﻿FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Chiang, TY
   Hsu, HC
   Jane, SW
   Chen, SC
AF Chiang, Ting-Yu
   Hsu, Hung-Chih
   Jane, Sui-Whi
   Chen, Shu-Ching
TI EGFRI-associated health-related quality of life by severity of skin
   toxicity in metastatic colorectal cancer patients receiving epidermal
   growth factor receptor inhibitor target therapy
SO SUPPORTIVE CARE IN CANCER
LA English
DT Article
DE Colorectal cancer; Molecular targeted therapy; Cetuximab; Body image;
   Skin toxic; Health-related quality of life
ID BODY-IMAGE; IMPACT; CETUXIMAB; QUESTIONNAIRE; MANAGEMENT; SYMPTOMS
AB Purpose The purposes of this study were to assess the levels of symptom distress, body image, and epidermal growth factor receptor inhibitors (EGFRI)-associated health-related quality of life (QoL); identify the factors related to EGFRI-associated health-related QoL; and examine the differences in EGFRI-associated health-related QoL by grade of skin toxicity in mCRC patients receiving target therapy. Methods This cross-sectional study examined mCRC patients who received cetuximab-based target therapy from the oncology and CRC inpatient and outpatient departments of a medical center in northern Taiwan. Structured questionnaires were used to measure patients' symptom distress, body image, and EGFRI-associated health-related QoL. Results Of the 111 mCRC patients studied, 79.2% reported acneiform eruption and 52.2% reported paronychia. The most common symptoms were dry skin and itching. Poor EGFRI-associated health-related QoL was associated with more symptom distress, more negative body image, a higher cumulative dose of target therapy, and being married; these factors explained 66.6% of the variance in EGFRI-associated health-related QoL. Conclusion Patient-specific skin care and emotional support are needed to relieve distressful dermatological symptoms and emotional distress during and post-treatment for mCRC.
C1 [Chiang, Ting-Yu] Chang Gung Mem Hosp Linkou, Dept Nursing, Taoyuan, Taiwan.
   [Hsu, Hung-Chih] Chang Gung Mem Hosp Linkou, Div Hematol Oncol, Taoyuan, Taiwan.
   [Hsu, Hung-Chih] Chang Gung Univ, Coll Med, Taoyuan, Taiwan.
   [Jane, Sui-Whi; Chen, Shu-Ching] Chang Gung Univ Sci & Technol, Coll Nursing, Sch Nursing, Taoyuan, Taiwan.
   [Jane, Sui-Whi] Linkou Chang Gung Mem Hosp, Dept Internal Med, Div Hematol Oncol, Taoyuan, Taiwan.
   [Jane, Sui-Whi; Chen, Shu-Ching] Chang Gung Univ, Coll Med, Sch Nursing, Taoyuan, Taiwan.
   [Jane, Sui-Whi; Chen, Shu-Ching] Chang Gung Univ Sci & Technol, Coll Nursing, Geriatr & Long Term Care Res Ctr, Taoyuan, Taiwan.
   [Chen, Shu-Ching] Chang Gung Mem Hosp Linkou, Dept Radiat Oncol, Taoyuan, Taiwan.
   [Chen, Shu-Ching] Chang Gung Mem Hosp Linkou, Proton & Radiat Therapy Ctr, Taoyuan, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung Memorial Hospital; Chang Gung
   University; Chang Gung University of Science & Technology; Chang Gung
   Memorial Hospital; Chang Gung University; Chang Gung University of
   Science & Technology; Chang Gung Memorial Hospital; Chang Gung Memorial
   Hospital
RP Chen, SC (corresponding author), Chang Gung Univ Sci & Technol, Coll Nursing, Sch Nursing, Taoyuan, Taiwan.; Chen, SC (corresponding author), Chang Gung Univ, Coll Med, Sch Nursing, Taoyuan, Taiwan.; Chen, SC (corresponding author), Chang Gung Univ Sci & Technol, Coll Nursing, Geriatr & Long Term Care Res Ctr, Taoyuan, Taiwan.; Chen, SC (corresponding author), Chang Gung Mem Hosp Linkou, Dept Radiat Oncol, Taoyuan, Taiwan.; Chen, SC (corresponding author), Chang Gung Mem Hosp Linkou, Proton & Radiat Therapy Ctr, Taoyuan, Taiwan.
EM shuching@gw.cgust.edu.tw
FU Chang Gung Memorial Hospital (CMRPG3G1591) Research Program in Taiwan
   [CMRPG3G1591] Funding Source: Medline
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NR 43
TC 7
Z9 7
U1 0
U2 5
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 OCT
PY 2020
VL 28
IS 10
BP 4771
EP 4779
DI 10.1007/s00520-020-05321-3
PG 9
WC Oncology; Health Care Sciences & Services; Rehabilitation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Health Care Sciences & Services; Rehabilitation
GA NL2KY
UT WOS:000567252100023
PM 31974771
DA 2025-01-04
ER

PT J
AU Alessandrini, L
   Perin, T
   Kadarè, S
   del Pup, L
   Memeo, L
   Steffan, A
   Colarossi, L
   Berretta, M
   De Paoli, P
   Canzonieri, V
AF Alessandrini, Lara
   Perin, Tiziana
   Kadare, Shahin
   del Pup, Lino
   Memeo, Lorenzo
   Steffan, Agostino
   Colarossi, Lorenzo
   Berretta, Massimiliano
   De Paoli, Paolo
   Canzonieri, Vincenzo
TI Cancer Targeted Therapy Strategy: The Pathologist's Perspectives
SO CURRENT CANCER DRUG TARGETS
LA English
DT Review
DE Target therapy; biomarker; pathologist's perspective;
   Immunohistochemistry; FFPE tissue; molecular analyses; traditional
   sequencing; next-generation sequencing
ID MALIGNANT PLEURAL MESOTHELIOMA; PARAFFIN-EMBEDDED TISSUE;
   QUALITY-ASSURANCE; GASTRIC-CANCER; NUCLEIC-ACIDS; BREAST-CANCER;
   COLON-CANCER; CELL; HER2; IMMUNOHISTOCHEMISTRY
AB The effectiveness of new personalized treatment procedures in oncology is based on the fact that certain tumors exhibit specific molecular features.
   More in detail, neoplastic tissues of patients should display a specific biomarker, most often a specific genetic alteration and/or under/overexpression of a definite protein, that could be the target of its respective drug Immunohistochemical and molecular analyses, which usually include examination of nucleic acids from either tissues or fluids, are common tests to define the status of a tumor.
   This review focuses on the pathologist's role in carefully controlling pre-analytic procedures and standard operating procedures that are a crucial prerequisite to reach reliable and reproducible results. Six paradigmatic applications of targeted therapy, for which pathological diagnosis plays a fundamental role, are summarized. Traditional and next-generation sequencing are also addressed from the pathologist's perspective as well as the importance pathologists have in this shift to more accurate definition of disease risk and prognostication of therapy response in the personalized medicine era.
C1 [Alessandrini, Lara; Perin, Tiziana; Canzonieri, Vincenzo] CRO IRCCS Natl Canc Inst, Div Pathol, Via Franco Gallini 2, I-33081 Aviano, PN, Italy.
   [Berretta, Massimiliano] CRO IRCCS Natl Canc Inst, Div Med Oncol A, Aviano, PN, Italy.
   [del Pup, Lino] CRO IRCCS Natl Canc Inst, Div Gynecol Oncol, Aviano, PN, Italy.
   [Perin, Tiziana; Steffan, Agostino; De Paoli, Paolo; Canzonieri, Vincenzo] CRO IRCCS Natl Canc Inst, Biobank, Aviano, PN, Italy.
   [De Paoli, Paolo] CRO IRCCS Natl Canc Inst, Sci Directorate, Aviano, PN, Italy.
   [Steffan, Agostino] CRO IRCCS Natl Canc Inst, Oncol Pathol Unit, Aviano, PN, Italy.
   [Kadare, Shahin] Univ Tirana, Pathol Dept, Tirana, Albania.
   [Kadare, Shahin] Diagnost Ctr Pathol Morphol, Tirana, Albania.
   [Memeo, Lorenzo; Colarossi, Lorenzo] Mediterranean Inst Oncol, Dept Expt Oncol, Catania, Italy.
C3 IRCCS Aviano (CRO); IRCCS Aviano (CRO); IRCCS Aviano (CRO); IRCCS Aviano
   (CRO); IRCCS Aviano (CRO); IRCCS Aviano (CRO); University of Tirana
   (UT); Mediterranean Institute of Oncology
RP Canzonieri, V (corresponding author), CRO IRCCS Natl Canc Inst, Div Pathol, Via Franco Gallini 2, I-33081 Aviano, PN, Italy.
EM vcanzonieri@cro.it
RI Canzonieri, Vincenzo/AAA-7951-2019; De Paoli, Paolo/AAG-2586-2021;
   Canzonieri, Vincenzo/K-3141-2018; Del Pup, Lino/AAC-3277-2020; Perin,
   Tiziana/AAC-2403-2020; Steffan, Agostino/ABE-5972-2020; Berretta,
   Massimiliano/S-5853-2019
OI Canzonieri, Vincenzo/0000-0001-6010-0976; Del Pup,
   Lino/0000-0003-2979-3844; Perin, Tiziana/0000-0002-9823-0167; De Paoli,
   Paolo/0000-0002-9502-1781; Memeo, Lorenzo/0000-0003-4251-7203; Steffan,
   Agostino/0000-0002-6320-3054; Berretta, Massimiliano/0000-0002-9837-9148
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NR 76
TC 3
Z9 3
U1 0
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 1568-0096
EI 1873-5576
J9 CURR CANCER DRUG TAR
JI Curr. Cancer Drug Targets
PY 2018
VL 18
IS 5
BP 410
EP 420
DI 10.2174/1568009618666171129145703
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GH0KY
UT WOS:000433092100003
PM 29189158
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Zhou, MY
   Yu, P
   Davin, DBH
   Li, YR
   Wang, YH
   Fu, LY
   Zhang, JD
AF Zhou, Mingyi
   Yu, Ping
   Davin, Dengue Bilibili Hernick
   Li, Yanrong
   Wang, Yuanhe
   Fu, Lingyu
   Zhang, Jingdong
TI Is FOLFOXIRI alone or combined with targeted therapy administered as
   first-line treatment a reasonable choice for most patients with mCRC?
   Systematic review and network meta-analysis
SO ONCOTARGET
LA English
DT Review
DE dose intensity; mCRC; prognosis; toxicities; network meta-anaylsis
ID METASTATIC COLORECTAL-CANCER; FOLFIRI PLUS BEVACIZUMAB; PHASE-III TRIAL;
   RAS MUTATIONS; INFUSIONAL FLUOROURACIL; CETUXIMAB TREATMENT; OPEN-LABEL;
   LEUCOVORIN; IRINOTECAN; OXALIPLATIN
AB Whether the intensive administration of folinic acid, 5-fluorouracil, oxaliplatin and irinotecan (FOLFOXIRI) alone or combined with target therapy as first-line treatment could improve the prognosis of metastatic colorectal cancer (mCRC) patients is controversial. PubMed, the Cochrane Collaboration Central Register of Controlled Clinical Trials, Cochrane Systematic Reviews, ClinicalTrials.gov, the databases of conferences were queried to identify RCTs evaluating the efficacies and toxicities of intensive therapies used for first-line treatment of mCRC patients. The search included articles dated from the inception of these resources until March 31, 2017. We estimated HRs for OS and PFS and RRs for ORR, the R0 resection rate, and toxicities. Ten RCTs comprising 2,506 patients were included in this network meta-analysis. The PFS of patients administered FOLFOXIRI plus target therapy experienced prolonged PFS and OS and improved ORRs compared with FOLFOX/FOLFIRI plus target therapy (PFS: HR 0.71, 95% CI 0.59-0.86; OS: HR 0.81, 95% CI 0.69-0.94; ORR: RR 1.66, 95% CI 0.96-2.88; R0 resection rate: RR 2.66, 95% CI 1.86-3.82). There were no significant differences between PFS, OS, ORRs, or R0 resection rates and toxicities of patients administered FOLFOXIRI and FOLFOX/FOLFIRI plus target therapy. Further, FOLFOXIRI plus target therapy did not increase toxicities compared with FOLFOX/ FOLFIRI plus target therapy. FOLFOXIRI plus target therapy when administered as first-line treatment of patients with mCRC is the best choice and did not increase toxicities. The patients with RAS/BRAF mutations could benefit from FOLFOXIRI plus Bev. FOLFOXIRI is as effective as FOLFOX/FOLFIRI plus target therapy.
C1 [Zhou, Mingyi] China Med Univ, Liaoning Canc Hosp & Inst, Canc Hosp, Dept Gynecol, Shenyang 110042, Liaoning, Peoples R China.
   [Yu, Ping] China Med Univ, Dept Med Oncol, Hosp 1, Shenyang 110001, Liaoning, Peoples R China.
   [Davin, Dengue Bilibili Hernick; Li, Yanrong; Wang, Yuanhe; Zhang, Jingdong] China Med Univ, Dept Med Oncol, Liaoning Canc Hosp & Inst, Canc Hosp, Shenyang 110042, Liaoning, Peoples R China.
   [Fu, Lingyu] China Med Univ, Dept Clin Epidemiol & Evidence Based Med, Hosp 1, Shenyang 110001, Liaoning, Peoples R China.
C3 China Medical University; China Medical University; China Medical
   University; China Medical University
RP Zhang, JD (corresponding author), China Med Univ, Dept Med Oncol, Liaoning Canc Hosp & Inst, Canc Hosp, Shenyang 110042, Liaoning, Peoples R China.
EM zhangjd0228@hotmail.com
FU Educational Commission of Liaoning Province of China [20060973]; Science
   and Technology Planning Project of Liaoning Province of China
   [2007225009-1, 2011404013-9, 2011225019, 2013225079]; National Natural
   Science Foundation of China [81372532]; Science and Technology Planning
   Project of Shenyang [F15-139-9-27]
FX This work was supported by the Educational Commission of Liaoning
   Province of China (No. 20060973), and the Science and Technology
   Planning Project of Liaoning Province of China (No. 2007225009-1,
   2011404013-9, 2011225019, 2013225079), and the National Natural Science
   Foundation of China (No. 81372532), and the Science and Technology
   Planning Project of Shenyang (No. F15-139-9-27).
CR [Anonymous], J CLIN ONCOL S
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NR 19
TC 8
Z9 8
U1 0
U2 4
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 5
PY 2017
VL 8
IS 37
BP 62339
EP 62348
DI 10.18632/oncotarget.17725
PG 10
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FF8GI
UT WOS:000409254200129
PM 28977949
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Coppola, R
   Santo, B
   Silipigni, S
   Panasiti, V
AF Coppola, Rosa
   Santo, Bianca
   Silipigni, Sonia
   Panasiti, Vincenzo
TI Symmetrical drug-related intertriginous and flexural exanthema and
   acneiform eruption in a patient with metastatic colorectal cancer
   treated with cetuximab
SO CLINICAL CANCER INVESTIGATION JOURNAL
LA English
DT Article
DE Acneiform eruption; cetuximab; skin toxicity; symmetrical drug-related
   intertriginous and flexural exanthema
AB Over recent years, targeted therapy has become one of the most important innovations in cancer treatment. Agents targeting the epidermal growth factor receptor (EGFR) are administered in patients with advanced, recurrent or metastatic malignancy. We reported the case of a 74 year-old male patient with metastatic colorectal cancer who developed an SDRIFE and acneiform eruption during molecular target therapy with cetuximab and FOLFOX.
C1 [Coppola, Rosa; Panasiti, Vincenzo] Campus Biomed Univ Rome, Dept Plast Reconstruct & Aesthet Surg, Rome, Italy.
   [Santo, Bianca; Silipigni, Sonia] Campus Biomed Univ Rome, Dept Radiat Oncol, Rome, Italy.
C3 University Campus Bio-Medico - Rome Italy; University Campus Bio-Medico
   - Rome Italy
RP Santo, B (corresponding author), Campus Biomed Univ Rome, Dept Radiat Oncol, Rome, Italy.
EM bianchia@hotmail.it
RI Santo, Bianca/HKW-0913-2023; Panasiti, Vincenzo/GPF-5731-2022
CR Allegra CJ, 2016, J CLIN ONCOL, V34, P179, DOI 10.1200/JCO.2015.63.9674
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NR 12
TC 3
Z9 3
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 2278-0513
J9 CLIN CANCER INVESTIG
JI Clin. Cancer Investig. J.
PD NOV-DEC
PY 2021
VL 10
IS 6
BP 331
EP 332
DI 10.4103/ccij.ccij_11_21
PG 2
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA XS2OW
UT WOS:000732755600010
DA 2025-01-04
ER

PT J
AU Berretta, M
   Romano, C
   Di Francia, R
   De Diviitis, C
   Canzonieri, V
   Caraglia, M
   Facchini, G
   Nasti, G
AF Berretta, Massimiliano
   Romano, Carmela
   Di Francia, Raffaele
   De Diviitis, Chiara
   Canzonieri, Vincenzo
   Caraglia, Michele
   Facchini, Gaetano
   Nasti, Guglielmo
TI The Role of Target Therapy in the Treatment of Gastrointestinal
   Noncolorectal Cancers: Clinical Impact and Cost Consideration
SO CURRENT CANCER DRUG TARGETS
LA English
DT Review
DE Gastrointestinal cancers; target therapy; clinical aspects; treatment;
   prognostic factors; metastases; costs
ID ADVANCED HEPATOCELLULAR-CARCINOMA; ENDOTHELIAL GROWTH-FACTOR;
   MULTICENTER PHASE-II; ADVANCED GASTRIC-CANCER; ERLOTINIB PLUS
   GEMCITABINE; ADVANCED PANCREATIC-CANCER; BILIARY-TRACT CANCER; 1ST-LINE
   THERAPY; FACTOR RECEPTOR; DOUBLE-BLIND
AB Gastrointestinal (GI) tumors are among the leading cause of death in cancer patients worldwide. Particularly, gastric cancer (GC) is the third cause of cancer deaths, whereas esophageal neoplasm is the eighth leading most common cancer worldwide and its incidence, especially adenocarcinoma type, is continuously increasing. Also, Hepatocellular carcinoma, Cholangiocarcinoma and pancreatic cancer represent a very interesting model to multidisciplinary approach and recently new drugs are used in their treatment. Currently, new clinical trials are designed including classic chemotherapy in association with either small molecule inhibitors (i.e. Tyrosine Kinase inhibitors) and/or monoclonal antibody (i.e. anti-EGFR antibody). Moreover, a comprehensive list of new molecules for target therapy is included in this issue. The development of new treatment modalities (multidisciplinary approach) and targeted therapy approaches have contributed to improving the outcome in these cancer diseases. During the past few years, remarkable progress in molecular biology of malignancy, the discovery of specific targets, and the resulting development of systemic drugs that block critical kinases and several molecular pathways have all contributed to progress in cancer treatment, also in GI non-colorectal cancer treatment.
C1 [Berretta, Massimiliano] Natl Canc Inst CRO, Div Med Oncol A, Dept Med Oncol, Aviano, PN, Italy.
   [Romano, Carmela; De Diviitis, Chiara] Natl Canc Inst G Pascale Fdn, Abdominal Dept, Med Oncol, Naples, Italy.
   [Di Francia, Raffaele] Natl Canc Inst G Pascale Fdn, Div Oncohematol, Naples, Italy.
   [Canzonieri, Vincenzo] Natl Canc Inst CRO, Anatomopathol Unit, Aviano, PN, Italy.
   [Caraglia, Michele] Univ Naples 2, Dept Biochem Biophys & Gen Pathol, Naples, Italy.
   [Facchini, Gaetano] Natl Canc Inst, Gynecol Oncol, Fdn G Pascale IRCCS, Naples, Italy.
C3 IRCCS Aviano (CRO); IRCCS Fondazione Pascale; IRCCS Fondazione Pascale;
   IRCCS Aviano (CRO); Universita della Campania Vanvitelli; IRCCS
   Fondazione Pascale
RP Berretta, M (corresponding author), Natl Canc Inst, Dept Med Oncol, Aviano, PN, Italy.
EM mberretta@cro.it
RI Canzonieri, Vincenzo/AAA-7951-2019; Caraglia, Michele/AAK-4569-2020;
   Berretta, Massimiliano/S-5853-2019; Canzonieri, Vincenzo/K-3141-2018;
   Caraglia, Michele/N-5670-2015; FACCHINI, GAETANO/P-4491-2015
OI Berretta, Massimiliano/0000-0002-9837-9148; Canzonieri,
   Vincenzo/0000-0001-6010-0976; Caraglia, Michele/0000-0003-2408-6091;
   FACCHINI, GAETANO/0000-0002-7430-001X
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NR 124
TC 1
Z9 1
U1 0
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 1568-0096
EI 1873-5576
J9 CURR CANCER DRUG TAR
JI Curr. Cancer Drug Targets
PY 2018
VL 18
IS 5
BP 430
EP 441
DI 10.2174/1568009617666170208162058
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GH0KY
UT WOS:000433092100005
PM 28183250
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Li, HX
   Zhang, XL
   Zhang, JQ
   Cai, M
   Li, SW
AF Li, Hong-Xia
   Zhang, Xiao-Lan
   Zhang, Jun-Qing
   Cai, Min
   Li, Sheng-Wen
TI Three-target treatment combined with surgery for BRAF V600E-mutant colon
   cancer with peritoneal metastasis: a case report
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE BRAF V600E mutation; colon cancer; peritoneal metastasis; targeted
   therapy; case report
ID PLUS CETUXIMAB; ENCORAFENIB
AB Background: BRAF V600E-mutant advanced colon cancer with peritoneal metastasis is associated with a poor prognosis. Surgery is not recommended by current guidelines, and there are few cases demonstrating the efficacy of targeted therapy combined with surgery in such patients. In the era of precision medicine, we apply aggressive surgery after successful conversion of triple-targeted drugs to prolong survival and provide a clinical basis for the treatment of such patients. Case Description: A 72-year-old male patient presented with abdominal distension and changes in bowel habits was admitted to the Department of Oncology, Shanxi Provincial People's Hospital. The patient was diagnosed with advanced ascending colon adenocarcinoma with peritoneal metastasis after relevant examinations such as abdominal enhanced computed tomography and tests of tumor markers. Later, further genetic testing was performed suggesting BRAF V600E mutation. We treated the patient with firstline three-target therapy (dabrafenib + trametinib + cetuximab). Repeat abdominal enhanced computed tomography after 6 weeks of three-target therapy revealed the disappearance of peritoneal metastases. Subsequently, after 3 months, the patient underwent resection of the primary lesion and removal of greater omental metastases. Three-target therapy continued after surgery until 4 months post-operation. However, carbohydrate antigen 199 was significantly increased at 9 months after medication discontinuation, and returned to normal after 4 months of re-initiation of three-target therapy. The three-target therapy was further adjusted to two-target therapy (dabrafenib + cetuximab) based on the results of circulating tumor cells, and the tumor markers are now normal. Conclusions: Patients with BRAF V600E colon cancer combined with peritoneal metastases are treated with targeted drug conversion therapy, and aggressive surgery may prolong survival depending on the conversion effect. Continued maintenance therapy after surgery may play a role in preventing recurrence.
C1 [Li, Hong-Xia; Zhang, Xiao-Lan; Zhang, Jun-Qing; Li, Sheng-Wen] Shanxi Prov Peoples Hosp, Dept Oncol, Taiyuan, Peoples R China.
   [Cai, Min] Shanxi Prov Peoples Hosp, Dept Nucl Med, Taiyuan, Peoples R China.
   [Li, Sheng-Wen] Shanxi Prov Peoples Hosp, Dept Oncol, Taiyuan 030012, Peoples R China.
C3 Shanxi People's Hospital; Shanxi People's Hospital; Shanxi People's
   Hospital
RP Li, SW (corresponding author), Shanxi Prov Peoples Hosp, Dept Oncol, Taiyuan 030012, Peoples R China.
EM liswww169@163.com
FU Shanxi Provincial Health Commission;  [2019022]
FX Funding: The study was supported by Shanxi Provincial Health Commission
   (No. 2019022) .
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NR 20
TC 0
Z9 0
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 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD OCT
PY 2022
VL 13
IS 5
BP 2647
EP 2653
DI 10.21037/jgo-22-748
EA SEP 2022
PG 7
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA 6M4BF
UT WOS:000873790100001
PM 36388686
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zheng, Y
   Peng, HL
   Hu, X
   Ou, Y
   Wang, D
   Wang, H
   Ren, SQ
AF Zheng, Yang
   Peng, Heling
   Hu, Xu
   Ou, Yong
   Wang, Dong
   Wang, Han
   Ren, Shangqing
TI Progress and prospects of targeted therapy and immunotherapy for urachal
   carcinoma
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE urachal carcinoma; immunotherapy; targeted therapy; EGFR; biomarker
ID GENERATION SEQUENCING NGS; MICROSATELLITE INSTABILITY; GENOMIC
   ALTERATIONS; CANCER-THERAPY; KRAS MUTATION; ADENOCARCINOMA; BLADDER;
   TUMORS; COLON; GENE
AB Introduction: Urachal carcinoma (UrC) is a rare and aggressive disease. Systematic chemotherapy shows limited efficacy in patients with advanced disease, while targeted therapy and immunotherapy may provide a reasonable alternative for specific populations. The molecular pattern of colorectal cancer (CRC) have recently been identified; this understanding has significantly influenced the clinical management of CRC in terms of molecular-targeted therapy. Although some genetic alterations have been associated with UrC, there is still no systematic overview of the molecular profile of this rare malignancy.Methods: In this review, we comprehensively discuss the molecular profile of UrC and further identify potential targets for the personalized treatment of UrC as well as immune checkpoint inhibitors that represent underlying biomarkers. A systematic literature search was carried out by searching the PubMed, EMBASE, and Web of Science databases to identify all literature related to targeted therapy and immunotherapy in urachal carcinoma from inception to February 2023.Results: A total of 28 articles were eligible, and most studies included were case report sand retrospective case series. Furthermore, 420 cases of UrC were identified to analyze the association between mutations and UrC. The most commonly mutated gene in UrC was TP53 with the prevalence of 70%, followed by KRAS mutations in 28.3%, MYC mutations in 20.3%, SMAD4 mutations in 18.2% and GNAS mutations in 18%, amongst other genes.Discussion: The molecular patterns of UrC and CRC are similar yet distinct. Notably, targeted therapy, especially EGFR-targeting therapy, might provide curative efficacy for patients with UrC by applying specific molecular markers. Additional potential biomarkers for the immunotherapy of UrC are mismatch repair (MMR) status and PD-L1 expression profile. In addition, combined regimens featuring targeted agents and immune checkpoint blockers might increase antitumor activity and exert better efficacy in UrC patients with specific mutational burden.
C1 [Zheng, Yang] Univ Elect Sci & Technol China, Sch Med, Chengdu, Peoples R China.
   [Zheng, Yang; Ou, Yong; Wang, Dong; Ren, Shangqing] Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Robot Minimally Invas Surg, Chengdu, Peoples R China.
   [Peng, Heling] Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Med Adm Dept, Chengdu, Peoples R China.
   [Hu, Xu] Sichuan Univ, West China Hosp, Inst Urol, Dept Urol, Chengdu, Peoples R China.
   [Wang, Han] Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Dept Gastroenterol, Chengdu, Peoples R China.
C3 University of Electronic Science & Technology of China; Sichuan
   Provincial People's Hospital; Sichuan Provincial People's Hospital;
   Sichuan University; Sichuan Provincial People's Hospital
RP Wang, D; Ren, SQ (corresponding author), Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Robot Minimally Invas Surg, Chengdu, Peoples R China.; Wang, H (corresponding author), Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Dept Gastroenterol, Chengdu, Peoples R China.
EM wangdong19690530@163.com; girlwh@163.com; rsq0516@163.com
RI Hu, Xu/JJD-9627-2023
FU Key Research and Development Projects of Sichuan Science and Technology
   Department [23ZDYF2070, 2022YFS0135]; Popular Application Project of
   Cadre Health Commission of Sichuan Province [SCR2023-210]
FX Funding This study was supported by the Key Research and Development
   Projects of Sichuan Science and Technology Department (23ZDYF2070 and
   2022YFS0135) and the Popular Application Project of Cadre Health
   Commission of Sichuan Province (SCR2023-210).
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NR 69
TC 2
Z9 2
U1 1
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD MAY 30
PY 2023
VL 14
AR 1199395
DI 10.3389/fphar.2023.1199395
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA J3FH7
UT WOS:001008496800001
PM 37324454
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Nishiyama, A
   Staub, Y
   Suga, Y
   Fujita, M
   Tanimoto, A
   Ohtsubo, K
   Yano, S
AF Nishiyama, Akihiro
   Staub, Yukiko
   Suga, Yukio
   Fujita, Mikiya
   Tanimoto, Azusa
   Ohtsubo, Koushiro
   Yano, Seui
TI Sarcopenia may Influence the Prognosis in Advanced Thyroid Cancer
   Patients Treated With Molecular Targeted Therapy
SO IN VIVO
LA English
DT Article
DE Sarcopenia; nutritional assessment; advanced thyroid cancer patient;
   molecular targeted therapy
ID NEUTROPHIL-TO-LYMPHOCYTE; COLORECTAL-CANCER; RATIO; IMPACT; LENVATINIB;
   INFECTION; RESECTION; SURVIVAL; OUTCOMES; SURGERY
AB Background/Aim: Reportedly, sarcopenia and nutritional status are associated with prognosis in cancer patients. However, data regarding the relationship of these factors with advanced thyroid cancer patients receiving molecular targeted therapy remains scarce. Therefore, we investigated the relationship between nutritional assessment, as well as sarcopenia, and prognosis in patients with advanced thyroid cancer undergoing molecular targeted therapy. Patients and Methods: In this retrospective study, sarcopenia and several markers of nutritional status were assessed in advanced thyroid cancer patients at the Kanazawa University Hospital, before the introduction of molecular targeted therapy. Results: Advanced thyroid cancer patients with sarcopenia presented a worse prognosis than those without sarcopenia. Additionally, sarcopenia strongly correlated with several markers of nutritional status, such as albumin, prognostic nutrition index, and Glasgow prognostic score. Conclusion: Sarcopenia could be a prognostic factor in patients with advanced thyroid cancer receiving molecular targeted therapy.
C1 [Nishiyama, Akihiro; Tanimoto, Azusa; Ohtsubo, Koushiro; Yano, Seui] Kanazawa Univ, Canc Res Inst, Div Med Oncol, 13-1 Takaramachi, Kanazawa, Ishikawa 9200934, Japan.
   [Staub, Yukiko; Suga, Yukio; Fujita, Mikiya] Kanazawa Univ, Fac Pharm, Inst Med Pharmaceut & Hlth Sci, Dept Clin Pharm & Healthcare Sci, Kanazawa, Ishikawa, Japan.
C3 Kanazawa University; Kanazawa University
RP Nishiyama, A (corresponding author), Kanazawa Univ, Canc Res Inst, Div Med Oncol, 13-1 Takaramachi, Kanazawa, Ishikawa 9200934, Japan.
EM an0510@staff.kanazawa-u.ac.jp
RI 谷本, 梓/JCF-0645-2023
OI Tanimoto, Azusa/0000-0002-6643-3867
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NR 28
TC 3
Z9 3
U1 0
U2 8
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0258-851X
EI 1791-7549
J9 IN VIVO
JI In Vivo
PD JAN-FEB
PY 2021
VL 35
IS 1
BP 401
EP 410
DI 10.21873/invivo.12271
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA PR5SY
UT WOS:000607297400003
PM 33402489
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, TL
   Sun, ZG
   Jiang, XM
   Guo, HF
AF Li, Tie-Ling
   Sun, Zhi-Guo
   Jiang, Xiaoming
   Guo, Hai-Feng
TI Clinical analysis of bevacizumab targeting therapy in treating early
   colorectal carcinoma after operation
SO ONCOLOGY LETTERS
LA English
DT Article
DE bevacizumab; early colorectal carcinoma; targeting therapy
ID CANCER; METAANALYSIS; SURVIVAL; EFFICACY
AB Clinical effects of bevacizumab target therapy in treating early colorectal carcinoma (CRC) after resection were analyzed. Ninety-two patients diagnosed with early CRC and treated with endoscopic mucosal resection for the first time were selected for the study. They were randomly divided into the control group and the observation group with 46 cases in each group. Control group was administered the chemotherapy regimen with oxaliplatin, calcium folinate and 5-fluorouracil, while bevacizumab targeting therapy was given to the observation group. The follow-up median time in these two groups was 30 months. In the observation group, objective response rate and disease control rate were higher than those in the control group, the adverse reaction rate was lower, and the differences were statistically significant (p< 0.05). In the observation group, disease-free survival was prolonged (38.6 vs. 30.5 months, p< 0.05); the recurrence rate was lower (13.0 vs. 30.4%, p< 0.05); the survival rate was improved (91.3 vs. 76.1%, p< 0.05). Vascular endothelial growth factor (VEGF) expressions of follow-up serum in these two groups were lower; VEGF expression in the observation group was lower than that in the control group, and the differences had statistical significance (p< 0.05). There was no statistical significance in comparison of positive expression in tissue VEGF (p> 0.05). In conclusion, after bevacizumab targeting therapy in treating early CRC, VEGF expression of serum was significantly lower; treatment effects improved; adverse drug reaction was reduced; survival time was prolonged; the recurrence rate was reduced; the survival rate improved. It has good application values.
C1 [Li, Tie-Ling] Mudanjiang Med Univ, Pathol Staff Room, Mudanjiang 157011, Heilongjiang, Peoples R China.
   [Sun, Zhi-Guo; Guo, Hai-Feng] Mudanjiang Med Univ, Hongqi Hosp, Normal Surg Dept, 1 Taiping Rd, Mudanjiang 157000, Heilongjiang, Peoples R China.
   [Jiang, Xiaoming] Mudanjiang Med Univ, Hongqi Hosp, Dept Intens Care Unit, Mudanjiang 157011, Heilongjiang, Peoples R China.
C3 Mudanjiang Medical University; Mudanjiang Medical University; Mudanjiang
   Medical University
RP Guo, HF (corresponding author), Mudanjiang Med Univ, Hongqi Hosp, Normal Surg Dept, 1 Taiping Rd, Mudanjiang 157000, Heilongjiang, Peoples R China.
EM haifengg6628@163.com
RI Li, xiaotong/GYV-4890-2022
CR [Anonymous], ASIAN PAC J SURG ONC
   [Anonymous], 2015, ASIAN PAC J SURG ONC
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NR 17
TC 2
Z9 2
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 JUN
PY 2017
VL 13
IS 6
BP 4675
EP 4678
DI 10.3892/ol.2017.6087
PG 4
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EY3XP
UT WOS:000403909200096
PM 28599469
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Coppola, R
   Santo, B
   Ramella, S
   Panasiti, V
AF Coppola, Rosa
   Santo, Bianca
   Ramella, Sara
   Panasiti, Vincenzo
TI Novel Skin Toxicity of Epidermal Growth Factor Receptor Inhibitors: A
   Case of Intertrigo-Like Eruption in a Patient with Metastatic Colorectal
   Cancer Treated with Cetuximab
SO CLINICAL CANCER INVESTIGATION JOURNAL
LA English
DT Article
DE Cetuximab; intertrigo-like eruption; skin toxicity
AB Over the recent years, targeted therapy has become one of the most important innovations in cancer treatment. Agents targeting the epidermal growth factor receptor (EGFR) are administered in patients with advanced, recurrent, and metastatic malignancy. Skin toxicity is one of the most common side effects of EGFR inhibitors. In this report, we present the case of a 70 year-old male patient with metastatic colorectal cancer who developed an intertrigo-like eruption during molecular target therapy with cetuximab treated with topical corticosteroid. A complete remission was obtained after 4 weeks.
C1 [Coppola, Rosa; Panasiti, Vincenzo] Campus Biomed Univ Rome, Dept Plast Reconstruct & Aesthet Surg, Rome, Italy.
   [Santo, Bianca; Ramella, Sara] Campus Biomed Univ Rome, Dept Radiat Oncol, Via Alvaro Portillo 200, I-00128 Rome, Italy.
C3 University Campus Bio-Medico - Rome Italy; University Campus Bio-Medico
   - Rome Italy
RP Santo, B (corresponding author), Campus Biomed Univ Rome, Dept Radiat Oncol, Via Alvaro Portillo 200, I-00128 Rome, Italy.
EM biancasanto.90@gmail.com
RI Santo, Bianca/HKW-0913-2023; Panasiti, Vincenzo/GPF-5731-2022; RAMELLA,
   SARA/AAC-6523-2022
CR Allegra CJ, 2016, J CLIN ONCOL, V34, P179, DOI 10.1200/JCO.2015.63.9674
   Balagula Y, 2011, INT J DERMATOL, V50, P129, DOI 10.1111/j.1365-4632.2010.04791.x
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NR 7
TC 5
Z9 5
U1 0
U2 4
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S  NO 1498A-2
   VILLAGE MAROL, ANDHERI EAST, MUMBAI, 400059, INDIA
SN 2278-0513
J9 CLIN CANCER INVESTIG
JI Clin. Cancer Investig. J.
PD MAR-APR
PY 2021
VL 10
IS 2
BP 91
EP 92
DI 10.4103/ccij.ccij_144_20
PG 2
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA RV6JG
UT WOS:000645936000007
DA 2025-01-04
ER

PT J
AU Ghani, S
   Bahrami, S
   Rafiee, B
   Eyvazi, S
   Yarian, F
   Ahangarzadeh, S
   Khalili, S
   Shahzamani, K
   Jafarisani, M
   Bandehpour, M
   Kazemi, B
AF Ghani, Sepideh
   Bahrami, Samira
   Rafiee, Behnam
   Eyvazi, Shirin
   Yarian, Fatemeh
   Ahangarzadeh, Shahrzad
   Khalili, Saeed
   Shahzamani, Kiana
   Jafarisani, Moslem
   Bandehpour, Mojgan
   Kazemi, Bahram
TI Recent developments in antibody derivatives against colorectal cancer; A
   review
SO LIFE SCIENCES
LA English
DT Review
DE Antibody derivatives; Colorectal cancer; Targeted therapy; Colorectal
   cancer markers
ID SINGLE-CHAIN ANTIBODY; CARCINOEMBRYONIC ANTIGEN; IN-VIVO;
   MONOCLONAL-ANTIBODIES; BISPECIFIC ANTIBODY; TARGETED THERAPY; GROWTH;
   FRAGMENT; IMMUNOTHERAPY; IDENTIFICATION
AB Colorectal cancer (CRC) is the fourth most common cause of cancer and mortality worldwide and is the third most common cancer in men and women. Surgery, radiotherapy, and chemotherapy are conventionally used for the treatment of colorectal cancer. However, these methods are associated with various side effects on normal cells. Thus, new studies are moving towards more effective and non-invasive methods for treatment of colorectal cancer. Targeted therapy of CRC is a promising new approach to enhance the efficiency and decrease the toxicity of the treatment. In targeted therapy of CRC, antibody fragments can directly inhibit tumor cell growth and proliferation. They also can act as an ideal carrier for targeted delivery of anticancer drugs. In the present study, the structure and function of different formats of antibody fragments, immune-targeted therapy of CRC using antibody fragments will be discussed.
C1 [Ghani, Sepideh] Shahid Beheshti Univ Med Sci, Sch Adv Technol Med, Dept Med Biotechnol, Student Res Comm, Tehran, Iran.
   [Ghani, Sepideh; Bahrami, Samira; Yarian, Fatemeh; Bandehpour, Mojgan; Kazemi, Bahram] Shahid Beheshti Univ Med Sci, Sch Adv Technol Med, Dept Med Biotechnol, Tehran, Iran.
   [Ghani, Sepideh; Yarian, Fatemeh; Bandehpour, Mojgan; Kazemi, Bahram] Shahid Beheshti Univ Med Sci, Cellular & Mol Biol Res Ctr, Tehran, Iran.
   [Rafiee, Behnam] Shahrekord Univ, Fac Vet Med, Dept Pathobiol, Shahrekord, Iran.
   [Eyvazi, Shirin] Tabriz Univ Med Sci, Biotechnol Res Ctr, Tabriz, Iran.
   [Ahangarzadeh, Shahrzad] Isfahan Univ Med Sci, Infect Dis & Trop Med Res Ctr, Esfahan, Iran.
   [Khalili, Saeed] Shahid Rajaee Teacher Training Univ, Dept Biol Sci, Tehran, Iran.
   [Shahzamani, Kiana] Isfahan Univ Med Sci, Isfahan Gastroenterol & Hepatol Res Ctr IGHRC, Esfahan, Iran.
   [Jafarisani, Moslem] Shahroud Univ Med Sci, Canc Prevent Res Ctr, Clin Biochem, Shahroud, Iran.
C3 Shahid Beheshti University Medical Sciences; Shahid Beheshti University
   Medical Sciences; Shahid Beheshti University Medical Sciences;
   Shahrekord University; Tabriz University of Medical Science; Isfahan
   University of Medical Sciences; Shahid Rajaee Teacher Training
   University (SRTTU); Isfahan University of Medical Sciences; Shahroud
   University Medical Sciences
RP Yarian, F (corresponding author), Shahid Beheshti Univ Med Sci, Sch Adv Technol Med, Dept Med Biotechnol, Tehran, Iran.
EM f.yarian@sbmu.ac.ir
RI yarian, fatemeh/P-2126-2019; Shahzamani, Kiana/R-9794-2017; Kazemi,
   Bahram/GRR-9838-2022; Eyvazi, Shirin/AAO-3828-2021; ghani,
   sepideh/ABC-3919-2021; Bahrami, Samira/AGV-2032-2022; bandehpour,
   mojgan/O-9744-2019; Ahangarzadeh, Shahrzad/AAD-3182-2020; Khalili,
   Saeed/IUN-4435-2023; Jafarisani, Moslem/AAZ-7290-2021
OI Khalili, Saeed/0000-0003-0493-9595; Jafarisani,
   Moslem/0000-0002-8341-6049; ghani, sepideh/0000-0003-2691-0523
FU Shahid Beheshti University of Medical Sciences [17047]
FX The project was financially supported by Shahid Beheshti University of
   Medical Sciences [grant number; 17047]. The authors would like to thank
   Cellular & Molecular Biology Research Center for kind supports.
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NR 98
TC 16
Z9 16
U1 0
U2 24
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 JAN 15
PY 2021
VL 265
AR 118791
DI 10.1016/j.lfs.2020.118791
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA PN4DK
UT WOS:000604430800047
PM 33220288
DA 2025-01-04
ER

PT J
AU Zhou, XY
   Zhao, Y
   Zhao, RC
   Shafi, S
   Yang, Y
   Liu, GX
   Liu, SB
AF Zhou, Xinying
   Zhao, Yu
   Zhao, Rongchuan
   Shafi, Shaheryar
   Yang, Yue
   Liu, Guangxing
   Liu, Song-Bai
TI Research progress of intestinal microbiota in targeted therapy and
   immunotherapy of colorectal cancer
SO JOURNAL OF CANCER METASTASIS AND TREATMENT
LA English
DT Review
DE CRC; gut microbiota; targeted therapy; immunotherapy
ID STREPTOCOCCUS-THERMOPHILUS; TUMOR-DEVELOPMENT; KAPPA-B; TUMORIGENESIS;
   CELLS; CARCINOGENESIS; PROLIFERATION; ANTIBACTERIAL; PROBIOTICS
AB Colorectal cancer (CRC) is one of the most common malignancies of the digestive tract, with increasing morbidity and mortality worldwide, and is the third most common malignancy in the world. At present, the main treatment methods for CRC include surgery, chemotherapy, targeted therapy, and immunotherapy. Regulation of the gut microbiota is one of the most promising new strategies for CRC treatment. Gut microbiota interacts with host cells to regulate many physiological processes, such as energy acquisition, metabolism, and immune responses. Recent studies have found that a combination of gut microbiota with targeted therapy and immunotherapy could improve the therapeutic effect of colon cancer compared with treatment alone. This article reviews the mechanism of microbiota regulation in CRC and the latest progress of intestinal microbiota in targeted therapy and immunotherapy of CRC, which is helpful in developing potential prevention or treatment strategies for colorectal cancer.
C1 [Zhou, Xinying; Zhao, Yu; Zhao, Rongchuan; Shafi, Shaheryar; Yang, Yue; Liu, Guangxing] Chinese Acad Sci, Suzhou Inst Biomed Engn & Technol, Suzhou 215163, Jiangsu, Peoples R China.
   [Liu, Song-Bai] Suzhou Vocat Hlth Coll, Jiangsu Prov Engn Res Ctr Mol Target Therapy & Com, Suzhou 215009, Jiangsu, Peoples R China.
   [Liu, Song-Bai] Suzhou Vocat Hlth Coll, Jiangsu Prov Engn Res Ctr Mol Target Therapy & Com, Kehua Rd 28, Suzhou 215009, Jiangsu, Peoples R China.
C3 Chinese Academy of Sciences; Suzhou Institute of Biomedical Engineering
   & Technology, CAS; Suzhou Vocational Health College; Suzhou Vocational
   Health College
RP Liu, GX (corresponding author), Chinese Acad Sci, Suzhou Inst Biomed Engn & Technol, Suzhou 215163, Jiangsu, Peoples R China.; Liu, SB (corresponding author), Suzhou Vocat Hlth Coll, Jiangsu Prov Engn Res Ctr Mol Target Therapy & Com, Kehua Rd 28, Suzhou 215009, Jiangsu, Peoples R China.
EM liugx@sibet.ac.cn; liusongbai@126.com
RI Zhang, Xueyang/HZI-0685-2023; Shafi, Shaheryar/GMW-4936-2022
OI Shafi, Shaheryar/0000-0002-1936-4838
FU Project of Jiangsu Province Engineering Research Center of Molecular
   Target Therapy and Companion Diagnostics in Oncology, Jiangsu higher
   education institution innovative research team for science and
   technology (2021); Program of Jiangsu vocational college engineering
   technology research center (2023); Key technology program of Suzhou
   people's livelihood technology projects [SZWZYTD202201]; Key Programs of
   the Suzhou Vocational Health College [SZWZYTD202201]; Qing-Lan Project
   of Jiangsu Province in China (2021, 2022)
FX This study was supported by the Project of Jiangsu Province Engineering
   Research Center of Molecular Target Therapy and Companion Diagnostics in
   Oncology, Jiangsu higher education institution innovative research team
   for science and technology (2021), Program of Jiangsu vocational college
   engineering technology research center ( 2023), Key technology program
   of Suzhou people's livelihood technology projects (Grant No.
   SKY2021029), Key Programs of the Suzhou Vocational Health College
   (SZWZYTD202201), Qing-Lan Project of Jiangsu Province in China (2021,
   2022).
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NR 74
TC 0
Z9 0
U1 5
U2 5
PU OAE PUBLISHING INC
PI ALHAMBRA
PA 245 E MAIN ST, ST122, ALHAMBRA, CA 91801 USA
SN 2394-4722
EI 2454-2857
J9 J CANCER METAS TREAT
JI J. Cancer Metastasis Treat.
PY 2024
VL 10
AR 12
DI 10.20517/2394-4722.2023.178
PG 12
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA LV9U8
UT WOS:001189702300001
OA gold
DA 2025-01-04
ER

PT J
AU Chang, JJ
   Xu, MD
   Wang, CC
   Huang, D
   Zhang, Z
   Chen, ZY
   Zhu, XD
   Li, WH
AF Chang, Jinjia
   Xu, Midie
   Wang, Chenchen
   Huang, Dan
   Zhang, Zhe
   Chen, Zhiyu
   Zhu, Xiaodong
   Li, Wenhua
TI Dual HER2 Targeted Therapy With Pyrotinib and Trastuzumab in Refractory
   HER2 Positive Metastatic Colorectal Cancer: A Result From HER2-FUSCC-G
   Study
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE mCRC; Trastuzumab; Pyrotinib; HER2; Target therapy
ID OPEN-LABEL; MULTICENTER
AB Background: Dual-HER2 targeted therapy has led to a promising antitumor effect in HER2 positive cancers including gastrointestinal cancer. The present data focus on patients with HER2 positive colorectal cancer who received pyrotinib and trastuzumab after failure to standard second-line treatment. Methods: Patients diagnosed of HER2 positive refractory or metastatic colorectal cancer were enrolled to receive trastuzumab in combination with pyrotinib as third-line and beyond therapy. Trastuzumab was given as a loading dose at 8 mg/kg followed by 6mg/kg once every 3 weeks, and oral pyrotinib as 400 mg per day until progression. ORR was set as the primary endpoint. PFS and OS were set as a secondary endpoints. This trial is registered with Clinical Trial.gov, NCT04960943, and is ongoing. Results: Between February 2020 to December 2021, 16 patients including 14 with RAS wild-type status were enrolled in this cohort. ORR was 50.0% in the overall population, and 57.1% in RAS wild-type patients. At a median follow-up of 11.2 months, median PFS and OS were 7.53 and 16.8 months, respectively. The RAS/BRAF wild-type patients had prolonged survival (PFS: 7.53 vs. 1.63 months, P = .02; OS: NR vs.4.13 months, P = .001) compared with RAS/BRAF mutant patients. The most common treatment-emergent adverse event (TEAE) reported is diarrhea. Five (31.3%) patients reported grade 3 TEAEs, and no death was reported. Conclusions: Trastuzumab in combination with pyrotinib demonstrated encouraging antitumor activity that translated to prolonged survival benefit in HER2 positive refractory or mCRC patients who are RAS wild-type with acceptable tolerance.
C1 [Chang, Jinjia; Wang, Chenchen; Chen, Zhiyu; Zhu, Xiaodong; Li, Wenhua] Fudan Univ Shanghai Ctr Shanghai, Dept Gastrointestinal Med Oncol, Shanghai 200032, Peoples R China.
   [Chang, Jinjia; Xu, Midie; Wang, Chenchen; Huang, Dan; Zhang, Zhe; Chen, Zhiyu; Zhu, Xiaodong; Li, Wenhua] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China.
   [Xu, Midie; Huang, Dan] Fudan Univ Shanghai Canc Ctr, Dept Pathol, Shanghai 200032, Peoples R China.
   [Zhu, Xiaodong; Li, Wenhua] Fudan Univ Shanghai Canc Ctr, Dept Med Oncol, 270 DongAn Rd, Shanghai, Peoples R China.
C3 Fudan University; Fudan University; Fudan University
RP Zhu, XD; Li, WH (corresponding author), Fudan Univ Shanghai Ctr Shanghai, Dept Gastrointestinal Med Oncol, Shanghai 200032, Peoples R China.; Zhu, XD; Li, WH (corresponding author), Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China.; Zhu, XD; Li, WH (corresponding author), Fudan Univ Shanghai Canc Ctr, Dept Med Oncol, 270 DongAn Rd, Shanghai, Peoples R China.
EM xddr001@163.com; whliiris@hotmail.com
RI xu, midie/AFS-3427-2022; Zhu, Xiao-Dong/A-8197-2010; Yang,
   Xueli/AAW-4792-2021
OI , Mi-die/0000-0003-1775-6608
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NR 25
TC 20
Z9 21
U1 0
U2 8
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 2022
VL 21
IS 4
BP 347
EP 353
DI 10.1016/j.clcc.2022.07.003
EA NOV 2022
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 7G0XK
UT WOS:000902258500008
PM 35941028
DA 2025-01-04
ER

PT J
AU Zarei, O
   Benvenuti, S
   Ustun-Alkan, F
   Hamzeh-Mivehroud, M
   Dastmalchi, S
AF Zarei, Omid
   Benvenuti, Silvia
   Ustun-Alkan, Fulya
   Hamzeh-Mivehroud, Maryam
   Dastmalchi, Siavoush
TI Strategies of targeting the extracellular domain of RON tyrosine kinase
   receptor for cancer therapy and drug delivery
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Review
DE Cancer; Drug conjugate; Monoclonal antibody; Peptide; Target therapy;
   Tumor; Tyrosine kinase receptor
ID MACROPHAGE-STIMULATING PROTEIN; HEPATOCYTE GROWTH-FACTOR; DORIGINE
   NANTAIS RON; HUMAN MONOCLONAL-ANTIBODIES; COLORECTAL-CARCINOMA CELLS;
   RESISTANT PROSTATE-CANCER; HUMAN-HUMAN HYBRIDOMAS; INHIBITS
   TUMOR-GROWTH; HUMAN GASTRIC-CANCER; BREAST-CANCER
AB Cancer is one of the most important life-threatening diseases in the world. The current efforts to combat cancer are being focused on molecular-targeted therapies. The main purpose of such approaches is based on targeting cancer cell-specific molecules to minimize toxicity for the normal cells. RON (Recepteur d'Origine Nantais) tyrosine kinase receptor is one of the promising targets in cancer-targeted therapy and drug delivery.
   In this review, we will summarize the available agents against extracellular domain of RON with potential antitumor activities.
   The presented antibodies and antibody drug conjugates against RON in this review showed wide spectrum of in vitro and in vivo antitumor activities promising the hope for them entering the clinical trials.
   Due to critical role of extracellular domain of RON in receptor activation, the development of therapeutic agents against this region could lead to fruitful outcome in cancer therapy.
C1 [Zarei, Omid] Tabriz Univ Med Sci, Fac Pharm, Dept Pharmaceut Biotechnol, Tabriz, Iran.
   [Zarei, Omid; Hamzeh-Mivehroud, Maryam; Dastmalchi, Siavoush] Tabriz Univ Med Sci, Biotechnol Res Ctr, Tabriz, Iran.
   [Zarei, Omid] Tabriz Univ Med Sci, Students Res Comm, Tabriz, Iran.
   [Benvenuti, Silvia] Candiolo Canc Inst FPO IRCCS, Mol Therapeut & Exploratory Res Lab, Turin, Italy.
   [Ustun-Alkan, Fulya] Istanbul Univ, Dept Pharmacol & Toxicol, Fac Vet Med, Istanbul, Turkey.
   [Hamzeh-Mivehroud, Maryam; Dastmalchi, Siavoush] Tabriz Univ Med Sci, Dept Med Chem, Fac Pharm, Tabriz, Iran.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science; Tabriz University of Medical Science; IRCCS Fondazione del
   Piemonte per l'Oncologia; Istanbul University; Tabriz University of
   Medical Science
RP Hamzeh-Mivehroud, M; Dastmalchi, S (corresponding author), Tabriz Univ Med Sci, Biotechnol Res Ctr, Tabriz, Iran.; Hamzeh-Mivehroud, M; Dastmalchi, S (corresponding author), Tabriz Univ Med Sci, Dept Med Chem, Fac Pharm, Tabriz, Iran.
EM hamzehm@tbzmed.ac.ir; dastmalchi.s@tbzmed.ac.ir
RI Zarei, Omid/C-2723-2018; USTUN ALKAN, Fulya/D-7406-2019
OI Benvenuti, Silvia/0000-0002-3041-4429; Zarei, Omid/0000-0002-9362-9240;
   USTUN ALKAN, Fulya/0000-0003-1782-9467
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NR 258
TC 16
Z9 17
U1 0
U2 31
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD DEC
PY 2016
VL 142
IS 12
BP 2429
EP 2446
DI 10.1007/s00432-016-2214-4
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EB6GJ
UT WOS:000387479400002
PM 27503093
DA 2025-01-04
ER

PT J
AU Ricco, G
   Seminerio, R
   Andrini, E
   Malvi, D
   Gruppioni, E
   Altimari, A
   Zagnoni, S
   Campana, D
   Lamberti, G
AF Ricco, Gianluca
   Seminerio, Renata
   Andrini, Elisa
   Malvi, Deborah
   Gruppioni, Elisa
   Altimari, Annalisa
   Zagnoni, Stefano
   Campana, Davide
   Lamberti, Giuseppe
TI BRAF V600E-mutated large cell neuroendocrine carcinoma responding to
   targeted therapy: a case report and review of the literature
SO ANTI-CANCER DRUGS
LA English
DT Review
DE BRAF V600E; carcinoma of unknown primary origin; circulating tumor DNA;
   immunotherapy; large cell neuroendocrine carcinoma; targeted therapy
ID DABRAFENIB PLUS TRAMETINIB; ALK-REARRANGEMENT; LUNG-CARCINOMA; EGFR
   MUTATION; NTRK FUSION; OPEN-LABEL; SURVIVAL; TUMORS; CANCER;
   CLASSIFICATION
AB Large cell neuroendocrine carcinoma (LCNEC) is a rare and aggressive high-grade neuroendocrine tumor, commonly arising in the lung or in the gastrointestinal tract, with a frequent proportion of unknown primary origin (20%). In the metastatic setting, platinum-based or fluoropyrimidine-based chemotherapeutic regimens are as considered the first-line treatment, despite the limited duration of response. To date, the prognosis of advanced high-grade neuroendocrine carcinoma remains poor, suggesting the need to explore new treatment strategies in this orphan tumor. The evolving molecular landscape of LCNEC, not yet been completely defined, could explain the heterogeneous response to different chemotherapeutic regimens and suggest that treatment strategy could be driven by molecular features. v-Raf murine sarcoma viral oncogene homolog B (BRAF) mutations, well described in melanoma, thyroid cancer, colon cancer and lung adenocarcinoma, account for approximately 2% of cases in lung LCNEC. Here, we describe the case of a patient with a BRAF V600E-mutated LCNEC of unknown primary origin who partially responded to BRAF/mitogen-activated protein kinase kinase inhibitors after standard treatment. Additionally, BRAF V600E circulating tumor DNA was used to monitor disease response. Thereafter, we reviewed the available literature about the role of targeted therapy in high-grade neuroendocrine neoplasms to provide insight for future research to identify patients with driver oncogenic mutations, who can potentially benefit from target therapy.
C1 [Ricco, Gianluca; Seminerio, Renata; Andrini, Elisa; Campana, Davide; Lamberti, Giuseppe] IRCCS Azienda Osped Univ Bologna, Div Med Oncol, Bologna, Italy.
   [Ricco, Gianluca; Seminerio, Renata; Andrini, Elisa; Campana, Davide; Lamberti, Giuseppe] SantOrsola Malpighi Univ Hosp, ENETS Ctr Excellence, Dept Expt Diagnost & Specialty Med, Bologna, Italy.
   [Malvi, Deborah] Azienda Osped Univ Bologna, Div Pathol, Bologna, Italy.
   [Gruppioni, Elisa; Altimari, Annalisa; Zagnoni, Stefano] IRCCS Azienda Osped Univ Bologna, Solid Tumor Mol Pathol Lab, Bologna, Italy.
   [Andrini, Elisa] IRCCS Azienda Osped Univ Bologna, ENETS Ctr Excellence, Div Med Oncol, NET Team Bologna, Via P Albertoni 15, I-40138 Bologna, Italy.
C3 IRCCS Azienda Ospedaliero-Universitaria di Bologna; IRCCS Azienda
   Ospedaliero-Universitaria di Bologna; IRCCS Azienda
   Ospedaliero-Universitaria di Bologna; University of Bologna; IRCCS
   Azienda Ospedaliero-Universitaria di Bologna; IRCCS Azienda
   Ospedaliero-Universitaria di Bologna
RP Andrini, E (corresponding author), IRCCS Azienda Osped Univ Bologna, ENETS Ctr Excellence, Div Med Oncol, NET Team Bologna, Via P Albertoni 15, I-40138 Bologna, Italy.
EM elisa.andrini3@unibo.it
RI Lamberti, Giuseppe/S-7497-2019; Malvi, Deborah/K-5424-2016; Campana,
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NR 72
TC 6
Z9 7
U1 1
U2 3
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 1076
EP 1084
DI 10.1097/CAD.0000000000001508
PG 9
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA U1PA5
UT WOS:001082579800003
PM 36847048
DA 2025-01-04
ER

PT J
AU Rong, BX
   Cai, XG
   Liu, H
   Yang, SY
AF Rong Biaoxue
   Cai Xiguang
   Liu Hua
   Yang Shuanying
TI Stathmin-dependent molecular targeting therapy for malignant tumor: the
   latest 5 years' discoveries and developments
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE Cancer; Stathmin; Drug target; Anticancer therapy; Molecular targeted
   therapy
ID COLORECTAL-CANCER METASTASIS; POOR-PROGNOSIS; GASTRIC-CANCER;
   MICROTUBULE DESTABILIZATION; CHEMOTHERAPY SENSITIVITY;
   CELL-PROLIFERATION; INDUCED APOPTOSIS; HIGH-RISK; IN-VITRO; EXPRESSION
AB Knowledge of the molecular mechanisms on malignant tumors is very critical for the development of new treatment strategies like molecularly targeted therapies. In last 5 years, many investigations suggest that stathmin is over-expressed in a variety of human malignant tumors, and potentially promotes the occurrence and development of tumors. Rather, down-regulation of stathmin can reduce cell proliferation, motility and metastasis and induce apoptosis of malignant tumors. Thus, a stathmin antagonist, such as a specific inhibitor (antibody, small molecule compound, peptide, or siRNA), may be a novel strategy of molecular targeted therapy. This review summarizes the research progress of recent 5 years on the role of stathmin in tumorigenesis, the molecular mechanisms and development of anti-stathmin treatment, which suggest that continued investigations into the function of stathmin in the tumorigenesis could lead to more rationally designed therapeutics targeting stathmin for treating human malignant tumors.
C1 [Rong Biaoxue] Xian Med Univ, Dept Resp Med, Affiliated Hosp 1, Xian, Peoples R China.
   [Cai Xiguang; Liu Hua] Gansu Prov Hosp, Dept Resp Med, Lanzhou, Peoples R China.
   [Yang Shuanying] Xi An Jiao Tong Univ, Dept Resp Med, Affiliated Hosp 2, Xian, Peoples R China.
C3 Xi'an Medical University; Xi'an Jiaotong University
RP Rong, BX (corresponding author), Xian Med Univ, Dept Resp Med, Affiliated Hosp 1, Xian, Peoples R China.
EM research568rbx@yeah.net
FU Technology Research and Development Plan of Gansu Province [0912TCYA016]
FX This work was supported by Technology Research and Development Plan of
   Gansu Province (0912TCYA016). The authors wish to thank Drs. Gao Wenlong
   and Wu Dianlei for their critical comments provided during the
   preparation of this manuscript and also wish to thank all authors of
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NR 92
TC 15
Z9 16
U1 2
U2 16
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD SEP 27
PY 2016
VL 14
AR 279
DI 10.1186/s12967-016-1000-z
PG 18
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA DX7WL
UT WOS:000384600000001
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Nakagiri, T
   Tokunaga, T
   Kunoh, H
   Noura, S
   Ishida, H
   Miyoshi, N
   Ohue, M
   Okami, J
   Higashiyama, M
AF Nakagiri, Tomoyuki
   Tokunaga, Toshiteru
   Kunoh, Hidenori
   Noura, Shingo
   Ishida, Hiroto
   Miyoshi, Norikatsu
   Ohue, Masayuki
   Okami, Jiro
   Higashiyama, Masahiko
TI Surgical Treatment following Chemo-Targeted Therapy with Bevacizumab for
   Lung Metastasis from Colorectal Carcinoma: Analysis of Safety and
   Histological Therapeutic Effects in Patients Treated at a Single
   Institution
SO CASE REPORTS IN ONCOLOGY
LA English
DT Article
DE Lung metastasis; Colorectal carcinoma; Surgical treatment; Safety;
   Chemo-targeted therapy; Histological result
ID CANCER; CHEMOTHERAPY; RECIST
AB Background: Recently, therapeutic strategies for a metastasectomy from colorectal carcinoma after chemo-targeted therapy with bevacizumab have been presented, with which some uncommon but serious adverse events have been reported. However, only few reports have investigated the safety of lung resection after such therapy or the histological effects. We retrospectively analyzed the both of them at our institute. Methods: Of 69 colorectal carcinoma patients who underwent pulmonary metastasectomy procedures from 2009 to 2014, we investigated 11 who also received chemo-targeted therapy prior to surgery. Results: In addition to bevacizumab, 5 fluorouracil (FU)/leucovorin + oxaliplatin or capecitabine was given in 6 cases and 5 FU/leucovorin + irinotecan in 5 cases. The mean period from the end of chemo-targeted therapy to surgery was 2.7 +/- 0.9 months. The response to therapy shown in imaging findings was progressive disease in 6, stable disease in 3, and partial response in 2 (response rate, 18.2%). The operation modes were wedge resection (n = 8, 72.3%), segmentectomy (n = 2, 1 in bilateral lobes, 1 in the right lobe, 18.2%), and lobectomy (n = 1, left lower lobectomy, 9.1%). All patients safely underwent a complete resection. As for postsurgical complications, chylothorax occurred in 1 case and prolonged pulmonary air leakage in 1 case. The histological effects of chemo-targeted therapy were slight. There was no relationship between histological findings with imaging findings obtained prior to the operation (p = 0.63). The 5-year disease-free survival rate after metastasectomy was 10.9%. Conclusions: Pulmonary metastasectomy after chemo-targeted therapy for colorectal carcinoma patients obtained acceptable results. In addition, there was no correlation between imaging and histopathologic results following chemo-targeted therapy. (C) 2018 The Author(s) Published by S. Karger AG, Basel
C1 [Nakagiri, Tomoyuki; Tokunaga, Toshiteru; Kunoh, Hidenori; Ishida, Hiroto; Okami, Jiro; Higashiyama, Masahiko] Osaka Int Canc Inst, Dept Thorac Surg, Osaka, Japan.
   [Noura, Shingo; Miyoshi, Norikatsu; Ohue, Masayuki] Osaka Int Canc Inst, Dept Surg, Osaka, Japan.
RP Nakagiri, T (corresponding author), Osaka Int Canc Inst, Dept Thorac Surg, Chuo Ku, 3-1-69 Otemae, Osaka 5418567, Japan.
EM gilly64@thoracic.med.osaka-u.ac.jp
RI Okami, Jiro/AAE-3837-2021
OI Nakagiri, Tomoyuki/0000-0001-9303-3773
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NR 14
TC 3
Z9 3
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1662-6575
J9 CASE REP ONCOL
JI Case Rep. Oncol.
PY 2018
VL 11
IS 1
BP 98
EP 108
DI 10.1159/000486825
PG 11
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA GG2SI
UT WOS:000432542500017
PM 29515416
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Inci, K
   Nilsson, B
   Ny, L
   Strömberg, U
   Wilking, N
   Lindskog, S
   Giglio, D
AF Inci, Kamuran
   Nilsson, Bengt
   Ny, Lars
   Stromberg, Ulf
   Wilking, Nils
   Lindskog, Stefan
   Giglio, Daniel
TI Targeted Therapy in the Palliative Setting of Colorectal Cancer-Survival
   and Medical Costs
SO CANCERS
LA English
DT Article
DE colorectal cancer; palliative; bevacizumab; EGFr; survival
ID CETUXIMAB PLUS IRINOTECAN; PHASE-III TRIAL; PRIMARY TUMOR; BASE-LINE;
   BEVACIZUMAB; CHEMOTHERAPY; FLUOROURACIL; LEUCOVORIN; PANITUMUMAB;
   COMBINATION
AB (1) Background: Targeted therapy is used alone or together with chemotherapy in metastatic colorectal cancer. The aim of this study was to assess overall survival and medical costs in a cohort of patients with metastatic colorectal cancer. (2) Methods: Demographic and clinical characteristics of 337 patients and pathological data of colorectal tumors were retrospectively collected in this population-based study. The overall survival and medical costs for patients receiving chemotherapy plus targeted therapy were compared with those for patients receiving chemotherapy only. (3) Results: Patients administered chemotherapy plus targeted therapy were less frail and had more often RAS wild-type tumors but had higher CEA levels than patients receiving chemotherapy only. No prolonged overall survival could be observed in patients receiving palliative targeted therapy. The medical costs for patients undergoing treatment with targeted therapy were significantly higher than for patients treated only with chemotherapy; they were especially higher in the group receiving targeted therapy early than late in the palliative setting. (4) Conclusions: The use of targeted therapy in metastatic colorectal cancer leads to significantly higher medical costs when used early in the palliative setting. No positive effects of the use of targeted therapy could be observed in this study; therefore, we suggest that targeted therapy be used in later lines of palliative therapy in metastatic colorectal cancer.
C1 [Inci, Kamuran; Nilsson, Bengt; Lindskog, Stefan] Univ Gothenburg, Inst Clin Sci, Sahlgrenska Acad, Dept Surg, S-40530 Gothenburg, Sweden.
   [Inci, Kamuran; Nilsson, Bengt; Lindskog, Stefan] Halland Hosp Varberg, Dept Surg, Reg Halland, S-43237 Varberg, Sweden.
   [Ny, Lars; Giglio, Daniel] Univ Gothenburg, Inst Clin Sci, Sahlgrenska Acad, Dept Oncol, S-40530 Gothenburg, Sweden.
   [Ny, Lars; Giglio, Daniel] Sahlgrens Univ Hosp, Dept Oncol, S-41345 Gothenburg, Sweden.
   [Stromberg, Ulf] Univ Gothenburg, Dept Res & Dev, Region Halland, S-40530 Gothenburg, Halland, Sweden.
   [Wilking, Nils] Karolinska Inst, Dept Oncol Pathol, S-17176 Stockholm, Sweden.
C3 University of Gothenburg; University of Gothenburg; Sahlgrenska
   University Hospital; University of Gothenburg; Karolinska Institutet
RP Giglio, D (corresponding author), Univ Gothenburg, Inst Clin Sci, Sahlgrenska Acad, Dept Oncol, S-40530 Gothenburg, Sweden.; Giglio, D (corresponding author), Sahlgrens Univ Hosp, Dept Oncol, S-41345 Gothenburg, Sweden.
EM kamuran.inci@regionhalland.se; lars.ny@oncology.gu.se;
   nils.wilking@ki.se; daniel.giglio@pharm.gu.se
OI Lindskog, Stefan/0000-0001-8055-5003; Giglio,
   Daniel/0000-0002-1349-9336; Ny, Lars/0000-0003-3864-5958
FU Region Halland
FX The study was sponsored by Region Halland.
CR Bennouna J, 2017, CLIN COLORECTAL CANC, V16, P129, DOI 10.1016/j.clcc.2016.07.013
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NR 33
TC 0
Z9 0
U1 0
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN 1
PY 2023
VL 15
IS 11
AR 3022
DI 10.3390/cancers15113022
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA I9RB6
UT WOS:001006069600001
PM 37296984
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Guadagni, S
   Fiorentini, G
   De Simone, M
   Masedu, F
   Zoras, O
   Mackay, AR
   Sarti, D
   Papasotiriou, I
   Apostolou, P
   Catarci, M
   Clementi, M
   Ricevuto, E
   Bruera, G
AF Guadagni, Stefano
   Fiorentini, Giammaria
   De Simone, Michele
   Masedu, Francesco
   Zoras, Odisseas
   Mackay, Andrew Reay
   Sarti, Donatella
   Papasotiriou, Ioannis
   Apostolou, Panagiotis
   Catarci, Marco
   Clementi, Marco
   Ricevuto, Enrico
   Bruera, Gemma
TI Precision oncotherapy based on liquid biopsies in multidisciplinary
   treatment of unresectable recurrent rectal cancer: a retrospective
   cohort study
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Rectal cancer; Recurrence; Perfusion; Precision oncotherapy; Liquid
   biopsy
ID CIRCULATING TUMOR-CELLS; LOCALLY RECURRENT; PELVIC PERFUSION; STOP-FLOW;
   THYMIDYLATE SYNTHASE; CHEMOTHERAPY; GUIDELINE; SOCIETY; COLON; PLUS
AB Background Third line innovative systemic treatments and loco-regional chemotherapy by hypoxic pelvic perfusion (HPP) have both been proposed for the treatment of unresectable not responsive recurrent rectal cancer (URRC). In the present study, we have compared the safety and efficacy of HPP/target therapy, using drug regimens selected by liquid biopsy precision oncotherapy, to third-line systemic therapy based on tissue specimens precision oncotherapy. Methods HPP/target therapy regimens were selected based on precision oncotherapy, including assays for chemosensitivity and viability, and qRT-PCR for tumor-related gene expression. In the control group, systemic third-line and further lines of therapy were defined according to clinical and biological parameters. Results From 2007 to 2019, 62 URRC patients were enrolled, comprised of 43 patients in the HPP/target-therapy group and 19 patients in the systemic therapy control group. No HPP related complications were reported and the most common adverse events were skin and bone marrow toxicity. In the HPP/target-therapy group, the ORR was 41.8% whereas in the systemic therapy control group was 15.8%. DCR of the HPP/target-therapy group was significantly improved over the systemic therapy group (P = 0.001), associated with a PFS of 8 vs 4 months (P = 0.009), and OS of 20 vs 8 months (P = 0.046). Conclusions The present data indicate that in URCC patients, the integration of HPP/target-therapy and precision oncotherapy based upon liquid biopsy is as effective and efficacious as third-line treatment in local disease control and, therefore, deserves to be further assessed and compared to conventional systemic treatments in future prospective randomized trials.
C1 [Guadagni, Stefano; Masedu, Francesco; Mackay, Andrew Reay; Clementi, Marco; Ricevuto, Enrico; Bruera, Gemma] Univ Aquila, Dept Appl Clin Sci & Biotechnol, I-67100 Laquila, Italy.
   [Fiorentini, Giammaria; Sarti, Donatella] Azienda Osped Osped Riuniti Marche Nord, Dept Oncol & Hematol, Pesaro, Italy.
   [De Simone, Michele] Inst Candiolo IRCCS, Dept Surg Oncol, Turin, Italy.
   [Zoras, Odisseas] Univ Crete, Dept Surg Oncol, Iraklion, Greece.
   [Papasotiriou, Ioannis] Res Genet Canc Ctr Int GmbH, Zug, Switzerland.
   [Apostolou, Panagiotis] Res Genet Canc Ctr SA, Florina, Greece.
   [Catarci, Marco] C&G Mazzoni Hosp, Gen Surg Unit, Ascoli Piceno, Italy.
   [Ricevuto, Enrico; Bruera, Gemma] Oncol Terr Care S Salvatore Hosp, Oncol Network ASL1 Abruzzo, Laquila, Italy.
C3 University of L'Aquila; IRCCS Fondazione del Piemonte per l'Oncologia;
   University of Crete
RP Guadagni, S (corresponding author), Univ Aquila, Dept Appl Clin Sci & Biotechnol, I-67100 Laquila, Italy.
EM stefano.guadagni@univaq.it
RI Catarci, Marco/AAC-6945-2020; Clementi, Marco/P-8582-2016; Guadagni,
   Stefano/P-6471-2016; MASEDU, Francesco/M-2989-2015
OI PAPASOTIRIOU, IOANNIS/0000-0002-6145-946X; Clementi,
   Marco/0000-0002-9652-5148; Catarci, Marco/0000-0002-6338-0114; Guadagni,
   Stefano/0000-0001-8525-084X; MASEDU, Francesco/0000-0003-0290-5324;
   Bruera, Gemma/0000-0002-8407-2479
CR Apostolou P., 2019, ONCOTARGET, V10, P3328, DOI 10.18632/oncotarget.26913
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NR 39
TC 16
Z9 16
U1 0
U2 3
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 JAN
PY 2020
VL 146
IS 1
BP 205
EP 219
DI 10.1007/s00432-019-03046-3
EA OCT 2019
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KH1SF
UT WOS:000491050900002
PM 31620896
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Piawah, S
   Venook, AP
AF Piawah, Sorbarikor
   Venook, Alan P.
TI Targeted therapy for colorectal cancer metastases: A review of current
   methods of molecularly targeted therapy and the use of tumor biomarkers
   in the treatment of metastatic colorectal cancer
SO CANCER
LA English
DT Review
DE colorectal cancer; immunotherapy; metastases; molecular targeted
   therapy; tumor biomarkers
ID CETUXIMAB PLUS IRINOTECAN; PHASE-III TRIAL; 1ST-LINE TREATMENT;
   OPEN-LABEL; MICROSATELLITE INSTABILITY; LIVER METASTASIS; PANITUMUMAB
   PLUS; WILD-TYPE; OXALIPLATIN; FLUOROURACIL
AB Despite recent advances in the management of colorectal cancer, metastatic disease remains challenging, and patients are rarely cured. However, a better understanding of the pathways implicated in the evolution and proliferation of cancer cells has led to the development of targeted therapies, that is, agents with action directed at these pathways/features. This approach is more specific to cells within which these pathways, such as epidermal growth factor receptor (EGFR), are overactive; this is in contrast to the relatively indiscriminate mechanism by which cytotoxic chemotherapy tends to affect rapidly dividing cells, regardless of their role. Although factors unique to a given patient, such as the location of the primary tumor (sidedness) or the presence of mutations that confer resistance, may limit the utility of these agents, targeted therapies are now a part of the treatment paradigm for metastatic colorectal cancer, and survival outcomes have significantly improved. This review provides an overview of the role of targeted therapy in the management of patients with colorectal cancer metastases as well as a discussion of issues in patient selection, with a focus on inhibitors of angiogenesis, EGFR-targeted therapy, BRAF mutation-targeted therapies, and other novel strategies, including immunotherapy.
C1 [Piawah, Sorbarikor; Venook, Alan P.] Univ Calif San Francisco, 1450 Third St,HD 376, San Francisco, CA 94158 USA.
C3 University of California System; University of California San Francisco
RP Venook, AP (corresponding author), Univ Calif San Francisco, 1450 Third St,HD 376, San Francisco, CA 94158 USA.
EM alan.venook@ucsf.edu
FU Maisin Foundation
FX Sorbarikor Piawah receives funding from the Maisin Foundation.
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NR 63
TC 341
Z9 366
U1 9
U2 124
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD DEC 1
PY 2019
VL 125
IS 23
BP 4139
EP 4147
DI 10.1002/cncr.32163
EA AUG 2019
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JM6RC
UT WOS:000482756100001
PM 31433498
OA Bronze
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Roberts, TJ
   Kehl, KL
   Brooks, GA
   Sholl, L
   Wright, AA
   Landrum, MB
   Keating, NL
AF Roberts, Thomas J.
   Kehl, Kenneth L.
   Brooks, Gabriel A.
   Sholl, Lynette
   Wright, Alexi A.
   Landrum, Mary Beth
   Keating, Nancy L.
TI Practice-Level Variation in Molecular Testing and Use of Targeted
   Therapy for Patients With Non-Small Cell Lung Cancer and Colorectal
   Cancer
SO JAMA NETWORK OPEN
LA English
DT Article
ID ASSOCIATION; MUTATIONS; SURVIVAL; KRAS
AB Key PointsQuestionHow do molecular testing and targeted therapy use for patients with colorectal cancer (CRC) and non-small cell lung cancer (NSCLC) vary across oncology practices? FindingsIn this cross-sectional study of 145740 Medicare beneficiaries, rates of molecular testing for NSCLC were ImportanceAll patients with newly diagnosed non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) should receive molecular testing to identify those who can benefit from targeted therapies. However, many patients do not receive recommended testing and targeted therapies. ObjectiveTo compare rates of molecular testing and targeted therapy use by practice type and across practices. Design, Setting, and ParticipantsThis cross-sectional study used 100% Medicare fee-for-service data from 2015 through 2019 to identify beneficiaries with new metastatic NSCLC or CRC diagnoses receiving systemic therapy and to assign patients to oncology practices. Hierarchical linear models were used to characterize variation by practice type and across practices. Data analysis was conducted from June 2019 to October 2022. ExposuresOncology practice providing care. OutcomesPrimary outcomes were rates of molecular testing and targeted therapy use for patients with NSCLC and CRC. Secondary outcomes were rates of multigene testing for NSCLC and CRC. ResultsThere were 106228 Medicare beneficiaries with incident NSCLC (31521 [29.7%] aged 65-69 years; 50348 [47.4%] female patients; 2269 [2.1%] Asian, 8282 [7.8%] Black, and 91215 [85.9%] White patients) and 39512 beneficiaries with incident CRC (14045 [35.5%] aged 65-69 years; 17518 [44.3%] female patients; 896 [2.3%] Asian, 3521 [8.9%] Black, and 32753 [82.9%] White patients) between 2015 and 2019. Among these beneficiaries, 18435 (12.9%) were treated at National Cancer Institute (NCI)-designated centers, 8187 (5.6%) were treated at other academic centers, and 94329 (64.7%) were treated at independent oncology practices. Molecular testing rates increased from 74% to 85% for NSCLC and 45% to 65% for CRC. First-line targeted therapy use decreased from 12% to 8% among patients with NSCLC and was constant at 5% for patients with CRC. For NSCLC, molecular testing rates were similar across practice types while rates of multigene panel use (13.2%) and targeted therapy use (16.6%) were highest at NCI-designated cancer centers. For CRC, molecular testing rates were 3.8 (95% CI: 1.2-6.5), 3.3 (95% CI, 0.4-6.1), and 12.2 (95% CI, 9.1-15.3) percentage points lower at hospital-owned practices, large independent practices, and small independent practices, respectively. Rates of targeted therapy use for CRC were similar across practice types. After adjusting for patient characteristics, there was moderate variation in molecular testing and targeted therapy use across oncology practices. Conclusions and RelevanceIn this cross-sectional study of Medicare beneficiaries, molecular testing rates for NSCLC and CRC increased in recent years but remained lower than recommended levels. Rates of targeted therapy use decreased for NSCLC and remained stable for CRC. Variation across practices suggests that where a patient was treated may have affected access to recommended testing and efficacious treatments.
C1 [Roberts, Thomas J.; Kehl, Kenneth L.; Wright, Alexi A.] Dana Farber Canc Inst, Div Populat Sci, Boston, MA USA.
   [Roberts, Thomas J.] Massachusetts Gen Hosp, Dept Med, Boston, MA USA.
   [Brooks, Gabriel A.] Dartmouth Hitchcock Med Ctr, Sect Med Oncol, Lebanon, NH USA.
   [Sholl, Lynette] Brigham & Womens Hosp, Dept Pathol, Boston, MA USA.
   [Landrum, Mary Beth; Keating, Nancy L.] Harvard Med Sch, Dept Hlth Care Policy, Boston, MA USA.
   [Keating, Nancy L.] Brigham & Womens Hosp, Div Gen Internal Med, Boston, MA USA.
C3 Harvard University; Dana-Farber Cancer Institute; Harvard University;
   Massachusetts General Hospital; Dartmouth College; Harvard University;
   Brigham & Women's Hospital; Harvard University; Harvard Medical School;
   Harvard University; Brigham & Women's Hospital
RP Keating, NL (corresponding author), Harvard Med Sch, Dept Hlth Care Policy, 180 Longwood Ave, Boston, MA 02115 USA.
EM keating@hcp.med.harvard.edu
RI Sholl, Lynette/ADI-7143-2022
FU Arnold Ventures [R01CA255035, 5T32CA092203]; National Cancer Institute
FX This research was supported by Arnold Ventures and by grant R01CA255035
   to Drs Keating and Landrum and grant 5T32CA092203 to Dr Roberts from the
   National Cancer Institute.
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NR 44
TC 14
Z9 14
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2574-3805
J9 JAMA NETW OPEN
JI JAMA Netw. Open
PD APR
PY 2023
VL 6
IS 4
AR e2310809
DI 10.1001/jamanetworkopen.2023.10809
PG 13
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA P0DZ0
UT WOS:001047443600011
PM 37115543
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Meric-Bernstam, F
   Johnson, AM
   Dumbrava, EEI
   Raghav, K
   Balaji, K
   Bhatt, M
   Murthy, RK
   Rodon, J
   Piha-Paul, SA
AF Meric-Bernstam, Funda
   Johnson, Amber M.
   Dumbrava, Ecaterina E. Ileana
   Raghav, Kanwal
   Balaji, Kavitha
   Bhatt, Michelle
   Murthy, Rashmi K.
   Rodon, Jordi
   Piha-Paul, Sarina A.
TI Advances in HER2-Targeted Therapy: Novel Agents and Opportunities Beyond
   Breast and Gastric Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Review
ID HER2 KINASE DOMAIN; SOLID TUMORS; LUNG-TUMORS; MUTATIONS; RESISTANCE;
   GENE; ADENOCARCINOMAS; AMPLIFICATION; TRASTUZUMAB; MECHANISMS
AB The introduction of HER2-targeted therapy for breast and gastric patients with ERBB2 (HER2) amplification/overexpression has led to dramatic improvements in oncologic outcomes. In the past 20 years, five HER2-targeted therapies have been FDA approved, with four approved in the past 8 years. HER2-targeted therapy similarly was found to improve outcomes in HER2-positive gastric cancer. Over the past decade, with the introduction of next-generation sequencing into clinical practice, our understanding of HER2 biology has dramatically improved. We have recognized that HER2 amplification is not limited to breast and gastric cancer but is also found in a variety of tumor types such as colon cancer, bladder cancer, and biliary cancer. Furthermore, HER2-targeted therapy has signal of activity in several tumor types. In addition to HER2 amplification and overexpression, there is also increased recognition of activating HER2 mutations and their potential therapeutic relevance. Furthermore, there is a rapidly growing number of new therapeutics targeting HER2 including small-molecule inhibitors, antibody-drug conjugates, and bispecific antibodies. Taken together, an increasing number of patients are likely to benefit from approved and emerging HER2-targeted therapies.
C1 [Meric-Bernstam, Funda; Dumbrava, Ecaterina E. Ileana; Balaji, Kavitha; Bhatt, Michelle; Rodon, Jordi; Piha-Paul, Sarina A.] Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, Houston, TX 77030 USA.
   [Meric-Bernstam, Funda; Johnson, Amber M.; Rodon, Jordi] Univ Texas MD Anderson Canc Ctr, Sheikh Khalifa Bin Zayed Al Nahyan Inst Personali, Houston, TX 77030 USA.
   [Meric-Bernstam, Funda; Murthy, Rashmi K.] Univ Texas MD Anderson Canc Ctr, Dept Breast Surg Oncol, Houston, TX 77030 USA.
   [Raghav, Kanwal] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center; University of Texas System;
   UTMD Anderson Cancer Center; University of Texas System; UTMD Anderson
   Cancer Center
RP Meric-Bernstam, F (corresponding author), Univ Texas MD Anderson Canc Ctr, 1400 Holcombe Blvd,Unit 455, Houston, TX 77030 USA.
EM fmeric@mdanderson.org
RI Meric-Bernstam, Funda/JRZ-1866-2023
OI Piha-Paul, Sarina/0000-0001-9455-1660; Rodon, Jordi/0000-0001-6467-3632;
   Murthy, Rashmi/0000-0002-0103-4718
FU Cancer Prevention & Research Institute of Texas [RP150535]; Sheikh
   Khalifa Al Nahyan Ben Zayed Institute for Personalized Cancer Therapy;
   Nellie B. Connally Breast Cancer Research Endowment; University of Texas
   MD Anderson Cancer Center Support Grant (NIH/NCI) [P30 CA016672]; AACR
FX This work was supported by the Cancer Prevention & Research Institute of
   Texas (grant number RP150535; to F. Meric-Bernstam, A.M. Johnson, and K.
   Balaji), the Sheikh Khalifa Al Nahyan Ben Zayed Institute for
   Personalized Cancer Therapy (to F. Meric-Bernstam), the Nellie B.
   Connally Breast Cancer Research Endowment (to F. Meric-Bernstam), and
   The University of Texas MD Anderson Cancer Center Support Grant (NIH/NCI
   grant number P30 CA016672; to F. Meric-Bernstam). The authors would also
   like to acknowledge the AACR and its financial and material support in
   the development of the AACR Project GENIE registry, as well as members
   of the consortium for their commitment to data sharing. Interpretations
   are the responsibility of study authors.
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NR 59
TC 235
Z9 247
U1 12
U2 128
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 APR 1
PY 2019
VL 25
IS 7
BP 2033
EP 2041
DI 10.1158/1078-0432.CCR-18-2275
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HR2UC
UT WOS:000462991900005
PM 30442682
OA Green Accepted, Green Submitted, Bronze
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Upadhyay, VA
   Johnson, BE
   Landman, AB
   Hassett, MJ
AF Upadhyay, Vivek A.
   Johnson, Bruce E.
   Landman, Adam B.
   Hassett, Michael J.
TI Real-World Analysis of Off-Label Use of Molecularly Targeted Therapy in
   a Large Academic Medical Center Cohort
SO JCO PRECISION ONCOLOGY
LA English
DT Article
ID CELL LUNG-CANCER; FDA APPROVAL; DABRAFENIB; MUTATIONS; PLATFORM;
   ONCOLOGY; TUMORS
AB PURPOSE The primary objective of this study is to quantify the use of off-label molecularly targeted therapy and describe the clinical situations in which off-label targeted therapy are used. A key secondary objective is to report the outcomes of patients treated with off-label use of targeted therapy. PATIENTS AND METHODS We searched the electronic health record between 2000 and 2020 at our center to characterize the volume, clinical settings, and outcomes associated with off-label use of targeted therapies in different types of solid tumors. RESULTS Among 46,712 patients who received targeted therapies, we identified 119 instances of off-label use of targeted therapy. Colon cancer was the most common cancer type to receive off-label targeted therapy in 18 patients (15.1%), followed by 13 with non-small-cell lung cancer (10.9%), eight with cholangiocarcinoma (6.7%), and seven with glioblastoma (5.9%). The most frequent molecular rationale for off-label therapy came from a comprehensive next-generation sequencing test (53.7%). The most frequently mutated gene that provided the rationale for targeted therapy was BRAF (20.1%), with BRAFV600E being the most common molecular alteration overall (15.1%). The median duration of off-label targeted therapy was 3.58 months, and the overall survival of treated patients was 7.59 months. There were 37 patients (31.1%) treated for longer than 6 months, 23 patients (19.3%) who survived >= 2 years, and 13 patients who were still on therapy as of June 2020. CONCLUSION In this large cohort study of patients with solid tumors, off-label use of targeted therapy was uncommon. With that said, a notable proportion of patients had treatment durations >= 6 months and survivals of >= 2 years.
C1 [Upadhyay, Vivek A.; Johnson, Bruce E.; Hassett, Michael J.] Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
   [Upadhyay, Vivek A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
   [Upadhyay, Vivek A.; Johnson, Bruce E.; Landman, Adam B.; Hassett, Michael J.] Harvard Med Sch, Boston, MA 02115 USA.
   [Landman, Adam B.] Brigham & Womens Hosp, 75 Francis St, Boston, MA 02115 USA.
C3 Harvard University; Dana-Farber Cancer Institute; Harvard University;
   Massachusetts General Hospital; Harvard University; Harvard Medical
   School; Harvard University; Brigham & Women's Hospital
RP Hassett, MJ (corresponding author), Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM Michael_hassett@dfci.harvard.edu
RI Landman, Adam/LTF-6000-2024; Johnson, Bruce/ACA-3897-2022; Hassett,
   Michael/M-5032-2019
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NR 21
TC 2
Z9 2
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2473-4284
J9 JCO PRECIS ONCOL
JI JCO Precis. Oncol.
PY 2022
VL 6
AR e2100232
DI 10.1200/PO.21.00232
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZT4ZR
UT WOS:000769166500021
PM 35050710
DA 2025-01-04
ER

PT J
AU Effendi, R
AF Effendi-Y S, Rustam
TI Cancer Stem Cells and Molecular Biology Test in Colorectal Cancer:
   Therapeutic Implications
SO ACTA MEDICA INDONESIANA
LA English
DT Article
DE colorectal cancer; cancer stem cells; biomarkers; chemoresistance;
   target therapy
ID CATENIN SIGNALING PATHWAY; TUMOR-INITIATING CELLS; SYSTEMIC THERAPY;
   SELF-RENEWAL; EXPRESSION; CHEMOTHERAPY; MECHANISM; CD133; MARKER; REPAIR
AB Colorectal cancer (CRC) is the third most frequent cancer in males, the second in females, and is the second leading cause of cancer related death worldwide. Within Indonesia's 250 million population, the incidence rates for CRC per 100,000 population were 15.2 for males and 10.2 for females, and estimated 63,500 cases per year. More than 50% of colorectal cancer patients will develop metastasis. CRC is still the main cause of tumor-related death, and although most CRC patients are treated with surgery to remove the tumor tissue, some of the CRC patients recurred. Chemotherapy used as adjuvant or neoadjuvant therapy also has several problems, in which these treatments are useless in tumor cells with chemo-resistance. Molecular testing of CRC from tumor tissues has important implications for the selection of treatment. Biomarkers can be used as prognostic value, molecular predictive factors, and targeted therapy. Recent research reported that, cancer stem cells (CSCs) are considered as the origin of tumorigenesis, development, metastasis and recurrence. At present, it has been shown that CSCs existed in many tumors including CRC. This review aims to summarize the issue on CSCs, and the future development of drugs that target colorectal cancer stem cells.
C1 [Effendi-Y S, Rustam] Univ Sumatera Utara, Pirngadi Hosp, Adam Malik Hosp, Dept Internal Med,Fac Med, Medan, Indonesia.
C3 University of North Sumatra
RP Effendi, R (corresponding author), Univ Sumatera Utara, Pirngadi Hosp, Adam Malik Hosp, Div Gastroenterol Hepatol,Dept Internal Med,Fac M, Jalan Sutrisno Sehati 754, Medan 20216, Indonesia.
EM effendiysr@yahoo.com
RI Effendi-YS, Rustam/HOC-7210-2023
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NR 53
TC 12
Z9 12
U1 0
U2 3
PU UNIV INDONESIA, FAC MEDICINE
PI JAKARTA PUSAT
PA JALAN SALEMBA 6, JAKARTA PUSAT, 10430, INDONESIA
SN 0125-9326
EI 2338-2732
J9 ACTA MED INDONES
JI Acta Med. Indones.
PD OCT
PY 2017
VL 49
IS 4
BP 351
EP 359
PG 9
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA GB7VK
UT WOS:000429283000011
PM 29348387
DA 2025-01-04
ER

PT J
AU Pranteda, A
   Piastra, V
   Stramucci, L
   Fratantonio, D
   Bossi, G
AF Pranteda, Angelina
   Piastra, Valentina
   Stramucci, Lorenzo
   Fratantonio, Deborah
   Bossi, Gianluca
TI The p38 MAPK Signaling Activation in Colorectal Cancer upon Therapeutic
   Treatments
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE p38 MAPK; colorectal cancer; therapeutic treatments; 5-fluorouracil;
   oxaliplatin; irinotecan; radiotherapy; target therapy
ID COLON-CANCER; PROTEIN-KINASE; CELL-LINES; KAPPA-B; EIF4E
   PHOSPHORYLATION; DEPENDENT PATHWAY; BREAST-CANCER; APOPTOSIS;
   INHIBITION; OXALIPLATIN
AB Pharmacological treatment of colorectal carcinoma currently proceeds through the administration of a combination of different chemotherapeutic agents. In the case of rectal carcinoma, radiation therapy also represents a therapeutic strategy. In an attempt at translating much-needed new targeted therapy to the clinics, p38 mitogen activated protein kinase (MAPK) inhibitors have been tested in clinical trials involving colorectal carcinoma patients, especially in combination with chemotherapy; however, despite the high expectations raised by a clear involvement of the p38 MAPK pathway in the response to therapeutic treatments, poor results have been obtained so far. In this work, we review recent insights into the exact role of the p38 MAPK pathway in response to currently available therapies for colorectal carcinoma, depicting an intricate scenario in which the p38 MAPK node presents many opportunities, as well as many challenges, for its perspective exploitation for clinical purposes.
C1 [Pranteda, Angelina; Piastra, Valentina; Stramucci, Lorenzo; Bossi, Gianluca] IRCCS Regina Elena Natl Canc Inst, Dept Diagnost Res & Technol Innovat, Oncogenom & Epigenet Unit, Via Elio Chianesi 53, I-00144 Rome, Italy.
   [Fratantonio, Deborah] Univ Bari Aldo Moro, Dept Biosci Biotechnol & Biopharmaceut, Via Orabona 4, I-70125 Bari, Italy.
C3 Universita degli Studi di Bari Aldo Moro
RP Bossi, G (corresponding author), IRCCS Regina Elena Natl Canc Inst, Dept Diagnost Res & Technol Innovat, Oncogenom & Epigenet Unit, Via Elio Chianesi 53, I-00144 Rome, Italy.
EM angelina.pranteda@ifo.gov.it; piastra.valentina@gmail.com;
   lorenzo.stramucci@gmail.com; deborah.fratantonio@uniba.it;
   gianluca.bossi@ifo.gov.it
RI Bossi, Gianluca/ABH-6846-2020; Bossi, Gianluca/G-8375-2016; Piastra,
   Valentina/AAC-2023-2022
OI Bossi, Gianluca/0000-0002-2947-1063; FRATANTONIO,
   Deborah/0000-0003-4835-0571; Piastra, Valentina/0000-0002-9427-2239
FU AIRC IG 2016 project from P.I. Bossi Gianluca [18449]; "Alice triangi"
   Pezcoller Foundation; 5x1000 funds from the Italian Ministry of Health
FX This research was funded by AIRC IG 2016-ID. 18449 project from P.I.
   Bossi Gianluca. L.S. was supported by the "Alice triangi" Pezcoller
   Foundation fellowship. B.G. was supported by 5x1000 funds from the
   Italian Ministry of Health (years 2011 and 2012).
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NR 71
TC 41
Z9 45
U1 0
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 APR
PY 2020
VL 21
IS 8
AR 2773
DI 10.3390/ijms21082773
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA LR3AC
UT WOS:000535565300115
PM 32316313
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kavousipour, S
   Khademi, F
   Zamani, M
   Vakili, B
   Mokarram, P
AF Kavousipour, Soudabeh
   Khademi, Fathemeh
   Zamani, Mozhdeh
   Vakili, Bahareh
   Mokarram, Pooneh
TI Novel biotechnology approaches in colorectal cancer diagnosis and
   therapy
SO BIOTECHNOLOGY LETTERS
LA English
DT Review
DE Colorectal cancer; Fragment antibody; Scaffold proteins; Targeted
   therapy
ID FACTOR-I RECEPTOR; DNA METHYLATION ANALYSIS; TARGETED DRUG-DELIVERY;
   GROWTH-FACTOR RECEPTOR; K-RAS MUTATIONS; COLON-CANCER; STEM-CELLS;
   BISPECIFIC ANTIBODIES; MONOCLONAL-ANTIBODY; BIOMARKER DISCOVERY
AB With ever-increasing molecular information about colorectal cancer (CRC), there is an expectation to detect more sensitive and specific molecular markers for new advanced diagnostic methods that can surpass the limitations of current screening tests. Moreover, enhanced molecular pathology knowledge about cancer has led to the development of targeted therapies, designed to interfere with specific aberrant biological pathways in cancer. Furthermore, biotechnology has opened a new window in CRC diagnosis and treatment by introducing different application of antibodies, antibody fragments, non-Ig scaffold proteins, and aptamers in targeted therapy and drug delivery. This review summarizes the molecular diagnostic and therapeutic approaches in CRC with a focus on genetic and epigenetic alterations, protein and metabolite markers as well as targeted therapy and drug delivery by Ig-scaffold proteins, non-Ig scaffold proteins, nanobodies, and aptamers.
C1 [Kavousipour, Soudabeh; Vakili, Bahareh] Shiraz Univ Med Sci, Dept Biotechnol, Sch Adv Med Sci & Technol, Shiraz, Iran.
   [Khademi, Fathemeh; Mokarram, Pooneh] Shiraz Univ Med Sci, Sch Med, Dept Biochem, POB 1167, Shiraz, Iran.
   [Zamani, Mozhdeh; Mokarram, Pooneh] Shiraz Univ Med Sci, Colorectal Res Ctr, Shiraz, Iran.
   [Mokarram, Pooneh] Shiraz Univ Med Sci, Sch Med, Nemazee Hosp, Gastroenterohepatol Res Ctr, Shiraz, Iran.
C3 Shiraz University of Medical Science; Shiraz University of Medical
   Science; Shiraz University of Medical Science; Shiraz University of
   Medical Science
RP Mokarram, P (corresponding author), Shiraz Univ Med Sci, Sch Med, Dept Biochem, POB 1167, Shiraz, Iran.
EM mokaram2@gmail.com
RI Mokarram, Pooneh/E-1613-2012; Vakili, Bahareh/ITV-6590-2023;
   Kavousipour, Soudabeh/AAC-5122-2020; Zamani, Mozhdeh/N-9607-2016
OI Mokarram, Pooneh/0000-0002-9717-0473; vakili,
   Bahareh/0000-0003-1900-5672; Kavousipour, Soudabeh/0000-0001-9724-9942;
   Zamani, Mozhdeh/0000-0001-7856-6029
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NR 180
TC 21
Z9 24
U1 2
U2 31
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0141-5492
EI 1573-6776
J9 BIOTECHNOL LETT
JI Biotechnol. Lett.
PD JUN
PY 2017
VL 39
IS 6
BP 785
EP 803
DI 10.1007/s10529-017-2303-8
PG 19
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA EV5WL
UT WOS:000401838900001
PM 28238060
DA 2025-01-04
ER

PT S
AU Pysz, I
   Andriollo, P
   Thurston, DE
AF Pysz, Ilona
   Andriollo, Paolo
   Thurston, David E.
BE Thurston, DE
   Jackson, PJM
TI Traditional Cytotoxic Agents as Antibody-Drug Conjugate (ADC) Payloads
SO CYTOTOXIC PAYLOADS FOR ANTIBODY-DRUG CONJUGATES
SE RSC Drug Discovery Series
LA English
DT Article; Book Chapter
ID MITOMYCIN-C NSC-26980; MONOCLONAL-ANTIBODY; BIOLOGICAL EVALUATION;
   ANTITUMOR-ACTIVITY; TARGETED THERAPY; HUMAN CARCINOMAS; COLON CANCER;
   METHOTREXATE; DOXORUBICIN; PACLITAXEL
C1 [Pysz, Ilona; Andriollo, Paolo; Thurston, David E.] Femtogenix Ltd, Lawes Open Innovat Hub, Rothamsted Res, Harpenden AL5 2JQ, Herts, England.
   [Pysz, Ilona; Andriollo, Paolo; Thurston, David E.] Kings Coll London, Inst Pharmaceut Sci, Sch Canc & Pharmaceut Sci, Fac Life Sci & Med, Franklin Wilkins Bldg,150 Stamford St, London SE1 9NH, England.
C3 UK Research & Innovation (UKRI); Biotechnology and Biological Sciences
   Research Council (BBSRC); Rothamsted Research; University of London;
   King's College London
RP Thurston, DE (corresponding author), Femtogenix Ltd, Lawes Open Innovat Hub, Rothamsted Res, Harpenden AL5 2JQ, Herts, England.; Thurston, DE (corresponding author), Kings Coll London, Inst Pharmaceut Sci, Sch Canc & Pharmaceut Sci, Fac Life Sci & Med, Franklin Wilkins Bldg,150 Stamford St, London SE1 9NH, England.
EM david.thurston@kcl.ac.uk
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NR 74
TC 1
Z9 1
U1 0
U2 2
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, CAMBRIDGE CB4 4WF, CAMBS, ENGLAND
SN 2041-3203
EI 2041-3211
BN 978-1-78801-289-8; 978-1-78801-077-1
J9 RSC DRUG DISCOV
JI RSC Drug Discov.
PY 2019
VL 71
BP 137
EP 165
D2 10.1039/9781788012898
PG 29
WC Pharmacology & Pharmacy; Toxicology
WE Book Citation Index – Science (BKCI-S)
SC Pharmacology & Pharmacy; Toxicology
GA BP2AC
UT WOS:000541670800008
OA Green Published
DA 2025-01-04
ER

PT J
AU Lairson, DR
   Parikh, RC
   Cormier, JN
   Chan, W
   Du, XLL
AF Lairson, David R.
   Parikh, Rohan C.
   Cormier, Janice N.
   Chan, Wenyaw
   Du, Xianglin L.
TI Cost-Utility Analysis of Treatments for Advanced Non-Small Cell Lung
   Cancer
SO AMERICAN JOURNAL OF PHARMACY BENEFITS
LA English
DT Article
ID ELDERLY-PATIENTS; ECONOMIC-EVALUATION; PROPENSITY SCORE;
   COLORECTAL-CANCER; CHEMOTHERAPY; CISPLATIN; BEVACIZUMAB; TRIALS; AGE;
   COMBINATION
AB Objectives: Chemotherapy combinations and biologics have increased the overall survival rate for patients with advanced non-small cell lung cancer (NSCLC), but at a very high cost. We evaluated the effectiveness of chemotherapy/targeted therapy among elderly patients with NSCLC stratified by age groups, and then assessed the cost utility of treatment.
   Study Design: Retrospective cohort study.
   Methods: SEER (Surveillance, Epidemiology, and End Results) program-and Medicare-linked data were used to estimate the total healthcare cost, life-years, and quality-adjusted life-years (QALYs) for elderly (aged 65-94 years) stage IIIB/IV NSCLC patients diagnosed between 2006 and 2009. Patients were grouped into "no chemotherapy," "platinum-based chemotherapy," and "platinum + targeted therapy" cohorts, and propensity score matching was performed. Cost-effectiveness was evaluated with the incremental cost-effectiveness ratio (ICER) and net monetary benefit. Uncertainty was accounted for by presenting cost-effectiveness acceptability curves (CEACs). A 3% discounting was applied to costs (2014 US$) and effectiveness.
   Results: A total of 4884 patients were included in the study, with 1628 in each treatment group. The ICER for platinum-based chemotherapy versus no chemotherapy was $124,645 per QALY gained; for platinum + targeted therapy versus platinum-based chemotherapy, it was $864,327 per QALY gained. Similar results were obtained for alternate scenarios and age groups. The CEAC showed that platinum-based chemotherapy was nearly 100% cost-effective at a willingness-to-pay threshold of $200,000 per QALY, while platinum + targeted therapy was 70% cost-effective at a willingness-to-pay threshold of $1 million per QALY.
   Conclusions: Platinum-based chemotherapy may be cost-effective compared with no chemotherapy for the overall elderly population and by age group. However, platinum + targeted therapy was not cost-effective compared with the use of platinum-based therapy alone.
C1 [Lairson, David R.; Parikh, Rohan C.; Du, Xianglin L.] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Dept Management Policy & Community Hlth, Houston, TX 77030 USA.
   [Du, Xianglin L.] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Dept Epidemiol Human Genet & Environm Sci, Houston, TX 77030 USA.
   [Chan, Wenyaw] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Div Biostat, Houston, TX 77030 USA.
   [Cormier, Janice N.] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX 77030 USA.
   [Cormier, Janice N.] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
C3 University of Texas System; University of Texas Health Science Center
   Houston; University of Texas School Public Health; University of Texas
   System; University of Texas Health Science Center Houston; University of
   Texas School Public Health; University of Texas System; University of
   Texas Health Science Center Houston; University of Texas School Public
   Health; University of Texas System; UTMD Anderson Cancer Center;
   University of Texas System; UTMD Anderson Cancer Center
RP Lairson, DR (corresponding author), 1200 Herman Pressler Dr,RAS E-307, Houston, TX 77030 USA.
EM David.R.Lairson@uth.tmc.edu
OI Parikh, Rohan/0000-0003-4516-9996
FU Agency for Healthcare Research and Quality (AHRQ) [R01-HS018956]; Cancer
   Prevention and Research Institute of Texas (CPRIT) [RP130051]
FX This study was supported in part by a grant from the Agency for
   Healthcare Research and Quality (AHRQ; R01-HS018956) and in part by a
   grant from the Cancer Prevention and Research Institute of Texas (CPRIT:
   RP130051).
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WC Health Care Sciences & Services
WE Emerging Sources Citation Index (ESCI)
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GA VA8LI
UT WOS:000410458500006
DA 2025-01-04
ER

PT J
AU Malla, M
   Parikh, AR
AF Malla, Midhun
   Parikh, Aparna R.
TI Evolving Role of Circulating Tumor DNA and Emerging Targeted Therapy in
   Colorectal Cancer
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Circulating tumor DNA; Response prediction; Minimal residual disease;
   Targeted therapy; Gene fusions; Precision medicine
ID EGFR MONOCLONAL-ANTIBODIES; III COLON-CANCER; MICROSATELLITE
   INSTABILITY; ACQUIRED-RESISTANCE; STAGE-II; CLINICAL-EFFICACY; LIQUID
   BIOPSIES; MUTATION STATUS; BRAF; PLASMA
C1 [Malla, Midhun] West Virginia Univ, Sect Hematol Oncol, Sch Med, 1 Med Ctr Dr, Morgantown, WV 26506 USA.
   [Parikh, Aparna R.] Harvard Med Sch, Tucker Gosnell Ctr Gastrointestinal Malignancies, Termeer Ctr Targeted Therapies, Massachusetts Gen Hosp,Canc Ctr, Boston, MA 02114 USA.
C3 West Virginia University; Harvard University; Massachusetts General
   Hospital; Harvard Medical School
RP Parikh, AR (corresponding author), Harvard Med Sch, Tucker Gosnell Ctr Gastrointestinal Malignancies, Termeer Ctr Targeted Therapies, Massachusetts Gen Hosp,Canc Ctr, Boston, MA 02114 USA.
EM Aparna.Parikh@mgh.harvard.edu
RI , midhun/AAH-6569-2019
FU National Institute of General Medical Sciences-NIH [5U54GM104942-05]
FX In the last 12 months, Dr A. Parikh has equity in c2i Genomics, DSMC
   Roche, consulting fees from Eli Lilly, Pfizer, Inivita. Research support
   to the institution from Puretech, PMV Pharmaceuticals, Plexxicon, BMS,
   Novartis, Mirati and Genentech, Natera. In the last 12 months, Dr M.
   Malla has received grant funding from the National Institute of General
   Medical Sciences-NIH (Grant #5U54GM104942-05). The content is solely the
   responsibility of the author and does not necessarily represent the
   official views of the National Institutes of Health. He received
   consulting fees from AstraZeneca, andand QED Therapeutics. He is on
   speakers bureau for natera and received honoraria from Omni Health, and
   Curio Science.
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NR 106
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PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8588
EI 1558-1977
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD JUN
PY 2022
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IS 3
BP 583
EP 601
DI 10.1016/j.hoc.2022.02.009
EA MAY 2022
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WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA 3E9WF
UT WOS:000830326100012
PM 35577710
OA Bronze
DA 2025-01-04
ER

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   Altucci, Lucia
   Tabernero, Josep
   Troiani, Teresa
   Ciardiello, Fortunato
   Kopetz, Scott
TI Antitumor Efficacy of Dual Blockade with Encorafenib plus Cetuximab in
   Combination with Chemotherapy in Human BRAFV6°°E-Mutant Colorectal
   Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CONSENSUS MOLECULAR SUBTYPES; BRAF MUTATION; COLON-CANCER; VEMURAFENIB;
   INHIBITION; IRINOTECAN; PROGNOSIS
AB Purpose: Encorafenib + cetuximab (E+C) is an effective thercancer (mCRC). However, there is a need to improve the efficacy of this molecular-targeted therapy and evaluate regimens suitable for Experimental Design: We performed a series of in vivo studies using BRAFV600E mCRC tumor xenografts. Mice were randomized to receive 5-fluoruracil (5-FU), irinotecan, or oxaliplatin regimens (FOLFIRI or FOLFOX), (E+C) or the combination. Patients received long-term treatment until disease progression, with deescalation strategies used to mimic maintenance therapy. Transcriptomic changes after progression on cytotoxic chemotherapy or targeted therapy were assessed. Results: Antitumor activity of either FOLFIRI or E+C was better as first-line treatment as compared with second-line, with partial cross-resistance seen between a cytotoxic regimen and targeted therapy with an average 62% loss of efficacy for FOLFIRI after E+C and a 45% loss of efficacy of E+C after FOLFIRI (P< 0.001 for both). FOLFIRI-treated models had upregulation of epithelial- mesenchymal transition (EMT) and MAPK pathway activation, where E+C treated models had suppressed MAPK signaling. In contrast, with chemotherapy with E+C, EMT and MAPK signaling remained suppressed. FOLFOX or FOLFIRI, each in combination with E+C, were the most active first-line treatments as compared with E+C or to chemotherapy alone. Furthermore, FOLFOX in combination with E+C as first-line induction therapy, followed by E+C f 5-FU as maintenance therapy, was the most effective strategy for long-term disease control. Conclusions: These results support the combination of cytotoxic chemotherapy and molecular-targeted therapy as a promising therapeutic approach in the first-line treatment of BRAFV600E mCRC.
C1 [Napolitano, Stefania; De Falco, Vincenzo; Martini, Giulia; Della Corte, Carminia Maria; Martinelli, Erika; Famiglietti, Vincenzo; Ciardiello, Davide; Altucci, Lucia; Troiani, Teresa; Ciardiello, Fortunato] Univ Campania Luigi Vanvitelli, Dept Precis Med, Naples, Italy.
   [Woods, Melanie; Lee, Hey Min; Anderson, Amanda; Villareal, Oscar Eduardo; Sorokin, Alexey; Kanikarla, Preeti; Coker, Olu; Morris, Van; Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, Dept Gastro Intestinal Med Oncol, Div Canc Med, Houston, TX USA.
   [Fowlkes, Natalie Wall] Univ Texas MD Anderson Canc Ctr, Vet Med & Surg Dept, Houston, TX USA.
   [Tabernero, Josep] Vall dHebron Hosp Campus, Med Oncol Dept, Barcelona, Spain.
   [Tabernero, Josep] Cent Univ Catalonia, Univ Vic, Inst Oncol, Barcelona, Spain.
   [Tabernero, Josep] Oncol Inst Barcelona Quironsalud, Biomed Res Ctr Canc, Barcelona, Spain.
   [Napolitano, Stefania] Univ Campania Luigi Vanvitelli, Dept Precis Med, Med Oncol, Via S Pansini 5, I-80131 Naples, Italy.
C3 Universita della Campania Vanvitelli; University of Texas System; UTMD
   Anderson Cancer Center; University of Texas System; UTMD Anderson Cancer
   Center; Universitat de Vic - Universitat Central de Catalunya
   (UVic-UCC); Universita della Campania Vanvitelli
RP Napolitano, S (corresponding author), Univ Campania Luigi Vanvitelli, Dept Precis Med, Med Oncol, Via S Pansini 5, I-80131 Naples, Italy.
EM Stefania.napolitano@unicampania.it
RI Napolitano, Stefania/AIB-9708-2022; Della Corte, Carminia/ABE-1377-2021;
   Ciardiello, Davide/AAC-4613-2022; Martini, Giulia/AIB-8246-2022; De
   Falco, Vincenzo/AAP-5495-2021; Altucci, Lucia/S-8031-2019
OI De Falco, Vincenzo/0000-0003-0261-0382; martinelli,
   erika/0000-0002-7108-0971; ciardiello, davide/0000-0003-1826-0305; Lee,
   Hey Min/0000-0001-7792-4226; Della Corte, Carminia
   Maria/0000-0002-3396-8099; MARTINI, Giulia/0000-0003-4093-2681;
   Villarreal, Oscar/0000-0002-4138-2696
FU Regione Campania (I -Cure Research Project) [Cup 21C17000030007]; Cancer
   Center Support Grant - Gastrointestinal Program [5P30 CA016672 - 46];
   CPRIT Training Program [RP210028]
FX A research grant that partially covered the costs of the study was
   provided by Regione Campania (I -Cure Research Project, grant number:
   Cup 21C17000030007, to F. Ciardiello and L. Altucci) . This work was
   also supported by Cancer Center Support Grant - Gastrointestinal Program
   (Project Number: 5P30 CA016672 - 46) . O.E. Villarreal was supported by
   the CPRIT Training Program (RP210028) .
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NR 38
TC 6
Z9 6
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 JUN 15
PY 2023
VL 29
IS 12
BP 2299
EP 2309
DI 10.1158/1078-0432.CCR-22-3894
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA K7ZV6
UT WOS:001018593400001
PM 37040395
OA Green Published, Green Submitted, hybrid
DA 2025-01-04
ER

PT J
AU Benevento, I
   De Felice, F
   Musio, D
   Tombolini, V
AF Benevento, Ilaria
   De Felice, Francesca
   Musio, Daniela
   Tombolini, Vincenzo
TI The Addition of Target Therapy to Neoadjuvant Chemoradiotherapy in
   Locally Advanced Rectal Cancer: A Review
SO CHEMOTHERAPY
LA English
DT Review
DE Rectal cancer; Locally advanced disease; Neoadjuvant treatment;
   Preoperative chemoradiotherapy; Target therapy; Epidermal growth factor
   receptor; Vascular endothelial growth factor receptor; Cetuximab;
   Bevacizumab
ID PHASE-II TRIAL; METASTATIC COLORECTAL-CANCER; PREOPERATIVE TREATMENT;
   RADIATION-THERAPY; DISEASE-CONTROL; CLINICAL-TRIAL; CAPECITABINE;
   RADIOTHERAPY; CETUXIMAB; BEVACIZUMAB
AB Currently, neoadjuvant fluoropyrimidine-based chemoradiotherapy (CRT) is standard practice in the management of locally advanced rectal cancer (LARC). In the last decade there has been a lively interest in the improvement of clinical outcomes by modifying this standard regimen by the addition of further agents. We review combinations of targeted therapies and conventional CRT currently under investigation in LARC patients. (C) 2017 S. Karger AG, Basel
C1 [Benevento, Ilaria; De Felice, Francesca; Musio, Daniela; Tombolini, Vincenzo] Sapienza Univ Rome, Policlin Umberto I, Dept Radiotherapy, Viale Regina Elena 326, IT-00161 Rome, Italy.
C3 Sapienza University Rome; University Hospital Sapienza Rome
RP De Felice, F (corresponding author), Sapienza Univ Rome, Policlin Umberto I, Dept Radiotherapy, Viale Regina Elena 326, IT-00161 Rome, Italy.
EM fradefelice@hotmail.it
RI De Felice, Francesca/I-2075-2017
OI De Felice, Francesca/0000-0002-5119-8358; Tombolini,
   Vincenzo/0000-0001-5359-9991
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NR 51
TC 6
Z9 6
U1 0
U2 3
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0009-3157
EI 1421-9794
J9 CHEMOTHERAPY
JI Chemotherapy
PY 2017
VL 62
IS 5
BP 314
EP 322
DI 10.1159/000476056
PG 9
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA FE0OJ
UT WOS:000407919300007
PM 28595169
DA 2025-01-04
ER

PT J
AU Abubakar, MB
   Gan, SH
AF Abubakar, Murtala B.
   Gan, Siew Hua
TI Molecular Targets in Advanced Therapeutics of Cancers: The Role of
   Pharmacogenetics
SO ONCOLOGY
LA English
DT Review
DE Targeted therapy; Molecular targets; Advanced therapeutics;
   Pharmacogenetics
ID CELL LUNG-CANCER; ENDOTHELIAL GROWTH-FACTOR; METASTATIC
   COLORECTAL-CANCER; ADVANCED HEPATOCELLULAR-CARCINOMA; TYROSINE KINASE
   INHIBITOR; ESTROGEN-RECEPTOR-ALPHA; EWING SARCOMA FAMILY;
   HUMAN-BREAST-CANCER; MONOCLONAL-ANTIBODY; ACQUIRED-RESISTANCE
AB The advent of advanced molecular targeted therapy has resulted in improved prognoses for patients with advanced malignancies. However, despite the significant success and specificity of this advocated targeted therapy, significant on-and off-target adverse effects and inter-individual variability in treatment responses have been reported. The interpatient variability in drug response has been suggested to be partly due to variations in patient genomes. Therefore, the identification of genetic biomarkers by conducting pharmacogenetics studies can help predict patient responses to targeted therapy and may serve as a basis for individualized treatment. In this review, both clinically established and potential molecular targets are highlighted. Overall, current literature suggests that individualization of targeted therapy is promising; however, integrating the clinical benefits of identified biomarkers into clinical practice for personalized medicine remains a major challenge, and further studies to validate these markers and identify novel therapeutic approaches are needed.
C1 [Abubakar, Murtala B.; Gan, Siew Hua] Univ Sains Malaysia, Sch Med Sci, Ctr Human Genome, Kelantan 16150, Kota Bharu, Malaysia.
   [Abubakar, Murtala B.] Usmanu Dan Fodiyo Univ, Coll Hlth Sci, Fac Basic Med Sci, Dept Physiol, Sokoto, Nigeria.
C3 Universiti Sains Malaysia
RP Abubakar, MB (corresponding author), Univ Sains Malaysia, Sch Med Sci, Ctr Human Genome, Kelantan 16150, Kota Bharu, Malaysia.
EM murtalaabubakar704@gmail.com
RI Abubakar, Murtala/G-8964-2016; gan, siew hua/A-6266-2011
OI gan, siew hua/0000-0001-6470-3651; Abubakar, Murtala/0000-0001-7666-4776
FU Universiti Sains Malaysia (USM) [1001/PPSP/853005]; USM Global
   Fellowship award [IPS/USMGF] [01/14]
FX This work was supported by grant No. 1001/PPSP/853005 from Universiti
   Sains Malaysia (USM). The authors acknowledge the USM Global Fellowship
   award [IPS/USMGF (01/14)] to the first author.
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NR 136
TC 12
Z9 12
U1 0
U2 12
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0030-2414
EI 1423-0232
J9 ONCOLOGY-BASEL
JI Oncology
PY 2016
VL 91
IS 1
BP 3
EP 12
DI 10.1159/000446437
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DT3KX
UT WOS:000381381000002
PM 27233906
DA 2025-01-04
ER

PT J
AU Johnson, KR
   Liauw, W
   Lassere, MND
AF Johnson, K. R.
   Liauw, W.
   Lassere, M. N. D.
TI Evaluating surrogacy metrics and investigating approval decisions of
   progression-free survival (PFS) in metastatic renal cell cancer: a
   systematic review
SO ANNALS OF ONCOLOGY
LA English
DT Review
DE metastatic renal cell; surrogate marker; targeted therapy; surrogate
   threshold effect; progression-free survival
ID RANDOMIZED PHASE-II; CLINICAL-TRIALS; END-POINTS; INTERFERON-ALPHA;
   SUBCUTANEOUS INTERLEUKIN-2; COLORECTAL-CANCER; 13-CIS-RETINOIC ACID;
   HIERARCHICAL LEVELS; EVALUATION SCHEMA; PLUS INTERFERON
AB Background: In metastatic renal cell cancer (mRCC) trials, progression-free survival (PFS) is increasingly used instead of overall survival (OS) as the approval end point. Unlike other solid tumors, there is no published demonstration of what PFS is needed across and by treatment class in mRCC. We determine this and evaluate drug approval decisions in mRCC targeted therapy.
   Methods: We identified all randomized, controlled trials reporting PFS and OS in mRCC. Surrogacy metrics were the coefficient of determination and surrogate threshold effect (STE)-the PFS difference needed to predict, with 95% confidence, an OS difference. Data from regulatory commentaries, briefing documents and transcripts were extracted.
   Results: No exclusively chemotherapy trial met criteria. Of 30 qualifying trials, 11 trials (13 comparisons) used targeted therapy. The all-trials and immunotherapy-only trials analysis failed to demonstrate a STE. The targeted trials, using the more conservative regression analysis demonstrated an STE of 3.9 months and an R-2 of 0.44. Crossover upon progression, control to active treatment, was common. Regulatory approval, accelerated or regular, labeling, interim analyses, and adjudication were context specific.
   Conclusions: A new targeted therapy trial showing a PFS difference of 3.9 months can claim an OS benefit in mRCC. PFS surrogacy for OS in metastatic renal cell is not generalizable across all drug classes.
C1 [Johnson, K. R.] Univ New S Wales, St George Clin Sch, Dept Rheumatol, Kogarah, NSW 2217, Australia.
   [Liauw, W.; Lassere, M. N. D.] Univ New S Wales, St George Clin Sch, Dept Oncol, Kogarah, NSW 2217, Australia.
C3 University of New South Wales Sydney; University of New South Wales
   Sydney
RP Johnson, KR (corresponding author), Univ New S Wales, Dept Rheumatol, St George Clin Sch, St George Hosp, Belgrave St, Kogarah, NSW 2217, Australia.
EM kent.johnson@unsw.edu.au
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NR 79
TC 18
Z9 18
U1 0
U2 5
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD MAR
PY 2015
VL 26
IS 3
BP 485
EP 496
DI 10.1093/annonc/mdu267
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CF0JE
UT WOS:000352228700006
PM 25057168
OA Bronze
DA 2025-01-04
ER

PT J
AU Liu, Y
   Zhang, X
   Xu, HF
   Shi, JH
   Zhao, YQ
   Du, LB
   Liu, YY
   Wang, WJ
   Cao, HL
   Ma, L
   Huang, JX
   Cao, J
   Li, L
   Fan, YP
   Gu, XF
   Feng, CY
   Zhu, Q
   Wang, XH
   Du, JC
   Zhang, JG
   Zhang, SK
   Qiao, YL
AF Liu, Yin
   Zhang, Xi
   Xu, Hui-Fang
   Shi, Ji-Hai
   Zhao, Yu-Qian
   Du, Ling-Bin
   Liu, Yun-Yong
   Wang, Wen-Jun
   Cao, He-Lu
   Ma, Li
   Huang, Juan-Xiu
   Cao, Ji
   Li, Li
   Fan, Yan-Ping
   Gu, Xiao-Fen
   Feng, Chang-Yan
   Zhu, Qian
   Wang, Xiao-Hui
   Du, Jing-Chang
   Zhang, Jian-Gong
   Zhang, Shao-Kai
   Qiao, You-Lin
CA China Working Grp Colorectal Can
TI Real-World Utilization, Barriers, and Factors Associated With the
   Targeted Treatment of Metastatic Colorectal Cancer Patients in China: A
   Multi-Center, Hospital-Based Survey Study
SO INTERNATIONAL JOURNAL OF PUBLIC HEALTH
LA English
DT Article
DE associated factors; utilization; barriers; metastatic colorectal cancer;
   targeted treatment
ID COST-EFFECTIVENESS ANALYSIS; RISK-FACTORS; FRUQUINTINIB; BEVACIZUMAB;
   REGORAFENIB; THERAPY; OXALIPLATIN; MANAGEMENT; SURVIVAL; PLACEBO
AB Objectives: To explore the utilization, barriers, and factors associated with the targeted treatment of Chinese metastatic colorectal cancer (mCRC) patients.Methods: A total of 1,688 mCRC patients from 19 hospitals in 14 cities were enrolled from March 2020 to March 2021 using stratified, multistage cluster sampling. The use of targeted therapy and any barriers patients experienced were collected. Logistic regression analyses were conducted to identify the factors associated with initiating targeted treatment.Results: About 51.6% of the patients initiated targeted therapy, of whom 44.5%, 20.2%, and 35.2% started first-, second-, and third-line treatment, respectively. The most reported barriers were high medical costs and a lack of belief in the efficacy of targeted therapy. Patients treated in the general hospital, diagnosed at an older age, less educated, and who had a lower family income, no medical insurance, poor health-related quality of life, metastasis outside the liver/lung or systemic metastasis, a shorter duration of mCRC were less likely to initiate targeted therapy.Conclusion: Reduced medical costs and interventional education to improve public awareness could facilitate the use of targeted treatment for mCRC.
C1 [Liu, Yin; Xu, Hui-Fang; Zhang, Jian-Gong; Zhang, Shao-Kai; Qiao, You-Lin] Zhengzhou Univ, Henan Engn Res Ctr Canc Prevent & Control, Affiliated Canc Hosp,Henan Canc Hosp, Dept Canc Epidemiol,Henan Int Joint Lab Canc Prev, Zhengzhou, Peoples R China.
   [Zhang, Xi] Peking Univ Canc Hosp & Inst, Minist Educ Beijing, Key Lab Carcinogenesis & Translat Res, Beijing Off Canc Prevent & Control, Beijing, Peoples R China.
   [Shi, Ji-Hai] Baotou Med Coll, Affiliated Hosp 1, Clin Epidemiol Res Ctr, Dept Dermatol, Baotou, Peoples R China.
   [Zhao, Yu-Qian] Univ Elect Sci & Technol China, Sichuan Canc Hosp & Inst, Sichuan Canc Ctr, Sch Med, Chengdu, Peoples R China.
   [Du, Ling-Bin] Univ Chinese Acad Sci, Zhejiang Canc Hosp, Dept Canc Prevent, Canc Hosp, Hangzhou, Peoples R China.
   [Liu, Yun-Yong] China Med Univ, Liaoning Canc Hosp & Inst, Liaoning Off Canc Control & Res, Canc Hosp, Shenyang, Peoples R China.
   [Wang, Wen-Jun] Jining Med Univ, Sch Nursing, Jining, Peoples R China.
   [Cao, He-Lu] Xinxiang Cent Hosp, Dept Prevent Hlth, Xinxiang, Peoples R China.
   [Ma, Li] Dalian Med Univ, Publ Hlth Sch, Dalian, Peoples R China.
   [Huang, Juan-Xiu] Wuzhou Red Cross Hosp, Dept Gastroenterol, Wuzhou, Peoples R China.
   [Cao, Ji] Guangxi Med Univ, Affiliated Hosp 1, Dept Canc Prevent & Control Off, Nanning, Guangxi, Peoples R China.
   [Li, Li] Jinan Univ, Affiliated Hosp 1, Dept Clin Res, Guangzhou, Peoples R China.
   [Fan, Yan-Ping] Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Canc Ctr, Guangzhou, Peoples R China.
   [Gu, Xiao-Fen] Xinjiang Med Univ, Affiliated Tumor Hosp, Dept Student Affairs, Urumqi, Xinjiang, Peoples R China.
   [Feng, Chang-Yan] Chongqing Univ, Chongqing Key Lab Translat Res Canc Metastasis &, Chongqing, Peoples R China.
   [Zhu, Qian] Chongqing Med Univ, Sch Publ Hlth & Management, Chongqing, Peoples R China.
   [Wang, Xiao-Hui] Gansu Prov Canc Hosp, Dept Publ Hlth, Lanzhou, Peoples R China.
   [Du, Jing-Chang] Chengdu Med Coll, Sch Publ Hlth, Chengdu, Peoples R China.
   [Qiao, You-Lin] Chinese Acad Med Sci & Peking Union Med Coll, Ctr Global Hlth, Sch Populat Med & Publ Hlth, Beijing, Peoples R China.
C3 Zhengzhou University; Baotou Medical College; University of Electronic
   Science & Technology of China; Chinese Academy of Sciences; University
   of Chinese Academy of Sciences, CAS; Zhejiang Cancer Hospital; China
   Medical University; Jining Medical University; Dalian Medical
   University; Guangxi Medical University; Jinan University; State Key Lab
   Oncology South China; Sun Yat Sen University; Xinjiang Medical
   University; Chongqing University; Chongqing Medical University; Chengdu
   Medical College; Chinese Academy of Medical Sciences - Peking Union
   Medical College; Peking Union Medical College
RP Zhang, JG; Zhang, SK; Qiao, YL (corresponding author), Zhengzhou Univ, Henan Engn Res Ctr Canc Prevent & Control, Affiliated Canc Hosp,Henan Canc Hosp, Dept Canc Epidemiol,Henan Int Joint Lab Canc Prev, Zhengzhou, Peoples R China.; Qiao, YL (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Ctr Global Hlth, Sch Populat Med & Publ Hlth, Beijing, Peoples R China.
EM zhangjg@zzu.edu.cn; shaokaizhang@126.com; qiaoy@cicams.ac.cn
RI Wang, Xiaohui/I-9861-2016; Qiao, You-Lin/B-4139-2012; zhao,
   yuqian/JED-8246-2023; Zhang, Bo/JVD-9890-2024
FU Beijing Love Book Cancer Foundation; Merck Serono Co., Ltd
FX This research was funded by Beijing Love Book Cancer Foundation. The
   authors declare that this study received funding from Merck Serono Co.,
   Ltd. The funder was not involved in the study design, collection,
   analysis, interpretation of data, the writing of this article, or the
   decision to submit it for publication.
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NR 41
TC 1
Z9 1
U1 5
U2 9
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1661-8556
EI 1661-8564
J9 INT J PUBLIC HEALTH
JI Int. J. Public Health
PD JUL 3
PY 2023
VL 68
AR 1606091
DI 10.3389/ijph.2023.1606091
PG 11
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Public, Environmental & Occupational Health
GA M4GV5
UT WOS:001029811500001
PM 37465051
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Mondaca, S
   Yaeger, R
AF Mondaca, Sebastian
   Yaeger, Rona
TI Colorectal cancer genomics and designing rational trials
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE Colorectal cancer (CRC); genomics; targeted therapies
ID CELL LUNG-CANCER; OPEN-LABEL; BRAF MUTATION; ACQUIRED-RESISTANCE;
   MICROSATELLITE INSTABILITY; RAS MUTATIONS; PREDICTIVE BIOMARKER;
   MONOCLONAL-ANTIBODY; 1ST-LINE TREATMENT; BREAST-CANCER
AB The widespread use of next generation sequencing (NGS) has led to a refined understanding of the genomics of colorectal cancer (CRC). However, progress in the use of molecular biomarkers in standard practice has been slow, and there is no approved targeted therapy for CRC based on a positive predictive marker yet. In this review, we will first summarize biomarkers with clinical utility in standard practice or targeted therapy trials and then consider how to rationally design clinical trials to more effectively target CRC. Specifically, we will discuss current clinical applications of genomic information consisting of the use of the MAPK (mitogen-activated protein kinase) pathway genes KRAS, NRAS, and BRAF as prognostic and predictive biomarkers for standard treatment, risk stratification by primary tumor site and consideration of tumor laterality in patient selection for epidermal growth factor receptor (EGFR) antibody treatment, and the evaluation for genomic biomarkers, including BRAF V600E, HER2 amplification, and gene rearrangements, for targeted therapies in clinical trials. Applying lessons from targeted therapy trials in CRC, we now appreciate that both tumor genomics and tissue of origin affect targeted therapy response and that the development of resistance to targeted therapies is dynamic and often subclonal. Based on these understandings, we propose the design of adaptive clinical trials that evaluate real-time pharmacodynamic markers and monitor tumor subpopulations during the course of treatment to overcome challenges targeting genetic drivers in CRC.
C1 [Mondaca, Sebastian; Yaeger, Rona] Mem Sloan Kettering Canc Ctr, Dept Med, 300 E 66th St,10th Floor, New York, NY 10065 USA.
C3 Memorial Sloan Kettering Cancer Center
RP Yaeger, R (corresponding author), Mem Sloan Kettering Canc Ctr, Dept Med, 300 E 66th St,10th Floor, New York, NY 10065 USA.
EM yaegerr@mskcc.org
FU National Institutes of Health Memorial Sloan Kettering Cancer Center
   Core Grant [P30 CA 008748]
FX Supported by the National Institutes of Health Memorial Sloan Kettering
   Cancer Center Core Grant (P30 CA 008748).
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NR 83
TC 20
Z9 20
U1 0
U2 11
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 MAY
PY 2018
VL 6
IS 9
SI SI
AR 159
DI 10.21037/atm.2018.03.27
PG 10
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA GG5EO
UT WOS:000432718400002
PM 29911107
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Mattinzoli, D
   Cacioppo, M
   Ikehata, M
   Armelloni, S
   Al, CM
   Castellano, G
   Barilani, M
   Arcudi, F
   Messa, P
   Prato, M
AF Mattinzoli, Deborah
   Cacioppo, Michele
   Ikehata, Masami
   Armelloni, Silvia
   Al, Carlo Maria
   Castellano, Giuseppe
   Barilani, Mario
   Arcudi, Francesca
   Messa, Piergiorgio
   Prato, Maurizio
TI Carbon dots conjugated to SN38 for improved colorectal anticancer
   therapy
SO MATERIALS TODAY BIO
LA English
DT Article
DE Carbon dots; Colorectal cancer therapy; Drug delivery; SN38; Cell cycle;
   Extracellular matrix
ID EXTRACELLULAR-MATRIX; IRINOTECAN CPT-11; TOPOISOMERASE-I; DRUG-DELIVERY;
   CANCER; CDK7; SN-38; DIFFERENTIATION; NANOCARRIERS; INHIBITION
AB Irinotecan (CTP-11) is one of the standard therapies for colorectal cancer (CRC). CTP-11 is enzymatically con-verted to the hydrophobic 7-ethyl-10-hydroxycamptothecin (SN38), a one hundred-fold more active metabolite. Conjugation of hydrophobic anticancer drugs to nanomaterials is a strategy to improve their solubility, efficacy, and selectivity. Carbon dots (CDs) have garnered interest for their small sizes (<10 nm), low toxicity, high water solubility, and bright fluorescence. This paper describes the use of CDs to improve drug vehiculation, stability, and chemotherapeutic efficiency of SN38 through a direct intracellular uptake in CRC. The covalent conjugation of SN38 to CDs via a carbamate bond provides a CD-SN38 hybrid material for slow, sustained, and pH-responsive drug release. CD-SN38 successfully penetrates the CRC cells with a release in the nucleus affecting first the cell cycle and then the cytoskeleton. Moreover, CD-SN38 leads to a deregulation of the extracellular matrix (ECM), one of the major components of the cancer niche considered a possible target therapy for reducing the cancer progression. This work shows the combined therapeutic and imaging potential of CD-based hybrid materials for the treatment of CRC. Future efforts for targeted therapy of chronic diseases characterized by altered ECM deposition, such as chronic kidney disease and chronic allograft nephropathy in kidney transplant patients are envisaged.
C1 [Mattinzoli, Deborah; Ikehata, Masami; Armelloni, Silvia] Fdn IRCCS CaGranda Osped Maggiore Policlin, Renal Res Lab, Via Pace 9, I-20122 Milan, Italy.
   [Cacioppo, Michele; Arcudi, Francesca; Prato, Maurizio] Univ Trieste, Dept Chem & Pharmaceut Sci, INSTM UdR Trieste, Via Licio Giorgieri 1, I-34127 Trieste, Italy.
   [Cacioppo, Michele; Prato, Maurizio] Ctr Cooperat Res Biomat CIC BiomaGUNE, Basque Res & Technol Alliance BRTA, Paseo Miramon 182, San Sebastian 20014, Spain.
   [Al, Carlo Maria; Castellano, Giuseppe; Messa, Piergiorgio] Dialysis & Renal Transplant Fdn IRCCS CaGranda Osp, Unit Nephrol, Via Commenda 15, I-20122 Milan, Italy.
   [Al, Carlo Maria; Castellano, Giuseppe; Messa, Piergiorgio] Univ Study Milan, Via Festa Perdono 7, I-20122 Milan, Italy.
   [Barilani, Mario] Univ Milan, Dept Clin Sci & Community Hlth, EPIGET LAB, I-20122 Milan, Italy.
   [Barilani, Mario] Fdn IRCCS CaGranda Osped Maggiore Policlin, Dept Transfus Med & Hematol, Regenerat Med Lab, Cell Factory, I-20122 Milan, Italy.
   [Prato, Maurizio] Basque Fdn Sci, Ikerbasque, Bilbao 48013, Spain.
C3 IRCCS Ca Granda Ospedale Maggiore Policlinico; University of Trieste;
   CIC biomaGUNE; University of Milan; University of Milan; IRCCS Ca Granda
   Ospedale Maggiore Policlinico; Basque Foundation for Science
RP Mattinzoli, D (corresponding author), Fdn IRCCS CaGranda Osped Maggiore Policlin, Renal Res Lab, Via Pace 9, I-20122 Milan, Italy.; Arcudi, F; Prato, M (corresponding author), Univ Trieste, Dept Chem & Pharmaceut Sci, INSTM UdR Trieste, Via Licio Giorgieri 1, I-34127 Trieste, Italy.; Prato, M (corresponding author), Ctr Cooperat Res Biomat CIC BiomaGUNE, Basque Res & Technol Alliance BRTA, Paseo Miramon 182, San Sebastian 20014, Spain.; Al, CM (corresponding author), Dialysis & Renal Transplant Fdn IRCCS CaGranda Osp, Unit Nephrol, Via Commenda 15, I-20122 Milan, Italy.; Al, CM (corresponding author), Univ Study Milan, Via Festa Perdono 7, I-20122 Milan, Italy.; Prato, M (corresponding author), Basque Fdn Sci, Ikerbasque, Bilbao 48013, Spain.
EM deborah.mattinzoli@policlinico.mi.it; carlo.alfieri@policlinico.mi.it;
   francescarcudi@gmail.com; prato@units.it
RI Armelloni, Silvia/AAP-8617-2021; Mattinzoli, Deborah/AAP-9152-2021;
   Barilani, Mario/O-6575-2015; castellano, giuseppe/H-1626-2012; Arcudi,
   Francesca/AAP-5518-2020; Cacioppo, Michele/AAO-6405-2021; Alfieri,
   Carlo/Q-8959-2016
OI Cacioppo, Michele/0000-0002-5610-3397; Mattinzoli,
   Deborah/0000-0003-0478-022X; Alfieri, Carlo/0000-0003-3860-5219;
   Armelloni, Silvia/0000-0001-6431-2642
FU AXA Chair for Bionanotechnology [2016-2023]; European Research Council
   [885323]; Spanish Ministerio de Ciencia, Innovacion y Universidades
   [PID2019-108523RB-I00]; IRCCS Ospedale Maggiore Policlinico; University
   of Trieste; Italian Ministry of Education MIUR [2017PBXPN4]; Maria de
   Maeztu Units of Excellence Program from the Spanish State Research
   Agency [MDM-2017-0720]; INSTM; European Research Council (ERC) [885323]
   Funding Source: European Research Council (ERC)
FX M.P. is the AXA Chair for Bionanotechnology (2016-2023) . The au-thors
   gratefully acknowledge the financial support from the European Research
   Council (ERC AdG-2019 n 885323, e-DOTS) , the Spanish Ministerio de
   Ciencia, Innovacion y Universidades (project PID2019-108523RB-I00) ,
   IRCCS Ospedale Maggiore Policlinico, the University of Trieste, INSTM,
   Italian Ministry of Education MIUR (cofin Prot. 2017PBXPN4) and the
   Maria de Maeztu Units of Excellence Program from the Spanish State
   Research Agency (Grant No. MDM-2017-0720) . The authors thank Dr.
   Lukaorevic for fruitful discussions.
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NR 61
TC 9
Z9 9
U1 5
U2 32
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2590-0064
J9 MATER TODAY BIO
JI Mater. Today Bio
PD DEC
PY 2022
VL 16
AR 100286
DI 10.1016/j.mtbio.2022.100286
EA SEP 2022
PG 12
WC Engineering, Biomedical; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Materials Science
GA 5I2HK
UT WOS:000868184300004
PM 36186846
OA Green Published
DA 2025-01-04
ER

PT J
AU Griffith, A
   Sanoff, H
AF Griffith, Anna
   Sanoff, Hanna
TI Current Trends in Systemic Therapies in Elderly Patients With Metastatic
   Colorectal Cancer
SO CURRENT COLORECTAL CANCER REPORTS
LA English
DT Article
DE Metastatic colorectal cancer; Elderly; Targeted therapy; Systemic
   therapy; Comprehensive geriatric assessment
ID QUALITY-OF-LIFE; OPEN-LABEL; POOLED ANALYSIS; PLUS CAPECITABINE;
   1ST-LINE THERAPY; PHASE-III; CHEMOTHERAPY; BEVACIZUMAB; OXALIPLATIN;
   COMBINATION
AB Purpose of ReviewThe incidence of colorectal cancer increases with age and the population is aging, making treatment of elderly patients with metastatic colorectal cancer (mCRC) an increasingly common part of oncology practice. We review the literature regarding systemic treatment of colorectal cancer in the elderly population.Recent FindingsMost of the data for toxicity and efficacy of systemic therapies for mCRC in older patients comes from subgroup analysis of pooled phase II and III trials of both chemotherapy and targeted agents. These studies suggest that combination chemotherapy and targeted therapy are well-tolerated in fit elderly patients with slightly increased risk of toxicity.SummaryAssessment of functional status independent of age can help differentiate which patients are candidates for combination chemotherapy, single-agent chemotherapy, targeted therapy, or supportive care. Fit, elderly patients should be treated as younger patients. Dose-reduced doublet therapy with dose escalation as tolerated is a safe and effective way to treat less-fit elderly patients. Most targeted therapies appear to be safe in the elderly population without significant concerns for increased toxicity.
C1 [Griffith, Anna; Sanoff, Hanna] UNC Hosp, Hematol Oncol, Phys Off Bldg,170 Manning Dr,3rd Floor, Chapel Hill, NC 27599 USA.
C3 University of North Carolina; University of North Carolina Chapel Hill;
   University North Carolina Hospital
RP Griffith, A (corresponding author), UNC Hosp, Hematol Oncol, Phys Off Bldg,170 Manning Dr,3rd Floor, Chapel Hill, NC 27599 USA.
EM anna.griffith@unchealth.unc.edu
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NR 31
TC 1
Z9 1
U1 0
U2 5
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 AUG
PY 2019
VL 15
IS 4
BP 105
EP 111
DI 10.1007/s11888-019-00436-0
PG 7
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA IL8ZP
UT WOS:000477575300001
DA 2025-01-04
ER

PT J
AU Li, D
   Jin, H
   Liu, Y
   Liu, JY
   Zhang, X
   Wang, L
   Fan, ZS
   Feng, L
   Zuo, J
   Han, J
   Wang, YD
AF Li, Dan
   Jin, Hui
   Liu, Yan
   Liu, Jiayin
   Zhang, Xue
   Wang, Long
   Fan, Zhisong
   Feng, Li
   Zuo, Jing
   Han, Jing
   Wang, Yudong
TI Identification of beneficial populations for targeted-immunotherapy
   combinations: tailoring later-line care for patients with pMMR/MSS
   metastatic colorectal cancer
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE microsatellite stable metastatic colorectal cancer; third-line or
   beyond; real-world; targeted-immunotherapy combination; beneficial
   population
ID LIVER METASTASIS; DOUBLE-BLIND; PLACEBO; MULTICENTER; FRUQUINTINIB;
   TRIAL; PLUS
AB Objective This study explores the benefits of targeted-immunotherapy combination in third-line or beyond treatment for microsatellite stable (MSS) metastatic colorectal cancer (mCRC) in a real-world setting.Methods Patients with MSS mCRC who were treated with either a targeted-immunotherapy combination or targeted therapy alone in the third-line or beyond setting at our hospital from August 2018 to August 2022 were included in the study. Inclusion criteria comprised patients treated with targeted therapy alone or in combination with immunotherapy. Effectiveness was compared between treatments, and patients with the potential to benefit from targeted-immunotherapy combination were identified.Results Among 71 patients, 31 received targeted therapies alone (TT group) and 40 received a combination of targeted therapy and immunotherapy (TI group). The TI group had higher objective response rates (20% vs 3.2%) and disease control rates (82.5% vs 58.1%). The median progression-free survival was significantly better in the TI group (4.6 vs 4.1 months, P = 0.027). Liver metastasis was associated with poor prognosis, while patients with only lung metastases had the longest median progression-free survival of 12.3 months with combination therapy.Conclusion The study indicates that targeted-immunotherapy combination offers more benefits than targeted therapy alone for MSS mCRC in the third-line or beyond setting.
C1 [Li, Dan; Jin, Hui; Liu, Yan; Liu, Jiayin; Zhang, Xue; Wang, Long; Fan, Zhisong; Feng, Li; Zuo, Jing; Han, Jing; Wang, Yudong] Hebei Med Univ, Hosp 4, Dept Med Oncol, Shijiazhuang, Peoples R China.
C3 Hebei Medical University
RP Wang, YD (corresponding author), Hebei Med Univ, Hosp 4, Dept Med Oncol, Shijiazhuang, Peoples R China.
EM wyd_999@hebmu.edu.cn
RI Fan, Zhisong/AAH-9736-2019; Wang, Yudong/JEZ-9111-2023
FX The author(s) declare that no financial support was received for the
   research, authorship, and/or publication of this article.
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NR 34
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 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD OCT 24
PY 2024
VL 15
AR 1462346
DI 10.3389/fimmu.2024.1462346
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA L1Q0Y
UT WOS:001348526700001
PM 39512338
OA gold
DA 2025-01-04
ER

PT J
AU Xu, WD
   Jing, HY
   Zhang, FL
AF Xu, WeiDong
   Jing, HuaYong
   Zhang, FuLi
TI Epidermal growth factor receptor-targeted therapy in colorectal cancer
SO FRONTIERS IN BIOSCIENCE-LANDMARK
LA English
DT Article
DE Cetuximab; Panitumumab; Colorectal Cancer; Review
ID HUMAN COLON-CANCER; 1ST-LINE TREATMENT; LIVER METASTASES;
   GENE-EXPRESSION; CETUXIMAB; PANITUMUMAB; ACTIVATION; OXALIPLATIN; CELLS;
   FLUOROURACIL
AB The epidermal growth factor receptor (EGFR) family plays an important role in colorectal cancer (CRC). EGFR participates in the key process of tumorigenesis and invasion, and its expression correlates with the prognosis of CRC. EGFR-targeted therapy has been widely utilized in stage III and IV CRC. The EGFR antibodies, cetuximab and panitumumab, are widely used in treatment of CRC. There are clinical trials and in vivo studies being carried out on the efficacy and mechanism of their action in CRC treatment. In this review, we will describe the EGFR-targeted therapy used in CRC, focusing on the efficacy and mechanisms of the most commonly used EGFR antibodies, cetuximab and panitumumab.
C1 [Xu, WeiDong; Jing, HuaYong; Zhang, FuLi] Beijing PLA, Mil Gen Hosp, Dept Radiat Oncol, 5 Nanmencang, Beijing 100700, Peoples R China.
RP Xu, WD (corresponding author), Beijing PLA, Mil Gen Hosp, Dept Radiat Oncol, 5 Nanmencang, Beijing 100700, Peoples R China.
EM xwddc@21cn.com
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NR 78
TC 10
Z9 10
U1 1
U2 15
PU IMR PRESS
PI ROBINSON
PA 112 ROBINSON RD, ROBINSON, SINGAPORE
SN 2768-6701
EI 2768-6698
J9 FRONT BIOSCI-LANDMRK
JI Front. Biosci.
PD JAN 1
PY 2016
VL 21
BP 410
EP 418
DI 10.2741/4397
PG 9
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA DC2WD
UT WOS:000369078400012
PM 26709782
OA Bronze
DA 2025-01-04
ER

PT J
AU Li, R
   Wu, YY
   Li, Y
   Shuai, W
   Wang, AX
   Zhu, YM
   Hu, XY
   Xia, Y
   Ouyang, L
   Wang, G
AF Li, Ru
   Wu, Yongya
   Li, Yan
   Shuai, Wen
   Wang, Aoxue
   Zhu, Yumeng
   Hu, Xiuying
   Xia, Yong
   Ouyang, Liang
   Wang, Guan
TI Targeted regulated cell death with small molecule compounds in
   colorectal cancer: Current perspectives of targeted therapy and
   molecular mechanisms
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE Colorectal cancer; Targeted therapy; Regulated cell death;
   Small-molecule compounds
ID SIGNALING PATHWAY; APOPTOSIS; GROWTH; COPPER; FERROPTOSIS; RESISTANCE;
   INHIBITOR; AUTOPHAGY; CASPASES; PROTEINS
AB Colorectal cancer (CRC), a tumor of the digestive system, is characterized by high malignancy and poor prognosis. Currently, targeted therapy of CRC is far away from satisfying. The molecular mechanisms of regulated cell death (RCD) have been clearly elucidated, which can be intervened by drug or genetic modification. Numerous studies have provided substantial evidence linking these mechanisms to the progression and treatment of CRC. The RCD includes apoptosis, autophagy-dependent cell death (ADCD), ferroptosis, necroptosis, and pyroptosis, and immunogenic cell death, etc, which provide potential targets for anti-cancer treatment. For the last several years, small-molecule compounds targeting RCD have been a well concerned therapeutic strategy for CRC. This present review aims to describe the function of small-molecule compounds in the targeted therapy of CRC via targeting apoptosis, ADCD, ferroptosis, necroptosis, immunogenic dell death and pyroptosis, and their mechanisms. In addition, we prospect the application of newly discovered cuproptosis and disulfidptosis in CRC. Our review may provide references for the targeted therapy of CRC using small-molecule compounds targeting RCD, including the potential targets and candidate compounds.
C1 [Li, Ru; Wu, Yongya; Li, Yan; Shuai, Wen; Wang, Aoxue; Zhu, Yumeng; Hu, Xiuying; Xia, Yong; Ouyang, Liang; Wang, Guan] Sichuan Univ, West China Hosp, Innovat Ctr Nursing Res, West China Sch Nursing,Nursing Key Lab Sichuan Pro, Chengdu 610041, Peoples R China.
   [Li, Ru; Wu, Yongya; Li, Yan; Shuai, Wen; Wang, Aoxue; Zhu, Yumeng; Hu, Xiuying; Xia, Yong; Ouyang, Liang; Wang, Guan] Sichuan Univ, West China Hosp, Canc Ctr, West China Sch Nursing,Management Dept Sci Res Lab, Chengdu 610041, Peoples R China.
   [Xia, Yong] Sichuan Univ, West China Hosp, Rehabil Med Ctr, Dept Rehabil Med, Chengdu 610041, Peoples R China.
   [Xia, Yong] Rehabil Med Res Inst, Key Lab Rehabil Med Sichuan Prov, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University
RP Xia, Y; Ouyang, L; Wang, G (corresponding author), Sichuan Univ, West China Hosp, Innovat Ctr Nursing Res, West China Sch Nursing,Nursing Key Lab Sichuan Pro, Chengdu 610041, Peoples R China.; Xia, Y; Ouyang, L; Wang, G (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, West China Sch Nursing,Management Dept Sci Res Lab, Chengdu 610041, Peoples R China.
EM yxia4@scu.edu.cn; ouyangliang@scu.edu.cn; guan8079@163.com
FU National Natural Science Foundation of China [22177083]; Sichuan Science
   and Technology Program [2022NSFSC1290]; The 1.3.5 project for
   disciplines of excellence-Clinical Research Incubation Project, West
   China Hospital, Sichuan University [ZYJC21016]; West China Nursing
   Discipline Development Special Fund Project, Sichuan University
   [HXHL21011]
FX This work was supported by grants from the National Natural Science
   Foundation of China (Grant 22177083) , Sichuan Science and Technology
   Program (Grant 2022NSFSC1290) , 1.3.5 project for disciplines of
   excellence-Clinical Research Incubation Project, West China Hospital,
   Sichuan University (ZYJC21016) , and West China Nursing Discipline
   Development Special Fund Project, Sichuan University (Grant HXHL21011) .
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NR 172
TC 5
Z9 5
U1 7
U2 25
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0223-5234
EI 1768-3254
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD FEB 5
PY 2024
VL 265
AR 116040
DI 10.1016/j.ejmech.2023.116040
EA DEC 2023
PG 25
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FI8S8
UT WOS:001145230000001
PM 38142509
DA 2025-01-04
ER

PT J
AU Mele, L
   del Vecchio, V
   Liccardo, D
   Prisco, C
   Schwerdtfeger, M
   Robinson, N
   Desiderio, V
   Tirino, V
   Papaccio, G
   La Noce, M
AF Mele, Luigi
   del Vecchio, Vitale
   Liccardo, Davide
   Prisco, Claudia
   Schwerdtfeger, Melanie
   Robinson, Nirmal
   Desiderio, Vincenzo
   Tirino, Virginia
   Papaccio, Gianpaolo
   La Noce, Marcella
TI The role of autophagy in resistance to targeted therapies
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE Autophagy; Drug resistance; Monoclonal antibodies; Targeted therapy;
   Tyrosine kinase inhibitors
ID ENDOPLASMIC-RETICULUM STRESS; SMALL-MOLECULE INHIBITORS; CHRONIC
   MYELOID-LEUKEMIA; PROSTATE-CANCER CELLS; BREAST-CANCER;
   HEPATOCELLULAR-CARCINOMA; MONOCLONAL-ANTIBODY; ANTITUMOR-ACTIVITY;
   COLORECTAL-CANCER; ER STRESS
AB Autophagy is a self-degradative cellular process, involved in stress response such as starvation, hypoxia, and oxidative stress. This mechanism balances macro-molecule recycling to regulate cell homeostasis. In cancer, autophagy play a role in the development and progression, while several studies describe it as one of the key processes in drug resistance. In the last years, in addition to standard anti-cancer treatments such as chemotherapies and irradiation, targeted therapy became one of the most adopted strategies in clinical practices, mainly due to high specificity and reduced side effects. However, similar to standard treatments, drug resistance is the main challenge in most patients. Here, we summarize recent studies that investigated the role of autophagy in drug resistance after targeted therapy in different types of cancers. We highlight positive results and limitations of pre-clinical and clinical studies in which autophagy inhibitors are used in combination with targeted therapies.
C1 [Mele, Luigi; del Vecchio, Vitale; Liccardo, Davide; Prisco, Claudia; Schwerdtfeger, Melanie; Desiderio, Vincenzo; Tirino, Virginia; Papaccio, Gianpaolo; La Noce, Marcella] Univ Campania L Vanvitelli Naples, Dept Expt Med, Naples, Italy.
   [Prisco, Claudia] Nottingham Trent Univ, Sch Sci & Technol, John van Geest Canc Res Ctr, Clifton Lane, Nottingham NG11 8NS, England.
   [Schwerdtfeger, Melanie] Univ Munich, Dept Med 4, Div Clin Pharmacol, Munich, Germany.
   [Robinson, Nirmal] SA Pathol, Ctr Canc Biol, GPO Box 2471, Adelaide, SA, Australia.
   [Robinson, Nirmal] Univ South Australia, GPO Box 2471, Adelaide, SA, Australia.
C3 Universita della Campania Vanvitelli; Nottingham Trent University;
   University of Munich; Centre for Cancer Biology; SA Pathology;
   University of South Australia
RP Papaccio, G (corresponding author), Dept Expt Med, Via L Armanni 5, I-80128 Naples, Italy.
EM gianpaolo.papaccio@unicampania.it
RI Mele, Luigi/AAC-9887-2019; desiderio, vincenzo/K-4244-2018; Robinson,
   Nirmal/AAJ-1996-2020; Del+Vecchio, Vitale/ACN-3410-2022; La Noce,
   Marcella/AAM-1750-2021; Papaccio, Gianpaolo/B-7150-2014
OI Mele, Luigi/0000-0002-6008-0802; La Noce, Marcella/0000-0002-8782-3821;
   Robinson, Nirmal/0000-0002-7361-9491; DEL VECCHIO,
   VITALE/0000-0002-7323-4444; Schwerdtfeger, Melanie/0000-0001-8193-3328;
   Papaccio, Gianpaolo/0000-0002-4014-5306
FU University of Campania "Luigi Vanvitelli" (Naples, Italy)
FX The costs of the open access publication were supported by the
   "Programma Valere 2020" of the University of Campania "Luigi Vanvitelli"
   (Naples, Italy).
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NR 139
TC 112
Z9 116
U1 0
U2 25
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0305-7372
EI 1532-1967
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD AUG
PY 2020
VL 88
AR 102043
DI 10.1016/j.ctrv.2020.102043
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MM6HO
UT WOS:000550255600007
PM 32505806
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Tong, GL
   Luo, QJ
   Pang, XH
   Chen, BR
   Lv, GQ
   Li, X
   Wang, SB
AF Tong, Gangling
   Luo, Qianjiang
   Pang, Xionghao
   Chen, Boran
   Lv, Guoqing
   Li, Xi
   Wang, Shubin
TI Retrospective Analyses of Complete Resection Combined with Systemic
   Chemotherapy and Targeted Therapy for Patients with Ovarian Metastases
   from Colorectal Cancer
SO CANCER BIOTHERAPY AND RADIOPHARMACEUTICALS
LA English
DT Article
DE chemotherapy; colorectal cancer; ovarian metastases; surgery
ID IMPACT
AB Background: The aim of the study is to evaluate clinical outcomes of patients with ovarian metastases from colorectal cancer (OM-CRC) treated with complete resection combined with chemotherapy and targeted therapy.
   Methods: Fifty female patients with OM-CRC who were treated in two different hospitals were categorized into three groups: 14 patients with OM-CRC received resection and chemotherapy combined with targeted therapy, 16 patients with OM-CRC only received chemotherapy combined with targeted therapy, and 20 patients with non-OM-CRC (NOM-CRC) received chemotherapy combined with targeted therapy. The primary outcomes, including overall survival (OS), the objective response rate (ORR), disease control rate (DCR), safety, and progression-free survival (PFS), were observed.
   Results: The ORR of OM-CRC was significantly lower compared with NOM-CRC (36.7% vs. 70.0%, p = 0.021), and the DCR of OM-CRC was also lower compared with NOM-CRC (76.7% vs. 90.0%, p = 0.229). The following chemotherapy and targeted therapy in the additional surgical resection of OM-CRC were positively associated with longer PFS and OS compared to no surgical resection (9.0 vs. 6.0 months and 21.0 vs. 15.0 months, respectively, p < 0.001), but the PFS and OS were best in patients with NOM-CRC (9.0 and 35.0 months). Improved OS was associated with R0 resection (23.0 vs. 17.0 months, p < 0.001). Multivariate analysis indicated that patients with well-differentiated pathology and unilateral ovarian metastasis had a better prognosis.
   Conclusion: Multidisciplinary treatment strategy, including systemic chemotherapy, targeted therapy, and complete surgery, may contribute to the prolongation of OS and be safe for treatment of OM-CRC.
C1 [Tong, Gangling; Chen, Boran; Lv, Guoqing; Wang, Shubin] Peking Univ, Dept Oncol, Shenzhen Hosp, Lianhua Rd North, Shenzhen 518036, Peoples R China.
   [Tong, Gangling; Chen, Boran; Lv, Guoqing; Wang, Shubin] Canc Inst Shenzhen PKU HKUST Med Ctr, Shenzhen Key Lab Gastrointestinal Canc Translat R, Shenzhen, Peoples R China.
   [Luo, Qianjiang; Li, Xi] Peking Univ, Dept Gastroenterol, Shenzhen Hosp, Lianhua Rd North, Shenzhen 518036, Peoples R China.
   [Pang, Xionghao] Shenzhen Second Peoples Hosp, Dept Oncol, Shenzhen, Peoples R China.
C3 Peking University; Peking University; Second People's Hospital of
   Shenzhen
RP Wang, SB (corresponding author), Peking Univ, Dept Oncol, Shenzhen Hosp, Lianhua Rd North, Shenzhen 518036, Peoples R China.; Li, X (corresponding author), Peking Univ, Dept Gastroenterol, Shenzhen Hosp, Lianhua Rd North, Shenzhen 518036, Peoples R China.
EM xili256@yeah.net; wangshubin2013@163.com
FU Shenzhen Sanming Project of Medicine [SZSM201612041]; Shenzhen Science
   and Technology Innovation Commission [JCYJ20190809100005672,
   GJHZ20180420180754917, ZDSYS20190902092855097]
FX This work was supported by Shenzhen Sanming Project of Medicine
   (No.SZSM201612041) and Shenzhen Science and Technology Innovation
   Commission (JCYJ201908091 00005672, GJHZ20180420180754917, and
   ZDSYS2019090 2092855097).
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NR 22
TC 3
Z9 3
U1 0
U2 15
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1084-9785
EI 1557-8852
J9 CANCER BIOTHER RADIO
JI Cancer Biother. Radiopharm.
PD SEP 1
PY 2022
VL 37
IS 7
BP 553
EP 559
DI 10.1089/cbr.2020.4013
EA MAR 2021
PG 7
WC Oncology; Medicine, Research & Experimental; Pharmacology & Pharmacy;
   Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine; Pharmacology & Pharmacy;
   Radiology, Nuclear Medicine & Medical Imaging
GA 6R2GD
UT WOS:000634742800001
PM 33764806
DA 2025-01-04
ER

PT J
AU Huang, JB
   Luo, QQ
   Xiao, Y
   Li, HY
   Kong, LQ
   Ren, GS
AF Huang, Jianbo
   Luo, Qingqing
   Xiao, Yun
   Li, Hongyuan
   Kong, Lingquan
   Ren, Guosheng
TI The implication from RAS/RAF/ERK signaling pathway increased activation
   in epirubicin treated triple negative breast cancer
SO ONCOTARGET
LA English
DT Article
DE TNBC; RAS/RAF/ERK signaling pathway; GSEA; epirubicin; targeting therapy
ID OPEN-LABEL; COLORECTAL-CANCER; MEK1/2 INHIBITOR; DRUG-RESISTANCE;
   PHASE-3 TRIAL; SELUMETINIB; MULTICENTER; ARRY-142886; METASTASIS;
   TRAMETINIB
AB Background: Triple negative breast cancer (TNBC) is not sensitive to RAS/RAF/ERK signaling pathway (ERK pathway) targeting therapy, due to the absence of excessive activation of ERK pathway. However, the kinase cascades might be activated after chemotherapy in TNBC. Here we aimed to predict whether ERK pathway targeting therapy could be used as an adjuvant therapy in TNBC.
   Methods: Within online GEO datasets (GSE43816 and GSE54326), gene set enrichment analysis (GSEA) was performed to detect molecular changes in epirubicin treated TNBC samples and cells, ERK pathway components and regulation genes changes were included.
   Results: In epirubicin treated TNBC samples and cells, we found ERK pathway components (eg. MAPK13, MAP3K1, MAPK12, MAPK11 and MAPKAPK3) were obviously enriched, also, expression of ERK pathway positive regulation genes significantly increased (P<0.05) and negative regulation genes decreased (P<0.05) in epirubicin resistant cells. Moreover, phosphorylated ERK levels were significantly elevated in MDA-MB-231 cells after epirubicin treatment.
   Conclusion: ERK signaling pathway was more activated in epirubicin treated TNBC, possibly contributing to the epirubicin resistance in TNBC, it implicated that ERK pathway could be used as an novel candidate for targeting therapy in refractory and relapse TNBC.
C1 [Huang, Jianbo; Luo, Qingqing; Li, Hongyuan; Kong, Lingquan; Ren, Guosheng] Chongqing Med Univ, Dept Endocrine & Breast Surg, Affiliated Hosp 1, Chongqing 400016, Peoples R China.
   [Xiao, Yun] Chongqing Med Univ, Dept Oncol, Yongchuan Hosp, Chongqing 402160, Peoples R China.
C3 Chongqing Medical University; Chongqing Medical University
RP Kong, LQ; Ren, GS (corresponding author), Chongqing Med Univ, Dept Endocrine & Breast Surg, Affiliated Hosp 1, Chongqing 400016, Peoples R China.
EM huihuikp@163.com; rengs726@126.com
OI Kong, Ling-quan/0000-0001-5705-9001; Huang, Jianbo/0000-0002-1662-2969
FU National Natural Science Foundation of China [31171243]
FX This work was supported by research grants from National Natural Science
   Foundation of China (31171243 to GS.R.).
CR [Anonymous], CLIN LYMPHOMA MYELOM
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NR 21
TC 20
Z9 20
U1 0
U2 15
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 8
PY 2017
VL 8
IS 64
BP 108249
EP 108260
DI 10.18632/oncotarget.22604
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FS1UR
UT WOS:000419564600070
PM 29296238
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Liu, GW
   Liu, JW
   Ren, WD
   Yang, LS
   Guo, QJ
   Ye, HP
AF Liu, Guiwei
   Liu, Jiawei
   Ren, Weidan
   Yang, Lisheng
   Guo, Qingjin
   Ye, Haopeng
TI Effects of natural orifice transluminal endoscopic radical resection of
   the colon and targeted therapy on immune response and blood CA199 and
   CA242 levels in colorectal cancer
SO MEDICINE
LA English
DT Article
DE colorectal cancer; immune function; natural orifice specimen extraction;
   targeted therapy
ID SURGERY
AB To examine the effect of natural orifice transluminal endoscopic radical resection combined with targeted therapy on the immune system and serum levels of CA199 and CA242 in individuals with colorectal cancer. We enrolled 90 patients admitted to our hospital with a diagnosis of colorectal cancer between February 2020 and May 2022 and divided them into 2 groups according to the treatment methods: observation group (n = 45) and control group (n = 45). Patients in the control group underwent conventional laparoscopic radical resection of the colon followed by targeted therapy, whereas those in the observation group underwent natural orifice transluminal endoscopic radical resection of the colon and targeted therapy. Serum CA199 and CA242 levels, incidence of adverse events, clinical efficacy, perioperative indicators, and immune function indicators were compared between the 2 groups. The objective response rate (ORR) and disease control rate (DCR) were significantly higher in the observation group than in the control group (60.00% vs 35.6%, P = .020, and 91.1% vs 64.44%, P = .002, respectively). Compared with the control group, the observation group was associated with less blood loss (P = .003), shorter operation time (P = .011), shorter first exhaust time (P = .042), shorter borborygmus recovery time (P = .042), and shorter length of hospital stay (P = .020). After treatment, the CD3 + (P = .020), CD4 + (P = .008), and CD4+/CD8 + (P = .035) counts were lower, whereas the IgG (P = .014), IgM (P = .019), and IgA (P = .038) counts were higher in the observation group than in the control group. CA199 (P = .009) and CA242 (P = .001) levels were lower in the observation group than in the control group. The groups did not differ significantly in the incidence of adverse events (P = .842). The combination of natural orifice transluminal endoscopic radical resection for colorectal cancer and targeted therapy can shorten hospital stay, improve immune function, lower serum levels of CA199 and CA242, and exhibit good clinical efficacy.
C1 [Liu, Guiwei; Liu, Jiawei; Ren, Weidan; Yang, Lisheng; Guo, Qingjin; Ye, Haopeng] Hebei Cangzhou Cent Hosp, Dept Anorectal Surg, Cangzhou, Hebei, Peoples R China.
   [Liu, Guiwei] Hebei Cangzhou Cent Hosp, Dept Anorectal Surg, Cangzhou 061000, Hebei, Peoples R China.
RP Liu, GW (corresponding author), Hebei Cangzhou Cent Hosp, Dept Anorectal Surg, Cangzhou 061000, Hebei, Peoples R China.
EM lgwcz1226@163.com; lgwcz1226@163.com; 1033806535@qq.com;
   1722886484@qq.com; 11886484@qq.com; 2658633458@qq.com
CR Bokor A, 2018, J MINIM INVAS GYN, V25, P1065, DOI 10.1016/j.jmig.2018.02.006
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NR 22
TC 0
Z9 0
U1 0
U2 0
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 NOV 24
PY 2023
VL 102
IS 47
AR e35949
DI 10.1097/MD.0000000000035949
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA AD3Z5
UT WOS:001116496400073
PM 38013346
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Guadagni, S
   Clementi, M
   Bencivenga, M
   Kusamura, S
   Fiorentini, C
   Masedu, F
AF Guadagni, Stefano
   Clementi, Marco
   Bencivenga, Maria
   Kusamura, Shigeki
   Fiorentini, Caterina
   Masedu, Francesco
TI Palliation with a multimodality treatment including hypoxic pelvic
   perfusion for unresectable recurrent rectal cancer: outcomes based on a
   retrospective study
SO UPDATES IN SURGERY
LA English
DT Article
DE Unresectable recurrent rectal cancer; Hypoxic pelvic perfusion;
   Mitomycin C; Cetuximab
ID LOCALLY RECURRENT; COLORECTAL-CANCER; LIVER METASTASES; MITOMYCIN-C;
   REIRRADIATION; TUMORS
AB Patients with unresectable recurrent rectal cancer that progresses after systemic chemotherapy and radiotherapy are candidates for palliation with hypoxic pelvic perfusion (HPP). The aim of this observational retrospective study was to evaluate if a multimodality treatment including HPP and targeted-therapy may be useful to prolong clinical responses and survival of these patients. From a cohort of 77 patients with unresectable recurrent rectal cancer in progression after standard treatments and submitted to HPP, 21 patients underwent repeat HPP using mitomycin C (MMC) at the dose of 25mg/m(2). After the last HPP, 7 patients received a targeted-therapy with cetuximab according to overexpression of epidermal growth factor receptor in recurrence cancer cells. The median overall survival of these 21 patients from the diagnosis of unresectable recurrent rectal cancer was 23months (iqr 18-24). After the first HPP, the median survival of the 21 patients until death or end of follow-up was 10months (iqr 9-13). The 1-year and 2-year survival rates were 71.4%, and 4.8%, respectively. From the first HPP, age>60years, a recurrence shrinkage of at least 30% (partial response), and the addition of a post-HPP targeted-therapy with cetuximab significantly affected survival (P<0.04). In conclusion, repeated MMC-HPP followed by targeted-therapy seems to be an effective palliative treatment for patients with unresectable recurrent rectal cancer in progression after systemic chemotherapy and radiation but the results of this study have to be confirmed by a larger phase III trial.
C1 [Guadagni, Stefano] Univ Aquila, Sect Gen Surg, Dept Appl Clin Sci & Biotechnol, Via Vetoio, I-67100 Laquila, Italy.
   [Clementi, Marco] Univ Aquila, Dept Life Hlth & Environm Sci, I-67100 Laquila, Italy.
   [Bencivenga, Maria] Univ Verona, Gen & Upper GI Surg Div, Piazzale Aristide Stefani 1, I-37126 Verona, Italy.
   [Kusamura, Shigeki] Fdn IRCCS, Ist Nazl Tumori Milano, Via Venezian 1, I-20133 Milan, Italy.
   [Fiorentini, Caterina] Univ Siena, Dept Med Biotechnol, Div Cardiol, I-53100 Siena, Italy.
   [Masedu, Francesco] Univ Aquila, Dept Appl Clin Sci & Biotechnol, I-67100 Laquila, Italy.
C3 University of L'Aquila; University of L'Aquila; University of Verona;
   Fondazione IRCCS Istituto Nazionale Tumori Milan; University of Siena;
   University of L'Aquila
RP Guadagni, S (corresponding author), Univ Aquila, Sect Gen Surg, Dept Appl Clin Sci & Biotechnol, Via Vetoio, I-67100 Laquila, Italy.
EM stefano.guadagni@univaq.it; marco.clementi@univaq.it;
   maria.benci@hotmail.it; shigeki.kusamura@istitutotumori.mi.it;
   caterina.fiorentini2891@gmail.com; francesco.masedu@cc.univaq.it
RI Kusamura, Shigeki/J-1868-2017; Bencivenga, Maria/AAR-1122-2020;
   Guadagni, Stefano/P-6471-2016; MASEDU, Francesco/M-2989-2015; Clementi,
   Marco/P-8582-2016
OI Guadagni, Stefano/0000-0001-8525-084X; MASEDU,
   Francesco/0000-0003-0290-5324; Clementi, Marco/0000-0002-9652-5148
CR Begossi G, 2008, SURG ONCOL CLIN N AM, V17, P825, DOI 10.1016/j.soc.2008.04.014
   Eisenhauer EA, 2009, EUR J CANCER, V45, P228, DOI 10.1016/j.ejca.2008.10.026
   Fiorentini G, 2004, J CHEMOTHERAPY, V16, P51, DOI 10.1080/1120009X.2004.11782385
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NR 16
TC 3
Z9 3
U1 0
U2 1
PU SPRINGER-VERLAG ITALIA SRL
PI MILAN
PA VIA DECEMBRIO, 28, MILAN, 20137, ITALY
SN 2038-131X
EI 2038-3312
J9 UPDATES SURG
JI Updates Surg.
PD DEC
PY 2018
VL 70
IS 4
BP 441
EP 447
DI 10.1007/s13304-018-0592-7
PG 7
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA HA5GZ
UT WOS:000450299500004
PM 30191532
DA 2025-01-04
ER

PT J
AU Cepero, A
   Luque, C
   Cabeza, L
   Perazzoli, G
   Quiñonero, F
   Mesas, C
   Melguizo, C
   Prados, J
AF Cepero, Ana
   Luque, Cristina
   Cabeza, Laura
   Perazzoli, Gloria
   Quinonero, Francisco
   Mesas, Cristina
   Melguizo, Consolacion
   Prados, Jose
TI Antibody-Functionalized Nanoformulations for Targeted Therapy of
   Colorectal Cancer: A Systematic Review
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Review
DE nanoformulation; colon carcinoma; monoclonal antibody; 5-fluorouracil;
   targeted therapy
ID MONOCLONAL-ANTIBODY; DRUG-DELIVERY; GOLD-NANOPARTICLES; CELLS;
   IMMUNOLIPOSOMES; OXALIPLATIN; EFFICACY; 5-FLUOROURACIL; LIPOSOMES
AB The failure of chemotherapeutic treatment in colorectal cancer (CRC), the second most mortal cancer worldwide, is associated with several drug limitations, such as non-selective distribution, short half-life, and development of multiple resistances. One of the most promising strategies in CRC therapy is the development of delivery systems based on nanomaterials that can transport antitumor agents to the tumor site more efficiently, increasing accumulation within the tumor and thus the antitumor effect. In addition to taking advantage of the increased permeability and retention effect (EPR) of solid tumors, these nanoformulations can be conjugated with monoclonal antibodies that recognize molecular markers that are specifically over-expressed on CRC cells. Active targeting of nanoformulations reduces the adverse effects associated with the cytotoxic activity of drugs in healthy tissues, which will be of interest for improving the quality of life of cancer patients in the future. This review focuses on in vitro and in vivo studies of drug delivery nanoformulations functionalized with monoclonal antibodies for targeted therapy of CRC.
C1 [Cepero, Ana; Luque, Cristina; Cabeza, Laura; Perazzoli, Gloria; Quinonero, Francisco; Mesas, Cristina; Melguizo, Consolacion; Prados, Jose] Univ Granada, Ctr Biomed Res CIBM, Inst Biopathol & Regenerat Med IBIMER, Granada 18100, Spain.
   [Cepero, Ana; Luque, Cristina; Cabeza, Laura; Perazzoli, Gloria; Quinonero, Francisco; Mesas, Cristina; Melguizo, Consolacion; Prados, Jose] Univ Granada, Fac Med, Dept Anat & Embryol, Granada 18071, Spain.
   [Cepero, Ana; Luque, Cristina; Cabeza, Laura; Quinonero, Francisco; Mesas, Cristina; Melguizo, Consolacion; Prados, Jose] SAS Univ Granada, Biosanit Inst Granada Ibs GRANADA, Granada 18014, Spain.
C3 University of Granada; University of Granada; Instituto de Investigacion
   Biosanitaria IBS Granada; University of Granada
RP Melguizo, C (corresponding author), Univ Granada, Ctr Biomed Res CIBM, Inst Biopathol & Regenerat Med IBIMER, Granada 18100, Spain.
EM melguizo@ugr.es
RI Mesas, Cristina/AAO-3126-2021; Cepero, Ana/HKV-1390-2023; Perazzoli,
   Gloria/AAI-7350-2020; Quinonero Munoz, Francisco Jose/T-3165-2018;
   Melguizo Alonso, Consolacion/E-9842-2016; Prados, Jose/J-7116-2017
OI Quinonero Munoz, Francisco Jose/0000-0002-9087-8161; Mesas,
   Cristina/0000-0001-6369-5485; Luque Uceda, Cristina/0000-0002-5269-8215;
   Melguizo Alonso, Consolacion/0000-0003-3990-806X; Cepero Martin,
   Ana/0000-0002-0242-5059; Prados, Jose/0000-0003-4303-7746
FU Ministerio de Educacion y Formacion Profesional (Spain) [FPU17/02977,
   FPU19/04112]; Ministerio de Ciencia, Innovacion y Universidades (Spain)
   [PI20-00284]; Junta de Andalucia [A-CTS-666-UGR20, P20_00540,
   B-CTS-122-UGR20, PYC20-RE-035 UGR]; FEDER program; Instituto de Salud
   Carlos III [PI19/01478-FEDER]
FX A.C. and F.Q. to acknowledge FPU2017 and FPU2019 grants (ref.
   FPU17/02977 and FPU19/04112) from the Ministerio de Educacion y
   Formacion Profesional (Spain) and C.L. a P-FIS (ref. PI20-00284) from
   the Ministerio de Ciencia, Innovacion y Universidades (Spain). This
   research was funded in part by Junta de Andalucia (A-CTS-666-UGR20,
   P20_00540, B-CTS-122-UGR20 and PYC20-RE-035 UGR) FEDER program and
   Instituto de Salud Carlos III(PI19/01478-FEDER).
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NR 86
TC 3
Z9 3
U1 3
U2 20
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 2022
VL 17
BP 5065
EP 5080
DI 10.2147/IJN.S368814
PG 16
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA 6A1QO
UT WOS:000880435800001
PM 36345508
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yang, L
   Atakhanova, N
   Arellano, MTC
   Mohamed, MY
   Hani, T
   Fahdil, AA
   Castillo-Acobo, RY
   Juyal, A
   Hussein, AK
   Amin, AH
   Pecho, RDC
   Akhavan-Sigari, R
AF Yang, Lei
   Atakhanova, Nigora
   Arellano, Meryelem Tania Churampi
   Mohamed, Mohammed Yassen
   Hani, Thamer
   Fahdil, Ali A.
   Castillo-Acobo, Roxana Yolanda
   Juyal, Ashima
   Hussein, Ahlam Kadhim
   Amin, Ali H.
   Pecho, Renzon Daniel Cosme
   Akhavan-Sigari, Reza
TI Translational research of new developments in targeted therapy of
   colorectal cancer
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Review
DE Colorectal cancer; Targeted therapies; Small molecule inhibitors;
   Monoclonal antibodies; CAR-T cells
ID ENDOTHELIAL GROWTH-FACTOR; ANTI-ANGIOGENIC THERAPY; MONOCLONAL-ANTIBODY;
   OPEN-LABEL; PHASE-II; CARCINOEMBRYONIC ANTIGEN; ACQUIRED-RESISTANCE;
   PLUS FLUOROURACIL; IMATINIB MESYLATE; TUMOR VASCULATURE
AB A severe global health concern is the rising incidence and mortality rate of colorectal cancer (CRC). Chemotherapy, which is typically used to treat CRC, is known to have limited specificity and can have noticeable side effects. A paradigm shift in cancer treatment has been brought about by the development of targeted therapies, which has led to the appearance of pharmacological agents with improved efficacy and decreased toxicity. Epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), human epidermal growth factor receptor 2 (HER2), and BRAF are among the molecular targets covered in this review that are used in targeted therapy for CRC. The current discussion also covers advancements in targeted therapeutic approaches, such as antibody-drug conjugates, immune checkpoint inhibitors, and chimeric antigen receptor (CAR) T-cell therapy. A review of the clinical trials and application of these particular therapies in treating CRC is also done. Despite the improvements in targeted therapy for CRC, problems such as drug resistance and patient selection remain to be solved. Despite this, targeted therapies have offered fresh possibilities for identifying and treating CRC, paving the way for the development of personalized medicine and extending the life expectancy and general well-being of CRC patients.
C1 [Yang, Lei] Peoples Hosp Chongqing Liangjiang New Area, Dept Clin Lab, Chongqing 401121, Peoples R China.
   [Atakhanova, Nigora] Tashkent Med Acad, Head Dept Oncol, Tashkent 100109, Uzbekistan.
   [Arellano, Meryelem Tania Churampi] UNIV LIMA, Lima, Peru.
   [Mohamed, Mohammed Yassen] AlNoor Univ Coll, Dept Anesthesia Tech, Nineveh, Iraq.
   [Hani, Thamer] Al Turath Univ Coll, Dent Dept, Baghdad, Iraq.
   [Fahdil, Ali A.] Al Farahidi Univ, Med Tech Coll, Baghdad, Iraq.
   [Castillo-Acobo, Roxana Yolanda] Univ Nacl San Agustin Arequipa, Arequipa, Peru.
   [Juyal, Ashima] Uttaranchal Univ, Uttaranchal Inst Technol, Dehra Dun 248007, India.
   [Hussein, Ahlam Kadhim] Al Zahrawi Univ Coll, Dept Nursing, Karbala, Iraq.
   [Amin, Ali H.] Umm Al Qura Univ, Deanship Sci Res, Mecca, Saudi Arabia.
   [Pecho, Renzon Daniel Cosme] Univ San Ignacio Loyola USIL, Dept Biochem, Lima, Peru.
   [Akhavan-Sigari, Reza] Univ Med Ctr Tuebingen, Dept Neurosurg, Tubingen, Germany.
   [Akhavan-Sigari, Reza] Warsaw Management Univ, Dept Hlth Care Management & Clin Res, Coll Humanum, Warsaw, Poland.
C3 Tashkent Medical Academy; Universidad de Lima; Alnoor University;
   Al-Turath University College; Universidad Nacional de San Agustin de
   Arequipa; Uttaranchal University; Al-Zahrawi University College; Umm Al
   Qura University; Universidad San Ignacio de Loyola; Eberhard Karls
   University of Tubingen; Eberhard Karls University Hospital
RP Pecho, RDC (corresponding author), Univ San Ignacio Loyola USIL, Dept Biochem, Lima, Peru.
EM cosmepechorenzondaniel@gmail.com
RI churampi arellano, meryelem/IWE-1260-2023; Amin, Ali/S-5328-2017; ,
   Al-Zahrawi University College/KEE-9430-2024; Castillo Acobo, Roxana
   Yolanda/AEK-2363-2022
OI , Al-Zahrawi University College/0009-0006-0211-3887; Castillo Acobo,
   Roxana Yolanda/0000-0002-6467-7796
FU Deputyship for Research & Innovation, Ministry of Education in Saudi
   Arabia [IFP22UQU4331100DSR002]
FX The authors extend their appreciation to the Deputyship for Research &
   Innovation, Ministry of Education in Saudi Arabia for funding this
   research work through the project number : IFP22UQU4331100DSR002".
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NR 153
TC 5
Z9 5
U1 2
U2 9
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
EI 1618-0631
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD DEC
PY 2023
VL 252
AR 154888
DI 10.1016/j.prp.2023.154888
EA NOV 2023
PG 12
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA Z5GX1
UT WOS:001112369100001
PM 37948996
DA 2025-01-04
ER

PT J
AU Zhu, MG
   Benson, AB III
AF Zhu, Mengou
   Benson III, Al B.
TI An update on pharmacotherapies for colorectal cancer: 2023 and beyond
SO EXPERT OPINION ON PHARMACOTHERAPY
LA English
DT Review
DE Colorectal cancer; dMMR/MSI; EGFR; immunotherapy; metastatic colorectal
   cancer; next-generation sequencing; pMMR/MSS; targeted therapy
ID RAS WILD-TYPE; MONOCLONAL-ANTIBODY THERAPY; CETUXIMAB PLUS IRINOTECAN;
   POSITIVE SOLID TUMORS; RANDOMIZED PHASE-III; 1ST-LINE TREATMENT;
   OPEN-LABEL; 1ST PROGRESSION; BRAF MUTATION; BEVACIZUMAB
AB Introduction: Colorectal cancer (CRC) is one of the most prevalent and lethal cancers worldwide. The treatment of metastatic colorectal cancer (mCRC) is difficult, and mCRC has a survival rate of only 13-17% compared with 70-90% in locoregional CRC. There is ongoing research effort on pharmacotherapy for CRC to improve the treatment outcome.Areas covered: We reviewed the current literature and ongoing clinical trials on CRC pharmacotherapy, with a focus on targeted therapy based on the results of genetic testing. The pharmacotherapies covered in this article include novel agents targeting EGFR and EGFR-related pathways, agents targeting the VEGF pathway, immunotherapy options depending on the MMR/MSI status, and new therapies targeting genetic fusions such as NTRK. We also briefly discuss the value of next-generation sequencing (NGS) in treatment selection and response monitoring.Expert opinion: We advocate for the early and routine use of NGS to genetically characterize CRC to assist with pharmacotherapy selection. Targeted therapy is a promising field of ongoing research and improves CRC treatment outcome.
C1 [Zhu, Mengou] Northwestern Univ, Dept Med, Feinberg Sch Med, Chicago, IL USA.
   [Benson III, Al B.] Northwestern Univ, Dept Med, Div Hematol & Oncol, Feinberg Sch Med, Chicago, IL USA.
   [Benson III, Al B.] Robert H Lurie Comprehens Canc Ctr, Chicago, IL USA.
   [Zhu, Mengou] Northwestern Univ, Dept Med, Feinberg Sch Med, 676 N St,Clair St Suite 850, Chicago, IL 60611 USA.
C3 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; Feinberg School of Medicine
RP Zhu, MG (corresponding author), Northwestern Univ, Dept Med, Feinberg Sch Med, 676 N St,Clair St Suite 850, Chicago, IL 60611 USA.
EM mengou.zhu@nm.org
RI Wang, Xueke/ABG-1310-2021
OI Zhu, Mengou/0000-0002-7969-3983
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NR 84
TC 2
Z9 2
U1 21
U2 30
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1465-6566
EI 1744-7666
J9 EXPERT OPIN PHARMACO
JI Expert Opin. Pharmacother.
PD JAN 2
PY 2024
VL 25
IS 1
BP 91
EP 99
DI 10.1080/14656566.2024.2304654
EA JAN 2024
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA GY2X8
UT WOS:001144283300001
PM 39023010
DA 2025-01-04
ER

PT J
AU da Silva, JL
   Paulino, E
   Dias, MF
   de Melo, AC
AF da Silva, Jesse Lopes
   Paulino, Eduardo
   Dias, Mariane Fontes
   de Melo, Andreia Cristina
TI Endometrial cancer: redefining the molecular-targeted approach
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Review
DE Cancer; Endometrium; Endometrial cancer; Chemotherapy; Targeted therapy;
   Molecular targets
ID PHASE-II TRIAL; K-RAS MUTATIONS; NONPOLYPOSIS COLORECTAL-CANCER;
   MICROSATELLITE INSTABILITY; BETA-CATENIN; PROMOTER HYPERMETHYLATION;
   RAPAMYCIN INHIBITOR; SEROUS CARCINOMA; HIGH-FREQUENCY; E-CADHERIN
AB Endometrial cancer (EC) is the most frequent gynecologic malignancy in the world. Metastatic and recurrent disease confers a worse prognosis, and the side effects of the current cytotoxic agents are the main cause of treatment disruption. Recently, the genetic alterations that facilitate the start, development and progression of EC have been elucidated, reclassifying the disease in distinct subtypes with different mechanisms of carcinogenesis. Targeted therapy aims to interfere specifically these mechanisms causing less toxicity, therefore opening new perspectives for a tailored treatment and improvement of response and survival rates for heavily treated recurrent disease. Treatment with hormone therapy was not addressed in this review because it is an extensively discussed issue and would divert the discussion about molecular-targeted therapy. The purpose of this paper was to review the available literature data regarding the main genetic abnormalities related to the carcinogenesis and evaluate the safety and efficacy of the molecular-targeted agents in the treatment of metastatic and recurrent EC.
C1 [da Silva, Jesse Lopes; Paulino, Eduardo; Dias, Mariane Fontes; de Melo, Andreia Cristina] Natl Canc Inst INCA, Hosp Canc II, Rio De Janeiro, Brazil.
C3 National Cancer Institute (Inca)
RP da Silva, JL (corresponding author), Natl Canc Inst INCA, Hosp Canc II, Rio De Janeiro, Brazil.
EM jessejeu@yahoo.com.br
RI ; Melo, Andreia Cristina de/C-8133-2019
OI da Silva, Jesse Lopes/0000-0002-0790-9917; Melo, Andreia Cristina
   de/0000-0002-1201-4333
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NR 95
TC 17
Z9 19
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD JUL
PY 2015
VL 76
IS 1
BP 1
EP 11
DI 10.1007/s00280-015-2758-z
PG 11
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA CL5XF
UT WOS:000357036500001
PM 25935126
DA 2025-01-04
ER

PT J
AU O'Hara, MH
   Hamilton, SR
   O'Dwyer, PJ
AF O'Hara, Mark H.
   Hamilton, Stanley R.
   O'Dwyer, Peter J.
TI Molecular Triage Trials in Colorectal Cancer
SO CANCER JOURNAL
LA English
DT Review
DE Clinical trials; molecular triage trials; colorectal cancer; genomic
   alterations; targeted therapy
ID PHASE-II; RAS MUTATIONS; PRECISION MEDICINE; CETUXIMAB; THERAPY; DESIGN;
   VEMURAFENIB; MELANOMA; SURVIVAL; EFFICACY
AB Advances in the understanding of genomic alterations in cancer, and the various therapies targeted to these alterations have permitted the design of trials directed to bringing this science to the clinic, with the ultimate goal of tailoring therapy to the individual. There is a high need for advances in targeted therapy in colorectal cancer, a disease in which only 2 classes of targeted therapies are approved for use in colorectal cancer, despite the majority of colorectal cancers containing a potentially targetable mutation. Here we outline the key elements to the design of these clinical trials and summarize the current active molecular triage trials in colorectal cancer.
C1 [O'Hara, Mark H.; O'Dwyer, Peter J.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
   [Hamilton, Stanley R.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
C3 University of Pennsylvania; University of Texas System; UTMD Anderson
   Cancer Center
RP O'Dwyer, PJ (corresponding author), Perelman Ctr Adv Med, 7 South Tower,3400 Spruce St, Philadelphia, PA 19104 USA.
EM peter.o'dwyer@uphs.upenn.edu
OI O'Hara, Mark/0000-0003-2751-6122
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NR 44
TC 2
Z9 2
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1528-9117
EI 1540-336X
J9 CANCER J
JI Cancer J.
PD MAY-JUN
PY 2016
VL 22
IS 3
BP 218
EP 222
DI 10.1097/PPO.0000000000000199
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DQ7EI
UT WOS:000379369300013
PM 27341602
DA 2025-01-04
ER

PT J
AU Nguyen, HT
   Duong, HQ
AF Ha Thi Nguyen
   Hong-Quan Duong
TI The molecular characteristics of colorectal cancer: Implications for
   diagnosis and therapy
SO ONCOLOGY LETTERS
LA English
DT Review
DE colorectal cancer; chromosomal instability; microsatellite instability;
   CpG island methylator phenotype; molecular characteristics; early
   diagnosis; targeted therapy
ID ISLAND METHYLATOR PHENOTYPE; DEFECTIVE MISMATCH REPAIR; POPULATION-BASED
   SAMPLE; PLURIPOTENT STEM-CELLS; MICROSATELLITE-INSTABILITY;
   COLON-CANCER; TUMOR-SUPPRESSOR; KRAS MUTATIONS; K-RAS; CHROMOSOMAL
   INSTABILITY
AB Colorectal cancer (CRC) results from the progressive accumulation of multiple genetic and epigenetic aberrations within cells. The progression from colorectal adenoma to carcinoma is caused by three major pathways: Microsatellite instability, chromosomal instability and CpG island methylator phenotype. A growing body of scientific evidences suggests that CRC is a heterogeneous disease, and genetic characteristics of the tumors determine their prognostic outcome and response to targeted therapies. Early diagnosis and effective targeted therapies based on a current knowledge of the molecular characteristics of CRC are essential to the successful treatment of CRC. Therefore, the present review summarized the current understanding of the molecular characteristics of CRC, and discussed its implications for diagnosis and targeted therapy.
C1 [Ha Thi Nguyen] Duy Tan Univ, Inst Res & Dev, Ctr Mol Biol, 03 Quang Trung, Danang 550000, Vietnam.
   [Hong-Quan Duong] Vinmec Res Inst Stem Cell & Gene Technol, Dept Canc Res, 458 Minh Khai, Hanoi 100000, Vietnam.
C3 Duy Tan University
RP Nguyen, HT (corresponding author), Duy Tan Univ, Inst Res & Dev, Ctr Mol Biol, 03 Quang Trung, Danang 550000, Vietnam.; Duong, HQ (corresponding author), Vinmec Res Inst Stem Cell & Gene Technol, Dept Canc Res, 458 Minh Khai, Hanoi 100000, Vietnam.
EM nguyenthiha23@dtu.edu.vn; quanvspt@gmail.com
RI Nguyen, Ha/Y-3064-2019
OI NGUYEN, Ha/0000-0001-9222-632X
FU National Foundation for Science and Technology Development (NAFOSTED)
   [106-YS.01-2015.12]
FX This study was supported by the National Foundation for Science and
   Technology Development (NAFOSTED; grant no. 106-YS.01-2015.12).
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NR 140
TC 192
Z9 207
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 JUL
PY 2018
VL 16
IS 1
BP 9
EP 18
DI 10.3892/ol.2018.8679
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GL4KQ
UT WOS:000437120300002
PM 29928381
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wong, AHN
   Ma, BGT
   Lui, RN
AF Wong, Ambrose H. N.
   Ma, Brigette
   Lui, Rashid N. N.
TI New developments in targeted therapy for metastatic colorectal cancer
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Review
DE BRAF inhibitor; colorectal cancer; EGFR inhibitor; personalized
   medicine; precision oncology; targeted therapy
ID EGFR MONOCLONAL-ANTIBODIES; POSITIVE SOLID TUMORS; 1ST-LINE TREATMENT;
   OPEN-LABEL; ACQUIRED-RESISTANCE; SUBGROUP ANALYSES; PLUS BEVACIZUMAB;
   NON-INFERIORITY; BRAF MUTATION; COLON-CANCER
AB Colorectal cancer (CRC) is the second most lethal cancer worldwide and the prognosis of metastatic CRC (mCRC) remains poor. Recent advancements in translational research have led to the identification of several new therapeutic targets and improved the treatment outcome of patients with tumours harbouring BRAF V600E mutation, (HER2) ErBB2 alterations, NTRK gene fusions and KRAS(G12C) mutation. Improved understanding towards the mechanism of resistance to targeted therapy such as anti-epidermal growth factor receptor antibodies and the evolving role of therapeutic monitoring with circulating tumour DNA (ctDNA) has enabled the longitudinal tracking of clonal evolution during treatment and the individualization of subsequent treatments. To broaden the community-based implementation of precision oncology in directing targeted therapies for patients with gastrointestinal cancers including mCRC, the feasibility of 'Master Protocols' that utilizes ctDNA-based genotyping platforms is currently being evaluated. Such protocols encompass both observational and interventional clinical trials of novel targeted therapies conducted within a large clinical trial network. In this review, we will discuss the latest developments in targeted therapies, and therapeutic strategies for overcoming acquired drug resistance in patients with mCRC.
C1 [Wong, Ambrose H. N.] Chinese Univ Hong Kong, Fac Med, Hong Kong, Peoples R China.
   [Ma, Brigette] Hong Kong Canc Inst, Sir YK Pao Ctr Canc, Dept Clin Oncol, State Key Lab Translat Oncol, Hong Kong, Peoples R China.
   [Lui, Rashid N. N.] Chinese Univ Hong Kong, Dept Clin Oncol, 9-F, Hong Kong, Peoples R China.
   [Lui, Rashid N. N.] Chinese Univ Hong Kong, Div Gastroenterol & Hepatol, Dept Med & Therapeut, Inst Digest Dis,Prince Wales Hosp, 9-F, Hong Kong, Peoples R China.
C3 Chinese University of Hong Kong; Chinese University of Hong Kong;
   Chinese University of Hong Kong; Prince of Wales Hospital
RP Lui, RN (corresponding author), Chinese Univ Hong Kong, Dept Clin Oncol, 9-F, Hong Kong, Peoples R China.; Lui, RN (corresponding author), Chinese Univ Hong Kong, Div Gastroenterol & Hepatol, Dept Med & Therapeut, Inst Digest Dis,Prince Wales Hosp, 9-F, Hong Kong, Peoples R China.
EM rashidlui@cuhk.edu.hk
RI Wong, Ambrose/LRT-3220-2024
OI Wong, Ambrose Hei Nam/0000-0002-8039-2643
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NR 153
TC 11
Z9 12
U1 0
U2 16
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PY 2023
VL 15
AR 17588359221148540
DI 10.1177/17588359221148540
PG 22
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA H8ZX7
UT WOS:000998788400001
PM 36687386
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Nishizaki, D
   Eskander, RN
AF Nishizaki, Daisuke
   Eskander, Ramez N.
TI Targeted Therapies, Biologics, and Immunotherapy in the Neoadjuvant and
   Adjuvant Settings: Perioperative Risks
SO SURGICAL ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Immune checkpoint inhibitors; Molecular targeted therapy; Biological
   products; Neoadjuvant therapy; Intraoperative complications
ID GASTROINTESTINAL STROMAL TUMORS; ACCESS PORT SYSTEMS; MAINTENANCE
   THERAPY; IMATINIB MESYLATE; COLORECTAL-CANCER; RANDOMIZED-TRIAL; ADVERSE
   EVENTS; OVARIAN-CANCER; DOUBLE-BLIND; OPEN-LABEL
C1 [Nishizaki, Daisuke] Univ Calif San Diego, Moores Canc Ctr, Div Hematol & Oncol, Ctr Personalized Canc Therapy,Dept Med, 3855 Hlth Sci Dr, La Jolla, CA 92037 USA.
   [Eskander, Ramez N.] Univ Calif San Diego, Moores Canc Ctr, Ctr Personalized Canc Therapy, Dept Obstet Gynecol & Reprod Sci,Div Gynecol Oncol, La Jolla, CA USA.
C3 University of California System; University of California San Diego;
   University of California System; University of California San Diego
RP Nishizaki, D (corresponding author), Univ Calif San Diego, Moores Canc Ctr, Div Hematol & Oncol, Ctr Personalized Canc Therapy,Dept Med, 3855 Hlth Sci Dr, La Jolla, CA 92037 USA.
EM dnishizaki@health.ucsd.edu
RI Nishizaki, Daisuke/LLK-6444-2024
OI Nishizaki, Daisuke/0000-0002-6746-3224
FU Clovis Oncology, United States; GlaxoSmithKline (GSK); Merck, United
   States; AstraZeneca
FX D. Nishizaki has nothing to disclose. R.N. Eskander reports research
   funding (institutional) from Clovis Oncology, United States,
   GlaxoSmithKline (GSK) , Merck, United States, AstraZeneca; consulting
   fees (including participation on Data Safety Moni- toring Board or
   Advisory Board) from AstraZeneca, Clovis, Eisai, GSK, Immunogen,
   Mersana, Myriad, Novocure, Onconova, Elevar Therapeutics, Daiichi
   Sankyo, IMV, Natera, Novartis, ORIC; payment for
   presentations/writing/educational events from Astra Zeneca, GSK,
   Immunogen, Merck, Medscape, CURIO, Great Debates and Updates; role as
   GOG P Associate Clinical Trial Advisor; role as Scientific and Medical
   Advisor to Clearity Foundation.
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NR 65
TC 0
Z9 0
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1055-3207
EI 1558-5042
J9 SURG ONCOL CLIN N AM
JI Surg. Oncol. Clin. N. Am.
PD APR
PY 2024
VL 33
IS 2
BP 279
EP 291
DI 10.1016/j.soc.2023.12.002
EA FEB 2024
PG 13
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA MW7J9
UT WOS:001196736200001
PM 38401910
DA 2025-01-04
ER

PT J
AU Gouverneur, A
   Bezin, J
   Jové, J
   Bosco-Lévy, P
   Fourrier-Réglat, A
   Noize, P
AF Gouverneur, Amandine
   Bezin, Julien
   Jove, Jeremy
   Bosco-Levy, Pauline
   Fourrier-Reglat, Annie
   Noize, Pernelle
TI Treatment Modalities and Survival in Older Adults with Metastatic
   Colorectal Cancer in Real Life
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE molecular targeted therapy; colorectal neoplasm; neoplasm metastasis;
   aged; frail older adults
ID 1ST-LINE COMBINATION CHEMOTHERAPY; ELDERLY-PATIENTS; TARGETED THERAPIES;
   CLINICAL-TRIAL; BEVACIZUMAB; CETUXIMAB; TOXICITY; DIAGNOSIS; SAFETY;
   CARE
AB OBJECTIVES Metastatic colorectal cancer (mCRC) is increasingly treated with targeted therapies, but little is known about real-life mCRC treatment in older adults. The aims were to describe the real-life first-line treatment modalities in older adult mCRC patients, to identify factors associated with treatment modalities, and to evaluate survival with regard to treatment modalities. PATIENTS AND METHODS A cohort of mCRC patients aged 65 years and older at diagnosis was identified between 2009 and 2013 using French national healthcare insurance system claims data. Treatment modalities were: treatment with one or more anticancer medication vs best supportive care and, among treated patients, treatment with targeted therapy vs conventional chemotherapy alone. Multivariate logistic regression was used to identify factors associated with treatment by anticancer medication and by targeted therapy. Cox proportional hazards models were used to assess the independent effect of treatment modalities on overall survival while adjusting for baseline covariates identified with logistic regression. RESULTS A total of 503 patients were included with a median age of 78 years (54% were men). Of these, 299 (59%) were treated with anticancer medications. Among treated patients, 131 (44%) received targeted therapy. In multivariate analysis, age 75 years or older, renal failure, malnutrition, and five or more concomitant medications were associated with a lower likelihood of treatment with anticancer medications. Among treated patients, age 75 years or older, history of cancer, lymph node metastases, and a single metastatic site were associated with a lower likelihood of treatment with targeted therapy. Multivariate Cox proportional hazards models found that treatment with any anticancer medication tended to be associated with a lower risk of death; treatment with targeted therapy was not significantly associated. CONCLUSION A more appropriate prescription of anticancer medications in the older adult will require the definition of more explicit criteria to avoid undertreatment. The real benefit of targeted therapies vs conventional chemotherapy alone needs to be confirmed in this population. J Am Geriatr Soc 67:913-919, 2019.
C1 [Gouverneur, Amandine; Bezin, Julien; Fourrier-Reglat, Annie; Noize, Pernelle] Univ Bordeaux, Bordeaux Populat Hlth Res Ctr, INSERM, Team Pharmacoepidemiol,UMR 1219, Bordeaux, France.
   [Gouverneur, Amandine; Fourrier-Reglat, Annie; Noize, Pernelle] CHU Bordeaux, Serv Pharmacol Med, Pole Sante Publ, Bordeaux, France.
   [Jove, Jeremy; Bosco-Levy, Pauline; Fourrier-Reglat, Annie; Noize, Pernelle] INSERM, Bordeaux PharmacoEpi, CIC1401, Bordeaux, France.
C3 Universite de Bordeaux; Institut National de la Sante et de la Recherche
   Medicale (Inserm); CHU Bordeaux; Universite de Bordeaux; Universite de
   Bordeaux; Institut National de la Sante et de la Recherche Medicale
   (Inserm)
RP Gouverneur, A (corresponding author), CHU Bordeaux, Serv Pharmacol Med, Batiment 1A,Case 36,146 Rue Leo Saignat, F-33076 Bordeaux, France.; Gouverneur, A (corresponding author), Univ Bordeaux, Batiment 1A,Case 36,146 Rue Leo Saignat, F-33076 Bordeaux, France.
EM amandine.gouverneur@u-bordeaux.fr
RI Bezin, Julien/T-1916-2019; Bosco-Lévy, Pauline/AAA-6256-2020; Noize,
   Pernelle/T-1955-2019; Gouverneur, Amandine/O-5332-2018
OI Bezin, Julien/0000-0002-2568-1928; Bosco-Levy,
   Pauline/0000-0001-9763-5974; Gouverneur, Amandine/0000-0001-6253-1833
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NR 31
TC 4
Z9 4
U1 1
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0002-8614
EI 1532-5415
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD MAY
PY 2019
VL 67
IS 5
BP 913
EP 919
DI 10.1111/jgs.15858
PG 7
WC Geriatrics & Gerontology; Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Geriatrics & Gerontology
GA HV7TT
UT WOS:000466184200009
PM 30840323
DA 2025-01-04
ER

PT J
AU Ray, T
   Kar, D
   Pal, A
   Mukherjee, S
   Das, C
   Pal, A
AF Ray, Tanusree
   Kar, Dwiprohi
   Pal, Ananda
   Mukherjee, Shravanti
   Das, Chandrima
   Pal, Amit
TI Molecular targeting of breast and colon cancer cells by PAR1 mediated
   apoptosis through a novel pro-apoptotic peptide
SO APOPTOSIS
LA English
DT Article
DE Pro-apoptotic peptide; Apoptosis; PAR1; Targeted therapy
ID EHRLICHS ASCITES-CARCINOMA; PROTEASE-ACTIVATED RECEPTORS; THROMBIN
   RECEPTOR; INVASION
AB A novel activating peptide was designed and synthesized from V. cholerae hemagglutinine protease (HAP) mediated cleavage site of mouse PAR1. The peptide PFISED interacts with PAR1 in a new site which is different from its thrombin mediated conventional activation site and induced a series of new downstream signaling pathways. The peptide showed apoptosis in human and mouse breast (MCF-7 and EAC) and colon (HT29 and CT26) cancer cells where as in the same peptide concentration in normal human breast epithelial cells (MCF-10A), normal human fibroblast cells (MRC-5), normal mouse peritoneal macrophage cells and normal mouse breast and colon tissues did not show any effect. Treatment with this peptide enhanced the survival kinetics of EAC induced mice. The peptide mediated apoptosis was inhibited in presence of PAR1 inhibitor and was significantly reduced in si-PAR1 treated cells that indicate the activating peptide PFISED induced PAR1 mediated apoptosis of colon and breast cancer cells. This peptide induced over expression and activation of PAR1 and its downstream MAP kinase and NFB signaling pathways. These signaling pathways enhanced the cellular ROS level to kill malignant cells. We report a novel pro-apoptotic peptide which can selectively kill malignant cells via its specific target receptor PAR1 which is over expressed in the malignant cells and can be used as a molecular target therapy for cancer treatment.
C1 [Ray, Tanusree; Kar, Dwiprohi; Pal, Amit] Natl Inst Cholera & Enter Dis, Div Pathophysiol, P-33,CIT Rd, Kolkata 700010, India.
   [Pal, Ananda] Natl Inst Cholera & Enter Dis, Div Clin Med, Kolkata, India.
   [Mukherjee, Shravanti; Das, Chandrima] Saha Inst Nucl Phys, Biophys & Struct Genom Div, Kolkata, India.
   [Das, Chandrima] Homi Bhaba Natl Inst, Bombay, Maharashtra, India.
C3 Indian Council of Medical Research (ICMR); ICMR - National Institute of
   Cholera & Enteric Diseases (NICED); Indian Council of Medical Research
   (ICMR); ICMR - National Institute of Cholera & Enteric Diseases (NICED);
   Saha Institute of Nuclear Physics; Homi Bhabha National Institute
RP Pal, A (corresponding author), Natl Inst Cholera & Enter Dis, Div Pathophysiol, P-33,CIT Rd, Kolkata 700010, India.
EM pala.niced@gov.in
RI Das, Chandrima/AAI-7398-2021
OI Pal, Ananda/0009-0001-1148-8465
FU DBT-India [BT/PR19713/BIC/101/237/2016]
FX Funding was provided by DBT-India with Grant No.
   [BT/PR19713/BIC/101/237/2016].
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NR 42
TC 11
Z9 12
U1 0
U2 18
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 2018
VL 23
IS 11-12
BP 679
EP 694
DI 10.1007/s10495-018-1485-4
PG 16
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA GX4NJ
UT WOS:000447710600010
PM 30196356
DA 2025-01-04
ER

PT J
AU Chen, DL
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AF Chen, Dong-Liang
   Xu, Rui-Hua
TI The emerging role of long non-coding RNAs in the drug resistance of
   colorectal cancer
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Review
DE CRC; lncRNA; drug resistance
ID OXALIPLATIN-BASED CHEMOTHERAPY; MOLECULAR-MECHANISMS; METASTATIC
   PROGRESSION; CISPLATIN RESISTANCE; MULTIDRUG-RESISTANCE; DECREASED
   EXPRESSION; SIGNALING PATHWAY; DOWN-REGULATION; CETUXIMAB; FLUOROURACIL
AB Colorectal cancer (CRC) remains one of the leading causes of cancer-related deaths in the world. Chemotherapy has been used to treat CRC patients in order to improve prognosis. Oxaliplatin and 5-Fluorouracil (5-FU) based chemotherapy is a first line treatment for locally advanced and metastatic CRC. For patients with wild-type KRAS metastatic CRC, cetuximab (an EGFR monoclonal antibody) is a commonly used targeted therapy. CRC is initially sensitive to chemotherapy and targeted therapy. However, drug resistance frequently arises, which significantly affect the treatment outcome in these patients. An increasing number of studies have indicated that lncRNAs are implicated in the drug resistance of CRC. This review aims to gain insights into the role and molecular mechanism of lncRNAs in CRC drug resistance.
C1 [Chen, Dong-Liang; Xu, Rui-Hua] Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, 651 Dong Feng East Rd, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; State Key Lab Oncology South China
RP Chen, DL; Xu, RH (corresponding author), Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, 651 Dong Feng East Rd, Guangzhou, Guangdong, Peoples R China.
EM chendl@sysucc.org.cn; xurh@sysucc.org.cn
RI Xu, Rui-Hua/AAW-4766-2021
OI Xu, Rui-Hua/0000-0001-9771-8534
FU National Natural Science Foundation of China [81372570, 81602053];
   Natural Science Foundation of Guangdong Province [2014A030312015,
   2016A030310195]; Science and Technology Program of Guangdong
   [2015B020232008]; Science and Technology Program of Guangzhou [15570006,
   158100066]; fourth outstanding young talents training plan of Sun Yatsen
   University Cancer Center [PT04141001]
FX This study was supported by the National Natural Science Foundation of
   China (no. 81372570; No 81602053), the Natural Science Foundation of
   Guangdong Province (no. 20-14A030312015; no. 2016A030310195), the
   Science and Technology Program of Guangdong (no. 2015B020232008), the
   Science and Technology Program of Guangzhou (nos. 15570006 and
   158100066), and the fourth outstanding young talents training plan of
   Sun Yatsen University Cancer Center (no. PT04141001).
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NR 70
TC 8
Z9 8
U1 0
U2 7
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 2018
VL 11
IS 10
BP 4735
EP 4743
PG 9
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA GY7ZK
UT WOS:000448836700001
PM 31949549
DA 2025-01-04
ER

PT B
AU Abdelrahim, M
   Kopetz, S
   Menter, D
AF Abdelrahim, Maen
   Kopetz, Scott
   Menter, David
BE Tsimberidou, AM
   Kurzrock, R
   Anderson, KC
TI Targeted Therapy in Solid Tumors: Colorectal Cancer
SO TARGETED THERAPY IN TRANSLATIONAL CANCER RESEARCH
SE Translational Oncology-Hoboken
LA English
DT Article; Book Chapter
ID GROWTH-FACTOR RECEPTOR; ISLAND METHYLATOR PHENOTYPE; CETUXIMAB PLUS
   IRINOTECAN; PHASE-III TRIAL; OXALIPLATIN-BASED CHEMOTHERAPY; 1ST-LINE
   TREATMENT; MICROSATELLITE INSTABILITY; COLON-CANCER; K-RAS; ADENOMATOUS
   POLYPOSIS
C1 [Abdelrahim, Maen] Baylor Coll Med, Dept Internal Med, Houston, TX 77030 USA.
   [Kopetz, Scott; Menter, David] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
C3 Baylor College of Medicine; University of Texas System; UTMD Anderson
   Cancer Center
RP Abdelrahim, M (corresponding author), Baylor Coll Med, Dept Internal Med, Houston, TX 77030 USA.
RI Kopetz, Scott/AAC-1387-2019
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NR 176
TC 6
Z9 6
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
BN 978-1-118-46868-5; 978-1-118-46857-9
J9 TRANSL ONCOL-HOBOKEN
PY 2016
BP 193
EP 204
PG 12
WC Oncology
WE Book Citation Index – Science (BKCI-S)
SC Oncology
GA BL8SM
UT WOS:000456964200023
DA 2025-01-04
ER

PT J
AU Belkhiri, A
   El-Rifai, W
AF Belkhiri, Abbes
   El-Rifai, Wael
TI Advances in targeted therapies and new promising targets in esophageal
   cancer
SO ONCOTARGET
LA English
DT Review
DE adenocarcinoma; esophageal; gastric; cancer; targeted therapy
ID PHASE-II TRIAL; SQUAMOUS-CELL CARCINOMA; METASTATIC COLORECTAL-CANCER;
   TO-MESENCHYMAL TRANSITION; ENDOTHELIAL GROWTH-FACTOR; AURORA-KINASE-A;
   GASTROESOPHAGEAL JUNCTION; BARRETTS-ESOPHAGUS; GASTRIC-CANCER;
   BREAST-CANCER
AB Esophageal cancer, comprising squamous carcinoma and adenocarcinoma, is a leading cause of cancer-related death in the world. Notably, the incidence of esophageal adenocarcinoma has increased at an alarming rate in the Western world. Unfortunately, the standard first-line chemo-radiotherapeutic approaches are toxic and of limited efficacy in the treatment of a significant number of cancer patients. The molecular analysis of cancer cells has uncovered key genetic and epigenetic alterations underlying the development and progression of tumors. These discoveries have paved the way for the emergence of targeted therapy approaches. This review will highlight recent progress in the development of targeted therapies in esophageal cancer. This will include a review of drugs targeting receptor tyrosine kinases and other kinases in esophageal cancer. Additional studies will be required to develop a rational integration of these targeted agents with respect to histologic types of esophageal cancer and the optimal selection of cancer patients who would most likely benefit from targeted therapy. Identification of AURKA and AXL as key molecular players in esophageal tumorigenesis and drug resistance strongly justifies the evaluation of the available drugs against these targets in clinical trials.
C1 [Belkhiri, Abbes; El-Rifai, Wael] Vanderbilt Univ, Med Ctr, Dept Surg, Nashville, TN 37232 USA.
   [El-Rifai, Wael] Tennessee Valley Healthcare Syst, Dept Vet Affairs, Nashville, TN 37212 USA.
C3 Vanderbilt University; US Department of Veterans Affairs; Veterans
   Health Administration (VHA); VA Tennessee Valley Healthcare System
RP El-Rifai, W (corresponding author), Vanderbilt Univ, Med Ctr, Dept Surg, Nashville, TN 37232 USA.
EM abbes.belkhiri@vanderbilt.edu; wael.el-rifai@vanderbilt.edu
FU NCI NIH HHS [R01 CA131225] Funding Source: Medline; NIDDK NIH HHS [P30
   DK058404] Funding Source: Medline
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NR 92
TC 41
Z9 45
U1 0
U2 18
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD JAN 30
PY 2015
VL 6
IS 3
BP 1348
EP 1358
DI 10.18632/oncotarget.2752
PG 11
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CF6TS
UT WOS:000352689800005
PM 25593196
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Xu, RH
   Qin, SK
   Guo, WJ
   Bai, YX
   Deng, YH
   Yang, L
   Chen, ZD
   Zhong, HJ
   Pan, HM
   Shu, YQ
   Yuan, Y
   Zhou, JF
   Xu, N
   Liu, TS
   Ma, D
   Wu, CP
   Cheng, Y
   Xu, JM
   Chen, DH
   Li, W
   Sun, SY
   Yu, Z
   Cao, PG
   Li, J
   Chen, HH
   Wang, JJ
   Wang, SB
   Wang, HB
   Wang, N
   Zhang, B
   Han, RB
   Su, WG
   Guo, XJ
   Li, J
AF Xu, Ruihua
   Qin, Shukui
   Guo, Weijian
   Bai, Yuxian
   Deng, Yanhong
   Yang, Lei
   Chen, Zhendong
   Zhong, Haijun
   Pan, Hongming
   Shu, Yongqian
   Yuan, Ying
   Zhou, Jianfeng
   Xu, Nong
   Liu, Tianshu
   Ma, Dong
   Wu, Changping
   Cheng, Ying
   Xu, Jianming
   Chen, Donghui
   Li, Wei
   Sun, Sanyuan
   Yu, Zhuang
   Cao, Peiguo
   Li, Jian
   Chen, Haihui
   Wang, Jiejun
   Wang, Shubin
   Wang, Hongbing
   Wang, Ning
   Zhang, Bin
   Han, Rubing
   Su, Weiguo
   Guo, Xiaojun
   Li, Jin
TI Subgroup analysis by prior anti-VEGF or anti-EGFR target therapy in
   FRESCO, a randomized, double-blind, Phase III trial
SO FUTURE ONCOLOGY
LA English
DT Article
DE anti-epidermal growth factor receptor; anti-vascular endothelial growth
   factor; fruquintinib; metastatic colorectal cancer; targeted therapy;
   VEGF receptor inhibitors
ID METASTATIC COLORECTAL-CANCER; 1ST-LINE TREATMENT; SUPPORTIVE CARE;
   FLUOROURACIL; PLACEBO; FRUQUINTINIB; OXALIPLATIN; BEVACIZUMAB;
   LEUCOVORIN; IRINOTECAN
AB Background: FRESCO study demonstrated efficacy and safety of fruquintinib in metastatic colorectal cancer patients. Impact of prior targeted therapy (PTT) on efficacy and safety of fruquintinib was evaluated. Materials & methods: In this subgroup analysis of FRESCO trial, patients were divided into PTT and non-PTT subgroups, and efficacy and safety of fruquintinib were assessed, respectively. Results: In non-PTT subgroup, fruquintinib significantly prolonged overall survival (OS) and progression free survival (PFS) of patients compared with placebo. In PTT subgroup, the median OS and PFS of patients in fruquintinib arm was significantly higher than those in placebo. Treatment-emergent adverse events (TEAEs) rates were similar in both subgroups. Conclusion: Fruquintinib demonstrated clinically meaningful improvement in OS, PFS, objective response rate, and disease control rate with manageable TEAEs in both subgroups.
   ClinicalTrial Registration: NCT02314819 (ClinicalTrials.gov)
   Lay abstract
   In this analysis of the FRESCO trial, we evaluated the efficacy and safety of fruquintinib in two different groups of patients (subgroups) with metastatic colorectal cancer - patients who received prior targeted therapy (PTT) and patients who did not (non-PTT). Of the 278 patients treated with fruquintinib, 111 patients received PTT. Patients treated with fruquintinib had longer overall survival and it took longer for their disease to worsen in both PTT and non-PTT subgroups compared with placebo. Patients in both subgroups treated with fruquintinib showed measurable reduction in their tumor size and disease control with similar side effects in patients of both the subgroups. These results suggest that fruquintinib is safe and effective in patients with metastatic colorectal cancer in both subgroups.
C1 [Xu, Ruihua] Sun Yat Sen Univ, Canc Ctr, State Key Lab Oncol South China, Dept Med Oncol, Guangzhou 510060, Peoples R China.
   [Qin, Shukui] Jinling Hosp, Canc Ctr, Dept Med Oncol, Nanjing 210093, Peoples R China.
   [Guo, Weijian] Fudan Univ, Shanghai Canc Ctr, Shanghai Med Coll, Dept Med Oncol, Shanghai 200032, Peoples R China.
   [Bai, Yuxian] Harbin Med Univ, Canc Hosp, Dept Gastrointestinal Oncol, Harbin 150040, Peoples R China.
   [Deng, Yanhong] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Med Oncol, Guangzhou 510655, Peoples R China.
   [Yang, Lei] Nantong Canc Hosp, Dept Med Oncol, Nantong 226361, Peoples R China.
   [Chen, Zhendong] Anhui Med Univ, Hosp 2, Dept Med Oncol, Hefei 230601, Peoples R China.
   [Zhong, Haijun] Zhejiang Canc Hosp, Dept Med Oncol, Hangzhou 310022, Peoples R China.
   [Pan, Hongming] Zhejiang Univ, Sir Run Run Shaw Hosp, Dept Med Oncol, Coll Med, Hangzhou 310020, Peoples R China.
   [Shu, Yongqian] Jiangsu Prov Hosp, Dept Med Oncol, Nanjing 210029, Peoples R China.
   [Yuan, Ying] Zhejiang Univ, Affiliated Hosp 2, Sch Med, Dept Med Oncol, Hangzhou 310009, Peoples R China.
   [Zhou, Jianfeng] Peking Union Med Coll Hosp, Dept Med Oncol, Beijing 100730, Peoples R China.
   [Xu, Nong] Zhejiang Univ, Affiliated Hosp 1, Sch Med, Dept Med Oncol, Hangzhou 310003, Peoples R China.
   [Liu, Tianshu] Fudan Univ, Zhongshan Hosp, Shanghai Med Coll, Dept Med Oncol, Shanghai 200032, Peoples R China.
   [Ma, Dong] Guangdong Prov Peoples Hosp, Dept Med Oncol, Guangzhou 510080, Peoples R China.
   [Wu, Changping] First Peoples Hosp Changzhou, Dept Med Oncol, Changzhou 213003, Jiangsu, Peoples R China.
   [Cheng, Ying] Jilin Prov Canc Hosp, Dept Med Oncol, Changchun 130012, Peoples R China.
   [Xu, Jianming] Chinese Peoples Liberat Army Gen Hosp, Med Ctr 5, Dept Gastrointestinal Oncol, Beijing 100039, Peoples R China.
   [Chen, Donghui] Shanghai Jiao Tong Univ Affiliated Peoples Hosp 1, Dept Med Oncol, Shanghai, Peoples R China.
   [Li, Wei] First Hosp Jilin Univ, Dept Med Oncol, Changchun 130021, Peoples R China.
   [Sun, Sanyuan] Xuzhou Cent Hosp, Dept Med Oncol, Xuzhou 221009, Jiangsu, Peoples R China.
   [Yu, Zhuang] Qingdao Univ, Affiliated Hosp, Dept Med Oncol, Qingdao 266000, Peoples R China.
   [Cao, Peiguo] Cent South Univ, Xiangya Hosp 3, Dept Med Oncol, Changsha 410013, Peoples R China.
   [Li, Jian] Peking Univ Canc Hosp & Inst, Key Lab Carcinogenesis & Translat Res, Minist Educ, Dept Gastrointestinal Oncol, Beijing, Peoples R China.
   [Chen, Haihui] Liuzhou Workers Hosp, Dept Med Oncol, Liuzhou 545001, Peoples R China.
   [Wang, Jiejun] Second Mil Med Univ, Shanghai Changzheng Hosp, Dept Med Oncol, Shanghai 200003, Peoples R China.
   [Wang, Shubin] Beijing Univ, Peking Univ, Shenzhen Hosp, Dept Med Oncol, Shenzhen 518036, Peoples R China.
   [Wang, Hongbing] Xuzhou Med Coll, Affiliated Hosp, Dept Med Oncol, Xuzhou 221002, Jiangsu, Peoples R China.
   [Wang, Ning; Zhang, Bin; Han, Rubing] Eli Lilly & Co, Shanghai 200041, Peoples R China.
   [Su, Weiguo; Guo, Xiaojun] Hutchison MediPharma Ltd, Shanghai 201203, Peoples R China.
   [Li, Jin] Tongji Univ, Shanghai East Hosp, Dept Med Oncol, Shanghai 200120, Peoples R China.
C3 Sun Yat Sen University; State Key Lab Oncology South China; Fudan
   University; Harbin Medical University; Sun Yat Sen University; Anhui
   Medical University; Zhejiang Cancer Hospital; Zhejiang University;
   Nanjing Medical University; Zhejiang University; Chinese Academy of
   Medical Sciences - Peking Union Medical College; Peking Union Medical
   College Hospital; Zhejiang University; Fudan University; Guangdong
   Academy of Medical Sciences & Guangdong General Hospital; Chinese
   People's Liberation Army General Hospital; Fifth Medical Center of
   Chinese PLA General Hospital; Shanghai Jiao Tong University; Jilin
   University; Qingdao University; Central South University; Naval Medical
   University; Peking University; Xuzhou Medical University; Eli Lilly;
   Tongji University
RP Li, J (corresponding author), Tongji Univ, Shanghai East Hosp, Dept Med Oncol, Shanghai 200120, Peoples R China.
EM lijin@csco.org.cn
RI l, j/HNC-5728-2023; Liu, Tianshu/H-6879-2019; Xu,
   Jianming/KWU-3367-2024; Shu, Yongqian/ABD-5698-2021; Wang,
   Ning/HKO-8446-2023; Chen, Dong-Hui/C-6618-2018; Xu,
   Rui-Hua/AAW-4766-2021
OI Cao, Peiguo/0000-0002-8828-9755; Xu, Rui-Hua/0000-0001-9771-8534
FU Eli Lilly; Hutchison MediPharma Limited; Eli Lilly, China
FX The study was funded by Eli Lilly and Hutchison MediPharma Limited. N
   Wang: employment: Eli Lilly; stock or other ownership: Eli Lilly. B
   Zhang: employment: Eli Lilly; stock or other ownership: Eli Lilly. R
   Han: employment: Eli Lilly; stock or other ownership: Eli Lilly. W Su:
   employment: Hutchison MediPharma Limited; stock or other ownership:
   Hutchison MediPharma Limited; X Guo: employment; Hutchison MediPharma
   Limited; stock or other ownership: Hutchison MediPharma Limited. 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.Medical writing support under the
   direction of authors was provided by A Nalli and V S (Indegene Pvt. Ltd,
   Bangalore) as funded by Eli Lilly, China.
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NR 24
TC 6
Z9 6
U1 1
U2 19
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PD APR
PY 2021
VL 17
IS 11
BP 1339
EP 1350
DI 10.2217/fon-2020-0875
EA DEC 2020
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QZ1HJ
UT WOS:000599189500001
PM 33325251
OA hybrid
DA 2025-01-04
ER

PT J
AU He, J
   Ahuja, N
AF He, Jin
   Ahuja, Nita
TI Personalized Approaches to Gastrointestinal Cancers Importance of
   Integrating Genomic Information to Guide Therapy
SO SURGICAL CLINICS OF NORTH AMERICA
LA English
DT Article
DE Tumor heterogeneity; Next-generation sequencing; Targeted therapy;
   Biomarkers
ID METASTATIC COLORECTAL-CANCER; CETUXIMAB PLUS IRINOTECAN; PHASE-III
   TRIAL; CIRCULATING TUMOR-CELLS; 1ST-LINE TREATMENT; STROMAL TUMORS;
   TYROSINE KINASE; IMATINIB MESYLATE; ADJUVANT IMATINIB; OXALIPLATIN
AB Cancers are characterized by complex tumor heterogeneity driven by subclones with differential genotypes and phenotypes, which then drives cancer behavior. As genomic strategies become feasible on smaller samples such as biopsies, coupled with decreasing costs of these approaches, clinicians will increasingly use genomic information to drive therapeutic decision making. Early applications of such personalized approaches are discussed. Genetic testing of high-risk family members may identify patients with germline mutations who can have prophylactic surgeries as a cancer prevention strategy. This article discusses examples of successful targeted therapy. Clinical trials need to incorporate genetic testing to stratify patients into different groups.
C1 [He, Jin; Ahuja, Nita] Johns Hopkins Univ, Sch Med, Dept Surg, Baltimore, MD 21287 USA.
C3 Johns Hopkins University
RP Ahuja, N (corresponding author), Johns Hopkins Univ, Sch Med, Dept Surg, 600 North Wolfe St,Blalock 685, Baltimore, MD 21287 USA.
EM nahuja1@jhmi.edu
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NR 55
TC 3
Z9 3
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 0039-6109
EI 1558-3171
J9 SURG CLIN N AM
JI Surg. Clin.-North Am.
PD OCT
PY 2015
VL 95
IS 5
BP 1081
EP +
DI 10.1016/j.suc.2015.05.002
PG 15
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA CS4OM
UT WOS:000362055300014
PM 26315525
DA 2025-01-04
ER

PT J
AU Su, D
   Liu, C
   Cui, J
   Tang, JB
   Ruan, YL
   Zhang, YQ
AF Su, Dan
   Liu, Chao
   Cui, Jie
   Tang, Jiebing
   Ruan, Yuli
   Zhang, Yanqiao
TI Advances and prospects of drug clinical research in colorectal cancer in
   2022
SO CANCER INNOVATION
LA English
DT Review
DE colorectal cancer; chemotherapy; targeted therapy; immunotherapy
ID KRAS G12C INHIBITOR; OPEN-LABEL; PHASE-III; PLUS CETUXIMAB; MCRC
   PATIENTS; CHEMOTHERAPY; TRASTUZUMAB; THERAPY; PANITUMUMAB; COMBINATION
AB Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer death worldwide. Clinical research results have provided more treatment opportunities for CRC patients, showing that an optimal combination of existing drugs and new drugs is needed to mitigate the burden of this disease. In this review, we have summarized recent advances in drug clinical research for CRC in 2022, including chemotherapy, targeted therapy, and immunotherapy, to find opportunities for substantial improvements in drug discovery and clinical development methods.
   Colorectal cancer (CRC) represents the leading cause of cancer-related death worldwide. The advent of fluorouracil in 1962 ushered in a new era of anticolorectal cancer drugs in the treatment of CRC; the rapid advancement of molecularly targeted therapy and immunotherapy has also offered a new therapeutic paradigm for patients. This article reviews the most recent studies in the field of CRC in 2022, which will be presented in terms of three aspects: chemotherapy, targeted therapy, and immunotherapy. image
C1 [Su, Dan; Liu, Chao; Cui, Jie; Tang, Jiebing; Ruan, Yuli; Zhang, Yanqiao] Harbin Med Univ, Canc Hosp, Dept Gastrointestinal Med Oncol, Harbin, Heilongjiang Pr, Peoples R China.
   [Su, Dan; Liu, Chao; Tang, Jiebing; Zhang, Yanqiao] Harbin Med Univ, Clin Res Ctr Colorectal Canc Heilongjiang, Canc Hosp, Harbin, Heilongjiang Pr, Peoples R China.
C3 Harbin Medical University; Harbin Medical University
RP Zhang, YQ (corresponding author), Harbin Med Univ, Canc Hosp, Dept Gastrointestinal Med Oncol, Harbin, Heilongjiang Pr, Peoples R China.
EM yanqiaozhang@ems.hrbmu.edu.cn
RI Zhang, Zixuan/JSL-3603-2023
FU National Natural Science Foundation of China [82102858, 82173233,
   U22A20330]
FX National Natural Science Foundation of China, Grant/Award Numbers:
   82102858, 82173233, U22A20330
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NR 68
TC 2
Z9 2
U1 7
U2 10
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 APR
PY 2023
VL 2
IS 2
BP 99
EP 113
DI 10.1002/cai2.62
PG 15
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA G8M7Q
UT WOS:001319119700005
PM 38090057
OA gold, Green Accepted
DA 2025-01-04
ER

PT J
AU Chen, JR
   Zhao, JT
   Xie, ZZ
AF Chen, Jian-Rui
   Zhao, Jing-Tong
   Xie, Zhen-Zhen
TI Integrin-mediated cancer progression as a specific target in clinical
   therapy
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Integrins; Cancer therapy; Anti -cancer drugs
ID ALPHA-V-INTEGRINS; NEWLY-DIAGNOSED GLIOBLASTOMA; HUMAN
   MONOCLONAL-ANTIBODY; SQUAMOUS-CELL CARCINOMA; LUNG-CANCER; PHASE-I;
   COLORECTAL-CANCER; ALPHA(V)BETA(3) INTEGRIN; RANDOMIZED PHASE-2;
   1ST-LINE TREATMENT
AB Integrins, a group of heterodimer receptors for cell-matrix and cell-cell adhesion, mediate various intracellular activities, including cell migration, polarity, survival, growth, and death. Multiple types of integrins are differentially expressed in various cancers during different stages of progression, which are involved in the regulation of cancer cell proliferation, invasion, migration, and angiogenesis. The crucial roles of integrins in tumor progression provide valuable clues for cancer diagnosis and targeted therapy. Numerous integrin inhibitors have been investigated in clinical trials to explore effective regimens and minimize side effects. Given the complexity of the integrin-mediated tumor-promoting effect, challenges and difficulties remain in the research and development of integrin inhibitors, which seriously restrict the efficacy and application of integrin-targeted therapy. Novel targeted therapy of integrins, however, is beneficial for patients as a potential avenue forward, which needs better pharmacological effect, valid experimental models, and in-depth understanding of integrins. This review provides the insight needed to elucidate the mechanisms underlying cancer progression and novel protocols for the clinical treatment of cancer.
C1 [Chen, Jian-Rui; Zhao, Jing-Tong; Xie, Zhen-Zhen] Nanchang Univ, Expt teaching Ctr Basic Med Coll, Nanchang 330006, Jiangxi, Peoples R China.
   [Chen, Jian-Rui; Zhao, Jing-Tong] Nanchang Univ, Queen Mary Sch, Med Dept, Nanchang 330006, Jiangxi, Peoples R China.
C3 Nanchang University; Nanchang University
RP Xie, ZZ (corresponding author), Nanchang Univ, Expt teaching Ctr Basic Med Coll, Nanchang 330006, Jiangxi, Peoples R China.
EM xiezhenzhengirl@163.com
RI 陈, 建芮/ISV-4420-2023
FU Fund of the National Natural Science Foundation of China [41966006]
FX This work was supported by the Fund of the National Natural Science
   Foundation of China (No. 41966006) . We are grateful for the critical
   revision of the manuscript by Anamika Dinesh (MD) , India. Fig. 4 was
   partly generated using Servier Medical Art, provided by Servier,
   licensed under a Creative Commons Attribution 3.0 unported license. We
   thank Accdon ( www.accdon.com ) for its linguistic assistance during the
   preparation of this manuscript.
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NR 149
TC 24
Z9 26
U1 1
U2 14
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD NOV
PY 2022
VL 155
AR 113745
DI 10.1016/j.biopha.2022.113745
EA SEP 2022
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 5B0ZH
UT WOS:000863304900006
PM 36182738
OA gold
DA 2025-01-04
ER

PT J
AU Sun, C
   España, S
   Buges, C
   Layos, L
   Hierro, C
   Manzano, JL
AF Sun, Chen
   Espana, Sofia
   Buges, Cristina
   Layos, Laura
   Hierro, Cinta
   Manzano, Jose Luis
TI Treatment of Advanced BRAF-Mutated Colorectal Cancer: Where We Are and
   Where We Are Going
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE BRAF-mutant; Colorectal cancer; Target therapy; BRAF gene; Treatment;
   Clinical Trials
ID FOLFOXIRI PLUS BEVACIZUMAB; MICROSATELLITE INSTABILITY; 1ST-LINE
   TREATMENT; COLON-CANCER; OPEN-LABEL; PHASE IB; INHIBITION; MUTATIONS;
   VEMURAFENIB; CETUXIMAB
AB In recent years, studies on the molecular typing of colorectal cancer have matured, and the V-raf murine sarcoma viral oncogene homolog B (BRAF) of the mitogen-activated protein kinase pathway has been shown to be an important effector molecule of this pathway and regulates the occurrence and development of colorectal cancer. Clinical observations indicate that colorectal cancer patients harboring the BRAF V600E mutation have a worse prognosis than BRAF wild type patients. Several resistance mechanisms have been identified that have led to the development of different treatment strategies, which have shown encouraging activity in early clinical trials. Therefore, a reasonable combination of targeted therapies is expected to further enhance the efficacy of selective BRAF inhibitors. Moreover, some CRC patients with high microsatellite instability or a mismatch repair deficiency seem to be susceptible to checkpoint inhibitors with objective and sustained clinical responses, providing new opportunities for patients with advanced disease. This article primarily explores 3 aspects of the treatment strategies for advanced BRAF-mutated colorectal cancer; chemotherapy, targeted therapy, and immunotherapy. (C) 2022 Elsevier Inc. All rights reserved.
C1 [Sun, Chen] Zhengzhou Univ, Affiliated Hosp 2, Dept Tumor Radiotherapy, Zhengzhou, Peoples R China.
   [Espana, Sofia; Buges, Cristina; Layos, Laura; Hierro, Cinta; Manzano, Jose Luis] Inst Catala Oncol Badalona, Catalan Inst Oncol, Dept Med Oncol, Barcelona, Spain.
C3 Zhengzhou University; Institut Catala d'Oncologia
RP España, S (corresponding author), Catalan Inst Oncol, Inst Catala Oncol Badalona, Med Oncol, Barcelona, Spain.
EM sofia.ef@iconcologia.net
RI Hierro, Cinta/HSG-4163-2023
OI Layos Romero, Laura/0000-0002-0537-6061; Sun, Chen/0000-0002-1611-3144
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NR 56
TC 4
Z9 4
U1 0
U2 9
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 2022
VL 21
IS 2
BP 71
EP 79
DI 10.1016/j.clcc.2022.01.009
EA MAY 2022
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 1Z9UE
UT WOS:000809159000004
PM 35277355
DA 2025-01-04
ER

PT J
AU Li, J
   Sun, AH
   Zhong, GF
   He, Y
   Xiong, HL
   Yuan, X
AF Li, Jun
   Sun, Aihua
   Zhong, Guofang
   He, Ying
   Xiong, Hailin
   Yuan, Xia
TI Mutation analysis of a 10-gene panel for colorectal cancer in Huizhou,
   Guangdong Province of China
SO JOURNAL OF INTERNATIONAL MEDICAL RESEARCH
LA English
DT Article
DE Colorectal cancer; gene panel; next-generation sequencing; targeted
   therapy; Huizhou; mutation
ID GROWTH; RESISTANCE; BIOMARKER; CETUXIMAB; MARKERS
AB Objective This study aimed to investigate the type and frequency of mutations in 10 genes in 85 colorectal cancer (CRC) patients in Huizhou and the guiding significance of targeted drug use. Methods The 10-gene panel next-generation sequencing (NGS) was used to assess genetic variants in 85 CRC patients from the Huizhou area combined with clinical information for a comprehensive analysis. Results Upon initial mutation testing, 68% (58/85) were positive. The mutation frequencies of these genes, including KRAS, PIK3CA, NRAS, ERBB2, BRAF, EGFR, and PDGFRA, were 51%, 20%, 5%, 4%, 4%, 1%, and 1%, respectively. Overall, 29 mutation types were detected from seven genes. More mutations were detected in more advanced cancers. There were three samples with multiple mutations of a single gene, including KRAS (n = 2) and ERBB2 (n = 2), 12 samples with multiple mutations of double genes, including KRAS/PIK3CA (n = 10), BRAF/PIK3CA (n = 1), and NRAS/PIK3CA (n = 1), and one sample with multiple mutations of three genes, including ERBB2/KRAS/PIK3CA (n = 1). Theoretically, 27 patients could receive targeted treatment. During the actual treatment, 10 patients received bevacizumab, cetuximab, or fruquintinib with no progression ranging from 12 to 24 months. Conclusion Gene mutations detected by a 10-gene panel were useful for targeting therapy of CRC in Huizhou.
C1 [Li, Jun; Yuan, Xia] Huizhou First Hosp, Dept Med Oncol, 20 Sanxin South Rd, Huizhou 516001, Guangdong, Peoples R China.
   [Sun, Aihua; Zhong, Guofang; He, Ying; Xiong, Hailin] Huizhou Municipal Ctr Hosp, Dept Med Oncol, Huizhou, Guangdong, Peoples R China.
RP Yuan, X (corresponding author), Huizhou First Hosp, Dept Med Oncol, 20 Sanxin South Rd, Huizhou 516001, Guangdong, Peoples R China.
EM Yuanxia_zlnk@163.com
FU Huizhou Science and Technology Program [20161128152026]
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and publication of this article: This study was
   funded by Huizhou Science and Technology Program (No. 20161128152026).
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NR 32
TC 2
Z9 2
U1 0
U2 3
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0300-0605
EI 1473-2300
J9 J INT MED RES
JI J. Int. Med. Res.
PD NOV
PY 2021
VL 49
IS 11
AR 03000605211061040
DI 10.1177/03000605211061040
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA XJ3ST
UT WOS:000726712900001
PM 34851763
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Leowattana, W
   Leowattana, P
   Leowattana, T
AF Leowattana, Wattana
   Leowattana, Pathomthep
   Leowattana, Tawithep
TI Systemic treatment for metastatic colorectal cancer
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Systemic treatment; Metastatic colorectal cancer; Personalized medicine;
   Biomarkers; Chemotherapy; Targeted therapy; Immunotherapy
ID ANTI-EGFR THERAPY; LIVER METASTASES; OPEN-LABEL; MICROSATELLITE
   INSTABILITY; PLUS BEVACIZUMAB; 1ST-LINE THERAPY; REPAIR-DEFICIENT; KRAS
   MUTATION; CETUXIMAB; BRAF
AB Significant progress has been achieved in the treatment of metastatic colorectal cancer (mCRC) patients during the last 20 years. There are currently numerous treatments available for the first-line treatment of mCRC. Sophisticated molecular technologies have been developed to reveal novel prognostic and predictive biomarkers for CRC. The development of next-generation sequencing and whole-exome sequencing, which are strong new tools for the discovery of predictive molecular biomarkers to facilitate the delivery of customized treatment, has resulted in tremendous breakthroughs in DNA sequencing technology in recent years. The appropriate adjuvant treatments for mCRC patients are determined by the tumor stage, presence of high-risk pathologic characteristics, microsatellite instability status, patient age, and performance status. Chemotherapy, targeted therapy, and immunotherapy are the main systemic treatments for patients with mCRC. Despite the fact that these novel treatment choices have increased overall survival for mCRC, survival remains optimal for individuals with non-metastatic disease. The molecular technologies currently being used to support our ability to practice personalized medicine; the practical aspects of applying molecular biomarkers to regular clinical practice; and the evolution of chemotherapy, targeted therapy, and immunotherapy strategies for the treatment of mCRC in the front-line setting are all reviewed here.
C1 [Leowattana, Wattana; Leowattana, Pathomthep] Mahidol Univ, Fac Trop Med, Clin Trop Med, 420-6 Rajavithi Rd, Bangkok 10400, Thailand.
   [Leowattana, Tawithep] Srinakharinwirot Univ, Fac Med, Dept Med, Bangkok 10110, Thailand.
C3 Mahidol University; Srinakharinwirot University
RP Leowattana, W (corresponding author), Mahidol Univ, Fac Trop Med, Clin Trop Med, 420-6 Rajavithi Rd, Bangkok 10400, Thailand.
EM wattana.leo@mahidol.ac.th
RI Leowattana, Wattana/V-8320-2019
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NR 100
TC 31
Z9 31
U1 1
U2 4
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAR 14
PY 2023
VL 29
IS 10
BP 1569
EP 1588
DI 10.3748/wjg.v29.i10.1569
PG 20
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA C3JV8
UT WOS:000960928500003
PM 36970592
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Chen, YC
   Huang, CW
   Li, CC
   Chang, TK
   Su, WC
   Chen, PJ
   Yeh, YS
   Chang, YT
   Tsai, HL
   Shih, MCP
   Wang, JY
AF Chen, Yen-Cheng
   Huang, Ching-Wen
   Li, Ching-Chun
   Chang, Tsung-Kun
   Su, Wei-Chih
   Chen, Po-Jung
   Yeh, Yung-Sung
   Chang, Yu-Tang
   Tsai, Hsiang-Lin
   Shih, Ming-Chen Paul
   Wang, Jaw-Yuan
TI Efficacy of transarterial chemoembolization with drug-eluting beads
   combined with systemic chemotherapy and targeted therapy in colorectal
   cancer liver metastasis
SO WORLD JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer with liver metastasis; Drug-eluting bead;
   Trans-arterial chemoembolization; Targeted therapy; Chemotherapy
ID TRANS-ARTERIAL CHEMOEMBOLIZATION; HEPATIC INTRAARTERIAL INJECTION;
   IRINOTECAN DOSE-ESCALATION; PHASE-II; 1ST-LINE BEVACIZUMAB; TACE;
   FOLFIRI; DEBIRI; POLYMORPHISM; CETUXIMAB
AB BackgroundSystemic therapy is the standard treatment for unresectable colorectal cancer with liver metastasis (CRCLM). Transarterial chemoembolization with drug-eluting beads (DEB-TACE) is considered an effective treatment option for CRCLM. Few studies have investigated the combination of DEB-TACE, chemotherapy, and targeted therapy for CRCLM. In the present study, we evaluated the disease control rate (DCR), adverse events, and survival among patients with CRCLM who underwent the combination of DEB-TACE and chemotherapy/targeted therapy.MaterialsWe retrospectively reviewed 35 patients with CRCLM who were treated between January 2015 and January 2021. Standard systemic chemotherapy, targeted therapy, and 66 DEB-TACE procedures were administered. Data were collected on each DEB-TACE procedure, including chemotherapy agents, tumor burden of liver metastasis, number of DEB-TACE courses, and adverse events. Patients who received DEB-TACE after failure of first-line systemic therapy were categorized into the first-line failure group. Patients who received DEB-TACE after the failure of second-line, third-line, or fourth-line therapy were categorized into the other group. Subgroup analysis was performed to compare overall survival (OS) and progression-free survival (PFS) between the two groups.ResultsIn total, 35 patients with CRCLM (34 patients with adenocarcinoma and 1 patient with neuroendocrine carcinoma) were enrolled. In total, 13 patients (37.1%) had extrahepatic metastases at initial diagnosis. In this study, 66 DEB-TACE procedures were performed. The DCR was 54.3%. The median OS period was 47.4 months, and the estimated 3-year OS rate was 59.5%. The median PFS period was 6.3 months, and the estimated 1-year PFS rate was 20.6%. The PFS period was longer in the first-line failure group than in the other group (7.2 vs. 6.3 months). No significant difference was observed in OS between the two groups. Four episodes (6.1%) of grade 3 intra-abdominal infection were observed.ConclusionThe combination of chemotherapy, targeted therapy, and DEB-TACE can lead to a favorable DCR and survival outcomes in patients with CRCLM. Early intervention with DEB-TACE (i.e., after the failure of first-line therapy) has the potential to extend the PFS period in patients with CRCLM. Severe adverse events were rare and manageable. Further prospective, randomized controlled studies are warranted to obtain more conclusive findings.
C1 [Chen, Yen-Cheng; Chang, Tsung-Kun; Su, Wei-Chih; Chen, Po-Jung; Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.
   [Chen, Yen-Cheng; Huang, Ching-Wen; Li, Ching-Chun; Chang, Tsung-Kun; Su, Wei-Chih; Chen, Po-Jung; Tsai, Hsiang-Lin; Wang, Jaw-Yuan] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, 100 Tzyou 1st Rd, Kaohsiung 807, Taiwan.
   [Huang, Ching-Wen; Chang, Yu-Tang; Tsai, Hsiang-Lin; Wang, Jaw-Yuan] Kaohsiung Med Univ, Coll Med, Fac Med, Dept Surg, Kaohsiung, Taiwan.
   [Chang, Tsung-Kun; Su, Wei-Chih] Kaohsiung Med Univ, Coll Med, Fac Postbaccalaureate Med, Dept Surg, Kaohsiung 80708, Taiwan.
   [Yeh, Yung-Sung] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Div Trauma & Surg Crit Care, Dept Surg, Kaohsiung 80708, Taiwan.
   [Yeh, Yung-Sung] Kaohsiung Med Univ, Coll Med, Fac Postbaccalaureate Med, Dept Emergency Med, Kaohsiung 80708, Taiwan.
   [Yeh, Yung-Sung] Taipei Med Univ, Grad Inst Injury Prevent & Control, Coll Publ Hlth, Taipei 11031, Taiwan.
   [Chang, Yu-Tang] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Pediat Surg, Kaohsiung 80708, Taiwan.
   [Shih, Ming-Chen Paul] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Med Imaging, Kaohsiung 80708, 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.
C3 Kaohsiung Medical University; Kaohsiung Medical University; Kaohsiung
   Medical University Hospital; Kaohsiung Medical University; Kaohsiung
   Medical University; Kaohsiung Medical University; Kaohsiung Medical
   University Hospital; Kaohsiung Medical University; Taipei Medical
   University; Kaohsiung Medical University; Kaohsiung Medical University
   Hospital; Kaohsiung Medical University; Kaohsiung Medical University
   Hospital; Kaohsiung Medical University; Kaohsiung Medical University
RP Wang, JY (corresponding author), Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, 100 Tzyou 1st Rd, Kaohsiung 807, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Coll Med, Fac Med, Dept Surg, Kaohsiung, Taiwan.; Shih, MCP (corresponding author), Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Med Imaging, 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.
EM stoneshih2007@gmail.com; Jawyuanwang@gmail.com
RI Wang, Xiuxing/HGU-0583-2022
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, KMUH109-9M33];
   Kaohsiung Medical University Research Center Grant [KMU-TC112A04]; Grant
   of Taiwan Precision Medicine Initiative and Taiwan Biobank, Academia
   Sinica, Taiwan
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, KMUH109-9M33) 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.
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NR 40
TC 2
Z9 2
U1 4
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 DEC 1
PY 2023
VL 21
IS 1
AR 378
DI 10.1186/s12957-023-03253-w
PG 11
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA Z4VL0
UT WOS:001112068600001
PM 38041083
OA gold
DA 2025-01-04
ER

PT J
AU Underwood, PW
   Pawlik, TM
AF Underwood, Patrick W.
   Pawlik, Timothy M.
TI Precision Medicine for Metastatic Colorectal Cancer: Where Do We Stand?
SO CANCERS
LA English
DT Review
DE targeted therapy; colon cancer; molecular profiling; personalized
   medicine
ID CETUXIMAB PLUS IRINOTECAN; CONSENSUS MOLECULAR SUBTYPES; MISMATCH
   REPAIR-DEFICIENT; POSITIVE SOLID TUMORS; PHASE-III TRIAL; OPEN-LABEL;
   1ST-LINE TREATMENT; COLON-CANCER; DOUBLE-BLIND; RANDOMIZED PHASE-3
AB Metastatic colorectal cancer is a leading cause of cancer-related death across the world. The treatment paradigm has shifted away from systemic chemotherapy alone to include targeted therapy and immunotherapy. The past two decades have been characterized by increased investigation into molecular profiling of colorectal cancer. These molecular profiles help physicians to better understand colorectal cancer biology among patients with metastatic disease. Additionally, improved data on genetic pathways allow for specific therapies to be targeted at the underlying molecular profile. Investigation of the EGFR, VEGF, HER2, and other pathways, as well as deficient mismatch repair, has led to the development of multiple targeted therapies that are now utilized in the National Comprehensive Cancer Network guidelines for colon and rectal cancer. While these new therapies have contributed to improved survival for metastatic colorectal cancer, long-term survival remains poor. Additional investigation to understand resistance to targeted therapy and development of new targeted therapy is necessary. New therapies are under development and are being tested in the preclinical and clinical settings. The aim of this review is to provide a comprehensive evaluation of molecular profiling, currently available therapies, and ongoing obstacles in the field of colorectal cancer.
C1 [Underwood, Patrick W.; Pawlik, Timothy M.] Ohio State Univ, Wexner Med Ctr, Dept Surg, 395 W 12th Ave,Suite 670, Columbus, OH 43210 USA.
C3 University System of Ohio; Ohio State University
RP Pawlik, TM (corresponding author), Ohio State Univ, Wexner Med Ctr, Dept Surg, 395 W 12th Ave,Suite 670, Columbus, OH 43210 USA.
EM patrick.underwood@osumc.edu; tim.pawlik@osumc.edu
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   Zheng SS, 2023, CANCERS, V15, DOI 10.3390/cancers15071948
   Zheng-Lin B, 2024, THER ADV MED ONCOL, V16, DOI 10.1177/17588359231225037
NR 115
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2024
VL 16
IS 22
AR 3870
DI 10.3390/cancers16223870
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA N4L4H
UT WOS:001364071100001
PM 39594824
OA gold
DA 2025-01-04
ER

PT J
AU Zhang, YQ
   Sun, J
   Song, YX
   Gao, P
   Wang, X
   Chen, M
   Li, Y
   Wu, ZH
AF Zhang, Yaqing
   Sun, Jie
   Song, Yongxi
   Gao, Peng
   Wang, Xin
   Chen, Miao
   Li, Yuan
   Wu, Zhonghua
TI Roles of fusion genes in digestive system cancers: Dawn for cancer
   precision therapy
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Fusion gene; Digestive system; Cancer; Targeted therapy
ID ONCOGENIC ALK FUSION; COLORECTAL-CANCER; CHROMOSOMAL TRANSLOCATIONS;
   CHIMERIC TRANSCRIPT; ACQUIRED-RESISTANCE; TARGETED THERAPY; TYROSINE
   KINASE; GASTRIC-CANCER; BETA-CATENIN; LUNG-CANCER
AB For advanced cancers of the digestive system, personalized, precise treatment can be life saving. With the development of next-generation sequencing technology, detection of fusion genes in solid tumors has become more extensive. Some fusion gene targeting therapies have been written into guidelines for digestive tract tumors, such as for neurotrophic receptor tyrosine kinase and fibroblast growth factor receptor 2. There are also many fusion genes being investigated as potential future therapeutic targets. This review focuses on the current detection methods for fusion genes, fusion genes written into the digestive system tumor guidelines, and potential fusion gene therapy targets in different organs to discuss the possibility of clinical treatments for these targets in digestive system cancers.
C1 [Zhang, Yaqing; Sun, Jie; Song, Yongxi; Gao, Peng; Wang, Xin; Chen, Miao; Li, Yuan; Wu, Zhonghua] First Hosp China Med Univ, Dept Surg Oncol & Gen Surg, 155 North Nanjing St, Shenyang 110001, Peoples R China.
   [Zhang, Yaqing; Sun, Jie; Gao, Peng; Wang, Xin; Chen, Miao; Li, Yuan; Wu, Zhonghua] China Med Univ, Minist Educ, Key Lab Precis Diag & Treatment Gastrointestinal, 155 North Nanjing St, Shenyang 110001, Peoples R China.
C3 China Medical University
RP Li, Y; Wu, ZH (corresponding author), First Hosp China Med Univ, Dept Surg Oncol & Gen Surg, 155 North Nanjing St, Shenyang 110001, Peoples R China.
EM 15942066533@163.com; wuzhonghua0728@126.com
RI Li, Yuan/GQQ-5806-2022; WU, Zhenduo/AAR-8317-2020
FU General program of National Natural Science Foundation of China
   [81872031, 82172657]; Youth program of National Natural Science
   Foundation of China [82002599]; Support plan for young and middle-aged
   scientific and technological talents in Shenyang [RC190202]
FX We thank very much for the support from the General program of National
   Natural Science Foundation of China (81872031 and82172657) , Youth
   program of National Natural Science Foundation of China (82002599) ,
   Support plan for young and middle-aged scientific and technological
   talents in Shenyang (RC190202) .
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NR 146
TC 10
Z9 10
U1 2
U2 17
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 MAR
PY 2022
VL 171
AR 103622
DI 10.1016/j.critrevonc.2022.103622
EA FEB 2022
PG 15
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA ZG5IU
UT WOS:000760292100010
PM 35124200
OA hybrid
DA 2025-01-04
ER

PT J
AU Jiang, YL
   Zhao, MY
   Tang, WX
   Zheng, XP
AF Jiang, Yunlin
   Zhao, Mingye
   Tang, Wenxi
   Zheng, Xueping
TI Comparison of systemic treatments for previously treated patients with
   unresectable colorectal liver metastases: a systematic review and
   network meta-analysis
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE metastatic colorectal cancer; unresectable liver metastases; network
   meta-analysis; treatment selection; overall survival
ID PHASE-III TRIAL; WILD-TYPE KRAS; DOUBLE-BLIND; 2ND-LINE TREATMENT;
   RANDOMIZED PHASE-3; OPEN-LABEL; 1ST-LINE THERAPY; SUPPORTIVE CARE;
   IRINOTECAN FOLFIRI; PANITUMUMAB PLUS
AB Background There is limited evidence of comparative results among different treatments for patients with unresectable colorectal liver metastases (CRLM) who have failed at least one line of previous systemic therapy. We aimed to compare the efficacy of systemic treatments among these patients through this investigation.Methods We collected randomized controlled trials (RCTs) reported in English up until July 2023, from databases including PubMed, Embase, Cochrane Library, ClinicalTrials.gov, and prominent conference databases, for this Bayesian network meta-analysis. Phase II or III trials that evaluated at least two therapeutic regimens were included. Primary outcome was overall survival (OS), secondary outcome was progression-free survival (PFS). Hazards ratios (HRs) with 95% confidence intervals (CIs) were used as effect size. Subgroup analysis was performed based on metastatic sites. The current systematic review protocol was registered on PROSPERO (CRD42023420498).Results 30 RCTs were included, with a total of 13,511 patients. Compared to chemotherapy, multi-targeted therapy (HR 0.57, 95% CI 0.37-0.87) and targeted therapy plus chemotherapy (HR 0.78, 95% CI 0.67-0.91) show significant advantages. Targeted therapy (HR 0.92, 95% CI 0.54-1.57) and local treatment plus chemotherapy (HR 1.03, 95% CI 0.85-1.23) had comparable performance. For patients with liver metastases, TAS-102 plus bevacizumab, aflibercept plus fluorouracil-based combination chemotherapy (CTFU), and bevacizumab plus capecitabine-based combination chemotherapy (CTCA) showed the best outcomes in terms of OS. Bevacizumab plus intensified CTFU, bevacizumab plus CTCA, and HAI followed by single-agent chemotherapy (SingleCT) performed the best regarding PFS. For patients with liver-limited metastases, aflibercept plus CTFU is the optimal choice in OS. For PFS, the best options were HAI followed by SingleCT, aflibercept plus CTFU, and panitumumab plus CTFU. For patients with multiple-site metastases, the best treatments were TAS-102 plus bevacizumab, bevacizumab plus CTCA, bevacizumab plus CTFU, and aflibercept plus CTFU.Conclusion Multi-targeted therapy and targeted therapy plus chemotherapy are the best treatment mechanisms. TAS-102 plus bevacizumab is superior in OS, the combination of anti-VEGF drugs like bevacizumab and aflibercept with standard chemotherapy is the preferred option for CRLM patients.
C1 [Jiang, Yunlin; Zheng, Xueping] Nanjing Univ Chinese Med, Nanjing Hosp Chinese Med, Nanjing, Peoples R China.
   [Jiang, Yunlin] Nanjing Univ Chinese Med, Grad Sch, Nanjing, Peoples R China.
   [Zhao, Mingye; Tang, Wenxi] China Pharmaceut Univ, Sch Int Pharmaceut Business, Dept Pharmacoecon, Nanjing, Jiangsu, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University of Chinese
   Medicine; China Pharmaceutical University
RP Zheng, XP (corresponding author), Nanjing Univ Chinese Med, Nanjing Hosp Chinese Med, Nanjing, Peoples R China.; Tang, WX (corresponding author), China Pharmaceut Univ, Sch Int Pharmaceut Business, Dept Pharmacoecon, Nanjing, Jiangsu, Peoples R China.
EM tokammy@cpu.edu.cn; zhengxp@njucm.edu.cn
FU National Natural Science Foundation of China10.13039/501100001809
FX No Statement Available
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NR 69
TC 0
Z9 0
U1 3
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 10
PY 2024
VL 14
AR 1293598
DI 10.3389/fonc.2024.1293598
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZI2A2
UT WOS:001274589400001
PM 39050571
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Effendi, YSR
AF Effendi, Y. S. Rustam
TI Colonoscopy, Biomarkers, and Targeted Therapy in Colorectal Cancer
SO ACTA MEDICA INDONESIANA
LA English
DT Review
DE Colonoscopy; colorectal cancer; biomarkers; cancer stem cells; targeted
   therapy
ID STEM-CELLS; PROGNOSIS; INSTABILITY; GUIDELINES; DIAGNOSIS; MICRORNAS;
   MARKERS
AB This review highlights the most versatile diagnostic test of colonoscopy for CRC. It remains the gold standard diagnostic tools for CRC, and to prevent CRC by screening and removing the polyp or premalignant lesions. This work also provides the most promising biomarkers, which highlights the application of the novel biomarkers in conjunction with clinical and pathologic features have allowed for more individualized approaches and targeted therapy to patients with CRC. CRC is the third most common cancer diagnosed, and the second leading cause of cancer-related deaths worldwide. With a population totaling 273,523,621 people, Indonesia has an estimated of 396,914 new cases of all cancers and 234,511 cancer-related deaths. Among those cancer cases, an estimated of 34,189 new CRC cases and 17,786 CRC deaths occurred in 2020. Most of CRC cases were located in the rectum compared to those in the distal colon or proximal colon. Clinical signs, symptoms and therapeutic approaches vary, depending on the stage and the location of CRC. Those cancer locations are different in terms of their associated molecular alterations. Biomarker tests of tumor tissue from colonoscopy biopsy can help doctors to select a specific CRC treatment, and the tests can be used to determine prognostic value, predictive factors and the targeted therapy. Targeted therapies are recommended for advanced or mCRC patients with KRAS/NRAS/BRAF mutated or wild-type tumors, HER2-amplified tumors, and NTRK gene fusion-positive, while immunotherapy is only offered for tumor with MSI-High (dMMR) status. The biomarkers and targeting approaches against colorectal CSCs are being developed and will be quite challenging.
C1 [Effendi, Y. S. Rustam] Univ Sumatera Utara, Adam Malik Hosp, Pirngadi Hosp, Dept Internal Med,Fac Med, Medan, Indonesia.
   [Effendi, Y. S. Rustam] Columbia Asia Hosp, Jl Listrik 2A, Medan 20112, Indonesia.
C3 University of North Sumatra
RP Effendi, YSR (corresponding author), Columbia Asia Hosp, Jl Listrik 2A, Medan 20112, Indonesia.
EM effendiysr@yahoo.com
RI Effendi-YS, Rustam/HOC-7210-2023
CR [Anonymous], 2015, INDONESIA J GASTROEN
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NR 48
TC 7
Z9 7
U1 0
U2 3
PU UNIV INDONESIA, FAC MEDICINE
PI JAKARTA PUSAT
PA JALAN SALEMBA 6, JAKARTA PUSAT, 10430, INDONESIA
SN 0125-9326
EI 2338-2732
J9 ACTA MED INDONES
JI Acta Med. Indones.
PD JUL
PY 2022
VL 54
IS 3
BP 476
EP 486
PG 11
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA 6C7GZ
UT WOS:000882179100016
PM 36156476
DA 2025-01-04
ER

PT J
AU Li, Y
   Xu, C
   Wang, B
   Xu, FJ
   Ma, FH
   Qu, YY
   Jiang, DX
   Li, K
   Feng, JW
   Tian, S
   Wu, XH
   Wang, YZ
   Liu, Y
   Qin, ZY
   Liu, YL
   Qin, J
   Song, Q
   Zhang, XL
   Sujie, A
   Huang, J
   Liu, TS
   Shen, KT
   Zhao, JY
   Hou, YY
   Ding, C
AF Li, Yan
   Xu, Chen
   Wang, Bing
   Xu, Fujiang
   Ma, Fahan
   Qu, Yuanyuan
   Jiang, Dongxian
   Li, Kai
   Feng, Jinwen
   Tian, Sha
   Wu, Xiaohui
   Wang, Yunzhi
   Liu, Yang
   Qin, Zhaoyu
   Liu, Yalan
   Qin, Jing
   Song, Qi
   Zhang, Xiaolei
   Sujie, Akesu
   Huang, Jie
   Liu, Tianshu
   Shen, Kuntang
   Zhao, Jian-Yuan
   Hou, Yingyong
   Ding, Chen
TI Proteomic characterization of gastric cancer response to chemotherapy
   and targeted therapy reveals new therapeutic strategies
SO NATURE COMMUNICATIONS
LA English
DT Article
ID COMPREHENSIVE MOLECULAR CHARACTERIZATION; EXTRACELLULAR-MATRIX PROTEIN;
   MULTICENTER PHASE-II; MICROSATELLITE INSTABILITY; PERIOPERATIVE
   CHEMOTHERAPY; NEOADJUVANT CHEMOTHERAPY; COLORECTAL-CANCER; 1ST-LINE
   THERAPY; OXALIPLATIN; DOCETAXEL
AB Chemotherapy and targeted therapy are the major treatments for gastric cancer (GC), but drug resistance limits its effectiveness. Here, we profile the proteome of 206 tumor tissues from patients with GC undergoing either chemotherapy or anti-HER2-based therapy. Proteome-based classification reveals four subtypes (G-I-G-IV) related to different clinical and molecular features. MSI-sig high GC patients benefit from docetaxel combination treatment, accompanied by anticancer immune response. Further study reveals patients with high T cell receptor signaling respond to anti-HER2-based therapy; while activation of extracellular matrix/PI3K-AKT pathway impair anti-tumor effect of trastuzumab. We observe CTSE functions as a cell intrinsic enhancer of chemosensitivity of docetaxel, whereas TKTL1 functions as an attenuator. Finally, we develop prognostic models with high accuracy to predict therapeutic response, further validated in an independent validation cohort. This study provides a rich resource for investigating the mechanisms and indicators of chemotherapy and targeted therapy in GC.
   The mechanisms of resistance to therapy in gastric cancer remain to be explored. Here, proteomic profiling of 206 tumour tissues from patients treated with chemotherapy and anti-HER2-based therapy results in the identification of four molecular subtypes and the development of prognostic models.
C1 [Li, Yan; Li, Kai; Feng, Jinwen; Tian, Sha; Wu, Xiaohui; Wang, Yunzhi; Liu, Yang; Qin, Zhaoyu; Song, Qi; Ding, Chen] Fudan Univ, State Key Lab Genet Engn, Shanghai 200433, Peoples R China.
   [Li, Yan; Li, Kai; Feng, Jinwen; Tian, Sha; Wu, Xiaohui; Wang, Yunzhi; Liu, Yang; Qin, Zhaoyu; Song, Qi; Ding, Chen] Fudan Univ, Inst Biomed Sci, Collaborat Innovat Ctr Genetics & Dev, Human Phenome Inst,Sch Life Sci, Shanghai 200433, Peoples R China.
   [Xu, Chen; Liu, Yalan; Zhang, Xiaolei; Sujie, Akesu; Huang, Jie; Hou, Yingyong] Fudan Univ, Zhongshan Hosp, Dept Pathol, Shanghai 200032, Peoples R China.
   [Wang, Bing] Henan Normal Univ, State Key Lab Cell Differentiat & Regulat, Henan Ctr outstanding overseas scientists Pulm fi, Henan Int Joint Lab Pulm Fibrosis,Coll Life Sci, Xinxiang 453007, Henan, Peoples R China.
   [Xu, Fujiang] Southwest Med Univ, Dept Oncol, Affiliated Hosp, Luzhou 646000, Peoples R China.
   [Qu, Yuanyuan] Fudan Univ, Dept Urol, Shanghai Canc Ctr, Shanghai 200032, Peoples R China.
   [Qu, Yuanyuan] Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China.
   [Qu, Yuanyuan] Shanghai Genitourinary Canc Inst, Shanghai 200032, Peoples R China.
   [Shen, Kuntang] Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Shanghai 200032, Peoples R China.
   [Liu, Tianshu] Fudan Univ, Zhongshan Hosp, Dept Oncol, Shanghai 200032, Peoples R China.
   [Zhao, Jian-Yuan] Shanghai Jiao Tong Univ, Inst Dev mental & Regenerat Cardiovasc, MOE Shanghai Key Lab Childrens Environm Hlth, Sch Med,Xinhua Hosp, Shanghai 200092, Peoples R China.
   [Zhao, Jian-Yuan] Zhengzhou Univ, Sch Basic Med Sci, Dept Anat & Neurosci, Res Inst, Zhengzhou 450001, Peoples R China.
C3 Fudan University; Fudan University; Fudan University; Henan Normal
   University; Southwest Medical University; Fudan University; Fudan
   University; Fudan University; Shanghai Jiao Tong University; Zhengzhou
   University
RP Ding, C (corresponding author), Fudan Univ, State Key Lab Genet Engn, Shanghai 200433, Peoples R China.; Ding, C (corresponding author), Fudan Univ, Inst Biomed Sci, Collaborat Innovat Ctr Genetics & Dev, Human Phenome Inst,Sch Life Sci, Shanghai 200433, Peoples R China.; Hou, YY (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Pathol, Shanghai 200032, Peoples R China.; Shen, KT (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Shanghai 200032, Peoples R China.; Liu, TS (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Oncol, Shanghai 200032, Peoples R China.; Zhao, JY (corresponding author), Shanghai Jiao Tong Univ, Inst Dev mental & Regenerat Cardiovasc, MOE Shanghai Key Lab Childrens Environm Hlth, Sch Med,Xinhua Hosp, Shanghai 200092, Peoples R China.; Zhao, JY (corresponding author), Zhengzhou Univ, Sch Basic Med Sci, Dept Anat & Neurosci, Res Inst, Zhengzhou 450001, Peoples R China.
EM liu.tianshu@zs-hospital.sh.cn; shen.kuntang@zs-hospital.sh.cn;
   zhaojy@fudan.edu.cn; hou.yingyong@zs-hospital.sh.cn; chend@fudan.edu.cn
RI Qin, Jing/U-1171-2019; ding, chen/KDN-1285-2024; Liu,
   Tianshu/H-6879-2019; Zhao, Jianyuan/G-8483-2012; Xu,
   Fujiang/AAG-1575-2019
OI Li, Yan/0000-0001-9041-7675; tian, sha/0000-0003-4407-8873; Feng,
   Jinwen/0000-0003-1683-4280; Li, Kai/0000-0001-6544-6052
FU National Key Research and Development Program of China [2017YFA0505102,
   2016YFA0502500, 2020YFE0201600, 2018YFE0201603, 2017YFA0505101,
   2018YFA0507501, 2017YFC0908404]; National Natural Science Foundation of
   China [31770886, 31972933, 31700682]; Science and Technology Commission
   of Shanghai Municipality [2017SHZDZX01]; Shanghai Science Technique
   Planning Foundation [19441904000]; Shanghai Municipal Key Clinical
   Specialty [shslczdzk 01302]; Shanghai Science and Technology Development
   Fund [19MC1911000]; Major Project of Special Development Funds of
   Zhangjiang National Independent Innovation Demonstration Zone
   [ZJ2019-ZD-004]; China Postdoctoral Science Foundation [2020T130114,
   2019M651268]
FX This work is supported by the National Key Research and Development
   Program of China (2017YFA0505102 [C.D.], 2016YFA0502500 [C.D.],
   2020YFE0201600 [C.D.], 2018YFE0201603 [C.D.], 2017YFA0505101 [C.D.],
   2018YFA0507501 [Z.Y.Q.], and 2017YFC0908404 [Z.Y.Q.]), the National
   Natural Science Foundation of China (31770886 [C.D.], 31972933 [C.D.],
   and 31700682 [C.D.]), the Science and Technology Commission of Shanghai
   Municipality (2017SHZDZX01 [C.D.]), Shanghai Science Technique Planning
   Foundation (no. 19441904000 [Y.Y.H.]), Shanghai Municipal Key Clinical
   Specialty (shslczdzk 01302 [Y.Y.H.]), Shanghai Science and Technology
   Development Fund (No. 19MC1911000 [Y.Y.H.]), the Major Project of
   Special Development Funds of Zhangjiang National Independent Innovation
   Demonstration Zone (ZJ2019-ZD-004 [C.D.]), and China Postdoctoral
   Science Foundation (2020T130114 [J.W.F.], 2019M651268 [Y.Z.W.]).
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NR 97
TC 28
Z9 29
U1 5
U2 51
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
EI 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD SEP 29
PY 2022
VL 13
IS 1
AR 5723
DI 10.1038/s41467-022-33282-0
PG 26
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 4Z2SM
UT WOS:000862065400026
PM 36175412
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Williams, CB
   McMahon, C
   Ali, SM
   Abramovitz, M
   Williams, KA
   Klein, J
   McKean, H
   Yelensky, R
   George, TJ
   Elvin, JA
   Soman, S
   Lipson, D
   Chmielecki, J
   Morosini, D
   Miller, VA
   Stephens, PJ
   Ross, JS
   Leyland-Jones, B
AF Williams, Casey B.
   McMahon, Caitlin
   Ali, Siraj M.
   Abramovitz, Mark
   Williams, Kirstin A.
   Klein, Jessica
   McKean, Heidi
   Yelensky, Roman
   George, Thomas J., Jr.
   Elvin, Julia A.
   Soman, Salil
   Lipson, Doron
   Chmielecki, Juliann
   Morosini, Deborah
   Miller, Vincent A.
   Stephens, Philip J.
   Ross, Jeffrey S.
   Leyland-Jones, Brian
TI A metastatic colon adenocarcinoma harboring <i>BRAF</i> V600E has a
   durable major response to dabrafenib/trametinib and chemotherapy
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE oxaliplatin; colorectal adenocarcinoma; combination targeted therapy;
   BRAF mutations
ID COLORECTAL-CANCER; INHIBITION; RESISTANCE; MUTATIONS
AB The subset of metastatic colorectal adenocarcinomas that harbor BRAF V600E mutations are aggressive tumors with significantly shortened survival and limited treatment options. Here we present a colorectal cancer patient whose disease progressed through standard chemotherapy and who developed liver metastasis. Comprehensive genomic profiling (FoundationOne (R)) identified a BRAF V600E mutation in the liver lesion, as well as other genomic alterations consistent with colorectal cancers. Combination therapy of dabrafenib and trametinib with standard cytotoxic chemotherapy resulted in a durable major ongoing response for the patient. This report illustrates the utility of comprehensive genomic profiling with personalized targeted therapy for aggressive metastatic colorectal adenocarcinomas.
C1 [Williams, Casey B.; Abramovitz, Mark; Williams, Kirstin A.; Klein, Jessica; McKean, Heidi; Leyland-Jones, Brian] Avera Canc Inst, Sioux Falls, SD USA.
   [McMahon, Caitlin; Ali, Siraj M.; Yelensky, Roman; Elvin, Julia A.; Lipson, Doron; Chmielecki, Juliann; Morosini, Deborah; Miller, Vincent A.; Stephens, Philip J.; Ross, Jeffrey S.] Fdn Med Inc, Cambridge, MA USA.
   [George, Thomas J., Jr.] Univ Florida, Coll Med, Gainesville, FL USA.
   [Soman, Salil] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
   [Ross, Jeffrey S.] Albany Med Coll, Albany, NY 12208 USA.
C3 Foundation Medicine; State University System of Florida; University of
   Florida; Harvard University; Beth Israel Deaconess Medical Center;
   Albany Medical College
RP Leyland-Jones, B (corresponding author), Avera Med Grp, Dept Mol & Expt Med, 1000 E 23rd St,Suite 200, Sioux Falls, SD 57105 USA.
EM bleylandj@aol.com
RI George, Thomas/L-9119-2019; Soman, Salil/LRS-7781-2024; Ali,
   Siraj/AAE-2958-2019
OI George, Thomas/0000-0002-6249-9180; Soman, Salil/0000-0002-5887-0717
FU Bristol-Myers Squibb; Bayer Oncology
FX CM, RY, DL, JC, DM, PJS, JSR, JAE, VAM, and SMA are employed by and have
   equity interest in Foundation Medicine, Inc. TJG has received research
   support from Bristol-Myers Squibb and Bayer Oncology. The authors report
   no other conflicts of interest in this work.
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NR 15
TC 9
Z9 9
U1 0
U2 2
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2015
VL 8
BP 3561
EP 3564
DI 10.2147/OTT.S90766
PG 4
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA CX9PY
UT WOS:000366039000001
PM 26664139
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Khiavi, MA
   Safary, A
   Somi, MH
AF Khiavi, Mostafa Akbarzadeh
   Safary, Azam
   Somi, Mohammad Hossein
TI Recent advances in targeted therapy of colorectal cancer: impacts of
   monoclonal antibodies nanoconjugates
SO BIOIMPACTS
LA English
DT Article
DE Monoclonal antibodies; Nanomedicines; Nanoconjugates; Colorectal cancer;
   Targeted therapy; Nanocarrier
ID GROWTH-FACTOR RECEPTOR; MULTIDRUG-RESISTANCE; DRUG-DELIVERY; EGFR;
   FUTURE; NANOPARTICLES; MECHANISMS; COLON; IMMUNOLIPOSOMES; NANOMEDICINE
AB Despite rapid advances in diagnostic and treatment approaches, the overall survival rate of cancer has not been improved. Colorectal cancer (CRC) is recognized as the third leading cause of neoplasm-related deaths worldwide, in large part due to its considerable metastasis and drug resistance. For developing new anticancer strategies, rapid progression of multimodal nanomedicines and nanoconjugates has provided promising treatment modalities for effective therapy of cancer. The limitations of cancer chemotherapy might be overcome through the use of such nanosized therapeutics, including nanoconjugates of monoclonal antibodies (mAbs) along with drugs and organic/inorganic nanoparticles. CRC cells express various molecular markers against which mAbs can be designed and used as targeting/therapeutic agents. This editorial highlights the importance of such targeted nanosystems against CRC.
C1 [Khiavi, Mostafa Akbarzadeh; Somi, Mohammad Hossein] Tabriz Univ Med Sci, Liver & Gastrointestinal Dis Res Ctr, Tabriz, Iran.
   [Khiavi, Mostafa Akbarzadeh; Safary, Azam] Tabriz Univ Med Sci, Res Ctr Pharmaceut Nanotechnol, Biomed Inst, Tabriz 5165665811, Iran.
   [Safary, Azam] Tabriz Univ Med Sci, Connect Tissue Dis Res Ctr, Tabriz, Iran.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science; Tabriz University of Medical Science
RP Somi, MH (corresponding author), Tabriz Univ Med Sci, Liver & Gastrointestinal Dis Res Ctr, Tabriz, Iran.
EM mhosseinsina@yahoo.com
RI Safary, Azam/W-2941-2017; Akbarzadeh Khiavi, Mostafa/AAU-1896-2020;
   Somi, Mohammad/B-1875-2009
OI Akbarzadeh Khiavi, Mostafa/0000-0002-1552-6537; Safary,
   Azam/0000-0002-8997-2003
FU Research Center for Liver and gastrointestinal diseases, Tabriz
   University of Medical Sciences [145/261]; Iran National Science
   Foundation (INSF) [96010102]
FX This work is a part of a Ph.D. thesis supported (grant No: 145/261) by
   the Research Center for Liver and gastrointestinal diseases, Tabriz
   University of Medical Sciences and Iran National Science Foundation
   (INSF) (grant #: 96010102).
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NR 60
TC 22
Z9 22
U1 0
U2 4
PU TABRIZ UNIV MEDICAL SCIENCES & HEALTH SERVICES
PI TABRIZ
PA DANESHGHAH ST, TABRIZ, REPUBLIC ISLAMIC 51664-14766, IRAN
SN 2228-5652
EI 2228-5660
J9 BIOIMPACTS
JI BioImpacts
PY 2019
VL 9
IS 3
BP 123
EP 127
DI 10.15171/bi.2019.16
PG 5
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA IU9UR
UT WOS:000483926500001
PM 31508327
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Sabanathan, D
   Eslick, GD
   Shannon, J
AF Sabanathan, Dhanusha
   Eslick, Guy D.
   Shannon, Jenny
TI Use of Neoadjuvant Chemotherapy Plus Molecular Targeted Therapy in
   Colorectal Liver Metastases: A Systematic Review and Meta-analysis
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE Adjuvant therapy; Combination therapy; Liver resection; Metastatic
   colorectal cancer; Surgery
ID PERIOPERATIVE CHEMOTHERAPY; PHASE-II; CETUXIMAB; BEVACIZUMAB; CANCER;
   IRINOTECAN; OXALIPLATIN; LEUCOVORIN; RESECTION; 5-FLUOROURACIL
AB Surgery remains the standard of care for patients with colorectal liver metastases (CLMs). The use of molecular targeted therapy combined with neoadjuvant chemotherapy for CLMs, however, remains controversial. Current evidence suggests that neoadjuvant chemotherapy plus molecular targeted agents for CLMs confers high overall response rates. Combination treatment might also increase the resectability rates in patients with initially unresectable CLMs.
   Background: Surgery remains the standard of care for patients with colorectal liver metastases (CLMs), with a 5- year survival rate approaching 35%. Perioperative chemotherapy confers a survival benefit in selected patients with CLMs. The use of molecular targeted therapy combined with neoadjuvant chemotherapy for CLMs, however, remains controversial. We reviewed the published data on combination neoadjuvant chemotherapy and molecular targeted therapy for resectable and initially unresectable CLMs. Materials and Methods: A literature search of the Medline and PubMed databases was conducted to identify studies of neoadjuvant chemotherapy plus molecular targeted therapy in the management of resectable or initially unresectable CLMs. We calculated the pooled proportion and 95% confidence intervals using a random effects model for the relationship of the combination neoadjuvant treatment on the overall response rate and performed a systematic review of all identified studies. The analysis was stratified according to the study design. Results: The data from 11 studies of 908 patients who had undergone systemic chemotherapy plus targeted therapy for CLM were analyzed. The use of combination neoadjuvant therapy was associated with an overall response rate of 68% (95% confidence interval, 63%- 73%), with significant heterogeneity observed in the studies (I-2 = 89.35; P < .001). Of the 11 studies, 4 used a combination that included oxaliplatin, 2 included irinotecan, and 5 included a combination of both. Also, 7 studies used cetuximab and 4 bevacizumab. The overall progression-free survival was estimated at 14.4 months. Conclusion: Current evidence suggests that neoadjuvant chemotherapy plus molecular targeted agents for CLM confers high overall response rates. Combination treatment might also increase the resectability rates in initially unresectable CLM. Further studies are needed to examine the survival outcomes, with a focus on the differential role of molecular targeted therapy in the neoadjuvant versus adjuvant setting.
C1 [Sabanathan, Dhanusha; Shannon, Jenny] Nepean Canc Care Ctr, Dept Med Oncol, Sydney, NSW, Australia.
   [Eslick, Guy D.] Univ Sydney, Sydney Med Sch, Whiteley Martin Res Ctr, Discipline Surg, Sydney, NSW, Australia.
C3 University of Sydney
RP Eslick, GD (corresponding author), Univ Sydney, Whiteley Martin Res Ctr, Discipline Surg, Nepean Hosp, Level 5,South Block, Penrith, NSW 2751, Australia.
EM eslickg@med.usyd.edu.au
RI Eslick, Guy/HMT-5739-2023
OI Eslick, Guy/0000-0002-0098-1705
CR Adam R, 2007, J CLIN ONCOL, V25, P4593, DOI 10.1200/JCO.2007.10.8126
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NR 25
TC 20
Z9 22
U1 0
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 DEC
PY 2016
VL 15
IS 4
BP E141
EP E147
DI 10.1016/j.clcc.2016.03.007
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EI7VQ
UT WOS:000392712600001
PM 27174607
DA 2025-01-04
ER

PT J
AU Udagawa, C
   Zembutsu, H
AF Udagawa, Chihiro
   Zembutsu, Hitoshi
TI Pharmacogenetics for severe adverse drug reactions induced by
   molecular-targeted therapy
SO CANCER SCIENCE
LA English
DT Review
DE adverse drug reaction; molecular-targeted drug; pharmacogenetics;
   polymorphism; precision medicine
ID RENAL-CELL CARCINOMA; SINGLE-NUCLEOTIDE POLYMORPHISMS; METASTATIC
   COLORECTAL-CANCER; SUNITINIB-INDUCED TOXICITY; BREAST-CANCER; INDUCED
   HYPERTENSION; DINUCLEOTIDE REPEAT; GENE POLYMORPHISMS; TRASTUZUMAB;
   ASSOCIATION
AB Molecular-targeted drugs specifically interfere with molecules that are frequently overexpressed or mutated in cancer cells. As such, these drugs are generally considered to precisely attack cancer cells, thereby inducing fewer adverse drug reactions (ADRs). However, molecular-targeted drugs can still cause characteristic ADRs that, although rarely severe, can be life-threatening. Therefore, it is becoming increasingly important to be able to predict which patients are at risk of developing ADRs after treatment with molecular-targeted therapy. The emerging field of pharmacogenetics aims to better distinguish the genetic variants associated with drug toxicity and efficacy to improve the selection of therapeutic strategies for each genetic profile. Here, we provide an overview of the current reports on the relationship between genetic variants and molecular-targeted drug-induced severe ADRs in oncology.
C1 [Udagawa, Chihiro] Natl Canc Ctr, Dept Genet Med & Serv, Tokyo, Japan.
   [Zembutsu, Hitoshi] Natl Canc Ctr, Dept Clin Genom, Res Inst, Tokyo, Japan.
C3 National Cancer Center - Japan; National Cancer Center - Japan
RP Zembutsu, H (corresponding author), Natl Canc Ctr, Dept Clin Genom, Res Inst, Chuo Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
EM hzenbuts@ncc.go.jp
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NR 73
TC 11
Z9 11
U1 1
U2 14
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 OCT
PY 2020
VL 111
IS 10
BP 3445
EP 3457
DI 10.1111/cas.14609
EA AUG 2020
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NX4CL
UT WOS:000563623900001
PM 32780457
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Valentini, AM
   Cavalcanti, E
   Di Maggio, M
   Caruso, ML
AF Valentini, Anna M.
   Cavalcanti, Elisabetta
   Di Maggio, Marianna
   Caruso, Maria L.
TI RAS-expanded Mutations and HER2 Expression in Metastatic Colorectal
   Cancer: A New Step of Precision Medicine
SO APPLIED IMMUNOHISTOCHEMISTRY & MOLECULAR MORPHOLOGY
LA English
DT Article
DE cetuximab; RAS; HER2; target therapy; colorectal cancer
ID RANDOMIZED PHASE-III; WILD-TYPE KRAS; MONOCLONAL-ANTIBODY;
   CONTROLLED-TRIALS; GASTRIC-CANCER; SCORING SYSTEM; PANITUMUMAB;
   RESISTANCE; EFFICACY; CARCINOMA
AB Cetuximab and panitumumab monoclonal antibodies are a milestone in the history of treatment of metastatic colorectal cancer (mCRC) and point toward future directions for personalized treatment. Recent studies have shown that broader RAS testing is needed to select patients for targeted therapy. The objectives of our study were to identify the prevalence of RAS mutations and evaluate human epidermal growth factor receptor 2 (HER2) expression in KRAS exon 2 wild-type (WT) mCRC patients, correlating the findings with objective response rate, progression-free survival, and overall survival. In total, 29 mCRC patients undergoing treatment with cetuximab therapy were enrolled in this study. By pyrosequencing, mutations were found in 17% of nonresponder patients, in KRAS codon 146 and NRAS codon 12. HER2 positivity was limited to only 1 responder carcinoma specimen. There was no correlation between RAS mutation, HER2/neu expression, and clinicopathologic findings. We highlighted significantly the differences between objective response rate and RAS gene status. The overall survival and progression-free survival of RAS WT patients were higher compared with those with RAS-mutated disease. Clinical response to cetuximab therapy is impaired in the presence of RAS-expanded mutations. In fact, our finding of 5 mutations in RAS-expanded genes allowed us to understand the resistance to cetuximab in 33% of KRAS WT exon 2 nonresponder patients. HER2 does not seem to be a potential biomarker for cetuximab-targeted therapy. These analyses suggest that the assessment of other biomarkers is needed to determine the best treatment for patients with mCRC, to maximize benefit and minimize harm.
C1 [Valentini, Anna M.; Cavalcanti, Elisabetta; Di Maggio, Marianna; Caruso, Maria L.] Sci Inst Digest Dis S de Bellis, Dept Pathol, Via Turi 27, I-70013 Castellana Grotte, BA, Italy.
C3 IRCCS Saverio de Bellis
RP Valentini, AM (corresponding author), Sci Inst Digest Dis S de Bellis, Dept Pathol, Via Turi 27, I-70013 Castellana Grotte, BA, Italy.
EM am.valentini@irccsdebellis.it
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NR 30
TC 2
Z9 2
U1 1
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 SEP
PY 2018
VL 26
IS 8
BP 539
EP 544
DI 10.1097/PAI.0000000000000475
PG 6
WC Anatomy & Morphology; Medical Laboratory Technology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anatomy & Morphology; Medical Laboratory Technology; Pathology
GA GV1RA
UT WOS:000445856700004
PM 30199395
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Su, C
   Olsen, KA
   Bond, CE
   Whitehall, VLJ
AF Su, Chang
   Olsen, Kelly A. A.
   Bond, Catherine E. E.
   Whitehall, Vicki L. J.
TI The Efficacy of Using Patient-Derived Organoids to Predict Treatment
   Response in Colorectal Cancer
SO CANCERS
LA English
DT Review
DE colorectal cancer; organoids; personalised medicine
ID SOLID TUMORS; COLON-CANCER; FLUOROURACIL; LEUCOVORIN; IRINOTECAN;
   CAPECITABINE; CHEMOTHERAPY; SENSITIVITY; MECHANISM; CETUXIMAB
AB Simple Summary Colorectal cancer is the third most commonly diagnosed cancer. Patients may receive chemotherapy, targeted therapy, immunotherapy, radiotherapy, and/or surgery. However, not all patients will benefit from each available treatment option. There has been rising interest in personalised medicine, which refers to tailoring treatment plans to the unique characteristics of each patient's cancer. Patient-derived tumour organoids are three-dimensional models of patients' cancer cells which can be tested for sensitivity to various treatment options in the laboratory. This review summarises studies which have explored whether the organoid's sensitivity in the laboratory corresponds to the patient's response in the clinic. Tumour organoids are promising models for personalised medicine in the context of selecting chemotherapy and radiotherapy options. Further advancements in organoid technology are required for testing immunotherapy and certain targeted therapy options. Overall, future clinical trials of organoid testing prior to treatment commencement will support the implementation of organoid-based personalised medicine in the clinic. Colorectal cancer is an important cause of morbidity and mortality worldwide. The current treatment landscape includes chemotherapy, targeted therapy, immunotherapy, radiotherapy, and surgery. A key challenge to improving patient outcomes is the significant inter-patient heterogeneity in treatment response. Tumour organoids derived from the patients' tumours via surgically resected or endoscopically biopsied tissue, have emerged as promising models for personalised medicine. This review synthesises the findings, to date, of studies which have explored the efficacy of ex vivo organoid sensitivity testing for predicting treatment response. Most studies have focused on predicting the response to standard-of-care radiotherapy and chemotherapy options. There is strong evidence to support organoid sensitivity testing of ionising radiation, 5-fluorouracil, and irinotecan, and to a lesser extent, oxaliplatin and TAS-102. Fewer studies have used organoids to identify patients who are likely to benefit from novel treatment options that otherwise remain in clinical trials. This review also summarises recent advancements in organoid culture to include non-epithelial components of the tumour microenvironment, to allow testing of immunotherapy and certain targeted therapy options. Overall, further prospective trials will support the implementation of organoid-based personalised medicine for colorectal cancer patients in the future.
C1 [Su, Chang; Olsen, Kelly A. A.; Bond, Catherine E. E.; Whitehall, Vicki L. J.] QIMR Berghofer Med Res Inst, Conjoint Gastroenterol Lab, Herston, QLD 4006, Australia.
   [Su, Chang; Whitehall, Vicki L. J.] Univ Queensland, Fac Med, Brisbane, QLD 4006, Australia.
   [Whitehall, Vicki L. J.] Conjoint Internal Med Lab, Pathol Queensland, Herston, QLD 4006, Australia.
C3 QIMR Berghofer Medical Research Institute; University of Queensland
RP Whitehall, VLJ (corresponding author), QIMR Berghofer Med Res Inst, Conjoint Gastroenterol Lab, Herston, QLD 4006, Australia.; Whitehall, VLJ (corresponding author), Univ Queensland, Fac Med, Brisbane, QLD 4006, Australia.; Whitehall, VLJ (corresponding author), Conjoint Internal Med Lab, Pathol Queensland, Herston, QLD 4006, Australia.
EM vicki.whitehall@qimrberghofer.edu.au
RI Whitehall, Vicki/E-5414-2019
FU Medical Research Future Fund Rapid Applied Research Translation Program
   (Centre for Personalised Analysis of Cancers) [GA59729]
FX This work was supported by funding from the Medical Research Future Fund
   Rapid Applied Research Translation Program (Centre for Personalised
   Analysis of Cancers; GA59729). We are grateful to the Garry Whyte Sea
   Angel PAF for generous financial support.
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NR 77
TC 13
Z9 13
U1 5
U2 25
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD FEB
PY 2023
VL 15
IS 3
AR 805
DI 10.3390/cancers15030805
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 8T5EN
UT WOS:000929285100001
PM 36765763
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Au, TH
   Wang, K
   Stenehjem, D
   Garrido-Laguna, I
AF Au, Trang H.
   Wang, Kai
   Stenehjem, David
   Garrido-Laguna, Ignacio
TI Personalized and precision medicine: integrating genomics into treatment
   decisions in gastrointestinal malignancies
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Next generation sequencing (NGS); targeted therapies; precision medicine
ID PHASE-III TRIAL; ADVANCED PANCREATIC-CANCER; CELL LUNG-CANCER;
   COLORECTAL-CANCER; TYROSINE KINASE; HEPATOCELLULAR-CARCINOMA;
   COLON-CANCER; DOUBLE-BLIND; 1ST-LINE TREATMENT; TARGETED THERAPY
AB The advent of next generation sequencing (NGS) technologies has advanced our understanding of the intrinsic biology of different gastrointestinal (GI) tumor types. The use of novel, more efficient sequencing platforms has improved turnaround times of sequencing results. This is providing real time opportunities to put precision medicine to the test. A number of early phase clinical trials are testing targeted therapies in unique molecularly characterized subsets of patients (baskets). While basket studies are gaining momentum, treatment failures serve to remind us that shifting from a histology-driven to a histologyagnostic approach is unlikely to be a failure-free strategy for a number of tumor types as recently learnt from vemurafenib failure in BRAF mutated metastatic colorectal cancer (mCRC). GI malignancies are clinically and molecularly heterogeneous. Unfortunately, development of biomarkers of response to therapy as well as targeted therapies for GI adenocarcinomas has fallen behind compared to other malignancies. Trastuzumab is the only FDA approved targeted therapy for GI adenocarcinomas for which a biomarker of response (HER2 amplifications) is available. In addition, RAS mutations are known to predict lack of response to epidermal growth factor receptor (EGFR) inhibitors in advanced colorectal cancer (CRC) patients. However, NGS has recently revealed that a number of actionable genetic aberrations are present at low prevalence across different GI malignancies. Prospective randomized clinical trials will determine whether matching actionable aberration with targeted therapy will contribute to improve survival in patients with GI malignancies. Here, we review current evidence for targeted therapies in GI malignancies, as well as application and pitfalls of NGS including tissue testing and liquid biopsies.
C1 [Au, Trang H.; Stenehjem, David] Univ Utah, Coll Pharm, Dept Pharmacotherapy, Salt Lake City, UT 84112 USA.
   [Wang, Kai] OrigiMed, Shanghai 200000, Peoples R China.
   [Stenehjem, David; Garrido-Laguna, Ignacio] Univ Utah, Sch Med, Ctr Invest Therapeut, Salt Lake City, UT USA.
   [Garrido-Laguna, Ignacio] Univ Utah, Sch Med, Huntsman Canc Inst, Div Oncol, Salt Lake City, UT 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; Huntsman Cancer Institute
RP Garrido-Laguna, I (corresponding author), Univ Utah, Sch Med, GI Oncol, 2000 Circle Hope,Suite 2100, Salt Lake City, UT 84112 USA.; Garrido-Laguna, I (corresponding author), Univ Utah, Sch Med, Huntsman Canc Inst, Dept Internal Med,Phase Program 1,Oncol Div, Salt Lake City, UT 84112 USA.
EM ignacio.garrido-laguna@hci.utah.edu
RI Garrido-Laguna, Ignacio/ABD-1875-2020
OI Stenehjem, David/0000-0002-1831-285X
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TC 19
Z9 20
U1 1
U2 11
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD JUN
PY 2017
VL 8
IS 3
BP 387
EP 404
DI 10.21037/jgo.2017.01.04
PG 18
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA FB4US
UT WOS:000406137900005
PM 28736627
OA Green Published
DA 2025-01-04
ER

PT J
AU Drilon, A
   Sharma, MR
   Johnson, ML
   Yap, TA
   Gadgeel, S
   Nepert, D
   Feng, G
   Reddy, MB
   Harney, AS
   Elsayed, M
   Cook, AW
   Wong, CE
   Hinklin, RJ
   Jiang, YT
   Brown, EN
   Neitzel, NA
   Laird, ER
   Wu, W
   Singh, A
   Wei, P
   Ching, KA
   Gaudino, JJ
   Lee, PA
   Hartley, DP
   Rothenberg, SM
AF Drilon, Alexander
   Sharma, Manish R.
   Johnson, Melissa L.
   Yap, Timothy A.
   Gadgeel, Shirish
   Nepert, Dale
   Feng, Gang
   Reddy, Micaela B.
   Harney, Allison S.
   Elsayed, Mohamed
   Cook, Adam W.
   Wong, Christina E.
   Hinklin, Ronald J.
   Jiang, Yutong
   Brown, Eric N.
   Neitzel, Nickolas A.
   Laird, Ellen R.
   Wu, Wen -, I
   Singh, Anurag
   Wei, Ping
   Ching, Keith A.
   Gaudino, John J.
   Lee, Patrice A.
   Hartley, Dylan P.
   Rothenberg, S. Michael
TI SHP2 Inhibition Sensitizes Diverse Oncogene-Addicted Solid Tumors to
   Re-treatment with Targeted Therapy
SO CANCER DISCOVERY
LA English
DT Article
ID PROTEIN-TYROSINE-PHOSPHATASE; LUNG-CANCER; RESISTANCE
AB Rationally targeted therapies have transformed cancer treatment, but many patients develop resistance through bypass signaling pathway activation. PF-07284892 (ARRY-558) is an allosteric SHP2 inhibitor designed to overcome bypass-signaling-mediated resist-ance when combined with inhibitors of various oncogenic drivers. Activity in this setting was confi rmed in diverse tumor models. Patients with ALK fusion-positive lung cancer, BRAFV600E-mutant colorectal cancer, KRASG12D-mutant ovarian cancer, and ROS1 fusion-positive pancreatic cancer who previously developed targeted therapy resistance were treated with PF-07284892 on the fi rst dose level of a fi rst-in-human clinical trial. After progression on PF-07284892 monotherapy, a novel study design allowed the addition of oncogene-directed targeted therapy that had previously failed. Combination therapy led to rapid tumor and circulating tumor DNA (ctDNA) responses and extended the duration of overall clinical benefi t. SIGNIFICANCE: PF-07284892-targeted therapy combinations overcame bypass-signaling-mediated resistance in a clinical setting in which neither component was active on its own. This provides proof of concept of the utility of SHP2 inhibitors in overcoming resistance to diverse targeted therapies and provides a paradigm for accelerated testing of novel drug combinations early in clinical development.
C1 [Drilon, Alexander] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10065 USA.
   [Drilon, Alexander] Weill Cornell Med Coll, New York, NY USA.
   [Sharma, Manish R.] START Midwest, Grand Rapids, MI USA.
   [Johnson, Melissa L.] Sarah Cannon Res Inst, Nashville, TN USA.
   [Yap, Timothy A.] Univ Texas MD Anderson Canc Ctr, Houston, TX USA.
   [Gadgeel, Shirish] Henry Ford Hlth, Henry Ford Canc Ctr, Detroit, MI USA.
   [Nepert, Dale; Reddy, Micaela B.; Harney, Allison S.; Elsayed, Mohamed; Cook, Adam W.; Wong, Christina E.; Hinklin, Ronald J.; Jiang, Yutong; Brown, Eric N.; Neitzel, Nickolas A.; Laird, Ellen R.; Wu, Wen -, I; Singh, Anurag; Gaudino, John J.; Lee, Patrice A.; Hartley, Dylan P.; Rothenberg, S. Michael] Pfizer Boulder Res Unit, Boulder, CO USA.
   [Feng, Gang] Pfizer Inc, Early Clin Dev, Massa, Italy.
   [Wei, Ping; Ching, Keith A.; Rothenberg, S. Michael] Pfizer Oncol Res & Dev, La Jolla, CA USA.
   [Rothenberg, S. Michael] Pfizer Inc, 3200 Walnut St, Boulder, CO 80301 USA.
C3 Memorial Sloan Kettering Cancer Center; Cornell University; Weill
   Cornell Medicine; Sarah Cannon Research Institute; University of Texas
   System; UTMD Anderson Cancer Center; Henry Ford Health System; Pfizer;
   Pfizer; Pfizer
RP Drilon, A (corresponding author), Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10065 USA.; Rothenberg, SM (corresponding author), Pfizer Inc, 3200 Walnut St, Boulder, CO 80301 USA.
EM drilona@mskcc.org; smichael.rothenberg@pfizer.com
RI Singh, Anurag/AAS-1727-2021; Jiang, Yutong/KUF-1282-2024; Yap,
   Timothy/AAV-3573-2020
OI Gadgeel, Shirish/0000-0001-5240-3811; Johnson,
   Melissa/0000-0001-9874-1314; Yap, Timothy/0000-0002-2154-3309; Wong,
   Christina/0009-0000-8597-7176; Sharma, Manish/0009-0000-9769-0850;
   Elsayed, Mohamed/0000-0002-1353-7259; Drilon,
   Alexander/0000-0001-6806-9061; Feng, Gang/0000-0002-0212-415X
FU NCI of the NIH [P30 CA008748, 1R01CA273224-01]
FX & nbsp;We thank Pfizer Boulder Research & Development and Array
   BioPharma colleagues, including Shannon L. Winski, James F. Blake, Mark
   Chicarelli, and Lauren Hanson. The study was funded by Pfizer, Inc. A.
   Drilon was supported in part by the NCI of the NIH under award numbers
   P30 CA008748 and 1R01CA273224-01.
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NR 28
TC 33
Z9 34
U1 3
U2 5
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 AUG
PY 2023
VL 13
IS 8
BP 1789
EP 1801
DI 10.1158/2159-8290.CD-23-0361
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA O9QG6
UT WOS:001047085800001
PM 37269335
OA Green Submitted, Green Published, hybrid
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Capuozzo, M
   Santorsola, M
   Landi, L
   Granata, V
   Perri, F
   Celotto, V
   Gualillo, O
   Nasti, G
   Ottaiano, A
AF Capuozzo, Maurizio
   Santorsola, Mariachiara
   Landi, Loris
   Granata, Vincenza
   Perri, Francesco
   Celotto, Venere
   Gualillo, Oreste
   Nasti, Guglielmo
   Ottaiano, Alessandro
TI Evolution of Treatment in Advanced Cholangiocarcinoma: Old and New
   towards Precision Oncology
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE cholangiocarcinoma; ivosidenib; pemigatinib; target therapy; genetics;
   precision oncology
ID POSITIVE SOLID TUMORS; OPEN-LABEL; INTRAHEPATIC CHOLANGIOCARCINOMAS;
   COLORECTAL-CANCER; TARGETED THERAPY; CHEMOTHERAPY; MULTICENTER;
   LAROTRECTINIB; TRASTUZUMAB; DABRAFENIB
AB Cholangiocarcinoma (CCA) is a malignant neoplasm arising in the epithelium of the biliary tract. It represents the second most common primary liver cancer in the world, after hepatocellular carcinoma, and it constitutes 10-15% of hepatobiliary neoplasms and 3% of all gastrointestinal tumors. As in other types of cancers, recent studies have revealed genetic alterations underlying the establishment and progression of CCA. The most frequently involved genes are APC, ARID1A, AXIN1, BAP1, EGFR, FGFRs, IDH1/2, RAS, SMAD4, and TP53. Actionable targets include alterations of FGFRs, IDH1/2, BRAF, NTRK, and HER2. "Precision oncology" is emerging as a promising approach for CCA, and it is possible to inhibit the altered function of these genes with molecularly oriented drugs (pemigatinib, ivosidenib, vemurafenib, larotrectinib, and trastuzumab). In this review, we provide an overview of new biologic drugs (their structures, mechanisms of action, and toxicities) to treat metastatic CCA, providing readers with panoramic information on the trajectory from "old" chemotherapies to "new" target-oriented drugs.
C1 [Capuozzo, Maurizio; Celotto, Venere] Coordinamento Farmaceut, I-80056 Ercolano, Italy.
   [Santorsola, Mariachiara; Granata, Vincenza; Perri, Francesco; Nasti, Guglielmo; Ottaiano, Alessandro] Ist Nazl Tumori Napoli, IRCCS G Pascale, Via M Semmola, I-80131 Naples, Italy.
   [Landi, Loris] Ds 58 ASL Naples 3, I-80056 Ercolano, Italy.
   [Gualillo, Oreste] Santiago Univ Clin Hosp, SERGAS Serv Galego Saude, Santiago De Compostela 15706, Spain.
   [Gualillo, Oreste] Santiago Univ Clin Hosp, Res Lab 9, NEIRID Lab Neuroendocrine Interact Rheumatol & Inf, IDIS, Santiago De Compostela 15706, Spain.
C3 IRCCS Fondazione Pascale; Complexo Hospitalario Universitario de
   Santiago de Compostela; Complexo Hospitalario Universitario de Santiago
   de Compostela
RP Ottaiano, A (corresponding author), Ist Nazl Tumori Napoli, IRCCS G Pascale, Via M Semmola, I-80131 Naples, Italy.
EM a.ottaiano@istitutotumori.na.it
RI Perri, Francesco/AAB-6392-2019; Capuozzo, Maurizio/IWM-1393-2023;
   Granata, Vincenza/K-6733-2016; GUALILLO, ORESTE/B-8223-2008
OI Ottaiano, Alessandro/0000-0002-2901-3855; Santorsola,
   Mariachiara/0000-0003-2689-3014; Capuozzo, Maurizio/0000-0001-9488-6057;
   Granata, Vincenza/0000-0002-6601-3221; GUALILLO,
   ORESTE/0000-0002-7154-1328; Perri, Francesco/0000-0001-8158-7509
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NR 87
TC 11
Z9 11
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD DEC
PY 2022
VL 23
IS 23
AR 15124
DI 10.3390/ijms232315124
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 6Y8FD
UT WOS:000897323400001
PM 36499450
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Richtig, G
   Kienzl, M
   Rittchen, S
   Roula, D
   Eberle, J
   Sarif, Z
   Pichler, M
   Hoefler, G
   Heinemann, A
AF Richtig, Georg
   Kienzl, Melanie
   Rittchen, Sonja
   Roula, David
   Eberle, Juergen
   Sarif, Zina
   Pichler, Martin
   Hoefler, Gerald
   Heinemann, Akos
TI Cannabinoids Reduce Melanoma Cell Viability and Do Not Interfere with
   Commonly Used Targeted Therapy in Metastatic Melanoma In Vivo and In
   Vitro
SO BIOLOGY-BASEL
LA English
DT Article
DE cannabinoid; melanoma; pharmacology; therapy
ID COLON-CANCER CELLS; TUMOR-GROWTH; PPAR-ALPHA; RECEPTOR; APOPTOSIS;
   ACTIVATION; EXPRESSION; DEATH; CB1; INHIBITION
AB Background: Cannabinoids are mainly used for recreational purposes, but also made their way into oncology, since these substances can be taken to increase appetite in tumour cachexia. Since there are some hints in the literature that cannabinoids might have some anti-cancerous effects, the aim of this study was to study if and how cannabinoids mediate pro-apoptotic effects in metastatic melanoma in vivo and in vitro and its value besides conventional targeted therapy in vivo.Methods: Several melanoma cell lines were treated with different concentrations of cannabinoids, and anti-cancerous efficacy was assessed by proliferation and apoptosis assays. Subsequent pathway analysis was performed using apoptosis, proliferation, flow cytometry and confocal microscopy data. The efficacy of cannabinoids in combination with trametinib was studied in NSG mice in vivo.Results: Cannabinoids reduced cell viability in multiple melanoma cell lines in a dose-dependent way. The effect was mediated by CB1, TRPV1 and PPARa receptors, whereby pharmacological blockade of all three receptors protected from cannabinoid-induced apoptosis. Cannabinoids initiated apoptosis by mitochondrial cytochrome c release with consecutive activation of different caspases. Essentially, cannabinoids significantly decreased tumour growth in vivo and were as potent as the MEK inhibitor trametinib.Conclusions: We could demonstrate that cannabinoids reduce cell viability in several melanoma cell lines, initiate apoptosis via the intrinsic apoptotic pathway by cytochrome c release and caspase activation and do not interfere with commonly used targeted therapy.
C1 [Richtig, Georg; Kienzl, Melanie; Rittchen, Sonja; Roula, David; Heinemann, Akos] Med Univ Graz, Otto Loewi Res Ctr Vasc Biol Immunol & Inflammat, Div Pharmacol, A-8010 Graz, Austria.
   [Richtig, Georg; Pichler, Martin] Med Univ Graz, Dept Internal Med, Div Oncol, A-8036 Graz, Austria.
   [Kienzl, Melanie] BioTechMed Graz, A-8010 Graz, Austria.
   [Eberle, Juergen; Sarif, Zina] Charite Univ med Berlin, Univ Med Ctr Charite, Skin Canc Ctr Charite, Dept Dermatol Venereol & Allergol, D-10117 Berlin, Germany.
   [Hoefler, Gerald] Med Univ Graz, Diag & Res Inst Pathol, A-8036 Graz, Austria.
C3 Medical University of Graz; Medical University of Graz; Berlin Institute
   of Health; Free University of Berlin; Humboldt University of Berlin;
   Charite Universitatsmedizin Berlin; Medical University of Graz
RP Richtig, G; Heinemann, A (corresponding author), Med Univ Graz, Otto Loewi Res Ctr Vasc Biol Immunol & Inflammat, Div Pharmacol, A-8010 Graz, Austria.; Richtig, G (corresponding author), Med Univ Graz, Dept Internal Med, Div Oncol, A-8036 Graz, Austria.
EM georg.richtig@medunigraz.at; melanie.kienzl@medunigraz.at;
   sonja.rittchen@medunigraz.at; juergen.eberle@charite.de;
   martin.pichler@medunigraz.at; gerald.hoefler@medunigraz.at;
   akos.heinemann@medunigraz.at
RI Hoefler, Gerald/B-7006-2008; Rittchen, Sonja/ISA-0643-2023; Hoefler,
   Gerald/H-1796-2016
OI Hoefler, Gerald/0000-0002-9056-3063; Eberle, Jurgen/0000-0001-8533-1519;
   Pichler, Martin/0000-0002-8701-9462; Rittchen,
   Sonja/0000-0002-8753-4384; Heinemann, Akos/0000-0002-8554-2372
FU Austrian Science Fund (FWF) [W1241]
FX G.R., S.R., M.K. and D.R. received funding from the Austrian Science
   Fund FWF (doctoral programs: DK-MOLIN (W1241)) and were trained within
   the frame of the Ph.D. Program Molecular Medicine of the Medical
   University of Graz.
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NR 79
TC 4
Z9 4
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2079-7737
J9 BIOLOGY-BASEL
JI Biology-Basel
PD MAY 12
PY 2023
VL 12
IS 5
AR 706
DI 10.3390/biology12050706
PG 19
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA H2LN9
UT WOS:000994333200001
PM 37237519
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Woo, J
   Cohen, SA
   Grim, JE
AF Woo, Janghee
   Cohen, Stacey A.
   Grim, Jonathan E.
TI Targeted therapy in gastroesophageal cancers: past, present and future
SO GASTROENTEROLOGY REPORT
LA English
DT Review
DE esophageal cancer; gastric cancer; targeted therapy; molecular oncology
ID ADVANCED GASTRIC-CANCER; PHASE-II TRIAL; ENDOTHELIAL GROWTH-FACTOR;
   JUNCTION ADENOCARCINOMA; ESOPHAGEAL CANCER; DOUBLE-BLIND; OPEN-LABEL;
   1ST-LINE TREATMENT; COLORECTAL-CANCER; 2ND-LINE TREATMENT
AB Gastroesophageal cancer is a significant global problem that frequently presents at an incurable stage and has very poor survival with standard chemotherapy approaches. This review will examine the epidemiology and molecular biology of gastroesophageal cancer and will focus on the key deregulated signaling pathways that have been targeted in the clinic. A comprehensive overview of clinical data highlighting successes and failures with targeted agents will be presented. Most notably, HER2-targeted therapy with the monoclonal antibody trastuzumab has proven beneficial in first-line therapy and has been incorporated into standard practice. Targeting the VEGF pathway has also proven beneficial, and the VEGFR-targeted monoclonal antibody ramucirumab is now approved for second-line therapy. In contrast to these positive results, agents targeting the EGFR and MET pathways have been evaluated extensively in gastroesophageal cancer but have repeatedly failed to show benefit. An increased understanding of the molecular predictors of response to targeted therapies is sorely needed. In the future, improved molecular pathology approaches should subdivide this heterogeneous disease entity to allow individualization of cancer therapy based on integrated and global identification of deregulated signaling pathways. Better patient selection, rational combinations of targeted therapies and incorporation of emerging immunotherapeutic approaches should further improve the treatment of this deadly disease.
C1 [Woo, Janghee; Cohen, Stacey A.; Grim, Jonathan E.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
   [Woo, Janghee; Cohen, Stacey A.; Grim, Jonathan E.] Univ Washington, Div Med Oncol, Seattle, WA 98195 USA.
   [Grim, Jonathan E.] VA Puget Sound Hlth Care Syst, Hosp & Specialty Med, 1660 S Columbian Way S-111 ONC, Seattle, WA 98108 USA.
C3 Fred Hutchinson Cancer Center; University of Washington; University of
   Washington Seattle; US Department of Veterans Affairs; Veterans Health
   Administration (VHA); Vet Affairs Puget Sound Health Care System
RP Grim, JE (corresponding author), VA Puget Sound Hlth Care Syst, Hosp & Specialty Med, 1660 S Columbian Way S-111 ONC, Seattle, WA 98108 USA.
EM jgrim@fhcrc.org
RI woo, janghee/CAG-2114-2022
OI Woo, Janghee/0000-0001-9617-4301
FU American Cancer Society [RSG-13-183-01]; National Cancer Institute, US
   NIH [5T32CA009515-30]; Conquer Cancer Foundation of the American Society
   for Clinical Oncology
FX Jonathan Ezra Grim was supported by American Cancer Society
   RSG-13-183-01. Janghee Woo was supported by 5T32CA009515-30 National
   Cancer Institute, US NIH. Stacey A. Cohen was supported by Young
   Investigator Award from the Conquer Cancer Foundation of the American
   Society for Clinical Oncology.
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NR 149
TC 19
Z9 19
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 2052-0034
J9 GASTROENTEROL REP
JI Gastroenterol. Rep.
PD NOV
PY 2015
VL 3
IS 4
SI SI
BP 316
EP 329
DI 10.1093/gastro/gov052
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CW9FX
UT WOS:000365305300006
PM 26510453
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Wu, YC
   Hsu, HH
   Chang, WC
   Tung, HJ
   Ko, KH
   Hsu, YC
   Huang, TW
   Ho, CL
   Chang, H
AF Wu, Yu-Cheng
   Hsu, Hsian-He
   Chang, Wei-Chou
   Tung, Ho-Jui
   Ko, Kai-Hsiung
   Hsu, Yi-Chih
   Huang, Tsai-Wang
   Ho, Ching-Liang
   Chang, Hung
TI Prognostic potential of initial CT changes for progression-free survival
   in gefitinib-treated patients with advanced adenocarcinoma of the lung:
   a preliminary analysis
SO EUROPEAN RADIOLOGY
LA English
DT Article
DE Targeted therapy; Tumour response assessment; Response criteria;
   Non-small cell lung cancer; Survival
ID METASTATIC COLORECTAL-CANCER; SURROGATE END-POINTS; TUMOR RESPONSE;
   TARGETED THERAPY; SOLID TUMORS; ERLOTINIB; CRITERIA; BEVACIZUMAB;
   PREDICTORS; REGRESSION
AB We aimed to determine whether initial tumour responses measured during short-term follow-up computed tomography (CT) examinations after baseline examinations would correlate with clinical outcomes in patients with non-small cell lung cancer (NSCLC) who received epidermal growth factor receptor (EGFR)-targeted therapy.
   A total of 86 gefitinib-treated patients with advanced adenocarcinoma of the lung were retrospectively reviewed. All patients underwent baseline and short-term follow-up CT examinations. The new response criteria (NRC) by Lee et al. were used for the response evaluations. A Cox proportional hazards multiple regression model and Kaplan-Meier survival analyses were used to evaluate correlations between the initial tumour changes and progression-free and overall survival (PFS, OS).
   Better separation and smaller p values were observed for both PFS and OS when good and poor disease responses (as defined by NRC) were compared after excluding tumours with characteristic morphologies. Early tumour changes correlated with PFS in a size-dependent manner. Moreover, a stronger association was observed between size changes and PFS when characteristic morphology was also considered.
   Initial changes in tumour size during short-term post-treatment CT examinations could act as a potential prognostic imaging surrogate for PFS in gefitinib-treated patients with advanced adenocarcinoma of the lung.
C1 [Wu, Yu-Cheng; Hsu, Hsian-He; Chang, Wei-Chou; Ko, Kai-Hsiung; Hsu, Yi-Chih] Triserv Gen Hosp, Dept Radiol, Natl Def Med Ctr, Taipei 114, Taiwan.
   [Tung, Ho-Jui] Asia Univ, Dept Healthcare Adm, Taichung, Taiwan.
   [Huang, Tsai-Wang; Chang, Hung] Triserv Gen Hosp, Div Thorac Surg, Natl Def Med Ctr, Dept Surg, Taipei 114, Taiwan.
   [Ho, Ching-Liang] Triserv Gen Hosp, Div Hematol Oncol, Natl Def Med Ctr, Dept Internal Med, Taipei 114, Taiwan.
C3 Tri-Service General Hospital; National Defense Medical Center; Asia
   University Taiwan; National Defense Medical Center; Tri-Service General
   Hospital; National Defense Medical Center; Tri-Service General Hospital
RP Hsu, HH (corresponding author), Triserv Gen Hosp, Dept Radiol, Natl Def Med Ctr, 325,Sect 2,Cheng Gong Rd, Taipei 114, Taiwan.
EM hsianhe@yahoo.com.tw
RI Chiang, Chi-Ling/O-3038-2016; Wu, Yu/KSL-9195-2024
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NR 38
TC 5
Z9 5
U1 0
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0938-7994
EI 1432-1084
J9 EUR RADIOL
JI Eur. Radiol.
PD JUN
PY 2015
VL 25
IS 6
BP 1801
EP 1813
DI 10.1007/s00330-014-3579-x
PG 13
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA CH5EC
UT WOS:000354056800033
PM 25577523
DA 2025-01-04
ER

PT J
AU Grassi, E
   Corbelli, J
   Papiani, G
   Barbera, MA
   Gazzaneo, F
   Tamberi, S
AF Grassi, Elisa
   Corbelli, Jody
   Papiani, Giorgio
   Barbera, Maria Aurelia
   Gazzaneo, Federica
   Tamberi, Stefano
TI Current Therapeutic Strategies in BRAF-Mutant Metastatic Colorectal
   Cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE colorectal cancer; BRAF mutation; microsatellites instability; targeted
   therapy; immunotherapy
ID FOLFOXIRI PLUS BEVACIZUMAB; 1ST-LINE TREATMENT; MUTATION STATUS; POOLED
   ANALYSIS; PHASE-II; INHIBITION; CHEMOTHERAPY; VEMURAFENIB; INSTABILITY;
   ACTIVATION
AB Around 8-12% of patients with advanced colon rectal cancer (CRC) present with BRAF alterations, in particular V600E mutation, which is associated with right-side, poorly differentiated and mucinous type tumors. The presence of BRAF mutation (BRAF-mt) has been identified as a hallmark of poor prognosis and treatment optimization in this patient subgroup is an important goal. Currently, the standard of care is an aggressive strategy involving triplet chemotherapy and anti-VEGF agents, but new therapeutic approaches are emerging. Very promising results have been obtained with targeted therapy combinations, such as anti-BRAF agents plus anti-EGFR agents. Furthermore, around 60% of BRAF-mt patients show a strong association with high microsatellite instability (MSI-H) and immune checkpoint inhibitors could represent the new standard of care for this subgroup. The focus of this review is to summarize current strategies for BRAF-mt CRC treatment and highlight new therapeutic options.
C1 [Grassi, Elisa; Corbelli, Jody; Papiani, Giorgio; Barbera, Maria Aurelia; Gazzaneo, Federica; Tamberi, Stefano] Azienda Unita Sanit Locale AUSL Romagna, Infermis Hosp, Dept Oncol, Faenza, Italy.
RP Grassi, E (corresponding author), Azienda Unita Sanit Locale AUSL Romagna, Infermis Hosp, Dept Oncol, Faenza, Italy.
EM elisa.grax@gmail.com
OI Tamberi, Stefano/0000-0002-7087-9116
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NR 42
TC 30
Z9 30
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 23
PY 2021
VL 11
AR 601722
DI 10.3389/fonc.2021.601722
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TE8HM
UT WOS:000670247300001
PM 34249672
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Pennel, K
   Dutton, L
   Melissourgou-Syka, L
   Roxburgh, C
   Birch, J
   Edwards, J
AF Pennel, Kathryn
   Dutton, Louise
   Melissourgou-Syka, Lydia
   Roxburgh, Campbell
   Birch, Joanna
   Edwards, Joanne
TI Novel radiation and targeted therapy combinations for improving rectal
   cancer outcomes
SO EXPERT REVIEWS IN MOLECULAR MEDICINE
LA English
DT Review
DE combination therapy; hallmarks of cancer; radiation;
   radio-sensitisation; rectal cancer; synergy; targeted therapy
ID SENSITIZES COLORECTAL-CANCER; IONIZING-RADIATION; PREOPERATIVE
   RADIOTHERAPY; TUMOR MICROENVIRONMENT; INDUCED SENESCENCE; IN-VITRO;
   CHEMORADIOTHERAPY; INHIBITION; EXPRESSION; HALLMARKS
AB Neoadjuvant radiotherapy (RT) is commonly used as standard treatment for rectal cancer. However, response rates are variable and survival outcomes remain poor, highlighting the need to develop new therapeutic strategies. Research is focused on identifying novel methods for sensitising rectal tumours to RT to enhance responses and improve patient outcomes. This can be achieved through harnessing tumour promoting effects of radiation or preventing development of radio-resistance in cancer cells. Many of the approaches being investigated involve targeting the recently published new dimensions of cancer hallmarks. This review article will discuss key radiation and targeted therapy combination strategies being investigated in the rectal cancer setting, with a focus on exploitation of mechanisms which target the hallmarks of cancer.
C1 [Pennel, Kathryn; Dutton, Louise; Melissourgou-Syka, Lydia; Roxburgh, Campbell; Birch, Joanna; Edwards, Joanne] Univ Glasgow, Wolfson Wohl Canc Res Ctr, Sch Canc Sci, Glasgow G61 1BD, Scotland.
   [Melissourgou-Syka, Lydia] CRUK Scotland Inst, Glasgow G61 1BD, Scotland.
   [Roxburgh, Campbell] Univ Glasgow, Glasgow Royal Infirm, Acad Unit Surg, Glasgow G4 0SF, Scotland.
C3 University of Glasgow; University of Glasgow
RP Pennel, K (corresponding author), Univ Glasgow, Wolfson Wohl Canc Res Ctr, Sch Canc Sci, Glasgow G61 1BD, Scotland.
EM Kathryn.Pennel@glasgow.ac.uk
OI Dutton, Louise/0000-0002-9336-7826; Pennel, Kathryn/0000-0003-0186-1331
FU Medical Research Council [EPD/22/13, TCS/22/02]; CRUK RadNet [GN21ON351,
   MR/T04358X/1]; NHS Endowment grant
FX The authors acknowledge funding from CRUK RadNet (J. E., K. P., C. R.),
   Chief Scientific Office (K. P., J. E.) (EPD/22/13, TCS/22/02), NHS
   Endowment grant (GN21ON351) (K. P., J. E.) and UKRI Future Leaders
   Fellowship (MR/T04358X/1) (L. D., J. B.). Biorender was used to
   construct both illustrative figures.
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NR 125
TC 1
Z9 1
U1 2
U2 3
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 16
PY 2024
VL 26
AR e14
DI 10.1017/erm.2024.15
PG 11
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA RF2M0
UT WOS:001226187200001
PM 38623751
OA hybrid, Green Published, Green Accepted
DA 2025-01-04
ER

PT J
AU Konieczkowski, DJ
   Johannessen, CM
   Garraway, LA
AF Konieczkowski, David J.
   Johannessen, Cory M.
   Garraway, Levi A.
TI A Convergence-Based Framework for Cancer Drug Resistance
SO CANCER CELL
LA English
DT Article
ID CELL LUNG-CANCER; METASTATIC BREAST-CANCER; NEUROENDOCRINE
   PROSTATE-CANCER; ACUTE LYMPHOBLASTIC-LEUKEMIA; BRAF INHIBITOR
   RESISTANCE; ANDROGEN-RECEPTOR GENE; ACQUIRED-RESISTANCE;
   COLORECTAL-CANCER; TARGETED THERAPY; RAF INHIBITION
AB Despite advances in cancer biology and therapeutics, drug resistance remains problematic. Resistance is often multifactorial, heterogeneous, and prone to undersampling. Nonetheless, many individual mechanisms of targeted therapy resistance may coalesce into a smaller number of convergences, including pathway reactivation (downstream re-engagement of original effectors), pathway bypass (recruitment of a parallel pathway converging on the same downstream output), and pathway indifference (development of a cellular state independent of the initial therapeutic target). Similar convergences may also underpin immunotherapy resistance. Such parsimonious, convergence-based frameworks may help explain resistance across tumor types and therapeutic categories and may also suggest strategies to overcome it.
C1 [Konieczkowski, David J.] Harvard Radiat Oncol Program, Boston, MA 02114 USA.
   [Johannessen, Cory M.] Broad Inst, Cambridge, MA 02142 USA.
   [Garraway, Levi A.] Eli Lilly & Co, Indianapolis, IN 46225 USA.
C3 Harvard University; Harvard Medical School; Harvard University;
   Massachusetts Institute of Technology (MIT); Broad Institute; Eli Lilly
RP Konieczkowski, DJ (corresponding author), Harvard Radiat Oncol Program, Boston, MA 02114 USA.
EM dkonieczkowski@partners.org
RI Garraway, Levi/M-7391-2014
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NR 173
TC 173
Z9 192
U1 1
U2 33
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 1535-6108
EI 1878-3686
J9 CANCER CELL
JI Cancer Cell
PD MAY 14
PY 2018
VL 33
IS 5
BP 801
EP 815
DI 10.1016/j.ccell.2018.03.025
PG 15
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA GG2BM
UT WOS:000432494500006
PM 29763622
OA Green Accepted, Bronze
DA 2025-01-04
ER

PT J
AU Tanabe, T
   Shida, D
   Boku, N
   Yoshida, T
   Tsukamoto, S
   Takashima, A
   Kanemitsu, Y
AF Tanabe, Taro
   Shida, Dai
   Boku, Narikazu
   Yoshida, Takefumi
   Tsukamoto, Shunsuke
   Takashima, Atsuo
   Kanemitsu, Yukihide
TI Primary Tumor-Related Complications Among Patients With Unresectable
   Stage IV Colorectal Cancer in the Era of Targeted Therapy: A Competing
   Risk Regression Analysis
SO DISEASES OF THE COLON & RECTUM
LA English
DT Article
DE Competing risk analysis; Primary tumor-related complications; Stage IV
   colorectal cancer; Targeted therapy; Unresectable colorectal cancer
ID COLON-CANCER; RESECTION; CHEMOTHERAPY; MANAGEMENT; SURVIVAL; SURGERY
AB BACKGROUND: Whether prolonged survival with current chemotherapy using molecular target agents has changed the rate of primary tumor-related complications in patients with unresectable stage IV colorectal cancer is unclear.
   OBJECTIVE: This study aimed to investigate the rate of primary tumor-related complications among patients receiving targeted therapy as compared with patients receiving chemotherapy without molecular target agents.
   DESIGN: This was a retrospective review of data from a prospectively maintained database.
   SETTINGS: The study was conducted at a high-volume multidisciplinary tertiary cancer center in Japan.
   PATIENTS: Subjects were 352 consecutive patients with unresectable stage IV colorectal cancer who received systemic chemotherapy without primary tumor resection from 2001 to 2015. Patients were categorized into nontargeted and targeted groups according to the use of molecular target agents.
   MAIN OUTCOME MEASURES: Complication rates attributed to primary tumors were measured.
   RESULTS: Of the 352 patients, 159 were categorized into the nontargeted group and 193 patients into the targeted group. Competing risk-adjusted univariate analysis revealed that the primary tumor-related complication rates in the nontargeted group were 6.9% (95% CI, 3.8%-11.9%) at 1 year and 8.2% (95% CI, 4.8%-13.8%) at 2 years, whereas the targeted group had complication rates of 11.5% (95% CI, 7.5%-16.6%) at 1 year and 16.7% (95% CI, 12.4%-23.3%) at 2 years. Multivariate analysis revealed that the targeted group was approximate to 2 times more likely to have primary tumor-related complications (subdistribution HR = 2.04 (95% CI, 1.12-4.01); p = 0.020). Median survival time was 12.0 months in the nontargeted group and 24.1 months in the targeted group (p < 0.001).
   LIMITATIONS: This study was limited by the retrospective design.
   CONCLUSIONS: Targeted therapy was associated with a significantly increased risk of primary tumor-related complications during chemotherapy. However, targeted therapy also improved overall survival, making it a tolerable therapy.
C1 [Tanabe, Taro; Shida, Dai; Yoshida, Takefumi; Tsukamoto, Shunsuke; Kanemitsu, Yukihide] Natl Canc Ctr, Dept Colorectal Surg, Tokyo, Japan.
   [Shida, Dai] Univ Tokyo, Inst Med Sci, Div Frontier Surg, Tokyo, Japan.
   [Boku, Narikazu; Takashima, Atsuo] Natl Canc Ctr, Gastrointestinal Med Oncol Div, Tokyo, Japan.
C3 National Cancer Center - Japan; University of Tokyo; National Cancer
   Center - Japan
RP Shida, D (corresponding author), Univ Tokyo, Inst Med Sci, Div Frontier Surg, Minato Ku, 4-6-1 Shirokanedai, Tokyo 1088639, Japan.
EM dshida@g.ecc.u-tokyo.ac.jp
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NR 27
TC 3
Z9 3
U1 0
U2 0
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 SEP
PY 2021
VL 64
IS 9
BP 1074
EP 1082
DI 10.1097/DCR.0000000000002010
PG 9
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA TY1CD
UT WOS:000683520900016
PM 34397558
DA 2025-01-04
ER

PT J
AU Oddo, D
   Siravegna, G
   Gloghini, A
   Vernieri, C
   Mussolin, B
   Morano, F
   Crisafulli, G
   Berenato, R
   Corti, G
   Volpi, CC
   Buscarino, M
   Niger, M
   Dunne, PD
   Rospo, G
   Valtorta, E
   Bartolini, A
   Fucà, G
   Lamba, S
   Martinetti, A
   Di Bartolomeo, M
   de Braud, F
   Bardelli, A
   Pietrantonio, F
   Di Nicolantonio, F
AF Oddo, Daniele
   Siravegna, Giulia
   Gloghini, Annunziata
   Vernieri, Claudio
   Mussolin, Benedetta
   Morano, Federica
   Crisafulli, Giovanni
   Berenato, Rosa
   Corti, Giorgio
   Volpi, Chiara Costanza
   Buscarino, Michela
   Niger, Monica
   Dunne, Philip D.
   Rospo, Giuseppe
   Valtorta, Emanuele
   Bartolini, Alice
   Fuca, Giovanni
   Lamba, Simona
   Martinetti, Antonia
   Di Bartolomeo, Maria
   de Braud, Filippo
   Bardelli, Alberto
   Pietrantonio, Filippo
   Di Nicolantonio, Federica
TI Emergence of <i>MET</i> hyper-amplification at progression to MET and
   BRAF inhibition in colorectal cancer
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE BRAF; colorectal cancer; crizotinib; drug resistance; target therapy;
   MET
ID ANTIBODY-DRUG CONJUGATE; ACQUIRED-RESISTANCE; C-MET; TARGETED THERAPY;
   LUNG-CANCER; NSCLC; EGFR; COMBINATIONS; CRIZOTINIB; ABBV-399
AB Background: Combined MET and BRAF inhibition showed clinical benefit in a patient with rectal cancer carrying BRAFV600E and MET amplification. However after 4 months, acquired resistance emerged and the patient deceased shortly after disease progression. The mechanism of resistance to this drug combination is unknown.
   Methods: We analysed plasma circulating tumour DNA obtained at progression by exome sequencing and digital PCR. MET gene and mRNA in situ hybridisation analyses in two bioptic specimens obtained at progression were used to confirm the plasma data.
   Results: We identified in plasma MET gene hyper-amplification as a potential mechanism underlying therapy resistance. Increased MET gene copy and transcript levels were detected in liver and lymph node metastatic biopsies. Finally, transduction of MET in BRAF mutant colorectal cancer cells conferred refractoriness to BRAF and MET inhibition.
   Conclusions: We identified in a rectal cancer patient MET gene hyper-amplification as mechanism of resistance to dual BRAF and MET inhibition.
C1 [Oddo, Daniele; Siravegna, Giulia; Crisafulli, Giovanni; Bardelli, Alberto; Di Nicolantonio, Federica] Univ Torino, Dept Oncol, I-10060 Candiolo, TO, Italy.
   [Oddo, Daniele; Siravegna, Giulia; Mussolin, Benedetta; Crisafulli, Giovanni; Corti, Giorgio; Buscarino, Michela; Rospo, Giuseppe; Bartolini, Alice; Lamba, Simona; Bardelli, Alberto; Di Nicolantonio, Federica] IRCCS, Candiolo Canc Inst FPO, I-10060 Candiolo, TO, Italy.
   [Siravegna, Giulia] FIRC Inst Mol Oncol IFOM, I-20139 Milan, Italy.
   [Gloghini, Annunziata; Volpi, Chiara Costanza] Fdn IRCCS Ist Nazl Tumori, Dept Diagnost Pathol & Lab Med, I-20133 Milan, Italy.
   [Vernieri, Claudio; Morano, Federica; Berenato, Rosa; Niger, Monica; Fuca, Giovanni; Martinetti, Antonia; Di Bartolomeo, Maria; de Braud, Filippo; Pietrantonio, Filippo] Fdn IRCCS Ist Nazl Tumori, Med Oncol Dept, I-20133 Milan, Italy.
   [Dunne, Philip D.] Queens Univ Belfast, Ctr Canc Res & Cell Biol, Belfast BT9 7AE, Antrim, North Ireland.
   [Valtorta, Emanuele] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, I-20162 Milan, Italy.
   [de Braud, Filippo] Univ Milan, Dept Oncol, I-20122 Milan, Italy.
C3 University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia; IFOM
   - FIRC Institute of Molecular Oncology; Fondazione IRCCS Istituto
   Nazionale Tumori Milan; Fondazione IRCCS Istituto Nazionale Tumori
   Milan; Queens University Belfast; University of Milan
RP Di Nicolantonio, F (corresponding author), Univ Torino, Dept Oncol, I-10060 Candiolo, TO, Italy.; Di Nicolantonio, F (corresponding author), IRCCS, Candiolo Canc Inst FPO, I-10060 Candiolo, TO, Italy.; Pietrantonio, F (corresponding author), Fdn IRCCS Ist Nazl Tumori, Med Oncol Dept, I-20133 Milan, Italy.
EM filippo.pietrantonio@istitutotumori.mi.it;
   federica.dinicolantonio@unito.it
RI Fuca, Giovanni/AAF-2378-2019; Niger, Monica/AAC-2452-2022; Rospo,
   Giuseppe/AAC-4523-2020; Dunne, Padraic/AAF-8128-2021; Siravegna,
   Giulia/Z-2826-2019; Gloghini, Annunziata/C-1992-2017; Crisafulli,
   Giovanni/AAB-6256-2019; Morano, Federica/B-7910-2018; Pietrantonio,
   Filippo/C-2180-2017; Vernieri, Claudio/J-7426-2018; Di Nicolantonio,
   Federica/A-2503-2011; Di Bartolomeo, Maria/D-1655-2017; BARTOLINI,
   ALICE/K-2534-2018; Volpi, Chiara Costanza/C-2002-2017; BARDELLI,
   Alberto/J-9721-2018; Martinetti, Antonia/L-4011-2017; de Braud, Filippo
   Guglielmo Maria/B-9997-2017
OI VALTORTA, EMANUELE/0000-0002-5087-6233; Gloghini,
   Annunziata/0000-0002-7226-1942; Dunne, Philip/0000-0001-9160-283X;
   Crisafulli, Giovanni/0000-0002-5511-1555; Siravegna,
   Giulia/0000-0002-7132-6484; Morano, Federica/0000-0002-5306-3596;
   Pietrantonio, Filippo/0000-0002-8530-8420; Vernieri,
   Claudio/0000-0003-1577-8176; Rospo, Giuseppe/0000-0002-1757-9085; Corti,
   Giorgio/0000-0001-6379-4117; Di Nicolantonio,
   Federica/0000-0001-9618-2010; Di Bartolomeo, Maria/0000-0002-7954-6609;
   BARTOLINI, ALICE/0000-0003-3492-0772; Volpi, Chiara
   Costanza/0000-0002-8306-6851; ODDO, DANIELE/0000-0001-6179-1668; Fuca,
   Giovanni/0000-0002-1560-2253; BARDELLI, Alberto/0000-0003-1647-5070;
   Martinetti, Antonia/0000-0002-8020-7751; MUSSOLIN,
   BENEDETTA/0000-0001-5723-5685; Niger, Monica/0000-0002-9055-5338; Lamba,
   Simona Elena/0000-0003-3207-1594; de Braud, Filippo Guglielmo
   Maria/0000-0003-0103-730X
FU AIRC IG [17707, 16788]; Fondo per la Ricerca Locale; Universita di
   Torino; AIRC 2010 Special Program Molecular Clinical Oncology 5 per
   mille, Targeting resistances to molecular therapies in metastatic
   colorectal carcinomas [9970]; Fondazione Piemontese per la Ricerca sul
   Cancro-ONLUS 5 per mille 2010 e 2011 Ministero della Salute; European
   Community's Seventh Framework Programme [602901, H2020, 635342-2]; IMI
   [115749]
FX This work was supported by grants AIRC IG n. 17707 (FDN); Fondo per la
   Ricerca Locale (ex 60%), Universita di Torino, 2014 (FDN). Partial
   support was also obtained from AIRC 2010 Special Program Molecular
   Clinical Oncology 5 per mille, Targeting resistances to molecular
   therapies in metastatic colorectal carcinomas, Project n. 9970 (A.
   Bardelli); the Fondazione Piemontese per la Ricerca sul Cancro-ONLUS 5
   per mille 2010 e 2011 Ministero della Salute (AB, FDN); and from the
   European Community's Seventh Framework Programme under grant agreement
   no. 602901 MErCuRIC (AB, FDN). H2020 grant agreement no. 635342-2
   MoTriColor (AB); AIRC IG n. 16788 (AB). IMI contract n. 115749 CANCER-ID
   (AB).
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NR 20
TC 29
Z9 30
U1 1
U2 6
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 JUL 25
PY 2017
VL 117
IS 3
BP 347
EP 352
DI 10.1038/bjc.2017.196
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FB5UL
UT WOS:000406207600008
PM 28654634
OA Green Submitted, Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Zhang, Y
   Hao, MQ
   Yang, XY
   Zhang, S
   Han, JH
   Wang, ZQ
   Chen, HN
AF Zhang, Yang
   Hao, Mengqiu
   Yang, Xuyang
   Zhang, Su
   Han, Junhong
   Wang, Ziqiang
   Chen, Hai-Ning
TI Reactive oxygen species in colorectal cancer adjuvant therapies
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
LA English
DT Review
DE Reactive oxygen species; Colorectal cancer; Adjuvant therapies;
   Oxidative stress; Antioxidant
ID DNA-DAMAGE RESPONSE; OXIDATIVE STRESS MARKERS; CELL-DEATH; MITOCHONDRIAL
   METABOLISM; PHYSIOLOGICAL FUNCTIONS; PHOTODYNAMIC THERAPY; ANTIOXIDANT
   VITAMINS; SIGNALING PATHWAYS; HYDROGEN-PEROXIDE; WNT/BETA-CATENIN
AB Colorectal cancer (CRC), a prevalent global malignancy, often necessitates adjuvant therapies such as chemotherapy, radiotherapy, targeted therapy, and immunotherapy to mitigate tumor burden in advanced stages. The efficacy of these therapies is significantly influenced by reactive oxygen species (ROS). Previous research underscores the pivotal role of ROS in gut pathology, targeted therapy, and drug resistance. ROS-mediated CRC adjuvant therapies encompass a myriad of mechanisms, including cell death and proliferation, survival and cell cycle, DNA damage, metabolic reprogramming, and angiogenesis. Preliminary clinical trials have begun to unveil the potential of ROS-manipulating therapy in enhancing CRC adjuvant therapies. This review aims to provide a comprehensive synthesis of studies exploring the role of ROS in CRC adjuvant therapies.
C1 [Zhang, Yang; Yang, Xuyang; Wang, Ziqiang; Chen, Hai-Ning] Sichuan Univ, West China Hosp, Colorectal Canc Ctr, Chengdu 610041, Peoples R China.
   [Zhang, Yang; Yang, Xuyang; Wang, Ziqiang; Chen, Hai-Ning] Sichuan Univ, West China Hosp, Dept Gen Surg, Chengdu 610041, Peoples R China.
   [Zhang, Yang; Hao, Mengqiu; Yang, Xuyang; Zhang, Su; Han, Junhong; Wang, Ziqiang; Chen, Hai-Ning] Sichuan Univ, West China Hosp, Frontiers Sci Ctr Dis related Mol Network, Dept Gen Surg,Res Lab Tumor Epigenet & Genom, Chengdu 610041, Peoples R China.
   [Zhang, Yang; Hao, Mengqiu; Yang, Xuyang; Zhang, Su; Han, Junhong; Wang, Ziqiang; Chen, Hai-Ning] Sichuan Univ, West China Hosp, Natl Clin Res Ctr Geriatr, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
   [Zhang, Yang; Hao, Mengqiu; Yang, Xuyang; Zhang, Su; Han, Junhong; Wang, Ziqiang; Chen, Hai-Ning] Sichuan Univ, West China Hosp, Canc Ctr, Chengdu, Peoples R China.
   [Wang, Ziqiang; Chen, Hai-Ning] Sichuan Univ, West China Hosp, Colorectal Canc Ctr, Dept Gen Surg, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University; Sichuan
   University; Sichuan University; Sichuan University
RP Wang, ZQ; Chen, HN (corresponding author), Sichuan Univ, West China Hosp, Colorectal Canc Ctr, Dept Gen Surg, Chengdu 610041, Peoples R China.
EM wangziqiang@scu.edu.cn; hnchen@scu.edu.cn
RI Han, Junhong/L-5264-2013; wang, ziqiang/JDV-9934-2023; Chen,
   Hai-Ning/AAR-8059-2021
FU Sichuan Science and Technology Program [2022JDRC0049, 2023YFS0277,
   2021YFS0025]; The 1.3.5 project for disciplines of excellence, West
   China Hospital, Sichuan University [20HXJS003]; The 1.3.5 project for
   disciplines of excellence-Clinical Research Incubation Project; West
   China Hospital, Sichuan University [22HXFH001, 2019HXFH031]; China
   Postdoctoral Science Foundation [2022M712264]; West China Hospital,
   Sichuan University [2021HXBH033]
FX This work was supported by Sichuan Science and Technology Program
   (2022JDRC0049, 2023YFS0277, 2021YFS0025) , 1.3.5 project for disciplines
   of excellence, West China Hospital, Sichuan University (20HXJS003) ,
   1.3.5 project for disciplines of excellence-Clinical Research Incubation
   Project, and West China Hospital, Sichuan Uni-versity (22HXFH001,
   2019HXFH031) , China Postdoctoral Science Foundation (2022M712264) ,
   Post-Doctor Research Project, West China Hospital, Sichuan University
   (2021HXBH033) . Figures in this review were created with the BioRender (
   www.biorender.com ) . The authors acknowledge BioRender.
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NR 199
TC 4
Z9 4
U1 3
U2 11
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 FEB
PY 2024
VL 1870
IS 2
AR 166922
DI 10.1016/j.bbadis.2023.166922
EA NOV 2023
PG 16
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA AE3F5
UT WOS:001116741100001
PM 37898425
DA 2025-01-04
ER

PT J
AU Howe, JR
AF Howe, James R.
TI The impact of DNA testing on management of patients with colorectal
   cancer
SO ANNALS OF GASTROENTEROLOGICAL SURGERY
LA English
DT Review
DE circulating tumor DNA; colorectal cancer; genetics; targeted therapy
ID MISMATCH REPAIR-DEFICIENT; III COLON-CANCER; GERMLINE MUTATIONS;
   OPEN-LABEL; MICROSATELLITE INSTABILITY; PLUS IRINOTECAN; COWDEN-DISEASE;
   GENE; OXALIPLATIN; PTEN
AB Knowledge of the genetic basis of colorectal cancer has evolved over the past decades, allowing for the pre-symptomatic identification of affected patients in those with familial syndromes and to the understanding of the multi-step progression to carcinogenesis in tumors. Knowledge of the genes and pathways involved in colorectal cancer has allowed for targeted therapies in patients in addition to standard chemotherapy for those with metastases. Next-generation sequencing technologies have now also allowed for the sensitive detection of circulating mutations derived from tumors, which can give insight into the presence of residual disease and has implications for changing the standard paradigms for treatment. This article will specifically review advances in targeted therapy in metastatic colon cancer and the progress being made in using circulating tumor DNA in patient management.
C1 [Howe, James R.] Univ Iowa, Dept Surg, Carver Coll Med, 200 Hawkins Dr, Iowa City, IA 52242 USA.
C3 University of Iowa
RP Howe, JR (corresponding author), Univ Iowa, Dept Surg, Carver Coll Med, 200 Hawkins Dr, Iowa City, IA 52242 USA.
EM james-howe@uiowa.edu
RI Howe, James/Q-8170-2018
OI Howe, James/0000-0001-5312-5972
FU National Institutes of Health [P50 CA174521-01]
FX National Institutes of Health, Grant/Award Number: P50 CA174521-01
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NR 73
TC 6
Z9 7
U1 0
U2 1
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 JAN
PY 2022
VL 6
IS 1
BP 17
EP 28
DI 10.1002/ags3.12526
EA NOV 2021
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA YL8PG
UT WOS:000717202400001
PM 35106411
OA Green Published
DA 2025-01-04
ER

PT J
AU Eriksen, M
   Pfeiffer, P
   Rohrberg, KS
   Yde, CW
   Petersen, LN
   Poulsen, LO
   Qvortrup, C
AF Eriksen, Martina
   Pfeiffer, Per
   Rohrberg, Kristoffer Staal
   Yde, Christina Westmose
   Petersen, Lone Norgard
   Poulsen, Laurids Ostergaard
   Qvortrup, Camilla
TI A phase II study of daily encorafenib in combination with biweekly
   cetuximab in patients with BRAF V600E mutated metastatic colorectal
   cancer: the NEW BEACON study
SO BMC CANCER
LA English
DT Article
DE Colorectal cancer; BRAF V600E mutation; BRAF targeted therapy; Biweekly
   cetuximab; Resistance; Genomic profiling
ID EVERY 2ND WEEK; 1ST-LINE TREATMENT; MICROSATELLITE INSTABILITY; PLUS
   CETUXIMAB; DOUBLE-BLIND; MELANOMA; RESISTANCE; VEMURAFENIB; INHIBITION;
   IRINOTECAN
AB BackgroundPatients with BRAF V600E mutated metastatic colorectal cancer (mCRC) have a poor prognosis. The introduction of BRAF targeted therapy with encorafenib and weekly administered cetuximab have shown improved survival with a median progression free survival (PFS) of 4.3 months. However, a regimen with cetuximab given every second week may have comparable efficacy and is more convenient for patients. While BRAF targeted therapy is a new standard therapy in pre-treated patients with BRAF V600E mutated mCRC, resistance invariably occurs and is an emerging challenge. The aim of this study is to investigate the efficacy and tolerability of cetuximab given every second week in combination with daily encorafenib and to explore the correlation between markers of resistance and outcome. MethodsThe study is an open label, single arm, phase II study, investigating the efficacy and tolerability of cetuximab given every second week in combination with encorafenib in patients with BRAF V600E mutated mCRC. Furthermore, we will be investigating mechanisms of response and resistance against BRAF targeted therapy though comprehensive genomic profiling on tumor tissue and blood for circulating tumor DNA analysis. A total of 53 patients (19 + 34 in two steps) will be included according to Simon's optimal two stage design. The primary end point of the study is 2 months PFS rate. DiscussionBy combining BRAF inhibitor with cetuximab given every second week we can halve the number of visits in the hospital compared to the currently approved regimen with weekly cetuximab. This seems particularly relevant in a group of patients with a median overall survival of 9.3 months. Resistance after initial response to targeted therapy can be either adaptive (e.g., epigenetic, or transcriptomic alterations) or acquired (selective genetic alterations - e.g., activating de novo mutations) resistance. It is of great importance to untangle these complex mechanisms of resistance in patients with BRAF V600E mutated mCRC to improve treatment strategies in the future potentially even further.
C1 [Eriksen, Martina; Rohrberg, Kristoffer Staal; Petersen, Lone Norgard; Qvortrup, Camilla] Rigshosp, Copenhagen Univ Hosp, Dept Oncol, Copenhagen, Denmark.
   [Eriksen, Martina; Qvortrup, Camilla] Univ Copenhagen, Fac Hlth & Med Sci, Copenhagen, Denmark.
   [Pfeiffer, Per] Odense Univ Hosp, Dept Oncol, Odense, Denmark.
   [Yde, Christina Westmose] Rigshosp, Dept Genom Med, Copenhagen Univ Hosp, Copenhagen, Denmark.
   [Poulsen, Laurids Ostergaard] Aalborg Univ Hosp, Dept Oncol, Aalborg, Denmark.
C3 Rigshospitalet; University of Copenhagen; University of Copenhagen;
   University of Southern Denmark; Odense University Hospital;
   Rigshospitalet; University of Copenhagen; Aalborg University; Aalborg
   University Hospital
RP Eriksen, M (corresponding author), Rigshosp, Copenhagen Univ Hosp, Dept Oncol, Copenhagen, Denmark.; Eriksen, M (corresponding author), Univ Copenhagen, Fac Hlth & Med Sci, Copenhagen, Denmark.
EM martina.amnitzboell.eriksen@regionh.dk
RI Qvortrup, Camilla/AAD-3366-2019; Poulsen, Laurids/K-6755-2019; Rohrberg,
   Kristoffer/HHZ-8445-2022
OI Pfeiffer, Per/0000-0002-2925-0586; Rohrberg,
   Kristoffer/0000-0002-5448-9003; Eriksen, Martina/0000-0002-4700-2615
FU Pierre Fabre Medicament; Danish Cancer Society
FX This work was supported financially by a grant from Pierre Fabre
   Medicament of 135,000 EUR and by covering of the expenses related to the
   medical product encorafenib. This work is further supported financially
   by a grant from the patient organization the Danish Cancer Society of
   2,500,000 DKK. Pierre Fabre has read and approved the final version of
   the original study protocol. Pierre Fabre and Danish Cancer Society has
   no role in the design of the study and collection, analysis, and
   interpretation of data and in writing the manuscript. The manuscript has
   not undergone any external peer review by the funding bodies.
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NR 40
TC 3
Z9 3
U1 1
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD DEC 16
PY 2022
VL 22
IS 1
AR 1321
DI 10.1186/s12885-022-10420-x
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 7C6ZL
UT WOS:000899958500003
PM 36527039
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Rao, W
   Liu, YT
   Li, Y
   Guo, L
   Qiu, T
   Dong, L
   Ying, JM
   Li, WH
AF Rao, Wei
   Liu, Yutao
   Li, Yan
   Guo, Lei
   Qiu, Tian
   Dong, Lin
   Ying, Jianming
   Li, Weihua
TI Potential unreliability of <i>ALK</i> variant allele frequency in the
   efficacy prediction of targeted therapy in NSCLC
SO FRONTIERS OF MEDICINE
LA English
DT Article
DE ALK fusion; next-generation sequencing; fluorescence in situ
   hybridization; immunohistochemistry; variant allele frequency;
   intratumoral heterogeneity; targeted therapy
ID COLORECTAL-CANCER; COPY NUMBER; LUNG; CRIZOTINIB; GENE; REARRANGEMENT;
   MUTATION; IMMUNOHISTOCHEMISTRY; HETEROGENEITY; CHEMOTHERAPY
AB Anaplastic lymphoma kinase (ALK) is the most common fusion gene involved in non-small cell lung cancer (NSCLC), and remarkable response has been achieved with the use of ALK tyrosine kinase inhibitors (ALK-TKIs). However, the clinical efficacy is highly variable. Pre-existing intratumoral heterogeneity (ITH) has been proven to contribute to the poor treatment response and the resistance to targeted therapies. In this work, we investigated whether the variant allele frequencies (VAFs) of ALK fusions can help assess ITH and predict targeted therapy efficacy. Through the application of next-generation sequencing (NGS), 7.2% (326/4548) of patients were detected to be ALK positive. On the basis of the adjusted VAF (adjVAF, VAF normalization for tumor purity) of four different threshold values (adjVAF < 50%, 40%, 30%, or 20%), the association of ALK subclonality with crizotinib efficacy was assessed. Nonetheless, no statistical association was observed between median progression-free survival (PFS) and ALK subclonality assessed by adjVAF, and a poor correlation of adjVAF with PFS was found among the 85 patients who received first-line crizotinib. Results suggest that the ALK VAF determined by hybrid capture-based NGS is probably unreliable for ITH assessment and targeted therapy efficacy prediction in NSCLC.
C1 [Rao, Wei; Li, Yan; Guo, Lei; Qiu, Tian; Dong, Lin; Ying, Jianming; Li, Weihua] Chinese Acad Med Sci & Peking Union Med Coll, Canc Hosp, Natl Canc Ctr, Natl Clin Res Ctr Canc,Dept Pathol, Beijing 100021, Peoples R China.
   [Liu, Yutao] Chinese Acad Med Sci & Peking Union Med Coll, Canc Hosp, Natl Canc Ctr, Natl Clin Res Ctr Canc,Dept Med Oncol, Beijing 100021, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Cancer Institute & Hospital - CAMS; Peking Union Medical College;
   Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College; Cancer Institute & Hospital - CAMS
RP Ying, JM; Li, WH (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Canc Hosp, Natl Canc Ctr, Natl Clin Res Ctr Canc,Dept Pathol, Beijing 100021, Peoples R China.
EM jmying@cicams.ac.cn; liweihua@cicams.ac.cn
RI Qiu, Tian/JGM-7268-2023; Guo, Lei/AAY-4929-2020
FU National Natural Science Foundation of China [81802294]; Beijing Hope
   Run Special Fund of Cancer Foundation of the People's Republic of China
   [LC2019L04]
FX AcknowledgementsThis work was supported by grants from the National
   Natural Science Foundation of China (No. 81802294) and the Beijing Hope
   Run Special Fund of Cancer Foundation of the People's Republic of China
   (No. LC2019L04).
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NR 43
TC 2
Z9 2
U1 1
U2 6
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 JUN
PY 2023
VL 17
IS 3
BP 493
EP 502
DI 10.1007/s11684-022-0946-x
EA APR 2023
PG 10
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA N6WB4
UT WOS:000962609400001
PM 37010729
DA 2025-01-04
ER

PT J
AU Li, XH
   Wang, HR
   Li, ZY
   Li, DD
   Lu, XF
   Ai, SC
   Dong, YX
   Liu, S
   Wu, JH
   Guan, WX
AF Li, Xianghui
   Wang, Haoran
   Li, Zhiyan
   Li, Dandan
   Lu, Xiaofeng
   Ai, Shichao
   Dong, Yuxiang
   Liu, Song
   Wu, Jinhui
   Guan, Wenxian
TI Oxygen tank for synergistic hypoxia relief to enhance
   mitochondria-targeted photodynamic therapy
SO BIOMATERIALS RESEARCH
LA English
DT Article
DE Organelle targeted therapy; Mitochondrial respiratory inhibition; PDT;
   Artificial red blood cells; Synergistic oxygen modulation; Tumor hypoxia
ID DELIVERY; METABOLISM; ATOVAQUONE; GENERATION; RELEASE; BLOOD; SELF
AB Background Mitochondria play an essential role in cellular redox homeostasis maintenance and meanwhile serve as an important target for organelle targeted therapy. Photodynamic therapy (PDT) is a promising strategy for organelle targeted therapy with noninvasive nature and highly spatiotemporal selectivity. However, the efficacy of PDT is not fully achieved due to tumor hypoxia. Moreover, aerobic respiration constantly consumes oxygen and leads to a lower oxygen concentration in mitochondria, which continuously limited the therapeutic effects of PDT. The lack of organelle specific oxygen delivery method remains a main challenge. Methods Herein, an Oxygen Tank is developed to achieve the organelle targeted synergistic hypoxia reversal strategy, which not only act as an oxygen storage tank to open sources and reduce expenditure, but also coated with red blood cell membrane like the tank with stealth coating. Within the oxygen tank, a mitochondrion targeted photosensitizer (IR780) and a mitochondria respiration inhibitor (atovaquone, ATO) are co-loaded in the RBC membrane (RBCm) coated perfluorocarbon (PFC) liposome core. Results Inside these bio-mimic nanoparticles, ATO effectively inhibits mitochondrial respiration and economized endogenous oxygen consumption, while PFC supplied high-capacity exogenous oxygen. These Oxygen modulators reverse the hypoxia status in vitro and in vivo, and exhibited a superior anti-tumor activity by mitochondria targeted PDT via IR780. Ultimately, the anti-tumor effects towards gastric cancer and colon cancer are elicited in vivo. Conclusions This oxygen tank both increases exogeneous oxygen supply and decreases endogenous oxygen consumption, may offer a novel solution for organelle targeted therapies.
C1 [Li, Xianghui; Li, Zhiyan; Lu, Xiaofeng; Ai, Shichao; Liu, Song; Guan, Wenxian] Nanjing Univ, Med Sch, Affiliated Nanjing Drum Tower Hosp, Dept Gastrointestinal Surg, Nanjing 210008, Peoples R China.
   [Li, Xianghui; Wang, Haoran; Li, Zhiyan; Li, Dandan; Wu, Jinhui] Nanjing Univ, Med Sch, State Key Lab Pharmaceut Biotechnol, Nanjing 210093, Peoples R China.
   [Li, Xianghui; Wang, Haoran; Li, Zhiyan; Li, Dandan; Wu, Jinhui] Nanjing Univ, Sch Life Sci, Nanjing 210093, Peoples R China.
   [Wang, Haoran] Nanjing Univ Chinese Med, Sch Pharm, Dept Pharmacol, Nanjing 210023, Peoples R China.
   [Dong, Yuxiang] Nanjing Med Univ, Clin Med Coll 1, Nanjing 210029, Peoples R China.
   [Wu, Jinhui] Nanjing Univ, Chem & Biomed Innovat Ctr, Nanjing 210023, Peoples R China.
   [Wu, Jinhui] Nanjing Univ, Jiangsu Key Lab Nano Technol, Nanjing 210093, Peoples R China.
C3 Nanjing University; Nanjing University; Nanjing University; Nanjing
   University of Chinese Medicine; Nanjing Medical University; Nanjing
   University; Nanjing University
RP Liu, S; Guan, WX (corresponding author), Nanjing Univ, Med Sch, Affiliated Nanjing Drum Tower Hosp, Dept Gastrointestinal Surg, Nanjing 210008, Peoples R China.; Wu, JH (corresponding author), Nanjing Univ, Med Sch, State Key Lab Pharmaceut Biotechnol, Nanjing 210093, Peoples R China.; Wu, JH (corresponding author), Nanjing Univ, Sch Life Sci, Nanjing 210093, Peoples R China.; Wu, JH (corresponding author), Nanjing Univ, Chem & Biomed Innovat Ctr, Nanjing 210023, Peoples R China.; Wu, JH (corresponding author), Nanjing Univ, Jiangsu Key Lab Nano Technol, Nanjing 210093, Peoples R China.
EM liusong@njglyy.com; wuj@nju.edu.cn; medguanwx@163.com
RI Wang, Haoran/GMW-4523-2022; Wu, Jinhui/J-9476-2012
OI Li, Xianghui/0000-0001-8352-0017; Wu, Jinhui/0000-0001-8809-1290; Wang,
   Haoran/0000-0002-1630-4813
FU National Natural Science Foundation of China [82172645]; Natural Science
   Foundation of Jiangsu Province [BK20200052, BK20220472]; Key project of
   Nanjing Health Commission [ZKX21013]; Bethune Charitable Foundation
   [05002]; Medical School of Nanjing University [2021-LCYJ-MS-09,
   2021-LCYJ-PY-17]
FX The authors acknowledge the support from the National Natural Science
   Foundation of China (82172645), Natural Science Foundation of Jiangsu
   Province (BK20200052, BK20220472), Key project of Nanjing Health
   Commission (ZKX21013), Bethune Charitable Foundation (05002), and
   Clinical Trials from the Affiliated Drum Tower Hospital, Medical School
   of Nanjing University (2021-LCYJ-MS-09 and 2021-LCYJ-PY-17).
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NR 72
TC 17
Z9 17
U1 5
U2 61
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1226-4601
EI 2055-7124
J9 BIOMATER RES
JI Biomater. Res.
PD SEP 22
PY 2022
VL 26
IS 1
AR 47
DI 10.1186/s40824-022-00296-0
PG 17
WC Engineering, Biomedical; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Materials Science
GA 4S0FY
UT WOS:000857129300001
PM 36138489
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ouyang, W
   Yu, J
   Nuerjiang, S
   Li, ZJ
   Wang, DJ
   Wang, XY
   Zhang, JH
   Xie, CH
AF Ouyang, Wen
   Yu, Jing
   Nuerjiang, Shuake
   Li, Zhijun
   Wang, Dajiang
   Wang, Xiaoyong
   Zhang, Junhong
   Xie, Conghua
TI Stereotactic body radiotherapy improves the survival of patients with
   oligometastatic non-small cell lung cancer
SO CANCER MEDICINE
LA English
DT Article
DE non-small cell lung cancer; oligometastases; stereotactic body
   radiotherapy
ID PHASE-II-TRIAL; 1ST-LINE SYSTEMIC THERAPY; RADIATION-THERAPY;
   MAINTENANCE THERAPY; COLORECTAL-CANCER; HEPATIC RESECTION; I/II TRIAL;
   STAGE-I; METASTASES; OUTCOMES
AB Purpose The aim of the study was to evaluate the efficacy and safety of stereotactic body radiotherapy (SBRT) for pulmonary lesions in oligometastatic non-small cell lung cancer (NSCLC) patients, to explore prognostic factors of progression-free survival (PFS) and overall survival (OS), to validate improved survival contributed by SBRT in oligometastatic NSCLC patients. Patients and methods A total of 71 oligometastatic NSCLC patients with 86 pulmonary lesions treated with SBRT in our institute between 2012 and 2018 were included. Local control (LC), progression-free survival (PFS), and overall survival (OS) were calculated using Kaplan-Meier method. Prognostic factors of PFS and OS were analyzed using univariate and multivariate Cox analyses. Subgroup analyses were performed to investigate the impact of SBRT on PFS and OS during first line systemic treatment. Results After a median follow-up of 17.6 months, 2-year LC and OS rates were 82.6% and 55.3%, respectively. No grade 4 or more toxicities were observed. Multivariate analysis showed systemic treatment regimen before SBRT was an independent prognostic factor of PFS, but not for OS. Among this cohort, patients receiving first line target therapy could show a better PFS and OS than those undergoing first line chemotherapy (target therapy vs chemotherapy, PFS, 26.4 m vs 6.9 m; OS, 34.8 m vs 15.5 m). Conclusions SBRT for pulmonary lesions was a feasible and tolerable option for oligometastatic NSCLC patients. Delivery of SBRT for pulmonary lesions improved outcomes of oligometastatic NSCLC patients. Finally, SBRT combined with first line target therapy might have optimal outcomes.
C1 [Ouyang, Wen; Yu, Jing; Nuerjiang, Shuake; Li, Zhijun; Wang, Dajiang; Wang, Xiaoyong; Zhang, Junhong; Xie, Conghua] Wuhan Univ, Dept Radiat & Med Oncol, Zhongnan Hosp, 169 Donghu Rd, Wuhan 430071, Hubei, Peoples R China.
   [Zhang, Junhong; Xie, Conghua] Wuhan Univ, Hubei Key Lab Tumor Biol Behav, Zhongnan Hosp, Wuhan, Hubei, Peoples R China.
   [Zhang, Junhong; Xie, Conghua] Wuhan Univ, Hubei Clin Canc Study Ctr, Zhongnan Hosp, Wuhan, Hubei, Peoples R China.
C3 Wuhan University; Wuhan University; Wuhan University
RP Zhang, JH; Xie, CH (corresponding author), Wuhan Univ, Dept Radiat & Med Oncol, Zhongnan Hosp, 169 Donghu Rd, Wuhan 430071, Hubei, Peoples R China.
EM zjhzhongnan@163.com; chxie_65@whu.edu.cn
OI Yu, Jing/0000-0003-2836-6373; Xie, Conghua/0000-0002-9324-8683
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NR 42
TC 18
Z9 19
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 AUG
PY 2019
VL 8
IS 10
BP 4605
EP 4614
DI 10.1002/cam4.2366
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IU7EY
UT WOS:000483748400010
PM 31245933
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Chen, YC
   Chuang, CH
   Miao, ZF
   Yip, KL
   Liu, CJ
   Li, LH
   Wu, DC
   Cheng, TL
   Lin, CY
   Wang, JY
AF Chen, Yen-Cheng
   Chuang, Chia-Hsien
   Miao, Zhi-Feng
   Yip, Kwan-Ling
   Liu, Chung-Jung
   Li, Ling-Hui
   Wu, Deng-Chyang
   Cheng, Tian-Lu
   Lin, Chung-Yen
   Wang, Jaw-Yuan
TI Gut microbiota composition in chemotherapy and targeted therapy of
   patients with metastatic colorectal cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE metastatic colorectal cancer; targeted therapy; Lactobacillus species;
   Bifidobacterium species; Fusobacterium nucleatum; Klebsiella
   quasipneumoniae
ID FUSOBACTERIUM-NUCLEATUM; RESPONSE EVALUATION; BEVACIZUMAB; METABOLITES;
   COLIBACTIN; GUIDELINES; IRINOTECAN; DIET
AB Studies have reported the effects of the gut microbiota on colorectal cancer (CRC) chemotherapy, but few studies have investigated the association between gut microbiota and targeted therapy. This study investigated the role of the gut microbiota in the treatment outcomes of patients with metastatic CRC (mCRC). We enrolled 110 patients with mCRC and treated them with standard cancer therapy. Stool samples were collected before administering a combination of chemotherapy and targeted therapy. Patients who had a progressive disease (PD) or partial response (PR) for at least 12 cycles of therapy were included in the study. We further divided these patients into anti-epidermal growth factor receptor (cetuximab) and anti-vascular endothelial growth factor (bevacizumab) subgroups. The gut microbiota of the PR group and bevacizumab-PR subgroup exhibited significantly higher alpha-diversity. The beta-diversity of bacterial species significantly differed between the bevacizumab-PR and bevacizumab-PD groups (P = 0.029). Klebsiella quasipneumoniae exhibited the greatest fold change in abundance in the PD group than in the PR group. Lactobacillus and Bifidobacterium species exhibited higher abundance in the PD group. The abundance of Fusobacterium nucleatum was approximately 32 times higher in the PD group than in the PR group. A higher gut microbiota diversity was associated with more favorable treatment outcomes in the patients with mCRC. Bacterial species analysis of stool samples yielded heterogenous results. K. quasipneumoniae exhibited the greatest fold change in abundance among all bacterial species in the PD group. This result warrants further investigation especially in a Taiwanese population.
C1 [Chen, Yen-Cheng; Miao, Zhi-Feng; Yip, Kwan-Ling; Wang, Jaw-Yuan] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, Kaohsiung, Taiwan.
   [Chen, Yen-Cheng; Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.
   [Chuang, Chia-Hsien; Lin, Chung-Yen] Acad Sinica, Inst Informat Sci, Taipei, Taiwan.
   [Liu, Chung-Jung] Kaohsiung Med Univ Hosp, Dept Internal Med, Div Gastroenterol, Kaohsiung, Taiwan.
   [Li, Ling-Hui] Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
   [Wu, Deng-Chyang; Cheng, Tian-Lu] Kaohsiung Med Univ, Dept Biomed Sci & Environm Biol, Kaohsiung, Taiwan.
   [Wu, Deng-Chyang] Kaohsiung Med Univ, Coll Med, Dept Med, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Coll Med, Fac Med,Dept Surg, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Ctr Canc Res, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Pingtung Hosp, Minist Hlth & Welf, Pingtung, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University; Academia Sinica - Taiwan; Kaohsiung
   Medical University; Kaohsiung Medical University Hospital; Academia
   Sinica - Taiwan; Kaohsiung Medical University; Kaohsiung Medical
   University; Kaohsiung Medical University; Kaohsiung Medical University;
   Kaohsiung Medical University Hospital; Kaohsiung Medical University
RP Wang, JY (corresponding author), Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.; Lin, CY (corresponding author), Acad Sinica, Inst Informat Sci, Taipei, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Coll Med, Fac Med,Dept Surg, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Ctr Canc Res, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Pingtung Hosp, Minist Hlth & Welf, Pingtung, Taiwan.
EM cylin@iis.sinica.edu.tw; jawyuanwang@gmail.com
RI Jaw-Yuan, Wang/AFS-8845-2022; Cheng, Tain-Lu/C-9645-2009; Liu,
   Chung-Jung/GPX-4530-2022; Lin, Chung-Yen/AAQ-3833-2021; , liu zhong
   rong/AAX-1889-2021
OI , liu zhong rong/0000-0002-2657-565X; Wang, Jaw-Yuan/0000-0002-7705-2621
FU Ministry of Science and Technology [MOST 109-2314-B-037-035, MOST
   109-2314-B-037-040, MOST 109-2314-B-037-046-MY3,
   MOST110-2314-B-037-097]; Ministry of Health and Welfare
   [MOHW109-TDU-B-212-134026, MOHW109-TDU-B-212-114006,
   MOHW110-TDU-B-212-1140026]; health and welfare surcharge of on tobacco
   products; Kaohsiung Medical University Hospital [KMUH110-0R37,
   KMUH110-0R38, KMUH110-0M34, KMUH110-0M35, KMUH110-0M36, KMUHSA11013,
   110010]; KMU Center for Cancer Research [KMU-TC111A04-1]; KMU Center for
   Liquid Biopsy [KMU-TC109B05]; KMU Office for Industry-Academic
   Collaboration [S109036]; Kaohsiung Medical University; Grant of Taiwan
   Precision Medicine Initiative
FX This work was supported by grants through funding from the Ministry of
   Science and Technology (MOST 109-2314-B-037-035, MOST
   109-2314-B-037-040, MOST 109-2314-B-037-046-MY3, MOST110-2314-B-037-097)
   and the Ministry of Health and Welfare (MOHW109-TDU-B-212-134026,
   MOHW109-TDU-B-212-114006, MOHW110-TDU-B-212-1140026) and funded by the
   health and welfare surcharge of on tobacco products, and the Kaohsiung
   Medical University Hospital (KMUH110-0R37, KMUH110-0R38, KMUH110-0M34,
   KMUH110-0M35, KMUH110-0M36, KMUHSA11013, KMUH-DK(C)110010,
   KMUH-DK(B)110004-3) and KMU Center for Cancer Research (KMU-TC111A04-1)
   and KMU Center for Liquid Biopsy and Cohort Research Center Grant
   (KMU-TC109B05) and KMU Office for Industry-Academic Collaboration
   (S109036),Kaohsiung Medical University. In addition, this study was
   supported by the Grant of Taiwan Precision Medicine Initiative and
   Taiwan Biobank, Academia Sinica, Taiwan, R.O.C.
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PD SEP 23
PY 2022
VL 12
AR 955313
DI 10.3389/fonc.2022.955313
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5D6AF
UT WOS:000865021300001
PM 36212420
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ruff, SM
   Pawlik, TM
AF Ruff, Samantha M.
   Pawlik, Timothy M.
TI A Review of Translational Research for Targeted Therapy for Metastatic
   Colorectal Cancer
SO CANCERS
LA English
DT Review
DE colorectal cancer; metastases; targeted therapy; KRAS; BRAF;
   microsatellite instability
ID GROWTH-FACTOR RECEPTOR; CETUXIMAB PLUS IRINOTECAN; COLON-CANCER; RAS
   MUTATIONS; 1ST-LINE TREATMENT; KRAS MUTATION; FLUOROURACIL; LEUCOVORIN;
   INHIBITION; SURVIVAL
AB Simple Summary Colorectal cancer is the third most common cause of cancer-related death in the United States with 20% of patients presenting with metastatic disease at time of diagnosis. Metastatic colon cancer is often treated with a combination of surgery, systemic therapy, and/or regional therapy. By utilizing the molecular and pathologic features of the primary tumor we can tailor treatment for patients to try and improve outcomes. Basic science work to elucidate new drug targets, understand mechanisms of evasion, and develop drugs and drug combinations is critical to inform clinical trials and identify novel, effective therapies for metastatic colorectal cancer. This review will focus on targeted therapy in the treatment of metastatic colorectal cancer and how the translational research has advanced the field to improve outcomes for patients. Colorectal cancer is the third most common cause of cancer-related death in the United States, with 20% of patients presenting with metastatic disease at the time of diagnosis. Metastatic colon cancer is often treated with a combination of surgery, systemic therapy (chemotherapy, biologic therapy, immunotherapy), and/or regional therapy (hepatic artery infusion pumps). Utilizing the molecular and pathologic features of the primary tumor to tailor treatment for patients may improve overall survival. Rather than a "one size fits all" approach, a more nuanced treatment plan guided by the unique features of a patient's tumor and the tumor's microenvironment can more effectively treat the disease. Basic science work to elucidate new drug targets, understand mechanisms of evasion, and develop drugs and drug combinations is critical to inform clinical trials and identify novel, effective therapies for metastatic colorectal cancer. Through the lens of key targets for metastatic colorectal cancer, this review discusses how work in the basic science lab translates into clinical trials.
C1 [Pawlik, Timothy M.] Ohio State Univ, Wexner Med Ctr, Dept Surg, Columbus, OH 43210 USA.
   James Comprehens Canc Ctr, Columbus, OH 43210 USA.
C3 University System of Ohio; Ohio State University; James Cancer Hospital
   & Solove Research Institute; University System of Ohio; Ohio State
   University
RP Pawlik, TM (corresponding author), Ohio State Univ, Wexner Med Ctr, Dept Surg, 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 65
TC 6
Z9 6
U1 2
U2 14
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 1395
DI 10.3390/cancers15051395
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9U1JD
UT WOS:000947475400001
PM 36900187
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, FR
   Lin, YP
   Li, R
   Shen, X
   Xiang, MY
   Xiong, GR
   Zhang, K
   Xia, TR
   Guo, JY
   Miao, ZH
   Liao, YD
   Zhang, X
   Xie, L
AF Li, Furong
   Lin, Yanping
   Li, Rong
   Shen, Xin
   Xiang, Mengying
   Xiong, Guangrui
   Zhang, Ke
   Xia, Tingrong
   Guo, Jiangyan
   Miao, Zhonghui
   Liao, Yedan
   Zhang, Xuan
   Xie, Lin
TI Molecular targeted therapy for metastatic colorectal cancer: current and
   evolving approaches
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE colorectal cancer; molecular targeted therapy; VEGF; epidermal growth
   factor receptor; RAS; Her-2
ID PHASE-III TRIAL; POSITIVE SOLID TUMORS; OPEN-LABEL; 1ST-LINE TREATMENT;
   GENOMIC LANDSCAPE; RAS MUTATIONS; MULTICENTER; FLUOROURACIL;
   BEVACIZUMAB; STATISTICS
AB Colorectal cancer (CRC) represents 10% of all cancer types, making it the third leading cause of cancer-related deaths globally. Metastasis is the primary factor causing mortality in CRC patients. Approximately 22% of CRC-related deaths have metastasis present at diagnosis, with approximately 70% of these cases recurring. Recently, with the application of novel targeted drugs, targeted therapy has become the first-line option for individualized and comprehensive treatment of CRC. The management of these patients remains a significant medical challenge. The most prevalent targeted therapies for CRC in clinical practice focus on anti-vascular endothelial growth factor and its receptor, epidermal growth factor receptor (EGFR), and multi-target kinase inhibitors. In the wake of advancements in precision diagnosis and widespread adoption of second-generation sequencing (NGS) technology, rare targets such as BRAF V600E mutation, KRAS mutation, HER2 overexpression/amplification, and MSI-H/dMMR in metastatic colorectal cancer (mCRC) are increasingly being discovered. Simultaneously, new therapeutic drugs targeting these mutations are being actively investigated. This article reviews the progress in clinical research for developing targeted therapeutics for CRC, in light of advances in precision medicine and discovery of new molecular target drugs.
C1 [Li, Furong; Zhang, Xuan] Kunming Med Univ, Yunnan Canc Hosp, Dept Colorectal Surg, Affiliated Hosp 3, Kunming, Peoples R China.
   [Lin, Yanping; Li, Rong; Shen, Xin; Xiang, Mengying; Xiong, Guangrui; Zhang, Ke; Xia, Tingrong; Miao, Zhonghui; Liao, Yedan; Xie, Lin] Kunming Med Univ, Yunnan Canc Hosp, Dept Gastroenterol & Internal Oncol, Affiliated Hosp 3, Kunming, Peoples R China.
   [Guo, Jiangyan] Kunming Med Univ, Yunnan Canc Hosp, Dept Oncol, Affiliated Hosp 3, Kunming, Peoples R China.
C3 Kunming Medical University; Kunming Medical University; Kunming Medical
   University
RP Zhang, X (corresponding author), Kunming Med Univ, Yunnan Canc Hosp, Dept Colorectal Surg, Affiliated Hosp 3, Kunming, Peoples R China.; Xie, L (corresponding author), Kunming Med Univ, Yunnan Canc Hosp, Dept Gastroenterol & Internal Oncol, Affiliated Hosp 3, Kunming, Peoples R China.
EM 1025415085@qq.com; xielinyanghan@163.com
FU This research was funded by the Key Project of Applied Basic Research in
   Yunnan Province (No. 202101AS070004) and the Joint Special Project of
   Applied Basic Research of Yunnan Provincial Science and Technology
   Department and Kunming Medical University (No. [202101AS070004]; Key
   Project of Applied Basic Research in Yunnan Province
   [202001AY070001-073]; Joint Special Project of Applied Basic Research of
   Yunnan Provincial Science and Technology Department and Kunming Medical
   University
FX This research was funded by the Key Project of Applied Basic Research in
   Yunnan Province (No. 202101AS070004) and the Joint Special Project of
   Applied Basic Research of Yunnan Provincial Science and Technology
   Department and Kunming Medical University (No. 202001AY070001-073).
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NR 75
TC 13
Z9 13
U1 0
U2 5
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 OCT 20
PY 2023
VL 14
AR 1165666
DI 10.3389/fphar.2023.1165666
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA W5RO7
UT WOS:001092200000001
PM 37927605
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Chen, N
   He, L
   Zou, Q
   Deng, HX
AF Chen, Na
   He, Ling
   Zou, Qiang
   Deng, Hongxin
TI HER2 targeted therapy in colorectal Cancer: Current landscape and future
   directions
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Review
DE Colorectal cancer; HER2-positive; ERBB2; Biomarker; Target therapy;
   Precision oncology
ID TRASTUZUMAB DERUXTECAN DS-8201; METASTATIC BREAST-CANCER; ANTIBODY-DRUG
   CONJUGATE; GROWTH-FACTOR RECEPTOR; CIRCULATING TUMOR DNA; PHASE-II
   TRIAL; GENOMIC LANDSCAPE; RECTAL-CANCER; OPEN-LABEL; T-CELLS
AB Colorectal cancer (CRC) is one of the most common causes of tumor -related deaths globally. Despite recent improvements in the comprehensive therapy of malignancy, metastatic CRC continues to have a poor prognosis. Human epidermal growth factor receptor 2 (HER2) is an established oncogenic driver, which is successfully targeted for breast and gastric cancers. Approximately 5% of CRC patients carry somatic HER2 mutations or gene amplification. In 2019, the U.S. Food and Drug Administration have approved trastuzumab and pertuzumab in combination with chemotherapy for the treatment of HER2 -positive metastatic CRC. This approval marked a significant milestone in the treatment of CRC, as HER2 -positive patients now have access to targeted therapies that can improve their outcomes. Yet, assessment for HER2 overexpression/ amplification in CRC has not been standardized. The resistance mechanisms to anti- HER2 therapy have been not clearly investigated in CRC. Although many unknowns remain, an improved understanding of these anti-HER2 agents will be essential for advanced CRC. In this review, we provide an overview of the role of HER2 in CRC as an oncogenic driver, a prognostic and predictive biomarker, and a clinically actionable target, as well as the current progress and challenges in the field.
C1 [Chen, Na; Deng, Hongxin] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
   [Chen, Na; Deng, Hongxin] Sichuan Univ, West China Hosp, Canc Ctr, Chengdu 610041, Sichuan, Peoples R China.
   [Chen, Na; Deng, Hongxin] Collaborat Innovat Ctr Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
   [He, Ling] Sichuan Univ, West China Hosp, Canc Ctr, Dept Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
   [Chen, Na; Zou, Qiang] Chengdu Med Coll, Ctr Sci & Res, Chengdu 610500, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University; Chengdu
   Medical College
RP Deng, HX (corresponding author), Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu 610041, Sichuan, Peoples R China.; Deng, HX (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, Chengdu 610041, Sichuan, Peoples R China.; Deng, HX (corresponding author), Collaborat Innovat Ctr Biotherapy, Chengdu 610041, Sichuan, Peoples R China.; Zou, Q (corresponding author), Chengdu Med Coll, Ctr Sci & Res, Chengdu 610500, Peoples R China.
EM qiangzou99@qq.com; denghongx@scu.edu.cn
FU Basic Research for Application of Sichuan Province, China program
   [2020YJ0066]; National Natural Science Foundation of China [81972607];
   West China Hospital of Sichuan University [2019HXBH033]
FX This work was supported by grant 2020YJ0066 by the Basic Research for
   Application of Sichuan Province, China program, grant 81972607 by the
   National Natural Science Foundation of China Pro- gram, grant
   2019HXBH033 of the Postdoctoral Research Project, West China Hospital of
   Sichuan University, and grant ZYGD20003 of the 1.3.5 project for
   disciplines of excellence, West China Hospital of Sichuan University.
   Figures created with BioRender.com .
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NR 125
TC 0
Z9 0
U1 5
U2 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD MAY
PY 2024
VL 223
AR 116101
DI 10.1016/j.bcp.2024.116101
EA MAR 2024
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA PU1F8
UT WOS:001216498800001
PM 38442793
DA 2025-01-04
ER

PT J
AU Seol, YM
   Kwon, CH
   Lee, SJ
   Lee, SJ
   Choi, Y
   Choi, YJ
   Kim, H
   Park, DY
AF Seol, Young Mi
   Kwon, Chae Hwa
   Lee, So Jeong
   Lee, Seon Jin
   Choi, Yuri
   Choi, Young Jin
   Kim, Hyojeong
   Park, Do Youn
TI A Pilot Prospective Study of Refractory Solid Tumor Patients for
   NGS-Based Targeted Anticancer Therapy
SO TRANSLATIONAL ONCOLOGY
LA English
DT Article
ID ADVANCED CANCER; CETUXIMAB; MULTICENTER; RESISTANCE; MUTATIONS; GROWTH;
   BASKET
AB With the advent of next-generation sequencing (NGS), targeted sequencing is now contributing to decision making for which chemotherapeutics to administer to cancer patients, especially in refractory and metastatic cancer. Given that most patients with refractory cancer develop resistance to chemotherapy and have few treatment options, we performed NGS test to evaluate the efficacy and clinical feasibility of NGS-based targeted anticancer therapy. We used a gene panel for capturing target regions covering 83 cancer-related genes. A total of 25 refractory metastatic solid tumor patients were enrolled in this study. Among the 25 patients, 7 had FDA-approved drug-responsive or -resistant alterations. However, the effectiveness of targeted therapy was assessed by follow-up in three patients (12%). These included crizotinib for ALK-EML4 fusion in a malignancy of undefined origin patient and everolimus for AKT3 amplification in a uterine sarcoma patient. In addition, we identified a KRAS codon 146 mutation (A146V), which is associated with resistance to anti-EGFR, in a cetuximab-resistant colon cancer patient with wild-type KRAS exons 2 and 12, and EGFR amplification. He received bevacizumab therapy. All three patients showed partial response after targeted therapy. Furthermore, we characterized KRAS A146V biologically using colon cancer cells. In conclusion, this study suggests that targeted therapy based on NGS test may be a good choice for improving the care of patients with refractory solid tumors.
C1 [Seol, Young Mi; Choi, Young Jin; Kim, Hyojeong] Pusan Natl Univ Hosp, Dept Hematooncol, 179 Gudeok Ro, Busan 49241, South Korea.
   [Seol, Young Mi; Lee, So Jeong; Lee, Seon Jin; Choi, Yuri; Choi, Young Jin; Kim, Hyojeong; Park, Do Youn] Pusan Natl Univ, Sch Med, 179 Gudeok Ro, Busan 49241, South Korea.
   [Seol, Young Mi; Kwon, Chae Hwa; Lee, So Jeong; Choi, Young Jin; Kim, Hyojeong; Park, Do Youn] Pusan Natl Univ Hosp, BioMed Res Inst, 1-10 AmiDong, Busan 602739, South Korea.
   [Lee, So Jeong; Lee, Seon Jin; Choi, Yuri; Park, Do Youn] Pusan Natl Univ Hosp, Dept Pathol, 179 Gudeok Ro, Busan 49241, South Korea.
C3 Pusan National University; Pusan National University Hospital; Pusan
   National University; Pusan National University; Pusan National
   University Hospital; Pusan National University; Pusan National
   University Hospital
RP Park, DY (corresponding author), Pusan Natl Univ, Sch Med, 179 Gudeok Ro, Busan 49241, South Korea.; Park, DY (corresponding author), Pusan Natl Univ Hosp, Dept Pathol, 179 Gudeok Ro, Busan 49241, South Korea.
EM pdy220@pusan.ac.kr
RI Kim, Ji-Soo/D-8744-2012
OI Park, Do Youn/0000-0001-7641-1509
FU Busan Cancer Center Research Grant (2018), Pusan National University
   Hospital
FX This study was supported by Busan Cancer Center Research Grant (2018),
   Pusan National University Hospital.
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NR 23
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Z9 9
U1 0
U2 1
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 FEB
PY 2019
VL 12
IS 2
BP 301
EP 307
DI 10.1016/j.tranon.2018.10.011
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HH1RI
UT WOS:000455497000012
PM 30448735
OA gold, Green Published
DA 2025-01-04
ER

PT S
AU Jung, A
AF Jung, Andreas
BE Lehmann, U
   Tost, J
TI Extended <i>KRAS</i> and <i>NRAS</i> Mutation Profiling by
   Pyrosequencing®
SO PYROSEQUENCING: METHODS AND PROTOCOLS, 2ND EDITION
SE Methods in Molecular Biology
LA English
DT Article; Book Chapter
DE Pyrosequencing (R); Colorectal cancer; anti-EGFR-targeted therapy; KRAS;
   NRAS; RAS-hypothesis
ID WILD-TYPE KRAS; 1ST-LINE TREATMENT; FLUOROURACIL; PANITUMUMAB;
   OXALIPLATIN; LEUCOVORIN; AMPLIFICATION; CETUXIMAB; RAS
AB With the advent of targeted therapies-drugs that specifically target molecules of tumor-driving signalling pathways-and the availability of biomarkers that predict the response of an individual patient on such a targeted therapy, the analysis of the status of the biomarker became an integral part of the therapy. For metastatic colorectal cancer, anti-EGFR-targeted antibodies (Cetuximab/Erbitux (R), Panitumumab/Vectibix (R)) fall into this category of drugs as it was shown in several clinical studies that oncogenic mutations in exons 2-4 of the RAS genes KRAS or NRAS result in therapeutic resistance of the metastatic colorectal cancers against the action of both targeted drugs. Therefore, mutations in the RAS genes exclude patients from this kind of targeted therapy (negative biomarker). Thus the molecular-pathological testing of the mutational status of KRAS and NRAS has become an important cornerstone in planning oncological strategies in the treatment of metastatic colorectal cancer. As the profile of mutations in the RAS genes is characterized by hotspot mutations in only a small number of codons (12, 13 in exon 2-59, 61 in exon 3-117, 146 in exon 4). Pyrosequencing (R) is an ideal and robust tool in the molecular-pathological detection. A detailed protocol for this detection procedure employing Pyrosequencing (R) is given here.
C1 [Jung, Andreas] Univ Munich, Inst Pathol, D-80539 Munich, Germany.
C3 University of Munich
RP Jung, A (corresponding author), Univ Munich, Inst Pathol, Thalkirchner Str 36, D-80539 Munich, Germany.
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NR 15
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U2 1
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
SN 1064-3745
EI 1940-6029
BN 978-1-4939-2715-9; 978-1-4939-2714-2
J9 METHODS MOL BIOL
JI Methods Mol. Biol.
PY 2015
VL 1315
BP 49
EP 61
DI 10.1007/978-1-4939-2715-9_5
D2 10.1007/978-1-4939-2715-9
PG 13
WC Genetics & Heredity
WE Book Citation Index – Science (BKCI-S)
SC Genetics & Heredity
GA BE0GH
UT WOS:000365987500006
PM 26103891
DA 2025-01-04
ER

PT J
AU Telang, N
AF Telang, Nitin
TI Drug-Resistant Stem Cells: Novel Approach for Colon Cancer Therapy
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE colon cancer; drug-resistant stem cells; natural products
ID FAMILIAL ADENOMATOUS POLYPOSIS; ESTROGEN-RECEPTOR BETA;
   COLORECTAL-CANCER; CYCLOOXYGENASE-2 INHIBITOR; CHEMOPREVENTIVE EFFICACY;
   CARCINOGENIC RISK; MOUSE MODEL; APC; PREVENTION; CELECOXIB
AB Background: Next to breast cancer, advanced stage metastatic colon cancer represents a major cause for mortality in women. Germline or somatic mutations in tumor suppressor genes or in DNA mismatch repair genes represent risk factors for genetic predisposition of colon cancer that are also detectable in sporadic colon cancer. Conventional chemotherapy for colon cancer includes combination of 5-fluoro-uracil with oxaliplatin and irinotecan or targeted therapy with non-steroid anti-inflammatory drugs and selective cyclooxygenase-2 inhibitors. Major limitations of these therapeutic interventions are associated with systemic toxicity, acquired tumor resistance and the emergence of drug resistant stem cells that favor initiation, progression and metastasis of therapy-resistant disease. These limitations emphasize an unmet need to identify tumor stem cell selective testable alternatives. Drug-resistant stem cell models facilitate the identification of new testable alternatives from natural phytochemicals and herbal formulations. The goal of this review is to provide an overview relevant to the current status of conventional/targeted therapy, the role of cancer stem cells and the status of testable alternatives for therapy-resistant colon cancer. Experimental models: Hyper-proliferative and tumorigenic cell lines from genetically predisposed colonic tissues of female mice represent experimental models. Chemotherapeutic agents select drug-resistant phenotypes that exhibit upregulated expressions of cellular and molecular stem cell markers. Mechanistically distinct natural phytochemicals effectively inhibit stem cell growth and downregulate the expressions of stem cell markers. Conclusions: The present review discusses the status of colon cancer therapy and inherent limitations, cancer stem cell biology, potential lead compounds and their advantages over chemotherapy. The present experimental approaches will facilitate the identification of pharmacological and naturally-occurring agents as lead compounds for stem cell targeted therapy of colon cancer.
C1 [Telang, Nitin] Palindrome Liaisons Consultants, Canc Prevent Res Program, Montvale, NJ 07645 USA.
RP Telang, N (corresponding author), Palindrome Liaisons Consultants, Canc Prevent Res Program, Montvale, NJ 07645 USA.
EM ntelang3@gmail.com
FU US National Cancer Institute (NCI) [CN 75029-63, CN 85141, CN 05107]
FX The research program "Preclinical models for genetically predisposed
   early onset colon cancer" has been funded in the past by US National
   Cancer Institute (NCI) Master Agreement CN 75029-63, Contracts CN 85141
   and CN 05107.
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NR 72
TC 13
Z9 13
U1 8
U2 45
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 2022
VL 23
IS 5
AR 2519
DI 10.3390/ijms23052519
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA ZW4RR
UT WOS:000771202700001
PM 35269660
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Guerrero, P
   Albarrán, V
   San Román, M
   González-Merino, C
   de Quevedo, CG
   Moreno, J
   Calvo, JC
   González, G
   Orejana, I
   Chamorro, J
   Martínez-Delfrade, I
   Morón, B
   de Frutos, B
   Ferreiro, MR
AF Guerrero, Patricia
   Albarran, Victor
   San Roman, Maria
   Gonzalez-Merino, Carlos
   de Quevedo, Coral Garcia
   Moreno, Jaime
   Calvo, Juan Carlos
   Gonzalez, Guillermo
   Orejana, Inmaculada
   Chamorro, Jesus
   Martinez-Delfrade, Inigo
   Moron, Blanca
   de Frutos, Belen
   Ferreiro, Maria Reyes
TI BRAF Inhibitors in Metastatic Colorectal Cancer and Mechanisms of
   Resistance: A Review of the Literature
SO CANCERS
LA English
DT Review
DE BRAF; inhibitors; resistance; colorectal cancer
ID MISMATCH REPAIR-DEFICIENT; MICROSATELLITE INSTABILITY;
   ACQUIRED-RESISTANCE; DRIVEN RESISTANCE; CLINICAL BENEFIT;
   DOSE-ESCALATION; PLUS CETUXIMAB; COLON-CANCER; PATIENTS PTS; OPEN-LABEL
AB Simple Summary The MAP kinases pathway has shown a key role in the pathogenesis of colorectal cancer. The development of targeted therapy against BRAF-mutated tumors is changing the management of advanced disease. A proper understanding of the mechanisms of acquired resistance is essential to optimize the results of systemic treatment. We aim to review the current knowledge and potential fields of research regarding the use of BRAF inhibitors in metastatic colorectal tumors.Abstract Metastatic colorectal cancer (mCRC) with mutated BRAF exhibits distinct biological and molecular features that set it apart from other subtypes of CRC. Current standard treatment for these tumors involves a combination of chemotherapy (CT) and VEGF inhibitors. Recently, targeted therapy against BRAF and immunotherapy (IT) for cases with microsatellite instability (MSI) have been integrated into clinical practice. While targeted therapy has shown promising results, resistance to treatment eventually develops in a significant portion of responsive patients. This article aims to review the available literature on mechanisms of resistance to BRAF inhibitors (BRAFis) and potential therapeutic strategies to overcome them.
C1 [Guerrero, Patricia; Albarran, Victor; San Roman, Maria; Gonzalez-Merino, Carlos; de Quevedo, Coral Garcia; Moreno, Jaime; Calvo, Juan Carlos; Gonzalez, Guillermo; Orejana, Inmaculada; Chamorro, Jesus; Martinez-Delfrade, Inigo; Moron, Blanca; de Frutos, Belen; Ferreiro, Maria Reyes] Ramon y Cajal Univ Hosp, Dept Med Oncol, Madrid 28034, Spain.
C3 Hospital Universitario Ramon y Cajal
RP Guerrero, P (corresponding author), Ramon y Cajal Univ Hosp, Dept Med Oncol, Madrid 28034, Spain.
EM patricia.guerrero@salud.madrid.org; valbarran@salud.madrid.org;
   mariavictoria.san@salud.madrid.org; cgmerino@salud.madrid.org;
   cgquevedosuero@salud.madrid.org; jmdoval@salud.madrid.org;
   jcalvop@salud.madrid.org; guillermo.gonzalez.martin@salud.madrid.org;
   inmaculada.orejana@salud.madrid.org; jchamorro@salud.madrid.org;
   imdelfrade@salud.madrid.org; blancaisabel.moron@salud.madrid.org;
   bfrutos@salud.madrid.org; mariareyes.ferreiro@salud.madrid.org
RI Gonzalez, Guillermo/HMV-7330-2023; San Roman, Maria/HNI-1169-2023;
   García de Quevedo Suero, Coral/HTS-6213-2023; Albarran Fernandez,
   Victor/HII-7609-2022
OI Calvo-Perez, Juan Carlos/0000-0001-7179-5363; San Roman-Gil,
   Maria/0000-0002-8810-6525; Garcia de Quevedo Suero,
   Coral/0000-0002-1342-9653; Gonzalez Merino, Carlos/0009-0008-2988-9751;
   de Frutos Gonzalez, Belen/0009-0009-0067-8595; Albarran Fernandez,
   Victor/0000-0001-6356-2551
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TC 5
Z9 5
U1 2
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2023
VL 15
IS 21
AR 5243
DI 10.3390/cancers15215243
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA X7XC5
UT WOS:001100523400001
PM 37958416
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yu, B
   O'Toole, SA
   Trent, RJ
AF Yu, Bing
   O'Toole, Sandra A.
   Trent, Ronald J.
TI Somatic DNA mutation analysis in targeted therapy of solid tumours
SO TRANSLATIONAL PEDIATRICS
LA English
DT Review
DE Somatic mutation; DNA testing; targeted therapy; multigene analysis;
   cancer genome; clinical implication; solid tumours
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; GASTROINTESTINAL STROMAL
   TUMORS; TYROSINE KINASE; C-KIT; ACQUIRED-RESISTANCE; MELANOMA PATIENTS;
   GENE-MUTATIONS; BRAF MUTATIONS; KRAS MUTATIONS
AB Cancer is a disease of the genome with diverse aetiologies including the accumulation of acquired mutations throughout the genome. There has been a flood of knowledge improving our understanding of the biology and molecular genetics of melanoma, lung and colorectal cancer since the genomics era started. Translation of this knowledge into a better understanding of cell proliferation, survival and apoptosis has produced a paradigm shift in medical oncology enabling gene-based cancer treatment (called personalised or precision medicine). Somatic mutation analysis is crucial for a genomics approach since it can identify driver mutations-the "Achilles' heel" of cancer, and support clinical decision-making through targeted therapy. Nevertheless, the applications of somatic DNA testing in cancer face many challenges such as obtaining comprehensive coverage of the cancer genome with limited DNA being available, and delivering an accurate report in a timely fashion without false-negative and false-positive results. Further advances in DNA technologies and bioinformatics will overcome these issues and maximise opportunities for targeted therapy. Somatic mutation analysis will then become an integral part of cancer management for all malignancies.
C1 [Yu, Bing; Trent, Ronald J.] Royal Prince Alfred Hosp, Dept Med Gen, Missenden Rd, Camperdown, NSW 2050, Australia.
   [Yu, Bing; O'Toole, Sandra A.; Trent, Ronald J.] Univ Sydney, Sydney Med Sch Cent, Sydney, NSW 2006, Australia.
   [O'Toole, Sandra A.] Royal Prince Alfred Hosp, Dept Tissue Pathol & Diagnost Oncol, Camperdown, NSW 2050, Australia.
C3 NSW Health; Royal Prince Alfred Hospital; University of Sydney;
   University of Sydney; NSW Health; Royal Prince Alfred Hospital;
   University of Sydney
RP Yu, B (corresponding author), Royal Prince Alfred Hosp, Dept Med Gen, Missenden Rd, Camperdown, NSW 2050, Australia.
EM bing.yu@sydney.edu.au
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NR 114
TC 19
Z9 21
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 2224-4336
EI 2224-4344
J9 TRANSL PEDIATR
JI Transl. Pediatr.
PD APR
PY 2015
VL 4
IS 2
BP 125
EP 138
DI 10.3978/j.issn.2224-4336.2015.04.04
PG 14
WC Pediatrics
WE Emerging Sources Citation Index (ESCI)
SC Pediatrics
GA V4F4T
UT WOS:000218883800007
PM 26835368
DA 2025-01-04
ER

PT J
AU Rong, DW
   Tang, WW
   Li, ZX
   Zhou, J
   Shi, JF
   Wang, HJ
   Cao, HY
AF Rong, Dawei
   Tang, Weiwei
   Li, Zhouxiao
   Zhou, Jian
   Shi, Junfeng
   Wang, Hanjin
   Cao, Hongyong
TI Novel insights into circular RNAs in clinical application of carcinomas
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE circular; targeted therapy; diagnosis; microRNA; noncoding RNA
ID PROFILING REVEALS; CELL-GROWTH; EXPRESSION; BIOMARKER; CANCER;
   IDENTIFICATION; PROLIFERATION; ABUNDANT
AB Circular RNAs (circRNAs), formed by nonsequential back-splicing of pre-messenger RNA (pre-mRNA) transcripts, have been widely concerned in recent years. With advances in high-throughput RNA sequencing (RNA-seq) technology, previous work has revealed that a large number of circRNAs, which are endogenous, abundant and stable in mammalian cells, may be involved in atherosclerotic vascular disease risk, neurological disorders, prion diseases and carcinomas. Remarkably, interaction between circRNAs and microRNA has already been observed to perform a significant role in a variety of cancers, including gastric cancer and colorectal cancer. Recent work has suggested that circRNAs may play critical roles in the initiation and development of cancers and could become potential new biomarkers for cancers. Herein, we review the current understanding of the roles of circRNAs in cancers and the potential implications of circRNAs in cancer-targeted therapy.
C1 [Rong, Dawei; Tang, Weiwei; Li, Zhouxiao; Wang, Hanjin; Cao, Hongyong] Nanjing Med Univ, Nanjing Hosp 1, Dept Gen Surg, Changle Rd 68, Nanjing 210006, Jiangsu, Peoples R China.
   [Li, Zhouxiao] Univ Hosp Munich, Dept Plast & Hand Surg, Munich, Germany.
   [Zhou, Jian] Nanjing Med Univ, Nanjing Hosp 1, Dept Oncol Surg, Nanjing, Jiangsu, Peoples R China.
   [Shi, Junfeng] Nanjing Med Univ, Nanjing Hosp 1, Dept Oncol, Nanjing, Jiangsu, Peoples R China.
C3 Nanjing Medical University; University of Munich; Nanjing Medical
   University; Nanjing Medical University
RP Wang, HJ; Cao, HY (corresponding author), Nanjing Med Univ, Nanjing Hosp 1, Dept Gen Surg, Changle Rd 68, Nanjing 210006, Jiangsu, Peoples R China.
EM whj_888@sohu.com; caohongy6167@163.com
RI Li, Zhouxiao/ABC-5800-2020; Tang, Weiwei/AAK-6878-2021
OI Li, Zhouxiao/0000-0002-5121-9681
FU Foundation of Nanjing City Committee of Science and Technology
FX This work was supported by the Foundation of Nanjing City Committee of
   Science and Technology to Professor Hongyong Cao. Dawei Rong, Weiwei
   Tang, and Zhouxiao Li are first authors.
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NR 53
TC 58
Z9 61
U1 1
U2 20
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 2183
EP 2188
DI 10.2147/OTT.S134403
PG 6
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA ES6TW
UT WOS:000399683600003
PM 28458561
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Schwarzenbach, H
AF Schwarzenbach, Heidi
TI The potential of circulating nucleic acids as components of companion
   diagnostics for predicting and monitoring chemotherapy response
SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS
LA English
DT Review
DE chemotherapy; circulating DNA; circulating miRNA; epigenetic
   alterations; genetic alterations; resistance; targeted therapy
ID COLORECTAL-CANCER; NONINVASIVE DETECTION; EGFR MUTATIONS; BREAST-CANCER;
   PLASMA DNA; IN-VITRO; TUMOR; MICRORNAS; THERAPY; SERUM
AB An effective personalized medicine is associated with the ability of identifying cancer patients who respond to anticancer targeted therapies. Therefore, new companion biomarkers that facilitate drug development are urgently needed. Since clinically relevant genetic and epigenetic alterations can be detected in cell-free nucleic acids in the blood circulation of cancer patients, these molecules may be a new promising class of potential liquid biomarkers. They can be obtained in real-time from blood, and their analyses could, consequently, facilitate treatment decisions. Screening of these liquid biopsies may provide information on the aberrant signaling pathway that should be blocked by the chosen targeted therapy. This article will discuss the potential of circulating nucleic acids as therapeutics for overcoming chemotherapeutic resistance in anticancer strategies.
C1 Univ Med Ctr Hamburg Eppendorf, Dept Tumour Biol, D-20246 Hamburg, Germany.
C3 University of Hamburg; University Medical Center Hamburg-Eppendorf
RP Schwarzenbach, H (corresponding author), Univ Med Ctr Hamburg Eppendorf, Dept Tumour Biol, Martinistr 52, D-20246 Hamburg, Germany.
EM hschwarz@uke.uni-hamburg.de
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NR 68
TC 11
Z9 11
U1 0
U2 27
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 267
EP 275
DI 10.1586/14737159.2015.980817
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA AZ7EA
UT WOS:000348380400012
PM 25382372
DA 2025-01-04
ER

PT J
AU Cho, DH
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AF Cho, Doah
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   Ward, Robyn
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   Mitchell, Andrew
   Thomas, David M.
   Cheyne, Saskia
   Martin, Andrew
   Morton, Rachael L.
   Simes, John
   Lee, Chee Khoon
TI Criteria for assessing evidence for biomarker-targeted therapies in rare
   cancers-an extrapolation framework
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Article
DE biomarker-driven trials; biomarker-guided therapy; biomarkers; clinical
   trials; companion diagnostics; predictive biomarkers; prognostic
   biomarkers; response biomarkers; targeted therapy
ID SURROGATE END-POINTS; METASTATIC COLORECTAL-CANCER;
   OF-AMERICAN-PATHOLOGISTS; FOR-MOLECULAR-PATHOLOGY; CLINICAL-TRIAL
   DESIGNS; HER2 SCORING SYSTEM; CELL LUNG-CANCER; BREAST-CANCER;
   ACCELERATED APPROVAL; DRUG DEVELOPMENT
AB Background: Advances in targeted therapy development and tumor sequencing technology are reclassifying cancers into smaller biomarker-defined diseases. Randomized controlled trials (RCTs) are often impractical in rare diseases, leading to calls for single-arm studies to be sufficient to inform clinical practice based on a strong biological rationale. However, without RCTs, favorable outcomes are often attributed to therapy but may be due to a more indolent disease course or other biases. When the clinical benefit of targeted therapy in a common cancer is established in RCTs, this benefit may extend to rarer cancers sharing the same biomarker. However, careful consideration of the appropriateness of extending the existing trial evidence beyond specific cancer types is required. A framework for extrapolating evidence for biomarker-targeted therapies to rare cancers is needed to support transparent decision-making.Objectives: To construct a framework outlining the breadth of criteria essential for extrapolating evidence for a biomarker-targeted therapy generated from RCTs in common cancers to different rare cancers sharing the same biomarker.Design: A series of questions articulating essential criteria for extrapolation.Methods: The framework was developed from the core topics for extrapolation identified from a previous scoping review of methodological guidance. Principles for extrapolation outlined in guidance documents from the European Medicines Agency, the US Food and Drug Administration, and Australia's Medical Services Advisory Committee were incorporated.Results: We propose a framework for assessing key assumptions of similarity of the disease and treatment outcomes between the common and rare cancer for five essential components: prognosis of the biomarker-defined cancer, biomarker test analytical validity, biomarker actionability, treatment efficacy, and safety. Knowledge gaps identified can be used to prioritize future studies.Conclusion: This framework will allow systematic assessment, standardize regulatory, reimbursement and clinical decision-making, and facilitate transparent discussions between key stakeholders in drug assessment for rare biomarker-defined cancers.
C1 [Cho, Doah; Lord, Sarah J.; Martin, Andrew; Morton, Rachael L.; Simes, John; Lee, Chee Khoon] Univ Sydney, Fac Med & Hlth, Natl Hlth & Med Res Council, Clin Trials Ctr, Locked Bag 77, Camperdown, NSW 1450, Australia.
   [Ward, Robyn] Univ Sydney, Fac Med & Hlth, Camperdown, NSW, Australia.
   [Ijzerman, Maarten] Univ Melbourne, Fac Med Dent & Hlth Sci, Ctr Hlth Policy, Ctr Canc Res, Parkville, Vic, Australia.
   [Ijzerman, Maarten] Erasmus Univ, Erasmus Sch Hlth Policy & Management, Rotterdam, Netherlands.
   [Mitchell, Andrew] Australian Natl Univ, Dept Hlth Econ Wellbeing & Soc, Canberra, ACT, Australia.
   [Thomas, David M.] Univ New South Wales, Ctr Mol Oncol, Sydney, NSW, Australia.
   [Martin, Andrew] Univ Queensland, Ctr Clin Res, St Lucia, Qld, Australia.
C3 National Health & Medical Research Council (NHMRC) of Australia;
   University of Sydney; University of Sydney; University of Melbourne;
   Erasmus University Rotterdam - Excl Erasmus MC; Erasmus University
   Rotterdam; Australian National University; University of New South Wales
   Sydney; University of Queensland
RP Cho, DH (corresponding author), Univ Sydney, Fac Med & Hlth, Natl Hlth & Med Res Council, Clin Trials Ctr, Locked Bag 77, Camperdown, NSW 1450, Australia.
EM doah.cho@sydney.edu.au
RI Lord, Sally/GZM-7796-2022; Morton, Rachael/AAB-7420-2020; IJzerman,
   Maarten/Q-8963-2016
OI IJzerman, Maarten/0000-0001-5788-5805; Lord, Sarah (Sally)
   J/0000-0003-2763-5949
FU NHMRC Postgraduate Research Scholarship (Medical-Dental) [SC0798];
   Postgraduate Research Supplementary Scholarship in Oncology;
   Postgraduate Research Supplementary Scholarship in Decision Making
   Frameworks in Rare Cancers; NHMRC Program Grant
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and/or publication of this article: This work was
   supported by an NHMRC Postgraduate Research Scholarship (Medical-Dental)
   (SC0798), Postgraduate Research Supplementary Scholarship in Oncology,
   Postgraduate Research Supplementary Scholarship in Decision Making
   Frameworks in Rare Cancers, and NHMRC Program Grant.
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NR 133
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PY 2024
VL 16
AR 17588359241273062
DI 10.1177/17588359241273062
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA E5M1N
UT WOS:001303431800001
PM 39229469
OA gold
DA 2025-01-04
ER

PT J
AU Zhu, XD
   Li, SL
AF Zhu, Xudong
   Li, Shenglong
TI Ferroptosis, Necroptosis, and Pyroptosis in Gastrointestinal Cancers:
   The Chief Culprits of Tumor Progression and Drug Resistance
SO ADVANCED SCIENCE
LA English
DT Review
DE drug resistance; ferroptosis; gastrointestinal cancers; necroptosis;
   pyroptosis; targeted therapy
ID COLORECTAL-CANCER; GASTRIC-CANCER; CELL-DEATH; HEPATOCELLULAR-CARCINOMA;
   DEPENDENT NECROPTOSIS; SIGNALING PATHWAY; ROS PRODUCTION; EMERGING ROLE;
   APOPTOSIS; GSDME
AB In recent years, the incidence of gastrointestinal cancers is increasing, particularly in the younger population. Effective treatment is crucial for improving patients' survival outcomes. Programmed cell death, regulated by various genes, plays a fundamental role in the growth and development of organisms. It is also critical for maintaining tissue and organ homeostasis and takes part in multiple pathological processes. In addition to apoptosis, there are other types of programmed cell death, such as ferroptosis, necroptosis, and pyroptosis, which can induce severe inflammatory responses. Notably, besides apoptosis, ferroptosis, necroptosis, and pyroptosis also contribute to the occurrence and development of gastrointestinal cancers. This review aims to provide a comprehensive summary on the biological roles and molecular mechanisms of ferroptosis, necroptosis, and pyroptosis, as well as their regulators in gastrointestinal cancers and hope to open up new paths for tumor targeted therapy in the near future.
C1 [Zhu, Xudong] Dalian Univ Technol, Canc Hosp, Liaoning Canc Hosp & Inst, Dept Gen Surg,China Med Univ, Shenyang 110042, Liaoning, Peoples R China.
   [Li, Shenglong] Dalian Univ Technol, Liaoning Canc Hosp & Inst, Ward Bone & Soft Tissue Tumor Surg 2, Canc Hosp,China Med Univ, Shenyang 110042, Liaoning, Peoples R China.
   [Li, Shenglong] Liaoning Prov Key Lab Interdisciplinary Res Gastro, Shenyang 110042, Liaoning, Peoples R China.
C3 China Medical University; Dalian University of Technology; Dalian
   University of Technology; China Medical University
RP Li, SL (corresponding author), Dalian Univ Technol, Liaoning Canc Hosp & Inst, Ward Bone & Soft Tissue Tumor Surg 2, Canc Hosp,China Med Univ, Shenyang 110042, Liaoning, Peoples R China.; Li, SL (corresponding author), Liaoning Prov Key Lab Interdisciplinary Res Gastro, Shenyang 110042, Liaoning, Peoples R China.
EM slli@cmu.edu.cn
RI zhu, xudong/LRT-1369-2024; Li, Shenglong/W-4929-2019
OI Li, Shenglong/0000-0003-2244-1184
FU Doctoral Start-up Foundation of Liaoning Province [2023-BS-048];
   Liaoning Cancer Hospital; Institute (Shenyang), China Medical
   University; Dalian University of Technology (Dalian)
FX This study was supported by Doctoral Start-up Foundation of Liaoning
   Province (2023-BS-048). This work was also supported by the Liaoning
   Cancer Hospital and Institute (Shenyang), China Medical University
   (Shenyang), and Dalian University of Technology (Dalian).
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NR 215
TC 34
Z9 34
U1 14
U2 58
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2198-3844
J9 ADV SCI
JI Adv. Sci.
PD SEP
PY 2023
VL 10
IS 26
DI 10.1002/advs.202300824
EA JUL 2023
PG 20
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA T6SC1
UT WOS:001026933300001
PM 37436087
OA Green Published, gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Tan, ZM
   Sun, WY
   Li, Y
   Jiao, XM
   Zhu, ML
   Zhang, JF
   Qing, C
   Jia, YN
AF Tan, Zhuomin
   Sun, Wenyan
   Li, Ya
   Jiao, Xingmeng
   Zhu, Mingliang
   Zhang, Junfei
   Qing, Chen
   Jia, Yinnong
TI Current Progress of EMT: A New Direction of Targeted Therapy for
   Colorectal Cancer with Invasion and Metastasis
SO BIOMOLECULES
LA English
DT Review
DE colorectal cancer; EMT; tumor invasion and metastasis; targeted therapy;
   signal pathway
ID EPITHELIAL-MESENCHYMAL TRANSITION; E-CADHERIN EXPRESSION; COLON-CANCER;
   CELL-MIGRATION; TGF-BETA; IN-VIVO; PATHWAY; CHEMORESISTANCE;
   POLYSACCHARIDE; INHIBITION
AB Colorectal cancer (CRC) is a common malignant tumor with a high frequency of recurrence and metastasis, which are the major causes of death in patients. The prerequisite for the invasion and metastasis is the strong mobility of CRC cells to transport far away from the original site to the distant organs and tissues, where they settle down and proliferate. It was reported that the epithelial-mesenchymal transition (EMT) is involved in the occurrence and development of various tumors in the entire process of tumor invasion and metastasis. Therefore, as a vital factor for the biological characteristics of tumor cells, EMT markers may serve as prognostic predictors and potential therapeutic targets in CRC. This article mainly reviews the current status of CRC with metastasis, the studies of EMT, the possible relationship of EMT with CRC, as well as the potential targeted therapy.
C1 [Tan, Zhuomin; Sun, Wenyan; Li, Ya; Zhu, Mingliang; Zhang, Junfei; Qing, Chen; Jia, Yinnong] Kunming Med Univ, Sch Pharmaceut Sci, Dept Pharmaceut Sci, Kunming 650500, Peoples R China.
   [Tan, Zhuomin; Sun, Wenyan; Li, Ya; Zhu, Mingliang; Zhang, Junfei; Qing, Chen; Jia, Yinnong] Kunming Med Univ, Yunnan Key Lab Pharmacol Nat Prod, Kunming 650500, Peoples R China.
   [Jiao, Xingmeng] Yunnan Univ Chinese Med, Coll Chinese Med, Kunming 650500, Peoples R China.
C3 Kunming Medical University; Kunming Medical University; Yunnan
   University of Chinese Medicine
RP Jia, YN (corresponding author), Kunming Med Univ, Sch Pharmaceut Sci, Dept Pharmaceut Sci, Kunming 650500, Peoples R China.; Jia, YN (corresponding author), Kunming Med Univ, Yunnan Key Lab Pharmacol Nat Prod, Kunming 650500, Peoples R China.
EM jiayinnong@kmmu.edu.cn
RI Qing, Chen/AFQ-7860-2022; Zhu, Mingliang/A-8000-2012; Zhang,
   Jun-Fei/JYP-7506-2024
OI jia, yinnong/0000-0001-5980-9275
FU NSFC project; Yunnan Fundamental Research Projects; Yunnan Provincial
   Department of S&T-KMU Joint Foundation Key Project of China; 
   [82160344];  [81860463];  [202001AU070141];  [202101AY070001-068]
FX This review was supported by NSFC project (grants no. 82160344 and no.
   81860463), Yunnan Fundamental Research Projects (grant no.
   202001AU070141), and Yunnan Provincial Department of S&T-KMU Joint
   Foundation Key Project of China (grant no. 202101AY070001-068).
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NR 79
TC 18
Z9 19
U1 3
U2 29
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD DEC
PY 2022
VL 12
IS 12
AR 1723
DI 10.3390/biom12121723
PG 15
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 7D3JW
UT WOS:000900392000001
PM 36551152
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Gmeiner, WH
AF Gmeiner, William H.
TI Recent Advances in Our Knowledge of mCRC Tumor Biology and Genetics: A
   Focus on Targeted Therapy Development
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE colorectal cancer; metastasis; mutation; whole exome sequencing;
   targeted therapy
ID METASTATIC COLORECTAL-CANCER; THYMIDYLATE SYNTHASE; COLON-CANCER;
   MICROSATELLITE INSTABILITY; DIHYDROPYRIMIDINE DEHYDROGENASE; MOLECULAR
   SUBTYPES; GENOMIC LANDSCAPE; CHEMOTHERAPY; SURVIVAL; EXPRESSION
AB Metastatic colorectal cancer (mCRC) remains a highly lethal malignancy although considerable progress has resulted from characterizing molecular alterations such as RAS mutation status and extent of microsatellite instability (MSI) to guide optimal use of available therapies. The availability of gene expression profiling, next generation sequencing technologies, proteomics analysis and other technologies provides high resolution information on individual tumors, including metastatic lesions to better define intra-tumor and inter-tumor heterogeneity. Recent literature applying this information to further customize personalized therapies is reviewed. Current biomarker-based stratification used to select optimal therapy that is personalized to the mutation profile of individual tumors is described. Recent literature using whole exome sequencing of metastatic lesions and primary CRC tumors and other advanced technologies to more fully elucidate the tumor biology specific to mCRC sub-types and to develop more precise therapies that improve outcomes is also reviewed.
C1 [Gmeiner, William H.] Wake Forest Sch Med, Dept Canc Biol, Winston Salem, NC 27101 USA.
C3 Wake Forest University
RP Gmeiner, WH (corresponding author), Wake Forest Sch Med, Dept Canc Biol, Winston Salem, NC 27101 USA.
EM bgmeiner@wakehealth.edu
FU NIH-NCI [R21 CA218933, P30 CA012197]; Wake Forest Baptist Comprehensive
   Cancer Center
FX This work was supported by NIH-NCI R21 CA218933, NIH-NCI P30 CA012197
   and Wake Forest Baptist Comprehensive Cancer Center.
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NR 91
TC 9
Z9 10
U1 0
U2 5
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2021
VL 14
BP 2121
EP 2130
DI 10.2147/OTT.S242224
PG 10
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA RB6VJ
UT WOS:000632247100001
PM 33790575
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ychou, M
   Rivoire, M
   Thezenas, S
   Guimbaud, R
   Ghiringhelli, F
   Mercier-Blas, A
   Mineur, L
   Francois, E
   Khemissa, F
   Chauvenet, M
   Kianmanesh, R
   Fonck, M
   Houyau, P
   Aparicio, T
   Galais, MP
   Audemar, F
   Assenat, E
   Lopez-Crapez, E
   Jouffroy, C
   Adenis, A
   Adam, R
   Bouché, O
AF Ychou, Marc
   Rivoire, Michel
   Thezenas, Simon
   Guimbaud, Rosine
   Ghiringhelli, Francois
   Mercier-Blas, Anne
   Mineur, Laurent
   Francois, Eric
   Khemissa, Faiza
   Chauvenet, Marion
   Kianmanesh, Reza
   Fonck, Marianne
   Houyau, Philippe
   Aparicio, Thomas
   Galais, Marie-Pierre
   Audemar, Franck
   Assenat, Eric
   Lopez-Crapez, Evelyne
   Jouffroy, Claire
   Adenis, Antoine
   Adam, Rene
   Bouche, Olivier
TI Chemotherapy (doublet or triplet) plus targeted therapy by <i>RAS</i>
   status as conversion therapy in colorectal cancer patients with
   initially unresectable liver-only metastases. The UNICANCER PRODIGE-14
   randomised clinical trial
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
ID 1ST-LINE TREATMENT; PHASE-II; OPEN-LABEL; BEVACIZUMAB; FOLFOXIRI;
   CETUXIMAB; OXALIPLATIN; FOLFIRINOX; SURVIVAL; CAPECITABINE
AB Background Colorectal cancer (CRC) patients have a better prognosis if metastases are resectable. Initially, unresectable liver-only metastases can be converted to resectable with chemotherapy plus a targeted therapy. We assessed which of chemotherapy doublet (2-CTx) or triplet (3-CTx), combined with targeted therapy by RAS status, would be better in this setting. Methods PRODIGE 14 was an open-label, multicenter, randomised Phase 2 trial. CRC patients with initially defined unresectable liver-only metastases received either, 2-CTx (FOLFOX or FOLFIRI) or 3-CTx (FOLFIRINOX), plus bevacizumab/cetuximab by RAS status. The primary endpoint was to increase the R0/R1 liver-resection rate from 50 to 70% with the 3-CTx. Results Patients (n = 256) were mainly men with an ECOG PS of 0, and a median age of 60 years. In total, 109 patients (42.6%) had RAS-mutated tumours. After a median follow-up of 45.6 months, the R0/R1 liver-resection rate was 56.9% (95% CI: 48-66) with the 3-CTx versus 48.4% (95% CI: 39-57) with the 2-CTx (P = 0.17). Median overall survival was 43.4 months with 3-CTx versus 40 months with 2-CTx. Conclusion We failed to increase from 50 to 70% the R0/R1 liver-resection rate with the use of 3-CTx combined with bevacizumab or cetuximab by RAS status in CRC patients with initially unresectable liver metastases.
C1 [Ychou, Marc; Adenis, Antoine] Inst Canc Montpellier, Dept Digest Oncol, Montpellier, France.
   [Rivoire, Michel] Leon Berard Canc Ctr, Dept Surg Oncol, Lyon, France.
   [Thezenas, Simon] Inst Canc Montpellier, Biometr Unit, Montpellier, France.
   [Guimbaud, Rosine] CHU Toulouse, Dept Digest Oncol IUCT Rangueil Larrey, Toulouse, France.
   [Ghiringhelli, Francois] Ctr Georges Francois Leclerc, Dept Med Oncol, Dijon, France.
   [Mercier-Blas, Anne] Ctr Hosp Prive St Gregoire, Dept Med Oncol, St Gregoire, France.
   [Mineur, Laurent] Inst St Catherine, Dept Digest Oncol, Avignon, France.
   [Francois, Eric] Ctr Antoine Lacassagne, Dept Med Oncol, Nice, France.
   [Khemissa, Faiza] Ctr Hosp St Jean, Gastroenterol Unit, Perpignan, France.
   [Chauvenet, Marion] Hop Lyon Sud, Dept Hepatogastroenterol & Digest Oncol, Lyon, France.
   [Kianmanesh, Reza] Hop Robert Debre, Dept Digest & Endocrine Surg, Reims, France.
   [Fonck, Marianne] Inst Bergonie, Dept Digest Oncol, Bordeaux, France.
   [Houyau, Philippe] Clin Claude Bernard, Dept Med Oncol, Albi, France.
   [Aparicio, Thomas] Hop St Louis, AP HP, Dept Gastroenterol & Digest Oncol, Paris, France.
   [Galais, Marie-Pierre] Ctr Francois Baclesse, Dept Med Oncol, Caen, France.
   [Audemar, Franck] Ctr Hosp Cote Basque, Gastroenterol Unit, Bayonne, France.
   [Assenat, Eric] CHU St Eloi, Dept Digest Oncol, Montpellier, France.
   [Lopez-Crapez, Evelyne] Inst Canc Montpellier, Translat Res Unit, Montpellier, France.
   [Lopez-Crapez, Evelyne] Univ Montpellier, Inst Rech Cancerol Montpellier, IRCM, INSERM U1194, Montpellier, France.
   [Jouffroy, Claire] R&D Unicanc, Paris, France.
   [Adam, Rene] Hop Paul Brousse, AP HP, Hepatobiliary Ctr, Villejuif, France.
   [Bouche, Olivier] Hop Robert Debre, Dept Hepatogastroenterol & Digest Oncol, Reims, France.
C3 UNICANCER; Universite de Montpellier; Institut Regional du Cancer
   Montpellier / Val d'Aurelle (ICM); UNICANCER; Centre Leon Berard;
   UNICANCER; Universite de Montpellier; Institut Regional du Cancer
   Montpellier / Val d'Aurelle (ICM); Universite de Toulouse; Universite
   Toulouse III - Paul Sabatier; CHU de Toulouse; UNICANCER; Centre
   Georges-Francois Leclerc; UNICANCER; Centre Antoine Lacassagne;
   UNICANCER; Centre Jean Perrin; CHU Lyon; Universite de Reims
   Champagne-Ardenne; CHU de Reims; UNICANCER; Institut Bergonie;
   Universite Paris Cite; Assistance Publique Hopitaux Paris (APHP);
   Hopital Universitaire Saint-Louis - APHP; UNICANCER; Centre Francois
   Baclesse; Universite de Montpellier; CHU de Montpellier; UNICANCER;
   Universite de Montpellier; Institut Regional du Cancer Montpellier / Val
   d'Aurelle (ICM); Institut National de la Sante et de la Recherche
   Medicale (Inserm); Universite de Montpellier; UNICANCER; Institut
   Regional du Cancer Montpellier / Val d'Aurelle (ICM); UNICANCER;
   Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
   Paul-Brousse - APHP; CHU de Reims; Universite de Reims Champagne-Ardenne
RP Ychou, M (corresponding author), Inst Canc Montpellier, Dept Digest Oncol, Montpellier, France.
EM marc.ychou@icm.unicancer.fr
RI ADENIS, ANTOINE/AFL-9835-2022
OI ghiringhelli, francois/0000-0002-5465-8305; Ychou,
   Marc/0000-0001-7378-9469
FU Merck-Serono France
FX This trial was made possible through an unrestricted grant from
   Merck-Serono France. Investigators list: INVESTIGATOR NAME: SITE, CITY.
   Pr. Marc YCHOU: Institut Regional du Cancer de Montpellier/Val d'Aurelle
   (ICM), Montpellier; Dr. Laurent MINEUR: Institut Ste Catherine, Avignon;
   Pr. Olivier BOUCHE: CHU de Reims, Reims; Dr. Pascale MARIANI: Institut
   Curie, Paris; Dr. Kartine BOUHIER-LEPORIER: CHU Cote de Nacre, Caen; Dr.
   Marianne FONCK: Institut Bergonie, Bordeaux; Dr. Roger FAROUX: CHD
   Vendee, La Roche sur Yon; Dr. Alice GAGNAIRE: CHU Dijon -Hopital Du
   Bocage, Dijon; Dr. Eric FRANCOIS: Centre Antoine Lacassagne, Nice; Dr.
   Julien FORESTIER: Hopital Edouard Herriot, Lyon; Pr Francois
   GHIRINGHELLI: Centre G. F. Leclerc, Dijon; Dr. Driffa MOUSSATA: Centre
   hospitalier Lyon Sud, Pierre-Benite; Dr. Gael DEPLANQUE: Centre
   Hospitalier Saint-Joseph, Paris; Dr. Jean-Louis LEGOUX: CHR d'Orleans
   -La Source, Orleans; Dr. Cedric LECAILLE: Polyclinique de Bordeaux Nord
   Aquitaine, Bordeaux; Pr. Nicole TUBIANA-MATHIEU: CHU Dupuytren, Limoges;
   Mr. Michel RIVOIRE: Centre Leon Berard, Lyon; Dr. Marie-Pierre GALAIS:
   Centre Francois Baclesse, Caen; Pr. Rosine GUIMBAUD: Centre hospitalier
   Rangueil, Toulouse; Dr. Francine FEIN: CHU Jean Minjoz, Besancon; Dr.
   Philippe HOUYAU: Clinique Claude Bernard, Albi; Pr. Thomas APARICIO:
   Hopital Avicenne, Bobigny; Pr. JeanFrancois SEITZ: CHU La Timone,
   Marseille; Dr. Stephen ELLIS: Centre Catalan d'oncologie, Perpignan; Dr.
   Stephane REMY: Centre d'oncologie et de radiotherapie du Pays basque,
   Bayonne; Dr. Faiza KHEMISSA -AKOUZ: Hopital Saint Jean, Perpignan; Dr.
   Mohammed RAMDANI: Centre Hospitalier de Beziers, Beziers; Dr. Anne
   MERCIER -BLAS: CHP Saint Gregoire, Saint Gregoire; Pr. Eric ASSENAT: CHU
   Saint Eloi -CHRU de Montpellier, Montpellier; Pr. Julien TAIEB: Hopital
   Europeen Georges Pompidou, Paris; Pr. Rene ADAM: Hopital Paul Brousse,
   Villejuif; Dr. Herve PERRIER: Hopital St Joseph, Marseille; Dr. Agnes
   PELAQUIER: Centre hospitalier Montelimar, Montelimar; Pr. Emmanuel
   MITRY: Hopital Huguenin -Institut Curie, Saint-Cloud; Dr. Serge FRATTE:
   CHBM -Site du Mittan, Montbeliard; Dr. Franck AUDEMAR: Centre
   hospitalier Cote Basque, Bayonne; Dr. JeanLuc LABOUREY: Centre
   hospitalier de Carcassonne, Carcassone; Dr. Mathilde MARTINEZ: Clinique
   Pasteur, Toulouse; Dr. Christian BOREL: Centre Paul Strauss, Strasbourg;
   Dr. Etienne SUC: Clinique St Jean du Languedoc, Toulouse; Dr. Christine
   LE FOLL: Centre hospitalier Marne la Vallee, Jossigny; Dr. Etienne
   MAURIAC: Polyclinique Cote Basque Sud, Saint Jean de Luz; Dr. Denis
   PERE-VERGE: Centre Hospitalier Saint-Joseph-Saint-Luc, Lyon.
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NR 26
TC 22
Z9 22
U1 0
U2 4
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD MAY 18
PY 2022
VL 126
IS 9
BP 1264
EP 1270
DI 10.1038/s41416-021-01644-y
EA JAN 2022
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0U6KE
UT WOS:000739827600001
PM 34992255
OA Green Published
DA 2025-01-04
ER

PT J
AU Li, WH
   Qiu, T
   Guo, L
   Ying, JM
   Zhou, AP
AF Li, Weihua
   Qiu, Tian
   Guo, Lei
   Ying, Jianming
   Zhou, Aiping
TI NGS-based oncogenic mutations analysis in advanced colorectal cancer
   patients improves targeted therapy prediction
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Article
DE Colorectal cancer; Next-generation sequencing; Oncogenic mutations;
   Targeted therapy; Concomitant mutation
ID ANTI-EGFR THERAPY; PIK3CA MUTATIONS; BRAF; KRAS; NRAS; MARKERS; COLON
AB Background. Characterization of genetic alterations has been revealed to be important to predict the outcomes of targeted therapy in cancer. We here aimed to assess the mutation profiling of 526 colorectal cancer (CRC) patients by next-generation sequencing (NGS) to enable a more personalized anti-EGFR treatment.
   Methods: Tumors were analyzed using NGS to determine hotspot mutations in 22 cancer-related genes.
   Results: Mutations were observed in 13 genes in 436 of 526 (82.9%) tumors, and the most common mutations occurred in TP53 and KRAS. PIK3CA mutations usually coexisted with KRAS, NRAS or BRAF mutations. A higher frequency of concomitant PIK3CA mutations was observed in tumors with KRAS outside codon 13 mutations, with NRAS codon 61 mutations and with BRAF kinase-activated mutations. Moreover, KRAS, PIK3CA, AKT1 and FBXW7 mutations were statistically associated with some clinicopathological features, including location, age or metastasis of CRC patients. For RAS wild-type patients treated with cetuximab, longer progression-free survival (PFS) was observed in patients identified as wild type in all 22 genes compared with patients with mutations in one or more genes.
   Conclusions: A wild-type result in all 22 cancer-related genes detected by NGS is associated with a better outcome of cetuximab treatment. Determining mutation patterns by NGS may aid to understand the molecular mechanisms of CRC and improve targeted therapy prediction.
C1 [Li, Weihua; Qiu, Tian; Guo, Lei; Ying, Jianming] Dept Pathol, Beijing 100021, Peoples R China.
   [Zhou, Aiping] Med Oncol, Beijing 100021, Peoples R China.
RP Ying, JM (corresponding author), Chinese Acad Med Sci, Canc Hosp, Dept Pathol, Natl Canc Ctr,Natl Clin Res Ctr Canc, 17 Panjiayuan Nanli, Beijing 100021, Peoples R China.; Ying, JM; Zhou, AP (corresponding author), Peking Union Med Coll, 17 Panjiayuan Nanli, Beijing 100021, Peoples R China.; Zhou, AP (corresponding author), Chinese Acad Med Sci, Dept Med Oncol, Natl Canc Ctr, Natl Clin Res Ctr Canc,Canc Hosp, 17 Panjiayuan Nanli, Beijing 100021, Peoples R China.
EM jmying@cicams.ac.cn; zhouap1825@126.com
RI Qiu, Tian/JGM-7268-2023; Guo, Lei/AEU-0178-2022
FU National Natural Science Foundation of China [81702436]; CAMS Innovation
   Fund for Medical Sciences [2017-I2M-1-006]
FX This work was supported by grants from the National Natural Science
   Foundation of China (81702436), and CAMS Innovation Fund for Medical
   Sciences (2017-I2M-1-006).
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NR 33
TC 8
Z9 8
U1 0
U2 9
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD MAR
PY 2019
VL 215
IS 3
BP 483
EP 489
DI 10.1016/j.prp.2018.12.037
PG 7
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA HO5WL
UT WOS:000460999500013
PM 30611619
DA 2025-01-04
ER

PT J
AU Zhang, M
   Zhao, SL
   Tan, C
   Gu, YZ
   He, XF
   Du, X
   Li, DW
   Wei, P
AF Zhang, Meng
   Zhao, Senlin
   Tan, Cong
   Gu, Yanzi
   He, Xuefeng
   Du, Xiang
   Li, Dawei
   Wei, Ping
TI RNA-binding protein IMP3 is a novel regulator of MEK1/ERK signaling
   pathway in the progression of colorectal Cancer through the
   stabilization of MEKK1 mRNA
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE IMP3; MEK1; ERK pathway; MEKK1; Colorectal Cancer
ID NEGATIVE BREAST-CANCER; CELL-MIGRATION; MAINTENANCE; METASTASIS;
   IGF2BP3; PROMOTE
AB Background MEK1/ERK signaling pathway plays an important role in most tumor progression, including colorectal cancer (CRC), however, MEK1-targeting therapy has little effective in treating CRC patients, indicating there may be a complex mechanism to activate MEK1/ERK signaling pathway except RAS activated mechanism. Methods To investigate the clinical significance of IMP3, we analyzed its expression levels in publicly available dataset and samples from Fudan University Shanghai Cancer Center. The effects of IMP3 on proliferation, migration, and invasion were determined by in vitro and in vivo experiments. To investigate the role of IMP3 in colon carcinogenesis, conditional IMP3 knockout C57BL/6 mice was generated. The IMP3/MEKK1/MEK/ERK signaling axis in CRC was screened and validated by RNA-sequencing, RNA immunoprecipitation, luciferase reporter and western blot assays. Results We find RNA binding protein IMP3 directly bind to MEKK1 mRNA 3 '-UTR, which regulates its stability, promote MEKK1 expression and sequentially activates MEK1/ERK signaling. Functionally, IMP3 promote the malignant biological process of CRC cells via MEKK1/MEK1/ERK signaling pathway both in vitro and in vivo, Moreover, IMP3(-/-) mice show decreased the expression of MEKK1 as well as colorectal tumors compared with wild-type mice after treatment with azoxymethane/dextran sodium sulfate. Clinically, the expression of IMP3 and MEKK1 are positive correlated, and concomitant IMP3 and MEKK1 protein levels negatively correlate with metastasis in CRC patients. In addition, MEK1 inhibitor in combination with shRNA-IMP3 have a synergistic effect both in vitro and in vivo. Conclusion Our study demonstrates that IMP3 regulates MEKK1 in CRC, thus activating the MEK1/ERK signaling in the progression of colorectal cancer, Furthermore, these results provide new insights into potential applications for combining MEK1 inhibitors with other target therapy such as IMP3 in preclinical trials for CRC patients.
C1 [Zhang, Meng; Tan, Cong; Du, Xiang; Wei, Ping] Fudan Univ, Dept Pathol, Shanghai Canc Ctr, Shanghai 200032, Peoples R China.
   [Zhang, Meng; Tan, Cong; Gu, Yanzi; Du, Xiang; Wei, Ping] Fudan Univ, Inst Pathol, Shanghai, Peoples R China.
   [Zhang, Meng; Zhao, Senlin; Tan, Cong; Gu, Yanzi; He, Xuefeng; Du, Xiang; Li, Dawei; Wei, Ping] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.
   [Zhao, Senlin; He, Xuefeng; Li, Dawei] Fudan Univ, Dept Colorectal Surg, Shanghai Canc Ctr, Shanghai 200032, Peoples R China.
   [Gu, Yanzi] Fudan Univ, Biobank, Shanghai Canc Ctr, Shanghai, Peoples R China.
   [Wei, Ping] Fudan Univ, Canc Inst, Shanghai Canc Ctr, Shanghai, Peoples R China.
C3 Fudan University; Fudan University; Fudan University; Fudan University;
   Fudan University; Fudan University
RP Du, X; Wei, P (corresponding author), Fudan Univ, Dept Pathol, Shanghai Canc Ctr, Shanghai 200032, Peoples R China.; Du, X; Li, DW; Wei, P (corresponding author), Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.
EM dx2008cn@163.com; li_dawei@fudan.edu.cn; weiping@fudan.edu.cn
FU National Science Foundation of China [81772583, 81972293, 81972185,
   81902430]; Shanghai Rising-Star Program [17QA1400900, 19QA1402200];
   Shanghai Natural Science Foundation [18ZR1407800]; Municipal Human
   Resources Development Program for Outstanding Young Talents in Medical
   and Health Sciences in Shanghai [2017YQ046]
FX This work was supported by the National Science Foundation of China
   (grant numbers 81772583, 81972293, 81972185, 81902430) and Shanghai
   Rising-Star Program (grant number17QA1400900, 19QA1402200), Shanghai
   Natural Science Foundation(grant numbers 18ZR1407800), Municipal Human
   Resources Development Program for Outstanding Young Talents in Medical
   and Health Sciences in Shanghai (grant number2017YQ046).
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NR 39
TC 14
Z9 14
U1 0
U2 11
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 JUN 21
PY 2021
VL 40
IS 1
AR 200
DI 10.1186/s13046-021-01994-8
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SX1EK
UT WOS:000664954300002
PM 34154626
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Nakayama, I
   Takahari, D
AF Nakayama, Izuma
   Takahari, Daisuke
TI The Role of Angiogenesis Targeted Therapies in Metastatic Advanced
   Gastric Cancer: A Narrative Review
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE gastric cancer; VEGF; target therapy; clinical trial
ID ENDOTHELIAL GROWTH-FACTOR; MULTICENTER PHASE-II; VASCULAR-PERMEABILITY
   FACTOR; S-1 PLUS CISPLATIN; CELL LUNG-CANCER; GASTROESOPHAGEAL JUNCTION;
   DOUBLE-BLIND; OPEN-LABEL; COLORECTAL-CANCER; 1ST-LINE THERAPY
AB Since bevacizumab was first approved by the U.S. Food and Drug Administration as an anti-angiogenic therapy in 2004, angiogenesis-targeted therapy has been developed for various types of solid tumors. To date, ramucirumab and apatinib are clinically available as treatments for metastatic advanced gastric cancer (AGC). Ramucirumab demonstrated prolonged survival as second-line therapy of metastatic AGC in the RAINBOW and REGARD trials. However, neither ramucirumab extended survival in treatment-naive patients with AGC in the RAINFALL or RAINSTORM trials nor bevacizumab in the AVAGAST and AVATAR trials. Apatinib demonstrated superior efficacy over the best supportive care in a Chinese phase III trial but not in an international phase III (ANGEL) trial. Currently, combination therapy of ramucirumab with irinotecan or FTD/TPI is being evaluated in the third-line setting, assessing the efficacy of continuous angiogenesis inhibition from second- to third-line therapy. Recently, the role of angiogenesis inhibition via immunomodulators is attractive to clinicians. Emerging results of several early-phase clinical trials indicated the promising antitumor activity of angiogenesis inhibition in combination with immune therapy. This review offers an overview of the history of clinical trials focused on anti-angiogenic for patients with AGC and presents future perspectives in this area.
C1 [Nakayama, Izuma; Takahari, Daisuke] Canc Inst Hosp Japanese Fdn Canc Res, Dept Gastroenterol Chemotherapy, Tokyo 1358550, Japan.
C3 Japanese Foundation for Cancer Research
RP Takahari, D (corresponding author), Canc Inst Hosp Japanese Fdn Canc Res, Dept Gastroenterol Chemotherapy, Tokyo 1358550, Japan.
EM izuma.nakayama@jfcr.or.jp; daisuke.takahari@jfcr.or.jp
RI Takahari, Daisuke/AAI-3955-2020; Takahari, Daisuke/ADQ-5466-2022
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NR 119
TC 7
Z9 8
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD APR 30
PY 2023
VL 12
IS 9
AR 3226
DI 10.3390/jcm12093226
PG 21
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA G2DK9
UT WOS:000987325400001
PM 37176668
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Tessitore, A
   Cicciarelli, G
   Mastroiaco, V
   Del Vecchio, F
   Capece, D
   Verzella, D
   Fischietti, M
   Vecchiotti, D
   Zazzeroni, F
   Alesse, E
AF Tessitore, Alessandra
   Cicciarelli, Germana
   Mastroiaco, Valentina
   Del Vecchio, Filippo
   Capece, Daria
   Verzella, Daniela
   Fischietti, Mariafausta
   Vecchiotti, Davide
   Zazzeroni, Francesca
   Alesse, Edoardo
TI Therapeutic Use of MicroRNAs in Cancer
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Article
DE Biomarker; cancer; chemotherapy; microRNA; radiation therapy; targeted
   therapy
ID CELL LUNG-CANCER; INCREASES DRUG-RESISTANCE; HEPATOCELLULAR-CARCINOMA
   CELLS; TUMOR-SUPPRESSOR PDCD4; NEGATIVE BREAST-CANCER; TREATED HCC CELL;
   COLORECTAL-CANCER; GASTRIC-CANCER; UP-REGULATION; COLON-CANCER
AB MicroRNAs are small non-coding RNAs which regulate gene expression and silence a wide set of target genes. Aberrant miRNA expression has been described in cancer cells and is at least in part responsible of cancer initiation, development and progression. Due to their role, miRNAs have emerged as therapeutic targets or molecules suitable at the therapeutic level as well as markers of the response to chemo/radio/targeted therapy. Restoration or repression of miRNAs expression and activity shows high potential in managing cancer, and many studies on pre-clinical models have demonstrated the feasibility and efficacy of miRNA-based therapy. However, despite the exciting potential, some limitations, due to the degree of delivery and biodistribution or to possible side effects, need to be taken into consideration and solved in order to accomplish transition to clinical application. In this review we report and discuss the role of miRNAs in cancer, focusing on their use as therapeutic agents and their involvement in modulating/affecting the response to chemo/radio/targeted therapy in some of the most frequent solid tumors.
C1 [Tessitore, Alessandra; Cicciarelli, Germana; Mastroiaco, Valentina; Del Vecchio, Filippo; Verzella, Daniela; Fischietti, Mariafausta; Vecchiotti, Davide; Zazzeroni, Francesca; Alesse, Edoardo] Univ Aquila, Dept Biotechnol & Appl Clin Sci, I-67100 Laquila, Italy.
   [Capece, Daria] Univ London Imperial Coll Sci Technol & Med, Ctr Cell Signalling & Inflammat, Dept Med, London W12 0NN, England.
C3 University of L'Aquila; Imperial College London
RP Tessitore, A (corresponding author), Univ Aquila, Dept Biotechnol & Appl Clin Sci, Via Vetoio,Coppito 2, I-67100 Laquila, Italy.
EM alessandra.tessitore@univaq.it
RI Fischietti, Mariafausta/Y-6449-2019; Capece, Daria/AFR-1769-2022; Del
   Vecchio, Filippo/AAL-7354-2021
OI Vecchiotti, Davide/0000-0003-1054-4565; tessitore,
   alessandra/0000-0002-7663-2210; Capece, Daria/0000-0003-3126-2014
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NR 160
TC 24
Z9 24
U1 0
U2 43
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 2016
VL 16
IS 1
BP 7
EP 19
DI 10.2174/1871520615666150824153358
PG 13
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA CW5NR
UT WOS:000365043100003
PM 26299662
DA 2025-01-04
ER

PT J
AU Matsuoka, T
   Yashiro, M
AF Matsuoka, Tasuku
   Yashiro, Masakazu
TI Molecular-targeted therapy toward precision medicine for
   gastrointestinal caner: Current progress and challenges
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Gastrointestinal cancer; Esophageal cancer; Gastric cancer; Colorectal
   cancer; Targeted therapy; Precision medicine
ID METASTATIC COLORECTAL-CANCER; TYROSINE KINASE INHIBITORS; PHASE-I TRIAL;
   GASTRIC-CANCER; ANTITUMOR-ACTIVITY; SIGNALING PATHWAY; COLON-CANCER;
   LUNG-CANCER; TGF-BETA; CHEMOTHERAPY
AB Gastrointestinal (GI) cancer remains the deadliest cancer in the world. The current standard treatment for GI cancer focuses on 5-fluorouracil-based chemotherapeutic regimens and surgery, and molecular-targeted therapy is expected to be a more effective and less toxic therapeutic strategy for GI cancer. There is well-established evidence for the use of epidermal growth factor receptor-targeted and vascular endothelial growth factor-targeted antibodies, which should routinely be incorporated into treatment strategies for GI cancer. Other potential therapeutic targets involve the PI3K/AKT pathway, tumor growth factor-beta pathway, mesenchymal-epithelial transition pathway, WNT pathway, poly (ADP-ribose) polymerase, and immune checkpoints. Many clinical trials assessing the agents of targeted therapy are underway and have presented promising and thought-provoking results. With the development of molecular biology techniques, we can identify more targetable molecular alterations in larger patient populations with GI cancer. Targeting these molecules will allow us to reach the goal of precision medicine and improve the outcomes of patients with GI cancer.
C1 [Matsuoka, Tasuku; Yashiro, Masakazu] Osaka City Univ, Dept Surg Oncol, Grad Sch Med, Osaka 5458585, Japan.
C3 Osaka Metropolitan University
RP Yashiro, M (corresponding author), Osaka City Univ, Dept Surg Oncol, Grad Sch Med, 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 KAKENHI (Grant-inAid for Scientific Research), No. 18H02883.
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NR 97
TC 4
Z9 4
U1 0
U2 18
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 MAY 15
PY 2021
VL 13
IS 5
DI 10.4251/wjgo.v13.i5.366
PG 26
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA SF1YT
UT WOS:000652559200004
PM 34040699
OA Green Published
DA 2025-01-04
ER

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   Lecaille, Cedric
   Louafi, Sami
   Lepage, Come
   Ducreux, Michel
   Taieb, Julien
   Akouz, Faiza Khemissa
   De Baere, Thierry
TI Phase III randomized trial comparing systemic versus intra-arterial
   oxaliplatin, combined with LV5FU2+/- irinotecan and a targeted therapy,
   in the first-line treatment of metastatic colorectal cancer restricted
   to the liver (OSCAR): PRODIGE 49
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Article
DE Colorectal neoplasm; Liver metastases; Hepatic arterial infusion;
   Randomized controlled trial
ID HEPATIC ARTERIAL INFUSION; FOLFOXIRI PLUS BEVACIZUMAB; EARLY TUMOR
   SHRINKAGE; PUMP CHEMOTHERAPY; OPEN-LABEL; FOLFIRI; 5-FLUOROURACIL;
   MULTICENTER; LEUCOVORIN; CONVERSION
AB Introduction: In patients with unresectable liver metastases from colorectal cancer (CRCLM), systemic doublet or triplet chemotherapy and targeted therapy is considered a standard first-line treatment. Hepatic arterial infusion of oxaliplatin (HAI-ox) generates a high response rate, but this still needs to be confirmed in a randomized trial. We incorporated HAI-ox in doublet or triplet + targeted therapy to validate its efficacy.
   Aim: The OSCAR study is an ongoing randomized phase III trial comparing FOLFOX + targeted therapy according to RAS status, or FOLFOXIRI + bevacizumab in patients eligible for triplet therapy, with the same regimen but with HAI-ox instead of IV-ox as the first-line treatment for CRCLM.
   Materials and methods: Main eligibility criteria are colorectal cancer, unresectable liver metastasis, no extra-hepatic metastases except pulmonary nodules if <= 3 and < 10 mm, ECOG performance status 0 or 1.
   Endpoint: The primary endpoint is progression-free survival (PFS). A difference of 4 months for the median PFS in favor of HAI-ox is expected (HR = 0.73). Secondary endpoints include overall survival, overall response rate, secondary liver resection, safety, and quality of life.
   Conclusion: This study is planned to include 348 patients to demonstrate the superiority of HAI-ox over systemic oxaliplatin in first-line CRCLM treatment (NCT02885753).
   (c) 2021 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Pernot, Simon] Inst Bergonie, Dept Med Oncol, 229 Cours Argonne, F-33076 Bordeaux, France.
   [Pellerin, Olivier] Univ Paris, Hop Europeen Georges Pompidou, Dept Intervent Radiol, SIRIC CARPEM, Paris, France.
   [Mineur, Laurent] Inst St Catherine, Dept Med Oncol, Avignon, France.
   [Monterymard, Carole; Lepage, Come] Univ Burgundy & Franche Comte, Federat Francophone Cancerol Digest FFCD, EPICAD INSERM LNC UMR 1231, Dijon, France.
   [Smith, Denis; Lepage, Come] Univ Bordeaux, Dept Gastroenterol & GI Oncol, CHU Haut Leveque, Pessac, France.
   [Lapuyade, Bruno; Lepage, Come] Univ Bordeaux, Dept Intervent Radiol, CHU Haut Leveque, Pessac, France.
   [Gallois, Claire; Lepage, Come; Taieb, Julien] Univ Paris, Hop Europeen Georges Pompidou, Dept Gastroenterol & GI Oncol, SIRIC CARPEM, Paris, France.
   [Lepage, Come; Akouz, Faiza Khemissa] CH St Jean, Dept Gastroenterol & GI Oncol, Perpignan, France.
   [Lepage, Come; De Baere, Thierry] Univ Paris Saclay, Dept Intervent Radiol, Gustave Roussy, BIOTHERIS, Villejuif, France.
   [Tougeron, David; Lepage, Come] Univ Poitiers, Dept Gastroenterol & Hepatol, CHU Mil, Poitiers, France.
   [Thirot-Bidault, Anne; Lepage, Come] Hop Prive Antony, Dept Med Oncol, Antony, France.
   [Audemar, Franck; Lepage, Come] CH Cote Basque, Dept Gastroenterol & GI Oncol, Bayonne, France.
   [Simon, Mireille; Lepage, Come] CH Pau, Dept Gastroenterol & GI Oncol, Pau, France.
   [Lecaille, Cedric; Lepage, Come] Polyclin Bordeaux Nord Aquitaine, Dept Gastroenterol & GI Oncol, Bordeaux, France.
   [Louafi, Sami; Lepage, Come] CH Corbeille Essonne, Dept Med Oncol, Corbeille Essonne, France.
   [Lepage, Come] Univ Burgundy & Franche Comte, Dept Gastroenterol & GI oncol, CHU Bocage, Dijon, France.
   [Ducreux, Michel] Univ Paris Saclay, Dept Med Oncol, Gustave Roussy, Inserm U1279, Villejuif, France.
C3 UNICANCER; Institut Bergonie; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris Cite; Hopital Universitaire Europeen Georges-Pompidou -
   APHP; Universite de Bourgogne; Institut Agro; AgroSup Dijon; Institut
   National de la Sante et de la Recherche Medicale (Inserm); CHU Bordeaux;
   Universite de Bordeaux; Universite de Bordeaux; CHU Bordeaux; Assistance
   Publique Hopitaux Paris (APHP); Universite Paris Cite; Hopital
   Universitaire Europeen Georges-Pompidou - APHP; Universite Paris Saclay;
   UNICANCER; Gustave Roussy; CHU Poitiers; Universite de Poitiers; CHU
   Dijon Bourgogne; UNICANCER; Gustave Roussy; Institut National de la
   Sante et de la Recherche Medicale (Inserm); Universite Paris Saclay
RP Pernot, S (corresponding author), Inst Bergonie, Dept Med Oncol, 229 Cours Argonne, F-33076 Bordeaux, France.
EM Simon.pernot@gmail.com
RI tougeron, david/ABF-3217-2020; Gallois, Claire/HLG-3074-2023
OI taieb, julien/0000-0002-9955-4753
FU AMGEN
FX Source of support: This trial is in part funded by AMGEN
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NR 32
TC 6
Z9 6
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD MAR
PY 2022
VL 54
IS 3
BP 324
EP 330
DI 10.1016/j.dld.2021.12.012
EA FEB 2022
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 0P5DI
UT WOS:000784240200006
PM 35027324
OA Bronze
DA 2025-01-04
ER

PT J
AU Wang, K
   Shen, RY
   Meng, TT
   Hu, FQ
   Yuan, H
AF Wang, Ke
   Shen, Ruoyu
   Meng, Tingting
   Hu, Fuqiang
   Yuan, Hong
TI Nano-Drug Delivery Systems Based on Different Targeting Mechanisms in
   the Targeted Therapy of Colorectal Cancer
SO MOLECULES
LA English
DT Review
DE targeted therapy; colorectal cancer; nanoparticles; drug delivery
   systems
ID CHITOSAN NANOPARTICLES; POTENTIAL TREATMENT; ORAL DELIVERY;
   COLON-CANCER; IN-VITRO; TUMOR; 5-FLUOROURACIL; COMBINATION; EFFICACY;
   DOXORUBICIN
AB Colorectal cancer (CRC) is a usual digestive tract malignancy and the third main cause of cancer death around the world, with a high occurrence rate and mortality rate. Conventional therapies for CRC have certain side effects and restrictions. However, the exciting thing is that with the rapid development of nanotechnology, nanoparticles have gradually become more valuable drug delivery systems than traditional therapies because of their capacity to control drug release and target CRC. This also promotes the application of nano-drug targeted delivery systems in the therapy of CRC. Moreover, to make nanoparticles have a better colon targeting effect, many approaches have been used, including nanoparticles targeting CRC and in response to environmental signals. In this review, we focus on various targeting mechanisms of CRC-targeted nanoparticles and their latest research progress in the last three years, hoping to give researchers some inspiration on the design of CRC-targeted nanoparticles.
C1 [Wang, Ke; Shen, Ruoyu; Meng, Tingting; Hu, Fuqiang; Yuan, Hong] Zhejiang Univ, Coll Pharmaceut Sci, 866 Yuhangtang Rd, Hangzhou 310058, Peoples R China.
C3 Zhejiang University
RP Yuan, H (corresponding author), Zhejiang Univ, Coll Pharmaceut Sci, 866 Yuhangtang Rd, Hangzhou 310058, Peoples R China.
EM wk1194229090@163.com; 3150101386@zju.edu.cn; mengtt@zju.edu.cn;
   hufq@zju.edu.cn; yuanhong70@zju.edu.cn
RI Shen, Ruoyu/IUP-5544-2023
OI Wang, Ke/0000-0002-6334-0200
FU National Natural Science Foundation of China [81773644, 81773648]
FX This research was funded by National Natural Science Foundation of China
   grant number 81773644 and 81773648.
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NR 96
TC 23
Z9 23
U1 12
U2 106
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD MAY
PY 2022
VL 27
IS 9
AR 2981
DI 10.3390/molecules27092981
PG 15
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 1E8SA
UT WOS:000794749900001
PM 35566331
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, NN
   Cao, YP
   Si, CS
   Shao, P
   Su, GQ
   Wang, K
   Bao, J
   Yang, L
AF Wang, Nannan
   Cao, Yuepeng
   Si, Chengshuai
   Shao, Peng
   Su, Guoqing
   Wang, Ke
   Bao, Jun
   Yang, Liu
TI Emerging Role of ERBB2 in Targeted Therapy for Metastatic Colorectal
   Cancer: Signaling Pathways to Therapeutic Strategies
SO CANCERS
LA English
DT Review
DE ERBB2; HER2; targeted therapy; colorectal cancer
ID HER2 GENE AMPLIFICATION; BREAST-CANCER; OPEN-LABEL; GROWTH;
   HETEROGENEITY; MUTATIONS; RECEPTOR; TRASTUZUMAB; DIFFERENTIATION; EGFR
AB Simple Summary Colorectal cancer (CRC) is the third most commonly diagnosed malignancy and the second most common cause of cancer-related mortality worldwide. Currently available targeted therapies for metastatic CRC mainly target vascular endothelial growth factor and epidermal growth factor receptor in RAS wild-type tumors. Although Erb-B2 receptor tyrosine kinase 2 (ERBB2/human epidermal growth factor receptor 2) plays a significant therapeutic role in breast and gastric cancers, there are no licensed ERBB2-targeted therapies for metastatic CRC. This review aims to outline the molecular biology of ERBB2-positive metastatic CRC and potential targeted therapeutic strategies. Despite recent improvements in the comprehensive therapy of malignancy, metastatic colorectal cancer (mCRC) continues to have a poor prognosis. Notably, 5% of mCRC cases harbor Erb-B2 receptor tyrosine kinase 2 (ERBB2) alterations. ERBB2, commonly referred to as human epidermal growth factor receptor 2, is a member of the human epidermal growth factor receptor family of protein tyrosine kinases. In addition to being a recognized therapeutic target in the treatment of gastric and breast malignancies, it is considered crucial in the management of CRC. In this review, we describe the molecular biology of ERBB2 from the perspective of biomarkers for mCRC-targeted therapy, including receptor structures, signaling pathways, gene alterations, and their detection methods. We also discuss the relationship between ERBB2 aberrations and the underlying mechanisms of resistance to anti-EGFR therapy and immunotherapy tolerance in these patients with a focus on novel targeted therapeutics and ongoing clinical trials. This may aid the development of a new standard of care in patients with ERBB2-positive mCRC.
C1 [Wang, Nannan; Cao, Yuepeng; Si, Chengshuai; Shao, Peng; Su, Guoqing; Wang, Ke; Yang, Liu] Nanjing Med Univ, Dept Colorectal Surg, Affiliated Canc Hosp, Nanjing 210009, Peoples R China.
   [Wang, Nannan; Cao, Yuepeng; Si, Chengshuai; Shao, Peng; Su, Guoqing; Wang, Ke; Bao, Jun; Yang, Liu] Jiangsu Canc Hosp, Nanjing 210009, Peoples R China.
   [Wang, Nannan; Cao, Yuepeng; Si, Chengshuai; Shao, Peng; Su, Guoqing; Wang, Ke; Bao, Jun; Yang, Liu] Jiangsu Inst Canc Res, Nanjing 210009, Peoples R China.
   [Bao, Jun] Nanjing Med Univ, Dept Med Oncol, Affiliated Canc Hosp, Nanjing 210009, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University; Nanjing Medical
   University; Nanjing Medical University
RP Yang, L (corresponding author), Nanjing Med Univ, Dept Colorectal Surg, Affiliated Canc Hosp, Nanjing 210009, Peoples R China.; Bao, J; Yang, L (corresponding author), Jiangsu Canc Hosp, Nanjing 210009, Peoples R China.; Bao, J; Yang, L (corresponding author), Jiangsu Inst Canc Res, Nanjing 210009, Peoples R China.; Bao, J (corresponding author), Nanjing Med Univ, Dept Med Oncol, Affiliated Canc Hosp, Nanjing 210009, Peoples R China.
EM baojun@jszlyy.com.cn; yangliu@njmu.edu.cn
OI Wang, Ke/0009-0004-9852-3842
FU National Natural Science Foundation of China [81602145, 8207270];
   Jiangsu Primary Research & Development Plan [SBE2021740280]; Jiangsu
   Province TCM science and technology development plan monographic project
   [ZT202118]; Jiangsu Province Natural Science Foundation [BK20171509];
   Jiangsu Province Medical Youth Talent, The Project of Invigorating
   Health Care through Science, Technology Education [QNRC2016649]; China
   Postdoctoral Science Foundation [2018M632265]; Talents Program of
   Jiangsu Cancer Hospital [2017-33]; Jiangsu Provincial Key Research and
   Development Program [BE2020723]; "333 Talents" Program of Jiangsu
   Province [BRA2020390]
FX This research was funded by the National Natural Science Foundation of
   China (81602145 and 8207270 to L.Y.), Jiangsu Primary Research &
   Development Plan (SBE2021740280), Jiangsu Province TCM science and
   technology development plan monographic project (ZT202118), Jiangsu
   Province Natural Science Foundation (BK20171509 to L.Y.), Jiangsu
   Province Medical Youth Talent, The Project of Invigorating Health Care
   through Science, Technology Education (QNRC2016649 to L.Y.), China
   Postdoctoral Science Foundation (2018M632265 to L.Y.) and the Talents
   Program of Jiangsu Cancer Hospital (2017-33 to L.Y.), Jiangsu Provincial
   Key Research and Development Program (BE2020723 to J.B.), The "333
   Talents" Program of Jiangsu Province (BRA2020390 to L.Y.).
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NR 126
TC 10
Z9 11
U1 3
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 20
AR 5160
DI 10.3390/cancers14205160
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5O3ZA
UT WOS:000872414500001
PM 36291943
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Patel, GS
   Ullah, S
   Beeke, C
   Hakendorf, P
   Padbury, R
   Price, TJ
   Karapetis, CS
AF Patel, Gargi S.
   Ullah, Shahid
   Beeke, Carol
   Hakendorf, Paul
   Padbury, Robert
   Price, Timothy J.
   Karapetis, Christos S.
TI Association of BMI with overall survival in patients with mCRC who
   received chemotherapy versus EGFR and VEGF-targeted therapies
SO CANCER MEDICINE
LA English
DT Article
DE Bevacizumab; BMI; colorectal cancer; metastatic; targeted therapies
ID BODY-MASS INDEX; COLORECTAL-CANCER; COLON-CANCER; ADJUVANT CHEMOTHERAPY;
   OBESITY; BEVACIZUMAB; OUTCOMES; OVERWEIGHT; AGE
AB Although a raised body mass index (BMI) is associated with increased risk of colorectal cancer (CRC) and recurrence after adjuvant treatment, data in the metastatic setting is limited. We compared overall survival (OS) across BMI groups for metastatic CRC, and specifically examined the effect of BMI within the group of patients treated with targeted therapies (TT). Retrospective data were obtained from the South Australian Registry for mCRC from February 2006 to October 2012. The BMI at first treatment was grouped as underweight <18.5kg/m(2), Normal=18.5 to <25kg/m(2), Overweight=25 to <30kg/m(2), Obese I=30 to <35kg/m(2), Obese II35kg/m(2). Of 1174 patients, 42 were underweight, 462 overweight, 175 Obese I, and 77 Obese II. The OS was shorter for patients who were underweight and overweight compared to normal (OS 13.7 and 22.3 vs. 24.1months, respectively, hazard ratio [HR] 2.21 and 1.23). The adjusted median OS was longer for normal versus overweight or obese I patients receiving chemotherapy + targeted therapy (35.7 vs 25.1 or 22.8months, HR 1.59 and 1.63, respectively) with no difference in OS for chemotherapy alone. On breakdown by type of targeted therapy, overweight and obese I patients had a poorer outcome with Bevacizumab. The BMI is predictive of a poorer outcome for underweight and overweight patients in the whole population. Of those receiving chemotherapy and targeted therapy, BMI is an independent predictor for OS for overweight and obese I patients, specifically for those treated with Bevacizumab. Patients who are overweight or obese (group I) may be a target group for lifestyle and nutrition advice to improve OS with TT.
C1 [Patel, Gargi S.; Karapetis, Christos S.] Flinders Med Ctr, Dept Med Oncol, Adelaide, SA 5042, Australia.
   [Beeke, Carol; Padbury, Robert; Karapetis, Christos S.] Flinders Univ S Australia, Flinders Ctr Innovat Canc, Adelaide, SA 5001, Australia.
   [Ullah, Shahid; Hakendorf, Paul] Flinders Univ S Australia, Sch Med, Flinders Ctr Epidemiol & Biostat, Adelaide, SA 5001, Australia.
   [Padbury, Robert] Flinders Med Ctr, Dept Surg, Adelaide, SA 5042, Australia.
   [Price, Timothy J.] Queen Elizabeth Hosp, Dept Med Oncol, Adelaide, SA, Australia.
   [Price, Timothy J.] Univ Adelaide, Sch Med, Adelaide, SA, Australia.
C3 Flinders Medical Centre; Flinders University South Australia; Flinders
   University South Australia; Flinders Medical Centre; University of
   Adelaide
RP Karapetis, CS (corresponding author), Flinders Med Ctr, Bedford Pk, Adelaide, SA 5042, Australia.
EM c.karapetis@flinders.edu.au
RI Patel, Gargi/AAG-2715-2019; Price, Timothy/AFN-1360-2022; Ullah,
   Shahid/AAC-3054-2020; Price, Timothy/G-1404-2012
OI Price, Timothy/0000-0002-3922-2693; Patel, Gargi/0000-0002-5268-4753;
   Ullah, Shahid/0000-0003-0010-2640; Karapetis,
   Christos/0000-0003-1741-996X
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NR 28
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U1 0
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD OCT
PY 2015
VL 4
IS 10
BP 1461
EP 1471
DI 10.1002/cam4.490
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CT4RI
UT WOS:000362794000001
PM 26211512
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Negulescu, AM
   Mehlen, P
AF Negulescu, Ana-Maria
   Mehlen, Patrick
TI Dependence receptors - the dark side awakens
SO FEBS JOURNAL
LA English
DT Review
DE apoptosis; caspase; dependence receptors; targeted therapy;
   tumorigenesis
ID NF-KAPPA-B; P75 NEUROTROPHIN RECEPTOR; TYROSINE KINASE RECEPTOR; LIPID
   RAFT LOCALIZATION; GROWTH-FACTOR RECEPTOR; TUMOR-SUPPRESSOR GENE; HUMAN
   COLON-CANCER; CELL-DEATH; COLORECTAL-CANCER; DCC GENE
AB Transmembrane receptors are usually seen as on and off switches: when the specific ligand is bound, the receptor is on and transduces a downstream signal, whereas when the ligand is absent, the receptor is off. Over the last two decades several reports have argued for an alternative view where some receptors, depending on the context, will be active both in the presence and in the absence of ligand, being sort of on(A) and on(B) switch rather than on and off. These receptors have been named dependence receptors (DR) and they share the ability to actively trigger cell death when unbound by their respective ligands. DRs have been shown to be important guardians of tissue homeostasis. In pathological settings such as cancer, DRs are seen as tumour suppressors and a clinical trial is ongoing to assay whether these DRs can be used to provide clinical benefit by triggering cancer cell death. In this review we are reviewing this functional family of receptors and underlying their promising potential for targeted therapy against cancer.
C1 [Negulescu, Ana-Maria; Mehlen, Patrick] Univ Claude Bernard Lyon 1, Apoptosis Canc & Dev Lab, Equipe Labelis La Ligue,Ctr Cancerol Lyon,Ctr Leo, LabEx DEVweCAN,INSERM U1052,CNRS UMR5286,Univ Lyo, F-69008 Lyon, France.
C3 Institut National de la Sante et de la Recherche Medicale (Inserm);
   Centre National de la Recherche Scientifique (CNRS); CNRS - National
   Institute for Biology (INSB); Universite Claude Bernard Lyon 1
RP Mehlen, P (corresponding author), Univ Claude Bernard Lyon 1, Apoptosis Canc & Dev Lab, Equipe Labelis La Ligue,Ctr Cancerol Lyon,Ctr Leo, LabEx DEVweCAN,INSERM U1052,CNRS UMR5286,Univ Lyo, F-69008 Lyon, France.
EM patrick.mehlen@lyon.unicancer.fr
FU INSERM; CNRS; ANR; ERC; Ligue Contre le Cancer; Centre Leon Berard;
   INCA; University of Lyon
FX The authors thank the members of Apoptosis, Cancer and Development
   Laboratory for their advice and contribution. The work in the authors'
   laboratory is funded by institutional grants from INSERM, CNRS,
   University of Lyon, Centre Leon Berard, INCA, ANR, ERC and from Ligue
   Contre le Cancer.
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NR 146
TC 28
Z9 31
U1 1
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1742-464X
EI 1742-4658
J9 FEBS J
JI FEBS J.
PD NOV
PY 2018
VL 285
IS 21
BP 3909
EP 3924
DI 10.1111/febs.14507
PG 16
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA GZ7UF
UT WOS:000449688600002
PM 29776009
OA hybrid
DA 2025-01-04
ER

PT J
AU Yao, FJ
   An, YC
   Li, XD
   Li, ZY
   Duan, JH
   Yang, XD
AF Yao, Fengjiao
   An, Yacong
   Li, Xundou
   Li, Zhaoyi
   Duan, Jinhong
   Yang, Xian-Da
TI Targeted Therapy of Colon Cancer by Aptamer-Guided Holliday Junctions
   Loaded with Doxorubicin
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE colon cancer; targeted therapy; aptamer; holliday junction; doxorubicin
ID DRUG-DELIVERY; OLIGONUCLEOTIDE AS1411; COLORECTAL-CANCER; CONJUGATE;
   GOVITECAN; TRIAL
AB Purpose: Chemotherapy is the primary treatment for advanced colon cancer, but its efficacy is often limited by severe toxicities. Targeted therapy in the form of selectively drug delivery system (SDDS) is an important strategy to reduce adverse effects. Here, we aim to design a novel SDDS with potential for practical application using biocompatible components and scalable production process, for targeted delivery of doxorubicin (Dox) to colon cancer cells.
   Methods: The SDDS was made of a self-assembled DNA nano-cross (Holliday junction, or HJ) functionalized by four AS1411 aptamers (Apt-HJ) and loaded with Dox.
   Results: Apt-HJ had an average size of 12.45 nm and a zeta potential of -11.6 mV. Compared with the monovalent AS1411 aptamer, the quadrivalent Apt-HJ showed stronger binding to target cancer cells (CT26). A complex of Apt-HJ and doxorubicin (Apt-HJ-Dox) was formed by intercalating Dox into the DNA structure of Apt-HJ, with each complex carrying approximately 17 Dox molecules. Confocal microscopy revealed that Apt-HJ-Dox selectively delivered Dox into CT26 colon cancer cells but not the control cells. Moreover, Apt-HJ-Dox achieved targeted killing of CT26 cancer cells in vitro and reduced the damage to control cells. Importantly, compared with free Dox, Apt-HJ-Dox significantly enhanced the antitumor efficacy in vivo without boosting the adverse effects.
   Conclusion: These results suggest that Apt-HJ-Dox has application potential in targeted treatment of colon cancer.
C1 [Yao, Fengjiao; An, Yacong; Li, Xundou; Li, Zhaoyi; Duan, Jinhong; Yang, Xian-Da] Chinese Acad Med Sci & Peking Union Med Coll, Inst Basic Med Sci, Beijing, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College
RP Yang, XD (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Inst Basic Med Sci, Beijing, Peoples R China.
EM ayangmd@hotmail.com
RI Yang, Xianda/G-5132-2018
FU Ministry of Science and Technology [2017YFA0205504]; CAMS Innovation
   Fund for Medical Sciences [CIFMS 2016-I2M-3-004]; Natural Science
   Foundation of China [81572997, 81602712]; Department of Pathology of
   PUMC
FX This work was supported by the Ministry of Science and Technology
   (2017YFA0205504), the CAMS Innovation Fund for Medical Sciences (CIFMS
   2016-I2M-3-004), the Natural Science Foundation of China (81572997,
   81602712), and the Research Fund to H.Y. from Department of Pathology of
   PUMC.
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NR 38
TC 29
Z9 29
U1 3
U2 42
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 2020
VL 15
BP 2119
EP 2129
DI 10.2147/IJN.S240083
PG 11
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA KX0SD
UT WOS:000521593000001
PM 32280210
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Choi, H
   Chang, JE
AF Choi, Ha Yeong
   Chang, Ji-Eun
TI Targeted Therapy for Cancers: From Ongoing Clinical Trials to
   FDA-Approved Drugs
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE cancer targeted therapy; lung cancer; colorectal cancer; prostate
   cancer; clinical trials; FDA-approved drugs
ID CELL LUNG-CANCER; RESISTANT PROSTATE-CANCER; METASTATIC
   COLORECTAL-CANCER; HUMAN MONOCLONAL-ANTIBODY; PHASE-III TRIAL;
   OPEN-LABEL; DOUBLE-BLIND; ABIRATERONE ACETATE; ACQUIRED-RESISTANCE;
   1ST-LINE TREATMENT
AB The development of targeted therapies has revolutionized cancer treatment, offering improved efficacy with reduced side effects compared with traditional chemotherapy. This review highlights the current landscape of targeted therapy in lung cancer, colorectal cancer, and prostate cancer, focusing on key molecular targets. Moreover, it aligns with US Food and Drug Administration (FDA)-approved drugs and drug candidates. In lung cancer, mutations in the epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) gene rearrangements have emerged as significant targets. FDA-approved drugs like osimertinib and crizotinib specifically inhibit these aberrant pathways, providing remarkable benefits in patients with EGFR-mutated or ALK-positive lung cancer. Colorectal cancer treatment has been shaped by targeting the vascular endothelial growth factor (VEGF) and EGFR. Bevacizumab and cetuximab are prominent FDA-approved agents that hinder VEGF and EGFR signaling, significantly enhancing outcomes in metastatic colorectal cancer patients. In prostate cancer, androgen receptor (AR) targeting is pivotal. Drugs like enzalutamide, apalutamide, and darolutamide effectively inhibit AR signaling, demonstrating efficacy in castration-resistant prostate cancer. This review further highlights promising targets like mesenchymal-epithelial transition (MET), ROS1, BRAF, and poly(ADP-ribose) polymeras (PARP) in specific cancer subsets, along with ongoing clinical trials that continue to shape the future of targeted therapy.
C1 [Choi, Ha Yeong; Chang, Ji-Eun] Dongduk Womens Univ, Coll Pharm, Seoul 02748, South Korea.
C3 Dongduk Women's University
RP Chang, JE (corresponding author), Dongduk Womens Univ, Coll Pharm, Seoul 02748, South Korea.
EM 201818@dongduk.ac.kr; jieun0515@dongduk.ac.kr
OI Chang, Ji-Eun/0000-0002-0037-1560
FU National Research Foundation of Korea (NRF) - Korea government (MSIT)
   [2022R1F1A1065569]
FX This work was supported by the National Research Foundation of Korea
   (NRF) grant funded by the Korea government (MSIT) (No.
   2022R1F1A1065569).
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NR 150
TC 28
Z9 28
U1 5
U2 32
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD SEP
PY 2023
VL 24
IS 17
AR 13618
DI 10.3390/ijms241713618
PG 27
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA R0GT6
UT WOS:001061216500001
PM 37686423
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Chen, J
   Chang, XA
   Li, XY
   Liu, JY
   Wang, N
   Wu, Y
   Zheng, LD
   Nie, X
AF Chen, Jie
   Chang, Xiaona
   Li, Xinyi
   Liu, Jiaying
   Wang, Na
   Wu, Ying
   Zheng, Liduan
   Nie, Xiu
TI The heterogeneous impact of targeted therapy on the prognosis of stage
   III/IV colorectal cancer patients with different subtypes of TP53
   mutations
SO CANCER MEDICINE
LA English
DT Article
DE colorectal neoplasms; genomic medicine; high-throughput nucleotide
   sequencing; mutation; survival analysis
ID MUTANT P53
AB BackgroundThe relationship between molecular characteristics and the prognosis of colorectal cancer (CRC) patients has not been fully understood. This study explored the impact of targeted therapy on the prognosis of CRC patients with different TP53 mutations, in the context of comprehensive treatment.MethodsThis study included patients with stage III/IV primary CRC from the electronic medical record system. TP53 mutations were detected via next-generation sequencing (NGS) using formalin-fixed paraffin-embedded (FFPE) tissues. Applying two methods, we classified TP53 mutations as gain of function (GOF)/non-GOF mutations or known/likely loss of function (LOF) mutations. Kaplan-Meier plot and parametric survival analysis were performed to evaluate the prognosis of CRC patients and identify potential predictors.ResultsThere were 286 patients included, of which 166 (58.04%) patients received targeted therapy and 120 (41.96%) did not. There were 286 patients in the TP53 GOF classification set and 247 in the TP53 LOF classification set. Parametric survival analysis, adjusted for sex, onset, KRAS mutation, sidedness, stage, and surgery, showed that receiving targeted therapy predicted better overall survival (OS) among patients who harbored TP53 GOF mutations (HR 0.40, 95% confidence interval (CI) [0.21, 0.76], p = 0.005) or known LOF mutations (HR 0.21, 95% CI [0.07, 0.60], p = 0.002). However, there was no significant impact of receiving targeted therapy on OS among patients harboring TP53 non-GOF mutations (HR 1.68, 95% CI [0.50, 5.63], p = 0.403) or likely LOF mutations (HR 0.90, 95% CI [0.34, 2.39], p = 0.837).ConclusionsReceiving targeted therapy had a heterogeneous impact on the prognosis of CRC patients harboring different TP53 mutations. These results provide promising value for future personalized treatment and precision medicine.
C1 [Chen, Jie; Chang, Xiaona; Li, Xinyi; Liu, Jiaying; Wang, Na; Wu, Ying; Zheng, Liduan; Nie, Xiu] Huazhong Univ Sci & Technol, Wuhan Union Hosp, Tongji Med Coll, Dept Pathol, Wuhan, Peoples R China.
   [Zheng, Liduan] Huazhong Univ Sci & Technol, Wuhan Union Hosp, Tongji Med Coll, Dept Pathol, 1277 Jiefang Rd, Wuhan 430022, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
   Science & Technology
RP Zheng, LD (corresponding author), Huazhong Univ Sci & Technol, Wuhan Union Hosp, Tongji Med Coll, Dept Pathol, 1277 Jiefang Rd, Wuhan 430022, Peoples R China.
EM ld_zheng@126.com
RI Chen, Jie/GNM-5503-2022; Li, Xinyi/AFU-7635-2022
OI Zheng, Liduan/0000-0001-5566-673X; Chen, Jie/0000-0002-4018-2502
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NR 44
TC 1
Z9 1
U1 2
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 DEC
PY 2023
VL 12
IS 24
BP 21920
EP 21932
DI 10.1002/cam4.6766
EA DEC 2023
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DD3K6
UT WOS:001116341200001
PM 38063316
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU González, NS
   Ros, J
   Baraibar, I
   Salvà, F
   Rodríguez-Castells, M
   Alcaraz, A
   García, A
   Tabernero, J
   Elez, E
AF Gonzalez, Nadia Saoudi
   Ros, Javier
   Baraibar, Iosune
   Salva, Francesc
   Rodriguez-Castells, Marta
   Alcaraz, Adriana
   Garcia, Ariadna
   Tabernero, Josep
   Elez, Elena
TI Cetuximab as a Key Partner in Personalized Targeted Therapy for
   Metastatic Colorectal Cancer
SO CANCERS
LA English
DT Review
DE cetuximab; colorectal cancer; KRASG12C; BRAFV600; personalized treatment
ID RAS WILD-TYPE; PHASE-1 DOSE-ESCALATION; PLUS CETUXIMAB; OPEN-LABEL;
   SINGLE-AGENT; SOLID TUMORS; ACQUIRED-RESISTANCE; 1ST-LINE TREATMENT;
   SUBGROUP ANALYSES; RANDOMIZED-TRIAL
AB Cetuximab, a chimeric IgG1 monoclonal antibody targeting the epidermal growth factor receptor (EGFR), has revolutionized personalized treatment of metastatic colorectal cancer (mCRC) patients. This review highlights the mechanism of action, characteristics, and optimal indications for cetuximab in mCRC. Cetuximab has emerged as a pivotal partner for novel therapies in specific molecular subgroups, including BRAF V600E, KRAS G12C, and HER2-altered mCRC. Combining cetuximab with immunotherapy and other targeted agents further expands the therapeutic landscape, offering renewed hope for mCRC patients who face the development of resistance to conventional therapies. Ongoing clinical trials have continued to uncover innovative cetuximab-based treatment strategies, promising a brighter future for mCRC patients. This review provides a comprehensive overview of cetuximab's role and its evolving importance in personalized targeted therapy of mCRC patients, offering valuable insights into the evolving landscape of colorectal cancer treatment.
C1 [Gonzalez, Nadia Saoudi; Ros, Javier; Baraibar, Iosune; Salva, Francesc; Rodriguez-Castells, Marta; Alcaraz, Adriana; Garcia, Ariadna; Tabernero, Josep; Elez, Elena] Vall dHebron Inst Oncol VHIO, Barcelona 08035, Spain.
   [Gonzalez, Nadia Saoudi; Ros, Javier; Baraibar, Iosune; Salva, Francesc; Rodriguez-Castells, Marta; Alcaraz, Adriana; Tabernero, Josep; Elez, Elena] Vall dHebron Hosp Campus, Barcelona 08035, Spain.
C3 Vall d'Hebron Institut d'Oncologia (VHIO)
RP Elez, E (corresponding author), Vall dHebron Inst Oncol VHIO, Barcelona 08035, Spain.; Elez, E (corresponding author), Vall dHebron Hosp Campus, Barcelona 08035, Spain.
EM nsaoudi@vhio.net; meelez@vhio.net
RI Baraibar, Iosune/GXF-7067-2022; Gonzalez, Nadia/GSN-4164-2022; Ros,
   Javier/HKF-1171-2023
OI Saoudi Gonzalez, Nadia/0000-0001-6044-1703; Tabernero,
   Josep/0000-0002-2495-8139; Ros, Javier/0000-0002-8137-5415; R Castells,
   Marta/0000-0003-1935-0951; Baraibar, Iosune/0000-0002-3500-9641
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NR 113
TC 5
Z9 5
U1 2
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2024
VL 16
IS 2
AR 412
DI 10.3390/cancers16020412
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GH9L1
UT WOS:001151894500001
PM 38254903
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Leiphrakpam, PD
   Are, C
AF Leiphrakpam, Premila D.
   Are, Chandrakanth
TI PI3K/Akt/mTOR Signaling Pathway as a Target for Colorectal Cancer
   Treatment
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colorectal cancer; PI3K; Akt; mTOR; cell survival; apoptosis;
   inhibitors; targeted therapy
ID ADVANCED SOLID TUMORS; I PI3K INHIBITOR; PHOSPHATIDYLINOSITOL 3-KINASE
   INHIBITOR; 1ST-IN-HUMAN PHASE-I; DOSE-ESCALATION; PI3K/MTOR INHIBITOR;
   PIK3CA MUTATIONS; DUAL INHIBITOR; BUPARLISIB BKM120; SAR245409 XL765
AB In the last decade, pathway-specific targeted therapy has revolutionized colorectal cancer (CRC) treatment strategies. This type of therapy targets a tumor-vulnerable spot formed primarily due to an alteration in an oncogene and/or a tumor suppressor gene. However, tumor heterogeneity in CRC frequently results in treatment resistance, underscoring the need to understand the molecular mechanisms involved in CRC for the development of novel targeted therapies. The phosphatidylinositol 3-kinase/protein kinase B/mammalian target of the rapamycin (PI3K/Akt/mTOR) signaling pathway axis is a major pathway altered in CRC. The aberrant activation of this pathway is associated with CRC initiation, progression, and metastasis and is critical for the development of drug resistance in CRC. Several drugs target PI3K/Akt/mTOR in clinical trials, alone or in combination, for the treatment of CRC. This review aims to provide an overview of the role of the PI3K/Akt/mTOR signaling pathway axis in driving CRC, existing PI3K/Akt/mTOR-targeted agents against CRC, their limitations, and future trends.
C1 [Leiphrakpam, Premila D.; Are, Chandrakanth] Univ Nebraska, Coll Med, Med Ctr, Grad Med Educ, Omaha, NE 68198 USA.
   [Leiphrakpam, Premila D.; Are, Chandrakanth] Univ Nebraska, Coll Med, Dept Surg, Div Surg Oncol,Med Ctr, Omaha, NE 68198 USA.
C3 University of Nebraska System; University of Nebraska Medical Center;
   University of Nebraska System; University of Nebraska Medical Center
RP Leiphrakpam, PD (corresponding author), Univ Nebraska, Coll Med, Med Ctr, Grad Med Educ, Omaha, NE 68198 USA.; Leiphrakpam, PD (corresponding author), Univ Nebraska, Coll Med, Dept Surg, Div Surg Oncol,Med Ctr, Omaha, NE 68198 USA.
EM pleiphrakpam@unmc.edu
RI Leiphrakpam, Premila/I-6685-2019
OI Leiphrakpam, Premila/0000-0002-2319-8844
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NR 142
TC 23
Z9 23
U1 30
U2 35
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 MAR
PY 2024
VL 25
IS 6
AR 3178
DI 10.3390/ijms25063178
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA MH4H1
UT WOS:001192715100001
PM 38542151
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Chen, JJ
   Dai, J
   Kang, ZM
   Yang, T
   Zhao, Q
   Zheng, JX
   Zhang, XX
   Zhang, JS
   Xu, J
   Sun, GQ
   Yang, LJ
   Yang, T
AF Chen, Junjun
   Dai, Jie
   Kang, Zhiming
   Yang, Ting
   Zhao, Qi
   Zheng, Jinxiu
   Zhang, Xinxin
   Zhang, Jisheng
   Xu, Jun
   Sun, Gongqin
   Yang, Lijun
   Yang, Tao
TI A combinatorial strategy for overcoming primary and acquired resistance
   of MEK inhibition in colorectal cancer
SO EXPERIMENTAL CELL RESEARCH
LA English
DT Article
DE Colorectal cancer; Trametinib; Targeted therapy resistance; Combination
   therapy
ID KRAS-MUTANT LUNG; COMBINED BRAF; ACTIVATION; MUTATIONS; MELANOMA;
   PATHWAY; HETEROGENEITY; TRAMETINIB; CETUXIMAB; THERAPY
AB Compared with traditional chemotherapeutic drugs, targeted therapeutic medicine has the advantages of high efficacy and less toxic side effects. However, in clinical practice for treatment of colorectal cancer, the primary and acquired resistance of these medicines limits their effectiveness in targeted therapy, therefore impedes the development of precision medicine and personalized therapy. Currently, there are limited number of drugs for targeted therapy of colorectal cancer, mainly monoclonal antibodies against EGFR or VEGFR inhibitors. Trametinib, a MEK inhibitor, has been applied in melanoma patient successfully, but not been used in clinical treatment of colorectal cancer because of its drug resistance. To identify the resistance mechanism of colorectal cancer cells to trametinib and find useful chemical combination to overcome the resistance, we screened primary and acquired cell line first and then tested multiple synergistic drug combinations by using the Chou-Talalay method. We obtained the primary resistant cell lines SW480, CW-2 and the acquired drug-resistant cell line RKO-R as well as a synergistic combination of trametinib and GSK2126458. This combination inhibits the colony formation of colorectal cancer cells and the growth of xenograft tumors in nude mice. Mechanistic analysis showed that trametinib can activate the alternative PI3K-AKT signaling pathway while inhibiting the MAPK pathway, which may be one of the molecular mechanisms of primary and acquired trametinib tolerance in colorectal cancer cells. Importantly, this bypass activation can be blocked by GSK2126458. These results suggest that a combination of trametinib and GSK2126458 is an effective approach for treating colorectal cancer resistance to trametinib.
C1 [Chen, Junjun; Dai, Jie; Kang, Zhiming; Yang, Ting; Yang, Tao] Shanxi Med Univ, Dept Biochem & Mol Biol, Taiyuan 030001, Shanxi, Peoples R China.
   [Zhao, Qi; Zheng, Jinxiu; Yang, Lijun] Shanxi Med Univ, Dept Pharmacol, Taiyuan 030001, Shanxi, Peoples R China.
   [Zhang, Xinxin] Shanxi Med Univ, Dept Med Expt Tech, Taiyuan 030001, Shanxi, Peoples R China.
   [Zhang, Jisheng] Qingdao Univ, Affiliated Hosp, Dept Otolaryngol Head & Neck Surg, Key Lab, Qingdao 266003, Shandong, Peoples R China.
   [Xu, Jun] Shanxi Med Univ, Dept Gen Surg, Affiliated Hosp 1, Taiyuan 030001, Shanxi, Peoples R China.
   [Sun, Gongqin] Univ Rhode Isl, Dept Cell & Mol Biol, Kingston, RI 02881 USA.
C3 Shanxi Medical University; Shanxi Medical University; Shanxi Medical
   University; Qingdao University; Shanxi Medical University; University of
   Rhode Island
RP Yang, LJ; Yang, T (corresponding author), 56 Xinjian South Rd, Taiyuan 030001, Shanxi, Peoples R China.; Sun, GQ (corresponding author), 120 Flag Rd, Kingston, RI 02881 USA.
EM gongqinsun@uri.edu; yang_lijun@sxmu.edu.cn; yangtao056cn@sxmu.edu.cn
RI Zhang, Jisheng/AAT-6495-2020; yang, lijun/E-6648-2012; Zhang,
   Xinxin/ABC-6731-2021
FU National Natural Science Foundation of China [81972325]; Shanxi
   Provincial Key Research and Development Project [201803D31072,
   201703D111029, 201703D321026-2]
FX This work was supported by grants from the National Natural Science
   Foundation of China (81972325), by the Shanxi Provincial Key Research
   and Development Project (201803D31072, 201703D111029 and
   201703D321026-2).
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NR 46
TC 6
Z9 8
U1 0
U2 13
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 1
PY 2020
VL 393
IS 1
AR 112060
DI 10.1016/j.yexcr.2020.112060
PG 10
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA LW8XS
UT WOS:000539427300008
PM 32407729
DA 2025-01-04
ER

PT J
AU Tang, YL
   Li, DD
   Duan, JY
   Sheng, LM
   Wang, X
AF Tang, Yuan-Ling
   Li, Dan-Dan
   Duan, Jia-Yu
   Sheng, Lei-Ming
   Wang, Xin
TI Resistance to targeted therapy in metastatic colorectal cancer: Current
   status and new developments
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Colorectal cancer; Targeted treatment; Resistance; New development
ID GROWTH-FACTOR RECEPTOR; FOLFIRI PLUS BEVACIZUMAB; WILD-TYPE KRAS;
   MISMATCH REPAIR-DEFICIENT; EGFR ANTIBODY MIXTURE; RANDOMIZED PHASE-II;
   1ST-LINE TREATMENT; OPEN-LABEL; COLON-CANCER; MICROSATELLITE INSTABILITY
AB Colorectal cancer (CRC) is one of the most lethal and common malignancies in the world. Chemotherapy has been the conventional treatment for metastatic CRC (mCRC) patients. However, the effects of chemotherapy have been unsatisfactory. With the advent of targeted therapy, the survival of patients with CRC have been prolonged. Over the past 20 years, targeted therapy for CRC has achieved substantial progress. However, targeted therapy has the same challenge of drug resistance as chemotherapy. Consequently, exploring the resistance mechanism and finding strategies to address the resistance to targeted therapy, along with searching for novel effective regimens, is a constant challenge in the mCRC treatment, and it is also a hot research topic. In this review, we focus on the current status on resistance to existing targeted therapies in mCRC and discuss future developments.
C1 [Tang, Yuan-Ling; Li, Dan-Dan; Duan, Jia-Yu; Sheng, Lei-Ming; Wang, Xin] Sichuan Univ, Canc Ctr, Dept Radiat Oncol, West China Hosp, 37 Guoxue Lane, Chengdu 610041, Sichuan, Peoples R China.
   [Tang, Yuan-Ling; Li, Dan-Dan; Duan, Jia-Yu; Sheng, Lei-Ming; Wang, Xin] Sichuan Univ, Canc Ctr, Dept Abdominal Canc, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University
RP Wang, X (corresponding author), Sichuan Univ, Canc Ctr, Dept Radiat Oncol, West China Hosp, 37 Guoxue Lane, Chengdu 610041, Sichuan, Peoples R China.
EM 2079248480@qq.com
RI Li, Dandan/HPH-9109-2023
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   Yaeger R, 2015, CLIN CANCER RES, V21, P1313, DOI 10.1158/1078-0432.CCR-14-2779
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   Yuan J, 2022, FRONT IMMUNOL, V13, DOI 10.3389/fimmu.2022.1022190
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NR 230
TC 15
Z9 16
U1 5
U2 14
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD FEB 14
PY 2023
VL 29
IS 6
BP 926
EP 948
DI 10.3748/wjg.v29.i6.926
PG 23
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 9L2HZ
UT WOS:000941377000003
PM 36844139
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Smith, DA
   Pfau, D
   Tirumani, SH
   Alessandrino, F
   Sadri, N
   Ramaiya, NH
AF Smith, Daniel A.
   Pfau, David
   Tirumani, Sree H.
   Alessandrino, Francesco
   Sadri, Navid
   Ramaiya, Nikhil H.
TI Decoding the Genomic Report for Radiologists
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Review
DE genomic report; molecular diagnostics; next-generation sequencing;
   oncologic imaging; targeted therapy
ID METASTATIC COLORECTAL-CANCER; MGMT PROMOTER METHYLATION; MISMATCH
   REPAIR; LUNG-CANCER; IMAGING PHENOTYPES; IMPROVED SURVIVAL; AMERICAN
   SOCIETY; TARGETED THERAPY; BRAF MUTATIONS; RAS MUTATIONS
AB OBJECTIVE. The purpose of this review is to provide a guide for radiologists that explains the language and format of modern genomic reports and summarizes the relevance of this information for modern oncologic imaging.
   CONCLUSION. Genomic testing plays a critical role in guiding oncologic therapies in the age of targeted treatments. Understanding and interpreting genomic reports is a valuable skill for radiologists involved with oncologic imaging interpretation.
C1 [Smith, Daniel A.; Pfau, David; Tirumani, Sree H.; Ramaiya, Nikhil H.] Case Western Reserve Univ, Dept Radiol, Univ Hosp Cleveland, Med Ctr, 11100 Euclid Ave, Cleveland, OH 44106 USA.
   [Alessandrino, Francesco] Harvard Med Sch, Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
   [Sadri, Navid] Case Western Reserve Univ, Univ Hosp Cleveland, Dept Pathol, Med Ctr, Cleveland, OH 44106 USA.
C3 University System of Ohio; Case Western Reserve University; Case Western
   Reserve University Hospital; University Hospitals of Cleveland; Harvard
   University; Brigham & Women's Hospital; Harvard Medical School;
   University System of Ohio; Case Western Reserve University; Case Western
   Reserve University Hospital; University Hospitals of Cleveland
RP Smith, DA (corresponding author), Case Western Reserve Univ, Dept Radiol, Univ Hosp Cleveland, Med Ctr, 11100 Euclid Ave, Cleveland, OH 44106 USA.
EM Daniel.Smith3@UHhospitals.org
RI Alessandrino, Francesco/H-8725-2019
OI sadri, navid/0000-0001-5051-717X
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NR 76
TC 1
Z9 1
U1 0
U2 2
PU AMER ROENTGEN RAY SOC
PI LEESBURG
PA 44211 SLATESTONE CT, LEESBURG, VA USA
SN 0361-803X
EI 1546-3141
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD MAY
PY 2020
VL 214
IS 5
BP 949
EP 961
DI 10.2214/AJR.19.21677
PG 13
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA LG7IN
UT WOS:000528270000011
PM 32182095
DA 2025-01-04
ER

PT J
AU Yeh, YS
   Tsai, HL
   Chen, YC
   Su, WC
   Chen, PJ
   Chang, TK
   Li, CC
   Huang, CW
   Wang, JY
AF Yeh, Yung-Sung
   Tsai, Hsiang-Lin
   Chen, Yen-Cheng
   Su, Wei-Chih
   Chen, Po-Jung
   Chang, Tsung-Kun
   LI, Ching-Chun
   Huang, Ching-Wen
   Wang, Jaw-Yuan
TI Effects of the number of neoadjuvant therapy cycles on clinicaloutcomes,
   safety, and survival in patients with metastatic colorectalcancer
   undergoing metastasectomy br
SO ONCOLOGY RESEARCH
LA English
DT Article
DE Metastatic colorectal cancer; Neoadjuvant chemotherapy; targeted
   therapy; Treatment cycles; Metastasectomy
ID CANCER; CHEMOTHERAPY; BEVACIZUMAB; RESECTION
AB The controversial outcomes in patients with metastatic colorectal cancer (mCRC) highlight the need fordeveloping effective systemic neoadjuvant treatment strategies to improve clinical results. The optimal treatment cyclesin patients with mCRC for metastasectomy remain undefined. This retrospective study compared the efficacy, safety,and survival of cycles of neoadjuvant chemotherapy/targeted therapy for such patients. Sixty-four patients with mCRCwho received neoadjuvant chemotherapy/targeted therapy following metastasectomy were enrolled between January2018 and April 2022. Twenty-eight patients received 6 cycles of chemotherapy/targeted therapy, whereas 36 patientsreceived >= 7 cycles (median, 13; range, 7-20). Clinical outcomes, including response, progression-free survival (PFS),overall survival (OS), and adverse events, were compared between these two groups. Of the 64 patients, 47 (73.4%) wereincluded in the response group, and 17 (26.6%) were included in the nonresponse group. The analysis revealedchemotherapy/targeted therapy cycle and pretreatment serum carcinoembryonic antigen (CEA) level as independentpredictors of the response as well as overall survival and chemotherapy/targeted therapy cycle as an independentpredictor of progression (allp< 0.05). Furthermore, our results revealed shorter operation time, lower estimatedoperative blood loss, higher response rate, lower progression rate, and higher survival rate in >= 7 cycles of chemotherapy/targeted therapy group (allp< 0.05), but no statistical differences in adverse events were observed between the twogroups (allp> 0.05). The median OS and PFS were 48 months (95% CI, 40.855-55.145) and 28 months (95% CI,18.952-37.48) in the >= 7-cycle group and 24 months (95% CI, 22.038-25.962) and 13 months (95% CI, 11.674-14.326)in the 6-cycle group, respectively (bothp< 0.001). The oncological outcomes in the >= 7-cycle group were significantlybetter than those in the 6-cycle group, without significant increases in adverse events. However, prospective randomizedtrials are mandatory to confirm the potential advantages of cycle numbers of neoadjuvant chemotherapy/targeted therapy
C1 [Yeh, Yung-Sung] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Trauma & Surg Crit Care, 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; Chen, Yen-Cheng; Su, Wei-Chih; Chen, Po-Jung; Chang, Tsung-Kun; LI, Ching-Chun; Huang, Ching-Wen; Wang, Jaw-Yuan] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, Kaohsiung, Taiwan.
   [Tsai, Hsiang-Lin; Huang, Ching-Wen; Wang, Jaw-Yuan] Kaohsiung Med Univ, Coll Med, Fac Med, Dept Surg, Kaohsiung, Taiwan.
   [Chen, Yen-Cheng; Su, Wei-Chih; Chen, Po-Jung; Chang, Tsung-Kun; Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.
   [Chang, Tsung-Kun] Kaohsiung Med Univ, Coll Med, Fac Postbaccalaureate Med, Dept Surg, 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.
C3 Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University; Taipei Medical University; Kaohsiung
   Medical University; Kaohsiung Medical University Hospital; Kaohsiung
   Medical University; Kaohsiung Medical University; Kaohsiung 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, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Coll Med, Fac Med, Dept Surg, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Ctr Canc Res, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Pingtung Hosp, Minist Hlth & Welf, Pingtung, Taiwan.
EM cy14112@ms14.hinet.net
RI Jaw-Yuan, Wang/AFS-8845-2022
OI Wang, Jaw-Yuan/0000-0002-7705-2621
FU 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]; Ministry of Health and Welfare
   [MOHW111-TDU-B-221-114014]; Healthand Welfare Surcharge of on Tobacco
   Products [KMUH110-0R37, KMUH110-0R38, KMUH110-0M34, KMUH110-0M35,
   KMUH110-0M36, KMUH-DK (B) 110004-3]; KMU Centerfor Cancer Research
   [KMU-TC111A04-1]; KMU Officefor Industry-Academic Collaboration,
   Kaohsiung Medical University [S109036]; Grant of Taiwan Precision
   Medicine Initiative; TaiwanBiobank, Academia Sinica, Taiwan, ROC
FX This work was supported by grantsthrough funding 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) and funded by the Healthand Welfare Surcharge
   of on Tobacco Products, and theKaohsiung Medical University Hospital
   (KMUH110-0R37,KMUH110-0R38, KMUH110-0M34, KMUH110-0M35,KMUH110-0M36,
   KMUH-DK (B) 110004-3) and KMU Centerfor Cancer Research (KMU-TC111A04-1)
   and KMU Officefor Industry-Academic Collaboration (S109036),
   KaohsiungMedical University. In addition, this study was supported bythe
   Grant of Taiwan Precision Medicine Initiative and TaiwanBiobank,
   Academia Sinica, Taiwan, ROC. This manuscript wasedited by Wallace
   Academic Editing.
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NR 26
TC 6
Z9 6
U1 0
U2 1
PU TECH SCIENCE PRESS
PI HENDERSON
PA 871 CORONADO CENTER DR, SUTE 200, HENDERSON, NV 89052 USA
SN 0965-0407
EI 1555-3906
J9 ONCOL RES
JI Oncol. Res.
PY 2022
VL 30
IS 2
BP 65
EP 76
DI 10.32604/or.2022.026659
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 8D3QR
UT WOS:000918212200002
PM 37305327
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Wang, ML
   Su, JY
   Lu, JH
   Yang, Z
   Wang, J
   Zhong, YZ
   Zeng, TN
   Shen, KZ
   Lin, SY
AF Wang, Menglei
   Su, Jingyang
   Lu, Jinhua
   Yang, Ze
   Wang, Jue
   Zhong, Yazhen
   Zeng, Tianni
   Shen, Kezhan
   Lin, Shengyou
TI Efficacy and safety of HER2-targeted therapy in patients with colorectal
   cancer: What should we expect from a meta-analysis?
SO CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY
LA English
DT Review
DE HER2; HER2-targeted therapy; Colorectal cancer; Efficacy; Safety
ID MULTICENTER
AB Background and objective: Human epidermal growth factor receptor 2 (HER2) is an effective therapeutic target for breast and stomach cancers. However, the application of HER2-targeted therapy in colorectal cancer (CRC) remains controversial. We sought to assess the efficacy and safety of HER2-targeted therapy in CRC by performing a meta-analysis of relevant studies. Methods: We searched PubMed, Embase, Cochrane Library, Web of Science, and the Clinical-Trials.gov database to retrieve relevant studies. STATA 16 was used for the statistical analysis. The objective response rate (ORR), disease control rate (DCR), progression-free survival (PFS), and incidence of treatment-related adverse events (TRAEs) were used as the outcome indicators analyzed by random-or fixed-effects models. Results: A total of 267 patients from nine studies were included in this meta-analysis. The overall ORR and DCR were 27.5% (95% CI 16.8% to 39.6%) and 68.9% (95% CI 55.4% to 81.0%), respectively. No significant heterogeneity was found in PFS among these studies and the over-all median PFS was 4.35 months (95% CI 3.70 to 4.99). The overall incidence of all-grade and grade 3 or higher adverse events were 93.5% (95% CI 88.4% to 97.4%) and 16.8% (95% CI 4.8% to 33.3%). Conclusions: HER2-targeted therapy was confirmed as a promising treatment for colorectal can-cer, warranting further high-quality clinical randomized controlled trials to verify. (c) 2023 Elsevier Masson SAS. All rights reserved.
C1 [Wang, Menglei; Su, Jingyang; Lu, Jinhua; Wang, Jue; Zhong, Yazhen; Zeng, Tianni; Shen, Kezhan; Lin, Shengyou] Zhejiang Chinese Med Univ, Hangzhou TCM Hosp, Hangzhou, Peoples R China.
   [Yang, Ze] Zhejiang Chinese Med Univ, Clin Coll 1, Hangzhou, Peoples R China.
   [Lin, Shengyou] Zhejiang Chinese Med Univ, Zhejiang Prov Hosp Chinese Med, Affiliated Hosp 1, Hangzhou, Peoples R China.
C3 Zhejiang Chinese Medical University; Zhejiang Chinese Medical
   University; Zhejiang Chinese Medical University
RP Lin, SY (corresponding author), Zhejiang Chinese Med Univ, Hangzhou TCM Hosp, Hangzhou, Peoples R China.; Lin, SY (corresponding author), Zhejiang Chinese Med Univ, Zhejiang Prov Hosp Chinese Med, Affiliated Hosp 1, Hangzhou, Peoples R China.
EM linsy0628@163.com
RI Lu, Jinhua/AAN-7228-2021
FU National Natural Science Foundation of China [81,904,197]; Science and
   technology planning projects of Zhejiang Province [2018C03025]; Zhejiang
   Lin Shengyou famous traditional Chinese medicine expert inheritance
   studio project [GZS202002]
FX This work was supported by the National Natural Science Foundation of
   China [grant number 81,904,197]; the science and technology planning
   projects of Zhejiang Province [grant number 2018C03025]; and Zhejiang
   Lin Shengyou famous traditional Chinese medicine expert inheritance
   studio project [grant number GZS202002].
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TC 2
Z9 2
U1 0
U2 3
PU ELSEVIER MASSON, CORP OFF
PI PARIS
PA 65 CAMILLE DESMOULINS CS50083 ISSY-LES-MOULINEAUX, 92442 PARIS, FRANCE
SN 2210-7401
EI 2210-741X
J9 CLIN RES HEPATOL GAS
JI Clin. Res. Hepatol. Gastroenterol.
PD FEB
PY 2023
VL 47
IS 2
AR 102078
DI 10.1016/j.clinre.2023.102078
EA JAN 2023
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA A4AK8
UT WOS:000954570200001
PM 36627051
DA 2025-01-04
ER

PT J
AU Bitterman, DS
   Du, KL
AF Bitterman, Danielle S.
   Du, Kevin L.
TI Safety and Efficacy of Combination Targeted Therapy and Radiotherapy
SO AMERICAN JOURNAL OF HEMATOLOGY-ONCOLOGY
LA English
DT Article
DE targeted therapies; radiation therapy; vascular endothelial growth
   factor inhibitors; PI3K; Akt; mTOR
ID PHASE-I TRIAL; SQUAMOUS-CELL CARCINOMA; EXTERNAL-BEAM RADIATION;
   RECTAL-CANCER; GLIOBLASTOMA-MULTIFORME; CONCURRENT CAPECITABINE;
   CONFORMAL RADIOTHERAPY; INHIBITOR NELFINAVIR; ESOPHAGEAL CANCER; PLUS
   TEMOZOLOMIDE
AB Targeted cancer therapies that act on specific drivers of oncogenesis are rapidly entering clinical use. While many of these agents are ineffective at improving cure rates as monotherapy, there is ample preclinical evidence that they are both chemosensitizing and radiosensitizing, and can improve cure rates when utilized in combination treatment regimens. There is therefore a need for high-quality safety and efficacy data on targeted therapy in combination with radiation therapy (RT). This article reviews the currently published clinical trials examining the combination of RT with commonly used targeted agents, such as vascular endothelial growth factor inhibitors, endothelial growth factor receptor inhibitors, and inhibitors of the PI3K/Akt/mTOR pathway. Continued efforts to develop high-quality clinical trial data combining targeted agents with RT are necessary for patient safety and to improve clinical outcomes.
C1 [Bitterman, Danielle S.; Du, Kevin L.] NYU, Langone Med Ctr, Dept Radiat Oncol, New York, NY USA.
C3 NYU Langone Medical Center; New York University
RP Du, KL (corresponding author), NYU, Langone Med Ctr, 160 East 34th St, New York, NY 10016 USA.
EM Kevin.Du@nyumc.org
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NR 66
TC 5
Z9 5
U1 0
U2 0
PU ROSSIISKII UNIV
PI NEW YORK
PA 114 W 26TH ST, 4TH FL, NEW YORK, NY 10001 USA
SN 1939-6163
EI 2334-0274
J9 AM J HEMATOL-ONCOL
JI Am. J. Hematol.-Oncol.
PD JAN
PY 2016
VL 12
IS 1
BP 23
EP 31
PG 9
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA FC2HF
UT WOS:000406657600005
DA 2025-01-04
ER

PT J
AU Zhao, YN
   Yang, J
   Luo, M
   Yang, YF
   Guo, XL
   Zhang, T
   Hao, JQ
   Yao, YQ
   Ma, XL
AF Zhao, Yunuo
   Yang, Jing
   Luo, Meng
   Yang, Yanfei
   Guo, Xinli
   Zhang, Tao
   Hao, Jianqi
   Yao, Yunqian
   Ma, Xuelei
TI Contrast-Enhanced CT-based Textural Parameters as Potential Prognostic
   Factors of Survival for Colorectal Cancer Patients Receiving Targeted
   Therapy
SO MOLECULAR IMAGING AND BIOLOGY
LA English
DT Article
DE Colorectal neoplasms; Multidetector computed tomography; Prognosis;
   Molecular targeted therapy
ID TUMOR HETEROGENEITY; FEATURES
AB Purpose This study was designed to estimate the clinical significance of the contrast-enhanced computed tomography (CT) textural features for prediction of survival in colorectal cancer (CRC) patients receiving targeted therapy (bevacizumab and cetuximab). Procedures The LifeX software was used to extract the textural parameters of the tumor lesions in the contrast-enhanced CT. We used the least absolute shrinkage and selection operator (LASSO) Cox regression and random forest method to screen the non-redundant radiomic features and constructed the CT imaging score. Univariate and multivariate analyses through the Cox proportional hazards model were performed to assess the prognostic clinical factor. Based on the result of multivariate analysis and CT imaging score, combined nomogram model was constructed to predict the overall survival (OS) of patients. Decision curves analysis was employed to evaluate the performance of the combined model and clinical model. Results After comparative analysis of the area under curve of the receiver operating characteristic (ROC) curve, we chose the result of random forest model as CT imaging score. Considering the clinical practice and the result of analysis, age, surgery, and lactate dehydrogenase (LDH) level have been introduced into clinical model. Based on the result of analysis and the CT imaging score, we constructed the nomogram combined model. C-index and calibration curve verified the goodness of fit and discrimination of the combined model. Decision curve analysis (DCA) demonstrated that the combined model showed the better net benefit for a 3-year OS than clinical model. Conclusions In conclusion, the study provides preliminary evidences that several radiomic parameters of tumor lesions derived from CT images were prognostic factors and predictive markers for CRC patients who are candidates for targeted therapy (bevacizumab and cetuximab).
C1 [Zhao, Yunuo; Luo, Meng; Yang, Yanfei; Ma, Xuelei] Sichuan Univ, West China Hosp, Dept Biotherapy, Canc Ctr,State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
   [Zhao, Yunuo; Luo, Meng; Yang, Yanfei; Guo, Xinli; Zhang, Tao; Hao, Jianqi; Yao, Yunqian] Sichuan Univ, West China Hosp, West China Sch Med, Chengdu 610041, Peoples R China.
   [Yang, Jing] Sun Yat Sen Univ Canc Ctr, Collaborat Innovat Ctr Canc Med, Melanoma & Sarcoma Med Oncol Unit, State Key Lab Oncol South China, 651 Dongfeng Rd East, Guangzhou 510060, Peoples R China.
   [Yang, Jing] Sun Yat Sen Univ Canc Ctr, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou 510060, Peoples R China.
C3 Sichuan University; Sichuan University; Sun Yat Sen University; State
   Key Lab Oncology South China; Sun Yat Sen University; State Key Lab
   Oncology South China
RP Ma, XL (corresponding author), Sichuan Univ, West China Hosp, Dept Biotherapy, Canc Ctr,State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
EM drmaxuelei@gmail.com
RI Zhang, Tao/KWU-2177-2024; guo, xin/KRP-4196-2024
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NR 28
TC 9
Z9 9
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1536-1632
EI 1860-2002
J9 MOL IMAGING BIOL
JI Mol. Imaging. Biol.
PD JUN
PY 2021
VL 23
IS 3
BP 427
EP 435
DI 10.1007/s11307-020-01552-2
EA OCT 2020
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA RY0WI
UT WOS:000584564000001
PM 33108800
DA 2025-01-04
ER

PT J
AU Rebersek, M
AF Rebersek, Martina
TI Consensus molecular subtypes (CMS) in metastatic colorectal cancer -
   personalized medicine decision
SO RADIOLOGY AND ONCOLOGY
LA English
DT Review
DE metastatic colorectal cancer; heterogeneity; biomarkers; consensus
   molecular subtypes; CMS1; CMS2; CMS3; CMS4
ID BIOMARKERS; EVOLUTION; THERAPY
AB Background. Colorectal cancer (CRC) is one of the most common types of cancer in the world. Metastatic disease is still incurable in most of these patients, but the survival rate has improved by treatment with novel systemic chemotherapy and targeted therapy in combination with surgery. New knowledge of its complex heterogeneity in terms of genetics, epigenetics, transcriptomics and microenvironment, including prognostic and clinical characteristics, led to its classification into various molecular subtypes of metastatic CRC, called consensus molecular subtypes (CMS). The CMS classification thus enables the medical oncologists to adjust the treatment from case to case. They can determine which type of systemic chemotherapy or targeted therapy is best suited to a specific patient, what dosages are needed and in what order.
   Conclusions. CMS in metastatic CRC are the new tool to include the knowledge of molecular factors, tumour stroma and signalling pathways for personalized, patient-orientated systemic treatment in precision medicine.
C1 [Rebersek, Martina] Inst Oncol Ljubljana, Dept Med Oncol, Zaloska 2, SI-1000 Ljubljana, Slovenia.
   [Rebersek, Martina] Univ Ljubljana, Fac Med, Ljubljana, Slovenia.
C3 Institute of Oncology - Slovenia; University of Ljubljana
RP Rebersek, M (corresponding author), Inst Oncol Ljubljana, Dept Med Oncol, Zaloska 2, SI-1000 Ljubljana, Slovenia.
EM mrebersek@onko-i.si
FU Slovenian Research Agency (ARRS) [P3-0321]
FX The research was financially supported by The Slovenian Research Agency
   (ARRS), grant number P3-0321.
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PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1318-2099
EI 1581-3207
J9 RADIOL ONCOL
JI Radiol. Oncol.
PD SEP
PY 2020
VL 54
IS 3
BP 272
EP 277
DI 10.2478/raon-2020-0031
PG 6
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA MV6CZ
UT WOS:000556444800003
PM 32463385
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lu, MH
   Fan, MF
   Yu, XD
AF Lu, M. -H.
   Fan, M. -F.
   Yu, X. -D.
TI NSD2 promotes osteosarcoma cell proliferation and metastasis by
   inhibiting E-cadherin expression
SO EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES
LA English
DT Article
DE NSD2; Osteosarcoma; Proliferation; Metastasis; E-cadherin
ID EPITHELIAL-MESENCHYMAL TRANSITION; SIGNALING PATHWAY; CANCER;
   RESISTANCE; RECEPTOR
AB OBJECTIVE: Osteosarcoma is one of the most common malignant bone tumors. The mechanisms of osteosarcoma development and invasion have been studied for periods of time, yet targeted therapy for improving survival has not been well established. Histone lysine methyltransferase NSD2 was frequently overexpressed in multiple types of cancer such as multiple myeloma, stomach and colon cancer, and the overexpression of it usually associated with aggressiveness tumor type. However, the expression status and function of NSD2 are still ambiguous in osteosarcoma.
   MATERIALS AND METHODS: Here, we evaluate the abnormal expression levels of NSD2 in osteosarcoma samples and cell lines. The higher expression of NSD2 in tumors resulted in a poorer outcome and a worse 5-year overall survival. To investigate the role of NSD2 in osteosarcoma cell proliferation and invasion in vitro, MTT assay, cell cycle distribution, wound healing, transwell assay was performed in relative cell lines, using a recombinant lentivirus expressing NSD2 short hairpin RNA or NSD2 construction. RESULTS: Our results imply that NSD2 promotes osteosarcoma cell proliferation and invasion, and the mechanism was possibly through the suppression of E-cadherin and induction of the epithelial mesenchymal transition, further to proceed invasion of osteosarcoma cells.
   CONCLUSIONS: NSD2 may work as a novel repression of E-cadherin; therefore, NSD2 has potential as a target of OS therapy. In the future, the monitoring of NSD2 in the serum/plasma from the RNA level may be used as a non-invasive method for selecting patients for target therapy.
C1 [Lu, M. -H.; Fan, M. -F.] Linyi Peoples Hosp, Dept Spinal Surg, Linyi, Shandong, Peoples R China.
   [Yu, X. -D.] Linyi Peoples Hosp, Dept Emergency Surg, Linyi, Shandong, Peoples R China.
RP Yu, XD (corresponding author), Linyi Peoples Hosp, Dept Emergency Surg, Linyi, Shandong, Peoples R China.
EM xiaodongyulinyi@163.com
CR Çolak H, 2013, EUR REV MED PHARMACO, V17, P2684
   Elles BD, 2005, ANN SURG ONCOL, V12, P1073
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NR 19
TC 21
Z9 24
U1 0
U2 4
PU VERDUCI PUBLISHER
PI ROME
PA VIA GREGORIO VII, ROME, 186-00165, ITALY
SN 1128-3602
J9 EUR REV MED PHARMACO
JI Eur. Rev. Med. Pharmacol. Sci.
PD MAR
PY 2017
VL 21
IS 5
BP 928
EP 936
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA ES0OS
UT WOS:000399226500005
PM 28338204
DA 2025-01-04
ER

PT J
AU Jansen, L
   Boakye, D
   Alwers, E
   Carr, PR
   Reissfelder, C
   Schneider, M
   Martens, UM
   Chang-Claude, J
   Hoffmeister, M
   Brenner, H
AF Jansen, Lina
   Boakye, Daniel
   Alwers, Elizabeth
   Carr, Prudence R.
   Reissfelder, Christoph
   Schneider, Martin
   Martens, Uwe M.
   Chang-Claude, Jenny
   Hoffmeister, Michael
   Brenner, Hermann
TI Uptake Rates of Novel Therapies and Survival Among Privately Insured
   Versus Publicly Insured Patients With Colorectal Cancer in Germany
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID INSURANCE STATUS; WAITING-TIMES; COST-EFFECTIVENESS; HEALTH-INSURANCE;
   BEVACIZUMAB; CARE; CHEMOTHERAPY
AB Background: In the era of personalized medicine, cancer care is subject to major changes and innovations. It is unclear, however, to what extent implementation of such innovations and their impact on patient outcomes differ by health insurance type. This study compared provision of treatment and survival outcomes among patients with colorectal cancer (CRC) who had statutory health insurance (SHI) versus private health insurance (PHI) in Germany. Methods: We an-alyzed patterns of CRC treatment (surgery, chemotherapy/radiotherapy, and targeted therapy) and survival in a large cohort of patients who were diagnosed with CRC in 2003 through 2014 and were observed for an average of 6 years. Associations of type of health insurance with treatment administration and with overall, CRC-specific, and recurrence-free survival were investigated using multivariable logistic and Cox proportional hazards models, respectively. Results: Of 3,977 patients with CRC, 427 (11%) had PHI. Although type of health insurance was not associated with treatment administration in patients with stage I-III disease, those with stage IV disease with PHI more often received targeted therapy (65% vs 40%; odds ratio, 2.43; 95% CI, 1.20-4.91), with differences decreasing over time because of catch-up of uptake rates in patients with SHI. Median overall survival was longer in patients with PHI than in those with SHI (137.0 vs 114.9 months; P=.010), but survival advantages were explained to a large extent by differences in sociodemographic factors. In patients with stage IV disease, survival advantages of PHI were nonsignificant and were restricted to the early years after diagnosis. Conclusions: We observed major differences in uptake of targeted therapy between patients with PHI and those with SHI but no differences in patient survival after adjusting for relevant sociodemographic, clinical, and tumor characteristics. Further studies are needed on factors associated with the uptake of therapeutic innovations and their impact on patient survival by health insurance type.
C1 [Jansen, Lina; Boakye, Daniel; Alwers, Elizabeth; Carr, Prudence R.; Hoffmeister, Michael; Brenner, Hermann] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Neuenheimer Feld 581, D-69120 Heidelberg, Germany.
   [Reissfelder, Christoph] Heidelberg Univ, Univ Hosp Mannheim, Med Fac Mannheim, Dept Surg, Mannheim, Germany.
   [Schneider, Martin] Heidelberg Univ Hosp, Clin Gen Visceral & Transplantat Surg, Heidelberg, Germany.
   [Martens, Uwe M.] Canc Ctr Heilbronn Franken, SLK Clin, Heilbronn, Germany.
   [Chang-Claude, Jenny] German Canc Res Ctr, Div Canc Epidemiol, Unit Genet Epidemiol, Heidelberg, Germany.
   [Chang-Claude, Jenny] Univ Med Ctr Hamburg Eppendorf UKE, Univ Canc Ctr Hamburg UCCH, Canc Epidemiol Grp, Hamburg, Germany.
   [Brenner, Hermann] German Canc Res Ctr, Div Prevent Oncol, Heidelberg, Germany.
   [Brenner, Hermann] German Canc Res Ctr, German Canc Consortium, Heidelberg, Germany.
C3 Helmholtz Association; German Cancer Research Center (DKFZ); Ruprecht
   Karls University Heidelberg; Ruprecht Karls University Heidelberg;
   Helmholtz Association; German Cancer Research Center (DKFZ); University
   of Hamburg; University Medical Center Hamburg-Eppendorf; Helmholtz
   Association; German Cancer Research Center (DKFZ); Helmholtz
   Association; German Cancer Research Center (DKFZ)
RP Jansen, L (corresponding author), German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Neuenheimer Feld 581, D-69120 Heidelberg, Germany.
EM l.jansen@dkfz.de
RI Schneider, Martin/H-3745-2011; Jansen, Lina/D-7255-2016; Rokohl,
   Alexander/K-6191-2019; Hoffmeister, Michael/T-7187-2019; Brenner,
   Hermann/ABE-6383-2020
OI Carr, Prudence/0000-0001-5671-7236; Reissfelder,
   Christoph/0000-0003-4591-1046; Boakye, Daniel/0000-0003-4684-0841;
   Brenner, Hermann/0000-0002-6129-1572; Hoffmeister,
   Michael/0000-0002-8307-3197
FU German Research Council [BR 1704/6-1, BR 1704/6-3, BR 1704/6-4, CH
   117/1-1]; German Federal Ministry of Education and Research [01KH0404,
   01ER0814, 01ER0815, 01ER1505A, 01ER1505B]; Ministry of Science, Research
   and Arts of Baden-Wuerttemberg
FX This work was supported by grants from the German Research Council (BR
   1704/6-1, BR 1704/6-3, BR 1704/6-4, CH 117/1-1), German Federal Ministry
   of Education and Research (01KH0404, 01ER0814, 01ER0815, 01ER1505A,
   01ER1505B), and the Ministry of Science, Research and Arts of
   Baden-Wuerttemberg.
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NR 38
TC 0
Z9 0
U1 1
U2 4
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 APR
PY 2021
VL 19
IS 4
BP 411
EP +
DI 10.6004/jnccn.2020.7636
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SJ1PX
UT WOS:000655302000006
PM 33578373
OA Bronze
DA 2025-01-04
ER

PT J
AU Johnson, D
   Chee, CE
   Wong, W
   Lam, RCT
   Tan, IBH
   Ma, BBY
AF Johnson, David
   Chee, Cheng Ean
   Wong, Wesley
   Lam, Rachel C. T.
   Tan, Iain Bee Huat
   Ma, Brigette B. Y.
TI Current advances in targeted therapy for metastatic colorectal cancer -
   Clinical translation and future directions
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE Metastatic colorectal cancer; Targeted therapy; Next generation
   sequencing
ID RAS WILD-TYPE; OPEN-LABEL; MISMATCH REPAIR; DOUBLE-BLIND; PHASE-III;
   1ST-LINE CHEMOTHERAPY; INTEGRATED ANALYSIS; PANITUMUMAB PLUS;
   RANDOMIZED-TRIAL; SUPPORTIVE CARE
AB The last two decades have witnessed major breakthroughs in the development of targeted therapy for patients with metastatic colorectal cancer (mCRC), an achievement which stems largely from advances in translational research. Precision medicine is now widely practiced in routine oncological care, where systemic therapy is individualized based on clinical factors such as primary tumor sidedness, location and number of metastases, as well as molecular factors such as the RAS and BRAF mutation status, mismatch repair / microsatellite status and presence of other actionable genomic alterations in the tumor. The optimal selection of patients with RAS and BRAF-wild type (WT), left-sided primary tumor for treatment with epidermal growth factor receptor (EGFR) and chemotherapy (chemo) has markedly improved survival in the first-line setting. The pivotal trials of cetuximab in combination with BRAF/ MEK inhibitor for BRAF V600E mutant mCRC, and panitumumab with KRAS G12C inhibitor in KRAS(G12C)-mutant mCRC have been practice-changing. Anti-HER2 small molecular inhibitor, antibodies and antibody-drug conjugates have significantly improved the treatment outcome of patients with HER2 amplified mCRC. Anti-angiogenesis agents are now used across all lines of treatment and novel combinations with immune-checkpoint inhibitors are under active investigation in MSS mCRC. The non-invasive monitoring of molecular resistance to targeted therapies using Next Generation Sequencing analysis of circulating tumor-derived DNA (ctDNA) and captured sequencing of tumors have improved patient selection for targeted therapies. This review will focus on how latest advances, challenges and future directions in the development of targeted therapies in mCRC.
C1 [Johnson, David; Wong, Wesley; Ma, Brigette B. Y.] Prince Wales Hosp, Dept Clin Oncol, Shatin, Ngan Shing St, Hong Kong, Peoples R China.
   [Chee, Cheng Ean] Natl Univ, Dept Hematol Oncol, Canc Inst, Singapore, Singapore.
   [Lam, Rachel C. T.] Chinese Univ Hong Kong, Fac Med, Hong Kong, Peoples R China.
   [Tan, Iain Bee Huat] Natl Canc Ctr Singapore, Singapore, Singapore.
   [Tan, Iain Bee Huat] Duke NUS, Grad Med Sch, Singapore, Singapore.
   [Tan, Iain Bee Huat] Genome Inst Singapore, Singapore, Singapore.
   [Ma, Brigette B. Y.] Chinese Univ Hong Kong, Hong Kong Canc Inst, Sir YK Pao Ctr Canc, State Key Lab Translat Oncol,Dept Clin Oncol, Hong Kong, Peoples R China.
C3 Chinese University of Hong Kong; Prince of Wales Hospital; National
   University of Singapore; Chinese University of Hong Kong; National
   Cancer Centre Singapore (NCCS); National University of Singapore; Agency
   for Science Technology & Research (A*STAR); A*STAR - Genome Institute of
   Singapore (GIS); Chinese University of Hong Kong
RP Ma, BBY (corresponding author), Prince Wales Hosp, Dept Clin Oncol, Shatin, Ngan Shing St, Hong Kong, Peoples R China.; Tan, IBH (corresponding author), Natl Canc Ctr Singapore, Singapore, Singapore.; Tan, IBH (corresponding author), Duke NUS, Grad Med Sch, Singapore, Singapore.; Tan, IBH (corresponding author), Genome Inst Singapore, Singapore, Singapore.
EM mdccce@nus.edu.sg; rachellam@link.cuhk.edu.hk;
   iain.tan.b.h@singhealth.com.sg; brigette@cuhk.edu.hk
RI B.Y., Brigette/H-4681-2017; Johnson, David/N-3193-2013
FU Kingboard Precision Oncology Program; Charlie Lee Precision
   Immuno-oncology program, The Chinese University of Hong Kong, Hong Kong
   SAR
FX This review is supported in part by the Kingboard Precision Oncology
   Program and the Charlie Lee Precision Immuno-oncology program, The
   Chinese University of Hong Kong, Hong Kong SAR. We thank Ms Alice Kong
   for clerical support.
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NR 122
TC 4
Z9 4
U1 5
U2 9
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0305-7372
EI 1532-1967
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD APR
PY 2024
VL 125
AR 102700
DI 10.1016/j.ctrv.2024.102700
EA FEB 2024
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OS7P6
UT WOS:001209337600001
PM 38422896
DA 2025-01-04
ER

PT J
AU Doostmohammadi, A
   Jooya, H
   Ghorbanian, K
   Gohari, S
   Dadashpour, M
AF Doostmohammadi, Ali
   Jooya, Hossein
   Ghorbanian, Kimia
   Gohari, Sargol
   Dadashpour, Mehdi
TI Potentials and future perspectives of multi-target drugs in cancer
   treatment: the next generation anti-cancer agents
SO CELL COMMUNICATION AND SIGNALING
LA English
DT Review
DE Cancer treatment; Drug resistance; Polypharmacology; Multi-target drugs
ID GROWTH-FACTOR RECEPTOR; NF-KAPPA-B; CELL LUNG-CANCER; PROTEIN-COUPLED
   RECEPTOR; RANDOMIZED PHASE-III; DOUBLE-BLIND; COLORECTAL-CANCER;
   PROSTATE-CANCER; THYROID-CANCER; BREAST-CANCER
AB Cancer is a major public health problem worldwide with more than an estimated 19.3 million new cases in 2020. The occurrence rises dramatically with age, and the overall risk accumulation is combined with the tendency for cellular repair mechanisms to be less effective in older individuals. Conventional cancer treatments, such as radiotherapy, surgery, and chemotherapy, have been used for decades to combat cancer. However, the emergence of novel fields of cancer research has led to the exploration of innovative treatment approaches focused on immunotherapy, epigenetic therapy, targeted therapy, multi-omics, and also multi-target therapy. The hypothesis was based on that drugs designed to act against individual targets cannot usually battle multigenic diseases like cancer. Multi-target therapies, either in combination or sequential order, have been recommended to combat acquired and intrinsic resistance to anti-cancer treatments. Several studies focused on multi-targeting treatments due to their advantages include; overcoming clonal heterogeneity, lower risk of multi-drug resistance (MDR), decreased drug toxicity, and thereby lower side effects. In this study, we'll discuss about multi-target drugs, their benefits in improving cancer treatments, and recent advances in the field of multi-targeted drugs. Also, we will study the research that performed clinical trials using multi-target therapeutic agents for cancer treatment.
C1 [Doostmohammadi, Ali] Semnan Univ Med Sci, Nervous Syst Stem Cells Res Ctr, Semnan, Iran.
   [Doostmohammadi, Ali; Ghorbanian, Kimia] Semnan Univ Med Sci, Student Res Comm, Semnan, Iran.
   [Jooya, Hossein] Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Biochem Grp, Mashhad, Iran.
   [Gohari, Sargol] Islamic Azad Univ, Dept Biol, Cent Tehran Branch, Tehran, Iran.
   [Dadashpour, Mehdi] Semnan Univ Med Sci, Fac Med, Dept Med Biotechnol, Semnan, Iran.
   [Dadashpour, Mehdi] Semnan Univ Med Sci, Canc Res Ctr, Semnan, Iran.
C3 Semnan University of Medical Sciences; Semnan University of Medical
   Sciences; Ferdowsi University Mashhad; Islamic Azad University; Semnan
   University of Medical Sciences; Semnan University of Medical Sciences
RP Dadashpour, M (corresponding author), Semnan Univ Med Sci, Fac Med, Dept Med Biotechnol, Semnan, Iran.; Dadashpour, M (corresponding author), Semnan Univ Med Sci, Canc Res Ctr, Semnan, Iran.
EM dadashpourmehdi1400@gmail.com
FU Semnan University of Medical Sciences, Semnan, Iran
FX The authors would like to express their gratitude to the Cancer Research
   Center, Semnan University of Medical Sciences, Semnan, Iran.
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NR 239
TC 11
Z9 11
U1 17
U2 26
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1478-811X
J9 CELL COMMUN SIGNAL
JI Cell Commun. Signal.
PD APR 15
PY 2024
VL 22
IS 1
AR 228
DI 10.1186/s12964-024-01607-9
PG 22
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA OB2I0
UT WOS:001204730700001
PM 38622735
OA gold
DA 2025-01-04
ER

PT J
AU Lupatov, AY
   Gisina, AM
   Kim, YS
   Bykasov, SA
   Volchenko, NN
   Sidorov, DV
   Yarygin, KN
   Kholodenko, RV
AF Lupatov, A. Yu.
   Gisina, A. M.
   Kim, Y. S.
   Bykasov, S. A.
   Volchenko, N. N.
   Sidorov, D. V.
   Yarygin, K. N.
   Kholodenko, R. V.
TI Expression of Ganglioside GD2 on Colorectal Adenocarcinoma Cells
SO BIOCHEMISTRY MOSCOW-SUPPLEMENT SERIES B-BIOMEDICAL CHEMISTRY
LA English
DT Article
DE colorectal cancer; ganglioside GD2; targeted therapy; CD133; EpCAM
ID CANCER STEM-CELLS
AB The expression of ganglioside GD2 on the cell lines of colorectal adenocarcinoma HT29 and CaCo-2, as well as on the tumor tissue samples of patients with colorectal cancer was analyzed by flow cytometry. The marker was found on EpCAM-positive tumor cell samples from 6 of 12 patients but not on the HT29 and CaCo-2 cell lines. GD2 expression was not associated with a cancer stem cell subpopulation as its expression level was similar on both CD133-positive and CD133-negative tumor cells. Thus, the presence of ganglioside GD2 was found for the first time on colorectal adenocarcinoma cells. This finding opens new opportunities for targeted therapy in the treatment of this disease.
C1 [Lupatov, A. Yu.; Gisina, A. M.; Kim, Y. S.; Yarygin, K. N.] Inst Biomed Chem, Pogodinskaya Ul 10, Moscow 119121, Russia.
   [Bykasov, S. A.; Volchenko, N. N.; Sidorov, D. V.] Natl Med Res Radiol Ctr, Hertsen Moscow Oncol Res Ctr, 2nd Botkinskiy Pr 3, Moscow 125284, Russia.
   [Kholodenko, R. V.] Russian Acad Sci, Shemyakin Ovchinnikov Inst Bioorgan Chem, Ul Mikhluho Maklaya 16-10, Moscow 117997, Russia.
C3 Russian Academy of Medical Sciences; Institute of Biomedical Chemistry;
   Russian Academy of Sciences; Pushchino Scientific Center for Biological
   Research (PSCBI) of the Russian Academy of Sciences; Institute of
   Bioorganic Chemistry of the Russian Academy of Sciences
RP Kholodenko, RV (corresponding author), Russian Acad Sci, Shemyakin Ovchinnikov Inst Bioorgan Chem, Ul Mikhluho Maklaya 16-10, Moscow 117997, Russia.
EM khol@mail.ru
RI Gisina, Alisa/AAO-3987-2020; Kim, Yan/S-1450-2016; Kholodenko,
   Roman/S-8412-2017; Yarygin, Konstantin/C-4047-2009; Lupatov,
   Alexey/ABF-7776-2020
OI Gisina, Alisa/0000-0001-7691-9265; Kim, Yan/0000-0002-7032-6781;
   Yarygin, Konstantin/0000-0002-2261-851X
FU Russian Science Foundation [18-15-00360]; Russian Science Foundation
   [18-15-00360] Funding Source: Russian Science Foundation
FX The study was supported by the Russian Science Foundation, project no.
   18-15-00360.
CR Battula VL, 2012, J CLIN INVEST, V122, P2066, DOI 10.1172/JCI59735
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NR 12
TC 0
Z9 0
U1 0
U2 0
PU MAIK NAUKA-INTERPERIODICA
PI MOSCOW
PA PROFSOYUZNAYA UL 90, MOSCOW, 117997, RUSSIA
SN 1990-7508
EI 1990-7516
J9 BIOCHEM MOSC-SUPPL S
JI Biochem. Mosc.-Suppl. Ser. B-Biomed. Chem.
PD JUL
PY 2020
VL 14
IS 3
BP 272
EP 276
DI 10.1134/S1990750820030099
PG 5
WC Biochemistry & Molecular Biology
WE Emerging Sources Citation Index (ESCI)
SC Biochemistry & Molecular Biology
GA ND3RS
UT WOS:000561821500009
DA 2025-01-04
ER

PT J
AU Legué, LM
   van Erning, FN
   Bernards, N
   Lemmens, VEPP
   de Hingh, IHJT
   Creemers, GJ
AF Legue, Laura M.
   van Erning, Felice N.
   Bernards, Nienke
   Lemmens, Valery E. P. P.
   de Hingh, Ignace H. J. T.
   Creemers, Geert-Jan
TI Addition of Bevacizumab to First-Line Palliative Chemotherapy in
   Patients with Metastatic Small Bowel Adenocarcinoma: A Population-Based
   Study
SO TARGETED ONCOLOGY
LA English
DT Article
ID PHASE-II; COLORECTAL-CANCER; PANITUMUMAB PLUS; SUPPORTIVE CARE;
   OPEN-LABEL; FLUOROURACIL; OXALIPLATIN; LEUCOVORIN; IRINOTECAN;
   CAPECITABINE
AB Background Data about the use and effectiveness of targeted therapy in metastatic small bowel adenocarcinoma (SBA) are scarce. Objective The aim of this population-based study was to obtain insights into the use and effectiveness of targeted therapy in patients with synchronous metastases of SBA. Patients and methods Data were retrieved from the Netherlands Cancer Registry. Patients treated with palliative chemotherapy and/or targeted therapy for synchronous metastatic SBA between 2007 and 2016 were included (n = 187). Differences in treatment and the subsequent effects on overall survival (OS) were evaluated. Results In first-line treatment, 25 patients (13%) received additional targeted therapy, exclusively bevacizumab, and mostly in combination with CAPOX/FOLFOX (n = 24). A primary ileal tumour was predictive for receiving bevacizumab in first-line treatment (odds ratio 3.2, 95% confidence interval (CI) 1.06-9.93). Median OS for patients in whom bevacizumab was added to first-line chemotherapy was 9.3 months, compared to 9.1 months with chemotherapy only (p = 0.85). Median OS for patients receiving first-line treatment only was 8.5 months with and 6.4 months without the addition of bevacizumab, respectively (p = 0.54). In multivariable survival analyses, the addition of bevacizumab was no prognostic factor (hazard ratio 1.01, 95% CI 0.65-1.59). Conclusions Bevacizumab was the only prescribed targeted therapy in first-line treatment. Considering the limited number of patients receiving first-line bevacizumab and the unknown reasons to prescribe additional targeted therapy, the corresponding survival rates of patients treated with and without additional bevacizumab in first-line treatment might suggest a limited clinical effect of bevacizumab in addition to first-line palliative chemotherapy on OS. Future research should focus on identifying the subgroup of patients who might benefit OR benefiting from anti-VEGF therapy in metastatic SBA.
C1 [Legue, Laura M.; Bernards, Nienke; Creemers, Geert-Jan] Catharina Hosp, Dept Med Oncol, Michelangelolaan 2, NL-5623 EJ Eindhoven, Netherlands.
   [Legue, Laura M.; van Erning, Felice N.; Lemmens, Valery E. P. P.; de Hingh, Ignace H. J. T.] Netherlands Comprehens Canc Org, Dept Res, Eindhoven, Netherlands.
   [Lemmens, Valery E. P. P.] Erasmus MC Univ, Med Ctr, Dept Publ Hlth, Rotterdam, Netherlands.
   [de Hingh, Ignace H. J. T.] Catharina Hosp, Dept Surg Oncol, Eindhoven, Netherlands.
   [de Hingh, Ignace H. J. T.] Maastricht Univ, Sch Oncol & Dev Biol, GROW, Maastricht, Netherlands.
C3 Catharina Hospital; Erasmus University Rotterdam; Erasmus MC; Catharina
   Hospital; Maastricht University
RP Legué, LM (corresponding author), Catharina Hosp, Dept Med Oncol, Michelangelolaan 2, NL-5623 EJ Eindhoven, Netherlands.; Legué, LM (corresponding author), Netherlands Comprehens Canc Org, Dept Res, Eindhoven, Netherlands.
EM laura.legue@catharinaziekenhuis.nl
OI Legue, Laura/0000-0003-0305-391X
FU Catharina Research Fund
FX This work was financially supported by a grant from the Catharina
   Research Fund, which was used for additional data collection, and had no
   involvement in relation to the presented outcomes.
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NR 26
TC 7
Z9 7
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 DEC
PY 2019
VL 14
IS 6
BP 699
EP 705
DI 10.1007/s11523-019-00681-1
EA OCT 2019
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JP8CP
UT WOS:000490840300002
PM 31625001
DA 2025-01-04
ER

PT J
AU Guadagni, S
   Clementi, M
   Mackay, AR
   Ricevuto, E
   Fiorentini, G
   Sarti, D
   Palumbo, P
   Apostolou, P
   Papasotiriou, I
   Masedu, F
   Valenti, M
   Giordano, AV
   Bruera, G
AF Guadagni, Stefano
   Clementi, Marco
   Mackay, Andrew R.
   Ricevuto, Enrico
   Fiorentini, Giammaria
   Sarti, Donatella
   Palumbo, Paola
   Apostolou, Panagiotis
   Papasotiriou, Ioannis
   Masedu, Francesco
   Valenti, Marco
   Giordano, Aldo Victor
   Bruera, Gemma
TI Real-life multidisciplinary treatment for unresectable colorectal cancer
   liver metastases including hepatic artery infusion with chemo-filtration
   and liquid biopsy precision oncotherapy: observational cohort study
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Liver metastases; Colorectal cancer; Third-line therapy; Hepatic artery
   infusion; Liquid biopsies; Precision oncotherapy; Chemo-filtration
ID CIRCULATING TUMOR-CELLS; SYSTEMIC CHEMOTHERAPY; PHASE-II;
   5-FLUOROURACIL; OXALIPLATIN; IRINOTECAN; COMBINATION; CONVERSION;
   RESECTION; SOCIETY
AB Background Hepatic artery infusion (HAI) and drug selection by liquid biopsy precision oncotherapy are under investigation for the multidisciplinary treatment of unresectable colorectal liver metastases (CRCLM) in progression after systemic therapy. Here, we compare the safety and efficacy of third-line HAI followed by target therapy with drug regimes selected by liquid biopsy precision oncotherapy to third-line systemic therapy with drug regimes selected partly by tissue biopsy precision oncotherapy, in a retrospective real-life study of 106 unresectable CRCLM patients. Methods Drug regimens for HAI/target therapy were selected by assessing the sensitivity of purified circulating tumor cell (CTCs) to 5-fluorouracil, carboplatin, cisplatin, oxaliplatin, irinotecan, doxorubicin, mitomycin, raltitrexed, and melphalan in-vitro and by real-time qRT-PCR gene expression assays, and for the Systemic therapy cohort were selected by age, comorbidity, performance status, and absence of RAS mutations. Therapeutic responses, adverse events, and quality of life were evaluated by RECIST 1.1, CTCAE 4.03, and ECOG criteria, respectively, and chemo-filtration performed following HAI to reduce systemic toxic effects. Results HAI/target therapy with drugs selected by liquid biopsy precision oncotherapy (44 patients), resulted in 2.27% CRs, 38.63% PRs, 56.81% SD,s and 2.27% PDs; ECOG 2 to 1 improvement, but no infusion-related technical or vascular complications, or deaths. Systemic therapy (62 patients) resulted in 1.6% CRs, 17.74% PRs, 37.09% SDs, and 45.16% PDs; more grade 1-2 adverse events and 4.84% ECOG 1 to 2 worsening. The median 5 month PFS in the HAI/target therapy cohort was significantly longer than 3 months in the systemic cohort (P < 0.007) and the median 14 month survival in the HAI/target therapy cohort was longer than 8.5 months in the systemic therapy cohort but not statistically significant. Multivariate analysis identified ECOG grade 2 as the most unfavourable survival prognostic factor in both cohorts. Conclusions HAI plus chemo-filtration followed by target therapy, with drug regimens selected by liquid biopsy precision oncotherapy, is a safe and efficacious alternative therapeutic strategy for unresectable CRCLM in progression after two lines of systemic therapy and should be considered for a multicentre prospective phase III study, to fully confirm this potential.
C1 [Guadagni, Stefano; Clementi, Marco; Mackay, Andrew R.; Ricevuto, Enrico; Masedu, Francesco; Valenti, Marco; Bruera, Gemma] Univ Aquila, Dept Appl Clin & Biotechnol Sci, I-67100 Laquila, Italy.
   [Ricevuto, Enrico; Bruera, Gemma] Oncol Territorial Care S Salvatore Hosp, Oncol Network ASL1 Abruzzo, Laquila, Italy.
   [Fiorentini, Giammaria; Sarti, Donatella] Osped Riuniti Marche Nord, Azienda Osped, Dept Hematol & Oncol, Pesaro, Italy.
   [Palumbo, Paola] Univ Aquila, Dept Life Hlth & Environm Sci, I-67100 Laquila, Italy.
   [Apostolou, Panagiotis] Res Genet Canc Ctr SA, Florina, Greece.
   [Papasotiriou, Ioannis] Res Genet Canc Ctr Int GmbH, Zug, Switzerland.
   [Giordano, Aldo Victor] S Salvatore Hosp, Intervent Radiol, I-67100 Laquila, Italy.
C3 University of L'Aquila; University of L'Aquila
RP Guadagni, S (corresponding author), Univ Aquila, Dept Appl Clin & Biotechnol Sci, I-67100 Laquila, Italy.
EM stefano.guadagni@univaq.it
RI VALENTI, MARCO/AAO-1383-2020; Guadagni, Stefano/P-6471-2016; MASEDU,
   Francesco/M-2989-2015; Clementi, Marco/P-8582-2016
OI Guadagni, Stefano/0000-0001-8525-084X; PAPASOTIRIOU,
   IOANNIS/0000-0002-6145-946X; MASEDU, Francesco/0000-0003-0290-5324;
   Clementi, Marco/0000-0002-9652-5148
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NR 37
TC 13
Z9 13
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD MAY
PY 2020
VL 146
IS 5
BP 1273
EP 1290
DI 10.1007/s00432-020-03156-3
EA FEB 2020
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LB8HJ
UT WOS:000516329400003
PM 32088781
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Yue, DL
   Zhang, Z
   Li, JY
   Chen, XF
   Ping, Y
   Liu, SS
   Shi, XJ
   Li, LF
   Wang, LP
   Huang, L
   Zhang, B
   Sun, Y
   Zhang, Y
AF Yue, Dongli
   Zhang, Zhen
   Li, Jieyao
   Chen, Xinfeng
   Ping, Yu
   Liu, Shasha
   Shi, Xiaojuan
   Li, Lifeng
   Wang, Liping
   Huang, Lan
   Zhang, Bin
   Sun, Yan
   Zhang, Yi
TI Transforming growth factor-beta1 promotes the migration and invasion of
   sphere-forming stem-like cell subpopulations in esophageal cancer
SO EXPERIMENTAL CELL RESEARCH
LA English
DT Article
DE Cancer stem cells (CSCs); Sphere-forming cells; Ultra low attachment
   surface culture; Esophageal cancer; TGF-beta 1
ID ACUTE MYELOID-LEUKEMIA; IN-VITRO PROPAGATION; BREAST-CANCER;
   SELF-RENEWAL; TGF-BETA; COLORECTAL-CANCER; INITIATING CELLS; SIDE
   POPULATION; CARCINOMA; IDENTIFICATION
AB Esophageal cancer is one of the most lethal solid malignancies. Mounting evidence demonstrates that cancer stem cells (CSCs) are able to cause tumor initiation, metastasis and responsible for chemotherapy and radiotherapy failures. As CSCs are thought to be the main reason of therapeutic failure, these cells must be effectively targeted to elicit long-lasting therapeutic responses. We aimed to enrich and identify the esophageal cancer cell subpopulation with stem-like properties and help to develop new target therapy strategies for CSCs. Here, we found esophageal cancer cells KYSE70 and TE1 could form spheres in ultra low attachment surface culture and be serially passaged. Sphere-forming cells could re-differentiate and acquire morphology comparable to parental cells, when return to adherent culture. The sphere-forming cells possessed the key criteria that define CSCs: persistent self-renewal, overexpression of stemness genes (SOX2, ALDH1A1 and KLF4), reduced expression of differentiation marker CK4, chemoresistance, strong invasion and enhanced tumorigenic potential. SB525334, transforming growth factor-beta 1(TGF-beta 1) inhibitor, significantly inhibited migration and invasion of sphere-forming stem-like cells and had no effect on sphere-forming ability. In conclusion, esophageal cancer sphere-forming cells from KYSE70 and TE1 cultured in ultra low attachment surface possess cancer stem cell properties, providing a model for CSCs targeted therapy. TGF-beta 1 promotes the migration and invasion of sphere-forming stem-like cells, which may guide future studies on therapeutic strategies targeting these cells. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Yue, Dongli; Zhang, Zhen; Li, Jieyao; Chen, Xinfeng; Ping, Yu; Liu, Shasha; Shi, Xiaojuan; Li, Lifeng; Huang, Lan; Zhang, Bin; Zhang, Yi] Zhengzhou Univ, Affiliated Hosp 1, Biotherapy Ctr, Zhengzhou 450052, Henan, Peoples R China.
   [Yue, Dongli; Zhang, Zhen; Li, Jieyao; Chen, Xinfeng; Shi, Xiaojuan; Li, Lifeng; Wang, Liping; Sun, Yan; Zhang, Yi] Zhengzhou Univ, Affiliated Hosp 1, Dept Oncol, Zhengzhou 450052, Henan, Peoples R China.
   [Ping, Yu; Liu, Shasha; Zhang, Yi] Zhengzhou Univ, Sch Life Sci, Zhengzhou 450000, Peoples R China.
   [Zhang, Bin] Northwestern Univ, Feinberg Sch Med, Robert H Lurie Comprehens Canc Ctr, Dept Med,Div Hematol Oncol, Chicago, IL 60611 USA.
   [Sun, Yan] Chinese Acad Med Sci, Canc Hosp, Dept Med Oncol, Beijing, Peoples R China.
   [Zhang, Yi] Zhengzhou Univ, Affiliated Hosp 1, Inst Clin Med, Zhengzhou 450052, Henan, Peoples R China.
C3 Zhengzhou University; Zhengzhou University; Zhengzhou University; Robert
   H. Lurie Comprehensive Cancer Center; Ann & Robert H. Lurie Children's
   Hospital of Chicago; Northwestern University; Feinberg School of
   Medicine; Chinese Academy of Medical Sciences - Peking Union Medical
   College; Cancer Institute & Hospital - CAMS; Zhengzhou University
RP Zhang, Y (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Biotherapy Ctr, 1 Jianshe Rd, Zhengzhou 450052, Henan, Peoples R China.
EM yizhang@zzu.edu.cn
RI Huang, Lingling/I-8722-2019; wang, chunping/KJL-6870-2024; Li,
   Donglin/JEF-4284-2023; zhang, yi/HKV-8165-2023
OI Li, Lifeng/0000-0002-7492-4017; Huang, Lan/0000-0001-9594-4722; Zhang,
   Yi/0000-0001-9861-4681
FU China-US (NFSCNIH) Program for Biomedical Collaborative Research
   [812111102]; National Natural Science Foundation of China [81171986];
   Ministry of Public Health [20110110001]; Basic and Advanced Technology
   Research Foundation from Science and Technology References Department of
   Henan Province [112300410153, 122300410155]; Funds for Creative Research
   Team of Henan Province, Creative Research Team of Higher Education of
   Henan Province; Innovation Team of the First Affiliated Hospital of
   Zhengzhou University
FX This study was supported by grants from the China-US (NFSCNIH) Program
   for Biomedical Collaborative Research (Grant no. 812111102), the
   National Natural Science Foundation of China (Grant no. 81171986),
   Research Grant from the Ministry of Public Health (Grant no.
   20110110001), the Basic and Advanced Technology Research Foundation from
   Science and Technology References Department of Henan Province (Grant
   nos. 112300410153 and 122300410155), Funds for Creative Research Team of
   Henan Province, Creative Research Team of Higher Education of Henan
   Province and the Innovation Team of the First Affiliated Hospital of
   Zhengzhou University.
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NR 43
TC 41
Z9 45
U1 0
U2 17
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 1
PY 2015
VL 336
IS 1
BP 141
EP 149
DI 10.1016/j.yexcr.2015.06.007
PG 9
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CO0EA
UT WOS:000358821700015
PM 26096658
DA 2025-01-04
ER

PT J
AU Sakata, S
   Larson, DW
AF Sakata, Shinichiro
   Larson, David W.
TI Targeted Therapy for Colorectal Cancer
SO SURGICAL ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Metastatic colorectal cancer; Targeted therapy; Bevacizumab; EGFR
ID SOCIETY TASK-FORCE; PHASE-III TRIAL; 1ST-LINE TREATMENT; PLUS
   OXALIPLATIN; LIVER METASTASES; RESECTION; CHEMOTHERAPY; BEVACIZUMAB;
   MUTATIONS; CETUXIMAB
C1 [Sakata, Shinichiro; Larson, David W.] Mayo Clin, Div Colon & Rectal Surg, Dept Surg, 200 First St SW, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Larson, DW (corresponding author), Mayo Clin, Div Colon & Rectal Surg, Dept Surg, 200 First St SW, Rochester, MN 55905 USA.
EM larson.david2@mayo.edu
OI Sakata, Shinichiro/0000-0002-9085-6755
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NR 53
TC 27
Z9 28
U1 2
U2 10
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1055-3207
EI 1558-5042
J9 SURG ONCOL CLIN N AM
JI Surg. Oncol. Clin. N. Am.
PD APR
PY 2022
VL 31
IS 2
SI SI
BP 255
EP 264
DI 10.1016/j.soc.2021.11.006
EA MAR 2022
PG 10
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA 1B9QG
UT WOS:000792764200010
PM 35351276
DA 2025-01-04
ER

PT J
AU Vermassen, T
   Geboes, K
   De Man, M
   Laurent, S
   Decoene, E
   Lumen, N
   Delanghe, J
   Rottey, S
AF Vermassen, Tijl
   Geboes, Karen
   De Man, Marc
   Laurent, Stephanie
   Decoene, Elsie
   Lumen, Nicolaas
   Delanghe, Joris
   Rottey, Sylvie
TI Neither creatinine- nor cystatin C-estimated glomerular filtration rate
   is optimal in oncology patients treated with targeted agents
SO NEPHROLOGY DIALYSIS TRANSPLANTATION
LA English
DT Article
DE cathepsin D; cystatin C; GFR; oncology; tyrosine kinase inhibitors
ID RENAL-CELL CARCINOMA; METASTATIC COLORECTAL-CANCER; CATHEPSIN-D
   EXPRESSION; BLIND PHASE-III; SERUM CREATININE; BEVACIZUMAB; SURVIVAL;
   SORAFENIB; SAFETY; SUNITINIB
AB In the last decade, there has been an increase in the use of anti-angiogenic drugs as treatment for metastatic malignancies. However, use of these targeted therapies could induce both glomerular and tubular damage. Also during targeted therapy, the lysosomal protease cathepsin D is released from the tumour, which is inhibited by the protease inhibitor cystatin C. The aim of this study is to determine if use of cystatin C-estimated glomerular filtration rate (eGFR) is applicable to a patient cohort treated with targeted agents.
   A cohort of 80 patients with various malignancies were continuously recruited and prospectively analysed. Serum and urinary biochemical analytes for renal toxicities were assessed at different time points during treatment. The association between serum cystatin C and cathepsin D was also determined.
   A decrease in serum cystatin C concentrations (1.03 versus 0.90 mg/L; P < 0.001), together with an increase in cystatin C-eGFR (71 versus 89 mL/min/1.73 m(2); P = 0.002) was observed during therapy, compared with baseline. This decrease in cystatin C concentrations was correlated with cathepsin D (r = 0.307; P < 0.001), which was released from the tumour during targeted therapy. Further analysis demonstrated cathepsin D-mediated proteolysis of cystatin C in serum.
   Cystatin C concentrations were decreased during targeted therapy due to cathepsin D-mediated proteolysis. Cystatin C-eGFR is therefore not considered a suitable marker for assessing kidney function in oncology patients, and other techniques to estimate the GFR have to be applied in this patient population.
C1 [Vermassen, Tijl; Decoene, Elsie; Rottey, Sylvie] Ghent Univ Hosp, Dept Med Oncol, Ghent, Belgium.
   [Geboes, Karen; De Man, Marc; Laurent, Stephanie] Ghent Univ Hosp, Dept Gastroenterol, Ghent, Belgium.
   [Lumen, Nicolaas] Ghent Univ Hosp, Dept Urol, Ghent, Belgium.
   [Delanghe, Joris] Ghent Univ Hosp, Dept Clin Chem, Ghent, Belgium.
C3 Ghent University; Ghent University Hospital; Ghent University; Ghent
   University Hospital; Ghent University; Ghent University Hospital; Ghent
   University; Ghent University Hospital
RP Rottey, S (corresponding author), Ghent Univ Hosp, Dept Med Oncol, Ghent, Belgium.
EM Sylvie.Rottey@UGent.be
RI Vermassen, Tijl/AHA-6274-2022; Geboes, Karen/E-1752-2018
OI Vermassen, Tijl/0000-0002-1335-9966
FU Pfizer; Bayer
FX This research was supported by a restricted grant from Bayer and Pfizer.
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NR 48
TC 9
Z9 9
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0931-0509
EI 1460-2385
J9 NEPHROL DIAL TRANSPL
JI Nephrol. Dial. Transplant.
PD MAR
PY 2018
VL 33
IS 3
BP 402
EP 408
DI 10.1093/ndt/gfx063
PG 7
WC Transplantation; Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Transplantation; Urology & Nephrology
GA FY5LC
UT WOS:000426868500009
PM 28482048
OA Bronze
DA 2025-01-04
ER

PT J
AU Wang, HT
   Tang, R
   Jiang, L
   Jia, YT
AF Wang, Haitao
   Tang, Rui
   Jiang, Ling
   Jia, Yingtian
TI The role of PIK3CA gene mutations in colorectal cancer and the selection
   of treatment strategies
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE PIK3CA gene mutation; colorectal cancer; pathogenesis; targeted therapy;
   immunotherapy
ID MISMATCH REPAIR-DEFICIENT; MICROSATELLITE INSTABILITY; PROGNOSTIC ROLE;
   PI3K PATHWAY; TUMOR-GROWTH; COLON-CANCER; OPEN-LABEL; WILD-TYPE; KRAS;
   BRAF
AB PIK3CA gene encodes the p110 alpha catalytic subunit of PI3K, which regulates the PI3K/AKT/mTOR signaling pathway. PIK3CA gene mutation is one of the most common mutations in colorectal cancer (CRC), affecting about 15%-20% of CRC patients. PIK3CA gene mutation leads to the persistent activation of the PI3K/AKT/mTOR signaling pathway, which promotes the proliferation, invasion, metastasis, and drug resistance of CRC. This article provides a summary of the key detection methods for PIK3CA gene mutation, and provides an introduction to the existing colorectal cancer treatments and their practical applications in the clinic. Besides, this article summarizes the role and mechanism of PIK3CA gene mutation in the occurrence and development of CRC. It also explores the relationship between PIK3CA gene mutation and the clinical features and prognosis of CRC. This article focuses on the influence and mechanism of PIK3CA gene mutation on the targeted therapy and immunotherapy of CRC, and discusses the potential value and future direction of PIK3CA gene mutation in the personalized therapy of CRC. We aim to provide new perspectives and ideas for the precise diagnosis and treatment of CRC.
C1 [Wang, Haitao] Southwest Med Univ, Sch Clin Med Sci, Luzhou, Sichuan, Peoples R China.
   [Tang, Rui; Jiang, Ling] Chengdu Anorectal Hosp, Chengdu, Peoples R China.
   [Jia, Yingtian] Southwest Med Univ, Affiliated Tradit Chinese Med Hosp, Dept Anorectal, Luzhou, Peoples R China.
C3 Southwest Medical University; Southwest Medical University
RP Jiang, L (corresponding author), Chengdu Anorectal Hosp, Chengdu, Peoples R China.; Jia, YT (corresponding author), Southwest Med Univ, Affiliated Tradit Chinese Med Hosp, Dept Anorectal, Luzhou, Peoples R China.
EM jianglingvic@163.com; shimutianhero@126.com
RI Wang, Haitao/LQK-3399-2024
OI Wang, Haitao/0009-0007-5486-8218
FU Southwest Medical University10.13039/501100014895
FX Figure drawing was supported by Figdraw.
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NR 164
TC 0
Z9 0
U1 0
U2 0
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 OCT 30
PY 2024
VL 15
AR 1494802
DI 10.3389/fphar.2024.1494802
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA M3M5M
UT WOS:001356618500001
PM 39555098
OA gold
DA 2025-01-04
ER

PT J
AU Siravegna, G
   Sartore-Bianchi, A
   Nagy, RJ
   Raghav, K
   Odegaard, JI
   Lanman, RB
   Trusolino, L
   Marsoni, S
   Siena, S
   Bardelli, A
AF Siravegna, Giulia
   Sartore-Bianchi, Andrea
   Nagy, Rebecca J.
   Raghav, Kanwal
   Odegaard, Justin I.
   Lanman, Richard B.
   Trusolino, Livio
   Marsoni, Silvia
   Siena, Salvatore
   Bardelli, Alberto
TI Plasma HER2 (<i>ERBB2</i>) Copy Number Predicts Response to
   HER2-targeted Therapy in Metastatic Colorectal Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CIRCULATING TUMOR DNA; COLON-CANCER; AMPLIFICATION; HETEROGENEITY;
   EXPRESSION; LAPATINIB; BLOCKADE
AB Purpose: ERBB2 (HER2) amplification is an emerging biomarker in colon cancer, conferring sensitivity to combination anti-HER2 therapy. Measurement of HER2 copy number is typically performed using surgical specimens, but cell-free circulating tumor DNA (ctDNA) analysis may be a noninvasive alternative. We determined the sensitivity of plasma copy number (pCN) for detecting ERBB2 amplifications and whether pCN correlated with tissue-detected copy number. We also assessed response to HER2-targeted therapy based onpCNand suggest a pCN threshold predictive of response.
   Experimental Design: Forty-eight pretreatment and progression plasma samples from 29 HER2-positive patients in the HERACLES A clinical trial were tested using the Guardant360 cfDNA assay. We correlated ERRB2 pCN with progression-free survival (PFS) and best objective response (BOR) and applied an adjustment method based on tumor DNA shedding using the maximum mutant allele fraction as a surrogate for tumor content to accurately determine the pCN threshold predictive of response.
   Results: Forty-seven of 48 samples had detectable ctDNA, and 46 of 47 samples were ERBB2-amplified on the basis of cfDNA [2.55-122 copies; 97.9% sensitivity (95% confidence interval, 87.2%-99.8%)]. An adjusted ERBB2 pCN of >= 25.82 copies correlated with BOR and PFS (P = 0.0347).
   Conclusions: cfDNA is a viable alternative to tissue-based genotyping in the metastatic setting. The cfDNA platform utilized correctly identified 28 of 29 (96.6%) of pretreatment samples as ERBB2-amplified and predicted benefit from HER2-targeted therapy. In this study, an observed pCN of 2.4 and an adjusted pCN of 25.82 copies of ERBB2 are proposed to select patients who will benefit from HER2 targeted therapy.
C1 [Siravegna, Giulia; Trusolino, Livio; Bardelli, Alberto] IRCCS, FPO, Candiolo Canc Inst, Turin, Italy.
   [Siravegna, Giulia; Trusolino, Livio; Bardelli, Alberto] Univ Torino, Dept Oncol, Turin, Italy.
   [Sartore-Bianchi, Andrea; Siena, Salvatore] ASST Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Sartore-Bianchi, Andrea; Siena, Salvatore] Univ Milan, Dept Oncol & Haematol Oncol, Milan, Italy.
   [Nagy, Rebecca J.; Odegaard, Justin I.; Lanman, Richard B.] Guardant Hlth Inc, Redwood City, CA USA.
   [Raghav, Kanwal] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Marsoni, Silvia] FIRC Inst Mol Oncol IFOM, Milan, Italy.
C3 IRCCS Fondazione del Piemonte per l'Oncologia; University of Turin;
   University of Milan; Guardant Health, Inc.; University of Texas System;
   UTMD Anderson Cancer Center; IFOM - FIRC Institute of Molecular Oncology
RP Bardelli, A (corresponding author), Univ Torino, Candiolo Canc Inst, IRCC SP 142 Km 3, I-10060 Turin, Italy.; Siena, S (corresponding author), Univ Milan, Via Festa Perdono 7, I-20122 Milan, Italy.
EM salvatore.siena@unimi.it; alberto.bardelli@unito.it
RI Lanman, Richard/D-8290-2016; Trusolino, Livio/A-3896-2011; SIENA,
   SALVATORE/AAC-5806-2019; Sartore-Bianchi, Andrea/AAB-9848-2019;
   Siravegna, Giulia/Z-2826-2019; BARDELLI, Alberto/J-9721-2018
OI Lanman, Richard/0000-0001-8122-4329; Trusolino,
   Livio/0000-0002-6379-3365; Sartore-Bianchi, Andrea/0000-0003-0780-0409;
   BARDELLI, Alberto/0000-0003-1647-5070; Marsoni,
   Silvia/0000-0002-5361-7122
FU European Community's Seventh Framework Programme [602901 MErCuRIC]; AIRC
   IG [18532, 16788]; Fondazione Piemontese per la Ricerca sul Cancro-ONLUS
   5 per mille 2014 e 2015 Ministero della Salute; Transcan, TACTIC; AIRC
   Special Program 5 per mille metastases Project [21091]; AIRC 3-year
   fellowship; Roche per la ricerca grant 2017; Terapia Molecolare Tumori
   by Fondazione Oncologia Niguarda Onlus; Genomic-Based Triage for Target
   Therapy in Colorectal Cancer Ministero della Salute [NET 02352137];
   H2020 grant [635342-2 MoTriColor]; IMI [115749 CANCER-ID]
FX This work was supported by European Community's Seventh Framework
   Programme under grant agreement no. 602901 MErCuRIC (to A. Bardelli);
   H2020 grant agreement no. 635342-2 MoTriColor (to A. Bardelli and S.
   Siena); IMI contract no. 115749 CANCER-ID (to A. Bardelli); AIRC IG no.
   16788 (to A. Bardelli); Fondazione Piemontese per la Ricerca sul
   Cancro-ONLUS 5 per mille 2014 e 2015 Ministero della Salute (to A.
   Bardelli, S. Siena, L. Trusolino, and S. Marsoni); AIRC IG no. 18532 (to
   L. Trusolino); Transcan, TACTIC (to L. Trusolino); AIRC Special Program
   5 per mille metastases Project n. 21091 (to A. Bardelli, S. Marsoni, S.
   Siena, and L. Trusolino); AIRC 3-year fellowship and Roche per la
   ricerca grant 2017 (to G. Siravegna); Terapia Molecolare Tumori by
   Fondazione Oncologia Niguarda Onlus (to A. Sartore-Bianchi and S.
   Siena); and Genomic-Based Triage for Target Therapy in Colorectal Cancer
   Ministero della Salute, project no. NET 02352137 (to A. Sartore-Bianchi,
   S. Siena, and S. Marsoni.).
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NR 27
TC 105
Z9 107
U1 0
U2 11
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 MAY 15
PY 2019
VL 25
IS 10
BP 3046
EP 3053
DI 10.1158/1078-0432.CCR-18-3389
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HY3YS
UT WOS:000468064200014
PM 30808777
OA Green Submitted, Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Santoni, M
   Conti, A
   Massari, F
   Di Nunno, V
   Faloppi, L
   Galizia, E
   Morbiducci, J
   Piva, F
   Buti, S
   Iacovelli, R
   Ferretti, B
   Cimadamore, A
   Scarpelli, M
   Lopez-Beltran, A
   Cheng, L
   Battelli, N
   Montironi, R
AF Santoni, Matteo
   Conti, Alessandro
   Massari, Francesco
   Di Nunno, Vincenzo
   Faloppi, Luca
   Galizia, Eva
   Morbiducci, Jarno
   Piva, Francesco
   Buti, Sebastiano
   Iacovelli, Roberto
   Ferretti, Benedetta
   Cimadamore, Alessia
   Scarpelli, Marina
   Lopez-Beltran, Antonio
   Cheng, Liang
   Battelli, Nicola
   Montironi, Rodolfo
TI Targeted therapy for solid tumors and risk of hypertension: a
   meta-analysis of 68077 patients from 93 phase III studies
SO EXPERT REVIEW OF CARDIOVASCULAR THERAPY
LA English
DT Article
DE Cancer; Cardiovascular events; Hypertension; Meta-analysis; Targeted
   therapy
ID CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER; RESISTANT
   PROSTATE-CANCER; ADVANCED BREAST-CANCER; BEVACIZUMAB PLUS CAPECITABINE;
   ENDOTHELIAL GROWTH-FACTOR; ADVANCED HEPATOCELLULAR-CARCINOMA;
   OXALIPLATIN-BASED CHEMOTHERAPY; DOUBLE-BLIND; 1ST-LINE TREATMENT
AB Objective: Hypertension is a common adverse event with targeted agents in cancer patients and can lead to serious and sometimes lethal cardiovascular complications. The authors performed a meta-analysis of clinical trials aiming to evaluate the incidence and Relative Risk (RR) of developing all-grade and high-grade Hypertension Events (HE) in patients with solid tumors receiving targeted therapy. Methods: A review of citations from PubMed was performed and studies were selected based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. The search was limited to randomized phase III trials published in English focused on the efficacy and safety of targeted agents in cancer patients, reporting data on HE. Incidence, RR and relative 95% CIs were analyzed using random or fixed-effects models. Overall incidences were calculated and further compared with the chi-squared test for proportions. Results: Ninety-three phase III trials were included, with a total of 68,077 patients. Prostate cancer was the most represented (18.9%), followed by breast cancer (17.3%) and colorectal cancer (16.4%). The incidence of all- and high-grade HE was 23.47% and 8.57%, respectively, with the highest incidence of serious HE reported by adjuvant Sunitib/Sorafenib (29.03%). The highest RR of high-grade HE was observed with Bevacizumab in patients with advanced cervical cancer. By drug category, the highest RR of high-grade HE was reported by VEGFR/EGFR TKIs. Conclusion: According to these data, monitoring this class of toxicities is of primary importance to avoid hypertension worsening and, thus, the risk of major cardiovascular events.
C1 [Santoni, Matteo; Faloppi, Luca; Galizia, Eva; Battelli, Nicola] Macerata Hosp, Oncol Unit, Macerata, Italy.
   [Conti, Alessandro] Azienda Osped Alto Adige, Bressanone Brixen Hosp, Bressanone, Italy.
   [Massari, Francesco; Di Nunno, Vincenzo] St Orsola Marcello Malpighi Hosp, Div Oncol, Bologna, Italy.
   [Morbiducci, Jarno] Area Vasta N 3, Dept Radiodiag, Macerata, Italy.
   [Piva, Francesco] Polytech Univ Marche, Dept Specialist Clin & Odontostomatol Sci, Ancona, Italy.
   [Buti, Sebastiano] Univ Hosp Parma, Div Oncol, Parma, Italy.
   [Iacovelli, Roberto] Univ Verona, AOUI, Dept Med Oncol, Verona, Italy.
   [Ferretti, Benedetta] Osped San Severino, Oncol Med, San Severino Marche, MC, Italy.
   [Cimadamore, Alessia; Scarpelli, Marina; Montironi, Rodolfo] Polytech Univ Marche Reg, United Hosp, Sch Med, Sect Pathol Anat, Ancona, Italy.
   [Lopez-Beltran, Antonio] Fac Med, Dept Pathol & Surg, Cordoba, Spain.
   [Cheng, Liang] Indiana Univ Sch Med, Dept Pathol & Lab Med, Indianapolis, IN 46202 USA.
C3 IRCCS Azienda Ospedaliero-Universitaria di Bologna; Marche Polytechnic
   University; University of Parma; University Hospital of Parma;
   University of Verona; Azienda Ospedaliera Universitaria Integrata
   Verona; Marche Polytechnic University; Indiana University System;
   Indiana University Bloomington
RP Montironi, R (corresponding author), Polytech Univ Marche Reg, United Hosp, Sch Med, Pathol Anat, Via Conca 71, I-60126 Ancona, Italy.
EM r.montironi@univpm.it
RI Faloppi, Luca/K-1030-2016; Cheng, Liang/E-9268-2011; López-Beltrán,
   António/AAK-7326-2020; CIMADAMORE, ALESSIA/AAT-1340-2021; DI NUNNO,
   VINCENZO/AAW-4446-2021; Iacovelli, Roberto/AAB-9850-2019; Buti,
   Sebastiano/S-1314-2017
OI Lopez-Beltran, Antonio/0000-0002-0724-1267; Buti,
   Sebastiano/0000-0003-0876-0226; CIMADAMORE, ALESSIA/0000-0001-5981-3514;
   Cheng, Liang/0000-0001-6049-5293; Iacovelli,
   Roberto/0000-0002-1750-2117; Montironi, Rodolfo/0000-0003-3938-610X
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NR 134
TC 4
Z9 5
U1 0
U2 6
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1477-9072
EI 1744-8344
J9 EXPERT REV CARDIOVAS
JI Expert Rev. Cardiovasc. Ther.
PD DEC 2
PY 2019
VL 17
IS 12
BP 917
EP 927
DI 10.1080/14779072.2019.1704626
EA DEC 2019
PG 11
WC Cardiac & Cardiovascular Systems
WE Emerging Sources Citation Index (ESCI)
SC Cardiovascular System & Cardiology
GA KB6TS
UT WOS:000503779200001
PM 31829045
DA 2025-01-04
ER

PT J
AU Erika, G
   Federica, Z
   Martina, S
   Anselmo, P
   Luigi, R
   Marina, M
   Davide, C
   Eleonora, Z
   Monica, V
   Silverio, T
AF Erika, Giordani
   Federica, Zoratto
   Martina, Strudel
   Anselmo, Papa
   Luigi, Rossi
   Marina, Minozzi
   Davide, Caruso
   Eleonora, Zaccarelli
   Monica, Verrico
   Silverio, Tomao
TI Old Tyrosine Kinase Inhibitors and Newcomers in Gastrointestinal Cancer
   Treatment
SO CURRENT CANCER DRUG TARGETS
LA English
DT Article
DE Approved tyrosine kinase inhibitors; efficacy data; experimental
   tyrosine kinase inhibitors; gastrointestinal cancers; personalized
   treatment
ID ADVANCED HEPATOCELLULAR-CARCINOMA; ENDOTHELIAL GROWTH-FACTOR; RANDOMIZED
   PHASE-III; METASTATIC COLORECTAL-CANCER; BEVACIZUMAB PLUS ERLOTINIB;
   ADVANCED PANCREATIC-CANCER; STROMAL TUMORS; DOUBLE-BLIND; IMATINIB
   MESYLATE; OPEN-LABEL
AB Gastrointestinal cancer treatment is based more on molecular biology that has provided increasing knowledge about cancer pathogenesis on which targeted therapy is being developed. Precisely, targeted therapy is defined as a "type of treatment that uses drugs, such as monoclonal antibodies or tyrosine kinase inhibitors, to identify and attack specific cancer cells". Nowadays, the United States Food and Drug Administration has approved many targeted therapies for gastrointestinal cancer treatment, as many are in various phases of development as well. In a previous review we discussed the main monoclonal antibodies used and studied in gastrointestinal cancer. In addition to monoclonal antibodies, tyrosine kinase inhibitors represent another class of targeted therapy and following the approval of imatinib for gastrointestinal stromal tumours, other tyrosine kinase inhibitors have been approved for gastrointestinal cancers treatment such as sunitinib, regoragenib, sorafenib and erlotinib. Moving forward, the purpose of this review is to focus on the efficacy data of main tyrosine kinase inhibitors commonly used in the personalized treatment of each gastrointestinal tumour and to provide a comprehensive overview about experimental targeted therapies ongoing in this setting.
C1 Univ Roma La Sapienza, Dept Med Surg Sci & Biotechnol, Via Faggiana 1668, I-04100 Latina, Italy.
   ICOT, Oncol Unit, Via Faggiana 1668, I-04100 Latina, Italy.
C3 Sapienza University Rome
RP Anselmo, P (corresponding author), Osped ICOT, Oncol Unit, Via Faggiana 1668, I-04100 Latina, Italy.
EM anselmo.papa@libero.it
OI Caruso, Davide/0000-0001-8622-8142
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NR 86
TC 8
Z9 10
U1 0
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 1568-0096
EI 1873-5576
J9 CURR CANCER DRUG TAR
JI Curr. Cancer Drug Targets
PY 2016
VL 16
IS 2
BP 175
EP 185
DI 10.2174/1568009615666150817120712
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DG5GJ
UT WOS:000372104500009
PM 26278713
DA 2025-01-04
ER

PT J
AU Ruiz-Saenz, A
   Atreya, CE
   Wang, CJ
   Pan, B
   Dreyer, CA
   Brunen, D
   Prahallad, A
   Muñoz, DP
   Ramms, DJ
   Burghi, V
   Spassov, DS
   Fewings, E
   Hwang, YC
   Cowdrey, C
   Moelders, C
   Schwarzer, C
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   Hann, B
   VandenBerg, SR
   Shokat, K
   Moasser, MM
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   Gutkind, JS
   van 't Veer, LJ
   Coppé, JP
AF Ruiz-Saenz, Ana
   Atreya, Chloe E.
   Wang, Changjun
   Pan, Bo
   Dreyer, Courtney A.
   Brunen, Diede
   Prahallad, Anirudh
   Munoz, Denise P.
   Ramms, Dana J.
   Burghi, Valeria
   Spassov, Danislav S.
   Fewings, Eleanor
   Hwang, Yeonjoo C.
   Cowdrey, Cynthia
   Moelders, Christina
   Schwarzer, Cecilia
   Wolf, Denise M.
   Hann, Byron
   VandenBerg, Scott R.
   Shokat, Kevan
   Moasser, Mark M.
   Bernards, Rene
   Gutkind, J. Silvio
   van 't Veer, Laura J.
   Coppe, Jean-Philippe
TI A reversible SRC-relayed COX2 inflammatory program drives resistance to
   BRAF and EGFR inhibition in BRAF<SUP>V600E</SUP> colorectal tumors
SO NATURE CANCER
LA English
DT Article
ID COLON-CANCER; PHASE-II; MUTATION STATUS; RAF; ACTIVATION; GROWTH;
   PHOSPHORYLATION; PROGRESSION; VEMURAFENIB; MECHANISM
AB Coppe and colleagues define a resistance mechanism to combination BRAF- and EGFR-targeted therapy in BRAF(V600E) colorectal cancers that could be overcome in vitro and in vivo by repurposing COX2 inhibitors.
   BRAF(V600E) mutation confers a poor prognosis in metastatic colorectal cancer (CRC) despite combinatorial targeted therapies based on the latest understanding of signaling circuitry. To identify parallel resistance mechanisms induced by BRAF-MEK-EGFR co-targeting, we used a high-throughput kinase activity mapping platform. Here we show that SRC kinases are systematically activated in BRAF(V600E) CRC following targeted inhibition of BRAF +/- EGFR and that coordinated targeting of SRC with BRAF +/- EGFR increases treatment efficacy in vitro and in vivo. SRC drives resistance to BRAF +/- EGFR targeted therapy independently of ERK signaling by inducing transcriptional reprogramming through beta-catenin (CTNNB1). The EGFR-independent compensatory activation of SRC kinases is mediated by an autocrine prostaglandin E-2 loop that can be blocked with cyclooxygenase-2 (COX2) inhibitors. Co-targeting of COX2 with BRAF + EGFR promotes durable suppression of tumor growth in patient-derived tumor xenograft models. COX2 inhibition represents a drug-repurposing strategy to overcome therapeutic resistance in BRAF(V600E) CRC.
C1 [Ruiz-Saenz, Ana; Atreya, Chloe E.; Wang, Changjun; Pan, Bo; Dreyer, Courtney A.; Munoz, Denise P.; Spassov, Danislav S.; Fewings, Eleanor; Hwang, Yeonjoo C.; Cowdrey, Cynthia; Moelders, Christina; Schwarzer, Cecilia; Wolf, Denise M.; Hann, Byron; VandenBerg, Scott R.; Shokat, Kevan; Moasser, Mark M.; van 't Veer, Laura J.; Coppe, Jean-Philippe] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94118 USA.
   [Ruiz-Saenz, Ana] Erasmus MC, Dept Cell Biol, Rotterdam, Netherlands.
   [Ruiz-Saenz, Ana] Erasmus MC, Dept Med Oncol, Rotterdam, Netherlands.
   [Brunen, Diede; Prahallad, Anirudh; Bernards, Rene] Netherlands Canc Inst, Div Mol Carcinogenesis, Amsterdam, Netherlands.
   [Brunen, Diede; Prahallad, Anirudh; Bernards, Rene] Netherlands Canc Inst, Oncode Inst, Amsterdam, Netherlands.
   [Ramms, Dana J.; Burghi, Valeria; Gutkind, J. Silvio] Univ Calif San Diego, Dept Pharmacol, La Jolla, CA USA.
   [Ramms, Dana J.; Burghi, Valeria; Gutkind, J. Silvio] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA USA.
   [Wang, Changjun; Pan, Bo] Peking Union Med Coll & Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Breast Surg, Beijing, Peoples R China.
   [Spassov, Danislav S.] Med Univ Sofia, Fac Pharm, Sofia, Bulgaria.
   [Fewings, Eleanor] Inst Computat Biomed, Heidelberg, Germany.
C3 University of California System; University of California San Francisco;
   UCSF Medical Center; UCSF Helen Diller Family Comprehensive Cancer
   Center; Erasmus University Rotterdam; Erasmus MC; Erasmus University
   Rotterdam; Erasmus MC; Netherlands Cancer Institute; Netherlands Cancer
   Institute; University of California System; University of California San
   Diego; University of California System; University of California San
   Diego; Chinese Academy of Medical Sciences - Peking Union Medical
   College; Peking Union Medical College Hospital; Peking Union Medical
   College; Medical University Sofia
RP Coppé, JP (corresponding author), Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94118 USA.
RI Spassov, Danislav/GQA-4368-2022; Gutkind, J Silvio/J-1201-2016;
   RUIZ-SAENZ, ANA/U-3220-2017
OI Spassov, Danislav/0000-0002-6680-877X; Ramms, Dana/0000-0002-7700-1728;
   Gutkind, J Silvio/0000-0002-5150-4482; Fewings,
   Eleanor/0000-0001-9012-3220; Hwang, Yeonjoo/0000-0002-3000-4710;
   RUIZ-SAENZ, ANA/0000-0001-6033-6153
FU Ramon Areces Fellowship; Natural Science Foundation of China [81001183];
   Dutch Cancer Society (KWF) through the Oncode Institute; Marcus Program
   in Precision Medicine Innovation Award; MSCA [882247];
   Sigma-Aldrich/UCSF T1 Catalyst Award; NIH [R01CA122216, UL1TR000005,
   R01CA229447]; Marie Curie Actions (MSCA) [882247] Funding Source: Marie
   Curie Actions (MSCA); National Cancer Institute [R01CA229447] Funding
   Source: NIH RePORTER
FX We thank E. Chow, at the Center for Advanced Technologies, UCSF, and M.
   Mori for support in setting up the HT-KAM liquid assay automation; J.
   Malato, D. Wang, P. Phojanakong, V. Steri and D. Banerji for their
   technical assistance with in vivo mouse studies; and J. Bolen and M.
   Nasser for providing details of IHC automation protocols, as well as the
   UCSF HDFCCC Histology and Biomarker Core for methods support. We thank
   Amgen for providing panitumumab. This work was supported by the
   following funding: the Ramon Areces Fellowship (to A.R.-S.), Natural
   Science Foundation of China grant no. 81001183 (to B.P.), the Dutch
   Cancer Society (KWF) through the Oncode Institute (to R.B.), a Marcus
   Program in Precision Medicine Innovation Award (to J.-P.C., C.E.A. and
   K.S.), MSCA grant no. 882247 (to D.S.S.), the Angela and Shu Kai Chan
   Endowed chair (to L.J.v.tV.), NIH R01CA122216 (to M.M.M.), NIH
   UL1TR000005, the Sigma-Aldrich/UCSF T1 Catalyst Award (to J.-P.C.) and
   NIH R01CA229447 (to C.E.A. and J.-P.C.).
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NR 61
TC 18
Z9 18
U1 3
U2 21
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
EI 2662-1347
J9 NAT CANCER
JI Nat. Cancer
PD FEB
PY 2023
VL 4
IS 2
BP 240
EP +
DI 10.1038/s43018-022-00508-5
EA FEB 2023
PG 27
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9F9DJ
UT WOS:000930680300001
PM 36759733
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Yonesaka, K
AF Yonesaka, Kimio
TI HER2-/HER3-Targeting Antibody-Drug Conjugates for Treating Lung and
   Colorectal Cancers Resistant to EGFR Inhibitors
SO CANCERS
LA English
DT Review
DE EGFR; HER2; HER3; ADC; trastuzumab deruxtecan (T-DXd); patritumab
   deruxtecan; NSCLC; CRC; HNSCC; EGFR-TKI
ID DERUXTECAN T-DXD; OPEN-LABEL; TRASTUZUMAB EMTANSINE; PREDICTIVE
   BIOMARKER; MONOCLONAL-ANTIBODY; ACQUIRED-RESISTANCE; MEDIATED
   RESISTANCE; 1ST-LINE TREATMENT; ANTITUMOR-ACTIVITY; ADVANCED BREAST
AB Simple Summary
   Epidermal growth factor receptor (EGFR) is one of the anticancer drug targets for certain malignancies including nonsmall cell lung cancer (NSCLC), colorectal cancer (CRC), and head and neck squamous cell carcinoma. However, the grave issue of drug resistance through diverse mechanisms persists. Since the discovery of aberrantly activated human epidermal growth factor receptor-2 (HER2) and HER3 mediating resistance to EGFR-inhibitors, intensive investigations on HER2- and HER3-targeting treatments have revealed their advantages and limitations. An innovative antibody-drug conjugate (ADC) technology, with a new linker-payload system, has provided a solution to overcome this resistance. HER2-targeting ADC trastuzumab deruxtecan or HER3-targeting ADC patritumab deruxtecan, using the same cleavable linker-payload system, demonstrated promising responsiveness in patients with HER2-positive CRC or EGFR-mutated NSCLC, respectively. The current manuscript presents an overview of the accumulated evidence on HER2- and HER3-targeting therapy and discussion on remaining issues for further improvement of treatments for cancers resistant to EGFR-inhibitors.
   Epidermal growth factor receptor (EGFR) is one of the anticancer drug targets for certain malignancies, including nonsmall cell lung cancer (NSCLC), colorectal cancer (CRC), and head and neck squamous cell carcinoma. However, the grave issue of drug resistance through diverse mechanisms persists, including secondary EGFR-mutation and its downstream RAS/RAF mutation. Since the discovery of the role of human epidermal growth factor receptor 2 (HER2) and HER3 in drug resistance, HER2- or HER3-targeting treatment strategies using monoclonal antibodies have been intensively examined and have demonstrated impressive responsiveness and limitations. Finally, an innovative targeted therapy called antibody drug conjugates (ADC) has provided a solution to overcome this resistance. Specifically, a new cleavable linker-payload system enables stable drug delivery to cancer cells, causing selective destruction. HER2-targeting ADC trastuzumab deruxtecan demonstrated promising responsiveness in patients with HER2-positive CRC, in a phase 2 clinical trial (objective response rate = 45.3%). Furthermore, HER3-targeting patritumab deruxtecan, another ADC, exhibited impressive tumor shrinkage in pretreated patients with EGFR-mutated NSCLC, in a phase 1 clinical trial. This manuscript presents an overview of the accumulated evidence on HER2- and HER3-targeting therapy, especially ADCs, and discussion of remaining issues for further improving these treatments in cancers resistant to EGFR inhibitors.
C1 [Yonesaka, Kimio] Kindai Univ, Fac Med, Dept Med Oncol, 377-2 Ohno Higashi Osaka Sayamashi, Osaka 5898511, Japan.
C3 Kindai University (Kinki University)
RP Yonesaka, K (corresponding author), Kindai Univ, Fac Med, Dept Med Oncol, 377-2 Ohno Higashi Osaka Sayamashi, Osaka 5898511, Japan.
EM yonesaka@med.kindai.ac.jp
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NR 61
TC 30
Z9 33
U1 2
U2 23
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2021
VL 13
IS 5
AR 1047
DI 10.3390/cancers13051047
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QV4TE
UT WOS:000627965300001
PM 33801379
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Huang, SC
   Lin, CC
   Teng, HW
   Lin, HH
   Chang, SC
   Lan, YT
   Wang, HS
   Yang, SH
   Chen, WS
   Jiang, JK
AF Huang, Sheng-Chieh
   Lin, Chun-Chi
   Teng, Hao-Wei
   Lin, Hung-Hsin
   Chang, Shih-Ching
   Lan, Yuan-Tzu
   Wang, Huann-Sheng
   Yang, Shung-Haur
   Chen, Wei-Shone
   Jiang, Jeng-Kai
TI A Long-Term and Large-Scale Real-World Study in Taiwan: Efficacy of
   Target Therapy in Stage IV Colorectal Cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; metastatic colorectal cancer; target therapy;
   cetuximab; bevacizumab; Taiwan; real-world study; metastectomy
ID PRIMARY TUMOR LOCATION; 1ST-LINE TREATMENT; BEVACIZUMAB; CHEMOTHERAPY;
   CETUXIMAB
AB This study expands the understanding of the role of target therapy in improving survival of patients with mCRC based on real-world study results. These data represent potential survival outcomes of Taiwanese patients with mCRC in clinical practice. CRC is the most commonly diagnosed cancer and the third leading cause of cancer-related death in Taiwan. The aim of this study was to evaluate the efficacy of target therapy in combination with chemotherapy for mCRC in Taiwan. This was a real-world, retrospective, observational study in patients diagnosed with mCRC (N=1583). A total of 792 patients received chemotherapy plus target therapy (anti-EGFR therapy, n=180; anti-VEGF therapy, n=612) and 791 patients who received chemotherapy alone. Overall survival (OS) and progression-free survival (PFS) were examined. For RAS wild-type patients, the median OS (mOS) was 34.3 months in the EGFR L (left-sided colon) group, 27.3 months in the VEGF L group, 18.4 months in VEGF R (right-sided colon) group, and 13.8 months in EGFR R group (P<0.001). Median PFS (mPFS) was 9.8 months in the EGFR L group, 8.9 months in the VEGF L group, 6.8 months in VEGF R group, and 5.8 months in EGFR R group. In patients with a RAS mutation, mOS was 25.4 months in the VEGF L group and 19.4 months in the VEGF R group (P=0.167). Judicious treatment allocation in Taiwanese patients with mCRC can result in an mOS of 34.3 months using cetuximab plus chemotherapy for left-sided tumors. An mOS of 48.5 months can be achieved using cetuximab plus chemotherapy in the neoadjuvant setting in mCRC patients with left-sided tumors. This study expands our understanding of the role of target therapy in improving survival of mCRC patients based on real-world study results.
C1 [Huang, Sheng-Chieh; Lin, Chun-Chi; Lin, Hung-Hsin; Chang, Shih-Ching; Lan, Yuan-Tzu; Wang, Huann-Sheng; Yang, Shung-Haur; Chen, Wei-Shone; Jiang, Jeng-Kai] Taipei Vet Gen Hosp, Dept Surg, Div Colon & Rectal Surg, Taipei, Taiwan.
   [Huang, Sheng-Chieh; Lin, Chun-Chi; Teng, Hao-Wei; Lin, Hung-Hsin; Chang, Shih-Ching; Lan, Yuan-Tzu; Wang, Huann-Sheng; Yang, Shung-Haur; Chen, Wei-Shone; Jiang, Jeng-Kai] Natl Yang Ming Univ, Sch Med, Taipei, Taiwan.
   [Teng, Hao-Wei] Taipei Vet Gen Hosp, Dept Oncol, Div Med Oncol, Taipei, Taiwan.
C3 Taipei Veterans General Hospital; National Yang Ming Chiao Tung
   University; Taipei Veterans General Hospital
RP Jiang, JK (corresponding author), Taipei Vet Gen Hosp, Dept Surg, Div Colon & Rectal Surg, Taipei, Taiwan.; Jiang, JK (corresponding author), Natl Yang Ming Univ, Sch Med, Taipei, Taiwan.
EM jkjiang@vghtpe.gov.tw
RI Chiang, Chi-Ling/O-3038-2016
OI Jiang, Jeng-Kai/0000-0001-8653-5476; Huang,
   Sheng-Chieh/0000-0003-2116-0989
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NR 20
TC 6
Z9 6
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 MAR 17
PY 2022
VL 12
AR 808808
DI 10.3389/fonc.2022.808808
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0H8CI
UT WOS:000778957400001
PM 35372058
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sandhu, J
   Lavingia, V
   Fakih, M
AF Sandhu, Jaideep
   Lavingia, Viraj
   Fakih, Marwan
TI Systemic treatment for metastatic colorectal cancer in the era of
   precision medicine
SO JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Review
DE biomarkers; chemotherapy; colorectal cancer; immunotherapy; targeted
   therapy
ID RANDOMIZED PHASE-III; KRAS WILD-TYPE; OXALIPLATIN-BASED CHEMOTHERAPY;
   UNRESECTABLE LIVER METASTASES; BEVACIZUMAB PLUS CAPECITABINE; 1ST-LINE
   TREATMENT; OPEN-LABEL; RAS MUTATIONS; COLON-CANCER; COMBINATION
   CHEMOTHERAPY
AB The treatment of metastatic colorectal cancer has evolved over the last two decades with the FDA approval of several cytotoxic, biological, and targeted agents. In this paper, we review the impact of sidedness, RAS, BRAF, HER-2, and other immune biomarkers on metastatic colorectal cancer treatment selection and sequencing in both the palliative and curative intent settings.
C1 [Sandhu, Jaideep] City Hope Natl Med Ctr, Natl Med Ctr, Dept Med Oncol, Duarte, CA USA.
   [Lavingia, Viraj] HCG Canc Ctr, Ahmadabad, Gujarat, India.
   [Fakih, Marwan] City Hope Natl Med Ctr, Comprehens Canc Ctr, Med Oncol & Therapeut Res, Briskin Ctr Clin Res,GI Med Oncol, Bldg 51,Room 112,1500E Duarte St, Duarte, CA 91010 USA.
C3 City of Hope; City of Hope
RP Fakih, M (corresponding author), City Hope Natl Med Ctr, Comprehens Canc Ctr, Med Oncol & Therapeut Res, Briskin Ctr Clin Res,GI Med Oncol, Bldg 51,Room 112,1500E Duarte St, Duarte, CA 91010 USA.
EM mfakih@coh.org
RI Sandhu, Jaideep/IZD-9934-2023
OI Fakih, Marwan/0000-0002-6554-5488; Sandhu, Jaideep/0000-0002-3165-6286;
   Lavingia, Viraj/0000-0003-1981-2693
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NR 130
TC 51
Z9 56
U1 0
U2 21
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-4790
EI 1096-9098
J9 J SURG ONCOL
JI J. Surg. Oncol.
PD APR
PY 2019
VL 119
IS 5
SI SI
BP 564
EP 582
DI 10.1002/jso.25421
PG 19
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA HP7SE
UT WOS:000461888500003
PM 30802315
DA 2025-01-04
ER

PT J
AU Jan, YH
   Tan, KT
   Chen, SJ
   Yip, TTC
   Lu, CT
   Lam, AKY
AF Jan, Yi-Hua
   Tan, Kien Thiam
   Chen, Shu-Jen
   Yip, Timothy Tak Chun
   Lu, Cu Tai
   Lam, Alfred King-Yin
TI Comprehensive assessment of actionable genomic alterations in primary
   colorectal carcinoma using targeted next-generation sequencing
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
ID CANCER; PD-1; BLOCKADE; TUMORS
AB Background The clinical utility of comprehensive genomic profiling (CGP) for guiding treatment has gradually become the standard-of-care procedure for colorectal carcinoma (CRC). Here, we comprehensively assess emerging targeted therapy biomarkers using CGP in primary CRC. Methods A total of 575 primary CRCs were sequenced by ACTOnco (R) assay for genomic alterations, tumour mutational burden (TMB), and microsatellite instability (MSI). Results Eighteen percent of patients were detected as MSI-High (MSI-H), and the remaining cases were classified as microsatellite stable (MSS). Driver mutation prevalence in MSS CRCs were APC (74%), TP53 (67%), KRAS (47%), PIK3CA (21%) and BRAF (13%). The median TMBs for MSI-H and MSS patients were 37.8 mutations per mega base (mut/Mb) and 3.9 mut/Mb, respectively. Forty-seven percent of MSI-H CRC harboured at least one loss-of-function mutations in genes that may hamper immune checkpoint blockade. Among MSS RAS/RAF wild-type CRCs, 59% had at least one actionable mutation that may compromise the efficacy of anti-EGFR therapy. For late-stage CRC, 51% of patients are eligible for standard care actionability and the remaining 49% could be enrolled in clinical trials with investigational drugs. Conclusions This study highlights the essential role of CGP for identifying rational targeted therapy options in CRC.
C1 [Jan, Yi-Hua; Tan, Kien Thiam; Chen, Shu-Jen] ACT Genom Co Ltd, Canc Genom, Taipei, Taiwan.
   [Yip, Timothy Tak Chun] ACT Genom Co Ltd, Med Sci, Hong Kong, Peoples R China.
   [Lu, Cu Tai] Gold Coast Univ Hosp, Dept Surg, Southport, Qld 4215, Australia.
   [Lam, Alfred King-Yin] Griffith Univ, Sch Med & Dent, Menzies Hlth Inst Queensland, Canc Mol Pathol, Gold Coast Campus, Gold Coast, Qld 4222, Australia.
   [Lam, Alfred King-Yin] Gold Coast Univ Hosp, Pathol Queensland, Southport, Qld 4215, Australia.
C3 Gold Coast University Hospital; Menzies Health Institute Queensland;
   Griffith University; Griffith University - Gold Coast Campus; Gold Coast
   University Hospital
RP Lam, AKY (corresponding author), Griffith Univ, Sch Med & Dent, Menzies Hlth Inst Queensland, Canc Mol Pathol, Gold Coast Campus, Gold Coast, Qld 4222, Australia.; Lam, AKY (corresponding author), Gold Coast Univ Hosp, Pathol Queensland, Southport, Qld 4215, Australia.
EM a.lam@griffith.edu.au
RI Lam, Alfred/C-1652-2008
OI Lam, Alfred/0000-0003-2771-564X
FU ELITE Research Grant Programme of Hong Kong Science & Technology Park;
   ACT Genomics, Co. Ltd.; CAUL
FX The study was supported by ELITE Research Grant Programme of Hong Kong
   Science & Technology Park and ACT Genomics, Co. Ltd. Open Access funding
   enabled and organized by CAUL and its Member Institutions.
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NR 28
TC 11
Z9 11
U1 0
U2 2
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD OCT 19
PY 2022
VL 127
IS 7
BP 1304
EP 1311
DI 10.1038/s41416-022-01913-4
EA JUL 2022
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4Y4JR
UT WOS:000826124000001
PM 35842545
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Ohhara, Y
   Fukuda, N
   Takeuchi, S
   Honma, R
   Shimizu, Y
   Kinoshita, I
   Dosaka-Akita, H
AF Ohhara, Yoshihito
   Fukuda, Naoki
   Takeuchi, Satoshi
   Honma, Rio
   Shimizu, Yasushi
   Kinoshita, Ichiro
   Dosaka-Akita, Hirotoshi
TI Role of targeted therapy in metastatic colorectal cancer
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Metastatic colorectal cancer; Aflibercept; Ramucirumab; Regorafenib;
   Cetuximab; Panitumumab; Targeted therapy; Bevacizumab
ID ENDOTHELIAL GROWTH-FACTOR; PHASE-III TRIAL; CETUXIMAB PLUS IRINOTECAN;
   WILD-TYPE KRAS; 1ST-LINE TREATMENT; OPEN-LABEL; RANDOMIZED PHASE-3;
   2ND-LINE TREATMENT; MONOCLONAL-ANTIBODY; RAS MUTATIONS
AB Colorectal cancer (CRC) is a significant cause of cancer-related morbidity and mortality all over the world. Improvements of cytotoxic and biologic agents have prolonged the survival in metastatic CRC (mCRC), with a median overall survival of approximately 2 years and more in the past two decades. The biologic agents that have proven clinical benefits in mCRC mainly target vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR). In particular, bevacizumab targeting VEGF and cetuximab and panitumumab targeting EGFR have demonstrated significant survival benefits in combination with cytotoxic chemotherapy in the first-line, second-line, or salvage setting. Aflibercept, ramucirumab, and regorafenib are also used in second-line or salvage therapy. Recent retrospective analyses have shown that KRAS or NRAS mutations were negative predictive markers for anti-EGFR therapy. Based on the evidence from large randomized clinical trials, personalized therapy is necessary for patients with mCRC according to their tumor biology and characteristics. The aim of this paper was to summarize the results of the major randomized clinical trials and highlight the benefits of the molecular targeted agents in patients with mCRC.
C1 [Ohhara, Yoshihito; Fukuda, Naoki; Takeuchi, Satoshi; Honma, Rio; Shimizu, Yasushi; Kinoshita, Ichiro; Dosaka-Akita, Hirotoshi] Hokkaido Univ, Grad Sch Med, Dept Med Oncol, Sapporo, Hokkaido 0608638, Japan.
C3 Hokkaido University
RP Ohhara, Y (corresponding author), Hokkaido Univ, Grad Sch Med, Dept Med Oncol, Kita Ku, North 15,West 7, Sapporo, Hokkaido 0608638, Japan.
EM yoshihito-ohhara@kkr-smc.com
RI Shimizu, Yasushi/D-8057-2012; Fukuda, Naoki/ABB-4440-2020; Akita,
   Hirotoshi/E-1356-2012
OI Shimizu, Yasushi/0000-0003-2624-4305; Fukuda, Naoki/0000-0002-5475-9309
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NR 96
TC 74
Z9 77
U1 0
U2 8
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD SEP 15
PY 2016
VL 8
IS 9
BP 642
EP 655
DI 10.4251/wjgo.v8.i9.642
PG 14
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA FE9TN
UT WOS:000408546200001
PM 27672422
OA Green Published, Green Submitted, hybrid
DA 2025-01-04
ER

PT J
AU Boileve, A
   Maillard, A
   Wagner, M
   Dromain, C
   Laurent, C
   Bierre, ED
   Le Sourd, S
   Audemar, F
   Ulusakarya, A
   Guerin-Meyer, V
   Smisth, D
   Pezzella, V
   De Baere, T
   Goere, D
   Gelli, M
   Taieb, J
   Boige, V
AF Boileve, Alice
   Maillard, Aline
   Wagner, Mathilde
   Dromain, Clarisse
   Laurent, Christophe
   Bierre, Eric Dupont
   Le Sourd, Samuel
   Audemar, Franck
   Ulusakarya, Ayhan
   Guerin-Meyer, Veronique
   Smisth, Denis
   Pezzella, Veronica
   De Baere, Thierry
   Goere, Diane
   Gelli, Maximiliano
   Taieb, Julien
   Boige, Valerie
TI Treatment intensification with hepatic arterial infusion chemotherapy in
   patients with liver-only colorectal metastases still unresectable after
   systemic induction chemotherapy - a randomized phase II study - SULTAN
   UCGI 30/PRODIGE 53 (NCT03164655)- study protocol
SO BMC CANCER
LA English
DT Article
DE Colorectal cancer; Liver metastases; Liver resection; Hepatic arterial
   infusion; Oxaliplatin; Randomized trial
ID QUALITY-OF-LIFE; INTRAARTERIAL FLOXURIDINE; FOLINIC ACID; CANCER;
   RESECTION; TRIAL; OXALIPLATIN; CARCINOMA; SURVIVAL; FLUOROURACIL
AB BackgroundApproximately 40% of colorectal cancer patients will develop colorectal liver metastases (CRLM). The most effective approach to increase long-term survival is CRLM complete resection. Unfortunately, only 10-15% of CRLM are initially considered resectable. The objective response rates (ORR) after current first-line systemic chemotherapy (sys-CT) regimens range from 40 to 80% and complete resection rates (CRR) range from 25 to 50% in patients with initially unresectable CRLM. When CRLM patients are not amenable to complete resection after induction of sys-CT, ORRs obtained with second-line sys-CT are much lower (between 10 and 30%) and consequently CRRs are also low (<10%). Hepatic arterial infusion (HAI) oxaliplatin may represent a salvage therapy in patients with CRLM unresectable after one or more sys-CT regimens with ORRs and CRRs up to 60 and 30%, respectively. This study is designed to evaluate the efficacy of an intensification strategy based on HAI oxaliplatin combined with sys-CT as a salvage treatment in patients with CRLM unresectable after at least 2 months of first-line induction sys-CT.Objectives and endpoints of the phase II studyOur main objective is to investigate the efficacy, in term of CRR (R0-R1), of treatment intensification in patients with liver-only CRLM not amenable to curative-intent resection (and/or ablation) after at least 2 months of induction sys-CT. Patients will receive either HAI oxaliplatin plus systemic FOLFIRI plus targeted therapy (i.e. anti-EGFR antibody or bevacizumab) or conventional sys-CT plus targeted therapy (i.e. anti-EGFR or antiangiogenic antibody). Secondary objectives are to compare: progression-free survival, overall survival, objective response rate, depth of response, feasibility of delivering HAI oxaliplatin including HAI catheter-related complications, and toxicity (NCI-CTCAE v4.0).MethodsThis study is a multicenter, randomized, comparative phase II trial (power, 80%; two-sided alpha-risk, 5%). Patients will be randomly assigned in a 1:1 ratio to receive HAI oxaliplatin combined with systemic FOLFIRI plus targeted therapy (experimental arm) or the best sys-CT plus targeted therapy on the basis of their first-line prior sys-CT history and current guidelines (control arm). One hundred forty patients are required to account for non-evaluable patients.Trial registrationClinicalTrials.gov, (NCT03164655). Trial registration date: 11th May 2017.
C1 [Boileve, Alice; Boige, Valerie] Gustave Roussy, Dept Med Oncol, 114 Rue Edouard Vaillant, F-94805 Villejuif, France.
   [Maillard, Aline] Dept Stat & Epidemiol, Villejuif, France.
   [Maillard, Aline] Paris Saclay Univ, INSERM U1018, Ctr Res Epidemiol & Populat Hlth Team 2, Villejuif, France.
   [Wagner, Mathilde] CHU Pitie Salpetriere, Dept Radiol, Paris, France.
   [Dromain, Clarisse] Ctr Hosp & Univ Vaudois, Dept Radiol, Lausanne, Switzerland.
   [Laurent, Christophe; Smisth, Denis] Hop Haut Leveque, Dept Hepatogastroenterol, Pessac, France.
   [Bierre, Eric Dupont] CHP St Gregoire, Dept Digest Surg, St Gregoire, France.
   [Le Sourd, Samuel] Ctr Eugene Marquis, Dept Med oncol, Rennes, France.
   [Audemar, Franck] Ctr Hosp Cote Basque, Dept Hepatogastroenterol, Bayonne, France.
   [Ulusakarya, Ayhan] Hop Paul Brousse, Dept Med Oncol, Villejuif, France.
   [Guerin-Meyer, Veronique] Inst Cancerol Ouest, Dept Med Oncol, Angers, France.
   [Pezzella, Veronica] R&D Unicancer, Paris, France.
   [De Baere, Thierry] Gustave Roussy, Dept Intervent Radiol, Villejuif, France.
   [Goere, Diane] Hop St Louis, Dept Surg Oncol, Paris, France.
   [Gelli, Maximiliano] Gustave Roussy, Dept Surg Oncol, Villejuif, France.
   [Taieb, Julien] Paris Descartes Univ, Sorbonne Paris Cite, Hop Europeen Georges Pompidou, Dept Digest Oncol, Paris, France.
C3 UNICANCER; Gustave Roussy; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Universite Paris Saclay; Sorbonne
   Universite; Assistance Publique Hopitaux Paris (APHP); Hopital
   Universitaire Pitie-Salpetriere - APHP; University of Lausanne; Centre
   Hospitalier Universitaire Vaudois (CHUV); CHU Bordeaux; Universite de
   Bordeaux; Universite de Rennes; UNICANCER; Centre Eugene Marquis;
   Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
   Paul-Brousse - APHP; UNICANCER; UNICANCER; Gustave Roussy; Universite
   Paris Cite; Assistance Publique Hopitaux Paris (APHP); Hopital
   Universitaire Saint-Louis - APHP; UNICANCER; Gustave Roussy; Universite
   Paris Cite; Assistance Publique Hopitaux Paris (APHP); Hopital
   Universitaire Europeen Georges-Pompidou - APHP
RP Boileve, A (corresponding author), Gustave Roussy, Dept Med Oncol, 114 Rue Edouard Vaillant, F-94805 Villejuif, France.
EM alice.boileve@gmail.com
RI Boilève, Alice/ABE-4470-2021; Gelli, Maximiliano/K-8340-2019
OI Boileve, Alice/0000-0003-3708-4909; Gelli,
   Maximiliano/0000-0001-9807-4021; , GOERE/0000-0001-6306-2354; taieb,
   julien/0000-0002-9955-4753; Wagner, Mathilde/0000-0003-1172-4592
FU National Institute of Cancer (INCa); UNICANCER; PRODIGE group
FX This study is financially supported by a governmental grant from the
   National Institute of Cancer (INCa). The authors declare that they have
   no competing interests relative to this study. The National Institute of
   Cancer (INCa) was not involved in the design of the study and
   collection, analysis, interpretation of data and in writing the
   manuscript.r This study is sponsored by UNICANCER and supported by
   PRODIGE group which regroup FFCD (Federation Francophone de Cancerologie
   Digestive), GERCOR (Groupe Cooperateur Multidisciplinaire en Oncologie)
   and UNICANCER gastrointestinal group.r The manuscript was peer reviewed
   by the funding body and the sponsor (UNICANCER).
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NR 39
TC 8
Z9 8
U1 0
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD JAN 30
PY 2020
VL 20
IS 1
AR 74
DI 10.1186/s12885-020-6571-7
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KV3UR
UT WOS:000520409000005
PM 32000724
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Börding, T
   Janik, T
   Bischoff, P
   Morkel, M
   Sers, C
   Horst, D
AF Boerding, Teresa
   Janik, Tobias
   Bischoff, Philip
   Morkel, Markus
   Sers, Christine
   Horst, David
TI GPA33 expression in colorectal cancer can be induced by WNT inhibition
   and targeted by cellular therapy
SO ONCOGENE
LA English
DT Article; Early Access
ID A33 ANTIGEN; MONOCLONAL-ANTIBODY; STEM-CELLS; CDX1; KRN330; TRIAL
AB GPA33 is a promising surface antigen for targeted therapy in colorectal cancer (CRC). It is expressed almost exclusively in CRC and intestinal epithelia. However, previous clinical studies have not achieved expected response rates. We investigated GPA33 expression and regulation in CRC and developed a GPA33-targeted cellular therapy. We examined GPA33 expression in CRC cohorts using immunohistochemistry and immunofluorescence. We analyzed GPA33 regulation by interference with oncogenic signaling in vitro and in vivo using inhibitors and conditional inducible regulators. Furthermore, we engineered anti-GPA33-CAR T cells and assessed their activity in vitro and in vivo. GPA33 expression showed consistent intratumoral heterogeneity in CRC with antigen loss at the infiltrative tumor edge. This pattern was preserved at metastatic sites. GPA33-positive cells had a differentiated phenotype and low WNT activity. Low GPA33 expression levels were linked to tumor progression in patients with CRC. Downregulation of WNT activity induced GPA33 expression in vitro and in GPA33-negative tumor cell subpopulations in xenografts. GPA33-CAR T cells were activated in response to GPA33 and reduced xenograft growth in mice after intratumoral application. GPA33-targeted therapy may be improved by simultaneous WNT inhibition to enhance GPA33 expression. Furthermore, GPA33 is a promising target for cellular immunotherapy in CRC.
C1 [Boerding, Teresa; Janik, Tobias; Bischoff, Philip; Morkel, Markus; Sers, Christine; Horst, David] Charite Univ Med Berlin, Berlin, Germany.
   [Boerding, Teresa; Janik, Tobias; Bischoff, Philip; Morkel, Markus; Sers, Christine; Horst, David] Free Univ Berlin, Berlin, Germany.
   [Boerding, Teresa; Janik, Tobias; Bischoff, Philip; Morkel, Markus; Sers, Christine; Horst, David] Humboldt Univ, Berlin, Germany.
   [Bischoff, Philip; Morkel, Markus; Sers, Christine; Horst, David] German Canc Res Ctr, German Canc Consortium DKTK, Partner Site Berlin, Heidelberg, Germany.
   [Bischoff, Philip] Charite Univ Med Berlin, Berlin Inst Hlth, BIH Biomed Innovat Acad, BIH Charite Clinician Scientist Program, 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; Helmholtz
   Association; German Cancer Research Center (DKFZ); Berlin Institute of
   Health; Free University of Berlin; Humboldt University of Berlin;
   Charite Universitatsmedizin Berlin
RP Horst, D (corresponding author), Charite Univ Med Berlin, Berlin, Germany.; Horst, D (corresponding author), Free Univ Berlin, Berlin, Germany.; Horst, D (corresponding author), Humboldt Univ, Berlin, Germany.; Horst, D (corresponding author), German Canc Res Ctr, German Canc Consortium DKTK, Partner Site Berlin, Heidelberg, Germany.
EM david.horst@charite.de
RI Bischoff, Philip/HHC-2955-2022; Morkel, Markus/HLQ-0079-2023
FU Wilhelm-Sander-Stiftung [2021.043.1]; Projekt DEAL
FX Funded in part by a grant from the Wilhelm-Sander-Stiftung (grant
   2021.043.1 to DH).Open Access funding enabled and organized by Projekt
   DEAL.
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NR 59
TC 0
Z9 0
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD 2024 OCT 29
PY 2024
DI 10.1038/s41388-024-03200-3
EA OCT 2024
PG 12
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 K6D0X
UT WOS:001344749500001
PM 39472498
DA 2025-01-04
ER

PT J
AU Biabangard, A
   Asoodeh, A
   Jaafari, MR
   Baigi, FM
AF Biabangard, Atefeh
   Asoodeh, Ahmad
   Jaafari, Mahmoud Reza
   Baigi, Fatemeh Moosavi
TI AR13 peptide-conjugated liposomes improve the antitumor efficacy of
   doxorubicin in mice bearing C26 colon carcinoma; <i>in silico</i>, <i>in
   vitro</i>, and in <i>vivo</i> study
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE AR13 peptide; Colon cancer; Drug delivery; PEGylated liposomal
   doxorubicin; Target therapy
ID DELIVERY; LESSONS; MUC1
AB Currently, liposomes have emerged as efficient and safer nano-carriers for targeted therapy in different cancers. This work aimed to employ PEGylated liposomal doxorubicin (Doxil (R)/PLD), modified with AR13 peptide, to target Muc1 on the surface of colon cancerous cells.
   We performed molecular docking and simulation studies (using Gromacs package) of AR13 peptide against Muc1 to analyze and visualize the peptide-Muc1 binding combination. For in vitro analysis, the AR13 peptide was post-inserted into Doxil (R) and verified by TLC, H-1 NMR, and HPLC techniques. The zeta potential, TEM, release, cell uptake, competition assay, and cytotoxicity studies were performed. In vivo antitumor activities and survival analysis on mice bearing C26 colon carcinoma were studied.
   Results showed that after 100 ns simulation, a stable complex between AR13 and Muc1 formed, and molecular dynamics analysis confirmed this interaction. In vitro analysis demonstrated significant enhancement of cellular binding and cell uptake.
   The results of in vivo study on BALB/c mice bearing C26 colon carcinoma, revealed an extended survival time to 44 days and higher tumor growth inhibition compared to Doxil (R). Thus, the AR13 peptide could be explored as a potent ligand for Muc1, improving therapeutic antitumor efficiency in colon cancer cells.
C1 [Biabangard, Atefeh; Asoodeh, Ahmad; Baigi, Fatemeh Moosavi] Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Iran.
   [Jaafari, Mahmoud Reza] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Nanotechnol Res Ctr, Sch Pharm, Mashhad, Iran.
   [Jaafari, Mahmoud Reza] Mashhad Univ Med Sci, Sch Pharm, Dept Pharmaceut Nanotechnol, Mashhad, Iran.
C3 Ferdowsi University Mashhad; Mashhad University of Medical Sciences;
   Mashhad University of Medical Sciences
RP Asoodeh, A (corresponding author), Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Iran.; Jaafari, MR (corresponding author), Mashhad Univ Med Sci, Pharmaceut Technol Inst, Nanotechnol Res Ctr, Sch Pharm, Mashhad, Iran.; Jaafari, MR (corresponding author), Mashhad Univ Med Sci, Sch Pharm, Dept Pharmaceut Nanotechnol, Mashhad, Iran.
EM asoodeh@um.ac.ir; jafarimr@mums.ac.ir
RI Asoodeh, Ahmad/H-1484-2011; Moosavi Baigi, Fatemeh/C-5676-2015
OI Moosavi Baigi, Fatemeh/0000-0001-9676-5881
FU Research and Technology Council of the Ferdowsi University of Mashhad,
   Mashhad-Iran [3/46317, 1396/12/22]
FX The authors appreciate the support provided by the Research and
   Technology Council of the Ferdowsi University of Mashhad, Mashhad-Iran
   (grant number: 3/46317, 1396/12/22).
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NR 57
TC 3
Z9 3
U1 1
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0041-008X
EI 1096-0333
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD MAY 1
PY 2023
VL 466
AR 116470
DI 10.1016/j.taap.2023.116470
EA MAR 2023
PG 10
WC Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Toxicology
GA D3NT3
UT WOS:000967833800001
PM 36933622
DA 2025-01-04
ER

PT J
AU Wang, D
   Wang, LW
   Zheng, LM
   Chen, JX
   Zhang, W
   Zhou, W
   Yang, XB
   Jiang, LF
   Jin, XQ
   Yu, XH
   Liu, X
   Chen, H
   Xu, JB
AF Wang, Di
   Wang, Liwei
   Zheng, Liming
   Chen, Jiaxin
   Zhang, Wei
   Zhou, Wei
   Yang, Xiaobo
   Jiang, Lifeng
   Jin, Xiaoqiang
   Yu, Xiaohua
   Liu, Xin
   Chen, Heng
   Xu, Jianbin
TI Enhancing the Management of Metastatic Tumors by Robust Co-Delivery of
   5-Fluorouracil/MicroRNA-10b Inhibitor Using EGFR-Targeted Nanovehicles
SO ADVANCED HEALTHCARE MATERIALS
LA English
DT Article
DE co-delivery; patient-derived xenograft model; targeted therapy; tumor
   metastasis
ID MICRORNA-B-10 PROMOTES MIGRATION; PATIENT-DERIVED XENOGRAFTS;
   COLORECTAL-CANCER; MEDIATED CODELIVERY; IN-VITRO; MODELS; NANOPARTICLES;
   MIR-B-10; THERAPY; DIFFERENTIATION
AB Invasion and metastasis are the leading causes of death of patients with CRC. 5-Fluorouracil is widely used in clinic practice as the basic chemotherapy drug for CRC. However, it is inefficient in inhibiting tumor metastasis. MicroRNA-10b is uninvolved in regulating the growth of primary tumors; however, it could induce early tumor metastases and is a key regulator of chemotherapeutic resistance to 5-FU. A multifunctional nanovehicle that can carry small molecule drugs not only through the hydrophobic pockets of conjugated beta-cyclodextrin but also through electrostatic interaction between the conjugated peptides and siRNA to target functional genes is previously developed. In this study, a nanovehicle, named GCD, with epithelium growth factor receptor (EGFR)-targeted characteristics to simultaneously deliver chemotherapeutic and nucleotide drugs to distinct targets in CRC, is employed. These data show that co-delivery of 5-FU and anti-miR-10b can be effectively applied to targeted therapy of EGFR-overexpressed CRC, particularly inhibiting the metastasis of CRC. Furthermore, the therapeutic effect of this combination on tumor xenograft models derived from patients with CRC is evaluated. Taken together, this study may provide insights into the inhibition of tumor growth and metastasis simultaneously.
C1 [Wang, Di; Wang, Liwei; Zheng, Liming; Chen, Jiaxin; Yang, Xiaobo; Jiang, Lifeng; Jin, Xiaoqiang; Yu, Xiaohua; Xu, Jianbin] Zhejiang Univ, Affiliated Hosp 2, Sch Med, Dept Orthoped Surg, Hangzhou 310000, Zhejiang, Peoples R China.
   [Wang, Di; Wang, Liwei; Zheng, Liming; Chen, Jiaxin; Yang, Xiaobo; Jiang, Lifeng; Jin, Xiaoqiang; Yu, Xiaohua; Xu, Jianbin] Zhejiang Univ, Orthoped Res Inst, Hangzhou 310000, Zhejiang, Peoples R China.
   [Wang, Di; Wang, Liwei; Zheng, Liming; Chen, Jiaxin; Yang, Xiaobo; Jiang, Lifeng; Jin, Xiaoqiang; Yu, Xiaohua; Xu, Jianbin] Key Lab Motor Syst Dis Res & Precis Therapy Zhejia, Hangzhou 310000, Zhejiang, Peoples R China.
   [Wang, Di; Wang, Liwei; Zheng, Liming; Chen, Jiaxin; Yang, Xiaobo; Jiang, Lifeng; Jin, Xiaoqiang; Yu, Xiaohua; Xu, Jianbin] Zhejiang Univ, Affiliated Hosp 2, Clin Res Ctr Motor Syst Dis Zhejiang Prov, Sch Med, Hangzhou 310000, Zhejiang, Peoples R China.
   [Zhang, Wei; Zhou, Wei] Zhejiang Univ, Sir Run Run Shaw Hosp, Dept Colorectal Surg, Sch Med, Hangzhou 310000, Zhejiang, Peoples R China.
   [Liu, Xin] Zhejiang Univ, Sir Run Run Shaw Hosp, Sch Med, Dept Orthopaed Surg, Hangzhou 310000, Zhejiang, Peoples R China.
   [Chen, Heng] Dongguan Univ Technol, Sch Mat Sci & Engn, Dongguan 523000, Guangdong, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang University; Zhejiang
   University; Zhejiang University; Dongguan University of Technology
RP Xu, JB (corresponding author), Zhejiang Univ, Affiliated Hosp 2, Sch Med, Dept Orthoped Surg, Hangzhou 310000, Zhejiang, Peoples R China.; Liu, X (corresponding author), Zhejiang Univ, Sir Run Run Shaw Hosp, Sch Med, Dept Orthopaed Surg, Hangzhou 310000, Zhejiang, Peoples R China.; Chen, H (corresponding author), Dongguan Univ Technol, Sch Mat Sci & Engn, Dongguan 523000, Guangdong, Peoples R China.
EM xinliuzju@zju.edu.cn; hchen@dgut.edu.cn; xu9709426@zju.edu.cn
RI zheng, liming/GWV-7646-2022; Yu, Xiaohua/J-9903-2014; Yang,
   Xiaobo/AAD-6333-2019; Xu, Jianbin/ISB-4232-2023
OI Zheng, Liming/0000-0002-7939-2152; Xu, Jianbin/0000-0003-0505-2160
FU National Natural Science Foundation of China [32071349, 81701820,
   52103059, 52003234]; Zhejiang Provincial Natural Science Foundation of
   China [LY20H180014, LQ21E030007]; Department of Health of Zhejiang
   Province [2018PY025]; Guangdong Basic and Applied Basic Research
   Foundation [2019A1515110433]; Shenzhen Science and Technology Planning
   Project [JCYJ20190808123207674]; China Postdoctoral Science Foundation
   [2022M722769]
FX Acknowledgements D.W. and L.W. contributed equally to this work. This
   work was supported by the National Natural Science Foundation of China
   (Grant Nos. 32071349, 81701820, 52103059, and 52003234), the Zhejiang
   Provincial Natural Science Foundation of China (Grant No. LY20H180014
   and LQ21E030007), the Department of Health of Zhejiang Province (Grant
   No. 2018PY025), the Guangdong Basic and Applied Basic Research
   Foundation (Grant No. 2019A1515110433), the Shenzhen Science and
   Technology Planning Project (Grant No. JCYJ20190808123207674). This work
   was funded by the China Postdoctoral Science Foundation (Grant No.
   2022M722769).
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NR 49
TC 1
Z9 2
U1 10
U2 26
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 JUN
PY 2023
VL 12
IS 15
DI 10.1002/adhm.202202989
EA FEB 2023
PG 14
WC Engineering, Biomedical; Nanoscience & Nanotechnology; Materials
   Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Science & Technology - Other Topics; Materials Science
GA J4FH9
UT WOS:000935131500001
PM 36740892
DA 2025-01-04
ER

PT J
AU Gulbake, A
   Jain, A
   Jain, A
   Jain, A
   Jain, SK
AF Gulbake, Arvind
   Jain, Aviral
   Jain, Ashish
   Jain, Ankit
   Jain, Sanjay K.
TI Insight to drug delivery aspects for colorectal cancer
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Colorectal cancer; Receptor based targeted therapy; Gene delivery
ID CARCINOEMBRYONIC ANTIGEN CEA; MONOCLONAL-ANTIBODY THERAPY; COLON-CANCER;
   GENE-THERAPY; ADJUVANT THERAPY; INTERFERON-ALPHA; TUMOR-CELLS;
   INCORPORATED NANOPARTICLES; INHIBITS ANGIOGENESIS; INTERLEUKIN-2 GENE
AB Colorectal cancer (CRC) is the third most common cancer diagnosed worldwide in human beings. Surgery, chemotherapy, radiotherapy and targeted therapies are the conventional four approaches which are currently used for the treatment of CRC. The site specific delivery of chemotherapeutics to their site of action would increase effectiveness with reducing side effects. Targeted oral drug delivery systems based on polysaccharides are being investigated to target and deliver chemotherapeutic and chemopreventive agents directly to colon and rectum. Site-specific drug delivery to colon increases its concentration at the target site, and thus requires a lower dose and hence abridged side effects. Some novel therapies are also briefly discussed in article such as receptor (epidermal growth factor receptor, folate receptor, wheat germ agglutinin, VEGF receptor, hyaluronic acid receptor) based targeting therapy; colon targeted proapoptotic anticancer drug delivery system, gene therapy. Even though good treatment options are available for CRC, the ultimate therapeutic approach is to avert the incidence of CRC. It was also found that CRCs could be prevented by diet and nutrition such as calcium, vitamin D, curcumin, quercetin and fish oil supplements. Immunotherapy and vaccination are used nowadays which are showing better results against CRC.
C1 [Gulbake, Arvind] DY Patil Univ, Ctr Interdisciplinary Res, Kolhapur 416006, Maharashtra, India.
   [Jain, Aviral] Ravishankar Coll Pharm, Dept Pharmaceut, Pharmaceut Res Lab, Bhopal 462010, Madhya Pradesh, India.
   [Jain, Ashish; Jain, Ankit; Jain, Sanjay K.] Dr Hari Singh Gour Cent Univ, Dept Pharmaceut Sci, Pharmaceut Res Projects Lab, Sagar 470003, Madhya Pradesh, India.
C3 Dr. Hari Singh Gour University
RP Jain, SK (corresponding author), Dr Hari Singh Gour Cent Univ, Dept Pharmaceut Sci, Pharmaceut Res Projects Lab, Sagar 470003, Madhya Pradesh, India.
EM drskjainin@yahoo.com
RI Jain, Siddharth/AFQ-0482-2022; Gulbake, Arvind/A-2115-2016; Jain,
   Ankit/P-8023-2018
OI Jain, Sanjay K/0000-0002-9241-3114; Gulbake, Arvind/0000-0001-7425-8125;
   Jain, Aviral/0000-0001-7808-6180; Jain, Ankit/0000-0001-8131-1860
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NR 154
TC 108
Z9 121
U1 2
U2 62
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 JAN 14
PY 2016
VL 22
IS 2
BP 582
EP 599
DI 10.3748/wjg.v22.i2.582
PG 18
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DA4YC
UT WOS:000367807700010
PM 26811609
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Sun, GC
   Yang, X
   Yu, Y
   Zhao, DW
AF Sun, Guang-Chun
   Yang, Xu
   Yu, Yan
   Zhao, Dai-Wei
TI The Applications of Targeting Anti-Cancer Agents in Cancer Therapeutics
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Article
DE Angiogenesis; cancer; combination therapy; signaling pathway; target
   therapy; tyrosine kinase
ID CELL LUNG-CANCER; EPIDERMAL-GROWTH-FACTOR; PHASE-II TRIAL; TYROSINE
   KINASE INHIBITORS; METASTATIC COLORECTAL-CANCER; CHRONIC
   MYELOID-LEUKEMIA; NON-HODGKINS-LYMPHOMA; QUALITY-OF-LIFE; FACTOR
   RECEPTOR; TRASTUZUMAB EMTANSINE
AB Anti-cancer targeting drugs appear to be a new and powerful "weapon" for cancer therapies. These targeting drugs are directed against specific molecules that are over-expressed or where certain unique factors are aberrantly expressed either in cancer cells or in diseased cell sites. Compared with traditional chemotherapeutic drugs, these targeting drugs have the advantages of high specificity, efficacy and less side effects. Target therapy is a breakthrough and revolutionary advance in the field of cancer therapy. Tumor angiogenesis plays a key role in tumor growth and metastasis and the mutation of tyrosine kinases is also strongly associated with cancer progression. Thus, in this review, we will discuss the advances in the development of targeting anti-cancer drugs by narrowing it down to small molecule tyrosine kinase inhibitors, monoclonal antibodies against epidermal growth factor receptors belonging to the ErbB family of receptor tyrosine kinases and angiogenic inhibitors. It will also address concerns for drug resistance and adverse events.
C1 [Sun, Guang-Chun; Yang, Xu; Yu, Yan] Fudan Univ, Peoples Hosp Shanghai 5, Dept Pharm, Shanghai 200240, Peoples R China.
   [Zhao, Dai-Wei] Guiyang Med Univ, Affiliated Hosp 2, Dept Surg, Kaili 556000, Peoples R China.
C3 Fudan University; Guizhou Medical University
RP Sun, GC (corresponding author), Fudan Univ, Peoples Hosp Shanghai 5, Dept Pharm, 801 He Qing Rd, Shanghai 200240, Peoples R China.
EM sunguangchun@5thhospital.com
FU Shanghai Committee of Science and Technology, China [14411972700]
FX The authors gratefully acknowledge the grant supported from the Shanghai
   Committee of Science and Technology, China (Grant No. 14411972700).
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NR 159
TC 6
Z9 7
U1 0
U2 13
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 2015
VL 15
IS 7
BP 869
EP 880
DI 10.2174/1871520615666150318101845
PG 12
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA CM8GW
UT WOS:000357937900007
PM 25783965
DA 2025-01-04
ER

PT J
AU Liang, GZ
   Wen, XF
   Song, YW
   Zhang, ZJ
   Chen, J
   Chen, YL
   Pan, WD
   He, XW
   Hu, T
   Xian, ZY
AF Liang, Guan-Zhan
   Wen, Xiao-Feng
   Song, Yi-Wen
   Zhang, Zong-Jin
   Chen, Jing
   Chen, Yong-Le
   Pan, Wei-Dong
   He, Xiao-Wen
   Hu, Tuo
   Xian, Zhen-Yu
TI Construction and Validation of a Novel Prognosis Model in Colon Cancer
   Based on Cuproptosis-Related Long Non-Coding RNAs
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE colon cancer; cuproptosis; long non-coding RNA; prognosis model;
   targeted therapy
ID COLORECTAL-CANCER; LNCRNA SIGNATURE; GENOME INSTABILITY; CELL-DEATH;
   SURVIVAL; IMMUNOTHERAPY; RECOMMENDATIONS; IDENTIFICATION; FERROPTOSIS;
   STATISTICS
AB Colon cancer (CC) is one of the most common (6%) malignancies and leading cause of cancer-associated death (more than 0.5 million) worldwide, which demands reliable prognostic biomarkers. Cuproptosis is a novel modality of regulated cell death triggered by the accumulation of intracellular copper. LncRNAs have been reported as prognostic signatures in different types of tumors. However, the correlation between cuproptosis-related lncRNAs (CRLs) and CC remains unclear. Data of CC patients were downloaded from public databases. The prognosis-associated CRLs were identified by co-expression analysis and univariate Cox. Least absolute shrinkage and selection operator were utilized to construct the CRLs-based prognostic signature in silico for CC patients. CRLs level was validated in human CC cell lines and patient tissues. ROC curve and Kaplan-Meier curve results revealed that high CRLs-risk score was associated with poor prognosis in CC patients. Moreover, the nomogram revealed that this model possessed a steady prognostic prediction capability with C-index as 0.68. More importantly, CC patients with high CRLs-risk score were more sensitive to eight targeted therapy drugs. The prognostic prediction power of the CRLs-risk score was further confirmed by cell lines, tissues and two independent CC cohorts. This study constructed a novel ten-CRLs-based prognosis model for CC patients. The CRLs-risk score is expected to serve as a promising prognostic biomarker and predict targeted therapy response in CC patients.
C1 [Liang, Guan-Zhan; Wen, Xiao-Feng; Zhang, Zong-Jin; Chen, Jing; Chen, Yong-Le; He, Xiao-Wen; Hu, Tuo; Xian, Zhen-Yu] Sun Yat Sen Univ, Affiliated Hosp 6, Dept Colorectal Surg, Dept Gen Surg,Guangdong Prov Key Lab Colorectal &, Guangzhou 510655, Peoples R China.
   [Song, Yi-Wen] Sun Yat Sen Univ, Affiliated Hosp 6, Dept Radiotherapy, Guangzhou 510655, Peoples R China.
   [Pan, Wei-Dong] Sun Yat Sen Univ, Affiliated Hosp 6, Dept Pancreat Hepatobiliary Surg, Dept Gen Surg, Guangzhou 510655, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University
RP Hu, T; Xian, ZY (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 6, Dept Colorectal Surg, Dept Gen Surg,Guangdong Prov Key Lab Colorectal &, Guangzhou 510655, Peoples R China.
EM hutuo3@mail.sysu.edu.cn; xianzhy@mail2.sysu.edu.cn
RI He, XW/JXN-0620-2024; Hu, Tuo/HDM-3005-2022; Zhang,
   Haiqing/KHU-5808-2024
OI Pan, Weidong/0000-0001-9519-7683; Hu, Tuo/0000-0001-7069-1466
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NR 67
TC 3
Z9 3
U1 4
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD FEB
PY 2023
VL 12
IS 4
AR 1528
DI 10.3390/jcm12041528
PG 18
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 9H2RN
UT WOS:000938684500001
PM 36836069
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU La Salvia, A
   Lopez-Gomez, V
   Garcia-Carbonero, R
AF La Salvia, Anna
   Lopez-Gomez, Victoria
   Garcia-Carbonero, Rocio
TI HER2-targeted therapy: an emerging strategy in advanced colorectal
   cancer
SO EXPERT OPINION ON INVESTIGATIONAL DRUGS
LA English
DT Article
DE Colorectal cancer; HER2 amplification; overexpression; mutation;
   personalized therapy; prognostic and predictive biomarker; EGFR
   resistance; mAbs
ID EGFR MONOCLONAL-ANTIBODIES; METASTATIC BREAST-CANCER; GENE
   AMPLIFICATION; TARGETED THERAPY; SOLID TUMORS; OPEN-LABEL; PHASE-I;
   HER2; OVEREXPRESSION; PROTEIN
AB Introduction: Colorectal cancer (CRC) is one of the most common malignant tumors; it is a focus of research globally, but the identification of clinically actionable oncogenic drivers remains elusive. Human epidermal growth factor receptor 2 (HER2) activation is present in approximately 5% of CRC and has acquired resistance to epidermal growth factor receptor (EGFR)-targeted therapy. Early clinical trials suggest an emerging role for personalized HER2-targeted therapy in a subset of metastatic CRC. Areas covered: This manuscript reviews the relevance of HER2 activation in CRC and its potential role as a target for therapy. A literature search was conducted in June 2018 of MEDLINE and EMBASE databases for published preclinical and clinical studies; abstracts of international cancer meetings (AACR, ASCO, and ESMO) were also reviewed. Expert opinion: HER2 is activated in a small but relevant proportion of CRC patients (particularly left-side, RAS wild-type, anti-EGFR resistant tumors). Dual HER2 blockade with monoclonal antibodies (mAbs) (trastuzumab and pertuzumab) or the combination of mAbs with tyrosine kinase inhibitors (trastuzumab and lapatinib) induces durable tumor responses in about one-third of HER2-positive CRC refractory to standard systemic therapy. Although immature, these results are remarkable and anticipate an expanding role for HER2 as a therapeutic target in CRC.
C1 [La Salvia, Anna; Lopez-Gomez, Victoria; Garcia-Carbonero, Rocio] Hosp Univ 12 Octubre, Oncol Dept, Madrid, Spain.
   [La Salvia, Anna] San Luigi Gonzaga Hosp, Oncol Dept, Orbassano, Italy.
   [Garcia-Carbonero, Rocio] UCM, Inst Invest Sanitaria Hosp 12 Octubre Imas12, Oncol Dept, CNIO,CIBERONC, Madrid, Spain.
C3 Hospital Universitario 12 de Octubre; Azienda Ospedaliero-Universitaria
   San Luigi Gonzaga; Centro Nacional de Investigaciones Oncologicas
   (CNIO); CIBER - Centro de Investigacion Biomedica en Red; CIBERONC;
   Complutense University of Madrid
RP Garcia-Carbonero, R (corresponding author), Hosp Univ 12 Octubre, Dept Med Oncol, Ave Cordoba Km 5-4, Madrid 28041, Spain.
EM rgcarbonero@gmail.com
RI La Salvia, Anna/C-6248-2019
OI LA SALVIA, ANNA/0000-0002-5020-8657; Garcia-Carbonero,
   Rocio/0000-0002-3342-397X
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NR 62
TC 30
Z9 33
U1 0
U2 9
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1354-3784
EI 1744-7658
J9 EXPERT OPIN INV DRUG
JI Expert Opin. Investig. Drugs
PD JAN 2
PY 2019
VL 28
IS 1
BP 29
EP 38
DI 10.1080/13543784.2019.1555583
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA HD8YR
UT WOS:000452847500004
PM 30513002
DA 2025-01-04
ER

PT J
AU Zheng, YL
   Cao, YQ
   Liu, JH
   Chen, H
   Peng, LM
AF Zheng, Yanling
   Cao, Yongqing
   Liu, Jiheng
   Chen, Hui
   Peng, Liming
TI Artificial Intelligence-Based Dynamic Contrast-Enhanced Magnetic
   Resonance Imaging for Quantitative Evaluation of the Efficacy of
   Targeted Therapy for Liver Metastasis from Colon Cancer and Nursing
SO SCIENTIFIC PROGRAMMING
LA English
DT Article
ID RESPONSE EVALUATION; NEURAL-NETWORKS; DCE-MRI
AB The purpose of this study was to quantitatively evaluate the targeted treatment and nursing effect of patients with liver metastasis of colon cancer by enhanced magnetic resonance imaging. First, Dynamic Contrast-Enhanced Magnetic Resonance Imaging (DCE-MRI) images were restored. 35 patients with liver metastases from colon cancer were selected as research subjects and treated by bevacizumab, and high-quality nursing methods were used to improve the psychophysiology of the patients. Enhanced CT examination and DCE-MRI scan were performed before and after the treatment. After the image was processed by the artificial intelligence algorithm, apparent diffusion coefficient (ADC), measurement transmission constant (Ktrans), reflux constant (Kep), extravascular extracellular volume fraction (Ve), and other data on the image were recorded. Two months after the treatment, 35 patients were divided into effective and ineffective groups. It was found that, after treatment, the Kep value and Ktrans value of the effective group were significantly reduced, showing statistically significant differences, and the P value was less than 0.05, and the Kep value and Ktrans value of the ineffective group showed no significant changes. The Ve value of the two groups gradually decreased with the progress of the treatment. In the effective group, the Ve values before the treatment, on the third day after the treatment, and on the seventh day after treatment were (0.235 +/- 0.134), (0.338 +/- 0.116), and (0.457 +/- 0.097), respectively. Compared with the Ve values of the ineffective group, there was a statistical difference, F =3.592, P = 0.0245; the ADC value was negatively correlated with the Ktrans and Kep values, and the results were statistically significant. It was concluded that the above indicators are effective in evaluating the efficacy of the targeted therapy of liver metastasis from colon cancer, and DCE-MRI is of great significance in predicting the efficacy of targeted therapy of liver metastasis from colon cancer.
C1 [Zheng, Yanling; Cao, Yongqing; Liu, Jiheng; Chen, Hui] Changsha First Hosp, Dept Hematol & Oncol, Changsha 410005, Peoples R China.
   [Peng, Liming] Changsha First Hosp, Dept Nursing, Changsha 410005, Peoples R China.
RP Peng, LM (corresponding author), Changsha First Hosp, Dept Nursing, Changsha 410005, Peoples R China.
EM zhengyanlingmds@yeah.net; caoyongqingzyh@163.com; liujihenglxb@126.com;
   chenhuiqeea@yeah.net; 1132037@mail.dhu.edu.cn
RI Peng, Liming/I-5030-2013
FU Scientific Research Projects of Hunan Health Commission [20200216]
FX This work was supported by Scientific Research Projects of Hunan Health
   Commission (Project no. 20200216).
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NR 20
TC 0
Z9 0
U1 0
U2 3
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1058-9244
EI 1875-919X
J9 SCI PROGRAMMING-NETH
JI Sci. Program.
PD AUG 29
PY 2021
VL 2021
AR 8734108
DI 10.1155/2021/8734108
PG 7
WC Computer Science, Software Engineering
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Computer Science
GA UL9BM
UT WOS:000692938200005
OA gold
DA 2025-01-04
ER

PT J
AU Sharma, R
   Kumar, S
   Kaushik, N
   Singh, B
AF Sharma, Raja
   Kumar, Satendra
   Kaushik, Niranjan
   Singh, Bahadur
TI Decoding the Mystery of Blood Cancer: Cause, Diagnosis, and Management
SO CURRENT CANCER THERAPY REVIEWS
LA English
DT Review
DE Blood cancer; leukemia; lymphoma; myeloma; genetics; environmental
   factors; medical conditions; symptoms; diagnosis; staging; chemotherapy;
   radiation therapy; stem cell transplant; targeted therapy;
   immunotherapy; supportive care; research; clinical trials; personalized
   medicine; emotional impact; psychological impact
ID QUALITY-OF-LIFE; STEM-CELL TRANSPLANTATION; CHRONIC MYELOID-LEUKEMIA;
   SIOP WORKING COMMITTEE; PHASE-II; PSYCHOSOCIAL ISSUES;
   COLORECTAL-CANCER; TARGETED THERAPY; PROSTATE-CANCER; ALL-CAUSE
AB Leukaemia, lymphoma, and myeloma are among the serious and frequently fatal conditions that impact thousands of people each year. Genetics, environmental factors, and medical problems can all affect the risk of developing blood cancer, however, the precise causes are still not entirely known. Fatigue, unexpected weight loss, and frequent infections are examples of common blood cancer symptoms. In the course of the diagnosis process, blood tests, imaging tests, and bone marrow biopsies are frequently combined. Blood cancer therapies include chemotherapy, radiation therapy, stem cell transplant, targeted therapy, and immunotherapy. Supportive care is also important for managing symptoms and improving quality of life. Ongoing research is exploring new treatments and therapies for blood cancer, as well as ways to improve supportive care and personalize treatment plans. Blood cancer patients and their families have severe emotional and psychological effects that must not be ignored. For improving outcomes and raising the general standard of living for people affected by this condition, it is essential to address these needs.
C1 [Sharma, Raja; Kumar, Satendra; Kaushik, Niranjan; Singh, Bahadur] Galgotias Univ, Sch Med & Allied Sci, Dept Pharm, Gautam Budh Nagar 201310, UP, India.
C3 Galgotias University
RP Kumar, S (corresponding author), Galgotias Univ, Sch Med & Allied Sci, Dept Pharm, Gautam Budh Nagar 201310, UP, India.
EM satendrakumarmaheshwaree@gmail.com
RI KUMAR, SATENDRA/KXS-1771-2024
FX Declared none.
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NR 101
TC 0
Z9 0
U1 0
U2 0
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1573-3947
EI 1875-6301
J9 CURR CANCER THER REV
JI Curr. Cancer Ther. Rev.
PY 2025
VL 21
IS 1
BP 40
EP 53
DI 10.2174/0115733947263279231114111550
EA AUG 2024
PG 14
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA M2V7W
UT WOS:001301853100001
DA 2025-01-04
ER

PT J
AU Ulrich-Pur, H
AF Ulrich-Pur, Herbert
TI New targets in metastatic colorectal cancer
SO MEMO-MAGAZINE OF EUROPEAN MEDICAL ONCOLOGY
LA English
DT Review
DE Metastatic Colorectal Cancer; Targeted Therapy; Therapeutic Options
ID 1ST-LINE TREATMENT; FLUOROURACIL; OXALIPLATIN; BEVACIZUMAB; LEUCOVORIN;
   FOLFIRI
AB At the moment, targeted therapy in metastatic colorectal cancer (mCRC) is a hot topic which is widely discussed in the scientific community. Approximately 25 % of all CRC patients present with metastases at the time of initial diagnosis, and an additional 50 % of them will develop metastases during the subsequent course of their disease, contributing to the high mortality rates reported. Novel targeted agents like monoclonal antibodies directed against vascular endothelial growth factors or against epidermal growth factor receptor combined with chemotherapy as well as multikinase inhibitors (in the salvage setting) have demonstrated to result in improved therapeutic outcome in patients with mCRC. Recent research efforts have focused to define patient subpopulations, who benefit most from the respective treatments. KRAS mutations in codons 12 and 13 are found in approximately 40 % of all patients with mCRC. These clinicopathologic characteristics generate consecutive activation of the mitogen-activated protein kinase pathway. Less frequent activating KRAS mutations occur in codons 61 and 146, and there are the NRAS mutations in codons 12, 13, and 61. The gene expression profiles of the RAS genes help to define those patients who are most likely to benefit from certain biological agents. This review discusses the therapeutic options based on recent publications.
C1 [Ulrich-Pur, Herbert] LKH Wiener Neustadt, Interne Abt, Corvinusring 3-5, A-2700 Wiener Neustadt, Austria.
RP Ulrich-Pur, H (corresponding author), LKH Wiener Neustadt, Interne Abt, Corvinusring 3-5, A-2700 Wiener Neustadt, Austria.
EM herbert.ulrichpur@yahoo.de
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NR 15
TC 0
Z9 0
U1 0
U2 0
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 JUN
PY 2015
VL 8
IS 2
BP 101
EP 104
DI 10.1007/s12254-014-0191-3
PG 4
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA V5I6U
UT WOS:000219643100005
DA 2025-01-04
ER

PT J
AU Chen, WZ
   Tong, KH
   Yu, JR
AF Chen, Wenzhong
   Tong, Kehui
   Yu, Jiren
TI MicroRNA-130a is upregulated in colorectal cancer and promotes cell
   growth and motility by directly targeting forkhead box F2
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article
DE microRNA-130a; colorectal cancer; growth; motility; forkhead box F2;
   microRNA-based targeted therapy
ID MIR-130A; PROLIFERATION; MIGRATION; INVASION; EXPRESSION; PATHWAYS;
   ONCOMIRS; ACTS
AB Colorectal cancer (CRC) is one of the most prevalent cancers among males and females worldwide. Despite progress in diagnostic and therapeutic strategies for CRC patients, the prognosis for patients with advanced CRC remains poor. MicroRNAs (miRNAs/miRs) are a class of highly conserved short, endogenously expressed and single-stranded non-coding RNAs. In recent years, increasing studies have demonstrated that dysregulation of miRNAs is closely associated with CRC carcinogenesis and progression. The aim of the present study was to explore the expression, roles and underlying molecular mechanism of miR-130a in CRC. The results indicated that miR-130a was significantly upregulated in CRC, and that miR-130a expression levels were correlated with TNM stage and lymph node metastasis of CRC. Inhibition of miR-130a markedly suppressed colorectal cancer cell proliferation, migration and invasion. Furthermore, forkhead box F2 (FOXF2) was identified as a direct downstream target gene of miR-130a in colorectal cancer. Downregulation of FOXF2 could partially reverse the functions induced by miR-130a under-expression in CRC cells. These findings suggested that miR-130a can regulate FOXF2 and function as an oncogene in CRC. Therefore, miR-130a may serve as a useful therapeutic agent for miRNA-based CRC targeted therapy.
C1 [Chen, Wenzhong; Yu, Jiren] Zhejiang Univ, Affiliated Hosp 1, Dept Gastroenterol Surg, 79 Qingchun Rd, Hangzhou 310009, Zhejiang, Peoples R China.
   [Chen, Wenzhong; Tong, Kehui] Ningbo Univ, Sch Med, Yinzhou Hosp, Dept Gastrointestinal Surg, Ningbo 315040, Zhejiang, Peoples R China.
C3 Zhejiang University; Ningbo University
RP Yu, JR (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Dept Gastroenterol Surg, 79 Qingchun Rd, Hangzhou 310009, Zhejiang, Peoples R China.
EM zhejiang_jirenyu@163.com
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NR 33
TC 20
Z9 22
U1 0
U2 3
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 OCT
PY 2017
VL 16
IS 4
BP 5241
EP 5248
DI 10.3892/mmr.2017.7257
PG 8
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA FG9JA
UT WOS:000410753800204
PM 28849155
OA Green Submitted, Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Kassouf, E
   Tabchi, S
   Tehfe, M
AF Kassouf, Elie
   Tabchi, Samer
   Tehfe, Mustapha
TI Anti-EGFR Therapy for Metastatic Colorectal Cancer in the Era of
   Extended RAS Gene Mutational Analysis
SO BIODRUGS
LA English
DT Review
ID PHASE-III TRIAL; CETUXIMAB PLUS IRINOTECAN; KRAS WILD-TYPE; 1ST-LINE
   TREATMENT; BRAF MUTATION; TARGETED THERAPY; COLON-CANCER; OPEN-LABEL;
   OXALIPLATIN; FLUOROURACIL
AB Colorectal cancer (CRC) is one of the leading causes of cancer-related mortality worldwide. In the past 2 decades, advances in cancer therapeutics allowed for a remarkable improvement in terms of survival for patients with metastatic CRC. The advent of targeted therapy, coupled with more efficient chemotherapy regimens, was the pillar achievement that contributed to the success of CRC therapy. Cetuximab and panitumumab, monoclonal antibodies targeting the epidermal growth factor receptor pathway, are the focus of this review since their mechanism of action and efficiency are closely related to the mutational status of a predictive biomarker, the Kristen rat Sarcoma viral oncogene (KRAS). More recently, another biomarker, the neuroblastoma rat sarcoma viral oncogene (NRAS), was found to be as valuable for the refinement of this targeted therapy. The arguments for the use of extended analysis of the RAS gene are thoroughly reviewed because they directly affect the choice of targeted agents and potentially the choice of backbone chemotherapy.
C1 [Kassouf, Elie; Tabchi, Samer; Tehfe, Mustapha] Ctr Hosp Univ Montreal, Hop Notre Dame, Dept Hematol Oncol, Hematol Oncol Div, 1560 Sherbrooke St East, Montreal, PQ H2L 4M1, Canada.
C3 Universite de Montreal
RP Tehfe, M (corresponding author), Ctr Hosp Univ Montreal, Hop Notre Dame, Dept Hematol Oncol, Hematol Oncol Div, 1560 Sherbrooke St East, Montreal, PQ H2L 4M1, Canada.
EM matohfe@gmail.com
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NR 45
TC 6
Z9 6
U1 0
U2 11
PU ADIS INT LTD
PI NORTHCOTE
PA 5 THE WAREHOUSE WAY, NORTHCOTE 0627, AUCKLAND, NEW ZEALAND
SN 1173-8804
EI 1179-190X
J9 BIODRUGS
JI Biodrugs
PD APR
PY 2016
VL 30
IS 2
BP 95
EP 104
DI 10.1007/s40259-016-0166-5
PG 10
WC Oncology; Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology; Pharmacology & Pharmacy
GA DM6ZG
UT WOS:000376501000004
PM 26927802
DA 2025-01-04
ER

PT J
AU Peters, NA
   Constantinides, A
   Ubink, I
   van Kuik, J
   Bloemendal, HJ
   van Dodewaard, JM
   Brink, MA
   Schwartz, TP
   Lolkema, MPJK
   Lacle, MM
   Moons, LM
   Geesing, J
   van Grevenstein, WMU
   Roodhart, JML
   Koopman, M
   Elias, SG
   Rinkes, IHMB
   Kranenburg, O
AF Peters, Niek A.
   Constantinides, Alexander
   Ubink, Inge
   van Kuik, Joyce
   Bloemendal, Haiko J.
   van Dodewaard, Joyce M.
   Brink, Menno A.
   Schwartz, Thijs P.
   Lolkema, Martijn P. J. K.
   Lacle, Miangela M.
   Moons, Leon M.
   Geesing, Joost
   van Grevenstein, Wilhelmina M. U.
   Roodhart, Jeanine M. L.
   Koopman, Miriam
   Elias, Sjoerd G.
   Rinkes, Inne H. M. Borel
   Kranenburg, Onno
TI Consensus molecular subtype 4 (CMS4)-targeted therapy in primary colon
   cancer: A proof-of-concept study
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; consensus molecular subtype 4; imatinib; ImPACCT;
   platelet-derived growth factor receptor (PDGFR)
ID COLORECTAL-CANCER; POOR-PROGNOSIS; EXPRESSION; GROWTH; COMBINATION;
   METASTASIS; IMATINIB; CELLS; MTOR; PROLIFERATION
AB BackgroundMesenchymal Consensus Molecular Subtype 4 (CMS4) colon cancer is associated with poor prognosis and therapy resistance. In this proof-of-concept study, we assessed whether a rationally chosen drug could mitigate the distinguishing molecular features of primary CMS4 colon cancer. MethodsIn the ImPACCT trial, informed consent was obtained for molecular subtyping at initial diagnosis of colon cancer using a validated RT-qPCR CMS4-test on three biopsies per tumor (Phase-1, n=69 patients), and for neoadjuvant CMS4-targeting therapy with imatinib (Phase-2, n=5). Pre- and post-treatment tumor biopsies were analyzed by RNA-sequencing and immunohistochemistry. Imatinib-induced gene expression changes were associated with molecular subtypes and survival in an independent cohort of 3232 primary colon cancer. ResultsThe CMS4-test classified 52/172 biopsies as CMS4 (30%). Five patients consented to imatinib treatment prior to surgery, yielding 15 pre- and 15 post-treatment samples for molecular analysis. Imatinib treatment caused significant suppression of mesenchymal genes and upregulation of genes encoding epithelial junctions. The gene expression changes induced by imatinib were associated with improved survival and a shift from CMS4 to CMS2. ConclusionImatinib may have value as a CMS-switching drug in primary colon cancer and induces a gene expression program that is associated with improved survival.
C1 [Peters, Niek A.; Constantinides, Alexander; Ubink, Inge; Roodhart, Jeanine M. L.; Rinkes, Inne H. M. Borel; Kranenburg, Onno] Univ Utrecht, Univ Med Ctr Utrecht, Div Imaging & Canc, Lab Translat Oncol, Utrecht, Netherlands.
   [van Kuik, Joyce; Lacle, Miangela M.] Univ Utrecht, Univ Med Ctr Utrecht, Dept Pathol, Utrecht, Netherlands.
   [Bloemendal, Haiko J.; van Dodewaard, Joyce M.] Meander Med Ctr, Dept Internal Med, Amersfoort, Netherlands.
   [Bloemendal, Haiko J.] Radboud Univ Nijmegen, Dept Internal Med Oncol, Med Ctr Nijmegen, Nijmegen, Netherlands.
   [Brink, Menno A.; Schwartz, Thijs P.] Meander Med Ctr, Dept Gastroenterol, Amersfoort, Netherlands.
   [Lolkema, Martijn P. J. K.] Erasmus MC, Dept Med Oncol, Rotterdam, Netherlands.
   [Moons, Leon M.] Univ Utrecht, Univ Med Ctr Utrecht, Dept Gastroenterol, Utrecht, Netherlands.
   [Geesing, Joost] Diakonessen Hosp, Dept Gastroenterol, Utrecht, Netherlands.
   [van Grevenstein, Wilhelmina M. U.; Rinkes, Inne H. M. Borel] Univ Utrecht, Univ Med Ctr Utrecht, Dept Surg Oncol, Div Imaging & Canc, Utrecht, Netherlands.
   [Roodhart, Jeanine M. L.; Koopman, Miriam] Univ Utrecht, Univ Med Ctr Utrecht, Dept Med Oncol, Utrecht, Netherlands.
   [Elias, Sjoerd G.] Univ Utrecht, Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
C3 Utrecht University; Utrecht University Medical Center; Utrecht
   University; Utrecht University Medical Center; Meander Medisch Centrum;
   Radboud University Nijmegen; Meander Medisch Centrum; Erasmus University
   Rotterdam; Erasmus MC; Utrecht University; Utrecht University Medical
   Center; Diakonessenhuis; Utrecht University; Utrecht University Medical
   Center; Utrecht University; Utrecht University Medical Center; Utrecht
   University; Utrecht University Medical Center
RP Rinkes, IHMB; Kranenburg, O (corresponding author), Univ Utrecht, Univ Med Ctr Utrecht, Div Imaging & Canc, Lab Translat Oncol, Utrecht, Netherlands.; Rinkes, IHMB (corresponding author), Univ Utrecht, Univ Med Ctr Utrecht, Dept Surg Oncol, Div Imaging & Canc, Utrecht, Netherlands.
EM i.h.m.borelrinkes@umcutrecht.nl; o.kranenburg@umcutrechl.nl
RI Constantinides, Alexander/M-6788-2019; Elias, Sjoerd/E-6057-2011;
   Lolkema, M.P./AAE-2906-2019
FU Dutch Cancer Society [UU-2014-6617]; ZonMw [95104001]
FX This work was supported by grants from the Dutch Cancer Society
   (UU-2014-6617 to IU) and ZonMw (95104001).
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NR 53
TC 15
Z9 15
U1 0
U2 2
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 6
PY 2022
VL 12
AR 969855
DI 10.3389/fonc.2022.969855
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4W4DR
UT WOS:000860116000001
PM 36147916
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hainsworth, JD
   Meric-Bernstam, F
   Swanton, C
   Hurwitz, H
   Spigel, DR
   Sweeney, C
   Burris, H
   Bose, R
   Yoo, B
   Stein, A
   Beattie, M
   Kurzrock, R
AF Hainsworth, John D.
   Meric-Bernstam, Funda
   Swanton, Charles
   Hurwitz, Herbert
   Spigel, David R.
   Sweeney, Christopher
   Burris, Howard
   Bose, Ron
   Yoo, Bongin
   Stein, Alisha
   Beattie, Mary
   Kurzrock, Razelle
TI Targeted Therapy for Advanced Solid Tumors on the Basis of Molecular
   Profiles: Results From MyPathway, an Open-Label, Phase IIa Multiple
   Basket Study
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; CELL LUNG-CANCER; BRAF V600E MUTATION;
   THYROID-CARCINOMA; HER2 EXPRESSION; AMPLIFICATION; VEMURAFENIB; TRIAL;
   GENE; OVEREXPRESSION
AB PurposeDetection of specific molecular alterations in tumors guides the selection of effective targeted treatment of patients with several types of cancer. These molecular alterations may occur in other tumor types for which the efficacy of targeted therapy remains unclear. The MyPathway study evaluates the efficacy and safety of selected targeted therapies in tumor types that harbor relevant genetic alterations but are outside of current labeling for these treatments.MethodsMyPathway (ClinicalTrials.gov identifier: NCT02091141) is a multicenter, nonrandomized, phase IIa multiple basket study. Patients with advanced refractory solid tumors harboring molecular alterations in human epidermal growth factor receptor-2, epidermal growth factor receptor, v-raf murine sarcoma viral oncogene homolog B1, or the Hedgehog pathway are treated with pertuzumab plus trastuzumab, erlotinib, vemurafenib, or vismodegib, respectively. The primary end point is investigator-assessed objective response rate within each tumor-pathway cohort.ResultsBetween April 1, 2014 and November 1, 2016, 251 patients with 35 different tumor types received study treatment. The efficacy population contains 230 treated patients who were evaluated for response or discontinued treatment before evaluation. Fifty-two patients (23%) with 14 different tumor types had objective responses (complete, n = 4; partial, n = 48). Tumor-pathway cohorts with notable objective response rates included human epidermal growth factor receptor-2-amplified/overexpressing colorectal (38% [14 of 37]; 95% CI, 23% to 55%) and v-raf murine sarcoma viral oncogene homolog B1 V600-mutated non-small-cell lung cancer (43% [six of 14]; 95% CI, 18% to 71%).ConclusionThe four currently approved targeted therapy regimens in the MyPathway study produced meaningful responses when administered without chemotherapy in several refractory solid tumor types not currently labeled for these agents.
C1 [Hainsworth, John D.; Spigel, David R.; Burris, Howard] Sarah Cannon Res Inst, 1100 Charlotte Ave,Suite 800, Nashville, TN 37203 USA.
   [Hainsworth, John D.; Spigel, David R.; Burris, Howard] Tennessee Oncol, Nashville, TN USA.
   [Meric-Bernstam, Funda] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Swanton, Charles] Francis Crick Inst, London, England.
   [Hurwitz, Herbert] Duke Univ, Med Ctr, Durham, NC USA.
   [Sweeney, Christopher] Harvard Med Sch, Dana Farber Canc Inst, Boston, MA USA.
   [Bose, Ron] Washington Univ, Sch Med, St Louis, MO USA.
   [Yoo, Bongin; Stein, Alisha; Beattie, Mary] Genentech Inc, San Francisco, CA 94080 USA.
   [Kurzrock, Razelle] Univ Calif San Diego, Moores Canc Ctr, San Diego, CA 92103 USA.
C3 Sarah Cannon Research Institute; Tennessee Oncology; University of Texas
   System; UTMD Anderson Cancer Center; Francis Crick Institute; Duke
   University; Harvard University; Dana-Farber Cancer Institute; Harvard
   Medical School; Washington University (WUSTL); Roche Holding; Genentech;
   University of California System; University of California San Diego
RP Hainsworth, JD (corresponding author), Sarah Cannon Res Inst, 1100 Charlotte Ave,Suite 800, Nashville, TN 37203 USA.
EM john.hainsworth@scresearch.net
RI Kurzrock, Razelle/AAU-9782-2020; Meric-Bernstam, Funda/JRZ-1866-2023;
   Swanton, Charles/AEY-0113-2022
OI Swanton, Charles/0000-0002-4299-3018
FU Roche/Genentech
FX The MyPathway study was supported by Roche/Genentech.
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NR 36
TC 343
Z9 359
U1 2
U2 37
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 FEB 20
PY 2018
VL 36
IS 6
BP 536
EP +
DI 10.1200/JCO.2017.75.3780
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FW6OF
UT WOS:000425437100005
PM 29320312
OA Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Passo, MD
   de Carvalho, GGC
AF Passo, Matheus dos Santos
   de Carvalho, Guilherme Graziany Camelo
TI In silico evaluation of potential drugs for the treatment of Colorectal
   Carcinoma
SO BRAZILIAN JOURNAL OF PHARMACEUTICAL SCIENCES
LA English
DT Article
DE Molecular Targeted Therapy; Colorectal Neoplasms; Anti Cancer Drug
   Screens; Antineoplastic Agents
ID CDC25B PHOSPHATASE; CIRCULAR RNA; CANCER; DISRUPTION; TOOLS
AB To evaluate possible new drugs for the treatment of Colorectal Carcinoma (CRC) using in silico tools was the main objective of this study. The method of analysis used was the in silico evaluation of tumor markers and their interaction with selected drugs, through the study of its pharmacokinetic and pharmacodynamic characteristics. A potential therapeutic target pointed out in this study was the Cell Division Cycle 25 B (CDC25B), belonging to the CDC25 phosphatase family. Overexpression of CDC25 phosphatases is often associated with a wide variety of cancers. In addition, CDC25B is an oncogenic protein that induces neoplastic transformation. In CRC, CDC25B is overexpressed to activate the CDC2/cyclin B complex and improve the growth and survival of these tumors. Four drugs were identified for evaluation, with alpha-amyrin being selected for docking, because it was that had the best characteristics according to the methodology used. The alpha-amyrin ligand obtained the interaction energy value of-7.6 G (Kcal/mol), while the standard CDC25B ligand obtained-10.0 G (Kcal/mol). TThe results showed that the CDC25B protein was the only structure cocrystallized with alpha-amyrin and presented favorable outcomes in docking, being a candidate for further studies for its use in the CRC targeted therapy.
C1 [Passo, Matheus dos Santos; de Carvalho, Guilherme Graziany Camelo] Univ Fed Maranhao, Social Sci Hlth & Technol Ctr, Med Sch, Imperatriz, MA, Brazil.
   [Passo, Matheus dos Santos] Univ Fed Maranhao, Unidade Avancada Bom Jesus, Coordenacao Curso Med, Av Univ S-N, BR-65915240 Imperatriz, MA, Brazil.
C3 Universidade Federal do Maranhao; Universidade Federal do Maranhao
RP Passo, MD (corresponding author), Univ Fed Maranhao, Unidade Avancada Bom Jesus, Coordenacao Curso Med, Av Univ S-N, BR-65915240 Imperatriz, MA, Brazil.
EM matheuspasso@hotmail.com
OI Carvalho, Guilherme/0000-0003-3994-9902
CR Arnold D, 2010, GUT, V59, P838, DOI 10.1136/gut.2009.196006
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NR 33
TC 0
Z9 0
U1 1
U2 3
PU UNIV SAO PAULO, CONJUNTO QUIMICAS
PI SAO PAULO
PA SERVICO PUBLICACOES E CIRCULACAO, CAIXA POSTAL 66083, SAO PAULO, 00000,
   BRAZIL
SN 1984-8250
EI 2175-9790
J9 BRAZ J PHARM SCI
JI Braz. J. Pharm. Sci.
PY 2022
VL 58
AR e20343
DI 10.1590/s2175-97902022e20343
PG 27
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 8J1JU
UT WOS:000922180400001
OA gold
DA 2025-01-04
ER

PT J
AU Zhang, YM
   Chen, ZY
   Li, J
AF Zhang, Yumei
   Chen, Zhiyu
   Li, Jin
TI The current status of treatment for colorectal cancer in China A
   systematic review
SO MEDICINE
LA English
DT Review
DE chemotherapy; colorectal cancer; maintenance therapy; radiotherapy;
   targeted therapy
ID ADVANCED RECTAL-CANCER; COMPLETE MESOCOLIC EXCISION; RANDOMIZED
   CONTROLLED-TRIAL; OPEN-LABEL; NEOADJUVANT CHEMOTHERAPY; MAINTENANCE
   THERAPY; 1ST-LINE TREATMENT; NON-INFERIORITY; OPEN SURGERY; DOUBLE-BLIND
AB Background: Colorectal cancer (CRC) is one of the most common cancers all over the world, but its epidemiology is obviously different in various regions.
   Methods: The treatment of CRC also has varying characteristics due to differences in economy, geography, disease onset, chemotherapy, and other factors, although international guidelines are used to guide the treatment of CRC in China.
   Results: This paper summarizes the current status of CRC treatment, including surgical therapy, neoadjuvant radiotherapy and chemotherapy, postoperative chemotherapy, targeted therapy, maintenance therapy, and immunotherapy, according to the clinical situation in China, so as to provide better therapy and improve clinical practice for patients with CRC.
   Conclusion: This research shows that the treatment of colorectal cancer continues to progress, and the patient's efficacy and quality of life have improved.
C1 [Zhang, Yumei; Li, Jin] Tongji Univ, Dept VIP Clin, South Branch, Shanghai East Hosp, Shanghai, Peoples R China.
   [Chen, Zhiyu] Fudan Univ, Dept Med Oncol, Shanghai Canc Ctr, Shanghai Med Coll, Shanghai, Peoples R China.
   [Li, Jin] Tongji Univ, Shanghai East Hosp, Dept Oncol, Shanghai, Peoples R China.
C3 Tongji University; Fudan University; Tongji University
RP Li, J (corresponding author), 150 Jimo Rd Pudong Dist, Shanghai 200120, Peoples R China.
EM tianyoulijin@163.com
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NR 63
TC 111
Z9 126
U1 0
U2 43
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 OCT
PY 2017
VL 96
IS 40
AR e8242
DI 10.1097/MD.0000000000008242
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA FO3UP
UT WOS:000416760800034
PM 28984783
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Bhattacharya, S
AF Bhattacharya, Sankha
TI An empirical review on the resistance mechanisms of epidermal growth
   factor receptor inhibitors and predictive molecular biomarkers in
   colorectal cancer
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Metastatic colorectal cancer (mCRC); K-Ras; Epidermal growth factor
   receptor (EGFR); Prognostic markers; Molecular markers;
   Mitogen-activated protein kinase (MAPK)
ID COLON-CANCER; TARGETED THERAPY; MUTATIONS; CELLS; KRAS; DNA;
   ADENOCARCINOMA; MANAGEMENT; EFFICACY; PATHWAY
AB Despite advances in cytotoxic treatments, colorectal cancer remains a leading cause of death. Metastatic colo -rectal cancer (mCRC) patients have a poor prognosis despite improved treatments and more prolonged median survival. Monoclonal antibodies like cetuximab and panitumumab target the epidermal growth factor receptor (EGFR). They play an essential role in the treatment of metastatic colorectal cancer (mCRC) due to their efficacy in multiple phase III clinical trials across multiple treatment lines. It was discovered that anti-EGFR moAbs were only effective for a small number of patients. Mutations in KRAS and NRAS have been identified as biomarkers of drug resistance. New molecular predictors and prognostic markers are used clinically. The K-Ras mutation is the first molecular marker of a lack of response to EGFR-targeted therapy in K-Ras-mutant patients. Validating predictive and prognostic markers will improve cancer treatments. This article examines molecular markers that can predict colorectal cancer prognosis.
C1 [Bhattacharya, Sankha] SVKMS NMIMS Deemed Univ, Sch Pharm & Technol Management, Dept Pharmaceut, Shirpur 425405, Maharashtra, India.
   [Bhattacharya, Sankha] SVKMS NMIMS Deemed Univ, Sch Pharm & Technol Management, Shirpur 425405, Maharashtra, India.
C3 SVKM's NMIMS (Deemed to be University); SVKM's NMIMS (Deemed to be
   University)
RP Bhattacharya, S (corresponding author), SVKMS NMIMS Deemed Univ, Sch Pharm & Technol Management, Shirpur 425405, Maharashtra, India.
EM sankhabhatt@gmail.com
RI Bhattacharya, Sankha/AAM-5111-2020
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   Zhou X, 2022, CANCER CELL INT, V22, DOI 10.1186/s12935-022-02478-1
NR 116
TC 7
Z9 7
U1 5
U2 17
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 MAR
PY 2023
VL 183
AR 103916
DI 10.1016/j.critrevonc.2023.103916
EA FEB 2023
PG 18
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA H0WV4
UT WOS:000993259900001
PM 36717006
DA 2025-01-04
ER

PT J
AU Ren, WQ
   Chen, H
   Huang, YJ
   Zuo, JQ
   Shu, XY
   Shu, P
AF Ren, Wenqin
   Chen, Hao
   Huang, Yujie
   Zuo, Jiaqian
   Shu, Xinyan
   Shu, Peng
TI The impact of different treatments on thromboelastography and other
   conventional parameters in patients with colorectal cancer
SO DISCOVER ONCOLOGY
LA English
DT Article
DE Colorectal cancer; Chemotherapy; Targeted therapy; Thromboelastography;
   Conventional coagulation parameters
ID BEVACIZUMAB
AB ObjectiveTo comprehend the effects of diverse therapeutic interventions on thromboelastography (TEG) and conventional coagulation parameters among individuals diagnosed with colorectal cancer, this study aims to explore the clinical relevance of both thromboelastography and conventional coagulation metrics in evaluating coagulation function and predicting the incidence of thrombotic and hemorrhagic events in patients with colorectal cancer.MethodsA cohort of 122 patients with colorectal cancer retrospectively recruited and divided into 2 groups: those undergoing surgical intervention (operation group) and those not subjected to surgery (non-operation group). According to the different types of treatment they received, the operation group was divided into chemotherapy-only group and a group receiving a combination of targeted therapy and chemotherapy. Blood samples were collected on admission and subjected to coagulation parameter assessment, including conventional coagulation tests and thromboelastography (TEG) assessment. Receiver operating characteristic (ROC) analysis was performed to predict the occurrence of complications in patients with colorectal cancer.ResultsCompared with the operation group, the non-operation group showed significant reductions in reaction time(R-time) and kinetics time (K-time), and significant elevation in angle, maximum amplitude (MA), fibrinogen and platelets. Patients receiving targeted therapy and chemotherapy had lower angle and maximum amplitude and higher R-time and K-time, activated partial thromboplastin time and fibrinogen. The area under the curve for TEG in patients without treatment was 0.802. The area under the curve for TEG and conventional coagulation parameters were 0.654 and 0.660 respectively.ConclusionDiverse treatments distinctly impact on the coagulation indicators of individuals diagnosed with colorectal cancer. The coagulation parameters observed in patients prior to operation suggest a hypercoagulable state. Nevertheless, following postoperative chemotherapy and targeted therapy, this hypercoagulable state demonstrates a notable improvement, occasionally leading to a propensity for hypocoagulation. The findings of this investigation underscore the unique clinical importance of thromboelastography (TEG) alongside traditional coagulation parameters, demonstrating that these diagnostic tools possess complementary value and cannot be substituted interchangeably.
C1 [Ren, Wenqin; Huang, Yujie; Zuo, Jiaqian; Shu, Xinyan] Nanjing Univ Chinese Med, Nanjing 210029, Jiangsu, Peoples R China.
   [Chen, Hao] Nanjing Univ Chinese Med, Jiangsu Prov Hosp Chinese Med, Dept Clin Lab, Affiliated Hosp, Nanjing 210029, Jiangsu, Peoples R China.
   [Shu, Peng] Nanjing Univ Chinese Med, Jiangsu Prov Hosp Chinese Med, Dept Oncol, Affiliated Hosp, Nanjing 210029, Jiangsu, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University of Chinese
   Medicine; Nanjing University of Chinese Medicine
RP Shu, P (corresponding author), Nanjing Univ Chinese Med, Jiangsu Prov Hosp Chinese Med, Dept Oncol, Affiliated Hosp, Nanjing 210029, Jiangsu, Peoples R China.
EM shupengnjucm@163.com
RI 舒, 鹏/HKD-9622-2023
CR Ades S, 2015, J THROMB HAEMOST, V13, P998, DOI 10.1111/jth.12910
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NR 23
TC 0
Z9 0
U1 0
U2 0
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 DEC 4
PY 2024
VL 15
IS 1
AR 748
DI 10.1007/s12672-024-01311-7
PG 9
WC Oncology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Endocrinology & Metabolism
GA O7A1E
UT WOS:001372599700005
PM 39633024
OA gold
DA 2025-01-04
ER

PT J
AU Qiu, TZ
   Chen, WS
   Li, P
   Sun, J
   Gu, YH
   Chen, XF
AF Qiu, Tianzhu
   Chen, Wensen
   Li, Ping
   Sun, Jing
   Gu, Yanhong
   Chen, Xiaofeng
TI Subsequent anti-VEGF therapy after first-line anti-EGFR therapy improved
   overall survival of patients with metastatic colorectal cancer
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE metastatic colorectal cancer; targeted therapy; overall survival
ID MUTATION STATUS; PLUS CETUXIMAB; RAS MUTATIONS; OPEN-LABEL; PHASE-III;
   BEVACIZUMAB; TRIAL; FLUOROURACIL; CHEMOTHERAPY; OXALIPLATIN
AB Colorectal cancer is one of the leading causes of cancer deaths worldwide. Due to targeted therapy, overall survival (OS) of metastatic colorectal cancer (mCRC) patients has been significantly increased over the past decade. However, the best sequencing of the therapeutic agents to be used in RAS wild-type subgroup is still under research. To determine the efficacy of targeted therapy, we collected randomized controlled trials which included patients receiving anti-epidermal growth factor receptor (EGFR) monoclonal antibody as first-line therapy in RAS/KRAS wild-type mCRC. In our study, we found that OS was significantly improved by anti-vascular endothelial growth factor (VEGF) agent after first-line anti-EGFR therapy. Our results revealed that it is a sensible treatment strategy to try anti-VEGF agent after first-line combination therapy with anti-EGFR monoclonal antibody for RAS/KRAS wild-type mCRC.
C1 [Qiu, Tianzhu; Li, Ping; Sun, Jing; Gu, Yanhong; Chen, Xiaofeng] Nanjing Med Univ, Dept Oncol, Affiliated Hosp 1, 300 Guangzhou Rd, Nanjing 210029, Jiangsu, Peoples R China.
   [Chen, Wensen] Nanjing Med Univ, Infect Management Off, Affiliated Hosp 1, Nanjing, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University
RP Gu, YH; Chen, XF (corresponding author), Nanjing Med Univ, Dept Oncol, Affiliated Hosp 1, 300 Guangzhou Rd, Nanjing 210029, Jiangsu, Peoples R China.
EM guluer@163.com; chenxiaofengnjmu@163.com
RI Shen, Yuchen/AAO-4015-2020
OI , Jing/0000-0003-4715-208X
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NR 25
TC 5
Z9 8
U1 0
U2 7
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 465
EP 471
DI 10.2147/OTT.S149110
PG 7
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA FU0LR
UT WOS:000423542900001
PM 29403291
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Benavides, M
   Gómez-España, A
   García-Alfonso, P
   González, CG
   Viéitez, JM
   Rivera, F
   Safont, MJ
   Abad, A
   Sastre, J
   Valladares-Ayerbes, M
   Carrato, A
   González-Flores, E
   Robles, L
   Salud, A
   Alonso-Orduña, V
   Montagut, C
   Asensio, E
   Díaz-Rubio, E
   Aranda, E
AF Benavides, Manuel
   Gomez-Espana, Auxiliadora
   Garcia-Alfonso, Pilar
   Garcia Gonzalez, Cristina
   Maria Vieitez, Jose
   Rivera, Fernando
   Jose Safont, Maria
   Abad, Albert
   Sastre, Javier
   Valladares-Ayerbes, Manuel
   Carrato, Alfredo
   Gonzalez-Flores, Encarnacion
   Robles, Luis
   Salud, Antonieta
   Alonso-Orduna, Vicente
   Montagut, Clara
   Asensio, Elena
   Diaz-Rubio, Eduardo
   Aranda, Enrique
CA Spanish Cooperative Grp Treatment
TI Upfront primary tumour resection and survival in synchronous metastatic
   colorectal cancer according to primary tumour location and RAS status:
   Pooled analysis of the Spanish Cooperative Group for the Treatment of
   Digestive Tumours (TTD)
SO EJSO
LA English
DT Article
DE Upfront primary tumour resection; Sidedness; RAS; Targeted therapy;
   Synchronous unresectable metastasis; Retrospective
ID UNRESECTABLE METASTASES; COLON-CANCER; LIVER METASTASES; PROGNOSTIC
   VALUE; PHASE-III; THERAPY; METAANALYSIS; MULTICENTER; BEVACIZUMAB;
   GUIDELINES
AB Introduction: Retrospective studies and meta-analyses suggest that upfront primary tumour resection (UPTR) confers a survival benefit in patients with asymptomatic unresectable metastatic colorectal cancer (mCRC) undergoing chemotherapy, however a consensus of its role in routine clinical practice in the current era of targeted therapies is lacking. This retrospective study aimed to analyse the survival benefit of UPTR in terms of tumour location and mutational status, in patients with synchronous mCRC receiving chemotherapy and targeted therapy.
   Patients and methods: Survival was analysed in a pooled cohort of synchronous mCRC patients treated with a first-line anti-VEGF or anti-EGFR inhibitor in seven trials of the Spanish TTD group, according to UPTR, tumour-sidedness and mutational profiling.
   Results: Of 1334 eligible patients, 642 (48%) had undergone UPTR. UPTR was associated with significantly longer overall survival (OS; 25.0 vs 20.3 months; HR 1.30, 95%CI 1.15-1.48; p < 0.0001). UPTR was associated with significant OS benefit in both left-sided (HR 1.38, 95%CI 1.13-1.69; p = 0.002) and right-sided (HR 1.39, 95%CI 1.00-1.94; p = 0.049) tumours, RASwt (HR 1.29, 95%CI 1.05-1.60; p = 0.016) and BRAFwt (HR 1.49, 95%CI 1.21-1.84; p = 0.0002) tumours, and treatment with anti-EGFRs (HR 1.47, 95%CI 1.13-1.92; p = 0.004) and anti-VEGFs (HR 1.25, 95%CI 1.08-1.44; p = 0.003). Multivariate analysis identified number of metastatic sites, RAS status, primary tumour location and UPTR as independent prognostic factors for OS.
   Conclusion: Considering the selection bias inherent to this study, our results support UPTR before first-line anti-EGFR or anti-VEGF targeted therapy in right and left-sided asymptomatic unresectable synchronous mCRC patients. RAS/BRAF mutational status may also influence UPTR function. (C) 2021 Elsevier Ltd, BASO - The Association for Cancer Surgery, and the European Society of Surgical Oncology. All rights reserved.
C1 [Benavides, Manuel; Garcia Gonzalez, Cristina] Hosp Univ Reg & Virgen de la Victoria, UGC Interctr Oncol Med, IBIMA, Ave Carlos Haya S-N, Malaga 29010, Spain.
   [Gomez-Espana, Auxiliadora; Aranda, Enrique] Univ Cordoba, Hosp Univ Reina Sofia, Inst Salud Carlos III, Dept Med Oncol,IMIBIC,CIBERONC, Cordoba, Spain.
   [Garcia-Alfonso, Pilar] Hosp Univ Gregorio Maranon, Dept Med Oncol, Madrid, Spain.
   [Maria Vieitez, Jose] Hosp Univ Cent Asturias, Dept Med Oncol, Oviedo, Spain.
   [Rivera, Fernando] Univ Hosp Marques de Valdecilla, Dept Med Oncol, IDIVAL, Santander, Spain.
   [Maria Vieitez, Jose] Univ Valencia, CIBERONC, Hosp Gen Univ Valencia, Dept Med Oncol, Valencia, Spain.
   [Abad, Albert] Inst Oncol Dr Rosell, Dept Med Oncol, Barcelona, Spain.
   [Sastre, Javier; Diaz-Rubio, Eduardo] Univ Complutense, CIBERONC, Inst Invest Hosp Clin San Carlos IdISSC, Dept Med Oncol,Hosp Clin San Carlos, Madrid, Spain.
   [Valladares-Ayerbes, Manuel] Hosp Virgen del Rocio, IBIS, Dept Med Oncol, Seville, Spain.
   [Carrato, Alfredo] Alcala Univ, Hosp Univ Ramon y Cajal, IRYCIS, Dept Med Oncol,CIBERONC, Madrid, Spain.
   [Gonzalez-Flores, Encarnacion] Hosp Virgen de las Nieves, Dept Med Oncol, Granada, Spain.
   [Robles, Luis] Hosp 12 Octubre, Dept Med Oncol, Madrid, Spain.
   [Salud, Antonieta] Hosp Lleida Arnau de Vilanova, Dept Med Oncol, Lerida, Spain.
   [Alonso-Orduna, Vicente] Hosp Univ Miguel Servet, IISA, Dept Med Oncol, Zaragoza, Spain.
   [Montagut, Clara] Hosp del Mar, Med Res Inst, CIBERONC, Dept Med Oncol, Barcelona, Spain.
   [Asensio, Elena] Hosp Gen Univ Elche, Dept Med Oncol, Alicante, Spain.
C3 Instituto de Investigacion Biomedica de Malaga y Plataforma en
   Nanomedicina (IBIMA); Universidad de Malaga; CIBER - Centro de
   Investigacion Biomedica en Red; CIBERONC; Instituto de Salud Carlos III;
   Universidad de Cordoba; General University Gregorio Maranon Hospital;
   Central University Hospital Asturias; Hospital Universitario Marques de
   Valdecilla (HUMV); University of Valencia; CIBER - Centro de
   Investigacion Biomedica en Red; CIBERONC; CIBER - Centro de
   Investigacion Biomedica en Red; CIBERONC; Hospital Clinico San Carlos;
   Complutense University of Madrid; Virgen del Rocio University Hospital;
   Consejo Superior de Investigaciones Cientificas (CSIC); University of
   Sevilla; CSIC-JA-USE - Instituto de Biomedicina de Sevilla (IBIS);
   Universidad de Alcala; Hospital Universitario Ramon y Cajal; CIBER -
   Centro de Investigacion Biomedica en Red; CIBERONC; Hospital
   Universitario Virgen de las Nieves; Hospital Universitario 12 de
   Octubre; Miguel Servet University Hospital; Hospital del Mar Research
   Institute; Hospital del Mar; CIBER - Centro de Investigacion Biomedica
   en Red; CIBERONC
RP Benavides, M (corresponding author), Hosp Univ Reg & Virgen de la Victoria, UGC Interctr Oncol Med, IBIMA, Ave Carlos Haya S-N, Malaga 29010, Spain.
EM manubenavidesor@gmail.com
RI Valladares'Ayerbes, MANUEL/LDG-3881-2024; Salvia, Antonieta/C-6531-2011;
   Valladares-Ayerbes, Manuel/K-8986-2014
OI Valladares-Ayerbes, Manuel/0000-0002-7950-9584; Benavides,
   Manuel/0000-0002-9817-1291; Aranda Aguilar, Enrique/0000-0002-5471-2842;
   Rivera, Fernando/0000-0001-8915-226X; Gonzalez Flores,
   Encarnacion/0000-0002-2077-5060
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NR 41
TC 3
Z9 3
U1 1
U2 10
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0748-7983
EI 1532-2157
J9 EJSO-EUR J SURG ONC
JI EJSO
PD MAY
PY 2022
VL 48
IS 5
BP 1123
EP 1132
DI 10.1016/j.ejso.2021.11.122
EA MAY 2022
PG 10
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA 1C1UM
UT WOS:000792912800025
PM 34872775
DA 2025-01-04
ER

PT J
AU Zhang, CM
   Lv, JF
   Gong, L
   Yu, LY
   Chen, XP
   Zhou, HH
   Fan, L
AF Zhang, Cong-Min
   Lv, Jin-Feng
   Gong, Liang
   Yu, Lin-Yu
   Chen, Xiao-Ping
   Zhou, Hong-Hao
   Fan, Lan
TI Role of Deficient Mismatch Repair in the Personalized Management of
   Colorectal Cancer
SO INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
LA English
DT Review
DE colorectal cancer; personalized treatment; mismatch repair system;
   microsatellite instability; adjuvant chemotherapy; targeted therapy;
   immune checkpoint inhibitor therapy
ID III COLON-CANCER; ENDOTHELIAL GROWTH-FACTOR; MICROSATELLITE-INSTABILITY
   STATUS; HMLH1 PROMOTER HYPERMETHYLATION; DISEASE-FREE SURVIVAL; ADJUVANT
   CHEMOTHERAPY; LYNCH-SYNDROME; STAGE-II; BRAF MUTATION; PREDICTIVE
   BIOMARKERS
AB Colorectal cancer (CRC) represents the third most common type of cancer in developed countries and one of the leading causes of cancer deaths worldwide. Personalized management of CRC has gained increasing attention since there are large inter-individual variations in the prognosis and response to drugs used to treat CRC owing to molecular heterogeneity. Approximately 15% of CRCs are caused by deficient mismatch repair (dMMR) characterized by microsatellite instability (MSI) phenotype. The present review is aimed at highlighting the role of MMR status in informing prognosis and personalized treatment of CRC including adjuvant chemotherapy, targeted therapy, and immune checkpoint inhibitor therapy to guide the individualized therapy of CRC.
C1 [Zhang, Cong-Min; Gong, Liang; Yu, Lin-Yu; Chen, Xiao-Ping; Zhou, Hong-Hao; Fan, Lan] Cent South Univ, Xiangya Hosp, Dept Clin Pharmacol, Changsha 410008, Hunan, Peoples R China.
   [Zhang, Cong-Min; Gong, Liang; Yu, Lin-Yu; Chen, Xiao-Ping; Zhou, Hong-Hao; Fan, Lan] Cent South Univ, Inst Clin Pharmacol, Hunan Key Lab Pharmacogenet, Changsha 410078, Hunan, Peoples R China.
   [Lv, Jin-Feng] Cent South Univ, Xiangya Hosp, Dept Pharm, Changsha 410008, Hunan, Peoples R China.
   [Lv, Jin-Feng] Cent South Univ, Inst Hosp Pharm, Changsha 410008, Hunan, Peoples R China.
C3 Central South University; Central South University; Central South
   University; Central South University
RP Fan, L (corresponding author), Cent South Univ, Xiangya Hosp, Dept Clin Pharmacol, Changsha 410008, Hunan, Peoples R China.; Fan, L (corresponding author), Cent South Univ, Inst Clin Pharmacol, Hunan Key Lab Pharmacogenet, Changsha 410078, Hunan, Peoples R China.
EM ZhangCM126126@126.com; lvjinfeng1990@163.com; gongliang3991@163.com;
   yulinhui19910530@163.com; chenxp74@hotmail.com; hhzhou2003@163.com;
   fanlan_038038@163.com
RI Zhou, Honghao/JWO-4641-2024; Zhang, Congmin/GWU-6900-2022
FU China Scholarship Council; National Natural Science Foundation of China
   [30901834]; Hunan Provincial Natural Science Foundation of China
   [12K005]; Research Funds of teachers for the Central South University; 
   [NCET-11-0509]
FX This work was supported by China Scholarship Council, the National
   Natural Science Foundation of China (No. 30901834), NCET-11-0509, Hunan
   Provincial Natural Science Foundation of China (No. 12K005) and Research
   Funds of teachers for the Central South University.
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NR 120
TC 43
Z9 46
U1 0
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1660-4601
J9 INT J ENV RES PUB HE
JI Int. J. Environ. Res. Public Health
PD SEP
PY 2016
VL 13
IS 9
AR 892
DI 10.3390/ijerph13090892
PG 17
WC Environmental Sciences; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
   Health
GA DX9EG
UT WOS:000384695800056
PM 27618077
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Harada, S
   Arend, R
   Dai, Q
   Levesque, JA
   Winokur, TS
   Guo, RJ
   Heslin, MJ
   Nabell, L
   Nabors, LB
   Limdi, NA
   Roth, KA
   Partridge, EE
   Siegal, GP
   Yang, ES
AF Harada, Shuko
   Arend, Rebecca
   Dai, Qian
   Levesque, Jessica A.
   Winokur, Thomas S.
   Guo, Rongjun
   Heslin, Martin J.
   Nabell, Lisle
   Nabors, L. Burt
   Limdi, Nita A.
   Roth, Kevin A.
   Partridge, Edward E.
   Siegal, Gene P.
   Yang, Eddy S.
TI Implementation and utilization of the molecular tumor board to guide
   precision medicine
SO ONCOTARGET
LA English
DT Review
DE precision medicine; targeted therapy; next generation sequencing;
   molecular tumor board
ID JOINT-CONSENSUS-RECOMMENDATION; SEQUENCE VARIANTS; CANCER GENOMICS;
   EXPERIENCE; ASSOCIATION; VALIDATION; MUTATIONS; CARCINOMA; STANDARDS;
   PATHOLOGY
AB Background: With rapid advances in genomic medicine, the complexity of delivering precision medicine to oncology patients across a university health system demanded the creation of a Molecular Tumor Board (MTB) for patient selection and assessment of treatment options. The objective of this report is to analyze our progress to date and discuss the importance of the MTB in the implementation of personalized medicine.
   Materials and Methods: Patients were reviewed in the MTB for appropriateness for comprehensive next generation sequencing (NGS) cancer gene set testing based on set criteria that were in place. Because profiling of stage IV lung cancer, colon cancer, and melanoma cancers were standard of care, these cancer types were excluded from this process. We subsequently analyzed the types of cases referred for testing and approved with regards to their results.
   Results: 191 cases were discussed at the MTB and 132 cases were approved for testing. Forty-six cases (34.8%) had driver mutations that were associated with an active targeted therapeutic agent, including BRAF, PIK3CA, IDH1, KRAS, and BRCA1. An additional 56 cases (42.4%) had driver mutations previously reported in some type of cancer. Twenty-two cases (16.7%) did not have any clinically significant mutations. Eight cases did not yield adequate DNA. 15 cases were considered for targeted therapy, 13 of which received targeted therapy. One patient experienced a near complete response. Seven of 13 had stable disease or a partial response.
   Conclusions: MTB at University of Alabama-Birmingham is unique because it reviews the appropriateness of NGS testing for patients with recurrent cancer and serves as a forum to educate our physicians about the pathways of precision medicine. Our results suggest that our detection of actionable mutations may be higher due to our careful selection. The application of precision medicine and molecular genetic testing for cancer patients remains a continuous educational process for physicians.
C1 [Harada, Shuko; Dai, Qian; Levesque, Jessica A.; Winokur, Thomas S.; Guo, Rongjun; Roth, Kevin A.; Siegal, Gene P.] Univ Alabama Birmingham, Dept Pathol, Birmingham, AL 35294 USA.
   [Heslin, Martin J.] Univ Alabama Birmingham, Dept Surg, Birmingham, AL 35294 USA.
   [Nabell, Lisle] Univ Alabama Birmingham, Dept Med, Birmingham, AL 35294 USA.
   [Nabors, L. Burt; Limdi, Nita A.] Univ Alabama Birmingham, Dept Neurol, UAB Stn, Birmingham, AL 35294 USA.
   [Arend, Rebecca] Univ Alabama Birmingham, Dept Obstet & Gynecol, Birmingham, AL 35294 USA.
   [Yang, Eddy S.] Univ Alabama Birmingham, Dept Radiat Oncol, Birmingham, AL 35487 USA.
   [Harada, Shuko; Arend, Rebecca; Heslin, Martin J.; Nabell, Lisle; Nabors, L. Burt; Partridge, Edward E.; Yang, Eddy S.] Univ Alabama Birmingham, Dept Comprehens Canc Ctr, Birmingham, AL 35294 USA.
C3 University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham
RP Yang, ES (corresponding author), Univ Alabama Birmingham, Dept Radiat Oncol, Birmingham, AL 35487 USA.; Yang, ES (corresponding author), Univ Alabama Birmingham, Dept Comprehens Canc Ctr, Birmingham, AL 35294 USA.
EM shyang@uabmc.edu
RI Nabors, Louis/ABB-8223-2021; Siegal, Gene/A-8653-2009
OI Arend, Rebecca/0000-0003-2108-3426
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NR 26
TC 56
Z9 57
U1 0
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 AUG 22
PY 2017
VL 8
IS 34
BP 57845
EP 57854
DI 10.18632/oncotarget.18471
PG 10
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FE3SI
UT WOS:000408135600170
PM 28915716
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hu, S
   Dai, HB
   Li, T
   Tang, Y
   Fu, WY
   Yuan, QN
   Wang, FF
   Lv, GJ
   Lv, YY
   Fan, XY
   Zhang, S
   Jin, RB
   Shen, YF
   Lin, FX
   Ye, XT
   Ding, M
   Yang, YJ
   Lei, CH
AF Hu, Shi
   Dai, Haibin
   Li, Tian
   Tang, Ying
   Fu, Wenyan
   Yuan, Qingning
   Wang, Feifei
   Lv, Gaojian
   Lv, Yuanyuan
   Fan, Xiaoyan
   Zhang, Sheng
   Jin, Ruobing
   Shen, Yafeng
   Lin, Fangxing
   Ye, Xuting
   Ding, Min
   Yang, Yongji
   Lei, Changhai
TI Broad RTK-targeted therapy overcomes molecular heterogeneity-driven
   resistance to cetuximab via vectored immunoprophylaxis in colorectal
   cancer
SO CANCER LETTERS
LA English
DT Article
DE Acquire resistance; CRC; Viral vectors; Broad targeted therapy
ID EPIDERMAL-GROWTH-FACTOR; FACTOR RECEPTOR EXPRESSION; CELL LUNG-CANCER;
   ACQUIRED-RESISTANCE; COLON-CANCER; INHIBITORY-ACTIVITY; GENE DELIVERY;
   NECK-CANCER; EGFR; AXL
AB The human epidermal growth factor receptor (EGFR) targeting chimeric monoclonal antibody, cetuximab (Erbitux (R)), is a widely used drug in the treatment of metastatic colorectal cancer. However, the activation of the extensive crosstalk among the EGFR family receptors as well as other tyrosine kinase receptors (RTKs) impairs the efficacy of the drug by fueling acquired resistance. To identify the responsible potential activation pathway underlying cetuximab resistance and generate novel treatment strategies, cetuximab-resistant colorectal cancer cell lines were generated and validated and a functional RNAi screen targeting human RTKs was used to identify extensive receptor tyrosine kinase signaling networks established in resistant cancer cells. MET, Axl, and IGF-1R were identified as contributors to the acquired resistance to cetuximab. Targeting vectored immunoprophylaxis (VIPs) to different RTKs were generated and characterized. Different VIP approaches were evaluated in vivo with parental and cetuximab-resistance xenografts and the RTKs in resistant cancer xenografts were inhibited with VIPs via resensitization to cetuximab treatment. Combination of VIPs was more broadly efficacious, mechanistically, due to co-blocking the EGFR/Axl/MET signaling pathway, which was cross-activated in the resistant cell lines. Moreover, a VIP-based procedural treatment strategy not only eliminated the tumor but also afforded long-lasting protection from tumor recurrence and resistance. Overall, EGFR-related RTK pathway-network activation represents a novel mechanism underlying cetuximab resistance. A broad VIP combination strategy and VIP-based procedural treatment strategy may be a recommended addition to cetuximab-based targeted therapy. Our results establish a new principle to achieve combined RTK inhibition and reverse drug resistance using a VIP approach. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
C1 [Hu, Shi; Li, Tian; Tang, Ying; Yuan, Qingning; Wang, Feifei; Lv, Gaojian; Lv, Yuanyuan; Fan, Xiaoyan; Shen, Yafeng; Lin, Fangxing; Ye, Xuting; Yang, Yongji; Lei, Changhai] Second Mil Med Univ, Dept Biophys, Coll Basic Med Sci, Shanghai 200433, Peoples R China.
   [Dai, Haibin] Nanjing Univ, Sch Med, Jinling Hosp, Dept Anesthesiol, Nanjing 210002, Jiangsu, Peoples R China.
   [Fu, Wenyan] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.
   [Zhang, Sheng] Second Mil Med Univ, Changzheng Hosp, Dept Emergency Med, Shanghai 200003, Peoples R China.
   [Jin, Ruobing] Second Mil Med Univ, Changzheng Hosp, Dept Nephrol, Shanghai 200003, Peoples R China.
   [Ding, Min] Fengchao Med Technol Shanghai Co Ltd, Mol Drug Discovery Ctr, Shanghai 200235, Peoples R China.
C3 Naval Medical University; Nanjing University; Fudan University; Naval
   Medical University; Naval Medical University
RP Hu, S; Lei, CH (corresponding author), Second Mil Med Univ, Dept Biophys, Coll Basic Med Sci, Shanghai 200433, Peoples R China.
EM hus@smmu.edu.cn; lei@smmu.edu.cn
RI lv, yuanyuan/JJC-4057-2023; ye, xu/HSH-7921-2023; Hu, Shi/ABF-4231-2020;
   王, 菲菲/R-1936-2019; Hu, Shi/A-2140-2015
OI Hu, Shi/0000-0002-7905-4284
FU China Postdoctoral Science Foundation [2016M593006]
FX We thank Dr. Cheng Chen, of Tianjin University, Dr. Junfeng Jiang, of
   Second Military Medical University, Dr. Xiaoze Wang, Nagoya University,
   and Dr. Tai An, of Union Medical College, for helpful discussions. This
   work was supported by the General Financial Grant from the China
   Postdoctoral Science Foundation (Grant Nos.:2016M593006).
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NR 56
TC 22
Z9 25
U1 1
U2 18
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 NOV 1
PY 2016
VL 382
IS 1
BP 32
EP 43
DI 10.1016/j.canlet.2016.08.022
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EA9SU
UT WOS:000386985800004
PM 27569653
DA 2025-01-04
ER

PT J
AU Leiphrakpam, PD
   Rajappa, SJ
   Krishnan, M
   Batra, R
   Murthy, SS
   Are, C
AF Leiphrakpam, Premila D.
   Rajappa, Senthil J.
   Krishnan, Mridula
   Batra, Rishi
   Murthy, Shilpa S.
   Are, Chandrakanth
TI Colorectal cancer: Review of signaling pathways and associated
   therapeutic strategies
SO JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Review
DE biomarkers; colorectal cancer; targeted therapy
ID RANDOMIZED PHASE-III; FOLFIRI PLUS BEVACIZUMAB; MOLECULAR SUBGROUP
   ANALYSES; FACTOR-BETA RECEPTOR; KRAS WILD-TYPE; OPEN-LABEL; 1ST-LINE
   TREATMENT; FOLFOXIRI PLUS; DOUBLE-BLIND; MAINTENANCE TREATMENT
AB Tumor profiling and targeted therapy revolutionized the treatment strategies of metastatic colorectal cancer (mCRC) in the last decade. The heterogeneity of CRC tumors plays a critical role in the development of treatment resistance, which underscores the need to understand the molecular mechanism involved in CRC to develop novel targeted therapeutic strategies. This review provides an overview of the signaling pathways driving CRC, the existing targeted agents, their limitations, and future trends.
C1 [Leiphrakpam, Premila D.; Are, Chandrakanth] Univ Nebraska Med Ctr, Coll Med, Grad Med Educ, Omaha, NE USA.
   [Leiphrakpam, Premila D.; Are, Chandrakanth] Univ Nebraska Med Ctr, Coll Med, Dept Surg, Div Surg Oncol, Omaha, NE USA.
   [Rajappa, Senthil J.] Basavatarakam Indo Amer Canc Hosp, Med Oncol, Hyderabad, Telangana, India.
   [Krishnan, Mridula] Univ Nebraska Med Ctr, Coll Med, Dept Internal Med, Div Oncol & Hematol, Omaha, NE USA.
   [Batra, Rishi] Univ Nebraska Med Ctr, Coll Med, Dept Surg, Div Gen Surg, Omaha, NE USA.
   [Murthy, Shilpa S.] Mem Sloan Kettering Canc Ctr, Div Surg Oncol, Global Canc Dispar Initiat, New York, NY USA.
   [Are, Chandrakanth] Univ Nebraska Med Ctr, Coll Med, Dept Surg, Div Surg Oncol, Omaha, NE 68198 USA.
C3 University of Nebraska System; University of Nebraska Medical Center;
   University of Nebraska System; University of Nebraska Medical Center;
   University of Nebraska System; University of Nebraska Medical Center;
   University of Nebraska System; University of Nebraska Medical Center;
   Memorial Sloan Kettering Cancer Center; University of Nebraska System;
   University of Nebraska Medical Center
RP Are, C (corresponding author), Univ Nebraska Med Ctr, Coll Med, Dept Surg, Div Surg Oncol, Omaha, NE 68198 USA.
EM care@unmc.edu
RI Leiphrakpam, Premila/I-6685-2019
OI Leiphrakpam, Premila/0000-0002-2319-8844; Murthy,
   Shilpa/0000-0001-7844-5227
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NR 98
TC 6
Z9 6
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-4790
EI 1096-9098
J9 J SURG ONCOL
JI J. Surg. Oncol.
PD JUN
PY 2023
VL 127
IS 8
SI SI
BP 1277
EP 1295
DI 10.1002/jso.27295
PG 19
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA H2KJ0
UT WOS:000994302000008
PM 37222698
DA 2025-01-04
ER

PT J
AU Schmidinger, M
   Danesi, R
AF Schmidinger, Manuela
   Danesi, Romano
TI Management of Adverse Events Associated with Cabozantinib Therapy in
   Renal Cell Carcinoma
SO ONCOLOGIST
LA English
DT Article
DE Cabozantinib; Renal cell carcinoma; Adverse events management
ID ENDOTHELIAL GROWTH-FACTOR; ANGIOTENSIN-II TYPE-1; NECROSIS-FACTOR-ALPHA;
   KINASE INHIBITORS; TARGETED THERAPY; DOUBLE-BLIND; OPEN-LABEL;
   PHASE-III; COLORECTAL-CANCER; LUNG-CANCER
AB Cabozantinib was recently approved for the treatment of advanced renal cell carcinoma (RCC) after treatment with vascular endothelial growth factor (VEGF)-targeted therapy. Cabozantinib is a multikinase inhibitor targeting VEGF receptor (VEGFR) 2, mesenchymal-epithelial transition receptor, and "anexelekto" receptor tyrosine kinase. A 60-mg daily dose led to improved overall survival and progression-free survival (PFS) versus everolimus in advanced RCC patients as a second- or later-line treatment in the METEOR trial. Improved PFS with cabozantinib versus sunitinib has also been demonstrated in the first-line setting in CABOSUN. However, cabozantinib, like other VEGFR inhibitors, is associated with toxicity that may affect the patient's quality of life. The most frequent adverse events (AEs) are diarrhea, fatigue, hypertension, hand-foot syndrome, weight loss, nausea, and stomatitis. This article summarizes the safety profile of cabozantinib in RCC patients and offers guidance for the management of these AEs. We discuss the underlying mechanisms of these AEs and, based on our experiences with cabozantinib and other multikinase inhibitors, we present approaches to manage toxicity. Prophylactic and therapeutic solutions are available to help with the management of toxicity associated with cabozantinib, and adequate interventions can ensure optimum adherence and maximize patient outcomes.
C1 [Schmidinger, Manuela] Med Univ Vienna, Dept Med 1, Clin Div Oncol, Vienna, Austria.
   [Danesi, Romano] Univ Pisa, Dept Clin & Expt Med, Clin Pharmacol & Pharmacogenet Unit, Pisa, Italy.
C3 Medical University of Vienna; University of Pisa
RP Schmidinger, M (corresponding author), Med Univ Vienna, Dept Med 1, Clin Div Oncol, Med, Waehringer Guertel 18-20, A-1090 Vienna, Austria.; Schmidinger, M (corresponding author), Comprehens Canc Ctr, Waehringer Guertel 18-20, A-1090 Vienna, Austria.
EM manuela.schmidinger@meduniwien.ac.at
RI Danesi, Romano/AAC-9410-2019
FU Ipsen
FX This study was supported by funding from Ipsen. Medical writing support
   was provided by Martin Gilmour and Thierry Deltheil at ESP Bioscience.
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NR 108
TC 54
Z9 58
U1 0
U2 11
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD MAR
PY 2018
VL 23
IS 3
BP 306
EP 315
DI 10.1634/theoncologist.2017-0335
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FY7DC
UT WOS:000427020800007
PM 29146618
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Serup-Hansen, E
   Linnemann, D
   Hogdall, E
   Geertsen, PF
   Havsteen, H
AF Serup-Hansen, Eva
   Linnemann, Dorte
   Hogdall, Estrid
   Geertsen, Poul Flemming
   Havsteen, Hanne
TI KRAS and BRAF mutations in anal carcinoma
SO APMIS
LA English
DT Article
DE Anal cancer; prognosis; survival; KRAS; BRAF
ID GROWTH-FACTOR RECEPTOR; METASTATIC COLORECTAL-CANCER; CETUXIMAB PLUS
   IRINOTECAN; III RANDOMIZED-TRIAL; PROGNOSTIC-FACTORS; PHASE-III;
   1ST-LINE TREATMENT; SURVIVAL; CHEMOTHERAPY; FLUOROURACIL
AB The EGF receptor (EGFR) is expressed in most cases of anal carcinomas. Anecdotal benefit from EGFR-targeted therapy has been reported in anal cancer and a negative correlation with Kirsten Ras (KRAS) mutation status has been proposed. The purpose of this retrospective study was to investigate the frequency and the prognostic value of KRAS and BRAF mutations in a large cohort of patients with anal cancer. One hundred and ninety-three patients with T1-4N0-3M0-1 anal carcinoma were included in the study. Patients were treated with curative (92%) or palliative intent (8%) between January 2000 and January 2010. KRAS mutations were detected using Therascreen((R))KRAS real-time PCR assay (Qiagen) and V600E or V600D/K BRAF mutations were uncovered using Pyrosequencing. The frequency of KRAS and BRAF mutations was low; KRAS mutations were detected in 1.6% and BRAF mutations in 4.7% of the biopsies. No impact of KRAS or BRAF status on survival was found. In conclusion, both KRAS and BRAF mutations are rare in anal cancer. The low frequency of KRAS mutations support protocols exploring EGFR-targeted therapy in patients with metastatic anal cancer, while treatment with BRAF inhibitors might be relevant for only a very few patients.
C1 [Serup-Hansen, Eva; Geertsen, Poul Flemming; Havsteen, Hanne] Herlev Hosp, Dept Oncol, DK-2730 Herlev, Denmark.
   [Linnemann, Dorte; Hogdall, Estrid] Herlev Hosp, Dept Pathol, DK-2730 Herlev, Denmark.
C3 University of Copenhagen; Herlev & Gentofte Hospital; University of
   Copenhagen; Herlev & Gentofte Hospital
RP Serup-Hansen, E (corresponding author), Dept Oncol RA54B1, Herlev Ringvej 75, DK-2730 Herlev, Denmark.
EM eva.serup-hansen@regionh.dk
OI Hogdall, Estrid/0000-0003-4689-5658
FU CIRRO - Lundbeck Foundation Center for Interventional Research in
   Radiation Oncology; Danish Council for Strategic Research; Fabrikant
   Einar Willumsens Mindelegat; Torben og Alice Frimodts Fond; Fabrikant
   Frands Kohler Nielsens og Hustrus Mindelegat
FX This study was supported by CIRRO - The Lundbeck Foundation Center for
   Interventional Research in Radiation Oncology and the Danish Council for
   Strategic Research, Fabrikant Einar Willumsens Mindelegat, Torben og
   Alice Frimodts Fond, and Fabrikant Frands Kohler Nielsens og Hustrus
   Mindelegat. They had no role in the study design, in the collection,
   analysis and interpretation of date, or in writing of the manuscript and
   in the decision to submit the manuscript for publication.
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NR 40
TC 20
Z9 20
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0903-4641
EI 1600-0463
J9 APMIS
JI APMIS
PD JAN
PY 2015
VL 123
IS 1
BP 53
EP 59
DI 10.1111/apm.12306
PG 7
WC Immunology; Microbiology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Microbiology; Pathology
GA AX6TY
UT WOS:000347055100007
PM 25244542
OA Bronze
DA 2025-01-04
ER

PT J
AU Zhang, ZF
   Lei, Y
   Wang, DZ
   Yang, L
   Lou, CJ
AF Zhang, Zhengfeng
   Lei, Yang
   Wang, Dazhen
   Yang, Liu
   Lou, Changjie
TI Case Report: A case of advanced duodenal adenocarcinoma in complete
   remission after chemotherapy combined with targeted therapy and
   radiotherapy
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE case report; duodenal adenocarcinoma; advanced stage; chemotherapy;
   radiotherapy; targeted therapy
ID SMALL-BOWEL; NEOADJUVANT TREATMENT; SINGLE-CENTER; CANCER; CAPECITABINE;
   OXALIPLATIN; FEATURES; AMPULLA; TUMORS; TRIAL
AB Duodenal adenocarcinoma (DA) is an extremely rare and highly aggressive malignant tumor of the digestive system. Due to the lack of specific clinical characteristics, it is easy to misdiagnosis and miss diagnosis, and the lack of specific consensus and recommendation for treatment, so it often refers to stomach cancer and colorectal cancer. Now, we report a case of a patient with advanced DA who achieved complete remission (CR) after undergoing chemoradiotherapy combined with targeted therapy. The patient was pathologically diagnosed with DA after radical surgery in October 2020, and he failed to undergo adjuvant chemotherapy on time due to the COVID-19 outbreak. The patient found multiple lymph node liver and abdominal metastases 6 months after the operation. Considering the progression of the disease, XELOX regimen (oxaliplatin + capecitabine) chemotherapy was given for 1 cycle. After 1 cycle of treatment, the tumor markers remained elevated; the carcinoembryonic antigen (CEA) was 5.03 ng/ml (0-5 ng/ml), and the carbohydrate antigen 19-9 (CA19-9) was 747.30 U/ml (0-37 U/ml). The patient also developed intolerable capecitabine-related treatment-related adverse events (TRAEs), namely, hand-foot syndrome. For the above reasons, capecitabine was replaced as S-1 at cycle 2, and the chemotherapy regimen became SOX (oxaliplatin + S-1); bevacizumab injection was also added to the SOX regimen, and it was further treated regularly for 7 cycles with the regimen of SOX plus bevacizumab. Liver metastases showed a continuous narrowing trend throughout the treatment period; tumor markers also showed a downward trend. Finally, the patient achieved complete remission (CR) at cycle 7. After completion of chemotherapy, radiotherapy was administered to the resistant metastatic lymph nodes present in the patient's abdominal cavity for a total of 10 times. However, the patient developed severe bone marrow suppression and obstructive jaundice during the course of radiotherapy and finally failed to complete the radiotherapy plan. Currently, the patient continued maintenance therapy with bevacizumab and S-1 and showed no recurrence or metastasis after review. In this case of advanced DA, we referred to both CRC and gastric cancer in the treatment regimen of the patient. At the same time, targeted drugs and radiotherapy were also added to the basis of chemotherapy, which has no clear consensus recommendation or case for reference in the treatment of advanced DA. Thankfully, the patient's disease was controlled and remained stable after treatment with this regimen. Therefore, for patients with advanced DA who lack standardized treatment regimens and guidelines, the combination of chemotherapy with targeted therapy and radiotherapy may be one of the effective treatment modalities.
C1 [Zhang, Zhengfeng; Lei, Yang; Wang, Dazhen; Yang, Liu; Lou, Changjie] Harbin Med Univ, Dept Gastroenterol, Canc Hosp, Harbin, Peoples R China.
C3 Harbin Medical University
RP Lou, CJ (corresponding author), Harbin Med Univ, Dept Gastroenterol, Canc Hosp, Harbin, Peoples R China.
EM 9337768@qq.com
FU Harbin Medical University Cancer Hospital Haiyan Scientific research
   fund;  [JJZD2020-03]
FX Funding Harbin Medical University Cancer Hospital Haiyan Scientific
   research fund (JJZD2020-03).
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NR 38
TC 4
Z9 4
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 OCT 24
PY 2022
VL 12
AR 968110
DI 10.3389/fonc.2022.968110
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 6A4KJ
UT WOS:000880625200001
PM 36353566
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Li, XS
   Wu, YM
   Tian, T
AF Li, Xiaoshuang
   Wu, Yanmin
   Tian, Tian
TI TGF-β Signaling in Metastatic Colorectal Cancer (mCRC): From Underlying
   Mechanism to Potential Applications in Clinical Development
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colorectal cancer; metastasis; TGF-beta signaling; targeting therapy;
   immune-suppressive
ID EPITHELIAL-MESENCHYMAL TRANSITION; TRANSFORMING-GROWTH-FACTOR;
   POOR-PROGNOSIS SUBTYPES; COLON-CANCER; DOWN-REGULATION; STEM-CELLS;
   IN-VIVO; LIVER; EXPRESSION; PATHWAY
AB Colorectal cancer (CRC) is a serious public health issue, and it has the leading incidence and mortality among malignant tumors worldwide. CRC patients with metastasis in the liver, lung or other distant sites always have poor prognosis. Thus, there is an urgent need to discover the underlying mechanisms of metastatic colorectal cancer (mCRC) and to develop optimal therapy for mCRC. Transforming growth factor-beta (TGF-beta) signaling plays a significant role in various physiologic and pathologic processes, and aberrant TGF-beta signal transduction contributes to mCRC progression. In this review, we summarize the alterations of the TGF-beta signaling pathway in mCRC patients, the functional mechanisms of TGF-beta signaling, its promotion of epithelial-mesenchymal transition, its facilitation of angiogenesis, its suppression of anti-tumor activity of immune cells in the microenvironment and its contribution to sternness of CRC cells. We also discuss the possible applications of TGF-beta signaling in mCRC diagnosis, prognosis and targeted therapies in clinical trials. Hopefully, these research advances in TGF-beta signaling in mCRC will improve the development of new strategies that can be combined with molecular targeted therapy, immunotherapy and traditional therapies to achieve better efficacy and benefit mCRC patients in the near future.
C1 [Li, Xiaoshuang; Wu, Yanmin; Tian, Tian] Beijing Jiaotong Univ, Coll Life Sci & Bioengn, Beijing 100044, Peoples R China.
C3 Beijing Jiaotong University
RP Tian, T (corresponding author), Beijing Jiaotong Univ, Coll Life Sci & Bioengn, Beijing 100044, Peoples R China.
EM ttian@bjtu.edu.cn
FU Natural Science Foundation of Beijing [5222019]
FX This research was funded by the Natural Science Foundation of Beijing
   (grant number 5222019).
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NR 228
TC 27
Z9 28
U1 4
U2 22
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 2022
VL 23
IS 22
AR 14436
DI 10.3390/ijms232214436
PG 28
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 6K2NT
UT WOS:000887346400001
PM 36430910
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, ZX
   Qi, FH
   Cui, YG
   Zhao, L
   Sun, XG
   Tang, W
   Cai, PP
AF Wang, Zhixue
   Qi, Fanghua
   Cui, Yangang
   Zhao, Lin
   Sun, Xiaogang
   Tang, Wei
   Cai, Pingping
TI An update on Chinese herbal medicines as adjuvant treatment of
   anticancer therapeutics
SO BIOSCIENCE TRENDS
LA English
DT Review
DE Chinese herbal medicine; adjuvant treatment; chemotherapy; radiotherapy;
   targeted therapy
ID CANCER-RELATED FATIGUE; SHENQI-FUZHENG INJECTION; JAVANICA OIL EMULSION;
   LUNG-CANCER; COLORECTAL-CANCER; SCUTELLARIA-BARBATA; GASTRIC-CANCER;
   PORIA-COCOS; BIOLOGICAL-ACTIVITIES; KANGLAITE INJECTION
AB Numerous studies have indicated that in cancer treatment Chinese herbal medicines in combination with chemo-, radio-, or targeted-therapy can be used to enhance the efficacy of and diminish the side effects and complications caused by these therapies. Therefore, an understanding of Chinese herbal medicines is needed by physicians and other health care providers. This review provides an update on Chinese herbal medicines as adjuvant treatment of anticancer therapeutics. First, some Chinese herbal medicines (e.g. Astragalus, Ginseng, Scutellaria barbata, TJ-41, TJ-48, PHY906, Huachansu injection, and Kanglaite injection) that are commonly used for treating the cancer and/or reducing the toxicity induced by chemo-, radio-, or targeted-therapy are discussed. These Chinese herbal medicines have been shown to possess great advantages in terms of suppressing tumor progression, increasing the sensitivity of chemo-, radio-, or targeted-therapeutics, improving an organism's immune system function, and lessening the damage caused by these therapeutics. Second, some clinical trials using Chinese herbal medicines as adjuvant improving cancer treatment related side effects and complications are reviewed. Some Chinese herbal medicines have a significant effect on reducing cancer-related fatigue and pain, improving peripheral neuropathy and gastrointestinal side effects including diarrhea, nausea, and vomiting, decrease the incidence of bone marrow suppression, protecting anthracycline-induced cardiotoxicity and radiation-induced pneumonitis, and relieving EGFR-TKIs related acneiform eruptions and other side effects. This review of those medicines should contribute to an understanding of Chinese herbal medicines as adjuvant treatment for cancer and provide useful information for the development of more effective anti-cancer drugs. However, rigorously designed trials on potential Chinese herbal medicine must be further examined involving cancer treatment especially molecular targeted-therapy in the future.
C1 [Wang, Zhixue; Qi, Fanghua; Zhao, Lin; Cai, Pingping] Shandong Univ, Shandong Prov Hosp, Dept Tradit Chinese Med, 324 Jingwuweiqi Rd, Jinan 250021, Shandong, Peoples R China.
   [Cui, Yangang] Shandong Univ, Shandong Prov Hosp, Dept Chemotherapy, Jinan, Shandong, Peoples R China.
   [Sun, Xiaogang] Shandong Univ, Shandong Prov Hosp, Dept Tumor Minimally Invas Surg, Jinan, Shandong, Peoples R China.
   [Tang, Wei] Natl Ctr Global Hlth & Med, Tokyo, Japan.
C3 Shandong First Medical University & Shandong Academy of Medical
   Sciences; Shandong University; Shandong University; Shandong First
   Medical University & Shandong Academy of Medical Sciences; Shandong
   First Medical University & Shandong Academy of Medical Sciences;
   Shandong University; National Center for Global Health & Medicine -
   Japan
RP Cai, PP (corresponding author), Shandong Univ, Shandong Prov Hosp, Dept Tradit Chinese Med, 324 Jingwuweiqi Rd, Jinan 250021, Shandong, Peoples R China.
EM pingpingcai@126.com
RI tang, wei/HZH-5205-2023
FU Shandong Provincial Natural Science Foundation, China [ZR2015HQ015];
   National Natural Science Foundation of China [81603449]
FX This study was funded by Shandong Provincial Natural Science Foundation,
   China (No. ZR2015HQ015) and National Natural Science Foundation of China
   (No. 81603449).
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NR 133
TC 127
Z9 139
U1 2
U2 73
PU IRCA-BSSA
PI TOKYO
PA PEARL CITY KOISHIKAWA 603, 2-4-5 KASUGA, BUNKYO-KU, TOKYO, 112-0003,
   JAPAN
SN 1881-7815
EI 1881-7823
J9 BIOSCI TRENDS
JI BioSci. Trends
PD JUN
PY 2018
VL 12
IS 3
BP 220
EP 239
DI 10.5582/bst.2018.01144
PG 20
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA GM4VC
UT WOS:000438122100002
PM 30012913
OA Bronze
DA 2025-01-04
ER

PT J
AU Matsunaga, Y
   Adachi, Y
   Sasaki, Y
   Koide, H
   Motoya, M
   Nosho, K
   Takagi, H
   Yamamoto, H
   Sasaki, S
   Arimura, Y
   Tokino, T
   Carbone, DP
   Imai, K
   Shinomura, Y
AF Matsunaga, Yasutaka
   Adachi, Yasushi
   Sasaki, Yasushi
   Koide, Hideyuki
   Motoya, Masayo
   Nosho, Katsuhiko
   Takagi, Hideyasu
   Yamamoto, Hiroyuki
   Sasaki, Shigeru
   Arimura, Yoshiaki
   Tokino, Takashi
   Carbone, David P.
   Imai, Kohzoh
   Shinomura, Yasuhisa
TI The effect of forced expression of mutated <i>K-RAS</i> gene on
   gastrointestinal cancer cell lines and the IGF-1R targeting therapy
SO MOLECULAR CARCINOGENESIS
LA English
DT Article
DE colorectal cancer; decoy; insulin-like growth factor-1 receptor
   (IGF-1R); K-RAS mutation; pancreatic cancer
ID GROWTH-FACTOR-I; RECEPTOR MONOCLONAL-ANTIBODY; HUMAN PANCREATIC-CANCER;
   COLORECTAL-CANCER; MATRIX METALLOPROTEINASE-7; TUMOR-GROWTH; PHASE-I;
   ACQUIRED-RESISTANCE; BINDING-PROTEINS; CARCINOMA CELLS
AB Mutation in K-RAS (K-RAS-MT) plays important roles in both cancer progression and resistance to anti-epidermal growth factor receptor (EGFR) therapy in gastrointestinal tumors. Insulin-like growth factor-1 receptor (IGF-1R) signaling is required for carcinogenicity and progression of many tumors as well. We have previously shown successful therapy for gastrointestinal cancer cell lines bearing a K-RAS mutation using an anti-IGF-1R monoclonal antibody. In this study, we sought to evaluate effects of forced K-RAS-MT expression on gastrointestinal cancer cell lines representing a possible second resistance mechanism for anti-EGFR therapy and IGF-1R-targeted therapy for these transfectants. We made stable transfectants of K-RAS-MT in two gastrointestinal cancer cell lines, colorectal RKO and pancreatic BxPC-3. We assessed the effect of forced expression of K-RAS-MT on proliferation, apoptosis, migration, and invasion in gastrointestinal cancer cells. Then we assessed anti-tumor effects of dominant negative IGF-1R (IGF-1R/dn) and an IGF-1R inhibitor, picropodophyllin, on the K-RAS-MT transfectants. Overexpression of K-RAS-MT in gastrointestinal cancer cell lines led to more aggressive phenotypes, with increased proliferation, decreased apoptosis, and increased motility and invasion. IGF-1R blockade suppressed cell growth, colony formation, migration, and invasion, and up-regulated chemotherapy-induced apoptosis of gastrointestinal cancer cells, even when K-RAS-MT was over-expressed. IGF-1R blockade inhibited the Akt pathway more than the extracellular signal-regulated kinase (ERK) pathway in the K-RAS-MT transfectants. IGF-1R/dn, moreover, inhibited the growth of murine xenografts expressing K-RAS-MT. Thus, K-RAS-MT might be important for progressive phonotype observed in gastrointestinal cancers. IGF-1R decoy is a candidate molecular therapeutic approach for gastrointestinal cancers even if K-RAS is mutated. (c) 2016 Wiley Periodicals, Inc.
C1 [Matsunaga, Yasutaka; Adachi, Yasushi; Koide, Hideyuki; Motoya, Masayo; Nosho, Katsuhiko; Takagi, Hideyasu; Sasaki, Shigeru; Arimura, Yoshiaki; Shinomura, Yasuhisa] Sapporo Med Univ, Dept Gastroenterol Rheumatol & Clin Immunol, Sapporo, Hokkaido, Japan.
   [Adachi, Yasushi] Sapporo Shirakaba Dai Hosp, Sapporo, Hokkaido, Japan.
   [Sasaki, Yasushi; Tokino, Takashi] Sapporo Med Univ, Res Inst Frontier Med, Med Genome Sci, Sapporo, Hokkaido, Japan.
   [Yamamoto, Hiroyuki] St Marianna Univ, Div Gastroenterol & Hepatol, Dept Internal Med, Sch Med, Kawasaki, Kanagawa, Japan.
   [Carbone, David P.] Ohio State Univ, Med Ctr, James Canc Ctr, Columbus, OH 43210 USA.
   [Imai, Kohzoh] Univ Tokyo, Inst Med Sci Hosp, Tokyo, Japan.
C3 Sapporo Medical University; Sapporo Medical University; Saint Marianna
   University; James Cancer Hospital & Solove Research Institute;
   University System of Ohio; Ohio State University; University of Tokyo
EM yadachi@sapmed.ac.jp
RI Tokino, Takashi/AAI-9887-2021; Yamamoto, Hiroyuki/GRF-4036-2022; Sasaki,
   Yasushi/AAA-3079-2019
OI Sasaki, Yasushi/0000-0002-3500-8059
FU Ministry of Health, Labour and Welfare, Japan; Ono Cancer Research Fund;
   Japanese Society of Strategies for Cancer Research and Therapy;
   Grants-in-Aid for Scientific Research [26460944, 16K07122, 16H06297,
   16H06276, 16H06277] Funding Source: KAKEN
FX Grant sponsor: Ministry of Health, Labour and Welfare, Japan; Grant
   sponsor: Ono Cancer Research Fund; Grant sponsor: Japanese Society of
   Strategies for Cancer Research and Therapy
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NR 49
TC 5
Z9 6
U1 0
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0899-1987
EI 1098-2744
J9 MOL CARCINOGEN
JI Mol. Carcinog.
PD FEB
PY 2017
VL 56
IS 2
BP 515
EP 526
DI 10.1002/mc.22513
PG 12
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA EI5GH
UT WOS:000392521800018
PM 27312358
DA 2025-01-04
ER

PT J
AU Steele, CW
   Whittle, T
   Smith, JJ
AF Steele, Colin W.
   Whittle, Thomas
   Smith, J. Joshua
TI Review: <i>KRAS</i> mutations are influential in driving hepatic
   metastases and predicting outcome in colorectal cancer
SO CHINESE CLINICAL ONCOLOGY
LA English
DT Review
DE KRAS; metastatic; colorectal; cancer
ID CONSENSUS MOLECULAR SUBTYPES; LIVER METASTASES; ACQUIRED-RESISTANCE;
   TARGETED THERAPY; RAS; RESECTION; SURVIVAL; TUMORS; CHEMOTHERAPY;
   PATTERNS
AB Metastatic colorectal cancer (CRC) is a topic of intense research. KRAS mutations have emerged as aggressive drivers of disease. Here we discuss the role of KRAS mutations in metastatic progression of CRC. We describe how KRAS has become a useful biomarker in metastatic CRC and examine where future trials may look to target KRAS mutant tumors for therapeutic benefit.
C1 [Steele, Colin W.; Whittle, Thomas] Glasgow Royal Infirm, Univ Dept Surg, Glasgow, Lanark, Scotland.
   [Smith, J. Joshua] Mem Sloan Kettering Canc Ctr, Dept Surg, Colorectal Serv, New York, NY 10021 USA.
C3 University of Glasgow; Memorial Sloan Kettering Cancer Center
RP Steele, CW (corresponding author), Glasgow Royal Infirm, Univ Dept Surg, Glasgow, Lanark, Scotland.
EM colin.steele@glasgow.ac.uk
RI Smith, Jesse Joshua/AAN-5440-2020
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NR 52
TC 6
Z9 7
U1 0
U2 17
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2304-3865
EI 2304-3873
J9 CHIN CLIN ONCOL
JI Chin. Clin. Oncol.
PD OCT
PY 2019
VL 8
IS 5
AR 53
DI 10.21037/cco.2019.08.16
PG 8
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA JC5PP
UT WOS:000489335700009
PM 31597434
OA gold
DA 2025-01-04
ER

PT J
AU Lin, LP
   Sabnis, AJ
   Chan, E
   Olivas, V
   Cade, L
   Pazarentzos, E
   Asthana, S
   Neel, D
   Yan, JJ
   Lu, XY
   Pham, L
   Wang, MXM
   Karachaliou, N
   Cao, MG
   Manzano, JL
   Ramirez, JL
   Torres, JMS
   Buttitta, F
   Rudin, CM
   Collisson, EA
   Algazi, A
   Robinson, E
   Osman, I
   Muñoz-Couselo, E
   Cortes, J
   Frederick, DT
   Cooper, ZA
   McMahon, M
   Marchetti, A
   Rosell, R
   Flaherty, KT
   Wargo, JA
   Bivona, TG
AF Lin, Luping
   Sabnis, Amit J.
   Chan, Elton
   Olivas, Victor
   Cade, Lindsay
   Pazarentzos, Evangelos
   Asthana, Saurabh
   Neel, Dana
   Yan, Jenny Jiacheng
   Lu, Xinyuan
   Pham, Luu
   Wang, Mingxue M.
   Karachaliou, Niki
   Gonzalez Cao, Maria
   Luis Manzano, Jose
   Luis Ramirez, Jose
   Sanchez Torres, Jose Miguel
   Buttitta, Fiamma
   Rudin, Charles M.
   Collisson, Eric A.
   Algazi, Alain
   Robinson, Eric
   Osman, Iman
   Munoz-Couselo, Eva
   Cortes, Javier
   Frederick, Dennie T.
   Cooper, Zachary A.
   McMahon, Martin
   Marchetti, Antonio
   Rosell, Rafael
   Flaherty, Keith T.
   Wargo, Jennifer A.
   Bivona, Trever G.
TI The Hippo effector YAP promotes resistance to RAF- and MEK-targeted
   cancer therapies
SO NATURE GENETICS
LA English
DT Article
ID SIGNALING PATHWAY; COLON-CANCER; INHIBITION; BRAF; KRAS; LUNG; MELANOMA;
   TRANSCRIPTION; ACTIVATION; SURVIVAL
AB Resistance to RAF-and MEK-targeted therapy is a major clinical challenge(1-4). RAF and MEK inhibitors are initially but only transiently effective in some but not all patients with BRAF gene mutation and are largely ineffective in those with RAS gene mutation because of resistance(5-14). Through a genetic screen in BRAF-mutant tumor cells, we show that the Hippo pathway effector YAP (encoded by YAP1) acts as a parallel survival input to promote resistance to RAF and MEK inhibitor therapy. Combined YAP and RAF or MEK inhibition was synthetically lethal not only in several BRAF-mutant tumor types but also in RAS-mutant tumors. Increased YAP in tumors harboring BRAF V600E was a biomarker of worse initial response to RAF and MEK inhibition in patients, establishing the clinical relevance of our findings. Our data identify YAP as a new mechanism of resistance to RAF-and MEK-targeted therapy. The findings unveil the synthetic lethality of combined suppression of YAP and RAF or MEK as a promising strategy to enhance treatment response and patient survival.
C1 [Lin, Luping; Sabnis, Amit J.; Chan, Elton; Olivas, Victor; Cade, Lindsay; Pazarentzos, Evangelos; Asthana, Saurabh; Neel, Dana; Yan, Jenny Jiacheng; Lu, Xinyuan; Pham, Luu; Wang, Mingxue M.; Collisson, Eric A.; Algazi, Alain; Bivona, Trever G.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
   [Lin, Luping; Sabnis, Amit J.; Chan, Elton; Olivas, Victor; Cade, Lindsay; Pazarentzos, Evangelos; Asthana, Saurabh; Neel, Dana; Yan, Jenny Jiacheng; Lu, Xinyuan; Pham, Luu; Wang, Mingxue M.; Collisson, Eric A.; Algazi, Alain; McMahon, Martin; Bivona, Trever G.] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
   [Sabnis, Amit J.] Univ Calif San Francisco, Dept Pediat, Div Pediat Hematol & Oncol, San Francisco, CA USA.
   [Karachaliou, Niki; Gonzalez Cao, Maria; Rosell, Rafael] Hosp Badalona Germans Trias & Pujol, Catalan Inst Oncol, Canc Biol & Precis Med Program, Badalona, Spain.
   [Luis Manzano, Jose] Hosp Badalona Germans Trias & Pujol, Calalan Inst Oncol, Med Oncol Serv, Badalona, Spain.
   [Luis Ramirez, Jose] Hosp Badalona Germans Trias & Pujol, Fundacio Inst Recerca Germans Trias & Pujol IGTP, Translat Oncol Lab, Catalan Inst Oncol, Barcelona, Spain.
   [Sanchez Torres, Jose Miguel] Hosp Univ La Princess, Med Oncol Serv, Madrid, Spain.
   [Buttitta, Fiamma] Univ Fdn, Ctr Predict Mol Med, Chieti, Italy.
   [Rudin, Charles M.] Mem Sloan Kettering Canc Ctr, Mol Chem & Pharmacol Program, New York, NY 10021 USA.
   [Rudin, Charles M.] Mem Sloan Kettering Canc Ctr, Thorac Oncol Serv, New York, NY 10021 USA.
   [Robinson, Eric; Osman, Iman] NYU, Inst Canc, Ronald O Perelman Dept Dermatol Med & Urol, New York, NY USA.
   [Munoz-Couselo, Eva; Cortes, Javier] Vall dHebron Inst Oncol, Barcelona, Spain.
   [Frederick, Dennie T.; Flaherty, Keith T.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
   [Frederick, Dennie T.; Flaherty, Keith T.] Massachusetts Gen Hosp, Ctr Comprehens Canc, Boston, MA 02114 USA.
   [Cooper, Zachary A.; Wargo, Jennifer A.] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX 77030 USA.
   [Cooper, Zachary A.; Wargo, Jennifer A.] Univ Texas MD Anderson Canc Ctr, Dept Genom Med, Houston, TX 77030 USA.
C3 University of California System; University of California San Francisco;
   University of California System; University of California San Francisco;
   UCSF Medical Center; UCSF Helen Diller Family Comprehensive Cancer
   Center; University of California System; University of California San
   Francisco; Hospital Germans Trias i Pujol; Institut Catala d'Oncologia;
   Hospital Germans Trias i Pujol; Institut Catala d'Oncologia; Fundacio
   Institut d'Investigacio en Ciencies de la Salut Germans Trias i Pujol
   (IGTP); Hospital Germans Trias i Pujol; Memorial Sloan Kettering Cancer
   Center; Memorial Sloan Kettering Cancer Center; New York University;
   Vall d'Hebron Institut d'Oncologia (VHIO); Harvard University;
   Massachusetts General Hospital; Harvard University; Massachusetts
   General Hospital; University of Texas System; UTMD Anderson Cancer
   Center; University of Texas System; UTMD Anderson Cancer Center
RP Bivona, TG (corresponding author), Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
EM tbivona@medicine.ucsf.edu
RI Rudin, Charles/R-2530-2019; Sabnis, Amit/KHV-6416-2024; Ramirez, Jose
   Luis/E-5161-2018
OI Rudin, Charles/0000-0001-5204-3465; Ramirez, Jose
   Luis/0000-0003-1447-2941; Pham, Luu/0000-0002-2437-5590; Cooper,
   Zachary/0000-0003-1059-0940; Sabnis, Amit/0000-0002-2061-5139;
   Pazarentzos, Evangelos/0000-0002-5453-1646
FU US National Institutes of Health (NIH) Director's New Innovator Award
   [DP2CA174497]; Howard Hughes Medical Institute; Doris Duke Charitable
   Foundation; American Lung Association; National Lung Cancer Partnership;
   Addario Foundation; Van Auken Private Foundation; Sidney Kimmel
   Foundation for Cancer Research; Searle Scholars Program; La Caixa
   Foundation; US NIH [R01CA131261]
FX We thank G. Bollag and P. Lin (Plexxikon) for providing PLX4720. We
   thank J. Weissman and members of the Bivona laboratory for critical
   review of the manuscript. The authors acknowledge funding support (to
   T.G.B.) from the following sources: US National Institutes of Health
   (NIH) Director's New Innovator Award (DP2CA174497), the Howard Hughes
   Medical Institute (Collaborative Innovation Award), the Doris Duke
   Charitable Foundation, the American Lung Association, the National Lung
   Cancer Partnership, the Addario and Van Auken Private Foundations, the
   Sidney Kimmel Foundation for Cancer Research and the Searle Scholars
   Program. The authors also acknowledge funding from La Caixa Foundation
   (to R.R.) and from US NIH grant R01CA131261 (to M.M.).
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TC 415
Z9 471
U1 1
U2 69
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD MAR
PY 2015
VL 47
IS 3
BP 250
EP +
DI 10.1038/ng.3218
PG 9
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA CC4MQ
UT WOS:000350327900016
PM 25665005
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Maimaitiyiming, Y
   Yang, C
   Wang, Y
   Hussain, L
   Naranmandura, H
AF Maimaitiyiming, Yasen
   Yang, Chang
   Wang, Yun
   Hussain, Liaqat
   Naranmandura, Hua
TI Selection and characterization of novel DNA aptamer against colorectal
   carcinoma Caco-2 cells
SO BIOTECHNOLOGY AND APPLIED BIOCHEMISTRY
LA English
DT Article
DE cell SELEX; Caco-2; CD133; ssDNA aptamer; targeted therapy
ID TARGETED THERAPY; CANCER
AB Aptamers are short, single-stranded nucleic acid (DNA or RNA) oligonucleotides that can be obtained by a technique called systematic evolution of ligands by exponential enrichment (SELEX) in vitro. Due to superior properties such as small size, high binding affinity, and stability, they are considered to be feasible tools for diagnosis and treatment of disease. In the current study, we attempted to screen a high-affinity DNA aptamer to selectively target the colorectal carcinoma Caco-2 cells by using cell-based SELEX approach. After 14 consecutive rounds of selection, aptamer ApC1 was identified. Confocal microscopy results revealed that ApC1 could rapidly internalize into Caco-2 cells but not HEK 293 cells. Moreover, it showed high specificity to Caco-2 cells rather than other cell lines such as 293T, HeLa, MCF-7, HL-60, and NB4. Collectively, our results demonstrated that aptamer ApC1 has high specificity to colorectal carcinoma Caco-2 cells, which could be further applied for targeted therapy of colorectal cancer in future studies.
C1 [Maimaitiyiming, Yasen; Yang, Chang; Wang, Yun; Hussain, Liaqat; Naranmandura, Hua] Zhejiang Univ, Sch Med, Dept Pharmacol, Hangzhou, Zhejiang, Peoples R China.
   [Naranmandura, Hua] Zhejiang Univ, Sch Med & Publ Hlth, Dept Toxicol, 866 Yu Hang Tang Rd,Zijingang Campus,Med Sci Bldg, Hangzhou 310058, Zhejiang, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP Naranmandura, H (corresponding author), Zhejiang Univ, Sch Med & Publ Hlth, Dept Toxicol, 866 Yu Hang Tang Rd,Zijingang Campus,Med Sci Bldg, Hangzhou 310058, Zhejiang, Peoples R China.
EM narenman@zju.edu.cn
RI Hussain, Liaqat/L-9974-2019; Naranmandura, Hua/C-6499-2015;
   Maimaitiyiming, Yasen/CAE-9627-2022
OI Maimaitiyiming, Yasen/0000-0002-1990-4857; Naranmandura,
   Hua/0000-0003-0799-2340; HUSSAIN, LIAQAT/0000-0001-7171-5917
FU National Natural Science Foundation of China [81673521, 81872942];
   Department of Science and Technology of Zhejiang Province [2015C33154];
   Key Project of Traditional Chinese Medicine Science and Technology of
   Zhejiang Province [2015ZZ006]; Zhejiang Provincial & National Health and
   Family Planning Commission Project for Medical Sciences [WKJ-ZJ-1512]
FX The authors wish to acknowledge the National Natural Science Foundation
   of China (Nos. 81673521; 81872942), Department of Science and Technology
   of Zhejiang Province (2015C33154); Key Project of Traditional Chinese
   Medicine Science and Technology of Zhejiang Province (2015ZZ006);
   Zhejiang Provincial & National Health and Family Planning Commission
   Project for Medical Sciences (WKJ-ZJ-1512).
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NR 29
TC 12
Z9 15
U1 0
U2 55
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0885-4513
EI 1470-8744
J9 BIOTECHNOL APPL BIOC
JI Biotechnol. Appl. Biochem.
PD MAY-JUN
PY 2019
VL 66
IS 3
BP 412
EP 418
DI 10.1002/bab.1737
PG 7
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA IK7SQ
UT WOS:000476792600016
PM 30746785
DA 2025-01-04
ER

PT J
AU Shida, D
   Yoshida, T
   Tanabe, T
   Tsukamoto, S
   Ochiai, H
   Kanemitsu, Y
AF Shida, Dai
   Yoshida, Takefumi
   Tanabe, Taro
   Tsukamoto, Shunsuke
   Ochiai, Hiroki
   Kanemitsu, Yukihide
TI Prognostic Impact of R0 Resection and Targeted Therapy for Colorectal
   Cancer with Synchronous Peritoneal Metastasis
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID III COLON-CANCER; CYTOREDUCTIVE SURGERY; INTRAPERITONEAL CHEMOTHERAPY;
   JAPANESE CLASSIFICATION; RANDOMIZED-TRIALS; OUTCOMES; CARCINOMATOSIS;
   FLUOROURACIL; BEVACIZUMAB; OXALIPLATIN
AB The National Comprehensive Cancer Network guidelines recommend R0 resection and targeted therapy, a combination of cytotoxic and molecular targeted agents, such as bevacizumab, cetuximab, and panitumumab, for colorectal cancer with synchronous peritoneal metastasis (M1c). While these therapeutic strategies are drawing attention, their efficacy has not been fully examined.
   The study population comprised 248 consecutive M1c patients who were treated at the National Cancer Center Hospital from 1997 to 2013. Multivariate analyses were performed to evaluate relationships between overall survival and R0 resection and targeted therapy using Cox proportional hazards regression models.
   The 3-year overall survival (3 yOS) was 19.5%, and median survival time (MST) was 16.2 months in 248 M1c patients. R0 resection was performed in 34 patients (14%), yielding a 3-year overall survival (OS) of 48.3% and median survival time (MST) of 29.9 months. Targeted therapy was performed in 54 patients (22%) at least once during the course of treatment, yielding a 3-yr OS of 38.2% and MST of 23.9 months. After adjusting for other key clinical factors, such as the number of organs involved with metastases, performance status, primary tumor site, and extent of peritoneal metastasis, both R0 resection and targeted therapy were independent factors associated with longer OS. Targeted therapy was associated with a significantly longer OS compared with multiple cytotoxic agent therapy [hazard ratio 0.65; 95% confidence interval (0.44-0.94); p = 0.02].
   If achievable, R0 resection is a desirable therapeutic strategy for patients with M1c colorectal cancer. Moreover, targeted therapy might be the optimal chemotherapy in this patient population.
C1 [Shida, Dai; Yoshida, Takefumi; Tanabe, Taro; Tsukamoto, Shunsuke; Ochiai, Hiroki; Kanemitsu, Yukihide] Natl Canc Ctr, Colorectal Surg Div, Tokyo, Japan.
C3 National Cancer Center - Japan
RP Shida, D (corresponding author), Natl Canc Ctr, Colorectal Surg Div, Tokyo, Japan.
EM dshida@ncc.go.jp
OI Shida, Dai/0000-0003-3294-1924
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U1 0
U2 5
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 JUN
PY 2018
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IS 6
BP 1646
EP 1653
DI 10.1245/s10434-018-6436-3
PG 8
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA GE4LZ
UT WOS:000431188700033
PM 29572704
DA 2025-01-04
ER

PT J
AU Nogales, JMS
   Parras, J
   Zazo, S
AF Nogales, Jose M. Sanz
   Parras, Juan
   Zazo, Santiago
TI DDQN-based optimal targeted therapy with reversible inhibitors to combat
   the Warburg effect
SO MATHEMATICAL BIOSCIENCES
LA English
DT Article
DE The Warburg effect; Optimal inhibition targeted therapy; Genistein;
   AR-C155858; Double Deep Q-networks
ID MONOCARBOXYLATE TRANSPORTERS; AEROBIC GLYCOLYSIS; DRUG-RESISTANCE;
   CLINICAL IMPACT; GASTRIC-CANCER; CELLS; EXPRESSION; LACTATE;
   HETEROGENEITY; MCT1
AB We cover the Warburg effect with a three-component evolutionary model, where each component represents a different metabolic strategy. In this context, a scenario involving cells expressing three different phenotypes is presented. One tumour phenotype exhibits glycolytic metabolism through glucose uptake and lactate secretion. Lactate is used by a second malignant phenotype to proliferate. The third phenotype represents healthy cells, which performs oxidative phosphorylation. The purpose of this model is to gain a better understanding of the metabolic alterations associated with the Warburg effect. It is suitable to reproduce some of the clinical trials obtained in colorectal cancer and other even more aggressive tumours. It shows that lactate is an indicator of poor prognosis, since it favours the setting of polymorphic tumour equilibria that complicates its treatment. This model is also used to train a reinforcement learning algorithm, known as Double Deep Q-networks, in order to provide the first optimal targeted therapy based on experimental tumour growth inhibitors as genistein and AR-C155858. Our in silico solution includes the optimal therapy for all the tumour state space and also ensures the best possible quality of life for the patients, by considering the duration of treatment, the use of low-dose medications and the existence of possible contraindications. Optimal therapies obtained with Double Deep Q-networks are validated with the solutions of the Hamilton-Jacobi-Bellman equation.
C1 [Nogales, Jose M. Sanz; Parras, Juan; Zazo, Santiago] Univ Politecn Madrid, Informat Proc & Telecommun Ctr, ETSI Telecomunicac, Av Complutense 30, Madrid 28040, Spain.
C3 Universidad Politecnica de Madrid; Centro de I+D+I en Procesado de la
   Informacion Telecomunicaciones (IPT)
RP Nogales, JMS (corresponding author), Univ Politecn Madrid, Informat Proc & Telecommun Ctr, ETSI Telecomunicac, Av Complutense 30, Madrid 28040, Spain.
EM jose.sanz.nogales@alumnos.upm.es
RI SANZ NOGALES, JOSE MARIA/ISV-6410-2023; Parras, Juan/Y-6229-2019
OI SANZ NOGALES, JOSE M./0000-0003-1396-8742
FU Spanish Ministry of Science and Innovation [PID2020-112502RB-C41]
FX This work was supported by the Spanish Ministry of Science and
   Innovation under the grant PID2020-112502RB-C41 (NAUTILUS) .
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NR 97
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0025-5564
EI 1879-3134
J9 MATH BIOSCI
JI Math. Biosci.
PD SEP
PY 2023
VL 363
AR 109044
DI 10.1016/j.mbs.2023.109044
EA JUL 2023
PG 14
WC Biology; Mathematical & Computational Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
   Biology
GA FS8A0
UT WOS:001147923700001
PM 37414271
OA hybrid
DA 2025-01-04
ER

PT J
AU Xing, ZY
   Sun, FB
   He, W
   Wang, ZW
   Song, XQ
   Zhang, FJ
AF Xing, Zhiyuan
   Sun, Fengbo
   He, Wang
   Wang, Zhiwei
   Song, Xiuqi
   Zhang, Fengjuan
TI Downregulation of ubiquitin-specific peptidase 39 suppresses the
   proliferation and induces the apoptosis of human colorectal cancer cells
SO ONCOLOGY LETTERS
LA English
DT Article
DE colorectal cancer; ubiquitin-specific peptidase 39; small hairpin RNA;
   cell apoptosis; targeted therapy
ID IN-VITRO; USP39; MUTATIONS; SPINDLE; GROWTH; GENES; SNRNP; SF3B1
AB Ubiquitin-specific peptidase 39 (USP39) has been reported to participate in the mitotic spindle checkpoint and the process of cytokinesis. and has been identified as a therapeutic target for various types of cancer. However, the effect of USP39 in colorectal cancer (CRC) has not been investigated. To explore the functional role of USP39 in CRC cell growth, lentivirus-mediated RNA interference was applied to inhibit USP39 expression in SW1116 and HCT116 cells. The relative USP39 mRNA and protein expression levels were significantly reduced in the USP39 knockdown cells, as verified by reverse transcription-quantitative polymerase chain reaction and western blot analysis. USP39 knockdown significantly reduced the proliferation and colony formation abilities of CRC cells, and induced apoptosis and cell cycle arrest in the G(2)/M phases, as determined by an MTT assay, a colony formation assay and flow cytometry analysis. Furthermore, western blot analysis demonstrated that USP39 knockdown may have induced apoptosis through the upregulation of p53, p-p53, PARP and caspase-3 expression in SW1116 cells. In conclusion, USP39 may be a novel biological marker for targeted therapy against CRC, and requires further investigation.
C1 [Xing, Zhiyuan; Wang, Zhiwei; Song, Xiuqi] Qingdao Univ, Affiliated Hosp 2, Med Coll, Dept Gen Surg, Qingdao 266000, Shandong, Peoples R China.
   [Sun, Fengbo] Qingdao Haici Med Grp, Dept Gen Surg, Qingdao 266000, Shandong, Peoples R China.
   [He, Wang] Qingdao Sixth Peoples Hosp, Dept Hepatopathy, Qingdao 266000, Shandong, Peoples R China.
   [Zhang, Fengjuan] Qingdao Univ, Affiliated Hosp 2, Med Coll, Dept Infect, 1677 Mt Wutai Rd, Qingdao 266000, Shandong, Peoples R China.
C3 Qingdao University; Qingdao University
RP Zhang, FJ (corresponding author), Qingdao Univ, Affiliated Hosp 2, Med Coll, Dept Infect, 1677 Mt Wutai Rd, Qingdao 266000, Shandong, Peoples R China.
EM 18661802286@163.com
RI Song, Xiuqi/KEH-5374-2024
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NR 23
TC 11
Z9 14
U1 0
U2 7
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD APR
PY 2018
VL 15
IS 4
BP 5443
EP 5450
DI 10.3892/ol.2018.808061
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GD9HA
UT WOS:000430822500188
PM 29556295
DA 2025-01-04
ER

PT J
AU Zhang, HY
   Zhang, JY
   Liu, YL
   Jiang, Y
   Li, ZM
AF Zhang, Huaiyu
   Zhang, Jiayu
   Liu, Yilun
   Jiang, Yang
   Li, Zhongmin
TI Molecular Targeted Agent and Immune Checkpoint Inhibitor Co-Loaded
   Thermosensitive Hydrogel for Synergistic Therapy of Rectal Cancer
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE molecular targeted therapy; immunotherapy; immune checkpoint blockade;
   thermosensitive hydrogel; cancer treatment; rectal cancer
ID CHEMOTHERAPY; MICELLE
AB Molecular targeted therapy has been proved effective in treatment of rectal cancer. Up-regulated expression of programmed death ligand-1 (PD-L1) was observed after the management of molecular targeted therapy, which made the therapeutic effect discounted. Tumors with higher PD-L1 expression were more sensitive and responsive to treatment of PD-L1 inhibitor. Therefore, the combination of molecular targeted therapy and immune checkpoint blockade makes sense. In this study, the copolymers of poly (ethylene glycol)-block-poly ((L)-leucine) (PEG-PLLeu) were synthesized as a thermosensitive hydrogel composite for consecutive release of regorafenib (REG) and BMS202. The mechanical properties of PEG-PLLeu were investigated, confirming that PEG-PLLeu (5 wt.%) was suitable for in situ injection as drug-delivery composite at low temperature and stable after sol-gel transition at body temperature. Importantly, the double drug loaded hydrogel showed superior antitumour activity over single drugs in an orthotopic rectal cancer model (CT26-Luc). Further analysis of the tumor tissues suggested that REG upregulated the expression of PD-L1 in tumor tissues. In addition, the immunosuppressive tumor microenvironment of CT26-Luc tumor was distinctly relieved under the effect of BMS202, as characterized by increased infiltration of CD8(+) T cells in tumors and enhanced secretion of antitumour cytokines (IFN-gamma and TNF-alpha). Moreover, the drug-loaded composite showed no obvious toxicity in histological analysis. Taken together, the administration of REG and BMS202 in the PEG-PLLeu composite could induce a synergistic effect in in situ treatment of rectal cancer without obvious toxicity, and thus represented a potential strategy for enhanced in situ therapeutic modality.
C1 [Zhang, Huaiyu; Zhang, Jiayu; Liu, Yilun; Jiang, Yang; Li, Zhongmin] Jilin Univ, China Japan Union Hosp, Dept Gastrointestinal Colorectal & Anal Surg, Changchun, Peoples R China.
C3 Jilin University
RP Jiang, Y; Li, ZM (corresponding author), Jilin Univ, China Japan Union Hosp, Dept Gastrointestinal Colorectal & Anal Surg, Changchun, Peoples R China.
EM jiangyang@jlu.edu.cn; lizhongmin1211@jlu.edu.cn
RI Zhang, Juan/GRX-2638-2022; Zhang, Zixuan/JSL-3603-2023; liang,
   YU/IYT-4334-2023
OI Li, Zhongmin/0000-0002-0865-4864; liang, YU/0009-0007-3922-3454
FU Medical and Health Program of Jilin Province [20190304047YY]; Jilin
   Provincial Science and Technology Department [20200201430JC]; Jilin
   Province Development and Reform Commission [2021C043-9]; Education
   Department of Jilin Province [JJKH20201034KJ]
FX This research was financially supported by the Medical and Health
   Program of Jilin Province (20190304047YY), Jilin Provincial Science and
   Technology Department (20200201430JC), Jilin Province Development and
   Reform Commission (2021C043-9), and Education Department of Jilin
   Province (JJKH20201034KJ).
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NR 32
TC 11
Z9 12
U1 5
U2 55
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 APR 16
PY 2021
VL 12
AR 671611
DI 10.3389/fphar.2021.671611
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA RV1OZ
UT WOS:000645611300001
PM 33935796
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Huang, JL
   Tseng, LH
   Parini, V
   Lokhandwala, PM
   Pallavajjala, A
   Rodriguez, E
   Xian, RN
   Chen, L
   Gocke, CD
   Eshleman, JR
   Lin, MT
AF Huang, Jialing
   Tseng, Li-Hui
   Parini, Vamsi
   Lokhandwala, Parvez M.
   Pallavajjala, Aparna
   Rodriguez, Erika
   Xian, Rena
   Chen, Liam
   Gocke, Christopher D.
   Eshleman, James R.
   Lin, Ming-Tseh
TI <i>IDH1</i> and <i>IDH2</i> Mutations in Colorectal Cancers
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE IDH1; IDH2; Colorectal cancer; BRAF p; V600E; Colitis-associated cancer
ID ISOCITRATE DEHYDROGENASE 1; MICROSATELLITE INSTABILITY; GENETIC
   ALTERATIONS; BRAF; ISOCITRATE-DEHYDROGENASE-1; LANDSCAPE; PROGNOSIS;
   PATHOLOGY; FEATURES; MUTANT
AB Objectives: To elucidate clinicopathologic and molecular characteristics of IDH1 and IDH2 (IDH1/2) mutations in colorectal cancers (CRCs).
   Methods: We evaluated IDH1/2 mutations in 1,623 CRCs using a next-generation sequencing assay.
   Results: IDH1/2 mutations, predominantly IDH1 p.R132C, were detected in 15 (0.9%) CRCs and in 5 (3.0%) of 167 BRAF p.V600E-mutated CRCs. Three IDH1/2-mutated CRCs were associated with inflammatory bowel disease. They were significantly associated with old age, mucinous or signet ring cell adenocarcinoma, and high-grade histomorphology. Concordance of variant allele frequency between IDH1/2 mutants and other trunk drivers in CRCs and presence of IDH1/2 mutation in the adenoma and early adenocarcinoma indicated IDH1/2 mutations could be trunk drivers suitable for targeted therapy.
   Conclusions: IDH1/2 mutations in CRCs were uncommon but enriched in BRAF p.V600E-mutated CRCs and perhaps colitis-associated CRCs. Further studies on IDH1/2-mutated CRCs are needed to clarify their clinicopathologic features and implications for targeted therapy.
C1 [Huang, Jialing; Tseng, Li-Hui; Parini, Vamsi; Lokhandwala, Parvez M.; Pallavajjala, Aparna; Rodriguez, Erika; Xian, Rena; Chen, Liam; Gocke, Christopher D.; Eshleman, James R.; Lin, Ming-Tseh] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
   [Xian, Rena; Gocke, Christopher D.; Eshleman, James R.] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
   [Huang, Jialing] Thomas Jefferson Univ, Dept Pathol, Philadelphia, PA 19107 USA.
   [Tseng, Li-Hui] Natl Taiwan Univ, Grad Inst Med Genom & Prote, Taipei, Taiwan.
C3 Johns Hopkins University; Johns Hopkins University; Jefferson
   University; National Taiwan University
RP Huang, JL (corresponding author), Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.; Huang, JL (corresponding author), Thomas Jefferson Univ, Dept Pathol, Philadelphia, PA 19107 USA.
EM jia-ling.huang@jefferson.edu
RI parini, vamsi/HZK-9008-2023
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NR 52
TC 16
Z9 16
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9173
EI 1943-7722
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD NOV
PY 2021
VL 156
IS 5
BP 777
EP 786
DI 10.1093/ajcp/aqab023
EA APR 2021
PG 10
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA WM6QH
UT WOS:000711207400006
PM 33929516
DA 2025-01-04
ER

PT J
AU Zhang, YB
   Xu, J
   Zhang, N
   Chen, M
   Wang, H
   Zhu, D
AF Zhang, Yunbin
   Xu, Jiang
   Zhang, Ning
   Chen, Ming
   Wang, Hua
   Zhu, Di
TI Targeting the tumour immune microenvironment for cancer therapy in human
   gastrointestinal malignancies
SO CANCER LETTERS
LA English
DT Article
DE Tumour microenvironment; Gastrointestinal cancer; Colorectal cancer;
   Drug resistance
ID REGULATORY T-CELLS; TYROSINE KINASE INHIBITOR; MEDIATED DRUG-RESISTANCE;
   COLORECTAL-CANCER; SUPPRESSOR-CELLS; MICROSATELLITE-INSTABILITY;
   HEPATOCELLULAR-CARCINOMA; INFILTRATING MACROPHAGES; CHRONIC
   INFLAMMATION; CHECKPOINT BLOCKADE
AB Gastrointestinal (GI) cancer is a malignancy of the GI tract and accessory digestive organs. GI cancer patients develop resistance to chemotherapy, targeted therapy drugs and immune therapies. Although immune checkpoint inhibitors have shown promising clinical results in melanoma, etc., immune checkpoint blockade responds in only a subset of colorectal cancer (CRC) patients with microsatellite instability-high (MSI-H) tumours. The tumour immune microenvironment (TIME) has a dynamic nature during malignant progression to which all the cells in the TIME contribute. Recent studies have highlighted the role of the TIME in the therapy resistance of cancer. Immune suppressive cells, such as tumour-associated macrophages, regulatory T cells, and myeloid derived suppressor cells, consist of a suppressive TIME to resist immune reactions. Combination approaches used to target the TIME, such as radiotherapy, chemotherapy, targeted therapy combined with checkpoint blockers or immune cell therapy, in addition to mono-immunotherapy, may provide better therapy responses. This review provides an analysis of recent developments regarding the role of the TIME in malignant progression, immunotherapy and the development of drug resistance in GI tract cancer, especially CRC, as well as approaches to overcome microenvironment-mediated resistance.
C1 [Zhang, Yunbin] Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai 200031, Peoples R China.
   [Xu, Jiang] Xuzhou Med Univ, Affiliated Hosp, Huaian Peoples Hosp 2, Dept Rehabil, Huaian, Peoples R China.
   [Zhang, Ning] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Urol, Shanghai 200020, Peoples R China.
   [Zhang, Yunbin; Chen, Ming] Yangzhou Univ, Affiliated Hosp 6, Dept Lab Med, Taizhou 225400, Jiangsu, Peoples R China.
   [Chen, Ming] Bengbu Med Coll, Affiliated Mixing Hosp, Dept Lab Med, Taizhou 225400, Jiangsu, Peoples R China.
   [Wang, Hua] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Orthoped, 58 Zhongshan Second Rd, Guangzhou 510080, Guangdong, Peoples R China.
   [Zhu, Di] Fudan Univ, Sch Pharm, Dept Pharmacol, Shanghai 201203, Peoples R China.
   [Zhu, Di] Fudan Univ, Minhang Hosp, Shanghai 201203, Peoples R China.
C3 Chinese Academy of Sciences; Xuzhou Medical University; Shanghai Jiao
   Tong University; Yangzhou University; Bengbu Medical University; Sun Yat
   Sen University; Fudan University; Fudan University
RP Wang, H (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 1, Dept Orthoped, 58 Zhongshan Second Rd, Guangzhou 510080, Guangdong, Peoples R China.; Zhu, D (corresponding author), Fudan Univ, Sch Pharm, Dept Pharmacol, Shanghai 201203, Peoples R China.; Zhu, D (corresponding author), Fudan Univ, Minhang Hosp, Shanghai 201203, Peoples R China.
EM wangxucheng@gmail.com; zhudi@fudan.edu.cn
RI Zhang, Ning/AHA-3443-2022
FU Science and Technology Commission of Shanghai, China [18ZR1403900];
   National Natural Science Foundation of China, China [81872895]; School
   of Pharmacy and Minhang Hospital, China [RO-MY201712]
FX The current study was supported by projects on the Science and
   Technology Commission of Shanghai, China (18ZR1403900) (Di Zhu); the
   National Natural Science Foundation of China, China (81872895) (Di Zhu);
   a project on joint translational research in the School of Pharmacy and
   Minhang Hospital, China (RO-MY201712) (Di Zhu).
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PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
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SN 0304-3835
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J9 CANCER LETT
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BP 123
EP 135
DI 10.1016/j.canlet.2019.05.017
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IF5KE
UT WOS:000473118900014
PM 31121212
DA 2025-01-04
ER

PT J
AU Chen, YT
   Tsao, SC
   Tsai, HP
   Wang, JY
   Chai, CY
AF Chen, Yi-Ting
   Tsao, Shu-Chuan
   Tsai, Hung-Pei
   Wang, Jaw-Yuan
   Chai, Chee-Yin
TI Serine protease inhibitor Kazal type 1 (SPINK1) as a prognostic marker
   in stage IV colon cancer patients receiving cetuximab based targeted
   therapy
SO JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE CARCINOMA; COLORECTAL CANCER; ONCOLOGY; RECTAL CANCER
ID EPIDERMAL-GROWTH-FACTOR; SECRETORY TRYPSIN-INHIBITOR; COLORECTAL-CANCER;
   BREAST-CANCER; EXPRESSION; FIBROBLASTS; METASTASIS; EGFR
AB Background Serine peptidase inhibitor Kazal type-1 (SPINK1), a trypsin kinase inhibitor, has well established associations with inflammation, cancer cell proliferation and carcinogenesis. However, the role of SPINK1 has not been investigated in stage IV colorectal cancer (CRC) patients receiving cetuximab based targeted therapy. The aim of this study was to evaluate the use of SPINK1 as a biomarker for predicting how patients with end stage CRC respond to anti-epidermal growth factor receptor (EGFR) therapies.
   Methods Immunohistochemical staining was used for semiquantitative analysis of SPINK1 protein expression in 51 CRC cases. Expression of SPINK1 protein was then analysed to identify correlations with clinicopathological variables.
   Results High SPINK1 expression was significantly associated with males (p=0.018). Kaplan-Meier analyses also showed that patients with high SPINK1 expression had significantly longer overall survival compared with controls (p=0.004). Multivariable analyses showed that SPINK1 expression and tumour size were significantly associated with prognosis (HR 0.416 and 0.437; 95% CI 0.217 to 0.797 and 0.236 to 0.810; p=0.008 and p=0.009, respectively) in these stage IV CRC cases.
   Conclusions High SPINK1 expression is associated with a good prognosis in stage IV CRC cases receiving cetuximab based targeted therapy. As SPINK1 expression is also an independent prognostic marker in these patients, it has potential use as a biomarker for clinical decision making and for designing personalised targeted therapies.
C1 [Chen, Yi-Ting; Tsao, Shu-Chuan; Chai, Chee-Yin] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Pathol, Kaohsiung, Taiwan.
   [Chen, Yi-Ting; Tsai, Hung-Pei; Wang, Jaw-Yuan; Chai, Chee-Yin] Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Municipal Hsiaokang Hosp, Dept Surg, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Dept Surg, Coll Med, Fac Med, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Div Gastroenterol & Gen Surg, Dept Surg, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Ctr Biomarkers & Biotech Drugs, Kaohsiung, Taiwan.
   [Chai, Chee-Yin] Kaohsiung Med Univ, Dept Pathol, Coll Med, Fac Med, Kaohsiung, Taiwan.
   [Chai, Chee-Yin] Natl Sun Yat Sen Univ, Inst Biomed Sci, Kaohsiung, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University; Kaohsiung Medical University; Kaohsiung
   Municipal Siao-Gang Hospital; Kaohsiung Medical University; Kaohsiung
   Medical University; Kaohsiung Medical University Hospital; Kaohsiung
   Medical University; Kaohsiung Medical University; Kaohsiung Medical
   University; National Sun Yat Sen University
RP Chai, CY (corresponding author), Kaohsiung Med Univ Hosp, Dept Pathol, 100 Tzyou 1st Rd, Kaohsiung 807, Taiwan.
EM cychai@kmu.edu.tw
RI Chai, Chee-Yin/D-5523-2009; Chen, Yuxuan/IWL-8267-2023; Jaw-Yuan,
   Wang/AFS-8845-2022
OI Wang, Jaw-Yuan/0000-0002-7705-2621; Chen, yiting/0000-0002-0817-1539;
   Chai, Chee-Yin/0000-0003-0486-9742; Tsai, Hung-Pei/0000-0001-9170-6268
FU Kaohsiung Medical University Hospital [KMUH 104-4T09]; Excellence for
   Cancer Research Centre Grant; Ministry of Health and Welfare, Health and
   Welfare Surcharge of Tobacco Products, Taiwan
   [MOHW105-TDU-B-212-134007]; Grant of Biosignature in Colorectal Cancers,
   Academia Sinica, Taiwan
FX This study was supported by a grant from the Kaohsiung Medical
   University Hospital (KMUH 104-4T09), the Excellence for Cancer Research
   Centre Grant, funded by the Ministry of Health and Welfare, Health and
   Welfare Surcharge of Tobacco Products, Taiwan (MOHW105-TDU-B-212-134007)
   and the Grant of Biosignature in Colorectal Cancers, Academia Sinica,
   Taiwan.
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NR 27
TC 7
Z9 7
U1 1
U2 9
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 NOV
PY 2016
VL 69
IS 11
BP 974
EP 978
DI 10.1136/jclinpath-2016-203638
PG 5
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA EC3DS
UT WOS:000388006000006
PM 27107100
DA 2025-01-04
ER

PT J
AU Dmello, RS
   To, SQ
   Chand, AL
AF Dmello, Rhynelle S.
   To, Sarah Q.
   Chand, Ashwini L.
TI Therapeutic Targeting of the Tumour Microenvironment in Metastatic
   Colorectal Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE metastatic colorectal cancer; targeted therapy; immunotherapy; tumour
   microenvironment; inflammation; cytokines; tumour heterogeneity
ID HEPATIC STELLATE CELLS; PREMETASTATIC NICHE FORMATION; CONSENSUS
   MOLECULAR SUBTYPES; IMMUNE CELLS; COLON-CANCER; OPEN-LABEL; MAINTENANCE
   THERAPY; ENDOTHELIAL-CELLS; LIVER METASTASIS; INITIAL THERAPY
AB Liver metastasis is the primary contributor to the death of patients with colorectal cancer. Despite the overall success of current treatments including targeted therapy, chemotherapy, and immunotherapy combinations in colorectal cancer patients, the prognosis of patients with liver metastasis remains poor. Recent studies have highlighted the importance of the tumour microenvironment and the crosstalk within that determines the fate of circulating tumour cells in distant organs. Understanding the interactions between liver resident cells and tumour cells colonising the liver opens new therapeutic windows for the successful treatment of metastatic colorectal cancer. Here we discuss critical cellular interactions within the tumour microenvironment in primary tumours and in liver metastases that highlight potential therapeutic targets. We also discuss recent therapeutic advances for the treatment of metastatic colorectal cancer.
C1 [Dmello, Rhynelle S.; To, Sarah Q.; Chand, Ashwini L.] La Trobe Univ, Olivia Newton John Canc Res Inst, Canc & Inflammat Program, Heidelberg, Vic 3084, Australia.
   [Dmello, Rhynelle S.; To, Sarah Q.; Chand, Ashwini L.] La Trobe Univ, Sch Canc Med, Heidelberg, Vic 3084, Australia.
C3 La Trobe University; Olivia Newton-John Cancer Research Institute; La
   Trobe University
RP Chand, AL (corresponding author), La Trobe Univ, Olivia Newton John Canc Res Inst, Canc & Inflammat Program, Heidelberg, Vic 3084, Australia.
EM Rhynelle.dmello@onjcri.org.au; Sarah.To@onjcri.org.au;
   ashwini.chand@onjcri.org.au
RI ; Chand, Ashwini/D-1531-2017
OI Dmello, Rhynelle/0000-0003-0202-7314; Chand, Ashwini/0000-0002-1245-729X
FU Cancer Council Victoria [1143036]; Austin Medical Research Fund; La
   Trobe RFA Scheme; Victorian Cancer Agency [19014]; Victorian State
   Government Operational Infrastructure Support Scheme; ONJCRI; La Trobe
   University Full-Fee Research Scholarship; La Trobe University
   Postgraduate Research Scholarship
FX The study was supported by the following grants and fellowship schemes:
   Cancer Council Victoria (1143036), Austin Medical Research Fund, La
   Trobe RFA Scheme, and the Victorian Cancer Agency (19014). Institutional
   funding from the Victorian State Government Operational Infrastructure
   Support Scheme and ONJCRI is acknowledged. R.S.D is supported by La
   Trobe University Full-Fee Research Scholarship and La Trobe University
   Postgraduate Research Scholarship.
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NR 110
TC 18
Z9 18
U1 8
U2 71
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD FEB
PY 2021
VL 22
IS 4
AR 2067
DI 10.3390/ijms22042067
PG 18
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA QP4HS
UT WOS:000623797900001
PM 33669775
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Suwaidan, AA
   Lau, DK
   Chau, I
AF Suwaidan, Ali Abdulnabi
   Lau, David K.
   Chau, Ian
TI HER2 targeted therapy in colorectal cancer: New horizons
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE Colorectal cancer; Targeted therapy; Human epidermal growth factor
   receptor; HER2; Precision medicine; ctDNA
ID MOLECULAR LANDSCAPE; PLUS-CETUXIMAB; RECTAL-CANCER; OPEN-LABEL;
   TRASTUZUMAB; OVEREXPRESSION; AMPLIFICATION; EXPRESSION; METASTASES;
   LAPATINIB
AB Despite recent advances in the treatment of metastatic colorectal cancer (mCRC), 5 years survival rates remain low. Chemotherapy remains as the mainstay of treatment with only few available targeted therapies. Human epidermal growth factor receptor 2 (HER2) amplification occurs in approximately 5% of metastatic colorectal cancer and it has been studied as a mechanism of resistance for anti-epidermal growth factor receptor (EGFR) therapy. Furthermore, several studies such as HERACLES-A, MyPathway and the DESTINY-CRCO1 trials have shown significant clinical benefit of HER2 blockade in patients with HER2 amplified mCRC. In this review, we provide an overview of the clinicopathological features of HER2 amplification and mutations in mCRC. In addition, we review HER2 as a biomarker of intrinsic and acquired anti-EGFR resistance as well as the preclinical, clinical and translational studies investigating the use of HER2 targeted therapies and future studies.
C1 [Suwaidan, Ali Abdulnabi; Lau, David K.; Chau, Ian] Royal Marsden NHS Fdn Trust, Gastrointestinal & Lymphoma Unit, London SM2 5PT, England.
   [Suwaidan, Ali Abdulnabi; Lau, David K.; Chau, Ian] Royal Marsden NHS Fdn Trust, Gastrointestinal & Lymphoma Unit, Downs Rd, Sutton SM2 5PT, Surrey, England.
C3 Royal Marsden NHS Foundation Trust; Royal Marsden NHS Foundation Trust
RP Chau, I (corresponding author), Royal Marsden NHS Fdn Trust, Gastrointestinal & Lymphoma Unit, Downs Rd, Sutton SM2 5PT, Surrey, England.
EM ian.chau@rmh.nhs.uk
RI Chau, Ian/ABC-2023-2020; Mohamed, Ali/HLX-3155-2023
OI Chau, Ian/0000-0003-0286-8703; Suwaidan, Ali
   Abdulnabi/0000-0002-5519-7432
FU National Institute for Health Research (NIHR) Biomedical Research Centre
   at The Royal Marsden NHS Foundation Trust, United Kingdom; Institute of
   Cancer Research, London, United Kingdom; Cancer Research UK Clinical
   Research Training Fellowship
FX We would like to acknowledge the National Institute for Health Research
   (NIHR) Biomedical Research Centre at The Royal Marsden NHS Foundation
   Trust, United Kingdom and the Institute of Cancer Research, London,
   United Kingdom. The views expressed are those of the author(s) and not
   necessarily those of the NIHR or the Department of Health and Social
   Care. AAM is the recipient of Cancer Research UK Clinical Research
   Training Fellowship.
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NR 90
TC 21
Z9 22
U1 3
U2 25
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0305-7372
EI 1532-1967
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD APR
PY 2022
VL 105
AR 102363
DI 10.1016/j.ctrv.2022.102363
EA FEB 2022
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3G0BT
UT WOS:000831023800002
PM 35228040
DA 2025-01-04
ER

PT J
AU Abedizadeh, R
   Majidi, F
   Khorasani, HR
   Abedi, H
   Sabour, D
AF Abedizadeh, Roya
   Majidi, Fateme
   Khorasani, Hamid Reza
   Abedi, Hassan
   Sabour, Davood
TI Colorectal cancer: a comprehensive review of carcinogenesis, diagnosis,
   and novel strategies for classified treatments
SO CANCER AND METASTASIS REVIEWS
LA English
DT Review
DE Colorectal cancer; Surgery; Chemotherapy; Targeted therapy;
   Immunotherapy; Nanomedicine
ID INTRAPERITONEAL AEROSOL CHEMOTHERAPY; COLON-CANCER; ADJUVANT
   CHEMOTHERAPY; RADIATION-THERAPY; LIVER METASTASES; RECTAL-CANCER;
   RADIOTHERAPY; IMMUNOTHERAPY; SURVIVAL; PHASE
AB Colorectal cancer is the third most common and the second deadliest cancer worldwide. To date, colorectal cancer becomes one of the most important challenges of the health system in many countries. Since the clinical symptoms of this cancer appear in the final stages of the disease and there is a significant golden time between the formation of polyps and the onset of cancer, early diagnosis can play a significant role in reducing mortality. Today, in addition to colonoscopy, minimally invasive methods such as liquid biopsy have received much attention. The treatment of this complex disease has been mostly based on traditional treatments including surgery, radiotherapy, and chemotherapy; the high mortality rate indicates a lack of success for current treatment methods. Moreover, disease recurrence is another problem of traditional treatments. Recently, new approaches such as targeted therapy, immunotherapy, and nanomedicine have opened new doors for cancer treatment, some of which have already entered the market, and many methods have shown promising results in clinical trials. The success of immunotherapy in the treatment of refractory disease, the introduction of these methods into neoadjuvant therapy, and the successful results in tumor shrinkage without surgery have made immunotherapy a tough competitor for conventional treatments. It seems that the combination of those methods with such targeted therapies will go through promising changes in the future of colorectal cancer treatment.
C1 [Abedizadeh, Roya; Majidi, Fateme; Khorasani, Hamid Reza; Sabour, Davood] ACECR, Royan Inst Stem Cell Biol & Technol, Cell Sci Res Ctr, Dept Canc Med, Isar 11, Babol 4713818983, Iran.
   [Abedizadeh, Roya; Majidi, Fateme; Khorasani, Hamid Reza; Sabour, Davood] ACECR, Royan Inst Stem Cell Biol & Technol, Cell Sci Res Ctr, Dept Stem Cells & Dev Biol, Bani Hashem Sq, Tehran 16635148, Iran.
   [Abedi, Hassan] Babol Univ Med Sci, Fac Med, Dept Internal Med, Babol, Iran.
C3 Academic Center for Education, Culture & Research (ACECR); Academic
   Center for Education, Culture & Research (ACECR); Babol University of
   Medical Sciences
RP Sabour, D (corresponding author), ACECR, Royan Inst Stem Cell Biol & Technol, Cell Sci Res Ctr, Dept Canc Med, Isar 11, Babol 4713818983, Iran.; Sabour, D (corresponding author), ACECR, Royan Inst Stem Cell Biol & Technol, Cell Sci Res Ctr, Dept Stem Cells & Dev Biol, Bani Hashem Sq, Tehran 16635148, Iran.; Abedi, H (corresponding author), Babol Univ Med Sci, Fac Med, Dept Internal Med, Babol, Iran.
EM h.abedi@mubabol.ac.ir; dsabour@royaninstitute.org
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NR 168
TC 10
Z9 10
U1 9
U2 24
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-7659
EI 1573-7233
J9 CANCER METAST REV
JI Cancer Metastasis Rev.
PD JUN
PY 2024
VL 43
IS 2
BP 729
EP 753
DI 10.1007/s10555-023-10158-3
EA DEC 2023
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TX3I0
UT WOS:001129251200001
PM 38112903
DA 2025-01-04
ER

PT J
AU Ciliberto, D
   Staropoli, N
   Caglioti, F
   Gualtieri, S
   Fiorillo, L
   Chiellino, S
   De Angelis, AM
   Mendicino, F
   Botta, C
   Caraglia, M
   Tassone, P
   Tagliaferri, P
AF Ciliberto, Domenico
   Staropoli, Nicoletta
   Caglioti, Francesca
   Gualtieri, Simona
   Fiorillo, Lucia
   Chiellino, Silvia
   De Angelis, Antonina Maria
   Mendicino, Francesco
   Botta, Cirino
   Caraglia, Michele
   Tassone, Pierfrancesco
   Tagliaferri, Pierosandro
TI A systematic review and meta-analysis of randomized trials on the role
   of targeted therapy in the management of advanced gastric cancer:
   Evidence does not translate?
SO CANCER BIOLOGY & THERAPY
LA English
DT Review
DE angiogenesis; gastric cancer; meta-analysis; randomized clinical trials;
   systemic chemotherapy; targeted pathways; targeted therapy
ID CELL-LUNG-CANCER; ENDOTHELIAL-GROWTH-FACTOR; ADVANCED ESOPHAGOGASTRIC
   CANCER; MEDULLARY-THYROID CANCER; PHASE-II TRIAL; OPEN-LABEL;
   DOUBLE-BLIND; JUNCTION ADENOCARCINOMA; 1ST-LINE TREATMENT;
   COLORECTAL-CANCER
AB It is still uncertain if targeted therapy-based regimens in advanced gastric cancer actually produce survival benefit. To shed light on this important question, we performed a systematic review and meta-analyses on each relevant targeted-pathway. By searching literature databases and proceedings of major cancer meetings in the time-frame 2005-2014, 22 randomized clinical trials exploring targeted therapy for a total of 7022 advanced gastric cancer patients were selected and included in the final analysis. Benefit was demonstrated for antiangiogenic agents in terms of overall survival (HR 0.759; 95% CI 0.655-0.880; p < 0.001). Conversely no benefit was found for EGFR pathway (HR 1.077; 95% CI 0.847-1.370; p = 0.543). Meta-analysis of HER-2 pathway confirmed improvement in terms of survival outcome, already known for this class of drugs (HR 0.823; 95% CI 0.722-0.939; p = 0.004). Pooled analysis demonstrated a significant survival benefit (OS: HR 0.823; PFS: HR 0.762) with acceptable tolerability profile for targeted-based therapies as compared to conventional treatments. This finding conflicts with the outcome of most individual studies, probably due to poor trial design or patients selection. In conclusion, our findings demonstrate a significant survival benefit for targeted therapy in its whole, which can be ascribed to anti-angiogenic and anti-HER2 agents.
C1 [Ciliberto, Domenico; Staropoli, Nicoletta; Caglioti, Francesca; Gualtieri, Simona; Fiorillo, Lucia; Chiellino, Silvia; De Angelis, Antonina Maria; Mendicino, Francesco; Botta, Cirino; Tassone, Pierfrancesco; Tagliaferri, Pierosandro] Magna Graecia Univ Catanzaro, Dept Expt & Clin Med, Catanzaro, Italy.
   [Caraglia, Michele] Univ Naples 2, Dept Biochem Biophys & Gen Pathol, Naples, Italy.
   [Caraglia, Michele; Tassone, Pierfrancesco] Temple Univ, Coll Sci & Technol, Ctr Biotechnol, Sbarro Inst Canc Res & Mol Med, Philadelphia, PA 19122 USA.
C3 Magna Graecia University of Catanzaro; Universita della Campania
   Vanvitelli; Pennsylvania Commonwealth System of Higher Education
   (PCSHE); Temple University
RP Caraglia, M (corresponding author), Univ Naples 2, Dept Biochem Biophys & Gen Pathol, Naples, Italy.
EM michele.caraglia@unina2.it; tassone@unicz.it; tagliaferri@unicz.it
RI Staropoli, Nicoletta/GZM-5038-2022; Tassone,
   Pierfrancesco/AIA-5373-2022; Caraglia, Michele/AAK-4569-2020;
   Tagliaferri, Pierosandro/K-9546-2016; Mendicino,
   Francesco/GZM-2793-2022; Caraglia, Michele/N-5670-2015; Ciliberto,
   Domenico/LTY-7873-2024; Botta, Cirino/K-8154-2017
OI Mendicino, Francesco/0000-0001-6339-632X; Caraglia,
   Michele/0000-0003-2408-6091; Staropoli, Nicoletta/0000-0001-9579-3960;
   Ciliberto, Domenico/0000-0003-1830-7070; Tassone,
   Pierfrancesco/0000-0002-8298-6787; Botta, Cirino/0000-0002-1522-4504
FU Magna Graecia University
FX This work is supported by PhD program of Magna Graecia University: PhD
   in molecular oncology and translational and innovative medical and
   surgical techniques.
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NR 115
TC 30
Z9 31
U1 0
U2 15
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 AUG
PY 2015
VL 16
IS 8
BP 1148
EP 1159
DI 10.1080/15384047.2015.1056415
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CO0LF
UT WOS:000358842000006
PM 26061272
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU El Bali, M
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   Mechita, MB
AF El Bali, Mouade
   Bakkach, Joaira
   Bennani Mechita, Mohcine
TI Colorectal Cancer: From Genetic Landscape to Targeted Therapy
SO JOURNAL OF ONCOLOGY
LA English
DT Review
ID CETUXIMAB PLUS IRINOTECAN; RANDOMIZED PHASE-III; CONSENSUS MOLECULAR
   SUBTYPES; ISLAND METHYLATOR PHENOTYPE; ANTI-EGFR THERAPY; KRAS CODON 12;
   COLON-CANCER; MICROSATELLITE INSTABILITY; ACQUIRED-RESISTANCE; 1ST-LINE
   TREATMENT
AB Colorectal cancer (CRC) is the third most common cancer type and the second cause of death worldwide. The advancement in understanding molecular pathways involved in CRC has led to new classifications based on the molecular characteristics of each tumor and also improved CRC management through the integration of targeted therapy into clinical practice. In this review, we will present the main molecular pathways involved in CRC carcinogenesis, the molecular classifications. The anti-VEGF and anti-EGFR therapies currently used in CRC treatment and those under clinical investigation will also be outlined, as well as the mechanisms of primary and acquired resistance to anti-EGFR monoclonal antibodies (cetuximab and panitumumab). Targeted therapy has led to great improvement in the treatment of metastatic CRC. However, there has been variability in CRC treatment outcomes due to molecular heterogeneity in colorectal tumors, which underscores the need for identifying prognostic and predictive biomarkers for CRC-targeted drugs.
C1 [El Bali, Mouade; Bakkach, Joaira; Bennani Mechita, Mohcine] Abdelmalek Essaadi Univ, Fac Sci & Tech Tangier, Biomed Genom & Oncogenet Res Lab, Tetouan, Morocco.
C3 Abdelmalek Essaadi University of Tetouan
RP El Bali, M (corresponding author), Abdelmalek Essaadi Univ, Fac Sci & Tech Tangier, Biomed Genom & Oncogenet Res Lab, Tetouan, Morocco.
EM mouade.elbali@etu.uae.ac.ma; j.bakkach@uae.ac.ma; mbennani@uae.ac.ma
RI Bakkach, Joaira/I-7022-2019
OI BENNANI MECHITA, Mohcine/0000-0002-8137-0665; EL BALI,
   Mouade/0000-0002-3096-9299
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NR 166
TC 31
Z9 31
U1 1
U2 19
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-8450
EI 1687-8469
J9 J ONCOL
JI J. Oncol.
PD JUL 6
PY 2021
VL 2021
AR 9918116
DI 10.1155/2021/9918116
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TM8UG
UT WOS:000675821000003
PM 34326875
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lakatos, G
   Köhne, CH
   Bodoky, G
AF Lakatos, Gabor
   Koehne, Claus-Henning
   Bodoky, Gyorgy
TI Current therapy of advanced colorectal cancer according to RAS/RAF
   mutational status
SO CANCER AND METASTASIS REVIEWS
LA English
DT Review
DE Colorectal cancer; RAS; BRAF; Targeted therapy; Biomarker
ID FOLFIRI PLUS BEVACIZUMAB; CIRCULATING TUMOR DNA; POST-HOC ANALYSIS; III
   COLON-CANCER; RAS MUTATIONS; KRAS MUTATIONS; 1ST-LINE TREATMENT; POOLED
   ANALYSIS; BRAF-MUTATION; GENETIC-HETEROGENEITY
AB Colorectal cancer is a clinically and molecularly heterogeneous disease. Currently, extended RAS and BRAF mutation testing is obligatory in routine clinical practice before starting any treatment in the metastatic setting. Treatment decision making also includes assessment of the clinical condition of the patient, definition of the treatment goal, and consideration of the primary tumor site. Biological treatment is part of the first-line drug combination unless contraindicated. Mutational status is significantly associated with the outcome of patients and is strongly predictive for anti-EGFR-targeted therapy. The prognosis of RAS mutant CRC is clearly inferior to wild-type cases. RAS remains an elusive target, and specific treatment options are not yet available. Recently, promising results of a direct KRAS G12C inhibitor have been reported; however, further confirmation is needed. The biomarker landscape in mCRC is evolving; new promising markers are awaited with the chance of more precise targeted treatment.
C1 [Lakatos, Gabor; Bodoky, Gyorgy] Natl Inst Infectol & Haematol, South Pest Hosp Ctr, Dept Oncol, Budapest, Hungary.
   [Koehne, Claus-Henning] Klinikum Oldenburg, Univ Clin Oncol & Haematol, Oldenburg, Germany.
C3 Klinikum Oldenburg
RP Lakatos, G (corresponding author), Natl Inst Infectol & Haematol, South Pest Hosp Ctr, Dept Oncol, Budapest, Hungary.
EM lakagab79@gmail.com
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NR 99
TC 18
Z9 19
U1 0
U2 9
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-7659
EI 1573-7233
J9 CANCER METAST REV
JI Cancer Metastasis Rev.
PD DEC
PY 2020
VL 39
IS 4
SI SI
BP 1143
EP 1157
DI 10.1007/s10555-020-09913-7
EA JUL 2020
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OU0UE
UT WOS:000546856300001
PM 32648137
DA 2025-01-04
ER

PT J
AU Taniguchi, G
   Kajino, K
   Momose, S
   Saeki, H
   Yue, L
   Ohtsuji, N
   Abe, M
   Shibuya, T
   Orimo, A
   Nagahara, A
   Watanabe, S
   Hino, O
AF Taniguchi, Gentaro
   Kajino, Kazunori
   Momose, Shuji
   Saeki, Harumi
   Yue, Liang
   Ohtsuji, Naomi
   Abe, Masaaki
   Shibuya, Tomoyoshi
   Orimo, Akira
   Nagahara, Akihito
   Watanabe, Sumio
   Hino, Okio
TI The Inhibitory Effects of Anti-ERC/Mesothelin Antibody 22A31 on
   Colorectal Adenocarcinoma Cells, within a Mouse Xenograft Model
SO CANCERS
LA English
DT Article
DE colorectal cancer; mesothelin; ERC; molecular targeting therapy;
   anti-ERC antibody
ID MESOTHELIN EXPRESSION; TARGET; PROLIFERATION; INVASION; BINDING;
   PROTEIN; TUMORS; TRIAL
AB Simple Summary The expression of Renal Carcinoma (ERC)/mesothelin is overexpressed in malignancies such as mesothelioma, pancreatic cancer, and ovarian cancer, and molecular-targeted therapies against ERC/mesothelin have been developed to treat them. Recently, it was revealed that ERC/mesothelin is also expressed in colorectal cancer; thus, this protein is expected to be a therapeutic target in colorectal cancer. In this study, we demonstrated that anti-ERC/mesothelin antibody 22A31 suppressed the growth of colorectal cancer cells subcutaneously xenografted on the back of mice. This is the first report to show the effectiveness of an anti-ERC/mesothelin antibody for the treatment of colorectal cancer in vivo. The expression of Renal Carcinoma (ERC)/mesothelin is enhanced in a variety of cancers. ERC/mesothelin contributes to cancer progression by modulating cell signals that regulate proliferation and apoptosis. Based on such biological insights, ERC/mesothelin has become a molecular target for the treatment of mesothelioma, pancreatic cancer, and ovarian cancer. Recent studies revealed about 50-60% of colorectal adenocarcinomas also express ERC/mesothelin. Therefore, colorectal cancer can also be a potential target of the treatment using an anti-ERC/mesothelin antibody. We previously demonstrated an anti-tumor effect of anti-ERC antibody 22A31 against mesothelioma. In this study, we investigated the effect of 22A31 on a colorectal adenocarcinoma cell line, HCT116. The cells were xenografted into BALB/c nu/nu mice. All mice were randomly allocated to either an antibody treatment group with 22A31 or isotype-matched control IgG1 kappa. We compared the volume of subsequent tumors, and tumors were pathologically assessed by immunohistochemistry. Tumors treated with 22A31 were significantly smaller than those treated with IgG1 kappa and contained significantly fewer mitotic cells with Ki67 staining. We demonstrated that 22A31 exhibited a growth inhibitory property on HCT116. Our results implied that ERC/mesothelin-targeted therapy might be a promising treatment for colorectal cancer.
C1 [Taniguchi, Gentaro; Kajino, Kazunori; Yue, Liang; Ohtsuji, Naomi; Abe, Masaaki; Orimo, Akira; Hino, Okio] Juntendo Univ, Grad Sch Med, Dept Mol Pathol, Bunkyo Ku, 2-1-1 Hongo, Tokyo 1138421, Japan.
   [Taniguchi, Gentaro; Shibuya, Tomoyoshi; Nagahara, Akihito; Watanabe, Sumio] Juntendo Univ, Dept Gastroenterol, Fac Med, Bunkyo Ku, 2-1-1 Hongo, Tokyo 1138421, Japan.
   [Kajino, Kazunori; Saeki, Harumi; Ohtsuji, Naomi] Juntendo Univ, Grad Sch Med, Dept Human Pathol, Bunkyo Ku, 2-1-1 Hongo, Tokyo 1138421, Japan.
   [Momose, Shuji] Saitama Med Univ, Dept Pathol, Saitama Med Ctr, 1981 Kamoda, Kawagoe, Saitama 3508550, Japan.
C3 Juntendo University; Juntendo University; Juntendo University; Saitama
   Medical University
RP Kajino, K (corresponding author), Juntendo Univ, Grad Sch Med, Dept Mol Pathol, Bunkyo Ku, 2-1-1 Hongo, Tokyo 1138421, Japan.; Kajino, K (corresponding author), Juntendo Univ, Grad Sch Med, Dept Human Pathol, Bunkyo Ku, 2-1-1 Hongo, Tokyo 1138421, Japan.
EM gtanigu@juntendo.ac.jp; kajino@juntendo.ac.jp; momose@saitama-med.ac.jp;
   haru-s@juntendo.ac.jp; l-yue@juntendo.ac.jp; kadowaki@juntendo.ac.jp;
   masa@juntendo.ac.jp; tomoyosi@juntendo.ac.jp; aorimo@juntendo.ac.jp;
   nagahara@juntendo.ac.jp; sumio@juntendo.ac.jp; ohino@juntendo.ac.jp
RI Nagahara, Akihito/L-4010-2016
OI Shibuya, Tomoyoshi/0000-0003-3558-7123
FU Japan Society for the Promotion of Science [221S0001]; Foundation of
   Strategic Research Projects in Private Universities of the Ministry of
   Education, Culture, Sports, Science and Technology of Japan (MEXT)
   [S1311011, S1511008L]; Promotion and Mutual Aid Corporation for Private
   Schools of Japan
FX This study was supported in part by a Grant-in-Aid (221S0001) for
   Scientific Research on Innovative Areas from the Japan Society for the
   Promotion of Science, Grants-in-Aid (S1311011 and S1511008L) from the
   Foundation of Strategic Research Projects in Private Universities of the
   Ministry of Education, Culture, Sports, Science and Technology of Japan
   (MEXT), and grants from Shizuoka Medical Research Center for Disaster of
   Juntendo University Shizuoka Hospital, and from the Institute for
   Environmental and Gender-Specific Medicine of Juntendo University
   Urayasu Hospital. This work was also supported by a Grant-in-Aid for
   Special Research in Subsidies for ordinary expenses of private schools
   from The Promotion and Mutual Aid Corporation for Private Schools of
   Japan.
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NR 33
TC 1
Z9 1
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 MAY
PY 2022
VL 14
IS 9
AR 2198
DI 10.3390/cancers14092198
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 1F6HK
UT WOS:000795267600001
PM 35565327
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, XY
   Zhao, CY
   Gong, Y
   Wang, Y
   Guo, F
AF Wang, Xiaoyan
   Zhao, Chenyi
   Gong, Yang
   Wang, Ying
   Guo, Feng
TI Multidrug resistance in the standardized treatment of colon cancer
   harboring a rare fibrosarcoma B-type (BRAF) p.N581I mutation: a case
   report
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE BRAF p; N581I; colorectal cancer metastasis; targeted therapy;
   immunotherapy; multidrug resistance; anti-EGFR monoclonal antibody
AB BRAF non-V600 mutations are a distinct molecular subset of colorectal cancer (CRC) that has little to no clinical similarity to the BRAF V600 mutations. It is generally considered that the BRAF non-V600 mutations correlate with better survival of CRC patients. In this report, we present an unusual case of that a midlife female patient who was initially diagnosed with stage IIIC colon cancer, and multiple metastases were found 25 months after radical surgery. Next-generation sequencing (NGS) revealed the BRAF p.N581I (c.1742A>T) mutation. She received chemotherapy, targeted therapy, and immunotherapy. However, the disease progressed rapidly with rare metastasis of the bone and cerebellum. This case highlights that the BRAF non-V600 mutations, such as BRAF p.N581I mutant, may lead to resistance to epidermal growth factor receptor (EGFR) inhibitors and result in a rapid course in colorectal cancer. The role of BRAF p.N581I mutation in colorectal cancer demands more attention.
C1 [Wang, Xiaoyan; Zhao, Chenyi; Gong, Yang; Wang, Ying; Guo, Feng] Nanjing Med Univ, Suzhou Municipal Hosp, Dept Oncol, Affiliated Suzhou Hosp, Suzhou, Peoples R China.
C3 Nanjing Medical University
RP Guo, F (corresponding author), Nanjing Med Univ, Suzhou Municipal Hosp, Dept Oncol, Affiliated Suzhou Hosp, Suzhou, Peoples R China.
EM guofeng27@gmail.com
RI GUO, FENG/JRX-3555-2023
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NR 27
TC 0
Z9 0
U1 1
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JUL 14
PY 2023
VL 13
AR 1175693
DI 10.3389/fonc.2023.1175693
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA N2FQ6
UT WOS:001035236900001
PM 37519790
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yang, YN
   Tang, J
   Zhang, M
   Gu, ZY
   Song, H
   Yang, Y
   Yu, CZ
AF Yang, Yannan
   Tang, Jie
   Zhang, Min
   Gu, Zhengying
   Song, Hao
   Yang, Yang
   Yu, Chengzhong
TI Responsively Aggregatable Sub-6 nm Nanochelators Induce Simultaneous
   Antiangiogenesis and Vascular Obstruction for Enhanced Tumor Vasculature
   Targeted Therapy
SO NANO LETTERS
LA English
DT Article
DE Ultrasmall nanochelators; organosilica; antiangiogenesis; vascular
   obstruction; copper depletion
ID ANGIOGENESIS; COPPER; CANCER; NANOPARTICLES; TETRATHIOMOLYBDATE; LIVER;
   COAGULOPATHY; RESISTANCE; MECHANISM; REMOVAL
AB Inhibiting the formation of new tumor blood vessels (so-called antiangiogenesis) and obstructing the established ones are two primary strategies in tumor vasculature targeted therapy. However, the therapeutic outcome of conventional methodologies relying on only one mechanism is rather limited. Herein, the first example of ultrasmall responsively aggregatable nanochelators that can intrinsically fulfill both antivasculature functions as well as high renal clearable efficiency is introduced. The nanochelators with sub-6 nm sizes exhibit not only systemic copper depletion activity for tumor antiangiogenesis but also, more surprisingly, the capability to transform from a "dispersed" state to an "aggregated" state to form large secondary particles in response to tumor microenvironment with elevated copper and phosphate levels for blood vessel obstruction. Compared to a benchmark antiangiogenic agent that can only inhibit the formation of tumor blood vessels, the nanochelators with unprecedented synergistic functions demonstrate significantly enhanced tumor inhibition activity in both breast cancer and colon cancer tumor models. Moreover, these ultrasmall nanochelators are noncytotoxic and renal clearable, ensuring superior biocompatibility. It is envisaged that the design of nanomaterials with ground-breaking properties and the synergistic antivasculature functions would offer a substantial conceptual advance for tumor vasculature targeted therapy and may provide vast opportunities for developing advanced nanomedicines.
C1 [Yang, Yannan; Tang, Jie; Zhang, Min; Gu, Zhengying; Song, Hao; Yang, Yang; Yu, Chengzhong] Univ Queensland, Australian Inst Bioengn & Nanotechnol, Brisbane, Qld 4072, Australia.
   [Zhang, Min; Yu, Chengzhong] East China Normal Univ, Sch Chem & Mol Engn, Shanghai 200241, Peoples R China.
C3 University of Queensland; East China Normal University
RP Yu, CZ (corresponding author), Univ Queensland, Australian Inst Bioengn & Nanotechnol, Brisbane, Qld 4072, Australia.; Yu, CZ (corresponding author), East China Normal Univ, Sch Chem & Mol Engn, Shanghai 200241, Peoples R China.
EM c.yu@uq.edu.au
RI Tang, Jie/CAJ-3829-2022; Yang, Yannan/KXR-8915-2024; Gu,
   Zhengying/E-5280-2019; Yu, Chengzhong/I-8663-2012; Song, Hao/C-5166-2019
OI Gu, Zhengying/0000-0002-8597-6752; Yu, Chengzhong/0000-0003-3707-0785;
   Song, Hao/0000-0002-6383-0605; Yang, Yannan/0000-0001-6696-3879
FU Australian Research Council; Queensland Government
FX The authors acknowledge the financial support from the Australian
   Research Council and the Queensland Government. We also thank the
   technical assistance from the Australian National Fabrication Facility,
   the Australian Microscopy and Microanalysis Research Facility at the
   Centre for Microscopy and Microanalysis, Centre for Advanced Imaging,
   The University of Queensland's Biological Resources, and QIMR Berghofer
   Medical Research Institute.
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NR 53
TC 27
Z9 31
U1 1
U2 98
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 NOV
PY 2019
VL 19
IS 11
BP 7750
EP 7759
DI 10.1021/acs.nanolett.9b02691
PG 10
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
   Nanotechnology; Materials Science, Multidisciplinary; Physics, Applied;
   Physics, Condensed Matter
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science;
   Physics
GA JO0EA
UT WOS:000497259300022
PM 31657578
DA 2025-01-04
ER

PT J
AU Koroukian, SM
   Booker, BD
   Vu, L
   Schumacher, FR
   Rose, J
   Cooper, GS
   Selfridge, JE
   Markt, SC
AF Koroukian, Siran M.
   Booker, Benjamin D.
   Vu, Long
   Schumacher, Fredrick R.
   Rose, Johnie
   Cooper, Gregory S.
   Selfridge, J. Eva
   Markt, Sarah C.
TI Receipt of Targeted Therapy and Survival Outcomes in Patients With
   Metastatic Colorectal Cancer
SO JAMA NETWORK OPEN
LA English
DT Article
ID 1ST-LINE TREATMENT; RACIAL DISPARITIES; PHASE-III; BEVACIZUMAB;
   FLUOROURACIL; LEUCOVORIN; CHEMOTHERAPY; OXALIPLATIN; PANITUMUMAB;
   IRINOTECAN
AB IMPORTANCE Professional society guidelines recommend treating patients with metastatic colorectal cancer with targeted therapies, including epithelial growth factor receptor (EGFR) inhibitors and vascular endothelial growth factor (VEGF) inhibitors, depending on the presence or absence of certain mutations. Since most studies of first-line targeted therapies have been limited by sample size, there is a need for larger studies using data from routine clinical care.
   OBJECTIVES To identify factors associated with receipt of first-line targeted therapies among patients with metastatic colorectal cancer for whom RAS or BRAF mutation data in the tumor were available and investigate whether targeted therapy is associated with survival.
   DESIGN, SETTING, AND PARTICIPANTS This cohort study used deidentified data from an electronic health record-derived database to include patients from 800 sites of patient care across the US who were diagnosed with de novo metastatic colorectal cancer between January 1, 2013, and March 31, 2020 (n = 9134).
   MAIN OUTCOMES AND MEASURES Receipt of first-line targeted therapy, categorized as ever having received EGFR inhibitors, VEGF inhibitors, or neither. The secondary outcome was overall survival.
   RESULTS The study population included 9134 patients. The median age at diagnosis was 62 years (IQR, 53-71 years), 5019 (54.9%) were male, and 5692 (62.3%) were White. The median follow-up period was 15 months. Overall, 713 patients (7.8%) received EGFR inhibitors and 5081 patients (55.6%) received VEGF inhibitors as part of their first-line treatment. Among patients with RAS wildtype (RAS-WT) tumors, 625 patients (15.5%) received EGFR inhibitors and 2053 patients (50.9%) received VEGF inhibitors. In patients with RAS mutant (RAS-Mut) tumors, 50 patients (1.1%) received EGFR inhibitors and 2682 patients (59.7%) received VEGF inhibitors; among those with BRAF mutant (BRAF-Mut) tumors, 38 patients (6.3%) received EGFR inhibitors and 346 patients (57.2%) received VEGF inhibitors. More than one-third of the patients (36.6%) received neither EGFR inhibitors nor VEGF inhibitors. Compared with patients younger than age 40 years, those aged 80 years or older had significantly lower odds to receive targeted therapies (EGFR or VEGF inhibitors in patients with RAS-WT tumors: adjusted odds ratio [aOR], 0.53; 95% CI, 0.36-0.79; and VEGF inhibitors in patients with RAS-Mut tumors: aOR, 0.62; 95% CI, 0.42-0.90). Improved survival was associated with EGFR inhibitor therapy in patients with RAS-WT tumors (adjusted hazard ratio [aHR], 0.85; 95% CI, 0.74-0.98). Unlike in clinical trials, however, no survival benefit was noted with use of VEGF inhibitors among patients with RAS-WT (aHR, 1.00; 95% CI, 0.91-1.11) or RAS-Mut (aHR, 1.01; 95% CI, 0.93-1.10) tumors.
   CONCLUSIONS AND RELEVANCE The findings of this study showed mixed results on survival benefits associated with targeted therapy. In addition, given that some of the results differed from those of randomized clinical trials, this study highlights the importance of using data originating from routine clinical care.
C1 [Koroukian, Siran M.; Booker, Benjamin D.; Vu, Long; Schumacher, Fredrick R.; Rose, Johnie; Cooper, Gregory S.; Markt, Sarah C.] Case Western Reserve Univ, Dept Populat & Quantitat Hlth Sci, Sch Med, Cleveland, OH USA.
   [Koroukian, Siran M.; Schumacher, Fredrick R.; Rose, Johnie; Cooper, Gregory S.; Selfridge, J. Eva; Markt, Sarah C.] Case Western Reserve Univ, Case Comprehens Canc Ctr, Sch Med, Cleveland, OH USA.
   [Rose, Johnie] Case Western Reserve Univ, Sch Med, Ctr Community Hlth Integrat, Cleveland, OH USA.
   [Cooper, Gregory S.] Univ Hosp Cleveland Med Ctr, Dept Internal Med, Cleveland, OH USA.
   [Selfridge, J. Eva] Univ Hosp Cleveland Med Ctr, Div Solid Tumor Oncol, Cleveland, OH USA.
C3 University System of Ohio; Case Western Reserve University; University
   System of Ohio; Case Western Reserve University; University System of
   Ohio; Case Western Reserve University; University Hospitals of
   Cleveland; University Hospitals of Cleveland
RP Koroukian, SM (corresponding author), Case Western Reserve Univ, Dept Populat & Quantitat Hlth Sci, Sch Med, 10900 Euclid Ave,WG-43, Cleveland, OH 44106 USA.
EM skoroukian@case.edu
RI Markt, Sarah/O-7554-2019
FU American Cancer Society [132678-RSGI-19-213-01-CPHPS, RWIA-20-1111-02
   RWIA]; National Cancer Institute [P30 CA043703, R37CA227865,
   R37CA222574, 1U54CA254566, K12CA076917, P50CA150964, R01CA256791];
   National Heart, Lung, and Blood Institute [R01HL153175]; National
   Institute of Dental and Craniofacial Research [UH2DE025487,
   UH3-DE025487]; National Institute of Nursing Research [R15 NR017792];
   National Institute of Diabetes, Digestive, and Kidney Disease [P30
   DK097948]; National Institute on Aging [R01 AG074946]; National
   Institute of Minority Health Disparities [R01HD105892]; Agency for
   Healthcare Research and Quality [U18 HS028742]; Centers for Disease
   Control and Prevention [U48 DP005030-05S1, U48 DP00640403S7]; Cleveland
   Clinic Foundation; Celgene Corporation; ERACE Concert AI; Bristol-Myers
   Squibb
FX This work was supported by funding from the American Cancer Society,
   grant RWIA-20-1111-02 RWIA. The authors report additional funding from
   the following sources: National Cancer Institute (grant P30 CA043703
   [Drs Koroukian, Cooper, Rose, and Schumacher, and Mr Vu]); grant
   R37CA227865 and R37CA222574 [Dr Markt]; grant 1U54CA254566 [Dr
   Schumacher]; and grant K12CA076917, P50CA150964, and R01CA256791 [Dr
   Selfridge]); the National Heart, Lung, and Blood Institute (grant
   R01HL153175 [Dr Rose]); the National Institute of Dental and
   Craniofacial Research (grant UH2DE025487 [Drs Koroukian and Rose], and
   grant UH3-DE025487 [Dr Koroukian]); the National Institute of Nursing
   Research (grant R15 NR017792 [Dr Koroukian]); the National Institute of
   Diabetes, Digestive, and Kidney Disease (grant P30 DK097948 [Dr
   Cooper]); the National Institute on Aging (grant R01 AG074946 [Dr
   Koroukian]); the National Institute of Minority Health Disparities
   (grant R01HD105892 [Dr Schumacher]); the Agency for Healthcare Research
   and Quality (grant U18 HS028742 [Dr Schumacher]); the Centers for
   Disease Control and Prevention (grant U48 DP005030-05S1 and U48
   DP00640403S7 [Dr Koroukian]); the American Cancer Society
   (132678-RSGI-19-213-01-CPHPS [Drs Koroukian and Cooper]); the Cleveland
   Clinic Foundation, including a subcontract from Celgene Corporation (Dr
   Koroukian); and ERACE Concert AI (Markt); and Bristol-Myers Squibb (Drs
   Markt and Schumacher).
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NR 43
TC 9
Z9 9
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2574-3805
J9 JAMA NETW OPEN
JI JAMA Netw. Open
PD JAN
PY 2023
VL 6
IS 1
AR e2250030
DI 10.1001/jamanetworkopen.2022.50030
PG 14
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA Q7PP9
UT WOS:001059410400001
PM 36656585
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yang, ML
   Yeatman, TJ
AF Yang, Mingli
   Yeatman, Timothy J.
TI Molecular stratification of colorectal cancer populations and its use in
   directing precision medicine
SO EXPERT REVIEW OF PRECISION MEDICINE AND DRUG DEVELOPMENT
LA English
DT Review
DE Colorectal cancer; genomic classification; driver genes; prognosis;
   adjuvant therapy; targeted therapy
ID ADENOMATOUS POLYPOSIS-COLI; MISMATCH REPAIR STATUS; CETUXIMAB PLUS
   IRINOTECAN; BRAF V600E MUTATION; MICROSATELLITE-INSTABILITY; CHROMOSOMAL
   INSTABILITY; ADJUVANT CHEMOTHERAPY; RAS MUTATIONS; SURVIVAL BENEFIT;
   TARGETED THERAPY
AB Introduction: The intrinsic heterogeneity of colorectal cancer (CRC) makes it difficult to determine which patients will benefit from adjuvant or systemic therapy and which patients will not require further treatment beyond surgical resection. This had led to a generalized 'one size fits all' approach to therapy. Such heterogeneity also makes it a great challenge to predict which patients might respond to targeted therapies. Precision medical diagnostics now hold promise to address these new challenges.
   Areas covered: The authors first review various molecular/genomic classification studies of colorectal cancer, including the prognostic role of MSI (microsatellite instability), CIN (chromosomal instability), and driver genes such as KRAS, NRAS, BRAF, PIK3CA and TP53, as well as our recent finding revealing a new prognostic role of APC and partnering mutations with KRAS and TP53. The authors then discuss prediction of treatment response for either adjuvant therapy or systemic targeted therapy (e.g. anti-EGFR therapy) as well as the effect of tumor sidedness.
   Expert commentary: There is an urgent need for more precise molecular classification to stratify adjuvant therapy and systemic targeted therapy to ultimately facilitate individualized treatments. Sequencing of APC may have clinical utility in the routine staging and potential therapeutic assignment for CRC patients.
C1 [Yang, Mingli; Yeatman, Timothy J.] Gibbs Canc Ctr & Res Inst, Gibbs Res Inst, Spartanburg, SC 29303 USA.
RP Yeatman, TJ (corresponding author), Gibbs Canc Ctr & Res Inst, Gibbs Res Inst, Spartanburg, SC 29303 USA.
EM Yeatman@gibbscc.org
RI Yeatman, Timothy/LJK-6730-2024
FU NIH [U01CA157960]
FX This paper was funded by NIH (U01CA157960 to TJ Yeatman).
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NR 145
TC 2
Z9 3
U1 0
U2 1
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 2380-8993
J9 EXPERT REV PRECIS ME
JI Expert Rev. Precis. Med. Drug Dev.
PY 2017
VL 2
IS 4
BP 205
EP 215
DI 10.1080/23808993.2017.1362316
PG 11
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA GX6DW
UT WOS:000447849200003
DA 2025-01-04
ER

PT J
AU Oliveres, H
   Cascante, M
   Maurel, J
AF Oliveres, Helena
   Cascante, Marta
   Maurel, Joan
TI Metabolic interventions to enhance immunotherapy and targeted therapy
   efficacy in advanced colorectal cancer
SO CURRENT OPINION IN CHEMICAL BIOLOGY
LA English
DT Review
DE Immunotherapy; Metabolism; Resistance
ID RESISTANCE; BLOCKADE; CELLS; GLYCOLYSIS; SUBTYPES; TUMORS
AB Current standard-of-care for metastatic colorectal cancer patients includes chemotherapy and anti-angiogenic or antiepider mal growth factor receptor for microsatellite stable tumors and pembrolizumab for microsatellite instable tumors. However, despite the available therapies, the prognosis remains poor. In recent years, new drugs combined with immune checkpoint inhibitors have been tested in microsatellite stable metastatic colorectal cancer patients, but the benefit was modest. Here, we review the metabolic interactions between the immune microenvironment and cancer cells. More specifically, we highlight potential correlatives of tumor immune and metabolic features with transcriptomic classifications such as the Consensus Molecular Subtype. Finally, we discuss the unmet need of immune-metabolic signatures and the value of a new signature (IMMETCOLS) for guiding new strategies in metastatic colorectal cancer. We conclude that the field is ready to propose customized strategies for modifying metabolism and improving immunotherapy and targeted therapy efficacy.
C1 [Oliveres, Helena; Maurel, Joan] Hosp Clin Barcelona, Med Oncol Dept, Translat Genom & Targeted Therapeut Solid Tumors G, IDIBAPS, Barcelona, Spain.
   [Cascante, Marta; Maurel, Joan] Inst Salud Carlos III ISCIII, Ctr Invest Biomed Red Enfermedades Hepat & Digest, Madrid, Spain.
   [Cascante, Marta] Univ Barcelona, Dept Biochem & Mol Biol, Barcelona, Spain.
   [Cascante, Marta] Univ Barcelona, Inst Biomed IBUB, Barcelona, Spain.
C3 University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS; CIBER -
   Centro de Investigacion Biomedica en Red; CIBEREHD; University of
   Barcelona; University of Barcelona
RP Maurel, J (corresponding author), Hosp Clin Barcelona, Med Oncol Dept, Translat Genom & Targeted Therapeut Solid Tumors G, IDIBAPS, Barcelona, Spain.; Cascante, M; Maurel, J (corresponding author), Inst Salud Carlos III ISCIII, Ctr Invest Biomed Red Enfermedades Hepat & Digest, Madrid, Spain.; Cascante, M (corresponding author), Univ Barcelona, Dept Biochem & Mol Biol, Barcelona, Spain.; Cascante, M (corresponding author), Univ Barcelona, Inst Biomed IBUB, Barcelona, Spain.
EM martacascante@ub.edu; jmaurel@clinic.cat
RI CASCANTE, MARTA/AFK-5991-2022
OI CASCANTE, MARTA/0000-0002-2062-4633
FU Spanish Ministry of Science and Innovation - MCIN/AEI
   [PID2020-115051RB-I00]; ICREA_Academiae Prize - ICREA Foundation;
   Foundation Olga Torres [A-2019/2020]; Spanish Association Against Cancer
   (AECC) [PROYE19040POST_001]; Instituto de Salud Carlos III [PI13/01728,
   PI19/0740]; Catalan Agency for the Management of University and Research
   Grants(AGAUR) [2021-SGR-01328, 2021- SGR-00350]
FX Grants from the Spanish Ministry of Science and Innovation
   PID2020-115051RB-I00 funded by MCIN/AEI/10.13039/501100011033 and the
   ICREA_Academiae Prize funded by ICREA Foundation to MC. Grants from
   Foundation Olga Torres (Biannual Grant A-2019/2020), Spanish Association
   Against Cancer (AECC, PROYE19040POST_001), and Instituto de Salud Carlos
   III (PI13/01728 and PI19/0740) to JM. Grants from the Catalan Agency for
   the Management of University and Research Grants(AGAUR) (2021-SGR-01328
   to JM and 2021- SGR-00350 to MC).
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NR 56
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 1367-5931
EI 1879-0402
J9 CURR OPIN CHEM BIOL
JI Curr. Opin. Chem. Biol.
PD DEC
PY 2023
VL 77
AR 102401
DI 10.1016/j.cbpa.2023.102401
EA OCT 2023
PG 8
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA W4YS5
UT WOS:001091704800001
PM 37806262
OA hybrid
DA 2025-01-04
ER

PT J
AU Shao, NY
   Wang, DX
   Wang, Y
   Li, Y
   Zhang, ZQ
   Jiang, Q
   Luo, WF
   Cao, C
AF Shao, Nai-yuan
   Wang, Dong-xing
   Wang, Yin
   Li, Ya
   Zhang, Zhi-qing
   Jiang, Qin
   Luo, Weifeng
   Cao, Cong
TI MicroRNA-29a-3p Downregulation Causes Gab1 Upregulation to Promote
   Glioma Cell Proliferation
SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
LA English
DT Article
DE Glioma; Gab1; MicroRNA-29a-3p; Cell proliferation
ID PIGMENT EPITHELIUM-CELLS; MACROPHAGE POLARIZATION; COLORECTAL-CANCER;
   TARGETED THERAPY; TNF-ALPHA; ACTIVATION; PROGRESSION; EXPRESSION;
   STATISTICS; PATHWAY
AB Background/Aims: Glioma causes significant human mortalities annually. Molecularly-targeted therapy is a focus of glioma research. Methods: Grb2-associated binding 1 (Gab1) expression and microRNA-29a-3p ("miR-29a-3p") expression in human glioma cells and tissues were tested by Western blotting assay and qRT-PCR assay. shRNA/siRNA strategy was applied to silence Gab1 in human glioma cells. miR-29a or anti-sense miR-29a construct was transfected to human glioma cells. Cell proliferation was tested by BrdU ELISA assay and cell counting assay. Results: We show that expression of Gab1 was significantly elevated in human glioma tissues and cells, which correlated with downregulation of its putative microRNA: miR29a-3p. In A172 glioma cells and primary human glioma cells, Gab1 shRNA/siRNA inhibited Akt-Erk activation and cell proliferation. Forced-expression of miR-29a-3p downregulated Gab1, inhibiting glioma cell proliferation, whereas miR-29a-3p was in-effective on cell proliferation in Gab1-silenced A172 cells. Furthermore, introduction of a 3'-untranslated region (3'-UTR) mutant Gab1 (UTR-G160A) blocked miR-29a-3p-induced inhibition on Akt signaling and A172 cell proliferation. Conclusions: miR-29a-3p downregulation leads to Gab1 upregulation to promote glioma cell proliferation. (C) 2018 The Author(s) Published by S. Karger AG, Basel
C1 [Shao, Nai-yuan] Soochow Univ, Affiliated Hosp 3, Dept Neurosurg, Changzhou, Peoples R China.
   [Wang, Dong-xing; Luo, Weifeng; Cao, Cong] Soochow Univ, Affiliated Hosp 2, Dept Neurol, Suzhou, Peoples R China.
   [Wang, Yin; Li, Ya; Zhang, Zhi-qing; Cao, Cong] Soochow Univ, Inst Neurosci, Suzhou, Peoples R China.
   [Jiang, Qin; Cao, Cong] Nanjing Med Univ, Affiliated Eye Hosp, 138 Han Zhong Rd, Nanjing 210029, Jiangsu, Peoples R China.
   [Cao, Cong] Municipal Hosp Suzhou, Suzhou, Peoples R China.
C3 Soochow University - China; Soochow University - China; Soochow
   University - China; Nanjing Medical University
RP Jiang, Q; Luo, WF; Cao, C (corresponding author), Nanjing Med Univ, Affiliated Eye Hosp, 138 Han Zhong Rd, Nanjing 210029, Jiangsu, Peoples R China.
EM Jqin710@vip.sina.com; Lwfwxx@126.com; caocong@suda.edu.cn
RI cao, cong/KCX-7547-2024; Shao, Nan/AAX-7528-2020
OI Shao, Naiyuan/0000-0001-5523-7142
FU National Natural Science Foundation of China [81371055, 81570859,
   81302195, 31371139, 81502162, 81571282]; Natural Science Foundation of
   Jiangsu Province [BK20130301, BK20151213, BK20170060]; Jiangsu province
   Six-Talent Peaks
FX This work was generously supported by grants from the National Natural
   Science Foundation of China (Nos. 81371055 and 81570859, 81302195,
   31371139 and 81502162, 81571282); Grants from Natural Science Foundation
   of Jiangsu Province (BK20130301, BK20151213, BK20170060), and Jiangsu
   province Six-Talent Peaks (To C.C.). The funders had no role in study
   design, data collection and analysis, decision to publish, or
   preparation of the manuscript. All authors carried out all the
   experiments, participated in the design of the project conceived of the
   study, and participated in its design and coordination and helped to
   draft the manuscript.
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NR 52
TC 31
Z9 31
U1 1
U2 5
PU Cell Physiol Biochem Press GmbH & Co
PI Dsseldorf
PA Herzogstr. 85, Dsseldorf, GERMANY
SN 1015-8987
EI 1421-9778
J9 CELL PHYSIOL BIOCHEM
JI Cell. Physiol. Biochem.
PY 2018
VL 48
IS 2
BP 450
EP 460
DI 10.1159/000491776
PG 11
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA GS4KH
UT WOS:000443610200003
PM 30016785
OA gold
DA 2025-01-04
ER

PT J
AU Takigawa, H
   Kitadai, Y
   Shinagawa, K
   Yuge, R
   Higashi, Y
   Tanaka, S
   Yasui, W
   Chayama, K
AF Takigawa, Hidehiko
   Kitadai, Yasuhiko
   Shinagawa, Kei
   Yuge, Ryo
   Higashi, Yukihito
   Tanaka, Shinji
   Yasui, Wataru
   Chayama, Kazuaki
TI Multikinase inhibitor regorafenib inhibits the growth and metastasis of
   colon cancer with abundant stroma
SO CANCER SCIENCE
LA English
DT Article
DE Colon cancer; mesenchymal stem cells; molecular target therapy;
   regorafenib; stroma
ID MESENCHYMAL STEM-CELLS; POSITRON-EMISSION-TOMOGRAPHY; COLORECTAL-CANCER;
   TUMOR-CELLS; BAY 73-4506; FACTOR RECEPTOR; BONE; ANGIOGENESIS;
   EXPRESSION; PATHWAY
AB Interaction between tumor cells and stromal cells plays an important role in the growth and metastasis of colon cancer. We previously found that carcinoma-associated fibroblasts (CAFs) expressed platelet-derived growth factor receptor-beta (PDGFR-beta) and that PDGFR targeted therapy using imatinib or nilotinib inhibited stromal reaction. Bone marrow-derived mesenchymal stem cells (MSCs) migrate to tumor stroma and differentiate into CAFs. A novel oral multikinase inhibitor regorafenib inhibits receptor tyrosine kinases expressed on stromal cells (vascular endothelial growth factor receptor 1-3, TIE2, PDGFR-beta, and fibroblast growth factors) and tumor cells (c-KIT, RET, and BRAF). These molecules are involved in tumor growth, angiogenesis, lymphangiogenesis, and stromal activation. Therefore, we examined whether regorafenib impaired the tumor-promoting effect of CAFs/MSCs. KM12SM human colon cancer cells alone or KM12SM cells with MSCs were transplanted into the cecal wall of nude mice. Co-implantation of KM12SM cells with MSCs into the cecal wall of nude mice produced tumors with abundant stromal component and promoted tumor growth and lymph node metastasis. Single treatment with regorafenib inhibited tumor growth and metastasis by inhibiting both tumor cells and stromal reaction. This tumor-inhibitory effect of regorafenib was more obvious in tumors developed by co-implanting KM12SM cells with MSCs. Our data suggested that targeting of the tumor microenvironment with regorafenib affected tumor cell-MSC interaction, which in turn inhibited the growth and metastasis of colon cancer.
C1 [Takigawa, Hidehiko; Kitadai, Yasuhiko; Yuge, Ryo; Chayama, Kazuaki] Hiroshima Univ, Dept Gastroenterol & Metab, Hiroshima, Japan.
   [Shinagawa, Kei] Hiroshima Prefectural Hosp, Dept Endoscopy, Hiroshima, Japan.
   [Higashi, Yukihito] Hiroshima Univ, Dept Cardiovasc Physiol & Med, Hiroshima, Japan.
   [Tanaka, Shinji] Hiroshima Univ Hosp, Dept Endoscopy, Hiroshima, Japan.
   [Yasui, Wataru] Hiroshima Univ, Dept Mol Pathol, Hiroshima, Japan.
C3 Hiroshima University; Hiroshima University; Hiroshima University;
   Hiroshima University
RP Kitadai, Y (corresponding author), 1-2-3 Kasumi,Minami Ku, Hiroshima 7348551, Japan.
EM kitadai@hiroshima-u.ac.jp
RI Tanaka, Shinji/G-5266-2019; chayama, Kazuaki/G-2917-2019; Kitadai,
   Yasuhiko/AAG-4389-2021; Higashi, Yukihito/G-5343-2019; Takigawa,
   Hidehiko/AAA-8321-2021
OI Chayama, Kazuaki/0000-0002-5530-5341; Takigawa,
   Hidehiko/0000-0001-6369-0641
FU Ministry of Education, Culture, Science, Sports and Technology of Japan
   [21590813]
FX Supported in part by grants-in-aid for cancer research from the Ministry
   of Education, Culture, Science, Sports and Technology of Japan. Grant
   Number: 21590813.
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NR 54
TC 40
Z9 44
U1 0
U2 16
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 2016
VL 107
IS 5
BP 601
EP 608
DI 10.1111/cas.12907
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DP7YH
UT WOS:000378714600005
PM 26865419
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Guadagni, S
   Fiorentini, G
   Palumbo, P
   Masedu, F
   Ricevuto, E
   Bruera, G
   Deraco, M
   Kusamura, S
   Sarti, D
   Fiorentini, C
   Gailhofer, S
   Clementi, M
AF Guadagni, Stefano
   Fiorentini, Giammaria
   Palumbo, Paola
   Masedu, Francesco
   Ricevuto, Enrico
   Bruera, Gemma
   Deraco, Marcello
   Kusamura, Shigeki
   Sarti, Donatella
   Fiorentini, Caterina
   Gailhofer, Sabine
   Clementi, Marco
TI Hypoxic pelvic perfusion with cisplatin and mitomycin C in
   multidisciplinary palliative treatment of patients with unresectable
   recurrent rectal cancer: a retrospective study
SO MINERVA CHIRURGICA
LA English
DT Article
DE Rectal neoplasms; Local neoplasms recurrence; Perfusion; Cetuximab
ID LOCALLY RECURRENT; COLORECTAL-CANCER; REIRRADIATION; GUIDELINE; TUMORS
AB BACKGROUND: Patients with unresectable recurrent rectal cancer that progresses after systemic chemotherapy and radiotherapy may be candidates for palliation with hypoxic pelvic perfusion (HPP). The aim of this observational retrospective study was to evaluate if a multimodality treatment including HPP and targeted-therapy may be useful to prolong clinical responses and survival of these patients.
   METHODS: Thirty-seven patients with unresectable recurrent rectal cancer in progression after standard treatments underwent repeated HPP with mitomycin C (25 mg/m(2)) and cisplatin (70 mg/m(2)). Twenty patients, exhibiting epidermal growth factor receptor (EGFR) overexpression, also received cetuximab targeted-therapy, following the ultimate HPP treatment.
   RESULTS: Following initial HPP treatment, median progression-free survival was 7 months (range: 5-19 months), median time-to-death or termination of follow-up was 13 months (range: 9-18 months), one-year survival-rate was 59.45%, two-year survival rate was 10.81%, and three-year survival rate was 2.7%. Survival was significantly influenced by cetuximab targeted-therapy post-HPP and the presence of additional metastatic sites (P<0.03).
   CONCLUSIONS: Repeated HPP treatments with mitomycin C plus cisplatin, followed by cetuximab targeted-therapy, may represent a safe and efficacious palliative therapy in patients with unresectable recurrent rectal cancer, in progression following standard systemic chemo- and radio-therapy, and thus warrants confirmation in a larger phase III study.
C1 [Guadagni, Stefano] Univ Aquila, Dept Appl Clin Sci & Biotechnol, Sect Gen Surg, Via Vetoio, I-67100 Laquila, Italy.
   [Fiorentini, Giammaria; Sarti, Donatella] Osped Riuniti Marche Nord, Unit Med Oncol, Dept Oncol & Hematol, Pesaro, Italy.
   [Palumbo, Paola] Univ Aquila, Dept Life Hlth & Environm Sci, Lab Immunopathol, Laquila, Italy.
   [Masedu, Francesco] Univ Aquila, Dept Appl Clin Sci & Biotechnol, Sect Biostat & Epidemiol, Laquila, Italy.
   [Ricevuto, Enrico; Bruera, Gemma] Univ Aquila, Dept Appl Clin Sci & Biotechnol, Sect Oncol, Laquila, Italy.
   [Deraco, Marcello; Kusamura, Shigeki] Natl Canc Inst Fdn, Unit Peritoneal Surface Malignancies Colon & Rect, Milan, Italy.
   [Fiorentini, Caterina] Univ Siena, Dept Med Biotechnol, Div Cardiol, Siena, Italy.
   [Gailhofer, Sabine] Medias Klinikum, Dept Surg Oncol, Burghausen, Germany.
   [Clementi, Marco] Univ Aquila, Dept Life Hlth & Environm Sci, Sect Gen Surg, Laquila, Italy.
C3 University of L'Aquila; University of L'Aquila; University of L'Aquila;
   University of L'Aquila; Fondazione IRCCS Istituto Nazionale Tumori
   Milan; University of Siena; University of L'Aquila
RP Guadagni, S (corresponding author), Univ Aquila, Dept Appl Clin Sci & Biotechnol, Sect Gen Surg, Via Vetoio, I-67100 Laquila, Italy.
EM stefano.guadagni@univaq.it
RI Kusamura, Shigeki/J-1868-2017; Guadagni, Stefano/P-6471-2016; Clementi,
   Marco/P-8582-2016; MASEDU, Francesco/M-2989-2015
OI Bruera, Gemma/0000-0002-8407-2479; Clementi, Marco/0000-0002-9652-5148;
   MASEDU, Francesco/0000-0003-0290-5324
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U1 0
U2 0
PU EDIZIONI MINERVA MEDICA
PI TURIN
PA CORSO BRAMANTE 83-85 INT JOURNALS DEPT., 10126 TURIN, ITALY
SN 0026-4733
EI 1827-1626
J9 MINERVA CHIR
JI Minerva Chir.
PD AUG
PY 2019
VL 74
IS 4
BP 304
EP 312
DI 10.23736/S0026-4733.19.07896-9
PG 9
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA IH0ZK
UT WOS:000474220900004
PM 31062943
DA 2025-01-04
ER

PT J
AU Tian, TD
   Chen, CL
   Yang, F
   Tang, JW
   Pei, JW
   Shi, B
   Zhang, N
   Zhang, JH
AF Tian, Tongde
   Chen, Chuanliang
   Yang, Feng
   Tang, Jingwen
   Pei, Junwen
   Shi, Bian
   Zhang, Ning
   Zhang, Jianhua
TI Establishment of apoptotic regulatory network for genetic markers of
   colorectal cancer and optimal selection of traditional Chinese medicine
   target
SO SAUDI JOURNAL OF BIOLOGICAL SCIENCES
LA English
DT Article
DE Colorectal cancer; Meta analysis; KEGG analysis; Traditional Chinese
   medicine
ID CURCUMIN
AB The paper aimed to screen out genetic markers applicable to early diagnosis for colorectal cancer and establish apoptotic regulatory network model for colorectal cancer, and to analyze the current situation of traditional Chinese medicine (TCM) target, thereby providing theoretical evidence for early diagnosis and targeted therapy of colorectal cancer. Taking databases including CNKI, VIP, Wanfang data, Pub Med, and MEDLINE as main sources of literature retrieval, literatures associated with genetic markers that are applied to early diagnosis of colorectal cancer were searched and performed comprehensive and quantitative analysis by Meta analysis, hence screening genetic markers used in early diagnosis of colorectal cancer. KEGG analysis was employed to establish apoptotic regulatory network model based on screened genetic markers, and optimization was conducted on TCM targets. Through Meta analysis, seven genetic markers were screened out, including WWOX, K-ras, COX-2, P53, APC, DCC and PTEN, among which DCC has the highest diagnostic efficiency. Apoptotic regulatory network was built by KEGG analysis. Currently, it was reported that TCM has regulatory function on gene locus in apoptotic regulatory network. The apoptotic regulatory model of colorectal cancer established in this study provides theoretical evidence for early diagnosis and TCM targeted therapy of colorectal cancer in clinic. (C) 2017 The Authors. Production and hosting by Elsevier B.V. on behalf of King Saud University.
C1 [Tian, Tongde; Yang, Feng; Tang, Jingwen; Pei, Junwen; Shi, Bian] Zhengzhou Univ, Canc Hosp, Integrated TCM & Western Med Dept, 127 Dongming Rd, Zhengzhou 450008, Henan Province, Peoples R China.
   [Chen, Chuanliang] Peoples Hosp Zhengzhou Univ, Hosp Off, 7 Weiwu Rd, Zhengzhou 450003, Henan Province, Peoples R China.
   [Zhang, Ning; Zhang, Jianhua] Zhengzhou Univ, Med Engn Technol & Data Mining Inst, 100 Sci Ave, Zhengzhou 450001, Henan Province, Peoples R China.
C3 Zhengzhou University; Zhengzhou University
RP Zhang, JH (corresponding author), Zhengzhou Univ, Med Engn Technol & Data Mining Inst, 100 Sci Ave, Zhengzhou 450001, Henan Province, Peoples R China.
EM petermails@zzu.edu.cn
RI chen, zhihao/GXM-3816-2022; Zhang, Ning/A-3217-2016; zhang,
   ying/HJB-1230-2022
FU National Natural Science Foundation of China [81373879]; Open
   cooperation project of Henan Province, China [132106000064]; Program of
   research in base and cutting-edge technologies of Henan Province, China
   [152300410151]; National 12th "Five-Year" Technology Support Programs
   [2013BAI02B00]
FX This study was supported by the National Natural Science Foundation of
   China (Grant: 81373879), the Open cooperation project of Henan Province,
   China (Grant No. 132106000064), the Program of research in base and
   cutting-edge technologies of Henan Province, China (152300410151), and
   the National 12th "Five-Year" Technology Support Programs
   (2013BAI02B00). I thank all authors who have contributed to this paper
   for advice and comments and thank Cancer Hospital Affiliated to
   Zhengzhou University for providing technical support.
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NR 67
TC 10
Z9 11
U1 0
U2 15
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1319-562X
EI 2213-7106
J9 SAUDI J BIOL SCI
JI Saudi J. Biol. Sci.
PD MAR
PY 2017
VL 24
IS 3
BP 634
EP 643
DI 10.1016/j.sjbs.2017.01.036
PG 10
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA EW4MF
UT WOS:000402474900024
PM 28386190
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Arai, H
   Minami, Y
   Chi, S
   Utsu, Y
   Masuda, S
   Aotsuka, N
AF Arai, Hironori
   Minami, Yosuke
   Chi, SungGi
   Utsu, Yoshikazu
   Masuda, Shinichi
   Aotsuka, Nobuyuki
TI Molecular-Targeted Therapy for Tumor-Agnostic Mutations in Acute Myeloid
   Leukemia
SO BIOMEDICINES
LA English
DT Review
DE acute myeloid leukemia; tumor agnostic; solid tumor; genomic profiling;
   hereditary breast and ovarian cancer; variant; molecular-targeted
   therapy; BRCA
ID GASTROINTESTINAL STROMAL TUMORS; ACUTE MYELOGENOUS LEUKEMIA; CELL
   LUNG-CANCER; FIBROBLAST GROWTH-FACTORS; MEK INHIBITOR TRAMETINIB;
   PHASE-II TRIAL; TYROSINE KINASE; OPEN-LABEL; COLORECTAL-CANCER;
   DOSE-ESCALATION
AB Comprehensive genomic profiling examinations (CGPs) have recently been developed, and a variety of tumor-agnostic mutations have been detected, leading to the development of new molecular-targetable therapies across solid tumors. In addition, the elucidation of hereditary tumors, such as breast and ovarian cancer, has pioneered a new age marked by the development of new treatments and lifetime management strategies required for patients with potential or presented hereditary cancers. In acute myeloid leukemia (AML), however, few tumor-agnostic or hereditary mutations have been the focus of investigation, with associated molecular-targeted therapies remaining poorly developed. We focused on representative tumor-agnostic mutations such as the TP53, KIT, KRAS, BRCA1, ATM, JAK2, NTRK3, FGFR3 and EGFR genes, referring to a CGP study conducted in Japan, and we considered the possibility of developing molecular-targeted therapies for AML with tumor-agnostic mutations. We summarized the frequency, the prognosis, the structure and the function of these mutations as well as the current treatment strategies in solid tumors, revealed the genetical relationships between solid tumors and AML and developed tumor-agnostic molecular-targeted therapies and lifetime management strategies in AML.
C1 [Arai, Hironori; Utsu, Yoshikazu; Masuda, Shinichi; Aotsuka, Nobuyuki] Japanese Red Cross Narita Hosp, Dept Hematol & Oncol, Iidacho 2860041, Japan.
   [Arai, Hironori; Minami, Yosuke; Chi, SungGi] Natl Canc Ctr Hosp East, Dept Hematol, Kashiwa 2778577, Japan.
C3 National Cancer Center - Japan
RP Minami, Y (corresponding author), Natl Canc Ctr Hosp East, Dept Hematol, Kashiwa 2778577, Japan.
EM yominami@east.ncc.go.jp
OI Chi, SungGi/0000-0002-5725-7187
FU National Cancer Research and Development expense grant; National Cancer
   Center, Japan;  [2021-A-11]
FX This paper was supported by a National Cancer Research and Development
   expense grant (2021-A-11), funded by the National Cancer Center, Japan.
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NR 206
TC 2
Z9 2
U1 0
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD DEC
PY 2022
VL 10
IS 12
AR 3008
DI 10.3390/biomedicines10123008
PG 23
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 7D5UB
UT WOS:000900554100001
PM 36551764
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Liu, J
   Hu, J
   Cheng, L
   Ren, W
   Yang, M
   Liu, BR
   Xie, L
   Qian, XP
AF Liu, Jiang
   Hu, Jing
   Cheng, Lei
   Ren, Wei
   Yang, Mi
   Liu, Baorui
   Xie, Li
   Qian, Xiaoping
TI Biomarkers predicting resistance to epidermal growth factor
   receptor-targeted therapy in metastatic colorectal cancer with wild-type
   KRAS
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE colorectal cancer; EGFR; BRAF; RAS; cetuximab; panitumumab
ID GENE COPY NUMBER; CETUXIMAB PLUS IRINOTECAN; EGFR MONOCLONAL-ANTIBODIES;
   PHASE-III TRIAL; CELL LUNG-CANCER; 1ST-LINE TREATMENT;
   ACQUIRED-RESISTANCE; COLON-CANCER; INHIBITOR CETUXIMAB; PIK3CA MUTATIONS
AB EGFR pathway is an important therapeutic target in human tumors, including metastatic colorectal cancer (mCRC). The advent of EGFR-targeted monoclonal antibodies panitumumab and cetuximab has generated promise for the treatment of mCRC and has largely improved patients' progression-free survival (PFS) and overall survival (OS). However, treatment with anti-EGFR monoclonal antibodies is only effective in a subset of mCRC patients with wild-type KRAS. This indicates that there are other factors affecting the efficacy of anti-EGFR monoclonal antibodies. Existing studies have demonstrated that among colorectal cancer patients with wild-type KRAS, harboring mutations of BRAF, PIK3CA, NRAS, or PTEN-null may demonstrate resistance to anti-EGFR-targeted therapy, and biomarkers detection can provide better-personalized treatment for mCRC patients. How to identify and reverse the secondary resistance to anti-EGFR monoclonal antibody therapy is also another great challenge to improve the anti-EGFR efficacy in wild-type KRAS mCRC patients. Finally, both of the molecular mechanisms of response and acquired resistance would be important for the directions of future research. This review focuses on how to further improve the predictive value of anti-EGFR therapies and how to also try and avoid futile treatment for wild-type KRAS colorectal cancer patients.
C1 [Liu, Jiang; Hu, Jing; Cheng, Lei; Ren, Wei; Yang, Mi; Liu, Baorui; Xie, Li; Qian, Xiaoping] Nanjing Univ, Drum Tower Hosp, Ctr Comprehens Canc, Med Sch,Clin Canc Inst, 321 Zhongshan Rd, Nanjing 210008, Jiangsu, Peoples R China.
C3 Nanjing University
RP Xie, L; Qian, XP (corresponding author), Nanjing Univ, Drum Tower Hosp, Ctr Comprehens Canc, Med Sch,Clin Canc Inst, 321 Zhongshan Rd, Nanjing 210008, Jiangsu, Peoples R China.
EM sheery01130@163.com; qianxiaoping211@hotmail.com
RI Cheng, Lei/AFT-2319-2022; Wei, Ren/J-7185-2019; Yang, Mi/GQA-8758-2022
FU National Science Foundation of China [81172094, 8110186]; Six Talents
   Peak Foundation of Jiangsu Province [2011-WS-005]
FX This work was supported by the Grants 81172094 and 8110186 from the
   National Science Foundation of China, and Grant 2011-WS-005 from the Six
   Talents Peak Foundation of Jiangsu Province.
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NR 98
TC 15
Z9 17
U1 0
U2 15
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 557
EP 565
DI 10.2147/OTT.S86966
PG 9
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA DB7GW
UT WOS:000368683800001
PM 26869800
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Muniz, TP
   Mason, WP
AF Muniz, Thiago P. P.
   Mason, Warren P. P.
TI <i>BRAF</i> Mutations in CNS Tumors-Prognostic Markers and Therapeutic
   Targets
SO CNS DRUGS
LA English
DT Review
ID DABRAFENIB PLUS TRAMETINIB; METASTATIC COLORECTAL-CANCER; HIGH-GRADE
   GLIOMA; CELL LUNG-CANCER; OPEN-LABEL; ADJUVANT TEMOZOLOMIDE;
   BRAF(V600E); VEMURAFENIB; INHIBITION; COBIMETINIB
AB Gliomas are a heterogeneous group of brain tumors with limited therapeutic options. However, identification of BRAF V600E mutations in a subset of gliomas has provided a genomic-targeted approach for management of these diseases. In this review, we aimed to review the role of BRAF V600E in gliomagenesis, to characterize concurrent genomic alterations and their potential prognostic implications, and to review comprehensively the efficacy data of BRAF inhibitors (combined or not with MEK inhibitors) for the treatment of low- and high-grade gliomas. We also provide a summary of the toxicity of these agents and describe resistance mechanisms that may be circumvented by alternative genomic approaches. Although the efficacy of targeted therapy for management of BRAF V600E-mutant gliomas has mostly been assessed in small retrospective and phase 2 studies with heterogeneous populations, the data generated so far are a proof of concept that genomic-directed therapies improve outcomes of patients with refractory/relapsed glioma and underpin the need of comprehensive genomic assessments for these difficult-to-treat diseases. In the future, the role of targeted therapy in the first-line setting and of genomic-directed therapies to overcome resistance mechanisms should be assessed in well-designed clinical trials.
C1 [Muniz, Thiago P. P.; Mason, Warren P. P.] Univ Toronto, Univ Hlth Network, Princess Margaret Canc Ctr, Div Med Oncol & Hematol, Toronto, ON, Canada.
C3 University of Toronto; University Health Network Toronto; Princess
   Margaret Cancer Centre
RP Muniz, TP (corresponding author), Univ Toronto, Univ Hlth Network, Princess Margaret Canc Ctr, Div Med Oncol & Hematol, Toronto, ON, Canada.
EM thiago.muniz@uhn.ca
OI P. Muniz, Thiago/0000-0001-5132-2403
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NR 94
TC 4
Z9 4
U1 0
U2 4
PU ADIS INT LTD
PI NORTHCOTE
PA 5 THE WAREHOUSE WAY, NORTHCOTE 0627, AUCKLAND, NEW ZEALAND
SN 1172-7047
EI 1179-1934
J9 CNS DRUGS
JI CNS Drugs
PD JUL
PY 2023
VL 37
IS 7
BP 587
EP 598
DI 10.1007/s40263-023-01016-5
EA JUN 2023
PG 12
WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA M9MF7
UT WOS:000999708300001
PM 37268805
DA 2025-01-04
ER

PT J
AU Henaine, AM
   Chahine, G
   Massoud, M
   Salameh, P
   Awada, S
   Lahoud, N
   Elias, E
   Salem, M
   Ballouts, S
   Hartmann, D
   Aulagner, G
   Armoiry, X
AF Henaine, Anna Maria
   Chahine, Georges
   Massoud, Marcel
   Salameh, Pascale
   Awada, Sanaa
   Lahoud, Nathalie
   Elias, Edward
   Salem, Mansour
   Ballouts, Souheir
   Hartmann, Daniel
   Aulagner, Gilles
   Armoiry, Xavier
TI Management of patients with metastatic colorectal cancer in Lebanese
   hospitals and associated direct cost: a multicentre cohort study
SO EASTERN MEDITERRANEAN HEALTH JOURNAL
LA English
DT Article
DE metastatic colorectal cancer; cytotoxic agents; targeted therapies;
   effectiveness; cost
ID RESPONSE EVALUATION CRITERIA; 1ST-LINE TREATMENT; INFUSIONAL
   FLUOROURACIL; TUMOR RESPONSE; CHEMOTHERAPY; BEVACIZUMAB; CETUXIMAB;
   OXALIPLATIN; COMBINATION; IRINOTECAN
AB Background: For metastatic colorectal cancer a series of novel therapies has emerged during the last decade but their use in routine clinical practice and their costs are not well documented.
   Aims: This study evaluated the clinical effectiveness of metastatic colorectal cancer patients in Lebanese oncologic units and estimated the costs.
   Methods: A prospective cohort study was conducted on metastatic colorectal cancer patients during 2008-2013. The type of medical management, overall survival and total costs from diagnosis to death were described. Cost analysis was performed using tariffs from 2013 in US dollars.
   Results: One hundred and seventy-nine metastatic patients were selected among which 84.9% had colorectal cancer involvement. The average follow-up from diagnosis until death or the latest news was 34.8 months. Around 49.7% were still alive at last follow-up date. Three lines of treatment accounted for 4.5%, 39.6% and 55.9% with an average duration of 14.5, 11.4 and 14.6 months respectively. A 73.2% of patients benefited from targeted therapy. The median overall survival was 20.8 months. The mean total costs of drugs was $22 256 in patients with standard therapy alone whereas the cost increased to $80 396 after the addition of targeted therapy. The mean global total cost was estimated at $64 805 per patient (min $3703; max $304 086).
   Conclusions: Targeted therapy associated to standard therapy is highly prevalent in Lebanon in metastatic disease and the associated medical cost substantial. This study is the first to show the clinical effectiveness and costs of targeted therapy in patients with metastatic colorectal cancer.
C1 [Henaine, Anna Maria; Hartmann, Daniel; Aulagner, Gilles; Armoiry, Xavier] Univ Claude Bernard Lyon, Lyon, France.
   [Hartmann, Daniel; Aulagner, Gilles; Armoiry, Xavier] UMR CNRS 5510 MATEIS, Lyon, France.
   [Henaine, Anna Maria; Aulagner, Gilles; Armoiry, Xavier] Hosp Civils Lyon, Hop Edouard Herriot, Serv Pharmaceut, Lyon, France.
   [Chahine, Georges; Massoud, Marcel; Elias, Edward; Salem, Mansour] Hotel Dieu France, Beirut, Lebanon.
   [Chahine, Georges; Massoud, Marcel; Elias, Edward; Salem, Mansour] St Joseph Univ, Beirut, Lebanon.
   [Chahine, Georges; Massoud, Marcel; Elias, Edward; Salem, Mansour] Hop Notre Dame Secours, Byblos, Lebanon.
   [Henaine, Anna Maria; Salameh, Pascale; Awada, Sanaa; Ballouts, Souheir] Lebanese Univ, Sch Pharm, Clin & Epidemiol Res Lab, Beirut, Lebanon.
   [Armoiry, Xavier] Univ Lyon, Claude Bernard Univ Lyon, Lyon, France.
   [Armoiry, Xavier] Lyon Sch Pharm, Publ Hlth Dept, Lyon, France.
   [Salameh, Pascale] Lebanese Amer Univ, Sch Pharm, Pharm Practice Dept, Beirut, Lebanon.
   [Lahoud, Nathalie] Lebanese Univ, Doctoral Sch Sci & Technol, Beirut, Lebanon.
   [Massoud, Marcel] Holy Spirit Univ, Kaslik, Lebanon.
C3 Universite Claude Bernard Lyon 1; Centre National de la Recherche
   Scientifique (CNRS); Institut National des Sciences Appliquees de Lyon -
   INSA Lyon; CHU Lyon; Lebanese University; Universite Claude Bernard Lyon
   1; Lebanese American University
RP Henaine, AM (corresponding author), Univ Claude Bernard Lyon, Lyon, France.; Henaine, AM (corresponding author), Hosp Civils Lyon, Hop Edouard Herriot, Serv Pharmaceut, Lyon, France.; Henaine, AM (corresponding author), Lebanese Univ, Sch Pharm, Clin & Epidemiol Res Lab, Beirut, Lebanon.
EM annamaria.henaine@gmail.com
RI Armoiry, Xavier/B-9600-2013; Chahine, Georges/A-2690-2011; Salameh,
   Pascale/F-9676-2011
OI Salameh, Pascale/0000-0002-4780-0772
FU Shiraz University of Medical Sciences, Shiraz, Islamic Republic of Iran
FX Shiraz University of Medical Sciences, Shiraz, Islamic Republic of Iran.
CR [Anonymous], 2016, J. Middle E. N. Afr. Sci
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NR 48
TC 3
Z9 3
U1 0
U2 2
PU WHO EASTERN MEDITERRANEAN REGIONAL OFFICE
PI NASR CITY, CAIRO
PA P. O. BOX 7608, NASR CITY, CAIRO, EGYPT
SN 1020-3397
EI 1687-1634
J9 E MEDITERR HEALTH J
JI East Mediterr. Health J.
PD JUL
PY 2019
VL 25
IS 7
BP 481
EP 494
DI 10.26719/emhj.18.063
PG 14
WC Health Care Sciences & Services; Health Policy & Services; Public,
   Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Health Care Sciences & Services; Public, Environmental & Occupational
   Health
GA JC0MV
UT WOS:000488974000006
PM 31612980
OA Bronze
DA 2025-01-04
ER

PT J
AU Wang, QY
   Shen, XF
   Chen, G
   Du, JF
AF Wang, Qianyu
   Shen, Xiaofei
   Chen, Gang
   Du, Junfeng
TI Drug Resistance in Colorectal Cancer: From Mechanism to Clinic
SO CANCERS
LA English
DT Review
DE colorectal cancer; drug resistance; chemotherapeutic agents; molecularly
   targeted therapy; immunotherapy; reversal strategies
ID GROWTH-FACTOR RECEPTOR; EGFR MONOCLONAL-ANTIBODY; MEDIATED
   MULTIDRUG-RESISTANCE; TUMOR-ASSOCIATED MACROPHAGES; CETUXIMAB PLUS
   IRINOTECAN; BH3 MIMETIC ABT-737; WILD-TYPE KRAS; COLON-CANCER;
   DIHYDROPYRIMIDINE DEHYDROGENASE; TGF-BETA
AB Simple Summary Chemotherapy, radiotherapy and molecularly targeted therapy could improve the prognosis of colorectal cancer (CRC) patients. Recently, immunotherapy, especially immune checkpoint inhibitors, has significantly improved the prognosis of some patients. However, drug resistance significantly reduces the usefulness of these drugs. Although research on the molecular mechanisms underlying the emergence of drug resistance is ongoing, the specific molecular mechanisms remain unclear. This article reviews the findings on the mechanisms of drug resistance in CRC patients in preclinical and clinical studies, which may provide valuable directions for future in-depth study of drug resistance. Colorectal cancer (CRC) is one of the leading causes of death worldwide. The 5-year survival rate is 90% for patients with early CRC, 70% for patients with locally advanced CRC, and 15% for patients with metastatic CRC (mCRC). In fact, most CRC patients are at an advanced stage at the time of diagnosis. Although chemotherapy, molecularly targeted therapy and immunotherapy have significantly improved patient survival, some patients are initially insensitive to these drugs or initially sensitive but quickly become insensitive, and the emergence of such primary and secondary drug resistance is a significant clinical challenge. The most direct cause of resistance is the aberrant anti-tumor drug metabolism, transportation or target. With more in-depth research, it is found that cell death pathways, carcinogenic signals, compensation feedback loop signal pathways and tumor immune microenvironment also play essential roles in the drug resistance mechanism. Here, we assess the current major mechanisms of CRC resistance and describe potential therapeutic interventions.
C1 [Wang, Qianyu] Shanxi Med Univ, Sch Clin Med 2, Taiyuan 030001, Peoples R China.
   [Shen, Xiaofei] Nanjing Univ, Dept Gen Surg, Affiliated Drum Tower Hosp, Med Sch, Nanjing 210008, Jiangsu, Peoples R China.
   [Chen, Gang; Du, Junfeng] Chinese Peoples Liberat Army Gen Hosp, Med Ctr 1, Med Dept Gen Surg, Beijing 100853, Peoples R China.
   [Chen, Gang; Du, Junfeng] Chinese Peoples Liberat Army Gen Hosp, Med Ctr 7, Dept Gen Surg, Beijing 100700, Peoples R China.
   [Du, Junfeng] Southern Med Univ, Sch Clin Med 2, Guangzhou 510515, Peoples R China.
C3 Shanxi Medical University; Nanjing University; Chinese People's
   Liberation Army General Hospital; Chinese People's Liberation Army
   General Hospital; Seventh Medical Center of Chinese PLA General
   Hospital; Southern Medical University - China
RP Chen, G; Du, JF (corresponding author), Chinese Peoples Liberat Army Gen Hosp, Med Ctr 1, Med Dept Gen Surg, Beijing 100853, Peoples R China.; Chen, G; Du, JF (corresponding author), Chinese Peoples Liberat Army Gen Hosp, Med Ctr 7, Dept Gen Surg, Beijing 100700, Peoples R China.; Du, JF (corresponding author), Southern Med Univ, Sch Clin Med 2, Guangzhou 510515, Peoples R China.
EM wangqy9264@163.com; dg1535058@smail.nju.edu.cn; chengdoctor@sina.com;
   dujf66@126.com
RI Shen, Xiaofei/HDL-7300-2022
OI Shen, Xiaofei/0000-0002-5816-1814; Wang, Qianyu/0000-0001-7048-8847; du,
   junfeng/0000-0002-8482-4271
FU National Natural Science Foundation of China [81970500, 81870393]
FX This work was supported by the National Natural Science Foundation of
   China (No. 81970500, X.S. and 81870393, J.D.).
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NR 345
TC 58
Z9 59
U1 3
U2 34
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN
PY 2022
VL 14
IS 12
AR 2928
DI 10.3390/cancers14122928
PG 38
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2K4SG
UT WOS:000816327100001
PM 35740594
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Mahmoudian, F
   Ahmari, A
   Shabani, S
   Sadeghi, B
   Fahimirad, S
   Fattahi, F
AF Mahmoudian, Fatemeh
   Ahmari, Azin
   Shabani, Shiva
   Sadeghi, Bahman
   Fahimirad, Shohreh
   Fattahi, Fahimeh
TI Aptamers as an approach to targeted cancer therapy
SO CANCER CELL INTERNATIONAL
LA English
DT Review
DE Aptamer; SELEX; Cancer; Targeted therapy
ID NUCLEIC-ACID APTAMERS; G-QUADRUPLEX APTAMER; CHITOSAN NANOPARTICLES;
   DRUG-DELIVERY; COLON-CANCER; NEXT-GENERATION; RNA APTAMERS;
   TUMOR-GROWTH; DNA APTAMER; T-CELLS
AB Conventional cancer treatments can cause serious side effects because they are not specific to cancer cells and can damage healthy cells. Aptamers often are single-stranded oligonucleotides arranged in a unique architecture, allowing them to bind specifically to target sites. This feature makes them an ideal choice for targeted therapeutics. They are typically produced through the systematic evolution of ligands by exponential enrichment (SELEX) and undergo extensive pharmacological revision to modify their affinity, specificity, and therapeutic half-life. Aptamers can act as drugs themselves, directly inhibiting tumor cells. Alternatively, they can be used in targeted drug delivery systems to transport drugs directly to tumor cells, minimizing toxicity to healthy cells. In this review, we will discuss the latest and most advanced approaches to using aptamers for cancer treatment, particularly targeted therapy overcoming resistance to conventional therapies.
C1 [Mahmoudian, Fatemeh] Semnan Univ Med Sci, Canc Res Ctr, Semnan, Iran.
   [Mahmoudian, Fatemeh; Ahmari, Azin; Shabani, Shiva; Sadeghi, Bahman; Fattahi, Fahimeh] Arak Univ Med Sci, Ayatollah Khansari Hosp, Clin Res Dev Unit, Arak, Iran.
   [Ahmari, Azin] Arak Univ Med Sci, Sch Med, Dept Radiat Oncol, Arak, Iran.
   [Shabani, Shiva] Arak Univ Med Sci, Sch Med, Dept Infect Dis, Arak, Iran.
   [Sadeghi, Bahman] Arak Univ Med Sci, Sch Med, Dept Community Med, Arak, Iran.
   [Fahimirad, Shohreh] Arak Univ Med Sci, Mol & Med Res Ctr, Arak, Iran.
   [Fattahi, Fahimeh] Iran Univ Med Sci, Oncopathol Res Ctr, Tehran, Iran.
C3 Semnan University of Medical Sciences; Iran University of Medical
   Sciences
RP Fattahi, F (corresponding author), Arak Univ Med Sci, Ayatollah Khansari Hosp, Clin Res Dev Unit, Arak, Iran.; Fahimirad, S (corresponding author), Arak Univ Med Sci, Mol & Med Res Ctr, Arak, Iran.; Fattahi, F (corresponding author), Iran Univ Med Sci, Oncopathol Res Ctr, Tehran, Iran.
EM sh_fahimirad@yahoo.com; ffattahi1@gmail.com
RI Fahimirad, Shohreh/ABA-4975-2020; Fattahi, Fahimeh/AAB-5019-2022
FU Cancer Research Center at Semnan University of Medical Sciences
FX The authors express gratitude for consultations from Arak Ayatollah
   Khansari Hospital's clinical research development unit and Cancer
   Research Center at Semnan University of Medical Sciences.
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NR 184
TC 11
Z9 11
U1 14
U2 25
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 16
PY 2024
VL 24
IS 1
AR 108
DI 10.1186/s12935-024-03295-4
PG 22
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LG9K5
UT WOS:001185752200001
PM 38493153
OA gold
DA 2025-01-04
ER

PT J
AU Willems, E
   Gerne, L
   George, C
   D'Hondt, M
AF Willems, E.
   Gerne, L.
   George, C.
   D'Hondt, M.
TI Adverse effects of bevacizumab in metastatic colorectal cancer : a case
   report and literature review
SO ACTA GASTRO-ENTEROLOGICA BELGICA
LA English
DT Review
DE Bevacizumab; metastatic colorectal cancer; bowel ischaemia;
   gastro-intestinal bleeding
ID GASTROINTESTINAL PERFORATION; RISK
AB Colorectal cancer is one of the most frequently diagnosed malignancies worldwide. One of the most important developments in the management of metastatic colorectal cancer is targeted therapy. Bevacizumab, a monoclonal antibody inhibiting VEGF induced angiogenesis, has been accepted as safe and efficient in the treatment of metastatic colorectal cancer for more than a decade. Addition of bevacizumab to fluorouracil-based chemotherapy is also associated with severe adverse events. We present a case of bevacizumab-induced bowel ischaemia associated with gastro-intestinal haemorrhage.
C1 [Willems, E.; Gerne, L.; D'Hondt, M.] AZ Groeninge Kortrijk, Dept Digest & Hepatobiliary Pancreat Surg, Kortrijk, Belgium.
   [George, C.] AZ Groeninge Kortrijk, Dept Gastroenterol, Kortrijk, Belgium.
RP Willems, E (corresponding author), President Kennedylaan 4, B-8500 Kortrijk, Belgium.
EM willems.edward@gmail.com
CR [Anonymous], 2014, PLOS ONE
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   ZHU X., INCREASED RISK HEMOR, P30
NR 12
TC 5
Z9 6
U1 0
U2 0
PU UNIV CATHOLIQUE LOUVAIN-UCL
PI BRUSSELS
PA CLIN UNIV SAINT LUC, AVE HIPPOCRATE 10, BRUSSELS, B-1200, BELGIUM
SN 1784-3227
J9 ACTA GASTRO-ENT BELG
JI Acta Gastro-Enterol. Belg.
PD APR-JUN
PY 2019
VL 82
IS 2
BP 322
EP 325
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA IH1KY
UT WOS:000474250900014
PM 31314196
DA 2025-01-04
ER

PT J
AU Kim, JS
   Kim, H
   Lee, SY
   Han, YD
   Han, K
   Min, BS
   Kim, MD
   Won, JY
   Beom, SH
   Shin, SJ
   Kim, HS
   Han, DH
   Ahn, JB
AF Kim, Ji Su
   Kim, Hyunwook
   Lee, Seo Young
   Han, Yoon Dae
   Han, Kichang
   Min, Byung Soh
   Kim, Man-Deuk
   Won, Jong Yun
   Beom, Seung-Hoon
   Shin, Sang Joon
   Kim, Han Sang
   Han, Dai Hoon
   Ahn, Joong Bae
TI Hepatic arterial infusion in combination with systemic chemotherapy in
   patients with hepatic metastasis from colorectal cancer: a randomized
   phase II study - (NCT05103020) - study protocol
SO BMC CANCER
LA English
DT Article
DE Colon cancer; Liver-only metastasis; Liver resection; Hepatic arterial
   infusion; Oxaliplatin; Randomized trial
ID UNRESECTABLE LIVER METASTASES; OXALIPLATIN; RESECTION; TRIAL; FOLFOXIRI;
   THERAPY
AB Background Although 80% of patients with metastatic colorectal cancer (CRC) experience liver metastases, only 10-25% undergo resection at the time of diagnosis. Even in initially unresectable conditions, if appropriate treatment is provided, such as surgical conversion through a combination of hepatic arterial infusion (HAI) chemotherapy and systemic chemotherapy (sys-CT), better overall survival can be expected. Therefore, this study aims to evaluate the efficacy of HAI oxaliplatin in combination with sys-CT plus targeted therapy in patients with unresectable CRC with liver-only metastasis.
   Methods This is a single-center, randomized, open-label phase II trial (NCT05103020). Patients with untreated CRC, who have liver-only metastases and for whom liver resection is potentially possible but deemed infeasible at the time of initial diagnosis by a multidisciplinary team, will be eligible. Patients will be randomly assigned in a 1:1 ratio to either the combined HAI oxaliplatin and modified systemic 5-fluorouracil, folinic acid, and irinotecan (FOLFIRI) plus targeted therapy group or the systemic FOLFIRI plus targeted therapy group. Both regimens will be repeated every 2 weeks for a total of 12 cycles. The primary objective of this study is to compare the rate of conversion to liver resection. The surgical conversion rate is expected to increase by 25% with HAI oxaliplatin in combination with sys-CT plus targeted therapy (40% in the experimental arm versus 15% in the control arm) (power, 80%; two-sided alpha-risk, 5%). The secondary objectives include overall survival, progression-free survival, and objective response rate.
   Discussion This is the first randomized controlled trial to investigate the efficacy of HAI oxaliplatin in combination with sys-CT plus targeted therapy as first-line treatment from the initial diagnosis in patients with unresectable CRC with liver-only metastasis, aiming to significantly increase the surgical conversion rate.
C1 [Kim, Ji Su] Catholic Univ, Incheon St Marys Hosp, Div Hepatobiliary & Pancreas Surg, Coll Med, Incheon, South Korea.
   [Kim, Hyunwook; Beom, Seung-Hoon; Shin, Sang Joon; Kim, Han Sang; Ahn, Joong Bae] Yonsei Univ, Div Med Oncol, Dept Internal Med, Yonsei Canc Ctr,Coll Med, 50-1 Yonsei Ro, Seoul 03722, South Korea.
   [Lee, Seo Young] Yonsei Univ, Gangnam Severance Hosp, Dept Med Oncol, Coll Med, Seoul, South Korea.
   [Han, Yoon Dae; Min, Byung Soh] Yonsei Univ, Severance Hosp, Dept Colorectal Surg, Coll Med, Seoul, South Korea.
   [Kim, Man-Deuk; Won, Jong Yun] Yonsei Univ, Severance Hosp, Dept Radiol, Coll Med, Seoul, South Korea.
   [Kim, Han Sang] Yonsei Univ, Severance Biomed Sci Inst, Grad Sch Med Sci, Brain Korea 21 Project,Coll Med, Seoul, South Korea.
   [Han, Dai Hoon] Yonsei Univ, Severance Hosp, Dept Hepatobiliary & Pancreat Surg, Coll Med, 50 Yonsei Ro, Seoul 03722, South Korea.
C3 Catholic University of Korea; Yonsei University; Yonsei University
   Health System; Yonsei University; Yonsei University Health System;
   Yonsei University; Yonsei University Health System; Yonsei University;
   Yonsei University Health System; Yonsei University; Yonsei University
   Health System; Yonsei University; Yonsei University Health System
RP Kim, HS; Ahn, JB (corresponding author), Yonsei Univ, Div Med Oncol, Dept Internal Med, Yonsei Canc Ctr,Coll Med, 50-1 Yonsei Ro, Seoul 03722, South Korea.; Han, DH (corresponding author), Yonsei Univ, Severance Hosp, Dept Hepatobiliary & Pancreat Surg, Coll Med, 50 Yonsei Ro, Seoul 03722, South Korea.
EM modeerfhs@yuhs.ac; DHHAN@yuhs.ac; vvswm513@yuhs.ac
RI Kim, Sang-Hyun/J-5402-2012; Han, Dai/AAS-3726-2021; Lee,
   Yoojin/AAB-9799-2022; Han, Yoondae/W-1325-2019; Kim, Han
   Sang/R-3768-2019
OI Beom, Seung-Hoon/0000-0001-7036-3753; Ahn, Joong
   Bae/0000-0001-6787-1503; Han, Yoondae/0000-0002-2136-3578; Kim,
   Hyunwook/0000-0002-4274-7562; Won, Jong Yun/0000-0002-8237-5628; Kim,
   Han Sang/0000-0002-6504-9927; Kim, Man-Deuk/0000-0002-3575-5847; Han,
   Kichang/0000-0002-9701-9757; Shin, Sang Joon/0000-0001-5350-7241; Han,
   Dai Hoon/0000-0003-2787-7876
FU Severance Hospital Research fund for Clinical excellence (SHRC)
   [C-2021-0002]; Yonsei University College of Medicine [2022-32-0062];
   National Research Foundation of Korea (NRF) - Korea government Ministry
   of Science and ICT (MSIT) [2022R1A2C4001879]
FX This study was supported by a Severance Hospital Research fund for
   Clinical excellence (SHRC) (C-2021-0002 to D.H.H.), and a new faculty
   research seed money grant of Yonsei University College of Medicine
   (2022-32-0062 to D.H.H.). This study was also supported in part by the
   National Research Foundation of Korea (NRF) grant, funded by the Korea
   government Ministry of Science and ICT (MSIT) (No. 2022R1A2C4001879 to
   H.S.K.).
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NR 26
TC 2
Z9 2
U1 0
U2 0
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD JUL 22
PY 2023
VL 23
IS 1
AR 691
DI 10.1186/s12885-023-11085-w
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GA7X6
UT WOS:001150013800001
PM 37481515
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhou, LH
   Li, Y
   Li, Q
AF Zhou, Li-Hong
   Li, Yan
   Li, Qi
TI Research hotspot and frontier progress of cancer under the background of
   precision medicine
SO TRADITIONAL MEDICINE RESEARCH
LA English
DT Review
DE Precision medicine; Cancer; Treatment methods; Detection technology;
   Traditional Chinese medicine
ID STEM-CELL TRANSPLANT; VEGF-TARGETED THERAPY; COLORECTAL-CANCER;
   GASTRIC-CANCER; LIQUID BIOPSY; LUNG-CANCER; COST-EFFECTIVENESS;
   HODGKIN-LYMPHOMA; HORMONE-THERAPY; PROSTATE-CANCER
AB The timely introduction and rapid development of precision medicine have provided strong theoretical support and technical support for tumor research. The treatment methods have been developed from single to multiple; the research technology has been transformed from macro to micro; the treatment drugs have been updated from systemic chemotherapy to targeted therapy and immunotherapy, and cancer has changed from a highly lethal disease to a "chronic disease". Based on the current international cancer research hotspots and treatment frontiers, this paper takes stock from five aspects, namely, treatment methods, detection technology, new drug research and development, information data and traditional Chinese medicine, with a view to "from the point to the surface", "from the outside to the inside", and "the combination of Chinese and western", so as to explore the overall picture of cancer treatment and research.
C1 [Zhou, Li-Hong; Li, Qi] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Med Oncol, Shanghai, Peoples R China.
   [Zhou, Li-Hong; Li, Qi] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Canc Inst, Shanghai, Peoples R China.
   [Zhou, Li-Hong; Li, Yan] Shanghai Univ Tradit Chinese Med, Shanghai Municipal Hosp Tradit Chinese Med, Dept Oncol, Shanghai, Peoples R China.
C3 Shanghai University of Traditional Chinese Medicine; Shanghai University
   of Traditional Chinese Medicine; Shanghai University of Traditional
   Chinese Medicine
RP Li, Q (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Med Oncol, Shanghai, Peoples R China.; Li, Q (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Canc Inst, Shanghai, Peoples R China.
EM lzwf@hotmail.com
FU National Natural Science Foundation of China [81673784, 81673783,
   81520108031, 81830120]; Science Foundation for Shanghai Committee of
   Science Project [18QA1404200, 17QA1404100]; Shanghai Health Bureau
   Science Foundation [ZY (2018-2020)-FWTX-4026]; Xinglin Young Scholar,
   Shanghai University of Traditional Chinese Medicine
FX This study is supported by the National Natural Science Foundation of
   China (Nos.81673784, 81673783, 81520108031, 81830120), the Science
   Foundation for Shanghai Committee of Science Project (Nos.18QA1404200,
   17QA1404100), the Shanghai Health Bureau Science Foundation (No.ZY
   (2018-2020)-FWTX-4026), and the Xinglin Young Scholar, Shanghai
   University of Traditional Chinese Medicine.
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NR 134
TC 4
Z9 4
U1 0
U2 13
PU TMR PUBLISHING GROUP
PI TIANJIN
PA BOLING BUILDING 902, DAZHIGU CENTER ST, TIANJIN, 00000, PEOPLES R CHINA
SN 2413-3973
J9 TRADIT MED RES
JI Tradit. Med. Res.
PD JAN 2
PY 2020
VL 5
IS 1
BP 22
EP 33
PG 12
WC Integrative & Complementary Medicine
WE Emerging Sources Citation Index (ESCI)
SC Integrative & Complementary Medicine
GA JZ6NY
UT WOS:000505221500005
DA 2025-01-04
ER

PT J
AU Simhadri, S
   Carrick, JN
   Murphy, S
   Kothari, OA
   Al-Hraishami, H
   Kulkarni, A
   Jalloul, N
   Stefanik, K
   Bandari, M
   Chettur, K
   Yao, M
   Ginjala, V
   Groisberg, R
   Hochster, H
   Mehnert, J
   Riedlinger, G
   Khiabanian, H
   Verzi, MP
   Tong, KV
   Ganesan, S
AF Simhadri, Srilatha
   Carrick, Jillian N.
   Murphy, Susan
   Kothari, Om A.
   Al-Hraishami, Husam
   Kulkarni, Atul
   Jalloul, Nahed
   Stefanik, Katarina
   Bandari, Manisha
   Chettur, Kavya
   Yao, Ming
   Ginjala, Vasudeva
   Groisberg, Roman
   Hochster, Howard
   Mehnert, Janice
   Riedlinger, Gregory
   Khiabanian, Hossein
   Verzi, Michael P.
   Tong, Kevin
   Ganesan, Shridar
TI Evolution of Rapid Clonal Dynamics and Non-Cross-Resistance in Response
   to Alternating Targeted Therapy and Chemotherapy in BRAF-V600E-Mutant
   Colon Cancer
SO JCO PRECISION ONCOLOGY
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; PROGNOSTIC-FACTOR; BRAF; INHIBITION;
   MUTATIONS; CETUXIMAB; SURVIVAL; EGFR; DIFFERENTIATION; VEMURAFENIB
AB PURPOSECombined BRAF, MEK, and EGFR inhibition can induce clinical responses in BRAF-V600E-mutant colon cancer, but rapid resistance often occurs.METHODSWe use serial monitoring of circulating tumor DNA cell-free plasma DNA (cfDNA) in a patient case study in addition to organoids derived from mouse models of BRAF-V600E-mutant intestinal cancer, which emulated the patient's mutational profile to assess drug treatment efficacy.RESULTSWe demonstrate dynamic evolution of resistance to combined EGFR/BRAF/MEK inhibition in a pediatric patient with metastatic BRAF-V600E-mutant, mismatch repair-stable colon cancer. Initial resistance to targeted therapy was associated with development of MET amplification. Sequential treatment with chemotherapy and targeted therapy resulted in clearing of the resistant MET-amplified clone. Rechallenge with combined BRAF/EGFR inhibition resulted in clinical and radiographic response, demonstrating these treatments may be non-cross-resistant. Tumor organoids were used to model clinical findings and demonstrated effectiveness of combined targeted therapy and chemotherapy.CONCLUSIONThese findings suggest rational strategies for combining sequential chemotherapy and BRAF-/EGFR-directed therapy in BRAF-V600E-mutant colon cancer to prevent resistance and improve outcome. The data demonstrate rapid clonal dynamics in response to effective therapies in BRAF-V600E-mutant colon cancer that can be monitored by serial cfDNA analysis. Moreover, in mismatch repair-proficient BRAF-V600E-mutant colon cancers, combined EGFR and BRAF/MEK therapy is not cross-resistant with standard chemotherapy, suggesting new rational combination treatment strategies.
C1 [Simhadri, Srilatha; Al-Hraishami, Husam; Kulkarni, Atul; Yao, Ming; Ginjala, Vasudeva; Groisberg, Roman; Hochster, Howard; Mehnert, Janice; Ganesan, Shridar] Rutgers State Univ, Rutgers Canc Inst New Jersey, Robert Wood Johnson Med Sch, Dept Med, New Brunswick, NJ USA.
   [Carrick, Jillian N.; Kothari, Om A.; Stefanik, Katarina; Verzi, Michael P.; Tong, Kevin] Rutgers State Univ, Human Genet Inst New Jersey, Dept Genet, Piscataway Township, NJ 08901 USA.
   [Carrick, Jillian N.; Bandari, Manisha; Chettur, Kavya] Hackensack Meridian Hlth Ctr Discovery & Innovat, Nutley, NJ USA.
   [Murphy, Susan] Rutgers State Univ, Rutgers Canc Inst New Jersey, Robert Wood Johnson Med Sch, Dept Med,Pediat Hematol Oncol Program, New Brunswick, NJ USA.
   [Jalloul, Nahed; Riedlinger, Gregory; Khiabanian, Hossein] Rutgers State Univ, Rutgers Canc Inst New Jersey, Robert Wood Johnson Med Sch, Dept Pathol, New Brunswick, NJ USA.
   [Stefanik, Katarina; Tong, Kevin] Coll New Jersey, Dept Biol, Ewing, NJ 08618 USA.
   [Chettur, Kavya] Tenafly High Sch, Tenafly, NJ USA.
   [Tong, Kevin] Hackensack Meridian Hlth Sch Med, Dept Med Sci, Nutley, NJ 07110 USA.
C3 Rutgers University System; Rutgers University New Brunswick; Rutgers
   University Biomedical & Health Sciences; Rutgers Cancer Institute of New
   Jersey; Rutgers University System; Rutgers University New Brunswick;
   Rutgers University System; Rutgers University New Brunswick; Rutgers
   University Biomedical & Health Sciences; Rutgers Cancer Institute of New
   Jersey; Rutgers University System; Rutgers University New Brunswick;
   Rutgers University Biomedical & Health Sciences; Rutgers Cancer
   Institute of New Jersey; College of New Jersey
RP Tong, KV (corresponding author), Rutgers State Univ, Human Genet Inst New Jersey, Dept Genet, Piscataway Township, NJ 08901 USA.; Tong, KV (corresponding author), Coll New Jersey, Dept Biol, Ewing, NJ 08618 USA.; Tong, KV (corresponding author), Hackensack Meridian Hlth Sch Med, Dept Med Sci, Nutley, NJ 07110 USA.
EM kevin.tong@hmh-cdi.org
RI Groisberg, Roman/X-2743-2019
OI Rusinak, Katarina/0000-0002-4683-7266
FU Ganesan laboratories
FX The authors thank the Verzi, Tong, and Ganesan laboratories for their
   constructive input and feedback on experimental designs and manuscript
   drafts.
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NR 31
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2473-4284
J9 JCO PRECIS ONCOL
JI JCO Precis. Oncol.
PD DEC
PY 2024
VL 8
AR e2300260
DI 10.1200/PO.23.00260
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA O6X2R
UT WOS:001372525000001
PM 39626159
DA 2025-01-04
ER

PT J
AU Joly, F
   Lefeuvre-Plesse, C
   Garnier-Tixidre, C
   Helissey, C
   Menneveau, N
   Zannetti, A
   Salas, S
   Houede, N
   Abadie-Lacourtoisie, S
   Stefani, L
   Nenan, S
   Rieger, I
   Durand-Zaleski, I
   Descotes, JM
   Anota, A
AF Joly, Florence
   Lefeuvre-Plesse, Claudia
   Garnier-Tixidre, Claire
   Helissey, Carole
   Menneveau, Nathalie
   Zannetti, Alain
   Salas, Sebastien
   Houede, Nadine
   Abadie-Lacourtoisie, Sophie
   Stefani, Laetitia
   Nenan, Soazig
   Rieger, Isabelle
   Durand-Zaleski, Isabelle
   Descotes, Jean-Marc
   Anota, Amelie
TI Feasibility and efficacy of a supervised home-based physical exercise
   program for metastatic cancer patients receiving oral targeted therapy:
   study protocol for the phase II/III - UNICANCER SdS 01 QUALIOR trial
SO BMC CANCER
LA English
DT Article
DE Oral targeted therapy; Metastatic cancer; Supervised physical exercise
   programs; Fatigue; Pain; Quality of life; Psychological and cognitive
   functions; Adherence to treatment; Supportive care; Medico-economy
ID BODY-MASS INDEX; FATIGUE; SORAFENIB
AB BackgroundCurrently, oral targeted therapies are known to be effective and are frequently used to treat metastatic cancer patients, but fatigue is a frequently reported early side effect of these treatments. This fatigue may impact the patient's treatment adherence and result in a negative impact on quality of life. Physical exercise significantly improved the general well-being and quality of life of advanced cancer patients. However, there is no specific physical activity program adapted for patients with advanced disease.MethodsQUALIOR is a two-part, randomized, open-label, and multicenter with two arms phase II/III trial. Patients (phase II: n=120; phase III: n=312) with metastatic cancer (breast cancer, kidney cancer, lung cancer, and other cancers [including but not limited to colon cancer, melanoma, sarcoma, or hepatocarcinoma]) treated with a first- or second-line oral targeted therapy without chemotherapy will be included. Patients will be randomized (2:1) to a 3-month supervised home-based standardized physical activity program or to a recommended adapted physical activity (via a booklet). The primary objective of the phase II is to evaluate the feasibility of the supervised program. The primary objective of the phase III is the evaluation of the benefit of the supervised home-based program compare to the recommended program in terms of fatigue and quality of life at 3months. The secondary objectives aim to evaluate the impact of the supervised program on fatigue over time, pain, physical capacities, psychosocial and cognitive functions, general quality of life, frequency of dose reduction and patients' adherence to the targeted therapy, overall survival, and progression-free survival. This study will also evaluate the medico-economic impact of supervised program compared to the recommended adapted physical activity program.DiscussionThe aim of this study is to evaluate home-based physical exercise program for metastatic cancer patients treated with oral targeted therapies to help patients to cope with fatigue and improve quality of life.Trial registrationThis trial was registered in ClinicalTrials.gov since May 2017 (NCT03169075).
C1 [Joly, Florence] Ctr Francois Baclesse, Caen, France.
   [Joly, Florence] CHU Cote Nacre, Caen, France.
   [Lefeuvre-Plesse, Claudia] Ctr Eugene Marquis, Rennes, France.
   [Garnier-Tixidre, Claire] Inst Daniel Hollard, Grenoble, France.
   [Helissey, Carole] HIA Begin, St Mande, France.
   [Menneveau, Nathalie; Anota, Amelie] CHRU Besancon, Besancon, France.
   [Zannetti, Alain] CH, Cholet, France.
   [Salas, Sebastien] CHU La Timone, Marseille, France.
   [Houede, Nadine] Inst Cancerol Gard, Nimes, France.
   [Abadie-Lacourtoisie, Sophie] ICO Rene Gauducheau, Nantes, France.
   [Stefani, Laetitia] CH Annecy Genevois, Pringy, France.
   [Nenan, Soazig; Rieger, Isabelle] Unicancer, Paris, France.
   [Durand-Zaleski, Isabelle] Hop Hotel Dieu, Paris, France.
   [Descotes, Jean-Marc] CAMI Sport & Canc, Neuilly Sur Seine, France.
C3 UNICANCER; Centre Francois Baclesse; Universite de Caen Normandie; CHU
   de Caen NORMANDIE; UNICANCER; Centre Eugene Marquis; Universite de
   Rennes; Universite de Franche-Comte; CHU Besancon; Aix-Marseille
   Universite; Assistance Publique-Hopitaux de Marseille; UNICANCER;
   Institut de Cancerologie de l'Ouest (ICO); Centre Hospitalier Annecy
   Genevois; UNICANCER; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris Cite; Hopital Universitaire Hotel-Dieu - APHP
RP Joly, F (corresponding author), Ctr Francois Baclesse, Caen, France.; Joly, F (corresponding author), CHU Cote Nacre, Caen, France.
EM f.joly@baclesse.unicancer.fr
RI Helissey, Carole/ABA-5343-2021; joly, florence/AAF-9191-2020;
   Durand-Zaleski, Isabelle/AFP-1493-2022
FU Ligue nationale Contre le cancer
FX This research was funded by the Ligue nationale Contre le cancer.
CR [Anonymous], 2000, ONCOLOGIST, DOI DOI 10.1634/THEONCOLOGIST.5-SUPPL_2-9
   [Anonymous], 2012, CHOICES METHODS EC E
   Antoun S, 2010, J CLIN ONCOL, V28, P1054, DOI 10.1200/JCO.2009.24.9730
   Aronson JK, 2007, BRIT J CLIN PHARMACO, V63, P383, DOI 10.1111/j.1365-2125.2007.02893.x
   Blauwhoff-Buskermolen S, 2016, SUPPORT CARE CANCER, V24, P661, DOI 10.1007/s00520-015-2826-2
   Bower JE, 2013, BRAIN BEHAV IMMUN, V30, pS48, DOI 10.1016/j.bbi.2012.06.011
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   Courneya KS, 2007, J CLIN ONCOL, V25, P4396, DOI 10.1200/JCO.2006.08.2024
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NR 23
TC 8
Z9 8
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 OCT 9
PY 2020
VL 20
IS 1
AR 975
DI 10.1186/s12885-020-07381-4
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OH6VR
UT WOS:000582734300001
PM 33036567
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Jiang, S
   Ren, R
   Gu, YY
   Jeet, V
   Liu, P
   Li, SP
AF Jiang, Shan
   Ren, Ru
   Gu, Yuanyuan
   Jeet, Varinder
   Liu, Ping
   Li, Shunping
TI Patient Preferences in Targeted Pharmacotherapy for Cancers: A
   Systematic Review of Discrete Choice Experiments
SO PHARMACOECONOMICS
LA English
DT Review
ID CDK4/6 INHIBITOR REGIMENS; BREAST-CANCER; MULTIPLE-MYELOMA; 1ST-LINE
   TREATMENT; COLORECTAL-CANCER; CANADIAN PATIENTS; DECISION-MAKING;
   PROSTATE-CANCER; THERAPY; HEALTH
AB Background Targeted pharmacotherapy has been increasingly applied in cancer treatment due to its breakthroughs. However, the unmet needs of cancer patients are still significant, highlighting the urgency to investigate patient preferences. It is unclear how patients deliberate their choices between different aspects of targeted therapy, including cost, efficacy, and adverse events. Since discrete choice experiments (DCEs) have been widely applied to patient preference elicitation, we reviewed DCEs on targeted therapy for different cancers. We also synthesized evidence on the factors influencing patients' choices and their willingness-to-pay (WTP) for survival when treated by targeted therapy. Methods We searched databases, including PubMed, EMBASE and MEDLINE, up to August 16, 2022, supplemented by a reference screening. The attributes from the selected studies were categorized into three groups: outcomes, costs, and process. We also calculated the relative importance of attributes and WTP for survival whenever possible. The purpose, respondents, explanation, findings, significance (PREFS) checklist was used to evaluate the quality of the included DCE studies. Results The review identified 34 eligible studies from 13 countries covering 14 cancers, such as breast, ovarian, kidney, prostate, and skin cancers. It also reveals a rising trend of DCEs on this topic, as most studies were published after 2018. We found that patients placed higher weights on the outcome (e.g., overall survival) and cost attributes than on process attributes. On average, patients were willing to pay $561 (95% confidence interval [CI]: $415-$758) and $716 (95% CI $524-$958) out-of-pocket for a 1-month increase in progression-free survival and overall survival, respectively. PREFS scores of the 34 studies ranged from 2 to 4, with a mean of 3.38 (SD: 0.65), suggesting a reasonable quality based on the checklist. However, most studies (n = 32, 94%) did not assess the impact of non-responses on the results. Conclusions This is the first systematic review focusing on patient preferences for targeted cancer therapy. We showcased novel approaches for evidence synthesis of DCE results, especially the attribute relative importance and WTP. The results may inform stakeholders about patient preferences toward targeted therapy and their WTP estimates. More studies with improved study design and quality are warranted to generate more robust evidence to assist decision making.
C1 [Jiang, Shan] Univ British Columbia, Sch Populat & Publ Hlth, Vancouver, BC, Canada.
   [Ren, Ru; Liu, Ping; Li, Shunping] Shandong Univ, Cheeloo Coll Med, Ctr Hlth Management & Policy Res, Sch Publ Hlth, Jinan 250012, Peoples R China.
   [Ren, Ru; Liu, Ping; Li, Shunping] Shandong Univ, NHC Key Lab Hlth Econ & Policy Res, Jinan 250012, Peoples R China.
   [Ren, Ru; Liu, Ping; Li, Shunping] Shandong Univ, Ctr Hlth Preference Res, Jinan 250012, Peoples R China.
   [Ren, Ru] Shandong Univ, Hosp 2, Cheeloo Coll Med, Inst Med Sci, 247 Beiyuan St, Jinan 250033, Peoples R China.
   [Gu, Yuanyuan; Jeet, Varinder] Macquarie Univ, Ctr Hlth Econ, Macquarie Business Sch, Sydney, NSW 2109, Australia.
   [Gu, Yuanyuan; Jeet, Varinder] Macquarie Univ, Australian Inst Hlth Innovat, Sydney, NSW 2109, Australia.
C3 University of British Columbia; Shandong University; Shandong
   University; Shandong University; Shandong University; Macquarie
   University; Macquarie University
RP Gu, YY (corresponding author), Macquarie Univ, Ctr Hlth Econ, Macquarie Business Sch, Sydney, NSW 2109, Australia.; Gu, YY (corresponding author), Macquarie Univ, Australian Inst Hlth Innovat, Sydney, NSW 2109, Australia.
EM yuanyuan.gu@mq.edu.au
RI Gu, Yuanyuan/JXM-6975-2024; Jiang, Shan/AAG-3456-2020
OI Jiang, Shan/0000-0003-1015-1278; Gu, Yuanyuan/0000-0002-3816-9106; Jeet,
   Varinder/0000-0003-3765-5310
FU CAUL
FX Open Access funding enabled and organized by CAUL and its Member
   Institutions.
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NR 87
TC 14
Z9 14
U1 6
U2 30
PU ADIS INT LTD
PI NORTHCOTE
PA 5 THE WAREHOUSE WAY, NORTHCOTE 0627, AUCKLAND, NEW ZEALAND
SN 1170-7690
EI 1179-2027
J9 PHARMACOECONOMICS
JI Pharmacoeconomics
PD JAN
PY 2023
VL 41
IS 1
BP 43
EP 57
DI 10.1007/s40273-022-01198-8
EA NOV 2022
PG 15
WC Economics; Health Care Sciences & Services; Health Policy & Services;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Business & Economics; Health Care Sciences & Services; Pharmacology &
   Pharmacy
GA 7U8JR
UT WOS:000882813800001
PM 36372823
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Chawla, A
   Peeples, M
   Li, NX
   Anhorn, R
   Ryan, J
   Signorovitch, J
AF Chawla, Anita
   Peeples, Miranda
   Li, Nanxin
   Anhorn, Rachel
   Ryan, Jason
   Signorovitch, James
TI Real-world utilization of molecular diagnostic testing and matched drug
   therapies in the treatment of metastatic cancers
SO JOURNAL OF MEDICAL ECONOMICS
LA English
DT Article
DE Claims analysis; molecular diagnostic testing; genomic profiling;
   metastatic cancer; real world; targeted therapy; utilization
ID CELL LUNG-CANCER; COST-EFFECTIVENESS; COLORECTAL-CANCER; PATHOLOGICAL
   EPIDEMIOLOGY; TARGETED THERAPY; EGFR MUTATIONS; STATISTICS; TRASTUZUMAB;
   BIOMARKER; PATTERNS
AB Aims: To assess the frequency of biopsies and molecular diagnostic testing (human DNA/RNA analysis), anti-cancer drug use (genomically-matched targeted therapy [GMTT], unmatched targeted therapy [UTT], endocrine therapy [ET], and chemotherapy [CT]), and medical service costs among adults with metastatic cancer.
   Methods: Adults diagnosed with metastatic breast, non-small cell lung (NSCLC), colorectal, head and neck, ovarian, and uterine cancer (2010Q1-2015Q1) were identified in the OptumHealth Care Solutions claims database and followed from first metastatic diagnosis for >= 1 month and until the end of data availability. Utilization was assessed for each cancer cohort (all and patients aged >= 65 years); per-patient-per-month (PPPM) medical service costs were assessed for all patients. Testing frequency estimates were applied to Surveillance, Epidemiology, and End Results Program data to estimate the number of untested patients (2010-2014).
   Results: Patients with metastatic cancer (n = 8,193; breast [n = 3 ,41 4], NSCLC [n = 2,231], colorectal [n=1,611], head and neck [n=511], ovarian [n=275], and uterine [n=151]) were 63 years old (mean), with 11.1-22.2 months of observation. Biopsy and molecular diagnostic testing frequencies ranged from 7% (uterine) to 73% (ovarian), and from 34% (head and neck) to 52% (breast), respectively. Few were treated with GMTT (breast, 11%; NSCLC, 9%; colorectal, 6%). Treatment with UTT ranged from 0.7% (uterine) to 21% (colorectal). Biopsy, diagnostic testing, and anti-cancer drug therapy were less frequent for those >= 65 years. Medical service costs (PPPM, mean) ranged from $6,618 (head and neck) to $9,940 (ovarian). The estimated number of untested new patients with metastatic cancer was 636,369 (all) and 341,397 (>65).
   Limitations: In addition to the limitations of claims analyses, diagnostic testing frequency may be under-estimated if patients underwent testing prior to study inclusion.
   Conclusions: The low frequency of molecular diagnostic testing suggests there are opportunities to better inform management of patients with advanced cancer, particularly decisions to treat with GMTT.
C1 [Chawla, Anita] Anal Grp Inc, Menlo Pk, CA USA.
   [Peeples, Miranda; Li, Nanxin; Signorovitch, James] Anal Grp Inc, Boston, MA USA.
   [Anhorn, Rachel; Ryan, Jason] Fdn Med Inc, Cambridge, MA USA.
C3 Analysis Group Inc.; Analysis Group Inc.; Foundation Medicine
RP Chawla, A (corresponding author), 1010 El Camino Real,Suite 310, Menlo Pk, CA 94025 USA.
EM anita.chawla@analysisgroup.com
RI Li, Nanxin/D-9755-2011
FU Foundation Medicine, Inc.
FX This study was funded by Foundation Medicine, Inc. The sponsor was
   involved in all parts of the study and in manuscript preparation.
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NR 57
TC 13
Z9 13
U1 1
U2 2
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1369-6998
EI 1941-837X
J9 J MED ECON
JI J. Med. Econ.
PY 2018
VL 21
IS 6
BP 543
EP 552
DI 10.1080/13696998.2017.1423488
PG 10
WC Economics; Health Care Sciences & Services; Health Policy & Services;
   Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Business & Economics; Health Care Sciences & Services; General &
   Internal Medicine
GA GH9JS
UT WOS:000433986300001
PM 29295635
DA 2025-01-04
ER

PT J
AU Shen, JY
   Li, L
   Yang, T
   Cheng, NL
   Sun, GQ
AF Shen, Jinyan
   Li, Li
   Yang, Tao
   Cheng, Niuliang
   Sun, Gongqin
TI Drug Sensitivity Screening and Targeted Pathway Analysis Reveal a
   Multi-Driver Proliferative Mechanism and Suggest a Strategy of
   Combination Targeted Therapy for Colorectal Cancer Cells
SO MOLECULES
LA English
DT Article
DE colorectal cancer; combination therapy; dose reduction index; protein
   kinase inhibitors; targeted therapy
ID SMALL-MOLECULE INHIBITOR; KINASE INHIBITOR; TYROSINE KINASE; INTRATUMOR
   HETEROGENEITY; COLON-CANCER; C-MET; GROWTH; SRC; ACTIVATION; DISCOVERY
AB Treatment of colorectal cancer mostly relies on traditional therapeutic approaches, such as surgery and chemotherapy. Limited options of targeted therapy for colorectal cancer narrowly focus on blocking cancer-generic targets VEGFR and EGFR. Identifying the oncogenic drivers, understanding their contribution to proliferation, and finding inhibitors to block such drivers are the keys to developing targeted therapy for colorectal cancer. In this study, ten colorectal cancer cell lines were screened against a panel of protein kinase inhibitors blocking key oncogenic signaling pathways. The results show that four of the 10 cell lines did not respond to any kinase inhibitors significantly, the other six were mildly inhibited by AZD-6244, BMS-754807, and/or dasatinib. Mechanistic analyses demonstrate that these inhibitors independently block the MAP kinase pathway, IR/IGF-1R/AKT pathway, and Src kinases, suggesting a multi-driver nature of proliferative signaling in these cells. Most of these cell lines were potently and synergistically inhibited by pair-wise combinations of these drugs. Furthermore, seven of the 10 cell lines were inhibited by the triple combination of AZD-6244/BMS-754807/dasatinib with IC50's between 10 and 84 nM. These results suggest that combination targeted therapy may be an effective strategy against colorectal cancer.
C1 [Shen, Jinyan; Yang, Tao; Cheng, Niuliang; Sun, Gongqin] Shanxi Med Univ, Dept Biochem & Mol Biol, Taiyuan 030001, Shanxi, Peoples R China.
   [Shen, Jinyan; Li, Li; Yang, Tao; Sun, Gongqin] Univ Rhode Isl, Dept Cell & Mol Biol, Kingston, RI 02881 USA.
   [Li, Li] Shanxi Med Univ, Dept Cell Biol & Med Genet, Taiyuan 030001, Shanxi, Peoples R China.
C3 Shanxi Medical University; University of Rhode Island; Shanxi Medical
   University
RP Cheng, NL; Sun, GQ (corresponding author), Shanxi Med Univ, Dept Biochem & Mol Biol, Taiyuan 030001, Shanxi, Peoples R China.; Sun, GQ (corresponding author), Univ Rhode Isl, Dept Cell & Mol Biol, Kingston, RI 02881 USA.
EM shen_jinyan@uri.edu; lili_5076@126.com; yangtao056cn@126.com;
   chengniuliang@126.com; gsun@uri.edu
OI Shen, Jinyan/0000-0002-1955-093X
FU College of Environment and Life Sciences; Shanxi Medical University,
   Taiyuan, Shanxi, China
FX This research was funded by College of Environment and Life Sciences.
   J.S., L.L. and T.Y. are supported by scholarships from Shanxi Medical
   University, Taiyuan, Shanxi, China.
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NR 53
TC 9
Z9 12
U1 1
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1420-3049
J9 MOLECULES
JI Molecules
PD FEB 1
PY 2019
VL 24
IS 3
AR 623
DI 10.3390/molecules24030623
PG 18
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA HL7PR
UT WOS:000458934000247
PM 30754629
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Neitzel, C
   Demuth, P
   Wittmann, S
   Fahrer, J
AF Neitzel, Carina
   Demuth, Philipp
   Wittmann, Simon
   Fahrer, Joerg
TI Targeting Altered Energy Metabolism in Colorectal Cancer: Oncogenic
   Reprogramming, the Central Role of the TCA Cycle and Therapeutic
   Opportunities
SO CANCERS
LA English
DT Review
DE colorectal cancer; cancer metabolism; mitochondria; TCA cycle; oncogenic
   signaling; tumor microenvironment; targeted therapy; CPI-613
ID HYPOXIA-INDUCIBLE FACTOR-1-ALPHA; MITOCHONDRIAL PYRUVATE CARRIER;
   ALPHA-LIPOIC ACID; COLON-CANCER; C-MYC; STEM-CELLS; TUMOR PROGRESSION;
   COPY-NUMBER; O-6-METHYLGUANINE-DNA METHYLTRANSFERASE;
   OXIDATIVE-PHOSPHORYLATION
AB Colorectal cancer (CRC) is among the most frequent cancer entities worldwide. Multiple factors are causally associated with CRC development, such as genetic and epigenetic alterations, inflammatory bowel disease, lifestyle and dietary factors. During malignant transformation, the cellular energy metabolism is reprogrammed in order to promote cancer cell growth and proliferation. In this review, we first describe the main alterations of the energy metabolism found in CRC, revealing the critical impact of oncogenic signaling and driver mutations in key metabolic enzymes. Then, the central role of mitochondria and the tricarboxylic acid (TCA) cycle in this process is highlighted, also considering the metabolic crosstalk between tumor and stromal cells in the tumor microenvironment. The identified cancer-specific metabolic transformations provided new therapeutic targets for the development of small molecule inhibitors. Promising agents are in clinical trials and are directed against enzymes of the TCA cycle, including isocitrate dehydrogenase, pyruvate dehydrogenase kinase, pyruvate dehydrogenase complex (PDC) and alpha-ketoglutarate dehydrogenase (KGDH). Finally, we focus on the alpha-lipoic acid derivative CPI-613, an inhibitor of both PDC and KGDH, and delineate its anti-tumor effects for targeted therapy.
C1 [Neitzel, Carina; Demuth, Philipp; Wittmann, Simon; Fahrer, Joerg] Tech Univ Kaiserslautern, Dept Chem, Div Food Chem & Toxicol, D-67663 Kaiserslautern, Germany.
C3 University of Kaiserslautern
RP Fahrer, J (corresponding author), Tech Univ Kaiserslautern, Dept Chem, Div Food Chem & Toxicol, D-67663 Kaiserslautern, Germany.
EM cneitzel@rhrk.uni-kl.de; pdemuth@rhrk.uni-kl.de;
   wittmans@rhrk.uni-kl.de; fahrer@chemie.uni-kl.de
FU Wilhelm Sander Foundation
FX This research was funded by the Wilhelm Sander Foundation (grant numbers
   2016.039.1 and 2016.039.2 to J.F.). The APC was funded by the Wilhelm
   Sander Foundation.
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NR 243
TC 38
Z9 39
U1 2
U2 30
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 1731
DI 10.3390/cancers12071731
PG 32
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MY3GO
UT WOS:000558308100001
PM 32610612
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Saad, AM
   Abdel-Rahman, O
AF Saad, Anas M.
   Abdel-Rahman, Omar
TI Initial systemic chemotherapeutic and targeted therapy strategies for
   the treatment of colorectal cancer patients with liver metastases
SO EXPERT OPINION ON PHARMACOTHERAPY
LA English
DT Review
DE Colon cancer; rectal cancer; liver metastases; chemotherapy; survival
ID HEPATIC-ARTERIAL-INFUSION; FOLFIRI PLUS BEVACIZUMAB; ADJUVANT
   CHEMOTHERAPY; PHASE-II; 1ST-LINE TREATMENT; PERIOPERATIVE CHEMOTHERAPY;
   PREOPERATIVE CHEMOTHERAPY; NEOADJUVANT CHEMOTHERAPY;
   SURGICAL-MANAGEMENT; COLON-CANCER
AB Introduction: The liver is the most common metastatic site in colorectal cancer with more than half the patients developing a liver metastasis either at the time of their diagnosis (synchronous) or later (metachronous). Surgical resection remains the principal curative approach that offers significant survival improvements. However, upfront surgery is only possible in about 10-20% of patients at the time of diagnosis, making the consideration of other treatment modalities essential. Areas covered: In this review, the authors provide an overview of the standard approaches for the initial management of patients with colorectal cancer with liver metastases. They then provide an up-to-date discussion of first-line systemic chemotherapy/targeted therapy options in the contexts of initially resectable and unresectable disease and review toxicities and complications following these options. Expert opinion: Advances in chemotherapeutic agents and biological targeted therapies have improved the prognosis of colorectal cancer with liver metastases. However, there is still no 'single best approach', making further trials necessary to provide more evidence.
C1 [Saad, Anas M.] Ain Shams Univ, Cairo, Egypt.
   [Abdel-Rahman, Omar] Ain Shams Univ, Clin Oncol Dept, Cairo, Egypt.
   [Abdel-Rahman, Omar] Univ Alberta, Cross Canc Inst, Dept Oncol, Edmonton, AB, Canada.
C3 Egyptian Knowledge Bank (EKB); Ain Shams University; Egyptian Knowledge
   Bank (EKB); Ain Shams University; University of Alberta
RP Abdel-Rahman, O (corresponding author), Univ Alberta, Cross Canc Inst, Dept Oncol, Edmonton, AB, Canada.
EM Omar.abdelrhman@med.asu.edu.eg
RI Saad, Anas/L-6672-2017
OI Saad, Anas/0000-0003-0101-0131
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NR 89
TC 13
Z9 13
U1 0
U2 14
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1465-6566
EI 1744-7666
J9 EXPERT OPIN PHARMACO
JI Expert Opin. Pharmacother.
PD SEP 22
PY 2019
VL 20
IS 14
BP 1767
EP 1775
DI 10.1080/14656566.2019.1642324
EA JUL 2019
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA IZ5JB
UT WOS:000476049700001
PM 31314604
DA 2025-01-04
ER

PT J
AU Maurea, N
   Spallarossa, P
   Cadeddu, C
   Madonna, R
   Mele, D
   Monte, I
   Novo, G
   Pagliaro, P
   Pepe, A
   Tocchetti, CG
   Zito, C
   Mercuro, G
AF Maurea, Nicola
   Spallarossa, Paolo
   Cadeddu, Christian
   Madonna, Rosalinda
   Mele, Donato
   Monte, Ines
   Novo, Giuseppina
   Pagliaro, Pasquale
   Pepe, Alessia
   Tocchetti, Carlo G.
   Zito, Concetta
   Mercuro, Giuseppe
TI A recommended practical approach to the management of target therapy and
   angiogenesis inhibitors cardiotoxicity: an opinion paper of the working
   group on drug cardiotoxicity and cardioprotection, Italian Society of
   Cardiology
SO JOURNAL OF CARDIOVASCULAR MEDICINE
LA English
DT Article
DE angiogenesis inhibitors; HER2; epidermal growth factor receptor 2;
   tyrosine kinase inhibitors
ID ARTERIAL THROMBOEMBOLIC EVENTS; GASTROINTESTINAL STROMAL TUMOR; ADJUVANT
   TRASTUZUMAB THERAPY; LEFT-VENTRICULAR DYSFUNCTION;
   CONGESTIVE-HEART-FAILURE; BREAST-CANCER; CARDIAC DYSFUNCTION;
   COLORECTAL-CANCER; KINASE INHIBITOR; CHEMOTHERAPY
AB The US National Cancer Institute estimates that cardiotoxicity (CTX) from target therapy refers mostly to four groups of drugs: epidermal growth factor receptor 2 inhibitors, angiogenic inhibitors, directed Abelson murine leukemia viral oncogene homolog inhibitors, and proteasome inhibitors. The main cardiotoxic side-effects related to antiepidermal growth factor receptor 2 therapy are left ventricular systolic dysfunction and heart failure. Angiogenesis inhibitors are associated with hypertension, left ventricular dysfunction/heart failure, myocardial ischemia, QT prolongation, and thrombosis. Moreover, other agents may be related to CTX induced by treatment. In this study, we review the guidelines for a practical approach for the management of CTX in patients under anticancer target therapy.
C1 [Maurea, Nicola] Ist Nazl Studio & Cura Tumori Fdn Giovanni Pascal, Div Cardiol, Via M Semmola 52, I-80123 Naples, Italy.
   [Spallarossa, Paolo] IRCCS San Martino IST, Clin Cardiovasc Dis, Genoa, Italy.
   [Cadeddu, Christian; Mercuro, Giuseppe] Univ Cagliari, Dept Med Sci Mario Aresu, Cagliari, Italy.
   [Madonna, Rosalinda] Univ G DAnnunzio, Ctr Excellence Aging, Inst Cardiol, Chieti, Italy.
   [Mele, Donato] Univ Hosp Ferrara, Cardiol Unit, Ferrara, Italy.
   [Monte, Ines] Univ Catania, Dept Gen Surg & Med Surg Specialties, Catania, Italy.
   [Novo, Giuseppina] Univ Palermo, Chair & Div Cardiol, Palermo, Italy.
   [Pagliaro, Pasquale] Univ Turin, Dept Clin & Biol Sci, Turin, Italy.
   [Pepe, Alessia] Fdn G Monasterio CNR, UOC Magnet Resonance Imaging, Pisa, Italy.
   [Tocchetti, Carlo G.] Univ Naples Federico II, Dept Translat Med Sci, Naples, Italy.
   [Zito, Concetta] Univ Messina, AOU Policlin G Martino, UOC Cardiol Intens Unit, Messina, Italy.
C3 University of Genoa; IRCCS AOU San Martino IST; University of Cagliari;
   G d'Annunzio University of Chieti-Pescara; University of Ferrara;
   Arcispedale Sant'Anna; University of Catania; University of Palermo;
   University of Turin; Consiglio Nazionale delle Ricerche (CNR);
   University of Naples Federico II; AOU Policlinico Gaetano Martino;
   University of Messina
RP Maurea, N (corresponding author), Ist Nazl Studio & Cura Tumori Fdn Giovanni Pascal, Div Cardiol, Via M Semmola 52, I-80123 Naples, Italy.
EM n.maurea@istitutotumori.na.it
RI Pagliaro, Pasquale/E-5239-2010; Cadeddu, Christian/AAI-9219-2020; Mele,
   Donato/K-2100-2018; PEPE, ALESSIA/A-7819-2012; Maurea,
   Nicola/AAC-2341-2022; Spallarossa, Paolo/AAC-8981-2019; novo,
   giuseppina/K-6580-2016; Tocchetti, Carlo Gabriele/AAG-5944-2020; Monte,
   Ines/G-8642-2013
OI Maurea, Nicola/0000-0003-3704-0092; Tocchetti, Carlo
   Gabriele/0000-0001-5983-688X; Madonna, Rosalinda/0000-0001-6455-2777;
   Pagliaro, Pasquale/0000-0002-4386-1383; Monte, Ines/0000-0001-7059-7525;
   Cadeddu, Christian/0000-0002-2823-1797; MELE, Donato/0000-0002-2823-4090
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NR 77
TC 33
Z9 33
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1558-2027
EI 1558-2035
J9 J CARDIOVASC MED
JI J. Cardiovasc. Med.
PD MAY
PY 2016
VL 17
SU 1
BP S93
EP S104
DI 10.2459/JCM.0000000000000383
PG 12
WC Cardiac & Cardiovascular Systems
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA DN2YW
UT WOS:000376930100012
PM 27183530
OA Green Published
DA 2025-01-04
ER

PT J
AU Yin, TC
   Chen, PJ
   Yeh, YS
   Li, CC
   Chen, YC
   Su, WC
   Chang, TK
   Huang, CW
   Huang, CM
   Tsai, HL
   Wang, JY
AF Yin, Tzu-Chieh
   Chen, Po-Jung
   Yeh, Yung-Sung
   Li, Ching-Chun
   Chen, Yen-Cheng
   Su, Wei-Chih
   Chang, Tsung-Kun
   Huang, Ching-Wen
   Huang, Chun-Ming
   Tsai, Hsiang-Lin
   Wang, Jaw-Yuan
TI Efficacy of concurrent radiotherapy in patients with locally advanced
   rectal cancer and synchronous metastasis receiving systemic therapy
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE metastatic rectal cancer; locally advanced rectal cancer; concurrent
   radiotherapy; primary tumor resection (PTR); systemic chemotherapy;
   systemic targeted therapy
ID CIRCULATING TUMOR-CELLS; TOTAL MESORECTAL EXCISION; COLORECTAL-CANCER;
   POSTOPERATIVE CHEMORADIOTHERAPY; PREOPERATIVE RADIOTHERAPY; HEPATIC
   RESECTION; SURGICAL RESECTION; SURVIVAL; LIVER; CHEMOTHERAPY
AB BackgroundNeoadjuvant chemoradiotherapy followed by total mesorectal excision is the standard treatment for patients with nonmetastatic locally advanced rectal cancer (LARC). However, for patients with LARC and synchronous metastasis, the optimal treatment strategy and sequence remain inconclusive. In the present study, we evaluated the efficacy and safety of concurrent radiotherapy in patients with de novo metastatic rectal cancer who received chemotherapy and targeted therapy. MethodsWe retrospectively reviewed the data of 63 patients with LARC and synchronous metastasis who received intensive therapy at the study hospital between April 2015 and November 2018. The included patients were divided into two groups: RT-CT, those who received systemic chemotherapy with targeted therapy and concurrent radiotherapy (for primary rectal cancer), and CT, those who received only systemic chemotherapy with targeted therapy. ResultsTreatment response was better in the RT-CT group than in the CT group. The rate of primary tumor resection (PTR) was higher in the RT-CT group than in the CT group (71.4% and 42.9%, respectively; P = .0286). The RT-CT group exhibited considerably longer local recurrence-free survival (P = .0453) and progression-free survival (PFS; from 13.3 to 22.5 months) than did the CT group (P = .0091); however, the groups did not differ in terms of overall survival (OS; P = .49). Adverse events were almost similar between the groups, except frequent diarrhea, the prevalence of which was higher in the RT-CT group than in the CT group (59.5% and 23.8%, respectively; P = .0075). ConclusionsIn the era of biologics, radiotherapy may increase the resectability of primary rectal tumors, reducing the risk of locoregional failure and prolonging PFS. Concurrent pelvic radiotherapy may not substantially improve OS, which is indicated by metastasis. Hence, the resection of the distant metastases may be essential for improving long-term OS. To further determine the efficacy of concurrent radiotherapy, additional prospective, randomized studies must combine preoperative pelvic radiotherapy with PTR and metastectomy to treat patients with stage IV LARC.
C1 [Yin, Tzu-Chieh; Li, Ching-Chun] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Gen & Digest Surg, Kaohsiung, Taiwan.
   [Yin, Tzu-Chieh] Kaohsiung Med Univ, Kaohsiung Municipal Tatung Hosp, Dept Surg, Kaohsiung, Taiwan.
   [Yin, Tzu-Chieh; Chen, Po-Jung; Chen, Yen-Cheng; Su, Wei-Chih; Chang, Tsung-Kun; Huang, Ching-Wen; Tsai, Hsiang-Lin; Wang, Jaw-Yuan] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, Kaohsiung, Taiwan.
   [Yeh, Yung-Sung] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Trauma & Surg Crit Care, 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.
   [Li, Ching-Chun] Kaohsiung Municipal Hsiaokang Hosp, Dept Surg, Kaohsiung, Taiwan.
   [Chen, Yen-Cheng; Su, Wei-Chih; Chang, Tsung-Kun; Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.
   [Chang, Tsung-Kun] Kaohsiung Med Univ, Coll Med, Fac Postbaccalaureate Med, Dept Surg, Kaohsiung, Taiwan.
   [Huang, Ching-Wen; Tsai, Hsiang-Lin; Wang, Jaw-Yuan] Kaohsiung Med Univ, Coll Med, Fac Med, Dept Surg, Kaohsiung, Taiwan.
   [Huang, Chun-Ming; Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung, Taiwan.
   [Huang, Chun-Ming] Kaohsiung Med Univ Hosp, Dept Radiat Oncol, Kaohsiung, Taiwan.
   [Huang, Chun-Ming] Kaohsiung Med Univ, Coll Med, Fac Med, Dept Radiat Oncol, Kaohsiung, Taiwan.
   [Huang, Chun-Ming] Kaohsiung Med Univ, Kaohsiung Municipal Ta Tung Hosp, Dept Radiat Oncol, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Ctr Canc Res, Kaohsiung, Taiwan.
   [Wang, Jaw-Yuan] Minist Hlth & Welf, Pingtung Hosp, Pingtung, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University; Kaohsiung Municipal Ta-Tung Hospital;
   Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University; Taipei Medical University; Kaohsiung
   Medical University; Kaohsiung Municipal Siao-Gang Hospital; Kaohsiung
   Medical University; Kaohsiung Medical University; Kaohsiung Medical
   University; Kaohsiung Medical University; Kaohsiung Medical University;
   Kaohsiung Medical University Hospital; Kaohsiung Medical University;
   Kaohsiung Medical University; Kaohsiung Municipal Ta-Tung Hospital;
   Kaohsiung Medical University
RP Tsai, HL; Wang, JY (corresponding author), Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Surg, Div Colorectal Surg, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung, Taiwan.; Tsai, HL; Wang, JY (corresponding author), Kaohsiung Med Univ, Coll Med, Fac Med, Dept Surg, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Grad Inst Med, Coll Med, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Ctr Canc Res, Kaohsiung, Taiwan.; Wang, JY (corresponding author), Minist Hlth & Welf, Pingtung Hosp, Pingtung, Taiwan.
EM chunpin870132@yahoo.com.tw; cy614112@ms14.hinet.net
RI Jaw-Yuan, Wang/AFS-8845-2022
OI Wang, Jaw-Yuan/0000-0002-7705-2621
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NR 45
TC 1
Z9 2
U1 1
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 MAR 30
PY 2023
VL 13
AR 1099168
DI 10.3389/fonc.2023.1099168
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA D3JM3
UT WOS:000967720400001
PM 37064097
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhao, F
   Liang, LY
   Wang, H
   Wang, C
   Su, D
   Ying, Y
   Li, WC
   Li, J
   Zheng, JW
   Qiao, L
   Mou, XZ
   Che, SL
   Yu, J
AF Zhao, Fan
   Liang, Liying
   Wang, Heng
   Wang, Chen
   Su, Dan
   Ying, Yao
   Li, Wangchang
   Li, Juan
   Zheng, Jingwu
   Qiao, Liang
   Mou, Xiaozhou
   Che, Shenglei
   Yu, Jing
TI H<sub>2</sub>S-Activated Ion-Interference Therapy: A Novel Tumor
   Targeted Therapy Based on Copper-Overload-Mediated Cuproptosis and
   Pyroptosis
SO ADVANCED FUNCTIONAL MATERIALS
LA English
DT Article
DE copper-overload; cuproptosis; H2S-activated cancer therapy;
   ion-interference therapy; pyroptosis
ID HYDROGEN-SULFIDE; UP-REGULATION; DETERMINES; METABOLISM
AB Copper overload is a novel way to achieve copper-ion-interference therapy by disrupting copper homeostasis and treating diseases through multiple cell death pathways. However, it is difficult to reach copper overload since excess intracellular copper ions will be pumped out. Herein, copper overload is achieved by both raising cellular uptake and reducing the efflux of copper ions using hydrogen sulfide (H2S)-responsive copper hydroxyphosphate nanoparticles (Cu-2(PO4)(OH) NPs). After immersion in an H2S-enriched colon cancer microenvironment, Cu-2(PO4)(OH) NPs can transform into copper sulfide NPs with reduced size for higher cell entering, resulting in improved Fenton activity as well as copper ion dissociation. Reactive oxygen species generated by the Fenton reaction not only activate inflammasomes and Caspase-1 proteins, cause the cleavage of gasdermin D to induce pyroptosis, but also affect mitochondrial function and down-regulate copper exporter ATP7A to further reduce the copper excretion. The combination of higher endocytosis and lower exportation leads to maximized copper overload. Together with the efficient copper ions release, mitochondrial tricarboxylic acid cycle can be disrupted and iron-sulfur cluster proteins are downregulated, ultimately triggering cuproptosis. As both pyroptosis and cuproptosis are efficient ways to induce cell death, this study provides a novel way to realize effective tumor-targeted therapy based on H2S-activated copper overload with simple Cu-2(PO4)(OH) NPs.
C1 [Zhao, Fan; Liang, Liying; Wang, Chen; Ying, Yao; Li, Wangchang; Li, Juan; Zheng, Jingwu; Qiao, Liang; Che, Shenglei; Yu, Jing] Zhejiang Univ Technol, Coll Mat Sci & Engn, Res Ctr Magnet & Elect Mat, Hangzhou 310014, Peoples R China.
   [Wang, Heng] Prov Peoples Hosp, Affiliated Peoples Hosp, Hangzhou Med Coll, Urol & Nephrol Ctr,Dept Urol, Hangzhou 310014, Zhejiang, Peoples R China.
   [Su, Dan] Hangzhou Med Coll, Dept Clin Med, Hangzhou 310014, Peoples R China.
   [Mou, Xiaozhou] Zhejiang Prov Peoples Hosp, Affiliated Peoples Hosp, Hangzhou Med Coll, Canc Ctr,Gen Surg,Minimally Invas Surg Key Lab Tum, Hangzhou 310014, Peoples R China.
C3 Zhejiang University of Technology; Hangzhou Medical College; Hangzhou
   Medical College; Hangzhou Medical College; Zhejiang Provincial People's
   Hospital
RP Che, SL; Yu, J (corresponding author), Zhejiang Univ Technol, Coll Mat Sci & Engn, Res Ctr Magnet & Elect Mat, Hangzhou 310014, Peoples R China.; Mou, XZ (corresponding author), Zhejiang Prov Peoples Hosp, Affiliated Peoples Hosp, Hangzhou Med Coll, Canc Ctr,Gen Surg,Minimally Invas Surg Key Lab Tum, Hangzhou 310014, Peoples R China.
EM mouxz@zju.edu.cn; cheshenglei@zjut.edu.cn; yujing@zjut.edu.cn
RI Liang, Liying/KDO-5300-2024; Shenglei, CHE/O-5902-2019
FU National Natural Science Foundation of China [52073258, 22278104];
   Natural Science Foundation of Zhejiang Province [LR22E010001,
   LY20E020017, LQ19H160016]; Fundamental Research Funds for the Provincial
   Universities of Zhejiang [RF-B2022006]; R&D program of Zhejiang
   University of Technology [KYY-HX-20190730]
FX This work was supported in part by the National Natural Science
   Foundation of China (52073258, 22278104), Natural Science Foundation of
   Zhejiang Province (LR22E010001, LY20E020017, and LQ19H160016), the
   Fundamental Research Funds for the Provincial Universities of Zhejiang
   (RF-B2022006), and R&D program of Zhejiang University of Technology
   (KYY-HX-20190730).
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NR 50
TC 41
Z9 42
U1 53
U2 284
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1616-301X
EI 1616-3028
J9 ADV FUNCT MATER
JI Adv. Funct. Mater.
PD SEP
PY 2023
VL 33
IS 38
DI 10.1002/adfm.202300941
EA JUN 2023
PG 13
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
   Nanotechnology; Materials Science, Multidisciplinary; Physics, Applied;
   Physics, Condensed Matter
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science;
   Physics
GA T9BL7
UT WOS:001001985700001
DA 2025-01-04
ER

PT J
AU Kamel, HFM
   Al-Amodi, HSAB
AF Kamel, Hala Fawzy Mohamed
   Al-Amodi, Hiba Saeed A. Bagader
TI Exploitation of Gene Expression and Cancer Biomarkers in Paving the Path
   to Era of Personalized Medicine
SO GENOMICS PROTEOMICS & BIOINFORMATICS
LA English
DT Review
DE Personalized medicine; Gene expression; Targeted therapy; Predictive
   biomarkers; Prognostic biomarkers
ID CELL LUNG-CANCER; METASTATIC BREAST-CANCER; CETUXIMAB PLUS IRINOTECAN;
   PATHOLOGICAL COMPLETE RESPONSE; ADVANCED COLORECTAL-CANCER; CIRCULATING
   TUMOR-CELLS; ADJUVANT CHEMOTHERAPY; PREDICTIVE BIOMARKERS; PHASE-II;
   EPIGENETIC CHANGES
AB Cancer therapy agents have been used extensively as cytotoxic drugs against tissue or organ of a specific type of cancer. With the better understanding of molecular mechanisms underlying carcinogenesis and cellular events during cancer progression and metastasis, it is now possible to use targeted therapy for these molecular events. Targeted therapy is able to identify cancer patients with dissimilar genetic defects at cellular level for the same cancer type and consequently requires individualized approach for treatment. Cancer therapy begins to shift steadily from the traditional approach of "one regimen for all patients" to a more individualized approach, through which each patient will be treated specifically according to their specific genetic defects. Personalized medicine accordingly requires identification of indicators or markers that guide in the decision making of such therapy to the chosen patients for more effective therapy. Cancer biomarkers are frequently used in clinical practice for diagnosis and prognosis, as well as identification of responsive patients and prediction of treatment response of cancer patient. The rapid breakthrough and development of microarray and sequencing technologies is probably the main tool for paving the way toward "individualized biomarker-driven cancer therapy" or "personalized medicine". In this review, we aim to provide an updated knowledge and overview of the current landscape of cancer biomarkers and their role in personalized medicine, emphasizing the impact of genomics on the implementation of new potential targeted therapies and development of novel cancer biomarkers in improving the outcome of cancer therapy.
C1 [Kamel, Hala Fawzy Mohamed; Al-Amodi, Hiba Saeed A. Bagader] Umm AL Qura Univ, Biochem Dept, Fac Med, Makhha 21955, Saudi Arabia.
   [Kamel, Hala Fawzy Mohamed] Ain Shams Univ, Med Biochem Dept, Fac Med, Cairo 11566, Egypt.
C3 Umm Al Qura University; Egyptian Knowledge Bank (EKB); Ain Shams
   University
RP Kamel, HFM (corresponding author), Umm AL Qura Univ, Biochem Dept, Fac Med, Makhha 21955, Saudi Arabia.; Kamel, HFM (corresponding author), Ain Shams Univ, Med Biochem Dept, Fac Med, Cairo 11566, Egypt.
EM kamelhala@msn.com
RI Nasif, Wesam/HPE-1237-2023; Kamel, Hala F.M./N-4622-2016
OI Kamel, Hala F.M./0000-0001-9960-4100; Alamodi, Hiba/0000-0003-1865-0004
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NR 213
TC 85
Z9 94
U1 0
U2 18
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1672-0229
EI 2210-3244
J9 GENOM PROTEOM BIOINF
JI Genom. Proteomics Bioinformatics
PD AUG
PY 2017
VL 15
IS 4
BP 220
EP 235
DI 10.1016/j.gpb.2016.11.005
PG 16
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA FG7PH
UT WOS:000410610300002
PM 28813639
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Bivona, TG
   Doebele, RC
AF Bivona, Trever G.
   Doebele, Robert C.
TI A framework for understanding and targeting residual disease in
   oncogene-driven solid cancers
SO NATURE MEDICINE
LA English
DT Article
ID CELL LUNG-CANCER; RANDOMIZED PHASE-II; ACQUIRED-RESISTANCE; COMBINED
   BRAF; COLORECTAL-CANCER; MEK INHIBITION; RAF INHIBITORS; FEEDBACK
   ACTIVATION; DRUG-RESISTANCE; EGFR
AB Molecular targeted therapy has the potential to dramatically improve survival in patients with cancer. However, complete and durable responses to targeted therapy are rare in individuals with advanced-stage solid cancers. Even the most effective targeted therapies generally do not induce a complete tumor response, resulting in residual disease and tumor progression that limits patient survival. We discuss the emerging need to more fully understand the molecular basis of residual disease as a prelude to designing therapeutic strategies to minimize or eliminate residual disease so that we can move from temporary to chronic control of disease, or a cure, for patients with advanced-stage solid cancers. Ultimately, we propose a shift from the current reactive paradigm of analyzing and treating acquired drug resistance to a pre-emptive paradigm of defining the mechanisms that result in residual disease, to target and limit this disease reservoir.
C1 [Bivona, Trever G.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
   [Bivona, Trever G.] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
   [Bivona, Trever G.] Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA.
   [Doebele, Robert C.] Univ Colorado, Dept Med & Med Oncol, Anschutz Med Campus, Aurora, CO USA.
C3 University of California System; University of California San Francisco;
   University of California System; University of California San Francisco;
   UCSF Medical Center; UCSF Helen Diller Family Comprehensive Cancer
   Center; University of California System; University of California San
   Francisco; University of Colorado System; University of Colorado
   Anschutz Medical Campus
RP Bivona, TG (corresponding author), Univ Calif San Francisco, Dept Med, San Francisco, CA USA.; Bivona, TG (corresponding author), Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.; Bivona, TG (corresponding author), Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA.
EM trever.bivona@ucsf.edu
RI Doebele, Robert/I-8230-2019
FU US National Institutes of Health Director's Office and Common Fund
   [DP2-CA174497]; National Cancer Institute [R01-CA169338]; HHMI
   Collaborative Innovation Award Program; Searle Scholars Program; Pew
   Charitable Trust; Addario Lung Cancer Foundation; V Foundation for
   Cancer Research; University of Colorado Lung Cancer SPORE; National
   Cancer Institute [R01CA169338] Funding Source: NIH RePORTER
FX T.G.B. acknowledges funding support from the US National Institutes of
   Health Director's Office and Common Fund (New Innovators Award
   DP2-CA174497), the National Cancer Institute (R01-CA169338), the HHMI
   Collaborative Innovation Award Program, the Searle Scholars Program, the
   Pew Charitable Trust, and the Addario Lung Cancer Foundation. R.C.D.
   acknowledges funding support from the V Foundation for Cancer Research
   and the University of Colorado Lung Cancer SPORE.
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NR 84
TC 133
Z9 154
U1 0
U2 15
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD MAY
PY 2016
VL 22
IS 5
BP 472
EP 478
DI 10.1038/nm.4091
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA DL3DI
UT WOS:000375514000009
PM 27149220
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Zeng, HL
   Wang, W
   Zhang, L
   Lin, ZH
AF Zeng, Huilan
   Wang, Wei
   Zhang, Lin
   Lin, Zhenghong
TI HER3-targeted therapy: the mechanism of drug resistance and the
   development of anticancer drugs
SO CANCER DRUG RESISTANCE
LA English
DT Review
DE HER3; molecular mechanism; drug resistance; targeted therapy; monoclonal
   antibody; molecular target
ID GROWTH-FACTOR-RECEPTOR; ANTI-HER3 MONOCLONAL-ANTIBODY; SQUAMOUS-CELL
   CARCINOMA; INHIBITS TUMOR-GROWTH; BREAST-CANCER CELLS; HEREGULIN-INDUCED
   ACTIVATION; UP-REGULATION; ANTITUMOR-ACTIVITY; COLORECTAL-CANCER;
   DOWN-REGULATION
AB Human epidermal growth factor receptor 3 (HER3), which is part of the HER family, is aberrantly expressed in various human cancers. Since HER3 only has weak tyrosine kinase activity, when HER3 ligand neuregulin 1 (NRG1) or neuregulin 2 (NRG2) appears, activated HER3 contributes to cancer development and drug resistance by forming heterodimers with other receptors, mainly including epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2). Inhibition of HER3 and its downstream signaling, including PI3K/AKT, MEK/MAPK, JAK/STAT, and Src kinase, is believed to be necessary to conquer drug resistance and improve treatment efficiency. Until now, despite multiple anti-HER3 antibodies undergoing preclinical and clinical studies, none of the HER3-targeted therapies are licensed for utilization in clinical cancer treatment because of their safety and efficacy. Therefore, the development of HER3-targeted drugs possessing safety, tolerability, and sensitivity is crucial for clinical cancer treatment. This review summarizes the progress of the mechanism of HER3 in drug resistance, the HER3-targeted therapies that are conducted in preclinical and clinical trials, and some emerging molecules that could be used as future designed drugs for HER3, aiming to provide insights for future research and development of anticancer drugs targeting HER3.
C1 [Zeng, Huilan; Lin, Zhenghong] Chongqing Univ, Sch Life Sci, South Rd 55,Univ Town, Chongqing 401331, Peoples R China.
   [Wang, Wei] Chongqing Univ, Three Gorges Hosp, Dept Canc Ctr, Sch Med, Xincheng Rd 165, Chongqing 404000, Peoples R China.
   [Zhang, Lin] Chongqing Univ, Jiangjin Hosp, Dept Gastroenterol, Dingshan St,Jiangzhou Rd 725, Chongqing 402260, Peoples R China.
C3 Chongqing University; Chongqing University; Chongqing University
RP Lin, ZH (corresponding author), Chongqing Univ, Sch Life Sci, South Rd 55,Univ Town, Chongqing 401331, Peoples R China.; Wang, W (corresponding author), Chongqing Univ, Three Gorges Hosp, Dept Canc Ctr, Sch Med, Xincheng Rd 165, Chongqing 404000, Peoples R China.; Zhang, L (corresponding author), Chongqing Univ, Jiangjin Hosp, Dept Gastroenterol, Dingshan St,Jiangzhou Rd 725, Chongqing 402260, Peoples R China.
EM wangwei929@cqu.edu.cn; brucezhanglin@cqu.edu.cn;
   zhenghonglin@cqu.edu.cdu.cn
FU National Natural Science Foundation of China [82172888]; Project the
   Fundamental Research Funds for the Central Universities
   [2023CDJYGRH-YB07, 2023CDJXY-009]
FX This work was supported by the National Natural Science Foundation of
   China (Grant No. 82172888) and Project the Fundamental Research Funds
   for the Central Universities (Grant No. 2023CDJYGRH-YB07 and Grant No.
   2023CDJXY-009) .
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NR 182
TC 0
Z9 0
U1 4
U2 6
PU OAE PUBLISHING INC
PI ALHAMBRA
PA 245 E MAIN ST, ST122, ALHAMBRA, CA 91801 USA
EI 2578-532X
J9 CANCER DRUG RESIST
JI Cancer Drug Resist.
PY 2024
VL 7
DI 10.20517/cdr.2024.11
PG 22
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA QY3U1
UT WOS:001224398200001
PM 38835349
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, DS
   Wang, Y
   Zhou, FX
AF Zhang, Desheng
   Wang, You
   Zhou, Fuxiang
TI Case report: Resolution of Guillain-Barré syndrome in a patient with
   dual primary tumors after treatment with rituximab
SO FRONTIERS IN NEUROLOGY
LA English
DT Article
DE Guillain-Barre syndrome; immune checkpoint inhibitors; tumor; targeted
   therapy; case report
ID CANCER
AB Guillain-Barre syndrome (GBS) is a rare immune-related adverse event (irAE) that can occur in solid tumors such as hepatocellular carcinoma, gastric cancer, breast cancer, and colorectal cancer. It is characterized by progressive myasthenia and mild sensory abnormalities. The emergence of immune checkpoint inhibitors (ICIs) has significantly improved cancer patients' life expectancy but can also trigger various irAEs, including GBS. We report a rare case of GBS in a 64-year-old male patient with dual primary tumors of the colon and stomach who received toripalimab and chemotherapy for liver metastases. After five treatments, the patient experienced weakness and numbness in his limbs. Lumbar puncture, electromyography, and other tests confirmed the diagnosis of GBS. Intravenous immunoglobulin (IVIG) and methylprednisolone did not improve the patient's symptoms, but rituximab, which is not a standard regimen for GBS, was effective in eliminating B cells and improving symptoms. Following this, we effectively shifted from a regimen combining immunotherapy and chemotherapy to a targeted therapy regimen, resulting in prolonged patient survival. Currently, limited studies have been undertaken to evaluate the efficacy of rituximab in managing refractory neurological adverse events associated with ICI therapy. Using this case, we reviewed similar cases and formed our views.
C1 [Zhang, Desheng; Wang, You; Zhou, Fuxiang] Wuhan Univ, Zhongnan Hosp, Dept Radiat & Med Oncol, Wuhan, Peoples R China.
C3 Wuhan University
RP Wang, Y; Zhou, FX (corresponding author), Wuhan Univ, Zhongnan Hosp, Dept Radiat & Med Oncol, Wuhan, Peoples R China.
EM youwang@whu.edu.cn; happyzhoufx@sina.com
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NR 21
TC 0
Z9 0
U1 2
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-2295
J9 FRONT NEUROL
JI Front. Neurol.
PD FEB 21
PY 2024
VL 15
AR 1348304
DI 10.3389/fneur.2024.1348304
PG 5
WC Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA JW2G8
UT WOS:001176127900001
PM 38450071
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Mazouji, O
   Ouhajjou, A
   Incitti, R
   Mansour, H
AF Mazouji, Omayma
   Ouhajjou, Abdelhak
   Incitti, Roberto
   Mansour, Hicham
TI Updates on Clinical Use of Liquid Biopsy in Colorectal Cancer Screening,
   Diagnosis, Follow-Up, and Treatment Guidance
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE colorectal cancer; liquid biopsy; biomarker; screening; diagnosis;
   prognosis; targeted therapy; circulating tumor DNA
ID CIRCULATING TUMOR-CELLS; ANTI-EGFR THERAPY; FREE DNA; TARGETED THERAPY;
   GENE METHYLATION; NUCLEIC-ACIDS; BIOMARKERS; STOOL; PLASMA; MANAGEMENT
AB Colorectal cancer (CRC) is one of the most common cancers worldwide, being the third most diagnosed in the world and the second deadliest. Solid biopsy provides an essential guide for the clinical management of patients with colorectal cancer; however, this method presents several limitations, in particular invasiveness, and cannot be used repeatedly. Recently, clinical research directed toward the use of liquid biopsy, as an alternative tool to solid biopsy, showed significant promise in several CRC clinical applications, as (1) detect CRC patients at early stage, (2) make treatment decision, (3) monitor treatment response, (4) predict relapses and metastases, (5) unravel tumor heterogeneity, and (6) detect minimal residual disease. The purpose of this short review is to describe the concept, the characteristics, the genetic components, and the technologies used in liquid biopsy in the context of the management of colorectal cancer, and finally we reviewed gene alterations, recently described in the literature, as promising potential biomarkers that may be specifically used in liquid biopsy tests.
C1 [Mazouji, Omayma; Mansour, Hicham] Mohamed First Univ, GES LCM2E, FPN, Oujda, Morocco.
   [Ouhajjou, Abdelhak] Al Azhar Oncol Ctr, Rabat, Morocco.
   [Incitti, Roberto] King Abdullah Univ Sci & Technol KAUST, Computat Biosci Res Ctr CBRC, Thuwal, Saudi Arabia.
C3 Mohammed First University of Oujda; King Abdullah University of Science
   & Technology
RP Mansour, H (corresponding author), Mohamed First Univ, GES LCM2E, FPN, Oujda, Morocco.
EM h.mansour@ump.ac.ma
RI Incitti, Roberto/KIG-7145-2024
OI Incitti, Roberto/0000-0001-6554-8489
FU Cancer Research Institute IRC, Kingdom of Morocco
FX The research funding of the university has supported this work.
   Publication fees supported by the Cancer Research Institute IRC, Kingdom
   of Morocco (www.irc.ma).
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NR 126
TC 35
Z9 35
U1 1
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD MAY 24
PY 2021
VL 9
AR 660924
DI 10.3389/fcell.2021.660924
PG 13
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA SU1YC
UT WOS:000662937000001
PM 34150757
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xue, WH
   Li, XW
   Ding, YQ
   Wu, N
   Pei, BB
   Ma, XY
   Xie, J
   Yang, WH
AF Xue, Wen-Hui
   Li, Xue-Wei
   Ding, Ya-Qian
   Wu, Na
   Pei, Bei-Bei
   Ma, Xiao-Yan
   Xie, Jun
   Yang, Wen-Hui
TI Efficacy and safety of third-line or later-line targeted treatment for
   patients with metastatic colorectal cancer: a meta-analysis
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE efficacy; safety; metastatic colorectal cancer; meta-analysis; targeted
   therapy
ID POSITIVE SOLID TUMORS; PHASE-II; SUPPORTIVE CARE; OPEN-LABEL; PLUS S-1;
   CHEMOTHERAPY; CETUXIMAB; THERAPY; IRINOTECAN; KRAS
AB Targeted therapy has been standardized in front-line therapies for metastatic colorectal cancer (mCRC), while explicit recommendations for third- or later-line are still lacking. This study evaluated the efficacy and safety of combining targeted therapy with chemotherapy in the third- or later-line treatment for mCRC via meta-analysis, providing evidence-based guidance for clinical or research practice. Comprehensive retrieval of related studies was conducted according to the PRISMA guideline. Studies were stratified with patient characteristics and pharmacological classification of the drugs. For the data available for quantitative analysis, pooled overall response rate, disease control rate, hazard ratios (HRs) for overall survival (OS) and progression-free survival (PFS), and adverse events rate with respective 95% confidence intervals (CIs) were calculated. A total of 22 studies (1,866 patients) were included in this meta-analysis. Data from 17 studies (1,769 patients) involving targets of epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) were extracted for meta-analyses. The overall response rates for monotherapy and combined therapy were 4% (95% CI: 3%, 5%) and 20% (95% CI: 11%, 29%). The pooled HRs (combined therapy vs. mono) for OS and PFS were 0.72 (95% CI: 0.53, 0.99) and 0.34 (95% CI: 0.26, 0.45). Another five studies were included in narrative depiction, involving targets of BRAF, HER-2, ROS1, and NTRK. The findings of this meta-analysis indicate that VEGF and EGFR inhibitors manifest promising clinical response rates and prolonged survival in the treatment of mCRC with acceptable adverse events.
C1 [Xue, Wen-Hui; Ding, Ya-Qian; Wu, Na; Pei, Bei-Bei; Ma, Xiao-Yan] Third Hosp Shanxi Med Univ, Shanxi Bethune Hosp, Tongji Shanxi Hosp, Shanxi Acad Med Sci,Dept Digest Oncol,Canc Ctr, Taiyuan, Shanxi, Peoples R China.
   [Li, Xue-Wei; Xie, Jun] Shanxi Med Univ, Dept Biochem & Mol Biol, Shanxi Key Lab Birth Defect & Cell Regenerat, Taiyuan, Shanxi, Peoples R China.
   [Yang, Wen-Hui] Shanxi Med Univ, Shanxi Prov Canc Hosp, Shanxi Hosp, Canc Hosp,Dept Gastroenterol,Chinese Acad Med Sci, Taiyuan, Shanxi, Peoples R China.
C3 Shanxi Medical University; Shanxi Medical University; Shanxi Medical
   University; Chinese Academy of Medical Sciences - Peking Union Medical
   College
RP Xie, J (corresponding author), Shanxi Med Univ, Dept Biochem & Mol Biol, Shanxi Key Lab Birth Defect & Cell Regenerat, Taiyuan, Shanxi, Peoples R China.; Yang, WH (corresponding author), Shanxi Med Univ, Shanxi Prov Canc Hosp, Shanxi Hosp, Canc Hosp,Dept Gastroenterol,Chinese Acad Med Sci, Taiyuan, Shanxi, Peoples R China.
EM junxie@sxmu.edu.cn; yangwenhui-10012@163.com
RI Ding, Yaqian/GVS-4870-2022; Yang, Wenhui/K-4599-2019
FU National Natural Science Foundation of China [82002619]; Key Medical
   Research Projects of Shanxi Province [2020XM55]; Talent introduction
   scientific research start-up fund of Shanxi Bethune Hospital [2020RC006]
FX Funding This work was supported by grants from the National Natural
   Science Foundation of China (No. 82002619), Key Medical Research
   Projects of Shanxi Province (No. 2020XM55), Talent introduction
   scientific research start-up fund of Shanxi Bethune Hospital (No.
   2020RC006).
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NR 49
TC 1
Z9 1
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 MAY 31
PY 2023
VL 13
AR 1165040
DI 10.3389/fonc.2023.1165040
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA I7GI1
UT WOS:001004429200001
PM 37324019
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Bashir, Z
   Ullah, B
   Jan, Z
   Ahmad, SU
   Khan, N
   Bashir, Z
   Zafar, I
   Sajjad, W
AF Bashir, Zainab
   Ullah, Basir
   Jan, Zainab
   Ahmad, Syed Umair
   Khan, Nayab
   Bashir, Zohaib
   Zafar, Imran
   Sajjad, Waseem
TI <i>In-silico</i> Studies of BRAF Signalling Network Expression in
   Colorectal Cancer; A systematic approach for multi-targeted therapy
SO BIOSCIENCE RESEARCH
LA English
DT Article
DE PPI network; Pathways analysis; BRAF; tumor; interactors; multi-target
ID RAS MUTATIONS; ONCOGENE; STAGE
AB Colorectal cancer is among third leading cause of death worldwide comprising the third most predominant cancer occurring in men and the second most predominant cancer occurring in women. Several genetic alterations and mutations in the cell pathway are the leading cause of the cancer. One such pathway is the MAPK pathway that is crucial for cell proliferation, differentiation, migration, survival, and angiogenesis. Alteration in this pathway leads to activation of the pathway hence in progression of tumors which is due to activating mutations in RAF and RAS. The BRAF oncogenic mutations in colorectal cancer, although occurring very rare up to 18%, shows no successful response hence shows poor prognosis. To understand the mechanism deeply, we analyse BRAF signalling network and analyse its interactions. Aims of the current study is to better understand the whole mechanism at gene network level to identify multiple targets for the cure of the respective cancer. We retrieved the BRAF signalling network, which consist of 65 nodes and 116 edges, followed by enrichment analysis. To identify the mutations and alterations at cancer level, Cbioportal was used which gives complete data about the alterations each gene have in the network contributing to the colorectal cancer. Statistical analysis was performed using cluster profiler platform to construct enrich map and bar plot to represent p values. We found that out of all the interactors of the network, many genetic alterations including amplification and mutations were observed in several genes of the network besides the main gene BRAF, which includes KRAS, EGFR, RAF1, ARAF and AKT1 suggesting a multi-target approach to the development of multi-targeted therapy in future for drug development.
C1 [Bashir, Zainab; Jan, Zainab; Ahmad, Syed Umair; Bashir, Zohaib] Hazara Univ Mansehra, Dept Bioinformat, Mansehra, Pakistan.
   [Ullah, Basir] Ayub Med Coll Abbottabad, Abbottabad, Pakistan.
   [Khan, Nayab] Univ Balochistan, Dept Zool, Quetta, Pakistan.
   [Zafar, Imran] Virtual Univ Pakistan, Dept Bioinformat & Computat Biol, Karachi, Pakistan.
   [Sajjad, Waseem] Hazara Univ Mansehra, Dept Biotechnol & Genet Engn, Mansehra, Pakistan.
C3 Hazara University; University of Balochistan; Virtual University of
   Pakistan; Hazara University
RP Bashir, Z; Ahmad, SU (corresponding author), Hazara Univ Mansehra, Dept Bioinformat, Mansehra, Pakistan.
EM zaini.khan552@gmail.com; ahmadumair927@gmail.com
RI Sajjad, Waseem/KFQ-2034-2024
CR Ahmad S.U., 2020, PURE APPL BIOL PAB, V9, P1583
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NR 23
TC 3
Z9 3
U1 0
U2 2
PU INNOVATIVE SCIENTIFIC INFORMATION & SERVICES NETWORK
PI FAISALABAD
PA INNOVATIVE SCIENTIFIC INFORMATION & SERVICES NETWORK, FAISALABAD, 00000,
   PAKISTAN
SN 1811-9506
EI 2218-3973
J9 BIOSCI RES
JI Biosci. Res.
PD JAN-MAR
PY 2021
VL 18
IS 1
BP 1015
EP 1023
PG 9
WC Biology
WE Emerging Sources Citation Index (ESCI)
SC Life Sciences & Biomedicine - Other Topics
GA SI5DC
UT WOS:000654843800102
DA 2025-01-04
ER

PT J
AU Tantoy, IY
   Cooper, BA
   Dhruva, A
   Cataldo, J
   Paul, SM
   Conley, YP
   Hammer, M
   Kober, KM
   Levine, JD
   Miaskowski, C
AF Tantoy, Ilufredo Y.
   Cooper, Bruce A.
   Dhruva, Anand
   Cataldo, Janine
   Paul, Steven M.
   Conley, Yvette P.
   Hammer, Marilyn
   Kober, Kord M.
   Levine, Jon D.
   Miaskowski, Christine
TI Quality of life of patients with gastrointestinal cancers undergoing
   chemotherapy
SO QUALITY OF LIFE RESEARCH
LA English
DT Article
DE Gastrointestinal cancer; Quality of life; Chemotherapy; Targeted therapy
ID METASTATIC COLORECTAL-CANCER; FORM HEALTH SURVEY; PHASE-III TRIAL;
   COLON-CANCER; MISSING-DATA; RECEIVING CHEMOTHERAPY;
   CONFIDENCE-INTERVALS; EVENING FATIGUE; GASTRIC-CANCER; BREAST-CANCER
AB Findings regarding changes in the quality of life (QOL) of patients with gastrointestinal cancers (GI) undergoing chemotherapy (CTX) are inconclusive. Purpose was to evaluate for changes in QOL scores of patients with GI cancers over two cycles of CTX.
   Patients (n = 397) completed disease-specific [i.e., Quality of Life-Scale-Patient Version (QOL-PV)] and generic [12-item Medical Outcomes Study Short Form Survey (SF-12)] measures of QOL a total of six times over two cycles of CTX. Changes in these QOL scores were evaluated using bootstrapped multilevel regression with full information maximum likelihood estimation. Treatment group (i.e., with or without targeted therapy), age, number of metastatic sites, time from cancer diagnosis, number of prior cancer treatments, GI cancer diagnosis (i.e., colon/rectum/anal vs. other), and CTX regimen were evaluated as covariates in the conditional models for each of the QOL scores.
   During the second cycle of CTX, QOL-PV scores decreased in the week following CTX administration, and then increased the following week. For both cycles of CTX, the physical component summary and mental component summary scores of the SF-12 decreased in the week following CTX administration and then increased the following week. Increased time from cancer diagnosis and a higher number of prior cancer treatments resulted in worse QOL-PV and SF-12 scores at enrollment.
   While changes in QOL scores over the two CTX cycles were statistically significant, the differences were not clinically meaningful. Future studies need to determine the optimal timing of QOL assessments to assess changes associated with cancer treatments.
C1 [Tantoy, Ilufredo Y.; Cooper, Bruce A.; Cataldo, Janine; Paul, Steven M.; Kober, Kord M.; Miaskowski, Christine] Univ Calif San Francisco, Sch Nursing, San Francisco, CA 94143 USA.
   [Dhruva, Anand; Levine, Jon D.] Univ Calif San Francisco, Sch Med, San Francisco, CA USA.
   [Conley, Yvette P.] Univ Pittsburgh, Sch Nursing, Pittsburgh, PA 15261 USA.
   [Hammer, Marilyn] Mt Sinai Hosp, Dept Nursing, New York, NY 10029 USA.
   [Miaskowski, Christine] Univ Calif San Francisco, Dept Physiol Nursing, 2 Koret Way,N631F, San Francisco, CA 94143 USA.
C3 University of California System; University of California San Francisco;
   University of California System; University of California San Francisco;
   Pennsylvania Commonwealth System of Higher Education (PCSHE); University
   of Pittsburgh; Icahn School of Medicine at Mount Sinai; University of
   California System; University of California San Francisco
RP Miaskowski, C (corresponding author), Univ Calif San Francisco, Sch Nursing, San Francisco, CA 94143 USA.; Miaskowski, C (corresponding author), Univ Calif San Francisco, Dept Physiol Nursing, 2 Koret Way,N631F, San Francisco, CA 94143 USA.
EM chris.miaskowski@ucsf.edu
RI Kober, Kord/ABF-2657-2020; Paul, Steve/ABE-5400-2020
OI Kober, Kord/0000-0001-9732-3321; Levine, Jon/0000-0003-0681-5545;
   Tantoy, Ilufredo/0000-0002-0193-0280; Conley, Yvette/0000-0002-1784-6067
FU National Cancer Institute (NCI) [CA134900]; NCI [CA168960]; National
   Institutes of Health (NIH) [NR007088]
FX This study was funded by a grant from the National Cancer Institute
   (NCI, CA134900). Dr. Christine Miaskowski is an American Cancer Society
   Clinical Research Professor and is funded by a K05 award from the NCI
   (CA168960). Mr. Tantoy was funded by a National Institutes of Health
   (NIH) T32 Grant (NR007088).
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NR 73
TC 16
Z9 17
U1 1
U2 12
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0962-9343
EI 1573-2649
J9 QUAL LIFE RES
JI Qual. Life Res.
PD JUL
PY 2018
VL 27
IS 7
BP 1865
EP 1876
DI 10.1007/s11136-018-1860-1
PG 12
WC Health Care Sciences & Services; Health Policy & Services; Public,
   Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Health Care Sciences & Services; Public, Environmental & Occupational
   Health
GA GJ2UK
UT WOS:000435128700018
PM 29679368
OA Green Accepted, Green Published
DA 2025-01-04
ER

PT J
AU Ma, J
   Liu, XH
   Chen, H
   Abbas, MK
   Yang, L
   Sun, HM
   Sun, TY
   Wu, B
   Yang, S
   Zhou, DS
AF Ma, Jian
   Liu, Xiaohui
   Chen, Hong
   Abbas, Muhammad Khawar
   Yang, Liu
   Sun, Haimei
   Sun, Tingyi
   Wu, Bo
   Yang, Shu
   Zhou, Deshan
TI c-KIT-ERK1/2 signaling activated ELK1 and upregulated carcinoembryonic
   antigen expression to promote colorectal cancer progression
SO CANCER SCIENCE
LA English
DT Article
DE CEA; c&#8208; KIT; colorectal cancer; ELK1; targeted therapy
ID CARCINOMA; GROWTH; GENE; IDENTIFICATION; TUMORIGENESIS; ADHESION;
   INVASION; ELEMENTS; SERVER; CELLS
AB Carcinoembryonic antigen (CEA) is highly expressed in embryo and colorectal cancer (CRC) and has been widely used as a marker for CRC. Emerging evidence has demonstrated that elevated CEA levels promote CRC progression. However, the mechanism of the increased CEA expression in patients with primary and recurrent CRC is still an open question. In this study, we showed that c-KIT, ELK1, and CEA were hyperexpressed in patients with CRC, especially patients with recurrent disease. From bioinformatics analysis, we picked ELK1 as a candidate transcription factor (TF) for CEA; the binding site of ELK1 within the CEA promoter was confirmed by chromatin immunoprecipitation and dual luciferase reporter assays. Overexpression of ELK1 increased CEA expression in vitro, while knockdown of ELK1 decreased CEA. Upregulated ELK1 promoted the adhesion, migration, and invasion of CRC cells, however knockdown of CEA blocked the activities of ELK1-overexpressed CRC cells. Furthermore, we explored the role of c-KIT-ERK1/2 signaling in activation of ELK1. Blocking c-KIT signaling using Imatinib or ISCK03 reduced p-ELK1 expression and consequently decreased CEA levels in CRC cells, as did blocking the ERK1/2 pathway by U0126. Compared with wild type littermates, the c-kit loss-of-functional Wads(m/m) mice showed lowered c-KIT, ELK1, and CEA expression. In conclusion, our study revealed that ELK1, which was activated by c-KIT-ERK1/2 signaling, was a key TF for CEA expression. Blocking ELK1 or its upstream signaling could be an alternative way to decelerate CRC progression. Besides being a biomarker for CRC, CEA could be used for guiding targeted therapy.
C1 [Ma, Jian; Liu, Xiaohui; Chen, Hong; Abbas, Muhammad Khawar; Yang, Liu; Sun, Haimei; Sun, Tingyi; Wu, Bo; Yang, Shu; Zhou, Deshan] Capital Med Univ, Sch Basic Med Sci, Dept Histol & Embryol, Beijing 100069, Peoples R China.
   [Ma, Jian; Liu, Xiaohui; Chen, Hong; Abbas, Muhammad Khawar; Yang, Liu; Sun, Haimei; Sun, Tingyi; Wu, Bo; Yang, Shu; Zhou, Deshan] Beijing Key Lab Canc Invas & Metastasis Res, Beijing, Peoples R China.
   [Wu, Bo; Yang, Shu; Zhou, Deshan] Capital Med Univ, Canc Inst, Beijing, Peoples R China.
C3 Capital Medical University; Capital Medical University
RP Yang, S; Zhou, DS (corresponding author), Capital Med Univ, Sch Basic Med Sci, Dept Histol & Embryol, Beijing 100069, Peoples R China.
EM yangshu@ccmu.edu.cn; zhouds08@ccmu.edu.cn
RI Abbas, Muhammad Khawar/GXW-0848-2022
OI , Liu/0009-0008-9410-2716; Ma, Jian/0000-0001-6921-5278; Abbas, Muhammad
   Khawar/0000-0001-7804-0748
FU Beijing Natural Science Foundation [5172008, 7172021]; Natural Science
   Foundation of Capital Medical University [PYZ19069]; Support Project of
   High-level Teachers in Beijing Municipal Universities in the Period of
   13th Five-year plan [IDHT20170516]; National Natural Science Foundation
   of China [31771332, 81572322]
FX Beijing Natural Science Foundation, Grant/Award Number: 5172008 and
   7172021; Natural Science Foundation of Capital Medical University,
   Grant/Award Number: PYZ19069; Support Project of High-level Teachers in
   Beijing Municipal Universities in the Period of 13th Five-year plan,
   Grant/Award Number: IDHT20170516; National Natural Science Foundation of
   China, Grant/Award Number: 31771332 and 81572322
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NR 41
TC 17
Z9 18
U1 0
U2 14
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 FEB
PY 2021
VL 112
IS 2
BP 655
EP 667
DI 10.1111/cas.14750
EA DEC 2020
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QK0RJ
UT WOS:000600053800001
PM 33247506
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Palma, S
   Zwenger, AO
   Croce, MV
   Abba, MC
   Lacunza, E
AF Palma, Sabina
   Zwenger, Ariel O.
   Croce, Maria V.
   abba, Martin C.
   Lacunza, Ezequiel
TI From Molecular Biology to Clinical Trials: Toward Personalized
   Colorectal Cancer Therapy
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE Clinical trials; Colorectal cancer; Genomic alterations; Signaling
   pathways; Targeted therapy
ID RECEPTOR MONOCLONAL-ANTIBODY; ENDOTHELIAL GROWTH-FACTOR; PHASE-III
   TRIAL; ACQUIRED-RESISTANCE; 1ST-LINE TREATMENT; PLUS BEVACIZUMAB;
   COLON-CANCER; KRAS STATUS; CETUXIMAB; EXPRESSION
AB During the past years, molecular studies through high-throughput technologies have led to the confirmation of critical alterations in colorectal cancer (CRC) and the discovery of some new ones, including mutations, DNA methylations, and structural chromosomal changes. These genomic alterations might act in concert to dysregulate specific signaling pathways that normally exert their functions on critical cell phenotypes, including the regulation of cellular metabolism, proliferation, differentiation, and survival. Targeted therapy against key components of altered signaling pathways has allowed an improvement in CRC treatment. However, a significant percentage of patients with CRC and metastatic CRC will not benefit from these targeted therapies and will be restricted to systemic chemotherapy. Mechanisms of resistance have been associated with specific gene alterations. To fully understand the nature and significance of the genetic and epigenetic defects in CRC that might favor a tumor evading a given therapy, much work remains. Therefore, a dynamic link between basic molecular research and preclinical studies, which ultimately constitute the prelude to standardized therapies, is very important to provide better and more effective treatments against CRC. We present an updated revision of the main molecular features of CRC and their associated therapies currently under study in clinical trials. Moreover, we performed an unsupervised classification of CRC clinical trials with the aim of obtaining an overview of the future perspectives of preclinical studies.
C1 [Palma, Sabina; Croce, Maria V.; abba, Martin C.; Lacunza, Ezequiel] Univ Nacl La Plata, Fac Ciencias Med, CINIBA, 60 & 120 SN, RA-1900 La Plata, Buenos Aires, Argentina.
   [Zwenger, Ariel O.] Hosp Prov Neuquen, Serv Oncol, Neuquen, Australia.
C3 National University of La Plata
RP Lacunza, E (corresponding author), Univ Nacl La Plata, Fac Ciencias Med, CINIBA, 60 & 120 SN, RA-1900 La Plata, Buenos Aires, Argentina.
EM ezequiellacunza@hotmail.com
RI Croce, Maria Virginia/GXZ-5151-2022
OI Lacunza, Ezequiel/0000-0002-6731-9820; Abba, Martin/0000-0002-9206-2369;
   Palma, Sabina/0000-0003-3212-4465
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NR 102
TC 19
Z9 21
U1 0
U2 13
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD JUN
PY 2016
VL 15
IS 2
BP 104
EP 115
DI 10.1016/j.clcc.2015.11.001
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DN9NR
UT WOS:000377407000011
PM 26777471
OA Green Published
DA 2025-01-04
ER

PT J
AU Elbadawy, M
   Usui, T
   Yamawaki, H
   Sasaki, K
AF Elbadawy, Mohamed
   Usui, Tatsuya
   Yamawaki, Hideyuki
   Sasaki, Kazuaki
TI Development of an Experimental Model for Analyzing Drug Resistance in
   Colorectal Cancer
SO CANCERS
LA English
DT Review
DE 3D cell culture; colorectal cancer; drug resistance; cancer stem cells
ID RESEARCH-AND-DEVELOPMENT; STEM-CELL NICHE; GROWTH-FACTOR; HUMAN COLON;
   TARGETED THERAPY; CHEMOTHERAPY; PRODUCTIVITY; STATISTICS; MECHANISMS;
   CETUXIMAB
AB Colorectal cancer (CRC) is one of the most common cancers, for which combination treatment of chemotherapy is employed. However, most patients develop drug resistance during the course of treatment. To clarify the mechanisms of drug resistance, various research models have been developed. Recently, we established a human CRC patients-derived three-dimensional (3D) culture system using an air-liquid interface organoid method. It contained numerous cancer stem cells and showed resistance to 5-fluorouracil and Irinotecan. In this review, we introduce conventional and our established models for studying drug resistance in CRC.
C1 [Elbadawy, Mohamed; Usui, Tatsuya; Sasaki, Kazuaki] Tokyo Univ Agr & Technol, Fac Agr, Dept Vet Med, Lab Vet Pharmacol, 3-5-8 Saiwai Cho, Fuchu, Tokyo 1838509, Japan.
   [Elbadawy, Mohamed] Benha Univ, Fac Vet Med, Dept Pharmacol, Toukh 13736, Elqaliobiya, Egypt.
   [Yamawaki, Hideyuki] Kitasato Univ, Sch Vet Med, Lab Vet Pharmacol, Towada, Aomori 0348628, Japan.
C3 Tokyo University of Agriculture & Technology; Egyptian Knowledge Bank
   (EKB); Benha University; Kitasato University
RP Usui, T (corresponding author), Tokyo Univ Agr & Technol, Fac Agr, Dept Vet Med, Lab Vet Pharmacol, 3-5-8 Saiwai Cho, Fuchu, Tokyo 1838509, Japan.
EM mohamed.elbadawy@fvtm.bu.edu.eg; fu7085@go.tuat.ac.jp;
   yamawaki@vmas.kitasato-u.ac.jp; skazuaki@cc.tuat.ac.jp
RI Usui, Tatsuya/Q-5170-2017; SASAKI, Kazuaki/G-1148-2013; Elbadawy,
   Mohamed/G-8841-2019
OI Elbadawy, Mohamed/0000-0001-9368-1535
FU Japan Society for the Promotion of Science [17K15370]; Grants-in-Aid for
   Scientific Research [17K15370] Funding Source: KAKEN
FX This study was supported in part by a Grant for Scientific Research from
   the Japan Society for the Promotion of Science (17K15370 TU).
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Z9 25
U1 1
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PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
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AR 164
DI 10.3390/cancers10060164
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WE Science Citation Index Expanded (SCI-EXPANDED)
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GA GK4KQ
UT WOS:000436128700011
PM 29843359
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Wang, WQ
   Jiang, KP
   Liu, X
   Li, J
   Zhou, WS
   Wang, C
   Cui, JW
   Liang, TT
AF Wang, Wanqing
   Jiang, Kaipeng
   Liu, Xue
   Li, Ju
   Zhou, Wenshuo
   Wang, Chang
   Cui, Jiuwei
   Liang, Tingting
TI FBXW7 and human tumors: mechanisms of drug resistance and potential
   therapeutic strategies
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE Fbxw7; human tumors; drug resistance; targeted therapy;
   ubiquitin-proteasome system (UPS)
ID F-BOX PROTEINS; EPITHELIAL-MESENCHYMAL TRANSITION; ACUTE
   LYMPHOBLASTIC-LEUKEMIA; CANCER STEM-CELLS; UBIQUITIN LIGASE;
   COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA; BREAST-CANCER; CYCLIN-E;
   C-MYC
AB Drug therapy, including chemotherapy, targeted therapy, immunotherapy, and endocrine therapy, stands as the foremost therapeutic approach for contemporary human malignancies. However, increasing drug resistance during antineoplastic therapy has become a substantial barrier to favorable outcomes in cancer patients. To enhance the effectiveness of different cancer therapies, an in-depth understanding of the unique mechanisms underlying tumor drug resistance and the subsequent surmounting of antitumor drug resistance is required. Recently, F-box and WD Repeat Domain-containing-7 (FBXW7), a recognized tumor suppressor, has been found to be highly associated with tumor therapy resistance. This review provides a comprehensive summary of the underlying mechanisms through which FBXW7 facilitates the development of drug resistance in cancer. Additionally, this review elucidates the role of FBXW7 in therapeutic resistance of various types of human tumors. The strategies and challenges implicated in overcoming tumor therapy resistance by targeting FBXW7 are also discussed.
C1 [Wang, Wanqing; Jiang, Kaipeng; Liu, Xue; Li, Ju; Zhou, Wenshuo; Wang, Chang; Cui, Jiuwei; Liang, Tingting] First Hosp Jilin Univ, Canc Ctr, Changchun, Jilin, Peoples R China.
C3 Jilin University
RP Liang, TT (corresponding author), First Hosp Jilin Univ, Canc Ctr, Changchun, Jilin, Peoples R China.
EM liangtt@jlu.edu.cn
RI li, tao/JVO-9006-2024
FU Jilin Provincial Education Department [3D5196778428]; Jilin Provincial
   Finance Department [3D5214495428]; First Hospital of Jilin University
FX The authors declare that the financial support was received for the
   research, authorship, and/or publication of this article. This study was
   funded by Jilin Provincial Education Department (Ref: 3D5196778428), and
   Jilin Provincial Finance Department (Ref: 3D5214495428). This work was
   supported from the First Hospital of Jilin University.
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NR 192
TC 4
Z9 4
U1 5
U2 11
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 NOV 13
PY 2023
VL 14
AR 1278056
DI 10.3389/fphar.2023.1278056
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA Y8AT6
UT WOS:001107438300001
PM 38027013
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Gluck, WL
   Martin, JC
   Edenfield, WJ
   Chung, KY
   Arguello, D
AF Gluck, W. Larry
   Martin, Julie C.
   Edenfield, W. Jeffrey
   Chung, Ki Y.
   Arguello, David
TI Prolonged response of widely metastatic HER2-positive colon cancer to
   trastuzumab therapy
SO COLORECTAL CANCER
LA English
DT Article
DE colon cancer; ERBB2; HER2; precision medicine; trastuzumab
ID COLORECTAL-CANCER; HER2; EXPRESSION
AB Emerging evidence suggests a small subset of late-stage colon cancer driven by HER2, a biomarker routinely evaluated in select breast and gastric cancers, may respond to HER2-targeted therapy. Herein, we describe a 49-year-old male with widely metastatic colon cancer originating in the sigmoid colon. After failing standard therapy, a biopsy specimen of the tumor was evaluated for novel biomarkers using molecular profiling. After identification of ERBB2 (HER2) amplification using in situ hybridization, the patient subsequently received a trial of trastuzumab monotherapy and experienced a dramatic and durable response. This report builds on our understanding of using precision oncology to improve survival in metastatic colon cancer.
C1 [Gluck, W. Larry; Martin, Julie C.; Edenfield, W. Jeffrey; Chung, Ki Y.] Greenville Hlth Syst, Inst Translat Oncol Res, Greenville, SC USA.
   [Arguello, David] Caris Life Sci, Phoenix, AZ 85040 USA.
C3 Greenville Health System
RP Arguello, D (corresponding author), Caris Life Sci, Phoenix, AZ 85040 USA.
EM darguello@carisls.com
RI Martin, Julie/KIK-5402-2024
OI Martin, Julie/0000-0003-1829-4994
CR [Anonymous], IJBMS
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NR 18
TC 2
Z9 2
U1 0
U2 2
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1758-194X
EI 1758-1958
J9 COLORECTAL CANCER
JI Colorectal Cancer
PD NOV
PY 2017
VL 6
IS 2
BP 57
EP 61
DI 10.2217/crc-2017-0006
PG 5
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA FQ7NA
UT WOS:000418548100003
OA hybrid
DA 2025-01-04
ER

PT J
AU Chen, GL
   Yang, ZH
   Eshleman, JR
   Netto, GJ
   Lin, MT
AF Chen, Guoli
   Yang, Zhaohai
   Eshleman, James R.
   Netto, George J.
   Lin, Ming-Tseh
TI Molecular Diagnostics for Precision Medicine in Colorectal Cancer:
   Current Status and Future Perspective
SO BIOMED RESEARCH INTERNATIONAL
LA English
DT Review
ID GROWTH-FACTOR RECEPTOR; ANTI-EGFR THERAPY; OF-AMERICAN-PATHOLOGISTS;
   CELL LUNG-CANCER; CLINICAL MUTATION DETECTION; MISMATCH REPAIR STATUS;
   BRAF V600E MUTATION; DEATH-LIGAND 1; MICROSATELLITE-INSTABILITY; KINASE
   INHIBITORS
AB Precision medicine, a concept that has recently emerged and has been widely discussed, emphasizes tailoring medical care to individuals largely based on information acquired from molecular diagnostic testing. As a vital aspect of precision cancer medicine, targeted therapy has been proven to be efficacious and less toxic for cancer treatment. Colorectal cancer (CRC) is one of the most common cancers and among the leading causes for cancer related deaths in the United States and worldwide. By far, CRC has been one of the most successful examples in the field of precision cancer medicine, applying molecular tests to guide targeted therapy. In this review, we summarize the current guidelines for anti-EGFR therapy, revisit the roles of pathologists in an era of precision cancer medicine, demonstrate the transition from traditional "one test-one drug" assays to multiplex assays, especially by using next-generation sequencing platforms in the clinical diagnostic laboratories, and discuss the future perspectives of tumor heterogeneity associated with anti-EGFR resistance and immune checkpoint blockage therapy in CRC.
C1 [Chen, Guoli; Yang, Zhaohai] Milton S Hershey Med Ctr, Penn State Coll Med, Dept Pathol, Hershey, PA USA.
   [Eshleman, James R.; Netto, George J.; Lin, Ming-Tseh] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE);
   Pennsylvania State University; Penn State Health; Johns Hopkins
   University
RP Lin, MT (corresponding author), Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
EM mlin36@jhmi.edu
RI Chen, Guoli/B-3624-2010; Zhang, Hongyang/IAR-1565-2023
OI Netto, George/0000-0003-3915-9134; Chen, Guoli/0000-0002-4426-6156
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NR 140
TC 19
Z9 22
U1 0
U2 1
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2314-6133
EI 2314-6141
J9 BIOMED RES INT-UK
JI Biomed Res. Int.
PY 2016
VL 2016
AR 9850690
DI 10.1155/2016/9850690
PG 12
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA DW3AJ
UT WOS:000383513900001
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Su, M
   Zhan, L
   Zhang, Y
   Zhang, JD
AF Su, Meng
   Zhan, Lei
   Zhang, Yong
   Zhang, Jingdong
TI Yes-activated protein promotes primary resistance of <i>BRAF</i> V600E
   mutant metastatic colorectal cancer cells to mitogen-activated protein
   kinase pathway inhibitors
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer (CRC); BRAF V600E mutation; yes-activated protein;
   mitogen-activated protein kinase pathway (MAPK pathway)
ID COLON-CANCER; YAP; CDK4/6; SGK1; RAF; MEK; APOPTOSIS; MELANOMA;
   STRATEGY; GROWTH
AB Background: Most colorectal cancer (CRC) patients with the BRAF V600E mutation display resistance to chemotherapy and targeted medicinal treatments. Thus, exploring new drugs and drug resistance mechanisms for the BRAF V600E mutation has become an urgent clinical priority.
   Methods: MTS experiment, cell cloning experiment, cell scratching experiment, Transwell experiment, chromatin immunoprecipitation (ChIP), quantitative polymerase chain reaction (qPCR) and flow cytometry are used. Detect the transcription and protein expression of YAP in colorectal cancer cell lines, establish a transient cell line with YAP gene overexpression and knockdown, and detect the effect of YAP gene expression on the biological functions of colorectal cancer cells RKO and HT-29. And further study the mechanism of YAP regulating the response of RAF and MEK targeted therapy.
   Results: In this study, for the first time, we verified that the expression of transcription factor yes-associated protein (YAP) was upregulated in BRAF V600E mutant CRC cells. After knocking down YAP, we observed a reduction in the growth rate, proliferation, and invasion ability of colon cancer cells. We further verified that YAP knockdown increased sensitivity of BRAF V600E mutant CRC cells to mitogen-activated protein kinase (MAPK) pathway inhibitors. In addition, we clarified the mechanism underlying YAP regulation of RAF and MAPK/extracellular signal- regulated kinase (MEK)-targeted therapy response: YAP cooperates with RAF -> MEK pathway inhibitors to regulate the cell cycle, increase cell G1/S phase arrest, and increase apoptosis.
   Conclusions: These results suggest that YAP expression may be related to the primary resistance of MAPK inhibitors in metastatic CRC with the BRAF V600E mutation. Therefore, the combination of YAP and MAPK pathway inhibitors in BRAF V600E mutant metastatic CRC may present a promising treatment method.
C1 [Su, Meng; Zhan, Lei; Zhang, Jingdong] China Med Univ, Liaoning Canc Hosp & Inst, Med Oncol Dept Gastrointestinal Canc, Canc Hosp, Shenyang, Peoples R China.
   [Zhang, Yong] China Med Univ, Liaoning Canc Hosp & Inst, Dept Pathol, Canc Hosp, Shenyang, Peoples R China.
C3 China Medical University; China Medical University
RP Zhang, JD (corresponding author), 44 Xiaoheyan Rd, Shenyang 110042, Peoples R China.
EM jdzhang@cancerhosp-ln-cmu.com
RI Zhang, Ran/HTT-1545-2023
OI Su, Meng/0009-0007-9511-1051
FU Science and Technology Planning Project of Shenyang [191124086,
   191124088]; Science and Technology Planning Project of Liaoning Province
   of China [20180530092]; National Key R&D Program of China
   [2018YFC1311600]; Scientific research foundation for the introduction of
   talents, Liaoning Cancer Hospital Institute [Z1702]
FX This study was supported by grants from the Science and Technology
   Planning Project of Shenyang (No. 191124088); Science and Technology
   Planning Project of Liaoning Province of China (No. 20180530092);
   National Key R&D Program of China (Grant #2018YFC1311600); Scientific
   research foundation for the introduction of talents, Liaoning Cancer
   Hospital & Institute (No. Z1702); and Science and Technology Planning
   Project of Shenyang (No. 191124086).
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NR 38
TC 7
Z9 7
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 JUN
PY 2021
VL 12
IS 3
BP 953
EP 963
DI 10.21037/jgo-21-258
PG 11
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA UN4ZL
UT WOS:000694025100005
PM 34295548
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xu, WT
   Yang, Z
   Lu, NH
AF Xu, Wenting
   Yang, Zhen
   Lu, Nonghua
TI Molecular targeted therapy for the treatment of gastric cancer
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Review
DE Molecular targeted therapy; Gastric cancer; Monoclonal antibody;
   Tyrosine kinase inhibitor
ID PHASE-II TRIAL; METASTATIC COLORECTAL-CANCER; GROWTH-FACTOR RECEPTORS;
   GASTROESOPHAGEAL JUNCTION; DOUBLE-BLIND; OPEN-LABEL; 1ST-LINE TREATMENT;
   ESOPHAGOGASTRIC CANCER; 2ND-LINE TREATMENT; MAMMALIAN TARGET
AB Despite the global decline in the incidence and mortality of gastric cancer, it remains one of the most common malignant tumors of the digestive system. Although surgical resection is the preferred treatment for gastric cancer, chemotherapy is the preferred treatment for recurrent and advanced gastric cancer patients who are not candidates for reoperation. The short overall survival and lack of a standard chemotherapy regimen make it important to identify novel treatment modalities for gastric cancer. Within the field of tumor biology, molecular targeted therapy has attracted substantial attention to improve the specificity of anti-cancer efficacy and significantly reduce non-selective resistance and toxicity. Multiple clinical studies have confirmed that molecular targeted therapy acts on various mechanisms of gastric cancer, such as the regulation of epidermal growth factor, angiogenesis, immuno-checkpoint blockade, the cell cycle, cell apoptosis, key enzymes, c-Met, mTOR signaling and insulin-like growth factor receptors, to exert a stronger anti-tumor effect. An in-depth understanding of the mechanisms that underlie molecular targeted therapies will provide new insights into gastric cancer treatment.
C1 [Xu, Wenting; Yang, Zhen; Lu, Nonghua] Nanchang Univ, Affiliated Hosp 1, Dept Gastroenterol, Nanchang 330006, Jiangxi, Peoples R China.
C3 Nanchang University
RP Yang, Z (corresponding author), Nanchang Univ, Affiliated Hosp 1, Dept Gastroenterol, Nanchang 330006, Jiangxi, Peoples R China.
EM zyang@ncu.edu.cn; lunonghua@ncu.edu.cn
FU National Natural Science Foundation of China [81460377]; Natural Science
   Foundation of Jiangxi Province, China [20142BAB215036, 20151BAB205041];
   Science and Technology Foundation of Department of Education of Jiangxi
   Province, China [GJJ14169]; Graduate Student Innovation Foundation of
   Jiangxi Province, China [YC2015-B021]; National Science and Technology
   Major Projects program for "Major New Drugs Innovation and Development"
   of China [2011ZX09302-007-03]; "Talent 555 Project" of Jiangxi Province,
   China
FX This work was supported in part by grants from the National Natural
   Science Foundation of China (81460377), the Natural Science Foundation
   of Jiangxi Province, China (20142BAB215036 and 20151BAB205041), the
   Science and Technology Foundation of Department of Education of Jiangxi
   Province, China (GJJ14169), the Graduate Student Innovation Foundation
   of Jiangxi Province, China (YC2015-B021), the National Science and
   Technology Major Projects program for "Major New Drugs Innovation and
   Development" of China (2011ZX09302-007-03), and the "Talent 555 Project"
   of Jiangxi Province, China.
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NR 79
TC 99
Z9 105
U1 4
U2 49
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 4
PY 2016
VL 35
AR 1
DI 10.1186/s13046-015-0276-9
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DA1CM
UT WOS:000367533900001
PM 26728266
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Guan, XY
   Guan, XL
   Zhu, JR
AF Guan, Xiao-ying
   Guan, Xiao-li
   Zhu, Jia-rui
TI Mechanisms and applications of ferroptosis-associated regulators in
   cancer therapy and drug resistance
SO JOURNAL OF CHEMOTHERAPY
LA English
DT Review
DE Ferroptosis; iron metabolism; lipid peroxidation; reactive oxygen
   specie; targeted therapy; drug resistance
ID CELL-DEATH; COLORECTAL-CANCER; IRON; TUMOR; INHIBITOR; PROTEIN;
   FERRITINOPHAGY; METABOLISM; XCT; SULFASALAZINE
AB Iron is an essential element for almost all living things. Both iron excess and iron deficiency can damage the body's health, but the body has developed complex mechanisms to regulate iron balance. The imbalance of iron homeostasis and lipid peroxidation are important features of ferroptosis. In this review, we summarize the latest regulatory mechanisms of ferroptosis, the roles of relevant regulators that target ferroptosis for cancer therapy, and their relationship to drug resistance. In conclusion, targeting ferroptosis is an important strategy for cancer therapy.
C1 [Guan, Xiao-ying] Lanzhou Univ Second Hosp, Pathol Dept, Lanzhou, Gansu, Peoples R China.
   [Guan, Xiao-li] Lanzhou Univ Second Hosp, Gen Med Dept, Lanzhou, Gansu, Peoples R China.
   [Zhu, Jia-rui] Lanzhou Univ Second Hosp, Cuiying Biomed Ctr, Lanzhou, Gansu, Peoples R China.
   [Guan, Xiao-ying] Lanzhou Univ Second Hosp, Pathol Dept, 82, Cuiying Gate, Lanzhou 730030, Gansu, Peoples R China.
RP Guan, XY (corresponding author), Lanzhou Univ Second Hosp, Pathol Dept, 82, Cuiying Gate, Lanzhou 730030, Gansu, Peoples R China.
EM guanxy18@lzu.edu.cn
FU Science and Technology Plan Project of Gansu Province [20JR5RA323];
   Health Industry Scientific Research Program of Gansu Province
   [GSWSKY2020-78]; Lanzhou Science and Technology Development Guiding Plan
   Project [2019-ZD-54]
FX This work was supported by Science and Technology Plan Project of Gansu
   Province (20JR5RA323), Health Industry Scientific Research Program of
   Gansu Province (GSWSKY2020-78), Lanzhou Science and Technology
   Development Guiding Plan Project (2019-ZD-54).
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NR 123
TC 4
Z9 4
U1 3
U2 12
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1120-009X
EI 1973-9478
J9 J CHEMOTHERAPY
JI J. Chemother.
PD NOV 17
PY 2023
VL 35
IS 8
BP 671
EP 688
DI 10.1080/1120009X.2023.2177808
EA FEB 2023
PG 18
WC Oncology; Infectious Diseases; Pathology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Infectious Diseases; Pathology; Pharmacology & Pharmacy
GA CB7Z4
UT WOS:000932090000001
PM 36764828
DA 2025-01-04
ER

PT J
AU Wu, YF
   Li, JJ
   Shu, LF
   Tian, ZY
   Wu, SR
   Wu, ZH
AF Wu, Yunfeng
   Li, Jiajia
   Shu, Linfeng
   Tian, Zhaoyu
   Wu, Siru
   Wu, Zuohui
TI Ultrasound combined with microbubble mediated immunotherapy for tumor
   microenvironment
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE ultrasound; cavitation effect; tumour microenvironment; immunotherapy;
   tumor cell
ID FOCUSED ULTRASOUND; DRUG-DELIVERY; HEPATOCELLULAR-CARCINOMA; CANCER;
   MACROPHAGES; THERAPY; CELLS; CAVITATION; VEGF; NANOPARTICLES
AB The tumor microenvironment (TME) plays an important role in dynamically regulating the progress of cancer and influencing the therapeutic results. Targeting the tumor microenvironment is a promising cancer treatment method in recent years. The importance of tumor immune microenvironment regulation by ultrasound combined with microbubbles is now widely recognized. Ultrasound and microbubbles work together to induce antigen release of tumor cell through mechanical or thermal effects, promoting antigen presentation and T cells' recognition and killing of tumor cells, and improve tumor immunosuppression microenvironment, which will be a breakthrough in improving traditional treatment problems such as immune checkpoint blocking (ICB) and himeric antigen receptor (CAR)-T cell therapy. In order to improve the therapeutic effect and immune regulation of TME targeted tumor therapy, it is necessary to develop and optimize the application system of microbubble ultrasound for organs or diseases. Therefore, the combination of ultrasound and microbubbles in the field of TME will continue to focus on developing more effective strategies to regulate the immunosuppression mechanisms, so as to activate anti-tumor immunity and/or improve the efficacy of immune-targeted drugs, At present, the potential value of ultrasound combined with microbubbles in TME targeted therapy tumor microenvironment targeted therapy has great potential, which has been confirmed in the experimental research and application of breast cancer, colon cancer, pancreatic cancer and prostate cancer, which provides a new alternative idea for clinical tumor treatment. This article reviews the research progress of ultrasound combined with microbubbles in the treatment of tumors and their application in the tumor microenvironment.
C1 [Wu, Yunfeng; Li, Jiajia; Shu, Linfeng; Tian, Zhaoyu; Wu, Siru; Wu, Zuohui] Zunyi Med Univ, Affiliated Hosp, Dept Ultrasound, Zunyi, Peoples R China.
C3 Zunyi Medical University
RP Wu, ZH (corresponding author), Zunyi Med Univ, Affiliated Hosp, Dept Ultrasound, Zunyi, Peoples R China.
EM csxfd12345@163.com
RI tian, zhaoyu/GYA-0475-2022
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NR 128
TC 1
Z9 1
U1 2
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 FEB 29
PY 2024
VL 15
AR 1304502
DI 10.3389/fphar.2024.1304502
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA LD3X3
UT WOS:001184813300001
PM 38487163
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Liu, DQ
   Che, XY
   Wu, GZ
AF Liu, Dequan
   Che, Xiangyu
   Wu, Guangzhen
TI Deciphering the role of neddylation in tumor microenvironment
   modulation: common outcome of multiple signaling pathways
SO BIOMARKER RESEARCH
LA English
DT Review
DE Neddylation; TME; NEDD8; Signaling pathway; MLN4924; Clinical trials
ID NEDD8-ACTIVATING ENZYME-INHIBITOR; NF-KAPPA-B; CULLIN-RING LIGASES; E3
   UBIQUITIN LIGASES; COLORECTAL-CANCER CELLS; ACUTE MYELOID-LEUKEMIA;
   GROWTH-FACTOR-BETA; TGF-BETA; TARGETING NEDDYLATION;
   EXTRACELLULAR-MATRIX
AB Neddylation is a post-translational modification process, similar to ubiquitination, that controls several biological processes. Notably, it is often aberrantly activated in neoplasms and plays a critical role in the intricate dynamics of the tumor microenvironment (TME). This regulatory influence of neddylation permeates extensively and profoundly within the TME, affecting the behavior of tumor cells, immune cells, angiogenesis, and the extracellular matrix. Usually, neddylation promotes tumor progression towards increased malignancy. In this review, we highlight the latest understanding of the intricate molecular mechanisms that target neddylation to modulate the TME by affecting various signaling pathways. There is emerging evidence that the targeted disruption of the neddylation modification process, specifically the inhibition of cullin-RING ligases (CRLs) functionality, presents a promising avenue for targeted therapy. MLN4924, a small-molecule inhibitor of the neddylation pathway, precisely targets the neural precursor cell-expressed developmentally downregulated protein 8 activating enzyme (NAE). In recent years, significant advancements have been made in the field of neddylation modification therapy, particularly the integration of MLN4924 with chemotherapy or targeted therapy. This combined approach has demonstrated notable success in the treatment of a variety of hematological and solid tumors. Here, we investigated the inhibitory effects of MLN4924 on neddylation and summarized the current therapeutic outcomes of MLN4924 against various tumors. In conclusion, this review provides a comprehensive, up-to-date, and thorough overview of neddylation modifications, and offers insight into the critical importance of this cellular process in tumorigenesis.
C1 [Liu, Dequan; Che, Xiangyu; Wu, Guangzhen] Dalian Med Univ, Affiliated Hosp 1, Dept Urol, Dalian 116011, Peoples R China.
C3 Dalian Medical University
RP Che, XY; Wu, GZ (corresponding author), Dalian Med Univ, Affiliated Hosp 1, Dept Urol, Dalian 116011, Peoples R China.
EM chexiangyu@firsthosp-dmu.com; wuguang0613@hotmail.com
OI guangzhen, wu/0000-0002-2300-8465; Liu, Dequan/0009-0003-1242-8792
FU Scientific Research Fund of the Liaoning Provincial Education Department
   [LZ2020071]; Doctoral Start-up Foundation of Liaoning Province
   [2021-BS-209]; Dalian Youth Science and Technology Star [2021RQ010]
FX This project is supported by the Scientific Research Fund of the
   Liaoning Provincial Education Department (No. LZ2020071), the Doctoral
   Start-up Foundation of Liaoning Province (No. 2021-BS-209), the Dalian
   Youth Science and Technology Star (No. 2021RQ010).
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NR 217
TC 7
Z9 8
U1 2
U2 7
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2050-7771
J9 BIOMARK RES
JI Biomark. Res.
PD JAN 8
PY 2024
VL 12
IS 1
AR 5
DI 10.1186/s40364-023-00545-x
PG 24
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA EI2W5
UT WOS:001138238900001
PM 38191508
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Dai, J
   Belum, VR
   Wu, SH
   Sibaud, V
   Lacouture, ME
AF Dai, Julia
   Belum, Viswanath R.
   Wu, Shenhong
   Sibaud, Vincent
   Lacouture, Mario E.
TI Pigmentary changes in patients treated with targeted anticancer agents:
   A systematic review and meta-analysis
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Review
DE cabozantinib; depigmentation; dyspigmentation; hyperpigmentation;
   hypopigmentation; imatinib; ipilimumab; nivolumab; pazopanib;
   pembrolizumab; pigmentary; repigmentation; sorafenib; sunitinib;
   vitiligo
ID RENAL-CELL CARCINOMA; PHASE-II TRIAL; TYROSINE KINASE INHIBITOR; CHRONIC
   MYELOID-LEUKEMIA; GASTROINTESTINAL STROMAL TUMORS; METASTATIC
   COLORECTAL-CANCER; CONTINUOUS DAILY SUNITINIB; VITILIGO-LIKE LESIONS;
   IMATINIB MESYLATE; HAIR DEPIGMENTATION
AB Background: The discovery of signaling networks that drive oncogenic processes has led to the development of targeted anticancer agents. The burden of pigmentary adverse events from these drugs is unknown.
   Objective: To conduct a systematic review and meta-analysis of published clinical trials and determine the incidence and risk of development of targeted therapye-induced pigmentary changes.
   Methods: A comprehensive search was conducted to identify studies reporting targeted therapy-induced pigmentary changes. The incidence and relative risk were calculated. Case reports and series were reviewed to understand clinical characteristics.
   Results: A total of 8052 patients from 36 clinical trials were included. The calculated overall incidences of targeted cancer therapy-induced all-grade pigmentary changes in the skin and hair were 17.7% (95% confidence interval [CI], 11.9-25.4) and 21.5% (95% CI, 14.9-30.1), respectively. The relative risk of all-grade pigmentary changes of skin and hair were 93.7 (95% CI, 5.86-1497.164) and 20.1 (95% CI, 8.35-48.248). Across 53 case reports/series (N = 75 patients), epidermal growth factor receptor and breakpoint cluster region-abelson inhibitors were the most common offending agents.
   Limitations: Potential under-reporting and variability in oncologists reporting these events.
   Conclusion: There is a significant risk of development of pigmentary changes during treatment with targeted anticancer therapies. Appropriate counseling and management are critical to minimize psychosocial impairment and deterioration in quality of life.
C1 [Dai, Julia; Belum, Viswanath R.; Lacouture, Mario E.] Mem Sloan Kettering Canc Ctr, Dept Med, Dermatol Serv, New York, NY 10021 USA.
   [Dai, Julia] Stanford Univ, Dept Dermatol, Stanford, CA 94305 USA.
   [Wu, Shenhong] SUNY Stony Brook, Dept Med, Div Med Oncol, Stony Brook, NY 11794 USA.
   [Wu, Shenhong] Northport Vet Adm Med Ctr, Dept Med, Div Hematol & Oncol, Northport, NY USA.
   [Sibaud, Vincent] Inst Univ Canc, Inst Claudius Regaud, Dept Dermatol, Toulouse Oncopole, Toulouse, France.
C3 Memorial Sloan Kettering Cancer Center; Stanford University; State
   University of New York (SUNY) System; Stony Brook University; UNICANCER;
   Institut Claudius Regaud
RP Lacouture, ME (corresponding author), Mem Sloan Kettering Canc Ctr, Dermatol Serv, 60th St Outpatient Ctr,Suite 407,Room 4312, New York, NY 10022 USA.
EM lacoutum@mskcc.org
RI Sibaud, Vincent/P-6270-2014
OI Lacouture, Mario/0000-0002-4818-3710
FU National Institutes of Health/National Cancer Institute Cancer Center
   [P20 CA008748]; RJR
FX Supported in part by the National Institutes of Health/National Cancer
   Institute Cancer Center Support Grant P20 CA008748. Drs Lacouture and
   Belum are supported by the RJR Oncodermatology Fund. Funders and
   sponsors were not involved in the design and conduct of the study;
   collection, management, analysis, and interpretation of the data;
   preparation, review, or approval of the manuscript; or the decision to
   submit the manuscript for publication.
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NR 112
TC 47
Z9 52
U1 1
U2 18
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0190-9622
J9 J AM ACAD DERMATOL
JI J. Am. Acad. Dermatol.
PD NOV
PY 2017
VL 77
IS 5
BP 902
EP +
DI 10.1016/j.jaad.2017.06.044
PG 11
WC Dermatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dermatology
GA FJ4AW
UT WOS:000412676800027
PM 28918974
OA Green Accepted
DA 2025-01-04
ER

PT J
AU DeStefanis, RA
   Kratz, JD
   Emmerich, PB
   Deming, DA
AF DeStefanis, Rebecca A.
   Kratz, Jeremy D.
   Emmerich, Philip B.
   Deming, Dustin A.
TI Targeted Therapy in Metastatic Colorectal Cancer: Current Standards and
   Novel Agents in Review
SO CURRENT COLORECTAL CANCER REPORTS
LA English
DT Review
DE Colon cancer; Rectal cancer; Targeted therapy; Molecular subtypes;
   Emerging subtypes chemotherapy
ID GROWTH-FACTOR RECEPTOR; CETUXIMAB PLUS IRINOTECAN; WILD-TYPE KRAS;
   1ST-LINE TREATMENT; OPEN-LABEL; MICROSATELLITE INSTABILITY;
   MONOCLONAL-ANTIBODY; CONTROLLED-TRIAL; POOLED ANALYSIS; RAS MUTATIONS
AB Purpose of Review Treatment options for patients with metastatic colorectal cancer continue to advance as the therapeutic implications of the molecular subtypes of this disease are becoming better understood. DNA sequencing and mismatch repair assessment are now standard of care analyses for patients with metastatic colorectal cancer This review describes important aspects of the biology of the clinically relevant molecular subtypes of colorectal cancer based on the current standard of care testing. In addition, the clinical treatment strategies available now and potentially in the future for these colorectal cancer subtypes are discussed.
   Recent Findings Currently, for metastatic colorectal cancer, standard of care molecular testing is done for mutations in exons 2, 3, and 4 of KRAS and NRAS, and BRAF V600E. Testing for mismatch repair (MMR) deficiency/microsatellite instability (MSI) status is also done. These aberrations are well known to change the clinical prognosis and guide patients' treatment strategies. Additionally, three new subtypes have emerged: PIK3CAmut, HER2 amplified, and NTRK fusions. With the addition of these emerging subtypes, tumor heterogeneity further validates the need to examine mCRC as a heterogeneous disease. Here, we present recent exciting data from translational research and clinical trials exhibiting possible distinct treatment strategies for these different subtypes.
   Summary Altogether, these data show promising treatment strategies for many of these well-known and emerging subtypes of mCRC. In addition, these also give better clinical prognostic and predictive information. We believe that as molecular testing expands, PIK3CA mutation, HER2 amplification, and NTRK fusion molecular testing will be included in standard of care analyses. This incorporation of testing in clinical practice will generate further information regarding prognostic and therapeutic options for these and other CRC subtypes in the future.
C1 [DeStefanis, Rebecca A.; Kratz, Jeremy D.; Emmerich, Philip B.; Deming, Dustin A.] Univ Wisconsin, Dept Med, Div Hematol & Oncol, Madison, WI 53706 USA.
   [Deming, Dustin A.] Univ Wisconsin, Carbone Canc Ctr, Madison, WI 53706 USA.
   [Deming, Dustin A.] Univ Wisconsin, McArdle Lab Canc Res, Dept Oncol, 6507 Wisconsin Inst Med Res, 1111 Highland Ave, Madison, WI 53705 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
RP Deming, DA (corresponding author), Univ Wisconsin, Dept Med, Div Hematol & Oncol, Madison, WI 53706 USA.; Deming, DA (corresponding author), Univ Wisconsin, Carbone Canc Ctr, Madison, WI 53706 USA.; Deming, DA (corresponding author), Univ Wisconsin, McArdle Lab Canc Res, Dept Oncol, 6507 Wisconsin Inst Med Res, 1111 Highland Ave, Madison, WI 53705 USA.
EM ddeming@medicine.wisc.edu
FU University of Wisconsin Carbone Cancer Center [P30 CA014520]
FX This project was supported by P30 CA014520 (Core Grant, University of
   Wisconsin Carbone Cancer Center).
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NR 87
TC 25
Z9 27
U1 0
U2 9
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1556-3790
EI 1556-3804
J9 CURR COLORECT CANC R
JI Curr. Colorectal Cancer Rep.
PD APR
PY 2019
VL 15
IS 2
BP 61
EP 69
DI 10.1007/s11888-019-00430-6
PG 9
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA HT9JD
UT WOS:000464884500003
PM 31130830
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Shen, TL
   Yang, SY
   Qu, XY
   Chen, ZL
   Zeng, LZ
   Sun, XJ
   Lin, YY
   Luo, M
   Lei, B
   Yue, CY
   Ma, CH
   Hu, N
   Wang, W
   Zhang, L
AF Shen, Tianli
   Yang, Shuanying
   Qu, Xiaoyan
   Chen, Zilu
   Zeng, Lizhong
   Sun, Xuejun
   Lin, Yuyao
   Luo, Meng
   Lei, Bo
   Yue, Chenyang
   Ma, Chunhong
   Hu, Nan
   Wang, Wei
   Zhang, Long
TI A bionic "Trojan horse"-like gene delivery system hybridized with tumor
   and macrophage cell membrane for cancer therapy
SO JOURNAL OF CONTROLLED RELEASE
LA English
DT Article
DE Gene delivery system; cancer therapy; Dual-membrane camouflage; Immune
   escape; Homologous targeting
ID COATED NANOPARTICLES
AB MiRNA-based gene therapy as a novel targeted therapy has yielded promising results in experimental cancer treatment, however, the inefficient delivery of miRNA to target tissues has limited its application in vivo. Here a unique dual-membrane-camouflaged miRNA21 antagomir delivery nanoplatform (M@NPs/miR21) with im-mune escape and homologous targeting properties was constructed by cancer cell membrane and macrophage membrane. Different from the single-cell membrane camouflage strategy, the dual-membrane camouflage miRNA21 antagomir delivery nanoplatform based on modification of CD47 protein with immune escape signal and galectin-3 protein with tumor cell aggregation enables efficient, safe and targeted therapy for colon cancer and lung metastases. Camouflaged with the dual-cell membrane, the "Trojan horse" like "pseudo-tumor cell" and/or "pseudo-macrophage" (M@NPs/miR21) carried the target gene miR21 antagomir to the tumor site and showed significant anti-tumor properties at the periphery and the core of subcutaneous tumor tissues. In addi-tion, M@NPs/miR21 was more likely to penetrate dense tumor tissues and function within the tumor mass than NPs/miR21 without membrane coating. M@NPs/miR21 can deliver miR21 antagomir into MC38 cancer cells and tumor tissues, promote tumor apoptosis, and regulate the expression of Bcl2 and Ki67. Moreover, the M@NPs/miR21 gene delivery system not only can effectively inhibit the progression of subcutaneous tumors and lung metastases, but also showed minimal toxicity and good biosafety, making this delivery system particularly attractive for future translational research.
C1 [Yang, Shuanying; Zeng, Lizhong; Zhang, Long] Xi An Jiao Tong Univ, Dept Resp & Crit Care Med, Affiliated Hosp 2, Xian 710004, Peoples R China.
   [Shen, Tianli; Chen, Zilu; Sun, Xuejun; Ma, Chunhong; Wang, Wei] Xi An Jiao Tong Univ, Dept Gen Surg, Affiliated Hosp 1, Xian 710061, Peoples R China.
   [Qu, Xiaoyan; Luo, Meng; Lei, Bo] Xi An Jiao Tong Univ, Frontier Inst Sci & Technol, Xian 710054, Peoples R China.
   [Lin, Yuyao] Xi An Jiao Tong Univ, Dept Plast Aesthet & Maxillofacial Surg, Affiliated Hosp 1, Xian 710061, Peoples R China.
   [Yue, Chenyang] York Univ, Dept Biol, Toronto, ON, Canada.
   [Hu, Nan] Xi An Jiao Tong Univ, Dept Rheumatol, Affiliated Hosp 1, Xian 710061, Peoples R China.
C3 Xi'an Jiaotong University; Xi'an Jiaotong University; Xi'an Jiaotong
   University; Xi'an Jiaotong University; York University - Canada; Xi'an
   Jiaotong University
RP Zhang, L (corresponding author), Xi An Jiao Tong Univ, Dept Resp & Crit Care Med, Affiliated Hosp 2, Xian 710004, Peoples R China.; Wang, W (corresponding author), Xi An Jiao Tong Univ, Dept Gen Surg, Affiliated Hosp 1, Xian 710061, Peoples R China.
EM wangwei@xjtufh.edu.cn; longzhang@xjtu.edu.cn
RI Lei, Bo/B-9463-2009; sun, xuejun/G-5212-2011; zhang, long/AAW-8390-2021;
   hu, nan/KHE-4563-2024; Yue, Chen/IAP-6501-2023; Chen, Zilu/JEF-2487-2023
OI Yue, Chenyang/0000-0003-0852-0409; , long/0000-0003-0091-6695; chen, zi
   lu/0000-0003-4315-9946
FU China Postdoctoral Science Foundation [2021M692578]; Fundamental
   Research Funds for the Central Uni [xzy012022114]
FX Acknowledgements This work was funded by China Postdoctoral Science
   Foundation (2021M692578) and Fundamental Research Funds for the Central
   Uni- versities (xzy012022114) . The picture materials in the schematic
   dia- gram are provided by "BioRender.com ".
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NR 47
TC 14
Z9 13
U1 12
U2 57
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-3659
EI 1873-4995
J9 J CONTROL RELEASE
JI J. Control. Release
PD JUN
PY 2023
VL 358
BP 204
EP 218
DI 10.1016/j.jconrel.2023.04.046
EA MAY 2023
PG 15
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA H7XL9
UT WOS:000998046500001
PM 37121518
DA 2025-01-04
ER

PT J
AU Akkad, J
   Bochum, S
   Martens, UM
AF Akkad, Jamil
   Bochum, Sylvia
   Martens, Uwe M.
TI Personalized treatment for colorectal cancer: novel developments and
   putative therapeutic strategies
SO LANGENBECKS ARCHIVES OF SURGERY
LA English
DT Review
DE Colorectal cancer; Targeted therapy; Biomarker; Precision medicine;
   Genomics; Cancer stem cells; NGS; RAS; KRAS; BRAF; PI3K; EGFR; VEGF;
   WNT; PD-1; Cetuximab; Panitumumab; Bevacizumab; Aflibercept; Regorafenib
ID WILD-TYPE KRAS; MICROSATELLITE-INSTABILITY; 1ST-LINE TREATMENT;
   ACQUIRED-RESISTANCE; GENE-EXPRESSION; BRAF MUTATION; COLON-CANCER;
   K-RAS; PLUS BEVACIZUMAB; MISMATCH REPAIR
AB Colorectal cancer (CRC) is the third most common cancer diagnosed worldwide and continues to be a major healthcare concern. Molecular heterogeneity of CRC is believed to be one of the main factors responsible for the considerable variability in treatment response. With the recent development of powerful genomic technologies, novel insights in tumor biology of CRC have now been provided, facilitating the recognition of new molecular subtypes with prognostic and predictive implications.
   The purpose of this review article is to summarize current knowledge about genomic, epigenomic, and proteomic characteristics of CRC, as well as their implications for biomarker identification and individualized targeted therapy.
   Supplementing the findings from several previous studies, the Cancer Genome Atlas (TCGA) project recently finalized the systematic characterization of CRC resulting in the first tumor dataset with complete molecular measurements at DNA, RNA, and protein levels. The challenge now is to translate these findings into a robust and reproducible CRC classification system linking molecular features of the tumor to precision medicine.
C1 [Akkad, Jamil; Bochum, Sylvia; Martens, Uwe M.] SLK Kliniken Heilbronn GmbH, Canc Ctr Heilbronn Franken, Heilbronn, Germany.
   [Akkad, Jamil; Martens, Uwe M.] SLK Kliniken Heilbronn GmbH, Dept Hematol & Oncol, Heilbronn, Germany.
   [Martens, Uwe M.] Heidelberg Univ, SLK Kliniken Heilbronn GmbH Acad Hosp, D-74078 Heilbronn, Germany.
C3 SLK-Kliniken Heilbronn GmbH; SLK-Kliniken Heilbronn GmbH; Ruprecht Karls
   University Heidelberg; SLK-Kliniken Heilbronn GmbH
RP Martens, UM (corresponding author), Heidelberg Univ, SLK Kliniken Heilbronn GmbH Acad Hosp, Gesundbrunnen 20-26, D-74078 Heilbronn, Germany.
EM uwe.martens@slk-kliniken.de
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NR 131
TC 15
Z9 16
U1 0
U2 15
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1435-2443
EI 1435-2451
J9 LANGENBECK ARCH SURG
JI Langenbecks Arch. Surg.
PD FEB
PY 2015
VL 400
IS 2
BP 129
EP 143
DI 10.1007/s00423-015-1276-0
PG 15
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA CC0PY
UT WOS:000350039200001
PM 25701352
DA 2025-01-04
ER

PT J
AU Riedesser, JE
   Ebert, MP
   Betge, J
AF Riedesser, Julian E.
   Ebert, Matthias P.
   Betge, Johannes
TI Precision medicine for metastatic colorectal cancer in clinical practice
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Review
DE chemotherapy; colorectal cancer; consensus molecular subtypes;
   immunotherapy; organoids; patient-derived xenografts; personalized
   oncology; precision medicine; targeted therapy
ID CONSENSUS MOLECULAR SUBTYPES; FOLFIRI PLUS BEVACIZUMAB; PHASE-III TRIAL;
   RANDOMIZED CONTROLLED-TRIAL; OPEN-LABEL; 1ST-LINE TREATMENT;
   BRAF-MUTATION; LIVER METASTASES; BREAST-CANCER; COLON-CANCER
AB Globally, metastatic colorectal cancer is one of the leading causes for cancer-related death. Treatment limited to conventional chemotherapeutics extended life for only a few months. However, advances in surgical approaches and medical treatment regimens have greatly increased survival, even leading to long-term remission in selected patients. Advances in multiomics analysis of tumors have built a foundation for molecular-targeted therapies. Furthermore, immunotherapies are on the edge of revolutionizing oncological practice. This review summarizes recent advances in the growing toolbox of personalized treatment for patients with metastatic colorectal cancer. We provide an overview of current multimodal therapy and explain novel immunotherapy and targeted therapy approaches in detail. We emphasize clinically relevant therapies, such as inhibitors of MAPK signaling, and give recommendations for clinical practice. Finally, we describe the potential predictive impact of molecular subtypes and provide an outlook on novel concepts, such as functional precision medicine.
C1 [Riedesser, Julian E.; Betge, Johannes] German Canc Res Ctr, Jr Clin Cooperat Unit Translat Gastrointestinal O, Neuenheimer Feld 580, D-69120 Heidelberg, Germany.
   [Riedesser, Julian E.; Betge, Johannes] Univ Med Ctr Mannheim, DKFZ Hector Canc Inst, Mannheim, Germany.
   [Riedesser, Julian E.; Ebert, Matthias P.; Betge, Johannes] Heidelberg Univ, Dept Med 2, Univ Med Ctr Mannheim, Med Fac Mannheim, Mannheim, Germany.
   [Riedesser, Julian E.; Ebert, Matthias P.; Betge, Johannes] Heidelberg Univ, Mannheim Canc Ctr, Univ Med Ctr Mannheim, Med Fac Mannheim, Mannheim, Germany.
C3 Helmholtz Association; German Cancer Research Center (DKFZ); Ruprecht
   Karls University Heidelberg; Ruprecht Karls University Heidelberg;
   Ruprecht Karls University Heidelberg
RP Betge, J (corresponding author), German Canc Res Ctr, Jr Clin Cooperat Unit Translat Gastrointestinal O, Neuenheimer Feld 580, D-69120 Heidelberg, Germany.; Betge, J (corresponding author), Univ Med Ctr Mannheim, DKFZ Hector Canc Inst, Mannheim, Germany.; Betge, J (corresponding author), Heidelberg Univ, Dept Med 2, Univ Med Ctr Mannheim, Med Fac Mannheim, Mannheim, Germany.; Betge, J (corresponding author), Heidelberg Univ, Mannheim Canc Ctr, Univ Med Ctr Mannheim, Med Fac Mannheim, Mannheim, Germany.
EM j.betge@dkfz.de
OI Betge, Johannes/0000-0001-9549-1866
FU Hector Foundation II, Weinheim, Germany
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and/or publication of this article: J.B. is
   supported by the Hector Foundation II, Weinheim, Germany.
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NR 231
TC 32
Z9 33
U1 2
U2 27
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PD JAN
PY 2022
VL 14
AR 17588359211072703
DI 10.1177/17588359211072703
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YP2XJ
UT WOS:000748489400001
PM 35237350
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Guadagni, S
   Masedu, F
   Fiorentini, G
   Sarti, D
   Fiorentini, C
   Guadagni, V
   Apostolou, P
   Papasotiriou, I
   Parsonidis, P
   Valenti, M
   Ricevuto, E
   Bruera, G
   Farina, AR
   Mackay, AR
   Clementi, M
AF Guadagni, Stefano
   Masedu, Francesco
   Fiorentini, Giammaria
   Sarti, Donatella
   Fiorentini, Caterina
   Guadagni, Veronica
   Apostolou, Panagiotis
   Papasotiriou, Ioannis
   Parsonidis, Panagiotis
   Valenti, Marco
   Ricevuto, Enrico
   Bruera, Gemma
   Farina, Antonietta R.
   Mackay, Andrew R.
   Clementi, Marco
TI Circulating tumour cell gene expression and chemosensitivity analyses:
   predictive accuracy for response to multidisciplinary treatment of
   patients with unresectable refractory recurrent rectal cancer or
   unresectable refractory colorectal cancer liver metastases
SO BMC CANCER
LA English
DT Article
DE Predictive accuracy; Precision oncotherapy; Liquid biopsies; Circulating
   tumor cells; Chemosensitivity tests; Tumor gene expressions analyses;
   Recurrent rectal cancer; Colorectal cancer liver metastases;
   Intraarterial chemotherapy; Targeted therapy
ID THYMIDYLATE SYNTHASE; CHEMOTHERAPY; BIOMARKERS; GUIDELINE
AB Background Patients with unresectable recurrent rectal cancer (RRC) or colorectal cancer (CRC) with liver metastases, refractory to at least two lines of traditional systemic therapy, may receive third line intraarterial chemotherapy (IC) and targeted therapy (TT) using drugs selected by chemosensitivity and tumor gene expression analyses of liquid biopsy-derived circulating tumor cells (CTCs). Methods In this retrospective study, 36 patients with refractory unresectable RRC or refractory unresectable CRC liver metastases were submitted for IC and TT with agents selected by precision oncotherapy chemosensitivity assays performed on liquid biopsy-derived CTCs, transiently cultured in vitro, and by tumor gene expression in the same CTC population, as a ratio to tumor gene expression in peripheral mononuclear blood cells (PMBCs) from the same individual. The endpoint was to evaluate the predictive accuracy of a specific liquid biopsy precision oncotherapy CTC purification and in vitro culture methodology for a positive RECIST 1.1 response to the therapy selected. Results Our analyses resulted in evaluations of 94.12% (95% CI 0.71-0.99) for sensitivity, 5.26% (95% CI 0.01-0.26) for specificity, a predictive value of 47.06% (95% CI 0.29-0.65) for a positive response, a predictive value of 50% (95% CI 0.01-0.98) for a negative response, with an overall calculated predictive accuracy of 47.22% (95% CI 0.30-0.64). Conclusions This is the first reported estimation of predictive accuracy derived from combining chemosensitivity and tumor gene expression analyses on liquid biopsy-derived CTCs, transiently cultured in vitro which, despite limitations, represents a baseline and benchmark which we envisage will be improve upon by methodological and technological advances and future clinical trials.
C1 [Guadagni, Stefano; Masedu, Francesco; Valenti, Marco; Ricevuto, Enrico; Bruera, Gemma; Farina, Antonietta R.; Mackay, Andrew R.; Clementi, Marco] Univ Aquila, Dept Appl Clin & Biotechnol Sci, I-67100 Laquila, Italy.
   [Fiorentini, Giammaria; Sarti, Donatella] Azienda Osped Osped Riuniti Marche Nord, Dept Hematol & Oncol, Pesaro, Italy.
   [Fiorentini, Caterina] Tech Univ Munich, Klinikum Rechts Isar, Univ Hosp, Dept Prevent & Sports Med, Munich, Germany.
   [Guadagni, Veronica] Univ Calgary, Cumming Sch Med, Dept Physiol & Pharmacol, Calgary, AB, Canada.
   [Apostolou, Panagiotis; Parsonidis, Panagiotis] Res Genet Canc Ctr SA, Florina, Greece.
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RP Guadagni, S (corresponding author), Univ Aquila, Dept Appl Clin & Biotechnol Sci, I-67100 Laquila, Italy.
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NR 44
TC 2
Z9 2
U1 1
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD JUN 16
PY 2022
VL 22
IS 1
AR 660
DI 10.1186/s12885-022-09770-3
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2E5IS
UT WOS:000812261600002
PM 35710393
OA gold, Green Published
DA 2025-01-04
ER

PT B
AU Bhaskar, LVKS
   Saikrishna, L
AF Bhaskar, L. V. K. S.
   Saikrishna, L.
BE Nagaraju, GP
TI Drug Resistance Against Tyrosine Kinase Inhibitor in Gastrointestinal
   Malignancies
SO ROLE OF TYROSINE KINASES IN GASTROINTESTINAL MALIGNANCIES
LA English
DT Article; Book Chapter
DE Gastrointestinal cancer; Tyrosine kinase inhibitors; TKI resistance;
   EGFR; VEGF; HER2
ID METASTATIC COLORECTAL-CANCER; PHASE-II TRIAL; GROWTH-FACTOR RECEPTOR;
   ADVANCED PANCREATIC-CANCER; ADVANCED HEPATOCELLULAR-CARCINOMA; ADVANCED
   GASTRIC-CANCER; RAMUCIRUMAB PLUS PACLITAXEL; ENHANCED
   ANTITUMOR-ACTIVITY; COOPERATIVE-ONCOLOGY-GROUP; 1ST-LINE THERAPY
AB Gastrointestinal cancers are heterogeneous and complex among the most common human cancers. In spite of this complexity, certain types of genetic alterations are linked to specific pathological lesions. Genomic and transcriptomic analyses have disclosed molecular subtypes that are characterized by specific genetic aberrations and expression signatures. Identification of better molecular markers to assist detection and prognostic evaluation of the cancer is therefore required. Tyrosine kinases are enzymes responsible for the activation of many proteins by signal transduction cascades. Inhibitors of tyrosine kinases (TKIs) have been effectively used for clinical treatment of certain types of cancer. Chronic exposure to gradually increasing concentrations of the TKI over a period of time, cells by activating modified signaling pathway can replace the lack of signal in target therapy, leading to the development of drug resistance. In recent years, researchers have specified different subsets of tyrosine kinase inhibitors' potential resistance mechanisms in various gastric cancers. This chapter intends to provide an overview of the most recently identified molecular mechanisms of acquired resistance to tyrosine kinase-targeted therapy in various gastrointestinal malignancies.
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NR 282
TC 0
Z9 0
U1 0
U2 12
PU SPRINGER-VERLAG SINGAPORE PTE LTD
PI SINGAPORE
PA 152 BEACH ROAD, #21-01/04 GATEWAY EAST, SINGAPORE, 189721, SINGAPORE
BN 978-981-13-1486-5; 978-981-13-1485-8
PY 2018
BP 191
EP 224
DI 10.1007/978-981-13-1486-5_14
D2 10.1007/978-981-13-1486-5
PG 34
WC Biochemistry & Molecular Biology; Gastroenterology & Hepatology
WE Book Citation Index – Science (BKCI-S)
SC Biochemistry & Molecular Biology; Gastroenterology & Hepatology
GA BO8QC
UT WOS:000529054600015
DA 2025-01-04
ER

PT J
AU Li, PH
   Dong, JD
   Zhou, X
   Sun, WJ
   Huang, H
   Chen, T
   Ye, B
   Zheng, ZQ
   Lu, MD
AF Li, Pihong
   Dong, Jianda
   Zhou, Xiang
   Sun, Weijian
   Huang, He
   Chen, Tong
   Ye, Bing
   Zheng, Zhiqiang
   Lu, Mingdong
TI Expression patterns of microRNA-329 and its clinical performance in
   diagnosis and prognosis of breast cancer
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE miR-329; diagnosis; prognosis; breast cancer; target therapy
ID CELL LUNG-CANCER; DOWN-REGULATION; COLORECTAL-CANCER; TUMOR-SUPPRESSOR;
   CERVICAL-CANCER; POOR-PROGNOSIS; BIOMARKER; WOMEN; METAANALYSIS;
   METASTASIS
AB This study was aimed to assess the expression and clinical performance of microRNA-329 (miR-329) in breast cancer. We recruited 134 breast cancer patients and 70 healthy volunteers for this study. MiR-329 expression was estimated by quantitative real-time polymerase chain reaction. A receiver operating characteristic assay was performed to evaluate the diagnostic value of serum miR-329. In addition, the prognostic significance of miR-329 was evaluated through Kaplan-Meier survival and Cox regression analyses. According to quantitative real-time polymerase chain reaction, miR-329 expression was downregulated in cancerous samples compared with healthy and normal controls (P<0.01), and its expression in serum specimens positively correlated with its expression in tissue samples (R=0.493, P<0.001). The decreased expression of miR-329 correlated with lymph node metastasis (P=0.015) and TNM stage (P=0.003). A receiver operating characteristic curve with an area under the curve of 0.932 was constructed, indicating the high diagnostic accuracy of miR-329. From the survival and multivariate Cox assays, we found that downregulated miR-329 expression was associated with poor overall survival (log-rank P<0.001) and served as an independent prognostic factor (hazard ratio = 2.987, 95% CI = 1.681-5.308, and P<0.001). In silico analysis using The Cancer Genome Atlas confirmed that miR-329 expression was lower in breast cancer cases compared with normal controls (P<0.001) and could be an efficient biomarker for cancer patients. Downregulated miR-329 expression was an effective diagnostic and prognostic biomarker, which could be used for targeted therapy in patients with breast cancer.
C1 [Lu, Mingdong] Wenzhou Med Univ, Dept Gen Surg, Affiliated Hosp 2, 109 West Xueyuan Rd, Wenzhou 325027, Peoples R China.
   [Lu, Mingdong] Wenzhou Med Univ, Yuying Childrens Hosp, 109 West Xueyuan Rd, Wenzhou 325027, Peoples R China.
C3 Wenzhou Medical University; Wenzhou Medical University
RP Lu, MD (corresponding author), Wenzhou Med Univ, Dept Gen Surg, Affiliated Hosp 2, 109 West Xueyuan Rd, Wenzhou 325027, Peoples R China.; Lu, MD (corresponding author), Wenzhou Med Univ, Yuying Childrens Hosp, 109 West Xueyuan Rd, Wenzhou 325027, Peoples R China.
EM lumingdong16@163.com
RI Huang, He/P-8935-2018; Li, Huihuang/GNM-7727-2022
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NR 36
TC 15
Z9 16
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 2017
VL 10
BP 5711
EP 5718
DI 10.2147/OTT.S147974
PG 8
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA FN7XH
UT WOS:000416231900003
PM 29238203
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Shen, JY
   Li, L
   Yang, T
   Cohen, PS
   Sun, GQ
AF Shen, Jinyan
   Li, Li
   Yang, Tao
   Cohen, Paul S.
   Sun, Gongqin
TI Biphasic Mathematical Model of Cell-Drug Interaction That Separates
   Target-Specific and Off-Target Inhibition and Suggests Potent Targeted
   Drug Combinations for Multi-Driver Colorectal Cancer Cells
SO CANCERS
LA English
DT Article
DE biphasic analysis; colorectal cancer; dose reduction index; protein
   kinase inhibitors; combination targeted therapy
ID PROTEIN-TYROSINE KINASE; SRC-FAMILY KINASES; LEUKEMIA CELL; LUNG-CANCER;
   HUMAN COLON; THERAPY; GROWTH; MUTATIONS; PHOSPHORYLATION; ACTIVATION
AB Quantifying the response of cancer cells to a drug, and understanding the mechanistic basis of the response, are the cornerstones for anti-cancer drug discovery. Classical single target-based IC50 measurements are inadequate at describing cancer cell responses to targeted drugs. In this study, based on an analysis of targeted inhibition of colorectal cancer cell lines, we develop a new biphasic mathematical model that accurately describes the cell-drug response. The model describes the drug response using three kinetic parameters: ratio of target-specific inhibition, F-1, potency of target-specific inhibition, K-d1, and potency of off-target toxicity, K-d2. Determination of these kinetic parameters also provides a mechanistic basis for predicting effective combination targeted therapy for multi-driver cancer cells. The experiments confirmed that a combination of inhibitors, each blocking a driver pathway and having a distinct target-specific effect, resulted in a potent and synergistic blockade of cell viability, improving potency over mono-agent treatment by one to two orders of magnitude. We further demonstrate that mono-driver cancer cells represent a special scenario in which F-1 becomes nearly 100%, and the drug response becomes monophasic. Application of this model to the responses of >400 cell lines to kinase inhibitor dasatinib revealed that the ratio of biphasic versus monophasic responses is about 4:1. This study develops a new mathematical model of quantifying cancer cell response to targeted therapy, and suggests a new framework for developing rational combination targeted therapy for colorectal and other multi-driver cancers.
C1 [Shen, Jinyan; Li, Li; Yang, Tao; Cohen, Paul S.; Sun, Gongqin] Univ Rhode Isl, Dept Cell & Mol Biol, Kingston, RI 02881 USA.
   [Shen, Jinyan; Yang, Tao] Shanxi Med Univ, Dept Biochem & Mol Biol, Taiyuan 030001, Peoples R China.
   [Li, Li] Shanxi Med Univ, Dept Cell Biol & Med Genet, Taiyuan 030001, Peoples R China.
C3 University of Rhode Island; Shanxi Medical University; Shanxi Medical
   University
RP Sun, GQ (corresponding author), Univ Rhode Isl, Dept Cell & Mol Biol, Kingston, RI 02881 USA.
EM jinyanshen201@163.com; lili_5076@126.com; yangtao056cn@126.com;
   pscohen@uri.edu; gsun@uri.edu
OI Shen, Jinyan/0000-0002-1955-093X; Li, Li/0000-0001-9208-6638
FU Shanxi Medical University in China; College of Environment and Life
   Sciences, University of Rhode Island; USDA National Institute of Food
   and Agriculture, Hatch Regional Project [1016896]
FX J. S., L.L. and T.Y. were supported by scholarships from Shanxi Medical
   University in China. The research was supported by the College of
   Environment and Life Sciences, University of Rhode Island, and by the
   USDA National Institute of Food and Agriculture, Hatch Regional Project
   1016896.
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NR 60
TC 14
Z9 19
U1 1
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD FEB
PY 2020
VL 12
IS 2
AR 436
DI 10.3390/cancers12020436
PG 22
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KY3ND
UT WOS:000522477300182
PM 32069833
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Elez, E
   Kopetz, S
   Tabernero, J
   Bekaii-Saab, T
   Taieb, J
   Yoshino, T
   Manji, G
   Fernandez, K
   Abbattista, A
   Zhang, XS
   Morris, VK
AF Elez, Elena
   Kopetz, Scott
   Tabernero, Josep
   Bekaii-Saab, Tanios
   Taieb, Julien
   Yoshino, Takayuki
   Manji, Gulam
   Fernandez, Kathrine
   Abbattista, Antonello
   Zhang, Xiaosong
   Morris, Van K.
TI SEAMARK: phase II study of first-line encorafenib and cetuximab plus
   pembrolizumab for MSI-H/dMMR <i>BRAFV600E</i>-mutant mCRC
SO FUTURE ONCOLOGY
LA English
DT Article
DE BRAF V600; cetuximab; dMMR; encorafenib; immunotherapy; metastatic
   colorectal cancer; MSI-H; pembrolizumab; targeted therapy; triplet
   combination therapy
ID METASTATIC COLORECTAL-CANCER; BRAF(V600E) INHIBITION; BRAF INHIBITION;
   MELANOMA; CONTRIBUTES; PATHWAY; COLON
AB Patients with both BRAF V600E mutations and microsatellite instability-high (MSI-H)/mismatch repair-deficient (dMMR) metastatic colorectal cancer (mCRC) have poor prognosis. Currently, there are no specifically targeted first-line treatment options indicated for patients with mCRC whose tumors harbor both molecular aberrations. Pembrolizumab is a checkpoint inhibitor approved for the treatment of MSI-H/dMMR mCRC, and the BRAF inhibitor encorafenib, in combination with cetuximab, is approved for previously treated BRAF V600E-mutant mCRC. Combination of pembrolizumab with encorafenib and cetuximab may synergistically enhance antitumor activity in patients with BRAF V600E-mutant, MSI-H/dMMR mCRC. SEAMARK is a randomized phase II study comparing the efficacy of the combination of pembrolizumab with encorafenib and cetuximab versus pembrolizumab alone in patients with previously untreated BRAF V600E-mutant, MSI-H/dMMR mCRC.
   Plain language summary - SEAMARK study: encorafenib & cetuximab plus pembrolizumab for people with BRAF V600E-mutant & DNA repair-deficient colorectal cancer: Colorectal cancer (CRC) occurs when there is an abnormal growth of cells (known as a tumor) in the colon or rectum. Some people with CRC have changes in their tumor genes (known as gene mutations). A gene is a piece of DNA that tells the cell to make specific molecules, such as proteins. Mutations in a gene called BRAF can turn on signals that help the cancer cells grow. Gene mutations that impair DNA repair mechanisms can also make the cancer cells grow more quickly and allow the immune system to detect the cancer cells as being foreign to the body. Targeted therapy is a type of cancer treatment that turns off specific genes and proteins involved in cancer cell survival and growth. BRAF and EGFR inhibitors are targeted therapies that work well together in treating people with BRAF-mutant CRC. BRAF proteins can help cancer cells grow, and BRAF inhibitors block these proteins to prevent, slow, or stop the growth of the cancer cells. Immunotherapy is a type of cancer treatment that helps a person's immune system fight cancer. Immunotherapy is effective for treating CRC that has mutations in the DNA repair mechanisms. By combining targeted therapy and immunotherapy, patients may be able to live longer without their disease getting worse. In the SEAMARK study, we will use a treatment combination including a BRAF inhibitor (encorafenib), an EGFR inhibitor (cetuximab) and an immunotherapy (pembrolizumab) in patients with CRC who have a BRAF mutation and deficiencies in the DNA repair mechanism.
C1 [Elez, Elena] Univ Autonoma Barcelona, Vall dHebron Hosp Campus, Barcelona, Spain.
   [Elez, Elena] Univ Autonoma Barcelona, Vall dHebron Inst Oncol, Barcelona, Spain.
   [Kopetz, Scott; Morris, Van K.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Tabernero, Josep] Univ Vic Univ Cent Catalunya, Vall dHebron Hosp Campus, Barcelona, Spain.
   [Tabernero, Josep] Univ Vic Univ Cent Catalunya, Vall dHebron Inst Oncol, Barcelona, Spain.
   [Bekaii-Saab, Tanios] Mayo Clin, Phoenix, AZ USA.
   [Taieb, Julien] Univ Paris, Georges Pompidou European Hosp, Paris, France.
   [Yoshino, Takayuki] Natl Canc Ctr Hosp East, Kashiwa, Chiba, Japan.
   [Manji, Gulam] Columbia Univ, Irving Med Ctr, New York, NY USA.
   [Manji, Gulam] NewYork Presbyterian Hosp, New York, NY USA.
   [Fernandez, Kathrine] Pfizer Global Prod Dev Oncol, Cambridge, MA USA.
   [Abbattista, Antonello] Pfizer Global Product Dev Oncol, Milan, Italy.
   [Zhang, Xiaosong] Pfizer, New York, NY USA.
C3 Autonomous University of Barcelona; Autonomous University of Barcelona;
   Vall d'Hebron Institut d'Oncologia (VHIO); University of Texas System;
   UTMD Anderson Cancer Center; Universitat de Vic - Universitat Central de
   Catalunya (UVic-UCC); Vall d'Hebron Institut d'Oncologia (VHIO);
   Universitat de Vic - Universitat Central de Catalunya (UVic-UCC); Mayo
   Clinic; Mayo Clinic Phoenix; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris Cite; Hopital Universitaire Europeen Georges-Pompidou -
   APHP; National Cancer Center - Japan; NewYork-Presbyterian Hospital;
   Columbia University; NewYork-Presbyterian Hospital; Pfizer; Pfizer
RP Morris, VK (corresponding author), Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
EM VKMorris@mdanderson.org
RI Morris, Van/KIE-0809-2024; Bekaii-Saab, Tanios/AGD-6851-2022
FU Pfizer, Inc.
FX The SEAMARK study was sponsored by Pfizer, Inc. This study is in
   collaboration with Merck Sharp & Dohme LLC, a subsidiary of Merck & Co.,
   Inc., Rahway, NJ, USA, Merck KGaA Darmstadt, Germany, and Eli Lilly and
   Company.
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NR 45
TC 5
Z9 5
U1 1
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PD APR
PY 2024
VL 20
IS 11
BP 653
EP 663
DI 10.2217/fon-2022-1249
EA OCT 2023
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PP6E2
UT WOS:001083403100001
PM 37815847
OA hybrid
DA 2025-01-04
ER

PT J
AU Jong, KXJ
   Mohamed, EHM
   Ibrahim, ZA
AF Jong, Kelly Xue Jing
   Mohamed, Elsa Haniffah Mejia
   Ibrahim, Zaridatul Aini
TI Escaping cell death via TRAIL decoy receptors: a systematic review of
   their roles and expressions in colorectal cancer
SO APOPTOSIS
LA English
DT Review
DE Colorectal cancer; Tumour necrosis factor (TNF)-related
   apoptosis-inducing ligand (TRAIL); Apoptosis; Decoy receptor;
   Osteoprotegerin (OPG); Targeted therapy
ID APOPTOSIS-INDUCING LIGAND; NF-KAPPA-B; COLON-CARCINOMA; OSTEOPROTEGERIN
   OPG; MONOCLONAL-ANTIBODY; DOWN-REGULATION; UP-REGULATION; TUMOR-CELLS;
   IMMUNE SURVEILLANCE; SIGNALING PATHWAY
AB The development of targeted therapy such as tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-based therapy has gained increasing attention as a promising new approach in cancer therapy. TRAIL specifically targets cancer cells while sparing the normal cells, thus, limiting the known side effects of the majority anti-cancer therapies. As more extensive research and clinical trials are conducted, resistance to TRAIL molecule has become one of the significant issues associated with the failure of TRAIL in treating colorectal cancer (CRC). To date, the exact mechanism by which TRAIL resistance may have occurred remains unknown. Interestingly, recent studies have revealed the critical role of the TRAIL decoy receptor family; consisting of decoy receptor 1 (DcR1; also known as TRAIL-R3), decoy receptor 2 (DcR2; also known as TRAIL-R4), and osteoprotegerin (OPG) in driving TRAIL resistance. This review highlights the expression of the decoy receptors in CRC and its possible association with the reduction in sensitivity towards TRAIL treatment based on the currently available in vitro, in vivo, and human studies. Additionally, discrepancies between the outcomes from different research groups are discussed, and essential areas are highlighted for future investigation of the roles of decoy receptors in modulating TRAIL-induced apoptosis. Overcoming TRAIL resistance through modulating the expression(s) and elucidating the role(s) of TRAIL decoy receptors hold great promise for TRAIL-based therapies to be extensively explored in treating human cancers including CRC.
C1 [Jong, Kelly Xue Jing; Mohamed, Elsa Haniffah Mejia; Ibrahim, Zaridatul Aini] Univ Malaya, Fac Med, Dept Pharmacol, Kuala Lumpur 50603, Malaysia.
C3 Universiti Malaya
RP Ibrahim, ZA (corresponding author), Univ Malaya, Fac Med, Dept Pharmacol, Kuala Lumpur 50603, Malaysia.
EM zaridatulaini@ummc.edu.my
RI MOHAMED, ELSA/B-8451-2010; Ibrahim, Zaridatul Aini/N-2626-2017
OI Mejia Mohamed, Elsa Haniffah/0000-0001-5091-2970
FU MAKNA Cancer Research Award [PV001-2021]
FX This research was supported by the MAKNA Cancer Research Award 2020
   (Grant Number: PV001-2021).
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NR 98
TC 10
Z9 10
U1 0
U2 12
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 2022
VL 27
IS 11-12
BP 787
EP 799
DI 10.1007/s10495-022-01774-5
EA OCT 2022
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 5U5OD
UT WOS:000864953100001
PM 36207556
DA 2025-01-04
ER

PT J
AU Wang, CK
   Fakih, MW
AF Wang, Chongkai
   Fakih, Marwan
TI Targeting KRAS in Colorectal Cancer
SO CURRENT ONCOLOGY REPORTS
LA English
DT Review
DE KRAS; Colorectal cancer; Targeting therapy
ID CELL LUNG-CANCER; TRANSFERASE INHIBITOR R115777; DABRAFENIB PLUS
   TRAMETINIB; ADVANCED SOLID TUMORS; AMG 510; KRAS(G12C) INHIBITOR;
   PROTEIN TRANSFERASE; DOSE-ESCALATION; RAS MUTATIONS; MUTANT KRAS
AB Purpose of ReviewMutations in kirsten rat sarcoma viral oncogene homolog (KRAS) are the most frequently observed genomic alterations in human cancers. No KRAS targeting therapy has been approved despite more than three decades of efforts. Encouraging progress has been made in targeting KRAS(G12C) with KRAS(G12C) specific covalent inhibitors in the past few years. Herein, we review the recent breakthroughs in KRAS targeting.Recent FindingsKRAS(G12C) mutation was found in 14% of non-small cell lung cancer (NSCLC) and 3% of colorectal cancer. Recently, highly potent KRAS(G12C) specific inhibitors have been developed and demonstrated potent activity in preclinical models. Early results from phase 1 clinical trials with sotorasib and MRTX849 show promising antitumor activity in NSCLC, colorectal cancer and other solid tumors harboring KRAS(G12C) mutation.SummaryFor the first time, the preclinical success of targeting KRAS has translated into clinical benefits, which holds the potential of transforming clinical management of KRAS mutated solid tumors. Additional efforts are needed to identify biomarkers that predict response to KRAS inhibition in patients with KRAS(G12C) as well as to develop strategies to overcome resistance.
C1 [Wang, Chongkai; Fakih, Marwan] City Hope Comprehens Canc Ctr, Dept Med Oncol & Therapeut Res, 1500 E Duarte Rd, Duarte, CA 91010 USA.
C3 City of Hope
RP Fakih, MW (corresponding author), City Hope Comprehens Canc Ctr, Dept Med Oncol & Therapeut Res, 1500 E Duarte Rd, Duarte, CA 91010 USA.
EM mfakih@coh.org
OI Fakih, Marwan/0000-0002-6554-5488
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NR 90
TC 27
Z9 30
U1 8
U2 66
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 FEB 13
PY 2021
VL 23
IS 3
AR 28
DI 10.1007/s11912-021-01022-0
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QK6QV
UT WOS:000620509800001
PM 33582927
DA 2025-01-04
ER

PT J
AU Yeh, JH
   Tsai, HL
   Chen, YC
   Li, CC
   Huang, CW
   Chang, TK
   Su, WC
   Chen, PJ
   Liu, YP
   Wang, JY
AF Yeh, Jen-Hao
   Tsai, Hsiang-Lin
   Chen, Yen-Cheng
   Li, Ching-Chun
   Huang, Ching-Wen
   Chang, Tsung-Kun
   Su, Wei-Chih
   Chen, Po-Jung
   Liu, Yu-Peng
   Wang, Jaw-Yuan
TI BRAF, MEK, and EGFR Triplet Inhibitors as Salvage Therapy in
   <i>BRAF</i>-Mutated Metastatic Colorectal Cancer-A Case Series Study
   <i>Target Therapy of</i> BRAF-<i>Mutated mCRC</i>
SO MEDICINA-LITHUANIA
LA English
DT Article
DE metastatic colorectal cancer; BRAF mutation; triple target therapy
ID KRAS MUTATIONS; COLON-CANCER; DABRAFENIB; TRAMETINIB; CETUXIMAB
AB Backgroundand objectives: Patients with BRAF-mutated metastatic colorectal cancer have considerably poorer responses to conventional systemic treatment. The real-world effects of triplet therapy with BRAF, mitogen-activated protein kinase kinase, and epidermal growth factor receptor inhibitors in Asia have not been well-reported. Materials and Methods: This single-center case series included patients with BRAF-mutated metastatic colorectal cancer undergoing triplet therapy after failure of prior systemic treatment from 2016 to 2020. The primary outcome was progression-free survival, and secondary outcomes were overall survival, response rate, disease control rate, and adverse events. Results: Nine eligible patients with BRAF-mutated metastatic colorectal cancer receiving triplet therapy were enrolled, with a median follow-up time of 14.5 months (range, 1-26). Most patients (88.8%) had two or more prior systemic treatments, and the triplet regimen was mainly dabrafenib, trametinib, and panitumumab. The overall response rate and disease control rate were 11.1% and 33.3%, respectively. Median progression-free survival and overall survival were 2.9 and 7.4 months, respectively, and a trend toward better overall survival was found with left-sided metastatic colorectal cancer compared with right-sided disease (9.2 vs. 6.9 months, p = 0.093). Adverse events were mostly Grade 1-2, including nausea, hypertension, gastrointestinal symptoms, and skin disorders. Conclusions: In this single-center case series, triplet therapy with BRAF, mitogen-activated protein kinase kinase, and epidermal growth factor receptor inhibitors in BRAF-mutated metastatic colorectal cancer had an acceptable safety profile and reasonable efficacy.
C1 [Yeh, Jen-Hao; Liu, Yu-Peng; Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung 80708, Taiwan.
   [Yeh, Jen-Hao] Dachang Hosp, Div Gastroenterol & Hepatol, Dept Internal Med, Kaohsiung 80794, Taiwan.
   [Yeh, Jen-Hao] I Shou Univ, Dept Med Technol, Coll Med, Kaohsiung 82445, Taiwan.
   [Yeh, Jen-Hao] E DA Hosp, Div Gastroenterol & Hepatol, Dept Internal Med, Kaohsiung 82445, Taiwan.
   [Tsai, Hsiang-Lin; Chen, Yen-Cheng; Li, Ching-Chun; Huang, Ching-Wen; Chang, Tsung-Kun; Su, Wei-Chih; Chen, Po-Jung; Wang, Jaw-Yuan] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Div Colorectal Surg, Dept Surg, Kaohsiung 80708, Taiwan.
   [Tsai, Hsiang-Lin; Huang, Ching-Wen; Wang, Jaw-Yuan] Kaohsiung Med Univ, Dept Surg, Coll Med, Fac Med, Kaohsiung 80708, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Ctr Canc Res, Kaohsiung 80708, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Ctr Liquid Biopsy & Cohort Res, Kaohsiung 80708, Taiwan.
   [Wang, Jaw-Yuan] Pingtung Hosp, Minist Hlth & Welf, Pingtung 90054, Taiwan.
C3 Kaohsiung Medical University; I Shou University; E-Da Hospital;
   Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University; Kaohsiung Medical University; Kaohsiung
   Medical University
RP Wang, JY (corresponding author), Kaohsiung Med Univ, Grad Inst Clin Med, Coll Med, Kaohsiung 80708, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Div Colorectal Surg, Dept Surg, Kaohsiung 80708, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Dept Surg, Coll Med, Fac Med, Kaohsiung 80708, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Ctr Canc Res, Kaohsiung 80708, Taiwan.; Wang, JY (corresponding author), Kaohsiung Med Univ, Ctr Liquid Biopsy & Cohort Res, Kaohsiung 80708, Taiwan.; Wang, JY (corresponding author), Pingtung Hosp, Minist Hlth & Welf, Pingtung 90054, Taiwan.
EM b9202078@gmail.com; chunpin870132@yahoo.com.tw; googoogi05@gmail.com;
   dobird05@yahoo.com.tw; baseball5824@yahoo.com.tw;
   tsungkunchang@gmail.com; lake0126@yahoo.com.tw; glaudiotennis@gmail.com;
   ypliu@kmu.edu.tw; cy614112@ms14.hinet.net
RI Liu, Yupeng/P-3181-2018; Jaw-Yuan, Wang/AFS-8845-2022
OI Liu, Yu-Peng/0000-0002-2716-0050; Wang, Jaw-Yuan/0000-0002-7705-2621;
   Chang, Tsung-Kun/0000-0001-9760-5070
FU Ministry of Science and Technology [MOST 109-2314-B-037-035, MOST
   109-2314-B-037-040, MOST 109-2314-B-037-046-MY3,
   MOST110-2314-B-037-097]; Ministry of Health and Welfare
   [MOHW109-TDU-B-212-134026, MOHW109-TDU-B-212-114006,
   MOHW110-TDU-B-212-1140026]; health and welfare surcharge of on tobacco
   products; Kaohsiung Medical University Hospital [KMUH109-9R32,
   KMUH109-9R33, KMUH109-9R34, KMUH109-9M30, KMUH-DK(C)110010,
   KMUH109-9M31, KMUH-DK(B)110004-3), KMUH109-9M32, KMUH109-9M33,
   KMU-TC109A04-1, KMU-TC109B05]; KMU Center for Cancer Research
   [KMUHSA11013]; KMU Center for Liquid Biopsy and Cohort Research Center
   Grant [110010]; Kaohsiung Medical University; Grant of Taiwan Precision
   Medicine Initiative, Academia Sinica, Taiwan, R.O.C;  [KMUHSA10903];
   Academy of Finland (AKA) [110004] Funding Source: Academy of Finland
   (AKA)
FX This work was supported by grants through funding from the Ministry of
   Science and Technology (MOST 109-2314-B-037-035, MOST
   109-2314-B-037-040, MOST 109-2314-B-037-046-MY3, MOST110-2314-B-037-097)
   and the Ministry of Health and Welfare (MOHW109-TDU-B-212-134026,
   MOHW109-TDU-B-212-114006, MOHW110-TDU-B-212-1140026) and funded by the
   health and welfare surcharge of on tobacco products, and the Kaohsiung
   Medical University Hospital (KMUH109-9R32, KMUH109-9R33, KMUH109-9R34,
   KMUH109-9M30, KMUH109-9M31, KMUH109-9M32, KMUH109-9M33, KMUHSA10903,
   KMUHSA11013, KMUH-DK(C)110010, KMUH-DK(B)110004-3) and KMU Center for
   Cancer Research (KMU-TC109A04-1) as well as and a KMU Center for Liquid
   Biopsy and Cohort Research Center Grant (KMU-TC109B05), Kaohsiung
   Medical University. In addition, this study was supported by the Grant
   of Taiwan Precision Medicine Initiative, Academia Sinica, Taiwan, R.O.C.
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NR 31
TC 8
Z9 8
U1 0
U2 2
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 DEC
PY 2021
VL 57
IS 12
AR 1339
DI 10.3390/medicina57121339
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA XW9DM
UT WOS:000735910400001
PM 34946284
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Liu, ZH
   Liu, H
   Cheng, JL
   Wang, HL
   Yang, YF
   Le, J
   Liu, YL
AF Liu, Zihan
   Liu, Han
   Cheng, Jialing
   Wang, Hongliang
   Yang, Yanfang
   Le, Jun
   Liu, Yuling
TI Strategies and opportunities of micro/nano delivery systems for targeted
   therapy of ulcerative colitis: Focus on underlying mechanisms and future
   perspectives
SO CHINESE CHEMICAL LETTERS
LA English
DT Article
DE Ulcerative colitis; Physiological characteristics; Colon-specific drug
   delivery; Mechanisms of action; Targeted therapy of UC
ID INFLAMMATORY-BOWEL-DISEASE; FECAL MICROBIOTA TRANSPLANTATION; ORAL-DRUG
   DELIVERY; GASTROINTESTINAL MUCUS; MAINTENANCE THERAPY; ECCO GUIDELINES;
   GUT MICROBIOME; COLON; NANOPARTICLES; MICROPARTICLES
AB Ulcerative colitis (UC) is a common progressive inflammatory disease whose incidence has increased rapidly in recent years, and can develop into colorectal cancer in severe cases. There are currently no adequate or effective treatments for UC due to the fact that some patients have found suboptimal results after repeated administration, while others have experienced adverse effects. With the rapid development of nanotechnology, developing innovative colon-targeting platforms is essential to improving efficacy, re-ducing side effects, and improving patient compliance. In this review, we summarize the pathophysiolog-ical characteristics of UC and the most recent status of numerous nanodrug delivery systems based on different tar geting mechanisms in treating UC. Oral, intravenous, and rectal drug delivery nanoparticles targeting the colon are discussed, which can provide ideas for the design of colon-targeting nanoparticles for the treatment of colon diseases, especially for the treatment of UC. Last but not least, we provide a glimpse into the future of colon-targeted delivery systems, as well as future advancements in the field.(c) 2023 Published by Elsevier B.V. on behalf of Chinese Chemical Society and Institute of Materia Medica, Chinese Academy of Medical Sciences.
C1 [Liu, Zihan; Liu, Han; Cheng, Jialing; Wang, Hongliang; Yang, Yanfang; Le, Jun; Liu, Yuling] Chinese Acad Med Sci & Peking Union Med Coll, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, Beijing 100050, Peoples R China.
   [Liu, Zihan; Liu, Han; Cheng, Jialing; Wang, Hongliang; Yang, Yanfang; Le, Jun; Liu, Yuling] Chinese Acad Med Sci & Peking Union Med Coll, Inst Mat Med, Beijing Key Lab Drug Delivery Technol & Novel Form, Beijing 100050, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College; Chinese Academy of Medical Sciences -
   Peking Union Medical College; Peking Union Medical College
RP Le, J; Liu, YL (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, Beijing 100050, Peoples R China.; Le, J; Liu, YL (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Inst Mat Med, Beijing Key Lab Drug Delivery Technol & Novel Form, Beijing 100050, Peoples R China.
EM yelinghao@imm.ac.cn; ylliu@imm.ac.cn
RI liu, qi/KHC-7509-2024
OI liu, han/0009-0003-8160-5780; Liu, Zihan/0009-0007-7831-4551; Ye,
   Jun/0000-0002-0536-6154
FU Beijing Nova Program [Z21110 0 0 02121127, 20220484219]; Beijing Natural
   Sci- ence Foundation [L212059]; Fundamental Research Funds for the
   Central Universities [3332021101]; CAMS Innovation Fund for Medical
   Sciences (CIFMS) [2021-I2M-1-026, 2021- I2M-1-028]
FX This work was financially supported by Beijing Nova Program (Nos. Z21110
   0 0 02121127 and 20220484219) , Beijing Natural Sci- ence Foundation
   (No. L212059) , Fundamental Research Funds for the Central Universities
   (No. 3332021101) , and CAMS Innovation Fund for Medical Sciences (CIFMS,
   Nos. 2021-I2M-1-026 and 2021- I2M-1-028) .
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NR 210
TC 5
Z9 6
U1 11
U2 31
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1001-8417
EI 1878-5964
J9 CHINESE CHEM LETT
JI Chin. Chem. Lett.
PD FEB
PY 2024
VL 35
IS 2
AR 109074
DI 10.1016/j.cclet.2023.109074
EA NOV 2023
PG 13
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA CL0U7
UT WOS:001125298000001
DA 2025-01-04
ER

PT J
AU Kawaguchi, Y
   De Bellis, M
   Panettieri, E
   Duwe, G
   Vauthey, JN
AF Kawaguchi, Yoshikuni
   De Bellis, Mario
   Panettieri, Elena
   Duwe, Gregor
   Vauthey, Jean-Nicolas
TI Debate Improvements in Systemic Therapies for Liver Metastases Will
   Increase the Role of Locoregional Treatments
SO SURGICAL ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Colorectal liver metastasis; Resection; Chemotherapy; Molecular-targeted
   therapy; Conversion therapy; Two-stage hepatectomy; Neuroendocrine liver
   metastasis; Gastric liver metastasis
ID HEPATIC VEIN EMBOLIZATION; RANDOMIZED PHASE-III; COLORECTAL-CANCER;
   2-STAGE HEPATECTOMY; GASTRIC-CANCER; NEUROENDOCRINE METASTASES; SURGICAL
   RESECTION; 1ST-LINE TREATMENT; MAJOR HEPATECTOMY; PLUS BEVACIZUMAB
C1 [Kawaguchi, Yoshikuni; De Bellis, Mario; Panettieri, Elena; Duwe, Gregor; Vauthey, Jean-Nicolas] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX 77030 USA.
   [Kawaguchi, Yoshikuni] Univ Tokyo, Grad Sch Med, Dept Surg, Hepatobiliary Pancreat Surg Div, Tokyo, Japan.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Tokyo
RP Vauthey, JN (corresponding author), 1515 Holcombe Blvd,Unit 1484, Houston, TX 77030 USA.
EM jvauthey@mdanderson.org
RI De Bellis, Mario/IQS-4997-2023; Panettieri, Elena/AAZ-1874-2020;
   Kawaguchi, Yoshikuni/AAB-1718-2022
OI Panettieri, Elena/0000-0001-7815-8092; DE BELLIS,
   MARIO/0000-0001-7932-5921; Duwe, Gregor/0000-0001-7008-1238
FU National Institutes of Health [T32 CA 009599]; MD Anderson Cancer Center
   Support Grant [CA016672]
FX This research was supported in part by the National Institutes of Health
   (T32 CA 009599) and the MD Anderson Cancer Center Support Grant,
   CA016672.
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NR 66
TC 4
Z9 4
U1 0
U2 8
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1055-3207
EI 1558-5042
J9 SURG ONCOL CLIN N AM
JI Surg. Oncol. Clin. N. Am.
PD JAN
PY 2021
VL 30
IS 1
BP 205
EP 218
DI 10.1016/j.soc.2020.08.009
PG 14
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA OY8XY
UT WOS:000594525000015
PM 33220806
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Chung, SS
   Adekoya, D
   Enenmoh, I
   Clarke, O
   Wang, P
   Sarkyssian, M
   Wu, Y
   Vadgama, JV
AF Chung, Seyung S.
   Adekoya, Debbie
   Enenmoh, Ikechukwu
   Clarke, Orette
   Wang, Piwen
   Sarkyssian, Marianna
   Wu, Yong
   Vadgama, Jaydutt V.
TI Salinomycin Abolished STAT3 and STAT1 Interactions and Reduced
   Telomerase Activity in Colorectal Cancer Cells
SO ANTICANCER RESEARCH
LA English
DT Article
DE Cancer stem cells; STAT3; STAT1; telomerase; salinomycin; MST-312
ID GROWTH; EXPRESSION; MST-312
AB Background: Colorectal cancer is the third leading cause of cancer-related mortality in most developed countries. This mortality is mainly due to the metastatic progression to the liver with frequent recurrence. Colorectal cancer remains a therapeutic challenge and this has intensified the search for new drug targets. In an effort to establish a novel targeted-therapy, we studied the molecular mechanisms of cancer stem cell inhibitor salinomycin. Materials and Methods: Co-immunoprecipitation was performed to examine STAT3-STAT1 protein interactions. Telomerase activity was measured by polymerase chain reaction (PCR) and ELISA assays. Apoptosis and cell stress arrays were analyzed to identify key proteins responding to salinomycin treatments. Results: IL-6 and TNF-alpha induced STAT3 and STAT1 interactions, however the interactions were abolished by salinomycin challenge. Salinomycin reduced cancer stem cell phenotype and decreased telomerase activity of colorectal cancer cells. Conclusion: Our work uncovers a new mechanism through which salinomycin inhibits cancer stemness suggesting a novel targeted-therapy for metastatic colorectal cancer.
C1 [Chung, Seyung S.; Adekoya, Debbie; Enenmoh, Ikechukwu; Clarke, Orette; Wang, Piwen; Sarkyssian, Marianna; Wu, Yong; Vadgama, Jaydutt V.] Dept Internal Med, Div Canc Res & Training, Los Angeles, CA USA.
   [Chung, Seyung S.; Adekoya, Debbie; Enenmoh, Ikechukwu; Clarke, Orette; Wang, Piwen; Sarkyssian, Marianna; Wu, Yong; Vadgama, Jaydutt V.] Charles R Drew Univ Med & Sci, Los Angeles, CA USA.
   [Chung, Seyung S.; Wang, Piwen; Sarkyssian, Marianna; Wu, Yong; Vadgama, Jaydutt V.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA USA.
   [Vadgama, Jaydutt V.] Jonsson Comprehens Canc Ctr, Los Angeles, CA USA.
C3 Charles R. Drew University of Medicine & Science; University of
   California System; University of California Los Angeles; University of
   California Los Angeles Medical Center; David Geffen School of Medicine
   at UCLA; UCLA Jonsson Comprehensive Cancer Center
RP Chung, SS; Vadgama, JV (corresponding author), Charles R Drew Univ Med & Sci, Div Canc Res & Training, 1731 East 120th St, Los Angeles, CA 90059 USA.; Vadgama, JV (corresponding author), Univ Calif Los Angeles, Sch Med, 1731 East 120th St, Los Angeles, CA 90059 USA.; Vadgama, JV (corresponding author), Charles R Drew Univ Med & Sci, Ctr Eliminate Canc Hlth Dispar, Dept Internal Med, 1731 East 120th St, Los Angeles, CA 90059 USA.
EM seyungchung@cdrewu.edu; jayvadgama@cdrewu.edu
OI Enenmoh, Ikechukwu/0000-0003-4158-5087
FU National Institutes of Health (NIH, NCI, NIMHD, NCATS) [U54 CA143931,
   U54MD007598, UL1TR000124]; NIMHD [R25 MD 007610]; pilot project [U54 MD
   007598]; Urban Health Institute-CDU [S21 MD 000103]; Accelerating
   Excellence in Translational Science Pilot [G0812D05]; National
   Institutes of Health ( NCI, NIMHD) [U54 CA143931, U54MD0075984]; NIH/NCI
   [SC1CA200517]
FX This work was supported by the National Institutes of Health (NIH, NCI,
   NIMHD, NCATS) Grants to J.V. Vadgama: U54 CA143931, U54MD007598,
   UL1TR000124. S. Steven Chung is a scholar supported by the Clinical
   Research Education and Career Development by the NIMHD R25 MD 007610,
   pilot project award from U54 MD 007598 and Emerging scientist award from
   the Urban Health Institute-CDU S21 MD 000103. Research reported in this
   publication was also supported by Accelerating Excellence in
   Translational Science Pilot Grants G0812D05, pilot project award from
   the National Institutes of Health ( NCI, NIMHD) Grants: U54 CA143931 and
   U54MD0075984, and NIH/NCI SC1CA200517 to Y. Wu. The content is solely
   the responsibility of the authors and does not necessarily represent the
   official views of the National Institutes of Health. We deeply
   appreciate the division of cancer research and training members for
   their helpful comments and suggestions.
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NR 22
TC 24
Z9 26
U1 0
U2 8
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 FEB
PY 2017
VL 37
IS 2
BP 445
EP 453
DI 10.21873/anticanres.11336
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EO7WQ
UT WOS:000396901200007
PM 28179289
OA Green Accepted, Bronze
DA 2025-01-04
ER

PT J
AU Fritz, J
   Lefebvre, O
   Fernandez, A
   Schmidt, J
   Bagnard, D
AF Fritz, Justine
   Lefebvre, Olivier
   Fernandez, Aurore
   Schmidt, Jordane
   Bagnard, Dominique
TI Prediction of Drug Efficacy in Colon Cancer Preclinical Models Using a
   Novel Ranking Method of Gene Expression
SO CANCERS
LA English
DT Article
DE gene expression; drug efficacy; targeted therapy selection; molecular
   profiling
ID MOLECULAR CLASSIFICATION; COLORECTAL-CANCER; RAS MUTATIONS;
   HETEROGENEITY; HALLMARKS; FLUOROURACIL; LEUCOVORIN; IRINOTECAN;
   SURVIVAL; TISSUES
AB The presence of stromal cells in tumors is altering the significance of molecular profiling when using standard methods of gene expression quantification. We developed a novel normalization method to rank target gene expression in tumor samples by comparisons with reference samples representing the different cell types found in a tumor. The score for each target gene obtained after normalization, is aimed to be predictive of targeted therapies efficiency. We performed this qPCR analysis on human colorectal cancers to demonstrate the importance of reference samples to obtain accurate data and on a collection of patient-derived xenografted (PDX) colon tumors treated with Cetuximab (anti-EGFR) to demonstrate that the calculated EGFR score is predictive of Cetuximab efficacy. Interestingly, the score allowed to select an efficient treatment in a PDX model refractory to standard of care. This method is opening a novel way to predict targeted therapy efficiency which could be extended to several tumor types, and to unlimited target genes.
C1 [Fritz, Justine; Lefebvre, Olivier; Fernandez, Aurore; Schmidt, Jordane; Bagnard, Dominique] Univ Strasbourg, INSERM U1109, Microenvironm Niche Tumorigenesis & Targeted Ther, Labex Medalis Federat Med Translat, F-67000 Strasbourg, France.
   [Bagnard, Dominique] Univ Strasbourg, INSERM U1119, BMNST Lab, Labex Medalis,Federat Med Translat, F-67000 Strasbourg, France.
C3 Universites de Strasbourg Etablissements Associes; Universite de
   Strasbourg; Institut National de la Sante et de la Recherche Medicale
   (Inserm); Institut National de la Sante et de la Recherche Medicale
   (Inserm); Universites de Strasbourg Etablissements Associes; Universite
   de Strasbourg
RP Bagnard, D (corresponding author), Univ Strasbourg, INSERM U1109, Microenvironm Niche Tumorigenesis & Targeted Ther, Labex Medalis Federat Med Translat, F-67000 Strasbourg, France.; Bagnard, D (corresponding author), Univ Strasbourg, INSERM U1119, BMNST Lab, Labex Medalis,Federat Med Translat, F-67000 Strasbourg, France.
EM jfritz@adaptherapy.com; lefebvre@unistra.fr; Aurore.Fernandez@chuv.ch;
   jordane.schmidt@unistra.fr; bagnard@unistra.fr
RI Bagnard, Dominique/I-6535-2013; Lefebvre, Olivier/I-2388-2016
OI fernandez, aurore/0000-0001-9780-5152; Lefebvre,
   Olivier/0000-0001-9130-9174; Bagnard, Dominique/0000-0002-5261-902X
FU French government; LABEX [ANR-10-LABX-0034_Medalis]
FX This work has been published within the LABEX ANR-10-LABX-0034_Medalis
   and received a financial support from the French government managed by
   the "Agence National de la Recherche" under the "Programme
   d'investissements d'avenir", SATT Conectus "PREDMED program".
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NR 36
TC 1
Z9 1
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2020
VL 12
IS 1
AR 149
DI 10.3390/cancers12010149
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KQ3KZ
UT WOS:000516826700149
PM 31936310
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Protsenko, SA
   Semionova, AI
   Komarov, YI
   Aleksakhina, SN
   Ivantsov, AO
   Iyevleva, AG
   Imyanitov, EN
AF Protsenko, Svetlana A.
   Semionova, Anna I.
   Komarov, Yuri I.
   Aleksakhina, Svetlana N.
   Ivantsov, Alexandr O.
   Iyevleva, Aglaya G.
   Imyanitov, Evgeny N.
TI BRAF-mutated clear cell sarcoma is sensitive to vemurafenib treatment
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Clear cell sarcoma; BRAF; Vemurafenib; Review
ID PAPILLARY THYROID-CANCER; METASTATIC COLORECTAL-CANCER; LUNG
   ADENOCARCINOMA; DRAMATIC RESPONSE; INHIBITOR DABRAFENIB; COMPLETE
   REMISSION; TARGETED THERAPY; V600E MUTATION; RAPID RESPONSE; LEUKEMIA
AB We report a patient with a metastatic relapse of clear cell sarcoma, whose tumor harbored BRAF V600E mutation. Standard chemotherapy with doxorubicin and ifosfamide failed to slow the disease progression. Subsequent administration of vemurafenib (960 mg twice a day) resulted in complete tumor response after 8 weeks of treatment. Literature data on the use of vemurafenib and dabrafenib in non-melanoma BRAF-mutated tumors are reviewed.
C1 [Protsenko, Svetlana A.; Semionova, Anna I.; Komarov, Yuri I.; Aleksakhina, Svetlana N.; Ivantsov, Alexandr O.; Imyanitov, Evgeny N.] NN Petrov Inst Oncol, Mol Oncol Lab, St Petersburg 197758, Russia.
   [Iyevleva, Aglaya G.; Imyanitov, Evgeny N.] St Petersburg Pediat Med Univ, St Petersburg 194100, Russia.
   [Imyanitov, Evgeny N.] II Mechnikov North Western Med Univ, St Petersburg 191015, Russia.
   [Imyanitov, Evgeny N.] St Petersburg State Univ, St Petersburg 199034, Russia.
C3 N.N. Petrov Research Institute of Oncology; Saint Petersburg State
   Pediatric Medical University; North-Western State Medical University
   named after I.I. Mechnikov; Saint Petersburg State University
RP Imyanitov, EN (corresponding author), NN Petrov Inst Oncol, Mol Oncol Lab, Pesochny 2, St Petersburg 197758, Russia.
EM evgeny@imyanitov.spb.ru
RI Ivantsov, Alexandr/Q-9953-2016; Iyevleva, Aglaya/P-8305-2016; Imyanitov,
   Evgeny/ABG-8619-2021; Aleksakhina, Svetlana/B-2136-2013; Komarov,
   Yuriy/A-7099-2015
OI Komarov, Yuriy/0000-0003-3256-0451; Aleksakhina,
   Svetlana/0000-0002-2149-7728
FU Russian Scientific Fund [14-15-00528]; Russian Science Foundation
   [14-15-00528] Funding Source: Russian Science Foundation
FX This work has been supported by the Russian Scientific Fund (grant
   number 14-15-00528). We are grateful to Dr. Hannah West (University of
   Cambridge School of Clinical Medicine, UK) for a critical reading of
   this manuscript.
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NR 54
TC 19
Z9 23
U1 0
U2 5
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 OCT
PY 2015
VL 33
IS 5
BP 1136
EP 1143
DI 10.1007/s10637-015-0280-0
PG 8
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA CW4PD
UT WOS:000364972700017
PM 26286452
DA 2025-01-04
ER

PT J
AU Elvas, F
   Boddaert, J
   Vangestel, C
   Pak, K
   Gray, B
   Kumar-Singh, S
   Staelens, S
   Stroobants, S
   Wyffels, L
AF Elvas, Filipe
   Boddaert, Jan
   Vangestel, Christel
   Pak, Koon
   Gray, Brian
   Kumar-Singh, Samir
   Staelens, Steven
   Stroobants, Sigrid
   Wyffels, Leonie
TI <SUP>99m</SUP>Tc-Duramycin SPECT Imaging of Early Tumor Response to
   Targeted Therapy: A Comparison with <SUP>18</SUP>F-FDG PET
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE cell death imaging; Tc-99m-duramycin SPECT; response evaluation;
   targeted therapy; colorectal cancer
ID POSITRON-EMISSION-TOMOGRAPHY; DEATH RECEPTOR 5; CELL-DEATH; FDG-PET;
   APOPTOSIS; CANCER; CONATUMUMAB; ACTIVATION; PHOSPHATIDYLETHANOLAMINE;
   LYMPHOMA
AB Molecular imaging of cell death may provide a detailed readout of the cellular response to novel therapies and prognostic information on tumor treatment efficacy, assisting in the design of individualized therapy. We compared the predictive power of cell death imaging using Tc-99m-duramycin with the current gold standard F-18-FDG for treatment response evaluation after targeted therapy. Methods: Early therapy response evaluation was assessed by Tc-99m-duramycin SPECT and F-18-FDG PET imaging in treatment-sensitive COL0205 and treatment-resistant HT29 human colorectal cancer xenografts 24 h after a single dose of conatumumab or IgG1 control. The specificity of Tc-99m-duramycin for apoptosis was assessed using Tc-99m-linear duramycin control radiotracer. Radiotracer uptake was validated ex vivo by gamma-counting and autoradiography and compared with cleaved caspase-3 (CC3) activation and DNA fragmentation (TdT-mediated dUTP nick-end labeling [TUNEL]). Data were analyzed with the Student t test and Pearson correlation. All statistical tests were 2-sided. Results: COL0205 tumor uptake of 88mTc-duramycin was increased 7-fold from baseline in conatumumab- versus IgG1-treated control mice (P < 0.001), in good correlation with histologic analysis of apoptosis (CC3, r = 0.842, and TUNEL, r = 0.894; P < 0.001). No response was detected in HT29 tumors. No change in Tc-99m-linear duramycin uptake could be detected in COL0205 tumors after treatment, indicating specificity of the Tc-99m-duramycin tumor signal. 18F-FDG uptake was not significantly increased from baseline in conatumumab-versus IgG1treated COL0205 and HT29 tumor bearing mice (P = 0.104 and 0.779, respectively) and did not correlate with immunohistochemical evidence of apoptosis, Conclusion: We have demonstrated that 88mTc-duramycin specifically accumulates in apoptotic tumors in which 18F-FDG was not able to differentiate responding from nonresponding tumors early after treatment. Tc-99m-duramycin holds promise as a noninvasive imaging radiotracer for early treatment evaluation in the clinic.
C1 [Elvas, Filipe; Vangestel, Christel; Staelens, Steven; Stroobants, Sigrid; Wyffels, Leonie] Univ Antwerp, Mol Imaging Ctr Antwerp, Antwerp, Belgium.
   [Elvas, Filipe; Vangestel, Christel; Stroobants, Sigrid; Wyffels, Leonie] Univ Antwerp Hosp, Dept Nucl Med, Wilrijkstr 10, B-2650 Edegem, Belgium.
   [Boddaert, Jan; Kumar-Singh, Samir] Univ Antwerp, Lab Mol Pathol Cell Biol & Histol, Antwerp, Belgium.
   [Pak, Koon; Gray, Brian] Mol Targeting Technol Inc, W Chester, PA USA.
C3 University of Antwerp; University of Antwerp; University of Antwerp
RP Elvas, F; Wyffels, L (corresponding author), Univ Antwerp Hosp, Dept Nucl Med, Wilrijkstr 10, B-2650 Edegem, Belgium.
EM filipe.elvas@uantwerpen.be; leonie.wyffels@uza.be
RI Elvas, Filipe/F-6280-2019; wyffels, Leonie/JFK-0743-2023; stroobants,
   sigrid/C-5640-2013; Staelens, Steven/D-8385-2017; Kumar-Singh,
   Samir/G-6280-2012
OI Elvas, Filipe/0000-0001-9790-3369; Staelens, Steven/0000-0003-3376-0519;
   Stroobants, Sigrid/0000-0002-6450-9944; wyffels,
   Leonie/0000-0002-5618-8191; Kumar-Singh, Samir/0000-0001-9466-6732
FU GOA [G.0135.13]
FX Financial support was provided by GOA (G.0135.13). Brian Gray and Koon
   Pak are employees of Molecular Targeting Technologies, Inc. No other
   potential conflict of interest relevant to this article was reported.
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NR 38
TC 34
Z9 41
U1 2
U2 19
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD APR
PY 2017
VL 58
IS 4
BP 665
EP 670
DI 10.2967/jnumed.116.182014
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA EQ7FP
UT WOS:000398249600031
PM 27879368
OA Bronze, Green Accepted
DA 2025-01-04
ER

PT J
AU Dienstmann, R
   Tabernero, J
AF Dienstmann, Rodrigo
   Tabernero, Josep
TI Spectrum of Gene Mutations in Colorectal Cancer <i>Implications for
   Treatment</i>
SO CANCER JOURNAL
LA English
DT Review
DE BRAF; colorectal cancer; ERBB2; hypermutation; immunotherapy; mutation;
   RAS; RNF43; targeted therapy
ID ANTI-EGFR THERAPY; KRAS WILD-TYPE; RAS MUTATIONS; CETUXIMAB TREATMENT;
   1ST-LINE TREATMENT; TARGETED THERAPY; PIK3CA MUTATION; PLUS CETUXIMAB;
   COLON-CANCER; OPEN-LABEL
AB Gene mutations acquired during colorectal carcinogenesis remain drivers of cancer progression in the metastatic setting. KRAS and NRAS mutations define a population refractory to anti-epidermal growth factor receptor (EGFR) antibodies, either as single agents or in combination with standard chemotherapy. High-sensitivity extended RAS testing is currently a requirement to select anti-EGFR therapy irrespective of treatment line, thus limiting unnecessary exposure and expense in patients unlikely to respond. Multiple genetic alterations driving resistance to anti-EGFR monoclonal antibodies have been described, with significant overlap in primary and acquired resistance mechanisms, in line with a clonal selection process. Some of them have been validated as targets for therapeutic intervention in clinical trials, such as ERBB2 amplifications. With advances in drug development and better understanding of the dynamics of target inhibition, additional gene alterations are now-promising positive predictive markers for matched targeted therapies in CRC, including BRAF V600E and RNF43 mutations. Furthermore, the micro-satellite instable hypermutated colorectal cancer population is particularly sensitive to immune checkpoint inhibitors. In this article, we review the expanding landscape of druggable gene alterations in metastatic colorectal cancer.
C1 [Dienstmann, Rodrigo; Tabernero, Josep] Univ Autonoma Barcelona, Dept Med Oncol, Vall dHebron Inst Oncol VHIO, Vall dHebron Univ Hosp, Barcelona, Spain.
   [Dienstmann, Rodrigo] Fred Hutchinson Canc Res Ctr, Sage Bionetworks, 1124 Columbia St, Seattle, WA 98104 USA.
C3 Autonomous University of Barcelona; Hospital Universitari Vall d'Hebron;
   Vall d'Hebron Institut d'Oncologia (VHIO); Fred Hutchinson Cancer Center
RP Dienstmann, R (corresponding author), Passeig Vall dHebron 119-129, Barcelona 08035, Spain.
EM rdienstmann@vhio.net
RI Tabernero, Josep/AAG-5026-2019
OI Tabernero, Josep/0000-0002-2495-8139
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NR 69
TC 24
Z9 30
U1 0
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1528-9117
EI 1540-336X
J9 CANCER J
JI Cancer J.
PD MAY-JUN
PY 2016
VL 22
IS 3
BP 149
EP 155
DI 10.1097/PPO.0000000000000191
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DQ7EI
UT WOS:000379369300002
PM 27341591
DA 2025-01-04
ER

PT J
AU Sommariva, S
   Berra, S
   Biddau, G
   Caviglia, G
   Benvenuto, F
   Piana, M
AF Sommariva, Sara
   Berra, Silvia
   Biddau, Giorgia
   Caviglia, Giacomo
   Benvenuto, Federico
   Piana, Michele
TI <i>In-silico</i> modelling of the mitogen-activated protein kinase
   (MAPK) pathway in colorectal cancer: mutations and targeted therapy
SO FRONTIERS IN SYSTEMS BIOLOGY
LA English
DT Article
DE colorectal cancer; MAPK pathway; mutations; targeted therapy; chemical
   reaction networks; dynamical systems
ID SIGNALING PATHWAYS; BEVACIZUMAB; APOPTOSIS; DIAGNOSIS; ROLES; PHASE;
   KRAS
AB Introduction: Chemical reaction networks (CRNs) are powerful tools for describing the complex nature of cancer's onset, progression, and therapy. The main reason for their effectiveness is in the fact that these networks can be rather naturally encoded as a dynamical system whose asymptotic solution mimics the proteins' concentration profile at equilibrium.Methods and Results: This paper relies on a complex CRN previously designed for modeling colorectal cells in their G1-S transition phase and presents a mathematical method to investigate global and local effects triggered on the network by partial and complete mutations occurring mainly in its mitogen-activated protein kinase (MAPK) pathway. Further, this same approach allowed the in-silico modeling and dosage of a multi-target therapeutic intervention that utilizes MAPK as its molecular target.Discussion: Overall the results shown in this paper demonstrate how the proposed approach can be exploited as a tool for the in-silico comparison and evaluation of different targeted therapies. Future effort will be devoted to refine the model so to incorporate more biologically sound partial mutations and drug combinations.
C1 [Sommariva, Sara; Berra, Silvia; Biddau, Giorgia; Caviglia, Giacomo; Benvenuto, Federico; Piana, Michele] Univ Genoa, Dipartimento Matemat, Methods Image & Data Anal Grp, Genoa, Italy.
   [Piana, Michele] Osped Policlin San Martino IRCCS, Life Sci Computat Lab, Genoa, Italy.
C3 University of Genoa
RP Sommariva, S (corresponding author), Univ Genoa, Dipartimento Matemat, Methods Image & Data Anal Grp, Genoa, Italy.
EM sommariva@dima.unige.it
RI Sommariva, Sara/L-1330-2019
FU Roche S.p.A., Italy; Gruppo Nazionale per il Calcolo Scientifico
   (GNCS-INdAM); Strengthening a person-centred ecosystem for the
   co-creation of digital health services for a smart community (DHEAL-COM)
   project [PNC E3-2022-23683267]
FX SB was granted a scholarship by Roche S.p.A., Italy. SS, MP, and FB have
   been partially supported by Gruppo Nazionale per il Calcolo Scientifico
   (GNCS-INdAM). MP acknowledges the support of the "Strengthening a
   person-centred ecosystem for the co-creation of digital health services
   for a smart community (DHEAL-COM)" project (PNC E3-2022-23683267).
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NR 59
TC 1
Z9 1
U1 0
U2 0
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2674-0702
J9 FRONT SYST BIOL
JI Front. Syst. Biol.
PD AUG 23
PY 2023
VL 3
AR 1207898
DI 10.3389/fsysb.2023.1207898
PG 14
WC Mathematical & Computational Biology
WE Emerging Sources Citation Index (ESCI)
SC Mathematical & Computational Biology
GA O3I6O
UT WOS:001370111100001
OA gold
DA 2025-01-04
ER

PT J
AU Grassilli, E
   Cerrito, MG
   Bonomo, S
   Giovannoni, R
   Conconi, D
   Lavitrano, M
AF Grassilli, Emanuela
   Cerrito, Maria Grazia
   Bonomo, Sara
   Giovannoni, Roberto
   Conconi, Donatella
   Lavitrano, Marialuisa
TI p65BTK Is a Novel Biomarker and Therapeutic Target in Solid Tumors
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE p65BTK; targeted therapy; drug resistance; colon cancer; lung cancer;
   ovarian cancer
ID BRUTONS TYROSINE KINASE; CHRONIC LYMPHOCYTIC-LEUKEMIA; POOR-PROGNOSIS;
   CANCER; BTK; RECEPTOR; IBRUTINIB; GLIOBLASTOMA; ACTIVATION; RESISTANCE
AB Bruton's tyrosine kinase (BTK) is a non-receptor intracellular kinase playing a key role in the proliferation and survival of normal and malignant B-lymphocytes. Its targeting by Ibrutinib, the first specific inhibitor, represented a turning point for the therapy of certain types of B-cell leukemias/lymphomas and several more BTK inhibitors are today in the clinic or advanced clinical trials. BTK expression was successively found to occur also outside of the hematopoietic compartment. In fact, we identified p65BTK, a novel 65 kDa isoform lacking an N-term stretch of 86 amino acids (compared to the 77 kDa protein expressed in B cells) as highly expressed in colon cancer patients. We demonstrated that p65BTK is a powerful oncogene acting downstream of the RAS/MAPK pathway and necessary for RAS-mediated transformation. Notably, the kinase domain is conserved and therefore inhibited by the available BTK-targeting drugs (Ibrutinib, Spebrutinib, etc.) which we used to demonstrate that p65BTK is an actionable target in drug-resistant colorectal carcinomas. We found p65BTK expressed also in >50% non-small cell lung cancers (NSCLC) and demonstrated that it is an actionable target in KRAS-mutated/EGFR-wild type drug-resistant NSCLC models (for which no targeted therapy is available). We also reported a significant correlation between p65BTK expression and low-grade tumors and overall survival of patients with grade III gliomas and showed that its targeting induced a significant decrease in the viability of in glioma stem cells. Finally, in ovarian cancer patients, p65BTK expression levels correlate with early relapse and shorter progression-free survival, both indicators of resistance to therapy. Remarkably, Ibrutinib is more effective than standard of care (SOC) therapeutics in in vitro and ex vivo settings. On the whole, our preclinical data indicate that, depending on the tumor type, BTK inhibitors used alone can induce cytotoxicity (gliomas), be more effective than SOC chemotherapy (ovarian cancer) or can kill drug-resistant tumor cells when used in combination with SOC chemotherapy (colon cancer and NSCLC) or targeted therapy (NSCLC and ovarian cancer), thus suggesting that p65BTK may be an actionable target in different solid tumors. In addition, our data also give the proof-of-concept for starting clinical trials using BTK inhibitors, alone or in combination, to improve the therapeutic options for solid tumors treatment.
C1 [Grassilli, Emanuela; Cerrito, Maria Grazia; Bonomo, Sara; Giovannoni, Roberto; Conconi, Donatella; Lavitrano, Marialuisa] Univ Milano Bicocca, Dept Med & Surg, Mol Med Lab, Monza, Italy.
C3 University of Milano-Bicocca
RP Grassilli, E (corresponding author), Univ Milano Bicocca, Dept Med & Surg, Mol Med Lab, Monza, Italy.
EM emanuela.grassilli@unimib.it
RI Cerrito, Maria/AAA-1190-2019; Giovannoni, Roberto/A-1413-2009;
   grassilli, emanuela/L-7296-2013
OI grassilli, emanuela/0000-0001-5387-5925; Cerrito, Maria
   Grazia/0000-0002-3347-5817
FU Italian Minister of University and Research [PON01_02782]; Ministry of
   Health [RF2010-2305526]; University of Milano-Bicocca [FAR
   2016-ATE-0599, 2014-ATE-0374, 2015-ATE-0447, 2016-ATE-0299]; Lung Cancer
   Research Foundation (LCRF) United States; Rivkin Foundation, United
   States
FX This work was supported by the Italian Minister of University and
   Research (PON01_02782 to ML); by the Ministry of Health (RF2010-2305526
   to ML); by the University of Milano-Bicocca (FAR 2016-ATE-0599 to ML and
   2014-ATE-0374, 2015-ATE-0447, and 2016-ATE-0299 to EG); by the Grant
   from the Lung Cancer Research Foundation (LCRF) United States
   -"Targeting p65BTK in Non-Small Cell Lung Cancer" to EG; by the Pilot
   Award from the Rivkin Foundation, United States -"p65BTK as an
   actionable target in ovarian cancer" to EG.
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NR 68
TC 9
Z9 9
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 JUN 7
PY 2021
VL 9
AR 690365
DI 10.3389/fcell.2021.690365
PG 9
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA SV4SK
UT WOS:000663811600001
PM 34164404
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Dienstmann, R
   Vermeulen, L
   Guinney, J
   Kopetz, S
   Tejpar, S
   Tabernero, J
AF Dienstmann, Rodrigo
   Vermeulen, Louis
   Guinney, Justin
   Kopetz, Scott
   Tejpar, Sabine
   Tabernero, Josep
TI Consensus molecular subtypes and the evolution of precision medicine in
   colorectal cancer
SO NATURE REVIEWS CANCER
LA English
DT Review
ID III COLON-CANCER; CIRCULATING TUMOR DNA; ACQUIRED-RESISTANCE; CETUXIMAB
   TREATMENT; RAS MUTATIONS; EGFR BLOCKADE; ANTITUMOR-ACTIVITY; TARGETED
   THERAPY; ANALYSIS REVEALS; MATCHED PRIMARY
AB Critical driver genomic events in colorectal cancer have been shown to affect the response to targeted agents that were initially developed under the 'one gene, one drug' paradigm of precision medicine. Our current knowledge of the complexity of the cancer genome, clonal evolution patterns under treatment pressure and pharmacodynamic effects of target inhibition support the transition from a one gene, one drug approach to a 'multi-gene, multi-drug' model when making therapeutic decisions. Better characterization of the transcriptomic subtypes of colorectal cancer, encompassing tumour, stromal and immune components, has revealed convergent pathway dependencies that mandate a 'multi-molecular' perspective for the development of therapies to treat this disease.
C1 [Dienstmann, Rodrigo; Tabernero, Josep] Univ Autonoma Barcelona, Vall dHebron Inst Oncol VHIO, Barcelona 08035, Spain.
   [Dienstmann, Rodrigo; Guinney, Justin] Sage Bionetworks, Fred Hutchinson Canc Res Ctr, 1100 Fairview Ave N, Seattle, WA 98109 USA.
   [Vermeulen, Louis] Univ Amsterdam, Acad Med Ctr, CEMM, Lab Expt Oncol & Radiobiol LEXOR, NL-1012 WX Amsterdam, Netherlands.
   [Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, 1515 Holcombe Blvd, Houston, TX 77030 USA.
   [Tejpar, Sabine] Univ Hosp Gasthuisberg, Digest Oncol Unit, Herestr 49, B-3000 Leuven, Belgium.
C3 Vall d'Hebron Institut d'Oncologia (VHIO); Autonomous University of
   Barcelona; Fred Hutchinson Cancer Center; University of Amsterdam;
   Academic Medical Center Amsterdam; University of Texas System; UTMD
   Anderson Cancer Center; KU Leuven; University Hospital Leuven
RP Dienstmann, R (corresponding author), Univ Autonoma Barcelona, Vall dHebron Inst Oncol VHIO, Barcelona 08035, Spain.; Dienstmann, R (corresponding author), Sage Bionetworks, Fred Hutchinson Canc Res Ctr, 1100 Fairview Ave N, Seattle, WA 98109 USA.
EM rdienstmann@vhio.net
RI Vermeulen, Louis/B-7488-2008; Tabernero, Josep/AAG-5026-2019; Kopetz,
   Scott/AAC-1387-2019
OI Kopetz, Scott/0000-0001-9647-3416; Guinney, Justin
   H/0000-0003-1477-1888; Tabernero, Josep/0000-0002-2495-8139
FU FERO Foundation; European Union [635342]; University of Leuven
   [GOA/12/2106]; Research Foundation Flanders; Belgian National Cancer
   Plan; KWF Kankerbestrijding (Dutch Cancer Society) [UVA2014-7245];
   European Research Council [ERG-StG 638193]; Netherlands Organisation for
   Health Research and Development [Vidi 016.156.308]; US National Cancer
   Institute [U54CA149237];  [3 P30 CA016672 41]; H2020 Societal Challenges
   Programme [635342] Funding Source: H2020 Societal Challenges Programme
FX R.D. and J.T. acknowledge the FERO Foundation for supporting research in
   gastrointestinal malignancies and the Cellex Foundation for providing
   research facilities and equipment. The work of R.D., S.T. and J.T. was
   supported by the European Union's Horizon 2020 research and innovation
   programme 2014-2020 under grant agreement number 635342 (MoTriColor
   project). The work of S.T. was supported by the University of Leuven
   (grant GOA/12/2106), the Research Foundation Flanders and the Belgian
   National Cancer Plan. The work of L.V. was supported by grants from KWF
   Kankerbestrijding (Dutch Cancer Society) (UVA2014-7245), the European
   Research Council (ERG-StG 638193) and the Netherlands Organisation for
   Health Research and Development (Vidi 016.156.308). The work of J.G. was
   supported by grant U54CA149237 from the US National Cancer Institute.
   The work of S.C. was supported by the generous philanthropic
   contributions to the University of Texas MD Anderson Moon Shots Program
   and Cancer Center Sipport Grants grant 3 P30 CA016672 41.
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NR 159
TC 683
Z9 746
U1 6
U2 240
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-175X
EI 1474-1768
J9 NAT REV CANCER
JI Nat. Rev. Cancer
PD FEB
PY 2017
VL 17
IS 2
BP 79
EP 92
DI 10.1038/nrc.2016.126
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EK2BZ
UT WOS:000393733600005
PM 28050011
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Skórzewska, M
   Geca, K
   Polkowski, WP
AF Skorzewska, Magdalena
   Geca, Katarzyna
   Polkowski, Wojciech P.
TI A Clinical Viewpoint on the Use of Targeted Therapy in Advanced Gastric
   Cancer
SO CANCERS
LA English
DT Review
DE targeted therapy; immunotherapy; gastric cancer
ID POSITIVE SOLID TUMORS; DABRAFENIB PLUS TRAMETINIB; GASTROESOPHAGEAL
   JUNCTION; OPEN-LABEL; MICROSATELLITE INSTABILITY; BISPECIFIC ANTIBODY;
   COLORECTAL-CANCER; PROGNOSTIC-FACTOR; PD-1 BLOCKADE; DOUBLE-BLIND
AB Simple Summary Outcomes for patients with advanced gastric cancer continue to be unsatisfactory despite the inclusion of new targeted therapies in the treatment options. The effectiveness of targeted therapies is limited for a particular subset of the population. This is related to the fact that specific biomarkers are present in a very small percentage of patients with advanced gastric cancer. It is paramount to conduct further research focused on identifying new molecular targets, as this can significantly improve the effectiveness of advanced-stage therapy.Abstract The development of therapies for advanced gastric cancer (GC) has made significant progress over the past few years. The identification of new molecules and molecular targets is expanding our understanding of the disease's intricate nature. The end of the classical oncology era, which relied on well-studied chemotherapeutic agents, is giving rise to novel and unexplored challenges, which will cause a significant transformation of the current oncological knowledge in the next few years. The integration of established clinically effective regimens in additional studies will be crucial in managing these innovative aspects of GC. This study aims to present an in-depth and comprehensive review of the clinical advancements in targeted therapy and immunotherapy for advanced GC.
C1 [Skorzewska, Magdalena; Geca, Katarzyna; Polkowski, Wojciech P.] Med Univ Lublin, Dept Surg Oncol, Radziwillowska 13 St, PL-20080 Lublin, Poland.
C3 Medical University of Lublin
RP Skórzewska, M; Geca, K (corresponding author), Med Univ Lublin, Dept Surg Oncol, Radziwillowska 13 St, PL-20080 Lublin, Poland.
EM magdalena.skorzewska@umlub.pl; katarzyna.geca@umlub.pl;
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RI Gęca, Katarzyna/AGW-9898-2022; Polkowski, Wojciech/AAN-5087-2021
OI Polkowski, Wojciech/0000-0001-6455-5636; Skorzewska,
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NR 190
TC 4
Z9 4
U1 2
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2023
VL 15
IS 22
AR 5490
DI 10.3390/cancers15225490
PG 34
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA Y9CR0
UT WOS:001108171400001
PM 38001751
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lu, M
   Hu, KW
AF Lu, Ming
   Hu, Kongwang
TI Correlation of HER2 and FOXM1 in human colorectal carcinoma and its
   clinical significance
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE Colorectal cancer; HER2; FOXM1; clinical significance; targeted therapy
ID PROGNOSTIC-FACTOR; MEDIATES RESISTANCE; HUMAN COLON; EXPRESSION; CANCER;
   OVEREXPRESSION; TARGET; FOXO3A; PROGRESSION; THERAPIES
AB Background: The human epidermal growth factor receptor 2 (HER2) and transcription factor forkhead box protein M1 (FOXM1) are proto-oncogenes and have expressed in various kinds of human solid malignancies. However, the clinical significance of HER2 and FOXM1 in colorectal cancer (CRC) remains controversial, and there is no related report of the connection between HER2 and FOXM1 in colorectal cancer. This study aims to investigate the clinical values based on the connection of HER2 with FOXM1 in colorectal cancer. Material/Methods: We retrospectively investigated HER2 and FOXM1 expressions of 130 paraffin embedded CRC and their adjacent paraneoplastic tissues through immunohistochemical assay. Western blot and RT-PCR assays were applied to measure the relative expressions of HER2 and FOXM1 in mRNA and the protein levels of 30 fresh CRC and the adjacent paraneoplastic tissues. Results: HER2 and FOXM1 expressions were significantly higher in colorectal cancer than those in paraneoplastic tissues (p<0.001). Similarly, the relative expression levels of HER2 and FOXM1 in mRNA and protein were also significantly higher in CRC tissues than those in paraneoplastic tissues (P<0.05). The HER2 expression was closely correlated with tumor size, degree of differentiation, presence of vascular invasion, lymph node metastasis, distant metastases, advanced TNM stage, and prognosis (P<0.05). The FOXM1 expression was related to tumor invasion, vascular invasion, lymph node metastasis, distant metastases, TNM stage, and prognosis (P<0.05). Besides, FOXM1 was an independent prognostic factor in CRC. There was a significant correlation between FOXM1 and HER2 expressions in colorectal cancer (r=0.335; P<0.01). Conclusions: The overexpressions of HER2 and FOXM1 protein in colorectal cancer correlate with their clinicopathological characteristics and prognosis. HER2 and FOXM1 are important diagnostic markers for colorectal cancer. Furthermore, FOXM1 may be a potential target for therapy especially in HER2-targeted therapy-resistant cancers.
C1 [Lu, Ming; Hu, Kongwang] Anhui Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Hefei, Anhui, Peoples R China.
C3 Anhui Medical University
RP Hu, KW (corresponding author), Anhui Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Hefei, Anhui, Peoples R China.
EM hukongwang@sina.com
FU Key Laboratory of natural immunity and chronic diseases, Chinese Academy
   of Sciences [20160526]
FX This work was funded by the Open Project Program of the Key Laboratory
   of natural immunity and chronic diseases, Chinese Academy of Sciences
   (number: 20160526) to Kongwang Hu.
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NR 38
TC 1
Z9 1
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 12
BP 11624
EP 11634
PG 11
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA FQ9UL
UT WOS:000418707100028
PM 31966520
DA 2025-01-04
ER

PT J
AU Liang, YH
   Chen, KH
   Shao, YY
AF Liang, Yi-Hsin
   Chen, Kuo-Hsing
   Shao, Yu-Yun
TI Treatment outcome comparisons of first-line targeted therapy in patients
   with <i>KRAS</i> wild-type metastatic colorectal cancer: A nationwide
   database study
SO CANCER MEDICINE
LA English
DT Article
DE bevacizumab; cetuximab; EGFR; metastatic colorectal cancer; panitumumab;
   secondary surgery
ID EARLY TUMOR SHRINKAGE; OPEN-LABEL; COLON-CANCER; ANTI-EGFR;
   CHEMOTHERAPY; BEVACIZUMAB; SURVIVAL; IMPACT; PANITUMUMAB; ANTIBODIES
AB Background: The first-line systemic therapy for metastatic colorectal cancer (mCRC) is a combination of one targeted therapy agent and a chemotherapy doublet. Whether bevacizumab or anti-epidermal growth factor receptor (anti-EGFR) monoclonal antibody (mAb) is the more effective addition to a chemotherapy doublet as the first-line treatment for inoperable KRAS wild-type mCRC remains controversial in prior clinical trials. Moreover, the association between the sidedness of primary tumors and the efficacy of anti-EGFR mAb needs to be addressed.Methods: We established a cohort of patients with KRAS wild-type mCRC who were treated with first-line targeted therapy plus doublet chemotherapy between 2013 and 2018 using Taiwan's National Health Insurance Research Database. Secondary surgery was defined as either resection of primary tumors, liver metastases, lung metastases, or radiofrequency ablation.Results: A total of 6482 patients were included; bevacizumab and anti-EGFR mAb were the first-line targeted therapies in 3334 (51.4%) and 3148 (48.6%) patients, respectively. Compared with those who received bevacizumab, patients who received anti-EGFR mAb exhibited significantly longer overall survival (OS; median, 23.1 vs. 20.2 months, p = 0.012) and time to treatment failure (TTF; median, 11.3 vs. 10 months, p < 0.001). Among left-sided primary tumors, the OS and TTF benefits of anti-EGFR mAb remained. Among right-sided primary tumors, the OS and TTF were similar regardless of the type of targeted therapy. In multivariate analyses, first-line anti-EGFR mAb therapy remained an independent predictor of longer OS and TTF for left-sided primary tumors. Patients who received anti-EGFR mAb were more likely to receive secondary surgery (29.6% vs. 22.6%, p < 0.0001) than patients who received bevacizumab.Conclusion: For patients who received first-line doublet chemotherapy for KRAS wild-type mCRC, adding anti-EGFR mAb was associated with significantly longer OS and TTF, especially for left-sided primary tumors.
C1 [Liang, Yi-Hsin; Chen, Kuo-Hsing; Shao, Yu-Yun] Natl Taiwan Univ, Coll Med, Grad Inst Oncol, Taipei, Taiwan.
   [Liang, Yi-Hsin; Chen, Kuo-Hsing] Natl Taiwan Univ, Ctr Genom & Precis Med, Coll Med, Taipei, Taiwan.
   [Liang, Yi-Hsin; Chen, Kuo-Hsing; Shao, Yu-Yun] Natl Taiwan Univ Hosp, Dept Oncol, 7 Chung Shan South Rd, Taipei 10002, Taiwan.
   [Liang, Yi-Hsin; Chen, Kuo-Hsing; Shao, Yu-Yun] Natl Taiwan Univ, Canc Ctr, Dept Med Oncol, Taipei, Taiwan.
C3 National Taiwan University; National Taiwan University; National Taiwan
   University; National Taiwan University Hospital; National Taiwan
   University
RP Shao, YY (corresponding author), Natl Taiwan Univ Hosp, Dept Oncol, 7 Chung Shan South Rd, Taipei 10002, Taiwan.
EM yuyunshao@gmail.com
RI chen, long/AAV-6276-2021; Shao, Yu-Yun/K-6434-2012
OI LIANG, YI-HSIN/0000-0002-7224-9687; Shao, Yu-Yun/0000-0001-7334-1912
FU Ministry of Science and Technology, Taiwan [MOST 105-2314-B-002-194,
   MOST 106-2314-B-002-213, MOST 108-2314-B-002-072-MY3, MOST
   111-2314-B-002-120]; National Taiwan University Hospital, Taipei, Taiwan
   [NTUH 108-S4150, NTUH 105-S2954]; Science and Technology Unit, Ministry
   of Health and Welfare, Taiwan [MOHW112-TDU-B-211-144-002,
   DOH102-NH-9002]
FX Ministry of Science and Technology, Taiwan, Grant/Award Number: MOST
   105-2314-B-002-194, MOST 106-2314-B-002-213, MOST 108-2314-B-002-072-MY3
   and MOST 111-2314-B-002-120; National Taiwan University Hospital,
   Taipei, Taiwan, Grant/Award Number: NTUH 108-S4150 and NTUH 105-S2954;
   the Science and Technology Unit, Ministry of Health and Welfare, Taiwan,
   Grant/Award Number: MOHW112-TDU-B-211-144-002 and DOH102-NH-9002
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NR 41
TC 0
Z9 0
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD JUL
PY 2023
VL 12
IS 14
BP 15176
EP 15186
DI 10.1002/cam4.6196
EA JUN 2023
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA W7QV8
UT WOS:001012827900001
PM 37325970
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wu, CC
   Su, CC
   Lee, PT
   Chen, YH
   Hsu, CW
   Su, YC
AF Wu, Chih-Chien
   Su, Chien -Chou
   Lee, Pei -Ting
   Chen, Yu-Hsun
   Hsu, Chao -Wen
   Su, Yi-Chia
TI Comparative effectiveness of primary tumor resection versus chemotherapy
   in patients with asymptomatic unresectable metastatic colorectal cancer:
   a retrospective cohort study using the trial emulation framework
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE Colorectal cancer; primary tumor resection; targeted therapy; survival;
   trial emulation; meta-analysis
ID COMORBIDITY INDEX; SURVIVAL; DATABASE; TAIWAN
AB Patients who undergo primary tumor resection (PTR) reportedly have significantly higher overall survival (OS) than those who do not undergo this procedure. However, this result is only evident in past retrospective studies, and clinical trial results did not show the same trend. Thus, it remains unclear whether primary tumor resection effectively increases survival in patients with metastatic colorectal cancer (mCRC) across different study designs. We compared the OS of patients with asymptomatic unresectable mCRC who underwent PTR with that of those who did not. This retrospective cohort study was designed to be a target trial emulation of a randomized controlled trial (RCT) that would have compared the effectiveness of PTR versus non-PTR in patients with asymptomatic unresectable mCRC from 2009 to 2017. A systematic review and meta -analysis were conducted to compare the efficacy of PTR and non-PTR in patients with mCRC, and corresponding results were compared. This cohort included 1,132 patients for a per -protocol analysis. The PTR group had non -significantly longer survival (adjusted hazard ratio: 0.70, 95% confidence interval: 0.62-1.01) than the non-PTR group in our cohort. A meta -analysis including five RCTs (1,016 patients) and our cohort found that the PTR group did not have a significantly lower mortality rate than the non-PTR group. The results of this cohort study and previous RCTs suggest that PTR is not associated with improved survival compared to systemic chemotherapy combined with targeted therapy among asymptomatic unresectable mCRC patients. Therefore, routine PTR is not recommended in these patients.
C1 [Wu, Chih-Chien; Chen, Yu-Hsun; Hsu, Chao -Wen] Kaohsiung Vet Gen Hosp, Dept Surg, Div Colorectal Surg, Kaohsiung 81362, Taiwan.
   [Wu, Chih-Chien; Hsu, Chao -Wen] Natl Yang Ming Chiao Tung Univ, Sch Med, Dept Surg, Taipei 11221, Taiwan.
   [Su, Chien -Chou] Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Clin Innovat & Res Ctr, Tainan 70403, Taiwan.
   [Su, Chien -Chou] Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Coll Med, Dept Pharm, Tainan 70101, Taiwan.
   [Lee, Pei -Ting; Su, Yi-Chia] Kaohsiung Vet Gen Hosp, Dept Pharm, 386,Dazhong 1st Rd, Kaohsiung 813414, Taiwan.
   [Lee, Pei -Ting] Natl Cheng Kung Univ, Coll Med, Dept Publ Hlth, Tainan 70101, Taiwan.
   [Su, Yi-Chia] Kaohsiung Med Univ, Sch Pharm, Dept Pharm, Kaohsiung 807378, Taiwan.
   [Su, Yi-Chia] Chia Nan Univ Pharm & Sci, Dept Pharm, Tainan 717301, Taiwan.
   [Su, Yi-Chia] Natl Cheng Kung Univ, Inst Clin Pharm & Pharmaceut Sci, Coll Med, Tainan 70101, Taiwan.
C3 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; Kaohsiung Veterans General Hospital; National Cheng
   Kung University; Kaohsiung Medical University; Chia Nan University of
   Pharmacy & Science; National Cheng Kung University
RP Su, YC (corresponding author), Kaohsiung Vet Gen Hosp, Dept Pharm, 386,Dazhong 1st Rd, Kaohsiung 813414, Taiwan.
EM jia.love70@gmail.com
RI Su, Yichia/HJI-3668-2023; chen, yuling/JMQ-4121-2023
FU Kaohsiung Veterans General Hospital [KSVGH112-137]; National Cheng Kung
   University Hospital, College of Medicine, National Cheng Kung University
   [NCKUH-11307007, NCKUH-11207009]
FX The authors wish to thank the Health Data Science Center, National Cheng
   Kung University Hospital for providing administrative and technical
   support and Ms. Hsiao-Ling Chiu of the Cancer Center, Kaohsiung Veterans
   General Hospital for her advisory comments on inter-preting the results.
   This research were funded by Kaohsiung Veterans General Hospital
   (KSVGH112-137) and National Cheng Kung University Hospital, College of
   Medicine, National Cheng Kung University (NCKUH-11307007 and
   NCKUH-11207009).
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NR 39
TC 0
Z9 0
U1 10
U2 14
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2156-6976
J9 AM J CANCER RES
JI Am. J. Cancer Res.
PY 2024
VL 14
IS 5
DI 10.62347/UGXA9515
PG 28
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SB5S2
UT WOS:001232018400010
PM 38859829
OA Bronze
DA 2025-01-04
ER

PT J
AU Miekus, K
AF Miekus, Katarzyna
TI The Met tyrosine kinase receptor as a therapeutic target and a potential
   cancer stem cell factor responsible for therapy resistance
SO ONCOLOGY REPORTS
LA English
DT Review
DE MET receptor; c-met; cancer stem cells; targeted therapy; therapy
   resistance
ID HEPATOCYTE GROWTH-FACTOR; FACTOR SCATTER FACTOR; C-MET;
   ACQUIRED-RESISTANCE; LUNG-CANCER; PROGNOSTIC-SIGNIFICANCE; GENE
   AMPLIFICATION; COLON-CANCER; HGF/C-MET; GEFITINIB RESISTANCE
AB The MET tyrosine kinase receptor plays an important role during tumor development and progression being responsible for proliferation, morphogenetic transformation, cell motility and invasiveness. High expression of the MET receptor has been shown to correlate with increased tumor growth and metastasis, poor prognosis and resistance to radiotherapy. Moreover, MET expression and activation has been shown to be associated with therapy resistance. The occurrence of resistance to targeted therapy might be related to the presence of cancer stem cells (CSCs). CSCs are a subpopulation of cells in the tumor that possess the ability of self-renewal, clonogenicity, radioresistanbe and self-sustained protection from apoptosis. Recently, MET has been postulated as an essential factor supporting the functional stem cell phenotype in some tumors and as a CSC factor is believed to be responsible for therapy resistance. This review presents the results from recent studies identifying MET as a potential marker of CSCs and tumor initiating cells, demonstrating pivotal role of MET in supporting stem cell phenotype and indicating the role of MET in acquiring resistance to antitumor therapy.
C1 [Miekus, Katarzyna] Jagiellonian Univ, Fac Biochem Biophys & Biotechnol, Dept Gen Biochem, Gronostajowa St 7, PL-30387 Krakow, Poland.
C3 Jagiellonian University
RP Miekus, K (corresponding author), Jagiellonian Univ, Fac Biochem Biophys & Biotechnol, Dept Gen Biochem, Gronostajowa St 7, PL-30387 Krakow, Poland.
EM katarzyna.miekus@uj.edu.pl
RI Miekus, Katarzyna/C-1264-2015
OI Miekus, Katarzyna/0000-0002-2716-203X
FU National Science Centre [2013/09/D/NZ5/00249]; European Union; Polish
   Ministry of Science and Higher Education [POIG.02.01.00-12-064/08,
   02.02.00-00-014/08]; Ministry of Science and Higher Education
FX The present study was supported by a grant from the National Science
   Centre (no. 2013/09/D/NZ5/00249) to K.M. The Faculty of Biochemistry,
   Biophysics and Biotechnology of the Jagiellonian University is a
   beneficiary of the structural funds from the European Union and the
   Polish Ministry of Science and Higher Education (grants nos.
   POIG.02.01.00-12-064/08 and 02.02.00-00-014/08) and is a partner of the
   Leading National Research Center (KNOW) supported by the Ministry of
   Science and Higher Education. I am very grateful to Mikolaj Przywara for
   language editing, proofreading and suggestions.
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NR 123
TC 16
Z9 19
U1 0
U2 14
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 647
EP 656
DI 10.3892/or.2016.5297
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EJ3BU
UT WOS:000393086900001
PM 27959446
OA Bronze
DA 2025-01-04
ER

PT J
AU Siddiqui, M
   Chand, M
   Eng, C
   Mehdizadeh, A
   Mirnezami, A
   Brown, G
AF Siddiqui, M.
   Chand, M.
   Eng, C.
   Mehdizadeh, A.
   Mirnezami, A.
   Brown, G.
TI Session 2: Mutational discordance: the big challenge in personalized
   treatments - any solutions?
SO COLORECTAL DISEASE
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; FOLFIRI PLUS BEVACIZUMAB; CIRCULATING
   TUMOR DNA; 1ST-LINE TREATMENT; OPEN-LABEL; KRAS
AB The great challenge for oncologists treating patients who are developing or progressing with metastatic disease is to be able to offer a truly personalized and targeted therapy that can have an early and meaningful effect on the course of the disease. At present the known molecular markers are limited in their frequency and reliability in determining the use of newer chemotherapies. Professor Eng discusses the challenges faced in ensuring timely and effective treatments based on the molecular profile of the tumour and the potential role of real-time analysis of mutational changes in the tumour when progression occurs.
C1 [Siddiqui, M.] Croydon Univ Hosp, Royal Marsden NHS Fdn Trust, Croydon, England.
   [Chand, M.] Univ Coll London Hosp, London, England.
   [Eng, C.; Mehdizadeh, A.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal GI Med Oncol, Div Canc Med, Houston, TX 77030 USA.
   [Mirnezami, A.] Univ Southampton, Southampton, Hants, England.
   [Brown, G.] Royal Marsden NHS Fdn Trust, London, England.
   [Brown, G.] Imperial Coll London, London, England.
C3 Croydon University Hospital; Royal Marsden NHS Foundation Trust;
   University College London Hospitals NHS Foundation Trust; University of
   London; University College London; University of Texas System; UTMD
   Anderson Cancer Center; University of Southampton; Royal Marsden NHS
   Foundation Trust; Imperial College London
RP Siddiqui, M; Brown, G (corresponding author), Royal Marsden NHS Fdn Trust, Dept Diagnost Imaging, Downs Rd, Sutton SM2 5PT, Surrey, England.
EM md0u812a@mac.com; Manish.chand@uclh.nhs.uk; ceng@mdanderson.org;
   AMehdizadeh@mdanderson.org; A.H.Mirnezami@soton.ac.uk;
   gina.brown@rmh.nhs.uk
RI BROWN, GINA/F-8081-2012; Brown, Gina/LFT-9453-2024
OI Brown, Gina/0000-0002-2336-622X; Eng, Cathy/0000-0003-2335-0612
CR Alix-Panabières C, 2016, CANCER DISCOV, V6, P479, DOI 10.1158/2159-8290.CD-15-1483
   Cremolini C, 2015, LANCET ONCOL, V16, P1306, DOI 10.1016/S1470-2045(15)00122-9
   Douillard JY, 2014, ANN ONCOL, V25, P1346, DOI 10.1093/annonc/mdu141
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NR 8
TC 0
Z9 0
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1462-8910
EI 1463-1318
J9 COLORECTAL DIS
JI Colorectal Dis.
PD MAY
PY 2018
VL 20
SU 1
SI SI
BP 49
EP 51
DI 10.1111/codi.14079
PG 3
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA GI0TG
UT WOS:000434081800011
PM 29878676
OA Bronze, Green Submitted, Green Accepted
DA 2025-01-04
ER

PT S
AU Martins, M
   Mansinho, A
   Cruz-Duarte, R
   Martins, SL
   Costa, L
AF Martins, Marta
   Mansinho, Andre
   Cruz-Duarte, Raquel
   Martins, Soraia Lobo
   Costa, Luis
BE Jordan, P
TI Anti-EGFR Therapy to Treat Metastatic Colorectal Cancer: Not for All
SO TARGETED THERAPY OF COLORECTAL CANCER SUBTYPES
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Book Chapter
DE Colorectal cancer; Epidermal growth factor receptor; Primary resistance;
   Secondary resistance; Targeted therapy
ID GROWTH-FACTOR RECEPTOR; CETUXIMAB PLUS IRINOTECAN; GENE COPY NUMBER;
   CONSENSUS MOLECULAR SUBTYPES; CELL LUNG-CANCER; K-RAS MUTATIONS;
   PHASE-III TRIAL; 1ST-LINE TREATMENT; ACQUIRED-RESISTANCE; COLON-CANCER
AB The development of monoclonal antibodies (mAbs) cetuximab and panitumumab, which target the transmembrane protein epidermal growth factor receptor (EGFR), mark a major step forward in the treatment of metastatic colorectal cancer (mCRC). However, this therapeutic progress proved to be effective only in a very restricted subset of patients. Although several mechanisms of resistance, both primary and acquired, have been identified, the only established predictive tumour biomarker for the treatment of mCRC patients is the RAS mutational status. RAS activating mutations predict a lack of response to these therapies while low levels of primary resistance characterize RAS wild type (WT) patients (only about 15%). However, even WT patients that initially respond to anti-EGFR therapy, eventually undergo tumour progression. In this context, there is still more to be done in the search for effective predictive markers with therapeutic applicability. In this chapter, we provide an overview on the mechanisms that contribute to resistance to EGFR-targeted therapy and highlight what is still missing in our understanding of these molecular mechanisms and approaches to overcome them.
C1 [Martins, Marta; Cruz-Duarte, Raquel; Costa, Luis] Univ Lisbon, Inst Med Mol Joao Lobo Antunes, Fac Med, Lisbon, Portugal.
   [Mansinho, Andre; Martins, Soraia Lobo; Costa, Luis] Santa Maria Hosp, Div Oncol, Ctr Hosp Lisboa Norte, Lisbon, Portugal.
C3 Universidade de Lisboa; Universidade de Lisboa; Hospital Santa Maria
RP Martins, M (corresponding author), Univ Lisbon, Inst Med Mol Joao Lobo Antunes, Fac Med, Lisbon, Portugal.
EM marta.martins@medicina.ulisboa.pt
RI Costa, Luis/E-5117-2015; Martins, Marta/A-9905-2013
OI Martins, Marta/0000-0003-0429-9380; Mansinho, Andre/0000-0001-8771-0838
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NR 110
TC 18
Z9 20
U1 0
U2 2
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 113
EP 131
DI 10.1007/978-3-030-02771-1_8
D2 10.1007/978-3-030-02771-1
PG 19
WC Oncology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA BL9PR
UT WOS:000458008800008
PM 30623369
DA 2025-01-04
ER

PT J
AU Korphaisarn, K
   Kopetz, S
AF Korphaisarn, Krittiya
   Kopetz, Scott
TI BRAF-Directed Therapy in Metastatic Colorectal Cancer
SO CANCER JOURNAL
LA English
DT Review
DE Biomarker; BRAF inhibitor; colorectal cancer; mutation; targeted therapy
ID RANDOMIZED CONTROLLED-TRIAL; DOSE-ESCALATION TRIAL; MICROSATELLITE
   INSTABILITY; COLON-CANCER; ACQUIRED-RESISTANCE; PIK3CA MUTATIONS; V600E
   MUTATION; MEK INHIBITORS; STAGE-III; MELANOMA
AB Activating BRAF (V-raf murine sarcoma viral oncogene homolog B) mutations occur in approximately 5% to 10% of patients with metastatic colorectal cancer, mostly V600E mutation, and it is associated with distinct clinical and pathological features. To date, there are no approved treatments to target this mutation. BRAF inhibitor monotherapy has limited efficacy, in contrast tometastatic melanoma. Combination strategies that block not only BRAF mutated kinase but other alternative pathways are ongoing and have demonstrated improved activity. This review aims to provide data about new strategies to target to BRAF gene mutation in metastatic colorectal cancer.
C1 [Korphaisarn, Krittiya] Siriraj Hosp, Div Med Oncol, Dept Med, Fac Med, Bangkok, Thailand.
   [Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, 1515 Holcombe Blvd, Houston, TX 77030 USA.
C3 Mahidol University; University of Texas System; UTMD Anderson Cancer
   Center
RP Kopetz, S (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Unit 426, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM Skopetz@mdanderson.org
RI Korphaisarn, Krittiya/GLV-2252-2022; Kopetz, Scott/AAC-1387-2019
OI Kopetz, Scott/0000-0001-9647-3416; Korphaisarn,
   Krittiya/0000-0001-5739-0175
FU  [ROI CA172670 + CA187238]
FX S.K. was supported by ROI CA172670 + CA187238.
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NR 39
TC 30
Z9 38
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1528-9117
EI 1540-336X
J9 CANCER J
JI Cancer J.
PD MAY-JUN
PY 2016
VL 22
IS 3
BP 175
EP 178
DI 10.1097/PPO.0000000000000189
PG 4
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DQ7EI
UT WOS:000379369300005
PM 27341594
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Shafiei, G
   Jafari-Gharabaghlou, D
   Farhoudi-Sefidan-Jadid, M
   Alizadeh, E
   Fathi, M
   Zarghami, N
AF Shafiei, Golchin
   Jafari-Gharabaghlou, Davoud
   Farhoudi-Sefidan-Jadid, Mahdi
   Alizadeh, Effat
   Fathi, Marziyeh
   Zarghami, Nosratollah
TI Targeted delivery of silibinin via magnetic niosomal nanoparticles:
   potential application in treatment of colon cancer cells
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE silibinin; niosome; targeted therapy; magnetic nanoparticle; drug
   delivery; colon cancer
ID BREAST-CANCER; GENE-EXPRESSION; SILYBUM-MARIANUM; SURFACE-CHARGE; MILK
   THISTLE; IN-VITRO; DRUG; RELEASE; ENCAPSULATION; CYTOTOXICITY
AB Introduction: In recent years, various nanoparticles (NPs) have been discovered and synthesized for the targeted therapy of cancer cells. Targeted delivery increases the local concentration of therapeutics and minimizes side effects. Therefore, NPs-mediated targeted drug delivery systems have become a promising approach for the treatment of various cancers. As a result, in the current study, we aimed to design silibinin-loaded magnetic niosomes nanoparticles (MNNPs) and investigate their cytotoxicity property in colorectal cancer cell treatment.Methods: MNPs ferrofluids were prepared and encapsulated into niosomes (NIOs) by the thin film hydration method. Afterward, the morphology, size, and chemical structure of the synthesized MNNPs were evaluated using the TEM, DLS, and FT-IR techniques, respectively.Results and Discussion: The distribution number of MNNPs was obtained at about 50 nm and 70 nm with a surface charge of -19.0 mV by TEM and DLS analysis, respectively. Silibinin loading efficiency in NIOs was about 90%, and the drug release pattern showed a controlled release with a maximum amount of about 49% and 70%, within 4 h in pH = 7.4 and pH = 5.8, respectively. To investigate the cytotoxicity effect, HT-29 cells were treated with the various concentration of the drugs for 24 and 48 h and evaluated by the MTT as well as flow cytometry assays. Obtained results demonstrated promoted cell cytotoxicity of silibinin-loaded MNNPs (5-fold decrease in cell viability) compared to pure silibinin (3-fold decrease in cell viability) while had no significant cytotoxic effect on HEK-293 (normal cell line) cells, and the cellular uptake level of MNNPs by the HT-29 cell line was enhanced compared to the control group. In conclusion, silibinin-loaded MNNPs complex can be considered as an efficient treatment approach for colorectal cancer cells.
C1 [Shafiei, Golchin; Alizadeh, Effat] Tabriz Univ Med Sci, Fac Adv Med Sci, Dept Med Biotechnol, Tabriz, Iran.
   [Shafiei, Golchin; Fathi, Marziyeh] Tabriz Univ Med Sci, Biomed Inst, Res Ctr Pharmaceut Nanotechnol, Tabriz, Iran.
   [Jafari-Gharabaghlou, Davoud; Farhoudi-Sefidan-Jadid, Mahdi; Zarghami, Nosratollah] Tabriz Univ Med Sci, Fac Med, Dept Clin Biochem & Lab Med, Tabriz, Iran.
   [Zarghami, Nosratollah] Istanbul Aydin Univ, Fac Med, Dept Med Biochem, Istanbul, Turkiye.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science; Tabriz University of Medical Science; Istanbul Aydin University
RP Zarghami, N (corresponding author), Tabriz Univ Med Sci, Fac Med, Dept Clin Biochem & Lab Med, Tabriz, Iran.; Zarghami, N (corresponding author), Istanbul Aydin Univ, Fac Med, Dept Med Biochem, Istanbul, Turkiye.
EM zarghami@tbzmed.ac.ir
RI Zarghami, Nosratollah/A-7821-2017; Alizadeh, Effat/L-7235-2017
OI Alizadeh, Effat/0000-0002-7481-0896
FU Research Vice-Chancellor of Tabriz University of Medical Sciences
   [68129]
FX This study is a part of an MSc thesis (Grant no: 68129) and the authors
   acknowledge the financial support provided by the Research
   Vice-Chancellor of Tabriz University of Medical Sciences.
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NR 73
TC 14
Z9 15
U1 2
U2 12
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 JUN 27
PY 2023
VL 14
AR 1174120
DI 10.3389/fphar.2023.1174120
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA M0PJ1
UT WOS:001027223800001
PM 37441534
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Leung, HKM
   Lo, EKK
   Zhang, FF
   Felicianna
   Ismaiah, MJ
   Chen, CJ
   El-Nezami, H
AF Leung, Hoi Kit Matthew
   Lo, Emily Kwun Kwan
   Zhang, Fangfei
   Felicianna, Marsena Jasiel
   Ismaiah, Marsena Jasiel
   Chen, Congjia
   El-Nezami, Hani
TI Modulation of Gut Microbial Biomarkers and Metabolites in Cancer
   Management by Tea Compounds
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE tea compounds; cancer; gut microbiota; metabolites; microbiome targeted
   therapy
ID HELICOBACTER-PYLORI; HYDROGEN-SULFIDE; GREEN TEA; COLORECTAL-CANCER;
   INFLAMMATION; POLYPHENOLS; AMMONIA; DYSBIOSIS; CHEMOPREVENTION;
   CARCINOGENESIS
AB Cancers are causing millions of deaths and leaving a huge clinical and economic burden. High costs of cancer drugs are limiting their access to the growing number of cancer cases. The development of more affordable alternative therapy could reach more patients. As gut microbiota plays a significant role in the development and treatment of cancer, microbiome-targeted therapy has gained more attention in recent years. Dietary and natural compounds can modulate gut microbiota composition while providing broader and more accessible access to medicine. Tea compounds have been shown to have anti-cancer properties as well as modulate the gut microbiota and their related metabolites. However, there is no comprehensive review that focuses on the gut modulatory effects of tea compounds and their impact on reshaping the metabolic profiles, particularly in cancer models. In this review, the effects of different tea compounds on gut microbiota in cancer settings are discussed. Furthermore, the relationship between these modulated bacteria and their related metabolites, along with the mechanisms of how these changes led to cancer intervention are summarized.
C1 [Leung, Hoi Kit Matthew; Lo, Emily Kwun Kwan; Zhang, Fangfei; Felicianna, Marsena Jasiel; Ismaiah, Marsena Jasiel; Chen, Congjia; El-Nezami, Hani] Univ Hong Kong, Sch Biol Sci, Pokfulam, Hong Kong 999077, Peoples R China.
   [El-Nezami, Hani] Univ Eastern Finland, Sch Med, Inst Publ Hlth & Clin Nutr, FI-70211 Kuopio, Finland.
C3 University of Hong Kong; University of Eastern Finland
RP El-Nezami, H (corresponding author), Univ Hong Kong, Sch Biol Sci, Pokfulam, Hong Kong 999077, Peoples R China.; El-Nezami, H (corresponding author), Univ Eastern Finland, Sch Med, Inst Publ Hlth & Clin Nutr, FI-70211 Kuopio, Finland.
EM lhkm1997@connect.hku.hk; emilylokwan@gmail.com; u3567792@connect.hku.hk;
   feli19@connect.hku.hk; marsena@hku.hk; nedchen2@gmail.com;
   elnezami@hku.hk
OI , Felicianna/0000-0003-1252-5667; Lo, Kwun Kwan
   Emily/0000-0001-9258-0716; Leung, Hoi Kit Matthew/0009-0001-6153-7245;
   Chen, Congjia/0009-0004-6800-3184
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NR 221
TC 0
Z9 0
U1 7
U2 7
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 JUN
PY 2024
VL 25
IS 12
AR 6348
DI 10.3390/ijms25126348
PG 22
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA WO1B5
UT WOS:001255715900001
PM 38928054
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Sorokin, M
   Zolotovskaia, M
   Nikitin, D
   Suntsova, M
   Poddubskaya, E
   Glusker, A
   Garazha, A
   Moisseev, A
   Li, XM
   Sekacheva, M
   Naskhletashvili, D
   Seryakov, A
   Wang, Y
   Buzdin, A
AF Sorokin, Maxim
   Zolotovskaia, Marianna
   Nikitin, Daniil
   Suntsova, Maria
   Poddubskaya, Elena
   Glusker, Alexander
   Garazha, Andrew
   Moisseev, Alexey
   Li, Xinmin
   Sekacheva, Marina
   Naskhletashvili, David
   Seryakov, Alexander
   Wang, Ye
   Buzdin, Anton
TI Personalized targeted therapy prescription in colorectal cancer using
   algorithmic analysis of RNA sequencing data
SO BMC CANCER
LA English
DT Article
DE Transcriptomics; RNA sequencing; Molecular diagnostics; Biomarkers
   detection; Colorectal cancer; Targeted therapy; Oncobox; Second opinion
   system; Personalized medicine; Bioinformatics
ID GROWTH-FACTOR RECEPTOR; FUTURE PERSPECTIVES; EXPRESSION; SURVIVAL;
   CHEMOTHERAPY; AFLIBERCEPT; INHIBITOR; KRAS; BRAF; ANGIOGENESIS
AB Background: Overall survival of advanced colorectal cancer (CRC) patients remains poor, and gene expression analysis could potentially complement detection of clinically relevant mutations to personalize CRC treatments. Methods: We performed RNA sequencing of formalin-fixed, paraffin-embedded (FFPE) cancer tissue samples of 23 CRC patients and interpreted the data obtained using bioinformatic method Oncobox for expression-based rating of targeted therapeutics. Oncobox ranks cancer drugs according to the efficiency score calculated using target genes expression and molecular pathway activation data. The patients had primary and metastatic CRC with metastases in liver, peritoneum, brain, adrenal gland, lymph nodes and ovary. Two patients had mutations in NRAS, seven others had mutated KRAS gene. Patients were treated by aflibercept, bevacizumab, bortezomib, cabozantinib, cetuximab, crizotinib, denosumab, panitumumab and regorafenib as monotherapy or in combination with chemotherapy, and information on the success of totally 39 lines of therapy was collected. Results: Oncobox drug efficiency score was effective biomarker that could predict treatment outcomes in the experimental cohort (AUC 0.77 for all lines of therapy and 0.91 for the first line after tumor sampling). Separately for bevacizumab, it was effective in the experimental cohort (AUC 0.87) and in 3 independent literature CRC datasets, n = 107 (AUC 0.84-0.94). It also predicted progression-free survival in univariate (Hazard ratio 0.14) and multivariate (Hazard ratio 0.066) analyses. Difference in AUC scores evidences importance of using recent biosamples for the prediction quality. Conclusion: Our results suggest that RNA sequencing analysis of tumor FFPE materials may be helpful for personalizing prescriptions of targeted therapeutics in CRC.
C1 [Sorokin, Maxim; Poddubskaya, Elena; Glusker, Alexander; Moisseev, Alexey] IM Sechenov First Moscow State Med Univ, Moscow 119991, Russia.
   [Sorokin, Maxim; Zolotovskaia, Marianna; Buzdin, Anton] Moscow Inst Phys & Technol, Moscow 141701, Moscow Region, Russia.
   [Sorokin, Maxim; Nikitin, Daniil; Garazha, Andrew] OmicsWay Corp, Walnut, CA 91789 USA.
   [Nikitin, Daniil; Buzdin, Anton] Shemyakin Ovchinnikov Inst Bioorgan Chem, Moscow 117997, Russia.
   [Suntsova, Maria; Sekacheva, Marina; Buzdin, Anton] Sechenov First Moscow State Med Univ, World Class Res Ctr Digital Biodesign & Personali, Moscow 119991, Russia.
   [Poddubskaya, Elena] Clin Ctr Vitamed, Moscow 121309, Russia.
   [Li, Xinmin] Univ Calif Los Angeles, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
   [Naskhletashvili, David] NN Blokhin Russian Canc Res Ctr, Moscow 115478, Russia.
   [Seryakov, Alexander] Med Holding SM Clin, Moscow, Russia.
   [Wang, Ye] Qingdao Univ, Core Lab, Affiliated Qingdao Cent Hosp, Qingdao, Peoples R China.
C3 Sechenov First Moscow State Medical University; Moscow Institute of
   Physics & Technology; Russian Academy of Sciences; Pushchino Scientific
   Center for Biological Research (PSCBI) of the Russian Academy of
   Sciences; Institute of Bioorganic Chemistry of the Russian Academy of
   Sciences; Sechenov First Moscow State Medical University; University of
   California System; University of California Los Angeles; N.N. Blokhin
   Russian Cancer Research Center; Qingdao University
RP Buzdin, A (corresponding author), Moscow Inst Phys & Technol, Moscow 141701, Moscow Region, Russia.; Buzdin, A (corresponding author), Shemyakin Ovchinnikov Inst Bioorgan Chem, Moscow 117997, Russia.; Buzdin, A (corresponding author), Sechenov First Moscow State Med Univ, World Class Res Ctr Digital Biodesign & Personali, Moscow 119991, Russia.; Li, XM (corresponding author), Univ Calif Los Angeles, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.; Wang, Y (corresponding author), Qingdao Univ, Core Lab, Affiliated Qingdao Cent Hosp, Qingdao, Peoples R China.
EM XinminLi@mednet.ucla.edu; yewang@gdu.edu.cn; buzdin@oncobox.com
RI Zolotovskaia, Marianna/AAE-2724-2019; Garazha, Andrew/L-2298-2016;
   Nikitin, Daniil/ABF-3553-2020; Poddubskaya, Elena/AAU-9664-2020
FU OmicsWay research program in oncology; Ministry of Science and Higher
   Education of the Russian Federation [075-15-2022-304]; National Natural
   Science Foundation of China [81800805]; Qingdao Key Research Project
   [17-3-3-10-nsh, 19-6-1-3-nsh]; Qingdao Key Health Discipline Development
   Fund
FX This study was supported by the OmicsWay research program in oncology
   and financed by the Ministry of Science and Higher Education of the
   Russian Federation within the framework of state support for the
   creation and development of World-Class Research Centers "Digital
   biodesign and personalized healthcare" No 075-15-2022-304 and by the
   National Natural Science Foundation of China (No. 81800805), Qingdao Key
   Research Project (No. 17-3-3-10-nsh and 19-6-1-3-nsh) and Qingdao Key
   Health Discipline Development Fund.
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   NAT BIOTECHNOL
NR 90
TC 5
Z9 5
U1 0
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD OCT 31
PY 2022
VL 22
IS 1
AR 1113
DI 10.1186/s12885-022-10177-3
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5V1HC
UT WOS:000876986600005
PM 36316649
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Gouda, MA
   Subbiah, V
AF Gouda, M. A.
   Subbiah, V.
TI Precision oncology for <i>BRAF</i>-mutant cancers with <i>BRAF</i> and
   <i>MEK</i> inhibitors: from melanoma to tissue-agnostic therapy
SO ESMO OPEN
LA English
DT Review
DE BRAF; MEK; cancer; precision oncology; targeted therapy
ID DABRAFENIB PLUS TRAMETINIB; CELL LUNG-CANCER; OPEN-LABEL; SINGLE-ARM;
   METASTATIC MELANOMA; IMPROVED SURVIVAL; RAF INHIBITION; LOW-GRADE;
   VEMURAFENIB; PHASE-2
AB BRAF activation occurs as part of the mitogen-activated protein kinase (MAPK) cellular signaling pathway which leads to increased cellular proliferation and survival. Mutations in BRAF can result in unbridled activation of downstream kinases with subsequent uncontrolled cellular growth that formulate the basis for oncogenesis in multiple tumor types. Targeting BRAF by selective inhibitors has been one of the early successes in precision oncology. Agents have been explored either as monotherapy or in combination with MEK inhibition in BRAF V600-mutant pan-cancers and with EGFR inhibition in colorectal cancer. Spectrum of BRAF inhibition has evolved from being melanoma-specific to being a pan-cancer target. In this article, we review BRAF and MEK inhibitor drug development journey from tissuespecific melanoma, non-small-cell lung cancer, and anaplastic thyroid cancer to tissue-agnostic approvals. Key words: BRAF, MEK, cancer, precision oncology, targeted therapy
C1 [Gouda, M. A.; Subbiah, V.] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Invest Canc Therapeut, Houston, TX 77030 USA.
   [Gouda, M. A.] Menoufia Univ, Dept Clin Oncol, Fac Med, Menoufia, Egypt.
   [Subbiah, V.] Univ Texas MD Anderson Canc Ctr, Div Pediat, Houston, TX 77030 USA.
   [Subbiah, V.] Univ Texas MD Anderson Canc Ctr, MD Anderson Canc Network, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; Egyptian
   Knowledge Bank (EKB); Menofia University; University of Texas System;
   UTMD Anderson Cancer Center; University of Texas System; UTMD Anderson
   Cancer Center
RP Subbiah, V (corresponding author), Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Invest Canc Therapeut, Phase 1 Clin Trials Program, Unit 455,1515 Holcombe Blvd, Houston, TX 77030 USA.
EM vsubbiah@mdanderson.org
FU United States National Institutes of Health (NIH) grant [R01CA242845,
   R01CA273168]; Cancer Prevention and Research Institute of Texas
   [RP1100584]; Sheikh Khalifa Bin Zayed Al Nahyan Institute for
   Personalized Cancer Therapy [1U01 CA180964]; NCATS (Center for Clinical
   and Translational Sciences) grant [UL1 TR000371]; MD Anderson Cancer
   Center Support Grant [P30 CA016672]
FX This work was supported by a United States National Institutes of Health
   (NIH) grant [grant numbers R01CA242845, R01CA273168 to VS]; MD Anderson
   Cancer Center Department of Investigational Cancer Therapeutics is
   supported by the Cancer Prevention and Research Institute of Texas
   [grant number RP1100584], the Sheikh Khalifa Bin Zayed Al Nahyan
   Institute for Personalized Cancer Therapy [grant number 1U01 CA180964],
   an NCATS (Center for Clinical and Translational Sciences) grant [grant
   number UL1 TR000371], and the MD Anderson Cancer Center Support Grant
   [grant number P30 CA016672].
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NR 87
TC 40
Z9 42
U1 9
U2 27
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PD APR
PY 2023
VL 8
IS 2
DI 10.1016/j.esmoop.2023.100788
EA FEB 2023
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA I0PF0
UT WOS:000999873700001
PM 36842301
OA Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Chen, ZQ
   Chen, JD
   Gao, Y
   Quan, M
AF Chen, Zhiqin
   Chen, Jinde
   Gao, Yong
   Quan, Ming
TI Heterogeneous clinical and pathological landscapes of HER2 positive
   colorectal cancer
SO EXPERT REVIEW OF ANTICANCER THERAPY
LA English
DT Review
DE Colorectal cancer; erbb2; clinicopathological features; targeted
   therapy; precision medicine
ID EXPRESSION; RESISTANCE; MUTATIONS; AFATINIB; DOMAIN
AB Introduction: Metastatic (m) colorectal cancer (CRC) can be divided into specific subgroups under the 'one gene, one drug' paradigm of precision medicine. Progress of targeted therapy in mCRC patients significantly improved the overall survival rate, notably by therapy targeting of EGFR signaling in RAS wild-type mCRC patients. Activation of the HER2 pathway is an important mechanism of resistance for anti-EGFR therapy. Area covered: Inhibition of HER2 with monoclonal antibodies and/or tyrosine kinase inhibitors induces tumor responses in partial HER2-positive CRC refractory to standard systemic therapy. This manuscript aimed to provide an overall insight of the HER2 expression pattern and highlighted specific clinicopathological and molecular features involved in mCRC. In addition, we summarize preclinical and clinical trials in HER2-positive mCRC. Expert opinion: The status and progression of HER2-positive gastric cancer and breast cancer and anti-HER2 therapy have been reported widely. However, the understanding of HER2-positive CRC models which may guide future therapeutic decision-making is poor. Therefore, it is essential to summarize the existing research to extract similarity and difference among various studies.
C1 [Chen, Zhiqin; Chen, Jinde; Gao, Yong; Quan, Ming] Tongji Univ, Shanghai East Hosp, Dept Oncol, Sch Med, Shanghai, Peoples R China.
C3 Tongji University
RP Quan, M (corresponding author), Tongji Univ, Shanghai East Hosp, Dept Oncol, Sch Med, Shanghai, Peoples R China.
EM mquan@tongji.edu.cn
RI Quan, Ming/KIC-9266-2024
FU National Natural Science Foundation of China [81972280]; Natural Science
   Foundation of Shanghai [19ZR1441800]; Outstanding Clinical Discipline
   Project of Shanghai Pudong [PWYgy2018-02]; Shanghai 'Rising Stars of
   Medical Talent' Youth Development Program [yyxx201901]
FX This work was supported by grants from the National Natural Science
   Foundation of China (81972280), the Natural Science Foundation of
   Shanghai (19ZR1441800), Outstanding Clinical Discipline Project of
   Shanghai Pudong (PWYgy2018-02) and Shanghai `Rising Stars of Medical
   Talent' Youth Development Program (yyxx201901).
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NR 52
TC 2
Z9 2
U1 0
U2 8
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1473-7140
EI 1744-8328
J9 EXPERT REV ANTICANC
JI Expert Rev. Anticancer Ther
PD OCT 3
PY 2021
VL 21
IS 10
BP 1097
EP 1104
DI 10.1080/14737140.2021.1944108
EA JUL 2021
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA US3SC
UT WOS:000673391800001
PM 34130577
DA 2025-01-04
ER

PT J
AU Ros, J
   Saoudi, N
   Salvà, F
   Baraibar, I
   Alonso, G
   Tabernero, J
   Elez, E
AF Ros, Javier
   Saoudi, Nadia
   Salva, Francesc
   Baraibar, Iosune
   Alonso, Guzman
   Tabernero, Josep
   Elez, Elena
TI Ongoing and evolving clinical trials enhancing future colorectal cancer
   treatment strategies
SO EXPERT OPINION ON INVESTIGATIONAL DRUGS
LA English
DT Review
DE BRAF; KRAS-G12C; HER2; MSI; targeted therapy; liquid biopsy; colorectal
   cancer
ID CIRCULATING-TUMOR DNA; MINIMAL RESIDUAL DISEASE; PLUS CETUXIMAB
   TREATMENT; ADVANCED COLON-CANCER; MICROSATELLITE INSTABILITY; RAS
   MUTATIONS; PHASE-II; COMBINED BRAF; OPEN-LABEL; PREOPERATIVE
   CHEMOTHERAPY
AB Introduction Molecular profiling has led to significantly longer survival in metastatic colorectal cancer (CRC) patients. Clinical guidelines recommend testing for KRAS/NRAS, BRAF, and MSI status, and over the last few years, several promising new biomarkers have also been identified. Circulating tumor DNA has reshaped the prognosis of localized CRC. These genomic findings can guide treatment management to improve clinical outcomes. Areas covered Preclinical and clinical data over the last decade were reviewed for known and novel biomarkers with clinical implications in refractory and metastatic CRC. In the localized stage, all clinical trials involving new approaches such as liquid biopsy or neoadjuvant immunotherapy are also discussed. Molecular alterations and targeted agents are described, and data from completed and ongoing studies with targeted therapy and immunotherapies are presented. Expert opinion The implementation of liquid biopsies in the localized CRC setting has reshaped management of this disease. The expanded use of biomarkers to guide CRC patients' treatment has revealed a level of complexity arising from interactions between different biomarkers. Prevalence of most established targetable biomarkers is low; however, the number of identified biomarkers in CRC is increasing. Thus, metastatic CRC may ultimately be considered an umbrella diagnosis encompassing numerous rare disease subtypes.
C1 [Ros, Javier; Saoudi, Nadia; Salva, Francesc; Baraibar, Iosune; Alonso, Guzman; Tabernero, Josep; Elez, Elena] Vall dHebron Univ Hosp, Med Oncol, Carrer Natzaret 115-117, Barcelona 08035, Spain.
   [Ros, Javier; Saoudi, Nadia; Salva, Francesc; Baraibar, Iosune; Alonso, Guzman; Tabernero, Josep; Elez, Elena] Vall dHebron Inst Oncol VHIO, Barcelona, Spain.
   [Ros, Javier] Univ Campania Luigi Vanvitelli, Med Oncol, Dept Precis Med, Naples, Italy.
C3 Hospital Universitari Vall d'Hebron; Vall d'Hebron Institut d'Oncologia
   (VHIO); Universita della Campania Vanvitelli
RP Ros, J (corresponding author), Vall dHebron Univ Hosp, Med Oncol, Carrer Natzaret 115-117, Barcelona 08035, Spain.; Ros, J (corresponding author), Vall dHebron Inst Oncol VHIO, Ctr Cellex, Carrer Natzaret 115-117, Barcelona 08035, Spain.
EM fjros@vhio.net
RI Baraibar, Iosune/GXF-7067-2022; Gonzalez, Nadia/AAM-9354-2021; Ros,
   Javier/HKF-1171-2023
OI Saoudi Gonzalez, Nadia/0000-0001-6044-1703; Salva,
   Francesc/0000-0001-9240-4907; Baraibar, Iosune/0000-0002-3500-9641; Ros,
   Javier/0000-0002-8137-5415
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NR 115
TC 6
Z9 6
U1 0
U2 10
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1354-3784
EI 1744-7658
J9 EXPERT OPIN INV DRUG
JI Expert Opin. Investig. Drugs
PD MAR 4
PY 2022
VL 31
IS 3
BP 235
EP 247
DI 10.1080/13543784.2022.2040016
EA FEB 2022
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA ZY7FR
UT WOS:000757774700001
PM 35133234
DA 2025-01-04
ER

PT J
AU Taghizadeh, H
   Mader, RM
   Mullauer, L
   Erhart, F
   Kautzky-Willer, A
   Prager, GW
AF Taghizadeh, Hossein
   Mader, Robert M.
   Mullauer, Leonhard
   Erhart, Friedrich
   Kautzky-Willer, Alexandra
   Prager, Gerald W.
TI Precision Medicine for the Management of Therapy Refractory Colorectal
   Cancer
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Article
DE molecular oncology; precision medicine; colorectal cancer; targeted
   therapy; molecular profiling
AB In this analysis, we examined the efficacy, feasibility, and limitations of molecular-based targeted therapies in heavily pretreated metastatic colorectal cancer (mCRC) patients after failure of all standard treatments. In this single-center, real-world retrospective analysis of our platform for precision medicine, we mapped the molecular profiles of 60 mCRC patients. Tumor samples of the patients were analyzed using next-generation sequencing panels of mutation hotspots, microsatellite instability testing, and immunohistochemistry. All profiles were reviewed by a multidisciplinary team to provide a targeted treatment recommendation after consensus discussion. In total, we detected 166 mutations in 53 patients. The five most frequently found mutations were TP53, KRAS, APC, PIK3CA, and PTEN. In 28 cases (47% of all patients), a molecularly targeted therapy could be recommended. Eventually, 12 patients (20%) received the recommended therapy. Six patients (10%) had a clinical benefit. The median time to treatment failure was 3.1 months. Our study demonstrates the feasibility and applicability of using targeted therapies in daily clinical practice for heavily pretreated mCRC patients. This could be used as a targeted treatment option in half of the patients.
C1 [Taghizadeh, Hossein; Mader, Robert M.; Prager, Gerald W.] Med Univ Vienna, Dept Med 1, Div Clin Oncol, A-1090 Vienna, Austria.
   [Taghizadeh, Hossein; Mader, Robert M.; Mullauer, Leonhard; Prager, Gerald W.] Comprehens Canc Ctr Vienna, A-1090 Vienna, Austria.
   [Mullauer, Leonhard] Med Univ Vienna, Clin Inst Pathol, A-1090 Vienna, Austria.
   [Erhart, Friedrich] Amstetten Reg State Clin, Dept Internal Med, A-3300 Amstetten, Austria.
   [Kautzky-Willer, Alexandra] Med Univ Vienna, Gender Med Unit, Dept Med 3, A-1090 Vienna, Austria.
C3 Medical University of Vienna; Medical University of Vienna; Medical
   University of Vienna
RP Prager, GW (corresponding author), Med Univ Vienna, Dept Med 1, Div Clin Oncol, A-1090 Vienna, Austria.; Prager, GW (corresponding author), Comprehens Canc Ctr Vienna, A-1090 Vienna, Austria.
EM seyed.taghizadehwaghefi@meduniwien.ac.at; robert.mader@meduniwien.ac.at;
   leonhard.muellauer@meduniwien.ac.at;
   Friedrich.Erhart@amstetten.lknoe.at;
   alexandra.kautzky-willer@meduniwien.ac.at;
   gerald.prager@meduniwien.ac.at
RI Prager, Gerald/AAS-8674-2021; Mullauer, Leonhard/GSN-9884-2022;
   Taghizadeh, Hossein/AAL-9334-2020
OI Kautzky-Willer, Alexandra/0000-0002-3520-4105; Mader,
   Robert/0000-0003-3017-8240; Mullauer, Leonhard/0000-0002-3399-078X;
   Taghizadeh, Hossein/0000-0002-0927-6498
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NR 35
TC 5
Z9 5
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 2020
VL 10
IS 4
AR 272
DI 10.3390/jpm10040272
PG 19
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA PJ6SB
UT WOS:000601893700001
PM 33322358
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, XL
   Ma, YM
   Ma, JH
   Yang, L
   Song, QZ
   Wang, HY
   Lv, GQ
AF Zhang, Xiaoli
   Ma, Yiming
   Ma, Jianhui
   Yang, Lan
   Song, Qingzhi
   Wang, Hongying
   Lv, Guoqing
TI Glutathione Peroxidase 4 as a Therapeutic Target for Anti-Colorectal
   Cancer Drug-Tolerant Persister Cells
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; drug tolerance; ferroptosis; glutathione peroxidase 4
   (GPX4); ferrous iron
ID STATE; FERROPTOSIS
AB BackgroundDespite the effectiveness of chemotherapy and targeted therapy for colorectal cancer, drug resistance drives therapy failure and tumor relapse. Increasing evidence has suggested that cancer cells can enter a reversible drug-tolerant persister state to survive chemotherapy or targeted agents. However, the traits and treatable vulnerabilities of anti-colorectal cancer drug-tolerant persister cells is not yet known. MethodsIn this study, we established 5-fluorouracil and AZ628-tolerant persister cell models in two colorectal cancer cell lines, namely HCT116 and SW620, and revealed the characteristics of colorectal cancer persister cells by cell viability assay and flow cytometry. We investigated the efficacy and mechanism of ferroptosis inducers RSL3 and FIN56 on persister cells, which are glutathione peroxidase 4 inhibitors. In the xenograft mouse model, we further evaluated the inhibitory effect of RSL3 on tumor regrowth. ResultsColorectal cancer persister cells, which were enriched in the residual cancer cell population, exhibited reduced drug sensitivity, were largely quiescent and expressed high levels of stem cell-related genes and mesenchymal markers but not epithelial markers. The persister cells were more sensitive and underwent ferroptosis induced by glutathione peroxidase 4 inhibitors. Mechanistically, glutathione peroxidase 4 and ferrous iron, which are pivotal ferroptosis regulators, were upregulated in residual cells or tumors, and were hence potential therapeutic targets of persister cells. In the xenograft model, we confirmed that inhibition of glutathione peroxidase 4 restrained tumor regrowth after discontinuation of anti-cancer drug treatment. Moreover, biopsies obtained from patients with colorectal cancer undergoing neoadjuvant chemoradiotherapy revealed upregulated glutathione peroxidase 4 and ferritin heavy chain 1. High glutathione peroxidase 4 expression correlates with a worse prognosis in colorectal cancer patients. ConclusionsOur work reveals that the upregulated glutathione peroxidase 4 and ferrous iron in anti-colorectal cancer drug-tolerant persister cells were potential therapeutic targets. Glutathione peroxidase 4 inhibition combined with chemotherapy or targeted therapy may be a promising therapy for colorectal cancer.
C1 [Zhang, Xiaoli; Song, Qingzhi; Lv, Guoqing] Hong Kong Univ Sci & Technol, Shenzhen Peking Univ, Peking Univ Shenzhen Hosp, Med Ctr, Shenzhen, Peoples R China.
   [Zhang, Xiaoli] Beijing Inst Technol, State Key Lab Explos Sci & Technol, Beijing, Peoples R China.
   [Zhang, Xiaoli; Ma, Yiming; Ma, Jianhui; Wang, Hongying] Chinese Acad Med Sci & Peking Union Med Coll, Canc Hosp, Natl Canc Ctr, Beijing, Peoples R China.
   [Yang, Lan] Shenzhen Univ, Dept Gastroenterol, Shenzhen Peoples Hosp 2, Hlth Sci Ctr,Affiliated Hosp 1, Shenzhen, Peoples R China.
C3 Peking University; Hong Kong University of Science & Technology; Beijing
   Institute of Technology; Chinese Academy of Medical Sciences - Peking
   Union Medical College; Peking Union Medical College; Cancer Institute &
   Hospital - CAMS; Shenzhen University
RP Lv, GQ (corresponding author), Hong Kong Univ Sci & Technol, Shenzhen Peking Univ, Peking Univ Shenzhen Hosp, Med Ctr, Shenzhen, Peoples R China.; Wang, HY (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Canc Hosp, Natl Canc Ctr, Beijing, Peoples R China.
EM hongyingwang@cicams.ac.cn; guoqinglv123@163.com
RI Ma, Yiming/AAG-3479-2019; lyu, guoqing/KEJ-5766-2024
OI Lv, Guoqing/0009-0006-5753-2472
FU Sanming Project of Medicine in Shenzhen [SZSM201612051]; opening project
   of State Key Laboratory of Explosion Science and Technology (Beijing
   Institute of Technology) [KFJJ22-16M]; National Nature Science
   Foundation of China [81970467]; CAMS Innovation Fund for Medical
   Sciences (CIFMS) [2019-I2M-1-003]
FX This work was supported by funding from the Sanming Project of Medicine
   in Shenzhen (SZSM201612051), the opening project of State Key Laboratory
   of Explosion Science and Technology (Beijing Institute of Technology,
   KFJJ22-16M), National Nature Science Foundation of China (81970467), and
   CAMS Innovation Fund for Medical Sciences (CIFMS, 2019-I2M-1-003).
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NR 34
TC 23
Z9 27
U1 2
U2 25
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 3
PY 2022
VL 12
AR 913669
DI 10.3389/fonc.2022.913669
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2F4EC
UT WOS:000812863800001
PM 35719967
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ohishi, T
   Kaneko, MK
   Yoshida, Y
   Takashima, A
   Kato, Y
   Kawada, M
AF Ohishi, Tomokazu
   Kaneko, Mika K.
   Yoshida, Yukihiro
   Takashima, Atsuo
   Kato, Yukinari
   Kawada, Manabu
TI Current Targeted Therapy for Metastatic Colorectal Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colorectal cancer; targeted therapy; clinical trial
ID GROWTH-FACTOR RECEPTOR; WILD-TYPE KRAS; MONOCLONAL-ANTIBODY THERAPY;
   FOLFIRI PLUS BEVACIZUMAB; POSITIVE SOLID TUMORS; 1ST-LINE TREATMENT;
   OPEN-LABEL; RAS MUTATIONS; PHASE-III; CETUXIMAB TREATMENT
AB Colorectal cancer (CRC) is the third most common type of cancer and the second leading cause of cancer deaths worldwide. Surgery or surgery plus radiotherapy and/or chemotherapy for patients with metastatic CRC (mCRC) were accepted as the main therapeutic strategies until the early 2000s, when targeted drugs, like cetuximab and bevacizumab, were developed. The use of targeted drugs in clinical practice has significantly increased patients' overall survival. To date, the emergence of several types of targeted drugs has opened new possibilities and revealed new prospects for mCRC treatment. Therapeutic strategies are continually being updated to select the most suitable targeted drugs based on the results of clinical trials that are currently underway. This review discusses the up-to date molecular evidence of targeted therapy for mCRC and summarizes the Food and Drug Administration-approved targeted drugs including the results of clinical trials. We also explain their mechanisms of action and how these affect the choice of a suitable targeted therapy.
C1 [Ohishi, Tomokazu] Microbial Chem Res Fdn, Inst Microbial Chem BIKAKEN, 18-24 Miyamoto, Numazu, Shizuoka 4100301, Japan.
   [Ohishi, Tomokazu; Kawada, Manabu] Microbial Chem Res Fdn, Inst Microbial Chem BIKAKEN, Lab Oncol, 3-14-23 Kamiosaki,Shinagawa Ku, Tokyo 1410021, Japan.
   [Kaneko, Mika K.; Kato, Yukinari] Tohoku Univ, Dept Antibody Drug Dev, Grad Sch Med, 2-1 Seiryo Machi,Aoba Ku, Sendai, Miyagi 9808575, Japan.
   [Yoshida, Yukihiro] Natl Canc Ctr, Dept Thorac Surg, 5-1-1 Tsukiji,Chuo Ku, Tokyo 1040045, Japan.
   [Takashima, Atsuo] Natl Canc Ctr, Dept Gastrointestinal Med Oncol, Chuo Ku, Tokyo 1040045, Japan.
   [Kato, Yukinari] Tohoku Univ, Dept Mol Pharmacol, Grad Sch Med, 2-1 Seiryo Machi,Aoba Ku, Sendai, Miyagi 9808575, Japan.
C3 Tohoku University; National Cancer Center - Japan; National Cancer
   Center - Japan; Tohoku University
RP Ohishi, T (corresponding author), Microbial Chem Res Fdn, Inst Microbial Chem BIKAKEN, 18-24 Miyamoto, Numazu, Shizuoka 4100301, Japan.; Ohishi, T (corresponding author), Microbial Chem Res Fdn, Inst Microbial Chem BIKAKEN, Lab Oncol, 3-14-23 Kamiosaki,Shinagawa Ku, Tokyo 1410021, Japan.; Kato, Y (corresponding author), Tohoku Univ, Dept Antibody Drug Dev, Grad Sch Med, 2-1 Seiryo Machi,Aoba Ku, Sendai, Miyagi 9808575, Japan.; Kato, Y (corresponding author), Tohoku Univ, Dept Mol Pharmacol, Grad Sch Med, 2-1 Seiryo Machi,Aoba Ku, Sendai, Miyagi 9808575, Japan.
EM ohishit@bikaken.or.jp; yukinari.kato.e6@tohoku.ac.jp
OI Kato, Yukinari/0000-0001-5385-8201; Ohishi, Tomokazu/0000-0002-9039-4474
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NR 167
TC 48
Z9 48
U1 31
U2 60
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 JAN
PY 2023
VL 24
IS 2
AR 1702
DI 10.3390/ijms24021702
PG 19
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 7X6EH
UT WOS:000914291800001
PM 36675216
OA Green Published, gold, Green Submitted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Siravegna, G
   Bardelli, A
AF Siravegna, Giulia
   Bardelli, Alberto
TI Blood circulating tumor DNA for non-invasive genotyping of colon cancer
   patients
SO MOLECULAR ONCOLOGY
LA English
DT Review
DE Liquid biopsy; Circulating tumor DNA; Colorectal cancer; Targeted
   therapy
ID ANTI-EGFR THERAPY; COLORECTAL-CANCER; CELL-FREE; ACQUIRED-RESISTANCE;
   KRAS MUTATIONS; LIQUID BIOPSY; PLASMA DNA; ORIGIN; EVOLUTION; MECHANISMS
AB Most solid tumors, including colorectal cancers, shed cell-free DNA (ctDNA) in the blood. ctDNA can be analyzed to generate molecular profiles which capture the heterogeneity of the disease more comprehensively then tumor tissue biopsies. This approach commonly called 'liquid biopsy' can be applied to monitor response to therapy, to assess minimal residual disease and to uncover the emergence of drug resistance. This review will discuss current and future developments of ctDNA analysis in the clinical management of colorectal cancer patients. (C) 2015 Published by Elsevier B.V. on behalf of Federation of European Biochemical Societies.
C1 [Siravegna, Giulia; Bardelli, Alberto] Univ Turin, Dept Oncol, SP 142,KM 3-95, I-10060 Turin, Italy.
   [Siravegna, Giulia; Bardelli, Alberto] IRCCS, Candiolo Canc Inst FPO, Turin, Italy.
   [Siravegna, Giulia] FIRC Inst Mol Oncol IFOM, Milan, Italy.
C3 University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia; IFOM
   - FIRC Institute of Molecular Oncology
RP Bardelli, A (corresponding author), Univ Turin, Dept Oncol, SP 142,KM 3-95, I-10060 Turin, Italy.; Bardelli, A (corresponding author), IRCCS, Candiolo Canc Inst FPO, Turin, Italy.
EM alberto.bardelli@unito.it
RI Siravegna, Giulia/Z-2826-2019; BARDELLI, Alberto/J-9721-2018
OI BARDELLI, Alberto/0000-0003-1647-5070; Siravegna,
   Giulia/0000-0002-7132-6484
FU European Community [602901 MErCuRIC]; IMI contract [115749 CANCER-ID];
   AIRC Special Program Molecular Clinical Oncology 5 per mille [9970];
   Fondazione Piemontese per la Ricerca sul Cancro-ONLUS 5 per mille
   Ministero della Salute; Ministero dell'Istruzione, dell'Universita e
   della Ricerca - progetto PRIN
FX This study was supported by the European Community's Seventh Framework
   Programme under grant agreement no. 602901 MErCuRIC; IMI contract n.
   115749 CANCER-ID; AIRC 2010 Special Program Molecular Clinical Oncology
   5 per mille, Project n. 9970; Fondazione Piemontese per la Ricerca sul
   Cancro-ONLUS 5 per mille 2010 e 2011 Ministero della Salute; Ministero
   dell'Istruzione, dell'Universita e della Ricerca - progetto PRIN
   2010-2011.
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NR 44
TC 49
Z9 49
U1 1
U2 31
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1878-0261
J9 MOL ONCOL
JI Mol. Oncol.
PD MAR
PY 2016
VL 10
IS 3
BP 475
EP 480
DI 10.1016/j.molonc.2015.12.005
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DG9CG
UT WOS:000372379800010
PM 26774880
OA hybrid, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Kim, TW
   Taieb, J
   Gurary, EB
   Lerman, N
   Cui, K
   Yoshino, T
AF Kim, Tae Won
   Taieb, Julien
   Gurary, Ellen B.
   Lerman, Nati
   Cui, Karen
   Yoshino, Takayuki
TI Olaparib with or without bevacizumab or bevacizumab and 5-fluorouracil
   in advanced colorectal cancer: Phase III LYNK-003
SO FUTURE ONCOLOGY
LA English
DT Review
DE 5-fluorouracil; bevacizumab; colorectal cancer; FOLFOX; folinic acid;
   irinotecan; maintenance therapy; olaparib; oxaliplatin; PARP inhibitor
ID FOLFIRI PLUS BEVACIZUMAB; 1ST-LINE TREATMENT; MAINTENANCE THERAPY;
   MAMMARY-TUMORS; OPEN-LABEL; COMBINATION; OXALIPLATIN; CHEMOTHERAPY;
   INHIBITION; CETUXIMAB
AB Oxaliplatin-based chemotherapy with a regimen such as FOLFOX with or without targeted therapy is a standard of care option for advanced colorectal cancer; however, long-term exposure to oxaliplatin is associated with cumulative toxicity. Growing evidence suggests maintenance therapy with a less intensive regimen after platinum-based induction therapy can provide continuing benefit with reduced toxicity. We describe the rationale and design of the Phase III LYNK-003 trial, which will evaluate the efficacy and safety of olaparib with or without bevacizumab compared with 5-fluoruracil plus bevacizumab in patients with unresectable or metastatic colorectal cancer that has not progressed on an induction course of FOLFOX plus bevacizumab. The primary end point is progression-free survival by independent central review; secondary end points include overall survival, objective response, duration of response and safety.
   Lay abstract Commonly used treatments for patients with advanced colorectal cancer are intensive chemotherapy-based combinations. However, long-term treatment with chemotherapy can cause significant toxic effects. To overcome this problem, patients with colorectal cancer are treated with chemotherapy for a short time, followed by a less aggressive maintenance regimen of the chemotherapy drug 5-fluorouracil and the targeted therapy drug bevacizumab. Here, we describe the rationale and design of the LYNK-003 study, which will investigate whether targeted therapy with olaparib alone or olaparib with bevacizumab compared with 5-fluorouracil and bevacizumab is effective and safe in patients with advanced colorectal cancer. Drugs like olaparib or bevacizumab specifically target proteins that promote cancer cell proliferation and have fewer toxic effects than chemotherapy. The results of LYNK-003 may lead to the availability of new chemotherapy-free maintenance options for patients with advanced colorectal cancer.
C1 [Kim, Tae Won] Univ Ulsan, Asan Med Ctr, Dept Oncol, Seoul 05505, South Korea.
   [Taieb, Julien] Univ Paris, Georges Pompidou European Hosp, SIRIC CARPEM, F-75015 Paris, France.
   [Gurary, Ellen B.; Lerman, Nati] Merck & Co Inc, Oncol Late Stage Dev, Kenilworth, NJ 07033 USA.
   [Cui, Karen] AstraZeneca, Oncol R&D, Late Dev Oncol, Gaithersburg, MD 20878 USA.
   [Yoshino, Takayuki] Natl Canc Ctr Hosp East, Dept Gastrointestinal Med, Kashiwa, Chiba 2778577, Japan.
C3 University of Ulsan; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris Cite; Hopital Universitaire Europeen Georges-Pompidou -
   APHP; Merck & Company; Merck & Company USA; AstraZeneca; National Cancer
   Center - Japan
RP Kim, TW (corresponding author), Univ Ulsan, Asan Med Ctr, Dept Oncol, Seoul 05505, South Korea.
EM twkimmd@amc.seoul.kr
RI Kim, Tae Won/GRX-7323-2022
OI Cui, Karen/0000-0003-3041-3706; Yoshino, Takayuki/0000-0002-0489-4756;
   Lerman, Nati/0000-0002-8744-7950; taieb, julien/0000-0002-9955-4753
FU Merck Sharp Dohme Corp.; AstraZeneca; Sanofi-Aventis; Merck Serono
FX This study is funded by Merck Sharp & Dohme Corp., a subsidiary of Merck
   & Co., Inc., NJ, USA, and AstraZeneca. TW Kim reports receiving grants
   to their institution from Sanofi-Aventis, Merck Serono, and AstraZeneca.
   J Taieb reports receiving consulting fees from Amgen, BMS, AstraZeneca,
   MSD, Merck, Pierre Fabre, Roche, Sanofi and Servier; and receiving
   payments or honoraria for lectures, presentations, speaker bureaus,
   manuscript writing, or education events from Amgen, BMS, AstraZeneca,
   MSD, Merck, Pierre Fabre, Roche, Sanofi and Servier. EB Gurary reports
   employment at Merck Sharp & Dohme Corp., a subsidiary of Merck & Co.,
   Inc., NJ, USA. N Lerman reports employment at Merck Sharp & Dohme Corp.,
   a subsidiary of Merck & Co., Inc., NJ, USA. K Cui has no conflicts to
   disclose. T Yoshino reports receiving grants to their institution from
   Taiho Pharmaceutical, Sumitomo Dainippon, Ono Pharmaceutical, Chugai
   Pharmaceutical, Amgen, Parexel International, MSD, Daiichi Sankyo, and
   Sanofi. 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.Medical writing and editorial
   assistance was provided by J Walker and D Mitra of ApotheCom (PA, USA).
   This assistance was funded by Merck Sharp & Dohme Corp., a subsidiary of
   Merck & Co., Inc., NJ, USA and AstraZeneca.
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NR 40
TC 4
Z9 4
U1 0
U2 4
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PD OCT 18
PY 2021
VL 17
IS 36
BP 5013
EP 5022
DI 10.2217/fon-2021-0899
EA NOV 2021
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XF7PK
UT WOS:000718445000001
PM 34779646
OA hybrid
DA 2025-01-04
ER

PT J
AU Hon, KW
   Abu, N
   Ab Mutalib, NS
   Jamal, R
AF Hon, Kha Wai
   Abu, Nadiah
   Ab Mutalib, Nurul-Syakima
   Jamal, Rahman
TI Exosomes As Potential Biomarkers and Targeted Therapy in Colorectal
   Cancer: A Mini-Review
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE exosomes; colorectal cancer; biomarkers; targeted therapy; molecular
   target
ID EXTRACELLULAR VESICLES; PURIFIED EXOSOMES; NONCODING RNAS; CIRCULAR
   RNAS; IN-VITRO; CELLS; SERUM; MICRORNA; PLASMA; EXPRESSION
AB The number of colorectal cancer (CRC) cases have increased gradually year by year. In fact, CRC is one of the most widely diagnosed cancer in men and women today. This disease is usually diagnosed at a later stage of the development, and by then, the chance of survival has declined significantly. Even though substantial progress has been made in understanding the basic molecular mechanism of CRC, there is still a lack of understanding in using the available information for diagnosing CRC effectively. Liquid biopsies are minimally invasive and have become the epitome of a good screening source for stage-specific diagnosis, measuring drug response and severity of the disease. There are various circulating entities that can be found in biological fluids, and among them, exosomes, have been gaining considerable attention. Exosomes can be found in almost all biological fluids including serum, urine, saliva, and breast milk. Furthermore, exosomes carry valuable molecular information such as proteins and nucleic acids that directly reflects the source of the cells. Nevertheless, the inconsistent yield and isolation process and the difficulty in obtaining pure exosomes have become major obstacles that need to be addressed. The potential usage of exosomes as biomarkers have not been fully validated and explored yet. This review attempts to uncover the potential molecules that can be derived from CRC-exosomes as promising biomarkers or molecular targets for effective diagnosing of CRC.
C1 [Hon, Kha Wai; Abu, Nadiah; Ab Mutalib, Nurul-Syakima; Jamal, Rahman] Univ Kebangsaan Malaysia, UKM Med Ctr, UKM Med Mol Biol Inst, Kuala Lumpur, Malaysia.
C3 Universiti Kebangsaan Malaysia
RP Abu, N (corresponding author), Univ Kebangsaan Malaysia, UKM Med Ctr, UKM Med Mol Biol Inst, Kuala Lumpur, Malaysia.
EM nadiah.abu@ppukm.ukm.edu.my
RI WAI, KHA/AAE-6785-2019; Mutalib, Nurul/C-2461-2014; Abu,
   Nadiah/N-8531-2016
OI Ab Mutalib, Nurul Syakima/0000-0001-6914-2224; Hon, Kha
   Wai/0000-0001-9548-3516; ABU, NADIAH/0000-0002-1488-2951
FU Universiti Kebangsaan Malaysia [DIP-2016-013]
FX This work was supported by the Dana Impak Perdana Grant, DIP-2016-013
   from Universiti Kebangsaan Malaysia.
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NR 69
TC 51
Z9 56
U1 1
U2 40
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 AUG 28
PY 2017
VL 8
AR 583
DI 10.3389/fphar.2017.00583
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FE9OA
UT WOS:000408531800001
PM 28894420
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ji, DB
   Wu, AW
AF Ji, Deng-Bo
   Wu, Ai-Wen
TI Organoid in colorectal cancer: progress and challenges
SO CHINESE MEDICAL JOURNAL
LA English
DT Review
DE Colorectal cancer; Patient-derived tumor organoids; Pre-clinical model
ID RANDOMIZED PHASE-III; TARGETED THERAPY; GENETIC-HETEROGENEITY; 1ST-LINE
   TREATMENT; TREATMENT RESPONSE; RAS MUTATIONS; SOLID TUMORS; STEM-CELLS;
   IN-VITRO; OXALIPLATIN
AB Patient-derived tumor organoids (PDOs) currently represent important modeling tools in pre-clinical investigation of malignancies. Organoid cultures conserve the genetic and phenotypic characteristics of the original tumor and maintain its heterogeneity, allowing their application in many research fields. PDOs derived from colorectal cancer (CRC) have been used for genetic modeling to investigate the function of driver genes. Some researchers have been exploring the value of CRC PDOs in chemotherapy, targeted therapy, and radiotherapy response prediction. The successful generation of PDOs derived from CRC could deepen our understanding of CRC biology and provide novel tools for cancer modeling, for realizing precision medicine by assessing specimens from individual patientsex vivo. The present review discusses recently reported advances in CRC PDOs and the challenges they face as pre-clinical models in CRC research.
C1 [Ji, Deng-Bo; Wu, Ai-Wen] Peking Univ Canc Hosp & Inst, Minist Educ, Dept Gastrointestinal Surg 3, Key Lab Carcinogenesis & Translat Res, 52 Fucheng Rd, Beijing 100142, Peoples R China.
RP Wu, AW (corresponding author), Peking Univ Canc Hosp & Inst, Minist Educ, Dept Gastrointestinal Surg 3, Key Lab Carcinogenesis & Translat Res, 52 Fucheng Rd, Beijing 100142, Peoples R China.
EM wuaw@sina.com
FU National Natural Science Foundation [81773214]
FX This work was supported by a grant from the National Natural Science
   Foundation (No. 81773214).
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EI 2542-5641
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JI Chin. Med. J.
PD AUG 20
PY 2020
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IS 16
BP 1971
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DI 10.1097/CM9.0000000000000882
PG 7
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WE Science Citation Index Expanded (SCI-EXPANDED)
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GA NP3NR
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PM 32826461
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Jones, L
   Cunningham, D
   Starling, N
AF Jones, Lauren
   Cunningham, David
   Starling, Naureen
TI HER-2 directed therapies across gastrointestinal tract cancers - A new
   frontier
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE HER-2; Gastrointestinal cancer; Gastric cancer; Biliary cancer;
   Pancreatic cancer; Colorectal cancer
ID CLINICAL-PRACTICE GUIDELINE; METASTATIC BREAST-CANCER; ADVANCED
   GASTRIC-CANCER; TRASTUZUMAB DERUXTECAN; OPEN-LABEL; GENE AMPLIFICATION;
   PROGNOSTIC-FACTOR; SCORING SYSTEM; SINGLE-ARM; RECEPTOR
AB Gastrointestinal (GI) cancers are common and in the metastatic setting they have a poor prognosis. The current mainstay of treatment of GI cancers is chemotherapy; however, the biomarker-directed treatment landscape is evolving. HER-2 is overexpressed in a portion of GI cancers and is an emerging target for therapy, with recent FDA tumor agnostic approval for trastuzumab deruxtecan. Testing for HER-2 expression is not standardized across GI cancers, methodology requires further optimization and standardization as HER-2 targeted therapy emerges into the treatment landscape. There is established rationale for use of HER-2 targeted therapy in first line treatment of metastatic gastric cancer, and emerging evidence with variable benefit in bile duct, pancreatic and colorectal cancers.
C1 [Jones, Lauren; Cunningham, David; Starling, Naureen] Royal Marsden NHS Fdn Trust, Gastrointestinal & Lymphoma Unit, London, England.
C3 Royal Marsden NHS Foundation Trust
RP Starling, N (corresponding author), Royal Marsden NHS Fdn Trust, Gastrointestinal & Lymphoma Unit, London, England.
EM Naureen.starling@rmh.nhs.uk
RI Starling, Naureen/JQV-9577-2023; Cunningham, David/ABT-0193-2022
OI Starling, Naureen/0000-0002-1496-6792; Cunningham,
   David/0000-0001-5158-1069; Jones, Lauren/0000-0001-8572-9359
FU National Institute for Health and Care Research (NIHR) Biomedical
   Research Centre at The Royal Marsden NHS Foundation Trust; Institute of
   Cancer Research, London; Small Business Research Initiative (SBRI); NHS
   England [SBRIC01P3008]; Goldman Sachs Gives Keenan Fellowship; NIHR;
   SBRI
FX This work is supported by the National Institute for Health and Care
   Research (NIHR) Biomedical Research Centre at The Royal Marsden NHS
   Foundation Trust and the Institute of Cancer Research, London. The views
   expressed are those of the authors and not necessarily those of the NIHR
   or the Department of Health and Social Care. LJ would like to
   acknowledge funding support from Small Business Research Initiative
   (SBRI) and NHS England (grant number SBRIC01P3008) and Goldman Sachs
   Gives Keenan Fellowship. DC would like to acknowledge funding support
   from NIHR. NS would like to acknowledge funding support from NIHR, SBRI
   and NHS England.
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NR 133
TC 1
Z9 1
U1 2
U2 2
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0305-7372
EI 1532-1967
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD SEP
PY 2024
VL 129
AR 102789
DI 10.1016/j.ctrv.2024.102789
EA JUL 2024
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XY2Z1
UT WOS:001265187800001
PM 38959629
OA hybrid
DA 2025-01-04
ER

PT J
AU Geissler, AL
   Geissler, M
   Kottmann, D
   Lutz, L
   Fichter, CD
   Fritsch, R
   Weddeling, B
   Makowiec, F
   Werner, M
   Lassmann, S
AF Geissler, Anna-Lena
   Geissler, Miriam
   Kottmann, Daniel
   Lutz, Lisa
   Fichter, Christiane D.
   Fritsch, Ralph
   Weddeling, Britta
   Makowiec, Frank
   Werner, Martin
   Lassmann, Silke
TI ATM mutations and E-cadherin expression define sensitivity to
   EGFR-targeted therapy in colorectal cancer
SO ONCOTARGET
LA English
DT Article
DE anti-EGFR therapy; next generation sequencing; predictive markers;
   colorectal cancer (CRC); E-cadherin
ID GROWTH-FACTOR RECEPTOR; IN-SITU HYBRIDIZATION; HUMAN COLON-CANCER; CELL
   LUNG-CANCER; WILD-TYPE; MICROSATELLITE INSTABILITY;
   MONOCLONAL-ANTIBODIES; CHEMOTHERAPY PLUS; CARCINOMA-CELLS; KRAS
   MUTATIONS
AB EGFR-targeted therapy is a key treatment approach in patients with RAS wildtype metastatic colorectal cancers (CRC). Still, also RAS wildtype CRC may be resistant to EGFR-targeted therapy, with few predictive markers available for improved stratification of patients. Here, we investigated response of 7 CRC cell lines (Caco2, DLD1, HCT116, HT29, LS174T, RKO, SW480) to Cetuximab and correlated this to NGS-based mutation profiles, EGFR promoter methylation and EGFR expression status as well as to E-cadherin expression. Moreover, tissue specimens of primary and/or recurrent tumors as well as liver and/or lung metastases of 25 CRC patients having received Cetuximab and/or Panitumumab were examined for the same molecular markers. In vitro and in situ analyses showed that EGFR promoter methylation and EGFR expression as well as the MSI and or CIMP-type status did not guide treatment responses. In fact, EGFR-targeted treatment responses were also observed in RAS exon 2 p.G13 mutated CRC cell lines or CRC cases and were further linked to PIK3CA exon 9 mutations. In contrast, non-response to EGFR-targeted treatment was associated with ATM mutations and low E-cadherin expression. Moreover, down-regulation of E-cadherin by siRNA in otherwise Cetuximab responding E-cadherin positive cells abrogated their response. Hence, we here identify ATM and E-cadherin expression as potential novel supportive predictive markers for EGFR-targeted therapy.
C1 [Geissler, Anna-Lena; Geissler, Miriam; Kottmann, Daniel; Lutz, Lisa; Fichter, Christiane D.; Weddeling, Britta; Werner, Martin; Lassmann, Silke] Univ Freiburg, Inst Surg Pathol, Freiburg, Germany.
   [Geissler, Anna-Lena; Geissler, Miriam; Kottmann, Daniel; Lutz, Lisa; Fichter, Christiane D.; Fritsch, Ralph; Makowiec, Frank; Werner, Martin; Lassmann, Silke] Univ Freiburg, Fac Med, Freiburg, Germany.
   [Geissler, Anna-Lena; Geissler, Miriam; Kottmann, Daniel; Fichter, Christiane D.] Univ Freiburg, Fac Biol, Freiburg, Germany.
   [Geissler, Anna-Lena; Werner, Martin; Lassmann, Silke] German Canc Consortium DKTK, Heidelberg, Germany.
   [Geissler, Anna-Lena; Werner, Martin; Lassmann, Silke] German Canc Res Ctr, Heidelberg, Germany.
   [Fritsch, Ralph] Univ Freiburg, Dept Internal Med, Freiburg, Germany.
   [Makowiec, Frank] Univ Freiburg, Dept Surg, Freiburg, Germany.
   [Fritsch, Ralph; Weddeling, Britta; Makowiec, Frank; Werner, Martin; Lassmann, Silke] Univ Freiburg, All Med Ctr, Comprehens Canc Ctr Freiburg, Freiburg, Germany.
   [Lassmann, Silke] Univ Freiburg, BIOSS Ctr Biol Signaling Studies, Freiburg, Germany.
C3 University of Freiburg; University of Freiburg; 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
RP Lassmann, S (corresponding author), Univ Freiburg, Inst Surg Pathol, Freiburg, Germany.; Lassmann, S (corresponding author), Univ Freiburg, Fac Med, 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, All Med Ctr, Comprehens Canc Ctr Freiburg, 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 Fritsch, Ralph/0000-0001-9639-3213; Makowiec, Frank/0000-0003-0012-3775;
   Kottmann, Daniel/0000-0002-1750-4016
FU German Consortium for Translational Cancer Research (DKTK Program
   Molecular Diagnostics); Mushett Family Foundation (Chester, NJ, USA)
FX This study was funded by the German Consortium for Translational Cancer
   Research (DKTK Program Molecular Diagnostics) and in part by the Mushett
   Family Foundation (Chester, NJ, USA) (grants to SL, MW).
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NR 72
TC 18
Z9 20
U1 0
U2 9
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD MAR 7
PY 2017
VL 8
IS 10
BP 17164
EP 17190
DI 10.18632/oncotarget.15211
PG 27
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EN5DA
UT WOS:000396024600086
PM 28199979
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Russo, V
   Lallo, E
   Munnia, A
   Spedicato, M
   Messerini, L
   D'Aurizio, R
   Ceroni, EG
   Brunelli, G
   Galvano, A
   Russo, A
   Landini, I
   Nobili, S
   Ceppi, M
   Bruzzone, M
   Cianchi, F
   Staderini, F
   Roselli, M
   Riondino, S
   Ferroni, P
   Guadagni, F
   Mini, E
   Peluso, M
AF Russo, Valentina
   Lallo, Eleonora
   Munnia, Armelle
   Spedicato, Miriana
   Messerini, Luca
   D'Aurizio, Romina
   Ceroni, Elia Giuseppe
   Brunelli, Giulia
   Galvano, Antonio
   Russo, Antonio
   Landini, Ida
   Nobili, Stefania
   Ceppi, Marcello
   Bruzzone, Marco
   Cianchi, Fabio
   Staderini, Fabio
   Roselli, Mario
   Riondino, Silvia
   Ferroni, Patrizia
   Guadagni, Fiorella
   Mini, Enrico
   Peluso, Marco
TI Artificial Intelligence Predictive Models of Response to Cytotoxic
   Chemotherapy Alone or Combined to Targeted Therapy for Metastatic
   Colorectal Cancer Patients: A Systematic Review and Meta-Analysis
SO CANCERS
LA English
DT Review
DE artificial intelligence; chemotherapy; targeted therapy; responders;
   radiomics; biomarkers; algorithm; colorectal cancer metastasis
ID THYMIDYLATE SYNTHASE EXPRESSION; MISMATCH REPAIR-DEFICIENT; CONSENSUS
   MOLECULAR SUBTYPES; AROMATIC DNA-ADDUCTS; WILD-TYPE; OPEN-LABEL;
   PRECISION MEDICINE; SUBGROUP ANALYSES; CASE-COHORT; CETUXIMAB
AB Simple Summary Metastatic colorectal cancer (mCRC) has high incidence and mortality. Nevertheless, innovative biomarkers have been developed for predicting the response to therapy. We have examined the ability of learning methods to build prognostic and predictive models to predict response to chemotherapy, alone or combined with targeted therapy in mCRC patients, by targeting specific narrative publications. After a literature search, 26 original articles met inclusion and exclusion criteria and were included in the study. We showed that all investigations conducted in this field provided generally promising results in predicting the response to therapy or toxic side-effects, using a meta-analytic approach. We found that radiomics and molecular biomarker signatures were able to discriminate response vs. non-response by correctly identifying up to 99% of mCRC patients who were responders and up to 100% of patients who were non-responders. Our study supports the use of computer science for developing personalized treatment decision processes for mCRC patients. Tailored treatments for metastatic colorectal cancer (mCRC) have not yet completely evolved due to the variety in response to drugs. Therefore, artificial intelligence has been recently used to develop prognostic and predictive models of treatment response (either activity/efficacy or toxicity) to aid in clinical decision making. In this systematic review, we have examined the ability of learning methods to predict response to chemotherapy alone or combined with targeted therapy in mCRC patients by targeting specific narrative publications in Medline up to April 2022 to identify appropriate original scientific articles. After the literature search, 26 original articles met inclusion and exclusion criteria and were included in the study. Our results show that all investigations conducted on this field have provided generally promising results in predicting the response to therapy or toxic side-effects. By a meta-analytic approach we found that the overall weighted means of the area under the receiver operating characteristic (ROC) curve (AUC) were 0.90, 95% C.I. 0.80-0.95 and 0.83, 95% C.I. 0.74-0.89 in training and validation sets, respectively, indicating a good classification performance in discriminating response vs. non-response. The calculation of overall HR indicates that learning models have strong ability to predict improved survival. Lastly, the delta-radiomics and the 74 gene signatures were able to discriminate response vs. non-response by correctly identifying up to 99% of mCRC patients who were responders and up to 100% of patients who were non-responders. Specifically, when we evaluated the predictive models with tests reaching 80% sensitivity (SE) and 90% specificity (SP), the delta radiomics showed an SE of 99% and an SP of 94% in the training set and an SE of 85% and SP of 92 in the test set, whereas for the 74 gene signatures the SE was 97.6% and the SP 100% in the training set.
C1 [Russo, Valentina; Lallo, Eleonora; Munnia, Armelle; Spedicato, Miriana; Peluso, Marco] ISPRO Study Prevent & Oncol Network Inst, Res & Dev Branch, Reg Canc Prevent Lab, I-50139 Florence, Italy.
   [Messerini, Luca; Cianchi, Fabio; Staderini, Fabio] Univ Florence, Dept Expt & Clin Med, I-50134 Florence, Italy.
   [D'Aurizio, Romina; Ceroni, Elia Giuseppe; Brunelli, Giulia] CNR, Inst Informat & Telemat, I-56124 Pisa, Italy.
   [Galvano, Antonio; Russo, Antonio] Univ Palermo, Dept Surg Oncol & Oral Sci, I-90127 Palermo, Italy.
   [Landini, Ida; Mini, Enrico] Univ Florence, Dept Hlth Sci, I-50139 Florence, Italy.
   [Nobili, Stefania] G DAnnunzio Chieti Pescara, Dept Neurosci Imaging & Clin Sci, I-66100 Chieti, Italy.
   [Ceppi, Marcello; Bruzzone, Marco] IRCCS Osped Policlin San Martino, Clin Epidemiol Unit, I-16131 Genoa, Italy.
   [Roselli, Mario; Riondino, Silvia] Tor Vergata Univ, Dept Syst Med, Med Oncol Unit, I-00133 Rome, Italy.
   [Ferroni, Patrizia; Guadagni, Fiorella] IRCCS San Raffaele Roma, BioBIM InterInst Multidisciplinary Biobank, I-00166 Rome, Italy.
   [Ferroni, Patrizia; Guadagni, Fiorella] San Raffaele Roma Open Univ, Dept Human Sci & Qual Life Promot, I-00166 Rome, Italy.
C3 University of Florence; Consiglio Nazionale delle Ricerche (CNR);
   Istituto di Informatica e Telematica (IIT-CNR); University of Palermo;
   University of Florence; G d'Annunzio University of Chieti-Pescara;
   University of Rome Tor Vergata; IRCCS San Raffaele Pisana
RP Peluso, M (corresponding author), ISPRO Study Prevent & Oncol Network Inst, Res & Dev Branch, Reg Canc Prevent Lab, I-50139 Florence, Italy.
EM m.peluso@ispro.toscana.it
RI Bruzzone, Marco/AAE-7591-2019; russo, valentina/AAB-9591-2022;
   D'Aurizio, Romina/J-8762-2016; Roselli, Mario/AAJ-5481-2020; Ceppi,
   Marcello/AAF-4733-2019; Riondino, Silvia/AAV-7126-2020; Ida,
   Ida/AAA-5304-2019; Brunelli, Giulia/HKO-1492-2023; Staderini,
   Fabio/AAM-4423-2020; Galvano, Antonio/K-7810-2016; Peluso,
   Marco/I-5187-2018; Ferroni, Patrizia/C-2705-2017
OI CIANCHI, FABIO/0000-0002-6936-8693; Brunelli,
   Giulia/0000-0002-4347-7074; Galvano, Antonio/0000-0003-4365-5683;
   Staderini, Fabio/0000-0002-2438-2563; Roselli,
   Mario/0000-0002-2431-6689; Peluso, Marco/0000-0001-7646-7967; Ceppi,
   Marcello/0000-0002-8177-8003; Russo, Valentina/0000-0002-5826-2455;
   Ferroni, Patrizia/0000-0002-9877-8712; Bruzzone,
   Marco/0000-0002-8821-4542; Riondino, Silvia/0000-0002-2965-402X
FU European Project Horizon 2020 SC1-BHC02-2019 [REVERT] [848098]; Tuscany
   Region (CRCSCREEN); Tuscany region (KNOWPAIN)
FX This work has been funded by a grant from the European Project Horizon
   2020 SC1-BHC02-2019 [REVERT, GA n. 848098], a grant of the Tuscany
   Region (CRCSCREEN) and a grant by the Tuscany region (KNOWPAIN).
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NR 137
TC 14
Z9 14
U1 2
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD AUG
PY 2022
VL 14
IS 16
AR 4012
DI 10.3390/cancers14164012
PG 38
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4B8VR
UT WOS:000846048000001
PM 36011003
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wei, B
   Huang, QY
   Zhong, XG
AF Wei, Bin
   Huang, Qiaoying
   Zhong, Xiaogang
TI RETRACTED: Upregulation of nucleostemin in colorectal cancer and its
   effects on cell malignancy (Retracted article. See vol. 9, pg. 2625,
   2016)
SO ONCOTARGETS AND THERAPY
LA English
DT Article; Retracted Publication
DE apoptosis; colorectal cancer; nucleostemin; small interfering RNA;
   Sw620; target therapy
ID EARLY-DIAGNOSIS; POOR-PROGNOSIS; UP-REGULATION; METAANALYSIS;
   EXPRESSION; MICRORNAS; SUSCEPTIBILITY; PROLIFERATION; ASSOCIATION;
   METASTASIS
AB Objective: Nucleostemin (NS) is a new protein localized in the nucleolus of most stem cells and tumor cells, which regulates their self-renewal and cell cycle progression. The aim of this study was to investigate the expression of NS in colorectal cancer (CRC) and the effects of NS knockdown in the Sw620 cell line to provide basis for clinical target therapy.
   Methods: NS expression in 372 patients with CRC and 367 normal participants was assessed using immunohistochemistry. The expression level of NS gene was evaluated by polymerase chain reaction. Then, the relationship among NS expression, clinicopathological features, and prognosis was analyzed. Silencing of NS expression was achieved by using NS-specific small-interfering RNAs. The viability and growth rate of Sw620 cells were determined by proliferation and invasion assays. Cell cycle distribution of the cells was analyzed by flow cytometry.
   Results: High NS expression was positively related with node metastasis, distant metastasis, and TNM stage. In Kaplan-Meier survival analysis, patients with low NS expression always had significantly longer survival time than those with high expression. Moreover, our results showed that knockdown of NS expression inhibited proliferation and viability of Sw620 cells in a time-dependent manner. Cell cycle studies revealed that NS depletion resulted in G1 cell cycle arrest at short times of transfection (24 hours), followed with apoptosis at longer times (48 hours and 72 hours), suggesting that post-G1 arrest apoptosis occurred in Sw620 cells.
   Conclusion: Overall, these results point to the essential role of NS in Sw620 cells; thus, this gene might be considered a promising target for treatment of CRC.
C1 [Wei, Bin; Zhong, Xiaogang] Peoples Hosp Guangxi Zhuang Autonomous Reg, Dept Gastroenterol & Peripheral Vasc Surg, Nanning 530021, Guangxi, Peoples R China.
   [Huang, Qiaoying] Guangxi Univ Chinese Med Res, Affiliated Hosp 1, Dept Med Mol Biol, Nanning, Guangxi, Peoples R China.
C3 Guangxi University of Chinese Medicine
RP Zhong, XG (corresponding author), Peoples Hosp Guangxi Zhuang Autonomous Reg, Dept Gastroenterol & Peripheral Vasc Surg, 6 Taoyuan Rd, Nanning 530021, Guangxi, Peoples R China.
EM zhongxiaogang1234@163.com
RI zhong, xiaogang/F-9642-2014
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NR 35
TC 3
Z9 4
U1 4
U2 20
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 2015
VL 8
BP 1805
EP 1814
DI 10.2147/OTT.S78461
PG 10
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA CN2CN
UT WOS:000358228100001
PM 26229488
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Zheng, ED
   Wlodarczyk, M
   Wegiel, A
   Osielczak, A
   Mozdzan, M
   Biskup, L
   Grochowska, A
   Wolyniak, M
   Gajewski, D
   Porc, M
   Marynczak, K
   Dziki,l
AF Zheng, Edward
   Wlodarczyk, Marcin
   Wegiel, Andrzej
   Osielczak, Aleksandra
   Mozdzan, Maria
   Biskup, Laura
   Grochowska, Agata
   Wolyniak, Maria
   Gajewski, Dominik
   Porc, Mateusz
   Marynczak, Kasper
   Dziki, Lukasz
TI Navigating through novelties concerning mCRC treatment-the role of
   immunotherapy, chemotherapy, and targeted therapy in mCRC
SO FRONTIERS IN SURGERY
LA English
DT Review
DE metastatic colorectal cancer (mCRC); immunotherapy; chemotherapy;
   targeted therapy; quality of life (QoL)
ID METASTATIC COLORECTAL-CANCER; POSITIVE SOLID TUMORS; RANDOMIZED
   PHASE-III; CAR-T CELLS; OPEN-LABEL; MICROSATELLITE INSTABILITY; 1ST-LINE
   TREATMENT; ELDERLY-PATIENTS; COLON-CANCER; DOUBLE-BLIND
AB Over the course of nearly six decades since the inception of initial trials involving 5-FU in the treatment of mCRC (metastatic colorectal cancer), our progressive comprehension of the pathophysiology, genetics, and surgical techniques related to mCRC has paved the way for the introduction of novel therapeutic modalities. These advancements not only have augmented the overall survival but have also positively impacted the quality of life (QoL) for affected individuals. Despite the remarkable progress made in the last two decades in the development of chemotherapy, immunotherapy, and target therapies, mCRC remains an incurable disease, with a 5-year survival rate of 14%. In this comprehensive review, our primary goal is to present an overview of mCRC treatment methods following the latest guidelines provided by the National Comprehensive Cancer Network (NCCN), the American Society of Clinical Oncology (ASCO), and the American Society of Colon and Rectal Surgeons (ASCRS). Emphasis has been placed on outlining treatment approaches encompassing chemotherapy, immunotherapy, targeted therapy, and surgery's role in managing mCRC. Furthermore, our review delves into prospective avenues for developing new therapies, offering a glimpse into the future of alternative pathways that hold potential for advancing the field.
C1 [Zheng, Edward; Wlodarczyk, Marcin; Wegiel, Andrzej; Osielczak, Aleksandra; Mozdzan, Maria; Biskup, Laura; Grochowska, Agata; Wolyniak, Maria; Gajewski, Dominik; Porc, Mateusz; Marynczak, Kasper; Dziki, Lukasz] Med Univ Lodz, Fac Med, Dept Gen & Oncol Surg, Lodz, Poland.
   [Wolyniak, Maria] Med Univ Lodz, Dept Biostat & Translat Med, Lodz, Poland.
C3 Medical University Lodz; Medical University Lodz
RP Wlodarczyk, M (corresponding author), Med Univ Lodz, Fac Med, Dept Gen & Oncol Surg, Lodz, Poland.
EM marcin.wlodarczyk@umed.lodz.pl
RI Wegiel, Andrzej/LCE-5358-2024; Grochowska, Agata/LUZ-2617-2024
OI Zheng, Edward/0009-0009-0496-293X; Grochowska,
   Agata/0009-0005-0158-8066; Wlodarczyk, Marcin/0000-0001-9118-4623;
   Dziki, Lukasz/0000-0002-0390-0827; Biskup, Laura/0009-0000-9336-3705
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NR 201
TC 1
Z9 1
U1 4
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-875X
J9 FRONT SURG
JI Front. Surg.
PD JUN 14
PY 2024
VL 11
AR 1398289
DI 10.3389/fsurg.2024.1398289
PG 22
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA WS4K4
UT WOS:001256848000001
PM 38948479
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, T
   Xu, Y
   Sun, LY
   He, B
   Hao, J
   Zhang, D
   Yang, YF
AF Zhang, Tong
   Xu, Yun
   Sun, Ling-yun
   He, Bin
   Hao, Jie
   Zhang, Da
   Yang, Yu-fei
TI Efficacy of Quxie Capsule in Metastatic Colorectal Cancer: Long-Term
   Survival Update of A Double-Blind, Randomized, Placebo Controlled Trial
SO CHINESE JOURNAL OF INTEGRATIVE MEDICINE
LA English
DT Article
DE Quxie capsule; metastatic colorectal cancer; randomited controlles
   trial; Chinese medicine
AB Objective To verify the efficacy of Quxie Capsule in patients with metastatic colorectal cancer (mCRC). Methods It was a block randomized, double-blind, placebo-controlled trial. Sixty patients with mCRC were randomized into 2 groups at a 1:1 ratio. The patients in the treatment group received conventional therapy including chemotherapy, radiotherapy, targeted therapy and supportive care, and Chinese herbal medicine combined with Quxie Capsule (each capsule of 0.4 g was orally administered at 50 mg/kg, twice daily, day 1-20, in a 30-day course) for 3 months. The patients in the control group received conventional therapy and Chinese herbal medicine combined with placebo for 3 months. Main outcome measures were overall survival (OS) and progression-free survival (PFS). Subgroup analysis was performed according to therapy lines, right or left-sided colon, targeted therapy and RAS gene status to determine the differences in PFS and OS between the two groups. Patients were followed up every 3 months until December 31st, 2018. Results Median follow-up time was 19.4 months. The median OS was 23.9 months in the treatment group [95% confidence interval (CI) 15.9-28.5] vs. 14.3 months in the control group (95% CI 11.3-21.4, P<;0.05). Hazard ratio (95% CI) was 0.55 (0.31-0.95, P=0.040). There were no significant differences between the two groups in PFS (P>0.05). In the subgroups of > second-line therapy, non-targeted therapy, RAS gene wild type and left-sided colon, the treatment group showed a significant survival benefit compared with the control group (PP<;0.01), respectively. Conclusion Quxie Capsule can reduce the risk of death and prolong the OS of patients with mCRC. (Registration No. ChiCTR-IOR-16009733)
C1 [Zhang, Tong; Xu, Yun; Sun, Ling-yun; He, Bin; Hao, Jie; Zhang, Da; Yang, Yu-fei] China Acad Chinese Med Sci, Xiyuan Hosp, Dept Oncol, Beijing 100091, Peoples R China.
C3 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 Sun, Lingyun/AFQ-4832-2022; Yang, yufei/KHW-2735-2024; Zhang,
   tong/IAP-2587-2023
FU National Natural Science Foundation of China [81573958]
FX Supported by National Natural Science Foundation of China (No. 81573958)
CR [Anonymous], Clinical Practice Guidelines in Oncology (NCCN Guidelines)
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   Zhang T, 2018, CHIN J INTEGR MED, V24, P171, DOI 10.1007/s11655-017-2962-2
NR 13
TC 5
Z9 7
U1 3
U2 7
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 NOV
PY 2022
VL 28
IS 11
BP 971
EP 974
DI 10.1007/s11655-021-3281-1
EA NOV 2021
PG 4
WC Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine
GA 5M9JQ
UT WOS:000716277600005
PM 34755287
DA 2025-01-04
ER

PT J
AU Gatalica, Z
   Vranic, S
   Xiu, J
   Swensen, J
   Reddy, S
AF Gatalica, Zoran
   Vranic, Semir
   Xiu, Joanne
   Swensen, Jeffrey
   Reddy, Sandeep
TI High microsatellite instability (MSI-H) colorectal carcinoma: a brief
   review of predictive biomarkers in the era of personalized medicine
SO FAMILIAL CANCER
LA English
DT Article
DE Colorectal cancer; Microsatellite instability; Lynch syndrome;
   Biomarkers; Conventional chemotherapy; Targeted therapy
ID GENE COPY NUMBERS; MISMATCH-REPAIR; THYMIDYLATE SYNTHASE;
   LYNCH-SYNDROME; ADJUVANT CHEMOTHERAPY; PD-1 BLOCKADE; CANCER;
   METHYLATION; ASSOCIATION; MUTATIONS
AB Approximately 15 % of colorectal carcinomas (CRC) display high level microsatellite instability (MSI-H) due to either a germline mutation in one of the genes responsible for DNA mismatch repair (Lynch syndrome, 3 %) or somatic inactivation of the same pathway, most commonly through hypermethylation of the MLH1 gene (sporadic MSI-H, 12 %). Although heterogeneous, MSI-H colorectal carcinomas as a group show some distinct biologic characteristics when compared to CRC with stable or low level microsatellite instability. In the present review we will highlight therapeutically relevant characteristics of MSI-H tumors which could lead to specific responses to some conventional chemotherapy or novel targeted therapy agents.
C1 [Gatalica, Zoran; Xiu, Joanne; Swensen, Jeffrey; Reddy, Sandeep] Caris Life Sci, 4610 South,44th Pl, Phoenix, AZ 85040 USA.
   [Vranic, Semir] Univ Clin Ctr Sarajevo, Dept Pathol, Sarajevo, Bosnia & Herceg.
C3 University of Sarajevo
RP Gatalica, Z (corresponding author), Caris Life Sci, 4610 South,44th Pl, Phoenix, AZ 85040 USA.
EM zgatalica@carisls.com
RI reddy, sandeep/HTT-0221-2023; Vranic, Semir/J-4113-2012
OI Vranic, Semir/0000-0001-9743-7265
CR [Anonymous], MOL GENETIC PATHOLOG
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NR 58
TC 92
Z9 107
U1 0
U2 15
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 JUL
PY 2016
VL 15
IS 3
SI SI
BP 405
EP 412
DI 10.1007/s10689-016-9884-6
PG 8
WC Oncology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Genetics & Heredity
GA DO6LO
UT WOS:000377895100007
PM 26875156
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Holch, JW
   Ricard, I
   Stintzing, S
   von Weikersthal, LF
   Decker, T
   Kiani, A
   Vehling-Kaiser, U
   Al-Batran, SE
   Heintges, T
   Lerchenmüller, C
   Kahl, C
   Kullmann, F
   Scheithauer, W
   Scholz, M
   Müller, S
   Link, H
   Rost, A
   Höffkes, HG
   Moehler, M
   Lindig, RU
   Miller-Phillips, L
   Kirchner, T
   Jung, A
   von Einem, JC
   Modest, DP
   Heinemann, V
AF Holch, Julian Walter
   Ricard, Ingrid
   Stintzing, Sebastian
   von Weikersthal, Ludwig Fischer
   Decker, Thomas
   Kiani, Alexander
   Vehling-Kaiser, Ursula
   Al-Batran, Salah-Eddin
   Heintges, Tobias
   Lerchenmueller, Christian
   Kahl, Christoph
   Kullmann, Frank
   Scheithauer, Werner
   Scholz, Michael
   Mueller, Sebastian
   Link, Hartmut
   Rost, Andreas
   Hoeffkes, Heinz-Gert
   Moehler, Markus
   Lindig, Reinhard Udo
   Miller-Phillips, Lisa
   Kirchner, Thomas
   Jung, Andreas
   von Einem, Jobst Christian
   Modest, Dominik Paul
   Heinemann, Volker
TI Relevance of liver-limited disease in metastatic colorectal cancer:
   Subgroup findings of the FIRE-3/AIO KRK0306 trial
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE metastatic colorectal cancer; clinical biomarker; liver-limited disease;
   bevacizumab; cetuximab
ID FOLFIRI PLUS CETUXIMAB; 1ST-LINE TREATMENT; OPEN-LABEL; CHEMOTHERAPY;
   BEVACIZUMAB; MANAGEMENT; SURVIVAL; IMPACT
AB In metastatic colorectal cancer (mCRC), liver-limited disease (LLD) is associated with a higher chance of metastectomy leading to long-term survival. However, limited data describes the prognostic and predictive relevance of initially unresectable LLD with regard to targeted first-line therapy. The present analysis investigated the relevance of initially unresectable LLD in mCRC patients treated with targeted therapy against either the epidermal growth factor receptor (EGFR) or vascular epithelial growth factor (VEGF). The analysis was performed based on FIRE-3, a randomized phase III trial comparing first-line chemotherapy with FOLFIRI plus either cetuximab (anti-EGFR) or bevacizumab (anti-VEGF) in RAS wild-type (WT) mCRC. Of 400 patients, 133 (33.3%) had LLD and 267 (66.8%) had non-LLD. Median overall survival (OS) was significantly longer in LLD compared to non-LLD patients (36.0 vs. 25.4 months; hazard ratio [HR] = 0.66; 95% confidence interval [CI]: 0.51-0.87; p = 0.002). In a multivariate analysis also including secondary hepatic resection as time-dependent variable, LLD status was independently prognostic for OS (HR = 0.67; 95% CI: 0.50-0.91; p = 0.01). As assessed by interaction tests, treatment benefit from FOLFIRI plus cetuximab compared to FOLFIRI plus bevacizumab was independent of LLD status with regard to objective response rate (ORR), early tumour shrinkage 20% (ETS), depth of response (DpR) and OS (all p > 0.05). In conclusion, LLD could be identified as a prognostic factor in RAS-WT mCRC, which was independent of hepatic resection in patients treated with targeted therapy. LLD had no predictive relevance since benefit from FOLFIRI plus cetuximab over bevacizumab was independent of LLD status.
C1 [Holch, Julian Walter; Stintzing, Sebastian; Miller-Phillips, Lisa; von Einem, Jobst Christian; Modest, Dominik Paul; Heinemann, Volker] Ludwig Maximilians Univ Munchen, Dept Internal Med Hematol & Oncol 3, Comprehens Canc Ctr Munich, Univ Hosp Grosshadern, Marchioninistr 15, D-81377 Munich, Germany.
   [Ricard, Ingrid] Univ Munich, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
   [von Weikersthal, Ludwig Fischer] Gesundheitszentrum St Marien GmbH, Onkol Haematol, Amberg, Germany.
   [Decker, Thomas] Onkol Ravensburg, Ravensburg, Germany.
   [Kiani, Alexander] Klinikum Bayreuth GmbH, Dept Med 4, Bayreuth, Germany.
   [Vehling-Kaiser, Ursula] Hamatoonkol Tagesklin, Landshut, Germany.
   [Al-Batran, Salah-Eddin] UCT Univ Canc Ctr, Inst Clin Canc Res, Krankenhaus Nordwest, Frankfurt, Germany.
   [Heintges, Tobias] Lukaskrankenhaus, Dept Med 2, Neuss, Germany.
   [Kahl, Christoph] Klinikum Magdeburg gGmbH, Dept Hematol Oncol & Palliat Care, Magdeburg, Germany.
   [Kullmann, Frank] Klinikum Weiden, Dept Internal Med 1, Weiden, Germany.
   [Scheithauer, Werner] Med Univ Vienna, Dept Internal Med 1, Vienna, Austria.
   [Scheithauer, Werner] Med Univ Vienna, CCC, Vienna, Austria.
   [Scholz, Michael] Krankenhaus Bad Cannstatt, Klinikum Stuttgart, Dept Med, Stuttgart, Germany.
   [Mueller, Sebastian] Ambulantes Onkol Zentrum, Ansbach, Germany.
   [Link, Hartmut] Westpfalz Klinikum, Dept Internal Med 1, Kaiserslautern, Germany.
   [Rost, Andreas] Clin Darmstadt GmbH, Med Clin Hematol Oncol 5, Darmstadt, Germany.
   [Hoeffkes, Heinz-Gert] Klinikum Fulda, Tumorklin, Fulda, Germany.
   [Moehler, Markus] Univ Med Ctr Mainz, Dept Internal Med 1, Mainz, Germany.
   [Lindig, Reinhard Udo] Univ Klinikum Jena, Klin Innere Med 2, Abt Hamatol Onkol, Jena, Germany.
   [Kirchner, Thomas; Jung, Andreas] Ludwig Maximilians Univ Munchen, Inst Pathol, Munich, Germany.
C3 University of Munich; University of Munich; Klinikum Bayreuth;
   Krankenhaus Nordwest; Medical University of Vienna; Medical University
   of Vienna; Klinikum Stuttgart; Westpfalz-Klinikum GmbH; Klinikum
   Darmstadt; Klinikum Fulda; Johannes Gutenberg University of Mainz;
   Friedrich Schiller University of Jena; University of Munich
RP Holch, JW (corresponding author), Ludwig Maximilians Univ Munchen, Dept Internal Med Hematol & Oncol 3, Comprehens Canc Ctr Munich, Univ Hosp Grosshadern, Marchioninistr 15, D-81377 Munich, Germany.
EM Julian.Holch@med.uni-muenchen.de
RI Modest, Dominik Paul/AAW-9756-2021; Rost, Andreas/F-3004-2011; Lerch,
   Markus/E-2206-2016; Link, Hartmut/AAP-8537-2020; Stintzing,
   Sebastian/I-4538-2016
OI Decker, Thomas/0000-0003-3814-8775; , Markus/0000-0003-2490-9131;
   Stintzing, Sebastian/0000-0002-3297-5801; Link,
   Hartmut/0000-0002-9659-0265
FU Merck KGaA [FIRE-3/AIO KRK0306]; Pfizer
FX Grant sponsor: FIRE-3/AIO KRK0306 was supported by Merck KGaA and Pfizer
CR [Anonymous], J CLIN ONCOL
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NR 22
TC 11
Z9 11
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD MAR 1
PY 2018
VL 142
IS 5
BP 1047
EP 1055
DI 10.1002/ijc.31114
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FR8ZC
UT WOS:000419362200018
PM 29047142
OA Bronze
DA 2025-01-04
ER

PT J
AU Cannon, TL
   Kokon, MA
   Shafqat, S
   Deeken, JF
AF Cannon, Timothy L.
   Kokon, Megan A.
   Shafqat, Sara
   Deeken, John F.
TI RAS Mutations Beyond KRAS Exon 2: A Review and Discussion of Clinical
   Trial Data
SO CURRENT TREATMENT OPTIONS IN ONCOLOGY
LA English
DT Review
DE Colorectal cancer; Other RAS mutations; Extended RAS; Review; EGFR
   inhibitors; Cetuximab; Panitumumab; Survival
ID METASTATIC COLORECTAL-CANCER; FOLFIRI PLUS BEVACIZUMAB; PHASE-III TRIAL;
   WILD-TYPE KRAS; 1ST-LINE TREATMENT; PANITUMUMAB PLUS; OPEN-LABEL;
   CETUXIMAB; CHEMOTHERAPY; FLUOROURACIL
AB The addition of targeted therapy to a 5-FU chemotherapy backbone is now a standard of care in metastatic colorectal cancer. Epidermal growth factor receptor (EGFR) inhibitors have been demonstrated to improve progression-free survival (PFS) and overall survival (OS) in the first line for patients with tumors that do not harbor KRAS exon 2 mutations. Eligibility criteria for most clinical trials involving EGFR inhibitors in recent years have used the absence of KRAS exon 2 mutation as the sole criteria for entry, as this specific mutation has been consistently shown to be predictive of a poor response to EGFR inhibitors. However, expanded analyses of first-line metastatic trials reveal that other RAS mutations, such as other KRAS mutations in exons 3 and 4, along with NRAS mutations, are predictive of poor responses to EGFR inhibitors as well. Testing for a full panel of these RAS mutations should be done prior to initiating treatment with an EGFR inhibitor. Further clinical trials are required to determine the predictive impact of each of these individual mutations. To date, they have been analyzed in the aggregate. The addition of targeted therapy, bevacizumab or an EGFR inhibitor, to a chemotherapy backbone should be considered for all appropriate patients. The relevant clinical trials that evaluated patients without any RAS mutation and compared an EGFR inhibitor to chemotherapy alone show a distinct advantage in overall survival and progression-free survival to the groups that received EGFR inhibition. The largest trial that compared bevacizumab with an EGFR inhibitor in the first line, CALGB/SWOG 80405, did not show a statistically significant difference between the two groups, making the use of bevacizumab, cetuximab, or panitumumab reasonable in the first line.
C1 [Cannon, Timothy L.; Kokon, Megan A.] INOVA Med Grp, Fairfax, VA 22031 USA.
   [Deeken, John F.] Virginia Commonwealth Univ, Fairfax, VA 22031 USA.
C3 Virginia Commonwealth University
RP Cannon, TL (corresponding author), INOVA Med Grp, 8505 Arlington Blvd,Suite 100, Fairfax, VA 22031 USA.
EM timothy.cannon@inova.org
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NR 59
TC 2
Z9 2
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1527-2729
EI 1534-6277
J9 CURR TREAT OPTION ON
JI Curr. Treat. Options Oncol.
PD JUL
PY 2015
VL 16
IS 7
AR 33
DI 10.1007/s11864-015-0350-8
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CM1HB
UT WOS:000357430800004
PM 26050230
DA 2025-01-04
ER

PT J
AU Pourhanifeh, MH
   Mehrzadi, S
   Hosseinzadeh, A
AF Pourhanifeh, Mohammad Hossein
   Mehrzadi, Saeed
   Hosseinzadeh, Azam
TI Melatonin and regulation of miRNAs: novel targeted therapy for cancerous
   and noncancerous disease
SO EPIGENOMICS
LA English
DT Review
DE angiogenesis; apoptosis; cancer; chemotherapy; gene expression;
   inflammation; melatonin; metastasis; microRNA; oxidative stress
ID COLORECTAL-CANCER; OXIDATIVE STRESS; DRUG-RESISTANCE; GENE-EXPRESSION;
   NONCODING RNA; BREAST-CANCER; UP-REGULATION; ORAL-CANCER; CELL-LINES;
   AUTOPHAGY
AB miRNAs, small noncoding RNAs with crucial diagnostic and prognostic capabilities, play essential therapeutic roles in different human diseases. These biomarkers are involved in several biological mechanisms and are responsible for the regulation of multiple genes expressions in cells. miRNA-based therapy has shown a very bright future in the case of clinical interventions. Melatonin, the main product of the pineal gland, is a multifunctional neurohormone with numerous therapeutic potentials in human diseases. Melatonin is able to regulate miRNAs in different pathologies such as malignant and nonmalignant diseases, which can be considered as a novel kind of targeted therapy. Herein, this review discusses possible therapeutic utility of melatonin for the regulation of miRNAs in various pathological conditions.
C1 [Pourhanifeh, Mohammad Hossein; Mehrzadi, Saeed; Hosseinzadeh, Azam] Iran Univ Med Sci, Razi Drug Res Ctr, Tehran, Iran.
C3 Iran University of Medical Sciences
RP Hosseinzadeh, A (corresponding author), Iran Univ Med Sci, Razi Drug Res Ctr, Tehran, Iran.
EM hosseinzadeazam@gmail.com
RI Mehrzadi, Saeed/AAY-8389-2020; Hosseinzadeh, Azam/AAN-6886-2021;
   hosseinzadeh, azam/K-5119-2018
OI Pourhanifeh, Mohammad Hossein/0000-0002-6752-2765; Mehrzadi,
   Saeed/0000-0001-6619-2330; hosseinzadeh, azam/0000-0001-6379-5769
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NR 156
TC 17
Z9 17
U1 0
U2 13
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1750-1911
EI 1750-192X
J9 EPIGENOMICS-UK
JI Epigenomics
PD JAN
PY 2021
VL 13
IS 1
BP 65
EP 81
DI 10.2217/epi-2020-0241
EA DEC 2020
PG 17
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA PV0YF
UT WOS:000600903800001
PM 33350862
DA 2025-01-04
ER

PT J
AU He, SQ
   Li, XW
   Zhou, XD
   Weng, WM
   Lai, JJ
AF He, Shengquan
   Li, Xiaowen
   Zhou, Xindong
   Weng, Weiming
   Lai, Jiajun
TI Role of epithelial cell-mesenchymal transition regulators in molecular
   typing and prognosis of colon cancer
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Epithelial-mesenchymal transition (EMT); molecular typing; random forest
   algorithm; PCOLCE2; CXCL1
ID METASTASIS; EXPRESSION; PROGRESSION; THERAPY; ZEB1; LUNG; EMT
AB Background: Despite advances in colon cancer screening, diagnosis, chemotherapy, and targeted therapy, the prognosis remains poor once colon cancer develops distant metastasis or local recurrence. To further improve the prognosis of colon cancer patients, researchers or clinicians may need to identify new indicators for predicting the prognosis and treatment of colon cancer.Methods: In order to discover the new mechanism of epithelial-mesenchymal transition (EMT) promoting tumor progression and to find new indicators of colon cancer diagnosis, targeted therapy and prognosis, this study conducted The Cancer Genome Atlas (TCGA) analysis, differential gene analysis, prognostic analysis, protein-protein interaction (PPI), enrichment analysis, molecular typing, and a machine algorithm were combined with data from TCGA and Gene Expression Omnibus (GEO) databases and EMT-related genes.Results: Our study identified 22 EMT-related genes with clinical prognostic value in colon cancer. On the basis of 22 EMT-related genes, we divided colon cancer into 2 different molecular subtypes by non-negative matrix factorization (NMF) model using 14 differentially expressed genes (DEGs), and the DEGs were enriched in multiple signaling pathways related to tumor metastasis process. Further analysis of EMT DEGs revealed that the PCOLCE2 and CXCL1 genes were characteristic genes for clinical prognosis of colon cancer. Conclusions: In this study, 22 prognostic genes were screened out from 200 EMT-related genes, and then the PCOLCE2 and CXCL1 molecules were finally focused on through the combination of the NMF molecular typing model and machine learning screening feature genes, suggesting that PCOLCE2 and CXCL1 may have good application potential. The findings provide a theoretical basis for the next clinical transformation in the treatment of colon cancer.
C1 [He, Shengquan; Li, Xiaowen; Zhou, Xindong; Weng, Weiming; Lai, Jiajun] Shantou Univ, Yuebei Peoples Hosp, Dept Gastrointestinal Surg, Yuebei Peoples Hosp,Med Coll, Shaoguan, Peoples R China.
   [Weng, Weiming; Lai, Jiajun] Shantou Univ, Yuebei Peoples Hosp, Dept Gastrointestinal Surg, Yuebei Peoples Hosp,Med Coll, 133 Huimin South Rd,Wu Jiang Dist, Shaoguan 512025, Peoples R China.
C3 Shantou University; Shantou University
RP Weng, WM; Lai, JJ (corresponding author), Shantou Univ, Yuebei Peoples Hosp, Dept Gastrointestinal Surg, Yuebei Peoples Hosp,Med Coll, 133 Huimin South Rd,Wu Jiang Dist, Shaoguan 512025, Peoples R China.
EM 1906694118@qq.com; sglaijiajun@163.com
RI lai, jiajun/GMW-9443-2022
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NR 51
TC 5
Z9 5
U1 1
U2 6
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD APR 29
PY 2023
VL 14
IS 2
BP 744
EP 757
DI 10.21037/jgo-23-49
EA APR 2023
PG 14
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA O2WM1
UT WOS:000978623800001
PM 37201067
OA gold
DA 2025-01-04
ER

PT J
AU Spiegelberg, D
   Mortensen, ACL
   Palupi, KD
   Micke, P
   Wong, J
   Vojtesek, B
   Lane, DP
   Nestor, M
AF Spiegelberg, Diana
   Mortensen, Anja Charlotte Lundgren
   Palupi, Kartika Dyah
   Micke, Patrick
   Wong, Julin
   Vojtesek, Borivoj
   Lane, David Philip
   Nestor, Marika
TI The Novel Anti-cMet Antibody seeMet 12 Potentiates Sorafenib Therapy and
   Radiotherapy in a Colorectal Cancer Model
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE radio-sensitization; chemo-sensitization; combination treatment;
   colorectal cancer; c-Met; HGFR; synergy
ID C-MET; SCATTER FACTOR; CELL-GROWTH; IN-VITRO; OVEREXPRESSION; INHIBITOR;
   SENSITIVITY; COMBINATION; EXPRESSION; RESISTANCE
AB Rational cMet is abnormally regulated in gastrointestinal cancer, and is associated with increased invasiveness of the disease and poor overall survival. There are indications that targeted therapy against cMet, alone or in combination with additional cancer therapies, can help improve treatment outcome. Thus, in the present study we investigated the therapeutic efficacy of a novel cMet-targeting antibody therapy in gastrointestinal cancer models, and assessed potential augmenting effects in combination with tyrosine kinase inhibitor (TKI) targeted therapy or radiotherapy. Methods Three different cMet-targeting antibodies were first characterized with respect to antigen binding and effects on cell viabilityin vitro. The best performing candidate seeMet 12 was then further assessed for effects on colorectal cancer cell growth, proliferation and migration. Combinations with the TKI-inhibitor sorafenib or external beam radiotherapy were then evaluated for potential additive or synergistic effectsin vitrousing monolayer- and multicellular tumor spheroid assays. Finally, the combination of seeMet 12 and radiotherapy was evaluatedin vivoin a proof-of-concept colorectal cancer xenograft study. Results Dose-dependent therapeutic effects were demonstrated for all three cMet-targeting antibodies. Monotherapy using seeMet 12 resulted in impaired cellular migration/proliferation and reduced tumor spheroid growth. Moreover, seeMet 12 was able to potentiate therapeutic effectsin vitrofor both sorafenib and radiotherapy treatments. Finally, thein vivotherapy study demonstrated promising results, where a combination of seeMet 12 and fractionated radiotherapy increased median survival by 79% compared to radiotherapy alone, and tripled maximum survival. Conclusion The novel anti-cMet antibody seeMet 12 demonstrated therapeutic effects in cMet positive gastrointestinal cancer cellsin vitro. Moreover, the addition of seeMet 12 augmented the effects of sorafenib and radiotherapy. Anin vivoproof-of-concept study of seeMet 12 and radiotherapy further validated the results. Thus, cMet-targeted therapy should be further explored as a promising approach to increase therapeutic effects, circumvent treatment resistance, and reduce side effects.
C1 [Spiegelberg, Diana; Mortensen, Anja Charlotte Lundgren; Palupi, Kartika Dyah; Micke, Patrick; Nestor, Marika] Uppsala Univ, Dept Immunol Genet & Pathol, Uppsala, Sweden.
   [Spiegelberg, Diana] Uppsala Univ, Dept Surg Sci, Uppsala, Sweden.
   [Wong, Julin; Lane, David Philip] ASTAR, Lab P53, Singapore, Singapore.
   [Vojtesek, Borivoj] Masaryk Mem Canc Inst, Res Ctr Appl Mol Oncol RECAMO, Brno, Czech Republic.
   [Lane, David Philip] Karolinska Inst, Sci Life Lab, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden.
C3 Uppsala University; Uppsala University; Agency for Science Technology &
   Research (A*STAR); Masaryk Memorial Cancer Institute; Karolinska
   Institutet
RP Spiegelberg, D (corresponding author), Uppsala Univ, Dept Immunol Genet & Pathol, Uppsala, Sweden.; Spiegelberg, D (corresponding author), Uppsala Univ, Dept Surg Sci, Uppsala, Sweden.
EM diana.spiegelberg@igp.uu.se
RI Lane, David/C-4920-2008; Spiegelberg, Diana/AAC-7174-2020; Nestor,
   Marika/HEZ-1169-2022
OI Mortensen, Anja/0000-0002-6771-3289; Spiegelberg,
   Diana/0000-0002-1509-2142; Palupi, Kartika Dyah/0000-0002-5999-122X
FU Swedish Cancer Society [CAN 2018/494, CAN 2015/1080]; Swedish Research
   Council [2013-30876-104113-30, 2013-8807]; project ENOCH
   [CZ.02.1.01/0.0/0.0/16_019/0000868]; project MH CZ -DRO (MMCI)
   [00209805]
FX This study was supported by grants from the Swedish Cancer Society (CAN
   2018/494 and CAN 2015/1080), and the Swedish Research Council
   (2013-30876-104113-30 and 2013-8807). BV was supported by projects ENOCH
   (No. CZ.02.1.01/0.0/0.0/16_019/0000868) and MH CZ -DRO (MMCI, 00209805).
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NR 45
TC 5
Z9 5
U1 0
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD SEP 11
PY 2020
VL 10
AR 1717
DI 10.3389/fonc.2020.01717
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NX8BQ
UT WOS:000575929900001
PM 33014851
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Amatu, A
   Sartore-Bianchi, A
   Bencardino, K
   Pizzutilo, EG
   Tosi, F
   Siena, S
AF Amatu, A.
   Sartore-Bianchi, A.
   Bencardino, K.
   Pizzutilo, E. G.
   Tosi, F.
   Siena, S.
TI Tropomyosin receptor kinase (TRK) biology and the role of <i>NTRK</i>
   gene fusions in cancer
SO ANNALS OF ONCOLOGY
LA English
DT Review
DE TRK; tropomyosin receptor kinase; NTRK gene fusions; TRK fusion cancer
ID NERVE GROWTH-FACTOR; TYROSINE PROTEIN-KINASE; NEUROTROPHIC FACTOR;
   MESOBLASTIC NEPHROMA; TARGETED THERAPY; CONGENITAL INSENSITIVITY;
   INHIBITOR ENTRECTINIB; PROTOONCOGENE PRODUCT; ACQUIRED-RESISTANCE;
   HIGH-FREQUENCY
AB The tropomyosin receptor kinase (TRK) family of receptor tyrosine kinases are encoded by NTRK genes and have a role in the development and normal functioning of the nervous system. Since the discovery of an oncogenic NTRK gene fusion in colorectal cancer in 1986, over 80 different fusion partner genes have been identified in a wide array of adult and paediatric tumours, providing actionable targets for targeted therapy. This review describes the normal function and physiology of TRK receptors and the biology behind NTRK gene fusions and how they act as oncogenic drivers in cancer. Finally, an overview of the incidence and prevalence of NTRK gene fusions in various types of cancers is discussed.
C1 [Amatu, A.; Sartore-Bianchi, A.; Bencardino, K.; Pizzutilo, E. G.; Tosi, F.; Siena, S.] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Dept Hematol & Oncol, Piazza Osped Maggiore 3, I-20162 Milan, Italy.
   [Sartore-Bianchi, A.; Pizzutilo, E. G.; Tosi, F.; Siena, S.] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
C3 University of Milan
RP Siena, S (corresponding author), Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Dept Hematol & Oncol, Piazza Osped Maggiore 3, I-20162 Milan, Italy.
EM salvatore.siena@unimi.it
RI Sartore-Bianchi, Andrea/AAB-9848-2019; TOSI, FEDERICA
   MARIA/AIA-1174-2022; Siena, Salvatore/ACK-2413-2022; Pizzutilo, Elio
   Gregory/KIG-8873-2024; Amatu, Alessio/K-2669-2018
OI Pizzutilo, Elio Gregory/0000-0002-1440-1820; Sartore-Bianchi,
   Andrea/0000-0003-0780-0409; TOSI, FEDERICA MARIA/0000-0001-6146-7411
FU Associazione Italiana Ricerca Cancro (AIRC) 5x1000 Special Program -
   Molecular Clinical Oncology [51000]; AIRC [20685]; AIRC 5x1000 Special
   Program - Metastases [21091]; Community Research and Development
   Information Service (CORDIS) Horizon 2020 - Molecularly Guided Trials
   with Specific Treatment Strategies in Patients with Advanced Newly
   Molecular Defined Subtypes of Colorectal Cancer (MoTriColor) [635342];
   Fondazione Regionale Ricerca Biomedica [IANG-CRC CP2_12/2018];
   Fondazione Oncologia Niguarda Onlus, grant Terapia Molecolare dei
   Tumori; Studies to Develop Therapies Against Colorectal Cancer in Young
   Adults [12018]; Bayer AG; Loxo Oncology, Inc.
FX This work is supported in part by the Associazione Italiana Ricerca
   Cancro (AIRC) 5x1000 Special Program - Molecular Clinical Oncology
   [grant number 51000]. SS is supported by the AIRC Investigator Grant
   [grant number 20685], the AIRC 5x1000 Special Program - Metastases
   [grant number 21091], Community Research and Development Information
   Service (CORDIS) Horizon 2020 - Molecularly Guided Trials with Specific
   Treatment Strategies in Patients with Advanced Newly Molecular Defined
   Subtypes of Colorectal Cancer (MoTriColor) [grant number 635342] and
   Fondazione Regionale Ricerca Biomedica [grant number IANG-CRC
   CP2_12/2018]. AS-B is supported by Fondazione Oncologia Niguarda Onlus,
   grant Terapia Molecolare dei Tumori to AS-B [no grant number
   applicable]. SS and AS-B are supported by the Studies to Develop
   Therapies Against Colorectal Cancer in Young Adults [grant number
   12018]. This paper was published as part of a supplement financially
   supported by Bayer AG and Loxo Oncology, Inc., a wholly owned subsidiary
   of Eli Lilly and Company.
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NR 121
TC 181
Z9 196
U1 4
U2 32
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD NOV
PY 2019
VL 30
SU 8
BP VIII5
EP VIII15
DI 10.1093/annonc/mdz383
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JU5PL
UT WOS:000501727600003
OA Green Published, hybrid
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Liu, WW
   Zheng, SQ
   Li, T
   Fei, YF
   Wang, C
   Zhang, S
   Wang, F
   Jiang, GM
   Wang, H
AF Liu, Wei-Wei
   Zheng, Si-Qing
   Li, Tian
   Fei, Yun-Fei
   Wang, Chen
   Zhang, Shuang
   Wang, Fei
   Jiang, Guan-Min
   Wang, Hao
TI RNA modifications in cellular metabolism: implications for
   metabolism-targeted therapy and immunotherapy
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID 18S RIBOSOMAL-RNA; PROMOTES TUMOR PROGRESSION; DEMETHYLASE FTO
   INHIBITORS; RESOLUTION MAPPING REVEALS; HEPATIC LIPID-METABOLISM; SITE
   RECOGNITION REGION; FATTY-ACID-METABOLISM; MESSENGER-RNA;
   COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA
AB Cellular metabolism is an intricate network satisfying bioenergetic and biosynthesis requirements of cells. Relevant studies have been constantly making inroads in our understanding of pathophysiology, and inspiring development of therapeutics. As a crucial component of epigenetics at post-transcription level, RNA modification significantly determines RNA fates, further affecting various biological processes and cellular phenotypes. To be noted, immunometabolism defines the metabolic alterations occur on immune cells in different stages and immunological contexts. In this review, we characterize the distribution features, modifying mechanisms and biological functions of 8 RNA modifications, including N6-methyladenosine (m6A), N6,2 '-O-dimethyladenosine (m6Am), N1-methyladenosine (m1A), 5-methylcytosine (m5C), N4-acetylcytosine (ac4C), N7-methylguanosine (m7G), Pseudouridine (psi), adenosine-to-inosine (A-to-I) editing, which are relatively the most studied types. Then regulatory roles of these RNA modification on metabolism in diverse health and disease contexts are comprehensively described, categorized as glucose, lipid, amino acid, and mitochondrial metabolism. And we highlight the regulation of RNA modifications on immunometabolism, further influencing immune responses. Above all, we provide a thorough discussion about clinical implications of RNA modification in metabolism-targeted therapy and immunotherapy, progression of RNA modification-targeted agents, and its potential in RNA-targeted therapeutics. Eventually, we give legitimate perspectives for future researches in this field from methodological requirements, mechanistic insights, to therapeutic applications.
C1 [Liu, Wei-Wei; Zheng, Si-Qing; Li, Tian; Fei, Yun-Fei; Wang, Chen; Zhang, Shuang; Wang, Hao] Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Lab Med, Div Life Sci & Med, Hefei, Peoples R China.
   [Liu, Wei-Wei] Shandong Univ, Sch Clin Med, Jinan, Peoples R China.
   [Zheng, Si-Qing; Li, Tian; Fei, Yun-Fei; Wang, Chen; Zhang, Shuang; Wang, Hao] Core Unit Natl Clin Res Ctr Lab Med, Hefei, Peoples R China.
   [Wang, Fei] Univ Sci & Technol China, Affiliated Hosp USTC 1, Neurosurg Dept, Div Life Sci & Med, Hefei, Peoples R China.
   [Jiang, Guan-Min] Sun Yat Sen Univ, Affiliated Hosp 5, Dept Clin Lab, Zhuhai, Peoples R China.
C3 Chinese Academy of Sciences; University of Science & Technology of
   China, CAS; Shandong University; Chinese Academy of Sciences; University
   of Science & Technology of China, CAS; Sun Yat Sen University
RP Wang, H (corresponding author), Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Lab Med, Div Life Sci & Med, Hefei, Peoples R China.; Wang, F (corresponding author), Univ Sci & Technol China, Affiliated Hosp USTC 1, Neurosurg Dept, Div Life Sci & Med, Hefei, Peoples R China.; Jiang, GM (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 5, Dept Clin Lab, Zhuhai, Peoples R China.
EM neurosurgeonwf1@ustc.edu.cn; jianggm3@mail.sysu.edu.cn; demo@ustc.edu.cn
FU the Scientific Research Project of Anhui Provincial Education Department
   (2022AH020079), the Natural Science Foundation of Anhui Province
   (2008085MH241). [2022AH020079]; Scientific Research Project of Anhui
   Provincial Education Department [2008085MH241]; Natural Science
   Foundation of Anhui Province
FX This study was supported by the Scientific Research Project of Anhui
   Provincial Education Department (2022AH020079), the Natural Science
   Foundation of Anhui Province (2008085MH241).
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WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
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UT WOS:001191287400001
PM 38531882
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Benson, A III
   Venook, AP
   Al-Hawary, MM
   Arain, MA
   Chen, YJ
   Ciombor, KK
   Cohen, S
   Cooper, HS
   Deming, D
   Garrido-Laguna, I
   Grem, JL
   Gunn, A
   Hoffe, S
   Hubbard, J
   Hunt, S
   Kirilcuk, N
   Krishnamurthi, S
   Messersmith, WA
   Meyerhardt, J
   Miller, ED
   Mulcahy, MF
   Nurkin, S
   Overman, MJ
   Parikh, A
   Patel, H
   Pedersen, K
   Saltz, L
   Schneider, C
   Shibata, D
   Skibber, JM
   Sofocleous, CT
   Stoffel, EM
   Stotsky-Himelfarb, E
   Willett, CG
   Johnson-Chilla, A
   Gurski, LA
AF Benson, Al B., III
   Venook, Alan P.
   Al-Hawary, Mahmoud M.
   Arain, Mustafa A.
   Chen, Yi-Jen
   Ciombor, Kristen K.
   Cohen, Stacey
   Cooper, Harry S.
   Deming, Dustin
   Garrido-Laguna, Ignacio
   Grem, Jean L.
   Gunn, Andrew
   Hoffe, Sarah
   Hubbard, Joleen
   Hunt, Steven
   Kirilcuk, Natalie
   Krishnamurthi, Smitha
   Messersmith, Wells A.
   Meyerhardt, Jeffrey
   Miller, Eric D.
   Mulcahy, Mary F.
   Nurkin, Steven
   Overman, Michael J.
   Parikh, Aparna
   Patel, Hitendra
   Pedersen, Katrina
   Saltz, Leonard
   Schneider, Charles
   Shibata, David
   Skibber, John M.
   Sofocleous, Constantinos T.
   Stoffel, Elena M.
   Stotsky-Himelfarb, Eden
   Willett, Christopher G.
   Johnson-Chilla, Alyse
   Gurski, Lisa A.
TI Rectal Cancer, Version 6.2020 <i>Featured Updates to the NCCN
   Guidelines</i>
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID CONCOMITANT CHEMORADIOTHERAPY; BRAF MUTATION; PHASE-II; CHEMOTHERAPY;
   SURGERY; CHEMORADIATION; CAPECITABINE; MANAGEMENT; CETUXIMAB
AB The NCCN Guidelines for Rectal Cancer provide recommendations for the diagnosis, evaluation, treatment, and follow-up of patients with rectal cancer. These NCCN Guidelines Insights summarize the panel discussion behind recent important updates to the guidelines. These updates include clarifying the definition of rectum and differentiating the rectum from the sigmoid colon; the total neoadjuvant therapy approach for localized rectal cancer; and biomarker-targeted therapy for metastatic colorectal cancer, with a focus on new treatment options for patients with BRAF V600E- or HER2 amplification- positive disease.
C1 [Benson, Al B., III; Mulcahy, Mary F.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
   [Venook, Alan P.; Arain, Mustafa A.] UCSF Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
   [Al-Hawary, Mahmoud M.; Stoffel, Elena M.] Univ Michigan, Rogel Canc Ctr, Ann Arbor, MI 48109 USA.
   [Chen, Yi-Jen] City Hope Natl Med Ctr, 1500 E Duarte Rd, Duarte, CA 91010 USA.
   [Ciombor, Kristen K.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
   [Cohen, Stacey] Seattle Canc Care Alliance, Fred Hutchinson Canc Res Ctr, Washington, DC USA.
   [Cooper, Harry S.] Fox Chase Canc Ctr, 7701 Burholme Ave, Philadelphia, PA 19111 USA.
   [Deming, Dustin] Univ Wisconsin, Carbone Canc Ctr, Madison, WI 53706 USA.
   [Garrido-Laguna, Ignacio] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
   [Grem, Jean L.] Fred & Pamela Buffett Canc Ctr, Omaha, NE USA.
   [Gunn, Andrew] ONeal Comprehens Canc Ctr UAB, Birmingham, AL USA.
   [Hoffe, Sarah] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
   [Hubbard, Joleen] Mayo Clin, Canc Ctr, Rochester, NY USA.
   [Hunt, Steven; Pedersen, Katrina] Washington Univ, Siteman Canc Ctr, Barnes Jewish Hosp, St Louis, MO USA.
   [Hunt, Steven; Pedersen, Katrina] Washington Univ, Sch Med, St Louis, MO USA.
   [Kirilcuk, Natalie] Stanford Canc Inst, Stanford, CA USA.
   [Krishnamurthi, Smitha] Univ Hosp Seidman Canc Ctr, Case Comprehens Canc Ctr, Cleveland, OH USA.
   [Krishnamurthi, Smitha] Cleveland Clin, Taussig Canc Inst, Cleveland, OH 44106 USA.
   [Messersmith, Wells A.] Univ Colorado, Canc Ctr, Boulder, CO 80309 USA.
   [Meyerhardt, Jeffrey] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
   [Miller, Eric D.] Ohio State Univ, Comprehens Canc Ctr, James Canc Hosp, Columbus, OH 43210 USA.
   [Miller, Eric D.] Ohio State Univ, Solove Res Inst, Columbus, OH 43210 USA.
   [Nurkin, Steven] Roswell Park Comprehens Canc Ctr, Buffalo, NY USA.
   [Overman, Michael J.; Skibber, John M.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Parikh, Aparna] Massachusetts Gen Hosp, Canc Ctr, Boston, MA 02114 USA.
   [Patel, Hitendra] UC San Diego Moores Canc Ctr, San Diego, CA USA.
   [Saltz, Leonard; Sofocleous, Constantinos T.] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
   [Schneider, Charles] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
   [Shibata, David] Univ Tennessee, Hlth Sci Ctr, Knoxville, TN 37996 USA.
   [Stotsky-Himelfarb, Eden] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
   [Willett, Christopher G.] Duke Canc Inst, Durham, NC USA.
   [Johnson-Chilla, Alyse; Gurski, Lisa A.] Natl Comprehens Canc Network, Plymouth Meeting, PA USA.
C3 Ann & Robert H. Lurie Children's Hospital of Chicago; Northwestern
   University; Robert H. Lurie Comprehensive Cancer Center; University of
   California System; University of California San Francisco; UCSF Medical
   Center; UCSF Helen Diller Family Comprehensive Cancer Center; University
   of Michigan System; University of Michigan; City of Hope; Vanderbilt
   University; Fred Hutchinson Cancer Center; Seattle Cancer Care Alliance;
   Fox Chase Cancer Center; University of Wisconsin System; University of
   Wisconsin Madison; Utah System of Higher Education; University of Utah;
   Huntsman Cancer Institute; H Lee Moffitt Cancer Center & Research
   Institute; Mayo Clinic; Siteman Cancer Center; Barnes-Jewish Hospital;
   Washington University (WUSTL); Washington University (WUSTL); Stanford
   Cancer Institute; University System of Ohio; Case Western Reserve
   University; Cleveland Clinic Foundation; University of Colorado System;
   University of Colorado Anschutz Medical Campus; University of Colorado
   Boulder; Harvard University; Dana-Farber Cancer Institute; University
   System of Ohio; Ohio State University; James Cancer Hospital & Solove
   Research Institute; University System of Ohio; Ohio State University;
   James Cancer Hospital & Solove Research Institute; Roswell Park
   Comprehensive Cancer Center; University of Texas System; UTMD Anderson
   Cancer Center; Harvard University; Massachusetts General Hospital;
   Memorial Sloan Kettering Cancer Center; University of Pennsylvania;
   University of Tennessee System; University of Tennessee Health Science
   Center; Johns Hopkins University; Johns Hopkins Medicine; Duke
   University
RP Benson, A III (corresponding author), Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
RI chen, yuling/JMQ-4121-2023; Pedersen, Katrina/KBA-8737-2024; Meyerhardt,
   Jeffrey/IAP-4528-2023; Garrido-Laguna, Ignacio/ABD-1875-2020;
   Krishnamurthi, Smitha/ABB-8593-2021
OI Pedersen, Katrina/0000-0003-2793-6901; Miller, Eric/0000-0002-4931-3521
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TC 334
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U1 8
U2 76
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 JUL
PY 2020
VL 18
IS 7
BP 807
EP 815
DI 10.6004/jnccn.2020.0032
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OA5JA
UT WOS:000577820100003
PM 32634771
OA Bronze
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Tichy, M
   Knopfová, L
   Jarkovsky, J
   Vlcek, P
   Katolická, J
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   Smarda, J
   Benes, P
AF Tichy, Michal
   Knopfova, Lucia
   Jarkovsky, Jiri
   Vlcek, Petr
   Katolicka, Jana
   Capov, Ivan
   Hermanova, Marketa
   Smarda, Jan
   Benes, Petr
TI High c-Myb Expression Associates with Good Prognosis in Colorectal
   Carcinoma
SO JOURNAL OF CANCER
LA English
DT Article
DE c-Myb; colorectal cancer; prognosis; survival
ID CANCER; OVEREXPRESSION; CLASSIFICATION; PROTOONCOGENE; TRANSCRIPTION;
   GALLBLADDER; SUPPRESSION; INCREASE; PUMA
AB Colorectal cancer (CRC) represents a serious challenge for oncologists due to high incidence and large heterogeneity. Prognostic factors are needed to stratify patients according to risk of disease progression. In this study, we report that high expression of c-Myb protein, determined by immunohistochemistry (IHC), associates with better overall and disease-free survival (OS, DFS) in a cohort of 103 patients. Although MYB has been previously considered to act as oncogene in CRC, our further analysis of datasets deposited in PrognoScan and SurvExpress databases confirmed that high MYB expression largely associates with good prognosis in CRC. As therapies targeting c-Myb have been developed and tested in preclinical studies, we believe that further studies are needed for detailed understanding of c-Myb function in CRC, before the c-Myb-targeted therapy enters clinical trials.
C1 [Tichy, Michal; Hermanova, Marketa] Masaryk Univ, St Annes Univ Hosp, Dept Pathol Anat 1, Brno, Czech Republic.
   [Tichy, Michal; Hermanova, Marketa] Masaryk Univ, Fac Med, Brno, Czech Republic.
   [Knopfova, Lucia; Smarda, Jan; Benes, Petr] Masaryk Univ, Fac Sci, Dept Expt Biol, Kamenice 5, Brno 62500, Czech Republic.
   [Knopfova, Lucia; Benes, Petr] St Annes Univ Hosp, Int Clin Res Ctr, Brno, Czech Republic.
   [Jarkovsky, Jiri] Masaryk Univ, Fac Med, Inst Biostat & Anal, Brno, Czech Republic.
   [Vlcek, Petr; Capov, Ivan] St Annes Univ Hosp Brno, Dept Surg 1, Brno, Czech Republic.
   [Katolicka, Jana] St Annes Univ Hosp Brno, Dept Oncol, Brno, Czech Republic.
C3 St. Anne's University Hospital Brno (FNUSA); Masaryk University Brno;
   Masaryk University Brno; Masaryk University Brno; St. Anne's University
   Hospital Brno (FNUSA); St. Anne's University Hospital Brno (FNUSA-ICRC);
   Institute of Biostatistics & Analyses; Masaryk University Brno; St.
   Anne's University Hospital Brno (FNUSA); St. Anne's University Hospital
   Brno (FNUSA)
RP Benes, P (corresponding author), Masaryk Univ, Fac Sci, Dept Expt Biol, Kamenice 5, Brno 62500, Czech Republic.
EM pbenes@sci.muni.cz
RI Benes, Petr/K-6369-2016
OI Knopfova, Lucia/0000-0003-4897-0404; Hermanova,
   Marketa/0000-0002-3889-0905; Benes, Petr/0000-0002-8297-9675
FU National Program of Sustainability II (Ministry of Education, Youth and
   Sports of the Czech Republic) [LQ1605]; Czech Science Foundation
   [17-08985Y]; Ministry of Health of the Czech Republic [NV18-07-00073]
FX This work was supported by project LQ1605 from the National Program of
   Sustainability II (Ministry of Education, Youth and Sports of the Czech
   Republic), 17-08985Y from Czech Science Foundation and NV18-07-00073
   from Ministry of Health of the Czech Republic.
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NR 33
TC 10
Z9 10
U1 1
U2 6
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2019
VL 10
IS 6
BP 1393
EP 1397
DI 10.7150/jca.29530
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HM8EM
UT WOS:000459711200007
PM 31031849
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Song, YQ
   Yan, XD
   Wang, Y
   Wang, ZZ
   Mao, XL
   Ye, LP
   Li, SW
AF Song, Ya-Qi
   Yan, Xiao-Dan
   Wang, Yi
   Wang, Zhen-Zhen
   Mao, Xin-Li
   Ye, Li-Ping
   Li, Shao-Wei
TI Role of ferroptosis in colorectal cancer
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Ferroptosis; Colorectal cancer; System X-c(-); Glutathione; Glutathione
   peroxidase 4
ID ERASTIN-INDUCED FERROPTOSIS; PROMOTES RSL3-INDUCED FERROPTOSIS;
   CYSTATHIONINE-BETA-SYNTHASE; LONG NONCODING RNA; SIGNALING PATHWAY;
   OXIDATIVE STRESS; CYSTINE/GLUTAMATE ANTIPORTER;
   HEPATOCELLULAR-CARCINOMA; TRANSSULFURATION PATHWAY; INHIBITS FERROPTOSIS
AB Colorectal cancer (CRC) is the second deadliest cancer and the third-most common malignancy in the world. Surgery, chemotherapy, and targeted therapy have been widely used to treat CRC, but some patients still develop resistance to these treatments. Ferroptosis is a novel non-apoptotic form of cell death. It is an iron-dependent non-apoptotic cell death characterized by the accumulation of lipid reactive oxygen species and has been suggested to play a role in reversing resistance to anticancer drugs. This review summarizes recent advances in the prognostic role of ferroptosis in CRC and the mechanism of action in CRC.
C1 [Song, Ya-Qi; Ye, Li-Ping] Zhejiang Univ, Taizhou Hosp Zhejiang Prov, Linhai 317000, Zhejiang, Peoples R China.
   [Yan, Xiao-Dan; Wang, Yi; Wang, Zhen-Zhen; Mao, Xin-Li; Ye, Li-Ping; Li, Shao-Wei] Wenzhou Med Univ, Taizhou Hosp Zhejiang Prov, Dept Gastroenterol, Linhai 317000, Zhejiang, Peoples R China.
   [Ye, Li-Ping; Li, Shao-Wei] Wenzhou Med Univ, Taizhou Hosp Zhejiang Prov, Inst Digest Dis, Linhai 317000, Zhejiang, Peoples R China.
   [Li, Shao-Wei] Wenzhou Med Univ, Taizhou Hosp Zhejiang Prov, Lab Minimally Invas Tech & Rapid Rehabil Digest Sy, Zhejiang 317000, Peoples R China.
   [Li, Shao-Wei] Wenzhou Med Univ, Taizhou Hosp Zhejiang Prov, Dept Gastroenterol, 150 Ximen St, Linhai 317000, Zhejiang, Peoples R China.
C3 Zhejiang University; Wenzhou Medical University; Wenzhou Medical
   University; Wenzhou Medical University; Wenzhou Medical University
RP Li, SW (corresponding author), Wenzhou Med Univ, Taizhou Hosp Zhejiang Prov, Dept Gastroenterol, 150 Ximen St, Linhai 317000, Zhejiang, Peoples R China.
EM li_shaowei81@hotmail.com
RI ye, li/KVY-5558-2024; WU, Yuying/ISB-0204-2023
FU Medical Health Science and Technology Project of Zhejiang Province
   [2021PY083]; Program of Taizhou Science and Technology Grant [22ywb09,
   1901ky18]; Key Technology Research and Development Program of Zhejiang
   Province [2019C03040]; Major Research Program of Taizhou Enze Medical
   Center Grant [19EZZDA2]
FX Supported by Medical Health Science and Technology Project of Zhejiang
   Province, No. 2021PY083; Program of Taizhou Science and Technology
   Grant, No. 22ywb09 and No. 1901ky18; Key Technology Research and
   Development Program of Zhejiang Province, No. 2019C03040; Major Research
   Program of Taizhou Enze Medical Center Grant, No. 19EZZDA2.
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NR 130
TC 5
Z9 5
U1 8
U2 36
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD FEB 15
PY 2023
VL 15
IS 2
BP 225
EP 239
DI 10.4251/wjgo.v15.i2.225
PG 15
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA 9S7NU
UT WOS:000946524900002
PM 36908317
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Cen, SY
   Liu, Z
   Pan, HM
   Han, WD
AF Cen, Shuyi
   Liu, Zhen
   Pan, Hongming
   Han, Weidong
TI Clinicopathologic features and treatment advances in cancers with HER2
   alterations
SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
LA English
DT Review
DE HER2; Immunotherapy; Targeted therapy; Immune checkpoint inhibitors
ID METASTATIC BREAST-CANCER; PHASE-II TRIAL; FACTOR RECEPTOR 2; CELL
   LUNG-CANCER; ADO-TRASTUZUMAB EMTANSINE; OPEN-LABEL; COLORECTAL-CANCER;
   GASTRIC-CANCER; TARGETED THERAPY; KINASE DOMAIN
AB HER2 is one of the most important proteins of the epidermal growth factor receptor (EGFR) family, whose alterations include amplification, overexpression and gene mutation. Growing attention has been given to HER2 as a biomarker for prognosis, an indicator for treatment response and a target for new drugs. Tumors with HER2 alterations have been well studied in multiple locations as distinct entities for treatment, especially breast cancer, gastric cancer, lung cancer and colorectal cancer. These four cancers are the leading causes of cancer incidence and cancer-related death worldwide. The present study details the landscape of HER2 amplification/overexpression and mutations and gives an up-to-date analysis of current clinical trials in the four cancers mentioned above. Different HER2-altered cancers not only respond differently to HER2-targeting therapies but also display diverse survival outcomes. Even in the same type of cancer, HER2 amplification/overexpression differs from HER2 mutation in terms of clinicopathologic features and treatment strategies. As an emerging strategy in cancer treatment, immune checkpoint inhibitors demonstrate distinct outcomes in HER2-altered breast cancer, gastric cancer and lung cancer.
C1 [Cen, Shuyi; Liu, Zhen; Pan, Hongming; Han, Weidong] Zhejiang Univ, Sir Run Run Shaw Hosp, Sch Med, Dept Med Oncol, Hangzhou, Zhejiang, Peoples R China.
C3 Zhejiang University
RP Pan, HM; Han, WD (corresponding author), Zhejiang Univ, Sir Run Run Shaw Hosp, Sch Med, 3 East Qinchun Rd, Hangzhou 310016, Zhejiang, Peoples R China.
EM panhongming@zju.edu.cn; hanwd@zju.edu.cn
OI Liu, Zhen/0000-0002-8910-9664
FU Zhejiang Medical Innovative Discipline Construction Project-2016; Ten
   Thousand Plan Youth Talent Support Program of Zhejiang Province
   [ZJWR0108009]
FX This work was supported by the Zhejiang Medical Innovative Discipline
   Construction Project-2016 and the Ten Thousand Plan Youth Talent Support
   Program of Zhejiang Province (ZJWR0108009).
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NR 141
TC 13
Z9 13
U1 0
U2 18
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 DEC
PY 2021
VL 1876
IS 2
AR 188605
DI 10.1016/j.bbcan.2021.188605
EA AUG 2021
PG 13
WC Biochemistry & Molecular Biology; Biophysics; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Oncology
GA US0WQ
UT WOS:000697158300014
PM 34358635
DA 2025-01-04
ER

PT J
AU Kano, Y
   Suenaga, M
   Uetake, H
AF Kano, Yoshihito
   Suenaga, Mitsukuni
   Uetake, Hiroyuki
TI Strategic Insight into the Combination Therapies for Metastatic
   Colorectal Cancer
SO CURRENT ONCOLOGY
LA English
DT Review
DE combination therapy; metastatic colorectal cancer; molecular targeted
   therapy; conversion surgery; liquid biopsy; RAS; KRAS(G12C)
ID RAS WILD-TYPE; MISMATCH REPAIR-DEFICIENT; PHASE-III TRIAL; LIVER
   METASTASES; OPEN-LABEL; PERITONEAL CARCINOMATOSIS; 1ST-LINE TREATMENT;
   PERIOPERATIVE CHEMOTHERAPY; INFUSIONAL FLUOROURACIL; CETUXIMAB
AB Colorectal cancer (CRC) is the second most common cause of cancer-related deaths worldwide. The 5-year survival rate after curative resection is almost 80%, however, it is still less than satisfactory for metastatic CRC (mCRC). The combination approach including surgery, chemotherapy, molecular targeted therapy, and immunotherapy is a promising strategy due to its synergistic anticancer effect. Moreover, circulating tumor DNA (ctDNA) analysis has been reported to stratify the post-operative risk of recurrence, thus providing clinically valuable information for deciding to conduct adjuvant chemotherapy. Furthermore, multiple new drugs that potentially target undruggable genes, including KRAS, have been developed. In this review, we discuss the current management of patients with mCRC and future perspectives in the light of a combination therapeutic strategy.
C1 [Kano, Yoshihito; Suenaga, Mitsukuni] Tokyo Med & Dent Univ TMDU, Grad Sch Med & Dent Sci, Dept Clin Oncol, Tokyo 1138510, Japan.
   [Uetake, Hiroyuki] Natl Hosp Org Disaster Med Ctr, Dept Clin Res, Tokyo 1900014, Japan.
C3 Institute of Science Tokyo; Tokyo Medical & Dental University (TMDU)
RP Suenaga, M (corresponding author), Tokyo Med & Dent Univ TMDU, Grad Sch Med & Dent Sci, Dept Clin Oncol, Tokyo 1138510, Japan.
EM kano.canc@tmd.ac.jp; suenaga.srg2@tmd.ac.jp; 7110srg2@tmd.ac.jp
RI Uetake, Hiroyuki/AAC-2669-2020; Kano, Yoshihito/AAQ-6031-2020
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NR 77
TC 3
Z9 3
U1 0
U2 3
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 JUL
PY 2023
VL 30
IS 7
BP 6546
EP 6558
DI 10.3390/curroncol30070480
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA N2DF9
UT WOS:001035174200001
PM 37504340
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sever, B
   Altintop, MD
   Çiftçi, GA
   Özdemir, A
AF Sever, Belgin
   Altintop, Mehlika Dilek
   Ciftci, Gulsen Akalin
   Ozdemir, Ahmet
TI A New Series of Triazolothiadiazines as Potential Anticancer Agents for
   Targeted Therapy of Non-small Cell Lung and Colorectal Cancers: Design,
   Synthesis, <i>In silico</i> and <i>In vitro</i> Studies Providing
   Mechanistic Insight into Their Anticancer Potencies
SO MEDICINAL CHEMISTRY
LA English
DT Article
DE Triazolothiadiazine; indole; colorectal cancer; non-small cell lung
   cancer; apoptosis; cell cycle arrest; COX-2
ID CYCLOOXYGENASE-2; INHIBITION; AKT
AB Background: Targeted therapies acting on specific molecular targets in cancer cells with better curative efficacy and lower toxicity have come into prominence for the management of non-small cell lung cancer (NSCLC) and colorectal cancer (CRC). COX-2 stands out as a plausible target for anticancer agents due to its pivotal role in tumor initiation, progression and invasion.
   Objectives: Due to the importance of triazolothiadiazine scaffold in targeted anticancer drug discovery, the aim of this work is the design of new triazolothiadiazines as potential anticancer agents for the targeted therapy of NSCLC and CRC.
   Methods: New triazolo[3,4-b]-1,3,4-thiadiazines (2a -g) were synthesized via the ring closure reac [Utions of 2-bromo-1-arylethanones with 4-amino-5-((5-methoxy-2-methyl-1H-indol-3-yl)methyl)-2,4-dihydro-3H-1,2,4-triazole-3-thione (1), which was obtained via the solvent-free reaction of 5-methoxy-2-methyl-3-indoleacetic acid with thiocarbohydrazide. MTT assay was performed to deter-mine their cytotoxic effects on A549 human lung adenocarcinoma, Caco-2 human colorectal adeno-carcinoma and CCD-19Lu human lung fibroblast cells. The most potent compounds were evaluated for their effects on apoptosis, caspase-3, mitochondrial membrane potential, cell cycle, ultrastructural morphological changes and COX-2 in A549 and Caco-2 cells. In silico docking and Absorption, Dis-tribution, Metabolism and Excretion (ADME) studies were also performed using Schrodinger's Maestro molecular modeling package.
   Results: 6-(4-Chlorophenyl)-3-[(5-methoxy-2-methyl-1H-indol-3-yl)methyl]-7H-[1,2,4]triazolo[3,4-b][1,3,4]thiadiazine (2e) was the most potent and selective anticancer agent in this series against A549 and Caco-2 cell lines. Compound 2e induced early apoptosis, caused mitochondrial membrane depolarization and arrested cell cycle at G0/G1 phase in A549 cells. On the other hand, compound 2e triggered intrinsic apoptotic pathway involving caspase-3 activation in Caco-2 cells. Compound 2e caused apoptotic morphological changes in both cancer cell lines. The cytotoxic and apoptotic effects of this compound on CRC were found to be related to its selective COX-2 inhibitory activity. According to molecular docking studies, compound 2e showed good affinity to the active site of COX-2 (PDB code: 4COX). Based on in silico ADME studies, the compound is predicted to possess a favor-able ADME profile.
   Conclusion: According to in vitro and in silico studies, compound 2e was identified as a potential orally bioavailable anticancer agent for COX-2-targeted therapy of CRC.
C1 [Sever, Belgin; Altintop, Mehlika Dilek; Ozdemir, Ahmet] Anadolu Univ, Fac Pharm, Dept Pharmaceut Chem, TR-26470 Eskisehir, Turkey.
   [Ciftci, Gulsen Akalin] Anadolu Univ, Fac Pharm, Dept Biochem, TR-26470 Eskisehir, Turkey.
C3 Anadolu University; Anadolu University
RP Altintop, MD (corresponding author), Anadolu Univ, Fac Pharm, Dept Pharmaceut Chem, TR-26470 Eskisehir, Turkey.
EM mdaltintop@anadolu.edu.tr
RI Altıntop, Mehlika/J-4787-2019; Özdemir, Ahmet/M-3803-2018; Sever,
   Belgin/V-8319-2017
OI Ozdemir, Ahmet/0000-0003-0280-5550; Altintop, Mehlika
   Dilek/0000-0002-8159-663X; Sever, Belgin/0000-0003-4847-9711
FU Anadolu University Scien-tific Research Projects Commission [1604S158]
FX Y This study was supported by Anadolu University Scien-tific Research
   Projects Commission under the grant no: 1604S158.
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NR 38
TC 12
Z9 12
U1 0
U2 11
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1573-4064
EI 1875-6638
J9 MED CHEM
JI Med. Chem.
PY 2021
VL 17
IS 10
BP 1104
EP 1128
DI 10.2174/1573406416666201021142832
PG 25
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA UR8JV
UT WOS:000696989400003
PM 33087032
DA 2025-01-04
ER

PT J
AU Melo, FDE
   Vermeulen, L
AF de Sousa e Melo, Felipe
   Vermeulen, Louis
TI Wnt Signaling in Cancer Stem Cell Biology
SO CANCERS
LA English
DT Review
DE Wnt signaling; cancer; stem cells; cancer stem cells; cancer stem cell
   niche; Wnt inhibition; targeted therapy
ID SMALL-MOLECULE INHIBITOR; GROWTH-FACTOR RECEPTOR; COLORECTAL-CANCER;
   COLON-CANCER; BREAST-CANCER; SELF-RENEWAL; INTESTINAL TUMORIGENESIS;
   INITIATING CELLS; TUMOR-GROWTH; MONOCLONAL-ANTIBODIES
AB Aberrant regulation of Wnt signaling is a common theme seen across many tumor types. Decades of research have unraveled the epigenetic and genetic alterations that result in elevated Wnt pathway activity. More recently, it has become apparent that Wnt signaling levels identify stem-like tumor cells that are responsible for fueling tumor growth. As therapeutic targeting of these tumor stem cells is an intense area of investigation, a concise understanding on how Wnt activity relates to cancer stem cell traits is needed. This review attempts at summarizing the intricacies between Wnt signaling and cancer stem cell biology with a special emphasis on colorectal cancer.
C1 [de Sousa e Melo, Felipe; Vermeulen, Louis] Acad Med Ctr, Lab Expt Oncol & Radiobiol LEXOR, Ctr Expt Mol Med, NL-1105 AZ Amsterdam, Netherlands.
C3 University of Amsterdam; Academic Medical Center Amsterdam
RP Vermeulen, L (corresponding author), Acad Med Ctr, Lab Expt Oncol & Radiobiol LEXOR, Ctr Expt Mol Med, NL-1105 AZ Amsterdam, Netherlands.
EM felipedesousamello@gmail.com; l.vermeulen@amc.uva.nl
RI Vermeulen, Louis/B-7488-2008
OI Vermeulen, Louis/0000-0002-6066-789X
FU Academic Medical Center (Amsterdam); European Research Council (ERG-StG)
   [638193]; Dutch Cancer Society (KWF) [UVA2014-7245]; Worldwide Cancer
   Research [14-1164]; Dutch Digestive Foundation [MLDS-CDG 14-03];
   Netherlands Organization for Scientific Research (NWO) [Vidi
   016.156.308]; European Research Council (ERC) [638193] Funding Source:
   European Research Council (ERC)
FX Louis Vermeulen is supported by the Academic Medical Center (Amsterdam),
   the European Research Council (ERG-StG 638193), the Dutch Cancer Society
   (KWF) (UVA2014-7245), Worldwide Cancer Research (14-1164), the Dutch
   Digestive Foundation (MLDS-CDG 14-03), and the Netherlands Organization
   for Scientific Research (NWO) (Vidi 016.156.308). The authors would like
   to thank Alison Bruce for generating the Figures and Evi Miguel for
   critical comments on the manuscript.
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NR 118
TC 148
Z9 156
U1 3
U2 44
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 2072-6694
J9 CANCERS
JI Cancers
PD JUL
PY 2016
VL 8
IS 7
AR 60
DI 10.3390/cancers8070060
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EO7SE
UT WOS:000396889600001
PM 27355964
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Ji, XY
   Sun, W
   Lv, CZ
   Huang, JP
   Zhang, H
AF Ji, Xiaoyu
   Sun, Wei
   Lv, Chengzhou
   Huang, Jiapeng
   Zhang, Hao
TI Circular RNAs Regulate Glucose Metabolism in Cancer Cells
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE circRNAs; glucose metabolism; Warburg effect; signaling pathway;
   targeted therapy
ID PYRUVATE-DEHYDROGENASE KINASE; ENDOTHELIAL GROWTH-FACTOR; BREAST-CANCER;
   LUNG-CANCER; AEROBIC GLYCOLYSIS; LACTATE-DEHYDROGENASE;
   HEPATOCELLULAR-CARCINOMA; COLORECTAL-CANCER; OXIDATIVE STRESS;
   LACTIC-ACIDOSIS
AB Circular RNAs (circRNAs) were originally thought to result from RNA splicing errors. However, it has been shown that circRNAs can regulate cancer onset and progression in various ways. They can regulate cancer cell proliferation, differentiation, invasion, and metastasis. Moreover, they modulate glucose metabolism in cancer cells through different mechanisms such as directly regulating glycolytic enzymes and glucose transporter (GLUT) or indirectly regulating signal transduction pathways. In this review, we elucidate on the role of circRNAs in regulating glucose metabolism in cancer cells, which partly explains the pathogenesis of malignant tumors, and provides new therapeutic targets or new diagnostic and prognostic markers for human cancers.
C1 [Ji, Xiaoyu; Sun, Wei; Lv, Chengzhou; Huang, Jiapeng; Zhang, Hao] China Med Univ, Affiliated Hosp 1, Dept Thyroid Surg, Shenyang 110001, Liaoning, Peoples R China.
C3 China Medical University
RP Zhang, H (corresponding author), China Med Univ, Affiliated Hosp 1, Dept Thyroid Surg, Shenyang 110001, Liaoning, Peoples R China.
EM haozhang@cmu.edu.cn
FU National Natural Science Foundation of China [81902726]; China
   Postdoctoral Science Foundation [2018M641739]; Natural Science
   Foundation of Liaoning Province [20180530090]
FX This study was financially supported by: The National Natural Science
   Foundation of China (grant number 81902726) ; The Project funded by
   China Postdoctoral Science Foundation (grant number 2018M641739) ; and
   Natural Science Foundation of Liaoning Province (grant number
   20180530090) .
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NR 195
TC 7
Z9 10
U1 1
U2 20
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2021
VL 14
BP 4005
EP 4021
DI 10.2147/OTT.S316597
PG 17
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA TD0DU
UT WOS:000669007600004
PM 34239306
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Takegawa, N
   Yonesaka, K
AF Takegawa, Naoki
   Yonesaka, Kimio
TI HER2 as an Emerging Oncotarget for Colorectal Cancer Treatment After
   Failure of Anti-Epidermal Growth Factor Receptor Therapy
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE Cetuximab; EGFR; Gastrointestinal; Panitumumab; Targeted therapy
ID WILD-TYPE KRAS; GASTRIC-CANCER; MONOCLONAL-ANTIBODIES; 1ST-LINE
   TREATMENT; PROGNOSTIC-FACTOR; SCORING SYSTEM; RAS MUTATIONS;
   HUMAN-BREAST; PHASE-II; CETUXIMAB
AB Amplification of the HER2 gene is an indicator of poor prognosis for several kinds of malignancies such as breast and gastric cancer, and anti-HER2 targeting therapies provide clinical benefits in these patients. In 2011, HER2 was identified as a resistance molecule for de novo and secondary anti-epidermal growth factor receptor (EGFR) antibody therapy. HER2 activation provides a bypass signaling pathway after anti-EGFR antibody treatment of colorectal cancer. Cell line-based screening revealed that HER2 genomic amplification induces resistance to the anti-EGFR antibody cetuximab in colorectal cancer. Recently, HER2 itself has been recognized as a target for oncotherapy in colorectal cancer. The first part of this review provides an update on the present state of knowledge about the role of HER2 in colorectal cancer, including its prognostic relevance and role in resistance to anti-EGFR antibody treatment. In the second part of the review, we discuss the results of preclinical and clinical studies that examined the potential utility of anti-HER2 targeted therapy in colorectal cancer. Although it acts as a barrier for other molecular targeting agents such as cetuximab, HER2 itself is a promising target for oncotherapy. Current research indicates that anti-HER2 drugs will be developed further and introduced into clinical practice for the treatment of patients with HER2-positive colorectal cancer. (C) 2017 Elsevier Inc. All rights reserved.
C1 [Takegawa, Naoki; Yonesaka, Kimio] Kindai Univ, Fac Med, Dept Med Oncol, 377-2 Ohno Higashi, Osaka Sayamashi, Osaka 5898511, Japan.
C3 Kindai University (Kinki University)
RP Yonesaka, K (corresponding author), Kindai Univ, Fac Med, Dept Med Oncol, 377-2 Ohno Higashi, Osaka Sayamashi, Osaka 5898511, Japan.
EM yonesaka@sakai.med.kindai.ac.jp
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NR 47
TC 39
Z9 42
U1 2
U2 13
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 2017
VL 16
IS 4
BP 247
EP 251
DI 10.1016/j.clcc.2017.03.001
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FN7FD
UT WOS:000416182900001
PM 28363756
DA 2025-01-04
ER

PT J
AU Van der Velden, DL
   Hoes, LR
   van der Wijngaart, H
   Henegouwen, JMV
   van Werkhoven, E
   Roepman, P
   Schilsky, RL
   de Leng, WWJ
   Huitema, ADR
   Nuijen, B
   Nederlof, PM
   van Herpen, CML
   de Groot, DJA
   Devriese, LA
   Hoeben, A
   de Jonge, MJA
   Chalabi, M
   Smit, EF
   de Langen, AJ
   Mehra, N
   Labots, M
   Kapiteijn, E
   Sleijfer, S
   Cuppen, E
   Verheul, HMW
   Gelderblom, H
   Voest, EE
AF van der Velden, D. L.
   Hoes, L. R.
   van der Wijngaart, H.
   Henegouwen, J. M. van Berge
   van Werkhoven, E.
   Roepman, P.
   Schilsky, R. L.
   de Leng, W. W. J.
   Huitema, A. D. R.
   Nuijen, B.
   Nederlof, P. M.
   van Herpen, C. M. L.
   de Groot, D. J. A.
   Devriese, L. A.
   Hoeben, A.
   de Jonge, M. J. A.
   Chalabi, M.
   Smit, E. F.
   de Langen, A. J.
   Mehra, N.
   Labots, M.
   Kapiteijn, E.
   Sleijfer, S.
   Cuppen, E.
   Verheul, H. M. W.
   Gelderblom, H.
   Voest, E. E.
TI The Drug Rediscovery protocol facilitates the expanded use of existing
   anticancer drugs
SO NATURE
LA English
DT Article
ID CLINICAL-TRIALS; OPEN-LABEL; PHASE-II; RESPONSE ASSESSMENT; TARGETED
   THERAPY; 2-STAGE DESIGNS; MULTICENTER; CRITERIA; CANCERS; TUMORS
AB The large-scale genetic profiling of tumours can identify potentially actionable molecular variants for which approved anticancer drugs are available(1-3). However, when patients with such variants are treated with drugs outside of their approved label, successes and failures of targeted therapy are not systematically collected or shared. We therefore initiated the Drug Rediscovery protocol, an adaptive, precision-oncology trial that aims to identify signals of activity in cohorts of patients, with defined tumour types and molecular variants, who are being treated with anticancer drugs outside of their approved label. To be eligible for the trial, patients have to have exhausted or declined standard therapies, and have malignancies with potentially actionable variants for which no approved anticancer drugs are available. Here we show an overall rate of clinical benefit-defined as complete or partial response, or as stable disease beyond 16 weeks-of 34% in 215 treated patients, comprising 136 patients who received targeted therapies and 79 patients who received immunotherapy. The overall median duration of clinical benefit was 9 months (95% confidence interval of 8-11 months), including 26 patients who were experiencing ongoing clinical benefit at data cut-off. The potential of the Drug Rediscovery protocol is illustrated by the identification of a successful cohort of patients with microsatellite instable tumours who received nivolumab (clinical benefit rate of 63%), and a cohort of patients with colorectal cancer with relatively low mutational load who experienced only limited clinical benefit from immunotherapy. The Drug Rediscovery protocol facilitates the defined use of approved drugs beyond their labels in rare subgroups of cancer, identifies early signals of activity in these subgroups, accelerates the clinical translation of new insights into the use of anticancer drugs outside of their approved label, and creates a publicly available repository of knowledge for future decision-making.
C1 [van der Velden, D. L.; Hoes, L. R.; Chalabi, M.; Voest, E. E.] Netherlands Canc Inst, Dept Mol Oncol & Immunol, Amsterdam, Netherlands.
   [van der Velden, D. L.; Hoes, L. R.; van der Wijngaart, H.; Henegouwen, J. M. van Berge; Smit, E. F.; Sleijfer, S.; Voest, E. E.] Ctr Personalized Canc Treatment, Rotterdam, Netherlands.
   [Hoes, L. R.; van der Wijngaart, H.; Henegouwen, J. M. van Berge; Cuppen, E.; Voest, E. E.] Oncode Inst, Utrecht, Netherlands.
   [van der Wijngaart, H.; Labots, M.; Verheul, H. M. W.] Vrije Univ Amsterdam, Amsterdam UMC, Canc Ctr Amsterdam, Dept Med Oncol, Amsterdam, Netherlands.
   [Henegouwen, J. M. van Berge; Kapiteijn, E.; Gelderblom, H.] Leiden Univ, Med Ctr, Dept Med Oncol, Leiden, Netherlands.
   [van Werkhoven, E.] Netherlands Canc Inst, Biometr Dept, Amsterdam, Netherlands.
   [Roepman, P.; Cuppen, E.] Hartwig Med Fdn, Amsterdam, Netherlands.
   [Schilsky, R. L.] Amer Soc Clin Oncol, Alexandria, VA USA.
   [de Leng, W. W. J.] Univ Med Ctr Utrecht, Dept Pathol, Utrecht, Netherlands.
   [Huitema, A. D. R.] Univ Utrecht, Univ Med Ctr Utrecht, Dept Clin Pharm, Utrecht, Netherlands.
   [Huitema, A. D. R.; Nuijen, B.] Netherlands Canc Inst, Dept Clin Pharmacol, Amsterdam, Netherlands.
   [Nederlof, P. M.] Netherlands Canc Inst, Mol Diagnost Lab, Dept Pathol, Amsterdam, Netherlands.
   [van Herpen, C. M. L.; Mehra, N.; Verheul, H. M. W.] Radboud Univ Nijmegen, Med Ctr, Dept Med Oncol, Nijmegen, Netherlands.
   [de Groot, D. J. A.] Univ Med Ctr Groningen, Dept Med Oncol, Groningen, Netherlands.
   [Devriese, L. A.] Univ Med Ctr Utrecht, Dept Med Oncol, Utrecht, Netherlands.
   [Hoeben, A.] Maastricht Univ, Med Ctr, Dept Med Oncol, Maastricht, Netherlands.
   [de Jonge, M. J. A.; Sleijfer, S.] Erasmus MC, Dept Med Oncol, Canc Inst, Rotterdam, Netherlands.
   [Chalabi, M.] Netherlands Canc Inst, Dept Gastrointestinal Oncol, Amsterdam, Netherlands.
   [Smit, E. F.; de Langen, A. J.] Netherlands Canc Inst, Dept Thorac Oncol, Amsterdam, Netherlands.
   [Cuppen, E.] Univ Med Ctr Utrecht, Ctr Mol Med, Utrecht, Netherlands.
C3 Netherlands Cancer Institute; University of Amsterdam; Vrije
   Universiteit Amsterdam; Leiden University; Leiden University Medical
   Center (LUMC); Leiden University - Excl LUMC; Netherlands Cancer
   Institute; American Society of Clinical Oncology; Utrecht University;
   Utrecht University Medical Center; Utrecht University; Utrecht
   University Medical Center; Netherlands Cancer Institute; Netherlands
   Cancer Institute; Radboud University Nijmegen; University of Groningen;
   Utrecht University; Utrecht University Medical Center; Maastricht
   University; Erasmus University Rotterdam; Erasmus MC; Erasmus MC Cancer
   Institute; Netherlands Cancer Institute; Netherlands Cancer Institute;
   Utrecht University; Utrecht University Medical Center
RP Voest, EE (corresponding author), Netherlands Canc Inst, Dept Mol Oncol & Immunol, Amsterdam, Netherlands.; Voest, EE (corresponding author), Ctr Personalized Canc Treatment, Rotterdam, Netherlands.; Voest, EE (corresponding author), Oncode Inst, Utrecht, Netherlands.
EM e.voest@nki.nl
RI Kapiteijn, Ellen/AAK-6065-2020; van Werkhoven, Erik/ABE-8062-2020; Smit,
   Egbert F./HJZ-3900-2023; van Herpen, Carla/N-3576-2014; Verheul,
   Henk/V-6462-2019; Labots, Mariette/J-9731-2013; Cuppen,
   Edwin/H-2389-2016; Mehra, Niven/B-7157-2017
OI Cuppen, Edwin/0000-0002-0400-9542; Smit, Egbert/0000-0002-7329-6995;
   Labots, Mariette/0000-0002-7095-1771; Gelderblom,
   Hans/0000-0001-9270-8636; Kapiteijn, Ellen/0000-0002-4814-6426; Mehra,
   Niven/0000-0002-4794-1831; van Berge Henegouwen, Jade
   Maxime/0000-0002-4112-9105
FU Barcode for Life Foundation; Dutch Cancer Society; Amgen; Astra Zeneca;
   Bayer; Boehringer Ingelheim; Bristol-Myers Squibb; Eisai; Merck Sharp
   and Dohme; Novartis; Pfizer; Roche
FX We thank the Barcode for Life Foundation and the Dutch Cancer Society
   for their financial support; Amgen, Astra Zeneca, Bayer, Boehringer
   Ingelheim, Bristol-Myers Squibb, Eisai, Merck Sharp and Dohme, Novartis,
   Pfizer and Roche for their in-kind and financial support; the HMF for
   their in-kind support by performing sequencing and biomarker analyses on
   baseline biopsies; the Center for Personalized Cancer Treatment
   Multidisciplinary Expert Board for supporting the central case-review
   process; the Independent Data Monitoring Committee for their advice on
   cohort decisions and the monitoring of preliminary safety data; the
   Netherlands Cancer Institute's Biobank Facility, Scientific Department
   and Pharmacy for their facilitating services; A. P. Hamberg, L. V.
   Beerepoot and J. M. MeerumTerwogt for their contributions to trial
   recruitment; and all participating hospitals for supporting and
   facilitating the conduct of the DRUP trial.
CR Bins S, 2017, ONCOLOGIST, V22, P33, DOI 10.1634/theoncologist.2016-0085
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NR 34
TC 171
Z9 175
U1 5
U2 34
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD OCT 3
PY 2019
VL 574
IS 7776
BP 127
EP +
DI 10.1038/s41586-019-1600-x
PG 16
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA JB8OZ
UT WOS:000488832500044
PM 31570881
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Heervä, E
   Lavonius, M
   Jaakkola, P
   Minn, H
   Ristamäki, R
AF Heerva, Eetu
   Lavonius, Maija
   Jaakkola, Panu
   Minn, Heikki
   Ristamaki, Raija
TI Overall Survival and Metastasis Resections in Patients with Metastatic
   Colorectal Cancer Using Electronic Medical Records
SO JOURNAL OF GASTROINTESTINAL CANCER
LA English
DT Article
DE Colorectal cancer; Electronic medical records; Chemotherapy; Targeted
   therapy; Dose reduction
ID 1ST-LINE TREATMENT; PLUS IRINOTECAN; RAS MUTATIONS; OPEN-LABEL;
   PHASE-III; FLUOROURACIL; LEUCOVORIN; OXALIPLATIN; BEVACIZUMAB; CETUXIMAB
AB Purpose Treatment for patients with metastatic colorectal cancer is chemotherapy commonly combined with monoclonal antibodies against vascular endothelial growth factor (bevacizumab) or epidermal growth factor receptor (cetuximab or panitumumab), the efficacy of which has been proven in randomized controlled trials. The objective of the current retrospective study was to analyze the impact of targeted therapy, adverse events, and dose reduction on overall survival (OS) and metastasis resection rates.
   Methods A hospital-based electronic informatics center was used to gather clinical data and outcome information in a Breal-life setting in a single academic hospital. A total of 178 patients were included in 2010-2013.
   Results In patients whose tumors expressed the KRAS wild type, the longest median OS was observed with irinotecanbased chemotherapy combined with bevacizumab (38 months), or with cetuximab (41 months). In the KRAS-mutated group, the longest median OS was observed with oxaliplatin with or without bevacizumab (34 months). Beneficial liver metastasis resections were observed in 12 out of 20 patients. Patients with KRAS wild-type tumors who received cetuximab were the most likely to undergo surgery. Age was a negative predictor of OS. Patients whose chemotherapy dose was reduced to below 80% had lower OS compared to those remaining above 80%. Treatment delays in chemotherapy did not affect OS. Pulmonary embolism and infections were common but did not have an impact on OS.
   Conclusions A hospital-based electronic informatics center provides comparable OS results, even though adverse events were frequently observed in the present study.
C1 [Heerva, Eetu; Jaakkola, Panu; Minn, Heikki; Ristamaki, Raija] Univ Turku, Dept Oncol, Hameentie 11, Turku 20521, Finland.
   [Heerva, Eetu; Lavonius, Maija; Jaakkola, Panu; Minn, Heikki; Ristamaki, Raija] Turku Univ Hosp, Hameentie 11, Turku 20521, Finland.
   [Lavonius, Maija] Univ Turku, Dept Digest Surg, Hameentie 11, Turku 20521, Finland.
   [Jaakkola, Panu] Turku Univ Hosp, Ctr Canc, Hameentie 11, Turku 20521, Finland.
C3 University of Turku; University of Turku; University of Turku;
   University of Turku
RP Heervä, E (corresponding author), Univ Turku, Dept Oncol, Hameentie 11, Turku 20521, Finland.; Heervä, E (corresponding author), Turku Univ Hosp, Hameentie 11, Turku 20521, Finland.
EM eaheer@utu.fi
RI Heervä, Eetu/AAU-2139-2021
OI Jaakkola, Panu/0000-0002-2365-4985; Minn, Heikki/0000-0002-5878-4333
FU Cancer Society of Finland; Turku University Hospital Foundation; Finnish
   Medical Foundation
FX The study was financially supported by the Cancer Society of Finland,
   Turku University Hospital Foundation and the Finnish Medical Foundation.
   The authors wish to thank the Centre of Clinical Informatics for
   managing the electronic patient data. Professor Tarja Laitinen, Anna
   Hammais MSc, and Mikhail Stephanov MSc are greatly appreciated for their
   expert opinions and technical support. The authors wish to thank
   Adelaide Lonnberg for language revision.
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NR 17
TC 6
Z9 7
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1941-6628
EI 1941-6636
J9 J GASTROINTEST CANC
JI J. Gastrointest. Cancer
PD SEP
PY 2018
VL 49
IS 3
BP 245
EP 251
DI 10.1007/s12029-017-9927-8
PG 7
WC Oncology; Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Oncology; Gastroenterology & Hepatology
GA GO5KN
UT WOS:000440060400003
PM 28229371
DA 2025-01-04
ER

PT J
AU Zettler, ME
AF Zettler, Marjorie E.
TI Dose Optimization of Targeted Therapies for Oncologic Indications
SO CANCERS
LA English
DT Review
DE dose optimization; dose-finding; drug development; targeted therapy;
   oncology drugs; cancer drugs
ID METASTATIC COLORECTAL-CANCER; PHASE-I; INHIBITOR; REGORAFENIB; OUTCOMES;
   PERSPECTIVES; MULTICENTER; FUTIBATINIB; ESCALATION; TOXICITIES
AB Simple Summary The majority of oncology drugs approved by the Food and Drug Administration over the past quarter century have been targeted therapies, designed to act on cancer cells with specific molecular abnormalities. Although these newer agents have different properties compared to cytotoxic chemotherapy, the same methodology used for dose-finding during drug development has continued to be used. Growing awareness of the inadequacy of traditional dose selection processes for modern cancer drugs has been the catalyst for the creation of new regulatory guidance aimed at reforming current practices. This review summarizes six cases, illustrating different approaches to targeted therapy dose optimization.Abstract Therapeutic advances in oncology in the 21st century have contributed to significant declines in cancer mortality. Notably, targeted therapies comprised the largest proportion of oncology drugs approved by the United States (US) Food and Drug Administration (FDA) over the past 25 years and have become the standard of care for the treatment of many cancers. However, despite the metamorphosis of the therapeutic landscape, some aspects of cancer drug development have remained essentially unchanged. In particular, the dose-finding methodology originally developed for cytotoxic chemotherapy drugs continues to be implemented, even though this approach no longer represents the most appropriate strategy for modern cancer therapies. In recognition of the need to reconsider assumptions, adapt the dose selection process for newer drugs, and design alternative strategies, the FDA has undertaken several initiatives in recent years to address these concerns. These actions include the launch of Project Optimus in 2021 and the issuance of draft guidance for industry on dose optimization of oncology drugs in 2023. Amid this evolving regulatory environment, the present manuscript reviews case studies for six different targeted cancer therapies, highlighting how dose-finding challenges have been managed to date by oncologists, sponsors, and regulators.
C1 [Zettler, Marjorie E.] Accutar Biotechnol Inc, Clin Sci, Cranbury, NJ 08512 USA.
RP Zettler, ME (corresponding author), Accutar Biotechnol Inc, Clin Sci, Cranbury, NJ 08512 USA.
EM marjoriezettler@accutarbio.com
OI Zettler, Marjorie/0000-0003-4332-0066
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NR 83
TC 0
Z9 0
U1 1
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN
PY 2024
VL 16
IS 12
AR 2180
DI 10.3390/cancers16122180
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WJ7K0
UT WOS:001254565800001
PM 38927886
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Kim, Y
   Kim, D
   Cao, BW
   Carvajal, R
   Kim, M
AF Kim, Youngchul
   Kim, Daewon
   Cao, Biwei
   Carvajal, Rodrigo
   Kim, Minjung
TI PDXGEM: patient-derived tumor xenograft-based gene expression model for
   predicting clinical response to anticancer therapy in cancer patients
SO BMC BIOINFORMATICS
LA English
DT Article
DE Patient-derived xenograft model; PDX; Gene expression; Predictive cancer
   biomarker; Chemotherapy; Targeted therapy; Drug response prediction
ID PANCREATIC DUCTAL ADENOCARCINOMA; NEOADJUVANT CHEMOTHERAPY; ADJUVANT
   TRASTUZUMAB; BIOMARKER DISCOVERY; RANDOMIZED-TRIAL; MUTATION STATUS;
   SIGNATURE; FLUOROURACIL; HETEROGENEITY; LEUCOVORIN
AB Background: Cancer is a highly heterogeneous disease with varying responses to anti-cancer drugs. Although several attempts have been made to predict the anti-cancer therapeutic responses, there remains a great need to develop highly accurate prediction models of response to the anti-cancer drugs for clinical applications toward a personalized medicine. Patient derived xenografts (PDXs) are preclinical cancer models in which the tissue or cells from a patient's tumor are implanted into an immunodeficient or humanized mouse. In the present study, we develop a bioinformatics analysis pipeline to build a predictive gene expression model (GEM) for cancer patients' drug responses based on gene expression and drug activity data from PDX models.
   Results: Drug sensitivity biomarkers were identified by performing an association analysis between gene expression levels and post-treatment tumor volume changes in PDX models. We built a drug response prediction model (called PDXGEM) in a random-forest algorithm by using a subset of the drug sensitvity biomarkers with concordant co-expression patterns between the PDXs and pretreatment cancer patient tumors. We applied the PDXGEM to several cytotoxic chemotherapies as well as targeted therapy agents that are used to treat breast cancer, pancreatic cancer, colorectal cancer, or non-small cell lung cancer. Significantly accurate predictions of PDXGEM for pathological response or survival outcomes were observed in extensive independent validations on multiple cancer patient datasets obtained from retrospective observational studies and prospective clinical trials.
   Conclusion: Our results demonstrated the strong potential of using molecular profiles and drug activity data of PDX tumors in developing a clinically translatable predictive cancer biomarkers for cancer patients. The PDXGEM web application is publicly available at http://pdxgem.moffitt.org.
C1 [Kim, Youngchul] H Lee Moffitt Canc Ctr & Res Inst, Dept Biostat & Bioinformat, 12902 Magnolia Dr, Tampa, FL 33612 USA.
   [Kim, Daewon] H Lee Moffitt Canc Ctr & Res Inst, Dept Gastrointestinal Oncol, Tampa, FL 33612 USA.
   [Cao, Biwei; Carvajal, Rodrigo] H Lee Moffitt Canc Ctr & Res Inst, Biostat & Bioinformat Shared Resource, 12902 Magnolia Dr, Tampa, FL 33612 USA.
   [Kim, Minjung] Univ S Florida, Dept Cell Biol Microbiol & Mol Biol, Tampa, FL 33620 USA.
C3 H Lee Moffitt Cancer Center & Research Institute; H Lee Moffitt Cancer
   Center & Research Institute; H Lee Moffitt Cancer Center & Research
   Institute; State University System of Florida; University of South
   Florida
RP Kim, Y (corresponding author), H Lee Moffitt Canc Ctr & Res Inst, Dept Biostat & Bioinformat, 12902 Magnolia Dr, Tampa, FL 33612 USA.
EM Youngchul.kim@moffitt.org
RI Carvajal, Ramon/F-7318-2016; Cao, Biwei/LKK-9764-2024
OI Kim, Minjung/0000-0002-5682-6640; kim, youngchul/0000-0002-2307-0330;
   Cao, Biwei/0009-0000-4255-8369; Carvajal, Rodrigo/0000-0002-7607-8272
FU H. Lee Moffitt Cancer Center and Research Institute, an NCI designated
   Comprehensive Cancer Center [P30-CA076292]
FX This study was supported by the Shared Resources at the H. Lee Moffitt
   Cancer Center and Research Institute, an NCI designated Comprehensive
   Cancer Center (P30-CA076292). The funding body did not play any roles in
   the design of the study and collection, analysis, and interpretation of
   data and in writing the manuscript.
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NR 51
TC 16
Z9 17
U1 0
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2105
J9 BMC BIOINFORMATICS
JI BMC Bioinformatics
PD JUL 6
PY 2020
VL 21
IS 1
AR 288
DI 10.1186/s12859-020-03633-z
PG 21
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Mathematical & Computational Biology
GA MM3XG
UT WOS:000550092500005
PM 32631229
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Haddad, J
   Slika, S
   Mahfouz, R
AF Haddad, Joseph
   Slika, Silva
   Mahfouz, Rami
TI Epidermal growth factor receptor (EGFR) in the era of Precision
   Medicine: The tale of a perfect example of targeted therapy. A review
SO META GENE
LA English
DT Review
DE EGFR; Precision; Medicine; Review
ID CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER; TYROSINE-KINASE
   INHIBITOR; SIGNALING NETWORKS; CLINICAL-TRIALS; GLIOBLASTOMA; MUTATIONS;
   RESISTANCE; CETUXIMAB; KRAS
AB Epidermal growth factor receptor has been under the lights for the past few years as a perfect and typical example of a success story of targeted therapy. In the era of Precision Medicine, such modalities of treatment are highly implicated in the adequate choice of therapy for a wide variety of oncological diseases. This review article is about the different aspects of detection, application, and analysis of the epidermal growth factor receptor genetic mutations that constitute a key element in the initiation of targeted therapy. (C) 2016 Elsevier B.V. All rights reserved.
C1 [Haddad, Joseph; Slika, Silva; Mahfouz, Rami] Amer Univ Beirut, Med Ctr, Dept Pathol & Lab Med, Beirut, Lebanon.
C3 American University of Beirut
RP Mahfouz, R (corresponding author), Amer Univ Beirut, Med Ctr, Dept Pathol & Lab Med, Mol Diagnost Lab, Cairo St, Beirut, Lebanon.
EM rm11@aub.edu.lb
RI Mahfouz, Rami/AGT-5804-2022
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NR 67
TC 3
Z9 4
U1 0
U2 15
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 2214-5400
J9 META GENE
JI Meta Gene
PD FEB
PY 2017
VL 11
BP 157
EP 163
DI 10.1016/j.mgene.2016.08.011
PG 7
WC Genetics & Heredity
WE Emerging Sources Citation Index (ESCI)
SC Genetics & Heredity
GA EM3ZZ
UT WOS:000395254400028
DA 2025-01-04
ER

PT J
AU Khondee, S
   Rabinsky, EF
   Owens, SR
   Joshi, BP
   Qiu, Z
   Duan, XY
   Zhao, LL
   Wang, TD
AF Khondee, Supang
   Rabinsky, Emily F.
   Owens, Scott R.
   Joshi, Bishnu P.
   Qiu, Zhen
   Duan, Xiyu
   Zhao, Lili
   Wang, Thomas D.
TI Targeted therapy of colorectal neoplasia with rapamycin in
   peptide-labeled pegylated octadecyl lithocholate micelles
SO JOURNAL OF CONTROLLED RELEASE
LA English
DT Article
DE Micelles; Targeted therapy; Colorectal cancer; Rapamycin; Endoscopy
ID SELF-ASSEMBLED NANOPARTICLES; MOUSE MODEL; CANCER; DELIVERY
AB Many powerful drugs have limited clinical utility because of poor water solubility and high systemic toxicity. Here, we formulated a targeted nanomedicine, rapamycin encapsulated in pegylated octadecyl lithocholate micelles labeled with a new ligand for colorectal neoplasia, LTTHYKL peptide. CPC; Apc mice that spontaneously develop colonic adenomas were treated with free rapamycin, plain rapamycin micelles, and peptide-labeled rapamycin micelles via intraperitoneal injection for 35 days. Endoscopy was performed to monitor adenoma regression in vivo. We observed complete adenoma regression at the end of therapy. The mean regression rate for peptide-labeled rapamycin micelles was significantly greater than that for plain rapamycin micelles, P < 0.01. On immunohistochemistry, we observed a significant reduction in phospho-S6 but not beta-catenin expression and reduced tumor cell proliferation, suggesting greater inhibition of downstreammTOR signaling. We observed significantly reduced renal toxicity for peptide-labeled rapamycin micelles compared to that of free drug, and no other toxicities were found on chemistries. Together, this unique targeted micelle represents a potential therapeutic for colorectal neoplasia with comparable therapeutic efficacy to rapamycin free drug and significantly less systemic toxicity. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Khondee, Supang; Rabinsky, Emily F.; Joshi, Bishnu P.; Wang, Thomas D.] Univ Michigan, Dept Med, Ann Arbor, MI 48109 USA.
   [Khondee, Supang] Univ Phayao, Sch Pharmaceut Sci, Phayao, Thailand.
   [Owens, Scott R.] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA.
   [Qiu, Zhen; Duan, Xiyu; Wang, Thomas D.] Univ Michigan, Dept Biomed Engn, Ann Arbor, MI 48109 USA.
   [Zhao, Lili] Univ Michigan, Dept Stat, Ann Arbor, MI 48109 USA.
   [Wang, Thomas D.] Univ Michigan, Dept Mech Engn, Ann Arbor, MI 48109 USA.
C3 University of Michigan System; University of Michigan; University of
   Phayao; 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
RP Wang, TD (corresponding author), Univ Michigan, Div Gastroenterol, 109 Zina Pitcher Pl,BSRB 1522, Ann Arbor, MI 48109 USA.
EM thomaswa@umich.edu
RI Zhao, Lili/JEO-7007-2023; Khondee, Supang/I-7440-2016
OI Khondee, Supang/0000-0003-2083-1779
FU US National Institutes of Health (NIH) [U54 CA13642, R01 CA142750, P30
   DK34933, P50 CA93990]; National Institute of Diabetes and Digestive and
   Kidney Diseases [P30DK034933] Funding Source: NIH RePORTER
FX We thank V.C. Yang and J.Y. Kao for technical support. This research was
   supported in part by the US National Institutes of Health (NIH) U54
   CA13642, R01 CA142750, P30 DK34933 (pilot award), and P50 CA93990 to
   TDW.
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NR 29
TC 15
Z9 18
U1 1
U2 28
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-3659
EI 1873-4995
J9 J CONTROL RELEASE
JI J. Control. Release
PD FEB 10
PY 2015
VL 199
BP 114
EP 121
DI 10.1016/j.jconrel.2014.11.034
PG 8
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA AZ8HR
UT WOS:000348456800013
PM 25483425
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Loria, R
   Vici, P
   Di Lisa, FS
   Soddu, S
   Maugeri-Sacca, M
   Bon, G
AF Loria, Rossella
   Vici, Patrizia
   Di Lisa, Francesca Sofia
   Soddu, Silvia
   Maugeri-Sacca, Marcello
   Bon, Giulia
TI Cross-Resistance Among Sequential Cancer Therapeutics: An Emerging Issue
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE targeted-therapy; cancer therapeutics resistance; cross-resistance;
   sequential therapeutics; personalized oncology
ID CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER; KINASE DOMAIN MUTATIONS;
   ANTI-EGFR THERAPY; BREAST-CANCER; ACQUIRED-RESISTANCE; DRUG-RESISTANCE;
   NEOADJUVANT CHEMOTHERAPY; COLLATERAL SENSITIVITY; MONOCLONAL-ANTIBODY
AB Over the past two decades, cancer treatment has benefited from having a significant increase in the number of targeted drugs approved by the United States Food and Drug Administration. With the introduction of targeted therapy, a great shift towards a new era has taken place that is characterized by reduced cytotoxicity and improved clinical outcomes compared to traditional chemotherapeutic drugs. At present, targeted therapies and other systemic anti-cancer therapies available (immunotherapy, cytotoxic, endocrine therapies and others) are used alone or in combination in different settings (neoadjuvant, adjuvant, and metastatic). As a result, it is not uncommon for patients affected by an advanced malignancy to receive subsequent anti-cancer therapies. In this challenging complexity of cancer treatment, the clinical pathways of real-life patients are often not as direct as predicted by standard guidelines and clinical trials, and cross-resistance among sequential anti-cancer therapies represents an emerging issue. In this review, we summarize the main cross-resistance events described in the diverse tumor types and provide insight into the molecular mechanisms involved in this process. We also discuss the current challenges and provide perspectives for the research and development of strategies to overcome cross-resistance and proceed towards a personalized approach.
C1 [Loria, Rossella; Soddu, Silvia; Bon, Giulia] Ist Ric & Cura Carattere Sci Regina Elena Natl Can, Cellular Network & Mol Therapeut Target Unit, Rome, Italy.
   [Vici, Patrizia; Di Lisa, Francesca Sofia] Cura Carattere Sci Regina Elena Natl Canc Inst, Ist Ric, Unit Phase Trials 4, Rome, Italy.
   [Di Lisa, Francesca Sofia] Univ Sapienza, Umberto I Univ Hosp, Dept Radiol Oncol & Anat Pathol Sci, Med Oncol A, Rome, Italy.
   [Maugeri-Sacca, Marcello] Ist Ric & Cura Carattere Sci Regina Elena Natl Can, Div Med Oncol 2, Rome, Italy.
C3 Sapienza University Rome; University Hospital Sapienza Rome
RP Bon, G (corresponding author), Ist Ric & Cura Carattere Sci Regina Elena Natl Can, Cellular Network & Mol Therapeut Target Unit, Rome, Italy.
EM giulia.bon@ifo.it
RI Bon, Giulia/CAJ-1801-2022; Loria, Rossella/ABH-7374-2020; Soddu,
   Silvia/K-2467-2018
FU Italian Ministry of Health
FX This work was supported by Funds Ricerca Corrente 2022 from Italian
   Ministry of Health.
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NR 193
TC 11
Z9 13
U1 0
U2 6
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JUN 23
PY 2022
VL 12
AR 877380
DI 10.3389/fonc.2022.877380
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3B5HU
UT WOS:000827972600001
PM 35814399
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Menyhart, O
   Kakisaka, T
   Pongor, LS
   Uetake, H
   Goel, A
   Gyorffy, B
AF Menyhart, Otilia
   Kakisaka, Tatsuhiko
   Pongor, Lorinc Sandor
   Uetake, Hiroyuki
   Goel, Ajay
   Gyorffy, Balazs
TI Uncovering Potential Therapeutic Targets in Colorectal Cancer by
   Deciphering Mutational Status and Expression of Druggable Oncogenes
SO CANCERS
LA English
DT Article
DE colon cancer; disruptive mutations; oncogenes; molecular targeted
   therapy; survival
ID TRANSCRIPTION FACTOR; MOLECULAR SUBTYPES; FLUOROURACIL; OXALIPLATIN;
   LEUCOVORIN; GENE; LUNG; MULTICENTER; BEVACIZUMAB; COMBINATION
AB Background: Numerous driver mutations have been identified in colorectal cancer (CRC), but their relevance to the development of targeted therapies remains elusive. The secondary effects of pathogenic driver mutations on downstream signaling pathways offer a potential approach for the identification of therapeutic targets. We aimed to identify differentially expressed genes as potential drug targets linked to driver mutations. Methods: Somatic mutations and the gene expression data of 582 CRC patients were utilized, incorporating the mutational status of 39,916 and the expression levels of 20,500 genes. To uncover candidate targets, the expression levels of various genes in wild-type and mutant cases for the most frequent disruptive mutations were compared with a Mann-Whitney test. A survival analysis was performed in 2100 patients with transcriptomic gene expression data. Up-regulated genes associated with worse survival were filtered for potentially actionable targets. The most significant hits were validated in an independent set of 171 CRC patients. Results: Altogether, 426 disruptive mutation-associated upregulated genes were identified. Among these, 95 were linked to worse recurrence-free survival (RFS). Based on the druggability filter, 37 potentially actionable targets were revealed. We selected seven genes and validated their expression in 171 patient specimens. The best independently validated combinations were DUSP4 (p = 2.6 x 10(-12)) in ACVR2A mutated (7.7%) patients; BMP4 (p = 1.6 x 10(-04)) in SOX9 mutated (8.1%) patients; TRIB2 (p = 1.35 x 10(-14)) in ACVR2A mutated patients; VSIG4 (p = 2.6 x 10(-05)) in ANK3 mutated (7.6%) patients, and DUSP4 (p = 7.1 x 10(-04)) in AMER1 mutated (8.2%) patients. Conclusions: The results uncovered potentially druggable genes in colorectal cancer. The identified mutations could enable future patient stratification for targeted therapy.
C1 [Menyhart, Otilia; Pongor, Lorinc Sandor; Gyorffy, Balazs] Semmelweis Univ, Dept Pediat 2, Tuzolto Utca 7-9, H-1094 Budapest, Hungary.
   [Menyhart, Otilia; Pongor, Lorinc Sandor; Gyorffy, Balazs] Hungarian Acad Sci, Inst Enzymol, MTA TTK Lendulet Canc Biomarker Res Grp, Magyar Tudosok Korutja 2, H-1117 Budapest, Hungary.
   [Kakisaka, Tatsuhiko; Goel, Ajay] Baylor Scott & White Res Inst, Ctr Gastrointestinal Res, 3410 Worth St,Suite 610, Dallas, TX 75246 USA.
   [Kakisaka, Tatsuhiko; Goel, Ajay] Baylor Scott & White Res Inst, Ctr Translat Genom & Oncol, 3410 Worth St,Suite 610, Dallas, TX 75246 USA.
   [Kakisaka, Tatsuhiko; Goel, Ajay] Charles A Sammons Canc Ctr, 3410 Worth St,Suite 610, Dallas, TX 75246 USA.
   [Kakisaka, Tatsuhiko; Goel, Ajay] Beckman Res Inst, City Hope Comprehens Canc Ctr, Dept Mol Diagnost Therapeut & Translat Oncol, 1218 S Fifth Ave,Suite 2226, Monrovia, CA 91016 USA.
   [Uetake, Hiroyuki] Tokyo Med & Dent Univ, Grad Sch Med & Dent Sci, Dept Specialized Surg, Tokyo 1138519, Japan.
C3 Semmelweis University; Hungarian Research Network; HUN-REN Research
   Centre for Natural Sciences; Hungarian Academy of Sciences; Baylor
   Health Care System; Baylor University Medical Center; Baylor Health Care
   System; Baylor University Medical Center; Baylor University Medical
   Center; Institute of Science Tokyo; Tokyo Medical & Dental University
   (TMDU)
RP Gyorffy, B (corresponding author), Semmelweis Univ, Dept Pediat 2, Tuzolto Utca 7-9, H-1094 Budapest, Hungary.; Gyorffy, B (corresponding author), Hungarian Acad Sci, Inst Enzymol, MTA TTK Lendulet Canc Biomarker Res Grp, Magyar Tudosok Korutja 2, H-1117 Budapest, Hungary.; Goel, A (corresponding author), Baylor Scott & White Res Inst, Ctr Gastrointestinal Res, 3410 Worth St,Suite 610, Dallas, TX 75246 USA.; Goel, A (corresponding author), Baylor Scott & White Res Inst, Ctr Translat Genom & Oncol, 3410 Worth St,Suite 610, Dallas, TX 75246 USA.; Goel, A (corresponding author), Charles A Sammons Canc Ctr, 3410 Worth St,Suite 610, Dallas, TX 75246 USA.
EM ajgoel@coh.org; gyorffy.balazs@ttk.mta.hu
RI Kakisaka, Tatsuhiko/JCO-2741-2023; Uetake, Hiroyuki/AAC-2669-2020;
   Gyorffy, Balazs/AAA-9135-2021; Goel, Ajay/ADO-9623-2022; Pongor,
   Lorinc/AAA-9835-2021
OI Gyorffy, Balazs/0000-0002-5772-3766; Kakisaka,
   Tatsuhiko/0000-0002-8556-5945; Menyhart, Otilia/0000-0003-4129-4589
FU National Research, Development and Innovation Office, Hungary
   [KH-129581, 2018-1.3.1-VKE-2018-00032, NVKP_16-1-2016-0037]; National
   Cancer Institute, National Institute of Health [CA72851, CA181572,
   CA184792, CA187956]; Cancer Prevention Research Institute of Texas
   [RP140784]; Sammons Cancer Center; Baylor Foundation; Baylor Research
   Institute, Dallas, TX, USA
FX The study was supported by the KH-129581, 2018-1.3.1-VKE-2018-00032 and
   the NVKP_16-1-2016-0037 grants of the National Research, Development and
   Innovation Office, Hungary awarded to Balazs Gyorffy. The present work
   was also supported by the CA72851, CA181572, CA184792 and CA187956
   grants from the National Cancer Institute, National Institute of Health;
   RP140784 from the Cancer Prevention Research Institute of Texas; grants
   from the Sammons Cancer Center and Baylor Foundation, as well as funds
   from the Baylor Research Institute, Dallas, TX, USA awarded to Ajay
   Goel.
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NR 50
TC 18
Z9 19
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN 26
PY 2019
VL 11
IS 7
AR 983
DI 10.3390/cancers11070983
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IO4AV
UT WOS:000479322800094
PM 31337155
OA gold, Green Accepted, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU González-Montero, J
   Burotto, M
   Valenzuela, G
   Mateluna, D
   Buen-Abad, F
   Toro, J
   Barajas, O
   Marcelain, K
AF Gonzalez-Montero, Jaime
   Burotto, Mauricio
   Valenzuela, Guillermo
   Mateluna, Debora
   Buen-Abad, Florencia
   Toro, Jessica
   Barajas, Olga
   Marcelain, Katherine
TI Classification of patients with metastatic colorectal cancer into
   consensus molecular subtypes into real-world: A pilot study
SO WORLD JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
DE Metastatic colorectal cancer; Targeted therapy; Consensus molecular
   subtypes; Personalized medicine
ID GENE-EXPRESSION; PCR
AB BACKGROUNDColorectal cancer is a complex disease with high mortality rates. Over time, the treatment of metastatic colorectal cancer (mCRC) has gradually improved due to the development of modern chemotherapy and targeted therapy regimens. However, due to the inherent heterogeneity of this condition, identifying reliable predictive biomarkers for targeted therapies remains challenging. A recent promising classification system-the consensus molecular subtype (CMS) system-offers the potential to categorize mCRC patients based on their unique biological and molecular characteristics. Four distinct CMS categories have been defined: immune (CMS1), canonical (CMS2), metabolic (CMS3), and mesenchymal (CMS4). Nevertheless, there is currently no standardized protocol for accurately classifying patients into CMS categories. To address this challenge, reverse transcription polymerase chain reaction (RT-qPCR) and next-generation genomic sequencing (NGS) techniques may hold promise for precisely classifying mCRC patients into their CMSs. AIMTo investigate if mCRC patients can be classified into CMS categories using a standardized molecular biology workflow. METHODSThis observational study was conducted at the University of Chile Clinical Hospital and included patients with unresectable mCRC who were undergoing systemic treatment with chemotherapy and/or targeted therapy. Molecular biology techniques were employed to analyse primary tumour samples from these patients. RT-qPCR was utilized to assess the expression of genes associated with fibrosis (TGF-beta and beta-catenin) and cell growth pathways (c-MYC). NGS using a 25-gene panel (TumorSec) was performed to identify specific genomic mutations. The patients were then classified into one of the four CMS categories according to the clinical consensus of a Tumour Board. Informed consent was obtained from all the patients prior to their participation in this study. All techniques were conducted at University of Chile. RESULTSTwenty-six patients were studied with the techniques and then evaluated by the Tumour Board to determine the specific CMS. Among them, 23% (n = 6), 19% (n = 5), 31% (n = 8), and 19% (n = 5) were classified as CMS1, CMS2, CMS3, and CMS4, respectively. Additionally, 8% of patients (n = 2) could not be classified into any of the four CMS categories. The median overall survival of the total sample was 28 mo, and for CMS1, CMS2, CMS3 and CMS4 it was 11, 20, 30 and 45 mo respectively, with no statistically significant differences between groups. CONCLUSIONA molecular biology workflow and clinical consensus analysis can be used to accurately classify mCRC patients. This classification process, which divides patients into the four CMS categories, holds significant potential for improving research strategies and targeted therapies tailored to the specific characteristics of mCRC.
C1 [Gonzalez-Montero, Jaime; Burotto, Mauricio] Bradford Hill Clin Res Ctr, Santiago 8420383, Chile.
   [Gonzalez-Montero, Jaime; Valenzuela, Guillermo; Mateluna, Debora; Buen-Abad, Florencia; Toro, Jessica; Barajas, Olga; Marcelain, Katherine] Univ Chile, Basic & Clin Oncol Dept, Santiago 8380453, Chile.
   [Gonzalez-Montero, Jaime] Bradford Hill Clin Res Ctr, Independencia 1027,Casilla 70058, Santiago 8380453, Chile.
C3 Universidad de Chile
RP González-Montero, J (corresponding author), Univ Chile, Basic & Clin Oncol Dept, Santiago 8380453, Chile.; González-Montero, J (corresponding author), Bradford Hill Clin Res Ctr, Independencia 1027,Casilla 70058, Santiago 8380453, Chile.
EM jagonzalez@ug.uchile.cl
RI Marcelain, Katherine/I-2791-2013; Garnacho-Montero, Jose/R-9496-2019
OI toro, jessica/0000-0002-7813-1380; Gonzalez-Montero,
   Jaime/0000-0003-0324-2948
FU Agencia Nacional de Investigacion y Desarrollo de Chile, Fondo Nacional
   de Investigacion en Salud (FONIS) [SA20I0059]
FX Supported by Agencia Nacional de Investigacion y Desarrollo de Chile,
   Fondo Nacional de Investigacion en Salud (FONIS), No. SA20I0059
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NR 26
TC 1
Z9 1
U1 0
U2 0
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2218-4333
J9 WORLD J CLIN ONCOL
JI World J. Clin. Oncol.
PD OCT 24
PY 2023
VL 14
IS 10
BP 409
EP 419
DI 10.5306/wjco.v14.i10.409
PG 11
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA Y1SG2
UT WOS:001103127900004
PM 37970108
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Razenberg, LGEM
   Creemers, GJ
   Beerepoot, LV
   Vos, AH
   van de Wouw, AJ
   Maas, HAAM
   Lemmens, VEPP
AF Razenberg, Lieke G. E. M.
   Creemers, Geert-Jan
   Beerepoot, Laurens V.
   Vos, Allert H.
   van de Wouw, Agnes J.
   Maas, Huub A. A. M.
   Lemmens, Valery E. P. P.
TI Age-related systemic treatment and survival of patients with
   metachronous metastases from colorectal cancer
SO ACTA ONCOLOGICA
LA English
DT Article
ID 1ST-LINE TREATMENT; ELDERLY-PATIENTS; COMBINATION CHEMOTHERAPY;
   OPEN-LABEL; FLUOROURACIL-LEUCOVORIN; CURATIVE RESECTION; IRINOTECAN;
   OXALIPLATIN; BEVACIZUMAB; PATTERNS
AB Background: Although the spectrum of systemic treatment for metastatic colorectal cancer (mCRC) has widened, there is a paucity of evidence for the feasibility and optimal use of these systemic agents in elderly patients. The present study provides real world data on the age-related systemic treatment and survival of CRC patients with non-resectable metachronous metastases.
   Methods: All consecutive patients with non-resectable metastases from primary resected CRC were extracted from the Eindhoven area of the Netherlands Cancer Registry (NCR). Patients receiving palliative systemic therapy were enrolled (n = 385). Systemic treatment and survival were analyzed according to age at diagnosis of metastases.
   Results: Patients aged >= 75 years more often received first-line single-agent chemotherapy than their younger counterparts (63% vs. 32%, p < .0001). First-line single-agent chemotherapy was often prescribed without additional targeted therapy (78%). Advanced age (>= 75 years) was associated with a lower probability of receiving all active cytotoxic agents compared to patients aged < 60 years at time of diagnosis of metastases (odds ratio (OR) 0.2, 95% CI 0.10-0.77). In a multivariable Cox regression analysis with adjustment for age and other relevant prognostic factors, the total number of received systemic agents was the only predictor of death (hazard ratio (HR) 0.7, 95% CI 0.61-0.81).
   Conclusion: The beneficial effect of treatment with all active systemic agents on survival (simultaneously or sequentially prescribed) should be taken into account when considering systemic therapy in patients with mCRC. In light of our results, future studies are warranted to clarify the role of potential targeted therapy in elderly mCRC patients, who are often not candidates for combination chemotherapy and treatment with all active cytotoxic agents.
C1 [Razenberg, Lieke G. E. M.; Creemers, Geert-Jan] Catharina Hosp, Dept Internal Med, Michelangelolaan 2, NL-5623 EJ Eindhoven, Netherlands.
   [Razenberg, Lieke G. E. M.; Lemmens, Valery E. P. P.] Netherlands Comprehens Canc Org, Dept Res, Eindhoven, Netherlands.
   [Beerepoot, Laurens V.] Elisabeth Tweesteden Hosp, Dept Oncol, Tilburg, Netherlands.
   [Vos, Allert H.] Bernhoven Hosp, Dept Oncol, Uden, Netherlands.
   [van de Wouw, Agnes J.] VieCuri Hosp, Dept Oncol, Venlo, Netherlands.
   [Maas, Huub A. A. M.] Elisabeth TweeSteden Hosp, Dept Geriatr Med, Tilburg, Netherlands.
   [Lemmens, Valery E. P. P.] Erasmus MC, Dept Publ Hlth, Rotterdam, Netherlands.
C3 Catharina Hospital; Elisabeth-TweeSteden Ziekenhuis (ETZ); VieCuri
   Medical Center; Elisabeth-TweeSteden Ziekenhuis (ETZ); Erasmus
   University Rotterdam; Erasmus MC
RP Razenberg, LGEM (corresponding author), Catharina Hosp, Dept Internal Med, Michelangelolaan 2, NL-5623 EJ Eindhoven, Netherlands.
EM lieke.razenberg@catharinaziekenhuis.nl
OI Beerepoot, Laurens Victor/0000-0002-3040-4626
FU Netherlands Organisation for Health Research and Development, Roche
   Pharmaceuticals [152002012, 152001022]
FX This work was supported by a grand from The Netherlands Organisation for
   Health Research and Development, 10.13039/501100001826 [project number
   152002012 and 152001022] Roche Pharmaceuticals [Unrestricted grand]
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NR 33
TC 6
Z9 6
U1 0
U2 0
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0284-186X
EI 1651-226X
J9 ACTA ONCOL
JI Acta Oncol.
PY 2016
VL 55
IS 12
BP 1443
EP 1449
DI 10.1080/0284186X.2016.1223880
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ED9IF
UT WOS:000389182700010
PM 27585122
OA Bronze
DA 2025-01-04
ER

PT J
AU Richiardone, E
   Al Roumi, R
   Lardinois, F
   Giolito, MV
   Ambroise, J
   Boidot, R
   Drotleff, B
   Ghesquière, B
   Bellahcène, A
   Bardelli, A
   Arena, S
   Corbet, C
AF Richiardone, Elena
   Al Roumi, Rim
   Lardinois, Fanny
   Giolito, Maria Virginia
   Ambroise, Jerome
   Boidot, Romain
   Drotleff, Bernhard
   Ghesquiere, Bart
   Bellahcene, Akeila
   Bardelli, Alberto
   Arena, Sabrina
   Corbet, Cyril
TI MCT1-dependent lactate recycling is a metabolic vulnerability in
   colorectal cancer cells upon acquired resistance to anti-EGFR targeted
   therapy
SO CANCER LETTERS
LA English
DT Article
DE Colorectal cancer; Metabolism; Therapy resistance; KRAS; Cetuximab;
   Lactate; Monocarboxylate transporter
ID 1ST-LINE TREATMENT; CETUXIMAB; GROWTH; KRAS; FLUOROURACIL; OXALIPLATIN;
   LEUCOVORIN; INHIBITION; EXPRESSION; MUTATIONS
AB Despite the implementation of personalized medicine, patients with metastatic CRC (mCRC) still have a dismal overall survival due to the frequent occurrence of acquired resistance mechanisms thereby leading to clinical relapse. Understanding molecular mechanisms that support acquired resistance to anti-EGFR targeted therapy in mCRC is therefore clinically relevant and key to improving patient outcomes. Here, we observe distinct metabolic changes between cetuximab-resistant CRC cell populations, with in particular an increased glycolytic activity in KRAS-mutant cetuximab-resistant CRC cells (LIM1215 and OXCO2) but not in KRAS-amplified resistant DiFi cells. We show that cetuximab-resistant LIM1215 and OXCO2 cells have the capacity to recycle glycolysisderived lactate to sustain their growth capacity. This is associated with an upregulation of the lactate importer MCT1 at both transcript and protein levels. Pharmacological inhibition of MCT1, with AR-C155858, reduces the uptake and oxidation of lactate and impairs growth capacity in cetuximab-resistant LIM1215 cells both in vitro and in vivo. This study identifies MCT1-dependent lactate utilization as a clinically actionable, metabolic vulnerability to overcome KRAS-mutant-mediated acquired resistance to anti-EGFR therapy in CRC.
C1 [Richiardone, Elena; Al Roumi, Rim; Giolito, Maria Virginia; Corbet, Cyril] UCLouvain, Inst Rech Expt & Clin IREC, Pole Pharmacol & Therapeut FATH, Ave Hippocrate 57,B1-57-04, B-1200 Brussels, Belgium.
   [Lardinois, Fanny; Bellahcene, Akeila] Univ Liege, Metastasis Res Lab, GIGA Canc, Liege, Belgium.
   [Ambroise, Jerome] UCLouvain, Inst Rech Expt & Clin IREC, Ctr Technol Mol Appl CTMA, Ave Hippocrate 54, B-1200 Brussels, Belgium.
   [Boidot, Romain] Georges Francois Leclerc Canc Ctr, Dept Biol & Pathol Tumors, Unit Mol Biol, UNICANCER, F-21079 Dijon, France.
   [Drotleff, Bernhard] EMBL Heidelberg, Metabol Core Facil, Heidelberg, Germany.
   [Ghesquiere, Bart] Katholieke Univ Leuven, Dept Cellular & Mol Med, Lab Appl Mass Spectrometry, Leuven, Belgium.
   [Ghesquiere, Bart] VIB, Metabol Core Facil Leuven, Ctr Canc Biol, Leuven, Belgium.
   [Bardelli, Alberto] Univ Torino, Mol Biotechnol Ctr, Dept Oncol, Turin, Italy.
   [Bardelli, Alberto] IFOM ETS AIRC Inst Mol Oncol, Milan, Italy.
   [Arena, Sabrina] Univ Torino, Dept Oncol, Candiolo, TO, Italy.
   [Arena, Sabrina] FPO IRCCS, Candiolo Canc Inst, Candiolo, TO, Italy.
C3 Universite Catholique Louvain; University of Liege; Universite
   Catholique Louvain; UNICANCER; Centre Georges-Francois Leclerc; European
   Molecular Biology Laboratory (EMBL); KU Leuven; Flanders Institute for
   Biotechnology (VIB); University of Turin; IFOM - FIRC Institute of
   Molecular Oncology; University of Turin; IRCCS Fondazione del Piemonte
   per l'Oncologia
RP Corbet, C (corresponding author), UCLouvain, Inst Rech Expt & Clin IREC, Pole Pharmacol & Therapeut FATH, Ave Hippocrate 57,B1-57-04, B-1200 Brussels, Belgium.; Arena, S (corresponding author), Univ Torino, Dept Oncol, Candiolo, TO, Italy.; Arena, S (corresponding author), FPO IRCCS, Candiolo Canc Inst, Candiolo, TO, Italy.
EM sabrina.arena@unito.it; cyril.corbet@uclouvain.be
RI Arena, Sabrina/H-4985-2012; Ghesquiere, Bart/HGU-8736-2022; Giolito,
   Maria Virginia/GPF-8613-2022
OI Ghesquiere, Bart/0000-0003-1547-1705; Lardinois,
   Fanny/0009-0001-9671-6569; Richiardone, Elena/0000-0002-6204-8347;
   Giolito, Maria Virginia/0000-0002-4888-7857; ARENA,
   Sabrina/0000-0002-1318-2494
FU AIRC [IG 2023-ID, 28922, 2022CHB9BA]
FX This work was supported by research grants from the Fonds National de la
   Recherche Scientifique (F.R.S.-FNRS) , the Belgian Foundation against
   Cancer, and the J. Maisin Foundation. The research leading to these
   results has also received funding from: AIRC under BRIDGE 2022-ID 27321
   project (S.A.) , MUR Dipartimento di Eccellenza 2023-2027 14586 DIORAMA
   (S.A.) , Finanziamento dell'Unione Europea Next-Generation EU M4 C2
   investimento 1.1.-PRIN 2022 PNRR P2022E3BTH (S.A.) , Italian Ministry of
   Health, Ricerca Corrente 2024 (S.A.) , AIRC under 5 per Mille 2018-ID.
   21091 program (A.Ba.) ; International Accelerator Award, ACRCelerate,
   jointly funded by Cancer Research UK (A26825 and A28223) , FC AECC
   (GEACC18004TAB) and AIRC (22795) (A.Ba.) ; AIRC under IG 2023-ID. 28922
   project (A.Ba.) and PRIN 2022-Prot. 2022CHB9BA (A.Ba.) . CC is a FNRS
   Research Associate. ER is a FNRS-FRIA PhD fellow. AB is a FNRS Research
   Director.r (A.Ba.) ; AIRC under IG 2023-ID. 28922 project (A.Ba.) and
   PRIN 2022-Prot. 2022CHB9BA (A.Ba.) . CC is a FNRS Research Associate. ER
   is a FNRS-FRIA PhD fellow. AB is a FNRS Research Director.
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NR 52
TC 3
Z9 3
U1 3
U2 3
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 AUG 28
PY 2024
VL 598
AR 217091
DI 10.1016/j.canlet.2024.217091
EA JUL 2024
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YJ3S6
UT WOS:001268089500001
PM 38964730
OA hybrid
DA 2025-01-04
ER

PT J
AU Diogo, V
   Teixeira, J
   Silva, PMA
   Bousbaa, H
AF Diogo, Vania
   Teixeira, Joana
   Silva, Patricia M. A.
   Bousbaa, Hassan
TI Spindle Assembly Checkpoint as a Potential Target in Colorectal Cancer:
   Current Status and Future Perspectives
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE Aneuploidy; Cancer; Gene expression; Spindle checkpoint genes; Targeted
   therapy
ID AURORA KINASE INHIBITOR; SMALL-MOLECULE INHIBITOR; POLO-LIKE KINASES;
   MITOTIC CHECKPOINT; CHROMOSOMAL INSTABILITY; ANTITUMOR-ACTIVITY;
   COLON-CANCER; PHASE-I; SELECTIVE INHIBITOR; EXPRESSION PROFILES
AB Colorectal cancer (CRC), one of the most common malignancies worldwide, is often diagnosed at an advanced stage, and resistance to chemotherapeutic and existing targeted therapy is a major obstacle to its successful treatment. New targets that offer alternative clinical options are therefore urgently needed. Recently, perturbation of the spindle assembly checkpoint (SAC), the surveillance mechanism that maintains anaphase inhibition until all chromosomes reach the metaphase plate, has been regarded as a promising target to fight cancer cells, either alone or in combination regimens. Consistent with this strategy, many cancers, including CRC, exhibit altered expression of SAC genes. In this article, we review our current knowledge on SAC activity status in CRC, and on current anti-CRC strategies and future therapeutic perspectives on the basis of SAC targeting experiments in vitro and in animal models. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Diogo, Vania; Teixeira, Joana; Silva, Patricia M. A.; Bousbaa, Hassan] CESPU, Inst Invest & Formacao Avancada Ciencias & Tecnol, Inst Univ Ciencias Saude, Gandra, Paredes, Portugal.
   [Diogo, Vania; Teixeira, Joana; Silva, Patricia M. A.] Univ Algarve, Dept Ciencias Biomed & Med, Faro, Portugal.
   [Silva, Patricia M. A.] Univ Algarve, Ctr Biomed Res CBMR, Faro, Portugal.
   [Bousbaa, Hassan] Univ Porto, Ctr Interdisciplinar Invest Marinha & Ambiental C, Oporto, Portugal.
C3 Universidade do Algarve; Universidade do Algarve; Universidade do Porto
RP Bousbaa, H (corresponding author), CESPU, Inst Invest & Formacao Avancada Ciencias & Tecnol, Rua Cent Gandra 1317, P-4585116 Gandra, Paredes, Portugal.
EM hassan.bousbaa@iscsn.cespu.pt
RI Silva, Patrícia/AAR-5774-2021; Teixeira, Joao/F-5445-2013; Bousbaa,
   Hassan/K-5947-2019
OI Silva, Patricia/0000-0002-0694-7321; Bousbaa, Hassan/0000-0002-4006-5779
FU CESPU [02-GCQF-CICS-2011N, CheckTax-CESPU-2014]; Foundation for Science
   and Technology (FCT); European Regional Development Fund; COMPETE
   [PEst-C/MAR/LA0015/2013, PTDC/MAR-BIO/4694/2014]; FCT
   [SFRH/BD/90744/2012]; Fundação para a Ciência e a Tecnologia
   [SFRH/BD/90744/2012, PEst-C/MAR/LA0015/2013] Funding Source: FCT
FX This work was funded by CESPU under the Projects 02-GCQF-CICS-2011N and
   CheckTax-CESPU-2014, and was partially supported through national funds
   provided by Foundation for Science and Technology (FCT) and European
   Regional Development Fund and COMPETE under the projects
   PEst-C/MAR/LA0015/2013 and PTDC/MAR-BIO/4694/2014. Patricia M.A. Silva
   is a PhD fellowship holder from FCT (SFRH/BD/90744/2012). The authors
   apologize to those colleagues whose contributions to this research field
   could not be cited due to space limitations, and thank both anonymous
   reviewers for their time, comments, and constructive criticism.
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NR 131
TC 13
Z9 16
U1 1
U2 8
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 2017
VL 16
IS 1
BP 1
EP 8
DI 10.1016/j.clcc.2016.06.006
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EQ3AY
UT WOS:000397944500001
PM 27435760
DA 2025-01-04
ER

PT J
AU Tao, BR
   Yi, CH
   Ma, Y
   Li, YT
   Zhang, B
   Geng, Y
   Chen, ZM
   Ma, XC
   Chen, JH
AF Tao, Baorui
   Yi, Chenhe
   Ma, Yue
   Li, Yitong
   Zhang, Bo
   Geng, Yan
   Chen, Zhenmei
   Ma, Xiaochen
   Chen, Jinhong
TI A Novel TGF-β-Related Signature for Predicting Prognosis, Tumor
   Microenvironment, and Therapeutic Response in Colorectal Cancer
SO BIOCHEMICAL GENETICS
LA English
DT Article; Early Access
DE Colorectal cancer; Liver metastasis; Tumor microenvironment; Prognosis;
   TGFBscore; Immunotherapy
ID GROWTH-FACTOR-BETA; REGULATORY T-CELLS; LIVER METASTASIS; BREAST-CANCER;
   RESISTANCE; SUBTYPES; EVASION; GENOME
AB The transforming growth factor beta (TGF-beta) signaling plays a critical role in immune evasion and tumor progression. However, its modulatory influences on prognosis, tumor microenvironment (TME), and therapeutic efficacy remain unknown in colorectal cancer (CRC). We summarized TGF-beta-related genes and comprehensively estimated their expression pattern in 2142 CRC samples from 9 datasets. Two distinct cluster patterns were divided and biological characteristics of each pattern were further analyzed. Then, to quantify the TGF-beta cluster pattern of individual CRC patient, we generated the TGF-beta score (TGFBscore) model based on TGF-beta cluster pattern-relevant differentially expressed genes (DEGs). Subsequently, we conducted correlation analysis for TGFBscore and clinical prognosis, consensus molecular subtypes (CMSs), TME characteristics, liver metastasis, drug response, and immunotherapeutic efficacy in CRC. We illustrated transcriptional and genetic alterations of TGF-beta-relevant genes, which were closely linked with carcinogenic pathways. We identified two different TGF-beta cluster patterns, characterized by a high and a low TGFBscore. The TGFBscore-high group was significantly linked with worse patient survival, epithelial-mesenchymal transition (EMT) activation, liver metastasis tendency, and the infiltration of immunosuppressive cells (regulatory T cells [Tregs], M2 macrophages, cancer-associated fibroblasts [CAFs], and myeloid-derived suppressor cells [MDSCs]), while the TGFBscore-low group was linked with a survival advantage, epithelial phenotype, early CRC staging, and the infiltration of immune-activated cells (B cell, CD4 T cell, natural killer T [NKT] cell, and T helper 1 [Th1] cell). In terms of predicting drug response, TGFBscore negatively correlated (sensitive to TGFBscore-high group) with drugs targeting PI3K/mTOR, JNK and p38, RTK signaling pathways, and positively correlated (sensitive to TGFBscore-low group) with drugs targeting EGFR signaling pathway. Also, TGFBscore could predict the efficacy of different anti-tumor therapies. TGFBscore-low patients might benefit more from anti-PDL1 immunotherapy, adjuvant chemotherapy (ACT), and ERBB targeted therapy, whereas TGFBscore-high patients might benefit more from antiangiogenic targeted therapy. Our study constructed a novel TGF-beta scoring model that could predict prognosis, liver metastasis tendency, and TME characteristics for CRC patients. More importantly, this work emphasizes the potential clinical utility of TGFBscore in evaluating the efficacy of chemotherapy, targeted therapy, and immunotherapy, guiding individualized precision treatment in CRC.
C1 [Tao, Baorui; Yi, Chenhe; Ma, Yue; Li, Yitong; Zhang, Bo; Geng, Yan; Chen, Zhenmei; Ma, Xiaochen; Chen, Jinhong] Fudan Univ, Huashan Hosp, Dept Gen Surg, 12 Middle Wulumuqi Rd, Shanghai 200040, Peoples R China.
   [Tao, Baorui; Yi, Chenhe; Ma, Yue; Li, Yitong; Zhang, Bo; Geng, Yan; Chen, Zhenmei; Ma, Xiaochen; Chen, Jinhong] Fudan Univ, Canc Metastasis Inst, Shanghai, Peoples R China.
C3 Fudan University; Fudan University
RP Chen, JH (corresponding author), Fudan Univ, Huashan Hosp, Dept Gen Surg, 12 Middle Wulumuqi Rd, Shanghai 200040, Peoples R China.; Chen, JH (corresponding author), Fudan Univ, Canc Metastasis Inst, Shanghai, Peoples R China.
EM jinhongch@hotmail.com
RI yi, chenhe/ABB-5145-2021; bo, zhang/KBB-8283-2024; li,
   jing/HNI-1304-2023
FU China National Science and Technology Major Project for Prevention and
   Treatment of Infectious Diseases [2017ZX10203207]
FX This work was funded by the China National Science and Technology Major
   Project for Prevention and Treatment of Infectious Diseases
   (2017ZX10203207).
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NR 85
TC 3
Z9 3
U1 0
U2 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0006-2928
EI 1573-4927
J9 BIOCHEM GENET
JI Biochem. Genet.
PD 2023 DEC 7
PY 2023
DI 10.1007/s10528-023-10591-7
EA DEC 2023
PG 31
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AI0I2
UT WOS:001117714500001
PM 38062276
DA 2025-01-04
ER

PT J
AU Alsuwaigh, R
   Lee, J
   Chan, G
   Chee, CE
   Choo, SP
AF Alsuwaigh, Rayan
   Lee, Joycelyn
   Chan, Gloria
   Chee, Cheng Ean
   Choo, Su Pin
TI RETRACTED: Response to targeted therapy or chemotherapy following
   immunotherapy in patients with gastrointestinal cancers - a case series
   (Retracted Article)
SO JOURNAL FOR IMMUNOTHERAPY OF CANCER
LA English
DT Article; Retracted Publication
DE Immunotherapy; Targeted therapy; Gastrointestinal cancers
ID MISMATCH REPAIR-DEFICIENT; INHIBITORS; NIVOLUMAB; RATES
AB Background: In non-small cell lung cancer, response rates to chemotherapy given after immune checkpoint inhibitors has been reported to be higher compared to response rates to chemotherapy given before immune checkpoint inhibitors. However, this phenomenon has not been reported in patients with gastrointestinal cancers nor with the use of multi-targeted kinase inhibitors.
   Case presentation: We present a series of six patients who received multi-targeted kinase inhibitors or chemotherapy after progression on immune checkpoint inhibitors and showed unexpected response. Five of these patients had metastatic hepatocellular carcinoma and received salvage multi-targeted kinase inhibitors. Two of these five patients had no response to initial multi-targeted kinase inhibitors but had unexpected response to re-challenge with multi-targeted kinase inhibitors after immune checkpoint inhibitors exposure. The sixth patient had metastatic rectal cancer and showed response to salvage chemotherapy following immune checkpoint inhibitors.
   Conclusion: We postulate that the sequencing of immune checkpoint inhibitors prior to other forms of systemic therapy may potentially lead to an immunomodulatory effect in gastrointestinal cancers with potential improvement in response rates.
C1 [Alsuwaigh, Rayan; Lee, Joycelyn; Choo, Su Pin] Natl Canc Ctr Singapore, Div Med Oncol, 11 Hosp Dr, Singapore 169610, Singapore.
   [Chan, Gloria; Chee, Cheng Ean] Natl Univ Canc Inst, Singapore, Singapore.
C3 National Cancer Centre Singapore (NCCS); National University of
   Singapore
RP Alsuwaigh, R (corresponding author), Natl Canc Ctr Singapore, Div Med Oncol, 11 Hosp Dr, Singapore 169610, Singapore.
EM Rayan.alsuwaigh@mohh.com.sg
RI Lee, joycelyn/KIG-1047-2024; CHOO, Su/ABB-3892-2020
CR Dwary AD, 2017, ONCOTARGET, V8, P91795, DOI 10.18632/oncotarget.20030
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NR 11
TC 14
Z9 13
U1 0
U2 3
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 2051-1426
J9 J IMMUNOTHER CANCER
JI J. Immunother. Cancer
PD JUN 27
PY 2019
VL 7
AR 162
DI 10.1186/s40425-019-0637-6
PG 6
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA IF5RL
UT WOS:000473139800001
PM 31248458
OA gold
DA 2025-01-04
ER

PT J
AU Howard, SAH
   Krajewski, KM
   Jagannathan, JP
   Braschi-Amirfarzan, M
   Tirumani, SH
   Shinagare, AB
   Ramaiya, NH
AF Howard, Stephanie A. Holler
   Krajewski, Katherine M.
   Jagannathan, Jyothi P.
   Braschi-Amirfarzan, Marta
   Tirumani, Sree H.
   Shinagare, Atul B.
   Ramaiya, Nikhil H.
TI A New Look at Toxicity in the Era of Precision Oncology: Imaging
   Findings, Their Relationship With Tumor Response, and Effect on
   Metastasectomy
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Review
DE adverse events; biomarker; metastasectomy; toxicity
ID METASTATIC COLORECTAL-CANCER; RENAL-CELL CARCINOMA; LONG-TERM SURVIVAL;
   LIVER RESECTION; HEPATIC RESECTION; TARGETED THERAPY; ADVERSE EVENTS;
   RADIOLOGIC MANIFESTATIONS; HEPATOCELLULAR-CARCINOMA; BEVACIZUMAB
   TREATMENT
AB OBJECTIVE. As cancer care becomes increasingly personalized and patients with metastatic disease live longer, oncologists' approach to drug toxicity is also evolving.
   CONCLUSION. This article aims to broaden the radiologist's understanding of imaging-evident toxicity by describing how oncologists grade toxicity, exploring toxicity as a biomarker of treatment response, discussing the effect of toxicity in patients who are candidates for metastasectomy, and illustrating how combining drugs of varying classes amplifies toxicity.
C1 [Howard, Stephanie A. Holler; Krajewski, Katherine M.; Jagannathan, Jyothi P.; Braschi-Amirfarzan, Marta; Tirumani, Sree H.; Shinagare, Atul B.; Ramaiya, Nikhil H.] Dana Farber Canc Inst, Dept Radiol, 450 Brookline Ave, Boston, MA 02115 USA.
   [Howard, Stephanie A. Holler; Krajewski, Katherine M.; Jagannathan, Jyothi P.; Braschi-Amirfarzan, Marta; Tirumani, Sree H.; Shinagare, Atul B.; Ramaiya, Nikhil H.] Brigham & Womens Hosp, 75 Francis St, Boston, MA 02115 USA.
C3 Harvard University; Dana-Farber Cancer Institute; Harvard University;
   Brigham & Women's Hospital
RP Howard, SAH (corresponding author), Dana Farber Canc Inst, Dept Radiol, 450 Brookline Ave, Boston, MA 02115 USA.; Howard, SAH (corresponding author), Brigham & Womens Hosp, 75 Francis St, Boston, MA 02115 USA.
EM sahoward@partners.org
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NR 66
TC 13
Z9 13
U1 0
U2 4
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
EI 1546-3141
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD JUL
PY 2016
VL 207
IS 1
BP 4
EP 14
DI 10.2214/AJR.15.15480
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA DP7DE
UT WOS:000378658500009
PM 27065346
DA 2025-01-04
ER

PT J
AU Park, CK
   Park, JS
   Kim, HS
   Rha, SY
   Hyung, WJ
   Cheong, JH
   Noh, SH
   Lee, SK
   Lee, YC
   Huh, YM
   Kim, H
AF Park, Cheol Keun
   Park, Ji Soo
   Kim, Hyo Song
   Rha, Sun Young
   Hyung, Woo Jin
   Cheong, Jae-Ho
   Noh, Sung Hoon
   Lee, Sang Kil
   Lee, Yong Chan
   Huh, Yong-min
   Kim, Hyunki
TI Receptor tyrosine kinase amplified gastric cancer: Clinicopathologic
   characteristics and proposed screening algorithm
SO ONCOTARGET
LA English
DT Article
DE gastric cancer; receptor tyrosine kinase; amplification; screening
   algorithm
ID MICROSATELLITE INSTABILITY; COLORECTAL-CARCINOMA;
   PROGNOSTIC-SIGNIFICANCE; GENE AMPLIFICATION; TARGETED THERAPIES; HER2;
   FGFR2; EGFR; MET; IMMUNOHISTOCHEMISTRY
AB Although targeted therapy for receptor tyrosine kinases (RTKs) of advanced gastric cancers (AGCs) has been in the spotlight, guidelines for the identification of RTK-amplified gastric cancers (RA-GCs) have not been established. In this study, we investigate clinicopathologic characteristics of RA-GCs and propose a screening algorithm for their identification. We performed immunohistochemistry (IHC) for MLH1, MSH2, PMS2, MSH6, key RTKs (EGFR, HER2, MET), and p53, in situ hybridization for Epstein-Barr virus encoding RNA, and silver in situ hybridization (SISH) for EGFR, HER2, and MET using tissue microarrays of 993 AGCs. On IHC, 157 (15.8%) 61, (6.15%), and 85 (8.56%) out of 993 cases scored 2+ or 3+ for EGFR, HER2, and MET, respectively. On SISH, 31.2% (49/157), 80.3% (49/61), and 30.6% (26/85) of 2+ or 3+ cases on IHC showed amplification of the corresponding genes. Of the 993 cases, 104 were classified as RA-GCs. RA-GC status correlated with older age (P<0.001), differentiated histology (P=0.001), intestinal or mixed type by Lauren classification (P<0.001), lymphovascular invasion (P=0.026), and mutant-pattern of p53 (P<0.001). The cases were divided into four subgroups using two classification systems, putative molecular classification and histologic-molecular classification, based on Lauren classification, IHC, and SISH results. The histologic-molecular classification showed higher sensitivity for identification of RA-GCs and predicted patient prognosis better than the putative molecular classification. In conclusion, RA-GCs show unique clinicopathologic features. The proposed algorithm based on histologic-molecular classification can be applied to select candidates for genetic examination and targeted therapy.
C1 [Park, Cheol Keun; Kim, Hyunki] Yonsei Univ, Coll Med, Dept Pathol, Seoul, South Korea.
   [Park, Ji Soo; Kim, Hyo Song; Rha, Sun Young] Yonsei Univ, Coll Med, Dept Internal Med, Div Med Oncol,Yonsei Canc Ctr, Seoul, South Korea.
   [Hyung, Woo Jin; Cheong, Jae-Ho; Noh, Sung Hoon] Yonsei Univ, Coll Med, Dept Surg, Seoul, South Korea.
   [Lee, Sang Kil; Lee, Yong Chan] Yonsei Univ, Coll Med, Dept Internal Med, Div Gastroenterol, Seoul, South Korea.
   [Huh, Yong-min] Yonsei Univ, Coll Med, Dept Radiol, YUMS KRIBB Med Convergence Res Inst, Seoul, South Korea.
C3 Yonsei University; Yonsei University Health System; Yonsei University;
   Yonsei University Health System; Yonsei University; Yonsei University
   Health System; Yonsei University; Yonsei University Health System;
   Yonsei University; Yonsei University Health System
RP Kim, H (corresponding author), Yonsei Univ, Coll Med, Dept Pathol, Seoul, South Korea.
EM kimhyunki@yuhs.ac
RI Kim, Hyon-Suk/R-4113-2017; Lee, Young/AAI-1932-2020; Lee,
   In/J-9324-2013; lee, wj/JNR-4926-2023; Park, Keunchil/ABD-5852-2021
OI Lee, Sang Kil/0000-0002-0721-0364; Kim, Hyunki/0000-0003-2292-5584; Noh,
   Sung Hoon/0000-0003-4386-6886; Park, Ji Soo/0000-0002-0023-7740; Lee,
   Yong Chan/0000-0001-8800-6906; Rha, Sun Young/0000-0002-2512-4531; Kim,
   Hyo Song/0000-0002-0625-9828; Huh, Yong-Min/0000-0002-9831-4475; Hyung,
   Woo Jin/0000-0002-8593-9214; Cheong, Jae-Ho/0000-0002-1703-1781
FU Basic Science Research Program through the National Research Foundation
   of Korea (NRF); Ministry of Science, ICT and Future Planning
   [2012R1A1A1004403]; Bio & Medical Technology Development Program of the
   NRF - Ministry of Science, ICT & Future Planning [NRF-2015M3A9D7029878]
FX This research was supported by the Basic Science Research Program
   through the National Research Foundation of Korea (NRF) and was funded
   by the Ministry of Science, ICT and Future Planning (Hyunki Kim;
   2012R1A1A1004403) and the Bio & Medical Technology Development Program
   of the NRF funded by the Ministry of Science, ICT & Future Planning
   (Yongmin Huh; NRF-2015M3A9D7029878).
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NR 43
TC 13
Z9 13
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 NOV 1
PY 2016
VL 7
IS 44
BP 72099
EP 72112
DI 10.18632/oncotarget.12291
PG 14
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EB5VQ
UT WOS:000387449100087
PM 27765925
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Li, H
   Lu, JB
   Yan, CQ
   Xu, LW
AF Li, Hui
   Lu, Jianbo
   Yan, Chengqiu
   Xu, Liwei
TI Tumor cell membrane-coated biomimetic nanoplatform for homologous
   targeted therapy of colorectal carcinoma
SO INTERNATIONAL JOURNAL OF POLYMERIC MATERIALS AND POLYMERIC BIOMATERIALS
LA English
DT Article
DE Biomimetic nanoplatform; colorectal carcinoma; homologous targeting;
   paclitaxel; targeted drug delivery; tumor cell membrane
ID DELIVERY; NANOPARTICLES; PACLITAXEL; NANOGELS; CLEARANCE; NETWORKS;
   CARRIERS
AB To avoid the clearance of reticuloendothelial system (RES) and realize tumor-specific targeting drug delivery are still the main challenges for nanodrug delivery systems in treatment of tumor. Recently, cell membranes coated nanoparticles have garnered more and more attention because of their mimic ability with their source cells, which are very effective in tumor therapy. Herein, we fabricated a biomimetic nanodrug delivery system composed of paclitaxel (PTX)-loaded gelatin nanogels (GN) as the inner cores and HT-29 tumor cell membranes (TCMs) as the outer shells, noted as TCM/GN/PTX for the targeted therapy of colorectal carcinoma. The TCM/GN/PTX showed obvious core-shell nanostructure and effectively reduced the release of laden PTX. Due to the homotypic targeting ability of coated TCM, the TCM/GN/PTX could realize the selective targeting of the homotypic tumor cells, therefore, obviously improving the accumulation of PTX at tumor sites. After administration in HT-29 xenografts mouse models, the TCM/GN/PTX significantly suppressed the tumor growth by inducing the necrosis and apoptosis of tumor cells. Moreover, due to the coated TCM effectively avoided the premature release of PTX, the TCM/GN/PTX showed minimal side effects. As a result, this bioinspired strategy-based biomimetic platform can be a promising nanodrug delivery system for unique targeted therapy of colorectal carcinoma.
C1 [Li, Hui; Yan, Chengqiu] Changchun Univ Tradit Chinese Med, Affiliated Hosp, Dept Anorectal Surg, Changchun, Jilin, Peoples R China.
   [Lu, Jianbo] Changchun Univ Tradit Chinese Med, Affiliated Hosp, Dept Ultrasound, Changchun, Jilin, Peoples R China.
   [Xu, Liwei] Changchun Univ Tradit Chinese Med, Affiliated Hosp, Dept Hematol & Oncol, Changchun, Jilin, Peoples R China.
C3 Changchun University of Chinese Medicine; Changchun University of
   Chinese Medicine; Changchun University of Chinese Medicine
RP Xu, LW (corresponding author), Changchun Univ Tradit Chinese Med, Affiliated Hosp, Dept Hematol & Oncol, Changchun, Jilin, Peoples R China.
EM liwei_xu45@sina.com
FU National Natural Science Foundation of China [31244208]
FX This work was supported by the National Natural Science Foundation of
   China [no. 31244208].
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NR 32
TC 10
Z9 10
U1 1
U2 38
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0091-4037
EI 1563-535X
J9 INT J POLYM MATER PO
JI Int. J. Polym. Mater. Polym. Biomat.
PD DEC 11
PY 2020
VL 69
IS 18
BP 1157
EP 1166
DI 10.1080/00914037.2019.1667804
EA SEP 2019
PG 10
WC Materials Science, Biomaterials; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Materials Science; Polymer Science
GA OA2EZ
UT WOS:000487523500001
DA 2025-01-04
ER

PT J
AU Feng, HR
   Jin, ZJ
   Liang, JY
   Zhao, QW
   Zhan, L
   Yang, ZY
   Yan, JQ
   Kuang, J
   Cheng, X
   Qiu, WH
AF Feng, Haoran
   Jin, Zhijian
   Liang, Juyong
   Zhao, Qiwu
   Zhan, Ling
   Yang, Zheyu
   Yan, Jiqi
   Kuang, Jie
   Cheng, Xi
   Qiu, Weihua
TI FOXK2 transcriptionally activating VEGFA induces apatinib resistance in
   anaplastic thyroid cancer through VEGFA/VEGFR1 pathway
SO ONCOGENE
LA English
DT Article
ID COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA; TYROSINE KINASE; INHIBITOR;
   CELLS; SUPPRESSES; EXPRESSION; PROGNOSIS; GROWTH
AB Anaplastic thyroid carcinoma (ATC) is a rare and extremely aggressive type of thyroid cancer, and the potential mechanisms involved in ATC progression remains unclarified. In this study, we found that forkhead box K2 (FOXK2) was upregulated in ATC tissues, and the expression of FOXK2 was associated with tumor size. Evidenced by RNA-seq and Chromatin immunoprecipitation (ChIP)-seq assays, FOXK2 positively regulated VEGF and VEGFR signaling network, among which only VEGFA could be noticed in both RNA-seq and ChIP-seq results. ChIP, dual-luciferase reporter system and functional experiments further confirmed that FOXK2 promoted angiogenesis by inducing the transcription of VEGFA. On VEGFR2 blockage by specific targeting agent, such as Apatinib, FOXK2 could rapidly trigger therapeutic resistance. Mechanical analyses revealed that VEGFA transcriptionally induced by FOXK2 could bind to VEGFR1 as a compensation for VEGFR2 blockage, which promoted angiogenesis by activating ERK, PI3K/AKT and P38/MAPK signaling in human umbilical vein endothelial cells (HUVECs). Synergic effect on anti-angiogenesis could be observed when VEGFR1 suppressor AF321 was included in VEGFR2 inhibition system, which clarified the pivot role of FOXK2 in VEGFR2 targeting therapy resistance. More importantly, the binding of VEGFA to VEGFR1 could further promoter FOXK2-mediated VEGFA transcription, which consequently constituted a positive feedback loop. Therefore, the novel loop VEGFA/VEGFR1/FOXK2 functioned importantly in resistance to VEGFR2 targeting therapy in FOXK2(+) ATCs. Altogether, FOXK2 plays critical roles in ATC angiogenesis and VEGFR2 blockage resistance by inducing VEGFA transcription. FOXK2 represents a potentially new therapeutic strategy and biomarker for anti-angiogenic therapy against ATC.
C1 [Feng, Haoran; Jin, Zhijian; Liang, Juyong; Zhao, Qiwu; Zhan, Ling; Yang, Zheyu; Yan, Jiqi; Kuang, Jie; Cheng, Xi; Qiu, Weihua] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Gen Surg, Shanghai, Peoples R China.
   [Feng, Haoran] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Shanghai Inst Digest Surg, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University; Shanghai Jiao Tong University
RP Kuang, J; Cheng, X; Qiu, WH (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Gen Surg, Shanghai, Peoples R China.
EM kuangjie823@msn.com; drchengxi@126.com; qwh11072@rjh.com.cn
RI feng, haoran/JJF-9894-2023; Yang, Zheyu/GRR-2329-2022; Xi,
   Cheng/AEY-6492-2022
OI Jin, Zhijian/0000-0002-0370-3698
FU National Natural Science Foundation of China [82072948, 82003169,
   82002475]; Shanghai Sailing Program [20YF1427700]
FX The study was supported by the National Natural Science Foundation of
   China, 82072948 (WQ); National Natural Science Foundation of China,
   82003169 (HF); National Natural Science Foundation of China, 82002475
   (XC) and Shanghai Sailing Program, 20YF1427700 (XC).
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NR 41
TC 17
Z9 19
U1 0
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 OCT 21
PY 2021
VL 40
IS 42
BP 6115
EP 6129
DI 10.1038/s41388-021-01830-5
EA SEP 2021
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 WK6OK
UT WOS:000692963000002
PM 34489549
DA 2025-01-04
ER

PT J
AU Moreira, RB
   Peixoto, RD
   Cruz, MRS
AF Moreira, Raphael Brandao
   Peixoto, Renata D'Alpino
   Sousa Cruz, Marcelo Rochade
TI Clinical Response to Sorafenib in a Patient with Metastatic Colorectal
   Cancer and FLT3 Amplification
SO CASE REPORTS IN ONCOLOGY
LA English
DT Article
DE Metastatic colorectal cancer; Sorafenib; FLT3 amplification
ID TYROSINE KINASE; HUMAN BREAST; CHEMOTHERAPY; COMBINATION; MUTATIONS;
   TRIAL; GENE; TRANSFORMATION; INHIBITOR; CETUXIMAB
AB Background: A considerable number of patients with metastatic colorectal cancer progress after exhausting all approved standard therapies but maintain an adequate performance status and could be candidates for further treatment. We aim at reviewing our experience with sorafenib treatment of a patient with FLT3 mutation in refractory metastatic colorectal cancer. Methods: Treatment with sorafenib of a patient with metastatic colorectal cancer and FLT3 translocation who had previously been heavily treated. Results: The patient with metastatic colorectal cancer, aged 51 years, showed significant symptomatic and laboratory improvement with sorafenib treatment (400 mg twice daily). Conclusion: The presented case illustrates how an aggressive and refractory colorectal tumor may respond well to targeted therapy. (C) 2015 S. Karger AG, Basel
C1 [Moreira, Raphael Brandao; Peixoto, Renata D'Alpino; Sousa Cruz, Marcelo Rochade] Ctr Oncol Antonio Ermirio Moraes, Sao Paulo, Brazil.
RP Moreira, RB (corresponding author), Marques Olinda St 401-18, BR-04277000 Sao Paulo, Brazil.
EM raphamoreira@gmail.com
OI Moreira, Raphael/0000-0002-7464-5544
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NR 39
TC 21
Z9 24
U1 1
U2 4
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1662-6575
J9 CASE REP ONCOL
JI Case Rep. Oncol.
PY 2015
VL 8
IS 1
BP 82
EP 86
DI 10.1159/000375483
PG 5
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA CU2SO
UT WOS:000363373900015
PM 25848357
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Hoffman, RM
AF Hoffman, Robert M.
TI Patient-Derived Orthotopic Xenograft (PDOX) Models of Melanoma
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE melanoma; patient-derived orthotopic xenografts; PDOX; targeted therapy;
   personalized therapy
ID SALMONELLA-TYPHIMURIUM A1-R; NUDE-MOUSE MODEL; HUMAN PANCREATIC-CANCER;
   SOFT-TISSUE SARCOMA; FLUORESCENCE-GUIDED SURGERY;
   GAMMA-MERCAPTOMETHANE-LYASE; HUMAN COLON-CANCER; ANTI-CEA ANTIBODY;
   SERUM METHIONINE; BREAST-CANCER
AB Metastatic melanoma is a recalcitrant tumor. Although targeted and immune therapies have been highly touted, only relatively few patients have had durable responses. To overcome this problem, our laboratory has established the melanoma patient-derived orthotopic xenograft (PDOX) model with the use of surgical orthotopic implantation (SOI). Promising results have been obtained with regard to identifying effective approved agents and experimental therapeutics, as well as combinations of the two using the melanoma PDOX model.
C1 [Hoffman, Robert M.] AntiCancer Inc, 7917 Ostrow St, San Diego, CA 92111 USA.
   [Hoffman, Robert M.] Univ Calif San Diego, Dept Surg, San Diego, CA 92103 USA.
C3 AntiCancer, Inc.; University of California System; University of
   California San Diego
RP Hoffman, RM (corresponding author), AntiCancer Inc, 7917 Ostrow St, San Diego, CA 92111 USA.; Hoffman, RM (corresponding author), Univ Calif San Diego, Dept Surg, San Diego, CA 92103 USA.
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NR 82
TC 27
Z9 29
U1 1
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD SEP
PY 2017
VL 18
IS 9
AR 1875
DI 10.3390/ijms18091875
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA FI4RW
UT WOS:000411963800054
PM 28858204
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Westin, JR
AF Westin, Jason R.
TI Busting robustness: using cancer's greatest strength to our advantage
SO FUTURE ONCOLOGY
LA English
DT Article
DE cancer; combination therapy; complexity; robustness; scale free
   networks; small molecule inhibitors; targeted therapy
ID COLON-CANCER; INHIBITION; NETWORKS; RESISTANCE
AB What do complex networks, such as those found in cancer cells, airplane flight patterns and the Internet have in common? A remarkable robustness with a surprising vulnerability. Complex networks follow remarkably similar patterns across seemingly unconnected fields, and it is possible that cancer researchers could thus learn from the advances in complex network theory. Very limited, yet coordinated, specific targeting of the most critical parts of a network can have dramatically outsized effects.At times, our strengths propel us so far forward we can no longer endure our weaknesses and perish from them.Nietzsche
RP Westin, JR (corresponding author), 1400 Holcombe Blvd,Unit 0429, Houston, TX 77030 USA.
EM jwestin@mdanderson.org
OI Westin, Jason/0000-0002-1824-2337
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NR 19
TC 7
Z9 7
U1 0
U2 3
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PY 2015
VL 11
IS 1
BP 73
EP 77
DI 10.2217/fon.14.49
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AY7AN
UT WOS:000347713800010
PM 24673642
DA 2025-01-04
ER

PT J
AU Mrowka, P
   Glodkowska-Mrowka, E
AF Mrowka, Piotr
   Glodkowska-Mrowka, Eliza
TI PPARγ Agonists in Combination Cancer Therapies
SO CURRENT CANCER DRUG TARGETS
LA English
DT Review
DE Peroxisome proliferator-activated receptor-gamma; PPAR gamma ligand;
   thiazolidinediones; cancer; leukemia; combination therapy; tyrosine
   kinase inhibitors; imatinib
ID ACTIVATED-RECEPTOR-GAMMA; CHRONIC MYELOID-LEUKEMIA; CELL-CYCLE ARREST;
   TROGLITAZONE INDUCES APOPTOSIS; PHASE-II TRIAL; BREAST-CANCER;
   GROWTH-INHIBITION; COLON-CANCER; LUNG-CANCER; ANTITUMOR-ACTIVITY
AB Peroxisome proliferator-activated receptor-gamma (PPAR gamma) is a nuclear receptor acting as a transcription factor involved in the regulation of energy metabolism, cell cycle, cell differentiation, and apoptosis. These unique properties constitute a strong therapeutic potential that place PPAR gamma agonists as one of the most interesting and widely studied anticancer molecules.
   Although PPAR gamma agonists exert significant, antiproliferative and tumoricidal activity in vitro, their anticancer efficacy in animal models is ambiguous, and their effectiveness in clinical trials in monotherapy is unsatisfactory. However, due to pleiotropic effects of PPAR gamma activation in normal and tumor cells, PPAR gamma ligands interact with many antitumor treatment modalities and synergistically potentiate their effectiveness. The most spectacular example is a combination of PPAR gamma ligands with tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML). In this setting, PPAR gamma activation sensitizes leukemic stem cells, resistant to any previous form of treatment, to targeted therapy. Thus, this combination is believed to be the first pharmacological therapy able to cure CML patients.
   Within the last decade, a significant body of data confirming the benefits of the addition of PPAR gamma ligands to various antitumor therapies, including chemotherapy, hormonotherapy, targeted therapy, and immunotherapy, has been published. Although the majority of these studies have been carried out in vitro or animal tumor models, a few successful attempts to introduce PPAR gamma ligands into anticancer therapy in humans have been recently made. In this review, we aim to summarize shines and shadows of targeting PPAR gamma in antitumor therapies.
C1 [Mrowka, Piotr] Med Univ Warsaw, Dept Biophys & Human Physiol, Warsaw, Poland.
   [Glodkowska-Mrowka, Eliza] Med Univ Warsaw, Dept Lab Diagnost & Clin Immunol Dev Age, Warsaw, Poland.
   [Glodkowska-Mrowka, Eliza] Inst Hematol & Transfus Med, Dept Expt Hematol, Warsaw, Poland.
C3 Medical University of Warsaw; Medical University of Warsaw
RP Glodkowska-Mrowka, E (corresponding author), Med Univ Warsaw, Dept Lab Diagnost & Clin Immunol Dev Age, Warsaw, Poland.; Glodkowska-Mrowka, E (corresponding author), Inst Hematol & Transfus Med, Dept Expt Hematol, Warsaw, Poland.
EM eliza.glodkowska@wum.edu.pl
RI Glodkowska-Mrowka, Eliza/AAR-8503-2021; Glodkowska-Mrowka,
   Eliza/AAC-7294-2020
OI Glodkowska-Mrowka, Eliza/0000-0002-5865-8425; Mrowka,
   Piotr/0000-0002-4300-7267
FU National Science Center [2012/05/N/NZ5/02616]; Polish Ministry of
   Science; Higher Education for Polish-Indian collaboration studies;
   Medical University of Warsaw; Scholarship for Outstanding Young
   Scientists
FX This work was supported by grant 2012/05/N/NZ5/02616 from National
   Science Center, Polish Ministry of Science (PM) and Higher Education for
   Polish-Indian collaboration studies (PM) and Medical University of
   Warsaw (PM, EGL). EGL is a recipient of Scholarship for Outstanding
   Young Scientists founded by the Polish Ministry of Science and Higher
   Education.
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NR 193
TC 13
Z9 13
U1 1
U2 21
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1568-0096
EI 1873-5576
J9 CURR CANCER DRUG TAR
JI Curr. Cancer Drug Targets
PY 2020
VL 20
IS 3
BP 197
EP 215
DI 10.2174/1568009619666191209102015
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KW2YN
UT WOS:000521034600003
PM 31814555
DA 2025-01-04
ER

PT J
AU Yuan, DP
   Tao, Y
   Wang, HY
   Wang, JW
   Cao, YP
   Cao, W
   Pan, S
   Yu, ZN
AF Yuan, Danping
   Tao, Yong
   Wang, Haoyi
   Wang, Jiawei
   Cao, Yuepeng
   Cao, Wen
   Pan, Shou
   Yu, Zhaonan
TI A comprehensive analysis of the microbiota composition and host driver
   gene mutations in colorectal cancer
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Microbiota; 16S; Colorectal cancer; Driver gene mutation; Target therapy
ID GUT MICROBIOTA
AB Studies of both, microbiota and target therapy associated with gene mutations in colorectal cancer, (CRC) have attracted increasing attention. However, only a few of them analyzed the combined effects on CRC. we analyzed differences in intestinal microbiota of 44 colorectal cancer patients and 20 healthy controls (HC) using 16S rRNA gene sequencing of fecal samples. For 39 of the CRC patients, targeted Next Generation Sequencing (NGS) was carried out at formalin fixed paraffin embedded (FFPE) samples to identify somatic mutation profiles. Compared to the HC group, the microbial diversity of CRC patients was significantly lower. In the CRC group, we found a microbiome that was significantly enriched for strains of Bifidobacterium, Bacteroides, and Megasphaera whereas in the HC group the abundance of Collinsella, Faecalibacterium, and Agathobacter strains was higher. Among the mutations detected in the CRC group, the APC gene had the highest mutation rate (77%, 30/39). We found that the KRAS mutant type was closely associated with Faecalibacterium, Roseburia, Megamonas, Lachnoclostridium, and Harryflintia. Notably, Spearman correlation analysis showed that KRAS mutations were negatively correlated with the existence of Bifidobacterium and positively correlated with Faecalibacterium. By employing 16S rRNA gene sequencing, we identified more unique features of microbiota profiles in CRC patients. For the first time, our study showed that gene mutations could directly be linked to the microbiota composition of CRC patients. We hypothesize that the effect of a targeted colorectal cancer therapy is also closely related to the colorectal flora, however, this requires further investigation.
C1 [Yuan, Danping; Tao, Yong; Cao, Yuepeng] Ningbo First Hosp, Dept Colorectal Surg, Ningbo, Peoples R China.
   [Wang, Haoyi; Wang, Jiawei; Cao, Wen; Pan, Shou; Yu, Zhaonan] Hangzhou DA Med Lab, Hangzhou 310030, Peoples R China.
C3 Ningbo University
RP Yuan, DP (corresponding author), Ningbo First Hosp, Dept Colorectal Surg, Ningbo, Peoples R China.; Yu, ZN (corresponding author), Hangzhou DA Med Lab, Hangzhou 310030, Peoples R China.
EM danpingyuan2021@163.com; yuzhaonan870213@163.com
RI Wang, Haoyi/GMX-2859-2022; Tao, Yong/AFG-9738-2022
OI yu, zhaonan/0000-0003-4725-1379
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NR 31
TC 11
Z9 11
U1 0
U2 8
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 OCT
PY 2022
VL 40
IS 5
BP 884
EP 894
DI 10.1007/s10637-022-01263-1
EA JUN 2022
PG 11
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA 3X6UQ
UT WOS:000813994200001
PM 35727391
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Foo, T
   Roy, A
   Karapetis, C
   Townsend, A
   Price, T
AF Foo, Tiffany
   Roy, Amitesh
   Karapetis, Christos
   Townsend, Amanda
   Price, Timothy
TI Metastatic colorectal cancer- third line therapy and beyond
SO EXPERT REVIEW OF ANTICANCER THERAPY
LA English
DT Review
DE Metastatic colorectal cancer; immunotherapy; targeted therapy;
   biomarkers; refractory disease
ID OPEN-LABEL; DOUBLE-BLIND; TAS-102 MONOTHERAPY; 1ST-LINE TREATMENT;
   REPAIR-DEFICIENT; ASIAN PATIENTS; SINGLE-ARM; PLACEBO; PLUS; REGORAFENIB
AB IntroductionThe outcome of patients with metastatic colorectal cancer (mCRC) has improved significantly in the last few decades. Metastatic colorectal cancer is a highly heterogenous cancer. Beyond second line chemotherapy, treatment decisions are often based on molecular testing.MethodIn this narrative review, we provide a comprehensive summary of data from key clinical trials and discuss how to integrate these agents into the current treatment landscape of metastatic colorectal cancer.Expert OpinionIn the era of precision medicine, molecular testing plays an increasingly important role in the management of mCRC. Efforts need to be made to target treatment based on molecular test results.
C1 [Foo, Tiffany; Townsend, Amanda; Price, Timothy] Queen Elizabeth Hosp, Dept Med Oncol, Woodville South, SA 5011, Australia.
   [Foo, Tiffany; Townsend, Amanda; Price, Timothy] Univ Adelaide, Woodville South, SA 5011, Australia.
   [Roy, Amitesh; Karapetis, Christos] FCIC, Dept Med Oncol, Bedford Pk, SA, Australia.
   [Roy, Amitesh; Karapetis, Christos] Flinders Univ S Australia, Bedford Pk, SA, Australia.
C3 University of Adelaide; Flinders University South Australia
RP Price, T (corresponding author), Queen Elizabeth Hosp, Dept Med Oncol, Woodville South, SA 5011, Australia.; Price, T (corresponding author), Univ Adelaide, Woodville South, SA 5011, Australia.
EM Timothy.Price@sa.gov.au
RI Price, Timothy/G-1404-2012; Roy, Amitesh/AGQ-4929-2022
OI Karapetis, Christos/0000-0003-1741-996X; Roy,
   Amitesh/0000-0002-3583-7981
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NR 66
TC 1
Z9 1
U1 5
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1473-7140
EI 1744-8328
J9 EXPERT REV ANTICANC
JI Expert Rev. Anticancer Ther
PD MAY 3
PY 2024
VL 24
IS 5
BP 219
EP 227
DI 10.1080/14737140.2024.2334784
EA APR 2024
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PS9Z4
UT WOS:001196486800001
PM 38526540
DA 2025-01-04
ER

PT J
AU Underwood, PW
   Ruff, SM
   Pawlik, TM
AF Underwood, Patrick W.
   Ruff, Samantha M.
   Pawlik, Timothy M.
TI Update on Targeted Therapy and Immunotherapy for Metastatic Colorectal
   Cancer
SO CELLS
LA English
DT Review
DE targeted therapy; personalized medicine; colorectal cancer; molecular
   profiling
ID RANDOMIZED PHASE-III; RAS WILD-TYPE; OXALIPLATIN-BASED CHEMOTHERAPY;
   CETUXIMAB PLUS IRINOTECAN; POSITIVE SOLID TUMORS; OPEN-LABEL; 1ST-LINE
   TREATMENT; COLON-CANCER; DOUBLE-BLIND; MICROSATELLITE INSTABILITY
AB Metastatic colorectal cancer remains a deadly malignancy and is the third leading cause of cancer-related death. The mainstay of treatment for metastatic colorectal cancer is chemotherapy, but unfortunately, even with recent progress, overall survival is still poor. Colorectal cancer is a heterogeneous disease, and the underlying genetic differences among tumors can define the behavior and prognosis of the disease. Given the limitations of cytotoxic chemotherapy, research has focused on developing targeted therapy based on molecular subtyping. Since the early 2000s, multiple targeted therapies have demonstrated efficacy in treating metastatic colorectal cancer and have received FDA approval. The epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and DNA mismatch repair pathways have demonstrated promising results for targeted therapies. As new gene mutations and proteins involved in the oncogenesis of metastatic colorectal cancer are identified, new targets will continue to emerge. We herein provide a summary of the updated literature regarding targeted therapies for patients with mCRC.
C1 [Underwood, Patrick W.; Ruff, Samantha M.; Pawlik, Timothy M.] Ohio State Univ, Wexner Med Ctr, Dept Surg, 395 W 12th Ave,Suite 670, Columbus, OH 43210 USA.
   [Underwood, Patrick W.; Ruff, Samantha M.; Pawlik, Timothy M.] James Comprehens Canc Ctr, 395 W 12th Ave,Suite 670, Columbus, OH 43210 USA.
C3 University System of Ohio; Ohio State University; James Cancer Hospital
   & Solove Research Institute; University System of Ohio; Ohio State
   University
RP Pawlik, TM (corresponding author), Ohio State Univ, Wexner Med Ctr, Dept Surg, 395 W 12th Ave,Suite 670, Columbus, OH 43210 USA.; Pawlik, TM (corresponding author), James Comprehens Canc Ctr, 395 W 12th Ave,Suite 670, Columbus, OH 43210 USA.
EM patrick.underwood@osumc.edu; samantha.ruff@osumc.edu;
   tim.pawlik@osumc.edu
RI Pawlik, Timothy/AAO-9335-2020
OI Pawlik, Timothy/0000-0002-7994-9870
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NR 89
TC 13
Z9 13
U1 37
U2 54
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD FEB
PY 2024
VL 13
IS 3
AR 245
DI 10.3390/cells13030245
PG 16
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA HO1Z8
UT WOS:001160367300001
PM 38334637
OA gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Zhang, T
   Liu, Z
   Lin, Q
AF Zhang, Tao
   Liu, Zhi
   Lin, Qian
TI Clinical effect and safety of targeted therapy combined with
   chemotherapy in the treatment of patients with advanced colon cancer
SO PAKISTAN JOURNAL OF MEDICAL SCIENCES
LA English
DT Article
DE Targeted therapy; Chemotherapy; Advanced colon cancer; Prognosis
ID ADJUVANT CHEMOTHERAPY
AB Objective: To evaluate the clinical effect and safety of immunotherapy combined with chemotherapy in patients with advanced colon cancer.Methods: This is a retrospective study. The subjects of this study were 120 patients with advanced colon cancer who were admitted to The No.2 Hospital of Baoding from November 30, 2019 to November 30, 2021. The enrolled patients were randomly divided into two groups, with 60 cases in each group. Patients in the control group were given F0LF0X4 regimen, while those in the study group were provided with Bevacizumab therapy on the basis of the method in the control group. All patients were evaluated after two cycles of treatment. The comparison of outcome measures included the curative effects, adverse drug reactions, improvement of quality-of-life scores and changes in tumor markers between the two groups.Results: The total effective rate of the study group was significantly better than that of the control group. There was no significant difference in the incidence of adverse drug reactions between the two groups. After treatment, the study group had a significantly higher rate of improved quality of life score, while the obviously lower rate of the aggravated score than those in the control group. The levels of CEA, CA19-9 and CA125 in the study group were significantly lower than those in the control group after treatment. Conclusion: Targeted therapy combined with chemotherapy is a safe and effective therapeutic option that has a definite curative effect in the treatment of patients with advanced colon cancer.
C1 [Zhang, Tao; Liu, Zhi] No 2 Hosp Baoding, Dept Gen Surg, Baoding 071051, Hebei, Peoples R China.
   [Lin, Qian] No 2 Hosp Baoding, Dept Nursing, Baoding 071051, Hebei, Peoples R China.
RP Zhang, T (corresponding author), No 2 Hosp Baoding, Dept Gen Surg, Baoding 071051, Hebei, Peoples R China.
EM zhangtao19882022@126.com
FU Baoding Science and technology plan project [2141ZF195]
FX This study is supported by Baoding Science and technology plan project
   task (No.: 2141ZF195).
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NR 32
TC 1
Z9 1
U1 1
U2 3
PU PROFESSIONAL MEDICAL PUBLICATIONS
PI SADDAR
PA PANORAMA CENTRE, RM 522, 5TH FLOOR, BLDG 2, RAJA GHAZANFAR ALI RD, PO
   BOX 8766, SADDAR, KARACHI 00000, PAKISTAN
SN 1682-024X
EI 1681-715X
J9 PAK J MED SCI
JI Pak. J. Med. Sci.
PD JUL-AUG
PY 2023
VL 39
IS 4
BP 1074
EP 1079
DI 10.12669/pjms.39.4.7105
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA N9TY7
UT WOS:001040363300031
PM 37492316
OA gold
DA 2025-01-04
ER

PT J
AU Wang, JF
   Liu, J
   Tian, F
   Zhan, Y
   Kong, DL
AF Wang, Jiefu
   Liu, Jia
   Tian, Fei
   Zhan, Yang
   Kong, Dalu
TI Cyclin-dependent kinase 9 expression and its association with
   CD8<SUP>+</SUP> T cell infiltration in microsatellite-stable colorectal
   cancer
SO ONCOLOGY LETTERS
LA English
DT Article
DE CDK9; immunotherapy; CD8(+) T cell exhaustion; microsatellite stable;
   colorectal cancer
ID KEY PLAYER; WEB SERVER; COLON; INHIBITION; PATHWAYS; TARGET; CDK9; PD-1;
   ACTIVATION; EXHAUSTION
AB Programmed death 1 (PD-1)-targeted therapy has benefited patients with microsatellite instability-high metastatic colorectal cancer (mCRC). However, the efficacy of PD-1-targeted therapy is poor in patients with microsatellite-stable (MSS) mCRC. Therefore, it is imperative to explore additional co-inhibitory molecular signalling pathways to improve the efficacy of immunotherapy in MSS mCRC treatment. In the present study, the association between cyclin-dependent kinase 9 (CDK9) expression and the survival of patients with CRC was analysed using RNA sequencing data from 605 patients, including 121 cases of mortality, from human cancer datasets. Furthermore, 35 clinical MSS stage III-IV CRC specimens were collected to assess CDK9 protein expression by immunohistochemistry, and the frequency of tumor-infiltrating CD8(+) T cells was assessed by flow cytometry. The human cancer datasets demonstrated that upregulation CDK9 significantly shortened the survival of patients with stage II-IV colon cancer. Additionally, CDK9 mRNA expression was positively correlated with the expression levels of genes associated with immune evasion in the tumor. Notably, CDK9 was expression was upregulated in stage IV CRC compared with para-cancerous tissues and early-stage tumors. Interestingly, CDK9 expression was negatively associated with the infiltration of CD8(+) T cells at the tumor site. In addition, the expression levels of T-cell immunoglobulin mucin family member 3 and CD39, proteins associated with exhaustion, on tumor-infiltrating CD8(+) T cells were significantly elevated in patients with abnormal CDK9 expression levels. The present study demonstrated that CDK9 expression was negatively associated with CD8(+) T cell infiltration and positively associated with CD8(+) T cell exhaustion in MSS mCRC. In conclusion, CDK9 may be utilized to evaluate the prognosis and the immune-type of the tumor microenvironment in patients with MSS mCRC.
C1 [Wang, Jiefu; Liu, Jia; Tian, Fei; Zhan, Yang; Kong, Dalu] Tianjin Med Univ Canc Inst & Hosp, Natl Clin Res Ctr Canc, Tianjins Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy, Huan Hu Xi Rd, Tianjin 300060, Peoples R China.
C3 Tianjin Medical University
RP Zhan, Y; Kong, DL (corresponding author), Tianjin Med Univ Canc Inst & Hosp, Natl Clin Res Ctr Canc, Tianjins Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy, Huan Hu Xi Rd, Tianjin 300060, Peoples R China.
EM zhanyang@tmu.edu.cn; kongdalu@tjmuch.com
RI Zhan, yang/AAV-7123-2020
FU Science and Technology Development Fund of Tianjin Education Commission
   for Higher Education [2017KJ204]; Scientific Research Foundation of
   Tianjin Medical University Cancer Institute and Hospital [B1704]
FX The present study was supported by grants from The Science and
   Technology Development Fund of Tianjin Education Commission for Higher
   Education (grant no. 2017KJ204) and Scientific Research Foundation of
   Tianjin Medical University Cancer Institute and Hospital (grant no.
   B1704), awarded to YZ.
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NR 51
TC 13
Z9 14
U1 0
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD DEC
PY 2019
VL 18
IS 6
BP 6046
EP 6056
DI 10.3892/ol.2019.10970
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KA1RN
UT WOS:000505576300042
PM 31788079
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Eng, C
   Rogers, JE
AF Eng, Cathy
   Rogers, Jane E.
TI Current synthetic pharmacotherapy for treatment-resistant colorectal
   cancer: when urgent action is required
SO EXPERT OPINION ON PHARMACOTHERAPY
LA English
DT Review
DE Antineoplastic agents; colorectal neoplasms; immunotherapy; molecular
   targeted therapy
ID CONSENSUS MOLECULAR SUBTYPES; OPEN-LABEL; MICROSATELLITE INSTABILITY;
   TARGETED THERAPY; PLUS BEVACIZUMAB; SOLID TUMORS; SURVIVAL; COLON;
   NIVOLUMAB; IMMUNOTHERAPY
AB Introduction: Colorectal cancer (CRC) remains a global concern. Fourteen antineoplastics are approved for metastatic CRC (mCRC); however, the 5-year overall survival remains poor for the overwhelming majority of patients. Poor outcomes continue to highlight the critical need for therapeutic advancement. Areas covered: mCRC represents a clinical and molecular complex malignancy with several treatment barriers. Prognostic and predictive factors have and continue to emerge anatomically, molecularly, and via patient-related factors. Herein, the authors review the current understanding and promising future directions amongst these different subtypes. Expert opinion: CRC is largely considered a common cancer. Consequently, treatment approaches have been rather homogenous with systemic chemotherapy combinations. Of significance is the recent identification of targetable rare subsets of mCRC, notably for microsatellite instability-high (MSI-H) patients and for BRAF mutated patients. As a result, we are at the forefront of interpreting biological differences that provide targetable approaches and/or additional insight. To continue to do so, future clinical trial developments must focus on diverse subtypes of mCRC rather than all-encompassing mCRC proposals. Yet of greatest need is identifying options for RAS-mutated and microsatellite-stable mCRC patients. For the majority of these patients, we continue to seek novel innovative approaches to improve the overall survival of these patients.
C1 [Eng, Cathy; Rogers, Jane E.] Univ Texas MD Anderson Canc Ctr, Gastrointestinal Med Oncol Dept, 1515 Holcombe Blvd,Unit 0426, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center
RP Eng, C (corresponding author), Univ Texas MD Anderson Canc Ctr, Gastrointestinal Med Oncol Dept, 1515 Holcombe Blvd,Unit 0426, Houston, TX 77030 USA.
EM ceng@mdanderson.org
OI Rogers, Jane/0000-0002-7275-7008; Eng, Cathy/0000-0003-2335-0612
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   [No title captured]
   [No title captured]
NR 88
TC 2
Z9 2
U1 0
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1465-6566
EI 1744-7666
J9 EXPERT OPIN PHARMACO
JI Expert Opin. Pharmacother.
PD MAR 24
PY 2019
VL 20
IS 5
BP 523
EP 534
DI 10.1080/14656566.2018.1561866
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA HP6QL
UT WOS:000461810500006
PM 30590946
DA 2025-01-04
ER

PT J
AU Li, WM
   Hu, TT
   Zhou, LL
   Feng, YM
   Wang, YY
   Fang, J
AF Li, Wan-Ming
   Hu, Ting-Ting
   Zhou, Lin-Lin
   Feng, Yi-Ming
   Wang, Yun-Yi
   Fang, Jin
TI Highly sensitive detection of the <i>PIK3CA<SUP>H1047R</SUP></i>
   mutation in colorectal cancer using a novel PCR-RFLP method
SO BMC CANCER
LA English
DT Article
DE PIK3CA; Low abundance mutation; Colorectal cancer; PCR-RFLP; Targeted
   therapy
ID RESOLUTION MELTING ANALYSIS; MONOCLONAL-ANTIBODIES; CETUXIMAB THERAPY;
   PIK3CA; KRAS; BRAF; GROWTH; RESISTANCE; GENE; CHEMOTHERAPY
AB Background: The PIK3CA(H1047R) mutation is considered to be a potential predictive biomarker for EGFR-targeted therapies. In this study, we developed a novel PCR-PFLP approach to detect the PIK3CA(H1047R) mutation in high effectiveness.
   Methods: A 126-bp fragment of PIK3CA exon-20 was amplified by PCR, digested with FspI restriction endonuclease and separated by 3 % agarose gel electrophoresis for the PCR-RFLP analysis. The mutant sequence of the PIK3CA(H1047R) was spiked into the corresponding wild-type sequence in decreasing ratios for sensitivity analysis. Eight-six cases of formalin-fixed paraffin-embedded colorectal cancer (CRC) specimens were subjected to PCR-RFLP to evaluate the applicability of the method.
   Results: The PCR-RFLP method had a capability to detect as litter as 0.4 % of mutation, and revealed 16.3 % of the PIK3CA(H1047R) mutation in 86 CRC tissues, which was significantly higher than that discovered by DNA sequencing (9. 3 %). A positive association between the PIK3CA(H1047R) mutation and the patients' age was first found, except for the negative relationship with the degree of tumor differentiation. In addition, the highly sensitive detection of a combinatorial mutation of PIK3CA, KRAS and BRAF was achieved using individual PCR-RFLP methods.
   Conclusions: We developed a sensitive, simple and rapid approach to detect the low-abundance PIK3CA(H1047R) mutation in real CRC specimens, providing an effective tool for guiding cancer targeted therapy.
C1 [Fang, Jin] China Med Univ, Dept Cell Biol, Key Lab Cell Biol, Minist Publ Hlth,Shenyang North New Area, 77 Puhe Rd, Shenyang 110122, Liaoning Provin, Peoples R China.
   China Med Univ, Minist Educ, Key Lab Med Cell Biol, Shenyang North New Area, 77 Puhe Rd, Shenyang 110122, Liaoning Provin, Peoples R China.
C3 China Medical University; China Medical University
RP Fang, J (corresponding author), China Med Univ, Dept Cell Biol, Key Lab Cell Biol, Minist Publ Hlth,Shenyang North New Area, 77 Puhe Rd, Shenyang 110122, Liaoning Provin, Peoples R China.
EM jfang61@netease.com
RI tingting, hu/AGX-8728-2022; Feng, Yiming/KZV-0094-2024; Fang,
   Jin/HKF-5214-2023
FU National Natural Science Foundation of China [21375149]; Shenyang
   Science and Technology Bureau [F13-220-9-29]; Program for Innovative
   Research Team in University of Ministry of Education of China [IRT13101]
FX The study was supported by the grants from the National Natural Science
   Foundation of China (Grant No. 21375149), Shenyang Science and
   Technology Bureau (Grant No. F13-220-9-29) and Program for Innovative
   Research Team in University of Ministry of Education of China
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NR 44
TC 8
Z9 9
U1 3
U2 24
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD JUL 12
PY 2016
VL 16
AR 454
DI 10.1186/s12885-016-2493-9
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DR6MO
UT WOS:000380016200001
PM 27405731
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Liu, GC
   Lin, WL
   Zhang, KF
   Chen, KX
   Niu, GL
   Zhu, YH
   Liu, YX
   Li, PK
   Li, ZH
   An, Y
AF Liu, Guangchao
   Lin, Wenlong
   Zhang, Kaifeng
   Chen, Kangxu
   Niu, Guanglin
   Zhu, Yonghao
   Liu, Yixuan
   Li, Pengkun
   Li, Zhihao
   An, Yang
TI Elucidating the prognostic and therapeutic significance of TOP2A in
   various malignancies
SO CANCER GENETICS
LA English
DT Article
DE TOP2A; Prognosis; Targeted therapy; Chemotherapy
ID TOPOISOMERASE-II-ALPHA; CELL LUNG-CANCER; ANDROGEN-RECEPTOR GENE;
   EPITHELIAL-MESENCHYMAL TRANSITION; ANTHRACYCLINE-BASED CHEMOTHERAPY;
   PROTEIN-CODING GENES; DNA-DAMAGE RESPONSE; BREAST-CANCER;
   PROSTATE-CANCER; MULTIDRUG-RESISTANCE
AB Topoisomerase II alpha (TOP2A) is a crucial enzyme that plays a vital role in DNA replication and transcription mechanisms. Dysregulated expression of TOP2A has been associated with various malignancies, including hepatocellular carcinoma, prostate cancer, colon cancer, lung cancer and breast cancer. In this review, we summarized the prognostic relevances of TOP2A in various types of cancer. The increased expression of TOP2A has been linked to resistance to therapy and reduced survival rates. Therefore, evaluating TOP2A levels could assist in identifying patients who may derive advantages from molecular targeted therapy. The amplification of TOP2A has been linked to a positive response to chemotherapy regimens that contain anthracycline. Nevertheless, the overexpression of TOP2A also indicates a heightened likelihood of disease recurrence and unfavorable prognosis. The prognostic significance of TOP2A has been extensively studied in various types of cancer. The increased expression of TOP2A is associated with poor clinical outcomes, indicating its potential as a valuable biomarker for assessing risk and stratifying treatment in these malignancies. However, further investigation is needed to elucidate the underlying mechanisms by which TOP2A influences cancer progression and to explore its potential as a therapeutic target.
C1 [Liu, Guangchao; Lin, Wenlong; Zhang, Kaifeng; Chen, Kangxu; Niu, Guanglin; Zhu, Yonghao; Liu, Yixuan; Li, Pengkun; Li, Zhihao; An, Yang] Henan Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, Kaifeng 475004, Peoples R China.
   [Liu, Guangchao; Lin, Wenlong; Zhang, Kaifeng; Chen, Kangxu; Niu, Guanglin; Zhu, Yonghao] Henan Univ, Sch Stomatol, Kaifeng 475004, Peoples R China.
   [Liu, Yixuan; Li, Pengkun; Li, Zhihao; An, Yang] Henan Univ, Henan Prov Engn Ctr Tumor Mol Med, Kaifeng Key Lab Cell Signal transduct, Kaifeng 475004, Peoples R China.
C3 Henan University; Henan University; Henan University
RP An, Y (corresponding author), Henan Univ, Sch Basic Med Sci, Jinming St, Kaifeng 475004, Henan, Peoples R China.
EM anyang@henu.edu.cn
RI Li, Zhi-Hao/GVU-9321-2022; LIU, GUANGCHAO/F-2810-2011
FU Program for Science and Technology Development in Henan Province
   [212102310616]; Innovation Project for College Students of Henan
   University
FX This work was supported by the Program for Science and Technology
   Development in Henan Province (No.212102310616) ; the Innovation Project
   for College Students of Henan University (No.XJ2024125;
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NR 211
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 2210-7762
EI 2210-7770
J9 CANCER GENET-NY
JI Cancer Genet.
PD NOV
PY 2024
VL 288-289
BP 68
EP 81
DI 10.1016/j.cancergen.2024.10.005
EA OCT 2024
PG 14
WC Oncology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Genetics & Heredity
GA L5Q5K
UT WOS:001351264200001
PM 39454521
DA 2025-01-04
ER

PT J
AU Schöche, J
   Niedersüss-Beke, D
AF Schoeche, Johannes
   Niedersuess-Beke, Dora
TI Treatment decision based on molecular profiling in metastatic colorectal
   cancer with a focus on <i>RAS</i> pathway mutations
SO MEMO-MAGAZINE OF EUROPEAN MEDICAL ONCOLOGY
LA English
DT Review
DE KRAS; NeoRAS; KRAS G12C; Targeted therapy; Precision medicine
ID WILD-TYPE; PREDICTIVE-VALUE; EGFR BLOCKADE; CETUXIMAB; CHEMOTHERAPY;
   ANTIBODIES; RESISTANCE; EVOLUTION; BENEFIT; TARGET
AB Agents targeting vascular endothelial growth factor (VEGF) or epidermal growth factor receptor (EGFR) are part of systemic therapy in advanced colorectal cancer. It is well known that only certain molecular subpopulations profit from EGFR antibodies, restricting those therapeutics to a smaller fraction of patients. Recently investigated, the monitoring of temporally changing RAS mutational status by liquid biopsy might allow the application of EGFR antibodies to an additional subset of patients. In addition, KRAS G12C inhibitors combined with anti-EGFR antibodies are currently under investigation in clinical trials and could provide another effective therapy in case of KRAS G12C mutations. Beyond RAS, therapy guided by microsatellite instability (MSI) status, BRAF mutations, HER2 overexpression and NTRK fusions are welcome additions to targeted treatment in advanced colorectal cancer.
C1 [Schoeche, Johannes; Niedersuess-Beke, Dora] Klin Ottakring, Dept Oncol Hematol & Palliat Care, Montleartstr 37, A-1160 Vienna, Austria.
RP Schöche, J (corresponding author), Klin Ottakring, Dept Oncol Hematol & Palliat Care, Montleartstr 37, A-1160 Vienna, Austria.
EM johannes.schoeche@gesundheitsverbund.at;
   dora.niedersuess-beke@gesundheitsverbund.at
OI Schoche, Johannes/0000-0002-4740-5166
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NR 42
TC 1
Z9 1
U1 0
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 FEB
PY 2022
VL 15
IS 1
BP 39
EP 44
DI 10.1007/s12254-021-00787-1
EA JAN 2022
PG 6
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA ZB4NE
UT WOS:000742562900001
DA 2025-01-04
ER

PT J
AU Ruff, SM
   Brown, ZJ
   Pawlik, TM
AF Ruff, Samantha M.
   Brown, Zachary J.
   Pawlik, Timothy M.
TI A review of targeted therapy and immune checkpoint inhibitors for
   metastatic colorectal cancer
SO SURGICAL ONCOLOGY-OXFORD
LA English
DT Review
DE Targeted therapy; EGFR; Colorectal cancer; Metastases; VEGF;
   Immunotherapy
ID GROWTH-FACTOR RECEPTOR; CETUXIMAB PLUS IRINOTECAN; III RANDOMIZED-TRIAL;
   KRAS WILD-TYPE; OPEN-LABEL; PHASE-III; 1ST-LINE TREATMENT; DOUBLE-BLIND;
   COLON-CANCER; LIVER METASTASES
AB Surgical resection is the cornerstone of treatment for metastatic colorectal cancer (CRC) and offers the best chance at long-term survival. Unfortunately, most patients do not present with resectable metastatic disease and, among patients who do undergo curative-intent resection, many will develop recurrence. In turn, patients require a multi-disciplinary treatment approach with a combination of chemotherapy, surgery, radiation, and/or liver directed therapies that is guided by patient disease burden and clinical status. The development of targeted therapies has led to varying success in other cancers and has emerged as a treatment option for patients with metastatic CRC. While cytotoxic chemotherapy aims to kill cells as they replicate, targeted therapies are directed at biologic features of cancers, like angiogenesis or immune checkpoints. Targeted therapy can facilitate a more treatment tailored approach to the unique genomic alterations of the tumor and hopefully deliver more personalized therapy. We herein provide a systematic review of approved targeted therapies and immune checkpoint inhibitors for metastatic CRC and provide an overview of the current literature.
C1 [Ruff, Samantha M.; Pawlik, Timothy M.] Ohio State Univ, Wexner Med Ctr, Dept Surg, Div Surg Oncol, Columbus, OH 43210 USA.
   [Ruff, Samantha M.; Pawlik, Timothy M.] James Comprehens Canc Ctr, Columbus, OH 43210 USA.
   [Brown, Zachary J.] New York Univ Long Isl, Dept Surg, Div Surg Oncol, Mineola, NY USA.
   [Pawlik, Timothy M.] Ohio State Univ, Dept Surg, Urban Meyer III & Shelley Meyer Chair Canc Res, Wexner Med Ctr, 395 W 12th Ave,Suite 670, Columbus, OH 43210 USA.
C3 University System of Ohio; Ohio State University; University System of
   Ohio; Ohio State University; James Cancer Hospital & Solove Research
   Institute; University System of Ohio; Ohio State University
RP Pawlik, TM (corresponding author), Ohio State Univ, Dept Surg, Urban Meyer III & Shelley Meyer Chair Canc Res, Wexner Med Ctr, 395 W 12th Ave,Suite 670, Columbus, OH 43210 USA.
EM tim.pawlik@osumc.edu
RI Pawlik, Timothy/AAO-9335-2020
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NR 86
TC 3
Z9 3
U1 0
U2 7
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 DEC
PY 2023
VL 51
AR 101993
DI 10.1016/j.suronc.2023.101993
EA SEP 2023
PG 9
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA U0OJ4
UT WOS:001081883400001
PM 37742544
DA 2025-01-04
ER

PT J
AU Meng, MJ
   Zhong, KY
   Jiang, T
   Liu, ZQ
   Kwan, HY
   Su, T
AF Meng, Mingjing
   Zhong, Keying
   Jiang, Ting
   Liu, Zhongqiu
   Kwan, Hiu Yee
   Su, Tao
TI The current understanding on the impact of KRAS on colorectal cancer
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Colorectal cancer; KRAS; Mutation; Therapy
ID CONSENSUS MOLECULAR SUBTYPES; ANTI-EGFR THERAPY; MUTANT KRAS; K-RAS;
   ONCOGENIC KRAS; MICROSATELLITE INSTABILITY; 1ST-LINE TREATMENT; MUTATION
   ANALYSIS; LIVER METASTASES; POOR-PROGNOSIS
AB KRAS (kirsten rat sarcoma viral oncogene) is a member of the RAS family. KRAS mutations are one of most dominant mutations in colorectal cancer (CRC). The impact of KRAS mutations on the prognosis and survival of CRC patients drives many research studies to explore potential therapeutics or target therapy for the KRAS mutant CRC. This review summarizes the current understanding of the pathological consequences of the KRAS mutations in the development of CRC; and the impact of the mutations on the response and the sensitivity to the current front-line chemotherapy. The current therapeutic strategies for treating KRAS mutant CRC, the difficulties and challenges will also be discussed.
C1 [Meng, Mingjing; Zhong, Keying; Jiang, Ting; Liu, Zhongqiu; Su, Tao] Guangzhou Univ Chinese Med, Sch Pharmaceut Sci, Int Inst Translat Chinese Med,Minist Educ Peoples, Guangdong Key Lab Translat Canc Res Chinese Med,J, Guangzhou, Guangdong, Peoples R China.
   [Liu, Zhongqiu; Su, Tao] Guangzhou Univ Chinese Med, Guangdong Hong Kong Macau Joint Lab Chinese Med &, Guangzhou, Guangdong, Peoples R China.
   [Kwan, Hiu Yee] Hong Kong Baptist Univ, Ctr Canc & Inflammat Res, Sch Chinese Med, Hong Kong, Peoples R China.
C3 Guangzhou University of Chinese Medicine; Guangzhou University of
   Chinese Medicine; Hong Kong Baptist University
RP Liu, ZQ; Su, T (corresponding author), Guangzhou Univ Chinese Med, Guangzhou 510006, Guangdong, Peoples R China.; Kwan, HY (corresponding author), Hong Kong Baptist Univ, Kowloon Tong, 7 Baptist Univ Rd, Hong Kong, Peoples R China.
EM liuzq@gzucm.edu.cn; hykwan@hkbu.edu.hk; sutao@gzucm.edu.cn
RI Su, Tao/T-4411-2019; Liu, Zhongqiu/AHC-9661-2022
OI KWAN, Hiu Yee/0000-0002-6088-7323
FU National Natural Science Foundation of China [SCM2016-NSFC-003,
   82074019, 81703705, 81930114, 81720108033]; Characteristic Innovation
   Projects of Universities in Guangdong Province [2020KTSCX030]; Guangdong
   Key Laboratory for Translational Cancer research of Chinese Medicine
   [2018B030322011]; Guangdong-Hong Kong-Macau Joint Lab on Chinese
   Medicine and Immune Disease Research, Guangzhou University of Chinese
   Medicine [2020B1212030006]; Key-Area Research and Development Program of
   Guangdong Province [2020B1111100004]; State Commission of Science
   Technology of China [2017YFE0119900]; Research Grant Council of HKSAR
   [HKBU-22103017-ECS]; Innovation & Technology Commission [PRP/015/19FX]
FX This work was supported by the National Natural Science Foundation of
   China (82074019, 81703705, 81930114 and 81720108033), Characteristic
   Innovation Projects of Universities in Guangdong Province
   (2020KTSCX030), Guangdong Key Laboratory for Translational Cancer
   research of Chinese Medicine (2018B030322011), and Guangdong-Hong
   Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research,
   Guangzhou University of Chinese Medicine (2020B1212030006), Key-Area
   Research and Development Program of Guangdong Province
   (2020B1111100004), State Commission of Science Technology of China
   (2017YFE0119900), Research Grant Council of HKSAR (HKBU-22103017-ECS),
   Innovation & Technology Commission (PRP/015/19FX), National Natural
   Science Foundation of China (SCM-2016-NSFC-003) and Natural Science
   Foundation of Guangdong Province (2018A0303130122).
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NR 164
TC 70
Z9 72
U1 0
U2 49
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 AUG
PY 2021
VL 140
AR 111717
DI 10.1016/j.biopha.2021.111717
EA MAY 2021
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA TE6HN
UT WOS:000670111900003
PM 34044280
OA gold
DA 2025-01-04
ER

PT J
AU Kavuri, SM
   Jain, N
   Galimi, F
   Cottino, F
   Leto, SM
   Migliardi, G
   Searleman, AC
   Shen, W
   Monsey, J
   Trusolino, L
   Jacobs, SA
   Bertotti, A
   Bose, R
AF Kavuri, Shyam M.
   Jain, Naveen
   Galimi, Francesco
   Cottino, Francesca
   Leto, Simonetta M.
   Migliardi, Giorgia
   Searleman, Adam C.
   Shen, Wei
   Monsey, John
   Trusolino, Livio
   Jacobs, Samuel A.
   Bertotti, Andrea
   Bose, Ron
TI HER2 Activating Mutations Are Targets for Colorectal Cancer Treatment
SO CANCER DISCOVERY
LA English
DT Article
ID LUNG-CANCER; EGFR; RESISTANCE; COLON; TRASTUZUMAB; AMPLIFICATION;
   COMBINATION; THERAPIES; PLATFORM
AB The Cancer Genome Atlas project identified HER2 somatic mutations and gene amplification in 7% of patients with colorectal cancer. Introduction of the HER2 mutations S310F, L755S, V777L, V842I, and L866M into colon epithelial cells increased signaling pathways and anchorage-independent cell growth, indicating that they are activating mutations. Introduction of these HER2 activating mutations into colorectal cancer cell lines produced resistance to cetuximab and panitumumab by sustaining MAPK phosphorylation. HER2 mutants are potently inhibited by low nanomolar doses of the irreversible tyrosine kinase inhibitors neratinib and afatinib. HER2 gene sequencing of 48 cetuximab-resistant, quadruple (KRAS, NRAS, BRAF, and PIK3CA) wild-type (WT) colorectal cancer patient-derived xenografts (PDX) identified 4 PDXs with HER2 mutations. HER2-targeted therapies were tested on two PDXs. Treatment with a single HER2-targeted drug (trastuzumab, neratinib, or lapatinib) delayed tumor growth, but dual HER2-targeted therapy with trastuzumab plus tyrosine kinase inhibitors produced regression of these HER2-mutated PDXs.
   SIGNIFICANCE: HER2 activating mutations cause EGFR antibody resistance in colorectal cell lines, and PDXs with HER2 mutations show durable tumor regression when treated with dual HER2-targeted therapy. These data provide a strong preclinical rationale for clinical trials targeting HER2 activating mutations in metastatic colorectal cancer. (C) 2015 AACR.
C1 [Kavuri, Shyam M.; Jain, Naveen; Searleman, Adam C.; Shen, Wei; Monsey, John; Bose, Ron] Washington Univ, Sch Med, Div Oncol, Dept Med, St Louis, MO 63110 USA.
   [Galimi, Francesco; Leto, Simonetta M.; Migliardi, Giorgia; Trusolino, Livio; Bertotti, Andrea] Univ Turin, Sch Med, Dept Oncol, Turin, Italy.
   [Galimi, Francesco; Cottino, Francesca; Leto, Simonetta M.; Migliardi, Giorgia; Trusolino, Livio; Bertotti, Andrea] Candiolo Canc Inst FPO IRCCS, Translat Canc Med, I-10060 Turin, Italy.
   [Jacobs, Samuel A.] NSABP Fdn, Pittsburgh, PA USA.
   [Bertotti, Andrea] Natl Inst Biostruct & Biosyst, Rome, Italy.
   [Bose, Ron] Washington Univ, Alvin J Siteman Canc Ctr, Sch Med, St Louis, MO 63110 USA.
C3 Washington University (WUSTL); University of Turin; IRCCS Fondazione del
   Piemonte per l'Oncologia; Pennsylvania Commonwealth System of Higher
   Education (PCSHE); University of Pittsburgh; National Surgical Adjuvant
   Breast & Bowel Project; Siteman Cancer Center; Washington University
   (WUSTL)
RP Bose, R (corresponding author), Washington Univ, Sch Med, 660 S Euclid Ave,Campus Box 8069, St Louis, MO 63110 USA.
EM andrea.bertotti@ircc.it; rbose@dom.wustl.edu
RI Migliardi, Giorgia/AAB-6619-2020; Trusolino, Livio/A-3896-2011
OI Migliardi, Giorgia/0000-0001-5770-8120; Trusolino,
   Livio/0000-0002-6379-3365; Cottino, Francesca/0000-0001-6715-1784; Jain,
   Naveen/0000-0001-9681-6618; Leto, Simonetta Maria/0000-0001-7580-6584;
   Bertotti, Andrea/0000-0001-8196-7608; GALIMI,
   Francesco/0000-0002-5939-6922; Searleman, Adam/0000-0003-1084-2415
FU NIH [R01CA161001]; Ohana Breast Cancer Research Fund; Foundation for
   Barnes-Jewish Hospital; Fight Colorectal Cancer-AACR Career Development
   Award; Associazione Italiana per la Ricerca sul Cancro (AIRC) [9970];
   AIRC [14205, 15571]; Fondazione Piemontese per la Ricerca sul
   Cancro-ONLUS; Ministero della Salute
FX This work was supported by the NIH (R01CA161001, to R. Bose); the Ohana
   Breast Cancer Research Fund and the Foundation for Barnes-Jewish
   Hospital (to R. Bose); the Fight Colorectal Cancer-AACR Career
   Development Award (to A. Bertotti); the Associazione Italiana per la
   Ricerca sul Cancro (AIRC) 2010 Special Program Molecular Clinical
   Oncology 5x1000, project 9970 (to L. Trusolino); AIRC Investigator
   Grants, project 14205 (to L. Trusolino); AIRC Investigator Grants,
   project 15571 (to A. Bertotti); and Fondazione Piemontese per la Ricerca
   sul Cancro-ONLUS, 5x1000 Ministero della Salute 2011 (to L. Trusolino).
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NR 34
TC 229
Z9 245
U1 0
U2 29
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 AUG
PY 2015
VL 5
IS 8
BP 832
EP 841
DI 10.1158/2159-8290.CD-14-1211
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CO7DF
UT WOS:000359317700016
PM 26243863
OA Green Submitted, Bronze, Green Accepted
DA 2025-01-04
ER

PT J
AU Zhang, C
   Liu, XY
   Jin, SD
   Chen, Y
   Guo, RH
AF Zhang, Chen
   Liu, Xinyin
   Jin, Shidai
   Chen, Yi
   Guo, Renhua
TI Ferroptosis in cancer therapy: a novel approach to reversing drug
   resistance
SO MOLECULAR CANCER
LA English
DT Review
DE Ferroptosis; Chemotherapy; Targeted therapy; Immunotherapy; Drug
   resistance
ID CELL-DEATH; COLORECTAL-CANCER; IRON; METABOLISM; IMMUNOTHERAPY;
   PEROXIDATION; DEGRADATION; MACROPHAGES; SENSITIVITY; MECHANISMS
AB Ferroptosis is an intracellular iron-dependent form of cell death that is distinct from apoptosis, necrosis, and autophagy. Extensive studies suggest that ferroptosis plays a pivotal role in tumor suppression, thus providing new opportunities for cancer therapy. The development of resistance to cancer therapy remains a major challenge. A number of preclinical and clinical studies have focused on overcoming drug resistance. Intriguingly, ferroptosis has been correlated with cancer therapy resistance, and inducing ferroptosis has been demonstrated to reverse drug resistance. Herein, we provide a detailed description of the mechanisms of ferroptosis and the therapeutic role of regulating ferroptosis in reversing the resistance of cancer to common therapies, such as chemotherapy, targeted therapy and immunotherapy. We discuss the prospect and challenge of regulating ferroptosis as a therapeutic strategy for reversing cancer therapy resistance and expect that our review could provide some references for further studies.
C1 [Zhang, Chen; Liu, Xinyin; Jin, Shidai; Chen, Yi; Guo, Renhua] Jiangsu Prov Hosp, 300 Guangzhou Rd, Nanjing, Jiangsu, Peoples R China.
   [Zhang, Chen; Liu, Xinyin; Jin, Shidai; Chen, Yi; Guo, Renhua] Nanjing Med Univ, Affiliated Hosp 1, 300 Guangzhou Rd, Nanjing, Jiangsu, Peoples R China.
   [Chen, Yi] Nanjing Pukou Cent Hosp, Hosp Jiangsu Prov Hosp, Pukou Branch, Nanjing, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University
RP Guo, RH (corresponding author), Jiangsu Prov Hosp, 300 Guangzhou Rd, Nanjing, Jiangsu, Peoples R China.; Guo, RH (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, 300 Guangzhou Rd, Nanjing, Jiangsu, Peoples R China.
EM rhguo@njmu.edu.cn
OI Guo, Renhua/0000-0003-4475-8617
FU National Natural Science Foundation of China [81972188]
FX This research was supported by the National Natural Science Foundation
   of China (No. 81972188).
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NR 66
TC 607
Z9 625
U1 44
U2 402
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD FEB 12
PY 2022
VL 21
IS 1
AR 47
DI 10.1186/s12943-022-01530-y
PG 12
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA YX8RD
UT WOS:000754362400001
PM 35151318
OA Green Published, gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Salim, EI
   Mahfouz, ME
   Kang, JS
   Hegazi, MM
   Helmy, HM
   Eltonouby, EA
AF Salim, Elsayed, I
   Mahfouz, Magdy E.
   Kang, Jin Seok
   Hegazi, Mona M.
   Helmy, Hager M.
   Eltonouby, Eman A.
TI Celecoxib Targeted Therapy Attenuates Mouse Colon Carcinogenesis through
   Modulation of Expression Patterns of Cancer Stem Cells
SO JOURNAL OF ENVIRONMENTAL PATHOLOGY TOXICOLOGY AND ONCOLOGY
LA English
DT Article
DE colorectal cancer; mice; cancer stem cells markers; targeted therapy
ID HUMAN HEMATOPOIETIC STEM; ALDEHYDE DEHYDROGENASE; SIGNALING PATHWAY;
   FLOW-CYTOMETRY; MARKER; LIVER; DNA; INHIBITION; CD133
AB This study was designated to explore the role of cancer stem cells (CSCs) during chemically induced mouse colon carcinogenesis (by 1,2- dimethylhydrazine dihydrochloride, DMH) with/or without the treatment with a targeted (anti-COX-2) therapeutic drug, celecoxib. Two experiments were conducted. The first, a short-term, 16-week mouse colon carcinogenesis bioassay, demonstrates the early stages of colon carcinogenesis. The other is a medium-teen, 32-week mouse colon cancer experiment that mimics an end point of colon malignancy. Colon tumors were detected in animals after 32 weeks; histopathologically, they varied from benign hyperplastic polyps and adenomas to dysplastic polyps, adenocarcinomas, and invasive carcinomas. The overall colon tumor incidences, multiplicities, and volumes were obviously reduced when treated with celecoxib after DMH initiation. The immunohistochemical (IHC) labeling indexes (L1%) of the proliferating cell nuclear antigen (PCNA) were lower in the colonic epithelium in both experiments after treatment with celecoxib. Also, the IHC expression patterns of CD133 and CD44, known to associate CSCs, showed differential changes depending on the end-point stage of carcinogenesis and celecoxib treatment. Moreover, the biochemical aldehyde dehydrogenase-1 (ALDH-1) activity levels, a known CSC marker in colonic epithelia, were downregulated after 16 weeks but were upregulated after 32 weeks. Flow cytometric analysis showed that numbers of CD133 cells increased in the colonic epithelia of mice after 16 weeks, while the numbers of CD44 but not CD133 cells increased after 32 weeks. Treatment with celecoxib after DMH induced significant increase in apoptotic cell numbers by 47% after 16 weeks, but these numbers had not changed after 32 weeks compared with the corresponding group treated DMH only. Thus, the specific markers and CSC populations targeted by this drug may vary depending on the genetic and phenotypic stages of carcinogenesis. This drug could be useful during targeted therapy for colon cancer patients.
C1 [Salim, Elsayed, I; Hegazi, Mona M.; Helmy, Hager M.; Eltonouby, Eman A.] Tanta Univ, Fac Sci, Zool Dept, Res Lab Mol Carcinogenesis, Tanta 31527, Egypt.
   [Mahfouz, Magdy E.] Kafrelsheikh Univ, Fac Sci, Dept Zool, Kafrelsheikh, Egypt.
   [Kang, Jin Seok] Namseoul Univ, Dept Biomed Lab Sci, Seoul, South Korea.
C3 Egyptian Knowledge Bank (EKB); Tanta University; Egyptian Knowledge Bank
   (EKB); Kafrelsheikh University; Namseoul University
RP Salim, EI (corresponding author), Tanta Univ, Fac Sci, Zool Dept, Res Lab Mol Carcinogenesis, Tanta 31527, Egypt.
EM elsayed.salim@science.tanta.edu.eg
RI Eltonouby, Eman/JUF-6382-2023
FU Egyptian Science and Technology Development Fund for basic and applied
   research (STDF) [7974]
FX This work was supported by a grant in aid by the Egyptian Science and
   Technology Development Fund for basic and applied research (STDF;
   project ID 7974). The authors wish to thank those responsible of the
   animal facility of the Zoology Department, Faculty of Science and the
   staff members of the Central Laboratory of Tanta University for their
   sincere technical assistance.
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Z9 6
U1 0
U2 7
PU BEGELL HOUSE INC
PI DANBURY
PA 50 NORTH ST, DANBURY, CT 06810 USA
SN 0731-8898
EI 2162-6537
J9 J ENVIRON PATHOL TOX
JI J. Environ. Pathol. Toxicol. Oncol.
PY 2019
VL 38
IS 4
BP 329
EP 343
DI 10.1615/JEnvironPatholToxicolOncol.2019030130
PG 15
WC Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Toxicology
GA KK7JF
UT WOS:000512914200003
PM 32464004
DA 2025-01-04
ER

PT J
AU Fleitas, T
   Ibarrola-Villava, M
   Ribas, G
   Cervantes, A
AF Fleitas, Tania
   Ibarrola-Villava, Maider
   Ribas, Gloria
   Cervantes, Andres
TI MassARRAY determination of somatic oncogenic mutations in solid tumors:
   Moving forward to personalized medicine
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE MassARRAY technology; OncoCarta panel v1.0; Somatic mutation profile;
   Solid tumors
ID CELL LUNG-CANCER; MASS-SPECTROMETRY; BREAST-CANCER; TARGETED THERAPY;
   NASOPHARYNGEAL CARCINOMA; GENOMIC CHARACTERIZATION; COLORECTAL-CANCER;
   GENE-MUTATIONS; BRAF MUTATIONS; OVARIAN-CANCER
AB This article will review the impact of the recently developed MassARRAY technology on our understanding of cancer biology and treatment. Analysis of somatic mutations is a useful tool in selecting personalized therapy, and for predicting the outcome of many solid tumors. Here, we review the literature on the application of MassARRAY technology (Sequenom Hamburg, Germany) to determine the mutation profile of solid tumors from patients. We summarize the use of commercially available panels of mutations - such as OncoCarta (TM) or other combinations - and their concordance with results obtained by using other technologies, such as next generation sequencing. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Fleitas, Tania; Ibarrola-Villava, Maider; Ribas, Gloria; Cervantes, Andres] Univ Valencia, Dept Hematol & Med Oncol, Biomed Res Inst INCLIVA, Av Blasco Ibafiez 17, Valencia 46010, Spain.
C3 University of Valencia
RP Ribas, G; Cervantes, A (corresponding author), Univ Valencia, Dept Hematol & Med Oncol, Biomed Res Inst INCLIVA, Av Blasco Ibafiez 17, Valencia 46010, Spain.
EM gribas@incliva.es; andres.cervantes@uv.es
RI Ribas-Despuig, Gloria/M-6190-2017; Ribas, Gloria/K-3379-2013; Cervantes,
   Andres/J-8713-2013
OI Ribas, Gloria/0000-0001-6883-4130; Cervantes,
   Andres/0000-0003-3806-3691; Fleitas-Kanonnikoff,
   Tania/0000-0002-2789-9082; Ibarrola-Villava, Maider/0000-0003-0946-8075;
   Bowcock, Anne/0000-0001-8691-9090
FU Spanish government Ministerio de Salud Carlos III [PI15/2180,
   PI13/00606]; Generalitat Valenciana Prometeo [Prometeo/2013/005]; Fondos
   FEDER; Ministerio de Salud Carlos III under a Rio Hortega contract
   [CM13/00193]; Ministerio de Salud Carlos III under a Sara Borrell
   contract [CD15/00153]; Ministerio de Salud Carlos III under a Miguel
   Servet II contract [CPII14-00013]
FX This work was supported in part by grants from the Spanish government
   Ministerio de Salud Carlos III [PI15/2180; PI13/00606]; the Generalitat
   Valenciana Prometeo [Prometeo/2013/005]; and Fondos FEDER. TF was funded
   by the Ministerio de Salud Carlos III under a Rio Hortega contract
   [CM13/00193]. MI-V is funded by the Ministerio de Salud Carlos III under
   a Sara Borrell contract [CD15/00153]. GR is funded by the Ministerio de
   Salud Carlos III under a Miguel Servet II contract [CPII14-00013].
CR [Anonymous], CANCER
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NR 93
TC 13
Z9 16
U1 2
U2 23
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0305-7372
EI 1532-1967
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD SEP
PY 2016
VL 49
BP 57
EP 64
DI 10.1016/j.ctrv.2016.07.007
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DV5YH
UT WOS:000383006100006
PM 27501018
DA 2025-01-04
ER

PT J
AU Clune, S
   Awolade, P
   Zhou, Q
   Esquer, H
   Matter, B
   Kearns, JT
   Kellett, T
   Akintayo, DC
   Kompella, UB
   LaBarbera, DV
AF Clune, Sophia
   Awolade, Paul
   Zhou, Qiong
   Esquer, Hector
   Matter, Brock
   Kearns, Jeffrey T.
   Kellett, Timothy
   Akintayo, Damilola Caleb
   Kompella, Uday B.
   V. LaBarbera, Daniel
TI The validation of new CHD1L inhibitors as a therapeutic strategy for
   cancer
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Cancer; CHD1L; CHD1Li; EMT; Hit to lead; Molecular modeling; Targeted
   therapy
ID DRUG DISCOVERY; HEPATOCELLULAR-CARCINOMA; PROGRESSION; METASTASIS;
   METABOLISM
AB Chromodomain helicase DNA-binding protein 1 like (CHD1L) is an oncogene that promotes tumor progression, metastasis, and multidrug resistance. CHD1L expression is indicative of poor outcomes and low survival in cancer patients with various cancer types. Herein, we report a set of CHD1L inhibitors (CHD1Li) discovered from highthroughput screening and evaluated using enzyme inhibition, 3D tumor organoid cytotoxicity and mechanistic assays. The structurally distinct compounds 8-11 emerged as hits with promising bioactivity by targeting CHD1L. CHD1Li were further examined for their stability in human and mouse liver microsomes, which showed compounds 9 and 11 to be the most metabolically stable. Additionally, molecular modeling studies of CHD1Li with the target protein shed light on key pharmacophore features driving CHD1L binding. Taken together, these results expand the chemical space of CHD1Li as a potential targeted therapy for colorectal cancer and other cancers.
C1 [Clune, Sophia; Awolade, Paul; Zhou, Qiong; Esquer, Hector; Matter, Brock; Kearns, Jeffrey T.; Kellett, Timothy; Akintayo, Damilola Caleb; Kompella, Uday B.; V. LaBarbera, Daniel] Univ Colorado CU, Skaggs Sch Pharm & Pharmaceut Sci, Dept Pharmaceut Sci, Anschutz Med Campus, Aurora, CO 80045 USA.
   [Awolade, Paul; Zhou, Qiong; Esquer, Hector; Kompella, Uday B.; V. LaBarbera, Daniel] CU Anschutz Ctr Drug Discovery, Aurora, CO USA.
   [Zhou, Qiong; Esquer, Hector; Kompella, Uday B.; V. LaBarbera, Daniel] CU Canc Ctr, Aurora, CO USA.
   [V. LaBarbera, Daniel] 12850 E Montview Blvd,Room V20-2101, Aurora, CO 80045 USA.
C3 University of Colorado System; University of Colorado Anschutz Medical
   Campus
RP LaBarbera, DV (corresponding author), 12850 E Montview Blvd,Room V20-2101, Aurora, CO 80045 USA.
EM daniel.labarbera@cuanschutz.edu
RI AKINTAYO, DAMILOLA CALEB/IYT-2243-2023; Awolade, Paul/GQY-9472-2022
OI LaBarbera, Daniel/0000-0001-9460-3862; Matter,
   Brock/0000-0002-6339-3820; Awolade, Paul/0000-0003-3995-121X; Esquer,
   Hector/0000-0002-1911-1523; Zhou, Qiong/0000-0002-8240-0440; Clune,
   Sophia/0009-0007-2734-972X; Kearns, Jeffrey/0009-0005-5691-5095
FU NIH NCI [R01-CA251361]
FX <B>Funding</B> This research was supported by a grant from the NIH NCI
   awarded to D.V.L. (R01-CA251361) .
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NR 45
TC 0
Z9 0
U1 3
U2 3
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 116037
DI 10.1016/j.biopha.2023.116037
EA DEC 2023
PG 11
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA FQ2G3
UT WOS:001147243400001
PM 38128184
OA gold, Green Accepted
DA 2025-01-04
ER

PT J
AU Kumar, R
   Harilal, S
   Carradori, S
   Mathew, B
AF Kumar, Rajesh
   Harilal, Seetha
   Carradori, Simone
   Mathew, Bijo
TI A Comprehensive Overview of Colon Cancer- A Grim Reaper of the 21st
   Century
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Colorectal cancer; targeted therapy; natural compounds; microbiota;
   multitherapies; morbidity from CRC
ID FACTOR-KAPPA-B; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; ENTEROPATHOGENIC
   ESCHERICHIA-COLI; CONSENSUS MOLECULAR SUBTYPES; GRAPE SEED
   PROANTHOCYANIDINS; CELL-CYCLE ARREST; COLORECTAL-CANCER; IN-VITRO;
   MICROSATELLITE INSTABILITY; ULCERATIVE-COLITIS
AB A few decades ago, the incidence of colorectal cancer (CRC) was low and is now the fourth in the list of deadly cancers producing nearly a million deaths annually. A population that is aging along with risk factors such as smoking, obesity, sedentary lifestyle with little or no physical activity, and non-healthy food habits of developed countries can increase the risk of colorectal cancer. The balance in gut microbiota and the metabolites produced during bacterial fermentation within the host plays a significant role in regulating intestinal diseases as well as colorectal cancer development. Recent progress in the understanding of illness resulted in multiple treatment options such as surgery, radiation, and chemotherapy, including targeted therapy and multitherapies. The treatment plan for CRC depends on the location, stage and grade of cancer as well as genomic biomarker tests. Despite all the advancements made in the genetic and molecular aspects of the disease, the knowledge seems inadequate as the drug action as well as the wide variation in drug response did not appear strongly correlated with the individual molecular and genetic characteristics, which suggests the requirement of comprehensive molecular understanding of this complex heterogeneous disease. Furthermore, multitherapies or a broad spectrum approach, which is an amalgamation of the various promising as well as effective therapeutic strategies that can tackle heterogeneity and act on several targets of the disease, need to be validated in clinical studies. The latest treatment options have significantly increased the survival of up to three years in the case of advanced disease. The fact that colorectal cancer is developed from a polypoid precursor, as well as the symptoms of the disease that occur at an advanced stage, underlines how screening programs can help early detection and decrease mortality as well as morbidity from CRC.
C1 [Kumar, Rajesh; Harilal, Seetha] Kerala Univ Hlth Sci, Dept Pharm, Trichur, Kerala, India.
   [Carradori, Simone] G dAnnunzio Univ Chieti Pescara, Dept Pharm, Via Vestini 31, I-66100 Chieti, Italy.
   [Mathew, Bijo] Amrita Vishwa Vidyapeetham, Dept Pharmaceut Chem, Amrita Sch Pharm, AIMS Hlth Sci Campus, Kochi 682041, Kerala, India.
C3 G d'Annunzio University of Chieti-Pescara; Amrita Vishwa Vidyapeetham;
   Amrita Vishwa Vidyapeetham Kochi
RP Carradori, S (corresponding author), G dAnnunzio Univ Chieti Pescara, Dept Pharm, Via Vestini 31, I-66100 Chieti, Italy.; Mathew, B (corresponding author), Amrita Vishwa Vidyapeetham, Dept Pharmaceut Chem, Amrita Sch Pharm, AIMS Hlth Sci Campus, Kochi 682041, Kerala, India.
EM simone.carradori@unich.it; bijomathew@aims.amrita.edu
RI Kumar, Rajesh/AAC-9303-2020; Harilal, Seetha/AAC-8619-2020; Carradori,
   Simone/S-4776-2019
OI K, Rajesh/0000-0002-8712-4705; Harilal, Seetha/0000-0002-8141-8649;
   mathew, bijo/0000-0002-6658-4497; Carradori, Simone/0000-0002-8698-9440
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NR 287
TC 24
Z9 26
U1 0
U2 21
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PY 2021
VL 28
IS 14
BP 2657
EP 2696
DI 10.2174/0929867327666201026143757
PG 40
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA TI4BW
UT WOS:000672743100001
PM 33106132
DA 2025-01-04
ER

PT J
AU Advani, S
   Kopetz, S
AF Advani, Shailesh
   Kopetz, Scott
TI Ongoing and future directions in the management of metastatic colorectal
   cancer: Update on clinical trials
SO JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Article
DE clinical trials; colorectal cancer; immunotherapy; metastatic; targeted
   therapy
ID 1ST-LINE TREATMENT; KINASE INHIBITORS; DOUBLE-BLIND; OPEN-LABEL;
   FLUOROURACIL; MULTICENTER; OXALIPLATIN; IRINOTECAN; FOLFIRI;
   HETEROGENEITY
AB Metastatic colorectal cancer (mCRC) continues to show poor outcomes, with many patients exhausting effective standard-of-care therapy. To explore the current landscape of clinical trials for mCRC, we reviewed over 600 clinical trials that are currently ongoing for mCRC patients. Immunotherapeutic agents form approximately 39% (includes monoclonal antibodies, viruses, vaccines, and immunomodulators) of all agents and targeted therapy forms 45% (tyrosine kinase inhibitors, epigenetic modulators, and others) of all agents being investigated for mCRC.
C1 [Advani, Shailesh] NHGRI, Social Behav Res Branch, NIH, Bethesda, MD 20892 USA.
   [Advani, Shailesh; Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, 1515 Holcombe Blvd,Unit 0426, Houston, TX 77030 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Human Genome
   Research Institute (NHGRI); University of Texas System; UTMD Anderson
   Cancer Center
RP Kopetz, S (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, 1515 Holcombe Blvd,Unit 0426, Houston, TX 77030 USA.
EM skopetz@mdanderson.org
RI Kopetz, Scott/AAC-1387-2019; Advani, Shailesh/AAA-2812-2020
OI Kopetz, Scott/0000-0001-9647-3416
CR [Anonymous], NAT CANC I DRUG DICT
   [Anonymous], COLLECTED STUDIES IM
   [Anonymous], Drug Dictionary
   [Anonymous], MON ANT APPR EMA FDA
   [Anonymous], CANC IMMUNOTHERAPY A
   [Anonymous], OPEN J GASTROENTEROL
   [Anonymous], VACC TREAT CANC
   [Anonymous], CLIN TRIALS INF
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NR 48
TC 28
Z9 29
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-4790
EI 1096-9098
J9 J SURG ONCOL
JI J. Surg. Oncol.
PD APR
PY 2019
VL 119
IS 5
SI SI
BP 642
EP 652
DI 10.1002/jso.25441
PG 11
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA HP7SE
UT WOS:000461888500012
PM 30852840
DA 2025-01-04
ER

PT J
AU Ahamed, SBB
   Ibrahim, FB
   Srinivasan, H
AF Ahamed, Shameera Begum Basheer
   Ibrahim, Faridha Begum
   Srinivasan, Hemalatha
TI Cancer nanomedicine: A review on approaches and applications towards
   targeted drug delivery
SO INTERNATIONAL JOURNAL OF NANO DIMENSION
LA English
DT Review
DE Antitumor Activity; Cancer; Drug Delivery; Nanomedicine; Targeted
   Therapy
ID LIGHT-RESPONSIVE NANOPARTICLES; BREAST-CANCER; FUNCTIONALIZED
   NANOPARTICLES; POLYMERIC NANOPARTICLES; PHOTOTHERMAL THERAPY; GOLD
   NANOPARTICLES; MESOPOROUS SILICA; INDOCYANINE GREEN; RECENT PROGRESS;
   COLON-CANCER
AB Cancer prevails to be one of the main reasons of death across the globe. A large group of drugs and other therapies exist in the market for cancer treatment, yet, these conventional therapies have huge drawbacks such as low-specificity, off-target toxicity, and multidrug resistance that impact the standard of living of the patients. The concept of nanomedicine for targeted cancer therapy was able to overcome these problems, enhance the antitumor activity, and reduce systemic toxicity. Nanomedicine aims at utilizing properties of materials in the range of 1 to 100 nm for the treatment of diseases. Nanomedicine can achieve targeted therapy owing to the uncommon properties of nanoparticles and cancer itself. Cancer nanomedicine is used not only for treatment but its potential can also be expanded for early cancer diagnosis and tumor imaging. Many nanomedicines are currently in various phases of clinical trials and a few have already been authorized by the Food and Drug Administration for clinical use. This review highlights different approaches to targeted delivery of drugs and summarizes the utilization of various nanoparticles in targeted drug delivery, combination therapy, diagnosis, and imaging. Finally, this review also discusses the challenges that need to be overcome and provides an insight into future perspectives in the area of cancer nanomedicine.
C1 [Ahamed, Shameera Begum Basheer; Ibrahim, Faridha Begum; Srinivasan, Hemalatha] BS Abdur Rahman Crescent Inst Sci & Technol, Sch Life Sci, Chennai 48, Tamil Nadu, India.
C3 B. S. Abdur Rahman Crescent Institute of Science & Technology
RP Srinivasan, H (corresponding author), BS Abdur Rahman Crescent Inst Sci & Technol, Sch Life Sci, Chennai 48, Tamil Nadu, India.
EM hemalatha.sls@crescent.education
RI Hemalatha, S/AAF-3638-2021
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NR 143
TC 3
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U1 1
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PU ISLAMIC AZAD UNIV, TONEKABON BRANCH
PI TONEKABON
PA DEPT FISHERIES SCIENCES & MARINE BIOLOGY, VALI ABAD, TONEKABON, IRAN
SN 2008-8868
EI 2228-5059
J9 INT J NANO DIMENS
JI Int. J. Nano Dimens.
PD FAL
PY 2021
VL 12
IS 4
BP 310
EP 327
PG 18
WC Nanoscience & Nanotechnology
WE Emerging Sources Citation Index (ESCI)
SC Science & Technology - Other Topics
GA UC0DI
UT WOS:000686205700001
DA 2025-01-04
ER

PT J
AU Picco, G
   Cattaneo, CM
   van Vliet, EJ
   Crisafulli, G
   Rospo, G
   Consonni, S
   Vieira, SF
   Rodríguez, IS
   Cancelliere, C
   Banerjee, R
   Schipper, LJ
   Oddo, D
   Dijkstra, KK
   Cinatl, J
   Michaelis, M
   Yang, FT
   Di Nicolantonio, F
   Sartore-Bianchi, A
   Siena, S
   Arena, S
   Voest, EE
   Bardelli, A
   Garnett, MJ
AF Picco, Gabriele
   Cattaneo, Chiara M.
   van Vliet, Esmee J.
   Crisafulli, Giovanni
   Rospo, Giuseppe
   Consonni, Sarah
   Vieira, Sara F.
   Rodriguez, Inigo Sanchez
   Cancelliere, Carlotta
   Banerjee, Ruby
   Schipper, Luuk J.
   Oddo, Daniele
   Dijkstra, Krijn K.
   Cinatl, Jindrich
   Michaelis, Martin
   Yang, Fengtang
   Di Nicolantonio, Federica
   Sartore-Bianchi, Andrea
   Siena, Salvatore
   Arena, Sabrina
   Voest, Emile E.
   Bardelli, Alberto
   Garnett, Mathew J.
CA Cell Model Network UK Grp
TI Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch
   RepairDeficient Colorectal Cancer Refractory to Targeted Therapies,
   Chemotherapy, and Immunotherapy
SO CANCER DISCOVERY
LA English
DT Article
ID ANTI-EGFR THERAPY; ACQUIRED-RESISTANCE; DRUG-SENSITIVITY;
   SMALL-MOLECULE; COLON-CANCER; DNA-DAMAGE; REPAIR; INHIBITION; BLOCKADE;
   TUMORS
AB Targeted therapies, chemotherapy, and immunotherapy are used to treat patients with mismatch repair-deficient (dMMR)/microsatellite instability-high (MSI-H) colorectal cancer. The clinical effectiveness of targeted therapy and chemotherapy is limited by resistance and drug toxicities, and about half of patients receiving immunotherapy have disease that is refractory to immune checkpoint inhibitors. Loss of Werner syndrome ATP-dependent helicase (WRN) is a synthetic lethality in dMMR/MSI-H cells. To inform the development of WRN as a therapeutic target, we performed WRN knockout or knockdown in 60 heterogeneous dMMR colorectal cancer preclinical models, demonstrating that WRN dependency is an almost universal feature and a robust marker for patient selection. Furthermore, models of resistance to clinically relevant targeted therapy, chemotherapy, and immunotherapy retain WRN dependency. These data show the potential of therapeutically targeting WRN in patients with dMMR/MSI-H colorectal cancer and support WRN as a therapeutic option for patients with dMMR/MSI-H cancers refractory to current treatment strategies.
   SIGNIFICANCE: We found that a large, diverse set of dMMR/MSI-H colorectal cancer preclinical models, including models of treatment-refractory disease, are WRN-dependent. Our results support WRN as a promising synthetic-lethal target in dMMR/MSI-H colorectal cancer tumors as a monotherapy or in combination with targeted agents, chemotherapy, or immunotherapy.
C1 [Picco, Gabriele; van Vliet, Esmee J.; Consonni, Sarah; Vieira, Sara F.; Banerjee, Ruby; Yang, Fengtang; Garnett, Mathew J.; Cell Model Network UK Grp] Wellcome Sanger Inst, Cambridge CB10 1SA, England.
   [Cattaneo, Chiara M.; Rodriguez, Inigo Sanchez; Schipper, Luuk J.; Dijkstra, Krijn K.; Voest, Emile E.] Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Dept Mol Oncol & Immunol, Amsterdam, Netherlands.
   [Cattaneo, Chiara M.; Rodriguez, Inigo Sanchez; Schipper, Luuk J.; Dijkstra, Krijn K.; Voest, Emile E.] Oncode Inst, Amsterdam, Netherlands.
   [Crisafulli, Giovanni; Rospo, Giuseppe; Cancelliere, Carlotta; Oddo, Daniele; Di Nicolantonio, Federica; Arena, Sabrina; Bardelli, Alberto] FPO IRCCS, Candiolo Canc Inst, Candiolo, TO, Italy.
   [Crisafulli, Giovanni; Rospo, Giuseppe; Oddo, Daniele; Di Nicolantonio, Federica; Arena, Sabrina; Bardelli, Alberto] Univ Turin, Dept Oncol, Candiolo, Italy.
   [Cinatl, Jindrich] Goethe Univ, Inst Med Virol, Frankfurt, Germany.
   [Michaelis, Martin] Univ Kent, Sch Biosci, Canterbury, Kent, England.
   [Sartore-Bianchi, Andrea; Siena, Salvatore] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Sartore-Bianchi, Andrea; Siena, Salvatore] Univ Milano Statale La Statale, Dipartimento Oncol Ematooncol, Milan, Italy.
C3 Wellcome Trust Sanger Institute; Netherlands Cancer Institute; IRCCS
   Fondazione del Piemonte per l'Oncologia; University of Turin; Goethe
   University Frankfurt; University of Kent
RP Garnett, MJ (corresponding author), Wellcome Sanger Inst, Cambridge CB10 1SA, England.
EM mg12@sanger.ac.uk
RI Sánchez Rodríguez, Iñigo/CAA-1966-2022; Sartore-Bianchi,
   Andrea/AAB-9848-2019; Bardelli, Alberto/J-9721-2018; Di Nicolantonio,
   Federica/A-2503-2011; Cattaneo, Chiara/LSK-7127-2024; Rospo,
   Giuseppe/AAC-4523-2020; Siena, Salvatore/ACK-2413-2022; Arena,
   Sabrina/H-4985-2012; Michaelis, Alexander/R-9240-2016; Crisafulli,
   Giovanni/AAB-6256-2019; Yang, Fengtang/LLK-1406-2024
OI van Vliet, Esmee/0000-0002-9301-1598; Sartore-Bianchi,
   Andrea/0000-0003-0780-0409; Sanchez Rodriguez,
   Inigo/0000-0002-6440-0922; Vieira, Sara/0000-0002-1021-3021; Rospo,
   Giuseppe/0000-0002-1757-9085; Cattaneo, Chiara
   Maria/0000-0002-8168-8649; Schipper, Luuk/0000-0002-8825-0113; picco,
   gabriele/0000-0001-8568-2781; Crisafulli, Giovanni/0000-0002-5511-1555;
   Yang, Fengtang/0000-0002-3573-2354; ARENA, Sabrina/0000-0002-1318-2494
FU SU2C-DCS International Translational Cancer Research Dream Team Grant
   [SU2C-AACR-DT1213]; Wellcome Trust [206194]; FONDAZIONE AIRC [21091];
   AIRC under MFAG [20236]; H2020 grant [635342-2]; AIRC [21923, 17707,
   21407]; Therapy in Colorectal Cancer Ministero della Salute [NET
   02352137]; TRANSCAN-2 JTC [TRS-2015-00000060 INTRACOLOR]; FPRC 5xmille
   2017 Ministero Salute PTCRC-Intra 2020 (REGENERATION-YIG 2020 project);
   AIRC-CRUK-FC AECC Accelerator Award [22795]; Fondazione Piemontese per
   la Ricerca sul Cancro-ONLUS 5 per mille 2015 Ministero della Salute;
   Ministero Salute, RC 2019; American Association for Cancer Research
FX We thank the Garnett laboratory, Cellular Genetics and Phenotyping
   facility, and drug screening teams at the Sanger Institute for data
   generation and assistance. We thank Annalisa Lorenzato (University of
   Torino, Candiolo, Italy) for technical help with sequenom analysis and
   Pamela Arcella (University of Torino) and Monica Montone (Candiolo
   Cancer Institute, FPOIRCCS) for preclinical models establishment. We
   thank Michael Linnebacher (University of Rostock, Germany) for providing
   the HROC cell models. The M.J. Garnett laboratory was supported by an
   SU2C-DCS International Translational Cancer Research Dream Team Grant
   (SU2C-AACR-DT1213) and the Wellcome Trust Grant 206194. Stand Up To
   Cancer is a division of the Entertainment Industry Foundation. The
   SU2C-DCS grant is administered by the American Association for Cancer
   Research. The research leading to these results has received funding
   from FONDAZIONE AIRC under 5 per Mille 2018-ID 21091 program (principal
   investigator: A. Bardelli (F. Di Nicolantonio and S. Siena), AIRC under
   MFAG 2017ID 20236 (principal investigator: S. Arena); H2020 grant
   agreement no. 635342-2 MoTriColor (to A. Bardelli); AIRC IG 2018-ID
   21923 project (to A. Bardelli), AIRC IG no. 17707, and IG no. 21407 (to
   F. Di Nicolantonio), Therapy in Colorectal Cancer Ministero della
   Salute, Project no. NET 02352137 (to A. Sartore-Bianchi, A. Bardelli, F.
   Di Nicolantonio, and S. Siena). TRANSCAN-2 JTC 2014 contract no.
   TRS-2015-00000060 INTRACOLOR (to S. Arena); FPRC 5xmille 2017 Ministero
   Salute PTCRC-Intra 2020 (REGENERATION-YIG 2020 project; to S. Arena);
   AIRC-CRUK-FC AECC Accelerator Award contract 22795 (to A. Bardelli);
   Fondazione Piemontese per la Ricerca sul Cancro-ONLUS 5 per mille 2015
   Ministero della Salute (to A. Bardelli and F. Di Nicolantonio);
   Ministero Salute, RC 2019 (to A. Bardelli and F. Di Nicolantonio). Hilfe
   fur krebskranke Kinder Frankfurt e.V., Frankfurter Stiftung fur
   krebskranke Kinder (to J. Cinatl). Kent Cancer Trust (to M. Michaelis).
   We thank Kong Xiangjun (Daniel Peeper lab) for providing the B2m-KO
   virus and Catrin Lutz (Jos Jonkers lab) for providing the luciferase
   virus. We thank Arno Velds (NKI) and Shriram Bhosle (Sanger Institute)
   for bioinformatic support. We thank Matthew Coelho for helpful advice.
   We thank Cibele Sotero-Caio and Kirsy Roberts (Sanger Institute) for
   technical help with karyotyping and PCR analysis.
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NR 64
TC 58
Z9 61
U1 2
U2 26
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 AUG
PY 2021
VL 11
IS 8
BP 1923
EP 1937
DI 10.1158/2159-8290.CD-20-1508
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TX3UX
UT WOS:000683016500025
PM 33837064
OA Green Submitted, Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Chaudhary, N
   Joshi, N
   Doloi, R
   Shivashankar, A
   Thorat, R
   Dalal, SN
AF Chaudhary, Nazia
   Joshi, Neha
   Doloi, Rinki
   Shivashankar, Anusha
   Thorat, Rahul
   Dalal, Sorab N.
TI Plakophilin3 loss leads to an increase in autophagy and radio-
   resistance
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Colorectal cancer; Plakophilin3; Autophagy; Radio-resistance
ID BREAST-CANCER CELLS; IONIZING-RADIATION; LUNG-CANCER; RADIORESISTANCE;
   INHIBITION; APOPTOSIS; EXPRESSION; SUBTYPES; DRIVEN; GROWTH
AB Loss of the desmosomal plaque protein plakophilin3 (PKP3) leads to increased tumor progression and metastasis. As metastatic tumors are often resistant to therapy, we wished to determine whether PKP3 loss led to increased radioresistance. PKP3 knockdown cells showed increased resistance to radiation in vitro and in vivo. The increase in resistance was accompanied by an increased ability to clear reactive oxygen species (ROS) and increased autophagy. The increase in autophagy was required for radio -resistance and ROS clearance as inhibiting autophagy using either chloroquine or knocking down ATG3 re-sensitized the PKP3 knockdown clones to radiotherapy. These experiments suggest that autophagy inhibitors could target therapy-resistant PKP3 deficient tumors.(c) 2022 Elsevier Inc. All rights reserved.
C1 [Thorat, Rahul] Tata Mem Hosp, Adv Ctr Treatment Res & Educ Canc, Cell & Tumor Biol & Lab Anim Facil, Navi Mumbai 410210, India.
   [Chaudhary, Nazia; Doloi, Rinki; Dalal, Sorab N.] Tata Mem Hosp, Adv Ctr Treatment Res & Educ Canc, Lab Anim Facil, Navi Mumbai 410210, India.
   [Dalal, Sorab N.] Homi Bhabha Natl Inst, Training Sch Complex, Mumbai 400085, India.
   [Dalal, Sorab N.] Tata Mem Hosp, Adv Ctr Treatment Res & Educ Canc ACTREC, Cell & Tumor Biol, KS216, Navi Mumbai 410210, India.
C3 Tata Memorial Centre (TMC); Tata Memorial Hospital; Advance Centre for
   Treatment, Research & Education in Cancer (ACTREC); Tata Memorial Centre
   (TMC); Advance Centre for Treatment, Research & Education in Cancer
   (ACTREC); Tata Memorial Hospital; Homi Bhabha National Institute; Tata
   Memorial Centre (TMC); Advance Centre for Treatment, Research &
   Education in Cancer (ACTREC); Tata Memorial Hospital
RP Dalal, SN (corresponding author), Tata Mem Hosp, Adv Ctr Treatment Res & Educ Canc, Lab Anim Facil, Navi Mumbai 410210, India.; Dalal, SN (corresponding author), Tata Mem Hosp, Adv Ctr Treatment Res & Educ Canc ACTREC, Cell & Tumor Biol, KS216, Navi Mumbai 410210, India.
EM sdalal@actrec.gov.in
RI Chaudhary, Nazia/JZC-6820-2024
OI Joshi, Neha/0000-0003-4133-2389; Shivashankar,
   Anusha/0000-0002-3692-3996; Doloi, Rinki/0000-0003-2062-8842
FU Department of Biotechnology [BT/PR8351/MED/30/995/2013]; ACTREC donation
   fund [4338]
FX The work was supported by a grant (BT/PR8351/MED/30/995/2013) from the
   Department of Biotechnology to SND and the ACTREC donation fund (4338)
   to SND. We want to thank the ACTREC digital imaging and electron
   microscope facilities for their help with image acquisition and ACTREC
   animal facility members for their help with animal maintenance.
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NR 39
TC 3
Z9 3
U1 0
U2 4
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 10
PY 2022
VL 620
BP 1
EP 7
DI 10.1016/j.bbrc.2022.06.060
PG 7
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 3E9MA
UT WOS:000830299500001
PM 35772211
DA 2025-01-04
ER

PT J
AU Li, Y
   Wang, B
   Ma, FH
   Jiang, DX
   Wang, Y
   Li, K
   Tan, SB
   Feng, JW
   Wang, YZ
   Qin, ZY
   Xu, GF
   Tian, S
   Zhang, XL
   Xu, C
   Wu, JX
   Xu, JM
   Hou, YY
   Ding, C
AF Li, Yan
   Wang, Bing
   Ma, Fahan
   Jiang, Dongxian
   Wang, Ying
   Li, Kai
   Tan, Subei
   Feng, Jinwen
   Wang, Yunzhi
   Qin, Zhaoyu
   Xu, Ganfei
   Tian, Sha
   Zhang, Xiaolei
   Xu, Chen
   Wu, Jiaxue
   Xu, Jianmin
   Hou, Yingyong
   Ding, Chen
TI Proteomic characterization of the colorectal cancer response to
   chemoradiation and targeted therapies reveals potential therapeutic
   strategies
SO CELL REPORTS MEDICINE
LA English
DT Article
ID PLUS CETUXIMAB TREATMENT; 1ST-LINE CHEMOTHERAPY; HUMAN COLON; CLASS
   DISCOVERY; RAS MUTATIONS; EXPRESSION; GENE; KRAS; LANDSCAPE;
   FLUOROURACIL
AB Chemoradiation and targeted therapies are the major treatments for colorectal cancer (CRC); however, molecular properties associated with therapy resistance are incompletely characterized. Here, we profile the proteome of 254 tumor tissues from patients with CRC undergoing chemotherapy, chemoradiation, or chemotherapy combined with targeted therapy. Proteome-based classification reveals four subtypes featured with distinct biological and therapeutic characteristics. The integrative analysis of CRC cell lines and clinical samples indicates that immune regulation is significantly associated with drug sensitivity. HSF1 can increase DNA damage repair and cell cycle, thus inducing resistance to radiation, while high expression of HDAC6 is negatively associated with response of cetuximab. Furthermore, we develop prognostic models with high accuracy to predict the therapeutic response, further validated by parallel reaction monitoring (PRM) assay in an independent validation cohort. This study provides a rich resource for investigating the mechanisms and indicators of chemoradiation and targeted therapy in CRC.
C1 [Li, Yan; Wang, Bing; Ma, Fahan; Wang, Ying; Li, Kai; Tan, Subei; Feng, Jinwen; Wang, Yunzhi; Qin, Zhaoyu; Xu, Ganfei; Tian, Sha; Wu, Jiaxue; Ding, Chen] Fudan Univ, Zhongshan Hosp, Inst Biomed Sci, Human Phenome Inst,Sch Life Sci,State Key Lab Gene, Shanghai 200433, Peoples R China.
   [Li, Yan; Wang, Bing; Ma, Fahan; Wang, Ying; Li, Kai; Tan, Subei; Feng, Jinwen; Wang, Yunzhi; Qin, Zhaoyu; Xu, Ganfei; Tian, Sha; Wu, Jiaxue; Ding, Chen] Fudan Univ, Zhongshan Hosp, Inst Biomed Sci, Human Phenome Inst,Collaborat Innovat Ctr Genet &, Shanghai 200433, Peoples R China.
   [Jiang, Dongxian; Zhang, Xiaolei; Xu, Chen; Hou, Yingyong] Fudan Univ, Zhongshan Hosp, Dept Pathol, Shanghai 200032, Peoples R China.
   [Xu, Jianmin] Fudan Univ, Dept Gen Surg, Zhongshan Hosp, Shanghai 200032, Peoples R China.
C3 Fudan University; Fudan University; Fudan University; Fudan University
RP Wu, JX; Ding, C (corresponding author), Fudan Univ, Zhongshan Hosp, Inst Biomed Sci, Human Phenome Inst,Sch Life Sci,State Key Lab Gene, Shanghai 200433, Peoples R China.; Wu, JX; Ding, C (corresponding author), Fudan Univ, Zhongshan Hosp, Inst Biomed Sci, Human Phenome Inst,Collaborat Innovat Ctr Genet &, Shanghai 200433, Peoples R China.; Xu, C; Hou, YY (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Pathol, Shanghai 200032, Peoples R China.; Xu, JM (corresponding author), Fudan Univ, Dept Gen Surg, Zhongshan Hosp, Shanghai 200032, Peoples R China.
EM xu.chen@zs-hospital.sh.cn; jiaxue@fudan.edu.cn; xujmin@aliyun.com;
   hou.yingyong@zs-hospital.sh.cn; xu.chen@zs-hospital.sh.cn
RI Yang, Yuxuan/JEZ-4150-2023; ding, chen/KDN-1285-2024; Xu,
   Ganfei/LVR-5290-2024
OI Ding, Chen/0000-0001-8673-3464; ying, wang/0009-0004-5264-9917
FU Special Development Funds of Zhangjiang National Independent Innovation
   Demonstration Zone [ZJ2019-ZD-004]; Science and Technology Commission of
   Shanghai Municipality [2017SHZDZX01]; Shanghai Science Technique
   Planning Foundation [19441904000]; Shanghai Municipal Key Clinical
   Specialty [shslczdzk 01302]; Shanghai Science and Technology Development
   Fund [19MC1911000]; Young Scientists Fund of the National Natural
   Science Foundation of China [32301236, 32201215, 32201212]; Shanghai
   Sailing Program [23YF1402800, 22YF1403100]
FX Special Development Funds of Zhangjiang National Independent Innovation
   Demonstration Zone (grant ZJ2019-ZD-004 [C.D.] ) , the Science and
   Technology Commission of Shanghai Municipality (grant 2017SHZDZX01
   [C.D.] ) , the Shanghai Science Technique Planning Foundation (grant
   19441904000 [Y.H.] ) , Shanghai Municipal Key Clinical Specialty
   (shslczdzk 01302 [Y.H.] ) , the Shanghai Science and Technology
   Development Fund (grant 19MC1911000 [Y.H.] ) , the Young Scientists Fund
   of the National Natural Science Foundation of China (grants 32301236
   [Y.L.] , 32201215 [J.F.] , and 32201212 [Yunzhi Wang] , the Shanghai
   Sailing Program (grants 23YF1402800 [Y.L.] and 22YF1403100 [J.F.] ) ,
   and the Fudan original research personalized support project.
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NR 74
TC 3
Z9 3
U1 6
U2 21
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 2666-3791
J9 CELL REP MED
JI Cell Rep. Med.
PD DEC 19
PY 2023
VL 4
IS 12
AR 101311
DI 10.1016/j.xcrm.2023.101311
EA DEC 2023
PG 29
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA ES0W6
UT WOS:001140804200001
PM 38086380
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Georgieva, M
   Gospodinova, Z
   Keremidarska-Markova, M
   Kamenska, T
   Gencheva, G
   Krasteva, N
AF Georgieva, Milena
   Gospodinova, Zlatina
   Keremidarska-Markova, Milena
   Kamenska, Trayana
   Gencheva, Galina
   Krasteva, Natalia
TI PEGylated Nanographene Oxide in Combination with Near-Infrared Laser
   Irradiation as a Smart Nanocarrier in Colon Cancer Targeted Therapy
SO PHARMACEUTICS
LA English
DT Article
DE nano-graphene oxide (nGO); nGO-PEG; near-infrared (NIR) light;
   phototherapy; colon cancer
ID REDUCED GRAPHENE OXIDE; POLY(ETHYLENE GLYCOL); PHOTOTHERMAL THERAPY;
   DELIVERY; AGGREGATION; SURFACE; NANOPARTICLES; DISPERSION; NANOSHEETS;
   REDUCTION
AB Anti-cancer therapies that integrate smart nanomaterials are the focus of cancer research in recent years. Here, we present our results with PEGylated nanographene oxide particles (nGO-PEG) and have studied their combined effect with near-infrared (NIR) irradiation on low and high invasive colorectal carcinoma cells. The aim is to develop nGO-PEG as a smart nanocarrier for colon cancer-targeted therapy. For this purpose, nGO-PEG nanoparticles' size, zeta potential, surface morphology, dispersion stability, aggregation, and sterility were determined and compared with pristine nGO nanoparticles (NPs). Our results show that PEGylation increased the particle sizes from 256.7 nm (pristine nGO) to 324.6 nm (nGO-PEG), the zeta potential from -32.9 to -21.6 mV, and wrinkled the surface of the nanosheets. Furthermore, nGO-PEG exhibited higher absorbance in the NIR region, as compared to unmodified nGO. PEGylated nGO demonstrated enhanced stability in aqueous solution, improved dispensability in the culture medium, containing 10% fetal bovine serum (FBS) and amended biocompatibility. A strong synergic effect of nGO-PEG activated with NIR irradiation for 5 min (1.5 W/cm(-2) laser) was observed on cell growth inhibition of low invasive colon cancer cells (HT29) and their wound closure ability while the effect of NIR on cellular morphology was relatively weak. Our results show that PEGylation of nGO combined with NIR irradiation holds the potential for a biocompatible smart nanocarrier in colon cancer cells with enhanced physicochemical properties and higher biological compatibility. For that reason, further optimization of the irradiation process and detailed screening of nGO-PEG in combination with NIR and chemotherapeutics on the fate of the colon cancer cells is a prerequisite for highly efficient combined nanothermal and photothermal therapy for colon cancer.
C1 [Georgieva, Milena] Bulgarian Acad Sci, Inst Mol Biol R Tsanev, Acad Georgi Bonchev Str,Bl 21, Sofia 1113, Bulgaria.
   [Gospodinova, Zlatina; Keremidarska-Markova, Milena; Kamenska, Trayana; Krasteva, Natalia] Bulgarian Acad Sci, Inst Biophys & Biomed Engn, Acad Georgi Bonchev Str,Bl 21, Sofia 1113, Bulgaria.
   [Gospodinova, Zlatina] Bulgarian Acad Sci, Inst Plant Physiol & Genet, Acad Georgi Bonchev Str,Bl 21, Sofia 1113, Bulgaria.
   [Keremidarska-Markova, Milena] Sofia Univ St Kliment Ohridski, Fac Biol, 8 Dragan Tsankov Blvd, Sofia 1164, Bulgaria.
   [Gencheva, Galina] Sofia Univ St Kliment Ohridski, Fac Chem & Pharm, 1 James Bourchier Blvd, Sofia 1164, Bulgaria.
C3 Bulgarian Academy of Sciences; Bulgarian Academy of Sciences; Bulgarian
   Academy of Sciences; University of Sofia; University of Sofia
RP Georgieva, M (corresponding author), Bulgarian Acad Sci, Inst Mol Biol R Tsanev, Acad Georgi Bonchev Str,Bl 21, Sofia 1113, Bulgaria.; Krasteva, N (corresponding author), Bulgarian Acad Sci, Inst Biophys & Biomed Engn, Acad Georgi Bonchev Str,Bl 21, Sofia 1113, Bulgaria.
EM milenageorgy@gmail.com; zlatina.go@abv.bg; m_keremidarska@abv.bg;
   trayanakamenska@abv.bg; gkissovsky@gmail.com; gkissovsky@gmail.com
RI Gencheva, Galina/AAM-4736-2021; Keremidarska-Markova,
   Milena/AAL-2383-2021; Georgieva, Milena/K-8427-2016
OI Georgieva, Milena/0000-0002-2371-7544; Krasteva,
   Natalia/0000-0001-7423-7412; Gencheva, Galina/0000-0003-1696-1589
FU Bulgarian Science Fund [KP-06-N31/15, K P-06 H31/15/2019]
FX This research and the APC are funded by the Bulgarian Science Fund,
   grant number KP-06-N31/15. (K P-06 H31/15/2019).
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NR 71
TC 22
Z9 23
U1 2
U2 14
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD MAR
PY 2021
VL 13
IS 3
AR 424
DI 10.3390/pharmaceutics13030424
PG 22
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA RE4AC
UT WOS:000634098100001
PM 33809878
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Tan, YJ
   Lee, YT
   Yeong, KY
   Petersen, SH
   Kono, K
   Tan, SC
   Oon, CE
AF Tan, Yi Jer
   Lee, Yeuan Ting
   Yeong, Keng Yoon
   Petersen, Sven H.
   Kono, Koji
   Tan, Soo Choon
   Oon, Chern Ein
TI Anticancer activities of a benzimidazole compound through sirtuin
   inhibition in colorectal cancer
SO FUTURE MEDICINAL CHEMISTRY
LA English
DT Article
DE BZD9L1; colorectal cancer; sirtuin; targeted therapy
ID COLON-CANCER; CELL-DEATH; APOPTOSIS; DEACETYLASE; EXPRESSION; P21;
   TRAF2; BCL-2; CYCLE
AB Aim: This study aims to investigate the mode of action of a novel sirtuin inhibitor (BZD9L1) and its associated molecular pathways in colorectal cancer (CRC) cells. Materials & methods: BZD9L1 was tested against metastatic CRC cell lines to evaluate cytotoxicity, cell cycle and apoptosis, senescence, apoptosis related genes and protein expressions, as well as effect against major cancer signaling pathways. Results & conclusion: BZD9L1 reduced the viability, cell migration and colony forming ability of both HCT 116 and HT-29 metastatic CRC cell lines through apoptosis. BZD9L1 regulated major cancer pathways differently in CRC with different mutation profiles. BZD9L1 exhibited anticancer activities as a cytotoxic drug in CRC and as a promising therapeutic strategy in CRC treatment.
   [GRAPHICS]
   .
C1 [Tan, Yi Jer; Lee, Yeuan Ting; Yeong, Keng Yoon; Tan, Soo Choon; Oon, Chern Ein] Univ Sains Malaysia, Inst Res Mol Med INFORMM, George Town 11800, Malaysia.
   [Yeong, Keng Yoon] Monash Univ, Sch Sci, Malaysia Campus,Jalan Lagoon Selatan, Bandar Sunway 47500, Selangor, Malaysia.
   [Petersen, Sven H.; Kono, Koji] Natl Univ Singapore, Canc Sci Inst Singapore, Singapore, Singapore.
   [Kono, Koji] Natl Univ Singapore, Dept Surg, Singapore, Singapore.
   [Kono, Koji] Fukushima Med Univ, Sch Med, Fukushima, Japan.
C3 Universiti Sains Malaysia; Monash University; Monash University
   Malaysia; National University of Singapore; National University of
   Singapore; Fukushima Medical University
RP Oon, CE (corresponding author), Univ Sains Malaysia, Inst Res Mol Med INFORMM, George Town 11800, Malaysia.
EM chern.oon@usm.my
RI Petersen, Sven/V-6315-2019; Yeong, Keng Yoon/JRR-8938-2023; Oon,
   Chern/B-3684-2013; Yeong, Keng Yoon/F-4287-2011; Lee, Yeuan
   Ting/Q-5720-2018
OI Yeong, Keng Yoon/0000-0003-0433-5070; Petersen, Sven
   H./0000-0001-8254-6100; Tan, Yi Jer/0000-0003-2145-2105; Lee, Yeuan
   Ting/0000-0001-9356-5681; Oon, Chern Ein/0000-0002-4685-6408
FU Ranjeet Bhagwan Singh Medical Research Grant [304/CIPPM/650708/K105];
   EScience Fund (MOSTI) [305/CIPPM/613620]; USM graduate assistant
   fellowship
FX This project was funded by Ranjeet Bhagwan Singh Medical Research Grant
   (304/CIPPM/650708/K105) and EScience Fund (MOSTI) (305/CIPPM/613620).
   Yeuan Ting Lee was supported by USM graduate assistant fellowship. The
   authors would also like to thank Warren Lee Xian Liang for technical
   advice on western blot. 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 62
TC 27
Z9 31
U1 0
U2 16
PU Newlands Press Ltd
PI London
PA 2 Albert Pl, London, UNITED KINGDOM
SN 1756-8919
EI 1756-8927
J9 FUTURE MED CHEM
JI Future Med. Chem.
PD SEP
PY 2018
VL 10
IS 17
BP 2039
EP 2057
DI 10.4155/fmc-2018-0052
PG 19
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA GS0HY
UT WOS:000443173800004
PM 30066578
DA 2025-01-04
ER

PT J
AU Wang, H
   Wang, LY
   Xie, ZX
   Zhou, S
   Li, Y
   Zhou, Y
   Sun, MY
AF Wang, Hao
   Wang, Liye
   Xie, Zuoxu
   Zhou, Shuang
   Li, Yan
   Zhou, Yue
   Sun, Meiyan
TI Nitric Oxide (NO) and NO Synthases (NOS)-Based Targeted Therapy for
   Colon Cancer
SO CANCERS
LA English
DT Review
DE nitric oxide; NO; NO synthases; NOS; iNOS; targeted therapy;
   chemoprevention; NO delivery system; colon cancer; clinical
   manifestation; clinical implication
ID HUMAN SERUM-ALBUMIN; ENHANCED VASCULAR-PERMEABILITY; SULFIDE-RELEASING
   HYBRID; ABERRANT CRYPT FOCI; NF-KAPPA-B; DONATING ASPIRIN;
   COLORECTAL-CANCER; TUMOR-GROWTH; MACROMOLECULAR THERAPEUTICS;
   INFLAMMATORY MEDIATORS
AB Colorectal cancer (CRC) is one of the most lethal malignancies worldwide and CRC therapy remains unsatisfactory. In recent decades, nitric oxide (NO)-a free-radical gas-plus its endogenous producer NO synthases (NOS), have attracted considerable attention. NO exerts dual effects (pro- and anti-tumor) in cancers. Endogenous levels of NO promote colon neoplasms, whereas exogenously sustained doses lead to cytotoxic functions. Importantly, NO has been implicated as an essential mediator in many signaling pathways in CRC, such as the Wnt/beta-catenin and extracellular-signal-regulated kinase (ERK) pathways, which are closely associated with cancer initiation, metastasis, inflammation, and chemo-/radio-resistance. Therefore, NO/NOS have been proposed as promising targets in the regulation of CRC carcinogenesis. Clinically relevant NO-donating agents have been developed for CRC therapy to deliver a high level of NO to tumor sites. Notably, inducible NOS (iNOS) is ubiquitously over-expressed in inflammatory-associated colon cancer. The development of iNOS inhibitors contributes to targeted therapies for CRC with clinical benefits. In this review, we summarize the multifaceted mechanisms of NO-mediated networks in several hallmarks of CRC. We review the clinical manifestation and limitations of NO donors and NOS inhibitors in clinical trials. We also discuss the possible directions of NO/NOS therapies in the immediate future.
C1 [Wang, Hao; Sun, Meiyan] Jilin Med Univ, Coll Lab Med, Jilin 132013, Jilin, Peoples R China.
   [Wang, Liye; Xie, Zuoxu; Zhou, Shuang; Li, Yan] Univ Houston, Coll Pharm, Dept Pharmacol & Pharmaceut Sci, Houston, TX 77204 USA.
   [Zhou, Yue] North Dakota Univ, Dept Stat, Fargo, ND 58105 USA.
C3 Jilin Medical University; University of Houston System; University of
   Houston
RP Sun, MY (corresponding author), Jilin Med Univ, Coll Lab Med, Jilin 132013, Jilin, Peoples R China.
EM 87115wh@163.com; lwang53@uh.edu; zxie3@Central.UH.EDU;
   goldenshuang1929@gmail.com; yli97@uh.edu; yue.zhou@ndsu.edu;
   sunmy990@163.com
RI Wang, Liye/AAK-2053-2020; sun, meiyan/AAW-4123-2020; xie,
   zuoxu/AAR-5443-2021
OI xie, zuoxu/0000-0003-3977-4006; sun, meiyan/0000-0002-5015-1224
FU Science and Technology Planning Project of Jilin Province
   [20200404099YY, 20200201623 JC]; National Natural Science Fund of the
   People's Republic of China [81601234, 81771304]; Traditional Chinese
   Medicine Science and Technology Fund of Jilin Province [2019140]; Health
   Science and Technology Innovation Project of Jilin Province [2018ZC032,
   20192C005]; Special Project for Health Research Talents of Jilin
   Province [2019SCZ037]; National Innovation and Entrepreneurship training
   Program for College Students [202013706062]
FX This work was supported by the Science and Technology Planning Project
   of Jilin Province (no. 20200404099YY), the National Natural Science Fund
   of the People's Republic of China (no. 81601234 and no. 81771304), the
   Traditional Chinese Medicine Science and Technology Fund of Jilin
   Province (no.2019140), the Health Science and Technology Innovation
   Project of Jilin Province (no.2018ZC032 and no.20192C005), the Special
   Project for Health Research Talents of Jilin Province (no. 2019SCZ037),
   National Innovation and Entrepreneurship training Program for College
   Students (no. 202013706062), the Science and Technology Planning Project
   of Jilin Province (No. 20200201623 JC).
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NR 162
TC 50
Z9 53
U1 1
U2 61
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 1881
DI 10.3390/cancers12071881
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MV6SJ
UT WOS:000556484800001
PM 32668616
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ye, J
   Lin, M
   Zhang, CM
   Zhu, XW
   Li, SM
   Liu, H
   Yin, JF
   Yu, H
   Zhu, KC
AF Ye, Jun
   Lin, Mei
   Zhang, Chuanmeng
   Zhu, Xiaowei
   Li, Sumeng
   Liu, Hui
   Yin, Jianfeng
   Yu, Hong
   Zhu, Kuichun
TI Tissue gene mutation profiles in patients with colorectal cancer and
   their clinical implications
SO BIOMEDICAL REPORTS
LA English
DT Article
DE colorectal cancer; gene mutation; targeted therapy; next-generation
   sequencing
ID BREAST-CANCER; TUMOR DNA; BRAF; INHIBITION; BIOMARKERS; RATIONALE;
   PATHOLOGY; EFFICACY; EGFR; MET
AB Colorectal cancer (CRC) is one of the most common types of cancer in the world, and targeted therapy is frequently used in the clinical management of the disease. A complete and accurate picture of tissue gene mutations is therefore critical. Tissue specimens from 117 patients with CRC were used for high throughput DNA next-generation sequencing (NGS) analysis. Hotspots from 50 genes frequently associated with the development and progression of solid tumors were targeted for sequencing. Characterization of tissue gene mutations was performed; the tissue mutation positive rates ofKRAS,KIT,PIK3CA,METandEGFRwere 52.1, 19.7, 29.9, 15.4 and 14.5%, respectively. The mutation positive rates ofTP53,APC,CDKN2A,STK11andFBXW7were 65.8, 39.3, 32.5, 19.7 and 19.7%, respectively. The most frequentKRASmutations were G12A/C/D/S/V, accounting for 61.2% of allKRASmutations. The most frequentTP53mutations were R273C/G/H/L, accounting for 8.5% of allTP53mutations. The most frequentAPCmutation was E1554fs, accounting for 19.7% of allAPCmutations.IDH1R132C/H,KITM541L,METN375S, andSMAD4R361C/H were also frequently identified.TP53mutations were more common in patients >= 60 years old (P<0.05), andIDH1mutations were more common in male patients (P<0.05). NGS 50 gene panel sequencing provides a comprehensive tissue gene mutation profile which may significantly improve clinical management.
C1 [Ye, Jun; Lin, Mei; Zhang, Chuanmeng; Zhu, Xiaowei; Li, Sumeng; Yu, Hong] Taizhou Peoples Hosp, Ctr Translat Med, 399 South Hailing Rd, Taizhou 225300, Jiangsu, Peoples R China.
   [Liu, Hui] Xuzhou Med Univ, Dept Pathol, Xuzhou 221000, Jiangsu, Peoples R China.
   [Yin, Jianfeng] Jianwei Med Lab, Taizhou 225300, Jiangsu, Peoples R China.
   [Zhu, Kuichun] Labway Clin Labs, R&D Dept, Shanghai 210000, Peoples R China.
   [Zhu, Kuichun] Wuxi Shenrui Biopharmaceut Co Ltd, R&D Dept, 1699 Huishan Blvd, Wuxi 214000, Jiangsu, Peoples R China.
C3 Xuzhou Medical University
RP Yu, H (corresponding author), Taizhou Peoples Hosp, Ctr Translat Med, 399 South Hailing Rd, Taizhou 225300, Jiangsu, Peoples R China.; Zhu, KC (corresponding author), Wuxi Shenrui Biopharmaceut Co Ltd, R&D Dept, 1699 Huishan Blvd, Wuxi 214000, Jiangsu, Peoples R China.
EM yuhongjianglin@163.com; kzhu68@hotmail.com
RI Liu, Zhiyong/ABK-5033-2022; Liu, Hui/AAJ-4339-2020
OI Zhu, Kuichun/0000-0002-3594-5616
FU 333 Plan Foundation of Jiangsu [BRA2017173]; Taizhou People's Hospital
   Medical Innovation Team Foundation [CXTDA201904, CXTDA201901]; 2018
   Taizhou People's Hospital Mandatory Project [ZL201733]
FX The work was funded in part by the 333 Plan Foundation of Jiangsu (grant
   no. BRA2017173), the Taizhou People's Hospital Medical Innovation Team
   Foundation (grant nos. CXTDA201904 and CXTDA201901), and the 2018
   Taizhou People's Hospital Mandatory Project (grant no. ZL201733).
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   2008, CLIN GASTROENT SER, P1
NR 50
TC 19
Z9 20
U1 0
U2 1
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 2049-9434
EI 2049-9442
J9 BIOMED REP
JI Biomed. Rep.
PD JUL
PY 2020
VL 13
IS 1
BP 43
EP 48
DI 10.3892/br.2020.1303
PG 6
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA MA1WK
UT WOS:000541708100006
PM 32440349
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kast, K
   Rhiem, K
AF Kast, Karin
   Rhiem, Kerstin
TI Familial Breast Cancer - Targeted Therapy in Secondary and Tertiary
   Prevention
SO BREAST CARE
LA English
DT Review
DE BRCA1; BRCA2; Breast cancer; Therapy; Carboplatin; PARPi
ID COMPLETE RESPONSE RATES; OVARIAN-CANCER; HEREDITARY BREAST; BRCA1;
   POLY(ADP-RIBOSE); MUTATIONS; REPAIR; CARBOPLATIN; WOMEN;
   CYCLOPHOSPHAMIDE
AB The introduction of an increasing number of individualized molecular targeted therapies into clinical routine mirrors their importance in modern cancer prevention and treatment. Well-known examples for targeted agents are the monoclonal antibody trastuzumab and the selective estrogen receptor modulator tamoxifen. The identification of an unaltered gene in tumor tissue in colon cancer (KRAS) is a predictor for the patient's response to targeted therapy with a monoclonal antibody (cetuximab). Targeted therapy for hereditary breast and ovarian cancer has become a reality with the approval of olaparib for platin-sensitive late relapsed BRCA-associated ovarian cancer in December 2014. This manuscript reviews the status quo of poly-ADP-ribose polymerase inhibitors (PARPi) in the therapy of breast and ovarian cancer as well as the struggle for carboplatin as a potential standard of care for triple-negative and, in particular, BRCA-associated breast cancer. Details of the mechanism of action with information on tumor development are provided, and an outlook for further relevant research is given. The efficacy of agents against molecular targets together with the identification of an increasing number of cancer-associated genes will open the floodgates to a new era of treatment decision-making based on molecular tumor profiles. Current clinical trials involving patients with BRCA-associated cancer explore the efficacy of the molecular targeted therapeutics platinum and PARPi.
C1 [Kast, Karin] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dept Gynecol & Obstet, D-01307 Dresden, Germany.
   [Rhiem, Kerstin] Univ Hosp Cologne, Ctr Familial Breast & Ovarian Canc, Dept Gynecol & Obstet, Cologne, Germany.
C3 Technische Universitat Dresden; Carl Gustav Carus University Hospital;
   University of Cologne
RP Kast, K (corresponding author), Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dept Gynecol & Obstet, Fetscherstr 74, D-01307 Dresden, Germany.
EM karin.kast@uniklinikum-dresden.de
CR Alsop K, 2012, J CLIN ONCOL, V30, P2654, DOI 10.1200/JCO.2011.39.8545
   [Anonymous], TNT TRIAL RANDOMIZED
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NR 37
TC 4
Z9 6
U1 1
U2 7
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1661-3791
EI 1661-3805
J9 BREAST CARE
JI Breast Care
PY 2015
VL 10
IS 1
BP 27
EP 31
DI 10.1159/000380756
PG 5
WC Oncology; Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Obstetrics & Gynecology
GA CD8HS
UT WOS:000351336400005
PM 25960722
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Boilève, A
   De Cuyper, A
   Larive, A
   Mahjoubi, L
   Najdawi, M
   Tazdait, M
   Gelli, M
   Tselikas, L
   Smolenschi, C
   Malka, D
   Pignon, JP
   Ducreux, M
   Boige, V
AF Boileve, Alice
   De Cuyper, Astrid
   Larive, Alicia
   Mahjoubi, Linda
   Najdawi, Milan
   Tazdait, Melodie
   Gelli, Maximiliano
   Tselikas, Lambros
   Smolenschi, Cristina
   Malka, David
   Pignon, Jean-Pierre
   Ducreux, Michel
   Boige, Valerie
TI Hepatic arterial infusion of oxaliplatin plus systemic chemotherapy and
   targeted therapy for unresectable colorectal liver metastases
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Colorectal cancer; Liver metastases; Hepatic arterial infusion;
   Oxaliplatin; Targeted therapy
ID RANDOMIZED-TRIAL; PHASE-II; CANCER; RESECTION; BEVACIZUMAB; SURVIVAL;
   RATES; FLUOROURACIL; COMBINATION; LEUCOVORIN
AB Background: Hepatic arterial infusion (HAI) combined with systemic chemotherapy has shown promising results in patients with unresectable colorectal liver metastases (CRLM), even after failure to systemic therapy. Addition of systemic targeted therapies has been investigated with controversial results regarding tolerance, especially with HAI-floruxidine when combined with systemic bevacizumab. Our study aimed to analyse feasibility, safety and efficacy of HAI-oxaliplatin plus systemic chemotherapy and targeted therapies.
   Methods: Between 2005 and 2016, single-centre consecutive patients with unresectable CRLM who received at least one cycle of HAI-oxaliplatin plus systemic chemotherapy and targeted therapies (cetuximab/panitumumab or bevacizumab) were analysed.
   Results: A total of 89 patients (median age 55 years (range, 26-76 years) who previously received a median number of one systemic chemotherapy regimen (range, 0-5) including oxaliplatin in 78% of cases were included. Median number of HAI-oxaliplatin cycles was 9 (range, 1-28) combined with systemic chemotherapy and targeted therapies (LV5FU2 [63%], FOLFIRI [36%]) plus anti-EGFR (30%), or bevacizumab (70%). Grade 3/4 toxicities included neutropenia (40%), HAI-related abdominal pain (43%) and neurotoxicity (12%). The intentto-treat objective response rate was 42%, and 45% had stable disease, allowing complete CRLM resection/ablation in 27% of patients. After a median follow-up of 72 months, median overall and progression-free survival was 20 and 9 months, respectively.
   Conclusion: Addition of targeted therapy to systemic chemotherapy combined with HAI-oxaliplatin is feasible, safe and shows promising activity, even after systemic chemotherapy failure. (C) 2020 Elsevier Ltd. All rights reserved.
C1 [Boileve, Alice; De Cuyper, Astrid; Mahjoubi, Linda; Najdawi, Milan; Smolenschi, Cristina; Malka, David; Ducreux, Michel; Boige, Valerie] Dept Med Oncol, Gustave Roussy Canc Campus, Villejuif, France.
   [De Cuyper, Astrid] Clin Univ St Luc, Dept Med Oncol, Brussels, Belgium.
   [Larive, Alicia; Pignon, Jean-Pierre] Univ Paris Saclay, Dept Biostat & Epidemiol, Gustave Roussy, Villejuif, France.
   [Tazdait, Melodie] Dept Radiol, Gustave Roussy Canc Campus, Villejuif, France.
   [Gelli, Maximiliano] Dept Surg, Gustave Roussy Canc Campus, Villejuif, France.
   [Tselikas, Lambros] Dept Intervent Radiol, Gustave Roussy Canc Campus, Villejuif, France.
   [Pignon, Jean-Pierre] Univ Paris Saclay, Labeled Ligue Canc, INSERM, Oncostat U1018, Villejuif, France.
   [Ducreux, Michel] Paris Saclay Univ, Villejuif, France.
C3 UNICANCER; Gustave Roussy; Universite Catholique Louvain; Cliniques
   Universitaires Saint-Luc; UNICANCER; Gustave Roussy; Universite Paris
   Saclay; UNICANCER; Gustave Roussy; UNICANCER; Gustave Roussy; UNICANCER;
   Gustave Roussy; Universite Paris Saclay; Institut National de la Sante
   et de la Recherche Medicale (Inserm); Universite Paris Saclay
RP Boilève, A (corresponding author), Inst Gustave Roussy, Med Oncol Dept, Digest Oncol Unit, 114 Rue Edouard Vaillant, F-94800 Villejuif, France.
EM alice.boileve@gmail.com
RI Boilève, Alice/ABE-4470-2021; Malka, David/HJA-5870-2022; Gelli,
   Maximiliano/K-8340-2019
OI Gelli, Maximiliano/0000-0001-9807-4021
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NR 42
TC 11
Z9 11
U1 1
U2 4
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 OCT
PY 2020
VL 138
BP 89
EP 98
DI 10.1016/j.ejca.2020.07.022
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NW2NO
UT WOS:000574846800011
PM 32871526
DA 2025-01-04
ER

PT J
AU Yeoh, Y
   Low, TY
   Abu, N
   Lee, PY
AF Yeoh, Yeelon
   Low, Teck Yew
   Abu, Nadiah
   Lee, Pey Yee
TI Regulation of signal transduction pathways in colorectal cancer:
   implications for therapeutic resistance
SO PEERJ
LA English
DT Article
DE Colorectal cancer; Drug resistance; Chemotherapy; Targeted therapy;
   Signalling pathways; Mitogen-activated protein kinases; Protein kinase
   B; Notch receptor
ID ACQUIRED DRUG-RESISTANCE; COLON-CANCER; 1ST-LINE TREATMENT;
   POOR-PROGNOSIS; GENE-MUTATIONS; CHEMOTHERAPY RESISTANCE; CETUXIMAB
   RESISTANCE; PIK3CA MUTATIONS; TARGETED THERAPY; MICROSATELLITE
   INSTABILITY
AB Resistance to anti-cancer treatments is a critical and widespread health issue that has brought serious impacts on lives, the economy and public policies. Mounting research has suggested that a selected spectrum of patients with advanced colorectal cancer (CRC) tend to respond poorly to both chemotherapeutic and targeted therapeutic regimens. Drug resistance in tumours can occur in an intrinsic or acquired manner, rendering cancer cells insensitive to the treatment of anti-cancer therapies. Multiple factors have been associated with drug resistance. The most well-established factors are the emergence of cancer stem cell-like properties and overexpression of ABC transporters that mediate drug efflux. Besides, there is emerging evidence that signalling pathways that modulate cell survival and drug metabolism play major roles in the maintenance of multidrug resistance in CRC. This article reviews drug resistance in CRC as a result of alterations in the MAPK, PI3K/PKB, Wnt/beta-catenin and Notch pathways.
C1 [Yeoh, Yeelon; Low, Teck Yew; Abu, Nadiah; Lee, Pey Yee] Univ Kebangsaan Malaysia, UKM Med Mol Biol Inst UMBI, Kuala Lumpur, Malaysia.
C3 Universiti Kebangsaan Malaysia
RP Lee, PY (corresponding author), Univ Kebangsaan Malaysia, UKM Med Mol Biol Inst UMBI, Kuala Lumpur, Malaysia.
EM leepeyyee@ukm.edu.my
RI Low, Teck/Q-5946-2019; Lee, Pey/Q-9961-2019; Abu, Nadiah/N-8531-2016
FU Fundamental Research Grant Scheme - Ministry of Higher Education,
   Malaysia [FRGS/1/2019/SKK08/UKM/03/5]
FX This work is supported by the Fundamental Research Grant Scheme
   (FRGS/1/2019/SKK08/UKM/03/5) awarded by the Ministry of Higher
   Education, Malaysia. 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 295
TC 9
Z9 9
U1 1
U2 12
PU PEERJ INC
PI LONDON
PA 341-345 OLD ST, THIRD FLR, LONDON, EC1V 9LL, ENGLAND
SN 2167-8359
J9 PEERJ
JI PeerJ
PD OCT 22
PY 2021
VL 9
AR e12338
DI 10.7717/peerj.12338
PG 55
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA WN0KH
UT WOS:000711465300001
PM 34733591
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lim, AR
   Rim, CH
AF Lim, Ah Reum
   Rim, Chai Hong
TI Oligometastasis: Expansion of Curative Treatments in the Field of
   Oncology
SO MEDICINA-LITHUANIA
LA English
DT Review
DE oligometastasis; immunotherapy; targeted therapy; radiation therapy;
   surgery; oligometastatic cancer; local treatment; lung cancer
ID CELL LUNG-CANCER; COLORECTAL-CARCINOMA METASTASES; STEREOTACTIC BODY
   RADIOTHERAPY; PHASE-II; RESECTION; THERAPY; DISEASE; MULTICENTER;
   RECURRENCE; SURVIVAL
AB Oligometastasis is defined as the presence of several limited metastatic lesions and is generally limited to three or fewer than five metastatic lesions. Previously, the treatment of metastatic cancer aimed to alleviate symptoms rather than cure them; however, the use of immunotherapy or targeted therapy has greatly improved patient life expectancy. Additionally, the effectiveness and safety of local treatment have recently been proven for oligometastatic cancers and have significantly improved patient survival and decreased recurrence rates. A few metastatic studies on lung cancer have demonstrated the usefulness of combining radiation therapy and immunotherapy. Recently, local and targeted therapy combinations have shown promising results in treating non-small cell lung cancer, predominantly caused by the epidermal growth factor receptor and anaplastic lymphoma kinase gene mutations, suggesting the potential of these new treatment strategies. It is well known that oligometastasis has better clinical results than polymetastasis; however, research on the biological profile of oligometastasis is still lacking. Studies using circulating tumor DNA and circulating tumor cells are at the initial stages of providing a better understanding of oligometastatic cancers, and the biological characteristics of these cancers may be revealed based on more diverse studies. With the development of these treatments, the prognosis for patients with oligometastatic cancers is steadily improving, and if the biological profile is revealed, customized treatment may be provided.
C1 [Lim, Ah Reum] Korea Univ, Ansan Hosp, Dept Internal Med, Div Cardiol, Ansan 15355, South Korea.
   [Rim, Chai Hong] Korea Univ, Ansan Hosp, Dept Radiat Oncol, Ansan 15355, South Korea.
C3 Korea University; Korea University Medicine (KU Medicine); Korea
   University; Korea University Medicine (KU Medicine)
RP Rim, CH (corresponding author), Korea Univ, Ansan Hosp, Dept Radiat Oncol, Ansan 15355, South Korea.
EM ahreumlim@korea.ac.kr; crusion3@naver.com
RI Rim, Chai/J-3455-2019
OI RIM, CHAI HONG/0000-0001-7431-4588; Lim, Ah Reum/0000-0001-9530-3204
FU Korea University Grant;  [K2125791]
FX This study is supported by Korea University Grant (K2125791).
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NR 39
TC 1
Z9 1
U1 0
U2 1
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 NOV
PY 2023
VL 59
IS 11
AR 1934
DI 10.3390/medicina59111934
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA Z7BV9
UT WOS:001113598600001
PM 38003982
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Strippoli, A
   Cocomazzi, A
   Basso, M
   Cenci, T
   Ricci, R
   Pierconti, F
   Cassano, A
   Fiorentino, V
   Barone, C
   Bria, E
   Ricci-Vitiani, L
   Tortora, G
   Larocca, LM
   Martini, M
AF Strippoli, Antonia
   Cocomazzi, Alessandra
   Basso, Michele
   Cenci, Tonia
   Ricci, Riccardo
   Pierconti, Francesco
   Cassano, Alessandra
   Fiorentino, Vincenzo
   Barone, Carlo
   Bria, Emilio
   Ricci-Vitiani, Lucia
   Tortora, Giampaolo
   Larocca, Luigi Maria
   Martini, Maurizio
TI c-MYC Expression Is a Possible Keystone in the Colorectal Cancer
   Resistance to EGFR Inhibitors
SO CANCERS
LA English
DT Article
DE c-MYC; colorectal cancer; EGFR inhibitor resistance; targeted therapy
ID CONSENSUS MOLECULAR SUBTYPES; ACQUIRED-RESISTANCE; THERAPY;
   OVEREXPRESSION; PROGNOSIS; EVOLUTION; BLOCKADE; MIR-145; CELLS
AB Alterations in the transcriptional factor c-MYC could be involved in the anti-EGFR resistance in metastatic colorectal cancer (mCRC). The c-MYC expression was evaluated in 121 RAS and BRAF wild-type mCRC before treatment with anti-EGFR+Folfiri therapy and in 33 subsequent metastases collected during target therapy (TT) or in TT resistance phase. We analyzed the expression and the functional role of some c-MYC linked miRNAs (miR-31-3p, miR-143 and miR-145) in our patient group and in two CRC cell lines, also performing a c-MYC target PCR array. Patients with higher c-MYC expression (HME) showed a significant lower PFS and OS when compared to those with low c-MYC expression (LME). HME pattern was significantly more frequent in the metastases after TT and significantly associated to anti-EGFR molecular resistance alterations. We also found a significant correlation between the expression of the above-mentioned c-MYC linked miRNAs, c-MYC level and anti-EGFR resistance. Moreover, expression gene profiling pointed out the pivotal role of c-MYC in CRC-related cell-cycle, apoptosis, signal transduction and cell-growth pathways. c-MYC expression might distinguish patients with a lower PFS and OS in anti-EGFR treated mCRC. The individuation of some miRNAs involved in the c-MYC pathway regulation and the downstream c-MYC effector genes could provide a new possible target to overcome the anti-EGFR resistance in mCRC.
C1 [Strippoli, Antonia; Basso, Michele; Ricci, Riccardo; Pierconti, Francesco; Cassano, Alessandra; Barone, Carlo; Bria, Emilio; Tortora, Giampaolo; Larocca, Luigi Maria; Martini, Maurizio] Fdn Policlin Univ A Gemelli IRCCS, Largo A Gemelli 8, Rome 00168, Italy.
   [Cocomazzi, Alessandra; Cenci, Tonia; Ricci, Riccardo; Pierconti, Francesco; Fiorentino, Vincenzo; Larocca, Luigi Maria; Martini, Maurizio] Univ Cattolica Sacro Cuore, Dept Life Sci & Publ Hlth, Largo F Vito 1, Rome 00168, Italy.
   [Cassano, Alessandra; Barone, Carlo; Bria, Emilio; Tortora, Giampaolo] Univ Cattolica Sacro Cuore, Dept Translat Med & Surg, Largo F Vito 1, Rome 00168, Italy.
   [Ricci-Vitiani, Lucia] Ist Super Sanita, Dept Oncol & Mol Med, Viale Regina Elena 299, Rome 00161, Italy.
C3 Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
   Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
   Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
   Istituto Superiore di Sanita (ISS)
RP Martini, M (corresponding author), Fdn Policlin Univ A Gemelli IRCCS, Largo A Gemelli 8, Rome 00168, Italy.; Martini, M (corresponding author), Univ Cattolica Sacro Cuore, Dept Life Sci & Publ Hlth, Largo F Vito 1, Rome 00168, Italy.
EM strefoantonia@gmail.com; alessandra.cocomazzi@libero.it;
   michele.basso@policlinicogemelli.it; tonia.cenci@gmail.com;
   riccardo.ricci@unicatt.it; francesco.pierconti@unicatt.it;
   alessandra.cassano@unicatt.it; vins8966@gmail.com;
   carlo.barone@unicatt.it; emilio.bria@unicatt.it; lriccivitiani@yahoo.it;
   giampaolo.tortora@unicatt.it; luigimaria.larocca@unicatt.it;
   maurizio.martini@unicatt.it
RI Cenci, Tonia/AAC-1372-2019; Martini, Maurizio/AAB-1564-2019; Larocca,
   Luigi Maria/M-9590-2019; Ricci, Riccardo/E-4411-2010; Tortora,
   Giampaolo/HGB-6261-2022; Basso, Michele/J-8607-2018; pierconti,
   francesco/AAC-7223-2022; Fiorentino, Vincenzo/JAX-8692-2023; Ricci
   Vitiani, Lucia/J-8320-2016; Larocca, Luigi Maria/A-1577-2008; Bria,
   Emilio/A-8574-2019
OI Fiorentino, Vincenzo/0000-0002-1132-1761; Ricci Vitiani,
   Lucia/0000-0001-7336-5615; Martini, Maurizio/0000-0002-6260-6310;
   Larocca, Luigi Maria/0000-0003-1739-4758; Tortora,
   Giampaolo/0000-0002-1378-4962; Bria, Emilio/0000-0002-2333-704X;
   Cassano, Alessandra/0009-0008-9392-2851
FU Associazione Italiana Ricerca sul Cancro [AIRC IG 20583]
FX This research was found by Universita Cattolica del Sacro Cuore, Fondi
   d'Ateneo, Linea D1 (M.M., E.B. and L.M.L.) and by the Associazione
   Italiana Ricerca sul Cancro (E.B.; AIRC IG 20583) (2018-2019).
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NR 38
TC 47
Z9 49
U1 1
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2020
VL 12
IS 3
AR 638
DI 10.3390/cancers12030638
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LJ5VG
UT WOS:000530232300114
PM 32164324
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Qi, YN
   Zhao, TT
   Han, MY
AF Qi, Yana
   Zhao, Tingting
   Han, Mingyong
TI The application of radiomics in predicting gene mutations in cancer
SO EUROPEAN RADIOLOGY
LA English
DT Article
DE Radiomics; Gene mutation; Precision medicine; Oncology; Radiological
   imaging
ID CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER; TYROSINE KINASE
   INHIBITORS; CT TEXTURE ANALYSIS; LOWER-GRADE GLIOMAS; MOLECULAR TESTING
   GUIDELINE; BREAST-CANCER; CLEAR-CELL; KRAS MUTATION; PRECISION MEDICINE
AB With the development of genome sequencing, the role of molecular targeted therapy in cancer is becoming increasingly important. However, genetic testing remains expensive, invasive, and time-consuming, and thus unavailable for all patients. Radiogenomics aims to correlate imaging characteristics with gene expression patterns, gene mutations, and other genome-related characteristics. Due to the noninvasive nature of medical imaging, the field of radiogenomics is rapidly developing and may serve as a substitute tool for genetic testing. In this article, we briefly summarise the current role of radiogenomics in predicting gene mutations in brain, lung, colorectal, breast, and kidney tumours.
C1 [Qi, Yana; Zhao, Tingting; Han, Mingyong] Shandong Univ, Shandong Prov Hosp, Cheeloo Coll Med, Canc Therapy & Res Ctr, 324 Jingwuweiqi Rd, Jinan 250021, Shandong, Peoples R China.
C3 Shandong University; Shandong First Medical University & Shandong
   Academy of Medical Sciences
RP Han, MY (corresponding author), Shandong Univ, Shandong Prov Hosp, Cheeloo Coll Med, Canc Therapy & Res Ctr, 324 Jingwuweiqi Rd, Jinan 250021, Shandong, Peoples R China.
EM hanmingyong@sina.com
RI Han, Ming-Yong/ABC-6398-2021
FU National Natural Science Foundation of China [81670046]
FX This study has received funding by the National Natural Science
   Foundation of China (ID: 81670046).
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NR 143
TC 35
Z9 40
U1 3
U2 39
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0938-7994
EI 1432-1084
J9 EUR RADIOL
JI Eur. Radiol.
PD JUN
PY 2022
VL 32
IS 6
BP 4014
EP 4024
DI 10.1007/s00330-021-08520-6
EA JAN 2022
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA 1J9ZO
UT WOS:000745735900001
PM 35048135
DA 2025-01-04
ER

PT J
AU Chen, JX
   Lan, JW
   Ye, ZW
   Duan, SY
   Hu, YK
   Zou, Y
   Zhou, J
AF Chen, Jianxiong
   Lan, Jiawen
   Ye, Zhiwei
   Duan, Shiyu
   Hu, Yukun
   Zou, Ying
   Zhou, Jun
TI Long noncoding RNA LRRC75A-AS1 inhibits cell proliferation and migration
   in colorectal carcinoma
SO EXPERIMENTAL BIOLOGY AND MEDICINE
LA English
DT Article
DE LRRC75A-AS1; colorectal cancer; long noncoding RNA; migration;
   proliferation
ID CANCER; EXPRESSION
AB With the continuous improvement of technology in the molecular field, more and more evidence indicated that long noncoding RNAs (lncRNAs) are widely expressed in a broad spectrum of human tumors, playing an important role in the development and progression of tumors. Most studies reported that lncRNAs might serve as reliable biomarkers and effective clinical therapeutic target. Leucine-rich repeat containing 75 A-antisense RNA1 (LRRC75A-AS1) was reported to be relevant to many types of cancers and indicated to do influence on colorectal carcinoma (CRC). This research firstly examined the role of LRRC75A-AS1 in CRC and analyzed its association with the biological behaviors of CRC cells. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) brought to light that LRRC75A-AS1 was remarkably expressed at low levels in CRC tissues. We also found that LRRC75A-AS1 was localized in the cytoplasm. In addition, LRRC75A-AS1 knockdown also notably promoted CRC cell proliferation, metastasis, invasion, and colony formation. To summarize, these experimental results showed that LRRC75A-AS1 might serve as an anti-oncogene for CRC tumorigenesis and advancement, and it may become a novel molecular marker for clinical diagnosis. Impact statement It is reported that colorectal cancer has seriously threatened human health. The incidence of colorectal cancer in China is increasing year by year. At present, the treatment of cancer is gradually developing towards individualized treatment whose core is targeted therapy, and molecular pathology is the basis of targeted therapy. Previous studies have shown that in addition to protein-coding genes that regulate tumor invasion and metastasis, there are also some non-coding genes involved in tumor encroachment and spread. Our study found that long noncoding RNA LRRC75A-AS1 is closely related to CRC and is related to its proliferation and migration. And it may become a novel molecular marker for clinical diagnosis and treatment.
C1 [Chen, Jianxiong; Lan, Jiawen; Ye, Zhiwei; Duan, Shiyu; Hu, Yukun; Zhou, Jun] Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.
   [Chen, Jianxiong; Lan, Jiawen; Ye, Zhiwei; Duan, Shiyu; Hu, Yukun; Zhou, Jun] Southern Med Univ, Sch Basic Med Sci, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.
   [Duan, Shiyu; Hu, Yukun; Zhou, Jun] Southern Med Univ, Guangdong Prov Key Lab Mol Oncol Pathol, Guangzhou 510515, Guangdong, Peoples R China.
   [Zou, Ying] Guangdong Med Univ, Sch Clin Med 2, Dept Tradit Chinese Med, Sci Res Platform, Dongguan 523808, Peoples R China.
C3 Southern Medical University - China; Southern Medical University -
   China; Southern Medical University - China; Guangdong Medical University
RP Zhou, J (corresponding author), Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.; Zhou, J (corresponding author), Southern Med Univ, Sch Basic Med Sci, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.; Zhou, J (corresponding author), Southern Med Univ, Guangdong Prov Key Lab Mol Oncol Pathol, Guangzhou 510515, Guangdong, Peoples R China.
EM chuhang127@163.com
RI Zou, Ying/KLC-9380-2024
FU Natural Science Foundation of China [81272763, 81672466]; Natural
   Science Foundation of Guangdong Province [2014A030313286,
   2017A030313550]; "Group-type" Special Support Project for Education
   Talents in Universities [G619080438, 4SG19044G]
FX This study was supported by the Natural Science Foundation of China
   (grant no. 81272763 and 81672466), the Natural Science Foundation of
   Guangdong Province (grant no. 2014A030313286 and 2017A030313550) and
   "Group-type" Special Support Project for Education Talents in
   Universities (grant no. G619080438 and 4SG19044G).
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U2 5
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1535-3702
EI 1535-3699
J9 EXP BIOL MED
JI Exp. Biol. Med.
PD OCT
PY 2019
VL 244
IS 14
BP 1137
EP 1143
DI 10.1177/1535370219874339
PG 7
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA JE3BO
UT WOS:000490569100001
PM 31505952
OA Green Published
DA 2025-01-04
ER

PT J
AU Guo, FZ
   Long, L
   Wang, JT
   Wang, YY
   Liu, YY
   Wang, L
   Luo, F
AF Guo, Fengzhu
   Long, Lang
   Wang, Jiantao
   Wang, Yuyi
   Liu, Yanyang
   Wang, Li
   Luo, Feng
TI Insights on CXC chemokine receptor 2 in breast cancer: An emerging
   target for oncotherapy
SO ONCOLOGY LETTERS
LA English
DT Review
DE breast cancer; CXC chemokine receptor 2; interleukin-8; molecular
   mechanism; targeted therapy
ID MESENCHYMAL STEM-CELLS; HOST CXCR2-DEPENDENT REGULATION;
   GROWTH-REGULATED ONCOGENE; MAMMARY-TUMOR GROWTH; NF-KAPPA-B;
   COLON-CANCER; ENDOTHELIAL-CELLS; MELANOMA GROWTH; IN-VITRO;
   INTERLEUKIN-8
AB Breast cancer is the most common malignant neoplasm in women worldwide, and the treatment regimens currently available are far from optimal. Targeted therapy, based on molecular typing of breast cancer, is the most precise form of treatment, and CXC chemokine receptor 2 (CXCR2) is one of the molecular markers used in targeted therapies. As a member of the seven transmembrane G-protein-coupled receptor family, CXCR2 and its associated ligands have been increasingly implicated in tumor-associated processes. These processes include proliferation, angiogenesis, invasion, metastasis, chemoresistance, and stemness and phenotypic maintenance of cancer stem cells. Thus, the inhibition of CXCR2 or its downstream signaling pathways could significantly attenuate tumor progression. Therefore, studies on the biological functions of CXCR2 and its association with neoplasia may help improve the prognosis of breast cancer. Furthermore, the targeting of CXCR2 could supplement the present clinical approaches of breast cancer treatment strategies. The present review discusses the structures and mechanisms of CXCR2 and its ligands. Additionally, the contribution of CXCR2 to the development of breast cancer and its potential therapeutic benefits are also discussed.
C1 [Guo, Fengzhu; Long, Lang; Wang, Jiantao; Wang, Yuyi; Liu, Yanyang; Wang, Li; Luo, Feng] Sichuan Univ, West China Hosp, Lung Canc Ctr, Canc Ctr,State Key Lab Biotherapy, 37 Guoxue Alley, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University
RP Wang, L; Luo, F (corresponding author), Sichuan Univ, West China Hosp, Lung Canc Ctr, Canc Ctr,State Key Lab Biotherapy, 37 Guoxue Alley, Chengdu 610041, Sichuan, Peoples R China.
EM wangli37029192@sina.com; hxluofeng@163.com
RI Liu, Yixuan/JFJ-2820-2023; wang, jiantao/GRS-9485-2022
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NR 116
TC 14
Z9 16
U1 1
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 DEC
PY 2019
VL 18
IS 6
BP 5699
EP 5708
DI 10.3892/ol.2019.10957
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KA1RN
UT WOS:000505576300005
PM 31788042
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kim, KT
   Lee, HW
   Lee, HO
   Song, HJ
   Jeong, DE
   Shin, S
   Kim, H
   Shin, Y
   Nam, DH
   Jeong, BC
   Kirsch, DG
   Joo, KM
   Park, WY
AF Kim, Kyu-Tae
   Lee, Hye Won
   Lee, Hae-Ock
   Song, Hye Jin
   Jeong, Da Eun
   Shin, Sang
   Kim, Hyunho
   Shin, Yoojin
   Nam, Do-Hyun
   Jeong, Byong Chang
   Kirsch, David G.
   Joo, Kyeung Min
   Park, Woong-Yang
TI Application of single-cell RNA sequencing in optimizing a combinatorial
   therapeutic strategy in metastatic renal cell carcinoma
SO GENOME BIOLOGY
LA English
DT Article
DE Single cell analysis; Renal cell carcinoma; Patient-derived xenograft;
   Tumor heterogeneity; Drug response
ID BREAST-CANCER; DRUG-SENSITIVITY; EXPRESSION ANALYSES; COLORECTAL-CANCER;
   TARGETED THERAPY; KINASE-ACTIVITY; GENETIC-BASIS; SRC FAMILY; SEQ DATA;
   TUMOR
AB Background: Intratumoral heterogeneity hampers the success of marker-based anticancer treatment because the targeted therapy may eliminate a specific subpopulation of tumor cells while leaving others unharmed. Accordingly, a rational strategy minimizing survival of the drug-resistant subpopulation is essential to achieve long-term therapeutic efficacy.
   Results: Using single-cell RNA sequencing (RNA-seq), we examine the intratumoral heterogeneity of a pair of primary renal cell carcinoma and its lung metastasis. Activation of drug target pathways demonstrates considerable variability between the primary and metastatic sites, as well as among individual cancer cells within each site. Based on the prediction of multiple drug target pathway activation, we derive a combinatorial regimen co-targeting two mutually exclusive pathways for the metastatic cancer cells. This combinatorial strategy shows significant increase in the treatment efficacy over monotherapy in the experimental validation using patient-derived xenograft platforms in vitro and in vivo.
   Conclusions: Our findings demonstrate the investigational application of single-cell RNA-seq in the design of an anticancer regimen. The approach may overcome intratumoral heterogeneity which hampers the success of precision medicine.
C1 [Kim, Kyu-Tae; Lee, Hae-Ock; Park, Woong-Yang] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Samsung Genome Inst, Seoul, South Korea.
   [Lee, Hye Won] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Inst Future Med, Seoul, South Korea.
   [Lee, Hae-Ock; Park, Woong-Yang] Sungkyunkwan Univ, Sch Med, Dept Mol Cell Biol, Seoul, South Korea.
   [Song, Hye Jin; Joo, Kyeung Min] Sungkyunkwan Univ, Sch Med, Dept Anat, Seoul, South Korea.
   [Song, Hye Jin; Joo, Kyeung Min] Sungkyunkwan Univ, Sch Med, Dept Cell Biol, Seoul, South Korea.
   [Jeong, Da Eun; Shin, Sang; Nam, Do-Hyun; Joo, Kyeung Min; Park, Woong-Yang] Sungkyunkwan Univ, Dept Hlth Sci & Technol, Samsung Adv Inst Hlth Sci & Technol, Seoul, South Korea.
   [Kim, Hyunho; Shin, Yoojin] Korea Univ, Sch Mech Engn, Seoul, South Korea.
   [Nam, Do-Hyun] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Neurosurg, Seoul, South Korea.
   [Jeong, Byong Chang] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Urol, Seoul, South Korea.
   [Kirsch, David G.] Duke Univ, Med Ctr, Dept Pharmacol, Durham, NC 27710 USA.
   [Kirsch, David G.] Duke Univ, Med Ctr, Dept Canc Biol, Durham, NC USA.
   [Kirsch, David G.] Duke Univ, Med Ctr, Dept Radiat Oncol, Durham, NC USA.
C3 Samsung; Sungkyunkwan University (SKKU); Samsung Medical Center;
   Sungkyunkwan University (SKKU); Samsung Medical Center; Sungkyunkwan
   University (SKKU); Sungkyunkwan University (SKKU); Sungkyunkwan
   University (SKKU); Sungkyunkwan University (SKKU); Samsung Medical
   Center; Korea University; Sungkyunkwan University (SKKU); Samsung
   Medical Center; Sungkyunkwan University (SKKU); Samsung Medical Center;
   Duke University; Duke University; Duke University
RP Park, WY (corresponding author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Samsung Genome Inst, Seoul, South Korea.; Park, WY (corresponding author), Sungkyunkwan Univ, Sch Med, Dept Mol Cell Biol, Seoul, South Korea.; Joo, KM (corresponding author), Sungkyunkwan Univ, Sch Med, Dept Anat, Seoul, South Korea.; Joo, KM (corresponding author), Sungkyunkwan Univ, Sch Med, Dept Cell Biol, Seoul, South Korea.; Joo, KM; Park, WY (corresponding author), Sungkyunkwan Univ, Dept Hlth Sci & Technol, Samsung Adv Inst Hlth Sci & Technol, Seoul, South Korea.
EM kmjoo@skku.edu; woongyang.park@samsung.com
RI Kim, Kyu/E-5500-2016; , Do Hyun Nam/C-9656-2011; Kim,
   Hyunho/GQH-5608-2022; Joo, Kyeung/A-1270-2018
OI Park, Woong-Yang/0000-0003-4234-0380
FU Samsung Medical Center and Health Technology R&D Project, Ministry of
   Health Welfare [HI13C2096000013]
FX We thank research fellows in the Samsung Genome Institute for
   experimental assistance and valuable comments on our work. This research
   was supported by the Samsung Medical Center and Health Technology R&D
   Project, Ministry of Health & Welfare (HI13C2096000013).
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NR 70
TC 158
Z9 178
U1 0
U2 34
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1474-760X
J9 GENOME BIOL
JI Genome Biol.
PD APR 29
PY 2016
VL 17
AR 80
DI 10.1186/s13059-016-0945-9
PG 17
WC Biotechnology & Applied Microbiology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA DN7TT
UT WOS:000377282700001
PM 27139883
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Douik, H
   Sahraoui, G
   Jemaà, M
   Doghri, R
   Charfi, L
   Mrad, K
AF Douik, Hayet
   Sahraoui, Ghada
   Jemaa, Mohamed
   Doghri, Raoudha
   Charfi, Lamia
   Mrad, Karima
TI Concurrent NRAS-BRAF variants in metastatic colorectal cancer: a
   Tunisian case report
SO ANTI-CANCER DRUGS
LA English
DT Article
DE BRAF; concomitant mutation; CRC; metastasis; NRAS
ID LIVER METASTASES; MUTATIONS; KRAS
AB Target therapy for metastatic colorectal cancer needs the determination of KRAS, NRAS, and BRAF mutation status to identify patients resistant to anti-EGFR treatment. RAS genes (KRAS/NRAS) are mutated in 40-60% of metastatic colorectal cancer and BRAF in 5-10%. The presence of a double mutation in RAS and BRAF is rare. Therefore, RAS and BRAF mutations were considered exclusive. Herein, we describe a novel concomitant NRAS/BRAF mutation identified in a series of 865 colorectal cancer patients.
C1 [Douik, Hayet; Sahraoui, Ghada; Doghri, Raoudha; Charfi, Lamia; Mrad, Karima] Salah Azaiz Inst, Pathol Dept, Tunis 1006, Tunisia.
   [Douik, Hayet; Jemaa, Mohamed] Tunis El Manar Univ, Human Genet Lab LR99ES10, Fac Med Tunis, Tunis, Tunisia.
   [Sahraoui, Ghada; Doghri, Raoudha; Charfi, Lamia; Mrad, Karima] Salah Azaiz Inst, Precis Med & Oncol Invest Lab LR21SP01, Tunis, Tunisia.
   [Jemaa, Mohamed] Tunis El Manar Univ, Fac Sci Tunis, Dept Biol, Tunis, Tunisia.
C3 Universite de Tunis-El-Manar; Institut Salah Azaiez; Universite de
   Tunis-El-Manar; Faculte de Medecine de Tunis (FMT); Universite de
   Tunis-El-Manar; Institut Salah Azaiez; Universite de Tunis-El-Manar;
   Faculte des Sciences de Tunis (FST)
RP Douik, H (corresponding author), Salah Azaiz Inst, Pathol Dept, Tunis 1006, Tunisia.
EM hayet.douik@rns.tn
RI JEMAA, Mohamed/J-7734-2019; JEMAA, Mohamed/K-3446-2015
OI JEMAA, Mohamed/0000-0003-4905-1020
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NR 18
TC 0
Z9 0
U1 0
U2 1
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 JUN
PY 2024
VL 35
IS 5
BP 462
EP 465
DI 10.1097/CAD.0000000000001586
PG 4
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA SJ0Z1
UT WOS:001233982000012
PM 38451831
DA 2025-01-04
ER

PT J
AU Gargalionis, AN
   Karamouzis, MV
   Adamopoulos, C
   Papavassiliou, AG
AF Gargalionis, Antonios N.
   Karamouzis, Michalis V.
   Adamopoulos, Christos
   Papavassiliou, Athanasios G.
TI Protein trafficking in colorectal carcinogenesis-targeting and bypassing
   resistance to currently applied treatments
SO CARCINOGENESIS
LA English
DT Review
ID GROWTH-FACTOR RECEPTOR; COLON-CANCER CELLS; ANTI-EGFR THERAPY;
   DOWN-REGULATION; E-CADHERIN; C-SRC; MEDIATED ENDOCYTOSIS; TUMOR-GROWTH;
   RAB GTPASES; INTEGRIN
AB Membrane receptors constitute novel targets during current treatment of metastatic colorectal cancer (CRC) due to the fact that their aberrant expression/activity favors cancer cell properties. Protein trafficking is responsible for the correct targeting of membrane receptors to the apical and basolateral surfaces, as well as to the adherent and tight junctions of the cell. Impaired availability or distribution of these receptors along the plasma membrane is not only associated with defective cellular homeostasis and tumor progression, but also to emerging mechanisms of resistance to CRC-targeted therapy. The present review describes how protein trafficking facilitates invasion and metastasis of CRC cells and focuses on receptor tyrosine kinases (RTKs) endocytic transport, providing thoughts for surpassing RTKs-centered mechanisms of resistance.
C1 [Gargalionis, Antonios N.; Karamouzis, Michalis V.; Adamopoulos, Christos; Papavassiliou, Athanasios G.] Univ Athens, Sch Med, Dept Biol Chem, Mol Oncol Unit, GR-11527 Athens, Greece.
C3 National & Kapodistrian University of Athens; Athens Medical School
RP Papavassiliou, AG (corresponding author), Univ Athens, Sch Med, Dept Biol Chem, Mol Oncol Unit, 75 M Asias St, GR-11527 Athens, Greece.
EM papavas@med.uoa.gr
RI Adamopoulos, Christos/JMQ-6589-2023; Koutsilieris,
   Michael/AAD-3648-2019; Gargalionis, Antonios/P-8374-2019
OI Adamopoulos, Christos/0000-0001-6323-4216; Papavassiliou,
   Athanasios/0000-0001-5803-4527
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NR 84
TC 10
Z9 12
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 JUN
PY 2015
VL 36
IS 6
BP 607
EP 615
DI 10.1093/carcin/bgv052
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CK4GK
UT WOS:000356181700001
PM 25863128
OA Bronze
DA 2025-01-04
ER

PT J
AU Sahin, IH
   Tan, E
   Kim, R
AF Sahin, Ibrahim Halil
   Tan, Elaine
   Kim, Richard
TI Regorafenib, an investigational agent for the treatment of
   cholangiocarcinoma
SO EXPERT OPINION ON INVESTIGATIONAL DRUGS
LA English
DT Article
DE Cholangiocarcinoma; biliary tumors; regorafenib; FGFR2; actionable
   genes; TKIs; targeted therapy
ID FOOT SKIN REACTION; PHASE-II; COLORECTAL-CANCER; DOUBLE-BLIND;
   OPEN-LABEL; MULTICENTER; TUMORS; SORAFENIB; EFFICACY; FAILURE
AB Introduction: Cholangiocarcinoma is a prevalent gastrointestinal cancer with a high mortality rate. A limited number of cholangiocarcinoma patients are diagnosed with early-stage disease but unfortunately, most patients present with an advanced-stage disease which is not amenable to curative surgical resection.
   Areas Covered:We discuss regorafenib, a multi-kinase inhibitor, which has been investigated as a therapeutic agent in advanced stage biliary tract cancer patients in phase II trials. We examined the efficacy and toxicity of this agent and its potential in this patient population in the future. We also provide further insights on novel approaches to optimize the efficacy of regorafenib in cholangiocarcinoma patients.
   Expert Opinion: The recent phase II trials of single-agent regorafenib in advanced stage biliary tumors revealed a modest activity in non enriched patient population and is currently part of the national comprehensive cancer network (NCCN) guidelines (Level 2B) in the refractory setting. However, more opportunities for this agent exist in combination approaches with other therapeutics such as immune checkpoint inhibitors. It is also important to recognize that the paradigm has significantly shifted for targeted therapy to more specific and more potent tyrosine kinase inhibitors targeting specific actionable genes.
C1 [Sahin, Ibrahim Halil; Tan, Elaine; Kim, Richard] H Lee Moffitt Canc Ctr & Res Inst, Dept Gastrointestinal Oncol, Tampa, FL USA.
C3 H Lee Moffitt Cancer Center & Research Institute
RP Kim, R (corresponding author), H Lee Moffitt Canc Ctr & Res Inst, Dept Gastrointestinal Med Oncol, Tampa, FL 33136 USA.
EM richard.kim@moffitt.org
RI Şahin, İbrahim/HHY-8303-2022
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NR 54
TC 7
Z9 7
U1 1
U2 8
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1354-3784
EI 1744-7658
J9 EXPERT OPIN INV DRUG
JI Expert Opin. Investig. Drugs
PD APR 3
PY 2021
VL 30
IS 4
SI SI
BP 333
EP 341
DI 10.1080/13543784.2021.1867537
EA DEC 2020
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA RW2YR
UT WOS:000603923500001
PM 33378249
DA 2025-01-04
ER

PT J
AU Ariyawutyakorn, W
   Saichaemchan, S
   Varella-Garcia, M
AF Ariyawutyakorn, Witthawat
   Saichaemchan, Siriwimon
   Varella-Garcia, Marileila
TI Understanding and Targeting MET Signaling in Solid Tumors - Are We There
   Yet?
SO JOURNAL OF CANCER
LA English
DT Review
DE MET; HGF; FISH; IHC; molecular testing; targeted therapy
ID CELL LUNG-CANCER; HEPATOCYTE GROWTH-FACTOR; PAPILLARY RENAL-CARCINOMAS;
   RECEPTOR TYROSINE KINASE; NEGATIVE BREAST-CANCER; METASTATIC
   COLORECTAL-CANCER; RANDOMIZED PHASE-II; GENE COPY NUMBER; NF-KAPPA-B;
   C-MET
AB The MET signaling pathway plays an important role in normal physiology and its deregulation has proved critical for development of numerous solid tumors. Different technologies have been used to investigate the genomic and proteomic status of MET in cancer patients and its association with disease prognosis. Moreover, with the development of targeted therapeutic drugs, there is an urgent need to identify potential biomarkers for selection of patients who are more likely to derive benefit from these agents. Unfortunately, the variety of technical platforms and analysis criteria for diagnosis has brought confusion to the field and a lack of agreement in the evaluation of MET status as a prognostic or predictive marker for targeted therapy agents. We review the molecular mechanisms involved in the deregulation of the MET signaling pathway in solid tumors, the different technologies used for diagnosis, and the main factors that affect the outcome, emphasizing the urge for completing analytical and clinical validation of these tests. We also review the current clinical studies with MET targeted agents, which mostly focus on lung cancer.
C1 [Ariyawutyakorn, Witthawat] Chiang Mai Univ, Fac Med, 110 Intavarorod Rd, Chiang Mai 50200, Thailand.
   [Saichaemchan, Siriwimon] Phramongkutklao Hosp, Dept Med, Div Oncol, 315 Phayathai Rd, Bangkok 10400, Thailand.
   [Saichaemchan, Siriwimon] Coll Med, 315 Phayathai Rd, Bangkok 10400, Thailand.
   [Ariyawutyakorn, Witthawat; Saichaemchan, Siriwimon; Varella-Garcia, Marileila] Univ Colorado, Dept Med, Anschutz Med Campus,12801 East 17th Ave,RC1 South, Aurora, CO 80045 USA.
C3 Chiang Mai University; Phramongkutklao Hospital; University of Colorado
   System; University of Colorado Anschutz Medical Campus
RP Varella-Garcia, M (corresponding author), Univ Colorado, Dept Med, Div Med Oncol, Anschutz Med Campus,12801 East 17th Ave,RC1 South, Aurora, CO 80045 USA.
EM marileila.garcia@ucdenver.edu
FU Thai Society of Clinical Oncology (TSCO); Phramongkutklao Hospital; NCI
   grant Colorado Lung Cancer SPORE [P50CA058187]; NCI grant CCSG
   [P30CA046934]
FX The authors acknowledge the Thai Society of Clinical Oncology (TSCO) for
   a fellowship to Witthawat Ariyawutyakorn, the Phramongkutklao Hospital
   for a fellowship to Siriwimon Saichamchan, and the support from NCI
   grants Colorado Lung Cancer SPORE (P50CA058187) and CCSG (P30CA046934)
   to Marileila Varella-Garcia.
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NR 119
TC 29
Z9 34
U1 0
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 2016
VL 7
IS 6
BP 633
EP 649
DI 10.7150/jca.12663
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DI3ZP
UT WOS:000373440000003
PM 27076844
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Larsson, K
   Jakobsson, PJ
AF Larsson, Karin
   Jakobsson, Per-Johan
TI Inhibition of microsomal prostaglandin E synthase-1 as targeted therapy
   in cancer treatment
SO PROSTAGLANDINS & OTHER LIPID MEDIATORS
LA English
DT Article
DE Prostaglandin E-2; Microsomal prostaglandin E synthase-1; Targeted
   therapy; Cancer treatment
ID LOW-DOSE ASPIRIN; GENETIC DELETION; COLON CARCINOGENESIS; MPGES-1
   INHIBITOR; E-2 SYNTHASE; TUMOR-GROWTH; IN-VIVO; PROSTATE;
   CHEMOPREVENTION; IDENTIFICATION
AB The bioactive lipid prostaglandin E-2 (PGE(2)) is involved in several steps of carcinogenesis in some of the most common cancers, e.g. colon cancer, lung cancer, prostate cancer and breast cancer. Non-steroidal anti-inflammatory drugs (NSAIDs) that target cyclooxygenase (COX) activity, the first step of the PGE2 biosynthesis, has been found to reduce the incidence of colon cancer. Due to severe adverse effects on the gastrointestinal tract and the cardiovascular system, their use as chemopreventing agent has been hampered. Genetic deletion of microsomal prostaglandin E synthase-1 (mPGES-1), the enzyme responsible for the second step of the PGE(2) biosynthesis, has resulted in reduced tumor progression in mouse models of colon cancer. Inhibition of mPGES-1 would potentially be beneficial to a great number of patients without the side effects associated with long-term treatment with traditional NSAIDs. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Larsson, Karin; Jakobsson, Per-Johan] Karolinska Inst, Dept Med, SE-17176 Stockholm, Sweden.
C3 Karolinska Institutet
RP Jakobsson, PJ (corresponding author), Karolinska Inst, Dept Med, SE-17176 Stockholm, Sweden.
EM per-johan.jakobsson@ki.se
RI Jakobsson, Per-Johan/ABC-5594-2021; Larsson, Karin/AAO-7701-2021
OI Jakobson, Per-Johan/0000-0001-7665-9715; Larsson,
   Karin/0000-0002-6403-2736
FU Swedish Childhood Cancer Foundation; Swedish Research Council; Swedish
   Rheumatism Association; King Gustaf V 80 years Foundation; Karolinska
   Institutet Foundation; Stockholm County Council
FX This study was supported by The Swedish Childhood Cancer Foundation, The
   Swedish Research Council, The Swedish Rheumatism Association, King
   Gustaf V 80 years Foundation, Karolinska Institutet Foundation and The
   Stockholm County Council.
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NR 62
TC 27
Z9 34
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1098-8823
EI 2212-196X
J9 PROSTAG OTH LIPID M
JI Prostaglandins Other Lipid Mediat.
PD JUL
PY 2015
VL 120
SI SI
BP 161
EP 165
DI 10.1016/j.prostaglandins.2015.06.002
PG 5
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA CS5UB
UT WOS:000362142700021
PM 26100239
DA 2025-01-04
ER

PT J
AU Yang, P
   Rui, Q
   Xu, ZP
   Chen, T
   He, ZY
AF Yang, Peng
   Rui, Qiang
   Xu, Zi-Peng
   Chen, Tao
   He, Zhen-Yu
TI Long non-coding RNA AK021444 correlates with poor prognosis and promotes
   cell proliferation in colorectal cancer
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
LA English
DT Article
DE LncRNA-AK021444; colorectal cancer; in situ hybridization
ID HIGH EXPRESSION; METASTASIS; MALAT-1
AB Long non-coding RNAs (lncRNAs) are aberrantly expressed in many diseases including cancer. Our previous studies suggested that lncRNA-AK021444 specificity expressed in Metastatic lymph node of colorectal cancer. However, the relationship between the clinical parameters and molecular mechanism of lncRNA-AK021444 in colorectal cancer (CRC) remain largely unknown. In the present study, we found that lncRNA-AK021444 was significantly related with CRC tumor size, lymph node metastasis, and increased death using in situ hybridization (ISH) method of 90 paired CRC specimens. Lentiviral vector-mediated lncRNA-AK021444 overexpression was employed in CRC cell line HCT116. Our study demonstrated that lncRNA-AK021444 overexpression regulated cell proliferation and apoptosis of CRC, which might be meaningful with regards to target therapy in CRC.
C1 [Yang, Peng; Rui, Qiang; Xu, Zi-Peng; Chen, Tao; He, Zhen-Yu] Nanjing Med Univ, Clin Med Coll 2, Nanjing, Jiangsu, Peoples R China.
   [He, Zhen-Yu] Nanjing Med Univ, Affiliated Hosp 2, Dept Gen Surg, 121 Jiangjiayuan Rd, Nanjing 210011, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University
RP He, ZY (corresponding author), Nanjing Med Univ, Affiliated Hosp 2, Dept Gen Surg, 121 Jiangjiayuan Rd, Nanjing 210011, Jiangsu, Peoples R China.
EM hezhenyu1968@126.com
RI xu, zipeng/GQP-9049-2022
FU Natural Science Foundation Project of Jiangsu Province [BK20-12872];
   Science and Technology Projects, Health Department of Jiangsu Province
   [H20-1207]; Research Innovation Program for College Graduates of Jiangsu
   Province [SJLX15_0427]
FX This work was supported by Natural Science Foundation Project of Jiangsu
   Province (BK20-12872), the Science and Technology Projects, Health
   Department of Jiangsu Province (H20-1207) and the Research Innovation
   Program for College Graduates of Jiangsu Province (SJLX15_0427).
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NR 18
TC 0
Z9 0
U1 0
U2 2
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1940-5901
J9 INT J CLIN EXP MED
JI Int. J. Clin. Exp. Med.
PY 2016
VL 9
IS 2
BP 3033
EP 3040
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA DK1EL
UT WOS:000374655200285
DA 2025-01-04
ER

PT J
AU Garmpis, N
   Damaskos, C
   Garmpi, A
   Nonni, A
   Georgakopoulou, VE
   Antoniou, E
   Schizas, D
   Sarantis, P
   Patsouras, A
   Syllaios, A
   Vallilas, C
   Koustas, E
   Kontzoglou, K
   Trakas, N
   Dimitroulis, D
AF Garmpis, Nikolaos
   Damaskos, Christos
   Garmpi, Anna
   Nonni, Afroditi
   Georgakopoulou, Vasiliki E.
   Antoniou, Efstathios
   Schizas, Dimitrios
   Sarantis, Panagiotis
   Patsouras, Alexandros
   Syllaios, Athanasios
   Vallilas, Christos
   Koustas, Evangelos
   Kontzoglou, Konstantinos
   Trakas, Nikolaos
   Dimitroulis, Dimitrios
TI Histone Deacetylases and their Inhibitors in Colorectal Cancer Therapy:
   Current Evidence and Future Considerations
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Histone; deacetylase; inhibitors; HDAC; HDACI; colorectal cancer;
   targeted therapy; epigenetics
ID ISLAND METHYLATOR PHENOTYPE; THYMIDYLATE SYNTHASE GENE; NEGATIVE
   BREAST-CANCER; CELL LUNG-CANCER; PHASE-I; HDAC INHIBITORS; VALPROIC
   ACID; PROTEASOME INHIBITORS; CIGARETTE-SMOKING; UP-REGULATION
AB Colorectal cancer (CRC) comprises a heterogeneous group of gastrointestinal tract tumors. It is a multifactorial disease, and a plethora of distinct factors are involved in its pathogenesis and pathophysiology. The development of CRC is not limited to genetic changes, but epigenetic and environmental factors are also involved. Among the epigenetic factors, histone deacetylases (HDACs), a group of epigenetic enzymes that regulate gene expression, have been reported to be over-expressed in CRC. HDACs and their inhibitors seem to play an important role in the molecular pathophysiology of CRC. The aim of this review was to define the role of HDAC inhibitors as potential anticancer agents against CRC.
C1 [Garmpis, Nikolaos; Antoniou, Efstathios; Kontzoglou, Konstantinos; Dimitroulis, Dimitrios] Natl & Kapodistrian Univ Athens, Laiko Gen Hosp, Med Sch, Dept Propedeut Surg 2, Athens, Greece.
   [Garmpis, Nikolaos; Damaskos, Christos; Antoniou, Efstathios; Patsouras, Alexandros; Kontzoglou, Konstantinos] Natl & Kapodistrian Univ Athens, Med Sch, NS Christeas Lab Expt Surg & Surg Res, Athens, Greece.
   [Damaskos, Christos] Laikon Gen Hosp, Renal Transplantat Unit, Athens, Greece.
   [Garmpi, Anna] Natl & Kapodistrian Univ Athens, Laiko Gen Hosp, Med Sch, Dept Propedeut Internal Med 1, Athens, Greece.
   [Nonni, Afroditi] Natl & Kapodistrian Univ Athens, Med Sch, Dept Pathol 1, Athens, Greece.
   [Georgakopoulou, Vasiliki E.] Laikon Gen Hosp, Dept Pulmonol, Athens, Greece.
   [Schizas, Dimitrios; Syllaios, Athanasios] Natl & Kapodistrian Univ Athens, Laiko Gen Hosp, Med Sch, Dept Surg 1, Athens, Greece.
   [Sarantis, Panagiotis; Vallilas, Christos; Koustas, Evangelos] Natl & Kapodistrian Univ Athens, Med Sch, Dept Biol Chem, Mol Oncol Unit, Athens, Greece.
   [Trakas, Nikolaos] Sismanogleio Hosp, Dept Biochem, Athens, Greece.
C3 Laiko General Hospital; National & Kapodistrian University of Athens;
   National & Kapodistrian University of Athens; Laiko General Hospital;
   Laiko General Hospital; National & Kapodistrian University of Athens;
   National & Kapodistrian University of Athens; Laiko General Hospital;
   Laiko General Hospital; National & Kapodistrian University of Athens;
   National & Kapodistrian University of Athens
RP Garmpis, N (corresponding author), Natl & Kapodistrian Univ Athens, Laiko Gen Hosp, Med Sch, Dept Propedeut Surg 2, Athens, Greece.; Damaskos, C (corresponding author), Natl & Kapodistrian Univ Athens, Med Sch, NS Christeas Lab Expt Surg & Surg Res, Athens, Greece.; Garmpi, A (corresponding author), Natl & Kapodistrian Univ Athens, Laiko Gen Hosp, Med Sch, Dept Propedeut Internal Med 1, Athens, Greece.
EM nikosg22@hotmail.com; x_damaskos@yahoo.gr; annagar@windowslive.com
RI SCHIZAS, DIMITRIOS/Z-3323-2019; Sarantis, Panagiotis/AAF-4774-2021;
   Georgakopoulou, Vasiliki/AAF-6885-2021
OI Damaskos, Christos/0000-0002-5454-2564; Syllaios,
   Athanasios/0000-0002-5053-0953
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NR 118
TC 12
Z9 12
U1 2
U2 10
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PY 2022
VL 29
IS 17
BP 2979
EP 2994
DI 10.2174/0929867328666210915105929
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 2U8TC
UT WOS:000823426200003
PM 34525905
DA 2025-01-04
ER

PT J
AU Cao, MN
   Chen, KT
   Li, QF
   Wang, L
   Jin, GW
   Na, RTY
   Ma, J
   Liu, YT
   Gao, JL
AF Cao, Mei-na
   Chen, Kai-ting
   Li, Quan-fu
   Wang, Li
   Jin, Gao-wa
   Na, Ren-tuya
   Ma, Jing
   Liu, Yu-ting
   Gao, Jin-liang
TI Development of BRAF V600E Mutation in NRAS Q61L Mutated Rectal Cancer
SO ANNALS OF CLINICAL AND LABORATORY SCIENCE
LA English
DT Article
DE BRAF; NRAS; concomitant mutation; colorectal cancer
ID METASTATIC COLORECTAL-CANCER; MOLECULAR-SPECTRUM; KRAS; PIK3CA; GENE;
   FREQUENCY
AB BRAF and NRAS are oncogenes in the RAS/RAF/MEK/MAP-kinase signaling pathway. Coexistent mutations of BRAF and NRAS in a single colorectal cancer patient have always been considered mutually exclusive or at least rare. The clinical outcome of these patients remains undetermined. Herein we report a 53-year-old man harboring an NRAS Q61L mutation in his primary rectal carcinoma, who presented with a concomitant mutation of BRAF V600E in his liver metastasis biopsy 55 months after the primary CRC surgical resection. Our findings suggest that a BRAF and NRAS developed co-mutation may lead to a distinct clinicopathological progression. BRAF-mutated CRCwill not benefit from anti-RAS targeted therapy.
C1 [Cao, Mei-na; Chen, Kai-ting; Liu, Yu-ting; Gao, Jin-liang] Ordos Cent Hosp, Lab Mol Med, Sudu Rd, Ordos 017000, Peoples R China.
   [Li, Quan-fu; Jin, Gao-wa] Ordos Cent Hosp, Dept Med Oncol, Ordos, Peoples R China.
   [Wang, Li; Na, Ren-tuya] Ordos Cent Hosp, Dept Pathol, Ordos, Peoples R China.
   [Ma, Jing; Gao, Jin-liang] Baotou Med Coll, Sch Publ Hlth, Baotou, Peoples R China.
C3 Baotou Medical College
RP Gao, JL (corresponding author), Ordos Cent Hosp, Lab Mol Med, Sudu Rd, Ordos 017000, Peoples R China.
EM golden_bright@hotmail.com
RI Gao, Jinliang/LRB-6330-2024
FU Program for Entrepreneurial and Innovative Talent Team of Ordos, China;
   Natural Science Foundation of Inner Mongolia Autonomous Region of China
   [2016MS08113]; National Natural Science Foundation of China (NSFC)
   [81760375]
FX This work was supported financially by the Program for Entrepreneurial
   and Innovative Talent Team of Ordos, China (2016), the Natural Science
   Foundation of Inner Mongolia Autonomous Region of China (Contract No.
   2016MS08113), and the National Natural Science Foundation of China
   (NSFC; Contract No. 81760375).
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NR 26
TC 2
Z9 2
U1 0
U2 3
PU ASSOC CLINICAL SCIENTISTS
PI MIDDLEBURY
PA PO BOX 1287, MIDDLEBURY, VT 05753 USA
SN 0091-7370
EI 1550-8080
J9 ANN CLIN LAB SCI
JI Ann. Clin. Lab. Sci.
PD MAR-APR
PY 2021
VL 51
IS 2
BP 262
EP 266
PG 5
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA SW8TI
UT WOS:000664786900016
PM 33941568
DA 2025-01-04
ER

PT J
AU Chen, SY
   Gu, J
   Wu, KC
   Zhao, XD
   Lu, YY
AF Chen, Shuyi
   Gu, Jing
   Wu, Kaichun
   Zhao, Xiaodi
   Lu, Yuanyuan
TI Progress in clinical diagnosis and treatment of colorectal cancer with
   rare genetic variants
SO CANCER BIOLOGY & MEDICINE
LA English
DT Article
DE KEYWORDS Genetic variation; gene mutation; gene amplification; gene
   rearrangement; targeted therapy; metastatic CRC (mCRC) therapy.
ID OPEN-LABEL; PLUS CETUXIMAB; SOLID TUMORS; ALK FUSION; ENTRECTINIB;
   MULTICENTER; MUTATIONS; IDENTIFICATION; REARRANGEMENT; TRASTUZUMAB
AB Targeted therapy is crucial for advanced colorectal cancer (CRC) positive for genetic drivers. With advances in deep sequencing technology and new targeted drugs, existing standard molecular pathological detection systems and therapeutic strategies can no longer meet the requirements for careful management of patients with advanced CRC. Thus, rare genetic variations require diagnosis and targeted therapy in clinical practice. Rare gene mutations, amplifications, and rearrangements are usually associated with poor prognosis and poor response to conventional therapy. This review summarizes the clinical diagnosis and treatment of rare genetic variations, in genes including erb-b2 receptor tyrosine kinase 2 (ERBB2), B-Raf proto-oncogene, serine/threonine kinase (BRAF), ALK receptor tyrosine kinase/ROS proto-oncogene 1, receptor tyrosine kinase (ALK/ROS1), neurotrophic receptor tyrosine kinases (NTRKs), ret proto-oncogene (RET), fibroblast growth factor receptor 2 (FGFR2), and epidermal growth factor receptor (EGFR), to enhance understanding and identify more accurate personalized treatments for patients with rare genetic variations.
C1 [Chen, Shuyi; Wu, Kaichun; Zhao, Xiaodi; Lu, Yuanyuan] Fourth Mil Med Univ, Xijing Hosp Digest Dis, State Key Lab Holist Integrat Management Gastroi, Xian 710032, Peoples R China.
   [Chen, Shuyi; Wu, Kaichun; Zhao, Xiaodi; Lu, Yuanyuan] Fourth Mil Med Univ, Xijing Hosp Digest Dis, Natl Clin Res Ctr Digest Dis, Xian 710032, Peoples R China.
   [Chen, Shuyi; Gu, Jing] Fourth Mil Med Univ, Sch Basic Med Sci, Xian 710032, Peoples R China.
C3 Air Force Military Medical University; Air Force Military Medical
   University; Air Force Military Medical University
RP Zhao, XD; Lu, YY (corresponding author), Fourth Mil Med Univ, Xijing Hosp Digest Dis, State Key Lab Holist Integrat Management Gastroi, Xian 710032, Peoples R China.; Zhao, XD; Lu, YY (corresponding author), Fourth Mil Med Univ, Xijing Hosp Digest Dis, Natl Clin Res Ctr Digest Dis, Xian 710032, Peoples R China.
EM leedyzhao@fmmu.edu.cn; luyuandreamer@aliyun.com
RI zhao, xd/HJX-9525-2023
OI Zhao, Xiaodi/0000-0002-1817-803X; Lu, Yuanyuan/0000-0003-0194-8074
FU National Natural Science Foundation of China [82073197, 82273142,
   82222058]
FX This work was supported by the National Natural Science Foundation of
   China (Grant Nos. 82073197, 82273142, and 82222058) .
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NR 87
TC 1
Z9 1
U1 1
U2 1
PU CHINA ANTI-CANCER ASSOC
PI TIANJIN
PA TIANJIN MEDICAL UNIV, CANCER INST & HOSPITAL  TI-YUAN-BEI, HUANHU XI LU,
   HEXIQU, TIANJIN, 300060, PEOPLES R CHINA
SN 2095-3941
J9 CANCER BIOL MED
JI Cancer Biol. Med.
PD JUN 15
PY 2024
VL 21
IS 6
BP 473
EP 483
DI 10.20892/j.issn.2095-3941.2024.0026
PG 11
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA XA3H8
UT WOS:001258917000003
PM 38940668
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Weng, WH
   Feng, JL
   Qin, HL
   Ma, YL
AF Weng, Wenhao
   Feng, Junlan
   Qin, Huanlong
   Ma, Yanlei
TI Molecular therapy of colorectal cancer: Progress and future directions
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Review
DE colorectal cancer; molecular therapy; progress
ID NF-KAPPA-B; GROWTH-FACTOR RECEPTOR; NONSTEROIDAL ANTIINFLAMMATORY DRUGS;
   BETA-CATENIN EXPRESSION; PHASE-II TRIAL; COLON-CANCER; TARGETED THERAPY;
   ENDOGENOUS INHIBITORS; MONOCLONAL-ANTIBODIES; RANDOMIZED-TRIALS
AB Colorectal cancer (CRC) remains one of the most common types of cancer and leading causes of cancer death worldwide. Although the introduction of cytotoxic drugs such as oxaliplatin, irinotecan and fluorouracil has improved the treatment of advanced CRC, the individual response to chemoradiotherapy varies tremendously from one patient to another. However, recent progress in CRC molecular therapies may provide new insight into the treatment of this disease. Currently, components of the EGFR, VEGF, Wnt and NF-kB pathways are the most important targets for CRC therapy. This review chronicles the development of molecular CRC therapies over the past few decades. We also provide an update on the current progress of research concerning the molecular pathways leading to CRC and discuss the possible implications for CRC therapy.
C1 [Weng, Wenhao] Tongji Univ, Dept Clin Lab, Shanghai Peoples Hosp 10, Shanghai 200072, Peoples R China.
   [Feng, Junlan] Shanghai Jiao Tong Univ, Peoples Hosp 6, Dept Surg, Shanghai 200030, Peoples R China.
   [Qin, Huanlong; Ma, Yanlei] Tongji Univ, Dept GI Surg, Shanghai Peoples Hosp 10, Shanghai 200072, Peoples R China.
C3 Tongji University; Shanghai Jiao Tong University; Tongji University
RP Ma, YL (corresponding author), Tongji Univ, Dept GI Surg, Shanghai Peoples Hosp 10, 301 Yanchang Rd, Shanghai 200072, Peoples R China.
EM yanleima@live.cn
RI huanlong, Qin/B-3844-2015
FU National Natural Science Foundation of China [81372615]; Shanghai
   Science and Technology Development Fund [12140902300, 12410707400];
   Shanghai Health System Outstanding Young Talent Training Plan
   [XYQ2013118]
FX Grant sponsor: National Natural Science Foundation of China; Grant
   number: 81372615; Grant sponsor: Shanghai Science and Technology
   Development Fund; Grant number: 12140902300 and 12410707400; Grant
   sponsor: Shanghai Health System Outstanding Young Talent Training Plan;
   Grant numbers: XYQ2013118
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NR 111
TC 58
Z9 61
U1 2
U2 133
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 FEB 15
PY 2015
VL 136
IS 3
BP 493
EP 502
DI 10.1002/ijc.28722
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AT2XD
UT WOS:000344796700001
PM 24420815
DA 2025-01-04
ER

PT J
AU Zhang, X
   Luo, MP
   Zhang, JH
   Guo, BZ
   Singh, S
   Lin, XX
   Xiong, HC
   Ju, SW
   Wang, LB
   Zhou, YL
   Zhou, JC
AF Zhang, Xun
   Luo, Mingpeng
   Zhang, Jiahang
   Guo, Bize
   Singh, Shreya
   Lin, Xixi
   Xiong, Hanchu
   Ju, Siwei
   Wang, Linbo
   Zhou, Yulu
   Zhou, Jichun
TI The role of lncRNA H19 in tumorigenesis and drug resistance of human
   Cancers
SO FRONTIERS IN GENETICS
LA English
DT Review
DE lncRNA H19; drug resistance; tumorigenesis; miRNA; chemotherapy;
   endocrine therapy; targeted therapy
ID LONG NONCODING RNA; CELL LUNG-CANCER; MCF-7 BREAST-CANCER;
   COLORECTAL-CANCER; SIGNALING PATHWAY; GENE-EXPRESSION; DOWN-REGULATION;
   OVARIAN-CANCER; CHEMOTHERAPY RESISTANCE; DOXORUBICIN RESISTANCE
AB Systemic therapy is one of the most significant cancer treatments. However, drug resistance often appears and has become the primary cause of cancer therapy failure. Regulation of drug target, drug metabolism and drug efflux, cell death escape (apoptosis, autophagy, et al.), epigenetic changes, and many other variables are complicatedly involved in the mechanisms of drug resistance. In various types of cancers, long non-coding RNA H19 (lncRNA H19) has been shown to play critical roles in tumor development, proliferation, metastasis, and multiple drug resistance as well. The efficacy of chemotherapy, endocrine therapy, and targeted therapy are all influenced by the expression of H19, especially in breast cancer, liver cancer, lung cancer and colorectal cancer. Here, we summarize the relationship between lncRNA H19 and tumorigenesis, and illustrate the drug resistance mechanisms caused by lncRNA H19 as well. This review may provide more therapeutic potential targets for future cancer treatments.
C1 [Zhang, Xun; Zhang, Jiahang; Lin, Xixi; Ju, Siwei; Wang, Linbo; Zhou, Yulu; Zhou, Jichun] Zhejiang Univ, Sir Run Run Shaw Affiliated Hosp, Dept Surg Oncol, Hangzhou, Peoples R China.
   [Zhang, Xun; Zhang, Jiahang; Lin, Xixi; Ju, Siwei; Wang, Linbo; Zhou, Yulu; Zhou, Jichun] Minist Educ, Key Lab Canc Prevent & Intervent, Hangzhou, Peoples R China.
   [Zhang, Xun; Zhang, Jiahang; Guo, Bize; Singh, Shreya; Lin, Xixi; Xiong, Hanchu; Ju, Siwei] Zhejiang Univ, Sch Med, Hangzhou, Peoples R China.
   [Luo, Mingpeng] Zhejiang Chinese Med Univ, Affiliated Hosp 1, Hangzhou, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang Chinese Medical
   University
RP Wang, LB; Zhou, YL; Zhou, JC (corresponding author), Zhejiang Univ, Sir Run Run Shaw Affiliated Hosp, Dept Surg Oncol, Hangzhou, Peoples R China.; Wang, LB; Zhou, YL; Zhou, JC (corresponding author), Minist Educ, Key Lab Canc Prevent & Intervent, Hangzhou, Peoples R China.
EM linbowang@zju.edu.cn; 11618390@zju.edu.cn; jichun-zhou@zju.edu.cn
RI lin, xi/GZL-4959-2022; LIN, WANG/JWA-3182-2024; Zhou, Jichun/F-3585-2011
OI Zhou, Jichun/0000-0002-0727-4034; Singh, Shreya/0000-0002-9524-9516
FU National Natural Science Foundation of China; Zhejiang Provincial
   Natural Science Foundation of China; Zhejiang Provincial Medical and
   Health Science and Technology (Youth Talent Program); Zheng Shu Medical
   Elite Scholarship Fund;  [81672729];  [81972597];  [81602471]; 
   [81972453];  [LY19H160059];  [LR22H160011];  [LY19H160055];  [2021RC016]
FX Funding This work was supported by the National Natural Science
   Foundation of China (No. 81672729, No. 81972597, No. 81602471, and No.
   81972453), Zhejiang Provincial Natural Science Foundation of China
   (Grant LY19H160059, LR22H160011, and LY19H160055), Zhejiang Provincial
   Medical and Health Science and Technology (Youth Talent Program) (Grant
   No. 2021RC016) and Zheng Shu Medical Elite Scholarship Fund.
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NR 161
TC 19
Z9 19
U1 2
U2 24
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD SEP 27
PY 2022
VL 13
AR 1005522
DI 10.3389/fgene.2022.1005522
PG 19
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 5I3SA
UT WOS:000868279500001
PM 36246634
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wu, BR
   Gan, ZH
   Tao, SC
   Wang, Q
   Song, YC
   Zhong, H
   Hu, F
AF Wu, Biru
   Gan, Zhuoheng
   Tao, Shengchang
   Wang, Qiang
   Song, Yuchen
   Zhong, Hua
   Hu, Fang
TI Dextran-Cholesterol Carrier Encapsulated Efficient Photosensitizer for
   the Photodynamic Killing of Cancer Cells
SO MOLECULES
LA English
DT Article
DE PDT; dextran; heavy atom
ID POLYSACCHARIDE; NANOPARTICLES; DELIVERY; SUBSTITUTION; PACLITAXEL
AB Selective photodynamic therapy (PDT) for cancer cells is more efficient and much safer. Most selective PDTs are realized by antigene-biomarker or peptide-biomarker interactions. Here, we modified dextran with hydrophobic cholesterol as a photosensitizer carrier to selectively target cancer cells, including colon cancer cells, and fulfilled selective PDT. The photosensitizer was designed with regular Aggregation-Induced Emission (AIE) units, including triphenylamine and 2-(3-cyano-4,5,5-trimethylfuran-2-ylidene)propanedinitrile. The AIE units can help to decrease the quenching effect in the aggregate state. The efficiency of the photosensitizer is further improved via the heavy atom effect after bromination modification. We found that the obtained photosensitizer nanoparticles could selectively target and ablate cancer cells after encapsulation into the dextran-cholesterol carrier. This study indicates that the polysaccharide-based carrier may have potential for cancer-targeting therapy beyond expectations.
C1 [Wu, Biru; Gan, Zhuoheng; Wang, Qiang; Song, Yuchen; Hu, Fang] Southern Med Univ, Biomat Res Ctr, Sch Biomed Engn, Guangzhou 510515, Peoples R China.
   [Tao, Shengchang] Southern Med Univ, Affiliated Dongguan Hosp, Dept Pharm, Dongguan 523059, Peoples R China.
   [Zhong, Hua] Southern Med Univ, Affiliated Hosp 5, Dept Orthopaed, Guangzhou 510900, Peoples R China.
   [Hu, Fang] Southern Med Univ, Zhujiang Hosp, Div Lab Med, Guangzhou 510282, Peoples R China.
C3 Southern Medical University - China; Southern Medical University -
   China; Southern Medical University - China; Southern Medical University
   - China
RP Hu, F (corresponding author), Southern Med Univ, Biomat Res Ctr, Sch Biomed Engn, Guangzhou 510515, Peoples R China.; Zhong, H (corresponding author), Southern Med Univ, Affiliated Hosp 5, Dept Orthopaed, Guangzhou 510900, Peoples R China.; Hu, F (corresponding author), Southern Med Univ, Zhujiang Hosp, Div Lab Med, Guangzhou 510282, Peoples R China.
EM zhong8099@163.com; hufang19@smu.edu.cn
RI Wu, Biru/KIA-3277-2024; Zhong, Hua/ACZ-5569-2022; Song,
   Yuchen/AAK-6951-2021; Hu, Fang/JPL-9115-2023
OI Hu, Fang/0000-0001-5062-0716; Wu, Biru/0000-0001-8506-8343
FU National Natural Science Foundation of China [22077060, 22205097]
FX This research was funded by the National Natural Science Foundation of
   China, grant number 22077060, 22205097.
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TC 0
Z9 0
U1 2
U2 20
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD MAY 28
PY 2023
VL 28
IS 11
AR 4404
DI 10.3390/molecules28114404
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA I5XG9
UT WOS:001003504600001
PM 37298877
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Li, RR
   Shen, JL
   Xu, YH
AF Li, Rongrong
   Shen, Jilu
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TI <i>Fusobacterium nucleatum</i> and Colorectal Cancer
SO INFECTION AND DRUG RESISTANCE
LA English
DT Review
DE Fusobacterium nucleatum; colorectal cancer; gut microbiome; mechanisms;
   biomarker
ID POTENTIATES INTESTINAL TUMORIGENESIS; ASSOCIATION; TUMORS; INFECTION;
   CATENIN; BINDING; CELLS; MICE
AB Fusobacterium nucleatum (F.n) is an oral anaerobic gram-negative bacillus that can colonize into the colon tissues through bloodstream infection. F.n have been found to be involved in both the occurrence and metastasis of colorectal cancer (CRC) through regulating immune response, virulence factor, oncogenic microRNAs, intestinal metabolites, DNA damage and other mechanisms. Therefore, F.n can be as an important pathogenic risk factor and a possible biomarker of CRC. Based on this, we have summarized the potential relationship between F.n and CRC to provide reference for the targeted therapy of CRC.
C1 [Li, Rongrong; Xu, Yuanhong] Anhui Med Univ, Affiliated Hosp 1, Dept Clin Lab, Hefei 230022, Peoples R China.
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C3 Anhui Medical University; Anhui Medical University
RP Xu, YH (corresponding author), Anhui Med Univ, Affiliated Hosp 1, Dept Clin Lab, Hefei 230022, Peoples R China.
EM 2073978993@qq.com
OI Yuanhong, Xu/0000-0002-1637-3800
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TC 21
Z9 22
U1 3
U2 26
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6973
J9 INFECT DRUG RESIST
JI Infect. Drug Resistance
PY 2022
VL 15
BP 1115
EP 1120
DI 10.2147/IDR.S357922
PG 6
WC Infectious Diseases; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Infectious Diseases; Pharmacology & Pharmacy
GA ZZ6AQ
UT WOS:000773349600001
PM 35321079
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yu, Y
   Jia, H
   Zhang, TS
   Zhang, W
AF Yu, Yue
   Jia, Hang
   Zhang, Tianshuai
   Zhang, Wei
TI Advances in DNA damage response inhibitors in colorectal cancer therapy
SO ACTA BIOCHIMICA ET BIOPHYSICA SINICA
LA English
DT Review
DE DNA damage response; colorectal cancer; targeted therapy; DDR inhibitor
ID STRAND BREAK REPAIR; GENOMIC INSTABILITY; REPLICATION STRESS; PHASE-I;
   ATR; OLAPARIB; COMBINATION; RADIATION; TUMORS; ACTIVATION
AB One potential cause of cancer is genomic instability that arises in normal cells due to years of DNA damage in the body. The clinical application of radiotherapy and cytotoxic drugs to treat cancer is based on the principle of damaging the DNA of cancer cells. However, the benefits of these treatments also have negative effects on normal tissue. While there have been notable advancements in molecular-driven therapy and immunotherapy for colorectal cancer (CRC), a considerable portion of patients with advanced CRC do not experience any benefits from these treatments, leading to a poor prognosis. In recent years, targeted therapy aimed at suppressing the DNA damage response (DDR) in cancer cells has emerged as a potential treatment option for CRC patients, offering them more choices for treatment. Currently, the integration of DDR and clinical intervention remains in the exploratory phase. This review primarily elucidates the fundamental principles of DDR inhibitors, provides an overview of their current clinical application status in CRC, and discusses the advancements as well as limitations observed in relevant studies.
C1 [Yu, Yue; Jia, Hang; Zhang, Tianshuai; Zhang, Wei] Naval Med Univ, Affiliated Hosp 1, Dept Colorectal Surg, Shanghai 200433, Peoples R China.
C3 Naval Medical University
RP Zhang, W (corresponding author), Naval Med Univ, Affiliated Hosp 1, Dept Colorectal Surg, Shanghai 200433, Peoples R China.
EM weizhang2000cn@163.com
FU National Natural Science Foundation of China [82072750]; Natural Science
   Foundation of Shanghai Municipality [20ZR1457200]
FX This work was supported by the grants from the National Natural Science
   Foundation of China (No. 82072750), and the Natural Science Foundation
   of Shanghai Municipality (No. 20ZR1457200).
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NR 80
TC 0
Z9 0
U1 3
U2 4
PU SCIENCE PRESS
PI BEIJING
PA 16 DONGHUANGCHENGGEN NORTH ST, Building 5, Room 411, BEIJING, 100009,
   PEOPLES R CHINA
SN 1672-9145
EI 1745-7270
J9 ACTA BIOCH BIOPH SIN
JI Acta Biochim. Biophys. Sin.
PD JAN
PY 2024
VL 56
IS 1
BP 15
EP 22
DI 10.3724/abbs.2023278
PG 8
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA JB8O9
UT WOS:001170788700002
PM 38115743
OA gold
DA 2025-01-04
ER

PT J
AU Kou, T
   Kanai, M
   Matsumoto, S
   Okuno, Y
   Muto, M
AF Kou, Tadayuki
   Kanai, Masashi
   Matsumoto, Shigemi
   Okuno, Yasushi
   Muto, Manabu
TI The possibility of clinical sequencing in the management of cancer
SO JAPANESE JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Review
DE precision medicine; next-generation sequencing; gene panel; actionable
   mutation; molecular targeted therapy
ID CIRCULATING TUMOR-CELLS; PRECISION MEDICINE; LUNG-CANCER; PERSONALIZED
   MEDICINE; TARGETED THERAPY; DNA; GENOME; ONCOLOGY; LANDSCAPE; TRIALS
AB Comprehensive genomic profiling using next-generation sequencing technologies provides insights into understanding the genomic architecture of human cancer. This new understanding of the cancer genome allows us to identify many more genomic alterations occurring within tumors than before, some of which could be potential therapeutic targets through molecular targeted agents. Currently, a large number of molecular targeted agents are being developed, and consequently, cancer treatment is rapidly shifting from empiric therapy employing cytotoxic anticancer drugs to genotype-directed therapy using molecular targeted agents. In current daily clinical practice, hotspot-based single-gene assays that detect RAS mutations in colorectal cancer or EGFR mutations in non-small cell lung cancer are widely used to identify variants. However, it is becoming evident that more comprehensive genomic analysis is crucial in identifying the patient population that may benefit from molecular targeted therapy and the accelerated development of novel drugs for early clinical trials. For these purposes, an increasing number of gene panel-based targeted sequencing is commercially available in clinical practice from sequencing companies. Despite several challenges in implementing this approach, comprehensive genomic profiling and identification of actionable mutations is likely to become one of the standard options in the management of cancer in the near future. The use of clinical sequencing has the potential to usher a new era in precision medicine for cancer diagnosis and treatment. In this review, we discuss the application of comprehensive genomic profiling using next-generation sequencing technologies in clinical oncology and address the current challenges for its implementation.
C1 [Kou, Tadayuki; Kanai, Masashi; Matsumoto, Shigemi; Muto, Manabu] Kyoto Univ, Grad Sch Med, Dept Therapeut Oncol, Kyoto, Japan.
   [Kou, Tadayuki; Kanai, Masashi; Matsumoto, Shigemi; Muto, Manabu] Kyoto Univ Hosp, Ctr Canc, Dept Clin Oncol, Kyoto, Japan.
   [Okuno, Yasushi] Kyoto Univ, Grad Sch Med, Dept Clin Syst Oncoinformat, Kyoto, Japan.
C3 Kyoto University; Kyoto University; Kyoto University
RP Muto, M (corresponding author), Kyoto Univ, Grad Sch Med, Dept Therapeut Oncol, Sakyo Ku, 54 Shogoin Kawaharacho, Kyoto 6068507, Japan.
EM mmuto@kuhp.kyoto-u.ac.jp
FU Practical Research for Innovative Cancer Control from Japan Agency for
   Medical Research and Development, AMED
FX This study is supported by the Practical Research for Innovative Cancer
   Control from Japan Agency for Medical Research and Development, AMED.
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NR 82
TC 22
Z9 23
U1 1
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0368-2811
EI 1465-3621
J9 JPN J CLIN ONCOL
JI Jpn. J. Clin. Oncol.
PD MAY
PY 2016
VL 46
IS 5
BP 399
EP 406
DI 10.1093/jjco/hyw018
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DR9YH
UT WOS:000380251600002
PM 26917600
OA Bronze
DA 2025-01-04
ER

PT J
AU Finnberg, N
   Gokare, P
   El-Deiry, WS
AF Finnberg, Niklas
   Gokare, Prashanth
   El-Deiry, Wafik S.
TI Novel and Emerging Targeted Therapies of Colorectal Cancer
SO CURRENT CLINICAL PHARMACOLOGY
LA English
DT Article
DE Clinical; colorectal cancer; DPYD; RAS; targeted therapy; TRAIL
ID GROWTH-FACTOR RECEPTOR; SMALL-CELL LUNG; PHASE-II TRIAL;
   OXALIPLATIN-RELATED NEUROTOXICITY; APOPTOSIS-INDUCING LIGAND; METASTATIC
   BREAST-CANCER; POLY(ADP-RIBOSE) POLYMERASE INHIBITORS; TRAIL-INDUCED
   APOPTOSIS; REGORAFENIB BAY 73-4506; ERBB FAMILY BLOCKER
AB The survival rate of patients with colorectal cancer (CRC) is steadily increasing over the past decade. However, CRC continue to be one of the leading causes of cancer-related fatality in the United States. Current targeted strategies offer limited clinical benefits and the overall survival rate for CRC remains low. Improved understanding of the molecular changes associated with CRC that control growth factor signaling and evasion of cell death allow for the development of improved targeted therapy. This review aims to discuss some of the emerging therapies aimed to target CRC.
C1 [Finnberg, Niklas] Fox Chase Canc Ctr, Lab Translat Oncol & Expt Canc Therapeut, Dept Med Oncol, 7701 Burholme Ave, Philadelphia, PA 19111 USA.
   [Finnberg, Niklas] Fox Chase Canc Ctr, Mol Therapeut Program, Philadelphia, PA 19111 USA.
C3 Fox Chase Cancer Center; Fox Chase Cancer Center
RP Finnberg, N (corresponding author), Fox Chase Canc Ctr, Lab Translat Oncol & Expt Canc Therapeut, Dept Med Oncol, 7701 Burholme Ave, Philadelphia, PA 19111 USA.
EM Niklas.Finnberg@FCCC.EDU
RI Gokare, Prashanth/U-7119-2019; El-Deiry, Wafik/AAJ-6080-2020
OI El-Deiry, Wafik/0000-0002-9577-8266
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NR 242
TC 4
Z9 4
U1 1
U2 8
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1574-8847
EI 2212-3938
J9 CURR CLIN PHARMACOL
JI Curr. Clin. Pharmacol.
PY 2015
VL 10
IS 4
BP 279
EP 298
DI 10.2174/1574884710666151020095911
PG 20
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA DJ6EP
UT WOS:000374303200004
PM 26548905
DA 2025-01-04
ER

PT J
AU He, YJ
   Zhang, X
   Zhu, M
   He, WG
   Hua, HJ
   Ye, F
   Zhou, XL
   Chen, N
   Li, YD
   Zhong, WX
   Wu, GS
   Cai, H
   Jiang, WQ
AF He, Yinjun
   Zhang, Xiang
   Zhu, Ming
   He, Wenguang
   Hua, Hanju
   Ye, Feng
   Zhou, Xile
   Chen, Nan
   Li, Yandong
   Zhong, Weixiang
   Wu, Guosheng
   Cai, Hui
   Jiang, Weiqin
TI Soluble PD-L1: a potential dynamic predictive biomarker for
   immunotherapy in patients with proficient mismatch repair colorectal
   cancer
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE sPD-L1; Colorectal cancer; Biomarker; Combination immunotherapy
ID CLINICAL-SIGNIFICANCE; CELL LYMPHOMA; EXPRESSION; LEVEL
AB BackgroundCirculating soluble programmed death ligand 1 (sPD-L1) can negatively regulate T-cell function and serve as a prognostic or predictive marker in a variety of cancers. However, rare studies have evaluated the potential roles of sPD-L1, and no study has estimated its predictive value for the efficacy of immune treatment in colorectal cancer (CRC).MethodsPlasma samples from 192 CRC patients were used to estimate correlations between clinicopathological features and sPD-L1, secreted PD-L1 (secPD-L1) and exosomal PD-L1 (exoPD-L1). Baseline and posttreatment sPD-L1 levels were also investigated in 55 patients with metastatic CRC (mCRC) treated with chemotherapy +/- targeted therapy and 40 patients with proficient mismatch repair (pMMR) mCRC treated with combination immunotherapy. Both sPD-L1 and secPD-L1 were quantified by enzyme-linked immunosorbent assay, while exoPD-L1 was analyzed using flow cytometry.ResultssecPD-L1 was the major component and positively correlated with sPD-L1 in CRC, while exoPD-L1 was almost undetectable. Higher levels of sPD-L1 were detected in patients with distant metastasis, especially those with distant lymph node metastasis and tissue combined positive score (CPS) instead of tumor proportion score (TPS). Chemotherapy or targeted therapy did not significantly impact sPD-L1 concentration. Progressive disease on combination immunotherapy was associated with an increase in sPD-L1 level, whereas no significant change was observed in patients with durable clinical benefit.ConclusionsPD-L1 mainly consisted of secPD-L1, and its level was higher in patients with distant metastasis, especially distant lymph node metastasis and positive CPS. sPD-L1 is a potential dynamic marker to identify rapid progression on combination immunotherapy and avoid ineffective treatment for pMMR CRC.
C1 [He, Yinjun; Hua, Hanju; Ye, Feng; Zhou, Xile; Li, Yandong; Wu, Guosheng; Jiang, Weiqin] Zhejiang Univ, Affiliated Hosp 1, Dept Colorectal Surg, Sch Med, Hangzhou, Peoples R China.
   [He, Yinjun; Zhu, Ming] Zhejiang Univ, Coll Med, Hangzhou, Peoples R China.
   [Zhang, Xiang; Cai, Hui] Gansu Prov Hosp, Gen Surg Clin Med Ctr, Lanzhou, Peoples R China.
   [Zhang, Xiang; Cai, Hui] Lanzhou Univ, Clin Med Coll 1, Lanzhou, 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, Ningbo, Peoples R China.
   [Zhong, Weixiang] Zhejiang Univ, Affiliated Hosp 1, Dept Pathol, Sch Med, Hangzhou, Peoples R China.
C3 Zhejiang University; Zhejiang University; Lanzhou University; Zhejiang
   University; Zhejiang University
RP Jiang, WQ (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Dept Colorectal Surg, Sch Med, Hangzhou, Peoples R China.
EM weiqinjiang@zju.edu.cn
RI Zhu, Mingjian/AGY-0163-2022; Wu, George/JCE-1302-2023
FU Natural Science Foundation of Zhejiang Province [LGF22H160007,
   LY22H160045, LD21H030001, LY20H030011]; National Natural Science
   Foundation of China [82,170,662]; Beijing Xisike Clinical Oncology
   Research Foundation [Y-Young2020-0471]
FX The work was supported by Natural Science Foundation of Zhejiang
   Province (LGF22H160007, LY22H160045, LD21H030001, LY20H030011), National
   Natural Science Foundation of China (82,170,662) and Beijing Xisike
   Clinical Oncology Research Foundation (Y-Young2020-0471).
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NR 59
TC 12
Z9 12
U1 5
U2 12
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD JAN 13
PY 2023
VL 21
IS 1
AR 25
DI 10.1186/s12967-023-03879-0
PG 13
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 9X7MK
UT WOS:000949950300001
PM 36639643
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, YJ
   Wang, XW
   Qin, XY
   Wang, XX
   Liu, F
   White, E
   Zheng, XFS
AF Zhang, Yanjie
   Wang, Xiaowen
   Qin, Xiaoyu
   Wang, Xinxin
   Liu, Feng
   White, Eileen
   Zheng, X. F. Steven
TI PP2AC Level Determines Differential Programming of p38-TSC-mTOR
   Signaling and Therapeutic Response to p38-Targeted Therapy in Colorectal
   Cancer
SO EBIOMEDICINE
LA English
DT Article
DE Targeted therapy; Cancer; Signal transduction; mTOR; p38; PDX
ID ACTIVATED PROTEIN-KINASE; P38 MAP KINASES; LY2228820 DIMESYLATE;
   SELECTIVE INHIBITOR; TUBEROUS SCLEROSIS; MAMMALIAN TARGET; COLON-CANCER;
   CELL-GROWTH; MTOR KINASE; AKT
AB The p38 MAP kinase is a promising cancer drug target but its therapeutic effect is not fully understood. Here we report that the response of colorectal cancer (CRC) to p38 inhibitors (p38i) is highly variable: while p38i induces regression of one subgroup of CRCs, it stimulates growth of another subgroup. We further show that PP2AC is differentially expressed in the two different CRC subgroups, which determines the programing of p38-TSC-mTORC1 signaling through differential TSC2 phosphorylation at S664, 1254 and 1798, and the antitumor activity by p38i. Remarkably, modulation of PP2AC level is sufficient to reprogram p38-to-mTORC1 signaling and antitumor response. PP2AC expression accurately predicts therapeutic response to p38i in several CRC models, including a large cohort of patient-derived xenografts (PDXs). Moreover, we demonstrate that combination of p38 and mTOR kinase inhibitors effectively overcomes resistance to either inhibitor in single agent therapy. These results demonstrate that alternative routing of signal transduction underlies differential response to p38 and mTOR targeted therapies. The biomarker-guided therapeutic strategies described herein provide a compelling reason for testing inmetastatic CRC patients who suffer very poor prognosis due to lack of efficacious drug therapies. (C) 2015 The Authors. Published by Elsevier B.V.
C1 [Zhang, Yanjie; Wang, Xiaowen; White, Eileen; Zheng, X. F. Steven] Rutgers State Univ, Rutgers Canc Inst New Jersey, New Brunswick, NJ 08903 USA.
   [Zhang, Yanjie; Qin, Xiaoyu; Wang, Xinxin; Liu, Feng] Shanghai Jiao Tong Univ, Sch Med, Shanghai Peoples Hosp 9, Dept Oncol, Shanghai 201900, Peoples R China.
   [White, Eileen] Rutgers State Univ, Dept Mol Biol & Biochem, Piscataway, NJ 08854 USA.
   [Zheng, X. F. Steven] Rutgers State Univ, Robert Wood Johnson Med Sch, Dept Pharmacol, Piscataway, NJ 08854 USA.
C3 Rutgers University System; Rutgers University New Brunswick; Rutgers
   University Biomedical & Health Sciences; Rutgers Cancer Institute of New
   Jersey; Shanghai Jiao Tong University; Rutgers University System;
   Rutgers University New Brunswick; Rutgers University System; Rutgers
   University New Brunswick; Rutgers University Biomedical & Health
   Sciences
RP Zhang, YJ (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Shanghai Peoples Hosp 9, Dept Oncol, Shanghai 201900, Peoples R China.
EM zhangyanjie@shsmu.edu.cn; zhengst@cinj.rutgers.edu
RI wang, xinxin/HIR-2598-2022; White, Eileen/ABD-6745-2021; Wang,
   Xiaowen/A-7236-2018
OI Wang, Xiaowen/0000-0003-3922-0126; White, Eileen/0000-0003-2961-3065;
   ZHANG, YANJIE/0000-0002-7425-8632
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NR 41
TC 24
Z9 27
U1 0
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 2352-3964
J9 EBIOMEDICINE
JI EBioMedicine
PD DEC
PY 2015
VL 2
IS 12
BP 1944
EP 1956
DI 10.1016/j.ebiom.2015.11.031
PG 13
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA DA1EC
UT WOS:000367538100027
OA Green Published
DA 2025-01-04
ER

PT J
AU Fabregas, JC
   Ramnaraign, B
   George, TJ
AF Fabregas, Jesus C.
   Ramnaraign, Brian
   George, Thomas J.
TI Clinical Updates for Colon Cancer Care in 2022
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE Immunotherapy; Clinical trials; Targeted therapy; Colon cancer;
   Circulating tumor DNA
ID COLORECTAL-CANCER; OPEN-LABEL; ADJUVANT CHEMOTHERAPY; MAINTENANCE
   TREATMENT; OXALIPLATIN; CETUXIMAB; SURVIVAL; RISK; PEMBROLIZUMAB;
   TRASTUZUMAB
AB Colon cancer needs better screening and treatment options. Its incidence in the young population is rising. Recent changes in guidelines recommend beginning screening for colon cancer at the age of 45. Circulating tumor DNA presents an opportunity to select patients for administration of adjuvant chemotherapy. Immunotherapy is an option for patients with a deficiency in mismatch repair proteins. However, its efficacy outside of this group of patients remains a challenge. Targeted therapies such as BRAF inhibitors are an option for patients with poor prognosis, for whom cytotoxic chemotherapy is not as effective. This review presents the recently published evidence regarding screening and treating patients with colon cancer. (C) 2022 Elsevier Inc. All rights reserved.
C1 [Fabregas, Jesus C.; Ramnaraign, Brian; George, Thomas J.] Univ Florida, Hlth Canc Ctr, Dept Med, Div Hematol Oncol, Gainesville, FL 32610 USA.
C3 State University System of Florida; University of Florida
RP Fabregas, JC (corresponding author), Univ Florida, Dept Med, POB 100278,1600 SW Archer Rd, Gainesville, FL 32610 USA.
EM Jesus.fabregas@medicine.ufl.edu
RI Ramnaraign, Brian/ABF-9031-2020; Fabregas, Jesus/GWM-5389-2022; George,
   Thomas/L-9119-2019
OI George, Thomas/0000-0002-6249-9180; Fabregas, Jesus/0000-0003-1120-1783;
   Ramnaraign, Brian/0000-0003-4051-4551
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NR 47
TC 67
Z9 71
U1 10
U2 25
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 2022
VL 21
IS 3
BP 198
EP 203
DI 10.1016/j.clcc.2022.05.006
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 7A7EP
UT WOS:000898614900011
PM 35729033
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Michiels, S
   Saad, ED
   Buyse, M
AF Michiels, Stefan
   Saad, Everardo D.
   Buyse, Marc
TI Progression-Free Survival as a Surrogate for Overall Survival in
   Clinical Trials of Targeted Therapy in Advanced Solid Tumors
SO DRUGS
LA English
DT Article
ID CELL LUNG-CANCER; INDIVIDUAL PATIENT DATA; END-POINTS; 1ST-LINE
   TREATMENT; CHEMOTHERAPY PLUS; OPEN-LABEL; APPROVAL; CRIZOTINIB;
   METAANALYSES; VALIDATION
AB Over the past 15 years, targeted therapy has revolutionized the systemic treatment of cancer. In parallel, there has been a growing debate on the choice of end points in clinical trials in oncology. This debate basically hinges on the choice between overall survival (OS) and progression-free survival (PFS). PFS is advantageous because it is measured earlier than OS, requires a smaller sample size than OS to achieve the desired power, and is not influenced by cross-over. On the other hand, PFS is prone to measurement error and bias, and may not capture the entire treatment effect on the outcomes of most interest to patients with an incurable disease: a prolonged survival and improved quality of life. Therefore, how can we choose between two imperfect end points? The answer to this question would certainly be made easier if PFS could be demonstrated to be a valid surrogate for OS. The validation of a surrogate end point is best made using individual-patient data (IPD) from randomized trials, which allows for standardized assessments of the patient-level and the trial-level correlations between surrogate and final end points. Proper IPD meta-analytical evaluations for targeted agents have still been rare, and to our knowledge only three studies on this topic are currently available in the metastatic setting: one in breast cancer, one in colorectal cancer and one in lung cancer. Although these three studies suffer from limitations inherent to the availability of IPD and the design of the original clinical trials, they have not been able to validate PFS as surrogate for OS, because only modest correlations were found between these two end points, both at the patient and at the trial level. Even if properly conducted surrogate-endpoint evaluations have thus far been unsuccessful, these evaluations are a step in the right direction and can be expected to be applied on a much larger scale in the era of data sharing of clinical trials.
C1 [Michiels, Stefan] Gustave Roussy, RDC B2M, Serv Biostat & Epidemiol, 114 Rue Edouard Vaillant, F-94805 Villejuif, France.
   [Michiels, Stefan] Univ Paris Sud, Univ Paris Saclay, UVSQ, CESP,INSERM,U1018, F-94805 Villejuif, France.
   [Michiels, Stefan] Gustave Roussy, Ligue Natl Canc Meta Anal Platform, F-94805 Villejuif, France.
   [Saad, Everardo D.] IDDI, Louvain, Belgium.
   [Buyse, Marc] Hasselt Univ, Interuniv Inst Biostat & Stat Bioinformat I BioSt, Hasselt, Belgium.
   [Buyse, Marc] IDDI, San Francisco, CA USA.
C3 UNICANCER; Gustave Roussy; Universite Paris Saclay; Institut National de
   la Sante et de la Recherche Medicale (Inserm); UNICANCER; Gustave
   Roussy; International Drug Development Institute; Hasselt University;
   International Drug Development Institute
RP Michiels, S (corresponding author), Gustave Roussy, RDC B2M, Serv Biostat & Epidemiol, 114 Rue Edouard Vaillant, F-94805 Villejuif, France.; Michiels, S (corresponding author), Univ Paris Sud, Univ Paris Saclay, UVSQ, CESP,INSERM,U1018, F-94805 Villejuif, France.; Michiels, S (corresponding author), Gustave Roussy, Ligue Natl Canc Meta Anal Platform, F-94805 Villejuif, France.
EM stefan.michiels@gustaveroussy.fr
RI Buyse, Marc/J-4658-2013; Michiels, Stefan/L-1516-2013
OI Michiels, Stefan/0000-0002-6963-2968
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NR 48
TC 32
Z9 33
U1 0
U2 4
PU ADIS INT LTD
PI NORTHCOTE
PA 5 THE WAREHOUSE WAY, NORTHCOTE 0627, AUCKLAND, NEW ZEALAND
SN 0012-6667
EI 1179-1950
J9 DRUGS
JI Drugs
PD MAY
PY 2017
VL 77
IS 7
BP 713
EP 719
DI 10.1007/s40265-017-0728-y
PG 7
WC Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Toxicology
GA ES9QV
UT WOS:000399895600001
PM 28337673
DA 2025-01-04
ER

PT J
AU Kang, Y
   Li, HT
   Liu, YP
   Li, Z
AF Kang, Yan
   Li, Huiting
   Liu, Yiping
   Li, Zheng
TI Regulation of VEGF-A expression and VEGF-A-targeted therapy in malignant
   tumors
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Review
DE VEGF-A; Angiogenesis; Expression regulation; Tumor immunity;
   Bevacizumab; Traditional Chinese medicine
ID ENDOTHELIAL GROWTH-FACTOR; RECEPTOR TYROSINE KINASES; NEGATIVE
   BREAST-CANCER; COLORECTAL-CANCER; ANTITUMOR-ACTIVITY; ANGIOGENESIS;
   BEVACIZUMAB; PROGRESSION; DIFFERENTIATION; PROLIFERATION
AB Vascular endothelial growth factor A (VEGF-A), a highly conserved dimeric glycoprotein, is a key regulatory gene and a marker molecule of angiogenesis. The upregulation of VEGF-A facilitates the process of tumor vascularization, thereby fostering the initiation and progression of malignant neoplasms. Many genes can adjust the angiogenesis of tumors by changing the expression of VEGF-A. In addition, VEGF-A also exhibits immune regulatory properties, which directly or indirectly suppresses the antitumor activity of immune cells. The emergence of VEGF-A-targeted therapy alone or in rational combinations has revolutionized the treatment of various cancers. This review discusses how diverse mechanisms in various tumors regulate VEGF-A expression to promote tumor angiogenesis and the role of VEGF-A in tumor immune microenvironment. The application of drugs targeting VEGF-A in tumor therapy is also summarized including antibody molecule drugs and traditional Chinese medicine.
C1 [Kang, Yan; Li, Huiting; Liu, Yiping; Li, Zheng] Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, NHC Key Lab Carcinogenesis,Key Lab Carcinogenesis,, Changsha, Hunan, Peoples R China.
   [Kang, Yan; Li, Huiting; Li, Zheng] Cent South Univ, Canc Res Inst, Sch Basic Med Sci, Changsha, Hunan, Peoples R China.
C3 Central South University; Central South University
RP Li, Z (corresponding author), Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, NHC Key Lab Carcinogenesis,Key Lab Carcinogenesis,, Changsha, Hunan, Peoples R China.; Li, Z (corresponding author), Cent South Univ, Canc Res Inst, Sch Basic Med Sci, Changsha, Hunan, Peoples R China.
EM lizheng@csu.edu.cn
FU National Natural Science Foundation of China [81972773]; Hunan Province
   Natural Sciences Foundation of China [S2022JJKWLH0203]
FX This study was supported by grants from the National Natural Science
   Foundation of China (No. 81972773), the Hunan Province Natural Sciences
   Foundation of China (No. S2022JJKWLH0203).
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NR 111
TC 8
Z9 8
U1 6
U2 10
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD APR 30
PY 2024
VL 150
IS 5
AR 221
DI 10.1007/s00432-024-05714-5
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PB0E2
UT WOS:001211494700002
PM 38687357
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Friedrich, T
   Leong, S
   Lieu, CH
AF Friedrich, Tyler
   Leong, Stephen
   Lieu, Christopher H.
TI Beyond RAS and BRAF: a target rich disease that is ripe for picking
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Colonic neoplasms; molecular targeted therapy; mitogen-activated protein
   kinases (MAPKs); protooncogene proteins B-raf
ID METASTATIC BREAST-CANCER; CELL LUNG-CANCER; COLORECTAL-CANCER;
   MICROSATELLITE INSTABILITY; ANTITUMOR-ACTIVITY; MEK INHIBITION;
   ACQUIRED-RESISTANCE; PRECLINICAL MODELS; PI3K INHIBITION; ONCOGENIC RAS
AB Despite numerous breakthroughs in the understanding of colorectal cancer and identification of many oncogenic mutations, the treatment of metastatic colorectal cancer remains relatively more empiric than targeted. Testing for mutations in rat sarcoma virus (RAS) and rapidly growing fibrosarcoma (RAF) are routinely performed, though identification of these mutations currently offers little more than a negative predictive marker for response to EGFR inhibitor treatment and, in the case of RAF mutation, a poor prognostic indicator. Next-generation sequencing has identified both common and rare mutations in colorectal cancer that offer options for more advanced, targeted therapy. With so much research invested in these targets, the treatment of metastatic colorectal cancer stands to become much more personalized in the near future. This review describes several of the more promising targets that are currently being investigated in advanced colorectal cancer.
C1 [Friedrich, Tyler; Leong, Stephen; Lieu, Christopher H.] Univ Colorado Denver, Div Med Oncol, Aurora, CO 80045 USA.
C3 Children's Hospital Colorado; University of Colorado System; University
   of Colorado Anschutz Medical Campus
RP Lieu, CH (corresponding author), Univ Colorado Denver, Div Med Oncol, Aurora, CO 80045 USA.
EM CHRISTOPHER.LIEU@ucdenver.edu
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NR 71
TC 3
Z9 3
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 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD OCT
PY 2016
VL 7
IS 5
BP 705
EP 712
DI 10.21037/jgo.2016.06.11
PG 8
WC Oncology; Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Oncology; Gastroenterology & Hepatology
GA EI5PN
UT WOS:000392546900004
PM 27747084
OA Green Published
DA 2025-01-04
ER

PT J
AU Wang, FT
   Sun, W
   Zhang, JT
   Fan, YZ
AF Wang, Fang-Tao
   Sun, Wei
   Zhang, Jing-Tao
   Fan, Yue-Zu
TI Cancer-associated fibroblast regulation of tumor neo-angiogenesis as a
   therapeutic target in cancer
SO ONCOLOGY LETTERS
LA English
DT Review
DE neoplasm; cancer-associated fibroblasts; tumor microenvironment;
   neo-angiogenesis; signaling pathway; target therapy
ID ENDOTHELIAL GROWTH-FACTOR; MEDIATED VASCULOGENIC MIMICRY; ACTIVATION
   PROTEIN-ALPHA; STROMAL FIBROBLASTS; CELL CARCINOMA; COLON-CANCER;
   TGF-BETA; VEGF-A; PODOPLANIN EXPRESSION; PROMOTE ANGIOGENESIS
AB Adequate blood supply is essential for tumor survival, growth and metastasis. The tumor microenvironment (TME) is dynamic and complex, comprising cancer cells, cancer-associated stromal cells and their extracellular products. The TME serves an important role in tumor progression. Cancer-associated fibroblasts (CAFs) are the principal component of stromal cells within the TME, and contribute to tumor neo-angiogenesis by altering the proteome and degradome. The present paper reviews previous studies of the molecular signaling pathways by which CAFs promote tumor neo-angiogenesis and highlights therapeutic response targets. Also discussed are potential strategies for antitumor neo-angiogenesis to improve tumor treatment efficacy.
C1 [Wang, Fang-Tao; Zhang, Jing-Tao; Fan, Yue-Zu] Tongji Univ, Sch Med, Tongji Hosp, Dept Surg, 389 Xincun Rd, Shanghai 200065, Peoples R China.
   [Sun, Wei] Tongji Univ, Shanghai Peoples Hosp 10, Sch Med, Dept Surg, Shanghai 200072, Peoples R China.
C3 Tongji University; Tongji University
RP Fan, YZ (corresponding author), Tongji Univ, Sch Med, Tongji Hosp, Dept Surg, 389 Xincun Rd, Shanghai 200065, Peoples R China.
EM fanyuezu@hotmail.com
RI LIU, YU/HTR-1607-2023; Wang, Fang-Tao/AAY-4463-2021; Li,
   Xiaoyang/AHI-7690-2022
OI Wang, Fang-Tao/0000-0003-3193-4108
FU National Natural Science Foundation of China [30672073, 81372614]
FX The present review was supported by the National Natural Science
   Foundation of China (grant nos. 30672073 and 81372614).
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NR 138
TC 99
Z9 103
U1 3
U2 64
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 3055
EP 3065
DI 10.3892/ol.2019.9973
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HN9YG
UT WOS:000460555900060
PM 30867734
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Cohen, R
   Svrcek, M
   Dreyer, C
   Cervera, P
   Duval, A
   Pocard, M
   Fléjou, JF
   de Gramont, A
   André, T
AF Cohen, Romain
   Svrcek, Magali
   Dreyer, Chantal
   Cervera, Pascale
   Duval, Alex
   Pocard, Marc
   Flejou, Jean-Francois
   de Gramont, Aimery
   Andre, Thierry
TI New Therapeutic Opportunities Based on DNA Mismatch Repair and
   <i>BRAF</i> Status in Metastatic Colorectal Cancer
SO CURRENT ONCOLOGY REPORTS
LA English
DT Review
DE Microsatellite instability; BRAF mutation; Immune checkpoint; PD-1;
   PD-L1
ID III COLON-CANCER; KRAS WILD-TYPE; MICROSATELLITE-INSTABILITY;
   LYNCH-SYNDROME; OPEN-LABEL; 1ST-LINE TREATMENT; STAGE-II; SURVIVAL;
   FLUOROURACIL; MUTATION
AB Recently, colorectal cancer (CRC) subtyping consortium identified four consensus molecular subtypes (CMS1-4). CMS1 is enriched for deficient mismatch repair (dMMR) and BRAF(V600E) tumors. Intriguingly, this subtype has better relapse-free survival but worse overall survival after relapse compared with the other subtypes. Growing evidence is accumulating on the benefit of specific therapeutic strategies such as immune checkpoint inhibition therapy in dMMR tumors and mitogen-activated protein kinase (MAPK) pathway targeted therapy in tumors harboring BRAF(V600E) mutation. After reviewing dMMR prognostic value, immune checkpoints as major targets for dMMR carcinomas will be highlighted. Following, BRAF(V600E) prognostic impact will be reviewed and therapeutic strategies with the combination of cytotoxic agents and especially the combinations of BRAF and MAPK inhibitors will be discussed.
C1 [Cohen, Romain; Dreyer, Chantal; Andre, Thierry] Hosp St Antoine, AP HP, Dept Med Oncol, 184 Rue Faubourg St Antoine, F-75012 Paris, France.
   [Svrcek, Magali; Cervera, Pascale; Flejou, Jean-Francois] Hosp St Antoine, AP HP, Dept Pathol, 184 Rue Faubourg St Antoine, F-75012 Paris, France.
   [Svrcek, Magali; Cervera, Pascale; Flejou, Jean-Francois; Andre, Thierry] Univ Paris 06, Paris 4, 4 Pl Jussieu, F-75005 Paris, France.
   [Duval, Alex; Andre, Thierry] INSERM, Ctr Rech St Antoine, Equipe Instabilite Microsatellites & Canc, Equipe Labellisee Ligue Natl Canc,Unite Mixte Rec, 184 Rue Faubourg St Antoine, F-75012 Paris, France.
   [Pocard, Marc; de Gramont, Aimery; Andre, Thierry] Oncol Multidisciplinary Grp, GERCOR, 151 Rue Faubourg St Antoine, F-75011 Paris, France.
   [Pocard, Marc] Hosp Lariboisiere, AP HP, Dept Digest & Oncol Surg, 2 Rue Ambroise Pare, F-75010 Paris, France.
   [de Gramont, Aimery] Inst Hosp Franco Britann, Dept Med Oncol, 4 Rue Kleber, F-92300 Levallois Perret, France.
C3 Assistance Publique Hopitaux Paris (APHP); Sorbonne Universite; Hopital
   Universitaire Saint-Antoine - APHP; Assistance Publique Hopitaux Paris
   (APHP); Sorbonne Universite; Hopital Universitaire Saint-Antoine - APHP;
   Sorbonne Universite; Institut National de la Sante et de la Recherche
   Medicale (Inserm); Assistance Publique Hopitaux Paris (APHP); Sorbonne
   Universite; Hopital Universitaire Saint-Antoine - APHP; Assistance
   Publique Hopitaux Paris (APHP); Universite Paris Cite; Hopital
   Universitaire Lariboisiere-Fernand-Widal - APHP
RP André, T (corresponding author), Hosp St Antoine, AP HP, Dept Med Oncol, 184 Rue Faubourg St Antoine, F-75012 Paris, France.; André, T (corresponding author), Univ Paris 06, Paris 4, 4 Pl Jussieu, F-75005 Paris, France.; André, T (corresponding author), INSERM, Ctr Rech St Antoine, Equipe Instabilite Microsatellites & Canc, Equipe Labellisee Ligue Natl Canc,Unite Mixte Rec, 184 Rue Faubourg St Antoine, F-75012 Paris, France.; André, T (corresponding author), Oncol Multidisciplinary Grp, GERCOR, 151 Rue Faubourg St Antoine, F-75011 Paris, France.
EM thierry.andre@aphp.fr
RI André, Thierry/N-8830-2017; Cohen, Romain/AAC-9089-2019
OI Cohen, Romain/0000-0001-9602-5162; Andre, Thierry/0000-0002-5103-7095;
   Duval, Alex/0000-0003-1534-1724
FU Bristol-Myers Squibb; Novartis; Roche
FX Thierry Andre is principal investigator for studies in metastatic
   colorectal cancer sponsored by Bristol-Myers Squibb, Novartis, and Roche
   and has received compensation from Roche, Amgen, and Bristol-Myers
   Squibb for service as a consultant.
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NR 74
TC 16
Z9 18
U1 0
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3790
EI 1534-6269
J9 CURR ONCOL REP
JI Curr. Oncol. Rep.
PD MAR
PY 2016
VL 18
IS 3
AR 18
DI 10.1007/s11912-016-0504-2
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DG0YB
UT WOS:000371790900001
PM 26861657
DA 2025-01-04
ER

PT J
AU Carreras, MJ
   Tomás-Guillén, E
   Farriols, A
   Renedo-Miró, B
   Valdivia, C
   Vidal, J
   Saura, C
   Carles, J
   Felip, E
   Gorgas, MQ
   Tabernero, J
   Monterde, J
AF Carreras, Maria-Josep
   Tomas-Guillen, Elena
   Farriols, Anna
   Renedo-Miro, Berta
   Valdivia, Carolina
   Vidal, Jana
   Saura, Cristina
   Carles, Joan
   Felip, Enriqueta
   Gorgas, Maria-Queralt
   Tabernero, Josep
   Monterde, Josep
TI Use of Drugs in Clinical Practice and the Associated Cost of Cancer
   Treatment in Adult Patients with Solid Tumors: A 10-Year Retrospective
   Cohort Study
SO CURRENT ONCOLOGY
LA English
DT Article
DE cancer; expenditure; antineoplastic agents; solid tumors; supportive
   care; retrospective cohort study; real word data
ID METASTATIC BREAST-CANCER; OF-POCKET COSTS; COLORECTAL-CANCER;
   EUROPEAN-UNION; PACLITAXEL; CATALONIA; MORTALITY; MELANOMA; BURDEN;
   PRICES
AB Background: Cancer is one of the leading causes of morbidity and mortality in the world. Its growing incidence and prevalence, as well as the advances in diagnostic and treatment tools, motivate an open debate about the economic burden it may place on health systems and have raised concerns about access to this technological innovation. There is a lack of information on the detailed costs of pharmacological treatment of cancer in our health setting. In this context, it is necessary to know the use of drugs in cancer treatment in conditions of real clinical practice. A real-word, evidence-based retrospective cohort study was conducted at Vall d'Hebron University Hospital (VHUH), the largest hospital complex in Catalonia, Spain, in order to determine the use of drugs and the associated cost in real clinical practice for the treatment of solid tumors in adult patients attended at this institution over 10 years (2010-2019). Methods: This was a single-center retrospective cohort study of adult cancer patients attended in clinical practice at the Medical Oncology Department of VHUH between 1 January 2010 and 31 December 2019. Data of prescription, preparation, and cost of antineoplastic treatments were analyzed by pharmacological class (cytotoxic drugs, immunotherapy, targeted therapy, radiopharmaceuticals, and others), by antineoplastic agent, and by type of tumor. The number of patients and the pharmaceutical expenditure corresponding to all these subgroups were recorded. The cost per patient in each tumor location was also calculated. Results: The study population included 13,209 patients with an overall pharmaceutical antineoplastic expenditure of EUR 120,396,097, increasing from 7.67% in relation to the total HUVH pharmaceutical expenditure in 2010 to 12.82% in 2019. By pharmacological class, the specific weight of the cost of targeted therapy is relevant (75.22% of pharmaceutical antineoplastic expenditure, 21.3% of patients) compared to the group of conventional cytotoxics (17.25% of pharmaceutical antineoplastic expenditure, 76.37% of patients), while immunotherapy has represented the largest relative increase, from 5% in 2014 to 12% in 2019. Eight targeted therapy drugs represented 50% of the costs of the targeted therapy drug class (palbociclib, trastuzumab, pertuzumab, bevacizumab, nivolumab, cetuximab, pembrolizumab, and trastuzumab emtansine). Eleven tumor sites accounted for 90% of the expenditure in 71% of all patients. Breast cancer had the highest expenditure during the study period (EUR 34,332,210) and at each individual year. Melanoma showed the highest increase, with 9.7% of total pharmaceutical antineoplastic expenditure in 2019 (2% of patients), representing a paradigm of the rising costs of cancer treatment due to the incorporation of new high-cost therapies. The average annual cost per patient was highly variable depending on the pathology. There was a growing increase in costs per patient in most tumor locations, particularly in patients with melanoma (from EUR 1922 in 2010 to EUR 37,020 in 2019), prostate cancer (from EUR 2992 in 2010 to EUR 14,118 in 2019), and non-small cell lung cancer (from EUR 3545 in 2010 to EUR 8371 in 2019). The relevance of the difference in monthly cost per patient that has been identified for the different intrinsic subtypes in breast cancer patients during 2019 (HER2+ EUR 2661/month, Luminal EUR 881/month, Triple negative EUR 386/month) makes us consider suggesting differentiated reimbursement rates for certain clinical conditions.
   Finally, support treatment with antiemetic drugs, erythropoietin stimulating agents, granulocyte-colony stimulating factor (G-CSF), and bone resorption inhibitors has involved a cost of EUR 5,751,910, which represents 4.6% of the overall pharmacological cost of cancer treatment. Conclusion: This study provides detailed insights on the oncological pharmaceutical expenditure for the treatment for solid tumors in the VHUH, based on real cost information from our hospital practice and for all antineoplastic therapies and types of solid tumors. This type of information on all the different types of cancer can be useful to better understand the economic burden of the disease and can be decisive for allocating public resources and funds for research, especially in those areas where information is scarce and therefore where further studies are needed. The contribution to knowledge of the cost of oncology therapy is of great value due to its realism and scope.
C1 [Carreras, Maria-Josep; Farriols, Anna; Renedo-Miro, Berta; Valdivia, Carolina; Vidal, Jana; Gorgas, Maria-Queralt] Vall dHebron Univ Hosp, Pharm Dept, E-08035 Barcelona, Spain.
   [Tomas-Guillen, Elena; Monterde, Josep] Asserta Global Healthcare Solut, Dept Oncol, E-08192 Sant Quirze Del Valles, Barcelona, Spain.
   [Saura, Cristina; Carles, Joan; Felip, Enriqueta; Tabernero, Josep] Vall dHebron Univ Hosp, Vall dHebron Inst Oncol VHIO, Med Oncol Dept, E-08035 Barcelona, Spain.
C3 Hospital Universitari Vall d'Hebron; Hospital Universitari Vall
   d'Hebron; Vall d'Hebron Institut d'Oncologia (VHIO)
RP Carreras, MJ (corresponding author), Vall dHebron Univ Hosp, Pharm Dept, E-08035 Barcelona, Spain.
EM mariajosep.carreras@vhebron.cat; elena.tomas@asserta.net;
   annamaria.farriols@vallhebron.cat; berta.renedo@vallhebron.cat;
   carolina.valdivia@vallhebron.cat; jana.vidal@vallhebron.cat;
   csaura@vhio.net; jcarles@vhio.net; efelip@vhio.net;
   mariaqueralt.gorgas@vallhebron.cat; jtabernero@vhio.net;
   j.monterde@asserta.net
RI Monterde, Juan/AAC-8796-2020; Saura, Carlos/AFM-9239-2022
OI Renedo-Miro, Berta/0000-0002-4502-1265; Gorgas, Maria
   Queralt/0000-0001-5523-5171; Tabernero, Josep/0000-0002-2495-8139;
   Tomas-Guillen, Elena/0009-0001-2522-2772; Saura Manich,
   Cristina/0000-0001-8296-5065
FU The authors thank Marta Pulido for editing the manuscript and editorial
   assistance.
FX The authors thank Marta Pulido for editing the manuscript and editorial
   assistance.
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NR 51
TC 3
Z9 3
U1 1
U2 3
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 SEP
PY 2023
VL 30
IS 9
BP 7984
EP 8004
DI 10.3390/curroncol30090580
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA S5CS4
UT WOS:001071350700001
PM 37754495
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wang, H
   Wang, RB
   Cai, KM
   He, H
   Liu, Y
   Yen, J
   Wang, ZY
   Xu, M
   Sun, YW
   Zhou, X
   Yin, Q
   Tang, L
   Dobrucki, IT
   Dobrucki, LW
   Chaney, EJ
   Boppart, SA
   Fan, TM
   Lezmi, S
   Chen, XS
   Yin, LC
   Cheng, JJ
AF Wang, Hua
   Wang, Ruibo
   Cai, Kaimin
   He, Hua
   Liu, Yang
   Yen, Jonathan
   Wang, Zhiyu
   Xu, Ming
   Sun, Yiwen
   Zhou, Xin
   Yin, Qian
   Tang, Li
   Dobrucki, Iwona T.
   Dobrucki, Lawrence W.
   Chaney, Eric J.
   Boppart, Stephen A.
   Fan, Timothy M.
   Lezmi, Stephane
   Chen, Xuesi
   Yin, Lichen
   Cheng, Jianjun
TI Selective <i>in vivo</i> metabolic cell-labeling-mediated cancer
   targeting
SO NATURE CHEMICAL BIOLOGY
LA English
DT Article
ID UNNATURAL AMINO-ACIDS; NEGATIVE BREAST-CANCER; PRECLINICAL MODELS;
   SURFACE RECEPTOR; CATHEPSIN-B; TRASTUZUMAB; GLYCANS; CHEMOTHERAPY;
   EXPRESSION; CHEMISTRY
AB Distinguishing cancer cells from normal cells through surface receptors is vital for cancer diagnosis and targeted therapy. Metabolic glycoengineering of unnatural sugars provides a powerful tool to manually introduce chemical receptors onto the cell surface; however, cancer-selective labeling still remains a great challenge. Herein we report the design of sugars that can selectively label cancer cells both in vitro and in vivo. Specifically, we inhibit the cell-labeling activity of tetraacetylN- azidoacetylmannosamine (Ac4ManAz) by converting its anomeric acetyl group to a caged ether bond that can be selectively cleaved by cancer-overexpressed enzymes and thus enables the overexpression of azido groups on the surface of cancer cells. Histone deacetylase and cathepsin L-responsive acetylated azidomannosamine, one such enzymatically activatable Ac4ManAz analog developed, mediated cancer-selective labeling in vivo, which enhanced tumor accumulation of a dibenzocyclooctyne- doxorubicin conjugate via click chemistry and enabled targeted therapy against LS174T colon cancer, MDAMB- 231 triple-negative breast cancer and 4T1 metastatic breast cancer in mice.
C1 [Wang, Hua; Wang, Ruibo; Cai, Kaimin; Liu, Yang; Wang, Zhiyu; Xu, Ming; Sun, Yiwen; Yin, Qian; Tang, Li; Cheng, Jianjun] Univ Illinois, Dept Mat Sci & Engn, Urbana, IL 61801 USA.
   [He, Hua; Yin, Lichen; Cheng, Jianjun] Soochow Univ, Inst Funct Nano & Soft Mat FUNSOM, Jiangsu Key Lab Carbon Based Funct Mat & Devices, Suzhou, Jiangsu, Peoples R China.
   [Yen, Jonathan; Dobrucki, Lawrence W.; Boppart, Stephen A.; Cheng, Jianjun] Univ Illinois, Dept Bioengn, Urbana, IL 61801 USA.
   [Zhou, Xin] Univ Sci & Technol China, Dept Chem, Hefei, Anhui, Peoples R China.
   [Dobrucki, Iwona T.; Chaney, Eric J.; Boppart, Stephen A.; Cheng, Jianjun] Univ Illinois, Beckman Inst Adv Sci & Technol, Urbana, IL 61801 USA.
   [Boppart, Stephen A.] Univ Illinois, Dept Elect & Comp Engn, Urbana, IL USA.
   [Boppart, Stephen A.] Univ Illinois, Dept Internal Med, Urbana, IL USA.
   [Fan, Timothy M.] Univ Illinois, Dept Vet Clin Med, Urbana, IL USA.
   [Lezmi, Stephane] Univ Illinois, Coll Vet Med, Dept Pathobiol, Urbana, IL USA.
   [Chen, Xuesi] Changchun Inst Appl Chem, Key Lab Polymer Ecomat, Changchun, Peoples R China.
   [Cheng, Jianjun] Univ Illinois, Dept Chem, Urbana, IL 61801 USA.
   [Cheng, Jianjun] Univ Illinois, Frederick Seitz Mat Res Lab, Urbana, IL 61801 USA.
   [Cheng, Jianjun] Univ Illinois, Carl R Woese Inst Genom Biol, Urbana, IL 61801 USA.
C3 University of Illinois System; University of Illinois Urbana-Champaign;
   Soochow University - China; University of Illinois System; University of
   Illinois Urbana-Champaign; Chinese Academy of Sciences; University of
   Science & Technology of China, CAS; University of Illinois System;
   University of Illinois Urbana-Champaign; University of Illinois System;
   University of Illinois Urbana-Champaign; University of Illinois System;
   University of Illinois Urbana-Champaign; University of Illinois System;
   University of Illinois Urbana-Champaign; University of Illinois System;
   University of Illinois Urbana-Champaign; Chinese Academy of Sciences;
   Changchun Institute of Applied Chemistry, CAS; University of Illinois
   System; University of Illinois Urbana-Champaign; University of Illinois
   System; University of Illinois Urbana-Champaign; University of Illinois
   System; University of Illinois Urbana-Champaign
RP Cheng, JJ (corresponding author), Univ Illinois, Dept Mat Sci & Engn, Urbana, IL 61801 USA.; Yin, LC; Cheng, JJ (corresponding author), Soochow Univ, Inst Funct Nano & Soft Mat FUNSOM, Jiangsu Key Lab Carbon Based Funct Mat & Devices, Suzhou, Jiangsu, Peoples R China.; Cheng, JJ (corresponding author), Univ Illinois, Dept Bioengn, Urbana, IL 61801 USA.; Cheng, JJ (corresponding author), Univ Illinois, Beckman Inst Adv Sci & Technol, Urbana, IL 61801 USA.; Chen, XS (corresponding author), Changchun Inst Appl Chem, Key Lab Polymer Ecomat, Changchun, Peoples R China.; Cheng, JJ (corresponding author), Univ Illinois, Dept Chem, Urbana, IL 61801 USA.; Cheng, JJ (corresponding author), Univ Illinois, Frederick Seitz Mat Res Lab, Urbana, IL 61801 USA.; Cheng, JJ (corresponding author), Univ Illinois, Carl R Woese Inst Genom Biol, Urbana, IL 61801 USA.
EM xschen@ciac.ac.cn; lcyin@suda.edu.cn; jianjunc@illinois.edu
RI Dobrucki, Wawrzyniec/D-3987-2009; Dobrucka, Iwona/LWJ-7552-2024; Cai,
   Kaimin/N-7363-2014; Chen, Xuesi/ABB-5039-2020; Wang,
   Zhiyu/AAZ-9437-2021; Tang, Li/A-6844-2013; Boppart, Stephen/C-7338-2009;
   Cheng, Jianjun/AAF-4301-2019; Wang, Ruibo/H-4832-2018
OI Lezmi, Stephane/0000-0002-3412-4058; Tang, Li/0000-0002-6393-982X;
   Cheng, Jianjun/0000-0003-2561-9291; Wang, Ruibo/0000-0002-8753-7163;
   Fan, Timothy/0000-0003-2510-7050; Boppart, Stephen/0000-0002-9386-5630;
   Wang, Hua/0000-0002-1157-8786; Dobrucki, Wawrzyniec/0000-0002-6807-217X;
   Yin, Qian/0000-0002-6535-9861
FU United States National Institute of Health [1DP2OD007246]; National
   Science Foundation [DMR 1309525]; National Natural Science Foundation of
   China [51403145, 51573123, 51528303]; Ministry of Science and Technology
   of China [2016YFA0201200]; Collaborative Innovation Center of Suzhou
   Nano Science and Technology; Priority Academic Program Development of
   Jiangsu Higher Education Institutions (PAPD); Howard Hughes Medical
   Institute International Student Research Fellowship; University of
   Illinois at Urbana-Champaign; NIH National Cancer Institute Alliance for
   Nanotechnology in Cancer "Midwest Cancer Nanotechnology Training Center"
   Grant [R25 CA154015A]; CSTAR/T32 Fellowship through the NIH T32 Tissue
   Microenvironment Training Program; Division Of Materials Research;
   Direct For Mathematical & Physical Scien [1309525] Funding Source:
   National Science Foundation
FX J.C. acknowledges support from the United States National Institute of
   Health (Director's New Innovator Award 1DP2OD007246), which partially
   supported the in vivo part of the research, and National Science
   Foundation (DMR 1309525), which partially supported the chemical design
   and synthesis of the work. L.Y. acknowledges the support from the
   National Natural Science Foundation of China (51403145 and 51573123),
   the Ministry of Science and Technology of China (2016YFA0201200), the
   Collaborative Innovation Center of Suzhou Nano Science and Technology,
   and the Priority Academic Program Development of Jiangsu Higher
   Education Institutions (PAPD). X.C. acknowledges the support from the
   National Natural Science Foundation of China (51528303). H.W. was
   supported via a Howard Hughes Medical Institute International Student
   Research Fellowship. K.C. and Q.Y. acknowledge Beckman Institute
   Graduate Fellowship support at the University of Illinois at
   Urbana-Champaign. K.C., Q.Y., and L.T. acknowledge support from the NIH
   National Cancer Institute Alliance for Nanotechnology in Cancer "Midwest
   Cancer Nanotechnology Training Center" Grant R25 CA154015A. R.W.
   acknowledges the support of a CSTAR/T32 Fellowship through the NIH T32
   Tissue Microenvironment Training Program. We acknowledge R. Tong and V.
   Mirshafiee for their early work related to the design of this project.
   We also acknowledge H. Ying and Y. Zhang for their useful discussions.
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NR 52
TC 376
Z9 409
U1 17
U2 549
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1552-4450
EI 1552-4469
J9 NAT CHEM BIOL
JI Nat. Chem. Biol.
PD APR
PY 2017
VL 13
IS 4
BP 415
EP +
DI 10.1038/nchembio.2297
PG 13
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA EO9IG
UT WOS:000397001800017
PM 28192414
OA Green Accepted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Li, JC
   Zhu, YZ
   Yang, L
   Wang, ZQ
AF Li, Junchuan
   Zhu, Yuzhou
   Yang, Lie
   Wang, Ziqiang
TI Effect of gut microbiota in the colorectal cancer and potential target
   therapy
SO DISCOVER ONCOLOGY
LA English
DT Review
DE Gut microbiota; Colorectal cancer; Gut dysbiosis; Methylation; Tumor
   proliferation; Pathogenesis
ID CULTURE-INDEPENDENT ANALYSIS; FUSOBACTERIUM-NUCLEATUM; ESCHERICHIA-COLI;
   MOLECULAR-FEATURES; PROMOTES; ASSOCIATION; COMMENSAL; PROBIOTICS;
   TUMORIGENESIS; LOCALIZATION
AB The symbiotic interaction between gut microbiota and the digestive tract is an important factor in maintaining the intestinal environment balance. Colorectal cancer (CRC) is a complex disease involving the interaction between tumour cells and a large number of microorganisms. The microbiota is involved in the occurrence, development and prognosis of colorectal cancer. Several microbiota species have been studied, such as Fusobacterium nucleatum (F.nucleatum), Enterotoxigenic Bacteroidesfragilis (ETBF), Streptococcus bovis (S. bovis), Lactobacillus, and Bifidobacterium. Studies about the interaction between microbiota and CRC were retrieved from Embase, PubMed, Ovid and Web of Science up to 21 Oct 2021. This review expounded on the effect of microbiota on CRC, especially the dysregulation of bacteria and carcinogenicity. The methods of gut microbiota modifications representing novel prognostic markers and innovative therapeutic strategies were also described.
C1 [Li, Junchuan; Zhu, Yuzhou; Yang, Lie; Wang, Ziqiang] Sichuan Univ, West China Hosp, Gastrointestinal Ctr, Chengdu, Sichuan, Peoples R China.
C3 Sichuan University
RP Yang, L (corresponding author), Sichuan Univ, West China Hosp, Gastrointestinal Ctr, Chengdu, Sichuan, Peoples R China.
EM 372644378@qq.com; 944875885@qq.com; lie_222@163.com;
   wangziqiang@scu.edu.cn
RI Zhiqiang, Wang/KEJ-2637-2024; li, junchuan/GXF-3124-2022; zhang,
   junfeng/JHT-7871-2023
FU Ministry of Science and Technology of the People's Republic of China
   [2017YFC0908204]; Department of Science and Technology of Sichuan
   Province [2021YFS0025]; 1.3.5 project for disciplines of excellence,
   West China Hospital, Sichuan University [20HXJS003]; 1.3.5 project for
   disciplines of excellence-Clinical Research Incubation Project; West
   China Hospital, Sichuan University [2019HXFH031]
FX This work was supported by the Ministry of Science and Technology of the
   People's Republic of China (No. 2017YFC0908204), Department of Science
   and Technology of Sichuan Province (No. 2021YFS0025), 1.3.5 project for
   disciplines of excellence, West China Hospital, Sichuan University (No.
   20HXJS003), 1.3.5 project for disciplines of excellence-Clinical
   Research Incubation Project, and West China Hospital, Sichuan University
   (No. 2019HXFH031).
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NR 135
TC 6
Z9 6
U1 2
U2 33
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 24
PY 2022
VL 13
IS 1
AR 51
DI 10.1007/s12672-022-00517-x
PG 11
WC Oncology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Endocrinology & Metabolism
GA 2J2LJ
UT WOS:000815495000001
PM 35749000
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Karlsson, S
   Nystrom, H
AF Karlsson, S.
   Nystrom, H.
TI The extracellular matrix in colorectal cancer and its metastatic
   settling-Alterations and biological implications
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Colorectal cancer; Metastases; Extracellular matrix; Tumour
   microenvironment; Stroma
ID PERITONEAL CARCINOMATOSIS; IV COLLAGEN; LIVER METASTASIS; LYSYL OXIDASE;
   TUMOR-MARKER; RISK-FACTORS; TENASCIN-C; EXPRESSION; ORIGIN;
   MICROENVIRONMENT
AB Colorectal cancer (CRC) remains one of the most common cancers worldwide. Metastatic disease is ultimately fatal when incurable. Cancer research has evolved to take the importance of the tumour microenvironment (TME) into account. The extracellular matrix (ECM) has been viewed merely as a structural scaffold, but it is now evident that the ECM is a highly active part of the TME and affects tumour cell behaviour and metastatic capability. The ECM context and composition are linked to patient outcome and the response to surgical and oncological therapy in CRC patients and may be an area for developing novel biomarkers and targeted therapy. In this review we focus on the components of the ECM in human primary and metastatic CRC. We discuss future aspects of the ECM for targeted therapy, as a source of novel biomarkers, current knowledge of the area and important considerations when studying the ECM in human CRC.
C1 [Karlsson, S.; Nystrom, H.] Umea Univ, Dept Surg, Dept Surg & Perioperat Sci, Umea, Sweden.
   [Nystrom, H.] Umea Univ, Wallenberg Ctr Mol Med, Umea, Sweden.
   [Nystrom, H.] Norrlands Univ Jukhus, Dept Surg 10 A, S-90185 Umea, Sweden.
C3 Umea University; Umea University; Umea University
RP Nystrom, H (corresponding author), Norrlands Univ Jukhus, Dept Surg 10 A, S-90185 Umea, Sweden.
EM hanna.nystrom@umu.se
RI Nystrom, Hanna/AAK-4743-2021
FU Wallenberg Foundations/Knut and Alice Wallenberg's Stiftelse;
   Vasterbotten County Council; Swedish Cancer Society; Ihre Foundation;
   Cancerforskningsfonden Norrland; Umea university, Sweden
FX This work was supported by the Wallenberg Foundations/Knut and Alice
   Wallenberg's Stiftelse, Vasterbotten County Council, The Swedish Cancer
   Society, Ihre Foundation, Cancerforskningsfonden Norrland and Umea
   university, Sweden.
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NR 126
TC 19
Z9 20
U1 4
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 JUL
PY 2022
VL 175
AR 103712
DI 10.1016/j.critrevonc.2022.103712
EA MAY 2022
PG 16
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA 3U7CO
UT WOS:000841125000006
PM 35588938
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Wu, SF
   Deng, CM
   Zhang, CY
   Xiong, JN
   Gu, XF
   Wang, Z
   Tu, JJ
   Xie, JM
AF Wu, Shuifa
   Deng, Cuimin
   Zhang, Caiyun
   Xiong, Jiani
   Gu, Xiaofan
   Wang, Ze
   Tu, Jingjing
   Xie, Jieming
TI Preparation of a novel EGFR specific immunotoxin and its efficacy of
   anti-colorectal cancer in vitro and in vivo
SO CLINICAL & TRANSLATIONAL ONCOLOGY
LA English
DT Article
DE Immunotoxin; C-CUS245C; Cetuximab; CUS245C; Targeted therapy; Colorectal
   neoplasms
ID PROTEIN
AB Objectives Epithelial growth factor receptor (EGFR), as a malignancy marker, is overly expressed in multiple solid tumors including colorectal neoplasms, one of the most prevalent malignancies worldwide. The main objective of this study is to enhance the efficacy of anti-tumor therapy targeting EGFR by constructing a novel EGFR-specific immunotoxin (C-CUS245C) based on Cetuximab and recombinant Cucurmosin (CUS245C). Methods E. coli BL21 (DE3) PlysS (E. coli) was used to express CUS245C with a cysteine residue inserting to the C-terminus of Cucurmosin. Then immobilized metal ion affinity chromatography (IMAC) was used to purify CUS245C. The chemical conjugation method was used for the preparation of C-CUS245C. Then dialysis and IMAC were used to purify C-CUS245C. Western blot as well as SDS-PAGE was carried out to characterize the formation of C-CUS245C. At last the anti-colorectal cancer activity of C-CUS245C was investigated in vitro and in vivo. Results CUS245C with high purity could be obtained from the prokaryotic system. C-CUS245C was successfully constructed and highly purified. The cytotoxicity assays in vitro showed a significant proliferation inhibition of C-CUS245C on EGFR-positive cells for 120 h with IC50 values less than 0.1 pM. Besides, the anti-tumor efficacy of C-CUS245C was remarkably more potent than that of Cetuximab, CUS245C, and C + CUS245C (P < 0.001). Whereas the cytotoxicity of C-CUS245C could hardly be detected on EGFR-null cell line. Our results also showed that C-CUS245C had efficacy of anti-colorectal cancer in mouse xenograft model, indicating the therapeutic potential of C-CUS245C for the targeted therapy of colorectal neoplasms. Conclusions C-CUS245C exhibits potent and EGFR-specific cytotoxicity. Insertional mutagenesis technique is worthy to be adopted in the preparation of immunotoxin. Immunotoxin can be highly purified through dialysis followed by IMAC.
C1 [Wu, Shuifa; Deng, Cuimin; Zhang, Caiyun; Gu, Xiaofan; Wang, Ze; Tu, Jingjing; Xie, Jieming] Fujian Med Univ, Coll Pharm, Dept Pharmacol, Fuzhou, Fujian, Peoples R China.
   [Wu, Shuifa] Fujian Med Univ, Dept Pharm, Quanzhou Hosp 1, Quanzhou, Fujian, Peoples R China.
   [Deng, Cuimin] QuanZhou Womens & Childrens Hosp, Dept Pharm, Quanzhou, Fujian, Peoples R China.
   [Xiong, Jiani] Fujian Canc Hosp, Dept Med Oncol, Fuzhou, Fujian, Peoples R China.
   [Xiong, Jiani] Fujian Med Univ, Canc Hosp, Fuzhou, Fujian, Peoples R China.
   [Xiong, Jiani] Fujian Canc Hosp, Canc Bioimmunotherapy Ctr, Fuzhou, Fujian, Peoples R China.
C3 Fujian Medical University; Fujian Medical University; Fujian Medical
   University
RP Xie, JM (corresponding author), Fujian Med Univ, Coll Pharm, Dept Pharmacol, Fuzhou, Fujian, Peoples R China.
EM jmxie@fjmu.edu.cn
OI Wu, Shuifa/0000-0002-8023-1874; Xie, Jieming/0000-0003-3884-0550
FU National Science Foundation of China [30772587]; Natural Science
   Foundation of Fujian Province [2016J01769]; Fujian Province health and
   family planning scientific research talent training project
   [2018-CX-40]; Startup Fund for scientific research, Fujian Medical
   University [2019 QH 1196]
FX This work was supported by the National Science Foundation of China (No.
   30772587), the Natural Science Foundation of Fujian Province (No.
   2016J01769), the Fujian Province health and family planning scientific
   research talent training project (No. 2018-CX-40), and Startup Fund for
   scientific research, Fujian Medical University (No. 2019 QH 1196).
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NR 57
TC 6
Z9 6
U1 1
U2 15
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 2021
VL 23
IS 8
BP 1549
EP 1560
DI 10.1007/s12094-020-02548-8
EA JAN 2021
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TB1HS
UT WOS:000609050300001
PM 33474678
DA 2025-01-04
ER

PT J
AU Wang, HY
   Diao, Y
   Tan, PZ
   Liang, H
AF Wang, Hui-Yan
   Diao, Yan
   Tan, Pei-Zhu
   Liang, Huan
TI Four centrosome-related genes to predict the prognosis and drug
   sensitivity of patients with colon cancer
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Colon cancer; Centrosome; Signature; Prognostic; Immune
   microenvironment; Therapy
ID COMPREHENSIVE ANALYSIS; POOR-PROGNOSIS; EXPRESSION; MTUS1; SURVIVAL
AB BACKGROUND As the primary microtubule organizing center in animal cells, centrosome abnormalities are involved in human colon cancer. AIM To explore the role of centrosome-related genes (CRGs) in colon cancer. METHODS CRGs were collected from public databases. Consensus clustering analysis was performed to separate the Cancer Genome Atlas cohort. Univariate Cox and least absolute shrinkage selection operator regression analyses were performed to identify candidate prognostic CRGs and construct a centrosome-related signature (CRS) to score colon cancer patients. A nomogram was developed to evaluate the CRS risk in colon cancer patients. An integrated bioinformatics analysis was conducted to explore the correlation between the CRS and tumor immune microenvironment and response to immunotherapy, chemotherapy, and targeted therapy. Single-cell transcriptome analysis was conducted to examine the immune cell landscape of core prognostic genes. RESULTS A total of 726 CRGs were collected from public databases. A CRS was constructed, which consisted of the following four genes: TSC1, AXIN2, COPS7A, and MTUS1. Colon cancer patients with a high-risk signature had poor survival. Patients with a high-risk signature exhibited decreased levels of plasma cells and activated memory CD4+ T cells. Regarding treatment response, patients with a high-risk signature were resistant to immunotherapy, chemotherapy, and targeted therapy. COPS7A expression was relatively high in endothelial cells and fibroblasts. MTUS1 expression was high in endothelial cells, fibroblasts, and malignant cells. CONCLUSION We constructed a centrosome-related prognostic signature that can accurately predict the prognosis of colon cancer patients, contributing to the development of individualized treatment for colon cancer.
C1 [Wang, Hui-Yan; Liang, Huan] Harbin Med Univ, Canc Hosp, Dept Clin Lab, 150 Haping Rd, Harbin 150086, Heilongjiang, Peoples R China.
   [Diao, Yan] Heilongjiang Prov Hosp, Dept Clin Lab, Harbin 150000, Heilongjiang, Peoples R China.
   [Tan, Pei-Zhu] Harbin Med Univ, Translat Med Ctr Northern China, Harbin 150081, Heilongjiang, Peoples R China.
C3 Harbin Medical University; Harbin Medical University
RP Liang, H (corresponding author), Harbin Med Univ, Canc Hosp, Dept Clin Lab, 150 Haping Rd, Harbin 150086, Heilongjiang, Peoples R China.
EM 601774@hrbmu.edu.cn
FU Heilongjiang Postdoctoral Fund [LBH-Z18214]; Haiyan Foundation of Harbin
   Medical University Cancer Hospital [JJQN2014-06]; Foundation of Health
   Commission of Heilongjiang Province [2016-096]
FX Supported by Heilongjiang Postdoctoral Fund, No. LBH-Z18214; Haiyan
   Foundation of Harbin Medical University Cancer Hospital, No.
   JJQN2014-06; and Foundation of Health Commission of Heilongjiang
   Province, No. 2016-096.
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NR 63
TC 1
Z9 1
U1 0
U2 0
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 MAY 15
PY 2024
VL 16
IS 5
DI 10.4251/wjgo.v16.i5.1908
PG 18
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA SH1P2
UT WOS:001233475700001
PM 38764831
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Chun, KS
   Joo, SH
AF Chun, Kyung-Soo
   Joo, Sang Hoon
TI Modulation of Reactive Oxygen Species to Overcome 5-Fluorouracil
   Resistance
SO BIOMOLECULES & THERAPEUTICS
LA English
DT Review
DE Reactive oxygen species; Cancer; Resistance; 5-Fluorouracil
ID HUMAN COLORECTAL-CANCER; CELL-CYCLE ARREST; LIVER-CANCER;
   CLINICAL-SIGNIFICANCE; OXIDATIVE STRESS; AMINOPEPTIDASE-N;
   ANTITUMOR-ACTIVITY; INDUCED APOPTOSIS; CARCINOMA CELLS; NADPH OXIDASE
AB 5-Fluorouracil (5-FU) remains to be an important chemotherapeutic drug for treating several cancers when targeted therapy is unavailable. Chemoresistance limits the clinical utility of 5-FU, and new strategies are required to overcome the resistance. Reactive oxygen species (ROS) and antioxidants are balanced differently in both normal and cancer cells. Modulating ROS can be one method of overcoming 5-FU resistance. This review summarizes selected compounds and endogenous cellular targets modulating ROS generation to overcome 5-FU resistance.
C1 [Chun, Kyung-Soo] Keimyung Univ, Coll Pharm, Daegu 42601, South Korea.
   [Joo, Sang Hoon] Daegu Catholic Univ, Dept Pharm, Gyongsan 38430, South Korea.
C3 Keimyung University; Catholic University of Daegu
RP Joo, SH (corresponding author), Daegu Catholic Univ, Dept Pharm, Gyongsan 38430, South Korea.
EM sjoo@cu.ac.kr
RI Joo, Sang/B-4116-2008
FU Daegu Catholic University
FX This work was supported by research grants from Daegu Catholic
   University in 2020.
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NR 110
TC 17
Z9 17
U1 1
U2 24
PU KOREAN SOC APPLIED PHARMACOLOGY
PI SEOUL
PA RM 805, KOREAN FEDERATION SCIENCE & TECHNOLOGY B/D, 635-4 YEOKSAM-DONG,
   KANGNAM-GU, SEOUL, 135-703, SOUTH KOREA
SN 1976-9148
EI 2005-4483
J9 BIOMOL THER
JI Biomol. Ther.
PD NOV
PY 2022
VL 30
IS 6
BP 479
EP 489
DI 10.4062/biomolther.2022.017
EA APR 2022
PG 11
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 7S1MS
UT WOS:000790313000001
PM 35440517
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Otieno, SB
   Nasir, S
   Weir, A
   Johnson, R
AF Otieno, Steve Biko
   Nasir, Syed
   Weir, Alva
   Johnson, Robert
TI Rapid Response in a Patient with Relapsed/Refractory Multiple Myeloma
   Treated with BRAF/MEK Inhibitors
SO CASE REPORTS IN HEMATOLOGY
LA English
DT Article
ID V600E MUTATION; ABSENCE
AB Patients with relapsed and refractory multiple myeloma have a poor prognosis. The mitogen-activated protein kinase (MAPK) pathway has been implicated in the pathogenesis of multiple myeloma. Several mutations in this pathway can lead to its constitutive activation leading to oncogenesis. One such mutation is BRAFV600E which is a therapeutic target in the treatment of melanoma, lung cancer, colon cancer, thyroid cancer, and hairy cell leukemia. BRAFV600E-directed therapy currently does not have approval in multiple myeloma. It has been proposed that this mutation leads to proteasome inhibitor resistance. About 4-10% of multiple myeloma cases harbor the BRAFV600E mutation. Herein, we report a case of a patient with relapsed and refractory multiple myeloma who had a progression-free survival (PFS) of 8.5 months on BRAF-targeted therapy.
C1 [Otieno, Steve Biko; Nasir, Syed; Weir, Alva; Johnson, Robert] Univ Tennessee, Hlth Sci Ctr, Dept Hematol Oncol, 19 S Manassas, Memphis, TN 38103 USA.
   [Otieno, Steve Biko; Weir, Alva] Vet Affairs Med Ctr, 1030 Jefferson Ave, Memphis, TN 38104 USA.
   [Otieno, Steve Biko; Nasir, Syed; Johnson, Robert] West Canc & Res Inst, 7945 Wolf River Blvd, Germantown, TN 38138 USA.
C3 University of Tennessee System; University of Tennessee Health Science
   Center; US Department of Veterans Affairs; Veterans Health
   Administration (VHA); Memphis VA Medical Center
RP Otieno, SB (corresponding author), Univ Tennessee, Hlth Sci Ctr, Dept Hematol Oncol, 19 S Manassas, Memphis, TN 38103 USA.; Otieno, SB (corresponding author), Vet Affairs Med Ctr, 1030 Jefferson Ave, Memphis, TN 38104 USA.; Otieno, SB (corresponding author), West Canc & Res Inst, 7945 Wolf River Blvd, Germantown, TN 38138 USA.
EM sotieno@uthsc.edu; snasir@westclinic.com; alva.weir@va.gov;
   rjohnson@westclinic.com
OI Otieno, Steve/0000-0002-7902-398X
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NR 14
TC 4
Z9 4
U1 0
U2 1
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2090-6560
EI 2090-6579
J9 CASE REP HEMATOL
JI Case Rep. Hematol.
PD DEC 11
PY 2020
VL 2020
AR 8821415
DI 10.1155/2020/8821415
PG 4
WC Hematology
WE Emerging Sources Citation Index (ESCI)
SC Hematology
GA PI6RF
UT WOS:000601215100001
PM 33381330
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Qiao, C
   Wang, HY
   Guan, QT
   Wei, MJ
   Li, ZH
AF Qiao, Chu
   Wang, Haiying
   Guan, Qiutong
   Wei, Minjie
   Li, Zhenhua
TI Ferroptosis-based nano delivery systems targeted therapy for colorectal
   cancer: Insights and future perspectives
SO ASIAN JOURNAL OF PHARMACEUTICAL SCIENCES
LA English
DT Review
DE Colorectal cancer; Ferroptosis; Iron metabolism; Lipid metabolism; Nano
   delivery system; Immunotherapy
ID FERRITIN NANOPARTICLES; TUMOR MICROENVIRONMENT; PHOTODYNAMIC THERAPY;
   STEM-CELLS; DOXORUBICIN; IRON; ACTIVATION; SORAFENIB
AB There are limited options for patients who develop liver metastasis from colorectal cancer (CRC), the leading cause of cancer-related mortality worldwide. Emerging evidence has provided insights into iron deficiency and excess in CRC. Ferroptosis is an iron-dependent form of programmed cell death characterized by aberrant iron and lipid metabolism, which play crucial roles in tumorigenesis, tumor progression, and treatment options. A better understanding of the underlying molecular mechanism of ferroptosis has shed light on the current findings of ferroptosis-based nanodrug targeting strategies, such as driving ferroptosis in tumor cells and the tumor microenvironment, emerging combination therapy and against multidrug resistance. Furthermore, this review highlights the challenge and perspective of a ferroptosis-driven nanodrug delivery system for CRC-targeted therapy.(c) 2022 Shenyang Pharmaceutical University. 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 [Qiao, Chu; Wang, Haiying; Guan, Qiutong; Wei, Minjie; Li, Zhenhua] China Med Univ, Sch Pharm, Shenyang 110122, Peoples R China.
C3 China Medical University
RP Wei, MJ; Li, ZH (corresponding author), China Med Univ, Sch Pharm, Shenyang 110122, Peoples R China.
EM mjwei@cmu.edu.cn; lizh@cmu.edu.cn
OI Li, Zhenhua/0000-0001-9871-2257
FU High-level Talents Research Start-up Fund [1210619010]; China Medical
   University, Double First -Class Scientific Research Fund [3110210603]
FX This work was supported by grants from High-level Talents Research
   Start-up Fund (# 1210619010) of China Medical University, Double First
   -Class Scientific Research Fund (# 3110210603) of China Medical
   University.
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NR 129
TC 27
Z9 28
U1 12
U2 62
PU SHENYANG PHARMACEUTICAL UNIV
PI SHENYANG
PA SHENYANG PHARMACEUTICAL UNIV, NO 103, WENHUA RD, SHENYANG, 110016,
   PEOPLES R CHINA
SN 1818-0876
J9 ASIAN J PHARM SCI
JI Asian J. Pharm. Sci.
PD AUG
PY 2022
VL 17
IS 5
BP 613
EP 629
DI 10.1016/j.ajps.2022.09.002
PG 17
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 6C6VA
UT WOS:000882148000001
PM 36382305
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zheng, SQ
   Zhang, X
   Pang, ZQ
   Liu, JD
   Liu, SY
   Sheng, R
AF Zheng, Shaoqin
   Zhang, Xi
   Pang, Zhongqiu
   Liu, Jidong
   Liu, Siyu
   Sheng, Ren
TI Anti-Pan-Rspo Chimeric Protein-Conjugated Albumin Nanoparticle Provides
   Promising Opportunities in Cancer Targeted Therapy
SO ADVANCED HEALTHCARE MATERIALS
LA English
DT Article
DE antitumor agents; cancer; nanoparticles; Rspo and Wnt signaling;
   targeted therapy
ID INTESTINAL STEM-CELL; COLORECTAL-CANCER; CRYSTAL-STRUCTURE;
   WNT/BETA-CATENIN; COLON; INTEGRIN; LGR5; WNT; DIFFERENTIATION;
   NANOMEDICINE
AB Rspos (R-spondins) belong to a family of secreted proteins that causes various cancers via interacting the corresponding receptors. However, targeted therapeutic approaches against Rspos are largely lacking. In this study, a chimeric protein Rspo-targeting anticancer chimeric protein (RTAC) is originally designed, engineered, and characterized. RTAC shows satisfactory anticancer effects through inhibition of pan-Rspo-mediated Wnt/& beta;-catenin signaling activation both in vitro and in vivo. Furthermore, a conceptually novel antitumor strategy distinct from traditional drug delivery systems that release drugs inside tumor cells is proposed. A special "firewall" nano-system is designed to enrich on tumor cell surface and cover the plasma membrane, rather than undergoing endocytosis, to block oncogenic Rspos from binding to receptors. Cyclic RGD (Arg-Gly-Asp) peptide-linked globular cluster serum albumin nanoparticles (SANP) are integrated as a vehicle for conjugating RTAC (SANP-RTAC/RGD) for tumor tissue targeting. These nanoparticles can adhere to the tumor cell surface and enable RTAC to locally capture free Rspos with high spatial efficiency and selectivity to antagonize cancer progression. Therefore, this approach offers a new nanomedical anticancer route and obtains the "dual-targeting" capability for effective tumor clearance and low potential toxicity. This study presents a proof-of-concept for anti-pan-Rspo therapy and a nanoparticle-integrated paradigm for targeted cancer treatment.
C1 [Zheng, Shaoqin; Pang, Zhongqiu; Liu, Jidong; Liu, Siyu; Sheng, Ren] Northeastern Univ, Coll Life & Hlth Sci, 195 Chuangxin Rd, Shenyang 110819, Liaoning, Peoples R China.
   [Zhang, Xi] Northeastern Univ, Coll Sci, 3-11 Wenhua Rd, Shenyang 110004, Liaoning, Peoples R China.
C3 Northeastern University - China; Northeastern University - China
RP Liu, SY; Sheng, R (corresponding author), Northeastern Univ, Coll Life & Hlth Sci, 195 Chuangxin Rd, Shenyang 110819, Liaoning, Peoples R China.
EM liusiyu@mail.neu.edu.cn; shengren@mail.neu.edu.cn
RI Liu, Siyu/GYV-4856-2022
OI Sheng, Ren/0000-0002-2293-8986; Shaoqin, Zheng/0000-0002-3027-7305
FU Fundamental Research Fund for the Central Universities, China
   [N182005006]; National Natural Science Foundation of China [31970721,
   81902830]; Liaoning Revitalization~Talents Program [XLYC1807239];
   General Project of Natural Science Funds of Liaoning Province
   [2020-MS-082]
FX S.Z. and X.Z. contributed equally to this work. R.S. acknowledges
   support by the Fundamental Research Fund for the Central Universities,
   China N182005006 (completed), the Starting Funds for 100-talent plan of
   Northeastern University, National Natural Science Foundation of China
   31970721 and 81902830, and Liaoning Revitalization & nbsp;Talents
   Program XLYC1807239 (completed). S.L. acknowledges support by the
   General Project of Natural Science Funds of Liaoning Province
   2020-MS-082.
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NR 38
TC 7
Z9 7
U1 5
U2 20
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 NOV
PY 2023
VL 12
IS 29
DI 10.1002/adhm.202301441
EA JUL 2023
PG 15
WC Engineering, Biomedical; Nanoscience & Nanotechnology; Materials
   Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Science & Technology - Other Topics; Materials Science
GA LJ6G6
UT WOS:001023050700001
PM 37414582
DA 2025-01-04
ER

PT J
AU Orlandi, A
   Calegari, MA
   Inno, A
   Berenato, R
   Caporale, M
   Niger, M
   Bossi, I
   Di Bartolomeo, M
   de Braud, F
   Pietrantonio, F
AF Orlandi, Armando
   Calegari, Maria Alessandra
   Inno, Alessandro
   Berenato, Rosa
   Caporale, Marta
   Niger, Monica
   Bossi, Ilaria
   Di Bartolomeo, Maria
   de Braud, Filippo
   Pietrantonio, Filippo
TI BRAF in metastatic colorectal cancer: the future starts now
SO PHARMACOGENOMICS
LA English
DT Review
DE BRAF; colorectal cancer; immunotherapy; target therapy
ID FOLFOXIRI PLUS BEVACIZUMAB; EGFR MONOCLONAL-ANTIBODIES; KRAS MUTATIONAL
   STATUS; COLON-CANCER; V600E MUTATION; MICROSATELLITE INSTABILITY;
   1ST-LINE TREATMENT; RAS MUTATIONS; POOR SURVIVAL; MAPK PATHWAY
AB BRAF mutations are detectable in about 5-15% of metastatic colorectal cancer (mCRC) patients and represent a clear negative prognostic factor. While in BRAF-mutated (BRAFmt) metastatic melanoma TKI target therapies (BRAF and MEK inhibitor), both alone or in combination, have shown significant efficacy, in BRAFmt CRC single-agent BRAF-inhibitors as well as chemotherapy seem to be ineffective. The critical role of EGFR in CRC and its multiple downstreaming pathways seem to be involved in this lack of response. In recent years, preclinical investigations and retrospective studies slowly increased our knowledge on BRAFmt CRC. This review analyses preclinical data and discusses several clinical trials in order to explore new therapeutic strategies targeting BRAFmt mCRC.
C1 [Orlandi, Armando; Calegari, Maria Alessandra] Univ Cattolica Sacro Cuore, Dept Med Oncol, Rome, Italy.
   [Inno, Alessandro] Sacro Cuore Don Calabria Hosp, Med Oncol, Verona, Italy.
   [Berenato, Rosa; Caporale, Marta; Niger, Monica; Bossi, Ilaria; Di Bartolomeo, Maria; de Braud, Filippo; Pietrantonio, Filippo] Fdn IRCCS Ist Nazl Tumori, Dept Med Oncol, Milan, Italy.
C3 Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
   IRCCS Sacro Cuore Don Calabria; Fondazione IRCCS Istituto Nazionale
   Tumori Milan
RP Pietrantonio, F (corresponding author), Fdn IRCCS Ist Nazl Tumori, Dept Med Oncol, Milan, Italy.
EM filippo.pietrantonio@istitutotumori.mi.it
RI Inno, Alessandro/AAA-8268-2022; Niger, Monica/AAC-2452-2022;
   Pietrantonio, Filippo/C-2180-2017; calegari, maria
   alessandra/K-3929-2018; de Braud, Filippo Guglielmo Maria/B-9997-2017;
   Inno, Alessandro/ISB-4184-2023; Di Bartolomeo, Maria/D-1655-2017;
   ORLANDI, Armando/A-1517-2015
OI Pietrantonio, Filippo/0000-0002-8530-8420; Niger,
   Monica/0000-0002-9055-5338; calegari, maria
   alessandra/0000-0001-6856-2593; de Braud, Filippo Guglielmo
   Maria/0000-0003-0103-730X; Inno, Alessandro/0000-0001-6331-6908; Di
   Bartolomeo, Maria/0000-0002-7954-6609; ORLANDI,
   Armando/0000-0001-5253-4678
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NR 65
TC 14
Z9 15
U1 1
U2 5
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1462-2416
EI 1744-8042
J9 PHARMACOGENOMICS
JI Pharmacogenomics
PD DEC
PY 2015
VL 16
IS 18
BP 2069
EP 2081
DI 10.2217/pgs.15.140
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CX9RP
UT WOS:000366043300007
PM 26615988
DA 2025-01-04
ER

PT J
AU Dréanic, J
   Dhooge, M
   Barret, M
   Brezault, C
   Mir, O
   Chaussade, S
   Coriat, R
AF Dreanic, Johann
   Dhooge, Marion
   Barret, Maximilien
   Brezault, Catherine
   Mir, Olivier
   Chaussade, Stanislas
   Coriat, Romain
TI Anti-epidermal or anti-vascular endothelial growth factor as first-line
   metastatic colorectal cancer in modified Glasgow prognostic score 2′
   patients
SO JOURNAL OF CACHEXIA SARCOPENIA AND MUSCLE
LA English
DT Article
DE Colorectal cancer; C-reactive protein; Glasgow prognostic score;
   Targeted therapy; Bevacizumab; Cetuximab; Vascular epithelial growth
   factor; Epidermal growth factor receptor
ID SYSTEMIC INFLAMMATORY RESPONSE; C-REACTIVE PROTEIN; PHASE-III;
   BEVACIZUMAB; SURVIVAL; FLUOROURACIL; PANITUMUMAB; LEUCOVORIN; ERA;
   CHEMOTHERAPY
AB Background In metastatic colorectal cancer, the modified Glasgow prognostic score (mGPS) has been approved as an independent prognostic indicator of survival. No data existed on poor prognosis patients treated with molecular-targeted agents.
   Methods From January 2007 to February 2012, patients with metastatic colorectal cancer and poor predictive survival score (mGPS=2), treated with 5-fluorouracil-based chemotherapy in addition to an anti-epidermal growth factor receptor (EGFR) or anti-vascular epidermal growth factor (VEGF) therapy, were included to assess the interest of targeted therapy within mGPS=2' patients.
   Results A total of 27 mGPS=2' patients were included and received a 5-fluorouracil-based systemic chemotherapy in addition to an anti-EGFR treatment (cetuximab; n=18) or an anti-VEGF treatment (bevacizumab; n=9). Median follow-up was 12.1months (interquartile range 4.9-22). Patients were Eastern Cooperative Oncology Group (ECOG) Performance Status 1, 2, and 3 in 66% (n=18), 26% (n=7), and 8% (n=2), respectively. Comparing anti-EGFR and anti-VEGF groups, median progression-free survival was 3.9 and 15.4months, respectively, and was significantly different (P=0.046). Conversely, the median overall survival was not significantly different between the two groups (P=0.15).
   Conclusion Our study confirmed the poor survival of patients with mGPS=2 despite the use of targeted therapy and identified the superiority of an anti-VEGF treatment in progression-free survival, without a significant benefit in the overall survival compared with the anti-EGFR therapy. Our results deserved confirmation by a prospective clinical trial.
C1 [Dreanic, Johann; Dhooge, Marion; Barret, Maximilien; Brezault, Catherine; Chaussade, Stanislas; Coriat, Romain] Univ Paris 05, Hop Cochin, Sorbonne Paris Cite, Gastroenterol & Endoscopy Unit,Fac Med, Paris, France.
   [Mir, Olivier] Gustave Roussy, Dept Canc Med, Med Oncol, Villejuif, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Cochin - APHP; UNICANCER; Gustave Roussy
RP Dréanic, J (corresponding author), Hop Cochin, Gastroenterol & Endoscopy Unit, 27 Rue Faubourg St Jacques, F-75014 Paris, France.
EM johann.dreanic@cch.aphp.fr
RI Mir, Olivier/GNP-7828-2022; Coriat, Romain/O-7902-2017; Barret,
   Maximilien/O-8341-2017; Mir, Olivier/N-9946-2017
OI Dhooge, Marion/0000-0002-7279-5549; Barret,
   Maximilien/0000-0002-0566-7870; Mir, Olivier/0000-0002-6761-4002
CR [Anonymous], J CLIN ONCOL
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NR 32
TC 7
Z9 8
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2190-5991
EI 2190-6009
J9 J CACHEXIA SARCOPENI
JI J. Cachexia Sarcopenia Muscle
PD SEP
PY 2015
VL 6
IS 3
BP 231
EP 236
DI 10.1002/jcsm.12022
PG 6
WC Geriatrics & Gerontology; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Geriatrics & Gerontology; General & Internal Medicine
GA CQ5EB
UT WOS:000360625000006
PM 26401469
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Qi, L
   Zhang, Y
   Song, FY
   Han, Y
   Ding, YQ
AF Qi, Lu
   Zhang, Ying
   Song, Fuyao
   Han, Yue
   Ding, Yanqing
TI A newly identified small molecular compound acts as a protein kinase
   inhibitor to suppress metastasis of colorectal cancer
SO BIOORGANIC CHEMISTRY
LA English
DT Article
DE Protein kinase; Colorectal cancer; Small molecular compound; Kalirin;
   KALRN
ID DATABASE; MUTATIONS; KALIRIN; GENES; MAP
AB Background: Targeted therapy has demonstrated high efficacy in the treatment of advanced cancer, and protein kinase inhibitors are a major focus of that therapy; therefore, our study aimed to identify a new protein kinase inhibitor that could be used in the treatment of advanced cancers.
   Methods: We analyzed the expression profile of colorectal cancer (CRC), combined the driver gene and drug target databases, and identified protein kinase kalirin RhoGEF kinase (kalirin/KALRN) which is related to CRC metastasis. Based on the structure of kalirin, we screened for the small molecular compound ZINC65387069. We first compared the kinase inhibitory activities and molecular properties of ZINC65387069 and tyrosine kinase inhibitors (TKIs). We then determined the effects of ZINC65387069 on the phosphorylation of protein kinase BRaf. Finally, we determined the effects of ZINC65387069 on migration and apoptosis of HCT116 cells as well as RKO cells. The cell cytoskeleton was also determined.
   Results: Compared with traditional TKIs, ZINC65387069 had stronger kinase inhibitory activity, a simpler structure, higher water solubility, a smaller polar surface area, and lower molecular weight and volume. In CRC cells, ZINC65387069 could significantly inhibit the phosphorylation of B-Raf as well as inhibit cell migration, destroy the cell cytoskeleton, and promote cell apoptosis.
   Conclusion: ZINC65387069 is a newly identified protein kinase inhibitor that deserves additional research as a lead compound for drug development to help create targeted therapy against CRC.
C1 [Qi, Lu; Song, Fuyao; Han, Yue; Ding, Yanqing] Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou 510515, Peoples R China.
   [Qi, Lu; Song, Fuyao; Han, Yue; Ding, Yanqing] Southern Med Univ, Sch Basic Med Sci, Dept Pathol, Guangzhou 510515, Peoples R China.
   [Qi, Lu; Song, Fuyao; Han, Yue; Ding, Yanqing] Guangdong Prov Key Lab Mol Oncol Pathol, Guangzhou 510515, Peoples R China.
   [Zhang, Ying] Southern Med Univ, Sch Publ Hlth, Dept Radiat Med, Guangzhou 510515, Peoples R China.
   [Zhang, Ying] Guangdong Prov Key Lab Trop Dis Res, Guangzhou 510515, Peoples R China.
C3 Southern Medical University - China; Southern Medical University -
   China; Southern Medical University - China
RP Qi, L; Ding, YQ (corresponding author), Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou 510515, Peoples R China.
EM kuuga888@qq.com; dyq@fimmu.com
RI Wang, Ziwen/AAG-9607-2021
FU Scientific Research Starting Foundation of Southern Medical University
   [PY2018N003]; National Natural Science Foundation of China [81972754,
   81773101]; National Key Basic Research Program of China (973 program)
   [2015CB554002]; China Postdoctoral Science Foundation [2020TQ0136,
   2020M672714]
FX This work was supported by the Scientific Research Starting Foundation
   of Southern Medical University (PY2018N003), the National Natural
   Science Foundation of China (81972754, 81773101), the National Key Basic
   Research Program of China (973 program, 2015CB554002), the China
   Postdoctoral Science Foundation (2020TQ0136, 2020M672714).
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NR 40
TC 6
Z9 6
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 0045-2068
EI 1090-2120
J9 BIOORG CHEM
JI Bioorganic Chem.
PD FEB
PY 2021
VL 107
AR 104625
DI 10.1016/j.bioorg.2021.104625
EA JAN 2021
PG 8
WC Biochemistry & Molecular Biology; Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA QH2KM
UT WOS:000618106100003
PM 33454506
DA 2025-01-04
ER

PT J
AU Li, DY
   Hu, CH
   Li, HB
AF Li, Dongyu
   Hu, Chenghao
   Li, Huibin
TI Survivin as a novel target protein for reducing the proliferation of
   cancer cells (Review)
SO BIOMEDICAL REPORTS
LA English
DT Review
DE survivin; cancer; programmed cell death; target therapy
ID SEPANTRONIUM BROMIDE YM155; UNRESECTABLE STAGE-III; GASTRIC-CANCER;
   BREAST-CANCER; STEM-CELL; COLON-CANCER; LUNG-CANCER; DNA-DAMAGE;
   PHASE-II; REGULATES SURVIVIN
AB Survivin, also known as baculoviral inhibitor of apoptosis repeat-containing 5, is a novel member of the inhibitor of apoptosis protein family. Survivin is highly expressed in tumors and embryonic tissues and is associated with tumor cell differentiation, proliferation, invasion and metastasis; however, survivin is expressed at low levels in normal terminally differentiated adult tissues. Meanwhile, the expression level of survivin is also a negative prognostic factor for patients with cancer. These unique characteristics of survivin make it an exciting potential therapeutic target for cancer treatment. This review will discuss the biological characteristics of survivin and its potential use as a treatment target to reduce cancer cell proliferation.
C1 [Li, Dongyu] Univ Wisconsin, Dept Genet, Coll Agr & Life Sci, Madison, WI 53706 USA.
   [Hu, Chenghao] Weifang Med Univ, Sch Clin Med, Weifang 261000, Shandong, Peoples R China.
   [Li, Huibin] Peoples Hosp Linyi, Dept Burns & Plast Surg, 27 Jiefang Rd, Linyi 276000, Shandong, Peoples R China.
C3 University of Wisconsin System; University of Wisconsin Madison;
   Shandong Second Medical University
RP Li, HB (corresponding author), Peoples Hosp Linyi, Dept Burns & Plast Surg, 27 Jiefang Rd, Linyi 276000, Shandong, Peoples R China.
EM lihuibin1234@163.com
RI Li, Huibin/V-1502-2019; Li, Dongyu/G-1380-2018
OI Li, Huibin/0000-0003-0170-7115; Li, Dongyu/0000-0001-7581-0276
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NR 99
TC 80
Z9 91
U1 0
U2 17
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 2049-9434
EI 2049-9442
J9 BIOMED REP
JI Biomed. Rep.
PD MAY
PY 2018
VL 8
IS 5
BP 399
EP 406
DI 10.3892/br.2018.1077
PG 8
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA GG5FG
UT WOS:000432720300001
PM 29725522
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Rogers, JE
   Dasari, A
   Eng, C
AF Rogers, Jane E.
   Dasari, Arvind
   Eng, Cathy
TI The Treatment of Colorectal Cancer During Pregnancy: Cytotoxic
   Chemotherapy and Targeted Therapy Challenges
SO ONCOLOGIST
LA English
DT Article
DE Pregnancy; Antineoplastics; Colorectal neoplasms; Monoclonal antibodies
ID COLON-CANCER; MONOCLONAL-ANTIBODIES; DESCENDING COLON; RECTAL-CANCER;
   IN-UTERO; IRINOTECAN; PHARMACOKINETICS; ERLOTINIB; AGENTS; IMPACT
AB Cancer diagnosed during pregnancy has increased because of delayed child-bearing and the known occurrence of age-dependent malignancies. Cases of colorectal cancer (CRC) in pregnancy have recently been reported. With the expected rise in CRC diagnosed in young adults coupled with the current trend of delayed child-bearing, CRC during pregnancy is likely to increase. Treating pregnant women with CRC by using antineoplastics presents a dilemma because there are many unknowns to guide treatment decisions. We review the issues regarding the use of 10 CRC-approved agents in pregnancy.
C1 [Rogers, Jane E.] Univ Texas MD Anderson Canc Ctr, Pharm Clin Programs, Houston, TX 77030 USA.
   [Dasari, Arvind; Eng, Cathy] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center
RP Rogers, JE (corresponding author), Univ Texas MD Anderson Canc Ctr, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM jerogers@mdanderson.org
OI Rogers, Jane/0000-0002-7275-7008; Eng, Cathy/0000-0003-2335-0612
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NR 69
TC 34
Z9 37
U1 0
U2 12
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD MAY
PY 2016
VL 21
IS 5
BP 563
EP 570
DI 10.1634/theoncologist.2015-0362
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DZ2IB
UT WOS:000385664400011
PM 27000464
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Miyamoto, Y
   Zhang, W
   Lenz, HJ
AF Miyamoto, Yuji
   Zhang, Wu
   Lenz, Heinz-Josef
TI Molecular Landscape and Treatment Options for Patients with Metastatic
   Colorectal Cancer
SO INDIAN JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Review
DE Colorectal cancer; Chemotherapy; Targeted therapy; Biomarker;
   Personalized therapy; Molecular pathway
ID MISMATCH REPAIR STATUS; MONOCLONAL-ANTIBODY THERAPY; FOLFOXIRI PLUS
   BEVACIZUMAB; DISEASE-FREE SURVIVAL; RAS GENE MUTATION; WILD-TYPE KRAS;
   CELL-FREE DNA; MICROSATELLITE-INSTABILITY; COLON-CANCER; BRAF MUTATION
AB Over the last 20 years, median survival for patients with metastatic colorectal cancer (CRC) has remarkably improved from about 12 to over 30 months, mainly because of the development of new agents and patient selection using predictive biomarkers. However, the identification of the most effective treatment for an individual patient is still a challenge. Molecular profiling of CRC has made great progress, but it is limited by tumor heterogeneity and absence of driver mutation. However, RAS, BRAF, and microsatellite instability are validated biomarker recommended by NCCN and ESMO. In this review, we discuss recent advances and future developments.
C1 [Miyamoto, Yuji; Zhang, Wu; Lenz, Heinz-Josef] Univ Southern Calif, Keck Sch Med, Div Med Oncol, Norris Comprehens Canc Ctr,Shanon A Carpenter Lab, 1441 Eastlake Ave, Los Angeles, CA 90033 USA.
   [Miyamoto, Yuji] Kumamoto Univ, Grad Sch Med Sci, Dept Gastroenterol Surg, Kumamoto, Japan.
C3 University of Southern California; Kumamoto University
RP Lenz, HJ (corresponding author), Univ Southern Calif, Keck Sch Med, Div Med Oncol, Norris Comprehens Canc Ctr,Shanon A Carpenter Lab, 1441 Eastlake Ave, Los Angeles, CA 90033 USA.
EM LENZ@med.usc.edu
OI Miyamoto, Yuji/0000-0003-3948-5044
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NR 109
TC 2
Z9 2
U1 0
U2 4
PU SPRINGER INDIA
PI NEW DELHI
PA 7TH FLOOR, VIJAYA BUILDING, 17, BARAKHAMBA ROAD, NEW DELHI, 110 001,
   INDIA
SN 0975-7651
EI 0976-6952
J9 INDIA J SURG ONCOL
JI India J. Surg. Oncol.
PD DEC
PY 2017
VL 8
IS 4
BP 580
EP 590
DI 10.1007/s13193-016-0543-z
PG 11
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA FO0VH
UT WOS:000416469300022
PM 29203992
OA Green Published
DA 2025-01-04
ER

PT J
AU Rong, Z
   Zheng, KF
   Chen, J
   Jin, XF
AF Rong, Ze
   Zheng, Kaifeng
   Chen, Jun
   Jin, Xiaofeng
TI The cross talk of ubiquitination and chemotherapy tolerance in
   colorectal cancer
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE CRC; Ubiquitination enzymes; Chemoresistance; Targeted therapy
ID SMALL-MOLECULE ANTAGONIST; X-LINKED INHIBITOR; III COLON-CANCER;
   STAGE-II; PHASE-I; MESENCHYMAL TRANSITION; MEDIATED DEGRADATION;
   PROTEASOME SYSTEM; APOPTOSIS PROTEIN; TUMOR-SUPPRESSOR
AB Ubiquitination, a highly adaptable post-translational modification, plays a pivotal role in maintaining cellular protein homeostasis, encompassing cancer chemoresistance-associated proteins. Recent findings have indicated a potential correlation between perturbations in the ubiquitination process and the emergence of drug resistance in CRC cancer. Consequently, numerous studies have spurred the advancement of compounds specifically designed to target ubiquitinates, offering promising prospects for cancer therapy. In this review, we highlight the role of ubiquitination enzymes associated with chemoresistance to chemotherapy via the Wnt/beta-catenin signaling pathway, epithelial-mesenchymal transition (EMT), and cell cycle perturbation. In addition, we summarize the application and role of small compounds that target ubiquitination enzymes for CRC treatment, along with the significance of targeting ubiquitination enzymes as potential cancer therapies.
C1 [Rong, Ze; Zheng, Kaifeng; Chen, Jun; Jin, Xiaofeng] Ningbo Univ, Affiliated Peoples Hosp, Dept Chemoradiotherapy, Ningbo 315040, Peoples R China.
   [Jin, Xiaofeng] Nngbo Univ, Hlth Sci Ctr, Dept Biochem & Mol Biol, Ningbo 315211, Peoples R China.
C3 Ningbo University
RP Rong, Z (corresponding author), Ningbo Univ, Affiliated Peoples Hosp, Dept Chemoradiotherapy, Ningbo 315040, Peoples R China.
EM 15058485619@163.com; zheng-kf@163.com; cjcj992@163.com;
   jinxiaofeng@nbu.edu.cn
RI zheng, kaifeng/ABH-1586-2021
FU The Natural Science Foundation of Ningbo
FX No Statement Available
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NR 233
TC 2
Z9 2
U1 0
U2 8
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 MAR 23
PY 2024
VL 150
IS 3
AR 154
DI 10.1007/s00432-024-05659-9
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LU4A6
UT WOS:001189289100001
PM 38521878
OA hybrid
DA 2025-01-04
ER

PT J
AU Magliacane, G
   Grassini, G
   Bartocci, P
   Francaviglia, I
   Dal Cin, E
   Barbieri, G
   Arrigoni, G
   Pecciarini, L
   Doglioni, C
   Cangi, MG
AF Magliacane, Gilda
   Grassini, Greta
   Bartocci, Paola
   Francaviglia, Ilaria
   Dal Cin, Elena
   Barbieri, Gianluca
   Arrigoni, Gianluigi
   Pecciarini, Lorenza
   Doglioni, Claudio
   Cangi, Maria Giulia
TI Rapid targeted somatic mutation analysis of solid tumors in routine
   clinical diagnostics
SO ONCOTARGET
LA English
DT Article
DE Pathology; molecular diagnostics; solid tumors; high throughput
   mass-spectrometry; target therapy; mutations
ID CELL LUNG-CANCER; K-RAS MUTATIONS; COLORECTAL-CANCER; BRAF MUTATIONS;
   MOLECULAR-PATHOLOGY; MELANOMA; VEMURAFENIB; INHIBITORS; FREQUENCY;
   PARADIGM
AB Tumor genotyping is an essential step in routine clinical practice and pathology laboratories face a major challenge in being able to provide rapid, sensitive and updated molecular tests.
   We developed a novel mass spectrometry multiplexed genotyping platform named PentaPanel to concurrently assess single nucleotide polymorphisms in 56 hotspots of the 5 most clinically relevant cancer genes, KRAS, NRAS, BRAF, EGFR and PIK3CA for a total of 221 detectable mutations. To both evaluate and validate the PentaPanel performance, we investigated 1025 tumor specimens of 6 different cancer types (carcinomas of colon, lung, breast, pancreas, and biliary tract, and melanomas), systematically addressing sensitivity, specificity, and reproducibility of our platform. Sanger sequencing was also performed for all the study samples.
   Our data showed that PentaPanel is a high throughput and robust tool, allowing genotyping for targeted therapy selection of 10 patients in the same run, with a practical turnaround time of 2 working days. Importantly, it was successfully used to interrogate different DNAs isolated from routinely processed specimens (formalin-fixed paraffin embedded, frozen, and cytological samples), covering all the requirements of clinical tests.
   In conclusion, the PentaPanel platform can provide an immediate, accurate and cost effective multiplex approach for clinically relevant gene mutation analysis in many solid tumors and its utility across many diseases can be particularly relevant in multiple clinical trials, including the new basket trial approach, aiming to identify appropriate targeted drug combination strategies.
C1 [Magliacane, Gilda; Grassini, Greta; Francaviglia, Ilaria; Dal Cin, Elena; Arrigoni, Gianluigi; Pecciarini, Lorenza; Doglioni, Claudio; Cangi, Maria Giulia] IRCCS San Raffaele Sci Inst, Unit Pathol, Milan, Italy.
   [Bartocci, Paola; Barbieri, Gianluca] Diatech Pharmacogenet Co, Jesi, Italy.
C3 Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele
RP Cangi, MG (corresponding author), IRCCS San Raffaele Sci Inst, Unit Pathol, Milan, Italy.
EM doglioni.claudio@hsr.it; cangi.mariagiulia@hsr.it
RI Pecciarini, Lorenza/GQI-3544-2022; Cangi, Maria Giulia/CAF-1459-2022
OI DOGLIONI, Claudio/0000-0002-4969-5216; Cangi, Maria
   Giulia/0000-0002-9472-0935; PECCIARINI, LORENZA/0009-0005-3864-1692
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NR 28
TC 12
Z9 13
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 OCT 13
PY 2015
VL 6
IS 31
BP 30592
EP 30603
DI 10.18632/oncotarget.5190
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CU0DD
UT WOS:000363185200027
PM 26435479
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Li, YJ
   Cheng, HM
   Zhang, Z
   Zhuang, XX
   Luo, JF
   Long, HY
   Zhou, Y
   Xu, Y
   Taghipouran, R
   Li, D
   Patterson, A
   Smaill, J
   Tu, ZC
   Wu, DH
   Ren, XM
   Ding, K
AF Li, Yingjun
   Cheng, Huimin
   Zhang, Zhang
   Zhuang, Xiaoxi
   Luo, Jinfeng
   Long, Huoyou
   Zhou, Yang
   Xu, Yong
   Taghipouran, Rana
   Li, Dan
   Patterson, Adam
   Smaill, Jeff
   Tu, Zhengchao
   Wu, Donghai
   Ren, Xiaomei
   Ding, Ke
TI <i>N</i>-(3-Ethynyl-2,4-difluorophenyl)sulfonamide Derivatives as
   Selective Raf Inhibitors
SO ACS MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE B-Raf; colon cancer; melanoma; kinase inhibitor; targeted therapy
ID BRAF INHIBITORS; CANCER-THERAPY; KINASE INHIBITORS; B-RAF; MUTATIONS;
   MELANOMA; RESISTANCE
AB A series of N-(3-ethynyl-2,4-difluorophenyl)sulfonamides were identified as new selective Raf inhibitors. The compounds potently inhibit B-Raf(V600E) with low nanomolar IC50 values and exhibit excellent target specificity in a selectivity profiling investigation against 468 kinases. They strongly suppress proliferation of a panel of human cancer cell lines and patient-derived melanoma cells with B-Raf(V600E) mutation while being significantly less potent to the cells with B-Raf(WT). The compounds also display favorable pharmacokinetic properties with a preferred example (3s) demonstrating significant in vivo antitumor efficacy in a xenograft mouse model of B-Raf(V600E) mutated Colo205 human colorectal cancer cells, supporting it as a promising lead compound for further anticancer drug discovery.
C1 [Li, Yingjun; Cheng, Huimin; Zhang, Zhang; Zhuang, Xiaoxi; Luo, Jinfeng; Long, Huoyou; Zhou, Yang; Xu, Yong; Tu, Zhengchao; Wu, Donghai; Ren, Xiaomei; Ding, Ke] Chinese Acad Sci, Guangzhou Inst Biomed & Hlth, State Key Lab Resp Dis, Guangzhou 510530, Guangdong, Peoples R China.
   [Li, Yingjun; Zhou, Yang] Univ Chinese Acad Sci, Beijing 100049, Peoples R China.
   [Zhang, Zhang] Jinan Univ, Biotechnol Inst Chinese Mat Med, Guangzhou 510632, Guangdong, Peoples R China.
   [Zhang, Zhang] Jinan Univ, Dept Pharmacol, Guangzhou 510632, Guangdong, Peoples R China.
   [Taghipouran, Rana; Li, Dan; Patterson, Adam; Smaill, Jeff] Univ Auckland, Auckland Canc Soc Res Ctr, Auckland 1142, New Zealand.
   [Patterson, Adam; Smaill, Jeff] Univ Auckland, Maurice Wilkins Ctr Mol Biodiscovery, Auckland 1142, New Zealand.
C3 Chinese Academy of Sciences; Guangzhou Institute of Biomedicine &
   Health, CAS; State Key Laboratory of Respiratory Disease; Chinese
   Academy of Sciences; University of Chinese Academy of Sciences, CAS;
   Jinan University; Jinan University; University of Auckland; University
   of Auckland
RP Ren, XM (corresponding author), Chinese Acad Sci, Guangzhou Inst Biomed & Hlth, State Key Lab Resp Dis, 190 Kaiyuan Ave, Guangzhou 510530, Guangdong, Peoples R China.
EM ren_xiaomei@gibh.ac.cn; ding_ke@gibh.ac.cn
RI Ding, Ke/B-3257-2010; Zou, Xiaoxin/ABD-6285-2021; Zhang,
   Zhang/JAX-2097-2023; li, yingjun/GWQ-2957-2022
OI Zhou, Yang/0000-0003-4167-6413; Patterson, Adam/0000-0001-5138-1227;
   Ding, Ke/0000-0001-9016-812X; li, yingjun/0000-0002-8376-1811
FU Ministry of Science and Technology of China [2014DFG32100]; National
   Natural Science Foundation [81425021, 21302186]; Health Research Council
   of New Zealand [13/1020]
FX We thank financial support from Ministry of Science and Technology of
   China (#2014DFG32100), the National Natural Science Foundation
   (#81425021, #21302186), and the Health Research Council of New Zealand
   (13/1020).
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NR 20
TC 30
Z9 32
U1 1
U2 35
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1948-5875
J9 ACS MED CHEM LETT
JI ACS Med. Chem. Lett.
PD MAY
PY 2015
VL 6
IS 5
BP 543
EP 547
DI 10.1021/acsmedchemlett.5b00039
PG 5
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Pharmacology & Pharmacy
GA CI6ZO
UT WOS:000354912900013
PM 26005530
OA Green Published
DA 2025-01-04
ER

PT J
AU Feng, M
   Zhao, ZW
   Yang, MX
   Ji, JS
   Zhu, D
AF Feng, Mei
   Zhao, Zhongwei
   Yang, Mengxuan
   Ji, Jiansong
   Zhu, Di
TI T-cell-based immunotherapy in colorectal cancer
SO CANCER LETTERS
LA English
DT Article
DE Cancer immunotherapy; Colorectal cancer; Immune checkpoint inhibitor;
   Tumor-specific antigen; Chimeric antigen receptor
ID ENCODING CARCINOEMBRYONIC ANTIGEN; NEWCASTLE-DISEASE VIRUS;
   TUMOR-SPECIFIC ANTIGENS; COLON-CANCER; MICROSATELLITE INSTABILITY;
   FRAMESHIFT-MUTATION; SUPPRESSOR-CELLS; POOR-PROGNOSIS; IMMUNE-SYSTEM;
   THERAPY
AB Colorectal cancer (CRC) is the leading cause of cancer death worldwide. CRC therapeutic strategies include surgical resection, chemotherapy, radiotherapy, and other approaches. However, patients with metastatic CRC have worse prognoses. In recent years, T-cell-based immunotherapy has elicited promising responses in B-cell malignancies, melanoma, and lung cancer, but most CRC patients are resistant to immunotherapy, chemotherapy, and targeted therapy. Immune checkpoint inhibitors have shown encouraging results in non-small cell lung cancer, melanoma, and other cancers, but immune checkpoint blockade is only effective for CRC subset with microsatellite instability. Other immunotherapies, such as cytokines, cancer vaccines, small molecules, oncolytic viruses, and chimeric antigen-receptor therapy, are currently in use against CRC. This review analyzes recent developments in immunotherapy for CRC treatment as well as the challenges in overcoming resistance.
C1 [Feng, Mei; Yang, Mengxuan; Zhu, Di] Fudan Univ, Minhang Hosp, Shanghai 201203, Peoples R China.
   [Feng, Mei; Yang, Mengxuan; Zhu, Di] Fudan Univ, Sch Pharm, Dept Pharmacol, Shanghai 201203, Peoples R China.
   [Zhao, Zhongwei; Ji, Jiansong] Zhejiang Univ, Key Lab Imaging Diag & Minimally Invas Intervent, Affiliated Lishui Hosp, Lishui 323000, Peoples R China.
   [Zhu, Di] Fudan Univ, Minist Educ, Key Lab Smart Drug Delivery, Shanghai 201203, Peoples R China.
   [Zhu, Di] Fudan Univ, Sch Pharm, State Key Lab Mol Engn Polymers, Shanghai 201203, Peoples R China.
   [Zhu, Di] Fudan Univ, Shanghai Engn Res Ctr ImmunoTherapeut, Shanghai 201203, Peoples R China.
C3 Fudan University; Fudan University; Zhejiang University; Fudan
   University; Fudan University; Fudan University
RP Zhu, D (corresponding author), Fudan Univ, Minhang Hosp, Shanghai 201203, Peoples R China.; Zhu, D (corresponding author), Fudan Univ, Sch Pharm, Dept Pharmacol, Shanghai 201203, Peoples R China.; Ji, JS (corresponding author), Zhejiang Univ, Key Lab Imaging Diag & Minimally Invas Intervent, Affiliated Lishui Hosp, Lishui 323000, Peoples R China.
EM jijiansong@zju.edu.cn; zhudi@fudan.edu.cn
RI Ji, Jiansong/AAG-9958-2020
OI , Jiansong/0000-0001-6975-620X
FU Science and Technology Commission of Shanghai [18ZR1403900]; National
   Natural Science Foundation of China [81872895]; project on joint
   translational research in the School of Pharmacy and Minhang Hospital
   [RO-MY201712]
FX The current study was supported by projects on the Science and
   Technology Commission of Shanghai (18ZR1403900) (D. Zhu), the National
   Natural Science Foundation of China (81872895) (D.Z.), and a project on
   joint translational research in the School of Pharmacy and Minhang
   Hospital (RO-MY201712) (D. Z.).
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NR 120
TC 54
Z9 56
U1 3
U2 38
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 FEB 1
PY 2021
VL 498
BP 201
EP 209
DI 10.1016/j.canlet.2020.10.040
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PH8TG
UT WOS:000600677200017
PM 33129958
DA 2025-01-04
ER

PT J
AU Su, CC
   Su, YC
   Wu, CC
   Lee, PT
AF Su, Chien-Chou
   Su, Yi-Chia
   Wu, Chih-Chien
   Lee, Pei-Ting
TI Explanatory Role of Conversion Surgery as a Mediator of the Mortality
   Risk Difference Between Patients With Unresectable Metastatic Colorectal
   Cancer Treated With First-Line Anti-EGFR Agents Versus Bevacizumab
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Antiepidermal growth factor receptor-blocking agents; Cetuximab; KRAS
   wild-type; Mediation analysis; Survival; Targeted therapy
ID COMORBIDITY INDEX; LIVER METASTASES; RESECTION; CHEMOTHERAPY; TAIWAN
AB This study investigated the impact of conversion surgery on mortality risk differences in metastatic colorectal cancer patients receiving anti-EGFR agents versus bevacizumab. Analyzing a cohort of 5,106 patients, the study found that conversion surgery played a significant role in improving survival outcomes, particularly in patients with KRAS wild-type tumors. These findings underscore the potential of conversion surgery to enhance overall survival in advanced colorectal cancer patients undergoing targeted therapies. Introduction: Bevacizumab and antiepidermal growth factor receptor-blocking (anti-EGFR) agents plus chemotherapy are first-line therapies for metastatic colorectal cancer (mCRC). Conversion surgery may improve outcomes; however, the extent to which it explains the difference in mortality rates among treatments is unclear. Herein, we aimed to assess the effects of conversion surger y on sur vival outcomes of patients with unresectable mCRC treated with bevacizumab and anti-EGFR agents. Materials and methods: This retrospective cohort study included patients with mCRC treated with bevacizumab and anti-EGFR agents as first-line therapy. We estimated the direct and indirect effects of treatments by comparing the mortality risk associated with targeted therapy type. Hazard ratios (HR) and the corresponding confidence intervals (CI) were estimated. Mediation analysis was used to estimate hazard ratio differences, and the proportion mediated. Results: A total of 5,106 patients were included. The natural indirect effect of conversion surgery reduced mortality risk (HR: 0.95; 95% CI, 0.93-0.97), with a mediated proportion of 42% after propensity score adjustment. In subgroup analyses, KRAS wild-type (HR: 0.94; 95% CI: 0.91-0.97), left tumor sidedness (HR: 0.94; 95% CI, 0.910.96), and liver resection (HR: 0.95; 95% CI, 0.93-0.98) were associated with reduced risks of mortality. The controlled and total direct effects of targeted therapy were associated with reduced mortality risk in the anti-EGFR-treated group compared to those in the bevacizumab-treated group; however, this effect was not statistically significant. Conclusion: Conversion surgery may account for the difference in survival outcomes between users of the anti-EGFR agents and bevacizumab.
C1 [Su, Chien-Chou] Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Coll Med, Clin Innovat & Res Ctr, Tainan, Taiwan.
   [Lee, Pei-Ting] Kaohsiung Vet Gen Hosp, Dept Pharm, Kaohsiung, Taiwan.
   [Su, Yi-Chia] Kaohsiung Med Univ, Sch Pharm, Coll Pharm, Kaohsiung, Taiwan.
   [Wu, Chih-Chien] Natl Cheng Kung Univ, Inst Clin Pharm & Pharmaceut Sci, Coll Med, Tainan, Taiwan.
   Chia Nan Univ Pharm & Sci, Dept Pharm, Tainan, Taiwan.
   [Wu, Chih-Chien] Kaohsiung Vet Gen Hosp, Dept Surg, Div Colorectal Surg, 386 Dazhong 1st Rd, Kaohsiung 813414, Taiwan.
   [Wu, Chih-Chien] Natl Yang Ming Chiao Tung Univ, Sch Med, Dept Surg, Taipei, Taiwan.
   Natl Cheng Kung Univ, Coll Med, Dept Publ Hlth, Tainan, Taiwan.
C3 National Cheng Kung University; National Cheng Kung University Hospital;
   Kaohsiung Veterans General Hospital; Kaohsiung Medical University;
   National Cheng Kung University; Chia Nan University of Pharmacy &
   Science; Kaohsiung Veterans General Hospital; National Yang Ming Chiao
   Tung University; National Cheng Kung University
RP Wu, CC (corresponding author), Kaohsiung Vet Gen Hosp, Dept Surg, Div Colorectal Surg, 386 Dazhong 1st Rd, Kaohsiung 813414, Taiwan.
EM pauleoswu@vghks.gov.tw
RI Su, Yichia/HJI-3668-2023
FU Kaohsiung Veterans General Hospital [KSVGH 113-129]
FX The authors wish to thank the Health Data Science Center, National Cheng
   Kung University Hospital, for providing admin-istrative and technical
   support, and Ms. Hsiao-Ling Chiu of the Cancer Center, Kaohsiung
   Veterans General Hospital, for her advisory comments on interpreting the
   results. This research was supported by Kaohsiung Veterans General
   Hospital (grant number KSVGH 113-129) .
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NR 23
TC 0
Z9 0
U1 0
U2 0
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD DEC
PY 2024
VL 23
IS 4
BP 364
EP 371
DI 10.1016/j.clcc.2024.05.008
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA O7R7E
UT WOS:001373059100001
PM 38879376
DA 2025-01-04
ER

PT J
AU Ahmed, M
   Chaudhari, K
   Babaei-Jadidi, R
   Dekker, LV
   Nateri, AS
AF Ahmed, Mehreen
   Chaudhari, Kritika
   Babaei-Jadidi, Roya
   Dekker, Lodewijk V.
   Nateri, Abdolrahman Shams
TI Concise Review: Emerging Drugs Targeting Epithelial Cancer Stem-Like
   Cells
SO STEM CELLS
LA English
DT Article
DE Cancer stem cells; Cell signaling; Differentiation; Self-renewal;
   Tissue-specific stem cells; Signal transduction; Targeted therapy; Drug
   targets
ID NEGATIVE BREAST-CANCER; TUMOR-INITIATING CELLS; SMALL-MOLECULE
   INHIBITOR; LUNG-CANCER; COLORECTAL-CANCER; IN-VITRO; MESENCHYMAL
   TRANSITION; SIDE POPULATION; SELF-RENEWAL; RESISTANCE
AB Increasing evidence suggests that cancer cell populations contain a small proportion of cells that display stem-like cell properties and which may be responsible for overall tumor maintenance. These cancer stem-like cells (CSCs) appear to have unique tumor-initiating ability and innate survival mechanisms that allow them to resist cancer therapies, consequently promoting relapses. Selective targeting of CSCs may provide therapeutic benefit and several recent reports have indicated this may be possible. In this article, we review drugs targeting CSCs, in selected epithelial cell-derived cancers.
C1 [Ahmed, Mehreen; Babaei-Jadidi, Roya; Nateri, Abdolrahman Shams] Univ Nottingham, Ctr Biomol Sci, Sch Pharm, Canc Genet & Stem Cell Grp, Nottingham, England.
   [Babaei-Jadidi, Roya] Univ Nottingham, Ctr Biomol Sci, Sch Med,Canc Biol, Tumor & Vasc Biol Labs,Div Canc & Stem Cells, Nottingham, England.
   [Dekker, Lodewijk V.] Univ Nottingham, Ctr Biomol Sci, Sch Pharm, Div Med Chem & Struct Biol, Nottingham, England.
   [Chaudhari, Kritika] Biomed Insights Ltd, Nottingham, England.
C3 University of Nottingham; University of Nottingham; University of
   Nottingham
RP Nateri, AS (corresponding author), Univ Nottingham, Sch Med, Canc Genet & Stem Cell Grp, Div Canc & Stem Cells,Canc Biol, Nottingham, England.
EM a.nateri@nottingham.ac.uk
RI ; Dekker, Lodewijk/J-6934-2013
OI Ahmed, Mehreen/0000-0002-0422-2343; Shams Nateri,
   Abdolrahman/0000-0002-6422-6813; Dekker, Lodewijk/0000-0001-5247-3297
FU Medical Research Council (MRC) [G0700763]; Cancer Research UK (CRUK)
   [A9275, A10247]; MRC [G0700763] Funding Source: UKRI
FX We thank B. Spencer-Dene and M. Ilyas for reading the manuscript, and
   the fantastic fundraising efforts of Alison Sims and her family in
   memory of Daz Sims to support the work in our laboratory. This study was
   supported by the Medical Research Council (MRC) Grant G0700763, and
   Cancer Research UK (CRUK) project Grants A9275 and A10247 to A. S. N.
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NR 102
TC 33
Z9 41
U1 1
U2 28
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
EI 1549-4918
J9 STEM CELLS
JI Stem Cells
PD APR
PY 2017
VL 35
IS 4
BP 839
EP 850
DI 10.1002/stem.2579
PG 12
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
   Oncology; Cell Biology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA EQ5DM
UT WOS:000398102000001
PM 28142204
OA Green Submitted, Bronze
DA 2025-01-04
ER

PT J
AU Gagto, JO
   Danguilan, JLJ
   Callueng, JMC
   Concejero, DAM
AF Gagto, Jesyl O.
   Danguilan, Jose Luis J.
   Callueng, Jose Miguel C.
   Concejero, Dante Allan M.
TI Hybrid approaches to pulmonary metastasectomy: a narrative review
SO VIDEO-ASSISTED THORACIC SURGERY
LA English
DT Review
DE Pulmonary metastasectomy (PM); oligometastases; hybrid approaches
ID STEREOTACTIC BODY RADIOTHERAPY; ISOLATED LUNG PERFUSION; MULTICENTER
   CLINICAL-TRIAL; BILATERAL PULMONARY; RADIOFREQUENCY ABLATION;
   CANCER-PATIENTS; COLORECTAL-CANCER; RADIATION-THERAPY; ARTERY PERFUSION;
   PHASE-I/II
AB Background and Objective: Pulmonary metastasectomy (PM) is a common surgical resective procedure performed by thoracic surgeons to improve long-term survival in selected patients with metastatic tumors in the lung. In the past, thoracotomy was the preferred surgical approach but in recent years, treatment options have expanded to include minimally invasive approaches, thermal ablation therapy, stereotactic body radiation therapy (SBRT), and combinations of these techniques. With rapid advances in chemotherapy, immunotherapy, and molecular-targeted therapy, thoracic surgeons should review the indications and approaches to pulmonary metastases. This article aims to review the evolution of PM and the different modalities currently available to the stage IV patient.Methods: A narrative review of the literature from 1959 to 2023 was conducted using a variable combination of the following terms: "lung metastasectomy" or "pulmonary metastasectomy", "thoracic surgery" or "lung surgery", "radiosurgery" or "stereotactic ablative radiotherapy" or "stereotactic body radiotherapy", "chemotherapy" and "ablation". Hand searching and citation chaining were used to include relevant articles that were not indexed in the initial search strategy. Included articles were those of human subjects and published in English language.Key Content and Findings: A hybrid approach to PM brought about by interdisciplinary collaboration between the fields of thoracic surgery, interventional radiology, radiation oncology and medical oncology has expanded the indications for which this potentially curative procedure can be applied.Conclusions: Open and minimally-invasive surgical resection, ablation, SBRT, chemotherapy, immunotherapy and targeted therapy can be used synergistically when applied in combination to provide local and systemic control of oligometastases. A highly individualized and multidisciplinary approach has the potential to maximize survival outcomes in patients with pulmonary metastases.
C1 [Gagto, Jesyl O.; Concejero, Dante Allan M.] Univ Philippines, Philippine Gen Hosp, Div Thorac Cardiac & Vasc Surg, Manila, Philippines.
   [Danguilan, Jose Luis J.] Lung Ctr Philippines, Dept Thorac Surg & Anesthesia, Quezon City, Philippines.
   [Callueng, Jose Miguel C.] Manila Doctors Hosp, Dept Radiat Oncol, Manila, Philippines.
   [Gagto, Jesyl O.] Univ Philippines, Philippine Gen Hosp, Div Thorac Cardiac & Vasc Surg, Taft Ave, Manila 1000, Philippines.
C3 University of the Philippines System; University of the Philippines
   Manila; Lung Center of the Philippines; University of the Philippines
   System; University of the Philippines Manila
RP Gagto, JO (corresponding author), Univ Philippines, Philippine Gen Hosp, Div Thorac Cardiac & Vasc Surg, Taft Ave, Manila 1000, Philippines.
EM jesylgagto@gmail.com
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NR 93
TC 0
Z9 0
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 2519-0792
J9 VIDEO-ASSIST THORAC
JI Video-Assist. Thorac. Surg.
PD JUN 30
PY 2024
VL 9
DI 10.21037/vats-23-28
EA AUG 2023
PG 11
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA XQ7U0
UT WOS:001056458500001
OA gold
DA 2025-01-04
ER

PT J
AU Lin, ZJ
   Ji, YQ
   Zhou, J
   Li, GQ
   Liu, WF
   Li, ZH
   Liu, T
AF Lin, Zhengjun
   Ji, Yuqiao
   Zhou, Jian
   Li, Guoqing
   Liu, Weifeng
   Li, Zhihong
   Liu, Tang
TI Exosomal circRNAs in cancer: Implications for therapy resistance and
   biomarkers
SO CANCER LETTERS
LA English
DT Article
DE Exosomes; circRNAs; Chemoresistance; Immunotherapy; Targeted therapy;
   Radiotherapy
ID CELL LUNG-CANCER; ENHANCES TEMOZOLOMIDE RESISTANCE; CIRCULAR RNA;
   COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA; TUMOR MICROENVIRONMENT;
   MOLECULAR-MECHANISMS; PROMOTES METASTASIS; PROMISING BIOMARKER; SERUM
   EXOSOMES
AB Despite the advances in cancer treatment in recent years, the development of resistance to cancer therapy remains the biggest hurdle towards curative cancer treatments. Therefore, investigating the molecular mechanisms underlying cancer therapy resistance is of paramount clinical importance. Circular RNAs (circRNAs), novel members of the noncoding RNA family, are endogenous biomolecules in eukaryotes characterized by a covalently closed loop structure with multiple biological functions. Significantly, circRNAs are abundant and stable in exosomes and can be packaged, secreted and transferred to targeted tumour cells, thereby modulating diverse hallmarks of cancer behaviours, such as proliferation, migration, and immune escape. Notably, a great number of exosomal circRNAs are abnormally expressed during cancer treatment and can mediate cancer therapy resistance through complex mechanisms; therefore, targeting exosomal circRNAs is a promising therapeutic method to reverse therapy resistance. This review aimed to elucidate the mechanisms underlying exosomal circRNAs controlling the resistance of cancer to common therapies, such as chemotherapy, targeted therapy, immunotherapy and radiotherapy, and we also discussed the therapeutic potential of exosomal circRNAs as clinical biomarkers and novel targets in cancer clinical management. We also discussed the prospects and challenges of targeting exosomal circRNAs as a novel therapeutic strategy for reversing cancer therapy resistance.
C1 [Lin, Zhengjun; Ji, Yuqiao; Zhou, Jian; Li, Guoqing; Li, Zhihong; Liu, Tang] Cent South Univ, Xiangya Hosp 2, Dept Orthoped, Changsha 410011, Hunan, Peoples R China.
   [Liu, Weifeng] Peking Univ, Beijing Jishuitan Hosp, Dept Orthopaed Oncol Surg, Beijing 100035, Peoples R China.
   [Lin, Zhengjun; Ji, Yuqiao; Li, Guoqing] Cent South Univ, Xiangya Sch Med, Changsha 410013, Hunan, Peoples R China.
C3 Central South University; Peking University; Central South University
RP Li, ZH; Liu, T (corresponding author), Cent South Univ, Xiangya Hosp 2, Dept Orthoped, Changsha 410011, Hunan, Peoples R China.; Liu, WF (corresponding author), Peking Univ, Beijing Jishuitan Hosp, Dept Orthopaed Oncol Surg, Beijing 100035, Peoples R China.
EM 2204170206@csu.edu.cn; liuweifengjst@126.com; lizhihong@csu.edu.cn;
   liutang1204@csu.edu.cn
FU National Natural Science Foundation of China, China [82072441]; Hunan
   Outstanding Youth Fund Project Grant [2022JJ10095]; Beijing Jishuitan
   Hospital Elite Young Scholar Program [XKGG202105]; Beijing Municipal
   Administration of Hospitals Incubating Program [PX2021015]; Beijing
   Natural Science Foundation, China [L212042]; Chinese Society of Clinical
   Oncology (CSCO) Research Foundation [Y- young2019-070, Y-2019GCTB-002]
FX This study was supported by grants from National Natural Science
   Foundation of China, China (NO.82072441) , Hunan Outstanding Youth Fund
   Project Grant (NO. 2022JJ10095) , Beijing Jishuitan Hospital Elite Young
   Scholar Program (NO. XKGG202105) , Beijing Municipal Administration of
   Hospitals Incubating Program (NO. PX2021015) , Beijing Natural Science
   Foundation, China (NO. L212042) , Chinese Society of Clinical Oncology
   (CSCO) Research Foundation (Y- young2019-070, Y-2019GCTB-002) .
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NR 215
TC 27
Z9 27
U1 5
U2 16
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 JUL 10
PY 2023
VL 566
AR 216245
DI 10.1016/j.canlet.2023.216245
EA MAY 2023
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA K5EB9
UT WOS:001016659000001
PM 37247772
DA 2025-01-04
ER

PT J
AU Suster, NK
   Virant-Klun, I
   Grazio, SF
   Smrkolj, S
AF Suster, N. Kenda
   Virant-Klun, I.
   Grazio, S. Frkovic
   Smrkolj, S.
TI The significance of the pluripotency and cancer stem cell-related marker
   NANOG in diagnosis and treatment of ovarian carcinoma
SO EUROPEAN JOURNAL OF GYNAECOLOGICAL ONCOLOGY
LA English
DT Review
DE Ovarian cancer; Cancer stem cells; NANOG; Chemoresistance; Target
   therapy
ID SELF-RENEWAL; ALDEHYDE DEHYDROGENASE; CLINICAL-IMPLICATIONS; SURFACE
   EPITHELIUM; COLORECTAL-CANCER; GENE-EXPRESSION; SOLID TUMORS;
   LUNG-CANCER; P53; IDENTIFICATION
AB Ovarian cancer is among the most common gynecologic cancers and unfortunately the most common cause of death from gynecologic malignancies. Due to few early symptoms and insufficient screening programs, an early diagnosis of ovarian cancer is very difficult and new biomarkers related to early ovarian carcinogenesis are needed. In the last years a growing scientific knowledge about cancer stem cells and their markers opened a new perspective on screening and early diagnosis of ovarian cancer. The transcription factor NANOG is not only a pluripotency and cancer stem cell-related marker, but also promotes cancer stem cell-like characteristics of tumor, tumor growth, dissemination, immune evasion, and resistance to conventional therapy. The recent data showed that small stem cells resembling very small embryonic-like stem cells are present in the ovarian surface epithelium of adult human ovaries. These cells expressed several genes related to primordial germ cells, germinal lineage, and pluripotency, including NANOG, therefore their involvement in the manifestation of ovarian cancer are not excluded. As majority of cancer cells within a tumor are non tumorigenic, the therapies targeting these cells cause tumor regression, but the survived cancer stem cells regenerate the tumor, so tumor relapse or reoccur. The eradication of cancer actually requires the elimination of cancer stem cells, therefore new strategies in treatment that specifically target cancer stem cells are urgently needed. Although the therapeutic efficacy of targeting NANOG as a cancer treatment method is still in experimental phase, the gene therapy with small interfering RNA or short hairpin RNA have already shown some promising therapeutic potential. The authors can conclude that NANOG represents a promising diagnostic marker and agent for target therapy of ovarian cancer.
C1 [Suster, N. Kenda; Smrkolj, S.] Univ Med Ctr Ljubljana, Dept Obstet & Gynecol, Slajmerjeva 3, SI-1000 Ljubljana, Slovenia.
   [Virant-Klun, I.] Univ Med Ctr Ljubljana, Dept Obstet & Gynecol, Reprod Unit, Ljubljana, Slovenia.
   [Grazio, S. Frkovic] Univ Med Ctr Ljubljana, Dept Obstet & Gynecol, Unit Gynecol Pathol & Cytol, Ljubljana, Slovenia.
C3 University Medical Centre Ljubljana; University Medical Centre Ljubljana
RP Smrkolj, S (corresponding author), Univ Med Ctr Ljubljana, Dept Obstet & Gynecol, Slajmerjeva 3, SI-1000 Ljubljana, Slovenia.
EM spela.smrkolj@mf.uni-lj.si
RI Smrkolj, Spela/AAI-5791-2020
OI SMRKOLJ, SPELA/0000-0001-9698-2130
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NR 93
TC 5
Z9 5
U1 0
U2 6
PU I R O G CANADA, INC
PI MONTREAL
PA 4900 COTE ST-LUC, APT#212, MONTREAL, QUEBEC H3W 2H3, CANADA
SN 0392-2936
J9 EUR J GYNAECOL ONCOL
JI Eur. J. Gynaecol. Oncol.
PY 2016
VL 37
IS 5
BP 604
EP 612
DI 10.12892/ejgo3121.2016
PG 9
WC Oncology; Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Obstetrics & Gynecology
GA DY4FX
UT WOS:000385055500002
PM 29786995
DA 2025-01-04
ER

PT J
AU Ham, NS
   Myung, SJ
AF Ham, Nam Seok
   Myung, Seung-Jae
TI Endoscopic molecular imaging in inflammatory bowel disease
SO INTESTINAL RESEARCH
LA English
DT Review
DE Molecular imaging; Intestinal diseases; Inflammatory bowel disease;
   Colitis; Neoplasm
ID CONFOCAL LASER ENDOMICROSCOPY; EVIDENCE-BASED CONSENSUS;
   ULCERATIVE-COLITIS; COLORECTAL-CANCER; SUBMUCOSAL DISSECTION;
   MICROSATELLITE INSTABILITY; DIAGNOSTIC-ACCURACY; DYSPLASTIC LESIONS;
   COLON-CANCER; PROBE
AB Molecular imaging is a technique for imaging the processes occurring in a living body at a molecular level in real-time, combining molecular cell biology with advanced imaging technologies using molecular probes and fluorescence. Gastrointestinal endoscopic molecular imaging shows great promise for improving the identification of neoplasms, providing characterization for patient stratification and assessing the response to molecular targeted therapy. In inflammatory bowel disease, endoscopic molecular imaging can be used to assess disease severity and predict therapeutic response and prognosis. Endoscopic molecular imaging is also able to visualize dysplasia in the presence of background inflammation. Several preclinical and clinical trials have evaluated endoscopic molecular imaging; however, this area is just beginning to evolve, and many issues have not been solved yet. In the future, it is expected that endoscopic molecular imaging will be of increasing interest among clinicians as a new technology for the identification and evaluation of colorectal neoplasm and colitis-associated cancer.
C1 [Ham, Nam Seok] Vet Hlth Serv Med Ctr, Dept Gastroenterol, Seoul, South Korea.
   [Myung, Seung-Jae] Univ Ulsan, Digest Dis Res Ctr, Asan Med Ctr, Dept Gastroenterol,Coll Med, Seoul, South Korea.
C3 Veterans Health Service Medical Center; University of Ulsan; Asan
   Medical Center
RP Myung, SJ (corresponding author), Univ Ulsan, Coll Med, Asan Med Ctr, Dept Gastroenterol, 88 Olymp Ro 43 Gil, Seoul 05505, South Korea.
EM sjmyung@amc.seoul.kr
RI Myung, Sun-Jung/J-5464-2012
OI Ham, Nam Seok/0000-0002-6661-4692
FU Ministry of Trade, Industry & Energy (MOTIE, Korea) under Industrial
   Technology Innovation Program [10063408]; Asan Institute for Life
   Sciences [2019-559, 2019-261]
FX This research was supported by grants of the Ministry of Trade, Industry
   & Energy (MOTIE, Korea) under Industrial Technology Innovation Program
   (No. 10063408) and the grants from Asan Institute for Life Sciences
   (Nos. 2019-559 and 2019-261).
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NR 75
TC 6
Z9 6
U1 0
U2 7
PU KOREAN ASSOC STUDY INTESTINAL DISEASES
PI SEOUL
PA LOTTEGOLDROSE 2-F, RM 305, 890-59, DAECHI-DONG, GANGNAM-GU, SEOUL,
   135-280, SOUTH KOREA
SN 1598-9100
J9 INTEST RES
JI Intest. Res.
PD JAN
PY 2021
VL 19
IS 1
BP 33
EP 44
DI 10.5217/ir.2019.09175
PG 12
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA QC0XG
UT WOS:000614557100004
PM 32299156
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Xie, T
   Huang, MX
   Wang, Y
   Wang, LY
   Chen, C
   Chu, XY
AF Xie, Tao
   Huang, Mengxi
   Wang, Ye
   Wang, Liya
   Chen, Cheng
   Chu, Xiaoyuan
TI MicroRNAs as Regulators, Biomarkers and Therapeutic Targets in the Drug
   Resistance of Colorectal Cancer
SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
LA English
DT Article
DE MicroRNA; Drug resistance; Colorectal cancer
ID EPITHELIAL-MESENCHYMAL TRANSITION; ENDOTHELIAL GROWTH-FACTOR; LOCKED
   NUCLEIC-ACID; WILD-TYPE KRAS; CELL-GROWTH; PROGNOSTIC INDICATOR;
   MOLECULAR-MECHANISMS; ABC TRANSPORTERS; OXALIPLATIN; EXPRESSION
AB Chemotherapy and targeted therapy are the main options for andvanced colorectal cancer (CRC). However, resistance to these therapies is a major challenge in the clinic. Understanding molecular mechanisms and developing effective strategies against the drug resistance are highly desired. Increasing evidence has revealed that microRNAs (miRNAs) are closely linked to drug resistance in CRC. The explosion of knowledge in this field has brought forward new predictive and therapeutic opportunities. In this review, we systemically summarize the roles of miRNAs as regulators, tissue or circulating biomarkers, and therapeutics in the CRC resistance to 5-fluorouracil (5-FU), oxaliplatin and anti-EGFR therapy. We also discuss the potential unsettled issues and future directions concerning these processes. (C) 2016 The Author(s) Published by S. Karger AG, Basel
C1 [Xie, Tao; Wang, Ye; Chu, Xiaoyuan] Southern Med Univ, Nanjing Clin Sch, Jinling Hosp, Dept Med Oncol, Nanjing, Jiangsu, Peoples R China.
   [Huang, Mengxi; Wang, Liya; Chen, Cheng; Chu, Xiaoyuan] Nanjing Univ, Sch Med, Jinling Hosp, Dept Med Oncol, Nanjing, Jiangsu, Peoples R China.
C3 Southern Medical University - China; Nanjing University
RP Chen, C; Chu, XY (corresponding author), 305 East Zhongshan Rd, Nanjing 210002, Jiangsu, Peoples R China.
EM chencheng1289@l26.com; chuxiaoyuan000@l63.com
RI Chen, Huanhuan/HTO-5007-2023; Wang, Liya/AAQ-8579-2021
FU National Natural Science Foundation of China [81272394]
FX This work was supported by grants from the National Natural Science
   Foundation of China (No.81272394)
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NR 86
TC 79
Z9 83
U1 0
U2 8
PU Cell Physiol Biochem Press GmbH & Co
PI Dsseldorf
PA Herzogstr. 85, Dsseldorf, GERMANY
SN 1015-8987
EI 1421-9778
J9 CELL PHYSIOL BIOCHEM
JI Cell. Physiol. Biochem.
PY 2016
VL 40
IS 1-2
BP 62
EP 76
DI 10.1159/000452525
PG 15
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA EE0DM
UT WOS:000389243900006
PM 27842308
OA gold
DA 2025-01-04
ER

PT J
AU He, K
   Wang, ZH
   Luo, MC
   Li, BW
   Ding, N
   Li, L
   He, B
   Wang, H
   Cao, JJ
   Huang, CH
   Yang, J
   Chen, HN
AF He, Kai
   Wang, Zhihan
   Luo, Maochao
   Li, Bowen
   Ding, Ning
   Li, Lei
   He, Bo
   Wang, Han
   Cao, Jiangjun
   Huang, Canhua
   Yang, Jun
   Chen, Hai-Ning
TI Metastasis organotropism in colorectal cancer: advancing toward
   innovative therapies
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE CRC; Organotropism; Metabolic reprogramming; Immune system; Cancer
   cell-organ interactions; Targeted therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; TUMOR-ASSOCIATED MACROPHAGES;
   PROMOTES LIVER METASTASIS; PERITONEAL CARCINOMATOSIS; COLON-CANCER;
   EXTRACELLULAR VESICLES; THERAPEUTIC TARGET; PHYSICAL-ACTIVITY;
   OPEN-LABEL; CELL
AB Distant metastasis remains a leading cause of mortality among patients with colorectal cancer (CRC). Organotropism, referring to the propensity of metastasis to target specific organs, is a well-documented phenomenon in CRC, with the liver, lungs, and peritoneum being preferred sites. Prior to establishing premetastatic niches within host organs, CRC cells secrete substances that promote metastatic organotropism. Given the pivotal role of organotropism in CRC metastasis, a comprehensive understanding of its molecular underpinnings is crucial for biomarker-based diagnosis, innovative treatment development, and ultimately, improved patient outcomes. In this review, we focus on metabolic reprogramming, tumor-derived exosomes, the immune system, and cancer cell-organ interactions to outline the molecular mechanisms of CRC organotropic metastasis. Furthermore, we consider the prospect of targeting metastatic organotropism for CRC therapy.
C1 [He, Kai; Ding, Ning; Li, Lei; Huang, Canhua] Chengdu Univ Tradit Chinese Med, Sch Basic Med Sci, Chengdu 611137, Peoples R China.
   [He, Kai; Ding, Ning; Li, Lei; Huang, Canhua] Chengdu Univ Tradit Chinese Med, State Key Lab Southwestern Chinese Med Resources, Chengdu 611137, Peoples R China.
   [He, Kai; Wang, Zhihan; Luo, Maochao; Li, Bowen; He, Bo; Wang, Han; Cao, Jiangjun; Huang, Canhua; Chen, Hai-Ning] Sichuan Univ, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
   [He, Kai; Wang, Zhihan; Luo, Maochao; Li, Bowen; He, Bo; Wang, Han; Cao, Jiangjun; Huang, Canhua; Chen, Hai-Ning] Sichuan Univ, West China Hosp, Canc Ctr, Chengdu 610041, Peoples R China.
   [He, Kai; Wang, Zhihan; Luo, Maochao; Li, Bowen; He, Bo; Wang, Han; Cao, Jiangjun; Huang, Canhua; Chen, Hai-Ning] Sichuan Univ, West China Sch Basic Med Sci & Forens Med, Chengdu 610041, Peoples R China.
   [He, Kai; Wang, Zhihan; Luo, Maochao; Li, Bowen; He, Bo; Wang, Han; Cao, Jiangjun; Huang, Canhua; Chen, Hai-Ning] Collaborat Innovat Ctr Biotherapy, Chengdu 610041, Peoples R China.
   [Yang, Jun] Kunming Med Univ, Affiliated Hosp 1, Dept Oncol, Kunming 650032, Peoples R China.
   [Chen, Hai-Ning] Sichuan Univ, Dept Gen Surg, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
   [Chen, Hai-Ning] Sichuan Univ, West China Hosp, Canc Ctr, Colorectal Canc Ctr, Chengdu 610041, Peoples R China.
C3 Chengdu University of Traditional Chinese Medicine; Chengdu University
   of Traditional Chinese Medicine; Sichuan University; Sichuan University;
   Sichuan University; Kunming Medical University; Sichuan University;
   Sichuan University
RP Chen, HN (corresponding author), Sichuan Univ, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.; Chen, HN (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, Chengdu 610041, Peoples R China.; Chen, HN (corresponding author), Sichuan Univ, West China Sch Basic Med Sci & Forens Med, Chengdu 610041, Peoples R China.; Chen, HN (corresponding author), Collaborat Innovat Ctr Biotherapy, Chengdu 610041, Peoples R China.; Yang, J (corresponding author), Kunming Med Univ, Affiliated Hosp 1, Dept Oncol, Kunming 650032, Peoples R China.; Chen, HN (corresponding author), Sichuan Univ, Dept Gen Surg, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.; Chen, HN (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, Colorectal Canc Ctr, Chengdu 610041, Peoples R China.
EM yangjun6@kmmu.edu.cn; hnchen@scu.edu.cn
RI Li, Bowen/LPP-4928-2024; Chen, Hai-Ning/AAR-8059-2021
OI Li, Bowen/0000-0001-8475-4800
FU 1.3.5 project for disciplines of excellence [ZYGD22007]; Sichuan Science
   and Technology Program [2022JDRC0049, 2022YFS0202]; National Natural
   Science Foundation of China [82200592, 82073246, 82160533]
FX This work was supported by 1 center dot 3 center dot 5 project for
   disciplines of excellence (ZYGD22007), Sichuan Science and Technology
   Program (2022JDRC0049, 2022YFS0202), and National Natural Science
   Foundation of China, (82200592, 82073246, 82160533).
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NR 216
TC 13
Z9 14
U1 3
U2 10
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD SEP 9
PY 2023
VL 21
IS 1
AR 612
DI 10.1186/s12967-023-04460-5
PG 23
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA R3ZH9
UT WOS:001063760600002
PM 37689664
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Salleh, EA
   Lee, YY
   Zakaria, AD
   Jalil, NAC
   Musa, M
AF Salleh, Elyn Amiela
   Lee, Yeong Yeh
   Zakaria, Andee Dzulkarnaen
   Jalil, Nur Asyilla che
   Musa, Marahaini
TI Cancer-associated fibroblasts of colorectal cancer: Translational
   prospects in liquid biopsy and targeted therapy
SO BIOCELL
LA English
DT Article
DE Activated fi broblast; Colon cancer; Liquid biopsy; Precision medicine
ID CIRCULATING TUMOR-CELLS; PROGENITOR CELLS; STROMAL CELLS; METASTASIS;
   CHALLENGES; PROGNOSIS; OPPORTUNITIES; PODOPLANIN; EXPRESSION; INVASION
AB Colorectal cancer (CRC) is a major global health concern. Accumulation of cancer-associated fibroblasts (CAFs) in CRC is associated with poor prognosis and disease recurrence. CAFs are the main cellular component of the tumor microenvironment. CAF-tumor cell interplay, which is facilitated by various secretomes, drives colorectal carcinogenesis. The complexity of CAF populations contributes to the heterogeneity of CRC and influences patient survival and treatment response. Due to their significant roles in colorectal carcinogenesis, different clinical applications utilizing or targeting CAFs have been suggested. Circulating CAFs (cCAFs) which can be detected in blood samples, have been proposed to help in determining patient prognosis and enables the detection of cancer through liquid biopsy. Liquid biopsy is gaining traction as it is non-invasive, allows frequent and easy sampling, and shows concordance to tissue biopsy analysis. In addition, CAF-targeted therapy is currently being studied extensively to be used as one of the treatment avenues for CRC. Various mechanisms of CAF-targeted therapy have been reported, including blocking the signaling pathways involving CAFs and cancer cells, thus abolishing the CAF-tumor cell crosstalk and subsequently hindering tumorigenesis. These translational applications of cCAFs and utilization of CAFs as key targets for CRC therapy, although still in the early phases of development, will potentially improve CRC patient management in the future.
C1 [Salleh, Elyn Amiela; Musa, Marahaini] Univ Sains Malaysia, Human Genome Ctr, Sch Med Sci, Kubang Kerian 16150, Malaysia.
   [Lee, Yeong Yeh] Univ Sains Malaysia, Sch Med Sci, Dept Internal Med, Kubang Kerian 16150, Malaysia.
   [Zakaria, Andee Dzulkarnaen] Univ Sains Malaysia, Sch Med Sci, Dept Surg, Kubang Kerian 16150, Malaysia.
   [Jalil, Nur Asyilla che] Univ Sains Malaysia, Sch Med Sci, Dept Pathol, Kubang Kerian 16150, Malaysia.
C3 Universiti Sains Malaysia; Universiti Sains Malaysia; Universiti Sains
   Malaysia; Universiti Sains Malaysia
RP Musa, M (corresponding author), Univ Sains Malaysia, Human Genome Ctr, Sch Med Sci, Kubang Kerian 16150, Malaysia.
EM marahaini.musa@usm.my
RI Musa, Marahaini/E-9987-2019; Zakaria, Andee/D-3676-2016; Lee, Yeong
   Yeh/G-2470-2010
FU Ministry of Higher Education Malaysia for Fundamental Research Grant
   Scheme [FRGS/1/2020/SKK0/USM/03/10]; USM
FX This work was supported by the Ministry of Higher Education Malaysia for
   Fundamental Research Grant Scheme with Project Code:
   FRGS/1/2020/SKK0/USM/03/10 and USM.
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NR 124
TC 0
Z9 0
U1 1
U2 1
PU TECH SCIENCE PRESS
PI HENDERSON
PA 871 CORONADO CENTER DR, SUTE 200, HENDERSON, NV 89052 USA
SN 0327-9545
EI 1667-5746
J9 BIOCELL
JI Biocell
PY 2023
VL 47
IS 10
BP 2233
EP 2244
DI 10.32604/biocell.2023.030541
PG 12
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA HE6F4
UT WOS:001157849500005
OA gold
DA 2025-01-04
ER

PT J
AU Fukui, S
   Umeda, K
   Kubota, H
   Iwai, A
   Akazawa, R
   Isobe, K
   Tanaka, K
   Kouzuki, K
   Kawabata, N
   Saida, S
   Kato, I
   Hiramatsu, H
   Itatani, Y
   Funakoshi, T
   Adachi, S
   Takita, J
AF Fukui, Sadahiro
   Umeda, Katsutsugu
   Kubota, Hirohito
   Iwai, Atsushi
   Akazawa, Ryo
   Isobe, Kiyotaka
   Tanaka, Kuniaki
   Kouzuki, Kagehiro
   Kawabata, Naoko
   Saida, Satoshi
   Kato, Itaru
   Hiramatsu, Hidefumi
   Itatani, Yoshiro
   Funakoshi, Taro
   Adachi, Souichi
   Takita, Junko
TI Use of Cabozantinib to Treat <i>MET</i>-amplified Pediatric Colorectal
   Cancer
SO JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY
LA English
DT Article
DE colorectal cancer; pediatric; cancer gene panel testing; MET inhibitor;
   cabozantinib
ID EXPRESSION; AMPLIFICATION; CARCINOMA; SMAD4
AB Pediatric colorectal cancer (CRC) is extremely rare, with little information about genetic profiles compared with adult CRC. Here, a 13-year-old male with advanced CRC underwent cancer gene panel testing, which detected 4 genetic abnormalities (MET amplification in addition to TP53, SMAD4, and CTNNA1 mutations) that might be associated with a poor prognosis. Based on high-level MET amplification, he received a multikinase inhibitor, cabozantinib, after failure of first-line and second-line chemotherapy, resulting in transient disease stabilization. Tailored targeted therapy based on molecular profiling can be an effective treatment strategy for rare cancers such as pediatric CRC.
C1 [Fukui, Sadahiro; Umeda, Katsutsugu; Kubota, Hirohito; Iwai, Atsushi; Akazawa, Ryo; Isobe, Kiyotaka; Tanaka, Kuniaki; Kouzuki, Kagehiro; Kawabata, Naoko; Saida, Satoshi; Kato, Itaru; Hiramatsu, Hidefumi; Takita, Junko] Kyoto Univ, Dept Pediat, Kyoto, Japan.
   [Itatani, Yoshiro] Kyoto Univ, Dept Surg, Kyoto, Japan.
   [Funakoshi, Taro] Kyoto Univ, Dept Clin Oncol, Kyoto, Japan.
   [Adachi, Souichi] Kyoto Univ, Grad Sch Med, Dept Human Hlth Sci, Kyoto, Japan.
   [Umeda, Katsutsugu] Kyoto Univ, Grad Sch Med, Dept Pediat, 54 Kawahara Cho,Shogoin,Sakyo ku, Kyoto 6068507, Japan.
C3 Kyoto University; Kyoto University; Kyoto University; Kyoto University;
   Kyoto University
RP Umeda, K (corresponding author), Kyoto Univ, Grad Sch Med, Dept Pediat, 54 Kawahara Cho,Shogoin,Sakyo ku, Kyoto 6068507, Japan.
EM sadasada1002@kuhp.kyoto-u.ac.jp; umeume@kuhp.kyoto-u.ac.jp;
   hirohito@kuhp.kyoto-u.ac.jp; atsu4i@kuhp.kyoto-u.ac.jp;
   akzwryo@kuhp.kyoto-u.ac.jp; kisobe@kuhp.kyoto-u.ac.jp;
   kuni0328@kuhp.kyoto-u.ac.jp; kagehiro@kuhp.kyoto-u.ac.jp;
   k.naoko@tsc.u-tokai.ac.jp; satoshi@kuhp.kyoto-u.ac.jp;
   itarkt@kuhp.kyoto-u.ac.jp; hiramatu@kuhp.kyoto-u.ac.jp;
   itatani@kuhp.kyoto-u.ac.jp; tarofun@kuhp.kyoto-u.ac.jp;
   adachiso@kuhp.kyoto-u.ac.jp; jtakita@kuhp.kyoto-u.ac.jp
RI Kubota, Hirohito/KVC-3023-2024
OI Kubota, Hirohito/0000-0002-6935-5120
FU Grants-in-Aid for Scientific Research [20H00528, 21K19405] Funding
   Source: KAKEN
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NR 20
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1077-4114
EI 1536-3678
J9 J PEDIAT HEMATOL ONC
JI J. Pediatr. Hematol. Oncol.
PD APR
PY 2023
VL 45
IS 3
BP E423
EP E426
DI 10.1097/MPH.0000000000002482
PG 4
WC Oncology; Hematology; Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology; Pediatrics
GA A8ZK6
UT WOS:000957943100036
PM 35536994
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Martino, E
   D'Onofrio, N
   Anastasio, C
   Abate, M
   Zappavigna, S
   Caraglia, M
   Balestrieri, ML
AF Martino, Elisa
   D'Onofrio, Nunzia
   Anastasio, Camilla
   Abate, Marianna
   Zappavigna, Silvia
   Caraglia, Michele
   Balestrieri, Maria Luisa
TI MicroRNA-nanoparticles against cancer: Opportunities and challenges for
   personalized medicine
SO MOLECULAR THERAPY-NUCLEIC ACIDS
LA English
DT Review
ID COLORECTAL-CANCER; ENHANCED PERMEABILITY; TARGETED THERAPY; DIAGNOSTIC
   BIOMARKERS; ORAL BIOAVAILABILITY; PHOTOTHERMAL THERAPY; OXIDE
   NANOPARTICLES; CO-DELIVERY; MIRNA; DRUG
AB Micro-RNAs (miRNAs) control gene expression at the posttranscriptional level and are widely involved in carcinogenesis, playing a role as both oncogenes and tumor suppressors. MiRNAs act as potent therapeutic weapon in cancer, but their potential therapeutic use is limited by the off-target effect due to their nonspecific distribution in normal tissues. The encapsulation of miRNAs in nanostructured carriers allows targeted effects aimed to destroy cancer cells, without affecting healthy tissues. Due to their small size and the optimal surface/size ratio, nanoparticles (NPs) envelop, protect, and release miRNAs, representing a promising strategy in cancer treatment. In the present review, we discuss the latest advances in the field of miRNA-encapsulating NPs in cancer, focusing on colorectal cancer and its metastatic forms, one of the most common malignancies worldwide.
C1 [Martino, Elisa; D'Onofrio, Nunzia; Anastasio, Camilla; Abate, Marianna; Zappavigna, Silvia; Caraglia, Michele; Balestrieri, Maria Luisa] Univ Campania Luigi Vanvitelli, Dept Precis Med, Naples, Italy.
C3 Universita della Campania Vanvitelli
RP D'Onofrio, N (corresponding author), Univ Campania Luigi Vanvitelli, Dept Precis Med, Naples, Italy.
EM nunzia.donofrio@unicampania.it
RI ABATE, MARIANNA/AAG-4679-2019; Caraglia, Michele/AFY-9729-2022;
   D'Onofrio, Nunzia/M-2081-2019
OI Martino, Elisa/0000-0003-4070-2894
FU PON Iamp;C [2014-2020-CAPSULE-F/200016/01-03/X45,
   2014-2020-TABAREZO-F/200085/01-03/X45];  [IZS ME 09/22 RC- STUPORANIMA]
FX This work was supported by PON I&C 2014-2020-CAPSULE-F/200016/01-03/X45;
   IZS ME 09/22 RC- STUPORANIMA "; PON I&C
   2014-2020-TABAREZO-F/200085/01-03/X45.
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NR 147
TC 12
Z9 12
U1 4
U2 12
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 2162-2531
J9 MOL THER-NUCL ACIDS
JI Mol. Ther.-Nucl. Acids
PD JUN 13
PY 2023
VL 32
DI 10.1016/j.omtn.2023.03.021
EA APR 2023
PG 14
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA O2KG2
UT WOS:001042153700001
PM 37128277
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, J
AF Li, Jian
TI Targeting claudins in cancer: diagnosis, prognosis and therapy
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Review
DE Claudins; cancer; diagnosis; prognosis; targeted therapy
ID CLOSTRIDIUM-PERFRINGENS ENTEROTOXIN; SQUAMOUS-CELL CARCINOMA; TIGHT
   JUNCTION PROTEIN; BLOOD-BRAIN-BARRIER; MONOCLONAL-ANTIBODIES;
   POOR-PROGNOSIS; GASTRIC-CANCER; LUNG-CANCER; COLON-CANCER; T-CELLS
AB Increasing evidence has linked claudins to signal transduction and tumorigenesis. The expression of claudins is frequently dysregulated in the context of neoplastic transformation, suggesting their promise as biomarkers for diagnosis and prognosis or targets for treatment. Claudin binders (Clostridium perfringens enterotoxin and monoclonal antibody) have been tested in preclinical experiments, and some of them have progressed into clinical trials involving patients with certain cancers. However, the clinical development of many of these agents has not advanced to clinical applications. Herein, I review the current status of preclinical and clinical investigations of agents targeting claudins for diagnosis, prognosis and therapy. I also discuss the potential of combining claudin binders with other currently approved therapeutic agents.
C1 [Li, Jian] Sichuan Mental Hlth Ctr, Hosp Mianyang 3, Dept Gen Surg, 190 East Sect Jiannan Rd, Mianyang 621000, Sichuan, Peoples R China.
RP Li, J (corresponding author), Sichuan Mental Hlth Ctr, Hosp Mianyang 3, Dept Gen Surg, 190 East Sect Jiannan Rd, Mianyang 621000, Sichuan, Peoples R China.
EM 654747973@qq.com
RI Li, Jian/L-8703-2019
FU Health Commission of Mianyang City; Science and Education Department of
   the Third Hospital of Mianyang
FX The author thanks the Health Commission of Mianyang City and the Science
   and Education Department of the Third Hospital of Mianyang for their
   support.
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NR 137
TC 24
Z9 24
U1 1
U2 9
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 2021
VL 11
IS 7
BP 3406
EP 3424
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TT0NO
UT WOS:000680048600002
PM 34354852
DA 2025-01-04
ER

PT J
AU Wu, DH
   Jiang, BH
   Lian, JN
   Liu, J
AF Wu, Denghai
   Jiang, Binhua
   Lian, Jianan
   Liu, Jian
TI SPARCL1 Modulates the Tumor Microenvironment and Suppresses Colorectal
   Cancer and Liver Metastasis through the CCL20/CCR6 Axis
SO JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
LA English
DT Article
DE colorectal cancer liver metastases; SPARCL1; tumor microenvironment;
   CCL20; CCR6 axis; Th17 cells
ID TH17 CELLS; TARGETS
AB Background and Purpose: To investigate the expression and biological functions of secreted protein acidic and rich in cysteine-like 1 (SPARCL1) in the tumor microenvironment of colorectal cancer liver metastases (CRCLM). More over the study aimed to provide a new molecular marker for targeted therapy.Methods: Thirty male C57BL6/J mice were randomly divided into the control group (n = 3), the CRCLM group (n = 7), the CRCLM+Lv-vector group (n = 5), the CRCLM+Lv-SPARCL1 group (n = 5), the CRCLM+Lv-vector shRNA group (n = 5), and the CRCLM+Lv-SPARCL1 shRNA group (n = 5). Mice liver tissues in each group was obtained. The histopathological changes and indexes were measured by hematoxylin and eosin (H&E) staining, Reverse transcription quantitative PCR (polymerase chain reaction) (RT-qPCR), western blot, Masson staining, Enzyme-linked immunosorbent assay (ELISA), and flow cytometry.Results: SPARCL1 mRNA and protein expression levels in the CRCLM group decreased compared to the control group (p < 0.05). Further SPARCL1 upregulation reduced the metastatic foci number, collagen area (%), expression of collagen I, collagen III, alpha-SMA (sarcomeric actin), CCL20 (chemokine CC-motif ligand 20), CCR6 (CC chemokine receptor 6), N-cadherin, and vi-mentin, percentage of Th17 cells, and IL (interleukin)-1 beta, IL-17, and TNF (tumor necrosis factor)-alpha content (p < 0.05). However, E-cadherin expression and IL-6, IL-8, and IL-10 content increased (p < 0.05). In contrast, downregulating SPARCL1 reversed the above index trends.Conclusions: SPARCL1 effectively reduced liver metastasis, collagen deposition, and liver fibrosis. Furthermore, it activated CCL20/CCR6 axis to inhibit immune responses and epithelial-to-mesenchymal transition (EMT), thus providing an experimen-tal basis for targeted therapy.
C1 [Wu, Denghai; Lian, Jianan; Liu, Jian] Zhejiang Chinese Med Univ, Affiliated Hosp 2, Deparment Hepatobiliary Surg, Hangzhou 310005, Zhejiang, Peoples R China.
   [Jiang, Binhua] Zhejiang Chinese Med Univ, Affiliated Hosp 2, Deparment Thorac Surg, Hangzhou 310005, Zhejiang, Peoples R China.
C3 Zhejiang Chinese Medical University; Zhejiang Chinese Medical University
RP Liu, J (corresponding author), Zhejiang Chinese Med Univ, Affiliated Hosp 2, Deparment Hepatobiliary Surg, Hangzhou 310005, Zhejiang, Peoples R China.
EM liujianxhdoc@163.com
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NR 36
TC 0
Z9 0
U1 0
U2 12
PU BIOLIFE SAS
PI SILVA MARINA (TE)
PA VIA S STEFANO 39 BIS, 64029 SILVA MARINA (TE), ITALY
SN 0393-974X
EI 1724-6083
J9 J BIOL REG HOMEOS AG
JI J. Biol. Regul. Homeost. Agents
PD MAR-APR
PY 2023
VL 37
IS 2
BP 987
EP 995
DI 10.23812/j.biol.regul.homeost.agents.20233702.101
PG 9
WC Endocrinology & Metabolism; Immunology; Medicine, Research &
   Experimental; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Immunology; Research & Experimental
   Medicine; Physiology
GA D0BJ2
UT WOS:000965463900001
DA 2025-01-04
ER

PT J
AU Kawaguchi, Y
   Kopetz, S
   Panettieri, E
   Hwang, H
   Wang, XM
   Cao, HST
   Tzeng, CWD
   Chun, YS
   Aloia, TA
   Vauthey, JN
AF Kawaguchi, Yoshikuni
   Kopetz, Scott
   Panettieri, Elena
   Hwang, Hyunsoo
   Wang, Xuemei
   Cao, Hop S. Tran
   Tzeng, Ching-Wei D.
   Chun, Yun Shin
   Aloia, Thomas A.
   Vauthey, Jean-Nicolas
TI Improved Survival over Time After Resection of Colorectal Liver
   Metastases and Clinical Impact of Multigene Alteration Testing in
   Patients with Metastatic Colorectal Cancer
SO JOURNAL OF GASTROINTESTINAL SURGERY
LA English
DT Article
DE Hepatectomy; Metastatic colorectal cancer; Chemotherapy; Molecular
   targeted therapy; Perioperative chemotherapy
ID 2-STAGE HEPATECTOMY; 1ST-LINE TREATMENT; HEPATIC RESECTION; PLUS
   IRINOTECAN; FLUOROURACIL; LEUCOVORIN; RECURRENCE; TRIAL; KRAS; BRAF
AB Background The past 20 years have seen advances in colorectal cancer management. We sought to determine whether survival in patients undergoing resection of colorectal liver metastases (CLM) has improved in association with three landmark advances: introduction of irinotecan- and/or oxaliplatin-containing regimens, molecular targeted therapy, and multigene alteration testing. Methods Patients undergoing CLM resection during 1998-2014 were identified and grouped by resection year. The influence of alterations in RAS, TP53, and SMAD4 was evaluated and validated in an external cohort including patients with unresectable metastatic colorectal cancer. Results Of 1961 patients, 1599 met the inclusion criteria. Irinotecan- and/or oxaliplatin-containing regimens and molecular targeted therapy were used for more than 50% of patients starting in 2001 and starting in 2006, respectively, so patients were grouped as undergoing resection during 1998-2000, 2001-2005, or 2006-2014. Liver resectability indications expanded over time. The 5-year overall survival (OS) rate was significantly better in 2006-2014, vs. 2001-2005 (56.5% vs. 44.1%, P < 0.001). RAS alteration was associated with worse 5-year OS than RAS wild-type (44.8% vs. 63.3%, P < 0.001). However, OS did not differ significantly between patients with RAS alteration and wild-type TP53 and SMAD4 and patients with RAS wild-type in our cohort (P = 0.899) or the external cohort (P = 0.932). Of 312 patients with genetic sequencing data, 178 (57.1%) had clinically actionable alterations. Conclusion OS after CLM resection has improved with advances in medical therapy and surgical technique. Multigene alteration testing is useful for prognostication and identification of potential therapeutic targets.
C1 [Kawaguchi, Yoshikuni; Panettieri, Elena; Cao, Hop S. Tran; Tzeng, Ching-Wei D.; Chun, Yun Shin; Aloia, Thomas A.; Vauthey, Jean-Nicolas] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, 1515 Holcombe Blvd,Unit 1484, Houston, TX 77030 USA.
   [Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
   [Hwang, Hyunsoo; Wang, Xuemei] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center; University of Texas System;
   UTMD Anderson Cancer Center
RP Vauthey, JN (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, 1515 Holcombe Blvd,Unit 1484, Houston, TX 77030 USA.
EM jvauthey@mdanderson.org
RI Panettieri, Elena/AAZ-1874-2020; Kawaguchi, Yoshikuni/AAB-1718-2022;
   Wang, Xuemei/GXF-3702-2022; Kopetz, Scott/AAC-1387-2019
OI Panettieri, Elena/0000-0001-7815-8092
FU National Institutes of Health through MD Anderson Cancer Center Support
   Grant [CA016672]
FX This research was supported in part by the National Institutes of Health
   through MD Anderson Cancer Center Support Grant, CA016672.
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NR 40
TC 19
Z9 19
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1091-255X
EI 1873-4626
J9 J GASTROINTEST SURG
JI J. Gastrointest. Surg.
PD MAR
PY 2022
VL 26
IS 3
BP 583
EP 593
DI 10.1007/s11605-021-05110-1
EA SEP 2021
PG 11
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA ZU8QJ
UT WOS:000694783300010
PM 34506029
DA 2025-01-04
ER

PT J
AU Abdel-Samad, R
   Aouad, P
   Darwiche, N
AF Abdel-Samad, Rana
   Aouad, Patrick
   Darwiche, Nadine
TI Natural and synthetic retinoids in preclinical colorectal cancer models
SO ANTI-CANCER DRUGS
LA English
DT Review
DE colorectal cancer; natural retinoids; preclinical models; retinoic acid;
   synthetic retinoids
ID ABERRANT CRYPT FOCI; ADENOMATOUS POLYPOSIS-COLI; UNION-OF-PHARMACOLOGY;
   CARBOXYLIC-ACID CD437; PPAR-GAMMA LIGANDS; CELL-LINES; BREAST-CANCER;
   X-RECEPTOR; RXR-ALPHA; INHIBITS PROLIFERATION
AB Colorectal cancer (CRC) remains a leading cause of cancer-related morbidity and mortality worldwide. Although targeted therapy in combination with chemotherapy in CRC prolongs the overall survival of patients with metastatic disease, acquired resistance and relapse hinder their clinical benefits. Moreover, patients with some specific genetic profile are unlikely to benefit from targeted therapy, suggesting the need for safe and effective treatment strategies. Retinoids, comprising of natural and synthetic analogs, are a class of chemical compounds that regulate cellular proliferation, differentiation, and cell death. Retinoids have been used in the clinic for several leukemias and solid tumors, either as single agents or in combination therapy. Furthermore, retinoids have shown potent chemotherapeutic and chemopreventive properties in different cancer models, including CRC. In this review, we summarize the major preclinical findings in CRC in which natural and synthetic retinoids showed promising antitumor activities and stress on the proposed mechanisms of action. Understanding of the retinoids' antitumor mechanisms would provide insights to support and warrant their development in the management of CRC. Copyright (C) 2019 Wolters Kluwer Health, Inc. All rights reserved.
C1 [Abdel-Samad, Rana] Univ Balamand, Fac Hlth Sci, Beirut, Lebanon.
   [Abdel-Samad, Rana; Aouad, Patrick; Darwiche, Nadine] Amer Univ Beirut, Dept Biochem & Mol Genet, Beirut, Lebanon.
C3 University Balamand; American University of Beirut
RP Darwiche, N (corresponding author), Amer Univ Beirut, Dept Biochem & Mol Genet, Fac Med, Bliss St,DTS Bldg,Room 419-E,POB 110236-41, Beirut 11072020, Lebanon.
EM nd03@aub.edu.lb
OI Abdel-Samad, Rana/0000-0002-7753-8779; Darwiche,
   Nadine/0000-0002-1862-5426
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NR 133
TC 9
Z9 9
U1 0
U2 13
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 AUG
PY 2019
VL 30
IS 7
BP 655
EP 669
DI 10.1097/CAD.0000000000000802
PG 15
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA IQ4SW
UT WOS:000480741900002
PM 31021825
DA 2025-01-04
ER

PT J
AU Liu, S
   Zhang, F
   Niu, J
   Liang, BJ
   Li, ZQ
   Wang, XL
   Jia, ZM
   Han, Y
   Wang, XH
   Cheng, K
   Yang, ZL
AF Liu Song
   Zhang Fan
   Niu Jun
   Liang Benjia
   Li Zequn
   Wang Xilong
   Jia Zhongming
   Han Yong
   Wang Xiaohong
   Cheng Kai
   Yang Zhenlin
TI Tumor specific delivery and therapy mediate by integrin β6-target
   immunoliposomes for β6-siRNA in colon carcinoma
SO ONCOTARGET
LA English
DT Article
DE colon carcinoma; integrin beta 6; target therapy; immunoliposomes; siRNA
ID CANCER CELLS; PROGNOSTIC INDICATOR; RNA INTERFERENCE; UP-REGULATION;
   EXPRESSION; ALPHA-V-BETA-6; MIGRATION; PROMOTES; SECRETION; LIPOSOMES
AB Adjuvant chemotherapy does not achieve the desired therapeutic efficacy in colon cancer as a result of the deficient reaction. Gene therapy using small interfering RNAs (siRNAs) delivered by target delivering system represents a potent and specific strategy in tumor therapy. Integrin beta 6 is exclusively expressed in malignant colonic epithelia, associated with the progression, metastasis, and chemotherapeutic resistance of colon cancer. Accordingly, designing an efficient and targeted delivery system for beta 6-siRNA could be a potential approach to improve therapeutic efficacy of colon cancer. Here, we designed the Integrin beta 6 target immunoliposomes for highly efficient and selective delivery of beta 6-siRNA in colon cancer, which consequently resulted in greatly growth suppression, invasion and metastasis of colon cancer cells. Moreover, it was able to greatly inhibit the tumor growing in vivo.
C1 [Liu Song; Wang Xilong; Jia Zhongming; Han Yong; Wang Xiaohong; Cheng Kai; Yang Zhenlin] Binzhou Med Coll Affiliated Hosp, Dept Thyroid & Breast Surg, Binzhou 256600, Shandong, Peoples R China.
   Binzhou Med Coll Affiliated Hosp, Dept Oncol, Binzhou 256600, Shandong, Peoples R China.
   [Niu Jun; Liang Benjia; Li Zequn] Shandong Univ, Qilu Hosp, Dept Hepatobiliary Surg, Jinan 250012, Shandong, Peoples R China.
C3 Binzhou Medical University; Binzhou Medical University; Shandong
   University
RP Yang, ZL (corresponding author), Binzhou Med Coll Affiliated Hosp, Dept Thyroid & Breast Surg, Binzhou 256600, Shandong, Peoples R China.
EM yzhlin@126.com
RI 杨, 镇霖/IXN-8059-2023
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NR 32
TC 9
Z9 11
U1 0
U2 10
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD DEC 20
PY 2016
VL 7
IS 51
BP 85163
EP 85175
DI 10.18632/oncotarget.13209
PG 13
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EG9BT
UT WOS:000391353200110
PM 27835891
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Hewitt, LC
   Hutchins, GG
   Melotte, V
   Saito, Y
   Grabsch, HI
AF Hewitt, Lindsay C.
   Hutchins, Gordon G.
   Melotte, Veerle
   Saito, Yuichi
   Grabsch, Heike I.
TI KRAS, BRAF and gastric cancer
SO TRANSLATIONAL GASTROINTESTINAL CANCER
LA English
DT Review
DE Gastric cancer (GC); KRAS; BRAF; mutation; gene amplification
ID K-RAS GENE; PHASE-II TRIAL; CETUXIMAB PLUS
   OXALIPLATIN/LEUCOVORIN/5-FLUOROURACIL; ISLAND METHYLATOR PHENOTYPE;
   COLORECTAL-CANCER; BIOMARKER ANALYSIS; OPEN-LABEL; B-RAF;
   CLINICOPATHOLOGICAL CHARACTERISTICS; COMPREHENSIVE SURVEY
AB Gastric cancer (GC) remains a major worldwide health problem and survival rates continue to be poor in patients with advanced stage disease despite multimodal treatment combining different chemo(radio) therapy regimens with surgery or best supportive care. Thus, there is an urgent clinical need to identify new potential drug targets in order to improve survival for GC patients. KRAS encodes a small guanosine triphosphatase and point mutations in codons 12 and 13 of KRAS have been detected in many human cancers. BRAF is a member of the RAF family of protein kinases and has a hotspot for mutations in codon 600 (so called V600E mutation). KRAS and BRAF proteins are both components of the MAPK/ERK pathway. When mutated, KRAS becomes constitutively active resulting in enhanced BRAF activity. KRAS and BRAF mutations in colorectal cancers (CRC) are known predictors of poor response to epidermal growth factor receptor (EGFR) targeting agents. This PubMed and Web of Science based review aimed to analyze and summarize the current literature on mutations in KRAS and BRAF in GC and their relationship to clinicopathological and molecular variables including KRAS amplification. In total, 69 studies were included in this review. The median incidence of a KRAS mutation was 6.5% ranging from 0-29%. The median incidence of KRAS mutations was similar in studies from the East and the West (East: 6%, ranging from 0-20%; West 7.5%, ranging from 0-29%). KRAS amplifications were reported at an incidence of 1-9%. The median BRAF mutation incidence in GC was 0%, ranging from 0% to 12%. Due to the low incidence and often small study size, many of the published studies had insufficient statistical power to detect a potential relationship between KRAS mutation status and clinicopathological variables including patient survival. In summary, the current literature on KRAS and BRAF in GC is still limited and very heterogeneous making any comparisons between different studies difficult. BRAF V600E mutations are very rare in GC. Interestingly, the incidence of KRAS mutations in GC is much lower than that in CRC and there appears to be no difference by ethnicity of the patients. KRAS mutations and KRAS amplifications seem to be mutually exclusive suggesting the need to screen GC patients for both genetic aberrations. So far, all clinical studies in unselected patients with metastatic GC have failed to show a significant benefit for EGFR targeting therapy. However, there has been a recent report indicating that the subgroup of signet ring cell GC, which is known to be resistant to standard cytotoxic chemotherapy, has a higher incidence of KRAS mutations (15%). Thus, EGFR targeted therapy in this particular histological subtype of GC could potentially be a promising treatment option in the future.
C1 [Hewitt, Lindsay C.; Melotte, Veerle; Saito, Yuichi; Grabsch, Heike I.] Maastricht Univ, Med Ctr, GROW Sch Oncol & Dev Biol, NL-6229 HX Maastricht, Netherlands.
   [Hewitt, Lindsay C.; Melotte, Veerle; Saito, Yuichi; Grabsch, Heike I.] Maastricht Univ, Med Ctr, Dept Pathol, NL-6229 HX Maastricht, Netherlands.
   [Hutchins, Gordon G.; Grabsch, Heike I.] Univ Leeds, Leeds Inst Canc & Pathol, Pathol & Tumour Biol, Leeds, W Yorkshire, England.
C3 Maastricht University; Maastricht University; University of Leeds
RP Grabsch, HI (corresponding author), Maastricht Univ, Med Ctr, GROW Sch Oncol & Dev Biol, P Debyelaan 25, NL-6229 HX Maastricht, Netherlands.
EM H.Grabsch@maastrichtuniversity.nl
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NR 140
TC 5
Z9 6
U1 0
U2 13
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 2224-476X
EI 2224-4778
J9 TRANSL GASTROIN CANC
JI Transl. Gastrointestin. Cancer
PD NOV
PY 2015
VL 4
IS 6
BP 429
EP 447
DI 10.3978/j.issn.2224-4778.2015.09.08
PG 19
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA CY9SH
UT WOS:000366746100004
DA 2025-01-04
ER

PT J
AU Kawaguchi, Y
   De Bellis, M
   Panettieri, E
   Duwe, G
   Vauthey, JN
AF Kawaguchi, Yoshikuni
   De Bellis, Mario
   Panettieri, Elena
   Duwe, Gregor
   Vauthey, Jean-Nicolas
TI Improvements in Systemic Therapies for Liver Metastases Will Increase
   the Role of Locoregional Treatments
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Colorectal liver metastasis; Resection; Chemotherapy; Molecular-targeted
   therapy; Conversion therapy; Two-stage hepatectomy; Neuroendocrine liver
   metastasis; Gastric liver metastasis
ID HEPATIC VEIN EMBOLIZATION; RANDOMIZED PHASE-III; COLORECTAL-CANCER;
   2-STAGE HEPATECTOMY; GASTRIC-CANCER; NEUROENDOCRINE METASTASES; SURGICAL
   RESECTION; 1ST-LINE TREATMENT; MAJOR HEPATECTOMY; PLUS BEVACIZUMAB
C1 [Kawaguchi, Yoshikuni; De Bellis, Mario; Panettieri, Elena; Duwe, Gregor; Vauthey, Jean-Nicolas] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX USA.
   [Kawaguchi, Yoshikuni] Univ Tokyo, Grad Sch Med, Dept Surg, Hepatobiliary Pancreat Surg Div, Tokyo, Japan.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Tokyo
RP Vauthey, JN (corresponding author), 1515 Holcombe Blvd,Unit 1484, Houston, TX 77030 USA.
EM jvauthey@mdanderson.org
RI Panettieri, Elena/AAZ-1874-2020
FU National Institutes of Health [T32 CA 009599]; MD Anderson Cancer Center
   Support Grant [CA016672]
FX Grant support: This research was supported in part by the National
   Institutes of Health (T32 CA 009599) and the MD Anderson Cancer Center
   Support Grant, CA016672.
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NR 66
TC 0
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U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8588
EI 1558-1977
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD FEB
PY 2025
VL 39
IS 1
BP 207
EP 220
DI 10.1016/j.hoc.2024.08.009
EA NOV 2024
PG 14
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA L7C4F
UT WOS:001352256800001
PM 39510674
DA 2025-01-04
ER

PT J
AU Chen, Y
   Bai, BJ
   Ying, KK
   Pan, HM
   Xie, BB
AF Chen, Yao
   Bai, Bingjun
   Ying, Kangkang
   Pan, Hongming
   Xie, Binbin
TI Anti-PD-1 combined with targeted therapy: Theory and practice in gastric
   and colorectal cancer
SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
LA English
DT Review
DE Immunotherapy Anti-PD-1; Targeted therapy; Combination Gastric Cancer;
   Colorectal Cancer
ID GASTROESOPHAGEAL JUNCTION CANCER; SINGLE-ARM; PHASE-II; RANDOMIZED
   PHASE-3; DOUBLE-BLIND; OPEN-LABEL; T-CELL; MONOCLONAL-ANTIBODY;
   ANTITUMOR-ACTIVITY; INDUCED APOPTOSIS
AB Gastric cancer (GC) and colorectal cancer (CRC) are frequent and aggressive malignancies worldwide. Despite the emergence of various therapeutic regimens, the prognosis of gastric and colorectal cancer is relatively poor. Immunotherapy targeting PD-1 is one of the most prevalent approaches, but it has a low response rate in most patients, particularly those with microsatellite stability (MSS). Recently, some targeted drugs have been found to remarkably enhance the anti-tumor immunity of cancer models, mainly through increasing the level of CD8(+) T cells, M1-type macrophages, expression of PD-L1, and decreasing the level of regulatory T cells and M2 macrophages. The above finding implies that the combination of anti-PD-1 and targeted therapies may be a potential treatment for gastric and colorectal cancer patients. Although many encouraging preclinical results have been shown, the clinical outcomes were not approving enough. To further enhance the therapeutic efficacy and improve the prognosis in GC and CRC patients, deeper and larger-scale studies should be done to determine the complicated interactions between the two therapies and the concrete use of combination regimens.
C1 [Chen, Yao; Ying, Kangkang; Pan, Hongming; Xie, Binbin] Zhejiang Univ, Sir Run Run Shaw Hosp, Sch Med, Dept Med Oncol, Hangzhou 310016, Peoples R China.
   [Bai, Bingjun] Zhejiang Univ, Sir Run Run Shaw Hosp, Sch Med, Dept Colorectal Surg, Hangzhou 310016, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP Pan, HM; Xie, BB (corresponding author), Zhejiang Univ, Sir Run Run Shaw Hosp, Sch Med, 3 East Qingchun Rd, Hangzhou 310016, Zhejiang, Peoples R China.
EM panhongming@zju.edu.cn; xieBB@zju.edu.cn
OI Bai, Bingjun/0000-0003-3763-638X
FU National Natural Science Foundation of China [82172908]; Zhejiang
   Provincial Natural Science Foundation of China [LQ21H160027]; China
   Postdoctoral Science Foundation [2020M681893]
FX This work was supported by grants from National Natural Science
   Foundation of China (grants 82100542 to B. Xie), Zhejiang Provincial
   Natural Science Foundation of China (Grant Nos. LQ21H160027 to B. Xie),
   the China Postdoctoral Science Foundation (Grant Nos. 2020M681893 to B.
   Xie), and National Natural Science Foundation of China (grants 82172908
   to H. Pan).
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JI Biochim. Biophys. Acta-Rev. Cancer
PD SEP
PY 2022
VL 1877
IS 5
DI 10.1016/j.bbcan.2022.188775
PG 12
WC Biochemistry & Molecular Biology; Biophysics; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Oncology
GA 7Q9SN
UT WOS:000909722000001
PM 35934154
DA 2025-01-04
ER

PT J
AU Zhang, H
   Lin, MB
   Dong, C
   Tang, Y
   An, LW
   Ju, JY
   Wen, FP
   Chen, F
   Wang, M
   Wang, WJ
   Chen, M
   Zhao, Y
   Li, JX
   Hou, SX
   Lin, XH
   Hu, LL
   Bu, WB
   Wu, DQ
   Li, L
   Jiao, S
   Zhou, ZC
AF Zhang, Hui
   Lin, Moubin
   Dong, Chao
   Tang, Yang
   An, Liwei
   Ju, Junyi
   Wen, Fuping
   Chen, Fan
   Wang, Meng
   Wang, Wenjia
   Chen, Min
   Zhao, Yun
   Li, Jixi
   Hou, Steven X.
   Lin, Xinhua
   Hu, Lulu
   Bu, Wenbo
   Wu, Dianqing
   Li, Lin
   Jiao, Shi
   Zhou, Zhaocai
TI An MST4-pβ-Catenin<SUP>Thr40</SUP> Signaling Axis Controls Intestinal
   Stem Cell and Tumorigenesis
SO ADVANCED SCIENCE
LA English
DT Article
DE cancer stem cells; colorectal cancer; intestinal stem cells; MST4-p
   beta-catenin(Thr40) signaling axis; targeted therapy
ID BETA-CATENIN PHOSPHORYLATION; WNT/BETA-CATENIN; HIPPO PATHWAY; APC;
   KINASE; PROTEIN; MST4; ACTIVATION; HOMEOSTASIS; IDENTIFICATION
AB Elevated Wnt/beta-catenin signaling has been commonly associated with tumorigenesis especially colorectal cancer (CRC). Here, an MST4-p beta-catenin(Thr40) signaling axis essential for intestinal stem cell (ISC) homeostasis and CRC development is uncovered. In response to Wnt3a stimulation, the kinase MST4 directly phosphorylates beta-catenin at Thr40 to block its Ser33 phosphorylation by GSK3 beta. Thus, MST4 mediates an active process that prevents beta-catenin from binding to and being degraded by beta-TrCP, leading to accumulation and full activation of beta-catenin. Depletion of MST4 causes loss of ISCs and inhibits CRC growth. Mice bearing either MST4(T178E) mutation with constitutive kinase activity or beta-catenin(T40D) mutation mimicking MST4-mediated phosphorylation show overly increased ISCs/CSCs and exacerbates CRC. Furthermore, the MST4-p beta-catenin(Thr40) axis is upregulated and correlated with poor prognosis of human CRC. Collectively, this work establishes a previously undefined machinery for beta-catenin activation, and further reveals its function in stem cell and tumor biology, opening new opportunities for targeted therapy of CRC.
C1 [Zhang, Hui; Wen, Fuping; Chen, Fan; Chen, Min; Zhao, Yun; Li, Lin] Chinese Acad Sci, Univ Chinese Acad Sci, Shanghai Inst Biochem & Cell Biol, CAS Ctr Excellence Mol Cell Sci,State Key Lab Mol, Shanghai 200031, Peoples R China.
   [Zhang, Hui; Wang, Meng; Wang, Wenjia; Li, Jixi; Hou, Steven X.; Lin, Xinhua; Jiao, Shi; Zhou, Zhaocai] Fudan Univ, Zhongshan Hosp, Sch Life Sci, Dept Cell & Dev Biol,State Key Lab Genet Engn, Shanghai 200438, Peoples R China.
   [Lin, Moubin] Tongji Univ, Sch Med, Yangpu Hosp, Dept Gen Surg, Shanghai 200090, Peoples R China.
   [Dong, Chao] Kunming Med Univ, Yunnan Tumor Hosp, Affiliated Hosp 3, Dept Med Oncol 2, Kunming 650118, Yunnan, Peoples R China.
   [Tang, Yang; An, Liwei; Ju, Junyi] Tongji Univ, Shanghai Peoples Hosp 10, Sch Med, Dept Med Ultrasound,Canc Ctr, Shanghai 200072, Peoples R China.
   [Hu, Lulu] Fudan Univ, Inst Biomed Sci, Shanghai Canc Ctr, State Key Lab Genet Engn, Shanghai 200032, Peoples R China.
   [Hu, Lulu] Fudan Univ, Shanghai Med Coll, Shanghai Lab Med Epigenet, Shanghai 200032, Peoples R China.
   [Bu, Wenbo] Fudan Univ, Dept Mat Sci, Shanghai 200433, Peoples R China.
   [Wu, Dianqing] Yale Sch Med, Dept Pharmacol, New Haven, CT 06520 USA.
C3 Chinese Academy of Sciences; Center for Excellence in Molecular Cell
   Science, CAS; University of Chinese Academy of Sciences, CAS; Fudan
   University; Tongji University; Kunming Medical University; Tongji
   University; Fudan University; Fudan University; Fudan University; Yale
   University
RP Jiao, S; Zhou, ZC (corresponding author), Fudan Univ, Zhongshan Hosp, Sch Life Sci, Dept Cell & Dev Biol,State Key Lab Genet Engn, Shanghai 200438, Peoples R China.
EM jiaoshi@sibcb.ac.cn; zhouzhaocai@fudan.edu.cn
RI DONG, CHAO/C-8318-2014; Li, xiaofei/GXF-7187-2022; Bu, Wenbo/G-1715-2012
OI An, Liwei/0000-0003-4514-5476; ju, junyi/0000-0002-9141-2363; Wen,
   Fuping/0009-0005-3153-9820
FU National Key R&D Program of China [2020YFA0803200, 2017YFA0504504];
   National Natural Science Foundation of China [81725014, 81822035,
   31930026, 82002493, 82060542, 81874201]; Youth Innovation Promotion
   Association of the Chinese Academic Sciences; Key Program for Basic
   Research of Shanghai [19JC1415600]; Shanghai Pujiang Program
   [19PJ1408300]; Open Research Fund of State Key Laboratory of Genetic
   Engineering, Fudan University [SKLGE-2103]; Talent Climbing Project from
   Shanghai Tenth People's Hospital [2021SYPDRC003]; China Postdoctoral
   Science Foundation [2020T130477]; top young talents of ten thousand
   talents plan in Yunnan Province [YNWR-QNBJ-2019-275]; medical discipline
   leader of Yunnan province [D-2019029]; general projects of basic
   research in Yunnan Province [2019FB113]
FX The authors thank Prof. Yi Arial Zeng and Prof. Bin Zhou at SIBCB, and
   Prof. Zhengquan Yu at China Agricultural University for kindly providing
   mice indicated in the method. This work was supported by the National
   Key R&D Program of China (2020YFA0803200 and 2017YFA0504504), the
   National Natural Science Foundation of China Grants (81725014, 81822035,
   31930026, 81822035, 82002493, 82060542, and 81874201), the Youth
   Innovation Promotion Association of the Chinese Academic Sciences, the
   Key Program for Basic Research of Shanghai (19JC1415600), Shanghai
   Pujiang Program (19PJ1408300), Open Research Fund of State Key
   Laboratory of Genetic Engineering, Fudan University (SKLGE-2103), Talent
   Climbing Project from Shanghai Tenth People's Hospital (2021SYPDRC003),
   and the China Postdoctoral Science Foundation (2020T130477). C.D. was
   sponsored by top young talents of ten thousand talents plan in Yunnan
   Province (YNWR-QNBJ-2019-275), the medical discipline leader of Yunnan
   province (D-2019029), and the general projects of basic research in
   Yunnan Province (2019FB113).
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NR 80
TC 14
Z9 15
U1 1
U2 37
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2198-3844
J9 ADV SCI
JI Adv. Sci.
PD SEP
PY 2021
VL 8
IS 17
AR 2004850
DI 10.1002/advs.202004850
EA JUL 2021
PG 17
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA UN0SK
UT WOS:000670837100001
PM 34240584
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, CK
   Sandhu, J
   Ouyang, C
   Ye, J
   Lee, PP
   Fakih, M
AF Wang, Chongkai
   Sandhu, Jaideep
   Ouyang, Ching
   Ye, Jian
   Lee, Peter P.
   Fakih, Marwan
TI Clinical Response to Immunotherapy Targeting Programmed Cell Death
   Receptor 1/Programmed Cell Death Ligand 1 in Patients With
   Treatment-Resistant Microsatellite Stable Colorectal Cancer With and
   Without Liver Metastases
SO JAMA NETWORK OPEN
LA English
DT Article
ID PHASE-II; SURVIVAL; MELANOMA; TUMORS
AB IMPORTANCE Microsatellite stable (MSS) metastatic colorectal cancer has been historically characterized as resistant to immunotherapy. Recent studies have demonstrated limited clinical activity of programmed cell death receptor 1/programmed death ligand 1 (PD-1/PD-L1) targeting in MSS metastatic colorectal cancer. The association of metastatic disease in the liver with treatment response has not been fully investigated.
   OBJECTIVE To investigate the association of liver metastases with response to PD-1/PD-L1-targeting therapy in MSS metastatic colorectal cancer.
   DESIGN, SETTING, AND PARTICIPANTS This single-center retrospective cohort study evaluated clinical responses to PD-1- or PD-L1-targeting therapy, with or without other investigational agents, in patients with MSS metastatic colorectal cancer and disease progression after standard of care therapy from January 1, 2014, to December 31, 2020.
   MAIN OUTCOMES AND MEASURES Objective response rate (ORR) and progression-free survival (PFS), measured from initiation of PD-1/PD-L1-targeting therapy.
   RESULTS Ninety-five patients with MSS metastatic colorectal cancer were identified (54 men [56.8%]; median age, 55 [interquartile range (IQR), 49-64] years). The overall ORR was 8.4%(8 of 95 patients). Eight of 41 patients without liver metastases achieved an ORR of 19.5%, and no response was observed in 54 patients with liver metastases. The disease control rate was 58.5%(24 of 41) in patients without liver metastasis and 1.9% (1 of 54) in patients with liver metastasis. Patients without liver metastases at the time of PD-1/PD-L1-targeting treatment had a superior median PFS compared with patients with liver metastases (4.0 [IQR, 2.0-7.5] vs 1.5 [IQR, 1.0-2.0] months; P < .001). In addition, median PFS was 5.5 (IQR, 2.0-11.5) months for patients without any prior or current liver involvement at the time of PD-1/PD-L1-targeting treatment initiation. Using a multivariate Cox regression model correcting for Eastern Cooperative Oncology Group status, primary tumor location, RAS and BRAF status, tumor mutation burden, and metastatic sites, liver metastases was the variable with the most significant association with faster progression after PD-1/PD-L1 treatment inhibition (hazard ratio, 7.00; 95% CI, 3.18-15.42; P < .001).
   CONCLUSIONS AND RELEVANCE Findings of this cohort study suggest that patients with MSS metastatic colorectal cancer and without liver metastases may derive clinical benefits from checkpoint inhibitors, whereas the presence of liver metastases was associated with resistance. Further prospective studies are needed to investigate PD-1/PD-L1 inhibitors in patients with MSS metastatic colorectal cancer without liver metastases.
C1 [Wang, Chongkai; Sandhu, Jaideep; Fakih, Marwan] City Hope Comprehens Canc Ctr, Dept Med Oncol & Therapeut Res, 1500 E Duarte Rd, Duarte, CA 91010 USA.
   [Ouyang, Ching] City Hope Natl Med Ctr, Ctr Informat, 1500 E Duarte Rd, Duarte, CA 91010 USA.
   [Ouyang, Ching] Beckman Res Inst City Hope, Dept Computat & Quantitat Med, Duarte, CA USA.
   [Ye, Jian; Lee, Peter P.] Beckman Res Inst City Hope, Dept Immunooncol, Duarte, CA USA.
C3 City of Hope; City of Hope; City of Hope; Beckman Research Institute of
   City of Hope; City of Hope; Beckman Research Institute of City of Hope
RP Fakih, M (corresponding author), City Hope Comprehens Canc Ctr, Dept Med Oncol & Therapeut Res, 1500 E Duarte Rd, Duarte, CA 91010 USA.
EM mfakih@coh.org
RI Sandhu, Jaideep/IZD-9934-2023; Lee, Peter/KXS-0736-2024
OI Sandhu, Jaideep/0000-0002-3165-6286
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NR 39
TC 80
Z9 83
U1 1
U2 13
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2574-3805
J9 JAMA NETW OPEN
JI JAMA Netw. Open
PD AUG 9
PY 2021
VL 4
IS 8
AR e2118416
DI 10.1001/jamanetworkopen.2021.18416
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA TZ7RR
UT WOS:000684670200001
PM 34369992
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhong, J
   Sun, ZJ
   Li, S
   Yang, L
   Cao, YP
   Bao, J
AF Zhong, Jie
   Sun, Zijian
   Li, Sheng
   Yang, Liu
   Cao, Yuepeng
   Bao, Jun
TI Immune checkpoint blockade therapy for <i>BRAF</i> mutant metastatic
   colorectal cancer: the efficacy, new strategies, and potential
   biomarkers
SO DISCOVER ONCOLOGY
LA English
DT Review
DE BRAF mutation; Colorectal cancer; Immune checkpoint blockade therapy;
   Targeted therapy; Predictive biomarkers
ID MISMATCH REPAIR-DEFICIENT; CONSENSUS MOLECULAR SUBTYPES; MICROSATELLITE
   INSTABILITY; OPEN-LABEL; 1ST-LINE TREATMENT; SUBGROUP ANALYSES; PD-L1
   EXPRESSION; PHASE-II; PEMBROLIZUMAB; INHIBITION
AB BRAF mutant metastatic colorectal cancer has long been considered a tumor with a poor prognosis and a poor response to chemotherapy. Despite the efficacy of targeted therapy with multi-targeted blockade of the mitogen-activated protein kinase (MAPK) signaling pathway has brought a glimmer of hope to this group of patients, the need to improve treatment efficacy remains unmet, especially for the microsatellite stability/DNA proficient mismatch repair (MSS/pMMR) subtype. BRAF mutant colorectal cancer patients with high microsatellite instability/DNA deficient mismatch repair (MSI-H/dMMR) have high tumor mutation burden and abundant neoantigen, who are deemed as ones that could receive expected efficacy from immunotherapy. Generally, it is believed that MSS/pMMR colorectal cancer is an immunologically "cold" tumor that is insensitive to immunotherapy. However, targeted therapy combined with immune checkpoint blockade therapy seems to bring light to BRAF mutant colorectal cancer patients. In this review, we provide an overview of clinical efficacy and evolving new strategies concerning immune checkpoint blockade therapy for both MSI-H/dMMR and MSS/pMMR BRAF mutant metastatic colorectal cancer and discuss the potential biomarkers in the tumor immune microenvironment for predicting immunotherapeutic response in BRAF mutant colorectal cancer.
C1 [Zhong, Jie; Sun, Zijian; Li, Sheng; Bao, Jun] Nanjing Med Univ, Affiliated Canc Hosp, Dept Med Oncol, Nanjing 210009, Peoples R China.
   [Yang, Liu; Cao, Yuepeng] Nanjing Med Univ, Affiliated Canc Hosp, Dept Colorectal Surg, Nanjing 210009, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University
RP Bao, J (corresponding author), Nanjing Med Univ, Affiliated Canc Hosp, Dept Med Oncol, Nanjing 210009, Peoples R China.
EM baojun@jszlyy.com.cn
FU Key R & D Plan of Jiangsu Provincial Department of Science and
   Technology [BE2020723]
FX This work was supported by Key R & D Plan of Jiangsu Provincial
   Department of Science and Technology (BE2020723).
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NR 106
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 11
PY 2023
VL 14
IS 1
AR 94
DI 10.1007/s12672-023-00718-y
PG 13
WC Oncology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Endocrinology & Metabolism
GA I5OI0
UT WOS:001003268300001
PM 37302081
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Rodenas, MC
   Peñas-Martínez, J
   Pardo-Sánchez, I
   Zaragoza-Huesca, D
   Ortega-Sabater, C
   Peña-García, J
   Espín, S
   Ricote, G
   Montenegro, S
   Ayala-De La Peña, F
   Luengo-Gil, G
   Nieto, A
   García-Molina, F
   Vicente, V
   Bernardi, F
   Lozano, ML
   Mulero, V
   Pérez-Sánchez, H
   Carmona-Bayonas, A
   Martínez-Martínez, I
AF Rodenas, Maria Carmen
   Penas-Martinez, Julia
   Pardo-Sanchez, Irene
   Zaragoza-Huesca, David
   Ortega-Sabater, Carmen
   Pena-Garcia, Jorge
   Espin, Salvador
   Ricote, Guillermo
   Montenegro, Sofia
   Ayala-De La Pena, Francisco
   Luengo-Gil, Gines
   Nieto, Andres
   Garcia-Molina, Francisco
   Vicente, Vicente
   Bernardi, Francesco
   Lozano, Maria Luisa
   Mulero, Victoriano
   Perez-Sanchez, Horacio
   Carmona-Bayonas, Alberto
   Martinez-Martinez, Irene
TI Venetoclax is a potent hepsin inhibitor that reduces the metastatic and
   prothrombotic phenotypes of hepsin-expressing colorectal cancer cells
SO FRONTIERS IN MOLECULAR BIOSCIENCES
LA English
DT Article
DE hepsin; colorectal cancer; metastasis; thrombosis; molecular-targeted
   therapy
ID FACTOR-VII; PROGNOSIS; PROMOTES; INVASION; TUMOR; RISK
AB Introduction: Hepsin is a type II transmembrane serine protease and its expression has been linked to greater tumorigenicity and worse prognosis in different tumors. Recently, our group demonstrated that high hepsin levels from primary tumor were associated with a higher risk of metastasis and thrombosis in localized colorectal cancer patients. This study aims to explore the molecular role of hepsin in colorectal cancer.Methods: Hepsin levels in plasma from resected and metastatic colorectal cancer patients were analyzed by ELISA. The effect of hepsin levels on cell migration, invasion, and proliferation, as well as on the activation of crucial cancer signaling pathways, was performed in vitro using colorectal cancer cells. A thrombin generation assay determined the procoagulant function of hepsin from these cells. A virtual screening of a database containing more than 2000 FDA-approved compounds was performed to screen hepsin inhibitors, and selected compounds were tested in vitro for their ability to suppress hepsin effects in colorectal cancer cells. Xenotransplantation assays were done in zebrafish larvae to study the impact of venetoclax on invasion promoted by hepsin.Results: Our results showed higher plasma hepsin levels in metastatic patients, among which, hepsin was higher in those suffering thrombosis. Hepsin overexpression increased colorectal cancer cell invasion, Erk1/2 and STAT3 phosphorylation, and thrombin generation in plasma. In addition, we identified venetoclax as a potent hepsin inhibitor that reduced the metastatic and prothrombotic phenotypes of hepsin-expressing colorectal cancer cells. Interestingly, pretreatment with Venetoclax of cells overexpressing hepsin reduced their invasiveness in vivo.Discussion: Our results demonstrate that hepsin overexpression correlates with a more aggressive and prothrombotic tumor phenotype. Likewise, they demonstrate the antitumor role of venetoclax as a hepsin inhibitor, laying the groundwork for molecular-targeted therapy for colorectal cancer.
C1 [Rodenas, Maria Carmen; Penas-Martinez, Julia; Zaragoza-Huesca, David; Ortega-Sabater, Carmen; Espin, Salvador; Ricote, Guillermo; Montenegro, Sofia; Ayala-De La Pena, Francisco; Vicente, Vicente; Lozano, Maria Luisa; Carmona-Bayonas, Alberto; Martinez-Martinez, Irene] Univ Murcia, Hosp Univ Morales Meseguer, Ctr Invest Biomed Red Enfermedades Raras, Ctr Reg Hemodonac,IMIB Pascual Parrilla,Dept Hemat, Murcia, Spain.
   [Pardo-Sanchez, Irene; Mulero, Victoriano] Univ Murcia, Fac Biol, Ctr Invest Biomed Red Enfermedades Raras, Dept Cell Biol,IMIB Pascual Parrilla, Murcia, Spain.
   [Pena-Garcia, Jorge; Perez-Sanchez, Horacio] UCAM Univ Catolica Murcia, Comp Engn Dept, Struct Bioinformat & High Performance Comp Res Grp, Guadalupe, Spain.
   [Luengo-Gil, Gines] Hosp Univ Santa Lucia, Clin Anal & Pathol Dept, Grp Mol Pathol & Pharmacogenet, IMIB Pascual Parrilla, Cartagena, Spain.
   [Nieto, Andres] Hosp Univ Morales Meseguer, Dept Pathol, Murcia, Spain.
   [Garcia-Molina, Francisco] Hosp Univ Reina Sofia, Dept Pathol, Murcia, Spain.
   [Bernardi, Francesco] Univ Ferrara, Dept Life Sci & Biotechnol, Ferrara, Italy.
C3 University of Murcia; CIBER - Centro de Investigacion Biomedica en Red;
   CIBERER; Meseguer General University Hospital Morales; CIBER - Centro de
   Investigacion Biomedica en Red; CIBERER; University of Murcia;
   Universidad Catolica de Murcia; Meseguer General University Hospital
   Morales; University of Ferrara
RP Carmona-Bayonas, A; Martínez-Martínez, I (corresponding author), Univ Murcia, Hosp Univ Morales Meseguer, Ctr Invest Biomed Red Enfermedades Raras, Ctr Reg Hemodonac,IMIB Pascual Parrilla,Dept Hemat, Murcia, Spain.; Pérez-Sánchez, H (corresponding author), UCAM Univ Catolica Murcia, Comp Engn Dept, Struct Bioinformat & High Performance Comp Res Grp, Guadalupe, Spain.
EM alberto.carmonabayonas@gmail.com
RI Ayala de la Peña, Francisco/C-5280-2011; De La Peña García,
   Jorge/O-8518-2016; ORTEGA, CARMEN/ABC-8616-2021; Lozano, Maria
   L/C-5886-2008; Rodenas, M.Carmen/AAE-8850-2022; Luengo-Gil,
   Ginés/AAB-6780-2019; Pérez-Sánchez, Horacio/O-5017-2016; Garcia-Molina,
   Francisco/S-6052-2019; Martínez-Martínez, Irene/AAM-8862-2020; Lozano,
   Maria L/J-8121-2012
OI Zaragoza Huesca, David/0000-0001-7330-7597; Garcia-Molina,
   Francisco/0000-0003-4481-7568; Martinez-Martinez,
   Irene/0000-0002-1067-6464; Mulero, Victoriano/0000-0001-9527-0211;
   Luengo-Gil, Gines/0000-0001-9940-0415; Montenegro Luis,
   Sofia/0000-0003-3849-327X; Lozano, Maria L/0000-0003-3148-7037
FU Carlos III Health Institute [PI17/00050 FEDER, PI21/00210 FEDER];
   Spanish Ministry of Economy and Competitiveness [2020-113660RB-I00,
   CTQ2017-87974-R]; Fundacion Seneca [20988/PI/18]
FX This research was funded by Carlos III Health Institute (Grant Number
   PI17/00050 & FEDER, PI21/00210 & FEDER), Spanish Ministry of Economy and
   Competitiveness (grant numbers 2020-113660RB-I00, FEDER, and
   CTQ2017-87974-R), Fundacion Seneca (Project 20988/PI/18), and generous
   donations to crowdfunding precipitation (FECYT).
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NR 50
TC 1
Z9 1
U1 0
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-889X
J9 FRONT MOL BIOSCI
JI Front. Mol. Biosci.
PD MAY 19
PY 2023
VL 10
AR 1182925
DI 10.3389/fmolb.2023.1182925
PG 14
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA I1FY9
UT WOS:001000314800001
PM 37275957
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Han, XW
   Huang, XD
   Zhang, JY
   Li, WD
   Ma, Z
   Ma, B
   Maswikiti, EP
   Yin, ZY
   Wang, YH
   Gao, L
   Chen, H
AF Han, Xiaowen
   Huang, Xiaodong
   Zhang, Jiayi
   Li, Weidong
   Ma, Zhen
   Ma, Bin
   Maswikiti, Ewestse Paul
   Yin, Zhenyu
   Wang, Yuhan
   Gao, Lei
   Chen, Hao
TI Case report: is necrotizing fasciitis in a rectal cancer patient after
   targeted systemic therapy related to the tumor site? - evidence from a
   hepatocellular carcinoma patient
SO INFECTIOUS AGENTS AND CANCER
LA English
DT Article
DE Rectal cancer; Hepatocellular carcinoma; Necrotizing fasciitis;
   Fournier's gangrene; Bevacizumab; Lenvatinib
ID FOURNIERS GANGRENE; COLORECTAL-CANCER; BEVACIZUMAB; MANAGEMENT
AB Necrotizing fasciitis (NF) is a rare and life-threatening serious infectious disease, characterized by acute onset and rapid progress, leading to extensive necrosis of skin, soft tissue as well as fascia by a variety of aerobic and anaerobic bacteria, localized on external genitalia, scrotum, groin and perianal areas in males. There exist numerous common etiologies for NF, yet NF induced by malignant neoplasms is exceedingly rare. Several studies have reported that NF may be associated with tumor site (rectal/sigmoid colon cancer) and blood supply dysfunction caused by targeted therapy drugs (bevacizumab, aflibercept, ramucirumab). The perforation of colorectal cancer poses a unique risk factor for NF. However, in our two cases, the patient with rectal cancer received CapeOX (oxaliplatin + capecitabine) + bevacizumab + tislelizumab for 3 cycles without perforation but did develop NF. One month after debridement, the patient continued immunotherapy with tislelizumab alone for the fourth cycle and maintained for an additional 3 cycles without any recurrence of NF. Therefore, does the occurrence of NF correlate with the tumor site (rectum) and targeted immunotherapy? Another patient with hepatocellular carcinoma also developed NF after receiving 2 cycles of lenvatinib + sintilimab treatment. The third cycle of sintilimab immunotherapy was administered on the 13th day after operation, which was subsequently maintained for an additional 2 cycles without recurrence of NF. The absence of a direct correlation between hepatocellular carcinoma and rectal tumor location as well as immunotherapy, suggests that NF may be closely linked to targeted therapy.
C1 [Han, Xiaowen; Huang, Xiaodong; Zhang, Jiayi; Li, Weidong; Maswikiti, Ewestse Paul; Yin, Zhenyu; Wang, Yuhan; Gao, Lei] Lanzhou Univ, Clin Med Coll 2, Lanzhou, Peoples R China.
   [Ma, Zhen; Ma, Bin; Chen, Hao] Lanzhou Univ, Dept Surg Oncol, Hosp 2, Lanzhou, Peoples R China.
   [Chen, Hao] Key Lab Environm Oncol Gansu Prov, Lanzhou, Peoples R China.
C3 Lanzhou University; Lanzhou University
RP Chen, H (corresponding author), Lanzhou Univ, Dept Surg Oncol, Hosp 2, Lanzhou, Peoples R China.; Chen, H (corresponding author), Key Lab Environm Oncol Gansu Prov, Lanzhou, Peoples R China.
EM ery_chenh@lzu.edu.cn
RI Zhang, Jiayi/GQQ-9674-2022; Huang, Xiaodong/KUC-6358-2024
FU National Natural Science Foundation of China
FX The authors of this article would like to acknowledge the patients and
   relatives for providing adequate case information and for consenting
   that this work be published.
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NR 18
TC 0
Z9 0
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U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1750-9378
J9 INFECT AGENTS CANCER
JI Infect. Agents Cancer
PD SEP 20
PY 2024
VL 19
IS 1
AR 45
DI 10.1186/s13027-024-00607-1
PG 10
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA G6A1F
UT WOS:001317432400001
PM 39304909
OA gold, Green Accepted
DA 2025-01-04
ER

PT J
AU Iyevleva, AG
   Imyanitov, EN
AF Iyevleva, Aglaya G.
   Imyanitov, Evgeny N.
TI Cytotoxic and targeted therapy for hereditary cancers
SO HEREDITARY CANCER IN CLINICAL PRACTICE
LA English
DT Review
DE Hereditary cancer syndromes; Familial cancer; Breast cancer; Ovarian
   cancer; Colorectal cancer; Cytotoxic therapy; Targeted therapy;
   Predictive markers; BRCA1; BRCA2
ID NEGATIVE BREAST-CANCER; PATHOLOGICAL COMPLETE RESPONSE; BRCA MUTATION
   CARRIERS; HIGH-DOSE CHEMOTHERAPY; HOMOLOGOUS RECOMBINATION DEFICIENCY;
   PEGYLATED LIPOSOMAL DOXORUBICIN; RIBOSE POLYMERASE INHIBITORS; RECURRENT
   EPITHELIAL OVARIAN; PLATINUM-BASED CHEMOTHERAPY; TUBEROUS SCLEROSIS
   COMPLEX
AB There is a number of drugs demonstrating specific activity towards hereditary cancers. For example, tumors in BRCA1/2 mutation carriers usually arise via somatic inactivation of the remaining BRCA allele, which makes them particularly sensitive to platinum-based drugs, PARP inhibitors (PARPi), mitomycin C, liposomal doxorubicin, etc. There are several molecular assays for BRCA-ness, which permit to reveal BRCA-like phenocopies among sporadic tumors and thus extend clinical indications for the use of BRCA-specific therapies. Retrospective data on high-dose chemotherapy deserve consideration given some unexpected instances of cure from metastatic disease among BRCA1/2-mutated patients. Hereditary non-polyposis colorectal cancer (HNPCC) is characterized by high-level microsatellite instability (MSI-H), increased antigenicity and elevated expression of immunosuppressive molecules. Recent clinical trial demonstrated tumor responses in HNPCC patients treated by the immune checkpoint inhibitor pembrolizumab. There are successful clinical trials on the use of novel targeted agents for the treatment or rare cancer syndromes, e.g. RET inhibitors for hereditary medullary thyroid cancer, mTOR inhibitors for tumors arising in patients with tuberous sclerosis (TSC), and SMO inhibitors for basal-cell nevus syndrome. Germ-line mutation tests will be increasingly used in the future for the choice of the optimal therapy, therefore turnaround time for these laboratory procedures needs to be significantly reduced to ensure proper treatment planning.
C1 [Iyevleva, Aglaya G.; Imyanitov, Evgeny N.] NN Petrov Inst Oncol, Pesochny 2, St Petersburg 197758, Russia.
   [Iyevleva, Aglaya G.; Imyanitov, Evgeny N.] St Petersburg Pediat Med Univ, St Petersburg 194100, Russia.
   [Imyanitov, Evgeny N.] II Mechnikov North Western Med Univ, St Petersburg 191015, Russia.
   [Imyanitov, Evgeny N.] St Petersburg State Univ, St Petersburg 199034, Russia.
C3 N.N. Petrov Research Institute of Oncology; Saint Petersburg State
   Pediatric Medical University; North-Western State Medical University
   named after I.I. Mechnikov; Saint Petersburg State University
RP Imyanitov, EN (corresponding author), NN Petrov Inst Oncol, Pesochny 2, St Petersburg 197758, Russia.; Imyanitov, EN (corresponding author), St Petersburg Pediat Med Univ, St Petersburg 194100, Russia.; Imyanitov, EN (corresponding author), II Mechnikov North Western Med Univ, St Petersburg 191015, Russia.; Imyanitov, EN (corresponding author), St Petersburg State Univ, St Petersburg 199034, Russia.
EM evgeny@imyanitov.spb.ru
RI Imyanitov, Evgeny/ABG-8619-2021; Iyevleva, Aglaya/P-8305-2016
FU Russian Scientific Fund [14-15-00528]; Russian Science Foundation
   [14-15-00528] Funding Source: Russian Science Foundation
FX This work has been supported by the Russian Scientific Fund (grant
   number 14-15-00528).
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NR 157
TC 36
Z9 45
U1 0
U2 22
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1731-2302
EI 1897-4287
J9 HERED CANCER CLIN PR
JI Hered. Cancer Clin. Pract.
PD AUG 23
PY 2016
VL 14
AR 17
DI 10.1186/s13053-016-0057-2
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DU9GN
UT WOS:000382524600001
PM 27555886
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Razenberg, LGEM
   van Gestel, YRBM
   Lemmens, VEPP
   de Hingh, IHJT
   Creemers, GJ
AF Razenberg, Lieke G. E. M.
   van Gestel, Yvette R. B. M.
   Lemmens, Valery E. P. P.
   de Hingh, Ignace H. J. T.
   Creemers, Geert-Jan
TI Bevacizumab in Addition to Palliative Chemotherapy for Patients With
   Peritoneal Carcinomatosis of Colorectal Origin: A Nationwide
   Population-Based Study
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Colorectal cancer; Palliative systemic therapy; Peritoneal metastases;
   Synchronous; Targeted therapy
ID OXALIPLATIN-BASED CHEMOTHERAPY; RANDOMIZED PHASE-III; ELDERLY-PATIENTS;
   COLON-CANCER; 1ST-LINE TREATMENT; INTRAPERITONEAL CHEMOTHERAPY; PLUS
   IRINOTECAN; GROWTH-FACTOR; FLUOROURACIL; LEUCOVORIN
AB Data on the use and effect of bevacizumab, in addition to palliative chemotherapy, are currently lacking for patients with colorectal cancer presenting with peritoneal carcinomatosis (PC). The present study involved 1235 patients with colorectal PC receiving only palliative systemic therapy. Bevacizumab was prescribed to 436 patients (35%) and was associated with an improved median overall survival (11 months).
   Background: Most patients with colorectal cancer (CRC) presenting with peritoneal carcinomatosis (PC) rely on palliative systemic treatment options. However, data on the use and effect of systemic treatment strategies, including targeted agents for the palliative treatment of colorectal PC, are lacking. We conducted a nationwide population-based study with data from the period in which the targeted agent bevacizumab was introduced in the Netherlands. Patients and Methods: The present study included all patients diagnosed from 2007 to 2014 with synchronous PC from CRC treated with only palliative systemic therapy. We assessed the use of bevacizumab, the standard choice of targeted treatment, in addition to first-line chemotherapy. Multivariable logistic regression analyses were performed to calculate the predictors for the additional prescription of bevacizumab. Survival estimates were calculated, and multivariable Cox analyses were performed to estimate the hazard ratios (HRs) of death stratified by the treatment received. Results: A total of 1235 patients received palliative chemotherapy, of whom 436 also received bevacizumab (35%). Patients aged >= 75 years and patients with PC from colonic tumors were less likely to receive chemotherapy plus bevacizumab. The addition of bevacizumab to palliative chemotherapy was associated with an improved overall median survival of 7.5 versus 11 months in both patients with isolated PC and those with concomitant extraperitoneal metastases. The improvement remained after adjustment for patient and tumor characteristics (HR, 0.7; 95% confidence interval, 0.64-0.83). Conclusion: The results of the present nationwide population-based study support the rationale for bevacizumab in addition to palliative chemotherapy for patients with PC of CRC and underline the need for ongoing efforts to precisely determine the role of targeted therapy in the treatment of PC.
C1 [Razenberg, Lieke G. E. M.; Creemers, Geert-Jan] Catharina Hosp, Dept Oncol, NL-5623 EJ Eindhoven, Netherlands.
   [Razenberg, Lieke G. E. M.; van Gestel, Yvette R. B. M.; Lemmens, Valery E. P. P.] Netherlands Comprehens Canc Org, Dept Registry & Res, Eindhoven, Netherlands.
   [Lemmens, Valery E. P. P.] Erasmus Med Ctr Univ, Med Ctr, Dept Publ Hlth, Rotterdam, Netherlands.
   [de Hingh, Ignace H. J. T.] Catharina Hosp, Dept Surg, NL-5623 EJ Eindhoven, Netherlands.
C3 Catharina Hospital; Erasmus University Rotterdam; Erasmus MC; Catharina
   Hospital
RP Razenberg, LGEM (corresponding author), Catharina Hosp, Dept Internal Med, Michelangelolaan 2, NL-5623 EJ Eindhoven, Netherlands.
EM lieke.razenberg@catharinaziekenhuis.nl
OI De Hingh, Ignace/0000-0003-3491-4268
FU Roche Pharmaceuticals
FX The present study was supported by an unrestricted grant from Roche
   Pharmaceuticals, manufacturer of the targeted agent Avastin
   (bevacizumab). The funder did not have any involvement in the study
   design, data collection, data analysis, data interpretation, writing of
   the report, or the decision to submit the report for publication, which
   was made independently by the authors. The authors thank the
   registration personnel of the Netherlands Cancer Registry for their
   dedicated data collection.
CR [Anonymous], 2013, International classification of diseases for oncology
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NR 37
TC 26
Z9 26
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 JUN
PY 2016
VL 15
IS 2
BP E41
EP E46
DI 10.1016/j.clcc.2015.12.006
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DN9NR
UT WOS:000377407000006
PM 26762572
DA 2025-01-04
ER

PT J
AU Patil, H
   Saxena, SG
   Barrow, CJ
   Kanwar, JR
   Kapat, A
   Kanwar, RK
AF Patil, Harshali
   Saxena, Shailaja Gada
   Barrow, Colin J.
   Kanwar, Jagat R.
   Kapat, Arnab
   Kanwar, Rupinder K.
TI Chasing the personalized medicine dream through biomarker validation in
   colorectal cancer
SO DRUG DISCOVERY TODAY
LA English
DT Review
ID METHYLENETETRAHYDROFOLATE REDUCTASE C677T; MOLECULAR PATHOLOGICAL
   EPIDEMIOLOGY; ISLAND METHYLATOR PHENOTYPE; MONOCLONAL-ANTIBODY THERAPY;
   DIHYDROPYRIMIDINE DEHYDROGENASE; MICROSATELLITE INSTABILITY; THYMIDINE
   PHOSPHORYLASE; A1298C POLYMORPHISMS; THYMIDYLATE SYNTHASE; PIK3CA
   MUTATION
AB Colorectal cancer (CRC) is a major health burden worldwide. The optimal approach to the diagnosis, management, and treatment of CRC involves multidisciplinary and integrated management practices. The field is rapidly changing because of recent advancements in delineating the molecular basis of tumorigenesis, introduction of targeted therapy, varied patient response to mainstay chemotherapeutics, biological drugs, and the effective combination regimes being used for treatment. Recent meta-analysis studies, which tend to establish few clinically useful predictor biomarkers, identify inconsistent results and limitations of the trials. Therefore, molecular pathological epidemiology discipline initiatives are promising. Here, we provide an overview of the potential of biomarker validation for personalized medicine by focusing largely on metastatic (m)CRC. We also highlight new candidate predictive and prognostic biomarkers.
C1 [Patil, Harshali; Saxena, Shailaja Gada; Kapat, Arnab] Reliance Life Sci Pvt Ltd, Dhirubhai Ambani Life Sci Ctr, Thane Belapur Rd, Navi Mumbai 400701, Maharashtra, India.
   [Patil, Harshali; Barrow, Colin J.] Deakin Univ, Ctr Chem & Biotechnol, Sch Life & Environm Sci, Locked Bag 20000, Geelong, Vic 3220, Australia.
   [Kanwar, Jagat R.; Kanwar, Rupinder K.] Deakin Univ, Fac Hlth, Ctr Mol & Med Res, Sch Med, Geelong, Vic 3216, Australia.
C3 Reliance Life Sciences Private Limited; Deakin University; Deakin
   University
RP Kapat, A (corresponding author), Reliance Life Sci Pvt Ltd, Dhirubhai Ambani Life Sci Ctr, Thane Belapur Rd, Navi Mumbai 400701, Maharashtra, India.; Kanwar, RK (corresponding author), Deakin Univ, Fac Hlth, Ctr Mol & Med Res, Sch Med, Geelong, Vic 3216, Australia.
EM arnab.kapat@ril.com; rupinder.kanwar@deakin.edu.au
RI Kanwar, Jagat/JDO-1829-2023; Barrow, Colin/LIC-4175-2024; Kanwar, Dr
   Rupinder Kaur/JBS-5937-2023
OI Barrow, Colin/0000-0002-2153-7267
FU Deakin India Research Initiative (DIRI) program; Reliance Institute of
   Life Sciences, India; Deakin University, Australia; Reliance Life
   Sciences Pvt. Ltd., Mumbai
FX The authors acknowledge the financial support of the Deakin India
   Research Initiative (DIRI) program initiated between the Reliance
   Institute of Life Sciences, India and Deakin University, Australia. The
   authors also gratefully acknowledge Reliance Life Sciences Pvt. Ltd.,
   Mumbai, for financial support for the project.
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NR 77
TC 20
Z9 20
U1 0
U2 11
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6446
EI 1878-5832
J9 DRUG DISCOV TODAY
JI Drug Discov. Today
PD JAN
PY 2017
VL 22
IS 1
BP 111
EP 119
DI 10.1016/j.drudis.2016.09.022
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EI8WB
UT WOS:000392787800012
PM 27693431
DA 2025-01-04
ER

PT J
AU Lee, H
   Lee, Y
   Song, C
   Cho, HR
   Ghaffari, R
   Choi, TK
   Kim, KH
   Lee, YB
   Ling, D
   Lee, H
   Yu, SJ
   Choi, SH
   Hyeon, T
   Kim, DH
AF Lee, Hyunjae
   Lee, Youngsik
   Song, Changyeong
   Cho, Hye Rim
   Ghaffari, Roozbeh
   Choi, Tae Kyu
   Kim, Kyung Hoon
   Lee, Young Bum
   Ling, Daishun
   Lee, Hyuk
   Yu, Su Jong
   Choi, Seung Hong
   Hyeon, Taeghwan
   Kim, Dae-Hyeong
TI An endoscope with integrated transparent bioelectronics and theranostic
   nanoparticles for colon cancer treatment
SO NATURE COMMUNICATIONS
LA English
DT Article
ID SILICA NANOPARTICLES; ORGANIC TRANSISTORS; THERAPY; ABLATION; DESIGN
AB The gastrointestinal tract is a challenging anatomical target for diagnostic and therapeutic procedures for bleeding, polyps and cancerous growths. Advanced endoscopes that combine imaging and therapies within the gastrointestinal tract provide an advantage over stand-alone diagnostic or therapeutic devices. However, current multimodal endoscopes lack the spatial resolution necessary to detect and treat small cancers and other abnormalities. Here we present a multifunctional endoscope-based interventional system that integrates transparent bioelectronics with theranostic nanoparticles, which are photoactivated within highly localized space near tumours or benign growths. These advanced electronics and nanoparticles collectively enable optical fluorescence-based mapping, electrical impedance and pH sensing, contact/temperature monitoring, radio frequency ablation and localized photo/chemotherapy, as the basis of a closed-loop solution for colon cancer treatment. In vitro, ex vivo and in vivo experiments highlight the utility of this technology for accurate detection, delineation and rapid targeted therapy of colon cancer or precancerous lesions.
C1 [Lee, Hyunjae; Lee, Youngsik; Song, Changyeong; Cho, Hye Rim; Choi, Tae Kyu; Kim, Kyung Hoon; Lee, Young Bum; Ling, Daishun; Choi, Seung Hong; Hyeon, Taeghwan; Kim, Dae-Hyeong] Inst for Basic Sci Korea, Ctr Nanoparticle Res, Seoul 151742, South Korea.
   [Lee, Hyunjae; Lee, Youngsik; Song, Changyeong; Choi, Tae Kyu; Kim, Kyung Hoon; Lee, Young Bum; Ling, Daishun; Hyeon, Taeghwan; Kim, Dae-Hyeong] Seoul Natl Univ, Inst Chem Proc, Sch Chem & Biol Engn, Seoul 151742, South Korea.
   [Cho, Hye Rim; Choi, Seung Hong] Seoul Natl Univ, Coll Med, Dept Radiol, Seoul 110744, South Korea.
   [Ghaffari, Roozbeh] MC10 Inc, Cambridge, MA 02140 USA.
   [Ling, Daishun] Zhejiang Univ, Inst Pharmaceut, Coll Pharmaceut Sci, Hangzhou 310058, Zhejiang, Peoples R China.
   [Lee, Hyuk] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Div Gastroenterol,Dept Med, Seoul 135710, South Korea.
   [Yu, Su Jong] Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 110744, South Korea.
C3 Institute for Basic Science - Korea (IBS); Seoul National University
   (SNU); Seoul National University (SNU); Zhejiang University;
   Sungkyunkwan University (SKKU); Samsung Medical Center; Seoul National
   University (SNU)
RP Choi, SH (corresponding author), Inst for Basic Sci Korea, Ctr Nanoparticle Res, Seoul 151742, South Korea.
EM verocay@snuh.org; thyeon@snu.ac.kr; dkim98@snu.ac.kr
RI LEE, KYUNG-HAN/HPD-9299-2023; Ling, Daishun/AAH-6088-2021; Kim,
   Dae-Hyeong/AFR-0566-2022; Ghaffari, Roozbeh/ABD-6718-2021
OI Yu, Su Jong/0000-0001-8888-7977; Ling, Daishun/0000-0002-9977-0237;
   Choi, Tae-Kyu/0000-0002-3058-9165; Kim, Dae-Hyeong/0000-0002-4722-1893;
   Lee, Young Bum/0009-0006-8996-0543; Lee, Hyunjae/0000-0003-1954-8124
FU Institute for Basic Science (IBS) in Republic of Korea [IBS-R006-D1]
FX This work was supported by IBS-R006-D1, a funding from the Institute for
   Basic Science (IBS) in Republic of Korea.
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NR 39
TC 156
Z9 162
U1 6
U2 128
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD NOV
PY 2015
VL 6
AR 10059
DI 10.1038/ncomms10059
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CY4KM
UT WOS:000366377000001
PM 26616435
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhang, Y
   Wang, X
AF Zhang, Ya
   Wang, Xin
TI Targeting the Wnt/β-catenin signaling pathway in cancer
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Review
DE Wnt/beta-catenin signaling pathway; Cancer; Targeted therapy; Cancer
   stem cell
ID PROTEIN-PROTEIN INTERACTION; ELEMENT-BINDING PROTEIN; TANKYRASE 1
   INHIBITIOR; AXIN-RGS DOMAIN; WNT PATHWAY; COLORECTAL-CANCER;
   BETA-CATENIN; STEM-CELLS; COLON-CANCER; SELF-RENEWAL
AB The aberrant Wnt/beta-catenin signaling pathway facilitates cancer stem cell renewal, cell proliferation and differentiation, thus exerting crucial roles in tumorigenesis and therapy response. Accumulated investigations highlight the therapeutic potential of agents targeting Wnt/beta-catenin signaling in cancer. Wnt ligand/ receptor interface, beta-catenin destruction complex and TCF/beta-catenin transcription complex are key components of the cascade and have been targeted with interventions in preclinical and clinical evaluations. This scoping review aims at outlining the latest progress on the current approaches and perspectives of Wnt/beta-catenin signaling pathway targeted therapy in various cancer types. Better understanding of the updates on the inhibitors, antagonists and activators of Wnt/beta-catenin pathway rationalizes innovative strategies for personalized cancer treatment. Further investigations are warranted to confirm precise and secure targeted agents and achieve optimal use with clinical benefits in malignant diseases.
C1 [Zhang, Ya; Wang, Xin] Shandong First Med Univ, Dept Hematol, Shandong Prov Hosp, Jinan 250021, Shandong, Peoples R China.
   [Zhang, Ya; Wang, Xin] Shandong Univ, Shandong Prov Hosp, Dept Hematol, Cheeloo Coll Med, Jinan 250021, Shandong, Peoples R China.
   [Zhang, Ya; Wang, Xin] Shandong Univ, Sch Med, Jinan 250021, Shandong, Peoples R China.
   [Zhang, Ya; Wang, Xin] Shandong Prov Engn Res Ctr Lymphoma, Jinan 250021, Shandong, Peoples R China.
   [Zhang, Ya; Wang, Xin] Branch Natl Clin Res Ctr Hematol Dis, Jinan 250021, Shandong, Peoples R China.
   [Zhang, Ya; Wang, Xin] Soochow Univ, Natl Clin Res Ctr Hematol Dis, Affiliated Hosp 1, Suzhou 250021, Peoples R China.
C3 Shandong First Medical University & Shandong Academy of Medical
   Sciences; Shandong First Medical University & Shandong Academy of
   Medical Sciences; Shandong University; Shandong University; Soochow
   University - China
RP Wang, X (corresponding author), Shandong First Med Univ, Dept Hematol, Shandong Prov Hosp, Jinan 250021, Shandong, Peoples R China.
EM xinw007@126.com
RI Wang, Min/JGL-8741-2023
OI Wang, Xin/0000-0001-8051-1481; Zhang, Ya/0000-0003-0894-4922
FU Translational Research Grant of National Clinical Research Center for
   Hematologic Diseases (NCRCH) [2020ZKMB01]; National Natural Science
   Foundation [82000195, 82070203, 81770210, 81473486, 81270598]; Key
   Research and Development Program of Shandong Province [2018CXGC1213];
   Technology Development Projects of Shandong Province [2017GSF18189];
   Taishan Scholars Program of Shandong Province; Shandong Provincial
   Natural Science Foundation [ZR201911140028]; Shandong Provincial
   Engineering Research Center of Lymphoma; Academic Promotion Programme of
   Shandong First Medical University; Shandong Provincial Hospital Youth
   Talent Plan; Shandong Provincial Hospital Research Incubation Fund
FX This study was funded by Translational Research Grant of National
   Clinical Research Center for Hematologic Diseases (NCRCH)
   (No.2020ZKMB01); National Natural Science Foundation (Nos. 82000195,
   82070203, 81770210, 81473486 and 81270598); Key Research and Development
   Program of Shandong Province (No. 2018CXGC1213); Technology Development
   Projects of Shandong Province (No. 2017GSF18189); Taishan Scholars
   Program of Shandong Province; Shandong Provincial Natural Science
   Foundation (No. ZR201911140028); Shandong Provincial Engineering
   Research Center of Lymphoma; Academic Promotion Programme of Shandong
   First Medical University; Shandong Provincial Hospital Youth Talent
   Plan; Shandong Provincial Hospital Research Incubation Fund.
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NR 164
TC 809
Z9 863
U1 41
U2 289
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 DEC 4
PY 2020
VL 13
IS 1
AR 165
DI 10.1186/s13045-020-00990-3
PG 16
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA PB5XT
UT WOS:000596394300001
PM 33276800
OA Green Published, gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Lederer, A
   Herrmann, P
   Seehofer, D
   Dietel, M
   Pratschke, J
   Schlag, P
   Stein, U
AF Lederer, Andri
   Herrmann, Pia
   Seehofer, Daniel
   Dietel, Manfred
   Pratschke, Johann
   Schlag, Peter
   Stein, Ulrike
TI Metastasis-associated in colon cancer 1 is an independent prognostic
   biomarker for survival in klatskin tumor patients
SO HEPATOLOGY
LA English
DT Article
ID LIVER-TRANSPLANTATION; MET EXPRESSION; CHOLANGIOCARCINOMA; MACC1;
   OVEREXPRESSION; RESECTION; PREDICTS; MARKER; GROWTH; RNA
AB Curative treatment of intrahepatic cholangiocarcinoma (ICC) and hilar cholangiocarcinoma (Klatskin tumors) is limited to surgical resection or orthotopic liver transplantation. However, not all patients benefit from a surgical approach and suffer from early tumor recurrence. Response to chemotherapy is generally poor and, until today, no targeted therapy could be established. Metastasis-associated in colon cancer 1 (MACC1) is a recently discovered regulator of the hepatocyte growth factor (HGF)/Met/mitogen-activated protein kinase pathway, which induces proliferation, migration, and invasion in cell culture, as well as metastasis in mice. MACC1 expression shows a significant correlation with Met expression in colon cancer tissue and is highly prognostic for occurrence of distant metastasis and survival in colon cancer patients. Thus, we aimed to measure the expression of MACC1, Met, and HGF messenger RNA in microdissected tumor tissue and corresponding normal liver tissue of 156 patients with Klatskin tumors (n=76) and ICC (n=80) using real-time quantitative reverse-transcriptase polymerase chain reaction. We used immunohistochemical staining to validate the results. MACC1 expression in tumor tissue of both tumor entities was significantly higher than in corresponding normal liver tissue (P<0.001). Klatskin tumor patients with a history of tumor recurrence had significantly higher MACC1 expression than those without tumor recurrence (P=0.005). Uni- und multivariate survival analysis showed that Klatskin tumor patients with high MACC1 had a significantly shorter overall (OS) and disease-free survival (DFS; P=0.001 and P<0.001, respectively). The multivariate analysis confirmed MACC1 to be an independent factor for overall survival in Klatskin tumor patients (hazard ratio: 2.777; 95% confidence interval: 1.389-5.555; P=0.004). Conclusion: Our study identified MACC1 as a highly prognostic biomarker for OS and DFS in Klatskin tumor patients. MACC1 expression could become an important diagnostic tool and might be a candidate for targeted therapy. (Hepatology 2015;62:841-850)
C1 [Lederer, Andri; Herrmann, Pia; Stein, Ulrike] Charite, Expt & Clin Res Ctr, D-13125 Berlin, Germany.
   [Lederer, Andri; Herrmann, Pia; Stein, Ulrike] Max Delbruck Ctr Mol Med, Berlin, Germany.
   [Lederer, Andri; Seehofer, Daniel] Charite, Dept Gen Visceral & Transplant Surg, D-13125 Berlin, Germany.
   [Dietel, Manfred] Charite, Dept Pathol, D-13125 Berlin, Germany.
   [Schlag, Peter] Charite Univ Med Berlin, Charite Comprehens Canc Ctr, Berlin, Germany.
   [Stein, Ulrike] German Canc Consortium, Heidelberg, Germany.
C3 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; Berlin Institute of Health; Free University
   of Berlin; Humboldt University of Berlin; Charite Universitatsmedizin
   Berlin; Helmholtz Association; German Cancer Research Center (DKFZ)
RP Stein, U (corresponding author), Charite, Univ Med Berlin, Expt & Clin Res Ctr, Robert Rossle Str 10, D-13125 Berlin, Germany.
EM ustein@mdc-berlin.de
RI Seehofer, Daniel/X-1933-2019
OI Stein, Ulrike/0000-0001-7006-282X
FU Bundesministerium fur Wirtschaft und Technologie (SIGNO program),
   Germany; German Cancer Consortium, Heidelberg
FX This work was supported by a grant from the Bundesministerium fur
   Wirtschaft und Technologie (SIGNO program), Germany, and by the German
   Cancer Consortium, Heidelberg.
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NR 36
TC 21
Z9 23
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD SEP
PY 2015
VL 62
IS 3
BP 841
EP 850
DI 10.1002/hep.27885
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CQ1RB
UT WOS:000360375100021
PM 25953673
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Linnekamp, JF
   Wang, X
   Medema, JP
   Vermeulen, L
AF Linnekamp, Janneke F.
   Wang, Xin
   Medema, Jan Paul
   Vermeulen, Louis
TI Colorectal Cancer Heterogeneity and Targeted Therapy: A Case for
   Molecular Disease Subtypes
SO CANCER RESEARCH
LA English
DT Review
ID COLON-CANCER; BREAST-CANCER; GROWTH-FACTOR; ADJUVANT TRASTUZUMAB;
   CETUXIMAB TREATMENT; CLASSIFICATION; CELLS; EGFR; MUTATION; KRAS
AB Personalized cancer medicine is becoming increasingly important in colorectal cancer treatment. Especially for targeted therapies, large variations between individual treatment responses exist. Predicting therapy response is of utmost significance, as it prevents overtreatment and adverse effects in patients. For EGFR-targeted therapy, many mechanisms of resistance have been uncovered, for example, mutations in KRAS and BRAF, and upregulation of alternative receptors. Currently, routine testing for all known modifiers of response is unpractical, and as a result, decision-making for anti-EGFR therapy is still largely based on assessing the mutation status of an individual gene (KRAS). Recently, comprehensive classifications of colorectal cancer have been presented that integrate many of the (epi-)genetic and microenvironmental factors that contribute to colorectal cancer heterogeneity. These classification systems are not only of prognostic value but also predict therapy efficacy, including the response to anti-EGFR agents. Therefore, molecular subtype-based stratification to guide therapeutic decisions is a promising new strategy that might overcome the shortcomings of single gene testing in colorectal cancer as well as in other malignancies. Furthermore, the development of new agents in a disease subtype-specific fashion has the potential to transform drug-discovery studies and generate novel, more effective therapies. (C) 2014 AACR.
C1 [Linnekamp, Janneke F.; Medema, Jan Paul; Vermeulen, Louis] Univ Amsterdam, Acad Med Ctr, Ctr Expt Mol Med, Lab Expt Oncol & Radiobiol, NL-1105 AZ Amsterdam, Netherlands.
   [Wang, Xin] Harvard Univ, Sch Med, Ctr Biomed Informat, Boston, MA USA.
C3 University of Amsterdam; Academic Medical Center Amsterdam; Harvard
   University; Harvard Medical School
RP Vermeulen, L (corresponding author), Univ Amsterdam, Acad Med Ctr, Ctr Expt Mol Med, Lab Expt Oncol & Radiobiol, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.
EM l.vermeulen@amc.nl
RI Vermeulen, Louis/B-7488-2008; Wang, Xin/A-1130-2012
OI Medema, Jan Paul/0000-0003-3045-2924; Wang, Xin/0000-0002-5122-2418;
   Vermeulen, Louis/0000-0002-6066-789X
FU Dutch Cancer Society (KWF); AICR grant [14-1164]
FX L. Vermeulen was supported by a Fellowship of the Dutch Cancer Society
   (KWF) and an AICR grant (14-1164).
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NR 37
TC 152
Z9 166
U1 0
U2 31
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD JAN 15
PY 2015
VL 75
IS 2
BP 245
EP 249
DI 10.1158/0008-5472.CAN-14-2240
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AZ0LT
UT WOS:000347937600002
PM 25593032
OA Bronze
DA 2025-01-04
ER

PT J
AU Nian, Q
   Li, JW
   Han, ZY
   Liang, Q
   Liu, MY
   Yang, C
   Rodrigues-Lima, F
   Jiang, T
   Zhao, LY
   Zeng, JH
   Liu, C
   Shi, JY
AF Nian, Qing
   Li, Jingwei
   Han, ZhongYu
   Liang, Qi
   Liu, Maoyu
   Yang, Chan
   Rodrigues-Lima, Fernando
   Jiang, Tao
   Zhao, Liyun
   Zeng, Jinhao
   Liu, Chi
   Shi, Jianyou
TI SPARC in hematologic malignancies and novel technique for hematological
   disease with its abnormal expression
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE SPARC; Targeted therapy; Hematologic malignancies; NAB
ID ALTERNATIVELY ACTIVATED MACROPHAGES; ALBUMIN-BOUND PACLITAXEL;
   INTEGRIN-LINKED KINASE; CELL LEUKEMIA-LYMPHOMA; ACUTE MYELOID-LEUKEMIA;
   NAB-PACLITAXEL; PULMONARY-FIBROSIS; PANCREATIC-CANCER; POTENTIAL ROLE;
   PROTEIN SPARC
AB Secreted protein acidic and rich in cysteine (SPARC), also known as osteonectin or BM-40, is a matricellular protein involved in several biological processes including cell adhesion, growth factor availability, extracellular matrix remodeling and immune-regulation. SPARC has also been associated with a variety of diseases including diabetes, colon cancer, and leukemia. The expression of SPARC in different diseases exhibits some degree of ambiguity, especially in hemopathies. Herein, we review the current expression and effects of SPARC in various hematologic disorders with respect to nanoparticle albumin bound innovative therapies and related diagnostic research, providing a clinical perspective on the use of NAB technology in the frontier treatment of hematologic diseases.
C1 [Nian, Qing; Li, Jingwei] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Chinese Acad Sci Sichuan Translat Med Res Hosp, Transfus Dept, Chengdu 610072, Peoples R China.
   [Han, ZhongYu] Chengdu Univ Tradit Chinese Med, Reprod & Women Children Hosp, Sch Med & Life Sci, Chengdu 610072, Peoples R China.
   [Liang, Qi] Southwest Jiaotong Univ, Coll Med, Chengdu 611756, Sichuan, Peoples R China.
   [Liu, Maoyu; Zhao, Liyun; Shi, Jianyou] Univ Elect Sci & Technol China, Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Sch Med, Dept Pharm,Personalized Drug Therapy Key Lab Sich, Chengdu 610072, Sichuan, Peoples R China.
   [Yang, Chan] Sichuan Univ, West China Hosp, Div Endocrinol & Metab, State Key Lab Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
   [Yang, Chan] Collaborat Innovat Ctr Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
   [Rodrigues-Lima, Fernando] Univ Paris, Unite Biol Fonct & Adaptat, F-75013 Paris, France.
   [Jiang, Tao] Chinese Acad Sci, Sichuan Prov Peoples Hosp, Univ Elect Sci & Technol China, Sichuan Translat Med Res Hosp, Chengdu 610072, Peoples R China.
   [Zeng, Jinhao] Hosp Chengdu Univ Tradit Chinese Med, Chengdu 610072, Peoples R China.
   [Liu, Chi] Univ Elect Sci & Technol China, Sichuan Clin Res Ctr Kidney Dis, Sch Med, Sichuan Prov Peoples Hosp,Renal Dept, Chengdu 610072, Peoples R China.
   [Liu, Chi] Univ Elect Sci & Technol China, Sichuan Clin Res Ctr Kidney Dis, Sch Med, Sichuan Prov Peoples Hosp,Nephrol Inst, Chengdu 610072, Peoples R China.
C3 Sichuan Provincial People's Hospital; University of Electronic Science &
   Technology of China; Chengdu University of Traditional Chinese Medicine;
   Southwest Jiaotong University; Sichuan Provincial People's Hospital;
   University of Electronic Science & Technology of China; Sichuan
   University; Universite Paris Cite; University of Electronic Science &
   Technology of China; Chinese Academy of Sciences; Sichuan Provincial
   People's Hospital; Chengdu University of Traditional Chinese Medicine;
   University of Electronic Science & Technology of China; Sichuan
   Provincial People's Hospital; Sichuan Provincial People's Hospital;
   University of Electronic Science & Technology of China
RP Shi, JY (corresponding author), Univ Elect Sci & Technol China, Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Sch Med, Dept Pharm,Personalized Drug Therapy Key Lab Sich, Chengdu 610072, Sichuan, Peoples R China.; Zeng, JH (corresponding author), Hosp Chengdu Univ Tradit Chinese Med, Chengdu 610072, Peoples R China.; Liu, C (corresponding author), Univ Elect Sci & Technol China, Sichuan Clin Res Ctr Kidney Dis, Sch Med, Sichuan Prov Peoples Hosp,Renal Dept, Chengdu 610072, Peoples R China.; Liu, C (corresponding author), Univ Elect Sci & Technol China, Sichuan Clin Res Ctr Kidney Dis, Sch Med, Sichuan Prov Peoples Hosp,Nephrol Inst, Chengdu 610072, Peoples R China.
EM zengjinhao@cdutcm.edu.cn; liuchi_1230@163.com; shijianyoude@126.com
RI Yang, Chan/JDC-4128-2023; Han, Zhongyu/KYQ-6838-2024
FU National Natural Science Foundation of China [82073311]; Natural Science
   Foundation of Sichuan Province [2022JDTD0025]; Key Research and
   Development Program of Science and Technology Department of Sichuan
   Province [2019YFS0514]; Key R & D projects in Sichuan Province
   [2020YFS0399]
FX This work was supported by the National Natural Science Foundation of
   China (No 82073311, 2021) ; Natural Science Foundation of Sichuan
   Province (No.2022JDTD0025, 2022) ; Key Research and Development Program
   of Science and Technology Department of Sichuan Province
   (No.2019YFS0514, 2019) ; the Key R & D projects in Sichuan Province
   (No.2020YFS0399, 2020) .
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NR 106
TC 4
Z9 4
U1 1
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 SEP
PY 2022
VL 153
AR 113519
DI 10.1016/j.biopha.2022.113519
EA AUG 2022
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 5C2GW
UT WOS:000864085000002
PM 36076604
OA gold
DA 2025-01-04
ER

PT J
AU Hong, HJ
   Shao, YF
   Zhang, S
   Yang, G
   Jia, HT
   Yang, X
   Huang, L
   Li, SC
   Aikemu, B
   Zhang, LY
   Ma, JJ
   Zang, L
   Sun, J
   Zheng, MH
AF Hong, Hi-Ju
   Shao, Yanfei
   Zhang, Sen
   Yang, Guang
   Jia, Hongtao
   Yang, Xiao
   Huang, Ling
   Li, Shuchun
   Aikemu, Batuer
   Zhang, Luyang
   Ma, Junjun
   Zang, Lu
   Sun, Jing
   Zheng, Minhua
TI ACACB is a novel metabolism-related biomarker in the prediction of
   response to cetuximab therapy in metastatic colorectal cancer
SO ACTA BIOCHIMICA ET BIOPHYSICA SINICA
LA English
DT Article
DE colorectal cancer; cetuximab; targeted therapy; ACACB; comprehensive
   analysis
ID FIBROBLAST-GROWTH-FACTOR; FATTY-ACID-METABOLISM; INHIBITION; SURVIVAL;
   CELLS; TRIAL; RISK; GENE; FGF2; KRAS
AB Cetuximab is one of the most valuable targeted therapy monoclonal antibodies in the treatment of metastatic colorectal cancer (CRC). However, the mechanisms affecting cetuximab resistance in CRC treatment remain unclear. Metabolism, especially fatty acid metabolism, has been reported to play an important role in tumor treatment. The correlation between cetuximab resistance and metabolism and whether it can be a new biomarker to evaluate the sensitivity of cetuximab in CRC treatment still need to be further explored. In this study, we perform a comprehensive analysis to confirm the relationship between fatty acid metabolism and cetuximab resistance, and the differentially expressed genes (DEGs) related to cetuximab drug resistance in CRC are screened by bioinformatics technology. We find that acetyl-CoA carboxylase beta (ACACB), ADH1C, CES1, MGLL, FMO5, and GPT are the hub DEGs, and ACACB is the most important biomarker among them. In addition, we systematically analyze the role of ACACB in the tumorigenesis of CRC, including tissue expression, CRC cell growth, cetuximab sensitivity, and potential downstream pathways, by using bioinformatics techniques, in vitro experiments and clinical cohort validation. Our results confirm that cetuximab resistance is correlated with metabolism. ACACB can lead to decreased sensitivity to cetuximab in CRC, and its mechanism may be related to EGFR phosphorylation, which could affect the activation of the mTOR/Akt signaling pathway and regulation of CDT1-, cyclin D1-, and p21-related cell cycle modulation.
C1 [Hong, Hi-Ju; Shao, Yanfei; Zhang, Sen; Yang, Guang; Jia, Hongtao; Yang, Xiao; Huang, Ling; Li, Shuchun; Aikemu, Batuer; Zhang, Luyang; Ma, Junjun; Zang, Lu; Sun, Jing; Zheng, Minhua] Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Gen Surg, Sch Med, Shanghai 200025, Peoples R China.
   [Hong, Hi-Ju; Zhang, Sen; Yang, Xiao; Aikemu, Batuer; Zhang, Luyang; Ma, Junjun; Zang, Lu; Sun, Jing; Zheng, Minhua] Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Gastrointestinal Surg, Sch Med, Shanghai 200025, Peoples R China.
   [Hong, Hi-Ju; Shao, Yanfei; Zhang, Sen; Yang, Guang; Jia, Hongtao; Yang, Xiao; Huang, Ling; Li, Shuchun; Aikemu, Batuer; Zhang, Luyang; Ma, Junjun; Zang, Lu; Sun, Jing; Zheng, Minhua] Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Minimally Invas Surg Ctr, Sch Med, Shanghai 200025, Peoples R China.
   [Sun, Jing] Ruijin Hosp, Wuxi Branch, Wuxi 213021, Jiangsu, Peoples R China.
C3 Shanghai Jiao Tong University; Shanghai Jiao Tong University; Shanghai
   Jiao Tong University
RP Zang, L; Sun, J; Zheng, MH (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Gen Surg, Sch Med, Shanghai 200025, Peoples R China.; Zang, L; Sun, J; Zheng, MH (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Gastrointestinal Surg, Sch Med, Shanghai 200025, Peoples R China.; Zang, L; Sun, J; Zheng, MH (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Minimally Invas Surg Ctr, Sch Med, Shanghai 200025, Peoples R China.; Sun, J (corresponding author), Ruijin Hosp, Wuxi Branch, Wuxi 213021, Jiangsu, Peoples R China.
EM zanglu@yeah.net; sj11788@rjh.com.cn; zmhtiger@yeah.net
RI yang, guang/AAV-2451-2021; huang, ling/KLC-7916-2024; Zang,
   Lu/JFK-0902-2023
OI Yang, Guang/0000-0001-6079-5093
FU National Natural Science Foundation of China [81871984, 82103207];
   Multicenter trial of Shanghai Jiao Tong University School of Medicine
   [DLY201504]; Shanghai Municipal Key Clinical Specialty [Shslczdzk00102];
   Research Physician Program of Shanghai Jiao Tong University School of
   Medicine [826304]
FX This work was supported by the grants from the National Natural Science
   Foundation of China (Nos. 81871984 and 82103207), the Multicenter trial
   of Shanghai Jiao Tong University School of Medicine (No. DLY201504),
   Shanghai Municipal Key Clinical Specialty (No. Shslczdzk00102), and
   Research Physician Program of Shanghai Jiao Tong University School of
   Medicine (No. 826304).
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NR 40
TC 2
Z9 2
U1 4
U2 16
PU SCIENCE PRESS
PI BEIJING
PA 16 DONGHUANGCHENGGEN NORTH ST, Building 5, Room 411, BEIJING, 100009,
   PEOPLES R CHINA
SN 1672-9145
EI 1745-7270
J9 ACTA BIOCH BIOPH SIN
JI Acta Biochim. Biophys. Sin.
PD NOV
PY 2022
VL 54
IS 11
BP 1671
EP 1683
DI 10.3724/abbs.2022121
PG 13
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 7O9YP
UT WOS:000908370800011
PM 36111743
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Cao, LR
   Meng, XY
   Zhang, ZY
   Liu, ZL
   He, Y
AF Cao, Liren
   Meng, Xiaoyan
   Zhang, Zhiyuan
   Liu, Zhonglong
   He, Yue
TI Macrophage heterogeneity and its interactions with stromal cells in
   tumour microenvironment
SO CELL AND BIOSCIENCE
LA English
DT Review
DE Single-cell study; Tumour-associated macrophage; Macrophage
   heterogeneity; Tumour stroma; Macrophage-stroma interactions
ID CANCER-ASSOCIATED FIBROBLASTS; MESENCHYMAL STEM-CELLS; INFLAMMATORY
   MONOCYTES; IMMUNE SUPPRESSION; COLORECTAL-CANCER; ENDOTHELIAL-CELLS; M2
   POLARIZATION; GENE-EXPRESSION; GROWTH-FACTOR; SINGLE-CELL
AB Macrophages and tumour stroma cells account for the main cellular components in the tumour microenvironment (TME). Current advancements in single-cell analysis have revolutionized our understanding of macrophage diversity and macrophage-stroma interactions. Accordingly, this review describes new insight into tumour-associated macrophage (TAM) heterogeneity in terms of tumour type, phenotype, metabolism, and spatial distribution and presents the association between these factors and TAM functional states. Meanwhile, we focus on the immunomodulatory feature of TAMs and highlight the tumour-promoting effect of macrophage-tumour stroma interactions in the immunosuppressive TME. Finally, we summarize recent studies investigating macrophage-targeted therapy and discuss their therapeutic potential in improving immunotherapy by alleviating immunosuppression.
C1 [Cao, Liren; Meng, Xiaoyan; Zhang, Zhiyuan; Liu, Zhonglong; He, Yue] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Oral Maxillofacial & Head & Neck Oncol, Sch Med,Natl Clin Res Ctr Oral Dis,Natl Ctr Stomat, Shanghai 200011, Peoples R China.
C3 Shanghai Jiao Tong University
RP Zhang, ZY; Liu, ZL; He, Y (corresponding author), Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Oral Maxillofacial & Head & Neck Oncol, Sch Med,Natl Clin Res Ctr Oral Dis,Natl Ctr Stomat, Shanghai 200011, Peoples R China.
EM zhzhy0502@163.com; zhonglong021@126.com; william5218@126.com
FU National Natural Science Foundation of China [82173451]; National
   Natural Science Foundation of China [YBKB202105]; Shanghai Ninth
   People's Hospital, Shanghai Jiao Tong University School of Medicine
   [2022LJ001]; Shanghai Municipal Health Commission
FX This work was financially supported by National Natural Science
   Foundation of China (No. 82173451), Biobank project by Shanghai Ninth
   People's Hospital, Shanghai Jiao Tong University School of Medicine (No.
   YBKB202105), and Shanghai Municipal Health Commission (No. 2022LJ001).
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NR 184
TC 3
Z9 3
U1 5
U2 16
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2045-3701
J9 CELL BIOSCI
JI Cell Biosci.
PD FEB 1
PY 2024
VL 14
IS 1
AR 16
DI 10.1186/s13578-024-01201-z
PG 22
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA GT7S8
UT WOS:001154993800001
PM 38303024
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Dorel, M
   Klinger, B
   Gross, T
   Sieber, A
   Prahallad, A
   Bosdriesz, E
   Wessels, LFA
   Blüthgen, N
AF Dorel, Mathurin
   Klinger, Bertram
   Gross, Torsten
   Sieber, Anja
   Prahallad, Anirudh
   Bosdriesz, Evert
   Wessels, Lodewyk F. A.
   Bluethgen, Nils
TI Modelling signalling networks from perturbation data
SO BIOINFORMATICS
LA English
DT Article
ID ACTIVATION; CANCER; ERK
AB Motivation: Intracellular signalling is realized by complex signalling networks, which are almost impossible to understand without network models, especially if feedbacks are involved. Modular Response Analysis (MRA) is a convenient modelling method to study signalling networks in various contexts.
   Results: We developed the software package STASNet (STeady-STate Analysis of Signalling Networks) that provides an augmented and extended version of MRA suited to model signalling networks from incomplete perturbation schemes and multi-perturbation data. Using data from the Dialogue on Reverse Engineering Assessment and Methods challenge, we show that predictions from STASNet models are among the top-performing methods. We applied the method to study the effect of SHP2, a protein that has been implicated in resistance to targeted therapy in colon cancer, using a novel dataset from the colon cancer cell line Widr and a SHP2-depleted derivative. We find that SHP2 is required for mitogen-activated protein kinase signalling, whereas AKT signalling only partially depends on SHP2.
C1 [Dorel, Mathurin; Klinger, Bertram; Gross, Torsten; Sieber, Anja; Bluethgen, Nils] Charite, Inst Pathol, D-10117 Berlin, Germany.
   [Dorel, Mathurin; Klinger, Bertram; Gross, Torsten; Sieber, Anja; Bluethgen, Nils] Humboldt Univ, IRI Life Sci, D-10115 Berlin, Germany.
   [Dorel, Mathurin; Bluethgen, Nils] Berlin Inst Hlth, D-10178 Berlin, Germany.
   [Prahallad, Anirudh; Bosdriesz, Evert; Wessels, Lodewyk F. A.] Netherlands Canc Inst, Div Mol Carcinogenesis, NL-1066 CX Amsterdam, Netherlands.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
   University of Berlin; Charite Universitatsmedizin Berlin; Humboldt
   University of Berlin; Berlin Institute of Health; Netherlands Cancer
   Institute
RP Blüthgen, N (corresponding author), Charite, Inst Pathol, D-10117 Berlin, Germany.; Blüthgen, N (corresponding author), Humboldt Univ, IRI Life Sci, D-10115 Berlin, Germany.; Blüthgen, N (corresponding author), Berlin Inst Hlth, D-10178 Berlin, Germany.
EM nils.bluethgen@charite.de
RI Bluthgen, Nils/A-1711-2011; Bosdriesz, Evert/K-6070-2013
OI Bluthgen, Nils/0000-0002-0171-7447; Klinger,
   Bertram/0000-0003-0242-1506; Bosdriesz, Evert/0000-0002-8788-9548;
   Dorel, Mathurin/0000-0002-1663-2075
FU Federal Ministry of Education and Research of Germany (BMBF) [02NUK047E,
   031A426A]; Berlin Institute of Health
FX This work was supported by the Federal Ministry of Education and
   Research of Germany (BMBF) through grants ZiSS-Trans (02NUK047E),
   ColoSys and MapTorNet (031A426A), as well as through funding by the
   Berlin Institute of Health.
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NR 25
TC 17
Z9 19
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
EI 1460-2059
J9 BIOINFORMATICS
JI Bioinformatics
PD DEC 1
PY 2018
VL 34
IS 23
BP 4079
EP 4086
DI 10.1093/bioinformatics/bty473
PG 8
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
   Computer Science, Interdisciplinary Applications; Mathematical &
   Computational Biology; Statistics & Probability
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Computer Science; Mathematical & Computational Biology; Mathematics
GA HE5TX
UT WOS:000453453300016
PM 29931053
OA Bronze, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Yu, Y
   Yang, J
   Li, QP
   Xu, BM
   Lian, YF
   Miao, L
AF Yu, Yang
   Yang, Jian
   Li, Quanpeng
   Xu, Boming
   Lian, Yifan
   Miao, Lin
TI LINC00152: A pivotal oncogenic long non-coding RNA in human cancers
SO CELL PROLIFERATION
LA English
DT Review
ID GASTRIC-CANCER; TUMOR-SUPPRESSOR; PROMOTES PROLIFERATION; TARGETED
   THERAPY; METASTASIS; STATISTICS; EXPRESSION; INVASION; GROWTH;
   BIOMARKERS
AB In recent years, increasing evidence has shown the potential role of long non-coding RNAs (lncRNAs) in multiple cancers. Deregulation of lncRNAs was detected being closely associated with many kinds of tumours where they can act as a tumour suppressor or accelerator. LINC00152 was identified as an oncogene involved in many kinds of cancers, such as gastric cancer, hepatocellular carcinoma, colon cancer, gallbladder cancer and renal cell carcinoma. Moreover, inhibition of LINC00152 can suppress proliferation, migration and invasion of the cancer cells. Increasing evidence has showed that LINC00152 may act as a diagnostic and prognostic biomarker for the above-mentioned cancers. In our review, we summarize the recent research progress of the expression and role of LINC00152 in various kinds of cancers.
C1 [Yu, Yang; Li, Quanpeng; Xu, Boming; Miao, Lin] Nanjing Med Univ, Affiliated Hosp 2, Med Ctr Digest Dis, 121 Jiangjiayuan, Nanjing 210011, Jiangsu, Peoples R China.
   [Yang, Jian] Nanjing Med Univ, Affiliated Hosp 2, Dept Urol, Nanjing, Jiangsu, Peoples R China.
   [Lian, Yifan] Nanjing Med Univ, Affiliated Hosp 2, Dept Oncol, Nanjing, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University; Nanjing Medical
   University
RP Miao, L (corresponding author), Nanjing Med Univ, Affiliated Hosp 2, Med Ctr Digest Dis, 121 Jiangjiayuan, Nanjing 210011, Jiangsu, Peoples R China.
EM miaolinxh@163.com
OI Yang, Jian/0000-0003-3033-1161; Miao, Lin/0000-0003-0248-2544
FU Project of Standard Diagnosis and Treatment of Key Disease of Jiangsu
   Province [BE2015722]; Project of the peak of the six talents of Jiangsu
   Province [WSN-018]; Scientific Research Foundation for Health of Jiangsu
   Province [H201408]
FX This study was supported by the: Project of Standard Diagnosis and
   Treatment of Key Disease of Jiangsu Province (BE2015722); Project of the
   peak of the six talents of Jiangsu Province (WSN-018) and Scientific
   Research Foundation for Health of Jiangsu Province (H201408).
CR [Anonymous], ONCOGENE
   [Anonymous], ONCOL RES
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NR 58
TC 66
Z9 68
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0960-7722
EI 1365-2184
J9 CELL PROLIFERAT
JI Cell Prolif.
PD AUG
PY 2017
VL 50
IS 4
AR e12349
DI 10.1111/cpr.12349
PG 6
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA FC9CS
UT WOS:000407139200011
PM 28464433
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Schmitz, R
   Valls, AF
   Yerbes, R
   von Richter, S
   Kahlert, C
   Loges, S
   Weitz, J
   Schneider, M
   de Almodovar, CR
   Ulrich, A
   Schmidt, T
AF Schmitz, Robin
   Valls, Aida Freire
   Yerbes, Rosario
   von Richter, Sophie
   Kahlert, Christoph
   Loges, Sonja
   Weitz, Jurgen
   Schneider, Martin
   de Almodovar, Carmen Ruiz
   Ulrich, Alexis
   Schmidt, Thomas
TI TAM receptors Tyro3 and Mer as novel targets in colorectal cancer
SO ONCOTARGET
LA English
DT Article
DE colorectal cancer; tyro3; Mer; Gas6; macrophages
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; ARREST-SPECIFIC GENE-6; K-DEPENDENT
   PROTEIN; HUMAN BREAST-CANCER; TYROSINE KINASES; GROWTH-ARREST;
   GLIOBLASTOMA-MULTIFORME; THERAPEUTIC TARGET; TAXOL RESISTANCE;
   GASTRIC-CANCER
AB Purpose: CRC remains the third most common cancer worldwide with a high 5-year mortality rate in advanced cases. Combined with chemotherapy, targeted therapy is an additional treatment option. However as CRC still escapes targeted therapy the vigorous search for new targets is warranted to increase patients' overall survival.
   Results: In this study we describe a new role for Gas6/protein S-TAM receptor interaction in CRC. Gas6, expressed by tumor-infiltrating M2-like macrophages, enhances malignant properties of tumor cells including proliferation, invasion and colony formation. Upon chemotherapy macrophages increase Gas6 synthesis, which significantly attenuates the cytotoxic effect of 5-FU chemotherapy on tumor cells. The anti-coagulant protein S has similar effects as Gas6. In CRC patient samples Tyro3 was overexpressed within the tumor. In-vitro inhibition of Tyro3 and Mer reduces tumor cell proliferation and sensitizes tumor cells to chemotherapy. Moreover high expression of Tyro3 and Mer in tumor tissue significantly shortens CRC patients' survival.
   Experimental design: Various in vitro models were used to investigate the role of Gas6 and its TAM receptors in human CRC cells, by stimulation (rhGas6) and knockdown (siRNA) of Axl, Tyro3 and Mer. In terms of a translational research, we additionally performed an expression analysis in human CRC tissue and analyzed the medical record of these patients.
   Conclusions: Tyro3 and Mer represent novel therapeutic targets in CRC and warrant further preclinical and clinical investigation in the future.
C1 [Schmitz, Robin; Valls, Aida Freire; von Richter, Sophie; Schneider, Martin; Ulrich, Alexis; Schmidt, Thomas] Heidelberg Univ, Univ Heidelberg Hosp, Dept Gen Visceral & Transplantat Surg, Heidelberg, Germany.
   [Valls, Aida Freire; Yerbes, Rosario; de Almodovar, Carmen Ruiz] Heidelberg Univ, Biochem Ctr, Heidelberg, Germany.
   [Kahlert, Christoph; Weitz, Jurgen] Univ Dresden, Dept Visceral Thorac & Vasc Surg, Dresden, Germany.
   [Loges, Sonja] Univ Med Ctr Hamburg Eppendorf, Ctr Med Expt, Dept Tumor Biol, Hamburg, Germany.
C3 Ruprecht Karls University Heidelberg; Ruprecht Karls University
   Heidelberg; Technische Universitat Dresden; University of Hamburg;
   University Medical Center Hamburg-Eppendorf
RP Schmidt, T (corresponding author), Heidelberg Univ, Univ Heidelberg Hosp, Dept Gen Visceral & Transplantat Surg, Heidelberg, Germany.
EM thomas.schmidt1@med.uni-heidelberg.de
RI Schmidt, Thomas/Y-8431-2019; Schneider, Martin/H-3745-2011; Schmitz,
   Robin/AAW-8046-2021; Loges, Sonja/ABE-9868-2021; Yerbes,
   Rosario/H-5649-2015
OI Yerbes, Rosario/0000-0002-4372-7619; Ruiz de Almodovar,
   Carmen/0000-0001-5975-7815; Schmidt, Thomas/0000-0002-7166-3675
FU Deutsche Forschungsgemeinschaft DFG [SCHM 2560/3-1]; Heidelberger
   Stiftung Chirurgie
FX This study was supported by a research grant of the Deutsche
   Forschungsgemeinschaft DFG (SCHM 2560/3-1) to TS and by the Heidelberger
   Stiftung Chirurgie.
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NR 55
TC 27
Z9 29
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 AUG 30
PY 2016
VL 7
IS 35
BP 56355
EP 56370
DI 10.18632/oncotarget.10889
PG 16
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA EA8TL
UT WOS:000386911600033
PM 27486820
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Lopez, G
   Boggio, F
   Ferrero, S
   Fusco, N
   Del Gobbo, A
AF Lopez, Gianluca
   Boggio, Francesca
   Ferrero, Stefano
   Fusco, Nicola
   Del Gobbo, Alessandro
TI Molecular and Immunohistochemical Markers with Prognostic and Predictive
   Significance in Liver Metastases from Colorectal Carcinoma
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE biomarkers; immunohistochemistry; molecular markers; colorectal cancer;
   liver metastases; prognostic; predictive
ID FOLATE RECEPTOR-ALPHA; CANCER PATIENTS; POOR-PROGNOSIS;
   CLINICAL-SIGNIFICANCE; BRAF MUTATIONS; PRIMARY TUMORS; BETA-CATENIN;
   COLON-CANCER; TGF-BETA; C-MET
AB Despite the significant recent achievements in the diagnosis and treatment of colorectal cancer (CRC), the prognosis of these patients has currently plateaued. During the past few years, the opportunity to consider multiple treatment modalities (including surgery and other locoregional treatments, systemic therapy, and targeted therapy) led to the research of novel prognostic and predictive biomarkers in CRC liver metastases (CRCLM) patients. In this review, we seek to describe the current state of knowledge of CRCLM biomarkers and to outline impending clinical perspectives, in particular focusing on the cutting-edge tools available for their characterization.
C1 [Lopez, Gianluca; Boggio, Francesca; Ferrero, Stefano; Fusco, Nicola; Del Gobbo, Alessandro] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Div Pathol, Via Francesco Sforza 35, I-20122 Milan, Italy.
   [Ferrero, Stefano; Fusco, Nicola] Univ Milan, Dept Biomed Surg & Dent Sci, Via Francesco Sforza 35, I-20122 Milan, Italy.
C3 IRCCS Ca Granda Ospedale Maggiore Policlinico; University of Milan
RP Fusco, N; Del Gobbo, A (corresponding author), Fdn IRCCS Ca Granda Osped Maggiore Policlin, Div Pathol, Via Francesco Sforza 35, I-20122 Milan, Italy.; Fusco, N (corresponding author), Univ Milan, Dept Biomed Surg & Dent Sci, Via Francesco Sforza 35, I-20122 Milan, Italy.
EM gianluca.lopez@outlook.com; francesca.boggio@hotmail.it;
   stefano.ferrero@unimi.it; nicola.fusco@unimi.it;
   alessandro.delgobbo@policlinico.mi.it
RI Lopez, Gianluca/AAM-1171-2021; Fusco, Nicola/D-6264-2016
OI Fusco, Nicola/0000-0002-9101-9131
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NR 110
TC 10
Z9 12
U1 1
U2 7
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 2018
VL 19
IS 10
AR 3014
DI 10.3390/ijms19103014
PG 18
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA GY9HB
UT WOS:000448951000169
PM 30282914
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, ZW
   Du, LT
   Dong, ZG
   Yang, YM
   Zhang, X
   Wang, LL
   Li, J
   Zheng, GX
   Qu, AL
   Wang, CX
AF Li, Zewu
   Du, Lutao
   Dong, Zhaogang
   Yang, Yongmei
   Zhang, Xin
   Wang, Lili
   Li, Juan
   Zheng, Guixi
   Qu, Ailin
   Wang, Chuanxin
TI RETRACTED: MiR-203 Suppresses ZNF217 Upregulation in Colorectal Cancer
   and Its Oncogenicity (Retracted Article)
SO PLOS ONE
LA English
DT Article; Retracted Publication
ID COPY NUMBER; CHROMOSOMAL REGION; BARRETTS-ESOPHAGUS; MICRORNAS; BREAST;
   IDENTIFICATION; RECOGNITION; TARGET; GENES; HYBRIDIZATION
AB Zinc finger protein 217 (ZNF217) is essential for cell proliferation and has been implicated in tumorigenesis. However, its expression and exact roles in colorectal cancer (CRC) remain unclear. In this study, we demonstrated that ZNF217 expression was aberrantly upregulated in CRC tissues and associated with poor overall survival of CRC patients. In addition, we found that ZNF217 was a putative target of microRNA (miR)-203 using bioinformatics analysis and confirmed that using luciferase reporter assay. Moreover, in vitro knockdown of ZNF217 or enforced expression of miR-203 attenuated CRC cell proliferation, invasion and migration. Furthermore, combined treatment of ZNF217 siRNA and miR-203 exhibited synergistic inhibitory effects. Taken together, our results provide new evidences that ZNF217 has an oncogenic role in CRC and is regulated by miR-203, and open up the possibility of ZNF217- and miR-203-targeted therapy for CRC.
C1 [Li, Zewu; Du, Lutao; Dong, Zhaogang; Yang, Yongmei; Zhang, Xin; Wang, Lili; Li, Juan; Zheng, Guixi; Qu, Ailin; Wang, Chuanxin] Shandong Univ, Qilu Hosp, Dept Clin Lab, Jinan 250100, Shandong, Peoples R China.
C3 Shandong University
RP Wang, CX (corresponding author), Shandong Univ, Qilu Hosp, Dept Clin Lab, Jinan 250100, Shandong, Peoples R China.
EM cxwang@sdu.edu.cn
RI Li, Zhenxing/ABD-0539-2022; Wang, Lili/ABH-8008-2020; Zhang,
   Xinxin/HZJ-1742-2023
OI ZHENG, GUIXI/0000-0003-2856-9592
FU China National Natural Science Foundation [81072406, 81271916, 31270971,
   81301506]; Research Fund for the Doctoral Program of Higher Education of
   China [20120131110055]; Shandong Province Natural Science Foundation
   [ZR2010HZ004]
FX The project was supported by the China National Natural Science
   Foundation Projects (Grant No. 81072406, 81271916, 31270971 and
   81301506), Research Fund for the Doctoral Program of Higher Education of
   China (Grant No. 20120131110055), and the Shandong Province Natural
   Science Foundation (Grant No. ZR2010HZ004). The funders had no role in
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
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Z9 37
U1 0
U2 7
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 JAN 26
PY 2015
VL 10
IS 1
AR e0116170
DI 10.1371/journal.pone.0116170
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA AZ8MR
UT WOS:000348470400003
PM 25621839
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Jiao, QL
   Ren, YD
   Gabrie, ANA
   Wang, Q
   Wang, YL
   Du, LT
   Liu, XY
   Wang, CX
   Wang, YS
AF Jiao, Qinlian
   Ren, Yidan
   Gabrie, Abakundana Nsenga Ariston
   Wang, Qin
   Wang, Yuli
   Du, Lutao
   Liu, Xiaoyan
   Wang, Chuanxin
   Wang, Yun-shan
TI Advances of immune checkpoints in colorectal cancer treatment
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Colorectal cancer; Immunotherapy; Immune checkpoints
ID T-LYMPHOCYTES; IMMUNOTHERAPY; PD-1; EXPRESSION; PATHWAY; CD28; TIL;
   COSTIMULATION; CHALLENGES; COMPONENT
AB Colorectal cancer (CRC) is a malignant gastrointestinal cancer that seriously threatens human health. Its morbidity and mortality are in the forefront of tumors. Chemotherapy and radiotherapy play an important role in the treatment of CRC, which can improve the survival time and quality of life of patients, but the treatment progress is slow, and the treatment effect is not satisfactory. In recent years, immunotherapy has been a new direction in the field of colorectal cancer treatment after radiotherapy, chemotherapy and targeted therapy. Immune checkpoints play a vital role in the immunotherapy of cancer, and take part in the immune escape of cancer, which is closely related to the occurrence and development of cancer. This article reviews the research progress of immune checkpoints and their blockers in the field of CRC, in order to help better use of the immune system to treat cancer.
C1 [Jiao, Qinlian; Ren, Yidan; Gabrie, Abakundana Nsenga Ariston; Wang, Yuli; Du, Lutao; Liu, Xiaoyan; Wang, Chuanxin; Wang, Yun-shan] Shandong Univ, Dept Clin Lab, Hosp 2, 247 Beiyuan St, Jinan 250033, Shandong, Peoples R China.
   [Jiao, Qinlian] Shandong Univ Sch Ocean, Int Biotechnol R&D Ctr, 180 Wenhua Xi Rd, Weihai 264209, Shandong, Peoples R China.
   [Wang, Qin] Shandong Univ, Qilu Hosp, Dept Anesthesiol, 107 Wenhua Xi Rd, Jinan 250012, Peoples R China.
C3 Shandong University; Shandong University
RP Wang, YS (corresponding author), Shandong Univ, Dept Clin Lab, Hosp 2, 247 Beiyuan St, Jinan 250033, Shandong, Peoples R China.
EM wangyunshan135@126.com
RI Wang, Yuli/AGJ-1891-2022; Liu, XiaoYan/GQA-7216-2022
FU National Natural Science Foundation of China [81874040]
FX This work was supported by the National Natural Science Foundation of
   China (No. 81874040).
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NR 82
TC 24
Z9 24
U1 0
U2 22
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 MAR
PY 2020
VL 123
AR 109745
DI 10.1016/j.biopha.2019.109745
PG 6
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA KF8HB
UT WOS:000509476800006
PM 31855736
OA gold
DA 2025-01-04
ER

PT J
AU Telang, NT
AF Telang, Nitin T.
TI Stem Cell Models for Breast and Colon Cancer: Experimental Approach for
   Drug Discovery
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE breast and colon cancer; cancer stem cells; therapeutic alternatives
ID COLORECTAL-CANCER; RESISTANCE; TUMORIGENESIS; MODIFIERS; MUTATION;
   BIOBANK; BETA; MLH1
AB The progression of the early stages of female breast and colon cancer to metastatic disease represents a major cause of mortality in women. Multi-drug chemotherapy and/or pathway selective targeted therapy are notable for their off-target effects and are associated with spontaneous and/or acquired chemotherapy resistance and the emergence of premalignant chemo-resistant cancer-initiating stem cells. The stem cell populations are responsible for the evolution of therapy-resistant metastatic disease. These limitations emphasize an unmet need to develop reliable drug-resistant cancer stem cell models as novel experimental approaches for therapeutic alternatives in drug discovery platforms. Drug-resistant stem cell models for breast and colon cancer subtypes exhibit progressive growth in the presence of cytotoxic chemo-endocrine therapeutics. The resistant cells exhibit upregulated expressions of stem cell-selective cellular and molecular markers. Dietary phytochemicals, nutritional herbs and their constituent bioactive compounds have documented growth inhibitory efficacy for cancer stem cells. The mechanistic leads for the stem cell-targeted efficacy of naturally occurring agents validates the present experimental approaches for new drug discovery as therapeutic alternatives for therapy-resistant breast and colon cancer. The present review provides a systematic discussion of published evidence on (i) conventional/targeted therapy for breast and colon cancer, (ii) cellular and molecular characterization of stem cell models and (iii) validation of the stem cell models as an experimental approach for novel drug discovery of therapeutic alternatives for therapy-resistant cancers.
C1 [Telang, Nitin T.] Palindrome Liaisons Consultants, Canc Prevent Res Program, Montvale, NJ 07645 USA.
RP Telang, NT (corresponding author), Palindrome Liaisons Consultants, Canc Prevent Res Program, Montvale, NJ 07645 USA.
EM ntelang3@gmail.com
FU US National Cancer Institute FIRST award [CA 44741]; US Department of
   Defense IDEA award [DAMD-17-94-J-4208]; US National Cancer Institute [CN
   75029-63, CN 85141, CN 05107]
FX The research programs "Cellular models for molecular subtypes of
   clinical breast cancer: Mechanistic approaches for lead compound
   efficacy" has received past support from US National Cancer Institute
   FIRST award CA 44741, and US Department of Defense IDEA award
   DAMD-17-94-J-4208 and "Preclinical models for genetically predisposed
   early onset colon cancer" has received past support from US National
   Cancer Institute Master Agreement CN 75029-63 and Contracts CN 85141 and
   CN 05107.
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NR 62
TC 6
Z9 6
U1 4
U2 23
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD AUG
PY 2022
VL 23
IS 16
AR 9223
DI 10.3390/ijms23169223
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 4B4QR
UT WOS:000845764600001
PM 36012489
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wang, ZY
   Shan, JH
   Zhou, XJ
   Wang, JW
   Yu, GY
   Dong, W
   Huai, F
   Sun, Q
   Lu, GL
   Ma, ZZ
   Liu, HC
AF Wang, Zhanyu
   Shan, Jiahui
   Zhou, Xinjie
   Wang, Jianwei
   Yu, Guangyang
   Dong, Wei
   Huai, Fei
   Sun, Qi
   Lu, Guoliang
   Ma, Zhenzhen
   Liu, Hechen
TI Surgery, radiotherapy, chemotherapy, targeted therapy, and immunotherapy
   of rectal adenocarcinoma with penile metastasis: a case report
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Metastatic rectal adenocarcinoma; penile metastasis; case report;
   prognosis; treatment
ID SIGMOID COLON-CANCER; METACHRONOUS METASTASIS; CARCINOMA; SECONDARY
AB Background: Despite the rich proximity and vascularization to the pelvic organs, metastatic lesions to the penis are incredibly uncommon. Most primary tumors are genitourinary cancers, and rectal origins are rare. Only 56 cases of metastatic penile tumors have been reported since 1870. Several palliative or curative methods, such as chemotherapy, total penectomy, and radiotherapy, have been applied to treat this condition in previous cases; however, the patient prognosis is poor. Immunotherapy is a beneficial treatment approach for multiple cancers, and recent investigations have shown that it may be beneficial for patients with advanced penile cancer. Case Description: Herein, we report the case of a 59-year-old Chinese man who had metastatic adenocarcinoma in the penile tissue 3 years after rectal cancer resection. The patient presented with penile pain and dysuria for 6 months when he was 54 years old, and Immunohistochemical staining showed that the origin was the rectum after total penectomy. The patient received surgery, chemotherapy, radiotherapy, targeted therapy and immunotherapy positively and still survived for a further 4 years and 6 months following penectomy despite the late metastasis of rectal cancer. There are two major changes and progress after penectomy, all of which have undergone surgical treatment during continuous treatment and followup, the patient completed right inguinal lymphadenectomy when his right regional nodes metastasis was found 23 months after penectomy. While the patient suffered from radiation injury after 47 months after penectomy, which led to radiation necrosis and hip soft tissue infection, and the patient tended to lay prone instead of lying on the back because of the hip pain. The patient ultimately died of multiple organ failure. Conclusions: All of the previously reported cases of penile metastasis from rectal cancer since 1870 have been reviewed. Yet, the metastatic prognosis remains poor regardless of the treatment options, except for lesions where metastasis is only limited to the penis. We found that the patient may derive more benefit from strategic therapies including surgery, radiotherapy, chemotherapy, targeted therapy, and immunotherapy.
C1 [Wang, Zhanyu; Wang, Jianwei; Yu, Guangyang; Dong, Wei; Huai, Fei; Sun, Qi; Lu, Guoliang; Ma, Zhenzhen; Liu, Hechen] Shandong Second Prov Gen Hosp, Dept Urol, Jinan, Peoples R China.
   [Shan, Jiahui; Zhou, Xinjie] Qingdao Univ, Dept Med, Qingdao, Peoples R China.
C3 Qingdao University
RP Liu, HC (corresponding author), Shandong Second Prov Gen Hosp, Dept Urol, Jinan, Peoples R China.
EM liuhechen_0828@163.com
RI Wang, Zhanyu/S-6815-2019; Wang, Jianwei/AAV-2918-2021; dong,
   wei/KVA-6898-2024
FU Traditional Chinese Medicine Science and Technology Project of Shandong
   Provincial Health Commission [2021Q133]
FX This work was supported by the Traditional Chinese Medicine Science and
   Technology Project of Shandong Provincial Health Commission (No.
   2021Q133) .
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NR 69
TC 1
Z9 1
U1 0
U2 4
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD APR 29
PY 2023
VL 14
IS 2
BP 1155
EP 1165
DI 10.21037/jgo-23-84
EA APR 2023
PG 11
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA O2WM1
UT WOS:000981992500001
PM 37201076
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Li, S
   Dong, DZ
   Geng, JH
   Zhu, XG
   Shi, C
   Zhang, YZ
   Wang, HZ
   Zhou, S
   Wu, H
   Cai, Y
   Li, YH
   Wang, WH
AF Li, Shuai
   Dong, Dezuo
   Geng, Jianhao
   Zhu, Xianggao
   Shi, Chen
   Zhang, Yangzi
   Wang, Hongzhi
   Zhou, Shun
   Wu, Hao
   Cai, Yong
   Li, Yongheng
   Wang, Weihu
TI Stereotactic body radiotherapy prolongs the progression-free survival
   and delays the change of systemic therapy regimen in patients with lung
   oligoprogressive metastatic colorectal cancer
SO ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
DE change of systemic therapy; colorectal cancer; lung oligoprogression;
   progression&#8208; free survival; stereotactic body radiotherapy
ID PROGNOSTIC-FACTORS; OLIGOMETASTASES; CHEMOTHERAPY; BEVACIZUMAB;
   CONSENSUS; DISEASE; RISK
AB Purpose To analyze the effect of stereotactic body radiotherapy (SBRT) on colorectal cancer (CRC) patients with lung oligoprogression (OP).
   Method Patients with lung OP from CRC treated by SBRT at our center were included in this retrospective analysis. The progression-free survival (PFS), change of systemic therapy (CST), local control (LC), and overall survival (OS) were analyzed. Cumulative incidence was used to report CST, and the Kaplan-Meier method was used to evaluate PFS and LC.
   Results A total of 17 patients with 38 lung OP lesions treated by SBRT from October 2012 to December 2018 were involved. All patients had undergone radical resection for primary CRC and administered with standard systemic therapy regimens (seven for the first line and 10 for the second line). Among them, nine (52.9%) had received targeted therapy before SBRT, 14 (82.4%) patients underwent chemotherapy, and 12 received targeted therapy after SBRT. Six patients (35.3%) underwent CST after a median time of 5.2 months (range: 1.7-27.5 months). The median follow-up was 9.9 months, and the 1-year OS rate for all patients was 73.5%. Progression was observed in of 14 of 17 patients (82.4%), and the 6-month PFS for all patients was 25.9%. Univariate analysis indicated that only targeted therapy before SBRT was a beneficial prognostic indicator for 6-month PFS (P = .026) and N-PFS (P = .013). The 1-year LC for all 38 lesions was 77.8%, and during and after SBRT, no grade 3 or higher toxicities were observed.
   Conclusion SBRT combined with systemic therapy made partial CRC patients with lung OP avoid the progress within 6 months and delayed the need for CST to 5.2 months, and targeted therapy before SBRT was a positive indicator of PFS.
C1 [Li, Shuai; Dong, Dezuo; Geng, Jianhao; Zhu, Xianggao; Shi, Chen; Zhang, Yangzi; Wang, Hongzhi; Zhou, Shun; Wu, Hao; Cai, Yong; Li, Yongheng; Wang, Weihu] Peking Univ, Key Lab Carcinogenesis & Translat Res, Canc Hosp & Inst, Dept Radiat Oncol,Minist Educ Beijing, Beijing 100142, Peoples R China.
C3 Peking University
RP Li, YH; Wang, WH (corresponding author), Peking Univ, Key Lab Carcinogenesis & Translat Res, Canc Hosp & Inst, Dept Radiat Oncol,Minist Educ Beijing, Beijing 100142, Peoples R China.
EM yonghenglee@163.com; wangweihu88@163.com
RI Dong, Dezuo/EUE-3308-2022
FU Science Foundation of Peking University Cancer Hospital [18-03];
   BeijingMunicipal Science& Technology Commission [Z181100001718192];
   Beijing Natural Science Foundation [7182028]; Beijing Municipal
   Administration of Hospitals' Youth Programme [QML20171104]; construction
   of advanced subjects of Peking University Health Science Center
   [BMU2019GJJXK021]
FX Science Foundation of Peking University Cancer Hospital, Grant/Award
   Number: 18-03; BeijingMunicipal Science& Technology Commission,
   Grant/Award Number: Z181100001718192; Beijing Natural Science
   Foundation, Grant/Award Number: 7182028; Beijing Municipal
   Administration of Hospitals' Youth Programme, Grant/Award Number:
   QML20171104; The construction of advanced subjects of Peking University
   Health Science Center, Grant/Award Number: BMU2019GJJXK021
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NR 35
TC 3
Z9 3
U1 0
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-7555
EI 1743-7563
J9 ASIA-PAC J CLIN ONCO
JI Asia-Pac. J. Clin. Oncol.
PD APR
PY 2022
VL 18
IS 2
BP E64
EP E72
DI 10.1111/ajco.13557
EA FEB 2021
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0L0GE
UT WOS:000621379000001
PM 33629479
DA 2025-01-04
ER

PT J
AU Holubec, L
   Polivka, J
   Safanda, M
   Karas, M
   Liska, V
AF Holubec, Lubos
   Polivka, Jiri, Jr.
   Safanda, Martin
   Karas, Michal
   Liska, Vaclav
TI The Role of Cetuximab in the Induction of Anticancer Immune Response in
   Colorectal Cancer Treatment
SO ANTICANCER RESEARCH
LA English
DT Review
DE Colorectal cancer; cetuximab; immune response; targeted therapy;
   immunomodulation; review
ID GAMMA RECEPTOR POLYMORPHISMS; CHECKPOINT INHIBITORS;
   MONOCLONAL-ANTIBODIES; THERAPY; EGFR; IMMUNOTHERAPY; PANITUMUMAB;
   SURVIVAL; MICROENVIRONMENT; CYTOTOXICITY
AB Monoclonal antibodies binding the epidermal growth factor receptor (EGFR), such as cetuximab or panitumumab, are widely used targeted therapeutics for the treatment of patients with colorectal cancer. The clinical significance of these drugs has so far been associated with combined chemotherapy or radiation. It has been shown that these treatment strategies have their clinical limitations and do not fully exploit the immunomodulatory effect of these drugs. In this review, we discuss the mechanisms of immunomodulation together with the anticancer immune response to the monoclonal antibodies targeted to the EGFR. The combination of anti-EGFR monoclonal antibodies with other immunotherapeutic treatment modalities certainly brings new opportunities for targeted therapy in patients with colorectal cancer.
C1 [Holubec, Lubos; Polivka, Jiri, Jr.; Liska, Vaclav] Charles Univ Prague, Biomed Ctr, Fac Med Plzen, Plzen, Czech Republic.
   [Polivka, Jiri, Jr.] Charles Univ Prague, Dept Histol & Embryol, Fac Med Plzen, Plzen, Czech Republic.
   [Karas, Michal] Charles Univ Prague, Dept Hematol & Oncol, Fac Med Plzen, Plzen, Czech Republic.
   [Holubec, Lubos; Safanda, Martin] Na Homolce Hosp, Dept Clin Oncol, Prague, Czech Republic.
C3 Charles University Prague; Charles University Prague; Charles University
   Prague; Na Homolce Hospital
RP Polivka, J (corresponding author), Charles Univ Prague, Dept Histol & Embryol, Fac Med Plzen, Husova 3, Plzen 30166, Czech Republic.
EM polivkajiri@gmail.com
RI Holubec, Lubos/O-3199-2017; Liska, Vaclav/Q-4402-2017
OI Holubec, Lubos/0000-0002-8566-0512; Liska, Vaclav/0000-0002-5226-0280
FU National Sustainability Program I (NPU I) by the Ministry of Education
   Youth and Sports of the Czech Republic [LO1503]
FX This work was supported by the National Sustainability Program I (NPU I)
   Nr. LO1503 provided by the Ministry of Education Youth and Sports of the
   Czech Republic.
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NR 45
TC 40
Z9 42
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 SEP
PY 2016
VL 36
IS 9
BP 4421
EP 4426
DI 10.21873/anticanres.10985
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DW9SB
UT WOS:000384001800005
PM 27630277
OA Bronze
DA 2025-01-04
ER

PT J
AU Yan, YY
   Grothey, A
AF Yan, Yiyi
   Grothey, Axel
TI Molecular profiling in the treatment of colorectal cancer: focus on
   regorafenib
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE metastatic colon cancer; targeted therapy; molecular profiling;
   regorafenib
ID RANDOMIZED PHASE-III; RENAL-CELL CARCINOMA; WILD-TYPE KRAS; 1ST-LINE
   TREATMENT; RAS MUTATIONS; BRAF MUTATION; COLON-CANCER; ANTI-PD-L1
   ANTIBODY; CLINICAL ACTIVITY; DOSE-ESCALATION
AB Metastatic colorectal cancer (mCRC) is a highly heterogeneous disease. Its treatment outcome has been significantly improved over the last decade with the incorporation of biological targeted therapies, including anti-EGFR antibodies, cetuximab and panitumumab, and VEGF inhibitors, bevacizumab, ramucirumab, and aflibercept. The identification of predictive biomarkers has further improved the survival by accurately selecting patients who are most likely to benefit from these treatments, such as RAS mutation profiling for EGFR antibodies. Regorafenib is a multikinase inhibitor currently used as late line therapy for mCRC. The molecular and genetic markers associated with regorafenib treatment response are yet to be characterized. Here, we review currently available clinical evidence of mCRC molecular profiling, such as RAS, BRAF, and MMR testing, and its role in targeted therapies with special focus on regorafenib treatment.
C1 [Yan, Yiyi; Grothey, Axel] Mayo Clin, Dept Med Oncol, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Grothey, A (corresponding author), Mayo Clin, Dept Med Oncol, 200 First St SW, Rochester, MN 55905 USA.
EM grothey.axel@mayo.edu
FU Bayer Oncology
FX The Mayo Clinic Foundation received grant funding from Bayer Oncology
   for research led by author AG. The authors report no other conflicts of
   interest in this work.
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NR 78
TC 19
Z9 22
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 2015
VL 8
BP 2949
EP 2957
DI 10.2147/OTT.S79145
PG 9
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA CT9UD
UT WOS:000363161200001
PM 26508880
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Kleist, B
   Poetsch, M
AF Kleist, Britta
   Poetsch, Micaela
TI Neuroendocrine differentiation: The mysterious fellow of colorectal
   cancer
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Neuroendocrine differentiation; Colorectal cancer; mTOR pathway;
   Neuroendocrine tumorigenesis; Targeted therapy
ID CHROMOGRANIN-A EXPRESSION; PROGNOSTIC-SIGNIFICANCE; ENDOCRINE-CELLS;
   ENTEROENDOCRINE CELLS; MTOR PATHWAY; INTESTINAL EPITHELIUM;
   CLINICAL-SIGNIFICANCE; PANCREATIC ENDOCRINE; TUMOR-CELLS; COLON
AB Neuroendocrine differentiation in sporadic colorectal cancer has been recognized since decades, but its clinical impact is still controversially discussed. Detailed parameter analyses hint at the possibility that probably not neuroendocrine differentiation itself, but its association with poor grade of tumor differentiation, lymph node metastases, distant metastases and other unfavorable features contribute to worse clinical outcome. However, other studies deny a relationship between neuroendocrine differentiation and prognosis of colorectal cancer. This review elucidates, whether new insights into the origin of neuroendocrine differentiation in the intestinal epithelium, its regulation by mTOR pathway components and its possible link to the intestinal stem cell compartment could determine a role of neuroendocrine cells as prognostic marker and putative therapeutic target in sporadic colorectal cancer.
C1 [Kleist, Britta] Southern Hosp Trust, Dept Pathol, N-4604 Kristiansand, Norway.
   [Poetsch, Micaela] Univ Hosp Essen, Inst Legal Med, D-45122 Essen, Germany.
C3 University of Duisburg Essen
RP Kleist, B (corresponding author), Southern Hosp Trust, Dept Pathol, Postbox 416, N-4604 Kristiansand, Norway.
EM britta.kleist@sshf.no
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NR 80
TC 29
Z9 31
U1 0
U2 11
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 NOV 7
PY 2015
VL 21
IS 41
BP 11740
EP 11747
DI 10.3748/wjg.v21.i41.11740
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CW5HA
UT WOS:000365025100019
PM 26556999
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Turker, S
   Cilbir, E
   Karacin, C
   Altinbas, M
AF Turker, Sema
   Cilbir, Ebru
   Karacin, Cengiz
   Altinbas, Mustafa
TI Hypertrichosis, trichomegaly, and androgenic alopecia related to
   cetuximab treatment
SO JOURNAL OF CANCER RESEARCH AND THERAPEUTICS
LA English
DT Article
DE Alopecia; cetuximab; colon cancer; hypertrichosis; trichomegaly
AB Anti-epidermal growth factor receptor (EGFR) antibodies are mainly used in the treatment of advanced stages of solid tumors as a targeted therapy to inhibit tumor proliferation. They cause many dermatological adverse reactions through inhibition of EGFR pathway in the skin. A 39-year-old female patient diagnosed with metastatic colon adenocarcinoma received oxaliplatin, fluorouracil, and folinic acid regimen with cetuximab. The patient noticed increase in fairy hair especially at facial area as well as in the whole body beginning after the first few cycles of treatment, after 3 months. Obvious hypertrichosis, androgenic alopecia, and trichomegaly were observed. Blood tests for androgenetic alopecia and hirsutism were studied. Hormonal levels were in normal range. Upper abdominal imaging to rule out any adrenal lesion was also normal. Previous studies reported found that cetuximab may cause alopecia, hypertrichosis on face and body, and trichomegaly. We have not encountered a combination of hypertrichosis, androgenic type alopecia, and trichomegaly in the literature.
C1 [Turker, Sema; Cilbir, Ebru; Karacin, Cengiz; Altinbas, Mustafa] SBU Diskapi Yildirim Beyazit Training & Res Hosp, Dept Med Oncol, TR-06110 Ankara, Turkey.
C3 Diskapi Yildirim Beyazit Training & Research Hospital
RP Turker, S (corresponding author), SBU Diskapi Yildirim Beyazit Training & Res Hosp, Dept Med Oncol, TR-06110 Ankara, Turkey.
EM sema.turker@yahoo.com
RI Karaçin, Cengiz/ABB-3650-2020; Turker, Sema/ABE-5926-2021
OI Karacin, Cengiz/0000-0002-7310-9328; Turker, Sema/0000-0001-9040-7266
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NR 10
TC 4
Z9 4
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, 400059, INDIA
SN 0973-1482
EI 1998-4138
J9 J CANCER RES THER
JI J. Canc. Res. Ther.
PD APR-JUN
PY 2020
VL 16
IS 3
BP 690
EP 692
DI 10.4103/jcrt.JCRT_343_17
PG 3
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OL5UJ
UT WOS:000585404400050
PM 32719294
OA gold
DA 2025-01-04
ER

PT J
AU Falcone, R
   Roberto, M
   Filetti, M
   Anselmi, E
   Marchetti, P
AF Falcone, Rosa
   Roberto, Michela
   Filetti, Marco
   Anselmi, Elisabetta
   Marchetti, Paolo
TI Anti epidermal growth factor receptor therapy in small bowel
   adenocarcinoma Case report and literature review
SO MEDICINE
LA English
DT Review
DE jejunum; panitumumab; small bowel adenocarcinoma; target therapy
ID PROTON PUMP INHIBITORS; PHASE-II; BEVACIZUMAB; CAPECITABINE;
   OXALIPLATIN; CANCER; CHEMOTHERAPY; CETUXIMAB; AMPULLA; PATIENT
AB Rationale: Small bowel adenocarcinoma (SBA) is an uncommon gastrointestinal cancer, thus limited data about treatment for advanced disease are available. The lack of specific guidelines has justified the use of therapeutic protocols usually applied in advanced colorectal cancer. Few and preliminary data have suggested possible clinical benefit from the use of target therapy such as bevacizumab and cetuximab.
   Patient concerns: We present the case of a young woman who was admitted to the emergency department for acute abdominal pain, nausea, and vomiting related to a jejunal stenosis.
   Diagnoses: An enteroscopy with jejunal biopsy showed poorly differentiated cancerous cells suggestive for primary intestinal cancer. There were no signs of metastatic disease at radiological evaluation. A jejunal resection was subsequently carried out and the diagnosis of mucinous adenocarcinoma of the jejunum was confirmed.
   Interventions: The computed tomography scan performed 1 month after surgery showed metastatic disease. Therefore, the patient received combined protocols of chemotherapy and either bevacizumab or the anti-epidermal growth factor receptor (EGFR) panitumumab.
   Outcomes: A partial response (PR) was achieved with Folfox plus panitumumab and a maintenance therapy with panitumumab is being conducted with a mild toxicity and a progression free survival of 19 months since the beginning of panitumumab.
   Lessons: This is, to the best of our knowledge, the first report in the literature of a patient with SBA who has benefitted from panitumumab with an overall survival of 83 months.
C1 [Falcone, Rosa; Roberto, Michela; Filetti, Marco; Anselmi, Elisabetta; Marchetti, Paolo] Sapienza Univ Rome, Dept Mol & Clin Med, Rome, Italy.
C3 Sapienza University Rome
RP Falcone, R (corresponding author), Sapienza Univ Rome, St Andrea Hosp, Dept Mol & Clin Med, Via Grottarossa 1035, I-00189 Rome, Italy.
EM falcone.rosa@hotmail.it
RI Marchetti, Paolo/J-9890-2018; Falcone, Rosa/GQB-2694-2022; Filetti,
   Marco/ABE-8668-2021; Roberto, Michela/AAC-2552-2022
OI FALCONE, ROSA/0000-0001-9679-4711
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NR 17
TC 11
Z9 11
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 2018
VL 97
IS 3
AR e9672
DI 10.1097/MD.0000000000009672
PG 3
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA FU8DE
UT WOS:000424082000045
PM 29505011
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhao, DZ
   Jiang, M
   Zhang, XC
   Hou, HL
AF Zhao, Deze
   Jiang, Man
   Zhang, Xiaochun
   Hou, Helei
TI The role of RICTOR amplification in targeted therapy and drug resistance
SO MOLECULAR MEDICINE
LA English
DT Review
DE RICTOR; TKIs; mTORC2; Drug resistance
ID RAPAMYCIN COMPLEX 2; TYROSINE KINASE COACTIVATION; REDUCES TUMOR-GROWTH;
   CELL LUNG-CANCER; MAMMALIAN TARGET; IN-VITRO; PI3K/MTOR INHIBITOR;
   TORC1/TORC2 INHIBITOR; SELECTIVE INHIBITOR; COLORECTAL-CANCER
AB The emergence of tyrosine kinase inhibitors (TKIs) has changed the current treatment paradigm and achieved good results in recent decades. However, an increasing number of studies have indicated that the complex network of receptor tyrosine kinase (RTK) co-activation could influence the characteristic phenotypes of cancer and the tumor response to targeted treatments. One of strategies to blocking RTK co-activation is targeting the downstream factors of RTK, such as PI3K-AKT-mTOR pathway. RICTOR, a core component of mTORC2, acts as a key effector molecule of the PI3K-AKT pathway; its amplification is often associated with poor clinical outcomes and resistance to TKIs. Here, we discuss the biology of RICTOR in tumor and the prospects of targeting RICTOR as a complementary therapy to inhibit RTK co-activation.
C1 [Zhao, Deze; Jiang, Man; Zhang, Xiaochun; Hou, Helei] Qingdao Univ, Affiliated Hosp, Dept Med Oncol, 16 Jiangsu Rd, Qingdao 266005, Peoples R China.
C3 Qingdao University
RP Hou, HL (corresponding author), Qingdao Univ, Affiliated Hosp, Dept Med Oncol, 16 Jiangsu Rd, Qingdao 266005, Peoples R China.
EM houhelei@qdu.edu.cn
RI xiang, li/JDN-4098-2023; zhao, deze/GYR-2200-2022
OI Zhao, Deze/0000-0002-4266-4214
FU Chinese Postdoctoral Science Foundation [2017 M622143]
FX This work was supported by a grant from Chinese Postdoctoral Science
   Foundation (2017 M622143 to Helei Hou).
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NR 125
TC 24
Z9 30
U1 0
U2 13
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1076-1551
EI 1528-3658
J9 MOL MED
JI Mol. Med.
PD FEB 10
PY 2020
VL 26
IS 1
AR 20
DI 10.1186/s10020-020-0146-6
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA KS4WA
UT WOS:000518309700001
PM 32041519
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU He, J
   Wu, WH
AF He, Jia
   Wu, Wenhan
TI A glimpse of research cores and frontiers on the relationship between
   long noncoding RNAs (lncRNAs) and colorectal cancer (CRC) using the
   VOSviewer tool
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE CRC; lncRNA; bibliometric analysis; research trend; precision treatment
ID EXTRACELLULAR VESICLES; IMMUNE ESCAPE; METASTASIS; MALAT1; GROWTH;
   CHEMORESISTANCE; PROLIFERATION; FIBROBLASTS; EXPRESSION; DISCOVERY
AB As lncRNAs are essential participants in colorectal carcinogenesis. This study aimed to use the VOSviewer tool to access the research cores and frontiers on the relationship between lncRNAs and CRC. Our findings showed that the mechanism of lncRNA in the occurrence and development of CRC was the core theme of the field. (1) Immunotherapy and immune microenvironment of CRC and lncRNAs, (2) CRC and lncRNAs in exosomes and (3) CRC and lncRNA-targeted therapy might represent three research frontiers. A comprehensive understanding of their existing mechanisms and the search for new regulatory paradigms are the core topics of future research. This knowledge will also help us select appropriate targeting methods and select appropriate preclinical models to promote clinical translation and ultimately achieve precise treatment of CRC.
C1 [He, Jia] Southwest Med Univ, Fac Affairs & Human Resources, Management Dept, Luzhou, Peoples R China.
   [Wu, Wenhan] Southwest Med Univ, Dept Gen Surg Gastrointestinal Surg, Affiliated Hosp, Luzhou, Peoples R China.
C3 Southwest Medical University; Southwest Medical University
RP Wu, WH (corresponding author), Southwest Med Univ, Dept Gen Surg Gastrointestinal Surg, Affiliated Hosp, Luzhou, Peoples R China.
EM wwh@wuwenhan.tech
RI Wu, Wenhan/HNQ-5653-2023
FU Doctoral Research Initiation Fund of Affiliated Hospital of Southwest
   Medical University [21041]
FX This study was supported by the Doctoral Research Initiation Fund of
   Affiliated Hospital of Southwest Medical University [No. 21041].
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TC 3
Z9 3
U1 2
U2 20
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD MAR 4
PY 2023
VL 58
IS 3
BP 254
EP 263
DI 10.1080/00365521.2022.2124537
EA SEP 2022
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 9G2VP
UT WOS:000857903500001
PM 36121831
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Kumarasamy, G
   Salim, NHM
   Afandi, NSM
   Habib, MAH
   Amin, NDM
   Ismail, MN
   Musa, M
AF Kumarasamy, Gaayathri
   Salim, Nurul Hakimah Mohd
   Afandi, Nur Syafiqah Mohd
   Habib, Mohd Afiq Hazlami
   Amin, Nor Datiakma Mat
   Ismail, Mohd Nazri
   Musa, Marahaini
TI Glycoproteomics-based liquid biopsy: translational outlook for
   colorectal cancer clinical management in Southeast Asia
SO FUTURE ONCOLOGY
LA English
DT Review
DE biomarker; colon cancer; glycoproteomics; liquid biopsy; screening
ID COLON
AB Colorectal cancer (CRC) signifies a significant healthcare challenge in Southeast Asia. Despite advancements in screening approaches and treatment modalities, significant medical gaps remain, ranging from prevention and early diagnosis to determining targeted therapy and establishing personalized approaches to managing CRC. There is a need to expand more validated biomarkers in clinical practice. An advanced technique incorporating high-throughput mass spectrometry as a liquid biopsy to unravel a repertoire of glycoproteins and glycans would potentially drive the development of clinical tools for CRC screening, diagnosis and monitoring, and it can be further adapted to the existing standard-of-care procedure. Therefore this review offers a perspective on glycoproteomics-driven liquid biopsy and its potential integration into the clinical care of CRC in the southeast Asia region.
   Colorectal cancer (CRC) is a significant concern in Southeast Asia, with gaps in prevention, diagnosis and therapy. Finding glycoproteins' and glycans' potentials as CRC biomarkers could revolutionize CRC care, from screening to treatment, across the region.
C1 [Kumarasamy, Gaayathri; Ismail, Mohd Nazri] Univ Sains Malaysia, Inst Res Mol Med, Gelugor 11800, Pulau Pinang, Malaysia.
   [Salim, Nurul Hakimah Mohd] Univ Sains Malaysia, Sch Med Sci, Dept Pathol, Kubang Kerian 16150, Kelantan, Malaysia.
   [Afandi, Nur Syafiqah Mohd; Habib, Mohd Afiq Hazlami; Amin, Nor Datiakma Mat; Ismail, Mohd Nazri] Univ Sains Malaysia, Analyt Biochem Res Ctr, Bayan Lepas 11900, Pulau Pinang, Malaysia.
   [Amin, Nor Datiakma Mat] Forest Res Inst Malaysia, Nat Prod Div, Kepong 52109, Selangor, Malaysia.
   [Musa, Marahaini] Univ Sains Malaysia, Human Genome Ctr, Sch Med Sci, Kubang Kerian 16150, Kelantan, Malaysia.
C3 Universiti Sains Malaysia; Universiti Sains Malaysia; Universiti Sains
   Malaysia; Institute Penyelidikan Perhutanan Malaysia; Universiti Sains
   Malaysia
RP Musa, M (corresponding author), Univ Sains Malaysia, Human Genome Ctr, Sch Med Sci, Kubang Kerian 16150, Kelantan, Malaysia.
EM marahaini.musa@usm.my
RI Ismail, Mohd Nazri/E-6842-2011; MAT AMIN, NOR DATIAKMA/GVU-8782-2022;
   Habib, Mohd Afiq Hazlami/D-1503-2019; Kumarasamy,
   Gaayathri/ISU-0069-2023; Musa, Marahaini/E-9987-2019
OI Habib, Mohd Afiq Hazlami/0000-0001-5258-6136; AMIN, NOR
   DATIAKMA/0000-0002-0607-8808; Kumarasamy, Gaayathri/0000-0001-6630-1218;
   Mohd Afandi, Nur Syafiqah/0000-0002-1631-2995; Musa,
   Marahaini/0000-0002-0165-5741
FU No writing assistance was utilized in the production of this manuscript.
FX Gaayathri Kumarasamy: writing- original draft preparation, reviewing,
   and editing. Nurul Hakimah Mohd Salim: writing- original draft
   preparation. Nur Syafiqah Mohd Afandi: writing- original draft
   preparation. Mohd Afiq Hazlami Habib: writing- original draft
   preparation. Nor Datiakma Mat Amin: writing- original draft preparation.
   Mohd Nazri Ismail: supervision, writing- reviewing, and editing.
   Marahaini Musa: conceptualisation, writing- reviewing and editing,
   supervision, project administration.r The authors would like to express
   their sincere appreciation to the following individuals who contributed
   valuable ideas and insights during the development of this review
   article: Hardiyanti Nirwan Ben, Khayrin Khairiz, Dr. Ley Hian Low, Dr.
   Kiat Yee Liow, Dr. Lee Cheng Siang, Dr. Thin-Thin Aye, Fadzhairi Jabar
   and Assoc. Prof. Dr. Nur Asyilla Che Jalil.r The authors have no
   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. This includes employment, consultancies, honoraria, stock
   ownership or options, expert testimony, grants or patents received or
   pending, or royalties.r The authors have no competing interests or
   relevant affiliations with any organization or entity with the subject
   matter or materials discussed in the manuscript. This includes
   employment, consultancies, honoraria, stock ownership or options, expert
   testimony, grants or patents received or pending, or royalties.r No
   writing assistance was utilized in the production of this manuscript.
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NR 163
TC 0
Z9 0
U1 0
U2 2
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PD NOV
PY 2023
VL 19
IS 34
BP 2313
EP 2332
DI 10.2217/fon-2023-0704
EA NOV 2023
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CN2P0
UT WOS:001096692100001
PM 37937446
DA 2025-01-04
ER

PT J
AU Zheng, DY
   Li, J
   Yan, H
   Zhang, G
   Li, W
   Chu, E
   Wei, N
AF Zheng, Dayong
   Li, Jun
   Yan, Han
   Zhang, Gang
   Li, Wei
   Chu, Edward
   Wei, Ning
TI Emerging roles of Aurora-A kinase in cancer therapy resistance
SO ACTA PHARMACEUTICA SINICA B
LA English
DT Review
DE Aurora-A; Therapy resistance; Chemoresistance; Targeted therapy;
   Radioresistance; Synthetic lethality; Alisertib; PROTAC
ID DNA-DAMAGE RESPONSE; SMALL-MOLECULE INHIBITOR; PROSTATE-CANCER;
   MESENCHYMAL TRANSITION; SELECTIVE INHIBITOR; DRUG-RESISTANCE; BREAST;
   PHOSPHORYLATION; CELLS; ACTIVATION
AB Aurora kinase A (Aurora-A), a serine/threonine kinase, plays a pivotal role in various cellular processes, including mitotic entry, centrosome maturation and spindle formation. Overexpression or gene-amplification/mutation of Aurora-A kinase occurs in different types of cancer, including lung cancer, colorectal cancer, and breast cancer. Alteration of Aurora-A impacts multiple cancer hallmarks, especially, immortalization, energy metabolism, immune escape and cell death resistance which are involved in cancer progression and resistance. This review highlights the most recent advances in the oncogenic roles and related multiple cancer hallmarks of Aurora-A kinase-driving cancer therapy resistance, including chemoresistance (taxanes, cisplatin, cyclophosphamide), targeted therapy resistance (osimertinib, imatinib, sorafenib, etc.), endocrine therapy resistance (tamoxifen, fulvestrant) and radioresistance. Specifically, the mechanisms of Aurora-A kinase promote acquired resistance through modulating DNA damage repair, feedback activation bypass pathways, resistance to apoptosis, necroptosis and autophagy, metastasis, and stemness. Noticeably, our review also summarizes the promising synthetic lethality strategy for Aurora-A inhibitors in RB1, ARID1A and MYC gene mutation tumors, and potential synergistic strategy for mTOR, PAK1, MDM2, MEK inhibitors or PD-L 1 antibodies combined with targeting Aurora-A kinase. In addition, we discuss the design and development of the novel class of Aurora-A inhibitors in precision medicine for cancer treatment.
C1 [Zheng, Dayong; Yan, Han; Li, Wei] North China Univ Sci & Technol, Sch Pharm, Tangshan 063210, Peoples R China.
   [Li, Jun] Liaoning Univ Tradit Chinese Med, Basic Med Sci Coll, Shenyang 110032, Peoples R China.
   [Zhang, Gang] CALTECH, Div Biol & Biol Engn, Pasadena, CA 91125 USA.
   [Chu, Edward; Wei, Ning] Albert Einstein Coll Med, Dept Oncol, Bronx, NY 10461 USA.
   [Chu, Edward; Wei, Ning] Albert Einstein Coll Med, Montefiore Einstein Canc Ctr, Canc Therapeut Program, Bronx, NY 10461 USA.
C3 North China University of Science & Technology; Liaoning University of
   Traditional Chinese Medicine; California Institute of Technology;
   Yeshiva University; Montefiore Medical Center; Albert Einstein College
   of Medicine; Yeshiva University; Montefiore Medical Center; Albert
   Einstein College of Medicine
RP Chu, E; Wei, N (corresponding author), Albert Einstein Coll Med, Dept Oncol, Bronx, NY 10461 USA.; Chu, E; Wei, N (corresponding author), Albert Einstein Coll Med, Montefiore Einstein Canc Ctr, Canc Therapeut Program, Bronx, NY 10461 USA.
EM edward.chu@einsteinmed.edu; ning.wei@einsteinmed.edu
RI WEI, NING/AAF-8368-2020
OI WEI, NING/0000-0003-2723-4061
FU Natural Science Foundation of Hebei Province [H2020209284]; Scientific
   Research Foundation of Higher Education Institutions of Hebei Province
   [QN2021120]; Department of Science and Technology of Liaoning province
   [2020 -MS -225]; Montefiore Einstein Cancer Center grant [NCI
   P30CA013330]
FX & nbsp;We want to apologize for those authors whose study we could not
   cite due to space constrains. The project was supported by the Natural
   Science Foundation of Hebei Province (No. H2020209284, China, Dayong
   Zheng) ; Scientific Research Foundation of Higher Education Institutions
   of Hebei Province (No. QN2021120, Day-ong Zheng) ; Department of Science
   and Technology of Liaoning province (No. 2020-MS-225, China, Jun Li) ;
   the Montefiore Einstein Cancer Center grant (NCI P30CA013330, USA,
   Edward Chu) .
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NR 159
TC 26
Z9 27
U1 10
U2 27
PU INST MATERIA MEDICA, CHINESE ACAD MEDICAL SCIENCES
PI BEIJING
PA C/O EDITORIAL BOARD OF ACTA PHARMACEUTICA SINICA, 1 XIANNONGTAN ST,
   BEIJING, 100050, PEOPLES R CHINA
SN 2211-3835
EI 2211-3843
J9 ACTA PHARM SIN B
JI Acta Pharm. Sin. B
PD JUL
PY 2023
VL 13
IS 7
BP 2826
EP 2843
DI 10.1016/j.apsb.2023.03.013
EA JUL 2023
PG 18
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA O7WL1
UT WOS:001045870500001
PM 37521867
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Makarem, M
   Garcia-Pardo, M
   Leighl, NB
AF Makarem, Maisam
   Garcia-Pardo, Miguel
   Leighl, Natasha B.
TI Plasma-Based Genotyping in Advanced Solid Tumors: A Comprehensive Review
SO CANCERS
LA English
DT Review
DE plasma genotyping; ctDNA; guideline recommendations
ID METASTATIC COLORECTAL-CANCER; MOLECULAR TESTING GUIDELINE;
   OF-AMERICAN-PATHOLOGISTS; CELL LUNG-CANCER; OVARIAN-CANCER; LIQUID
   BIOPSY; CLINICAL-ONCOLOGY; DNA ANALYSIS; BREAST; THERAPY
AB Simple Summary: Targeted therapy is at the forefront of cancer diagnosis and treatment today for multiple advanced tumors. Although molecular testing of tumour tissue biopsies remains the gold standard for molecular diagnosis, it has certain limitations. There have been major advances in the use of plasma, also referred to as a "liquid biopsy," to identify changes in the genome associated with approved targeted therapies. Here, we review key studies that have led to these approvals and a paradigm shift toward greater use of liquid biopsy in precision oncology.
   Molecular genotyping for advanced solid malignancies has transformed the clinical management of patients with metastatic disease. Treatment decisions in a growing number of tumors require knowledge of molecularly driven alterations in order to select optimal targeted therapy. Although genomic testing of tumor tissue is the gold standard for identifying targetable genomic alterations, biopsy samples are often limited or difficult to access. This has paved the way for the development of plasma-based approaches for genomic profiling. Recent advances in the detection of plasma-circulating tumor DNA (ctDNA) have enabled the integration of plasma-based molecular profiling into clinical practice as an alternative or complementary tool for genomic testing in the setting of advanced cancer, to facilitate the identification of driver mutations to guide initial treatment and diagnose resistance. Several guidelines now recommend the use of plasma where tumor tissue is limited to identify a targetable genomic alteration. Current plasma-based assays can evaluate multiple genes in comprehensive panels, and their application in advanced disease will be increasingly incorporated into standard practice. This review focuses on current and future applications of plasma ctDNA-based assays in advanced solid malignancies, while highlighting some limitations in implementing this technology into clinical practice.
C1 [Makarem, Maisam; Garcia-Pardo, Miguel; Leighl, Natasha B.] Princess Margaret Canc Ctr, Dept Med Oncol, Toronto, ON M5G 2C1, Canada.
C3 University of Toronto; University Health Network Toronto; Princess
   Margaret Cancer Centre
RP Leighl, NB (corresponding author), Princess Margaret Canc Ctr, Dept Med Oncol, Toronto, ON M5G 2C1, Canada.
EM natasha.leighl@uhn.ca
RI ; Garcia Pardo, Miguel/HNC-4200-2023
OI Makarem, Maisam/0000-0002-5659-1095; Garcia Pardo,
   Miguel/0000-0001-6339-8501
FU Princess Margaret Cancer Foundation; Division of Medical Oncology,
   Princess Margaret Cancer Centre
FX N.B.L. is supported through the Princess Margaret Cancer Foundation (OSI
   Pharmaceuticals Foundation Chair). M.G.-P. is supported by the Division
   of Medical Oncology, Princess Margaret Cancer Centre.
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NR 98
TC 3
Z9 3
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2021
VL 13
IS 21
AR 5299
DI 10.3390/cancers13215299
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WX5YN
UT WOS:000718671400001
PM 34771462
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lodewijk, I
   Duenas, M
   Paramio, JM
   Rubio, C
AF Lodewijk, Iris
   Duenas, Marta
   Paramio, Jesus M.
   Rubio, Carolina
TI CD44v6, STn & O-GD2: promising tumor associated antigens paving the way
   for new targeted cancer therapies
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE CD44v6; STn; O-GD2; Cancer; Targeted Therapy; O-glycans; Tn; GD2
ID SQUAMOUS-CELL CARCINOMA; CAR-T-CELLS; IMMUNOCONJUGATE BIVATUZUMAB
   MERTANSINE; ACTIVE SPECIFIC IMMUNOTHERAPY; METASTATIC BREAST-CANCER;
   MONOCLONAL-ANTIBODY U36; PHASE-I TRIAL; SIALYL-TN; COLORECTAL-CANCER;
   CLINICAL-TRIAL
AB Targeted therapies are the state of the art in oncology today, and every year new Tumor-associated antigens (TAAs) are developed for preclinical research and clinical trials, but few of them really change the therapeutic scenario. Difficulties, either to find antigens that are solely expressed in tumors or the generation of good binders to these antigens, represent a major bottleneck. Specialized cellular mechanisms, such as differential splicing and glycosylation processes, are a good source of neo-antigen expression. Changes in these processes generate surface proteins that, instead of showing decreased or increased antigen expression driven by enhanced mRNA processing, are aberrant in nature and therefore more specific targets to elicit a precise anti-tumor therapy. Here, we present promising TAAs demonstrated to be potential targets for cancer monitoring, targeted therapy and the generation of new immunotherapy tools, such as recombinant antibodies and chimeric antigen receptor (CAR) T cell (CAR-T) or Chimeric Antigen Receptor-Engineered Natural Killer (CAR-NK) for specific tumor killing, in a wide variety of tumor types. Specifically, this review is a detailed update on TAAs CD44v6, STn and O-GD2, describing their origin as well as their current and potential use as disease biomarker and therapeutic target in a diversity of tumor types.
C1 [Lodewijk, Iris; Duenas, Marta; Paramio, Jesus M.; Rubio, Carolina] Univ Hosp 12 Octubre, Biomed Res Inst 1 12, Madrid, Spain.
   [Lodewijk, Iris; Duenas, Marta; Paramio, Jesus M.; Rubio, Carolina] CIEMAT Ctr Invest Energet Medioambientales & Tecno, Mol Oncol Unit, Madrid, Spain.
   [Lodewijk, Iris; Duenas, Marta; Paramio, Jesus M.; Rubio, Carolina] Biomed Res Networking Ctr Oncol CIBERONC, Madrid, Spain.
C3 Hospital Universitario 12 de Octubre
RP Rubio, C (corresponding author), Univ Hosp 12 Octubre, Biomed Res Inst 1 12, Madrid, Spain.; Rubio, C (corresponding author), CIEMAT Ctr Invest Energet Medioambientales & Tecno, Mol Oncol Unit, Madrid, Spain.; Rubio, C (corresponding author), Biomed Res Networking Ctr Oncol CIBERONC, Madrid, Spain.
EM Carolina.Rubio@externos.ciemat.es
RI Rubio Martin, Carolina/H-4709-2015; Paramio, Jesus M/M-8482-2014
OI Paramio, Jesus M/0000-0001-7520-3177; Lodewijk, Iris/0000-0002-5208-8249
FU Instituto de Salud Carlos III (ISCIII) [PI20/00813]; European Union;
   European Regional Development Fund (FEDER) Grants from Science and
   Innovation [SAF2015-66015-R, PID2019-110758RB-I00]; Instituto de Salud
   Carlos III (CIBERONC) [CB16/12/00228, DTS20/00043, DTS22/00002]; CARLOS
   III HEALTH INSTITUTE (ISCIII); ISCIII [AC22/00015]; Scientific
   Foundation of the Spanish Association Against Cancer (FCAECC)
   [TRNSC213883DUEN]; Fundacion Eugenio Rodriguez Pascual [FERP-2022-79];
   AECC (Spanish Ass. against Cancer) [PRDMA19024LODE]
FX This study was cofounded by Instituto de Salud Carlos III (ISCIII)
   through the Project PI20/00813 to MD and co-funded by the European
   Union; European Regional Development Fund (FEDER) Grants from Science
   and Innovation (SAF2015-66015-R, and PID2019-110758RB-I00 to JMP),
   Instituto de Salud Carlos III (CIBERONC no. CB16/12/00228 to JMP;
   DTS20/00043; DTS22/00002 to MD), Project "FINANCED BY NEXTGENERATIONEU
   FUNDS, WHICH FINANCE THE ACTIONS OF THE RECOVERY AND RESILIENCE
   MECHANISM (MRR)". Funding entity: CARLOS III HEALTH INSTITUTE (ISCIII).
   ISCIII project code: AC22/00015 - Title: "Circulating tumor
   microenvironment components as predictors of response to immunotherapy
   in urothelial cancer" - PI: Marta Duenas Porto. Project also funded by
   the Scientific Foundation of the Spanish Association Against Cancer
   (FCAECC) with project ID TRNSC213883DUEN, Transcan-3 JTC2022 and
   Fundacion Eugenio Rodriguez Pascual (FERP-2022-79 to CR). IL is
   supported by a predoctoral fellowship from AECC (Spanish Ass. against
   Cancer), Predoctoral AECC 2019 grant number PRDMA19024LODE.
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NR 184
TC 5
Z9 5
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 OCT 3
PY 2023
VL 14
AR 1272681
DI 10.3389/fimmu.2023.1272681
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA U4AY9
UT WOS:001084250300001
PM 37854601
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lindenberg, L
   Adler, S
   Turkbey, IB
   Mertan, F
   Ton, A
   Do, K
   Kummar, S
   Gonzalez, EM
   Bhattacharyya, S
   Jacobs, PM
   Choyke, P
AF Lindenberg, Liza
   Adler, Stephen
   Turkbey, Ismail B.
   Mertan, Francesca
   Ton, Anita
   Do, Khanh
   Kummar, Shivaani
   Gonzalez, Esther Mena
   Bhattacharyya, Sibaprasad
   Jacobs, Paula M.
   Choyke, Peter
TI Dosimetry and first human experience with <SUP>89</SUP>Zr-panitumumab
SO AMERICAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Article
DE Zr-89-panitumumab; human dosimetry; PET
ID GROWTH-FACTOR RECEPTOR; COLORECTAL-CANCER; TARGETED THERAPY;
   PANITUMUMAB; PET; CETUXIMAB; LIFE
AB Zr-89-panitumumab is a novel immuno-PET radiotracer. A fully humanized IgG2 antibody, panitumumab binds with high affinity to the extracellular ligand binding domain of EGFR. Immuno-PET with radiolabeled panitumumab is a non-invasive method that could characterize EGFR expression in tumors and metastatic lesions. It might also assist in selecting patients likely to benefit from targeted therapy as well as monitor response and drug biodistribution for dosing guidance. Our objective was to calculate the maximum dosing for effective imaging with minimal radiation exposure in a small subset. Three patients with metastatic colon cancer were injected with approximately 1 mCi (37 MBq) of Zr-89-panitumumab IV. Whole body static images were then obtained at 2-6 hours, 1-3 days and 5-7 days post injection. Whole organ contours were applied to the liver, kidneys, spleen, stomach, lungs, bone, gut, heart, bladder and psoas muscle. From these contours, time activity curves were derived and used to calculate mean resident times which were used as input into OLINDA 1.1 software for dosimetry estimates. The whole body effective dose was estimated between 0.264 mSv/MBq (0.97 rem/mCi) and 0.330 mSv/MBq (1.22 rem/mCi). The organ which had the highest dose was the liver which OLINDA estimated between 1.9 mGy/MBq (7.2 rad/mCi) and 2.5 mGy/MBq (9 rad/mCi). The effective dose is within range of extrapolated estimates from mice studies. Zr-89-panitumumab appears safe and dosimetry estimates are reasonable for clinical imaging.
C1 [Lindenberg, Liza; Turkbey, Ismail B.; Mertan, Francesca; Gonzalez, Esther Mena; Choyke, Peter] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Adler, Stephen; Ton, Anita] Leidos Biomed Res Inc, Clin Res Directorate, Clin Monitoring Res Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
   [Do, Khanh] Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Kummar, Shivaani] Stanford Univ, Sch Med, Palo Alto, CA 94304 USA.
   [Bhattacharyya, Sibaprasad] US FDA, Off Pharmaceut Qual, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
   [Jacobs, Paula M.] NCI, Canc Imaging Program, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); National Institutes of Health (NIH) - USA; NIH National Cancer
   Institute (NCI); Frederick National Laboratory for Cancer Research;
   Harvard University; Dana-Farber Cancer Institute; Stanford University;
   US Food & Drug Administration (FDA); National Institutes of Health (NIH)
   - USA; NIH National Cancer Institute (NCI)
RP Lindenberg, L (corresponding author), NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM liza.lindenberg@nih.gov
RI Jacobs, Paula/HHN-1964-2022; Choyke, Peter/C-8809-2011
FU National Cancer Institute, National Institutes of Health
   [HHSN261200800001E]
FX This project has been funded in whole or in part with federal funds from
   the National Cancer Institute, National Institutes of Health, under
   Contract No. HHSN261200800001E. The content of this publication does not
   necessarily reflect the views or policies of the Department of Health
   and Human Services, nor does mention of trade names, commercial
   products, or organizations imply endorsement by the U.S. Government. The
   authors wish to thank Dr Gary Griffiths and Dr G. Craig Hill for
   assistance in editing the manuscript.
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NR 16
TC 35
Z9 39
U1 0
U2 15
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 2017
VL 7
IS 4
BP 195
EP 203
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
WE Emerging Sources Citation Index (ESCI)
SC Radiology, Nuclear Medicine & Medical Imaging
GA FF9XN
UT WOS:000409372300006
PM 28913158
DA 2025-01-04
ER

PT J
AU Niu, LR
   Yang, WL
   Duan, LL
   Wang, XQ
   Li, YD
   Xu, CC
   Liu, C
   Zhang, YJ
   Zhou, W
   Liu, JQ
   Zhao, QC
   Hong, L
   Fan, DM
AF Niu, Liaoran
   Yang, Wanli
   Duan, Lili
   Wang, Xiaoqian
   Li, Yiding
   Xu, Chengchao
   Liu, Chao
   Zhang, Yujie
   Zhou, Wei
   Liu, Jinqiang
   Zhao, Qingchuan
   Hong, Liu
   Fan, Daiming
TI Biological Implications and Clinical Potential of Metastasis-Related
   miRNA in Colorectal Cancer
SO MOLECULAR THERAPY NUCLEIC ACIDS
LA English
DT Review
ID EPITHELIAL-MESENCHYMAL TRANSITION; ADENOMATOUS POLYPOSIS-COLI; INHIBITS
   TUMOR-GROWTH; LONG NONCODING RNAS; MOLECULAR-MECHANISMS; PATHOLOGICAL
   STAGE; LIVER METASTASIS; DOWN-REGULATION; MICRORNAS; PROMOTES
AB Colorectal cancer (CRC), ranking as the third commonest cancer, leads to extremely high rates of mortality. Metastasis is the major cause of poor outcome in CRC. When metastasis occurs, 5-year survival rates of patients decrease sharply, and strategies to enhance a patient's lifetime seem limited. MicroRNAs (miRNAs) are evolutionarily conserved small non-coding RNAs that are significantly involved in manipulation of CRC malignant phenotypes, including proliferation, invasion, and metastasis. To date, accumulating studies have revealed the mechanisms and functions of certain miRNAs in CRC metastasis. However, there is no systematic discussion about the biological implications and clinical potential (diagnostic role, prognostic role, and targeted therapy potential) of metastasis-related miRNAs in CRC. This review mainly summarizes the recent advances of miRNA-mediated metastasis in CRC. We also discuss the clinical values of metastasis-related miRNAs as potential biomarkers or therapeutic targets in CRC. Moreover, we envisage the future orientation and challenges in translating these findings into clinical applications.
C1 [Niu, Liaoran; Yang, Wanli; Duan, Lili; Wang, Xiaoqian; Li, Yiding; Zhang, Yujie; Zhou, Wei; Liu, Jinqiang; Zhao, Qingchuan; Hong, Liu; Fan, Daiming] Fourth Mil Med Univ, Xijing Hosp Digest Dis, State Key Lab Canc Biol, Xian 710032, Shaanxi, Peoples R China.
   [Niu, Liaoran; Yang, Wanli; Duan, Lili; Wang, Xiaoqian; Li, Yiding; Zhang, Yujie; Zhou, Wei; Liu, Jinqiang; Zhao, Qingchuan; Hong, Liu; Fan, Daiming] Fourth Mil Med Univ, Xijing Hosp Digest Dis, Natl Clin Res Ctr Digest Dis, Xian 710032, Shaanxi, Peoples R China.
   [Xu, Chengchao] 94719 Mil Hosp, Jian 343700, Jiangxi, Peoples R China.
   [Liu, Chao] Fourth Mil Med Univ, Sch Basic Med Sci, Xian 710032, Shaanxi, Peoples R China.
C3 Air Force Military Medical University; Air Force Military Medical
   University; Air Force Military Medical University
RP Hong, L (corresponding author), Fourth Mil Med Univ, Xijing Hosp Digest Dis, State Key Lab Canc Biol, Xian 710032, Shaanxi, Peoples R China.; Hong, L (corresponding author), Fourth Mil Med Univ, Xijing Hosp Digest Dis, Natl Clin Res Ctr Digest Dis, Xian 710032, Shaanxi, Peoples R China.
EM hongliufmmu@163.com
RI Xu, Chengchao/HJB-0692-2022
FU Scientific Foundation of Shaanxi Province [2019ZDLSF01-02-01,
   2018SF240]; National Clinical Research Center for Digestive Diseases
   [2015BAI13B07]; State Key Laboratory of Cancer Biology [CBSKL2014Z13]
FX This work was supported in part by grants from the Scientific Foundation
   of Shaanxi Province (nos. 2019ZDLSF01-02-01 and 2018SF240), the National
   Clinical Research Center for Digestive Diseases (no. 2015BAI13B07), and
   the State Key Laboratory of Cancer Biology (no. CBSKL2014Z13).
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NR 141
TC 38
Z9 41
U1 0
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 2162-2531
J9 MOL THER NUCL ACIDS
JI Mol. Ther. Nucl. Acids
PD MAR 5
PY 2021
VL 23
BP 42
EP 54
DI 10.1016/j.omtn.2020.10.030
PG 13
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA RB1FX
UT WOS:000631863200004
PM 33335791
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Garcia-Padilla, C
   Lozano-Velasco, E
   Muñoz-Gallardo, MD
   Castillo-Casas, JM
   Caño-Carrillo, S
   Martínez-Amaro, FJ
   García-López, V
   Aránega, A
   Franco, D
   García-Martínez, V
   López-Sánchez, C
AF Garcia-Padilla, Carlos
   Lozano-Velasco, Estefania
   del Mar Munoz-Gallardo, Maria
   Manuel Castillo-Casas, Juan
   Cano-Carrillo, Sheila
   Jose Martinez-Amaro, Francisco
   Garcia-Lopez, Virginio
   Aranega, Amelia
   Franco, Diego
   Garcia-Martinez, Virginio
   Lopez-Sanchez, Carmen
TI LncRNA H19 Impairs Chemo and Radiotherapy in Tumorigenesis
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE lncRNA H19; chemo-resistance; radio-resistance; tumorigenesis
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; LONG NONCODING RNAS; HUMAN
   GLIOMA-CELLS; COLORECTAL-CANCER; GENE-EXPRESSION; ERLOTINIB RESISTANCE;
   TARGETED THERAPY; UP-REGULATION; TEMOZOLOMIDE
AB Various treatments based on drug administration and radiotherapy have been devoted to preventing, palliating, and defeating cancer, showing high efficiency against the progression of this disease. Recently, in this process, malignant cells have been found which are capable of triggering specific molecular mechanisms against current treatments, with negative consequences in the prognosis of the disease. It is therefore fundamental to understand the underlying mechanisms, including the genes-and their signaling pathway regulators-involved in the process, in order to fight tumor cells. Long non-coding RNAs, H19 in particular, have been revealed as powerful protective factors in various types of cancer. However, they have also evidenced their oncogenic role in multiple carcinomas, enhancing tumor cell proliferation, migration, and invasion. In this review, we analyze the role of lncRNA H19 impairing chemo and radiotherapy in tumorigenesis, including breast cancer, lung adenocarcinoma, glioma, and colorectal carcinoma.
C1 [Garcia-Padilla, Carlos; Lozano-Velasco, Estefania; Garcia-Lopez, Virginio; Garcia-Martinez, Virginio; Lopez-Sanchez, Carmen] Univ Extremadura, Fac Med, Inst Mol Pathol Biomarkers, Dept Human Anat & Embryol, Badajoz 06006, Spain.
   [Garcia-Padilla, Carlos; Lozano-Velasco, Estefania; del Mar Munoz-Gallardo, Maria; Manuel Castillo-Casas, Juan; Cano-Carrillo, Sheila; Jose Martinez-Amaro, Francisco; Aranega, Amelia; Franco, Diego] Univ Jaen, Dept Expt Biol, Jaen 23071, Spain.
   [Lozano-Velasco, Estefania; Aranega, Amelia; Franco, Diego] Fdn Medina, Granada 18016, Spain.
C3 Universidad de Extremadura; Universidad de Jaen
RP Garcia-Padilla, C; López-Sánchez, C (corresponding author), Univ Extremadura, Fac Med, Inst Mol Pathol Biomarkers, Dept Human Anat & Embryol, Badajoz 06006, Spain.; Garcia-Padilla, C (corresponding author), Univ Jaen, Dept Expt Biol, Jaen 23071, Spain.
EM carlogp@unex.es; evelasco@ujaen.es; mmmg0012@red.ujaen.es;
   jmcc0028@red.ujaen.es; scano@ujaen.es; fmamaro@ujaen.es;
   garcialopez@unex.es; aaranega@ujaen.es; dfranco@ujaen.es;
   virginio@unex.es; clopez@unex.es
RI Garcia-Lopez, Virginio/KTI-8545-2024; Velasco, Estefanía/B-2209-2017;
   Lopez-Sanchez, Carmen/K-5458-2014; Garcia-Martinez,
   Virginio/K-5180-2014; Aranega, Amelia/AAA-8908-2019
OI Lozano Velasco, Estefania/0000-0002-5615-2754; Lopez-Sanchez,
   Carmen/0000-0003-3296-2071; Garcia-Padilla, Carlos/0000-0003-2061-3157;
   Garcia-Martinez, Virginio/0000-0002-7760-1985; Cano Carrillo,
   Sheila/0000-0002-3746-877X; Garcia-Lopez, Virginio/0000-0003-1489-7296;
   Castillo-Casas, Juan Manuel/0009-0005-0984-3543; Franco,
   Diego/0000-0002-5669-7164; Aranega, Amelia/0000-0002-0046-9410
FU Junta de Extremadura [IB18123, GR21174, CTS005]; FEDER [CTS-446]; Junta
   de Andalucia Regional Council
FX This work has been financed with research grants IB18123 (to C.L.-S.)
   and GR21174 (to V.G.-M., CTS005) from the Junta de Extremadura, with
   FEDER co-financing, and CTS-446 (to D.F. and A.A.) from the Junta de
   Andalucia Regional Council.
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NR 113
TC 8
Z9 10
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD AUG
PY 2022
VL 23
IS 15
AR 8309
DI 10.3390/ijms23158309
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 3T3EN
UT WOS:000840162100001
PM 35955440
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wu, C
AF Wu, Christina
TI Systemic Therapy for Colon Cancer
SO SURGICAL ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Irinotecan; Oxaliplatin; 5-fluorouracil; Antiepidermal growth factor
   receptor antibody; Vascular endothelial growth factor antibody;
   Immunotherapy; Regorafenib; Trifluridine/tipiracil
ID ADVANCED COLORECTAL-CANCER; SUBGROUP ANALYSES; ADJUVANT THERAPY;
   STAGE-II; MISMATCH-REPAIR; FLUOROURACIL; LEUCOVORIN; OXALIPLATIN;
   CHEMOTHERAPY; IRINOTECAN
AB Systemic treatments for patients with colon cancer has expanded broadly beyond 5-fluorouracil-based chemotherapy. For patients with early-stage colon cancer who are considering adjuvant chemotherapy, multiple factors such as the risk of disease recurrence, absolute survival benefit of chemotherapy, treatment toxicity, and patient comorbid medical conditions must be taken into account. In the metastatic setting, biomarkers such as KRAS/NRAS/BRAF mutation, microsatellite instability status, and left- versus right-sided colon cancer have helped oncologists to tailor systemic treatment regimens, which include chemotherapy, targeted therapy, and immunotherapy.
C1 [Wu, Christina] Winship Canc Inst, Dept Hematol Oncol, 1365-C Clifton Rd Northeast, Atlanta, GA 30322 USA.
RP Wu, C (corresponding author), Winship Canc Inst, Dept Hematol Oncol, 1365-C Clifton Rd Northeast, Atlanta, GA 30322 USA.
EM Christina.Wu@emoryhealthcare.org
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NR 22
TC 111
Z9 116
U1 0
U2 19
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1055-3207
EI 1558-5042
J9 SURG ONCOL CLIN N AM
JI Surg. Oncol. Clin. N. Am.
PD APR
PY 2018
VL 27
IS 2
BP 235
EP +
DI 10.1016/j.soc.2017.11.001
PG 9
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA GB5DQ
UT WOS:000429083000003
PM 29496087
DA 2025-01-04
ER

PT J
AU Woff, E
   Hendlisz, A
   Garcia, C
   Deleporte, A
   Delaunoit, T
   Maréchal, R
   Holbrechts, S
   Van den Eynde, M
   Demolin, G
   Vierasu, I
   Lhommel, R
   Gauthier, N
   Guiot, T
   Ameye, L
   Flamen, P
AF Woff, Erwin
   Hendlisz, Alain
   Garcia, Camilo
   Deleporte, Amelie
   Delaunoit, Thierry
   Marechal, Raphae
   Holbrechts, Stephane
   Van den Eynde, Marc
   Demolin, Gauthier
   Vierasu, Irina
   Lhommel, Renaud
   Gauthier, Namur
   Guiot, Thomas
   Ameye, Lieveke
   Flamen, Patrick
TI Monitoring metabolic response using FDG PET-CT during targeted therapy
   for metastatic colorectal cancer
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Article
DE Early metabolic response assessment; FDG PET-CT; Tumoral heterogeneity;
   Metastatic colorectal cancer; Targeted therapy
ID POSITRON-EMISSION-TOMOGRAPHY; REGORAFENIB BAY 73-4506; EARLY PREDICTION;
   TUMOR RESPONSE; 1ST-LINE CHEMOTHERAPY; LIVER METASTASES; GUIDELINES;
   LYMPHOMA; CRITERIA; FLARE
AB The introduction of targeted drugs has had a significant impact on the approach to assessing tumour response. These drugs often induce a rapid cytostatic effect associated with a less pronounced and slower tumoural volume reduction, thereby impairing the correlation between the absence of tumour shrinkage and the patient's unlikelihood of benefit. The aim of the study was to assess the predictive value of early metabolic response (mR) evaluation after one cycle, and its interlesional heterogeneity to a later metabolic and morphological response assessment performed after three cycles in metastatic colorectal cancer (mCRC) patients treated with combined sorafenib and capecitabine.
   This substudy was performed within the framework of a wider prospective multicenter study on the predictive value of early FDG PET-CT response assessment (SoMore study). A lesion-based response analysis was performed, including all measurable lesions identified on the baseline PET. On a per-patient basis, a descriptive 4-class response categorization was applied based upon the presence and proportion of non-responding lesions. For dichotomic response comparison, all patients with at least one resistant lesion were classified as non-responding.
   On baseline FDG PET-CT, 124 measurable "target" lesions were identified in 38 patients. Early mR assessments showed 18 patients (47 %) without treatment resistant lesions and 12 patients (32 %) with interlesional response heterogeneity. The NPV and PPV of early mR were 85 % (35/41) and 84 % (70/83), respectively, on a per-lesion basis and 95 % (19/20) and 72 % (13/18), respectively, on a dichotomized per-patient basis.
   Early mR assessment performed after one cycle of sorafenib-capecitabine in mCRC is highly predictive of non-response at a standard response assessment time. The high NPV (95 %) of early mR could be useful as the basis for early treatment discontinuation or adaptation to spare patients from exposure to non-effective drugs.
C1 [Woff, Erwin; Garcia, Camilo; Guiot, Thomas; Flamen, Patrick] Univ Libre Bruxelles, Inst Jules Bordet, Dept Nucl Med, 1 Rue Heger Bordet, B-1000 Brussels, Belgium.
   [Hendlisz, Alain; Deleporte, Amelie] Univ Libre Bruxelles, Inst Jules Bordet, Dept Med Oncol, Brussels, Belgium.
   [Delaunoit, Thierry] Jolimont Hosp, Dept Oncol, Haine St Paul, Belgium.
   [Marechal, Raphae] Univ Libre Bruxelles, Erasme Univ Hosp, Gastroenterol Medicosurg Dept, Brussels, Belgium.
   [Holbrechts, Stephane] CHU Ambroise Pare, Dept Oncol, Mons, Belgium.
   [Van den Eynde, Marc] Catholic Univ Louvain, Clin Univ St Luc, Dept Oncol, Brussels, Belgium.
   [Demolin, Gauthier] CHC St Joseph, Dept Gastroenterol, Liege, Belgium.
   [Vierasu, Irina] Univ Libre Bruxelles, Erasme Univ Hosp, Dept Nucl Med, Brussels, Belgium.
   [Lhommel, Renaud] Catholic Univ Louvain, Clin Univ St Luc, Dept Nucl Med, Brussels, Belgium.
   [Gauthier, Namur] CHC St Joseph, Dept Nucl Med, Liege, Belgium.
   [Ameye, Lieveke] Univ Libre Bruxelles, Inst Jules Bordet, Data Ctr Dept, Brussels, Belgium.
C3 Universite Libre de Bruxelles; Institut Jules Bordet; Universite
   Catholique Louvain; Cliniques Universitaires Saint-Luc; Universite Libre
   de Bruxelles; Institut Jules Bordet; Groupe Jolimont; Universite Libre
   de Bruxelles; Universite Catholique Louvain; Cliniques Universitaires
   Saint-Luc; Universite Catholique Louvain; Cliniques Universitaires
   Saint-Luc; Universite Libre de Bruxelles; Universite Catholique Louvain;
   Cliniques Universitaires Saint-Luc; Universite Libre de Bruxelles;
   Institut Jules Bordet; Universite Libre de Bruxelles
RP Woff, E (corresponding author), Univ Libre Bruxelles, Inst Jules Bordet, Dept Nucl Med, 1 Rue Heger Bordet, B-1000 Brussels, Belgium.
EM erwin.woff@bordet.be
RI Ameye, Lieveke/LWI-3661-2024; Woff, Erwin/ABH-1616-2020; Garcia,
   Camilo/HIZ-5830-2022
OI Woff, Erwin/0000-0001-9290-8929; Lhommel, Renaud/0000-0003-0668-6122;
   Ameye, Lieveke/0000-0001-5153-1766; hendlisz, alain/0000-0003-2122-1948
FU Jules Bordet Institute; Bayer
FX This academic work was supported and sponsored by the Jules Bordet
   Institute. The main study was financed by a research grant from Bayer.
   The results were presented at the EANM'14 - Annual Congress of the
   European Association of Nuclear Medicine as a poster presentation during
   the general poster session (abstract 2087).
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NR 38
TC 15
Z9 17
U1 0
U2 6
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 SEP
PY 2016
VL 43
IS 10
BP 1792
EP 1801
DI 10.1007/s00259-016-3365-x
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA DS3RJ
UT WOS:000380700100006
PM 27072811
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Tantoy, IY
   Dhruva, A
   Cataldo, J
   Venook, A
   Cooper, BA
   Paul, SM
   Levine, JD
   Conley, YP
   Cartwright, F
   Lee, K
   Wright, F
   Miaskowski, C
AF Tantoy, Ilufredo Y.
   Dhruva, Anand
   Cataldo, Janine
   Venook, Alan
   Cooper, Bruce A.
   Paul, Steven M.
   Levine, Jon D.
   Conley, Yvette P.
   Cartwright, Frances
   Lee, Kathryn
   Wright, Fay
   Miaskowski, Christine
TI Differences in symptom occurrence, severity, and distress ratings
   between patients with gastrointestinal cancers who received chemotherapy
   alone or chemotherapy with targeted therapy
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Gastrointestinal cancer; symptoms; chemotherapy (CTX); targeted therapy
   (TT)
ID QUALITY-OF-LIFE; METASTATIC COLORECTAL-CANCER; DISORDERS IDENTIFICATION
   TEST; ADVANCED GASTRIC-CANCER; PHASE-II TRIAL; INTERFERENCE MEASURES;
   1ST-LINE TREATMENT; ASSESSMENT SCALE; BEVACIZUMAB; PREVALENCE
AB Background: Approximately 28% of patients with gastrointestinal (GI) cancers will receive targeted therapy (TT) because of the associated increases in survival. Only four studies have examined the symptom experience of these patients. To date, no studies have evaluated for differences in symptom occurrence, severity, and distress between patients who received chemotherapy (CTX) alone (n=304) or CTX with TT (n=93).
   Methods: Patients completed self-report questionnaires, approximately one week after they received CTX. A modified version of the Memorial Symptom Assessment Scale (MSAS) was used to obtain data on symptom occurrence, severity, and distress. Binary logistic regression analyses were used to test for differences in symptom occurrence rates between the two treatment groups. Ordinal logistic regression analyses were used to test for differences in severity and distress ratings between the two treatment groups.
   Results: Patients who received CTX with TT were significantly younger (P=0.009); were diagnosed with cancer longer (P=0.004); had a higher number of prior treatments (P=0.024); had metastatic disease, specifically to the liver (P<0.001); had a diagnosis of anal, colon, rectum, or colorectal cancer (CRC) (P<0.001); and were positive for detection of B-Raf proto-oncogene, serine/threonine kinase (BRAF) and Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations (both P<0.001). In addition, CTX treatment regimens were significantly different between the two groups (P<0.001). After controlling for significant covariates, patients who received TT reported lower occurrence rates for lack of energy, cough, feeling drowsy, and difficulty sleeping (all, P<0.05). Patients who received TT reported lower severity scores for dry mouth (P=0.034) and change in the way food tastes (P=0.035). However, they reported higher severity scores for "I don't look like myself" (P=0.026). No differences in symptom distress scores were found between the two treatment groups.
   Conclusions: This study is the first to evaluate for differences in the symptom experience of GI cancer patients who received CTX alone or CTX with TT using a multidimensional symptom assessment scale. While between group differences in patients' symptom experiences were identified, both treatment groups warrant ongoing assessments to optimally manage their symptoms.
C1 [Tantoy, Ilufredo Y.; Cataldo, Janine; Cooper, Bruce A.; Paul, Steven M.; Lee, Kathryn; Miaskowski, Christine] Univ Calif San Francisco, Sch Nursing, Dept Physiol Nursing, San Francisco, CA 94143 USA.
   [Dhruva, Anand; Venook, Alan; Levine, Jon D.] Univ Calif San Francisco, Sch Med, Dept Med, San Francisco, CA USA.
   [Conley, Yvette P.] Univ Pittsburgh, Sch Nursing, Dept Hlth Promot & Dev, Pittsburgh, PA 15261 USA.
   [Cartwright, Frances] Mt Sinai Hosp, Dept Nursing, New York, NY 10029 USA.
   [Wright, Fay] Yale Univ, Sch Nursing, Dept Nursing & Acute Care Hlth Syst, New Haven, CT 06536 USA.
C3 University of California System; University of California San Francisco;
   University of California System; University of California San Francisco;
   Pennsylvania Commonwealth System of Higher Education (PCSHE); University
   of Pittsburgh; Icahn School of Medicine at Mount Sinai; Yale University
RP Miaskowski, C (corresponding author), Univ Calif San Francisco, Dept Physiol Nursing, 2 Koret Way,N631F, San Francisco, CA 94143 USA.
EM chris.miaskowski@ucsf.edu
RI Wright, Fay/AAH-9449-2020; Paul, Steve/ABE-5400-2020
OI Wright, Fay/0000-0001-9636-0411; Conley, Yvette/0000-0002-1784-6067;
   Levine, Jon/0000-0003-0681-5545; Tantoy, Ilufredo/0000-0002-0193-0280
FU National Cancer Institute (NCI) [CA134900]; K05 award from the NCI
   [CA168960]; National Institutes of Health (NIH) [T32NR007088]
FX This study was supported by a grant from the National Cancer Institute
   (NCI, CA134900). Dr. Christine Miaskowski is an American Cancer Society
   Clinical Research Professor and is funded by a K05 award from the NCI
   (CA168960). Mr. Tantoy is funded by a National Institutes of Health
   (NIH) T32 grant (T32NR007088).
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NR 60
TC 20
Z9 24
U1 0
U2 4
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 FEB
PY 2017
VL 8
IS 1
BP 109
EP 126
DI 10.21037/jgo.2017.01.09
PG 18
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA EP5HI
UT WOS:000397409200022
PM 28280616
OA Green Published
DA 2025-01-04
ER

PT J
AU Fusco, N
   Bosari, S
AF Fusco, Nicola
   Bosari, Silvano
TI <i>HER2</i> aberrations and heterogeneity in cancers of the digestive
   system: Implications for pathologists and gastroenterologists
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE HER2; Digestive system; Gastrointestinal tract; Gastric cancer; Colon
   cancer; Esophageal cancer; Gastroesophageal junction cancer; Biliary
   tract cancer; Gallbladder cancer; Liver cancer; Pancreas cancer
ID GROWTH-FACTOR RECEPTOR; IN-SITU HYBRIDIZATION; ADVANCED
   HEPATOCELLULAR-CARCINOMA; MOLECULAR TARGETED THERAPY; DIGITAL
   IMAGE-ANALYSIS; C-ERB B2; GASTRIC-CANCER; BILIARY-TRACT; BREAST-CANCER;
   PROGNOSTIC-SIGNIFICANCE
AB Management of cancers of the digestive system has progressed rapidly into the molecular era. Despite the significant recent achievements in the diagnosis and treatment of these patients, the number of deaths for these tumors has currently plateaued. Many investigations have assessed the role of HER2 in tumors of the digestive system in both prognostic and therapeutic settings, with heterogeneous results. Novel testing and treatment guidelines are emerging, in particular in gastric and colorectal cancers. However, further advances are needed. In this review we provide a comprehensive overview of the current state-of-knowledge of HER2 alterations in the most common tumors of the digestive system and discuss the operational implications of HER2 testing.
C1 [Fusco, Nicola; Bosari, Silvano] Fdn IRCCS Ca Granda, Osped Maggiore Policlin, Div Pathol, Via Francesco Sforza 35, I-20122 Milan, Italy.
   [Fusco, Nicola; Bosari, Silvano] Univ Milan, Dept Pathophysiol & Organ Transplantat, I-20122 Milan, Italy.
C3 IRCCS Ca Granda Ospedale Maggiore Policlinico; University of Milan
RP Bosari, S (corresponding author), Fdn IRCCS Ca Granda, Osped Maggiore Policlin, Div Pathol, Via Francesco Sforza 35, I-20122 Milan, Italy.
EM silvano.bosari@unimi.it
RI Bosari, Silvano/K-7744-2016; Fusco, Nicola/D-6264-2016
OI Bosari, Silvano/0000-0002-9744-6951; Fusco, Nicola/0000-0002-9101-9131
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NR 117
TC 37
Z9 37
U1 0
U2 7
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD SEP 21
PY 2016
VL 22
IS 35
BP 7926
EP 7937
DI 10.3748/wjg.v22.i35.7926
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DW9LT
UT WOS:000383981800006
PM 27672288
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Amann, A
AF Amann, A.
TI ESMO 2019-personal highlights in gastrointestinal cancer
SO MEMO-MAGAZINE OF EUROPEAN MEDICAL ONCOLOGY
LA English
DT Review
DE Molecular phenotyping; Targeted therapy; ESMO meeting 2019;
   Gastrointestinal cancer; Precision medicine
ID PHASE-III; IDEA-FRANCE
AB This article summarizes important highlights regarding gastrointestinal cancer at the 2019 ESMO annual meeting. The choice of the abstracts was based on a personal view with a focus on different tumor entities of the gastrointestinal tract. Precision-medicine-guided therapy for cancer entities was one of the main topics at this year's ESMO. Furthermore, circulating tumor DNA (ctDNA) by performing liquid biopsy was again another hot topic, especially in guiding adjuvant chemotherapy in stage III colorectal cancer (CRC) patients. Finally, hope was stirred up again for immunotherapy in the indication of first-line treatment in nonresectable hepatocellular cancer (HCC). In summary, the astonishing progress in new drugs that has been made in recent years is still ongoing and will lead to better treatment for cancer patients.
C1 [Amann, A.] Med Univ Innsbruck, Dept Hematol & Oncol, Internal Med 5, Anichstr 35, A-6020 Innsbruck, Austria.
C3 Medical University of Innsbruck
RP Amann, A (corresponding author), Med Univ Innsbruck, Dept Hematol & Oncol, Internal Med 5, Anichstr 35, A-6020 Innsbruck, Austria.
EM arno.amann@tirol-kliniken.at
RI Amann, Arno/LRU-5258-2024
FU University of Innsbruck; Medical University of Innsbruck
FX Open access funding provided by University of Innsbruck and Medical
   University of Innsbruck.
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   Tabernero J, 2019, ANN ONCOL, V30, P868
   Taieb J, 2019, ANN ONCOL, V30, P867
   Vogel A, 2019, ANN ONCOL, V30, P876
NR 7
TC 1
Z9 1
U1 0
U2 1
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 1865-5041
EI 1865-5076
J9 MEMO-MAG EUR MED ONC
JI Memo-Mag. Eur. Med. Oncol.
PD JUN
PY 2020
VL 13
IS 2
BP 154
EP 156
DI 10.1007/s12254-020-00603-2
EA APR 2020
PG 3
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA LV2CA
UT WOS:000528502600001
OA hybrid
DA 2025-01-04
ER

PT J
AU Hu, AN
   Wang, H
   Xu, QQ
   Pan, YQ
   Jiang, ZY
   Li, S
   Qu, Y
   Hu, YL
   Wu, H
   Wang, XZ
AF Hu, Anni
   Wang, Hang
   Xu, Qianqian
   Pan, Yuqi
   Jiang, Zeyu
   Li, Sheng
   Qu, Yi
   Hu, Yili
   Wu, Hao
   Wang, Xinzhi
TI A novel CPT1A covalent inhibitor modulates fatty acid oxidation and
   CPT1A-VDAC1 axis with therapeutic potential for colorectal cancer
SO REDOX BIOLOGY
LA English
DT Article
DE Colorectal cancer; 26-Dihydroxypeperomin B; CPT1A; Covalent inhibitor;
   VDAC1
ID LIPID-METABOLISM; CYTOCHROME-C; OLIGOMERIZATION; RELEASE; TARGET
AB Colorectal cancer (CRC) is a common and deadly disease of the digestive system, but its targeted therapy is hampered by the lack of reliable and specific biomarkers. Hence, discovering new therapeutic targets and agents for CRC is an urgent and challenging task. Here we report that carnitine palmitoyltransferase 1A (CPT1A), a mitochondrial enzyme that catalyzes fatty acid oxidation (FAO), is a potential target for CRC treatment. We show that CPT1A is overexpressed in CRC cells and that its inhibition by a secolignan-type compound, 2,6-dihydrox-ypeperomin B (DHP-B), isolated from the plant Peperomia dindygulensis, suppresses tumor cell growth and in-duces apoptosis. We demonstrate that DHP-B covalently binds to Cys96 of CPT1A, blocks FAO, and disrupts the mitochondrial CPT1A-VDAC1 interaction, leading to increased mitochondrial permeability and reduced oxygen consumption and energy metabolism in CRC cells. We also reveal that CPT1A expression correlates with the survival of tumor-bearing animals and that DHP-B exhibits anti-CRC activity in vitro and in vivo. Our study uncovers the molecular mechanism of DHP-B as a novel CPT1A inhibitor and provides a rationale for its pre-clinical development as well as a new strategy for CRC targeted therapy.
C1 [Hu, Anni; Wang, Hang; Xu, Qianqian; Pan, Yuqi; Jiang, Zeyu; Li, Sheng; Qu, Yi; Wu, Hao; Wang, Xinzhi] Nanjing Univ Chinese Med, Coll Pharm, Xianlin Ave 138, Nanjing 210046, Peoples R China.
   [Hu, Anni; Wang, Hang; Xu, Qianqian; Pan, Yuqi; Jiang, Zeyu; Li, Sheng; Qu, Yi; Wang, Xinzhi] Jiangsu Key Lab Res & Dev Marine Bioresource Pharm, Nanjing 210046, Peoples R China.
   [Hu, Yili] Nanjing Univ Chinese Med, Expt Ctr Sci & Technol, Nanjing 210046, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University of Chinese
   Medicine
RP Wang, XZ (corresponding author), Nanjing Univ Chinese Med, Coll Pharm, Xianlin Ave 138, Nanjing 210046, Peoples R China.
EM xinzhiwang@njucm.edu.cn
RI Hu, Yili/HLG-3795-2023
FU National Natural Science Foundation of China [82074067]
FX This work was supported by grants from the National Natural Science
   Foundation of China (82074067) .
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Z9 3
U1 3
U2 9
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2213-2317
J9 REDOX BIOL
JI Redox Biol.
PD DEC
PY 2023
VL 68
AR 102959
DI 10.1016/j.redox.2023.102959
EA NOV 2023
PG 19
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA FZ6V1
UT WOS:001149724800001
PM 37977042
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sirvent, A
   Lafitte, M
   Roche, S
AF Sirvent, Audrey
   Lafitte, Marie
   Roche, Serge
TI DDR1 inhibition as a new therapeutic strategy for colorectal cancer
SO MOLECULAR & CELLULAR ONCOLOGY
LA English
DT Article
DE colorectal cancer; invasion; metastasis; DDR1 tyrosine kinase receptor;
   collagen; targeted therapy; nilotinib
ID BCR-ABL
AB The clinical management of metastatic colorectal cancer (mCRC) is still a major challenge. Recently, we discovered that nilotinib, an approved treatment for chronic myeloid leukaemia, inhibits invasive and metastatic properties of CRC cells by targeting the kinase activity of receptor for collagens DDR1 (Discoidin Domain Receptor tyrosine kinase 1), suggesting that nilotinib could be an effective strategy to treat mCRC.
C1 [Sirvent, Audrey; Lafitte, Marie; Roche, Serge] Univ Montpellier, CNRS, Ctr Rech Biol Cellulaire Montpellier CRBM, 1919 Route Mende, F-34293 Montpellier, France.
C3 Universite de Montpellier; Centre National de la Recherche Scientifique
   (CNRS)
RP Sirvent, A (corresponding author), Univ Montpellier, CNRS, Ctr Rech Biol Cellulaire Montpellier CRBM, 1919 Route Mende, F-34293 Montpellier, France.
EM audrey.sirvent@crbm.cnrs.fr; marie.lafitte@crbm.cnrs.fr;
   serge.roche@crbm.cnrs.fr
OI roche, serge/0000-0003-3413-3859
FU ARC (Association pour la Recherche sur le Cancer); Montpellier SIRIC
   (Site de Recherche Integree sur le Cancer; INCa-DGOS-Inserm grant);
   Ligue Nationale contre le Cancer; Fondation de France; CNRS (Centre
   National de la Recherche Scientifique); University of Montpellier
FX This work was supported by ARC (Association pour la Recherche sur le
   Cancer), Montpellier SIRIC (Site de Recherche Integree sur le Cancer;
   INCa-DGOS-Inserm 6045 grant), Ligue Nationale contre le Cancer,
   Fondation de France, CNRS (Centre National de la Recherche Scientifique)
   and the University of Montpellier.
CR Ambrogio C, 2016, ESMO OPEN, V1, DOI 10.1136/esmoopen-2016-000076
   Gao H, 2016, CELL, V166, P47, DOI 10.1016/j.cell.2016.06.009
   Grillet F, 2017, GUT, V66, P1802, DOI 10.1136/gutjnl-2016-311447
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NR 10
TC 15
Z9 17
U1 0
U2 4
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 2372-3556
EI 2372-3548
J9 MOL CELL ONCOL
JI MOL. CELL ONCOL.
PY 2018
VL 5
IS 4
AR e1465882
DI 10.1080/23723556.2018.1465882
PG 3
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA GT6GN
UT WOS:000444608900007
PM 30250919
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Parikh, AR
   Leshchiner, I
   Elagina, L
   Goyal, L
   Levovitz, C
   Siravegna, G
   Livitz, D
   Rhrissorrakrai, K
   Martin, EE
   Van Seventer, EE
   Hanna, M
   Slowik, K
   Utro, F
   Pinto, CJ
   Wong, A
   Danysh, BP
   de la Cruz, FF
   Fetter, IJ
   Nadres, B
   Shahzade, HA
   Allen, JN
   Blaszkowsky, LS
   Clark, JW
   Giantonio, B
   Murphy, JE
   Nipp, RD
   Roeland, E
   Ryan, DP
   Weekes, CD
   Kwak, EL
   Faris, JE
   Wo, JY
   Aguet, F
   Dey-Guha, I
   Hazar-Rethinam, M
   Dias-Santagata, D
   Ting, DT
   Zhu, AX
   Hong, TS
   Golub, TR
   Iafrate, AJ
   Adalsteinsson, VA
   Bardelli, A
   Parida, L
   Juric, D
   Getz, G
   Corcoran, RB
AF Parikh, Aparna R.
   Leshchiner, Ignaty
   Elagina, Liudmila
   Goyal, Lipika
   Levovitz, Chaya
   Siravegna, Giulia
   Livitz, Dimitri
   Rhrissorrakrai, Kahn
   Martin, Elizabeth E.
   Van Seventer, Emily E.
   Hanna, Megan
   Slowik, Kara
   Utro, Filippo
   Pinto, Christopher J.
   Wong, Alicia
   Danysh, Brian P.
   de la Cruz, Ferran Fece
   Fetter, Isobel J.
   Nadres, Brandon
   Shahzade, Heather A.
   Allen, Jill N.
   Blaszkowsky, Lawrence S.
   Clark, Jeffrey W.
   Giantonio, Bruce
   Murphy, Janet E.
   Nipp, Ryan D.
   Roeland, Eric
   Ryan, David P.
   Weekes, Colin D.
   Kwak, Eunice L.
   Faris, Jason E.
   Wo, Jennifer Y.
   Aguet, Francois
   Dey-Guha, Ipsita
   Hazar-Rethinam, Mehlika
   Dias-Santagata, Dora
   Ting, David T.
   Zhu, Andrew X.
   Hong, Theodore S.
   Golub, Todd R.
   Iafrate, A. John
   Adalsteinsson, Viktor A.
   Bardelli, Alberto
   Parida, Laxmi
   Juric, Dejan
   Getz, Gad
   Corcoran, Ryan B.
TI Liquid versus tissue biopsy for detecting acquired resistance and tumor
   heterogeneity in gastrointestinal cancers
SO NATURE MEDICINE
LA English
DT Article
ID ANTI-EGFR THERAPY; COLORECTAL-CANCER; TARGETED THERAPY; INTRATUMOR
   HETEROGENEITY; GENOMIC LANDSCAPE; EVOLUTION; BLOCKADE; DNA; INHIBITION;
   MUTATIONS
AB During cancer therapy, tumor heterogeneity can drive the evolution of multiple tumor subclones harboring unique resistance mechanisms in an individual patient(1-3). Previous case reports and small case series have suggested that liquid biopsy (specifically, cell-free DNA (cfDNA)) may better capture the heterogeneity of acquired resistance(4-8). However, the effectiveness of cfDNA versus standard single-lesion tumor biopsies has not been directly compared in larger-scale prospective cohorts of patients following progression on targeted therapy. Here, in a prospective cohort of 42 patients with molecularly defined gastrointestinal cancers and acquired resistance to targeted therapy, direct comparison of post-progression cfDNA versus tumor biopsy revealed that cfDNA more frequently identified clinically relevant resistance alterations and multiple resistance mechanisms, detecting resistance alterations not found in the matched tumor biopsy in 78% of cases. Whole-exome sequencing of serial cfDNA, tumor biopsies and rapid autopsy specimens elucidated substantial geographic and evolutionary differences across lesions. Our data suggest that acquired resistance is frequently characterized by profound tumor heterogeneity, and that the emergence of multiple resistance alterations in an individual patient may represent the 'rule' rather than the 'exception'. These findings have profound therapeutic implications and highlight the potential advantages of cfDNA over tissue biopsy in the setting of acquired resistance.
C1 [Parikh, Aparna R.; Goyal, Lipika; Van Seventer, Emily E.; Pinto, Christopher J.; de la Cruz, Ferran Fece; Fetter, Isobel J.; Nadres, Brandon; Shahzade, Heather A.; Allen, Jill N.; Blaszkowsky, Lawrence S.; Clark, Jeffrey W.; Giantonio, Bruce; Murphy, Janet E.; Nipp, Ryan D.; Roeland, Eric; Ryan, David P.; Weekes, Colin D.; Kwak, Eunice L.; Faris, Jason E.; Wo, Jennifer Y.; Dey-Guha, Ipsita; Hazar-Rethinam, Mehlika; Dias-Santagata, Dora; Ting, David T.; Zhu, Andrew X.; Hong, Theodore S.; Iafrate, A. John; Juric, Dejan; Getz, Gad; Corcoran, Ryan B.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
   [Parikh, Aparna R.; Goyal, Lipika; Van Seventer, Emily E.; Pinto, Christopher J.; de la Cruz, Ferran Fece; Fetter, Isobel J.; Nadres, Brandon; Shahzade, Heather A.; Allen, Jill N.; Blaszkowsky, Lawrence S.; Clark, Jeffrey W.; Giantonio, Bruce; Murphy, Janet E.; Nipp, Ryan D.; Roeland, Eric; Ryan, David P.; Weekes, Colin D.; Kwak, Eunice L.; Faris, Jason E.; Wo, Jennifer Y.; Dey-Guha, Ipsita; Hazar-Rethinam, Mehlika; Dias-Santagata, Dora; Ting, David T.; Zhu, Andrew X.; Hong, Theodore S.; Iafrate, A. John; Juric, Dejan; Getz, Gad; Corcoran, Ryan B.] Harvard Med Sch, Dept Med, Boston, MA 02115 USA.
   [Leshchiner, Ignaty; Elagina, Liudmila; Livitz, Dimitri; Martin, Elizabeth E.; Hanna, Megan; Slowik, Kara; Wong, Alicia; Danysh, Brian P.; Aguet, Francois; Golub, Todd R.; Adalsteinsson, Viktor A.; Getz, Gad] Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.
   [Levovitz, Chaya; Rhrissorrakrai, Kahn; Utro, Filippo; Parida, Laxmi] IBM Res, Yorktown Hts, NY USA.
   [Siravegna, Giulia; Bardelli, Alberto] Candiolo Canc Inst, Turin, Italy.
   [Siravegna, Giulia; Bardelli, Alberto] Univ Torino, Dept Oncol, Turin, Italy.
   [Golub, Todd R.] Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Golub, Todd R.] Howard Hughes Med Inst, Boston, MA 02115 USA.
   [Getz, Gad] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
C3 Harvard University; Massachusetts General Hospital; Harvard University;
   Harvard Medical School; Harvard University; Massachusetts Institute of
   Technology (MIT); Broad Institute; International Business Machines
   (IBM); IRCCS Fondazione del Piemonte per l'Oncologia; University of
   Turin; Harvard University; Dana-Farber Cancer Institute; Howard Hughes
   Medical Institute; Harvard University; Massachusetts General Hospital
RP Getz, G; Corcoran, RB (corresponding author), Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.; Getz, G; Corcoran, RB (corresponding author), Harvard Med Sch, Dept Med, Boston, MA 02115 USA.; Getz, G (corresponding author), Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.; Getz, G (corresponding author), Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
EM gadgetz@broadinstitute.org; rbcorcoran@partners.org
RI Juric, Dejan/C-5214-2008; Siravegna, Giulia/Z-2826-2019; Wo,
   Jennifer/Y-6074-2018; Getz, Gad/ABW-5118-2022; Roeland,
   Eric/N-4229-2019; BARDELLI, Alberto/J-9721-2018; Ting, David/F-4389-2017
OI Leshchiner, Ignaty/0000-0001-8942-9265; Fece de la Cruz,
   Ferran/0000-0003-2694-4838; Danysh, Brian/0000-0001-6839-6337; Livitz,
   Dimitri/0000-0003-2528-1446; Fetter, Isobel/0000-0002-6021-2713;
   Roeland, Eric/0000-0002-3674-3573; BARDELLI,
   Alberto/0000-0003-1647-5070; Ting, David/0000-0002-3261-2322
FU NIH/NCI [CA127003, R01CA208437, K08CA166510, U54CA224068]; Damon Runyon
   Clinical Investigator Award; Stand Up To Cancer Colorectal Dream Team
   Translational Research Grant [SU2C-AACR-DT22-17]; Broad/IBM Cancer
   Resistance Research Project; Susan Eid Tumor Heterogeneity Initiative;
   FONDAZIONE AIRC [21091, 16788]; AIRC [21923]; AIRC-CRUK-FC AECC
   Accelerator Award [22795]; European Community [602901 MErCuRIC, 635342-2
   MoTriColor, 115749 CANCER-ID]; Ministero della Salute
   [NET-2011-02352137]; Fondazione Piemontese per la Ricerca sul
   Cancro-ONLUS 5 per Mille 2014; 2015 Ministero della Salute; Roche; AIRC
FX This work is partially supported by the NIH/NCI Gastrointestinal Cancer
   Specialized Program of Research Excellence P50 (CA127003, R01CA208437,
   K08CA166510 and U54CA224068), a Damon Runyon Clinical Investigator Award
   and a Stand Up To Cancer Colorectal Dream Team Translational Research
   Grant (grant number SU2C-AACR-DT22-17 to R.B.C.). Research grants are
   administered by the American Association of Cancer Research, the
   scientific partners of Stand Up To Cancer. The work is partially
   supported by the Broad/IBM Cancer Resistance Research Project (G.G. and
   L.P.) and the Susan Eid Tumor Heterogeneity Initiative (D.J.). The
   research leading to these results has received funding from FONDAZIONE
   AIRC under 5 per Mille 2018 ID. 21091 program - P. I. Bardelli Alberto.
   The research leading to these results has received funding from
   FONDAZIONE AIRC: AIRC Investigator Grant 2015 - ID. 16788; AIRC
   Investigator Grant 2018 - ID. 21923; AIRC-CRUK-FC AECC Accelerator Award
   - contract 22795. This work was also supported by the European
   Community's Seventh Framework Programme (grant agreement number 602901
   MErCuRIC), H2020 (grant agreement number 635342-2 MoTriColor), IMI
   (contract number 115749 CANCER-ID), Ministero della Salute (project
   NET-2011-02352137) and Fondazione Piemontese per la Ricerca sul
   Cancro-ONLUS 5 per Mille 2014 and 2015 Ministero della Salute. G.S. was
   funded by a Roche per la Ricerca grant (2017) and AIRC three-year
   fellowship (2017).
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NR 47
TC 343
Z9 360
U1 2
U2 102
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD SEP
PY 2019
VL 25
IS 9
BP 1415
EP +
DI 10.1038/s41591-019-0561-9
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA IW2TC
UT WOS:000484832800025
PM 31501609
OA Green Accepted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Grassilli, E
   Cerrito, MG
AF Grassilli, Emanuela
   Cerrito, Maria Grazia
TI Emerging actionable targets to treat therapy-resistant colorectal
   cancers
SO CANCER DRUG RESISTANCE
LA English
DT Review
DE Colorectal cancer; resistance; chemotherapy; target therapy; EGFR;
   ERBB2; MET; BRAF; kinase inhibitors; immune checkpoint inhibitors; gut
   microbiota
ID EGFR MONOCLONAL-ANTIBODIES; WILD-TYPE KRAS; COLON-CANCER;
   DRUG-RESISTANCE; ACQUIRED-RESISTANCE; MISMATCH REPAIR; PHASE-II;
   THYMIDYLATE SYNTHASE; TUMOR RESISTANCE; COMBINED BRAF
AB In the last two decades major improvements have been reached in the early diagnosis of colorectal cancer ( CRC) and, besides chemotherapy, an ampler choice of therapeutic approaches is now available, including targeted and immunotherapy. Despite that, CRC remains a "big killer" mainly due to the development of resistance to therapies, especially when the disease is diagnosed after it is already metastatic. At the same time, our knowledge of the mechanisms underlying resistance has been rapidly expanding which allows the development of novel therapeutic options in order to overcome it. As far as resistance to chemotherapy is concerned, several contributors have been identified such as: intake/efflux systems upregulation; alterations in the DNA damage response, due to defect in the DNA checkpoint and repair systems; dysregulation of the expression of apoptotic/anti-apoptotic members of the BCL2 family; overexpression of oncogenic kinases; the presence of cancer stem cells; and the composition of the tumoral microenvironment and that of the gut microbiota. Interestingly, several mechanisms are also involved in the resistance to targeted and/or immunotherapy. For example, overexpression and/or hyperactivation and/or amplification of oncogenic kinases can sustain resistance to targeted therapy whereas the composition of the gut microbiota, as well as that of the tumoral niche, and defects in DNA repair systems are crucial for determining the response to immunotherapy. In this review we will make an overview of the main resistance mechanisms identified so far and of the new therapeutic approaches to overcome it.
C1 [Grassilli, Emanuela; Cerrito, Maria Grazia] Univ Milano Bicocca, Dept Med & Surg, Via Cadore 48, I-20900 Monza, Italy.
C3 University of Milano-Bicocca
RP Grassilli, E (corresponding author), Univ Milano Bicocca, Dept Med & Surg, Via Cadore 48, I-20900 Monza, Italy.
EM emanuela.grassilli@unimib.it
RI Cerrito, Maria/AAA-1190-2019; grassilli, emanuela/L-7296-2013
OI grassilli, emanuela/0000-0001-5387-5925; Cerrito, Maria
   Grazia/0000-0002-3347-5817
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NR 174
TC 16
Z9 16
U1 1
U2 6
PU OAE PUBLISHING INC
PI ALHAMBRA
PA 245 E MAIN ST, ST122, ALHAMBRA, CA 91801 USA
EI 2578-532X
J9 CANCER DRUG RESIST
JI Cancer Drug Resist.
PY 2022
VL 5
IS 1
BP 36
EP 63
DI 10.20517/cdr.2021.96
PG 28
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA 4H1FC
UT WOS:000849626900004
PM 35582524
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Maity, P
   Halder, A
   Ghosh, R
   Chatterjee, U
   Barman, S
   Sarkar, R
AF Maity, Priyanka
   Halder, Aniket
   Ghosh, Ranajoy
   Chatterjee, Uttara
   Barman, Shibsankar
   Sarkar, Ruchirendra
TI Immunohistochemistry as a Surrogate Marker of Underlying Molecular
   Derangements in Sporadic Colorectal Carcinoma in Children - A Series of
   Three Cases
SO FETAL AND PEDIATRIC PATHOLOGY
LA English
DT Article
DE IHC; pediatric tumors; colorectal carcinoma; BRAF; MSI
ID COLON; ADENOCARCINOMA; FEATURES
AB Background:Colorectal carcinomas (CRCs) are uncommon tumors in children. Here, we elucidate three cases of childhood CRCs with their underlying molecular derangements using immunohistochemistry (IHC) with emphasis on BRAF mutation.Case summary:All three CRCs were sporadic tumors involving the left colon with two of them having a mucinous phenotype. We performed IHC for BRAF, p53 and beta-catenin along with markers of microsatellite instability (MSI) in all three tumors. All the tumors had diffuse strong cytoplasmic BRAF positivity, with focal p53 positivity in two cases and cytoplasmic beta-catenin staining in one case. One case showed CpG island hypermethylation with isolated loss of PMS2 staining. None of the cases had any family history of CRC.Conclusions:IHC can be used as a surrogate marker for determining the underlying molecular derangements in CRC. Sporadic CRCs in children are a cumulative effect of multiple mutations, of which BRAF mutation is significant and critical for planning targeted therapy.
C1 [Maity, Priyanka; Chatterjee, Uttara] Inst Postgrad Med Educ & Res, Dept Pathol, Kolkata, India.
   [Halder, Aniket; Ghosh, Ranajoy] Inst Postgrad Med Educ & Res, Dept GI Pathol, Kolkata, India.
   [Barman, Shibsankar; Sarkar, Ruchirendra] Inst Postgrad Med Educ & Res, Dept Pediat Surg, Kolkata, India.
C3 Institute of Post Graduate Medical Education & Research (IPGMER),
   Kolkata; Institute of Post Graduate Medical Education & Research
   (IPGMER), Kolkata; Institute of Post Graduate Medical Education &
   Research (IPGMER), Kolkata
RP Halder, A (corresponding author), Inst Postgrad Med Educ & Res, Dept GI Pathol, Kolkata, India.
EM aniket.halder@gmail.com
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NR 16
TC 1
Z9 1
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1551-3815
EI 1551-3823
J9 FETAL PEDIATR PATHOL
JI Fetal Pediatr. Pathol.
PD FEB 7
PY 2022
VL 41
IS 1
BP 98
EP 106
DI 10.1080/15513815.2020.1765918
EA MAY 2020
PG 9
WC Pathology; Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Pediatrics
GA YU1DV
UT WOS:000539146900001
PM 32441577
DA 2025-01-04
ER

PT J
AU Mo, YZ
   Wang, YM
   Zhang, LS
   Yang, LT
   Zhou, M
   Li, XL
   Li, Y
   Li, GY
   Zeng, ZY
   Xiong, W
   Xiong, F
   Guo, C
AF Mo, Yongzhen
   Wang, Yumin
   Zhang, Lishen
   Yang, Liting
   Zhou, Ming
   Li, Xiaoling
   Li, Yong
   Li, Guiyuan
   Zeng, Zhaoyang
   Xiong, Wei
   Xiong, Fang
   Guo, Can
TI The role of Wnt signaling pathway in tumor metabolic reprogramming
SO JOURNAL OF CANCER
LA English
DT Review
DE tumor metabolic reprogramming; Wnt signaling; targeted therapy
ID PENTOSE-PHOSPHATE PATHWAY; CANCER STEM-CELL; T-CELL; NASOPHARYNGEAL
   CARCINOMA; COLORECTAL-CANCER; C-MYC; GLUCOSE-METABOLISM;
   LIPID-METABOLISM; BREAST-CANCER; MITOCHONDRIAL DYNAMICS
AB The occurrence and development of tumors is a complex process involving long-term multi-factor participation. In this process, tumor cells from a set of abnormal metabolic patterns that are different from normal cells. This abnormal metabolic change is called metabolic reprogramming of tumors. Wnt signaling pathway is one of the critical signaling pathways regulating cell proliferation and differentiation. In recent years, it has been found that Wnt signaling participates in the occurrence and development of malignant tumors by affecting metabolic reprogramming. This paper reviews the role of Wnt signaling in tumor metabolic reprogramming to provide crucial theoretical guidance for targeted therapy and drug response of tumors.
C1 [Mo, Yongzhen; Wang, Yumin; Yang, Liting; Zhou, Ming; Li, Guiyuan; Zeng, Zhaoyang; Xiong, Wei; Xiong, Fang; Guo, Can] Cent South Univ, Xiangya Hosp, Dept Neurosurg, NHC Key Lab Carcinogenesis, Changsha 410078, Hunan, Peoples R China.
   [Mo, Yongzhen; Wang, Yumin; Zhang, Lishen; Zhou, Ming; Li, Xiaoling; Li, Guiyuan; Zeng, Zhaoyang; Xiong, Wei; Xiong, Fang; Guo, Can] Cent South Univ, Chinese Minist Educ, Canc Res Inst, Key Lab Carcinogenesis & Canc Invas, Changsha 410078, Hunan, Peoples R China.
   [Mo, Yongzhen; Wang, Yumin; Zhang, Lishen; Zhou, Ming; Li, Xiaoling; Li, Guiyuan; Zeng, Zhaoyang; Xiong, Wei; Xiong, Fang; Guo, Can] Cent South Univ, Sch Basic Med Sci, Changsha 410078, Hunan, Peoples R China.
   [Mo, Yongzhen; Zhou, Ming; Li, Guiyuan; Zeng, Zhaoyang; Xiong, Wei; Xiong, Fang; Guo, Can] Cent SouthUniv, Hunan Key Lab Nonresolving Inflammat & Canc, Dis Genome Res Ctr, Xiangya Hosp 3, Changsha, Hunan, Peoples R China.
   [Li, Yong] Cleveland Clin, Lerner Res Inst, Dept Canc Biol, Cleveland, OH 44195 USA.
C3 Central South University; Central South University; Central South
   University; Central South University; Cleveland Clinic Foundation
RP Xiong, F; Guo, C (corresponding author), Cent South Univ, Xiangya Hosp, Dept Neurosurg, NHC Key Lab Carcinogenesis, Changsha 410078, Hunan, Peoples R China.; Xiong, F; Guo, C (corresponding author), Cent South Univ, Key Lab Carcinogenesis & Canc Invas, Chinese Minist Educ, Canc Res Inst, Changsha 410078, Hunan, Peoples R China.; Xiong, F; Guo, C (corresponding author), Cent South Univ, Sch Basic Med Sci, Changsha 410078, Hunan, Peoples R China.; Xiong, F; Guo, C (corresponding author), Cent SouthUniv, Hunan Key Lab Nonresolving Inflammat & Canc, Dis Genome Res Ctr, Xiangya Hosp 3, Changsha, Hunan, Peoples R China.
EM xiongf@csu.edu.cn; guocde@csu.edu.cn
RI Li, Ye/JBS-2949-2023; chen, yuying/JNS-9778-2023; Wang,
   Yumin/C-9551-2014; Zeng, Zhaoyang/LLL-3057-2024; li,
   yuanyuan/GZA-4435-2022; xiong, wei/GXZ-9586-2022
OI Li, Yong/0000-0001-8838-1714
FU National Natural Science Foundation of China [81572787, 81672683,
   81672993, 81672688, 81702907, 81772901, 81772928, 81803025, 81872278];
   Overseas Expertise Introduction Project for Discipline Innovation (111
   Project) [111-2-12]; Natural Science Foundation of Hunan Province
   [2016JC2035, 2017SK2105, 2018JJ3704, 2018JJ3815, 2018SK21210,
   2018SK21211]
FX This study was supported by grants from The National Natural Science
   Foundation of China (81572787, 81672683, 81672993, 81672688, 81702907,
   81772901, 81772928, 81803025 and 81872278), the Overseas Expertise
   Introduction Project for Discipline Innovation (111 Project, No.
   111-2-12), and the Natural Science Foundation of Hunan Province
   (2016JC2035, 2017SK2105, 2018JJ3704, 2018JJ3815, 2018SK21210 and
   2018SK21211).
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NR 183
TC 81
Z9 83
U1 2
U2 33
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 3789
EP 3797
DI 10.7150/jca.31166
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IC9AH
UT WOS:000471273000022
PM 31333796
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Janas, K
   Boniewska-Bernacka, E
   Dyrda, G
   Slota, R
AF Janas, Katarzyna
   Boniewska-Bernacka, Ewa
   Dyrda, Gabriela
   Slota, Rudolf
TI Porphyrin and phthalocyanine photosensitizers designed for targeted
   photodynamic therapy of colorectal cancer
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE Photodynamic therapy; Colorectal cancer; Porphyrins; Phthalocyanines;
   Targeted therapy
ID SUBCELLULAR-LOCALIZATION; ZINC(II) PHTHALOCYANINE; DELIVERY;
   DERIVATIVES; NANOPARTICLES; DOXORUBICIN; MEMBRANE; MICELLES; PORPHIN;
   OXYGEN
AB Colorectal cancer is of particular concern due to its high mortality rate count. Recent investigations on targeted phototherapy involving novel photosensitizers and drug-delivery systems have provided promising results and realistic prospects for a successful medical treatment. New research trends have been focused particularly on development of advanced molecular systems offering effective photoactive species which could be selectively delivered directly into the affected cells. Porphyrins and phthalocyanines have been considered extremely attractive for this purpose due to their molecular versatility, excellent photochemical properties and multi-functional nature. In this review it has been demonstrated that such macrocyclic compounds may effectively contribute to the inhibition of the growth of colon cancer cells and eventually to their photonecrosis. Purposely designed and tailored porphyrin and phthalocyanine derivatives in combination with smart drug-carriers have proved suitable for photodynamic therapy (PDT) and related antitumor treatments. This survey comprises a choice of potentially applicable ideas developed since 2010 involving 9 different tumor cell lines and featuring 32 photosensitizers.
C1 [Janas, Katarzyna; Dyrda, Gabriela; Slota, Rudolf] Univ Opole, Inst Chem, Ul Oleska 48, PL-45052 Opole, Poland.
   [Boniewska-Bernacka, Ewa] Univ Opole, Inst Med Sci, Ul Oleska 48, PL-45052 Opole, Poland.
C3 University of Opole; University of Opole
RP Slota, R (corresponding author), Univ Opole, Inst Chem, Ul Oleska 48, PL-45052 Opole, Poland.
EM kbarchiewicz@gmail.com; Ewa.Boniewska@uni.opole.pl; gaba@uni.opole.pl;
   rslota@uni.opole.pl
OI Boniewska-Bernacka, Ewa/0000-0002-4424-8409; Slota,
   Rudolf/0000-0001-7059-6602
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NR 61
TC 50
Z9 51
U1 3
U2 34
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 JAN 15
PY 2021
VL 30
AR 115926
DI 10.1016/j.bmc.2020.115926
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
   Organic
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA QE2NF
UT WOS:000616047600011
PM 33341498
DA 2025-01-04
ER

PT J
AU Ivanova, M
   Venetis, K
   Guerini-Rocco, E
   Bottiglieri, L
   Mastropasqua, MG
   Garrone, O
   Fusco, N
   Ghidini, M
AF Ivanova, Mariia
   Venetis, Konstantinos
   Guerini-Rocco, Elena
   Bottiglieri, Luca
   Mastropasqua, Mauro Giuseppe
   Garrone, Ornella
   Fusco, Nicola
   Ghidini, Michele
TI HER2 in Metastatic Colorectal Cancer: Pathology, Somatic Alterations,
   and Perspectives for Novel Therapeutic Schemes
SO LIFE-BASEL
LA English
DT Review
DE HER2; colorectal cancer; pathology; biomarkers; targeted therapy
ID TRASTUZUMAB; SYSTEM; SAFETY
AB Simple Summary In the current clinical practice, HER2 status is tested in breast and gastroesophageal cancers to select patients eligible for anti-HER2 treatment. However, HER2 is an emerging biomarker in colorectal cancer (CRC), one of the big killers in oncology. The most frequent types of HER2 alterations in CRC include gene amplification and mutations and often involve protein overexpression. In this review, we discuss the current knowledge of HER2 testing in CRC and the immediate future perspectives for HER2 targeting in the metastatic setting. HER2 is an emerging biomarker in colorectal cancer (CRC). This oncogene plays an essential role in regulating cell proliferation, differentiation, migration, and, more in general, tumorigenesis and tumor progression. The most frequent types of HER2 alterations in CRC include gene amplification and missense mutations in 7-8% of CRC, often being mirrored by HER2 protein overexpression, representing founder events in solid tumors, including CRC. There are currently no approved HER2-targeted therapy guidelines for CRC; however, several studies have shown that HER2 can be effectively targeted in meta-static CRC settings. In this review, we discuss the current knowledge of HER2 testing in CRC and the immediate future perspectives for HER2 targeting in the metastatic setting.
C1 [Ivanova, Mariia; Venetis, Konstantinos; Guerini-Rocco, Elena; Bottiglieri, Luca; Fusco, Nicola] Univ Milan, European Inst Oncol IRCCS, Div Pathol, IEO, Via Giuseppe Ripamonti 435, I-20141 Milan, Italy.
   [Mastropasqua, Mauro Giuseppe] Univ Bari Aldo Moro, Sch Med, Dept Emergency & Organ Transplantat, Piazza G Cesare 11, I-70124 Bari, Italy.
   [Garrone, Ornella; Ghidini, Michele] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Med Oncol Unit, I-20122 Milan, Italy.
C3 University of Milan; IRCCS European Institute of Oncology (IEO);
   Universita degli Studi di Bari Aldo Moro; IRCCS Ca Granda Ospedale
   Maggiore Policlinico
RP Fusco, N (corresponding author), Univ Milan, European Inst Oncol IRCCS, Div Pathol, IEO, Via Giuseppe Ripamonti 435, I-20141 Milan, Italy.
EM nicola.fusco@ieo.it
RI MASTROPASQUA, Mauro/AAK-8813-2020; Ivanova, Mariia/ACC-9004-2022;
   Garrone, Ornella/HHS-9402-2022; Venetis, Konstantinos/AAA-6077-2021;
   Fusco, Nicola/D-6264-2016; MASTROPASQUA, Mauro Giuseppe/I-4649-2018;
   Ghidini, Michele/I-7362-2018
OI Fusco, Nicola/0000-0002-9101-9131; MASTROPASQUA, Mauro
   Giuseppe/0000-0002-8306-0839; Ivanova, Mariia/0000-0002-7636-1000;
   Ghidini, Michele/0000-0001-5435-1218; Garrone,
   Ornella/0000-0001-7359-5410
FU Italian Ministry of Health
FX This research was partially funded by Grant Ricerca Corrente 2021,
   Italian Ministry of Health.
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NR 71
TC 11
Z9 11
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-1729
J9 LIFE-BASEL
JI Life-Basel
PD SEP
PY 2022
VL 12
IS 9
AR 1403
DI 10.3390/life12091403
PG 13
WC Biology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Microbiology
GA 4R6YJ
UT WOS:000856906500001
PM 36143438
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lee, JJX
   Choo, SP
   Chua, C
AF Lee, Joycelyn Jie Xin
   Choo, Su Pin
   Chua, Clarinda
TI Novel Targets in Advanced Colorectal Cancer
SO CURRENT COLORECTAL CANCER REPORTS
LA English
DT Review
DE Colon cancer; Rectal cancer; Targeted therapy; Oncogenic gene fusions;
   Immunotherapy; Microbiome
ID COLON-CANCER; INHIBITION; FUSIONS; PLUS; TRK; GENE; EGFR
AB Purpose of ReviewAlthough current guidelines suggest only testing for RAS and BRAF mutations as well as MMR deficiency in metastatic colon cancer, there are many other promising therapeutic targets that are being studied. We aim to review the recent literature and evidence behind some of these novel targets.Recent FindingsMany of these targets such as NTRK, ROS, ALK, and HER2 are being studied in current clinical trials and hold great potential in changing the treatment landscape for metastatic colorectal cancer.SummaryCurrent molecular testing algorithms may need to be expanded to allow better target discovery and for patients to benefit from more therapeutic options.
C1 [Lee, Joycelyn Jie Xin; Choo, Su Pin; Chua, Clarinda] Natl Canc Ctr Singapore, Div Med Oncol, 11 Hosp Dr, Singapore 169610, Singapore.
C3 National Cancer Centre Singapore (NCCS)
RP Chua, C (corresponding author), Natl Canc Ctr Singapore, Div Med Oncol, 11 Hosp Dr, Singapore 169610, Singapore.
EM clarinda.chua.w.l@singhealth.com.sg
RI Lee, joycelyn/KIG-1047-2024; CHOO, Su/ABB-3892-2020
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NR 43
TC 1
Z9 1
U1 0
U2 7
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 DEC
PY 2018
VL 14
IS 6
BP 192
EP 198
DI 10.1007/s11888-018-0422-9
PG 7
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA HC4FO
UT WOS:000451758500004
DA 2025-01-04
ER

PT J
AU Lee, WR
   Shen, SC
   Shih, YH
   Chou, CL
   Tseng, JTP
   Chin, SY
   Liu, KH
   Chen, YC
   Jiang, MC
AF Lee, Woan-Ruoh
   Shen, Shing-Chuan
   Shih, Yi-Hsien
   Chou, Chia-Lun
   Tseng, Jonathan Te-Peng
   Chin, Szu-Ying
   Liu, Kao-Hui
   Chen, Yen-Chou
   Jiang, Ming-Chung
TI Early decline in serum phospho-CSE1L levels in
   vemurafenib/sunitinib-treated melanoma and sorafenib/lapatinib-treated
   colorectal tumor xenografts
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE ERK1/2; Monitoring; Phospho-CSE1L; Serum; Targeted drug; Targeted
   therapy
ID CELLULAR APOPTOSIS; MOLECULAR-BASIS; CANCER; PROTEIN; ACTIVATION;
   INHIBITORS; BREAST; GROWTH; CSE1L; BRAF(V600E)
AB Background: Although targeted therapies have improved the clinical outcomes of cancer treatment, tumors resistance to targeted drug are often detected too late and cause mortality. CSE1L is secreted from tumor and its phosphorylation is regulated by ERK1/2. ERK1/2 is located downstream of various growth factor receptors and kinases, the targets of most targeted drugs. Serum phospho-CSE1L may be a marker for monitoring the efficacy of targeted therapy.
   Methods: We used mice tumor xenograft model to study the assay of serum phosphorylated CSE1L for early detecting the efficacy of targeted drugs. The phosphorylation status of CSE1L in vemurafenib and sorafenib treated tumor cells were assayed by immunoblotting with antibody against phosphorylated CSE1L.
   Results: Ras activation increased phospho-CSE1L expression in B16F10 melanoma cells. Vemurafenib and sorafenib treatment did not significantly reduce the total CSE1L levels; however, they inhibited ERK1/2 and CSE1L phosphorylation in A375 melanoma cells and HT-29 colorectal cancer cells. In the melanoma xenograft model, serum phospho-CSE1L level declined 5 days after vemurafenib/sunitinib treatment and 3 days after sorafenib/lapatinib treatment in the HT-29 colon cancer xenograft model. Vemurafenib/sunitinib and sorafenib/lapatinib treatments resulted in tumor regression.
   Conclusions: Our results indicated that serum phospho-CSE1L is useful for early detecting the efficacy of targeted therapy in initial treatment and for monitoring emerging secondary drug resistance to facilitate timely therapeutic decision making.
C1 [Lee, Woan-Ruoh; Shih, Yi-Hsien; Chou, Chia-Lun; Tseng, Jonathan Te-Peng; Chin, Szu-Ying; Jiang, Ming-Chung] Taipei Med Univ, Shuang Ho Hosp, Dept Dermatol, New Taipei, Taiwan.
   [Lee, Woan-Ruoh; Shih, Yi-Hsien; Chou, Chia-Lun; Tseng, Jonathan Te-Peng; Chin, Szu-Ying; Jiang, Ming-Chung] Taipei Med Univ, Coll Med, Sch Med, Dept Dermatol, Taipei 11031, Taiwan.
   [Lee, Woan-Ruoh; Shen, Shing-Chuan; Shih, Yi-Hsien; Tseng, Jonathan Te-Peng; Chin, Szu-Ying; Liu, Kao-Hui; Chen, Yen-Chou] Taipei Med Univ, Coll Med, Grad Inst Med Sci, Taipei, Taiwan.
C3 Taipei Medical University; Shuang Ho Hospital; Taipei Medical
   University; Taipei Medical University
RP Jiang, MC (corresponding author), Taipei Med Univ, Coll Med, Sch Med, Dept Dermatol, 252 Wu Hsing St, Taipei 11031, Taiwan.
EM jiangmwd@gmail.com
RI Lee, William/B-5836-2011
OI SHIH, YI-HSIEN/0000-0003-2095-7064
FU National Science Council [NSC 103-2314-B-038-023-MY2, NSC
   101-2314-B-038-038]
FX This study was supported by grants from the National Science Council
   (NSC 103-2314-B-038-023-MY2) and (NSC 101-2314-B-038-038).
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NR 50
TC 13
Z9 14
U1 0
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD JUN 13
PY 2015
VL 13
AR 191
DI 10.1186/s12967-015-0553-6
PG 12
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA CK4SC
UT WOS:000356212500001
PM 26070816
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Morganti, S
   Curigliano, G
AF Morganti, Stefania
   Curigliano, Giuseppe
TI Combinations using checkpoint blockade to overcome resistance
SO ECANCERMEDICALSCIENCE
LA English
DT Review
DE chemo-immunotherapy; immune-checkpoint inhibitors; immunotherapy
   combinations; immunotherapy resistance; next-generation immune
   modulators; NGIM; targeted therapy
ID METASTATIC COLORECTAL-CANCER; SUPPRESSOR-CELLS; T-CELLS; ANTITUMOR
   IMMUNITY; PD-L1 EXPRESSION; BRAF INHIBITION; DENDRITIC CELLS;
   BREAST-CANCER; UP-REGULATION; PATIENTS PTS
AB The advent of immunotherapy for cancer represented a paradigm shift in the treatment approach of neoplasia. Immune-checkpoint inhibitors (ICIs) were demonstrated to significantly improve outcomes, including overall survival across several cancer types, with yearly-durable responses. Nevertheless, many patients derive minor or no benefit with immune checkpoint (IC)-blockade, including patients with cancer types traditionally considered immunogenic. Combination strategies of ICIs with chemotherapy, radiotherapy, targeted therapies or other immunotherapy compounds have been conceived in order to boost the immune-responses and potentially overcome resistance to ICIs. This review focuses on mechanisms underlying resistance to IC-blockade and provides an overview of potential advantages and limitations of combination strategies currently under investigation.
C1 [Morganti, Stefania; Curigliano, Giuseppe] IRCCS, Div Early Drug Dev Innovat Therapies, European Inst Oncol IEO, Via Ripamonti 435, I-20141 Milan, Italy.
   [Morganti, Stefania; Curigliano, Giuseppe] Univ Milan, Dept Oncol & Hematooncol, Via Festa Perdono 7, I-20122 Milan, Italy.
C3 IRCCS European Institute of Oncology (IEO); University of Milan
RP Curigliano, G (corresponding author), IRCCS, Div Early Drug Dev Innovat Therapies, European Inst Oncol IEO, Via Ripamonti 435, I-20141 Milan, Italy.; Curigliano, G (corresponding author), Univ Milan, Dept Oncol & Hematooncol, Via Festa Perdono 7, I-20122 Milan, Italy.
EM Giuseppe.curigliano@ieo.it
RI Curigliano, Giuseppe/D-3371-2018; Morganti, Stefania/AAB-1145-2021
OI Morganti, Stefania/0000-0001-5284-9944
FU Italian Ministry of Health
FX This work was partially supported by the Italian Ministry of Health with
   Ricerca Corrente and 5x1000 funds.
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NR 142
TC 12
Z9 14
U1 0
U2 6
PU CANCER INTELLIGENCE LTD
PI BRISTOL
PA 11 ALMA VALE RD,, BRISTOL, BS8 2HL, ENGLAND
SN 1754-6605
J9 ECANCERMEDICALSCIENC
JI eCancerMedicalScience
PD DEC 3
PY 2020
VL 14
AR 1148
DI 10.3332/ecancer.2020.1148
PG 19
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA PB5UT
UT WOS:000596386500001
PM 33574893
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Qiu, QQ
   Wang, QY
   Deng, CX
   Sun, YQ
   Chen, TL
   Guo, LL
   Zhang, F
AF Qiu, Qianqian
   Wang, Qiongyao
   Deng, Changxu
   Sun, Yanqin
   Chen, Taoliang
   Guo, Linlang
   Zhang, Fan
TI Small molecular peptide-ScFv αvβ3 conjugates specifically inhibit lung
   cancer cell growth <i>in</i> <i>vitro</i> and <i>in</i> <i>vivo</i>
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE Lung cancer; cdGIGPQc; integrin alpha v beta 3; ScFv; targeted therapy
ID INTEGRIN ALPHA(V)BETA(3); TARGETED THERAPY; BLOOD-VESSELS; COLON-CANCER;
   ALPHA-V; ANGIOGENESIS; ANTIBODY; EXPRESSION; FRAGMENT; VITAXIN
AB Integrin alpha v beta 3 (ITG) is highly expressed in various cancers and is considered a major target for anti-angiogensis cancer therapy. The single chain fragment variable of which (ScFv alpha v beta 3) has been reported to inhibit tumor growth both in vitro and in vivo. Here, we conjugated cdGIGPQc which can exclusively bind to NSCLC cells according to our previous study synthesized by SPPS with ScFv alpha v beta 3 expressed in E. coli BL21 (DE3) to develop a novel lung cancer specific targeted drug. Specific cell targeting of cdGIGPQc-ScFv was assessed in parallel with the single ScFv and a control nonspecific peptide-ScFv through immunofluorescence and flow cytometry while the alpha v beta 3-binding property was examined by Western blot. Our results showed that cdGIGPQc-ScFv retained both the lung cancer-binding activity of cdGIGPQc and the antigen-recognizing ability of ScFv alpha v beta 3 in vitro. CCK8 assays and in animal experiments suggested that cdGIGPQc-ScFv possessed a superior antitumor effect than ScFv and nonspecific peptide-ScFv both in vitro and vivo. Further immunohistochemical staining revealed that cdGIGPQc-ScFv retarded lung cancer growth through inhibiting tumor angiogensis and proliferation. Therefore, cdGIGPQc delivery of ScFv alpha v beta 3 to lung cancer may be a hopeful new strategy for enhancing specific antitumor efficacy and cdGIGPQc-ScFv could be a potential drug for lung cancer targeted treatment.
C1 [Qiu, Qianqian; Wang, Qiongyao; Guo, Linlang] Southern Med Univ, Zhujiang Hosp, Dept Pathol, 253 Gongye Rd, Guangzhou 510282, Guangdong, Peoples R China.
   [Chen, Taoliang] Southern Med Univ, Zhujiang Hosp, Dept Neurosurg, Guangzhou, Guangdong, Peoples R China.
   [Zhang, Fan] Southern Med Univ, Zhujiang Hosp, Dept Dermatol, 253 Gongye Rd, Guangzhou 510282, Guangdong, Peoples R China.
   [Deng, Changxu] Southern Med Univ, Wuhan Gen Hosp Guangzhou Mil Reg, Dept Orthoped, Wuhan, Peoples R China.
   [Sun, Yanqin] Guangdong Med Univ, Dept Pathol, Dongguan, Peoples R China.
C3 Southern Medical University - China; Southern Medical University -
   China; Southern Medical University - China; Southern Medical University
   - China; Guangdong Medical University
RP Guo, LL (corresponding author), Southern Med Univ, Zhujiang Hosp, Dept Pathol, 253 Gongye Rd, Guangzhou 510282, Guangdong, Peoples R China.; Zhang, F (corresponding author), Southern Med Univ, Zhujiang Hosp, Dept Dermatol, 253 Gongye Rd, Guangzhou 510282, Guangdong, Peoples R China.
EM linlangg@yahoo.com; mr.zhangfan@163.com
RI Fan, Zhang/AAZ-3509-2021
FU Science and Technology Planning Project of Guangdong Province, China
   [2013B021800146]; Guangdong Provincial Key Laboratory of Malignant Tumor
   Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun
   Yat-sen University
FX This work was supported by Science and Technology Planning Project of
   Guangdong Province, China Grant (2013B021800146) and by Guangdong
   Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene
   Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University.
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NR 39
TC 1
Z9 3
U1 0
U2 8
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2156-6976
J9 AM J CANCER RES
JI Am. J. Cancer Res.
PY 2016
VL 6
IS 12
BP 2846
EP 2858
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EF8PR
UT WOS:000390591800008
PM 28042504
DA 2025-01-04
ER

PT J
AU Li, J
   Chen, YX
   Guo, X
   Zhou, L
   Jia, ZM
   Peng, Z
   Tang, YP
   Liu, WD
   Zhu, B
   Wang, L
   Ren, CP
AF Li, Jian
   Chen, Yuxiang
   Guo, Xiong
   Zhou, Lin
   Jia, Zeming
   Peng, Zha
   Tang, Yaping
   Liu, Weidong
   Zhu, Bin
   Wang, Lei
   Ren, Caiping
TI GPC1 exosome and its regulatory miRNAs are specific markers for the
   detection and target therapy of colorectal cancer
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE colorectal cancer; exosome; biomarker; GPC1; miRNA
ID HEPATOCELLULAR-CARCINOMA; CELL-PROLIFERATION; GLYPICAN-1; INHIBITION;
   INVASION; GROWTH
AB Colorectal cancer (CRC) is the second leading cause of cancer-related deaths worldwide. However, a biomarker for a sensitive and simple diagnostic test and highly effective target therapy of CRC is still clinically unavailable. This study is to investigate the evidence and significance of plasma GPC1 positive exosomes as a biomarker of CRC. Results showed that GPC1(+) exosomes were successfully isolated from tissues and plasma. The percentage of GPC1(+) exosomes and the GPC1 protein expression in exosomes from tumour tissues and plasma of CRC patients before surgical treatment was significantly elevated compared to that in the peritumoural tissues and the plasma of healthy controls. miR-96-5p and miR-149 expression in tumour tissues and plasma of CRC patients as well as in the GPC1(+) exosomes from CRC patients were significantly decreased compared to that in the peritumoural tissues and the plasma of healthy controls. Two months after surgical treatment, levels of all tested markers significantly normalized. Overexpression of miR-96-5p and miR-149 significantly decreased GPC1 expression in HT-29 and HCT-116 cells, xenograft tumours, plasma in mice bearing HT-29 and HCT-116 tumours, and the secretion of GPC1(+) exosomes from the HT-29 and HCT-116 cells and xenograft tumours. Overexpression of miR-96-5p and miR-149 significantly decreased cell viability and increased cell apoptosis in HT-29 and HCT-116 cells, and inhibited the growth of xenograft HT-29 and HCT-116 tumours. In conclusion, the increased plasma GPC1(+) exosomes and reduced plasma miR-96-5p and miR-149 expression are specific markers for the diagnosis of CRC and targets for the therapy of CRC.
C1 [Li, Jian; Guo, Xiong; Zhou, Lin; Jia, Zeming; Peng, Zha; Tang, Yaping] Cent S Univ, Xiangya Hosp, Hepatobiliary & Enter Surg Res Ctr, Changsha, Hunan, Peoples R China.
   [Chen, Yuxiang] Cent S Univ, Sch Pharmaceut Sci, Changsha, Hunan, Peoples R China.
   [Liu, Weidong; Zhu, Bin; Wang, Lei; Ren, Caiping] Cent S Univ, Canc Res Inst, Sch Basic Med Sci,Chinese Minist Hlth, Collaborat Innovat Ctr Canc Med,Key Lab Carcinoge, Changsha, Hunan, Peoples R China.
C3 Central South University; Central South University; Central South
   University
RP Chen, YX (corresponding author), Cent S Univ, Sch Pharmaceut Sci, Changsha, Hunan, Peoples R China.; Ren, CP (corresponding author), Cent S Univ, Canc Res Inst, Sch Basic Med Sci,Chinese Minist Hlth, Collaborat Innovat Ctr Canc Med,Key Lab Carcinoge, Changsha, Hunan, Peoples R China.
EM chenyx08@yahoo.com; rencaiping@csu.edu.cn
RI Zhu, Bin/HHZ-1819-2022
FU National 863 Hi-tech Project of China [2007AA021803, 2007AA021901,
   2007AA021809, 2007AA021811]; National Natural Science Foundation of
   China [81272972, 81472355]; National Basic Research Program of China
   [2010CB833605]; Hunan Provincial Nature Science Foundation [16JJ3056];
   Hunan Provincial Science Department Program [2014FJ6006]; Incubation
   Program for National Natural Science Funds for Distinguished Young
   Scholar of Central South University [2010QYZD006]; Open-End Fund for the
   Valuable and Precision Instruments of Central South University
   [CSUZC201638, CSUZC201634]
FX This study was supported by the National 863 Hi-tech Project of China
   (2007AA021803, 2007AA021901, 2007AA021809, 2007AA021811), the National
   Natural Science Foundation of China (81272972, 81472355), National Basic
   Research Program of China (2010CB833605), Hunan Provincial Nature
   Science Foundation (16JJ3056), Hunan Provincial Science Department
   Program (2014FJ6006), Incubation Program for National Natural Science
   Funds for Distinguished Young Scholar of Central South University
   (2010QYZD006), and Open-End Fund for the Valuable and Precision
   Instruments of Central South University (CSUZC201638, CSUZC201634).
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NR 23
TC 134
Z9 142
U1 0
U2 48
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 1582-4934
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD MAY
PY 2017
VL 21
IS 5
BP 838
EP 847
DI 10.1111/jcmm.12941
PG 10
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA EU9GY
UT WOS:000401348400001
PM 28233416
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Gu, RQ
   Fang, HS
   Wang, RJ
   Dai, WX
   Cai, GX
AF Gu, Ruiqi
   Fang, Hongsheng
   Wang, Renjie
   Dai, Weixing
   Cai, Guoxiang
TI A comprehensive overview of the molecular features and therapeutic
   targets in <i>BRAF</i><SUP><i>V600E</i></SUP>-mutant colorectal cancer
SO CLINICAL AND TRANSLATIONAL MEDICINE
LA English
DT Review
DE BRAF; colorectal cancer; molecular features; target therapy
ID FOLFOXIRI PLUS BEVACIZUMAB; MEK INHIBITION; COMBINED BRAF; OPEN-LABEL;
   MICROSATELLITE INSTABILITY; COLON-CANCER; PHASE-II; B-RAF; INTRINSIC
   RESISTANCE; 1ST-LINE TREATMENT
AB As one of the most prevalent digestive system tumours, colorectal cancer (CRC) poses a significant threat to global human health. With the emergence of immunotherapy and target therapy, the prognosis for the majority of CRC patients has notably improved. However, the subset of patients with BRAF exon 15 p.V600E mutation (BRAF(V600E)) has not experienced remarkable benefits from these therapeutic advancements. Hence, researchers have undertaken foundational investigations into the molecular pathology of this specific subtype and clinical effectiveness of diverse therapeutic drug combinations. This review comprehensively summarised the distinctive molecular features and recent clinical research advancements in BRAF-mutant CRC. To explore potential therapeutic targets, this article conducted a systematic review of ongoing clinical trials involving patients with BRAF(V600E)-mutant CRC.
C1 [Gu, Ruiqi; Fang, Hongsheng; Wang, Renjie; Dai, Weixing; Cai, Guoxiang] Fudan Univ, Dept Colorectal Surg, Shanghai Canc Ctr, Shanghai, Peoples R China.
   [Gu, Ruiqi; Fang, Hongsheng; Wang, Renjie; Dai, Weixing; Cai, Guoxiang] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.
C3 Fudan University; Fudan University
RP Dai, WX; Cai, GX (corresponding author), Fudan Univ, Shanghai Med Coll, Dept Oncol, Dept Colorectal Surg,Shanghai Canc Ctr, 270 Dongan Rd, Shanghai 200032, Peoples R China.
EM daiweixing2015@163.com; gxcaifuscc@163.com
RI CAI, GUOXIANG/LKK-9614-2024
OI Cai, Guoxiang/0000-0002-7772-7078
FU Shanghai Municipal Health Commission [2022XD012]; Shanghai Municipal
   Hospital Development Center [SHDC2022CRD046]
FX Figures were created with the help of . This work was supported by
   Shanghai Municipal Health Commission (2022XD012) and Shanghai Municipal
   Hospital Development Center (SHDC2022CRD046).
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NR 194
TC 0
Z9 0
U1 3
U2 3
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 JUL
PY 2024
VL 14
IS 7
AR e1764
DI 10.1002/ctm2.1764
PG 27
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA A2D5O
UT WOS:001280689600001
PM 39073010
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Devon, KM
   Lerner-Ellis, JP
   Ganai, S
   Angelos, P
AF Devon, Karen M.
   Lerner-Ellis, Jordan P.
   Ganai, Sabha
   Angelos, Peter
TI Ethics and Genomic Medicine, How to Navigate Decisions in Surgical
   Oncology
SO JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Review
DE genetics; ethics; personalized medicine
ID BILATERAL PROPHYLACTIC MASTECTOMY; METASTATIC COLORECTAL-CANCER;
   BREAST-CANCER; PERSONALIZED MEDICINE; GENETIC INFORMATION; BRCA2
   MUTATIONS; FAMILY-HISTORY; INSURANCE DISCRIMINATION; INCIDENTAL
   FINDINGS; EFFICACY
AB Using genetic information to make medical decisions and tailor treatments to individuals will likely provide major benefits and become an important part of health care. Surgical oncologists must ethically apply scientific genetic information in a complex and evolving environment to the benefit of their patients. In this review we address ethical issues associated with: indications for genetic testing, informed consent for testing and therapy, confidentiality, targeted therapy, prophylactic surgery, and genetic testing in children. J. Surg. Oncol. 2015 111:18-23. (c) 2014 Wiley Periodicals, Inc.
C1 [Devon, Karen M.] Univ Toronto, Dept Surg, Toronto, ON, Canada.
   [Devon, Karen M.] Univ Toronto, Womens Coll Hosp, Dept Surg, Toronto, ON M5S 1B2, Canada.
   [Devon, Karen M.] Univ Hlth Network, Dept Surg, Toronto, ON, Canada.
   [Lerner-Ellis, Jordan P.] Univ Toronto, Lab Med & Pathobiol, Toronto, ON, Canada.
   [Lerner-Ellis, Jordan P.] Mt Sinai Hosp, Dept Pathol & Lab Med, Toronto, ON M5G 1X5, Canada.
   [Lerner-Ellis, Jordan P.] Ontario Inst Canc Res, Toronto, ON, Canada.
   [Ganai, Sabha] Simmons Canc Inst SIU, Springfield, IL USA.
   [Ganai, Sabha] So Illinois Univ, Sch Med, Springfield, IL USA.
   [Angelos, Peter] MacLean Ctr Clin Med Eth, Chicago, IL USA.
C3 University of Toronto; University of Toronto; Womens College Hospital;
   University of Toronto; University Health Network Toronto; University of
   Toronto; University of Toronto; Sinai Health System Toronto; Lunenfeld
   Tanenbaum Research Institute; University of Toronto; Ontario Institute
   for Cancer Research; Southern Illinois University System; Southern
   Illinois University
RP Devon, KM (corresponding author), Univ Toronto, Womens Coll Hosp, 76 Grenville St Rm 6227, Toronto, ON M5S 1B2, Canada.
EM karen.devon@wchospital.ca
RI Lerner-Ellis, Jordan/J-5559-2016; Ganai, Sabha/M-8022-2016
OI Ganai, Sabha/0000-0001-6160-3559
CR Allain DC, 2012, FAM CANCER, V11, P637, DOI 10.1007/s10689-012-9564-0
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NR 34
TC 5
Z9 7
U1 0
U2 25
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-4790
EI 1096-9098
J9 J SURG ONCOL
JI J. Surg. Oncol.
PD JAN 1
PY 2015
VL 111
IS 1
BP 18
EP 23
DI 10.1002/jso.23771
PG 6
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA AX5OF
UT WOS:000346975300004
PM 25183289
DA 2025-01-04
ER

PT J
AU Baeumer, N
   Scheller, A
   Wittmann, L
   Faust, A
   Apel, M
   Nimmagadda, SC
   Geyer, C
   Grunert, K
   Kellmann, N
   Peipp, M
   Kailayangiri, S
   Suburu, MEG
   Strassert, CA
   Schenk, M
   Greune, L
   Rueter, C
   Dersch, P
   Hartmann, W
   Rossig, C
   Neri, D
   Mueller-Tidow, C
   Schwoeppe, C
   Schliemann, C
   Khandanpour, C
   Lenz, G
   Berdel, WE
   Baeumer, S
AF Baeumer, Nicole
   Scheller, Annika
   Wittmann, Lisa
   Faust, Andreas
   Apel, Mara
   Nimmagadda, Subbaiah Chary
   Geyer, Christiane
   Grunert, Katharina
   Kellmann, Neele
   Peipp, Matthias
   Kailayangiri, Sareetha
   Gutierrez Suburu, Matias Ezequiel
   Strassert, Cristian A.
   Schenk, Mathias
   Greune, Lilo
   Rueter, Christian
   Dersch, Petra
   Hartmann, Wolfgang
   Rossig, Claudia
   Neri, Dario
   Mueller-Tidow, Carsten
   Schwoeppe, Christian
   Schliemann, Christoph
   Khandanpour, Cyrus
   Lenz, Georg
   Berdel, Wolfgang E.
   Baeumer, Sebastian
TI Electrostatic anti-CD33-antibody-protamine nanocarriers as platform for
   a targeted treatment of acute myeloid leukemia
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Article
DE RNA interference; Gemtuzumab; DNMT3A inhibition; Ibrutinib; Molecular
   targeted therapy
ID DNMT3A MUTATIONS; GEMTUZUMAB OZOGAMICIN; CLONAL HEMATOPOIESIS; RNA
   INTERFERENCE; CANCER; DELIVERY; SIRNA; MALIGNANCIES; INHIBITOR;
   RELEVANCE
AB Background: Acute myeloid leukemia (AML) is a fatal clonal hematopoietic malignancy, which results from the accumulation of several genetic aberrations in myeloid progenitor cells, with a worldwide 5-year survival prognosis of about 30%. Therefore, the development of more effective therapeutics with novel mode of action is urgently demanded. One common mutated gene in the AML is the DNA-methyltransferase DNMT3A whose function in the development and maintenance of AML is still unclear. To specifically target "undruggable " oncogenes, we initially invented an RNAi-based targeted therapy option that uses the internalization capacity of a colorectal cancer specific anti-EGFR-antibody bound to cationic protamine and the anionic siRNA. Here, we present a new experimental platform technology of molecular oncogene targeting in AML.Methods: Our AML-targeting system consists of an internalizing anti-CD33-antibody-protamine conjugate, which together with anionic molecules such as siRNA or ibrutinib-Cy3.5 and cationic free protamine spontaneously assembles into vesicular nanocarriers in aqueous solution. These nanocarriers were analyzed concerning their physical properties and relevant characteristics in vitro in cell lines and in vivo in xenograft tumor models and patient-derived xenograft leukemia models with the aim to prepare them for translation into clinical application.Results: The nanocarriers formed depend on a balanced electrostatic combination of the positively charged cationic protamine-conjugated anti-CD33 antibody, unbound cationic protamine and the anionic cargo. This nanocarrier transports its cargo safely into the AML target cells and has therapeutic activity against AML in vitro and in vivo. siRNAs directed specifically against two common mutated genes in the AML, the DNA-methyltransferase DNMT3A and FLT3-ITD lead to a reduction of clonal growth in vitro in AML cell lines and inhibit tumor growth in vivo in xenotransplanted cell lines. Moreover, oncogene knockdown of DNMT3A leads to increased survival of mice carrying leukemia patient-derived xenografts. Furthermore, an anionic derivative of the approved Bruton's kinase (BTK) inhibitor ibrutinib, ibrutinib-Cy3.5, is also transported by this nanocarrier into AML cells and decreases colony formation.Conclusions: We report important results toward innovative personalized, targeted treatment options via electrostatic nanocarrier therapy in AML. xenotransplanted cell lines. Moreover, oncogene knockdown of DNMT3A leads to increased survival of mice carrying leukemia patient-derived xenografts. Furthermore, an anionic derivative of the approved Bruton's kinase (BTK) inhibitor ibrutinib, ibrutinib-Cy3.5, is also transported by this nanocarrier into AML cells and decreases colony formation.
C1 [Baeumer, Nicole; Scheller, Annika; Wittmann, Lisa; Apel, Mara; Nimmagadda, Subbaiah Chary; Grunert, Katharina; Kellmann, Neele; Schwoeppe, Christian; Schliemann, Christoph; Khandanpour, Cyrus; Lenz, Georg; Berdel, Wolfgang E.; Baeumer, Sebastian] Univ Hosp Muenster, Dept Med A Hematol Oncol & Pneumol, Albert Schweitzer Campus 1, D-48149 Munster, Germany.
   [Faust, Andreas] Univ Munster, European Inst Mol Imaging, Waldeyerstr 15, D-48159 Munster, Germany.
   [Geyer, Christiane] Univ Hosp Munster, Inst Clin Radiol, Albert Schweitzer Campus 1, D-48149 Munster, Germany.
   [Peipp, Matthias] Univ Kiel, Div Antibody Based Immunotherapy, Arnold Heller Str 3, D-24105 Kiel, Germany.
   [Kailayangiri, Sareetha; Rossig, Claudia] Univ Childrens Hosp Muenster, Dept Pediat Hematol & Oncol, Albert Schweitzer Campus 1, D-48149 Munster, Germany.
   [Gutierrez Suburu, Matias Ezequiel; Strassert, Cristian A.] Univ Munster, Dept Inorgan & Analyt Chem, Corrensstrasse 28-30, D-48149 Munster, Germany.
   [Schenk, Mathias] Fraunhofer Inst Cell Therapy & Immunol IZI, Dept Drug Design & Target Validat, Weinbergweg 22, D-06120 Halle, Germany.
   [Greune, Lilo; Rueter, Christian; Dersch, Petra] Univ Munster, Inst Infectiol, Ctr Mol Biol Inflammat ZMBE, Von Esmarch Str 56, D-48149 Munster, Germany.
   [Hartmann, Wolfgang] Univ Munster, Gerhard Domagk Inst Pathol, Albert Schweitzer Campus 1, D-48149 Munster, Germany.
   [Neri, Dario] Swiss Fed Inst Technol, Inst Pharmaceut Sci, Vladimir Prelog Weg 1-5-10, CH-8093 Zurich, Switzerland.
   [Mueller-Tidow, Carsten] Heidelberg Univ, Dept Med 5, Neuenheimer Feld 410, D-69120 Heidelberg, Germany.
C3 University of Munster; University of Munster; University of Munster;
   University of Kiel; University of Munster; University of Munster;
   Fraunhofer Gesellschaft; University of Munster; University of Munster;
   Swiss Federal Institutes of Technology Domain; ETH Zurich; Ruprecht
   Karls University Heidelberg
RP Baeumer, S (corresponding author), Univ Hosp Muenster, Dept Med A Hematol Oncol & Pneumol, Albert Schweitzer Campus 1, D-48149 Munster, Germany.
EM baumers@uni-muenster.de
RI Geyer, Christiane/E-7495-2010; Müller-Tidow, Carsten/L-4062-2015;
   Rossig, Claudia/HKN-4057-2023; Neri, Diana/N-1002-2019; Peipp,
   Matthias/A-8775-2013; Muller-Tidow, Carsten/O-7207-2018; Ruter,
   Christian/B-5127-2017; Strassert, Cristian Alejandro/M-6459-2014
OI Rossig, Claudia/0000-0002-8672-5285; Gutierrez Suburu, Matias
   Ezequiel/0000-0002-9133-3614; Peipp, Matthias/0000-0002-5088-3804;
   Muller-Tidow, Carsten/0000-0002-7166-5232; Ruter,
   Christian/0000-0003-1982-4811; Khandanpour, Cyrus/0000-0003-4655-6269;
   Strassert, Cristian Alejandro/0000-0002-1964-0169
FU Projekt DEAL; Deutsche Jose Carreras Leukamie-Stiftung [DJCLS 04 R/2017,
   DJCLS 04 R/2020]; Deutsche Krebshilfe [70112282]; Wilhelm
   Sander-Stiftung [2014.054.1, 2017.071.1]; Innovative Medical Research of
   the University of Munster Medical School [111418, 211502, 121314,
   111501, 12 18 02]; Deutsche Forschungsgemeinschaft [DFG EXC1003,
   6103/3-1, DFG CRC1009B03]; Interdisciplinary Centre for Clinical
   Research [IZKF Bau2/009/19]; ForTra gGmbH [2021_EKTP13]
FX Open Access funding enabled and organized by Projekt DEAL. This study
   was supported by the Deutsche Jose Carreras Leukamie-Stiftung (DJCLS 04
   R/2017 and DJCLS 04 R/2020 given to N. Baumer and S. Baumer). This study
   was also funded by Deutsche Krebshilfe (No. 70112282, N. Baumer and S.
   Baumer), Wilhelm Sander-Stiftung (2014.054.1 and 2017.071.1, W. E.
   Berdel, S. Baumer), Innovative Medical Research of the University of
   Munster Medical School (111418, S. Baumer; 211502, S. Baumer; 121314, N.
   Baumer; 111501 and 12 18 02, S. Baumer, N. Baumer) and Deutsche
   Forschungsgemeinschaft (DFG EXC1003, W. E. Berdel, G. Lenz; 6103/3-1, S.
   Baumer; DFG CRC1009B03, C. Ruter). SB and NB gratefully acknowledge the
   Interdisciplinary Centre for Clinical Research (IZKF Bau2/009/19 & core
   unit PIX) for financial support. The translational work bringing this
   project to clinical application was funded by the ForTra gGmbH for
   research transfer of the Else Kroner-Fresenius-Stiftung to S. Baumer, W.
   E. Berdel and C. Schwoppe (2021_EKTP13).
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NR 70
TC 11
Z9 12
U1 2
U2 15
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 DEC 1
PY 2022
VL 15
IS 1
AR 171
DI 10.1186/s13045-022-01390-5
PG 26
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA 7V5GZ
UT WOS:000912843400001
PM 36457063
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Créancier, L
   Vandenberghe, I
   Gomes, B
   Dejean, C
   Blanchet, JC
   Meilleroux, J
   Guimbaud, R
   Selves, J
   Kruczynski, A
AF Creancier, Laurent
   Vandenberghe, Isabelle
   Gomes, Bruno
   Dejean, Caroline
   Blanchet, Jean-Christophe
   Meilleroux, Julie
   Guimbaud, Rosine
   Selves, Janick
   Kruczynski, Anna
TI Chromosomal rearrangements involving the NTRK1 gene in colorectal
   carcinoma
SO CANCER LETTERS
LA English
DT Article
DE NTRK1; TRKA; Gene rearrangement; Colon cancer
ID TARGETED THERAPY; LUNG-CANCER; KINASE; ONCOGENE; FUSION
AB Chromosomal rearrangements of the NTRK1 gene, which encodes the high affinity nerve growth factor receptor (tropomyosin related kinase, TRKA), have been observed in several epithelial cancers, such as colon cancer, papillary thyroid carcinoma or non small cell lung cancer. The various NTRK1 fusions described so far lead to constitutive activation of TRKA kinase activity and are oncogenic. We further investigated here the existence and the frequency of NTRK1 gene rearrangements in colorectal cancer. Using immunohistochemistry and quantitative reverse transcriptase PCR, we analyzed a series of human colorectal cancers. We identified two TRKA positive cases over 408, with NTRK1 chromosomal rearrangements. One of these rearrangements is a TPM3-NTRK1 fusion already observed in colon cancer, while the second one is a TPR-NTRK1 fusion never described in this type of cancer. These findings further confirm that translocations in the NTRK1 gene are recurring events in colorectal cancer, although occurring at a low frequency (around 0.5%). (C) 2015 Elsevier Ireland Ltd. All rights reserved.
C1 [Creancier, Laurent; Vandenberghe, Isabelle; Gomes, Bruno; Dejean, Caroline; Blanchet, Jean-Christophe; Kruczynski, Anna] Inst Rech Pierre Fabre, Ctr Rech Oncol Expt, F-31035 Toulouse 1, France.
   [Meilleroux, Julie; Guimbaud, Rosine; Selves, Janick] Ctr Hosp Univ Toulouse, F-31300 Toulouse, France.
   [Guimbaud, Rosine; Selves, Janick] Univ Toulouse 3, INSERM, Ctr Rech Cancerol Toulouse, Unite Mixte Rech 1037, F-31062 Toulouse, France.
C3 CHU de Toulouse; Universite de Toulouse; Universite Toulouse III - Paul
   Sabatier; Institut National de la Sante et de la Recherche Medicale
   (Inserm)
RP Kruczynski, A (corresponding author), Inst Rech Pierre Fabre, Ctr Rech Oncol Expt, 3 Ave Hubert Curien BP13562, F-31035 Toulouse 1, France.
EM anna.kruczynski@pierre-fabre.com
RI Selves, Janick/M-7719-2014
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NR 18
TC 74
Z9 92
U1 0
U2 9
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 AUG 28
PY 2015
VL 365
IS 1
BP 107
EP 111
DI 10.1016/j.canlet.2015.05.013
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CL8LV
UT WOS:000357227100012
PM 26001971
DA 2025-01-04
ER

PT J
AU Xiong, MH
   Lei, Q
   You, XY
   Gao, TT
   Song, XJ
   Xia, Y
   Ye, TH
   Zhang, LD
   Wang, NY
   Yu, LT
AF Xiong, Menghua
   Lei, Qian
   You, Xinyu
   Gao, Tiantao
   Song, Xuejiao
   Xia, Yong
   Ye, Tinghong
   Zhang, Lidan
   Wang, Ningyu
   Yu, Luoting
TI Mannosylated liposomes improve therapeutic effects of paclitaxel in
   colon cancer models
SO JOURNAL OF MICROENCAPSULATION
LA English
DT Article
DE Liposomes; modified liposomes; targeted drug delivery; colon cancer;
   mannose receptor
ID MANNOSE RECEPTOR; DRUG-DELIVERY
AB Mannose receptor (MR) is a highly effective endocytic receptor. It is closely related to tumour immune escape and metastasis. We found that MR was highly expressed in some colon cancer cell lines such as CT26 and HCT116 cells. Therefore, MR might be a potential target in colon cancer therapy. In this study, we aimed to develop mannosylated liposomes containing anticancer drug paclitaxel and investigate the potential effects on targeted therapy for colon cancer. Mannosylated liposomes were prepared by film dispersion method. Characterisation, drug release behaviour, cytotoxicity, cellular uptake, anti-tumour efficacy and safety profiles of liposomes were investigated. The results showed that mannosylated liposomes had a higher CT26 cells uptake efficiency and tumour inhibition rate, which might be due to the target effect to MR. And no notable toxicity was observed. Taken together, these data demonstrated that mannosylated liposomes could target colon cancer and improve the efficacy of chemotherapy.
C1 [Xiong, Menghua; Lei, Qian; Gao, Tiantao; Song, Xuejiao; Xia, Yong; Ye, Tinghong; Zhang, Lidan; Wang, Ningyu; Yu, Luoting] Sichuan Univ, West China Hosp, Canc Ctr, Lab Chem, Chengdu, Sichuan, Peoples R China.
   [Xiong, Menghua; Lei, Qian; Gao, Tiantao; Song, Xuejiao; Xia, Yong; Ye, Tinghong; Zhang, Lidan; Wang, Ningyu; Yu, Luoting] Sichuan Univ, Collaborat Innovat Ctr, Chengdu, Sichuan, Peoples R China.
   [You, Xinyu] Sichuan Univ, Sch Chem Engn, Chengdu, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University
RP Yu, LT (corresponding author), Sichuan Univ, West China Med Sch, State Key Lab Biotherapy, 17,3rd Sect Ren Min South Rd, Chengdu 610041, Peoples R China.
EM yuluot@scu.edu.cn
RI Liu, XiaoYan/GQA-7216-2022; Xia, Yong/E-8689-2013; Xiong,
   Menghua/JXN-1494-2024; YE, Ting-Hong/HLW-3123-2023
OI Wang, Ning-Yu/0000-0003-3571-4903
FU National Natural Science Foundation of China [81602398]; China
   Postdoctoral Science Foundation [2015M582561, 2016T90861]
FX We appreciate the funding support from the National Natural Science
   Foundation of China (No. 81602398) and the China Postdoctoral Science
   Foundation (No. 2015M582561 and No. 2016T90861).
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NR 23
TC 37
Z9 38
U1 4
U2 54
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0265-2048
EI 1464-5246
J9 J MICROENCAPSUL
JI J. Microencapsul.
PY 2017
VL 34
IS 6
BP 513
EP 521
DI 10.1080/02652048.2017.1339739
PG 9
WC Chemistry, Applied; Engineering, Chemical; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Engineering; Pharmacology & Pharmacy
GA FN0ID
UT WOS:000415660600001
PM 28705043
DA 2025-01-04
ER

PT J
AU Hazra, A
   Chatterjee, S
   Mohanta, A
   Paul, P
   Samanta, A
AF Hazra, Ahana
   Chatterjee, Sohini
   Mohanta, Abhishek
   Paul, Pankaj
   Samanta, Amalesh
TI A review on fungal pullulan as a natural polymer focusing on targeted
   therapy for colon cancer and other pharmaceutical applications
SO POLYMERS FOR ADVANCED TECHNOLOGIES
LA English
DT Review
DE anticolon cancer activity; application; drug targeting; pullulan;
   sources
ID AUREOBASIDIUM-PULLULANS; DRUG-DELIVERY; GUM ODINA; HYDROPHOBIZED
   POLYSACCHARIDE; MOLECULAR-WEIGHT; NANOPARTICLES; HYDROGELS;
   MICROSPHERES; CHEMOTHERAPY; OXALIPLATIN
AB Colon cancer is the second most invasive cancer and fourth most common malignant neoplasm worldwide. Targeted oral colonic drug delivery systems have attracted considerable attention in the treatment of colon cancer due to their superior properties. However, the delivery of drugs safely and effectively to the target site of the colon tumor is a hindrance due to the complexity of the gastrointestinal structure. Herein, to achieve an effective delivery system specifically targeting the colon, we have taken concern by using natural polymer such as pullulan, signifying its flexibility and relevance in biomaterials science to design antineoplastic approaches. Here, we summarize the physicochemical properties, different pullulan derivatives and their biomedical application, several colon cancer-related treatment, and pullulan and its derivatives-based delivery systems towards colonic tissue.
C1 [Hazra, Ahana; Chatterjee, Sohini; Mohanta, Abhishek; Paul, Pankaj; Samanta, Amalesh] Jadavpur Univ, Dept Pharmaceut Technol, Div Microbiol & Pharmaceut Biotechnol, 188 Raja SC Mullick Rd, Kolkata 700032, India.
C3 Jadavpur University
RP Samanta, A (corresponding author), Jadavpur Univ, Dept Pharmaceut Technol, Div Microbiol & Pharmaceut Biotechnol, 188 Raja SC Mullick Rd, Kolkata 700032, India.
EM asamanta61@yahoo.co.in
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NR 96
TC 2
Z9 2
U1 1
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1042-7147
EI 1099-1581
J9 POLYM ADVAN TECHNOL
JI Polym. Adv. Technol.
PD OCT
PY 2023
VL 34
IS 10
BP 3183
EP 3192
DI 10.1002/pat.6139
EA JUL 2023
PG 10
WC Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Polymer Science
GA R1PK5
UT WOS:001023561000001
DA 2025-01-04
ER

PT J
AU Di Nicolantonio, F
   Vitiello, PP
   Marsoni, S
   Siena, S
   Tabernero, J
   Trusolino, L
   Bernards, R
   Bardelli, A
AF Di Nicolantonio, Federica
   Vitiello, Pietro Paolo
   Marsoni, Silvia
   Siena, Salvatore
   Tabernero, Josep
   Trusolino, Livio
   Bernards, Rene
   Bardelli, Alberto
TI Precision oncology in metastatic colorectal cancer - from biology to
   medicine
SO NATURE REVIEWS CLINICAL ONCOLOGY
LA English
DT Review
AB Progress in precision medicine for colorectal cancer continues to lag behind the rapid improvements seen in patients with certain other solid tumour types. Nonetheless, owing largely to the availability of better translational models, novel and effective targeted therapy strategies based on tumour biology are beginning to be developed for subsets of patients. In this Review, the authors summarize these developments and discuss future directions in this rapidly evolving area of research.
   Remarkable progress has been made in the development of biomarker-driven targeted therapies for patients with multiple cancer types, including melanoma, breast and lung tumours, although precision oncology for patients with colorectal cancer (CRC) continues to lag behind. Nonetheless, the availability of patient-derived CRC models coupled with in vitro and in vivo pharmacological and functional analyses over the past decade has finally led to advances in the field. Gene-specific alterations are not the only determinants that can successfully direct the use of targeted therapy. Indeed, successful inhibition of BRAF or KRAS in metastatic CRCs driven by activating mutations in these genes requires combinations of drugs that inhibit the mutant protein while at the same time restraining adaptive resistance via CRC-specific EGFR-mediated feedback loops. The emerging paradigm is, therefore, that the intrinsic biology of CRC cells must be considered alongside the molecular profiles of individual tumours in order to successfully personalize treatment. In this Review, we outline how preclinical studies based on patient-derived models have informed the design of practice-changing clinical trials. The integration of these experiences into a common framework will reshape the future design of biology-informed clinical trials in this field.
C1 [Di Nicolantonio, Federica; Vitiello, Pietro Paolo; Trusolino, Livio; Bardelli, Alberto] Univ Torino, Dept Oncol, Candiolo, Italy.
   [Di Nicolantonio, Federica; Trusolino, Livio; Bardelli, Alberto] IRCCS, FPO, Candiolo Canc Inst, Candiolo, Italy.
   [Vitiello, Pietro Paolo] Univ Campania Luigi Vanvitelli, Med Oncol Unit, Dept Precis Med, Naples, Italy.
   [Marsoni, Silvia] Ist FIRC Oncol Mol, Milan, Italy.
   [Marsoni, Silvia; Siena, Salvatore] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Siena, Salvatore] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
   [Tabernero, Josep] Vall Hebron Univ Hosp, Barcelona, Spain.
   [Tabernero, Josep] UVic UCC, IOB Quiron, Inst Oncol, Barcelona, Spain.
   [Bernards, Rene] Netherlands Canc Inst, Oncode Inst, Div Mol Carcinogenesis, Amsterdam, Netherlands.
C3 University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia;
   Universita della Campania Vanvitelli; IFOM - FIRC Institute of Molecular
   Oncology; University of Milan; Hospital Universitari Vall d'Hebron;
   Universitat de Vic - Universitat Central de Catalunya (UVic-UCC);
   Netherlands Cancer Institute
RP Di Nicolantonio, F; Bardelli, A (corresponding author), Univ Torino, Dept Oncol, Candiolo, Italy.; Di Nicolantonio, F; Bardelli, A (corresponding author), IRCCS, FPO, Candiolo Canc Inst, Candiolo, Italy.
EM federica.dinicolantonio@unito.it; alberto.bardelli@unito.it
RI Giardina, Giorgio/Y-5513-2019; Siena, Salvatore/ACK-2413-2022; Di
   Nicolantonio, Federica/A-2503-2011; Vitiello, Pietro
   Paolo/HKN-2581-2023; Trusolino, Livio/A-3896-2011; BARDELLI,
   Alberto/J-9721-2018
OI Bernards, Rene/0000-0001-8677-3423; Trusolino,
   Livio/0000-0002-6379-3365; BARDELLI, Alberto/0000-0003-1647-5070;
   Marsoni, Silvia/0000-0002-5361-7122
FU Fondazione AIRC, Associazione Italiana per la Ricerca sul Cancro [20685,
   21923, 21407, 22802]; Fondazione AIRC under 5 per Mille 2018 program
   [21091]; Instituto de Salud Carlos III (European Regional Development
   Fund/European Social Fund "A way to make Europe"/"Investing in your
   future") [AC15/00018]; AIRC-CRUK-FC AECC Accelerator Award [22795];
   Fondazione Piemontese per la Ricerca sul Cancro-ONLUS, 5x1000 Ministero
   della Salute 2015 Project "STRATEGY"; Fondazione Piemontese per la
   Ricerca sul Cancro-ONLUS, 5x1000 Ministero della Salute 2015 Project
   "IMMUNOGENOMICA"; BiLiGeCT [PON ARS01_00492]; Fondazione Piemontese per
   la Ricerca sul Cancro-ONLUS, 5x1000 Ministero della Salute 2014;
   Fondazione Piemontese per la Ricerca sul Cancro-ONLUS, 5x1000 Ministero
   della Salute 2016; H2020 grant [754923 COLOSSUS]; CORDIS Community
   Research and Development Information Service, Horizon 2020 grant,
   Molecularly Guided Trials with Specific Treatment Strategies in Patients
   with Advanced Newly Molecular Defined Subtypes of Colorectal Cancer
   (MoTriColor) [635342]; Fondazione Oncologia Niguarda Onlus, grant
   Terapia Molecolare dei Tumori
FX This work is supported by Fondazione AIRC, Associazione Italiana per la
   Ricerca sul Cancro, Investigator Grants 20685 (S.S.), 21923 (A.B.),
   21407 (F.D.N.) and 22802 (L.T.); Fondazione AIRC under 5 per Mille
   2018-ID 21091 program (to A.B., F.D.N., S.M., S.S. and L.T); Instituto
   de Salud Carlos III through the project "AC15/00018" (co-funded by the
   European Regional Development Fund/European Social Fund "A way to make
   Europe"/"Investing in your future") (J.T.). AIRC-CRUK-FC AECC
   Accelerator Award contract 22795 (A.B., L.T. and J.T); Fondazione
   Piemontese per la Ricerca sul Cancro-ONLUS, 5x1000 Ministero della
   Salute 2015 Project "STRATEGY" (F.D.N.); Fondazione Piemontese per la
   Ricerca sul Cancro-ONLUS, 5x1000 Ministero della Salute 2015 Project
   "IMMUNOGENOMICA" (A.B. and L.T.); BiLiGeCT - Progetto PON ARS01_00492
   (A.B.); Fondazione Piemontese per la Ricerca sul Cancro-ONLUS, 5x1000
   Ministero della Salute 2014 and 2016 (L.T.); H2020 grant agreement no.
   754923 COLOSSUS (L.T. and J.T.); CORDIS Community Research and
   Development Information Service, Horizon 2020 (project ID 635342) grant,
   Molecularly Guided Trials with Specific Treatment Strategies in Patients
   with Advanced Newly Molecular Defined Subtypes of Colorectal Cancer
   (MoTriColor) (J.T.); and Fondazione Oncologia Niguarda Onlus, grant
   Terapia Molecolare dei Tumori (S.S.).
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NR 279
TC 137
Z9 138
U1 4
U2 68
PU NATURE RESEARCH
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1759-4774
EI 1759-4782
J9 NAT REV CLIN ONCOL
JI Nat. Rev. Clin. Oncol.
PD AUG
PY 2021
VL 18
IS 8
BP 506
EP 525
DI 10.1038/s41571-021-00495-z
EA APR 2021
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TM2UP
UT WOS:000640731700001
PM 33864051
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Wang, XL
   Ouyang, XM
   Chen, JL
   Hu, Y
   Sun, XY
   Yu, ZW
AF Wang, Xiaoling
   Ouyang, Xumei
   Chen, Jinliang
   Hu, Ying
   Sun, Xiaoyi
   Yu, Zhenwei
TI Nanoparticulate photosensitizer decorated with hyaluronic acid for
   photodynamic/photothermal cancer targeting therapy
SO NANOMEDICINE
LA English
DT Article
DE chlorin e6; hyaluronic acid; peritumoral injection; photodynamic
   therapy; photothermal therapy; polydopamine nanoparticles
ID CORE-SHELL NANOPARTICLES; PHOTODYNAMIC THERAPY; CHLORIN E6;
   POLYDOPAMINE; AGENT; PENETRATION; NANOSPHERES; MEMBRANE
AB Aim: A photomedicine consisting of a core for photothermal therapy, a photosensitizer for photodynamic therapy, and a cancer-targeting moiety was fabricated to improve photosensitizer selectivity and antitumor efficiency. Materials & methods: Hyaluronic acid-decorated polydopamine nanoparticles with conjugated chlorin e6 (HA-PDA-Ce6) were synthesized and characterized. Cell uptake, phototoxicity, penetration, distribution and therapeutic effects were evaluated. Results: HA-PDA-Ce6 had high photoactivities for photodynamic therapy/photothermal therapy and was readily internalized via CD44-mediated endocytosis. Enhanced accumulation and deeper penetration into tumors were achieved by the diffusion molecular retention tumor targeting effect following peritumoral injection. In the combination therapy, HA-PDA-Ce6 displayed the highest tumor growth inhibition in HCT-116 tumor-bearing mice. Conclusion: HA-PDA-Ce6 is promising for targeted colorectal cancer therapy.
C1 [Wang, Xiaoling; Ouyang, Xumei; Sun, Xiaoyi] Zhejiang Univ City Coll, Dept Pharm, Hangzhou 310015, Zhejiang, Peoples R China.
   [Wang, Xiaoling; Ouyang, Xumei] Zhejiang Univ, Coll Pharmaceut Sci, Dept Pharmaceut, Hangzhou 310058, Zhejiang, Peoples R China.
   [Chen, Jinliang] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Clin Pharmacol, Hangzhou 310009, Zhejiang, Peoples R China.
   [Hu, Ying] Zhejiang Pharmaceut Coll, Dept Pharm, Ningbo 315000, Zhejiang, Peoples R China.
   [Yu, Zhenwei] Zhejiang Univ, Sir Run Run Shaw Hosp, Coll Med, Dept Pharm, Hangzhou 310016, Zhejiang, Peoples R China.
C3 Hangzhou City University; Zhejiang University; Zhejiang University;
   Zhejiang University
RP Sun, XY (corresponding author), Zhejiang Univ City Coll, Dept Pharm, Hangzhou 310015, Zhejiang, Peoples R China.; Yu, ZW (corresponding author), Zhejiang Univ, Sir Run Run Shaw Hosp, Coll Med, Dept Pharm, Hangzhou 310016, Zhejiang, Peoples R China.
EM sunxiaoyi@zucc.edu.cn; zhenweiyu84@126.com
RI Yu, Zhenwei/JTL-3981-2023
FU National Natural Science Foundation of China [81402872]; Natural Science
   Foundation of Zhejiang Province, China [LY17H160002, LY17H300001];
   Zhejiang Provincial Department of Health Medical Research Foundation of
   China [2018KY649]; Science and Technology Innovation Team Project of
   Ningbo Science and Technology Bureau, China [2015C110027]
FX This study is supported by the National Natural Science Foundation of
   China (81402872), Natural Science Foundation of Zhejiang Province, China
   (LY17H160002, LY17H300001), Zhejiang Provincial Department of Health
   Medical Research Foundation of China (2018KY649), Science and Technology
   Innovation Team Project of Ningbo Science and Technology Bureau, China
   (2015C110027). Writing support was provided by Liwen Bianji, Edanz
   Editing China. 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 38
TC 28
Z9 29
U1 5
U2 168
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1743-5889
EI 1748-6963
J9 NANOMEDICINE-UK
JI Nanomedicine
PD JAN
PY 2019
VL 14
IS 2
BP 151
EP 167
DI 10.2217/nnm-2018-0204
PG 17
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Science & Technology - Other
   Topics
GA HH3CV
UT WOS:000455597400003
PM 30511886
DA 2025-01-04
ER

PT J
AU Chung, SS
   Oliva, B
   Dwabe, S
   Vadgama, JV
AF Chung, Seyung S.
   Oliva, Bryant
   Dwabe, Sami
   Vadgama, Jaydutt V.
TI Combination treatment with flavonoid morin and telomerase inhibitor
   MST-312 reduces cancer stem cell traits by targeting STAT3 and
   telomerase
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE cancer stem cell; telomerase; combination treatment; colorectal cancer;
   STAT3
ID SIGNAL TRANSDUCER; GENE-EXPRESSION; GROWTH; FAMILY; ACTIVATION;
   PHOSPHORYLATION; IDENTIFICATION; PATHWAY; MEMBER
AB Colorectal cancer (CRC) is one of the most commonly diagnosed cancers worldwide. The malignant CRC that undergoes metastasis in the advanced stage is usually refractory to existing chemotherapy and shows a poor prognosis. However, to date, efficient targeted-therapy for metastatic CRC is ill-defined. We tested the hypothesis that combined treatment of flavonoid morin and telomerase inhibitor MST-312 may reduce the cancer stem cell (CSC) traits. To characterize CSC phenotype, we performed the CD133/CD44 subpopulation profiling, tumorsphere formation assay, cell invasion assay and wound healing assay. We have examined the augmenting effects of the combined treatment of morin and MST-312 for 5-FU (5-fluorouracil) efficacy in human colorectal cancer. Morin and MST-312 combined treatment reduced CD133 (+) and CD44 (+) subpopulations in human colorectal and breast cancer cells, respectively. Tumorsphere formation and cell invasiveness were decreased with the morin and MST-312 combination treatment. Consistent with these data, morin and MST-312 treatment decreased the wound healing capacity of human breast cancer cells. Stress and apoptosis antibody arrays revealed that there were specific upregulated and downregulated proteins resulting from different treatments. Phosphorylation levels of BAD, p53 and Chkl were enhanced upon morin/MST-312 treatments in HT-29 cells, whereas caspase-3 cleavage level and expression of IKBa were down regulated by combined morin/MST-312 treatment in SW620 cells. Finally, morin and MST-312 co-treatment further augmented the 5-FU efficacy, chemosensitizing the 5-FU resistant human colorectal cancer cells. Taken together, our study suggests that novel targeted-therapy can be implemented by using flavonoid morin and telomerase inhibitor MST-312 for improved cancer prognosis.
C1 [Chung, Seyung S.; Oliva, Bryant; Dwabe, Sami; Vadgama, Jaydutt V.] Charles R Drew Univ Med & Sci, Div Canc Res & Training, 1731 East 120th St, Los Angeles, CA 90059 USA.
   [Chung, Seyung S.; Oliva, Bryant; Dwabe, Sami; Vadgama, Jaydutt V.] Charles R Drew Univ Med & Sci, Dept Internal Med, 1731 East 120th St, Los Angeles, CA 90059 USA.
   [Vadgama, Jaydutt V.] Jonsson Comprehens Canc Ctr, Los Angeles, CA 90034 USA.
   [Chung, Seyung S.; Vadgama, Jaydutt V.] David Geffen UCLA Sch Med, Los Angeles, CA 90059 USA.
C3 Charles R. Drew University of Medicine & Science; Charles R. Drew
   University of Medicine & Science; UCLA Jonsson Comprehensive Cancer
   Center; University of California System; University of California Los
   Angeles; University of California Los Angeles Medical Center; David
   Geffen School of Medicine at UCLA
RP Chung, SS (corresponding author), Charles R Drew Univ Med & Sci, Div Canc Res & Training, 1731 East 120th St, Los Angeles, CA 90059 USA.
EM seyungchung@cdrewu.edu
FU National Institutes of Health (NIH, NCI) [U54 CA143931, U54MD007598,
   UL1TR000124]; National Institutes of Health (NIH, NIMHD) [U54 CA143931,
   U54MD007598, UL1TR000124]; National Institutes of Health (NIH, NCATS)
   [U54 CA143931, U54MD007598, UL1TR000124]; Clinical Research Education
   and Career Development by the NIMHD [R25 MD 007610, U54 MD 007598]; Life
   Science Institute-CDU [S21 MD 000103]
FX This study was supported by the National Institutes of Health (NIH, NCI,
   NIMHD, NCATS) grants to J.V. Vadgama: U54 CA143931, U54MD007598,
   UL1TR000124. S. Steven Chung is a scholar supported by the Clinical
   Research Education and Career Development by the NIMHD R25 MD 007610,
   pilot project award from U54 MD 007598 and Emerging scientist award from
   the Life Science Institute-CDU S21 MD 000103. We thank the division of
   cancer research and training members for their helpful suggestions. We
   also thank Dr Robert Gelfand for careful reading and proofreading of the
   manuscript.
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NR 36
TC 43
Z9 44
U1 0
U2 21
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 AUG
PY 2016
VL 49
IS 2
BP 487
EP 498
DI 10.3892/ijo.2016.3546
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DP1QD
UT WOS:000378263600006
PM 27279256
OA Green Published, hybrid, Green Submitted
DA 2025-01-04
ER

EF