﻿FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Lim, JR
   Mouawad, J
   Gorton, OK
   Bubb, WA
   Kwan, AH
AF Lim, Jacqueline R.
   Mouawad, Josette
   Gorton, Olivia K.
   Bubb, William A.
   Kwan, Ann H.
TI Cancer stem cell characteristics and their potential as therapeutic
   targets
SO MEDICAL ONCOLOGY
LA English
DT Review
DE Cancer stem cells; CSCs; Treatment resistance; Self-renewal; Targeted
   therapy; Clinical significance
ID BREAST-CANCER; COLORECTAL-CANCER; SELF-RENEWAL; METFORMIN; EXPRESSION;
   PLASTICITY; CURCUMIN; MARKERS; HEAD; PROLIFERATION
AB Cancer stem cells (CSCs) are a tumour subpopulation whose capacity for self-renewal, differentiation and proliferation generates unfavourable patient outcomes, including therapeutic resistance and metastasis. Much research has focused on the generation, biomarkers and therapeutic resistance of CSCs, as well as the development of CSC-targeted therapies. Reviews to date have either addressed general CSC characteristics or focused on CSCs from a well-studied cancer. Increasingly, specific treatment plans based on identification of molecular features and biomarkers of a patient's cancer, rather than classification according to tissue origin or bulk tumour properties, are leading to better patient outcomes. Here, we compare CSC characteristics, specifically their biomarkers and molecular features, and identify those that are common to a number of cancers. Identification of CSC markers that suggest therapeutic strategies has led to several successful in vitro and animal tests, recommending clinical trials of treatments with potentially enhanced therapeutic benefits, especially for recurring cancers.
C1 [Lim, Jacqueline R.; Mouawad, Josette; Gorton, Olivia K.; Bubb, William A.; Kwan, Ann H.] Univ Sydney, Sydney, NSW, Australia.
C3 University of Sydney
RP Kwan, AH (corresponding author), Univ Sydney, Sydney, NSW, Australia.
EM ann.kwan@sydney.edu.au
OI Lim, Jacqueline R/0009-0007-5574-4866; Kwan, Ann/0000-0002-1506-2226
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NR 97
TC 24
Z9 25
U1 0
U2 12
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1357-0560
EI 1559-131X
J9 MED ONCOL
JI Med. Oncol.
PD JUL
PY 2021
VL 38
IS 7
AR 76
DI 10.1007/s12032-021-01524-8
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SK1EK
UT WOS:000655964000001
PM 34050825
DA 2025-01-04
ER

PT J
AU Duan, LL
   Yang, WL
   Feng, WB
   Cao, L
   Wang, XQ
   Niu, LR
   Li, YD
   Zhou, W
   Zhang, YJ
   Liu, JQ
   Zhang, HW
   Zhao, QC
   Hong, L
   Fan, DM
AF Duan, Lili
   Yang, Wanli
   Feng, Weibo
   Cao, Lu
   Wang, Xiaoqian
   Niu, Liaoran
   Li, Yiding
   Zhou, Wei
   Zhang, Yujie
   Liu, Jinqiang
   Zhang, Hongwei
   Zhao, Qingchuan
   Hong, Liu
   Fan, Daiming
TI Molecular mechanisms and clinical implications of miRNAs in drug
   resistance of colorectal cancer
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Review
DE biomarkers; colorectal cancer; drug resistance; miRNAs; targeted therapy
ID INHIBITS TUMOR-GROWTH; X-LINKED INHIBITOR; CONFERS 5-FLUOROURACIL
   RESISTANCE; EPITHELIAL-MESENCHYMAL TRANSITION; MEDIATES METHOTREXATE
   RESISTANCE; PROGRAMMED CELL-DEATH; COLON-CANCER; DOWN-REGULATION;
   OXALIPLATIN RESISTANCE; MULTIDRUG-RESISTANCE
AB Systemic chemotherapy is identified as a curative approach to prolong the survival time of patients with colorectal cancer (CRC). Although great progress in therapeutic approaches has been achieved during the last decades, drug resistance still extensively persists and serves as a major hurdle to effective anticancer therapy for CRC. The mechanism of multidrug resistance remains unclear. Recently, mounting evidence suggests that a great number of microRNAs (miRNAs) may contribute to drug resistance in CRC. Certain of these miRNAs may thus be used as promising biomarkers for predicting drug response to chemotherapy or serve as potential targets to develop personalized therapy for patients with CRC. This review mainly summarizes recent advances in miRNAs and the molecular mechanisms underlying miRNA-mediated chemoresistance in CRC. We also discuss the potential role of drug resistance-related miRNAs as potential biomarkers (diagnostic and prognostic value) and envisage the future orientation and challenges in translating the findings on miRNA-mediated chemoresistance of CRC into clinical applications.
C1 [Duan, Lili; Yang, Wanli; Feng, Weibo; Wang, Xiaoqian; Niu, Liaoran; Li, Yiding; Zhou, Wei; Zhang, Yujie; Liu, Jinqiang; Zhang, Hongwei; Zhao, Qingchuan; Hong, Liu; Fan, Daiming] Fourth Mil Med Univ, Natl Clin Res Ctr Digest Dis, State Key Lab Canc Biol, Xian 710032, Peoples R China.
   [Duan, Lili; Yang, Wanli; Feng, Weibo; Wang, Xiaoqian; Niu, Liaoran; Li, Yiding; Zhou, Wei; Zhang, Yujie; Liu, Jinqiang; Zhang, Hongwei; Zhao, Qingchuan; Hong, Liu; Fan, Daiming] Fourth Mil Med Univ, Xijing Hosp Digest Dis, Xian 710032, Peoples R China.
   [Cao, Lu] Fourth Mil Med Univ, Dept Biomed Engn, Xian, 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, Natl Clin Res Ctr Digest Dis, State Key Lab Canc Biol, Xian 710032, Peoples R China.; Hong, L (corresponding author), Fourth Mil Med Univ, Xijing Hosp Digest Dis, Xian 710032, Peoples R China.
EM hongliufmmu@163.com
RI feng, weibo/F-9183-2018
OI Cao, Lu/0000-0002-5159-7615
FU Scientific Foundation of Shaanxi Province [2019ZDLSF01-02-01,
   2018SF-240]; State Key Laboratory of Cancer Biology [CBSKL2014Z13];
   National Clinical Research Center for Digestive Diseases [2015BAI13B07]
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and/or publication of this article: This study was
   supported in part by grant from the Scientific Foundation of Shaanxi
   Province (Grant number 2019ZDLSF01-02-01, 2018SF-240), grant from the
   State Key Laboratory of Cancer Biology (Grant number CBSKL2014Z13) and
   grant from the National Clinical Research Center for Digestive Diseases
   (Grant number 2015BAI13B07). It was not supported by any private or
   public company or organization.
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NR 194
TC 14
Z9 14
U1 1
U2 12
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 AUG
PY 2020
VL 12
AR 1758835920947342
DI 10.1177/1758835920947342
PG 28
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NI6UW
UT WOS:000565487300001
PM 32922521
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Huang, ZY
   Wen, L
   Ye, LF
   Lu, YT
   Fong, WP
   Zhang, RJ
   Wu, SX
   Chen, ZG
   Cai, YY
   Xu, RH
   Li, YH
   Du, ZM
   Wang, DS
AF Huang, Zi-Yao
   Wen, Lei
   Ye, Liu-Fang
   Lu, Yu-Ting
   Fong, William Pat
   Zhang, Ren-Jing
   Wu, Si-Xian
   Chen, Zhi-Gang
   Cai, Yan-Yu
   Xu, Rui-Hua
   Li, Yu-Hong
   Du, Zi-Ming
   Wang, De-Shen
TI Clinical and molecular characteristics of <i>RNF43</i> mutations as
   promising prognostic biomarkers in colorectal cancer
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Article
DE colorectal cancer; predictive biomarker; prognosis; R117fs variant;
   RNF43 mutations
ID SERRATED PATHWAY; WNT; LANDSCAPE
AB Background: Transmembrane E3 ubiquitin ligase (RNF43) mutations are present in approximately 6-18% of colorectal cancers (CRC) and could enhance Wnt/beta-catenin signaling, which is emerging as a promising therapeutic target. This study aims to investigate the clinical and molecular characteristics and potential heterogeneity of RNF43-mutant CRC.Methods: A total of 78 patients with RNF43-mutant CRC were enrolled from July 2013 to November 2022. Demographic data, clinical characteristics, treatment regimens used, and survival outcomes were collected and analyzed.Results: Our study uncovered that patients with RNF43 mutations in the N-terminal domain (NTD; n = 50) exhibited shorter overall survival (OS; median months, 50.80 versus not reached; p = 0.043) compared to those in the C-terminal domain (CTD; n = 17). Most RNF43 mutations in NTD had positive primary lymph node status, low tumor mutation burden (TMB-L), and correlated with proficient mismatch repair (pMMR)/microsatellite stable (MSS) status. By contrast, RNF43 mutations in CTD were significantly enriched in deficient MMR (dMMR)/microsatellite instability (MSI-H) tumors with high TMB (TMB-H). N-terminal RNF43-mutated tumors harbored a hotspot variant (RNF43 R117fs), which independently predicted a significantly worse outcome in pMMR/MSS CRC with a median OS of 18.9 months. Patients with RNF43 mutations and the BRAF V600E alterations demonstrated sensitivity to BRAF/EGFR inhibitors. Moreover, we observed that pMMR/MSS patients with RNF43 R117fs mutation had a higher incidence of stage IV, >= 2 metastatic sites, low TMB, and none of them received PD-1/PD-L1 inhibitor therapy.Conclusion: Our findings provide the first evidence that RNF43 mutations in NTD and the R117fs variant correlate with a poorer prognosis in CRC patients, providing strategies for Wnt-targeted therapy to improve clinical efficacy.
C1 [Huang, Zi-Yao; Wen, Lei; Ye, Liu-Fang; Lu, Yu-Ting; Zhang, Ren-Jing; Wu, Si-Xian; Chen, Zhi-Gang; Cai, Yan-Yu; Xu, Rui-Hua; Li, Yu-Hong; Du, Zi-Ming; Wang, De-Shen] Sun Yat Sen Univ Canc Ctr, Guangdong Prov Clin Res Ctr Canc, Dept Med Oncol, State Key Lab Oncol South China, Guangzhou 510060, Peoples R China.
   [Huang, Zi-Yao; Wen, Lei; Ye, Liu-Fang; Wu, Si-Xian; Chen, Zhi-Gang; Cai, Yan-Yu; Xu, Rui-Hua; Li, Yu-Hong; Wang, De-Shen] Chinese Acad Med Sci, Res Unit Precis Diag & Treatment Gastrointestinal, Guangzhou 510060, Peoples R China.
   [Zhang, Ren-Jing; Du, Zi-Ming] Sun Yat Sen Univ Canc Ctr, Dept Mol Diagnost, Guangzhou 510060, Peoples R China.
C3 Sun Yat Sen University; State Key Lab Oncology South China; Chinese
   Academy of Medical Sciences - Peking Union Medical College; Sun Yat Sen
   University
RP Li, YH; Du, ZM; Wang, DS (corresponding author), Sun Yat Sen Univ Canc Ctr, Guangdong Prov Clin Res Ctr Canc, Dept Med Oncol, State Key Lab Oncol South China, Guangzhou 510060, Peoples R China.; Li, YH; Wang, DS (corresponding author), Chinese Acad Med Sci, Res Unit Precis Diag & Treatment Gastrointestinal, Guangzhou 510060, Peoples R China.
EM liyh@sysucc.org.cn; duzm1@sysucc.org.cn; wangdsh@sysucc.org.cn
RI Lu, Yuting/GQI-0554-2022; Fong, William/IYJ-6068-2023; you,
   wenlong/GYU-5216-2022; Wang, De-shen/JBR-7938-2023; Xu,
   Rui-Hua/AAW-4766-2021
OI Pat Fong, William/0000-0003-1259-6406; Wang,
   De-shen/0000-0001-9657-4380; Xu, Rui-Hua/0000-0001-9771-8534
FU Guangdong Basic and Applied Basic Research Foundation [2023B1515020015];
   National Natural Science Foundation of China [82073302, 81930065,
   82173128]; Fundamental Research Funds for the Central Universities, Sun
   Yat-sen University [22qntd4001]; CAMS Innovation Fund for Medical
   Sciences (CIFMS) [2019-I2M-5-036]; Beijing Health Alliance Charitable
   Foundation [BJHA-CRP-058]
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and/or publication of this article: This work was
   supported, in part, by the Guangdong Basic and Applied Basic Research
   Foundation (Grand number: 2023B1515020015); National Natural Science
   Foundation of China (Grant numbers: 82073302, 81930065, 82173128); the
   Fundamental Research Funds for the Central Universities, Sun Yat-sen
   University (Grand number: 22qntd4001); the CAMS Innovation Fund for
   Medical Sciences (CIFMS) (Grant number: 2019-I2M-5-036); Beijing Health
   Alliance Charitable Foundation (Grand number: BJHA-CRP-058). The funders
   played no role in designing the study, collecting, analyzing, or
   interpreting data, nor did they contribute to the writing of the
   manuscript.
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NR 46
TC 2
Z9 2
U1 0
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PY 2024
VL 16
AR 17588359231220600
DI 10.1177/17588359231220600
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EN4V8
UT WOS:001139600600001
PM 38205077
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Keikes, L
   van Oijen, MGH
   Lemmens, VEPP
   Koopman, M
   Punt, CJA
AF Keikes, Lotte
   van Oijen, Martijn G. H.
   Lemmens, Valery E. P. P.
   Koopman, Miriam
   Punt, Cornelis J. A.
TI Evaluation of Guideline Adherence in Colorectal Cancer Treatment in The
   Netherlands: A Survey Among Medical Oncologists by the Dutch Colorectal
   Cancer Group
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Adjuvant chemotherapy; Colorectal neoplasms; Molecular targeted therapy;
   Practice guidelines as topic; Quality of health care
ID CLINICAL-PRACTICE GUIDELINES; III COLON-CANCER; ADJUVANT CHEMOTHERAPY;
   STAGE-II; COST-EFFECTIVENESS; BEVACIZUMAB; OXALIPLATIN; FLUOROURACIL;
   COMBINATION; LEUCOVORIN
AB Guideline adherence for the systemic treatment of (metastatic) colorectal cancer was surveyed among oncologists in The Netherlands. Reported overtreatment patterns (adjuvant setting) and undertreatment patterns for targeted therapies (metastatic setting) were identified, possibly explained by unawareness or disagreement with the guidelines, or local financial restrictions. Additional support for guideline implementation and monitoring besides investigating underlying causes for nonadherence is recommended.
   Background: Clinical guidelines are generated to preserve high-quality evidence-based care. Data on the implementation of guidelines into clinical practice are scarce, despite that guideline adherence prevents over-and undertreatment and correlates with survival. Therefore, we investigated guideline adherence for the systemic treatment in high-risk stage II and stage III colon cancer and metastatic colorectal cancer. Patients and Methods: In all Dutch hospitals (n = 88) 1 medical oncologist involved in colorectal cancer care was approached to participate. An online survey was conducted regarding the local standard of care for adjuvant chemotherapy in high-risk stage II and stage III colon cancer and first-line treatment regimens in metastatic colorectal cancer. Frequency tables were provided for categorical variables and compared for differences in guideline adherence according to hospital type (academic/teaching/regional). Results: The overall response rate was 70% (62 of 88). Reported guideline adherence was at least 60% of all presented settings. For high-risk stage II and stage III colon cancer, treatment strategies agreed with national guidelines in 66% and 84% of hospitals, and overtreatment patterns were identified in 28% and 13%, respectively. Targeted therapy was not routinely administered as first-line treatment in metastatic colorectal cancer (range from 63% to 71% in different settings). No differences in guideline adherence were observed among different hospital types. Conclusion: Guideline adherence as reported by medical oncologists in The Netherlands is suboptimal. Possible explanations include unawareness or disagreement with the guidelines, or local financial restrictions. Our results recommend additional support of guideline implementation and monitoring in clinical practice, and investigating underlying causes in case of nonadherence. (C) 2017 The Authors. Published by Elsevier Inc.
C1 [Keikes, Lotte; van Oijen, Martijn G. H.; Punt, Cornelis J. A.] Acad Med Ctr, Canc Ctr Amsterdam, Dept Med Oncol, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.
   [Lemmens, Valery E. P. P.] Netherlands Comprehens Canc Org, Utrecht, Netherlands.
   [Koopman, Miriam] Univ Med Ctr, Dept Med Oncol, Utrecht, Netherlands.
C3 University of Amsterdam; Academic Medical Center Amsterdam; Vrije
   Universiteit Amsterdam; Utrecht University; Utrecht University Medical
   Center
RP Keikes, L (corresponding author), Acad Med Ctr, Canc Ctr Amsterdam, Dept Med Oncol, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.
EM l.keikes@amc.uva.nl
FU Amgen; Roche; Merck Serono
FX The authors thank all medical oncologists in The Netherlands who
   participated in this study. This study was funded with an unrestricted
   research grant by Amgen, Roche, and Merck Serono.
CR Abdelsattar ZM, 2015, CANCER-AM CANCER SOC, V121, P783, DOI 10.1002/cncr.29124
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NR 20
TC 27
Z9 27
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 MAR
PY 2018
VL 17
IS 1
BP 58
EP 64
DI 10.1016/j.clcc.2017.10.007
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FY0HC
UT WOS:000426490300027
PM 29157662
OA hybrid
DA 2025-01-04
ER

PT J
AU Mas, L
   Bachet, JB
   Jooste, V
   Lepage, C
   Bouvier, AM
AF Mas, Leo
   Bachet, Jean-Baptiste
   Jooste, Valerie
   Lepage, Come
   Bouvier, Anne-Marie
TI Chemotherapy of metastatic colon cancer in France: A population-based
   study
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Article
DE Metastatic colorectal cancer; Chemotherapy; Population-based
ID FOLFIRI PLUS BEVACIZUMAB; COLORECTAL-CANCER; 1ST-LINE TREATMENT;
   SYSTEMIC THERAPY; ELDERLY-PATIENTS; OPEN-LABEL; OLDER PATIENTS;
   SURVIVAL; CETUXIMAB; FLUOROURACIL
AB Aims: to describe, using data from a cancer registry in a well-defined French population, the therapeutic strategies and survival of patients with metastatic colon cancer (mCC). Methods: all patients with synchronous mCC diagnosed within the 2005-2014 period recorded in the digestive cancers registry of Burgundy were included. Results: 1286 mCC patients were included (57% male), of which 34.5% did not receive any antitumor treatment. Both, advanced age ( >75 years) and the Charlson comorbidity score >2 were significantly associated with the absence of antitumor treatment. Among the patients treated with chemotherapy, 59 and 33% received at least two and three lines, respectively. Most patients treated with chemotherapy (68%) did not receive first-line targeted therapy. Of patients aged >75 years, 57% received no chemotherapy and 56% of treated patients had first-line treatment only. Conclusion: this population-based study shows that more than one-third of patients with mCC receive no chemotherapy and that only 59% of treated patients receive treatment beyond the first line. This study also highlights the fact that more than half of patients >75 years do not get any antitumor treatment. In patients < 75 years, the proportion of patients receiving chemotherapy and/or undergoing curative intent surgery tended to increase over time. (c) 2021 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Mas, Leo; Bachet, Jean-Baptiste] Hop La Pitie Salpetriere, AP HP, Dept Hepatogastroenterol & Digest Oncol, 47-83 Blvd Hop, F-75013 Paris, France.
   [Bachet, Jean-Baptiste] UPMC Univ, Sorbonne Univ, 15-21 Rue Ecole Med, F-75006 Paris, France.
   [Jooste, Valerie; Lepage, Come; Bouvier, Anne-Marie] Digest Canc Registry Burgundy, Dijon, France.
   [Jooste, Valerie; Lepage, Come; Bouvier, Anne-Marie] Dijon Univ Hosp, 2 Blvd Marechal Lattre de Tassigny, F-21000 Dijon, France.
   [Jooste, Valerie; Lepage, Come; Bouvier, Anne-Marie] INSERM UMR 1231, Dijon, France.
   [Jooste, Valerie; Lepage, Come; Bouvier, Anne-Marie] Univ Burgundy, Maison Univ, F-21078 Dijon, France.
C3 Sorbonne Universite; Assistance Publique Hopitaux Paris (APHP); Hopital
   Universitaire Pitie-Salpetriere - APHP; Sorbonne Universite; Universite
   de Bourgogne; Institut Agro; AgroSup Dijon; CHU Dijon Bourgogne;
   Institut Agro; AgroSup Dijon; Universite de Bourgogne; Institut National
   de la Sante et de la Recherche Medicale (Inserm); Universite de
   Bourgogne
RP Bachet, JB (corresponding author), Hop La Pitie Salpetriere, AP HP, Dept Hepatogastroenterol & Digest Oncol, 47-83 Blvd Hop, F-75013 Paris, France.
EM jean-baptiste.bachet@aphp.fr
RI BACHET, Jean-Baptiste/N-6943-2017; Bouvier, Anne-Marie/R-6600-2017;
   Jooste, Valerie/AFW-1362-2022
OI Bouvier, Anne-Marie/0000-0001-9070-1027
FU Merck Serono s.a.s. (France), an affiliate of Merck KGaA (Darmstadt,
   Germany)
FX This study was supported by a grant from Merck Serono s.a.s. (France),
   an affiliate of Merck KGaA (Darmstadt, Germany). Merck Serono s.a.s.
   (France) had no role in study design, data collection, data analysis,
   data interpretation, or writing of the report.
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NR 42
TC 2
Z9 2
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD OCT
PY 2021
VL 53
IS 10
BP 1334
EP 1342
DI 10.1016/j.dld.2021.03.019
EA SEP 2021
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA WH0QU
UT WOS:000707394700019
PM 33865721
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Sur, D
   Lungulescu, C
   Dumitrescu, EA
   Afrasanie, V
   Spinu, S
   Lungulescu, CV
   Schmoll, HJ
AF Sur, Daniel
   Lungulescu, Cristina
   Dumitrescu, Elena Adriana
   Afrasanie, Vlad
   Spinu, Stefan
   Lungulescu, Cristian Virgil
   Schmoll, Hans-Joachim
TI A systematic review of clinical trials of treatment regimens in
   HER2-amplified metastatic colorectal cancer
SO EXPERT REVIEW OF ANTICANCER THERAPY
LA English
DT Review
DE mCRC; HER2 overexpression; targeted therapy; overall survival; toxicity
ID HER2; EGFR
AB Introduction: Targeting HER2 has led to a revolution in therapy for cancers such as breast and gastric cancer, HER2 amplification is rarer (just 2-6%) in colorectal cancer (CRC) and efforts to target this receptor have lagged. Despite recent FDA approval for the first directed therapy combination for HER2 amplified metastatic CRC, the EMA has not yet authorized any such treatment and this represents a persistent unmet need in Europe and beyond. Here, we review data from trials targeting HER2 amplification, the latest target for CRC therapy.Areas covered: PubMed, Cochrane Library, EMBASE, and clinicaltrials.gov were reviewed systematically for possible manuscripts from inception to 1 July 2022. Results: A total of seven studies comprised of 284 locally advanced/mCRC patients receiving HER2 targeting agents were included in this systematic review. Most of the studies (n = 5) were non-randomized phase 2 trials, one phase 2/3 randomized controlled trial, and one phase 2a multiple-basket study. The outcomes consisted in the analysis of HER2 targeting agents and ORR, PFS, OS benefit, and toxicities of the therapy.Expert opinion: Anti-HER2 therapy exhibits a favorable toxicity profile compared with other targeted approaches; however, there is work to be done on optimizing patient selection and understanding resistance mechanisms.
C1 [Sur, Daniel] Univ Med & Pharm Iuliu Hatieganu, Dept Med Oncol 11, Cluj Napoca, Romania.
   [Lungulescu, Cristina] Univ Med & Pharm Craiova, Doctoral Sch, Craiova, Romania.
   [Dumitrescu, Elena Adriana] Oncol Inst Prof Dr Alexandru Trestioreanu, Dept Med Oncol, Bucharest, Romania.
   [Afrasanie, Vlad] Univ Med & Pharm Grigore T Popa, Iasi, Romania.
   [Spinu, Stefan] Oncol Inst Prof Dr Ion Chiricuta, Dept Med Oncol, Cluj Napoca, Romania.
   [Lungulescu, Cristian Virgil] Univ Med & Pharm Craiova, Oncol Dept, 2-4 Petru Rares Str, Craiova 200349, Romania.
   [Schmoll, Hans-Joachim] Martin Luther Univ Halle Wittenberg Germany, Univ Clin, Dept Hematol Oncol, Clin Internal Med Hematol Oncol 4, Halle, Germany.
C3 Iuliu Hatieganu University of Medicine & Pharmacy; University of
   Medicine & Pharmacy of Craiova; Institute of Oncology "Prof. Dr. Al
   Trestioreanu"; Grigore T Popa University of Medicine & Pharmacy;
   Oncology Institute Prof. Dr. Ion Chiricuta; University of Medicine &
   Pharmacy of Craiova
RP Lungulescu, CV (corresponding author), Univ Med & Pharm Craiova, Oncol Dept, 2-4 Petru Rares Str, Craiova 200349, Romania.
EM cristilungulescu@yahoo.com
RI Lungulescu, Cristina/IUO-9050-2023; Lungulescu, Cristian/AAE-1833-2021;
   schmoll, hans-joachim/AAO-5219-2021; Sur, Daniel/X-5257-2018
OI Sur, Daniel/0000-0002-0926-4614; Spinu, Stefan/0000-0002-9526-5620
FU Ministry of Research, Innovation and Digitization, CNCS - UEFISCDI,
   within PNCDI III [PN-III-P1-1.1-PD-2021-0669]
FX This work was supported by a grant of the Ministry of Research,
   Innovation and Digitization, CNCS - UEFISCDI, project number
   PN-III-P1-1.1-PD-2021-0669, within PNCDI III.
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NR 30
TC 1
Z9 1
U1 1
U2 4
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 JUN 3
PY 2023
VL 23
IS 6
BP 633
EP 641
DI 10.1080/14737140.2023.2207830
EA MAY 2023
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA G7MJ0
UT WOS:000982055500001
PM 37127555
DA 2025-01-04
ER

PT J
AU Chen, YT
   Hsu, HC
   Lee, YS
   Liu, H
   Tan, BCM
   Chin, CY
   Chang, IYF
   Yang, CY
AF Chen, Yi-Tung
   Hsu, Hung-Chih
   Lee, Yun-Shien
   Liu, Hsuan
   Tan, Bertrand Chin-Ming
   Chin, Chia-Yin
   Chang, Ian Yi-Feng
   Yang, Chia-Yu
TI Longitudinal High-Throughput Sequencing of the T-Cell Receptor
   Repertoire Reveals Dynamic Change and Prognostic Significance of
   Peripheral Blood TCR Diversity in Metastatic Colorectal Cancer During
   Chemotherapy
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE T cell repertoire; metastatic colorectal cancer; prognosis; peripheral
   blood; chemotherapy
ID CARCINOEMBRYONIC ANTIGEN; INTRATUMOR HETEROGENEITY; COMBINATION; DEEP;
   AGE
AB Colorectal cancer (CRC) is a major cause of cancer mortality and morbidity. Despite advances in chemotherapy and targeted therapy, unsustainable clinical benefit was noted due to recurrence and therapy resistance. The immune status of the cancer patient may affect the effectiveness of disease treatments. The dynamic change in the T-cell receptor (TCR) repertoire might be a clinical parameter for monitoring treatment responses. In this study, we aimed to determine the characteristics and clinical significance of the TCR repertoire in patients with unresectable metastatic colorectal cancer (mCRC). Herein, we comprehensively profile 103 peripheral blood samples from 20 healthy controls and 16 CRC patients with a follow-up of 98 to 452 days to identify hypervariable rearrangements of the TCR alpha and TCR beta repertoires using high-throughput sequencing. We found that TCR alpha repertoires, TCR beta repertoires, and CDR3 clonotypes were altered in mCRC patients compared with healthy controls. The diversity of TCR repertoires and CDR3 clonotypes decreased in most mCRC patients after therapy. Furthermore, compared with baseline TCR diversity, patients whose TCR diversity dropped considerably during therapy had better treatment responses, including lower CEA and CA19-9 levels and smaller tumor sizes. TCR baseline diversity was also significantly associated with partial response (PR) status (odds ratio: 5.29, p = 0.04). In conclusion, the present study demonstrated the association between dynamic changes in TCR diversity during chemotherapy and clinical outcomes as well as the potential utility of the TCR repertoire in predicting the prognosis of cancer treatment.
C1 [Chen, Yi-Tung; Liu, Hsuan; Chin, Chia-Yin; Chang, Ian Yi-Feng; Yang, Chia-Yu] Chang Gung Univ, Mol Med Res Ctr, Taoyuan, Taiwan.
   [Chen, Yi-Tung; Tan, Bertrand Chin-Ming] Chang Gung Univ, Res Ctr Emerging Viral Infect, 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.
   [Lee, Yun-Shien] Ming Chuan Univ, Dept Biotechnol, Taoyuan, Taiwan.
   [Liu, Hsuan] Chang Gung Univ, Coll Med, Dept Cell & Mol Biol, Taoyuan, Taiwan.
   [Liu, Hsuan; Tan, Bertrand Chin-Ming; Yang, Chia-Yu] Chang Gung Univ, Coll Med, Grad Inst Biomed Sci, Taoyuan, Taiwan.
   [Liu, Hsuan] Chang Gung Mem Hosp, Div Colon & Rectal Surg, Taoyuan, Taiwan.
   [Tan, Bertrand Chin-Ming] Chang Gung Univ, Coll Med, Dept Biomed Sci, Taoyuan, Taiwan.
   [Tan, Bertrand Chin-Ming; Chang, Ian Yi-Feng] Chang Gung Mem Hosp, Lin Kou Med Ctr, Dept Neurosurg, Taoyuan, Taiwan.
   [Yang, Chia-Yu] Chang Gung Univ, Coll Med, Dept Microbiol & Immunol, Taoyuan, Taiwan.
   [Yang, Chia-Yu] Chang Gung Mem Hosp, Dept Otolaryngol Head & Neck Surg, Taoyuan, Taiwan.
C3 Chang Gung University; Chang Gung University; Chang Gung Memorial
   Hospital; Chang Gung University; Ming Chuan University; Chang Gung
   University; Chang Gung University; Chang Gung Memorial Hospital; Chang
   Gung University; Chang Gung Memorial Hospital; Chang Gung University;
   Chang Gung Memorial Hospital
RP Yang, CY (corresponding author), Chang Gung Univ, Mol Med Res Ctr, Taoyuan, Taiwan.; Yang, CY (corresponding author), Chang Gung Univ, Coll Med, Grad Inst Biomed Sci, Taoyuan, Taiwan.; Yang, CY (corresponding author), Chang Gung Univ, Coll Med, Dept Microbiol & Immunol, Taoyuan, Taiwan.; Yang, CY (corresponding author), Chang Gung Mem Hosp, Dept Otolaryngol Head & Neck Surg, Taoyuan, Taiwan.
EM chiayu-yang@mail.cgu.edu.tw
RI Chang, Ian/U-3571-2019
OI Chen, Yi-Tung/0000-0001-9715-648X; Chang, Ian/0000-0001-5840-2051
FU Ministry of Science and Technology of Taiwan [107-2314-B-182-075-MY3,
   110-2314-B-182-046]; Chang Gung Memorial Hospital [CMRPG3I0311,
   CMRPG3G2071, CMRPD1K0402]; Ministry of Education (MOE) in Taiwan
   [MOST108-3017-F182-001]; Ministry of Science and Technology (MOST),
   Taiwan [MOST108-3017-F182-001]; Genomics NGS Laboratory Molecular
   Medicine Research Center, Chang Gung University, Taiwan [EMRPD1L0281,
   CLRPD1J0013]
FX This work was supported by grants from the Ministry of Science and
   Technology of Taiwan (107-2314-B-182-075-MY3, 110-2314-B-182-046 to
   C-YY) and Chang Gung Memorial Hospital (CMRPG3I0311 and CMRPG3G2071 to
   H-CH, CMRPD1K0402 to C-YY). This work was also financially supported by
   the "Research Center for Emerging Viral Infections" and the "Molecular
   Medicine Research Center" from the Featured Areas Research Center
   Program within the framework of the Higher Education Sprout Project by
   the Ministry of Education (MOE) in Taiwan and the Ministry of Science
   and Technology (MOST), Taiwan (MOST108-3017-F182-001). NGS experiments
   and bioinformatics analyses were performed at the Genomics NGS
   Laboratory Molecular Medicine Research Center, Chang Gung University,
   Taiwan (EMRPD1L0281, CLRPD1J0013).
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NR 35
TC 9
Z9 10
U1 0
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JAN 12
PY 2022
VL 12
AR 743448
DI 10.3389/fimmu.2021.743448
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 2C5AR
UT WOS:000810881700001
PM 35095836
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Schmitt, M
   Greten, FR
AF Schmitt, Mark
   Greten, Florian R.
TI The inflammatory pathogenesis of colorectal cancer
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT Review
ID TUMOR-ASSOCIATED NEUTROPHILS; POOR-PROGNOSIS SUBTYPES; KAPPA-B
   ACTIVATION; BODY-MASS INDEX; MOUSE MODEL; INTESTINAL INFLAMMATION;
   FUSOBACTERIUM-NUCLEATUM; COLON CARCINOGENESIS; TARGETED THERAPY; IMMUNE
   LANDSCAPE
AB The mutational landscape of colorectal cancer (CRC) does not enable predictions to be made about the survival of patients or their response to therapy. Instead, studying the polarization and activation profiles of immune cells and stromal cells in the tumour microenvironment has been shown to be more informative, thus making CRC a prototypical example of the importance of an inflammatory microenvironment for tumorigenesis. Here, we review our current understanding of how colon cancer cells interact with their microenvironment, comprised of immune cells, stromal cells and the intestinal microbiome, to suppress or escape immune responses and how inflammatory processes shape the immune pathogenesis of CRC.
   Mark Schmitt and Florian Greten describe the mechanisms by which chronic inflammation can initiate tumorigenesis and by which tumour-elicited and therapy-induced inflammation can promote colorectal cancer, as well as the role of extrinsic factors such as diet, the microbiota and the mycobiota.
C1 [Schmitt, Mark; Greten, Florian R.] Georg Speyer Haus, Inst Tumor Biol & Expt Therapy, Frankfurt, Germany.
   [Schmitt, Mark; Greten, Florian R.] Goethe Univ Frankfurt, Frankfurt Canc Inst, Frankfurt, Germany.
   [Greten, Florian R.] German Canc Consortium DKTK, Heidelberg, Germany.
   [Greten, Florian R.] German Canc Res Ctr, Heidelberg, Germany.
C3 Octapharma; Goethe University Frankfurt; Helmholtz Association; German
   Cancer Research Center (DKFZ); Helmholtz Association; German Cancer
   Research Center (DKFZ)
RP Greten, FR (corresponding author), Georg Speyer Haus, Inst Tumor Biol & Expt Therapy, Frankfurt, Germany.; Greten, FR (corresponding author), Goethe Univ Frankfurt, Frankfurt Canc Inst, Frankfurt, Germany.; Greten, FR (corresponding author), German Canc Consortium DKTK, Heidelberg, Germany.; Greten, FR (corresponding author), German Canc Res Ctr, Heidelberg, Germany.
EM greten@gsh.uni-frankfurt.de
RI Schmitt, Mark/LQJ-7638-2024; Greten, Florian/AAF-5196-2020
OI Greten, Florian/0000-0002-3928-6080
FU Georg-Speyer-Haus; LOEWE Center Frankfurt Cancer Institute (FCI) -
   Hessen State Ministry for Higher Education, Research and the Arts [III L
   5-519/03/03.001-(0015)]; Deutsche Forschungsgemeinschaft [FOR2438:
   Gr1916/11-1, SFB 815, SFB 1177, SFB 1292, GRK 2336]; German Federal
   Ministry of Health; Ministry of Higher Education, Research and the Arts
   of the State of Hessen (HMWK)
FX Work in the laboratory of F.R.G. is supported by institutional funds
   from the Georg-Speyer-Haus, by the LOEWE Center Frankfurt Cancer
   Institute (FCI) funded by the Hessen State Ministry for Higher
   Education, Research and the Arts [III L 5 -519/03/03.001 -(0015)], and
   by the Deutsche Forschungsgemeinschaft (FOR2438: Gr1916/11-1; SFB 815,
   1177 and 1292 as well as GRK 2336). The Institute for Tumor Biology and
   Experimental Therapy, Georg-Speyer-Haus, is funded jointly by the German
   Federal Ministry of Health and the Ministry of Higher Education,
   Research and the Arts of the State of Hessen (HMWK).
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PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1474-1733
EI 1474-1741
J9 NAT REV IMMUNOL
JI Nat. Rev. Immunol.
PD OCT
PY 2021
VL 21
IS 10
BP 653
EP 667
DI 10.1038/s41577-021-00534-x
EA APR 2021
PG 15
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA UX9XG
UT WOS:000645174200002
PM 33911231
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Li, XW
   Xu, M
   Ding, L
   Tang, JH
AF Li, Xingwang
   Xu, Min
   Ding, Li
   Tang, Jinhai
TI MiR-27a: A Novel Biomarker and Potential Therapeutic Target in Tumors
SO JOURNAL OF CANCER
LA English
DT Review
DE miRNA; miR-27a; cancer
ID GASTRIC-CANCER SUSCEPTIBILITY; CELL-PROLIFERATION; GENETIC VARIANT;
   GROWTH-FACTOR; UP-REGULATION; ONCOGENIC MICRORNA-27A; ESOPHAGEAL CANCER;
   BLADDER-CANCER; RS11671784 G/A; EXPRESSION
AB MicroRNAs (miRNAs) are endogenous, time sequencing, conserved and small non-coding RNA molecules (19-25 bp long) that regulate gene expression at the post-transcriptional level by binding to the partial sequence homology of the 3'-untranslated region of target messenger (m)RNA. The miRNA-27 family consists of miR-27a and miR-27b, which are transcribed from different chromosomes and different in nucleotide at the 3' end. It has been reported that miR-27a was located on chromosome 19 and played a vital role in tumor development. Increasing evidences support a vital role for miR-27a in modulating polymorphisms, tumorigenesis, proliferation, apoptosis, invasion, migration and angiogenesis. Apart from it, miR-27a could affect drug sensitivity, treatment of cancer and patients prognosis. The miR-27a could be an oncogene or a tumor suppressor in several types of cancer, including colon cancer, pancreatic cancer, breast cancer, bladder cancer and hepatocellular carcinoma. In this review, we discuss the role of miR-27a in tumor biology and clinical significance in detail and offer novel insights into molecular targeting therapy for human cancers.
C1 [Li, Xingwang; Xu, Min; Tang, Jinhai] Xuzhou Med Univ, Sch Clin Med, 209 Tongshan Rd, Xuzhou 221004, Jiangsu, Peoples R China.
   [Ding, Li; Tang, Jinhai] Nanjing Med Univ, Affiliated Hosp 1, Dept Gen Surg, Nanjing 210029, Jiangsu, Peoples R China.
C3 Xuzhou Medical University; Nanjing Medical University
RP Tang, JH (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, Dept Gen Surg, Nanjing 210029, Jiangsu, Peoples R China.
EM jhtang@njmu.edu.cn
RI Li, Xingwang/K-8678-2019
FU National Key Research and Development Program of China [2016YFC0905900];
   National Natural Science Foundation of China [81872365]; "333" Talent
   Project of Jiangsu Province [4(2016)]; Innovation Team Construction
   Project of Nanjing Medical University [JX102GSP201727]
FX This research was supported by the National Key Research and Development
   Program of China (No. 2016YFC0905900), National Natural Science
   Foundation of China (No. 81872365), the "333" Talent Project of Jiangsu
   Province [No. 4(2016)] and Innovation Team Construction Project of
   Nanjing Medical University (No. JX102GSP201727).
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NR 82
TC 85
Z9 86
U1 0
U2 8
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 12
BP 2836
EP 2848
DI 10.7150/jca.31361
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IB2HC
UT WOS:000470089300026
PM 31258791
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Li, L
   Xu, Y
   Yang, Y
   Ye, F
   Zhang, HM
   Zhou, AP
   Zhao, XM
AF Li, Lu
   Xu, Ying
   Yang, Yi
   Ye, Feng
   Zhang, Hongmei
   Zhou, Aiping
   Zhao, Xinming
TI RECIST 1.1, Choi and mChoi criteria in the evaluation of tumor response
   in patients with metastatic colorectal cancer treated with Regorafenib
   and anti-PD-1 antibody
SO EUROPEAN JOURNAL OF RADIOLOGY
LA English
DT Article
DE Metastatic colorectal cancer; Targeted therapy; Immunotherapy; Tumor
   response; Overall survival
ID HEPATOCELLULAR-CARCINOMA; CELL CARCINOMA; NIVOLUMAB
AB Purpose: No comparative study on evaluating performance of radiological criteria has been investigated in metastatic colorectal cancer (mCRC) patients treated with the combination of Regorafenib and anti-programmed cell death 1(PD-1) antibody. We aimed to compare the performance of different radiological criteria in evaluating response in mCRC patients treated with the combination of Regorafenib plus anti-PD-1 antibody. Method: We retrospectively recruited patients treated with Regorafenib and anti-PD-1 antibody in a single institution. Baseline and the first tumor evaluation of contrast-enhanced computed tomography (CE-CT) were assessed by three evaluation criteria: RECIST 1.1, Choi, modified Choi (mChoi). Overall survival (OS) was defined as endpoint event. Results: Twenty-three mCRC patients [age: 58.8 +/- 10.6 years, 18 (78.3 %) males] were assessed. The median overall survival was 11.8 months. According to RECIST 1.1, 8 (34.8 %) patients were stable disease (SD) and 15 (65.2 %) were progressive disease (PD). According to Choi and mChoi, 5 (21.7 %) and 1(4.3 %) patient was responders, respectively. All non-PD patients showed significantly better overall survival than PD patients by all criteria. According to Choi, those identified as responders showed better overall survival than non-responders though significant statistics were not reached (P=0.262). Conclusions: RECIST 1.1, Choi and mChoi criteria could identify survival benefit from Regorafenib plus anti-PD-1 antibody in mCRC patients. However, the value of responders detected by Choi remains to be validated in further studies.
C1 [Li, Lu; Xu, Ying; Yang, Yi; Ye, Feng; Zhang, Hongmei; Zhao, Xinming] Chinese Acad Med Sci, Dept Diagnost Radiol, Natl Canc Ctr, Natl Clin Res Ctr Canc,Canc Hosp, Beijing 100021, Peoples R China.
   [Yang, Yi] Chinese Acad Med Sci, Dept Intervent Therapy, Natl Canc Ctr, Natl Clin Res Ctr Canc,Canc Hosp, Beijing 100021, Peoples R China.
   [Zhou, Aiping] Chinese Acad Med Sci, Dept Med Oncol, Natl Canc Ctr, Natl Clin Res Ctr Canc,Canc Hosp, Beijing 100021, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Cancer Institute & Hospital - CAMS; Chinese Academy of Medical Sciences
   - Peking Union Medical College; Cancer Institute & Hospital - CAMS;
   Chinese Academy of Medical Sciences - Peking Union Medical College;
   Cancer Institute & Hospital - CAMS
RP Ye, F; Zhou, AP (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Canc Hosp, 17 Pan Jia Yuan South Lane, Beijing 100021, Peoples R China.
EM dr_fengye_ncc@163.com; zhouaiping2021@yeah.net
RI Yang, Yi/AAR-2728-2020
OI Yang, Yi/0000-0002-9835-4098
FU Peking Union Medical College Youth Fund [2017320014]
FX This paper is supported by the Peking Union Medical College Youth Fund
   under Grant Nos. 2017320014.
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NR 20
TC 5
Z9 5
U1 0
U2 1
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0720-048X
EI 1872-7727
J9 EUR J RADIOL
JI Eur. J. Radiol.
PD AUG
PY 2021
VL 141
AR 109823
DI 10.1016/j.ejrad.2021.109823
EA JUN 2021
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA TL2AP
UT WOS:000674656400003
PM 34146911
DA 2025-01-04
ER

PT J
AU Yee, NS
AF Yee, Nelson S.
TI Update in Systemic and Targeted Therapies in Gastrointestinal Oncology
SO BIOMEDICINES
LA English
DT Article
DE biliary tract carcinoma; chemotherapy; clinical trial; colorectal
   carcinoma; gastric carcinoma; gastrointestinal oncology; hepatocellular
   carcinoma; immunotherapy; pancreatic carcinoma; targeted therapy
ID MOLECULAR-GENETICS; OPEN-LABEL; CANCER; MULTICENTER
AB Progress has been made in the treatment of gastrointestinal cancers through advances in systemic therapies, surgical interventions, and radiation therapy. At the Multi-Disciplinary Patient Care in Gastrointestinal Oncology conference, the faculty members of the Penn State Health Milton S. Hershey Medical Center presented a variety of topics that focused on this sub-specialty. This conference paper highlights the new development in systemic treatment of various malignant diseases in the digestive system. Results of the recent clinical trials that investigated the clinical efficacy of pegylated hyaluronidase, napabucasin, and L-asparaginase in pancreatic carcinoma are presented. The use of peri-operative chemotherapy comprised of 5-fluorouracil or capecitabine, leucovorin, oxaliplatin, and docetaxel (FLOT), and immunotherapy including pembrolizumab, nivolumab, and ipilimumab in gastroesophageal carcinoma are discussed. Data from clinical trials that investigated the targeted therapeutics including nivolumab, ramucirumab, lenvatinib, and BLU-554 are reported. The role of adjuvant capecitabine in resected biliary tract carcinoma (BTC) and nab-paclitaxel in combination with gemcitabine and cisplatin in advanced BTC are presented. In colorectal carcinoma, the efficacy of nivolumab, adjuvant FOLFOX or CAPOX, irinotecan/cetuximab/vemurafenib, and trifluridine/tipiracil/bevacizumab, is examined. In summary, some of the above systemic therapies have become or are expected to become new standard of care, while the others demonstrate the potential of becoming new treatment options.
C1 [Yee, Nelson S.] Penn State Univ, Penn State Hlth Milton S Hershey Med Ctr, Expt Therapeut Program, Penn State Canc Inst,Coll Med,Dept Med,Div Hemato, Hershey, PA 17033 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE);
   Pennsylvania State University; Penn State Health
RP Yee, NS (corresponding author), Penn State Univ, Penn State Hlth Milton S Hershey Med Ctr, Expt Therapeut Program, Penn State Canc Inst,Coll Med,Dept Med,Div Hemato, Hershey, PA 17033 USA.
EM nyee@pennstatehealth.psu.edu
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NR 30
TC 13
Z9 14
U1 0
U2 10
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD MAR
PY 2018
VL 6
IS 1
AR 34
DI 10.3390/biomedicines6010034
PG 14
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 GA7GY
UT WOS:000428505300033
PM 29547556
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Mammatas, LH
   Verheul, HMW
   Hendrikse, NH
   Yaqub, M
   Lammertsma, AA
   van Oordt, CWMV
AF Mammatas, Lemonitsa H.
   Verheul, Henk M. W.
   Hendrikse, N. Harry
   Yaqub, Maqsood
   Lammertsma, Adriaan A.
   van Oordt, C. Willemien Menke-van der Houven
TI Molecular imaging of targeted therapies with positron emission
   tomography: the visualization of personalized cancer care
SO CELLULAR ONCOLOGY
LA English
DT Review
DE Positron emission tomography; Molecular imaging; Radiolabelled drugs;
   Targeted therapy; Response prediction; Personalized medicine
ID SQUAMOUS-CELL CARCINOMA; ENDOTHELIAL GROWTH-FACTOR; TRANSGENIC MOUSE
   MODEL; IN-VIVO EVALUATION; BREAST-CANCER; EGFR EXPRESSION; LUNG-CANCER;
   RECEPTOR-BINDING; COLORECTAL-CANCER; QUANTITATIVE PET
AB Molecular imaging has been defined as the visualization, characterization and measurement of biological processes at the molecular and cellular level in humans and other living systems. In oncology it enables to visualize (part of) the functional behaviour of tumour cells, in contrast to anatomical imaging that focuses on the size and location of malignant lesions.
   Available molecular imaging techniques include single photon emission computed tomography (SPECT), positron emission tomography (PET) and optical imaging. In PET, a radiotracer consisting of a positron emitting radionuclide attached to the biologically active molecule of interest is administrated to the patient.
   Several approaches have been undertaken to use PET for the improvement of personalized cancer care. For example, a variety of radiolabelled ligands have been investigated for intratumoural target identification and radiolabelled drugs have been developed for direct visualization of the biodistibution in vivo, including intratumoural therapy uptake. First indications of the clinical value of PET for target identification and response prediction in oncology have been reported. This new imaging approach is rapidly developing, but uniformity of scanning processes, standardized methods for outcome evaluation and implementation in daily clinical practice are still in progress. In this review we discuss the available literature on molecular imaging with PET for personalized targeted treatment strategies.
   Molecular imaging with radiolabelled targeted anticancer drugs has great potential for the improvement of personalized cancer care. The non-invasive quantification of drug accumulation in tumours and normal tissues provides understanding of the biodistribution in relation to therapeutic and toxic effects.
C1 [Mammatas, Lemonitsa H.; Verheul, Henk M. W.; van Oordt, C. Willemien Menke-van der Houven] Vrije Univ Amsterdam, Med Ctr, Dept Med Oncol, VUmc Canc Ctr Amsterdam, NL-1081 HV Amsterdam, Netherlands.
   [Hendrikse, N. Harry; Yaqub, Maqsood; Lammertsma, Adriaan A.] Vrije Univ Amsterdam, Med Ctr, Dept Radiol & Nucl Med, VUmc Canc Ctr Amsterdam, NL-1081 HV Amsterdam, Netherlands.
   [Hendrikse, N. Harry] Vrije Univ Amsterdam, Med Ctr, Dept Clin Pharmacol & Pharm, VUmc Canc Ctr Amsterdam, NL-1081 HV Amsterdam, Netherlands.
C3 Vrije Universiteit Amsterdam; VU UNIVERSITY MEDICAL CENTER; Vrije
   Universiteit Amsterdam; VU UNIVERSITY MEDICAL CENTER; Vrije Universiteit
   Amsterdam; VU UNIVERSITY MEDICAL CENTER
RP van Oordt, CWMV (corresponding author), Vrije Univ Amsterdam, Med Ctr, Dept Med Oncol, VUmc Canc Ctr Amsterdam, De Boelelaan 1117, NL-1081 HV Amsterdam, Netherlands.
EM c.menke@vumc.nl
RI Verheul, Henk/V-6462-2019; van+der+Houven+van+Oordt, C./AAE-8064-2020;
   Lammertsma, Adriaan/HNJ-3740-2023
OI Menke-van der Houven van Oordt, C. Willemien/0000-0002-5404-5883;
   Verheul, Henk/0000-0001-5981-922X; Lammertsma,
   Adriaan/0000-0003-1237-2891; Mammatas, Lemonitsa/0000-0001-9720-7769
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NR 133
TC 24
Z9 27
U1 0
U2 27
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 2211-3428
EI 2211-3436
J9 CELL ONCOL
JI Cell. Oncol.
PD FEB
PY 2015
VL 38
IS 1
BP 49
EP 64
DI 10.1007/s13402-014-0194-4
PG 16
WC Oncology; Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology; Pathology
GA CD7YQ
UT WOS:000351312400006
PM 25248503
DA 2025-01-04
ER

PT J
AU Toomey, S
   Gunther, J
   Carr, A
   Weksberg, DC
   Thomas, V
   Salvucci, M
   Bacon, O
   Sherif, EM
   Fay, J
   Kay, EW
   Sheehan, KM
   McNamara, DA
   Sanders, KL
   Mathew, G
   Breathnach, OS
   Grogan, L
   Morris, PG
   Foo, WC
   You, YQN
   Prehn, JH
   O'Neill, B
   Krishnan, S
   Hennessy, BT
   Furney, SJ
AF Toomey, Sinead
   Gunther, Jillian
   Carr, Aoife
   Weksberg, David C.
   Thomas, Valentina
   Salvucci, Manuela
   Bacon, Orna
   Sherif, El-Masry
   Fay, Joanna
   Kay, Elaine W.
   Sheehan, Katherine M.
   McNamara, Deborah A.
   Sanders, Keith L.
   Mathew, Geena
   Breathnach, Oscar S.
   Grogan, Liam
   Morris, Patrick G.
   Foo, Wai C.
   You, Yi-Qian N.
   Prehn, Jochen H.
   O'Neill, Brian
   Krishnan, Sunil
   Hennessy, Bryan T.
   Furney, Simon J.
TI Genomic and Transcriptomic Characterisation of Response to Neoadjuvant
   Chemoradiotherapy in Locally Advanced Rectal Cancer
SO CANCERS
LA English
DT Article
DE locally advanced rectal cancer; neoadjuvant chemoradiotherapy; whole
   exome sequencing; RNA-seq; microbiome; microsatellite instability
ID GENE COPY NUMBER; COLORECTAL-CANCER; AURORA KINASE; COLON-CANCER;
   CHEMORADIATION THERAPY; MUTATIONS; SUBTYPES; KRAS; RADIOTHERAPY;
   RESISTANCE
AB Standard treatment for locally advanced rectal cancer (LARC) is neoadjuvant chemoradiotherapy (NACRT), followed by surgical resection. However, >70% of patients do not achieve a complete pathological response and have higher rates of relapse and death. There are no validated pre- or on-treatment factors that predict response to NACRT besides tumour stage and size. We characterised the response of 33 LARC patients to NACRT, collected tumour samples from patients prior to, during and after NACRT, and performed whole exome, transcriptome and high-depth targeted sequencing. The pre-treatment LARC genome was not predictive of response to NACRT. However, in line with the increasing recognition of microbial influence in cancer, RNA analysis of pre-treatment tumours suggested a greater abundance ofFusobacteriain intermediate and poor responders. In addition, we investigated tumour heterogeneity and evolution in response to NACRT. While matched pre-treatment, on-treatment and post-treatment tumours revealed minimal genome evolution overall, we identified cases in which microsatellite instability developed or was selected for during NACRT. Recent research has suggested a role for adaptive mutability to targeted therapy in colorectal cancer cells. We provide preliminary evidence of selection for mismatch repair deficiency in response to NACRT. Furthermore, pre-NACRT genomic landscapes do not predict treatment response but pre-NACRT microbiome characteristics may be informative.
C1 [Toomey, Sinead; Carr, Aoife; Hennessy, Bryan T.] Royal Coll Surgeons Ireland, Dept Mol Med, Med Oncol Grp, Dublin 9, Ireland.
   [Gunther, Jillian; Weksberg, David C.; Sanders, Keith L.; Mathew, Geena; Krishnan, Sunil] Univ Texas MD Anderson Canc Ctr, Dept Radiat Oncol, Houston, TX 77030 USA.
   [Weksberg, David C.] UPMC Pinnacle, Harrisburg, PA 17101 USA.
   [Thomas, Valentina; Furney, Simon J.] Royal Coll Surgeons Ireland, Dept Physiol & Med Phys, Genom Oncol Res Grp, Dublin 2, Ireland.
   [Thomas, Valentina; Salvucci, Manuela; Bacon, Orna; Prehn, Jochen H.; Furney, Simon J.] Royal Coll Surgeons Ireland, Ctr Syst Med, Dept Physiol & Med Phys, Dublin 2, Ireland.
   [Sherif, El-Masry] Our Lady Lourdes Hosp Drogheda, Dept Surg, Drogheda, Co Louth, Ireland.
   [Sherif, El-Masry; McNamara, Deborah A.] Beaumont Hosp, Dept Surg, Dublin 9, Ireland.
   [Fay, Joanna; Kay, Elaine W.; Sheehan, Katherine M.] Royal Coll Surgeons Ireland, Dept Pathol, Dublin 9, Ireland.
   [Breathnach, Oscar S.; Grogan, Liam; Morris, Patrick G.; Hennessy, Bryan T.] Beaumont Hosp, Dept Med Oncol, Dublin 9, Ireland.
   [Foo, Wai C.] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
   [You, Yi-Qian N.] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX 77030 USA.
   [O'Neill, Brian] Beaumont Hosp, St Lukes Radiat Oncol Ctr, Dept Radiat Oncol, Dublin 9, Ireland.
C3 Royal College of Surgeons - Ireland; University of Texas System; UTMD
   Anderson Cancer Center; Royal College of Surgeons - Ireland; Royal
   College of Surgeons - Ireland; Royal College of Surgeons - Ireland;
   University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center
RP Hennessy, BT (corresponding author), Royal Coll Surgeons Ireland, Dept Mol Med, Med Oncol Grp, Dublin 9, Ireland.; Krishnan, S (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Radiat Oncol, Houston, TX 77030 USA.; Furney, SJ (corresponding author), Royal Coll Surgeons Ireland, Dept Physiol & Med Phys, Genom Oncol Res Grp, Dublin 2, Ireland.; Furney, SJ (corresponding author), Royal Coll Surgeons Ireland, Ctr Syst Med, Dept Physiol & Med Phys, Dublin 2, Ireland.; Hennessy, BT (corresponding author), Beaumont Hosp, Dept Med Oncol, Dublin 9, Ireland.
EM sineadtoomey@rcsi.ie; JGunther@mdanderson.org; aoifecarr@rcsi.ie;
   davidweks@gmail.com; valentinathomas@rcsi.ie; manuelasalvucci@rcsi.ie;
   ornabacon@rcsi.ie; selmasry@rcsi.ie; joannafay@rcsi.ie;
   elainewkay@gmail.com; ksheehan@rcsi.ie; deborahmcnamara@rcsi.ie;
   KLSanders@mdanderson.org; geenag@mdanderson.org;
   osbreathnach@beaumont.ie; liamgrogan@beaumont.ie;
   patrickmorris@beaumont.ie; WFoo@mdanderson.org; YNYou@mdanderson.org;
   JPrehn@rcsi.ie; Brian.Oneill@slh.ie; krishnan.sunil@mayo.edu;
   bryanhennessy74@gmail.com; simonfurney@rcsi.ie
RI O'Neill, Brian/B-8702-2015; Furney, Simon/C-6248-2011; Prehn,
   Jochen/A-3928-2010; Krishnan, Sunil/HKF-3238-2023
OI Hennessy, Bryan/0000-0002-7871-6477; Toomey, Sinead/0000-0002-1365-8173;
   Furney, Simon/0000-0002-8920-6800; Foo, Wai Chin/0000-0002-0471-4911;
   Sanders, Keith/0000-0003-0161-5384; McNamara,
   Deborah/0000-0003-3975-0485
FU North East Cancer Research and Education Trust (NECRET); Science
   Foundation Ireland [08-SRC-B1410, 13/IA/1881]; St. Luke's Institute of
   Cancer Research; Fox and Kerins families; European Commission
   [FP7-PEOPLE-2013-IEF-6270270]; Royal College of Surgeons in Ireland StAR
   programme
FX This work was supported by the North East Cancer Research and Education
   Trust (NECRET), the Science Foundation Ireland funded Molecular
   Therapeutics for Cancer Ireland (08-SRC-B1410) and investigator award
   13/IA/1881, St. Luke's Institute of Cancer Research and the Fox and
   Kerins families. SJF acknowledges support from the European Commission
   (FP7-PEOPLE-2013-IEF-6270270) and the Royal College of Surgeons in
   Ireland StAR programme.
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NR 57
TC 16
Z9 16
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUL
PY 2020
VL 12
IS 7
AR 1808
DI 10.3390/cancers12071808
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MX4PH
UT WOS:000557705900001
PM 32640573
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Dienstmann, R
   Elez, E
   Argiles, G
   Matos, I
   Sanz-Garcia, E
   Ortiz, C
   Macarulla, T
   Capdevila, J
   Alsina, M
   Sauri, T
   Verdaguer, H
   Vilaro, M
   Ruiz-Pace, F
   Viaplana, C
   Garcia, A
   Landolfi, S
   Palmer, HG
   Nuciforo, P
   Rodon, J
   Vivancos, A
   Tabernero, J
AF Dienstmann, Rodrigo
   Elez, Elena
   Argiles, Guillem
   Matos, Ignacio
   Sanz-Garcia, Enrique
   Ortiz, Carolina
   Macarulla, Teresa
   Capdevila, Jaume
   Alsina, Maria
   Sauri, Tamara
   Verdaguer, Helena
   Vilaro, Marta
   Ruiz-Pace, Fiorella
   Viaplana, Cristina
   Garcia, Ariadna
   Landolfi, Stefania
   Palmer, Hector G.
   Nuciforo, Paolo
   Rodon, Jordi
   Vivancos, Ana
   Tabernero, Josep
TI Analysis of mutant allele fractions in driver genes in colorectal cancer
   - biological and clinical insights
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE clonality; colorectal cancer; driver gene; mutant allele fraction
ID TARGETED THERAPY; HETEROGENEITY; MUTATIONS; PATTERNS; PREDICTS; KRAS
AB Sequencing of tumors is now routine and guides personalized cancer therapy. Mutant allele fractions (MAFs, or the 'mutation dose') of a driver gene may reveal the genomic structure of tumors and influence response to targeted therapies. We performed a comprehensive analysis of MAFs of driver alterations in unpaired primary and metastatic colorectal cancer (CRC) at our institution from 2010 to 2015 and studied their potential clinical relevance. Of 763 CRC samples, 622 had detailed annotation on overall survival in the metastatic setting (OSmet) and 89 received targeted agents matched to KRAS (MEK inhibitors), BRAF (BRAF inhibitors), or PIK3CA mutations (PI3K pathway inhibitors). MAFs of each variant were normalized for tumor purity in the sample (adjMAFs). We found lower adjMAFs for BRAF (V600E) and PIK3CA than for KRAS, NRAS, and BRAF non-V600 variants. TP53 and BRAF(V600E) adjMAFs were higher in metas-tases as compared to primary tumors, and high KRAS adjMAFs were found in CRC metastases of patients with KRAS wild-type primary tumors previously exposed to EGFR antibodies. Patients with RAS-or BRAF (V600E)-mutated tumors, irrespective of adjMAFs, had worse OSmet. There was no significant association between adjMAFs and time to progression on targeted therapies matched to KRAS, BRAF, or PIK3CA mutations, potentially related to the limited antitumor activity of the employed drugs (overall response rate of 4.5%). In conclusion, the lower BRAF (V600E) and PIK3CA adjMAFs in subsets of primary CRC tumors indicate subclonality of these driver genes. Differences in adjMAFs between metastases and primary tumors suggest that approved therapies may result in selection of BRAF (V600E)-and KRAS-resistant clones and an increase in genomic heterogeneity with acquired TP53 alterations. Despite significant differences in prognosis according to mutations in driver oncogenes, adjMAFs levels did not impact on survival and did not help predict benefit with matched targeted agents in the metastatic setting.
C1 [Dienstmann, Rodrigo; Vilaro, Marta; Ruiz-Pace, Fiorella; Viaplana, Cristina; Garcia, Ariadna] VHIO, Oncol Data Sci ODysSey Grp, P Vall dHebron 119-129, Barcelona 08035, Spain.
   [Elez, Elena; Argiles, Guillem; Matos, Ignacio; Sanz-Garcia, Enrique; Ortiz, Carolina; Macarulla, Teresa; Capdevila, Jaume; Alsina, Maria; Sauri, Tamara; Verdaguer, Helena; Tabernero, Josep] Vall Hebron Univ Hosp, VHIO, Med Oncol Dept, Barcelona, Spain.
   [Landolfi, Stefania] Univ Autonoma Barcelona, Vall Hebron Univ Hosp, Pathol Dept, Barcelona, Spain.
   [Palmer, Hector G.] VHIO, Stem Cells & Canc Lab, Barcelona, Spain.
   [Nuciforo, Paolo] VHIO, Mol Oncol Lab, Barcelona, Spain.
   [Rodon, Jordi] VHIO, Mol Therapeut Res Unit, Barcelona, Spain.
   [Vivancos, Ana] VHIO, Canc Genom Lab, Barcelona, Spain.
C3 Vall d'Hebron Institut d'Oncologia (VHIO); Hospital Universitari Vall
   d'Hebron; Vall d'Hebron Institut d'Oncologia (VHIO); Hospital
   Universitari Vall d'Hebron; Autonomous University of Barcelona; Vall
   d'Hebron Institut d'Oncologia (VHIO); Vall d'Hebron Institut d'Oncologia
   (VHIO); Vall d'Hebron Institut d'Oncologia (VHIO); Vall d'Hebron
   Institut d'Oncologia (VHIO)
RP Dienstmann, R (corresponding author), VHIO, Oncol Data Sci ODysSey Grp, P Vall dHebron 119-129, Barcelona 08035, Spain.
EM rdienstmann@vhio.net
RI Palmer, Héctor/AAG-8332-2019; Élez, Elena/AAH-2945-2019; Nuciforo,
   Paolo/Q-2885-2019; Tabernero, Josep/AAG-5026-2019; Macarulla,
   Teresa/AAG-9230-2019; ALSINA, MARIA/ACJ-5958-2022; Argiles,
   Guillem/KQU-7406-2024; Vivancos, Ana/AAG-8331-2019
OI Palmer, Hector/0000-0002-9823-5638; Sanz Garcia,
   Enrique/0000-0002-3119-3832; Elez, Elena/0000-0002-4653-6324; Macarulla,
   Teresa/0000-0002-5856-4082; Argiles, Guillem/0000-0002-1487-7108; Rodon,
   Jordi/0000-0001-6467-3632; Landolfi, Stefania/0000-0002-1059-635X;
   Tabernero, Josep/0000-0002-2495-8139; Sauri Nadal,
   Tamara/0000-0002-7479-5120; Ruiz Pace, Fiorella/0000-0002-3932-0170;
   Vivancos, Ana/0000-0003-2888-6512
FU FERO Foundation
FX The authors acknowledge the FERO Foundation for supporting research in
   gastrointestinal malignancies and the Cellex Foundation for providing
   research facilities and equipment.
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NR 16
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Z9 26
U1 0
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1574-7891
EI 1878-0261
J9 MOL ONCOL
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PD SEP
PY 2017
VL 11
IS 9
BP 1263
EP 1272
DI 10.1002/1878-0261.12099
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FF3UR
UT WOS:000408847000010
PM 28618197
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Guo, YL
   Xie, YJ
   Luo, Y
AF Guo, Yingli
   Xie, Yajuan
   Luo, Yao
TI The Role of Long Non-Coding RNAs in the Tumor Immune Microenvironment
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE long non-coding RNAs; tumor immune microenvironment; cancer
   immunotherapy; biomarker; targeted therapy
ID CANCER STEM-CELLS; EPITHELIAL-MESENCHYMAL TRANSITION;
   CARCINOMA-ASSOCIATED FIBROBLASTS; DENDRITIC CELLS; COLORECTAL-CANCER;
   SUPPRESSOR-CELLS; CRNDE PROMOTES; MYELOID CELLS; LIVER-CANCER; IFN-GAMMA
AB Tumorigenesis is a complicated process caused by successive genetic and epigenetic alterations. The past decades demonstrated that the immune system affects tumorigenesis, tumor progression, and metastasis. Although increasing immunotherapies are revealed, only a tiny proportion of them are effective. Long non-coding RNAs (lncRNAs) are a class of single-stranded RNA molecules larger than 200 nucleotides and are essential in the molecular network of oncology and immunology. Increasing researches have focused on the connection between lncRNAs and cancer immunotherapy. However, the in-depth mechanisms are still elusive. In this review, we outline the latest studies on the functions of lncRNAs in the tumor immune microenvironment. Via participating in various biological processes such as neutrophil recruitment, macrophage polarization, NK cells cytotoxicity, and T cells functions, lncRNAs regulate tumorigenesis, tumor invasion, epithelial-mesenchymal transition (EMT), and angiogenesis. In addition, we reviewed the current understanding of the relevant strategies for targeting lncRNAs. LncRNAs-based therapeutics may represent promising approaches in serving as prognostic biomarkers or potential therapeutic targets in cancer, providing ideas for future research and clinical application on cancer diagnosis and therapies.
C1 [Guo, Yingli; Luo, Yao] Sichuan Univ, State Key Lab Biotherapy & Canc Ctr, West China Hosp, Chengdu, Peoples R China.
   [Guo, Yingli; Luo, Yao] Collaborat Innovat Ctr Biotherapy, Chengdu, Peoples R China.
   [Xie, Yajuan] Sun Yat Sen Univ, Hosp Stomatol, Dept Orthdnt, Guangzhou, Peoples R China.
C3 Sichuan University; Sun Yat Sen University
RP Luo, Y (corresponding author), Sichuan Univ, State Key Lab Biotherapy & Canc Ctr, West China Hosp, Chengdu, Peoples R China.; Luo, Y (corresponding author), Collaborat Innovat Ctr Biotherapy, Chengdu, Peoples R China.
EM luoyao@scu.edu.cn
RI Guo, Yingli/GQH-6216-2022; Luo, Yao/HSE-6408-2023
OI Guo, Yingli/0000-0003-4117-6865; Luo, Yao/0000-0002-4542-3504
FU National Natural Science Foundation of China [31771102, 82003262]; China
   Postdoctoral Science Foundation [2019TQ0221, 2019M663517]; West China
   Hospital, Sichuan University [2019HXBH059]
FX Funding This work was supported by the National Natural Science
   Foundation of China (No. 31771102, 82003262), China Postdoctoral Science
   Foundation (No. 2019TQ0221, 2019M663517), and Post-Doctor Research
   Project, West China Hospital, Sichuan University (No. 2019HXBH059).
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NR 266
TC 26
Z9 29
U1 2
U2 18
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD FEB 9
PY 2022
VL 13
AR 851004
DI 10.3389/fimmu.2022.851004
PG 23
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA ZH1VB
UT WOS:000760732900001
PM 35222443
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Prijovich, ZM
   Burnouf, PA
   Chou, HC
   Huang, PT
   Chen, KC
   Cheng, TL
   Leu, YL
   Roffler, SR
AF Prijovich, Zeljko M.
   Burnouf, Pierre-Alain
   Chou, Hua-Cheng
   Huang, Ping-Ting
   Chen, Kai-Chuan
   Cheng, Tian-Lu
   Leu, Yu-Lin
   Roffler, Steve R.
TI Synthesis and Antitumor Properties of BQC-Glucuronide, a Camptothecin
   Prodrug for Selective Tumor Activation
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE camptothecin; glucuronide; prodrug; cancer; targeted therapy;
   beta-glucuronidase; albumin influence; ADEPT
ID HUMAN SERUM-ALBUMIN; CANCER DRUG TOXICITY; HUMAN OVARIAN-CANCER;
   BETA-GLUCURONIDASE; TARGETED ACTIVATION; MEDIATED EXPRESSION;
   MELANOMA-CELLS; HUMAN BLOOD; NUDE-MICE; METASTASIS
AB Major limitations of camptothecin anticancer drugs (toxicity, nonselectivity, water insolubility, inactivation by human serum albumin) may be improved by creating glucuronide prodrugs that rely on beta-glucuronidase for their activation. We found that the camptothecin derivative 5,6dihydro-4H-benzo [de] quinoline-camptothecin (BQC) displays greater cytotoxicity against cancer cells than the clinically used Norma tissue camptothecin derivatives SN-38 and topotecan even in the presence of human serum albumin. We synthesized the prodrug BQC-glucuronide (BQC-G), which was 4000 times more water soluble and 20-40 times less cytotoxic than BQC. Importantly, even in the presence of human serum albumin, BQC-G was efficiently hydrolyzed by beta-glucuronidase and produced greater cytotoxicity (IC50 = 13 nM) than camptothecin, 9-aminocamptothecin, SN-38, or topotecan (IC50 > 3000, 1370, 48, and 28 nM, respectively). BQC-G treatment of mice bearing human colon cancer xenografts with naturally or artificially elevated beta-glucuronidase activity produced significant antitumor activity, showing that BQC-G is a potent prodrug suitable for selective intratumoral drug activation.
C1 [Prijovich, Zeljko M.; Burnouf, Pierre-Alain; Huang, Ping-Ting; Chen, Kai-Chuan; Roffler, Steve R.] Acad Sinica, Inst Biomed Sci, Acad Rd,Sect 2 128, Taipei 11529, Taiwan.
   [Burnouf, Pierre-Alain] Natl Yang Ming Univ, Taiwan Int Grad Program Mol Med, Taipei 112, Taiwan.
   [Burnouf, Pierre-Alain] Acad Sinica, Acad Rd,Sect 2 128, Taipei 11529, Taiwan.
   [Cheng, Tian-Lu] Kaohsiung Med Univ, Fac Biomed Sci & Environm Biol, Kaohsiung 80708, Taiwan.
   [Chou, Hua-Cheng; Leu, Yu-Lin] Chia Nan Univ, Erh Jen Rd,Sect 1 60, Tainan 71710, Taiwan.
C3 Academia Sinica - Taiwan; National Yang Ming Chiao Tung University;
   Academia Sinica - Taiwan; Kaohsiung Medical University; Chia Nan
   University of Pharmacy & Science
RP Roffler, SR (corresponding author), Acad Sinica, Inst Biomed Sci, Acad Rd,Sect 2 128, Taipei 11529, Taiwan.; Leu, YL (corresponding author), Chia Nan Univ, Erh Jen Rd,Sect 1 60, Tainan 71710, Taiwan.
EM yulin@mail.cnu.edu.tw; sroff@ibms.sinica.edu.tw
RI Roffler, Steve/N-7791-2018; chen, huan/GXZ-8858-2022; Chen,
   Hao/JHT-2948-2023; Burnouf, Pierre-Alain/ABD-5452-2020; Cheng,
   Tain-Lu/C-9645-2009; Prijovic, Zeljko/T-9825-2018
OI Burnouf, Pierre-Alain/0000-0002-6135-1547; Cheng,
   Tian-Lu/0000-0002-7263-2766; Prijovic, Zeljko/0000-0003-1069-2453;
   Roffler, Steve/0000-0003-2543-7295
FU Academia Sinica [AS-98-TP-B09]; Ministry of Science and Technology,
   Taipei, Taiwan [NSC102-2320-B-001-013-MY3]
FX This work was supported by a grant from Academia Sinica (AS-98-TP-B09)
   and the Ministry of Science and Technology, Taipei, Taiwan
   (NSC102-2320-B-001-013-MY3).
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NR 45
TC 22
Z9 27
U1 0
U2 64
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1543-8384
J9 MOL PHARMACEUT
JI Mol. Pharm.
PD APR
PY 2016
VL 13
IS 4
BP 1242
EP 1250
DI 10.1021/acs.molpharmaceut.5b00771
PG 9
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA DI5PH
UT WOS:000373550600005
PM 26824303
DA 2025-01-04
ER

PT J
AU Ebrahimi, N
   Manavi, MS
   Faghihkhorasani, F
   Fakhr, SS
   Baei, FJ
   Khorasani, FF
   Zare, MM
   Far, NP
   Rezaei-Tazangi, F
   Ren, J
   Reiter, RJ
   Nabavi, N
   Aref, AR
   Chen, C
   Ertas, YN
   Lu, Q
AF Ebrahimi, Nasim
   Manavi, Mahdokht Sadat
   Faghihkhorasani, Ferdos
   Fakhr, Siavash Seifollahy
   Baei, Fatemeh Jafari
   Khorasani, Fereshteh Faghih
   Zare, Mohammad Mehdi
   Far, Nazanin Pazhouhesh
   Rezaei-Tazangi, Fatemeh
   Ren, Jun
   Reiter, Russel J.
   Nabavi, Noushin
   Aref, Amir Reza
   Chen, Chu
   Ertas, Yavuz Nuri
   Lu, Qi
TI Harnessing function of EMT in cancer drug resistance: a metastasis
   regulator determines chemotherapy response
SO CANCER AND METASTASIS REVIEWS
LA English
DT Review
DE Mesenchymal-to-epithelial transition (MET); Targeting therapy;
   Non-coding RNAs; Signaling pathways; Multidrug-resistance (MDR)
ID EPITHELIAL-MESENCHYMAL TRANSITION; BLADDER-CANCER; COLORECTAL-CANCER;
   CELL CARCINOMA; BREAST-CANCER; INCREASES RADIOSENSITIVITY; SIGNALING
   PATHWAY; TWIST EXPRESSION; CERVICAL-CANCER; LUNG METASTASIS
AB Epithelial-mesenchymal transition (EMT) is a complicated molecular process that governs cellular shape and function changes throughout tissue development and embryogenesis. In addition, EMT contributes to the development and spread of tumors. Expanding and degrading the surrounding microenvironment, cells undergoing EMT move away from the main location. On the basis of the expression of fibroblast-specific protein-1 (FSP1), fibroblast growth factor (FGF), collagen, and smooth muscle actin (-SMA), the mesenchymal phenotype exhibited in fibroblasts is crucial for promoting EMT. While EMT is not entirely reliant on its regulators like ZEB1/2, Twist, and Snail proteins, investigation of upstream signaling (like EGF, TGF-beta, Wnt) is required to get a more thorough understanding of tumor EMT. Throughout numerous cancers, connections between tumor epithelial and fibroblast cells that influence tumor growth have been found. The significance of cellular crosstalk stems from the fact that these events affect therapeutic response and disease prognosis. This study examines how classical EMT signals emanating from various cancer cells interfere to tumor metastasis, treatment resistance, and tumor recurrence.
C1 [Ebrahimi, Nasim] Univ Isfahan, Fac Sci & Technol, Dept Cell & Mol Biol & Microbiol, Genet Div, Esfahan, Iran.
   [Manavi, Mahdokht Sadat] Univ Tehran Med Sci, Otolaryngol Dept, Tehran, Iran.
   [Faghihkhorasani, Ferdos] Xi An Jiao Tong Univ, Med Campus, Xian, Shaanxi, Peoples R China.
   [Fakhr, Siavash Seifollahy] Inland Norway Univ Appl Sci, Fac Appl Ecol Agr Sci & Biotechnol, Dept Biotechnol, Campus Hamar, Hamar, Norway.
   [Baei, Fatemeh Jafari] Amol Univ Special Modern Technol, Amol, Iran.
   [Khorasani, Fereshteh Faghih; Zare, Mohammad Mehdi] Shahid Sadoughi Univ Med Sci, Fac Med, Yazd, Iran.
   [Far, Nazanin Pazhouhesh] Islamic Azad Univ, Fac Adv Sci & Technol, Dept Microbiol, Tehran Med Sci, Tehran, Iran.
   [Rezaei-Tazangi, Fatemeh] Fasa Univ Med Sci, Sch Med, Dept Anat, Fasa, Iran.
   [Ren, Jun] Fudan Univ, Zhongshan Hosp, Shanghai Inst Cardiovasc Dis, Dept Cardiol, Shanghai 200032, Peoples R China.
   [Reiter, Russel J.] UT Hlth Sci Ctr, Dept Cellular & Struct Biol, San Antonio, TX 77030 USA.
   [Nabavi, Noushin] Univ British Columbia, Dept Urol Sci, Vancouver, BC V6H 3Z6, Canada.
   [Nabavi, Noushin] Univ British Columbia, Vancouver Prostate Ctr, Vancouver, BC V6H 3Z6, Canada.
   [Aref, Amir Reza] Xsphera Biosci, Translat Med Grp, 6 Tide St, Boston, MA 02210 USA.
   [Aref, Amir Reza] Harvard Med Sch, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
   [Chen, Chu; Lu, Qi] Nantong Univ, Dept Cardiol, Affiliated Hosp, Nantong 226001, Jiangsu, Peoples R China.
   [Ertas, Yavuz Nuri] Erciyes Univ, ERNAM Nanotechnol Res & Applicat Ctr, TR-38039 Kayseri, Turkiye.
   [Ertas, Yavuz Nuri] Erciyes Univ, Dept Biomed Engn, TR-38039 Kayseri, Turkiye.
C3 University of Isfahan; Tehran University of Medical Sciences; Xi'an
   Jiaotong University; Inland Norway University of Applied Sciences; Amol
   University of Special Modern Technologies - Iran; Islamic Azad
   University; Fudan University; University of Texas System; University of
   Texas Health Science Center at San Antonio; University of British
   Columbia; University of British Columbia; Harvard University; Harvard
   Medical School; Dana-Farber Cancer Institute; Nantong University;
   Erciyes University; Erciyes University
RP Aref, AR (corresponding author), Xsphera Biosci, Translat Med Grp, 6 Tide St, Boston, MA 02210 USA.; Aref, AR (corresponding author), Harvard Med Sch, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.; Lu, Q (corresponding author), Nantong Univ, Dept Cardiol, Affiliated Hosp, Nantong 226001, Jiangsu, Peoples R China.; Ertas, YN (corresponding author), Erciyes Univ, ERNAM Nanotechnol Res & Applicat Ctr, TR-38039 Kayseri, Turkiye.; Ertas, YN (corresponding author), Erciyes Univ, Dept Biomed Engn, TR-38039 Kayseri, Turkiye.
EM amir@xspherabio.com; yavuznuri@gmail.com; luqint@sina.com
RI Rezaei-Tazangi, Fatemeh/ABE-2421-2021; Reiter, Russel/D-3221-2009;
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OI Manavi, Mahdokht sadat/0000-0003-4114-1371
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NR 217
TC 16
Z9 16
U1 8
U2 14
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 MAR
PY 2024
VL 43
IS 1
SI SI
BP 457
EP 479
DI 10.1007/s10555-023-10162-7
EA JAN 2024
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WX6J9
UT WOS:001152233500002
PM 38227149
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Gray, EJ
   Darvishzadeh, A
   Sharma, A
   Ganeshan, D
   Faria, SC
   Lall, C
AF Gray, Eric J.
   Darvishzadeh, Ayeh
   Sharma, Ankush
   Ganeshan, Dhakshinamoorthy
   Faria, Silvana C.
   Lall, Chandana
TI Cancer therapy-related complications in the bowel and mesentery: an
   imaging perspective
SO ABDOMINAL RADIOLOGY
LA English
DT Article
DE Antineoplastic agents; Molecular targeted therapy; Drug-induced
   complications; Gastrointestinal toxicity; Gastrointestinal tract
ID METASTATIC COLORECTAL-CANCER; PHASE-I TRIAL; PNEUMATOSIS-INTESTINALIS;
   SCLEROSING MESENTERITIS; NEUTROPENIC ENTEROCOLITIS; RANDOMIZED-TRIAL;
   OVARIAN-CANCER; BREAST-CANCER; GASTROINTESTINAL COMPLICATIONS;
   SURGICAL-MANAGEMENT
AB Cancer therapy-induced complications in the bowel and mesentery are fairly common. It is important for clinicians to be aware of these complications and the agents most frequently implicated. Cancer therapy is rapidly evolving and often encompasses both classic cytotoxic drugs and newer molecular targeted agents. Drugs from both broad classes can have numerous adverse effects on the bowel and mesentery that can be detected on imaging. These adverse effects include ileus, various forms of enterocolitis, gastrointestinal perforation, pneumatosis intestinalis, secretory diarrhea, and sclerosing mesenteritis. These complications are diverse and range from relatively benign to life threatening. The management is also variable, but many of these conditions are easily controlled and reversed with supportive care and cessation of the particular cancer therapy. The objective of this pictorial essay is to demonstrate some of the more common cancer therapy-induced complications of the bowel and mesentery, with a focus on the radiographic findings.
C1 [Gray, Eric J.; Darvishzadeh, Ayeh; Lall, Chandana] Univ Calif Irvine, Sch Med, Dept Radiol Sci, 101 City Dr South, Orange, CA 92868 USA.
   [Sharma, Ankush] Univ Calif Irvine, Sch Med, Dept Internal Med, Orange, CA 92668 USA.
   [Ganeshan, Dhakshinamoorthy; Faria, Silvana C.] Univ Texas MD Anderson Canc Ctr, Dept Diagnost Radiol, Houston, TX 77030 USA.
C3 University of California System; University of California Irvine;
   University of California System; University of California Irvine;
   University of Texas System; UTMD Anderson Cancer Center
RP Gray, EJ (corresponding author), Univ Calif Irvine, Sch Med, Dept Radiol Sci, 101 City Dr South, Orange, CA 92868 USA.
EM ejgray@uci.edu
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Z9 12
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 2366-004X
EI 2366-0058
J9 ABDOM RADIOL
JI Abdom. Radiol.
PD OCT
PY 2016
VL 41
IS 10
BP 2031
EP 2047
DI 10.1007/s00261-016-0799-3
PG 17
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA DV4TF
UT WOS:000382917300017
PM 27277528
DA 2025-01-04
ER

PT J
AU Bidard, FC
   Kiavue, N
   Ychou, M
   Cabel, L
   Stern, MH
   Madic, J
   Saliou, A
   Rampanou, A
   Decraene, C
   Bouché, O
   Rivoire, M
   Ghiringhelli, F
   Francois, E
   Guimbaud, R
   Mineur, L
   Khemissa-Akouz, F
   Mazard, T
   Moussata, D
   Proudhon, C
   Pierga, JY
   Stanbury, T
   Thezenas, S
   Mariani, P
AF Bidard, Francois-Clement
   Kiavue, Nicolas
   Ychou, Marc
   Cabel, Luc
   Stern, Marc-Henri
   Madic, Jordan
   Saliou, Adrien
   Rampanou, Aurore
   Decraene, Charles
   Bouche, Olivier
   Rivoire, Michel
   Ghiringhelli, Francois
   Francois, Eric
   Guimbaud, Rosine
   Mineur, Laurent
   Khemissa-Akouz, Faiza
   Mazard, Thibault
   Moussata, Driffa
   Proudhon, Charlotte
   Pierga, Jean-Yves
   Stanbury, Trevor
   Thezenas, Simon
   Mariani, Pascale
TI Circulating Tumor Cells and Circulating Tumor DNA Detection in
   Potentially Resectable Metastatic Colorectal Cancer: A Prospective
   Ancillary Study to the Unicancer Prodige-14 Trial
SO CELLS
LA English
DT Article
DE circulating tumor cells; circulating tumor DNA; liquid biopsy;
   metastatic colorectal cancer; FOLFIRINOX
ID 1ST-LINE TREATMENT; PROGRESSION-FREE; CHEMOTHERAPY; MUTATIONS; KRAS;
   RESECTION; SURVIVAL; BLOOD
AB The management of patients with colorectal cancer (CRC) and potentially resectable liver metastases (LM) requires quick assessment of mutational status and of response to pre-operative systemic therapy. In a prospective phase II trial (NCT01442935), we investigated the clinical validity of circulating tumor cell (CTC) and circulating tumor DNA (ctDNA) detection. CRC patients with potentially resectable LM were treated with first-line triplet or doublet chemotherapy combined with targeted therapy. CTC (Cellsearch((R))) and Kirsten RAt Sarcoma (KRAS) ctDNA (droplet digital polymerase chain reaction (PCR)) levels were assessed at inclusion, after 4 weeks of therapy and before LM surgery. 153 patients were enrolled. The proportion of patients with high CTC counts (>= 3 CTC/7.5mL) decreased during therapy: 19% (25/132) at baseline, 3% (3/108) at week 4 and 0/57 before surgery. ctDNA detection sensitivity at baseline was 91% (N=42/46) and also decreased during treatment. Interestingly, persistently detectable KRAS ctDNA (p = 0.01) at 4 weeks was associated with a lower R0/R1 LM resection rate. Among patients who had a R0/R1 LM resection, those with detectable ctDNA levels before liver surgery had a shorter overall survival (p < 0.001). In CRC patients with limited metastatic spread, ctDNA could be used as liquid biopsy tool. Therefore, ctDNA detection could help to select patients eligible for LM resection.
C1 [Bidard, Francois-Clement; Kiavue, Nicolas; Cabel, Luc; Pierga, Jean-Yves] PSL Res Univ, Inst Curie, Dept Med Oncol, F-75005 Paris, France.
   [Bidard, Francois-Clement; Cabel, Luc; Madic, Jordan; Saliou, Adrien; Rampanou, Aurore; Decraene, Charles; Proudhon, Charlotte; Pierga, Jean-Yves] PSL Res Univ, Inst Curie, Circulating Tumor Biomarkers Lab, F-75005 Paris, France.
   [Bidard, Francois-Clement; Cabel, Luc] Paris Saclay Univ, UVSQ, F-92210 St Cloud, France.
   [Ychou, Marc; Mazard, Thibault] ICM Reg Canc Inst Montpellier, Dept Digest Oncol, F-34298 Montpellier, France.
   [Ychou, Marc] Montpellier Univ, Dept Oncol, F-34000 Montpellier, France.
   [Stern, Marc-Henri] PSL Res Univ, Inst Curie, INSERM U830, F-75005 Paris, France.
   [Decraene, Charles] PSL Res Univ, Inst Curie, CNRS UMR144, F-75005 Paris, France.
   [Bouche, Olivier] Reims Univ Hosp, Hop Robert Debre, Dept Med Oncol, F-51100 Reims, France.
   [Rivoire, Michel] Ctr Leon Berard, Dept Digest Oncol, F-69008 Lyon, France.
   [Ghiringhelli, Francois] Ctr Georges Francois Leclerc, INSERM U866, F-21000 Dijon, France.
   [Francois, Eric] Ctr Antoine Lacassagne, Dept Med Oncol, F-06189 Nice, France.
   [Guimbaud, Rosine] CHU Toulouse, Dept Digest Oncol, F-31059 Toulouse, France.
   [Mineur, Laurent] Inst St Catherine, Dept Digest Oncol, F-84000 Avignon, France.
   [Khemissa-Akouz, Faiza] Hop St Jean, Dept Gastroenterol, F-66000 Perpignan, France.
   [Moussata, Driffa] CHRU Tours, Dept Gastroenterol, F-37044 Tours, France.
   [Pierga, Jean-Yves] Univ Paris 05, F-75270 Paris, France.
   [Stanbury, Trevor] R&D UNICANCER, UCGI Grp, F-75654 Paris, France.
   [Thezenas, Simon] ICM Reg Canc Inst Montpellier, Biometr Unit, F-34298 Montpellier, France.
   [Mariani, Pascale] PSL Res Univ, Inst Curie, Dept Surg Oncol, F-75005 Paris, France.
C3 UNICANCER; Universite PSL; Institut Curie; UNICANCER; Universite PSL;
   Institut Curie; Universite Paris Saclay; Universite de Montpellier;
   Universite de Montpellier; Universite PSL; UNICANCER; Institut Curie;
   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 PSL; UNICANCER; Institut Curie;
   Universite de Reims Champagne-Ardenne; CHU de Reims; UNICANCER; Centre
   Leon Berard; Institut National de la Sante et de la Recherche Medicale
   (Inserm); UNICANCER; Centre Georges-Francois Leclerc; Universite de
   Bourgogne; Institut Agro; AgroSup Dijon; UNICANCER; Centre Antoine
   Lacassagne; Universite de Toulouse; Universite Toulouse III - Paul
   Sabatier; CHU de Toulouse; CHU Tours; Universite Paris Cite; UNICANCER;
   Universite de Montpellier; UNICANCER; Universite PSL; Institut Curie
RP Kiavue, N (corresponding author), PSL Res Univ, Inst Curie, Dept Med Oncol, F-75005 Paris, France.
EM francois-clement.bidard@curie.fr; nicolas.kiavue@curie.fr;
   marc.ychou@icm.unicancer.fr; luc.cabel@curie.fr;
   marc-henri.stern@curie.fr; jordanmadic@yahoo.fr;
   saliou.adrien@gmail.com; aurore.rampanou@curie.fr;
   charles.decraene@curie.fr; obouche@chu-reims.fr;
   michel.rivoire@lyon.unicancer.fr; fghiringhelli@cgfl.fr;
   eric.francois@nice.unicancer.fr; guimbaud.r@chu-toulouse.fr;
   l.mineur@isc84.org; faiza.khemissa@ch-perpignan.fr;
   t-mazard@chu-montpellier.fr; d.moussata@chu-tours.fr;
   charlotte.proudhon@curie.fr; jean-yves.pierga@curie.fr;
   t-stanbury@unicancer.fr; simon.thezenas@icm.unicancer.fr;
   pascale.mariani@curie.fr
RI MAZARD, Thibault/ABH-6334-2020; Moussata, Driffa/D-1351-2014; CABEL,
   LUC/S-4336-2019; Stern, Marc-Henri/A-2728-2011
OI ghiringhelli, francois/0000-0002-5465-8305; Bidard,
   Francois-Clement/0000-0001-5932-8949; Stern,
   Marc-Henri/0000-0002-8100-2272; Proudhon, Charlotte/0000-0002-4649-4574
FU French Ministry of Health (Programme hospitalier de recherche clinique);
   pharmaceutical company Merck
FX This research was funded by the French Ministry of Health (Programme
   hospitalier de recherche clinique) and the pharmaceutical company Merck.
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NR 39
TC 77
Z9 81
U1 0
U2 16
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD JUN
PY 2019
VL 8
IS 6
DI 10.3390/cells8060516
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA II6MY
UT WOS:000475309200004
PM 31142037
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Khan, U
   Shah, MA
AF Khan, Uqba
   Shah, Manish A.
TI Ramucirumab for the treatment of gastric or gastro-esophageal junction
   cancer
SO EXPERT OPINION ON BIOLOGICAL THERAPY
LA English
DT Article
DE Ramucirumab; gastric cancer; gastroesophageal adenocarcinoma; VEGFR-2
   inhibitors; targeted therapy
ID ENDOTHELIAL GROWTH-FACTOR; DOUBLE-BLIND; 1ST-LINE THERAPY;
   COLORECTAL-CARCINOMA; ADENOCARCINOMA; PLACEBO; CHEMOTHERAPY;
   MULTICENTER; COMBINATION; AFFINITY
AB Introduction: Gastric cancer remains one of the most lethal malignancy, accounting for an estimated 783,000 deaths worldwide in 2018. Although there are several approved drugs for the treatment of gastric cancer, the survival of patients with advanced disease remains dismal. Ramucirumab, a vascular endothelial growth factor receptor-2 inhibitor, is an important new targeted drug approved for gastric and gastroesophageal adenocarcinoma (GEJ) in second-line setting. Areas covered: In this article, we have reviewed the role of ramucirumab in the management of gastric and GEJ adenocarcinoma. A comprehensive review of various clinical trials is presented that support the use of ramucirumab in gastric cancer. Expert opinion: In our opinion, ramucirumab should be considered as a standard of care option, either alone or with paclitaxel, after progression on first-line therapy for advanced or metastatic disease. The results of large, randomized phase III clinical trials show benefit of ramucirumab on median overall survival (OS). However, the benefit is limited, with only about two months OS benefit of using ramucirumab with paclitaxel compared to paclitaxel alone. Novel combination therapies, such as ramucirumab with other targeted agents and immune checkpoint inhibitors in ongoing clinical trials, may provide important information to further improve the patient outcomes.
C1 [Khan, Uqba; Shah, Manish A.] Weill Cornell Med, Div Hematol & Oncol, New York Presbyterian Hosp, New York, NY USA.
C3 NewYork-Presbyterian Hospital; Cornell University; Weill Cornell
   Medicine
RP Shah, MA (corresponding author), Weill Cornell Med, Div Hematol & Med Oncol, New York Presbyterian Hosp, 1305 York Ave,Room Y1247, New York, NY 10021 USA.
EM mas9313@med.cornell.edu
RI Shah, Manish/AHI-4322-2022; Khan, Uqba/N-4069-2019
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NR 38
TC 22
Z9 23
U1 0
U2 7
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1471-2598
EI 1744-7682
J9 EXPERT OPIN BIOL TH
JI Expert Opin. Biol. Ther.
PY 2019
VL 19
IS 11
BP 1135
EP 1141
DI 10.1080/14712598.2019.1656715
EA AUG 2019
PG 7
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA MA9XO
UT WOS:000483818900001
PM 31452409
DA 2025-01-04
ER

PT J
AU Chen, YH
   Wei, MF
   Wang, CW
   Lee, HW
   Pan, SL
   Gao, M
   Kuo, SH
   Cheng, AL
   Teng, CM
AF Chen, Yu-Hsuan
   Wei, Ming-Feng
   Wang, Chun-Wei
   Lee, Hsiao-Wei
   Pan, Shiow-Lin
   Gao, Ming
   Kuo, Sung-Hsin
   Cheng, Ann-Lii
   Teng, Che-Ming
TI Dual Phosphoinositide 3-kinase/mammalian target of rapamycin inhibitor
   is an effective radiosensitizer for colorectal cancer
SO CANCER LETTERS
LA English
DT Article
DE PI3K/Akt/mTOR; BEZ235; Radiation; Colorectal cancer
ID RESECTABLE RECTAL-CANCER; DOUBLE-STRAND BREAKS; PREOPERATIVE
   RADIOTHERAPY; SIGNALING PATHWAY; NVP-BEZ235; RAS; GLIOBLASTOMA;
   ACTIVATION; KINASE; CELLS
AB The present study was aimed to investigate whether combination of molecular targeting therapy, a dual PI3K/mTOR inhibitor (BEZ235), with radiation can enhance the radiosensitivity of colorectal cancer cells (CRC). K-RAS mutant CRC cells (HCT 116 and SW 620) and wild type CRC cells (HT 29) were irradiated with different dose of radiation (0-6 Gy). The synergistic effects of combining radiation with different concentration of BEZ235 (0-10 nM) pretreatment were demonstrated by cell survival assay. When comparing with radiation alone and BEZ235 alone, the combination of BEZ235 pretreatment and radiation resulted in an increased percentage of sub-G1 phase cells, and an increased number of gamma-H2AX/cell (DNA double strand breaks). Radiation up-regulated AKT/mTOR signaling pathway, including the activation of phospho (p)AKT, p-mTOR, p-eIF4E, and p-rpS6; and this activated AKT/mTOR signaling pathway was attenuated by BEZ235 pretreatment. In addition, BEZ235 blocked double strand break repair induced by radiation through attenuating the activation of ATM and DNA-PKcs and sensitized CRC cells to radiation. In vivo model, the tumor size and the expression pattern of p-mTOR, p-eIF4E, and p-rpS6 were significantly decreased in combined group than radiation alone or BEZ235 alone. Our findings indicate that the administration of BEZ235 before radiation enhances the radiotherapeutic effect of CRC cells both in vitro and in vivo. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Chen, Yu-Hsuan; Wang, Chun-Wei; Lee, Hsiao-Wei; Kuo, Sung-Hsin; Cheng, Ann-Lii] Natl Taiwan Univ, Dept Oncol, Natl Taiwan Univ Hosp, Taipei 10764, Taiwan.
   [Chen, Yu-Hsuan; Wang, Chun-Wei; Lee, Hsiao-Wei; Gao, Ming; Kuo, Sung-Hsin; Cheng, Ann-Lii] Natl Taiwan Univ, Coll Med, Taipei, Taiwan.
   [Chen, Yu-Hsuan; Wang, Chun-Wei; Lee, Hsiao-Wei; Gao, Ming; Kuo, Sung-Hsin; Cheng, Ann-Lii] Natl Taiwan Univ, Canc Res Ctr, Taipei 10764, Taiwan.
   [Chen, Yu-Hsuan; Pan, Shiow-Lin; Teng, Che-Ming] Natl Taiwan Univ, Inst Pharmacol, Taipei, Taiwan.
   [Wei, Ming-Feng] Natl Taiwan Univ, Inst Biomed Engn, Taipei 10764, Taiwan.
   [Kuo, Sung-Hsin; Cheng, Ann-Lii] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Dept Internal Med, Taipei 10764, Taiwan.
   [Kuo, Sung-Hsin; Cheng, Ann-Lii] Natl Taiwan Univ, Coll Med, Grad Inst Oncol, Taipei, Taiwan.
C3 National Taiwan University; National Taiwan University Hospital;
   National Taiwan University; National Taiwan University; National Taiwan
   University; National Taiwan University; National Taiwan University;
   National Taiwan University Hospital; National Taiwan University
RP Kuo, SH (corresponding author), Natl Taiwan Univ, Dept Oncol, Natl Taiwan Univ Hosp, Taipei 10764, Taiwan.
EM shkuo101@ntu.edu.tw
RI Pan, Shiow-Lin/C-1372-2010; Cheng, Ann-Lii/ACM-0936-2022
OI CHEN, YU-HSUAN/0000-0002-6634-2746; Kuo, Sung-Hsin/0000-0003-0054-887X;
   Cheng, Ann-Lii/0000-0002-9152-6512; TENG, CHE-MING/0000-0002-9719-7334
FU Ministry of Science and Technology, Taiwan [MOST
   101-2314-B-002-157-MY3]; National Health Research Institutes, Taiwan
   [NHRI-EX103-10239BI]; National Taiwan University Hospital, Taiwan [NTUH
   103-S2387]; Ministry of Health and Welfare, Taiwan [MOHW103-TD-B-111-04]
FX The authors thank Novartis for great support of BEZ235. This study was
   supported by research grants MOST 101-2314-B-002-157-MY3 from the
   Ministry of Science and Technology, Taiwan, NHRI-EX103-10239BI from the
   National Health Research Institutes, Taiwan, NTUH 103-S2387 from the
   National Taiwan University Hospital, Taiwan, and MOHW103-TD-B-111-04
   from the Ministry of Health and Welfare, Taiwan.
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NR 37
TC 41
Z9 41
U1 0
U2 5
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 28
PY 2015
VL 357
IS 2
BP 582
EP 590
DI 10.1016/j.canlet.2014.12.015
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CB4IU
UT WOS:000349592200019
PM 25497009
DA 2025-01-04
ER

PT J
AU Zheng, Z
   Lu, X
   Zhou, D
   Deng, XF
   Liu, QX
   Liu, XB
   Zhang, J
   Li, YQ
   Zheng, H
   Dai, JG
AF Zheng, Zhi
   Lu, Xiao
   Zhou, Dong
   Deng, Xu-feng
   Liu, Quan-xing
   Liu, Xiao-bing
   Zhang, Jiao
   Li, Yan-qi
   Zheng, Hong
   Dai, Ji-gang
TI A novel enemy of cancer: recent investigations into protozoan anti-tumor
   properties
SO FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
LA English
DT Review
DE protozoa; protozoan components; anti-tumor; immune response;
   angiogenesis
ID TRYPANOSOMA-CRUZI CALRETICULIN; EHRLICH SOLID CARCINOMA; CENTRAL
   NERVOUS-SYSTEM; TOXOPLASMA-GONDII; IMMUNE-RESPONSE; TUMOR-GROWTH;
   INTRAVENOUS IMMUNIZATION; BREAST-CANCER; COLON-CANCER; CELLS
AB Cancer remains a significant global health issue, despite advances in screening and treatment. While existing tumor treatment protocols such as surgery, chemotherapy, radiotherapy, targeted therapy, and immunotherapy have proven effective in enhancing the prognosis for some patients, these treatments do not benefit all patients. Consequently, certain types of cancer continue to exhibit a relatively low 5-year survival rate. Therefore, the pursuit of novel tumor intervention strategies may help improve the current effectiveness of tumor treatment. Over the past few decades, numerous species of protozoa and their components have exhibited anti-tumor potential via immune and non-immune mechanisms. This discovery introduces a new research direction for the development of new and effective cancer treatments. Through in vitro experiments and studies involving tumor-bearing mice, the anti-tumor ability of Toxoplasma gondii, Plasmodium, Trypanosoma cruzi, and other protozoa have unveiled diverse mechanisms by which protozoa combat cancer, demonstrating encouraging prospects for their application. In this review, we summarize the anti-tumor ability and anti-tumor mechanisms of various protozoa and explore the potential for their clinical development and application.
C1 [Zheng, Zhi; Lu, Xiao; Zhou, Dong; Deng, Xu-feng; Liu, Quan-xing; Liu, Xiao-bing; Zhang, Jiao; Li, Yan-qi; Zheng, Hong; Dai, Ji-gang] Army Third Mil Med Univ, Xinqiao Hosp, Dept Thorac Surg, Chongqing, Peoples R China.
C3 Army Medical University
RP Zheng, H; Dai, JG (corresponding author), Army Third Mil Med Univ, Xinqiao Hosp, Dept Thorac Surg, Chongqing, Peoples R China.
EM ziecoe@tmmu.edu.cn; daijigang@tmmu.edu.cn
RI li, yanqi/IVH-6058-2023; Zheng, Hong/O-9604-2018
OI Zheng, Hong/0000-0003-3725-4541; zheng, zhi/0009-0008-0423-9015
FU National Natural Science Foundation of China [81972190, 81702247]; Key
   Projects on Technological Innovation and Application Development of
   Chongqing [195]; Excellent Talent Program of Chongqing
   [cstc2022ycjh-bgzxm0109]; Key Projects of Talent Incubation Plan of
   Xinqiao Hospital [2022YQB012]
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This work was supported
   by grants from the National Natural Science Foundation of China (No.
   81972190 and 81702247), the Key Projects on Technological Innovation and
   Application Development of Chongqing (195), the Excellent Talent Program
   of Chongqing (cstc2022ycjh-bgzxm0109), and the Key Projects of Talent
   Incubation Plan of Xinqiao Hospital (2022YQB012).
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NR 146
TC 2
Z9 2
U1 32
U2 48
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2235-2988
J9 FRONT CELL INFECT MI
JI Front. Cell. Infect. Microbiol.
PD JAN 11
PY 2024
VL 13
AR 1325144
DI 10.3389/fcimb.2023.1325144
PG 14
WC Immunology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Microbiology
GA FU1I0
UT WOS:001148273100001
PM 38274735
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, WG
   Li, JS
   Ding, ZY
   Li, YZ
   Wang, JL
   Chen, SJ
   Miao, JL
AF Wang, Weiguo
   Li, Jinsong
   Ding, Zhiyu
   Li, Yuezhan
   Wang, Jianlong
   Chen, Shijie
   Miao, Jinglei
TI Tanshinone I inhibits the growth and metastasis of osteosarcoma via
   suppressing JAK/STAT3 signalling pathway
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE JAK; STAT3 signalling pathway; osteosarcoma; tanshinone I; tumour growth
   and metastasis
ID PROSTATE-CANCER CELLS; COLON-CANCER; MESENCHYMAL TRANSITION; APOPTOSIS
   INDUCTION; ANTICANCER ACTIVITY; TARGETED THERAPY; FREE SURVIVAL;
   UP-REGULATION; STAT3; IIA
AB Tanshinone I (Tan I) is a widely used diterpene compound derived from the traditional Chinese herb Danshen. Increasing evidence suggests that it exhibits anti-cancer activity in various human cancers. However, the in vitro and in vivo effects of Tan I on osteosarcoma (OS) remain inadequately elucidated, especially those against tumour metastasis. Our results showed that Tan I significantly inhibited OS cancer cell proliferation, migration and invasion and induced cell apoptosis in vitro. Moreover, treatment with 10 and 20 mg/kg Tan I effectively suppressed tumour growth in subcutaneous xenografts and orthotopic xenograft mouse models. In addition, Tan I significantly inhibited tumour metastasis in intracardiac inoculation xenograft models. The results also showed that Tan I-induced increased expression of the proapoptotic gene Bax and decreased expression of the anti-apoptotic gene Bcl-2 is the possible mechanism of its anti-cancer effects. Tan I was also found to abolish the IL-6-mediated activation of the JAK/STAT3 signalling pathway. Conclusively, this study is the first to show that Tan I suppresses OS growth and metastasis in vitro and in vivo, suggesting it may be a potential novel and efficient drug candidate for the treatment of OS progression.
C1 [Wang, Weiguo; Li, Jinsong; Ding, Zhiyu; Li, Yuezhan; Wang, Jianlong; Chen, Shijie; Miao, Jinglei] Cent S Univ, Xiangya Hosp 3, Dept Orthopaed, 138 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China.
C3 Central South University
RP Chen, SJ; Miao, JL (corresponding author), Cent S Univ, Xiangya Hosp 3, Dept Orthopaed, 138 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China.
EM shijiechencsu@163.com; miaojinglei999@sina.com
RI Wang, Jianlong/AAG-9425-2020; Li, Jinsong/AAT-4230-2020
FU New Xiangya Talent Project of the Third Xiangya Hospital of Central
   South University [JY201510]
FX New Xiangya Talent Project of the Third Xiangya Hospital of Central
   South University, Grant/Award Number: JY201510
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NR 58
TC 39
Z9 44
U1 2
U2 28
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1582-1838
EI 1582-4934
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD SEP
PY 2019
VL 23
IS 9
BP 6454
EP 6465
DI 10.1111/jcmm.14539
EA JUL 2019
PG 12
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA IZ0EQ
UT WOS:000485016300001
PM 31293090
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Gu, ZC
   Lin, SX
   Yu, JH
   Jin, F
   Zhang, QQ
   Xia, KL
   Chen, L
   Li, Y
   He, B
AF Gu, Zhicheng
   Lin, Shuxian
   Yu, Junhui
   Jin, Fei
   Zhang, Qingqing
   Xia, Keli
   Chen, Lei
   Li, Yan
   He, Bin
TI Advances in dual-targeting inhibitors of HDAC6 for cancer treatment
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Review
DE HDAC6; Hybrid molecules; Dual-targeting inhibitors
ID HISTONE DEACETYLASE INHIBITORS; KINASE 2 JAK2; STRUCTURAL REQUIREMENTS;
   ANTITUMOR-ACTIVITY; BIOLOGICAL EVALUATION; THERAPEUTIC TARGETS; ANDROGEN
   RECEPTOR; COLORECTAL-CANCER; PROSTATE-CANCER; MOLECULAR-BASIS
AB Histone Deacetylase 6 (HDAC6) is an essential regulator of histone acetylation processes, exerting influence on a multitude of cellular functions such as cell motility, endocytosis, autophagy, apoptosis, and protein trafficking through its deacetylation activity. The significant implications of HDAC6 in diseases such as cancer, neurodegenerative disorders, and immune disorders have motivated extensive investigation into the development of specific inhibitors targeting this enzyme for therapeutic purposes. Single targeting drugs carry the risk of inducing drug resistance, thus prompting exploration of dual targeting therapy which offers the potential to impact multiple signaling pathways simultaneously, thereby lowering the likelihood of resistance development. While pharmacological studies have exhibited promise in combined therapy involving HDAC6, challenges related to potential drug interactions exist. In response to these challenges, researchers are investigating HDAC6 hybrid molecules which enable the concomitant targeting of HDAC6 and other key proteins, thus enhancing treatment efficacy while mitigating side effects and reducing the risk of resistance compared to traditional combination therapies. The published design strategies for dual targeting inhibitors of HDAC6 are summarized and discussed in this review. This will provide some valuable insights into more novel HDAC6 dual targeting inhibitors to meet the urgent need for innovative therapies in oncology and other related fields.
C1 [Gu, Zhicheng; Lin, Shuxian; Yu, Junhui; Jin, Fei; Zhang, Qingqing; Xia, Keli; Chen, Lei; He, Bin] Guizhou Med Univ, Engn Res Ctr Dev & Applicat Ethn Med & TCM, State Key Lab Funct & Applicat Med Plants, Sch Pharm,Minist Educ,Guizhou Prov Key Lab Pharmac, Guiyang 550004, Peoples R China.
   [Lin, Shuxian] Guizhou Prov Peoples Hosp, Dept Pharm, Guiyang 550002, Peoples R China.
   [Li, Yan] Guizhou Med Univ, Sch Basic Med Sci, Guiyang 550004, Guizhou, Peoples R China.
C3 Guizhou Medical University; Guizhou Medical University
RP He, B (corresponding author), Guizhou Med Univ, Engn Res Ctr Dev & Applicat Ethn Med & TCM, State Key Lab Funct & Applicat Med Plants, Sch Pharm,Minist Educ,Guizhou Prov Key Lab Pharmac, Guiyang 550004, Peoples R China.
EM binhe@gmc.edu.cn
FU Guizhou Science and Technology Department of China [82160655]; GCC
   [[2022] 030-1, [2022] 005, ZK [2022] 035]; Guizhou Provincial Health
   Care Commission of China;  [gzwkj2023-081]
FX This work was supported by the National Natural Science Foundation of
   China (no. 82160655) , Guizhou Science and Technology Department of
   China (no. GCC [2022] 030-1, CXTD [2022] 005, ZK [2022] 035) and the
   Guizhou Provincial Health Care Commission of China (gzwkj2023-081) .r of
   China (no. 82160655) , Guizhou Science and Technology Department of
   China (no. GCC [2022] 030-1, CXTD [2022] 005, ZK [2022] 035) and the
   Guizhou Provincial Health Care Commission of China (gzwkj2023-081) .
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NR 212
TC 4
Z9 4
U1 25
U2 29
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 SEP 5
PY 2024
VL 275
AR 116571
DI 10.1016/j.ejmech.2024.116571
EA JUN 2024
PG 33
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA WB6D9
UT WOS:001252439100001
PM 38857566
DA 2025-01-04
ER

PT J
AU Chen, L
   Wu, Y
   Tang, Q
   Tang, FQ
AF Chen, Lin
   Wu, Yao
   Tang, Qi
   Tang, Faqing
TI Oncogenic-tsRNA: A novel diagnostic and therapeutic molecule for cancer
   clinic
SO JOURNAL OF CANCER
LA English
DT Review
DE tsRNAs; tumor; diagnosis; targeted therapy; biomarker
ID PROMOTES CELL-PROLIFERATION; RNA-DERIVED FRAGMENTS; STRESS;
   IDENTIFICATION; ANGIOGENIN; TRANSLATION; BIOMARKERS; CLEAVAGE; REVEALS
AB tsRNA (tRNA-derived small RNA) is derived from mature tRNA or precursor tRNA (pre-tRNAs). It is lately found that tsRNA's aberrant expression is associated with tumor occurrence and development, it may be used a molecule of diagnosis and therapy. Based on the cleavage position of pre-tRNAs or mature tRNAs, tsRNAs are classified into two categories: tRNA-derived fragments (tRFs) and tRNA halves (also named tiRNAs or tRHs). tsRNAs display more stability within cells, tissues, and peripheral blood than other small non-coding RNAs (sncRNAs), and play a role of stable entities that function in various biological contexts, thus, they may serve as functional molecules in human disease. Recently, tsRNAs have been found in a large number of tumors including such as lung cancer, breast cancer, gastric cancer, colorectal cancer, liver cancer, and prostate cancer. Although the biological function of tsRNAs is still poorly understood, increasing evidences have indicated that tsRNAs have a great significance and potential in early tumor screening and diagnosis, therapeutic targets and application, and prognosis. In the present review, we mainly describe tsRNAs in tumors and their potential clinical value in early screening and diagnosis, therapeutic targets and application, and prognosis, it provides theoretical support and guidance for further revealing the therapeutic potential of tsRNAs in tumor.
C1 [Chen, Lin; Wu, Yao; Tang, Qi; Tang, Faqing] Hunan Univ Chinese Med, Clin Coll 1, Changsha 410007, Peoples R China.
   [Chen, Lin; Wu, Yao; Tang, Qi; Tang, Faqing] Hunan Canc Hosp, Changsha 410007, Peoples R China.
   [Chen, Lin; Tang, Faqing] Cent South Univ, Hunan Key Lab Oncotarget Gene, Changsha 410013, Peoples R China.
   [Chen, Lin; Tang, Faqing] Cent South Univ, Clin Lab Affiliated Canc Hosp, Xiangya Sch Med, Changsha 410013, Peoples R China.
C3 Hunan University of Chinese Medicine; Central South University; Central
   South University
RP Tang, FQ (corresponding author), Cent South Univ, Clin Lab Hunan Canc Hosp, Affiliated Canc Hosp, Hunan Key Lab Oncotarget Gene,Xiangya Sch Med, Changsha 410013, Peoples R China.
EM tangfq@hnca.org.cn
FU Research Projects of Hunan Health Commission [kg1801107, kq2004136]; 
   [B2019084]
FX This work was supported in part by Major Scientific and Technological
   Innovation Project of Hunan Province (2021SK1020-4), Natural Science
   Foundation of Hunan Province (2018JJ6131, 2019JJ40175, and 2021JJ70098)
   , Changsha Science and Technology Project (kg1801107 and kq2004136) ,
   and Research Projects of Hunan Health Commission (B2019084) .r
   Technology Project (kg1801107 and kq2004136) , and Research Projects of
   Hunan Health Commission (B2019084) .
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NR 85
TC 0
Z9 0
U1 6
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 2024
VL 15
IS 16
BP 5403
EP 5414
DI 10.7150/jca.98656
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA E2O7F
UT WOS:001301452000006
PM 39247588
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yamaga, Y
   Fukuda, A
   Nakanishi, Y
   Goto, N
   Matsumoto, Y
   Yoshioka, T
   Maruno, T
   Chiba, T
   Seno, H
AF Yamaga, Yuichi
   Fukuda, Akihisa
   Nakanishi, Yuki
   Goto, Norihiro
   Matsumoto, Yoshihide
   Yoshioka, Takuto
   Maruno, Takahisa
   Chiba, Tsutomu
   Seno, Hiroshi
TI Gene expression profile of Dclk1<SUP>+</SUP> cells in intestinal tumors
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Article
DE Colorectal cancer; Microarray analysis; Tumor stem cells
ID PROTEIN-TYROSINE KINASE; CANCER STEM-CELLS; TUFT CELLS; THERAPEUTIC
   TARGET; CYCLE PROGRESSION; MICROARRAY DATA; FAMILY; HCK; IDENTIFICATION;
   REVEALS
AB Background: Accumulating evidence has shown the existence of tumor stem cells with therapeutic potential. Previously, we reported that doublecortin like kinase I (Dclk1) marks tumor stem cells but not normal stem cells in the intestine of Apc(Min/+) mice, and that Dclk1- and Lgr5-double positive tumor cells are the tumor stem cells of intestinal tumors.
   Aim: To investigate molecules highly expressed in the Dclk1(+) normal intestinal and Dclk1(+) tumor cells in Apc(Min/+) mice.
   Methods: We used microarray analyses to examine the gene expression profile of Dclk1(+) cells in both mouse normal intestinal epithelium and Apc(Min/+) mouse intestinal tumors. We also performed immunofluorescence analyses.
   Results: Genes related to microtubules and the actin cytoskeleton (e.g., Rac2), and members of the Src family kinases (i.e., Hck, Lyn, Csk, and Ptpn6) were highly expressed in both Dclk1(+) normal intestinal and Dclk1(+) tumor cells. Phosphorylated Hck and phosphorylated Lyn were expressed in Lgr5(+) cells in the intestinal tumors of Lgr(5EGFP-IRES- CreERT2/+); Apc(Min/+) mice.
   Conclusion: We revealed factors that are highly expressed in Dclk1(+) intestinal tumor cells, which may help to develop cancer stem cell-targeted therapy in future. (C) 2018 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Yamaga, Yuichi; Fukuda, Akihisa; Nakanishi, Yuki; Goto, Norihiro; Matsumoto, Yoshihide; Yoshioka, Takuto; Maruno, Takahisa; Chiba, Tsutomu; Seno, Hiroshi] Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Kyoto, Japan.
C3 Kyoto University
RP Seno, H (corresponding author), Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Sakyo Ku, 54 Shogoin Kawahara Cho, Kyoto 6068507, Japan.
EM seno@kuhp.kyoto-u.ac.jp
RI Goto, Norihiro/LXB-2981-2024; ç¥è²´, ä¸­è¥¿/KJD-4998-2024
FU KAKENHI [15J03212, 25112707, 26293173, 16K09394, 16K15427, 17H04157];
   Kobayashi Foundation for Cancer Research; Naito Foundation; Princess
   Takamatsu Cancer Research Fund [13-24514]; Mitsubishi Foundation;
   Mochida Foundation; Japanese Society of Gastroenterology; Grants-in-Aid
   for Scientific Research [16K15427, 15J03212, 26293173, 16K09394,
   17H04157, 25112707] Funding Source: KAKEN
FX This work was supported partly by Grants-in-Aid KAKENHI (15J03212,
   25112707, 26293173, 16K09394, 16K15427, and 17H04157). This work was
   also supported by the Kobayashi Foundation for Cancer Research, Naito
   Foundation, Princess Takamatsu Cancer Research Fund13-24514, Mitsubishi
   Foundation, Mochida Foundation, and Japanese Society of
   Gastroenterology.
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NR 45
TC 9
Z9 9
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD DEC
PY 2018
VL 50
IS 12
BP 1353
EP 1361
DI 10.1016/j.dld.2018.06.011
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HC4HO
UT WOS:000451764100017
PM 30001952
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Yilmaz, F
   Karabulut, CC
   Ozdemir, F
   Aydin, F
AF Yilmaz, Feride
   Karabulut, Cevriye Ceyda
   Ozdemir, Feyyaz
   Aydin, Fazil
TI Prognostic Factors for Survival in Patients with Metastatic Colon
   Carcinoma
SO UHOD-ULUSLARARASI HEMATOLOJI-ONKOLOJI DERGISI
LA English
DT Article
DE Metastatic colorectal cancer; Survival; Prognostic factors
ID COLORECTAL-CANCER; MULTIVARIATE-ANALYSIS; LIVER METASTASES; TUMOR
   RESECTION; CHEMOTHERAPY; MANAGEMENT; SURGERY
AB Colorectal cancers are the most common cancers of the gastrointestinal system. They rank third after prostate and lung cancer in men and after breast and lung cancer in women. In Turkiye, colon cancer is the third most common among all cancers. In such cancer, beyond the stage of the disease, there are many biological, molecular, genetic, and tissue-related factors that determine the prognosis. Among these, vascular invasion, the number of affected regional lymph nodes, and the levels of preoperative carcinoembryonic antigen (CEA) are prominent factors. In this study, we investigated the personal, clinical, tumoral, metastatic, and treatment characteristics of metastatic colon cancer (MCC) that may be associated with long survival. This study included the data of 103 patients diagnosed with MCC who were followed at the Medical Oncology Department of Karadeniz Technical University Faculty of Medicine between 2010 and 2016. In univariate analyses, primary surgery (p< 0.001), targeted therapy (p= 0.01), being less than 65 years old (p=0.02), having normal CEA levels (p= 0.03), and not having elevated platelet counts (p= 0.001) were significant factors associated with prolonged survival. Multivariate analysis indicated that survival was longer in patients who underwent primary surgery (p= 0.001, 95% CI: 0.07-0.52) and had normal or low platelet levels at the time of diagnosis (p= 0.001, 95% CI: 1.77-9.16), regardless of other factors. In patients diagnosed with MCC, those who had primary tumor surgery and had normal or low platelet levels at the time of diagnosis had a better prognosis regardless of other factors. Therefore, prognostic factors are important in MCC, and more comprehensive studies are needed on this subject.
C1 [Yilmaz, Feride] Hacettepe Univ, Dept Med Oncol, Oncol Inst, Ankara, Turkiye.
   [Karabulut, Cevriye Ceyda] Prov Hlth Directorate, Publ Hlth Dept, Bingol, Turkiye.
   [Ozdemir, Feyyaz] Karadeniz Tech Univ, Fac Med, Dept Med Oncol, Trabzon, Turkiye.
   [Aydin, Fazil] Private Imperial Hosp, Dept Med Oncol, Trabzon, Turkiye.
C3 Hacettepe University; Karadeniz Technical University
RP Yilmaz, F (corresponding author), Hacettepe Univ, Onkoloji Enstitusu, Tibbi Onkoloji Bolumu, Ankara, Turkiye.
EM doktorferide@gmail.com
RI YILMAZ, Feride/ABG-3580-2021
OI YILMAZ, Feride/0000-0001-5848-3381
CR Altekruse S, 2010, SEER cancer statistics review, 1975-2007, V7
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NR 16
TC 0
Z9 0
U1 0
U2 0
PU AKAD DOKTORLAR YAYINEVI
PI HILAL CANKAYA
PA 4 CADDE 56, SOKAK, NO 49-E, HILAL CANKAYA, ANKARA 06550, Turkiye
SN 1306-133X
J9 UHOD-ULUSLAR HEMATOL
JI UHOD-Uluslar. Hematol.-Onkol. De.
PY 2024
VL 34
IS 3
BP 148
EP 154
DI 10.4999/uhod.247610
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA K2G8K
UT WOS:001342121900005
DA 2025-01-04
ER

PT J
AU Song, HN
   Lee, C
   Kim, ST
   Kim, SY
   Kim, NKD
   Jang, J
   Kang, M
   Jang, H
   Ahn, S
   Kim, SH
   Park, Y
   Cho, YB
   Heo, JW
   Lee, WY
   Park, JO
   Lim, HY
   Kang, WK
   Park, YS
   Park, WY
   Lee, J
   Kim, HC
AF Song, Haa-Na
   Lee, Chung
   Kim, Seung Tae
   Kim, Sun Young
   Kim, Nayoung K. D.
   Jang, Jiryeon
   Kang, Mihyun
   Jang, Hyojin
   Ahn, Soomin
   Kim, Seok Hyeong
   Park, Yoona
   Cho, Yong Beom
   Heo, Jeong Wook
   Lee, Woo Yong
   Park, Joon Oh
   Lim, Ho Yeong
   Kang, Won Ki
   Park, Young Suk
   Park, Woong-Yang
   Lee, Jeeyun
   Kim, Hee Cheol
TI Molecular characterization of colorectal cancer patients and concomitant
   patient-derived tumor cell establishment
SO ONCOTARGET
LA English
DT Article
DE colorectal cancer; patient-derived cell; somatic mutation
ID III COLON-CANCER; XENOGRAFT MODELS; STAGE-II; MUTATION; OXALIPLATIN;
   CETUXIMAB; BIOLOGY; KRAS; BRAF
AB Background: We aimed to establish a prospectively enrolled colorectal cancer (CRC) cohort for targeted sequencing of primary tumors from CRC patients. In parallel, we established collateral PDC models from the matched primary tumor tissues, which may be later used as preclinical models for genome-directed targeted therapy experiments.
   Results: In all, we identified 27 SNVs in the 6 genes such as PIK3CA (N = 16), BRAF (N = 6), NRAS (N = 2), and CTNNB1 (N = 1), PTEN (N = 1), and ERBB2 (N = 1). RET-NCOA4 translocation was observed in one out of 105 patients (0.9%). PDC models were successfully established from 62 (55.4%) of the 112 samples. To confirm the genomic features of various tumor cells, we compared variant allele frequency results of the primary tumor and progeny PDCs. The Pearson correlation coefficient between the variants from primary tumor cells and PDCs was 0.881.
   Methods: Between April 2014 and June 2015, 112 patients with CRC who underwent resection of the primary tumor were enrolled in the SMC Oncology Biomarker study. The PDC culture protocol was performed for all eligible patients. All of the primary tumors from the 112 patients who provided written informed consent were genomically sequenced with targeted sequencing. In parallel, PDC establishment was attempted for all sequenced tumors.
   Conclusions: We have prospectively sequenced a CRC cohort of 105 patients and successfully established 62 PDC in parallel. Each genomically characterized PDCs can be used as a preclinical model especially in rare genomic alteration event.
C1 [Song, Haa-Na; Kim, Seung Tae; Kim, Sun Young; Jang, Jiryeon; Kang, Mihyun; Jang, Hyojin; Park, Joon Oh; Lim, Ho Yeong; Kang, Won Ki; Park, Young Suk; Lee, Jeeyun] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Med,Div Hematol Oncol, Seoul, South Korea.
   [Lee, Chung; Kim, Nayoung K. D.; Park, Woong-Yang] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Samsung Genome Inst, Seoul, South Korea.
   [Ahn, Soomin; Kim, Seok Hyeong] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol & Translat Genom, Seoul, South Korea.
   [Park, Yoona; Cho, Yong Beom; Heo, Jeong Wook; Lee, Woo Yong; Kim, Hee Cheol] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Surg, Seoul, South Korea.
   [Park, Woong-Yang] Sungkyunkwan Univ, Sch Med, Dept Mol Cell Biol, Seoul, South Korea.
   [Song, Haa-Na] Gyeongsang Natl Univ, Sch Med, Dept Internal Med, Jinju, South Korea.
   [Lee, Chung; Park, Woong-Yang] Sungkyunkwan Univ, SAIHST, Dept Hlth Sci & Technol, Seoul, South Korea.
C3 Sungkyunkwan University (SKKU); Samsung Medical Center; Samsung;
   Sungkyunkwan University (SKKU); Samsung Medical Center; Sungkyunkwan
   University (SKKU); Samsung Medical Center; Sungkyunkwan University
   (SKKU); Samsung Medical Center; Sungkyunkwan University (SKKU);
   Gyeongsang National University; Sungkyunkwan University (SKKU)
RP Lee, J (corresponding author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Med,Div Hematol Oncol, Seoul, South Korea.; Park, WY (corresponding author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Samsung Genome Inst, Seoul, South Korea.; Kim, HC (corresponding author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Surg, Seoul, South Korea.; Park, WY (corresponding author), Sungkyunkwan Univ, Sch Med, Dept Mol Cell Biol, Seoul, South Korea.; Park, WY (corresponding author), Sungkyunkwan Univ, SAIHST, Dept Hlth Sci & Technol, Seoul, South Korea.
EM woongyang@skku.edu; jyunlee@skku.edu; hckim@skku.edu
RI Lee, Chung/KRP-3824-2024; Kim, Nam Hoon/HNS-5794-2023; kim,
   st/O-5928-2014; Lee, Jee/C-9646-2011; Lim, Ho Yeong/KBA-8868-2024; Park,
   Susan/JRY-5671-2023; Cho, Yong/F-4606-2014; Kim, Kyunga/LCL-2839-2024
OI Lee, Chung/0000-0003-0855-4553; Park, Woong-Yang/0000-0003-4234-0380
FU Korean Health Technology R & D Project, Ministry of Health & Welfare,
   Republic of Korea [HI13C1951, HI13C2096, HI14C3418]; 20 by 20 Project of
   Samsung Medical Center [GF01140111]
FX This work was supported by funding from the Korean Health Technology R &
   D Project, Ministry of Health & Welfare, Republic of Korea (HI13C1951,
   HI13C2096, and HI14C3418). Support was also provided by a grant from the
   20 by 20 Project of Samsung Medical Center (GF01140111).
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NR 31
TC 12
Z9 12
U1 0
U2 3
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD APR 12
PY 2016
VL 7
IS 15
BP 19610
EP 19619
DI 10.18632/oncotarget.7526
PG 10
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DL7ES
UT WOS:000375804000040
PM 26909603
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Qi, J
   Cui, CH
   Deng, QW
   Wang, LF
   Chen, RH
   Zhai, DY
   Xie, L
   Yu, JL
AF Qi, Jia
   Cui, Chunhui
   Deng, Quanwen
   Wang, Lifeng
   Chen, Rihong
   Zhai, Duanyang
   Xie, Lang
   Yu, Jinlong
TI Downregulated SIRT6 and upregulated NMNAT2 are associated with the
   presence, depth and stage of colorectal cancer
SO ONCOLOGY LETTERS
LA English
DT Article
DE colorectal carcinoma; nicotinamide mononucleotide adenylyltransferase 2;
   sirtuin 6
ID HISTONE DEACETYLASE SIRT6; HEPATOCELLULAR-CARCINOMA; CELL-GROWTH;
   METABOLISM; EXPRESSION; HYPERTROPHY; PROTECTS; SIRTUINS; PATHWAY
AB Colorectal cancer (CRC) is an important cause of morbidity and mortality worldwide, and is difficult to detect in its early stages. Diagnostic and prognostic biomarkers are required, which may also be the basis for improving the targeted therapy for CRC. Sirtuin 6 (SIRT6) is a member of the sirtuin family of gene regulators, which have specific functions in genomic stability, gene transcription and energy metabolism in tumorigenesis. Nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) is a metabolic enzyme which can be deacetylated by sirtuins. In this study, tissue samples from 29 patients with histologically confirmed CRC of varying grade and stage were studied for SIRT6 and NMNAT2 expression by western blotting and reverse transcription-quantitative polymerase chain reaction. Immunohistochemistry was performed for SIRT6 and NMNAT2 expression in 113 paired (CRC and adjacent) tissue sections. SIRT6 protein and mRNA expression levels were significantly reduced in CRC tissues; NMNAT2 protein and mRNA expression levels were significantly increased in CRC tissues (P<0.01). A negative correlation between the expression of SIRT6 and NMNAT2 in CRC tissue samples was identified (r=-0.246, P<0.01). The reduced expression of SIRT6 and increased expression of NMNAT2 were associated with the tumor depth invasion, stage, differentiation grade (SIRT6 only) and the presence of lymph node metastasis (P<0.05). In conclusion, the findings of the present preliminary study demonstrated that the increased expression of NMNAT2 and reduced expression of SIRT6 may be associated with the progression of CRC. The downregulation of SIRT6 may promote the expression of NMNAT2. Further studies are indicated on the role of NMNAT2 and SIRT6 as potential diagnostic and prognostic biomarkers and as targets for therapy in CRC and other malignant tumors.
C1 [Qi, Jia; Cui, Chunhui; Chen, Rihong; Zhai, Duanyang; Xie, Lang; Yu, Jinlong] Southern Med Univ, Zhujiang Hosp, Dept Gen Surg, 253 Ind Ave, Guangzhou 510280, Guangdong, Peoples R China.
   [Deng, Quanwen] Southern Med Univ, Nanfang Hosp, Dept Pharm, Guangzhou 510515, Guangdong, Peoples R China.
   [Wang, Lifeng] Southern Med Univ, Zhujiang Hosp, Dept Gastroenterol, Guangzhou 510280, Guangdong, Peoples R China.
C3 Southern Medical University - China; Southern Medical University -
   China; Southern Medical University - China
RP Yu, JL (corresponding author), Southern Med Univ, Zhujiang Hosp, Dept Gen Surg, 253 Ind Ave, Guangzhou 510280, Guangdong, Peoples R China.
EM projinlongyu@sina.com
RI Zhai, Cathy/JGX-0083-2023
FU Natural Science Foundation of Guangdong Province, China [2014
   a030313295]
FX The present study was supported by the Natural Science Foundation of
   Guangdong Province, China (grant no., 2014 a030313295).
CR [Anonymous], INT BANK RECONSTRUCT
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NR 41
TC 26
Z9 29
U1 0
U2 9
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD NOV
PY 2018
VL 16
IS 5
BP 5829
EP 5837
DI 10.3892/ol.2018.9400
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GY3FG
UT WOS:000448433500040
PM 30333863
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Gouverneur, A
   Coutureau, J
   Jové, J
   Rouyer, M
   Grelaud, A
   Duc, S
   Gerard, S
   Smith, D
   Ravaud, A
   Droz, C
   Bernard, MA
   Lassalle, R
   Forrier-Réglat, A
   Noize, P
   Smith, D
   Tubiana-Mathieu, N
   Michel, P
   Guimbaud, R
   Becouarn, Y
   Viret, F
   Guimbaud, R
   Larregain-Fournier, D
   Botreau, Y
   Texereau, P
   Auby, D
   Gautier-Felizot, L
   Loury-Lariviere, I
   Brudieux, E
   Cany, L
   Lecaille, C
   Jaubert, D
   Guichard, P
   Bernard, O
   Vives, L
   Taoubi, N
   Martinez, M
   Burki, F
   Roque, I
   Thouveny, F
   Gaspard, MH
AF Gouverneur, Amandine
   Coutureau, Juliette
   Jove, Jeremy
   Rouyer, Magali
   Grelaud, Angela
   Duc, Sophie
   Gerard, Stephane
   Smith, Denis
   Ravaud, Alain
   Droz, Cecile
   Bernard, Marie-Agnes
   Lassalle, Regis
   Forrier-Reglat, Annie
   Noize, Pernelle
   Smith, D.
   Tubiana-Mathieu, N.
   Michel, P.
   Guimbaud, R.
   Becouarn, Y.
   Viret, F.
   Guimbaud, R.
   Larregain-Fournier, D.
   Botreau, Y.
   Texereau, P.
   Auby, D.
   Gautier-Felizot, L.
   Loury-Lariviere, I
   Brudieux, E.
   Cany, L.
   Lecaille, C.
   Jaubert, D.
   Guichard, P.
   Bernard, O.
   Vives, L.
   Taoubi, N.
   Martinez, M.
   Burki, F.
   Roque, I
   Thouveny, F.
   Gaspard, M. H.
CA ETNA Study Grp
   EREBUS Study Grp
TI Patterns of Use, Safety, and Effectiveness of Targeted Therapies in
   First-Line Treatment of Metastatic Colorectal Cancer According to Age:
   The STROMBOLI Cohort Study
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Aged; Colorectal neoplasm; Frail elderly; Molecular targeted therapy;
   Neoplasm metastasis
ID ELDERLY-PATIENTS; PERFORMANCE STATUS; BEVACIZUMAB; SURVIVAL; OUTCOMES
AB Elderly patients are excluded from clinical trials, yet they can be treated in clinical practice. This large cohort of metastatic colorectal cancer patients treated in first-line with targeted therapies reinforces their benefit in elderly patients. Safety and effectiveness of targeted therapies are similar between elderly and younger metastatic colorectal cancer patients.
   Background: Metastatic colorectal cancer (mCRC) is increasingly treated using targeted therapies. Their real-life evaluation is insufficient, especially in elderly and frail patients. The aim was to describe use, safety, and effectiveness of targeted therapies in first-line mCRC treatment according to age. Patients and Methods: Two field cohorts of patients initiating bevacizumab or cetuximab for first-line mCRC were pooled. Patients characteristics, use, and safety were compared between younger and elderly patients (< 75 vs. >= 75 years). Two-year overall survival (OS) and progression-free survival (PFS) were estimated in both age groups using the KaplaneMeier method adjusted on factors associated with death or progression identified with Cox multivariate modeling. Results: Eight hundred patients (n = 411, 51.4% bevacizumab) were included: 498 (62.3%) male, median age 64 years, 118 (14.8%) Eastern Cooperative Oncology Group performance status (ECOG-PS) >= 2. Elderly patients (n = 126, 15.8%) were more often treated with 5-fluorouracil alone than younger. Severe adverse events were equivalent across age groups. ECOGPS >= 1, abnormal hemoglobin, and abnormal alkaline phosphatases were associated with a higher risk of death; OS adjusted on these factors was similar between elderly and younger patients. ECOGPS >= 1, lung metastases, abnormal hemoglobin, and abnormal creatinine clearance were associated with a higher risk of progression or death; PFS adjusted on these factors was similar across groups. Conclusion: Despite treatment adaptations, elderly patients could benefit from targeted therapies as younger without safety warning. (C) 2018 Elsevier Inc. All rights reserved.
C1 [Gouverneur, Amandine; Coutureau, Juliette; Forrier-Reglat, Annie; Noize, Pernelle] Univ Bordeaux, Bordeaux Populat Hlth Res Ctr, Team Pharmacoepidemiol, INSERM,UMR 1219, Bordeaux, France.
   [Gouverneur, Amandine; Jove, Jeremy; Rouyer, Magali; Grelaud, Angela; Droz, Cecile; Bernard, Marie-Agnes; Lassalle, Regis; Forrier-Reglat, Annie; Noize, Pernelle] INSERM, Bordeaux PharmacoEpi, CIC1401, Bordeaux, France.
   [Gouverneur, Amandine; Coutureau, Juliette; Forrier-Reglat, Annie; Noize, Pernelle] CHU Bordeaux, Pole Sante Publ, Serv Pharmacol Med, Bordeaux, France.
   [Jove, Jeremy; Rouyer, Magali; Grelaud, Angela; Droz, Cecile; Bernard, Marie-Agnes; Lassalle, Regis] ADERA, Pessac, France.
   [Duc, Sophie] CHU Bordeaux, Serv Geriatr, Bordeaux, France.
   [Gerard, Stephane] CHU Toulouse, Serv Geriatr, Toulouse, France.
   [Smith, Denis; Ravaud, Alain] CHU Bordeaux, Serv Oncol Med, Bordeaux, France.
   [Smith, D.] CHU Bordeaux, Bordeaux, France.
   [Tubiana-Mathieu, N.] CHU Limoges, Limoges, France.
   [Michel, P.] CHU Rouen, Rouen, France.
   [Guimbaud, R.] CHU Toulouse, Toulouse, France.
   [Becouarn, Y.] Inst Bergonie Bordeaux, Bordeaux, France.
   [Viret, F.] Inst Paoli Calmettes Marseille, Marseille, France.
   [Guimbaud, R.] Inst Claudius Regaud Toulouse, Toulouse, France.
   [Larregain-Fournier, D.] CH Bayonne, Bayonne, France.
   [Botreau, Y.] CH Cahors, Cahors, France.
   [Texereau, P.] CH Mont Marsan, Mont De Marsan, France.
   [Auby, D.] CH Libourne, Libourne, France.
   [Gautier-Felizot, L.] CH Dax, Dax, France.
   [Loury-Lariviere, I] CH Pau, Pau, France.
   [Brudieux, E.] CH Villeneuve sur Lot, Villeneuve Sur Lot, France.
   [Cany, L.] Polyclin Francheville Perigueux, Perigueux, France.
   [Lecaille, C.] Polyclin Bordeaux Nord, Bordeaux, France.
   [Jaubert, D.] Clin Tivoli Bordeaux, Bordeaux, France.
   [Guichard, P.] Polyclin Bordeaux Rive Droite, Lormont, France.
   [Bernard, O.] Clin Calabet Agen, Agen, France.
   [Vives, L.] CH St Gaudens, St Gaudens, France.
   [Taoubi, N.] CH Ville Franche Rouergue, Villefranche De Rouergue, France.
   [Martinez, M.] Clin Parc Toulouse, Toulouse, France.
   [Burki, F.] Clin Union Toulouse, Toulouse, France.
   [Roque, I] Clin Cedres Cornebarrieu, Cornebarrieu, France.
   [Thouveny, F.] Clin Pont Chaume Montauban, Montauban, France.
   [Gaspard, M. H.] Clin Claude Bernard Albi, Albi, France.
C3 Institut National de la Sante et de la Recherche Medicale (Inserm);
   Universite de Bordeaux; Universite de Bordeaux; Institut National de la
   Sante et de la Recherche Medicale (Inserm); CHU Bordeaux; Universite de
   Bordeaux; Universite de Bordeaux; CHU Bordeaux; CHU de Toulouse;
   Universite de Toulouse; Universite Toulouse III - Paul Sabatier;
   Universite de Bordeaux; CHU Bordeaux; Universite de Bordeaux; CHU
   Bordeaux; CHU Limoges; Universite de Rouen Normandie; CHU de Rouen; CHU
   de Toulouse; Universite de Toulouse; Universite Toulouse III - Paul
   Sabatier; UNICANCER; Institut Bergonie; UNICANCER; Institut
   Paoli-Calmette (IPC); UNICANCER; Institut Claudius Regaud
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-bordreux.fr
RI Bernard, Olivier/E-5721-2016; Noize, Pernelle/T-1955-2019; Gouverneur,
   Amandine/O-5332-2018
OI Ravaud, Alain/0000-0001-9455-6744; Angela, Grelaud/0000-0002-3480-3405;
   Gouverneur, Amandine/0000-0001-6253-1833; Droz-Perroteau,
   Cecile/0000-0002-7697-1167
FU French National Clinical Research Programme (Programme Hospitalier de
   Recherche Clinique) from the French Ministry of Health
   [2005/PHRC/INCa/DHOS]; Roche SAS; Merck Sante s.a.s. (rue St Romain,
   Lyon 1, France)
FX The ETNA cohort was supported by partial funding from the French
   National Clinical Research Programme (Programme Hospitalier de Recherche
   Clinique) from the French Ministry of Health (grant number
   2005/PHRC/INCa/DHOS), and an additional unconditional grant from Roche
   SAS, manufacturers of bevacizumab, who had no role in study design; in
   the collection, analysis, and interpretation of data; in the writing of
   the report; and in the decision to submit the report for publication.
   The EREBUS cohort was supported by an unconditional grant from Merck
   Sante s.a.s. (37, rue St Romain, 69008 Lyon 1, France).
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NR 21
TC 3
Z9 4
U1 0
U2 7
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD MAR
PY 2019
VL 18
IS 1
BP E150
EP E162
DI 10.1016/j.clcc.2018.11.005
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HP9VM
UT WOS:000462041100015
PM 30630730
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Ota, Y
   Nakamura, A
   Elboray, EE
   Itoh, Y
   Suzuki, T
AF Ota, Yosuke
   Nakamura, Arisa
   Elboray, Elghareeb E.
   Itoh, Yukihiro
   Suzuki, Takayoshi
TI Design, Synthesis, and Biological Evaluation of a Conjugate of
   5-Fluorouracil and an LSD1 Inhibitor
SO CHEMICAL & PHARMACEUTICAL BULLETIN
LA English
DT Article
DE anticancer drug; prodrug; 5-fluorouracil; targeted therapy; epigenetics
ID CANCER; INACTIVATOR
AB Prodrug approaches are useful for enhancing the efficacies and reducing the side effects of anticancer drugs. Previously, we proposed a prodrug strategy for targeting cancers over expressing lysine-specific demethylase 1 (LSD1), namely, conjugates of trans-2-phenylcyclopropylamine (PCPA, an LSD1 inhibitor) and anticancer drugs. In this study, we applied this prodrug strategy to the anticancer agent 5-fluorouracil (5-FU). In vitro assays showed that the PCPA-5-FU conjugate (1) released 5-FU upon the inhibition of LSD1. Furthermore, the conjugate (1) exerted an antiproliferative effect on colon cancer HCT116 cells. Thus, the PCPA-5-FU conjugate (1) was able to function as a prodrug of 5-FU, activated by LSD1 inhibition, and provided a useful new lead structure for further development.
C1 [Ota, Yosuke; Nakamura, Arisa; Elboray, Elghareeb E.; Itoh, Yukihiro; Suzuki, Takayoshi] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Sakyo Ku, 1-5 Shimogamo Hangi Cho, Kyoto 6030823, Japan.
   [Elboray, Elghareeb E.] South Valley Univ, Fac Sci, Dept Chem, Qena 83523, Egypt.
   [Suzuki, Takayoshi] Japan Sci & Technol Agcy JST, CREST, 4-1-8 Honcho Kawaguchi, Kawaguchi, Saitama 3320012, Japan.
C3 Kyoto Prefectural University of Medicine; Egyptian Knowledge Bank (EKB);
   South Valley University Egypt; Japan Science & Technology Agency (JST)
RP Ota, Y; Suzuki, T (corresponding author), Kyoto Prefectural Univ Med, Grad Sch Med Sci, Sakyo Ku, 1-5 Shimogamo Hangi Cho, Kyoto 6030823, Japan.; Suzuki, T (corresponding author), Japan Sci & Technol Agcy JST, CREST, 4-1-8 Honcho Kawaguchi, Kawaguchi, Saitama 3320012, Japan.
EM y-ota@koto.kpu-m.ac.jp; suzukit@koto.kpu-m.ac.jp
RI Itoh, Yukihiro/GQP-4681-2022; Elboray, Elghareeb E./ACO-6994-2022
OI Elboray, Elghareeb E./0000-0003-2261-0355; Itoh,
   Yukihiro/0000-0002-3410-2924
FU Japan Society for the Promotion of Science [JP14J10025, JP15K14982]; JST
   CREST program [JPMJCR14L2]; Takeda Science Foundation; Research
   Foundation for Pharmaceutical Sciences
FX The authors would like to thank Dr. Miki Suzuki and Dr. Yasunao Hattori
   for their technical support. This work was supported in part by a
   Grant-in-Aid from the Japan Society for the Promotion of Science (Y.O.,
   T.S.) (JP14J10025, JP15K14982), the JST CREST program (T.S.)
   (JPMJCR14L2), the Takeda Science Foundation, and the Research Foundation
   for Pharmaceutical Sciences (T.S.).
CR Chari RVJ, 2014, ANGEW CHEM INT EDIT, V53, P3796, DOI 10.1002/anie.201307628
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NR 18
TC 6
Z9 7
U1 2
U2 27
PU PHARMACEUTICAL SOC JAPAN
PI TOKYO
PA 2-12-15 SHIBUYA, SHIBUYA-KU, TOKYO, 150-0002, JAPAN
SN 0009-2363
J9 CHEM PHARM BULL
JI Chem. Pharm. Bull.
PD MAR
PY 2019
VL 67
IS 3
BP 192
EP 195
DI 10.1248/cpb.c18-00577
PG 4
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Pharmacology & Pharmacy; Chemistry
GA HN7JX
UT WOS:000460366300005
PM 30369513
OA gold
DA 2025-01-04
ER

PT J
AU Mohamed, AH
   Ahmed, AT
   Al Abdulmonem, W
   Bokov, DO
   Shafie, A
   Al-Hetty, HRAK
   Hsu, CY
   Alissa, M
   Nazir, S
   Jamali, MC
   Mudhafar, M
AF Mohamed, Asma'a H.
   Ahmed, Abdulrahman T.
   Al Abdulmonem, Waleed
   Bokov, Dmitry Olegovich
   Shafie, Alaa
   Al-Hetty, Hussein Riyadh Abdul Kareem
   Hsu, Chou-Yi
   Alissa, Mohammed
   Nazir, Shahid
   Jamali, Mohammad Chand
   Mudhafar, Mustafa
TI Interleukin-6 serves as a critical factor in various cancer progression
   and therapy
SO MEDICAL ONCOLOGY
LA English
DT Review
DE IL-6; Cancer; Inflammatory cytokines; Targeted therapy; STAT3
ID SMALL-MOLECULE INHIBITOR; SQUAMOUS-CELL CARCINOMA; ANTI-INTERLEUKIN-6
   MONOCLONAL-ANTIBODY; SILTUXIMAB CNTO 328; COLORECTAL-CANCER;
   BREAST-CANCER; SIGNAL TRANSDUCER; GASTRIC-CANCER; IL-6 PROMOTES;
   LUNG-CANCER
AB Interleukin-6 (IL-6), a pro-inflammatory cytokine, plays a crucial role in host immune defense and acute stress responses. Moreover, it modulates various cellular processes, including proliferation, apoptosis, angiogenesis, and differentiation. These effects are facilitated by various signaling pathways, particularly the signal transducer and activator of transcription 3 (STAT3) and Janus kinase 2 (JAK2). However, excessive IL-6 production and dysregulated signaling are associated with various cancers, promoting tumorigenesis by influencing all cancer hallmarks, such as apoptosis, survival, proliferation, angiogenesis, invasiveness, metastasis, and notably, metabolism. Emerging evidence indicates that selective inhibition of the IL-6 signaling pathway yields therapeutic benefits across diverse malignancies, such as multiple myeloma, prostate, colorectal, renal, ovarian, and lung cancers. Targeting key components of IL-6 signaling, such as IL-6Rs, gp130, STAT3, and JAK via monoclonal antibodies (mAbs) or small molecules, is a heavily researched approach in preclinical cancer studies. The purpose of this study is to offer an overview of the role of IL-6 and its signaling pathway in various cancer types. Furthermore, we discussed current preclinical and clinical studies focusing on targeting IL-6 signaling as a therapeutic strategy for various types of cancer.
C1 [Mohamed, Asma'a H.] Al Mustaqbal Univ, Coll Engn & Technol, Biomed Engn Dept, Hilla 51001, Iraq.
   [Ahmed, Abdulrahman T.] Al Maarif Univ Coll, Dept Nursing, Ramadi, AL Anbar Govern, Iraq.
   [Al Abdulmonem, Waleed] Qassim Univ, Coll Med, Dept Pathol, Buraydah, Saudi Arabia.
   [Bokov, Dmitry Olegovich] Sechenov First Moscow State Med Univ, Inst Pharm, Inst Pharm, 8 Trubetskaya St,Bldg 2, Moscow 119991, Russia.
   [Bokov, Dmitry Olegovich] Fed Res Ctr Nutr Biotechnol & Food Safety, Lab Food Chem, 2-14 Ustyinsky Pr, Moscow 109240, Russia.
   [Shafie, Alaa] Taif Univ, Coll Appl Med Sci, Dept Clin Lab Sci, POB 11099, Taif 21944, Saudi Arabia.
   [Al-Hetty, Hussein Riyadh Abdul Kareem] Univ Anbar, Coll Educ Pure Sci, Dept Biol, Ramadi 31001, Iraq.
   [Hsu, Chou-Yi] Arizona State Univ, Thunderbird Sch Global Management, Tempe Campus, Phoenix, AZ 85004 USA.
   [Alissa, Mohammed] Prince Sattam bin Abdulaziz Univ, Coll Appl Med Sci, Dept Med Lab, Al Kharj 11942, Saudi Arabia.
   [Nazir, Shahid] Univ New England, Sch Sci & Technol, Armidale, NSW, Australia.
   [Jamali, Mohammad Chand] Liwa Coll, Fac Med & Hlth Sci, Al Ain, Abu Dhabi, U Arab Emirates.
   [Mudhafar, Mustafa] Univ Kerbala, Coll Appl Med Sci, Dept Med Phys, Karbala 56001, Iraq.
   [Mudhafar, Mustafa] Al Taff Univ Coll, Dept Anesthesia Tech & Intens Care, Kerbala 56001, Iraq.
C3 Al-Mustaqbal University College; Al-Maarif University; Qassim
   University; Sechenov First Moscow State Medical University; Federal
   Research Center of Nutrition, Biotechnology & Food Safety; Taif
   University; University of Anbar; Arizona State University; Arizona State
   University-Downtown Phoenix; Prince Sattam Bin Abdulaziz University;
   University of New England; United Arab Emirates University; University
   of Kerbala
RP Ahmed, AT (corresponding author), Al Maarif Univ Coll, Dept Nursing, Ramadi, AL Anbar Govern, Iraq.; Al-Hetty, HRAK (corresponding author), Univ Anbar, Coll Educ Pure Sci, Dept Biol, Ramadi 31001, Iraq.
EM Abdulrahman.dheyab@uoa.edu.iq; hussin.riyadh@uoanbar.edu.iq
RI Hsu, Chou-Yi/HTM-7154-2023; Shafie, Alaa/ABE-1826-2021; Al-Heety,
   Hussein/ACI-5584-2022; Alissa, Mohammed/AHD-9636-2022; Al Abdulmonem,
   Waleed/LUY-1192-2024; Mudhafar, Mustafa/GNM-6487-2022; Jamali, Mohammad
   Chand/A-8536-2019
OI Alissa, Mohammed/0000-0002-4045-0810; Riyadh Abdul Kareem Al-Hetty,
   Hussein/0000-0002-4861-9377; Al Abdulmonem, Waleed/0000-0003-2984-9262;
   T. Ahmed, Abdulrahman/0009-0007-9181-0904; Hsu,
   Chou-Yi/0000-0001-7105-1161; Mudhafar, Mustafa/0000-0002-3785-7396;
   Jamali, Mohammad Chand/0000-0002-1990-0610; Hsu,
   Chou-Yi/0009-0009-1616-3203
FU Prince Sattam bin Abdulaziz University [PSAU/2024/R/1445]; Prince Sattam
   bin Abdulaziz University
FX This study is supported via funding from Prince Sattam bin Abdulaziz
   University project number (PSAU/2024/R/1445).
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NR 236
TC 2
Z9 2
U1 13
U2 14
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1357-0560
EI 1559-131X
J9 MED ONCOL
JI Med. Oncol.
PD JUN 20
PY 2024
VL 41
IS 7
AR 182
DI 10.1007/s12032-024-02422-5
PG 24
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UX0B5
UT WOS:001251234800003
PM 38900329
DA 2025-01-04
ER

PT J
AU Ruszkowska-Ciastek, B
   Kwiatkowska, K
   Marques-da-Silva, D
   Lagoa, R
AF Ruszkowska-Ciastek, Barbara
   Kwiatkowska, Katarzyna
   Marques-da-Silva, Dorinda
   Lagoa, Ricardo
TI Cancer Stem Cells from Definition to Detection and Targeted Drugs
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE cancer stem cells; leukaemia stem cells; cancer progression; solid
   tumours; haematological malignancies; tumour microenvironment;
   artificial intelligence; targeted therapy; polyphenols
ID ACUTE MYELOID-LEUKEMIA; INITIATING CELLS; BREAST-CANCER; HEMATOPOIETIC
   STEM; COLORECTAL-CANCER; SELF-RENEWAL; SIGNAL TRANSDUCER; PROGENITOR
   CELLS; UP-REGULATION; MARKERS CD44
AB Cancers remain the second leading cause of mortality in the world. Preclinical and clinical studies point an important role of cancer/leukaemia stem cells (CSCs/LSCs) in the colonisation at secondary organ sites upon metastatic spreading, although the precise mechanisms for specific actions are still not fully understood. Reviewing the present knowledge on the crucial role of CSCs/LSCs, their plasticity, and population heterogeneity in treatment failures in cancer patients is timely. Standard chemotherapy, which acts mainly on rapidly dividing cells, is unable to adequately affect CSCs with a low proliferation rate. One of the proposed mechanisms of CSC resistance to anticancer agents is the fact that these cells can easily shift between different phases of the cell cycle in response to typical cell stimuli induced by anticancer drugs. In this work, we reviewed the recent studies on CSC/LSC alterations associated with disease recurrence, and we systematised the functional assays, markers, and novel methods for CSCs screening. This review emphasises CSCs' involvement in cancer progression and metastasis, as well as CSC/LSC targeting by synthetic and natural compounds aiming at their elimination or modulation of stemness properties.
C1 [Ruszkowska-Ciastek, Barbara] Nicolaus Copernicus Univ, Fac Pharm, Dept Pathophysiol, Coll Med, PL-85094 Bydgoszcz, Poland.
   [Kwiatkowska, Katarzyna] Jan Biziel Univ Hosp 2, Dept Lab Diagnost, PL-85168 Bydgoszcz, Poland.
   [Marques-da-Silva, Dorinda; Lagoa, Ricardo] Polytech Inst Leiria, Lab Separat & React Engn, Lab Catalysis & Mat LSRE LCM, P-2411901 Leiria, Portugal.
   [Marques-da-Silva, Dorinda; Lagoa, Ricardo] Univ Porto, Fac Engn, Associate Lab Chem Engn ALiCE, Rua Dr Roberto Frias, P-4200465 Porto, Portugal.
   [Marques-da-Silva, Dorinda; Lagoa, Ricardo] Polytech Inst Leiria, Sch Technol & Management, Morro Lena Alto Vieiro, P-2411901 Leiria, Portugal.
C3 Nicolaus Copernicus University; Universidade do Porto
RP Ruszkowska-Ciastek, B (corresponding author), Nicolaus Copernicus Univ, Fac Pharm, Dept Pathophysiol, Coll Med, PL-85094 Bydgoszcz, Poland.
EM ruszkowska.basia@gmail.com; katarzynakwiatkowska@abs.umk.pl;
   dorinda.silva@ipleiria.pt; ricardo.lagoa@ipleiria.pt
RI Lagoa, Ricardo/AEV-0520-2022
OI /0000-0003-0460-5421; Lagoa, Ricardo/0000-0003-2375-6612; Ciastek,
   Barbara/0000-0003-4245-2403
FU Fundao para a Cincia e Tecnologia (FCT-Portugal)
FX No Statement Available
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NR 208
TC 2
Z9 2
U1 10
U2 18
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD APR
PY 2024
VL 25
IS 7
AR 3903
DI 10.3390/ijms25073903
PG 35
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA NN0B5
UT WOS:001201002000001
PM 38612718
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhu, YM
   Zang, YW
   Zhao, F
   Li, ZX
   Zhang, JB
   Fang, L
   Li, MH
   Xing, LG
   Xu, ZH
   Yu, JM
AF Zhu, Yingming
   Zang, Yuanwei
   Zhao, Fen
   Li, Zhenxiang
   Zhang, Jianbo
   Fang, Liang
   Li, Minghuan
   Xing, Ligang
   Xu, Zhonghua
   Yu, Jinming
TI Inhibition of HIF-1α by PX-478 suppresses tumor growth of esophageal
   squamous cell cancer in vitro and in vivo
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE Esophageal squamous cell cancer (ESCC); hypoxia inducible factor-1 alpha
   (HIF-1 alpha) inhibitors; PX-478; tumor growth; epithelial-mesenchymal
   transition (EMT)
ID HYPOXIA-INDUCIBLE FACTOR; MOLECULAR-MECHANISMS; PROGNOSTIC-SIGNIFICANCE;
   COLORECTAL-CANCER; EXPRESSION; CARCINOMA; CYCLOOXYGENASE-2; PD-L1;
   FACTOR-1-ALPHA; INTERVENTION
AB The aim of this study is to investigate the clinical significance of hypoxia inducible factor-1 alpha (HIF-1 alpha) expression in esophageal squamous cell cancer (ESCC) and clarify the effects of PX-478, a selective HIF-1a inhibitor, on ESCC both in vitro and in vivo. HIF-1 alpha, cyclooxygenase-2 (COX-2) and programmed death ligand-1 (PD-L1) were markedly overexpressed in ESCC tissue and associated with poorer survival. In vitro, both COX-2 and PD-L1 expression of ESCC cells were significantly induced by CoCl2 treatment, but inhibited by HIF-1 alpha knock-down or PX-478 treatment. Furthermore, PX-478 significantly inhibited tumor cell proliferation by inhibiting the G2/M transition and promoting apoptosis of ESCC cells. In addition, inhibited epithelial-mesenchymal transition was observed after PX-478 treatment. In vivo, PX-478 significantly decreased tumor volume following subcutaneous implantation. Together, our results indicated that PX-478 had significant antitumor activity against HIF-1 alpha over-expressing ESCC tumors in vitro and in vivo. These results opened up the possibility of inhibiting HIF-1 alpha for targeted therapy of ESCC.
C1 [Zhu, Yingming; Zhao, Fen; Li, Zhenxiang; Li, Minghuan; Xing, Ligang; Yu, Jinming] Shandong Univ, Shandong Canc Hosp & Inst, Dept Radiat Oncol, 440 Jiyan Rd, Jinan 250117, Peoples R China.
   [Zhang, Jianbo] Shandong Univ, Shandong Canc Hosp & Inst, Dept Pathol, Jinan, Peoples R China.
   [Zang, Yuanwei; Fang, Liang; Xu, Zhonghua] Shandong Univ, Qilu Hosp, Dept Urol, Jinan, Peoples R China.
C3 Shandong University; Shandong First Medical University & Shandong
   Academy of Medical Sciences; Shandong First Medical University &
   Shandong Academy of Medical Sciences; Shandong University; Shandong
   University
RP Yu, JM (corresponding author), Shandong Univ, Shandong Canc Hosp & Inst, Dept Radiat Oncol, 440 Jiyan Rd, Jinan 250117, Peoples R China.
EM yujinmingsd@126.com
RI Fang, Liang/AGI-2303-2022; Li, Yilin/JCD-8027-2023
OI Zang, Yuanwei/0000-0002-2265-3198
FU Natural Science Foundation of Shandong Province [ZR2015HZ004]; National
   Natural Science Foundation of China [81372335]
FX This study was supported by grant number ZR2015HZ004 from the Natural
   Science Foundation of Shandong Province and grant number 81372335 from
   the National Natural Science Foundation of China. We are also grateful
   to Dr. Yufeng Cheng (Qilu hospital, Shandong University) for kindly
   providing the EC109 and EC9706 cells.
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NR 33
TC 54
Z9 55
U1 0
U2 10
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2156-6976
J9 AM J CANCER RES
JI Am. J. Cancer Res.
PY 2017
VL 7
IS 5
BP 1198
EP +
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EW1NK
UT WOS:000402257100013
PM 28560067
DA 2025-01-04
ER

PT J
AU Dobre, M
   Dinu, DE
   Panaitescu, E
   Bîrla, RD
   Iosif, CI
   Boeriu, M
   Constantinoiu, S
   Ivan, RN
   Ardeleanu, CM
   Costache, M
AF Dobre, Maria
   Dinu, Daniela Elena
   Panaitescu, Eugenia
   Birla, Rodica Daniela
   Iosif, Cristina-Ileana
   Boeriu, Marius
   Constantinoiu, Silviu
   Ivan, Roxana Nicoleta
   Ardeleanu, Carmen Maria
   Costache, Marieta
TI KRAS gene mutations - prognostic factor in colorectal cancer?
SO ROMANIAN JOURNAL OF MORPHOLOGY AND EMBRYOLOGY
LA English
DT Article
DE colorectal cancer; KRAS gene; prognostic; gene mutation; targeted
   therapy
ID K-RAS GENE; ABERRANT CRYPT FOCI; PREDICTIVE FACTORS; POINT MUTATIONS;
   STAGE-II; TUMORIGENESIS; BRAF; FREQUENCY; COLON; APC
AB The colorectal cancer (CRC) modern therapy is using adjuvant and neoadjuvant companion therapeutic agents, part of them having an anti-angiogenic action. Their benefic effect can be annulated by some gene mutations, which are interfering in signal transduction pathways. One of the more frequent activating mutations is occurring in the KRAS gene. We assessed the KRAS mutations by two molecular methods, in a group of patients with a follow-up until 144 months, aiming to establish eventual correlations between the presence of mutations and the evolution of patients. We tried to appreciate the prognostic value of these mutations. A retrospective study was conducted on 74 patients treated by radical surgery; the surgical specimens were analyzed macroscopically and the histopathological type and degree were established. PCR-RFLP (polymerase chain reaction restriction fragment length polymorphism) and pyrosequencing were performed on paraffin-embedded tumor specimens. Statistical analysis showed significant differences in survival between patients with wild type gene and patients with mutation in codon 13; the same results were also obtained regarding TNM I, II stages or Dukes type A and B cases. However, for the patients in stage IV pTNM, the evolution was slightly better in association with a KRAS mutation than in wild type cases.
C1 [Dobre, Maria; Ivan, Roxana Nicoleta; Ardeleanu, Carmen Maria] Victor Babes Natl Inst Res & Dev Pathol & Biomed, Dept Pathol, Bucharest 050096, Romania.
   [Dobre, Maria; Costache, Marieta] Univ Bucharest, Fac Biol, Bucharest, Romania.
   [Dinu, Daniela Elena; Birla, Rodica Daniela; Boeriu, Marius; Constantinoiu, Silviu] Carol Davila Univ Med & Pharm, Dept Gen & Esophageal Surg, Bucharest, Romania.
   [Dinu, Daniela Elena; Birla, Rodica Daniela; Boeriu, Marius; Constantinoiu, Silviu] Sf Maria Clin Hosp, Bucharest, Romania.
   [Panaitescu, Eugenia] Carol Davila Univ Med & Pharm, Dept Biostat & Med Informat, Bucharest, Romania.
   [Iosif, Cristina-Ileana] Sf Maria Clin Hosp, Dept Pathol, Bucharest, Romania.
C3 Victor Babes National Institute of Pathology; University of Bucharest;
   Carol Davila University of Medicine & Pharmacy; Carol Davila University
   of Medicine & Pharmacy
RP Ardeleanu, CM (corresponding author), Victor Babes Natl Inst Res & Dev Pathol & Biomed, 99-101 Independentei Ave,Sect 5, Bucharest 050096, Romania.
EM cmardeleanu@yahoo.com
RI Panaitescu, Eugenia/AAI-5524-2021; Dobre, Maria/AAT-1781-2021; SILVIU,
   CONSTANTINOIU/HMD-3237-2023; Costache, Marieta/F-2806-2016; birla,
   rodica/AAI-2857-2020
OI Dobre, Maria/0000-0002-1376-4021; Costache, Marieta/0000-0002-8103-3693;
   birla, rodica/0000-0002-8799-4524; Panaitescu,
   Eugenia/0000-0002-0083-8992
FU POSCCE [173/2010];  [POSDRU/159/1.5/S/133391]
FX This work was supported by the strategic grant POSDRU/159/1.5/S/133391
   and POSCCE 173/2010.
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NR 31
TC 21
Z9 23
U1 0
U2 6
PU EDITURA ACAD ROMANE
PI BUCURESTI
PA CALEA 13 SEPTEMBRIE NR 13, SECTOR 5, BUCURESTI 050711, ROMANIA
SN 1220-0522
J9 ROM J MORPHOL EMBRYO
JI Rom. J. Morphol. Embryol.
PY 2015
VL 56
IS 2
SU S
BP 671
EP 678
PG 8
WC Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Developmental Biology
GA CT4UA
UT WOS:000362801600005
PM 26429158
DA 2025-01-04
ER

PT J
AU Zhou, J
   Wu, XY
   Li, G
   Gao, X
   Zhai, M
   Chen, WC
   Hu, HG
   Tang, ZX
AF Zhou, Jin
   Wu, Xiaoyu
   Li, Gang
   Gao, Xin
   Zhai, Min
   Chen, Weichang
   Hu, Huagang
   Tang, Zaixiang
TI Prediction of radiosensitive patients with gastric cancer by developing
   gene signature
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE cross-validation; gene signature; radiosensitive genes; individualized
   radiotherapy; gastric cancer
ID 3-DIMENSIONAL CONFORMAL RADIOTHERAPY; INTENSITY-MODULATED RADIOTHERAPY;
   ADVANCED RECTAL-CANCER; PHASE-III TRIAL; PREOPERATIVE CHEMORADIOTHERAPY;
   EXTERNAL VALIDATION; RADIATION-THERAPY; CLINICAL-TRIAL; ADENOCARCINOMA;
   FLUOROURACIL
AB Adjuvant radiotherapy is an important clinical treatment for the majority of gastric cancer, a common cancer. However, radiotherapy is a double-edged sword. It is necessary to develop a method to predict radiosensitive patients who are most likely to benefit from radiotherapy. Using the publicly available data of gastric cancer from The Cancer Genome Atlas (TCGA), we developed a gene signature that predicts radiosensitive patients through estimating a new index, nominal HR (nHR) (HR product of sensitive genes), for each patient. In this study, we provided several results to validate our prediction. Cross-validation results showed that the predicted radiosensitive patients who received radiotherapy had significantly better survival than predicted radiosensitive patients who did not receive radiotherapy. After adjusting for other clinical factors, including age, sex, target therapy, histologic diagnosis, tumor stage, the benefit of radiotherapy on predicted radiosensitive patient remained significant. In addition, predicted radiosensitive patients who received radiotherapy had a significantly reduced rate of disease progression. Taken together, we have obtained a set of genes, to identify radiosensitive patients with gastric cancer. These genes may be potential biomarkers for diagnosis and treatment of gastric cancer, which could give new insight for revealing the underlying mechanism of radiosensitivity of gastric cancer.
C1 [Zhou, Jin; Gao, Xin; Zhai, Min] Soochow Univ, Affiliated Hosp 1, Dept Gen Surg, Suzhou 215006, Jiangsu, Peoples R China.
   [Wu, Xiaoyu] Nanjing Univ Chinese Med, Affiliated Hosp, Dept Surg Oncol, Nanjing 210029, Jiangsu, Peoples R China.
   [Li, Gang] Nanjing Med Univ, Affiliated Canc Hosp, Jiangsu Canc Hosp, Dept Gen Surg, Nanjing 210009, Jiangsu, Peoples R China.
   [Chen, Weichang] Soochow Univ, Affiliated Hosp 1, Dept Gastroenterol, Suzhou 215006, Jiangsu, Peoples R China.
   [Hu, Huagang] Soochow Univ, Med Coll, Sch Nursing, Suzhou 215123, Jiangsu, Peoples R China.
   [Hu, Huagang; Tang, Zaixiang] Soochow Univ, Med Coll, Jiangsu Key Lab Prevent & Translat Med Geriatr Di, Suzhou 215123, Jiangsu, Peoples R China.
   [Hu, Huagang; Tang, Zaixiang] Soochow Univ, Med Coll, Ctr Genet Epidemiol & Genom, Suzhou 215123, Jiangsu, Peoples R China.
   [Tang, Zaixiang] Soochow Univ, Med Coll, Dept Biostat, Sch Publ Hlth, 199 Renai Rd, Suzhou 215123, Jiangsu, Peoples R China.
C3 Soochow University - China; Nanjing University of Chinese Medicine;
   Nanjing Medical University; Soochow University - China; Soochow
   University - China; Soochow University - China; Soochow University -
   China; Soochow University - China
RP Hu, HG (corresponding author), Soochow Univ, Med Coll, Sch Nursing, Suzhou 215123, Jiangsu, Peoples R China.; Tang, ZX (corresponding author), Soochow Univ, Med Coll, Dept Biostat, Sch Publ Hlth, 199 Renai Rd, Suzhou 215123, Jiangsu, Peoples R China.
EM huhuagang@suda.edu.cn; tangzx@suda.edu.cn
RI Gao, Xin/D-5487-2013; Zhou, Jin/JEF-3922-2023; wu, 晓煜/HIK-3475-2022
OI Chen, Wei-Chang/0000-0001-8849-6204
FU National Natural Science Foundation of China [81573253, 81773541];
   Jiangsu Provincial Medical Youth Talent; Suzhou Science and Technology
   Bureau [SYS201672]; Priority Academic Program Development of Jiangsu
   Higher Education Institutions at Soochow University
FX We acknowledge the contributions of the TCGA Research Network. This
   study was supported by the National Natural Science Foundation of China
   (no. 81573253 and 81773541) to Z.-X.T., a project funded by Jiangsu
   Provincial Medical Youth Talent to J.Z., a project funded by Suzhou
   Science and Technology Bureau (no. SYS201672) to H.-G.H., and a project
   funded by the Priority Academic Program Development of Jiangsu Higher
   Education Institutions at Soochow University.
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TC 16
Z9 17
U1 0
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PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD OCT
PY 2017
VL 51
IS 4
BP 1067
EP 1076
DI 10.3892/ijo.2017.4107
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FI3HW
UT WOS:000411849600007
PM 28902346
OA Green Submitted, Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Alrushaid, N
   Khan, FA
   Al-Suhaimi, E
   Elaissari, A
AF Alrushaid, Noor
   Khan, Firdos Alam
   Al-Suhaimi, Ebtesam
   Elaissari, Abdelhamid
TI Progress and Perspectives in Colon Cancer Pathology, Diagnosis, and
   Treatments
SO DISEASES
LA English
DT Review
DE colorectal cancer; development of colorectal cancer; colorectal cancer
   pathology; colorectal cancer diagnosis; molecular markers; cancer
   treatments
ID HORMONE REPLACEMENT THERAPY; DRUG-DELIVERY SYSTEMS; COLORECTAL-CANCER;
   PHOTODYNAMIC THERAPY; GENE-THERAPY; RISK; RESVERATROL; BIOMARKERS;
   STATISTICS; EXPRESSION
AB Worldwide, colon cancer is the third most frequent malignancy and the second most common cause of death. Although it can strike anybody at any age, colon cancer mostly affects the elderly. Small, non-cancerous cell clusters inside the colon, commonly known as polyps, are typically where colon cancer growth starts. But over time, if left untreated, these benign polyps may develop into malignant tissues and develop into colon cancer. For the diagnosis of colon cancer, with routine inspection of the colon region for polyps, several techniques, including colonoscopy and cancer scanning, are used. In the case identifying the polyps in the colon area, efforts are being taken to surgically remove the polyps as quickly as possible before they become malignant. If the polyps become malignant, then colon cancer treatment strategies, such as surgery, chemotherapy, targeted therapy, and immunotherapy, are applied to the patients. Despite the recent improvements in diagnosis and prognosis, the treatment of colorectal cancer (CRC) remains a challenging task. The objective of this review was to discuss how CRC is initiated, and its various developmental stages, pathophysiology, and risk factors, and also to explore the current state of colorectal cancer diagnosis and treatment, as well as recent advancements in the field, such as new screening methods and targeted therapies. We examined the limitations of current methods and discussed the ongoing need for research and development in this area. While this topic may be serious and complex, we hope to engage and inform our audience on this important issue.
C1 [Alrushaid, Noor; Elaissari, Abdelhamid] Univ Claude Bernard Lyon 1, CNRS, ISA, UMR 5280, F-69100 Villeurbanne, France.
   [Alrushaid, Noor; Khan, Firdos Alam] Imam Abdulrahman Bin Faisal Univ, Inst Res & Med Consultat IRMC, Dept Stem Cell Res, Dammam 31441, Saudi Arabia.
   [Al-Suhaimi, Ebtesam] Imam Abdulrahman Bin Faisal Univ, Inst Res & Med Consultat IRMC, Coll Sci, Biol Dept, Dammam 31441, Saudi Arabia.
C3 Universite Claude Bernard Lyon 1; Centre National de la Recherche
   Scientifique (CNRS); CNRS - Institute of Chemistry (INC); Imam
   Abdulrahman Bin Faisal University; Imam Abdulrahman Bin Faisal
   University
RP Elaissari, A (corresponding author), Univ Claude Bernard Lyon 1, CNRS, ISA, UMR 5280, F-69100 Villeurbanne, France.
EM naalrushaid@iau.edu.sa; fakhan@iau.edu.sa; ealsuhaimi@iau.edu.sa;
   abdelhamid.elaissari@univ-lyon1.fr
RI Elaissari, Abdelhamid/M-3312-2017; KHAN, FIRDOS/A-5190-2017; Al-Suhaimi,
   Ebtesam/C-6054-2015
OI Elaissari, Abdelhamid/0000-0002-2151-9894; KHAN,
   FIRDOS/0000-0002-6892-1530; Al-Suhaimi, Ebtesam/0000-0003-1614-0211
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NR 89
TC 6
Z9 6
U1 16
U2 52
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2079-9721
J9 DISEASES-BASEL
JI Diseases
PD DEC
PY 2023
VL 11
IS 4
AR 148
DI 10.3390/diseases11040148
PG 22
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA DI0C5
UT WOS:001131273900001
PM 37987259
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Matos, I
   Elez, E
   Capdevila, J
   Tabernero, J
AF Matos, Ignacio
   Elez, Elena
   Capdevila, Jaume
   Tabernero, Josep
TI Emerging tyrosine kinase inhibitors for the treatment of metastatic
   colorectal cancer
SO EXPERT OPINION ON EMERGING DRUGS
LA English
DT Review
DE Metastatic colorectal cancer; targeted therapies; biomarkers; emerging
   resistance; tyrosine kinase inhibitors; molecular subtypes
ID PHASE-III TRIAL; PREVIOUSLY TREATED PATIENTS; BEVACIZUMAB PLUS MFOLFOX6;
   ENDOTHELIAL GROWTH-FACTOR; 1ST-LINE TREATMENT; OPEN-LABEL;
   ACQUIRED-RESISTANCE; DOUBLE-BLIND; EGFR BLOCKADE; CETUXIMAB RESISTANCE
AB Introduction: Colorectal cancer (CRC) is a leading cause of cancer death worldwide. Over the last decade, the addition of antibodies that block the epidermal growth factor receptor (EGFR) or angiogenesis to the classic chemotherapy backbone has improved overall survival in metastatic colorectal cancer (mCRC). However, the role of the other major targeted therapy, the tyrosine kinase inhibitors (TKIs), is not yet fully clarified.
   Areas covered: This review discusses key published and ongoing studies with TKIs in mCRC, the mechanisms of resistance to standard treatments that are potentially targetable with these small molecules, along with the role of biomarkers in therapeutic decision-making process.
   Expert opinion: The current effectiveness of TKIs is limited by two principal reasons, firstly the use of combination chemotherapy necessitates lower dose-density to manage the toxicity profile and secondly, development of these drugs has mainly been performed in molecularly unselected populations. mCRC is a heterogeneous and dynamic disease, and clinical trials with TKIs must be designed on the basis of specific molecular alterations targeted by these drugs. Success with this approach relies on identifying mutations at the time of progression, raising the importance of minimally-invasive monitoring tools. Liquid biopsies are a promising option, although this technique remains to be validated. Overall, this approach contributes to the move towards personalized and precision therapeutic strategies.
C1 [Matos, Ignacio; Elez, Elena; Capdevila, Jaume; Tabernero, Josep] Vail dHebron Univ Hosp, Spain Med Oncol Dept, Barcelona, Spain.
C3 Hospital Universitari Vall d'Hebron
RP Tabernero, J (corresponding author), Hosp Valle De Hebron, Dept Med Oncol, Pg Vall dHebron 119-129, Barcelona 08035, Spain.
EM jtabernero@vhebron.net
RI Tabernero, Josep/AAG-5026-2019; Élez, Elena/AAH-2945-2019
OI Elez, Elena/0000-0002-4653-6324; Tabernero, Josep/0000-0002-2495-8139
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NR 100
TC 7
Z9 9
U1 0
U2 13
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1472-8214
EI 1744-7623
J9 EXPERT OPIN EMERG DR
JI Expert Opin Emerg. Drugs
PD SEP
PY 2016
VL 21
IS 3
BP 267
EP 282
DI 10.1080/14728214.2016.1220535
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DV9ZQ
UT WOS:000383301100004
PM 27578253
DA 2025-01-04
ER

PT J
AU Yan, HX
   Ou, QL
   Chang, YL
   Liu, JH
   Chen, LZ
   Guo, DY
   Zhang, SF
AF Yan, Haixia
   Ou, Qinling
   Chang, Yonglong
   Liu, Jinhui
   Chen, Linzi
   Guo, Duanyang
   Zhang, Sifang
TI 5-Fluorouracil resistance-based immune-related gene signature for COAD
   prognosis
SO HELIYON
LA English
DT Article
DE Colon adenocarcinoma; 5-FU-Related genes; Gene signature; Prognostic
   model; Immune infiltration; 5FRRDEGs
ID COLORECTAL-CANCER; COLON-CANCER; INVASION
AB Background: Drug resistance is the primary obstacle to advanced tumor therapy and the key risk factor for tumor recurrence and death. 5-Fluorouracil (5-FU) chemotherapy is the most common chemotherapy for individuals with colorectal cancer, despite numerous options. Methods: The Gene Expression Omnibus database was utilized to extract expression profile data of HCT-8 human colorectal cancer wild-type cells and their 5-FU-induced drug resistance cell line. These data were used to identify 5-FU resistance-related differentially expressed genes (5FRRDEGs), which intersected with the colorectal adenocarcinoma (COAD) transcriptome data provided by the Cancer Genome Atlas Program database. A prognostic signature containing five 5FRRDEGs (GOLGA8A, KLC3, TIGD1, NBPF1, and SERPINE1) was established after conducting a Cox regression analysis. We conducted nomogram development, drug sensitivity analysis, tumor immune microenvironment analysis, and mutation analysis to assess the therapeutic value of the prognostic qualities. Results: We identified 166 5FRRDEGs in patients with COAD. Subsequently, we created a prognostic model consisting of five 5FRRDEGs using Cox regression analysis. The patients with COAD were divided into different risk groups by risk score; the high-risk group demonstrated a worse prognosis than the low-risk group. Conclusion: In summary, the 5FRRDEG-based prognostic model is an effective tool for targeted therapy and chemotherapy in patients with COAD. It can accurately predict the survival prognosis of these patients as well as to provide the direction for exploring the resistance mechanism underlying COAD.
C1 [Yan, Haixia; Ou, Qinling; Chang, Yonglong; Chen, Linzi; Zhang, Sifang] Cent South Univ, Xiangya Hosp 2, Dept Integrated Tradit Chinese & Western Med, Changsha 410011, Hunan, Peoples R China.
   [Liu, Jinhui; Guo, Duanyang] Hunan Univ Chinese Med, Coll Integrated Tradit Chinese & Western Med, Changsha 410208, Hunan, Peoples R China.
C3 Central South University; Hunan University of Chinese Medicine
RP Zhang, SF (corresponding author), Cent South Univ, Xiangya Hosp 2, Dept Integrated Tradit Chinese & Western Med, Changsha 410011, Hunan, Peoples R China.
EM sifangzhang2005@csu.edu.cn
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NR 61
TC 0
Z9 0
U1 1
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
EI 2405-8440
J9 HELIYON
JI Heliyon
PD JUL 30
PY 2024
VL 10
IS 14
AR e34535
DI 10.1016/j.heliyon.2024.e34535
PG 17
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA ZK3Y6
UT WOS:001275165700001
PM 39130472
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Jiao, X
   Xing, FZ
   Zhai, MM
   Sun, P
AF Jiao, Xin
   Xing, Fang-Zhou
   Zhai, Mi-Mi
   Sun, Peng
TI Successful treatment of breast metastasis from primary transverse colon
   cancer: A case report
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Article
DE Colon cancer; Breast metastasis; Tumor markers; FOLFIRI; Cetuximab;
   Prognosis; Case report
ID COLORECTAL-CANCER; CARCINOMA
AB BACKGROUND The incidence of colon cancer is increasing worldwide. Treatments for colon cancer include surgery and surgery combined with chemotherapy and radiotherapy, but the median survival rate is still poor. Colon cancer most commonly metastasizes to the lymph nodes, lungs, liver, peritoneum, and brain, but breast metastasis is rare. There is no agreement on its treatment.CASE SUMMARY A 23-year-old woman was admitted to our hospital for further treatment with a history of acute abdominal pain, nausea, and vomiting. Her physical examination and computed tomography scan revealed an abdominal tumor. Transverse colectomy was successfully performed. Histopathological examination revealed that the tumor was a mucosecretory adenocarcinoma with signet ring cells. The patient inadvertently found a mass in the outer upper quadrant of the right breast after four cycles of XELOX chemotherapy [oxaliplatin 130 mg/m(2), d1, intravenous (iv) drip for 2 h; capecitabine 1000 mg/m(2), po, bid, d1-d14]. After discussion with the patient, we performed a lumpectomy and frozen biopsy. The latter revealed that the breast tumor was intestinal metastasis. Genetic testing showed wild-type RAS and BRAF. So we replaced the original chemotherapy with FOLFIRI [irinotecan 180 mg/m(2), d1, iv drip for 3-90 min; leucovorin 400 mg/m(2), d1, iv drip for 2 h; 5-fluorouracil (5-FU) 400 mg/m(2), d1 and 5-FU 1200 mg/(m(2) d) x 2 d, continuous iv drip for 46-48 h] + cetuximab (500 mg/m(2), d1, iv drip for 2 h). Serum levels of tumor markers returned to normal after several treatment cycles, and there was no evidence of tumor recurrence or metastasis.CONCLUSION Breast metastasis from colon cancer is rare. Radical breast surgery should be avoided unless needed for palliation. Chemotherapy combined with targeted therapy should be the first choice.
C1 [Jiao, Xin; Xing, Fang-Zhou; Sun, Peng] Weifang Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp, 2428 Yuhe Rd, Weifang 261041, Shandong, Peoples R China.
   [Zhai, Mi-Mi] Weifang Peoples Hosp, Dept Digest Syst, Weifang 261041, Shandong, Peoples R China.
C3 Shandong Second Medical University
RP Sun, P (corresponding author), Weifang Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp, 2428 Yuhe Rd, Weifang 261041, Shandong, Peoples R China.
EM 1105031456@qq.com
RI Sun, Peng/KDO-4243-2024
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NR 19
TC 0
Z9 0
U1 0
U2 1
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD APR 16
PY 2023
VL 11
IS 11
DI 10.12998/wjcc.v11.i11.2559
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA F4HL9
UT WOS:000981973000024
PM 37123317
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Nevala-Plagemann, C
   Iyengar, S
   Trunk, AD
   Pappas, L
   Haaland, B
   Garrido-Laguna, I
AF Nevala-Plagemann, Christopher
   Iyengar, Siddharth
   Trunk, Andrew D.
   Pappas, Lisa
   Haaland, Benjamin
   Garrido-Laguna, Ignacio
TI Treatment Trends and Clinical Outcomes of Left-Sided<i> RAS/RAF</i>
   Wild-Type Metastatic Colorectal Cancer in the United States
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID PRIMARY TUMOR LOCATION; PHASE-III TRIAL; OPEN-LABEL;
   MONOCLONAL-ANTIBODIES; 1ST-LINE TREATMENT; PLUS IRINOTECAN; CETUXIMAB;
   CHEMOTHERAPY; BEVACIZUMAB; PANITUMUMAB
AB Background: Post hoc analysis of the CALGB/SWOG 80405 trial suggests that anti-EGFR therapy may be superior to bevacizumab when added to first-line chemotherapy in patients with metastatic colorectal cancer (mCRC) who have left-sided primary tumors. We evaluated trends in use of anti-EGFR agents in patients with left-sided RAS/RAF wild-type (WT) mCRC and compared clinical outcomes among the most commonly used treatment strategies. Methods: A nationwide electronic health record (EHR)-derived deidentified database was reviewed for patients with left-sided RAS/RAF WT mCRC. Treatment trends over time were assessed by fitting a linear model to the percentage of patients receiving anti-EGFR therapy. A propensity score weighted Cox model was used to compare overall survival (OS) stratified by first-line targeted therapy received. Results: A total of 1,607 patients with left-sided RAS/RAF WT mCRC received standard first line chemotherapy. Of these, 965 (60%) received bevacizumab and 186 (12%) received an anti-EGFR agent. The percentage of patients receiving an anti-EGFR increased from 9% in 2013 to 16% in 2018. Median OS for patients treated with chemotherapy alone was 27.3 months (95% CI, 24.8-32.3), 27.5 months with bevacizumab (95% CI, 25.8-28.9; hazard ratio [HR], 0.88; P=.33), and 42.9 months with an anti-EGFR agent (95% CI, 36.0 to not reached; HR, 0.52; P=.005). Conclusions: This analysis suggests that chemotherapy with bevacizumab remained the most widely used first-line treatment strategy for patients with left-sided RAS/RAF WT mCRC in the United States in 2018. Despite this preference, treatment with an anti-EGFR agent was associated with improved OS.
C1 [Nevala-Plagemann, Christopher; Garrido-Laguna, Ignacio] Univ Utah, Div Med Oncol, Huntsman Canc Inst, Salt Lake City, UT USA.
   [Iyengar, Siddharth; Trunk, Andrew D.] Univ Utah, Dept Internal Med, Salt Lake City, UT USA.
   [Pappas, Lisa; Haaland, Benjamin] Univ Utah, Dept Populat Hlth Sci, Salt Lake City, UT USA.
C3 Utah System of Higher Education; University of Utah; Huntsman Cancer
   Institute; Utah System of Higher Education; University of Utah; Utah
   System of Higher Education; University of Utah
RP Garrido-Laguna, I (corresponding author), Huntsman Canc Inst, Div Med Oncol, 2000 Circle Hope,Suite 5507, Salt Lake City, UT 84112 USA.
EM Ignacio.Garrido-Laguna@hci.utah.edu
RI Garrido-Laguna, Ignacio/ABD-1875-2020
FU NCI of the NIH [P30CA042014-23]
FX Research reported in this publication was supported by the NCI of the
   NIH under award number P30CA042014-23.
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NR 28
TC 4
Z9 4
U1 0
U2 1
PU HARBORSIDE PRESS
PI HUNTINGTON
PA 94 NORTH WOODHULL RD, HUNTINGTON, NY 11743 USA
SN 1540-1405
EI 1540-1413
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD MAR
PY 2022
VL 20
IS 3
BP 268
EP 275
DI 10.6004/jnccn.2021.7079
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZZ5XP
UT WOS:000773341700010
PM 35120306
OA Bronze
DA 2025-01-04
ER

PT J
AU Sgarbura, O
   Samalin, E
   Carrere, S
   Mazard, T
   de Forges, H
   Alline, M
   Pissas, MH
   Portales, F
   Ychou, M
   Quenet, F
AF Sgarbura, Olivia
   Samalin, Emmanuelle
   Carrere, Sebastien
   Mazard, Thibault
   de Forges, Helene
   Alline, Mathias
   Pissas, Marie-Helene
   Portales, Fabienne
   Ychou, Marc
   Quenet, Francois
TI Preoperative intraperitoneal oxaliplatin for unresectable peritoneal
   carcinomatosis of colorectal origin: a pilot study
SO PLEURA AND PERITONEUM
LA English
DT Article
DE colorectal cancer; intraperitoneal treatment; oxaliplatin; peritoneal
   carcinomatosis; preoperative chemotherapy
ID ADVANCED GASTRIC-CANCER; CYTOREDUCTIVE SURGERY; INTRAVENOUS PACLITAXEL;
   SYSTEMIC CHEMOTHERAPY; LIVER METASTASES; OVARIAN-CANCER; PHASE-I; S-1;
   DISSEMINATION; COMBINATION
AB Background: Peritoneal carcinomatosis in colorectal cancer is an advanced stage of the disease where improved survival can be attained whenever the resection associated with hyperthermic intreperitoneal chemotherapy is possible. In unresectable cases, systemic chemotherapy is administered to obtain conversion to resectability but results have not yet been clearly evaluated. Local chemotherapy in this setting has been proven useful in several similar situations. The aim of the present pilot study was to evaluate the feasibility of preoperative intraperitoneal chemotherapy with oxaliplatin in these patients.
   Methods: Six patients with unresectable peritoneal disease of colorectal origin were included in the study. An intraperitoneal implantable chamber catheter was inserted during the laparotomy that evaluated the extent of the peritoneal disease (peritoneal carcinomatosis index 25 to 39). Patients then underwent intraperitoneal chemotherapy with oxaliplatin 85 mg/m(2) in combination with systemic chemotherapy (FOLFIRI or simplified LV5FU) and a targeted therapy every 2 weeks.
   Results: Two catheter perfusion incidents were reported due to the abdominal wall thickness. Two patients completed the four intraperitoneal (IP) chemotherapy cycles without major toxicity. One patient developed grade 3 or 4 diarrhea requiring a short intensive care unit (ICU) stay, though it is not clear whether the event was induced by intravenous irinotecan, IP oxaliplatin or the combination of both. Grade 3 fatigue and abdominal pain were also recorded. For one patient with aggressive disease, best supportive care was initiated after the first course of chemotherapy.
   Conclusions: Our study is the first to assess intraperitoneal oxaliplatin-based chemotherapy in the preoperative setting for patients with unresectable peritoneal metastases. The tolerance was acceptable for 85 mg/m2 IP oxaliplatin combined with systemic therapy in these patients. Our results justify carrying on with a phase I/II trial to determine the recommended dose of oxaliplatin in this clinical context and its efficacy.
C1 [Sgarbura, Olivia; Carrere, Sebastien; Alline, Mathias; Pissas, Marie-Helene; Quenet, Francois] Inst Reg Canc Montpellier ICM, Surg Oncol Dept, 208 Ave Apothicaires, F-34298 Montpellier, France.
   [Samalin, Emmanuelle; Mazard, Thibault; Portales, Fabienne; Ychou, Marc] Inst Reg Canc Montpellier ICM, Med Oncol Dept, Montpellier, France.
   [de Forges, Helene] Inst Reg Canc Montpellier ICM, Clin Res Unit, Montpellier, France.
C3 Universite de Montpellier; Universite de Montpellier; Universite de
   Montpellier
RP Sgarbura, O (corresponding author), Inst Reg Canc Montpellier ICM, Surg Oncol Dept, 208 Ave Apothicaires, F-34298 Montpellier, France.
EM olivia.sgarbura@icm.unicancer.fr
RI MAZARD, Thibault/ABH-6334-2020; SGARBURA, Olivia/L-7546-2013
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NR 43
TC 8
Z9 8
U1 0
U2 1
PU DE GRUYTER OPEN LTD
PI WARSAW
PA BOGUMILA ZUGA 32A ST, 01-811 WARSAW, POLAND
SN 2364-7671
EI 2364-768X
J9 PLEURA PERITONEUM
JI Pleura Peritoneum
PD DEC
PY 2016
VL 1
IS 4
BP 209
EP 215
DI 10.1515/pap-2016-0018
PG 7
WC Oncology; Surgery
WE Emerging Sources Citation Index (ESCI)
SC Oncology; Surgery
GA FF4CV
UT WOS:000408878100006
PM 30911625
DA 2025-01-04
ER

PT J
AU Wang, DW
   Zhang, WH
   Danil, G
   Yang, K
   Hu, JK
AF Wang, De-Wen
   Zhang, Wei-Han
   Danil, Galiullin
   Yang, Kun
   Hu, Jian-Kun
TI The role and mechanism of claudins in cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE claudin; signaling pathways; cancer; molecular targeted therapy; tumor
   diagnosis
ID CLOSTRIDIUM-PERFRINGENS ENTEROTOXIN; SQUAMOUS-CELL CARCINOMA; TIGHT
   JUNCTION PROTEIN; GASTRIC-CANCER; UP-REGULATION;
   PROGNOSTIC-SIGNIFICANCE; COLORECTAL-CANCER; LUNG-CANCER; MESENCHYMAL
   TRANSITION; EXPRESSION PATTERNS
AB Claudins are a tetraspan membrane protein multigene family that plays a structural and functional role in constructing tight junctions. Claudins perform crucial roles in maintaining cell polarity in epithelial and endothelial cell sheets and controlling paracellular permeability. In the last two decades, increasing evidence indicates that claudin proteins play a major role in controlling paracellular permeability and signaling inside cells. Several types of claudins are dysregulated in various cancers. Depending on where the tumor originated, claudin overexpression or underexpression has been shown to regulate cell proliferation, cell growth, metabolism, metastasis and cell stemness. Epithelial-to-mesenchymal transition is one of the most important functions of claudin proteins in disease progression. However, the exact molecular mechanisms and signaling pathways that explain why claudin proteins are so important to tumorigenesis and progression have not been determined. In addition, claudins are currently being investigated as possible diagnostic and treatment targets. Here, we discuss how claudin-related signaling pathways affect tumorigenesis, tumor progression, and treatment sensitivity.
C1 [Wang, De-Wen; Zhang, Wei-Han; Danil, Galiullin; Yang, Kun; Hu, Jian-Kun] Sichuan Univ, West China Hosp, Gastr Canc Ctr, Chengdu, Peoples R China.
   [Wang, De-Wen; Zhang, Wei-Han; Danil, Galiullin; Yang, Kun; Hu, Jian-Kun] Sichuan Univ, West China Hosp, Dept Gen Surg, Lab Gastr Canc, Chengdu, Peoples R China.
   [Wang, De-Wen; Zhang, Wei-Han; Danil, Galiullin; Yang, Kun; Hu, Jian-Kun] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu, Peoples R China.
   [Danil, Galiullin] Bashkir State Med Univ, Cent Res Lab, Ufa, Russia.
C3 Sichuan University; Sichuan University; Sichuan University; Bashkir
   State Medical University
RP Hu, JK (corresponding author), Sichuan Univ, West China Hosp, Gastr Canc Ctr, Chengdu, Peoples R China.; Hu, JK (corresponding author), Sichuan Univ, West China Hosp, Dept Gen Surg, Lab Gastr Canc, Chengdu, Peoples R China.; Hu, JK (corresponding author), Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu, Peoples R China.
EM hujkwch@126.com
RI Zhang, Wei-Han/AAS-3536-2021; Hu, Jiankun/D-9856-2012
OI Galiullin, Danil/0000-0002-5795-6375
FU National Natural Science Foundation of China; Foundation of Science &
   Technology Department of Sichuan Province; Medical Science and Technique
   Project of Health Commission of Sichuan Province;  [82072688]; 
   [81902437];  [2020YJ3357];  [2021YJ0475];  [21PJ043]
FX Funding National Natural Science Foundation of China (No. 82072688, No.
   81902437). Foundation of Science & Technology Department of Sichuan
   Province (No. 2020YJ3357, No. 2021YJ0475). Medical Science and Technique
   Project of Health Commission of Sichuan Province (No. 21PJ043).
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NR 195
TC 28
Z9 29
U1 1
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD DEC 22
PY 2022
VL 12
AR 1051497
DI 10.3389/fonc.2022.1051497
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 7O1HP
UT WOS:000907783000001
PM 36620607
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhang, WJ
   Li, Y
   Wei, MN
   Chen, Y
   Qiu, JG
   Jiang, QW
   Yang, Y
   Zheng, DW
   Qin, WM
   Huang, JR
   Wang, K
   Zhang, WJ
   Wang, YJ
   Yang, DH
   Chen, ZS
   Shi, Z
AF Zhang, Wen-Ji
   Li, Yong
   Wei, Meng-Ning
   Chen, Yao
   Qiu, Jian-Ge
   Jiang, Qi-Wei
   Yang, Yang
   Zheng, Di-Wei
   Qin, Wu-Ming
   Huang, Jia-Rong
   Wang, Kun
   Zhang, Wen-Juan
   Wang, Yi-Jun
   Yang, Dong-Hua
   Chen, Zhe-Sheng
   Shi, Zhi
TI Synergistic antitumor activity of regorafenib and lapatinib in
   preclinical models of human colorectal cancer
SO CANCER LETTERS
LA English
DT Article
DE Regorafenib; Lapatinib; Targeted therapy; Combination chemotherapy;
   Colorectal cancer
ID MULTIDRUG-RESISTANCE; BREAST-CANCER; DRUG-SENSITIVITY; PHASE-3 TRIAL;
   TUMOR-GROWTH; COLON-CANCER; INHIBITOR; CELLS; COMBINATION; MULTICENTER
AB Regorafenib significantly prolongs overall survival in patients with metastatic colorectal cancer (mCRC), but the overall clinical efficacy of regorafenib remains quite limited. Combination chemotherapy is a potentially promising approach to enhance anticancer activity, overcome drug resistance, and improve disease-free and overall survival. The current study investigates the antitumor activity of regorafenib in combination with lapatinib in preclinical models of human CRC. Our results show improved antitumor efficacy when regorafenib is combined with lapatinib both in vitro and in vivo. Furthermore, pharmacokinetic analyses revealed that regorafenib and lapatinib do not influence on each plasma concentration. The finding that regorafenib in combination with lapatinib have synergistic activity warrants further clinical investigation of this beneficial combination as a potential treatment strategy for CRC patients. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
C1 [Zhang, Wen-Ji; Wei, Meng-Ning; Chen, Yao; Qiu, Jian-Ge; Jiang, Qi-Wei; Yang, Yang; Zheng, Di-Wei; Qin, Wu-Ming; Huang, Jia-Rong; Wang, Kun; Shi, Zhi] Jinan Univ, Dept Cell Biol, Guangzhou 510632, Guangdong, Peoples R China.
   [Zhang, Wen-Ji; Wei, Meng-Ning; Chen, Yao; Qiu, Jian-Ge; Jiang, Qi-Wei; Yang, Yang; Zheng, Di-Wei; Qin, Wu-Ming; Huang, Jia-Rong; Wang, Kun; Shi, Zhi] Jinan Univ, Inst Biomed, Natl Engn Res Ctr Genet Med, Guangdong Prov Key Lab Bioengn Med,Coll Life Sci, Guangzhou 510632, Guangdong, Peoples R China.
   [Li, Yong] Guangdong Acad Med Sci, Guangdong Gen Hosp, Dept Gastrointestinal Surg & Gen Surg, Guangzhou 510080, Guangdong, Peoples R China.
   [Zhang, Wen-Juan] Jinan Univ, Dept Prevent Med, Coll Med, Guangzhou 510632, Guangdong, Peoples R China.
   [Wang, Yi-Jun; Yang, Dong-Hua; Chen, Zhe-Sheng] St Johns Univ, Dept Pharmaceut Sci, Coll Pharm & Hlth Sci, Queens, NY 11439 USA.
   [Chen, Zhe-Sheng] Jinan Univ, Coll Pharm, Guangdong Prov Key Lab Pharmacodynam Constituents, Guangzhou 510632, Guangdong, Peoples R China.
C3 Jinan University; Jinan University; Guangdong Academy of Medical
   Sciences & Guangdong General Hospital; Southern Medical University -
   China; Jinan University; Saint John's University; Jinan University
RP Chen, ZS (corresponding author), 8000 Utopia Pkwy, Jamaica, NY 11439 USA.; Shi, Z (corresponding author), 601 Huangpu Rd West, Guangzhou 510632, Guangdong, Peoples R China.
EM chenz@stjohns.edu; tshizhi@jnu.edu.cn
RI Wang, Yijun/GXW-1763-2022; Chen, Yuxuan/IWL-8267-2023; Huang,
   Jiarong/M-2374-2019; YANG, DH/C-4905-2008
OI Chen, Zhe-Sheng/0000-0002-8289-097X; Yang, Dong-Hua/0000-0001-8649-5531;
   Zhang, Wenji/0000-0003-1500-6627
FU NIH [1R15CA143701]; St. John's University Research Seed Grant
   [579-1110-7002]; National Natural Science Foundation of China [31271444,
   81201726, 81473014]; Science and Technology Program of Guangzhou
   [2014J4100009]; Guangdong Natural Science Funds for Distinguished Young
   Scholar [2014A030306001]; Guangdong Special Support Program for Young
   Talent [2015TQ01R350]; Science and Technology Program of Guangdong
   [2016A050502027]; Foundation for Research Cultivation and Innovation of
   Jinan University [21616119]
FX This work was supported by funds from the NIH No. 1R15CA143701 and St.
   John's University Research Seed Grant No. 579-1110-7002 (Z.S.C), the
   National Natural Science Foundation of China No. 31271444, No. 81201726
   (Z.S.) and No. 81473014 (W.J.Z.), the Science and Technology Program of
   Guangzhou No. 2014J4100009 (Z.S.), the Guangdong Natural Science Funds
   for Distinguished Young Scholar No. 2014A030306001 (Z.S.), the Guangdong
   Special Support Program for Young Talent No. 2015TQ01R350 (Z.S.), the
   Science and Technology Program of Guangdong No. 2016A050502027 (Z.S.),
   and the Foundation for Research Cultivation and Innovation of Jinan
   University No. 21616119 (Z.S.).
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NR 47
TC 30
Z9 30
U1 0
U2 37
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
PY 2017
VL 386
BP 100
EP 109
DI 10.1016/j.canlet.2016.11.011
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EI8QV
UT WOS:000392773500010
PM 27864115
DA 2025-01-04
ER

PT J
AU Ree, AH
   Nygaard, V
   Boye, K
   Heinrich, D
   Dueland, S
   Bergheim, IR
   Johansen, C
   Beiske, K
   Negård, A
   Lund-Iversen, M
   Nygaard, V
   Hovig, E
   Nakken, S
   Nasser, S
   Julsrud, L
   Reisse, CH
   Ruud, EA
   Kristensen, VN
   Florenes, VA
   Geitvik, GA
   Lingjærde, OC
   Borresen-Dale, AL
   Russnes, HG
   Mælandsmo, GM
   Flatmark, K
AF Ree, Anne Hansen
   Nygaard, Vigdis
   Boye, Kjetil
   Heinrich, Daniel
   Dueland, Svein
   Bergheim, Inger Riise
   Johansen, Christin
   Beiske, Klaus
   Negard, Anne
   Lund-Iversen, Marius
   Nygaard, Vegard
   Hovig, Eivind
   Nakken, Sigve
   Nasser, Salah
   Julsrud, Lars
   Reisse, Claudius H.
   Ruud, Espen A.
   Kristensen, Vessela N.
   Florenes, Vivi A.
   Geitvik, Gry A.
   Lingjaerde, Ole Christian
   Borresen-Dale, Anne-Lise
   Russnes, Hege G.
   Maelandsmo, Gunhild M.
   Flatmark, Kjersti
TI Molecularly matched therapy in the context of sensitivity, resistance,
   and safety; patient outcomes in end-stage cancer - the MetAction study
SO ACTA ONCOLOGICA
LA English
DT Article
ID TARGETED THERAPY; TRIALS; TUMORS; HETEROGENEITY; CRIZOTINIB; GUIDELINES;
   ONCOLOGY; FUSIONS
AB Background: In precision cancer medicine, the challenge is to prioritize DNA driver events, account for resistance markers, and procure sufficient information for treatment that maintains patient safety. The MetAction project, exploring how tumor molecular vulnerabilities predict therapy response, first established the required workflow for DNA sequencing and data interpretation (2014-2015). Here, we employed it to identify molecularly matched therapy and recorded outcome in end-stage cancer (2016-2019). Material and methods: Metastatic tissue from 26 patients (16 colorectal cancer cases) was sequenced by the Oncomine assay. The study tumor boards interpreted called variants with respect to sensitivity or resistance to matched therapy and recommended single-agent or combination treatment if considered tolerable. The primary endpoint was the rate of progression-free survival 1.3-fold longer than for the most recent systemic therapy. The objective response rate and overall survival were secondary endpoints. Results: Both common and rare actionable alterations were identified. Thirteen patients were found eligible for therapy following review of tumor sensitivity and resistance variants and patient tolerability. The interventions were inhibitors of ALK/ROS1-, BRAF-, EGFR-, FGFR-, mTOR-, PARP-, or PD-1-mediated signaling for 2-3 cases each. Among 10 patients who received treatment until radiologic evaluation, 6 (46% of the eligible cases) met the primary endpoint. Four colorectal cancer patients (15% of the total study cohort) had objective response. The only serious adverse event was a transient colitis, which appeared in 1 of the 2 patients given PD-1 inhibitor with complete response. Apart from those two, overall survival was similar for patients who did and did not receive study treatment. Conclusions: The systematic MetAction approach may point forward to a refined framework for how to interpret the complexity of sensitivity versus resistance and patient safety that resides in tumor sequence data, for the possibly improved outcome of precision cancer medicine in future studies. ClinicalTrials.gov, identifier: NCT02142036
C1 [Ree, Anne Hansen; Heinrich, Daniel; Johansen, Christin] Akershus Univ Hosp, Dept Oncol, Lorenskog, Norway.
   [Ree, Anne Hansen; Beiske, Klaus; Negard, Anne; Kristensen, Vessela N.; Borresen-Dale, Anne-Lise; Flatmark, Kjersti] Univ Oslo, Inst Clin Med, Oslo, Norway.
   [Nygaard, Vigdis; Boye, Kjetil; Hovig, Eivind; Nakken, Sigve; Maelandsmo, Gunhild M.; Flatmark, Kjersti] Oslo Univ Hosp, Dept Tumor Biol, Oslo, Norway.
   [Boye, Kjetil; Dueland, Svein] Oslo Univ Hosp, Dept Oncol, Oslo, Norway.
   [Bergheim, Inger Riise; Kristensen, Vessela N.; Geitvik, Gry A.; Lingjaerde, Ole Christian; Borresen-Dale, Anne-Lise; Russnes, Hege G.] Oslo Univ Hosp, Dept Canc Genet, Oslo, Norway.
   [Beiske, Klaus; Lund-Iversen, Marius; Florenes, Vivi A.; Russnes, Hege G.] Oslo Univ Hosp, Dept Pathol, Oslo, Norway.
   [Negard, Anne; Nasser, Salah; Ruud, Espen A.] Akershus Univ Hosp, Dept Radiol, Lorenskog, Norway.
   [Nygaard, Vegard] Oslo Univ Hosp, Dept Core Facil, Oslo, Norway.
   [Hovig, Eivind] Univ Oslo, Ctr Bioinformat, Oslo, Norway.
   [Hovig, Eivind; Nakken, Sigve] Norwegian Canc Genom Consortium, Oslo, Norway.
   [Nakken, Sigve] Univ Oslo, Ctr Canc Cell Reprogramming, Oslo, Norway.
   [Julsrud, Lars; Reisse, Claudius H.] Oslo Univ Hosp, Dept Radiol, Oslo, Norway.
   [Maelandsmo, Gunhild M.] Arctic Univ Norway, Univ Tromso, Inst Med Biol, Tromso, Norway.
   [Flatmark, Kjersti] Oslo Univ Hosp, Dept Gastroenterol Surg, Oslo, Norway.
C3 University of Oslo; University of Oslo; University of Oslo; University
   of Oslo; University of Oslo; University of Oslo; University of Oslo;
   University of Oslo; University of Oslo; University of Oslo; University
   of Oslo; UiT The Arctic University of Tromso; University of Oslo
RP Ree, AH (corresponding author), Akershus Univ Hosp, Dept Oncol, Lorenskog, Norway.
EM a.h.ree@medisin.uio.no
RI Flatmark, Kjersti/JVO-0068-2024; Nakken, Sigve/H-2898-2019; Boye,
   Kjetil/AAM-8753-2021; Mælandsmo, Gunhild Mari/AFV-4446-2022; Russnes,
   Hege G/N-6170-2015; Nygaard, Vigdis/A-8100-2014; Hovig,
   Eivind/H-2474-2011
OI Ree, Anne H./0000-0002-8264-3223; Hovig, Eivind/0000-0002-9103-1077;
   Flatmark, Kjersti/0000-0001-7409-0780; Dueland,
   Svein/0000-0002-6125-6689; Maelandsmo, Gunhild Mari/0000-0002-4797-1600;
   Nakken, Sigve/0000-0001-8468-2050; Boye, Kjetil/0000-0002-5552-6283
FU Research Council of Norway [218325]; South-Eastern Norway Regional
   Health Authority [2017109]
FX This work was supported by the Research Council of Norway under Grant
   218325 (to GMM); the South-Eastern Norway Regional Health Authority
   under Grant 2017109 (to AHR); and patient donations in support of this
   specific research (to AHR).
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NR 32
TC 10
Z9 10
U1 0
U2 4
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0284-186X
EI 1651-226X
J9 ACTA ONCOL
JI Acta Oncol.
PD JUL 2
PY 2020
VL 59
IS 7
BP 733
EP 740
DI 10.1080/0284186X.2020.1742377
EA MAR 2020
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MI5ZZ
UT WOS:000524044100001
PM 32208873
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Kula, A
   Dawidowicz, M
   Mielcarska, S
   Kiczmer, P
   Chrabanska, M
   Rynkiewicz, M
   Swietochowska, E
   Waniczek, D
AF Kula, Agnieszka
   Dawidowicz, Miriam
   Mielcarska, Sylwia
   Kiczmer, Pawel
   Chrabanska, Magdalena
   Rynkiewicz, Magdalena
   Swietochowska, Elzbieta
   Waniczek, Dariusz
TI Periostin in Angiogenesis and Inflammation in CRC-A Preliminary
   Observational Study
SO MEDICINA-LITHUANIA
LA English
DT Article
DE periostin; colorectal cancer; tumor microenvironment
ID TUMOR-NECROSIS-FACTOR; COLORECTAL-CANCER; POTENTIAL ROLE; CELL-SURVIVAL;
   TNF-ALPHA; EXPRESSION; GROWTH; FIBROBLASTS; METASTASIS; CARCINOMA
AB Background and Objectives: To assess the periostin level and the concentrations of pro-inflammatory cytokines: TNF alpha, IFN-gamma, IL-1 beta and IL-17 in tumor and marginal tissues of CRC and to investigate the influence of periostin on angiogenesis by MVD (microvessel density) and concentration of VEGF-A in relation to clinicopathological parameters of patients. Materials and Methods: The study used 47 samples of tumor and margin tissues derived from CRC patients. To determinate the concentration of periostin, VEGF-A, TNF alpha, IFN gamma, IL-1 beta and IL-17, we used the commercially available enzyme- linked immunosorbent assay kit. MVD was assessed on CD34-stained specimens. The MVD and budding were assessed using a light microscope Results: We found significantly higher concentrations of periostin, VEGF-A, IFN-gamma, IL-1 beta, IL-17 and TNF alpha in the tumor samples compared with surgical tissue margins. The tumor concentrations of periostin were correlated with tumor levels of VEGF-A, IFN-gamma, IL-1 beta and TNF alpha. We observed significant correlation between margin periostin and VEGF-A, IFN-gamma, IL-17 and TNF alpha in tumor and margin specimens. Additionally, we found a significantly negative correlation between periostin tumor concentration and microvessel density at the invasive front. Tumor periostin levels were also correlated positively with tumor budding. Conclusions: Periostin activity may be associated with pro-inflammatory cytokine levels: TNF alpha, IFN-gamma, IL-1 beta and IL-17. Our results also suggest the role of periostin in angiogenesis in CRC and its upregulation in poorly vascularized tumors. Further research on the regulations between periostin and cytokines are necessary to understand the interactions between tumor and immune tumor microenvironment, which could be helpful in the development of new targeted therapy.
C1 [Kula, Agnieszka; Dawidowicz, Miriam; Waniczek, Dariusz] Univ Silesia, Fac Med Sci Zabrze, Dept Surg Oncol, 35 Ceglana, PL-40514 Katowice, Poland.
   [Mielcarska, Sylwia; Swietochowska, Elzbieta] Med Univ Silesia, Fac Med Sci Zabrze, Dept Med & Mol Biol, 19 Jordana, PL-41800 Zabrze, Poland.
   [Kiczmer, Pawel; Chrabanska, Magdalena; Rynkiewicz, Magdalena] Med Univ Silesia, Fac Med Sci Zabrze, Dept & Chair Pathomorphol, 13-15 3 Maja, PL-41800 Zabrze, Poland.
C3 University of Silesia in Katowice; Medical University Silesia; Medical
   University Silesia
RP Kula, A (corresponding author), Univ Silesia, Fac Med Sci Zabrze, Dept Surg Oncol, 35 Ceglana, PL-40514 Katowice, Poland.
EM agnieszkakula20@gmail.com; miriamdawidowicz@o2.pl;
   sylwiamielcarska@gmail.com; Pawel.kiczmer@protonmail.com;
   hannaonyszczuk@sum.edu.pl; mrynkiewicz@sum.edu.pl; elaswieta@interia.pl;
   dariusz.waniczek@gmail.com
RI Waniczek, Dariusz/ABD-1692-2020; Kiczmer, Paweł/ABB-8445-2021
OI Dawidowicz, Miriam/0000-0002-6629-7711; Onyszczuk,
   Magdalena/0000-0001-7704-1124; Kiczmer, Pawel/0000-0001-9060-0154; Kula,
   Agnieszka/0000-0002-6659-8653; Swietochowska,
   Elzbieta/0000-0001-5787-7880; Waniczek, Dariusz/0000-0002-0410-8604;
   Mielcarska, Sylwia/0000-0003-4228-9343
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NR 59
TC 6
Z9 7
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 JAN
PY 2022
VL 58
IS 1
AR 96
DI 10.3390/medicina58010096
PG 15
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA ZB7RL
UT WOS:000757034800001
PM 35056404
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ni, WF
   Li, ZY
   Liu, ZQ
   Ji, YT
   Wu, LJ
   Sun, SZ
   Jian, XQ
   Gao, XJ
AF Ni, Wenfeng
   Li, Zhengye
   Liu, Zengquan
   Ji, Yuting
   Wu, Lijia
   Sun, Sizhe
   Jian, Xiqi
   Gao, Xiujun
TI Dual-Targeting Nanoparticles: Codelivery of Curcumin and 5-Fluorouracil
   for Synergistic Treatment of Hepatocarcinoma
SO JOURNAL OF PHARMACEUTICAL SCIENCES
LA English
DT Article
DE nanoparticles; targeted drug delivery; cancer chemotherapy; polyglycolic
   acid; polyethylene glycol
ID GASTRIC-CANCER CELLS; CO-DELIVERY; POLYMERIC NANOPARTICLES;
   COLON-CANCER; HEPATOCELLULAR-CARCINOMA; CHITOSAN NANOPARTICLES; PLGA
   NANOPARTICLES; IN-VITRO; DOXORUBICIN; PACLITAXEL
AB Chemotherapy has been the standard for cancer therapy, but the nonspecific cytotoxicity of chemotherapeutic agents and drug resistance of tumor cells has limited its efficacy. However, multidrug combination therapy and targeting therapy have resulted in enhanced anticancer effects and have become increasingly important strategies in clinical applications. In this study, a biotin-/lactobionic acid-modified poly(ethylene glycol)-poly(lactic-co-glycolic acid)-poly(ethylene glycol) (BLPP) copolymer was synthesized, and curcumin-and 5-fluorouracil-loaded nanoparticles (BLPPNPs/C + F) were prepared to enhance the treatment of hepatocellular carcinoma. Blank BLPPNPs were shown to have great biocompatibility via both in vitro and in vivo studies. Good targeting of tumor cells of BLPPNPs was confirmed by flow cytometry, fluorescence microscopy, and biodistribution. The synergistic anticancer effects of BLPPNPs/C + F were demonstrated by cytotoxicity and animal studies, while western blotting was used to further verify the synergistic effect of curcumin and 5-fluorouracil. The dual-targeting and drug-loaded codelivery nanosystem demonstrated higher cellular uptake and stronger cytotoxicity for tumor cells. Therefore, these dual-targeting NPs are a promising codelivery carrier that could be made available for cellular targeting of anticancer drugs to achieve better intracellular delivery and synergistic anticancer efficacy. (c) 2019 American Pharmacists Association (R). Published by Elsevier Inc. All rights reserved.
C1 [Ni, Wenfeng; Li, Zhengye; Liu, Zengquan; Ji, Yuting; Wu, Lijia; Sun, Sizhe; Jian, Xiqi; Gao, Xiujun] Tianjin Med Univ, Inst Biomed Engn, Tianjin 300070, Peoples R China.
C3 Tianjin Medical University; Chinese Academy of Medical Sciences - Peking
   Union Medical College; Institute of BioMedical Engineering - CAMS
RP Gao, XJ (corresponding author), Tianjin Med Univ, Inst Biomed Engn, Tianjin 300070, Peoples R China.
EM gaoxiujun201007@163.com
RI Gao, Xiujun/ISV-1206-2023; Zhao, Yong/Z-3231-2019
FU Natural Science Foundation of China [81272495]; Natural Science
   Foundation of Tianjin [16JC2DJC32200]
FX This study was supported by the Natural Science Foundation of China
   (grant no. 81272495) and a grant from the Natural Science Foundation of
   Tianjin (grant no. 16JC2DJC32200).
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NR 54
TC 52
Z9 52
U1 0
U2 60
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0022-3549
EI 1520-6017
J9 J PHARM SCI-US
JI J. Pharm. Sci.
PD MAR
PY 2019
VL 108
IS 3
BP 1284
EP 1295
DI 10.1016/j.xphs.2018.10.042
PG 12
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Chemistry
GA HN2IW
UT WOS:000460009900025
PM 30395829
DA 2025-01-04
ER

PT J
AU Gakinya, S
   Njau, A
   Abdallah, A
   Nzioka, A
   Ogutu, J
AF Gakinya, Samuel
   Njau, Allan
   Abdallah, Abdulkarim
   Nzioka, Ancent
   Ogutu, James
TI Frequency of <i>KRAS</i> and <i>BRAF</i> mutations in colorectal
   carcinoma and their association with clinical-pathological
   characteristics in a tertiary hospital in Kenya
SO FRONTIERS IN MEDICINE
LA English
DT Article
DE KRAS; BRAF V600E; colorectal carcinoma; Kenya; Africa
ID OF-AMERICAN-PATHOLOGISTS; PROGNOSTIC-FACTORS; CANCER; SURVIVAL; ROLES
AB Introduction: Colorectal carcinoma is a leading cause of cancer morbidity and mortality globally. Its management includes the use of targeted therapy which require assessment for biomarkers to choose eligible patients. KRAS and BRAF mutations are biomarkers predictive of response to anti-EGFR therapy. This study aimed at determining the frequency of BRAF V600E and KRAS exon 2,3,4 mutations in colorectal carcinoma patients at the Aga Khan University Hospital Nairobi, Kenya. Methods: Study participants were patients who had colectomy for colorectal carcinoma. They were identified from the laboratory information system. The patients age, gender and tumor location were determined from the medical records. The histological diagnosis, pathological tumor and nodal stage were confirmed by examining hematoxylin and eosin-stained slides prepared from the colectomy specimen. DNA was extracted from the specimens using Qiagen QIAamp DNA FFPE Tissue Kit and PCR performed using EntroGen KRAS/BRAF mutation analysis kit following manufacturer's protocol. Results: One hundred fourteen patients were enrolled. Colorectal carcinoma was significantly more common in males than females. The mean age at diagnosis was 58 years. Majority of the tumors were in the right colon, were of pathological tumor stage T3 and had nodal involvement. Forty six percent (46%) of the cases had KRAS mutations while 5.3% had BRAF V600E mutation. KRAS mutation was associated with a high pathological tumor stage and nodal involvement. Conclusion: Colorectal carcinoma in our patients is more common in males and tend to occur at a younger age. The patients tend to have a high tumor pathological stage and nodal involvement at diagnosis. The high frequency of KRAS exon 2,3,4 mutation and low frequency of BRAF V600E mutations is similar to what has been reported in literature.
C1 [Gakinya, Samuel; Njau, Allan] Aga Khan Univ, Dept Pathol, Nairobi, Kenya.
   [Abdallah, Abdulkarim] Aga Khan Univ, Dept Surg, Nairobi, Kenya.
   [Nzioka, Ancent] Kenyatta Univ Teaching, Referral & Res Hosp, Dept Pathol, Nairobi, Kenya.
   [Ogutu, James] Kenyatta Univ, Sch Med, Dept Microbiol, Nairobi, Kenya.
C3 Aga Khan University; Aga Khan University; Kenyatta University
RP Gakinya, S (corresponding author), Aga Khan Univ, Dept Pathol, Nairobi, Kenya.; Ogutu, J (corresponding author), Kenyatta Univ, Sch Med, Dept Microbiol, Nairobi, Kenya.
EM samuel.mukono@aku.edu; ogutu.james@ku.ac.ke
FU Aga Khan University's University Research Council (URC); Aga Khan
   University Hospital, Department of Pathology
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This work was supported
   by the Aga Khan University's University Research Council (URC) and Aga
   Khan University Hospital, Department of Pathology.
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NR 26
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 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD SEP 19
PY 2024
VL 11
AR 1433120
DI 10.3389/fmed.2024.1433120
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA I5S6R
UT WOS:001330860400001
PM 39364024
OA gold
DA 2025-01-04
ER

PT J
AU Reyland, ME
   Jones, DNM
AF Reyland, Mary E.
   Jones, David N. M.
TI Multifunctional roles of PKCδ: Opportunities for targeted therapy in
   human disease
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE Protein kinase C; Signal transduction; Cancer; Apoptosis; Therapeutics
ID PROTEIN-KINASE-C; PROSTATE-CANCER CELLS; ESTER-INDUCED APOPTOSIS;
   TUMOR-NECROSIS-FACTOR; HUMAN COLON-CANCER; PHASE-II TRIAL; PHORBOL
   ESTER; TYROSINE PHOSPHORYLATION; SALIVARY-GLAND; DNA-DAMAGE
AB The serine-threonine protein kinase, protein kinase C-delta (PKC delta), is emerging as a bi-functional regulator of cell death and proliferation. Studies in PKC delta-/- mice have confirmed :a pro-apoptotic role for this kinase in response to DNA damage and a tumor promoter role in some oncogenic contexts. In non-transformed cells, inhibition of PKC delta suppresses the release of cytochrome c and caspase activation, indicating a function upstream of apoptotic pathways. Data from PKG delta-/- mice demonstrate a role for PKC delta in the execution of DNA damage-induced and physiologic apoptosis. This has led to the important finding that inhibitors of PKC delta can be used therapeutically to reduce irradiation and chemotherapy-induced toxicity. By contrast, PKC delta is a tumor promoter in mouse models of mammary gland and lung cancer, and increased PKC delta expression is a negative prognostic indicator in Her2+ and other subtypes of human breast cancer. Understanding how these distinct functions of PM are regulated is critical for the design of therapeutics to target this pathway. This review will discuss what is currently known about biological roles of PKC delta and prospects for targeting ARCS in human disease. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Reyland, Mary E.] Univ Colorado, Dept Craniofacial Biol, Sch Dent Med, Anschutz Med Campus, Aurora, CO 80045 USA.
   [Jones, David N. M.] Univ Colorado, Dept Pharmacol, Sch Med, Anschutz Med Campus, Aurora, CO 80045 USA.
C3 University of Colorado System; University of Colorado Anschutz Medical
   Campus; University of Colorado System; University of Colorado Anschutz
   Medical Campus
RP Reyland, ME (corresponding author), 12801 E 17th Ave,Mail Stop 8120, Aurora, CO 80045 USA.
EM Mary.Reyland@ucdenver.edu
FU NIDCR NIH HHS [R21 DE024309, R01 DE015648] Funding Source: Medline
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NR 225
TC 35
Z9 44
U1 0
U2 16
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD SEP
PY 2016
VL 165
BP 1
EP 13
DI 10.1016/j.pharmthera.2016.05.001
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DW7GH
UT WOS:000383818700001
PM 27179744
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Carr, RM
   Qiao, GL
   Qin, JZ
   Jayaraman, S
   Prabhakar, BS
   Maker, AV
AF Carr, Ryan M.
   Qiao, Guilin
   Qin, Jianzhong
   Jayaraman, Sundararajan
   Prabhakar, Bellur S.
   Maker, Ajay, V
TI Targeting the metabolic pathway of human colon cancer overcomes
   resistance to TRAIL-induced apoptosis
SO CELL DEATH DISCOVERY
LA English
DT Article
ID DOSE-ESCALATION; DEATH; 2-DEOXY-D-GLUCOSE; RECEPTORS; EXPRESSION; CELLS;
   RADIOTHERAPY; COMBINATION; ACTIVATION; GENE
AB Colon cancer is a leading cause of cancer-related mortality for which targeted therapy is needed; however, trials using apoptosis-inducing ligand monotherapy to overcome resistance to apoptosis have not shown clinical responses. Since colon cancer cells selectively uptake and rapidly metabolize glucose, a property utilized for clinical staging, we investigated mechanisms to alter glucose metabolism in order to selectively target the cancer cells and to overcome evasion of apoptosis. We demonstrate TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) resistance in the majority of human colon cancers tested and utilize the glucose analog 2-deoxy-D-glucose to sensitize TRAIL-resistant gastrointestinal adenocarcinoma cells, and not normal gastrointestinal epithelial cells, to TRAIL-induced apoptosis through enhanced death receptor 5 expression, downstream modulation of MAPK signaling and subsequent miRNA expression modulation by increasing the expression of miR-494 via MEK activation. Further, established human colon cancer xenografts treated with this strategy experience anti-tumor responses. These findings in colon adenocarcinoma support further investigation of manipulation of cellular energetics to selectively overcome resistance to apoptosis and to impart tumor regressions in established colon cancer tumors.
C1 [Carr, Ryan M.; Qiao, Guilin; Qin, Jianzhong; Jayaraman, Sundararajan; Maker, Ajay, V] Univ Illinois, Dept Surg, Div Surg Oncol, Chicago, IL 60612 USA.
   [Carr, Ryan M.; Prabhakar, Bellur S.; Maker, Ajay, V] Univ Illinois, Dept Microbiol & Immunol, Coll Med, 835S Wolcott Ave,MC790, Chicago, IL 60612 USA.
   [Maker, Ajay, V] Advocate Illinois Masonic Med Ctr, Creticos Canc Ctr, Chicago, IL 60657 USA.
C3 University of Illinois System; University of Illinois Chicago;
   University of Illinois Chicago Hospital; University of Illinois System;
   University of Illinois Chicago; University of Illinois Chicago Hospital
RP Maker, AV (corresponding author), Univ Illinois, Dept Surg, Div Surg Oncol, Chicago, IL 60612 USA.; Maker, AV (corresponding author), Univ Illinois, Dept Microbiol & Immunol, Coll Med, 835S Wolcott Ave,MC790, Chicago, IL 60612 USA.; Maker, AV (corresponding author), Advocate Illinois Masonic Med Ctr, Creticos Canc Ctr, Chicago, IL 60657 USA.
EM amaker@uic.edu
OI Carr, Ryan/0000-0001-5762-367X; Jayaraman,
   Sundararajan/0000-0002-7026-5958
FU University of Illinois Cancer Center Junior Cancer Investigator Grant
   from the National Center for Advancing Translational Sciences, National
   Institutes of Health [UL1TR000050]; NIH/NCI [K08CA190855]
FX We acknowledge Dr. Yves Lussier from the Center for Research
   Informatics, University of Illinois at Chicago, for his assistance in
   miRNA analysis; and Mark Maienschein-Cline, Bioinformatics Specialist in
   the Research Informatics Core, Center for Clinical and Translational
   Science, for his generation of miRNA heat maps. This work was supported
   in part by the University of Illinois Cancer Center Junior Cancer
   Investigator Grant from the National Center for Advancing Translational
   Sciences, National Institutes of Health, through Grant UL1TR000050
   (AVM). AVM is supported by the NIH/NCI K08CA190855.
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NR 33
TC 23
Z9 26
U1 0
U2 2
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2058-7716
J9 CELL DEATH DISCOV
JI Cell Death Discov.
PY 2016
VL 2
AR 16067
DI 10.1038/cddiscovery.2016.67
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA VI2GA
UT WOS:000463076300071
PM 27648301
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kuan, YD
   Lee, CH
AF Kuan, Yu-Diao
   Lee, Che-Hsin
TI <i>Salmonella</i> overcomes tumor immune tolerance by inhibition of
   tumor indoleamine 2, 3-dioxygenase 1 expression
SO ONCOTARGET
LA English
DT Article
DE salmonella; tumor-targeting; indoleamine 2; 3-dioxygenase 1; immune
   tolerance
ID TYPHIMURIUM A1-R; COLORECTAL-CANCER; TARGETED THERAPY; STEM-LIKE;
   2,3-DIOXYGENASE; AUTOPHAGY; BACTERIAL; CELLS; METASTASIS; EFFICACY
AB Over the past decades, Salmonella has been proven capable of inhibiting tumor growth. It can specifically target tumors and due to its facultative anaerobic property, can be more penetrative than other drug therapies. However, the molecular mechanism by which Salmonella inhibits tumor growth is still incompletely known. The antitumor therapeutic effect mediated by Salmonella is associated with an inflammatory immune response at the tumor site and a T cell-dependent immune response. Many tumors have been proven to have a high expression of indoleamine 2, 3-dioxygenase 1 (IDO), which is a rate-limiting enzyme that catalyzes tryptophan to kynurenine, thus causing immune tolerance within the tumor microenvironment. With decreased expression of IDO, increased immune response can be observed, which might be helpful when developing cancer immunotherapy. The expression of IDO was decreased after tumor cells were infected with Salmonella. In addition, Western blot analysis showed that the expression levels of phospho-protein kinase B (P-AKT), phospho-mammalian targets of rapamycin (P-mTOR), and phospho-p70 ribosomal s6 kinase (P-p70s6K) in tumor cells were decreased after Salmonella infection. In conclusion, our results indicate that Salmonella inhibits IDO expression and plays a crucial role in anti-tumor therapy, which might be a promising strategy combined with other cancer treatments.
C1 [Kuan, Yu-Diao; Lee, Che-Hsin] China Med Univ, Grad Inst Basic Med Sci, Sch Med, Taichung, Taiwan.
   [Lee, Che-Hsin] China Med Univ, Sch Med, Dept Microbiol, Taichung, Taiwan.
C3 China Medical University Taiwan; China Medical University Taiwan
RP Lee, CH (corresponding author), China Med Univ, Grad Inst Basic Med Sci, Sch Med, Taichung, Taiwan.; Lee, CH (corresponding author), China Med Univ, Sch Med, Dept Microbiol, Taichung, Taiwan.
EM chlee@mail.cmu.edu.tw
OI Kuan, Yu-Diao/0000-0002-6591-4706
FU Ministry of Science and Technology, Taiwan [MOST 104-2320-B-039-042-MY3]
FX This work was supported by grants from the Ministry of Science and
   Technology, Taiwan (MOST 104-2320-B-039-042-MY3).
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NR 58
TC 37
Z9 43
U1 1
U2 13
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 5
PY 2016
VL 7
IS 1
BP 374
EP 385
DI 10.18632/oncotarget.6258
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DD5GI
UT WOS:000369950300030
PM 26517244
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Xu, FF
   Sun, HM
   Fang, RP
   Zhang, L
   Shi, H
   Wang, X
   Fu, XL
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   Shi, XH
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   Ye, K
   Zhang, WY
   Ye, LH
AF Xu, Fei-fei
   Sun, Hui-min
   Fang, Run-ping
   Zhang, Lu
   Shi, Hui
   Wang, Xue
   Fu, Xue-li
   Li, Xian-meng
   Shi, Xu-he
   Wu, Yue
   Ye, Kai
   Zhang, Wei-ying
   Ye, Li-hong
TI The modulation of PD-L1 induced by the oncogenic HBXIP for breast cancer
   growth
SO ACTA PHARMACOLOGICA SINICA
LA English
DT Article
DE HBXIP; breast cancer; PD-L1; transcription activation; protein
   acetylation
ID COLORECTAL-CANCER; POSTTRANSLATIONAL MODIFICATIONS; TARGETED-THERAPY;
   IMMUNE EVASION; UP-REGULATION; ASPIRIN USE; ACETYLATION; ACTIVATION;
   EXPRESSION; INHIBITION
AB Programmed death ligand-1 (PD-L1)/PD-1 checkpoint extensively serves as a central mediator of immunosuppression. A tumor-promoting role for abundant PD-L1 in several cancers is revealed. However, the importance of PD-L1 and how the PD-L1 expression is controlled in breast cancer remains obscure. Here, the mechanisms of controlling PD-L1 at the transcription and protein acetylation levels in promoting breast cancer growth are presented. Overexpressed PD-L1 accelerates breast cancer growth in vitro and in vivo. RNA-seq uncovers that PD-L1 can induce some target genes affecting many cellular processes, especially cancer development. In clinical breast cancer tissues and cells, PD-L1 and HBXIP are both increased, and their expressions are positively correlated. Mechanistic exploration identifies that HBXIP stimulates the transcription of PD-L1 through co-activating ETS2. Specifically, HBXIP induces PD-L1 acetylation at K270 site through interacting with acetyltransferase p300, leading to the stability of PD-L1 protein. Functionally, depletion of HBXIP attenuates PD-L1-accelerated breast tumor growth. Aspirin alleviates breast cancer via targeting PD-L1 and HBXIP. Collectively, the findings display new light into the mechanisms of controlling tumor PD-L1 and broaden the utility for PD-L1 as a target in breast cancer therapy.
C1 [Xu, Fei-fei; Sun, Hui-min; Fang, Run-ping; Zhang, Lu; Shi, Hui; Wang, Xue; Fu, Xue-li; Li, Xian-meng; Shi, Xu-he; Wu, Yue; Ye, Kai; Zhang, Wei-ying; Ye, Li-hong] Nankai Univ, Tianjin Key Lab Prot Sci, State Key Lab Med Chem Biol, Dept Biochem,Coll Life Sci, Tianjin 300071, Peoples R China.
C3 Nankai University
RP Zhang, WY; Ye, LH (corresponding author), Nankai Univ, Tianjin Key Lab Prot Sci, State Key Lab Med Chem Biol, Dept Biochem,Coll Life Sci, Tianjin 300071, Peoples R China.
EM zhwybao@nankai.edu.cn; yelihong@nankai.edu.cn
RI Fang, Runping/AAF-6835-2020; SHI, HUI/KXQ-4873-2024; Yu,
   Yan/GYV-4514-2022
FU National Natural Science Foundation of China [82072943, 82072929,
   31870752]; Project of Prevention and Control of Key Chronic
   Non-Infectious Diseases [2016YFC1303401]
FX This work was supported by National Natural Science Foundation of China
   (82072943, 82072929, and 31870752), and Project of Prevention and
   Control of Key Chronic Non-Infectious Diseases (No. 2016YFC1303401).
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NR 76
TC 9
Z9 10
U1 3
U2 43
PU NATURE PUBL GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1671-4083
EI 1745-7254
J9 ACTA PHARMACOL SIN
JI Acta Pharmacol. Sin.
PD FEB
PY 2022
VL 43
IS 2
BP 429
EP 445
DI 10.1038/s41401-021-00631-6
EA APR 2021
PG 17
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA YN4TG
UT WOS:000637476300004
PM 33824459
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Pecero, ML
   Salvador-Bofill, J
   Molina-Pinelo, S
AF Luisa Pecero, Ma
   Salvador-Bofill, Javier
   Molina-Pinelo, Sonia
TI Long non-coding RNAs as monitoring tools and therapeutic targets in
   breast cancer
SO CELLULAR ONCOLOGY
LA English
DT Review
DE LncRNAs; Breast cancer; Chemotherapy; Radiotherapy; Endocrine therapy;
   Targeted therapy
ID TAMOXIFEN RESISTANCE; PROSTATE-CANCER; POOR-PROGNOSIS;
   COLORECTAL-CANCER; DOWN-REGULATION; TUMOR-GROWTH; CELLS; EXPRESSION;
   IDENTIFICATION; CHEMOTHERAPY
AB BackgroundCurrent therapeutic strategies that are used to combat breast cancer vary widely and largely depend on its clinicopathological features, including tumor subtype, size, stage, lymph node involvement, the presence of hormone receptors and/or HER2, as well as the degree of proliferative activity. Recent work has focused on improving our knowledge on the molecular mechanisms that underlie this complex disease. Most of the human genome is transcribed into RNAs that do not encode proteins. These noncoding RNAs may act as mediators in the regulation of gene expression. Based on their size and function, noncoding RNAs are classified into small noncoding RNAs (sncRNAs) and long noncoding RNAs (lncRNAs). LncRNAs have been found to play key roles in relevant biological processes, including breast cancer. As such, lncRNAs have been proposed as diagnostic and prognostic biomarkers, as predictive biomarkers and as putative therapeutic targets.ConclusionsIn this review, we discuss the potential application of lncRNAs for the monitoring and treatment of breast cancer. We conclude that lncRNAs play important roles in the pathophysiology of this disease and may serve as putative therapeutic targets. As such, tumor-specific lncRNAs may be instrumental for improving current breast cancer clinical practices.
C1 [Luisa Pecero, Ma; Salvador-Bofill, Javier; Molina-Pinelo, Sonia] Univ Seville, CSIC, HUVR, Unit Integral Oncol,Inst Biomed Sevilla IBIS, Seville, Spain.
   [Molina-Pinelo, Sonia] Ctr Invest Biomed Red Canc CIBERONC, Madrid, Spain.
   [Molina-Pinelo, Sonia] Inst Biomed Sevilla IBIS, Campus Hosp Univ Virgen del Rocio, Seville 41013, Spain.
C3 Consejo Superior de Investigaciones Cientificas (CSIC); University of
   Sevilla; CSIC-JA-USE - Instituto de Biomedicina de Sevilla (IBIS); CIBER
   - Centro de Investigacion Biomedica en Red; CIBERONC; Consejo Superior
   de Investigaciones Cientificas (CSIC); University of Sevilla;
   CSIC-JA-USE - Instituto de Biomedicina de Sevilla (IBIS)
RP Molina-Pinelo, S (corresponding author), Univ Seville, CSIC, HUVR, Unit Integral Oncol,Inst Biomed Sevilla IBIS, Seville, Spain.; Molina-Pinelo, S (corresponding author), Ctr Invest Biomed Red Canc CIBERONC, Madrid, Spain.; Molina-Pinelo, S (corresponding author), Inst Biomed Sevilla IBIS, Campus Hosp Univ Virgen del Rocio, Seville 41013, Spain.
EM smolina-ibis@us.es
RI Molina-Pinelo, Sonia/M-4643-2015
OI Molina-Pinelo, Sonia/0000-0002-5726-2453
FU Consejeria de Salud y Bienestar Social of Junta de Andalucia through the
   "Nicolas Monardes" program [C-0040-2016]
FX SMP was supported by the Consejeria de Salud y Bienestar Social of Junta
   de Andalucia through the "Nicolas Monardes" program [C-0040-2016].
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NR 98
TC 48
Z9 52
U1 0
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 2211-3428
EI 2211-3436
J9 CELL ONCOL
JI Cell. Oncol.
PD FEB
PY 2019
VL 42
IS 1
BP 1
EP 12
DI 10.1007/s13402-018-0412-6
PG 12
WC Oncology; Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology; Pathology
GA HL1WR
UT WOS:000458495300001
PM 30361825
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Kou, FR
   Li, J
   Wang, ZH
   Xu, T
   Qian, JJ
   Zhang, EL
   Zhang, LJ
   Shen, L
   Wang, XC
AF Kou, Fu-Rong
   Li, Jian
   Wang, Zheng-Hang
   Xu, Ting
   Qian, Juan-Juan
   Zhang, En-Li
   Zhang, Li-Jun
   Shen, Lin
   Wang, Xi-Cheng
TI Analysis of actionable gene fusions in a large cohort of Chinese
   patients with colorectal cancer
SO GASTROENTEROLOGY REPORT
LA English
DT Article
DE actionable gene fusions; colorectal cancer; Chinese population
ID POSITIVE SOLID TUMORS; ENTRECTINIB; GUIDELINES; PATHOLOGY; BRAF
AB Background The prevalence of gene fusion is extremely low in unselected patients with colorectal cancer (CRC). Published data on gene fusions are limited by relatively small sample sizes, with a primary focus on Western populations. This study aimed to analyse actionable gene fusions in a large consecutive Chinese CRC population. Methods This study included 5,534 consecutive CRC patients from the Genecast database. Genomic profiling was performed using a panel of 769 cancer-related genes. Data for 34 CRC patients with actionable gene fusions were also collected from cBioPortal and ChimerSeq. Results Among 5,534 CRC patients, 54 (0.98%) had actionable gene fusions, with NTRK1/2/3 being the most common fusion (0.38%), accounting for 38.9% (21/54) of those with fusions. Actionable gene fusion enrichment was higher in patients with microsatellite instability-high (MSI-H) (6.7% vs. 0.5%, P < 0.001), RAS/BRAF wildtype (2.0% vs. 0.2%, P < 0.001) and RNF43 mutation (7.7% vs. 0.4%, P < 0.001) than in patients with microsatellite stability/MSI-low, RAS/BRAF mutation and RNF43 wildtype, respectively. When these markers were combined, the fusion detection rate increased. Among patients with RAS/BRAF wildtype and MSI-H, fusions were detected in 20.3% of patients. The fusion detection rate further increased to 37.5% when RNF43 mutation was added. The fusion detection rate was also higher in colon cancer than in rectal cancer. No significant differences in clinical or molecular features were found in patients with actionable gene fusions between the Genecast, cBioPortal, and ChimerSeq databases. Conclusions Approximately 1% of the unselected Chinese CRC population carries actionable gene fusions, mostly involving NTRK. Actionable gene fusions are more prevalent in MSI-H, RAS/BRAF wildtype, or RNF43-mutated CRC, as well as in colon cancer. Mapping of these molecular markers can markedly increase the fusion detection rate, which can help clinicians select candidates for fusion testing and targeted therapy.
C1 [Kou, Fu-Rong; Li, Jian; Wang, Zheng-Hang; Xu, Ting; Shen, Lin; Wang, Xi-Cheng] Peking Univ Canc Hosp & Inst, Dept Gastrointestinal Oncol, Key Lab Carcinogenesis & Translat Res, Minist Educ, Fu Cheng Rd 52, Beijing 100142, Peoples R China.
   [Kou, Fu-Rong] Peking Univ Canc Hosp & Inst, Minist Educ, Dept Comprehens Clin Trial Ward, Key Lab Carcinogenesis & Translat Res, Beijing, Peoples R China.
   [Qian, Juan-Juan; Zhang, En-Li; Zhang, Li-Jun] Genecast Biotechnol Co Ltd, Dept Med, Wuxi, Jiangsu, Peoples R China.
RP Wang, XC (corresponding author), Peking Univ Canc Hosp & Inst, Dept Gastrointestinal Oncol, Key Lab Carcinogenesis & Translat Res, Minist Educ, Fu Cheng Rd 52, Beijing 100142, Peoples R China.
EM xicheng_wang@hotmail.com
RI wang, xicheng/IXX-0974-2023
FU  [2022-2-7083]
FX This work was financially supported by the capital health research and
   development of special (2022-2-7083).
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NR 38
TC 1
Z9 1
U1 1
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 2052-0034
J9 GASTROENTEROL REP
JI Gastroenterol. Rep.
PD OCT 9
PY 2024
VL 12
AR goae092
DI 10.1093/gastro/goae092
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA J2U1M
UT WOS:001335659200001
PM 39391592
OA gold
DA 2025-01-04
ER

PT J
AU Obaid, NM
   Bedard, K
   Huang, WY
AF Obaid, Nourah Mohammad
   Bedard, Karen
   Huang, Weei-Yuarn
TI Strategies for Overcoming Resistance in Tumours Harboring <i>BRAF</i>
   Mutations
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE BRAF; acquired resistance
ID MUTANT COLORECTAL-CANCER; PHASE-II TRIAL; B-RAF; INHIBITOR RESISTANCE;
   ACQUIRED-RESISTANCE; KINASE PATHWAY; MAPK PATHWAY; COLON-CANCER;
   BRAF(V600E) INHIBITION; CLINICAL BEHAVIOR
AB The development of resistance to previously effective treatments has been a challenge for health care providers and a fear for patients undergoing cancer therapy. This is an unfortunately frequent occurrence for patients undergoing targeted therapy for tumours harboring the activating V600E mutation of the BRAF gene. Since the initial identification of the BRAF mutation in 2002, a series of small molecular inhibitors that target the BRAFV600E have been developed, but intrinsic and acquired resistance to these drugs has presented an ongoing challenge. More recently, improvements in therapy have been achieved by combining the use of BRAF inhibitors with other drugs, such as inhibitors of the downstream effector mitogen activated protein kinase (MAPK)/extracellular-signal regulated kinase (ERK) kinase (MEK). Despite improved success in response rates and in delaying resistance using combination therapy, ultimately, the acquisition of resistance remains a concern. Recent research articles have shed light on some of the underlying mechanisms of this resistance and have proposed numerous strategies that might be employed to overcome or avoid resistance to targeted therapies. This review will explore some of the resistance mechanisms, compare what is known in melanoma cancer to colorectal cancer, and discuss strategies under development to manage the development of resistance.
C1 [Obaid, Nourah Mohammad; Bedard, Karen; Huang, Weei-Yuarn] Dalhousie Univ, Dept Pathol, Halifax, NS B3H 4R2, Canada.
   [Huang, Weei-Yuarn] Nova Scotia Hlth Author, Dept Pathol, Halifax, NS B3H 1V8, Canada.
C3 Dalhousie University
RP Huang, WY (corresponding author), Dalhousie Univ, Dept Pathol, Halifax, NS B3H 4R2, Canada.; Huang, WY (corresponding author), Nova Scotia Hlth Author, Dept Pathol, Halifax, NS B3H 1V8, Canada.
EM nourah-m-obaid@Dal.Ca; kbedard@gmail.com; huangw@nshealth.ca
OI Bedard, Karen/0000-0001-5864-5344
FU Ministry of Higher Education of Saudi Arabia
FX Funding for Nourah Mohammad Obaid was kindly provided by the Ministry of
   Higher Education of Saudi Arabia.
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NR 126
TC 26
Z9 27
U1 1
U2 17
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 2017
VL 18
IS 3
AR 585
DI 10.3390/ijms18030585
PG 15
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA EN8ME
UT WOS:000396253700116
PM 28282860
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Luo, MC
   Huang, Z
   Yang, XY
   Chen, Y
   Jiang, JW
   Zhang, L
   Zhou, L
   Qin, SY
   Jin, P
   Fu, SY
   Peng, LY
   Li, BW
   Fang, YT
   Pu, WC
   Gong, YQ
   Liu, Y
   Ren, ZX
   Liu, QL
   Wang, C
   Xiao, FQ
   He, D
   Zhang, HY
   Li, CL
   Xu, H
   Dai, LZ
   Peng, Y
   Zhou, ZG
   Huang, CH
   Chen, HN
AF Luo, Maochao
   Huang, Zhao
   Yang, Xingyue
   Chen, Yan
   Jiang, Jingwen
   Zhang, Lu
   Zhou, Li
   Qin, Siyuan
   Jin, Ping
   Fu, Shuyue
   Peng, Liyuan
   Li, Bowen
   Fang, Yongting
   Pu, Wenchen
   Gong, Yanqiu
   Liu, Yu
   Ren, Zhixiang
   Liu, Qiu-Luo
   Wang, Cun
   Xiao, Fangqiong
   He, Du
   Zhang, Hongying
   Li, Changlong
   Xu, Heng
   Dai, Lunzhi
   Peng, Yong
   Zhou, Zong-Gung
   Huang, Canhua
   Chen, Hai-Ning
TI PHLDB2 Mediates Cetuximab Resistance via Interacting With EGFR in Latent
   Metastasis of Colorectal Cancer
SO CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE EGFR; Latent Metastasis; Cetuximab Resistance; PHLDB2; Colorectal Cancer
ID GROWTH-FACTOR RECEPTOR; COLON-CANCER; INHIBITION; TUMORS
AB BACKGROUND & AIMS: Latent metastasis of colorectal cancer (CRC) frequently develops months or years after primary surgery, followed by adjuvant therapies, and may progress rapidly even with targeted therapy administered, but the underlying mecha-nism remains unclear. Here, we aim to explore the molecular basis for the aggressive behavior of latent metastasis in CRC.& nbsp;METHODS: Transcriptional profiling and pathway enrichment analysis of paired primary and metastatic tumor samples were performed. The underlying mechanisms of pleckstrin homol-ogy-like domain, family B, member 2 (PHLDB2) in CRC were investigated by RNA immunoprecipitation assay, immunohis-tochemistry, mass spectrometry analysis, and Duolink in situ proximity ligation assay (Sigma-Aldrich, Shanghai, China). The efficacy of targeting PHLDB2 in cetuximab treatment was elucidated in CRC cell lines and mouse models.& nbsp;RESULTS: Based on the transcriptional profile of paired primary and metastatic tumor samples, we identified PHLDB2 as a potential regulator in latent liver metastasis. A detailed mechanistic study showed that chemotherapeutic agent-induced oxidative stress promotes methyltransferase-like 14 (METTL14)-mediated N6-methyladenosine modification of PHLDB2 messenger RNA, facili-tating its protein expression. Up-regulated PHLDB2 stabilizes epidermal growth factor receptor (EGFR) and promotes its nuclear translocation, which in turn results in EGFR signaling activation and consequent cetuximab resistance. Moreover, Arg1163 (R1163) of PHLDB2 is crucial for interaction with EGFR, and the R1163A mutation abrogates its regulatory function in EGFR signaling.& nbsp;CONCLUSIONS: PHLDB2 plays a crucial role in cetuximab resis-tance and is proposed to be a potential target for the treatment of CRC.& nbsp;
C1 [Luo, Maochao; Huang, Zhao; Yang, Xingyue; Chen, Yan; Jiang, Jingwen; Zhang, Lu; Zhou, Li; Qin, Siyuan; Jin, Ping; Fu, Shuyue; Peng, Liyuan; Li, Bowen; Fang, Yongting; Pu, Wenchen; Gong, Yanqiu; Liu, Yu; Ren, Zhixiang; Xu, Heng; Dai, Lunzhi; Peng, Yong; Huang, Canhua] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu, Peoples R China.
   [Luo, Maochao; Huang, Zhao; Yang, Xingyue; Chen, Yan; Jiang, Jingwen; Zhang, Lu; Zhou, Li; Qin, Siyuan; Jin, Ping; Fu, Shuyue; Peng, Liyuan; Li, Bowen; Fang, Yongting; Pu, Wenchen; Gong, Yanqiu; Liu, Yu; Ren, Zhixiang; Liu, Qiu-Luo; Wang, Cun; Xu, Heng; Dai, Lunzhi; Peng, Yong; Zhou, Zong-Gung; Huang, Canhua; Chen, Hai-Ning] Sichuan Univ, West China Sch Basic Med Sci & Forens Med, Chengdu, Peoples R China.
   [Luo, Maochao; Huang, Zhao; Yang, Xingyue; Chen, Yan; Jiang, Jingwen; Zhang, Lu; Zhou, Li; Qin, Siyuan; Jin, Ping; Fu, Shuyue; Peng, Liyuan; Li, Bowen; Fang, Yongting; Pu, Wenchen; Gong, Yanqiu; Liu, Yu; Ren, Zhixiang; Xu, Heng; Dai, Lunzhi; Peng, Yong; Huang, Canhua; Chen, Hai-Ning] Sichuan Univ, West China Hosp, Dept Gastrointestinal Surg, State Key Lab Biotherapy, Chengdu, Peoples R China.
   [He, Du; Zhang, Hongying] Sichuan Univ, West China Hosp, Dept Pathol, Chengdu, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University; Sichuan
   University
RP Huang, CH (corresponding author), Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu, Peoples R China.; Huang, CH (corresponding author), Sichuan Univ, West China Sch Basic Med Sci & Forens Med, Chengdu, Peoples R China.; Chen, HN (corresponding author), Sichuan Univ, West China Hosp, Dept Gastrointestinal Surg, State Key Lab Biotherapy, Chengdu, Peoples R China.
EM hcanhua@hotmail.com
RI Jiang, Jing/AAP-5996-2021; Qin, Siyuan/AER-9460-2022; Chen,
   Hai-Ning/AAR-8059-2021; Ren, Zhixiang/LJM-3888-2024; jiang,
   lei/IWE-1124-2023; Li, Bowen/LPP-4928-2024; Pu, Wenchen/E-9537-2018;
   Huang, Zhao/ABE-8698-2022; Xu, Heng/AAS-3465-2021
OI Li, Bowen/0000-0001-8475-4800; Chen, Hai-Ning/0000-0003-0104-8498; Dai,
   Lunzhi/0000-0002-3003-8910; Jiang, Jingwen/0009-0006-9768-0314
FU National Key Research and Development Project of China [2020YFA0509400,
   2020YFC2002705]; national natural science foundation of china [81702378,
   82073246, 81821002, 81790251, 82130082, 82003098]; Guangdong Basic and
   Applied Basic Research Foundation [2019B030302012]; Sichuan Science and
   Technology Program [22CXRC0248, 2020YJ0105, 2020YJ0094]; 1.3.5 project
   for disciplines of excellence, West China Hospital, Sichuan University
   [2016105, ZYGD20006, ZYYC20003]
FX Funding This work was supported by grants from the National Key Research
   and Development Project of China (2020YFA0509400 and 2020YFC2002705) ,
   the national natural science foundation of china (81702378, 82073246,
   81821002, 81790251, 82130082, and 82003098) , Guangdong Basic and
   Applied Basic Research Foundation (2019B030302012) , Sichuan Science and
   Technology Program (22CXRC0248, 2020YJ0105, and 2020YJ0094) , and the
   1.3.5 project for disciplines of excellence, West China Hospital,
   Sichuan University (2016105, ZYGD20006, and ZYYC20003) .
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NR 43
TC 19
Z9 20
U1 3
U2 21
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 2352-345X
J9 CELL MOL GASTROENTER
JI Cell. Mol. Gastroenterol. Hepatol.
PY 2022
VL 13
IS 4
BP 1223
EP 1242
DI 10.1016/j.jcmgh.2021.12.011
EA FEB 2022
PG 20
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 0M0KY
UT WOS:000781854400005
PM 34952201
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Jerin, S
   Harvey, AJ
   Lewis, A
AF Jerin, Samanta
   Harvey, Amanda J.
   Lewis, Annabelle
TI Therapeutic Potential of Protein Tyrosine Kinase 6 in Colorectal Cancer
SO CANCERS
LA English
DT Review
DE PTK6; colorectal cancer; tyrosine kinase inhibitors
ID CELL-MIGRATION; DISTINCT FAMILY; PLASMA-MEMBRANE; GENE-EXPRESSION;
   LUNG-CANCER; SH3 DOMAIN; BRK; PTK6; GROWTH; STAT3
AB Simple Summary Protein tyrosine kinase 6 (PTK6) is a biomarker of poor prognosis in breast cancer, but its importance in other cancer types is unclear. In this review, we explore a potential role for PTK6 in colorectal cancer. PTK6 phosphorylates multiple substrates, including signal transduction proteins, RNA binding proteins, and transcription factors, many of which are involved in key colorectal cancer pathways. PTK6 is overexpressed in colorectal tumors vs. normal tissue and activates WNT signaling when localized to the membrane in colorectal cancer cells. It is also upregulated and promotes cell survival under DNA-damaging conditions. We propose that targeting PTK6 therapeutically in colorectal cancer could increase cancer cell sensitivity to standard chemotherapy treatment. PTK6, a non-receptor tyrosine kinase, modulates the pathogenesis of breast and prostate cancers and is recognized as a biomarker of breast cancer prognosis. There are over 30 known substrates of PTK6, including signal transducers, transcription factors, and RNA-binding proteins. Many of these substrates are known drivers of other cancer types, such as colorectal cancer. Colon and rectal tumors also express higher levels of PTK6 than the normal intestine suggesting a potential role in tumorigenesis. However, the importance of PTK6 in colorectal cancer remains unclear. PTK6 inhibitors such as XMU-MP-2 and Tilfrinib have demonstrated potency and selectivity in breast cancer cells when used in combination with chemotherapy, indicating the potential for PTK6 targeted therapy in cancer. However, most of these inhibitors are yet to be tested in other cancer types. Here, we discuss the current understanding of the function of PTK6 in normal intestinal cells compared with colorectal cancer cells. We review existing PTK6 targeting therapeutics and explore the possibility of PTK6 inhibitory therapy for colorectal cancer.
C1 [Jerin, Samanta; Lewis, Annabelle] Brunel Univ London, Coll Hlth & Life Sci, Ctr Genome Engn & Maintenance, Dept Life Sci,Div Biosci, Uxbridge UB8 3PH, England.
   [Harvey, Amanda J.] Brunel Univ London, Inst Hlth Med & Environm, Ctr Genome Engn & Maintenance, Uxbridge UB8 3PH, England.
C3 Brunel University; Brunel University
RP Lewis, A (corresponding author), Brunel Univ London, Coll Hlth & Life Sci, Ctr Genome Engn & Maintenance, Dept Life Sci,Div Biosci, Uxbridge UB8 3PH, England.
EM 2138092@brunel.ac.uk; amanda.harvey@brunel.ac.uk;
   annabelle.lewis@brunel.ac.uk
OI Lewis, Annabelle/0000-0003-1876-1927
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NR 118
TC 5
Z9 5
U1 1
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUL
PY 2023
VL 15
IS 14
AR 3703
DI 10.3390/cancers15143703
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA N1XH1
UT WOS:001035019100001
PM 37509364
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Pezeshkian, Z
   Nobili, S
   Peyravian, N
   Shojaee, B
   Nazari, H
   Soleimani, H
   Asadzadeh-Aghdaei, H
   Bonab, MA
   Nazemalhosseini-Mojarad, E
   Mini, E
AF Pezeshkian, Zahra
   Nobili, Stefania
   Peyravian, Noshad
   Shojaee, Bahador
   Nazari, Haniye
   Soleimani, Hiva
   Asadzadeh-Aghdaei, Hamid
   Ashrafian Bonab, Maziar
   Nazemalhosseini-Mojarad, Ehsan
   Mini, Enrico
TI Insights into the Role of Matrix Metalloproteinases in Precancerous
   Conditions and in Colorectal Cancer
SO CANCERS
LA English
DT Review
DE Matrix Metalloproteinases (MMPs); polyp; colorectal cancer; TIMPs; MMP
   polymorphisms; MMP targeting
ID MACROPHAGE METALLOELASTASE GENE; TUMOR-GROWTH; TISSUE INHIBITOR;
   PROGNOSTIC-SIGNIFICANCE; PLASMA MMP-2; EXPRESSION; POLYMORPHISMS;
   CARCINOMA; METASTASIS; TIMP-2
AB Simple Summary Colorectal cancer (CRC) is one of the most common cancer worldwide. CRC is derived from polyps and many factors, such as Matrix Metalloproteinases (MMPs) can gain the progression of colorectal carcinogenesis. Many investigations have indicated the role of MMPs in CRC development while there is not enough knowledge about the function of MMPs in precancerous conditions. This review summarizes the current information about the role of MMPs in polyps and CRC progression. Colorectal cancer (CRC) is the third and second cancer for incidence and mortality worldwide, respectively, and is becoming prevalent in developing countries. Most CRCs derive from polyps, especially adenomatous polyps, which can gradually transform into CRC. The family of Matrix Metalloproteinases (MMPs) plays a critical role in the initiation and progression of CRC. Prominent MMPs, including MMP-1, MMP-2, MMP-7, MMP-8, MMP-9, MMP-12, MMP-13, MMP-14, and MMP-21, have been detected in CRC patients, and the expression of most of them correlates with a poor prognosis. Moreover, many studies have explored the inhibition of MMPs and targeted therapy for CRC, but there is not enough information about the role of MMPs in polyp malignancy. In this review, we discuss the role of MMPs in colorectal cancer and its pathogenesis
C1 [Pezeshkian, Zahra; Peyravian, Noshad; Shojaee, Bahador; Asadzadeh-Aghdaei, Hamid] Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Basic & Mol Epidemiol Gastrointestinal Disorders, Tehran 19835178, Iran.
   [Nobili, Stefania] G DAnnunzio Univ Chieti Pescara, Dept Neurosci Imaging & Clin Sci, I-66100 Chieti, Italy.
   [Nobili, Stefania] Univ G dAnnunzio, Ctr Adv Studies & Technol CAST, I-66100 Chieti, Italy.
   [Nazari, Haniye] Islamic Azad Univ, Tehran Med Sci, Fac Adv Sci & Technol, Dept Microbiol, Tehran 193951495, Iran.
   [Soleimani, Hiva] Islamic Azad Univ Shahr E Qods, Fac Fundamental Sci, Dept Gen Biol, Tehran 37515374, Iran.
   [Ashrafian Bonab, Maziar] Univ Sunderland, Sch Med, City Campus,Chester Rd, Sunderland SR1 3SD, England.
   [Nazemalhosseini-Mojarad, Ehsan] Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Gastroenterol & Liver Dis Res Ctr, Tehran 19835178, Iran.
   [Mini, Enrico] Univ Florence, Dept Hlth Sci, I-50139 Florence, Italy.
   [Mini, Enrico] Univ Florence, DENOTHE Excellence Ctr, I-50139 Florence, Italy.
C3 Shahid Beheshti University Medical Sciences; G d'Annunzio University of
   Chieti-Pescara; G d'Annunzio University of Chieti-Pescara; Islamic Azad
   University; University of Sunderland; Shahid Beheshti University Medical
   Sciences; University of Florence; University of Florence
RP Nazemalhosseini-Mojarad, E (corresponding author), Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Gastroenterol & Liver Dis Res Ctr, Tehran 19835178, Iran.; Mini, E (corresponding author), Univ Florence, Dept Hlth Sci, I-50139 Florence, Italy.; Mini, E (corresponding author), Univ Florence, DENOTHE Excellence Ctr, I-50139 Florence, Italy.
EM zahrapezeshkian@yahoo.com; stefania.nobili@unich.it;
   peyravian.n@iums.ac.ir; bahadorshojaee@ufl.edu; hani7311926@gmail.com;
   M_hivi@yahoo.com; hamid.asadzadeh@sbmu.ac.ir;
   maziar.bonab@sunderland.ac.uk; E.nazemalhosseini@sbmu.ac.ir;
   enrico.mini@unifi.it
RI Bonab, Maziar/AAG-1686-2019; Asadzadeh-Aghdaei, Hamid/AAD-4494-2022;
   Nazemalhosseini-Moja, ehsan/HGF-3165-2022; Pezeshkian,
   Zahra/GPC-5089-2022
OI nazemalhosseini-mojarad, ehsan/0000-0001-8914-004X; Pezeshkian,
   Zahra/0000-0002-8945-9971; Ashrafian Bonab, Maziar/0000-0002-9833-7976
FU Fondo Beneficenza Intesa Sanpaolo S.p.A. (Milan, Italy); Associazione
   Giacomo Onlus (Castiglioncello, Italy)
FX This research was supported by Fondo Beneficenza Intesa Sanpaolo S.p.A.
   (Milan, Italy) and Associazione Giacomo Onlus (Castiglioncello, Italy)
   to E.M.
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NR 149
TC 32
Z9 35
U1 0
U2 16
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD DEC
PY 2021
VL 13
IS 24
AR 6226
DI 10.3390/cancers13246226
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XX1LV
UT WOS:000736067400001
PM 34944846
OA gold, Green Published, Green Accepted
DA 2025-01-04
ER

PT J
AU Yang, C
   Xie, N
   Luo, ZF
   Ruan, XL
   Zhang, YX
   Wang, WJ
   Huang, YS
AF Yang, Cheng
   Xie, Na
   Luo, Zhifei
   Ruan, Xiling
   Zhang, Yixin
   Wang, Weijiang
   Huang, Yousheng
TI The Effect of High CDC6 Levels on Predicting Poor Prognosis in
   Colorectal Cancer
SO CHEMOTHERAPY
LA English
DT Article
DE Cell division cycle 6; Colorectal cancer; Cell cycle; Lentivirus;
   Prognosis
ID DNA-REPLICATION; EXPRESSION; PROLIFERATION; INITIATION
AB Introduction: We investigated the function of cell division cycle 6 (CDC6) on the prognosis in colorectal carcinoma (CRC). Methods: CDC6 protein expression levels in 121 patients with colorectal cancer and adjacent normal mucosa were detected by immunohistochemistry. Results: Compared to adjacent normal tissues, CDC6 mRNA level was overexpressed in CRC tissues. Moreover, CDC6 protein levels were expressed up to 93.39% (113/121) in CRC tissues in the cell nucleus or cytoplasm. However, there were only 5.79% (7/121) in normal mucosal tissues with nuclear expression. CDC6 expression was significantly correlated with TNM stage and tumor metastasis. The 5-year survival rate was lower in the high CDC6 expression group than the low group. After silencing of CDC6 expression in SW620 cells, cell proliferation was slowed, the tumor clones were decreased, and the cell cycle was arrested in G1 phase. In multivariate analysis, increased CDC6 protein expression levels in colon cancer tissues were associated with cancer metastasis, TNM stage, and patient survival time. Conclusion: CDC6 is highly expressed in CRC, and downregulation of CDC6 can slow the growth of CRC cells in vitro. It is also an independent predictor for poor prognosis and may be a useful biomarker for targeted therapy and prognostic evaluation.
C1 [Yang, Cheng; Xie, Na; Luo, Zhifei; Wang, Weijiang; Huang, Yousheng] Hainan Med Univ, Dept Pathol, Haikou, Hainan, Peoples R China.
   [Yang, Cheng; Xie, Na; Luo, Zhifei; Ruan, Xiling; Zhang, Yixin; Huang, Yousheng] Hainan Med Univ, Dept Pathol, Affiliated Hosp 1, Haikou, Hainan, Peoples R China.
C3 Hainan Medical University; Hainan Medical University
RP Huang, YS (corresponding author), Hainan Med Univ, Dept Pathol, Haikou, Hainan, Peoples R China.; Huang, YS (corresponding author), Hainan Med Univ, Dept Pathol, Affiliated Hosp 1, Haikou, Hainan, Peoples R China.
EM huangyousheng@hainmc.edu.cn
RI Huang, Yousheng/JKH-8317-2023
FU Education Department of Hainan Province [Hnky2019-50]; Natural Science
   Foundation of Hainan Province [818MS142]
FX This project was supported by the Education Department of Hainan
   Province (Hnky2019-50) and the Natural Science Foundation of Hainan
   Province (818MS142).
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NR 18
TC 8
Z9 8
U1 0
U2 8
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0009-3157
EI 1421-9794
J9 CHEMOTHERAPY
JI Chemotherapy
PD FEB
PY 2022
VL 67
IS 1
BP 47
EP 56
DI 10.1159/000519913
EA JAN 2022
PG 10
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA 8P3DT
UT WOS:000745868300001
PM 35034031
DA 2025-01-04
ER

PT J
AU Corsini, LR
   Fanale, D
   Passiglia, F
   Incorvaia, L
   Gennusa, V
   Bazan, V
   Russo, A
AF Corsini, Lidia Rita
   Fanale, Daniele
   Passiglia, Francesco
   Incorvaia, Lorena
   Gennusa, Vincenzo
   Bazan, Viviana
   Russo, Antonio
TI Monoclonal antibodies for the treatment of non-hematological tumors: a
   safety review
SO EXPERT OPINION ON DRUG SAFETY
LA English
DT Review
DE Adverse events; CTLA-4; EGFR; HER-2; immunotherapy; moAbs; PD-1; PD-L1;
   target therapy; VEGF
ID METASTATIC BREAST-CANCER; CETUXIMAB PLUS IRINOTECAN; ENDOTHELIAL
   GROWTH-FACTOR; RANDOMIZED PHASE-III; WILD-TYPE KRAS; COLORECTAL-CANCER;
   DOUBLE-BLIND; OPEN-LABEL; TRASTUZUMAB EMTANSINE; 1ST-LINE TREATMENT
AB Introduction: The introduction of monoclonal antibodies (moAbs) into clinical practice revolutionized the treatment strategies in several solid tumors. These agents differ from cytotoxic chemotherapy for their mechanism of action and toxicity. By targeting specific antigens present on healthy cells and modulating immune system activity, these biological drugs are able to generate a wide spectrum of peculiar adverse events that can negatively impact on patients' quality of life. Areas covered: In this review, the main side effects associated with the use of moAbs have been described to show their incidence and current management strategies, which may drive clinicians in their daily practice. Expert opinion: The majority of these drugs represents an example of successful innovation, since they are able to induce a significant improvement of patients' survival and quality of life without any increase in related side effects as compared to standard cancer treatments. For this reason, they have become new milestones in personalized therapy for different non-hematological malignancies. With the increasing use of moAbs in treatment regimens, it is strongly recommended that clinicians are knowledgeable about the side effects associated with these agents, their management and monitoring, to optimize the clinical treatment of cancer patients.
C1 [Corsini, Lidia Rita; Fanale, Daniele; Passiglia, Francesco; Incorvaia, Lorena; Gennusa, Vincenzo; Bazan, Viviana; Russo, Antonio] Univ Palermo, Sect Med Oncol, Dept Surg Oncol & Oral Sci, Via Vespro 129, I-90127 Palermo, Italy.
C3 University of Palermo
RP Russo, A (corresponding author), Univ Palermo, Sect Med Oncol, Dept Surg Oncol & Oral Sci, Via Vespro 129, I-90127 Palermo, Italy.
EM antonio.russo@usa.net
RI Passiglia, Francesco/AAC-7794-2022; Fanale, Daniele/K-8630-2016
OI Passiglia, Francesco/0000-0002-0244-5738
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NR 159
TC 7
Z9 7
U1 0
U2 5
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1474-0338
EI 1744-764X
J9 EXPERT OPIN DRUG SAF
JI Expert Opin. Drug Saf.
PD DEC 2
PY 2018
VL 17
IS 12
BP 1197
EP 1209
DI 10.1080/14740338.2018.1550068
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA HF5RT
UT WOS:000454291800007
PM 30457416
DA 2025-01-04
ER

PT J
AU Liu, YC
   Liu, Z
   Peng, R
   Xiao, RT
   Wang, JJ
   Wang, H
   Ma, LL
AF Liu, Yunchong
   Liu, Zhuo
   Peng, Ran
   Xiao, Ruotao
   Wang, Junjie
   Wang, Hao
   Ma, Lulin
TI Preoperative stereotactic body radiotherapy combined with surgical
   treatment for renal cell carcinoma and inferior vena cava tumour
   thrombus: study protocol for a single-arm cohort trial
SO BMJ OPEN
LA English
DT Article
DE radiotherapy; urological tumours; kidney tumours
ID RADIOSURGERY ONCOLOGY CONSORTIUM; RADIATION-THERAPY; RECTAL-CANCER;
   EXPERIENCE; MANAGEMENT; KIDNEY; COMPLICATIONS; IRRADIATION; IMPACT
AB Introduction Although surgery is currently the first choice for patients with renal cell carcinoma and vena cava tumour thrombus, the surgery is difficult, with many complications, and the prognosis of patients is not ideal. Renal cell carcinoma is not sensitive to traditional radiotherapy, but the development of stereotactic ablative body radiotherapy (SABR) technology with the characteristics of high precision, dose and conformity has made the radiotherapy of renal cell carcinoma reexamined. Methods and analysis Study design This trial is a single-arm cohort study sponsored by Peking University Third Hospital. Study treatment Preoperative stereotactic ablative radiotherapy combined with surgical treatment. Primary endpoints (1) Adverse reactions after 4-6 weeks of SABR. (2) Mayo staging of tumour thrombus. (3) The length of the tumour thrombus from the corresponding anatomical mark. (4) Invasion of the inferior vena cava wall. (5) Recurrent-free survival rate of the tumour. (6) Cancer-specific survival rate. (7) Overall survival rate. (8) Perioperative indicators including operation time, intraoperative bleeding volume and postoperative complications. Secondary endpoints (1) The longest diameter of the tumour and (2) Lymph node condition. Main inclusion criteria Patients with renal cell carcinoma and inferior vena cava tumour thrombus graded from Mayo II to IV and eligible for radical nephrectomy and inferior vena cava thrombectomy. Main exclusion criteria Patients with previous targeted therapy, chemotherapy or other interventions, or who cannot tolerate SABR or surgery. Planned sample size 20 patients. Ethics and dissemination The trial protocol and the informed consent of the subjects were submitted and approved by the Peking University Biomedical Ethics Committee.
C1 [Liu, Yunchong; Liu, Zhuo; Xiao, Ruotao; Ma, Lulin] Peking Univ Third Hosp, Dept Urol, Beijing, Peoples R China.
   [Peng, Ran; Wang, Junjie; Wang, Hao] Peking Univ Third Hosp, Dept Radiat Oncol, Beijing, Peoples R China.
C3 Peking University
RP Ma, LL (corresponding author), Peking Univ Third Hosp, Dept Urol, Beijing, Peoples R China.; Wang, H (corresponding author), Peking Univ Third Hosp, Dept Radiat Oncol, Beijing, Peoples R China.
EM hhbysy@126.com; malulinpkw@163.com
RI peng, budian/HNB-6730-2023
OI Liu, Yunchong/0000-0002-8851-457X
FU Peking University; 'Double First-Class' Advantage Discipline
   Construction Project of Peking University [BMU2017YS001-2]
FX This work was supported by Peking University. The costs incurred in the
   research process are derived from the following funding: Project No.
   BMU2017YS001-2, which is detailed as the 'Double First-Class' Advantage
   Discipline Construction Project of Peking University.
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NR 38
TC 3
Z9 3
U1 0
U2 7
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 2044-6055
J9 BMJ OPEN
JI BMJ Open
PD JAN
PY 2022
VL 12
IS 1
AR e055364
DI 10.1136/bmjopen-2021-055364
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA YQ0HX
UT WOS:000749001500009
PM 35105644
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Badawy, AAG
   El-Hindawi, A
   Hammam, O
   Moussa, M
   Gabal, S
   Said, N
AF Badawy, Afkar Abdel-Ghany
   El-Hindawi, Ali
   Hammam, Olfat
   Moussa, Mona
   Gabal, Samia
   Said, Noha
TI Impact of epidermal growth factor receptor and transforming growth
   factor-α on hepatitis C virus-induced hepatocarcinogenesis
SO APMIS
LA English
DT Review
DE Epidermal growth factor receptor; transforming growth factor-alpha;
   chronic hepatitis C; immunohistochemistry; fluorescence insitu
   hybridization
ID CHRONIC LIVER-DISEASE; GENE COPY NUMBER; HEPATOCELLULAR-CARCINOMA;
   RISK-FACTORS; COLORECTAL-CANCER; HEPATOCYTE GROWTH; VIRAL-HEPATITIS;
   MESSENGER-RNA; EXPRESSION; EGFR
AB Epidermal growth factor receptor system plays a central hepato-protective and pro-regenerative role in liver. Transforming growth factor- (TGF-) is an important autocrine growth regulator of hepatocytes that plays a role in development of hepatocellular carcinoma (HCC) among patients with chronic hepatitis C (CHC). This study was done on 40 core liver biopsies from patients with CHC, 20 liver specimens from HCC cases on top of CHC as well as five normal controls. All were immunohistochemically stained with epidermal growth factor receptor (EGFR) and TGF- antibodies. Some selected HCC cases were submitted for FISH technique to detect EGFR gene alteration. By immunohistochemistry EGFR and TGF- were overexpressed in HCC and cirrhotic cases compared to CHC cases without cirrhosis. Also, their expression was stronger in CHC cases with higher grades of activity and stages of fibrosis compared to lower ones. FISH positive results for EGFR were detected in 33.3% of the examined HCC cases. EGFR and TGF- can be used as predictive markers for activity, fibrosis, and carcinogenesis in CHC patients. Overexpression of EGFR in HCC patients can be promising in selecting those who can get benefit from anti-EGFR target therapy.
C1 [Badawy, Afkar Abdel-Ghany; Hammam, Olfat; Moussa, Mona; Said, Noha] Theodor Bilharz Res Inst, Dept Pathol, Imbaba, Egypt.
   [El-Hindawi, Ali; Gabal, Samia] Cairo Univ, Fac Med, Giza, Egypt.
C3 Egyptian Knowledge Bank (EKB); Theodor Bilharz Research Institute
   (TBRI); Egyptian Knowledge Bank (EKB); Cairo University
RP Said, N (corresponding author), Theodor Bilharz Res Inst, Dept Pathol, El Nile St,POB 30, Giza 12411, Egypt.
EM nohasaidhelal@yahoo.com
RI Gabal, Samia/L-8389-2019; Helal, Noha/E-8377-2019; Hammam,
   Olfat/D-4613-2015
OI Hammam, Olfat/0000-0002-4965-5804
FU TBRI internal project [90T]
FX This work was financed by TBRI internal project No. 90T. Principle
   investigator: Prof. Dr. Afkar A. Badawy.
CR [Anonymous], J GASTROENTEROL
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NR 48
TC 25
Z9 26
U1 1
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0903-4641
EI 1600-0463
J9 APMIS
JI APMIS
PD OCT
PY 2015
VL 123
IS 10
BP 823
EP 831
DI 10.1111/apm.12431
PG 9
WC Immunology; Microbiology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Microbiology; Pathology
GA CS5OM
UT WOS:000362127600001
PM 26279457
DA 2025-01-04
ER

PT J
AU Xu, JY
   Liu, MT
   Tao, T
   Zhu, X
   Fei, FQ
AF Xu, Jia-Yi
   Liu, Min-Ting
   Tao, Tao
   Zhu, Xiao
   Fei, Fang-Qin
TI The role of gut microbiota in tumorigenesis and treatment
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Gut microbiota; Cancer; Immune system; Immunotherapy; Biomarkers; Fecal
   microbiota transplantation
ID COLORECTAL-CANCER; BACTERIA; CELLS; TRANSPLANTATION; GROWTH
AB A large number of microbial communities exist in normal human intestinal tracts, which maintain a relatively stable dynamic balance under certain conditions. Gut microbiota are closely connected with human health and the occurrence of tumors. The colonization of certain intestinal bacteria on specific sites, gut microbiota disturbance and intestinal immune disorders can induce the occurrence of tumors. Meanwhile, gut microbiota can also play a role in tumor therapy by participating in immune regulation, influencing the efficacy of antitumor drugs, targeted therapy of engineered probiotics and fecal microbiota transplantation. This article reviews the role of gut microbiota in the occurrence, development, diagnosis and treatment of tumors. A better understanding of how gut microbiota affect tumors will help us find more therapies to treat the disease.
C1 [Xu, Jia-Yi; Liu, Min-Ting; Zhu, Xiao] Guangdong Med Univ, Marine Biomed Res Inst, Guangdong Key Lab Res & Dev Nat Drugs, Zhanjiang, Peoples R China.
   [Tao, Tao] Zibo Cent Hosp, Dept Gastroenterol, Zibo, Peoples R China.
   [Fei, Fang-Qin] Huzhou Univ, Affiliated Hosp 1, Dept Endocrinol, Huzhou, Peoples R China.
C3 Guangdong Medical University; Huzhou University
RP Zhu, X (corresponding author), Guangdong Med Univ, Marine Biomed Res Inst, Guangdong Key Lab Res & Dev Nat Drugs, Zhanjiang, Peoples R China.; Fei, FQ (corresponding author), Huzhou Univ, Affiliated Hosp 1, Dept Endocrinol, Huzhou, Peoples R China.
EM xzhu@gdmu.edu.cn; feifangqin@139.com
RI Zhu, Xiao/ABZ-7449-2022
OI Fei, Fangqin/0000-0002-0506-8958
FU National Natural Science Foundation of China [81541153]; Guangdong
   Science and Technology Department [2016B030309002, 2019B090905011]; Fund
   of Southern Marine Science and Engineering Guangdong Laboratory
   (Zhanjiang) [ZJW-2019-007]; Public Service Platform of South China Sea
   for R&D Marine Biomedicine Resources [GDMUK201808]
FX This work was supported partly by National Natural Science Foundation of
   China (81541153); Guangdong Science and Technology Department
   (2016B030309002 and 2019B090905011); The Fund of Southern Marine Science
   and Engineering Guangdong Laboratory (Zhanjiang) (ZJW-2019-007); The
   Public Service Platform of South China Sea for R&D Marine Biomedicine
   Resources (GDMUK201808).
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NR 105
TC 24
Z9 27
U1 4
U2 55
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD JUN
PY 2021
VL 138
AR 111444
DI 10.1016/j.biopha.2021.111444
EA MAR 2021
PG 8
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA RP0BZ
UT WOS:000641403600009
PM 33662679
OA gold
DA 2025-01-04
ER

PT J
AU Elamin, YY
   Rafee, S
   Toomey, S
   Hennessy, BT
AF Elamin, Yasir Y.
   Rafee, Shereen
   Toomey, Sinead
   Hennessy, Bryan T.
TI Immune Effects of Bevacizumab: Killing Two Birds with One Stone
SO CANCER MICROENVIRONMENT
LA English
DT Review
DE Bevacizumab; Immunomodulation; Antiangiogenesis; Tumour microenvironment
ID ENDOTHELIAL GROWTH-FACTOR; RENAL-CELL CARCINOMA; METASTATIC
   COLORECTAL-CANCER; ANTI-VEGF THERAPY; PHASE-III TRIAL; DENDRITIC CELLS;
   SUPPRESSOR-CELLS; T-CELLS; TARGETED THERAPY; 1ST-LINE THERAPY
AB Angiogenesis or new vessel formation is essential for tumour growth and progression. Therefore, targeting angiogenesis has been an attractive strategy in the treatment ofcancer. Bevacizumab is a recombinant humanized monoclonal IgG1 antibody thattargets vascular endothelial growth factor-A (VEGF-A) - a key molecular player inangiogenesis. Bevacizumumab has shown clinical efficacy in phase III clinical trials inseveral advanced solid malignancies. The clinical efficacy of bevacizumumab isprimarily due to its antiangiogenic effects; however, there are direct antitumor effectsand immunomodulatory effects. Enhancing the immune system to restore itsantitumour activity has been utilized successfully in clinical setting. In this article we willdiscuss the possible immunomodulatory effects of the most clinically usedantiangiogenic agent; bevacizumumab.
C1 [Elamin, Yasir Y.; Toomey, Sinead; Hennessy, Bryan T.] Beaumont Hosp, Royal Coll Surg, Dept Med Oncol, Dublin, Ireland.
   [Rafee, Shereen] St James Hosp, Dept Med Oncol, Dublin, Ireland.
C3 Royal College of Surgeons - Ireland; Trinity College Dublin
RP Elamin, YY (corresponding author), Beaumont Hosp, Royal Coll Surg, Dept Med Oncol, Dublin, Ireland.
EM elaminy@tcd.ie
OI Toomey, Sinead/0000-0002-1365-8173; Hennessy, Bryan/0000-0002-7871-6477
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NR 63
TC 48
Z9 51
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1875-2292
EI 1875-2284
J9 CANCER MICROENVIRON
JI Cancer Microenviron.
PD APR
PY 2015
VL 8
IS 1
BP 15
EP 21
DI 10.1007/s12307-014-0160-8
PG 7
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA V5D5G
UT WOS:000219509100002
PM 25326055
OA Green Published
DA 2025-01-04
ER

PT J
AU Feng, WZ
   Shi, P
   Lei, BA
   Chai, XQ
   Tan, CE
AF Feng, Wenzhe
   Shi, Peng
   Lei, Biao
   Chai, Xiaoqin
   Tan, Conge
TI IL-33 influenced the development of colorectal cancer via regulating
   Fra-1
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE Colorectal cancer; Fra-1; IL-33; invasion; migration
ID EPITHELIAL-MESENCHYMAL TRANSITION; IN-VITRO; EXPRESSION; CELLS;
   METASTASIS; VIVO
AB Colorectal cancer is a common digestive tract malignant tumor with the leading morbidity and mortality among all digestive system tumors. It is only second to gastric cancer and esophageal cancer. It was found that Fra-1 was overexpressed in colorectal cancer tissue, especially in the adjacent tissue with inflammatory cells infiltration. At present, the mechanism of Fra-1 in colorectal cancer has not been fully clarified. Interleukin-33 (IL-33) is a type of Th2 cytokine with anti-tumor activity. Exogenous IL-33 can promote tumor specific killer T cell response, thus to enhance antitumor effect. There is still lack of report about the impact of IL-33 in inducing Fra-1 expression on colorectal cancer metastasis. This study intends to investigate the role of Fra-1 in IL-33 mediated colorectal cancer. IL-33 eukaryotic expression vector was constructed and transfected to colorectal cancer cell HCT-116. After transfected for 24 h, the cells were tested by Western blot to determine Fra-1 and IL-33 expression. Wound healing assay and Transwell assay were applied to detect HCT-116 cells migration and invasion. Fra-1 protein obviously declined after IL-33 transfection compared with control (P < 0.05). Cell invasion and migration significantly reduced compared with control after transfection (P < 0.05). IL-33 plays an inhibitory role on colorectal cancer HCT-116 cell migration and invasion through suppressing Fra-1 expression. It provides theoretical basis for colorectal cancer metastasis related biomarker selection and targeted therapy.
C1 [Feng, Wenzhe; Shi, Peng; Lei, Biao; Chai, Xiaoqin; Tan, Conge] Shaanxi Univ Chinese Med, Affiliated Hosp, Dept Anorectal Surg, Xianyang 712000, Shaanxi, Peoples R China.
C3 Shaanxi University of Chinese Medicine
RP Tan, CE (corresponding author), Shaanxi Univ Chinese Med, Basic Med Coll, 2 West Weiyang Rd, Xianyang 712000, Shaanxi, Peoples R China.
EM tanzime@163.com
RI Tan, Chong Eng/AFI-7735-2022
FU Projects of National Natural Science Foundation of China [81473559]
FX Research supported by the Projects of National Natural Science
   Foundation of China (NO. 81473559).
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NR 20
TC 1
Z9 2
U1 0
U2 6
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1936-2625
J9 INT J CLIN EXP PATHO
JI Int. J. Clin. Exp. Pathol.
PY 2017
VL 10
IS 1
BP 467
EP 472
PG 6
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA EH8DO
UT WOS:000392002100052
DA 2025-01-04
ER

PT J
AU Dreikhausen, L
   Klupsch, A
   Wiest, I
   Xiao, QY
   Schulte, N
   Betge, J
   Boch, T
   Brochhausen, C
   Gaiser, T
   Hofheinz, RD
   Ebert, M
   Zhan, TZ
AF Dreikhausen, Lena
   Klupsch, Anna
   Wiest, Isabella
   Xiao, Qiyun
   Schulte, Nadine
   Betge, Johannes
   Boch, Tobias
   Brochhausen, Christoph
   Gaiser, Timo
   Hofheinz, Ralf-Dieter
   Ebert, Matthias
   Zhan, Tianzuo
TI Clinical impact of panel gene sequencing on therapy of advanced cancers
   of the digestive system: a retrospective, single center study
SO BMC CANCER
LA English
DT Article
DE Targeted therapy; Panel gene sequencing; Cancer therapy; Precision
   oncology
ID PRECISION MEDICINE; PRACTICE GUIDELINE; DIAGNOSIS; VARIANTS
AB Background Panel gene sequencing is an established diagnostic tool for precision oncology of solid tumors, but its utility for the treatment of cancers of the digestive system in clinical routine is less well documented.Methods We retrospectively identified patients with advanced or metastatic gastrointestinal, pancreaticobiliary or hepatic cancers who received panel gene sequencing at a tertiary university hospital from 2015 to 2022. For these cases, we determined the spectrum of genetic alterations, clinicopathological parameters and treatment courses. Assessment of actionability of genetic alterations was based on the OncoKB database, cancer-specific ESMO treatment guidelines, and recommendations of the local molecular tumor board.Results In total, 155 patients received panel gene sequencing using either the Oncomine Focus (62 cases), Comprehensive (91 cases) or Childhood Cancer Research Assay (2 cases). The mean age of patients was 61 years (range 24-90) and 37% were female. Most patients suffered from either colorectal cancer (53%) or cholangiocellular carcinoma (19%). 327 genetic alterations were discovered in 123 tumor samples, with an average number of 2.1 alterations per tumor. The most frequently altered genes were TP53, KRAS and PIK3CA. Actionable gene alterations were detected in 13.5-56.8% of tumors, according to ESMO guidelines or the OncoKB database, respectively. Thirteen patients were treated with targeted therapies based on identified molecular alterations, with a median progression-free survival of 8.8 months.Conclusions Actionable genetic alterations are frequently detected by panel gene sequencing in patients with advanced cancers of the digestive tract, providing clinical benefit in selected cases. However, for the majority of identified actionable alterations, sufficient clinical evidence for targeted treatments is still lacking.
C1 [Dreikhausen, Lena; Klupsch, Anna; Wiest, Isabella; Xiao, Qiyun; Schulte, Nadine; Betge, Johannes; Ebert, Matthias; Zhan, Tianzuo] Heidelberg Univ, Med Fac Mannheim, Dept Med 2, Mannheim, Germany.
   [Betge, Johannes] German Canc Res Ctr, Jr Clin Cooperat Unit Translat Gastrointestinal On, Heidelberg, Germany.
   [Betge, Johannes; Hofheinz, Ralf-Dieter; Ebert, Matthias; Zhan, Tianzuo] Heidelberg Univ, Med Fac Mannheim, Mannheim Canc Ctr, Mannheim, Germany.
   [Boch, Tobias; Hofheinz, Ralf-Dieter] Heidelberg Univ, Med Fac Mannheim, Dept Med 3, Mannheim, Germany.
   [Brochhausen, Christoph; Gaiser, Timo] Heidelberg Univ, Med Fac Mannheim, Inst Pathol, Mannheim, Germany.
   [Betge, Johannes; Boch, Tobias; Ebert, Matthias; Zhan, Tianzuo] Heidelberg Univ, DKFZ Hector Canc Inst, Med Fac Mannheim, Mannheim, Germany.
C3 Ruprecht Karls University Heidelberg; Helmholtz Association; German
   Cancer Research Center (DKFZ); Ruprecht Karls University Heidelberg;
   Ruprecht Karls University Heidelberg; Ruprecht Karls University
   Heidelberg; Ruprecht Karls University Heidelberg
RP Zhan, TZ (corresponding author), Heidelberg Univ, Med Fac Mannheim, Dept Med 2, Mannheim, Germany.; Zhan, TZ (corresponding author), Heidelberg Univ, Med Fac Mannheim, Mannheim Canc Ctr, Mannheim, Germany.; Zhan, TZ (corresponding author), Heidelberg Univ, DKFZ Hector Canc Inst, Med Fac Mannheim, Mannheim, Germany.
EM tianzuo.zhan@medma.uni-heidelberg.de
OI Betge, Johannes/0000-0001-9549-1866; Zhan, Tianzuo/0000-0002-9346-3180
FU Medizinische Fakultt Mannheim der Universitt Heidelberg (8990)
FX We thank Dr. Fabian Siegel from the Department of Medical Bioinformatics
   for assistance in identification of patients.
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NR 45
TC 0
Z9 0
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 APR 25
PY 2024
VL 24
IS 1
AR 526
DI 10.1186/s12885-024-12261-2
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OY9G8
UT WOS:001210950200004
PM 38664720
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Li, ZR
   Zhao, BB
   Qin, C
   Wang, YY
   Li, TH
   Wang, WB
AF Li, Zeru
   Zhao, Bangbo
   Qin, Cheng
   Wang, Yuanyang
   Li, Tianhao
   Wang, Weibin
TI Chromatin Dynamics in Digestive System Cancer: Commander and Regulator
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE digestive system tumor; epigenetics; chromatin dynamics; targeted
   therapy; clinical trials
ID I HYPERSENSITIVE SITES; COLORECTAL-CANCER; HISTONE ACETYLATION; DNASE-I;
   PANCREATIC-CANCER; GENE-EXPRESSION; NUCLEOSOME; BINDING; PROTEIN;
   ACCESSIBILITY
AB Digestive system tumors have a poor prognosis due to complex anatomy, insidious onset, challenges in early diagnosis, and chemoresistance. Epidemiological statistics has verified that digestive system tumors rank first in tumor-related death. Although a great number of studies are devoted to the molecular biological mechanism, early diagnostic markers, and application of new targeted drugs in digestive system tumors, the therapeutic effect is still not satisfactory. Epigenomic alterations including histone modification and chromatin remodeling are present in human cancers and are now known to cooperate with genetic changes to drive the cancer phenotype. Chromatin is the carrier of genetic information and consists of DNA, histones, non-histone proteins, and a small amount of RNA. Chromatin and nucleosomes control the stability of the eukaryotic genome and regulate DNA processes such as transcription, replication, and repair. The dynamic structure of chromatin plays a key role in this regulatory function. Structural fluctuations expose internal DNA and thus provide access to the nuclear machinery. The dynamic changes are affected by various complexes and epigenetic modifications. Variation of chromatin dynamics produces early and superior regulation of the expression of related genes and downstream pathways, thereby controlling tumor development. Intervention at the chromatin level can change the process of cancer earlier and is a feasible option for future tumor diagnosis and treatment. In this review, we introduced chromatin dynamics including chromatin remodeling, histone modifications, and chromatin accessibility, and current research on chromatin regulation in digestive system tumors was also summarized.
C1 [Li, Zeru; Zhao, Bangbo; Qin, Cheng; Wang, Yuanyang; Li, Tianhao; Wang, Weibin] Peking Union Med Coll Hosp, Chinese Acad Med Sci & Peking Union Med Coll, Dept Gen Surg, State Key Lab Complex Severe & Rare Dis, Beijing, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College; Peking Union Medical College Hospital
RP Wang, WB (corresponding author), Peking Union Med Coll Hosp, Chinese Acad Med Sci & Peking Union Med Coll, Dept Gen Surg, State Key Lab Complex Severe & Rare Dis, Beijing, Peoples R China.
RI qin, cheng/KHC-3344-2024
FU National Natural Science Foundation of China; CAMS Innovation Fund for
   Medical Science (CIFMS);  [81773215];  [82173074];  [2021-12M-1-002]
FX Funding The research was funded by the National Natural Science
   Foundation of China, grant number (Nos. 81773215 and 82173074) and CAMS
   Innovation Fund for Medical Science (CIFMS), grant number
   (2021-12M-1-002).
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NR 174
TC 2
Z9 2
U1 0
U2 10
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JUL 29
PY 2022
VL 12
AR 935877
DI 10.3389/fonc.2022.935877
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3T8QB
UT WOS:000840533200001
PM 35965507
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Schiavon, G
   Hrebien, S
   Garcia-Murillas, I
   Cutts, RJ
   Pearson, A
   Tarazona, N
   Fenwick, K
   Kozarewa, I
   Lopez-Knowles, E
   Ribas, R
   Nerurkar, A
   Osin, P
   Chandarlapaty, S
   Martin, LA
   Dowsett, M
   Smith, IE
   Turner, NC
AF Schiavon, Gaia
   Hrebien, Sarah
   Garcia-Murillas, Isaac
   Cutts, Rosalind J.
   Pearson, Alex
   Tarazona, Noelia
   Fenwick, Kerry
   Kozarewa, Iwanka
   Lopez-Knowles, Elena
   Ribas, Ricardo
   Nerurkar, Ashutosh
   Osin, Peter
   Chandarlapaty, Sarat
   Martin, Lesley-Ann
   Dowsett, Mitch
   Smith, Ian E.
   Turner, Nicholas C.
TI Analysis of <i>ESR1</i> mutation in circulating tumor DNA demonstrates
   evolution during therapy for metastatic breast cancer
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID ESTROGEN-RECEPTOR-ALPHA; COLORECTAL-CANCER; GENOMIC INSTABILITY;
   ACQUIRED-RESISTANCE; KRAS MUTATIONS; EGFR BLOCKADE; EMERGENCE
AB Acquired ESR1 mutations are a major mechanism of resistance to aromatase inhibitors (AIs). We developed ultra high-sensitivity multiplex digital polymerase chain reaction assays for ESR1 mutations in circulating tumor DNA (ctDNA) and investigated the clinical relevance and origin of ESR1 mutations in 171 women with advanced breast cancer. ESR1 mutation status in ctDNA showed high concordance with contemporaneous tumor biopsies and was accurately assessed in samples shipped at room temperature in preservative tubes. ESR1 mutations were found exclusively in estrogen receptor-positive breast cancer patients previously exposed to AI. Patients with ESR1 mutations had a substantially shorter progression-free survival on subsequent AI-based therapy [hazard ratio, 3.1; 95% confidence interval (CI), 1.9 to 23.1; P = 0.0041]. ESR1 mutation prevalence differed markedly between patients who were first exposed to AI during the adjuvant and metastatic settings [5.8% (3 of 52) versus 36.4% (16 of 44), respectively; P = 0.0002]. In an independent cohort, ESR1 mutations were identified in 0% (0 of 32; 95% CI, 0 to 10.9) tumor biopsies taken after progression on adjuvant AI. In a patient with serial sampling, ESR1 mutation was selected during metastatic AI therapy to become the dominant clone in the cancer. ESR1 mutations can be robustly identified with ctDNA analysis and predict for resistance to subsequent AI therapy. ESR1 mutations are rarely acquired during adjuvant AI but are commonly selected by therapy for metastatic disease, providing evidence that mechanisms of resistance to targeted therapy may be substantially different between the treatment of micrometastatic and overt metastatic cancer.
C1 [Schiavon, Gaia; Hrebien, Sarah; Garcia-Murillas, Isaac; Cutts, Rosalind J.; Pearson, Alex; Tarazona, Noelia; Fenwick, Kerry; Kozarewa, Iwanka; Lopez-Knowles, Elena; Ribas, Ricardo; Martin, Lesley-Ann; Dowsett, Mitch; Smith, Ian E.; Turner, Nicholas C.] Inst Canc Res, Breast Canc Now Res Ctr, London SW3 6JB, England.
   [Schiavon, Gaia; Nerurkar, Ashutosh; Osin, Peter; Dowsett, Mitch; Smith, Ian E.; Turner, Nicholas C.] Royal Marsden Hosp, Breast Unit, London SW3 6JJ, England.
   [Chandarlapaty, Sarat] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10065 USA.
C3 Royal Marsden NHS Foundation Trust; University of London; Institute of
   Cancer Research - UK; Royal Marsden NHS Foundation Trust; Memorial Sloan
   Kettering Cancer Center
RP Turner, NC (corresponding author), Inst Canc Res, Breast Canc Now Res Ctr, London SW3 6JB, England.
EM nicholas.turner@icr.ac.uk
RI Dowsett, MItch/AGC-4236-2022; Martin, Lesley-Ann/AAA-1841-2020;
   TARAZONA, NOELIA/ISU-2610-2023
OI Lopez Knowles, Elena/0000-0002-0893-3361; garcia-murillas,
   isaac/0000-0001-8183-7969; Cheang, Maggie Chon U/0000-0001-5718-2501;
   Dowsett, Mitch/0000-0003-4122-744X; Turner, Nicholas/0000-0001-8937-0873
FU National Health Service; Institute of Cancer Research, Cancer Research
   UK [C30746/A16642]; Mary-Jean Mitchell Green Foundation; Cridlan Trust;
   Susan G. Komen Foundation
FX This research was funded by National Health Service funding to the NIHR
   Biomedical Research Centre at The Royal Marsden and the Institute of
   Cancer Research, Cancer Research UK C30746/A16642, Breast Cancer Now
   with support from the Mary-Jean Mitchell Green Foundation, the Cridlan
   Trust, and the Susan G. Komen Foundation.
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NR 22
TC 371
Z9 426
U1 4
U2 48
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
EI 1946-6242
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD NOV 11
PY 2015
VL 7
IS 313
AR 313ra182
DI 10.1126/scitranslmed.aac7551
PG 8
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA CW8GL
UT WOS:000365237400007
PM 26560360
OA Green Accepted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Modest, DP
   Pant, S
   Sartore-Bianchi, A
AF Modest, D. P.
   Pant, S.
   Sartore-Bianchi, A.
TI Treatment sequencing in metastatic colorectal cancer
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Review
DE Metastatic colorectal cancer; Treatment sequencing; Molecular markers;
   Rechallenge
ID FOLFIRI PLUS BEVACIZUMAB; KRAS WILD-TYPE; RANDOMIZED PHASE-III;
   ANTI-EGFR THERAPY; CLINICAL-PRACTICE GUIDELINES; 1ST-LINE TREATMENT;
   OPEN-LABEL; 2ND-LINE TREATMENT; INFUSIONAL FLUOROURACIL; TARGETED
   THERAPY
AB Metastatic colorectal cancer (mCRC) remains incurable in most cases, but survival has improved with advances in cytotoxic chemotherapy and targeted agents. However, the optimal use and sequencing of these agents across multiple lines of treatment is unclear. Here, we review current treatment approaches and optimal treatment sequencing across the first-, second-and third-line settings in mCRC, including biological aspects affecting sequencing and rechallenge. Effective first-line therapy is a key determinant of treatment outcomes and should be selected after considering both clinical factors and biological markers, notably RAS and BRAF. The second-line regimen choice depends on the systemic therapies given in first-line. Anti-angiogenic agents (e.g. bevacizumab, ramucirumab and aflibercept) are indicated for most patients, whereas epidermal growth factor receptor (EGFR) inhibitors do not improve survival in the second-line setting. Molecular profiling is important in third-line treatment, with options in RAS wild-type patients including EGFR inhibitors (cetuximab or panitumumab), regorafenib and trifluridine/tipiracil. Immunotherapy with pembrolizumab or nivolumab +/- ipilimumab may be considered for patients with high microsatellite instability disease. Targeting HER2/neu amplification shows promise for the subset of CRC tumours displaying this abnormality. Sequencing decisions are complicated by the potential for any treatment break or de-escalation to evoke a distinct clinical progression type. Ongoing trials are investigating the optimal sequencing and timing of therapies for mCRC. Molecular profiling has established new targets, and increasing knowledge of tumour evolution under drug pressure will possibly impact on sequencing. (C) 2018 Elsevier Ltd. All rights reserved.
C1 [Modest, D. P.] Ludwig Maximilians Univ Munchen, Univ Hosp, Dept Med 3, Marchioninistr 15, D-81377 Munich, Germany.
   [Pant, S.] Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, Houston, TX 77030 USA.
   [Sartore-Bianchi, A.] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Piazza Osped Maggiore 3, I-20162 Milan, Italy.
   [Sartore-Bianchi, A.] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
C3 University of Munich; University of Texas System; UTMD Anderson Cancer
   Center; University of Milan
RP Modest, DP (corresponding author), Ludwig Maximilians Univ Munchen, Univ Hosp, Dept Med 3, Marchioninistr 15, D-81377 Munich, Germany.
EM dominik.modest@med.uni-muenchen.de
RI Sartore-Bianchi, Andrea/AAB-9848-2019; Modest, Dominik
   Paul/AAW-9756-2021
OI Sartore-Bianchi, Andrea/0000-0003-0780-0409
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NR 121
TC 230
Z9 238
U1 4
U2 69
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD MAR
PY 2019
VL 109
BP 70
EP 83
DI 10.1016/j.ejca.2018.12.019
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HM0RN
UT WOS:000459154800008
PM 30690295
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Ocansey, DKW
   Qian, F
   Cai, PP
   Ocansey, S
   Amoah, S
   Qian, YC
   Mao, F
AF Ocansey, Dickson Kofi Wiredu
   Qian, Fei
   Cai, Peipei
   Ocansey, Stephen
   Amoah, Samuel
   Qian, Yingchen
   Mao, Fei
TI Current evidence and therapeutic implication of PANoptosis in cancer
SO THERANOSTICS
LA English
DT Review
DE PANoptosis; cancer; regulated cell death; therapy; immunity
ID PROGRAMMED CELL-DEATH; INFLAMMASOME ACTIVATION; COLORECTAL-CANCER;
   APOPTOSIS; NECROPTOSIS; MECHANISMS; PYROPTOSIS; AUTOPHAGY; CASPASE-8;
   IMMUNITY
AB Regulated cell death (RCD) is considered a critical pathway in cancer therapy, contributing to eliminating cancer cells and influencing treatment outcomes. The application of RCD in cancer treatment is marked by its potential in targeted therapy and immunotherapy. As a type of RCD, PANoptosis has emerged as a unique form of programmed cell death (PCD) characterized by features of pyroptosis, apoptosis, and necroptosis but cannot be fully explained by any of these pathways alone. It is regulated by a multi-protein complex called the PANoptosome. As a relatively new concept first described in 2019, PANoptosis has been shown to play a role in many diseases, including cancer, infection, and inflammation. This study reviews the application of PCD in cancer, particularly the emergence and implication of PANoptosis in developing therapeutic strategies for cancer. Studies have shown that the characterization of PANoptosis patterns in cancer can predict survival and response to immunotherapy and chemotherapy, highlighting the potential for PANoptosis to be used as a therapeutic target in cancer treatment. It also plays a role in limiting the spread of cancer cells. PANoptosis allows for the elimination of cancer cells by multiple cell death pathways and has the potential to address various challenges in cancer treatment, including drug resistance and immune evasion. Moreover, active investigation of the mechanisms and potential therapeutic agents that can induce PANoptosis in cancer cells is likely to yield effective cancer treatments and improve patient outcomes. Research on PANoptosis is still ongoing, but it is a rapidly evolving field with the potential to lead to new treatments for various diseases, including cancer.
C1 [Ocansey, Dickson Kofi Wiredu; Mao, Fei] Jiangsu Univ, Lianyungang Clin Coll, Dept Lab Med, Lianyungang 222006, Jiangsu, Peoples R China.
   [Ocansey, Dickson Kofi Wiredu; Ocansey, Stephen] Univ Cape Coast, Directorate Univ Hlth Serv, CC0959347, Cape Coast, Central Region, Ghana.
   [Qian, Fei] Nantong Univ, Affiliated Danyang Hosp, Peoples Hosp Danyang, Zhenjiang 212300, Jiangsu, Peoples R China.
   [Ocansey, Stephen] Univ Cape Coast, Coll Hlth & Allied Sci, Sch Allied Hlth Sci, Dept Optometry & Vis Sci, CC0959347, Cape Coast, Central Region, Ghana.
   [Qian, Yingchen] Nanjing Jiangning Hosp, Dept Pathol, Nanjing 211100, Jiangsu, Peoples R China.
   [Qian, Yingchen] Nanjing Jiangning Hosp, Dept Pathol, 168 Gushan Rd,Dongshan St, Nanjing 211100, Jiangsu, Peoples R China.
C3 Jiangsu University; University of Cape Coast; Nantong University;
   University of Cape Coast
RP Mao, F (corresponding author), Jiangsu Univ, Lianyungang Clin Coll, Dept Lab Med, Lianyungang 222006, Jiangsu, Peoples R China.; Qian, YC (corresponding author), Nanjing Jiangning Hosp, Dept Pathol, 168 Gushan Rd,Dongshan St, Nanjing 211100, Jiangsu, Peoples R China.
EM qianyingchen@jnyy10.wecom.work; maofei2003@ujs.edu.cn
RI Ocansey, Dickson/AAO-5984-2020
OI Qian, Yingchen/0000-0001-5928-4456; Ocansey, Stephen/0000-0002-3992-0969
FU National Natural Science Fund of China [82250410378]; The 2022 Jiangsu
   Excellent postdoctoral program [2022ZB634]; Project of Zhenjiang key
   research and development plan (social development) [SH2023050]; Project
   of Suzhou Science and Technology [SKY2022027]
FX This study was sponsored by the National Natural Science Fund of China
   (Grant no. 82250410378) , 2022 Jiangsu Excellent postdoctoral program
   (Grant no. 2022ZB634) , Project of Zhenjiang key research and
   development plan (social development) (Grant No. SH2023050) , and
   Project of Suzhou Science and Technology (Grant no. SKY2022027) .
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NR 150
TC 15
Z9 15
U1 22
U2 44
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2024
VL 14
IS 2
BP 640
EP 661
DI 10.7150/thno.91814
PG 22
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA EW2P8
UT WOS:001141907600008
PM 38169587
OA Green Published, gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Hou, JB
   Cui, HJ
AF Hou, Jianbing
   Cui, Hongjuan
TI CSN6: a promising target for cancer prevention and therapy
SO HISTOLOGY AND HISTOPATHOLOGY
LA English
DT Review
DE CSN6; Ubiquitin; Signaling transduction; Targeted therapy
ID REGULATES C-JUN; COP9 SIGNALOSOME; UBIQUITIN LIGASE; MEDIATED
   DEGRADATION; CRYSTAL-STRUCTURE; SUBUNIT-6; EXPRESSION; CELLS;
   DENEDDYLATION; P27(KIP1)
AB CSN6 has recently received increased attention as a multifunctional protein involved in protein stability. CSN6 plays an important role in controlling cellular proliferation, apoptosis and metastasis, modulating signal transduction, as well as regulating DNA damage and repair. Most studies have demonstrated that CSN6 is significantly upregulated in human malignant tumors such as cervical cancer, papillary thyroid cancer, colorectal cancer, breast cancer, lung adenocarcinoma, and glioblastoma, and its expression is usually correlated with poor prognosis. In this review, we summarize recent available findings regarding the oncogenic role of CSN6 in tumors, and provide a better understanding of CSN6 function at the molecular level and its potential therapeutic implications in combating human cancers.
C1 [Hou, Jianbing; Cui, Hongjuan] Southwest Univ, Coll Biotechnol, State Key Lab Silkworm Genome Biol, Key Lab Sericulture Biol & Genet Breeding,Minist, Chongqing, Peoples R China.
   [Hou, Jianbing; Cui, Hongjuan] Southwest Univ, Canc Ctr, Med Res Inst, Chongqing, Peoples R China.
   [Hou, Jianbing; Cui, Hongjuan] Chongqing Engn & Technol Res Ctr Silk Biomat & Re, Chongqing, Peoples R China.
C3 Southwest University - China; Southwest University - China
RP Cui, HJ (corresponding author), Southwest Univ, Cell Biol Lab, State Key Lab Silkworm Genome Biol, Chongqing 400716, Peoples R China.
EM hcui@swu.edu.cn
FU National Key Research and Development Program of China [2016YFC1302204,
   2017YFC1308600]; Fundamental Research Funds for the Central Universities
   [swu118097]; National Natural Science Foundation of China [81872071and
   81672502]
FX This work was supported by the National Key Research and Development
   Program of China (2016YFC1302204 and 2017YFC1308600), the Fundamental
   Research Funds for the Central Universities (swu118097) and the National
   Natural Science Foundation of China (81872071and 81672502).
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NR 55
TC 5
Z9 5
U1 0
U2 5
PU F HERNANDEZ
PI MURCIA
PA PLAZA FUENSANTA 2-7 C, 30008 MURCIA, SPAIN
SN 0213-3911
EI 1699-5848
J9 HISTOL HISTOPATHOL
JI Histol. Histopath.
PD JUL
PY 2020
VL 35
IS 7
BP 645
EP 652
DI 10.14670/HH-18-206
PG 8
WC Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Pathology
GA MQ1CY
UT WOS:000552635700003
PM 32016946
DA 2025-01-04
ER

PT J
AU Chen, JF
   Wu, SW
   Shi, ZM
   Hu, B
AF Chen, Jin-Fang
   Wu, Shi-Wei
   Shi, Zi-Man
   Hu, Bing
TI Traditional Chinese medicine for colorectal cancer treatment: potential
   targets and mechanisms of action
SO CHINESE MEDICINE
LA English
DT Review
DE Colorectal cancer; Traditional Chinese medicine; Signaling pathway;
   Mechanism of action
ID NF-KAPPA-B; CELL-CYCLE ARREST; OXYMATRINE SUPPRESSES PROLIFERATION; ACID
   INHIBITS PROLIFERATION; COLON ADENOCARCINOMA CELLS; TO-MESENCHYMAL
   TRANSITION; WNT SIGNALING PATHWAYS; PHASE-III TRIAL; ZUO JIN WAN;
   TGF-BETA
AB Colorectal cancer (CRC) is a disease with complex pathogenesis, it is prone to metastasis, and its development involves abnormalities in multiple signaling pathways. Surgery, chemotherapy, radiotherapy, target therapy, and immunotherapy remain the main treatments for CRC, but improvement in the overall survival rate and quality of life is urgently needed. Traditional Chinese medicine (TCM) has a long history of preventing and treating CRC. It could affect CRC cell proliferation, apoptosis, cell cycle, migration, invasion, autophagy, epithelial-mesenchymal transition, angiogenesis, and chemoresistance by regulating multiple signaling pathways, such as PI3K/Akt, NF-kappa B, MAPK, Wnt/beta-catenin, epidermal growth factor receptors, p53, TGF-beta, mTOR, Hedgehog, and immunomodulatory signaling pathways. In this paper, the main signaling pathways and potential targets of TCM and its active ingredients in the treatment of CRC were systematically summarized, providing a theoretical basis for treating CRC with TCM and new ideas for further exploring the pathogenesis of CRC and developing new anti-CRC drugs.
C1 [Chen, Jin-Fang; Wu, Shi-Wei; Shi, Zi-Man; Hu, Bing] Shanghai Univ Tradit Chinese Med, Longhua Hosp, Inst Tradit Chinese Med Oncol, Shanghai 200032, Peoples R China.
   [Chen, Jin-Fang; Wu, Shi-Wei; Shi, Zi-Man; Hu, Bing] Shanghai Univ Tradit Chinese Med, Longhua Hosp, Dept Oncol, Shanghai 200032, Peoples R China.
C3 Shanghai University of Traditional Chinese Medicine; Shanghai University
   of Traditional Chinese Medicine
RP Hu, B (corresponding author), Shanghai Univ Tradit Chinese Med, Longhua Hosp, Inst Tradit Chinese Med Oncol, Shanghai 200032, Peoples R China.; Hu, B (corresponding author), Shanghai Univ Tradit Chinese Med, Longhua Hosp, Dept Oncol, Shanghai 200032, Peoples R China.
EM beearhu@shutcm.edu.cn
RI CHEN, Jinfang/LKK-1408-2024
OI /0000-0003-0810-6670
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NR 272
TC 32
Z9 34
U1 12
U2 50
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1749-8546
J9 CHIN MED-UK
JI Chin. Med.
PD FEB 13
PY 2023
VL 18
IS 1
AR 14
DI 10.1186/s13020-023-00719-7
PG 31
WC Integrative & Complementary Medicine; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Integrative & Complementary Medicine; Pharmacology & Pharmacy
GA 9A9IR
UT WOS:000934363000001
PM 36782251
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Han, S
   Cao, YY
   Guo, TY
   Lin, QL
   Luo, FJ
AF Han, Shuai
   Cao, Yunyun
   Guo, Tianyi
   Lin, Qinlu
   Luo, Feijun
TI Targeting lncRNA/Wnt axis by flavonoids: A promising therapeutic
   approach for colorectal cancer
SO PHYTOTHERAPY RESEARCH
LA English
DT Review
DE colorectal cancer; epigenetic therapy; flavonoids; lncRNA; Wnt axis
ID LONG NONCODING RNA; SIGNALING PATHWAY; CELL-PROLIFERATION;
   POOR-PROGNOSIS; PROMOTES; METASTASIS; RESISTANCE; PROGRESSION;
   TUMORIGENESIS; TRANSCRIPTION
AB Despite the dramatic advances in our understanding of the etiology of colorectal cancer (CRC) in recent decades, effective therapeutic strategies are still urgently needed. Oncogenic mutations in the Wnt/beta-Catenin pathway are hallmarks of CRC. Moreover, long non-coding RNAs (lncRNAs) as molecular managers are involved in the initiation, progression, and metastasis of CRC. Therefore, it is important to further explore the interaction between lncRNAs and Wnt/beta-Catenin signaling pathway for targeted therapy of CRC. Natural phytochemicals have not toxicity and can target carcinogenesis-related pathways. Growing evidences suggest that flavonoids are inversely associated with CRC risk. These bioactive compounds could target carcinogenesis pathways of CRC and reduced the side effects of anti-cancer drugs. The review systematically summarized the progress of flavonoids targeting lncRNA/Wnt axis in the investigations of CRC, which will provide a promising therapeutic approach for CRC and develop nutrition-oriented preventive strategies for CRC based on epigenetic mechanisms. In the field, more epidemiological and clinical trials are required in the future to verify feasibility of targeting lncRNA/Wnt axis by flavonoids in the therapy and prevention of CRC.
C1 [Han, Shuai; Cao, Yunyun; Guo, Tianyi; Lin, Qinlu; Luo, Feijun] Cent South Univ Forestry & Technol, Coll Food Sci & Engn, Hunan Key Lab Grain Oil Deep Proc & Qual Control, Hunan Key Lab Forestry Edible Resources Safety &, Changsha, Hunan, Peoples R China.
C3 Central South University of Forestry & Technology
RP Luo, FJ (corresponding author), Cent South Univ Forestry & Technol, Coll Food Sci & Engn, 498 Shaoshan Rd, Changsha 410004, Peoples R China.
EM luofeijun888@cusft.edu.cn
RI Lin, Qinlu/B-1732-2019; Luo, Feijun/B-1424-2012
OI Lin, Qinlu/0000-0003-2043-4220; Luo, Feijun/0000-0001-7489-544X
FU Natural Science Foundation of Hunan Province [2019JJ50984];
   Post-graduate Scientific Research Innovations Project of Hunan Province
   [CX20200699, CX20201018, CX20210862]; Program for Science & Technology
   Innovation Platform of Hunan Province [2019TP1029]; Scientific
   Innovation Fund for Post-graduate of Central South University of
   Forestry and Technology [CX202101027]
FX Natural Science Foundation of Hunan Province, Grant/Award Number:
   2019JJ50984; Post-graduate Scientific Research Innovations Project of
   Hunan Province, Grant/Award Numbers: CX20200699, CX20201018, CX20210862;
   Program for Science & Technology Innovation Platform of Hunan Province,
   Grant/Award Number: 2019TP1029; Scientific Innovation Fund for
   Post-graduate of Central South University of Forestry and Technology,
   Grant/Award Number: CX202101027
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NR 183
TC 6
Z9 6
U1 2
U2 26
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0951-418X
EI 1099-1573
J9 PHYTOTHER RES
JI Phytother. Res.
PD NOV
PY 2022
VL 36
IS 11
BP 4024
EP 4040
DI 10.1002/ptr.7550
EA OCT 2022
PG 17
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 6F1JM
UT WOS:000866538500001
PM 36227024
DA 2025-01-04
ER

PT J
AU Son, B
   Lee, W
   Kim, H
   Shin, H
   Park, HH
AF Son, Boram
   Lee, Wonhwa
   Kim, Hyeonjeong
   Shin, Heungsoo
   Park, Hee Ho
TI Targeted therapy of cancer stem cells: inhibition of mTOR in
   pre-clinical and clinical research
SO CELL DEATH & DISEASE
LA English
DT Review
ID PHASE-I TRIAL; PI3K/AKT/MTOR SIGNALING PATHWAY; PANCREATIC-CANCER;
   MAMMALIAN TARGET; ALPHA-FETOPROTEIN; TGF-BETA; HEPATOCELLULAR-CARCINOMA;
   COLORECTAL-CANCER; TUMOR-GROWTH; MATRIX METALLOPROTEINASES
AB Cancer stem cells (CSCs) are a type of stem cell that possesses not only the intrinsic abilities of stem cells but also the properties of cancer cells. Therefore, CSCs are known to have self-renewal and outstanding proliferation capacity, along with the potential to differentiate into specific types of tumor cells. Cancers typically originate from CSCs, making them a significant target for tumor treatment. Among the related cascades of the CSCs, mammalian target of rapamycin (mTOR) pathway is regarded as one of the most important signaling pathways because of its association with significant upstream signaling: phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway and mitogen-activated protein kinase (MAPK) cascade, which influence various activities of stem cells, including CSCs. Recent studies have shown that the mTOR pathway not only affects generation of CSCs but also the maintenance of their pluripotency. Furthermore, the maintenance of pluripotency or differentiation into specific types of cancer cells depends on the regulation of the mTOR signal in CSCs. Consequently, the clinical potential and importance of mTOR in effective cancer therapy are increasing. In this review, we demonstrate the association between the mTOR pathway and cancer, including CSCs. Additionally, we discuss a new concept for anti-cancer drug development aimed at overcoming existing drawbacks, such as drug resistance, by targeting CSCs through mTOR inhibition.
C1 [Son, Boram; Kim, Hyeonjeong; Shin, Heungsoo; Park, Hee Ho] Hanyang Univ, Dept Bioengn, Seoul 04763, South Korea.
   [Son, Boram] Kookmin Univ, Dept Bio & Fermentat Convergence Technol, Seoul 02707, South Korea.
   [Lee, Wonhwa] Sungkyunkwan Univ, Dept Chem, Suwon 16419, South Korea.
   [Park, Hee Ho] Hanyang Univ, Res Inst Convergence Basic Sci, Seoul 04763, South Korea.
C3 Hanyang University; Kookmin University; Sungkyunkwan University (SKKU);
   Hanyang University
RP Shin, H (corresponding author), Hanyang Univ, Dept Bioengn, Seoul 04763, South Korea.
EM hshin@hanyang.ac.kr; parkhh@hanyang.ac.kr
RI Lee, Wonhwa/GLQ-6506-2022; Son, Boram/HNB-4995-2023
OI Park, Hee Ho/0000-0003-1498-5624; Lee, Wonhwa/0000-0003-4336-5221
FU National Research Foundation of Korea (NRF) [RS-2023-00207746,
   2021R1C1C1014606]; Korea Institute of Planning and Evaluation for
   Technology in Food, Agriculture and Forestry (IPET) through High
   Value-added Food Technology Development Program; Ministry of
   Agriculture, Food and Rural Affairs (MAFRA) [RS-2024-00402798];
   Institute of Information & Communications Technology Planning &
   Evaluation (IITP) - Korea government (MSIT) [2020-0-01373]; Hanyang
   University
FX This work was supported by the National Research Foundation of Korea
   (NRF)grant funded by the Korea government (MSIT) (No.
   RS-2023-00207746,2021R1C1C1014606). This work was supported by Korea
   Institute of Planning and Evaluation for Technology in Food, Agriculture
   and Forestry (IPET) through High Value-added Food Technology Development
   Program, funded by Ministry of Agriculture, Food and Rural Affairs
   (MAFRA) (RS-2024-00402798). This work was partly supported by Institute
   of Information & Communications Technology Planning & Evaluation (IITP)
   grant funded by the Korea government (MSIT)(No.2020-0-01373, Artificial
   Intelligence Graduate School Program (Hanyang University)) and the
   research fund of Hanyang University (HY-2024).
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NR 321
TC 2
Z9 2
U1 3
U2 3
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD SEP 30
PY 2024
VL 15
IS 9
AR 696
DI 10.1038/s41419-024-07077-8
PG 18
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA H8J6N
UT WOS:001325851100017
PM 39349424
OA gold
DA 2025-01-04
ER

PT J
AU Chavez-Dominguez, R
   Perez-Medina, M
   Lopez-Gonzalez, JS
   Galicia-Velasco, M
   Aguilar-Cazares, D
AF Chavez-Dominguez, Rodolfo
   Perez-Medina, Mario
   Lopez-Gonzalez, Jose S.
   Galicia-Velasco, Miriam
   Aguilar-Cazares, Dolores
TI The Double-Edge Sword of Autophagy in Cancer: From Tumor Suppression to
   Pro-tumor Activity
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE autophagy; cell death; metabolic reprograming; metastasis;
   carcinogenesis; tumor microenvironment; immune evasion; chemotherapy and
   targeted therapy resistance
ID HYPOXIA-INDUCED AUTOPHAGY; CELL-DEATH; MOLECULAR-MECHANISMS; ANOIKIS
   RESISTANCE; MITOCHONDRIAL METABOLISM; GLUTAMINE-METABOLISM;
   GLUCOSE-METABOLISM; INHIBITS AUTOPHAGY; REGULATE AUTOPHAGY;
   COLORECTAL-CANCER
AB During tumorigenesis, cancer cells are exposed to a wide variety of intrinsic and extrinsic stresses that challenge homeostasis and growth. Cancer cells display activation of distinct mechanisms for adaptation and growth even in the presence of stress. Autophagy is a catabolic mechanism that aides in the degradation of damaged intracellular material and metabolite recycling. This activity helps meet metabolic needs during nutrient deprivation, genotoxic stress, growth factor withdrawal and hypoxia. However, autophagy plays a paradoxical role in tumorigenesis, depending on the stage of tumor development. Early in tumorigenesis, autophagy is a tumor suppressor via degradation of potentially oncogenic molecules. However, in advanced stages, autophagy promotes the survival of tumor cells by ameliorating stress in the microenvironment. These roles of autophagy are intricate due to their interconnection with other distinct cellular pathways. In this review, we present a broad view of the participation of autophagy in distinct phases of tumor development. Moreover, autophagy participation in important cellular processes such as cell death, metabolic reprogramming, metastasis, immune evasion and treatment resistance that all contribute to tumor development, is reviewed. Finally, the contribution of the hypoxic and nutrient deficient tumor microenvironment in regulation of autophagy and these hallmarks for the development of more aggressive tumors is discussed.
C1 [Chavez-Dominguez, Rodolfo; Perez-Medina, Mario; Lopez-Gonzalez, Jose S.; Galicia-Velasco, Miriam; Aguilar-Cazares, Dolores] Inst Nacl Enfermedades Resp Ismael Cosio Villegas, Dept Enfermedades Cronicodegenerat, Mexico City, DF, Mexico.
   [Chavez-Dominguez, Rodolfo] Univ Nacl Autonoma Mexico, Posgrad Ciencias Biol, Mexico City, DF, Mexico.
   [Perez-Medina, Mario] Inst Politecn Nacl, Dept Bioquim, Lab Quimioterapia Expt, Escuela Nacl Ciencias Biol, Mexico City, DF, Mexico.
C3 Universidad Nacional Autonoma de Mexico; Instituto Politecnico Nacional
   - Mexico
RP Aguilar-Cazares, D (corresponding author), Inst Nacl Enfermedades Resp Ismael Cosio Villegas, Dept Enfermedades Cronicodegenerat, Mexico City, DF, Mexico.
EM doloresaguilarcazares@yahoo.com.mx
RI Perez, MArio/LUY-7383-2024; Chavez-Dominguez, Rodolfo L/JLM-3143-2023;
   Aguilar-Cazares, Dolores/AAA-4774-2021; Lopez-Gonzalez, Jose
   Sullivan/GZK-6775-2022
OI Aguilar-Cazares, Dolores/0000-0002-7475-0969; /0000-0002-9308-2521;
   Lopez-Gonzalez, Jose Sullivan/0000-0003-0746-2286; Chavez,
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NR 183
TC 196
Z9 201
U1 8
U2 34
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 7
PY 2020
VL 10
AR 578418
DI 10.3389/fonc.2020.578418
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OD4WU
UT WOS:000579853600001
PM 33117715
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Mohr, P
   van Sluis, J
   Hooge, MNLD
   Lammertsma, AA
   Brouwers, AH
   Tsoumpas, C
AF Mohr, Philipp
   van Sluis, Joyce
   Lub-de Hooge, Marjolijn N.
   Lammertsma, Adriaan A.
   Brouwers, Adrienne H.
   Tsoumpas, Charalampos
TI Advances and challenges in immunoPET methodology
SO FRONTIERS IN NUCLEAR MEDICINE
LA English
DT Review
DE monoclonal antibody; immunoPET; quantification; kinetic modeling;
   zirconium; imaging; PET/CT
ID POSITRON-EMISSION-TOMOGRAPHY; STANDARDIZED UPTAKE VALUE; BREAST-CANCER;
   MONOCLONAL-ANTIBODY; RADIATION-DOSIMETRY; NECK-CANCER; ZR-89-BEVACIZUMAB
   PET; COLORECTAL-CARCINOMA; RECEPTOR OCCUPANCY; TUMOR PENETRATION
AB Immuno-positron emission tomography (immunoPET) enables imaging of specific targets that play a role in targeted therapy and immunotherapy, such as antigens on cell membranes, targets in the disease microenvironment, or immune cells. The most common immunoPET applications use a monoclonal antibody labeled with a relatively long-lived positron emitter such as 89Zr (T1/2 = 78.4 h), but smaller antibody-based constructs labeled with various other positron emitting radionuclides are also being investigated. This molecular imaging technique can thus guide the development of new drugs and may have a pivotal role in selecting patients for a particular therapy. In early phase immunoPET trials, multiple imaging time points are used to examine the time-dependent biodistribution and to determine the optimal imaging time point, which may be several days after tracer injection due to the slow kinetics of larger molecules. Once this has been established, usually only one static scan is performed and semi-quantitative values are reported. However, total PET uptake of a tracer is the sum of specific and nonspecific uptake. In addition, uptake may be affected by other factors such as perfusion, pre-/co-administration of the unlabeled molecule, and the treatment schedule. This article reviews imaging methodologies used in immunoPET studies and is divided into two parts. The first part summarizes the vast majority of clinical immunoPET studies applying semi-quantitative methodologies. The second part focuses on a handful of studies applying pharmacokinetic models and includes preclinical and simulation studies. Finally, the potential and challenges of immunoPET quantification methodologies are discussed within the context of the recent technological advancements provided by long axial field of view PET/CT scanners.
C1 [Mohr, Philipp; van Sluis, Joyce; Lub-de Hooge, Marjolijn N.; Lammertsma, Adriaan A.; Brouwers, Adrienne H.; Tsoumpas, Charalampos] Univ Groningen, Univ Med Ctr Groningen, Dept Nucl Med & Mol Imaging, Groningen, Netherlands.
   [Lub-de Hooge, Marjolijn N.] Univ Groningen, Univ Med Ctr Groningen, Dept Clin Pharm & Pharmacol, Groningen, Netherlands.
C3 University of Groningen; University of Groningen
RP Mohr, P (corresponding author), Univ Groningen, Univ Med Ctr Groningen, Dept Nucl Med & Mol Imaging, Groningen, Netherlands.
EM p.mohr@umcg.nl
OI Brouwers, Adrienne/0000-0003-2698-1516; Mohr,
   Philipp/0000-0001-9391-3287; van Sluis, Joyce/0000-0003-1908-4518;
   Lub-de Hooge, Marjolijn/0000-0002-5390-2791
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NR 197
TC 1
Z9 1
U1 1
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2673-8880
J9 FRONT NUCL MED
JI Front. Nucl. Med.
PD FEB 19
PY 2024
VL 4
AR 1360710
DI 10.3389/fnume.2024.1360710
PG 24
WC Radiology, Nuclear Medicine & Medical Imaging
WE Emerging Sources Citation Index (ESCI)
SC Radiology, Nuclear Medicine & Medical Imaging
GA N3W2Z
UT WOS:001363675400001
PM 39355220
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Jackson, K
   Samaddar, S
   Markiewicz, MA
   Bansal, A
AF Jackson, Katy
   Samaddar, Sohini
   Markiewicz, Mary A.
   Bansal, Ajay
TI Vaccination-Based Immunoprevention of Colorectal Tumors A Primer for the
   Clinician
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Review
DE cancer immunoprevention; vaccines; colorectal cancers
ID IMMUNE CELLS; CANCER PREVENTION; MOLECULAR-ORIGINS; LYNCH SYNDROME; MUC1
   VACCINE; DOUBLE-BLIND; FOLLOW-UP; ASPIRIN; ANTIGENS; COLON
AB Colorectal cancer (CRC) continues to be a significant public health problem worldwide. CRC screening programs have reduced the incidence rates of CRCs but still suffer from the problems of missed lesions and interval cancers. Chemopreventive strategies against CRC would benefit high-risk populations but trials testing synthetic and naturally occurring compounds have not yielded a front runner. Immune mechanisms promoting cancer have been modulated to develop immunotherapy for cancer treatment that has revolutionized cancer management, but could also be applied to cancer interception, that is, cancer immunoprevention. Cancer immunoprevention refers to approaches that can enhance the immune system, either directly or by removing natural breaks such as immune checkpoints, to survey and destroy tumor cells. In this primer, we aim to explain the concepts behind vaccine-based cancer immunoprevention. Multiple cancer vaccines have been tried in advanced cancer populations, but most have failed primarily because of an immunosuppressive environment that accompanies advanced cancers. Preventive vaccines in immunocompetent hosts may have a better clinical response compared with therapeutic vaccines in immunosuppressed hosts. The first randomized controlled trial testing the mucin1 vaccine against CRC in the prevention setting has been successfully completed. For the benefit of the clinician, we briefly discuss important concepts related to the workings of preventive vaccines. Prevention with vaccines is a highly attractive approach because of the potential for highly targeted therapy with minimal side effects that could theoretically provide lifelong protection.
C1 [Jackson, Katy] Univ Kansas Hlth Syst, Dept Med, Kansas City, KS USA.
   [Samaddar, Sohini; Bansal, Ajay] Univ Kansas, Med Ctr, Div Gastroenterol & Hepatol, Kansas City, KS USA.
   [Markiewicz, Mary A.] Univ Kansas, Med Ctr, Dept Microbiol Mol Genet & Immunol, Kansas City, KS USA.
   [Bansal, Ajay] Univ Kansas Canc Ctr, Kansas City, KS USA.
   [Bansal, Ajay] Univ Kansas, Sch Med, Dept Med, 3901 Rainbow Blvd, Kansas City, KS USA.
C3 University of Kansas; University of Kansas Medical Center; University of
   Kansas; University of Kansas Medical Center; University of Kansas;
   University of Kansas Medical Center
RP Bansal, A (corresponding author), Univ Kansas, Sch Med, Dept Med, 3901 Rainbow Blvd, Kansas City, KS USA.
EM kjackson18@kumc.edu; sohini.samaddar@gmail.com; mmarkiewicz@kumc.edu;
   abansal@kumc.edu
OI Markiewicz, Mary/0000-0001-5685-8573
FU NIH/NCI Cancer Center Support Grant [P30 CA168524]; Freenome Holdings
   and Stella Diagnostics
FX This work was supported in part by the NIH/NCI Cancer Center Support
   Grant P30 CA168524 to AB. M.A.M. is a paid consultant for Design-Zyme,
   LLC. A.B. has received research support from Freenome Holdings and
   Stella Diagnostics.
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NR 68
TC 3
Z9 3
U1 2
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD MAR
PY 2023
VL 57
IS 3
BP 246
EP 252
DI 10.1097/MCG.0000000000001808
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 9C0TE
UT WOS:000935139400004
PM 36730670
OA Green Published
DA 2025-01-04
ER

PT J
AU Gouverneur, A
   Favary, C
   Jové, J
   Rouyer, M
   Bignon, E
   Salvo, F
   Tchalla, A
   Paillaud, E
   Aparicio, T
   Noize, P
AF Gouverneur, Amandine
   Favary, Clelia
   Jove, Jeremy
   Rouyer, Magali
   Bignon, Emmanuelle
   Salvo, Francesco
   Tchalla, Achille
   Paillaud, Elena
   Aparicio, Thomas
   Noize, Pernelle
TI Impact of Cardiovascular Comorbidities on the Effectiveness and Safety
   of Bevacizumab in Older Patients with Metastatic Colorectal Cancer
SO TARGETED ONCOLOGY
LA English
DT Article
ID ELDERLY-PATIENTS; PLUS CHEMOTHERAPY; PRODIGE 20; FRANCE; IDENTIFICATION;
   THERAPY; SOCIETY; HOSPITALIZATION; ASSOCIATION; PREVALENCE
AB BackgroundCardiovascular comorbidities are not contraindications of bevacizumab for metastatic colorectal cancer.ObjectiveWe aimed to evaluate the impact of cardiovascular comorbidities before bevacizumab treatment on overall survival and cardiovascular safety in older patients with metastatic colorectal cancer.MethodsA 2009-2015 cohort of patients with metastatic colorectal cancer aged & GE; 65 years administered first-line bevacizumab was extracted from the French healthcare reimbursement claims database. Baseline heart failure, hypertension, and venous/arterial thromboembolic events were identified. The 36-month overall survival rate was evaluated using the Kaplan-Meier method, and the impact of cardiovascular comorbidities on the 36-month overall survival using a time-dependent, multivariable, Cox proportional hazards model. The 36-month cumulative incidence of cardiovascular events, and the impact of cardiovascular comorbidities on the likelihood of cardiovascular events were evaluated using the Fine and Gray model, with death as a competing risk.ResultsWe included 9222 patients (56.4% male; median age 73 years). Two-thirds (66.7%) had baseline cardiovascular comorbidities. The median 36-month overall survival was 20.4 [95% confidence interval (CI) 19.9-21.0] and 21.8 [95% CI 21.1-22.6] months in patients with and without cardiovascular comorbidities, respectively. Age & GE; 75 years, dependency in activities of daily living, radiotherapy, and another targeted therapy were identified as death risk factors, but not cardiovascular comorbidities. At 36 months, cardiovascular events had occurred in 60.2% [95% CI 58.9-61.4] and 44.1% [95% CI 42.3-45.9] of patients with and without cardiovascular comorbidities. Baseline venous thrombosis, female, three or more cardiovascular medications, another targeted therapy, and more than six bevacizumab injections were identified as risk factors for cardiovascular events.ConclusionsIn clinical practice, cardiovascular comorbidities before administering bevacizumab to older patients with metastatic colorectal cancer impacted the cardiovascular safety, but not overall survival. Unless they limit functional independency, older patients with cardiovascular comorbidities should be treated with bevacizumab under close monitoring.
C1 [Gouverneur, Amandine; Salvo, Francesco; Noize, Pernelle] Univ Bordeaux, Team AHeaD, INSERM, BPH,U1219, F-33000 Bordeaux, France.
   [Gouverneur, Amandine; Salvo, Francesco; Noize, Pernelle] CHU Bordeaux, Serv Pharmacol Med, Pole Sante Publ, F-33000 Bordeaux, France.
   [Favary, Clelia; Jove, Jeremy; Rouyer, Magali; Bignon, Emmanuelle] Univ Bordeaux, INSERM CIC P 1401, Bordeaux PharmacoEpi, F-33000 Bordeaux, France.
   [Tchalla, Achille] Univ Limoges, Inst OMEGA Hlth, Lab VieSante UR 24134 Vieillissement Fragil Preven, F-87042 Limoges, France.
   [Tchalla, Achille] CHU Limoges, Serv Med Geriatr, Pole HU Gerontol Clin, F-87042 Limoges, France.
   [Paillaud, Elena] Univ Paris Cite, Paris Canc Inst CARPEM, F-75015 Paris, France.
   [Paillaud, Elena] Hop Europeen Georges Pompidou, AP HP, Serv Geriatrie, F-75015 Paris, France.
   [Aparicio, Thomas] Univ Paris, F-75010 Paris, France.
   [Aparicio, Thomas] Hop St Louis, AP HP, Serv Gastroenterol, F-75010 Paris, France.
C3 Institut National de la Sante et de la Recherche Medicale (Inserm);
   Universite de Bordeaux; Universite de Bordeaux; CHU Bordeaux; Universite
   de Bordeaux; Institut National de la Sante et de la Recherche Medicale
   (Inserm); Universite de Limoges; CHU Limoges; Universite Paris Cite;
   Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Europeen Georges-Pompidou - APHP; Universite Paris
   Cite; Universite Paris Cite; Assistance Publique Hopitaux Paris (APHP);
   Hopital Universitaire Saint-Louis - APHP
RP Noize, P (corresponding author), Univ Bordeaux, Team AHeaD, INSERM, BPH,U1219, F-33000 Bordeaux, France.
EM pernelle.noize@u-bordeaux.fr
RI Paillaud, Elena/K-5616-2017; Gouverneur, Amandine/O-5332-2018
OI Gouverneur, Amandine/0000-0001-6253-1833
FU French Ministry of Health; French National Cancer Institute, INCa
   [INCa-DGOS_11409]
FX This study was supported by a grant from the French Ministry of Health
   and managed by the French National Cancer Institute, INCa (Grant number:
   INCa-DGOS_11409). The funding source had no role in the design, methods,
   subject recruitment, data collections, analysis, and preparation of the
   paper.
CR ameli, ETUDE ALGORITHMES DE
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NR 42
TC 0
Z9 0
U1 0
U2 0
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 SEP
PY 2023
VL 18
IS 5
BP 717
EP 726
DI 10.1007/s11523-023-00986-2
EA SEP 2023
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA S4KW1
UT WOS:001064347100002
PM 37682504
DA 2025-01-04
ER

PT J
AU Wang, YY
   Xin, ZC
   Wang, K
AF Wang, Yan-Yan
   Xin, Ze-Chang
   Wang, Kun
TI Impact of Molecular Status on Metastasectomy of Colorectal Cancer Liver
   Metastases
SO CLINICS IN COLON AND RECTAL SURGERY
LA English
DT Article
DE colorectal cancer liver metastases; molecular status; hepatectomy;
   prognosis
ID CIRCULATING TUMOR DNA; MUTATION PREDICTS; BRAF MUTATION; MICROSATELLITE
   INSTABILITY; PROGNOSTIC-FACTORS; RAS MUTATIONS; KRAS STATUS; RESECTION;
   RECURRENCE; SURVIVAL
AB Although surgical resection could provide better survival for patients with colorectal cancer liver metastases (CRLM), the recurrence rate after resection of CRLM remains high. The progress of genome sequencing technologies has greatly improved the molecular understanding of colorectal cancer. In the era of genomics and targeted therapy, genetic mutation analysis is of great significance to guide systemic treatment and identify patients who can benefit from resection of CRLM. RAS and BRAF mutations and microsatellite instability/deficient deoxyribonucleic acid (DNA) mismatch repair status have been incorporated into current clinical practice. Other promising molecular biomarkers such as coexisting gene mutations and circulating tumor DNA are under active investigation. This study aimed to review the prognostic significance of molecular biomarkers in patients with CRLM undergoing metastasectomy based on the current evidence.
C1 [Wang, Yan-Yan; Xin, Ze-Chang; Wang, Kun] Peking Univ, Beijing Canc Hosp & Inst, Sch Oncol, Hepatopancreatobiliary Surg Dept 1,Key Lab Carcino, 52 Fucheng Rd, Beijing 100142, Peoples R China.
C3 Peking University
RP Wang, K (corresponding author), Peking Univ, Beijing Canc Hosp & Inst, Sch Oncol, Hepatopancreatobiliary Surg Dept 1,Key Lab Carcino, 52 Fucheng Rd, Beijing 100142, Peoples R China.
EM wang-kun@vip.sina.com.cn
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NR 88
TC 0
Z9 0
U1 0
U2 1
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 1531-0043
EI 1530-9681
J9 CLIN COLON RECT SURG
JI Clin. Colon Rectal Surg.
PD NOV
PY 2023
VL 36
IS 06
BP 423
EP 429
DI 10.1055/s-0043-1767700
EA APR 2023
PG 7
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA EX9H1
UT WOS:000967465500001
PM 37795466
OA Green Published
DA 2025-01-04
ER

PT J
AU Piercey, O
   Tie, J
   Hollande, F
   Wong, HL
   Mariadason, J
   Desai, J
AF Piercey, Oliver
   Tie, Jeanne
   Hollande, Frederic
   Wong, Hui-Li
   Mariadason, John
   Desai, Jayesh
TI <i>BRAFV600E-Mutant</i> V600E-Mutant Metastatic Colorectal Cancer:
   Current Evidence, Future Directions, and Research Priorities
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE Targeted therapy; Resistance mechanisms; Bowel cancer; Predictive
   biomarkers; MAPK pathway
ID NEGATIVE FEEDBACK-REGULATION; ACQUIRED-RESISTANCE; COMBINED BRAF;
   MICROSATELLITE INSTABILITY; ERK1/2 INHIBITOR; DOSE-ESCALATION; SUBGROUP
   ANALYSES; PROGNOSTIC-FACTOR; ALLELE FRACTION; EGFR INHIBITION
AB BRAFV600E-mutant V600E-mutant metastatic colorectal cancer represents a distinct molecular phenotype known for its aggressive biological behavior, resistance to standard therapies, and poor survival rates. Improved understanding of the biology of the BRAF oncogene has led to the development of targeted therapies that have paved the way for a paradigm shift in managing this disease. However, despite significant recent advancements, responses to targeted therapies are shortlived, and several challenges remain. In this review, we discuss how progress in treating BRAFV600E-mutant V600E-mutant metastatic colorectal cancer has been made through a better understanding of its unique biological and clinical features. We provide an overview of the evidence to support current treatment approaches and discuss critical areas of need and future research strategies that hold the potential to refine clinical practice further. We also discuss some challenging aspects of managing this disease, particularly the complexity of acquired resistance mechanisms that develop under the selective pressure of targeted therapies and rational strategies being investigated to overcome them.
C1 [Piercey, Oliver; Tie, Jeanne; Wong, Hui-Li; Desai, Jayesh] Peter MacCallum Canc Ctr, 305 Grattan St, Melbourne, Vic 3000, Australia.
   [Piercey, Oliver; Hollande, Frederic] Univ Melbourne, Ctr Canc Res, Melbourne, Australia.
   [Piercey, Oliver; Hollande, Frederic] Univ Melbourne, Dept Clin Pathol, Melbourne, Australia.
   [Tie, Jeanne; Wong, Hui-Li; Desai, Jayesh] Univ Melbourne, Sir Peter MacCallum Dept Oncol, Melbourne, Australia.
   [Tie, Jeanne; Wong, Hui-Li] Walter & Eliza Hall Inst Med Res, Parkville, Australia.
   [Mariadason, John] Olivia Newton John Canc Wellness & Res Ctr, Heidelberg, Australia.
   [Mariadason, John] La Trobe Univ, Sch Med, Melbourne, Australia.
C3 Peter Maccallum Cancer Center; University of Melbourne; University of
   Melbourne; University of Melbourne; Peter Maccallum Cancer Center;
   Walter & Eliza Hall Institute; La Trobe University; Olivia Newton-John
   Cancer Research Institute; La Trobe University
RP Piercey, O (corresponding author), Peter MacCallum Canc Ctr, 305 Grattan St, Melbourne, Vic 3000, Australia.
EM Oliver.piercey@petermac.org
RI Desai, Jayesh/AAV-1237-2021; Mariadason, John/N-2003-2013
OI Mariadason, John/0000-0001-9123-7684
FX This research did not receive any specific grant from funding agencies
   in the public, commercial, or not-for-profit sectors.
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NR 122
TC 0
Z9 0
U1 2
U2 2
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD SEP
PY 2024
VL 23
IS 3
BP 215
EP 229
DI 10.1016/j.clcc.2024.04.004
EA AUG 2024
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA E9L5X
UT WOS:001306144200001
PM 38816264
DA 2025-01-04
ER

PT J
AU Zhang, HM
   Zhong, H
   Li, L
   Ji, WS
   Zhang, XQ
AF Zhang, Hongmei
   Zhong, Hua
   Li, Lei
   Ji, Wansheng
   Zhang, Xiaoqian
TI Overexpressed transcription factor FOXM1 contributes to the progression
   of colorectal cancer
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article
DE colorectal cancer; forkhead box M1; small interfering RNA;
   proliferation; invasion; targeted therapy
ID OVARIAN-CANCER; EXPRESSION; CARCINOGENESIS; TARGET; CELLS
AB Forkhead box M1 (FOXM1) is a characteristic proliferation-associated transcription factor, which is overexpressed in various types of human cancer. The aim of the present study was to determine the expression of FOXM1 in a large collection of colorectal cancer (CRC) samples. Between March 2012 and January 2014, 96 patients with histologically diagnosed CRC were recruited into the current study. Using immunohistochemistry, reverse transcription-quantitative polymerase chain reaction and western blotting, mRNA and protein expression levels of FOXM1 in CRC tissue samples were determined. The function of FOXM1 in the CRC cells was evaluated by small interfering RNA-mediated depletion of FOXM1, followed by analyses of cell proliferation and invasion. High levels of staining for FOXM1 were observed in significantly more CRC tissue samples: 85.42% (82/96) of CRC tissue samples compared with 18.75% (18/96) of adjacent normal mucosa tissue samples. Silencing FOXM1 inhibited the proliferation of LoVo cells, which express a relatively high level of FOXM1, and the invasion and migration of LoVo cells were also markedly suppressed. The data from the present study suggested that the pathogenesis of human CRC may be mediated by FOXM1, and that FOXM1 inhibition may provide a promising therapeutic strategy for CRC.
C1 [Zhang, Hongmei; Zhong, Hua; Li, Lei; Ji, Wansheng; Zhang, Xiaoqian] Weifang Med Univ, Affiliated Hosp, Dept Gastroenterol, 2428 Yuhe Rd, Weifang 261031, Shandong, Peoples R China.
C3 Shandong Second Medical University
RP Zhang, XQ (corresponding author), Weifang Med Univ, Affiliated Hosp, Dept Gastroenterol, 2428 Yuhe Rd, Weifang 261031, Shandong, Peoples R China.
EM drzhxq@163.com
RI zhong, hua/JRW-4786-2023
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NR 26
TC 17
Z9 19
U1 0
U2 5
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 MAR
PY 2016
VL 13
IS 3
BP 2696
EP 2700
DI 10.3892/mmr.2016.4875
PG 5
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA DF8TS
UT WOS:000371633000099
PM 26861549
OA Bronze
DA 2025-01-04
ER

PT J
AU Zhou, Q
   Xiong, W
   Zhou, X
   Gao, RS
   Lin, QF
   Liu, HY
   Li, JN
   Tian, XF
AF Zhou, Qing
   Xiong, Wei
   Zhou, Xing
   Gao, Rui-Song
   Lin, Qun-Fang
   Liu, Hui-Ying
   Li, Juan-Ni
   Tian, Xue-Fei
TI CTHRC1 and PD-1/PD-L1 expression predicts tumor recurrence in prostate
   cancer
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article
DE prostate cancer; collagen triple helix repeat containing 1; tumor
   microenvironment; program death receptor-1
ID TRIPLE-HELIX REPEAT; PROMOTES CELL-PROLIFERATION; COLORECTAL-CANCER; WEB
   SERVER; E-CADHERIN; METASTASIS; MICROENVIRONMENT; OVEREXPRESSION;
   INVASIVENESS; CONTAINING-1
AB Collagen triple helix repeat containing 1 (CTHRC1) is a gene that has been associated with tumor progression in human prostate cancer (PC). The tumor immune microenvironment has been linked with disease outcome in PC. In the present study, the correlation between CTHRC1 with PC recurrence and the tumor immunological microenvironment was investigated. Using the data supplied by the Tumor Immune Estimation Resource (TIMER), the expression of CTHRC1, programmed cell death protein 1 (PD-1), and programmed cell death 1 ligand 1 (PD-L1) were analyzed. Immunohistochemical staining of CTHRC1, PD-1 and PD-L1 was performed using a tissue microarray construction of prostate adenocarcinoma (PRAD) specimens. In PRAD, an association was reported between the CTHRC1 expression and the disease free survival (DFS) rate (P=0.022). Overexpression of CTHRC1 was correlated with increased levels of PD-1 (R=0.272, P=0.021) and PD-L1 (R=0.298, P=0.016), elevated levels of infiltrating B cells (P=9.51e(-11)), CD4(+) cells (P=1.51e(-11)), macrophages (P=8.25e(-5)), neutrophils (P=2.17e(-9)) and dendritic cells (P=3.13e(-13)). Bioinformatics analysis revealed that CTHRC1 was correlated with the expression levels of matrix metalloproteinase-9, mucin 1 and solute carrier organic anion transporter family member 2B1 genes, which exert an influence in PRAD. The occurrence of this condition is most likely to be associated with regulation of the tumor microenvironment. Taken together, we demonstrated that the prognosis and immunity of PC are closely linked to CTHRC1 upregulation. Furthermore, these results suggest that the immune function of PC may be suppressed by CTHRC1-targeting therapy.
C1 [Zhou, Qing; Xiong, Wei; Zhou, Xing; Gao, Rui-Song; Lin, Qun-Fang; Liu, Hui-Ying] Hunan Univ Chinese Med, Affiliated Hosp 1, Dept Androl, Changsha 410007, Hunan, Peoples R China.
   [Li, Juan-Ni] Cent South Univ, Xiangya Hosp, Dept Pathol, Changsha 410005, Hunan, Peoples R China.
   [Tian, Xue-Fei] Hunan Univ Chinese Med, Coll Integrated Chinese & Western Med, Dept Internal Med, 300 Xueshi Rd, Changsha 410208, Hunan, Peoples R China.
C3 Hunan University of Chinese Medicine; Central South University; Hunan
   University of Chinese Medicine
RP Tian, XF (corresponding author), Hunan Univ Chinese Med, Coll Integrated Chinese & Western Med, Dept Internal Med, 300 Xueshi Rd, Changsha 410208, Hunan, Peoples R China.
EM 003640@hnucm.edu.cn
OI TIAN, xuefei/0000-0003-4786-0844
FU National Natural Science Foundation of China [81573988, 81704093,
   81473617]; Hunan Science and Technology Department of China
   [2015JC3075]; Innovation Platform Open Foundation of Hunan Educational
   office [16K066]
FX The present study was supported by grants from the National Natural
   Science Foundation of China (grant nos. 81573988, 81704093 and
   81473617), the Hunan Science and Technology Department of China (grant
   no. 2015JC3075), and the Innovation Platform Open Foundation of Hunan
   Educational office (grant no. 16K066).
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NR 49
TC 17
Z9 18
U1 0
U2 11
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD NOV
PY 2019
VL 20
IS 5
BP 4244
EP 4252
DI 10.3892/mmr.2019.10690
PG 9
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA JF4YL
UT WOS:000491393100027
PM 31545446
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Cherradi, S
   Ayrolles-Torro, A
   Vezzo-Vié, N
   Gueguinou, N
   Denis, V
   Combes, E
   Boissière, F
   Busson, M
   Canterel-Thouennon, L
   Mollevi, C
   Pugnière, M
   Bibeau, F
   Ychou, M
   Martineau, P
   Gongora, C
   Del Rio, M
AF Cherradi, S.
   Ayrolles-Torro, A.
   Vezzo-Vie, N.
   Gueguinou, N.
   Denis, V.
   Combes, E.
   Boissiere, F.
   Busson, M.
   Canterel-Thouennon, L.
   Mollevi, C.
   Pugniere, M.
   Bibeau, F.
   Ychou, M.
   Martineau, P.
   Gongora, C.
   Del Rio, M.
TI Antibody targeting of claudin-1 as a potential colorectal cancer therapy
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE Metastatic; Colorectal cancer; Claudin-1; Antibody; Targeted therapy
ID TIGHT JUNCTION PROTEINS; PLUS IRINOTECAN; EXPRESSION; OVEREXPRESSION;
   PROLIFERATION; FLUOROURACIL; METASTASIS; LEUCOVORIN; CETUXIMAB; SEQUENCE
AB Background: Metastatic colorectal cancer (mCRC) is one of the major causes of cancer-related death. Despite the substantial progress in mCRC management, it remains important to identify new therapeutic options and biological markers for personalized medicine. Here, we investigated the expression of claudin-1 (CLDN1), a major tight junction transmembrane protein, in the different colorectal cancer (CRC) molecular subtypes and then assessed the anti-tumor effect of a new anti-CLDN1 monoclonal antibody (mAb).
   Methods: Gene expression profiling and immunochemistry analysis of normal and tumor tissue samples from patients with stage IV CRC were used to determine CLDN1 gene expression. Then, the 6F6 mAb against CLDN1 extracellular part was generated. Its effect on CRC cell cycle, proliferation, survival and migration was assessed in vitro, using a 3D cell culture system, flow cytometry, clonogenic and migration assays. In vivo, 6 F6 mAb efficacy was evaluated in nude mice after subcutaneous xenografts or intrasplenic injection of CRC cells.
   Results: Compared with normal mucosa where it was almost exclusively cytoplasmic, in CRC samples CLDN1 was overexpressed (p < 0.001) and mainly localized at the membrane. Moreover, it was differentially expressed in the various CRC molecular subtypes. The strongest expressions were found in the consensus molecular subtype CMS2 (p < 0.001), the transit-ampliflying (p < 0.001) and the C5 subtypes (p < 0.001). Lower CLDN1 expression predicted a better outcome in the molecular subtypes C3 and C5 (p = 0.012 and p = 0.004, respectively). CLDN1 targeting with the 6 F6 mAb led to reduction of survival, growth and migration of CLDN1-positive cells. In preclinical mouse models, the 6F6 mAb decreased tumor growth and liver metastasis formation.
   Conclusion: Our data indicate that CLDN1 targeting with an anti-CLDN1 mAb results in decreased growth and survival of CRC cells. This suggests that CLDN1 could be a new potential therapeutic target.
C1 [Cherradi, S.; Ayrolles-Torro, A.; Vezzo-Vie, N.; Gueguinou, N.; Denis, V.; Combes, E.; Busson, M.; Canterel-Thouennon, L.; Mollevi, C.; Pugniere, M.; Bibeau, F.; Ychou, M.; Martineau, P.; Gongora, C.; Del Rio, M.] Univ Montpellier, Inserm U1194, IRCM, Inst Reg Canc Montpellier ICM, 208 Rue Apothicaires, F-34298 Montpellier 5, France.
   [Vezzo-Vie, N.; Boissiere, F.; Canterel-Thouennon, L.; Mollevi, C.; Bibeau, F.; Ychou, M.; Del Rio, M.] Inst Reg Canc Montpellier ICM, F-34298 Montpellier, France.
C3 Institut National de la Sante et de la Recherche Medicale (Inserm);
   Universite de Montpellier; Universite de Montpellier
RP Del Rio, M (corresponding author), Univ Montpellier, Inserm U1194, IRCM, Inst Reg Canc Montpellier ICM, 208 Rue Apothicaires, F-34298 Montpellier 5, France.; Del Rio, M (corresponding author), Inst Reg Canc Montpellier ICM, F-34298 Montpellier, France.
EM maguy.delrio@icm.unicancer.fr
RI Mollevi, Caroline/AAA-6839-2019; PUGNIERE, Martine/AAD-4315-2020;
   Martineau, Pierre/N-4386-2017; PUGNIERE, Martine/T-1355-2017
OI GONGORA, Celine/0000-0001-9034-4031; Martineau,
   Pierre/0000-0002-7993-7183; Ychou, Marc/0000-0001-7378-9469; PUGNIERE,
   Martine/0000-0002-2049-2909
FU French National Research Agency [LabEx MAbImprove: ANR-10-LABX-53];
   SIRIC Montpellier Cancer [INCa-DGOS-Inserm 6045]; Inca [INCA-RECF0356];
   Ligue Regionale Contre le Cancer (comite du Gard); GEFLUC
FX This work was supported by grants from the French National Research
   Agency under the program "Investissements d'avenir" Grant Agreement
   LabEx MAbImprove: ANR-10-LABX-53, SIRIC Montpellier Cancer Grant <<
   INCa-DGOS-Inserm 6045 >>, Inca grant INCA-RECF0356, Ligue Regionale
   Contre le Cancer (comite du Gard) and GEFLUC.
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NR 40
TC 45
Z9 46
U1 1
U2 8
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD JUN 28
PY 2017
VL 36
AR 89
DI 10.1186/s13046-017-0558-5
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EZ0OL
UT WOS:000404405300002
PM 28659146
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sardu, C
   Santamaria, M
   Paolisso, G
   Marfella, R
AF Sardu, Celestino
   Santamaria, Matteo
   Paolisso, Giuseppe
   Marfella, Raffaele
TI microRNA expression changes after atrial fibrillation catheter ablation
SO PHARMACOGENOMICS
LA English
DT Review
DE atrial fibrillation; catheter ablation; microRNA
ID EXPERT CONSENSUS STATEMENT; DELAYED RECTIFIER CURRENT; MEAN PLATELET
   VOLUME; DOWN-REGULATION; CARDIAC CONTRACTILITY; COLORECTAL-CANCER;
   SURGICAL ABLATION; EUROPEAN-SOCIETY; OUTWARD CURRENT; MIR-133
AB Atrial fibrillation (AF) is most common arrhythmia in general population, with increasing trend in mortality and morbidity. Electrophysiological and structural abnormalities, promoting abnormal impulse formation and propagation, lead to this disease. AF catheter ablation is related to a not small percentage of nonresponder patients. microRNAs (miRs) have been used as AF fibrotic and electrical alterations biomarkers. miRs may differentiate responders patients to ablative approach. Selective miR target therapy, as upregulation by adenovirus transfection and/or miR downregulation by antagomiR, may be used to treat AF patients. Catheter ablation of triggering electrical pulmonary veins activity or fibrotic areas defragmentation may be upgraded by miR therapy to prevent cardiac electrical and fibrotic remodeling after AF ablation.
C1 [Sardu, Celestino; Paolisso, Giuseppe; Marfella, Raffaele] Second Univ Study Naples, Med Surg Neurol Metab & Aging Sci Dept, Naples, Italy.
   [Sardu, Celestino; Santamaria, Matteo] Giovanni Paolo II Res & Care Fdn, Cardiovasc & Arrhythmias Dept, Campobasso, Italy.
RP Sardu, C (corresponding author), Second Univ Study Naples, Med Surg Neurol Metab & Aging Sci Dept, Naples, Italy.
EM drsarducele@gmail.com
RI Santamaria, Matteo/U-4066-2019; Sardu, Celestino/AAA-7451-2019;
   Marfella, Raffaele/AAH-2595-2019; paolisso, giuseppe/AAP-8516-2020
OI marfella, raffaele/0000-0003-3960-9270; Santamaria,
   Matteo/0000-0003-1000-0592; Paolisso, Giuseppe/0000-0002-2137-455X;
   Sardu, Celestino/0000-0001-5099-3790
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NR 105
TC 47
Z9 48
U1 0
U2 12
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1462-2416
EI 1744-8042
J9 PHARMACOGENOMICS
JI Pharmacogenomics
PY 2015
VL 16
IS 16
BP 1863
EP 1877
DI 10.2217/pgs.15.117
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CX3AO
UT WOS:000365568100009
PM 26554530
DA 2025-01-04
ER

PT J
AU Lazar, V
   Zhang, BL
   Magidi, S
   Le Tourneau, C
   Raymond, E
   Ducreux, M
   Bresson, C
   Raynaud, J
   Wunder, F
   Onn, A
   Felip, E
   Tabernero, J
   Batist, G
   Kurzrock, R
   Rubin, E
   Schilsky, RL
AF Lazar, Vladimir
   Zhang, Baolin
   Magidi, Shai
   Le Tourneau, Christophe
   Raymond, Eric
   Ducreux, Michel
   Bresson, Catherine
   Raynaud, Jacques
   Wunder, Fanny
   Onn, Amir
   Felip, Enriqueta
   Tabernero, Josep
   Batist, Gerald
   Kurzrock, Razelle
   Rubin, Eitan
   Schilsky, Richard L.
TI A transcriptomics approach to expand therapeutic options and optimize
   clinical trials in oncology
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Article
DE analogous normal tissue biopsies; clinical trials; oncology;
   transcriptomics; tumor biopsies
ID TARGETED THERAPY; SOLID TUMORS; MET; BIOMARKERS; MEDICINE; RESISTANCE
AB Background:The current model of clinical drug development in oncology displays major limitations due to a high attrition rate in patient enrollment in early phase trials and a high failure rate of drugs in phase III studies. Objective:Integrating transcriptomics for selection of patients has the potential to achieve enhanced speed and efficacy of precision oncology trials for any targeted therapies or immunotherapies. Methods:Relative gene expression level in the metastasis and normal organ-matched tissues from the WINTHER database was used to estimate in silico the potential clinical benefit of specific treatments in a variety of metastatic solid tumors. Results:As example, high mRNA expression in tumor tissue compared to analogous normal tissue of c-MET and its ligand HGF correlated in silico with shorter overall survival (OS; p < 0.0001) and may constitute an independent prognostic marker for outcome of patients with metastatic solid tumors, suggesting a strategy to identify patients most likely to benefit from MET-targeted treatments. The prognostic value of gene expression of several immune therapy targets (PD-L1, CTLA4, TIM3, TIGIT, LAG3, TLR4) was investigated in non-small-cell lung cancers and colorectal cancers (CRCs) and may be useful to optimize the development of their inhibitors, and opening new avenues such as use of anti-TLR4 in treatment of patients with metastatic CRC. Conclusion:This in silico approach is expected to dramatically decrease the attrition of patient enrollment and to simultaneously increase the speed and detection of early signs of efficacy. The model may significantly contribute to lower toxicities. Altogether, our model aims to overcome the limits of current approaches.
C1 [Lazar, Vladimir] WIN Consortium, Worldwide Innovat Network WIN Assoc, 24 rue Albert Thuret, F-94550 Villejuif, France.
   [Magidi, Shai; Le Tourneau, Christophe; Raynaud, Jacques; Wunder, Fanny; Kurzrock, Razelle; Schilsky, Richard L.] WIN Consortium, Worldwide Innovat Network WIN Assoc, Villejuif, France.
   [Zhang, Baolin] Food & Drug Adm FDA, Ctr Drug Evaluat & Res CDER, Off Biotechnol Prod OBP, Silver Spring, MA USA.
   [Le Tourneau, Christophe] Paris Saclay Univ, Inst Curie, Dept Drug Dev & Innovat D3i, INSERM U900 Res Unit, Paris, France.
   [Raymond, Eric] Grp Hosp Paris St Joseph, Oncol Dept, Paris, France.
   [Ducreux, Michel] Univ Paris Saclay, Dept Med Oncol, Gustave Roussy, Inserm U1279, Villejuif, France.
   [Onn, Amir] Sheba Med Ctr, Inst Pulmonol, Tel Hashomer, Israel.
   [Felip, Enriqueta; Tabernero, Josep] Vall Hebron Hosp Campus, Oncol Dept, Barcelona, Spain.
   [Felip, Enriqueta; Tabernero, Josep] UV UCC, Inst Oncol VHIO, Barcelona, Spain.
   [Batist, Gerald] McGill Univ, Jewish Gen Hosp, Segal Canc Ctr, Dept Oncol, Montreal, PQ, Canada.
   [Rubin, Eitan] Ben Gurion Univ Negev, Shraga Segal Dept Microbiol & Immunol, Fac Hlth Sci, Beer Sheva, Israel.
C3 US Food & Drug Administration (FDA); Institut National de la Sante et de
   la Recherche Medicale (Inserm); Universite Paris Saclay; UNICANCER;
   Universite PSL; Institut Curie; Universite Paris Cite; Hopital Paris
   Saint-Joseph; Institut National de la Sante et de la Recherche Medicale
   (Inserm); Universite Paris Saclay; UNICANCER; Gustave Roussy; Chaim
   Sheba Medical Center; Vall d'Hebron Institut d'Oncologia (VHIO); McGill
   University; Ben Gurion University
RP Lazar, V (corresponding author), WIN Consortium, Worldwide Innovat Network WIN Assoc, 24 rue Albert Thuret, F-94550 Villejuif, France.
EM vladimir.lazar@winconsortium.org
RI Zhang, Baolin/L-5768-2017; Lazar, Vladimir/AAV-2087-2020; Kurzrock,
   Razelle/AAU-9782-2020; BRESSON, CATHERINE/AAQ-2084-2020
OI Zhang, Baolin/0000-0002-7859-0843
CR [Anonymous], 2017, JCO Precis Oncol
   [Anonymous], 2000, Modeling Survival Data: Extending the Cox Model
   [Anonymous], 2019, FDA APPROVED TARGETE
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NR 43
TC 4
Z9 4
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PY 2023
VL 15
AR 17588359231156382
DI 10.1177/17588359231156382
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C2WH4
UT WOS:000960576100001
PM 37025260
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Huang, YJ
   Zheng, DT
   Zhou, ZM
   Wang, HT
   Li, YP
   Zheng, HH
   Tan, JH
   Wu, JY
   Yang, QP
   Tian, HT
   Lin, LM
   Li, ZY
   Li, TY
AF Huang, Yujie
   Zheng, Daitian
   Zhou, Zhongming
   Wang, Haiting
   Li, Yanpo
   Zheng, Huihui
   Tan, Jianhui
   Wu, Jingyao
   Yang, Qiuping
   Tian, Huiting
   Lin, Liuming
   Li, Zhiyang
   Li, Tianyu
TI The research advances in Kirsten rat sarcoma viral oncogene homolog
   (KRAS)-related cancer during 2013 to 2022: a scientometric analysis
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE KRAS; cancer; scientometrics; Bibliometrix; VOSviewer; Citespace
ID METASTATIC COLORECTAL-CANCER; PLUS CETUXIMAB; MUTATIONS; KRAS;
   PUBLICATION; IRINOTECAN
AB Introduction Cancer represents a significant global public health concern. In recent years, the incidence of cancer has been on the rise worldwide due to various factors, including diet, environment, and an aging population. Simultaneously, advancements in tumor molecular biology and genomics have led to a shift from systemic chemotherapy focused on disease sites and morphopathology towards precise targeted therapy for driver gene mutations. Therefore, we propose a comprehensive review aimed at exploring the research hotspots and directions in the field of Kirsten rat sarcoma viral oncogene homolog (KRAS)-mutant cancers over the past decade, providing valuable insights for cancer treatment strategies. Specifically, we aim to present an intellectual landscape using data obtained from the Web of Science (WoS) regarding KRAS mutation. Methods Bibliometrix, VOSviewer, CiteSpace, and HistCite were employed to conduct scientometric analyses on national publications, influential authors, highly cited articles, frequent keywords, etc. Results A total of 16,609 publications met the screening criteria and exhibited a consistent annual growth trend overall. Among 102 countries/regions, the United States occupied the vast majority share of the published volume. The journal Oncotarget had the highest circulation among all scientific publications. Moreover, the most seminal articles in this field primarily focus on biology and targeted therapies, with overcoming drug resistance being identified as a future research direction. Conclusion The findings of the thematic analysis indicate that KRAS mutation in lung cancer, the prognosis following B-Raf proto-oncogene, serine/threonine kinase (BRAF) or rat sarcoma (RAS) mutations, and anti-epidermal growth factor receptor (EGFR)-related lung cancer are the significant hotspots in the given field. Considering the significant advancements made in direct targeting drugs like sotorasib, it is anticipated that interest in cancers associated with KRAS mutations will remain steadfast.
C1 [Huang, Yujie; Zheng, Daitian; Zhou, Zhongming; Wang, Haiting; Li, Yanpo; Zheng, Huihui; Tan, Jianhui; Wu, Jingyao; Yang, Qiuping; Tian, Huiting; Lin, Liuming; Li, Zhiyang; Li, Tianyu] Shantou Univ, Dept Thyroid Breast & Hernia Surg, Affiliated Hosp 2, Med Coll, Shantou, Guangdong, Peoples R China.
C3 Shantou University
RP Li, ZY; Li, TY (corresponding author), Shantou Univ, Dept Thyroid Breast & Hernia Surg, Affiliated Hosp 2, Med Coll, Shantou, Guangdong, Peoples R China.
EM s_zyli4@stu.edu.cn; 17f2tyli@stu.edu.cn
RI Li, Tianyu/AAG-6648-2021; Wang, Haiting/AEV-6398-2022; Huang,
   Yujie/LVR-2899-2024; Zhou, Zhongming/GWC-9382-2022
FU Special Fund Project of Guangdong Science and Technology
   [210728156901524, 210728156901519]; Medical Scientific Research
   Foundation of Guangdong Province, China [A2023481]; Shantou Medical
   Science and Technology Planning Project [220518116490772,
   220518116490933]
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This work was supported
   by the Special Fund Project of Guangdong Science and Technology
   (210728156901524, 210728156901519), Medical Scientific Research
   Foundation of Guangdong Province, China (grant number A2023481), Shantou
   Medical Science and Technology Planning Project (grant number
   220518116490772, 220518116490933).
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NR 57
TC 0
Z9 0
U1 2
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD APR 19
PY 2024
VL 14
AR 1345737
DI 10.3389/fonc.2024.1345737
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QK7N0
UT WOS:001220833500001
PM 38706597
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xu, XM
   Wang, JZ
AF Xu, Xiaoming
   Wang, Jingzhi
TI Multi-omics analysis reveals focal adhesion characteristic associated
   tumor immune microenvironment in colon adenocarcinoma
SO FRONTIERS IN GENETICS
LA English
DT Article
DE focal adhesion genes; gene signature; colon cancer; GEO database; TCGA
   data base
ID REGULARIZATION PATHS; CANCER; EXPRESSION; FAK; CONTRIBUTES; ACTIVATION
AB Colon adenocarcinoma (COAD) is one of the most frequent malignant lesions of the digestive system in humans, with an insidious onset. At the time of diagnosis, most of them have developed to the middle and late stages, and cancer cells have metastasized, and the prognosis is poor. Treatment options for progressive COAD are limited, and despite the promise of immunotherapy, immunotherapy response rates are low. The assembly and disaggregation of focal adhesion are critical for the directional migration of tumor cells to different sites, and it is unclear whether focal adhesion-related genes are involved in the development and prognosis of colon adenocarcinoma. This study aimed to investigate the role of focal adhesion genes in the occurrence and prognosis of COAD. We obtained datasets of COAD patients, including RNA-sequencing data and clinical information, from the TCGA and GEO databases (GSE17538 and GSE39582). Through CNMF clustering, two molecular subtypes with different expression patterns of focal adhesion genes were identified, and it was found that the molecular subtype with low expression of focal adhesion genes had better prognosis. Then the prediction signature was constructed by LASSO-Cox regression model, and the receiver operating characteristic (ROC) curve showed that the 4-gene signature had a good prediction effect on COAD 1-, 2-, and 3-year OS. Gene function enrichment analysis showed that the high-risk group was mainly enriched in immune and adhesion-related signaling pathways, suggesting that focal adhesion genes may affect the development and prognosis of COAD by regulating the immune microenvironment and tumor metastasis. The interaction between focal adhesion genes and immunity during the occurrence of COAD may help improve the response rate of immunotherapy, which also provides new ideas for the molecular mechanism and targeted therapy in COAD.
C1 [Xu, Xiaoming] Jining First Peoples Hosp, Dept Gastroenterol, Jining, Peoples R China.
   [Wang, Jingzhi] Nanjing Univ, Affiliated Yancheng Hosp 1, Peoples Hosp Yancheng 1, Dept Radiotherapy Oncol,Med Sch, Yancheng, Peoples R China.
C3 Nanjing University
RP Wang, JZ (corresponding author), Nanjing Univ, Affiliated Yancheng Hosp 1, Peoples Hosp Yancheng 1, Dept Radiotherapy Oncol,Med Sch, Yancheng, Peoples R China.
EM wangjzjs@163.com
RI xu, xiaoming/GRX-8854-2022; song, yu/KCZ-2003-2024
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NR 36
TC 2
Z9 2
U1 0
U2 1
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 MAR 6
PY 2023
VL 14
AR 1088091
DI 10.3389/fgene.2023.1088091
PG 11
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA A3VG2
UT WOS:000954434900001
PM 36950136
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Tam, C
   Wong, JH
   Tsui, SKW
   Zuo, T
   Chan, TF
   Ng, TB
AF Tam, Chit
   Wong, Jack Ho
   Tsui, Stephen Kwok Wing
   Zuo, Tao
   Chan, Ting Fung
   Ng, Tzi Bun
TI LncRNAs with miRNAs in regulation of gastric, liver, and colorectal
   cancers: updates in recent years
SO APPLIED MICROBIOLOGY AND BIOTECHNOLOGY
LA English
DT Review
DE lncRNA; miRNA; Epigenetic alteration; Microbiota meditation; Tumor
   proliferation; Metastasis; Targeted therapy design
ID LONG NONCODING RNA; PROMOTES CELL-PROLIFERATION; EPITHELIAL-MESENCHYMAL
   TRANSITION; HEPATOCELLULAR-CARCINOMA CELLS; PREDICTS POOR-PROGNOSIS;
   HELICOBACTER-PYLORI INFECTION; WNT/BETA-CATENIN PATHWAY; FACILITATES
   TUMOR-GROWTH; GENOME-WIDE ANALYSIS; COLON-CANCER
AB Long noncoding RNA (lncRNA) is a kind of RNAi molecule composed of hundreds to thousands of nucleotides. There are several major types of functional lncRNAs which participate in some important cellular pathways. LncRNA-RNA interaction controls mRNA translation and degradation or serves as a microRNA (miRNA) sponge for silencing. LncRNA-protein interaction regulates protein activity in transcriptional activation and silencing. LncRNA guide, decoy, and scaffold regulate transcription regulators of enhancer or repressor region of the coding genes for alteration of expression. LncRNA plays a role in cellular responses including the following activities: regulation of chromatin structural modification and gene expression for epigenetic and cell function control, promotion of hematopoiesis and maturation of immunity, cell programming in stem cell and somatic cell development, modulation of pathogen infection, switching glycolysis and lipid metabolism, and initiation of autoimmune diseases. LncRNA, together with miRNA, are considered the critical elements in cancer development. It has been demonstrated that tumorigenesis could be driven by homeostatic imbalance of lncRNA/miRNA/cancer regulatory factors resulting in biochemical and physiological alterations inside the cells. Cancer-driven lncRNAs with other cellular RNAs, epigenetic modulators, or protein effectors may change gene expression level and affect the viability, immortality, and motility of the cells that facilitate cancer cell cycle rearrangement, angiogenesis, proliferation, and metastasis. Molecular medicine will be the future trend for development. LncRNA/miRNA could be one of the potential candidates in this category. Continuous studies in lncRNA functional discrepancy between cancer cells and normal cells and regional and rational genetic differences of lncRNA profiles are critical for clinical research which is beneficial for clinical practice.
C1 [Tam, Chit; Wong, Jack Ho; Tsui, Stephen Kwok Wing; Ng, Tzi Bun] Chinese Univ Hong Kong, Sch Biomed Sci, Fac Med, Shatin, Lo Kwee Seong Integrated Biomed Sci Bldg,Area 39, Hong Kong, Peoples R China.
   [Zuo, Tao] Chinese Univ Hong Kong, Dept Med & Therapeut, Fac Med, Shatin, Hong Kong, Peoples R China.
   [Chan, Ting Fung] Chinese Univ Hong Kong, Sch Life Sci, Fac Sci, Shatin, Run Run Shaw Sci Bldg, Hong Kong, Peoples R China.
C3 Chinese University of Hong Kong; Chinese University of Hong Kong;
   Chinese University of Hong Kong
RP Tam, C; Ng, TB (corresponding author), Chinese Univ Hong Kong, Sch Biomed Sci, Fac Med, Shatin, Lo Kwee Seong Integrated Biomed Sci Bldg,Area 39, Hong Kong, Peoples R China.; Chan, TF (corresponding author), Chinese Univ Hong Kong, Sch Life Sci, Fac Sci, Shatin, Run Run Shaw Sci Bldg, Hong Kong, Peoples R China.
EM 1155059540@link.cuhk.edu.hk; tf.chan@cuhk.edu.hk; tzibunng@cuhk.edu.hk
RI Zuo, Tao/AAB-9328-2020; TAM, Chit/IQU-3939-2023; Chan,
   TingFung/A-6161-2013; Tsui, Stephen Kwok-Wing/E-4385-2015
OI Zuo, Tao/0000-0001-8450-5281; TAM, Chit/0000-0002-8719-1190; Chan,
   TingFung/0000-0002-0489-3884; WONG, Jack/0000-0002-9732-986X; Tsui,
   Stephen Kwok-Wing/0000-0003-0686-4259
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NR 406
TC 108
Z9 116
U1 1
U2 51
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0175-7598
EI 1432-0614
J9 APPL MICROBIOL BIOT
JI Appl. Microbiol. Biotechnol.
PD JUN
PY 2019
VL 103
IS 12
BP 4649
EP 4677
DI 10.1007/s00253-019-09837-5
PG 29
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA HZ9QN
UT WOS:000469192100001
PM 31062053
DA 2025-01-04
ER

PT J
AU Ohhara, Y
   Suenaga, M
   Matsusaka, S
   Shinozaki, E
   Mizunuma, N
   Yamaguchi, T
AF Ohhara, Yoshihito
   Suenaga, Mitsukuni
   Matsusaka, Satoshi
   Shinozaki, Eiji
   Mizunuma, Nobuyuki
   Yamaguchi, Toshiharu
TI Comparison between three oxaliplatin-based regimens with bevacizumab in
   patients with metastatic colorectal cancer
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE bevacizumab; early tumor objective response; oxaliplatin; colorectal
   cancer
ID CAPECITABINE PLUS OXALIPLATIN; RANDOMIZED PHASE-III; EARLY TUMOR
   SHRINKAGE; 1ST-LINE TREATMENT; ORAL CAPECITABINE; RETROSPECTIVE
   ANALYSIS; JAPANESE PATIENTS; TARGETED THERAPY; COLON-CANCER; TRIAL
AB Background: A previous pivotal Phase III study (NO16966) demonstrated the benefit of the addition of bevacizumab (BV) to oxaliplatin-based regimens in metastatic colorectal cancer (MCRC). Our study evaluated the safety and efficacy of three oxaliplatin-based chemotherapy regimens (FOLFOX4 [intravenous twice-bolus and twice-infusional 5-fluorouracil/folinic acid plus oxaliplatin], mFOLFOX6 [intravenous once-bolus and once-infusional 5-fluorouracil/folinic acid plus oxaliplatin], and XELOX [capecitabine plus oxaliplatin]) plus BV in the first-line treatment of MCRC patients.
   Methods: Patients with MCRC who started treatment between June 2007 and September 2010 were evaluated in this retrospective cohort study. We also evaluated early objective tumor response (EOTR) within 12 weeks, which was defined as a relative change of >= 30% in the sum of the longest diameters of target lesions when compared with baseline. The primary study endpoints were progression-free survival (PFS) and response rate.
   Results: A total of 185 patients received the following chemotherapy: FOLFOX4 + BV (FF4 arm, n=85), mFOLFOX6 + BV (FF6 arm, n=40), and XELOX + BV (XELOX arm, n=60). The overall response rates were 61.2%, 72.5%, and 75.0% (95% confidence interval: 50.6%-71.8%, 58.0%-87.0%, and 63.7%-86.3%). Median PFS was 18.0, 15.5, and 13.7 months, respectively (log-rank: P=0.254; data cut-off: May 2013). Patients with EOTR (n=117) had significantly better PFS than those without-EOTR (n=68) (17.5 versus 12.7 months, P=0.004).
   Conclusion: This study suggests that these three BV plus oxaliplatin-based treatments might have comparable benefit in terms of tumor response and PFS. Moreover, EOTR may be a predictive factor for PFS in patients with MCRC.
C1 [Ohhara, Yoshihito; Suenaga, Mitsukuni; Matsusaka, Satoshi; Shinozaki, Eiji; Mizunuma, Nobuyuki] Japanese Fdn Canc Res, Canc Inst Hosp, Dept Gastroenterol, Tokyo 1358550, Japan.
   [Ohhara, Yoshihito] Hokkaido Univ, Grad Sch Med, Dept Med Oncol, Sapporo, Hokkaido, Japan.
   [Yamaguchi, Toshiharu] Japanese Fdn Canc Res, Canc Inst Hosp, Dept Gastroenterol Surg, Tokyo 1358550, Japan.
C3 Japanese Foundation for Cancer Research; Hokkaido University; Japanese
   Foundation for Cancer Research
RP Ohhara, Y (corresponding author), Japanese Fdn Canc Res, Canc Inst Hosp, Dept Gastroenterol, Koto Ku, 3-8-31 Ariake, Tokyo 1358550, Japan.
EM yoshihito-ohhara@kkr-smc.com
CR [Anonymous], J CLIN ONCOL S
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NR 36
TC 8
Z9 8
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 529
EP 537
DI 10.2147/OTT.S77190
PG 9
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA CC3DZ
UT WOS:000350226600003
PM 25767397
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Gao, F
   Li, M
   Liu, WB
   Li, W
AF Gao, Feng
   Li, Ming
   Liu, Wenbin
   Li, Wei
TI Inhibition of EGFR Signaling and Activation of Mitochondria! Apoptosis
   Contribute to Tanshinone IIA-Mediated Tumor Suppression in Non-Small
   Cell Lung Cancer Cells
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE non-small cell lung cancer; Tanshinone IIA; epidermal growth factor
   receptor; Mcl-1; ubiquitination
ID COLORECTAL-CANCER; TARGETED THERAPY; RESISTANCE; MCL-1; FBW7
AB Background: Deregulation of epidermal growth factor receptor (EGFR) signaling plays a critical role in non-small cell lung cancer (NSCLC) tumorigenesis. The natural product Tanshinone HA (Tan HA) exhibits significant anti-tumor effect in various human cancers, however, the mechanism remains elusive.
   Methods: The inhibitory effect of Tan HA NSCLC cells was determined by MTS and soft agar assays. The activation of EGFR signaling and the protein level of myeloid cell leukemia 1 (Mcl-1) were examined by immunoblot (IB), immunohistochemical staining (IHC), and ubiquitination analysis. The in vivo anti-tumor effect was validated by the xenograft mouse model.
   Results: Tan HA inhibits NSCLC cells through suppression of EGFR signaling. Tan HA decreases cell viability and colony formation in EGFR wild type and activating mutant cell lines. The IB data further confirmed that Tan HA suppresses EGFR phosphorylation timeand dose-dependently. Tan HA destabilizes Mcl-1 and shortens the half-life. Ubiquitination analysis showed that treatment with Tan HA promotes Mcl-1 ubiquitination and degradation. Further study showed that the downregulation of EGFR-Akt signaling is required for Tan IIA-induced Mcl-1 reduction. Ectopic overexpression of constitutively activated Akt1 compromised these antitumor efficacies in Tan HA-treated NSCLC cells. Finally, Tan HA inhibited the in vivo tumor growth.
   Conclusion: Our data indicate that Tan HA acts as an EGFR signaling inhibitor, and targeting EGFR-Akt-Mcl1 axis could provide a new option for NSCLC treatment.
C1 [Gao, Feng; Li, Ming] Cent South Univ, Xiangya Hosp 3, Cell Transplantat & Gene Therapy Inst, Changsha 410013, Hunan, Peoples R China.
   [Gao, Feng; Li, Wei] Cent South Univ, Xiangya Hosp 3, Dept Ultrasonog, Changsha 410013, Hunan, Peoples R China.
   [Li, Ming] Hunan Univ Chinese Med, Sch Stomatol, Changsha 410208, Hunan, Peoples R China.
   [Li, Ming] Hunan Univ Chinese Med, Changsha Stomatol Hosp, Changsha 410004, Hunan, Peoples R China.
   [Liu, Wenbin] Cent South Univ, Dept Pathol, Affiliated Hunan Canc Hosp, Changsha 410013, Hunan, Peoples R China.
   [Li, Wei] Cent South Univ, Dept Radiol, Xiangya Hosp 3, Changsha 410013, Hunan, Peoples R China.
C3 Central South University; Central South University; Hunan University of
   Chinese Medicine; Hunan University of Chinese Medicine; Central South
   University; Central South University
RP Li, W (corresponding author), Cent South Univ, Xiangya Hosp 3, Dept Ultrasonog, Changsha 410013, Hunan, Peoples R China.; Li, W (corresponding author), Cent South Univ, Dept Radiol, Xiangya Hosp 3, Changsha 410013, Hunan, Peoples R China.
EM weililx@csu.edu.cn
RI Liu, Wenbin/GVU-0680-2022
OI li, wei/0000-0002-7267-6494
FU National Natural Science Foundation of China [81904262, 81972837];
   Natural Science Foundation of Hunan Province [2018JJ3787, 2018JJ2604,
   2019JJ50682]
FX This work was supported by the National Natural Science Foundation of
   China (No.81904262, and No.81972837), the Natural Science Foundation of
   Hunan Province (2018JJ3787, 2018JJ2604, 2019JJ50682).
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NR 41
TC 21
Z9 21
U1 2
U2 18
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 2020
VL 13
BP 2757
EP 2769
DI 10.2147/OTT.S246606
PG 13
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA KZ0SF
UT WOS:000522981200001
PM 32308411
OA Green Published, gold
DA 2025-01-04
ER

PT J
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   Fröhling, S
AF Horak, Peter
   Klink, Barbara
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   Hutter, Barbara
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   Huebschmann, Daniel
   Schlesner, Matthias
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   Pfuetze, Katrin
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   Wolf, Stephan
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   Penzel, Roland
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   Kirchner, Martina
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   Endris, Volker
   Singer, Stephan
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   Stenzinger, Albrecht
   Schlenk, Richard F.
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   Brors, Benedikt
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   Glimm, Hanno
   Froehling, Stefan
TI Precision oncology based on omics data: The NCT Heidelberg experience
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE next-generation sequencing; precision oncology; whole-exome sequencing;
   clinical trial design; personalized medicine
ID KINASE INHIBITOR TREATMENT; PHASE PROTEIN ARRAYS; GENE COPY NUMBER;
   COLORECTAL-CANCER; TARGETED THERAPY; XENOGRAFT MODELS; BREAST-CANCER;
   PATIENT; TRIALS; RESISTANCE
AB Precision oncology implies the ability to predict which patients will likely respond to specific cancer therapies based on increasingly accurate, high-resolution molecular diagnostics as well as the functional and mechanistic understanding of individual tumors. While molecular stratification of patients can be achieved through different means, a promising approach is next-generation sequencing of tumor DNA and RNA, which can reveal genomic alterations that have immediate clinical implications. Furthermore, certain genetic alterations are shared across multiple histologic entities, raising the fundamental question of whether tumors should be treated by molecular profile and not tissue of origin. We here describe MASTER (Molecularly Aided Stratification for Tumor Eradication Research), a clinically applicable platform for prospective, biology-driven stratification of younger adults with advanced-stage cancer across all histologies and patients with rare tumors. We illustrate how a standardized workflow for selection and consenting of patients, sample processing, whole-exome/genome and RNA sequencing, bioinformatic analysis, rigorous validation of potentially actionable findings, and data evaluation by a dedicated molecular tumor board enables categorization of patients into different intervention baskets and formulation of evidence-based recommendations for clinical management. Critical next steps will be to increase the number of patients that can be offered comprehensive molecular analysis through collaborations and partnering, to explore ways in which additional technologies can aid in patient stratification and individualization of treatment, to stimulate clinically guided exploratory research projects, and to gradually move away from assessing the therapeutic activity of targeted interventions on a case-by-case basis toward controlled clinical trials of genomics-guided treatments.
C1 [Horak, Peter; Heining, Christoph; Groeschel, Stefan; Richter, Daniela; Pfuetze, Katrin; Geoerg, Christina; Meissburger, Bettina; von Kalle, Christof; Glimm, Hanno; Froehling, Stefan] German Canc Res Ctr, Natl Ctr Tumor Dis NCT Heidelberg, Dept Translat Oncol, Heidelberg, Germany.
   [Horak, Peter; Heining, Christoph; Groeschel, Stefan; von Kalle, Christof; Glimm, Hanno; Froehling, Stefan] Heidelberg Univ Hosp, Sect Personalized Oncol, Heidelberg, Germany.
   [Klink, Barbara; Schroeck, Evelin] Tech Univ Dresden, Inst Clin Genet, Fac Med Carl Gustav Carus, Dresden, Germany.
   [Klink, Barbara; Schroeck, Evelin] German Canc Consortium DKTK, Dresden, Germany.
   [Klink, Barbara; Schroeck, Evelin] German Canc Res Ctr, Heidelberg, Germany.
   [Klink, Barbara; Schroeck, Evelin] Natl Ctr Tumor Dis NCT, Dresden, Germany.
   [Groeschel, Stefan] German Canc Res Ctr, Res Grp Mol Leukemogenesis, Heidelberg, Germany.
   [Groeschel, Stefan] NCT Heidelberg, Dept Med Oncol, Heidelberg, Germany.
   [Groeschel, Stefan] Heidelberg Univ Hosp, Heidelberg, Germany.
   [Groeschel, Stefan; Schirmacher, Peter; Stenzinger, Albrecht; Brors, Benedikt; von Kalle, Christof; Glimm, Hanno; Froehling, Stefan] DKTK, Heidelberg, Germany.
   [Hutter, Barbara; Froehlich, Martina; Uhrig, Sebastian; Brors, Benedikt] DKFZ, Div Appl Bioinformat, Heidelberg, Germany.
   [Hutter, Barbara; Froehlich, Martina; Uhrig, Sebastian; Brors, Benedikt] NCT Heidelberg, Heidelberg, Germany.
   [Huebschmann, Daniel; Schlesner, Matthias; Eils, Roland] DKFZ, Div Theoret Bioinformat, Heidelberg, Germany.
   [Eils, Roland] Heidelberg Univ, Inst Pharm & Mol Biotechnol & BioQuant, Dept Bioinformat & Funct Genom, Heidelberg, Germany.
   [Huebschmann, Daniel] Heidelberg Univ Hosp, Dept Pediat Immunol Hematol & Oncol, Heidelberg, Germany.
   [Pfuetze, Katrin; Geoerg, Christina; Meissburger, Bettina; von Kalle, Christof] DKFZ Heidelberg Ctr Personalized Oncol HIPO, Heidelberg, Germany.
   [Wolf, Stephan; Schulz, Angela] DKFZ, Genom & Prote Core Facil, Heidelberg, Germany.
   [Penzel, Roland; Herpel, Esther; Kirchner, Martina; Lier, Amelie; Endris, Volker; Singer, Stephan; Schirmacher, Peter; Stenzinger, Albrecht] Heidelberg Univ Hosp, Inst Pathol, Heidelberg, Germany.
   [Weichert, Wilko] Tech Univ Munich, Inst Pathol, Munich, Germany.
   [Weichert, Wilko] DKTK, Munich, Germany.
   [Schlenk, Richard F.] NCT Heidelberg, NCT Trial Ctr, Heidelberg, Germany.
C3 Helmholtz Association; German Cancer Research Center (DKFZ); Ruprecht
   Karls University Heidelberg; Ruprecht Karls University Heidelberg;
   Technische Universitat Dresden; Helmholtz Association; German Cancer
   Research Center (DKFZ); Helmholtz Association; German Cancer Research
   Center (DKFZ); Helmholtz Association; German Cancer Research Center
   (DKFZ); Ruprecht Karls University Heidelberg; Helmholtz Association;
   German Cancer Research Center (DKFZ); Helmholtz Association; German
   Cancer Research Center (DKFZ); Ruprecht Karls University Heidelberg;
   Ruprecht Karls University Heidelberg; Helmholtz Association; German
   Cancer Research Center (DKFZ); Helmholtz Association; German Cancer
   Research Center (DKFZ); Ruprecht Karls University Heidelberg; Helmholtz
   Association; German Cancer Research Center (DKFZ); Ruprecht Karls
   University Heidelberg; Ruprecht Karls University Heidelberg; Helmholtz
   Association; German Cancer Research Center (DKFZ); Ruprecht Karls
   University Heidelberg; Technical University of Munich; Helmholtz
   Association; German Cancer Research Center (DKFZ); Ruprecht Karls
   University Heidelberg
RP Glimm, H; Fröhling, S (corresponding author), German Canc Res Ctr, Natl Ctr Tumor Dis NCT Heidelberg, Dept Translat Oncol, Heidelberg, Germany.
EM hanno.glimm@nct-heidelberg.de
RI Heining, Christoph/IUO-2974-2023; Schlenk, Richard/AAG-3218-2019; Horak,
   Peter/ABC-1587-2021; Brors, Benedikt/E-5620-2013; Schlesner,
   Matthias/I-4030-2013; Eils, Roland/B-6121-2009
OI Klink, Barbara/0000-0002-8753-8238; Horak, Peter/0000-0003-4536-9306;
   Brors, Benedikt/0000-0001-5940-3101; Hubschmann,
   Daniel/0000-0002-6041-7049; von Kalle, Christof/0000-0001-9221-3297;
   Schlesner, Matthias/0000-0002-5896-4086; Eils,
   Roland/0000-0002-0034-4036
FU PharmaMar; AstraZeneca; Pfizer; Novartis; Thermo Fisher; Illumina
FX SF and RFS have received research support from PharmaMar, AstraZeneca,
   and Pfizer. AS is an advisory board member for Novartis, AstraZeneca,
   and Thermo Fisher and has received honoraria for speeches from Novartis,
   AstraZeneca, Thermo Fisher, and Illumina. WW has worked as advisor for
   Roche, BMS, MSD, Novartis, AstraZeneca, Boehringer, and Pfizer and has
   joint research projects with Roche and Bruker. The other authors declare
   no financial disclosures or conflicts of interest.
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NR 61
TC 126
Z9 126
U1 0
U2 22
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD SEP 1
PY 2017
VL 141
IS 5
BP 877
EP 886
DI 10.1002/ijc.30828
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EZ6QJ
UT WOS:000404842200003
PM 28597939
OA Green Submitted, Bronze
DA 2025-01-04
ER

PT J
AU Moryoussef, F
   Dhooge, M
   Volet, J
   Barbe, C
   Brezault, C
   Hoeffel, C
   Coriat, R
   Bouché, O
AF Moryoussef, Frederick
   Dhooge, Marion
   Volet, Julien
   Barbe, Coralie
   Brezault, Catherine
   Hoeffel, Christine
   Coriat, Romain
   Bouche, Olivier
TI Reversible sarcopenia in patients with gastrointestinal stromal tumor
   treated with imatinib
SO JOURNAL OF CACHEXIA SARCOPENIA AND MUSCLE
LA English
DT Article
DE Imatinib; C-kit inhibitors; Sarcopenia; Gastrointestinal stromal
   tumours; Toxicity; Body composition
ID BODY-MASS INDEX; RENAL-CELL CARCINOMA; SKELETAL-MUSCLE; CANCER-PATIENTS;
   CHEMOTHERAPY TOXICITY; COLORECTAL-CANCER; CACHEXIA; IMPACT; DETERMINANT;
   SURVIVAL
AB Background Imatinib is a long-term, oral, targeted therapy for high-risk resected and advanced gastrointestinal stromal tumours (GIST). It is known that sarcopenia affects prognosis and treatment tolerance in patients with various solid cancers. We analysed lumbar skeletal muscle index changes in imatinib-treated GIST patients. Imatinib tolerance was also assessed to evaluate the influence of pre-treatment sarcopenia.
   Methods Thirty-one patients with advanced (n = 16) or high-risk resected (n = 15) GIST treated with imatinib (400 mg/day) were analysed retrospectively. Lumbar skeletal muscle indexes were evaluated on computed tomography images obtained before starting imatinib for all patients and at 6 months for those initially sarcopenic. Sarcopenia was defined using consensual cutoffs. Imatinib-induced toxicities were assessed after 3 months of administration.
   Results Twelve (38.7%) of the 31 patients were sarcopenic, including one unassessable at 6 months. Seven (63.6%) of the 11 assessable sarcopenic patients became non-sarcopenic after 6 months of imatinib. Pre-treatment sarcopenia was not associated with grades 3-4 toxicities, but the mean number of all-grade toxicities per sarcopenic patient was significantly higher for those non-sarcopenic (4.1 vs. 1.7, respectively, p < 0.01) after 3 months of treatment. Grades 1-2 anaemia and grades 1-2 fatigue were more frequent for sarcopenic than non-sarcopenic patients (83% vs. 26%, P < 0.01 and 42% vs. 5%, P = 0.02, respectively).
   Conclusions Sarcopenia is reversible in some GIST patients treated with imatinib. Pre-imatinib sarcopenia is predictive of non-severe toxicities, particularly anaemia and fatigue.
C1 [Moryoussef, Frederick; Volet, Julien; Bouche, Olivier] Hop Robert Debre, CHU Reims, Dept Gastroenterol & Digest Oncol, F-51092 Reims, France.
   [Dhooge, Marion; Barbe, Coralie; Brezault, Catherine; Coriat, Romain] Univ Paris 05, Sorbonne Paris Cite, Cochin Teaching Hosp, AP HP,Dept Gastroenterol, Paris, France.
   [Barbe, Coralie] Hop Robert Debre, CHU Reims, Clin Res Unit, F-51092 Reims, France.
   [Hoeffel, Christine] Hop Robert Debre, CHU Reims, Dept Radiol, F-51092 Reims, France.
C3 CHU de Reims; Universite de Reims Champagne-Ardenne; Universite Paris
   Cite; Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
   Cochin - APHP; Universite de Reims Champagne-Ardenne; CHU de Reims; CHU
   de Reims; Universite de Reims Champagne-Ardenne
RP Moryoussef, F (corresponding author), Hop Robert Debre, CHU Reims, Dept Gastroenterol & Digest Oncol, Ave Gen Koenig, F-51092 Reims, France.
EM Fr.moryoussef@gmail.com
RI Coriat, Romain/O-7902-2017
OI Dhooge, Marion/0000-0002-7279-5549
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NR 39
TC 33
Z9 35
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2190-5991
EI 2190-6009
J9 J CACHEXIA SARCOPENI
JI J. Caxhexia Sarcopenia Muscle
PD DEC
PY 2015
VL 6
IS 4
BP 343
EP 350
DI 10.1002/jcsm.12047
PG 8
WC Geriatrics & Gerontology; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Geriatrics & Gerontology; General & Internal Medicine
GA CX2OP
UT WOS:000365536800012
PM 26673372
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Gonzalez, NS
   López, D
   Gómez, D
   Ros, J
   Baraibar, I
   Salva, F
   Tabernero, J
   Élez, E
AF Saoudi Gonzalez, Nadia
   Lopez, Daniel
   Gomez, Diego
   Ros, Javier
   Baraibar, Iosune
   Salva, Francesc
   Tabernero, Josep
   Elez, Elena
TI Pharmacokinetics and pharmacodynamics of approved monoclonal antibody
   therapy for colorectal cancer
SO EXPERT OPINION ON DRUG METABOLISM & TOXICOLOGY
LA English
DT Review
DE Bispecific antibody; colorectal cancer; monoclonal antibody;
   pharmacodynamics; pharmacokinetics
ID TRASTUZUMAB DERUXTECAN DS-8201; PROGRESSION-FREE SURVIVAL; CONTROLLED
   PHASE-II; GROWTH-FACTOR VEGF; OPEN-LABEL; CLINICAL PHARMACOKINETICS;
   DOUBLE-BLIND; MICROSATELLITE INSTABILITY; PANITUMUMAB MONOTHERAPY;
   1ST-LINE TREATMENT
AB IntroductionThe introduction of monoclonal antibodies to the chemotherapy backbone treatment has challenged the paradigm of metastatic colorectal cancer (mCRC) treatment. Their mechanism of action and pharmacokinetics are complex but important to understand in order to improve patient selection and treatment outcomes for mCRC population.Areas coveredThis review examines the scientific data, pharmacodynamics, and pharmacokinetics of approved monoclonal antibodies used to treat mCRC patients, including agents targeting signaling via VEGFR (bevacizumab and ramucirumab), EGFR (cetuximab and panitumumab), HER2/3 target therapy, and immunotherapy agents such as pembrolizumab or nivolumab. Efficacy and mechanism of action of bispecific antibodies are also covered.Expert opinionmCRC is a heterogeneous disease and the optimal selection and sequence of treatments is challenging. Monoclonal antibodies have complex pharmacokinetics and pharmacodynamics, with important interactions between them. The arrival of bioequivalent molecules to the market increases the need for the characterization of pharmacokinetics and pharmacodynamics of classic monoclonal antibodies to reach bioequivalent novel molecules.
C1 [Saoudi Gonzalez, Nadia; Lopez, Daniel; Gomez, Diego; Ros, Javier; Baraibar, Iosune; Salva, Francesc; Tabernero, Josep; Elez, Elena] Med Oncol Dept, Vall dHebron Barcelona Hosp Campus, Barcelona, Spain.
   [Saoudi Gonzalez, Nadia; Ros, Javier; Baraibar, Iosune; Salva, Francesc; Tabernero, Josep; Elez, Elena] Vall dHebron Inst Oncol, Vhio Barcelona, Med Oncol Dept, Barcelona, Spain.
C3 Vall d'Hebron Institut d'Oncologia (VHIO)
RP Élez, E (corresponding author), Med Oncol Dept, Vall dHebron Barcelona Hosp Campus, Barcelona, Spain.; Élez, E (corresponding author), Vall dHebron Inst Oncol, Vhio Barcelona, Med Oncol Dept, Barcelona, Spain.
EM meelez@vhio.net
RI Baraibar, Iosune/GXF-7067-2022; Ros, Javier/HKF-1171-2023
OI Ros, Javier/0000-0002-8137-5415; Salva, Francesc/0000-0001-9240-4907;
   Baraibar, Iosune/0000-0002-3500-9641; Lopez-Valbuena,
   Daniel/0000-0002-8458-516X
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NR 120
TC 5
Z9 5
U1 6
U2 23
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1742-5255
EI 1744-7607
J9 EXPERT OPIN DRUG MET
JI Expert Opin. Drug Metab. Toxicol.
PD NOV 2
PY 2022
VL 18
IS 11
BP 755
EP 767
DI 10.1080/17425255.2022.2160316
EA DEC 2022
PG 13
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA 7P3ZK
UT WOS:000905224700001
PM 36582117
DA 2025-01-04
ER

PT J
AU Campbell, BK
   Gao, ZJ
   Corcoran, NM
   Stylli, SS
   Hovens, CM
AF Campbell, Bethany K.
   Gao, Zijie
   Corcoran, Niall M.
   Stylli, Stanley S.
   Hovens, Christopher M.
TI Molecular Mechanisms Driving the Formation of Brain Metastases
SO CANCERS
LA English
DT Review
DE brain metastases; genomics; secondary brain tumor; primary tumor;
   metastasis
ID BREAST-CANCER CELLS; MELANOMA; REVEALS; EVOLUTION; DIAGNOSIS; TISSUE
AB Simple Summary Brain metastases are the most common brain tumor in adults and are associated with poor prognosis. The propensity of different solid tumors to metastasize varies greatly, with lung, breast, and melanoma primary tumors commonly leading to brain metastases, while other primaries such as prostate rarely metastasize to the brain. The molecular mechanisms that predispose and facilitate brain metastasis development are poorly understood. In this review, we present the current data on the genomic landscape of brain metastases that arise from various primary cancers and also outline potential molecular mechanisms that drive the formation of distant metastases in the brain. Targeted therapies for cancers have improved primary tumor response rates, but concomitantly, brain metastases (BM) have become the most common brain tumors in adults and are associated with a dismal prognosis of generally less than 6 months, irrespective of the primary cancer type. They most commonly occur in patients with primary breast, lung, or melanoma histologies; however, they also appear in patients with other primary cancers including, but not limited to, prostate cancer, colorectal cancer, and renal cell carcinoma. Historically, molecular biomarkers have normally been identified from primary tumor resections. However, clinically informative genomic alterations can occur during BM development and these potentially actionable alterations are not always detected in the primary tumor leading to missed opportunities for effective targeted therapy. The molecular mechanisms that facilitate and drive metastasis to the brain are poorly understood. Identifying the differences between the brain and other extracranial sties of metastasis, and between primary tumors and BM, is essential to improving our understanding of BM development and ultimately patient management and survival. In this review, we present the current data on the genomic landscape of BM from various primary cancers which metastasize to the brain and outline potential mechanisms which may play a role in promoting the formation of the distant metastases in the brain.
C1 [Campbell, Bethany K.; Gao, Zijie; Corcoran, Niall M.; Stylli, Stanley S.; Hovens, Christopher M.] Univ Melbourne, Dept Surg, Parkville, Vic 3050, Australia.
   [Campbell, Bethany K.; Corcoran, Niall M.; Hovens, Christopher M.] Univ Melbourne, Victorian Comprehens Canc Ctr, Ctr Canc Res, Parkville, Vic 3050, Australia.
   [Corcoran, Niall M.] Royal Melbourne Hosp, Dept Urol, Parkville, Vic 3050, Australia.
   [Corcoran, Niall M.] Western Hlth, Dept Urol, Footscray, Vic 3011, Australia.
   [Corcoran, Niall M.] Victorian Comprehens Canc Ctr, Melbourne, Vic 3000, Australia.
   [Stylli, Stanley S.] Royal Melbourne Hosp, Dept Neurosurg, Parkville, Vic 3050, Australia.
C3 University of Melbourne; University of Melbourne; Melbourne Health;
   Royal Melbourne Hospital; University of Melbourne; Melbourne Health;
   Royal Melbourne Hospital
RP Hovens, CM (corresponding author), Univ Melbourne, Dept Surg, Parkville, Vic 3050, Australia.; Hovens, CM (corresponding author), Univ Melbourne, Victorian Comprehens Canc Ctr, Ctr Canc Res, Parkville, Vic 3050, Australia.
EM chovens@unimelb.edu.au
RI stylli, stanley/R-7540-2019; Corcoran, Niall/AAO-6295-2021; Stylli,
   Stanley/N-5982-2016
OI Stylli, Stanley/0000-0002-3505-7387; Campbell,
   Bethany/0000-0001-6859-8158
FU NHMRC [1162514]; PRECEPT program grant; Movember; Australian Federal
   Government; Movember-Distinguished Gentleman's Ride Clinician Scientist
   Award through the Prostate Cancer Foundation of Australia's Research
   Program
FX Support for this work was provided through the NHMRC project grant
   1162514 to C.M.H. and the PRECEPT program grant, co-funded by Movember
   and the Australian Federal Government to N.M.C. N.M.C. was also
   supported by a David Bickart Clinician Researcher Fellowship from the
   Faculty of Medicine, Dentistry and Health Sciences, University of
   Melbourne, and more recently by a Movember-Distinguished Gentleman's
   Ride Clinician Scientist Award through the Prostate Cancer Foundation of
   Australia's Research Program.
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NR 71
TC 10
Z9 10
U1 2
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD OCT
PY 2022
VL 14
IS 19
AR 4963
DI 10.3390/cancers14194963
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5G0LE
UT WOS:000866698900001
PM 36230886
OA gold, Green Published
DA 2025-01-04
ER

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   Hashimoto, D
   Chikamoto, A
   Baba, H
AF Hayashi, Hiromitsu
   Beppu, Toru
   Sakamoto, Yasuo
   Miyamoto, Yuji
   Yokoyama, Naomi
   Higashi, Takaaki
   Nitta, Hidetoshi
   Hashimoto, Daisuke
   Chikamoto, Akira
   Baba, Hideo
TI Prognostic value of Ki-67 expression in conversion therapy for
   colorectal liver-limited metastases
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE Colorectal cancer; liver metastasis; conversion therapy; Ki-67 index
ID RANDOMIZED PHASE-III; LONG-TERM SURVIVAL; PLUS FOLINIC ACID; TARGETED
   THERAPY; CANCER PATIENTS; CHEMOTHERAPY; SURGERY; RESECTION;
   FLUOROURACIL; IRINOTECAN
AB Introduction: The objective of this study was to examine the prognostic value of Ki-67 expression in conversion therapy for colorectal liver-confined metastases. Methods: We enrolled a total of 96 patients including 54 patients who received oxaliplatin-or irinotecan-based chemotherapy and curative hepatectomy for initially unresectable metastases (conversion group) and 42 patients with initially resectable liver metastases (straight hepatectomy group). Ki-67 expression was examined in 96 resected specimens but excluded the 2 specimens that revealed no residual cancer cells in conversion group. Results: Conversion therapy leads to greater survival that is equivalent to that straight hepatectomy group. In conversion group, high Ki-67 expression (> 30%) levels were detectable in 33 patients (64%) after chemotherapy prior to conversion therapy. High Ki-67 expression was significantly associated with shorter disease-free survival and worse overall survival (P < 0.01 in both), and was an independent worse prognostic factor of disease-free survival and overall survival (hazard ratio [HR] and P-values were 5.608, 0.001 and 5.366, 0.04, respectively) in patients with conversion therapy. Interestingly, even in the patients with RECIST PR (n = 32), high Ki-67 expression was significantly shorter disease-free survival compared to low Ki-67 expression (P < 0.001). In contrast to conversion group, there was no significant difference in disease free survival and overall survival between low (n = 14, 33%) and high (n = 28, 67%) Ki-67 expressions in patients with straight hepatectomy (P = 0.14 and 0.74, respectively). Conclusions: Residual Ki-67 expression is a useful biomarker for worse prognostic outcomes after conversion therapy. High Ki-67 expression may be a biomarker of micrometastases containing aggressive cancer cells.
C1 [Hayashi, Hiromitsu; Beppu, Toru; Sakamoto, Yasuo; Miyamoto, Yuji; Yokoyama, Naomi; Higashi, Takaaki; Nitta, Hidetoshi; Hashimoto, Daisuke; Chikamoto, Akira; Baba, Hideo] Kumamoto Univ, Grad Sch Life Sci, Dept Gastroenterol Surg, Kumamoto 8608556, Japan.
C3 Kumamoto University
RP Baba, H (corresponding author), Kumamoto Univ, Grad Sch Life Sci, Dept Gastroenterol Surg, 1-1-1 Honjo, Kumamoto 8608556, Japan.
EM hdoba-ba@kumamoto-u.ac.jp
RI Hashimoto, Daisuke/AAE-7134-2020
FU Ministry of Education, Culture, Sports, Science, and Technology of Japan
   [24791434]; Japanese Foundation for Multidisciplinary Treatment of
   Cancer, Japan; Grants-in-Aid for Scientific Research [24791434] Funding
   Source: KAKEN
FX This work was supported by Grant-in-Aid for Young Scientists (B); the
   Ministry of Education, Culture, Sports, Science, and Technology of
   Japan, No. 24791434 (to H.H.); and Japanese Foundation for
   Multidisciplinary Treatment of Cancer, Japan (to H.H.).
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NR 32
TC 16
Z9 18
U1 0
U2 3
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 2015
VL 5
IS 3
BP 1225
EP +
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CI5DJ
UT WOS:000354772800028
PM 26046001
DA 2025-01-04
ER

PT J
AU Perkhofer, L
   Ettrich, TJ
   Seufferlein, T
AF Perkhofer, Lukas
   Ettrich, Thomas J.
   Seufferlein, Thomas
TI Pancreatic Cancer: Progress in Systemic Therapy
SO GASTROINTESTINAL TUMORS
LA English
DT Review
DE Chemotherapy; Pancreas; Pancreatic cancer; Therapy
ID PHASE-II TRIAL; METASTATIC COLORECTAL-CANCER; GEMCITABINE-BASED
   CHEMORADIATION; COOPERATIVE-ONCOLOGY-GROUP; NAB-PACLITAXEL; ADJUVANT
   CHEMOTHERAPY; RESECTABLE ADENOCARCINOMA; OXALIPLATIN FOLFIRINOX;
   2ND-LINE CHEMOTHERAPY; FOLINIC ACID
AB Background: Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer-related deaths in the Western world. Due to lack of specific symptoms and no accessible precursor lesions, primary diagnosis is commonly delayed, resulting in the identification of only 15-20% of patients with potentially curable disease. The major limiting factor is an already locally advanced or metastatic disease at the time of diagnosis. Consequently, systemic therapy forms the backbone of treatment strategy for the majority of patients. Summary: A deeper understanding of the molecular characteristics of pancreatic cancer has led to the identification of several potential therapeutic targets. A variety of targeted therapies are currently under clinical evaluation as single agents or in combination with chemotherapy for PDAC. This review highlights the current state of chemotherapy in pancreatic cancer and provides an outlook on its future perspectives. Key Message: This review focuses on the current chemotherapy regimens for the systemic treatment of PDAC. Practical Implications: Various neoadjuvant approaches have been explored, including chemoradiation, chemotherapy followed by chemoradiation or intensified chemotherapy without defining a standard of care so far. The standard of care is gemcitabine or 5-fluorouracil. The oral fluoropyrimidine S-1 may be a promising new agent in this setting. For first-line treatment of metastatic pancreatic cancer, no targeted therapy has yet demonstrated clinical benefit apart from the combination of the tyrosine kinase inhibitor erlotinib plus gemcitabine. Recently, novel chemotherapeutic regimens such as FOLFIRINOX and gemcitabine plus nanoparticle albumin-bound paclitaxel have been introduced. Both combinations have proved to be superior to the standard gemcitabine regimen. For second-line treatment the combination of 5-fluorouracil/leucovorin and oxaliplatin yields improved results compared to best supportive care. (C) 2015 S. Karger AG, Basel
C1 [Perkhofer, Lukas; Ettrich, Thomas J.; Seufferlein, Thomas] Ulm Univ Hosp, Dept Internal Med 1, Albert Einstein Allee 23, DE-89081 Ulm, Germany.
C3 Ulm University
RP Seufferlein, T (corresponding author), Ulm Univ Hosp, Dept Internal Med 1, Albert Einstein Allee 23, DE-89081 Ulm, Germany.
EM thomas.seufferlein@uniklinik-ulm.de
RI Seufferlein, Thomas/P-7147-2018; Ettrich, Thomas/JZE-1092-2024
OI Ettrich, Thomas J./0000-0002-7654-2442
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NR 80
TC 10
Z9 12
U1 1
U2 6
PU Maximum Academic Press
PI Fayetteville
PA 1833 Highway 85 S, Fayetteville, Georgia, UNITED STATES
SN 2296-3774
EI 2296-3766
J9 GASTROINTEST TUMORS
JI Gastrointest. Tumors
PY 2015
VL 1
IS 4
BP 167
EP 179
DI 10.1159/000380785
PG 13
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA V3W7G
UT WOS:000218656300001
PM 26672477
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Rosati, G
   Montrone, M
   Pacilio, C
   Colombo, A
   Cicero, G
   Paragliola, F
   Vaia, A
   Annunziata, L
   Bilancia, D
AF Rosati, Gerardo
   Montrone, Michele
   Pacilio, Carmen
   Colombo, Alfredo
   Cicero, Giuseppe
   Paragliola, Fernando
   Vaia, Angelo
   Annunziata, Luigi
   Bilancia, Domenico
TI An Update on the Role of Anti-EGFR in the Treatment of Older Patients
   with Metastatic Colorectal Cancer
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE cetuximab; metastatic colorectal cancer; older patients; panitumumab
ID CETUXIMAB PLUS CAPECITABINE; SINGLE-AGENT PANITUMUMAB; FRAIL
   ELDERLY-PATIENTS; RANDOMIZED PHASE-III; 1ST-LINE TREATMENT;
   INTERNATIONAL-SOCIETY; OPEN-LABEL; GERIATRIC ASSESSMENT; POOLED
   ANALYSIS; IRINOTECAN
AB Although colorectal cancer is increasingly being diagnosed in older patients, their number is largely underrepresented in phase II or III clinical trials. Consequently, guidelines and the SIOG recommendations are not sufficiently clear regarding the treatment of these patients, particularly when chemotherapy is combined with monoclonal antibodies (bevacizumab, cetuximab, and panitumumab). Targeted therapy based on the use of anti-epidermal growth factor receptors (EGFRs) is conditioned by the potential for increased toxicity, making it more difficult to treat an older, rat sarcoma virus (RAS) and B rapidly accelerated fibrosarcoma (BRAF) wild-type patient. In light of a more detailed characterization of the older population, modernly differentiable between fit, vulnerable, or frail patients on the basis of the comprehensive geriatric assessment, and of the analysis of more recent studies, this review fully collects data from the literature, differentiating the results on functional status patients.
C1 [Rosati, Gerardo; Paragliola, Fernando; Vaia, Angelo; Annunziata, Luigi; Bilancia, Domenico] San Carlo Hosp, Med Oncol Unit, I-85100 Potenza, Italy.
   [Montrone, Michele] IRCCS Ist Tumori Giovanni Paolo 2, Med Thorac Oncol Unit, I-70124 Bari, Italy.
   [Pacilio, Carmen] IRCCS Ist Tumori G Pascale, Med Breast Canc Dept, I-80131 Naples, Italy.
   [Colombo, Alfredo] CDC Macchiarella, Med Oncol Unit, I-90138 Palermo, Italy.
   [Cicero, Giuseppe] Univdegli Studi Palermo, Med Oncol, I-90133 Palermo, Italy.
RP Rosati, G (corresponding author), San Carlo Hosp, Med Oncol Unit, I-85100 Potenza, Italy.
EM oncogerry@yahoo.it
RI Rosati, Gerardo/AAH-5676-2020; Colombo, Alfredo/KOD-1042-2024; Montrone,
   Michele/AAD-8560-2020
OI Rosati, Gerardo/0000-0001-7004-6862
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NR 45
TC 1
Z9 1
U1 1
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 DEC
PY 2022
VL 11
IS 23
AR 7108
DI 10.3390/jcm11237108
PG 15
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 6X3BP
UT WOS:000896292900001
PM 36498683
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Underwood, JJ
   Quadri, RS
   Kalva, SP
   Shah, H
   Sanjeeviah, AR
   Beg, MS
   Sutphin, PD
AF Underwood, Jacob J.
   Quadri, Rehan S.
   Kalva, Sanjeeva P.
   Shah, Hriday
   Sanjeeviah, Aravind R.
   Beg, Muhammad S.
   Sutphin, Patrick D.
TI Liquid Biopsy for Cancer: Review and Implications for the Radiologist
SO RADIOLOGY
LA English
DT Review
ID CIRCULATING TUMOR-CELLS; METASTATIC BREAST-CANCER; KRAS MUTATION STATUS;
   LUNG-CANCER; PANCREATIC-CANCER; ACQUIRED-RESISTANCE; COLORECTAL-CANCER;
   PERIPHERAL-BLOOD; RECTAL-CANCER; DIGITAL PCR
AB Imaging and image-guided procedures play an imperative role in the screening, diagnosis, and surveillance of cancer. Although emerging imaging techniques now enable more precise molecular characterization of tumors, to multigenetic tumor profiling for targeted therapeutic selection remains limited to direct tissue acquisition. Even in the context of targeted therapy, tumors adapt to acquire resistance. This necessitates serial monitoring, traditionally through tissue acquisition, to identify the molecular mechanism of resistance and to guide second-line therapy. An alternative to tissue acquisition is the collection of circulating tumor markers such as cell-free nucleic acids and circulating tumor cells in the peripheral blood. This noninvasive diagnostic approach is referred to as the liquid biopsy. The liquid biopsy is currently used clinically for therapeutic guidance when tissue acquisition is impossible or when the specimen is inadequate. It is also being studied in the context of screening, diagnosis, and surveillance. As cancer treatment continues to move toward a focus on precision medicine, this developing technology may alter and/or augment the role of imaging in the management of cancer. This review aims to outline the use of liquid biopsy in cancer and its potential impact on diagnostic imaging and image-guided procedures. (C) RSNA, 2019
C1 [Underwood, Jacob J.] Univ North Texas, Texas Coll Osteopath Med, Hlth Sci Ctr, Ft Worth, TX USA.
   [Quadri, Rehan S.; Shah, Hriday; Sutphin, Patrick D.] Univ Texas Southwestern Med Ctr Dallas, Dept Radiol, Div Intervent Radiol, Dallas, TX 75390 USA.
   [Kalva, Sanjeeva P.; Sutphin, Patrick D.] Massachusetts Gen Hosp, Dept Radiol, Div Intervent Radiol, 55 Fruit Sr,GRB 290, Boston, MA 02114 USA.
   [Sanjeeviah, Aravind R.; Beg, Muhammad S.] Univ Texas Southwestern Med Ctr Dallas, Dept Internal Med, Div Hematol Oncol, Dallas, TX 75390 USA.
   [Underwood, Jacob J.] Spokane Teaching Hlth Ctr, Transit Year Program, Spokane, WA USA.
   [Quadri, Rehan S.] Univ Virginia, Dept Radiol, Div Intervent Nal Radiol, Charlottesville, VA USA.
   [Kalva, Sanjeeva P.] Huron Valley Radiol, Ypsilanti, MI USA.
C3 University of North Texas System; University of North Texas Denton;
   University of Texas System; University of Texas Southwestern Medical
   Center Dallas; Harvard University; Massachusetts General Hospital;
   University of Texas System; University of Texas Southwestern Medical
   Center Dallas; University of Virginia
RP Sutphin, PD (corresponding author), Univ Texas Southwestern Med Ctr Dallas, Dept Radiol, Div Intervent Radiol, Dallas, TX 75390 USA.; Sutphin, PD (corresponding author), Massachusetts Gen Hosp, Dept Radiol, Div Intervent Radiol, 55 Fruit Sr,GRB 290, Boston, MA 02114 USA.
EM psutphin@mgh.harvard.edu
OI Sutphin, Patrick/0000-0001-9393-1952; Kalva,
   Sanjeeva/0000-0002-4988-5714
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NR 100
TC 52
Z9 57
U1 1
U2 23
PU RADIOLOGICAL SOC NORTH AMERICA (RSNA)
PI OAK BROOK
PA 820 JORIE BLVD, SUITE 200, OAK BROOK, ILLINOIS, UNITED STATES
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD JAN
PY 2020
VL 294
IS 1
BP 5
EP 17
DI 10.1148/radiol.2019182584
PG 13
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA JW6UV
UT WOS:000503185400003
PM 31746691
DA 2025-01-04
ER

PT J
AU Deshmukh, R
AF Deshmukh, Rohitas
TI Modulation of Intestinal Flora as an Emerging Therapeutic Approach for
   the Treatment of Colon Cancer
SO CURRENT CANCER THERAPY REVIEWS
LA English
DT Review; Early Access
DE Gut microbiota; dysbiosis; microbiome; antibiotics; anticancer; drug
   delivery; colorectal cancer
ID ISLAND METHYLATOR PHENOTYPE; COLORECTAL-CANCER; CARCINOMA; CETUXIMAB;
   PATHWAYS; BEVACIZUMAB; RESISTANCE; MICROBIOTA; MUTATIONS; DISEASE
AB The five-year survival rate for people with colon cancer has increased explosively over the last two decades due to major advances in treatment. Colon cancer survival rates have improved significantly over the past few decades, with some of this success owing to aggressive surgical care and breakthroughs in other complementary treatments. As a new option for Colorectal Cancer (CRC) patients, targeted therapy has been shown to be effective in extending the overall life. A dramatic increase in the number of novel drugs targeting multiple key pathways and immunological checkpoints has been observed after the success of cetuximab (an EGFR inhibitor) and bevacizumab (an anti-angiogenic agent). Neutralizing an already present dysbiosis in the gut microbiome is a novel strategy for combating colorectal cancer and its metastases. Several methods have been employed to date, such as prebiotics, postbiotics, antibiotics, and the transplantation of faecal microbiota. An overview of the epidemiological study and possible mechanisms of colon cancer is presented in this review. We have covered a wide range of targeted treatments for CRC in addition to diagnostic biomarkers as therapeutic targets.
C1 [Deshmukh, Rohitas] GLA Univ, Inst Pharmaceut Res, Mathura 281406, India.
C3 GLA University
RP Deshmukh, R (corresponding author), GLA Univ, Inst Pharmaceut Res, Mathura 281406, India.
EM rahi18rahi@gmail.com
RI Deshmukh, Rohitas/AAU-3455-2021
OI Deshmukh, Rohitas/0000-0002-8962-6821
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NR 114
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.
PD 2024 OCT 8
PY 2024
DI 10.2174/0115733947302126240924050845
EA OCT 2024
PG 14
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA I3E4H
UT WOS:001329119400001
DA 2025-01-04
ER

PT J
AU Shin, W
   Yun, JS
   Han, KYD
   Park, DG
AF Shin, Wonseok
   Yun, Jeongseok
   Han, Kyudong
   Park, Dong-Guk
TI Comparison of genetic variation between primary colorectal cancer and
   metastatic peritoneal cancer
SO GENES & GENOMICS
LA English
DT Article
DE Primary colorectal cancer; Peritoneal metastasis; Comprehensive Cancer
   Panel; Next-generation sequencing
ID HETEROGENEITY; THERAPY
AB BackgroundAmong cancer metastases by primary colorectal cancer (CRC), peritoneal metastasis is the second most common metastatic lesion after liver metastasis. In treating metastatic CRC, it is very important to differentiate targeted-therapy and chemotherapy according to the characteristics of each lesion because the genetic variation of the primary and metastatic lesions are different. However, there are few studies of genetic characteristics on peritoneal metastasis caused by primary CRC, so molecular-level studies are continuously required.ObjectiveWe propose an appropriate peritoneal metastasis treatment policy by identifying the genetic characteristics between primary CRC and synchronous peritoneal metastatic lesions.MethodsPrimary CRC and synchronous peritoneal metastasis samples were analyzed in pairs from six patients using Comprehensive Cancer Panel (409 cancer-related genes, Thermo Fisher Scientific, USA) and next-generation sequencing (NGS).ResultsThe mutations were commonly found on the KMT2C and THBS1 genes in both primary CRC and peritoneal metastasis. The PDE4DIP gene was mutated in all cases except for on a sample of peritoneal metastasis. As a result of analysis using the mutation database, we confirmed that the gene mutations of primary CRC and the peritoneal metastasis derived from it showed the same tendency, although we did not accompany the gene expression level or epigenetic study.ConclusionIt is thought that the treatment policy through molecular genetic testing of primary CRC can also be applied to peritoneal metastasis treatment. Our study is expected to be the basis for further peritoneal metastasis research.
C1 [Shin, Wonseok; Han, Kyudong; Park, Dong-Guk] Dankook Univ Hosp, NGS Clin Lab, Cheonan, South Korea.
   [Yun, Jeongseok; Park, Dong-Guk] Dankook Univ, Coll Med, Dept Surg, Cheonan, South Korea.
   [Han, Kyudong] Dankook Univ, Dept Microbiol, Cheonan, South Korea.
   [Han, Kyudong] Dankook Univ, Ctr Biomed Engn Core Facil, Cheonan, South Korea.
   [Han, Kyudong] HuNbiome Co Ltd, R&D Ctr, Seoul, South Korea.
C3 Dankook University; Dankook University Hospital; Dankook University;
   Dankook University; Dankook University
RP Han, KYD; Park, DG (corresponding author), Dankook Univ Hosp, NGS Clin Lab, Cheonan, South Korea.; Park, DG (corresponding author), Dankook Univ, Coll Med, Dept Surg, Cheonan, South Korea.; Han, KYD (corresponding author), Dankook Univ, Dept Microbiol, Cheonan, South Korea.; Han, KYD (corresponding author), Dankook Univ, Ctr Biomed Engn Core Facil, Cheonan, South Korea.; Han, KYD (corresponding author), HuNbiome Co Ltd, R&D Ctr, Seoul, South Korea.
EM kyudong.han@gmail.com; dkp21876@gmail.com
RI Han, Kyudong/AAF-1788-2019
OI Park, Dong-Guk/0000-0002-9894-9104; Han, Kyudong/0000-0001-6791-2408;
   Shin, Wonseok/0000-0001-5964-1425
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NR 42
TC 2
Z9 2
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1976-9571
EI 2092-9293
J9 GENES GENOM
JI Genes Genom.
PD AUG
PY 2023
VL 45
IS 8
BP 989
EP 1001
DI 10.1007/s13258-023-01408-3
EA JUN 2023
PG 13
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Genetics & Heredity
GA L8BS8
UT WOS:001000767500002
PM 37277571
DA 2025-01-04
ER

PT J
AU Xu, FH
   Xiao, ZF
   Fan, LQ
   Ruan, GC
   Cheng, Y
   Tian, YT
   Chen, MJ
   Chen, DF
   Wei, YL
AF Xu, Fenghua
   Xiao, Zhifeng
   Fan, Liqin
   Ruan, Guangcong
   Cheng, Yi
   Tian, Yuting
   Chen, Minjia
   Chen, Dongfeng
   Wei, Yanling
TI RFWD3 Participates in the Occurrence and Development of Colorectal
   Cancer <i>via</i> E2F1 Transcriptional Regulation of BIRC5
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Article
DE colorectal cancer; RFWD3; BIRC5; cell proliferation; cell apoptosis
ID TARGETED THERAPY; GROWTH-FACTOR; SURVIVIN; CHEMOTHERAPY; BIOMARKERS;
   DIAGNOSIS; CELLS; RPA
AB Objectives: Colorectal cancer (CRC) is one of the most common human malignancies. It was reported that the alterations in the DNA damage response (DDR) pathways are emerging as novel targets for treatment across different cancer types including CRC. RFWD3 plays a critical role in replication protein A (RPA)-mediated DNA damage in cancer cells. More importantly, RFWD3 can response to DNA damage by positively regulating p53 stability when the G1 cell cycle checkpoint is activated. However, the functional significance of RFWD3 in CRC has not been reported in the existing documents.
   Materials and Methods: Here, we revealed high expression of RFWD3 in CRC tissues by IHC analysis and The Cancer Genome Atlas (TCGA) database. Besides, overexpression of RFWD3 in CRC cell lines was also confirmed by qRT-PCR and western blot assay. The Celigo cell counting method and wound-healing/transwell migration assay were applied to evaluate CRC cell proliferation and migration. The tumor growth indicators were quantified in nude mice xenografted with shRFWD3 and shCtrl RKO cells.
   Results: The results indicated that RFWD3 knockdown restricted CRC development in vitro and in vivo. In exploring the downstream mechanism of RFWD3's action, we found that RFWD3 could transcriptionally activate BIRC5 by interacting with E2F transcription factor 1 (E2F1). Accordingly, we identified BIRC5 as a downstream gene of RFWD3 regulating CRC. Subsequent loss- and gain- of function experiments demonstrated that upon overexpressing BIRC5 in RKO cells with down-regulated RFWD3, the inhibitory effects of cell proliferation, migration and colony formation could be reversed, while the capacity of cell apoptosis was ameliorated, suggesting that the effects of RFWD3 depletion was mainly due to BIRC5 suppression.
   Conclusion: Taken together, this study revealed that RFWD3 participates in the occurrence and development of colorectal cancer via E2F1 transcriptional regulation of BIRC5.
C1 [Xu, Fenghua; Xiao, Zhifeng; Fan, Liqin; Ruan, Guangcong; Cheng, Yi; Tian, Yuting; Chen, Minjia; Chen, Dongfeng; Wei, Yanling] Third Mil Med Univ, Army Med Univ, Daping Hosp, Dept Gastroenterol, Chongqing, Peoples R China.
C3 Army Medical University
RP Chen, DF; Wei, YL (corresponding author), Third Mil Med Univ, Army Med Univ, Daping Hosp, Dept Gastroenterol, Chongqing, Peoples R China.
EM chendf1981@126.com; lingzi016@126.com
RI Tian, Yuting/AAV-8200-2020
OI Ruan, Guangcong/0000-0002-1918-2305
FU Second-Class Program of Talent Research and Training of Army Medical
   University [2018XLC2028]
FX Funding This work was financially supported by The Second-Class Program
   of Talent Research and Training of Army Medical University
   (2018XLC2028).
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NR 38
TC 8
Z9 8
U1 1
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 OCT 12
PY 2021
VL 9
AR 675356
DI 10.3389/fcell.2021.675356
PG 12
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA WP6GV
UT WOS:000713228600001
PM 34712656
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Amagai, Y
   Fujiyuki, T
   Yoneda, M
   Shoji, K
   Furukawa, Y
   Sato, H
   Kai, C
AF Amagai, Yosuke
   Fujiyuki, Tomoko
   Yoneda, Misako
   Shoji, Koichiro
   Furukawa, Yoichi
   Sato, Hiroki
   Kai, Chieko
TI Oncolytic Activity of a Recombinant Measles Virus, Blind to Signaling
   Lymphocyte Activation Molecule, Against Colorectal Cancer Cells
SO SCIENTIFIC REPORTS
LA English
DT Article
ID RECEPTOR; NECTIN-4; PANITUMUMAB; EXPRESSION; MUTATIONS; CETUXIMAB;
   MARKER; PIK3CA; SPREAD; KRAS
AB Oncolytic virotherapy is a distinctive antitumor therapy based on the cancer-cell-specific infectivity and killing activity of viruses, which exert a considerable antitumor effect with only a few treatments. Because colorectal cancer cells often acquire resistance to the molecular-targeted therapies and alternative treatments are called for, in this study, we evaluated the oncolytic activity against colorectal cancer cells of a recombinant measles virus (rMV-SLAMblind), which is blind to signaling lymphocytic activation molecule (SLAM) and infects target cells via nectin-4/poliovirus receptor-related 4 protein. We examined 10 cell lines including 8 cell lines that were resistant to epidermal-growth-factor-receptor (EGFR) targeted therapy. rMV-SLAMblind infected and lysed the nectin-4-positive cell lines dependently on nectin-4 expression, in spite of mutation in EGFR cascade. Tumour progression in xenograft models was also abrogated by the virus, and the infection of cancer cells in vivo by the virus was demonstrated with both flow cytometry and a histological analysis. Therefore, rMV-SLAMblind is considered a novel therapeutic agent for colorectal cancers, including those resistant to molecular-targeted therapies.
C1 [Amagai, Yosuke; Fujiyuki, Tomoko; Yoneda, Misako; Shoji, Koichiro; Sato, Hiroki; Kai, Chieko] Univ Tokyo, Inst Med Sci, Lab Anim Res Ctr, Tokyo 108, Japan.
   [Furukawa, Yoichi] Univ Tokyo, Inst Med Sci, Div Clin Genome Res, Tokyo, Japan.
C3 University of Tokyo; University of Tokyo
RP Kai, C (corresponding author), Univ Tokyo, Inst Med Sci, Lab Anim Res Ctr, Tokyo 108, Japan.
EM ckai@ims.u-tokyo.ac.jp
RI Sato, Hiroki/IRZ-1683-2023; Fujiyuki, Tomoko/GYD-6398-2022
FU Health and Labour Sciences Research Grants; Grants-in-Aid for Scientific
   Research [16J10993, 16H02587] Funding Source: KAKEN
FX This work was supported by Health and Labour Sciences Research Grants.
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NR 33
TC 23
Z9 26
U1 0
U2 4
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD APR 19
PY 2016
VL 6
AR 24572
DI 10.1038/srep24572
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA DJ6TN
UT WOS:000374346100001
PM 27090874
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Pu, K
   Gao, JY
   Feng, Y
   Hu, J
   Tang, SL
   Yang, GD
   Xu, C
AF Pu, Ke
   Gao, Jingyuan
   Feng, Yang
   Hu, Jian
   Tang, Shunli
   Yang, Guodong
   Xu, Chuan
TI Comprehensive evaluation of immunological attributes and immunotherapy
   responses of positive T cell function regulators in colorectal cancer
SO BMC GASTROENTEROLOGY
LA English
DT Article
DE T-cell function positive regulators; Immunotherapy; Colorectal Cancer;
   Tumor microenvironment; Risk score model
ID MICROSATELLITE INSTABILITY; EXPRESSION; CELLMINER; FEATURES; THERAPY;
   PD-L1
AB BackgroundPositive regulators of T-cell function (PTFRs), integral to T-cell proliferation and activation, have been identified as potential prognostic markers in colorectal cancer (CRC). Despite this, their role within the tumor microenvironment (TME) and their response to immunotherapy are not yet fully understood.MethodsThis study delved into PTFR-related CRC subtypes by analyzing four independent transcriptome datasets, emphasizing the most significant prognostic PTFRs. We identified differentially expressed genes (DEGs) between two subtypes and developed a PTFR risk model using LASSO and Cox regression methods. The model's associations with survival time, clinical features, TME characteristics, tumor mutation profiles, microsatellite instability (MSI), cancer stem cell (CSC) index, and responses to chemotherapy, targeted therapy, and immunotherapy were subsequently explored.ResultsThe PTFR risk model demonstrated a strong predictive capacity for CRC. It facilitated the estimation of immune cell composition, HLA expression levels, immune checkpoint expression, mutation burden, CSC index features, and the effectiveness of immunotherapy.ConclusionsThis study enhances our understanding of the role of PTFRs in CRC progression and introduces an innovative assessment framework for CRC immunotherapy. This framework improves the prediction of treatment outcomes and aids in the customization of therapeutic strategies.
C1 [Pu, Ke; Yang, Guodong] North Sichuan Med Coll, Dept Gastroenterol, Affiliated Hosp, Nanchong 637000, Sichuan, Peoples R China.
   [Gao, Jingyuan] Shaanxi Univ Chinese Med, Dept Immunol, Xianyang 712046, Shaanxi, Peoples R China.
   [Feng, Yang] Northwest Univ, Xian Hosp No 3, Affiliated Hosp, Dept Neurosurg, Xian 710018, Shaanxi, Peoples R China.
   [Hu, Jian] Dazhou Second Peoples Hosp, Integrated TCM & Western Med Hosp, Dept Thorac & Cardiovasc Surg, Dazhou 635000, Peoples R China.
   [Tang, Shunli] Dazhou Second Peoples Hosp, Integrated TCM & Western Med Hosp, Dept Pathol, Dazhou 635000, Peoples R China.
   [Xu, Chuan] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Sichuan Acad Med Sci, Dept Oncol, Chengdu 610072, Peoples R China.
   [Xu, Chuan] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Canc Inst, Sichuan Acad Med Sci, Chengdu 610072, Peoples R China.
   [Xu, Chuan] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Dept Lab Med, Chengdu 610072, Peoples R China.
   [Xu, Chuan] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Sichuan Prov Key Lab Human Dis Gene Study, Chengdu 610072, Peoples R China.
C3 North Sichuan Medical University; Shaanxi University of Chinese
   Medicine; Northwest University Xi'an; University of Electronic Science &
   Technology of China; Sichuan Provincial People's Hospital; University of
   Electronic Science & Technology of China; Sichuan Provincial People's
   Hospital; University of Electronic Science & Technology of China;
   Sichuan Provincial People's Hospital; University of Electronic Science &
   Technology of China; Sichuan Provincial People's Hospital
RP Yang, GD (corresponding author), North Sichuan Med Coll, Dept Gastroenterol, Affiliated Hosp, Nanchong 637000, Sichuan, Peoples R China.; Xu, C (corresponding author), Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Sichuan Acad Med Sci, Dept Oncol, Chengdu 610072, Peoples R China.; Xu, C (corresponding author), Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Canc Inst, Sichuan Acad Med Sci, Chengdu 610072, Peoples R China.; Xu, C (corresponding author), Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Dept Lab Med, Chengdu 610072, Peoples R China.; Xu, C (corresponding author), Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Sichuan Prov Key Lab Human Dis Gene Study, Chengdu 610072, Peoples R China.
EM ygd_ld2006@163.com; xuchuan19860530@163.com
RI Pu, Ke/KOC-8921-2024
FU The Intramural Fund of North Sichuan Medical College
FX Not applicable.
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NR 46
TC 0
Z9 0
U1 1
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-230X
J9 BMC GASTROENTEROL
JI BMC Gastroenterol.
PD OCT 1
PY 2024
VL 24
IS 1
AR 339
DI 10.1186/s12876-024-03409-2
PG 20
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA H9Q8J
UT WOS:001326714200006
PM 39354362
OA gold
DA 2025-01-04
ER

PT J
AU Zhou, JF
   Wang, HG
   Ma, TH
   Yan, W
   Wu, SN
   Shi, YT
   Yang, XZ
AF Zhou, J-F
   Wang, H-G
   Ma, T-H
   Yan, W.
   Wu, S-N
   Shi, Y-T
   Yang, X-Z
TI Long noncoding RNA LINC01510 is highly expressed in colorectal cancer
   and predicts favorable prognosis
SO EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES
LA English
DT Article
DE LINC01510; Long non-coding RNA; Colorectal cancer; Prognosis
ID CELL-PROLIFERATION; TARGETED THERAPY; BIOMARKERS; DIAGNOSIS; AFAP1-AS1;
   BIOLOGY
AB OBJECTIVE: Long noncoding RNAs (IncRNAs) have recently emerged as important regulators in governing fundamental biological processes, as well as in tumorigenesis. LncRNA LINC01510 (LINC01510) was recently shown to be involved in colorectal cancer (CRC); however, its role in CRC remains unknown. The objective of this study was to evaluate LINC01510 expression and its relevance to the prognosis of CRC.
   PATIENTS AND METHODS: LINC01510 expression was detected in CRC tissues and cell lines by using quantitative real-time PCR (qRT-PCR). The correction between LINC01510 expression and clinical characteristics was evaluated with x(2)-test. Survival curves and log-rank test were used to analyze patients' survival. A Cox proportional hazard model was constructed to evaluate the association of LINC01510 expression with overall survival and disease-free survival, respectively.
   RESULTS: Here, we found that the levels of LINC01510 in CRC tissues were significantly higher than those in matched tumor-adjacent tissues. Moreover, high LINC01510 expression was observed to be closely correlated with histology/differentiation (p = 0.001), depth of invasion (p = 0.004) and TNM stage (p = 0.003). From the Kaplan-Meier survival curves, it was observed that patients with high expression of LINC01510 had shorter overall survival (p = 0.004) and disease-free survival (p = 0.000) as compared with the LINC01510-low group. In the multivariate analysis, high LINC01510 expression was an independent prognostic factor for both overall survival (p = 0.001) and disease-free survival (p = 0.001).
   CONCLUSIONS: We demonstrated that low LINC01510 expression was associated with the progression of CRC and could serve as a potential independent prognostic biomarker for patients with CRC.
C1 [Zhou, J-F; Wang, H-G; Ma, T-H; Yan, W.; Wu, S-N; Shi, Y-T; Yang, X-Z] Nanjing Med Univ, Dept Gastroenterol, Affiliated Huaian 1 Peoples Hosp, Huaian, Peoples R China.
C3 Nanjing Medical University
RP Yang, XZ (corresponding author), Nanjing Med Univ, Dept Gastroenterol, Affiliated Huaian 1 Peoples Hosp, Huaian, Peoples R China.
EM yxz3176@163.com
CR Ahmed S, 2014, INT J COLORECTAL DIS, V29, P1031, DOI 10.1007/s00384-014-1928-5
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NR 26
TC 17
Z9 17
U1 0
U2 1
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 NOV
PY 2018
VL 22
IS 22
BP 7710
EP 7715
PG 6
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA HD8AA
UT WOS:000452774900015
PM 30536314
DA 2025-01-04
ER

PT J
AU She, TS
   Shi, QX
   Li, Z
   Feng, YR
   Yang, H
   Tao, Z
   Li, H
   Chen, J
   Wang, SS
   Liang, Y
   Cheng, JQ
   Lu, XF
AF She, Tianshan
   Shi, Qiuxiao
   Li, Zhao
   Feng, Yanru
   Yang, Hao
   Tao, Ze
   Li, Heng
   Chen, Jie
   Wang, Shisheng
   Liang, Yan
   Cheng, Jingqiu
   Lu, Xiaofeng
TI Combination of long-acting TRAIL and tumor cell-targeted photodynamic
   therapy as a novel strategy to overcome chemotherapeutic multidrug
   resistance and TRAIL resistance of colorectal cancer
SO THERANOSTICS
LA English
DT Article
DE Tumor necrosis factor-related apoptosis-inducing ligand; Photodynamic
   therapy; Multidrug resistance; Cancer targeted therapy; Colorectal
   cancer
ID AFFINITY
AB Chemotherapeutic multidrug resistance (MDR) is the major hindrance for clinical therapy of colorectal cancer (CRC). Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) with selective cytotoxicity might overcome MDR of CRC cells. Unfortunately, cross-resistance to TRAIL has been detected in many CRC cells, suggesting the need to combine TRAIL with sensitizers to combat refractory CRC. Our purpose is to explore the potential of combination therapy of TRAIL and tumor-cell targeted photodynamic therapy (PDT) in combating CRC with both chemotherapeutic MDR and TRAIL resistance.
   Methods: Tumor cell-targeted PDT was performed using a Ze-IR700 photosensitizer with high affinity for epidermal growth factor receptor (EGFR). The impact of PDT on the gene expression of CRC cells was revealed by RNA sequencing. The synergistic antitumor effect of long-acting TRAIL and PDT was evaluated in mice bearing tumor grafts of CRC cells with both chemotherapeutic MDR and TRAIL resistance.
   Results: Chemotherapeutic MDR and TRAIL resistance are common in CRC cells. Pretreatment of CRC cells with tumor cell-targeted PDT significantly (10-60 times) increased the sensitivity of these CRC cells to TRAIL by upregulating death receptors. Combination therapy, but not monotherapy, of long-acting TRAIL and PDT greatly induced apoptosis of CRC cells, thus efficiently eradicated large (similar to 150 mm(3)) CRC tumor xenografts in mice.
   Conclusions: Tumor cell-targeted PDT extensively sensitizes CRC cells to TRAIL. Combination therapy of long-acting TRAIL and PDT is promising to combat CRC with both chemotherapeutic MDR and TRAIL resistance, which might be developed as a novel strategy for precision therapy of refractory CRC.
C1 [She, Tianshan; Shi, Qiuxiao; Li, Zhao; Feng, Yanru; Yang, Hao; Tao, Ze; Li, Heng; Chen, Jie; Cheng, Jingqiu; Lu, Xiaofeng] Sichuan Univ, West China Hosp, Regenerat Med Res Ctr, Key Lab Transplant Engn & Immunol,MOH, Chengdu 610041, Peoples R China.
   [Yang, Hao; Cheng, Jingqiu; Lu, Xiaofeng] Sichuan Univ, West China Hosp, Frontiers Sci Ctr Dis Related Mol Network, Chengdu 610041, Peoples R China.
   [Wang, Shisheng] Sichuan Univ, West China Hosp, West China Washington Mitochondria & Metab Res Ct, Chengdu 610041, Peoples R China.
   [Liang, Yan] Sichuan Univ, West China Hosp, Histopathol Platforms Expt Ctr, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University; Sichuan
   University
RP Cheng, JQ; Lu, XF (corresponding author), Sichuan Univ, West China Hosp, Regenerat Med Res Ctr, Key Lab Transplant Engn & Immunol,MOH, Chengdu 610041, Peoples R China.; Cheng, JQ; Lu, XF (corresponding author), Sichuan Univ, West China Hosp, Frontiers Sci Ctr Dis Related Mol Network, Chengdu 610041, Peoples R China.
EM jqcheng@scu.edu.cn; xiaofenglu@scu.edu.cn
RI Feng, YanRu/AAA-2183-2020; Wang, Shisheng/CAG-7844-2022; Chen,
   Yi/HPD-0595-2023; Lu, Xiaofeng/ABD-9075-2021; li, zhao/IYS-8424-2023
OI li, zhao/0000-0003-0302-1635; Tao, Ze/0000-0002-0726-192X
FU National Natural Science Fund of China [82073362, 81871475]; Key R&D
   Program of Sichuan Province [2020YFS0072]; International Cooperation
   Program of Sichuan Province [2020YFH0029]; 1.3.5 Project for Disciplines
   of Excellence, West China Hospital, Sichuan University [ZYGD18014]
FX This study was funded by the National Natural Science Fund of China
   (82073362 and 81871475), the Key R&D Program of Sichuan Province
   (2020YFS0072), the International Cooperation Program of Sichuan Province
   (2020YFH0029), and the "1.3.5 Project for Disciplines of Excellence,
   West China Hospital, Sichuan University" (ZYGD18014). The authors thank
   Yang Yang and Xijing Yang (Animal Center of West China Hospital, Sichuan
   University) for their assistance in animal administration.
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NR 38
TC 19
Z9 20
U1 2
U2 31
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2021
VL 11
IS 9
BP 4281
EP 4297
DI 10.7150/thno.51193
PG 17
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA QP9DW
UT WOS:000624130200017
PM 33754061
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Cui, JP
   Ding, RM
   Liu, HF
   Ma, MX
   Zuo, RX
   Liu, X
AF Cui, Junpeng
   Ding, Rongmei
   Liu, Haifeng
   Ma, Mingxiu
   Zuo, Ruixue
   Liu, Xun
TI Trends in the incidence and survival of cancer in individuals aged 55
   years and older in the United States, 1975-2019
SO BMC PUBLIC HEALTH
LA English
DT Article
DE Cancer; Incidence rate; Older population; Cancer prevention; Survival
   rate
ID COLORECTAL-CANCER; CIGARETTE-SMOKING; TOBACCO CONTROL; US; POPULATION;
   STATISTICS; MORTALITY; IMPACT; COUNTRIES; PATTERNS
AB BackgroundIn ageing societies such as the United States, evaluating the incidence and survival rates of cancer in older adults is essential. This study aimed to analyse the incidence and survival rates of cancer in individuals aged 55 years or older in the United States.MethodsThis retrospective study (1975-2019) was conducted using combined registry data from the Surveillance, Epidemiology, and End Results database. Data from the 9, 12, and 17 Registries (Nov 2021 Sub) datasets were used.ResultsIn 2019, the incidence of cancer in individuals older than 55 years and the overall population was 1322.8 and 382.1 per 100,000 population, respectively. From 2000 to 2019, the incidence of cancer in individuals older than 55 years showed a decreasing trend, whereas their five-year survival rates showed an increasing trend. The incidence of cancer in the 75-79 and 80-84 year age groups was the highest among all age groups.ConclusionsThe incidence of colon cancer declined significantly, whereas that of intrahepatic bile duct cancer increased considerably. These trends may be due to increased screening for cancers with high incidence rates and improved control of the risk factors for cancer. Rapid development of targeted therapy and immunotherapy combined with early tumour detection may be an important reason for the improved survival rates.
C1 [Cui, Junpeng; Liu, Haifeng; Ma, Mingxiu; Zuo, Ruixue; Liu, Xun] China Med Univ, Dept Gen Surg, Shengjing Hosp, 36 Sanhao St, Shenyang 110004, Liaoning, Peoples R China.
   [Ding, Rongmei] China Med Univ, Dept Oncol, Shengjing Hosp, 36 Sanhao St, Shenyang 110004, Liaoning, Peoples R China.
C3 China Medical University; China Medical University
RP Liu, X (corresponding author), China Med Univ, Dept Gen Surg, Shengjing Hosp, 36 Sanhao St, Shenyang 110004, Liaoning, Peoples R China.
EM liuxun@sj-hospital.org
RI Liu, Haifeng/ITU-7594-2023
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NR 59
TC 3
Z9 3
U1 1
U2 2
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2458
J9 BMC PUBLIC HEALTH
JI BMC Public Health
PD JAN 3
PY 2024
VL 24
IS 1
AR 72
DI 10.1186/s12889-023-17571-x
PG 12
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Public, Environmental & Occupational Health
GA EA2P5
UT WOS:001136118300005
PM 38172749
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Montero, JC
   del Carmen, S
   Abad, M
   Sayagués, JM
   Barbáchano, A
   Fernández-Barral, A
   Muñoz, A
   Pandiella, A
AF Montero, Juan Carlos
   del Carmen, Sofia
   Abad, Mar
   Sayagues, Jose M.
   Barbachano, Antonio
   Fernandez-Barral, Asuncion
   Munoz, Alberto
   Pandiella, Atanasio
TI An amino acid transporter subunit as an antibody-drug conjugate target
   in colorectal cancer
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE CD98hc; Antibody-drug conjugates; Colorectal cancer; Targeted therapy
ID CD98 EXPRESSION; BIOMARKER; PROTEIN; MARKER; CELLS; ASCT2; LAT1
AB BackgroundAdvanced colorectal cancer (CRC) is difficult to treat. For that reason, the development of novel therapeutics is necessary. Here we describe a potentially actionable plasma membrane target, the amino acid transporter protein subunit CD98hc.MethodsWestern blot and immunohistochemical analyses of CD98hc protein expression were carried out on paired normal and tumoral tissues from patients with CRC. Immunofluorescence and western studies were used to characterize the action of a DM1-based CD98hc-directed antibody-drug conjugate (ADC). MTT and Annexin V studies were performed to evaluate the effect of the anti-CD98hc-ADC on cell proliferation and apoptosis. CRISPR/Cas9 and shRNA were used to explore the specificity of the ADC. In vitro analyses of the antitumoral activity of the anti-CD98hc-ADC on 3D patient-derived normal as well as tumoral organoids were also carried out. Xenografted CRC cells and a PDX were used to analyze the antitumoral properties of the anti-CD98hc-ADC.ResultsGenomic as well proteomic analyses of paired normal and tumoral samples showed that CD98hc expression was significantly higher in tumoral tissues as compared to levels of CD98hc present in the normal colonic tissue. In human CRC cell lines, an ADC that recognized the CD98hc ectodomain, reached the lysosomes and exerted potent antitumoral activity. The specificity of the CD98hc-directed ADC was demonstrated using CRC cells in which CD98hc was decreased by shRNA or deleted using CRISPR/Cas9. Studies in patient-derived organoids verified the antitumoral action of the anti-CD98hc-ADC, which largely spared normal tissue-derived colon organoids. In vivo studies using xenografted CRC cells or patient-derived xenografts confirmed the antitumoral activity of the anti-CD98hc-ADC.ConclusionsThe studies herewith reported indicate that CD98hc may represent a novel ADC target that, upon well-designed clinical trials, could be used to increase the therapeutic armamentarium against CRC.
C1 [Montero, Juan Carlos; Pandiella, Atanasio] Univ Salamanca, CSIC, Inst Biol Mol & Celular Canc, Inst Biomed Res Salamanca IBSAL, Salamanca, Spain.
   [Montero, Juan Carlos; del Carmen, Sofia; Abad, Mar; Sayagues, Jose M.] Univ Hosp Salamanca, Dept Pathol, Salamanca, Spain.
   [Montero, Juan Carlos; del Carmen, Sofia; Abad, Mar; Sayagues, Jose M.] Univ Hosp Salamanca, IBSAL, Salamanca, Spain.
   [Montero, Juan Carlos; Sayagues, Jose M.; Barbachano, Antonio; Fernandez-Barral, Asuncion; Munoz, Alberto; Pandiella, Atanasio] CIBERONC, Madrid, Spain.
   [Barbachano, Antonio; Fernandez-Barral, Asuncion; Munoz, Alberto] Autonomous Univ Madrid, CSIC, Inst Invest Biomed Alberto Sols, Madrid, Spain.
   [Barbachano, Antonio; Fernandez-Barral, Asuncion; Munoz, Alberto] Hosp Univ La Paz, Inst Invest Sanitaria, Madrid, Spain.
C3 University of Salamanca; Consejo Superior de Investigaciones Cientificas
   (CSIC); CSIC-USAL - Instituto de Biologia Molecular y Celular del Cancer
   de Salamanca (IBMCC); University of Salamanca; CIBER - Centro de
   Investigacion Biomedica en Red; CIBERONC; Autonomous University of
   Madrid; Consejo Superior de Investigaciones Cientificas (CSIC); CSIC -
   Instituto de Investigaciones Biomedicas Alberto Sols (IIBM); Hospital
   Universitario La Paz
RP Montero, JC; Pandiella, A (corresponding author), Univ Salamanca, CSIC, Inst Biol Mol & Celular Canc, Inst Biomed Res Salamanca IBSAL, Salamanca, Spain.; Montero, JC (corresponding author), Univ Hosp Salamanca, Dept Pathol, Salamanca, Spain.; Montero, JC (corresponding author), Univ Hosp Salamanca, IBSAL, Salamanca, Spain.; Montero, JC; Pandiella, A (corresponding author), CIBERONC, Madrid, Spain.
EM jcmon@usal.es; atanasio@usal.es
RI Montero, Juan Carlos/AEL-5598-2022; Pandiella, Atanasio/O-5180-2014;
   Munoz, Alberto/O-6393-2014; Barbachano Becerril, Antonio/O-7731-2015
OI Munoz, Alberto/0000-0003-3890-4251; Montero, Juan
   Carlos/0000-0003-4773-053X; Barbachano Becerril,
   Antonio/0000-0002-1248-5143; del Carmen, Sofia/0000-0001-9565-2009
FU  [PT20/00004]
FX AcknowledgementsWe want to particularly acknowledge the patients and the
   Biobank IdiPAZ (PT20/00004) integrated in the Spanish National Biobanks
   Network for their collaboration. We thank Maria del Carmen Rodriguez
   Gonzalez for help with immunohistochemical stainings and David
   Albandea-Rodriguez for helping us with immunofluorescence staining of
   organoids.
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NR 58
TC 3
Z9 3
U1 4
U2 10
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD AUG 9
PY 2023
VL 42
IS 1
AR 200
DI 10.1186/s13046-023-02784-0
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA O6XH8
UT WOS:001045208000003
PM 37559159
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Rodrigues, JG
   Duarte, HO
   Gomes, C
   Balmaña, M
   Martins, AM
   Hensbergen, PJ
   de Ru, AH
   Lima, J
   Albergaria, A
   van Veelen, PA
   Wuhrer, M
   Gomes, J
   Reis, CA
AF Rodrigues, Joana G.
   Duarte, Henrique O.
   Gomes, Catarina
   Balmana, Meritxell
   Martins, Alvaro M.
   Hensbergen, Paul J.
   de Ru, Arnoud H.
   Lima, Jorge
   Albergaria, Andre
   van Veelen, Peter A.
   Wuhrer, Manfred
   Gomes, Joana
   Reis, Celso A.
TI Terminal α2,6-sialylation of epidermal growth factor receptor modulates
   antibody therapy response of colorectal cancer cells
SO CELLULAR ONCOLOGY
LA English
DT Article
DE Colorectal cancer; alpha 2,6-sialylation; Cetuximab; EGFR; ST6Gal1
ID PROTECTS TUMOR-CELLS; N-GLYCOSYLATION; EXPRESSION; SIALYLATION;
   RESISTANCE; CETUXIMAB; PANITUMUMAB; PROGRESSION; INHIBITION; MECHANISMS
AB Background The epidermal growth factor receptor (EGFR) is a key protein involved in cancer development. Monoclonal antibodies targeting EGFR are approved for the treatment of metastatic colorectal cancer (CRC). Despite the beneficial clinical effects observed in subgroups of patients, the acquisition of resistance to treatment remains a major concern. Protein N-glycosylation of cellular receptors is known to regulate physiological processes leading to activation of downstream signaling pathways. In the present study, the role of EGFR-specific terminal alpha 2,6-sialylation was analyzed in modulation of the malignant phenotype of CRC cells and their resistance to monoclonal antibody Cetuximab-based therapy.
   Methods Glycoengineered CRC cell models with specific sialyltransferase ST6GAL1 expression levels were applied to evaluate EGFR activation, cell surface glycosylation and therapeutic response to Cetuximab.
   Results Glycoproteomic analysis revealed EGFR as a major target of ST6Gal1-mediated alpha 2,6-sialylation in a glycosite-specific manner. Mechanistically, CRC cells with increased ST6Gal1 expression and displaying terminal alpha 2,6-sialylation showed a marked resistance to Cetuximab-induced cytotoxicity. Moreover, we found that this resistance was accompanied by downregulation of EGFR expression and its activation.
   Conclusions Our data indicate that EGFR alpha 2,6-sialylation is a key factor in modulating the susceptibility of CRC cells to antibody targeted therapy, thereby disclosing a potential novel biomarker and providing key molecular information for tailor made anti-cancer strategies.
C1 [Rodrigues, Joana G.; Duarte, Henrique O.; Gomes, Catarina; Balmana, Meritxell; Martins, Alvaro M.; Lima, Jorge; Albergaria, Andre; Gomes, Joana; Reis, Celso A.] Univ Porto, i3S Inst Invest & Inovacao Saude, P-4200135 Porto, Portugal.
   [Rodrigues, Joana G.; Duarte, Henrique O.; Gomes, Catarina; Balmana, Meritxell; Martins, Alvaro M.; Lima, Jorge; Albergaria, Andre; Gomes, Joana; Reis, Celso A.] Univ Porto, IPATIMUP Inst Mol Pathol & Immunol, P-4200135 Porto, Portugal.
   [Rodrigues, Joana G.; Duarte, Henrique O.; Reis, Celso A.] Univ Porto, Inst Ciencias Biomed Abel Salazar, P-4050313 Porto, Portugal.
   [Balmana, Meritxell] Austrian Acad Sci IMBA, Inst Mol Biotechnol, A-1030 Vienna, Austria.
   [Hensbergen, Paul J.; de Ru, Arnoud H.; van Veelen, Peter A.; Wuhrer, Manfred] Leiden Univ, Ctr Proteom & Metabol, Med Ctr, Leiden, Netherlands.
   [Lima, Jorge; Albergaria, Andre; Reis, Celso A.] Univ Porto, Fac Med, P-4200319 Porto, Portugal.
C3 Universidade do Porto; i3S - Instituto de Investigacao e Inovacao em
   Saude, Universidade do Porto; Universidade do Porto; Universidade do
   Porto; Austrian Academy of Sciences; Vienna Biocenter (VBC); Institute
   of Molecular Biotechnology (IMBA); Leiden University; Leiden University
   Medical Center (LUMC); Leiden University - Excl LUMC; Universidade do
   Porto
RP Rodrigues, JG; Reis, CA (corresponding author), Univ Porto, i3S Inst Invest & Inovacao Saude, P-4200135 Porto, Portugal.; Rodrigues, JG; Reis, CA (corresponding author), Univ Porto, IPATIMUP Inst Mol Pathol & Immunol, P-4200135 Porto, Portugal.; Rodrigues, JG; Reis, CA (corresponding author), Univ Porto, Inst Ciencias Biomed Abel Salazar, P-4050313 Porto, Portugal.; Reis, CA (corresponding author), Univ Porto, Fac Med, P-4200319 Porto, Portugal.
EM joanag@ipatimup.pt; celsor@ipatimup.pt
RI Gomes, Catarina/CAJ-5505-2022; Martins, Álvaro/HTQ-7771-2023; Wuhrer,
   Manfred/ABE-9168-2020; Albergaria, André/J-6162-2013; REIS,
   Celso/B-9969-2008; Oliveira Duarte, Henrique/AAZ-7387-2021; Lima,
   Jorge/J-5975-2013; Gomes, Joana/K-9031-2013
OI Lima, Jorge/0000-0001-7780-0901; Hensbergen, Paul/0000-0002-3193-5445;
   Balmana, Meritxell/0000-0001-6587-3900; Gomes,
   Joana/0000-0002-8832-2703; Duarte, Henrique/0000-0001-8641-8368; M.
   Martins, Alvaro/0000-0003-0266-9093; Rodrigues,
   Joana/0000-0001-5890-6620; van Veelen, Peter/0000-0002-7898-9408
FU Merck KGaA, Darmstadt, Germany; FEDER funds through the Operational
   Programme for Competitiveness Factors COMPETE 2020
   [POCI-01-0145-FEDER-016585, POCI-01-0145-FEDER-007274]; Foundation for
   Science and Technology (FCT) - Norte Portugal Regional Programme (NORTE
   2020), under the PORTUGAL 2020 Partnership Agreement, through the
   European Regional Development Fund (ERDF) [PTDC/BBB-EBI/0567/2014,
   UID/BIM/04293/2013, PTDC/MED-QUI/29,780/2017,
   NORTE-01-0145-FEDER-000029]; Programa Operacional Potencial Humano
   (POPH); FCT [PD/0016/2012, SFRH/BD/136,736/2018, PD/BD/128,407/2017];
   European Union [748,880]
FX This research was funded by Merck KGaA, Darmstadt, Germany, and by FEDER
   funds through the Operational Programme for Competitiveness Factors
   COMPETE 2020 (POCI-01-0145-FEDER-016585; POCI-01-0145-FEDER-007274) and
   national funds through the Foundation for Science and Technology (FCT),
   under the projects: PTDC/BBB-EBI/0567/2014 to C.A. R and
   UID/BIM/04293/2013; PTDC/MED-QUI/29,780/2017 to C. G., and the project
   NORTE-01-0145-FEDER-000029, supported by Norte Portugal Regional
   Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement,
   through the European Regional Development Fund (ERDF). J.G. R. was
   supported by a FCT PhD grant (SFRH/BD/136,736/2018); H.O.D. was
   supported by a FCT PhD grant (PD/BD/128,407/2017) through the FCT PhD
   Programmes and by Programa Operacional Potencial Humano (POPH),
   specifically by the BiotechHealth Programme (Doctoral Programme on
   Cellular and Molecular Biotechnology Applied to Health Sciences), with
   the reference PD/0016/2012 funded by FCT. M.B. was supported by the
   European Union's Horizon 2020 research and innovation program under the
   Marie Sklodowska-Curie grant agreement n.o 748,880.
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NR 52
TC 20
Z9 22
U1 2
U2 13
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 2211-3428
EI 2211-3436
J9 CELL ONCOL
JI Cell. Oncol.
PD AUG
PY 2021
VL 44
IS 4
BP 835
EP 850
DI 10.1007/s13402-021-00606-z
EA APR 2021
PG 16
WC Oncology; Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology; Pathology
GA TU9FY
UT WOS:000639724700001
PM 33847896
DA 2025-01-04
ER

PT J
AU Jebelli, A
   Baradaran, B
   Mosafer, J
   Baghbanzadeh, A
   Mokhtarzadeh, A
   Tayebi, L
AF Jebelli, Asiyeh
   Baradaran, Behzad
   Mosafer, Jafar
   Baghbanzadeh, Amir
   Mokhtarzadeh, Ahad
   Tayebi, Lobat
TI Recent developments in targeting genes and pathways by RNAi-based
   approaches in colorectal cancer
SO MEDICINAL RESEARCH REVIEWS
LA English
DT Review
DE colorectal cancer; molecular target; shRNA; signaling pathway; siRNA
ID SYNTHETIC LETHAL INTERACTIONS; DOWN-REGULATION; PLGA NANOPARTICLES;
   BCL-XL; MICROSATELLITE INSTABILITY; SERINE/THREONINE KINASE; MEDIATED
   DELIVERY; IMPRINTED SITES; FEEDBACK LOOP; TUMOR-GROWTH
AB A wide spectrum of genetic and epigenetic variations together with environmental factors has made colorectal cancer (CRC), which involves the colon and rectum, a challenging and heterogeneous cancer. CRC cannot be effectively overcomed by common conventional therapies including surgery, chemotherapy, targeted therapy, and hormone replacement which highlights the need for a rational design of novel anticancer therapy. Accumulating evidence indicates that RNA interference (RNAi) could be an important avenue to generate great therapeutic efficacy for CRC by targeting genes that are responsible for the viability, cell cycle, proliferation, apoptosis, differentiation, metastasis, and invasion of CRC cells. In this review, we underline the documented benefits of small interfering RNAs and short hairpin RNAs to target genes and signaling pathways related to CRC tumorigenesis. We address the synergistic effects of RNAi-mediated gene knockdown and inhibitors/chemotherapy agents to increase the sensitivity of CRC cells to common therapies. Finally, this review points new delivery systems/materials for improving the cellular uptake efficiency and reducing off-target effects of RNAi.
C1 [Jebelli, Asiyeh] Higher Educ Inst Rab Rashid, Fac Basic Sci, Dept Biol Sci, Tabriz, Iran.
   [Baradaran, Behzad; Baghbanzadeh, Amir; Mokhtarzadeh, Ahad] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz 5166614731, Iran.
   [Mosafer, Jafar] Torbat Heydariyeh Univ Med Sci, Res Ctr Adv Technol Med, Torbat Heydariyeh, Iran.
   [Tayebi, Lobat] Marquette Univ, Sch Dent, Milwaukee, WI 53233 USA.
C3 Tabriz University of Medical Science; Marquette University
RP Mokhtarzadeh, A (corresponding author), Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz 5166614731, Iran.; Tayebi, L (corresponding author), Marquette Univ, Sch Dent, Milwaukee, WI 53233 USA.
EM ahad.mokhtarzadeh@gmail.com; lobat.tayebi@marquette.edu
RI Jebelli, Asiyeh/IAP-3359-2023; Mosafer, Jafar/O-1493-2017; Baradaran,
   Behzad/AAQ-5177-2020; Mokhtarzadeh, Ahad/V-3748-2017
OI Tayebi, Lobat/0000-0003-1947-5658; mokhtarzadeh, Amir
   Ali/0000-0002-4515-8675; baradaran, behzad/0000-0002-8642-6795; Mosafer,
   Jafar/0000-0002-2897-0039; baghbanzadeh, amir/0000-0002-1261-3213;
   jebelli, asiyeh/0000-0001-9494-2207
FU Tabriz University of Medical Sciences [61733]
FX Tabriz University of Medical Sciences, Grant/Award Number: 61733
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NR 178
TC 14
Z9 15
U1 0
U2 25
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0198-6325
EI 1098-1128
J9 MED RES REV
JI Med. Res. Rev.
PD JAN
PY 2021
VL 41
IS 1
BP 395
EP 434
DI 10.1002/med.21735
EA SEP 2020
PG 40
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA PE3BJ
UT WOS:000573353300001
PM 32990372
DA 2025-01-04
ER

PT J
AU Liu, JH
   Zeng, WQ
   Huang, CZ
   Wang, JJ
   Yang, DY
   Ma, D
AF Liu, Jianhua
   Zeng, Weiqiang
   Huang, Chengzhi
   Wang, Junjiang
   Yang, Dongyang
   Ma, Dong
TI Predictive and Prognostic Implications of Mutation Profiling and
   Microsatellite Instability Status in Patients with Metastatic Colorectal
   Carcinoma
SO GASTROENTEROLOGY RESEARCH AND PRACTICE
LA English
DT Article
ID PIK3CA MUTATIONS; CANCER PATIENTS; CLINICOPATHOLOGICAL CHARACTERISTICS;
   RAS ONCOGENE; BRAF; KRAS; NRAS; PATHWAY; MODEL
AB To investigate whether mutation profiling and microsatellite instability (MSI) status were associated with clinicopathological features and the prognosis in metastatic colorectal cancer (mCRC), mutations in RAS (including KRAS, NRAS, and HRAS) and BRAF were determined by Sanger sequencing. Tumor mismatch repair proteins and MSI status were examined using immunohistochemistry and polymerase chain reaction, respectively. The clinical value of these abnormalities was statistically analyzed, and prognostic value of different treatment regimens was also evaluated. Among 461 mCRC patients, mutations in RAS, BRAF, and MSI- high (MSI-H) status were observed in 45.3% (209/461), 5.6% (26/461), and 6.5% (30/461) of cases, respectively. Brain metastasis and high carcinoembryonic antigen level were highly correlated with KRAS mutation (P = 0 011 and P < 0 001), and tumors from females or located in the right colon tended to harbor BRAF mutation (P = 0 039 and P = 0 001). RAS/BRAF mutations may predict brain and/or lung metastases. Although neither clinical nor prognostic importance of MSI status was identified in our study, KRAS and BRAF mutations were demonstrated to be independent prognostic factors for overall survival and progression-free survival. Besides, in wild-type group, patients treated with chemotherapy plus targeted therapy exhibited the most favorable prognosis. Therefore, RAS/BRAF mutations may serve as indicators for prognosis and treatment options in mCRC.
C1 [Liu, Jianhua; Yang, Dongyang; Ma, Dong] Guangdong Acad Med Sci, Guangdong Gen Hosp, Dept Gastrointestinal Oncol, Canc Ctr, Guangzhou, Guangdong, Peoples R China.
   [Zeng, Weiqiang] Guangdong Acad Med Sci, Guangdong Gen Hosp, Dept Pharm, Guangzhou, Guangdong, Peoples R China.
   [Huang, Chengzhi; Wang, Junjiang] Guangdong Acad Med Sci, Guangdong Gen Hosp, Dept Gastrointestinal Surg, Guangzhou, Guangdong, Peoples R China.
C3 Southern Medical University - China; Guangdong Academy of Medical
   Sciences & Guangdong General Hospital; Guangdong Academy of Medical
   Sciences & Guangdong General Hospital; Southern Medical University -
   China; Southern Medical University - China; Guangdong Academy of Medical
   Sciences & Guangdong General Hospital
RP Ma, D (corresponding author), Guangdong Acad Med Sci, Guangdong Gen Hosp, Dept Gastrointestinal Oncol, Canc Ctr, Guangzhou, Guangdong, Peoples R China.
EM madong8005@126.com
FU Program of Health and Family Planning Commission Foundation of Guangzhou
   City, Guangdong Province, China [A2017418]; Program of Science and
   Technology Commission Foundation of Guangzhou City, Guangdong Province,
   China [20140705]
FX This work was supported by a grant from the Program of Health and Family
   Planning Commission Foundation of Guangzhou City, Guangdong Province,
   China (Grant no. A2017418), and a grant from the Program of Science and
   Technology Commission Foundation of Guangzhou City, Guangdong Province,
   China (Grant no. 20140705).
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NR 36
TC 13
Z9 15
U1 0
U2 10
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-6121
EI 1687-630X
J9 GASTROENT RES PRACT
JI Gastroenterol. Res. Pract.
PY 2018
VL 2018
AR 4585802
DI 10.1155/2018/4585802
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FV8GL
UT WOS:000424824100001
PM 29643917
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Chen, ZG
   Jiang, LL
AF Chen, Zhongguang
   Jiang, Lili
TI The clinical application of fruquintinib on colorectal cancer
SO EXPERT REVIEW OF CLINICAL PHARMACOLOGY
LA English
DT Article
DE Fruquintinib; EGFR; VEGF; VEGFR; CRC
ID CELL LUNG-CANCER; ENDOTHELIAL GROWTH-FACTOR; PLASMA-PROTEIN BINDING;
   SELECTIVE VEGFR INHIBITOR; CHRONIC INFLAMMATION; PRACTICE GUIDELINES;
   TYROSINE KINASES; DRUG DISCOVERY; GUT MICROBIOTA; P53 STATUS
AB Introduction: Anti-angiogenetic agents are currently the most commonly used drugs for the treatment of colorectal cancer (CRC) patients, including various inhibitors targeting the epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and VEGF receptors (VEGFRs). Fruquintinib (HMPL-013), a highly selective and long-term small-molecule inhibitor of VEGFR (VEGFR1, 2, and 3) was recently approved in China for CRC treatment. Clinical studies have shown it has many advantages, such as low off-target toxicity, good drug tolerance, and strong effect. Areas covered: In the review, the molecular structure, mechanism of action, pharmacokinetics, clinical efficacy, and safety of fruquintinib are introduced in detail. The potential clinic application on non-small cell lung cancer (NSCLC) and gastric cancer is also discussed. Expert commentary: Fruquintinib was approved for patients with metastatic colorectal cancer (RAS wild type) who have previously received fluorouracil, oxaliplatin, and irinotecan-based chemotherapy and who have received or are not suitable for anti- VEGF therapy and anti- EGFR therapy. As a novel, therapeutic approach to CRC, Fruquintinib could be used as a third-line drug for the treatment of CRC patients. Due to drug resistance during the long-term therapy, the combination of fruquintinib with other targeted therapy drugs may be an effective option for CRC treatment.
C1 [Chen, Zhongguang] Cent Hosp Linyi City, Dept Pharmaceut, Clin Pharmaceut Room,Huakang Bldg 22 Floor, Yishui 276400, Shandong, Peoples R China.
   [Jiang, Lili] Shandong Univ, Jinan Cent Hosp, Ultrasound Med Dept, Jinan, Shandong, Peoples R China.
C3 Shandong First Medical University & Shandong Academy of Medical
   Sciences; Shandong University
RP Chen, ZG (corresponding author), Cent Hosp Linyi City, Dept Pharmaceut, Clin Pharmaceut Room,Huakang Bldg 22 Floor, Yishui 276400, Shandong, Peoples R China.
EM czg1129@126.com
RI Chen, zhongguang/AAV-7085-2020
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NR 84
TC 19
Z9 24
U1 3
U2 29
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1751-2433
EI 1751-2441
J9 EXPERT REV CLIN PHAR
JI Expert Rev. Clin. Pharmacol.
PD AUG 3
PY 2019
VL 12
IS 8
BP 713
EP 721
DI 10.1080/17512433.2019.1630272
EA JUN 2019
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA IN9ZR
UT WOS:000472394900001
PM 31177854
DA 2025-01-04
ER

PT J
AU Taira, K
   Okazaki, S
   Akiyoshi, K
   Machida, H
   Ikeya, T
   Kimura, A
   Nakata, A
   Nadatani, Y
   Ohminami, M
   Fukunaga, S
   Otani, K
   Hosomi, S
   Tanaka, F
   Kamata, N
   Nagami, Y
   Fujiwara, Y
AF Taira, Koichi
   Okazaki, Shunsuke
   Akiyoshi, Kohei
   Machida, Hirohisa
   Ikeya, Tetsuro
   Kimura, Akie
   Nakata, Akinobu
   Nadatani, Yuji
   Ohminami, Masaki
   Fukunaga, Shusei
   Otani, Koji
   Hosomi, Shuhei
   Tanaka, Fumio
   Kamata, Noriko
   Nagami, Yasuaki
   Fujiwara, Yasuhiro
TI Short bevacizumab infusion as an effective and safe treatment for
   colorectal cancer
SO MOLECULAR AND CLINICAL ONCOLOGY
LA English
DT Article
DE bevacizumab; infusion; colorectal cancer; target therapy; PFS
ID FLUOROURACIL; FEASIBILITY; PACLITAXEL; LEUCOVORIN
AB Bevacizumab is a humanized monoclonal antibody that contains <10% murine protein. To prevent infusion-related hypersensitivity reactions (HSRs), the initial bevacizumab infusion is delivered for 90 min, the second for 60 min and subsequent doses for 30 min. Several previous studies have shown that short bevacizumab infusions are safe and do not result in severe HSRs in patients with colorectal, lung, ovarian and brain cancer. However, the efficacy of short bevacizumab infusions for colorectal cancer management remains unclear. Therefore, to investigate this issue, a prospective multicenter study was conducted using 23 patients enrolled between June 2017 and March 2019. The initial infusion of bevacizumab was for 30 min followed by a second infusion rate of 0.5 mg/kg/min (5 mg/kg over 10 min and 7.5 mg/kg over 15 min. The primary endpoint was progression-free survival (PFS). The overall response and disease control rates were 57 and 87%, respectively. The median PFS time was 306 days (interquartile range, 204-743 days). No HSRs were noted. Adverse events associated with bevacizumab included grade 4 small intestinal perforation and grade 3 stroke in 1 patient each. These results suggest that a short bevacizumab infusion regime comprising an initial infusion for 30 min followed by a second infusion at 0.5 mg/kg/min is safe and efficacious for the management of colorectal cancer.
C1 [Taira, Koichi; Kimura, Akie; Nakata, Akinobu; Nadatani, Yuji; Ohminami, Masaki; Fukunaga, Shusei; Otani, Koji; Hosomi, Shuhei; Tanaka, Fumio; Kamata, Noriko; Nagami, Yasuaki; Fujiwara, Yasuhiro] Osaka Metropolitan Univ, Grad Sch Med, Dept Gastroenterol, Osaka 5458585, Japan.
   [Okazaki, Shunsuke; Akiyoshi, Kohei] Osaka City Gen Hosp, Dept Clin Oncol, Osaka 5340021, Japan.
   [Okazaki, Shunsuke] Nara Med Univ Hosp, Dept Med Oncol, Nara 6348521, Japan.
   [Machida, Hirohisa] Machida Gastrointestinal Hosp, Dept Gastroenterol, Osaka 5570001, Japan.
   [Ikeya, Tetsuro] Osaka Ekisaikai Hosp, Dept Surg, Osaka 5500022, Japan.
C3 Osaka Metropolitan University; Osaka City General Hospital; Nara Medical
   University
RP Taira, K (corresponding author), Osaka Metropolitan Univ, Grad Sch Med, Dept Gastroenterol, Osaka 5458585, Japan.
EM koichit0802@gmail.com
RI Hosomi, Shuhei/LEL-9155-2024; Fujiwara, Yasuhiro/AAM-5504-2020; Tanaka,
   Fumio/HCI-5442-2022
OI Tanaka, Fumio/0000-0002-9186-1249
CR Aljehani MA, 2018, JAMA SURG, V153, P60, DOI 10.1001/jamasurg.2017.3466
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NR 23
TC 2
Z9 2
U1 0
U2 2
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 2049-9450
EI 2049-9469
J9 MOL CLIN ONCOL
JI Mol. Clin. Oncol.
PD SEP
PY 2022
VL 17
IS 3
AR 139
DI 10.3892/mco.2022.2572
PG 5
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA 3U2WW
UT WOS:000840835800001
PM 35949896
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Arakawa, K
   Hata, K
   Nozawa, H
   Kawai, K
   Tanaka, T
   Nishikawa, T
   Sasaki, K
   Shuno, Y
   Kaneko, M
   Hiyoshi, M
   Emoto, S
   Murono, K
   Sonoda, H
   Okada, S
   Ishihara, S
AF Arakawa, Keiichi
   Hata, Keisuke
   Nozawa, Hiroaki
   Kawai, Kazushige
   Tanaka, Toshiaki
   Nishikawa, Takeshi
   Sasaki, Kazuhito
   Shuno, Yasutaka
   Kaneko, Manabu
   Hiyoshi, Masaya
   Emoto, Shigenobu
   Murono, Koji
   Sonoda, Hirofumi
   Okada, Satoshi
   Ishihara, Soichiro
TI Molecular Subtypes Are Frequently Discordant Between Lesions in Patients
   With Synchronous Colorectal Cancer: Molecular Analysis of 59 Patients
SO ANTICANCER RESEARCH
LA English
DT Article
DE Colorectal cancer; MSI; MLH1 methylation; BRAF
ID HMLH1 PROMOTER HYPERMETHYLATION; ISLAND METHYLATOR PHENOTYPE;
   MICROSATELLITE INSTABILITY; CLINICOPATHOLOGICAL FEATURES; CARCINOMA;
   EXPRESSION; PROTEIN; HETEROGENEITY; SUBSET
AB Background: We aimed to investigate the molecular features of synchronous colorectal cancer (CRC). Materials and Methods: Out of 1,262 patients with CRC, 130 lesions in 59 patients with synchronous CRC were retrospectively analyzed. Microsatellite, v-Ki-Ras2 Kristen rat sarcoma viral oncogene homolog (KRAS), v-raf murine sarcoma viral oncogene homolog B1 (BRAF), tumor protein 53 (TP53) and beta-catenin status were evaluated and compared between synchronous CRC lesions in each patient. Results: The subtypes of instability, BRAF and beta-catenin subtypes was significant but low. Patients with discordant KRAS and TP53 were not concordant between lesions in the same patient, and concordance of microsatellite KRAS/BRAF subtypes comprised 50.8% of those with synchronous CRC. The rate of patients with lesions containing both mutL homolog 1 (MLH1) methylation and microsatellite stable status was 66.7% in those with synchronous CRC, with at least one lesion with high microsatellite instability. Conclusion: The present study on synchronous CRC demonstrated a low concordance of molecular subtypes between lesions in the same patient. A molecular analysis of metastatic lesions is warranted for molecular targeted therapy of metastatic synchronous CRC.
C1 [Arakawa, Keiichi; Hata, Keisuke; Nozawa, Hiroaki; Kawai, Kazushige; Tanaka, Toshiaki; Nishikawa, Takeshi; Sasaki, Kazuhito; Shuno, Yasutaka; Kaneko, Manabu; Hiyoshi, Masaya; Emoto, Shigenobu; Murono, Koji; Sonoda, Hirofumi; Okada, Satoshi; Ishihara, Soichiro] Univ Tokyo, Dept Surg Oncol, Tokyo, Japan.
C3 University of Tokyo
RP Arakawa, K (corresponding author), Univ Tokyo Hosp, Dept Surg Oncol, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan.
EM Keiichiarakawa@hotmail.com
RI Ishihara, Soichiro/AFK-1375-2022; Okada, Satoshi/N-3058-2014; Murono,
   Koji/AAC-3958-2020; Kawai, Kazushige/AAF-4334-2020
OI Sonoda, Hirofumi/0000-0003-3353-1783; Arakawa,
   Keiichi/0000-0002-9424-4481; Hata, Keisuke/0000-0003-4064-8701
FU Japan Society for the Promotion of Science [16K07143, 16K07161,
   17K10620, 17K10621, 17K10623, 18K07194]; Project for Cancer Research and
   Therapeutic Evolution from the Japan Agency for Medical Research and
   Development [18cm0106502h0003]; Grants-in-Aid for Scientific Research
   [17K10623] Funding Source: KAKEN
FX ;This research was supported by Grants-in-Aid for Scientific Research
   (C) (grant numbers: 16K07143, 16K07161, 17K10620, 17K10621, 17K10623,
   and 18K07194) from the Japan Society for the Promotion of Science and by
   the Project for Cancer Research and Therapeutic Evolution (grant number:
   18cm0106502h0003) from the Japan Agency for Medical Research and
   Development.
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NR 39
TC 3
Z9 3
U1 0
U2 3
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 MAR
PY 2019
VL 39
IS 3
BP 1425
EP 1432
DI 10.21873/anticanres.13258
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HN7WN
UT WOS:000460403800041
PM 30842178
OA Bronze
DA 2025-01-04
ER

PT J
AU Jiang, FQ
   Chen, YD
   Ren, S
   Li, ZZ
   Sun, K
   Xing, YW
   Zhu, YK
   Piao, DX
AF Jiang, Fengqi
   Chen, Yaodong
   Ren, Shuo
   Li, Zizhuo
   Sun, Kan
   Xing, Yanwei
   Zhu, Yuekun
   Piao, Daxun
TI Cyclovirobuxine D inhibits colorectal cancer tumorigenesis via the
   CTHRC1-AKT/ERK-Snail signaling pathway
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Article
DE cyclovirobuxine D; colorectal cancer; collagen triple helix repeat
   containing 1-AKT; ERK-Snail signaling pathway; epithelial-to-mesenchymal
   transition
ID EPITHELIAL-MESENCHYMAL TRANSITION; TRIPLE-HELIX REPEAT; CYCLIN D1;
   EXPRESSION; MIGRATION; PROLIFERATION; GLIOBLASTOMA; PROGRESSION;
   METASTASIS; APOPTOSIS
AB Cyclovirobuxine D (CVB-D) is an alkaloid, which is mainly derived fromBuxus microphylla. It has been reported that CVB-D has positive effects on breast cancer, gastric cancer and other malignant tumors. However, to the best of our knowledge, there are no reports regarding the effects of CVB-D on colorectal cancer (CRC). The purpose of the present study was to determine the anticancer effects of CVB-D and further elucidate its molecular mechanism(s). DLD-1 and LoVo cell lines were selected to evaluate the antitumor effect of CVB-D. Cytotoxicity, viability and proliferation were evaluated by the MTT and colony formation assays. Flow cytometry was used to detect the effects on apoptosis and the cell cycle in CVB-D-treated CRC cells. The migration and invasion abilities of CRC cells were examined by wound healing and Transwell assays. In addition, RNA sequencing, bioinformatics analysis and western blotting were performed to investigate the target of drug action and clarify the molecular mechanisms. A xenograft model was established using nude mice, and ultrasound was employed to assess the preclinical therapeutic effects of CVB-Din vivo. It was identified that CVB-D inhibited the proliferation, migration, stemness, angiogenesis and epithelial-mesenchymal transition of CRC cells, and induced apoptosis and S-phase arrest. In addition, CVB-D significantly inhibited the growth of xenografts. It is notable that CVB-D exerted anticancer effects in CRC cells partly by targeting collagen triple helix repeat containing 1 (CTHRC1), which may be upstream of the AKT and ERK pathways. CVB-D exerted anticancer effects through the CTHRC1-AKT/ERK-Snail signaling pathway. Targeted therapy combining CTHRC1 with CVB-D may offer a promising novel therapeutic approach for CRC treatment.
C1 [Jiang, Fengqi; Ren, Shuo; Li, Zizhuo; Xing, Yanwei; Zhu, Yuekun; Piao, Daxun] Harbin Med Univ, Affiliated Hosp 1, Dept Colorectal Surg, 23 Youzheng St, Harbin 150001, Heilongjiang, Peoples R China.
   [Chen, Yaodong] Shanxi Med Univ, Dept Ultrason Imaging, Clin Med Coll 1, Taiyuan 030001, Shanxi, Peoples R China.
   [Sun, Kan] Heilongjiang Prov Hosp, Dept Gen Surg, Harbin 150001, Heilongjiang, Peoples R China.
C3 Harbin Medical University; Shanxi Medical University
RP Piao, DX (corresponding author), Harbin Med Univ, Affiliated Hosp 1, Dept Colorectal Surg, 23 Youzheng St, Harbin 150001, Heilongjiang, Peoples R China.
EM piaodaxun@sina.com
FU Scientific Planning Project of Heilongjiang Province [201713];
   Innovation Project of Harbin Medical University [YJSKYCX2018-37HYD]
FX This work was supported by the Scientific Planning Project of
   Heilongjiang Province (grant. no. 201713) and the Innovation Project of
   Harbin Medical University (grant. no. YJSKYCX2018-37HYD).
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NR 63
TC 21
Z9 23
U1 1
U2 18
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1019-6439
EI 1791-2423
J9 INT J ONCOL
JI Int. J. Oncol.
PD JUL
PY 2020
VL 57
IS 1
BP 183
EP 196
DI 10.3892/ijo.2020.5038
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ME9OB
UT WOS:000544982500015
PM 32319595
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Sadeghi, M
   Mestivier, D
   Sobhani, I
AF Sadeghi, Mohammad
   Mestivier, Denis
   Sobhani, Iradj
TI Contribution of pks plus <i>Escherichia coli</i> (<i>E</i>. <i>coli</i>)
   to Colon Carcinogenesis
SO MICROORGANISMS
LA English
DT Review
DE pks plus E. coli; colorectal cancer; colon; gut microbiota; diagnosis;
   therapy
ID CYTOLETHAL DISTENDING TOXIN; CYTOTOXIC NECROTIZING FACTOR-1;
   ASSEMBLY-LINE ENZYMOLOGY; PERSISTENT DNA-DAMAGE; CELL-CYCLE;
   NONRIBOSOMAL PEPTIDE; COLORECTAL-CANCER; COLIBACTIN BIOSYNTHESIS;
   INTESTINAL INFLAMMATION; BACTERIAL GENOTOXIN
AB Colorectal cancer (CRC) stands as a significant global health concern, ranking second in mortality and third in frequency among cancers worldwide. While only a small fraction of CRC cases can be attributed to inherited genetic mutations, the majority arise sporadically due to somatic mutations. Emerging evidence reveals gut microbiota dysbiosis to be a contributing factor, wherein polyketide synthase-positive Escherichia coli (pks+ E. coli) plays a pivotal role in CRC pathogenesis. pks+ bacteria produce colibactin, a genotoxic protein that causes deleterious effects on DNA within host colonocytes. In this review, we examine the role of the gut microbiota in colon carcinogenesis, elucidating how colibactin-producer bacteria induce DNA damage, promote genomic instability, disrupt the gut epithelial barrier, induce mucosal inflammation, modulate host immune responses, and influence cell cycle dynamics. Collectively, these actions foster a microenvironment conducive to tumor initiation and progression. Understanding the mechanisms underlying pks+ bacteria-mediated CRC development may pave the way for mass screening, early detection of tumors, and therapeutic strategies such as microbiota modulation, bacteria-targeted therapy, checkpoint inhibition of colibactin production and immunomodulatory pathways.
C1 [Sadeghi, Mohammad; Mestivier, Denis; Sobhani, Iradj] Paris East Creteil Univ UPEC, EA7375 EC2M3 Early, Detect Colon Canc Using Microbial & Mol Markers, F-94010 Creteil, France.
   [Sobhani, Iradj] Henri Mondor Hosp, APHP, Dept Gastroenterol, F-94010 Creteil, France.
C3 Universite Paris-Est-Creteil-Val-de-Marne (UPEC); Assistance Publique
   Hopitaux Paris (APHP); Universite Paris-Est-Creteil-Val-de-Marne (UPEC);
   Hopital Universitaire Henri-Mondor - APHP
RP Sadeghi, M; Sobhani, I (corresponding author), Paris East Creteil Univ UPEC, EA7375 EC2M3 Early, Detect Colon Canc Using Microbial & Mol Markers, F-94010 Creteil, France.; Sobhani, I (corresponding author), Henri Mondor Hosp, APHP, Dept Gastroenterol, F-94010 Creteil, France.
EM mohammad.sadeghi@u-pec.fr; denis.mestivier@u-pec.fr;
   iradj.sobhani@aphp.fr
RI SOBHANI, Iradj/A-3973-2013; SADEGHI, Mohammad/LKL-4249-2024
OI SADEGHI, Mohammad/0000-0003-2524-2279
FU EPIMECHA [5 R01 CA264048-03]; MicroTEND study (GTE French
   Gastrointestinal endocrine tumours); National Institutes of Health
   [1C06MH264048-20A5]
FX EPIMECHA (Grant 5 R01 CA264048-03) and MicroTEND study (GTE French
   Gastrointestinal endocrine tumours). National Institutes of Health:
   1C06MH264048-20A5.
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NR 143
TC 3
Z9 3
U1 4
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-2607
J9 MICROORGANISMS
JI Microorganisms
PD JUN
PY 2024
VL 12
IS 6
AR 1111
DI 10.3390/microorganisms12061111
PG 23
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA WU5E2
UT WOS:001257392200001
PM 38930493
OA gold
DA 2025-01-04
ER

PT J
AU Imyanitov, E
   Kuligina, E
AF Imyanitov, Evgeny
   Kuligina, Ekaterina
TI Molecular testing for colorectal cancer: Clinical applications
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Colorectal cancer; Anti-epidermal growth factor receptor therapy; KRAS;
   NRAS; BRAF; HER2; Microsatellite instability; MUTYH; Hereditary cancer
ID MICROSATELLITE INSTABILITY; FAMILIAL PREDISPOSITION; INTERNATIONAL
   CRITERIA; INSTITUTE WORKSHOP; RAS MUTATIONS; BRAF; GUIDELINES; BLOCKADE;
   THERAPY; PIK3CA
AB Molecular genetic analysis is an integral part of colorectal cancer (CRC) management. The choice of systemic therapy for CRC is largely based on the results of tumor molecular testing. Evaluation of the KRAS and NRAS gene status is mandatory for consideration of anti-epidermal growth factor receptor (EGFR) therapy. Tumors with the BRAF V600E substitution are characterized by aggressive behaviour, may require intensified cytotoxic regimens and benefit from combined BRAF and EGFR inhibition. The inactivation of DNA mismatch repair (MMR), or MUTYH gene, or DNA polymerase epsilon results in excessive tumor mutational burden; these CRCs are highly antigenic and therefore sensitive to immune checkpoint inhibitors. Some CRCs are characterized by overexpression of the HER2 oncogene and respond to the appropriate targeted therapy. There are CRCs with clinical signs of hereditary predisposition to this disease, which require germline genetic testing. Liquid biopsy is an emerging technology that has the potential to assist CRC screening, control the efficacy of surgical intervention and guide disease monitoring. The landscape of CRC molecular diagnosis is currently undergoing profound changes due to the increasing use of next generation sequencing.
C1 [Imyanitov, Evgeny; Kuligina, Ekaterina] NN Petrov Inst Oncol, Dept Tumor Biol, St Petersburg 197758, Russia.
   [Imyanitov, Evgeny] St Petersburg Pediat Med Univ, Dept Med Genet, St Petersburg 194100, Russia.
   [Imyanitov, Evgeny] II Mechnikov North Western Med Univ, Dept Oncol, St Petersburg 191015, 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
RP Imyanitov, E (corresponding author), NN Petrov Inst Oncol, Dept Tumor Biol, St Petersburg 197758, Russia.
EM evgeny@imyanitov.spb.ru
RI Kuligina, Ekaterina/P-4449-2016
FU Ministry of Science and Higher Education of the Russian Federation
   [075-15-2020-789]
FX Supported by Ministry of Science and Higher Education of the Russian
   Federation, No. 075-15-2020-789.
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NR 96
TC 10
Z9 10
U1 0
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD OCT 15
PY 2021
VL 13
IS 10
BP 1288
EP 1301
DI 10.4251/wjgo.v13.i10.1288
PG 14
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA XB8VS
UT WOS:000721601200005
PM 34721767
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Marginean, EC
   Melosky, B
AF Marginean, Esmeralda Celia
   Melosky, Barbara
TI Is There a Role for Programmed Death Ligand-1 Testing and Immunotherapy
   in Colorectal Cancer With Microsatellite Instability? Part I-Colorectal
   Cancer: Microsatellite Instability, Testing, and Clinical Implications
SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
ID LYNCH-SYNDROME; ADJUVANT CHEMOTHERAPY; BETHESDA GUIDELINES; HEREDITARY;
   COLON; CLASSIFICATION; CARCINOMAS; PREDICT; TUMORS; RISK
AB Context.-Colorectal cancer (CRC) represents the third most-common cancer in developed countries and is a leading cause of cancer deaths worldwide. Two recognized pathways contribute to CRC development: a more-common chromosomal instability pathway and, in 15% of cases, a deficient mismatch repair or microsatellite instability-high (MSI-H) pathway. The MSI-H CRC can be associated with somatic or germline mutations. Microsatellite status has been recognized as a prognostic and predictive biomarker.
   Objectives.-To summarize the molecular pathways of CRC, with an emphasis on the MSI (mismatch repair) pathway; the recommended MSI testing algorithms and interpretation; and the prognostic and predictive role of MSI-H status in personalized treatment, including adjuvant chemotherapy, targeted therapy, and immune checkpoint inhibitor therapy.
   Data Sources.-A PubMed (US National Library of Medicine, Bethesda, Maryland) review was performed for articles pertaining to CRC, MSI and mismatch repair systems, molecular classification, immune response, programmed death receptor-1/programmed death ligand-1, and immunotherapy.
   Conclusions.-Although the TNM classification of malignant tumor stage remains the key determinant of CRC prognosis and treatment, there are considerable stage-independent, interindividual differences in clinical outcome and therapy response by patients. In addition, MSI-H status has an important role in CRC management and can be reliably detected by molecular and immunohistochemistry techniques and genetic testing. Efforts must be made to identify whether MSI-H CRC is germline or sporadic to ensure appropriate treatment, accurate prognosis, and risk assessment for relatives. Microsatellite status has been recognized as a good prognostic indicator and is predictive of a poor response to 5-fluorouracil-based chemotherapy and a good response to programmed death ligand-1 inhibitor pembrolizumab in metastatic/refractory MSI-H CRC.
C1 [Marginean, Esmeralda Celia] Univ Ottawa, Dept Pathol, Ottawa, ON, Canada.
   [Marginean, Esmeralda Celia] Ottawa Hosp, Gastrointestinal Pathol Sect, CCW Room 4251,501 Smyth Rd, Ottawa, ON K1H 8L6, Canada.
   [Melosky, Barbara] Univ British Columbia, Dept Med Oncol, Vancouver, BC, Canada.
   [Melosky, Barbara] British Columbia Canc Agcy, Dept Oncol, Vancouver, BC, Canada.
C3 University of Ottawa; University of Ottawa; Ottawa Hospital Research
   Institute; University of British Columbia; British Columbia Cancer
   Agency
RP Marginean, EC (corresponding author), Ottawa Hosp, Gastrointestinal Pathol Sect, CCW Room 4251,501 Smyth Rd, Ottawa, ON K1H 8L6, Canada.
EM cmarginean@toh.on.ca
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NR 51
TC 30
Z9 34
U1 1
U2 5
PU COLL AMER PATHOLOGISTS
PI NORTHFIELD
PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA
SN 0003-9985
EI 1543-2165
J9 ARCH PATHOL LAB MED
JI Arch. Pathol. Lab. Med.
PD JAN
PY 2018
VL 142
IS 1
BP 17
EP 25
DI 10.5858/arpa.2017-0040-RA
PG 9
WC Medical Laboratory Technology; Medicine, Research & Experimental;
   Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology; Research & Experimental Medicine;
   Pathology
GA FT9FP
UT WOS:000423457800006
PM 29144791
OA gold
DA 2025-01-04
ER

PT J
AU Cheng, HH
   Shao, YC
   Lin, CY
   Chiang, TW
   Chen, MC
   Chiu, TY
   Huang, YL
   Chen, CC
   Chen, CP
   Chiang, FF
AF Cheng, H. -H.
   Shao, Y. -C.
   Lin, C. -Y.
   Chiang, T. -W.
   Chen, M. -C.
   Chiu, T. -Y.
   Huang, Y. -L.
   Chen, C. -C.
   Chen, C. -P.
   Chiang, F. -F.
TI Impact of chemotherapy on surgical outcomes in ileostomy reversal: a
   propensity score matching study from a single centre
SO TECHNIQUES IN COLOPROCTOLOGY
LA English
DT Article
DE Rectal cancer; Adjuvant chemotherapy; Target therapy; Ileostomy; Stoma;
   Morbidity; Complication
ID LOW ANTERIOR RESECTION; RECTAL-CANCER; LOOP ILEOSTOMY; ADJUVANT
   CHEMOTHERAPY; COLONIC ANASTOMOSES; DEFUNCTIONING STOMA; 5-FLUOROURACIL;
   CLOSURE; MORBIDITY
AB PurposeIn patients with chemotherapy, there is no consensus on the timing of ileostomy closure. Ileostomy reversal could improve the quality of life and minimise the long-term adverse events of delayed closure. In this study, we evaluated the impact of chemotherapy on ileostomy closure and searched for the predictive factors for complications.MethodsWe retrospectively analysed 212 patients with rectal cancer who underwent ileostomy closure surgery during and without chemotherapy and were consecutively enrolled between 2010 and 2016. As a result of the heterogeneity of the two groups, propensity score matching (PSM) was performed with a 1:1 PSM cohort.ResultsA total of 162 patients were included in the analysis. The overall stoma closure-related complications (12.4% vs. 11.1%, p = 1.00) and major complications (2.5% vs. 6.2%, p = 0.44) were not significantly different between the two groups. Multivariate analysis demonstrated that chronic kidney disease and bevacizumab use are risk factors for major complications.ConclusionPatients with oral or intravenous chemotherapy can safely have ileostomy closure with an adequate time delay from chemotherapy. When patients use bevacizumab, major complications related to ileostomy closure should still be cautioned.
C1 [Cheng, H. -H.] Taipei Vet Gen Hosp, Dept Surg, Div Colon & Rectal Surg, Taipei, Taiwan.
   [Cheng, H. -H.; Shao, Y. -C.; Lin, C. -Y.; Chiang, T. -W.; Chen, M. -C.; Chiu, T. -Y.; Huang, Y. -L.; Chen, C. -C.; Chen, C. -P.; Chiang, F. -F.] Taichung Vet Gen Hosp, Dept Surg, Div Colorectal Surg, Taichung, Taiwan.
   [Cheng, H. -H.; Shao, Y. -C.; Lin, C. -Y.] Natl Yang Ming Chiao Tung Univ, Fac Med, Sch Med, Dept Surg, Taipei, Taiwan.
   [Shao, Y. -C.] China Med Univ, Dept Surg, Div Colorectal Surg, Hsinchu Hosp, Hsinchu, Taiwan.
C3 Taipei Veterans General Hospital; Taichung Veterans General Hospital;
   National Yang Ming Chiao Tung University; China Medical University
   Taiwan
RP Cheng, HH (corresponding author), Taipei Vet Gen Hosp, Dept Surg, Div Colon & Rectal Surg, Taipei, Taiwan.; Cheng, HH (corresponding author), Taichung Vet Gen Hosp, Dept Surg, Div Colorectal Surg, Taichung, Taiwan.; Cheng, HH (corresponding author), Natl Yang Ming Chiao Tung Univ, Fac Med, Sch Med, Dept Surg, Taipei, Taiwan.
EM samhhtenn@gmail.com
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NR 34
TC 3
Z9 3
U1 1
U2 2
PU SPRINGER-VERLAG ITALIA SRL
PI MILAN
PA VIA DECEMBRIO, 28, MILAN, 20137, ITALY
SN 1123-6337
EI 1128-045X
J9 TECH COLOPROCTOL
JI Tech. Coloproctology
PD DEC
PY 2023
VL 27
IS 12
BP 1227
EP 1234
DI 10.1007/s10151-023-02790-6
EA MAR 2023
PG 8
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA Y2LO9
UT WOS:000959335200002
PM 36973527
DA 2025-01-04
ER

PT J
AU Ceccon, C
   Angerilli, V
   Rasola, C
   Procaccio, L
   Sabbadin, M
   Bergamo, F
   Malapelle, U
   Lonardi, S
   Fassan, M
AF Ceccon, Carlotta
   Angerilli, Valentina
   Rasola, Cosimo
   Procaccio, Letizia
   Sabbadin, Marianna
   Bergamo, Francesca
   Malapelle, Umberto
   Lonardi, Sara
   Fassan, Matteo
TI Microsatellite Instable Colorectal Adenocarcinoma Diagnostics: The
   Advent of Liquid Biopsy Approaches
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE liquid biopsy; colorectal cancer; microsatellite Instability;
   immunotherapy; circulating tumor DNA; cancer screening; early detection
ID TUMOR MUTATIONAL BURDEN; ACQUIRED-RESISTANCE; CLINICAL-PRACTICE; EGFR
   BLOCKADE; COLON-CANCER; INSTABILITY; DNA; PLASMA; HETEROGENEITY;
   VALIDATION
AB The introduction of immunotherapy has revolutionized the oncological targeted therapy paradigm. Microsatellite instability (MSI) identifies a subgroup of colorectal cancers (CRCs) which respond to treatment with immune checkpoint inhibitors. Tissue biopsy is currently the gold standard for the assessment of MSI/Mismatch Repair deficiency (MMRd) by means immunohistochemistry or molecular assays. However, the application of liquid biopsy in the clinic may help to overcome several limitations of tissue analysis and may provide great benefit to the diagnostic scenario and therapeutic decision-making process. In the context of MSI/MMRd CRC, the use of liquid biopsy may allow to establish MSI/MMR status if tissue sampling cannot be performed or in case of discordant tissue biopsies. Liquid biopsy may also become a powerful tool to monitor treatment response and the onset resistance to immunotherapy over time and to stratify of MSI/MMRd patients according to their risk of relapse and metastases. The aim of this review is to summarize the main technical aspects and clinical applications, the benefits, and limitations of the use of liquid biopsy in MSI/MMRd colorectal cancer patients.
C1 [Ceccon, Carlotta; Angerilli, Valentina; Fassan, Matteo] Univ Padua, Dept Med DIMED, Padua, Italy.
   [Rasola, Cosimo; Procaccio, Letizia; Sabbadin, Marianna; Bergamo, Francesca; Lonardi, Sara; Fassan, Matteo] IRCCS, Veneto Inst Oncol IOV, Padua, Italy.
   [Rasola, Cosimo] Univ Padua, Dept Surg Oncol & Gastroenterol, Padua, Italy.
   [Malapelle, Umberto] Univ Naples Federico II, Dept Publ Hlth, Naples, Italy.
C3 University of Padua; IRCCS Istituto Oncologico Veneto (IOV); University
   of Padua; University of Naples Federico II
RP Fassan, M (corresponding author), Univ Padua, Dept Med DIMED, Padua, Italy.; Fassan, M (corresponding author), IRCCS, Veneto Inst Oncol IOV, Padua, Italy.
EM matteo.fassan@unipd.it
RI Fassan, Matteo/F-5152-2012; Procaccio, Letizia/AAV-8916-2021; Bergamo,
   Francesca/AAB-9010-2019; Lonardi, Sara/F-4228-2014
OI Lonardi, Sara/0000-0002-7593-8138; Ceccon, Carlotta/0009-0004-5478-9550;
   Sabbadin, Marianna/0009-0004-7795-415X
FU Italian Health Ministry/Veneto Region Research Programme
   [NET-2016-02363853]; Italian Health Ministrys Research Program
   [GR-2019-12368903]; AIRC 5 per mille 2019 [22759]
FX MF is supported by a grant from the Italian Health Ministry/Veneto
   Region Research Programme NET-2016-02363853, AIRC 5 per mille 2019 (ID.
   22759 programme) and Italian Health Ministrys Research Program
   GR-2019-12368903.
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NR 85
TC 5
Z9 5
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 JUN 28
PY 2022
VL 12
AR 930108
DI 10.3389/fonc.2022.930108
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2W4VO
UT WOS:000824523500001
PM 35837109
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Clifton, K
   Rich, TA
   Parseghian, C
   Raymond, VM
   Dasari, A
   Pereira, AAL
   Willis, J
   Loree, JM
   Bauer, TM
   Chae, YK
   Sherrill, G
   Fanta, P
   Grothey, A
   Hendifar, A
   Henry, D
   Mahadevan, D
   Nezami, MA
   Tan, B
   Wainberg, ZA
   Lanman, R
   Kopetz, S
   Van Morris
AF Clifton, Katherine
   Rich, Thereasa A.
   Parseghian, Christine
   Raymond, Victoria M.
   Dasari, Arvind
   Pereira, Allan Andresson Lima
   Willis, Jason
   Loree, Jonathan M.
   Bauer, Todd M.
   Chae, Young Kwang
   Sherrill, Gary
   Fanta, Paul
   Grothey, Axel
   Hendifar, Andrew
   Henry, David
   Mahadevan, Daruka
   Nezami, Mohammad Amin
   Tan, Benjamin
   Wainberg, Zev A.
   Lanman, Richard
   Kopetz, Scott
   Van Morris
TI Identification of Actionable Fusions as an Anti-EGFR Resistance
   Mechanism Using a Circulating Tumor DNA Assay
SO JCO PRECISION ONCOLOGY
LA English
DT Article
ID ACQUIRED-RESISTANCE; GENOMIC LANDSCAPE; TARGETED THERAPY; BLOCKADE
AB PURPOSE Gene fusions are established oncogenic drivers and emerging therapeutic targets in advanced colorectal cancer. This study aimed to detail the frequencies and clinicopathological features of gene fusions in colorectal cancer using a circulating tumor DNA assay.
   METHODS Circulating tumor DNA samples in patients with advanced colorectal cancer were analyzed at 4,581 unique time points using a validated plasma-based multigene assay that includes assessment of fusions in FGFR2, FGFR3, RET, ALK, NTRK1, and ROS1. Associations between fusions and clinicopathological features were measured using Fisher's exact test. Relative frequencies of genomic alterations were compared between fusion-present and fusion-absent cases using an unpaired t test.
   RESULTS Forty-four unique fusions were identified in 40 (1.1%) of the 3,808 patients with circulating tumor DNA detected: RET(n = 6; 36% of all fusions detected), FGFR3 (n = 2; 27%), ALK(n = 10, 23%), NTRK1 (n = 3; 7%), ROS1 (n = 2; 5%), and FGFR2 (n = 1; 2%). Relative to nonfusion variants detected, fusions were more likely to be subclonal (odds ratio, 8.2; 95% CI, 2.94 to 23.00; P < .001). Mutations associated with a previously reported anti-epidermal growth factor receptor (anti-EGFR) therapy resistance signature (subclonal RAS and EGFR mutations) were found with fusions in FGFR3 (10 of 12 patients), RET(nine of 16 patients), and ALK(seven of 10 patients). For the 27 patients with available clinical histories, 21 (78%) had EGFR monoclonal antibody treatment before fusion detection.
   CONCLUSION Diverse and potentially actionable fusions can be detected using a circulating tumor DNA assay in patients with advanced colorectal cancer. Distribution of coexisting subclonal mutations in EGFR, KRAS, and NRAS in a subset of the patients with fusion-present colorectal cancer suggests that these fusions may arise as a novel mechanism of resistance to anti-EGFR therapies in patients with metastatic colorectal cancer. (C) 2019 by American Society of Clinical Oncology
C1 [Clifton, Katherine; Parseghian, Christine; Dasari, Arvind; Pereira, Allan Andresson Lima; Willis, Jason; Kopetz, Scott; Van Morris] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Rich, Thereasa A.; Raymond, Victoria M.; Lanman, Richard] GuardantHealth, Redwood City, CA USA.
   [Loree, Jonathan M.] BC Canc, Vancouver, BC, Canada.
   [Bauer, Todd M.] Tennessee Oncol Sarah Cannon Res Inst, Nashville, TN USA.
   [Chae, Young Kwang] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
   [Sherrill, Gary] Cone Hlth Canc Ctr, Greensboro, NC USA.
   [Fanta, Paul] Univ San Diego, Moores Canc Ctr, La Jolla, CA USA.
   [Grothey, Axel] Univ Tennessee, West Canc Ctr, Memphis, TN USA.
   [Hendifar, Andrew] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
   [Henry, David] Univ Penn, Philadelphia, PA 19104 USA.
   [Mahadevan, Daruka] Univ Arizona, Ctr Canc, Tucson, AZ USA.
   [Nezami, Mohammad Amin] Pacific Med Ctr Hope, Fresno, CA USA.
   [Tan, Benjamin] Washington Univ, Sch Med, St Louis, MO USA.
   [Wainberg, Zev A.] Univ Calif Los Angeles, Los Angeles, CA USA.
C3 University of Texas System; UTMD Anderson Cancer Center; Sarah Cannon
   Research Institute; Tennessee Oncology; Northwestern University;
   Feinberg School of Medicine; University of San Diego; University of
   Tennessee System; University of Tennessee Health Science Center; Cedars
   Sinai Medical Center; University of Pennsylvania; University of Arizona;
   Washington University (WUSTL); University of California System;
   University of California Los Angeles
RP Van Morris (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, 1400 Holcombe Blvd,Unit 426, Houston, TX 77030 USA.
EM vkmorris@mdanderson.org
RI Kopetz, Scott/AAC-1387-2019; Henry, David/AAJ-4332-2020; PEREIRA,
   ALLAN/N-7773-2016; Morris, Van/KIE-0809-2024; Lanman,
   Richard/D-8290-2016
OI Bauer, Todd/0000-0002-3078-5043
FU National Cancer Institute T32 Grant [CA009666]; National Cancer
   Institute K12 Grant [CA088084]
FX Supported by funding support from the National Cancer Institute T32
   Grant No. CA009666 (K.C.) and K12 Grant No. CA088084 (V.K.M.).
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NR 33
TC 21
Z9 21
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
EI 2473-4284
J9 JCO PRECIS ONCOL
JI JCO Precis. Oncol.
PD OCT 3
PY 2019
VL 3
DI 10.1200/PO.19.00141
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JC4YY
UT WOS:000489285700001
PM 33015522
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Janssens, K
   Lambrechts, C
   Geerinckx, B
   Op de Beeck, K
   Van Camp, G
   Oliveres, H
   Prenen, H
   Vandamme, T
   Peeters, M
AF Janssens, Katleen
   Lambrechts, Chinouk
   Geerinckx, Barbara
   Op de Beeck, Ken
   Van Camp, Guy
   Oliveres, Helena
   Prenen, Hans
   Vandamme, Timon
   Peeters, Marc
TI New Developments in Treating <i>RAS</i>-Mutated Metastatic Colorectal
   Cancer
SO CURRENT TREATMENT OPTIONS IN ONCOLOGY
LA English
DT Review
DE Metastatic colorectal cancer; RAS mutation; Targeted therapy;
   KRAS(G12C)-inhibitors
ID PHASE-III TRIAL; DOUBLE-BLIND; OPEN-LABEL; PLUS BEVACIZUMAB;
   ACQUIRED-RESISTANCE; ADAGRASIB MRTX849; SUBGROUP ANALYSES; 1ST-LINE
   THERAPY; RANDOMIZED-TRIAL; NON-INFERIORITY
AB Opinion statementOne of the great challenges in digestive oncology is choosing the optimal therapy for RAS-mutated metastatic colorectal cancer (mCRC). Even though the RAS genes and accompanying pathway were identified decades ago and extensive knowledge exists on their role in carcinogenesis, it has proven challenging to translate these insights into new therapies and clinical benefit for patients. However, recently, new drugs targeting this pathway (for example, KRAS(G12C) inhibitors) have shown promising results in clinical trials, as monotherapy or in combination regimens. Although resistance remains an important issue, more knowledge on adaptive resistance and feedback loops in the RAS-pathway has led to strategical combination regimens to overcome this problem. In the past year, many encouraging results have been published or presented at conferences. Even though some of the data is still preliminary, these studies may bring practice-changing results and can lead to a clinical benefit for patients over the coming years. Because of these recent developments, the treatment of RAS-mutated mCRC has become a topic of great interest. Therefore, in this review, we will summarize the standard of care and discuss the most important emerging therapies for this patient population.
C1 [Janssens, Katleen; Op de Beeck, Ken; Van Camp, Guy] Univ Antwerp, Ctr Med Genet, Prins Boudewijnlaan 43-6, B-2650 Edegem, Belgium.
   [Janssens, Katleen; Op de Beeck, Ken; Van Camp, Guy] Antwerp Univ Hosp, Prins Boudewijnlaan 43-6, B-2650 Edegem, Belgium.
   [Janssens, Katleen; Op de Beeck, Ken; Prenen, Hans; Vandamme, Timon; Peeters, Marc] Univ Antwerp, Ctr Oncol Res CORE, Integrated Personalized & Precis Oncol Network IPP, Univ Pl 1, B-2610 Antwerp, Belgium.
   [Janssens, Katleen; Op de Beeck, Ken; Prenen, Hans; Vandamme, Timon; Peeters, Marc] Antwerp Univ Hosp, Univ Pl 1, B-2610 Antwerp, Belgium.
   [Lambrechts, Chinouk; Geerinckx, Barbara; Oliveres, Helena; Prenen, Hans; Vandamme, Timon; Peeters, Marc] Antwerp Univ Hosp, Dept Oncol, Drie Eikenstr 655, B-2650 Edegem, Belgium.
   [Lambrechts, Chinouk; Geerinckx, Barbara; Oliveres, Helena; Prenen, Hans; Vandamme, Timon; Peeters, Marc] Antwerp Univ Hosp, Drie Eikenstr 655, B-2650 Edegem, Belgium.
C3 University of Antwerp; University of Antwerp; University of Antwerp;
   University of Antwerp; University of Antwerp; University of Antwerp
RP Vandamme, T (corresponding author), Univ Antwerp, Ctr Oncol Res CORE, Integrated Personalized & Precis Oncol Network IPP, Univ Pl 1, B-2610 Antwerp, Belgium.; Vandamme, T (corresponding author), Antwerp Univ Hosp, Univ Pl 1, B-2610 Antwerp, Belgium.; Vandamme, T (corresponding author), Antwerp Univ Hosp, Dept Oncol, Drie Eikenstr 655, B-2650 Edegem, Belgium.; Vandamme, T (corresponding author), Antwerp Univ Hosp, Drie Eikenstr 655, B-2650 Edegem, Belgium.
EM timon.vandamme@uza.be
RI Peeters, Marc/C-5525-2013; Van Camp, Guy/F-3386-2013; Vandamme,
   Timon/C-4961-2013
OI Prenen, Hans/0000-0001-8802-7352; Peeters, Marc/0000-0003-4969-2303;
   janssens, katleen/0000-0003-3987-4592; Van Camp,
   Guy/0000-0001-5105-9000; Vandamme, Timon/0000-0003-3701-5305; Geerinckx,
   Barbara/0000-0002-7687-2273
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NR 91
TC 0
Z9 0
U1 0
U2 5
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 AUG
PY 2023
VL 24
IS 8
BP 965
EP 987
DI 10.1007/s11864-023-01095-y
EA MAY 2023
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA M1EB8
UT WOS:000992360900002
PM 37212934
DA 2025-01-04
ER

PT J
AU Lo, L
   Patel, D
   Townsend, AR
   Price, TJ
AF Lo, Louisa
   Patel, Dainik
   Townsend, Amanda R.
   Price, Timothy J.
TI Pharmacokinetic and pharmacodynamic evaluation of panitumumab in the
   treatment of colorectal cancer
SO EXPERT OPINION ON DRUG METABOLISM & TOXICOLOGY
LA English
DT Review
DE colorectal cancer; panitumumab; pharmacokinetics; resistance
ID EPIDERMAL-GROWTH-FACTOR; KRAS WILD-TYPE; RECEPTOR MONOCLONAL-ANTIBODY;
   BEVACIZUMAB PLUS MFOLFOX6; LIVER-ONLY METASTASES; RANDOMIZED PHASE-III;
   1ST-LINE TREATMENT; OPEN-LABEL; SUPPORTIVE CARE; POOLED ANALYSIS
AB Introduction: Integration of targeted therapy and additional chemotherapy options has improved median overall survival (OS) in patients with unresectable metastatic colorectal cancer (mCRC). Cetuximab and panitumumab are examples of targeted therapies, specifically against the epidermal growth factor receptor (EGFR). This review focuses on Panitumumab, a fully human IgG2 monoclonal antibody, which inhibits key oncogenic downstream cell signalling pathways. Panitumumab and cetuximab have improved tumour response rate, progression-free survival, and OS in mCRC patients in whom the RAS (Rat Sarcoma) gene is of Wild Type (WT) status.Areas covered: The EGFR signalling pathway and preclinical, Phase I and Phase II clinical studies on the pharmacokinetic, pharmacodynamic and safety evaluation of panitumumab are presented. Phase III studies utilising panitumumab in the first, second and third line setting in mCRC are also described.Expert opinion: Panitumumab exhibits excellent pharmacokinetics and pharmacodynamics by way of uncomplicated dosing, non-existent drug interactions, minimal infusion reactions and manageable side effects, making it a suitable target for combination treatments. However, innate and acquired resistances are still obstacles. To overcome this, experimented strategies are ongoing, particularly in patients with Her-2 and BRAF gene alterations. Novel biomarkers to improve patient selection and second-generation targeted antibodies are in development.
C1 [Lo, Louisa; Patel, Dainik; Townsend, Amanda R.; Price, Timothy J.] Queen Elizabeth Hosp, Dept Med Oncol, Woodville, SA 5011, Australia.
   [Townsend, Amanda R.; Price, Timothy J.] Univ Adelaide, Sch Med, Adelaide, SA 5000, Australia.
C3 University of Adelaide
RP Price, TJ (corresponding author), Queen Elizabeth Hosp, Dept Med Oncol, Woodville, SA 5011, Australia.
EM timothy.price@sa.gov.au
RI Price, Timothy/G-1404-2012
OI Lo, Louisa/0000-0001-7426-7953
FU Amgen; Novartis
FX TJ Price is an advisory board member for Merck, AMGEN and Roche. AR
   Townsend has received sponsorship from Amgen and Novartis for
   investigator-led clinical trials. 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 102
TC 11
Z9 12
U1 0
U2 12
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1742-5255
EI 1744-7607
J9 EXPERT OPIN DRUG MET
JI Expert Opin. Drug Metab. Toxicol.
PD DEC 2
PY 2015
VL 11
IS 12
BP 1907
EP 1924
DI 10.1517/17425255.2015.1112787
PG 18
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA CX5XI
UT WOS:000365775400001
PM 26572750
DA 2025-01-04
ER

PT J
AU Aleksakhina, SN
   Imyanitov, EN
AF Aleksakhina, Svetlana N.
   Imyanitov, Evgeny N.
TI Cancer Therapy Guided by Mutation Tests: Current Status and Perspectives
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE mutations; genetic testing; lung cancer; melanoma; colorectal cancer;
   targeted therapy; TMB; HRD; MSI-H
ID PHASE-II TRIAL; COLORECTAL-CANCER; OPEN-LABEL; MICROSATELLITE
   INSTABILITY; LUNG CARCINOMAS; MULTICENTER; EFFICACY; VEMURAFENIB;
   CRIZOTINIB; MANAGEMENT
AB The administration of many cancer drugs is tailored to genetic tests. Some genomic events, e.g., alterations of EGFR or BRAF oncogenes, result in the conformational change of the corresponding proteins and call for the use of mutation-specific compounds. Other genetic perturbations, e.g., HER2 amplifications, ALK translocations or MET exon 14 skipping mutations, cause overproduction of the entire protein or its kinase domain. There are multilocus assays that provide integrative characteristics of the tumor genome, such as the analysis of tumor mutation burden or deficiency of DNA repair. Treatment planning for non-small cell lung cancer requires testing for EGFR, ALK, ROS1, BRAF, MET, RET and KRAS gene alterations. Colorectal cancer patients need to undergo KRAS, NRAS, BRAF, HER2 and microsatellite instability analysis. The genomic examination of breast cancer includes testing for HER2 amplification and PIK3CA activation. Melanomas are currently subjected to BRAF and, in some instances, KIT genetic analysis. Predictive DNA assays have also been developed for thyroid cancers, cholangiocarcinomas and urinary bladder tumors. There is an increasing utilization of agnostic testing which involves the analysis of all potentially actionable genes across all tumor types. The invention of genomically tailored treatment has resulted in a spectacular improvement in disease outcomes for a significant portion of cancer patients.</p>
C1 [Aleksakhina, Svetlana N.; Imyanitov, Evgeny N.] NN Petrov Inst Oncol, Dept Tumor Growth Biol, St Petersburg 197758, Russia.
   [Aleksakhina, Svetlana N.; Imyanitov, Evgeny N.] St Petersburg Pediat Med Univ, Dept Med Genet, St Petersburg 194100, Russia.
C3 N.N. Petrov Research Institute of Oncology; Saint Petersburg State
   Pediatric Medical University
RP Imyanitov, EN (corresponding author), NN Petrov Inst Oncol, Dept Tumor Growth Biol, St Petersburg 197758, Russia.; Imyanitov, EN (corresponding author), St Petersburg Pediat Med Univ, Dept Med Genet, St Petersburg 194100, Russia.
EM abyshevasv@gmail.com; evgeny@imyanitov.spb.ru
RI Imyanitov, Evgeny/ABG-8619-2021; Aleksakhina, Svetlana/B-2136-2013
FU Ministry of Science and Higher Education of the Russian Federation [?
   075-15-2020-789]
FX FundingThis research was funded by the Ministry of Science and Higher
   Education of the Russian Federation [grant ? 075-15-2020-789].
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NR 130
TC 24
Z9 25
U1 0
U2 9
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 2021
VL 22
IS 20
AR 10931
DI 10.3390/ijms222010931
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA WN0UE
UT WOS:000711491100001
PM 34681592
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lin, CY
   Yang, SJ
   Peng, CL
   Shieh, MJ
AF Lin, Chun-Yen
   Yang, Shu-Jyuan
   Peng, Cheng-Liang
   Shieh, Ming-Jium
TI Panitumumab-Conjugated and Platinum-Cored pH-Sensitive Apoferritin
   Nanocages for Colorectal Cancer-Targeted Therapy
SO ACS APPLIED MATERIALS & INTERFACES
LA English
DT Article
DE apoferritin; oxaliplatin; panitumumab; EGFR; colorectal cancer
ID WILD-TYPE KRAS; DRUG-DELIVERY; TUMOR MICROENVIRONMENT; ANTIBODY THERAPY;
   NANOPARTICLES; OXALIPLATIN; CYTOTOXICITY; CHEMOTHERAPY; CISPLATIN;
   NIVOLUMAB
AB Apoferritin (AF) is a natural nontoxic iron carrier and has a natural hollow structure that can be used to deliver small molecules. The surface of AF has many amine functional groups that can be modified to create targeted ligands. We loaded oxaliplatin onto AF, which was then used as a template to conjugate with panitumumab via a polyethylene glycol linker. The oxaliplatin-loaded AF conjugated with panitumumab (AFPO) was designed to specifically target cell lines expressing epidermal growth factor receptor (EGFR). AFPO efficiently released oxaliplatin and suppressed tumor cell growth. Furthermore, the novel AFPO nanocages showed significant inhibition and greater accumulation in tumor models with high EGFR expression in vivo. Our study revealed that combining panitumumab and oxaliplatin into one formulation (AFPO nanocage) could be a promising shortcut in clinical applications.
C1 [Lin, Chun-Yen; Yang, Shu-Jyuan; Shieh, Ming-Jium] Natl Taiwan Univ, Coll Med, Inst Biomed Engn, 1,Sect 1,Jen Ai Rd, Taipei 100, Taiwan.
   [Lin, Chun-Yen; Yang, Shu-Jyuan; Shieh, Ming-Jium] Natl Taiwan Univ, Coll Engn, 1,Sect 1,Jen Ai Rd, Taipei 100, Taiwan.
   [Yang, Shu-Jyuan] Genee Tech Co Ltd, 2F,661,Bannan Rd, New Taipei 235, Taiwan.
   [Peng, Cheng-Liang] Inst Nucl Energy Res, Isotope Applicat Div, Taoyuan 32546, Taiwan.
   [Shieh, Ming-Jium] Natl Taiwan Univ Hosp, Dept Oncol, 7 Chung Shan South Rd, Taipei 100, Taiwan.
   [Shieh, Ming-Jium] Natl Taiwan Univ Hosp, Coll Med, 7 Chung Shan South Rd, Taipei 100, Taiwan.
C3 National Taiwan University; National Taiwan University; Institute of
   Nuclear Energy Research - Taiwan; National Taiwan University; National
   Taiwan University Hospital; National Taiwan University; National Taiwan
   University Hospital
RP Shieh, MJ (corresponding author), Natl Taiwan Univ, Coll Med, Inst Biomed Engn, 1,Sect 1,Jen Ai Rd, Taipei 100, Taiwan.; Shieh, MJ (corresponding author), Natl Taiwan Univ Hosp, Dept Oncol, 7 Chung Shan South Rd, Taipei 100, Taiwan.; Shieh, MJ (corresponding author), Natl Taiwan Univ Hosp, Coll Med, 7 Chung Shan South Rd, Taipei 100, Taiwan.
EM soloman@ntu.edu.tw
FU Ministry of Science and Technology, R.O.C. [MOST 102-2221-E-002-037-MY3]
FX This work was financially supported by the Ministry of Science and
   Technology, R.O.C. (MOST 102-2221-E-002-037-MY3).
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NR 47
TC 33
Z9 33
U1 0
U2 41
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1944-8244
EI 1944-8252
J9 ACS APPL MATER INTER
JI ACS Appl. Mater. Interfaces
PD FEB 21
PY 2018
VL 10
IS 7
BP 6096
EP 6106
DI 10.1021/acsami.7b13431
PG 11
WC Nanoscience & Nanotechnology; Materials Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Materials Science
GA FX5TS
UT WOS:000426143900006
PM 29368506
DA 2025-01-04
ER

PT J
AU Yao, S
   Zheng, P
   Wu, H
   Song, LM
   Ying, XF
   Xing, C
   Li, Y
   Xiao, ZQ
   Zhou, XN
   Shen, T
   Chen, L
   Liu, YH
   Lai, MD
   Mei, L
   Gao, TM
   Li, JM
AF Yao, Su
   Zheng, Ping
   Wu, Hua
   Song, Li-Ming
   Ying, Xiao-Fang
   Xing, Cheng
   Li, Ying
   Xiao, Zheng-Quan
   Zhou, Xing-Ni
   Shen, Tong
   Chen, Lin
   Liu, Yu-Hong
   Lai, Mao-De
   Mei, Lin
   Gao, Tian-Ming
   Li, Jian-Ming
TI Erbin interacts with c-Cbl and promotes tumourigenesis and tumour growth
   in colorectal cancer by preventing c-Cbl-mediated ubiquitination and
   down-regulation of EGFR
SO JOURNAL OF PATHOLOGY
LA English
DT Article
DE Erbin; EGFR; ubiquitination; tumourigenesis; tumour growth; colorectal
   cancer
ID ACTIVATION; BINDING; IDENTIFICATION; SUPPRESSES; EXPRESSION; RECEPTORS;
   PROTEIN; CELLS
AB The epidermal growth factor receptor (EGFR) is implicated in many types of cancer, including colorectal cancer (CRC), and has become one of the most common candidates for targeted therapy. Here, we found that Erbin, a member of the leucine-rich repeat and PDZ domain (LAP) family, plays a key role in EGFR signalling. Erbin inhibited EGFR ubiquitination and stabilized the EGFR protein by interacting with c-Cbl. Moreover, the PDZ domain of Erbin was critical for the interaction between Erbin and c-Cbl and EGFR ubiquitination. Interestingly, Erbin expression was elevated in tumour samples from CRC patients, increased in advanced clinical stage disease and correlated with EGFR expression. In vivo studies using mouse xenograft models of CRC showed that Erbin promotes tumour growth, and that the effects of Erbin on tumour growth are mainly related to the regulatory effects of Erbin on EGFR. The azoxymethane (AOM)-induced colon carcinogenesis model in Erbin(C/C) mice, with the PDZ domain of Erbin deleted, demonstrated that the PDZ domain of Erbin and its regulation of EGFR signalling are necessary for the tumourigenesis and tumour growth of CRC. We found that Erbin promotes tumourigenesis and tumour growth in CRC by stabilizing EGFR. Our study sheds light on developing Erbin, especially its PDZ domain, as a potential target for CRC treatment. Copyright (c) 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
C1 [Yao, Su; Zheng, Ping; Song, Li-Ming; Ying, Xiao-Fang; Xing, Cheng; Li, Ying; Xiao, Zheng-Quan; Zhou, Xing-Ni; Chen, Lin; Li, Jian-Ming] Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.
   [Wu, Hua; Shen, Tong; Li, Jian-Ming] Soochow Univ, Sch Med, Dept Pathol, Suzhou, Peoples R China.
   [Liu, Yu-Hong] Southern Med Univ, Baoan Hosp, Dept Pathol, Shenzhen, Peoples R China.
   [Lai, Mao-De] Zhejiang Univ, Sch Med, Dept Pathol, Hangzhou 310003, Zhejiang, Peoples R China.
   [Mei, Lin] Georgia Regents Univ, Med Coll Georgia, Dept Neurosci & Regenerat Med, Augusta, GA USA.
   [Gao, Tian-Ming] Southern Med Univ, State Key Lab Organ Failure Res, Key Lab Psychiat Disorders Guangdong Prov, Sch Basic Med Sci,Dept Neurobiol, Guangzhou 510515, Guangdong, Peoples R China.
C3 Southern Medical University - China; Soochow University - China;
   Southern Medical University - China; Zhejiang University; University
   System of Georgia; Augusta University; Southern Medical University -
   China
RP Li, JM (corresponding author), Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou 510515, Guangdong, Peoples R China.
EM tgao@fimmu.com; lixinyue@fimmu.com
RI Yang, Zhaohui/T-5687-2019; Wu, Hua/W-4204-2019
FU National Nature Science Foundation of China [81090422, 81329003,
   81272300, 81001110, 81372574, 31300630, 30971361]; Programme for New
   Century Excellent Talents in the University of China [NCET-10-0092];
   Natural Science Foundation of Jiangsu Province [BK20130337]; China
   Postdoctoral Science Foundation [2013 M541727]
FX This study was supported by the National Nature Science Foundation of
   China (Grant Nos 81090422, 81329003, 81272300, 81001110, 81372574,
   31300630 and 30971361), the Programme for New Century Excellent Talents
   in the University of China (Grant No. NCET-10-0092), the Natural Science
   Foundation of Jiangsu Province (Grant No. BK20130337) and the China
   Postdoctoral Science Foundation (Grant No. 2013 M541727).
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NR 31
TC 37
Z9 46
U1 0
U2 37
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3417
EI 1096-9896
J9 J PATHOL
JI J. Pathol.
PD MAY
PY 2015
VL 236
IS 1
BP 65
EP 77
DI 10.1002/path.4502
PG 13
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA CG1OF
UT WOS:000353041900007
PM 25521828
DA 2025-01-04
ER

PT J
AU Jia, JQ
   Morse, MA
   Nagy, RJ
   Lanman, RB
   Strickler, JH
AF Jia, Jingquan
   Morse, Michael A.
   Nagy, Rebecca J.
   Lanman, Richard B.
   Strickler, John H.
TI Cell-Free DNA Profiling to Discover Mechanisms of Exceptional Response
   to Cabozantinib Plus Panitumumab in a Patient With Treatment Refractory
   Metastatic Colorectal Cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE MET amplification; metastatic colorectal cancer; cabozantinib; cell-free
   DNA; ctDNA
ID WILD-TYPE KRAS; ACQUIRED-RESISTANCE; MET AMPLIFICATION; C-MET; TYROSINE
   KINASE; LUNG-CANCER; COPY NUMBER; OPEN-LABEL; CETUXIMAB; THERAPY
AB MET amplification is rare in treatment-naive metastatic colorectal cancer (CRC) tumors, but can emerge as a mechanism of resistance to anti-EGFR therapies. Preclinical and clinical data suggest that patients with MET amplified tumors benefit from MET-targeted therapy. Cabozantinib is an inhibitor of multiple tyrosine kinases, included c-MET. Panitumumab is an inhibitor of EGFR. This report describes a patient with KRAS, NRAS, and BRAF wild-type metastatic CRC who experienced disease progression on all standard chemotherapy and anti-EGFR antibody therapy. The patient was enrolled in a clinical trial evaluating the combination of cabozantinib plus panitumumab. After only 6 weeks of treatment, the patient experienced a significant anti-tumor response. Although tumor tissue was negative for MET amplification, molecular profiling of cell-free DNA (cfDNA) revealed MET amplification. This case represents the first report showing the activity of cabozantinib in combination with panitumumab in a patient with metastatic CRC, and suggests that MET amplification in cfDNA may be a biomarker of response. A clinical trial targeting MET amplified metastatic CRC is currently underway.
C1 [Jia, Jingquan; Morse, Michael A.; Strickler, John H.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
   [Nagy, Rebecca J.; Lanman, Richard B.] Guardant Hlth Inc, Redwood City, CA USA.
   [Jia, Jingquan] Duke Univ, Med Ctr, Dept Med, Div Hematol, Durham, NC 27710 USA.
   [Jia, Jingquan] Duke Univ, Med Ctr, Dept Med, Div Cellular Therapy, Durham, NC 27710 USA.
   [Jia, Jingquan] Duke Univ, Med Ctr, Dept Med, Div Med Oncol, Durham, NC 27710 USA.
C3 Duke University; Guardant Health, Inc.; Duke University; Duke
   University; Duke University
RP Strickler, JH (corresponding author), Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
EM john.strickler@dm.duke.edu
RI Lanman, Richard/D-8290-2016
OI Strickler, John/0000-0001-7579-1175
FU Exelixis, Inc.
FX This work is supported by Exelixis, Inc.
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NR 49
TC 14
Z9 14
U1 0
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD AUG 28
PY 2018
VL 8
AR 305
DI 10.3389/fonc.2018.00305
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GR7HD
UT WOS:000442858700001
PM 30211110
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Kashyap, MK
   Mangrulkar, SV
   Kushwaha, S
   Ved, A
   Kale, MB
   Wankhede, NL
   Taksande, BG
   Upaganlawar, AB
   Umekar, MJ
   Koppula, S
   Kopalli, SR
AF Kashyap, Monu Kumar
   Mangrulkar, Shubhada V.
   Kushwaha, Sapana
   Ved, Akash
   Kale, Mayur B.
   Wankhede, Nitu L.
   Taksande, Brijesh G.
   Upaganlawar, Aman B.
   Umekar, Milind J.
   Koppula, Sushruta
   Kopalli, Spandana Rajendra
TI Recent Perspectives on Cardiovascular Toxicity Associated with
   Colorectal Cancer Drug Therapy
SO PHARMACEUTICALS
LA English
DT Review
DE colorectal cancer; cardiotoxicity; chemotherapy; oxidative stress;
   apoptosis; 5-fluorouracil
ID TYROSINE KINASE INHIBITORS; INDUCED CARDIOTOXICITY; CARDIAC DYSFUNCTION;
   RADIATION-THERAPY; CHEMOTHERAPY; ANGIOGENESIS; PREVALENCE; MECHANISMS;
   STRATEGIES; SAFETY
AB Cardiotoxicity is a well-known adverse effect of cancer-related therapy that has a significant influence on patient outcomes and quality of life. The use of antineoplastic drugs to treat colorectal cancers (CRCs) is associated with a number of undesirable side effects including cardiac complications. For both sexes, CRC ranks second and accounts for four out of every ten cancer deaths. According to the reports, almost 39% of patients with colorectal cancer who underwent first-line chemotherapy suffered cardiovascular impairment. Although 5-fluorouracil is still the backbone of chemotherapy regimen for colorectal, gastric, and breast cancers, cardiotoxicity caused by 5-fluorouracil might affect anywhere from 1.5% to 18% of patients. The precise mechanisms underlying cardiotoxicity associated with CRC treatment are complex and may involve the modulation of various signaling pathways crucial for maintaining cardiac health including TKI ErbB2 or NRG-1, VEGF, PDGF, BRAF/Ras/Raf/MEK/ERK, and the PI3/ERK/AMPK/mTOR pathway, resulting in oxidative stress, mitochondrial dysfunction, inflammation, and apoptosis, ultimately damaging cardiac tissue. Thus, the identification and management of cardiotoxicity associated with CRC drug therapy while minimizing the negative impact have become increasingly important. The purpose of this review is to catalog the potential cardiotoxicities caused by anticancer drugs and targeted therapy used to treat colorectal cancer as well as strategies focused on early diagnosing, prevention, and treatment of cardiotoxicity associated with anticancer drugs used in CRC therapy.
C1 [Kashyap, Monu Kumar] Goel Inst Pharmaceut Sci, Faizabad Rd, Lucknow 226028, Uttar Pradesh, India.
   [Kashyap, Monu Kumar; Ved, Akash] Dr A P J Abdul Kalam Tech Univ, Lucknow 222001, Uttar Pradesh, India.
   [Mangrulkar, Shubhada V.; Kale, Mayur B.; Wankhede, Nitu L.; Taksande, Brijesh G.; Umekar, Milind J.] Smt Kishoritai Bhoyar Coll Pharm, Nagpur 441002, Maharashtra, India.
   [Kushwaha, Sapana] Natl Inst Pharmaceut Educ & Res, Raebareli 229010, Uttar Pradesh, India.
   [Upaganlawar, Aman B.] SNJBs Shriman Sureshdada Jain Coll Pharm, Chandwad 423101, Maharashtra, India.
   [Koppula, Sushruta] Konkuk Univ, Coll Biomed & Hlth Sci, Chungju Si 27478, Chungcheongbuk, South Korea.
   [Kopalli, Spandana Rajendra] Sejong Univ, Dept Biosci & Biotechnol, Seoul 05006, South Korea.
C3 Dr. A.P.J. Abdul Kalam Technical University (AKTU); National Institute
   of Pharmaceutical Education & Research, S.A.S. Nagar (Mohali); Konkuk
   University; Sejong University
RP Kopalli, SR (corresponding author), Sejong Univ, Dept Biosci & Biotechnol, Seoul 05006, South Korea.
EM monukumarkashyap95@gmail.com; shubhadamangrulkar@yahoo.com;
   akashved@gmail.com; mayur.kale28@gmail.com;
   nitu.wankhede211994@gmail.com; amanrxy@gmail.com;
   spandanakopalli@gmail.com
RI Kushwaha, Sapana/AAA-7852-2020; MANGRULKAR, SHUBHADA/N-8899-2019;
   Kashyap, Monu Kumar/JJE-4614-2023; Koppula, Sushruta/JRW-6571-2023;
   Kale, Mayur/GQI-0968-2022; MANGRULKAR, SHUBHADA/C-4985-2019; VED,
   AKASH/JBJ-3605-2023; Koppula, Sushruta/F-2817-2013
OI Taksande, Brijesh/0000-0002-6132-8822; Kopalli, Spandana
   Rajendra/0000-0003-0908-4178; Kushwaha, Sapana/0000-0001-8825-3034;
   MANGRULKAR, SHUBHADA/0000-0003-4795-308X; VED,
   AKASH/0000-0001-8487-3885; Kopalli, Spandana
   Rajendra/0000-0002-3379-4797; Kale, Mayur/0000-0001-5881-7927; Koppula,
   Sushruta/0000-0002-8597-7763
FU This work was supported by Sejong University, Republic of Korea.; Sejong
   University, Republic of Korea
FX This work was supported by Sejong University, Republic of Korea.
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NR 95
TC 3
Z9 3
U1 1
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1424-8247
J9 PHARMACEUTICALS-BASE
JI Pharmaceuticals
PD OCT
PY 2023
VL 16
IS 10
AR 1441
DI 10.3390/ph16101441
PG 25
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA W1SU9
UT WOS:001089509900001
PM 37895912
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Raimondi, L
   Raimondi, FM
   Di Benedetto, L
   Cimino, G
   Spinelli, GP
AF Raimondi, Lucrezia
   Raimondi, Filippo Maria
   Di Benedetto, Laura
   Cimino, Giuseppe
   Spinelli, Gian Paolo
TI PD-L1 Expression on Circulating Tumour Cells May Be Predictive of
   Response to Regorafenib in Patients Diagnosed with Chemorefractory
   Metastatic Colorectal Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE chemorefractory metastatic colorectal cancer; regorafenib; circulating
   tumour cells; PD-L1; PLR; liquid biopsy; acquired resistance; targeted
   therapy
ID LUNG-CANCER
AB Regorafenib, targeting a broad range of receptor tyrosine kinases (RTKs), is an oral multikinase inhibitor which improves the progression-free survival (PFS) and overall survival (OS) of patients diagnosed with chemorefractory metastatic colorectal cancer (mCRC), making an immunosuppressive tumour microenvironment. The correlation between PD-1/PD-L1 expression and RTKs inhibition has been studied in several tumour types but has not been analyzed extensively in mCRC in the era of regorafenib. In this study, using liquid biopsy, we evaluated the opportunity to reveal if PD-L1 expression on circulating tumour cells (CTCs) could serve as a predictive biomarker of response and clinical benefit in patients treated with regorafenib as the third line of treatment. We analyzed a cohort of forty chemorefractory metastatic colorectal cancer patients, of whom twenty-sixKRASmutated, treated with regorafenib, all as the third line of treatment. Blood samples were collected from patients prior to treatment and longitudinally four and eight weeks after initiation of therapy. CTCs were identified using multiparametric flow cytometry; therefore, PD-L1 expression was evaluated. Objective responses were defined following the RECIST criteria v.1.1. Moreover, focusing on peripheral blood biomarkers, we found that high platelet-to-lymphocyte ratio (PLR) was an independent prognostic indicator of poor OS. For the first time, our study showed the usefulness of sequential assessments of CTCs as a non-invasive real-time biopsy to evaluate PD-L1 expression in patients diagnosed with mCRC and treated with regorafenib. Our analysis suggests that by assessing PD-L1 expression on CTCs, we could predict who will benefit from regorafenib, offering highly individualized treatment plans.
C1 [Raimondi, Lucrezia; Cimino, Giuseppe; Spinelli, Gian Paolo] Univ Rome Sapienza, AUSL Latina, UOC Terr Oncol Aprilia, I-04011 Aprilia, Italy.
   [Di Benedetto, Laura] BIOS SpA, I-00197 Rome, Italy.
C3 Sapienza University Rome
RP Spinelli, GP (corresponding author), Univ Rome Sapienza, AUSL Latina, UOC Terr Oncol Aprilia, I-04011 Aprilia, Italy.
EM lucrezia.raimondi@uniroma1.it; filippo3006@gmail.com;
   lauradibenedetto.ldb@gmail.com; giuseppe.cimino@uniroma1.it;
   gianpaolo.spinelli@uniroma1.it
OI Spinelli, Gian Paolo/0000-0002-4363-6274; Raimondi, Filippo
   Maria/0000-0001-7600-687X; Raimondi, Lucrezia/0000-0002-7313-7732
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NR 28
TC 12
Z9 15
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 SEP
PY 2020
VL 21
IS 18
AR 6907
DI 10.3390/ijms21186907
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA OE1QO
UT WOS:000580314200001
PM 32962309
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Huang, TH
   Mokgautsi, N
   Huang, YJ
   Wu, ATH
   Huang, HS
AF Huang, Tse-Hung
   Mokgautsi, Ntlotlang
   Huang, Yan-Jiun
   Wu, Alexander T. H.
   Huang, Hsu-Shan
TI Comprehensive Omics Analysis of a Novel Small-Molecule Inhibitor of
   Chemoresistant Oncogenic Signatures in Colorectal Cancer Cell with
   Antitumor Effects
SO CELLS
LA English
DT Article
DE chemoresistance; small molecule; bioinformatics; cancer stem cells
   (CSCs); RV59; immune checkpoint
ID C-MYC; TISSUE INHIBITOR; TUMOR-GROWTH; STEM-CELLS; GENE; EXPRESSION;
   SURVIVAL; TIMP-1; METALLOPROTEINASES; 5-FLUOROURACIL
AB Tumor recurrence from cancer stem cells (CSCs) and metastasis often occur post-treatment in colorectal cancer (CRC), leading to chemoresistance and resistance to targeted therapy. MYC is a transcription factor in the nuclei that modulates cell growth and development, and regulates immune response in an antitumor direction by mediating programmed death ligand 1 (PD-L1) and promoting CRC tumor recurrence after adjuvant chemotherapy. However, the molecular mechanism through which c-MYC maintains stemness and confers treatment resistance still remains elusive in CRC. In addition, recent reports demonstrated that CRC solid colon tumors expresses C-X-C motif chemokine ligand 8 (CXCL8). Expression of CXCL8 in CRC was reported to activate the expression of PD-L1 immune checkpoint through c-MYC, this ultimately induces chemoresistance in CRC. Accumulating studies have also demonstrated increased expression of CXCL8, matrix metalloproteinase 7 (MMP7), tissue inhibitor of metalloproteinase 1 (TIMP1), and epithelial-to-mesenchymal transition (EMT) components, in CRC tumors suggesting their potential collaboration to promote EMT and CSCs. TIMP1 is MMP-independent and regulates cell development and apoptosis in various cancer cell types, including CRC. Recent studies showed that TIMP1 cleaves CXCL8 on its chemoattractant, thereby influencing its mechanistic response to therapy. This therefore suggests crosstalk among the c-MYC/CXCL8/TIMP1 oncogenic signatures. In this study, we explored computer simulations through bioinformatics to identify and validate that the MYC/CXCL8/TIMP1 oncogenic signatures are overexpressed in CRC, Moreover, our docking results exhibited putative binding affinities of the above-mentioned oncogenes, with our novel small molecule, RV59, Finally, we demonstrated the anticancer activities of RV59 against NCI human CRC cancer cell lines both as single-dose and dose-dependent treatments, and also demonstrated the MYC/CXCL8/TIMP1 signaling pathway as a potential RV59 drug target.
C1 [Huang, Tse-Hung] Chang Gung Mem Hosp, Dept Tradit Chinese Med, Keelung 20401, Taiwan.
   [Huang, Tse-Hung] Chang Gung Univ, Sch Tradit Chinese Med, Taoyuan 333, Taiwan.
   [Huang, Tse-Hung] Natl Taipei Univ Nursing & Hlth Sci, Sch Nursing, Taipei 112, Taiwan.
   [Huang, Tse-Hung] Chang Gung Univ Sci & Technol, Grad Inst Hlth Ind Technol, Taoyuan 333, Taiwan.
   [Huang, Tse-Hung] Chang Gung Univ Sci & Technol, Res Ctr Chinese Herbal Med, Taoyuan 333, Taiwan.
   [Huang, Tse-Hung] Ming Chi Univ Technol, Dept & Grad Inst Chem Engn, New Taipei 243, Taiwan.
   [Huang, Tse-Hung] Ming Chi Univ Technol, Grad Inst Biochem Engn, New Taipei 243, Taiwan.
   [Mokgautsi, Ntlotlang; Huang, Hsu-Shan] Taipei Med Univ, Coll Med Sci & Technol, PhD Program Canc Mol Biol & Drug Discovery, Taipei 11031, Taiwan.
   [Mokgautsi, Ntlotlang; Huang, Hsu-Shan] Acad Sinica, Taipei 11031, Taiwan.
   [Mokgautsi, Ntlotlang; Huang, Hsu-Shan] Taipei Med Univ, Coll Med Sci & Technol, Grad Inst Canc Biol & Drug Discovery, Taipei 11031, Taiwan.
   [Huang, Yan-Jiun] Taipei Med Univ, Taipei Med Univ Hosp, Dept Surg, Div Colorectal Surg, Taipei 110, Taiwan.
   [Huang, Yan-Jiun] Taipei Med Univ, Coll Med, Sch Med, Dept Surg, Taipei 110, Taiwan.
   [Wu, Alexander T. H.] Taipei Med Univ, TMU Res Ctr Canc Translat Med, Taipei 11031, Taiwan.
   [Wu, Alexander T. H.] Taipei Med Univ, Coll Sci & Technol, PhD Program Translat Med, Taipei 11031, Taiwan.
   [Wu, Alexander T. H.] Taipei Med Univ, Taipei Med Univ Hosp, Clin Res Ctr, Taipei 11031, Taiwan.
   [Wu, Alexander T. H.] Natl Def Med Ctr, Grad Inst Med Sci, Taipei 11490, Taiwan.
   [Huang, Hsu-Shan] Natl Def Med Ctr, Sch Pharm, Taipei 11490, Taiwan.
   [Huang, Hsu-Shan] Taipei Med Univ, Coll Pharm, PhD Program Drug Discovery & Dev Ind, Taipei 11031, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung University; National Taipei
   University of Nursing & Health Science (NTUNHS); Chang Gung University
   of Science & Technology; Chang Gung University of Science & Technology;
   Ming Chi University of Technology; Ming Chi University of Technology;
   Taipei Medical University; Academia Sinica - Taiwan; Taipei Medical
   University; Taipei Medical University; Taipei Medical University
   Hospital; Taipei Medical University; Taipei Medical University; Taipei
   Medical University; Taipei Medical University Hospital; Taipei Medical
   University; National Defense Medical Center; National Defense Medical
   Center; Taipei Medical University
RP Huang, HS (corresponding author), Taipei Med Univ, Coll Med Sci & Technol, PhD Program Canc Mol Biol & Drug Discovery, Taipei 11031, Taiwan.; Huang, HS (corresponding author), Acad Sinica, Taipei 11031, Taiwan.; Huang, HS (corresponding author), Taipei Med Univ, Coll Med Sci & Technol, Grad Inst Canc Biol & Drug Discovery, Taipei 11031, Taiwan.; Wu, ATH (corresponding author), Taipei Med Univ, TMU Res Ctr Canc Translat Med, Taipei 11031, Taiwan.; Wu, ATH (corresponding author), Taipei Med Univ, Coll Sci & Technol, PhD Program Translat Med, Taipei 11031, Taiwan.; Wu, ATH (corresponding author), Taipei Med Univ, Taipei Med Univ Hosp, Clin Res Ctr, Taipei 11031, Taiwan.; Wu, ATH (corresponding author), Natl Def Med Ctr, Grad Inst Med Sci, Taipei 11490, Taiwan.; Huang, HS (corresponding author), Natl Def Med Ctr, Sch Pharm, Taipei 11490, Taiwan.; Huang, HS (corresponding author), Taipei Med Univ, Coll Pharm, PhD Program Drug Discovery & Dev Ind, Taipei 11031, Taiwan.
EM tsehunghuang_1089@yahoo.com.tw; d621108006@tmu.edu.tw;
   d622101001@tmu.edu.tw; chaw1211@tmu.edu.tw; huanghs99@tmu.edu.tw
RI Wu, Alexander/AAD-8826-2022; Huang, Tse-Hung/N-5989-2019
OI Huang, Hsu-Shan/0000-0001-8162-5608; Wu, Alexander/0000-0002-0178-6530;
   Huang, Hsu-Shan/0000-0001-6193-5182
FU Ministry of Science and Technology [MOST 109-2113-M-038-003, MOST
   110-2314-B-038-120]; Ministry of Education, Taipei Medical University
   [DP2-110-21121-03-C-09, DP2-110-21121-01-H-03-03, CMRPG2H0121,
   CMRPG2H0362]
FX Hsu-Shan Huang is funded by the Ministry of Science and Technology (MOST
   109-2113-M-038-003 and MOST 110-2314-B-038-120). Alexander TH Wu is
   funded by the Ministry of Education, Taipei Medical University
   (DP2-110-21121-03-C-09 and DP2-110-21121-01-H-03-03). Tse-Hung Huang is
   funded by CMRPG2H0121 and CMRPG2H0362 research grants.
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NR 75
TC 11
Z9 11
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD AUG
PY 2021
VL 10
IS 8
AR 1970
DI 10.3390/cells10081970
PG 21
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA UG0EQ
UT WOS:000688937400001
PM 34440739
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hu, L
   Zhu, JY
   Fang, L
   Yu, XC
   Yan, ZL
AF Hu, Li
   Zhu, Ji-Yun
   Fang, Lei
   Yu, Xiu-Chong
   Yan, Zhi-Long
TI Isolated metachronous splenic multiple metastases after colon cancer
   surgery: A case report and literature review
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Review
DE Colon cancer; Isolated; Metachronous; Splenic metastasis; Literature
   review; Case report
ID COLORECTAL-CARCINOMA; RECTAL-CARCINOMA; SPLENECTOMY
AB BACKGROUND Isolated splenic metastasis is a rare clinical entity. Multiple metastases in the spleen after radical colon resection in a patient who subsequently underwent a second local resection for isolated metachronous splenic metastasis are exceedingly rare.
   CASE SUMMARY We report a colon cancer patient who underwent laparoscopic radical colon resection 14 mo previously, and subsequently underwent a second local resection due to local recurrence detected by elevated serum carcinoembryonic antigen (CEA) and positron emission tomography (PET). However, multiple metastases in the spleen were found 7 mo later by elevated serum CEA and PET-magnetic resonance imaging. Then the patient underwent total laparoscopic splenectomy. Local tumor recurrence and splenic metastasis from colorectal cancer (CRC) were found by postoperative pathology. Genetic analysis of these recurrent and metastatic tissues showed KRAS exon2, APC exon16 and TP53 exon6 missense mutations, but no mutations of NRAS, KRAF, EGFR, ERBB2, MET, MLH1, MSH2 and MSH6 were detected. Chemotherapy and target therapy were administered after multiple disciplinary team (MDT) consultation, and no tumor recurrence has been observed to date. We also reviewed the literature by conducting a search of the PubMed database using the following key words: CRC, splenic metastasis, isolated, and review. We identified 34 relevant papers, which included 28 cases of metachronous metastasis and 6 cases of simultaneous metastasis.
   CONCLUSION Close monitoring of serum CEA levels is crucial for the detection of isolated splenic metastases after colon surgery. In terms of overall survival and progression-free survival, MDT plays an important role in the entire process of disease management.
C1 [Hu, Li; Zhu, Ji-Yun; Fang, Lei; Yu, Xiu-Chong; Yan, Zhi-Long] Ningbo First Hosp, Dept Gastrointestinal Surg, 59 Liuting Rd, Ningbo 315000, Zhejiang, Peoples R China.
C3 Ningbo University
RP Yan, ZL (corresponding author), Ningbo First Hosp, Dept Gastrointestinal Surg, 59 Liuting Rd, Ningbo 315000, Zhejiang, Peoples R China.
EM yanzhilong@nbu.edu.cn
RI Fang, Lei/C-1084-2008
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NR 37
TC 6
Z9 7
U1 0
U2 3
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD AUG 6
PY 2020
VL 8
IS 15
BP 3320
EP U222
DI 10.12998/wjcc.v8.i15.3320
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA NZ4QD
UT WOS:000577079200021
PM 32874988
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Belaid, I
   Ben Moussa, C
   Melliti, R
   Limam, M
   Ben Ahmed, T
   Ezzaari, F
   Elghali, MA
   Bouazzi, A
   Ben Mabrouk, M
   Bourigua, R
   Ammar, N
   Hochlaf, M
   Ben Fatma, L
   Chabchoub, I
   Ben Ahmed, S
AF Belaid, Imtinene
   Ben Moussa, Chaimaa
   Melliti, Rihab
   Limam, Manel
   Ben Ahmed, Tarek
   Ezzaari, Faten
   Elghali, Mohamed Amine
   Bouazzi, Amal
   Ben Mabrouk, Mohamed
   Bourigua, Rym
   Ammar, Nouha
   Hochlaf, Makrem
   Ben Fatma, Leila
   Chabchoub, Imene
   Ben Ahmed, Slim
TI Quality of life in Tunisian colorectal cancer patients: a
   cross-sectional study
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Colorectal tumors; Chemotherapy; Colorectal surgery; Quality of life
ID TOTAL MESORECTAL EXCISION; RECTAL-CANCER; RADIOTHERAPY; POPULATION;
   DIAGNOSIS; SURVIVORS; IMPACT; LONG
AB Purpose Quality of life (QOL) of colorectal cancer (CRC) patients has been little studied in Tunisia. The aim of this work was to evaluate the QOL of CRC patients and to identify factors that may influence it. Methods A cross-sectional, study spread was made over a period of 6 months on patients with CRC treated in the department of Medical Oncology of Farhat Hached University Hospital of Sousse. The EORTC questionnaires translated and validated in Arabic (QLQ-C30 and QLQ-CR29) were used. Results 142 patients diagnosed with colon or rectal cancer were enrolled. The overall QOL score was 58.5 +/- 29.1. The emotional and sexual functional dimensions were the most affected, especially in women and patients under 50 years of age. QOL scores were higher in patients who were in complete remission (71.4 +/- 24.7) and in good general condition (63.7 +/- 26.6) physical activity may have a significant influence on all functional dimensions of QOL (p < 0.001). Fatigue was significantly (p < 0.001) more present when there was a sedentary lifestyleradiotherapy, palliative chemotherapy (1st and 2nd line) and targeted therapy. Conclusion Evaluating quality of life of patients with colorectal cancer in Tunisia is necessary especially those under 50 years old and in women. Laparoscopic surgery with restoration of intestinal continuity, less toxic palliative chemotherapy protocols, more accessibility to new radiotherapy technics will improve QOL of CRC patients. Physical activity and nutrition support are also essential in promoting QOL of these patients.
C1 [Belaid, Imtinene; Melliti, Rihab; Ben Ahmed, Tarek; Ezzaari, Faten; Bourigua, Rym; Ammar, Nouha; Hochlaf, Makrem; Ben Fatma, Leila; Chabchoub, Imene; Ben Ahmed, Slim] Univ Sousse, Hop Farhat Hached, Fac Med Sousse, Assoc Recherhe & Informat,Canc Ctr Tunisien,Dept, Sousse 4000, Tunisia.
   [Ben Moussa, Chaimaa; Limam, Manel] Univ Sousse, Fac Med Sousse, Dept Epidemiol, Sousse 4000, Tunisia.
   [Elghali, Mohamed Amine] Univ Sousse, Hop Farhat Hached, Fac Med Sousse, Dept Surg, Sousse 4000, Tunisia.
   [Bouazzi, Amal; Ben Mabrouk, Mohamed] Univ Sousse, Hop Sahloul, Fac Med Sousse, Dept Surg, Sousse 4000, Tunisia.
C3 Universite de Sousse; Hopital Farhat Hached; Universite de Sousse;
   Universite de Sousse; Hopital Farhat Hached; Universite de Sousse;
   Hopital Sahloul
RP Belaid, I (corresponding author), Univ Sousse, Hop Farhat Hached, Fac Med Sousse, Assoc Recherhe & Informat,Canc Ctr Tunisien,Dept, Sousse 4000, Tunisia.
EM belaid_im@hotmail.fr
RI chabchoub, imene/GRY-0691-2022; GHALI, Mohamed/AAE-6952-2021; belaid,
   Imtinene/A-6586-2019
OI belaid, Imtinene/0000-0003-1673-321X; Ben Ahmed,
   Tarek/0000-0002-8302-4694; Manel, Limam/0000-0002-4220-8825
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NR 40
TC 1
Z9 1
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD JUL
PY 2023
VL 149
IS 7
BP 2735
EP 2742
DI 10.1007/s00432-022-04154-3
EA JUN 2022
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA L4OB8
UT WOS:000819301000002
PM 35771260
DA 2025-01-04
ER

PT S
AU Francies, HE
   Barthorpe, A
   McLaren-Douglas, A
   Barendt, WJ
   Garnett, MJ
AF Francies, Hayley E.
   Barthorpe, Andrew
   McLaren-Douglas, Anne
   Barendt, William J.
   Garnett, Mathew J.
BE Turksen, K
TI Drug Sensitivity Assays of Human Cancer Organoid Cultures
SO ORGANOIDS: Stem Cells, Structure, and Function
SE Methods in Molecular Biology
LA English
DT Article; Book Chapter
DE Drug screening; Organoids; Cancer; Cell lines; Cancer models; Drugs;
   Targeted therapy; Preclinical
ID LUNG-CANCER; CELL-LINES; STEM-CELLS; MUTATIONS; MODELS
AB Drug sensitivity testing utilizing preclinical disease models such as cancer cell lines is an important and widely used tool for drug development. Importantly, when combined with molecular data such as gene copy number variation or somatic coding mutations, associations between drug sensitivity and molecular data can be used to develop markers to guide patient therapies. The use of organoids as a preclinical cancer model has become possible following recent work demonstrating that organoid cultures can be derived from patient tumors with a high rate of success. A genetic analysis of colon cancer organoids found that these models encompassed the majority of the somatic variants present within the tumor from which it was derived, and capture much of the genetic diversity of colon cancer observed in patients. Importantly, the systematic sensitivity testing of organoid cultures to anticancer drugs identified clinical gene-drug interactions, suggestive of their potential as preclinical models for testing anticancer drug sensitivity. In this chapter, we describe how to perform medium/high-throughput drug sensitivity screens using 3D organoid cell cultures.
C1 [Francies, Hayley E.; Barthorpe, Andrew; McLaren-Douglas, Anne; Barendt, William J.; Garnett, Mathew J.] Wellcome Trust Sanger Inst, Cambridge, England.
C3 Wellcome Trust Sanger Institute
RP Francies, HE (corresponding author), Wellcome Trust Sanger Inst, Cambridge, England.
FU Wellcome Trust [102696]; Stand Up To Cancer [SU2C-AACR-DT1213]; Dutch
   Cancer Society [H1/2014-6919]; Cancer Research UK [C44943/A22536]
FX We would like to thank the Wellcome Trust Sanger Institute cell line
   drug screening team for their help in developing these protocols and
   Stacey Price for critical reading of this manuscript. This work was
   funded with Awards from the Wellcome Trust (102696), Stand Up To Cancer
   (SU2C-AACR-DT1213), The Dutch Cancer Society (H1/2014-6919), and Cancer
   Research UK (C44943/A22536).
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NR 18
TC 50
Z9 53
U1 0
U2 18
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 USA
SN 1064-3745
EI 1940-6029
BN 978-1-4939-7617-1; 978-1-4939-7616-4
J9 METHODS MOL BIOL
JI Methods Mol. Biol.
PY 2019
VL 1576
BP 339
EP 351
DI 10.1007/7651_2016_10
D2 10.1007/978-1-4939-7617-1
PG 13
WC Biochemical Research Methods; Cell & Tissue Engineering; Medicine,
   Research & Experimental
WE Book Citation Index – Science (BKCI-S)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA BS1AA
UT WOS:000685760200029
PM 27628132
OA hybrid, Green Accepted
DA 2025-01-04
ER

PT J
AU Ekblad, L
   Welinder, C
   Kjellén, E
   Brun, E
   Wennerberg, J
AF Ekblad, Lars
   Welinder, Charlotte
   Kjellen, Elisabeth
   Brun, Eva
   Wennerberg, Johan
TI Anti-or pro-proliferation - Conditional options for TGF-α and cetuximab
   in head and neck squamous cell carcinoma
SO ORAL ONCOLOGY
LA English
DT Article
DE Epidermal growth factor receptor; Transforming growth factor alpha;
   Squamous cell carcinoma of the head and neck; Cetuximab;
   Molecular-targeted therapy
ID EPIDERMAL-GROWTH-FACTOR; METASTATIC COLORECTAL-CANCER; CHEMOTHERAPY PLUS
   CETUXIMAB; PHORBOL ESTERS; RECEPTORS; EGF; EXPRESSION; AFFINITY;
   PROTEIN; LINES
AB Objectives: Cetuximab is an epidermal growth factor receptor (EGFR)-targeting drug that has shown effects in head and neck squamous cell carcinoma (HNSCC). The effects are, however, small and have mainly been proven in a subset of patients, and the cost-effectiveness has been questioned. For this reason, we need to know more about the basic mechanisms controlling the effect of EGFR signalling on tumour growth.
   Materials and methods: We investigated the effect of the EGFR ligand transforming growth factor alpha (TGF-alpha) and cetuximab, alone and in combination, on HNSCC cell lines, measuring proliferation and the activity of intracellular signalling pathways.
   Results: In line with previous reports we found the majority of the cell lines to be growth-inhibited by TGF-alpha. Surprisingly, two of the cell lines, which were more thoroughly investigated, were either growth-inhibited or stimulated by both cetuximab and TGF-alpha, depending on the presence or absence of the other substance. We also present data indicating the existence of two different receptor activities emanating from the EGFR protein.
   Conclusion: We therefore show that TGF-alpha can have both growth-stimulating and growth-inhibiting effects in the same cell line and that EGFR-targeting drugs can be similarly double-edged. The implication for such drugs is that the micro-environment within a tumour, and possibly within portions of a tumour, may influence the growth-inhibiting effect of the drug. There may also be important implications for our understanding of EGFR signalling and its influence on growth and development. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Ekblad, Lars; Welinder, Charlotte; Kjellen, Elisabeth; Brun, Eva] Lund Univ, Div Oncol & Pathol, Lund, Sweden.
   [Ekblad, Lars; Welinder, Charlotte; Kjellen, Elisabeth; Brun, Eva; Wennerberg, Johan] Skane Univ Hosp, Lund, Sweden.
   [Wennerberg, Johan] Lund Univ, Div Otorhinolaryngol Head & Neck Surg, Lund, Sweden.
C3 Lund University; Lund University; Skane University Hospital; Lund
   University
RP Ekblad, L (corresponding author), Div Oncol, Barngatan 2b, SE-22185 Lund, Sweden.
EM Lars.Ekblad@med.lu.se
RI Ekblad, Lars/O-8932-2014; Welinder, Charlotte/G-1144-2014
OI Ekblad, Lars/0000-0003-0152-786X; Welinder,
   Charlotte/0000-0001-9626-0576
FU Swedish Cancer Society [08 0686, 08 0709]; National Health Service in
   Sweden; Mrs. Berta Kamprad's Foundation; Crafoord Foundation; Laryng
   Foundation
FX This work was supported by the Swedish Cancer Society (08 0686 and 08
   0709), governmental funding of clinical research within the National
   Health Service in Sweden, Mrs. Berta Kamprad's Foundation, the Crafoord
   Foundation, and the Laryng Foundation.
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NR 29
TC 2
Z9 3
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1368-8375
EI 1879-0593
J9 ORAL ONCOL
JI Oral Oncol.
PD JAN
PY 2015
VL 51
IS 1
BP 46
EP 52
DI 10.1016/j.oraloncology.2014.08.019
PG 7
WC Oncology; Dentistry, Oral Surgery & Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Dentistry, Oral Surgery & Medicine
GA AW3UG
UT WOS:000346210900010
PM 25261297
DA 2025-01-04
ER

PT J
AU Wang, CY
   Zhou, SC
   Li, XW
   Li, BH
   Zhang, JJ
   Ge, Z
   Zhang, Q
   Hu, JH
AF Wang, Chen-Yu
   Zhou, Shi-Can
   Li, Xing-Wang
   Li, Bing-Hui
   Zhang, Jun-Jie
   Ge, Zheng
   Zhang, Quan
   Hu, Jun-Hong
TI Bibliometric analysis of randomized controlled trials of colorectal
   cancer over the last decade
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Article
DE Colorectal cancer; Randomized controlled trial; Bibliometrics; China
ID PHASE-III; CHEMOTHERAPY; MULTICENTER; FLUOROURACIL; BEVACIZUMAB;
   PANITUMUMAB; LEUCOVORIN; CETUXIMAB; SURGERY; CHINA
AB BACKGROUND Colorectal cancer is one of the most common cancers globally. In China, its prevalence ranks fourth and fifth among females and males, respectively. Presently, treatment of rectal cancer follows a multidisciplinary comprehensive treatment approach involving surgery, radiotherapy, chemotherapy, and targeted therapy. With deepening theoretical and molecular research on colorectal cancer, randomized controlled trials (RCTs) on colorectal cancer have made significant progress. However, many RCTs have shortfalls. AIM To investigate the RCTs of global colorectal cancer spanning from 2008 to 2018. To provide suggestions for conducting Chinese RCTs of colorectal cancer. METHODS PubMed and Web of Science databases were searched to obtain RCTs of colorectal cancer carried out between January 1, 2008, and January 1, 2018. The bibliometric method was used for statistical analysis of the publication years, countries/regions, authors, institutions, source journals, quoted times, key words, and authors. RESULTS Colorectal cancer RCTs showed an upward trend between 2008 to 2018; the top 10 research institutions in the included literature were from the United States, the United Kingdom, and other countries with a high incidence of colorectal cancer. Most of the related research journals are sponsored by European and American countries. The 15 most cited studies involved international multicenter clinical research, having few participants from Chinese research institutions. Network visualization using key words showed that RCTs on colorectal cancer focus on screening, disease-free survival, drug treatment, surgical methods, clinical trials, quality of life, and prognosis. The result of the coauthorship network analysis showed that Chinese researchers are less involved in international exchanges compared to those from leading publication countries. CONCLUSION High-quality RCTs are increasingly favored by leading international journals. However, there is still a large gap in clinical research between China and leading countries. Researchers should implement standardized and accurate clinical trials, strengthen international multicenter cooperation, and emphasize quality control.
C1 [Wang, Chen-Yu; Zhou, Shi-Can; Li, Xing-Wang; Li, Bing-Hui; Zhang, Jun-Jie; Ge, Zheng; Zhang, Quan; Hu, Jun-Hong] Henan Univ, Huaihe Hosp, Dept Anorectal Surg, 8 Baobei Rd, Kaifeng 47500, Henan, Peoples R China.
C3 Henan University
RP Hu, JH (corresponding author), Henan Univ, Huaihe Hosp, Dept Anorectal Surg, 8 Baobei Rd, Kaifeng 47500, Henan, Peoples R China.
EM hjh-8282@163.com
RI Li, Xingwang/K-8678-2019
FU Key Research and Promotion Projects of Henan Province [202102310094]; Wu
   Jieping Medical Foundation of Clinical Research Special Fund
   [320.2710.1836]; Henan University [SYL18060141]; Henan Province Medical
   Science and Technology Project Joint Development Project [2018020331]
FX Supported by Key Research and Promotion Projects of Henan Province, No.
   202102310094; Wu Jieping Medical Foundation of Clinical Research Special
   Fund, No. 320.2710.1836; Henan University Graduate "Excellence Program",
   No. SYL18060141; Henan Province Medical Science and Technology Project
   Joint Development Project, No. 2018020331.
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NR 22
TC 3
Z9 3
U1 3
U2 31
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD JUL 26
PY 2020
VL 8
IS 14
BP 3021
EP 3030
DI 10.12998/wjcc.v8.i14.3021
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA MW2SF
UT WOS:000556892700012
PM 32775383
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Luo, XJ
   Lu, YX
   Wang, Y
   Huang, RJ
   Liu, J
   Jin, Y
   Liu, ZK
   Liu, ZX
   Huang, QT
   Pu, HY
   Zeng, ZL
   Xu, RH
   Zhao, Q
   Wu, QN
AF Luo, Xiao-Jing
   Lu, Yun-Xin
   Wang, Yun
   Huang, Runjie
   Liu, Jia
   Jin, Ying
   Liu, Ze-Kun
   Liu, Ze-Xian
   Huang, Qi-Tao
   Pu, Heng-Ying
   Zeng, Zhao-Lei
   Xu, Ruihua
   Zhao, Qi
   Wu, Qi-Nian
TI M6A-modified lncRNA<i> FAM83H-AS1</i> promotes colorectal cancer
   progression through PTBP1
SO CANCER LETTERS
LA English
DT Article
DE CRC; FAM83H-AS1; PTBP1; m6A modification; RNA splicing
ID LONG NONCODING RNAS; MESSENGER-RNA; LNCRNA FAM83H-AS1; M(6)A
   MODIFICATION; CARCINOMA; PROTEINS; BINDING
AB LncRNA plays a crucial role in cancer progression and targeting, but it has been difficult to identify the critical lncRNAs involved in colorectal cancer (CRC) progression. We identified FAM83H-AS1 as a tumor-promoting associated lncRNA using 21 pairs of stage IV CRC tissues and adjacent normal tissues. In vitro and in vivo experiments revealed that knockdown of FAM83H-AS1 in CRC cells inhibited tumor proliferation and metastasis, and vice versa. M6A modification is critical for FAM83H-AS1 RNA stability through the writer METTL3 and the readers IGF2BP2/IGFBP3. PTBP1-an RNA binding protein-is responsible for the FAM83H-AS1 function in CRC. T4 (1770-2440 nt) and T5 (2440-2743 nt) on exon 4 of FAM83H-AS1 provide a platform for PTBP1 RRM2 interactions. Our results demonstrated that m6A modification dysregulated the FAM83H-AS1 oncogenic role by phosphorylated PTBP1 on its RNA splicing effect. In patient-derived xenograft models, ASO-FAM83H-AS1 significantly suppressed the growth of gastrointestinal (GI) tumors, not only CRC but also GC and ESCC. The combination of ASO-FAM83H-AS1 and oxaliplatin/cisplatin significantly suppressed tumor growth compared with treatment with either agent alone. Notably, there was pathological complete response in all these three GI cancers. Our findings suggest that FAM83H-AS1 targeted therapy would benefit patients primarily receiving platinum-based therapy in GI cancers.
C1 [Luo, Xiao-Jing; Huang, Qi-Tao; Wu, Qi-Nian] Sun Yat Sen Univ, Guangdong Prov Clin Res Ctr Canc, Dept Pathol, State Key Lab Oncol South China,Canc Ctr, Guangzhou 510060, Peoples R China.
   [Lu, Yun-Xin; Wang, Yun; Huang, Runjie; Liu, Jia; Jin, Ying; Xu, Ruihua] Sun Yat Sen Univ, Guangdong Prov Clin Res Ctr Canc, Dept Med Oncol, State Key Lab Oncol South China,Canc Ctr, Guangzhou 510060, Peoples R China.
   [Liu, Ze-Kun] Sun Yat Sen Univ, Guangdong Prov Clin Res Ctr Canc, Dept Radiol, State Key Lab Oncol South China,Canc Ctr, Guangzhou 510060, Peoples R China.
   [Liu, Ze-Xian; Pu, Heng-Ying; Zeng, Zhao-Lei; Zhao, Qi] Sun Yat Sen Univ, Guangdong Prov Clin Res Ctr Canc, State Key Lab Oncol South China, Canc Ctr, Guangzhou 510060, Peoples R China.
   [Xu, Ruihua] Chinese Acad Med Sci, Res Unit Precis Diag & Treatment Gastrointestinal, Guangzhou 510060, Peoples R China.
C3 State Key Lab Oncology South China; Sun Yat Sen University; State Key
   Lab Oncology South China; Sun Yat Sen University; Sun Yat Sen
   University; State Key Lab Oncology South China; State Key Lab Oncology
   South China; Sun Yat Sen University; Chinese Academy of Medical Sciences
   - Peking Union Medical College
RP Xu, RH; Zhao, Q; Wu, QN (corresponding author), Sun Yat Sen Univ, Canc Ctr, Guangzhou 510060, Peoples R China.
EM xurh@sysucc.org.cn; zhaoqi@sysucc.org.cn; wuqn@sysucc.org.cn
RI Zhang, Zixuan/JSL-3603-2023; Zhao, Qi/X-7899-2019
FU National Natural Science Foundation of China [82321003, 81930065,
   82173128, 82173096, 81802438]; CAMS Innovation Fund for Medical Sciences
   (CIFMS) [2019-I2M-5-036]; Cancer Innovative Research Program of Sun
   Yat-sen University Cancer Center [CIRP-SYSUCC-0004]; Sun Yat-sen
   University clinical research 5010 program [84000-31630002]; Youth Talent
   Support Program of Guangdong Provincial Association for Science and
   Technology [SKXRC202313]; Young Talents Program of Sun Yat-sen
   University Cancer Center [YTP-SYSUCC-0033]
FX This study was supported by National Natural Science Foundation of China
   [82321003, 81930065, 82173128 to RH.X., 82173096 to QN.W., 81802438 to
   Q.Z.] , CAMS Innovation Fund for Medical Sciences (CIFMS)
   (2019-I2M-5-036) ; Cancer Innovative Research Program of Sun Yat-sen
   University Cancer Center (CIRP-SYSUCC-0004) ; Sun Yat-sen University
   clinical research 5010 program (84000-31630002) . The Youth Talent
   Support Program of Guangdong Provincial Association for Science and
   Technology (SKXRC202313 to Q.Z.) ; The Young Talents Program of Sun
   Yat-sen University Cancer Center (YTP-SYSUCC-0033 to Q.Z) .
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NR 55
TC 0
Z9 0
U1 8
U2 8
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 217085
DI 10.1016/j.canlet.2024.217085
EA JUL 2024
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YO8Z2
UT WOS:001269531700001
PM 38964733
OA hybrid
DA 2025-01-04
ER

PT J
AU Gao, Y
   Liu, C
   Xu, XY
   Wang, YJ
   Jiang, YY
AF Gao, Yang
   Liu, Chen
   Xu, Xiaoyun
   Wang, Yijing
   Jiang, Yuanyuan
TI Circular RNA sterile alpha motif domain containing 4A contributes to
   cell 5-fluorouracil resistance in colorectal cancer by regulating the
   miR-545-3p/6-phosphofructo-2-kinase/fructose-2,6-bisphosphataseisotype 3
   axis
SO ANTI-CANCER DRUGS
LA English
DT Article
DE 5-fluorouracil; CircSAMD4A; miR-545-3p; PFKFB3
ID PROLIFERATION
AB Colorectal cancer (CRC) is one of the most fatal cancers in the world. Circular RNA sterile alpha motif domain containing 4A (circSAMD4A) was found to be highly expressed in CRC and promoted the tumorigenesis of CRC. However, the role of circSAMD4A in 5-fluorouracil (5-Fu) resistance of CRC is yet to be clarified. This study is designed to investigate the function of circSAMD4A in 5-Fu resistance of CRC and its potential molecular mechanism. Quantitative real-time PCR was used to detect the expression levels of circSAMD4A, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase isotype 3 (PFKFB3) mRNA, and miR-545-3p, and western blot was used to detect the protein expression. For functional analysis, 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay, colony formation/5-ethynyl-2 '-deoxyuridine assay, flow cytometry analysis, and glycolysis metabolism analysis were used to assess the capacities of cell viability, proliferation, apoptosis, and glycolysis in 5-Fu-resistant cells of CRC. The dual-luciferase reporter assay was used to verify the interaction between miR-545-3p and circSAMD4A or PFKFB3. Xenograft tumor model was established to confirm the biological role of circSAMD4A in 5-Fu resistance of CRC in vivo. CircSAMD4A was upregulated in 5-Fu-resistant CRC tissues and cells. Functionally, circSAMD4A knockdown inhibited the proliferation and glycolysis mechanism but promoted apoptosis in 5-Fu-resistant cells of CRC. CircSAMD4A was identified as a molecular sponge of miR-545-3p to upregulate PFKFB3 expression. Mechanistically, circSAMD4A knockdown-induced 5-Fu sensitivity was mediated by miR-545-3p/PFKFB3 axis. Moreover, circSAMD4A knockdown improved 5-Fu sensitivity of CRC in vivo. CircSAMD4A contributed to 5-Fu resistance of CRC cells partly through upregulating PFKFB3 expression by sponging miR-545-3p, providing a possible circRNA-targeted therapy for CRC.
C1 [Gao, Yang; Liu, Chen; Xu, Xiaoyun; Wang, Yijing] Suzhou Vocat Univ, Coll Educ & Humanities, Suzhou, Peoples R China.
   [Jiang, Yuanyuan] Zhengzhou Univ, Dept Gastroenterol, Zhengzhou Cent Hosp, 195 Tongbai Rd, Zhengzhou 215000, Henan, Peoples R China.
C3 Suzhou Vocational University; Zhengzhou University
RP Jiang, YY (corresponding author), Zhengzhou Univ, Dept Gastroenterol, Zhengzhou Cent Hosp, 195 Tongbai Rd, Zhengzhou 215000, Henan, Peoples R China.
EM 15937102930@126.com
RI jiang, anyi/GPT-0379-2022
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NR 23
TC 7
Z9 7
U1 0
U2 4
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 JUL
PY 2022
VL 33
IS 6
BP 553
EP 563
DI 10.1097/CAD.0000000000001285
PG 11
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA 1I0NQ
UT WOS:000796935000005
PM 35276696
DA 2025-01-04
ER

PT J
AU Ozkan, M
   Oflazoglu, U
   Yildiz, Y
   Güc, ZG
   Salman, T
   Ünal, S
   Kücükzeybek, Y
   Alacacioglu, A
AF Ozkan, Merve
   Oflazoglu, Utku
   Yildiz, Yasar
   Guc, Zeynep G.
   Salman, Tarik
   Unal, Sinan
   Kucukzeybek, Yuksel
   Alacacioglu, Ahmet
TI Regorafenib therapy as a third-line treatment for metastatic colorectal
   cancer: A single center long term experience
SO MEDICINE
LA English
DT Article
DE effectiveness; metastatic colorectal carcinoma; regorafenib; safety
ID DOUBLE-BLIND; EFFICACY
AB This study examined the effects of regorafenib (Reg) on progression-free survival (PFS), overall survival (OS), and adverse events (AEs) in metastatic colorectal cancer (mCRC) patients who underwent targeted treatment and chemotherapy. Reg was administered as a third-line treatment to 84 patients who had undergone 2 rounds of chemotherapy and targeted therapy and subsequently experienced progression. Treatment was initiated with a daily dose of 80 or 120 mg, based on the patient's ability to tolerate the medication, which was increased to 160 mg/day. The median PFS with Reg was 4 +/- 0.2 months, while the median OS was 9 +/- 1.2 months. When compared to patients who started Reg treatment at 80 mg, patients starting at 160 mg had longer median PFS and OS (PFS:6 +/- 2.1 months vs 4 +/- 0.2 months; P = .05; OS:13 +/- 0.7 months vs 6 +/- 1.3 months; P = .069). Patients with right-sided colon cancer who received Reg as third-line therapy had a significantly longer mPFS than those with left-sided colon cancer (8 months +/- 4 vs 4 months +/- 0.3, P = .039). Patients with KRAS mutations had a prolonged mPFS than those with panRAS-wild type (6 +/- 1.6 months vs 4 +/- 0.3 months, P = .06). The mPFS contribution in the BRAF mutant subgroup with poor prognosis is promising, as it is similar to that of patients without BRAF mutations (4 months +/- 0.8 x 4 months +/- 0.5, P = .74). The most common AEs reported were elevated liver enzyme levels and dermatological toxicities.
C1 [Ozkan, Merve; Oflazoglu, Utku; Yildiz, Yasar; Guc, Zeynep G.; Salman, Tarik; Unal, Sinan; Kucukzeybek, Yuksel; Alacacioglu, Ahmet] Izmir Katip Celebi Univ, Dept Med Oncol, TR-35100 Izmir, Turkiye.
C3 Izmir Katip Celebi University
RP Ozkan, M (corresponding author), Izmir Katip Celebi Univ, Dept Med Oncol, TR-35100 Izmir, Turkiye.
EM drmerveozkan88@gmail.com; u.oflaz35@gmail.com; dryasar2706@yahoo.co.uk;
   drtariksalman@gmail.com; dralaca2000@yahoo.com
RI Yildiz, Yasar/HKN-6909-2023; SALMAN, TARIK/HNI-1984-2023; Kucukzeybek,
   Yuksel/HKN-6361-2023; oflazoglu, utku/HJP-4039-2023
OI OZKAN, MERVE/0000-0002-2202-5159
CR Ciardiello D, 2021, CANCERS, V13, DOI 10.3390/cancers13225715
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NR 27
TC 0
Z9 0
U1 8
U2 13
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD DEC 15
PY 2023
VL 102
IS 50
AR e36435
DI 10.1097/MD.0000000000036435
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA CR7E9
UT WOS:001127027700034
PM 38115370
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Räsänen, K
   Lehtinen, E
   Nokelainen, K
   Kuopio, T
   Hautala, L
   Itkonen, O
   Stenman, UH
   Koistinen, H
AF Rasanen, Kati
   Lehtinen, Elina
   Nokelainen, Kristiina
   Kuopio, Teijo
   Hautala, Laura
   Itkonen, Outi
   Stenman, Ulf-Hakan
   Koistinen, Hannu
TI Interleukin-6 increases expression of serine protease inhibitor Kazal
   type 1 through STAT3 in colorectal adenocarcinoma
SO MOLECULAR CARCINOGENESIS
LA English
DT Article
DE SPINK1; inflammation; fibroblast; tumor microenvironment; colorectal
   cancer
ID TUMOR-ASSOCIATED TRYPSIN; COLON-CANCER; INFLAMMATION; PROLIFERATION;
   FIBROBLASTS; ACTIVATION; CARCINOMA; TATI; IL-6; IDENTIFICATION
AB Inflammation promotes colorectal cancer (CRC) tumorigenesis, but the underlying molecular mechanisms are still being uncovered. Proinflammatory cytokine interleukin-6 (IL-6) stimulates survival signaling in CRC; inflammatory signals also regulate production and activity of proteases and their inhibitors. Over-expression of serine protease inhibitor Kazal type 1 (SPINK1) predicts an unfavorable outcome in colon cancer. The SPINK1 gene contains an IL-6 responsive element, suggesting it could act as an acute phase reactant. We assessed the connection between IL-6 and SPINK1, and the function and mechanism of this signaling. Our results show that Colo205 and HT-29 cells express and secrete SPINK1, and both fibroblast-derived and recombinant IL-6 further increased the SPINK1 levels. Concurrently CRC cells augmented the IL-6 production in fibroblasts. In CRC tissues cancer cells were positive for SPINK1, whereas IL-6 was found in stromal cells. In Colo205 cells IL-6 also stimulated the secretion of trypsin-1 and -2, the key targets of SPINK1 protease inhibition, whereas in HT-29 cells trypsin-1 and -2 levels remained constantly low. Functionally, both IL-6 and SPINK1 increased the motility of the CRC cells. Mechanistically, IL-6 activated the canonical STAT3 pathway and inhibition of STAT3 phosphorylation decreased the levels of SPINK1, trypsin-1 and -2. Taken together, our results indicate a novel link between inflammatory signals originating from the tumor microenvironment and increased SPINK1 levels. This finding has potential therapeutic implications for targeted therapy, as it confirms that SPINK1 acts as an acute phase reactant and that it participates in the paracrine crosstalk with the tumor microenvironment of colon cancer. (c) 2015 Wiley Periodicals, Inc.
C1 [Rasanen, Kati; Lehtinen, Elina; Nokelainen, Kristiina; Hautala, Laura; Stenman, Ulf-Hakan; Koistinen, Hannu] Univ Helsinki, Dept Clin Chem, Medicum, Helsinki, Finland.
   [Kuopio, Teijo] Cent Finland Cent Hosp, Dept Pathol, Jyvaskyla, Finland.
   [Kuopio, Teijo] Univ Jyvaskyla, Dept Biol & Environm Sci, Div Cell & Mol Biol, Jyvaskyla, Finland.
   [Itkonen, Outi] Univ Helsinki, HUSLAB, Cent Hosp, Helsinki, Finland.
C3 University of Helsinki; Central Finland Central Hospital; University of
   Jyvaskyla; University of Helsinki; Helsinki University Central Hospital
RP Räsänen, K (corresponding author), Univ Helsinki, Dept Clin Chem, POB 63 Haartmaninkatu 8, FIN-00014 Helsinki, Finland.
EM kati.rasanen@helsinki.fi
RI Koistinen, Hannu/AGU-1279-2022; Räsänen, Kati/I-5769-2014; Kuopio,
   Teijo/HNB-7797-2023
OI Koistinen, Hannu/0000-0003-0926-3109; Hautala,
   Laura/0000-0002-5501-2792; Kuopio, Teijo/0000-0003-3503-4094; Stenman,
   Ulf-Hakan/0000-0002-2695-3454
FU Academy of Finland; Sigrid Juselius Foundation; Finska Lakaresallskapet;
   Helsinki University Central Hospital Research Fund; Orion Research
   Foundation
FX Grant sponsor: Academy of Finland; Grant sponsor: Sigrid Juselius
   Foundation; Grant sponsor: Finska Lakaresallskapet; Grant sponsor:
   Helsinki University Central Hospital Research Fund; Grant sponsor: Orion
   Research Foundation
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NR 53
TC 13
Z9 14
U1 2
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0899-1987
EI 1098-2744
J9 MOL CARCINOGEN
JI Mol. Carcinog.
PD DEC
PY 2016
VL 55
IS 12
BP 2010
EP 2023
DI 10.1002/mc.22447
PG 14
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA EC1GY
UT WOS:000387854100011
PM 26663388
DA 2025-01-04
ER

PT J
AU Liang, YH
   Tsai, JH
   Cheng, YM
   Chan, KY
   Hsu, WL
   Lee, CC
   Chen, KH
   Yeh, KH
AF Liang, Yi-Hsin
   Tsai, Jia-Huei
   Cheng, Yung-Ming
   Chan, Kuang-Yu
   Hsu, Wen-Ling
   Lee, Chang-Cheng
   Chen, Kuo-Hsing
   Yeh, Kun-Huei
TI Chemotherapy agents stimulate dendritic cells against human colon cancer
   cells through upregulation of the transporter associated with antigen
   processing
SO SCIENTIFIC REPORTS
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; IMMUNE; CARCINOMA; ANTIBODY;
   5-FLUOROURACIL; PEMBROLIZUMAB; BEVACIZUMAB; EXPRESSION; INHIBITOR;
   RECURRENT
AB Single immunotherapy fails to demonstrate efficacy in patients with microsatellite stable (MSS) metastatic colorectal cancer (mCRC). Research on immune reactions before and after systemic agents for mCRC is warranted. Our study examined cell line models to compare the expression of immune surface markers on colon cancer cells before and after chemotherapy agents. We also elucidated mechanisms underlying the effects of chemotherapy agents on immune surface markers. We used real-world clinical samples with NanoString analysis and the Perkin-Elmer Opal multiplex system. We established that chemotherapy agents, particularly 7-ethyl-10-hydroxycamptothecin (SN-38), the active metabolite of irinotecan, stimulated the expression of stimulatory MHC class I alleles through stimulation the pathway of transporters associated with antigen processing 1 and 2 (TAP1 and TAP2) in cell line models. Application of infected cell protein 47 (ICP-47), a specific inhibitor of the TAP1/TAP2, significantly inhibited expression of TAP1/TAP2 and also inhibited the expression of the downstream MHC class I. In the functional assay, SN-38 significantly promoted the phagocytosis of colon cancer cells by monocyte-derived dendritic cells (MoDCs). We confirmed that the expression of major histocompatibility complex (MHC) class I, significantly increased after first-line chemotherapy and targeted therapy in the samples of real-world patients with de novo mCRC. Our study provides new insights for novel immunotherapy combinations.
C1 [Liang, Yi-Hsin; Chan, Kuang-Yu; Lee, Chang-Cheng; Chen, Kuo-Hsing; Yeh, Kun-Huei] Natl Taiwan Univ, Grad Inst Oncol, Taipei, Taiwan.
   [Lee, Chang-Cheng; Yeh, Kun-Huei] Natl Taiwan Univ, Clin Med, Taipei, Taiwan.
   [Liang, Yi-Hsin; Hsu, Wen-Ling] Natl Taiwan Univ, Coll Med, Ctr Genom & Precis Med, Taipei, Taiwan.
   [Liang, Yi-Hsin; Chen, Kuo-Hsing; Yeh, Kun-Huei] Natl Taiwan Univ Hosp, Dept Oncol, 7 Chung Shan South Rd, Taipei 10002, Taiwan.
   [Tsai, Jia-Huei; Cheng, Yung-Ming] Natl Taiwan Univ Hosp, Dept Pathol, Taipei, Taiwan.
   [Liang, Yi-Hsin; Chen, Kuo-Hsing; Yeh, Kun-Huei] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Canc Ctr, Taipei, Taiwan.
C3 National Taiwan University; National Taiwan University; National Taiwan
   University; National Taiwan University; National Taiwan University
   Hospital; National Taiwan University; National Taiwan University
   Hospital; National Taiwan University; National Taiwan University
   Hospital
RP Yeh, KH (corresponding author), Natl Taiwan Univ, Grad Inst Oncol, Taipei, Taiwan.; Yeh, KH (corresponding author), Natl Taiwan Univ, Clin Med, Taipei, Taiwan.; Yeh, KH (corresponding author), Natl Taiwan Univ Hosp, Dept Oncol, 7 Chung Shan South Rd, Taipei 10002, Taiwan.; Yeh, KH (corresponding author), Natl Taiwan Univ, Natl Taiwan Univ Hosp, Canc Ctr, Taipei, Taiwan.
EM khyeh@ntu.edu.tw
RI chen, long/AAV-6276-2021; Yeh, Kun-Huei/HGD-3316-2022
OI LIANG, YI-HSIN/0000-0002-7224-9687
FU Ministry of Science and Technology, Taiwan [MOST-106-2314-B-002-222-MY3,
   MOST 109-2634-F-002-043]; Ministry of Education, Taiwan
   [NTU-109L901403]; National Taiwan University Hospital, Taipei, Taiwan
   [NTUH.106-N3634]
FX This study was supported by the Ministry of Science and Technology,
   Taiwan (MOST-106-2314-B-002-222-MY3, MOST 109-2634-F-002-043); the
   Ministry of Education, Taiwan (NTU-109L901403); and the National Taiwan
   University Hospital, Taipei, Taiwan (NTUH.106-N3634).
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NR 41
TC 6
Z9 8
U1 0
U2 7
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD APR 27
PY 2021
VL 11
IS 1
AR 9080
DI 10.1038/s41598-021-88648-z
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA RX3OD
UT WOS:000647135600009
PM 33907276
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Boussios, S
   Ozturk, MA
   Moschetta, M
   Karathanasi, A
   Zakynthinakis-Kyriakou, N
   Katsanos, KH
   Christodoulou, DK
   Pavlidis, N
AF Boussios, Stergios
   Ozturk, Mehmet Akif
   Moschetta, Michele
   Karathanasi, Afroditi
   Zakynthinakis-Kyriakou, Nikolaos
   Katsanos, Konstantinos H.
   Christodoulou, Dimitrios K.
   Pavlidis, Nicholas
TI The Developing Story of Predictive Biomarkers in Colorectal Cancer
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Review
DE colorectal cancer; biomarkers; prognostic and predictive markers;
   treatment resistance
ID CIRCULATING TUMOR-CELLS; KIRSTEN RAS MUTATIONS; DNA MISMATCH REPAIR;
   TO-LYMPHOCYTE RATIO; II COLON-CANCER; 1ST-LINE TREATMENT; STAGE-III;
   MICROSATELLITE INSTABILITY; PROGNOSTIC-SIGNIFICANCE; OPEN-LABEL
AB Colorectal cancer (CRC) is the third most common malignancy worldwide. Surgery remains the most important treatment for non-metastatic CRC, and the administration of adjuvant chemotherapy depends mainly on the disease stage, which is still the strongest prognostic factor. A refined understanding of the genomics of CRC has recently been achieved thanks to the widespread use of next generation sequencing with potential future therapeutic implications. Microsatellite instability (MSI) has been suggested as a predictive marker for response to anti-programmed-cell-death protein 1 (PD-1) therapy in solid tumors, including CRC. It should be noted that not all cancers with MSI phenotype respond to anti-PD-1 immunotherapy, highlighting the urgent need for even better predictive biomarkers. Mitogen-Activated Protein Kinase (MAPK) pathway genes KRAS, NRAS, and BRAF represent important molecular targets and could serve as independent prognostic biomarkers in CRC, and identify those who potentially benefit from anti-epidermal growth factor receptor (EGFR) treatment. Emerging evidence has attributed a significant role to inflammatory markers including blood cell ratios in the prognosis and survival of CRC patients; these biomarkers can be easily assessed in routine blood exams and be used to identify high-risk patients or those more likely to benefit from chemotherapy, targeted therapies and potentially immunotherapy. Analysis of cell-free DNA (cfDNA), circulating tumor cells (CTC) and/or micro RNAs (miRNAs) could provide useful information for the early diagnosis of CRC, the identification of minimal residual disease and, the evaluation of the risk of recurrence in early CRC patients. Even the selection of patients suitable for the new targeted therapy is becoming possible with the use of predictive miRNA biomarkers. Finally, the development of treatment resistance with the emergence of chemo-resistance clones after treatment remains the most important challenge in the clinical practice. In this context it is crucial to identify potential biomarkers and therapeutic targets which could lead to development of new and more effective treatments.
C1 [Boussios, Stergios; Karathanasi, Afroditi] Medway NHS Fdn Trust, Acute Oncol Assessment Unit, Windmill Rd, Gillingham ME7 5NY, Kent, England.
   [Boussios, Stergios] AELIA Org, 9th Km Thessaloniki Thermi, Thessaloniki 57001, Greece.
   [Ozturk, Mehmet Akif] Bahcesehir Univ, Sch Med, Dept Internal Med, TR-34353 Istanbul, Turkey.
   [Moschetta, Michele] Sarah Cannon Res Inst, Drug Dev Unit, 93 Harley St, London W1G 6AD, England.
   [Zakynthinakis-Kyriakou, Nikolaos] Leicester Diabet Res Ctr, Gwendolen Rd, Leicester LE5 4PW, Leics, England.
   [Katsanos, Konstantinos H.; Christodoulou, Dimitrios K.] Univ Ioannina, Sch Hlth Sci, Dept Gastroenterol, Univ Hosp Ioannina,Fac Med, Ioannina 45110, Greece.
   [Pavlidis, Nicholas] Univ Ioannina, Med Sch, Stavros Niarchou Ave, Ioannina 45110, Greece.
C3 Bahcesehir University; University Hospital Ioannina; University of
   Ioannina; University of Ioannina
RP Boussios, S (corresponding author), Medway NHS Fdn Trust, Acute Oncol Assessment Unit, Windmill Rd, Gillingham ME7 5NY, Kent, England.; Boussios, S (corresponding author), AELIA Org, 9th Km Thessaloniki Thermi, Thessaloniki 57001, Greece.
EM stergiosboussios@gmail.com; ozturkakif@yahoo.com;
   michelemoschetta1@gmail.com; a.karathanasi@nhs.net;
   nikolaoszakynthinakis@gmail.com; khkostas@hotmail.com;
   dchristodoulou@gmail.com; npavlid@uoi.gr
RI Boussios, Stergios/AAH-2933-2019; OZTURK, MEHMET AKIF/C-2218-2013
OI Boussios, Stergios/0000-0002-2512-6131; Christodoulou,
   Dimitrios/0000-0001-9694-1160; OZTURK, MEHMET AKIF/0000-0003-1365-7944
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NR 175
TC 129
Z9 130
U1 1
U2 23
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 MAR
PY 2019
VL 9
IS 1
AR 12
DI 10.3390/jpm9010012
PG 23
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA HS6SI
UT WOS:000464001200011
PM 30736475
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Xing, Q
   Cui, Y
   Liu, M
   Gu, XL
   Li, XT
   Xing, BC
   Sun, YS
AF Xing, Qian
   Cui, Yong
   Liu, Ming
   Gu, Xiao-Lei
   Li, Xiao-Ting
   Xing, Bao-Cai
   Sun, Ying-Shi
TI Preoperative CT-based morphological heterogeneity for predicting
   survival in patients with colorectal cancer liver metastases after
   surgical resection: a retrospective study
SO BMC MEDICAL IMAGING
LA English
DT Article
DE Colorectal cancer; Liver metastases; Heterogeneity; Prognosis; CT
ID RESPONSE EVALUATION; HEPATIC RESECTION; CHEMOTHERAPY; CRITERIA
AB ObjectiveTo explore the value of preoperative CT-based morphological heterogeneity (MH) for predicting local tumor disease-free survival (LTDFS) and progression-free survival (PFS) in patients with colorectal cancer liver metastases (CRLM).MethodsThe latest CT data of 102 CRLM patients were retrospectively analyzed. The morphological score of each liver metastasis was obtained, and the morphological heterogeneity difference (MHD) was calculated. The receiver operating characteristic (ROC) curve was drawn, and the cutoff value was found. The Kaplan-Meier method was used to draw survival curves of patients with or without MH. The Cox regression analysis was used to build the model with MH and clinical characteristics for predicting PFS.ResultsIn 78 patients without MH, median PFS was 9.0 months (95% CI:6.5-11.5), while in 24 patients with MH, median PFS was 6.0 months (95% CI:4.0-8.1), indicating that MH significantly affected PFS (p = 0.001). MH affected PFS in both the chemotherapy group and the chemotherapy combined with targeted therapy group (p = 0.005, p = 0.043). MH, preoperative carcinoembryonic antigen (CEA) and chemotherapy after surgery were independent predictors for postoperative PFS in patients with CRLM.ConclusionPreoperative CT-based MH had good efficacy for predicting LTDFS and PFS of CRLM patients after surgical resection, regardless of preoperative treatment. MH is one of the independent predictors of PFS.
C1 [Xing, Qian; Cui, Yong; Gu, Xiao-Lei; Li, Xiao-Ting; Sun, Ying-Shi] Peking Univ Canc Hosp & Inst, Dept Radiol, Minist Educ Beijing, Key Lab Carcinogenesis & Translat Res, 52 Fucheng Rd, Beijing 100142, Peoples R China.
   [Liu, Ming; Xing, Bao-Cai] Peking Univ, Minist Educ Beijing, Hepatopancreatobiliary Surg Dept 1, Key Lab Carcinogenesis & Translat Res,Canc Hosp In, 52 Fu Cheng Rd, Beijing 100142, Peoples R China.
RP Sun, YS (corresponding author), Peking Univ Canc Hosp & Inst, Dept Radiol, Minist Educ Beijing, Key Lab Carcinogenesis & Translat Res, 52 Fucheng Rd, Beijing 100142, Peoples R China.; Xing, BC (corresponding author), Peking Univ, Minist Educ Beijing, Hepatopancreatobiliary Surg Dept 1, Key Lab Carcinogenesis & Translat Res,Canc Hosp In, 52 Fu Cheng Rd, Beijing 100142, Peoples R China.
EM xingbaocai88@sina.com; sys27@163.com
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NR 21
TC 0
Z9 0
U1 0
U2 0
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2342
J9 BMC MED IMAGING
JI BMC Med. Imag.
PD DEC 18
PY 2024
VL 24
IS 1
AR 343
DI 10.1186/s12880-024-01524-w
PG 12
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA P9K3A
UT WOS:001381000800010
PM 39696033
DA 2025-01-04
ER

PT J
AU Kim, S
   Lim, Y
   Kang, JK
   Kim, HP
   Roh, H
   Kim, SY
   Lee, D
   Bang, D
   Jeong, SY
   Park, KJ
   Han, SW
   Kim, TY
AF Kim, Sheehyun
   Lim, Yoojoo
   Kang, Jun-Kyu
   Kim, Hwang-Phill
   Roh, Hanseong
   Kim, Su Yeon
   Lee, Dongin
   Bang, Duhee
   Jeong, Seung-Yong
   Park, Kyu Joo
   Han, Sae-Won
   Kim, Tae-You
TI Dynamic changes in longitudinal circulating tumour DNA profile during
   metastatic colorectal cancer treatment
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
ID CELL-FREE DNA; LIQUID BIOPSY; HETEROGENEITY; MUTATIONS; THERAPY; KRAS;
   BRAF
AB Background Circulating tumour DNA (ctDNA) has been spotlighted as an attractive biomarker because of its easy accessibility and real-time representation of tumour genetic profile. However, the clinical utility of longitudinal ctDNA monitoring has not been clearly defined. Methods Serial blood samples were obtained from metastatic colorectal cancer patients undergoing first-line chemotherapy. ctDNA was sequenced using a targeted next-generation sequencing platform which included 106 genes. Changes in ctDNA profile and treatment outcome were comprehensively analysed. Results A total of 272 samples from 62 patients were analysed. In all, 90.3% of patients had detectable ctDNA mutation before treatment. ctDNA clearance after chemotherapy was associated with longer progression-free survival which was independent of radiological response (adjusted hazard ratio 0.22, 95% confidence interval 0.10-0.46). Longitudinal monitoring was able to detect ctDNA progression which preceded radiological progressive disease (PD) in 58.1% (median 3.3 months). Diverse resistant mutations (34.9%) and gene amplification (7.0%) at the time of PD were discovered. For 16.3% of the PD patients, the newly identified mutations could be potential candidates of targeted therapy or clinical trial. Conclusion ctDNA profile provided a more accurate landscape of tumour and dynamic changes compared to radiological evaluation. Longitudinal ctDNA monitoring may improve personalised treatment decision-making.
C1 [Kim, Sheehyun] Seoul Natl Univ Hosp, Dept Genom Med, Seoul, South Korea.
   [Lim, Yoojoo; Kang, Jun-Kyu; Kim, Hwang-Phill; Roh, Hanseong; Kim, Su Yeon; Kim, Tae-You] IMBdx Inc, Seoul, South Korea.
   [Lee, Dongin; Bang, Duhee] Yonsei Univ, Dept Chem, Seoul, South Korea.
   [Jeong, Seung-Yong; Park, Kyu Joo] Seoul Natl Univ Hosp, Dept Surg, Seoul, South Korea.
   [Han, Sae-Won; Kim, Tae-You] Seoul Natl Univ Hosp, Dept Internal Med, Seoul, South Korea.
   [Han, Sae-Won; Kim, Tae-You] Seoul Natl Univ, Canc Res Inst, Seoul, South Korea.
C3 Seoul National University (SNU); Seoul National University Hospital;
   Yonsei University; Seoul National University (SNU); Seoul National
   University Hospital; Seoul National University (SNU); Seoul National
   University Hospital; Seoul National University (SNU)
RP Kim, TY (corresponding author), IMBdx Inc, Seoul, South Korea.; Han, SW; Kim, TY (corresponding author), Seoul Natl Univ Hosp, Dept Internal Med, Seoul, South Korea.; Han, SW; Kim, TY (corresponding author), Seoul Natl Univ, Canc Res Inst, Seoul, South Korea.
EM saewon1@snu.ac.kr; kimty@snu.ac.kr
RI Kim, Chang Gon/IAP-6721-2023; Park, Kyu/J-5480-2012
OI Kim, Sheehyun/0000-0002-4347-4420; Lim, Yoojoo/0000-0002-4181-2916
FU Korea Health Technology R&D Project through the Korea Health Industry
   Development Institute (KHIDI) - Ministry of Health & Welfare, Republic
   of Korea [HI18C2282]
FX This study was supported by grants from the Korea Health Technology R&D
   Project through the Korea Health Industry Development Institute (KHIDI),
   funded by the Ministry of Health & Welfare, Republic of Korea (grant
   number: HI18C2282).
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NR 37
TC 18
Z9 18
U1 0
U2 6
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD SEP 1
PY 2022
VL 127
IS 5
BP 898
EP 907
DI 10.1038/s41416-022-01837-z
EA MAY 2022
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4E3AZ
UT WOS:000803302500001
PM 35643791
OA Green Published
DA 2025-01-04
ER

PT J
AU Lin, WC
   Lin, CC
   Lin, YY
   Yang, WH
   Twu, YC
   Teng, HW
   Hwang, WL
AF Lin, Wen-Chun
   Lin, Chun-Chi
   Lin, Yen-Yu
   Yang, Wen-Hao
   Twu, Yuh-Ching
   Teng, Hao-Wei
   Hwang, Wei-Lun
TI Molecular actions of exosomes and their theragnostics in colorectal
   cancer: current findings and limitations
SO CELLULAR ONCOLOGY
LA English
DT Review
DE Colorectal Cancer; Tumor Heterogeneity; Tumor Microenvironment;
   Extracellular Vesicles; Cancer Biomarker
ID EXTRACELLULAR VESICLES; TRANSFERRIN RECEPTOR; STEM-CELLS; FIBROBLASTS;
   RNA; CHEMORESISTANCE; BIOGENESIS; MATURATION; SECRETION; PROMOTE
AB Extracellular vesicles (EVs) are cell-released, membranous structures essential for intercellular communication. The biochemical compositions and physiological impacts of exosomes, lipid-bound, endosomal origin EVs, have been focused on, especially on the tumor-host interactions in a defined tumor microenvironment (TME). Despite recent progress in targeted therapy and cancer immunotherapy in colorectal cancer (CRC), cancer patients still suffer from distal metastasis and tumor relapse, suggesting unmet needs for biomarkers directing therapeutic interventions and predicting treatment responsiveness. As exosomes are indispensable for intercellular communication and high exosome abundance makes them feasible biomarker molecules, this review discusses exosome heterogeneity and how exosomes orchestrate the interplay among tumor cells, cancer stem cells (CSCs) and host cells, including stromal cells, endothelial cells and immunocytes, in the CRC TME. This review also discusses mechanisms for loading exosomal contents and potential exosomal DNA, RNA and protein biomarkers for early CRC detection. Finally, we summarize the diagnostic and therapeutic exosomes in clinical trials. We envision that detecting and targeting cancer-specific exosomes could provide therapeutic advances in developing personalized cancer medicine.
C1 [Lin, Wen-Chun; Twu, Yuh-Ching; Hwang, Wei-Lun] Natl Yang Ming Chiao Tung Univ, Dept Biotechnol & Lab Sci Med, 155,Sec 2,Li Nong St, Taipei 112, Taiwan.
   [Lin, Chun-Chi] Taipei Vet Gen Hosp, Dept Surg, Div Colon Sr Rectal Surg, Taipei 112, Taiwan.
   [Lin, Chun-Chi] Natl Yang Ming Chiao Tung Univ, Fac Med, Sch Med, Dept Surg, Taipei 112, Taiwan.
   [Lin, Yen-Yu] Fu Ten Catholic Univ, Fu Ten Catholic Univ Hosp, Div Pathol, New Taipei 24352, Taiwan.
   [Yang, Wen-Hao] China Med Univ, Res Ctr Canc Biol, Grad Inst Biomed Sci, Taichung 406, Taiwan.
   [Yang, Wen-Hao] China Med Univ, Ctr Mol Med, Taichung 406, Taiwan.
   [Teng, Hao-Wei] Taipei Vet Gen Hosp, Dept Oncol, Div Med Oncol, 112,201,Sec 2,Shipai Rd, Taipei, Taiwan.
   [Teng, Hao-Wei] Natl Yang Ming Chiao Tung Univ, Sch Med, Taipei 112, Taiwan.
   [Hwang, Wei-Lun] Natl Yang Ming Chiao Tung Univ, Canc Progress Res Ctr, Taipei 112, Taiwan.
C3 National Yang Ming Chiao Tung University; Taipei Veterans General
   Hospital; National Yang Ming Chiao Tung University; China Medical
   University Taiwan; China Medical University Taiwan; Taipei Veterans
   General Hospital; National Yang Ming Chiao Tung University; National
   Yang Ming Chiao Tung University
RP Hwang, WL (corresponding author), Natl Yang Ming Chiao Tung Univ, Dept Biotechnol & Lab Sci Med, 155,Sec 2,Li Nong St, Taipei 112, Taiwan.; Teng, HW (corresponding author), Taipei Vet Gen Hosp, Dept Oncol, Div Med Oncol, 112,201,Sec 2,Shipai Rd, Taipei, Taiwan.; Teng, HW (corresponding author), Natl Yang Ming Chiao Tung Univ, Sch Med, Taipei 112, Taiwan.; Hwang, WL (corresponding author), Natl Yang Ming Chiao Tung Univ, Canc Progress Res Ctr, Taipei 112, Taiwan.
EM hwteng1971@gmail.com; wlhwang@nycu.edu.tw
RI Yang, wenhao/GXG-5965-2022; Chiang, Chi-Ling/O-3038-2016
OI Yang, Wen-Hao/0000-0002-6292-9048; Hwang, Wei-Lun/0000-0002-8694-877X
FU Ministry of Science and Technology [109-2320-B-010-021,
   111-2628-B-A49-017, 109-2314-B-075-081-MY3, 109-2314-B-075-026]; Yen
   Tjing Ling Medical Foundation [CI-111-15]; Ministry of Health and
   Welfare, Center of Excellence for Cancer Research
   [MOHW107-TDU-B-211-114019, 111 W31208]; Higher Education Sprout Project
   by the Ministry of Education (MOE) [110AC-D303]; Taipei Veterans General
   Hospital [V111C-069, V110C-189]; Innovative Research Grant of the
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TC 3
Z9 3
U1 1
U2 14
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 2211-3428
EI 2211-3436
J9 CELL ONCOL
JI Cell. Oncol.
PD DEC
PY 2022
VL 45
IS 6
BP 1043
EP 1052
DI 10.1007/s13402-022-00711-7
EA SEP 2022
PG 10
WC Oncology; Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology; Pathology
GA 7B1QK
UT WOS:000848494100001
PM 36048363
DA 2025-01-04
ER

PT J
AU Ishida, R
   Koyanagi-Aoi, M
   Oshima, N
   Kakeji, Y
   Aoi, T
AF Ishida, Ryo
   Koyanagi-Aoi, Michiyo
   Oshima, Nobu
   Kakeji, Yoshihiro
   Aoi, Takashi
TI The Tissue-Reconstructing Ability of Colon CSCs Is Enhanced by FK506 and
   Suppressed by GSK3 Inhibition
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID GLYCOGEN-SYNTHASE KINASE-3; HUMAN COLORECTAL-CANCER; STEM-CELL NICHE;
   SIDE-POPULATION; CYCLOSPORINE-A; IN-VITRO; GROWTH; TRANSPLANTATION;
   ZAKI-4; VIVO
AB Cancer stem cells (CSC) are capable of reconstructing cancer tissues, are involved in both recurrence and metastasis, and contribute to therapeutic resistance. Therefore, elucidating the molecular mechanism in CSCs is important to successfully treat unresectable cancers. Previously, we observed that colon cancer stem-like cells can be induced from human colon cancer cell lines by retrovirally introducing OCT3/4, SOX2, and KLF4, and we have designated such cells as induced cancer stem cells (iCSC). In the current study, we used iCSCs to evaluate the molecular mechanism of colon CSCs and developed new methods to control them. The spheres that were derived in vitro from the iCSCs, but not those from parental cells, mimicked human colon cancer tissues in terms of their immunohistologic patterns; therefore, sphere-forming ability was assessed as a measure of the tissuere-constructing ability of iCSCs. Interestingly, the calcineurin inhibitor FK506 enhanced the sphere-forming ability of iCSCs, whereas GSK3 inhibition by RNAi, CHIR99021, and valproic acid (VPA) impeded the sphere-forming ability and expansion of iCSCs. FK506 and GSK3 inhibition showed the opposite effect regarding the NFATc3 localization of iCSCs. These data reveal the crucial role that NFAT localization, as regulated by calcineurin and GSK3, plays in the tissue-reconstructing ability of colon cancer stem cells and the potential of GSK3 inhibitors, such as VPA, in colon cancer stem cell-targeting therapy. (C) 2017 AACR.
C1 [Ishida, Ryo; Koyanagi-Aoi, Michiyo; Aoi, Takashi] Kobe Univ, Grad Sch Sci Technol & Innovat, Div Adv Med Sci, Kobe, Hyogo, Japan.
   [Ishida, Ryo; Koyanagi-Aoi, Michiyo; Aoi, Takashi] Kobe Univ, Grad Sch Med, Dept iPS Cell Applicat, Kobe, Hyogo, Japan.
   [Ishida, Ryo; Kakeji, Yoshihiro] Kobe Univ, Grad Sch Med, Div Gastrointestinal Surg, Dept Surg, Kobe, Hyogo, Japan.
   [Koyanagi-Aoi, Michiyo; Aoi, Takashi] Kobe Univ Hosp, Ctr Human Resource Dev Regenerat Med, Kobe, Hyogo, Japan.
   [Oshima, Nobu] Kyoto Univ, Grad Sch Med, Dept Surg, Kyoto, Japan.
C3 Kobe University; Kobe University; Kobe University; Kobe University;
   Kyoto University
RP Aoi, T (corresponding author), Kobe Univ, Grad Sch Sci Technol & Innovat, Chuo Ku, 7-5-1 Kusunoki Cho, Kobe, Hyogo 6500017, Japan.
EM takaaoi@med.kobe-u.ac.jp
FU Japan Agency for Medical Research and Development, AMED [16817073]
FX This work was supported by a grant for Research Center Network for
   Realization of Regenerative Medicine (16817073) from Japan Agency for
   Medical Research and Development, AMED.
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U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
EI 1557-3125
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD OCT
PY 2017
VL 15
IS 10
BP 1455
EP 1466
DI 10.1158/1541-7786.MCR-17-0071
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FI7FD
UT WOS:000412161400015
PM 28710230
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Kim, CW
AF Kim, Chan Wook
TI Update on Diagnosis and Treatment of Colorectal Cancer
SO EWHA MEDICAL JOURNAL
LA English
DT Review
DE Colorectal neoplasms; Screening; Metastatic; Neoadjuvant therapy;
   Precision medicine
ID HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY; ADVANCED RECTAL-CANCER; TOTAL
   MESORECTAL EXCISION; LIVER METASTASES; PULMONARY METASTASECTOMY;
   CYTOREDUCTIVE SURGERY; OPEN-LABEL; RESECTION; OUTCOMES; WATCH
AB The rate of colorectal cancer (CRC) has altered. Early-onset CRC patients are increasing, and it is one of the main causes of cancer-related death. Based on epidemiologic change, the CRC screening program needs to be changed. To increase compliance, non-invasive screening techniques are developed. Although CRC survival has increased, the oncologic prognosis of metastatic CRC is remains poor. Even in metastatic CRC, which is the most difficult to treat, attempts are being made to increase the survival rate by active surgical therapy with the creation of chemotherapeutic regimens and targeted treatment based on genomic information. Due to the introduction of aggressive chemotherapy regimens, targeted therapy based on genomic features, and improvements in surgical technique, the role of surgical treatment in metastatic CRC has expanded. Metastatic CRC surgery was indicated for liver, lung, and even peritoneal seeding. Local ablation therapy was also effectively used for liver and lung metastasis. Cytoreductive surgery and intraperitoneal chemotherapy were tried for peritoneal seeding and demonstrated good results in a subgroup of patients, although the right indication was carefully assessed. At the same time, one of the key goals of treatment for CRC was to maintain functional outcomes. Neoadjuvant treatment, in particular, helped rectal cancer patients preserve functional results while maintaining oncologic safety. Rectal cancer organ preservation techniques are now being researched heavily in a variety of neoadjuvant treatment settings, including immunotherapy and whole neoadjuvant therapy. Precision medicine based on patient and disease characteristics is currently being used for the diagnosis and treatment of CRC.
C1 [Kim, Chan Wook] Univ Ulsan, Asan Med Ctr, Dept Colon & Rectal Surg, Coll Med, 88 Olymp Ro 43 Gil, Seoul 05505, South Korea.
C3 University of Ulsan
RP Kim, CW (corresponding author), Univ Ulsan, Asan Med Ctr, Dept Colon & Rectal Surg, Coll Med, 88 Olymp Ro 43 Gil, Seoul 05505, South Korea.
EM crscwkim@amc.seoul.kr
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NR 48
TC 1
Z9 1
U1 0
U2 4
PU EWHA WOMANS UNIV SCH MEDICINE
PI SEOUL
PA 52, EWHAYEODAE-GIL, SEODAEMUN-GU, SEOUL, 03760, SOUTH KOREA
SN 2234-3180
EI 2234-2591
J9 EWHA MED J
JI Ewha Med. J.
PD OCT
PY 2022
VL 45
IS 4
AR e8
DI 10.12771/emj.2022.e8
PG 9
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA 5Z3GS
UT WOS:000879865200006
OA gold
DA 2025-01-04
ER

PT J
AU Pan, GX
   Li, DN
   Li, X
   Peng, Y
   Wang, T
   Zuo, CJ
AF Pan, Guixia
   Li, Danni
   Li, Xiao
   Peng, Ye
   Wang, Tao
   Zuo, Changjing
TI SPECT/CT imaging of HER2 expression in colon cancer-bearing nude mice
   using <SUP>125</SUP>I-Herceptin
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE HER2; Targeting; Colon cancer; SPECT imaging
ID BREAST-CANCER; MONOCLONAL-ANTIBODY; OVEREXPRESSION
AB An accurate assessment of HER2 status in patients with colorectal cancer is very important, because only the patients overexpressing HER2 can benefit most from the anti-HER2 targeted therapy. In this study, we investigated the feasibility of detecting HER2 expression in colon cancer by SPECT imaging using I-125-Herceptin, which showed high labeling rate, good in vitro stability and high binding specificity for HER2. HER2-positive mouse colon adenocarcinoma cell line (MC 38) was chosen as the colon caner cell model, and used for the establishment of colon cancer-bearing nude mice model. SPECT/CT imaging suggested that the tumors can be visualized at 12 h after the injection of I-125-Herceptin, and the uptake of tracer in tumors reached the peak at 24 h after injection, and can be attenuated significantly by pretreatment with an excess of nonlabeled Herceptin. These results indicates that I-125-Herceptin can be considered as an effective SPECT probe for the non-invasive detection of HER2 expression in colon cancer. (C) 2018 Elsevier Inc. All rights reserved.
C1 [Pan, Guixia; Li, Danni; Li, Xiao; Peng, Ye; Wang, Tao; Zuo, Changjing] Second Mil Med Univ, Changhai Hosp, Dept Nucl Med, Shanghai 200433, Peoples R China.
C3 Naval Medical University
RP Wang, T; Zuo, CJ (corresponding author), Second Mil Med Univ, Changhai Hosp, Dept Nucl Med, Shanghai 200433, Peoples R China.
EM wangtao2086@smmu.edu.cn; cjzuo@smmu.edu.cn
RI Peng, Ye/JIE-7238-2023
OI Li, Danni/0000-0002-8151-2803; Wang, Tao/0000-0001-8797-9765
FU National Natural Science Foundation of China [81471714, 81701761];
   Staring Foundation for Young Researcher of Changhai Hospital [CH201714];
   Scientific Research Foundation of the Second Military Medical University
   [2012QN15]
FX This work is supported by the National Natural Science Foundation of
   China (Grant No. 81471714, 81701761), the Staring Foundation for Young
   Researcher of Changhai Hospital (Grant No. CH201714) and the Scientific
   Research Foundation of the Second Military Medical University (Grant No.
   2012QN15).
CR Abrahao-Machado LF, 2016, WORLD J GASTROENTERO, V22, P4619, DOI 10.3748/wjg.v22.i19.4619
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NR 22
TC 3
Z9 3
U1 0
U2 12
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 OCT 12
PY 2018
VL 504
IS 4
BP 765
EP 770
DI 10.1016/j.bbrc.2018.08.201
PG 6
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA GX4EU
UT WOS:000447681200023
PM 30217443
DA 2025-01-04
ER

PT J
AU Li, S
   Wang, F
   Zhang, G
   Chou, TF
AF Li, Shan
   Wang, Feng
   Zhang, Gang
   Chou, Tsui-Fen
TI NMS-873 Leads to Dysfunctional Glycometabolism in A p97-Independent
   Manner in HCT116 Colon Cancer Cells
SO PHARMACEUTICS
LA English
DT Article
DE p97 inhibitor; glycometabolism; resistance; protein stability;
   proteomics
ID THERMAL SHIFT ASSAY; INDUCED RESISTANCE; INDOLE INHIBITORS; P97; TARGET;
   COMBINATION; 2-DEOXY-D-GLUCOSE; POLYPHARMACOLOGY; DISRUPTION; METABOLISM
AB Adenosine triphosphate (ATP)-competitive p97 inhibitor CB-5339, the successor of CB-5083, is being evaluated in Phase 1 clinical trials for anti-cancer therapy. Different modes-of-action p97 inhibitors such as allosteric inhibitors are useful to overcome drug-induced resistance, one of the major problems of targeted therapy. We previously demonstrated that allosteric p97 inhibitor NMS-873 can overcome CB-5083-induced resistance in HCT116. Here we employed chemical proteomics and drug-induced thermal proteome changes to identify drug targets, in combination with drug-resistant cell lines to dissect on- and off-target effects. We found that NMS-873 but not CB-5083 affected glycometabolism. By establishing NMS-873-resistant HCT116 cell lines and performing both cell-based and proteomic analysis, we confirmed that NMS-873 dysregulates glycometabolism in a p97-independent manner. We then used proteome integral solubility alteration with a temperature-based method (PISA T) to identify NDUFAF5 as one of the potential targets of NMS-873 in the mitochondrial complex I. We also demonstrated that glycolysis inhibitor 2-DG enhanced the anti-proliferative effect of NMS-873. The polypharmacology of NMS-873 can be advantageous for anti-cancer therapy for colon cancer.
C1 [Li, Shan; Wang, Feng; Zhang, Gang; Chou, Tsui-Fen] CALTECH, Div Biol & Biol Engn, Pasadena, CA 91125 USA.
   [Chou, Tsui-Fen] CALTECH, Proteome Explorat Lab, Beckman Inst, Pasadena, CA 91125 USA.
C3 California Institute of Technology; California Institute of Technology
RP Li, S; Chou, TF (corresponding author), CALTECH, Div Biol & Biol Engn, Pasadena, CA 91125 USA.; Chou, TF (corresponding author), CALTECH, Proteome Explorat Lab, Beckman Inst, Pasadena, CA 91125 USA.
EM lflshan@caltech.edu; fengwang@caltech.edu; gzhang2@caltech.edu;
   tfchou@caltech.edu
OI Chou, Tsui-Fen/0000-0003-2410-2186
FU National Institute of Neurological Disorders and Stroke [R01NS100815,
   R01NS102279]; National Institute on Aging; National Institute of
   Neurological Disorders and Stroke [R01NS102279] Funding Source: NIH
   RePORTER
FX This work was supported in part with funds from the National Institute
   of Neurological Disorders and Stroke, R01NS100815, and R01NS102279.
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NR 62
TC 6
Z9 6
U1 1
U2 20
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD APR
PY 2022
VL 14
IS 4
AR 764
DI 10.3390/pharmaceutics14040764
PG 17
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 0T6GN
UT WOS:000787065100001
PM 35456598
OA gold, Green Accepted, Green Published
DA 2025-01-04
ER

PT J
AU Dawood, S
AF Dawood, Shaheenah
TI The evolving role of immune oncology in colorectal cancer
SO CHINESE CLINICAL ONCOLOGY
LA English
DT Review
DE Colorectal cancer; immunotherapy; immune checkpoint inhibitors;
   microsatellite instability (MSI)
ID TUMOR MICROSATELLITE-INSTABILITY; MISMATCH REPAIR DEFICIENCY; CELL
   BISPECIFIC ANTIBODY; T-CELL; CARCINOEMBRYONIC ANTIGEN; MOLECULAR
   SUBTYPES; CLINICAL ACTIVITY; PD-1 BLOCKADE; SOLID TUMORS; PATIENTS PTS
AB Metastatic colorectal cancer still remains an essentially non curable disease. However, with advances in chemotherapeutic and personalizing therapeutic approaches with the incorporation of targeted therapy such as anti-EGFR and anti-VEGF agents survival associated with metastatic colorectal cancer has certainly improved over the last two decades. Patients who are not amenable to surgery median survival remain approximately 2 to 3 years. In an attempt to improve prognostic outcome over the last decade research has focused on therapeutic options geared towards harnessing the immune system with success observed with the use of immune checkpoint inhibitors in the realm of a number of solid tumors including lung and renal cancer. The use of immunomodulatory therapeutic approaches for the management of unselected advanced colorectal cancer has not seen the same success with low response rates reported. The turning point was our recent understanding that efficacy of immunotherapy was limited to a subset of patients with hyper mutated microsatellite instability-high (MSI-H) tumors. This review will focus on summarizing available knowledge on the immunological and molecular landscape of colorectal cancer that can help determine subsets of immunogenic CRC, determine potential predictive markers to help select patients for immunotherapeutic approaches as well looking at the existing evidence of incorporating immune checkpoint inhibitors to the therapeutic management of patients with mCRC.
C1 [Dawood, Shaheenah] Mediclin City Hosp, Dept Med Oncol, Dubai Hlth Care City, Comprehens Canc Ctr, POB 8179, Dubai, U Arab Emirates.
RP Dawood, S (corresponding author), Mediclin City Hosp, Dept Med Oncol, Dubai Hlth Care City, Comprehens Canc Ctr, POB 8179, Dubai, U Arab Emirates.
EM Shaheenah@post.harvard.edu
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NR 58
TC 9
Z9 11
U1 0
U2 6
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2304-3865
EI 2304-3873
J9 CHIN CLIN ONCOL
JI Chin. Clin. Oncol.
PD APR
PY 2018
VL 7
IS 2
AR 17
DI 10.21037/cco.2018.04.07
PG 10
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA GF0PQ
UT WOS:000431633600006
PM 29764162
DA 2025-01-04
ER

PT J
AU Sad, LM
   Elsaka, AM
   Zamzam, YA
   Khairallah, FG
AF Sad, Lamiss Mohamed
   Elsaka, Ayman Mohamed
   Zamzam, Yomna Abdelmonem
   Khairallah, Fatma Gharib
TI Phase angle, body mass index and KRAS status of metastatic colorectal
   cancer in response to chemotherapy with and without target therapy:
   clinical impact and survival
SO JOURNAL OF BUON
LA English
DT Article
DE phase angle; BIA; BMI; metastatic; colorectal cancer; KRAS
ID MUTATION STATUS; CETUXIMAB
AB Purpose: KRAS mutations are associated with colorectal cancer survival whereas the role of body mass index (BMI) is less defined. Phase angle, which is more an indicator of cell integrity also has not been studied as prognostic and predictive factor. We evaluated the association between BMI, phase angle and colorectal cancer overall survival (OS), by KRAS mutation status and other prognostic for metastatic colorectal cancer.
   Methods: This prospective study included 89 patients diagnosed with metastatic colorectal cancer in oncology and pathology departments. BMI and phase angle alpha were reported from the TANITA MC-780U mutifrequency segmental body composition analyzer at presentation at our department. KRAS mutation status was analyzed. Multivariate analysis was estimated from Cox proportional hazards models.
   Results: High phase angle which indicated proper cell integrity was associated with good performance status, low T stage, low fat percent and high BMI. Overall response was statistically significant with left sided colon cancer and high BMI. On multivariate analysis, the factors maintaining statistical significance with OS were KRAS and overall response. High BMI was associated with higher OS in both mutated and wild groups without statistical significance. As regard progression free survival (PFS), surgery, T stage, and lymphovascular invasion maintained statistical significance on multivariate analysis.
   Conclusion: High phase angle was associated with improved performance status. High BMI was associated with improved OS in all KRAS subgroups.
C1 [Sad, Lamiss Mohamed; Khairallah, Fatma Gharib] Tanta Univ Hosp, Clin Oncol Dept, Tanta, Egypt.
   [Elsaka, Ayman Mohamed; Zamzam, Yomna Abdelmonem] Tanta Univ Hosp, Anat Pathol Dept, Tanta, Egypt.
C3 Egyptian Knowledge Bank (EKB); Tanta University; Egyptian Knowledge Bank
   (EKB); Tanta University
RP Sad, LM (corresponding author), Tanta Univ Hosp, Oncol Dept, 42 Metwaly Elshawray Abrag Afiti, Tanta, Egypt.
EM lamissmohamed2@yahoo.commail
RI sad, Lamiss/AAO-5420-2020
OI Zamzam, Yomna/0000-0003-0270-3140; sad, lamiss/0000-0002-1569-600X
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NR 33
TC 5
Z9 5
U1 1
U2 2
PU IMPRIMATUR PUBLICATIONS
PI ATHENS
PA 30 DEM POLIORKETES ST, ATHENS, 136 76, GREECE
SN 1107-0625
EI 2241-6293
J9 J BUON
JI J. BUON
PD MAR-APR
PY 2020
VL 25
IS 2
BP 914
EP 926
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NE1TJ
UT WOS:000562380000018
PM 32521886
DA 2025-01-04
ER

PT J
AU Nakamura, S
   Fukui, T
   Suzuki, S
   Takeda, H
   Watanabe, K
   Yoshioka, T
AF Nakamura, Sho
   Fukui, Tadahisa
   Suzuki, Shuhei
   Takeda, Hiroyuki
   Watanabe, Kaname
   Yoshioka, Takashi
TI Long-term survival after a favorable response to anti-EGFR antibody plus
   chemotherapy to treat bone marrow metastasis: a case report of
   <i>KRAS</i>-wildtype rectal cancer
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE colorectal cancer; anti-epidermal growth factor receptor antibody;
   molecular targeted therapies; disseminated intravascular coagulation;
   standard of care
ID DISSEMINATED CARCINOMATOSIS
AB Bone marrow metastasis is a rare consequence of colorectal cancer that results in a poor prognosis; few reports describe a favorable response to doublet chemotherapy combined with targeted therapy, which is currently the standard treatment. We experienced a case where anti-epidermal growth factor receptor (EGFR) antibody produced a marked anti-tumor response to bone marrow metastasis that led to long-term survival. A 51-year-old man was diagnosed with a primary KRAS-wildtype rectal cancer with multiple metastases, including the bone marrow. Disease control was achieved for 10.8 months following chemotherapy with a modified FOLFOX6 regimen combined with an anti-EGFR antibody. He died of cancer 22.7 and 16.6 months after disease onset and first-line chemotherapy, respectively. This case shows that early tumor shrinkage and deepness of response to the anti-EGFR antibody were observed even in a patient with bone marrow metastasis. Anti-EGFR antibody therapy should therefore be considered even when a patient's medical condition appears to be poor owing to bone marrow metastasis. Moreover, tumors that are likely to be sensitive to chemotherapy, such as RAS-wildtype colorectal cancers, can be considered for anti-EGFR antibody therapy even if the patient is considered unfit for chemotherapy.
C1 [Nakamura, Sho; Fukui, Tadahisa; Suzuki, Shuhei; Takeda, Hiroyuki; Watanabe, Kaname; Yoshioka, Takashi] Yamagata Univ, Dept Clin Oncol, Fac Med, 2-2-2 Iida Nishi, Yamagata 9909585, Japan.
C3 Yamagata University
RP Yoshioka, T (corresponding author), Yamagata Univ, Dept Clin Oncol, Fac Med, 2-2-2 Iida Nishi, Yamagata 9909585, Japan.
EM ytakashi@med.id.yamagata-u.ac.jp
RI Takeda, Hiroyuki/AAQ-9288-2020; suzuki, shuhei/AAB-9564-2021; Nakamura,
   Sho/O-2107-2014
OI Nakamura, Sho/0000-0002-5378-9477; Watanabe, Kaname/0000-0002-6155-5283
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NR 11
TC 5
Z9 5
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 2017
VL 10
BP 1143
EP 1147
DI 10.2147/OTT.S129275
PG 5
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA EL9BM
UT WOS:000394914100001
PM 28260928
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Iranpour, S
   Bahrami, AR
   Dayyani, M
   Saljooghi, AS
   Matin, MM
AF Iranpour, Sonia
   Bahrami, Ahmad Reza
   Dayyani, Mahdieh
   Saljooghi, Amir Sh.
   Matin, Maryam M.
TI A potent multifunctional ZIF-8 nanoplatform developed for colorectal
   cancer therapy by triple-delivery of chemo/radio/targeted therapy agents
SO JOURNAL OF MATERIALS CHEMISTRY B
LA English
DT Article
ID GRAPHENE QUANTUM DOTS; IMIDAZOLATE FRAMEWORK-8 NANOPARTICLES;
   METAL-ORGANIC FRAMEWORKS; DRUG-DELIVERY; RADIATION-THERAPY; DNA
   APTAMERS; RELEASE; SIZE
AB Background: Multimodal cancer therapy has garnered significant interest due to its ability to target tumor cells from various perspectives. The advancement of novel nano-delivery platforms represents a promising approach for improving treatment effectiveness while minimizing detrimental effects on healthy tissues. Methods: This study aimed to develop a multifunctional nano-delivery system capable of simultaneously delivering an anti-cancer drug, a radiosensitizer agent, and a targeting moiety (three-in-one) for the triple combination therapy of colorectal cancer (CRC). This unique nano-platform, called Apt-PEG-DOX/ZIF-8@GQD, encapsulated both doxorubicin (DOX) and graphene quantum dots (GQDs) within the zeolitic imidazolate framework-8 (ZIF-8). To enhance the safety and anti-cancer potential of the platform, heterobifunctional polyethylene glycol (PEG) and an epithelial cell adhesion molecule (EpCAM) aptamer were conjugated with the system, resulting in the formation of targeted Apt-PEG-DOX/ZIF-8@GQD NPs. The physical and chemical characteristics of Apt-PEG-DOX/ZIF-8@GQD were thoroughly examined, and its therapeutic efficacy was evaluated in combination with radiotherapy (RT) against both EpCAM-positive HT-29 and EpCAM-negative CHO cells. Furthermore, the potential of Apt-PEG-DOX/ZIF-8@GQD as a tumor-specific, radio-enhancing, non-toxic, and controllable delivery system for in vivo cancer treatment was explored using immunocompromised C57BL/6 mice bearing human HT-29 tumors. Results: The large surface area of ZIF-8 (1013 m2 g-1) enabled successful loading of DOX with an encapsulation efficiency of approximately similar to 90%. The synthesis of Apt-PEG-DOX/ZIF-8@GQD resulted in uniform particles with an average diameter of 100 nm. This targeted platform exhibited rapid decomposition under acidic conditions, facilitating an on-demand release of DOX after endosomal escape. In vitro experiments revealed that the biocompatible nano-platform induced selective toxicity in HT-29 cells by enhancing X-ray absorption. Moreover, in vivo experiments demonstrated that the therapeutic efficacy of Apt-PEG-ZIF-8/DOX@GQD against HT-29 tumors was enhanced through the synergistic effects of chemotherapy, radiotherapy, and targeted therapy, with minimal side effects. Conclusion: The combination of Apt-PEG-DOX/ZIF-8@GQD with RT as a multimodal therapy approach demonstrated promising potential for the targeted treatment of CRC and enhancing therapeutic effectiveness. The co-delivery of DOX and GQD using this nano-platform holds great promise for improving the outcome of CRC treatment.
   Background: Multimodal cancer therapy has garnered significant interest due to its ability to target tumor cells from various perspectives.
C1 [Iranpour, Sonia; Bahrami, Ahmad Reza; Matin, Maryam M.] Ferdowsi Univ Mashhad, Fac Sci, Dept Biol, Mashhad, Iran.
   [Bahrami, Ahmad Reza] Ferdowsi Univ Mashhad, Inst Biotechnol, Ind Biotechnol Res Grp, Mashhad, Iran.
   [Dayyani, Mahdieh] Reza Radiotherapy & Oncol Ctr, Radiat Oncol Dept, Mashhad, Iran.
   [Saljooghi, Amir Sh.] Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Iran.
   [Saljooghi, Amir Sh.; Matin, Maryam M.] Ferdowsi Univ Mashhad, Inst Biotechnol, Novel Diagnost & Therapeut Res Grp, Mashhad, Iran.
C3 Ferdowsi University Mashhad; Ferdowsi University Mashhad; Ferdowsi
   University Mashhad; Ferdowsi University Mashhad
RP Matin, MM (corresponding author), Ferdowsi Univ Mashhad, Fac Sci, Dept Biol, Mashhad, Iran.; Saljooghi, AS; Matin, MM (corresponding author), Ferdowsi Univ Mashhad, Inst Biotechnol, Novel Diagnost & Therapeut Res Grp, Mashhad, Iran.
EM saljooghi@um.ac.ir; matin@um.ac.ir
RI Saljooghi, Amir/AAB-6042-2021; M. Matin, Maryam/W-1884-2017
OI M. Matin, Maryam/0000-0002-7949-7712
FU Ferdowsi University of Mashhad [3.51537]; Ferdowsi University of Mashhad
FX The authors would like to thank Mr Khalili-Hezarjaribi, Mr Malaekeh, Dr
   Noroozpour and Dr Shaterzade for their excellent support and technical
   assistance. We are also grateful to the Reza Radiotherapy and Oncology
   Center for their technical help. This work was supported by Ferdowsi
   University of Mashhad, grant number: 3.51537.
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NR 84
TC 9
Z9 9
U1 14
U2 44
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2050-750X
EI 2050-7518
J9 J MATER CHEM B
JI J. Mat. Chem. B
PD JAN 24
PY 2024
VL 12
IS 4
BP 1096
EP 1114
DI 10.1039/d3tb02571c
EA JAN 2024
PG 19
WC Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Materials Science
GA GE3M6
UT WOS:001143087800001
PM 38229578
OA Bronze
DA 2025-01-04
ER

PT J
AU Van den Eynde, M
   Mlecnik, B
   Bindea, G
   Galon, JM
AF Van den Eynde, Marc
   Mlecnik, Bernhard
   Bindea, Gabriela
   Galon, Jerome
TI Multiverse of immune microenvironment in metastatic colorectal cancer
SO ONCOIMMUNOLOGY
LA English
DT Article
DE Immunoscore; colorectal cancer; metastases; tumor microenvironment;
   biopsy; prognosis; chemotherapy; targeted therapy
AB The comprehensive analysis of patients with a complete resection of all metastases reveals the heterogeneity of the colorectal metastatic disease and its clinical impact. Complex tumor immune interrelations shape the metastatic landscape, not only in terms of number and size of lesions, or mutational pattern, but also in terms of immune cell infiltrate. Significantly higher densities of T-cells and lower density of B-cells were quantified in the tumor microenvironment of metastases compared with primary tumors. A high T cell infiltration and Immunoscore measured in the least-infiltrated metastasis were associated with a significantly lower number of metastases, larger metastasis, and prolonged survival while patients with increased metastatic burden had a lower Immunoscore. Immunoscore was evaluated on a biopsy, in a random metastasis or as the mean value of all metastases significantly predicting outcome. However, the most immune-infiltrated metastasis was not significantly predicting outcome, whereas the least immune-infiltrated metastasis was best in predicting clinical outcome. A good likelihood of concordance of Immunoscore was observed between one biopsy and complete metastasis, but the overall intra-metastatic immune infiltrate might be better estimated with multiple biopsies or sampling of larger tumor areas. This intra-metastatic adaptive immune reaction increases following aneoadjuvant treatment containing anti-EGFR monoclonal antibody, an effect that is currently therapeutically evaluated in clinical trials to improve the survival of metastatic patients.
C1 [Van den Eynde, Marc] Univ Catholique Louvain Uclouvain, Inst Roi Albert II, Clin Univ St Luc, Dept Med Oncol & Hepatogastroenterol, Brussels, Belgium.
   [Mlecnik, Bernhard; Bindea, Gabriela; Galon, Jerome] INSERM, Lab Integrat Canc Immunol, Paris, France.
   [Mlecnik, Bernhard; Bindea, Gabriela; Galon, Jerome] Equipe Labellisee Ligue Le Canc, Paris, France.
   [Mlecnik, Bernhard; Bindea, Gabriela; Galon, Jerome] Univ Paris, Sorbonne Univ, Ctr Rech Cordeliers, Paris, France.
   [Mlecnik, Bernhard] Inovarion, Paris, France.
C3 Universite Catholique Louvain; Cliniques Universitaires Saint-Luc;
   Institut National de la Sante et de la Recherche Medicale (Inserm);
   Institut National de la Sante et de la Recherche Medicale (Inserm);
   Universite Paris Cite; Sorbonne Universite
RP Galon, JM (corresponding author), INSERM, Lab Integrat Canc Immunol, Cordeliers Res Ctr, F-75006 Paris, France.
EM jerome.galon@crc.jussieu.fr
RI mlecnik, bernhard/AAT-7467-2021
FU INSERM; LabEx Immuno-oncology; Transcan ERAnet European project; Society
   for Immunotherapy of Cancer (SITC); Association pour la Recherche contre
   le Cancer (ARC); CARPEM; AP-HP; HalioDx; Institut National du Cancer,
   France (INCa). [UMRS1138]; Qatar National Research Fund (QNRF)
   [NPRP11S-0121-180351]
FX This work was supported by the INSERM, LabEx Immuno-oncology, Transcan
   ERAnet European project, Society for Immunotherapy of Cancer (SITC),
   Association pour la Recherche contre le Cancer (ARC), CARPEM, AP-HP,
   HalioDx, and Institut National du Cancer, France (INCa). [UMRS1138];
   Qatar National Research Fund (QNRF) [NPRP11S-0121-180351].
CR Angell HK, 2020, CLIN CANCER RES, V26, P332, DOI 10.1158/1078-0432.CCR-18-1851
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NR 15
TC 10
Z9 10
U1 1
U2 2
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 2162-402X
J9 ONCOIMMUNOLOGY
JI OncoImmunology
PY 2020
VL 9
IS 1
AR 1824316
DI 10.1080/2162402X.2020.1824316
PG 3
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA NY5WN
UT WOS:000576459500001
PM 33457100
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Fiori, E
   Crocetti, D
   Lamazza, A
   De Felice, F
   Tarallo, M
   Sterpetti, AV
   Mingoli, A
   Sapienza, P
   De Toma, G
AF Fiori, Enrico
   Crocetti, Daniele
   Lamazza, Antonietta
   De Felice, Francesca
   Tarallo, Mariarita
   Sterpetti, Antonio V.
   Mingoli, Andrea
   Sapienza, Paolo
   De Toma, Giorgio
TI Resection or Stenting in the Treatment of Symptomatic Advanced
   Metastatic Rectal Cancer: A Dilemma
SO ANTICANCER RESEARCH
LA English
DT Article
DE Rectal cancer; targeted therapy; stent positioning
ID IV COLORECTAL-CANCER; OXALIPLATIN-BASED CHEMOTHERAPY; PRIMARY TUMOR
   RESECTION; COMBINATION CHEMOTHERAPY; PLUS BEVACIZUMAB; POOLED ANALYSIS;
   COLON-CANCER; SURGERY; STATISTICS; PLACEMENT
AB Background/Aim: Patients affected with Stage IV colorectal cancer and unresectable metastases represent a heterogeneous group. Resection of the primary tumor or stent positioning followed by chemotherapy and/or targeted therapies still represent a difficult choice for surgeons. Patients and Methods: From February 2013 to September 2019, 46 patients were enrolled into a prospective randomized open label parallel trial presenting with Stage IVA and IVB rectal cancer, unresectable metastases and symptoms of subacute large bowel obstruction. Our population was divided into two groups: Group 1 included 20 patients who underwent placement of a self-expandable metal stent and Group 2 included 26 patients in whom primary tumor resection was performed. Results: One-year actuarial survival rate of Group 1 was significantly lower compared to Group 2. Overall 17 patients had survival longer than 1-year (3 in Group 1 and 14 in Group 2). Cox regression analysis showed that endoscopic stent positioning and the suspension of the chemotherapy because of deterioration of liver function tests were the two most important factors negatively influencing survival. Conclusion: Patients affected with stage IVA and IVB rectal cancer and symptoms of bowel obstruction had a significant longer survival rate when submitted to surgical rectal resection followed by chemotherapy.
C1 [Fiori, Enrico; Crocetti, Daniele; Lamazza, Antonietta; Tarallo, Mariarita; Sterpetti, Antonio V.; Mingoli, Andrea; Sapienza, Paolo; De Toma, Giorgio] Sapienza Univ Rome, Dept Surg Pietro Valdoni, Viale Policlin 155, I-00166 Rome, Italy.
   [De Felice, Francesca] Sapienza Univ Rome, Dept Radiol Radiotherapy Oncol & Anatomopathol, Rome, Italy.
C3 Sapienza University Rome; Sapienza University Rome
RP Crocetti, D (corresponding author), Sapienza Univ Rome, Dept Surg Pietro Valdoni, Viale Policlin 155, I-00166 Rome, Italy.
EM danielecrocetti@hotmail.it
RI Mingoli, Andrea/A-2889-2010; Crocetti, Daniele/G-8694-2014; Sapienza,
   Paolo/AAL-7381-2020; De Felice, Francesca/I-2075-2017
OI Tarallo, Mariarita/0000-0003-3783-4749; De Felice,
   Francesca/0000-0002-5119-8358; Crocetti, Daniele/0000-0001-9950-3553;
   Sapienza, Paolo/0000-0002-0198-7930
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NR 41
TC 5
Z9 6
U1 0
U2 1
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD DEC
PY 2019
VL 39
IS 12
BP 6781
EP 6786
DI 10.21873/anticanres.13893
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KY7AG
UT WOS:000522725300038
PM 31810943
OA Bronze, Green Submitted
DA 2025-01-04
ER

PT J
AU Dörk, T
   Hillemanns, P
   Tempfer, C
   Breu, J
   Fleisch, MC
AF Dork, Thilo
   Hillemanns, Peter
   Tempfer, Clemens
   Breu, Julius
   Fleisch, Markus C.
TI Genetic Susceptibility to Endometrial Cancer: Risk Factors and Clinical
   Management
SO CANCERS
LA English
DT Review
DE endometrium; carcinoma; genetics; Lynch syndrome; Cowden syndrome;
   targeted therapy
ID NONPOLYPOSIS COLORECTAL-CANCER; GENOME-WIDE ASSOCIATION; DNA MISMATCH
   REPAIR; BODY-MASS INDEX; LYNCH SYNDROME IMPLICATIONS; PROTEIN
   EXPRESSION; FAMILY-HISTORY; GERMLINE MUTATIONS; BRCA2 MUTATIONS; COWDEN
   SYNDROME
AB Endometrial cancer (EC) is the most common cancer affecting the female reproductive organs in higher-income states. Apart from reproductive factors and excess weight, genetic predisposition is increasingly recognized as a major factor in endometrial cancer risk. Endometrial cancer is genetically heterogeneous: while a subgroup of patients belongs to cancer predisposition syndromes (most notably the Lynch Syndrome) with high to intermediate lifetime risks, there are also several common genomic polymorphisms contributing to the spectrum of germline predispositions. Germline variants and somatic events may act in concert to modulate the molecular evolution of the tumor, where mismatch-repair deficiency is common in endometrioid endometrial tumors whereas homologous recombinational repair deficiency has been described for non-endometrioid endometrial tumors. In this review, we will survey the currently known genomic predispositions for endometrial cancer and discuss their relevance for clinical management in terms of counseling, screening and novel treatments.
C1 [Dork, Thilo; Hillemanns, Peter] Hannover Med Sch, Ctr Comprehens Canc, Dept Gynecol & Obstet, D-30625 Hannover, Germany.
   [Tempfer, Clemens] Ruhr Univ Bochum, Marien Hosp, Dept Gynaecol, D-44625 Herne, Germany.
   [Breu, Julius; Fleisch, Markus C.] Univ Witten Herdecke, Dept Gynecol & Obstet, D-42283 Wuppertal, Germany.
C3 Hannover Medical School; St. Marien Hospital; Ruhr University Bochum;
   Witten Herdecke University
RP Dörk, T (corresponding author), Hannover Med Sch, Ctr Comprehens Canc, Dept Gynecol & Obstet, D-30625 Hannover, Germany.
EM doerk.thilo@mh-hannover.de; hillemanns.peter@mh-hannover.de;
   Clemens.Tempfer@elisabethgruppe.de; Julius.Breu@helios-gesundheit.de;
   Markus.Fleisch@helios-gesundheit.de
RI Fleisch, Markus/E-4134-2014; Dork, Thilo/J-8620-2012
OI Hillemanns, Peter/0000-0001-9829-3531; Tempfer,
   Clemens/0000-0002-6904-3258; Dork, Thilo/0000-0002-9458-0282
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NR 129
TC 37
Z9 38
U1 2
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD SEP
PY 2020
VL 12
IS 9
AR 2407
DI 10.3390/cancers12092407
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OG6XQ
UT WOS:000582024900001
PM 32854222
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Seo, HI
   Kim, DI
   Chung, Y
   Choi, CI
   Kim, M
   Yun, S
   Kim, S
   Park, DY
AF Seo, Hyung-Il
   Kim, Dong-Il
   Chung, Youngsoo
   Choi, Chang In
   Kim, Minjoo
   Yun, Sungpil
   Kim, Suk
   Park, Do Youn
TI Multimodal treatments of right gastroepiploic arterial leiomyosarcoma
   with hepatic metastasis: A case report and review of the literature
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Review
DE Multimodal treatments; Intra-abdominal arterial leiomyosarcoma; Hepatic
   metastasis; Arterial leiomyosarcoma; Surgical resection
ID COMMON ILIAC ARTERY
AB Leiomyosarcoma of an artery is very rare, and cases with hepatic metastasis are even rarer. We describe a case of a 70-year-old man who after follow up due to rectal cancer, presented with an intra-abdominal hypervascular mass and a hepatic mass. After surgical resection, it was diagnosed as a leiomyosarcoma of the right gastroepiploic artery with hepatic metastasis. Multiple metastases had recurred at the liver. He has survived more than 53 mo through multimodal treatments (three surgical resections, radiofrequency ablation, transarterial chemoembolization, chemotherapies, and targeted therapy). Multimodal treatments, including active surgical resection, may be helpful in the treatment of aggressive diseases such as arterial leiomyosarcoma with metastasis.
C1 [Seo, Hyung-Il; Chung, Youngsoo; Choi, Chang In; Kim, Minjoo] Pusan Natl Univ Hosp, Biomed Res Inst, Dept Surg, Busan 49241, South Korea.
   [Kim, Dong-Il] Pusan Natl Univ, Yangsan Hosp, Dept Surg, 20 Geumo Ro, Yangsan 50612, Gyeongsangnam D, South Korea.
   [Yun, Sungpil] Dept Surg, Busan 49241, South Korea.
   [Kim, Suk] Pusan Natl Univ Hosp, Biomed Res Inst, Dept Radiol, Busan 49241, South Korea.
   [Park, Do Youn] Pusan Natl Univ Hosp, Biomed Res Inst, Dept Pathol, Busan 49241, South Korea.
C3 Pusan National University; Pusan National University Hospital; Pusan
   National University; Pusan National University Hospital; Pusan National
   University; Pusan National University Hospital; Pusan National
   University; Pusan National University Hospital
RP Kim, DI (corresponding author), Pusan Natl Univ, Yangsan Hosp, Dept Surg, 20 Geumo Ro, Yangsan 50612, Gyeongsangnam D, South Korea.
EM led117@naver.com
RI Choi, Chang/ABH-6588-2020
CR BIRKENSTOCK WE, 1976, BRIT J SURG, V63, P81, DOI 10.1002/bjs.1800630119
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NR 11
TC 1
Z9 1
U1 0
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD AUG 16
PY 2018
VL 6
IS 8
BP 219
EP 223
DI 10.12998/wjcc.v6.i8.219
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA GQ6HC
UT WOS:000441806500009
PM 30148151
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Magadhi, M
   Panigrahi, R
   Rath, J
AF Magadhi, Malvika
   Panigrahi, Ranjita
   Rath, Jayasree
TI Stromal Expression of CD10 in Colorectal Carcinoma and its Correlation
   with Lymph Node Metastasis and Other Prognostic Factors
SO JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH
LA English
DT Article
DE Adenocarcinomas; Adenomas; Stromal CD10; Tissue microarray
ID MATRIX METALLOPROTEINASES MMPS; INVASION; CELLS
AB Introduction: Colorectal Carcinoma (CRC) is an important public health problem. The study has been one of the main pre-occupation for researchers worldwide and continuous research is going on to find out methods for the early detection, control and drugs for targeted therapy to improve the survival rate.
   Aim: To study the expression of stromal CD10 (sCD10) in colorectal neoplasia and to find out if there is any significant difference between sCD10 expression in adenomas versus carcinoma and association of sCD10 expression with age, tumour grade, depth of invasion and nodal status in CRC.
   Materials and Methods: The present study was a prospective and retrospective observational study conducted in the Department of Pathology, Kalinga Institute of Medical Sciences, Bhubaneswar, Odisha, India, from August 2014 to July 2016. Expression of sCD10 in 71 cases including adenomas (12 cases) and adenocarcinomas (59 cases) were studied. Five tissues from proximal margin were included in the tissue microarray to study the pattern of sCD10 expression in the normal areas.
   Results: The age of patients ranged from 19-74 years with a male to female ratio of 1.62: 1. The stromal expression of CD10 did not show any statistically significant association with any specific age group. In the present study, low grade adenoma was found to be negative for sCD10 but 50% (4/8) cases of high grade adenoma were positive for sCD10 expression. However, the values were not statistically significant. Of the total cases of CRC, 50.85% (30/59) cases showed no expression of sCD10 whereas 49.15% (29/59) cases were positive for sCD10 expression. Evaluation of sCD10 and lymph node status showed that 44.12% (15/34) node negative cases were sCD10 positive where as only 40.00% (10/25) node positive cases were sCD10 positive and these values were not statistically significant.
   Conclusion: In different grades of CRC sCD10 positivity did not show any statistically significant correlation, but the sCD10 expression was found to be increased with increased depth of tumour.
C1 [Magadhi, Malvika] KIMS, Dept Pathol, Bhubaneswar, Odisha, India.
   [Magadhi, Malvika] Inst Neurosci, Dept Pathol, Kolkata, W Bengal, India.
   [Panigrahi, Ranjita; Rath, Jayasree] Kalinga Inst Med Sci, Dept Pathol, Bhubaneswar, Odisha, India.
C3 Kalinga Institute of Industrial Technology (KIIT); Kalinga Institute of
   Industrial Technology (KIIT)
RP Panigrahi, R (corresponding author), Kalinga Inst Med Sci, Kushabhadra Campus 5, Bhubaneswar 751024, Odisha, India.
EM ranjita_panigrahi@yahoo.com
CR [Anonymous], 2010, WHO CLASSIFICATION T
   Bernescu I, 2016, DIS COLON RECTUM, V59, P22, DOI 10.1097/DCR.0000000000000651
   Choi CH, 2012, KOREAN J PATHOL, V46, P562, DOI 10.4132/KoreanJPathol.2012.46.6.562
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NR 18
TC 1
Z9 1
U1 0
U2 1
PU PREMCHAND SHANTIDEVI RESEARCH FOUNDATION
PI DELHI
PA 71 JAIN COLONY, VEER NAGAR, DELHI, 110 007, INDIA
SN 2249-782X
EI 0973-709X
J9 J CLIN DIAGN RES
JI J. Clin. Diagn. Res.
PD FEB
PY 2019
VL 13
IS 2
DI 10.7860/JCDR/2019/37679.12560
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA HO0CV
UT WOS:000460569000011
OA gold
DA 2025-01-04
ER

PT J
AU Cohen, R
   Raeisi, M
   Chibaudel, B
   Shi, Q
   Yoshino, T
   Zalcberg, JR
   Adams, R
   Cremolini, C
   Van Cutsem, E
   Heinemann, V
   Tabernero, J
   Punt, CJA
   Arnold, D
   Hurwitz, HI
   Douillard, JY
   Venook, AP
   Saltz, LB
   Maughan, TS
   Kabbinavar, F
   Bokemeyer, C
   Grothey, A
   Mayer, RJ
   Kaplan, R
   Tebbutt, NC
   Hecht, JR
   Giantonio, BJ
   Díaz-Rubio, E
   Sobrero, AF
   Peeters, M
   Koopman, M
   Goldberg, RM
   Andre, T
   de Gramont, A
AF Cohen, Romain
   Raeisi, Morteza
   Chibaudel, Benoist
   Shi, Qian
   Yoshino, Takayuki
   Zalcberg, John R.
   Adams, Richard
   Cremolini, Chiara
   Van Cutsem, Eric
   Heinemann, Volker
   Tabernero, Josep
   Punt, Cornelis J. A.
   Arnold, Dirk
   Hurwitz, Herbert I.
   Douillard, Jean-Yves
   Venook, Alan P.
   Saltz, Leonard B.
   Maughan, Timothy S.
   Kabbinavar, Fairooz
   Bokemeyer, Carsten
   Grothey, Axel
   Mayer, Robert J.
   Kaplan, Richard
   Tebbutt, Niall C.
   Hecht, J. Randolph
   Giantonio, Bruce J.
   Diaz-Rubio, Eduardo
   Sobrero, Alberto F.
   Peeters, Marc
   Koopman, Miriam
   Goldberg, Richard M.
   Andre, Thierry
   de Gramont, Aimery
TI Prognostic value of liver metastases in colorectal cancer treated by
   systemic therapy: An ARCAD pooled analysis
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Liver metastatic colorectal cancer; Prognostic value; Chemotherapy;
   Targeted therapy
ID RANDOMIZED PHASE-III; FOLFIRI PLUS BEVACIZUMAB; 1ST-LINE TREATMENT;
   PERITONEAL CARCINOMATOSIS; HEPATIC RESECTION; OPEN-LABEL; CHEMOTHERAPY;
   OXALIPLATIN; CETUXIMAB; FLUOROURACIL
AB Background: The liver is the most frequent site of metastases in colorectal cancer (CRC). This study aimed to assess the response rate and survival outcomes in metastatic CRC patients with non-liver metastases (NLM) compared to those with liver metastases (LM) across different lines of treatment. Methods: A total of 17,924 mCRC patients included in 26 trials from the ARCAD CRC database were analyzed. The analysis was conducted based on the presence or absence of LM across different treatment groups: chemotherapy (CT) alone, CT + anti-VEGF, CT + anti-EGFR in KRAS wild-type tumors, within the first-line (1 L) and second-line (2 L), and patients enrolled in third-line (>= 3 >= 3 L) trials treated with trifluridine/tipiracil or regorafenib or placebo. The endpoints were overall survival (OS), progression-free survival (PFS), and overall response rate (ORR). Results: Out of the 17,924 patients, 14,066 had LM (30.6 % with only liver involvement and 69.4 % with liver and other metastatic sites), while 3858 patients had NLM. In the CT alone and CT + anti-VEGF subgroups, NLM patients showed better OS and PFS in the 1 L and 2 L settings. However, in the CT + anti-EGFR 1 L and 2 L subgroups, there was no significant difference in OS and PFS between NLM and LM patients. In the >= 3 L subgroups, better OS and PFS were observed in NLM patients. ORRs were higher in LM patients than in NLM patients across all cohorts treated in the 1 L and only in the anti-EGFR cohort in the 2 L. Conclusion: LM is a poor prognostic factor for mCRC increasing from 1 L to >= 3 L except for patients in 1 L and 2 L receiving CT+anti-EGFR. +anti-EGFR. These data justify using LM as a stratification factor in future trials for patients with unresectable mCRC.
C1 [Cohen, Romain; Andre, Thierry] Sorbonne Univ, Hop St Antoine, AP HP, Dept Med Oncol, Paris, France.
   [Cohen, Romain; Andre, Thierry] Ctr Rech St Antoine, Equipe Instabil Microsatell & Canc, Equipe Labellisee Ligue Natl Canc, SIRIC CURAMUS,INSERM,UMRS 938, Paris, France.
   [Raeisi, Morteza] ARCAD Fdn, Stat Unit, 45 Rue Croulebarbe, F-75013 Paris, France.
   [Chibaudel, Benoist] Franco British Hosp, Dept Med Oncol, Fdn Cognacq Jay, Levallois Perret, France.
   [Shi, Qian] Mayo Clin, Dept Quantitat Hlth Sci, Rochester, MN USA.
   [Yoshino, Takayuki] Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa, Chiba, Japan.
   [Zalcberg, John R.] Monash Univ, Sch Publ Hlth & Prevent Med, Melbourne, Vic, Australia.
   [Zalcberg, John R.] Alfred Hlth, Dept Med Oncol, Melbourne, Vic, Australia.
   [Adams, Richard] Cardiff Univ, Cardiff, Wales.
   [Adams, Richard] Velindre Canc Ctr, Cardiff, Wales.
   [Cremolini, Chiara] Univ Pisa, Dept Translat Res & New Technol, Pisa, Italy.
   [Van Cutsem, Eric] Univ Hosp Leuven, Dept Gastrointestinal & Liver Dis, Digest Oncol Unit, Leuven, Belgium.
   [Van Cutsem, Eric] Katholieke Univ Leuven, Leuven, Belgium.
   [Heinemann, Volker] Univ Munich, LMU Hosp, Dept Med Oncol, Munich, Germany.
   [Tabernero, Josep] Vall dHebron Univ Hosp, Barcelona, Spain.
   [Tabernero, Josep] Vall dHebron Inst Oncol VHIO, IOB Quiron, Barcelona, Spain.
   [Punt, Cornelis J. A.; Koopman, Miriam] Univ Med Ctr Utrecht, Utrecht, Netherlands.
   [Arnold, Dirk] Asklepios Klin Altona, Asklepios Tumorzentrum Hamburg, Hamburg, Germany.
   [Hurwitz, Herbert I.] Duke Univ, Durham, NC USA.
   [Douillard, Jean-Yves] Integrated Ctr Oncol Nantes, Med Oncol Dept, Nantes, France.
   [Venook, Alan P.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
   [Saltz, Leonard B.] Mem Sloan Kettering Canc Ctr, New York, NY USA.
   [Maughan, Timothy S.] Univ Liverpool, Liverpool, Merseyside, England.
   [Kabbinavar, Fairooz] Cardiff Oncol, San Diego, CA USA.
   [Bokemeyer, Carsten] Univ Med Ctr Hamburg Eppendorf, Dept Oncol & Hematol, Hamburg, Germany.
   [Grothey, Axel] West Canc Ctr, Germantown, TN USA.
   [Mayer, Robert J.] Dana Farber Canc Inst, Boston, MA USA.
   [Kaplan, Richard] MRC Clin Trials Unit UCL, London, England.
   [Tebbutt, Niall C.] Austin Hlth, Wellness & Res Ctr, Dept Med Oncol, Olivia Newton John Canc, Heidelberg, Vic, Australia.
   [Hecht, J. Randolph] Univ Calif Angeles, David Geffen Sch Med, Los Angeles, CA USA.
   [Giantonio, Bruce J.] Massachusetts Gen Hosp, Boston, MA USA.
   [Diaz-Rubio, Eduardo] Hosp Clin San Carlos, Madrid 28040, Spain.
   [Sobrero, Alberto F.] Osped San Martino Genova, Dept Med Oncol, Genoa, Italy.
   [Peeters, Marc] Univ Hosp Ghent, Ghent, Belgium.
   [Goldberg, Richard M.] West Virginia Univ, Dept Med, Canc Inst, Morgantown, WV USA.
   [Andre, Thierry; de Gramont, Aimery] ARCAD Fdn, Paris, France.
   [de Gramont, Aimery] Franco British Hosp, Dept Med Oncol, Levallois Perret, France.
C3 Assistance Publique Hopitaux Paris (APHP); Sorbonne Universite; Hopital
   Universitaire Saint-Antoine - APHP; Sorbonne Universite; Institut
   National de la Sante et de la Recherche Medicale (Inserm); Mayo Clinic;
   National Cancer Center - Japan; Monash University; Cardiff University;
   Velindre Cancer Centre; University of Pisa; KU Leuven; University
   Hospital Leuven; KU Leuven; University of Munich; Hospital Universitari
   Vall d'Hebron; Vall d'Hebron Institut d'Oncologia (VHIO); Utrecht
   University; Utrecht University Medical Center; Asklepios Klinik Altona;
   Duke University; University of California System; University of
   California San Francisco; Memorial Sloan Kettering Cancer Center;
   University of Liverpool; University of Hamburg; University Medical
   Center Hamburg-Eppendorf; Harvard University; Dana-Farber Cancer
   Institute; Medical Research Council Clinical Trials Unit; Austin
   Research Institute; Florey Institute of Neuroscience & Mental Health;
   University of California System; University of California Los Angeles;
   University of California Los Angeles Medical Center; David Geffen School
   of Medicine at UCLA; Harvard University; Massachusetts General Hospital;
   Hospital Clinico San Carlos; University of Genoa; IRCCS AOU San Martino
   IST; Ghent University; Ghent University Hospital; West Virginia
   University
RP Raeisi, M (corresponding author), ARCAD Fdn, Stat Unit, 45 Rue Croulebarbe, F-75013 Paris, France.
EM morteza.raeisi@fondationarcad.org
RI Raeisi, Morteza/KOC-0922-2024; Cremolini, Chiara/AAC-1889-2019
OI Raeisi, Morteza/0000-0002-9999-4097
FU ARCAD Foundation
FX This work was supported by ARCAD Foundation (no grant number).
   Independently of this work, the ARCAD Foundation received donation in
   the 3 past years from Bristol Myers Squibb, Sanofi, AstraZeneca and
   dotation funds.
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NR 41
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD AUG
PY 2024
VL 207
AR 114160
DI 10.1016/j.ejca.2024.114160
EA JUN 2024
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA J0T6N
UT WOS:001334286300001
PM 38896997
DA 2025-01-04
ER

PT J
AU Murphy, AG
   Casey, R
   Maguire, A
   Tosetto, M
   Butler, CT
   Conroy, E
   Reynolds, AL
   Sheahan, K
   O'Donoghue, D
   Gallagher, WM
   Fennelly, D
   Kennedy, BN
   O'Sullivan, J
AF Murphy, Adrian G.
   Casey, Rory
   Maguire, Aoife
   Tosetto, Miriam
   Butler, Clare T.
   Conroy, Emer
   Reynolds, Alison L.
   Sheahan, Kieran
   O'Donoghue, Diarmuid
   Gallagher, William M.
   Fennelly, David
   Kennedy, Breandan N.
   O'Sullivan, Jacintha
TI Preclinical validation of the small molecule drug quininib as a novel
   therapeutic for colorectal cancer
SO SCIENTIFIC REPORTS
LA English
DT Article
ID IN-VIVO; ANTIANGIOGENIC COMPOUNDS; ANTITUMOR-ACTIVITY; TARGETED THERAPY;
   BEVACIZUMAB; ANGIOGENESIS; ZEBRAFISH; GROWTH; CAPECITABINE; FLUOROURACIL
AB Colorectal cancer (CRC) is a leading cause of cancer deaths. Molecularly targeted therapies (e.g. bevacizumab) have improved survival rates but drug resistance ultimately develops and newer therapies are required. We identified quininib as a small molecule drug with anti-angiogenic activity using in vitro, ex vivo and in vivo screening models. Quininib (2-[(E)-2-(Quinolin-2-yl)vinyl] phenol), is a small molecule drug (molecular weight 283.75 g/mol), which significantly inhibited blood vessel development in zebrafish embryos (p < 0.001). In vitro, quininib reduced endothelial tubule formation (p < 0.001), cell migration was unaffected by quininib and cell survival was reduced by quininib ( p < 0.001). Using ex vivo human CRC explants, quininib significantly reduced the secretions of IL-6, IL-8, VEGF, ENA-78, GRO-alpha, TNF, IL-1 beta and MCP-1 ex vivo (all values p < 0.01). Quininib is well tolerated in mice when administered at 50 mg/kg intraperitoneally every 3 days and significantly reduced tumour growth of HT-29-luc2 CRC tumour xenografts compared to vehicle control. In addition, quininib reduced the signal from a alpha(V)beta(3) integrin fluorescence probe in tumours 10 days after treatment initiation, indicative of angiogenic inhibition. Furthermore, quininib reduced the expression of angiogenic genes in xenografted tumours. Collectively, these findings support further development of quininib as a novel therapeutic agent for CRC.
C1 [Murphy, Adrian G.; Tosetto, Miriam; Sheahan, Kieran; O'Donoghue, Diarmuid; Fennelly, David] St Vincents Univ Hosp, Ctr Colorectal Dis, Elm Pk, Dublin 4, Ireland.
   [Murphy, Adrian G.; Butler, Clare T.; Conroy, Emer; Reynolds, Alison L.; Gallagher, William M.; Kennedy, Breandan N.] Univ Coll Dublin, UCD Sch Biomol, Dublin 4, Ireland.
   [Murphy, Adrian G.; Butler, Clare T.; Conroy, Emer; Reynolds, Alison L.; Gallagher, William M.; Kennedy, Breandan N.] Univ Coll Dublin, Biomed Sci Conway Inst, Dublin 4, Ireland.
   [Casey, Rory; O'Sullivan, Jacintha] Trinity Coll Dublin, Trinity Translat Med Inst, St Jamess Hosp, Dept Surg, Dublin 8, Ireland.
   [Maguire, Aoife] St James Hosp, Dept Histopathol, Dublin 8, Ireland.
C3 University College Dublin; Saint Vincent's University Hospital;
   University College Dublin; University College Dublin; Trinity College
   Dublin; Trinity College Dublin
RP O'Sullivan, J (corresponding author), Trinity Coll Dublin, Trinity Translat Med Inst, St Jamess Hosp, Dept Surg, Dublin 8, Ireland.
EM osullij4@tcd.ie
RI kennedy, Breandan/H-5643-2019; Conroy, Emer/T-2878-2019; Reynolds,
   Alison/KOZ-8938-2024
OI O'Sullivan, Jacintha/0000-0001-8622-9858; Gallagher,
   William/0000-0002-4307-5999; Conroy, Emer/0000-0002-6158-229X; Reynolds,
   Alison/0000-0002-3147-0094; Kennedy, Breandan/0000-0001-7991-4689;
   Maguire, Aoife/0000-0002-9120-6383
FU Newman Fellowship from the University College Dublin Newman Foundation;
   Science Foundation Ireland TIDA grant [11/TIDA/B1966]; Science
   Foundation Ireland (SFI) [11/TIDA/B1966] Funding Source: Science
   Foundation Ireland (SFI)
FX Adrian Murphy was funded by a Newman Fellowship from the University
   College Dublin Newman Foundation to conduct this work. This work was
   also funded by a Science Foundation Ireland TIDA grant 11/TIDA/B1966.
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NR 53
TC 14
Z9 14
U1 0
U2 12
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD OCT 14
PY 2016
VL 6
AR 34523
DI 10.1038/srep34523
PG 10
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA DY7FE
UT WOS:000385294200001
PM 27739445
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Chen, TW
   Zhang, XL
   Ding, XF
   Feng, J
   Zhang, XL
   Xie, D
   Wang, X
AF Chen, Tianwei
   Zhang, Xilin
   Ding, Xufen
   Feng, Jing
   Zhang, Xueli
   Xie, Dong
   Wang, Xiang
TI Ryanodine receptor 2 promotes colorectal cancer metastasis by the
   ROS/<i>BACH1</i> axis
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE colorectal cancer; metastasis; ROS; RyR2
ID CALCIUM; CA2+
AB There is no targeted therapy for KRAS proto-oncogene, GTPase (KRAS)-mutant metastatic colorectal cancer (mCRC) because the underlying mechanism remains obscure. Based on bioinformatic analysis, this study aims to elucidate a potential gene target for which an approved drug is available, and to reveal the function as well as the underlying mechanism of the candidate gene. Here, we identified that ryanodine receptor 2 (RyR2) expression was upregulated in KRAS-mutant mCRC, and that this promoted cancer cell metastasis. S107, an approved drug to inhibit calcium release from RyR2 in the clinic, inhibited cancer cell metastasis both in vitro and in vivo. High expression of RyR2 predicts poor survival in our patient cohort. CRC patients with serosa invasion and vascular tumor thrombus are characterized by high RyR2 expression. Analysis of expression profiles upon RyR2 knockdown and inhibition, revealed a set of metastasis-related molecules, and identified BTB domain and CNC homolog 1 (BACH1) as the main transcription factor regulated by RyR2. RyR2 regulates cellular reactive oxygen species (ROS) levels, which activates nuclear factor erythroid 2-related factor 2 (Nrf2; also known as NFE2L2) and HMOX1 expression, and thus BACH1 accumulation. Collectively, this study provides evidence that the RyR2/ROS/BACH1 axis may be a potential intervention target for CRC metastasis.
C1 [Chen, Tianwei; Wang, Xiang] Zhejiang Univ, Affiliated Hangzhou Peoples Hosp 1, Dept Hepatobiliary & Pancreat Surg, Key Lab Integrated Oncol & Intelligent Med Zhejian, Hangzhou, Peoples R China.
   [Zhang, Xilin] Huzhou Univ, Affiliated Hosp 1, Dept Cent Lab, Huzhou, Peoples R China.
   [Ding, Xufen; Xie, Dong] Shanghai Inst Nutr & Hlth, Shanghai Inst Biol Sci, Chinese Acad Sci, CAS Key Lab Nutr Metab & Food Safety, Shanghai, Peoples R China.
   [Feng, Jing; Zhang, Xueli] Southern Med Univ, Fengxian Hosp, Dept Gen Surg, 6600 Nanfeng Rd, Shanghai 201499, Peoples R China.
   [Wang, Xiang] Zhejiang Univ, Affiliated Hangzhou Peoples Hosp 1, Ctr Integrated Oncol & Precis Med, Sch Med, Hangzhou 310006, Peoples R China.
   [Xie, Dong] Chinese Acad Sci, Inst Nutr Sci, Shanghai Inst Biol Sci, Lab Mol Oncol, 320 Yue Yang Rd, Shanghai 200031, Peoples R China.
C3 Zhejiang University; Huzhou University; Chinese Academy of Sciences;
   Shanghai Institute of Nutrition & Health, CAS; Southern Medical
   University - China; Zhejiang University; Chinese Academy of Sciences
RP Zhang, XL (corresponding author), Southern Med Univ, Fengxian Hosp, Dept Gen Surg, 6600 Nanfeng Rd, Shanghai 201499, Peoples R China.; Wang, X (corresponding author), Zhejiang Univ, Affiliated Hangzhou Peoples Hosp 1, Ctr Integrated Oncol & Precis Med, Sch Med, Hangzhou 310006, Peoples R China.; Xie, D (corresponding author), Chinese Acad Sci, Inst Nutr Sci, Shanghai Inst Biol Sci, Lab Mol Oncol, 320 Yue Yang Rd, Shanghai 200031, Peoples R China.
EM zhangxl2017@smu.edu.cn; dxie@sibs.ac.cn; wangxiang2021@zju.edu.cn
RI ding, xufen/A-6161-2019
OI Wang, Xiang/0000-0003-0440-6203
FU National Natural Science Foundation of China [81970570, 82003076,
   81870377, 82172361]; China Postdoctoral Science Foundation; Shanghai
   Super Postdoctoral Program; Huzhou Science and Technology Fund
   [2018GY04]; Special Research Assistant of Chinese Academy of Sciences
FX This work was supported by National Natural Science Foundation of China
   (81970570, 82003076, 81870377, 82172361), China Postdoctoral Science
   Foundation, Shanghai Super Postdoctoral Program and Special Research
   Assistant of Chinese Academy of Sciences, Huzhou Science and Technology
   Fund under grant no. 2018GY04.
CR Atakpa P, 2018, CELL REP, V25, P3180, DOI 10.1016/j.celrep.2018.11.064
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NR 33
TC 7
Z9 7
U1 2
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1574-7891
EI 1878-0261
J9 MOL ONCOL
JI Mol. Oncol.
PD APR
PY 2023
VL 17
IS 4
BP 695
EP 709
DI 10.1002/1878-0261.13350
EA DEC 2022
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C7TM4
UT WOS:000900767500001
PM 36453019
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Gershenson, DM
AF Gershenson, David M.
TI Molecular targeting of low-grade serous and mucinous carcinomas of the
   ovary or peritoneum
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Review
DE Ovarian cancer; low-grade serous carcinoma; mucinous carcinoma; targeted
   therapy
ID BORDERLINE TUMORS; BRAF MUTATION; CLINICAL BEHAVIOR; INTESTINAL-TYPE;
   GROWTH-FACTOR; CANCER; EXPRESSION; KRAS; SURVIVAL; PATHWAY
AB Over the past decade, the strategy for clinical trial design in making progress against epithelial cancers of the ovary/peritoneum/fallopian tube has changed dramatically. The NRG [the Gynecologic Oncology Group (GOG)] Rare Tumor Committee has been a leader in this transformation. No longer does "one size fit all". Rather, separate clinical trials for rare subtypes have been developed, and, in some cases, completed. An enhanced understanding of their pathologic diagnosis, molecular biology, and clinical behavior has galvanized this change. Pathology studies have led to replacement of the International Federation of Gynecology and Obstetrics (FIGO) grading system of low-grade serous carcinoma to the binary grading system, and immunohistochemical studies have assisted in distinguishing mucinous carcinoma of the ovary from colorectal cancer. Historically, conventional chemotherapy has demonstrated very limited activity in both histologic subtypes. Preclinical studies have identified and elucidated genes and pathways in both-MAP kinase pathway, IGF1-R, the angiogenesis pathway, and possibly, the PI3K/AKT/mTOR pathway in low-grade serous carcinoma, and KRAS, HER-2/neu amplification, src, and the angiogenesis pathway in mucinous carcinoma-that may serve as targets for novel therapies. MEK inhibitor (MEKi) therapy has shown promising activity in patients with recurrent low-grade serous carcinoma, and the current emphasis is focused on the second generation of MEKi trials and combinations of MEKi and inhibitors of the PI3K/AKT/mTOR pathway. For mucinous carcinoma, mEOC/GOG 0241 was designed to test both a colorectal cancer-type chemotherapy regimen and anti-angiogenesis therapy but closed prematurely due to slow accrual related to the rarity of this subtype. The experience with targeted therapy is otherwise extremely limited to date. The hope is that lessons learned from the failure of the mEOC/GOG 0241 trial will inform future trials. In summary, there is tremendous potential for progress against these two rare histologic subtypes by leveraging our knowledge of their molecular biology and translating this understanding into improved, novel therapeutics.
C1 [Gershenson, David M.] Univ Texas MD Anderson Canc Ctr, Dept Gynecol Oncol & Reprod Med, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center
RP Gershenson, DM (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Gynecol Oncol, Unit 1362, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM dgershen@mdanderson.org
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NR 84
TC 1
Z9 1
U1 1
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 2218-676X
EI 2219-6803
J9 TRANSL CANCER RES
JI Transl. Cancer Res.
PD FEB
PY 2015
VL 4
IS 1
BP 29
EP 39
DI 10.3978/j.issn.2218-676X.2015.01.05
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DE4QZ
UT WOS:000370616100004
DA 2025-01-04
ER

PT J
AU Tajima, JY
   Futamura, M
   Gaowa, S
   Mori, R
   Tanahashi, T
   Tanaka, Y
   Matsuhashi, N
   Takahashi, T
   Yamaguchi, K
   Miyazaki, T
   Yoshida, K
AF Tajima, Jesse Yu
   Futamura, Manabu
   Gaowa, Siqin
   Mori, Ryutaro
   Tanahashi, Toshiyuki
   Tanaka, Yoshihiro
   Matsuhashi, Nobuhisa
   Takahashi, Takao
   Yamaguchi, Kazuya
   Miyazaki, Tatsuhiko
   Yoshida, Kazuhiro
TI Clinical Significance of Glycoprotein Non-metastatic B and Its
   Association with EGFR/HER2 in Gastrointestinal Cancer
SO JOURNAL OF CANCER
LA English
DT Article
DE GPNMB; gastrointestinal cancer; cross-talk; molecular-targeted therapy;
   drug resistance
ID CONJUGATE GLEMBATUMUMAB VEDOTIN; METASTATIC BREAST-CANCER; TYROSINE
   KINASE RECEPTOR; GROWTH-FACTOR RECEPTOR; RANDOMIZED PHASE-II; MELANOMA
   PROTEIN-B; DIFFERENTIAL EXPRESSION; GEFITINIB RESISTANCE; THERAPEUTIC
   TARGET; GASTRIC-CANCER
AB Glycoprotein non-metastatic B (GPNMB), a type I transmembrane glycoprotein, is overexpressed in melanoma and breast cancer and promotes cancer-cell invasion and motility. We previously reported cross-talk between GPNMB and human epidermal growth factor receptor 2 (HER2) in breast cancer, suggesting that GPNMB might play an important role in resistance to anti-HER2 therapy in breast cancer. Here, we clarified the association between GPNMB and HER-family proteins in gastrointestinal cancer by examining their relationships using gastric and colorectal cancer cell lines. We found that GPNMB depletion of by small-interfering RNA increased epidermal growth factor receptor (EGFR) expression and phosphorylation through AKT8 virus oncogene cellular homolog (AKT) and mitogen-activated protein kinase (MAPK) pathways. Additionally, treatment with cetuximab (CTX) also increased GPNMB expression, and combination therapy consisting of GPNMB depletion and CTX treatment significantly suppressed cell growth in colorectal cancer cell lines, but not in gastric cancer cell lines. Furthermore, we also evaluated changes in GPNMB expression in vivo, with immunohistochemistry detecting GPNMB overexpression in a colorectal cancer patient following anti-EGFR therapy. These results suggested possible cross-talk between GPNMB and EGFR, and that GPNMB might play an important role in resistance to anti-EGFR therapy in gastrointestinal cancer.
C1 [Tajima, Jesse Yu; Futamura, Manabu; Gaowa, Siqin; Mori, Ryutaro; Tanahashi, Toshiyuki; Tanaka, Yoshihiro; Matsuhashi, Nobuhisa; Takahashi, Takao; Yamaguchi, Kazuya; Yoshida, Kazuhiro] Gifu Univ, Grad Sch Med, Dept Surg Oncol, Gifu, Japan.
   [Miyazaki, Tatsuhiko] Gifu Univ Hosp, Div Pathol, Gifu, Japan.
C3 Gifu University; Gifu University
RP Futamura, M (corresponding author), Gifu Univ, Grad Sch Med, Dept Surg Oncol, Gifu, Japan.
EM mfutamur@gifu-u.ac.jp
FU Taiho Pharmaceutical Co., Ltd.; Pfizer Inc.; Chugai Pharmaceutical Co.,
   Ltd.; Yakult Honsha Co., Ltd.; Bristol-Myers Squibb; Kyowa Hakko Kirin
   Co., Ltd.
FX KY has received grants and personal fees from Taiho Pharmaceutical Co.,
   Ltd., Pfizer Inc., Chugai Pharmaceutical Co., Ltd., and Yakult Honsha
   Co., Ltd., grants from Bristol-Myers Squibb and Kyowa Hakko Kirin Co.,
   Ltd., honoraria from Taiho Pharmaceutical Co., Ltd., Pfizer Inc., Chugai
   Pharmaceutical Co., Ltd., Kyowa Hakko Kirin Co., Ltd., and Yakult Honsha
   Co., Ltd., and had a consultant or advisory relationship with Taiho
   Pharmaceutical Co., Ltd. and La Roche, Ltd. All remaining authors
   declare that they have no conflicts of interest.
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NR 42
TC 8
Z9 11
U1 1
U2 4
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2018
VL 9
IS 2
BP 358
EP 366
DI 10.7150/jca.20266
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FY1IX
UT WOS:000426566500016
PM 29344282
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Kopetz, S
   Murphy, DA
   Pu, J
   Ciardiello, F
   Desai, J
   Van Cutsem, E
   Wasan, HS
   Yoshino, T
   Saffari, H
   Zhang, XS
   Hamilton, P
   Xie, T
   Yaeger, R
   Tabernero, J
AF Kopetz, Scott
   Murphy, Danielle A.
   Pu, Jie
   Ciardiello, Fortunato
   Desai, Jayesh
   Van Cutsem, Eric
   Wasan, Harpreet Singh
   Yoshino, Takayuki
   Saffari, Hedieh
   Zhang, Xiaosong
   Hamilton, Phineas
   Xie, Tao
   Yaeger, Rona
   Tabernero, Josep
TI Molecular profiling of BRAF-V600E-mutant metastatic colorectal cancer in
   the phase 3 BEACON CRC trial
SO NATURE MEDICINE
LA English
DT Article
ID MUTATIONAL SIGNATURES; ACQUIRED-RESISTANCE; COMBINED BRAF; INHIBITION;
   SUBTYPES; COMBINATION; DABRAFENIB; MECHANISMS; TRAMETINIB; SUBSETS
AB The BEACON CRC study demonstrated that encorafenib (Enco)+cetuximab (Cetux)+/- binimetinib (Bini) significantly improved overall survival (OS) versus Cetux + chemotherapy in previously treated patients with BRAF-V600E-mutant mCRC, providing the basis for the approval of the Enco+Cetux regimen in the United States and the European Union. A greater understanding of biomarkers predictive of response to Enco+Cetux +/- Bini treatment is of clinical relevance. In this prespecified, exploratory biomarker analysis of the BEACON CRC study, we characterize genomic and transcriptomic correlates of clinical outcomes and acquired resistance mechanisms through integrated clinical and molecular analysis, including whole-exome and -transcriptome tissue sequencing and circulating tumor DNA genomic profiling. Tumors with higher immune signatures showed a trend towards increased OS benefit with Enco+Bini+Cetux. RAS, MAP2K1 and MET alterations were most commonly acquired with Enco+Cetux +/- Bini, and more frequent in patients with a high baseline cell-cycle gene signature; baseline TP53 mutation was associated with acquired MET amplification. Acquired mutations were subclonal and polyclonal, with evidence of increased tumor mutation rate with Enco+Cetux +/- Bini and mutational signatures (SBS17a/b). These findings support treatment with Enco+Cetux +/- Bini for patients with BRAF-V600E-mutant mCRC and provide insights into the biology of response and resistance to MAPK-pathway-targeted therapy. ClinicalTrials.gov registration: NCT02928224
   Prespecified exploratory genomic and transcriptomic profiling of tumor tissues and circulating tumor DNA from patients with BRAF-V600E-mutant metastatic colorectal cancer who participated in the phase 3 BEACON CRC trial identifies biomarkers of response and mechanisms of acquired resistance to treatment with the BRAF inhibitor encorafenib plus the anti-EGFR antibody cetuximab, with or without the MEK inhibitor binimetinib.
C1 [Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Murphy, Danielle A.; Hamilton, Phineas; Xie, Tao] Pfizer, La Jolla, CA USA.
   [Pu, Jie] Pfizer, New York, NY USA.
   [Ciardiello, Fortunato] Univ Campania Luigi Vanvitelli, Naples, Italy.
   [Desai, Jayesh] Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
   [Van Cutsem, Eric] Univ Hosp Gasthuisberg, Leuven, Belgium.
   [Van Cutsem, Eric] Katholieke Univ Leuven, Leuven, Belgium.
   [Wasan, Harpreet Singh] Hammersmith Hosp, Imperial Coll London, Div Canc, London, England.
   [Yoshino, Takayuki] Natl Canc Ctr Hosp East, Kashiwa, Japan.
   [Saffari, Hedieh; Zhang, Xiaosong] Pfizer, South San Francisco, CA USA.
   [Yaeger, Rona] Mem Sloan Kettering Canc Ctr, New York, NY USA.
   [Tabernero, Josep] Cent Univ Catalonia, Univ Vic, Vall dHebron Hosp Campus, Barcelona, Spain.
   [Tabernero, Josep] Cent Univ Catalonia, Univ Vic, Vall dHebron Inst Oncol VHIO, Barcelona, Spain.
C3 University of Texas System; UTMD Anderson Cancer Center; Pfizer; Pfizer;
   Universita della Campania Vanvitelli; Peter Maccallum Cancer Center; KU
   Leuven; University Hospital Leuven; KU Leuven; Imperial College London;
   National Cancer Center - Japan; Pfizer; Memorial Sloan Kettering Cancer
   Center; Universitat de Vic - Universitat Central de Catalunya
   (UVic-UCC); Universitat de Vic - Universitat Central de Catalunya
   (UVic-UCC); Vall d'Hebron Institut d'Oncologia (VHIO)
RP Kopetz, S (corresponding author), Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
EM SKopetz@mdanderson.org
RI Kopetz, Scott/AAC-1387-2019; Desai, Jayesh/AAV-1237-2021
OI Desai, Jayesh/0000-0003-4246-9344; Yoshino,
   Takayuki/0000-0002-0489-4756; Kopetz, Scott/0000-0001-9647-3416
FU This study was also supported by a Cancer Center Core Grant P30 CA008748
   to MSK. Medical writing support was provided by Qing Yun Chong, PhD, and
   Asu Erden, PhD, of Nucleus Global, an Inizio Company, and was funded by
   Pfizer.; Vall d'Hebron Institute of Oncology; Pfizer; Merck KGaA,
   Darmstadt, Germany; ONO Pharmaceutical and Pierre Fabre [P30 CA008748];
   Cancer Center Core Grant
FX We thank the participating patients and their families, as well as the
   staff at the participating sites. Additionally, we acknowledge E. Elez
   from the Vall d'Hebron Institute of Oncology and Vall d'Hebron
   University Hospital, for her contributions to patient recruitment and
   trial conduct. The BEACON CRC trial was sponsored by Pfizer and was
   conducted with support from Merck KGaA, Darmstadt, Germany (for sites
   outside of North America), ONO Pharmaceutical and Pierre Fabre. This
   study was also supported by a Cancer Center Core Grant P30 CA008748 to
   Memorial Sloan Kettering Cancer Center. Medical writing support was
   provided by Q.Y. Chong and A. Erden of Nucleus Global, an Inizio
   Company, and was funded by Pfizer.
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NR 57
TC 1
Z9 1
U1 3
U2 3
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 NOV
PY 2024
VL 30
IS 11
DI 10.1038/s41591-024-03235-9
EA SEP 2024
PG 29
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 M2I8S
UT WOS:001318200400002
PM 39313594
OA hybrid
DA 2025-01-04
ER

PT J
AU Rühlmann, F
   Windhof-Jaidhauser, IM
   Menze, C
   Beissbarth, T
   Bohnenberger, H
   Ghadimi, M
   Dango, S
AF Ruehlmann, Felix
   Windhof-Jaidhauser, Indra Maria
   Menze, Cornelius
   Beissbarth, Tim
   Bohnenberger, Hanibal
   Ghadimi, Michael
   Dango, Sebastian
TI The prognostic capacities of CBP and p300 in locally advanced rectal
   cancer
SO WORLD JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer; Biomarkers; Targeted therapy; Histone
   acetyltransferase
ID ACUTE MYELOID-LEUKEMIA; CREB-BINDING PROTEIN; HISTONE
   ACETYLTRANSFERASES; HETEROZYGOSITY; ACETYLATION; INHIBITOR; MUTATIONS;
   EXPRESSION; DISCOVERY; CBP/P300
AB Background: CREB-binding protein (CBP) and p300 represent histone acetyltransferases (HATs) and transcriptional coactivators that play essential roles in tumour initiation and progression. Both proteins are generally thought to function as tumour suppressors, although their distinct roles in colorectal cancer (CRC) remain inconsistent and ambiguous. Thus, we analysed the expression of these two HATs in human tissue samples from patients with locally advanced rectal cancer via immunohistochemistry and evaluated their potential impacts on future CRC diagnosis and treatment.
   Methods: In our analysis, we included ninety-three (n = 93) patients diagnosed with adenocarcinoma in the upper third of the rectum. None of the patients received preoperative chemoradiotherapy, but the patients did undergo primary resection of the tumour within the phase II GAST-05 trial. By using H-scores, the expression of both proteins was visualised via immunohistochemistry in resected specimens from the patients. CBP and p300 expression were correlated with clinical and follow-up data.
   Results: Our analysis showed that high expression of CBP was significantly associated with prolonged cancer-specific survival (CSS; p = 0.002). In univariate analysis, CBP was an independent prognostic parameter for CSS (p = 0.042). High nuclear CBP expression was observed in two-thirds of patients. In contrast, we could not find any significant correlation between the expression of p300 and cancer-specific survival in this cohort of patients (p = 0.09). We did not observe any cooperation between CBP and p300 in our analysis.
   Conclusions: High expression of CBP was significantly associated with improved oncological outcomes. This finding could help to stratify patients in the future for CRC treatment. Histone deacetylase (HDAC) inhibitors are increasingly playing a role in oncological treatment and could additionally become therapeutic options in CRC. Our findings need to be further evaluated and verified in future clinical analyses.
C1 [Ruehlmann, Felix; Windhof-Jaidhauser, Indra Maria; Menze, Cornelius; Ghadimi, Michael; Dango, Sebastian] Univ Med Ctr, Dept Gen Visceral & Pediat Surg, Robert Koch Str 40, D-37075 Gottingen, Germany.
   [Beissbarth, Tim] Univ Med Ctr, Dept Med Stat, Gottingen, Germany.
   [Bohnenberger, Hanibal] Univ Med Ctr, Dept Pathol, Gottingen, Germany.
   [Dango, Sebastian] Kreisklinikum Siegen, Dept Gen & Visceral Surg, Weidenauer Str 76, D-57076 Siegen, Germany.
C3 University of Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; University of
   Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; University of Gottingen;
   UNIVERSITY GOTTINGEN HOSPITAL
RP Rühlmann, F (corresponding author), Univ Med Ctr, Dept Gen Visceral & Pediat Surg, Robert Koch Str 40, D-37075 Gottingen, Germany.
EM felix.ruehlmann@med.uni-goettingen.de
RI Bohnenberger, Hanibal/F-2317-2013; Beissbarth, Tim/B-3129-2013
FU Department of General, Visceral and Paediatric Surgery at University
   Medical Center Gottingen, Germany
FX Funding was provided by the Department of General, Visceral and
   Paediatric Surgery at University Medical Center Gottingen, Germany. This
   funding body did not participate in the study design, data analysis or
   manuscript preparation.
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NR 48
TC 10
Z9 12
U1 1
U2 1
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 19
PY 2019
VL 17
IS 1
AR 224
DI 10.1186/s12957-019-1764-8
PG 8
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA KI4ZL
UT WOS:000511359300003
PM 31856851
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Necula, L
   Matei, L
   Dragu, D
   Pitica, I
   Neagu, A
   Bleotu, C
   Diaconu, CC
   Chivu-Economescu, M
AF Necula, Laura
   Matei, Lilia
   Dragu, Denisa
   Pitica, Ioana
   Neagu, Ana
   Bleotu, Coralia
   Diaconu, Carmen C.
   Chivu-Economescu, Mihaela
TI Collagen Family as Promising Biomarkers and Therapeutic Targets in
   Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE collagens; cancer; targeted therapy; extracellular matrix; biomarkers
ID INTEGRATED BIOINFORMATICS ANALYSIS; GASTRIC-CANCER;
   EXTRACELLULAR-MATRIX; CELL-PROLIFERATION; BREAST-CANCER; IV COLLAGEN;
   COLORECTAL-CANCER; PREDICTIVE-VALUE; DRUG-RESISTANCE; GENE-EXPRESSION
AB Despite advances in cancer detection and therapy, it has been estimated that the incidence of cancers will increase, while the mortality rate will continue to remain high, a fact explained by the large number of patients diagnosed in advanced stages when therapy is often useless. Therefore, it is necessary to invest knowledge and resources in the development of new non-invasive biomarkers for the early detection of cancer and new therapeutic targets for better health management. In this review, we provided an overview on the collagen family as promising biomarkers and on how they may be exploited as therapeutic targets in cancer. The collagen family tridimensional structure, organization, and functions are very complex, being in a tight relationship with the extracellular matrix, tumor, and immune microenvironment. Moreover, accumulating evidence underlines the role of collagens in promoting tumor growth and creating a permissive tumor microenvironment for metastatic dissemination. Knowledge of the molecular basis of these interactions may help in cancer diagnosis and prognosis, in overcoming chemoresistance, and in providing new targets for cancer therapies.
C1 [Necula, Laura; Matei, Lilia; Dragu, Denisa; Pitica, Ioana; Neagu, Ana; Bleotu, Coralia; Diaconu, Carmen C.; Chivu-Economescu, Mihaela] Stefan S Nicolau Inst Virol, Dept Cellular & Mol Pathol, Bucharest 030304, Romania.
   [Necula, Laura] Titu Maiorescu Univ, Fac Med, Bucharest 040441, Romania.
C3 Romanian Academy; Stefan S. Nicolau Institute of Virology; Carol Davila
   University of Medicine & Pharmacy; Titu Maiorescu University
RP Necula, L (corresponding author), Stefan S Nicolau Inst Virol, Dept Cellular & Mol Pathol, Bucharest 030304, Romania.; Necula, L (corresponding author), Titu Maiorescu Univ, Fac Med, Bucharest 040441, Romania.
EM laura.necula@virology.ro
RI Coralia, Bleotu/B-5976-2011; Dragu, Denisa/I-3095-2015; Necula,
   Laura/I-1668-2015; Economescu, Mihaela/B-4323-2011; Diaconu, Carmen
   Cristina/B-9119-2011; Neagu, Ana/O-2238-2016; Matei, Lilia/O-8008-2014;
   Pitica, Ioana Madalina/AAB-6056-2019
OI Economescu, Mihaela/0000-0001-7512-4700; Diaconu, Carmen
   Cristina/0000-0002-2259-1425; Neagu, Ana/0000-0001-6126-8973; Matei,
   Lilia/0000-0003-4479-655X; Pitica, Ioana Madalina/0000-0001-7440-9798
FU Ministry of Research, Innovation and Digitization; CNCS/CCCDI-UEFISCDI
   [PN-III-P4-ID-PCCF-2016-0158, PCCF 17/2018]; PNCDI III [TE 36/2020,
   PN-III-P1-1.1-TE-2019-1864, P_37_798 MyeloAL-EDiaProT, 149/26.10.2016,
   106774]
FX This research was funded by the projects from the Ministry of Research,
   Innovation and Digitization; CNCS/CCCDI-UEFISCDI; project number
   PN-III-P4-ID-PCCF-2016-0158 (contract PCCF 17/2018) within PNCDI III;
   project number TE 36/2020 (PN-III-P1-1.1-TE-2019-1864) within PNCDI III;
   and the following project: Regional Development Fund (ERDF),
   Competitiveness Op-erational Programme (COP) A1.1.4. ID: P_37_798
   MyeloAL-EDiaProT, Contract 149/26.10.2016, (SMIS: 106774).
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NR 119
TC 29
Z9 30
U1 4
U2 28
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 2022
VL 23
IS 20
AR 12415
DI 10.3390/ijms232012415
PG 15
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 5S5OH
UT WOS:000875238600001
PM 36293285
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Andersen, IR
   Olesen, R
   Boysen, AK
   Jensen, LH
   Mortensen, FV
   Nielsen, DT
   Rasmussen, F
AF Andersen, Iben R.
   Olesen, Rene
   Boysen, Anders K.
   Jensen, Lars H.
   Mortensen, Frank, V
   Nielsen, Dennis T.
   Rasmussen, Finn
TI Dynamic contrast-enhanced computed tomography as a potential biomarker
   in patients with metastatic colorectal cancer treated with regorafenib
SO ACTA RADIOLOGICA
LA English
DT Article
DE CT quantitative; dynamic contrast-enhanced computed tomography;
   metastatic colorectal cancer; patient outcome; angiogenesis inhibitors
ID LIVER METASTASES; HEPATOCELLULAR-CARCINOMA; PERFUSION; CHEMOTHERAPY;
   TUMOR; BEVACIZUMAB; CRITERIA; VOLUME
AB Background RECIST 1.1 presents challenges when evaluating treatment response to angiogenesis inhibitors. The objective response rate, when evaluating the treatment effect of regorafenib, using RECIST 1.1, is < 2% and beneficial treatment could erroneously be terminated. Dynamic contrast-enhanced computed tomography (DCE-CT) has potential as a non-invasive functional imaging biomarker, by quantifying the treatment effect of this targeted therapy. Purpose To evaluate three-dimensional (3D) tumor dynamic parameters representing tumor microcirculation assessed by DCE-CT during the treatment with regorafenib in a cohort of patients with treatment-refractory metastatic colorectal cancer. Material and Methods Thirty-three patients with colorectal metastases (27 liver lesions, three abdominal lesions, and three pulmonary lesions) were treated with regorafenib and evaluated using DCE-CT. A total of 112 DCE-CT scans were analyzed using Advanced Perfusion and Permeability Application and correlated to standard contrast-enhanced computed tomography (CE-CT) evaluated using RECIST 1.1. Results A significant decrease in most DCE-CT parameters, a simultaneous decrease in tumor attenuation and an increase in tumor volume were detected during treatment. However, no associations were found between the DCE-CT parameters and PFS or OS using simple COX proportional hazards regression. Conclusion In this exploratory study, a significant decrease in most dynamic parameters suggests an overall treatment effect of regorafenib in tumor vasculature. DCE-CT may assist in an objective evaluation of these responses compared to RECIST. The anti-angiogenic changes could not be associated with treatment outcome in terms of PFS and OS, which might be due to the small cohort or a rather limited survival benefit in this pre-medicated treatment-refractory group of patients.
C1 [Andersen, Iben R.; Nielsen, Dennis T.; Rasmussen, Finn] Aarhus Univ Hosp, Dept Radiol, Norrebrogade 44, DK-8000 Aarhus, Denmark.
   [Olesen, Rene; Boysen, Anders K.] Aarhus Univ Hosp, Dept Oncol, Aarhus, Denmark.
   [Jensen, Lars H.] Lillebaelt Hosp, Dept Oncol, Vejle, Denmark.
   [Mortensen, Frank, V] Aarhus Univ Hosp, Dept Surg, Aarhus, Denmark.
C3 Aarhus University; Aarhus University; Aarhus University
RP Andersen, IR (corresponding author), Aarhus Univ Hosp, Dept Radiol, Norrebrogade 44, DK-8000 Aarhus, Denmark.
EM iben.rahbek.andersen@rm.dk
RI Andersen, Iben/LTF-6085-2024; Jensen, Lars Henrik/P-6252-2018
OI Mortensen, Frank Viborg/0000-0001-7580-8037; Jensen, Lars
   Henrik/0000-0002-0020-1537
FU Memorial Foundation of Eva and Henry Fraenkel; Health Research Fund of
   Central Denmark Region; Bayer Healthcare
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: IRA
   received research grants from the Memorial Foundation of Eva and Henry
   Fraenkel and the Health Research Fund of Central Denmark Region. Bayer
   Healthcare supported the imaging part of the study but did not have any
   involvement in the clinical decisions regarding the treatment. Bayer was
   given the opportunity to comment on the first draft of this manuscript,
   but the authors made the final decisions about the content. Philips
   Healthcare provided the APPA software for the DCE-CT analysis.
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NR 30
TC 3
Z9 3
U1 0
U2 2
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0284-1851
EI 1600-0455
J9 ACTA RADIOL
JI Acta Radiol.
PD JUL
PY 2019
VL 60
IS 7
BP 836
EP 845
DI 10.1177/0284185118806652
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA IF6OJ
UT WOS:000473199700004
PM 30348001
DA 2025-01-04
ER

PT J
AU Li, J
   Hu, QZ
   Li, ZY
   Feng, KY
   Li, KB
AF Li, Jie
   Hu, Qiaozhen
   Li, Zhongyan
   Feng, Kaiyu
   Li, Kangbao
TI MT1G Regulates c-MYC/P53 Signal to Inhibit Proliferation, Invasion and
   Migration and Promote Apoptosis in Colon Cancer Cells
SO CURRENT MOLECULAR MEDICINE
LA English
DT Article
DE Colon cancer; MT1G; c-MYC; P53; LoVo cells; HCT116
ID METALLOTHIONEIN 1G; COLORECTAL-CANCER; GENE
AB Introduction Colon cancer is a common and malignant cancer featuring high morbidity and poor prognosis.Aims This study was performed to explore the regulatory role of MT1G in colon cancer as well as its unconcealed molecular mechanism.Methods The expressions of MT1G, c-MYC, and p53 were assessed with the application of RT-qPCR and western blot. The impacts of MT1G overexpression on the proliferative ability of HCT116 and LoVo cells were measured by CCK-8 and BrdU incorporation assays. Additionally, transwell wound healing, and flow cytometry assays were employed to evaluate the invasive and migrative capacities as well as the apoptosis level of HCT116 and LoVo cells. Moreover, the activity of the P53 promoter region was assessed with the help of a luciferase reporter assay.Results It was found that the expressions of MT1G at both mRNA and protein levels were greatly decreased in human colon cancer cell lines, particularly in HCT116 and LoVo cell lines. After transfection, it was discovered that the MT1G overexpression suppressed the proliferation, migration and invasion but promoted the apoptosis of HCT116 and LoVo cells, which were then partially reversed after overexpressing c-MYC. Additionally, MT1G overexpression reduced c-MYC expression but enhanced the p53 expression, revealing that the MT1G overexpression could regulate c-MYC/P53 signal. Elsewhere, it was also shown that c-MYC overexpression suppressed the regulatory effects of MT1G on P53.Conclusion To conclude, MT1G was verified to regulate c-MYC/P53 signal to repress the proliferation, migration and invasion but promote the apoptosis of colon cancer cells, which might offer a novel targeted-therapy for the improvement of colon cancer.
C1 [Li, Jie; Hu, Qiaozhen; Li, Zhongyan; Feng, Kaiyu; Li, Kangbao] South China Univ Technol, Guangzhou Peoples Hosp 1, Sch Med, Dept Geriatr,Natl Clin Key Specialty, Guangzhou 510180, Guangdong, Peoples R China.
   [Li, Kangbao] South China Univ Technol, Guangzhou Peoples Hosp 1, Sch Med, Dept Geriatr,Natl Clin Key Specialty, 1 Panfu Rd, Guangzhou 510180, Guangdong, Peoples R China.
C3 South China University of Technology; South China University of
   Technology
RP Li, KB (corresponding author), South China Univ Technol, Guangzhou Peoples Hosp 1, Sch Med, Dept Geriatr,Natl Clin Key Specialty, 1 Panfu Rd, Guangzhou 510180, Guangdong, Peoples R China.
EM likangbao721@163.com
RI Hu, Qiaozhen/IQT-7468-2023; Li, Yuesheng/F-6728-2019
FU Science and Technology Project of Guangdong Provincial Science and
   Technology Department [01548280218329 060, 0445091120222 076]
FX This study was supported by the Science and Technology Project of
   Guangdong Provincial Science and Technology Department: (1) Relationship
   between cannabinoid receptor 1 (CNR1) gene polymorphism and irritable
   bowel syndrome (No. 01548280218329 060); (2) Study of NF-kB signaling
   pathway in the anti-colon cancer effect of curcumin (No. 0445091120222
   076).
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NR 25
TC 0
Z9 0
U1 3
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 1566-5240
EI 1875-5666
J9 CURR MOL MED
JI Curr. Mol. Med.
PY 2024
VL 24
IS 3
BP 379
EP 388
DI 10.2174/1566524023666230329085557
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA LF2R2
UT WOS:001185306400004
PM 36999424
DA 2025-01-04
ER

PT J
AU Ding, L
   Ni, J
   Yang, F
   Huang, LL
   Deng, H
   Wu, Y
   Ding, XS
   Tang, JH
AF Ding, Li
   Ni, Jie
   Yang, Fan
   Huang, Lingli
   Deng, Heng
   Wu, Yang
   Ding, Xuansheng
   Tang, Jinhai
TI Promising therapeutic role of miR-27b in tumor
SO TUMOR BIOLOGY
LA English
DT Review
DE MicroRNA; microRNA-27b; cancer; therapy; biomarker
ID MICRORNA EXPRESSION; GROWTH-FACTOR; COLORECTAL-CANCER; UP-REGULATION;
   ANGIOGENESIS INHIBITOR; MULTIDRUG-RESISTANCE; MYELOID-LEUKEMIA;
   CARCINOMA CELLS; PROGRESSION; GENE
AB MicroRNAs are small nonprotein-encoding RNAs ranging from 18 to 25 nucleotides in size and regulate multiple biological pathways via directly targeting a variety of associated genes in cancers. MicroRNA-27b is a highly conserved MicroRNA throughout vertebrates and there are two homologs (hsa-miR-27a and hsa-miR-27b) in humans. MicroRNA-27b is an intragenic microRNA located on chromosome 9q22.1 within the C9orf3 gene, clustering with miR-23b and miR-24-1 in human. As a frequently dysregulated microRNA in human cancers, microRNA-27b could function as a tumor suppressor or an oncogenic microRNA. More and more studies indicate that microRNA-27b is involved in affecting various biological processes, such as angiogenesis, proliferation, metastasis, and drug resistance, and thus may act as a promising therapeutic target in human cancers. In this review, we discuss the role of microRNA-27b in detail and offer novel insights into molecular targeting therapy for cancers.
C1 [Ding, Li; Ding, Xuansheng] China Pharmaceut Univ, Sch Basic Med & Clin Pharm, Nanjing, Jiangsu, Peoples R China.
   [Ding, Li; Ni, Jie; Yang, Fan; Huang, Lingli; Wu, Yang; Tang, Jinhai] Nanjing Med Univ, Jiangsu Canc Hosp, Nanjing, Jiangsu, Peoples R China.
   [Ni, Jie] Nanjing Med Univ, Sch Clin Med 4, Nanjing, Jiangsu, Peoples R China.
   [Deng, Heng] AnHui Univ Tradit Chinese Med, Grad Sch, Hefei, Peoples R China.
   [Tang, Jinhai] Nanjing Med Univ, Affiliated Hosp 1, Dept Gen Surg, Nanjing 210029, Jiangsu, Peoples R China.
C3 China Pharmaceutical University; Nanjing Medical University; Nanjing
   Medical University; Anhui University of Chinese Medicine; Nanjing
   Medical University
RP Tang, JH (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, Dept Gen Surg, Nanjing 210029, Jiangsu, Peoples R China.
EM jhtang@njmu.edu.cn
RI HUANG, LING/HTR-1819-2023
OI Huang, Lingli/0000-0002-6686-5942
FU National High Technology Research and Development Program of China
   [2014AA020604]; National Natural Science Foundation of China [81272470];
   National Key Clinical Specialist Construction Programs of China
   [2013[544]]; Major Program of Natural Science Foundation of Jiangsu
   Province [BL2014090]; Natural Science Foundation of Jiangsu Province
   [BK20151579]
FX This work was supported by the National High Technology Research and
   Development Program of China (no. 2014AA020604), the National Natural
   Science Foundation of China (no. 81272470), the National Key Clinical
   Specialist Construction Programs of China (no. 2013[544]), the Major
   Program of Natural Science Foundation of Jiangsu Province (no.
   BL2014090), and the Natural Science Foundation of Jiangsu Province (no.
   BK20151579).
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NR 90
TC 25
Z9 27
U1 0
U2 19
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1010-4283
EI 1423-0380
J9 TUMOR BIOL
JI Tumor Biol.
PD MAR
PY 2017
VL 39
IS 3
AR 691657
DI 10.1177/1010428317691657
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ET4OS
UT WOS:000400263700008
PM 28351320
OA gold
DA 2025-01-04
ER

PT J
AU Li, SL
   Yang, XM
   Lu, T
   Yuan, L
   Zhang, YT
   Zhao, J
   Deng, J
   Xue, CQ
   Sun, Q
   Liu, XW
   Zhang, WJ
   Zhou, JL
AF Li, Shenglin
   Yang, Xinmei
   Lu, Ting
   Yuan, Long
   Zhang, Yuting
   Zhao, Jun
   Deng, Juan
   Xue, Caiqiang
   Sun, Qiu
   Liu, Xianwang
   Zhang, Wenjuan
   Zhou, Junlin
TI Extracellular volume fraction can predict the treatment response and
   survival outcome of colorectal cancer liver metastases
SO EUROPEAN JOURNAL OF RADIOLOGY
LA English
DT Article
DE Colorectal cancer; Metastasis; Molecular targeted therapy; Treatment
   outcome
ID ARTERIAL ENHANCEMENT FRACTION; PREOPERATIVE CHEMOTHERAPY; BEVACIZUMAB;
   SELECTION; RESECTION; CRITERIA; THERAPY; RECIST; MRI
AB Objective: To assess the prognostic value of pre- and post-therapeutic changes in extracellular volume (ECV) fraction of liver metastases (LMs) for treatment response (TR) and survival outcomes in colorectal cancer liver metastases (CRLM). Methods: 186 LMs were confirmed by pathology or follow-up (Training: 130; Test: 56). We analyzed the changes in ECV fraction of LMs before and after 2 cycles of chemotherapy combined with bevacizumab. After 12 cycles, we evaluated the TR on LMs based on the RECIST v1.1. Relative changes in ECV fraction and Hounsfield Units (HU), defined as Delta ECV and Delta HU, were associated with progression-free survival (PFS), overall survival (OS), and TR. We identified TR predictors with multivariate logistic regression and PFS, OS risk factors with COX analysis. Results: 186 LMs were classified as TR lesions (TR+: 84) and non-TR lesions (TR-:102). Delta ECV, Delta HUA-E, and texture could distinguish the TR of LMs in training and test set (P < 0.05). Delta ECV [Odds ratio (OR): 1.03; 95% Confidence interval (CI): 1.02-1.05, P < 0.01] was an independent predictor of TR-. Area under the curve (AUC), sensitivity and specificity of TR model in training and test set were 0.87, 0.84, 90.14%, 90.32%, 72.88%, 64.00%, respectively. High CRD_score indicates that patients have shorter PFS [Hazard ratio (HR): 2.01; 95%CI: 1.02-3.98, P = 0.045)] and OS (HR: 1.89, 95%CI: 1.04-3.42, P = 0.038). Conclusion: Delta ECV can be used as an independent predictor of TR of CRLM chemotherapy combined with bevacizumab.
C1 [Li, Shenglin; Yang, Xinmei; Lu, Ting; Yuan, Long; Zhao, Jun; Deng, Juan; Xue, Caiqiang; Sun, Qiu; Liu, Xianwang; Zhang, Wenjuan; Zhou, Junlin] Lanzhou Univ Second Hosp, Dept Radiol, Cuiyingmen 82, Lanzhou 730030, Peoples R China.
   [Li, Shenglin; Yang, Xinmei; Lu, Ting; Yuan, Long; Deng, Juan; Xue, Caiqiang; Sun, Qiu; Liu, Xianwang; Zhou, Junlin] Lanzhou Univ, Clin Sch 2, Lanzhou, Peoples R China.
   [Li, Shenglin; Yang, Xinmei; Lu, Ting; Yuan, Long; Deng, Juan; Xue, Caiqiang; Liu, Xianwang; Zhou, Junlin] Key Lab Med Imaging Gansu Prov, Lanzhou, Peoples R China.
   [Li, Shenglin; Yang, Xinmei; Lu, Ting; Yuan, Long; Deng, Juan; Xue, Caiqiang; Liu, Xianwang; Zhou, Junlin] Gansu Int Sci & Technol Cooperat Base Med Imaging, Lanzhou, Peoples R China.
C3 Lanzhou University
RP Zhou, JL (corresponding author), Lanzhou Univ Second Hosp, Dept Radiol, Cuiyingmen 82, Lanzhou 730030, Peoples R China.
EM lishl21@lzu.edu.cn; ery_zhoujl@lzu.edu.cn
RI Zhou, Junlin/LWH-5467-2024; Zhang, Wei-Ming/L-5761-2017; zhang,
   weidi/JEF-7121-2023
FU National Youth Science Foundation Project [82102151]; Cuiying Scientific
   and Technological Innovation Program of Lanzhou University Second
   Hospital [CY2021-ZD-01]
FX This study was supported by grants of the National Youth Science
   Foundation Project (82102151) and the Cuiying Scientific and
   Technological Innovation Program of Lanzhou University Second Hospital
   (CY2021-ZD-01) .
CR Benson AB III, 2022, J NATL COMPR CANC NE, V20, P1139, DOI 10.6004/jnccn.2022.0051
   Boonsirikamchai P, 2011, AM J ROENTGENOL, V197, pW1060, DOI 10.2214/AJR.11.6459
   Cao YH, 2023, NAT REV DRUG DISCOV, V22, P476, DOI 10.1038/s41573-023-00671-z
   Chang YC, 2012, J MAGN RESON IMAGING, V36, P387, DOI 10.1002/jmri.23660
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   Dohan A, 2020, GUT, V69, P531, DOI 10.1136/gutjnl-2018-316407
   Eisenhauer EA, 2009, EUR J CANCER, V45, P228, DOI 10.1016/j.ejca.2008.10.026
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   Froelich MF, 2018, EUR RADIOL, V28, P5284, DOI 10.1007/s00330-018-5454-7
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NR 32
TC 0
Z9 0
U1 3
U2 4
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0720-048X
EI 1872-7727
J9 EUR J RADIOL
JI Eur. J. Radiol.
PD JUN
PY 2024
VL 175
AR 111444
DI 10.1016/j.ejrad.2024.111444
EA MAR 2024
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA QV5T1
UT WOS:001223664400001
PM 38531223
DA 2025-01-04
ER

PT J
AU Gu, ZE
   Wang, L
   Ma, JZ
   Zhang, T
   Yang, YF
AF Gu, Zhien
   Wang, Lei
   Ma, Jiawei Zhai
   Zhang, Tong
   Yang, Yufei
TI Conventional Therapy Combined With Quxie Capsule Modulating Gut
   Microbiome in Metastatic Colorectal Cancer Patients With the Third or
   Above Line Setting: Result From an Investigator-Initiated, Open-Label,
   Single-Arm, Phase II Study
SO INTEGRATIVE CANCER THERAPIES
LA English
DT Article
DE metastatic colorectal cancer (mCRC); third or above line treatment;
   traditional Chinese medicine; gut microbiome; Quxie capsule
ID MULTICENTER; PLACEBO
AB Background: In patients with metastatic colorectal cancer (mCRC), Quxie Cap-sule (QX)-a combination of conventional therapy (including chemotherapy, targeted therapy or supportive care)-has shown a significant overall survival benefit compared with placebo and might have the property of dual effects of antitumor and immunity enhancement, both mediated by the microbiome. In preclinical models, QX has also shown activity against colorectal cancer. This study aimed to describe how the aforementioned effects of QX look after when focusing on the patients in third or above line setting.Methods: A Simon's Minimax two-stage phase II design was used in this study, which enrolled mCRC patients who progressed after second-line treatment. Patients received conventional therapy plus QX until disease progression or unacceptable toxicity. Before and after 1-month intervention, we collected patients' stool samples for microbiome analysis by 16s rRNA sequencing approaches. And the microbiome analysis before and after 1-month intervention was done through bioinformation analysis platform.Results: Fifteen patients were enrolled and gut microbiome were analyzed from 7 of 10 patients that with PFS over 3.7 months. Microbiome community analysis on genus level showed that the proportion of Lachnospiraceae_UCG-001 (0.04% vs 1.06%, P = .02249) significantly increased after conventional therapy plus QX while the proportion of Alistipes (2.96% vs 1.35%, P = .03461), Flavonifractor (0.04% vs 0.02%, P = .02249), Bifidobacterium (6.11% vs 1.14%, P = .02249) and Butyricimonas (0.24% vs 0.11%, P = .03603) significantly decreased after intervention . LEfSe analysis showed that after intervention, samples were highly related with unclassified-f-lachnospiraceae, Eubacterium and Lachnospiraceae_UCG-001.Conclusions: Decrease of gut bacteria with potential roles in carcinogenesis of colorectal cancer and increase in the abundance of gut anticancer bacteria such as Lachnospiraceae may partly explain how conventional therapy combined with QX can influence carcinogenesis and tumor progression in colon cancer.Trial registration: Chinese Clinical Trial Registry (ChiCTR2100053874).
C1 [Gu, Zhien; Zhang, Tong; Yang, Yufei] China Acad Chinese Med Sci, Beijing, Peoples R China.
   [Wang, Lei] Chongqing Univ, Three Gorges Hosp, Chongqing, Peoples R China.
   [Ma, Jiawei Zhai] Beijing Chaoyang Integrat Medicinerescue & First A, Beijing, Peoples R China.
C3 China Academy of Chinese Medical Sciences; Chongqing University
RP Zhang, T; Yang, YF (corresponding author), China Acad Chinese Med Sci Xiyuan, Xiyuan Hosp, Oncol Dept, Xiyuan Caochang Rd, Beijing 100091, Peoples R China.
EM ashtray7654@126.com; yyf93@vip.sina.com
RI Yang, yufei/KHW-2735-2024
OI Gu, Zhien/0009-0006-3849-0764
FU National Natural Science Foundation of China [82174461]; Hospital
   capability enhancement project of Xiyuan Hospital, CACMS [XYZX0201-22]
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: The study
   was funded by grants from National Natural Science Foundation of China
   (General program 2021, No. 82174461) and Hospital capability enhancement
   project of Xiyuan Hospital, CACMS. (NO. XYZX0201-22).
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NR 33
TC 0
Z9 0
U1 1
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1534-7354
EI 1552-695X
J9 INTEGR CANCER THER
JI Integr. Cancer Ther.
PY 2024
VL 23
AR 15347354241280390
DI 10.1177/15347354241280390
PG 13
WC Oncology; Integrative & Complementary Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Integrative & Complementary Medicine
GA G9H6T
UT WOS:001319669000001
PM 39313964
OA gold
DA 2025-01-04
ER

PT J
AU Ding, YW
   Wang, J
   Zhu, N
   Xu, D
   Ding, KF
   Yuan, Y
AF Ding, Yuwei
   Wang, Juan
   Zhu, Ning
   Xu, Dong
   Ding, Kefeng
   Yuan, Ying
TI Fruquintinib effectively controlled the advanced small bowel
   adenocarcinoma progressed after multiple lines of palliative treatment:
   a case report and literature review
SO CANCER BIOLOGY & THERAPY
LA English
DT Review
DE Fruquintinib; Small bowel adenocarcinoma; HER-2 amplification;
   Cetuximab; Palliative treatment
ID ENDOTHELIAL GROWTH-FACTOR; COLORECTAL-CANCER; EXPRESSION; INHIBITOR;
   POTENT
AB Small bowel cancer is a very rare disease. It can be treated by surgery at early stages; however, there is no standard therapeutic strategy established for the treatment of unresectable and/or metastatic diseases.
   Here we present a case of metastatic small bowel adenocarcinoma, which progressed after sequential treatment with XELOX (capecitabine and oxaliplatin), FOLFIRI (fluorouracil, leucovorin, and irinotecan), cetuximab, HER-2 targeted therapy and apatinib and was then effectively controlled by fruquintinib. Genetic testing showed wild-type KRAS/NRAS/BRAF, HER-2 amplification, and microsatellite stable. Then the patient started to receive fruquintinib and has already achieved a 6-month progression-free survival. Till Jun 2019, the treatment with fruquintinib is still ongoing and no severe adverse effect has been seen so far.
   Although fruquintinib is not, at present, a standard therapeutic strategy recommended by the treatment guideline for advanced small bowel adenocarcinoma, the significant curative effect has been seen in our clinical practice.
C1 [Ding, Yuwei; Wang, Juan; Zhu, Ning; Yuan, Ying] Zhejiang Univ, Key Lab Canc Prevent & Intervent, Affiliated Hosp 2, Dept Med Oncol,Minist Educ,Sch Med, Hangzhou, Zhejiang, Peoples R China.
   [Xu, Dong; Ding, Kefeng] Zhejiang Univ, Affiliated Hosp 2, Dept Colorectal Surg, Sch Med, Hangzhou, Peoples R China.
   [Ding, Yuwei; Wang, Juan; Zhu, Ning; Xu, Dong; Ding, Kefeng; Yuan, Ying] Zhejiang Univ, Key Lab Canc Prevent & Intervent, Canc Inst, Minist Educ,Affiliated Hosp 2,Sch Med, Hangzhou, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang University
RP Yuan, Y (corresponding author), Zhejiang Univ, Sch Med, Dept Med Oncol, Hangzhou 310009, Zhejiang, Peoples R China.
EM yuanying1999@zju.edu.cn
OI Ying, Yuan/0000-0002-3922-9553
FU Natural Science Foundation of China [81872481, 81902956]; National Key
   R&D Program of China [2017YFC0908200]
FX This work was supported by Natural Science Foundation of China under
   Grant 81872481 and 81902956; and National Key R&D Program of China under
   Grant 2017YFC0908200.
CR Chen XF, 2019, ONCOLOGIST, V24, P883, DOI 10.1634/theoncologist.2019-0164
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NR 20
TC 0
Z9 0
U1 1
U2 11
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4047
EI 1555-8576
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD DEC 1
PY 2020
VL 21
IS 12
BP 1105
EP 1108
DI 10.1080/15384047.2020.1836549
EA NOV 2020
PG 4
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PA2KN
UT WOS:000586091800001
PM 33151122
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Li, QZ
   Zhang, X
   Fan, BQ
   Yang, YD
   Cui, XA
   Zhang, J
   Jiang, KT
   Zhang, CX
   Zhang, B
AF Li, Qizheng
   Zhang, Xia
   Fan, Buqun
   Yang, Yudie
   Cui, Xiaonan
   Zhang, Jie
   Jiang, Kaiteng
   Zhang, Chunxia
   Zhang, Bin
TI Anlotinib combined with TAS-102 as the third-line treatment for a
   patient with metastatic colon cancer: A case report
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE TAS-102; anlotinib; third-line; case report; metastatic colon cancer;
   mCRC
ID COLORECTAL-CANCER; OPEN-LABEL; TRIFLURIDINE/TIPIRACIL TAS-102; ASIAN
   PATIENTS; DOUBLE-BLIND; PLACEBO; MONOTHERAPY; MULTICENTER; BEVACIZUMAB;
   SURVIVAL
AB Chemotherapy combined with targeted therapy is a first-line and second-line treatment for metastatic colorectal cancer(mCRC), which has brought survival benefits to mCRC patients, however, disease progression is inevitable. More than 60% of patients still needed third-line treatment after the progress of second-line treatment. After the failure of second-line chemotherapy, treatment compliance and the physical tolerance of patients both decrease. Therefore, choosing an appropriate third-line treatment regimen is key to prolonging survival and improving quality of life. As a novel cytotoxic antitumor drug, trifluridine/tipiracil (TAS-102) is composed of trifluridine (FTD) and tipiracil hydrochloride (TPI). FTD can directly bind to the DNA of cancer cells to cause DNA dysfunction, thereby exerting antitumor effects. TPI can inhibit the degradation of FTD, thereby increasing its cytotoxicity. The few side effects of TAS-102 has become an important reason why clinicians present it as a treatment option to the patient for consideration, clinical trial data for progression free survival are lacking. The exploration of third-line treatment regimens with drug combinations has attracted much attention. This article reports a case of metastatic colon cancer (RAS/BRAF wild type, pMMR/Non-MSI-H), after failure of first-line and second-line therapies, the patient was eventually treated with anlotinib combined with TAS-102 as the third-line treatment. The treatment has shown good efficacy, with a long PFS benefit for more than 20 months and mild adverse reactions. This case reports demonstrates that anlotinib combined with TAS-102 is a promising third-line treatment regimen for refractory mCRC, and provides proof-of-concept for the clinical exploration of optimal third-line combination treatment regimens.
C1 [Li, Qizheng; Zhang, Xia; Fan, Buqun; Yang, Yudie; Cui, Xiaonan; Zhang, Jie; Zhang, Chunxia; Zhang, Bin] Dalian Med Univ, Affiliated Hosp 1, Dept Oncol, Dalian, Peoples R China.
   [Zhang, Xia] Dalian Fifth Peoples Hosp, Dept Oncol, Dalian, Peoples R China.
   [Jiang, Kaiteng] Nanchang Univ, Queen Mary Coll, Nanchang, Peoples R China.
C3 Dalian Medical University; Nanchang University
RP Zhang, CX; Zhang, B (corresponding author), Dalian Med Univ, Affiliated Hosp 1, Dept Oncol, Dalian, Peoples R China.
EM qm1210zcx@aliyun.com; Zhangbin_dlmu@163.com
RI zhang, chunmei/IUQ-7038-2023
FU Scientific research fund project of Education Department of Liaoning
   Province; Dalian Medical Science Research Project; Natural Science
   Foundation of Liaoning province;  [LJKZ0861];  [2011012]; 
   [20180550077];  [20180550937]
FX Funding This work was supported by the Scientific research fund project
   of Education Department of Liaoning Province (LJKZ0861) and the Dalian
   Medical Science Research Project (No. 2011012) and the Natural Science
   Foundation of Liaoning province (Nos. 20180550077 and 20180550937).
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NR 22
TC 1
Z9 1
U1 2
U2 7
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD NOV 30
PY 2022
VL 12
AR 978005
DI 10.3389/fonc.2022.978005
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 6Y3GY
UT WOS:000896987700001
PM 36531025
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Nwosu, ZC
   Song, MG
   di Magliano, MP
   Lyssiotis, CA
   Kim, SE
AF Nwosu, Zeribe Chike
   Song, Mun Gu
   di Magliano, Marina Pasca
   Lyssiotis, Costas A. A.
   Kim, Sung Eun
TI Nutrient transporters: connecting cancer metabolism to therapeutic
   opportunities
SO ONCOGENE
LA English
DT Review
ID MITOCHONDRIAL PYRUVATE CARRIER; AMINO-ACID-METABOLISM; PRIMARY LUNG
   CANCERS; MONOCARBOXYLATE TRANSPORTER; TUMOR PROGRESSION;
   COLORECTAL-CANCER; GENE-EXPRESSION; CELL-GROWTH; DIFFERENTIAL
   EXPRESSION; FUNCTIONAL EXPRESSION
AB Cancer cells rely on certain extracellular nutrients to sustain their metabolism and growth. Solute carrier (SLC) transporters enable cells to acquire extracellular nutrients or shuttle intracellular nutrients across organelles. However, the function of many SLC transporters in cancer is unknown. Determining the key SLC transporters promoting cancer growth could reveal important therapeutic opportunities. Here we summarize recent findings and knowledge gaps on SLC transporters in cancer. We highlight existing inhibitors for studying these transporters, clinical trials on treating cancer by blocking transporters, and compensatory transporters used by cancer cells to evade treatment. We propose targeting transporters simultaneously or in combination with targeted therapy or immunotherapy as alternative strategies for effective cancer therapy.
C1 [Nwosu, Zeribe Chike; Lyssiotis, Costas A. A.] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI USA.
   [Nwosu, Zeribe Chike; Lyssiotis, Costas A. A.] Univ Michigan, Rogel Canc Ctr, Ann Arbor, MI USA.
   [Song, Mun Gu; Kim, Sung Eun] Korea Univ, Coll Hlth Sci, Dept Biosyst & Biomed Sci, Seoul 02841, South Korea.
   [Song, Mun Gu; Kim, Sung Eun] Korea Univ, Coll Hlth Sci, Dept Integrated Biomed & Life Sci, Seoul 02841, South Korea.
   [di Magliano, Marina Pasca] Univ Michigan, Dept Surg, Ann Arbor, MI USA.
   [Lyssiotis, Costas A. A.] Univ Michigan, Dept Internal Med, Div Gastroenterol, Ann Arbor, MI USA.
C3 University of Michigan System; University of Michigan; University of
   Michigan System; University of Michigan; Korea University; Korea
   University; University of Michigan System; University of Michigan;
   University of Michigan System; University of Michigan
RP Kim, SE (corresponding author), Korea Univ, Coll Hlth Sci, Dept Biosyst & Biomed Sci, Seoul 02841, South Korea.; Kim, SE (corresponding author), Korea Univ, Coll Hlth Sci, Dept Integrated Biomed & Life Sci, Seoul 02841, South Korea.
EM sek19@korea.ac.kr
RI Kim, Hyeon/F-8796-2019; Nwosu, Zeribe/AAD-9820-2020; Lyssiotis,
   Costas/AAI-1923-2019
OI Kim, Sung Eun/0000-0002-4281-5625; Lyssiotis, Costas/0000-0001-9309-6141
FU Michigan Postdoctoral Pioneer Program at the University of Michigan
   Medical School, NIH/NCI [K99CA267176]; NIH/NIGMS [R25GM143298]; NIH/NCI
   [R37CA237421, R01CA248160, R01CA244931, R01CA151588, R01CA198074]; UMCCC
   Core Grant [P30CA046592]; National Research Foundation of Korea (NRF)
   [2020R1C1C1013220]; National Cancer Institute [R01CA248160, R37CA237421,
   K99CA267176, R01CA244931, P30CA046592] Funding Source: NIH RePORTER
FX ZCN was supported by the Michigan Postdoctoral Pioneer Program at the
   University of Michigan Medical School, NIH/NCI grant K99CA267176 and
   NIH/NIGMS grant R25GM143298. MP was supported by NIH/NCI grants
   R01CA151588 and R01CA198074. CAL was supported by the NIH/NCI grants
   R37CA237421, R01CA248160, and R01CA244931, and MP and CAL by UMCCC Core
   Grant (P30CA046592). SEK was supported by the National Research
   Foundation of Korea (NRF) grant (2020R1C1C1013220). The funders had no
   role in the content and publication of this manuscript. The authors
   apologize to researchers whose relevant work could not be cited in this
   review due to space limitations.
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NR 170
TC 13
Z9 15
U1 2
U2 18
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD MAR 3
PY 2023
VL 42
IS 10
BP 711
EP 724
DI 10.1038/s41388-023-02593-x
EA FEB 2023
PG 14
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 9O3RS
UT WOS:000926056700001
PM 36739364
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Harrold, E
   Keane, F
   Walch, H
   Chou, JF
   Sinopoli, J
   Palladino, S
   Al-Rawi, DH
   Chadalavada, K
   Manca, P
   Chalasani, S
   Yang, J
   Cercek, A
   Shia, J
   Capanu, M
   Bakhoum, SF
   Schultz, N
   Chatila, WK
   Yaeger, R
AF Harrold, Emily
   Keane, Fergus
   Walch, Henry
   Chou, Joanne F.
   Sinopoli, Jenna
   Palladino, Silvia
   Al-Rawi, Duaa H.
   Chadalavada, Kalyani
   Manca, Paolo
   Chalasani, Sree
   Yang, Jessica
   Cercek, Andrea
   Shia, Jinru
   Capanu, Marinela
   Bakhoum, Samuel F.
   Schultz, Nikolaus
   Chatila, Walid K.
   Yaeger, Rona
TI Molecular and Clinical Determinants of Acquired Resistance and Treatment
   Duration for Targeted Therapies in Colorectal Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID ANTI-EGFR THERAPY; COMBINED BRAF; INHIBITION; CETUXIMAB; MUTATION; DNA;
   HETEROGENEITY; CHEMOTHERAPY; PANITUMUMAB; COMBINATION
AB Purpose: Targeted therapies have improved outcomes for patients with metastatic colorectal cancer, but their impact is limited by rapid emergence of resistance. We hypothesized that an understanding of the underlying genetic mechanisms and intrinsic tumor features that mediate resistance to therapy will guide new therapeutic strategies and ultimately allow the prevention of resistance. Experimental Design: We assembled a series of 52 patients with paired pretreatment and progression samples who received therapy targeting EGFR (n = 17), BRAF V600E (n = 17), KRAS G12C (n = 15), or amplified HER2 (n = 3) to identify molecular and clinical factors associated with time on treatment (TOT). Results: All patients stopped treatment for progression and TOT did not vary by oncogenic driver (P = 0.5). Baseline disease burden (>= 3 vs. <3 sites, P = 0.02), the presence of hepatic metastases (P = 0.02), and gene amplification on baseline tissue (P = 0.03) were each associated with shorter TOT. We found evidence of chromosomal instability (CIN) at progression in patients with baseline MAPK pathway amplifications and those with acquired gene amplifications. At resistance, copy-number changes (P = 0.008) and high number (>= 5) of acquired alterations (P = 0.04) were associated with shorter TOT. Patients with hepatic metastases demonstrated both higher number of emergent alterations at resistance and enrichment of mutations involving receptor tyrosine kinases. Conclusions: Our genomic analysis suggests that high baseline CIN or effective induction of enhanced mutagenesis on targeted therapy underlies rapid progression. Longer response appears to result from a progressive acquisition of genomic or chromosomal instability in the underlying cancer or from the chance event of a new resistance alteration.
C1 [Harrold, Emily; Keane, Fergus; Sinopoli, Jenna; Palladino, Silvia; Al-Rawi, Duaa H.; Manca, Paolo; Chalasani, Sree; Yang, Jessica; Cercek, Andrea; Yaeger, Rona] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10065 USA.
   [Walch, Henry; Chou, Joanne F.; Capanu, Marinela; Schultz, Nikolaus; Chatila, Walid K.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol Biostat, New York, NY 10065 USA.
   [Walch, Henry; Schultz, Nikolaus; Chatila, Walid K.] Mem Sloan Kettering Canc Ctr, Marie Josee & Henry R Kravis Ctr Mol Oncol, New York, NY 10065 USA.
   [Chadalavada, Kalyani] Mem Sloan Kettering Canc Ctr, Dept Surg, New York, NY 10065 USA.
   [Chalasani, Sree; Yang, Jessica; Cercek, Andrea; Yaeger, Rona] Weill Cornell Med Coll, Dept Med, New York, NY USA.
   [Shia, Jinru] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10065 USA.
   [Bakhoum, Samuel F.; Schultz, Nikolaus] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10065 USA.
   [Bakhoum, Samuel F.] Mem Sloan Kettering Canc Ctr, Dept Radiat Oncol, New York, NY 10065 USA.
   [Yaeger, Rona] Mem Sloan Kettering Canc Ctr, 300 East 66th St, New York, NY 10065 USA.
C3 Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering Cancer
   Center; Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering
   Cancer Center; Cornell University; Weill Cornell Medicine; Memorial
   Sloan Kettering Cancer Center; Memorial Sloan Kettering Cancer Center;
   Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering Cancer
   Center
RP Yaeger, R (corresponding author), Mem Sloan Kettering Canc Ctr, 300 East 66th St, New York, NY 10065 USA.
EM yaegerr@mskcc.org
RI Schultz, Nikolaus/ABE-6347-2020
OI , Jenna/0000-0003-0167-2792; Al-Rawi, Duaa/0000-0002-9218-6513;
   Chalasani, Sree/0009-0007-2815-8466; Harrold, Emily/0000-0003-1733-7593;
   Manca, Paolo/0000-0002-3813-6339; Walch, Henry/0000-0003-1188-350X; ,
   Kalyani/0000-0001-9097-3989
FU National Institutes of Health (NIH) [R01 CA233736]; NIH [P30 CA008748];
   Cancer Center Core Grant
FX Supported by NIH R01 CA233736 (R. Yaeger) and Cancer Center Core Grant
   P30 CA008748. This research is the responsibility of the authors and
   does not necessarily represent the official views of the NIH. We thank
   the Molecular Cytology core facility and Eric Rosiek for help with
   digital imaging.
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NR 56
TC 2
Z9 2
U1 2
U2 3
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 14
PY 2024
VL 30
IS 12
BP 2672
EP 2683
DI 10.1158/1078-0432.CCR-23-4005
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UI8D1
UT WOS:001247510400002
PM 38502113
OA hybrid
DA 2025-01-04
ER

PT J
AU Ryska, A
AF Ryska, Ales
TI Molecular pathology in real time
SO CANCER AND METASTASIS REVIEWS
LA English
DT Review
DE Tumor heterogeneity; Evolution; Liquid biopsy.; Limitation; Molecular
   pathology; Targeted therapy; Predictive marker; Resistance
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; CIRCULATING TUMOR-CELLS;
   PRIMARY BREAST-CANCER; TYROSINE KINASE INHIBITORS; HER2 GENE
   AMPLIFICATION; MUIR-TORRE-SYNDROME; LYMPH-NODE METASTASES; REGULATORY
   T-CELLS; COLORECTAL-CANCER
AB With the development of sophisticated individualized therapeutic approaches, the role of pathology in classification of tumors is enormously increasing. The solely morphological characterization of neoplastic process is no more sufficient for qualified decision on optimal therapeutic approach. Thus, morphologic diagnosis must be supplemented by molecular analysis of the lesion with emphasis on the detection of status of certain markers used as predictive factors for targeted therapy. Both intrinsic and acquired types of intratumor heterogeneity have an impact at various moments of cancer diagnostics and therapy. The primary heterogeneity of neoplastic tissue represents a significant problem in patients, where only limited biopsy samples from the primary tumor are available for diagnosis, such as core needle biopsy specimens in breast cancer, transthoracic or endobronchial biopsies in lung cancer, or endoscopic biopsies in gastric cancer. Detection of predictive markers may be influenced by this heterogeneity, and the marker detection may be falsely negative or (less probably) falsely positive. In addition, as these markers are often detected in the tissue samples from primary tumor, the differences between molecular features of the primary lesion and its metastases may be responsible for failure of systemic therapy in patients with discordant phenotype between primary and metastatic disease. The fact of tumor heterogeneity must be taken into consideration already in establishing pathological diagnosis. One has to be aware that limited biopsy specimen must not always be fully representative of the entire tumor volume. To overcome these limitations, there does not exist one single simple solution. Examination of more tissue (preference of surgical resection specimens over biopsies, whenever possible), use of ultra-sensitive methods able to identify the minute subclones as a source of possible resistance to treatment, and detection of secondary molecular events from the circulating tumor cells or circulating cell-free DNA are potential solutions how to handle this issue.
C1 [Ryska, Ales] Charles Univ Prague, Med Fac Hosp, Fingerland Dept Pathol, Hradec Kralove 50005, Czech Republic.
C3 Charles University Prague; University Hospital Hradec Kralove
RP Ryska, A (corresponding author), Charles Univ Prague, Med Fac Hosp, Fingerland Dept Pathol, Hradec Kralove 50005, Czech Republic.
EM ryskaale@gmail.com
RI Ryska, Ales/L-9671-2017
OI Ryska, Ales/0000-0002-3051-2280
FU program PRVOUK [P37/11]; Czech Ministry of Health IGA [NT14150-3/2013]; 
   [LM2010004]
FX This study was supported by the program PRVOUK P37/11, by the project
   LM2010004, and by grant of the Czech Ministry of Health IGA No.
   NT14150-3/2013.
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NR 112
TC 9
Z9 11
U1 0
U2 13
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 MAR
PY 2016
VL 35
IS 1
BP 129
EP 140
DI 10.1007/s10555-016-9607-3
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DI6YE
UT WOS:000373645300011
PM 26931654
DA 2025-01-04
ER

PT J
AU Gurzu, S
   Silveanu, C
   Fetyko, A
   Butiurca, V
   Kovacs, Z
   Jung, I
AF Gurzu, Simona
   Silveanu, Camelia
   Fetyko, Annamaria
   Butiurca, Vlad
   Kovacs, Zsolt
   Jung, Ioan
TI Systematic review of the old and new concepts in the
   epithelial-mesenchymal transition of colorectal cancer
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Angiogenesis; Colorectal cancer; Budding; Epithelial-mesenchymal
   transition; Chemoresistance
ID COLON-CANCER; BETA-CATENIN; E-CADHERIN; PROGNOSTIC PARAMETER; CELLULAR
   SENESCENCE; DOWN-REGULATION; POOR SURVIVAL; GROWTH-FACTOR; CELLS;
   EXPRESSION
AB Epithelial-to-mesenchymal transition (EMT) is defined as the transformation of an epithelial cell into a spindle cell with the loss of membrane E-cadherin expression and the gain of mesenchymal markers positivity. In the field of colorectal cancer (CRC), first data about EMT was published in 1995 and more than 400 papers had been written up to March 2016. Most of them are focused on the molecular pathways and experimentally-proved chemoresistance. In the present article, an update in the field of EMT in CRC based on the review of the literature and personal experience of the authors is presented. The information about the molecular and immunohistochemical (IHC) particularities of these processes and their possible role in the prognosis of CRC were also up-dated. This article focuses on the IHC quantification of the EMT, the immunoprofile of tumor buds and on the relation between EMT, angiogenesis, and stem cells activation. The EMT-induced chemoresistance vs chemotherapy- or radiotherapy-induced EMT and cellular senescence was also synthesized for both conventional and targeted therapy. As a future perspective, the EMT-angiogenesis-stemness link could be used as a possible valuable parameter for clinical follow-up and targeted therapeutic oncologic management of patients with CRC. Association of dexamethasone and angiotensin converting enzyme inhibitors combined with conventional chemotherapies could have clinical benefits in patients with CRC. The main conclusion is that, although many studies have been published, the EMT features are still incompletely elucidated and newly discovered EMT markers provide confusing data in understanding this complicated process, which might have significant clinical impact.
C1 [Gurzu, Simona; Silveanu, Camelia; Fetyko, Annamaria; Jung, Ioan] Univ Med & Pharm Tirgu Mures, Dept Pathol, Targu Mures 540139, Romania.
   [Butiurca, Vlad] Univ Med & Pharm Tirgu Mures, Dept Surg, Targu Mures 540139, Romania.
   [Kovacs, Zsolt] Univ Med & Pharm Tirgu Mures, Dept Biochem & Genet, Targu Mures 540139, Romania.
C3 George Emil Palade University of Medicine, Pharmacy, Science, &
   Technology of Targu Mures; George Emil Palade University of Medicine,
   Pharmacy, Science, & Technology of Targu Mures; George Emil Palade
   University of Medicine, Pharmacy, Science, & Technology of Targu Mures
RP Gurzu, S (corresponding author), Univ Med & Pharm, Res Ctr, Dept Pathol, 38 Ghe Marinescu, Targu Mures 540139, Romania.
EM simonagurzu@yahoo.com
RI GURZU, SIMONA/AAD-2710-2019; KOVACS, ZSOLT/P-2666-2017; Butiurca,
   Vlad-Olimpiu/B-3859-2018
OI gurzu, simona/0000-0003-3968-5118; KOVACS, ZSOLT/0000-0002-1038-7769;
   Butiurca, Vlad-Olimpiu/0000-0002-9900-5375
FU University of Medicine and Pharmacy of Tirgu-Mures, Romania
   [UMFTGM-PO-CC-02-F01, 19/2014]
FX Supported by University of Medicine and Pharmacy of Tirgu-Mures,
   Romania, Team Research Projects Frame: UMFTGM-PO-CC-02-F01, No. 19/2014.
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NR 74
TC 85
Z9 89
U1 0
U2 26
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 AUG 14
PY 2016
VL 22
IS 30
BP 6764
EP 6775
DI 10.3748/wjg.v22.i30.6764
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DS4SC
UT WOS:000380770400002
PM 27570416
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Zheng, NX
   Wang, H
   Yu, Q
   Wang, C
   Bai, CG
   Pan, AF
   Jiang, JJ
   Lu, J
   Dai, SM
   Mei, ZB
   Zhang, W
   Gao, XH
AF Zheng, Nanxin
   Wang, Hao
   Yu, Qing
   Wang, Chen
   Bai, Chen Guang
   Pan, An Fu
   Jiang, Jianjun
   Lu, Jian
   Dai, Si Min
   Mei, Zubing
   Zhang, Wei
   Gao, Xian Hua
TI Changing trends, clinicopathological characteristics, surgical treatment
   patterns, and prognosis of schistosomiasis-associated versus
   non-schistosomiasis-associated colorectal cancer: a large retrospective
   cohort study of 31 153 cases in Shanghai, China (2001-2021)
SO INTERNATIONAL JOURNAL OF SURGERY
LA English
DT Article
DE clinicopathological features; cohort study; comparative study;
   prognosis; schistosomiasis-associated colorectal cancer; trends
ID JAPONICUM; CARCINOMA
AB Background:With the elimination of schistosomiasis in China, its role in the pathogenesis of colorectal cancer (CRC) has decreased. However, the trends, clinicopathological features, surgical treatment patterns, and prognosis of schistosomiasis-associated CRC (SACRC) versus non-schistosomiasis-associated CRC (NSACRC) in China remain unclear. Materials and methods:The percentage trend of SACRC in CRC patients in China was analyzed using data retrieved from the Pathology Registry of Changhai Hospital (2001-2021). Clinicopathological characteristics, surgical treatment patterns, and prognosis-related parameters were compared between the two groups. Multivariate Cox regression analyses were performed for disease-free survival (DFS) and overall survival (OS). Results:A total of 31 153 CRC cases were included, with 823 (2.6%) cases of SACRC and 30 330 (97.4%) cases of NSACRC. The average percentage of SACRC cases has decreased continuously from 3.8 to 1.7% (from 2001 to 2021). Compared with the NSACRC group, the SACRC group had more men, older age at diagnosis, lower BMI, fewer symptoms; higher rates of rectal cancer, comorbidities, KRAS mutation, multiple primary CRC and concomitant polyps; less lymph node metastasis, distant metastasis, vascular invasion, and tumor budding; less preoperative radiotherapy and preoperative chemotherapy; and more positive resection margins and postoperative targeted therapy. There were no significant differences between the two groups regarding laparoscopic surgery, palliative resection, extended radical resection, or ostomy. Moreover, the SACRC group had adverse DFS and similar OS compared with the NSACRC group. In multivariate analyses, schistosomiasis was not an independent predictor of DFS or OS. Conclusion:The percentage of SACRC in CRC (2.6%) in our hospital was very low, and it decreased continuously over the last two decades, indicating that schistosomiasis is no longer an important risk factor for CRC in Shanghai, China. Patients with SACRC have distinct clinicopathological, molecular, and treatment-related features and survival rates similar to those with NSACRC.
C1 [Zheng, Nanxin; Wang, Hao; Wang, Chen; Pan, An Fu; Zhang, Wei; Gao, Xian Hua] Naval Med Univ, Changhai Hosp, Dept Colorectal Surg, Shanghai, Peoples R China.
   [Zheng, Nanxin; Wang, Hao; Wang, Chen; Zhang, Wei; Gao, Xian Hua] Changhai Hosp, Hereditary Colorectal Canc Ctr, Ctr Familial Canc, Shanghai, Peoples R China.
   [Zheng, Nanxin; Wang, Hao; Wang, Chen; Zhang, Wei; Gao, Xian Hua] Changhai Hosp, Genet Block Ctr Familial Canc, Shanghai, Peoples R China.
   [Yu, Qing; Dai, Si Min] Shanghai Municipal Ctr Dis Control & Prevent, Dept Parasit Dis, Shanghai, Peoples R China.
   [Bai, Chen Guang] Naval Med Univ, Changhai Hosp, Dept Pathol, Shanghai, Peoples R China.
   [Jiang, Jianjun; Lu, Jian] Kongjiang Hosp, Dept Anorectal Surg, Shanghai, Peoples R China.
   [Mei, Zubing] Shanghai Univ Tradit Chinese Med, Dept Anorectal Surg, Shuguang Hosp, Shanghai, Peoples R China.
   [Mei, Zubing] Anorectal Dis Inst Shuguang Hosp, Shanghai, Peoples R China.
   [Zhang, Wei; Gao, Xian Hua] Changhai Hosp, Dept Colorectal Surg, 168 Changhai Rd, Shanghai 200433, Peoples R China.
   [Mei, Zubing] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Anorectal Dis Inst Shuguang Hosp, Dept Anorectal Surg, 528 Zhangheng Rd, Shanghai 201203, Peoples R China.
C3 Naval Medical University; Naval Medical University; Naval Medical
   University; Shanghai Center for Disease Control & Prevention; Naval
   Medical University; Shanghai University of Traditional Chinese Medicine;
   Naval Medical University; Shanghai University of Traditional Chinese
   Medicine
RP Zhang, W; Gao, XH (corresponding author), Changhai Hosp, Dept Colorectal Surg, 168 Changhai Rd, Shanghai 200433, Peoples R China.; Mei, ZB (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Anorectal Dis Inst Shuguang Hosp, Dept Anorectal Surg, 528 Zhangheng Rd, Shanghai 201203, Peoples R China.
EM nanxin_zheng@163.com; wanghaohh@vip.126.com; yuqing_1@scdc.sh.cn;
   1291339217@qq.com; bcg709@126.com; 1265306963@qq.com;
   jiangjj06@vip.qq.com; 13601744929@163.com; daisimin@scdc.sh.cn;
   herrmayor@126.com; weizhang2000cn@163.com; gxh505@126.com
RI Gao, Xian Hua/HJA-0052-2022; Mei, Zubing/H-7879-2019; Yu,
   Qing/KIG-5023-2024
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NR 37
TC 1
Z9 1
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1743-9191
EI 1743-9159
J9 INT J SURG
JI Int. J. Surg.
PD APR
PY 2023
VL 109
IS 4
BP 772
EP 784
DI 10.1097/JS9.0000000000000293
PG 13
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA H9YF4
UT WOS:000999427500014
PM 36999800
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Park, YS
   Kim, J
   Ryu, YS
   Moon, JH
   Shin, YJ
   Kim, JH
   Hong, SW
   Jung, SA
   Lee, S
   Kim, SM
   Lee, DH
   Kim, DY
   Yun, H
   You, JE
   Yoon, DI
   Kim, CH
   Koh, DI
   Jin, DH
AF Park, Yoon Sun
   Kim, Joseph
   Ryu, Yea Seong
   Moon, Jai-Hee
   Shin, Yu Jin
   Kim, Jeong Hee
   Hong, Seung-Woo
   Jung, Soo-A
   Lee, Seul
   Kim, Seung-Mi
   Lee, Dae Hee
   Kim, Do Yeon
   Yun, Hyeseon
   You, Ji-Eun
   Yoon, Dong Il
   Kim, Chul Hee
   Koh, Dong-In
   Jin, Dong-Hoon
TI Mutant PIK3CA as a negative predictive biomarker for treatment with a
   highly selective PIM1 inhibitor in human colon cancer
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE PIM1; PIK3CA; mutant KRAS; colorectal cancer; predictive marker
ID SERINE/THREONINE KINASE-ACTIVITY; I PI3 KINASE; REGULATES GLYCOLYSIS;
   ACQUIRED-RESISTANCE; TUMOR-GROWTH; OPEN-LABEL; THERAPY; PATHWAY;
   IDENTIFICATION; POTENT
AB Significant improvement in targeted therapy for colorectal cancer (CRC) has occurred over the past few decades since the approval of the EGFR inhibitor cetuximab. However, cetuximab is used only for patients possessing the wild-type oncogene KRAS, NRAS, and BRAF, and even most of these eventually acquire therapeutic resistance, via activation of parallel oncogenic pathways such as RAS-MAPK or PI3K/Akt/mTOR. The two aforementioned pathways also contribute to the development of therapeutic resistance in CRC patients, due to compensatory and feedback mechanisms. Therefore, combination drug therapies (versus monotherapy) targeting these multiple pathways may be necessary for further efficacy against CRC. In this study, we identified PIK3CA mutant (PIK3CA MT) as a determinant of resistance to SMI-4a, a highly selective PIM1 kinase inhibitor, in CRC cell lines. In CRC cell lines, SMI-4a showed its effect only in PIK3CA wild type (PIK3CA WT) cell lines, while PIK3CA MT cells did not respond to SMI-4a in cell death assays. In vivo xenograft and PDX experiments confirmed that PIK3CA MT is responsible for the resistance to SMI-4a. Inhibition of PIK3CA MT by PI3K inhibitors restored SMI-4a sensitivity in PIK3CA MT CRC cell lines. Taken together, these results demonstrate that sensitivity to SMI-4a is determined by the PIK3CA genotype and that co-targeting of PI3K and PIM1 in PIK3CA MT CRC patients could be a promising and novel therapeutic approach for refractory CRC patients.
C1 [Park, Yoon Sun; Kim, Joseph; Ryu, Yea Seong; Moon, Jai-Hee; Shin, Yu Jin; Kim, Jeong Hee; Hong, Seung-Woo; Jung, Soo-A; Lee, Seul; Kim, Seung-Mi; Lee, Dae Hee; Kim, Do Yeon; Yun, Hyeseon; You, Ji-Eun; Yoon, Dong Il; Kim, Chul Hee; Koh, Dong-In] Asan Med Ctr, Asan Inst Life Sci, Seoul, South Korea.
   [Park, Yoon Sun; Kim, Joseph; Kim, Do Yeon; Yun, Hyeseon; You, Ji-Eun; Yoon, Dong Il; Kim, Chul Hee] Univ Ulsan, Asan Med Inst Convergence Sci & Technol, Asan Med Ctr, Dept Med Sci,Coll Med, Seoul, South Korea.
   [Jin, Dong-Hoon] Univ Ulsan, Dept Pharmacol, Coll Med, Seoul, South Korea.
   [Jin, Dong-Hoon] Asan Med Ctr, Asan Inst Life Sci, Dept Convergence Med, Seoul, South Korea.
C3 University of Ulsan; Asan Medical Center; University of Ulsan; Asan
   Medical Center; University of Ulsan; University of Ulsan; Asan Medical
   Center
RP Jin, DH (corresponding author), Asan Med Ctr, Asan Inst Life Sci, Dept Convergence Med, Seoul, South Korea.
EM inno183@amc.seoul.kr
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   DAE-HEE/O-5243-2018
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NR 59
TC 1
Z9 1
U1 3
U2 9
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4047
EI 1555-8576
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD DEC 31
PY 2023
VL 24
IS 1
AR 2246208
DI 10.1080/15384047.2023.2246208
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA Q0RI1
UT WOS:001054669300001
PM 37621144
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Adamowicz, K
   Baczkowska-Waliszewska, Z
AF Adamowicz, Krzysztof
   Baczkowska-Waliszewska, Zuzanna
TI Prognostic Value of Knowledge of Cancer and Used Unconventional Therapy
   Methods on Quality of Life in Advanced, Metastatic Colorectal Cancer in
   Clinical Practice
SO JOURNAL OF CANCER EDUCATION
LA English
DT Article
DE Colorectal cancer; Chemotherapy; Treatment outcomes; Quality of life;
   Knowledge of cancer
ID RANDOMIZED PHASE-III; 1ST-LINE TREATMENT; FLUOROURACIL; LEUCOVORIN;
   FOLFIRI
AB Colorectal cancer (CRC) is the third most common malignancy in the world and the second cause of cancer-related deaths. Despite the search for new therapeutic agents, there are still many doubts concerning the quality of life (QOL) improvement in palliative patients. In this study, we assessed the impact of oncology knowledge on QOL and the relationship between QOL and various environmental factors and unconventional treatment methods in patients with CRC treated with chemotherapy and targeted therapy. The results of first-line palliative chemotherapy in 330 patients with colorectal cancer treated between January 2010 and December 2016 in two centers were analyzed. The average age of patients was 66 +/- 11.7 years. Median survival time was 25 months. In multivariate analysis, the performance status and response to treatment had a significant effect on survival time. A trend towards shorter survival was also observed in patients receiving 5-FU monotherapy, in elderly patients and in patients with less oncology knowledge. A relationship between general quality of life and performance status (PS 0 vs. PS > 0), response to treatment and oncology knowledge was found. Patients with limited oncology knowledge more often used unconventional therapy methods in parallel with the treatment. In patients over 70 years of age and in patients with worse overall condition, 5-FU monotherapy was more commonly used (p < 0.01). The level of oncology knowledge of the treated patients observed in everyday clinical practice may be related to some parameters of treatment effectiveness assessment, such as QOL and may be related to the use of unconventional treatment methods. Those, in turn may have an impact on the QOL of the treated patients.
C1 [Adamowicz, Krzysztof] Reg Oncol Ctr, Gdansk, Poland.
   [Adamowicz, Krzysztof] Reg Hosp Wejherowo, Pomeranian Hosp, Dept Oncol, Wejherowo, Poland.
   [Baczkowska-Waliszewska, Zuzanna] 7th Naval Hosp, Gdansk, Poland.
RP Adamowicz, K (corresponding author), Reg Oncol Ctr, Gdansk, Poland.; Adamowicz, K (corresponding author), Reg Hosp Wejherowo, Pomeranian Hosp, Dept Oncol, Wejherowo, Poland.
EM krzys.adamowicz@gmail.com
OI Baczkowska-Waliszewska, Zuzanna/0000-0002-1303-1506
CR Adamowicz K, 2011, J ONCOLOGY, V61, P449
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NR 17
TC 2
Z9 2
U1 1
U2 3
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0885-8195
EI 1543-0154
J9 J CANCER EDUC
JI J. Cancer Educ.
PD FEB
PY 2020
VL 35
IS 1
BP 151
EP 158
DI 10.1007/s13187-018-1454-1
PG 8
WC Oncology; Education, Scientific Disciplines; Public, Environmental &
   Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Education & Educational Research; Public, Environmental &
   Occupational Health
GA KJ2XQ
UT WOS:000511921700021
PM 30523599
DA 2025-01-04
ER

PT J
AU Orlov-Slavu, C
   Parosanu, A
   Olaru, M
   Serban, D
   Paunica, I
   Nitipir, C
AF Orlov-Slavu, Cristina
   Parosanu, Andreea
   Olaru, Mihaela
   Serban, Dragos
   Paunica, Ioana
   Nitipir, Cornelia
TI How opportune is multigene testing in metastatic colorectal cancer? A
   review
SO JOURNAL OF MIND AND MEDICAL SCIENCES
LA English
DT Article
DE multigene assay; metastatic; colorectal cancer; targeted therapy
ID 1ST-LINE TREATMENT; RAS MUTATIONS; COLON-CANCER; TUMOR; BRAF;
   FLUOROURACIL; LEUCOVORIN; INHIBITION; IRINOTECAN; SURVIVAL
AB Personalized treatment in oncology is the most innovative method of care. The best method to establish personalized treatment is by genetic characterization of the malignant cell.
   Theoretically, the more detailed the characterization, the more effective the choice of treatment becomes. Currently, there are fast and relatively low-cost options that allow such genetic characterization. However, test results sometimes do not detect targetable alterations and, even if they do detect, the use of the treatment-alteration combination does not always generate a satisfactory oncological response.
   The present paper aims to answer two questions. First, how targetable can the most common gene alterations in colorectal cancer be. Second, whether it makes sense to use broad molecular testing as a standard in all metastatic patients.
C1 [Orlov-Slavu, Cristina; Parosanu, Andreea; Olaru, Mihaela; Nitipir, Cornelia] Carol Davila Univ Med & Pharm, Fac Gen Med, Dept Oncol, Bucharest, Romania.
   [Orlov-Slavu, Cristina; Parosanu, Andreea; Olaru, Mihaela; Nitipir, Cornelia] Elias Univ Emergency Hosp, Dept Med Oncol, Bucharest, Romania.
   [Serban, Dragos] Carol Davila Univ Med & Pharm, Emergency Univ Hosp Bucharest, Dept Surg 4, Bucharest, Romania.
   [Paunica, Ioana] Carol Davila Univ Med & Pharm, Fac Gen Med, Bucharest, Romania.
C3 Carol Davila University of Medicine & Pharmacy; Carol Davila University
   of Medicine & Pharmacy; Carol Davila University of Medicine & Pharmacy
RP Parosanu, A (corresponding author), Carol Davila Univ Med & Pharm, Fac Gen Med, Dept Oncol, Bucharest, Romania.
EM aparosanu@yahoo.com
RI SERBAN, DRAGOS/AAD-5874-2020; OLARU, CRISTINA/AAM-3495-2021
CR Alecu L, 2015, CHIRURGIA-BUCHAREST, V110, P525
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NR 42
TC 6
Z9 6
U1 0
U2 1
PU VALPOSCHOLAR-VALPRAISO UNIV
PI BUCHAREST
PA STRADA DIONISE LUPU 37, BUCHAREST, 70183, ROMANIA
SN 2392-7674
J9 J MIND MED SCI
JI J. Mind Med. Sci.
PY 2021
VL 8
IS 2
AR 7
DI 10.22543/7674.82.P215220
PG 8
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA WG7SS
UT WOS:000707195500008
OA gold
DA 2025-01-04
ER

PT J
AU Patel, AK
   Singh, S
AF Patel, Ankit Kumar
   Singh, Sandeep
TI Cancer associated fibroblasts: phenotypic and functional heterogeneity
SO FRONTIERS IN BIOSCIENCE-LANDMARK
LA English
DT Article
DE Cancer Associated Fibroblasts; Tumor Microenvironment; alpha-Smooth
   muscle actin; Cancer Stem Cells; Heterogeneity; metastasis; Review
ID CARCINOMA-ASSOCIATED FIBROBLASTS; ENDOTHELIAL-CELLS; STROMAL
   FIBROBLASTS; COLON-CANCER; STEM-CELLS; MATRIX METALLOPROTEINASES;
   MOLECULAR CLASSIFICATION; TUMOR MICROENVIRONMENT; GENETIC ALTERATIONS;
   GRANULATION-TISSUE
AB Cancer associated fibroblasts (CAFs) are the most abundant stromal cell-type in solid tumor-microenvironment (TME) and have emerged as key player in tumor progression. CAFs establish communication with cancer cells through paracrine mechanisms or via direct cell adhesion as well as influence the cancer cell behaviour indirectly by remodelling the extracellular matrix. Although numerous studies have strongly suggested the tumor promoting role of CAFs, few recent reports have revealed the heterogeneity in CAFs. Here, we have summarized the recent findings on the mechanisms related to the heterogeneous behaviour of CAFs serving as positive or negative regulator of tumor progression. Further, reports related to the targeted therapy against CAF-mediated mechanisms are also summarized briefly.
C1 [Patel, Ankit Kumar; Singh, Sandeep] Natl Inst Biomed Genom, Kalyani 741251, W Bengal, India.
C3 Department of Biotechnology (DBT) India; National Institute of
   Biomedical Genomics (NIBMG)
RP Singh, S (corresponding author), Natl Inst Biomed Genom, Kalyani 741251, W Bengal, India.
EM ss5@nibmg.ac.in
RI Patel, Ankit/ABB-4196-2021
OI Patel, Ankit Kmar/0000-0003-0150-2769; Singh,
   Sandeep/0000-0002-2589-4835
FU Wellcome Trust-DBT India Alliance [IA/I/13/1/500908]; NIBMG; ICMR, India
FX This work was supported by the grant received from Wellcome Trust-DBT
   India Alliance (#IA/I/13/1/500908) and NIBMG-intramural grant. AKP thank
   ICMR, India for fellowship support.
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NR 98
TC 19
Z9 20
U1 0
U2 5
PU FRONTIERS IN BIOSCIENCE INC
PI IRVINE
PA 16471 SCIENTIFIC WAY, IRVINE, CA 92618 USA
SN 1093-9946
EI 1093-4715
J9 FRONT BIOSCI-LANDMRK
JI Front. Biosci.
PD MAR 1
PY 2020
VL 25
BP 961
EP 978
AR PMID 32114420
DI 10.2741/4843
PG 18
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA NG7EV
UT WOS:000564144300002
PM 32114420
OA Bronze
DA 2025-01-04
ER

PT J
AU Duta-Ion, SG
   Juganaru, IR
   Hotinceanu, IA
   Dan, A
   Burtavel, LM
   Coman, MC
   Focsa, IO
   Zaruha, AG
   Codreanu, PC
   Bohiltea, LC
   Radoi, VE
AF Duta-Ion, Simona Gabriela
   Juganaru, Ioana Ruxandra
   Hotinceanu, Iulian Andrei
   Dan, Andra
   Burtavel, Livia Malina
   Coman, Madalin Codrut
   Focsa, Ina Ofelia
   Zaruha, Andra Giorgiana
   Codreanu, Patricia Christina
   Bohiltea, Laurentiu Camil
   Radoi, Viorica Elena
TI Redefining Therapeutic Approaches in Colorectal Cancer: Targeting
   Molecular Pathways and Overcoming Resistance
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colon cancer; targeted therapy; immunotherapy; BRAF mutations; MSI/dMMR;
   PI3K/AKT/mTOR pathway; KRAS mutations; APC pathway
ID ADVANCED SOLID TUMORS; CAR-T-CELLS; PREDICTIVE BIOMARKERS; COLON-CANCER;
   INHIBITOR; MUTATIONS; KRAS; ATR; ACTIVATION; STRATEGIES
AB Colorectal cancer (CRC) arises through a combination of genetic and epigenetic alterations that affect key pathways involved in tumor growth and progression. This review examines the major molecular pathways driving CRC, including Chromosomal Instability (CIN), Microsatellite Instability (MSI), and the CpG Island Methylator Phenotype (CIMP). Key mutations in genes such as APC, KRAS, NRAS, BRAF, and TP53 activate signaling pathways like Wnt, EGFR, and PI3K/AKT, contributing to tumorigenesis and influencing responses to targeted therapies. Resistance mechanisms, including mutations that bypass drug action, remain challenging in CRC treatment. This review highlights the role of molecular profiling in guiding the use of targeted therapies such as tyrosine kinase inhibitors and immune checkpoint inhibitors. Novel combination treatments are also discussed as strategies to improve outcomes and overcome resistance. Understanding these molecular mechanisms is critical to advancing personalized treatment approaches in CRC and improving patient prognosis.
C1 [Duta-Ion, Simona Gabriela; Juganaru, Ioana Ruxandra; Hotinceanu, Iulian Andrei; Dan, Andra; Burtavel, Livia Malina; Coman, Madalin Codrut; Focsa, Ina Ofelia; Zaruha, Andra Giorgiana; Codreanu, Patricia Christina; Bohiltea, Laurentiu Camil; Radoi, Viorica Elena] Carol Davila Univ Med & Pharm, Dept Med Genet, Bucharest 020021, Romania.
   [Bohiltea, Laurentiu Camil; Radoi, Viorica Elena] Alessandrescu Rusescu Natl Inst Maternal & Child H, Bucharest 20382, Romania.
C3 Carol Davila University of Medicine & Pharmacy
RP Juganaru, IR (corresponding author), Carol Davila Univ Med & Pharm, Dept Med Genet, Bucharest 020021, Romania.
EM simona-gabriela.duta@rez.umfcd.ro; ioana-ruxandra.calapod@rez.umfcd.ro;
   iulian.hotinceanu@s.unibuc.ro; andra.dan@rez.umfcd.ro;
   livia-malina.burtavel@rez.umfcd.ro; madalin-codrut.coman@rez.umfcd.ro;
   ina.focsa@umfcd.ro; andra-giorgiana.zaruha@rez.umfcd.ro;
   patricia-christina.codreanu@rez.umfcd.ro; laurentiu.bohiltea@umfcd.ro;
   viorica.radoi@umfcd.ro
FU The "Carol Davila" University of Medicine and Pharmacy
FX The publication of this paper was supported by "Carol Davila" University
   of Medicine and Pharmacy, through the institutional program Publish not
   Perish.
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TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD DEC
PY 2024
VL 25
IS 23
AR 12507
DI 10.3390/ijms252312507
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA P2P9Q
UT WOS:001376406300001
PM 39684219
OA gold
DA 2025-01-04
ER

PT J
AU Lubner, SJ
   Uboha, NV
   Deming, DA
AF Lubner, Sam J.
   Uboha, Nataliya V.
   Deming, Dustin A.
TI Primary and acquired resistance to biologic therapies in
   gastrointestinal cancers
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Targeted therapy; resistance; gastrointestinal cancers
ID METASTATIC COLORECTAL-CANCER; ADVANCED GASTRIC-CANCER; RECEPTOR ANTIBODY
   THERAPY; INHIBITOR TRAMETINIB T; GROWTH-FACTOR-D; COLON-CANCER; 1ST-LINE
   TREATMENT; DOUBLE-BLIND; PHASE-II; TRASTUZUMAB-RESISTANT
AB Improvements in the understanding of cancer biology have led to therapeutic advances in the treatment of gastrointestinal cancers. Drugs which target the vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR) pathways have led the way in colon cancer. Monoclonal antibodies (mAbs) such as bevacizumab, ramucirumab, cetuximab, and panitumumab, have improved progression free survival and overall survival (OS) for colorectal cancers and were quickly adopted. Human epidermal growth factor receptor 2 (HER2) has demonstrated significant benefit for gastroesophageal cancers and in the setting of HER2 amplification, trastuzumab in combination with chemotherapy has become the standard of care. However, responses have not been as durable nor as robust as once hoped. Mechanisms of resistance for each of these biologic compounds have been hypothesized and are in the process of being better elucidated. This review will approach the innate and acquired mechanisms of resistance of the above compounds. Additionally, we will explore some ongoing clinical trials to capitalize on the mechanisms of resistance in the hopes of retaining the promise of targeting these pathways.
C1 [Lubner, Sam J.; Uboha, Nataliya V.; Deming, Dustin A.] Univ Wisconsin, Dept Med, Carbone Canc Ctr, Hematol Oncol Sect, K4-528 CSC,600 Highland Ave, Madison, WI 53792 USA.
C3 University of Wisconsin System; University of Wisconsin Madison
RP Lubner, SJ (corresponding author), Univ Wisconsin, Dept Med, Carbone Canc Ctr, Hematol Oncol Sect, K4-528 CSC,600 Highland Ave, Madison, WI 53792 USA.
EM sjlubner@medicine.wisc.edu
OI Lubner, Sam/0000-0002-5732-2938
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EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD JUN
PY 2017
VL 8
IS 3
BP 499
EP 512
DI 10.21037/jgo.2017.01.16
PG 14
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA FB4US
UT WOS:000406137900015
PM 28736637
OA Green Published
DA 2025-01-04
ER

PT J
AU Mihai, MM
   Ion, A
   Giurcaneanu, C
   Nitipir, C
   Popa, AM
   Chifiriuc, MC
   Popa, MI
   Ricar, J
   Popa, LG
   Sârbu, I
   Lazar, V
AF Mihai, Mara Madalina
   Ion, Ana
   Giurcaneanu, Calin
   Nitipir, Cornelia
   Popa, Ana-Maria
   Chifiriuc, Mariana-Carmen
   Popa, Mircea Ioan
   Ricar, Jan
   Popa, Liliana Gabriela
   Sarbu, Ionela
   Lazar, Veronica
TI The Impact of Long-Term Antibiotic Therapy of Cutaneous Adverse
   Reactions to EGFR Inhibitors in Colorectal Cancer Patients
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE gut microbiome dysbiosis; Fusobacterium nucleatum; metastatic colorectal
   cancer; EGFR inhibitors; tetracyclines; papulo-pustular rash; acneiform
   rash; long-term antibiotic therapy
ID GROWTH-FACTOR RECEPTOR; CETUXIMAB PLUS IRINOTECAN; QUALITY-OF-LIFE;
   PHASE-II TRIAL; FUSOBACTERIUM-NUCLEATUM; SKIN TOXICITY; COLON-CANCER;
   1ST-LINE TREATMENT; RANDOMIZED-TRIAL; ORAL MINOCYCLINE
AB Colorectal cancer (CRC) is an important public health issue, in terms of incidence and mortality, with approximately 1.8 million new cases reported worldwide in 2018. Advancements in understanding pathophysiological key steps in CRC tumorigenesis have led to the development of new targeted therapies such as those based on epidermal growth factor receptor inhibitors (EGFR inhibitors). The cutaneous adverse reactions induced by EGFR inhibitors, particularly papulopustular rash, often require long-term antibiotic treatment with tetracycline agents (mostly minocycline and doxycycline). However, this raises several issues of concern: possible occurrence of gut dysbiosis in already vulnerable CRC patients, selection of highly antibiotic resistant and/or virulent clones, development of adverse reactions related to tetracyclines, interference of antibiotics with the response to oncologic therapy, with a negative impact on disease prognosis etc. In the context of scarce information regarding these issues and controversial opinions regarding the role of tetracyclines in patients under EGFR inhibitors, our aim was to perform a thorough literature review and discuss the main challenges raised by long-term use of tetracyclines in advanced CRC patients receiving this targeted therapy.
C1 [Mihai, Mara Madalina; Giurcaneanu, Calin; Popa, Liliana Gabriela] Carol Davila Univ Med & Pharm, Elias Emergency Univ Hosp, Dept Oncol Dermatol, Bucharest 020021, Romania.
   [Mihai, Mara Madalina; Ion, Ana; Giurcaneanu, Calin; Popa, Liliana Gabriela] Elias Emergency Univ Hosp, Dept Dermatol, Bucharest 011461, Romania.
   [Mihai, Mara Madalina; Chifiriuc, Mariana-Carmen; Lazar, Veronica] Univ Bucharest, Fac Biol, Dept Microbiol, ICUB Res Inst, Bucharest 050657, Romania.
   [Nitipir, Cornelia; Popa, Ana-Maria] Carol Davila Univ Med & Pharm, Elias Emergency Univ Hosp, Dept Oncol, Bucharest 020021, Romania.
   [Popa, Mircea Ioan] Carol Davila Univ Med & Pharm, Fac Med, Dept Microbiol, Bucharest 020021, Romania.
   [Ricar, Jan] Charles Univ Prague, Med Sch & Teaching Hosp Pilsen, Dept Dermatol & Venereol, Plzen 30599, Czech Republic.
   [Sarbu, Ionela] Univ Bucharest, Fac Biol, Dept Genet, ICUB Res Inst, Bucharest 050657, Romania.
C3 Carol Davila University of Medicine & Pharmacy; University of Bucharest;
   Carol Davila University of Medicine & Pharmacy; Carol Davila University
   of Medicine & Pharmacy; Charles University Prague; University of
   Bucharest
RP Mihai, MM (corresponding author), Carol Davila Univ Med & Pharm, Elias Emergency Univ Hosp, Dept Oncol Dermatol, Bucharest 020021, Romania.; Mihai, MM; Ion, A (corresponding author), Elias Emergency Univ Hosp, Dept Dermatol, Bucharest 011461, Romania.; Mihai, MM (corresponding author), Univ Bucharest, Fac Biol, Dept Microbiol, ICUB Res Inst, Bucharest 050657, Romania.
EM mara.mihai@umfcd.ro; anaion00@yahoo.com; calin.giurcaneanu@gmail.com;
   cornelia.nitipir@umfcd.ro; ana-maria.popa@umfcd.ro;
   carmen.chifiriuc@bio.unibuc.ro; mircea.ioan.popa@umfcd.ro;
   ricarj@fnplzen.cz; liliana.popa@umfcd.ro; ionela24avram@yahoo.com;
   veronica.lazar2009@gmail.com
RI Ricar, Jan/JKJ-1688-2023; Popa, Liliana/IWD-6082-2023; POPA,
   ANA/AAL-3244-2021; Chifiriuc, Mariana/AFP-0825-2022; Mihai,
   Mara/K-1349-2014; Popa, Mircea Ioan/A-4830-2011; Avram,
   Ionela/A-2891-2014
OI Popa, Liliana Gabriela/0000-0002-1702-7280; Ion,
   Ana/0000-0002-4214-4446; Popa, Mircea Ioan/0000-0002-0794-9329;
   Chifiriuc, Mariana Carmen/0000-0001-6098-1857; Mihai,
   Mara/0000-0002-1436-0088; Lazar, Veronica/0009-0000-3754-4288; Avram,
   Ionela/0000-0002-9171-0846
FU Ministry of Research, Innovation and Digitization, CNCS/CCCDI-UEFISCDI
   [PN-III-P1-1.1-PD-2019-1225]
FX This work was supported by a grant of the Ministry of Research,
   Innovation and Digitization, CNCS/CCCDI-UEFISCDI, project number
   PN-III-P1-1.1-PD-2019-1225, within PNCDI III.
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NR 138
TC 16
Z9 17
U1 1
U2 7
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 AUG
PY 2021
VL 10
IS 15
AR 3219
DI 10.3390/jcm10153219
PG 19
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA TW0FO
UT WOS:000682087700001
PM 34362003
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Nannini, M
   Ravegnini, G
   Angelini, S
   Astolfi, A
   Biasco, G
   Pantaleo, MA
AF Nannini, Margherita
   Ravegnini, Gloria
   Angelini, Sabrina
   Astolfi, Annalisa
   Biasco, Guido
   Pantaleo, Maria A.
TI miRNA profiling in gastrointestinal stromal tumors: implication as
   diagnostic and prognostic markers
SO EPIGENOMICS
LA English
DT Review
DE gastrointestinal stromal tumors; KIT; microRNA; PDGFRA; wild-type
ID MICRORNA EXPRESSION SIGNATURE; CELL LUNG-CANCER; DOWN-REGULATION;
   UP-REGULATION; UNFAVORABLE PROGNOSIS; THERAPEUTIC TARGET;
   COLORECTAL-CANCER; GASTRIC-CANCER; PROGRESSION; IMATINIB
AB MicroRNAs are a class of short noncoding RNAs, that play a relevant role in multiple biological processes, such as differentiation, proliferation and apoptosis. Gastrointestinal stromal tumors (GIST) are considered as a paradigm of molecular biology in solid tumors worldwide, and after the discovery of specific alterations in the KIT and PDGFRA genes, they have emerged from anonymity to become a model for targeted therapy. Epigenetics have an emerging and relevant role in different steps of GIST biology such as tumorigenesis, disease progression, prognosis and drug resistance. The aim of the present review was to summarize the current evidence about the role of microRNAs in GIST, including their potential application as well as their limits.
C1 [Nannini, Margherita; Biasco, Guido; Pantaleo, Maria A.] Univ Bologna, St Orsola Malpighi Hosp, Dept Specialized Expt & Diagnost Med, Bologna, Italy.
   [Ravegnini, Gloria; Angelini, Sabrina] Univ Bologna, FaBit, Dept Pharm & Biotechnol, Bologna, Italy.
   [Astolfi, Annalisa; Biasco, Guido; Pantaleo, Maria A.] Univ Bologna, Giorgio Prodi Canc Res Ctr, Bologna, Italy.
C3 University of Bologna; IRCCS Azienda Ospedaliero-Universitaria di
   Bologna; University of Bologna; University of Bologna
RP Nannini, M (corresponding author), Univ Bologna, St Orsola Malpighi Hosp, Dept Specialized Expt & Diagnost Med, Bologna, Italy.
EM margherita.nannini@unibo.it
RI Nannini, Margherita/J-9866-2016; Angelini, Sabrina/AAB-5220-2022;
   Pantaleo, Maria/AAE-1101-2021; Ravegnini, Gloria/K-1330-2016; Astolfi,
   Annalisa/K-3034-2016
OI Ravegnini, Gloria/0000-0002-7774-402X; PANTALEO, MARIA
   ABBONDANZA/0000-0002-0177-6957; Astolfi, Annalisa/0000-0002-2732-0747;
   NANNINI, MARGHERITA/0000-0002-2103-1960
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NR 89
TC 22
Z9 24
U1 0
U2 13
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1750-1911
EI 1750-192X
J9 EPIGENOMICS-UK
JI Epigenomics
PY 2015
VL 7
IS 6
BP 1033
EP 1049
DI 10.2217/epi.15.52
PG 17
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA CW7FO
UT WOS:000365163600014
PM 26447534
DA 2025-01-04
ER

PT J
AU Zhang, YB
   Gao, S
   Mao, JM
   Song, YY
   Wang, XT
   Jiang, JW
   Lv, L
   Zhou, ZC
   Wang, JH
AF Zhang, Yuebin
   Gao, Shan
   Mao, Jiaming
   Song, Yuyao
   Wang, Xueting
   Jiang, Jingwei
   Lv, Li
   Zhou, Zunchun
   Wang, Jihong
TI The Inhibitory Effect and Mechanism of the Histidine-Rich Peptide
   rAj-HRP from <i>Apostichopus japonicus</i> on Human Colon Cancer HCT116
   Cells
SO MOLECULES
LA English
DT Article
DE rAj-HRP; <italic>Apostichopus japonicus</italic>; histidine-rich
   peptide; HCT116 cells; EGFR
ID MESENCHYMAL TRANSITION; COLORECTAL-CANCER; TUMOR-GROWTH; GLYCOPROTEIN;
   EXPRESSION; METASTASIS; PROTEIN; ASSOCIATION; MODULATION; DRUGS
AB Colon cancer is a common and lethal malignancy, ranking second in global cancer-related mortality, highlighting the urgent need for novel targeted therapies. The sea cucumber (Apostichopus japonicus) is a marine organism known for its medicinal properties. After conducting a bioinformatics analysis of the cDNA library of Apostichopus japonicus, we found and cloned a cDNA sequence encoding histidine-rich peptides, and the recombinant peptide was named rAj-HRP. Human histidine-rich peptides are known for their anti-cancer properties, raising questions as to whether rAj-HRP might exhibit similar effects. To investigate whether rAj-HRP can inhibit colon cancer, we used human colon cancer HCT116 cells as a model and studied the tumor suppressive activity in vitro and in vivo. The results showed that rAj-HRP inhibited HCT116 cell proliferation, migration, and adhesion to extracellular matrix (ECM) proteins in vitro. It also disrupted the cytoskeleton and induced apoptosis in these cells. In vivo, rAj-HRP significantly inhibited the growth of HCT116 tumors in BALB/c mice, reducing tumor volume and weight without affecting the body weight of the tumor-bearing mice. Western blot analysis showed that rAj-HRP inhibited HCT116 cell proliferation and induced apoptosis by upregulating BAX and promoting PARP zymogen degradation. Additionally, rAj-HRP inhibited HCT116 cell adhesion and migration by reducing MMP2 levels. Further research showed that rAj-HRP downregulated EGFR expression in HCT116 cells and inhibited key downstream molecules, including AKT, P-AKT, PLC gamma, P38 MAPK, and c-Jun. In conclusion, rAj-HRP exhibits significant inhibitory effects on HCT116 cells in both in vitro and in vivo, primarily through the EGFR and apoptosis pathways. These findings suggest that rAj-HRP has the potential as a novel targeted therapy for colon cancer.
C1 [Zhang, Yuebin; Mao, Jiaming; Song, Yuyao; Wang, Jihong] Liaoning Normal Univ, Sch Life Sci, Dalian 116081, Peoples R China.
   [Gao, Shan; Jiang, Jingwei; Zhou, Zunchun] Liaoning Ocean & Fisheries Sci Res Inst, Liaoning Key Lab Marine Fishery Mol Biol, Dalian 116023, Peoples R China.
   [Wang, Xueting; Lv, Li] Dalian Med Univ, Coll Pharm, Dept Pharmacol, Dalian 116044, Peoples R China.
C3 Liaoning Normal University; Dalian Medical University
RP Wang, JH (corresponding author), Liaoning Normal Univ, Sch Life Sci, Dalian 116081, Peoples R China.; Zhou, ZC (corresponding author), Liaoning Ocean & Fisheries Sci Res Inst, Liaoning Key Lab Marine Fishery Mol Biol, Dalian 116023, Peoples R China.
EM yuebinz@hotmail.com; gs_070920@hotmail.com; jiamingmao@hotmail.com;
   yolanda_songyy@hotmail.com; wxt1344943824@hotmail.com;
   weijingjiang@live.cn; lvli@dmu.edu.cn; zunchunz@hotmail.com;
   jihongwang999@lnnu.edu.cn
RI Wang, Xueting/AAT-2534-2021
FU Liaoning Revitalization Talents Program; Science & Technology Project of
   Liaoning Province [2023JH1/10200007, 2022JH2/101300287]; Dalian Science
   and Technology Talent Innovation Support Program [2023RJ007]; Innovation
   and Entrepreneurship Program for High-level Talent of Dalian [2021RT08];
   Key R&D Program of Dalian [2022YF16SN068]; Presidential Foundation of
   the Liaoning Academy of Agricultural Sciences [2022BS0703]; 
   [XLYC2203191]
FX The Liaoning Revitalization Talents Program (No. XLYC2203191); the
   Science & Technology Project of Liaoning Province (No. 2023JH1/10200007,
   No. 2022JH2/101300287); the Dalian Science and Technology Talent
   Innovation Support Program (No. 2023RJ007); the Innovation and
   Entrepreneurship Program for High-level Talent of Dalian (No. 2021RT08);
   the Key R&D Program of Dalian (No. 2022YF16SN068); The Presidential
   Foundation of the Liaoning Academy of Agricultural Sciences (No.
   2022BS0703).
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NR 63
TC 0
Z9 0
U1 1
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD NOV
PY 2024
VL 29
IS 21
AR 5214
DI 10.3390/molecules29215214
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA L6N0G
UT WOS:001351851900001
PM 39519855
OA gold
DA 2025-01-04
ER

PT J
AU Weng, WH
   Leung, WH
   Pang, YJ
   Kuo, LW
   Hsu, HH
AF Weng, Wen-Hui
   Leung, Wai-Hung
   Pang, Yeu Jye
   Kuo, Li-Wei
   Hsu, Hsi-Hsien
TI EPA significantly improves anti-EGFR targeted therapy by regulating
   miR-378 expression in colorectal cancer
SO ONCOLOGY LETTERS
LA English
DT Article
DE colorectal cancer; eicosapentaenoic acid; anti-EGFR
ID BRAF MUTATION; FATTY-ACIDS; 1ST-LINE TREATMENT; INDUCED APOPTOSIS;
   GENE-EXPRESSION; CELL-DEATH; K-RAS; CETUXIMAB; ACTIVATION; KRAS
AB It is known that colorectal cancer (CRC) cells containing mutations of the genes KRAS and BRAF are predominate mechanisms causing resistance to epidermal growth factor receptor (EGFR) inhibitors, and commonly exhibit a lower expression of microRNA-378 (miR-378) when compared with the wild type. In the present study, the aim was to determine the possible mechanism which associates miR-378 with the mitogen-activated protein kinase pathway, and to determine the efficiency of eicosapentaenoic acid ethyl ester (EPA) in its ability to restore sensitivity towards cetuximab, an EGFR inhibitor. The results demonstrated that a combined treatment of 40 mu M EPA with 0.2 mu M cetuximab can significantly suppress the cell growth in KRAS-mutant and control wild-type cells. Furthermore, the higher phosphorylated protein level of extracellular-signal-regulated kinase 1/2 was notable in KRAS EPA-treated cells (P=0.006-0.047) and resulted in significantly increased cell death; however, inconsistent results were indicated in EPA-treated BRAF-mutant cells, compared with the original cells (without treatment). KRAS-mutant and wild-type Caco-2 cells treated with EPA exhibited increased cetuximab response rates, but these response rates were reduced in the BRAF-mutant cells. In conclusion, upregulation of miR-378 induced by EPA may result in the significant restoration of sensitivity to cetuximab in the KRAS-mutant cells. The present data will contribute to a notable potential therapeutic solution for future clinical CRC treatments.
C1 [Weng, Wen-Hui; Leung, Wai-Hung; Kuo, Li-Wei] Natl Taipei Univ Technol, Grad Inst Biochem & Biomed Engn, Dept Chem Engn & Biotechnol, 3 Zhongxiao East Rd, Taipei 10608, Taiwan.
   [Leung, Wai-Hung; Hsu, Hsi-Hsien] Mackay Mem Hosp, Dept Surg, Div Colorectal Surg, Taipei 10491, Taiwan.
   [Pang, Yeu Jye] Queen Elizabeth Queen Mother Hosp, Dept Internal Med, Margate CT9 4AN, England.
C3 National Taipei University of Technology; Mackay Memorial Hospital
RP Weng, WH (corresponding author), Natl Taipei Univ Technol, Grad Inst Biochem & Biomed Engn, Dept Chem Engn & Biotechnol, 3 Zhongxiao East Rd, Taipei 10608, Taiwan.
EM wwhlab@gmail.com
RI Weng, Wen/AAV-7260-2021
FU National Taipei University of Technology, Mackay Memorial Hospital Joint
   Research Program [NTUT-MMH-107-03]
FX The present study was supported by the National Taipei University of
   Technology, Mackay Memorial Hospital Joint Research Program
   (NTUT-MMH-107-03).
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NR 46
TC 14
Z9 15
U1 0
U2 2
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD NOV
PY 2018
VL 16
IS 5
BP 6188
EP 6194
DI 10.3892/ol.2018.9408
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GY3FG
UT WOS:000448433500088
PM 30333883
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Nair, M
   Sandhu, SS
   Sharma, AK
AF Nair, Meera
   Sandhu, Sardul Singh
   Sharma, Anil Kumar
TI Cancer molecular markers: A guide to cancer detection and management
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Article
DE Biomarkers; Molecular markers; Personalized cancer medicine; Genomics;
   NGS
ID EPITHELIAL OVARIAN-CANCER; TOPOISOMERASE II-ALPHA; IN-SITU
   HYBRIDIZATION; KAPPA-B P65; COLORECTAL-CANCER; BLADDER-CANCER;
   BREAST-CANCER; PROSTATE-CANCER; PROGNOSTIC VALUE; PREDICTIVE BIOMARKERS
AB Cancer is generally caused by the molecular alterations which lead to specific mutations. Advances in molecular biology have provided an impetus to the study of cancers with valuable prognostic and predictive significance. Over the hindsight various attempts have been undertaken by scientists worldwide, in the management of cancer; where, we have witnessed a number of molecular markers which allow the early detection of cancers and lead to a decrease in its mortality rate. Recent advances in oncology have led to the discovery of cancer markers that has allowed early detection and targeted therapy of tumors. In this context, current review provides a detail outlook on various molecular markers for diagnosis, prognosis and management of therapeutic response in cancer patients.
C1 [Nair, Meera] Peoples Univ, Stem Cell Technol Lab, Ctr Sci Res & Dev, Bhopal 462037, MP, India.
   [Nair, Meera; Sandhu, Sardul Singh] Rani Durgavati Univ, Biol Sci Dept, Jabalpur 482001, MP, India.
   [Sharma, Anil Kumar] MM Univ Mullana, Dept Biotechnol, Ambala 133207, Haryana, India.
C3 People's University; People's College of Medical Sciences & Research
   Centre; Maharishi Markandeshwar University
RP Nair, M (corresponding author), Rani Durgavati Univ, Biol Sci Dept, Jabalpur 482001, MP, India.
EM meera.nair3@gmail.com
RI Sharma, Anil/AAP-1909-2020; Sandhu, Sardul/HKV-8224-2023
OI Sharma, Anil/0000-0002-9768-1644
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NR 137
TC 51
Z9 54
U1 0
U2 38
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
EI 1096-3650
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD OCT
PY 2018
VL 52
BP 39
EP 55
DI 10.1016/j.semcancer.2018.02.002
PN 1
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GV7EW
UT WOS:000446285800006
PM 29428478
DA 2025-01-04
ER

PT J
AU Srinivas, NR
AF Srinivas, Nuggehally R.
TI Pharmacology of Pimasertib, A Selective MEK1/2 Inhibitor
SO EUROPEAN JOURNAL OF DRUG METABOLISM AND PHARMACOKINETICS
LA English
DT Review
ID COLORECTAL-CANCER CELLS; ADVANCED SOLID TUMORS; PHASE-I;
   ANTITUMOR-ACTIVITY; PRECLINICAL MODELS; KINASE INHIBITORS; TARGETED
   THERAPY; COMBINATION; PATHWAY; RESISTANCE
AB Pimasertib belongs to the growing family of mitogen activated protein kinase (MEK1/2) inhibitors undergoing clinical development for various cancer indications. Since the MEK inhibition in several cell signalling transduction cascades within tumours was considered therapeutically beneficial, number of clinical investigations of pimasertib have been reported. Despite being orally bioavailable in cancer patients, pimasertib undergoes faster clearance with a short elimination half-life. In addition, due to occurrence of toxicity, the development of pimasertib appears to be stalled. Case studies are provided on the possible utilization of pimasertib in combination therapies with other approved drugs. Based on the review, it appeared that there was the need to identify the optimal dose and the dosing regimen of pimasertib to provide a balance between safety and efficacy when combined with approved therapies.
C1 [Srinivas, Nuggehally R.] Zydus Res Ctr, Ahmadabad 382210, Gujarat, India.
RP Srinivas, NR (corresponding author), Zydus Res Ctr, Ahmadabad 382210, Gujarat, India.
EM nuggehally.srinivas@zyduscadila.com
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NR 48
TC 7
Z9 8
U1 0
U2 3
PU SPRINGER FRANCE
PI PARIS
PA 22 RUE DE PALESTRO, PARIS, 75002, FRANCE
SN 0378-7966
EI 2107-0180
J9 EUR J DRUG METAB PH
JI Eur. J. Drug Metabol. Pharmacokinet.
PD AUG
PY 2018
VL 43
IS 4
BP 373
EP 382
DI 10.1007/s13318-018-0466-x
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA GM8JZ
UT WOS:000438475000001
PM 29488172
DA 2025-01-04
ER

PT J
AU Jiang, GY
   Wu, QH
   Li, BL
AF Jiang, Genyi
   Wu, Qianhua
   Li, Bilan
TI Evaluation of immunotherapy efficacy in gynecologic cancer
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE gynecologic cancer; immunotherapy; DNA mismatch repair (MMR); programmed
   cell death protein 1 (PD-1); tumor mutational burden (TMB)
ID TUMOR MUTATIONAL BURDEN; COLORECTAL-CANCER; OVARIAN-CANCER; IMMUNE;
   CELL; EXPRESSION; PHENOTYPE; CEMIPLIMAB; BIOMARKERS; RECURRENT
AB Various immunotherapies have demonstrated remarkable success over the past few decades, and have been approved for the treatment of different cancer types. However, patient responses to immunotherapy are variable, and approximately 50% of cases are refractory to these agents. Tumor biomarker-based stratification of cases may therefore help identify subpopulations that are sensitive/resistant to immunotherapy; it may also improve prediction of response in various cancers including gynecologic cancer. These biomarkers include the tumor mutational burden, microsatellite instability, mismatch repair deficiency, T cell-inflamed gene expression profile, programmed cell death protein 1 ligand 1, tumor-infiltrating lymphocytes, and numerous other genomic alterations. Future directions in the treatment of gynecologic cancer include the utilization of these biomarkers to select ideal candidates. This review focused on recent advances in the predictive ability of molecular biomarkers in patients with gynecologic cancer who undergo immunotherapy. The most recent developments in combined immunotherapy and targeted therapy strategies and novel immune interventions against gynecologic cancers have also been discussed.
C1 [Jiang, Genyi; Li, Bilan] Tongji Univ, Shanghai Matern & Infant Hosp 1, Sch Med, Dept Gynecol, Shanghai, Peoples R China.
   [Wu, Qianhua] Tongji Univ, Sch Med, Shanghai, Peoples R China.
C3 Tongji University; Tongji University
RP Li, BL (corresponding author), Tongji Univ, Shanghai Matern & Infant Hosp 1, Sch Med, Dept Gynecol, Shanghai, Peoples R China.
EM libilan@51mch.com
OI Li, Bilan/0000-0002-7239-2109
FU National Natural Science Foundation of China [82172714]; Natural Science
   Foundation of Shanghai [20ZR1443900]; Clinical Research Plan of SHDC
   [SHDC2020CR4086]
FX Funding This study was supported by grants from the National Natural
   Science Foundation of China (No. 82172714), Natural Science Foundation
   of Shanghai (No. 20ZR1443900), Clinical Research Plan of SHDC (No.
   SHDC2020CR4086).
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NR 104
TC 5
Z9 5
U1 4
U2 12
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JAN 31
PY 2023
VL 14
AR 1061761
DI 10.3389/fimmu.2023.1061761
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 8W1YQ
UT WOS:000931124000001
PM 36793735
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yu, T
   Wu, C
   Zhu, CH
   He, YH
   Yang, DK
   Cheng, YZ
   Gao, X
AF Yu, Ting
   Wu, Cong
   Zhu, Changhui
   He, Yihong
   Yang, Daoke
   Cheng, Yongzhong
   Gao, Xiang
TI Oral Administration of Liposome-Apatinib and Locally Delivery of
   Docetaxel/MPEG-PCL by Fibrin Glue Synergistically Improve Therapeutic
   Effect in Colorectal Cancer
SO JOURNAL OF BIOMEDICAL NANOTECHNOLOGY
LA English
DT Article
DE Apatinib; Liposome; Docetaxel; MPEG/PCL; Angiogenesis; Colorectal Cancer
ID PHASE-II TRIAL; MULTIDRUG-RESISTANCE; BREAST-CANCER; COLON-CANCER;
   CHEMOTHERAPY; PHARMACOKINETICS; HYDROGEL; COMBINATION; STATISTICS;
   INHIBITOR
AB Colorectal cancer is one of the most common and malignant cancer in the world wide. Recently, combination of target therapy and chemotherapy has generated new promise for colorectal cancer. Apatinib mesylate is a novel and highly selective VEGFR-2 inhibitor, presented with an outstanding activity of anti-angiogensis, which has the potential for treating various tumors. As a traditional chemotherapeutic drug, docetaxel (Taxotere) is a widely used semisynthetic taxoid in solid tumors. In this study, Liposome and Methoxy poly(ethylene glycol)-poly(epsilon-caprolactone) (MPEG-PCL) were constructed as drug delivery system for the delivery of apatinib (Lipo-Apa) and docetaxel (DOC/M), respectively. Co-administration of Lipo-Apa and DOC/M showed synergistically effects on inhibiting cell proliferation and inducing cell apoptosis of CT26 cells in vitro. Moreover, fibrin glue, as a biocompatible adherent hemostat, was used as a kind of vehicle for locally delivery of DOCIM in animal models, for achieving locally high concentration and prolonging releasing time. Combination of Lipo-Apa by gavage and locally delivery of DOC/M showed significantly improved anti-tumor activity in a subcutaneous xenograft model as well as in the abdominal metastasis model of colorectal cancer. In addition, promoted tumor apoptosis, inhibited proliferation and decreased tumor angiogenesis were presented by the co-administration. Finally, our study suggested that combination of oral administration of Lipo-Apa and locally delivery of DOC/M by fibrin glue, has the potential to be applied clinically in colorectal cancer therapy.
C1 [Yu, Ting; Wu, Cong; He, Yihong; Cheng, Yongzhong; Gao, Xiang] Sichuan Univ, Collaborat Innovat Ctr Biotherapy, West China Med Sch, Dept Neurosurg,West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
   [Yu, Ting; Wu, Cong; He, Yihong; Cheng, Yongzhong; Gao, Xiang] Sichuan Univ, Collaborat Innovat Ctr Biotherapy, West China Med Sch, Inst Neurosurg,State Key Lab Biotherapy,West Chin, Chengdu 610041, Sichuan, Peoples R China.
   [Yang, Daoke] Zhengzhou Univ, Affiliated Hosp 1, Tumor Hosp, Zhengzhou 450052, Henan, Peoples R China.
   [Zhu, Changhui] Heilongjiang Prov Acad TCM, Dept Pharm, Harbin 150036, Heilongjiang, Peoples R China.
C3 Sichuan University; Sichuan University; Zhengzhou University
RP Cheng, YZ; Gao, X (corresponding author), Sichuan Univ, Collaborat Innovat Ctr Biotherapy, West China Med Sch, Dept Neurosurg,West China Hosp, Chengdu 610041, Sichuan, Peoples R China.; Cheng, YZ; Gao, X (corresponding author), Sichuan Univ, Collaborat Innovat Ctr Biotherapy, West China Med Sch, Inst Neurosurg,State Key Lab Biotherapy,West Chin, Chengdu 610041, Sichuan, Peoples R China.
EM eeecheng@163.com; xianggao@scu.edu.cn
RI yu, ting/KBD-0922-2024
FU National Natural Science Foundation of China [81602075]
FX This work was financially supported by the National Natural Science
   Foundation of China (No. 81602075).
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NR 64
TC 20
Z9 20
U1 2
U2 89
PU AMER SCIENTIFIC PUBLISHERS
PI VALENCIA
PA 26650 THE OLD RD, STE 208, VALENCIA, CA 91381-0751 USA
SN 1550-7033
EI 1550-7041
J9 J BIOMED NANOTECHNOL
JI J. Biomed. Nanotechnol.
PD DEC
PY 2018
VL 14
IS 12
BP 2077
EP 2091
DI 10.1166/jbn.2018.2651
PG 15
WC Nanoscience & Nanotechnology; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Materials Science
GA GW5NT
UT WOS:000446983100007
PM 30305215
DA 2025-01-04
ER

PT J
AU Li, HX
   Li, JH
   Feng, LM
AF Li, Haixia
   Li, Jinghua
   Feng, Limin
TI Hedgehog signaling pathway as a therapeutic target for ovarian cancer
SO CANCER EPIDEMIOLOGY
LA English
DT Article
DE Ovarian cancer; Hedgehog; Targeted therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; TUMOR-FORMATION ABILITY; BASAL-CELL
   CARCINOMA; TAXANE RESISTANCE; SONIC HEDGEHOG; COLON-CANCER; GLI GENES;
   IN-VIVO; INHIBITION; GROWTH
AB Ovarian cancer is the most lethal cause of death among gynecological malignancies. Despite advancements in surgery and chemotherapy treatment strategies, the prognosis of ovarian cancer patients remains poor; a majority of patients relapse and eventually succumb to this disease. Therefore, novel therapeutic approaches to improve patient outcome are urgently needed. The hedgehog signaling pathway is vital for embryonic development and tissue homeostasis, and its deregulation is implicated in cancer cell growth, survival, differentiation, and metastasis. The critical role of hedgehog signaling in multiple biologic processes raises concerns about its potential therapeutic use in cancer. Consequently, many studies are focusing on hedgehog signaling as an attractive target in cancer treatment. In this review, we present an overview of the hedgehog pathway and its pathological aberrations in ovarian cancer. We also discuss inhibitors of the hedgehog signaling pathway that are currently being investigated in the laboratory and in early clinical trials; as well as the clinical challenges these inhibitors face. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Li, Haixia; Li, Jinghua; Feng, Limin] Capital Med Univ, Beijing TianTan Hosp, Dept Obstet & Gynecol, Beijing, Peoples R China.
C3 Capital Medical University
RP Feng, LM (corresponding author), Capital Med Univ, Beijing TianTan Hosp, Dept Obstet & Gynecol, Beijing, Peoples R China.
EM lucyfeng1966@163.com
RI Li, Huang/IZE-8023-2023
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NR 65
TC 25
Z9 30
U1 0
U2 20
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1877-7821
EI 1877-783X
J9 CANCER EPIDEMIOL
JI Cancer Epidemiol.
PD FEB
PY 2016
VL 40
BP 152
EP 157
DI 10.1016/j.canep.2015.11.014
PG 6
WC Oncology; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Public, Environmental & Occupational Health
GA DD8HM
UT WOS:000370167000021
PM 26724464
DA 2025-01-04
ER

PT J
AU Yekedüz, E
   Aktas, EG
   Köksoy, EB
   Dogan, N
   Ürün, Y
   Utkan, G
AF Yekeduz, Emre
   Aktas, Elif Gizem
   Koksoy, Elif Berna
   Dogan, Neslihan
   Urun, Yuksel
   Utkan, Gungor
TI The prognostic role of polypharmacy in metastatic colorectal cancer
   patients treated with regorafenib
SO FUTURE ONCOLOGY
LA English
DT Article
DE colon cancer; drug interaction; rectal cancer; regorafenib
ID COMPREHENSIVE GERIATRIC ASSESSMENT; POTENTIAL-DRUG INTERACTIONS;
   PALLIATIVE CARE; ELDERLY-PATIENTS; RISK-FACTORS; CHEMOTHERAPY; SURVIVAL;
   MEDICATIONS
AB Aim: To evaluate polypharmacy (PP) in patients with metastatic colorectal cancer receiving regorafenib. Methods: Patients with metastatic colorectal cancer receiving regorafenib were included and divided into two categories by their PP status: PP- (<5 regular drug use/day) and PP+ (>= 5 regular drug use/day). Results: 80 patients were included. 31 (38.7%) patients had PP. The median number of drugs used was three and seven in PP- and PP+ patients, respectively. Antiemetics (26.5%) and antacids (48.4%) were the most common drugs used by PP- and PP+ patients, respectively. In multivariate analysis, the risk of death was higher in PP+ patients (hazard ratio: 2.1; 95% CI: 1.2-3.7; p = 0.005). Conclusion: PP was an independent prognostic factor for overall survival in patients with metastatic colorectal cancer receiving regorafenib.
   Plain language summary Regorafenib is a targeted therapy option that is used in patients with chemotherapy-refractory metastatic colorectal cancer. Because of the chemotherapy-refractory stage of the disease, patients are prone to use more medications for symptom palliation. Polypharmacy (PP) refers to the drug burden in an individual, and the use of five or more drugs in a day is usually considered to represent PP. In this study, the authors assessed the impact of PP in patients with metastatic colorectal cancer treated with regorafenib. The authors' study found that PP had a negative impact on survival outcomes in these patients. This is why inappropriate drug use should be assessed at each visit and the medication discontinued if it is not an essential part of the treatment.
C1 [Yekeduz, Emre; Koksoy, Elif Berna; Urun, Yuksel; Utkan, Gungor] Ankara Univ, Fac Med, Dept Med Oncol, TR-06590 Ankara, Turkey.
   [Yekeduz, Emre; Koksoy, Elif Berna; Urun, Yuksel; Utkan, Gungor] Ankara Univ, Canc Res Inst, TR-06590 Ankara, Turkey.
   [Aktas, Elif Gizem] Ankara Univ, Fac Med, Dept Internal Med, TR-06590 Ankara, Turkey.
   [Dogan, Neslihan] Giresun Univ, Prof Dr A Ilhan Ozdemir Training & Res Hosp, Med Oncol Clin, TR-28100 Giresun, Turkey.
C3 Ankara University; Ankara University; Ankara University; Giresun
   University
RP Yekedüz, E (corresponding author), Ankara Univ, Fac Med, Dept Med Oncol, TR-06590 Ankara, Turkey.; Yekedüz, E (corresponding author), Ankara Univ, Canc Res Inst, TR-06590 Ankara, Turkey.
EM emreyekeduz@gmail.com
RI Yekedüz, Emre/ABA-5814-2020; Ürün, Yüksel/AAQ-3612-2020
OI Ozyurt, Neslihan/0000-0002-1404-8983; URUN, YUKSEL/0000-0002-9152-9887;
   Yekeduz, Emre/0000-0001-6819-5930; UTKAN, GUNGOR/0000-0001-8445-6993;
   koksoy, elif berna/0000-0002-6590-4444
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   UpToDate, LEXICOMP DRUG INTERA
   US DepartmentofHealthandHumanServices, 2017, COMMON TERMINOLOGY C
NR 33
TC 3
Z9 3
U1 1
U2 10
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 MAR
PY 2022
VL 18
IS 9
BP 1067
EP 1076
DI 10.2217/fon-2021-1182
EA FEB 2022
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZO5HD
UT WOS:000750441300001
PM 35109668
DA 2025-01-04
ER

PT J
AU Conradi, LC
   Spitzner, M
   Metzger, AL
   Kisly, M
   Middel, P
   Bohnenberger, H
   Gaedcke, J
   Ghadimi, MB
   Liersch, T
   Rüschoff, J
   Beissbarth, T
   König, A
   Grade, M
AF Conradi, Lena-Christin
   Spitzner, Melanie
   Metzger, Anna-Lena
   Kisly, Merle
   Middel, Peter
   Bohnenberger, Hanibal
   Gaedcke, Jochen
   Ghadimi, Michael B.
   Liersch, Torsten
   Rueschoff, Joseph
   Beissbarth, Tim
   Koenig, Alexander
   Grade, Marian
TI Combined targeting of HER-2 and HER-3 represents a promising therapeutic
   strategy in colorectal cancer
SO BMC CANCER
LA English
DT Article
DE Colorectal cancer; HER-2; HER-3; Targeted therapy; Inhibitors
ID LIVER METASTASES; RECTAL-CANCER; GASTRIC-CANCER; COPY NUMBER;
   CHEMORADIOTHERAPY; AMPLIFICATION; VALIDATION; MECHANISMS; EXPRESSION;
   STANDARD
AB Background Abrogation of growth factor-dependent signaling represents an effective therapeutic strategy for patients with colorectal cancer (CRC). Here we evaluated the effectiveness of targeting the epidermal growth factor (EGF) receptors HER-2 and HER-3 in the three cell lines LS513, LS1034 and SW837. Methods Treatment with HER-2-specific antibodies trastuzumab and pertuzumab resulted in a mild reduction of cellular viability. In contrast, the antibody-drug conjugate T-DM1 mediated a strong and dose-dependent decrease of viability and Akt phosphorylation. Results The most striking effects were observed with the dual tyrosine kinase inhibitor lapatinib, and the Pan-ErbB inhibitor afatinib. Selectively, the effect of EGF receptor inhibition was augmented by a combination with 5-fluorouracil and oxaliplatin. Finally, high expression of HER-3 was detected in 121 of 172 locally advanced rectal cancers (70.3%). In conclusion, inhibition of EGF receptors effectively blocks downstream signaling and significantly impairs viability of CRC cells. However, the effectiveness of receptor inhibition highly depends on the inhibitors' mode of action, as targeting HER-2 alone is not sufficient. Conclusion Since HER-2 and HER-3 are expressed in a relevant number of patients, targeting both receptors may represent a promising therapeutic strategy for CRC.
C1 [Conradi, Lena-Christin; Spitzner, Melanie; Metzger, Anna-Lena; Kisly, Merle; Gaedcke, Jochen; Ghadimi, Michael B.; Liersch, Torsten; Grade, Marian] Univ Med Ctr Goettingen, Dept Gen Visceral & Pediat Surg, Robert Koch Str 40, D-37075 Gottingen, Germany.
   [Middel, Peter; Rueschoff, Joseph] Pathol Nordhessen, Dept Pathol, Kassel, Germany.
   [Bohnenberger, Hanibal] Univ Med Ctr Goettingen, Dept Pathol, Gottingen, Germany.
   [Beissbarth, Tim] Univ Med Ctr Goettingen, Dept Med Stat, Gottingen, Germany.
   [Koenig, Alexander] Univ Med Ctr Goettingen, Dept Gastroenterol & Gastrointestinal Oncol, Gottingen, Germany.
C3 University of Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; University of
   Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; University of Gottingen;
   UNIVERSITY GOTTINGEN HOSPITAL; University of Gottingen; UNIVERSITY
   GOTTINGEN HOSPITAL
RP Grade, M (corresponding author), Univ Med Ctr Goettingen, Dept Gen Visceral & Pediat Surg, Robert Koch Str 40, D-37075 Gottingen, Germany.
EM marian.grade@med.uni-goettingen.de
RI Bohnenberger, Hanibal/F-2317-2013; Beissbarth, Tim/B-3129-2013
OI Spitzner, Melanie/0000-0002-3673-0625
FU Deutsche Forschungsgemeinschaft [KFO 179]; Fritz Thyssen Foundation
FX This work was supported by the Deutsche Forschungsgemeinschaft, KFO 179
   (M.G.) and the Fritz Thyssen Foundation (L-C.C.) for consumables and to
   cover personal costs. The design of the study and collection, analysis
   and interpretation of data and writing the manuscript was done by the
   authors idenpendently of the funding body.
CR [Anonymous], PRECISION MED METAST
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NR 52
TC 15
Z9 15
U1 1
U2 9
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD SEP 5
PY 2019
VL 19
IS 1
AR 880
DI 10.1186/s12885-019-6051-0
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IW4ON
UT WOS:000484959600004
PM 31488078
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhuang, Y
   Liu, K
   He, QY
   Gu, XS
   Jiang, CP
   Wu, JH
AF Zhuang, Yan
   Liu, Kua
   He, Qinyu
   Gu, Xiaosong
   Jiang, Chunping
   Wu, Junhua
TI Hypoxia signaling in cancer: Implications for therapeutic interventions
SO MEDCOMM
LA English
DT Review
DE hyperoxia; hypoxia-inducible factor (HIF); immunotherapy; targeted
   theraphy; tumor hypoxia
ID ENDOTHELIAL GROWTH-FACTOR; HYPERBARIC-OXYGEN THERAPY; WHOLE-BODY
   HYPERTHERMIA; RENAL-CELL CARCINOMA; COMBINED PHOTODYNAMIC THERAPY;
   METASTATIC COLORECTAL-CANCER; TUMOR-ASSOCIATED MACROPHAGES; INTERSTITIAL
   FLUID PRESSURE; EXPERIMENTAL BLADDER-TUMOR; DOSE-ESCALATION TRIAL
AB Hypoxia is a persistent physiological feature of many different solid tumors and a key driver of malignancy, and in recent years, it has been recognized as an important target for cancer therapy. Hypoxia occurs in the majority of solid tumors due to a poor vascular oxygen supply that is not sufficient to meet the needs of rapidly proliferating cancer cells. A hypoxic tumor microenvironment (TME) can reduce the effectiveness of other tumor therapies, such as radiotherapy, chemotherapy, and immunotherapy. In this review, we discuss the critical role of hypoxia in tumor development, including tumor metabolism, tumor immunity, and tumor angiogenesis. The treatment methods for hypoxic TME are summarized, including hypoxia-targeted therapy and improving oxygenation by alleviating tumor hypoxia itself. Hyperoxia therapy can be used to improve tissue oxygen partial pressure and relieve tumor hypoxia. We focus on the underlying mechanisms of hyperoxia and their impact on current cancer therapies and discuss the prospects of hyperoxia therapy in cancer treatment.
C1 [Zhuang, Yan; Liu, Kua; He, Qinyu; Jiang, Chunping; Wu, Junhua] Nanjing Univ, Med Sch, Natl Inst Healthcare Data Sci, State Key Lab Pharmaceut Biotechnol,Jiangsu Key La, Nanjing, Peoples R China.
   [Gu, Xiaosong; Jiang, Chunping; Wu, Junhua] Jinan Microecol Biomed Shandong Lab, Microecol Regenerat & Microfabricat Tech Platform, Jinan, Peoples R China.
   [Jiang, Chunping; Wu, Junhua] Nanjing Univ, Med Sch, Mengminwei Bldg, 22 Hankou Rd, Nanjing 210093, Jiangsu, Peoples R China.
C3 Nanjing University; Jinan Microecological Biomedicine Shandong
   Laboratory; Nanjing University
RP Jiang, CP; Wu, JH (corresponding author), Nanjing Univ, Med Sch, Mengminwei Bldg, 22 Hankou Rd, Nanjing 210093, Jiangsu, Peoples R China.
EM chunpingjiang@nju.edu.cn; wujunhua@nju.edu.cn
RI Gu, Xiao-song/ABD-5166-2021; WU, Junhua/JTT-4742-2023
OI Wu, Junhua/0000-0003-4753-2648
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NR 460
TC 34
Z9 34
U1 4
U2 49
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2688-2663
J9 MEDCOMM
JI MedComm
PD FEB
PY 2023
VL 4
IS 1
AR e203
DI 10.1002/mco2.203
PG 37
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA 8C3IX
UT WOS:000917507400001
PM 36703877
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Cheng, YF
   Shen, P
AF Cheng, Yanfeng
   Shen, Peng
TI miR-335 Acts as a Tumor Suppressor and Enhances Ionizing
   Radiation-Induced Tumor Regression by Targeting ROCK1
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE melanoma; ionizing radiation; resistance; apoptosis; miR-335; ROCK1
ID CELL LUNG-CANCER; COLORECTAL-CANCER; MIGRATION; PROLIFERATION; INVASION;
   MELANOMA; EXPRESSION
AB Recent development of integrative therapy against melanoma combines surgery, radiotherapy, targeted therapy, and immunotherapy; however, the clinical outcomes of advanced stage and recurrent melanoma are poor. As a skin cancer, melanoma is generally resistant to radiotherapy. Hence, there is an urgent need for evaluation of the mechanisms of radioresistance. The present study identified miR-335 as one of the differential expression of miRNAs in recurrent melanoma biopsies post-radiotherapy. The expression of miR-335 declined in melanoma tissues compared to the adjacent tissues. Moreover, miR-335 expression correlated with advanced stages of melanoma negatively. Consistent with the prediction of STARBASE and miRDB database, miR-335 targeted ROCK1 via binding with 3 '-UTR of ROCK1 directly, resulting in attenuation of proliferation, migration, and radioresistance of melanoma cells. The authors validated that overexpression of miR-335 enhanced X-ray-induced tumor regression by B16 mouse models. Briefly, the present findings gained insights into miR-335/ROCK1-mediated radiosensitivity and provided a promising therapeutic strategy for improving radiotherapy against melanoma.
C1 [Cheng, Yanfeng; Shen, Peng] China Med Univ, Dept Dermatol, Shengjing Hosp, Shenyang, Peoples R China.
C3 China Medical University
RP Shen, P (corresponding author), China Med Univ, Dept Dermatol, Shengjing Hosp, Shenyang, Peoples R China.
EM sp4239@163.com
RI Chen, Shanshan/M-5985-2013
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NR 34
TC 11
Z9 12
U1 0
U2 0
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD MAR 11
PY 2020
VL 10
AR 278
DI 10.3389/fonc.2020.00278
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LC9HL
UT WOS:000525644000001
PM 32219065
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Telekes, A
   Horváth, A
AF Telekes, Andras
   Horvath, Anna
TI The Role of Cell-Free DNA in Cancer Treatment Decision Making
SO CANCERS
LA English
DT Review
DE circulating tumor DNA (ctDNA); cell-free DNA (cfDNA); solid tumor;
   clinical decision making
ID CIRCULATING TUMOR DNA; RESIDUAL DISEASE MRD; BREAST-CANCER; LUNG-CANCER;
   LIQUID BIOPSY; ACQUIRED-RESISTANCE; COLORECTAL-CANCER; GENOMIC
   ALTERATIONS; TARGETED THERAPY; BLOOD-PLASMA
AB Simple Summary The aim of this review is to evaluate the present status of the use of cell-free DNA and its fraction of circulating tumor DNA (ctDNA) because this year July 2022, an ESMO guideline was published regarding the application of ctDNA in patient care. In the near future the data obtained from ctDNA may routinely be used for finding minimal residual disease, detecting relapse, determining either the unknown primary tumor, or the site of metastases. It can also be used for deciding upon the appropriate efficiency of the therapy and/or emerging resistance to the therapy. Therefore, clinicians should be aware of the potentials and the limitations of the assays. Of course, several open questions are still under research and as a result, cfDNA and ctDNA testing are not part of routine care yet. The aim of this review is to evaluate the present status of the use of cell-free DNA and its fraction of circulating tumor DNA (ctDNA) because this year July 2022, an ESMO guideline was published regarding the application of ctDNA in patient care. This review is for clinical oncologists to explain the concept, the terms used, the pros and cons of ctDNA; thus, the technical aspects of the different platforms are not reviewed in detail, but we try to help in navigating the current knowledge in liquid biopsy. Since the validated and adequately sensitive ctDNA assays have utility in identifying actionable mutations to direct targeted therapy, ctDNA may be used for this soon in routine clinical practice and in other different areas as well. The cfDNA fragments can be obtained by liquid biopsy and can be used for diagnosis, prognosis, and selecting among treatment options in cancer patients. A great proportion of cfDNA comes from normal cells of the body or from food uptake. Only a small part (<1%) of it is related to tumors, originating from primary tumors, metastatic sites, or circulating tumor cells (CTCs). Soon the data obtained from ctDNA may routinely be used for finding minimal residual disease, detecting relapse, and determining the sites of metastases. It might also be used for deciding appropriate therapy, and/or emerging resistance to the therapy and the data analysis of ctDNA may be combined with imaging or other markers. However, to achieve this goal, further clinical validations are inevitable. As a result, clinicians should be aware of the limitations of the assays. Of course, several open questions are still under research and because of it cfDNA and ctDNA testing are not part of routine care yet.
C1 [Telekes, Andras] Omnimed Etosz Ltd, 81 Szeher Rd, H-1021 Budapest, Hungary.
   [Telekes, Andras] Semmelweis Univ, 26 Ulloi Rd, H-1085 Budapest, Hungary.
   [Horvath, Anna] Semmelweis Univ, Dept Internal Med & Haematol, 46 Szentkiralyi Rd, H-1088 Budapest, Hungary.
C3 Semmelweis University; Semmelweis University
RP Telekes, A (corresponding author), Omnimed Etosz Ltd, 81 Szeher Rd, H-1021 Budapest, Hungary.; Telekes, A (corresponding author), Semmelweis Univ, 26 Ulloi Rd, H-1085 Budapest, Hungary.
EM prof.andras.telekes@gmail.com
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   US
NR 271
TC 15
Z9 16
U1 0
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD DEC
PY 2022
VL 14
IS 24
AR 6115
DI 10.3390/cancers14246115
PG 31
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 7G2LS
UT WOS:000902363300001
PM 36551600
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lv, KK
   He, TL
AF Lv, Keke
   He, Tianlin
TI Cancer-associated fibroblasts: heterogeneity, tumorigenicity and
   therapeutic targets
SO MOLECULAR BIOMEDICINE
LA English
DT Review
DE Cancer associated fibroblasts; Tumor microenvironment; Extracellular
   matrix; Immune cells; Mechanisms; Cancer cell; Cancer targeting therapy
ID PANCREATIC DUCTAL ADENOCARCINOMA; CARCINOMA-ASSOCIATED FIBROBLASTS;
   ENDOTHELIAL GROWTH-FACTOR; LYSYL HYDROXYLASE 2; CROSS-LINK SWITCH; TUMOR
   MICROENVIRONMENT; MESENCHYMAL TRANSITION; COLORECTAL-CANCER;
   EXTRACELLULAR-MATRIX; STROMAL FIBROBLASTS
AB Cancer, characterized by its immune evasion, active metabolism, and heightened proliferation, comprises both stroma and cells. Although the research has always focused on parenchymal cells, the non-parenchymal components must not be overlooked. Targeting cancer parenchymal cells has proven to be a formidable challenge, yielding limited success on a broad scale. The tumor microenvironment(TME), a critical niche for cancer cell survival, presents a novel way for cancer treatment. Cancer-associated fibroblast (CAF), as a main component of TME, is a dynamically evolving, dual-functioning stromal cell. Furthermore, their biological activities span the entire spectrum of tumor development, metastasis, drug resistance, and prognosis. A thorough understanding of CAFs functions and therapeutic advances holds significant clinical implications. In this review, we underscore the heterogeneity of CAFs by elaborating on their origins, types and function. Most importantly, by elucidating the direct or indirect crosstalk between CAFs and immune cells, the extracellular matrix, and cancer cells, we emphasize the tumorigenicity of CAFs in cancer. Finally, we highlight the challenges encountered in the exploration of CAFs and list targeted therapies for CAF, which have implications for clinical treatment.
C1 [Lv, Keke; He, Tianlin] Changhai Hosp, Dept Hepatopanreatobiliary Surg, 168 Changhai Rd, Shanghai 200433, Peoples R China.
C3 Naval Medical University
RP He, TL (corresponding author), Changhai Hosp, Dept Hepatopanreatobiliary Surg, 168 Changhai Rd, Shanghai 200433, Peoples R China.
EM tlhe@smmu.edu.cn
RI he, tianlin/K-7614-2015
FU National Natural Science Foundation of China; National Natural Science
   Foundation of China; Shanghai "Rising Stars of Medical Talent" Youth
   Development
FX We express our gratitude to all authors for their contributions to the
   manuscript. Meanwhile, we thank The National Natural Science Foundation
   of China and Shanghai "Rising Stars of Medical Talent" Youth Development
   for supporting this work. Besides, the Fig. 1, 2, 3, 4 in the review
   were created with BioRender.com. The Artificial Intelligence (AI) was
   used to improve the words of some paragraphs, but not to generate new
   content.
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NR 208
TC 0
Z9 0
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2662-8651
J9 MOL BIOMED
JI Mol. Biomed.
PD DEC 16
PY 2024
VL 5
IS 1
AR 70
DI 10.1186/s43556-024-00233-8
PG 22
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
WE Emerging Sources Citation Index (ESCI)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA P5Q5C
UT WOS:001378453200001
PM 39680287
OA gold
DA 2025-01-04
ER

PT J
AU Mogavero, A
   Bironzo, P
   Righi, L
   Merlini, A
   Benso, F
   Novello, S
   Passiglia, F
AF Mogavero, Andrea
   Bironzo, Paolo
   Righi, Luisella
   Merlini, Alessandra
   Benso, Federica
   Novello, Silvia
   Passiglia, Francesco
TI Deciphering Lung Adenocarcinoma Heterogeneity: An Overview of
   Pathological and Clinical Features of Rare Subtypes
SO LIFE-BASEL
LA English
DT Review
DE pulmonary enteric carcinoma; colorectal cancer; immunochemistry;
   mutation analyses; colloid carcinoma; fetal carcinoma; NOS carcinoma
ID PULMONARY ENTERIC ADENOCARCINOMA; DIFFERENTIATED FETAL ADENOCARCINOMA;
   COLLOID CARCINOMA; CANCER; DIAGNOSIS; MARKER; IMPACT
AB Lung cancer is one of the most frequently diagnosed cancers worldwide and the leading cause of cancer-related death. The 2021 World Health Organization (WHO) classification provided a detailed and updated categorization of lung adenocarcinomas with a special focus on rare histological types, including enteric, fetal and colloid types, as well as not otherwise specified adenocarcinoma, overall accounting for about 5-10% of all cases. However, rare entities are nowadays difficult to diagnose in most centers, and evidence of optimal therapeutic management for these patients is still lacking. In recent years, increasing knowledge about the mutational profile of lung cancer, in addition to the spreading diffusion of next-generation sequencing (NGS) in different centers, have been helpful in the identification of rare variants of lung cancer. Hence, the hope is that several new drugs will be available in the near future to treat these rare lung tumors, such as in targeted therapy and immunotherapy, which are often used in clinical practice for several malignancies. The aim of this review is to summarize the current knowledge about the molecular pathology and clinical management of the most common rare adenocarcinoma subtypes in order to provide a concise and updated report that can drive clinicians' choices in their routine practice.
C1 [Mogavero, Andrea; Bironzo, Paolo; Righi, Luisella; Merlini, Alessandra; Benso, Federica; Novello, Silvia; Passiglia, Francesco] Univ Turin, San Luigi Gonzaga Hosp, Dept Oncol, I-10043 Orbassano, Italy.
C3 University of Turin; Azienda Ospedaliero-Universitaria San Luigi Gonzaga
RP Bironzo, P (corresponding author), Univ Turin, San Luigi Gonzaga Hosp, Dept Oncol, I-10043 Orbassano, Italy.
EM mogavero.andrea@gmail.com; pbironzo@gmail.com
RI Merlini, Alessandra/ABB-4487-2021; novello, silvia/K-6335-2016; Righi,
   Luisella/K-4583-2018
OI Righi, Luisella/0000-0002-8927-204X; Mogavero,
   Andrea/0000-0001-8718-6773; Merlini, Alessandra/0000-0002-5280-1411;
   Bironzo, Paolo/0000-0002-2784-5076
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NR 43
TC 3
Z9 3
U1 1
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-1729
J9 LIFE-BASEL
JI Life-Basel
PD JUN
PY 2023
VL 13
IS 6
AR 1291
DI 10.3390/life13061291
PG 11
WC Biology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Microbiology
GA K3IM4
UT WOS:001015407900001
PM 37374074
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Liu, GH
   Chen, T
   Zhang, X
   Ma, XL
   Shi, HS
AF Liu, Gui-Hong
   Chen, Tao
   Zhang, Xin
   Ma, Xue-Lei
   Shi, Hua-Shan
TI Small molecule inhibitors targeting the cancers
SO MEDCOMM
LA English
DT Review
DE combination therapy; multikinase molecule inhibitors; resistance; small
   molecule inhibitors; small molecule kinase inhibitors
ID CELL LUNG-CANCER; GROWTH-FACTOR RECEPTOR; ACUTE MYELOID-LEUKEMIA;
   CHRONIC LYMPHOCYTIC-LEUKEMIA; GASTROINTESTINAL STROMAL TUMOR;
   1ST-IN-HUMAN PHASE-I; DABRAFENIB PLUS TRAMETINIB; HISTONE DEACETYLASE
   INHIBITOR; METASTATIC COLORECTAL-CANCER; QUALITY-OF-LIFE
AB Compared with traditional therapies, targeted therapy has merits in selectivity, efficacy, and tolerability. Small molecule inhibitors are one of the primary targeted therapies for cancer. Due to their advantages in a wide range of targets, convenient medication, and the ability to penetrate into the central nervous system, many efforts have been devoted to developing more small molecule inhibitors. To date, 88 small molecule inhibitors have been approved by the United States Food and Drug Administration to treat cancers. Despite remarkable progress, small molecule inhibitors in cancer treatment still face many obstacles, such as low response rate, short duration of response, toxicity, biomarkers, and resistance. To better promote the development of small molecule inhibitors targeting cancers, we comprehensively reviewed small molecule inhibitors involved in all the approved agents and pivotal drug candidates in clinical trials arranged by the signaling pathways and the classification of small molecule inhibitors. We discussed lessons learned from the development of these agents, the proper strategies to overcome resistance arising from different mechanisms, and combination therapies concerned with small molecule inhibitors. Through our review, we hoped to provide insights and perspectives for the research and development of small molecule inhibitors in cancer treatment.
C1 [Liu, Gui-Hong; Zhang, Xin; Ma, Xue-Lei; Shi, Hua-Shan] Sichuan Univ, West China Hosp, Canc Ctr, Dept Biotherapy,State Key Lab Biotherapy, 17,Block 3,Southern Renmin Rd, Chengdu 610041, Sichuan, Peoples R China.
   [Chen, Tao] China Med Univ, Dept Cardiol, Affiliated Hosp 1, Shenyang, Liaoning, Peoples R China.
C3 Sichuan University; China Medical University
RP Shi, HS (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, Dept Biotherapy,State Key Lab Biotherapy, 17,Block 3,Southern Renmin Rd, Chengdu 610041, Sichuan, Peoples R China.
EM shihuashan@scu.edu.cn
RI Liu, Guihong/AAA-8293-2020
OI ZHANG, Xin/0000-0003-1816-0953
FU National Natural Science Foundation of China [81201788]
FX This work was financially supported by National Natural Science
   Foundation of China (81201788).
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NR 786
TC 59
Z9 64
U1 10
U2 82
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2688-2663
J9 MEDCOMM
JI MedComm
PD DEC
PY 2022
VL 3
IS 4
AR e181
DI 10.1002/mco2.181
PG 74
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA 5G1OY
UT WOS:000866776600001
PM 36254250
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU McFall, T
   Schomburg, NK
   Rossman, KL
   Stites, EC
AF McFall, Thomas
   Schomburg, Noah K.
   Rossman, Kent L.
   Stites, Edward C.
TI Discernment between candidate mechanisms for KRAS G13D colorectal cancer
   sensitivity to EGFR inhibitors
SO CELL COMMUNICATION AND SIGNALING
LA English
DT Article
DE KRAS; GTPase; EGFR; Cancer; Targeted therapy
ID STRUCTURAL-ANALYSIS; ERBB RECEPTORS; RAS MUTATIONS; NEUROFIBROMIN;
   NETWORK; ACTIVATION
AB Phase three clinical trial evidence suggests that colorectal cancers with the KRAS G13D mutation may benefit from EGFR inhibitors, like cetuximab, in contrast to the other most common KRAS mutations. A mechanism to explain why this mutation behaves differently from other KRAS mutations had long been lacking. Two recent studies have reproduced KRAS G13D specific sensitivity to cetuximab in cellular models, and both have implicated the tumor suppressor NF1 as a critical variable in determining sensitivity and resistance. One study proposes a mechanism that focuses on the inhibition of active, GTP-bound wild-type RAS, which is proposed to occur to a greater extent in KRAS G13D tumors due to the inability of KRAS G13D to bind NF1 well. The other study suggests NF1 can convert GTP-bound KRAS G13D to inactive, GDP-bound KRAS G13D. Here, we report an inability to reproduce cellular and biophysical studies that suggested NF1 has strong GTPase activity on KRAS G13D. We also report additional data that further suggests only WT RAS-GTP levels are reduced with EGFR inhibition and that KRAS G13D is impaired in binding to NF1. These new experiments further support a mechanism in which cetuximab inhibits wild-type (HRAS and NRAS) signals in KRAS G13D colorectal cancers.
C1 [McFall, Thomas; Stites, Edward C.] Salk Inst Biol Studies, Integrat Biol Lab, 10010 N Torrey Pines Rd, La Jolla, CA 92037 USA.
   [Schomburg, Noah K.; Rossman, Kent L.] Univ N Carolina, Sch Med, Dept Surg, Chapel Hill, NC 27599 USA.
   [Schomburg, Noah K.; Rossman, Kent L.] Univ N Carolina, Sch Med, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
C3 Salk Institute; University of North Carolina School of Medicine;
   University of North Carolina; University of North Carolina Chapel Hill;
   University of North Carolina School of Medicine; University of North
   Carolina; University of North Carolina Chapel Hill
RP Stites, EC (corresponding author), Salk Inst Biol Studies, Integrat Biol Lab, 10010 N Torrey Pines Rd, La Jolla, CA 92037 USA.
EM estites@salk.edu
OI Stites, Edward/0000-0002-3783-7336
FU National Cancer Institute of the National Institutes of Health
   [R01CA223495, K22CA216318, P30CA014195, T32CA009370]
FX Research reported in this publication was supported by the National
   Cancer Institute of the National Institutes of Health under award number
   R01CA223495 (K. L. Rossman), K22CA216318 and P30CA014195 (E. C. Stites),
   and T32CA009370 (T. McFall).
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NR 23
TC 10
Z9 11
U1 0
U2 6
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 NOV 5
PY 2020
VL 18
IS 1
AR 179
DI 10.1186/s12964-020-00645-3
PG 7
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA OS3HQ
UT WOS:000590056800001
PM 33153459
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Gao, F
   Dong, J
   Zeng, DL
   Rong, A
   Ibrahim, JG
AF Gao, Fei
   Dong, Jun
   Zeng, Donglin
   Rong, Alan
   Ibrahim, Joseph G.
TI Pattern mixture models for clinical validation of biomarkers in the
   presence of missing data
SO STATISTICS IN MEDICINE
LA English
DT Article
DE clinical trials; companion diagnostics; missing data
ID THERAPY; EM
AB Targeted therapies for cancers are sometimes only effective in a subset of patients with a particular biomarker status. In clinical development, the biomarker status is typically determined by an investigational-use-only/laboratory-developed test. A market ready test (MRT) is developed later to meet regulatory requirements and for future commercial use. In the USA, the clinical validation of MRT showing efficacy and safety profile of the targeted therapy in the biomarker subgroups determined by MRT is needed for pre-market approval. One of the major challenges in carrying out clinical validation is that the biomarker status per MRT is often missing for many subjects. In this paper, we treat biomarker status as a missing covariate and develop a novel pattern mixture model in the setting of a proportional hazards model for the time-to-event outcome variable. We specify a multinomial regression model for the missing biomarker statuses, and develop an expectation-maximization algorithm by the Method of Weights (Ibrahim, Journal of the American Statistical Association, 1990) to estimate the parameters in the regression model. We use Louis' formula (Louis, Journal of the Royal Statistical Society. Series B, 1982) to obtain standard errors estimates. We examine the performance of our method in extensive simulation studies and apply our method to a clinical trial in metastatic colorectal cancer. Copyright (c) 2017 John Wiley & Sons, Ltd.
C1 [Gao, Fei; Zeng, Donglin; Ibrahim, Joseph G.] Univ N Carolina, Dept Biostat, CB7420, Chapel Hill, NC 27599 USA.
   [Dong, Jun] Amgen Inc, One Amgen Ctr Dr, Thousand Oaks, CA 91320 USA.
   [Rong, Alan] Astellas Pharma Inc, Northbrook, IL USA.
C3 University of North Carolina; University of North Carolina Chapel Hill;
   Amgen; Astellas Pharmaceuticals
RP Ibrahim, JG (corresponding author), Univ N Carolina, Dept Biostat, CB7420, Chapel Hill, NC 27599 USA.
EM ibrahim@bios.unc.edu
RI a, r/JSL-6459-2023; Gao, Fei/U-7821-2019
OI Gao, Fei/0000-0001-6797-5468
FU NCI NIH HHS [P01 CA142538] Funding Source: Medline; NIGMS NIH HHS [R01
   GM070335] Funding Source: Medline
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NR 12
TC 2
Z9 2
U1 0
U2 5
PU WILEY
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PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-6715
EI 1097-0258
J9 STAT MED
JI Stat. Med.
PD AUG 30
PY 2017
VL 36
IS 19
BP 2994
EP 3004
DI 10.1002/sim.7328
PG 11
WC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Medicine, Research &
   Experimental; Statistics & Probability
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Mathematical & Computational Biology; Public, Environmental &
   Occupational Health; Medical Informatics; Research & Experimental
   Medicine; Mathematics
GA EZ8HS
UT WOS:000404966200003
PM 28464562
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Zangouei, AS
   Ghasaban, FT
   Dalili, A
   Akhlaghipour, I
   Moghbeli, M
AF Zangouei, Amir Sadra
   Ghasaban, Faezeh Tolue
   Dalili, Amin
   Akhlaghipour, Iman
   Moghbeli, Meysam
TI MicroRNAs as the pivotal regulators of Forkhead box protein family
   during gastrointestinal tumor progression and metastasis
SO GENE REPORTS
LA English
DT Article
DE Gastrointestinal; Cancer; microRNA; Forkhead box; Marker; Diagnosis
ID EPITHELIAL-MESENCHYMAL TRANSITION; GASTRIC-CANCER CELLS; HUMAN
   COLORECTAL-CANCER; TRANSCRIPTION FACTORS; EMERGING ROLES;
   HEPATOCELLULAR-CARCINOMA; CISPLATIN RESISTANCE; FOXP3 EXPRESSION;
   NONCODING RNA; IN-VITRO
AB Gastrointestinal (GI) tumors are among the most common causes of cancer related mortalities in the world. Despite various treatment modalities, there are still significant high mortality rates in these patients. Late diagnosis in advanced tumor stages is one of the major reasons for the high mortality rate that results in treatment failure and tumor relapse among these patients. Therefore, it is required to assess the molecular mechanisms involved in GI tumor progression to introduce novel efficient early detection markers. Forkhead box (FOX) is a family of transcription factors that have critical roles in regulation of cellular processes. MicroRNAs (miRNAs) are pivotal regulators of FOX gene expressions during tumor progressions. In the present review, we discussed the role of miRNAs-FOX axis during GI tumor progression and metastasis. This review paves the way to introduce the miRNAs-FOX axis as a novel candidate for the early detection and targeted therapy in GI tumors.
C1 [Zangouei, Amir Sadra; Akhlaghipour, Iman] Mashhad Univ Med Sci, Student Res Comm, Fac Med, Mashhad, Iran.
   [Ghasaban, Faezeh Tolue; Moghbeli, Meysam] Mashhad Univ Med Sci, Sch Med, Dept Med Genet & Mol Med, Mashhad, Iran.
   [Ghasaban, Faezeh Tolue; Moghbeli, Meysam] Mashhad Univ Med Sci, Med Genet Res Ctr, Mashhad, Iran.
   [Dalili, Amin] Mashhad Univ Med Sci, Sch Med, Dept Gen Surg, Mashhad, Iran.
C3 Mashhad University of Medical Sciences; Mashhad University of Medical
   Sciences; Mashhad University of Medical Sciences; Mashhad University of
   Medical Sciences
RP Moghbeli, M (corresponding author), Mashhad Univ Med Sci, Sch Med, Dept Med Genet & Mol Med, Mashhad, Iran.
EM moghbelim@mums.ac.ir
RI Akhlaghipour, Iman/AHB-8277-2022; Dalili, Amin/AAL-3994-2020; Moghbeli,
   Meysam/Q-7916-2019
OI Dalili, Amin/0000-0001-6695-8551; Tolue Ghasaban,
   Faezeh/0009-0004-8567-9637; Akhlaghipour, Iman/0000-0001-5379-4607
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NR 189
TC 3
Z9 3
U1 0
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2452-0144
J9 GENE REP
JI Gene Rep.
PD DEC
PY 2022
VL 29
AR 101694
DI 10.1016/j.genrep.2022.101694
EA OCT 2022
PG 12
WC Genetics & Heredity
WE Emerging Sources Citation Index (ESCI)
SC Genetics & Heredity
GA 5K5JM
UT WOS:000869762500001
DA 2025-01-04
ER

PT J
AU Heravi, G
   Yazdanpanah, O
   Podgorski, I
   Matherly, LH
   Liu, WQ
AF Heravi, Gioia
   Yazdanpanah, Omid
   Podgorski, Izabela
   Matherly, Larry H.
   Liu, Wanqing
TI Lipid metabolism reprogramming in renal cell carcinoma
SO CANCER AND METASTASIS REVIEWS
LA English
DT Review
DE Metabolic reprogramming; Cholesterol; Free fatty acids; PUFA; Renal cell
   carcinoma
ID FATTY-ACID SYNTHASE; PANCREATIC-CANCER CELLS; CHOLESTEROL-METABOLISM;
   COLORECTAL-CANCER; DELTA-5-DESATURASE PROMOTES; MEVALONATE PATHWAY;
   OPEN-LABEL; BODY-SIZE; INHIBITION; RISK
AB Metabolic reprogramming is recognized as a hallmark of cancer. Lipids are the essential biomolecules required for membrane biosynthesis, energy storage, and cell signaling. Altered lipid metabolism allows tumor cells to survive in the nutrient-deprived environment. However, lipid metabolism remodeling in renal cell carcinoma (RCC) has not received the same attention as in other cancers. RCC, the most common type of kidney cancer, is associated with almost 15,000 death in the USA annually. Being refractory to conventional chemotherapy agents and limited available targeted therapy options has made the treatment of metastatic RCC very challenging. In this article, we review recent findings that support the importance of synthesis and metabolism of cholesterol, free fatty acids (FFAs), and polyunsaturated fatty acids (PUFAs) in the carcinogenesis and biology of RCC. Delineating the detailed mechanisms underlying lipid reprogramming can help to better understand the pathophysiology of RCC and to design novel therapeutic strategies targeting this malignancy.
C1 [Heravi, Gioia; Liu, Wanqing] Wayne State Univ, Eugene Applebaum Coll Pharm & Hlth Sci, Dept Pharmaceut Sci, Detroit, MI 48202 USA.
   [Yazdanpanah, Omid] Wayne State Univ, Sch Med, Dept Internal Med, Detroit, MI 48201 USA.
   [Podgorski, Izabela; Matherly, Larry H.; Liu, Wanqing] Wayne State Univ, Sch Med, Dept Pharmacol, Detroit, MI 48201 USA.
   [Podgorski, Izabela; Matherly, Larry H.; Liu, Wanqing] Wayne State Univ, Sch Med, Dept Oncol, Detroit, MI 48202 USA.
   [Podgorski, Izabela; Matherly, Larry H.; Liu, Wanqing] Karmanos Canc Inst, Detroit, MI 48201 USA.
C3 Wayne State University; Wayne State University; Wayne State University;
   Wayne State University; Barbara Ann Karmanos Cancer Institute
RP Liu, WQ (corresponding author), Wayne State Univ, Eugene Applebaum Coll Pharm & Hlth Sci, Dept Pharmaceut Sci, Detroit, MI 48202 USA.; Liu, WQ (corresponding author), Wayne State Univ, Sch Med, Dept Pharmacol, Detroit, MI 48201 USA.; Liu, WQ (corresponding author), Wayne State Univ, Sch Med, Dept Oncol, Detroit, MI 48202 USA.; Liu, WQ (corresponding author), Karmanos Canc Inst, Detroit, MI 48201 USA.
EM wliu@wayne.edu
OI Liu, Wanqing/0000-0001-7727-6900
FU NIH/NIDDK [R01DK106540, R01DK124612]; Office of Vice President for
   Research of Wayne State University; Eunice and Milton Ring Endowed Chair
   for Cancer Research; NCI [T32-CA009531]; National Cancer Institute
   [T32CA009531] Funding Source: NIH RePORTER
FX This study is supported in part by the NIH/NIDDK grants (R01DK106540 and
   R01DK124612) (W.L.), the start-up fund of the Office of Vice President
   for Research of Wayne State University (W.L.), the Eunice and Milton
   Ring Endowed Chair for Cancer Research (L.H.M), and a NCI T32-CA009531
   (L.H.M.) Pre-doctoral Training fellowship to G.H.
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NR 136
TC 48
Z9 53
U1 2
U2 21
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 MAR
PY 2022
VL 41
IS 1
BP 17
EP 31
DI 10.1007/s10555-021-09996-w
EA NOV 2021
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZT9AV
UT WOS:000715003900001
PM 34741716
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Lehmann-Che, J
   Poirot, B
   Boyer, JC
   Evrard, A
AF Lehmann-Che, Jacqueline
   Poirot, Brigitte
   Boyer, Jean-Christophe
   Evrard, Alexandre
TI Cancer genomics guide clinical practice in personalized medicine
SO THERAPIE
LA English
DT Article
DE Theranostic biomarkers; Targeted therapy; Personalized medicine
ID GASTROINTESTINAL STROMAL TUMORS; NONSMALL CELL LUNG; METASTATIC
   COLORECTAL-CANCER; TYROSINE KINASE INHIBITORS; EORTC-SOFT-TISSUE;
   MONOCLONAL-ANTIBODY; BREAST-CANCER; ACQUIRED-RESISTANCE; IMATINIB
   MESYLATE; ONCOGENIC KIT
AB Targeted therapies have revolutionized the treatment of many cancers. Widely developed over the last decade, this new concept of precision medicine relies on the use of genomic technologies to analyze tumor samples in order to identify actionable targets and biomarkers of resistance. The goal is to optimize treatment by identifying which therapeutic approach is best for each patient, i.e. the treatment that is effective, has minimal adverse effects, and avoids unnecessary intervention and cost. The purpose of this review is to highlight, using a few seminal examples of therapeutic targets, the important contribution of appropriate analysis of key oncogenes or driver genes in making clinical decisions. Cancer genomics is now an indispensable part of clinical management. Furthermore, the development of next generation sequencing (NGS) will enable exploration of more and more genes of interest, leading to new treatment options for personalized medicine. (C) 2017 Societe francaise de pharmacologie et de therapeutique. Published by Elsevier Masson SAS. All rights reserved.
C1 [Lehmann-Che, Jacqueline; Poirot, Brigitte] Hop St Louis, Lab Oncol Mol, 1 Ave Claude Vellefaux, F-75475 Paris 10, France.
   [Lehmann-Che, Jacqueline; Poirot, Brigitte] Unite CNRS UMR7212 U944, Equipe Rech Translationnelle Oncol Batiment Jean, F-75475 Paris, France.
   [Boyer, Jean-Christophe; Evrard, Alexandre] CHU Nimes Caremeau, Lab Biochim, F-30029 Nimes, France.
   [Boyer, Jean-Christophe] IURC, Fac Med Montpellier, Aide a Decis Med Personnalisee Aspects Methodol, EA 2415, F-34093 Montpellier, France.
   [Evrard, Alexandre] IRCM, Unite Inserm U1194, F-34298 Montpellier, France.
C3 Centre National de la Recherche Scientifique (CNRS); CNRS - National
   Institute for Biology (INSB); Universite Paris Cite; Universite de
   Montpellier; CHU de Nimes; Universite de Montpellier; Universite de
   Montpellier; UNICANCER; Institut Regional du Cancer Montpellier / Val
   d'Aurelle (ICM); Institut National de la Sante et de la Recherche
   Medicale (Inserm)
RP Lehmann-Che, J (corresponding author), Hop St Louis, Lab Oncol Mol, 1 Ave Claude Vellefaux, F-75475 Paris 10, France.
EM jacqueline.lehmann-che@aphp.fr
RI Evrard, Alexandre/C-4269-2013
OI Lehmann-Che, jacqueline/0000-0001-6685-3354
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NR 90
TC 9
Z9 9
U1 0
U2 5
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0040-5957
EI 1958-5578
J9 THERAPIE
JI Therapie
PD SEP
PY 2017
VL 72
IS 4
BP 439
EP 451
DI 10.1016/j.therap.2016.09.015
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FK6XX
UT WOS:000413649600005
PM 28258721
DA 2025-01-04
ER

PT J
AU Yang, LP
   Jiang, TJ
   He, MM
   Ling, YH
   Wang, ZX
   Wu, HX
   Zhang, Z
   Xu, RH
   Wang, F
   Yuan, SQ
   Zhao, Q
AF Yang, Lu-Ping
   Jiang, Teng-Jia
   He, Ming-Ming
   Ling, Yi-Hong
   Wang, Zi-Xian
   Wu, Hao-Xiang
   Zhang, Zhen
   Xu, Rui-Hua
   Wang, Feng
   Yuan, Shu-Qiang
   Zhao, Qi
TI Comprehensive genomic characterization of sporadic synchronous
   colorectal cancer: Implications for treatment optimization and clinical
   outcome
SO CELL REPORTS MEDICINE
LA English
DT Article
ID NEUTRAL TUMOR EVOLUTION; MICROSATELLITE INSTABILITY; MOLECULAR
   CHARACTERISTICS; HETEROGENEITY; MUTATIONS; CARCINOMA; VARIANTS; PATHWAY;
   ADULT
AB Sporadic synchronous colorectal cancer (SCRC) refers to multiple primary CRC tumors detected simultaneously in an individual without predisposing hereditary conditions, which accounts for the majority of multiple CRCs while lacking a profound understanding of the genomic landscape and evolutionary dynamics to optimize its treatment. In this study, 103 primary tumor samples from 51 patients with SCRC undergo wholeexome sequencing. The germline and somatic mutations and evolutionary and clinical features are comprehensively investigated. Somatic genetic events are largely inconsistent between paired tumors. Compared with solitary CRC, SCRCs have higher prevalence of tumor mutation burden high (TMB-H; 33.3%) and micro satellite-instability high (MSI-H; 29.4%) and different mutation frequencies in oncogenic signaling pathways. Moreover, neutrally evolving SCRC tumors are associated with higher intratumoral heterogeneity and better prognosis. These findings unveil special molecular features, carcinogenesis, and prognosis of sporadic SCRC. Strategies for targeted therapy and immunotherapy should be optimized accordingly.
C1 [Yang, Lu-Ping; Jiang, Teng-Jia; He, Ming-Ming; Ling, Yi-Hong; Wang, Zi-Xian; Wu, Hao-Xiang; Zhang, Zhen; Xu, Rui-Hua; Wang, Feng; Yuan, Shu-Qiang; Zhao, Qi] Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou 510060, Peoples R China.
   [He, Ming-Ming; Wang, Zi-Xian; Wu, Hao-Xiang; Xu, Rui-Hua] Chinese Acad Med Sci, Res Unit Precis Diag & Treatment Gastrointestinal, Guangzhou 510060, Peoples R China.
C3 Sun Yat Sen University; State Key Lab Oncology South China; Chinese
   Academy of Medical Sciences - Peking Union Medical College
RP Yuan, SQ; Zhao, Q (corresponding author), Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou 510060, Peoples R China.
EM yuanshq@sysucc.org.cn; zhaoqi@sysucc.org.cn
RI He, Mingming/AAY-5609-2021; Xu, Rui-Hua/AAW-4766-2021
OI Xu, Rui-Hua/0000-0001-9771-8534
FU National Key R&D Program of China [2021YFA1302100]; National Natural
   Science Foundation of China [82172861]; Guangdong Basic and Applied
   Basic Research Foundation [2021A1515011743]; Youth Talent Support
   Program of Guangdong Provincial Association for Science and Technology
   [SKXRC202313]
FX The work was supported by the National Key R&D Program of China
   (2021YFA1302100 to Q.Z.) ; the National Natural Science Foundation of
   China (82172861 to Q.Z.) ; the Guangdong Basic and Applied Basic
   Research Foundation (2021A1515011743 to Q.Z.) ; and the Youth Talent
   Support Program of Guangdong Provincial Association for Science and
   Technology (SKXRC202313 to Q.Z.) . We also sincerely show gratitude to
   Dr. Seeruttun Sharvesh Raj from the Sun Yat-sen University Cancer Center
   for his writing assistance. Part of the graphical abstract was created
   with BioRender.com .
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NR 55
TC 0
Z9 1
U1 1
U2 4
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 OCT 17
PY 2023
VL 4
IS 10
AR 101222
DI 10.1016/j.xcrm.2023.101222
EA OCT 2023
PG 16
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA Y0GE3
UT WOS:001102131600001
PM 37794586
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Cherri, S
   Libertini, M
   Zaniboni, A
AF Cherri, Sara
   Libertini, Michela
   Zaniboni, Alberto
TI New drugs for the treatment of metastatic colorectal cancer
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Colon cancer; Colon rectal cancer; New drugs; Drug resistance;
   Metastatic colorectal cancer
ID COLON-CANCER; FRUQUINTINIB; INSTABILITY; POPULATION; INHIBITION;
   CETUXIMAB; SURVIVAL
AB Colorectal cancer (CRC) represents one of the most frequent malignancies in terms of incidence and mortality, thus representing the third leading cause of cancer death worldwide. In the last decade, few drugs have enriched the treatment landscape of metastatic CRC and have significantly affected prognosis. Unlike other neoplasms, metastatic CRC patients who have exhausted treatment options often still maintain a good performance status. There are many challenges to increasing potential treatment options, notably a better understanding of disease biology and the mechanisms of resistance underlying cancer treatment failure. The development of new drugs for metastatic CRC certainly represents one of the most important challenges in medical oncology. This article discusses the main limitations in the development of new drugs and potential future scenarios. In particular, we addressed three questions: (1) The main limitations of targeted therapy in the treatment of metastatic CRC (mCRC); (2) New target armamentarium that could escape primary and secondary resistance and lead to more personalized mCRC therapy; and (3) Future directions.
C1 [Cherri, Sara; Libertini, Michela; Zaniboni, Alberto] Fdn Poliambulanza, Dept Oncol, Via L Bissolati 57, I-25124 Brescia, Italy.
RP Cherri, S (corresponding author), Fdn Poliambulanza, Dept Oncol, Via L Bissolati 57, I-25124 Brescia, Italy.
EM sara.cherri@poliambulanza.it
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NR 45
TC 3
Z9 3
U1 2
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 NOV 15
PY 2021
VL 13
IS 11
BP 1551
EP 1560
DI 10.4251/wjgo.v13.i11.1551
PG 10
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA XL4WF
UT WOS:000728144900002
PM 34853636
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Saponaro, C
   Sergio, S
   Coluccia, A
   De Luca, M
   La Regina, G
   Mologni, L
   Famiglini, V
   Naccarato, V
   Bonetti, D
   Gautier, C
   Gianni, S
   Vergara, D
   Salzet, M
   Fournier, I
   Bucci, C
   Silvestri, R
   Passerini, CG
   Maffia, M
   Coluccia, AML
AF Saponaro, Concetta
   Sergio, Sara
   Coluccia, Antonio
   De Luca, Maria
   La Regina, Giuseppe
   Mologni, Luca
   Famiglini, Valeria
   Naccarato, Valentina
   Bonetti, Daniela
   Gautier, Candice
   Gianni, Stefano
   Vergara, Daniele
   Salzet, Michel
   Fournier, Isabelle
   Bucci, Cecilia
   Silvestri, Romano
   Passerini, Carlo Gambacorti
   Maffia, Michele
   Coluccia, Addolorata Maria Luce
TI β-catenin knockdown promotes NHERF1-mediated survival of colorectal
   cancer cells: implications for a double-targeted therapy
SO ONCOGENE
LA English
DT Article
ID SMALL-MOLECULE INHIBITION; REGULATORY FACTOR-1; NUCLEAR NHERF1; PROTEIN;
   GROWTH; COLON; PTEN; PHOSPHORYLATION; ASSOCIATION; ACTIVATION
AB Nuclear activated beta-catenin plays a causative role in colorectal cancers (CRC) but remains an elusive therapeutic target. Using human CRC cells harboring different Wnt/beta-catenin pathway mutations in APC/KRAS or beta-catenin/KRAS genes, and both genetic and pharmacological knockdown approaches, we show that oncogenic beta-catenin signaling negatively regulates the expression of NHERF1 (Na+/H+ exchanger 3 regulating factor 1), a PDZ-adaptor protein that is usually lost or downregulated in early dysplastic adenomas to exacerbate nuclear beta-catenin activity. Chromatin immunoprecipitation (ChIP) assays demonstrated that beta-catenin represses NHERF1 via TCF4 directly, while the association between TCF1 and the Nherf1 promoter increased upon beta-catenin knockdown. To note, the occurrence of a cytostatic survival response in settings of single beta-catenin-depleted CRC cells was abrogated by combining NHERF1 inhibition via small hairpin RNA (shRNA) or RS5517, a novel PDZ1-domain ligand of NHERF1 that prevented its ectopic nuclear entry. Mechanistically, dual NHERF1/beta-catenin targeting promoted an autophagy-to-apoptosis switch consistent with the activation of Caspase-3, the cleavage of PARP and reduced levels of phospho-ERK1/2, Beclin-1, and Rab7 autophagic proteins compared with beta-catenin knockdown alone. Collectively, our data unveil novel beta-catenin/TCF-dependent mechanisms of CRC carcinogenesis, also offering preclinical proof of concept for combining beta-catenin and NHERF1 pharmacological inhibitors as a mechanism-based strategy to augment apoptotic death of CRC cells refractory to current Wnt/beta-catenin-targeted therapeutics.
C1 [Saponaro, Concetta; Sergio, Sara; Vergara, Daniele; Maffia, Michele; Coluccia, Addolorata Maria Luce] Giovanni Paolo II Oncol Hosp, Lab Clin Prote, I-73100 Lecce, Italy.
   [Saponaro, Concetta] IRCCS Ist Tumori Giovanni Paolo II, Funct Biomorphol Lab, Bari, Italy.
   [Sergio, Sara; De Luca, Maria; Vergara, Daniele; Bucci, Cecilia; Maffia, Michele; Coluccia, Addolorata Maria Luce] Univ Salento, Dept Biol & Environm Sci & Technol, I-73100 Lecce, Italy.
   [Coluccia, Antonio; La Regina, Giuseppe; Famiglini, Valeria; Naccarato, Valentina; Silvestri, Romano] Sapienza Univ Rome, Ist Pasteur Italia, Fdn Cenci Bolognetti, Dept Drug Chem & Technol, Piazzale Aldo Moro 5, I-00185 Rome, Italy.
   [Mologni, Luca; Passerini, Carlo Gambacorti] Univ Milano Bicocca, San Gerardo Hosp, Dept Clin Med, I-20052 Monza, Italy.
   [Bonetti, Daniela; Gautier, Candice; Gianni, Stefano] Sapienza Univ Rome, Ist Pasteur Italia, Fdn Cenci Bolognetti, Dept Biochem, Piazzale Aldo Moro 5, I-00185 Rome, Italy.
   [Salzet, Michel; Fournier, Isabelle] U1192 Lab Prote Reponse Inflammatoire & Spectrome, F-59000 Lille, France.
C3 IRCCS Istituto Tumori Bari Giovanni Paolo II; University of Salento;
   Sapienza University Rome; Fondazione Cenci Bolognetti; San Gerardo
   Hospital; University of Milano-Bicocca; Sapienza University Rome;
   Fondazione Cenci Bolognetti; Universite de Lille
RP Coluccia, AML (corresponding author), Giovanni Paolo II Oncol Hosp, Lab Clin Prote, I-73100 Lecce, Italy.; Coluccia, AML (corresponding author), Univ Salento, Dept Biol & Environm Sci & Technol, I-73100 Lecce, Italy.
EM michele.maffia@unisalento.it; malu.coluccia@unisalento.it
RI Coluccia, Antonio/K-3114-2018; Mologni, Luca/AAC-1065-2022; Bucci,
   Cecilia/F-6699-2012; MAFFIA, MICHELE/AAC-2943-2020; Saponaro,
   Concetta/K-7886-2018; La Regina, Giuseppe/I-2161-2012; sergio,
   sara/AAC-3849-2019; gianni, stefano/C-8536-2009; Vergara,
   Daniele/K-3831-2014; Salzet, Michel/A-7675-2011; FOURNIER,
   Isabelle/H-9195-2015
OI Mologni, Luca/0000-0002-6365-5149; Gautier, Candice/0000-0002-6125-662X;
   Vergara, Daniele/0000-0002-2396-7674; Saponaro,
   Concetta/0000-0002-8196-3583; Salzet, Michel/0000-0003-4318-0817;
   Sergio, Sara/0000-0002-4490-4189; FOURNIER, Isabelle/0000-0003-1096-5044
FU Italian Association for Cancer Research (AIRC)-Investigator Grant (IG)
   [14236]; Italian Grant PRIN 2015 [2015FCHJ8E]; European Union's Horizon
   2020 Research and Innovation program under the Marie Sklodowska-Curie
   grant [675341]; AIRC IG 2016 [19068]; Apulia Regione Cluster Project
   SISTEMA [T7WGSJ3]; Veronesi Foundation fellowship
FX We thank Dr. Hans Clevers (Hubrecht Laboratory, Utrecht, The
   Netherlands) for providing the pcDNA<INF>6</INF>TR and pTER vectors. We
   gratefully acknowledge funding from Italian Association for Cancer
   Research (AIRC)-Investigator Grant (IG) 2014 No. 14236 (AMLC). This work
   was partially supported by Italian Grant PRIN 2015 (2015FCHJ8E) (RS),
   European Union's Horizon 2020 Research and Innovation program under the
   Marie Sklodowska-Curie grant agreement No. 675341 (SG), AIRC IG 2016 No.
   19068 (CB) and Apulia Regione Cluster Project SISTEMA No. T7WGSJ3 (MM).
   MDL was recipient of a Veronesi Foundation fellowship. We warmly thank
   Dr. Antonio Danieli for his technical assistance.
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NR 50
TC 19
Z9 19
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD JUN 14
PY 2018
VL 37
IS 24
BP 3301
EP 3316
DI 10.1038/s41388-018-0170-y
PG 16
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 GJ6XB
UT WOS:000435526600009
PM 29551770
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Lee, KC
   Ou, YC
   Hu, WH
   Liu, CC
   Chen, HH
AF Lee, Ko-Chao
   Ou, Yu-Che
   Hu, Wan-Hsiang
   Liu, Chia-Cheng
   Chen, Hong-Hwa
TI Meta-analysis of outcomes of patients with stage IV colorectal cancer
   managed with chemotherapy/radiochemotherapy with and without primary
   tumor resection
SO ONCOTARGETS AND THERAPY
LA English
DT Article
DE chemotherapy; colorectal cancer; outcomes; tumor resection
ID ASYMPTOMATIC PATIENTS; SURGICAL RESECTION; INTESTINAL COMPLICATIONS;
   SYNCHRONOUS METASTASES; COLON-CANCER; SURVIVAL; CHEMOTHERAPY;
   OXALIPLATIN; SURGERY; BEVACIZUMAB
AB Background: Colorectal cancer is the third leading cause of death worldwide. Currently, novel chemotherapeutic agents are first-line therapy for unresectable stage IV colorectal cancer, while benefits of noncurative primary tumor resection in advanced disease remain debatable.
   Objective: This meta-analysis evaluated outcomes of patients with unresectable stage IV colorectal cancer receiving systemic chemotherapy with or without primary tumor resection.
   Materials and methods: A database search of PubMed and Cochrane Library databases identified 167 studies that were screened for relevance. After 119 were excluded, 48 were assessed for eligibility and 26 were included for meta-analysis, including 24 retrospective studies, one prospective study, and one randomized, controlled trial. Extracted data included patient demographics (age, sex), clinical data (tumor stage, metastasis), targeted therapy agents, and surgical data (with/without tumor resection). Patients' overall and progression-free survival was compared between groups with/without primary tumor resection.
   Results: The 26 studies included 43,903 patients with colorectal cancer, with 29,639 receiving chemotherapy/radiotherapy plus primary tumor resection, and 14,264 managed medically with chemotherapy/chemoradiotherapy alone without primary tumor resection. Patients receiving primary tumor resection plus chemotherapy/radiotherapy had longer overall survival (hazard ratio [HR 0.59], 95% confidence interval [CI] 0.51-0.68; P < 0.001), with significant differences in overall survival between patients with and without primary tumor resection (HR 0.58, 95% CI 0.49-0.68; P < 0.001). Longer overall survival was also found among patients receiving primary tumor resection who were treated with bevacizumab/cetuximab targeted therapy agents (HR 0.63, 95% CI 0.46-0.86; P=0.003). Patients from three studies who received primary tumor resection had longer progression-free survival (HR 0.73, 95% CI 0.58-0.91; P=0.005). Results are limited by retrospective data, inconsistent complications data, and publication bias.
   Conclusion: Study results support primary tumor resection in stage IV colorectal cancer, but significant biases in studies suggest that randomized trials are warranted to confirm findings.
C1 [Lee, Ko-Chao; Hu, Wan-Hsiang; Chen, Hong-Hwa] Chang Gung Univ, Coll Med, Kaohsiung Med Ctr, Div Colorectal Surg,Dept Surg,Chang Gung Mem Hosp, Kaohsiung, Taiwan.
   [Ou, Yu-Che] Chang Gung Univ, Coll Med, Kaohsiung Med Ctr, Dept Obstet & Gynecol,Chang Gung Mem Hosp, Kaohsiung, Taiwan.
   [Liu, Chia-Cheng] Pingtung Christian Hosp, Dept Surg, Pingtung, Taiwan.
C3 Chang Gung University; Chang Gung Memorial Hospital; Chang Gung
   University; Chang Gung Memorial Hospital
RP Lee, KC; Chen, HH (corresponding author), Kaohsiung Chang Gung Mem Hosp, Dept Surg, Div Colorectal Surg, 123 Ta Pei Rd, Kaohsiung, Taiwan.
EM kclee@adm.cgmh.org.tw; kmch4329@gmail.com
RI Lee, Ko-Chao/AHC-2415-2022
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NR 46
TC 22
Z9 24
U1 0
U2 1
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 7059
EP 7069
DI 10.2147/OTT.S112965
PG 11
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA EC1XJ
UT WOS:000387901800001
PM 27895498
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Zhang, XM
   Yang, G
   Zhao, Y
   Dai, XY
   Liu, WJ
   Qu, F
   Huang, YY
AF Zhang, Xiaomin
   Yang, Ge
   Zhao, Yi
   Dai, Xuyan
   Liu, Wenjing
   Qu, Feng
   Huang, Yuanyu
TI Selection and Identification of an ssDNA Aptamer for Fibroblast
   Activation Protein
SO MOLECULES
LA English
DT Article
DE FAP; aptamer; CE; SELEX; cancer-associated fibroblasts
ID NONEQUILIBRIUM CAPILLARY-ELECTROPHORESIS; EQUILIBRIUM MIXTURES;
   IMMUNITY; GROWTH; POTENT; STROMA; CELLS
AB As a type II transmembrane serine protease, fibroblast activation protein (FAP) is specifically expressed on the surface of fibroblasts associated with a variety of epithelial-derived malignancies such as pancreatic cancer, breast cancer, and colon cancer. It participates in the processes of tumorigenesis, progression, and immunosuppression. FAP constitutes an important target for tumor treatment; however, the current studies on FAP are mainly related to structural characteristics, enzymatic properties, and biological functions, and aptamers of FAP have not been investigated. In this work, by using recombinant human FAP as the target, five candidate aptamers, which are AptFAP-A1, AptFAP-A2, AptFAP-A3, AptFAP-A4, and AptFAP-A5, were selected by capillary electrophoresis-systematic evolution of ligands by exponential enrichment (CE-SELEX), and their secondary structures were predicted to be mainly stem-loop. Moreover, the CE-laser-induced fluorescence (LIF) method was used to determine the equilibrium dissociation constant K-D values between the FAP protein and candidate aptamers, and the K-D value was in the low molar range. Finally, Cy5-labeled aptamers were co-incubated with human pancreatic cancer-associated fibroblasts highly expressing FAP protein, and confocal microscopy imaging showed that aptamer AptFAP-A4 had the highest affinities with the cells. The FAP aptamers screened in this study provide a promising direction for the development of rapid tumor diagnosis and targeted therapy.
C1 [Zhang, Xiaomin; Yang, Ge; Zhao, Yi; Qu, Feng; Huang, Yuanyu] Beijing Inst Technol, Adv Res Inst Multidisciplinary Sci, Sch Life Sci, Key Lab Mol Med & Biotherapy,Key Lab Med Mol Sci &, Beijing 100081, Peoples R China.
   [Yang, Ge] Chinese Acad Med Sci & Peking Union Med Coll, CAMS Key Lab Antiviral Drug Res, Beijing Key Lab Antimicrobial Agents, Inst Med Biotechnol,NHC Key Lab Biotechnol Antibio, Beijing 100050, Peoples R China.
   [Dai, Xuyan] Hunan Agr Univ, Econ Coll, Changsha 410128, Peoples R China.
   [Liu, Wenjing] Capital Med Univ, Beijing Chest Hosp, Beijing TB & Thorac Tumor Res Inst, Beijing Key Lab Drug Resistance TB Res, Beijing 101125, Peoples R China.
C3 Beijing Institute of Technology; Chinese Academy of Medical Sciences -
   Peking Union Medical College; Peking Union Medical College; Hunan
   Agricultural University; Capital Medical University
RP Yang, G; Huang, YY (corresponding author), Beijing Inst Technol, Adv Res Inst Multidisciplinary Sci, Sch Life Sci, Key Lab Mol Med & Biotherapy,Key Lab Med Mol Sci &, Beijing 100081, Peoples R China.; Yang, G (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, CAMS Key Lab Antiviral Drug Res, Beijing Key Lab Antimicrobial Agents, Inst Med Biotechnol,NHC Key Lab Biotechnol Antibio, Beijing 100050, Peoples R China.
EM yangge@imb.cams.cn; yyhuang@bit.edu.cn
RI zhang, xiaomin/IQX-1078-2023; Liu, Wenjing/B-3816-2019; Huang,
   Yuanyu/H-8466-2014
OI Huang, Yuanyu/0000-0003-3935-7245
FU National Natural Science Foundation of China [21874010, 32101148];
   Beijing Nova Program from Beijing Municipal Science & Technology
   Commission [Z201100006820005]; Beijing Municipal Natural Science
   Foundation [7222310]; Fundamental Research Funds for the Central
   Universities [3332022055]
FX This research was funded by the National Natural Science Foundation of
   China (21874010, 32101148), the Beijing Nova Program from Beijing
   Municipal Science & Technology Commission (Z201100006820005), Beijing
   Municipal Natural Science Foundation (7222310), and the Fundamental
   Research Funds for the Central Universities (3332022055).
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NR 65
TC 5
Z9 5
U1 4
U2 30
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD FEB
PY 2023
VL 28
IS 4
AR 1682
DI 10.3390/molecules28041682
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 9L9EJ
UT WOS:000941845200001
PM 36838669
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Loilome, W
   Dokduang, H
AF Loilome, Watcharin
   Dokduang, Hasaya
TI Protein Kinases as Targets for <i>Opisthorchis viverrini</i>- Associated
   Cholangiocarcinoma Therapy
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
DE Protein kinases; signal transduction; kinase inhibitors;
   cholangiocarcinoma (CCA); targeted therapy; cholangiocarcinoma therapy
ID RECEPTOR TYROSINE KINASE; PI3K/AKT SIGNALING PATHWAY; NITRATIVE
   DNA-DAMAGE; LUNG-CANCER; COLORECTAL-CANCER; STAT PROTEINS; PERIHILAR
   CHOLANGIOCARCINOMA; TRANSCRIPTION FACTORS; NORTHEAST THAILAND;
   BETA-CATENIN
AB Protein kinases are enzymes that catalyze the transfer of phosphate from ATP to the serine/threonine or tyrosine residues of target molecules. These are key important mediators in a signaling cascade involved in several biological processes. Dysregulation of their activity has been found in various tumors. From the increased understanding of kinase structure and activation mechanisms emerged new strategies for targeting kinase in cancer treatment. Nowadays, kinase specific inhibitors are developed and widely used for clinical cancer treatment. In this review, we focus on protein kinases that are involved in cholangiocarcinoma (CCA). CCA is a slow progression tumor that is recognized as a major public health issue in northeastern Thailand. The standard regimen for CCA treatment is surgical resection. However, the patient's clinical outcome is still problematic. Therefore, the search to identify molecular mechanisms and molecules that are involved in carcinogenesis and the progression of CCA that can be used as therapeutic targets is urgently required. Aberrant expression and activation, as well as the functions of protein kinases in CCA, have been extensively studied in order to apply them as therapeutic targets. This review provides the information on protein kinases and their activity in CCA, as well as the preclinical data on kinase inhibitors that have been evaluated for this cancer.
C1 [Loilome, Watcharin] Khon Kaen Univ, Fac Med, Dept Biochem, Khon Kaen, Thailand.
   [Loilome, Watcharin; Dokduang, Hasaya] Khon Kaen Univ, Cholangiocarcinoma Res Inst, Khon Kaen, Thailand.
   [Loilome, Watcharin; Dokduang, Hasaya] Khon Kaen Univ, Fac Med, Cholangiocarcinoma Screening & Care Program CASCA, Khon Kaen, Thailand.
C3 Khon Kaen University; Khon Kaen University; Khon Kaen University
RP Loilome, W (corresponding author), Khon Kaen Univ, Fac Med, Dept Biochem, Khon Kaen, Thailand.; Loilome, W (corresponding author), Khon Kaen Univ, Cholangiocarcinoma Res Inst, Khon Kaen, Thailand.; Loilome, W (corresponding author), Khon Kaen Univ, Fac Med, Cholangiocarcinoma Screening & Care Program CASCA, Khon Kaen, Thailand.
EM watloi@yahoo.com
RI Loilome, Watcharin/AAW-6203-2021
OI Dokduang, Hasaya/0009-0004-4765-333X
FU Thailand Research Fund; Faculty of Medicine, Khon Kaen University
FX This article is dedicated to Professor Puangrat Yongvanit, the scientist
   who intensively studied and provided the link of liver fluke-induced
   inflammation in relation to CCA development. We would like to thank all
   granting agencies, including the grants from the Thailand Research Fund
   and Faculty of Medicine, Khon Kaen University. We also thank Professor
   Trevor N. Petney for editing the initial submission via Publication
   Clinic KKU, Thailand.
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NR 94
TC 3
Z9 3
U1 0
U2 1
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1381-6128
EI 1873-4286
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PY 2017
VL 23
IS 29
BP 4281
EP 4289
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FM8YM
UT WOS:000415378600006
PM 28699535
DA 2025-01-04
ER

PT J
AU Chapdelaine, AG
   Ku, GC
   Sun, GQ
   Ayrapetov, MK
   Roche, S
AF Chapdelaine, Abygail G.
   Ku, Geng Chia
   Sun, Gongqin
   Ayrapetov, Marina K.
   Roche, Serge
TI The Targeted Degradation of BRAF V600E Reveals the Mechanisms of
   Resistance to BRAF-Targeted Treatments in Colorectal Cancer Cells
SO CANCERS
LA English
DT Article
DE proteolysis targeting chimera; PROTAC; BRAF V600E mutation; colorectal
   cancer; triple-negative breast cancer; intrinsic resistance;
   mitogen-activated protein kinase pathway
ID ACQUIRED-RESISTANCE; MEK INHIBITION; RAF INHIBITION; MUTATIONS;
   MELANOMA; THERAPY; PATHWAY; GENE; VEMURAFENIB; DABRAFENIB
AB The BRAF V600E mutation is frequently found in cancer. It activates the MAPK pathway and promotes cancer cell proliferation, making BRAF an excellent target for anti-cancer therapy. While BRAF-targeted therapy is highly effective for melanoma, it is often ineffective against other cancers harboring the BRAF mutation. In this study, we evaluate the effectiveness of a proteolysis targeting chimera (PROTAC), SJF-0628, in directing the degradation of mutated BRAF across a diverse panel of cancer cells and determine how these cells respond to the degradation. SJF-0628 treatment results in the degradation of BRAF V600E and a decrease in Mek activation in all cell lines tested, but the effects of the treatment on cell signaling and cell proliferation are cell-line-specific. First, BRAF degradation killed DU-4475 and Colo-205 cells via apoptosis but only partially inhibited the proliferation of other cancer cell lines. Second, SJF-0628 treatment resulted in co-degradation of MEK in Colo-205 cells but did not have the same effect in other cell lines. Finally, cell lines partially inhibited by BRAF degradation also contain other oncogenic drivers, making them multi-driver cancer cells. These results demonstrate the utility of a PROTAC to direct BRAF degradation and reveal that multi-driver oncogenesis renders some colorectal cancer cells resistant to BRAF-targeted treatment.
C1 [Chapdelaine, Abygail G.; Ku, Geng Chia; Sun, Gongqin; Ayrapetov, Marina K.] Univ Rhode Isl, Dept Cell & Mol Biol, Kingston, RI 02881 USA.
C3 University of Rhode Island
RP Sun, GQ; Ayrapetov, MK (corresponding author), Univ Rhode Isl, Dept Cell & Mol Biol, Kingston, RI 02881 USA.
EM agchapdelaine@uri.edu; gengchia_ku@uri.edu; gsun@uri.edu;
   ayrapetov@uri.edu
FU the United States Department of Defense Peer-Reviewed Cancer Research
   Program [P20GM103430]; Rhode Island Institutional Development Award
   (IDeA) Network of Biomedical Research Excellence from the National
   Institute of General Medical Sciences of the National Institutes of
   Health
FX We appreciate the generous access to important research equipment in the
   laboratories of Matthew Ramsey, Niall Howlett, and Arnob Dutta in the
   Department of Cell and Molecular Biology at URI. Research reported in
   this publication was also supported, in part, by the Rhode Island
   Institutional Development Award (IDeA) Network of Biomedical Research
   Excellence from the National Institute of General Medical Sciences of
   the National Institutes of Health under grant number P20GM103430.
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NR 61
TC 2
Z9 2
U1 3
U2 16
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD DEC
PY 2023
VL 15
IS 24
AR 5805
DI 10.3390/cancers15245805
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DM1A8
UT WOS:001132357000001
PM 38136350
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Coronel-Hernández, J
   Salgado-García, R
   Cantú-De León, D
   Jacobo-Herrera, N
   Millan-Catalan, O
   Delgado-Waldo, I
   Campos-Parra, AD
   Rodríguez-Morales, M
   Delgado-Buenrostro, NL
   Pérez-Plasencia, C
AF Coronel-Hernandez, Jossimar
   Salgado-Garcia, Rebeca
   Cantu-De Leon, David
   Jacobo-Herrera, Nadia
   Millan-Catalan, Oliver
   Delgado-Waldo, Izamary
   Campos-Parra, Alma D.
   Rodriguez-Morales, Miguel
   Delgado-Buenrostro, Norma L.
   Perez-Plasencia, Carlos
TI Combination of Metformin, Sodium Oxamate and Doxorubicin Induces
   Apoptosis and Autophagy in Colorectal Cancer Cells <i>via</i>
   Downregulation HIF-1α
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE HIF-1 alpha; autophagy; ULK1; mir-26a; AKT; proliferation
ID NEGATIVE BREAST-CANCER; HYPOXIA; INHIBITION; EXPRESSION; MIR-26A; AKT;
   PROLIFERATION; INVOLVEMENT; DEPRIVATION; PANITUMUMAB
AB Colorectal cancer (CRC) is the third leading cause of cancer-related death worldwide in both sexes. Current therapies include surgery, chemotherapy, and targeted therapy; however, prolonged exposure to chemical agents induces toxicity in patients and drug resistance. So, we implemented a therapeutic strategy based on the combination of doxorubicin, metformin, and sodium oxamate called triple therapy (Tt). We found that Tt significantly reduced proliferation by inhibiting the mTOR/AKT pathway and promoted apoptosis and autophagy in CRC derived cells compared with doxorubicin. Several autophagy genes were assessed by western blot; ULK1, ATG4, and LC3 II were overexpressed by Tt. Interestingly, ULK1 was the only one autophagy-related protein gradually overexpressed during Tt administration. Thus, we assumed that there was a post-transcriptional mechanism mediating by microRNAs that regulate UKL1 expression during autophagy activation. Through bioinformatics approaches, we ascertained that ULK1 could be targeted by mir-26a, which is overexpressed in advanced stages of CRC. In vitro experiments revealed that overexpression of mir-26a decreased significantly ULK1, mRNA, and protein expression. Contrariwise, the Tt recovered ULK1 expression by mir-26a decrease. Due to triple therapy repressed mir-26a expression, we hypothesized this drug combination could be involved in mir-26a transcription regulation. Consequently, we analyzed the mir-26a promoter sequence and found two HIF-1 alpha transcription factor recognition sites. We developed two different HIF-1 alpha stabilization models. Both showed mir-26a overexpression and ULK1 reduction in hypoxic conditions. Immunoprecipitation experiments were performed and HIF-1 alpha enrichment was observed in mir-26a promoter. Surprisingly, Tt diminished HIF-1 alpha detection and restored ULK1 mRNA expression. These results reveal an important regulation mechanism controlled by the signaling that activates HIF-1 alpha and that in turn regulates mir-26a transcription.
C1 [Coronel-Hernandez, Jossimar; Perez-Plasencia, Carlos] UNAM, FES Iztacala, Unidad Biomed, Lab Genom Func, Tlalnepantla, Mexico.
   [Coronel-Hernandez, Jossimar; Salgado-Garcia, Rebeca; Cantu-De Leon, David; Millan-Catalan, Oliver; Delgado-Waldo, Izamary; Campos-Parra, Alma D.; Rodriguez-Morales, Miguel; Perez-Plasencia, Carlos] Inst Nacl Cancerol, Lab Genomica, Tlalpan, Mexico.
   [Jacobo-Herrera, Nadia] INCMNSZ, Unidad Bioquimca, Tlalpan, Mexico.
   [Delgado-Buenrostro, Norma L.] UNAM, FES IZTACALA, Lab Toxicol, Unidad Biomed, Tlalnepantla, Mexico.
C3 Universidad Nacional Autonoma de Mexico; Instituto Nacional de
   Cancerologia (INCAN); Universidad Nacional Autonoma de Mexico
RP Pérez-Plasencia, C (corresponding author), UNAM, FES Iztacala, Unidad Biomed, Lab Genom Func, Tlalnepantla, Mexico.; Pérez-Plasencia, C (corresponding author), Inst Nacl Cancerol, Lab Genomica, Tlalpan, Mexico.
EM carlos.pplas@gmail.com
RI Jacobo-Herrera, Nadia/AGG-8009-2022; Perez-Plasencia,
   Carlos/P-2372-2019; Rodriguez, Miguel/AGY-0751-2022
OI Rodriguez, Miguel/0000-0002-4302-1069; Coronel-Hernandez,
   Jossimar/0000-0001-6543-5310; Delgado-Waldo,
   Izamary/0000-0002-3688-9775; Jacobo-Herrera, Nadia/0000-0002-1026-3774
FU CONACYT [402278]; COMECYT [2019ND0005-11]; UNAM [PAPIIT-IN231420]
FX JC-H is a doctoral student from Programa de Doctorado en Ciencias
   Biomedicas, Universidad Nacional Autonoma de Mexico (UNAM) and received
   fellowship 402278 from CONACYT and 2019ND0005-11 from COMECYT. This
   study was supported by UNAM PAPIIT-IN231420 research funds granted to
   CP-P.
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NR 78
TC 22
Z9 22
U1 0
U2 12
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 26
PY 2021
VL 11
AR 594200
DI 10.3389/fonc.2021.594200
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SO6MK
UT WOS:000659084500001
PM 34123772
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kaboli, PJ
   Chen, HF
   Babaeizad, A
   Geraylow, KR
   Yamaguchi, H
   Hung, MC
AF Kaboli, Parham Jabbarzadeh
   Chen, Hsiao-Fan
   Babaeizad, Ali
   Geraylow, Kiarash Roustai
   Yamaguchi, Hirohito
   Hung, Mien-Chie
TI Unlocking c-MET: A comprehensive journey into targeted therapies for
   breast cancer
SO CANCER LETTERS
LA English
DT Article
DE c-MET receptor; Breast cancer; Hepatocyte growth factor receptor;
   Targeted therapy; Tumorigenesis; Clinical approach
ID HEPATOCYTE GROWTH-FACTOR; CELL LUNG-CANCER; CAR-T-CELLS; PHASE-II;
   ANTITUMOR-ACTIVITY; COLORECTAL-CANCER; TYROSINE KINASE;
   ACQUIRED-RESISTANCE; MEDIATED RESISTANCE; TUMOR PROGRESSION
AB Breast cancer is the most common malignancy among women, posing a formidable health challenge worldwide. In this complex landscape, the c-MET (cellular-mesenchymal epithelial transition factor) receptor tyrosine kinase (RTK), also recognized as the hepatocyte growth factor (HGF) receptor (HGFR), emerges as a prominent protagonist, displaying overexpression in nearly 50% of breast cancer cases. Activation of c-MET by its ligand, HGF, secreted by neighboring mesenchymal cells, contributes to a cascade of tumorigenic processes, including cell proliferation, metastasis, angiogenesis, and immunosuppression. While c-MET inhibitors such as crizotinib, capmatinib, tepotinib and cabozantinib have garnered FDA approval for non-small cell lung cancer (NSCLC), their potential within breast cancer therapy is still undetermined. This comprehensive review embarks on a journey through structural biology, multifaceted functions, and intricate signaling pathways orchestrated by cMET across cancer types. Furthermore, we highlight the pivotal role of c-MET-targeted therapies in breast cancer, offering a clinical perspective on this promising avenue of intervention. In this pursuit, we strive to unravel the potential of c-MET as a beacon of hope in the fight against breast cancer, unveiling new horizons for therapeutic innovation.
C1 [Kaboli, Parham Jabbarzadeh; Chen, Hsiao-Fan; Yamaguchi, Hirohito; Hung, Mien-Chie] China Med Univ, Grad Inst Biomed Sci, Inst Biochem & Mol Biol, Res Ctr Canc Biol,Ctr Canc Biol,Canc Biol & Precis, Taichung 406, Taiwan.
   [Kaboli, Parham Jabbarzadeh; Chen, Hsiao-Fan; Yamaguchi, Hirohito; Hung, Mien-Chie] China Med Univ, Ctr Mol Med, Taichung 406, Taiwan.
   [Babaeizad, Ali; Geraylow, Kiarash Roustai] Semnan Univ Med Sci, Fac Med, Semnan, Iran.
   [Hung, Mien-Chie] Asia Univ, Dept Biotechnol, Taichung 413, Taiwan.
C3 China Medical University Taiwan; China Medical University Taiwan; Semnan
   University of Medical Sciences; Asia University Taiwan
RP Hung, MC (corresponding author), China Med Univ, Grad Inst Biomed Sci, Inst Biochem & Mol Biol, Res Ctr Canc Biol,Ctr Canc Biol,Canc Biol & Precis, Taichung 406, Taiwan.; Hung, MC (corresponding author), China Med Univ, Ctr Mol Med, Taichung 406, Taiwan.
EM mhung@cmu.edu.tw
RI Chen, Hsiao-Fan/E-9532-2012; Hung, Mien-Chie/ABD-5911-2021; Jabbarzadeh
   Kaboli, Parham/H-9623-2019
OI Jabbarzadeh Kaboli, Parham/0000-0002-4157-7901
FU National Science and Technology Council (NSTC) [112-2639-B-039-001 -ASP,
   111-2314-B-039-007]; Ministry of Health and Welfare Taiwan Grant
   [MOHW112-TDU-B-222-124016]; Ministry of Education (MOE) in Taiwan
FX The authors extend their gratitude to China Medical University,
   Taichung, Taiwan, whose generous financial support has been pivotal in
   the inception and successful completion of this article. Additionally,
   we acknowledge the invaluable contributions from the following funding
   agencies: the National Science and Technology Council (NSTC) Grant
   112-2639-B-039-001 -ASP (M.-C.H.) and 111-2314-B-039-007 (H.Y.) , the
   Ministry of Health and Welfare Taiwan Grant MOHW112-TDU-B-222-124016
   (M.-C.H.) , and The Featured Areas Research Center Program by the
   Ministry of Education (MOE) in Taiwan.r agencies: the National Science
   and Technology Council (NSTC) Grant 112-2639-B-039-001 -ASP (M.-C.H.)
   and 111-2314-B-039-007 (H.Y.) , the Ministry of Health and Welfare
   Taiwan Grant MOHW112-TDU-B-222-124016 (M.-C.H.) , and The Featured Areas
   Research Center Pro-gram by the Ministry of Education (MOE) in Taiwan.
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NR 188
TC 6
Z9 6
U1 8
U2 15
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD APR 28
PY 2024
VL 588
AR 216780
DI 10.1016/j.canlet.2024.216780
EA MAR 2024
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PA4K0
UT WOS:001211343700001
PM 38462033
DA 2025-01-04
ER

PT J
AU Bahmad, HF
   Gogola, S
   Rejzer, M
   Stoyanov, K
   Gomez, AS
   Valencia, AK
   Cummings, A
   Skerry, T
   Alloush, F
   Aljamal, AA
   Deb, A
   Alghamdi, S
   Poppiti, R
AF Bahmad, Hisham F.
   Gogola, Samantha
   Rejzer, Michael
   Stoyanov, Kalin
   Gomez, Aaron S.
   Valencia, Ann-Katrin
   Cummings, Adonicah
   Skerry, Timothy
   Alloush, Ferial
   Aljamal, Abed A.
   Deb, Arunima
   Alghamdi, Sarah
   Poppiti, Robert
TI Unraveling the Mysteries of Perineural Invasion in Benign and Malignant
   Conditions
SO CURRENT ONCOLOGY
LA English
DT Review
DE perineural invasion; TNM classification; staging; College of American
   Pathologists; World Health Organization
ID EPITHELIAL SHEATH NEUROMA; INFILTRATING SYRINGOMATOUS ADENOMA; RADICAL
   PROSTATECTOMY SPECIMENS; GRANULAR-CELL TUMOR; BLUE NEVUS;
   PANCREATIC-CANCER; ADENOMYOMATOUS HYPERPLASIA; PROGNOSTIC-SIGNIFICANCE;
   INTRANEURAL INVASION; COLORECTAL-CANCER
AB Perineural invasion (PNI) is defined as the dissemination of neoplastic cells within the perineural space. PNI can be a strong indicator of malignancy and is linked to poor prognosis and adverse outcomes in various malignant neoplasms; nevertheless, it can also be seen in benign pathologic conditions. In this review article, we discuss various signaling pathways and neurotrophic factors implicated in the development and progression of PNI. We also describe the methodology, benefits, and limitations of different in vitro, ex vivo, and in vivo models of PNI. The spectrum of presentation for PNI can range from diffuse spread within large nerves ("named" nerves) all the way through localized spread into unnamed microscopic nerves. Therefore, the clinical significance of PNI is related to its extent rather than its mere presence or absence. In this article, we discuss the guidelines for the identification and quantification of PNI in different malignant neoplasms based on the College of American Pathologists (CAP) and World Health Organization (WHO) recommendations. We also describe benign pathologic conditions and neoplasms demonstrating PNI and potential mimics of PNI. Finally, we explore avenues for the future development of targeted therapy options via modulation of signaling pathways involved in PNI.
C1 [Bahmad, Hisham F.; Alloush, Ferial; Deb, Arunima; Alghamdi, Sarah; Poppiti, Robert] Mt Sinai Med Ctr, Arkadi M Rywlin M D Dept Pathol & Lab Med, Miami Beach, FL 33140 USA.
   [Gogola, Samantha; Rejzer, Michael; Stoyanov, Kalin; Gomez, Aaron S.; Valencia, Ann-Katrin; Cummings, Adonicah; Skerry, Timothy] Florida Int Univ, Herbert Wertheim Coll Med, Miami, FL 33199 USA.
   [Aljamal, Abed A.] Med Univ South Carolina, Dept Med, Div Hematol Oncol, Charleston, SC 29425 USA.
   [Alghamdi, Sarah; Poppiti, Robert] Florida Int Univ, Herbert Wertheim Coll Med, Dept Pathol, Miami, FL 33199 USA.
C3 Mount Sinai Medical Center; State University System of Florida; Florida
   International University; Medical University of South Carolina; State
   University System of Florida; Florida International University
RP Bahmad, HF (corresponding author), Mt Sinai Med Ctr, Arkadi M Rywlin M D Dept Pathol & Lab Med, Miami Beach, FL 33140 USA.
EM hfbahmad@gmail.com; sgogo002@med.fiu.edu; mrejz001@med.fiu.edu;
   kstoy002@med.fiu.edu; agome399@med.fiu.edu; avale115@med.fiu.edu;
   acumm012@med.fiu.edu; tsker001@med.fiu.edu; ferial.alloush@msmc.com;
   aljamal@musc.edu; arunima.deb@msmc.com; sarah.alghamdi@msmc.com;
   robert.poppiti@msmc.com
RI Stoyanov, Kalin/JDM-9982-2023; Bahmad, Hisham/A-5369-2019
OI Bahmad, Hisham/0000-0003-3799-2595; Gogola,
   Samantha/0000-0003-2979-9648; Alloush, Ferial/0009-0000-3270-5898;
   Gomez, Aaron/0000-0002-4738-705X
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NR 156
TC 1
Z9 2
U1 1
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1198-0052
EI 1718-7729
J9 CURR ONCOL
JI Curr. Oncol.
PD OCT
PY 2023
VL 30
IS 10
BP 8948
EP 8972
DI 10.3390/curroncol30100647
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA W5ZY6
UT WOS:001092418500001
PM 37887547
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Nagaraja, V
   Eslick, GD
AF Nagaraja, Vinayak
   Eslick, Guy D.
TI HER2 expression in gastric and oesophageal cancer: a meta-analytic
   review
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Human epidermal growth factor receptor 2 (HER2); gastric cancer;
   esophageal cancer
ID EPITHELIAL OVARIAN-CANCER; HER-2/NEU EXPRESSION; COLORECTAL-CANCER;
   PROGNOSTIC-SIGNIFICANCE; OVEREXPRESSION; AMPLIFICATION; SURVIVAL
AB Background: Since the advent and the success of adjuvant medical therapy for human epidermal growth factor receptor 2 (HER2)-positive breast cancer in the form of trastuzumab there has been increasing interest in the development of similar therapies in other solid organ malignancies including gastric cancer and oesophageal cancer. Over the years, multiple observational studies have been inconsistent. Several meta-analyses have been published looking at the association between HER2 and gastric cancer and oesophageal cancer. This review aims to summarize the meta-analytic evidence for the association between HER2 in gastric and oesophageal cancer.
   Methods: A systematic search was conducted using MEDLINE, PubMed, EMBASE, Current Contents Connect, Cochrane Library, Google Scholar, Science Direct, and Web of Science.
   Results: Of the articles selected, only nine studies met full criteria. Six of them reviewed the role of HER2 in gastric cancer and the remaining three reviewed its role in oesophageal cancer.
   Conclusions: The current evidence regarding the role of HER2 is unclear. However, it clearly plays a key role in the pathogenesis of gastric and oesophageal carcinomas. Targeted therapy towards this subgroup (despite variable frequency and association with survival) would offer a mortality benefit and improve survival.
C1 [Nagaraja, Vinayak; Eslick, Guy D.] Sydney Med Sch Nepean, Discipline Surg, Whiteley Martin Res Ctr, Penrith, NSW 2751, Australia.
C3 University of Sydney
RP Eslick, GD (corresponding author), Univ Sydney, Nepean Hosp, Discipline Surg, Whiteley Martin Res Ctr, Level 5,South Block,POB 63, Penrith, NSW 2751, Australia.
EM guy.eslick@sydney.edu.au
RI Nagaraja, Vinayak/AAX-9728-2020; Eslick, Guy/HMT-5739-2023
OI Eslick, Guy/0000-0002-0098-1705
CR [Anonymous], GASTRIC CANC
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Z9 20
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
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SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
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VL 6
IS 2
BP 143
EP 154
DI 10.3978/j.issn.2078-6891.2014.107
PG 12
WC Oncology; Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Oncology; Gastroenterology & Hepatology
GA CS4YH
UT WOS:000362081700014
PM 25830034
DA 2025-01-04
ER

PT J
AU Sun, YQ
   Wang, RF
   Qiao, M
   Xu, YC
   Guan, WB
   Wang, LF
AF Sun, Yeqi
   Wang, Ruifen
   Qiao, Meng
   Xu, Yanchun
   Guan, Wenbin
   Wang, Lifeng
TI Cancer associated fibroblasts tailored tumor microenvironment of therapy
   resistance in gastrointestinal cancers
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Review
DE cancer associated fibroblasts; crosstalk; gastrointestinal cancer;
   signaling pathway; therapy resistance
ID EPITHELIAL-MESENCHYMAL TRANSITION; CARCINOMA-ASSOCIATED FIBROBLASTS;
   STROMAL CAVEOLIN-1 EXPRESSION; STEM-LIKE CELLS; PANCREATIC-CANCER;
   COLORECTAL-CANCER; GASTRIC-CANCER; ACTIVATION PROTEIN; ESOPHAGEAL
   CANCER; DOWN-REGULATION
AB Gastrointestinal cancers (GI), are a group of highly aggressive malignancies with heavy cancer-related mortalities. Even if continued development of therapy methods, therapy resistance has been a great obstruction for cancer treatment and thereby inevitably leads to depressed final mortality. Peritumoral cancer associated fibroblasts (CAFs), a versatile population assisting cancer cells to build a facilitated tumor microenvironment (TME), has been demonstrated exerting a promotion influence on cancer proliferation, migration, invasion, metastasis, and also therapy resistance. In this review, we provide an update progress in describing how CAFs mediate therapy resistance in GI by various means, meanwhile highlight the crosstalk between CAFs and cancer cells and present some vital signaling pathways activated by CAFs in this resistant process. Furthermore, we discuss the current advances in adopting novel drugs against CAFs and how the knowledge contributing to improved therapy efficacy in clinical practice. In sum, CAFs create a therapy-resistant TME in several aspects of GI progression, although some key problems about distinguishing CAFs subpopulations and controversial issues on pleiotropic CAFs in medication need to be solved for subsequent clinical application. Predictably, targeting therapy-resistant CAFs is a promising adjunctive treatment to benefit GI patients.
C1 [Sun, Yeqi; Wang, Ruifen; Qiao, Meng; Xu, Yanchun; Guan, Wenbin; Wang, Lifeng] Shanghai Jiao Tong Univ, Xinhua Hosp, Sch Med, Dept Pathol, 1665 Kongjiang Rd, Shanghai 200092, Peoples R China.
C3 Shanghai Jiao Tong University
RP Guan, WB; Wang, LF (corresponding author), Shanghai Jiao Tong Univ, Xinhua Hosp, Sch Med, Dept Pathol, 1665 Kongjiang Rd, Shanghai 200092, Peoples R China.
EM guanwenbin@xinhuamed.com.cn; wanglifeng@xinhuamed.com.cn
FU Shanghai Municipal Commission of Health and Family Planning
   [20154Y0145]; Medicine-Engineering Crossed Fund of Shanghai Jiao Tong
   University [YG2016QN72]; Xinhua Hospital, School of Medicine, Shanghai
   Jiao Tong University [15YJ10]
FX Shanghai Municipal Commission of Health and Family Planning, Grant
   number: 20154Y0145; Medicine-Engineering Crossed Fund of Shanghai Jiao
   Tong University, Grant number: YG2016QN72; Xinhua Hospital, School of
   Medicine, Shanghai Jiao Tong University, Grant number: 15YJ10
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NR 99
TC 23
Z9 25
U1 0
U2 72
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD SEP
PY 2018
VL 233
IS 9
BP 6359
EP 6369
DI 10.1002/jcp.26433
PG 11
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA GI1JX
UT WOS:000434127700005
PM 29334123
DA 2025-01-04
ER

PT J
AU Iranpour, S
   Bahrami, AR
   Saljooghi, AS
   Matin, MM
AF Iranpour, Sonia
   Bahrami, Ahmad Reza
   Saljooghi, Amir Sh
   Matin, Maryam M.
TI Application of smart nanoparticles as a potential platform for effective
   colorectal cancer therapy
SO COORDINATION CHEMISTRY REVIEWS
LA English
DT Review
DE Nanotechnology; Nanocarriers; Mesoporous silica nanoparticle;
   Superparamagnetic iron oxide nanoparticle; Metal organic framework;
   Colorectal cancer; Targeted therapy; Theranostic
ID MESOPOROUS SILICA NANOPARTICLES; METAL-ORGANIC-FRAMEWORK; IRON-OXIDE
   NANOPARTICLES; TARGETED DRUG-DELIVERY; ONE-POT SYNTHESIS; COLON-CANCER;
   CONTROLLED-RELEASE; IN-VITRO; MAGNETIC NANOPARTICLES; PHOTODYNAMIC
   THERAPY
AB Nowadays, nanomedicine has emerged as one of the most interesting fields of biomedical research, combining nanotechnology and medicine to offer a better prospect to design therapeutic agents with improved safety and efficacy for diagnosis and treatment of various diseases. A variety of inorganic, organic and hybrid organic-inorganic nanoparticles (NPs) with unique properties have been introduced in this field. In this review, we focus on applications of mesoporous silica nanoparticles (MSNs), superparamagnetic iron oxide nanoparticles (SPIONs) and metal organic frameworks (MOFs) as suitable inorganic nanocarriers in colorectal cancer (CRC) therapy. Furthermore, we summarize their advantages and disadvantages and review challenges related to use of these nanocarriers in cancer therapy. Then, the most recent theranostic applications of mentioned NPs in singular and combinatorial therapy for CRC are presented to provide a better context for further research in this field. Despite the wide variety of researches done, there are still serious challenges that must be taken into account in the design of true drug delivery systems (DDSs) in order to maximize the therapeutic index. Finally, use of advanced methods such as computational techniques, bioinformatics tools, applying appropriate models, and optimized mapping of treatment can result in an effective model based on nanocarriers for future CRC therapeutics. (C) 2021 Elsevier B.V. All rights reserved.
C1 [Iranpour, Sonia; Bahrami, Ahmad Reza; Matin, Maryam M.] Ferdowsi Univ Mashhad, Fac Sci, Dept Biol, Mashhad, Razavi Khorasan, Iran.
   [Bahrami, Ahmad Reza] Ferdowsi Univ Mashhad, Inst Biotechnol, Ind Biotechnol Res Grp, Mashhad, Razavi Khorasan, Iran.
   [Saljooghi, Amir Sh] Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Razavi Khorasan, Iran.
   [Matin, Maryam M.] Ferdowsi Univ Mashhad, Inst Biotechnol, Novel Diagnost & Therapeut Res Grp, Mashhad, Razavi Khorasan, Iran.
C3 Ferdowsi University Mashhad; Ferdowsi University Mashhad; Ferdowsi
   University Mashhad; Ferdowsi University Mashhad
RP Matin, MM (corresponding author), Ferdowsi Univ Mashhad, Fac Sci, Dept Biol, Mashhad, Razavi Khorasan, Iran.; Saljooghi, AS (corresponding author), Ferdowsi Univ Mashhad, Fac Sci, Dept Chem, Mashhad, Razavi Khorasan, Iran.
EM saljooghi@um.ac.ir; matin@um.ac.ir
RI Saljooghi, Amir/AAB-6042-2021; Bahrami, Ahmad Reza/AAA-4090-2020; M.
   Matin, Maryam/W-1884-2017
OI Sh. Saljooghi, Amir/0000-0001-5764-469X; Bahrami, Ahmad
   Reza/0000-0001-9122-7216; M. Matin, Maryam/0000-0002-7949-7712
FU Ferdowsi University of Mashhad [51537]
FX This work was supported by Ferdowsi University of Mashhad, grant number:
   51537.
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NR 381
TC 37
Z9 37
U1 2
U2 82
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 0010-8545
EI 1873-3840
J9 COORDIN CHEM REV
JI Coord. Chem. Rev.
PD SEP 1
PY 2021
VL 442
AR 213949
DI 10.1016/j.ccr.2021.213949
EA MAY 2021
PG 25
WC Chemistry, Inorganic & Nuclear
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA SK3VQ
UT WOS:000656147400001
DA 2025-01-04
ER

PT J
AU Tanaka, H
   Saigo, C
   Iwata, Y
   Yasufuku, I
   Kito, Y
   Yoshida, K
   Takeuchi, T
AF Tanaka, Hideharu
   Saigo, Chiemi
   Iwata, Yoshinori
   Yasufuku, Itaru
   Kito, Yusuke
   Yoshida, Kazuhiro
   Takeuchi, Tamotsu
TI Human colorectal cancer-associated carbohydrate antigen on annexin A2
   protein
SO JOURNAL OF MOLECULAR MEDICINE-JMM
LA English
DT Article
DE Colorectal cancer; Monoclonal antibody; Carbohydrate antigen; Annexin
   A2; Prognosis
AB Cancer-associated antigens are not only a good marker for monitoring cancer progression but are also useful for molecular target therapy. In this study, we aimed to generate a monoclonal antibody that preferentially reacts with colorectal cancer cells relative to noncancerous gland cells. We prepared antigens composed of HT-29 colorectal cancer cell lysates that were adsorbed by antibodies to sodium butyrate-induced enterocytically differentiated HT-29 cells. Subsequently, we generated a monoclonal antibody, designated 12G5A, which reacted with HT-29 colon cancer cells, but not with sodium butyrate-induced differentiated HT-29 cells. Immunohistochemical staining revealed 12G5A immunoreactivity in all 73 colon cancer tissue specimens examined at various degrees, but little or no immunoreactivity in noncancerous gland cells. Notably, high 12G5A immunoreactivity, which was determined as more than 50% of colon cancer cells intensively stained with 12G5A antibody, exhibited significantly higher association with a poor overall survival rate of patients with colorectal cancer (P = 0.0196) and unfavorable progression-free survival rate of patients with colorectal cancer (P = 0.0418). Matrix-assisted laser desorption ionization time-of-flight mass spectrometry, si-RNA silencing analysis, enzymatic deglycosylation, and tunicamycin treatment revealed that 12G5A recognized the glycosylated epitope on annexin A2 protein. Our findings indicate that 12G5A identified a cancer-associated glycosylation epitope on annexin A2, whose expression was related to unfavorable colorectal cancer behavior. Key message center dot 12G5A monoclonal antibody recognized a colorectal cancer-associated epitope. center dot 12G5A antibody recognized the N-linked glycosylation epitope on annexin A2. center dot 12G5A immunoreactivity was related to unfavorable colorectal cancer behavior.
C1 [Tanaka, Hideharu; Iwata, Yoshinori; Yasufuku, Itaru; Yoshida, Kazuhiro] Gifu Univ, Sch Med, Dept Surg Oncol, Gifu, Japan.
   [Saigo, Chiemi; Kito, Yusuke; Takeuchi, Tamotsu] Gifu Univ, Grad Sch Med, Dept Pathol & Translat Res, Gifu, Japan.
C3 Gifu University; Gifu University
RP Takeuchi, T (corresponding author), Gifu Univ, Grad Sch Med, Dept Pathol & Translat Res, Gifu, Japan.
EM takeutit08@gmail.com
OI , Tamotsu/0000-0002-4264-3632
FU Ministry of Education of Japan [K07406]; Grants-in-Aid for Scientific
   Research [20K07406] Funding Source: KAKEN
FX This study was supported by grants from the Ministry of Education of
   Japan (Grant nos. KAKEN 20 K07406).
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NR 33
TC 7
Z9 7
U1 0
U2 7
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0946-2716
EI 1432-1440
J9 J MOL MED
JI J. Mol. Med.
PD AUG
PY 2021
VL 99
IS 8
BP 1115
EP 1123
DI 10.1007/s00109-021-02077-z
EA APR 2021
PG 9
WC Genetics & Heredity; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Research & Experimental Medicine
GA TP8KJ
UT WOS:000644768400001
PM 33904933
DA 2025-01-04
ER

PT J
AU Hanly, EK
   Bednarczyk, RB
   Tuli, NY
   Moscatello, AL
   Halicka, HD
   Li, JW
   Geliebter, J
   Darzynkiewicz, Z
   Tiwari, RK
AF Hanly, Elyse K.
   Bednarczyk, Robert B.
   Tuli, Neha Y.
   Moscatello, Augustine L.
   Halicka, H. Dorota
   Li, Jiangwei
   Geliebter, Jan
   Darzynkiewicz, Zbigniew
   Tiwari, Raj K.
TI mTOR inhibitors sensitize thyroid cancer cells to cytotoxic effect of
   vemurafenib
SO ONCOTARGET
LA English
DT Article
DE vemurafenib; mTOR; thyroid cancer; cytotoxic effect; drug resistance
ID BRAF V600E MUTATION; BRAF(V600E) INHIBITION; MAMMALIAN PROTEIN; TARGETED
   THERAPY; APOPTOTIC CELLS; COLON-CANCER; METFORMIN; RAPAMYCIN; GROWTH;
   ASSOCIATION
AB Treatment options for advanced metastatic thyroid cancer patients are limited. Vemurafenib, a BRAFV600E inhibitor, has shown promise in clinical trials although cellular resistance occurs. Combination therapy that includes BRAFV600E inhibition and avoids resistance is a clinical need. We used an in vitro model to examine combination treatment with vemurafenib and mammalian target of rapamycin ( mTOR) inhibitors, metformin and rapamycin. Cellular viability and apoptosis were analyzed in thyroid cell lines by trypan blue exclusion and TUNEL assays. Combination of vemurafenib and metformin decreased cell viability and increased apoptosis in both BCPAP papillary thyroid cancer cells and 8505c anaplastic thyroid cancer cells. This combination was also found to be active in vemurafenib-resistant BCPAP cells. Changes in expression of signaling molecules such as decreased mTOR expression in BCPAP and enhanced inhibition of phospho-MAPK in resistant BCPAP and 8505c were observed. The second combination of vemurafenib and rapamycin amplified cell death in BCPAP cells. We conclude that combination of BRAFV600E and mTOR inhibition forms the basis of a treatment regimen that should be further investigated in in vivo model systems. Metformin or rapamycin adjuvant treatment may provide clinical benefits with minimal side effects to BRAFV600E-positive advanced thyroid cancer patients treated with vemurafenib.
C1 [Hanly, Elyse K.; Bednarczyk, Robert B.; Tuli, Neha Y.; Geliebter, Jan; Tiwari, Raj K.] New York Med Coll, Dept Microbiol & Immunol, Valhalla, NY 10595 USA.
   [Moscatello, Augustine L.] New York Med Coll, Dept Otolaryngol Head & Neck Surg, Valhalla, NY 10595 USA.
   [Halicka, H. Dorota; Li, Jiangwei; Darzynkiewicz, Zbigniew] New York Med Coll, Dept Pathol, Valhalla, NY 10595 USA.
C3 New York Medical College; New York Medical College; New York Medical
   College
RP Tiwari, RK (corresponding author), New York Med Coll, Dept Microbiol & Immunol, Valhalla, NY 10595 USA.
EM Raj_Tiwari@nymc.edu
OI Darzynkiewicz, Zbigniew/0000-0002-2040-7081
FU National Cancer Institute [1R01CA131946]; Andrew Welke Cancer Research
   Foundation
FX This study was supported by grants from National Cancer Institute
   1R01CA131946 (RKT) and Andrew Welke Cancer Research Foundation (ZD).
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NR 51
TC 25
Z9 28
U1 0
U2 6
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD NOV 24
PY 2015
VL 6
IS 37
BP 39702
EP 39713
DI 10.18632/oncotarget.4052
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CY0RW
UT WOS:000366114400030
PM 26284586
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Yu, SH
   Wang, SY
   Wang, XY
   Xu, XM
AF Yu, Shuhong
   Wang, Siyu
   Wang, Xuanyu
   Xu, Ximing
TI The axis of tumor-associated macrophages, extracellular matrix proteins,
   and cancer-associated fibroblasts in oncogenesis
SO CANCER CELL INTERNATIONAL
LA English
DT Review
DE Extracellular matrix; Tumor microenvironment; Cancer-associated
   fibroblasts; Tumor-associated macrophages; Targeted therapy
ID CARCINOMA-ASSOCIATED FIBROBLASTS; MESENCHYMAL STEM-CELLS; PHASE-II
   TRIAL; ACTIVATION PROTEIN; TGF-BETA; BREAST-CANCER; TENASCIN-C;
   MONOCLONAL-ANTIBODY; COLORECTAL-CANCER; SIGNALING PATHWAY
AB The extracellular matrix (ECM) is a complex, dynamic network of multiple macromolecules that serve as a crucial structural and physical scaffold for neighboring cells. In the tumor microenvironment (TME), ECM proteins play a significant role in mediating cellular communication between cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs). Revealing the ECM modification of the TME necessitates the intricate signaling cascades that transpire among diverse cell populations and ECM proteins. The advent of single-cell sequencing has enabled the identification and refinement of specific cellular subpopulations, which has substantially enhanced our comprehension of the intricate milieu and given us a high-resolution perspective on the diversity of ECM proteins. However, it is essential to integrate single-cell data and establish a coherent framework. In this regard, we present a comprehensive review of the relationships among ECM, TAMs, and CAFs. This encompasses insights into the ECM proteins released by TAMs and CAFs, signaling integration in the TAM-ECM-CAF axis, and the potential applications and limitations of targeted therapies for CAFs. This review serves as a reliable resource for focused therapeutic strategies while highlighting the crucial role of ECM proteins as intermediates in the TME.
C1 [Yu, Shuhong; Wang, Siyu; Xu, Ximing] Wuhan Univ, Dept Oncol, Renmin Hosp, Wuhan 430060, Peoples R China.
   [Wang, Xuanyu] Wuhan Univ, Dept Urol, Zhongnan Hosp, Wuhan 430071, Peoples R China.
C3 Wuhan University; Wuhan University
RP Xu, XM (corresponding author), Wuhan Univ, Dept Oncol, Renmin Hosp, Wuhan 430060, Peoples R China.
EM doctorxu120@aliyun.com
RI wang, xuanyu/JXO-5246-2024
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NR 384
TC 0
Z9 0
U1 9
U2 9
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1475-2867
J9 CANCER CELL INT
JI Cancer Cell Int.
PD OCT 7
PY 2024
VL 24
IS 1
AR 335
DI 10.1186/s12935-024-03518-8
PG 30
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA I1E0F
UT WOS:001327745500001
PM 39375726
OA gold
DA 2025-01-04
ER

PT J
AU Khorsandi, D
   Yang, JW
   Foster, S
   Khosravi, S
   Kouchehbaghi, NH
   Zarei, F
   Lee, YB
   Runa, F
   Gangrade, A
   Voskanian, L
   Adnan, D
   Zhu, YZ
   Wang, ZH
   Jucaud, V
   Dokmeci, MR
   Shen, XL
   Bishehsari, F
   Kelber, JA
   Khademhosseini, A
   de Barros, NR
AF Khorsandi, Danial
   Yang, Jia-Wei
   Foster, Samuel
   Khosravi, Safoora
   Hosseinzadeh Kouchehbaghi, Negar
   Zarei, Fahimeh
   Lee, Yun Bin
   Runa, Farhana
   Gangrade, Ankit
   Voskanian, Leon
   Adnan, Darbaz
   Zhu, Yangzhi
   Wang, Zhaohui
   Jucaud, Vadim
   Dokmeci, Mehmet Remzi
   Shen, Xiling
   Bishehsari, Faraz
   Kelber, Jonathan A.
   Khademhosseini, Ali
   de Barros, Natan Roberto
TI Patient-Derived Organoids as Therapy Screening Platforms in Cancer
   Patients
SO ADVANCED HEALTHCARE MATERIALS
LA English
DT Review
DE cancer treatment; clinical translation; microfabrication technologies;
   patient-derived organoids; therapeutic screening
ID COLORECTAL-CANCER; TREATMENT RESPONSE; TARGETED THERAPY; CELL-LINES;
   TUMOR; MODELS; DORMANCY; CULTURE; BIOPSY; METASTASIS
AB Patient-derived organoids (PDOs) developed ex vivo and in vitro are increasingly used for therapeutic screening. They provide a more physiologically relevant model for drug discovery and development compared to traditional cell lines. However, several challenges remain to be addressed to fully realize the potential of PDOs in therapeutic screening. This paper summarizes recent advancements in PDO development and the enhancement of PDO culture models. This is achieved by leveraging materials engineering and microfabrication technologies, including organs-on-a-chip and droplet microfluidics. Additionally, this work discusses the application of PDOs in therapy screening to meet diverse requirements and overcome bottlenecks in cancer treatment. Furthermore, this work introduces tools for data processing and analysis of organoids, along with their microenvironment. These tools aim to achieve enhanced readouts. Finally, this work explores the challenges and future perspectives of using PDOs in drug development and personalized screening for cancer patients.
   This article highlights PDOs for therapeutic screening in cancer, emphasizing physiological relevance over traditional cell lines. It discusses advancements in PDO development and culture enhancement through materials engineering, including organs-on-a-chip technology. The paper explores PDO applications in screening and cancer treatment challenges. It discusses the future of PDOs in drug development and personalized treatment. image
C1 [Khorsandi, Danial; Yang, Jia-Wei; Foster, Samuel; Khosravi, Safoora; Hosseinzadeh Kouchehbaghi, Negar; Zarei, Fahimeh; Lee, Yun Bin; Gangrade, Ankit; Voskanian, Leon; Zhu, Yangzhi; Wang, Zhaohui; Jucaud, Vadim; Dokmeci, Mehmet Remzi; Shen, Xiling; Khademhosseini, Ali; de Barros, Natan Roberto] Terasaki Inst Biomed Innovat TIBI, Dept Bioengn, 1018 Westwood Blvd, Los Angeles, CA 91367 USA.
   [Khosravi, Safoora] Univ British Columbia, Dept Elect & Comp Engn, Vancouver, BC V6T 1Z4, Canada.
   [Hosseinzadeh Kouchehbaghi, Negar] Amirkabir Univ Technol, Tehran Polytech, Dept Text Engn, Hafez Ave, Tehran 1591634311, Iran.
   [Runa, Farhana; Kelber, Jonathan A.] Calif State Univ Northridge, Dept Biol, 18111 Nordhoff St, Northridge, CA 91330 USA.
   [Adnan, Darbaz; Bishehsari, Faraz] Rush Univ, Rush Med Coll, Rush Ctr Integrated Microbiome & Chronobiol Res, Med Ctr, Chicago, IL 60612 USA.
   [Wang, Zhaohui] Duke Univ, Sch Med, Dept Pathol, Durham, NC 27710 USA.
   [Bishehsari, Faraz] Rush Univ, Rush Ctr Integrated Microbiome & Chronobiol Res, Div Digest Dis, Med Ctr, Chicago, IL 60612 USA.
   [Kelber, Jonathan A.] Baylor Univ, Dept Biol, 101 Bagby Ave, Waco, TX 76706 USA.
C3 University of British Columbia; Amirkabir University of Technology;
   California State University System; California State University
   Northridge; Rush University; Duke University; Rush University; Baylor
   University
RP Khademhosseini, A; de Barros, NR (corresponding author), Terasaki Inst Biomed Innovat TIBI, Dept Bioengn, 1018 Westwood Blvd, Los Angeles, CA 91367 USA.; Kelber, JA (corresponding author), Calif State Univ Northridge, Dept Biol, 18111 Nordhoff St, Northridge, CA 91330 USA.; Kelber, JA (corresponding author), Baylor Univ, Dept Biol, 101 Bagby Ave, Waco, TX 76706 USA.
EM jonathan_kelber@baylor.edu; khademh@terasaki.org; nbarros@terasaki.org
RI Gangrade, Ankit/AAE-3507-2021; Zhu, Yangzhi/S-3400-2019; Lee,
   Yoojin/AAB-9799-2022; Khorsandi, Danial/ABC-9562-2021; Kelber,
   Jonathan/K-1023-2012; adnan, darbaz/JJE-4854-2023; Gangrade,
   Ankit/AAJ-3462-2020
OI Forster, Samuel/0009-0006-3116-2418; Gangrade,
   Ankit/0000-0002-9169-7450; KHORSANDI, DANIAL/0000-0002-5245-5555
FU National Institutes of Health, National Cancer Institute [CA257558];
   National Institutes of Health; Terasaki Institute for Biomedical
   Innovation [112-2917-I-564-015]; National Science and Technology Council
   (NSTC) [CA279487, CA277110]; NIH
FX The authors acknowledge funding from the National Institutes of Health
   (CA257558) and the Terasaki Institute for Biomedical Innovation. J.-W.Y.
   would like to acknowledge financial support from the National Science
   and Technology Council (NSTC 112-2917-I-564-015), Taiwan. F.B. is
   supported by NIH CA279487 and CA277110.
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NR 113
TC 4
Z9 5
U1 17
U2 39
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 AUG
PY 2024
VL 13
IS 21
SI SI
DI 10.1002/adhm.202302331
EA MAR 2024
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 D4I6G
UT WOS:001175717300001
PM 38359321
DA 2025-01-04
ER

PT J
AU Zhang, ZC
   Li, D
   Yun, H
   Tong, J
   Liu, W
   Chai, KQ
   Zeng, TW
   Gao, ZH
   Xie, YQ
AF Zhang, Zhengchao
   Li, Dong
   Yun, Heng
   Tong, Jie
   Liu, Wei
   Chai, Keqiang
   Zeng, Tongwei
   Gao, Zhenghua
   Xie, Yongqiang
TI Opportunities and challenges of targeting c-Met in the treatment of
   digestive tumors
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE c-Met; digestive system tumors; gastric cancer; hepatocellular
   carcinoma; pancreatic cancer; colorectal cancer; targeted therapy;
   adoptive immunotherapy
ID HEPATOCYTE GROWTH-FACTOR; RECEPTOR TYROSINE KINASE; EPITHELIAL
   MORPHOGENESIS DOWNSTREAM; RANDOMIZED PHASE-II; TIVANTINIB ARQ 197;
   CANCER STEM-CELLS; GASTRIC-CANCER; LUNG-CANCER;
   HEPATOCELLULAR-CARCINOMA; PANCREATIC-CANCER
AB At present, a large number of studies have demonstrated that c-Met generally exerts a crucial function of promoting tumor cells proliferation and differentiation in digestive system tumors. c-Met also mediates tumor progression and drug resistance by signaling interactions with other oncogenic molecules and then activating downstream pathways. Therefore, c-Met is a promising target for the treatment of digestive system tumors. Many anti-tumor therapies targeting c-Met (tyrosine kinase inhibitors, monoclonal antibodies, and adoptive immunotherapy) have been developed in treating digestive system tumors. Some drugs have been successfully applied to clinic, but most of them are defective due to their efficacy and complications. In order to promote the clinical application of targeting c-Met drugs in digestive system tumors, it is necessary to further explore the mechanism of c-Met action in digestive system tumors and optimize the anti-tumor treatment of targeting c-Met drugs. Through reading a large number of literatures, the author systematically reviewed the biological functions and molecular mechanisms of c-Met associated with tumor and summarized the current status of targeting c-Met in the treatment of digestive system tumors so as to provide new ideas for the treatment of digestive system tumors.
C1 [Zhang, Zhengchao; Li, Dong; Yun, Heng; Tong, Jie; Liu, Wei; Chai, Keqiang; Zeng, Tongwei; Gao, Zhenghua; Xie, Yongqiang] Gansu Univ Tradit Chinese Med, Dept Gen Surg, Affiliated Hosp 3, Baiyin, Peoples R China.
   [Zhang, Zhengchao] Lanzhou Univ, Dept Gen Surg, Hosp 2, Lanzhou, Peoples R China.
C3 Gansu University of Chinese Medicine; Lanzhou University
RP Gao, ZH; Xie, YQ (corresponding author), Gansu Univ Tradit Chinese Med, Dept Gen Surg, Affiliated Hosp 3, Baiyin, Peoples R China.
EM zhangzcmnwk@163.com; 398815535@qq.com
FU Third Affiliated Hospital of Gansu University of Chinese Medicine
   [2016YG-06]; Baiyin City 2019 Science and technology plan project
   [20191-22Y]
FX This study was funded by the Third Affiliated Hospital of Gansu
   University of Chinese Medicine (Project Approval Number: 2016YG-06) and
   Baiyin City 2019 Science and technology plan project (Project Approval
   Number: 20191-22Y).
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NR 146
TC 9
Z9 9
U1 1
U2 21
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 AUG 1
PY 2022
VL 12
AR 923260
DI 10.3389/fonc.2022.923260
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3V4NP
UT WOS:000841639900001
PM 35978812
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Nie, J
   Zhao, CL
   Deng, L
   Chen, J
   Yu, B
   Wu, XL
   Pang, P
   Chen, XY
AF Nie, Jiao
   Zhao, Changlin
   Deng, Li
   Chen, Jia
   Yu, Bin
   Wu, Xianlin
   Pang, Peng
   Chen, Xiaoyin
TI Efficacy of traditional Chinese medicine in treating cancer (Review)
SO BIOMEDICAL REPORTS
LA English
DT Article
DE cancer; herbal medicines; cellular and molecular level; survival time;
   side effects; quality of life
ID MULTIDRUG-RESISTANCE PROTEINS; INHIBITS TUMOR ANGIOGENESIS;
   P-GLYCOPROTEIN; BREAST-CANCER; MOUSE MODEL; CELL-DEATH; APOPTOSIS
   INDUCTION; COLORECTAL-CANCER; SIGNALING PATHWAY; BEARING MICE
AB The morbidity associated with cancer has rapidly increased in recent years, and in the previous 5 years has had a tendency to be the leading cause of fatality compared with cardiovascular disease. Therefore, effective measures are required with an aim to reduce the incidence. Based on the results of clinical investigation, a multidisciplinary treatment strategy for cancer, which includes radiotherapy, chemotherapy, surgery, targeted therapy and immunotherapy, are prominently used in clinical practice. However, the therapies are insufficient due to multidrug resistance, adverse effects and the presence of the root of the cancer. Therefore, there is a necessity to develop more effective or adjunctive therapies for cancer prevention and treatment. Cancer is now widely recognized as a systemic humoral disease. Similarly, the function of herbal drugs is to modulate the whole body system in a more holistic way. Recently, herbal drugs have been applied to one of the efficient approaches for cancer therapy. Furthermore, there is evidence that various herbal medicines have been proven to be useful and effective in sensitizing the conventional agents against the various factors at the cellular and molecular levels that are associated with the occurrence of cancer and in prolonging survival time, alleviating side effects of chemotherapy and radiotherapy and improving the quality of life in cancer patients.
C1 [Nie, Jiao; Zhao, Changlin; Deng, Li; Chen, Jia; Yu, Bin; Wu, Xianlin; Pang, Peng; Chen, Xiaoyin] Jinan Univ, Coll Med, Dept Tradit Chinese Med, 601 Huangpu Rd West, Guangzhou 510632, Guangdong, Peoples R China.
   [Zhao, Changlin] Guangzhou Univ Tradit Chinese Med, Clifford Hosp, Dept Oncol, Guangzhou 510632, Guangdong, Peoples R China.
   [Yu, Bin] Jining Med Univ, Inst Clin, Jining 272013, Shandong, Peoples R China.
   [Wu, Xianlin] Jinan Univ, Affiliated Hosp 1, Dept Pancreat Dis Ctr, Guangzhou 510632, Guangdong, Peoples R China.
C3 Jinan University; Guangzhou University of Chinese Medicine; Jining
   Medical University; Jinan University
RP Chen, XY (corresponding author), Jinan Univ, Coll Med, Dept Tradit Chinese Med, 601 Huangpu Rd West, Guangzhou 510632, Guangdong, Peoples R China.
EM tchenxiaoyin@jnu.edu.cn
RI Zhao, changlin/AAE-9022-2019; yu, bin/AAJ-8592-2021
OI Zhao, Changlin/0000-0002-8668-1075
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NR 74
TC 93
Z9 103
U1 0
U2 15
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 JAN
PY 2016
VL 4
IS 1
BP 3
EP 14
DI 10.3892/br.2015.537
PG 12
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA DC1ZT
UT WOS:000369017700001
PM 26870326
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Song, N
   Qu, XJ
   Liu, SZ
   Zhang, SM
   Liu, J
   Qu, JL
   Zheng, HC
   Liu, YP
   Che, XF
AF Song, Na
   Qu, Xiujuan
   Liu, Shizhou
   Zhang, Simeng
   Liu, Jing
   Qu, Jinglei
   Zheng, Huachuan
   Liu, Yunpeng
   Che, Xiaofang
TI Dual inhibition of MET and SRC kinase activity as a combined targeting
   strategy for colon cancer
SO EXPERIMENTAL AND THERAPEUTIC MEDICINE
LA English
DT Article
DE MET; SRC; colon cancer; targeted therapy
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; C-SRC; THERAPEUTIC TARGETS;
   RESISTANCE; ACTIVATION; THERAPIES; IDENTIFICATION; REGORAFENIB;
   ERLOTINIB
AB Hepatocyte growth factor (HGF)/MET signaling is implicated in the development of colorectal cancer (CRC) and possesses therapeutic value for various types of cancer. However, inhibition of MET alone has been demonstrated to have limited efficacy. The present study examined the combined inhibition of MET and SRC kinase activity in colon cancer cells. Furthermore, the role of the HGF/MET pathway in ligand-dependent and-independent activation was demonstrated. The single inhibition of MET by knockdown small interfering RNA or inhibitor indicated a limited anti-viability effects without inhibiting the basal phosphorylation levels of SRC, protein kinase B (AKT) or extracellular signal-regulated kinase (ERK). In view of the strong association between MET and SRC identified by direct regulation, growth factor-induced MET activation was suppressed by pretreatment with the SRC inhibitor, dasatinib, and downstream phosphorylation of AKT and ERK partially decreased, which suggested that SRC activation was essential for ligand-dependent and independent activation of MET. Considering that both the activation of MET and SRC was required in ligand-dependent and -independent MET activation, the antitumor effect of concurrent inhibition of MET and SRC was examined, and it was demonstrated that combination treatment exerted increased viability inhibition and apoptosis enhancement in mutant and wild type RAS colon cancer cells. Therefore, combinational inhibition of MET and SRC may be a promising strategy for the treatment of CRC.
C1 [Song, Na; Qu, Xiujuan; Zhang, Simeng; Liu, Jing; Qu, Jinglei; Liu, Yunpeng; Che, Xiaofang] China Med Univ, Hosp 1, Dept Med Oncol, 155 North Nanjing St, Shenyang 110001, Liaoning, Peoples R China.
   [Liu, Shizhou] Zhejiang Univ, Inst Translat Med, Hangzhou 310029, Zhejiang, Peoples R China.
   [Zheng, Huachuan] China Med Univ, Shengjing Hosp, Dept Expt Oncol, Shenyang 110001, Liaoning, Peoples R China.
C3 China Medical University; Zhejiang University; China Medical University
RP Liu, YP; Che, XF (corresponding author), China Med Univ, Hosp 1, Dept Med Oncol, 155 North Nanjing St, Shenyang 110001, Liaoning, Peoples R China.
EM cmuliuyunpeng@hotmail.com; xf_che@hotmail.com
RI wang, wei/JYP-7819-2024; Xiaofang, Che/J-9430-2019
OI liu, Yunpeng/0000-0001-9800-4373
FU Chinese National Foundation of National Sciences Grants [81401938,
   81372546]; National Science and Technology Major Project of the Ministry
   of Science and Technology of China [2013JX09303002]; Science and
   Technology Plan Project of Liaoning Province [2014225013, 2014021089]
FX The present study was supported by grants from the Chinese National
   Foundation of National Sciences Grants (grant nos. 81401938 and
   81372546), the National Science and Technology Major Project of the
   Ministry of Science and Technology of China (grant no. 2013JX09303002)
   and the Science and Technology Plan Project of Liaoning Province (grant
   nos. 2014225013 and 2014021089).
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NR 34
TC 5
Z9 8
U1 0
U2 7
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-0981
EI 1792-1015
J9 EXP THER MED
JI Exp. Ther. Med.
PD AUG
PY 2017
VL 14
IS 2
BP 1357
EP 1366
DI 10.3892/etm.2017.4692
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA FB7BY
UT WOS:000406297300066
PM 28810597
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Baretti, M
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   Santoro, A
   Rimassa, L
AF Baretti, M.
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   Santoro, A.
   Rimassa, L.
TI Emergence of KRAS-mutation in liver metastases after an anti-EGFR
   treatment in patient with colorectal cancer: Are we aware of the
   therapeutic impact of intratumor heterogeneity?
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE Colorectal cancer; Cancer Biology; Heterogeneity; Mutation; Liver
   metastases; RAS; Target therapy; Treatment resistance; Tumor Metastases
ID ACQUIRED-RESISTANCE; CLONAL EVOLUTION; CHEMOTHERAPY; CETUXIMAB; PIK3CA;
   TRIAL; BRAF
AB Tumors represent a dynamic system where the genomic plasticity permits to adapt to the perturbation induced by environmental pressures, supporting the importance of longitudinal tumor sampling strategies to deciphering the temporal acquisition of driver event that could impact treatment outcome. We describe the case of a metastatic colorectal cancer (mCRC) patient, RAS wild-type, who responded to anti-EGFR therapy and underwent liver surgery, revealing a KRAS mutations in the metastatic lesion, not detectable prior to initiation of therapy in the colonic biopsy. After liver surgery, the patient received chemotherapy alone, then underwent left colectomy and the final pathological report confirmed the KRAS wild-type status. We can speculate the existence of two distinct populations of KRAS wild-type and mutant CRC cells sharing the same genetic origin. The anti-EGFR treatment represented a selective pressure which allowed the selection of KRAS mutant subclones. The prognostic and /or predictive role of intratumor heterogeneity has not been assessed prospectively. Our case report is of clinical relevance because patients with mCRC who respond to anti-EGFR antibodies often develop resistance within several months of initiating therapy, thus outlining the importance to better ascertain the molecular landscape of tumors to design better therapeutic strategies.
C1 [Baretti, M.; Personenia, N.; Santoro, A.; Rimassa, L.] Humanitas Clin & Res Ctr, Humanitas Canc Ctr, Med Oncol & Hematol Unit, Rozzano, Milan, Italy.
   [Personenia, N.] Univ Milan, Dept Med Biotechnol & Translat Med, Milan, Italy.
   [Destro, A.] Humanitas Clin & Res Ctr, Pathol Unit, Rozzano, Milan, Italy.
   [Santoro, A.] Humanitas Univ, Rozzano, Milan, Italy.
C3 IRCCS Humanitas Research Hospital; University of Milan; IRCCS Humanitas
   Research Hospital; Humanitas University; IRCCS Humanitas Research
   Hospital
RP Baretti, M (corresponding author), Humanitas Clin & Res Ctr, Humanitas Canc Ctr, Via Manzoni 56 Rozzano, I-20089 Milan, Italy.
EM marina.baretti@gmail.com
RI Baretti, Marina/AAM-4481-2021; Personeni, Nicola/ABG-7925-2020; DESTRO,
   ANNARITA/HII-7324-2022; Baretti, Marina/F-3231-2018; Rimassa,
   Lorenza/N-4884-2016; Santoro, Armando/J-9594-2018
OI DESTRO, ANNARITA/0000-0001-5388-0353; Baretti,
   Marina/0000-0003-0125-2405; Rimassa, Lorenza/0000-0001-9957-3615;
   Santoro, Armando/0000-0003-1709-9492; Personeni,
   Nicola/0000-0002-7995-272X
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NR 19
TC 8
Z9 9
U1 0
U2 4
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.
PY 2018
VL 19
IS 8
BP 659
EP 663
DI 10.1080/15384047.2018.1450117
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GN9ZO
UT WOS:000439574300003
PM 29580164
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Wang, H
   Zhang, Y
   Zhang, H
   Cao, H
   Mao, JN
   Chen, XX
   Wang, LC
   Zhang, N
   Luo, P
   Xue, J
   Qi, XY
   Dong, XC
   Liu, GD
   Cheng, Q
AF Wang, Hao
   Zhang, Yi
   Zhang, Hao
   Cao, Hui
   Mao, Jinning
   Chen, Xinxin
   Wang, Liangchi
   Zhang, Nan
   Luo, Peng
   Xue, Ji
   Qi, Xiaoya
   Dong, Xiancheng
   Liu, Guodong
   Cheng, Quan
TI Liquid biopsy for human cancer: cancer screening, monitoring, and
   treatment
SO MEDCOMM
LA English
DT Review
DE Circulating tumor cell; Circulating tumor DNA; Exosomes; ICI;
   Immunotherapy; Liquid biopsy; Noninvasive tumor detection; PD-L1;
   Tumor-related circulating cells
ID CIRCULATING TUMOR-CELLS; COLORECTAL-CANCER; PD-L1 EXPRESSION;
   HEPATOCELLULAR-CARCINOMA; BREAST-CANCER; CLINICAL-SIGNIFICANCE; ANTI-PD1
   RESISTANCE; MATERNAL PLASMA; DNA; IMMUNOTHERAPY
AB Currently, tumor treatment modalities such as immunotherapy and targeted therapy have more stringent requirements for obtaining tumor growth information and require more accurate and easy-to-operate tumor information detection methods. Compared with traditional tissue biopsy, liquid biopsy is a novel, minimally invasive, real-time detection tool for detecting information directly or indirectly released by tumors in human body fluids, which is more suitable for the requirements of new tumor treatment modalities. Liquid biopsy has not been widely used in clinical practice, and there are fewer reviews of related clinical applications. This review summarizes the clinical applications of liquid biopsy components (e.g., circulating tumor cells, circulating tumor DNA, extracellular vesicles, etc.) in tumorigenesis and progression. This includes the development process and detection techniques of liquid biopsies, early screening of tumors, tumor growth detection, and guiding therapeutic strategies (liquid biopsy-based personalized medicine and prediction of treatment response). Finally, the current challenges and future directions for clinical applications of liquid biopsy are proposed. In sum, this review will inspire more researchers to use liquid biopsy technology to promote the realization of individualized therapy, improve the efficacy of tumor therapy, and provide better therapeutic options for tumor patients.
   Application of liquid biopsy in immunotherapy of tumors. This schematic illustrates the advantages of liquid biopsy over tissue biopsy, such as minimally invasive and reproducible. As an essential alternative or complementary tool to tissue biopsy, liquid biopsy obtains a tumor profile by analyzing tumor-derived components from the circulation (e.g., circulating tumor cells, circulating tumor DNA, exosomes, etc.) and can be used in critical fields, such as screening for immunotherapy beneficiaries, indicating disease progression, predicting prognosis, and so on. image
C1 [Wang, Hao; Zhang, Yi; Zhang, Hao; Chen, Xinxin; Liu, Guodong] Chongqing Med Univ, Affiliated Hosp 2, Dept Neurosurg, Chongqing 400000, Peoples R China.
   [Cao, Hui] Hunan Univ Chinese Med, Sch Clin Med, Dept Psychiat, Changsha, Peoples R China.
   [Cao, Hui] Brain Hosp Hunan Prov, Peoples Hosp Hunan Prov 2, Dept Psychiat, Changsha, Peoples R China.
   [Mao, Jinning; Qi, Xiaoya] Chongqing Med Univ, Affiliated Hosp 2, Hlth Management Ctr, Chongqing, Peoples R China.
   [Wang, Liangchi] Fengdu Peoples Hosp, Dept Neurosurg, Chongqing, Peoples R China.
   [Zhang, Nan] Huazhong Univ Sci & Technol, Coll Life Sci & Technol, Wuhan, Peoples R China.
   [Luo, Peng] Southern Med Univ, Zhujiang Hosp, Dept Oncol, Guangzhou, Peoples R China.
   [Xue, Ji] Tradit Chinese Med Hosp Dianjiang Chongqing, Dept Neurosurg, Chongqing, Peoples R China.
   [Dong, Xiancheng] Dazhou Cent Hosp, Dept Cerebrovasc Dis, Sichuan, Peoples R China.
   [Cheng, Quan] Cent South Univ, Xiangya Hosp, Dept Neurosurg, Changsha 410008, Peoples R China.
   [Cheng, Quan] Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha, Peoples R China.
C3 Chongqing Medical University; Hunan University of Chinese Medicine;
   Chongqing Medical University; Huazhong University of Science &
   Technology; Southern Medical University - China; Central South
   University; Central South University
RP Liu, GD (corresponding author), Chongqing Med Univ, Affiliated Hosp 2, Dept Neurosurg, Chongqing 400000, Peoples R China.; Cheng, Q (corresponding author), Cent South Univ, Xiangya Hosp, Dept Neurosurg, Changsha 410008, Peoples R China.
EM 304678@hospital.cqmu.edu.cn; chengquan@csu.edu.cn
RI LUO, PENG/KYP-5865-2024
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NR 202
TC 5
Z9 5
U1 7
U2 8
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2688-2663
J9 MEDCOMM
JI MedComm
PD JUN
PY 2024
VL 5
IS 6
AR e564
DI 10.1002/mco2.564
PG 24
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA SB9E2
UT WOS:001232108400001
PM 38807975
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Jin, Q
   Zhang, N
   Zhan, Y
   Xu, XH
   Han, C
   Zhao, H
   Hu, XD
   Tang, HB
   Wu, YM
AF Jin, Qiong
   Zhang, Ning
   Zhan, Yang
   Xu, Xiaohong
   Han, Chao
   Zhao, Hui
   Hu, Xiaodi
   Tang, Hongbo
   Wu, Yumei
TI MicroRNA-592 Inhibits the Growth of Ovarian Cancer Cells by Targeting
   ERBB3
SO TECHNOLOGY IN CANCER RESEARCH & TREATMENT
LA English
DT Article
DE ovarian cancer; ERBB3; oncology; MicroRNA-592; cell signaling
ID HUMAN COLORECTAL-CANCER; MIR-592; PROLIFERATION; STATISTICS
AB Objectives: Ovarian cancer is the most lethal gynecologic malignancy, and targeted therapy for different pathological types and molecular phenotypes is urgent to be studied. Studies have shown that MicroRNA-592 (miR-592) plays an important negative regulatory role in the occurrence of gastrointestinal malignancies, breast cancer, non-small cell lung cancer, and glioma, but the expression of miR-592 in ovarian cancer and the mechanism of action are still unclear. Methods: The expressions of miR-592 were examined by RT-PCR and Western Blot. Cell viability and migratory capacity were detected by CCK-8 and transwell assay. TargetScan () was analyzed to predict potential targets of miR-592. Then Dual-luciferase reporter gene assay was performed to verify the targeting relationship between miR-592 and ERBB3. A mouse xenograft model was applied to confirm the effect of miR-592. Results: In our study, we found that the expression of miR-592 is reduced in epithelial ovarian cancer tissues. The exogenous expression of miR-592 inhibits the proliferation, migration, and invasion in epithelial ovarian cancer tumor cells. Furthermore, the exogenous expression of miR-592 inhibits tumor growth in the nude mouse xenograft model. Therefore, miR-592 may play a role of tumor suppressor miRNA in the occurrence and development of ovarian cancer. Further experiments demonstrated that tumor-related ERBB3 is a target gene mediated by miRNA-592. The dual-luciferase reporter system was used to identify miRNA-592 target genes; qPCR and Western Blot were used to detect the expression of ERBB3. Mechanical experiments confirmed that miRNA-592 negatively regulated ERBB3.Conclusion: Together, these findings identify a heretofore unrecognized link between miR-592 and ERBB3 and suggest that targeting on miR-592 warrants attention as a novel and potential therapeutic strategy for ovarian cancer.
C1 [Jin, Qiong; Xu, Xiaohong; Han, Chao; Zhao, Hui; Hu, Xiaodi; Wu, Yumei] Capital Med Univ, Beijing Obstet & Gynecol Hosp, Beijing Maternal & Child Hlth Care Hosp, Dept Gynecol Oncol, Beijing, Peoples R China.
   [Zhang, Ning] Yantai Penglai Tradit Chinese Med Hosp, Dept Intens Care Med, Yantai, Peoples R China.
   [Zhan, Yang] Capital Med Univ, Beijing Obstet & Gynecol Hosp, Beijing Maternal & Child Hlth Care Hosp, Dept Pathol, Beijing, Peoples R China.
   [Tang, Hongbo] Capital Med Univ, Beijing Obstet & Gynecol Hosp, Beijing Maternal & Child Hlth Care Hosp, Dept Pharm, Beijing, Peoples R China.
C3 Capital Medical University; Capital Medical University; Capital Medical
   University
RP Wu, YM (corresponding author), Capital Med Univ, Beijing Obstet & Gynecol Hosp, Beijing Maternal & Child Hlth Care Hosp, Dept Gynecol Oncol, Beijing, Peoples R China.
EM wym597118@ccmu.edu.cn
RI Zhao, Hui/AAS-7145-2020
FU Capital Medical University, Beijing Obstetrics and Gynecology Hospital
   [17JL27, FCYY201921]
FX <STRONG> </STRONG>The authors disclosed receipt of the following
   financial support for the research, authorship, and/or publication of
   this article: This work was supported by the Capital Medical University,
   Beijing Obstetrics and Gynecology Hospital (grant number No. 17JL27, No.
   FCYY201921).
CR Amin DN, 2010, SEMIN CELL DEV BIOL, V21, P944, DOI 10.1016/j.semcdb.2010.08.007
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NR 31
TC 3
Z9 3
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1533-0346
EI 1533-0338
J9 TECHNOL CANCER RES T
JI Technol. Cancer Res. Treat.
PY 2023
VL 22
AR 15330338231157156
DI 10.1177/15330338231157156
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9Y5WF
UT WOS:000950528000001
PM 36916303
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Módos, O
   Reis, H
   Niedworok, C
   Rübben, H
   Szendröi, A
   Szász, MA
   Tímár, J
   Baghy, K
   Kovalszky, I
   Golabek, T
   Chlosta, P
   Okon, K
   Peyronnet, B
   Mathieu, R
   Shariat, SF
   Hollósi, P
   Nyirády, P
   Szarvas, T
AF Modos, Orsolya
   Reis, Henning
   Niedworok, Christian
   Ruebben, Herbert
   Szendroi, Attila
   Szasz, Marcell A.
   Timar, Jozsef
   Baghy, Kornelia
   Kovalszky, Ilona
   Golabek, Tomasz
   Chlosta, Piotr
   Okon, Krzysztof
   Peyronnet, Benoit
   Mathieu, Romain
   Shariat, Shahrokh F.
   Hollosi, Peter
   Nyirady, Peter
   Szarvas, Tibor
TI Mutations of KRAS, NRAS, BRAF, EGFR, and PIK3CA genes in urachal
   carcinoma - occurence and prognostic significance
SO ONCOTARGET
LA English
DT Article
DE urachal carcinoma; urachal cancer; urachus; mutation; EGFR; Pathology
   Section
ID METASTATIC COLORECTAL-CANCER; GROWTH-FACTOR RECEPTOR; COMPREHENSIVE
   MOLECULAR CHARACTERIZATION; BLADDER-CANCER; KINASE DOMAIN; METAANALYSIS;
   THERAPY; ADENOCARCINOMA; DIAGNOSIS; OUTCOMES
AB Purpose: Targeted therapy represents an attractive alternative for rare tumors such as urachal carcinoma (UrC). The aim of this study was to assess the mutations of the most commonly affected 5 genes in the targetable EGFR-pathway in UrC and comapre their frequencies to those of found in urothelial and colorectal cancer.
   Materials and Methods: Mutational hot-spots of selected genes were tested in 22 UrC samples by pyrosequencing. Mutational patterns were compared to those published for colorectal and urothelial cancers. Furthermore, we sought correlations between mutations and clinicopathological and follow-up data.
   Results: We found 11 mutations in 10 of 22 (45%) patients. The most frequently mutated gene was KRAS (27%) followed by BRAF (18%) and NRAS (5%), while no mutations were detected in the EGFR and PIK3CA genes. No correlation was found between the mutation status and clinicopathological parameters (Sheldon/Mayo stage, tumor grade, metastases). Furthermore, none of the mutations correlated with progression-free or overall survival.
   Conclusions: The mutation pattern of UrC is more similar to colorectal than to urothelial cancer. However, the mutation characteristics of UrC seems to be unique suggesting that clinical decision-making for UrC cannot be simply adopted from urothelial or colorectal carcinoma. The high occurence of EGFR-pathway mutations warrants the testing for KRAS and BRAF mutations when considering anti-EGFR therapy in UrC.
C1 [Modos, Orsolya; Szendroi, Attila; Nyirady, Peter; Szarvas, Tibor] Semmelweis Univ, Dept Urol, H-1085 Budapest, Hungary.
   [Reis, Henning] Univ Duisburg Essen, Inst Pathol, Essen, Germany.
   [Niedworok, Christian; Ruebben, Herbert; Szarvas, Tibor] Univ Duisburg Essen, Dept Urol, Essen, Germany.
   [Szasz, Marcell A.; Timar, Jozsef] Semmelweis Univ, Dept Pathol 2, H-1085 Budapest, Hungary.
   [Baghy, Kornelia; Kovalszky, Ilona; Hollosi, Peter] Semmelweis Univ, Dept Pathol & Expt Canc Res 1, H-1085 Budapest, Hungary.
   [Golabek, Tomasz; Chlosta, Piotr] Jagiellonian Univ, Dept Urol, Krakow, Poland.
   [Okon, Krzysztof] Jagiellonian Univ, Dept Pathomorphol, Krakow, Poland.
   [Peyronnet, Benoit; Mathieu, Romain] Rennes Univ Hosp, Dept Urol, Rennes, France.
   [Shariat, Shahrokh F.] Med Univ Vienna, Vienna Gen Hosp, Dept Urol, Vienna, Austria.
   [Hollosi, Peter] Hungarian Acad Sci, Tumor Progress Res Grp, Budapest, Hungary.
C3 Semmelweis University; University of Duisburg Essen; University of
   Duisburg Essen; Semmelweis University; Semmelweis University;
   Jagiellonian University; Jagiellonian University; CHU Rennes; Universite
   de Rennes; Medical University of Vienna; Hungarian Academy of Sciences
RP Szarvas, T (corresponding author), Semmelweis Univ, Dept Urol, H-1085 Budapest, Hungary.; Szarvas, T (corresponding author), Univ Duisburg Essen, Dept Urol, Essen, Germany.
EM sztibusz@gmail.com
RI Okon, Krzysztof/D-1345-2011; Reis, Henning/AAX-9545-2020; Kovalszky,
   Ilona/ABH-2832-2020; Baghy, Kornélia/ABH-2549-2020; VIEILLARD,
   Philippe/B-8544-2008; Peyronnet, benoit/AGV-9053-2022; Szarvas,
   Tibor/L-4422-2017
OI Okon, Krzysztof/0000-0002-1921-5007; Szarvas, Tibor/0000-0002-6321-0799;
   Reis, Henning/0000-0003-1373-5295; Baghy, Kornelia/0000-0002-5323-2775
FU Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences;
   National Research, Development and Innovation Office [NKFIH/PD 115616];
   Hungarian Association of Urology
FX We thank for Ms Krisztina Egedi and Ms Krisztina Csaszar for their
   technical assistance. Thank you for Dr. Nathalie Rioux-Leclercq for her
   help in retrieving samples. Macell A. Szasz and Tibor Szarvas were
   supported by Janos Bolyai Research Scholarship of the Hungarian Academy
   of Sciences. This study was supported by the National Research,
   Development and Innovation Office (Grant number: NKFIH/PD 115616) and
   the Hungarian Association of Urology.
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NR 42
TC 44
Z9 45
U1 0
U2 5
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD JUN 28
PY 2016
VL 7
IS 26
BP 39293
EP 39301
DI 10.18632/oncotarget.9828
PG 9
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DP6NV
UT WOS:000378614700027
PM 27283768
OA Green Submitted, Green Published, Green Accepted, gold
DA 2025-01-04
ER

PT J
AU Sheffield, BS
   Beharry, A
   Diep, J
   Perdrizet, K
   Iafolla, MAJ
   Raskin, W
   Dudani, S
   Brett, MA
   Starova, B
   Olsen, B
   Cheema, PK
AF Sheffield, Brandon S.
   Beharry, Andrea
   Diep, Joanne
   Perdrizet, Kirstin
   Iafolla, Marco A. J.
   Raskin, William
   Dudani, Shaan
   Brett, Mary Anne
   Starova, Blerta
   Olsen, Brian
   Cheema, Parneet K.
TI Point of Care Molecular Testing: Community-Based Rapid Next-Generation
   Sequencing to Support Cancer Care
SO CURRENT ONCOLOGY
LA English
DT Article
DE NGS; precision medicine; targeted therapy
ID CELL LUNG-CANCER
AB Purpose: Biomarker data are critical to the delivery of precision cancer care. The average turnaround of next-generation sequencing (NGS) reports is over 2 weeks, and in-house availability is typically limited to academic centers. Lengthy turnaround times for biomarkers can adversely affect outcomes. Traditional workflows involve moving specimens through multiple facilities. This study evaluates the feasibility of rapid comprehensive NGS using the Genexus integrated sequencer and a novel streamlined workflow in a community setting. Methods: A retrospective chart review was performed to assess the early experience and performance characteristics of a novel approach to biomarker testing at a large community center. This approach to NGS included an automated workflow utilizing the Genexus integrated sequencer, validated for clinical use. NGS testing was further integrated within a routine immunohistochemistry (IHC) service, utilizing histotechnologists to perform technical aspects of NGS, with results reported directly by anatomic pathologists. Results: Between October 2020 and October 2021, 578 solid tumor samples underwent genomic profiling. Median turnaround time for biomarker results was 3 business days (IQR: 2-5). Four hundred eighty-one (83%) of the cases were resulted in fewer than 5 business days, and 66 (11%) of the cases were resulted simultaneously with diagnosis. Tumor types included lung cancer (310), melanoma (97), and colorectal carcinoma (68), among others. NGS testing detected key driver alterations at expected prevalence rates: lung EGFR (16%), ALK (3%), RET (1%), melanoma BRAF (43%), colorectal RAS/RAF (67%), among others. Conclusion: This is the first study demonstrating clinical implementation of rapid NGS. This supports the feasibility of automated comprehensive NGS performed and interpreted in parallel with diagnostic histopathology and immunohistochemistry. This novel approach to biomarker testing offers considerable advantages to clinical cancer care.
C1 [Sheffield, Brandon S.; Beharry, Andrea; Diep, Joanne; Brett, Mary Anne; Starova, Blerta; Olsen, Brian] William Osler Hlth Syst, Dept Lab Med, Brampton, ON L6R 3J7, Canada.
   [Perdrizet, Kirstin; Iafolla, Marco A. J.; Raskin, William; Dudani, Shaan; Cheema, Parneet K.] William Osler Hlth Syst, Div Med Oncol, Brampton, ON L6R 3J7, Canada.
   [Perdrizet, Kirstin; Iafolla, Marco A. J.; Raskin, William; Cheema, Parneet K.] Univ Toronto, Dept Med, Toronto, ON M5S 1A1, Canada.
C3 University of Toronto
RP Sheffield, BS (corresponding author), William Osler Hlth Syst, Dept Lab Med, Brampton, ON L6R 3J7, Canada.
EM brandon.sheffield@williamoslerhs.ca; andrea.beharry@williamoslerhs.ca;
   joanne.diep@williamoslerhs.ca; kirstin.perdrizet@williamoslerhs.ca;
   marco.iafolla@williamoslerhs.ca; william.raskin@williamoslerhs.ca;
   shaan.dudani@williamoslerhs.ca; maryanne.brett@williamoslerhs.ca;
   blerta.starova@williamoslerhs.ca; brian.olsen@williamoslerhs.ca;
   parneet.cheema@williamoslerhs.ca
RI Iafolla, Marco/AAA-2344-2021
OI Perdrizet, Kirstin/0000-0002-8746-665X; Dudani,
   Shaan/0000-0003-4958-381X
FU Eli Lilly Canada; Pfizer Canada
FX This research was funded by Eli Lilly Canada and Pfizer Canada.
CR Akahane T, 2021, DIAGN CYTOPATHOL, V49, P1078, DOI 10.1002/dc.24841
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NR 18
TC 26
Z9 28
U1 0
U2 2
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 MAR
PY 2022
VL 29
IS 3
BP 1326
EP 1334
DI 10.3390/curroncol29030113
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0E9BP
UT WOS:000776968000001
PM 35323313
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Patil, R
   Shanthala, PR
   Saldanha, P
AF Patil, Renuka
   Shanthala, P. R.
   Saldanha, Prema
TI IMMUNOHISTOCHEMICAL MARKERS OF CLINICAL SIGNIFICANCE IN CARCINOMA OF THE
   COLON AND RECTUM
SO JOURNAL OF EVOLUTION OF MEDICAL AND DENTAL SCIENCES-JEMDS
LA English
DT Article
DE Colorectal Carcinoma; Ki-67; Her2/neu
ID PROLIFERATION; EXPRESSION; KI-67
AB BACKGROUND Ki-67, a proliferative cell marker has a potential to distinguish rapidly proliferative tumours that are more likely to respond to chemotherapy. The Her2/neu is a marker of prognostic and therapeutic significance that has been in clinical use for breast carcinomas. Similar studies related to other tumours like colorectal carcinomas are needed to explore the significance. The aim of the present study was to analyse the expression of Ki-67 and Her2/neu status in colorectal carcinomas in correlation with parameters like histological type, grade, tumour size and lymph node status.
   MATERIALS AND METHODS The retrospective study included 30 histologically diagnosed cases of colorectal carcinomas. The clinical and pathological findings were recorded. Immunohistochemical study was performed with Ki-67 and Her2/neu markers on all cases and the findings were independently interpreted by two observers.
   RESULTS The cases were in the age range of 30-75 yrs. with a M:F ratio of 1.2 :1. Most of the tumours were in the left colon with rectum being the commonest site. Adenocarcinoma, NOS was the commonest type (86%). High Ki-67 labelling (> 50%) was seen in 18 cases (60%) of adenocarcinomas. The Her2/neu positivity was observed only in 3 cases of grade I adenocarcinomas.
   CONCLUSION The Ki-67 marker study would precisely define the cases with higher proliferative rate. Their predictive role could be of potential use for individualisation of adjuvant therapy. Her2/neu expression is low in colorectal carcinomas and need larger studies with combination of IHC and molecular methods along with clinical approach to determine the possible use in targeted therapy for colorectal carcinomas.
C1 [Patil, Renuka; Shanthala, P. R.; Saldanha, Prema] Yenepoya Univ, Yenepoya Med Coll, Dept Pathol, Mangaluru 575018, India.
C3 Yenepoya (Deemed to be University)
RP Patil, R (corresponding author), Yenepoya Univ, Yenepoya Med Coll, Dept Pathol, Mangaluru 575018, India.
EM renu83r@gmail.com
RI Saldanha, Prema/AAD-9591-2019
CR [Anonymous], IJBMS
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NR 15
TC 0
Z9 0
U1 0
U2 0
PU JOURNAL EVOLUTION MEDICAL & DENTAL SCIENCES
PI KARNATAKA
PA C/O AKSHANTALA ENTERPRISES, NO 65, 1ST FL, SAHUKAR CHENNIAH RD, MYSORE,
   KARNATAKA, 570 009, INDIA
SN 2278-4748
EI 2278-4802
J9 J EVOL MED DENT SCI-
JI J. Evol. Med. Dent. Sci.-JEMDS
PD DEC 1
PY 2016
VL 5
IS 96
BP 7087
EP 7090
DI 10.14260/jemds/2016/1603
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA EL5SZ
UT WOS:000394682600009
OA gold
DA 2025-01-04
ER

PT J
AU Tampellini, M
   La Salvia, A
   Scagliotti, GV
AF Tampellini, M.
   La Salvia, A.
   Scagliotti, G. V.
TI Novel investigational therapies for treating biliary tract carcinoma
SO EXPERT OPINION ON INVESTIGATIONAL DRUGS
LA English
DT Review
DE Cholangiocarcinoma review; target therapy; next generation sequencing;
   prognostic biomarker
ID PHASE-II TRIAL; SRC INHIBITOR SARACATINIB; TYROSINE KINASE INHIBITOR;
   METASTATIC BREAST-CANCER; ADVANCED SOLID TUMORS; CELL LUNG-CANCER;
   OPEN-LABEL; COLORECTAL-CANCER; 1ST-LINE TREATMENT; IN-VITRO
AB Introduction: Cholangiocarcinoma (CCA) is an epithelial cell malignancy arising from bile ducts and/or peribiliary glands. Even though it is considered as a rare neoplasm, its incidence is raising, particularly in developed countries. Prognosis is generally poor with few patients who present the inclusion criteria for surgery (the mainstay treatment for this tumour). Several genetic alterations potentially driving tumour progression have been described, representing a possible target for new compounds.
   Areas covered: A clinical trial search in Clinicaltrials. gov encompassing a literature search in PubMed and ASCO/ESMO Websites was undertaken in March 2016.
   Expert opinion: Notwithstanding a large number of drug tested, results are still disappointing. The main reasons could be the low number of patients enrolled in trials, and the lack of a patient selection based on the biological profile of the tumours. Potential active drugs could have been discharged simply because beneficial in a particular subgroup of patients and not in un unselected population. The future direction of the research should consider biomarker evaluation in order to describe the genetic alteration/s that drive tumour progression and aggressiveness and the mechanisms of drug resistance. Finally, it will be of great interest to consider the results of immunotherapy whenever available.
C1 [Tampellini, M.; La Salvia, A.; Scagliotti, G. V.] Univ Turin, AOU San Luigi di Orbassano, Dept Oncol, Reg Gonzole 10, I-10043 Turin, Italy.
C3 University of Turin
RP Tampellini, M (corresponding author), Univ Turin, AOU San Luigi di Orbassano, Dept Oncol, Reg Gonzole 10, I-10043 Turin, Italy.
EM marco.tampellini@unito.it
RI Scagliotti, Giorgio/K-6359-2016; La Salvia, Anna/C-6248-2019
OI Scagliotti, Giorgio/0000-0001-6646-958X; LA SALVIA,
   ANNA/0000-0002-5020-8657
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NR 131
TC 5
Z9 5
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 DEC
PY 2016
VL 25
IS 12
BP 1423
EP 1436
DI 10.1080/13543784.2016.1252330
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA ED6JU
UT WOS:000388962700008
PM 27771967
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Caputo, F
   Santini, C
   Bardasi, C
   Cerma, K
   Casadei-Gardini, A
   Spallanzani, A
   Andrikou, K
   Cascinu, S
   Gelsomino, F
AF Caputo, Francesco
   Santini, Chiara
   Bardasi, Camilla
   Cerma, Krisida
   Casadei-Gardini, Andrea
   Spallanzani, Andrea
   Andrikou, Kalliopi
   Cascinu, Stefano
   Gelsomino, Fabio
TI BRAF-Mutated Colorectal Cancer: Clinical and Molecular Insights
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colorectal cancer; BRAF mutation; BRAF inhibitors; molecular targets;
   targeted therapy
ID III COLON-CANCER; DNA MISMATCH REPAIR; FOLFOXIRI PLUS BEVACIZUMAB; KRAS
   WILD-TYPE; 1ST-LINE TREATMENT; MICROSATELLITE INSTABILITY;
   DOSE-ESCALATION; POOLED ANALYSIS; STAGE-II; PROGNOSTIC-FACTORS
AB Colorectal cancer (CRC) is one of the leading causes of mortality and morbidity in the world. It is a heterogeneous disease, which can be classified into different subtypes, characterized by specific molecular and morphological alterations. In this context, BRAF mutations are found in about 10% of CRC patients and define a particular subtype, characterized by a dismal prognosis, with a median survival of less than 12 months. Chemotherapy plus bevacizumab is the current standard therapy in first-line treatment of BRAF-mutated metastatic CRC (mCRC), with triplet (FOLFOXIRI) plus bevacizumab as a valid option in patients with a good performance status. BRAF inhibitors are not so effective as compared to melanoma, because of various resistance mechanisms. However, the recently published results of the BEACON trial will establish a new standard of care in this setting. This review provides insights into the molecular underpinnings underlying the resistance to standard treatment of BRAF-mutated CRCs, with a focus on their molecular heterogeneity and on the research perspectives both from a translational and a clinical point of view.
C1 [Caputo, Francesco; Santini, Chiara; Bardasi, Camilla; Cerma, Krisida; Casadei-Gardini, Andrea; Spallanzani, Andrea; Andrikou, Kalliopi; Cascinu, Stefano; Gelsomino, Fabio] Univ Modena & Reggio Emilia, Div Oncol, Dept Oncol & Hematol, I-41121 Modena, Italy.
   [Cascinu, Stefano] IRCCS San Raffaele Sci Inst Hosp, I-20019 Milan, Italy.
C3 Universita di Modena e Reggio Emilia
RP Casadei-Gardini, A (corresponding author), Univ Modena & Reggio Emilia, Div Oncol, Dept Oncol & Hematol, I-41121 Modena, Italy.
EM francesco1990.caputo@libero.it; santinic_90@libero.it;
   camilla.bardasi@gmail.com; kridi90@gmail.com; casadeigardini@gmail.com;
   andrea.spallanzani@gmail.com; k.andrikou@hotmail.com;
   cascinu.stefano@hsr.it; fabiogelsomino83@yahoo.it
RI Cascinu, Stefano/AAN-1923-2020; Gardini, Andrea/AAA-6985-2022;
   gelsomino, fabio/AAB-8967-2022; Spallanzani, Andrea/LRU-8788-2024;
   Caputo, Francesco/HSF-6337-2023; Casadei gardini, Andrea/F-1830-2016;
   Cascinu, Stefano/G-2399-2017
OI gelsomino, fabio/0000-0001-7979-4795; Caputo,
   Francesco/0000-0003-0331-3582; Spallanzani, Andrea/0000-0001-6955-7139;
   Casadei gardini, Andrea/0000-0001-6289-7202; Bardasi,
   Camilla/0000-0002-0692-2546; Cascinu, Stefano/0000-0003-2215-0731
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NR 91
TC 102
Z9 104
U1 0
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD NOV
PY 2019
VL 20
IS 21
AR 5369
DI 10.3390/ijms20215369
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA JQ4VU
UT WOS:000498946100127
PM 31661924
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Su, HH
   Pan, HW
   Lu, CP
   Chuang, JJ
   Yang, T
AF Su, Hsing-Hao
   Pan, Hung-Wei
   Lu, Chuan-Pin
   Chuang, Jyun-Jie
   Yang, Tsan
TI Automatic Detection Method for Cancer Cell Nucleus Image Based on
   Deep-Learning Analysis and Color Layer Signature Analysis Algorithm
SO SENSORS
LA English
DT Article
DE nucleus; mitosis; micronuclei; artificial intelligence; computer vision;
   convolutional neural network
ID CHROMOSOMAL INSTABILITY; SEGREGATION; ANEUPLOIDY
AB Exploring strategies to treat cancer has always been an aim of medical researchers. One of the available strategies is to use targeted therapy drugs to make the chromosomes in cancer cells unstable such that cell death can be induced, and the elimination of highly proliferative cancer cells can be achieved. Studies have reported that the mitotic defects and micronuclei in cancer cells can be used as biomarkers to evaluate the instability of the chromosomes. Researchers use these two biomarkers to assess the effects of drugs on eliminating cancer cells. However, manual work is required to count the number of cells exhibiting mitotic defects and micronuclei either directly from the viewing window of a microscope or from an image, which is tedious and creates errors. Therefore, this study aims to detect cells with mitotic defects and micronuclei by applying an approach that can automatically count the targets. This approach integrates the application of a convolutional neural network for normal cell identification and the proposed color layer signature analysis (CLSA) to spot cells with mitotic defects and micronuclei. This approach provides a method for researchers to detect colon cancer cells in an accurate and time-efficient manner, thereby decreasing errors and the processing time. The following sections will illustrate the methodology and workflow design of this study, as well as explain the practicality of the experimental comparisons and the results that were used to validate the practicality of this algorithm.
C1 [Su, Hsing-Hao] Kaohsiung Vet Gen Hosp, Dept Otorhinolaryngol Head & Neck Surg, Kaohsiung 81362, Taiwan.
   [Su, Hsing-Hao] Tajen Univ, Dept Pharm, Pingtung 90741, Taiwan.
   [Su, Hsing-Hao] Tajen Univ, Grad Inst Pharmaceut Technol, Pingtung 90741, Taiwan.
   [Pan, Hung-Wei] I Shou Univ, Coll Med, Sch Med Int Students, Kaohsiung 84001, Taiwan.
   [Lu, Chuan-Pin; Chuang, Jyun-Jie] Meiho Univ, Dept Informat Technol, Pingtung 91202, Taiwan.
   [Yang, Tsan] Meiho Univ, Dept Hlth Business Adm, Pingtung 91202, Taiwan.
C3 Kaohsiung Veterans General Hospital; I Shou University
RP Lu, CP (corresponding author), Meiho Univ, Dept Informat Technol, Pingtung 91202, Taiwan.
EM shsu@vghks.gov.tw; hwpan@isu.edu.tw; x00002174@meiho.edu.tw;
   d40614139@go.meiho.edu.tw; x00002115@meiho.edu.tw
OI Chuang, Jyun-Jie/0000-0003-2678-3528; SU, HSING-HAO/0000-0002-3905-8870
FU Kaohsiung Veterans General Hospital [VGHMHU109-005]; Ministry of Science
   and Technology, Taiwan [MOST108-2637-E-276-001]
FX This research was funded in part by Kaohsiung Veterans General Hospital,
   grant number VGHMHU109-005, and the Ministry of Science and Technology,
   Taiwan, under grant MOST108-2637-E-276-001.
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PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1424-8220
J9 SENSORS-BASEL
JI Sensors
PD AUG
PY 2020
VL 20
IS 16
AR 4409
DI 10.3390/s20164409
PG 19
WC Chemistry, Analytical; Engineering, Electrical & Electronic; Instruments
   & Instrumentation
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Engineering; Instruments & Instrumentation
GA NL2TP
UT WOS:000567274600001
PM 32784663
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ti, WQ
   Wang, JB
   Cheng, YF
AF Ti, Wenqi
   Wang, Jianbo
   Cheng, Yufeng
TI The Interaction Between Long Non-Coding RNAs and Cancer-Associated
   Fibroblasts in Lung Cancer
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE cancer-associated fibroblasts (CAFs); long non-coding RNAs (lncRNAs);
   tumor microenvironment; exosomes; lung cancer; targeted therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; CARCINOMA-ASSOCIATED FIBROBLASTS;
   TUMOR-GROWTH; TGF-BETA; COLORECTAL-CANCER; CELLS; CHEMORESISTANCE;
   INVASION; PROMOTE; MYOFIBROBLASTS
AB Despite great advances in research and treatment, lung cancer is still one of the most leading causes of cancer-related deaths worldwide. Evidence is mounting that dynamic communication network in the tumor microenvironment (TME) play an integral role in tumor initiation and development. Cancer-associated fibroblasts (CAFs), which promote tumor growth and metastasis, are the most important stroma component in the tumor microenvironment. Consequently, in-depth identification of relevant molecular mechanisms and biomarkers related to CAFs will increase understanding of tumor development process, which is of great significance for precise treatment of lung cancer. With the development of sequencing technologies such as microarray and next-generation sequencing, lncRNAs without protein-coding ability have been found to act as communicators between tumor cells and CAFs. LncRNAs participate in the activation of normal fibroblasts (NFs) to CAFs. Moreover, activated CAFs can influence the gene expression and secretion characteristics of cells through lncRNAs, enhancing the malignant biological process in tumor cells. In addition, lncRNA-loaded exosomes are considered to be another important form of crosstalk between tumor cells and CAFs. In this review, we focus on the interaction between tumor cells and CAFs mediated by lncRNAs in the lung cancer microenvironment, and discuss the analysis of biological function and molecular mechanism. Furthermore, it contributes to paving a novel direction for the clinical treatment of lung cancer.
C1 [Ti, Wenqi; Wang, Jianbo; Cheng, Yufeng] Shandong Univ, Qilu Hosp, Cheeloo Coll Med, Dept Radiat Oncol, Jinan, Peoples R China.
C3 Shandong University
RP Wang, JB; Cheng, YF (corresponding author), Shandong Univ, Qilu Hosp, Cheeloo Coll Med, Dept Radiat Oncol, Jinan, Peoples R China.
EM qlwjb2008@163.com; qlcyf@sdu.edu.cn
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NR 85
TC 14
Z9 14
U1 0
U2 7
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 JAN 11
PY 2022
VL 9
AR 714125
DI 10.3389/fcell.2021.714125
PG 10
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA YO6BE
UT WOS:000748023700001
PM 35087824
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kelly, RJ
   Forde, PM
   Elnahal, SM
   Forastiere, AA
   Rosner, GL
   Smith, TJ
AF Kelly, Ronan J.
   Forde, Patrick M.
   Elnahal, Shereef M.
   Forastiere, Arlene A.
   Rosner, Gary L.
   Smith, Thomas J.
TI Patients and Physicians Can Discuss Costs of Cancer Treatment in the
   Clinic
SO JOURNAL OF ONCOLOGY PRACTICE
LA English
DT Article
ID PATIENTS NEEDS; CARE; INSURANCE; SATISFACTION; ASSOCIATION; PREFERENCES;
   VIEWS
AB Purpose: As one solution to reducing costs and medical bankruptcies, experts have suggested that patients and physicians should discuss the cost of care up front. Whether these discussions are possible in an oncology setting and what their effects on the doctor-patient relationship are is not known.
   Methods: We used the National Comprehensive Cancer Network (NCCN) Guidelines and the eviti Advisor platform to show patients with metastatic breast, lung, or colorectal cancer the costs associated with their chemotherapy and/or targeted therapy options during an oncology consultation. We measured provider attitudes and assessed patient satisfaction when consultations included discussion of costs.
   Results: We approached 107 patients; 96 (90%) enrolled onto the study, three (3%) asked if they could be interviewed at a later date, and eight (7%) did not want to participate. Only five of 18 oncologists (28%) felt comfortable discussing costs, and only one of 18 (6%) regularly asked patients about financial difficulties. The majority of patients (80%) wanted cost information, and 84% reported that these conversations would be even more important if their co-pays were to increase. In total, 72% of patients responded that no health care professional has ever discussed costs with them. The majority of patients (80%) had no negative feelings about hearing cost information.
   Conclusion: In an era of rising co-pays, patients with cancer want cost-of-treatment discussions, and these conversations do not lead to negative feelings in the majority of patients. Additional training to prepare clinicians for how to discuss costs with their patients is needed.
C1 Johns Hopkins, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
   Eviti, Philadelphia, PA USA.
C3 Johns Hopkins University; Johns Hopkins Medicine
RP Smith, TJ (corresponding author), Johns Hopkins Med Inst, Sidney Kimmel Comprehens Canc Ctr, 600 N Wolfe St,Blalock 369, Baltimore, MD 21287 USA.
EM tsmit136@jhmi.edu
RI Rosner, Gary/ABG-8161-2021; Forde, Patrick/AAX-2936-2021; Smith,
   Thomas/A-9640-2010
OI Forde, Patrick/0000-0001-6925-6344; Smith, Thomas/0000-0003-3040-6434
FU National Comprehensive Cancer Network Young Investigator Award; National
   Cancer Institute [P 30 006973]
FX Supported by a National Comprehensive Cancer Network Young Investigator
   Award (R.J.K.) and by National Cancer Institute Grant No. P 30 006973 to
   Sidney Kimmel Comprehensive Cancer Center.
CR [Anonymous], J CLIN ONCOL
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NR 22
TC 53
Z9 57
U1 0
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 1554-7477
EI 1935-469X
J9 J ONCOL PRACT
JI J. Oncol. Pract.
PD JUL
PY 2015
VL 11
IS 4
BP 308
EP +
DI 10.1200/JOP.2015.003780
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CY1PQ
UT WOS:000366180100017
PM 26015459
OA Green Published, Green Accepted
DA 2025-01-04
ER

PT J
AU Liu, ZZ
   Gao, ZY
   Yang, W
   Zhang, LX
   Xiao, N
   Qu, DM
   Su, ZJ
   Xu, KB
   Liu, GW
   Wang, YL
   Ren, Q
   Yu, S
   Cheng, Y
   Zhou, YN
   Deng, QH
   Zhao, YC
   Wang, ZY
   Yang, HM
AF Liu, Zhengzhi
   Gao, Zhenyue
   Yang, Wei
   Zhang, Lixiu
   Xiao, Nan
   Qu, Dongmei
   Su, Zhengjie
   Xu, Kaibo
   Liu, Guangwen
   Wang, Yanli
   Ren, Qing
   Yu, Shuang
   Cheng, Yang
   Zhou, Yannan
   Deng, Qiaohuan
   Zhao, Yicheng
   Wang, Zeyu
   Yang, Haimiao
TI A randomized, double-blind, single-dose, parallel phase I clinical trial
   to compare the bioequivalence, immunogenicity, and safety of bevacizumab
   biosimilar and bevacizumab in healthy Chinese subjects
SO EXPERT OPINION ON DRUG METABOLISM & TOXICOLOGY
LA English
DT Article
DE Bevacizumab; bioequivalence; biosimilars; cancer; vascular endothelial
   growth factor
ID CANCER; CHEMOTHERAPY; COMBINATION; CARCINOMA; SURVIVAL; THERAPY;
   GLIOBLASTOMA; TEMOZOLOMIDE; CETUXIMAB; RECURRENT
AB Background: Bevacizumab, a humanized monoclonal antibody against VEGF, can be used as a target therapy for colorectal cancer. A phase I clinical trial was conducted to compare the bioequivalence, immunogenicity, and safety of bevacizumab biosimilar (Chia Tai Tianqing Pharmaceutical Group Co., Ltd.) and Bevacizumab (Roche Diagnostics GmbH) in healthy Chinese males.
   Research design & method: Healthy Chinese subjects (N = 98) were randomly divided into two groups. A single-dose bevacizumab biosimilar or Bevacizumab was given per cycle. Plasma drug concentrations were detected by liquid chromatography-tandem mass spectrometry (LC-MC/MS) assay. We detected the levels of anti-drug antibody (ADA) to evaluate drug immunogenicity and the safety of drugs throughout the study.
   Results: The geometric mean ratios (GMRs) of AUC(0-t), C-max, and AUC(0-infinity) for bevacizumab biosimilar and Bevacizumab were 96.27%, 93.69%, and 97.01%, respectively. The 90% CIs were all within 80-125%, meeting the bioequivalence standards. The levels of ADA were similar. In addition, the two drugs both demonstrated excellent safety in the trial.
   Conclusion: This study showed that bevacizumab biosimilar and Bevacizumab had similar pharmacokinetics (PK) parameters and safety in healthy Chinese subjects.
C1 [Liu, Zhengzhi; Yang, Wei; Zhang, Lixiu; Su, Zhengjie; Xu, Kaibo; Liu, Guangwen; Wang, Yanli; Ren, Qing; Yu, Shuang; Cheng, Yang; Zhou, Yannan; Deng, Qiaohuan; Wang, Zeyu; Yang, Haimiao] Changchun Univ Chinese Med, Phase I Clin Trial Lab, Affiliated Hosp, Changchun, Peoples R China.
   [Gao, Zhenyue; Xiao, Nan] Chia Tai Tianqing Pharmaceut Grp Co Ltd, Dept Clin Res Ctr, Nanjing, Peoples R China.
   [Qu, Dongmei] Ansiterui Med Technol Consulting Co Ltd, Cin Tial Qual Control Ctr, Changchun, Peoples R China.
   [Zhao, Yicheng] First Hosp Jilin Univ, Ctr Pathogen Biol & Infect Dis, Key Lab Organ Regenerat & Transplantat, Minist Educ, Changchun, Peoples R China.
   [Zhao, Yicheng] Changchun Univ Chinese Med, Clin Med Coll, Changchun, Peoples R China.
   [Wang, Zeyu] Changchun Univ Chinese Med, Sci Res Dept, Changchun, Peoples R China.
C3 Changchun University of Chinese Medicine; Jilin University; Changchun
   University of Chinese Medicine; Changchun University of Chinese Medicine
RP Wang, ZY; Yang, HM (corresponding author), Changchun Univ Chinese Med, Phase I Clin Trial Lab, Affiliated Hosp, Changchun, Peoples R China.
EM zeyu781022@163.com; haimiaoyang@outlook.com
RI Zhao, Yicheng/GNP-3908-2022; Wang, lili/IXD-9828-2023; Yang,
   Haimiao/HNS-8599-2023; Li, Shanshan/HLH-7747-2023
OI Zhao, Yicheng/0000-0002-1691-323X
FU Chia Tai Tianqing Pharmaceutical Group Co., Ltd., Jiangsu, China [I
   2017-01]
FX This work was supported by Chia Tai Tianqing Pharmaceutical Group Co.,
   Ltd., Jiangsu, China (funding number: phase I 2017-01). The founder
   helps pay for this study and has no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 40
TC 0
Z9 0
U1 2
U2 2
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1742-5255
EI 1744-7607
J9 EXPERT OPIN DRUG MET
JI Expert Opin. Drug Metab. Toxicol.
PD AUG 3
PY 2022
VL 18
IS 7-8
BP 519
EP 527
DI 10.1080/17425255.2022.2113382
EA AUG 2022
PG 9
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA 4L9KR
UT WOS:000841817700001
PM 35961948
DA 2025-01-04
ER

PT J
AU Sepay, N
   Kim, TW
   Singh, T
   Paul, M
   Kong, HJ
   Ryu, JS
   Ghosh, N
   Jeon, S
   Lee, S
   Ahn, TS
   Baek, MJ
   Kang, DH
   Im, J
AF Sepay, Nasim
   Kim, Tae Wan
   Singh, Tejinder
   Paul, Mohuya
   Kong, Hye Jeong
   Ryu, Jae Sung
   Ghosh, Nandan
   Jeon, Seob
   Lee, Soohyeon
   Ahn, Tae Sung
   Baek, Moo-Jun
   Kang, Dong Hyun
   Im, Jungkyun
TI Targeted delivery of oxaliplatin to colorectal cancer using the
   cancer-specific cell-penetrating peptide BR2
SO JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
LA English
DT Article
DE Cell-penetrating peptide; BR2; Oxaliplatin; Drug delivery; Targeted
   therapy; Colorectal cancer
ID BIODEGRADABLE POLYMER; MECHANISM; APOPTOSIS; COMPLEX; CARRIER
AB Oxaliplatin is one of the main drugs used in chemotherapy to treat advanced colorectal cancer (CRC), but its effectiveness is limited by its weak cellular uptake, and poor targeting to cancer cells, which can lead to drug resistance and adverse effects in patients. To address these issues, we tested a cell-penetrating, cancer-specific peptide called BR2 as a new peptide-drug conjugate. We conjugated oxaliplatin with BR2 covalently using a heterobifunctional linker. The resulting conjugate (BR2-Oxal) was examined for in vitro and in vivo effectiveness against human colon cancer cells and tumors. Compared with the parent drug, the in vitro investigations showed selective cellular uptake of BR2-Oxal in cancer cells rather than in normal cells and a significantly greater reduction in colon cancer cell viability due to a higher ratio of apoptosis. We also found that BR2-Oxal exhibited a higher accumulation in tumors and greater tumor suppression than oxaliplatin in a xenograft mouse model, suggesting that BR2-Oxal was efficiently and specifically delivered to tumors in vivo. These findings indicate that using the BR2 peptide for the intracellular delivery of oxaliplatin is a promising drug-delivery strategy. This approach also has the potential to enhance the efficiency of oxaliplatin prodrugs or derivatives.
C1 [Sepay, Nasim; Singh, Tejinder; Paul, Mohuya; Ghosh, Nandan; Im, Jungkyun] Soonchunhyang Univ, Dept Elect Mat Devices & Equipment Engn, Asan 31538, South Korea.
   [Kim, Tae Wan; Kong, Hye Jeong; Ryu, Jae Sung] Soonchunhyang Univ, Dept Med Life Sci, Asan 31538, South Korea.
   [Jeon, Seob] Soonchunhyang Univ, Cheonan Hosp, Coll Med, Dept Obstet & Gynecol, Cheonan 31151, South Korea.
   [Lee, Soohyeon; Ahn, Tae Sung; Baek, Moo-Jun; Kang, Dong Hyun] Soonchunhyang Univ, Cheonan Hosp, Coll Med, Dept Surg, Cheonan 31151, South Korea.
   [Im, Jungkyun] Soonchunhyang Univ, Dept Chem Engn, Asan 31538, South Korea.
C3 Soonchunhyang University; Soonchunhyang University; Soonchunhyang
   University; Soonchunhyang University; Soonchunhyang University
RP Im, J (corresponding author), Soonchunhyang Univ, Dept Elect Mat Devices & Equipment Engn, Asan 31538, South Korea.; Kang, DH (corresponding author), Soonchunhyang Univ, Cheonan Hosp, Coll Med, Dept Surg, Cheonan 31151, South Korea.
EM mctoms@naver.com; jkim5279@sch.ac.kr
RI Baek, Moo-Jun/W-1736-2019
OI Paul, Mohuya/0000-0001-6017-2160
FU National Research Foundation of Korea (NRF) - Korean government (MSIT)
   [2021R1F1A1062951, 2019M3E5D1A02069058]; Soonchunhyang University
   research fund
FX This work was supported by the National Research Foundation of Korea
   (NRF) grants funded by the Korean government (MSIT) (No.
   2021R1F1A1062951, and No. 2019M3E5D1A02069058) . This work was also
   supported by Soonchunhyang University research fund.
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NR 54
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1773-2247
EI 2588-8943
J9 J DRUG DELIV SCI TEC
JI J. Drug Deliv. Sci. Technol.
PD NOV
PY 2024
VL 101
AR 106261
DI 10.1016/j.jddst.2024.106261
EA OCT 2024
PN B
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA J1L9T
UT WOS:001334767600001
DA 2025-01-04
ER

PT J
AU Fadlallah, H
   El Masri, J
   Fakhereddine, H
   Youssef, J
   Chemaly, C
   Doughan, S
   Abou-Kheir, W
AF Fadlallah, Hiba
   El Masri, Jad
   Fakhereddine, Hiam
   Youssef, Joe
   Chemaly, Chrystelle
   Doughan, Samer
   Abou-Kheir, Wassim
TI Colorectal cancer: Recent advances in management and treatment
SO WORLD JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Review
DE Colorectal cancer; Treatment; Surgery; Chemotherapy; Targeted therapy;
   Immunotherapy
ID ADVANCED RECTAL-CANCER; III COLON-CANCER; CETUXIMAB PLUS IRINOTECAN;
   MISMATCH REPAIR-DEFICIENT; ASTRO PRACTICE PARAMETER; PROTON-BEAM
   THERAPY; RADIATION-THERAPY; OPEN-LABEL; 1ST-LINE TREATMENT; DOUBLE-BLIND
AB Colorectal cancer (CRC) is the third most common cancer worldwide, and the second most common cause of cancer-related death. In 2020, the estimated number of deaths due to CRC was approximately 930000, accounting for 10% of all cancer deaths worldwide. Accordingly, there is a vast amount of ongoing research aiming to find new and improved treatment modalities for CRC that can potentially increase survival and decrease overall morbidity and mortality. Current management strategies for CRC include surgical procedures for resectable cases, and radiotherapy, chemotherapy, and immunotherapy, in addition to their combination, for non-resectable tumors. Despite these options, CRC remains incurable in 50% of cases. Nonetheless, significant improvements in research techniques have allowed for treatment approaches for CRC to be frequently updated, leading to the availability of new drugs and therapeutic strategies. This review summarizes the most recent therapeutic approaches for CRC, with special emphasis on new strategies that are currently being studied and have great potential to improve the prognosis and lifespan of patients with CRC.
C1 [Fadlallah, Hiba; El Masri, Jad; Fakhereddine, Hiam; Youssef, Joe; Chemaly, Chrystelle; Abou-Kheir, Wassim] Amer Univ Beirut, Dept Anat Cell Biol & Physiol Sci, Bliss St, Beirut 11072020, Lebanon.
   [Doughan, Samer] Amer Univ Beirut, Med Ctr, Dept Surg, Beirut 11072020, Lebanon.
C3 American University of Beirut; American University of Beirut
RP Abou-Kheir, W (corresponding author), Amer Univ Beirut, Dept Anat Cell Biol & Physiol Sci, Bliss St, Beirut 11072020, Lebanon.
EM wa12@aub.edu.lb
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NR 184
TC 3
Z9 3
U1 2
U2 2
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 SEP 24
PY 2024
VL 15
IS 9
DI 10.5306/wjco.v15.i9.1136
PG 22
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA H6T8F
UT WOS:001324753800009
PM 39351451
DA 2025-01-04
ER

PT J
AU Xin, R
   Shen, B
   Jiang, YJ
   Liu, JB
   Li, S
   Hou, LK
   Wu, W
   Jia, CY
   Wu, CY
   Fu, D
   Ma, YS
   Jiang, GX
AF Xin, Rui
   Shen, Biao
   Jiang, Ying-Jie
   Liu, Ji-Bin
   Li, Sha
   Hou, Li-Kun
   Wu, Wei
   Jia, Cheng-You
   Wu, Chun-Yan
   Fu, Da
   Ma, Yu-Shui
   Jiang, Geng-Xi
TI Comprehensive analysis to identify a novel PTEN-associated ceRNA
   regulatory network as a prognostic biomarker for lung adenocarcinoma
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE ceRNA network; LINC00460; miR-150-3p; LUAD; PTEN
ID COLON-CANCER; PROGRESSION; EXPRESSION; CARCINOMA; PROMOTES; GENES
AB Lung adenocarcinoma (LUAD) is one of the most prevalent forms of lung cancer. Competitive endogenous RNA (ceRNA) plays an important role in the pathogenesis of lung cancer. Phosphatase and tensin homolog (PTEN) is one of the most frequently deleted tumour suppressor genes in LUAD. The present study aimed to identify a novel PTEN-associated-ceRNA regulatory network and identify potential prognostic markers associated with LUAD. Transcriptome sequencing profiles of 533 patients with LUAD were obtained from TCGA database, and differentially expressed genes (DEGs) were screened in LUAD samples with PTEN high- (PTENhigh) and low- (PTENlow) expression. Eventually, an important PTEN-related marker was identified, namely, the LINC00460/miR-150-3p axis. Furthermore, the predicted target genes (EME1/HNRNPAB/PLAUR/SEMA3A) were closely related to overall survival and prognosis. The LINC00460/miR-150-3p axis was identified as a clinical prognostic factor through Cox regression analysis. Methylation analyses suggested that abnormal regulation of the predicted target genes might be caused by hypomethylation. Furthermore, immune infiltration analysis showed that the LINC00460/miR-150-3p axis could alter the levels of immune infiltration in the tumour immune microenvironment, and promote the clinical progression of LUAD. To specifically induce PTEN deletion in the lungs, we constructed an STP mouse model (SFTPC-rtTA/tetO-cre/Pten(flox/+)). Quantitative PCR (qPCR) and immunohistochemical (IHC) analysis were used to detect predicted target genes. Therefore, we revealed that the PTEN-related LINC00460/miR-150-3p axis based on ceRNA mechanism plays an important role in the development of LUAD and provides a new direction and theoretical basis for its targeted therapy.
C1 [Xin, Rui; Li, Sha; Wu, Wei; Jia, Cheng-You; Fu, Da; Ma, Yu-Shui] Tongji Univ, Shanghai Peoples Hosp 10, Dept Nucl Med, Sch Med, Shanghai, Peoples R China.
   [Shen, Biao] Nantong Univ, Dept Thorac Surg, Affiliated Tumor Hosp, Nantong, Peoples R China.
   [Jiang, Ying-Jie] Navy Mil Med Univ, Dept Pathol, Affiliated Changhai Hosp, Shanghai, Peoples R China.
   [Liu, Ji-Bin] Nantong Univ, Inst Oncol, Affiliated Tumor Hosp, Nantong, Jiangsu, Peoples R China.
   [Hou, Li-Kun; Wu, Chun-Yan] Tongji Univ, Shanghai Pulm Hosp, Dept Pathol, Sch Med, Shanghai, Peoples R China.
   [Fu, Da] Shanghai Jiaotong Univ Sch Med, Ruijin Hosp, Inst Pancreat Dis, Sch Med, Shanghai, Peoples R China.
   [Ma, Yu-Shui] Shanghai Univ Tradit Chinese Med, Longhua Hosp, Canc Inst, Shanghai, Peoples R China.
   [Jiang, Geng-Xi] Navy Mil Med Univ, Dept Thorac Surg, Affiliated Changhai Hosp, Shanghai, Peoples R China.
C3 Tongji University; Nantong University; Naval Medical University; Nantong
   University; Tongji University; Shanghai Jiao Tong University; Shanghai
   University of Traditional Chinese Medicine; Naval Medical University
RP Fu, D; Ma, YS (corresponding author), Tongji Univ, Shanghai Peoples Hosp 10, Dept Nucl Med, Sch Med, Shanghai, Peoples R China.; Fu, D (corresponding author), Shanghai Jiaotong Univ Sch Med, Ruijin Hosp, Inst Pancreat Dis, Sch Med, Shanghai, Peoples R China.; Ma, YS (corresponding author), Shanghai Univ Tradit Chinese Med, Longhua Hosp, Canc Inst, Shanghai, Peoples R China.; Jiang, GX (corresponding author), Navy Mil Med Univ, Dept Thorac Surg, Affiliated Changhai Hosp, Shanghai, Peoples R China.
EM fu80da90@163.com; mayushui@tongji.edu.cn; jiang9909@hotmail.com
RI WU, CHUNYAN/HMO-6771-2023; Fu, Da/F-1763-2013; Fu, Da/GXF-2656-2022;
   liu, James/E-9699-2014
OI Ma, Yu-Shui/0000-0002-5728-7458; Jiang, Yingjie/0009-0003-7031-2448; Fu,
   Da/0000-0002-0878-2575
FU Natural Science Foundation of Jiangsu Province; Shanghai Natural Science
   Foundation; Key Program of Hunan Provincial Department of Science and
   Technology;  [BK20201442];  [20ZR1472400];  [2020WK2020]
FX Funding This study was supported partly by grants from Natural Science
   Foundation of Jiangsu Province (BK20201442), Shanghai Natural Science
   Foundation (20ZR1472400), Key Program of Hunan Provincial Department of
   Science and Technology (2020WK2020).
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NR 60
TC 4
Z9 4
U1 2
U2 13
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD AUG 24
PY 2022
VL 12
AR 923026
DI 10.3389/fonc.2022.923026
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4I7DN
UT WOS:000850735500001
PM 36091160
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lu, XQ
   Zhang, JQ
   Zhang, SX
   Qiao, J
   Qiu, MT
   Liu, XR
   Chen, XX
   Gao, C
   Zhang, HH
AF Lu, Xiao-Qing
   Zhang, Jia-Qian
   Zhang, Sheng-Xiao
   Qiao, Jun
   Qiu, Meng-Ting
   Liu, Xiang-Rong
   Chen, Xiao-Xia
   Gao, Chong
   Zhang, Huan-Hu
TI Identification of novel hub genes associated with gastric cancer using
   integrated bioinformatics analysis
SO BMC CANCER
LA English
DT Article
DE Gastric cancer; Bioinformatics analysis; Differentially expressed genes
ID PROTEIN-INTERACTION NETWORKS; CELL-PROLIFERATION; CYCLIN A2;
   HEPATOCELLULAR-CARCINOMA; COLORECTAL-CANCER; EXPRESSION; PROMOTES;
   INVASION; SURVIVAL; INTERLEUKIN-8
AB BackgroundGastric cancer (GC) is one of the most common solid malignant tumors worldwide with a high-recurrence-rate. Identifying the molecular signatures and specific biomarkers of GC might provide novel clues for GC prognosis and targeted therapy.MethodsGene expression profiles were obtained from the ArrayExpress and Gene Expression Omnibus database. Differentially expressed genes (DEGs) were picked out by R software. The hub genes were screened by cytohubba plugin. Their prognostic values were assessed by Kaplan-Meier survival analyses and the gene expression profiling interactive analysis (GEPIA). Finally, qRT-PCR in GC tissue samples was established to validate these DEGs.ResultsTotal of 295 DEGs were identified between GC and their corresponding normal adjacent tissue samples in E-MTAB-1440, GSE79973, GSE19826, GSE13911, GSE27342, GSE33335 and GSE56807 datasets, including 117 up-regulated and 178 down-regulated genes. Among them, 7 vital upregulated genes (HMMR, SPP1, FN1, CCNB1, CXCL8, MAD2L1 and CCNA2) were selected. Most of them had a significantly worse prognosis except SPP1. Using qRT-PCR, we validated that their transcriptions in our GC tumor tissue were upregulated except SPP1 and FN1, which correlated with tumor relapse and predicts poorer prognosis in GC patients.ConclusionsWe have identified 5 upregulated DEGs (HMMR, CCNB1, CXCL8, MAD2L1, and CCNA2) in GC patients with poor prognosis using integrated bioinformatical methods, which could be potential biomarkers and therapeutic targets for GC treatment.
C1 [Lu, Xiao-Qing; Liu, Xiang-Rong; Chen, Xiao-Xia] Shanxi Canc Hosp, Dept Breast Surg, Taiyuan, Shanxi, Peoples R China.
   [Zhang, Jia-Qian; Zhang, Sheng-Xiao; Qiao, Jun; Qiu, Meng-Ting] Shanxi Med Univ, Hosp 2, Dept Rheumatol, Taiyuan, Shanxi, Peoples R China.
   [Gao, Chong] Harvard Med Sch, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
   [Zhang, Huan-Hu] Shanxi Canc Hosp, Dept Gastroenterol, Taiyuan 030001, Shanxi, Peoples R China.
C3 Shanxi Medical University; Harvard University; Brigham & Women's
   Hospital; Harvard Medical School
RP Zhang, HH (corresponding author), Shanxi Canc Hosp, Dept Gastroenterol, Taiyuan 030001, Shanxi, Peoples R China.
EM zhhh31@163.com
RI gao, chong/JUF-7924-2023
OI Zhang, Sheng-Xiao/0000-0003-1341-7588
FU Graduate Students Outstanding Innovation Project Foundation of Shanxi
   Province [2C592020079]
FX This project was supported by Graduate Students Outstanding Innovation
   Project Foundation of Shanxi Province (2C592020079). The funding bodies
   played no role in the design of the study and collection, analysis, and
   interpretation of data and in writing the manuscript.
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NR 75
TC 26
Z9 28
U1 0
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 JUN 14
PY 2021
VL 21
IS 1
AR 697
DI 10.1186/s12885-021-08358-7
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SW9BM
UT WOS:000664809100001
PM 34126961
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Jang, M
   Pak, HY
   Heo, JY
   Lim, H
   Choi, YL
   Shim, HS
   Kim, EK
AF Jang, Mi
   Pak, Hae Yong
   Heo, Ja Yoon
   Lim, Hyunsun
   Choi, Yoon-La
   Shim, Hyo Sup
   Kim, Eun Kyung
TI Trends and Clinical Characteristics of Next-Generation Sequencing-Based
   Genetic Panel Tests: An Analysis of Korean Nationwide Claims Data
SO CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Next-generation sequencing; Population-based; Claims data; National
   health insurance; Anticancer drug; Targeted therapy
ID CENTRAL-NERVOUS-SYSTEM; CLASSIFICATION; TUMORS
AB Purpose In the modern era of precision medicine, next-generation sequencing (NGS) is employed for a variety of clinical purposes. The aim of this study was to investigate the trends and clinical characteristics of NGS testing in South Korea.Materials and Methods This nationwide, population-based, retrospective cohort study examined National Health Insurance Service claims data from 2017 to 2021 for NGS and from 2008 to 2021 for gene-targeted anticancer drugs.Results Among the total 98,748 claims, there were 51,407 (52.1%) solid cancer panels, 30,173 (30.5%) hereditary disease panels, and 17,168 (17.4%) hematolymphoid cancer panels. The number of annual claims showed a persistent upward trend, exhibiting a 5.4-fold increase, from 5,436 in 2017 to 29,557 in 2021. In the solid cancer panel, colorectal cancer was the most common (19.2%), followed by lung cancer (18.8%). The annual claims for targeted cancer drugs have increased 25.7-fold, from 3,932 in 2008 to 101,211 in 2020. Drugs for the treatment of lung cancer accounted for 488,819 (71.9%) claims. The number of patients who received non-hereditary NGS testing has substantially increased, and among them, the count of patients prescribed targeted anticancer drugs consistently rose from 508 (13.9%) in 2017 to 2,245 (12.3%) in 2020. Conclusion This study highlights the rising nationwide demand for comprehensive genetic testing for disease diagnosis and treatment following NGS reimbursement by the National Health Insurance in South Korea, in addition to the need for greater utilization of targeted anticancer drugs.
C1 [Jang, Mi; Kim, Eun Kyung] Ilsan Hosp, Dept Pathol, Natl Hlth Insurance Serv, Goyang, South Korea.
   [Pak, Hae Yong; Lim, Hyunsun] Ilsan Hosp, Dept Policy Res Affairs, Natl Hlth Insurance Serv, Goyang, South Korea.
   [Heo, Ja Yoon] Ilsan Hosp, Dept Oncol, Natl Hlth Insurance Serv, Goyang, South Korea.
   [Choi, Yoon-La] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol & Translat Genom, Seoul, South Korea.
   [Shim, Hyo Sup] Yonsei Univ, Dept Pathol, Coll Med, Seoul, South Korea.
   [Kim, Eun Kyung] Ilsan Hosp, Natl Hlth Insurance Serv, Dept Pathol, 100 Ilsan Ro, Goyang 10444, South Korea.
C3 NHIS Ilsan Hospital; National Health Insurance Service; National Health
   Insurance Service; NHIS Ilsan Hospital; NHIS Ilsan Hospital; National
   Health Insurance Service; Sungkyunkwan University (SKKU); Samsung
   Medical Center; Yonsei University; Yonsei University Health System; NHIS
   Ilsan Hospital; National Health Insurance Service
RP Kim, EK (corresponding author), Ilsan Hosp, Natl Hlth Insurance Serv, Dept Pathol, 100 Ilsan Ro, Goyang 10444, South Korea.
EM dalsoon2@nhimc.or.kr
RI Shim, Hyo/ABI-6190-2020
OI Shim, Hyo Sup/0000-0002-5718-3624
FU National Health Insurance Service Ilsan Hospital [NHIMC-2022-PR-014];
   National Research Foundation of Korea [NRF-2022R1C1C1008494]
FX <STRONG> </STRONG>The National Health Information Database was provided
   by the National Health Insurance Service of Korea. The authors would
   like to thank the National Health Insurance Service for their
   cooperation. This work was supported by the National Health Insurance
   Service Ilsan Hospital [NHIMC-2022-PR-014] and the National Research
   Foundation of Korea (NRF-2022R1C1C1008494).
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NR 24
TC 0
Z9 0
U1 0
U2 0
PU KOREAN CANCER ASSOCIATION
PI SEOUL
PA RM 1824, GWANGHWAMUN OFFICIA, 92 SAEMUNAN-RO, JONGNO-GU, SEOUL, 110-999,
   SOUTH KOREA
SN 1598-2998
EI 2005-9256
J9 CANCER RES TREAT
JI Cancer Res. Treat.
PD JAN
PY 2024
VL 56
IS 1
BP 27
EP 36
DI 10.4143/crt.2023.844
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FS9L4
UT WOS:001147961100001
PM 37680123
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Gymnopoulos, M
   Betancourt, O
   Blot, V
   Fujita, R
   Galvan, D
   Lieuw, V
   Nguyen, S
   Snedden, J
   Stewart, C
   Villicana, J
   Wojciak, J
   Wong, E
   Pardo, R
   Patel, N
   D'Hooge, F
   Vijayakrishnan, B
   Barry, C
   Hartley, JA
   Howard, PW
   Newman, R
   Coronella, J
AF Gymnopoulos, Marco
   Betancourt, Oscar
   Blot, Vincent
   Fujita, Ryo
   Galvan, Diana
   Lieuw, Vincent
   Nguyen, Sophie
   Snedden, Jeanette
   Stewart, Christine
   Villicana, Jose
   Wojciak, Jon
   Wong, Eley
   Pardo, Raul
   Patel, Neki
   D'Hooge, Francois
   Vijayakrishnan, Balakumar
   Barry, Conor
   Hartley, John A.
   Howard, Philip W.
   Newman, Roland
   Coronella, Julia
TI TR1801-ADC: a highly potent cMet antibody-drug conjugate with high
   activity in patient-derived xenograft models of solid tumors
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE antibody; drug conjugate; cMet; gastrointestinal cancer;
   pyrrolobenzodiazepine; solid tumors
ID C-MET; CHROMOSOMAL INSTABILITY; ROVALPITUZUMAB TESIRINE; CANCER;
   EXPRESSION; PHARMACOKINETICS; STRATEGIES; RECEPTOR; PROGRESS; SAFETY
AB cMet is a well-characterized oncogene that is the target of many drugs including small molecule and biologic pathway inhibitors, and, more recently, antibody-drug conjugates (ADCs). However, the clinical benefit from cMet-targeted therapy has been limited. We developed a novel cMet-targeted 'third-generation' ADC, TR1801-ADC, that was optimized at different levels including specificity, stability, toxin-linker, conjugation site, and in vivo efficacy. Our nonagonistic cMet antibody was site-specifically conjugated to the pyrrolobenzodiazepine (PBD) toxin-linker tesirine and has picomolar activity in cancer cell lines derived from different solid tumors including lung, colorectal, and gastric cancers. The potency of our cMet ADC is independent of MET gene copy number, and its antitumor activity was high not only in high cMet-expressing cell lines but also in medium-to-low cMet cell lines (40 000-90 000 cMet/cell) in which a cMet ADC with tubulin inhibitor payload was considerably less potent. In vivo xenografts with low-medium cMet expression were also very responsive to TR1801-ADC at a single dose, while a cMet ADC using a tubulin inhibitor showed a substantially reduced efficacy. Furthermore, TR1801-ADC had excellent efficacy with significant antitumor activity in 90% of tested patient-derived xenograft models of gastric, colorectal, and head and neck cancers: 7 of 10 gastric models, 4 of 10 colorectal cancer models, and 3 of 10 head and neck cancer models showed complete tumor regression after a single-dose administration. Altogether, TR1801-ADC is a new generation cMet ADC with best-in-class preclinical efficacy and good tolerability in rats.
C1 [Gymnopoulos, Marco; Betancourt, Oscar; Blot, Vincent; Fujita, Ryo; Galvan, Diana; Lieuw, Vincent; Nguyen, Sophie; Snedden, Jeanette; Stewart, Christine; Villicana, Jose; Wojciak, Jon; Wong, Eley; Newman, Roland; Coronella, Julia] Tanabe Res Labs USA Inc, 4540 Towne Ctr Court, San Diego, CA 92121 USA.
   [Pardo, Raul; Patel, Neki; D'Hooge, Francois; Vijayakrishnan, Balakumar; Barry, Conor; Hartley, John A.; Howard, Philip W.] Spirogen, London, England.
RP Gymnopoulos, M (corresponding author), Tanabe Res Labs USA Inc, 4540 Towne Ctr Court, San Diego, CA 92121 USA.
EM mgymnopoulos@trlusa.com
RI Hartley, John/GRY-6691-2022
OI Gymnopoulos, Marco/0000-0001-6885-5951
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NR 53
TC 43
Z9 47
U1 0
U2 16
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1574-7891
EI 1878-0261
J9 MOL ONCOL
JI Mol. Oncol.
PD JAN
PY 2020
VL 14
IS 1
BP 54
EP 68
DI 10.1002/1878-0261.12600
EA DEC 2019
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KA5ZE
UT WOS:000500056700001
PM 31736230
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Nguyen, MT
   Nguyen, VM
   Tran, VH
   Pham, AV
AF Minh Thao Nguyen
   Van Mao Nguyen
   Van Huy Tran
   Anh Vu Pham
TI A case report of anorectal malignant melanoma in the transitional zone
SO INTERNATIONAL JOURNAL OF SURGERY CASE REPORTS
LA English
DT Article
DE Anorectal melanoma; Transitional zone; Case report
ID MANAGEMENT
AB INTRODUCTION: Anorectal malignant melanoma is an uncommon and highly malignant disease with a greater incidence in females. Many patients were misdiagnosed as hemorrhoids, benign polyps, and rectal cancer. They were often diagnosed in an advanced stage. Wide local excision and abdominoperineal resection are the main treatments of rectal melanoma.
   PRESENTATION OF CASE: A case report is a 77-year-old man who has blood in the stool for 4 months without clinical examination. He admitted to the emergency room with sudden syndromes that related to bowel perforation. Rectal examination detected a large anorectal polyp. Computer tomography showed free air and fluid in the peritoneal cavity. He was received laparoscopic surgery and found the fishbone penetrated the sigmoid colon without polyp resection. The polyp was treated by local excision a few days later. The histology examination was a primary malignant melanoma. Due to the pigmented lesion that remained from the resected polyp's root, the abdominoperineal resection was performed as a radical treatment.
   DISCUSSION: Diagnosis of anorectal malignant melanoma is difficult because of atypical signs, that are confused with bleeding hemorrhoids especially an amelanotic melanoma. Treatment is controversial, including surgery, radiotherapy, chemotherapy, and target therapy. A present case is an option in radical surgery.
   CONCLUSION: Anorectal melanoma is a rare disease with poor results and prognosis. A lack of large-data leads to a missing evidence-based guideline in this disease. Early-staging diagnosis and surgical treatment help patients improve their overall survival. (C) 2020 The Author(s). Published by Elsevier Ltd on behalf of IJS Publishing Group Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
C1 [Minh Thao Nguyen; Anh Vu Pham] Hue Univ, Hue Univ Med & Pharm, Hue Univ Med & Pharm Hosp, Digest Surg Dept, Hue City 49126, Vietnam.
   [Van Mao Nguyen] Hue Univ, Hue Univ Med & Pharm, Hue Univ Med & Pharm Hosp, Pathol Dept, Hue City 49126, Vietnam.
   [Van Huy Tran] Hue Univ, Hue Univ Med & Pharm, Dept Internal Med, Hue City 49126, Vietnam.
C3 Hue University; Hue University; Hue University
RP Pham, AV (corresponding author), Hue Univ, Hue Univ Med & Pharm, Hue Univ Med & Pharm Hosp, Digest Surg Dept, Hue City 49126, Vietnam.
EM nmthao@huemed-univ.edu.vn; nvmao@huemed-univ.edu.vn;
   tvhuy@huemed-univ.edu.vn; pavu@huemed-univ.edu.vn
RI Tran, Huy/KYP-9992-2024; Nguyen, Thao/AAR-4201-2021
OI Nguyen, Thao Minh/0000-0003-0311-2019
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NR 21
TC 3
Z9 3
U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 2210-2612
J9 INT J SURG CASE REP
JI Int. J. Surg. Case Rep.
PY 2020
VL 75
BP 264
EP 268
DI 10.1016/j.ijscr.2020.09.091
PG 5
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA OC9BO
UT WOS:000579450100062
PM 32979823
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Benedetto, R
   Massicano, AVF
   Silva, JJ
   Boas, CAWV
   Mengatti, J
   de Araújo, EB
AF Benedetto, Raquel
   Fernandes Massicano, Adriana Vidal
   Silva, Jefferson Jesus
   Wieczorek Villas Boas, Cristian Antonio
   Mengatti, Jair
   de Araujo, Elaine Bortoleti
TI Development of radioimmunoconjugate for diagnosis and management of
   head-and-neck subclinical cancer and colorectal carcinoma
SO BRAZILIAN JOURNAL OF PHARMACEUTICAL SCIENCES
LA English
DT Article
DE Radioimmunoconjugate/development; Head and neck cancer/diagnosis; Tumors
   diagnosis; Cetuximab; SPECT; In-111
ID PHASE-I; MONOCLONAL-ANTIBODIES; PROTEINS; TRIAL; RADIOIMMUNOTHERAPY;
   AGENTS
AB Scientific innovations in diagnostic methods are important drivers of cancer control and prevention. Noninvasive imaging of the epidermal growth factor receptor (EGFR) in head-and-neck squamous, cell carcinoma and colorectal cancer could be valuable to select patients for EGFR-targeted therapy, as well as to monitor the efficacy and occurrence of resistance to immunotherapy. In order to develop the first Brazilian radioimmunoconjugate for diagnosis, Cetuximab has been conjugated to p-SCN-Bn-DTPA chelator and radiolabeled with Indium-111. The conjugation methodology was optimized using different mAb: DTPA molar ratios, time was then reduced for immunoconjugate preparation, besides the protein recovery' percentage increased after purification (m = 83.8 +/- 0.91 %). The stability of Cetuximab-DTPA at -20 degrees C was evaluated for six months, and its integrity was greater than 90% (m = 93.9 +/- 1.5%, N = 24). The radioimmunoconjugate with specific activity of 185 MBq/mg showed radiochemical purity above 95% (m=96.8 +/- 1.31 %, N = 15). We conclude that the radioimmunoconjugate In-111-DTPA-cetuximab is stable and may be applied to the diagnosis of EGFR-positive tumors.
C1 [Benedetto, Raquel; Fernandes Massicano, Adriana Vidal; Silva, Jefferson Jesus; Wieczorek Villas Boas, Cristian Antonio; Mengatti, Jair; de Araujo, Elaine Bortoleti] IPEN Inst Energy & Nucl Res, Radiopharm Ctr, Av Prof Lineu Prestes 2242,Cidade Univ, BR-05508000 Sao Paulo, SP, Brazil.
C3 Comissao Nacional de Energia Nuclear (CNEN); Instituto de Pesquisas
   Energeticas e Nucleares (IPEN)
RP Benedetto, R (corresponding author), IPEN Inst Energy & Nucl Res, Radiopharm Ctr, Av Prof Lineu Prestes 2242,Cidade Univ, BR-05508000 Sao Paulo, SP, Brazil.
EM benedettoraquel@yahoo.com.br
RI Massicano, Adriana/AAM-4617-2020; Boas, Cristian/K-1998-2019; ARAUJO,
   ELAINE/J-9818-2015; Villas Boas, Cristian/B-6135-2017
OI Villas Boas, Cristian/0000-0003-0048-4749; BORTOLETI DE ARAUJO,
   ELAINE/0000-0003-0456-5589
FU scientific cooperation of Marycel Rosa Felisa Figols Barboza; National
   Commission of Nuclear Energy - CNEN
FX The author is grateful to scientific cooperation of Marycel Rosa Felisa
   Figols Barboza and the National Commission of Nuclear Energy - CNEN, for
   financial support.
CR Brady ED, 2004, NUCL MED BIOL, V31, P795, DOI 10.1016/j.nucmedbio.2004.04.004
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NR 26
TC 3
Z9 3
U1 0
U2 4
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 2017
VL 53
IS 4
AR e170039
DI 10.1590/s2175-97902017000417039
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA GC3NK
UT WOS:000429690600001
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Tian, X
   Wang, Q
   Cai, WS
AF Tian, Xin
   Wang, Qian
   Cai, Weisong
TI A Novel Mutation in <i>MYH</i> Gene Associated with Aggressive
   Colorectal Cancer in a Child: A Case Report and Review of Literature
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE pediatric; colorectal cancer; heredity; MYH; gene mutations
ID CARCINOMA; MUTYH; RISK; MANAGEMENT; CARRIERS; COLON
AB Colorectal cancer is a rare pediatric tumor. Pediatric patients with colorectal cancer present with more aggressive tumor biology and at later stages of the disease, higher proportions of signet ring and mucinous histology, and less differentiation. The effective treatment is same as that received by adults. The overall prognosis of pediatric colorectal cancer is generally poor. Genetic mutations have been identified as the cause of inherited cancer risk in some colorectal cancers. Here, we presented a case of a pediatric patient carrying a maternally derived, heterozygous MYH germline mutation (c.934-2A>G,intron), the mutation was not reported in pediatric patients before. Also, the patient carried somatic mutations of proto-oncogene SMAD4 (R361C) and TP53 (Y234H). The patient underwent surgical resection, chemotherapy and targeted therapy, but the prognosis was not good. We also review the literature to summarize clinical features, gene mutations, management, and outcomes of pediatric colorectal cancer patient. Our results suggest that the genetic mutation of MYH together with somatic mutations of proto-oncogene SMAD4 and TP53 may lead to the early onset colorectal cancer of the patient. Although the overall prognosis of pediatric colorectal cancer is generally poor, the pathogenesis may be related to hereditary genetic mutations as was found with the MYH gene mutation in our case. Genetic screening can provide early diagnosis and improve prognosis.
C1 [Tian, Xin; Wang, Qian; Cai, Weisong] China Med Univ, Dept Clin Oncol, Shengjing Hosp, 39 Huaxiang Rd, Shenyang 110022, Liaoning, Peoples R China.
C3 China Medical University
RP Cai, WS (corresponding author), China Med Univ, Dept Clin Oncol, Shengjing Hosp, 39 Huaxiang Rd, Shenyang 110022, Liaoning, Peoples R China.
EM caiweisongvip@163.com
FU foundation of research on accurate diagnosis, treatment and clinical
   guidelines in pediatric major fatal diseases of Liaoning Province
FX The study was funded by the foundation of research on accurate
   diagnosis, treatment and clinical guidelines in pediatric major fatal
   diseases of Liaoning Province.
CR Ahnen DJ, 2014, MAYO CLIN PROC, V89, P216, DOI 10.1016/j.mayocp.2013.09.006
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   Win AK, 2014, GASTROENTEROLOGY, V146, P1208, DOI 10.1053/j.gastro.2014.01.022
   Win AK, 2011, INT J CANCER, V129, P2256, DOI 10.1002/ijc.25870
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NR 25
TC 2
Z9 2
U1 0
U2 4
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 2020
VL 13
BP 8557
EP 8565
DI 10.2147/OTT.S259587
PG 9
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA OH7DA
UT WOS:000582753400001
PM 32904697
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Song, ZY
   Gao, ZH
   Chu, JH
   Han, XZ
   Qu, XJ
AF Song, Zhi-Yu
   Gao, Zu-Hua
   Chu, Jia-Hui
   Han, Xiu-Zhen
   Qu, Xian-Jun
TI Downregulation of the CXCR4/CXCL12 axis blocks the activation of the
   Wnt/β-catenin pathway in human colon cancer cells
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Colon cancer; CXCR4/CXCL12 axis; Wnt/beta-catenin pathway;
   CXCL12-induced cell migration; MMP-2; MMP-9
ID COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA; BLADDER-CANCER;
   RECTAL-CANCER; EXPRESSION; GROWTH; WNT; INDUCTION; MIGRATION; HYPOXIA
AB Chemokine CXCL12 is an extracellular chemokine, which binds to its cell surface receptor CXCR4. High expressions of CXCR4 and CXCL12 are associated with biological malignant potential in colon cancers. We aimed to investigate the roles of the CXCR4/CXCL12 axis in activation of the Wnt/beta-catenin pathway in the development of colon cancers. Using colon cancer cell line, we performed the RNA interference assay to downregulate the expression of CXCR4. Cells were exposed to CXCL12 and their growth and metastatic activity were examined. Matrix metalloproteinases (MMPs) activity were analyzed by the gelatin zymography assay. Cell migration ability was estimated by assays of scratch wound and transwell chamber. The expression of CXCR4 and molecules relevant to the Wnt/beta-catenin pathway were analyzed by the western blotting and real-time PCR assays. Human colon cancer HT-29 cells identified high expression of CXCR4. HT-29 cells highly responded to CXCL12 stimulation, showing the increase of cell proliferation, invasion and migration through the Matrigeal. The secretion and activity of MMP-2 and MMP-9 were also stimulated in HT-29 cells exposure to CXCL12. However, the CXCR4 knockdown HT-29 cells did not response to CXCL12 stimulation. We suggested that the activation of the CXCR4/CXCL12 axis be blocked in the CXCR4 knockdown cells. This study indicated that one key to the role of the CXCR4/CXCL12 axis is activation of the Wnt/beta-catenin pathway. Downregulation of the CXCR4/CXCL12 axis thus reduces cancer growth and metastasis. Targeted therapy utilizing the CXCR4/CXCL12 axis could be an effective strategy for treatment of colon cancers. (C) 2015 Elsevier Masson SAS. All rights reserved.
C1 [Song, Zhi-Yu; Chu, Jia-Hui; Han, Xiu-Zhen; Qu, Xian-Jun] Shandong Univ, Sch Pharmaceut Sci, Jinan 250100, Peoples R China.
   [Gao, Zu-Hua] McGill Univ, Dept Pathol, Montreal, PQ, Canada.
C3 Shandong University; McGill University
RP Han, XZ (corresponding author), Shandong Univ, Sch Pharmaceut Sci, Jinan 250100, Peoples R China.
EM qxj@sdu.edu.cn
FU Natural Science Foundation of China [81173090, 91229113, 81373435];
   Beijing Science Foundation [7142017]; Research Institute McGill
   University Health Centre
FX This project was supported by the grants from Natural Science Foundation
   of China (grant nos. 81173090, 91229113, 81373435) and from Beijing
   Science Foundation (7142017). We behold genuine thankfulness to Research
   Institute McGill University Health Centre for financial support.
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NR 31
TC 32
Z9 34
U1 0
U2 23
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 APR
PY 2015
VL 71
BP 46
EP 52
DI 10.1016/j.biopha.2015.01.020
PG 7
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA CH6XK
UT WOS:000354179500008
PM 25960214
DA 2025-01-04
ER

PT J
AU Zheng-Lin, B
   Graham, RP
   Bekaii-Saab, TS
AF Zheng-Lin, Binbin
   Graham, Rondell P.
   Bekaii-Saab, Tanios S.
TI Targeting ERBB2/HER2 genetic alterations: an expanding therapeutic
   opportunity in gastrointestinal cancers
SO CHINESE CLINICAL ONCOLOGY
LA English
DT Review
DE HER2; gastroesophageal cancer (GEC); colorectal cancer (CRC); biliary
   tract cancer (BTC); targeted therapy
ID GASTROESOPHAGEAL ADENOCARCINOMA GUIDELINE; CLINICAL DECISION-MAKING;
   OF-AMERICAN-PATHOLOGISTS; ADVANCED GASTRIC-CANCER; COLORECTAL-CANCER;
   OPEN-LABEL; HER2 EXPRESSION; AMPLIFICATION; JUNCTION; TRASTUZUMAB
AB HER2 amplification and/or activating variations of its protein, human epidermal growth factor receptor 2 (HER2), are associated with distinct clinical and pathological features in gastrointestinal tumors, including a worse overall prognosis and a higher incidence of metastastic lesions in the central nervous system. Notably, the role of HER2 as a therapeutic target continues to expand beyond the scope of breast and gastroesophageal tumors, now encompassing colorectal and biliary tract cancers (BTCs), among others. In parallel, there is a burgeoning array of therapeutic agents designed to inhibit the activity of the HER2 and antibody-drug conjugate compounds. In this comprehensive review, we will explore the current body of evidence that supports the implementation of HER2-targeting strategies in the treatment of patients with gastric, esophageal, colorectal, and biliary tract tumors. We will also describe testing methods for HER2 status in clinical practice, including immunohistochemistry (IHC), and its correlation with next-generation sequencing-based techniques. Additionally, we will review the key treatment-related adverse events associated with specific anti-HER2 agents, emphasizing the need for early diagnosis and effective management. Furthermore, a critical aspect of this exploration is determining the optimal treatment sequencing among the available therapies, which will be pivotal in enhancing treatment outcomes
C1 [Zheng-Lin, Binbin; Bekaii-Saab, Tanios S.] Mayo Clin, Div Hematol & Oncol, 5881 East Mayo Blvd, Phoenix, AZ 85054 USA.
   [Graham, Rondell P.] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
C3 Mayo Clinic; Mayo Clinic Phoenix; Mayo Clinic
RP Bekaii-Saab, TS (corresponding author), Mayo Clin, Div Hematol & Oncol, 5881 East Mayo Blvd, Phoenix, AZ 85054 USA.
EM Bekaii-Saab.Tanios@mayo.edu
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NR 60
TC 1
Z9 1
U1 0
U2 0
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2304-3865
EI 2304-3873
J9 CHIN CLIN ONCOL
JI Chin. Clin. Oncol.
PD OCT 31
PY 2023
VL 12
IS 5
AR 55
DI 10.21037/cco-23-72
PG 11
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA IE7U9
UT WOS:001164724600006
PM 37964543
OA gold
DA 2025-01-04
ER

PT S
AU Truffi, M
   Sorrentino, L
   Corsi, F
AF Truffi, Marta
   Sorrentino, Luca
   Corsi, Fabio
BE Birbrair, A
TI Fibroblasts in the Tumor Microenvironment
SO TUMOR MICROENVIRONMENT: NON-HEMATOPOIETIC CELLS
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Book Chapter
DE Cancer-associated fibroblasts; Epithelial-to-mesenchymal transition;
   Tumor microenvironment; Pro-tumorigenic cytokines; Extracellular matrix
   remodeling; Tumor neoangiogenesis; Immunosuppression; Cancer-stroma
   crosstalk; Chemoresistance; Targeted therapy; Cancer treatment
ID CANCER-ASSOCIATED FIBROBLASTS; ACTIVATION PROTEIN-ALPHA; PHASE-II TRIAL;
   INHIBITOR BIBF 1120; TGF-BETA; MATRIX METALLOPROTEINASES;
   COLORECTAL-CANCER; GROWTH-FACTOR; COLON-CANCER; EXTRACELLULAR-MATRIX
AB The implications of a tumor microenvironment in cancer initiation and progression have drawn interest in recent years. Within the tumor stroma, fibroblasts represent a predominant cell type and are responsible for the majority of extracellular components within the tumor microenvironment, such as matrix and soluble factors. A switch from quiescent fibroblasts to cancer-associated fibroblasts triggers a large variety of pro-tumorigenic signals that support tumor progression and shape the surrounding pathological stroma, with the remodeling of tissue architecture and repression of the local immune response. The heterogeneous nature of cancer-associated fibroblasts and their multiple functions are subject of active research as they could repre- sent promising targets for cutting-edge therapeutic approaches to cancer and the tumor microenvironment.
C1 [Truffi, Marta; Corsi, Fabio] Ist Clin Sci Maugeri IRCCS, Pavia, Italy.
   [Truffi, Marta; Sorrentino, Luca; Corsi, Fabio] Univ Milan, Dept Biomed & Clin Sci Luigi Sacco, Milan, Italy.
C3 University of Milan; Luigi Sacco Hospital
RP Corsi, F (corresponding author), Ist Clin Sci Maugeri IRCCS, Pavia, Italy.; Corsi, F (corresponding author), Univ Milan, Dept Biomed & Clin Sci Luigi Sacco, Milan, Italy.
EM marta.truffi@icsmaugeri.it; luca.sorrentino1@unimi.it;
   fabio.corsi@icsmaugeri.it
RI Corsi, Fabio/ABH-9554-2020; Sorrentino, Luca/KHT-6228-2024; Corsi,
   Fabio/E-9204-2017; Truffi, Marta/AAB-2272-2019
OI Corsi, Fabio/0000-0002-6469-4086; Truffi, Marta/0000-0002-1095-4188
FU Associazione Italiana per la Ricerca sul Cancro [AIRC IG 20172]
FX The authors thank Associazione Italiana per la Ricerca sul Cancro for
   research support (AIRC IG 20172 to F.C.)
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NR 124
TC 84
Z9 91
U1 6
U2 40
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 0065-2598
EI 2214-8019
BN 978-3-030-37184-5; 978-3-030-37183-8
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2020
VL 1234
BP 15
EP 29
DI 10.1007/978-3-030-37184-5_2
D2 10.1007/978-3-030-37184-5
PG 15
WC Oncology; Cell Biology; Medicine, Research & Experimental
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology; Research & Experimental Medicine
GA BP1EF
UT WOS:000539023500003
PM 32040852
DA 2025-01-04
ER

PT J
AU Roudi, R
   Barodabi, M
   Madjd, Z
   Roviello, G
   Corona, SP
   Panahei, M
AF Roudi, Raheleh
   Barodabi, Mahboubeh
   Madjd, Zahra
   Roviello, Giandomenico
   Corona, Silvia Paola
   Panahei, Mahshid
TI Expression patterns and clinical significance of the potential cancer
   stem cell markers OCT4 and NANOG in colorectal cancer patients
SO MOLECULAR & CELLULAR ONCOLOGY
LA English
DT Article
DE Colorectal cancer; cancer stem cells; neoplastic stem cells; NANOG;
   OCT4; immunohistochemistry; tissue microarray
ID PROGNOSTIC VALUE; CD133
AB Colorectal cancer (CRC) is one of the most important malignancies and causes of cancer-related deaths worldwide. Cancer stem cell markers identification could be helpful to acquire important prognostic information and develop new treatment regimens. This study aimed to evaluate the expression of OCT4 and NANOG in CRC patients and their clinical significance. Totally 359 CRC samples were stained for OCT4 and NANOG expression using tissue microarray. The correlation between their expression and clinical and pathological features was explored. The majority of CRC cases showed low-level expression of OCT4 (80%) and NANOG (75%). Lower expression of OCT4 was more often detected in CRC cases with no vascular involvement (P= .01). Also, a trend found between low level of OCT4 expression and absence of distant metastasis or lymph node involvement (P= .07 andP= .09, respectively). Surprisingly, a significant positive correlation was observed between NANOG expression and cellular differentiation (P= .05). Our combined analysis demonstrated that OCT4(low)/NANOG(low)phenotype has frequently seen in colorectal cancer cases with no vascular invasion (P= .05). Our observations indicated that higher expression of OCT4 and NANOG can confer malignant and aggressive behavior to CRC. Evaluation of the co-expression of these cancer stem cell markers can serve a new diagnostic and prognostic approach in CRC patients. These findings also suggested that simultaneous expression of OCT4 and NANOG can be considered as a therapeutic marker for targeted therapy of CRC, especially in advanced stages.
C1 [Roudi, Raheleh; Barodabi, Mahboubeh; Madjd, Zahra; Panahei, Mahshid] Iran Univ Med Sci, Oncopathol Res Ctr, Tehran, Iran.
   [Roudi, Raheleh] Univ Texas Hlth San Antonio, Dept Cell Syst & Anat, San Antonio, TX USA.
   [Barodabi, Mahboubeh; Madjd, Zahra; Panahei, Mahshid] Iran Univ Med Sci, Fac Med, Dept Pathol, Tehran, Iran.
   [Madjd, Zahra] Iran Univ Med Sci, Fac Adv Technol Med, Dept Mol Med, Tehran, Iran.
   [Roviello, Giandomenico] Univ Florence, Dept Hlth Sci, Florence, Italy.
   [Corona, Silvia Paola] Univ Trieste, Cattinara Hosp, Dept Med Surg & Hlth Sci, Trieste, Italy.
   [Panahei, Mahshid] Iran Univ Med Sci, Firoozgar Hosp, Dept Pathol, Tehran, Iran.
C3 Iran University of Medical Sciences; University of Texas System;
   University of Texas Health Science Center at San Antonio; Iran
   University of Medical Sciences; Iran University of Medical Sciences;
   University of Florence; University of Trieste; Iran University of
   Medical Sciences
RP Panahei, M (corresponding author), Iran Univ Med Sci, Firoozgar Hosp, Dept Pathol, Tehran, Iran.
EM Panahei.M@iums.ac.ir
RI Corona, Silvia/ABD-2358-2020; Madjd, Zahra/ABA-5018-2020; Roviello,
   Giandomenico/AAA-5310-2019; Roudi, Raheleh/J-2587-2018
OI Roviello, Giandomenico/0000-0001-5504-8237; Roudi,
   Raheleh/0000-0001-5023-4743
FU Deputy for Research and Technology, Ministry of Health and Medical
   Education, IR Iran [700/169]
FX We acknowledge the grant by Deputy for Research and Technology, Ministry
   of Health and Medical Education, IR Iran (Grant no: 700/169).
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NR 46
TC 28
Z9 29
U1 0
U2 4
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
EI 2372-3556
J9 MOL CELL ONCOL
JI MOL. CELL ONCOL.
PD SEP 2
PY 2020
VL 7
IS 5
AR 1788366
DI 10.1080/23723556.2020.1788366
EA JUL 2020
PG 6
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA NI8QH
UT WOS:000552079700001
PM 32944642
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Wang, Y
   Zhu, LM
   Guo, M
   Sun, G
   Zhou, K
   Pang, WJ
   Cao, DC
   Tang, X
   Meng, XJ
AF Wang, Yu
   Zhu, Liming
   Guo, Mei
   Sun, Gang
   Zhou, Kun
   Pang, Wenjing
   Cao, Dachun
   Tang, Xin
   Meng, Xiangjun
TI Histone methyltransferase WHSC1 inhibits colorectal cancer cell
   apoptosis via targeting anti-apoptotic BCL2
SO CELL DEATH DISCOVERY
LA English
DT Article
ID SYNDROME CANDIDATE 1; EXPRESSION; METHYLATION; CARCINOGENESIS;
   PROLIFERATION; STABILIZATION; GROWTH; EZH2
AB WHSC1 is a histone methyltransferase that facilitates histone H3 lysine 36 dimethylation (H3K36me2), which is a permissive mark associated with active transcription. In this study, we revealed how WHSC1 regulates tumorigenesis and chemosensitivity of colorectal cancer (CRC). Our data showed that WHSC1 as well as H3K36me2 were highly expressed in clinical CRC samples, and high WHSC1 expression is associated with poorer prognosis in OS patients. WHSC1 reduction promoted colon cancer cell apoptosis both in vivo and in vitro. We found that B cell lymphoma-2 (BCL2) expression, an anti-apoptotic protein, is markedly decreased in after WHSC1 depletion. Mechanistic characterization indicated that WHSC1 directly binds to the promoter region of BCL2 gene and regulate its H3K36 dimethylation level. What's more, our study indicated that WHSC1 depletion promotes chemosensitivity in CRC cells. Together, our results suggested that WHSC1 and H3K36me2 modification might be optimal therapeutic targets to disrupt CRC progression and WHSC1-targeted therapy might potentially overcome the resistance of chemotherapeutic agents.
C1 [Wang, Yu; Zhu, Liming; Guo, Mei; Sun, Gang; Zhou, Kun; Pang, Wenjing; Cao, Dachun; Meng, Xiangjun] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Gastroenterol, Sch Med, Shanghai, Peoples R China.
   [Tang, Xin] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Geriatr, Sch Med, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University; Shanghai Jiao Tong University
RP Cao, DC; Meng, XJ (corresponding author), Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Gastroenterol, Sch Med, Shanghai, Peoples R China.; Tang, X (corresponding author), Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Geriatr, Sch Med, Shanghai, Peoples R China.
EM lily_cao2000@hotmail.com; dancingtx@126.com; xiangjunmeng@tom.com
RI zhou, kun/KRP-1631-2024; Wang, Jingya/HZM-1570-2023; PANG,
   Wenjing/AAB-8990-2022
FU National Natural Science Foundation of China [81872419]
FX This work was supported by the National Natural Science Foundation of
   China (81872419).
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NR 33
TC 18
Z9 19
U1 3
U2 16
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2058-7716
J9 CELL DEATH DISCOV
JI Cell Death Discov.
PD JAN 19
PY 2021
VL 7
IS 1
AR 19
DI 10.1038/s41420-021-00402-6
PG 9
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA PU0HO
UT WOS:000608988800001
PM 33469000
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kiran, NS
   Yashaswini, C
   Maheshwari, R
   Bhattacharya, S
   Prajapati, BG
AF Kiran, Neelakanta Sarvashiva
   Yashaswini, Chandrashekar
   Maheshwari, Rahul
   Bhattacharya, Sankha
   Prajapati, Bhupendra G.
TI Advances in Precision Medicine Approaches for Colorectal Cancer: From
   Molecular Profiling to Targeted Therapies
SO ACS PHARMACOLOGY & TRANSLATIONAL SCIENCE
LA English
DT Review
DE precision medicine; colorectal cancer; biomarkers; immunotherapy;
   personalized treatment
ID PROGNOSTIC BIOMARKER; HETEROGENEITY; DIAGNOSIS; PROGRESS; CELLS; RAS
AB Precision medicine is transforming colorectal cancer treatment through the integration of advanced technologies and biomarkers, enhancing personalized and effective disease management. Identification of key driver mutations and molecular profiling have deepened our comprehension of the genetic alterations in colorectal cancer, facilitating targeted therapy and immunotherapy selection. Biomarkers such as microsatellite instability (MSI) and DNA mismatch repair deficiency (dMMR) guide treatment decisions, opening avenues for immunotherapy. Emerging technologies such as liquid biopsies, artificial intelligence, and machine learning promise to revolutionize early detection, monitoring, and treatment selection in precision medicine. Despite these advancements, ethical and regulatory challenges, including equitable access and data privacy, emphasize the importance of responsible implementation. The dynamic nature of colorectal cancer, with its tumor heterogeneity and clonal evolution, underscores the necessity for adaptive and personalized treatment strategies. The future of precision medicine in colorectal cancer lies in its potential to enhance patient care, clinical outcomes, and our understanding of this intricate disease, marked by ongoing evolution in the field. The current reviews focus on providing in-depth knowledge on the various and diverse approaches utilized for precision medicine against colorectal cancer, at both molecular and biochemical levels.
C1 [Kiran, Neelakanta Sarvashiva; Yashaswini, Chandrashekar] REVA Univ, Sch Appl Sci, Dept Biotechnol, Bengaluru 560064, Karnataka, India.
   [Maheshwari, Rahul] Deemed Univ, SVKMs Narsee Monjee Inst Management Studies NMIMS, Sch Pharm & Technol Management, Hyderabad 509301, India.
   [Bhattacharya, Sankha] SVKMS NMIMS Deemed Univ, Sch Pharm & Technol Management, Shirpur 425405, Maharashtra, India.
   [Prajapati, Bhupendra G.] Ganpat Univ, Shree S K Patel Coll Pharmaceut Educ & Res, Kherva 384012, Gujarat, India.
C3 REVA University; SVKM's NMIMS (Deemed to be University); SVKM's NMIMS
   (Deemed to be University); Ganpat University
RP Bhattacharya, S (corresponding author), SVKMS NMIMS Deemed Univ, Sch Pharm & Technol Management, Shirpur 425405, Maharashtra, India.; Prajapati, BG (corresponding author), Ganpat Univ, Shree S K Patel Coll Pharmaceut Educ & Res, Kherva 384012, Gujarat, India.
EM sankhabhatt@gmail.com; bhupendra.prajapati@ganpatuniversity.ac.in
RI Bhattacharya, Sankha/AAM-5111-2020; Maheshwari, Rahul/GPK-8456-2022;
   Prajapati, Dr. Bhupendra/A-3088-2015
OI Prajapati, Dr. Bhupendra/0000-0001-8242-4541
FU REVA University, SVKM'S NMIMS Deemed-to-be University; Ganpat University
FX We the authors greatly acknowledge REVA University, SVKM'S NMIMS
   Deemed-to-be University, and Ganpat University for providing a platform
   and opportunity for research.
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NR 245
TC 5
Z9 6
U1 4
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
EI 2575-9108
J9 ACS PHARMACOL TRANSL
JI ACS Pharmacol. Transl. Sci.
PD MAR 19
PY 2024
VL 7
IS 4
BP 967
EP 990
DI 10.1021/acsptsci.4c00008
EA MAR 2024
PG 24
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA NR7T5
UT WOS:001187676700001
PM 38633600
OA hybrid
DA 2025-01-04
ER

PT J
AU Cervantes, B
   Andre, T
   Cohen, R
AF Cervantes, Baptiste
   Andre, Thierry
   Cohen, Romain
TI Deficient mismatch repair/microsatellite unstable colorectal cancer:
   therapeutic advances and questions
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Review
DE checkpoint inhibitor; colorectal cancer; diagnostic; immunotherapy; MSI
ID IMMUNE CHECKPOINT INHIBITORS; MICROSATELLITE INSTABILITY; COLON-CANCER;
   REPAIR DEFICIENCY; HMLH1 PROMOTER; BRAF MUTATION; OPEN-LABEL;
   CHEMOTHERAPY; PEMBROLIZUMAB; KEYNOTE-177
AB The microsatellite instability (MSI) phenotype is related to a deficiency of the DNA mismatch repair (dMMR) system and is observed in 5% of metastatic colorectal cancers (mCRCs). MSI/dMMR phenotype testing should be routine for all CRCs regardless of stage. Two complementary techniques with a high concordance (90-97%) allow us to determine the MSI/dMMR status of a tumor: immunohistochemistry and polymerase chain reaction. Since 2020 and the results of the phase III KEYNOTE 177 trial, pembrolizumab [anti-programmed cell death protein 1 (PD1)] is the new standard of care in first-line MSI/dMMR mCRC. To date, no combination of chemtotherapy +/- targeted therapy with immune checkpoint inhibitors (ICIs) has been validated in the management of MSI/dMMR mCRC, and it is not known whether this combination would be beneficial. It is also unclear whether dual therapy with two ICIs is more effective than monotherapy. Several phase III trials are ongoing to answer these questions. Despite a high response rate and long-term benefit of a first line by anti-PD1, 30-50% of patients with MSI/dMMR mCRC experience an early or secondary progression. There are currently no validated predictive biomarkers of anti-PD1 +/- anti-cytotoxic T lymphocyte antigen-4 resistance in patients with MSI/dMMR mCRC. In case of early progression on ICIs, the first two questions to consider are the possibility of pseudoprogression and the correct diagnosis of MSI/dMMR status. To date, there are no data on the use of adjuvant ICIs for MSI/dMMR resected colon cancers. By contrast, data are accumulating regarding the efficacy of neoadjuvant ICIs, with at least two-thirds of patients in the different trials in pathological complete response, making it possible to envisage 'Watch and wait' strategies in future.
C1 [Cervantes, Baptiste] Sorbonne Univ, St Antoine Hosp, AP HP, Dept Med Oncol, Paris, France.
   [Andre, Thierry; Cohen, Romain] Sorbonne Univ, St Antoine Hosp, Dept Med Oncol, Paris, France.
   [Andre, Thierry] Ctr Rech St Antoine, AP HP,Unite Mixte Rech Sci 938, Equipe Instabil Microsatell & Canc,SIRIC CURAMUS, Equipe Labellisee Ligue Natl Contre Canc,INSERM, Paris, France.
   [Cohen, Romain] St Antoine Hosp, AP HP,Ctr Rech St Antoine, Unite Mixte Rech Sci 938,SIRIC CURAMUS, Equipe Instabil Microsatell & Canc,Equipe Labellis, 184 Rue Fg St Antoine, F-75012 Paris, France.
C3 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); Sorbonne Universite; Hopital Universitaire Saint-Antoine - APHP;
   Assistance Publique Hopitaux Paris (APHP); Sorbonne Universite; Hopital
   Universitaire Saint-Antoine - APHP; Institut National de la Sante et de
   la Recherche Medicale (Inserm); Assistance Publique Hopitaux Paris
   (APHP); Sorbonne Universite; Hopital Universitaire Saint-Antoine - APHP
RP Cohen, R (corresponding author), Sorbonne Univ, St Antoine Hosp, Dept Med Oncol, Paris, France.; Cohen, R (corresponding author), St Antoine Hosp, AP HP,Ctr Rech St Antoine, Unite Mixte Rech Sci 938,SIRIC CURAMUS, Equipe Instabil Microsatell & Canc,Equipe Labellis, 184 Rue Fg St Antoine, F-75012 Paris, France.
EM romain.cohen@aphp.fr
RI Cohen, Romain/AAC-9089-2019; André, Thierry/N-8830-2017
OI Cohen, Romain/0000-0001-9602-5162
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NR 44
TC 4
Z9 4
U1 0
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PY 2024
VL 16
AR 17588359231170473
DI 10.1177/17588359231170473
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EJ9T7
UT WOS:001138682600001
PM 38205076
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Qi, L
   Zhang, Y
   Zhang, WJ
   Wang, YQ
   Han, Y
   Ding, YQ
AF Qi, Lu
   Zhang, Ying
   Zhang, Wenjuan
   Wang, Yiqing
   Han, Yue
   Ding, Yanqing
TI The inhibition of colorectal cancer growth by the natural product
   macrocarpal I
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Colorectal cancer; Targeted intervention; Multi-target; Small molecule
   compounds
AB Background: Presently, few small molecule compounds are used as targeted therapy drugs in the treatment of colorectal cancer (CRC). It is important to identify new small molecule compounds, which can be used in the treatment of CRC.
   Methods: In this study, we selected four protein molecules as drug targets: PRL-3 (Phosphatase of regenerating liver 3), CLIC4 (Chloride intracellular channel 4), THBS2 (Thrombospondin 2), and BGN (Biglycan). These protein molecules were associated with the growth and metastasis of CRC cells. Small molecular compounds were screened on the basis of their target structures. Thus, five small molecule compounds were screened from each target structure, and three small molecule compounds (macrocarpal I, sildenafil, and neoandrographolide) were found to bind with two drug targets at the same time. Further experiments revealed that the inhibition rate of macrocarpal I was the highest in CRC cells. Therefore, we determined the effects of macrocarpal I on proliferation, apoptosis, cytoskeleton of CRC cells, and subcutaneous tumorigenesis in nude mice. Furthermore, RNA-seq analysis was performed to determine the molecular mechanism through which macrocarpal I inhibited the progression of CRC.
   Results: We found that macrocarpal I could effectively inhibit proliferation, colony formation of CRC cells, and subcutaneous tumorigenesis in nude mice. Moreover, it also destroyed the cytoskeleton of CRC cells and promoted apoptosis. The effects on kinase activity, cytoskeleton, and DNA repair is the mechanism of macrocarpal I to inhibiting CRC growth.
   Conclusion: Macrocarpal I is a small molecule compound that can effectively inhibit the progression of CRC. Thus, macrocarpal I is a therapeutic compound that shows promising results in the treatment of advanced CRC.
C1 [Qi, Lu; Zhang, Wenjuan; Wang, Yiqing; Han, Yue; Ding, Yanqing] Southern Med Univ, Nanfang Hosp, Dept Pathol, Guangzhou 510515, Peoples R China.
   [Qi, Lu; Zhang, Wenjuan; Wang, Yiqing; Han, Yue; Ding, Yanqing] Southern Med Univ, Sch Basic Med Sci, Dept Pathol, Guangzhou 510515, Peoples R China.
   [Qi, Lu; Zhang, Wenjuan; Wang, Yiqing; 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 National Key Basic Research Program of China (973 program)
   [2015CB554002]; National Natural Science Foundation of China [81972754,
   81773101]; Scientific Research Starting Foundation of Southern Medical
   University [PY2018N003]; China Postdoctoral Science Foundation
   [2020TQ0136, 2020M672714]
FX This work was supported by the National Key Basic Research Program of
   China (973 program, 2015CB554002), the National Natural Science
   Foundation of China (81972754, 81773101), the Scientific Research
   Starting Foundation of Southern Medical University (PY2018N003), the
   China Postdoctoral Science Foundation (2020TQ0136, 2020M672714).
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NR 42
TC 4
Z9 5
U1 0
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD JAN
PY 2021
VL 162
BP 383
EP 391
DI 10.1016/j.freeradbiomed.2020.10.317
EA FEB 2021
PG 9
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA QH9XI
UT WOS:000618628700006
PM 33137468
DA 2025-01-04
ER

PT J
AU Ma, K
   Shao, ZF
   Xu, XX
   Guo, SF
   Wang, YJ
   Wang, ZQ
AF Ma, Kun
   Shao, Zefeng
   Xu, Xiangxian
   Guo, Shanfeng
   Wang, Youjin
   Wang, Zhongqiu
TI LINC00178 promotes cell growth, migration, and invasion in colorectal
   cancer in vitro and in vivo
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE LINC00178; colorectal cancer (CRC); invasion; migration
ID PROLIFERATION; METASTASIS
AB Background: This study aimed to determine the role of LINC00178 in colorectal cancer (CRC) cell invasion and migration by examining its expression in CRC cells and tissues.Methods: Cancer tissues and corresponding adjacent tissue specimens were collected from 45 patients who experienced radical CRC resection in the hospital from March to September 2021. The expression of LINC00178 was measured in both CRC cells and tissues and normal human colorectal mucosal cells using quantitative fluorescence polymerase chain reaction (QF-PCR). Cell Counting Kit-8 (CCK-8), clonogenic, and transwell assays were used to assess the impact of LINC00178 overexpression or knockdown on the CRC cells invasion and proliferation. In addition, the expression levels of vimentin, E-cadherin, and N-cadherin in CRC cells were determined after either LINC00178 knock down or overexpression was performed using western blotting.Results: The experiments revealed that LINC00178 was over expressed in CRC cells and tissues. Overexpression of LINC00178 could significantly promote the propagation, clone formation, invasion, and transportation of CRC, whereas knockdown of LINC00178 had the opposite function. When LINC00178 was expressed at high levels, it suppressed the vimentin and N-cadherin expression and prevented the upregulation of E-cadherin. In vivo (nude mouse) studies showed that the over expression of LINC00178 could significantly promote the propagation in CRC cells.Conclusions: LINC00178 is overexpressed in CRC cells and tissues. In vivo and in vitro experiments showed that LINC00178 can significantly promote the propagation of CRC cells, so it may develop a potential biological site for targeted therapy of CRC patients.
C1 [Ma, Kun; Shao, Zefeng; Xu, Xiangxian; Guo, Shanfeng; Wang, Youjin] Nanjing Univ Chinese Med, Affiliated Hosp, Jiangsu Prov Hosp Chinese Med, Dept Intervent Med, Nanjing, Peoples R China.
   [Wang, Zhongqiu] Nanjing Univ Chinese Med, Affiliated Hosp, Jiangsu Prov Hosp Chinese Med, Dept Radiol, Nanjing, Peoples R China.
   [Wang, Zhongqiu] Nanjing Univ Chinese Med, Affiliated Hosp, Jiangsu Prov Hosp Chinese Med, Dept Radiol, Chaotiangong St, Nanjing, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University of Chinese
   Medicine; Nanjing University of Chinese Medicine
RP Wang, ZQ (corresponding author), Nanjing Univ Chinese Med, Affiliated Hosp, Jiangsu Prov Hosp Chinese Med, Dept Radiol, Chaotiangong St, Nanjing, Peoples R China.
EM zhq2001us@163.com
RI Wang, Zhong-Qiu/ABC-5782-2021
CR Ali T, 2020, ELIFE, V9, DOI 10.7554/eLife.60583
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NR 30
TC 0
Z9 0
U1 1
U2 2
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD OCT
PY 2022
VL 13
IS 5
BP 2415
EP 2425
DI 10.21037/jgo-22-940
PG 11
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA 6A7BG
UT WOS:000880805800010
PM 36388674
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Battisti, NML
   Liposits, G
   De Glas, NA
   Gomes, F
   Baldini, C
   Mohile, S
AF Battisti, Nicolo Matteo Luca
   Liposits, Gabor
   De Glas, Nienke Aafke
   Gomes, Fabio
   Baldini, Capucine
   Mohile, Supriya
TI Systemic Therapy of Common Tumours in Older Patients: Challenges and
   Opportunities. A Young International Society of Geriatric Oncology
   Review Paper
SO CURRENT ONCOLOGY REPORTS
LA English
DT Review
DE Older adults; Geriatric assessment; Chemotherapy; Targeted therapy;
   Immunotherapy; Survivorship
ID CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER; III COLON-CANCER;
   POSITIVE BREAST-CANCER; QUALITY-OF-LIFE; CLINICAL-PRACTICE GUIDELINES;
   GROUP PERFORMANCE STATUS; RANDOMIZED PHASE-II; ELDERLY-PATIENTS;
   ADJUVANT CHEMOTHERAPY
AB Purpose of ReviewDecision-making for systemic treatments in older patients with cancer is difficult because of concerns for decreased organ function, risk of toxicity, limited life expectancy due to comorbidities and the lack of evidence available to guide its management in this population. Here, we review the data on the role of systemic agents for the treatment of common malignancies in this age group.Recent FindingsEvidence on the use of systemic treatments for older patients with cancer is increasing, especially for newer options including immune checkpoint inhibitors and targeted agents that provide comparable benefit in older and younger patients. Nonetheless, the risks for short- and long-term toxicities need to be considered. More research is warranted and represents a unique opportunity to increase the knowledge on cancer treatment for older adults.SummaryHealthy, older individuals should be considered for standard systemic treatment options, whereas those at risk based on geriatric assessments require adjusted plans. Geriatric assessments are key for decision-making.
C1 [Battisti, Nicolo Matteo Luca] Royal Marsden NHS Fdn Trust, Dept Med, Downs Rd, London SM2 5PT, England.
   [Battisti, Nicolo Matteo Luca] Inst Canc Res, Breast Canc Res Div, 15 Cotswold Rd, London SM2 5NG, England.
   [Liposits, Gabor] Reg Hosp West Jutland, Dept Oncol, Gl Landevej 61, DK-7400 Herning, Denmark.
   [De Glas, Nienke Aafke] Leiden Univ, Med Ctr, Dept Med Oncol, Albinusdreef 2, NL-2333 ZA Leiden, Netherlands.
   [Gomes, Fabio] Christie NHS Fdn Trust, Med Oncol, Wilmslow Rd, Manchester M20 4BX, Lancs, England.
   [Baldini, Capucine] Inst Gustave Roussy, Drug Dev Dept, Gustave Roussy Canc Campus, F-94800 Villejuif, France.
   [Mohile, Supriya] Univ Rochester, James P Wilmot Canc Inst, Div Hematol Oncol, Med Ctr, 601 Elmwood Ave 704, Rochester, NY 14642 USA.
C3 Royal Marsden NHS Foundation Trust; Royal Marsden NHS Foundation Trust;
   University of London; Institute of Cancer Research - UK; Leiden
   University - Excl LUMC; Leiden University; Leiden University Medical
   Center (LUMC); Christie NHS Foundation Trust; UNICANCER; Gustave Roussy;
   University of Rochester
RP Battisti, NML (corresponding author), Royal Marsden NHS Fdn Trust, Dept Med, Downs Rd, London SM2 5PT, England.; Battisti, NML (corresponding author), Inst Canc Res, Breast Canc Res Div, 15 Cotswold Rd, London SM2 5NG, England.
EM nicolo.battisti@rmh.nhs.uk; gabor.liposits@rm.dk; n.a.de_glas@lumc.nl;
   fabio.gomes@christie.nhs.uk; capucine.baldini@gustaveroussy.fr;
   supriya_mohile@urmc.rochester.edu
RI Liposits, Gabor/ABC-9408-2021; Mohile, Supriya/AHD-3603-2022; de Glas,
   Nienke/AAL-3546-2021; Battisti, Nicolo Matteo Luca/M-3652-2014
OI Gomes, Fabio/0000-0003-0922-2665; Battisti, Nicolo Matteo
   Luca/0000-0002-1063-1717; de Glas, Nienke/0000-0001-8350-4252; Liposits,
   Gabor/0000-0002-8204-3949
FU Royal Marsden NIHR Biomedical Research Centre for Cancer; Cridlan Ross
   Smith Charitable Trust
FX Dr. Battisti wishes to acknowledge the support of The Royal Marsden NIHR
   Biomedical Research Centre for Cancer and The Cridlan Ross Smith
   Charitable Trust.
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NR 189
TC 4
Z9 4
U1 1
U2 11
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 JUL 28
PY 2020
VL 22
IS 10
AR 98
DI 10.1007/s11912-020-00958-z
PG 26
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MW0DZ
UT WOS:000556719100001
PM 32725503
DA 2025-01-04
ER

PT J
AU Ni, XH
   Feng, YJ
   Fu, XW
AF Ni, Xiaohong
   Feng, Yongjiang
   Fu, Xiangwei
TI Role of salt-inducible kinase 2 in the malignant behavior and glycolysis
   of colorectal cancer cells
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article
DE salt-inducible kinase 2; tripartite motif containing 28; colorectal
   cancer; glycolysis; malignancy
ID ESMO CONSENSUS GUIDELINES; MESORECTAL EXCISION; BIOMARKERS; MANAGEMENT;
   TRIAL
AB Colorectal cancer (CRC) is the third most common type of cancer worldwide. Currently, surgery, chemotherapy and radiation therapy are the conventional approaches used to treat CRC. However, these therapy strategies cause several side effects. The present study aimed to develop an alternative and more effective treatment approach for patients with CRC. It has been reported that salt-inducible kinase 2 (SIK2) acts as an oncogene. Therefore, in the present study, the expression levels of SIK2 were determined in CRC cells using western blot analysis and reverse transcription-quantitative PCR. In addition, SIK2 was knocked down in CRC cells to evaluate its role in cell proliferation, migration, invasion and glycolysis using Cell Counting Kit-8, wound healing, Transwell assays and glycolysis cell-based assay kit, respectively. Additionally, the target genes of SIK2 were identified using bioinformatics analysis, while SIK2 overexpression experiments were carried out to determine whether SIK2 could regulate CRC cell malignant behavior and glycolysis. The results revealed that SIK2 was upregulated in CRC cells. Furthermore, SIK2 knockdown attenuated CRC cell proliferation, migration, invasion and glycolysis. Bioinformatics analysis predicted that SIK2 could interact with tripartite motif containing 28 (TRIM28), while TRIM28 overexpression could reverse the effects of SIK2 silencing on cell proliferation, migration, invasion and glycolysis. This finding indicated that the aforementioned effects of SIK2 were mediated by regulating TRIM28. In conclusion, the findings of the present study suggested that SIK2 may be involved in CRC carcinogenesis and glycolysis by regulating TRIM28 expression. These findings could provide a novel approach to targeted therapy and clinical diagnosis of CRC in the future.
C1 [Ni, Xiaohong; Feng, Yongjiang] Yancheng Dafeng Peoples Hosp, Dept Gastrointestinal Surg, Yancheng 224100, Jiangsu, Peoples R China.
   [Fu, Xiangwei] Hainan Med Univ, Affiliated Hosp 2, Dept Gen Surg, 368 Yehai Ave, Haikou 570105, Hainan, Peoples R China.
C3 Hainan Medical University
RP Fu, XW (corresponding author), Hainan Med Univ, Affiliated Hosp 2, Dept Gen Surg, 368 Yehai Ave, Haikou 570105, Hainan, Peoples R China.
EM fuxiangwei12@126.com
RI Deng, Shou-Long/GWV-0452-2022
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   Zong S., 2020, BIOSCIENCE REP
NR 45
TC 5
Z9 5
U1 0
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD NOV
PY 2021
VL 24
IS 5
AR 822
DI 10.3892/mmr.2021.12460
PG 11
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA WC1XO
UT WOS:000704057100001
PM 34558647
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Bhat, AA
   Nisar, S
   Singh, M
   Ashraf, B
   Masoodi, T
   Prasad, CP
   Sharma, A
   Maacha, S
   Karedath, T
   Hashem, S
   Yasin, SB
   Bagga, P
   Reddy, R
   Frennaux, MP
   Uddin, S
   Dhawan, P
   Haris, M
   Macha, MA
AF Bhat, Ajaz A.
   Nisar, Sabah
   Singh, Mayank
   Ashraf, Bazella
   Masoodi, Tariq
   Prasad, Chandra P.
   Sharma, Atul
   Maacha, Selma
   Karedath, Thasni
   Hashem, Sheema
   Yasin, Syed Besina
   Bagga, Puneet
   Reddy, Ravinder
   Frennaux, Michael P.
   Uddin, Shahab
   Dhawan, Punita
   Haris, Mohammad
   Macha, Muzafar A.
TI Cytokine- and chemokine-induced inflammatory colorectal tumor
   microenvironment: Emerging avenue for targeted therapy
SO CANCER COMMUNICATIONS
LA English
DT Review
DE chemokine; colorectal cancer; cytokine; drug resistance;
   epithelial-mesenchymal transition; immunosuppression; immunotherapy;
   inflammation; metastasis; tumor microenvironment
ID EPITHELIAL-MESENCHYMAL TRANSITION; NECROSIS-FACTOR-ALPHA; COLON-CANCER
   CELLS; BETA SIGNALING ALTERATIONS; LYMPH-NODE METASTASIS; LINKS INNATE
   IMMUNITY; LIVER METASTASIS; SUPPRESSOR-CELLS; KAPPA-B; TNF-ALPHA
AB Colorectal cancer (CRC) is a predominant life-threatening cancer, with liver and peritoneal metastases as the primary causes of death. Intestinal inflammation, a known CRC risk factor, nurtures a local inflammatory environment enriched with tumor cells, endothelial cells, immune cells, cancer-associated fibroblasts, immunosuppressive cells, and secretory growth factors. The complex interactions of aberrantly expressed cytokines, chemokines, growth factors, and matrix-remodeling enzymes promote CRC pathogenesis and evoke systemic responses that affect disease outcomes. Mounting evidence suggests that these cytokines and chemokines play a role in the progression of CRC through immunosuppression and modulation of the tumor microenvironment, which is partly achieved by the recruitment of immunosuppressive cells. These cells impart features such as cancer stem cell-like properties, drug resistance, invasion, and formation of the premetastatic niche in distant organs, promoting metastasis and aggressive CRC growth. A deeper understanding of the cytokine- and chemokine-mediated signaling networks that link tumor progression and metastasis will provide insights into the mechanistic details of disease aggressiveness and facilitate the development of novel therapeutics for CRC. Here, we summarized the current knowledge of cytokine- and chemokine-mediated crosstalk in the inflammatory tumor microenvironment, which drives immunosuppression, resistance to therapeutics, and metastasis during CRC progression. We also outlined the potential of this crosstalk as a novel therapeutic target for CRC. The major cytokine/chemokine pathways involved in cancer immunotherapy are also discussed in this review.
C1 [Bhat, Ajaz A.; Nisar, Sabah; Masoodi, Tariq; Haris, Mohammad] Sidra Med, Dept Canc Res, Lab Mol & Metab Imaging, Doha 26999, Qatar.
   [Singh, Mayank; Prasad, Chandra P.; Sharma, Atul] All India Inst Med Sci AIIMS, Dr BR Ambedkar Inst Rotary Canc Hosp, Dept Med Oncol, New Delhi 110029, India.
   [Ashraf, Bazella] Cent Univ Kashmir, Sch Life Sci, Dept Biotechnol, Ganderbal 191201, Jammu & Kashmir, India.
   [Maacha, Selma] Sidra Med, Div Translat Med, Res Branch, Doha 26999, Qatar.
   [Karedath, Thasni] Qatar Fdn, Genom Core Facil, QBRI, Doha 34110, Qatar.
   [Yasin, Syed Besina] Sher Kashmir Inst Med Sci, Dept Pathol, Srinagar 191201, Jammu & Kashmir, India.
   [Bagga, Puneet] St Jude Childrens Res Hosp, Dept Diagnost Imaging, Memphis, TN 38105 USA.
   [Reddy, Ravinder] Univ Penn, Perelman Sch Med, Dept Radiol, Ctr Adv Metab Imaging Precis Med, Philadelphia, PA 19104 USA.
   [Frennaux, Michael P.] Hamad Med Corp, Acad Hlth Syst, Doha 3050, Qatar.
   [Uddin, Shahab] Hamad Med Corp, Res Inst, Doha 3050, Qatar.
   [Dhawan, Punita] Univ Nebraska Med Ctr, Dept Biochem & Mol Biol, Omaha, NE 68198 USA.
   [Haris, Mohammad] Qatar Univ, Anim Res Ctr, Doha 2713, Qatar.
   [Macha, Muzafar A.] Islamic Univ Sci & Technol, Watson Crick Ctr Mol Med, Awantipora 192122, Jammu & Kashmir, India.
C3 Sidra Medical & Research Center; All India Institute of Medical Sciences
   (AIIMS) New Delhi; DR. B.R.A. Institute Rotary Cancer Hospital; Central
   University of Kashmir; Sidra Medical & Research Center; Qatar Foundation
   (QF); Hamad Bin Khalifa University-Qatar; Qatar Biomedical Research
   Institute (QBRI); Sher-i-Kashmir Institute of Medical Sciences; St Jude
   Children's Research Hospital; University of Pennsylvania; Hamad Medical
   Corporation; Hamad Medical Corporation; University of Nebraska System;
   University of Nebraska Medical Center; Qatar University
RP Haris, M (corresponding author), Sidra Med, Dept Canc Res, Lab Mol & Metab Imaging, Doha 26999, Qatar.; Macha, MA (corresponding author), Islamic Univ Sci & Technol, Watson Crick Ctr Mol Med, Awantipora 192122, Jammu & Kashmir, India.
EM mharis@sidra.org; muzafar.macha@islamicuniversity.edu.in
RI Karedath, Thasni/AAQ-6925-2020; Mir, Mohammad/AAF-7967-2020; Bagga,
   Puneet/AAA-5433-2020; Bhat, A./AEK-4320-2022; MACHA,
   MUZAFAR/AAN-5735-2020; Singh, Mayank/ABE-5733-2021; Sharma,
   Atul/ISS-2723-2023; Masoodi, Tariq/C-9843-2012; Prasad, Chandra
   Prakash/B-6404-2015; Uddin, Shahab/AFH-8541-2022
OI karedath abdul azis, Thasni/0000-0001-5482-5954; Prasad, Chandra
   Prakash/0000-0002-4911-7483; Singh, Mayank/0000-0003-0728-1936; Uddin,
   Shahab/0000-0003-1886-6710; Bhat, Ajaz Ahmad/0000-0003-3079-5097;
   Masoodi, Tariq/0000-0002-9186-6349
FU Ramalingaswami Fellowship [BT/HRD/35/02/2006]; Department of
   Biotechnology; Core Research grant [CRG/2021/003805]; Science and
   Engineering Research Board (SERB), Govt. of India, New Delhi; Sidra
   Medicine Precision Program [5081012003, 5081012002]
FX Ramalingaswami Fellowship, Grant/Award Number: D.O.
   NO.BT/HRD/35/02/2006; the Department of Biotechnology, & Core Research
   grant, Grant/Award Number: CRG/2021/003805; Science and Engineering
   Research Board (SERB), Govt. of India, New Delhi; Sidra Medicine
   Precision Program, Grant/Award Numbers: 5081012003, 5081012002
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NR 289
TC 75
Z9 81
U1 26
U2 68
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2523-3548
J9 CANCER COMMUN
JI Cancer Commun.
PD AUG
PY 2022
VL 42
IS 8
BP 689
EP 715
DI 10.1002/cac2.12295
EA JUL 2022
PG 27
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3W9WP
UT WOS:000820927900001
PM 35791509
OA Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Xiong, YF
   Zhou, H
   Huang, XJ
   Huang, JM
   Yang, G
   Lei, ZX
   Li, JD
AF Xiong Yongfu
   Zhou He
   Huang Xujian
   Huang Jiemei
   Yang Gang
   Lei, Zhixiong
   Li Jingdong
TI PLHPP2 inhibits the stemness of colorectal cancer by inactivating the
   Nrf2 signaling pathway
SO JOURNAL OF CANCER
LA English
DT Article
DE colorectal cancer; stemness; PHLPP2; Nrf2
AB Pleckstrin homology (PH) domain leucine-rich repeat protein phosphatase 2 (PHLPP2) is a critical regulator of cellular homeostasis and acts as a tumor suppressor in multiple human cancers. However, its exact biological function in colorectal cancer (CRC) and the underlying molecular mechanism remain poorly understood. The correlation between the transcription and protein abundance of PHLPP2 was analyzed using proteomic and corresponding transcriptional data. Immunohistochemistry was used to validate the protein expression and the role of PHLPP2 in patient prognosis. In addition, a series of experiments in vitro and in vivo were performed to investigate the underlying molecular mechanism. Immunohistochemical staining of a CRC tissue microarray revealed that PHLPP2 protein expression was significantly downregulated compared to that in adjacent normal tissues. Low expression of PHLPP2 was an independent prognostic risk factor for poor survival. A nomogram established by integrating PHLPP2 expression and traditional clinicopathological factors achieved more reliable prognostic assessment in CRC patients. Additionally, PHLPP2 overexpression suppressed CRC cell migration, invasion and stemness in vitro as well as tumorigenesis in vivo. Further experiments revealed that upregulation of PHLPP2 increased ROS levels by suppressing the Nrf2-ARE signaling pathway, which inhibited the stemness of CRC cells. Moreover, incubation with sulforaphane, a selective chemical agonist of Nrf2, reversed this inhibitory effect in CRC. PHLPP2 acts as a tumor suppressor gene in CRC by restraining the Nrf2-ARE signaling pathway and increasing ROS levels, affecting the stemness of CRC cells. These anticancer molecular mechanisms indicate PHLLPP2's significant clinical value in prognosis prediction and targeted therapy.
C1 [Xiong Yongfu; Huang Xujian; Yang Gang; Li Jingdong] North Sichuan Med Coll, Dept Hepatobiliary Surg, Affiliated Hosp, Nanchong 637007, Peoples R China.
   [Xiong Yongfu; Lei, Zhixiong] Wusheng Cty Peoples Hosp, Dept Thorac & Hepatobiliary Surg, Guangan 638400, Peoples R China.
   [Xiong Yongfu; Huang Xujian; Yang Gang; Li Jingdong] North Sichuan Med Coll, Inst Hepatobiliary Pancreat Intestinal Dis, Nanchong 637007, Peoples R China.
   [Xiong Yongfu; Zhou He; Yang Gang] North Sichuan Med Coll, Affiliated Hosp, Res Off Hepatobiliary Pancreat Intestinal Dis, Nanchong 637007, Peoples R China.
   [Zhou He] Chongqing Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Chongqing, Peoples R China.
   North Sichuan Med Coll, Affiliated Hosp, Dept Gastrointestinal Surg, Nanchong 637007, Peoples R China.
   [Huang Jiemei] North Sichuan Med Coll, Affiliated Hosp, Weikang Technol, Nanchong 637007, Peoples R China.
C3 North Sichuan Medical University; North Sichuan Medical University;
   North Sichuan Medical University; Chongqing Medical University; North
   Sichuan Medical University; North Sichuan Medical University
RP Xiong, YF; Li, JD (corresponding author), North Sichuan Med Coll, Affiliated Hosp, Dept Hepatobiliary Surg, Nanchong 637000, Peoples R China.
EM Xiong-Yongfu@nsmc.edu.cn; Li-Jingdong@hotmail.com
RI 黄, 旭/JFJ-8744-2023
OI Xiong, Yongfu/0000-0001-9016-8509
FU Youth National Natural Science foundation of China [82003147]; Free
   Exploring Basic Research Project of Science and Technology of Sichuan
   province [2020YJ0186, 2021YJ0456]; Scientific Research Project of
   Affiliated Hospital of North Sichuan Medical College [2021ZD001];
   Nanchong City [19SXHZ0290]; NSMC [19SXHZ0290]; Nanchong Science and
   Technology Bureau National Natural Science Foundation Project
   Cultivation Special [20SXZRKX0004]; Doctoral Research Startup Fund
   Project of North Sichuan Medical College [CBY20-QD03]
FX This work was financially supported by grants from the Youth National
   Natural Science foundation of China (Grant No. 82003147) ; Free
   Exploring Basic Research Project of Science and Technology of Sichuan
   province (Grant No. 2020YJ0186) ; Free Exploring Basic Research Project
   of Science and Technology of Sichuan Province (Grant No.2021YJ0456) ;
   Scientific Research Project of Affiliated Hospital of North Sichuan
   Medical College (Grant No.2021ZD001) ; Cooperation Project Between
   Nanchong City and NSMC (Grant No. 19SXHZ0290) ; Nanchong Science and
   Technology Bureau National Natural Science Foundation Project
   Cultivation Special (NO.20SXZRKX0004) ; The Doctoral Research Startup
   Fund Project of North Sichuan Medical College (NO.CBY20-QD03) .
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NR 27
TC 1
Z9 1
U1 1
U2 11
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2022
VL 13
IS 4
BP 1313
EP 1323
DI 10.7150/jca.65444
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YW6SX
UT WOS:000753545900001
PM 35281874
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Eslami, M
   Memarsadeghi, O
   Davarpanah, A
   Arti, A
   Nayernia, K
   Behnam, B
AF Eslami, Maryam
   Memarsadeghi, Omid
   Davarpanah, Ali
   Arti, Afshin
   Nayernia, Karim
   Behnam, Babak
TI Overcoming Chemotherapy Resistance in Metastatic Cancer: A Comprehensive
   Review
SO BIOMEDICINES
LA English
DT Review
DE chemotherapy resistance; metastatic cancer cells; combination therapy;
   targeted therapy; immunotherapy; drug repurposing; personalized
   medicine; predictive biomarkers; clinical trials
ID MULTIDRUG-RESISTANCE; DRUG-RESISTANCE; MOLECULAR-MECHANISMS;
   CO-DELIVERY; PROSTATE-CANCER; STEM-CELL; EPIGENETIC MODIFICATIONS;
   PERSONALIZED MEDICINE; MULTIPLE-MYELOMA; COLON-CANCER
AB The management of metastatic cancer is complicated by chemotherapy resistance. This manuscript provides a comprehensive academic review of strategies to overcome chemotherapy resistance in metastatic cancer. The manuscript presents background information on chemotherapy resistance in metastatic cancer cells, highlighting its clinical significance and the current challenges associated with using chemotherapy to treat metastatic cancer. The manuscript delves into the molecular mechanisms underlying chemotherapy resistance in subsequent sections. It discusses the genetic alterations, mutations, and epigenetic modifications that contribute to the development of resistance. Additionally, the role of altered drug metabolism and efflux mechanisms, as well as the activation of survival pathways and evasion of cell death, are explored in detail. The strategies to overcome chemotherapy resistance are thoroughly examined, covering various approaches that have shown promise. These include combination therapy approaches, targeted therapies, immunotherapeutic strategies, and the repurposing of existing drugs. Each strategy is discussed in terms of its rationale and potential effectiveness. Strategies for early detection and monitoring of chemotherapy drug resistance, rational drug design vis-a-vis personalized medicine approaches, the role of predictive biomarkers in guiding treatment decisions, and the importance of lifestyle modifications and supportive therapies in improving treatment outcomes are discussed. Lastly, the manuscript outlines the clinical implications of the discussed strategies. It provides insights into ongoing clinical trials and emerging therapies that address chemotherapy resistance in metastatic cancer cells. The manuscript also explores the challenges and opportunities in translating laboratory findings into clinical practice and identifies potential future directions and novel therapeutic avenues. This comprehensive review provides a detailed analysis of strategies to overcome chemotherapy resistance in metastatic cancer. It emphasizes the importance of understanding the molecular mechanisms underlying resistance and presents a range of approaches for addressing this critical issue in treating metastatic cancer.
C1 [Eslami, Maryam; Memarsadeghi, Omid; Davarpanah, Ali] Islamic Azad Univ, Appl Biotechnol Res Ctr, Tehran Med Sci, Tehran 1949635881, Iran.
   [Eslami, Maryam; Memarsadeghi, Omid; Davarpanah, Ali] Islamic Azad Univ, Int Fac, Tehran Med Sci, Tehran 1949635881, Iran.
   [Eslami, Maryam; Davarpanah, Ali] Islamic Azad Univ, Fac Adv Sci & Technol, Dept Genet, Tehran Med Sci, Tehran 1949635881, Iran.
   [Arti, Afshin] Islamic Azad Univ, Dept Biomed Engn, Cent Tehran Branch, Tehran 1469669191, Iran.
   [Nayernia, Karim] Int Ctr Personalized Med P7Med, D-40235 Dusseldorf, Germany.
   [Behnam, Babak] NSF Int, Dept Regulatory Affairs, Amarex Clin Res, Germantown, MD 20874 USA.
C3 Islamic Azad University; Islamic Azad University; Islamic Azad
   University; Islamic Azad University; National Science Foundation (NSF)
RP Nayernia, K (corresponding author), Int Ctr Personalized Med P7Med, D-40235 Dusseldorf, Germany.; Behnam, B (corresponding author), NSF Int, Dept Regulatory Affairs, Amarex Clin Res, Germantown, MD 20874 USA.
EM drmaryam.eslami2020@gmail.com; omemarsadeghi@gmail.com;
   davarpanah.alii94@gmail.com; afshinarti@yahoo.com; nayernia@icpm.center;
   bbehnam@nsf.org
OI Behnam, Babak/0000-0002-1266-1602; Davarpanah jazi,
   Ali/0009-0006-8009-9152
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NR 161
TC 14
Z9 14
U1 4
U2 15
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD JAN
PY 2024
VL 12
IS 1
AR 183
DI 10.3390/biomedicines12010183
PG 28
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 FY0N5
UT WOS:001149296400001
PM 38255288
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Pinto, C
   Normanno, N
   Orlandi, A
   Fenizia, F
   Damato, A
   Maiello, E
   Tamburini, E
   Di Costanzo, F
   Tonini, G
   Bilancia, D
   Corsi, D
   Pisconti, S
   Ferrau, F
   Gori, S
   Daniele, B
   Zaniboni, A
   Parra, HS
   Frassinetti, GL
   Iaffaioli, RV
   Cassata, A
   Zampino, MG
   Repetto, L
   Calegari, MA
   Barone, C
AF Pinto, Carmine
   Normanno, Nicola
   Orlandi, Armando
   Fenizia, Francesca
   Damato, Angela
   Maiello, Evaristo
   Tamburini, Emiliano
   Di Costanzo, Francesco
   Tonini, Giuseppe
   Bilancia, Domenico
   Corsi, Domenico
   Pisconti, Salvatore
   Ferrau, Francesco
   Gori, Stefania
   Daniele, Bruno
   Zaniboni, Alberto
   Parra, Hector Soto
   Frassinetti, Giovanni Luca
   Iaffaioli, Rosario Vincenzo
   Cassata, Antonio
   Zampino, Maria Giulia
   Repetto, Lazzaro
   Calegari, Maria Alessandra
   Barone, Carlo
TI Phase III study with FOLFIRI plus cetuximab versus FOLFIRI plus
   cetuximab followed by cetuximab alone in <i>RAS</i> and <i>BRAF</i> WT
   mCRC
SO FUTURE ONCOLOGY
LA English
DT Review
DE cetuximab; colorectal cancer; de-escalation therapy; RAS and BRAF
   wild-type
ID METASTATIC COLORECTAL-CANCER; 1ST-LINE TREATMENT; NON-INFERIORITY;
   MUTATION STATUS; OPEN-LABEL; BEVACIZUMAB; TRIAL; KRAS; FLUOROURACIL;
   LEUCOVORIN
AB The optimal duration and intensity of first-line therapy in metastatic colorectal cancer patients once they have achieved an objective response is controversial. In a molecularly selected RAS and BRAF wild-type (wt) population, this concern is amplified. Once disease control has been achieved with a combination therapy including an anti-EGFR antibody, further exposure both to cytotoxic drugs and targeted therapy might result only in increased toxicity. In unresectable metastatic RAS and BRAF wt colorectal cancer patients, a deintensified therapy could represent a valuable option that might preserve quality of life. We designed a study to compare FOLFIRI/cetuximab to FOLFIRI/cetuximab for eight cycles followed by cetuximab alone in first-line treatment of RAS and BRAF (wt) metastatic colorectal cancer patients.
C1 [Pinto, Carmine; Damato, Angela] Azienda USL IRCCS, Ctr Clin Canc, Med Oncol, Reggio Emilia, Italy.
   [Normanno, Nicola; Fenizia, Francesca] Ist Nazl Tumori IRCCS Fdn Pascale, Cell Biol & Biotherapy Unit, Naples, Campania, Italy.
   [Orlandi, Armando; Calegari, Maria Alessandra; Barone, Carlo] Fdn Policlin Univ A Gemelli, Oncol Unit, Rome, Lazio, Italy.
   [Maiello, Evaristo] Osped Casa Sollievo Sofferenza, Oncol Unit, San Giovanni Rotondo, Puglia, Italy.
   [Tamburini, Emiliano] Azienda Unita Sanit Locale Romagna, Oncol Unit, Rimini, Emilia Romagna, Italy.
   [Di Costanzo, Francesco] Azienda Osped Univ Careggi Firenze, Oncol Unit, Toscana, Italy.
   [Tonini, Giuseppe] Univ Campus Biomed Roma, Oncol Unit, Rome, Lazio, Italy.
   [Bilancia, Domenico] Osped San Carlo Potenza, Oncol Unit, Basilicata, Italy.
   [Corsi, Domenico] San Giovanni Calabita Hosp, Oncol Unit, Rome, Lazio, Italy.
   [Pisconti, Salvatore] SG Moscati Hosp Taranto, Oncol Unit, Taranto, Italy.
   [Ferrau, Francesco] Osped San Vicenzo, Oncol Unit, Taormina, Sicilia, Italy.
   [Gori, Stefania] Osped Sacro Cuore Don Calabria, Ctr Clin Canc, Med Oncol, Negrar, Veneto, Italy.
   [Daniele, Bruno] Azienda Osped Gaetano Rummo, Oncol Unit, Benevento, Campania, Italy.
   [Zaniboni, Alberto] Fdn Poliambulanza Ist Osped, Oncol Unit, Brescia, Lombardia, Italy.
   [Parra, Hector Soto] Univ Catania Scuola Fac Med, Oncol Unit, Catania, Sicilia, Italy.
   [Frassinetti, Giovanni Luca] IRCCS Ist Sci Romagnolo Studio & Cura Tumori Med, Oncol Unit, Emilia Romagna, Italy.
   [Iaffaioli, Rosario Vincenzo; Cassata, Antonio] Inst Nazl Tumori IRCCS Fdn Pascale, Oncol Clin Sperimentale Addome, Naples, Campania, Italy.
   [Zampino, Maria Giulia] Ist Europeo Oncol, Oncol Unit, Milan, Lombardia, Italy.
   [Repetto, Lazzaro] Osped Civile G Borea, Oncol Unit, San Remo, Liguria, Italy.
C3 IRCCS Fondazione Pascale; Catholic University of the Sacred Heart; IRCCS
   Policlinico Gemelli; IRCCS Casa Sollievo Della Sofferenza; University
   Campus Bio-Medico - Rome Italy; IRCCS Sacro Cuore Don Calabria;
   University of Catania; IRCCS European Institute of Oncology (IEO)
RP Orlandi, A (corresponding author), Fdn Policlin Univ A Gemelli, Oncol Unit, Rome, Lazio, Italy.
EM armando.orlandi@policlinicogemelli.it
RI Maiello, Evaristo/C-5224-2017; Pisconti, Salvatore/ADD-8059-2022;
   Damato, Angela/AAC-1343-2019; de Rosa, Francesco/AAC-5935-2022; Zampino,
   Maria/AAQ-4795-2020; Di Costanzo, Francesco/HMV-6214-2023; Fenizia,
   Francesca/AAC-1394-2019; Normanno, Nicola/AAT-1107-2021; Tamburini,
   Emiliano/LQJ-8211-2024; Daniele, Bruno/IAR-5511-2023; GORI,
   Stefania/AAB-4802-2022; Bilancia, Domenico/AAO-9167-2021; SOTO PARRA,
   HECTOR/IZE-2180-2023; Pinto, Carmine/AAC-2184-2020; ORLANDI,
   Armando/A-1517-2015; calegari, maria alessandra/K-3929-2018
OI SOTO PARRA, HECTOR/0000-0001-7966-4472; Di Costanzo,
   Francesco/0000-0002-6858-7827; Fenizia, Francesca/0000-0003-0523-1919;
   Tamburini, Emiliano/0000-0003-4619-7091; Normanno,
   Nicola/0000-0002-7158-2605; Damato, Angela/0000-0001-8286-1274; Pinto,
   Carmine/0000-0002-3159-5268; Frassineti, Giovanni
   Luca/0000-0002-0277-5622; Pisconti, Salvatore/0000-0002-1658-523X; Gori,
   Stefania/0000-0001-6320-405X; ORLANDI, Armando/0000-0001-5253-4678;
   calegari, maria alessandra/0000-0001-6856-2593
FU Merck
FX The study is partially supported by an unrestricted grant provided by
   Merck. Merck KGaA reviewed the manuscript for medical accuracy only
   before journal submission. 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 14
TC 6
Z9 6
U1 0
U2 4
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 JUN
PY 2018
VL 14
IS 14
BP 1339
EP 1346
DI 10.2217/fon-2017-0592
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GM2NU
UT WOS:000437925300002
PM 29846100
DA 2025-01-04
ER

PT J
AU Talar-Wojnarowska, R
   Fabisiak, A
   Zatorski, H
   Ploszka, K
   Blaziak, K
   Fendler, W
   Rydzewska, G
   Malecka-Wojciesko, E
   Eder, P
AF Talar-Wojnarowska, Renata
   Fabisiak, Adam
   Zatorski, Hubert
   Ploszka, Katarzyna
   Blaziak, Katarzyna
   Fendler, Wojciech
   Rydzewska, Grazyna
   Malecka-Wojciesko, Ewa
   Eder, Piotr
TI Comparison of ustekinumab, infliximab and combination therapy in
   moderately to severely active ulcerative colitis - a study protocol of a
   randomized, multicenter, head-to-head COMBO-UC trial
SO FRONTIERS IN MEDICINE
LA English
DT Article
DE inflammatory bowel diseases; ulcerative colitis; dual biological
   therapy; infliximab; ustekinumab
ID INFLAMMATORY-BOWEL-DISEASE; MAINTENANCE THERAPY; ECCO GUIDELINES;
   THERAPEUTICS; INDUCTION
AB Background Ulcerative colitis (UC) is a chronic inflammatory bowel disease with a complex etiology that affects the large intestine. Characterized by chronic, bloody diarrhea, UC can lead to severe complications, including an increased risk of colorectal cancer. Despite advancements in conservative treatment, including biologics like anti-TNF agents and ustekinumab (UST), many patients do not achieve full remission. Dual targeted therapy (DTT) combining infliximab (IFX) and UST is a promising approach to improve treatment outcomes. Methods This prospective, randomized, multicenter, head-to-head controlled trial will evaluate the efficacy and safety of UST, IFX, and combination therapy (UST + IFX) in 172 patients with moderate to severe active UC across eight gastroenterology centers in Poland. The study includes a 14-16 week remission induction period followed by a 52-week maintenance phase. Patients will be randomly assigned to one of three treatment arms: IFX monotherapy, UST monotherapy, or IFX + UST combination therapy. Primary endpoint is clinical and endoscopic remission post-induction. Secondary endpoints include clinical response, biochemical remission, histological remission, and quality of life assessments using the Inflammatory Bowel Diseases Questionnaire and 36-Item Short Form Survey. Safety will be monitored through adverse event and serious adverse event reporting. Discussion This trial aims to determine whether combining IFX and UST can achieve higher remission rates and better long-term outcomes compared to monotherapy. The results could provide crucial insights into the optimal use of biologic agents in UC treatment, potentially establishing DTT as a standard therapy. The study's design, including extensive follow-up and robust endpoint measures, will contribute to understanding the therapeutic potential and safety profile of this combination therapy.
C1 [Talar-Wojnarowska, Renata; Fabisiak, Adam; Zatorski, Hubert; Malecka-Wojciesko, Ewa] Med Univ Lodz, Dept Digest Tract Dis, Lodz, Poland.
   [Ploszka, Katarzyna; Blaziak, Katarzyna; Fendler, Wojciech] Med Univ Lodz, Dept Biostat & Translat Med, Lodz, Poland.
   [Rydzewska, Grazyna] Minist Interior & Adm, Natl Med Inst, Clin Dept Internal Med & Gastroenterol, Inflammatory Bowel Dis Unit, Warsaw, Poland.
   [Eder, Piotr] Poznan Univ Med Sci, Dept Gastroenterol Dietet & Internal Med, Poznan, Poland.
C3 Medical University Lodz; Medical University Lodz; National Medicines
   Institute Lekow (NIL); Poznan University of Medical Sciences
RP Fabisiak, A (corresponding author), Med Univ Lodz, Dept Digest Tract Dis, Lodz, Poland.
EM adam.fabisiak@umed.lodz.pl
RI Malecka-Panas, Ewa/AFN-7115-2022; Talar-Wojnarowska, Renata/T-1009-2016;
   Fabisiak, Adam/U-1144-2019; Eder, Piotr/JLL-6119-2023
OI Talar-Wojnarowska, Renata/0000-0003-3887-2712; Zatorski,
   Hubert/0000-0002-4932-9013; Malecka-Wojciesko, Ewa/0000-0002-1825-1807;
   Ploszka, Katarzyna/0000-0002-9573-2719
FU Medical Research Agency (Agencja Badan Medycznych) [2022/ABM/03/00013]
FX The author(s) declare that financial support was received for the
   research, authorship, and/or publication of this article. This work was
   supported by Medical Research Agency (Agencja Badan Medycznych) grant
   no. 2022/ABM/03/00013.
CR Atreya R, 2022, J CROHNS COLITIS, V16, DOI 10.1093/ecco-jcc/jjac007
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NR 25
TC 0
Z9 0
U1 1
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD SEP 19
PY 2024
VL 11
AR 1458998
DI 10.3389/fmed.2024.1458998
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA I5S7M
UT WOS:001330862500001
PM 39364021
OA gold
DA 2025-01-04
ER

PT J
AU Gurzu, S
   Fetyko, A
   Bara, T
   Banias, L
   Butiurca, VO
   Bara, T
   Tudorache, V
   Jung, L
AF Gurzu, Simons
   Fetyko, Annamaria
   Bara, Tivadar
   Banias, Laura
   Butiurca, Vlad Olimpiu
   Bara, Tivadar, Jr.
   Tudorache, Vlad
   Jung, Loan
TI Gastrointestinal mixed adenoneuroendocrine carcinoma (MANEC): An
   immunohistochemistry study of 13 microsatellite stable cases
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Article
DE MANEC; Epithelial mesenchymal transition; CD44; Maspin; Beta-catenin;
   Lymph node architecture
ID DIFFERENTIATED NEUROENDOCRINE CARCINOMAS; COLORECTAL-CANCER; RECTUM;
   TRACT; COLON
AB Background: Mixed adenoneuroendocrine carcinoma (MANEC) is currently included in the category of neuroendocrine carcinomas but the therapeutically management is not yet defined.
   Aims: To present the immunohistochemical (IHC) features of the epithelial mesenchymal transition (EMT) of MANEC.
   Materials and methods: The clinicopathological features of 13 consecutive cases of MANEC (6 gastric and 7 colorectal) were correlated with the IHC expression of the biomarkers E-cadherin, beta-catenin, N-cadherin, vimentin, maspin, CD44 and S100. In all of the cases open surgery was performed.
   Results: All of the cases showed microsatellite stable status, expressed E-cadherin and membrane beta-catenin in both components (neuroendocrine and adenocarcinoma) and were negative for N-cadherin, vimentin and S-100. The colorectal MANECs were negative for maspin. In gastric MANECs, maspin showed cytoplasm positivity in the neuroendocrine component and nuclear translocation in the adenocarcinoma cells. CD44 was positive in all of the cases, in both components. No tumor buddings were identified. Three of the 13 patients survived for at least 32 months, all of them showing lymphatic emboli but not lymph node metastases. Pure neuroendocrine lymph node metastases were seen in only four of the cases: one from stomach, two of the ascending colon and two cases of the upper rectum.
   Conclusions: Gastrointestinal MANEC is a microsatellite stable tumor with nodular growth, which components might originate from a CD44-positive stem-like precursor cell. Lymph node status remains the most reliable prognostic parameter and agressivity seems to not be influenced by tumor budding degree or EMT-related features. The histologic aspect of metastatic component (neuroendocrine versus adenocarcinoma) should be included in the histopathological reports and might be used for establishing the proper-targeted therapy of MANEC.
C1 [Gurzu, Simons; Banias, Laura; Tudorache, Vlad; Jung, Loan] Univ Med Pharm Sci & Technol, Dept Pathol, Targu Mures, Romania.
   [Gurzu, Simons; Fetyko, Annamaria] Clin Cty Emergency Hosp, Dept Pathol, Targu Mures, Romania.
   [Gurzu, Simons] Univ Med Pharm Sci & Technol, Res Ctr, Dept Pathol, Targu Mures, Romania.
   [Bara, Tivadar; Butiurca, Vlad Olimpiu; Bara, Tivadar, Jr.] Univ Med Pharm Sci & Technol, Dept Surg, Targu Mures, Romania.
C3 George Emil Palade University of Medicine, Pharmacy, Science, &
   Technology of Targu Mures; George Emil Palade University of Medicine,
   Pharmacy, Science, & Technology of Targu Mures; George Emil Palade
   University of Medicine, Pharmacy, Science, & Technology of Targu Mures
RP Gurzu, S (corresponding author), Univ Med Pharm Sci & Technol, 38 Ghe Marinescu St, Targu Mures 540139, Romania.
EM simonagurzu@yahoo.com
RI Tudorache, Valentina/D-2743-2012; Bara, Tivadar Jr/C-4943-2017; Banias,
   Laura/AAB-9233-2022; Butiurca, Vlad-Olimpiu/B-3859-2018
OI BANIAS, LAURA/0000-0002-2240-2540; Butiurca,
   Vlad-Olimpiu/0000-0002-9900-5375
FU Romanian National Authority for Scientific Research, CNCSIS - UEFISCDI
   [20 PCCF/2018, PN-III-P4-ID-PCCF-2016-0006]
FX This work was supported by a grant of the Romanian National Authority
   for Scientific Research, CNCSIS - UEFISCDI, project number 20 PCCF/2018,
   code: PN-III-P4-ID-PCCF-2016-0006.
CR [Anonymous], 2010, WHO CLASSIFICATION T
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NR 30
TC 15
Z9 17
U1 0
U2 11
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PY 2019
VL 215
IS 12
AR 152697
DI 10.1016/j.prp.2019.152697
PG 6
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA KK1BP
UT WOS:000512485400015
PM 31704155
DA 2025-01-04
ER

PT J
AU Huang, KB
   Liu, RY
   Peng, QH
   Li, ZS
   Jiang, LJ
   Guo, SJ
   Zhou, QH
   Liu, TY
   Deng, CZ
   Yao, K
   Qin, ZK
   Liu, ZW
   Li, YH
   Han, H
   Zhou, FJ
AF Huang, Kang-bo
   Liu, Ran-yi
   Peng, Qi-hua
   Li, Zai-shang
   Jiang, Li-juan
   Guo, Sheng-jie
   Zhou, Qiang-hua
   Liu, Ting-yu
   Deng, Chuang-zhong
   Yao, Kai
   Qin, Zi-ke
   Liu, Zhuo-wei
   Li, Yong-hong
   Han, Hui
   Zhou, Fang-jian
TI EGFR mono-antibody salvage therapy for locally advanced and distant
   metastatic penile cancer: Clinical outcomes and genetic analysis
SO UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS
LA English
DT Article
DE EGFR mono-antibody; Penile cancer; Salvage therapy; Genetic alterations;
   Human papillomavirus
ID SQUAMOUS-CELL CARCINOMA; GROWTH-FACTOR RECEPTOR; HUMAN-PAPILLOMAVIRUS;
   COLORECTAL-CANCER; CHEMOTHERAPY; EXPRESSION; PACLITAXEL; RESISTANCE;
   CISPLATIN; BLOCKADE
AB Purpose: There are limited therapeutic options for patients with advanced penile squamous cell carcinoma (PSCC) after chemotherapy failure. Thus, we evaluated the feasibility of salvage treatment using the epidermal growth factor receptor (EGFR) mono-antibody nimotuzumab in chemotherapy-failed PSCC patients and explored potential response or resistance biomarkers.
   Materials and methods: Six chemotherapy-failed PSCC patients with locally advanced disease or distant metastasis were enrolled consecutively to nimotuzumab treatment. Clinical responses and side effects were evaluated, and genetic characteristics of cancer specimens were analyzed through the next-generation sequencing of hotspot regions in cancer-related genes.
   Results: Two of 6 patients showed partial responses, one was identified as having stable disease, while the other 3 had disease progression after nimotuzumab therapy. Side effects were all welltolerated. Genetic analysis revealed that TP53, CDKN2A, RB1, SMAD4, FLT3, and PIK3CA were the most frequently mutated genes in PSCC specimens, while altered KRAS, HRAS, EGFR, ERBB2, and FLT3 may be correlated with nimotuzumab resistance. Furthermore, 3 patients that were human papillomavirus-positive each showed clinical response or stable disease.
   Conclusions: EGFR mono-antibody may be a potential modality for locally advanced PSCC patients after chemotherapy failure. Further large-scale clinical studies are needed to elucidate the role of human papillomavirus status and critical gene mutations in the clinical response to EGFR-targeted therapy. (C) 2018 The Authors. Published by Elsevier Inc.
C1 [Huang, Kang-bo; Liu, Ran-yi; Peng, Qi-hua; Li, Zai-shang; Jiang, Li-juan; Guo, Sheng-jie; Zhou, Qiang-hua; Liu, Ting-yu; Deng, Chuang-zhong; Yao, Kai; Qin, Zi-ke; Liu, Zhuo-wei; Li, Yong-hong; Han, Hui; Zhou, Fang-jian] Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Canc Ctr, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; State Key Lab Oncology South China
RP Liu, RY; Han, H (corresponding author), Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Canc Ctr, Guangzhou, Guangdong, Peoples R China.
EM liury@sysucc.org.cn; hanhui@sysucc.org.cn
RI Liu, Ran-yi/L-1008-2019; Zhou, Qianghua/AAQ-1973-2021; Li,
   Zaishang/KOD-0673-2024; Liu, Tingyu/AAI-7945-2020
FU National Natural Science Foundation of China [81772755]; Guangdong
   Province Science and Technology Project [2015A030302018]; Guangzhou
   Municipal Science and Technology Project [201704030037]
FX We thank Prof. Yan-xia Shi for his valuable suggestions, this work was
   supported by the National Natural Science Foundation of China (No.
   81772755), Guangdong Province Science and Technology Project (No.
   2015A030302018), and Guangzhou Municipal Science and Technology Project
   (No. 201704030037). The authenticity of this article has been validated
   by uploading the key raw data onto the Research Data Deposit public
   platform (www.researchdata.org.cn), with the approval number
   RDDB2018000441.
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NR 30
TC 8
Z9 8
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1078-1439
EI 1873-2496
J9 UROL ONCOL-SEMIN ORI
JI Urol. Oncol.-Semin. Orig. Investig.
PD JAN
PY 2019
VL 37
IS 1
BP 71
EP 77
DI 10.1016/j.urolonc.2018.10.016
PG 7
WC Oncology; Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Urology & Nephrology
GA HD2ON
UT WOS:000452350100010
PM 30446465
OA hybrid
DA 2025-01-04
ER

PT J
AU Liu, J
   Zhang, XB
   Yang, MJ
   Zhang, XH
AF Liu, Jia
   Zhang, Xianbo
   Yang, Meijian
   Zhang, Xianghong
TI CircCOL1A1 promotes proliferation, migration, and invasion of colorectal
   cancer (CRC) cells and glutamine metabolism through GLS1 up-regulation
   by sponging miR-214-3p
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer; miR-214-3p/GLS1 axis
ID TARGETED THERAPY; OXIDATIVE STRESS; METASTASIS
AB Background Circular ribose nucleic acids (circRNAs), an abundant type of noncoding RNAs, are widely expressed in eukaryotic cells and exert a significant impact on the initiation and progression of various disorders, including different types of cancer. However, the specific role of various circRNAs in colorectal cancer (CRC) pathology is still not fully understood.Methods The initial step involved the use of quantitative reverse transcription polymerase chain reaction (RT-qPCR) to assess the expression levels of circRNAs and messenger RNA (mRNA) in CRC cell lines and tissues. Subsequently, functional analyses of circCOL1A1 knockdown were conducted in vitro and in vivo through cell counting kit (CCK)-8, colony formation and transwell assays, as well as xenograft mouse model of tumor formation. Molecular expression and interactions were investigated using luciferase reporter assays, Western blot analysis, RNA immunoprecipitation (RIP), and immunohistochemical staining.Results The RT-qPCR results revealed elevated levels of circCOL1A1 expressions in CRC tissues and cell lines as compared to the normal counterparts. In addition, circCOL1A1 expression level was found to be correlated with TNM stage, lymph node metastases, distant metastases, and invasion. Knockdown of circCOL1A1 resulted in impaired invasion, migration, and proliferation of CRC cells, and suppressed tumor generation in the animal model. We further demonstrated that circCOL1A1 could act as a sponge for miR-214-3p, suppressing miR-214-3p activity and leading to the upregulation of GLS1 protein to promote glutamine metabolism.Conclusion These findings suggest that circCOL1A1 functions as an oncogenic molecule to promote CRC progression via miR-214-3p/GLS1 axis, hinting on the potential of circCOL1A1 as a therapeutic target for CRC.
C1 [Liu, Jia] Hebei Med Univ, Oncol Teaching & Res Off, 361 Zhongshan East Rd, Shijiazhuang 050017, Hebei, Peoples R China.
   [Liu, Jia; Zhang, Xianbo; Yang, Meijian] Hebei Gen Hosp, Dept Oncol 2, 348 Heping West Rd, Shijiazhuang 050051, Hebei, Peoples R China.
   [Zhang, Xianghong] Hebei Med Univ, Hosp 2, Dept Pathol, 215 Heping West Rd, Shijiazhuang 050000, Hebei, Peoples R China.
C3 Hebei Medical University; Hebei Medical University
RP Zhang, XH (corresponding author), Hebei Med Univ, Hosp 2, Dept Pathol, 215 Heping West Rd, Shijiazhuang 050000, Hebei, Peoples R China.
EM zhangxianghong3210@163.com
RI Zhang, Xianbo/JNS-2212-2023
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NR 44
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
SN 0171-5216
EI 1432-1335
J9 J CANCER RES CLIN
JI J. Cancer Res. Clin. Oncol.
PD APR 25
PY 2024
VL 150
IS 4
AR 211
DI 10.1007/s00432-024-05736-z
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OU2Z4
UT WOS:001209742600001
PM 38662258
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Yoon, J
   Oh, DY
AF Yoon, Jeesun
   Oh, Do-Youn
TI HER2-targeted therapies beyond breast cancer - an update
SO NATURE REVIEWS CLINICAL ONCOLOGY
LA English
DT Review
ID ANTIBODY-DRUG CONJUGATE; ANTI-HER2 BISPECIFIC ANTIBODY; METASTATIC
   COLORECTAL-CANCER; ADVANCED GASTRIC-CANCER; ACTIVATED T-CELLS; PHASE-II
   TRIAL; TRASTUZUMAB DERUXTECAN; OPEN-LABEL; LUNG-CANCER; SINGLE-ARM
AB The receptor tyrosine-kinase HER2 (also known as ErbB2) is a well-established therapeutic target in patients with breast or gastric cancer selected on the basis of HER2 overexpression on immunohistochemistry and/or ERBB2 amplification on in situ hybridization. With advances in cancer molecular profiling and increased implementation of precision medicine approaches into oncology practice, actionable HER2 alterations in solid tumours have expanded to include ERBB2 mutations in addition to traditional HER2 overexpression and ERBB2 amplification. These various HER2 alterations can be found in solid tumour types beyond breast and gastric cancer, although few HER2-targeted therapeutic options have been established for the other tumour types. Nevertheless, during the 5 years since our previous Review on this topic was published in this journal, obvious and fruitful progress in the development of HER2-targeted therapies has been made, including new disease indications, innovative drugs with diverse mechanisms of action and novel frameworks for approval by regulatory authorities. These advances have culminated in the recent histology-agnostic approval of the anti-HER2 antibody-drug conjugate trastuzumab deruxtecan for patients with HER2-overexpressing solid tumours. In this new Review, we provide an update on the current development landscape of HER2-targeted therapies beyond breast cancer, as well as anticipated future HER2-directed treatment strategies to overcome resistance and thereby improve efficacy and patient outcomes.
   Anti-HER2 therapy has revolutionized the treatment of HER2-positive breast cancer. However, HER2 has emerged as a driver of various other cancers and the indications for HER2-targeted therapy have expanded to include diverse HER2-overexpressing as well as HER2-mutant tumour types beyond breast cancer, facilitated by the advent of novel agents with greater potency and distinct mechanisms of action. Some of these agents have demonstrated promising activity even against HER2-low cancers. Herein, Yoon and Oh describe the landscape of HER2 alterations and HER2-targeted drug development beyond breast cancer. They also discuss new insights into mechanisms of resistance and potential strategies by which they might be overcome.
   Over the past few years, the indications for HER2-targeted therapy have expanded beyond breast cancer and gastric or gastroesophageal junction cancer (G/GEJC) to include various other solid tumour types.The anti-HER2 antibody-drug conjugate trastuzumab deruxtecan has become a new standard of care for patients with treatment-refractory HER2-positive G/GEJC, HER2-mutant non-small-cell lung cancer or any HER2-overexpressing (immunohistochemistry 3+) solid tumour, owing to its potent antitumour activity and impressive clinical efficacy.Ten years after the ToGA study established the anti-HER2 antibody trastuzumab in combination with chemotherapy as the standard of care for patients with previously untreated advanced-stage HER2-positive G/GEJC, the addition of an immune-checkpoint inhibitor (the anti-PD-1 antibody pembrolizumab) to this regimen has presented a new first-line treatment option for this disease.Several potential mechanisms of resistance to HER2-targeted therapies have been identified, such as alterations that impaired drug binding to HER2 or that constitutively activate signalling pathways downstream of or parallel to HER2.Novel agents targeting HER2 and new combinations HER2-target therapies with various agents, including inhibitors of other receptor tyrosine kinases, immunotherapies and DNA damage repair inhibitors, are under investigation in clinical trials.
C1 [Yoon, Jeesun; Oh, Do-Youn] Seoul Natl Univ Hosp, Dept Internal Med, Div Med Oncol, Seoul, South Korea.
   [Oh, Do-Youn] Seoul Natl Univ, Coll Med, Canc Res Inst, Seoul, South Korea.
   [Oh, Do-Youn] Seoul Natl Univ, Integrated Major Innovat Med Sci, Grad Sch, Seoul, South Korea.
C3 Seoul National University (SNU); Seoul National University Hospital;
   Seoul National University (SNU); Seoul National University (SNU)
RP Oh, DY (corresponding author), Seoul Natl Univ Hosp, Dept Internal Med, Div Med Oncol, Seoul, South Korea.; Oh, DY (corresponding author), Seoul Natl Univ, Coll Med, Canc Res Inst, Seoul, South Korea.; Oh, DY (corresponding author), Seoul Natl Univ, Integrated Major Innovat Med Sci, Grad Sch, Seoul, South Korea.
EM ohdoyoun@snu.ac.kr
OI Yoon, Jeesun/0000-0002-1456-2392
FU National Research Foundation of Korea - Korea government (MSIT)
   [2021R1A2C2007430]; Institute of Smart Healthcare Innovative Medical
   Sciences, a Brain Korea 21 four programme, Seoul National University
FX The work of the authors is supported by a National Research Foundation
   of Korea grant funded by the Korea government (MSIT; grant no.
   2021R1A2C2007430 to D.-Y.O.) and the Institute of Smart Healthcare
   Innovative Medical Sciences, a Brain Korea 21 four programme, Seoul
   National University (to D.-Y.O.).
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NR 232
TC 5
Z9 5
U1 15
U2 15
PU NATURE PORTFOLIO
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 SEP
PY 2024
VL 21
IS 9
BP 675
EP 700
DI 10.1038/s41571-024-00924-9
EA JUL 2024
PG 26
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA D4S1Q
UT WOS:001274313800002
PM 39039196
DA 2025-01-04
ER

PT J
AU Manchun, S
   Dass, CR
   Cheewatanakornkool, K
   Sriamornsak, P
AF Manchun, Somkamol
   Dass, Crispin R.
   Cheewatanakornkool, Kamonrak
   Sriamornsak, Pornsak
TI Enhanced anti-tumor effect of pH-responsive dextrin nanogels delivering
   doxorubicin on colorectal cancer
SO CARBOHYDRATE POLYMERS
LA English
DT Article
DE Colorectal cancer; pH-responsive; Dextrin; Nanogels; Doxorubicin; Drug
   delivery
ID TUMOR EXTRACELLULAR PH; DRUG-DELIVERY; POLYMERIC MICELLES; TARGETED
   THERAPY; ANTICANCER DRUG; NANOPARTICLES; CELLS; CYTOTOXICITY;
   COMBINATION; NANOCARRIER
AB Efficacy of doxorubicin (DOX) in colorectal cancer treatment is limited by undesirable side-effects, which are partially due to nonspecific delivery DOX to the tumor target site. This study aimed to develop pH-responsive dextrin nanogels (DNGs) as anticancer drug carriers with pH-controlled drug release. DNGs prepared with formaldehyde as a cross-linker (FDNGs) exhibited smaller size, compared to that using glyoxal (GDNGs). Both DNGs showed pH-dependent drug release properties; drug release was slow at neutral pH but increased significantly in acidic medium. The cytotoxicity of empty and DOX-loaded FDNGs was lower than free DOX and GDNGs, against two commonly used colorectal cancer cells. Intracellular uptake studies indicated that the DOX-loaded FDNGs could efficiently deliver DOX into the nuclei. In vivo, DOX-loaded FDNGs substantially enhanced anti-tumor efficacy, compared to free DOX, exhibiting much higher effects on inhibiting proliferation and inducing apoptosis, as confirmed by mice weight shifts, tumor weight, tumor volume and histological assessment. Therefore, FDNGs are promising as a potential drug delivery vehicle for colorectal cancer therapy. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Manchun, Somkamol; Cheewatanakornkool, Kamonrak; Sriamornsak, Pornsak] Silpakorn Univ, Fac Pharm, Dept Pharmaceut Technol, Nakhon Pathom 73000, Thailand.
   [Manchun, Somkamol; Cheewatanakornkool, Kamonrak; Sriamornsak, Pornsak] Silpakorn Univ, Fac Pharm, Pharmaceut Biopolymer Grp PBiG, Nakhon Fathom 73000, Thailand.
   [Dass, Crispin R.] Curtin Univ, Fac Hlth Sci, Sch Pharm, Perth, WA 6845, Australia.
   [Dass, Crispin R.] Curtin Hlth Innovat Res Inst Ageing & Chron Dis, Bentley, WA 6102, Australia.
C3 Silpakorn University; Curtin University
RP Sriamornsak, P (corresponding author), Silpakorn Univ, Fac Pharm, Dept Pharmaceut Technol, Nakhon Pathom 73000, Thailand.
EM sriamornsak_p@su.ac.th
RI Sriamornsak, Pornsak/F-5850-2010
OI Dass, Crispin/0000-0001-7087-7957
FU Higher Education Research Promotion; National Research University
   project of Thailand, Office of the Higher Education Commission; Royal
   Golden jubilee Ph.D. Program [PHD/0361/2551]; Thailand Research Fund;
   Curtin Academic50 grant scheme
FX This work was financially supported by the Higher Education Research
   Promotion and National Research University project of Thailand, Office
   of the Higher Education Commission. SM is supported by the Royal Golden
   jubilee Ph.D. Program (Grant No. PHD/0361/2551), The Thailand Research
   Fund. Thanks to Siam Modified Starch Co., Ltd. (Pathumthani, Thailand)
   who kindly provided dextrin samples. CRD is supported by a Curtin
   Academic50 grant scheme.
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NR 53
TC 62
Z9 66
U1 1
U2 95
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0144-8617
EI 1879-1344
J9 CARBOHYD POLYM
JI Carbohydr. Polym.
PD AUG 1
PY 2015
VL 126
BP 222
EP 230
DI 10.1016/j.carbpol.2015.03.018
PG 9
WC Chemistry, Applied; Chemistry, Organic; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Polymer Science
GA CI8PN
UT WOS:000355034300029
PM 25933543
DA 2025-01-04
ER

PT J
AU Rowe, SP
   Hawasli, H
   Fishman, EK
   Johnson, PT
AF Rowe, Steven P.
   Hawasli, Hazem
   Fishman, Elliot K.
   Johnson, Pamela T.
TI Advances in the Treatment of Oligometastatic Disease: What the
   Radiologist Needs to Know to Guide Patient Management
SO ACADEMIC RADIOLOGY
LA English
DT Article
DE Cancer imaging; Oligometastatic disease
ID CELL LUNG-CANCER; MEMBRANE ANTIGEN; BREAST-CANCER; METASTASES;
   RESECTION; SURVIVAL; THERAPY
AB Rationale and Objectives: An ever-expanding body of biological, genetic, and clinical evidence has brought to light the presence of the oligometastatic state of cancer, which is considered between localized disease and widespread metastases. Indeed, in some patients with oligometastatic disease, curative therapy is possible.
   Conclusions: For select cancer histologies, aggressive focal therapy of oligometastatic lesions is already the clinical standard of care (i.e. colorectal cancer and sarcomas), while for other tumor types the evidence is still emerging (i.e. prostate, breast, etc.). It is increasingly important, therefore, for the radiologist interpreting oncology patients' staging or restaging examinations to be aware of those diseases for which targeted therapy of oligometastases may be undertaken to effectively guide such management. The improved imaging resolution provided by technological advances promise to aid in the detection of subtle sites of disease to ensure the identification of patients with oligometastases amenable to targeted treatment.
C1 [Rowe, Steven P.; Hawasli, Hazem; Fishman, Elliot K.; Johnson, Pamela T.] Johns Hopkins Univ Hosp, Russell H Morgan Dept Radiol & Radiol Sci, 600 N Wolfe St, Baltimore, MD 21287 USA.
C3 Johns Hopkins University; Johns Hopkins Medicine
RP Johnson, PT (corresponding author), Johns Hopkins Univ Hosp, Russell H Morgan Dept Radiol & Radiol Sci, 600 N Wolfe St, Baltimore, MD 21287 USA.
EM pjohnso5@jhmi.edu
CR [Anonymous], RAD ONCOL
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NR 22
TC 3
Z9 3
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1076-6332
EI 1878-4046
J9 ACAD RADIOL
JI Acad. Radiol.
PD MAR
PY 2016
VL 23
IS 3
BP 326
EP 328
DI 10.1016/j.acra.2015.11.006
PG 3
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA DE2PK
UT WOS:000370469000010
PM 26781202
DA 2025-01-04
ER

PT J
AU Sun, ZQ
   Zhang, QG
   Yuan, WT
   Li, XL
   Chen, C
   Guo, YX
   Shao, B
   Dang, Q
   Zhou, QB
   Wang, QS
   Wang, GX
   Liu, JB
   Kan, QC
AF Sun, Zhenqiang
   Zhang, Qiuge
   Yuan, Weitang
   Li, Xiaoli
   Chen, Chen
   Guo, Yaxin
   Shao, Bo
   Dang, Qin
   Zhou, Quanbo
   Wang, Qisan
   Wang, Guixian
   Liu, Jinbo
   Kan, Quancheng
TI MiR-103a-3p promotes tumour glycolysis in colorectal cancer via
   hippo/YAP1/HIF1A axis
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Article
DE MiR-103a-3p; Hippo pathway; Glycolysis; Colorectal cancer
ID YES-ASSOCIATED PROTEIN; HIPPO PATHWAY; EXPRESSION; YAP; HYPOXIA;
   TUMORIGENESIS; REGENERATION; METABOLISM; KINASES; TARGETS
AB Background Glycolysis plays an essential role in the growth and metastasis of solid cancer and has received increasing attention in recent years. However, the complex regulatory mechanisms of tumour glycolysis remain elusive. This study aimed to explore the molecular effect and mechanism of the noncoding RNA miR-103a-3p on glycolysis in colorectal cancer (CRC). Methods We explored the effects of miR-103a-3p on glycolysis and the biological functions of CRC cells in vitro and in vivo. Furthermore, we investigated whether miR-103a-3p regulates HIF1A expression through the Hippo/YAP1 pathway, and evaluated the role of the miR-103a-3p-LATS2/SAV1-YAP1-HIF1A axis in promoting glycolysis and angiogenesis in CRC cells and contributed to invasion and metastasis of CRC cells. Results We found that miR-103a-3p was highly expressed in CRC tissues and cell lines compared with matched controls and the high expression of miR-103a-3p was associated with poor patient prognosis. Under hypoxic conditions, a high level of miR-103a-3p promoted the proliferation, invasion, migration, angiogenesis and glycolysis of CRC cells. Moreover, miR-103a-3p knockdown inhibited the growth, proliferation, and glycolysis of CRC cells and promoted the Hippo-YAP1 signalling pathway in nude mice in a xenograft model. Here, we demonstrated that miR-103a-3p could directly target LATS2 and SAV1. Subsequently, we verified that TEAD1, a transcriptional coactivator of Yes-associated protein 1 (YAP1), directly bound to the HIF1A promoter region and the YAP1 and TEAD1 proteins co-regulated the expression of HIF1A, thus promoting tumour glycolysis. Conclusions MiR-103a-3p, which is highly expressed in CRC cells, promotes HIF1A expression by targeting the core molecules LATS2 and SAV1 of the Hippo/YAP1 pathway, contributing to enhanced proliferation, invasion, migration, glycolysis and angiogenesis in CRC. Our study revealed the functional mechanisms of miR-103a-3p/YAP1/HIF1A axis in CRC glycolysis, which would provide potential intervention targets for molecular targeted therapy of CRC.
C1 [Sun, Zhenqiang; Yuan, Weitang; Shao, Bo; Dang, Qin; Zhou, Quanbo; Wang, Guixian; Liu, Jinbo] Zhengzhou Univ, Affiliated Hosp 1, Dept Colorectal Surg, Zhengzhou 450052, Henan, Peoples R China.
   [Sun, Zhenqiang; Zhang, Qiuge; Chen, Chen; Shao, Bo] Zhengzhou Univ, Acad Med Sci, Zhengzhou 450052, Henan, Peoples R China.
   [Zhang, Qiuge; Li, Xiaoli] Zhengzhou Univ, Affiliated Hosp 1, Dept Geriatr Med, Zhengzhou 450052, Henan, Peoples R China.
   [Chen, Chen] Zhengzhou Univ, Sch Life Sci, Zhengzhou 450001, Henan, Peoples R China.
   [Guo, Yaxin] Zhengzhou Univ, Sch Basic Med Sci, Zhengzhou 450002, Henan, Peoples R China.
   [Guo, Yaxin] Zhengzhou Univ, Henan Acad Med & Pharmaceut Sci, Zhengzhou 450052, Henan, Peoples R China.
   [Wang, Qisan] Xinjiang Med Univ, Affiliated Tumor Hosp, Dept Gastrointestinal Surg, Urumqi 830000, Peoples R China.
   [Kan, Quancheng] Zhengzhou Univ, Affiliated Hosp 1, Dept Pharm, Zhengzhou 450052, Henan, Peoples R China.
C3 Zhengzhou University; Zhengzhou University; Zhengzhou University;
   Zhengzhou University; Zhengzhou University; Zhengzhou University;
   Xinjiang Medical University; Zhengzhou University
RP Sun, ZQ; Liu, JB (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Colorectal Surg, Zhengzhou 450052, Henan, Peoples R China.; Sun, ZQ (corresponding author), Zhengzhou Univ, Acad Med Sci, Zhengzhou 450052, Henan, Peoples R China.; Kan, QC (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Pharm, Zhengzhou 450052, Henan, Peoples R China.
EM zqsun82@csu.edu.cn; 1999liujb@163.com; kanqc@zzu.edu.cn
RI Chen, Siqi/IZE-8631-2023; Dang, Qin/GLT-0336-2022; zhou,
   bolin/KHX-0072-2024; Li, Xiaoli/GYQ-7384-2022
OI Dang, Qin/0000-0002-2521-625X
FU National Natural Science Foundation of China [81560385, 81972663]; Key
   Scientific Research Projects of Institutions of Higher Education in
   Henan Province [19A310024]; Medical Scientific and Technological
   Research Project of Henan Province [201702027]; China Postdoctoral
   Science Foundation [2019 T120648, 2017 M610462]; National Natural
   Science Foundation of Henan Province [182300410342]; Health Commission
   Technology Talents Overseas Training Project of Henan Province
   [2018140]; Key Scientific Research Project of Henan Higher Education
   Institutions [20A310024]
FX This study was supported by The National Natural Science Foundation of
   China (81560385, 81972663), Key Scientific Research Projects of
   Institutions of Higher Education in Henan Province (19A310024), The
   Medical Scientific and Technological Research Project of Henan Province
   (201702027), The China Postdoctoral Science Foundation (2019 T120648,
   2017 M610462), The National Natural Science Foundation of Henan Province
   (182300410342), The Health Commission Technology Talents Overseas
   Training Project of Henan Province (2018140) and The Key Scientific
   Research Project of Henan Higher Education Institutions (20A310024).
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NR 49
TC 60
Z9 61
U1 2
U2 28
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1756-9966
J9 J EXP CLIN CANC RES
JI J. Exp. Clin. Cancer Res.
PD DEC 20
PY 2020
VL 39
IS 1
AR 250
DI 10.1186/s13046-020-01705-9
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OT8QF
UT WOS:000591103500001
PM 33218358
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Zheng, BH
   He, ZX
   Zhang, J
   Ma, JJ
   Zhang, HW
   Zhu, W
   Shao, ZM
   Ni, XJ
AF Zheng, Bo-Hao
   He, Zhi-Xian
   Zhang, Juan
   Ma, Jing-Jing
   Zhang, Hong-Wei
   Zhu, Wei
   Shao, Zhi-Min
   Ni, Xiao-Jian
TI The Biological Function of TUSC7/miR-1224-3p Axis in Triple-Negative
   Breast Cancer
SO CANCER MANAGEMENT AND RESEARCH
LA English
DT Article
ID NONCODING RNAS; TUMOR-SUPPRESSOR; GENE-EXPRESSION; LNCRNA; P53;
   TRANSCRIPTION; LOC285194; PATTERNS; REVEAL; MAPS
AB Background: Triple-negative breast cancers (TNBC), comprising about 20% of breast cancers, have a poor prognosis. Currently, there is no effective target therapy for TNBC. LncRNA TUSC7 has been identified as a tumor suppressor in osteosarcoma and colorectal cancer. In this study, we investigated the clinical significance and the biological function of TUSC7 in breast cancer. Methods: We retrospectively evaluated the expression level and clinical significance of TUSC7 in 90 paired breast cancer tissues and normal tissues. The proliferation, migration, and invasion assays were performed to investigate the biological function of TUSC7 in breast cancer. Finally, microarray, a luciferase reporter assay, and quantitative real-time polymerase chain reaction (qPCR) were used to explore the potential underlying mechanism of tumor suppressor role of TUSC7. Results: Low TUSC7 expression was found to be an independent prognostic factor of poor overall survival (OS) in TNBC patients. Ectopic expression of TUSC7 inhibited tumor cell growth both in vitro and in vivo. TUSC7 overexpression significantly promoted the sensitivity of MDA-MB-468 cells to paclitaxel and carboplatin. In terms of the mechanism, TUSC7 might perform its biological function through binding with miR-1224-3P and regulating its expression level. Besides, genes in cell cycle pathways, such as BUB3 (budding uninhibited by benzimidazoles 3) and TGF-ss (targeting transforming growth factor beta) pathways were downregulated, and genes involved in the MAPK (mitogen-activated protein kinase) (TGFBR2, transforming growth factor-beta receptor 2), PI3K-AKT (phosphoinositide 3-kinase-AKT serine/threonine kinase 1) and NF-kappa B (nuclear factor-kappa B subunit) pathways were upregulated in TUSC7 knockdown MDA-MB-231 cells. Conclusion: The low TUSC7 expression is an independent prognostic factor of poor OS of TNBC patients. TUSC7 might inhibit breast cancer cell growth and metastasis both in vitro and vivo through binding with miR-1224-3P and regulating MAPK, PI3K/AKT, and NF-kappa B signaling pathways.
C1 [Zheng, Bo-Hao; Zhang, Hong-Wei; Zhu, Wei; Ni, Xiao-Jian] Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Shanghai 200032, Peoples R China.
   [Zheng, Bo-Hao; Zhang, Hong-Wei; Zhu, Wei; Ni, Xiao-Jian] Fudan Univ, Zhongshan Hosp, Canc Ctr, Shanghai 200032, Peoples R China.
   [He, Zhi-Xian] Nantong Univ, Affiliated Hosp, Dept Gen Surg, Nantong 226001, Peoples R China.
   [Zhang, Juan] Fudan Univ, Zhongshan Hosp, Liver Canc Inst, Key Lab Carcinogenesis & Canc Invas,Minist Educ, Shanghai 200032, Peoples R China.
   [Ma, Jing-Jing] Nanjing Med Univ, Nanjing Matern & Child Hlth Care Hosp, Dept Breast Surg, State Key Lab Reprod Med, Nanjing 210004, Peoples R China.
   [Shao, Zhi-Min] Fudan Univ, Dept Breast Surg, Key Lab Breast Canc Shanghai, Ctr Canc, Shanghai 200032, Peoples R China.
   [Shao, Zhi-Min] Fudan Univ, Inst Canc, Shanghai 200032, Peoples R China.
C3 Fudan University; Fudan University; Nantong University; Fudan
   University; Nanjing Medical University; Fudan University; Fudan
   University
RP Ni, XJ (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Shanghai 200032, Peoples R China.; Shao, ZM (corresponding author), Fudan Univ, Dept Breast Surg, Key Lab Breast Canc Shanghai, Ctr Canc, Shanghai 200032, Peoples R China.; Shao, ZM (corresponding author), Fudan Univ, Inst Canc, Shanghai 200032, Peoples R China.
EM shaozhimingfd@163.com; ni.xiaojian@zs-hospital.sh.cn
RI Zhang, Hw/HPD-4999-2023; 郑, 博豪/JXM-7394-2024
OI Zheng, Bohao/0000-0003-0934-8209
FU National Natural Science Foundation of China [81902687, 81702586]; 2016
   Zhongshan Hospital, Fudan University, Qingnian Funds [2016ZSQN59];
   Shanghai key clinical medical center and construction of key disciplines
FX The study was supported by grants from the National Natural Science
   Foundation of China (81702586); the National Natural Science Foundation
   of China (81902687); and the 2016 Zhongshan Hospital, Fudan University,
   Qingnian Funds (2016ZSQN59); and Shanghai key clinical medical center
   and construction of key disciplines.
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NR 35
TC 7
Z9 7
U1 0
U2 7
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1179-1322
J9 CANCER MANAG RES
JI Cancer Manag. Res.
PY 2021
VL 13
BP 5763
EP 5774
DI 10.2147/CMAR.S305865
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TK8ID
UT WOS:000674396000006
PM 34305410
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU de Ridder, JAM
   van der Stok, EP
   Mekenkamp, LJ
   Wiering, B
   Koopman, M
   Punt, CJA
   Verhoef, C
   de Wilt, JH
AF de Ridder, Jannemarie A. M.
   van der Stok, Eric P.
   Mekenkamp, Leonie J.
   Wiering, Bastiaan
   Koopman, Miriam
   Punt, Cornelis J. A.
   Verhoef, Cornelis
   de Wilt, Johannes H.
TI Management of liver metastases in colorectal cancer patients: A
   retrospective case-control study of systemic therapy versus liver
   resection
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Colorectal liver metastases; Survival; Treatment; Surgical treatment;
   Liver resection; Systemic therapy
ID CLINICAL RISK SCORE; LONG-TERM SURVIVAL; HEPATIC RESECTION; NEOADJUVANT
   CHEMOTHERAPY; TREATMENT STRATEGIES; PROGNOSTIC-FACTORS; DECISION-MAKING;
   PHASE-III; BEVACIZUMAB; SURGERY
AB Objective: To evaluate and compare the overall survival (OS) in case-matched patient groups treated either with systemic therapy or surgery for colorectal liver metastases (CRLM).
   Methods: Patients with CRLM, without extra-hepatic disease, treated with chemotherapy with or without targeted therapy in two phase III studies (n = 480) were selected and case-matched to patients who underwent liver resection (n = 632). Matching criteria were sex, age, established prognostic factors for survival (clinical risk score). Available computed tomography (CT)-scans of patients treated with systemic therapies were reviewed by three independent liver surgeons for resectability. Survival was compared between patients with resectable CRLM (based on CT-scan review) who were treated with systemic therapy versus patients who underwent liver resection.
   Results: A total of 96 patients treated with systemic therapy were included. Pre-treatment CT-scans of the liver were available for review in 56 of the systemically treated patients, and metastases were unanimously considered resectable in 36 patients (64.3%) (complex resectable: n = 25; 69%). These 36 patients were case-matched with 36 patients who underwent liver resection (wedge resection or segmentectomy: n = 26; 72%). Median OS in the patient group treated with systemic therapy was 26.5 months (range 0-81 months), which was significantly lower than that in case-matched patients who underwent liver resection (median OS 56 months; range 6-116) (p = 0.027).
   Conclusions: In this case-matched control study, surgery provided superior OS rates compared to systemic therapy for CRLM. Resection of CRLM should always be considered, preferably in a dedicated liver centre, since not all patients that qualify for resection are identified as such. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [de Ridder, Jannemarie A. M.; de Wilt, Johannes H.] Radboud Univ Nijmegen, Med Ctr, Dept Surg Oncol, Nijmegen, Netherlands.
   [van der Stok, Eric P.; Verhoef, Cornelis] Erasmus MC Canc Inst, Dept Surg Oncol, Rotterdam, Netherlands.
   [Mekenkamp, Leonie J.; Punt, Cornelis J. A.] Univ Amsterdam, Acad Med Ctr, Dept Med Oncol, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.
   [Wiering, Bastiaan] Slingeland Hosp, Dept Surg, Doetinchem, Netherlands.
   [Koopman, Miriam] Univ Med Ctr Utrecht, Dept Med Oncol, Utrecht, Netherlands.
C3 Radboud University Nijmegen; Erasmus University Rotterdam; Erasmus MC;
   Erasmus MC Cancer Institute; University of Amsterdam; Utrecht
   University; Utrecht University Medical Center
RP de Ridder, JAM (corresponding author), Radboud Univ Nijmegen, Med Ctr, Dept Surg, POB 9101, NL-6500 HB Nijmegen, Netherlands.
EM jannemarie.deridder@radboudumc.nl
RI Wilt, J.H.W./H-8121-2014; van der Stok, Eric/GYD-6548-2022; Verhoef,
   Cornelis/ABD-3648-2020
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NR 43
TC 52
Z9 53
U1 0
U2 5
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 MAY
PY 2016
VL 59
BP 13
EP 21
DI 10.1016/j.ejca.2016.02.003
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DK7WT
UT WOS:000375138200002
PM 26994469
DA 2025-01-04
ER

PT J
AU Alburquerque-González, B
   López-Calderón, FF
   López-Abellán, MD
   Esteban-Gil, A
   García-Solano, J
   Conesa-Zamora, P
AF Alburquerque-Gonzalez, Begona
   Lopez-Calderon, Fernando F.
   Dolores Lopez-Abellan, Maria
   Esteban-Gil, Angel
   Garcia-Solano, Jose
   Conesa-Zamora, Pablo
TI Biology and Therapeutic Targets of Colorectal Serrated Adenocarcinoma;
   Clues for a Histologically Based Treatment against an Aggressive Tumor
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colorectal cancer; serrated adenocarcinoma; angiogenesis; immune
   response; invasive front; molecular targets
ID REPAIR PROTEIN EXPRESSION; BETA-CATENIN; COLON-CANCER;
   ENDOTHELIAL-CELLS; DENDRITIC CELLS; IMMUNE CELLS; E-CADHERIN; BRAF;
   ANGIOGENESIS; PROGRESSION
AB Serrated adenocarcinoma (SAC) is a tumor recognized by the WHO as a histological subtype accounting for around 9% of colorectal carcinomas. Compared to conventional carcinomas, SACs are characterized by a worse prognosis, weak development of the immune response, an active invasive front and a frequent resistance to targeted therapy due to a high occurrence of KRAS or BRAF mutation. Nonetheless, several high-throughput studies have recently been carried out unveiling the biology of this cancer and identifying potential molecular targets, favoring a future histologically based treatment. This review revises the current evidence, aiming to propose potential molecular targets and specific treatments for this aggressive tumor.
C1 [Alburquerque-Gonzalez, Begona; Lopez-Calderon, Fernando F.; Garcia-Solano, Jose; Conesa-Zamora, Pablo] Univ Catolica Murcia UCAM, Fac Life Sci, Dept Histol & Pathol, Murcia 30107, Spain.
   [Alburquerque-Gonzalez, Begona; Lopez-Calderon, Fernando F.; Garcia-Solano, Jose] Santa Lucia Gen Univ Hosp HGUSL, Dept Pathol, Calle Mezquita SN, Cartagena 30202, Spain.
   [Dolores Lopez-Abellan, Maria; Conesa-Zamora, Pablo] Santa Lucia Gen Univ Hosp HGUSL, Dept Clin Anal, Calle Mezquita SN, Cartagena 30202, Spain.
   [Esteban-Gil, Angel] Fdn Healthcare Training & Res Reg Murcia FFIS, Inst Biomed Res Murcia IMIB, Biomed Informat & Bioinformat Platform, Murcia 30003, Spain.
   [Garcia-Solano, Jose; Conesa-Zamora, Pablo] Inst Biomed Res Murcia IMIB, Res Grp Mol Pathol & Pharmacogenet, Calle Mezquita SN, Cartagena 30202, Spain.
C3 Universidad Catolica de Murcia
RP Conesa-Zamora, P (corresponding author), Univ Catolica Murcia UCAM, Fac Life Sci, Dept Histol & Pathol, Murcia 30107, Spain.; Conesa-Zamora, P (corresponding author), Santa Lucia Gen Univ Hosp HGUSL, Dept Clin Anal, Calle Mezquita SN, Cartagena 30202, Spain.; Conesa-Zamora, P (corresponding author), Inst Biomed Res Murcia IMIB, Res Grp Mol Pathol & Pharmacogenet, Calle Mezquita SN, Cartagena 30202, Spain.
EM begoalbur@gmail.com; davolef@gmail.com;
   mariadolores.lopezabellan@outlook.es; angel.esteban@ffis.es;
   jgarcia652@ucam.edu; pablo.conesa@carm.es
RI Alburquerque González, Begoña/HKW-3633-2023
OI Conesa-Zamora, Pablo/0000-0003-0190-3044; Alburquerque Gonzalez,
   Begona/0000-0003-3413-5889; Esteban Gil, Angel/0000-0002-9777-1906
FU UCAM [FPI05-UCAM/17]; Junta Provincial Murcia Predoctoral Asociacion
   Espanola Contra el Cancer (AECC) [PRDMU19002]; Instituto de Salud Carlos
   III (Spanish Ministry of Health); FEDER [PI15/00626, PI18/00144]
FX B.A.-G. and F.F.L.-C. belong to the Programa de Doctorado en Ciencias de
   la Salud from the Catholic University of Murcia (UCAM). B.A.-G. holds a
   predoctoral grant from UCAM (FPI05-UCAM/17). F.F.L.-C. was supported by
   the Junta Provincial Murcia Predoctoral Asociacion Espanola Contra el
   Cancer (AECC) (ref: PRDMU19002) grant. This work has been funded by
   Instituto de Salud Carlos III (Spanish Ministry of Health) and FEDER
   funds (refs: PI15/00626 and PI18/00144).
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NR 117
TC 7
Z9 7
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD MAR
PY 2020
VL 21
IS 6
AR 1991
DI 10.3390/ijms21061991
PG 19
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA LJ0UU
UT WOS:000529890200087
PM 32183342
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Brar, B
   Ranjan, K
   Palria, A
   Kumar, R
   Ghosh, M
   Sihag, S
   Minakshi, P
AF Brar, Basanti
   Ranjan, Koushlesh
   Palria, Ankur
   Kumar, Rajesh
   Ghosh, Mayukh
   Sihag, Sweety
   Minakshi, Prasad
TI Nanotechnology in Colorectal Cancer for Precision Diagnosis and Therapy
SO FRONTIERS IN NANOTECHNOLOGY
LA English
DT Review
DE colorectal cancer; nanotechnology; detection; treatment; targeted
   therapy
AB Colorectal cancer (CRC) is the third most frequently occurring tumor in the human population. CRCs are usually adenocarcinomatous and originate as a polyp on the inner wall of the colon or rectum which may become malignant in the due course of time. Although the therapeutic options of CRC are limited, the early diagnosis of CRC may play an important role in preventive and therapeutic interventions to decrease the mortality rate. The CRC-affected tissues exhibit several molecular markers that may be exploited as the novel strategy to develop newer approaches for the treatment of the disease. Nanotechnology consists of a wide array of innovative and astonishing nanomaterials with both diagnostics and therapeutic potential. Several nanomaterials and nano formulations such as Carbon nanotubes, Dendrimer, Liposomes, Silica Nanoparticles, Gold nanoparticles, Metal-organic frameworks, Core-shell polymeric nano-formulations, Nano-emulsion System, etc can be used to targeted anticancer drug delivery and diagnostic purposes in CRC. The light-sensitive photosensitizer drugs loaded gold and silica nanoparticles can be used to diagnose as well as the killing of CRC cells by the targeted delivery of anticancer drugs to cancer cells. This review is focused on the recent advancement of nanotechnology in the diagnosis and treatment of CRC.
C1 [Brar, Basanti] CCS Haryana Agr Univ, Biofertilizer Prod Unit, HABITAT, GIPPCL, Hisar, India.
   [Ranjan, Koushlesh] Sardar Vallabhbhai Patel Univ Agr & Technol, Dept Vet Physiol & Biochem, Meerut, India.
   [Palria, Ankur] Chaudhary Bansi Lal Univ, Dept Zool, Bhiwani, India.
   [Kumar, Rajesh] Lala Lajpat Rai Univ Vet & Anim Sci, Dept Vet Physiol & Biochem, Hisar, India.
   [Ghosh, Mayukh] Banaras Hindu Univ, Dept Vet Physiol & Biochem, RGSC, Varanasi, India.
   [Sihag, Sweety] CCS Haryana Agr Univ, Dept Chem & Biochem, Hisar, India.
   [Minakshi, Prasad] Lala Lajpat Rai Univ Vet & Anim Sci, Dept Anim Biotechnol, Hisar, India.
C3 CCS Haryana Agricultural University; Sardar Vallabhbhai Patel University
   of Agriculture & Technology; Lala Lajpat Rai University of Veterinary &
   Animal Sciences; Banaras Hindu University (BHU); CCS Haryana
   Agricultural University; Lala Lajpat Rai University of Veterinary &
   Animal Sciences
RP Brar, B (corresponding author), CCS Haryana Agr Univ, Biofertilizer Prod Unit, HABITAT, GIPPCL, Hisar, India.; Minakshi, P (corresponding author), Lala Lajpat Rai Univ Vet & Anim Sci, Dept Anim Biotechnol, Hisar, India.
EM basantibrar@gmail.com; minakshi.abt@luvas.edu.in
RI Ranjan, Koushlesh/V-6683-2019; Brar, Basanti/JFL-0154-2023
OI Ranjan, Dr. Koushlesh/0000-0003-3238-8057; kumar,
   Rajesh/0000-0003-4586-1923; Kumari, Ankur/0000-0003-2136-7437
NR 0
TC 43
Z9 43
U1 3
U2 7
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2673-3013
J9 FRONT NANOTECHNOL
JI Front. Nanotechnol.
PD SEP 16
PY 2021
VL 3
AR 699266
DI 10.3389/fnano.2021.699266
PG 21
WC Nanoscience & Nanotechnology; Materials Science, Multidisciplinary
WE Emerging Sources Citation Index (ESCI)
SC Science & Technology - Other Topics; Materials Science
GA G7ME0
UT WOS:000990947200001
OA gold
DA 2025-01-04
ER

PT J
AU Wang, Y
   Zhao, T
   Huang, CY
   Liu, F
   Zhang, Y
   Kong, DS
   Fan, ZM
AF Wang, Yi
   Zhao, Tong
   Huang, Chuyue
   Liu, Fei
   Zhang, Yang
   Kong, Desong
   Fan, Zhimin
TI Effect and mechanism of Banxia Xiexin decoction in colorectal cancer: A
   network pharmacology approach
SO PHYTOMEDICINE
LA English
DT Article
DE Banxia Xiexin decoction; Colorectal cancer; Network pharmacology;
   PI3K/AKT/mTOR
ID PI3K/MTOR INHIBITOR; AUTOPHAGY
AB Background: Banxia Xiexin decoction (BXD) is a traditional Chinese medicine with anti-colorectal cancer (CRC) activity. However, its bioactive constituents and its mechanism of action remain unclear. Herein, we explored the mechanism of action of BXD against CRC using a network pharmacology approach.
   Methods: First, the targets of the main chemical components of BXD were predicted and collected through a database, and the intersection of compound targets and disease targets was obtained. Subsequently, protein-protein interaction network analysis, Gene Ontology enrichment, and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis were performed to explore the potential mechanisms underlying the effects of BXD on CRC. Finally, a CRC cell model and a CRC xenograft model in nude mice were utilized to further determine the mechanism of action.
   Results: A compound-therapeutic target network of BXD was constructed, revealing 146 cellular targets of BXD. The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling axis was identified as the main target of BXD. Using in vitro and in vivo models, the activity of BXD against CRC was found to be mediated through ferritinophagy by targeting the PI3K/AKT/mTOR axis, leading to intracellular iron accumulation, reactive oxygen species activation, and finally ferroptosis.
   Conclusions: Through the application of network pharmacology and in vitro/in vivo validation experiments, we discovered that BXD exerts anti-CRC effects via the ferritinophagy pathway. Furthermore, we elucidated the potential mechanism underlying its induction of ferritinophagy. These findings demonstrate the significant potential of traditional drugs in managing CRC and support their wider clinical application in combination chemotherapy, targeted therapy, and immunotherapy.
C1 [Wang, Yi; Liu, Fei; Zhang, Yang; Fan, Zhimin] Nanjing Univ Chinese Med, Colon & Rectal Surg, Nanjing Hosp Chinese Med, Nanjing 210022, Peoples R China.
   [Zhao, Tong] Nanjing Univ Chinese Med, Sch Chinese Med, Sch Integrated Chinese & Western Med, Nanjing 210023, Peoples R China.
   [Kong, Desong] Nanjing Univ Chinese Med, Nanjing Hosp Chinese Med, Chinese Med Modernizat & Big Data Res Ctr, Nanjing 210022, Peoples R China.
   [Huang, Chuyue; Kong, Desong; Fan, Zhimin] Nanjing Univ Chinese Med, Jiangsu Clin Innovat Ctr Anorectal Dis TCM, Nanjing Hosp Chinese Med, Nanjing 210022, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University of Chinese
   Medicine; Nanjing University of Chinese Medicine; Nanjing University of
   Chinese Medicine
RP Zhang, Y; Fan, ZM (corresponding author), Nanjing Univ Chinese Med, Colon & Rectal Surg, Nanjing Hosp Chinese Med, Nanjing 210022, Peoples R China.; Kong, DS (corresponding author), Nanjing Univ Chinese Med, Nanjing Hosp Chinese Med, Chinese Med Modernizat & Big Data Res Ctr, Nanjing 210022, Peoples R China.; Kong, DS; Fan, ZM (corresponding author), Nanjing Univ Chinese Med, Jiangsu Clin Innovat Ctr Anorectal Dis TCM, Nanjing Hosp Chinese Med, Nanjing 210022, Peoples R China.
EM 21670235@qq.com; kongds@njucm.edu.cn; fanzm711@163.com
RI huang, chuyue/JKH-8373-2023
FU Science and Technology Innovation Project for Overseas Students in
   Nanjing 2020 [WY2020190]; Nanjing Chinese Medicine Young Talents
   Training Program [NJSZYYQNRC-2020-WY2]; Training Plan of Clinical
   Medical Research Center Jointly Built by Ministry and Province in
   Nanjing [GCYJZX-2019]; Jiangsu provincial key research and development
   program [BE2021611]
FX This research was funded by the "Science and Technology Innovation
   Project for Overseas Students in Nanjing 2020, grant number WY2020190,"
   the "Nanjing Chinese Medicine Young Talents Training Program, grant
   number NJSZYYQNRC-2020-WY2," the "Training Plan of Clinical Medical
   Research Center Jointly Built by Ministry and Province in Nanjing, grant
   number GCYJZX-2019," and the "Jiangsu provincial key research and
   development program, grant number BE2021611".
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NR 35
TC 7
Z9 7
U1 22
U2 45
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0944-7113
EI 1618-095X
J9 PHYTOMEDICINE
JI Phytomedicine
PD JAN
PY 2024
VL 123
AR 155174
DI 10.1016/j.phymed.2023.155174
EA NOV 2023
PG 12
WC Plant Sciences; Chemistry, Medicinal; Integrative & Complementary
   Medicine; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Pharmacology & Pharmacy; Integrative & Complementary
   Medicine
GA CW4Q4
UT WOS:001128262500001
PM 38039904
OA hybrid
DA 2025-01-04
ER

PT J
AU Koldenhof, JJ
   Langenberg, MHG
   Witteveen, PO
   Teunissen, SCCM
AF Koldenhof, J. J.
   Langenberg, M. H. G.
   Witteveen, P. O.
   Teunissen, S. C. C. M.
TI Patient-reported symptoms and stepwise symptom management in patients on
   epidermal growth factor inhibitors: A retrospective, descriptive cohort
   study
SO EUROPEAN JOURNAL OF CANCER CARE
LA English
DT Article
DE cancer; EGFR inhibitor; patient reported outcome; symptom management;
   symptom monitoring; targeted therapy
ID FACTOR RECEPTOR INHIBITORS; METASTATIC COLORECTAL-CANCER;
   QUALITY-OF-LIFE; PHASE-II TRIAL; SKIN TOXICITY; DERMATOLOGICAL
   TOXICITIES; ASSESSMENT SYSTEM; NECK-CANCER; CETUXIMAB; THERAPY
AB Adverse events (AEs) of epidermal growth factor inhibitors (EGFRi) influence well-being with a risk to dose modifications (DMs). Hereby, clinical benefit of treatment might be affected. This retrospective cohort study was set up to gain insight into the suitability and added value of a patient-reported outcome measurement tool (PROM), together with a stepwise intervention management plan for EGFRi-related AEs in daily practice. The primary objective was to gain insight into total treatment duration and DMs, and the secondary objective to gain insight into patient-reported symptoms and well-being as well as healthcare professional-reported AEs. Sixty-eight patients on cetuximab and 19 on panitumumab treatment were included for analysis; 69% had squamous cell carcinoma of head and neck (SCCHN) and 26% metastatic colorectal carcinoma. DMs due to AEs occurred in 39% of the patients and dose discontinuations in 22%. Especially anorexia, dysphagia, oral pain and skin changes led to a decreased well-being. In patients on EGFRi, application of PROMs together with a stepwise symptom management plan enhances early recognition of symptom burden, pro-active symptom management and effect evaluation of interventions performed whereby well-being recovers. Since only SCCHN patients discontinued treatment due to AEs, patient-centred care focused on radiotherapy-related AEs, creates opportunities for amelioration.
C1 [Koldenhof, J. J.; Langenberg, M. H. G.] Univ Med Ctr Utrecht, Dept Med Oncol, Ctr Canc, Utrecht, Netherlands.
   [Witteveen, P. O.] Univ Med Ctr Utrecht, Dept Med Oncol, Ctr Canc, Med Oncol, Utrecht, Netherlands.
   [Teunissen, S. C. C. M.] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Dept Primary Care, Hosp Care Palliat Care, Utrecht, Netherlands.
C3 Utrecht University; Utrecht University Medical Center; Utrecht
   University; Utrecht University Medical Center; Utrecht University;
   Utrecht University Medical Center
RP Koldenhof, JJ (corresponding author), Univ Med Ctr Utrecht, Dept Med Oncol, Ctr Canc, Utrecht, Netherlands.
EM j.koldenhof@umcutrecht.nl
OI Teunissen, Charlotte/0000-0002-4061-0837; Teunissen,
   Saskia/0000-0001-8827-461X
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NR 35
TC 3
Z9 3
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0961-5423
EI 1365-2354
J9 EUR J CANCER CARE
JI Eur. J. Cancer Care
PD MAR
PY 2018
VL 27
IS 2
AR e12800
DI 10.1111/ecc.12800
PG 13
WC Oncology; Health Care Sciences & Services; Nursing; Rehabilitation
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Oncology; Health Care Sciences & Services; Nursing; Rehabilitation
GA GA4SH
UT WOS:000428321300037
PM 29314360
OA gold
DA 2025-01-04
ER

PT J
AU Choi, JH
   Jang, TY
   Jeon, SE
   Kim, JH
   Lee, CJ
   Yun, HJ
   Jung, JY
   Park, SY
   Nam, JS
AF Choi, Jang-Hyun
   Jang, Tae-Young
   Jeon, So-El
   Kim, Jee-Heun
   Lee, Choong-Jae
   Yun, Hyeon-Ji
   Jung, Ji-Youn
   Park, So-Yeon
   Nam, Jeong-Seok
TI The Small-Molecule Wnt Inhibitor ICG-001 Efficiently Inhibits Colorectal
   Cancer Stemness and Metastasis by Suppressing MEIS1 Expression
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE colorectal cancer; cancer stem-like cells; metastasis; Wnt; ICG-001;
   MEIS1
ID CELLS; GROWTH
AB Recurrence and metastasis remain major obstacles in colorectal cancer (CRC) treatment. Recent studies suggest that a small subpopulation of cells with a self-renewal ability, called cancer stem-like cells (CSCs), promotes recurrence and metastasis in CRC. Unfortunately, no CSC inhibitor has been demonstrated to be more effective than existing chemotherapeutic drugs, resulting in a significant unmet need for effective CRC therapies. In this study, transcriptomic profiling of metastatic tumors from CRC patients revealed significant upregulation in the Wnt pathway and stemness genes. Thus, we examined the therapeutic effect of the small-molecule Wnt inhibitor ICG-001 on cancer stemness and metastasis. The ICG-001 treatment efficiently attenuated self-renewal activity and metastatic potential. Mechanistically, myeloid ecotropic viral insertion site 1 (MEIS1) was identified as a target gene of ICG-001 that is transcriptionally regulated by Wnt signaling. A series of functional analyses revealed that MEIS1 enhanced the CSC behavior and metastatic potential of the CRC cells. Collectively, our findings suggest that ICG-001 efficiently inhibits CRC stemness and metastasis by suppressing MEIS1 expression. These results provide a basis for the further clinical investigation of ICG-001 as a targeted therapy for CSCs, opening a new avenue for the development of novel Wnt inhibitors for the treatment of CRC metastasis.
C1 [Choi, Jang-Hyun; Jang, Tae-Young; Jeon, So-El; Kim, Jee-Heun; Lee, Choong-Jae; Yun, Hyeon-Ji; Park, So-Yeon; Nam, Jeong-Seok] Gwangju Inst Sci & Technol, Sch Life Sci, Gwangju 61005, South Korea.
   [Jung, Ji-Youn] Kongju Natl Univ, Dept Compan & Lab Anim Sci, Gongju 32439, South Korea.
   [Park, So-Yeon; Nam, Jeong-Seok] Gwangju Inst Sci & Technol, Cell Logist Res Ctr, Gwangju 61005, South Korea.
C3 Gwangju Institute of Science & Technology (GIST); Kongju National
   University; Gwangju Institute of Science & Technology (GIST)
RP Park, SY; Nam, JS (corresponding author), Gwangju Inst Sci & Technol, Sch Life Sci, Gwangju 61005, South Korea.; Park, SY; Nam, JS (corresponding author), Gwangju Inst Sci & Technol, Cell Logist Res Ctr, Gwangju 61005, South Korea.
EM wkdgus1216@gist.ac.kr; gistjty1300@gm.gist.ac.kr;
   thdpf8939@gm.gist.ac.kr; jeeheun.kim@gist.ac.kr; cjlee7847@gist.ac.kr;
   hyeon1540@gm.gist.ac.kr; wangza@kongju.ac.kr; sypark0125@gist.ac.kr;
   namje@gist.ac.kr
RI Park, So-Yeon/ABC-4767-2021; Lee, Choong/AAD-9230-2020; Kim,
   Jee-Heun/ABC-7132-2021; Choi, Jang-Hyun/JGE-1924-2023
OI Nam, Jeong-Seok/0000-0001-9753-6095; JUNG, JI-YOUN/0000-0002-8153-4455;
   Park, So-Yeon/0000-0002-5749-3120; Kim, Jee-Heun/0000-0002-4619-3966
FU National Research Foundation of Korea through the Korean government
   (Ministry of Science, ICT and Future Planning)
   [NRF-2020R1A2B5B-03094382, 2020R1C1C1010758]; Cell Logistics Research
   Center of the National Research Foundation of Korea
   [NRF-2016R1A5A1007318]; "GIST Research Institute (GRI) IIBR" - GIST in
   2021; GIST Young Scientist Research Project - GIST in 2021
FX This work was supported by the National Research Foundation of Korea
   through grants funded by the Korean government (Ministry of Science, ICT
   and Future Planning; NRF-2020R1A2B5B-03094382, 2020R1C1C1010758), by a
   grant from the Cell Logistics Research Center of the National Research
   Foundation of Korea (NRF-2016R1A5A1007318), by a "GIST Research
   Institute (GRI) IIBR" grant funded by the GIST in 2021, and by the GIST
   Young Scientist Research Project grant funded by the GIST in 2021.
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NR 31
TC 12
Z9 14
U1 0
U2 5
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 2021
VL 22
IS 24
AR 13413
DI 10.3390/ijms222413413
PG 10
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA YA8BL
UT WOS:000738551800001
PM 34948208
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Sperti, C
   Merigliano, S
   Moletta, L
AF Sperti, C.
   Merigliano, S.
   Moletta, L.
TI Metastatic pancreatic tumors: what is the optimal treatment?
SO MINERVA CHIRURGICA
LA English
DT Review
DE Neoplasm metastasis; Pancreas; Pancreatic neoplasms; Pancreatectomy;
   Carcinoma, renal cell
ID RENAL-CELL CARCINOMA; SINGLE-CENTER-EXPERIENCE; LONG-TERM SURVIVAL;
   PHASE-III TRIAL; PROGNOSTIC-FACTORS; INTERFERON-ALPHA; BREAST-CANCER;
   OBSTRUCTIVE-JAUNDICE; COLORECTAL-CANCER; RECTAL-CANCER
AB Although rare, metastases to the pancreas from other primary tumors are increasingly recognized in clinical practice, but the optimal treatment remains unclear. When a careful staging is performed and widespread disease is excluded, the indication of pancreatectomy may arise. This study was designated to review the published literature on the results of surgical treatment for the most common malignancies metastasizing to the pancreas. Analysis of the reports show that resection can be performed safely, but long term survival is substantially influenced by the tumor's biology. There are convincing evidences that pancreatic resection for metastasis from renal cell cancer may offer excellent results in term of prolonged survival, while for other type of cancer, pancreatic resection should be considered only a palliative procedure, with only anedoctical reported long-term survivors. So, comparison of the results of surgical and non-surgical management of metastatic tumors to the pancreas is very difficult to perform. There is a need of studies evaluating the role of chemotherapy in the neoadjuvant setting or the best sequential use of multimodality treatment (targeted therapy, radiotherapy, surgery, etc.). At the moment, pancreatic resection for metastasis should be reserved to patients in good health conditions, with isolated disease from renal cell cancer. For other types of tumor, surgery should be performed only in individual basis.
C1 [Sperti, C.; Merigliano, S.; Moletta, L.] Univ Padua, Dept Surg Oncol & Gastroenterol, Surg Clin 3, Padua, Italy.
C3 University of Padua
RP Sperti, C (corresponding author), 3rd Surg Clin, Dept Surg Oncol & Gastroenterol, Via Giustiniani 2, I-35128 Padua, Italy.
EM csperti@libero.it
RI Merigliano, Stefano/AAY-3023-2021; Moletta, Lucia/ABD-7200-2020
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NR 85
TC 3
Z9 3
U1 0
U2 2
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 APR
PY 2015
VL 70
IS 2
BP 131
EP 139
PG 9
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA CI6ZB
UT WOS:000354911600008
PM 25645113
DA 2025-01-04
ER

PT J
AU Kim, N
   Cho, D
   Kim, H
   Kim, S
   Cha, YJ
   Greulich, H
   Bass, A
   Cho, HS
   Cho, J
AF Kim, Nayoung
   Cho, Daseul
   Kim, Hyunjin
   Kim, Sujin
   Cha, Young-je
   Greulich, Heidi
   Bass, Adam
   Cho, Hyun-Soo
   Cho, Jeonghee
TI Colorectal adenocarcinoma-derived EGFR mutants are oncogenic and
   sensitive to EGFR-targeted monoclonal antibodies, cetuximab and
   panitumumab
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE epidermal growth factor receptor (EGFR); cetuximab (Erbitux);
   panitumumab; colon cancer; EGFR mutation; receptor dimerization;
   targeted therapy
ID GROWTH-FACTOR RECEPTOR; LUNG-CANCER; ASYMMETRIC DIMERIZATION;
   ACQUIRED-RESISTANCE; KRAS MUTATIONS; THERAPY; CELLS
AB Somatic mutations of epidermal growth factor receptor (EGFR) occur in similar to 3% of colorectal cancer (CRC) patients. Here, through systematic functional screening of 21 recurrent EGFR mutations selected from public data sets, we show that 11 colon cancer-derived EGFR mutants (G63R, E114K, R165Q, R222C, S492R, P596L, K708R, E709K, G719S, G724S and L858R) are oncogenic and able to transform cells in a ligand-independent manner. We demonstrate that cellular transformation by these mutants requires receptor dimerization. Importantly, the EGF-induced and constitutive oncogenic potential of these EGFR mutants are inhibited by cetuximab or panitumumab in vivo and in vitro. Taken together, we propose that a subset of EGFR mutations can serve as genomic predictors for response to anti-EGFR antibodies and that metastatic CRC patients with such mutations may benefit from these drugs as part of the first-line therapy.
C1 [Kim, Nayoung; Cho, Daseul; Kim, Hyunjin; Kim, Sujin; Cho, Jeonghee] Dankook Univ, Dept Nanobiomed Sci, 119 Dandae Ro, Cheonan 31116, South Korea.
   [Kim, Nayoung] Sungkyunkwan Univ, Dept Hlth Sci & Technol, SAIHST, Seoul, South Korea.
   [Cha, Young-je; Cho, Hyun-Soo] Yonsei Univ, Dept Syst Biol, Coll Life Sci & Biotechnol, Seoul, South Korea.
   [Greulich, Heidi] Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.
   [Greulich, Heidi; Bass, Adam] Dana Farber Canc Inst, Div Mol & Cellular Oncol, Boston, MA 02115 USA.
C3 Dankook University; Sungkyunkwan University (SKKU); Yonsei University;
   Harvard University; Massachusetts Institute of Technology (MIT); Broad
   Institute; Harvard University; Dana-Farber Cancer Institute
RP Cho, J (corresponding author), Dankook Univ, Dept Nanobiomed Sci, 119 Dandae Ro, Cheonan 31116, South Korea.
EM jeonghee.cho@dankook.ac.kr
OI Cho, Jeonghee/0000-0003-4422-6266
FU Korea Health Technology R&D Project through the Korea Health Industry
   Development Institute (KHIDI) - Ministry of Health & Welfare, Republic
   of Korea [HI15C2353]; National Research Foundation of Korea (NRF) -
   Korea government (MEST) [2016R1A2B2011100]
FX The authors would like to thank to Joshua Francis for constructive
   criticism of the manuscript. This work was in part supported by the
   Korea Health Technology R&D Project through the Korea Health Industry
   Development Institute (KHIDI), funded by the Ministry of Health &
   Welfare, Republic of Korea (HI15C2353; J.C.) and by the National
   Research Foundation of Korea (NRF) grant funded by the Korea government
   (MEST) (2016R1A2B2011100; J.C.).
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NR 27
TC 26
Z9 27
U1 4
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD APR 15
PY 2020
VL 146
IS 8
BP 2194
EP 2200
DI 10.1002/ijc.32499
EA JUL 2019
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KM5FL
UT WOS:000477369200001
PM 31290142
OA Bronze
DA 2025-01-04
ER

PT J
AU Hasegawa, H
   Miyo, M
   Mori, K
   Mano, M
   Ishida, H
   Mita, E
AF Hasegawa, Hiroko
   Miyo, Masaaki
   Mori, Kiyoshi
   Mano, Masayuki
   Ishida, Hisashi
   Mita, Eiji
TI A Rare BRAF Fusion in Advanced Rectal Cancer Treated with Anti-Epidermal
   Growth Factor Receptor Therapy
SO CASE REPORTS IN ONCOLOGY
LA English
DT Article
DE Advanced rectal cancer; Comprehensive genomic profiling; BRAF fusion;
   Anti-epidermal growth factor receptor therapy
ID GENE FUSIONS; TUMORS
AB Recently, v-raf murine sarcoma viral oncogene homologue B (BRAF) fusions have been identified in multiple cancer types using comprehensive genomic profiling (CGP) assays. BRAF fusions are extremely rare, occurring in <0.5% of patients with metastatic colorectal cancer (mCRC). Until now, there is no standard treatment for mCRC with BRAF fusions. Here, we report a recurrent colorectal cancer case that harbored an EXOC4-BRAF fusion. A 40-year-old female patient with a 2-year history of type 2 diabetes was diagnosed with pathologically confirmed stage IV rectal adenocarcinoma with liver metastasis. She underwent R0 resection after neoadjuvant therapy; however, her disease recurred at multiple metastatic sites (lymph nodes, ovary, and peritoneal gland). A rectal cancer surgical specimen was submitted for CGP (Foundation One) to identify potential targets to develop treatment strategies. An EXOC4-BRAF fusion was identified, and she achieved partial response to FOLFOX + panitumumab which is a fully human antibody directed against epidermal growth factor receptor. No EXOC4-BRAF fusions in colorectal cancer cases have been reported to date. Further studies investigating molecular mechanisms and novel targeted therapy approaches are required.
C1 [Hasegawa, Hiroko; Ishida, Hisashi; Mita, Eiji] Natl Hosp Org, Osaka Natl Hosp, Dept Gastroenterol & Hepatol, Osaka, Japan.
   [Miyo, Masaaki] Natl Hosp Org, Osaka Natl Hosp, Dept Surg, Osaka, Japan.
   [Mori, Kiyoshi; Mano, Masayuki] Natl Hosp Org, Osaka Natl Hosp, Dept Pathol, Osaka, Japan.
C3 Osaka National Hospital; Osaka National Hospital; Osaka National
   Hospital
RP Hasegawa, H (corresponding author), Natl Hosp Org, Osaka Natl Hosp, Dept Gastroenterol & Hepatol, Osaka, Japan.
EM hasegawa.hiroko.yr@mail.hosp.go.jp
RI Miyo, Masaaki/LBI-5534-2024
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NR 15
TC 1
Z9 1
U1 0
U2 1
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1662-6575
J9 CASE REP ONCOL
JI Case Rep. Oncol.
PY 2021
VL 14
IS 2
BP 938
EP 943
DI 10.1159/000517007
PG 6
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA UK7OG
UT WOS:000692155100040
PM 34267639
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Palmioli, A
   Forcella, M
   Oldani, M
   Angotti, I
   Sacco, G
   Fusi, P
   Airoldi, C
AF Palmioli, Alessandro
   Forcella, Matilde
   Oldani, Monica
   Angotti, Irene
   Sacco, Grazia
   Fusi, Paola
   Airoldi, Cristina
TI Adjuvant Effect of Cinnamon Polyphenolic Components in Colorectal Cancer
   Cell Lines
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE colorectal cancer (CRC); cinnamon metabolic profiling; flavonoids;
   procyanidins; cetuximab; adjuvant therapy
ID GROWTH-FACTOR RECEPTOR; PANITUMUMAB; CETUXIMAB; BARK
AB Colorectal cancer (CRC) is the second-leading cause of cancer death, with a worldwide incidence rate constantly increasing; thus, new strategies for its prevention or treatment are needed. Here, we describe the adjuvant effect of the polyphenol-enriched fractions of cinnamon, from cinnamon bark and buds, when co-administered with a potent anticancer drug, cetuximab, used for CRC therapy. The co-administration significantly reduces the cetuximab dose required for the antiproliferative activity against colorectal cancer cell line E705, which is sensitive to EGFR-targeted therapy. The anticancer activity of these cinnamon-derived fractions, whose major components (as assessed by UPLC-HRMS analysis) are procyanidins and other flavonoids, strictly correlates with their ability to induce apoptosis in cancer cell lines through ERK activation and the mitochondrial membrane potential impairment. Due to the severe side effects of cetuximab administration, our results suggest the use of nutraceuticals based on the polyphenolic fractions of cinnamon extracts as adjuvants in the therapy of CRC.
C1 [Palmioli, Alessandro; Forcella, Matilde; Oldani, Monica; Angotti, Irene; Sacco, Grazia; Fusi, Paola; Airoldi, Cristina] Univ Milano Bicocca, Dept Biotechnol & Biosci, Pzza Sci 2, I-20126 Milan, Italy.
C3 University of Milano-Bicocca
RP Fusi, P; Airoldi, C (corresponding author), Univ Milano Bicocca, Dept Biotechnol & Biosci, Pzza Sci 2, I-20126 Milan, Italy.
EM alessandro.palmioli@unimib.it; matilde.forcella@unimib.it;
   m.oldani12@campus.unimib.it; paola.fusi@unimib.it;
   cristina.airoldi@unimib.it
RI Airoldi, Cristina/A-6521-2010; Palmioli, Alessandro/A-8695-2013
OI Palmioli, Alessandro/0000-0002-5287-1663; OLDANI,
   MONICA/0000-0002-1512-8926; FORCELLA, Matilde/0000-0002-9706-4654;
   Airoldi, Cristina/0000-0002-3670-6262
FU Italian Ministry for Instruction, University and Research-Fondo per il
   finanziamento delle attivit base di ricerca
FX No Statement Available
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NR 35
TC 2
Z9 2
U1 2
U2 4
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 2023
VL 24
IS 22
AR 16117
DI 10.3390/ijms242216117
PG 18
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA AT8O1
UT WOS:001120799900001
PM 38003308
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Montaseri, H
   Simelane, NWN
   Abrahamse, H
AF Montaseri, Hanieh
   Simelane, Nokuphila Winifred Nompumelelo
   Abrahamse, Heidi
TI Zinc Phthalocyanine Tetrasulfonate-Loaded Ag@mSiO<sub>2</sub>
   Nanoparticles for Active Targeted Photodynamic Therapy of Colorectal
   Cancer
SO FRONTIERS IN NANOTECHNOLOGY
LA English
DT Article
DE colorectal cancer; Ag@mSiO2 nanoparticles; photodynamic therapy; ZnPcS4
   photosensitizer; targeted therapy
ID CELL-DEATH; DELIVERY; MECHANISMS
AB Colorectal cancer has high morbidity and mortality rate, with a high level of metastasis and recurrence due to the poor therapeutic effects. Photodynamic therapy (PDT) as an emerging clinical modality for cancer treatment provides remarkable advantages over existing treatments by generating reactive oxygen species (ROS) through light irradiating photosensitizers (PSs) in the presence of oxygen. PDT can induce immunity against recurrence and destruction of metastases. The application of nanoparticles (NPs) in targeted cancer therapy is coming to light to circumvent the limitations associated with low physiological solubility and lack of selectivity of the PS towards tumor sites. In this in vitro study, we proved the added value of NP systems on PS efficacy and a tumor-targeting ligand. Using core/shell Ag@mSiO(2) NPs loaded with ZnPcS4 PS and folic acid (FA), stronger cellular localization in the human colorectal cancer cell line (Caco-2) was observed compared to the passive NC and free PS. Additionally, light-induced photodynamic activation of the ZnPcS4/Ag@mSiO(2)-FA nanoconjugate (NC) elicited a strong cytotoxicity effect mediated by post-PDT. The results also revealed that the active NC was able to decrease the cell viability remarkably to 38.0% +/- 4.2 *** compared to the passive NC (67.0% +/- 7.4*) under 0.125 mu M ZnPcS4 (IC50). More importantly, the actively targeted NC-induced apoptosis where cell cycle analysis elaborated on cell death through the G0 phase, indicating the final NC's efficacy 20 hr post-PDT treatment.
C1 [Montaseri, Hanieh; Simelane, Nokuphila Winifred Nompumelelo; Abrahamse, Heidi] Univ Johannesburg, Fac Hlth Sci, Laser Res Ctr, Doornfontein, South Africa.
C3 University of Johannesburg
RP Montaseri, H (corresponding author), Univ Johannesburg, Fac Hlth Sci, Laser Res Ctr, Doornfontein, South Africa.
EM haniehm@uj.ac.za
RI Montaseri, Hanieh/U-4485-2019; Abrahamse, Heidi/U-7763-2019; Simelane,
   Nokuphila/AEG-3318-2022
FU South African Research Chairs Initiative of the Department of Science
   and Technology and National Research Foundation of South Africa [98337];
   University of Johannesburg; National Laser Centre; National Research
   Foundation-South African Research Chairs Initiative (NRF-SARChI); Global
   Excellence Stature 4.0
FX This research was funded by the South African Research Chairs Initiative
   of the Department of Science and Technology and National Research
   Foundation of South Africa, grant number 98337. The authors sincerely
   thank the University of Johannesburg, the National Laser Centre, and the
   National Research Foundation-South African Research Chairs Initiative
   (NRF-SARChI) and Global Excellence Stature 4.0 for their financial grant
   support.
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NR 32
TC 9
Z9 9
U1 2
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2673-3013
J9 FRONT NANOTECHNOL
JI Front. Nanotechnol.
PD JUL 12
PY 2022
VL 4
AR 928010
DI 10.3389/fnano.2022.928010
PG 11
WC Nanoscience & Nanotechnology; Materials Science, Multidisciplinary
WE Emerging Sources Citation Index (ESCI)
SC Science & Technology - Other Topics; Materials Science
GA G9AW1
UT WOS:000992008500001
OA gold
DA 2025-01-04
ER

PT J
AU Mosaad, H
   Ahmed, MM
   Elaidy, MM
   Elfarargy, OM
AF Mosaad, Hala
   Ahmed, Mona Mostafa
   Elaidy, Mostafa M.
   Elfarargy, Ola M.
TI Down-regulated MiRNA 29-b as a diagnostic marker in colorectal cancer
   and its correlation with ETV4 and Cyclin D1 immunohistochemical
   expression
SO CANCER BIOMARKERS
LA English
DT Article
DE Colon cancer; miR-29b; ETV4; cyclin D1
ID OVEREXPRESSION; PROGRESSION; METASTASIS; MIR-29B; INVASION; BREAST
AB BACKGROUND: Colorectal cancer (CRC) is the most common malignant tumor of the gastrointestinal tract with unfavorable prognosis. Therefore, novel biomarkers that may be used for new diagnostic strategies and drug-targeting therapy should be developed.
   OBJECTIVES: To investigate the expression of miR-29b in CRC and its association with ETV4 and cyclin D1 expression. Moreover, the current work aims to investigate the association between them and the clinicopathological features of CRC.
   METHODS: The expression of miR-29b and ETV4 (by qRT-PCR) and ETV4 and cyclin D1 (immunohistochemistry) was investigated in 65 cases of colon cancer and surrounding healthy tissues.
   RESULTS: MiR-29b down-regulated and ETV4 and Cyclin D1 up-regulated significantly in colon cancer tissues compared to normal nearby colonic tissues. In addition, significant associations between ETV4 and cyclin D1 expressions and progressive stage and lymph node (LN) metastasis (P < 0.001 for each) were found. Furthermore, there was a negative correlation between miR-29b gene expression and ETV4 gene expression (r = 0.298, P < 0.016).
   CONCLUSION: Down-regulation of miR-29b and over-expression of ETV4 and cyclin D1 may be utilized as early diagnostic marker for development of colon cancer. ETV4 and cyclin D1 correlate with poor prognostic indicators and considered as a possible target for therapy in colon cancer.
C1 [Mosaad, Hala] Zagazig Univ, Fac Med, Dept Biochem, Zagazig, Egypt.
   [Ahmed, Mona Mostafa] Zagazig Univ, Fac Med, Dept Pathol, Zagazig, Egypt.
   [Elaidy, Mostafa M.] Zagazig Univ, Fac Med, Dept Gen Surg, Zagazig, Egypt.
   [Elfarargy, Ola M.] Zagazig Univ, Fac Med, Dept Med Oncol, Zagazig, Egypt.
C3 Egyptian Knowledge Bank (EKB); Zagazig University; Egyptian Knowledge
   Bank (EKB); Zagazig University; Egyptian Knowledge Bank (EKB); Zagazig
   University; Egyptian Knowledge Bank (EKB); Zagazig University
RP Ahmed, MM (corresponding author), Zagazig Univ, Fac Med, Dept Pathol, Zagazig, Egypt.
EM mostafamona90@yahoo.com
RI Ahmed, Mona/AAK-9849-2021; Mostafa AHMED, Mona/ADZ-3749-2022
OI Mostafa AHMED, Mona/0000-0003-2149-5439
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NR 38
TC 2
Z9 2
U1 2
U2 2
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 1574-0153
EI 1875-8592
J9 CANCER BIOMARK
JI Cancer Biomark.
PY 2023
VL 37
IS 3
BP 179
EP 189
DI 10.3233/CBM-220349
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA M3GJ1
UT WOS:001029092900004
PM 37248886
DA 2025-01-04
ER

PT J
AU Chen, JR
   Li, ZY
   Yue, CF
   Ma, JH
   Cao, LX
   Lin, JX
   Zhu, DD
   An, R
   Lai, JX
   Guo, YM
   Gu, B
AF Chen, Jierong
   Li, Ziyue
   Yue, Caifeng
   Ma, Jianhong
   Cao, Lixue
   Lin, Jiaxin
   Zhu, Dandan
   An, Ran
   Lai, Jinxin
   Guo, Yunmiao
   Gu, Bing
TI Human umbilical cord mesenchymal stem cell-derived exosomes carrying
   miR-1827 downregulate SUCNR1 to inhibit macrophage M2 polarization and
   prevent colorectal liver metastasis
SO APOPTOSIS
LA English
DT Article
DE Colorectal cancer; microRNA-1827; Succinate receptor 1; Human umbilical
   cord mesenchymal stem cells; Exosomes; Macrophages; M2 polarization;
   Liver metastasis
ID CANCER; CONTRIBUTE; CAMP; MDM2
AB microRNA-1827 (miR-1827) is proposed to be enriched in exosomes from mesenchymal stem cells (MSCs-Exos). A recent study has addressed the suppressive effect of exosomes from human umbilical cord mesenchymal stem cells (hUC-MSCs-Exos) on colorectal cancer (CRC) metastasis. Hence, our study aims at investigating whether hUC-MSCs-Exos can modulate the liver metastasis in CRC by mediating miR-1827. Transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA) were used to identify hUC-MSCs-Exos. Using gain- and loss-of-function approaches, the expression of miR-1827 and succinate receptor 1 (SUCNR1) was altered. Consequently, the biological functions of CRC cells were assessed by CCK-8 and Transwell assays and macrophage M2 polarization was assayed by flow cytometry. Dual-luciferase reporter assay was applied to clarify interaction between miR-1827 and SUCNR1. CRC cells were incubated with hUC-MSCs-Exos and tumor-bearing mice were injected with hUC-MSCs-Exos to examine the effects on CRC cell growth and metastasis. SUCNR1, lowly expressed in CRC, could promote CRC cell growth and macrophage M2 polarization. miR-1827 could target SUCNR1 and hence suppress the progression and metastasis of CRC. hUC-MSCs-Exos carried miR-1827 to inhibit M2 macrophage polarization by downregulating SUCNR1 expression, and inhibited proliferating, migrating and invading properties of CRC cells. Furthermore, hUC-MSCs-Exos carrying miR-1827 blocked CRC liver metastasis in vivo. These findings indicate hUC-MSCs-Exos as an inhibitor of M2 macrophage polarization and liver metastasis in CRC through inducing miR-1827-targeted inhibition of SUCNR1. This provides a theoretical basis for understanding the mechanisms underlying Exos-based target therapy for CRC.
C1 [Chen, Jierong; Ma, Jianhong; Lin, Jiaxin; Zhu, Dandan; Lai, Jinxin; Gu, Bing] Guangdong Acad Med Sci, Guangdong Prov Peoples Hosp, Dept Lab Med, 106 Zhongshan 2nd Rd, Guangzhou 510080, Guangdong, Peoples R China.
   [Li, Ziyue] Guangzhou Med Univ, Prenatal Diagnost Ctr, Guangzhou 510000, Peoples R China.
   [Li, Ziyue] Guangzhou Med Univ, Guangzhou Women & Childrens Med Ctr, Cord Blood Bank, Guangzhou 510000, Peoples R China.
   [Yue, Caifeng] Guangdong Med Univ, Cent Peoples Hosp Zhanjiang, Zhanjiang Cent Hosp, Dept Lab Med, Zhanjiang 524045, Peoples R China.
   [Cao, Lixue; An, Ran] Guangdong Acad Med Sci, Guangdong Prov Peoples Hosp, Res Ctr Med Sci, Guangzhou 510080, Peoples R China.
   [Guo, Yunmiao] Guangdong Med Univ, Cent Peoples Hosp Zhanjiang, Zhanjiang Cent Hosp, Zhanjiang Inst Clin Med, Zhanjiang 524045, Guangdong, Peoples R China.
C3 Guangdong Academy of Medical Sciences & Guangdong General Hospital;
   Southern Medical University - China; Guangzhou Medical University;
   Guangzhou Medical University; Guangdong Medical University; Guangdong
   Academy of Medical Sciences & Guangdong General Hospital; Southern
   Medical University - China; Guangdong Medical University
RP Gu, B (corresponding author), Guangdong Acad Med Sci, Guangdong Prov Peoples Hosp, Dept Lab Med, 106 Zhongshan 2nd Rd, Guangzhou 510080, Guangdong, Peoples R China.; Guo, YM (corresponding author), Guangdong Med Univ, Cent Peoples Hosp Zhanjiang, Zhanjiang Cent Hosp, Zhanjiang Inst Clin Med, Zhanjiang 524045, Guangdong, Peoples R China.
EM yunmiaoguo@163.com; gubing@gdph.org.cn
RI Cao, Lixue/AAM-9316-2020; CF, Yue/AAT-9821-2021; Guo,
   Yun-Miao/KYR-7770-2024; Lin, Jiaxing/Q-3555-2018
CR Chakedis J, 2018, SURG ONCOL CLIN N AM, V27, P377, DOI 10.1016/j.soc.2017.11.010
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NR 46
TC 25
Z9 25
U1 1
U2 15
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1360-8185
EI 1573-675X
J9 APOPTOSIS
JI Apoptosis
PD APR
PY 2023
VL 28
IS 3-4
BP 549
EP 565
DI 10.1007/s10495-022-01798-x
EA JAN 2023
PG 17
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA M7QP6
UT WOS:000914896000001
PM 36652132
DA 2025-01-04
ER

PT J
AU Cho, E
   Mun, SJ
   Jeon, M
   Kim, HK
   Baek, H
   Ham, YS
   Gil, WJ
   Kim, JW
   Yang, CS
AF Cho, Euni
   Mun, Seok-Jun
   Jeon, Minha
   Kim, Hyo Keun
   Baek, Hwira
   Ham, Yu Seong
   Gil, Woo Jin
   Kim, Jin Woong
   Yang, Chul-Su
TI Tumor-targeted liposomes with platycodin D2 promote apoptosis in
   colorectal cancer
SO MATERIALS TODAY BIO
LA English
DT Article
DE Platycosides; Liposomes; Apoptosis; Colorectal cancer; Xenograft
ID DELIVERY; PEPTIDE; NANOMEDICINE; STRATEGIES
AB Conventional chemotherapy for colorectal cancer (CRC), though efficacious, is discouraging due to its limited targeting capability, lack of selectivity, and chemotherapy-associated side effects. With the advent of nanomedicines, a liposomal delivery system making use of a combination of anticancer phytochemicals is fast gaining popularity as one of the most promising nanoplatforms for CRC treatment. Rising evidence supports phytochemicals such as platycosides for their anticancer potency. To this end, a combination therapy including tumortargeted liposomes along with phytochemicals might have a greater therapeutic potential against cancer. In this study, we developed acidity-triggered rational membrane (ATRAM) along with conjugated platycodin D2 (PCD2) and liposomes (PCD2-Lipo-ATRAM) as a tumor-targeting therapy. The PCD2-Lipo-ATRAM treatment demonstrated a successful tumor-targeting ability in the CRC xenografts, in which PCD2 not only exerted a potent antitumor effect by inducing apoptotic cell death and but also functioned as a liposome membrane stabilizer. Moreover, PCD2-Lipo-ATRAM suppressed antiapoptotic BCL-2 family proteins, resulting in enhanced cytotoxicity toward CRC cells by inducing intrinsic caspase-9/-3 mediated apoptosis. Thus, our data has shown that tumor-targeting PCD2-based liposomal systems represent a promising strategy for CRC therapy, since they directly target the tumors, unlike other therapies that can miss the target.
C1 [Cho, Euni; Mun, Seok-Jun] Hanyang Univ, Dept Bionano Engn Technol, Seoul 04673, South Korea.
   [Cho, Euni; Mun, Seok-Jun; Kim, Hyo Keun; Ham, Yu Seong; Gil, Woo Jin; Yang, Chul-Su] Ctr Bionano Intelligence Educ & Res, Ansan 15588, South Korea.
   [Jeon, Minha; Baek, Hwira; Kim, Jin Woong] Sungkyunkwan Univ, Sch Chem Engn, Suwon 16419, South Korea.
   [Kim, Hyo Keun; Ham, Yu Seong; Gil, Woo Jin; Yang, Chul-Su] Hanyang Univ, Dept Mol & Life Sci, Ansan 15588, South Korea.
   [Yang, Chul-Su] Hanyang Univ, Dept Med & Life Sci, Ansan 15588, South Korea.
   [Yang, Chul-Su] 55 Hanyangdaehak Ro, Ansan 15588, Gyeonggi Do, South Korea.
   [Kim, Jin Woong] 2066 Seobu Ro, Suwon 16419, Gyeonggi Do, South Korea.
C3 Hanyang University; Sungkyunkwan University (SKKU); Hanyang University;
   Hanyang University
RP Yang, CS (corresponding author), 55 Hanyangdaehak Ro, Ansan 15588, Gyeonggi Do, South Korea.; Kim, JW (corresponding author), 2066 Seobu Ro, Suwon 16419, Gyeonggi Do, South Korea.
EM jinwoongkim@skku.edu; chulsuyang@hanyang.ac.kr
RI Yang, Chul-Su/J-3833-2013
OI Yang, Chul-Su/0000-0003-4918-961X
FU NRF - Korea government (MSIP) [2019R1A2C1086383, 2019R1I1A2A01064237,
   2021R1A4A5032463]
FX This work was supported by the NRF grant funded by the Korea government
   (MSIP) (2019R1A2C1086383, 2019R1I1A2A01064237 and 2021R1A4A5032463). We
   would like to thank all members of the Infection Biology Lab for
   critical reading and discussion of the manuscript.
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NR 45
TC 4
Z9 4
U1 5
U2 13
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2590-0064
J9 MATER TODAY BIO
JI Mater. Today Bio
PD OCT
PY 2023
VL 22
AR 100745
DI 10.1016/j.mtbio.2023.100745
EA AUG 2023
PG 10
WC Engineering, Biomedical; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Materials Science
GA P8DH0
UT WOS:001052916500001
PM 37576871
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Liu, SY
   Huang, F
   Ye, Q
   Li, YM
   Chen, JH
   Huang, H
AF Liu, Shengyuan
   Huang, Feng
   Ye, Qing
   Li, Yangming
   Chen, Jinhu
   Huang, Hong
TI SPRY4-IT1 promotes survival of colorectal cancer cells through
   regulating PDK1-mediated glycolysis
SO ANIMAL CELLS AND SYSTEMS
LA English
DT Article
DE SPRY4-IT1; colorectal cancer (CRC); proliferation; glycolysis; molecular
   target
ID NONCODING RNA SPRY4-IT1; PREDICTS POOR-PROGNOSIS; LNCRNA SPRY4-IT1;
   UP-REGULATION; INVASION; PROLIFERATION; MIGRATION
AB Colorectal cancer (CRC) becomes the third leading cause of cancer-related deaths worldwide recently. The prognosis of CRC is still poor in decades, and targeted therapy is still a potential effective treatment. Long non-coding RNAs (lncRNAs) could regulate series of cellular functions and developmental processes. LncRNA-SPRY4-IT1 (GenBank ID AK024556) is derived from an intron of the SPRY4 gene, which was highly expressed in melanoma cells and affected the progression of multiple types of cancers. However, the mechanism of SPRY4-IT1 in CRC progression remains unclear. Herein, we found the high level of SPRY4-IT1 in human colorectal cancer (CRC) tissues and cells, and correlated with patients' prognosis. We further noticed that SPRY4-IT1 regulated CRC cell growth and glycolysis, and promoting PDK1 expression. Our data further confirmed that SPRY4-IT1 regulated CRC progression targeting PDK1. We therefore thought SPRY4-IT1 could serve as a promising molecular target for the treatment of CRC.
C1 [Liu, Shengyuan; Huang, Feng; Ye, Qing; Li, Yangming; Chen, Jinhu; Huang, Hong] Fujian Med Univ Canc Hosp, Fujian Canc Hosp, Dept Gastroenterol, 420 Fuma Rd, Fuzhou 350014, Fujian, Peoples R China.
RP Huang, F (corresponding author), Fujian Med Univ Canc Hosp, Fujian Canc Hosp, Dept Gastroenterol, 420 Fuma Rd, Fuzhou 350014, Fujian, Peoples R China.
EM fenghuangfkl@163.com
RI YE, QING/KIG-8170-2024; Liu, Shengyuan/AAC-2359-2019
FU Starup Fund for scientific research, Fujian Medical University
   [2018QH1227]
FX This work was supported by Starup Fund for scientific research, Fujian
   Medical University [grant number 2018QH1227].
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NR 36
TC 10
Z9 10
U1 0
U2 9
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1976-8354
EI 2151-2485
J9 ANIM CELLS SYST
JI Anim. Cells Syst.
PD JUL 3
PY 2020
VL 24
IS 4
BP 220
EP 227
DI 10.1080/19768354.2020.1784274
EA JUN 2020
PG 8
WC Cell Biology; Zoology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Zoology
GA NG4IV
UT WOS:000548143900001
PM 33029299
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ben Brahim, E
   Ayari, I
   Jouini, R
   Atafi, S
   Koubaa, W
   Elloumi, H
   Chadli, A
AF Ben Brahim, Ehsen
   Ayari, Imen
   Jouini, Raja
   Atafi, Salsabil
   Koubaa, Wafa
   Elloumi, Hela
   Chadli, Aschraf
TI Expression of epidermal growth factor receptor (EGFR) in colorectal
   cancer: An immunohistochemical study
SO ARAB JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Colorectal cancer; EGFR; Immunohistochemistry
ID IMPACT
AB Background and study aim: The epidermal growth factor receptor (EGFR) plays an important role in tumourigenesis and tumour progression of colorectal cancer (CRC) and leads to the activation of intracellular signaling pathways. The use of anti-EGFR-targeted therapy has increased for patients with metastatic CRC. Today, the clinical utility of immunohistochemistry has remained somewhat inconclusive. It is based on EGFR screening methods using paraffin-embedded tumour specimen to select patients eligible for treatment. There is still lack of agreement on reproducible scoring criteria for EGFR immunohistochemistry has in various clinical trials.
   Patients and methods: We retrospectively reviewed 36 CRC patients who underwent surgeries during 2011 in Habib Thameur hospital in Tunis. We analyzed the immunohistochemical overexpression of EGFR using a score based on immunostaining intensity. In addition, we analyzed the correlation between this overexpression and patients' clinicopathologic parameters.
   Results: The positive expression rate of EGFR was 78% (28/36). Using the immunoreactivity score, 21 cases were considered low grade expression and 15 tumours were high grade. Immunohistochemical expression of EGFR showed a significant difference with tumour's location (p = 0.034) and vascular invasion (p = 0.03). This expression was not significantly associated with age, gender, tumour size, histological type, grade, TNM staging and perineural invasion.
   Conclusions: EGFR expression by immunohistochemistry in CRC is variably correlated with clinicopathological parameters. Its assessment by this method has still not proved its predictive value. (C) 2018 Pan-Arab Association of Gastroenterology. Published by Elsevier B.V. All rights reserved.
C1 [Ben Brahim, Ehsen; Ayari, Imen; Jouini, Raja; Atafi, Salsabil; Koubaa, Wafa; Chadli, Aschraf] Univ Tunis El Manar, Pathol Dept, Habib Thameur Hosp, Tunis, Tunisia.
   [Ben Brahim, Ehsen; Ayari, Imen; Jouini, Raja; Atafi, Salsabil; Koubaa, Wafa; Elloumi, Hela; Chadli, Aschraf] Univ Tunis El Manar, Fac Med, Tunis, Tunisia.
   [Elloumi, Hela] Univ Tunis El Manar, Gastroenterol Dept, Habib Thameur Hosp, Tunis, Tunisia.
C3 Universite de Tunis-El-Manar; Hopital Habib Thameur; Universite de
   Tunis-El-Manar; Faculte de Medecine de Tunis (FMT); Universite de
   Tunis-El-Manar; Hopital Habib Thameur
RP Ben Brahim, E (corresponding author), Univ Tunis El Manar, Pathol Dept, Habib Thameur Hosp, Tunis, Tunisia.; Ben Brahim, E (corresponding author), Univ Tunis El Manar, Fac Med, Tunis, Tunisia.
EM benbrahim_ehsen@yahoo.fr
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NR 20
TC 6
Z9 8
U1 0
U2 4
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1687-1979
EI 2090-2387
J9 ARAB J GASTROENTEROL
JI Arab J. Gastroenterol.
PD SEP
PY 2018
VL 19
IS 3
BP 121
EP 124
DI 10.1016/j.ajg.2018.08.002
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GW8AL
UT WOS:000447194800004
PM 30243897
DA 2025-01-04
ER

PT J
AU Hu, YW
   Pan, C
   Hu, JY
   Zhang, SZ
AF Hu, Yiwang
   Pan, Chi
   Hu, Jiyi
   Zhang, Suzhan
TI The role of Reg IV in colorectal cancer, as a potential therapeutic
   target
SO WSPOLCZESNA ONKOLOGIA-CONTEMPORARY ONCOLOGY
LA English
DT Review
DE Reg IV; colorectal cancer; Cdx2; EGFR/Akt/AP-1 pathway; targeted therapy
ID GENE FAMILY; EXPRESSION PROFILE; PROTEIN; CDX2; COLON; MEMBER;
   OVEREXPRESSION; 5-FLUOROURACIL; IRINOTECAN; RESISTANCE
AB Regenerating islet-derived family, member 4 (Reg IV), a member of the Reg gene family, has been reported to be overexpressed in gastrointestinal tract cancers. Reg IV overexpression in tumor cells has been associated with carcinogenesis, tissue regeneration, proliferation and resistance to apoptosis. Reg IV activates the epidermal growth factor receptor (EGFR) signaling pathway in colon cancer and increases expression of B-cell lymphoma- 2 (Bcl-2) and B-cell lymphoma- extra large (Bcl-xl), which are associated with the inhibition of apoptosis, results in mitogenic signaling in colon cancer cells, increase cell proliferation, metastasis and decreased apoptosis. Reg IV treatment inhibits 5-fluorouracil induced apoptosis, at least two mechanisms are involved in inhibition of apoptosis by Reg IV, including Bcl-2 and dihydropyrimidine dehydrogenase (DPD). These studies may lead to novel therapeutic strategies for cancers expressing Reg IV. Recently, one proteoglycan was confirmed to disrupt this signaling pathway to perform antitumor effect. This review summaries current knowledge of the expression and roles of Reg IV in human colorectal cancer, describes the possible signaling pathway which Reg IV activates, and discusses the relevance of Reg IV as a potential therapeutic target for cancer treatment.
C1 [Hu, Yiwang; Pan, Chi; Zhang, Suzhan] Zhejiang Univ, China Natl Minist Educ, Sch Med, Canc Inst Key Lab Canc Prevent & Intervent, Hangzhou 310000, Peoples R China.
   [Hu, Jiyi] Zhejiang Univ, Affiliated Hosp 2, Sch Med, Med Oncol, Hangzhou, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP Zhang, SZ (corresponding author), Zhejiang Univ, China Natl Minist Educ, Sch Med, Canc Inst Key Lab Canc Prevent & Intervent, Hangzhou 310000, Peoples R China.
EM Zhangscy07@gmail.com
RI Pan, Chi/GRR-6330-2022
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NR 36
TC 6
Z9 7
U1 0
U2 1
PU TERMEDIA PUBLISHING HOUSE LTD
PI POZNAN
PA KLEEBERGA 2, POZNAN, 61-615, POLAND
SN 1428-2526
EI 1897-4309
J9 WSPOLCZESNA ONKOL
JI Wspolczesna Onkol.
PY 2015
VL 19
IS 4
BP 261
EP 264
DI 10.5114/wo.2015.54385
PG 4
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA V8Y7J
UT WOS:000422088600001
PM 26557771
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Cui, YF
   Cui, XE
   Yang, XT
   Zhuo, ZZ
   Du, XS
   Xin, L
   Yang, Z
   Cheng, XT
AF Cui, Yanfen
   Cui, Xue'e
   Yang, Xiaotang
   Zhuo, Zhizheng
   Du, Xiaosong
   Xin, Lei
   Yang, Zhao
   Cheng, Xintao
TI Diffusion kurtosis imaging-derived histogram metrics for prediction of
   KRAS mutation in rectal adenocarcinoma: Preliminary findings
SO JOURNAL OF MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE diffusion kurtosis imaging; histogram; rectal cancer; mutations
ID METASTATIC COLORECTAL-CANCER; RAS MUTATIONS; HETEROGENEITY; PARAMETERS;
   CARCINOMA; PET/CT
AB Background Although histological examination is the standard method for assessing genetic status, the development of a noninvasive method, which can display the heterogeneity of the whole tumor to supplement genotype analysis, might be important for personalized treatment strategies. Purpose To evaluate the potential role of diffusion kurtosis imaging (DKI)-derived parameters using histogram analysis derived from whole-tumor volumes for prediction of the status of KRAS mutations in patients with rectal adenocarcinoma. Study Type Retrospective. Subjects In all, 148 consecutive patients with histologically confirmed rectal adenocarcinoma who were treated at our institution. Sequence DKI was performed with a 3.0 T MRI system using a single-shot echo-planar imaging sequence with b values of 0, 700, 1400, and 2100 sec/mm(2). Assessment D, K, and apparent diffusion coefficient (ADC) values were measured using whole-tumor volume histogram analysis and were compared between different KRAS mutations status. Statistical Tests Student's t-test or Mann-Whitney U-test, and receiver operating characteristic (ROC) curves were used for statistical analysis. Results All the percentile metrics of ADC and D values were significantly lower in the mutated group than those in the wildtype group (all P < 0.05), except for the minimum value of ADC and D (both P > 0.05), while K-related percentile metrics were higher in the mutated group compared with those in the wildtype group (all P < 0.05). Regarding the comparison of the diagnostic performance of all the histogram metrics, K-75th showed the highest AUC value of 0.871, and the corresponding values for sensitivity, specificity, positive predictive value, and negative predictive value were 81.43%, 78.21%, 77.03%, and 82.43%, respectively. Data Conclusion DKI metrics with whole-tumor volume histogram analysis is associated with KRAS mutations, and thus may be useful for predicting the KRAS status of rectal cancers for guiding targeted therapy. Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2019;50:930-939.
C1 [Cui, Yanfen; Yang, Xiaotang; Du, Xiaosong; Xin, Lei; Yang, Zhao; Cheng, Xintao] Shanxi Med Univ, Shanxi Prov Canc Hosp, Dept Radiol, Taiyuan 030013, Shanxi, Peoples R China.
   [Cui, Xue'e] Shanghai Jiao Tong Univ, Xinhua Hosp, Sch Med, Dept Radiol, Shanghai, Peoples R China.
   [Zhuo, Zhizheng] Philips Healthcare Greater China, MR Clin Sci, Beijing, Peoples R China.
C3 Shanxi Medical University; Shanghai Jiao Tong University; Philips;
   Philips Healthcare
RP Yang, XT (corresponding author), Shanxi Med Univ, Shanxi Prov Canc Hosp, Dept Radiol, Taiyuan 030013, Shanxi, Peoples R China.
EM yangxt210@126.com
OI Cui, Yanfen/0000-0001-6631-5687
CR Allegra CJ, 2016, J CLIN ONCOL, V34, P179, DOI 10.1200/JCO.2015.63.9674
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NR 33
TC 22
Z9 23
U1 0
U2 18
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1053-1807
EI 1522-2586
J9 J MAGN RESON IMAGING
JI J. Magn. Reson. Imaging
PD SEP
PY 2019
VL 50
IS 3
BP 930
EP 939
DI 10.1002/jmri.26653
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA IQ2MT
UT WOS:000480583900026
PM 30637861
DA 2025-01-04
ER

PT J
AU Long, JY
   Lin, JZ
   Wang, AQ
   Wu, LC
   Zheng, YC
   Yang, XB
   Wan, XS
   Xu, HF
   Chen, SG
   Zhao, HT
AF Long, Junyu
   Lin, Jianzhen
   Wang, Anqiang
   Wu, Liangcai
   Zheng, Yongchang
   Yang, Xiaobo
   Wan, Xueshuai
   Xu, Haifeng
   Chen, Shuguang
   Zhao, Haitao
TI PD-1/PD-L blockade in gastrointestinal cancers: lessons learned and the
   road toward precision immunotherapy
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Review
DE Precision immunotherapy; Immune checkpoint blockade; PD-1/PD-L blockade;
   Gastrointestinal cancer; Biomarker; Combination therapy; Adverse effect;
   Treatment evaluation; Drug resistance; Cost-effectiveness
ID SQUAMOUS-CELL CARCINOMA; IMMUNE-RELATED RESPONSE; METASTATIC
   MALIGNANT-MELANOMA; EPSTEIN-BARR-VIRUS; PROGRAMMED DEATH 1;
   HEPATOCELLULAR-CARCINOMA; COLORECTAL-CANCER; MICROSATELLITE INSTABILITY;
   GASTRIC-CANCER; PEMBROLIZUMAB MK-3475
AB Gastrointestinal (GI) malignancies are the most prevalent tumors worldwide, with increasing incidence and mortality. Although surgical resection, chemotherapy, radiotherapy, and molecular targeted therapy have led to significant advances in the treatment of GI cancer patients, overall survival is still low. Therefore, alternative strategies must be identified to improve patient outcomes. In the tumor microenvironment, tumor cells can escape the host immune response through the interaction of PD-1 and PD-L, which inhibits the function of T cells and tumor-infiltrating lymphocytes while increasing the function of immunosuppressive T regulatory cells. The use of an anti-PD-1/PD-L blockade enables reprogramming of the immune system to efficiently identify and kill tumor cells. In recent years, the efficacy of PD-1/PD-L blockade has been demonstrated in many tumors, and this treatment is expected to be a pan-immunotherapy for tumors. Here, we review the signaling pathway underlying the dysregulation of PD-1/PD-L in tumors, summarize the current clinical data for PD-1/PD-L inhibitors in GI malignancies, and discuss road toward precision immunotherapy in relation to PD-1/PD-L blockade. The preliminary data for PD-1/PD-L inhibitors are encouraging, and the precision immunotherapy of PD-1/PD-L inhibitors will be a viable and pivotal clinical strategy for GI cancer therapy.
C1 [Long, Junyu; Lin, Jianzhen; Wang, Anqiang; Wu, Liangcai; Zheng, Yongchang; Yang, Xiaobo; Wan, Xueshuai; Xu, Haifeng; Zhao, Haitao] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Liver Surg, Beijing, Peoples R China.
   [Long, Junyu; Lin, Jianzhen; Wang, Anqiang; Wu, Liangcai; Zheng, Yongchang; Yang, Xiaobo; Wan, Xueshuai; Xu, Haifeng; Chen, Shuguang; Zhao, Haitao] Peking Union Med Coll, Beijing, Peoples R China.
   [Chen, Shuguang] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Gen Surg, Beijing, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College Hospital; 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 Hospital
RP Xu, HF; Zhao, HT (corresponding author), Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Liver Surg, Beijing, Peoples R China.; Xu, HF; Chen, SG; Zhao, HT (corresponding author), Peking Union Med Coll, Beijing, Peoples R China.; Chen, SG (corresponding author), Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Gen Surg, Beijing, Peoples R China.
EM xuhf781120@sina.com; shuguang9@btmail.net.cn; zhaoht@pumch.cn
RI Xu, Haifeng/AIC-5767-2022; Zheng, Yongchang/KDO-5062-2024
OI Zhao, Haitao/0000-0002-3444-8044; long, junyu/0000-0001-5745-7165
FU International Science and Technology Cooperation Projects [2015DFA30650,
   2016YFE0107100]; Capital Special Research Project for Clinical
   Application [Z151100004015170]; Capital Special Research Project for
   Health Development [2014-2-4012]; Beijing Nature Science Foundation for
   Young Scholars Project [7164293]; Program for New Century Excellent
   Talents in University [NCET-11-0288]
FX This work was supported by International Science and Technology
   Cooperation Projects (2015DFA30650 and 2016YFE0107100), the Capital
   Special Research Project for Clinical Application (Z151100004015170),
   the Capital Special Research Project for Health Development
   (2014-2-4012), the Beijing Nature Science Foundation for Young Scholars
   Project (7164293), and the Program for New Century Excellent Talents in
   University (NCET-11-0288).
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NR 165
TC 81
Z9 87
U1 2
U2 45
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 AUG 3
PY 2017
VL 10
AR 146
DI 10.1186/s13045-017-0511-2
PG 21
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA FC6QX
UT WOS:000406967200001
PM 28774337
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, C
   Xiu, YT
   Zhang, YJ
   Wang, YH
   Xu, JZ
   Yu, WP
   Xing, DM
AF Wang, Chao
   Xiu, Yutao
   Zhang, Yujing
   Wang, Yanhong
   Xu, Jiazhen
   Yu, Wanpeng
   Xing, Dongming
TI Recent advances in biotin-based therapeutic agents for cancer therapy
SO NANOSCALE
LA English
DT Review; Early Access
ID BIOLOGICAL EVALUATION; TARGETED DELIVERY; COLORECTAL-CANCER; PAMAM
   DENDRIMER; CROSS-LINKING; FOLIC-ACID; DRUG; DESIGN; CELLS; NANOPARTICLES
AB Biotin receptors, as biomarkers for cancer cells, are overexpressed in various tumor types. Compared to other vitamin receptors, such as folate receptors and vitamin B12 receptors, biotin receptor-based targeting strategies exhibit superior specificity and broader potential in treating aggressive cancers, including ovarian cancer, leukemia, colon cancer, breast cancer, kidney cancer, and lung cancer. These strategies promote biotin transport via receptor-mediated endocytosis, which is triggered upon ligand binding. Biotin, as the ligand of the biotin receptor, can be conjugated to anti-cancer drugs to form targeted therapies that bind to receptors overexpressed on tumor cells, thus increasing drug uptake. Despite these advantages, many candidate drugs have progressed slowly and remain in the preclinical stage, impeding clinical translation. This is mainly due to the effects of various conjugation methods and drug formulations on their functionality and efficacy. Therefore, developing novel biotin-based therapeutics is crucial. The innovation of this strategy lies in its multifunctionality-researchers can use different conjugation methods to design and synthesize these drugs, enabling precise targeting of various tumor types while minimizing toxicity to normal cells. These drugs include small-molecule-biotin conjugates (SMBCs) and nano-biotin conjugates (NBCs). This dual-platform approach represents a significant advancement in targeted therapy, offering unprecedented flexibility in drug design and delivery. Compared to chemotherapy drugs and traditional delivery systems, biotin-based drugs with tumor-specific targeting demonstrate enhanced targeting, improved efficacy, and reduced toxicity. This review examines strategies and applications for enhancing the delivery of chemotherapy drugs to cancer cells, highlighting the need for high-quality conjugates and strategies. It not only summarizes the latest progress but also provides key insights into how this emerging field could revolutionize personalized cancer treatment, especially in the context of precision medicine. Additionally, it offers perspectives on future research directions in this field.
C1 [Wang, Chao; Xiu, Yutao; Wang, Yanhong; Xu, Jiazhen; Xing, Dongming] Qingdao Univ, Affiliated Hosp, Canc Inst, Qingdao 266071, Peoples R China.
   [Zhang, Yujing; Xing, Dongming] Qingdao Univ, Affiliated Cardiovasc Hosp, Qingdao 266071, Peoples R China.
   [Yu, Wanpeng] Qingdao Univ, Qingdao Med Coll, Qingdao 266071, Peoples R China.
   [Xing, Dongming] Tsinghua Univ, Sch Life Sci, Beijing 100084, Peoples R China.
RP Xing, DM (corresponding author), Qingdao Univ, Affiliated Hosp, Canc Inst, Qingdao 266071, Peoples R China.; Xing, DM (corresponding author), Qingdao Univ, Affiliated Cardiovasc Hosp, Qingdao 266071, Peoples R China.; Yu, WP (corresponding author), Qingdao Univ, Qingdao Med Coll, Qingdao 266071, Peoples R China.; Xing, DM (corresponding author), Tsinghua Univ, Sch Life Sci, Beijing 100084, Peoples R China.
EM yuwanpeng1987@163.com; xdm_tsinghua@163.com
FU National Natural Science Foundation of China [82303590]; National
   Natural Science Foundation of China [ZR2021MC189]; Natural Science
   Foundation of Shandong [23-2-1-141-zyyd-jch]; Natural Science Foundation
   of Qingdao [2023KJ227]; Youth Innovation Team Development Program of
   Shandong Province [2023M741867]; China Postdoctoral Science Foundation
   [QDBSH20230202076]; Qingdao Postdoctoral Application Project
FX This work was supported by grants from the National Natural Science
   Foundation of China (82303590), the Natural Science Foundation of
   Shandong (ZR2021MC189), the Natural Science Foundation of Qingdao
   (23-2-1-141-zyyd-jch), the Youth Innovation Team Development Program of
   Shandong Province (2023KJ227), the China Postdoctoral Science Foundation
   (2023M741867), and the Qingdao Postdoctoral Application Project
   (QDBSH20230202076). The author thanks Dongming Xing and Wanpeng Yu for
   the support in preparing figures.
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NR 155
TC 0
Z9 0
U1 2
U2 2
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2040-3364
EI 2040-3372
J9 NANOSCALE
JI Nanoscale
PD 2024 DEC 6
PY 2024
DI 10.1039/d4nr03729d
EA DEC 2024
PG 62
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary; Physics, Applied
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science;
   Physics
GA P4P0D
UT WOS:001377734400001
PM 39676680
DA 2025-01-04
ER

PT J
AU Oyallon, B
   Brachet-Botineau, M
   Logé, C
   Robert, T
   Bach, S
   Ibrahim, S
   Raoul, W
   Croix, C
   Berthelot, P
   Guillon, J
   Pinaud, N
   Gouilleux, F
   Viaud-Massuard, MC
   Denevault-Sabourin, C
AF Oyallon, Bruno
   Brachet-Botineau, Marie
   Loge, Cedric
   Robert, Thomas
   Bach, Stephane
   Ibrahim, Sajida
   Raoul, William
   Croix, Cecile
   Berthelot, Pascal
   Guillon, Jean
   Pinaud, Noel
   Gouilleux, Fabrice
   Viaud-Massuard, Marie-Claude
   Denevault-Sabourin, Caroline
TI New Quinoxaline Derivatives as Dual Pim-1/2 Kinase Inhibitors: Design,
   Synthesis and Biological Evaluation
SO MOLECULES
LA English
DT Article
DE quinoxaline; Pim kinases; kinase inhibitor; anticancer targeted therapy
ID SUBSTITUTED PHENYL GROUP; PIM KINASES; SERINE/THREONINE KINASE;
   DRUG-RESISTANCE; PHOSPHATASE; GLYCOLYSIS; VALIDATION; FAMILY; GROWTH;
   ACIDS
AB Proviral integration site for Moloney murine leukemia virus (Pim)-1/2 kinase overexpression has been identified in a variety of hematologic (e.g., multiple myeloma or acute myeloid leukemia (AML)) and solid (e.g., colorectal carcinoma) tumors, playing a key role in cancer progression, metastasis, and drug resistance, and is linked to poor prognosis. These kinases are thus considered interesting targets in oncology. We report herein the design, synthesis, structure-activity relationships (SAR) and in vitro evaluations of new quinoxaline derivatives, acting as dual Pim1/2 inhibitors. Two lead compounds (5c and 5e) were then identified, as potent submicromolar Pim-1 and Pim-2 inhibitors. These molecules were also able to inhibit the growth of the two human cell lines, MV4-11 (AML) and HCT-116 (colorectal carcinoma), expressing high endogenous levels of Pim-1/2 kinases.
C1 [Oyallon, Bruno; Croix, Cecile; Viaud-Massuard, Marie-Claude; Denevault-Sabourin, Caroline] Univ Tours, EA GICC ERL 7001 CNRS, Team IMT, F-37200 Tours, France.
   [Brachet-Botineau, Marie; Gouilleux, Fabrice] Univ Tours, CNRS ERL7001 LNOx EA GICC, F-37000 Tours, France.
   [Loge, Cedric] Univ Nantes, Dept Med Chem, IICIMED EA1155, IRS2, F-44200 Nantes, France.
   [Robert, Thomas; Bach, Stephane] Sorbonne Univ, CNRS, Integrat Biol Marine Models Lab LBI2M, UMR8227, F-29680 Roscoff, France.
   [Robert, Thomas; Bach, Stephane] Sorbonne Univ, CNRS, Kinase Inhibitor Specialized Screening Facil KISS, FR2424, F-29680 Roscoff, France.
   [Bach, Stephane] North West Univ, Ctr Excellence Pharmaceut Sci, Private Bag X6001, ZA-2520 Potchefstroom, South Africa.
   [Ibrahim, Sajida; Raoul, William] Univ Tours, EA GICC ERL 7001 CNRS, Team PATCH, F-37200 Tours, France.
   [Raoul, William] Univ Tours, N2C, INSERM, UMR 1069, F-37032 Tours, France.
   [Berthelot, Pascal] Univ Lille, UMR S 1172 JPArc, INSERM, CHU Lille, F-59000 Lille, France.
   [Guillon, Jean] Univ Bordeaux, INSERM U12132 UMR CNRS 5320, ARNA Lab, F-33076 Bordeaux, France.
   [Pinaud, Noel] Univ Bordeaux, ISM, CNRS, UMR 5255, F-33405 Talence, France.
C3 Universite de Tours; Universite de Tours; Nantes Universite; Sorbonne
   Universite; Centre National de la Recherche Scientifique (CNRS); CNRS -
   National Institute for Biology (INSB); Sorbonne Universite; Centre
   National de la Recherche Scientifique (CNRS); North West University -
   South Africa; Universite de Tours; Universite de Tours; Institut
   National de la Sante et de la Recherche Medicale (Inserm); Universite de
   Lille; CHU Lille; Institut National de la Sante et de la Recherche
   Medicale (Inserm); Universite de Bordeaux; Universite de Bordeaux;
   Centre National de la Recherche Scientifique (CNRS); CNRS - Institute of
   Chemistry (INC)
RP Denevault-Sabourin, C (corresponding author), Univ Tours, EA GICC ERL 7001 CNRS, Team IMT, F-37200 Tours, France.
EM bruno.oyallon@gmail.com; marie.brachet.botineau@gmail.com;
   cedric.loge@univ-nantes.fr; trobert@sb-roscoff.fr; bach@sb-roscoff.fr;
   sajidaibrahim@hotmail.com; william.raoul@univ-tours.fr;
   cecile.croix@univ-tours.fr; pascal.berthelot@univ-lille2.fr;
   jean.guillon@u-bordeaux.fr; noel.pinaud@u-bordeaux.fr;
   fabrice.gouilleux@univ-tours.fr;
   marie-claude.viaud-massuard@univ-tours.fr;
   caroline.denevault@univ-tours.fr
RI /ABD-5865-2020; Raoul, William/IUM-9329-2023; Raoul, William/H-2118-2018
OI Bach, Stephane/0000-0002-7186-7483; Gouilleux,
   Fabrice/0000-0001-6047-1718; loge, cedric/0000-0001-5113-6547; Guillon,
   Jean/0000-0001-8577-3894; IBRAHIM, sajida/0000-0002-3441-7942; Raoul,
   William/0000-0002-5040-3372; Pinaud, Noel/0000-0001-7646-5312
FU "Association pour le Developpement de la Recherche et de l'Innovation
   dans le NORD PAS DE CALAIS" (ADRINORD); Region Centre Val de Loire;
   LabEx SynOrg [ANR-11-LABX-0029]
FX This research was funded by a grant from the "Association pour le
   Developpement de la Recherche et de l'Innovation dans le NORD PAS DE
   CALAIS" (ADRINORD) (to B.O.). The authors also thank the Canceropole
   Grand Ouest (3MC network-Marine Molecules, Metabolism and Cancer), GIS
   IBiSA (Infrastructures en Biologie Sante et Agronomie) and Biogenouest
   (Western France life science and environment core facility network) for
   supporting the KISSf screening facility. The authors wish to thank the
   Region Centre Val de Loire and LabEx SynOrg (ANR-11-LABX-0029) for
   financial support.
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NR 43
TC 19
Z9 19
U1 1
U2 17
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD FEB
PY 2021
VL 26
IS 4
AR 867
DI 10.3390/molecules26040867
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA QQ0BE
UT WOS:000624191300001
PM 33562106
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Oliveira, AF
   Bretes, L
   Furtado, I
AF Oliveira, Andre F.
   Bretes, Luis
   Furtado, Irene
TI Review of PD-1/PD-L1 Inhibitors in Metastatic dMMR/MSI-H Colorectal
   Cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE immunotherapy; colorectal cancer; PD-1; inhibitors; PD-L1;
   microsatellite instability; MSI-H; dMMR
ID MOLECULAR SUBTYPES; PD-1 BLOCKADE; IMMUNE; IMMUNOTHERAPY; NIVOLUMAB;
   OPPORTUNITIES; IPILIMUMAB; PROGNOSIS; SAFETY; TUMORS
AB There are a wide range of therapies for metastatic colorectal cancer (CRC) available, but outcomes remain suboptimal. Learning the role of the immune system in cancer development and progression led to advances in the treatment over the last decade. While the field is rapidly evolving, PD-1, and PD-L1 inhibitors have a leading role amongst immunomodulatory agents. They act against pathways involved in adaptive immune suppression resulting in immune checkpoint blockade. Immunotherapy has been slow to impact the management of this patient population due to disappointing results, mainly when used broadly. Nevertheless, some patients with microsatellite-instability-high (MSI-H) or mismatch repair-deficient (dMMR) CRC appear to be susceptible to checkpoint inhibitors with objective and sustained clinical responses, providing a new therapeutic option for patients with advanced disease. This article provides a comprehensive review of the early and late phase trials with the updated data of PD-1/PD-L1 inhibitors alone or in combination with other therapies (immunotherapy, targeted therapy and chemotherapy). While data is still limited, many ongoing trials are underway, testing the efficacy of these agents in CRC. Current and future challenges of PD-1 and PD-L1 inhibitors are also discussed.
C1 [Oliveira, Andre F.; Bretes, Luis; Furtado, Irene] Ctr Hosp Univ Algarve, Serv Oncol Med, Faro, Portugal.
RP Oliveira, AF (corresponding author), Ctr Hosp Univ Algarve, Serv Oncol Med, Faro, Portugal.
EM afoliveira@chalgarve.min-saude.pt
OI Oliveira, Andre Filipe/0000-0002-1118-3610
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NR 38
TC 139
Z9 161
U1 3
U2 28
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 14
PY 2019
VL 9
AR 396
DI 10.3389/fonc.2019.00396
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HY1LD
UT WOS:000467877600001
PM 31139574
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Liu, Z
   Ji, MM
   Jin, FT
   Jiang, F
   Liu, XP
AF Liu, Zheng
   Ji, Mengmeng
   Jin, Fangtong
   Jiang, Feng
   Liu, Xiaoping
TI Expression and clinical significance of miR-17-5p in tumor tissues of
   patients with colorectal cancer
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer (CRC); miR-17-5p; proliferation; invasion; apoptosis
ID MICRORNAS; CELLS
AB Background: At present, there is a lack of novel biomarkers for the early diagnosis and targeted therapy of colorectal cancer (CRC). The current study investigated the expression of miR-17-5p in colorectal tumors and adjacent tissues, and examined the effects of miR-17-5p on the cellular growth of the colon cancer cell line HCT-116. Methods: A total of 30 paired tissue specimens were obtained from patients with CRC who were admitted to the Department of General Surgery V of the First Affiliated Hospital, Gannan Medical College between December 2019 and January 2021. The clinical information for the corresponding patients was collated. Real-time fluorescence quantitative polymerase chain reaction ( RT- qPCR) was performed to detect the expression of miR-17-5p in tumor tissues and the paracancerous tissues. The relationship between miR-175p and clinicopathology was analyzed. The CRC cell line HCT-116 was transfected with miR-17-5p mimics and inhibitors using liposomes. The effects of miR-17-5p on cell proliferation, invasion and migration, and apoptosis were determined using colon formation assays, transwell and scratch assays, and flow cytometry, respectively. The effects of miR-17-5p on CD44 (homing cell adhesion molecule), MMP2 (matrix metalloproteinase 2), BCL2 (B-cell lymphoma-2), BAX (BCL2-associated X), and E-cadherin protein and gene expression were investigated using Western blot and RT-qPCR, respectively. Results: MiR-17-5p expression was higher in tumor tissues compared to the normal adjacent tissues. While miR-17-5p expression levels were unrelated to age nor gender, they were related to the degree of differentiation, stage, lymph node metastasis, and tumor size in patients with CRC. Upregulation of miR17- 5p promoted CRC cell proliferation, metastasis, and invasion, while inhibiting apoptosis. However, downregulation of miR-17-5p had the opposite effect. Furthermore, miR-17-5p upregulation increased E-cadherin, CD44, MMP2, and BCL2 expression while decreasing BAX expression, whereas miR-17-5p downregulation had the opposite effect. Conclusions: MiR-17-5p is highly expressed in tumor tissues and correlates with increased proliferation, invasion, and migration, as well as reduced apoptosis in HCT- 116 cells. Indeed, miR- 17-5p may be a potential indicator for the early diagnosis of CRC and may guide clinical targeted therapy.
C1 [Liu, Zheng; Ji, Mengmeng; Jin, Fangtong; Jiang, Feng; Liu, Xiaoping] Gannan Med Coll, Dept Gen Surg, Affiliated Hosp 1, Ganzhou 341000, Peoples R China.
   [Liu, Zheng; Ji, Mengmeng; Jin, Fangtong; Liu, Xiaoping] Ganzhou City Key Lab Colorectal & Anal Dis Res, Ganzhou 341000, Peoples R China.
C3 Gannan Medical University
RP Liu, XP (corresponding author), Gannan Med Coll, Dept Gen Surg, Affiliated Hosp 1, Ganzhou 341000, Peoples R China.; Liu, XP (corresponding author), Ganzhou City Key Lab Colorectal & Anal Dis Res, Ganzhou 341000, Peoples R China.
EM xiaoxiaoliu1982@163.com
RI JIANG, Feng/HTP-2862-2023; Liu, Xiaoping/F-8791-2013
FU Ganzhou City Key Laboratory of Colorectal and Anal Diseases Research
   [20220101-25]; project of Jiangxi Provincial Education Department
   [GJJ180810]; Jiangxi Provincial Health Commission [202210908]
FX The study was supported by the Ganzhou City Key Laboratory of Colorectal
   and Anal Diseases Research (No. 20220101-25), the project of Jiangxi
   Provincial Education Department (No. GJJ180810), and Jiangxi Provincial
   Health Commission (No. 202210908).
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NR 21
TC 1
Z9 1
U1 0
U2 9
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD DEC
PY 2022
VL 13
IS 6
BP 3067
EP +
DI 10.21037/jgo-22-1185
PG 14
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA D6UP6
UT WOS:000970063500001
PM 36636078
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zheng, GW
   Tang, MM
   Shu, CY
   Xin, WX
   Zhang, YH
   Chi, BB
   Shi, MR
   Guo, X
   Zhang, ZZ
   Lian, XY
AF Zheng, Guo-Wan
   Tang, Ming-Min
   Shu, Chen-Yan
   Xin, Wen-Xiu
   Zhang, Yan-Hua
   Chi, Bin-Bin
   Shi, Mu-Ran
   Guo, Xing
   Zhang, Zhi-Zhen
   Lian, Xiao-Yuan
TI A small natural molecule CADPE kills residual colorectal cancer cells by
   inhibiting key transcription factors and translation initiation factors
SO CELL DEATH & DISEASE
LA English
DT Article
ID TUMOR-GROWTH; RESISTANCE; MEK; PATHWAYS; MYC; METASTASIS; CHALLENGES;
   DIVERSE; DISEASE; ESTER
AB Residual disease is the major cause for colorectal cancer (CRC) relapse. Herein, we explore whether and how a natural molecule CADPE killed heterogenic populations in a panel of CRC cell lines with KRAS/BRAF mutations that are natively resistant to EGFR- or VEGFR-targeted therapy, without sparing persistent cells, a reservoir of the disease relapse. Results showed that CADPE killed the tumor bulk and residual cells in the panel of CRC cell lines, rapidly inactivated c-Myc, STAT3, and NF-kappa B, and then decreased the protein levels of key signaling molecules for CRC, such as beta-catenin, Notch1, and the nodes of mTOR pathways; eukaryotic translation initiation factors (eIF4F); anti-apoptotic proteins (Bcl-xl, Mcl-1, and survivin); and stemness-supporting molecules (CD133, Bim-1, and VEGF). In terms of mechanism of action, concurrent downregulation of Mcl-1, Bcl-xl, and survivin was necessary for CADPE to kill CRC bulk cells, while additional depletion of CD133 and VEGF proteins was required for killing the residual CRC cells. Moreover, the disabled c-Myc, STAT3, NF-kappa B, and eIF4F were associated with the broadly decreased levels of anti-apoptosis proteins and pro-stemness proteins. Consistently, CADPE suppressed CRC tumor growth associated with robust apoptosis and depleted levels of c-Myc, STAT3, NF-kappa B, eIF4F, anti-apoptotic proteins, and pro-stemness proteins. Our findings showed the promise of CADPE for treating CRC and suggested a rational polytherapy that disables c-Myc, STAT3, NF-kappa B, and eIF4F for killing CRC residual disease.
C1 [Zheng, Guo-Wan; Tang, Ming-Min; Shu, Chen-Yan; Zhang, Yan-Hua; Chi, Bin-Bin; Shi, Mu-Ran; Guo, Xing; Lian, Xiao-Yuan] Zhejiang Univ, Coll Pharmaceut Sci, Hangzhou 310058, Zhejiang, Peoples R China.
   [Xin, Wen-Xiu] Zhejiang Canc Hosp, Dept Pharm, Hangzhou 310022, Zhejiang, Peoples R China.
   [Zhang, Zhi-Zhen] Zhejiang Univ, Ocean Coll, Zhoushan Campus, Zhoushan 316021, Zhejiang, Peoples R China.
C3 Zhejiang University; Zhejiang Cancer Hospital; Zhejiang University
RP Lian, XY (corresponding author), Zhejiang Univ, Coll Pharmaceut Sci, Hangzhou 310058, Zhejiang, Peoples R China.; Zhang, ZZ (corresponding author), Zhejiang Univ, Ocean Coll, Zhoushan Campus, Zhoushan 316021, Zhejiang, Peoples R China.
EM zzhang88@zju.edu.cn; xylian@zju.edu.cn
RI Zheng, Guowan/HNP-7979-2023; ZHANG, ZHIZHEN/GYA-3230-2022; Liu,
   Xiaoyang/JUV-8314-2023; Xin, Wenxiu/AAH-1348-2021
OI Zheng, Guowan/0000-0001-5731-8325
FU National Major Scientific Research Program [2012CB966600]; National
   Natural Science Foundations of China [81072617, 81274137, 81773769]
FX This study was financially supported by the National Major Scientific
   Research Program (No. 2012CB966600) and the National Natural Science
   Foundations of China (Nos. 81072617, 81274137, and 81773769).
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NR 48
TC 4
Z9 4
U1 2
U2 14
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD NOV 15
PY 2020
VL 11
IS 11
AR 982
DI 10.1038/s41419-020-03191-5
PG 14
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA OY4JE
UT WOS:000594213800003
PM 33191401
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Song, MY
   Zhou, XL
   Hou, RN
   Sigdel, M
   Liu, YM
   Zhang, CZ
   Xu, KH
   Han, XW
   Jiao, DC
AF Song, Mengyao
   Zhou, Xueliang
   Hou, Rongna
   Sigdel, Milan
   Liu, Yiming
   Zhang, Chengzhi
   Xu, Kaihao
   Han, Xinwei
   Jiao, Dechao
TI CT-guided radioactive <SUP>125</SUP>I seeds brachytherapy for lung
   oligometastases from colorectal cancer: initial results
SO BMC CANCER
LA English
DT Article
DE Lung oligometastases; Colorectal cancer; I-125 brachytherapy; Clinical
   study
ID STEREOTACTIC BODY RADIOTHERAPY; ABLATIVE RADIATION-THERAPY;
   PROGNOSTIC-FACTORS; METASTASES; IMPLANTATION; RESECTION; EFFICACY
AB Objectives: To evaluate the safety and effectiveness of computed tomography (CT)-guided radioactive I-125 seeds brachytherapy (RISB) for lung oligometastases (LO) from colorectal cancer (CRC). Methods: Data for 144 LOs from 70 CRC patients who underwent CT-guided RISB were retrospectively analyzed. The primary endpoints were progression-free survival (PFS) and overall survival (OS), and the secondary endpoints were technical success, local control rate (LCR), and complications. Kaplan-Meier method was used for survival analysis. Cox model was used to identify the independent predictors of poor prognosis. Results: The RISB procedures were successfully performed in all patients, and the success rate was 100%. The median follow-up was 27.8 months. The median PFS was 10.0 months (95% CI: 8.9-11.1) and the 1- and 2-year PFS rates were 32.9% and 5.9%, respectively. On multivariate analysis, serum carcinoembryonic antigen (CEA) <= 15 ng/ml (P = 0.048), middle-high differentiated pathological classification (P = 0.015), primary TNM stages I-III (P = 0.001), LO number <= 2 (P < 0.001) and cumulative gross tumor volume (GTV) <= 40 cm(3) (P < 0.001) showed superior PFS. The median OS was 30.8 months (95% CI: 27.1-34.4) and the 1-, 2-, and 3-year OS rates were 95.7%, 67.4%, and 42.5%, respectively. On multivariate analysis, serum CEA <= 15 ng/ml (P = 0.004), middle-high differentiated pathological classification (P < 0.001), primary TNM stages I-III (P < 0.001), LO number <= 2 (P < 0.001), cumulative GTV <= 40 cm(3) (P < 0.001) and system treatments combined with chemotherapy and target therapy (P < 0.001) showed superior OS. The LCR for 3, 6, and 12 months was 97.9%, 91.0%, and 83.6%, respectively. There were 4 cases of pneumothorax at 5.7% that required drainage. Conclusions: RISB for LO from CRC is safe and effective, and serum CEA, TNM stage, LO number, cumulative GTV, and system treatments should be emphasized for long OS.
C1 [Song, Mengyao; Zhou, Xueliang; Hou, Rongna; Sigdel, Milan; Liu, Yiming; Zhang, Chengzhi; Xu, Kaihao; Han, Xinwei; Jiao, Dechao] Zhengzhou Univ, Affiliated Hosp 1, Dept Intervent Radiol, 1 Jianshe East Rd, Zhengzhou 450052, Peoples R China.
C3 Zhengzhou University
RP Jiao, DC (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Intervent Radiol, 1 Jianshe East Rd, Zhengzhou 450052, Peoples R China.
EM jiaodechao007@126.com
RI Zhou, Xueliang/HLQ-3595-2023; Dechao, Jiao/ABH-1680-2021
OI Sigdel, Milan/0009-0009-7930-2303
FU Major Science and Technology Projects of Henan Province in 2022
FX We thank the patients enrolled in this study.
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PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
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AR 265
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PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KC0X1
UT WOS:001177654500001
PM 38403626
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Varghese, C
   Wells, CI
   Bissett, IP
   O'Grady, G
   Keane, C
AF Varghese, Chris
   Wells, Cameron I.
   Bissett, Ian P.
   O'Grady, Gregory
   Keane, Celia
TI The role of colonic motility in low anterior resection syndrome
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE low anterior resection syndrome (LARS); colonic motility; rectosigmoid
   brake; rectal cancer; low anterior resection
ID TOTAL MESORECTAL EXCISION; SACRAL NERVE-STIMULATION; POUCH-ANAL
   ANASTOMOSIS; RECTAL-CANCER SURGERY; TO-END ANASTOMOSIS; QUALITY-OF-LIFE;
   FECAL INCONTINENCE; PREOPERATIVE RADIOTHERAPY; MOTOR PATTERNS; COLOANAL
   ANASTOMOSIS
AB Low anterior resection syndrome (LARS) describes the symptoms and experiences of bowel dysfunction experienced by patients after rectal cancer surgery. LARS is a complex and multifactorial syndrome exacerbated by factors such as low anastomotic height, defunctioning of the colon and neorectum, and radiotherapy. There has recently been growing awareness and understanding regarding the role of colonic motility as a contributing mechanism for LARS. It is well established that rectosigmoid motility serves an important role in coordinating rectal filling and maintaining continence. Resection of the rectosigmoid may therefore contribute to LARS through altered distal colonic and neorectal motility. This review evaluates the role of colonic motility within the broader pathophysiology of LARS and outlines future directions of research needed to enable targeted therapy for specific LARS phenotypes.
C1 [Varghese, Chris; Wells, Cameron I.; Bissett, Ian P.; O'Grady, Gregory; Keane, Celia] Univ Auckland, Fac Med & Hlth Sci, Dept Surg, Auckland, New Zealand.
   [Wells, Cameron I.] Counties Manukau Dist Hlth Board, Dept Gen Surg, Auckland, New Zealand.
   [Bissett, Ian P.] Auckland City Hosp, Dept Surg, Auckland, New Zealand.
   [Keane, Celia] Whangarei Hosp, Dept Surg, Whangarei, New Zealand.
C3 University of Auckland; Auckland City Hospital
RP Keane, C (corresponding author), Univ Auckland, Fac Med & Hlth Sci, Dept Surg, Auckland, New Zealand.; Keane, C (corresponding author), Whangarei Hosp, Dept Surg, Whangarei, New Zealand.
EM celia.keane@auckland.ac.nz
RI Keane, Celia/AAV-7779-2020; Varghese, Chris/AAL-5156-2020; Bissett,
   Ian/A-4529-2016
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NR 143
TC 5
Z9 5
U1 4
U2 13
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD SEP 16
PY 2022
VL 12
AR 975386
DI 10.3389/fonc.2022.975386
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4Z8PI
UT WOS:000862462900001
PM 36185226
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wang, MT
   Xu, T
   Shen, L
   Li, J
   Zhu, L
   Wang, C
   Hu, ZY
   Li, P
   Yang, YL
   Wang, XC
AF Wang, Mengting
   Xu, Ting
   Shen, Lin
   Li, Jian
   Zhu, Ling
   Wang, Chen
   Hu, Zhiyuan
   Li, Ping
   Yang, Yanlian
   Wang, Xicheng
TI HER2 Expression in Circulating Tumor Cells as Prognostic and Predictive
   Biomarkers for Anti-HER2 Therapy in Previously Treated Metastatic
   Colorectal Cancer
SO ADVANCED THERAPEUTICS
LA English
DT Article
DE circulating tumor cells; colorectal cancer; human epidermal growth
   factor receptor 2 phenotyping; human epidermal growth factor receptor
   2-targeted therapy; peptide nanomaterials
ID BREAST-CANCER; AMERICAN-PATHOLOGISTS; PROGRESSION-FREE; CHEMOTHERAPY;
   GUIDELINE; SURVIVAL; SOCIETY; PLUS
AB For human epidermal growth factor receptor 2-positive metastatic colorectal cancer (HER2+ mCRC), anti-HER2 therapy shows benefits, while current HER2 testing using tumor biopsy remains controversial. Noninvasive circulating tumor cells (CTCs) may achieve more accurate HER2 diagnosis . Herein, enumeration and HER2 phenotyping on CTCs (HER2((0/1+/2+/3+)) CTCs) are assessed using TUMORFISHER for 40 mCRC patients (20 HER2+; 20 HER2-negative). Positive/negative HER2 phenotypes on CTCs (ctcHER2+/-) are determined with or without > 5% HER2((2+/3+)) CTCs. After anti-HER2 therapy, HER2+ patients without baseline CTCs show significantly better survivals than those with 1 & LE; CTCs & LE; 51 or & GE; 52 CTCs at baseline (mPFS; 5.6, 4.2, and 2.0 months; p = 0.0021) (mOS; not yet reached, 18.0 and 9.1 months; p = 0.0002). Among HER2+ patients with 1 & LE; CTCs & LE; 51 at baseline, ctcHER2+ has more favorable survivals than ctcHER2- (mPFS; 5.1 and 2.3 months; p = 0.0257) (mOS; not yet reached, 14.7 months; p = 0.0400). HER2+ patients with & GE; 52 CTCs or (with 1 & LE; CTCs & LE; 51 and maintained ctcHER2-) show a higher progression disease rate (60.0%, 0.0%; p = 0.0106). Therefore, CTC enumeration and ctcHER2 phenotyping may be prognostic and predictive biomarkers for HER2+ mCRC with anti-HER2 therapy.
C1 [Wang, Mengting; Zhu, Ling; Wang, Chen; Hu, Zhiyuan; Li, Ping; Yang, Yanlian] Natl Ctr Nanosci & Technol, CAS Ctr Excellence Nanosci, CAS Key Lab Standardizat & Measurement Nanotechnol, CAS Key Lab Biol Effects Nanomat & Nanosafety, 11 Beiyitiao, Beijing 100190, Peoples R China.
   [Xu, Ting; Shen, Lin; Li, Jian; Wang, Xicheng] Peking Univ Canc Hosp & Inst, Dept Gastrointestinal Oncol, Key Lab Carcinogenesis & Translat Res, Minist Educ Beijing, Beijing 100142, Peoples R China.
   [Wang, Mengting; Zhu, Ling; Wang, Chen; Hu, Zhiyuan; Li, Ping; Yang, Yanlian] Univ Chinese Acad Sci, 19 Yuquan Rd, Beijing 100049, Peoples R China.
C3 Chinese Academy of Sciences; National Center for Nanoscience &
   Technology, CAS; Chinese Academy of Sciences; University of Chinese
   Academy of Sciences, CAS
RP Hu, ZY; Li, P; Yang, YL (corresponding author), Natl Ctr Nanosci & Technol, CAS Ctr Excellence Nanosci, CAS Key Lab Standardizat & Measurement Nanotechnol, CAS Key Lab Biol Effects Nanomat & Nanosafety, 11 Beiyitiao, Beijing 100190, Peoples R China.; Wang, XC (corresponding author), Peking Univ Canc Hosp & Inst, Dept Gastrointestinal Oncol, Key Lab Carcinogenesis & Translat Res, Minist Educ Beijing, Beijing 100142, Peoples R China.; Hu, ZY; Li, P; Yang, YL (corresponding author), Univ Chinese Acad Sci, 19 Yuquan Rd, Beijing 100049, Peoples R China.
EM huzy@nanoctr.cn; lip@nanoctr.cn; yangyl@nanoctr.cn;
   xicheng_wang@hotmail.com
RI Xu, Ting/AAW-7829-2021; yang, yanlian/N-1892-2014; Shen,
   Lin/JPX-7656-2023; Zhu, Ling/AFZ-9657-2022; wang, xicheng/IXX-0974-2023
OI Yang, Yanlian/0000-0003-4318-7672
FU Strategic Priority Research Program of Chinese Academy of Science
   [XDB36000000]; National Natural Science Foundation of China
   [51861135103, 31971295]; Key Research Program of Frontier Sciences
   [QYZDJ-SSW-SLH048]; Youth Innovation Promotion Association of Chinese
   Academy of Science [2018048]
FX M.W. and T.X. are co-first authors and contributed equally to this work.
   Z.H., P.L., Y.Y., and X.W. are co-corresponding authors. The authors are
   grateful to the financial support from the Strategic Priority Research
   Program of Chinese Academy of Science (XDB36000000), the National
   Natural Science Foundation of China (Nos. 51861135103, 31971295), the
   Key Research Program of Frontier Sciences (QYZDJ-SSW-SLH048), and the
   Youth Innovation Promotion Association of Chinese Academy of Science
   (2018048). Besides, the authors are sincerely grateful to all the
   patients in the work, whose clinical blood samples greatly helped
   explore the clinical utility of TUMORFISHER-based CTC enumeration and
   ctcHER2 phenotyping in pretreated HER2+ mCRC during anti-HER2 therapy.
   In addition, the authors also express sincere thanks to Liang's
   laboratory, which presented colorectal cancer cell lines as a gift for
   this trial.
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NR 53
TC 1
Z9 1
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2366-3987
J9 ADV THER-GERMANY
JI Adv. Therap.
PD OCT
PY 2023
VL 6
IS 10
DI 10.1002/adtp.202300044
EA JUL 2023
PG 11
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA IT7S9
UT WOS:001022695800001
DA 2025-01-04
ER

PT J
AU Yang, YN
   Zhang, R
   Du, JW
   Yuan, HH
   Li, YJ
   Wei, XL
   Du, XX
   Jiang, SL
   Han, Y
AF Yang, Ying-nan
   Zhang, Rui
   Du, Jing-wen
   Yuan, Heng-heng
   Li, Yan-jing
   Wei, Xiao-li
   Du, Xiao-xue
   Jiang, Shu-lin
   Han, Yu
TI Predictive role of UCA1-containing exosomes in cetuximab-resistant
   colorectal cancer
SO CANCER CELL INTERNATIONAL
LA English
DT Article
DE UCA1; Exosomes; Cetuximab; Metastatic colorectal cancer; Biomarker
ID LONG NONCODING RNA; HEPATOCELLULAR-CARCINOMA; EXTRACELLULAR VESICLES;
   BREAST-CANCER; UCA1; MICROENVIRONMENT; PROLIFERATION; CHEMOTHERAPY;
   CELLS; PANITUMUMAB
AB BackgroundPrimary or acquired resistance to cetuximab often occurs during targeted therapy in metastatic colorectal cancer (mCRC) patients. In many cancers, the key role of the long noncoding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) in anticancer drug resistance has been confirmed. Emerging evidence has shown that specific exosomal lncRNAs may serve as meaningful biomarkers. In this study, we hypothesize that exosomal UCA1 might predict the response to cetuximab in CRC patients.MethodsFirst, acquired cetuximab-resistant cell lines were generated, and UCA1 expressions in these cells and their exosomes were compared. We also systematically evaluate the stability of exosomal UCA1. Thereafter, the predictive value of exosomal UCA1 in CRC patients treated with cetuximab was evaluated. Finally, through cell apoptosis assays and immunofluorescence staining, we analyzed the role of UCA1-containing exosomes in conferring cetuximab resistance.ResultsUCA1 expression was markedly higher in cetuximab-resistant cancer cells and their exosomes. Exosomal UCA1 was shown to be detectable and stable in serum from CRC patients. In addition, circulating UCA1-containing exosomes could predict the clinical outcome of cetuximab therapy in CRC patients, and UCA1 expression was considerably higher in the progressive disease/stable disease patients than in the partial response/complete response patients. Furthermore, exosomes derived from cetuximab-resistant cells could alter UCA1 expression and transmit cetuximab resistance to sensitive cells.ConclusionsWe discovered a novel role of UCA1-containing exosomes, showed their capability to transmit drug resistance and investigated their potential clinical use in predicting cetuximab resistance.
C1 [Yang, Ying-nan] Harbin Med Univ, Dept Thorac Surg, Canc Hosp, Harbin, Heilongjiang, Peoples R China.
   [Zhang, Rui] China Med Univ, Liaoning Canc Hosp & Inst, Dept Colorectal Surg, Canc Hosp, Shenyang, Liaoning, Peoples R China.
   [Du, Jing-wen; Yuan, Heng-heng; Li, Yan-jing; Wei, Xiao-li; Du, Xiao-xue; Han, Yu] Harbin Med Univ, Dept Gastrointestinal Oncol, Canc Hosp, 150 Haping Rd, Harbin 150081, Heilongjiang, Peoples R China.
   [Jiang, Shu-lin] Harbin Med Univ, Dept Cardiovasc Surg, Affiliated Hosp 2, 246 Xuefu Rd, Harbin 150001, Heilongjiang, Peoples R China.
C3 Harbin Medical University; China Medical University; Harbin Medical
   University; Harbin Medical University
RP Han, Y (corresponding author), Harbin Med Univ, Dept Gastrointestinal Oncol, Canc Hosp, 150 Haping Rd, Harbin 150081, Heilongjiang, Peoples R China.; Jiang, SL (corresponding author), Harbin Med Univ, Dept Cardiovasc Surg, Affiliated Hosp 2, 246 Xuefu Rd, Harbin 150001, Heilongjiang, Peoples R China.
EM sljiang36@163.com; hanyu_2017@126.com
RI WANG, JIAXUAN/JMP-8599-2023
OI Han, Yu/0000-0002-5910-6307
FU Key Project of Haiyan Research Fund of Harbin Medical University Cancer
   Hospital [JJZD2018-06]; WU Jieping Medical Foundation [320.6750.16172]
FX This study was supported by the Key Project of Haiyan Research Fund of
   Harbin Medical University Cancer Hospital (No. JJZD2018-06) and WU
   Jieping Medical Foundation (No. 320.6750.16172).
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NR 46
TC 75
Z9 85
U1 0
U2 12
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1475-2867
J9 CANCER CELL INT
JI Cancer Cell Int.
PD OCT 22
PY 2018
VL 18
AR 164
DI 10.1186/s12935-018-0660-6
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GX8JM
UT WOS:000448031200003
PM 30377411
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ma, R
   Li, T
AF Ma, Rui
   Li, Tao
TI Conversion therapy combined with individualized surgical treatment
   strategy improves survival in patients with colorectal cancer liver
   metastases
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE Colorectal cancer; liver metastasis; initially resectable; initially
   unresectable; conversion therapy
ID HEPATIC METASTASES; SURGERY; RESECTION; CHEMOTHERAPY; MANAGEMENT;
   CONSENSUS; ABLATION; OUTCOMES; TERM
AB Objective: To explore surgical treatment strategies for patients with liver metastases from colorectal cancer (CRLM), and analyze the prognosis and influencing factors. Methods: The clinical data of 156 inpatients with CRLM admitted to our hospital from January 2009 to June 2019 were retrospectively analyzed. Patients were divided into initially resectable group (80 cases) and initially unresectable group (76 cases). For patients with initially unresectable CRLM, conversion therapy (chemotherapy plus targeted therapy) combined with individualized surgical treatment strategy was used. The individualized surgical treatment strategy mainly included hepatectomy combined with ablation. Portal vein ligation and staged resection were adopted according to the patients? specific conditions. All patients were followed up until death. The Kaplan-Meier method and Log-rank test were used for survival analysis. Results: Median overall survival (OS) time of patients in the initially resectable group and initially unresectable group were 36 months and 17 months, respectively (P = 0.001). Median OS time of 24 patients who underwent surgical resection after successful conversion therapy was significantly longer than that of 52 patients with unsuccessful conversion therapy (20 months versus 15 months, respectively, P = 0.034). Univariate analysis showed that a maximum diameter of liver metastases < 6 cm and a number of metastases ? 4 were independent factors associated with successful conversion therapy. According to patients? specific conditions, 6 cases accepted hepatectomy combined with ablation, and 1 case accepted portal vein ligation and staged resection. Conclusion: Treatment of patients with CRLM should follow the principles of standardization and individualization. For patients with initially unresectable CRLM, successful conversion therapy should be pursued whenever possible. The maximum size and number of liver metastases were significantly associated with successful conversion therapy. Surgical resection-based comprehensive treatment is key.
C1 [Ma, Rui] Peking Univ Peoples Hosp, Dept Crit Med, 11 Xizhimen South St, Beijing 100044, Peoples R China.
   [Li, Tao] Peking Univ Peoples Hosp, Dept Hepatobiliary Surg, 11 Xizhimen South St, Beijing 100044, Peoples R China.
C3 Peking University
RP Li, T (corresponding author), Peking Univ Peoples Hosp, Dept Hepatobiliary Surg, 11 Xizhimen South St, Beijing 100044, Peoples R China.
EM ltlitao@hotmail.com
RI Li, Tingting/HKE-0812-2023
FU Beijing Natural Science Foundation [7192212]
FX This research was supported by Beijing Natural Science Foundation
   (7192212).
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NR 30
TC 4
Z9 4
U1 0
U2 0
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 2021
VL 14
IS 3
BP 314
EP 321
PG 8
WC Oncology; Pathology
WE Emerging Sources Citation Index (ESCI)
SC Oncology; Pathology
GA QW8FB
UT WOS:000628882300002
PM 33786148
DA 2025-01-04
ER

PT J
AU Franchi, M
   Garau, D
   Kirchmayer, U
   Di Martino, M
   Romero, M
   De Carlo, I
   Scondotto, S
   Corrao, G
AF Franchi, Matteo
   Garau, Donatella
   Kirchmayer, Ursula
   Di Martino, Mirko
   Romero, Marilena
   De Carlo, Ilenia
   Scondotto, Salvatore
   Corrao, Giovanni
TI Effectiveness and Costs Associated to Adding Cetuximab or Bevacizumab to
   Chemotherapy as Initial Treatment in Metastatic Colorectal Cancer:
   Results from the Observational FABIO Project
SO CANCERS
LA English
DT Article
DE colorectal cancer; target therapy; effectiveness; cost-effectiveness;
   survival; long-term outcomes
ID MEAN SURVIVAL-TIME; FLUOROURACIL; OXALIPLATIN; COMBINATION; LEUCOVORIN
AB Evidence available on the effectiveness and costs of biological therapies for the initial treatment of metastatic colorectal cancer (mCRC) is scarce and contrasting. We conducted a population-based cohort investigation for assessing overall survival and costs associated with their use in a real-world setting. Healthcare utilization databases were used to select patients newly diagnosed with mCRC between 2010 and 2016. Those initially treated with biological therapy (bevacizumab or cetuximab) added to chemotherapy were propensity-score-matched to those treated with standard chemotherapy alone, and were followed up to June 30th, 2018. Kaplan-Meier survival estimates, restricted mean survival time (RMST) and cumulative costs were compared between the two treatment arms. The study cohort included 1896 mCRC patients treated with biological therapy matched to 5678 patients treated with chemotherapy alone. Median overall survival was 21.8 and 20.2 months, respectively. After 84 months of follow-up, RMSTs were 30.9 and 31.9 months (p = 0.193), indicating no differences between the average survival time between treatment arms. Patients treated with biological therapy were associated with higher costs. Cumulative per capita costs were Euro59,663 and Euro44,399, respectively. In our study, first-line biological therapy did not improve long-term overall survival and was associated with higher costs as compared to standard chemotherapy.
C1 [Franchi, Matteo; Corrao, Giovanni] Natl Ctr Healthcare Res & Pharmacoepidemiol, I-20126 Milan, Italy.
   [Franchi, Matteo; Corrao, Giovanni] Univ Milano Bicocca, Dept Stat & Quantitat Methods, Lab Healthcare Res & Pharmacoepidemiol, I-20126 Milan, Italy.
   [Garau, Donatella] Gen Directorate Hlth, I-09123 Cagliari, Sardinia Region, Italy.
   [Kirchmayer, Ursula; Di Martino, Mirko] Lazio Reg Hlth Serv, Dept Epidemiol ASL Roma 1, I-00154 Rome, Italy.
   [Romero, Marilena] Univ G dAnnunzio, Dept Med Oral & Biotechnol Sci, Sect Pharmacol & Toxicol, I-66100 Chieti, Italy.
   [De Carlo, Ilenia] Reg Hlth Author, Reg Ctr Pharmacovigilance, I-60125 Ancona, Marche Region, Italy.
   [Scondotto, Salvatore] Reg Hlth Author, Dept Hlth Serv & Epidemiol Observ, I-90145 Palermo, Sicily Region, Italy.
C3 University of Milano-Bicocca; G d'Annunzio University of Chieti-Pescara
RP Franchi, M (corresponding author), Natl Ctr Healthcare Res & Pharmacoepidemiol, I-20126 Milan, Italy.; Franchi, M (corresponding author), Univ Milano Bicocca, Dept Stat & Quantitat Methods, Lab Healthcare Res & Pharmacoepidemiol, I-20126 Milan, Italy.
EM matteo.franchi@unimib.it
RI Franchi, Matteo/AAN-5991-2020; Kirchmayer, Ursula/L-7847-2016;
   Scondotto, Salvatore/KLD-5149-2024
OI De Carlo, Ilenia/0000-0002-4638-296X; FRANCHI,
   MATTEO/0000-0001-9620-8057; Scondotto, Salvatore/0000-0001-7620-3080
FU AIFA-the Italian Medicines Agency [H56J16000500005]; Sardinia Region
   [H56D15000030005]; Italian Ministry of Education, University and
   Research ('Fondo d'Ateneo per la Ricerca' portion)
FX This research was funded by a research grant from the AIFA-the Italian
   Medicines Agency-(project AIFA-Fondi Farmacovigilanza Attiva; CUP code
   H56J16000500005) and from the Sardinia Region (CUP code
   H56D15000030005). Data analyses were performed at the Laboratory of
   Healthcare Research & Pharmacoepidemiology, University of Milano-Bicocca
   with grants from the Italian Ministry of Education, University and
   Research ('Fondo d'Ateneo per la Ricerca' portion, year 2018).
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NR 24
TC 10
Z9 10
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 APR
PY 2020
VL 12
IS 4
AR 839
DI 10.3390/cancers12040839
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LR3IP
UT WOS:000535587400068
PM 32244478
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lee, JW
   Lee, JH
   Shim, BY
   Kim, SH
   Chung, MJ
   Kye, BH
   Kim, HJ
   Cho, HM
   Jang, HS
AF Lee, Jeong Won
   Lee, Jong Hoon
   Shim, Byoung Yong
   Kim, Sung Hwan
   Chung, Mi-Joo
   Kye, Bong-Hyeon
   Kim, Hyung Jin
   Cho, Hyeon Min
   Jang, Hong Seok
TI KRAS Mutation Status Is Not a Predictor for Tumor Response and Survival
   in Rectal Cancer Patients Who Received Preoperative Radiotherapy With
   5-Fluoropyrimidine Followed by Curative Surgery
SO MEDICINE
LA English
DT Article
ID COLORECTAL-CANCER; TARGETED THERAPY; RAS MUTATIONS; CHEMORADIOTHERAPY;
   RADIATION; CHEMORADIATION; CETUXIMAB; CHEMOTHERAPY; RECURRENCE;
   BIOMARKERS
AB We evaluated the tumor response and survival according to the KRAS oncogene status in locally advanced rectal cancer. One hundred patients with locally advanced rectal cancer (cT3-4N0-2M0) received preoperative radiation of 50.4Gy in 28 fractions with 5-fluorouracil and total mesorectal excision. Tumor DNA from each patient was obtained from pretreatment biopsy tissues. A Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation was found in 26 (26%) of the 100 patients. Downstaging (ypT0-2N0M0) rates after preoperative chemoradiotheray were not statistically different between the wild-type and mutant-type KRAS groups (30.8% vs 27.0%, P=0.715, respectively). After a median follow-up time of 34 months, there was no statistically significant difference in the 3-year relapse-free survival (82.2% vs 82.6%, P=0.512) and overall survival (94.7% vs 92.3%, P=0.249) rates between wild-type and mutant-type KRAS groups, respectively. The KRAS mutation status does not influence the tumor response to the radiotherapy and survival in locally advanced rectal cancer patients who received preoperative chemoradiotherapy and curative surgery.
C1 [Lee, Jeong Won; Jang, Hong Seok] Catholic Univ Korea, Seoul St Marys Hosp, Dept Radiat Oncol, Seoul, South Korea.
   [Lee, Jong Hoon; Kim, Sung Hwan; Chung, Mi-Joo] Catholic Univ Korea, St Vincents Hosp, Coll Med, Dept Radiat Oncol, Seoul, South Korea.
   [Shim, Byoung Yong] Catholic Univ Korea, St Vincents Hosp, Coll Med, Dept Med Oncol, Seoul, South Korea.
   [Kye, Bong-Hyeon; Kim, Hyung Jin; Cho, Hyeon Min] Catholic Univ Korea, St Vincents Hosp, Coll Med, Dept Colorectal Surg, Seoul, South Korea.
C3 Catholic University of Korea; Seoul St. Mary's Hospital; Catholic
   University of Korea; Catholic University of Korea; Catholic University
   of Korea
RP Lee, JW (corresponding author), St Vincents Hosp, Dept Radiat Oncol, 93 Ji Dong, Seoul, South Korea.
EM koppul@catholic.ac.kr; hsjang11@catholic.ac.kr
RI Kim, Sung Hwan/GQQ-1731-2022; Lee, Heejin/HTT-4810-2023
FU Catholic Medical Center Research Foundation
FX The authors thank the financial support of the Catholic Medical Center
   Research Foundation made in the program year of 2015. Financial support
   of the Catholic Medical Center Research Foundation made in the program
   year of 2015. Jeong Won Lee, Byoung Yong Shim, and Sung Hwan Kim equally
   contributed to this work.
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NR 31
TC 19
Z9 19
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD AUG
PY 2015
VL 94
IS 31
AR e1284
DI 10.1097/MD.0000000000001284
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA CV5IU
UT WOS:000364304000001
PM 26252300
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Geva, R
   Vecchione, L
   Kalogeras, KT
   Jensen, BV
   Lenz, HJ
   Yoshino, T
   Paez, D
   Montagut, C
   Souglakos, J
   Cappuzzo, F
   Cervantes, A
   Frattini, M
   Fountzilas, G
   Johansen, JS
   Hogdall, EV
   Zhang, W
   Yang, DY
   Yamazaki, K
   Nishina, T
   Papamichael, D
   Vincenzi, B
   Macarulla, T
   Loupakis, F
   De Schutter, J
   Spindler, KLG
   Pfeiffer, P
   Ciardiello, F
   Piessevaux, H
   Tejpar, S
AF Geva, Ravit
   Vecchione, Loredana
   Kalogeras, Konstantinos T.
   Jensen, Benny Vittrup
   Lenz, Heinz-Josef
   Yoshino, Takayuki
   Paez, David
   Montagut, Clara
   Souglakos, John
   Cappuzzo, Federico
   Cervantes, Andres
   Frattini, Milo
   Fountzilas, George
   Johansen, Julia S.
   Hogdall, Estrid Vilma
   Zhang, Wu
   Yang, Dongyun
   Yamazaki, Kentaro
   Nishina, Tomohiro
   Papamichael, Demetris
   Vincenzi, Bruno
   Macarulla, Teresa
   Loupakis, Fotios
   De Schutter, Jef
   Spindler, Karen Lise Garm
   Pfeiffer, Per
   Ciardiello, Fortunato
   Piessevaux, Hubert
   Tejpar, Sabine
TI FCGR polymorphisms and cetuximab efficacy in chemorefractory metastatic
   colorectal cancer: an international consortium study
SO GUT
LA English
DT Article
DE Antibody Targeted Therapy; Colorectal Cancer; Genetic Polymorphisms;
   Immune Response
ID GROWTH-FACTOR-RECEPTOR; SINGLE-AGENT CETUXIMAB; B-CELL LYMPHOMA; PLUS
   IRINOTECAN; BREAST-CANCER; FOLLICULAR LYMPHOMA; PREDICT RESPONSE; KRAS
   MUTATIONS; K-RAS; THERAPY
AB Objective We aimed to better clarify the role of germline variants of the FCG2 receptor, FCGR2A-H131R and FCGR3A-V158F, on the therapeutic efficacy of cetuximab in metastatic colorectal cancer (mCRC). A large cohort with sufficient statistical power was assembled.
   Design To show a HR advantage of 0.6 in progression-free survival (PFS) for FCGR2A-HH versus the rest and FCGR3A-VV versus the rest, with an 80% power, 80 Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) wild-type (KRAS-WT) and 52 KRAS-WT patients are required, respectively. This leads to a total sample size of 952 and 619 patients, respectively. Samples were collected from 1123 mCRC patients from 15 European centres treated with cetuximab alone or in combination with chemotherapy. Fc gamma receptor (FCGR) status was centrally genotyped. Two additional externally genotyped series were included.
   Results Incidences of FCGR2A-HH and FCGR3A-VV in KRAS-WT patients were 220/660 (33%) and 109/676 (16.1%) respectively. There was no difference in median PFS (mPFS) for KRAS-WT patients with FCGR2A-HH (22.0weeks; 95% CI18.8 to 25.2) versus non-HH (22.0weeks; 95% CI 19.4 to 24.6) or for FCGR3A-VV (16.4weeks; 95% CI 13.0 to 19.8) versus non-VV (23weeks; 95% CI 21.1 to 24.9) (p=0.06). Median overall survival, response rate and disease control rate assessments showed no benefit for either HH or VV.
   Conclusions No differences in mPFS were found between the FCGR polymorphisms HH and the others and VV versus the others in KRAS-WT mCRC patients refractory to irinotecan, oxaliplatin and 5-fluorouracil treated with cetuximab. We cannot confirm the effects of other IgG1 antibodies, which may be weaker than previously suggested. Other markers may be needed to study the actual host antibody response to cetuximab.
C1 [Geva, Ravit] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, Dept Oncol, IL-69978 Tel Aviv, Israel.
   [Vecchione, Loredana; De Schutter, Jef; Tejpar, Sabine] Univ Hosp Gasthuisberg, Lab Mol Digest Oncol, B-3000 Leuven, Belgium.
   [Kalogeras, Konstantinos T.; Fountzilas, George] Hellen Cooperat Oncol Grp HeCOG, Athens, Greece.
   [Jensen, Benny Vittrup; Johansen, Julia S.] Herlev Hosp, Copenhagen, Denmark.
   [Lenz, Heinz-Josef; Zhang, Wu; Yang, Dongyun] USC Norris Comprehens Canc Ctr & Hosp, Los Angeles, CA USA.
   [Yoshino, Takayuki] Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa, Chiba, Japan.
   [Paez, David] Hosp Santa Creu & Sant Pau, Barcelona, Spain.
   [Montagut, Clara] Univ Hosp del Mar IMIM, Dept Oncol, Barcelona, Spain.
   [Souglakos, John] Univ Crete, Univ Gen Hosp Heraklion, Dept Med Oncol, Iraklion, Greece.
   [Souglakos, John] Univ Crete, Tumor Cell Biol Lab, Sch Med, Iraklion, Greece.
   [Cappuzzo, Federico] Osped Civile Livorno, Livorno, Italy.
   [Cervantes, Andres] Univ Valencia, INCLIVA, Dept Hematol & Med Oncol, Valencia, Spain.
   [Frattini, Milo] Inst Pathol, Lab Mol Pathol, Locarno, Switzerland.
   [Hogdall, Estrid Vilma] Herlev Univ Hosp, Dept Pathol, Copenhagen, Denmark.
   [Yamazaki, Kentaro] Shizuoka Canc Ctr, Div Gastrointestinal Oncol, Shizuoka, Japan.
   [Nishina, Tomohiro] Shikoku Canc Ctr, Natl Hosp Org, Dept Gastrointestinal Med Oncol, Matsuyama, Ehime, Japan.
   [Papamichael, Demetris] BO Cyprus Oncol Ctr, Nicosia, Cyprus.
   [Vincenzi, Bruno] Univ Campus Biomed, Rome, Italy.
   [Macarulla, Teresa] Hosp Valle De Hebron, Barcelona, Spain.
   [Loupakis, Fotios] Azienda Osped Univ Pisana, Ist Toscano, UO Oncol Med 2, Pisa, Italy.
   [Spindler, Karen Lise Garm] Vejle Hosp, Dept Oncol, Vejle, Denmark.
   [Pfeiffer, Per] Odense Univ Hosp, Dept Oncol, DK-5000 Odense, Denmark.
   [Ciardiello, Fortunato] Univ Naples 2, Dept Expt & Clin Med, Div Med Oncol, Naples, Italy.
   [Piessevaux, Hubert] Clin Univ St Luc, B-1200 Brussels, Belgium.
C3 Tel Aviv University; Tel Aviv Sourasky Medical Center; KU Leuven;
   University Hospital Leuven; Hellenic Cooperative Oncology Group;
   University of Copenhagen; Herlev & Gentofte Hospital; University of
   Southern California; National Cancer Center - Japan; Hospital of Santa
   Creu i Sant Pau; Hospital del Mar Research Institute; Hospital del Mar;
   University of Crete; University Hospital of Heraklion; University of
   Crete; University of Valencia; University of Copenhagen; Herlev &
   Gentofte Hospital; Shizuoka Cancer Center; University Campus Bio-Medico
   - Rome Italy; Hospital Universitari Vall d'Hebron; University of Pisa;
   Azienda Ospedaliero Universitaria Pisana; University of Southern
   Denmark; Lillebaelt Hospital; University of Southern Denmark; Odense
   University Hospital; Universita della Campania Vanvitelli; Universite
   Catholique Louvain; Cliniques Universitaires Saint-Luc
RP Tejpar, S (corresponding author), Univ Hosp Gasthuisberg, Lab Mol Digest Oncol, Herestr 49, B-3000 Leuven, Belgium.
EM sabine.tejpar@uzleuven.be
RI Piessevaux, Hubert/N-9558-2019; Fountzilas, George/ABF-2139-2020;
   Macarulla, Teresa/AAG-9230-2019; Yang, Dongyun/M-2579-2019; Cappuzzo,
   Federico/R-2827-2016; Cervantes, Andres/J-8713-2013; Loupakis,
   Fotios/I-7243-2012
OI Ciardiello, Fortunato/0000-0002-3369-4841; Hogdall,
   Estrid/0000-0003-4689-5658; Pfeiffer, Per/0000-0002-2925-0586; Cappuzzo,
   Federico/0000-0002-6295-6767; Fountzilas, George/0000-0001-8045-2186;
   vecchione, loredana/0000-0003-3942-5498; Cervantes,
   Andres/0000-0003-3806-3691; Macarulla, Teresa/0000-0002-5856-4082;
   Loupakis, Fotios/0000-0001-9651-0395; Yang, Dongyun/0000-0003-0736-4977;
   Piessevaux, Hubert/0000-0003-1193-0601
FU ESMO fellowship for Translational Research; Ministry of Health, Labour
   and Welfare of Japan [21 S4-5]; Associazione italiana per la ricerca sul
   cancro (AIRC); Ministero dell'Istruzione, dell'Universita della Ricerca
   (MIUR); progetti di ricerca di interesse nazionale (PRIN); Instituto de
   Salud Carlos III [FIS/1101711]; Belgian Federation against Cancer
   (Stichting tegen Kanker); Belgian National Cancer Plan (Nationaal
   Kankerplan);  [PI12/00989];  [AECC 11964]
FX LV is supported by an ESMO fellowship for Translational Research. TY is
   supported by the Grant-in-Aid for Cancer Research (21 S4-5) from the
   Ministry of Health, Labour and Welfare of Japan. FC is sponsored by a
   grant from Associazione italiana per la ricerca sul cancro (AIRC) and
   from Ministero dell'Istruzione, dell'Universita della Ricerca (MIUR) and
   progetti di ricerca di interesse nazionale (PRIN). DP is supported by
   the Instituto de Salud Carlos III (FIS/1101711). CMV is supported by
   PI12/00989 and AECC 11964. ST is a Senior Clinical Investigator of the
   Fund for Scientific Research Flanders (FWO-Vlaanderen) and has received
   research grants from the Belgian Federation against Cancer (Stichting
   tegen Kanker) and from the Belgian National Cancer Plan (Nationaal
   Kankerplan).
CR Ahlgrimm M, 2011, BLOOD, V118, P4657, DOI 10.1182/blood-2011-04-346411
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NR 28
TC 19
Z9 21
U1 0
U2 9
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD JUN
PY 2015
VL 64
IS 6
BP 921
EP 928
DI 10.1136/gutjnl-2014-307234
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CH9TT
UT WOS:000354380000012
PM 25011934
DA 2025-01-04
ER

PT J
AU Deng, YM
   Zhao, C
   Wu, L
   Qu, Z
   Wang, XY
AF Deng, You-Ming
   Zhao, Cheng
   Wu, Lei
   Qu, Zhan
   Wang, Xin-Yu
TI Cannabinoid Receptor-1 suppresses M2 macrophage polarization in
   colorectal cancer by downregulating EGFR
SO CELL DEATH DISCOVERY
LA English
DT Article
ID TUMOR-ASSOCIATED MACROPHAGES; EPITHELIAL-MESENCHYMAL TRANSITION;
   GROWTH-FACTOR RECEPTOR; COLON-CANCER; INFILTRATING MACROPHAGES;
   PANCREATIC-CANCER; CELLS; ACTIVATION; EXPRESSION; MICROENVIRONMENT
AB Cannabinoid receptors, CB1 and CB2, have been implicated as emerging targets for cancer therapy. Herein, we investigated the potential regulation mechanism of CB1 and its implications in colorectal cancer. CB1 and EGFR expression were examined in colorectal cancer cell lines. The effects of CB1 agonist ACEA and its antagonist AM251 on the proliferation, migration and invasion of colorectal cancer cells and the expression of M1 and M2 macrophage markers were examined. EGFR overexpression was performed with plasmids containing EGFR gene. Tumor xenografts were constructed to explore the effects of CB1 activation on tumorigenesis. We showed that CB1 was downregulated while EGFR was upregulated in colorectal cancer cells. The activation of CB1 suppressed the proliferation, migration and invasion of colorectal cancer cells and the differentiation of M2 macrophages, while CB1 inhibition had opposite effects. Moreover, the alterations in tumorigenesis and M2 macrophage activation induced by CB1 activation were counteracted by EGFR overexpression. Besides, CB1 silencing promoted tumor cell proliferation and M2 polarization which was counteracted by EGFR knockdown. In vivo, CB1 activation also repressed tumorigenesis and M2 macrophage activation. The present study demonstrated that CB1 activation suppressed M2 macrophage through EGFR downregulation in colorectal cancers. These findings first unveiled the potential avenue of CB1 as a targeted therapy for colorectal cancer.
C1 [Deng, You-Ming; Qu, Zhan; Wang, Xin-Yu] Cent South Univ, Xiangya Hosp, Dept Essential Surg, Changsha 410008, Peoples R China.
   [Zhao, Cheng] Shenzhen Univ, Dept Endocrinol, Affiliated Hosp 1, Shenzhen 518037, Peoples R China.
   [Wu, Lei] Nanjing Univ, Res Inst Gen Surg, Jinling Hosp, Nanjing 210093, Peoples R China.
C3 Central South University; Shenzhen University; Nanjing University
RP Qu, Z (corresponding author), Cent South Univ, Xiangya Hosp, Dept Essential Surg, Changsha 410008, Peoples R China.
EM quzhan@csu.edu.cn
RI Wang, Xinyu/O-4266-2015
OI , Zhan/0000-0002-0936-3284
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NR 39
TC 10
Z9 11
U1 2
U2 23
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2058-7716
J9 CELL DEATH DISCOV
JI Cell Death Discov.
PD MAY 31
PY 2022
VL 8
IS 1
AR 273
DI 10.1038/s41420-022-01064-8
PG 10
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 1S2XH
UT WOS:000803918700001
PM 35641479
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Liu, DX
   Wang, FF
   Yue, J
   Jing, XB
   Huang, YB
AF Liu, Daxing
   Wang, Feifei
   Yue, Jun
   Jing, Xiabin
   Huang, Yubin
TI Metabolism targeting therapy of dichloroacetate-loaded electrospun mats
   on colorectal cancer
SO DRUG DELIVERY
LA English
DT Article
DE Colorectal cancer; diisopropylamine dichloroacetate (DADA); electrospun
   mats; metabolism targeting; sodium dichloroacetate (DCA)
ID TUMOR; APOPTOSIS; TRANSPORTER; RESISTANCE; INHIBITORS; GROWTH; STROMA;
   DCA
AB Differences in energy metabolism between tumor cells and normal cells offer an attractive avenue of research into drug targets for tumor therapy. The use of a metabolic modulator (sodium dichloroacetate, DCA), administered in situ, to reverse the "Warburg effect'' of tumor cells has been demonstrated as an effective tumor therapy. Herein, DCA and diisopropylamine dichloroacetate (DADA) were incorporated separately into polylactide (PLA) electrospun mats and applied to C26 tumor-bearing mice via in situ administration. After 12 d of treatment, the tumor suppression rates of 75% and 84% were achieved in the DC group (treated with a DCA-loaded mat) and the DA group (treated with a DADA-loaded mat), respectively. With tolerable physiologic toxicity under high local concentration, the DA group showed a 95% tumor suppression rate without any recurrence after 15 d of therapy. The desirable therapeutic effects of these metabolic modulators should ascribe to the energy-central metabolism-targeting effects of DCA and DADA, which were demonstrated both in vitro and in vivo. Therefore, DCA-and DADA-loaded mats are the effective anti-cancer drugs dosages to discriminate between tumor cells and normal cells for minimizing systemic toxicity.
C1 [Liu, Daxing; Wang, Feifei; Yue, Jun; Jing, Xiabin; Huang, Yubin] Chinese Acad Sci, Changchun Inst Appl Chem, State Key Lab Polymer Phys & Chem, Changchun 130022, Peoples R China.
   [Liu, Daxing; Wang, Feifei; Yue, Jun; Jing, Xiabin] Chinese Acad Sci, Grad Sch, Beijing, Peoples R China.
C3 Chinese Academy of Sciences; Changchun Institute of Applied Chemistry,
   CAS; Chinese Academy of Sciences; University of Chinese Academy of
   Sciences, CAS
RP Huang, YB (corresponding author), Chinese Acad Sci, Changchun Inst Appl Chem, State Key Lab Polymer Phys & Chem, Changchun 130022, Peoples R China.
EM ybhuang@ciac.ac.cn
RI Liu, Daxing/A-7665-2017; , Jun/M-1049-2018
OI Liu, Daxing/0000-0001-8532-9611; , Jun/0000-0001-8038-3555
FU National Natural Science Foundation of China [51273194, 51021003,
   50733003, 21174143]; Ministry of Science and Technology of China
   [2009CB930102, 2012AA021900]; Jilin Provincial Science and Technology
   Department [20100588]
FX The authors would like to thank the financial support from the National
   Natural Science Foundation of China (Nos. 51273194, 51021003, 50733003,
   and 21174143), the Ministry of Science and Technology of China (Nos.
   2009CB930102 and 2012AA021900), and Jilin Provincial Science and
   Technology Department (No. 20100588).
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NR 36
TC 15
Z9 19
U1 2
U2 36
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1071-7544
EI 1521-0464
J9 DRUG DELIV
JI Drug Deliv.
PD JAN
PY 2015
VL 22
IS 1
BP 136
EP 143
DI 10.3109/10717544.2013.870258
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA AX5OC
UT WOS:000346975000015
PM 24359441
DA 2025-01-04
ER

PT J
AU Sun, XL
   Li, SW
   Shen, BZ
AF Sun, Xilin
   Li, Shaowei
   Shen, Baozhong
TI Identification of Disease States and Response to Therapy in Humans by
   Utilizing the Biomarker EGFR for Targeted Molecular Imaging
SO CURRENT PROTEIN & PEPTIDE SCIENCE
LA English
DT Review
DE Molecular imaging; cancer; biomarker; EGFR; positron emission
   tomography; molecular medicine
ID GROWTH-FACTOR RECEPTOR; LUNG-CANCER; IRREVERSIBLE INHIBITOR;
   COLORECTAL-CANCER; TUMOR RESPONSE; PET; DRUG; AGENTS; NANOPARTICLES;
   BIODISTRIBUTION
AB The epidermal growth factor receptor (EGFR) plays important roles in cell proliferation, suppression of apoptosis, increased motility, and recruitment of neovasculature. Overexpressed or mutated EGFR has been an important biomarker for cancer diagnosis and molecular target for many anticancer drugs because it frequently occurs in many common human cancers. Localizing and estimating the expression of EGFR can potentially identify patients who have tumors that overexpress EGFR and would, therefore, most likely benefit from a targeted treatment to avoid overtreatment and undertreatment. Traditional biopsy methods are invasive, and analysis of the specimens is not sufficient for real-time detection of the lesions or for monitoring the therapeutic efficacy of anticancer drugs. Molecular imaging, a technology of in vivo characterization and measurement of biological processes at the cellular and molecular level, can fulfill these goals. In this review, we summarize current molecular imaging techniques including optical imaging, magnetic resonance imaging, single photon emission computed tomography, and positron emission tomography for in vivo EGFR visualization and discuss their advantages and disadvantages. Special emphasis is placed on noninvasive imaging mutant EGFR with emerging new agents and new imaging technologies to distinguish the maximum benefit to cancer patients for molecular targeted therapy.
C1 [Sun, Xilin; Li, Shaowei; Shen, Baozhong] Harbin Med Univ, TOF PET CT MR Ctr, Hosp 4, 31 Yinhang St, Harbin 150001, Heilongjiang, Peoples R China.
   [Sun, Xilin; Li, Shaowei; Shen, Baozhong] Harbin Med Univ, Mol Imaging Res Ctr, Harbin, Heilongjiang, Peoples R China.
C3 Harbin Medical University; Harbin Medical University
RP Shen, BZ (corresponding author), Harbin Med Univ, TOF PET CT MR Ctr, Hosp 4, 31 Yinhang St, Harbin 150001, Heilongjiang, Peoples R China.
EM shenbzh@vip.sina.com
RI Li, Shaowei/O-4531-2019; Sun, Xilin/GXH-0270-2022
FU National Natural Science Foundation of China [81471724, 81101088,
   81130028, 31210103913]; National Basic Research Program of China
   [2015CB931800]; Innovation Fund Designated of Harbin [2014RFQGJ011];
   Heilongjiang Postdoctoral Science Foundation [LBH-Q15089, LBH-TZ0414,
   LBH-Z12199]; Heilongjiang Province Department of Education Science and
   Technology Research Projects [12521184]; China Postdoctoral Science
   Foundation [2013T60388, 2012M510095]; Youth Science WU LIANDE Foundation
   of Harbin Medical University [WLD-QN1119]; Fourth Hospital of Harbin
   Medical University Fund for Distinguished Young Scholars; Key Grant
   Project of Heilongjiang Province [GA12C302]
FX This work was supported by the National Natural Science Foundation of
   China (81471724, 81101088, 81130028, 31210103913), the National Basic
   Research Program of China (2015CB931800), Innovation Fund Designated of
   Harbin (2014RFQGJ011), Heilongjiang Postdoctoral Science Foundation
   (LBH-Q15089, LBH-TZ0414, LBH-Z12199), Heilongjiang Province Department
   of Education Science and Technology Research Projects (12521184), China
   Postdoctoral Science Foundation (2013T60388, 2012M510095), the Youth
   Science WU LIANDE Foundation of Harbin Medical University (WLD-QN1119),
   the Fourth Hospital of Harbin Medical University Fund for Distinguished
   Young Scholars, and the Key Grant Project of Heilongjiang Province
   (GA12C302).
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NR 84
TC 5
Z9 5
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 1389-2037
EI 1875-5550
J9 CURR PROTEIN PEPT SC
JI Curr. Protein Pept. Sci.
PY 2016
VL 17
IS 6
BP 534
EP 542
DI 10.2174/1389203717666160101123610
PG 9
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA DS4VL
UT WOS:000380779600003
PM 26721405
DA 2025-01-04
ER

PT J
AU Ochoa-Sanchez, A
   Sahare, P
   Pathak, S
   Banerjee, A
   Estevez, M
   Duttaroy, AK
   Luna-Bárcenas, G
   Paul, S
AF Ochoa-Sanchez, Adriana
   Sahare, Padmavati
   Pathak, Surajit
   Banerjee, Antara
   Estevez, Miriam
   Duttaroy, Asim K.
   Luna-Barcenas, Gabriel
   Paul, Sujay
TI Evaluation of the synergistic effects of curcumin-resveratrol co-loaded
   biogenic silica on colorectal cancer cells
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE colorectal cancer; curcumin; resveratrol; bioformulation; biogenic
   silica; therapy
ID DRUG-DELIVERY SYSTEM; MESOPOROUS SILICA; TARGETED THERAPY; NANOPARTICLES
AB Colorectal cancer (CRC) remains a significant global health concern, being the third most diagnosed cancer in men and the second most diagnosed cancer in women, with alarming mortality rates. Natural phytochemicals have gained prominence among various therapeutic avenues explored due to their diverse biological properties. Curcumin, extracted from turmeric, and resveratrol, a polyphenol found in several plants, have exhibited remarkable anticancer activities. However, their limited solubility and bioavailability hinder their therapeutic efficacy. To enhance the bioavailability of these compounds, nanomaterials work as effective carriers with biogenic silica (BS) attracting major attention owing to their exceptional biocompatibility and high specific surface area. In this study, we developed Curcumin-resveratrol-loaded BS (Cur-Res-BS) and investigated their effects on colorectal cancer cell lines (HCT-116 and Caco-2). Our results demonstrated significant concentration-dependent inhibition of cell viability in HCT-116 cells and revealed a complex interplay of crucial proto-onco or tumor suppressor genes, such as TP53, Bax, Wnt-1, and CTNNB1, which are commonly dysregulated in colorectal cancer. Notably, Cur-Res-BS exhibited a synergistic impact on key signaling pathways related to colorectal carcinogenesis. While these findings are promising, further investigations are essential to comprehensively understand the mechanisms and optimize the therapeutic strategy. Moreover, rigorous safety assessments and in vitro studies mimicking the in vivo environment are imperative before advancing to in vivo experiments, ensuring the potential of Cur-Res-BS as an efficient treatment for CRC.
C1 [Ochoa-Sanchez, Adriana; Paul, Sujay] Tecnol Monterrey, Sch Engn & Sci, NatProLab, Queretaro, Mexico.
   [Sahare, Padmavati; Luna-Barcenas, Gabriel] Tecnol Monterrey, Inst Adv Mat Sustainable Mfg, Sch Engn & Sci, Queretaro, Mexico.
   [Pathak, Surajit; Banerjee, Antara] Chettinad Acad Res & Educ CARE, Chettinad Hosp & Res Inst CHRI, Fac Allied Hlth Sci, Dept Med Biotechnol, Chennai, India.
   [Estevez, Miriam] Univ Nacl Autonoma Mexico, Ctr Appl Phys & Adv Technol CFATA, Queretaro, Mexico.
   [Duttaroy, Asim K.] Univ Oslo, Inst Basic Med Sci, Fac Med, Dept Nutr, Oslo, Norway.
C3 Tecnologico de Monterrey; Tecnologico de Monterrey; Universidad Nacional
   Autonoma de Mexico; University of Oslo
RP Paul, S (corresponding author), Tecnol Monterrey, Sch Engn & Sci, NatProLab, Queretaro, Mexico.; Luna-Bárcenas, G (corresponding author), Tecnol Monterrey, Inst Adv Mat Sustainable Mfg, Sch Engn & Sci, Queretaro, Mexico.; Duttaroy, AK (corresponding author), Univ Oslo, Inst Basic Med Sci, Fac Med, Dept Nutr, Oslo, Norway.
EM a.k.duttaroy@medisin.uio.no; spaul@tec.mx
RI Paul, Sujay/R-7572-2019; Banerjee, Antara/AAH-4044-2020
OI Paul, Sujay/0000-0001-5024-7261
FU Tecnologico de Monterrey
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. The authors are grateful
   to Tecnologico de Monterrey for the financial support during this
   study.r The author(s) declare financial support was received for the
   research, authorship, and/or publication of this article. The authors
   are grateful to Tecnologico de Monterrey for the financial support
   during this study.
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NR 94
TC 0
Z9 0
U1 7
U2 7
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 11
PY 2024
VL 15
AR 1341773
DI 10.3389/fphar.2024.1341773
PG 18
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA WD0S6
UT WOS:001252820500001
PM 38919255
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, Q
   Geng, S
   Luo, H
   Wang, W
   Mo, YQ
   Luo, Q
   Wang, L
   Song, GB
   Sheng, JP
   Xu, B
AF Li, Qing
   Geng, Shan
   Luo, Hao
   Wang, Wei
   Mo, Ya-Qi
   Luo, Qing
   Wang, Lu
   Song, Guan-Bin
   Sheng, Jian-Peng
   Xu, Bo
TI Signaling pathways involved in colorectal cancer: pathogenesis and
   targeted therapy
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID ISLAND METHYLATOR PHENOTYPE; GROWTH-FACTOR RECEPTOR; CIRCULATING
   TUMOR-CELLS; NF-KAPPA-B; COLON-CANCER; T-CELL; WNT/BETA-CATENIN;
   MICROSATELLITE INSTABILITY; DNA METHYLATION; 1ST-LINE TREATMENT
AB Colorectal cancer (CRC) remains one of the leading causes of cancer-related mortality worldwide. Its complexity is influenced by various signal transduction networks that govern cellular proliferation, survival, differentiation, and apoptosis. The pathogenesis of CRC is a testament to the dysregulation of these signaling cascades, which culminates in the malignant transformation of colonic epithelium. This review aims to dissect the foundational signaling mechanisms implicated in CRC, to elucidate the generalized principles underpinning neoplastic evolution and progression. We discuss the molecular hallmarks of CRC, including the genomic, epigenomic and microbial features of CRC to highlight the role of signal transduction in the orchestration of the tumorigenic process. Concurrently, we review the advent of targeted and immune therapies in CRC, assessing their impact on the current clinical landscape. The development of these therapies has been informed by a deepening understanding of oncogenic signaling, leading to the identification of key nodes within these networks that can be exploited pharmacologically. Furthermore, we explore the potential of integrating AI to enhance the precision of therapeutic targeting and patient stratification, emphasizing their role in personalized medicine. In summary, our review captures the dynamic interplay between aberrant signaling in CRC pathogenesis and the concerted efforts to counteract these changes through targeted therapeutic strategies, ultimately aiming to pave the way for improved prognosis and personalized treatment modalities in colorectal cancer.
C1 [Li, Qing] Chongqing Univ, Shapingba Hosp, Chongqing, Peoples R China.
   [Li, Qing; Mo, Ya-Qi; Wang, Lu; Xu, Bo] Chongqing Univ, Canc Hosp, Chongqing Key Lab Intelligent Oncol Breast Canc, Chongqing, Peoples R China.
   [Li, Qing; Mo, Ya-Qi; Wang, Lu; Xu, Bo] Chongqing Univ, Sch Med, Chongqing, Peoples R China.
   [Li, Qing; Luo, Hao; Luo, Qing; Song, Guan-Bin] Chongqing Univ, Coll Bioengn, Minist Educ, Minist Educ, Chongqing, Peoples R China.
   [Geng, Shan] Chongqing Med Univ, Affiliated Dazu Hosp, Cent Lab, Chongqing, Peoples R China.
   [Luo, Hao] Army Med Univ, Daping Hosp, Canc Ctr, Chongqing, Peoples R China.
   [Wang, Wei] Chongqing Municipal Hlth & Hlth Comm, Chongqing, Peoples R China.
   [Sheng, Jian-Peng] Nanjing Univ Aeronaut & Astronaut, Coll Artificial Intelligence, Nanjing, Peoples R China.
C3 Chongqing University; Chongqing University; Chongqing University;
   Chongqing University; Chongqing Medical University; Army Medical
   University; Nanjing University of Aeronautics & Astronautics
RP Xu, B (corresponding author), Chongqing Univ, Canc Hosp, Chongqing Key Lab Intelligent Oncol Breast Canc, Chongqing, Peoples R China.; Song, GB (corresponding author), Chongqing Univ, Coll Bioengn, Minist Educ, Minist Educ, Chongqing, Peoples R China.; Sheng, JP (corresponding author), Nanjing Univ Aeronaut & Astronaut, Coll Artificial Intelligence, Nanjing, Peoples R China.
EM song@cqu.edu.cn; jp@infinityscope.cn; xubo731@cqu.edu.cn
RI Li, Qing/A-6285-2018
OI Li, Qing/0000-0003-2652-6070
FU National Natural Science Foundation of China (National Science
   Foundation of China) [61906022]; National Natural Science Foundation of
   China [2024NSCQ-MSX3327]; Chongqing Natural Science Foundation
   [2021CDJXKJC004]; Chongqing University Research Fund
FX This study is supported by the National Natural Science Foundation of
   China (82203066, to Q.L.) and the Chongqing Natural Science Foundation
   (2024NSCQ-MSX3327, to Q.L.) and the National Natural Science Foundation
   of China (61906022, to B.X.) and Chongqing University Research Fund
   2021CDJXKJC004.
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NR 537
TC 2
Z9 2
U1 16
U2 16
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD OCT 7
PY 2024
VL 9
IS 1
AR 266
DI 10.1038/s41392-024-01953-7
PG 48
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA I3T7P
UT WOS:001329521500001
PM 39370455
OA gold
DA 2025-01-04
ER

PT J
AU El Hajj, J
   Reddy, S
   Verma, N
   Huang, EH
   Kazmi, SM
AF El Hajj, Joanna
   Reddy, Sarah
   Verma, Nilesh
   Huang, Emina H.
   Kazmi, Syed M.
TI Immune Checkpoint Inhibitors in pMMR/MSS Colorectal Cancer
SO JOURNAL OF GASTROINTESTINAL CANCER
LA English
DT Review
DE Colorectal cancer; Microsaetllite stable; Immunotherapy
ID MICROSATELLITE INSTABILITY DETECTION; NIVOLUMAB PLUS IPILIMUMAB; TUMOR
   MUTATIONAL BURDEN; LYNCH-SYNDROME; OPEN-LABEL; 1ST-LINE TREATMENT;
   DOUBLE-BLIND; PHASE-II; DNA; IMMUNOHISTOCHEMISTRY
AB BackgroundImmune checkpoint inhibitors have recently replaced over chemotherapy as the first-line treatment for microsatellite instability-high or mismatch repair deficient (dMMR/MSI-H) stage 4 colorectal cancers. Considering this success, many studies have tried to replicate the use of immune checkpoint inhibitors, either as a single agent or in combination with other therapeutic agents, in the treatment of proficient mismatch repair (pMMR/MSS) stage 4 colorectal cancers. This review summarizes the seminal clinical data about the immune checkpoint inhibitors used in pMMR/MSS colorectal cancers and some future directions.ResultsStudies concerning the use of immune checkpoint inhibitors as a single agent or in combination with other immune checkpoint inhibitors, targeted therapy, chemotherapy, or radiotherapy have proven inefficient in the treatment of pMMR/MSS colorectal cancer. However, a small subset of patients with pMMR/MSS colorectal cancer who has a mutation in POLE and POLD1 enzymes may respond to immunotherapy. Moreover, patients without liver metastasis appear to have a better chance of response. New immune checkpoint targets are being identified, such as VISTA, TIGIT, LAG3, STING signal pathway, and BTLA, and studies are ongoing to determine their efficiency in this disease type.ConclusionImmune checkpoint inhibitor-based regimens have not yet shown any meaningful positive outcomes for most pMMR/MSS colorectal cancers. A beneficial effect among a minority of these patients has been observed, but concrete biomarkers of response are lacking. Understanding the underlying mechanisms of immune resistance should guide further research for overcoming these obstacles.
C1 [El Hajj, Joanna; Reddy, Sarah; Verma, Nilesh; Kazmi, Syed M.] UT Southwestern Med Ctr, Dept Internal Med, Dallas, TX 75390 USA.
   [El Hajj, Joanna; Verma, Nilesh; Kazmi, Syed M.] UT Southwestern Med Ctr, Div Hematol & Oncol, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
   [Huang, Emina H.] UT Southwestern Med Ctr, Dept Surg, Div Surg Oncol, Dallas, TX USA.
C3 University of Texas System; University of Texas Southwestern Medical
   Center Dallas; University of Texas System; University of Texas
   Southwestern Medical Center Dallas; University of Texas System;
   University of Texas Southwestern Medical Center Dallas
RP Kazmi, SM (corresponding author), UT Southwestern Med Ctr, Dept Internal Med, Dallas, TX 75390 USA.; Kazmi, SM (corresponding author), UT Southwestern Med Ctr, Div Hematol & Oncol, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM Syed.Kazmi@UTSouthwestern.edu
OI Kazmi, Syed/0000-0002-3367-367X; El Hajj, Joanna/0000-0002-8675-1766; ,
   Nilesh Verma/0009-0002-3011-2874
FU National Center for Advancing Translational Sciences of the National
   Institutes of Health [R01 CA237304, U01214300]
FX Research reported in this publication was supported by the National
   Center for Advancing Translational Sciences of the National Institutes
   of Health under the CTSA Program award number R01 CA237304 and
   U01214300. The content is solely the responsibility of the authors and
   does not necessarily represent the official views of the NIH.
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NR 106
TC 4
Z9 4
U1 3
U2 11
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1941-6628
EI 1941-6636
J9 J GASTROINTEST CANC
JI J. Gastrointest. Cancer
PD DEC
PY 2023
VL 54
IS 4
BP 1017
EP 1030
DI 10.1007/s12029-023-00927-2
EA APR 2023
PG 14
WC Oncology; Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Oncology; Gastroenterology & Hepatology
GA DA1P8
UT WOS:000961771100001
PM 37009977
DA 2025-01-04
ER

PT J
AU Liu, XM
   Fu, Q
   Du, Y
   Yang, YX
   Cho, WC
AF Liu, Xiaoming
   Fu, Qi
   Du, Yong
   Yang, Yinxue
   Cho, William C.
TI MicroRNA as Regulators of Cancer Stem Cells and Chemoresistance in
   Colorectal Cancer
SO CURRENT CANCER DRUG TARGETS
LA English
DT Review
DE Cancer stem cells; chemoresistance; colorectal cancer; microRNA;
   targeted therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; NEGATIVE FEEDBACK LOOP; PROMOTES
   TUMOR-GROWTH; ANTI-EGFR THERAPY; MUTS HOMOLOG 2; COLON-CANCER;
   DOWN-REGULATION; DRUG-RESISTANCE; IN-VITRO; CIRCULATING MICRORNAS
AB Colorectal cancer (CRC) is one of the most common cancers worldwide. The development of resistance to anti-cancer treatment is one of the major challenges in the treatment of CRC, which limits the efficacy of both conventional and targeted therapies in clinical settings. Understanding the mechanisms underpinning resistances is therefore critical in developing novel agents to reverse drug resistance and for more specific targeted treatments. Accumulating studies have reported that microRNAs (miRNAs) are key players in the regulation of cancer cells with intrinsic/acquired drug resistance through varied mechanisms that endow cells with a drug-resistant phenotype. miRNAs have been evolved in the regulation of chemoresistance to various CRC treatments and the stemness of CRC stem cells (CRSCs), sequentially modulating the sensitivity of CRC cells to anti-cancer treatments. Targeting miRNAs may be a novel strategy for eradicating CRSCs, re-sensitizing drug-resistant cells to anti-cancer agents, improving drug efficiency and developing novel biological agents for CRC treatment. This paper highlights the role of miRNAs in the regulation of chemoresistance and CRSCs in CRC, with focus on the mechanisms underlying how miRNAs alter CRSCs fate, and the process of epithelial-to-mesenchymal transition, cell cycle and apoptosis in CRC cells.
C1 [Liu, Xiaoming; Fu, Qi; Du, Yong; Yang, Yinxue] Ningxia Med Univ, Gen Hosp, Human Stem Cell Inst, Yinchuan 750004, Peoples R China.
   [Liu, Xiaoming; Fu, Qi; Du, Yong; Yang, Yinxue] Ningxia Med Univ, Gen Hosp, Dept Colorectal Surg, Yinchuan 750004, Peoples R China.
   [Cho, William C.] Queen Elizabeth Hosp, Dept Clin Oncol, Hong Kong, Hong Kong, Peoples R China.
C3 Ningxia Medical University; Ningxia Medical University
RP Yang, YX (corresponding author), Ningxia Med Univ, Gen Hosp, Dept Colorectal Surg, Yinchuan 750004, Peoples R China.; Cho, WC (corresponding author), Queen Elizabeth Hosp, Dept Clin Oncol, Hong Kong, Hong Kong, Peoples R China.
EM nyfyyyx@126.com; chocs@ha.org.hk
RI Cho, William/H-7429-2019; Liu, Xiaoyan/ACD-3429-2022; Fu,
   Qi/HTT-2030-2023
OI LIU, XIAOMING/0000-0002-3902-9105
FU National Natural Science Foundation of China [81260309]
FX This work was supported by a grant from the National Natural Science
   Foundation of China (No. 81260309).
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NR 169
TC 28
Z9 29
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PU BENTHAM SCIENCE PUBL LTD
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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 9
BP 738
EP 754
DI 10.2174/1568009616666151118114759
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EB0AM
UT WOS:000387005800001
PM 26577538
DA 2025-01-04
ER

PT J
AU Li, PW
   Chen, WS
   Wang, YZ
   Fu, X
   Wen, KM
   Qian, J
   Huang, C
   Fu, ZX
AF Li, Peiwu
   Chen, Wangsheng
   Wang, Yingzhen
   Fu, Xu
   Wen, Kunming
   Qian, Jiang
   Huang, Chun
   Fu, Zhongxue
TI Effects of ephrinB2 gene siRNA on the biological behavior of human
   colorectal cancer cells
SO ONCOLOGY REPORTS
LA English
DT Article
DE colorectal cancer; SW480 cell; ephrinB2; small interfering RNA
ID MATRIX METALLOPROTEINASES; TYROSINE KINASE; EPH RECEPTORS;
   SMOOTH-MUSCLE; TUMOR ANGIOGENESIS; ENDOTHELIAL-CELLS; TARGETED THERAPY;
   RNA INTERFERENCE; EXPRESSION; GROWTH
AB Colorectal cancer (CRC) is a common gastrointestinal malignancy worldwide and is a lethal and aggressive malignancy with a dismal prognosis. EphrinB2 is a membrane-bound ligand and has an intracellular domain that also possesses an intrinsic signaling capacity called 'reverse signaling'. In the present study, CRC cell lines were screened for high expression of ephrinB2. Small interfering RNA (siRNA) knockdown of ephrinB2 was performed in human SW480 CRC cells. The levels of expression of ephrinB2, VEGF, CD105 and matrix metalloproteinase 9 (MMP9) protein were measured by western blotting, and messenger RNA (mRNA) levels were measured using real-time PCR. Apoptosis and cell cycle distribution were determined using flow cytometry. Cell proliferation was measured by a methyl thiazole tetrazolium (MTT) test and a scratch healing experiment was used to measure the extent of cell migration. A Transwell assay was used to detect the extent of cell invasion. The results showed that RNA interference (RNAi) of ephrinB2 effectively silenced the ephrinB2 gene at both the mRNA and protein levels in SW480 cells and inhibited the proliferation, invasion, migration and angiogenesis and induced apoptosis in SW480 cells. These effects may be attributed to VEGF and MMP9 regulation.
C1 [Li, Peiwu; Chen, Wangsheng; Wen, Kunming; Qian, Jiang; Huang, Chun; Fu, Zhongxue] Chongqing Med Univ, Affiliated Hosp 1, Dept Gen Surg, Chongqing 400010, Peoples R China.
   [Li, Peiwu; Wang, Yingzhen; Fu, Xu] Lanzhou Univ, Hosp 2, Dept Emergency, Lanzhou 730000, Peoples R China.
   [Chen, Wangsheng] Luzhou Med Coll, Affiliated Hosp, Dept Gen Surg, Luzhou 646000, Peoples R China.
C3 Chongqing Medical University; Lanzhou University; Southwest Medical
   University
RP Fu, ZX (corresponding author), Chongqing Med Univ, Affiliated Hosp 1, Dept Gen Surg, 1 Coll Rd, Chongqing 400010, Peoples R China.
EM fuzhongxue08@163.com
OI Li, Peiwu/0000-0003-3127-930X
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SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD FEB
PY 2015
VL 33
IS 2
BP 758
EP 766
DI 10.3892/or.2014.3633
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AZ6OJ
UT WOS:000348338500033
PM 25434750
OA Bronze
DA 2025-01-04
ER

PT J
AU Chauhan, S
   Sharma, S
AF Chauhan, Sonia
   Sharma, Sakshi
TI Recent Approaches on Molecular Markers, Treatment and Novel Drug
   Delivery System Used for the Management of Colorectal Cancer: A
   Comprehensive Review
SO CURRENT PHARMACEUTICAL BIOTECHNOLOGY
LA English
DT Review
DE PVT1; colorectal cancer; diagnosis; biomarkers; carcinoma; mutation;
   antibody; gene expression
ID PH-SENSITIVE NANOPARTICLES; POLYMERIC NANOPARTICLES; THERAPEUTIC
   STRATEGIES; ULCERATIVE-COLITIS; TARGETED THERAPY; GENE-THERAPY;
   IN-VITRO; BIOMARKER; KRAS; COMBINATION
AB Colorectal cancer affects 1 in 25 females and 1 in 24 males, making it the third most frequent cancer with over 6,08,030 deaths worldwide, despite advancements in detection and treatments, including surgery, chemotherapeutics, radiotherapy, and immune therapeutics. Novel potential agents have increased survival in acute and chronic disease conditions, with a higher risk of side effects and cost. However, metastatic disease has an insignificant long-term diagnosis, and significant challenges remain due to last-stage diagnosis and treatment failure. Early detection, survival, and treatment efficacy are all improved by biomarkers. The advancement of cancer biomarkers' molecular pathology and genomics during the last three decades has improved therapy. Clinically useful prognostic biomarkers assist clinical judgment, for example, by predicting the success of EGFR-inhibiting antibodies in the presence of KRAS gene mutations. Few biomarkers are currently used in clinical settings, so further research is still needed. Nanocarriers, with materials like Carbon nanotubes and gold nanoparticles, provide targeted CRC drug delivery and diagnostics. Light-responsive drugs with gold and silica nanoparticles effectively target and destroy CRC cells. We evaluate the potential use of the long non-coding RNA (non-coding RNA) oncogene plasmacytoma variant translocation 1 (PVT1) as a diagnostic, prognostic, and therapeutic biomarker, along with the latest nanotech breakthroughs in CRC diagnosis and treatment.
C1 [Chauhan, Sonia; Sharma, Sakshi] Noida Inst Engn & Technol, Pharm Inst, Greater Noida 201306, Uttar Pradesh, India.
C3 Noida Institute of Engineering & Technology
RP Sharma, S (corresponding author), Noida Inst Engn & Technol, Pharm Inst, Greater Noida 201306, Uttar Pradesh, India.
EM sakshi.sharma1964@gmail.com
FX Declared none.
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NR 124
TC 0
Z9 0
U1 6
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 1389-2010
EI 1873-4316
J9 CURR PHARM BIOTECHNO
JI Curr. Pharm. Biotechnol.
PY 2024
VL 25
IS 15
BP 1969
EP 1985
DI 10.2174/0113892010270975231208113157
PG 17
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA A6B4V
UT WOS:001283366100009
PM 38275054
DA 2025-01-04
ER

PT J
AU Zhang, JT
   Deng, YL
   Zuo, YL
   Wang, J
   Zhao, Y
AF Zhang, Jiting
   Deng, Yulan
   Zuo, Yuanli
   Wang, Jin
   Zhao, Yun
TI Analysis of Colorectal Cancer-Associated Alternative Splicing Based on
   Transcriptome
SO DNA AND CELL BIOLOGY
LA English
DT Article
DE colorectal cancer; alternative splicing; splicing factor; RNA-seq
ID TUMOR-SUPPRESSOR; PROGNOSIS; APOPTOSIS; FRAMEWORK; GROWTH; COLON
AB Colorectal cancer (CRC) is a severe risk to public health, and there is growing evidence that alternative splicing (AS) plays a crucial role in cancer. However, the AS biomarkers in CRC are seldom reported. In this study, we perform transcriptome analysis of colorectal samples for cancer-specific AS and transcriptomic alterations. We identify 1577 splice events in 885 genes, enriched in CRC-associated pathways and functions. In parallel, we find 10 splicing factors (SFs) with transcriptome variation or significant differential expression. Based on co-expression and binding motif, we construct an SF-AS regulatory network, revealing the association between cancer-specific AS and aberrant SF. Integrating The Cancer Genome Atlas and published sources, we observed that some recurrent AS is an indicator of poor prognosis. Through further experimental verification, we found that the AS of six genes showed significant differences between the tumor sample and the normal sample, and AS of TCF7, COL12A1, GK, and UBA1 can be used as new potential biomarkers in CRC. Our study provides an important analysis of CRC-associated AS, which could act as a starting point for future functional explorations, the development of biomarkers and AS-based target therapy.
C1 [Zhang, Jiting; Zuo, Yuanli; Zhao, Yun] Sichuan Univ, Coll Life Sci, Minist Educ, Key Lab Bioresource & Ecoenvironm, 29 Wangjiang Rd, Chengdu 610064, Sichuan, Peoples R China.
   [Deng, Yulan] Sichuan Univ, West China Hosp, Dept Thorac Surg, Chengdu, Sichuan, Peoples R China.
   [Wang, Jin] Sichuan Univ, State Natl Key Lab Biotherapy, Chengdu, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University
RP Zhao, Y (corresponding author), Sichuan Univ, Coll Life Sci, Minist Educ, Key Lab Bioresource & Ecoenvironm, 29 Wangjiang Rd, Chengdu 610064, Sichuan, Peoples R China.
EM zhaoyun@scu.edu.cn
RI zhao, yun/AAJ-4105-2020; Wang, Jin/GYA-2019-2022
OI Zhang, Jiting/0000-0001-6069-5906
FU National Natural Science Foundation of China [31801119]; China
   Postdoctoral Science Foundation [2019T120835, 2019M650243]; West China
   Hospital, Sichuan University [2019HXBH047]
FX This study was supported by the National Natural Science Foundation of
   China (Grant No. 31801119), project funded by China Postdoctoral Science
   Foundation (Grant Nos. 2019T120835 and 2019M650243), and Post-Doctor
   Research Project, West China Hospital, Sichuan University (Grant No.
   2019HXBH047).
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NR 39
TC 5
Z9 5
U1 0
U2 15
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1044-5498
EI 1557-7430
J9 DNA CELL BIOL
JI DNA Cell Biol.
PD JAN 1
PY 2020
VL 39
IS 1
BP 16
EP 24
DI 10.1089/dna.2019.5111
EA DEC 2019
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity
GA KB8KQ
UT WOS:000504865300001
PM 31808724
DA 2025-01-04
ER

PT J
AU Asif, PJ
   Longobardi, C
   Hahne, M
   Medema, JP
AF Asif, Paris Jabeen
   Longobardi, Ciro
   Hahne, Michael
   Medema, Jan Paul
TI The Role of Cancer-Associated Fibroblasts in Cancer Invasion and
   Metastasis
SO CANCERS
LA English
DT Review
DE cancer-associated fibroblast; invasion; metastasis; colorectal cancer;
   extracellular matrix; epithelial-to-mesenchymal transition; CAF-targeted
   therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; HEDGEHOG SIGNALING PATHWAY;
   COLORECTAL-CANCER; TGF-BETA; GROWTH-FACTOR; EXTRACELLULAR-MATRIX; TUMOR
   PROGRESSION; CARCINOMA-CELLS; DOWN-REGULATION; MOUSE MODEL
AB Simple Summary Cancer metastasis is often associated with a dismal prognosis for the patient. It is, therefore, crucial to understand the mechanisms behind the cascade of events that lead to metastatic disease. Cancer-associated fibroblasts (CAFs) play a key role in cancer progression. Therefore, it is of importance to understand the roles of CAFs in invasion, metastasis, and therapy resistance. Here, we reviewed the crosstalk between CAFs and tumor cells to summarize the current knowledge on CAF roles in cancers to provide the necessary structure to advance the field. Cancer-associated fibroblasts (CAFs) play a key role in cancer progression by contributing to extracellular matrix (ECM) deposition and remodeling, extensive crosstalk with cancer cells, epithelial-to-mesenchymal transition (EMT), invasion, metastasis, and therapy resistance. As metastasis is a main reason for cancer-related deaths, it is crucial to understand the role of CAFs in this process. Colorectal cancer (CRC) is a heterogeneous disease and lethality is especially common in a subtype of CRC with high stromal infiltration. A key component of stroma is cancer-associated fibroblasts (CAFs). To provide new perspectives for research on CAFs and CAF-targeted therapeutics, especially in CRC, we discuss the mechanisms, crosstalk, and functions involved in CAF-mediated cancer invasion, metastasis, and protection. This summary can serve as a framework for future studies elucidating these roles of CAFs.
C1 [Asif, Paris Jabeen; Longobardi, Ciro; Medema, Jan Paul] Univ Amsterdam, Ctr Expt & Mol Med, Canc Ctr Amsterdam, Amsterdam UMC, NL-1105 AZ Amsterdam, Netherlands.
   [Asif, Paris Jabeen; Longobardi, Ciro; Medema, Jan Paul] Univ Amsterdam, Oncode Inst, Amsterdam UMC, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.
   [Hahne, Michael] Univ Montpellier, CNRS, Inst Genet Mol Montpellier, F-34090 Montpellier, France.
C3 Vrije Universiteit Amsterdam; University of Amsterdam; University of
   Amsterdam; Centre National de la Recherche Scientifique (CNRS);
   Universite de Montpellier
RP Medema, JP (corresponding author), Univ Amsterdam, Ctr Expt & Mol Med, Canc Ctr Amsterdam, Amsterdam UMC, NL-1105 AZ Amsterdam, Netherlands.; Medema, JP (corresponding author), Univ Amsterdam, Oncode Inst, Amsterdam UMC, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.
EM p.j.asif@amsterdamumc.nl; c.longobardi@amsterdamumc.nl;
   michael.hahne@igmm.cnrs.fr; j.p.medema@amsterdamumc.nl
OI Asif, Paris/0000-0003-0238-9876; Longobardi, Ciro/0000-0003-4965-9976
FU Oncode and Dutch Cancer Society [10150]; INSERM [21CM047-00]; INCA
   [PLBIO21-222]; ANR [CE14 CILCOL]
FX Paris J Asif: Ciro Longobardi, and Jan Paul Medema were funded by Oncode
   and Dutch Cancer Society grant 10150. Michael Hahne was funded by INSERM
   (21CM047-00), INCA (PLBIO21-222), and ANR (CE14 CILCOL).
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NR 148
TC 125
Z9 129
U1 10
U2 56
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD SEP
PY 2021
VL 13
IS 18
AR 4720
DI 10.3390/cancers13184720
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UU8OQ
UT WOS:000699054700001
PM 34572947
OA Green Published, gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Rühlmann, F
   Nietert, M
   Sprenger, T
   Wolff, HA
   Homayounfar, K
   Middel, P
   Bohnenberger, H
   Beissbarth, T
   Ghadimi, BM
   Liersch, T
   Conradi, LC
AF Ruehlmann, Felix
   Nietert, Manuel
   Sprenger, Thilo
   Wolff, Hendrik A.
   Homayounfar, Kia
   Middel, Peter
   Bohnenberger, Hanibal
   Beissbarth, Tim
   Ghadimi, B. Michael
   Liersch, Torsten
   Conradi, Lena-Christin
TI The Prognostic Value of Tyrosine Kinase SRC Expression in Locally
   Advanced Rectal Cancer
SO JOURNAL OF CANCER
LA English
DT Article
DE SRC; rectal cancer; tyrosine kinase; preoperative chemoradiotherapy;
   biomarker; targeted therapy
ID PHASE-III TRIAL; PREOPERATIVE CHEMORADIOTHERAPY; POSTOPERATIVE
   CHEMOTHERAPY; COLORECTAL-CANCER; C-SRC; GERMAN CAO/ARO/AIO-04;
   TUMOR-REGRESSION; OXALIPLATIN; RADIOTHERAPY; CHEMORADIATION
AB The cellular sarcoma gene (SRC) is a proto-oncogene encoding for a tyrosine kinase. SRC expression was determined in locally advanced rectal adenocarcinoma tissue from pretreatment biopsies and resection specimens. The expression level was correlated with clinicopathological parameters to evaluate the predictive and prognostic capacity.
   For this monocentric analysis 186 patients with locally advanced rectal cancer (median: 63.7 years; 130 men (69.9%), 56 women (30.1%)) were included. Patients with a carcinoma of the upper third of the rectum were treated with primary tumor resection (n=27; 14.5%). All other patients received a preoperative chemoradiotherapy (CRT) with 50.4 Gy and concomitant 5-fluorouracil (5-FU) or 5-FU+oxaliplatin followed by postoperative chemotherapy with 5-FU or 5-FU+ oxaliplatin. SRC expression was determined with immunohistochemical staining from pretreatment biopsies (n=152) and residual tumor tissue from the resection specimens (n=163). The results were correlated with clinicopathological parameters and long-term follow-up.
   The expression of SRC was determined in pretherapeutic biopsies (mean H-Score: 229) and resection specimens (mean H-Score: 254). High SRC expression in pretherapeutic tumor samples significantly correlated with a negative postoperative nodal status (p=0.005). Furthermore an increased protein expression in residual tumor tissue was associated with fewer distant metastases (p=0.04). The overexpression of SRC in pretreatment tumor biopsies showed also a trend for a longer cancer-specific survival (CSS; p=0.05) and fewer local relapses (p=0.06) during long-term follow-up.
   High SRC expression in rectal cancer seems to be associated with a better long-term outcome. This finding could help in the future to stratify patients for a recurrence risk adapted postoperative treatment.
C1 [Ruehlmann, Felix; Sprenger, Thilo; Homayounfar, Kia; Ghadimi, B. Michael; Liersch, Torsten; Conradi, Lena-Christin] Univ Med Ctr, Dept Gen Visceral & Pediat Surg, Gottingen, Germany.
   [Nietert, Manuel; Beissbarth, Tim] Univ Med Ctr, Dept Med Stat, Gottingen, Germany.
   [Wolff, Hendrik A.] Univ Med Ctr, Gottingen, Germany.
   [Wolff, Hendrik A.] Radiol Munchen, Munich, Germany.
   [Middel, Peter] Pathol Nordhessen, Kassel, Germany.
   [Bohnenberger, Hanibal] Univ Med Ctr, Dept Pathol, Gottingen, Germany.
C3 University of Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; University of
   Gottingen; UNIVERSITY GOTTINGEN HOSPITAL; University of Gottingen;
   UNIVERSITY GOTTINGEN HOSPITAL; University of Gottingen; UNIVERSITY
   GOTTINGEN HOSPITAL
RP Conradi, LC (corresponding author), Univ Med Ctr Gottingen, Gen Visceral & Pediat Surg, Robert Koch Str 40, D-37075 Gottingen, Germany.
EM lena.conradi@med.uni-goettingen.de
RI Bohnenberger, Hanibal/F-2317-2013; Beissbarth, Tim/B-3129-2013
OI Nietert, Manuel/0000-0001-5443-7943
CR [Anonymous], 2007, STUDIES CLASSIFICATI
   [Anonymous], ONCOTARGET
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NR 55
TC 1
Z9 1
U1 0
U2 1
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2017
VL 8
IS 7
BP 1229
EP 1237
DI 10.7150/jca.16980
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EW4LW
UT WOS:000402474000015
PM 28607598
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Zheng, Y
   Zou, JY
   Sun, C
   Peng, F
   Peng, C
AF Zheng, Yang
   Zou, Jiayu
   Sun, Chen
   Peng, Fu
   Peng, Cheng
TI Ado-tratuzumab emtansine beyond breast cancer: therapeutic role of
   targeting other HER2-positive cancers
SO FRONTIERS IN MOLECULAR BIOSCIENCES
LA English
DT Review
DE T-DM1; HER2(+); cancer; therapeutic potential; targeted therapy
ID CELL LUNG-CANCER; ANTIBODY-DRUG CONJUGATE; UROTHELIAL BLADDER-CANCER;
   PHASE-II TRIAL; TRASTUZUMAB-EMTANSINE; GASTRIC-CANCER;
   COLORECTAL-CANCER; RESISTANCE MECHANISMS; ANTITUMOR-ACTIVITY;
   OVARIAN-CANCER
AB Ado-trastuzumab emtansine (T-DM1) is an antibody-drug conjugate approved by the FDA in 2013 for advanced HER2-positive breast cancer treatment exhibiting promising clinical benefits. However, HER2 overexpression and gene amplification have also been reported in other cancers like gastric cancer, non-small cell lung cancer (NSCLC), and colorectal cancer. Numerous preclinical studies have also revealed the significant antitumor effect of T-DM1 on HER2-positive tumors. With the advancement in research, several clinical trials have been conducted to investigate the antitumor effect of T-DM1. In this review, we briefly introduced the pharmacological effects of T-DM1. We reviewed its preclinical and clinical studies, especially on other HER2-positive cancers, establishing what has been encountered between its preclinical and clinical studies. In clinical studies, we found that T-DM1 has a therapeutic value on other cancers. An insignificant effect was observed on gastric cancer and NSCLC, inconsistent with the preclinical studies.
C1 [Zheng, Yang; Zou, Jiayu; Sun, Chen; Peng, Cheng] Chengdu Univ Tradit Chinese Med, State Key Lab Southwestern Chinese Med Resources, Chengdu, Sichuan, Peoples R China.
   [Peng, Fu] Chengdu Univ Tradit Chinese Med, Chengdu, Sichuan, Peoples R China.
   [Peng, Fu] Sichuan Univ, Chengdu, Sichuan, Peoples R China.
C3 Chengdu University of Traditional Chinese Medicine; Chengdu University
   of Traditional Chinese Medicine; Sichuan University
RP Peng, C (corresponding author), Chengdu Univ Tradit Chinese Med, State Key Lab Southwestern Chinese Med Resources, Chengdu, Sichuan, Peoples R China.; Peng, F (corresponding author), Chengdu Univ Tradit Chinese Med, Chengdu, Sichuan, Peoples R China.; Peng, F (corresponding author), Sichuan Univ, Chengdu, Sichuan, Peoples R China.
EM pengchengchengdu@126.com; pengf@scu.edu.cn
RI Zhang, Juan/GRX-2638-2022; PENG, Fu/KRQ-8632-2024; shengyue,
   chen/JPL-8966-2023
OI PENG, Fu/0000-0003-0289-4426
FU National Natural Science Foundation of China [82003879, U19A2010]; Key
   Project of Science and Technology Department of Sichuan Province
   [2021YFS0044]; National Natural Science Foundation of Science and
   Technology Department of Sichuan Province [2023NSFSC 1928]; Project of
   State Administration of Traditional Chinese Medicine of China
   [ZYYCXTD-D-202209]; Young Elite Scientist Sponsorship Program by China
   Association for Science and Technology [CACM-2020-QNRC1-01]; Traditional
   Chinese Medicine Science and Technology Industry Innovation Team of
   Sichuan Province; Multi-dimensional Evaluation and product Development
   Innovation Team of Characteristic Traditional Chinese Medicine Resources
   [2022C001]
FX The study was supported by the National Natural Science Foundation of
   China (Nos. 82003879 and U19A2010), the Key Project of Science and
   Technology Department of Sichuan Province (No. 2021YFS0044), the
   National Natural Science Foundation of Science and Technology Department
   of Sichuan Province (No. 2023NSFSC 1928), the Project of State
   Administration of Traditional Chinese Medicine of China (No.
   ZYYCXTD-D-202209), Young Elite Scientist Sponsorship Program by China
   Association for Science and Technology (no. CACM-2020-QNRC1-01), the
   Traditional Chinese Medicine Science and Technology Industry Innovation
   Team of Sichuan Province, and the Multi-dimensional Evaluation and
   product Development Innovation Team of Characteristic Traditional
   Chinese Medicine Resources (No. 2022C001).
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NR 105
TC 2
Z9 2
U1 2
U2 14
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 11
PY 2023
VL 10
AR 1165781
DI 10.3389/fmolb.2023.1165781
PG 13
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA I1IO9
UT WOS:001000386100001
PM 37251081
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Cheng, LS
   Cheng, YF
   Liu, WT
   Shen, AL
   Zhang, DY
   Xu, TJ
   Yin, W
   Cheng, M
   Ma, XP
   Wang, FR
   Zhao, Q
   Zeng, XL
   Zhang, Y
   Shen, GD
AF Cheng, Lian-sheng
   Cheng, Yong-feng
   Liu, Wen-ting
   Shen, Aolin
   Zhang, Dayan
   Xu, Tingjuan
   Yin, Wu
   Cheng, Min
   Ma, Xiaopeng
   Wang, Fengrong
   Zhao, Qun
   Zeng, Xiaoli
   Zhang, Yan
   Shen, Guodong
TI A humanized 4-1BB-targeting agonistic antibody exerts potent antitumor
   activity in colorectal cancer without systemic toxicity
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE 4-1BB; CD137; Monoclonal antibody; Targeted therapy; Cancer
   immunotherapy; Antitumor immunity; Toxicity
ID T-CELL FUNCTION; MONOCLONAL-ANTIBODY; 4-1BB; URELUMAB; AFFINITY
AB Background Colorectal cancer (CRC) is one of the most common malignancies and the patient survival rate remains unacceptably low. The anti-programmed cell death-1 (PD-1)/programmed cell death ligand 1 (PD-L1) antibody-based immune checkpoint inhibitors have been added to CRC treatment regimens, however, only a fraction of patients benefits. As an important co-stimulatory molecule, 4-1BB/CD137 is mainly expressed on the surface of immune cells including T and natural killer (NK) cells. Several agonistic molecules targeting 4-1BB have been clinically unsuccessful due to systemic toxicity or weak antitumor effects. We generated a humanized anti-4-1BB IgG4 antibody, HuB6, directed against a unique epitope and hypothesized that it would promote antitumor immunity with high safety. Methods The antigen binding specificity, affinity and activity of HuB6 were determined by enzyme-linked immunosorbent assay (ELISA), surface plasmon resonance (SPR), biolayer interferometry (BLI) and flow cytometry. The antitumor effects were evaluated in humanized mice bearing syngeneic tumors, and possible toxicity was evaluated in humanized mice and cynomolgus monkeys. Results HuB6 showed high specificity and affinity for a binding epitope distinct from those of other known 4-1BB agonists, including utomilumab and urelumab, and induced CD8 + T, CD4 + T and NK cell stimulation dependent on Fc gamma receptor (Fc gamma R) crosslinking. HuB6 inhibited CRC tumor growth in a dose-dependent manner, and the antitumor effect was similar with urelumab and utomilumab in humanized mouse models of syngeneic CRC. Furthermore, HuB6 combined with an anti-PD-L1 antibody significantly inhibited CRC growth in vivo. Additionally, HuB6 induced antitumor immune memory in tumor model mice rechallenged with 4 x 10(6) tumor cells. Toxicology data for humanized 4-1BB mice and cynomolgus monkeys showed that HuB6 could be tolerated up to a 180 mg/kg dose without systemic toxicity. Conclusions This study demonstrated that HuB6 should be a suitable candidate for further clinical development and a potential agent for CRC immunotherapy.
C1 [Cheng, Lian-sheng; Xu, Tingjuan; Yin, Wu; Cheng, Min; Shen, Guodong] Univ Sci & Technol China, Div Life Sci & Med, Gerontol Inst Anhui Prov, Dept Geriatr,Affiliated Hosp 1, Hefei 230001, Anhui, Peoples R China.
   [Cheng, Lian-sheng; Liu, Wen-ting; Zhang, Dayan; Wang, Fengrong; Zhao, Qun; Zeng, Xiaoli] Hefei HankeMab Biotechnol Ltd, Hefei 230088, Anhui, Peoples R China.
   [Cheng, Lian-sheng; Shen, Aolin; Xu, Tingjuan; Yin, Wu; Cheng, Min; Shen, Guodong] Anhui Prov Key Lab Tumor Immunotherapy & Nutr, Hefei 230001, Anhui, Peoples R China.
   [Cheng, Yong-feng] Anhui Med Univ, Dept Genet, Sch Life Sci, Hefei 230032, Anhui, Peoples R China.
   [Shen, Aolin] Anhui Med Univ, Affiliated Hosp 1, Dept Gen Surg, Hefei 230032, Anhui, Peoples R China.
   [Ma, Xiaopeng] Univ Sci & Technol China, Div Life Sci & Med, Affiliated Hosp 1, Dept Thyroid & Breast Surg, Hefei 230001, Anhui, Peoples R China.
   [Zhang, Yan] Anhui Med Univ, Sch Hlth Serv Management, Hefei 230032, Anhui, Peoples R China.
C3 Chinese Academy of Sciences; University of Science & Technology of
   China, CAS; Anhui Medical University; Anhui Medical University; Chinese
   Academy of Sciences; University of Science & Technology of China, CAS;
   Anhui Medical University
RP Shen, GD (corresponding author), Univ Sci & Technol China, Div Life Sci & Med, Gerontol Inst Anhui Prov, Dept Geriatr,Affiliated Hosp 1, Hefei 230001, Anhui, Peoples R China.; Shen, GD (corresponding author), Anhui Prov Key Lab Tumor Immunotherapy & Nutr, Hefei 230001, Anhui, Peoples R China.; Ma, XP (corresponding author), Univ Sci & Technol China, Div Life Sci & Med, Affiliated Hosp 1, Dept Thyroid & Breast Surg, Hefei 230001, Anhui, Peoples R China.; Zhang, Y (corresponding author), Anhui Med Univ, Sch Hlth Serv Management, Hefei 230032, Anhui, Peoples R China.
EM xiaopengma@fsyy.ustc.edu.cn; zhangymail@ahmu.edu.cn; gdshen@ustc.edu.cn
RI Wang, Jinwu/AAG-4431-2021; 沈, 国栋/ABA-5925-2021
OI Yin, Wu/0000-0002-9988-4939
FU Key Project of Science and Technology of Anhui Province
   [202004b11020019, 202004j07020020]; Hefei Municipal Natural Science
   Foundation [2021005]; Natural Science Foundation for the Higher
   Education Institutions of Anhui Province [KJ2019A0943]
FX This work was supported by the Key Project of Science and Technology of
   Anhui Province (202004b11020019, 202004j07020020), the Hefei Municipal
   Natural Science Foundation (2021005) and the Natural Science Foundation
   for the Higher Education Institutions of Anhui Province (KJ2019A0943).
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NR 32
TC 8
Z9 8
U1 3
U2 16
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 8
PY 2022
VL 20
IS 1
AR 415
DI 10.1186/s12967-022-03619-w
PG 18
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 4L1OB
UT WOS:000852403500004
PM 36076251
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Liu, YK
   Cai, J
   Yang, XJ
   Xiong, Z
   Zou, D
   Jiao, DL
   Xu, KX
   Wei, HJ
   Zhao, HY
AF Liu, Yukun
   Cai, Jie
   Yang, Xinjiao
   Xiong, Zhe
   Zou, Di
   Jiao, Deling
   Xu, Kaixiang
   Wei, Hong-Jiang
   Zhao, Hong-Ye
TI Role of P53 Mediated Molecular Regulation in Starvation-Induced
   Autophagy in HCT-116 and HT-29 Colorectal Carcinoma Cells
SO BIOLOGY BULLETIN
LA English
DT Article
DE colorectal carcinoma cells; P53; autophagy signaling pathway genes,
   autophagy related genes (ATG); autophagy flux
ID CANCER-CELLS; MUTANT P53; INDUCED APOPTOSIS; MECHANISM; GROWTH;
   INHIBITION; INDUCTION; MODULATOR; TARGET; STRESS
AB The tumor suppressor P53 is a known regulator of autophagy, which has been reported to be associated with colorectal cancer (CRC) cells' drug resistance. However, the molecular mechanisms of P53 regulating autophagic responses remain incompletely clear in CRC. HCT-116 and HT-29 cell line are colorectal cancer cell line with wild type and mutant P53 gene. Here, we aimed to investigate the mechanisms of P53 regulating the starvation-induced autophagy in HCT-116 and HT-29 cells. After P53 was inhibited by siRNA following treatment with EBSS or EBSS combination with bafilomycin A1, the hallmarks of autophagy were examined by real-time PCR and western blot. We found that P53 knockdown led to the accumulation of p62 in HCT-116 cells, indicating the autophagy flux was blocked. In addition, P53 knockdown caused the decreased p62 in HT-29 cells and the autophagy flux was activated. Furthermore, the expression of signaling pathway genes and autophagy related genes (ATG) showed an opposite pattern between two cell lines after P53 inhibition. Specially, the expression of autophagy regulating genes ATG14, VPS34 and TSC1 were significantly decreased by P53 knockdown in HCT-116 cells, and the expression of PTEN, DRAM1 and ULK2 were dramatically increased in HT-29 cells. In conclusion, our results demonstrated that P53 can promote autophagy by increasing the expression of signaling pathway genes and ATG in HCT-116 cells but inhibit autophagy by an opposite pattern in HT-29 cell line. These findings might be hopeful for the targeting therapy of different types of CRC.
C1 [Liu, Yukun; Cai, Jie; Yang, Xinjiao; Xiong, Zhe; Zou, Di; Jiao, Deling; Xu, Kaixiang; Wei, Hong-Jiang; Zhao, Hong-Ye] Key Lab Porcine Gene Editing & Xenotransplantat, Kunming 650201, Yunnan, Peoples R China.
   [Liu, Yukun; Cai, Jie; Yang, Xinjiao; Xiong, Zhe; Zou, Di; Jiao, Deling; Xu, Kaixiang; Wei, Hong-Jiang; Zhao, Hong-Ye] Yunnan Agr Univ, Xenotransplantat Res Engn Ctr, Kunming 650201, Yunnan, Peoples R China.
   [Jiao, Deling; Xu, Kaixiang; Wei, Hong-Jiang; Zhao, Hong-Ye] Yunnan Agr Univ, Coll Vet Med, Kunming 650201, Peoples R China.
   [Wei, Hong-Jiang] Yunnan Agr Univ, Fac Anim Sci & Technol, Kunming 650201, Peoples R China.
   [Cai, Jie] Yunnan Agr Univ, Coll Plant Protect, Kunming 650201, Peoples R China.
   [Liu, Yukun] Chuxiong Med Coll, Chuxiong 675005, Peoples R China.
   [Yang, Xinjiao] Dali Univ, Coll Pharm & Chem, Dali 671000, Peoples R China.
C3 Yunnan Agricultural University; Yunnan Agricultural University; Yunnan
   Agricultural University; Yunnan Agricultural University; Dali University
RP Zhao, HY (corresponding author), Key Lab Porcine Gene Editing & Xenotransplantat, Kunming 650201, Yunnan, Peoples R China.; Zhao, HY (corresponding author), Yunnan Agr Univ, Xenotransplantat Res Engn Ctr, Kunming 650201, Yunnan, Peoples R China.; Zhao, HY (corresponding author), Yunnan Agr Univ, Coll Vet Med, Kunming 650201, Peoples R China.
EM hyzhao2000@126.com
RI Liu, Yukun/LIG-7414-2024; Cai, Jie/LOR-7320-2024
FU Major Science and Technology Project of Yunnan Province; National
   Natural Science Foundation of China
FX We thank for the Major Science and Technology Project of Yunnan Province
   and National Natural Science Foundation of China.
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NR 52
TC 1
Z9 1
U1 2
U2 2
PU PLEIADES PUBLISHING INC
PI NEW YORK
PA PLEIADES HOUSE, 7 W 54 ST, NEW YORK,  NY, UNITED STATES
SN 1062-3590
EI 1608-3059
J9 BIOL BULL+
JI Biol. Bull
PD DEC
PY 2023
VL 50
IS SUPPL 4
SU 4
BP S522
EP S533
DI 10.1134/S1062359023602823
PG 12
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA JK2A5
UT WOS:001172984100012
DA 2025-01-04
ER

PT J
AU Wu, CC
   Wang, JH
   Chang, MC
   Chen, YH
   Wang, YC
   Lee, MH
   Lin, CY
   Su, YC
   Lin, PC
   Hsu, CW
AF Wu, Chih-Chien
   Wang, Jui-Ho
   Chang, Min-Chi
   Chen, Yu-Hsun
   Wang, Yung-Chang
   Lee, Ming-Hung
   Lin, Chien-Yuan
   Su, Yi-Chia
   Lin, Pei-Chin
   Hsu, Chao-Wen
TI Shared decision-making and patient decision aids in choosing first-line
   targeted therapy for metastatic colorectal cancer in Taiwan
SO JOURNAL OF ONCOLOGY PHARMACY PRACTICE
LA English
DT Article
DE Cancer; treatment; decision aids; insurance
ID PHASE-III TRIAL; PLUS CETUXIMAB; OPEN-LABEL; FLUOROURACIL; CHEMOTHERAPY;
   BEVACIZUMAB; LEUCOVORIN; KRAS; MORTALITY; PANITUMUMAB
AB Introduction
   In Taiwan, given the discrepancy between current treatment guidelines and reimbursement options, patients might require a tool to support their decision-making process when selecting a regimen for metastatic colorectal cancer, especially therapeutic strategies, and subsequent costs, along with efficacy and safety outcomes. Therefore, we developed a patient decision aid (PDA) to support patients in choosing between treatment options recommended based on the current evidence and those reimbursed by the Taiwanese National Health Insurance.
   Methods
   By carefully reviewing the updated data and then interpreting the clinical tool, we conducted a needs assessment using a serial questionnaire to test for a step-by-step adjustment of the PDA.
   Results
   Patients, their relatives, and medical team members were most concerned about outcomes, such as overall survival, progression-free survival, objective response rate, tumor shrinkage to resectable status, total medical cost, severe gastrointestinal perforation, and severe skin reaction. After a serial alpha test for quality, we performed quantitative evaluation and beta tests, revealing average scores of more than 4 points (on a scale of 1-5) for both perceptibility and utility.
   Conclusions
   The present findings suggest that PDAs are useful and supplement the shared decision-making practice, helping patients make decisions about preferences and consider the pros and cons of treatment regimens, along with insurance reimbursement options.
C1 [Wu, Chih-Chien; Wang, Jui-Ho; Chang, Min-Chi; Chen, Yu-Hsun; Wang, Yung-Chang; Lee, Ming-Hung; Lin, Chien-Yuan; Hsu, Chao-Wen] Kaohsiung Vet Gen Hosp, Div Colorectal Surg, Dept Surg, 386,Dazhong 1st Rd, Kaohsiung 81362, Taiwan.
   [Wu, Chih-Chien; Hsu, Chao-Wen] Natl Yang Ming Chiao Tung Univ, Sch Med, Taipei, Taiwan.
   [Chang, Min-Chi] Meiho Univ, Dept Hlth Business Adm, Pingtung, Taiwan.
   [Su, Yi-Chia] Kaohsiung Vet Gen Hosp, Dept Pharm, 386,Dazhong 1st Rd, Kaohsiung 81362, Taiwan.
   [Su, Yi-Chia] Natl Cheng Kung Univ, Inst Clin Pharm & Pharmaceut Sci, Coll Med, Tainan, Taiwan.
   [Su, Yi-Chia] Shu Zen Jr Coll Med & Management, Dept Nursing, Kaohsiung, Taiwan.
   [Lin, Pei-Chin] Kaohsiung Vet Gen Hosp, Dept Med Educ & Res, Kaohsiung, Taiwan.
C3 Kaohsiung Veterans General Hospital; National Yang Ming Chiao Tung
   University; Kaohsiung Veterans General Hospital; National Cheng Kung
   University; Kaohsiung Veterans General Hospital
RP Hsu, CW (corresponding author), Kaohsiung Vet Gen Hosp, Div Colorectal Surg, Dept Surg, 386,Dazhong 1st Rd, Kaohsiung 81362, Taiwan.; Su, YC (corresponding author), Kaohsiung Vet Gen Hosp, Dept Pharm, 386,Dazhong 1st Rd, Kaohsiung 81362, Taiwan.
EM jia.love70@gmail.com; s19101080@gm.ym.edu.tw
RI Su, Yichia/HJI-3668-2023; Lin, Pei-Chin/AAW-9869-2020; chen,
   yuling/JMQ-4121-2023
OI Wu, Chih-Chien/0000-0001-5791-4047
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NR 38
TC 4
Z9 4
U1 2
U2 12
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1078-1552
EI 1477-092X
J9 J ONCOL PHARM PRACT
JI J. Oncol. Pharm. Pract.
PD SEP
PY 2022
VL 28
IS 6
BP 1293
EP 1302
AR 10781552211020806
DI 10.1177/10781552211020806
EA JUN 2021
PG 10
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA 3S5AZ
UT WOS:000657880900001
PM 34060351
DA 2025-01-04
ER

PT J
AU Ke, WW
   Lu, ZM
   Zhao, XX
AF Ke, Weiwei
   Lu, Zaiming
   Zhao, Xiangxuan
TI NOB1: A Potential Biomarker or Target in Cancer
SO CURRENT DRUG TARGETS
LA English
DT Review
DE Cancer; NIN1/RPN12 binding protein 1 homolog (NOB1); signaling pathway;
   targeted therapy; RNA metabolism; anticancer therapy
ID ONE BINDING-PROTEIN; CARCINOMA IN-VITRO; 18S RIBOSOMAL-RNA;
   CLINICAL-SIGNIFICANCE; INHIBITS PROLIFERATION; DOWN-REGULATION; 26S
   PROTEASOME; PIN DOMAIN; COLORECTAL-CANCER; TUMOR-GROWTH
AB Human NIN1/RPN12 binding protein 1 homolog (NOB1), an RNA binding protein, is expressed ubiquitously in normal tissues such as the lung. liver, and spleen. Its core physiological function is to regulate protease activities and participate in maintaining RNA metabolism and stability. NOB1 is overexpressed in a variety of cancers, including pancreatic cancer, non-small cell lung cancer, ovarian cancer, prostate carcinoma, osteosarcoma, papillary thyroid carcinoma, colorectal cancer, and glioma. Although existing data indicate that NOB1 overexpression is associated with cancer growth, invasion, and poor prognosis, the molecular mechanisms behind these effects and its exact roles remain unclear. Several studies have confirmed that NOB1 is clinically relevant in different cancers, and further research at the molecular level will help evaluate the role of NOB1 in tumors. NOB1 has become an attractive target in anticancer therapy because it is overexpressed in many cancers and mediates different stages of tumor development. Elucidating the role of NOB1 in different signaling pathways as a potential cancer treatment will provide new ideas for existing cancer treatment methods. This review summarizes the research progress made into NOB1 in cancer in the past decade; this information provides valuable clues and theoretical guidance for future anticancer therapy by targeting NOB1.
C1 [Ke, Weiwei; Lu, Zaiming; Zhao, Xiangxuan] China Med Univ, Dept Radiol, Shengjing Hosp, 36 Sanhao St, Shenyang 110004, Liaoning, Peoples R China.
C3 China Medical University
RP Zhao, XX (corresponding author), China Med Univ, Dept Radiol, Shengjing Hosp, 36 Sanhao St, Shenyang 110004, Liaoning, Peoples R China.
EM xiangxuanzhao@163.com
OI Ke, Weiwei/0000-0002-3849-0514
FU National Natural Science Foundation of China [81771947, 31371425];
   Liaoning Provincial Natural Science Foundation of China [20180551061]
FX This work was partially supported by National Natural Science Foundation
   of China [81771947] to Z Lu and [31371425] to X Zhao; Liaoning
   Provincial Natural Science Foundation of China [20180551061] to X Zhao.
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NR 83
TC 9
Z9 10
U1 0
U2 29
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1389-4501
EI 1873-5592
J9 CURR DRUG TARGETS
JI Curr. Drug Targets
PY 2019
VL 20
IS 10
BP 1081
EP 1089
DI 10.2174/1389450120666190308145346
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA II6HR
UT WOS:000475295400008
PM 30854959
DA 2025-01-04
ER

PT J
AU Yu, JH
   Xiao, BY
   Tang, JH
   Wang, F
   Ding, Y
   Han, K
   Kong, LH
   Ling, YH
   Mei, WJ
   Hong, ZG
   Liao, LE
   Yang, WJ
   Pan, ZZ
   Zhang, XS
   Jiang, W
   Ding, PR
AF Yu, Jie-Hai
   Xiao, Bin-Yi
   Tang, Jing-Hua
   Wang, Fang
   Ding, Ya
   Han, Kai
   Kong, Ling-Heng
   Ling, Yi-Hong
   Mei, Wei-Jian
   Hong, Zhi-Gang
   Liao, Le -En
   Yang, Wan -Jun
   Pan, Zhi-Zhong
   Zhang, Xiao-Shi
   Jiang, Wu
   Ding, Pei-Rong
TI Efficacy of PD-1 inhibitors for colorectal cancer and polyps in Lynch
   syndrome patients
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Colorectal cancer; Lynch syndrome; Colorectal polyp; PD-1 inhibitors
ID MISMATCH REPAIR-DEFICIENT; MICROSATELLITE INSTABILITY; TUMORS; NIVOLUMAB
AB Background: Programmed death-1 (PD-1) inhibitor is effective for colorectal cancer (CRC) with deficient mismatch repair (dMMR) or high microsatellite instability (MSI-H). We aimed to explore its effects on CRCs and colonic polyps in Lynch syndrome (LS) patients. Methods: LS patients with CRC who had evaluable tumours and received at least 2 cycles of PD-1 inhibitors were retrospectively included. PD-1 inhibitors were given as a monotherapy or in combination with other therapies, including anticytotoxic T-lymphocyte-associated antigen -4 treatment, radiotherapy, chemotherapy, and targeted therapy. Correlations of treatment re-sponses with clinicopathological characteristics and genomic profiles were analysed.Four of five cases of LS CRCs displaying proficient MMR (pMMR) or microsatellite stable (MSS) were not responsive. Mucinous/signet-ring cell differentiation was associated with a lower ORR (P = 0.013). The 3-year overall survival and progression-free survival were 91.2% and 82.2%, respectively. A polyp was detected in 26 patients during surveillance. Seven adenomas disappeared after treatment, and they were all larger than 7 mm.Conclusion: PD-1 inhibitors are highly effective for dMMR and MSI-H LS CRCs, but not for pMMR or MSS LS CRCs or mucinous/signet-ring cell CRC. Large LS adenomas may also be eliminated by anti-PD-1 treatment.Data Availability Statement: Due to the privacy of patients, the related data cannot be available for public access but can be obtained from Pei-Rong Ding (dingpr@sysucc.org.cn) upon reasonable request. The key raw data have been uploaded to the Research Data Deposit public platform (www.researchdata.org.cn).& COPY; 2023 Elsevier Ltd. All rights reserved.
C1 [Yu, Jie-Hai; Xiao, Bin-Yi; Tang, Jing-Hua; Wang, Fang; Ding, Ya; Han, Kai; Kong, Ling-Heng; Ling, Yi-Hong; Mei, Wei-Jian; Hong, Zhi-Gang; Liao, Le -En; Yang, Wan -Jun; Pan, Zhi-Zhong; Zhang, Xiao-Shi; Jiang, Wu; Ding, Pei-Rong] Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Canc Ctr, Guangzhou, Peoples R China.
   [Yu, Jie-Hai; Xiao, Bin-Yi; Tang, Jing-Hua; Han, Kai; Kong, Ling-Heng; Mei, Wei-Jian; Hong, Zhi-Gang; Liao, Le -En; Yang, Wan -Jun; Pan, Zhi-Zhong; Jiang, Wu; Ding, Pei-Rong] Sun Yat Sen Univ, Canc Ctr, Dept Colorectal Surg, 651 Dongfeng East Rd, Guangzhou 510060, Peoples R China.
   [Ding, Ya; Zhang, Xiao-Shi] Sun Yat Sen Univ, Dept Biol Therapy Ctr, Canc Ctr, Guangzhou, Peoples R China.
   [Wang, Fang] Sun Yat Sen Univ, Dept Mol Diag, Canc Ctr, Guangzhou 510060, Peoples R China.
   [Ling, Yi-Hong] Sun Yat sen Univ, Dept Pathol, Canc Ctr, Guangzhou, Peoples R China.
C3 State Key Lab Oncology South China; Sun Yat Sen University; Sun Yat Sen
   University; Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen
   University
RP Ding, PR (corresponding author), Sun Yat Sen Univ, Canc Ctr, Dept Colorectal Surg, 651 Dongfeng East Rd, Guangzhou 510060, Peoples R China.
EM dingpr@sysucc.org.cn
RI Mei, Wei-Jian/HGD-6868-2022; ä¹æ©, å»–/KRO-7885-2024; Han,
   Kai/E-5689-2015; Yu, Jiehai/KHW-2380-2024; Zhang, Xiaoshi/AAW-9866-2020;
   Li, Dandan/JJE-6222-2023
OI Li, Dandan/0000-0001-9346-3212; leen, liao/0000-0001-8716-0653; Mei,
   Wei-Jian/0000-0002-0025-2908; Yu, Jiehai/0000-0001-7554-0018
FU National Natural Science Foundation of China [82073159]; Guangdong Basic
   and Applied Basic Research Foundation [2020A1515110544]
FX This study was supported by the National Natural Science Foundation of
   China (grant number 82073159) and the Guangdong Basic and Applied Basic
   Research Foundation (2020A1515110544).
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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 2023
VL 192
AR 113253
DI 10.1016/j.ejca.2023.113253
EA AUG 2023
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA R5VB9
UT WOS:001065017700001
PM 37625240
DA 2025-01-04
ER

PT J
AU Yang, ZY
   Wu, GC
   Zhang, X
   Gao, JL
   Meng, C
   Liu, YS
   Wei, Q
   Sun, LT
   Wei, PY
   Bai, ZG
   Yao, HW
   Zhang, ZT
AF Yang, Zhengyang
   Wu, Guocong
   Zhang, Xiao
   Gao, Jiale
   Meng, Cong
   Liu, Yishan
   Wei, Qi
   Sun, Liting
   Wei, Pengyu
   Bai, Zhigang
   Yao, Hongwei
   Zhang, Zhongtao
TI Current progress and future perspectives of neoadjuvant anti-PD-1/PD-L1
   therapy for colorectal cancer
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE colorectal cancer; PD-1; PD-L1 inhibitors; neoadjuvant; microsatellite
   instability; mismatch repair
ID IMMUNE CHECKPOINT INHIBITORS; MISMATCH REPAIR-DEFICIENT; ADVANCED
   RECTAL-CANCER; REGULATORY T-CELLS; MICROSATELLITE INSTABILITY; PD-1
   BLOCKADE; PD-1/PD-L1 BLOCKADE; POOLED ANALYSIS; OPEN-LABEL;
   IMMUNOTHERAPY
AB Immunotherapies, especially the programmed cell death 1/programmed cell death ligand 1 (PD-1/PD-L1) inhibitors, have revolutionized the therapeutic strategies of various cancers. As for colorectal cancer (CRC), the current clinical application of PD-1/PD-L1 inhibitors are mainly used according to the mutation pattern, which is categorized into deficient mismatch repair (dMMR)/high levels of microsatellite instability (MSI-H) and proficient mismatch repair (pMMR), or non-high levels of microsatellite instability (non-MSI-H). PD-1/PD-L1 inhibitors have been proven to have favorable outcomes against dMMR/MSI-H CRC because of more T-cell infiltration into tumor tissues. Nevertheless, the effectiveness of PD-1/PD-L1 inhibitors in pMMR/non-MSI-H CRC is still uncertain. Because of the quite-lower proportion of dMMR/MSI-H in CRC, PD-1/PD-L1 inhibitors have been reported to combine with other antitumor treatments including chemotherapy, radiotherapy, and targeted therapy for better therapeutic effect in recent clinical trials. Neoadjuvant therapy, mainly including chemotherapy and radiotherapy, not only can reduce clinical stage but also benefit from local control, which can improve clinical symptoms and the quality of life. Adding immunotherapy into neoadjuvant therapy may change the treatment strategy of primary resectable or some metastatic CRC. In this review, we focus on the development of neoadjuvant anti-PD-1/PD-L1 therapy and discuss the future perspectives in CRC.
C1 [Bai, Zhigang; Yao, Hongwei; Zhang, Zhongtao] Capital Med Univ, Beijing Friendship Hosp, Dept Gen Surg, Beijing, Peoples R China.
   Natl Clin Res Ctr Digest Dis, Beijing, Peoples R China.
C3 Capital Medical University
RP Bai, ZG; Yao, HW; Zhang, ZT (corresponding author), Capital Med Univ, Beijing Friendship Hosp, Dept Gen Surg, Beijing, Peoples R China.
EM baizhigang@ccmu.edu.cn; yaohongwei@ccmu.edu.cn; zhangzht@ccmu.edu.cn
RI Yang, Zhengyang/V-6233-2019; Wei, Qi/JJF-3393-2023; Bai,
   Zhi-Gang/C-3872-2011
OI Yang, Zhengyang/0000-0002-2640-9619; Yao, Hongwei/0000-0003-3995-6520;
   Wei, Qi/0000-0001-6613-9425; Bai, Zhi-Gang/0000-0001-9234-9354; Zhang,
   Zhongtao/0000-0002-4718-6821
FU National Key Technologies RD Program [2015BAI13B09]; National Key
   Technologies R&D Program of China [2017YFC0110904]; Clinical Center for
   Colorectal Cancer, Capital Medical University [1192070313]
FX This work was supported by grants from the National Key Technologies R&D
   Program (No. 2015BAI13B09), National Key Technologies R&D Program of
   China (No. 2017YFC0110904), and Clinical Center for Colorectal Cancer,
   Capital Medical University (No. 1192070313).
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NR 91
TC 35
Z9 38
U1 5
U2 37
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 9
PY 2022
VL 13
AR 1001444
DI 10.3389/fimmu.2022.1001444
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 4X7IX
UT WOS:000861012500001
PM 36159842
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Shen, J
   Li, ZJ
   Li, LF
   Lu, L
   Xiao, ZG
   Wu, WKK
   Zhang, L
   Li, MX
   Hu, W
   Chan, KM
   Cho, CH
AF Shen, Jing
   Li, Zhi Jie
   Li, Long Fei
   Lu, Lan
   Xiao, Zhan Gang
   Wu, William Ka Kei
   Zhang, Lin
   Li, Ming Xing
   Hu, Wei
   Chan, Kam Ming
   Cho, Chi Hin
TI Vascular-targeted TNFα and IFNγ inhibits orthotopic colorectal tumor
   growth
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Vascular targeting; TNF alpha; IFN gamma; Colorectal cancer; Drug
   delivery
ID NECROSIS-FACTOR-ALPHA; NF-KAPPA-B; ISOLATED LIMB PERFUSION; PHASE-I
   TRIAL; INTERFERON-GAMMA; INDUCED APOPTOSIS; FACTOR RECEPTORS;
   CANCER-THERAPY; DRUG-DELIVERY; CELL-LINES
AB Background: Tumor necrosis factor alpha (TNF alpha) and interferon gamma (IFN gamma) were originally identified to show potent anti-tumor activity and immunomodulatory capability. Unfortunately, several clinical studies of relevant cancer therapy did not observe significant response in maximum tolerated dose whether given alone or in combination. We have identified a tumor vasculature homing peptide (TCP-1 peptide) which targets only the vasculature of colorectal tumors but not normal blood vessels in animals and humans. In the current study, the antitumor effect of TCP-1/TNF alpha and TCP-1/IFN gamma alone or in combination was studied in orthotopic colorectal tumor model.
   Methods: TCP-1/TNF alpha and TCP-1/IFN gamma recombinant proteins were prepared and i.v. injected to study the in vivo anticancer effect in orthotopic colorectal tumor model. Tumor apoptosis was determined by TUNEL staining and cleaved caspase-3 immunofluorescent staining. Tumor infiltrating lymphocytes were analyzed by immunofluorescent staining and flow cytometry. Western-blot was performed to examine the expression of proteins. Cell apoptosis was measured by Annexin V/PI flow cytometry.
   Results: Targeted delivery of TNF alpha or IFN gamma by TCP-1 peptide exhibited better antitumor activity than unconjugated format by inducing more tumor apoptosis and also enhancing antitumor immunity shown by increased infiltration of T lymphocytes inside the tumor. More importantly, combination therapy of TCP-1/TNF alpha and TCP-1/IFN gamma synergistically suppressed tumor growth and alleviated systematic toxicity associated with untargeted therapy. This combination therapy induced massive apoptosis/secondary necrosis in the tumor.
   Conclusions: Taken together, our data demonstrate TCP-1 is an efficient drug carrier for targeted therapy of colorectal cancer (CRC). TCP-1/TNF alpha combined with TCP-1/IFN gamma is a promising combination therapy for CRC.
C1 [Shen, Jing; Li, Zhi Jie; Li, Long Fei; Lu, Lan; Xiao, Zhan Gang; Li, Ming Xing; Cho, Chi Hin] Southwest Med Univ, Sch Pharm, Dept Pharmacol, Mol Pharmacol Lab, Luzhou, Peoples R China.
   [Lu, Lan; Zhang, Lin; Hu, Wei; Chan, Kam Ming; Cho, Chi Hin] Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Shatin, Hong Kong, Peoples R China.
   [Wu, William Ka Kei] Chinese Univ Hong Kong, Dept Anaesthesia & Intens Care, Hong Kong, Hong Kong, Peoples R China.
   [Li, Zhi Jie] Univ Western Australia, Harry Perkins Inst Med Res, Crawley, WA 6009, Australia.
C3 Southwest Medical University; Chinese University of Hong Kong; Chinese
   University of Hong Kong; University of Western Australia; Harry Perkins
   Institute of Medical Research
RP Li, ZJ; Cho, CH (corresponding author), Southwest Med Univ, Sch Pharm, Dept Pharmacol, Mol Pharmacol Lab, Luzhou, Peoples R China.; Cho, CH (corresponding author), Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Shatin, Hong Kong, Peoples R China.; Li, ZJ (corresponding author), Univ Western Australia, Harry Perkins Inst Med Res, Crawley, WA 6009, Australia.
EM jackylizhijie@gmail.com; chcho@cuhk.edu.hk
RI Chan, K/AAH-4084-2019; LI, ZHIJIE/HJG-6926-2022; Cho, Chi/C-6543-2014;
   ZHANG, Lin/O-9109-2015; Wu, William K.K./A-3277-2009
OI Zhang, Lin/0000-0003-1634-3780; Wu, William K.K./0000-0002-5662-5240;
   LI, Longfei/0009-0000-7872-2175
FU Innovation and Technology Support Programme; Innovation and Technology
   Commission; Research Grant Council from Hong Kong; Southwest Medical
   University
FX The study was supported by the Innovation and Technology Support
   Programme and the General Research Fund from the Innovation and
   Technology Commission, the Research Grant Council from Hong Kong and the
   start-up fund from Southwest Medical University. We thank Chun Yin for
   the technical assistance in this study.
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NR 44
TC 15
Z9 17
U1 3
U2 21
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1479-5876
J9 J TRANSL MED
JI J. Transl. Med.
PD JUN 24
PY 2016
VL 14
AR 187
DI 10.1186/s12967-016-0944-3
PG 13
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA DP7LH
UT WOS:000378680200001
PM 27342639
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lenz, HJ
   Ou, FS
   Venook, AP
   Hochster, HS
   Niedzwiecki, D
   Goldberg, RM
   Mayer, RJ
   Bertagnolli, MM
   Blanke, CD
   Zemla, T
   Qu, XP
   Wirapati, P
   Tejpar, S
   Innocenti, F
   Kabbarah, O
AF Lenz, Heinz-Josef
   Ou, Fang-Shu
   Venook, Alan P.
   Hochster, Howard S.
   Niedzwiecki, Donna
   Goldberg, Richard M.
   Mayer, Robert J.
   Bertagnolli, Monica M.
   Blanke, Charles D.
   Zemla, Tyler
   Qu, Xueping
   Wirapati, Pratyaksha
   Tejpar, Sabine
   Innocenti, Federico
   Kabbarah, Omar
TI Impact of Consensus Molecular Subtype on Survival in Patients With
   Metastatic Colorectal Cancer: Results From CALGB/SWOG 80405 (Alliance)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID FOLFIRI PLUS BEVACIZUMAB; 1ST-LINE TREATMENT; OPEN-LABEL; STATISTICS;
   CLASSIFICATION; CHEMOTHERAPY; INHIBITION; CETUXIMAB; FIRE-3; MODELS
AB PURPOSETo determine the predictive and prognostic value of the consensus molecular subtypes (CMSs) of colorectal cancer (CRC) that represent a merging of gene expression-based features largely in primary tumors from six independent classification systems and provide a framework for capturing the intrinsic heterogeneity of CRC in patients enrolled in CALGB/SWOG 80405.PATIENTS AND METHODSCALGB/SWOG 80405 is a phase III trial that compared the addition of bevacizumab or cetuximab to infusional fluorouracil, leucovorin, and oxaliplatin or fluorouracil, leucovorin, and irinotecan as first-line treatment of advanced CRC. We characterized the CMS classification using a novel NanoString gene expression panel on primary CRCs from 581 patients enrolled in this study to assess the prognostic and predictive value of CMSs in these patients.RESULTSThe CMSs are highly prognostic for overall survival (OS; P < .001) and progression-free survival (PFS; P < .001). Furthermore, CMSs were predictive for both OS (P for interaction < .001) and PFS (P for interaction = .0032). In the CMS1 cohort, patients treated with bevacizumab had a significantly longer OS than those treated with cetuximab (P < .001). In the CMS2 cohort, patients treated with cetuximab had a significantly longer OS than patients treated with bevacizumab (P = .0046).CONCLUSIONThese findings highlight the possible clinical utility of CMSs and suggests that refinement of the CMS classification may provide a path toward identifying patients with metastatic CRC who are most likely to benefit from specific targeted therapy as part of the initial treatment.
C1 [Lenz, Heinz-Josef] Univ Southern Calif, Norris Comprehens Canc Ctr, 1441 Eastlake Ave,Suite 3456, Los Angeles, CA 90089 USA.
   [Ou, Fang-Shu; Zemla, Tyler] Mayo Clin, Canc Ctr, Rochester, MN USA.
   [Venook, Alan P.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
   [Hochster, Howard S.] Yale Canc Ctr, New Haven, CT USA.
   [Niedzwiecki, Donna] Duke Univ, Med Ctr, Durham, NC USA.
   [Goldberg, Richard M.] West Virginia Univ, Canc Inst, Morgantown, WV 26506 USA.
   [Mayer, Robert J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Bertagnolli, Monica M.] Brigham & Womens Hosp, 75 Francis St, Boston, MA 02115 USA.
   [Blanke, Charles D.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
   [Qu, Xueping; Kabbarah, Omar] Genentech Inc, San Francisco, CA USA.
   [Wirapati, Pratyaksha] Swiss Inst Bioinformat, Lausanne, Switzerland.
   [Tejpar, Sabine] Univ Ziekenhuis Leuven, Leuven, Belgium.
   [Innocenti, Federico] Univ N Carolina, Chapel Hill, NC 27515 USA.
C3 University of Southern California; Mayo Clinic; University of California
   System; University of California San Francisco; Yale University; Duke
   University; West Virginia University; Harvard University; Dana-Farber
   Cancer Institute; Harvard University; Brigham & Women's Hospital; Oregon
   Health & Science University; Roche Holding; Genentech; Swiss Institute
   of Bioinformatics; KU Leuven; University Hospital Leuven; University of
   North Carolina; University of North Carolina Chapel Hill
RP Lenz, HJ (corresponding author), Univ Southern Calif, Norris Comprehens Canc Ctr, 1441 Eastlake Ave,Suite 3456, Los Angeles, CA 90089 USA.
EM lenz@usc.edu
RI Innocenti, Federico/G-3206-2018
OI Niedzwiecki, Donna/0000-0002-3566-0450
FU National Cancer Institute [U10CA180821, U10CA180882, U10CA180790,
   U10CA180791, U10CA180795, U10CA180799, U10CA180830, U10CA180836,
   U10CA180838, U10CA180850, U10CA180867, U10CA180888]; Bristol-Myers
   Squibb; Eli Lilly; Genentech; Pfizer; Sanofi
FX Supported by National Cancer Institute grants U10CA180821 and
   U10CA180882 (Alliance for Clinical Trials in Oncology), U10CA180790
   (Mayo Clinic), U10CA180791 (Memorial Sloan Kettering), U10CA180795
   (Indiana University), U10CA180799 (University of Wisconsin), U10CA180830
   (University of Southern California Norris Cancer Hospital), U10CA180836
   (The University of Chicago), U10CA180838 (The University of North
   Carolina), U10CA180850 (The Ohio State University), U10CA180867
   (Dana-Farber Cancer Institute), and U10CA180888 (SWOG). The trial was
   also supported in part by Bristol-Myers Squibb, Eli Lilly, Genentech,
   Pfizer, and Sanofi.
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NR 35
TC 168
Z9 177
U1 0
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD AUG 1
PY 2019
VL 37
IS 22
BP 1876
EP +
DI 10.1200/JCO.18.02258
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IS7VC
UT WOS:000482356400008
PM 31042420
OA Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Xiang, D
   Li, HY
   Pan, J
   Chen, YT
AF Xiang, Dan
   Li, Huiyu
   Pan, Jun
   Chen, Yitian
TI <i>SLC4A4</i> Moulds the Inflammatory Tumor Microenvironment and
   Predicts Therapeutic Expectations in Colorectal Cancer
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Article; Early Access
DE Colorectal cancer; prognosis; immunotherapy; immunogenicity
ID PPAR-GAMMA; EXPRESSION; CELLS; PROLIFERATION; MIGRATION; INVASION;
   COLON; METASTASIS; PROGNOSIS; IMMUNITY
AB Background Colorectal cancer (CRC) cases with advanced or distal metastases experience a survival rate of less than 20%, with the lack of spectral therapeutic targets and prognostic markers posing a significant challenge for CRC treatment. SLC4A4 may be a CRC-targeted therapy for which there is currently inadequate evidence. Aim In this report, we performed a comprehensive analysis of data on colorectal cancer (CRC) to elucidate the association among Solute Carrier Family 4 Member 4 (SLC4A4) and the abundance of immunological features and immune cell infiltration in CRC and to explore the impact of SLC4A4 on the CRC tumor microenvironment. Objective The objective of this study was to systematically reveal the characteristics of the tumor microenvironment created by SLC4A4. Methods We downloaded RNA sequencing files from the Cancer Genome Atlas (TCGA-COADREAD). The correlations of SLC4A4 with immune-related characteristics were analyzed. A Limma package was applied for selecting SLC4A4/immunity-related differentially expressed genes (DEGs). An assessment system for predicting CRC prognosis was constructed based on univariate COX and multivariate COX analyses. A nomogram was also designed to assess the survival risk status of CRC. Besides, we evaluated the potential association of SLC4A4 to immunotherapy through TIDE analysis. Results We found that SLC4A4 expression was positively correlated with immune checkpoint expression (PD-L1). SLC4A4 promoted the infiltration of CD8 T cells, dendritic cells, macrophages, NK cells, and Th1 cells in CRC, shaping the inflammatory tumor microenvironment. Up-regulated SLC4A4 might improve drug response to anti-FGFR3 therapy, anti-PPARG therapy, nivolumab, and ipilimumab in CRC patients, and down-regulated SLC4A4 might promote drug response to anti-EGFR therapy and Aflibercept drug response. The constructed RiskScore model showed excellent predictive effect and robustness. RiskScore presented a trend of negative correlation with SLC4A4, which was consistent with the trend of the effect of SLC4A4 on CRC survival. TIDE analysis further disclosed that high-risk groups with high levels of SLC4A4 were possible for immune escape. Finally, the constructed nomogram also showed potential clinical value. Conclusion Overall, upregulation of SLC4A4 expression promoted an inflammatory tumor microenvironment in CRC, and RiskScore predicted therapeutic expectancy. SLC4A4 could be a potentially clinically valuable target for CRC therapy.
C1 [Xiang, Dan; Li, Huiyu; Pan, Jun; Chen, Yitian] Nanjing Univ, Med Sch, Affiliated Jinling Hosp, Dept Med Oncol, 305 Zhongshan East Rd, Nanjing 210008, Jiangsu, Peoples R China.
C3 Nanjing University
RP Pan, J; Chen, YT (corresponding author), Nanjing Univ, Med Sch, Affiliated Jinling Hosp, Dept Med Oncol, 305 Zhongshan East Rd, Nanjing 210008, Jiangsu, Peoples R China.
EM yitianchen@126.com
RI Li, Huiyu/ABA-9096-2021
FU National Natural Science Foundation of China (NSFC ) [81972332,
   81702442]
FX This work was supported by grants from the National Natural Science
   Foundation of China (NSFC numbers 81972332 and 81702442).
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NR 64
TC 2
Z9 2
U1 0
U2 1
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.
PD 2024 FEB 15
PY 2024
DI 10.2174/0109298673277357231218070812
EA FEB 2024
PG 18
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA JY7B0
UT WOS:001176773700001
PM 38310390
DA 2025-01-04
ER

PT J
AU Ou, SY
   Xu, RC
   Li, K
   Chen, Y
   Kong, Y
   Liu, HC
   Li, JL
   Ouyang, YZ
   Yu, XP
AF Ou, Shuangyan
   Xu, Ruocai
   Li, Ke
   Chen, Yong
   Kong, Yi
   Liu, Hanchun
   Li, Jianliang
   Ouyang, Yongzhong
   Yu, Xiaoping
TI Radiofrequency ablation with systemic chemotherapy in the treatment of
   colorectal cancer liver metastasis: a 10-year single-center study
SO CANCER MANAGEMENT AND RESEARCH
LA English
DT Article
DE radiofrequency assay; systemic chemotherapy; liver metastasis;
   colorectal cancer; ultrasound; survival
ID PERCUTANEOUS ETHANOL INJECTION; LONG-TERM SURVIVAL;
   HEPATOCELLULAR-CARCINOMA; HEPATIC METASTASES; SURGICAL RESECTION; 5-YEAR
   SURVIVAL; 1ST-LINE TREATMENT; THERMAL ABLATION; SOLITARY; FLUOROURACIL
AB Objective: To retrospectively evaluate the long-term efficacy and safety of radiofrequency ablation (RFA) with systemic chemotherapy (CT) in treatment of solitary liver metastasis after surgery for colorectal cancer (CRC).
   Methods: This single-center study was conducted at the Hunan Provincial Cancer Hospital from June 2006 to December 2015 with median follow-up time of 26 months. Percutaneous ultrasound-guided RFA was carried out on eligible patients with solitary liver metastasis after surgery for CRC. After a week, ablation status was confirmed by MRI. Post MRI, all patients received systemic CT with or without molecular-targeted therapy. Survival rate was evaluated and survival curve was constructed with Kaplan-Meier analysis. Log-rank test and Cox regression model were used for univariate and multivariate analysis, respectively, to determine the independent prognostic factors for survival rate.
   Results: A total of 109 eligible patients (mean age, 53.84 +/- 11.71; mean tumor mass diameter, 3.4+2.01 cm) were enrolled in this 10-year study. After RFA, 95 patients achieved complete ablation, and 14 patients achieved partial ablation, with median ablation time of 26 minutes (range: 12-120 minutes). The median survival time required for achieving complete and partial ablation was 56.0 and 19.0 months, respectively (P<.01). After RFA and adjuvant systemic CT, the 1-, 3-, and 5-year survival rates were 92.3%, 50.7%, and 41.6%, respectively, with the median (mean) survival time of 39.0 (56.5) months. Age was the only significant independent prognostic factor with better survival rate observed in patients aged >= 50 years than those aged <50 years (P<0.05). The incidence of complications was minimal (1.8%) with only two cases: one biliary fistula and one liver hemorrhage.
   Conclusion: RFA combination with systemic CT was safe; it showed long-term efficacy in patients with solitary liver metastasis after surgery for CRC and can be a preferred treatment.
C1 [Ou, Shuangyan; Xu, Ruocai; Li, Ke; Chen, Yong; Kong, Yi; Liu, Hanchun; Li, Jianliang] Hunan Canc Hosp, Dept Hepatobiliary & Pancreat Med, Changsha, Hunan, Peoples R China.
   [Ouyang, Yongzhong] Hunan Prov Canc Hosp, Dept Gastroduodenal Surg, Changsha, Hunan, Peoples R China.
   [Yu, Xiaoping] Hunan Canc Hosp, Dept Radiol, Changsha, Hunan, Peoples R China.
RP Ou, SY (corresponding author), Dept Hepatobiliary & Pancreat Med, 283 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China.
EM oushuangyan@gmail.com
OI yu, xiaoping/0000-0003-4502-1027
FU Medtronic China Co Ltd.
FX The authors would like to acknowledge Wu Shengqi, Chief Physician, Hunan
   Provincial Cancer Hospital, China, who helped in the treatment protocol
   and has extended support in carrying out the statistical analysis for
   the study. All the investigators involved in the study contributed in
   development and approval of the manuscript. The authors acknowledge Dr
   Priyanka Nair and Dr Anuradha Nalli's support (Indegene Pvt Ltd) in
   providing medical writing assistance in the development of this
   manuscript, funded by Medtronic China Co Ltd. The study was funded by
   Medtronic China Co Ltd.
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NR 61
TC 15
Z9 15
U1 0
U2 3
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1179-1322
J9 CANCER MANAG RES
JI Cancer Manag. Res.
PY 2018
VL 10
BP 5227
EP 5237
DI 10.2147/CMAR.S170160
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GZ0KP
UT WOS:000449051800004
PM 30464620
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Aranda, E
   Polo, E
   Camps, C
   Carrato, A
   Diaz-Rubio, E
   Guillem, 
   Lopez, R
   Anton, A
AF Aranda, E.
   Polo, E.
   Camps, C.
   Carrato, A.
   Diaz-Rubio, E.
   Guillem, V
   Lopez, R.
   Anton, A.
TI Treatment patterns for metastatic colorectal cancer in Spain
SO CLINICAL & TRANSLATIONAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer; Metastatic; Treatment patterns; KRAS; BRAF mutation
   status; Clinical practice guideline
ID TREATMENT GUIDELINES; ADHERENCE; SURVIVAL; COLON; DIAGNOSIS; THERAPY;
   RAS
AB Purpose The primary aim of this retrospective study was to describe the treatment patterns according to the type of treatment received by patients with metastatic colorectal cancer (mCRC) in Spain. Methods This was a retrospective, observational, multicenter study performed by 33 sites throughout Spain that included consecutive patients aged 18 years or older who had received or were receiving treatment for mCRC. Results At the time of inclusion, of the 873 evaluable patients, 507 (58%) had received two lines, 235 (27%) had received three lines, 106 (12%) had received four lines, and the remaining patients had received up to ten lines. The most frequent chemotherapy schemes were the FOLFOX or CAPOX regimens (66%) for first-line treatment, FOLFOX, CAPOX or FOLFIRI (70%) for second-line treatment, and FOLFOX, FOLFIRI or other fluoropyrimidine-based regimens for third- and fourth-line (over 60%) treatment. Sixty percent of patients received targeted therapy as part of their first-line treatment, and this proportion increased up to approximately 70% of patients as part of the second-line of treatment. A relevant proportion of patients were treated with unknown KRAS, and especially the BRAF, mutation statuses. Conclusions This study reveals inconsistencies regarding adherence to the recommendations of the ESMO guidelines for the management of mCRC in Spain. Improved adherence to the standard practice described in such guidelines for the determination of RAS and BRAF mutation statuses and the use of targeted therapies in first-line treatment should be considered to guarantee that patients can benefit from the best therapeutic approaches available.
C1 [Aranda, E.] Univ Cordoba, Reina Sofia Hosp, Maimonides Inst Biomed Res IMIBIC, Oncol Dept, Cordoba, Spain.
   [Aranda, E.; Carrato, A.; Diaz-Rubio, E.; Lopez, R.] Inst Salud Carlos III, CIBERONC, Madrid, Spain.
   [Polo, E.; Anton, A.] Miguel Servet Univ Hosp, IIS Aragon, Med Oncol Dept, Zaragoza, Spain.
   [Camps, C.] Fdn Invest Hosp Gen Univ Valencia, Mol Oncol Lab, Valencia, Spain.
   [Camps, C.] CIBERONC, Valencia, Spain.
   [Camps, C.] Consorcio Hosp Gen Univ Valencia, Dept Med Oncol, Valencia, Spain.
   [Camps, C.] Univ Valencia, Dept Med, Valencia, Spain.
   [Carrato, A.] Alcala Univ, Ramon y Cajal Univ Hosp, IRYCIS, Med Oncol, Madrid, Spain.
   [Diaz-Rubio, E.] Hosp Clin San Carlos, Med Oncol, Madrid, Spain.
   [Guillem, V] Fdn Inst Valenciano Oncol, Med Oncol Dept, Valencia, Spain.
   [Lopez, R.] Hosp Clin Univ, Serv Oncol Med, Santiago De Compostela, Spain.
   [Lopez, R.] Hosp Clin Univ, Grp Oncol Med Traslac Oncomet, Santiago De Compostela, Spain.
   [Lopez, R.] Inst Invest Sanitaria IDIS Santiago, Santiago De Compostela, Spain.
   [Aranda, E.] Hosp Univ Reina Sofia, Oncol Dapartment, Av Menendez Pidal S-N, Cordoba 14004, Spain.
C3 Universidad de Cordoba; Instituto de Salud Carlos III; CIBER - Centro de
   Investigacion Biomedica en Red; CIBERONC; Miguel Servet University
   Hospital; CIBER - Centro de Investigacion Biomedica en Red; CIBERONC;
   University of Valencia; Universidad de Alcala; Hospital Universitario
   Ramon y Cajal; Hospital Clinico San Carlos; Instituto Valenciano De
   Oncologia; Complexo Hospitalario Universitario de Santiago de
   Compostela; Complexo Hospitalario Universitario de Santiago de
   Compostela
RP Aranda, E (corresponding author), Univ Cordoba, Reina Sofia Hosp, Maimonides Inst Biomed Res IMIBIC, Oncol Dept, Cordoba, Spain.; Aranda, E (corresponding author), Inst Salud Carlos III, CIBERONC, Madrid, Spain.; Aranda, E (corresponding author), Hosp Univ Reina Sofia, Oncol Dapartment, Av Menendez Pidal S-N, Cordoba 14004, Spain.
EM earandaa@seom.org
RI Anton, Antonio/AAP-6563-2020
OI Aranda Aguilar, Enrique/0000-0002-5471-2842; Lopez Lopez,
   Rafael/0000-0003-1315-655X; CARRATO, ALFREDO/0000-0001-7749-8140
CR Abrams TA, 2014, JNCI-J NATL CANCER I, V106, DOI 10.1093/jnci/djt371
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NR 23
TC 12
Z9 12
U1 0
U2 1
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 SEP
PY 2020
VL 22
IS 9
BP 1455
EP 1462
DI 10.1007/s12094-019-02279-5
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MP1OE
UT WOS:000551980000004
PM 31974819
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Faizullin, D
   Valiullina, Y
   Salnikov, V
   Zelenikhin, P
   Zuev, Y
   Ilinskaya, O
AF Faizullin, Dzhigangir
   Valiullina, Yuliya
   Salnikov, Vadim
   Zelenikhin, Pavel
   Zuev, Yuriy
   Ilinskaya, Olga
TI Fibrin-Rhamnogalacturonan I Composite Gel for Therapeutic Enzyme
   Delivery to Intestinal Tumors
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE drug delivery; colorectal cancer; binase; fibrin; rhamnogalacturonan I
ID PREBIOTIC PROPERTIES; CELL-PROLIFERATION; DRUG-DELIVERY; RIBONUCLEASE;
   TURBIDITY; HYDRATION; POLYSACCHARIDES; POLYMERIZATION; HYDROGELS;
   VESICLES
AB Therapy of colorectal cancer with protein drugs, including targeted therapy using monoclonal antibodies, requires the preservation of the drug's structure and activity in the gastrointestinal tract or bloodstream. Here, we confirmed experimentally the fundamental possibility of creating composite protein-polysaccharide hydrogels based on non-degrading rhamnogalacturonan I (RG) and fibrin as a delivery vehicle for antitumor RNase binase. The method is based on enzymatic polymerization of fibrin in the presence of RG with the inclusion of liposomes, containing an encapsulated enzyme drug, into the gel network. The proposed method for fabricating a gel matrix does not require the use of cytotoxic chemical cross-linking agents and divalent cations, and contains completely biocompatible and biodegradable components. The process proceeds under physiological conditions, excluding the effect of high temperatures, organic solvents and ultrasound on protein components. Immobilization of therapeutic enzyme binase in the carrier matrix by encapsulating it in liposomes made from uncharged lipid made it possible to achieve its prolonged release with preservation of activity for a long time. The release time of binase from the composite carrier can be regulated by variation of the fibrin and RG concentration.
C1 [Faizullin, Dzhigangir; Valiullina, Yuliya; Salnikov, Vadim; Zuev, Yuriy] FRC Kazan Sci Ctr RAS, Kazan Inst Biochem & Biophys, Kazan 420111, Russia.
   [Zelenikhin, Pavel; Ilinskaya, Olga] Kazan Fed Univ, Inst Fundamental Med & Biol, Kazan 420008, Russia.
C3 Russian Academy of Sciences; Kazan Scientific Centre of the Russian
   Academy of Sciences; Kazan Institute of Biochemistry & Biophysics; Kazan
   Federal University
RP Zuev, Y (corresponding author), FRC Kazan Sci Ctr RAS, Kazan Inst Biochem & Biophys, Kazan 420111, Russia.
EM zuev@kibb.knc.ru
RI salnikova, vera/AAH-3126-2020; Faizullin, Dzhigangir/AAO-9872-2021;
   Zelenikhin, Pavel/E-7042-2014; Ilinskaya, Olga/A-7458-2014; Zuev,
   Yuriy/A-7761-2016
OI Faizullin, Dzhigangir/0000-0002-2872-732X; Ilinskaya,
   Olga/0000-0001-6936-2032; Zuev, Yuriy/0000-0002-6715-2530; Zelenikhin,
   Pavel/0000-0003-1971-1745
FU Kazan Federal University Strategic Academic Leadership Program
   [PRIORITY-2030]
FX The work of D.F., Y.V., V.S. and Y.Z. was supported by the government
   assignment for FRC Kazan Scientific Center of RAS (122011800137-0).
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NR 70
TC 3
Z9 3
U1 1
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JAN
PY 2023
VL 24
IS 2
AR 926
DI 10.3390/ijms24020926
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 7Y8JT
UT WOS:000915119000001
PM 36674440
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Alqahtani, QM
   Crowley, A
   Rapp, S
   Cushman-Vokoun, AM
AF Alqahtani, Qamra M.
   Crowley, Ann
   Rapp, Sharleen
   Cushman-Vokoun, Allison M.
TI QIAGEN Therascreen <i>KRAS</i> RGQ Assay, QIAGEN <i>KRAS</i> Pyro Assay,
   and Dideoxy Sequencing for Clinical Laboratory Analysis of <i>KRAS</i>
   Mutations in Tumor Specimens
SO LABORATORY MEDICINE
LA English
DT Article
DE real-time PCR; pyrosequencing; EGFR inhibitor; colorectal cancer; DNA;
   formalin-fixed paraffin embedded; targeted therapy; biomarker
ID METASTATIC COLORECTAL-CANCER; RAS MUTATIONS; CETUXIMAB; PANITUMUMAB;
   ONCOGENES; THERAPY; GENE; PCR
AB Objective: To compare the performance of assays used to assess KRAS mutations in tumor specimens.
   Methods: We analyzed DNA extracted from 30 formalin-fixed paraffin-embedded (FFPE) tumor specimens using the QIAGEN Therascreen KRAS RGQ and QIAGEN Pyro reagents, with dideoxy sequencing (colloquially considered to be the gold standard) as the reference method.
   Results: We detected 22 codon 12 or 13 KRAS mutations using the Pyro assay, whereas the RGQ assay detected 19 mutations. For mutation detection, the clinical sensitivity was 86% for the RGQ assay compared with 100% for the Pyro but 100% for the KRAS mutations that the RGQ was predesigned to detect. The Pyro could detect rare mutations. The RGQ demonstrated a lower limit of detection compared with the Pyro; However, the Pyro required less DNA input than the RGQ.
   Conclusion: The 2 assays that we tested yielded comparable performance in detecting KRAS mutations, as we had expected based on assay design. Overall, the Pyro assay detects more mutations and requires less DNA input but is less analytically sensitive, compared with the RGQ assay.
C1 [Alqahtani, Qamra M.; Crowley, Ann; Rapp, Sharleen; Cushman-Vokoun, Allison M.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
C3 University of Nebraska System; University of Nebraska Medical Center
RP Cushman-Vokoun, AM (corresponding author), Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
EM acushman@unmc.edu
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NR 18
TC 3
Z9 3
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0007-5027
EI 1943-7730
J9 LAB MED
JI Lab. Med.
PD FEB
PY 2016
VL 47
IS 1
BP 30
EP 38
DI 10.1093/labmed/lmv009
PG 9
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA DF1WK
UT WOS:000371129800008
PM 26732779
OA Bronze
DA 2025-01-04
ER

PT J
AU Craig, SG
   Humphries, MP
   Alderdice, M
   Bingham, V
   Richman, SD
   Loughrey, MB
   Coleman, HG
   Viratham-Pulsawatdi, A
   McCombe, K
   Murray, GI
   Blake, A
   Domingo, E
   Robineau, J
   Brown, L
   Fisher, D
   Seymour, MT
   Quirke, P
   Bankhead, P
   McQuaid, S
   Lawler, M
   McArt, DG
   Maughan, TS
   James, JA
   Salto-Tellez, M
AF Craig, Stephanie G.
   Humphries, Matthew P.
   Alderdice, Matthew
   Bingham, Victoria
   Richman, Susan D.
   Loughrey, Maurice B.
   Coleman, Helen G.
   Viratham-Pulsawatdi, Amelie
   McCombe, Kris
   Murray, Graeme I.
   Blake, Andrew
   Domingo, Enric
   Robineau, James
   Brown, Louise
   Fisher, David
   Seymour, Matthew T.
   Quirke, Phil
   Bankhead, Peter
   McQuaid, Stephen
   Lawler, Mark
   McArt, Darragh G.
   Maughan, Tim S.
   James, Jacqueline A.
   Salto-Tellez, Manuel
TI Immune status is prognostic for poor survival in colorectal cancer
   patients and is associated with tumour hypoxia
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
ID CARCINOMA; MICROENVIRONMENT
AB Background Immunohistochemical quantification of the immune response is prognostic for colorectal cancer (CRC). Here, we evaluate the suitability of alternative immune classifiers on prognosis and assess whether they relate to biological features amenable to targeted therapy. Methods Overall survival by immune (CD3, CD4, CD8, CD20 and FOXP3) and immune-checkpoint (ICOS, IDO-1 and PD-L1) biomarkers in independent CRC cohorts was evaluated. Matched mutational and transcriptomic data were interrogated to identify associated biology. Results Determination of immune-cold tumours by combined low-density cell counts of CD3, CD4 and CD8 immunohistochemistry constituted the best prognosticator across stage II-IV CRC, particularly in patients with stage IV disease (HR 1.98 [95% CI: 1.47-2.67]). These immune-cold CRCs were associated with tumour hypoxia, confirmed using CAIX immunohistochemistry (P = 0.0009), which may mediate disease progression through common biology (KRASmutations, CRIS-B subtype andSPP1mRNA overexpression). Conclusions Given the significantly poorer survival of immune-cold CRC patients, these data illustrate that assessment of CD4-expressing cells complements low CD3 and CD8 immunohistochemical quantification in the tumour bulk, potentially facilitating immunophenotyping of patient biopsies to predict prognosis. In addition, we found immune-cold CRCs to associate with a difficult-to-treat, poor prognosis hypoxia signature, indicating that these patients may benefit from hypoxia-targeting clinical trials.
C1 [Craig, Stephanie G.; Humphries, Matthew P.; Alderdice, Matthew; Bingham, Victoria; Viratham-Pulsawatdi, Amelie; McCombe, Kris; McQuaid, Stephen; Lawler, Mark; McArt, Darragh G.; James, Jacqueline A.; Salto-Tellez, Manuel] Queens Univ Belfast, Ctr Cell Res & Cell Biol, Precis Med Ctr Excellence, Belfast, Antrim, North Ireland.
   [Richman, Susan D.; Seymour, Matthew T.; Quirke, Phil] Univ Leeds, Leeds Inst Med Res St Jamess, Leeds, W Yorkshire, England.
   [Loughrey, Maurice B.; McQuaid, Stephen; James, Jacqueline A.; Salto-Tellez, Manuel] Royal Victoria Hosp, Belfast Hlth & Social Care Trust, Dept Cellular Pathol, Belfast, Antrim, North Ireland.
   [Loughrey, Maurice B.; Coleman, Helen G.] Queens Univ Belfast, Ctr Publ Hlth, Belfast, Antrim, North Ireland.
   [Murray, Graeme I.] Univ Aberdeen, Sch Med Med Sci & Nutr, Pathol, Aberdeen, Scotland.
   [Blake, Andrew; Domingo, Enric; Robineau, James; Maughan, Tim S.] Univ Oxford, CRUK MRC Oxford Inst Radiat Oncol, Oxford, England.
   [Brown, Louise; Fisher, David] UCL, MRC Clin Trials Unit, London, England.
   [Bankhead, Peter] Univ Edinburgh, Div Pathol, Edinburgh, Midlothian, Scotland.
C3 Queens University Belfast; University of Leeds; Queens University
   Belfast; University of Aberdeen; University of Oxford; Medical Research
   Council Clinical Trials Unit; University of London; University College
   London; University of Edinburgh
RP Salto-Tellez, M (corresponding author), Queens Univ Belfast, Ctr Cell Res & Cell Biol, Precis Med Ctr Excellence, Belfast, Antrim, North Ireland.; Salto-Tellez, M (corresponding author), Royal Victoria Hosp, Belfast Hlth & Social Care Trust, Dept Cellular Pathol, Belfast, Antrim, North Ireland.
EM m.salto-tellez@qub.ac.uk
RI Maughan, Tim/AAV-7636-2021; Bankhead, Peter/AAA-7915-2020; Craig,
   Stephanie/AAX-2060-2020; Domingo, Enric/JDV-9587-2023; Fisher,
   David/KLC-7622-2024; Coleman, Helen/G-3373-2011; Domingo,
   Enric/A-9099-2018
OI Salto-Tellez, Manuel/0000-0001-8586-282X; Blake,
   Andrew/0000-0002-8154-6253; Brown, Louise/0000-0003-2827-6634; Craig,
   Stephanie/0000-0002-5476-751X; Maughan, Timothy
   Stanley/0000-0002-0580-5065; Richman, Susan/0000-0003-3993-5041;
   Domingo, Enric/0000-0003-4390-8767; Seymour,
   Matthew/0000-0002-2441-9629; Bankhead, Peter/0000-0003-4851-8813;
   Quirke, Philip/0000-0002-3597-5444; Lawler, Mark/0000-0002-3930-8470;
   Fisher, David/0000-0002-2512-2296
FU Cancer Research UK Accelerator grant; Cancer Research UK; Medical
   Research Council; MRC [MR/M016587/1] Funding Source: UKRI
FX The funders had no role in study design, collection, data analysis or
   interpretation of the data. This study was supported by a Cancer
   Research UK Accelerator grant and carried out in collaboration with the
   stratified medicine consortium in colorectal cancer (S:CORT), which is
   jointly funded by the Medical Research Council and Cancer Research UK.
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NR 33
TC 51
Z9 53
U1 0
U2 6
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 13
PY 2020
VL 123
IS 8
BP 1280
EP 1288
DI 10.1038/s41416-020-0985-5
EA JUL 2020
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OH6JV
UT WOS:000550125400004
PM 32684627
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Pranteda, A
   Piastra, V
   Serra, M
   Bernardini, R
   Lo Sardo, F
   Carpano, S
   Diodoro, MG
   Bartolazzi, A
   Milella, M
   Blandino, G
   Bossi, G
AF Pranteda, Angelina
   Piastra, Valentina
   Serra, Martina
   Bernardini, Roberta
   Lo Sardo, Federica
   Carpano, Silvia
   Diodoro, Maria Grazia
   Bartolazzi, Armando
   Milella, Michele
   Blandino, Giovanni
   Bossi, Gianluca
TI Activated MKK3/MYC crosstalk impairs dabrafenib response in BRAFV600E
   colorectal cancer leading to resistance
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Colorectal Cancer (CRC); MYC; BRAF target therapy; MKK3 / p38MAPK
ID KINASE KINASE 3; ACQUIRED-RESISTANCE; COLON-CANCER; INHIBITION; MYC;
   IDENTIFICATION; COMBINATIONS; VEMURAFENIB; CONTRIBUTES; DISCOVERY
AB Colorectal cancer (CRC) patients with BRAF mutations develop resistance to BRAF inhibitors at a very early stage. Understanding the molecular mechanisms involved in BRAF inhibitor resistance is critical for the devel-opment of novel therapeutic opportunities for this subtype of CRC patients. CRC cells bearing BRAF mutations are mostly sensitive to the abrogation of Mitogen-Activated Protein Kinase Kinase 3 (MKK3), a specific activator of p38MAPKs signaling, suggesting that BRAF alterations might addict CRC cells to the MKK3/p38MAPK signaling. Interestingly, publicly available gene expression profiling data show significantly higher MKK3 transcript levels in CRC lines with acquired resistance to BRAF inhibitors. Herein, we investigated the roles of MKK3 in the response to BRAF targeting (dabrafenib) with COLO205 and HT29 BRAFV600E CRC lines and derived dabrafenib-resistant (DABR) sublines. Dabrafenib treatments reduce MKK3 activation by inducing autophagy in parental but not DABR cells. The MKK3 knockdown induces cell death in DABR cells, whereas ectopic MKK3 expression reduces dabrafenib sensitivity in parental cells. Mechanistically, activated MKK3 interacts and co -localizes with c-Myc oncoprotein (MYC), sustaining MYC protein stability and thus preventing the dabrafenib induced effects in CRC DABR cells both in vitro and in vivo. Overall, we identify a novel molecular mechanism beyond the dabrafenib resistance, shedding light on an uncovered vulnerability for the development of novel therapeutic opportunities in BRAFV600E CRC.
C1 [Pranteda, Angelina; Piastra, Valentina; Lo Sardo, Federica; Blandino, Giovanni; Bossi, Gianluca] IRCCS Regina Elena Natl Canc Inst, Dept Diagnost Res & Technol Innovat, Translat Oncol Res Unit, Via Elio Chianesi 53, I-00144 Rome, Italy.
   [Pranteda, Angelina; Piastra, Valentina] Univ Roma TRE, Dept Sci, Viale G Marconi,446 I, I-00146 Rome, Italy.
   [Serra, Martina; Bernardini, Roberta] Univ Roma Tor Vergata, Interdept Ctr Comparat Med Alternat Tech & Aquacul, Via Montpellier 1, I-00133 Rome, Italy.
   [Bernardini, Roberta] Univ Roma La Sapienza, Ctr Res & Serv Preclin Experimentat & Anim Welf SP, Piazzale Aldo Moro 5, I-00185 Rome, Italy.
   [Carpano, Silvia] IRCCS Regina Elena Natl Canc Inst, Div Med Oncol 2, Via Elio Chianesi 53, I-00144 Rome, Italy.
   [Diodoro, Maria Grazia] IRCCS Regina Elena Natl Canc Inst, Dept Pathol, Via Elio Chianesi 53, I-00144 Rome, Italy.
   [Bartolazzi, Armando] St Andrea Univ Hosp, Pathol Res Lab, Via Grottarossa 1035, I-00189 Rome, Italy.
   [Milella, Michele] Verona Univ & Hosp Trust, Azienda Osped Univ Integrata AOUI Verona, UOC Oncol, Piazzale Aristide Stefani 1, I-37126 Verona, Italy.
C3 Roma Tre University; Italfarmaco; University of Rome Tor Vergata;
   Sapienza University Rome; Sapienza University Rome; Azienda Ospedaliera
   Sant'Andrea; University of Verona; Azienda Ospedaliera Universitaria
   Integrata Verona
RP Bossi, G (corresponding author), IRCCS Regina Elena Natl Canc Inst, Dept Diagnost Res & Technol Innovat, Translat Oncol Res Unit, Via Elio Chianesi 53, I-00144 Rome, Italy.
EM gianluca.bossi@ifo.it
RI Bernardini, Roberta/AAC-1301-2019; Bossi, Gianluca/B-9394-2017; Milella,
   Michele/ABH-8606-2020; Blandino, Giovanni/LLM-1397-2024; Bossi,
   Gianluca/G-8375-2016; Lo Sardo, Federica/AAC-1757-2019; Piastra,
   Valentina/AAC-2023-2022
OI Bossi, Gianluca/0000-0002-2947-1063; Lo Sardo,
   Federica/0000-0002-2912-079X; Piastra, Valentina/0000-0002-9427-2239;
   Serra, Martina/0000-0002-3932-9861
FU Italian Ministry of Health [18449, RF-2021-12372851]; Italian Ministry
   of Health [18449, RF-2021-12372851]
FX This work was financially supported by following grants to G. Bossi:
   Italian Association for Cancer Research (AIRC) (ID. 18449 project) ;
   Lega Italiana per la Lotta contro i Tumori (LILT) 5 x 1000 year 2019;
   Ricerca Corrente and Ricerca Finalizzata (RF-2021-12372851) granted by
   the Italian Ministry of Health.
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NR 43
TC 2
Z9 2
U1 2
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 NOV
PY 2023
VL 167
AR 115480
DI 10.1016/j.biopha.2023.115480
EA SEP 2023
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA T8MV2
UT WOS:001080478500001
PM 37713993
OA gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Abdulrazaq, JA
   Zakari, MA
   Ibrahim, Y
   Ahmad, H
AF Abdulrazaq, Jimoh Ajanaku
   Zakari, Mohammed Aminu
   Ibrahim, Yusuf
   Ahmad, Hamza
TI Expression of cyclooxygenase-2 (COX-2) in colorectal carcinoma in an
   indigenous African population of Kano, Nigeria
SO ECANCERMEDICALSCIENCE
LA English
DT Article
DE COX-2 expression; colorectal cancer; indigenous Africa population; Kano;
   Nigeria
ID BETA-CATENIN; EARLY-ONSET; PROGNOSTIC-SIGNIFICANCE; ASPIRIN USE;
   LOW-PREVALENCE; RECTAL-CANCER; RISK; GENE; OVEREXPRESSION; METASTASIS
AB Background: cyclooxygenases-2 (COX-2) over-expression has been noticed in colorectal cancers (CRCs) with adverse outcomes, serving as a potential marker for prognosis, targeted therapy and as a window in CRC prevention. Unfortunately, there are scarce data regarding COX-2 expression in CRC in Africa where CRC incidence is on the increase with younger age affectation and unfavourable outcomes. Aims: This retrospective study aims to determine the proportion of CRCs that over- express COX-2 and document any relationship between COX-2 over-expression with clinicopathological features such as histologic subtype, tumour grade, age and sex. Methods: All the 139 CRCs that were histologically diagnosed at Aminu Kano Teaching Hospital over a 5-year period were included, but only 124 Formalin-fixed paraffin embedded tissue blocks were sectioned and stained with COX-2 antibody. COX-2 expression was scored for distribution (no cells = 0, 1%-10% = 1, 11%-50% = 2, 51%- 80% = 3, 81%-100% = 4) and intensity (no stain = 0; weak = 1; moderate = 2, strong = 3). The immunoreactive score (IRS) is a product of intensity (I) and distribution (D) as: 9-12 strongly +, 5-8 moderately +, 1-4 weakly + and 0 negative. Over-expression of COX-2 is an IRS of 5-12. Outcomes were statistically evaluated with clinicopathological data. Results: The CRCs occurred more commonly in males (M: F, 2:1), in the middle age group (mostly between 30 and 59 years), and 51.1% of cases occurred before 50 years and peaked in the 6th decade. Over-expression of COX-2 was observed in 46.8% (58/124) and was strongly associated with adenocarcinoma (ADC) not otherwise specified (NOS) (moderately and poorly differentiated tumours) but not with age or sex. Conclusion: The over-expression of COX-2 was significantly associated with ADC NOS (moderately and poorly differentiated tumours), indicating that it may influence the outcome of CRCs with possible variation in tumour subtype.
C1 [Abdulrazaq, Jimoh Ajanaku] Fed Univ Hlth Sci Azare, Dept Pathol, Azare 751101, Bauchi, Nigeria.
   [Zakari, Mohammed Aminu; Ibrahim, Yusuf; Ahmad, Hamza] Aminu Kano Teaching Hosp, Dept Pathol, Kano 700101, Nigeria.
RP Abdulrazaq, JA (corresponding author), Fed Univ Hlth Sci Azare, Dept Pathol, Azare 751101, Bauchi, Nigeria.
EM jimmeeq@gmail.com
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NR 81
TC 0
Z9 0
U1 0
U2 0
PU eCancer Global Foundation
PI Bristol
PA 13 King Square Avenue, Bristol, UNITED KINGDOM
SN 1754-6605
J9 ECANCERMEDICALSCIENC
JI eCancerMedicalScience
PD DEC 6
PY 2024
VL 18
AR 1816
DI 10.3332/ecancer.2024.1816
PG 16
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA O7B7N
UT WOS:001372642200001
OA gold
DA 2025-01-04
ER

PT J
AU Triki, M
   Kallel, R
   Feki, J
   Mellouli, M
   Charfi, S
   Ayadi, L
   Boudawara, T
AF Triki, Meriam
   Kallel, Rim
   Feki, Jihene
   Mellouli, Manel
   Charfi, Slim
   Ayadi, Lobna
   Boudawara, Tahya
TI Prognostic significance of E-cadherin and Cox 2 expression in Tunisian
   patients with colorectal mutinous adenocarcinoma
SO ANNALS OF DIAGNOSTIC PATHOLOGY
LA English
DT Article
DE Mucinous colorectal carcinoma; E-Cadherin; Cox-2; Prognosis; Survival
ID MUCINOUS ADENOCARCINOMA; CLINICOPATHOLOGICAL FEATURES; BETA-CATENIN;
   CYCLOOXYGENASE-2; CARCINOMA; COLON; CANCER; SURVIVAL; INHIBITORS;
   PROTEIN
AB Introduction: Mucinous colorectal carcinoma (MC) is a rare subtype of colorectal adenocarcinoma known to be associated with bad prognosis. Lately, research has turned to identify new prognostic markers allowing the use of targeted therapy. The aim of our study is to evaluate the prognostic impact of E-cadherin and Cox-2expression in MC.
   Materials and method: A total of 40 formalin-fixed, paraffin-embedded MC specimens were collected within a period of 13 years and were studied for the expression of the two proteins. We used SPSS 22 software to study associations with clinicopathological parameters and overall survival (OS).
   Results: A reduced or absent E-cadherin expression was noted in 52.5% of cases. It was associated with distant metastases (p = 0.049) and venous invasion (p = 0.049). Cox-2 was overexpressed in 17.5% of cases. It was associated with negative lymph node status (p = 0.020) and with early stage tumor (p = 0.020). A significant association between the two proteins was also noted (p = 0.04). No significant association with OS was found; However, there was an improvement in the survival of patients overexpressing Cox-2 (p = 0.16).
   Conclusion: Our findings link the loss of E-cadherin expression with spread and aggressiveness in MC and Cox-2 overexpression with better prognosis and survival. Because MC has a distinct genetic pathway we encourage the analysis of MSI and Cox-2 expression in all MC. Cox-2 inhibitors may not be effective chemopreventative agents in the setting of defective DNA mismatch repair. More molecular studies are needed to better understand the role of these markers and their prognostic significance in MC.
C1 [Triki, Meriam; Kallel, Rim; Mellouli, Manel; Charfi, Slim; Ayadi, Lobna; Boudawara, Tahya] Habib Bourguiba Univ Hosp, Dept Pathol, El Ain Rd Km 0-5, Sfax 3029, Tunisia.
   [Feki, Jihene] Habib Bourguiba Univ Hosp, Dept Oncol, Sfax, Tunisia.
C3 Universite de Sfax; Hopital Habib Bourguiba; Universite de Sfax; Hopital
   Habib Bourguiba
RP Triki, M (corresponding author), Habib Bourguiba Univ Hosp, Dept Pathol, El Ain Rd Km 0-5, Sfax 3029, Tunisia.
EM meriamtriki@yahoo.fr
RI ; Mellouli, Manel/Q-2425-2018
OI Triki, Meriam/0000-0003-1961-7601; Mellouli, Manel/0000-0002-8892-6734
CR Alshenawy HA, 2013, ANN DIAGN PATHOL, V17, P476, DOI 10.1016/j.anndiagpath.2013.05.007
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NR 32
TC 3
Z9 3
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1092-9134
EI 1532-8198
J9 ANN DIAGN PATHOL
JI Ann. Diagn. Pathol.
PD DEC
PY 2020
VL 49
AR 151624
DI 10.1016/j.anndiagpath.2020.151624
PG 6
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA PI8BI
UT WOS:000601309200012
PM 32919337
DA 2025-01-04
ER

PT J
AU Jang, BG
   Kim, HS
   Chang, WY
   Bae, JM
   Oh, HJ
   Wen, X
   Jeong, S
   Cho, NY
   Kim, WH
   Kang, GH
AF Jang, Bo Gun
   Kim, Hye Sung
   Chang, Weon Young
   Bae, Jeong Mo
   Oh, Hyeon Jeong
   Wen, Xianyu
   Jeong, Seorin
   Cho, Nam Yun
   Kim, Woo Ho
   Kang, Gyeong Hoon
TI Prognostic significance of strornal GREM1 expression in colorectal
   cancer
SO HUMAN PATHOLOGY
LA English
DT Article
DE GnMl1; Cancer-associated fibroblasts; Colorectal cancers; In situ
   hybridization; Prognosis
ID ISLAND METHYLATOR PHENOTYPE; STEM-CELL NICHE; TUMOR MICROENVIRONMENT;
   FIBROBLASTS; PROGRESSION; ANTAGONISTS; PATTERNS; PROTEASE; MARKERS;
   STROMA
AB Cancer-associated fibroblasts are the dominant cell population in the cancer stroma. Gremlin 1 (GREM1), an antagonist of the bone morphogenetic protein pathway, is expressed by cancer-associated fibroblasts in a variety of human cancers. However, its biological significance for cancer patients is largely unknown. We applied RNA in situ hybridization to evaluate the prognostic value of stromal GREM1 expression in a large cohort of 670 colorectal cancers (CRCs). Overall, GREM1 expression in CRCs was lower than that of the matched normal mucosa, and GREM1 expression had a strong positive correlation with BMI1 and inverse correlations with EPHB2 and OLFM4. RNA in situ hybridization localized the GREM expression to smooth muscle cells of the muscularis mucosa and fibroblasts around crypt bases and in the submucosal space of a normal colon. In various colon polyps, epithelial GREM1 expression was exclusively observed in traditional serrated adenomas. In total, 44% of CRCs were positive for stromal GREM1, which was associated with decreased lymphovascular invasion, a lower cancer stage, and nuclear beta-catenin staining. Stromal GREM1 was significantly associated with improved recurrence-free and overall survival, although it was not found to be an independent prognostic marker in multivariate analyses. In addition, for locally advanced stage II and III CRC, it was associated with better, stage-independent clinical outcomes. In summary, CRCs are frequently accompanied by GERM1-expressing fibroblasts, which are closely associated with low lymphovascular invasion and a better prognosis, suggesting stromal GREM1 as a potential biomarker and possible candidate for targeted therapy in the treatment of CRCs. (C) 2017 Elsevier Inc. All rights reserved.
C1 [Jang, Bo Gun; Kim, Hye Sung] Jeju Natl Univ, Sch Med, Dept Pathol, Jeju 690767, South Korea.
   [Jang, Bo Gun; Kim, Hye Sung; Chang, Weon Young] Jeju Natl Univ Hosp, Jeju 690767, South Korea.
   [Chang, Weon Young] Jeju Natl Univ, Sch Med, Dept Gen Surg, Jeju 690767, South Korea.
   [Bae, Jeong Mo; Oh, Hyeon Jeong; Wen, Xianyu; Kim, Woo Ho; Kang, Gyeong Hoon] Seoul Natl Univ, Coll Med, Dept Pathol, 103 Daehak Ro, Seoul 110799, South Korea.
   [Bae, Jeong Mo; Wen, Xianyu; Jeong, Seorin; Cho, Nam Yun; Kang, Gyeong Hoon] Seoul Natl Univ, Coll Med, Canc Res Inst, Lab Epigenet, Seoul 110799, South Korea.
C3 Jeju National University; Jeju National University; Jeju National
   University; Seoul National University (SNU); Seoul National University
   (SNU)
RP Kang, GH (corresponding author), Seoul Natl Univ, Coll Med, Dept Pathol, 103 Daehak Ro, Seoul 110799, South Korea.
EM ghkang@snu.ac.kr
RI Jang, Bo-Gun/ADZ-5252-2022; Kang, Gyeong Hoon/F-1051-2010
OI Kang, Gyeong Hoon/0000-0003-2380-6675
FU SNUH Research Fund [0420150260 [2015-117]]; NRF - Korean Ministry of
   Science, ICT and Future Planning [2011-0030049, 2016M3A9B6026921,
   2009-0093820]; Priority Research Centers Program through the NRF; Korea
   Health Technology R&D Project through the Korea Health Industry
   Development Institute; Korean Ministry of Health and Welfare
   [11114C1277]; Jeju National University Hospital
FX This work was supported by a grant from the SNUH Research Fund
   (0420150260 [2015-117]); an NRF grant funded by the Korean Ministry of
   Science, ICT and Future Planning (2011-0030049; 2016M3A9B6026921); a
   grant (2009-0093820) from the Priority Research Centers Program through
   the NRF; a grant from the Korea Health Technology R&D Project through
   the Korea Health Industry Development Institute funded by the Korean
   Ministry of Health and Welfare (11114C1277); and a research grant of the
   Jeju National University Hospital in 2015.
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NR 30
TC 21
Z9 21
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 0046-8177
EI 1532-8392
J9 HUM PATHOL
JI Hum. Pathol.
PD APR
PY 2017
VL 62
BP 56
EP 65
DI 10.1016/j.humpath.2016.12.018
PG 10
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA ET4DZ
UT WOS:000400230800008
PM 28041973
DA 2025-01-04
ER

PT J
AU Bai, YB
   Li, TZ
   Wang, QS
   You, WQ
   Yang, HC
   Xu, XT
   Li, ZY
   Zhang, Y
   Yan, CS
   Yang, L
   Qiu, JQ
   Liu, YH
   Chen, SY
   Wang, DF
   Huang, BL
   Liu, KX
   Song, BL
   Wang, ZZ
   Li, K
   Liu, X
   Wang, GC
   Yang, WW
   Chen, JF
   Hao, P
   Zhang, ZM
   Wang, ZG
   Zhu, ZJ
   Xu, CQ
AF Bai, Yibing
   Li, Tongzhou
   Wang, Qinshu
   You, Weiqiang
   Yang, Haochen
   Xu, Xintian
   Li, Ziyi
   Zhang, Yu
   Yan, Chengsong
   Yang, Lei
   Qiu, Jiaqian
   Liu, Yuanhua
   Chen, Shiyang
   Wang, Dongfang
   Huang, Binlu
   Liu, Kexin
   Song, Bao- Liang
   Wang, Zhuozhong
   Li, Kang
   Liu, Xin
   Wang, Guangchuan
   Yang, Weiwei
   Chen, Jianfeng
   Hao, Pei
   Zhang, Zemin
   Wang, Zhigang
   Zhu, Zheng-Jiang
   Xu, Chenqi
TI Shaping immune landscape of colorectal cancer by cholesterol metabolites
SO EMBO MOLECULAR MEDICINE
LA English
DT Article
DE Colorectal Cancer with Microsatellite Stability; Asynchronous
   Cholesterol Biosynthesis; Distal Cholesterol Precursors; Th17; Cyp51
   Targeted Therapy
ID CELLS; IDENTIFICATION; DIFFERENTIATION; DESMOSTEROL; MECHANISMS;
   CHECKPOINT; IMPACT; TH17
AB Cancer immunotherapies have achieved unprecedented success in clinic, but they remain largely ineffective in some major types of cancer, such as colorectal cancer with microsatellite stability (MSS CRC). It is therefore important to study tumor microenvironment of resistant cancers for developing new intervention strategies. In this study, we identify a metabolic cue that determines the unique immune landscape of MSS CRC. Through secretion of distal cholesterol precursors, which directly activate ROR gamma t, MSS CRC cells can polarize T cells toward Th17 cells that have well-characterized pro-tumor functions in colorectal cancer. Analysis of large human cancer cohorts revealed an asynchronous pattern of the cholesterol biosynthesis in MSS CRC, which is responsible for the abnormal accumulation of distal cholesterol precursors. Inhibiting the cholesterol biosynthesis enzyme Cyp51, by pharmacological or genetic interventions, reduced the levels of intratumoral distal cholesterol precursors and suppressed tumor progression through a Th17-modulation mechanism in preclinical MSS CRC models. Our study therefore reveals a novel mechanism of cancer-immune interaction and an intervention strategy for the difficult-to-treat MSS CRC.
   A metabolic cue shaping the unique immune landscape of colorectal cancer with microsatellite stability (MSS CRC) is identified. Tumor-secreted distal cholesterol precursors (DCPs) polarize type 17 T cells, thereby inducing an immunosuppressive microenvironment to favor tumor progression.MSS CRC cells secreted DCPs to polarize Th17 cells. The accumulation of DCPs was induced by an asynchronous pattern of the cholesterol biosynthesis in MSS CRC cells. Inhibiting the cholesterol biosynthesis enzyme Cyp51 reshaped tumor immune microenvironment and reduced MSS CRC progression.
   A metabolic cue shaping the unique immune landscape of colorectal cancer with microsatellite stability (MSS CRC) is identified. Tumor-secreted distal cholesterol precursors (DCPs) polarize type 17 T cells, thereby inducing an immunosuppressive microenvironment to favor tumor progression.
C1 [Bai, Yibing; Yang, Haochen; Zhang, Yu; Yan, Chengsong; Yang, Lei; Chen, Shiyang; Huang, Binlu; Liu, Kexin; Liu, Xin; Wang, Guangchuan; Yang, Weiwei; Chen, Jianfeng; Xu, Chenqi] Chinese Acad Sci, Univ Chinese Acad Sci, Shanghai Inst Biochem & Cell Biol, CAS Ctr Excellence Mol Cell Sci, Shanghai, Peoples R China.
   [Li, Tongzhou; Qiu, Jiaqian; Zhu, Zheng-Jiang] Chinese Acad Sci, Univ Chinese Acad Sci, Shanghai Inst Organ Chem, Interdisciplinary Res Ctr Biol & Chem, Shanghai, Peoples R China.
   [Wang, Qinshu; Xu, Chenqi] ShanghaiTech Univ, Sch Life Sci & Technol, Shanghai, Peoples R China.
   [You, Weiqiang; Wang, Zhigang] Shanghai Jiao Tong Univ Affiliated Peoples Hosp 6, Dept Gen Surg, Shanghai, Peoples R China.
   [Xu, Xintian; Liu, Yuanhua; Hao, Pei] Chinese Acad Sci, Inst Pasteur Shanghai, Ctr Biosafety Mega Sci, CAS Key Lab Mol Virol & Immunol, Shanghai, Peoples R China.
   [Li, Ziyi; Wang, Dongfang; Zhang, Zemin] Peking Univ, Beijing Adv Innovat Ctr Genom, BIOPIC, Beijing, Peoples R China.
   [Li, Ziyi; Wang, Dongfang; Zhang, Zemin] Peking Univ, Sch Life Sci, Beijing, Peoples R China.
   [Song, Bao- Liang] Wuhan Univ, Coll Life Sci, Hubei Key Lab Cell Homeostasis, Wuhan, Peoples R China.
   [Wang, Zhuozhong] Harbin Med Univ, Affiliated Hosp 2, Harbin, Peoples R China.
   [Li, Kang] Harbin Med Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Harbin, Peoples R China.
C3 Chinese Academy of Sciences; Center for Excellence in Molecular Cell
   Science, CAS; University of Chinese Academy of Sciences, CAS; Chinese
   Academy of Sciences; Shanghai Institute of Organic Chemistry, CAS;
   University of Chinese Academy of Sciences, CAS; ShanghaiTech University;
   Shanghai Jiao Tong University; Chinese Academy of Sciences; Shanghai
   Institute of Immunity and Infection, CAS; Pasteur Network; Peking
   University; Peking University; Wuhan University; Harbin Medical
   University; Harbin Medical University
RP Xu, CQ (corresponding author), Chinese Acad Sci, Univ Chinese Acad Sci, Shanghai Inst Biochem & Cell Biol, CAS Ctr Excellence Mol Cell Sci, Shanghai, Peoples R China.; Zhu, ZJ (corresponding author), Chinese Acad Sci, Univ Chinese Acad Sci, Shanghai Inst Organ Chem, Interdisciplinary Res Ctr Biol & Chem, Shanghai, Peoples R China.; Xu, CQ (corresponding author), ShanghaiTech Univ, Sch Life Sci & Technol, Shanghai, Peoples R China.; Wang, ZG (corresponding author), Shanghai Jiao Tong Univ Affiliated Peoples Hosp 6, Dept Gen Surg, Shanghai, Peoples R China.
EM wangzhigang72@sjtu.edu.cn; jiangzhu@sioc.ac.cn; cqxu@sibcb.ac.cn
RI Chen, Shiyang/HPD-6687-2023; xu, xintian/AAB-3809-2021; Wang,
   Dongfang/IWM-5676-2023; chang, hao/JNF-0325-2023; Li,
   Ruoyan/GRX-9551-2022; Zhu, Zheng-Jiang/C-5306-2011; bai,
   yibing/KHU-1907-2024; chen, jianfeng/ITU-6686-2023
OI Bai, Yibing/0000-0002-2944-5367; Yang, Haochen/0000-0003-4273-5411
FU National Key R&D Program of China [2018YFA0800700]; CAS grant
   [YSBR-014]; NSFC [31830026, 92057201, 92157301, 92169212, 91857000];
   Shanghai Pilot Program for Basic Research - Chinese Academy of Sciences,
   Shanghai Branch [JCYJ-SHFY-2022-009]; STSMC Fundamental Research Program
   [21JC1405900]; China Postdoctoral Science Foundation [2020M671260]
FX The authors sincerely thank Youcun Qian for ROR gamma t-KO mice and
   Haopeng Wang and Xinyu Ke for critical reading of the manuscript. The
   following core facilities enabled our study: CEMCS Core Facility of
   Molecular Biology, Core Facility for Cell Biology, Chemical Biology Core
   Facility, Animal Core Facility. CX is funded by National Key R&D Program
   of China (2018YFA0800700), CAS grant (YSBR-014), NSFC grants (31830026,
   92057201, 92157301), Shanghai Pilot Program for Basic Research - Chinese
   Academy of Sciences, Shanghai Branch (JCYJ-SHFY-2022-009) and STSMC
   Fundamental Research Program (21JC1405900). B-LS is funded by the NSFC
   grant 91857000. YB is funded by National Key R&D Program of China
   (2022YFC2505004), CAS grant (Excellent Research Associate Program
   2020000001), China Postdoctoral Science Foundation (2020M671260), and
   NSFC grant (92169212).
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NR 57
TC 2
Z9 2
U1 9
U2 18
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1757-4676
EI 1757-4684
J9 EMBO MOL MED
JI EMBO Mol. Med.
PD FEB 15
PY 2024
VL 16
IS 2
BP 334
EP 360
DI 10.1038/s44321-023-00015-9
PG 27
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA QJ2B8
UT WOS:001220431600004
PM 38177537
OA gold
DA 2025-01-04
ER

PT J
AU Liu, WJ
   Luo, XT
   Zhang, ZL
   Chen, YP
   Dai, YL
   Deng, JZ
   Yang, CY
   Liu, H
AF Liu, Wenjun
   Luo, Xitu
   Zhang, Zilang
   Chen, Yepeng
   Dai, Yongliang
   Deng, Jianzhong
   Yang, Chengyu
   Liu, Hao
TI Construction of an immune predictive model and identification of TRIP6
   as a prognostic marker and therapeutic target of CRC by integration of
   single-cell and bulk RNA-seq data
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE Colorectal cancer; Single-cell RNA sequencing; Prognosis; Immune
   landscape; TRIP6
ID COLORECTAL-CANCER; PROLIFERATION; HETEROGENEITY; METASTASIS; SURVIVAL;
   SUBTYPES; PROTEIN
AB BackgroundInvestigations elucidating the complex immunological mechanisms involved in colorectal cancer (CRC) and accurately predicting patient outcomes via bulk RNA-Seq analysis have been notably limited. This study aimed to identify the immune status of CRC patients, construct a prognostic model, and identify prognostic signatures via bulk RNA sequencing (RNA-seq) and single-cell RNA-seq (scRNA-seq).MethodsThe scRNA-seq data of CRC were downloaded from Gene Expression Omnibus (GEO). The UCSC Xena database was used to obtain bulk RNA-seq data. Differentially expressed gene (DEG), functional enrichment, and random forest analyses were conducted in order to identify core genes associated with colorectal cancer (CRC) that were relevant to prognosis. A molecular immune prediction model was developed using logistic regression after screening features using the least absolute shrinkage and selection operator (LASSO). The differences in immune cell infiltration, mutation, chemotherapeutic drug sensitivity, cellular senescence, and communication between patients who were at high and low risk of CRC according to the predictive model were investigated. The prognostic genes that were closely associated with CRC were identified by random survival forest (RSF) analysis. The expression levels and clinical significance of the hub genes were analyzed in vitro. The LoVo cell line was employed to ascertain the biological role of thyroid hormone receptor-interacting protein 6 (TRIP6).ResultsA total of seven main cell subtypes were identified by scRNA-seq analysis. A molecular immune predictive model was constructed based on the risk scores. The risk score was significantly associated with OS, stage, mutation burden, immune cell infiltration, response to immunotherapy, key pathways, and cell-cell communication. The functions of the six hub genes were determined and further utilized to establish a regulatory network. Our findings unequivocally confirmed that TRIP6 upregulation was verified in the CRC samples. After knocking down TRIP6, cell proliferation, migration, and invasion of LoVo cells were inhibited, and apoptosis was promoted.ConclusionsThe molecular predictive model reliably distinguished the immune status of CRC patients. We further revealed that TRIP6 may act as an oncogene in CRC, making it a promising candidate for targeted therapy and as a prognostic marker for CRC.
C1 [Liu, Wenjun; Luo, Xitu; Chen, Yepeng; Dai, Yongliang; Yang, Chengyu] Guangzhou Med Univ, Dept Gen Surg 1, Affiliated Hosp 3, Guangzhou 510150, Guangdong, Peoples R China.
   [Zhang, Zilang; Deng, Jianzhong] First Peoples Hosp Foshan, Dept Anorectal Surg, Foshan 528010, Guangdong, Peoples R China.
   [Liu, Hao] Southern Med Univ, Nanfang Hosp, Dept Gen Surg, Div Vasc & Intervent Radiol, Guangzhou 510000, Guangdong, Peoples R China.
C3 Guangzhou Medical University; Southern Medical University - China
RP Liu, H (corresponding author), Southern Med Univ, Nanfang Hosp, Dept Gen Surg, Div Vasc & Intervent Radiol, Guangzhou 510000, Guangdong, Peoples R China.
EM droctorliu24@163.com
RI LIU, Wenjun/F-1892-2010
OI liu, wenjun/0000-0003-4237-5604
FU Guangzhou Municipal Health Commission
FX We would like to thank Nature Research Editing Service
   (https://authorservices.springernature.com) for English language
   editing.
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NR 73
TC 0
Z9 0
U1 3
U2 7
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0340-7004
EI 1432-0851
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD MAR 2
PY 2024
VL 73
IS 4
AR 69
DI 10.1007/s00262-024-03658-w
PG 18
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA KU7Y5
UT WOS:001182555200004
PM 38430268
OA hybrid
DA 2025-01-04
ER

PT J
AU Zhu, GM
   Pei, LJ
   Xia, HW
   Tang, QL
   Bi, F
AF Zhu, Gongmin
   Pei, Lijiao
   Xia, Hongwei
   Tang, Qiulin
   Bi, Feng
TI Role of oncogenic KRAS in the prognosis, diagnosis and treatment of
   colorectal cancer
SO MOLECULAR CANCER
LA English
DT Review
DE Colorectal cancer; KRAS; G12C; Prognosis; Targeted therapy; Combination
   therapy
ID GROWTH-FACTOR RECEPTOR; TRANSFERASE INHIBITOR R115777; CONSENSUS
   MOLECULAR SUBTYPES; CETUXIMAB PLUS IRINOTECAN; ANTITUMOR-ACTIVITY; RAS
   MUTATIONS; COLON-CANCER; K-RAS; BRAF-MUTATION; STAGE-II
AB Colorectal cancer (CRC) is a heterogeneous disease at the cellular and molecular levels. Kirsten rat sarcoma (KRAS) is a commonly mutated oncogene in CRC, with mutations in approximately 40% of all CRC cases; its mutations result in constitutive activation of the KRAS protein, which acts as a molecular switch to persistently stimulate downstream signaling pathways, including cell proliferation and survival, thereby leading to tumorigenesis. Patients whose CRC harbors KRAS mutations have a dismal prognosis. Currently, KRAS mutation testing is a routine clinical practice before treating metastatic cases, and the approaches developed to detect KRAS mutations have exhibited favorable sensitivity and accuracy. Due to the presence of KRAS mutations, this group of CRC patients requires more precise therapies. However, KRAS was historically thought to be an undruggable target until the development of KRAS(G12C) allele-specific inhibitors. These promising inhibitors may provide novel strategies to treat KRAS-mutant CRC. Here, we provide an overview of the role of KRAS in the prognosis, diagnosis and treatment of CRC.
C1 [Zhu, Gongmin; Xia, Hongwei; Tang, Qiulin; Bi, Feng] Sichuan Univ, West China Hosp, Dept Abdominal Oncol, Canc Ctr, 37 Guoxue Lane, Chengdu 610041, Sichuan, Peoples R China.
   [Zhu, Gongmin; Xia, Hongwei; Tang, Qiulin; Bi, Feng] Sichuan Univ, West China Hosp, Lab Mol Targeted Therapy Oncol, 37 Guoxue Lane, Chengdu 610041, Sichuan, Peoples R China.
   [Pei, Lijiao] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University
RP Bi, F (corresponding author), Sichuan Univ, West China Hosp, Dept Abdominal Oncol, Canc Ctr, 37 Guoxue Lane, Chengdu 610041, Sichuan, Peoples R China.; Bi, F (corresponding author), Sichuan Univ, West China Hosp, Lab Mol Targeted Therapy Oncol, 37 Guoxue Lane, Chengdu 610041, Sichuan, Peoples R China.
EM bifeng@scu.edu.cn
RI Bi, Feng/J-7459-2015
FU Science and Technology Department of Sichuan Province [2019YJ0056];
   National Natural Science Foundation of China [82073314, 82073059,
   81621003, 81872020]; 1.3.5 Project for Disciplines of Excellence, West
   China Hospital, Sichuan University [ZYGD18005]
FX This study was supported by grants from Science and Technology
   Department of Sichuan Province (No. 2019YJ0056), the National Natural
   Science Foundation of China (No. 82073059), the National Natural Science
   Foundation of China (No. 81872020), 1.3.5 Project for Disciplines of
   Excellence, West China Hospital, Sichuan University (No. ZYGD18005), the
   National Natural Science Foundation of China (No. 81621003), and the
   National Natural Science Foundation of China (No. 82073314).
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NR 135
TC 179
Z9 196
U1 8
U2 47
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD NOV 6
PY 2021
VL 20
IS 1
AR 143
DI 10.1186/s12943-021-01441-4
PG 17
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA WS2OA
UT WOS:000715025400001
PM 34742312
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Julka, PK
   Arya, D
   Gupta, K
AF Julka, Pramod Kumar
   Arya, Deepika
   Gupta, Kush
TI Long-Term 5-Year Response to Pembrolizumab, Bevacizumab, and
   Capecitabine Regimen in a Metastatic Colon Cancer Patient with MSI-High
   and KRAS Mutation: Case Report
SO CASE REPORTS IN ONCOLOGY
LA English
DT Article
DE MSI-high; Pembrolizumab; Bevacizumab; Capecitabine; Metatstatic colon
   cancer
ID COLORECTAL-CANCER; PLUS IRINOTECAN; OPEN-LABEL; TRIAL; FLUOROURACIL;
   MULTICENTER
AB With an estimated 1.88 million new cases and 0.92 million deaths in 2020, colorectal cancer accounts for nearly one-tenth of all new cancer and cancer-related deaths worldwide. Nearly half of the patients of colorectal cancer are diagnosed with metastatic or inoperable disease with a very dismal 5-year survival rate. Chemotherapy, targeted therapy, and immunotherapy have been used to treat metastatic disease, either alone or in combination. We present a case of recurrent metastatic colon carcinoma with KRAS exon 2 mutation and high microsatellite instability that was treated with a combination regimen of bevacizumab, capecitabine oral chemotherapy, and pembrolizumab immunotherapy. At nearly 5 years of treatment, the patient is alive with good performance status and improved quality of life owing to a favorable response to the molecular profiling-based treatment approach.
C1 [Julka, Pramod Kumar; Arya, Deepika] Max Inst Canc Care, Dept Med Oncol, Delhi, India.
   [Gupta, Kush] Catalyst Clin Serv Pvt Ltd, Dept Clin Operat, Delhi, India.
RP Julka, PK (corresponding author), Max Inst Canc Care, Dept Med Oncol, Delhi, India.
EM pkjulka18@yahoo.co.in
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NR 23
TC 0
Z9 0
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 2023
VL 16
IS 1
BP 1020
EP 1027
DI 10.1159/000533760
PG 8
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA NW4F6
UT WOS:001203472100136
PM 37900837
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lee, HS
   Kim, WH
   Kwak, Y
   Koh, J
   Bae, JM
   Kim, KM
   Chang, MS
   Han, HS
   Kim, JM
   Kim, HW
   Chang, HK
   Choi, YH
   Park, JY
   Gu, MJ
   Lhee, MJ
   Kim, JY
   Kim, HS
   Cho, MY
AF Lee, Hye Seung
   Kim, Woo Ho
   Kwak, Yoonjin
   Koh, Jiwon
   Bae, Jeong Mo
   Kim, Kyoung-Mee
   Chang, Mee Soo
   Han, Hye Seung
   Kim, Joon Mee
   Kim, Hwal Woong
   Chang, Hee Kyung
   Choi, Young Hee
   Park, Ji Y.
   Gu, Mi Jin
   Lhee, Min Jin
   Kim, Jung Yeon
   Kim, Hee Sung
   Cho, Mee-Yon
CA Gastrointestinal Pathology Study G
   Mol Pathology Study Grp Korean Soc
TI Molecular Testing for Gastrointestinal Cancer
SO JOURNAL OF PATHOLOGY AND TRANSLATIONAL MEDICINE
LA English
DT Review
DE Gastric neoplasms; Colorectal neoplasms; Molecular diagnosis; Prognosis;
   Targeted therapy
ID EPSTEIN-BARR-VIRUS; TUMOR PIK3CA MUTATION; IN-SITU HYBRIDIZATION;
   ALLELE-SPECIFIC PCR; K-RAS MUTATIONS; COLORECTAL-CANCER; GASTRIC-CANCER;
   MICROSATELLITE INSTABILITY; KRAS MUTATIONS; CLINICAL-SIGNIFICANCE
AB With recent advances in molecular diagnostic methods and targeted cancer therapies, several molecular tests have been recommended for gastric cancer (GC) and colorectal cancer (CRC). Microsatellite instability analysis of gastrointestinal cancers is performed to screen for Lynch syndrome, predict favorable prognosis, and screen patients for immunotherapy. The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor has been approved in metastatic CRCs with wildtype RAS (KRAS and NRAS exon 2-4). A BRAF mutation is required for predicting poor prognosis. Additionally, amplification of human epidermal growth factor receptor 2 (HER2) and MET is also associated with resistance to EGFR inhibitor in metastatic CRC patients. The BRAF V600E mutation is found in sporadic microsatellite unstable CRCs, and thus is helpful for ruling out Lynch syndrome. In addition, the KRAS mutation is a prognostic biomarker and the PIK3CA mutation is a molecular biomarker predicting response to phosphoinositide 3-kinase/AKT/mammalian target of rapamycin inhibitors and response to aspirin therapy in CRC patients. Additionally, HER2 testing should be performed in all recurrent or metastatic GCs. If the results of HER2 immunohistochemistry are equivocal, HER2 silver or fluorescence in situ hybridization testing are essential for confirmative determination of HER2 status. Epstein-Barr virus-positive GCs have distinct characteristics, including heavy lymphoid stroma, hypermethylation phenotype, and high expression of immune modulators. Recent advances in next-generation sequencing technologies enable us to examine various genetic alterations using a single test. Pathologists play a crucial role in ensuring reliable molecular testing and they should also take an integral role between molecular laboratories and clinicians.
C1 [Lee, Hye Seung; Kwak, Yoonjin] Seoul Natl Univ, Bundang Hosp, Dept Pathol, Seongnam, South Korea.
   [Lee, Hye Seung; Kim, Woo Ho; Kwak, Yoonjin; Koh, Jiwon; Chang, Mee Soo] Seoul Natl Univ, Coll Med, Seoul, South Korea.
   [Bae, Jeong Mo; Chang, Mee Soo] SMG SNU Boramae Med Ctr, Seoul, South Korea.
   [Kim, Kyoung-Mee] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Seoul, South Korea.
   [Han, Hye Seung] Konkuk Univ, Sch Med, Seoul, South Korea.
   [Kim, Joon Mee] Inha Univ, Sch Med, Incheon, South Korea.
   [Kim, Hwal Woong] Seegene Med Fdn, Busan, South Korea.
   [Chang, Hee Kyung] Kosin Univ, Coll Med, Gospel Hosp, Busan, South Korea.
   [Choi, Young Hee] Hallym Univ, Dongtan Sacred Heart Hosp, Hwaseong, South Korea.
   [Park, Ji Y.] Catholic Univ Daegu, Sch Med, Daegu, South Korea.
   [Gu, Mi Jin] Yeungnam Univ, Coll Med, Daegu, South Korea.
   [Lhee, Min Jin] Seoul Red Cross Hosp, Seoul, South Korea.
   [Kim, Jung Yeon] Inje Univ, Sanggye Paik Hosp, Seoul, South Korea.
   [Kim, Hee Sung] Chung Ang Univ, Coll Med, Seoul, South Korea.
   [Cho, Mee-Yon] Yonsei Univ, Wonju Coll Med, Wonju Severance Christian Hosp, Wonju, South Korea.
C3 Seoul National University (SNU); Seoul National University (SNU); Seoul
   National University (SNU); Seoul National University Hospital;
   Sungkyunkwan University (SKKU); Samsung Medical Center; Konkuk
   University; Konkuk University Medical Center; Inha University; Hallym
   University; Catholic University of Daegu; Yeungnam University; Inje
   University; Chung Ang University; Chung Ang University Hospital; Yonsei
   University
RP Kim, WH (corresponding author), Seoul Natl Univ, Coll Med, Dept Pathol, 103 Daehak Ro, Seoul 03080, South Korea.
EM woohokim@snu.ac.kr
RI Kim, Kyung/N-6095-2017; Kwak, Yoonjin/HOI-0139-2023; Kim,
   Han/C-4709-2011; Lee, Hye Seung/G-6419-2011
OI Kim, Kyoung Min/0000-0001-8150-0266; Lee, Hye Seung/0000-0002-1667-7986
FU Korean Society of Pathologists
FX This research was supported by The Korean Society of Pathologists Grant
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NR 131
TC 59
Z9 59
U1 1
U2 9
PU KOREAN SOC PATHOLOGISTS
PI SEOUL
PA 1209 GWANGHWAMUN OFFICIA, 92 SAEMUNAN-RO, JONGNO-GU, SEOUL, 03186, SOUTH
   KOREA
SN 2383-7837
EI 2383-7845
J9 J PATHOL TRANSL MED
JI J. Pathol. Transl. Med.
PD MAR
PY 2017
VL 51
IS 2
BP 103
EP 121
DI 10.4132/jptm.2017.01.24
PG 19
WC Pathology
WE Emerging Sources Citation Index (ESCI)
SC Pathology
GA ER7WA
UT WOS:000399024300001
PM 28219002
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Tang, YF
   Zong, SQ
   Zeng, HL
   Ruan, XF
   Yao, LT
   Han, SS
   Hou, FG
AF Tang, Yufei
   Zong, Shaoqi
   Zeng, Hailun
   Ruan, Xiaofeng
   Yao, Liting
   Han, Susu
   Hou, Fenggang
TI MicroRNAs and angiogenesis: a new era for the management of colorectal
   cancer
SO CANCER CELL INTERNATIONAL
LA English
DT Review
DE MiRNA; Colorectal cancer; Angiogenesis
ID EPITHELIAL-MESENCHYMAL TRANSITION; INHIBITS TUMOR-GROWTH;
   CELL-PROLIFERATION; DOWN-REGULATION; COLON-CANCER; DISRUPTING
   ANGIOGENESIS; PROMOTES ANGIOGENESIS; TGF-BETA; METASTASIS; BEVACIZUMAB
AB MicroRNAs (miRNAs) are a class of small noncoding RNA molecules containing only 20-22 nucleotides. MiRNAs play a role in gene silencing and translation suppression by targeting and binding to mRNA. Proper control of miRNA expression is very important for maintaining a normal physiological environment because miRNAs can affect most cellular pathways, including cell cycle checkpoint, cell proliferation, and apoptosis pathways, and have a wide range of target genes. With these properties, miRNAs can modulate multiple signalling pathways involved in cancer development, such as cell proliferation, apoptosis, and migration pathways. MiRNAs that activate or inhibit the molecular pathway related to tumour angiogenesis are common topics of research. Angiogenesis promotes tumorigenesis and metastasis by providing oxygen and diffusible nutrients and releasing proangiogenic factors and is one of the hallmarks of tumour progression. CRC is one of the most common tumours, and metastasis has always been a difficult issue in its treatment. Although comprehensive treatments, such as surgery, radiotherapy, chemotherapy, and targeted therapy, have prolonged the survival of CRC patients, the overall response is not optimistic. Therefore, there is an urgent need to find new therapeutic targets to improve CRC treatment. In a series of recent reports, miRNAs have been shown to bidirectionally regulate angiogenesis in colorectal cancer. Many miRNAs can directly act on VEGF or inhibit angiogenesis through other pathways (HIF-1a, PI3K/AKT, etc.), while some miRNAs, specifically many exosomal miRNAs, are capable of promoting CRC angiogenesis. Understanding the mechanism of action of miRNAs in angiogenesis is of great significance for finding new targets for the treatment of tumour angiogenesis. Deciphering the exact role of specific miRNAs in angiogenesis is a challenge due to the high complexity of their actions. Here, we describe the latest advances in the understanding of miRNAs and their corresponding targets that play a role in CRC angiogenesis and discuss possible miRNA-based therapeutic strategies.
C1 [Tang, Yufei; Zong, Shaoqi; Zeng, Hailun; Ruan, Xiaofeng; Yao, Liting; Han, Susu; Hou, Fenggang] Shanghai Univ Tradit Chinese Med, Shanghai Municipal Hosp Tradit Chinese Med, Shanghai 200071, Peoples R China.
   [Zong, Shaoqi] Univ Tradit Chinese Med, Grad Sch Shanghai, Shanghai, Peoples R China.
C3 Shanghai University of Traditional Chinese Medicine
RP Hou, FG (corresponding author), Shanghai Univ Tradit Chinese Med, Shanghai Municipal Hosp Tradit Chinese Med, Shanghai 200071, Peoples R China.
EM fghou555@126.com
FU Scientific Research Foundation of Traditional Chinese Medicine of the
   Shanghai Health Bureau [ZY (2018-2020)-FWTX-6008]; Scientific Research
   Plan Project of the Shanghai Science and Technology Committee
   [16401970503]
FX This work was supported by the Scientific Research Foundation of
   Traditional Chinese Medicine of the Shanghai Health Bureau, ZY
   (2018-2020)-FWTX-6008 and the Scientific Research Plan Project of the
   Shanghai Science and Technology Committee (16401970503).
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NR 132
TC 32
Z9 33
U1 2
U2 17
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1475-2867
J9 CANCER CELL INT
JI Cancer Cell Int.
PD APR 17
PY 2021
VL 21
IS 1
AR 221
DI 10.1186/s12935-021-01920-0
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RP5CC
UT WOS:000641744900001
PM 33865381
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Walker-Samuel, S
   Roberts, TA
   Ramasawmy, R
   Burrell, JS
   Johnson, SP
   Siow, BM
   Richardson, S
   Calves, MRGC
   Pendse, D
   Robinson, SP
   Pedley, RB
   Lythgoe, MF
AF Walker-Samuel, Simon
   Roberts, Thomas A.
   Ramasawmy, Rajiv
   Burrell, Jake S.
   Johnson, Sean Peter
   Siow, Bernard M.
   Richardson, Simon
   Calves, Miguel R. Gon Comma
   Pendse, Douglas
   Robinson, Simon P.
   Pedley, R. Barbara
   Lythgoe, Mark F.
TI Investigating Low-Velocity Fluid Flow in Tumors with Convection-MRI
SO CANCER RESEARCH
LA English
DT Article
ID LYMPH-NODE METASTASIS; ALTERNATING INVERSION-RECOVERY; BLOOD-FLOW; SOLID
   TUMORS; INTERSTITIAL PRESSURE; BREAST-CANCER; PERFUSION; TRANSPORT;
   MICROENVIRONMENT; MACROMOLECULES
AB Several distinct fluid flow phenomena occur in solid tumors, including intravascular blood flow and interstitial convection. Interstitial fluid pressure is often raised in solid tumors, which can limit drug delivery. To probe low-velocity flow in tumors resulting from raised interstitial fluid pressure, we developed a novel MRI technique named convection-MRI, which uses a phase-contrast acquisition with a dual-inversion vascular nulling preparation to separate intra-and extravascular flow. Here, we report the results of experiments in flow phantoms, numerical simulations, and tumor xenograft models to investigate the technical feasibility of convec-tion-MRI. We observed a significant correlation between estimates of effective fluid pressure fromconvection-MRI with gold-standard, invasive measurements of interstitial fluid pressure in mouse models of human colorectal carcinoma. Our results show how convection-MRI can provide insights into the growth and responsiveness to vascular-targeting therapy in colorectal cancers. Significance: A noninvasive method for measuring lowvelocity fluid flow caused by raised fluid pressure can be used to assess changes caused by therapy. (C) 2018 AACR.
C1 [Walker-Samuel, Simon; Roberts, Thomas A.; Ramasawmy, Rajiv; Siow, Bernard M.; Richardson, Simon; Calves, Miguel R. Gon Comma; Lythgoe, Mark F.] UCL Ctr Adv Biomed Imaging, Div Med, London, England.
   [Burrell, Jake S.; Robinson, Simon P.] Inst Canc Res, Div Radiotherapy & Imaging, Sutton, Surrey, England.
   [Johnson, Sean Peter; Pedley, R. Barbara] UCL Canc Inst, London, England.
   [Pendse, Douglas] Univ Coll Hosp, London, England.
C3 University of London; University College London; University of London;
   Institute of Cancer Research - UK; University of London; University
   College London; University of London; University College London
RP Walker-Samuel, S (corresponding author), UCL, Ctr Adv Biomed Imaging, Lower Ground Floor,Paul OGorman Bldg,72 Huntley, London WC1 6DD, England.
EM simon.walkersamuel@ucl.ac.uk
RI Pendse, Doug/L-5354-2019; Siow, Bernard/ABC-4414-2020
OI Roberts, Tom/0000-0003-0385-1057; Robinson, Simon/0000-0003-4101-7274;
   Pendse, Douglas/0000-0002-6326-4658; Siow, Bernard/0000-0002-8687-8783
FU Kings College London; UCL CR-UK; EPSRC Comprehensive Cancer Imaging
   Centre; MRC; Department of Health (England) [C1519/A10331];
   BBSRC/AstraZeneca Industrial Partnership Studentship [BB/E528979/1]; UK
   Regenerative Medicine Platform Safety Hub [MRC: MR/K026739/1]; Eli Lilly
   and Company; EPSRC [EP/N034864/1]; Wellcome Trust [WT100247MA,
   091763/Z/10/Z]; Wellcome Trust [091763/Z/10/Z] Funding Source: Wellcome
   Trust; EPSRC [EP/N034864/1] Funding Source: UKRI; MRC [G1001497,
   MR/K026739/1] Funding Source: UKRI
FX S. Walker-Samuel, R.B. Pedley, M.F. Lythgoe, and S.P. Robinson
   acknowledge the support received for the Kings College London and UCL
   CR-UK and EPSRC Comprehensive Cancer Imaging Centre, in association with
   the MRC and Department of Health (England; C1519/A10331). M.F. Lythgoe
   was supported by BBSRC/AstraZeneca Industrial Partnership Studentship
   (BB/E528979/1), the UK Regenerative Medicine Platform Safety Hub (MRC:
   MR/K026739/1), Eli Lilly and Company, and the EPSRC (EP/N034864/1). S.
   Walker-Samuel is supported by a Wellcome Trust Senior Fellowship
   (WT100247MA). S.P. Robinson was supported by the Wellcome Trust
   (091763/Z/10/Z). We thank OXiGENE for supplying CA4P.
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NR 59
TC 30
Z9 35
U1 2
U2 16
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 APR 1
PY 2018
VL 78
IS 7
BP 1859
EP 1872
DI 10.1158/0008-5472.CAN-17-1546
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GB4CU
UT WOS:000429008900022
PM 29317434
OA Green Submitted, Bronze, Green Accepted, Green Published
DA 2025-01-04
ER

PT J
AU Tummala, S
   Gowthamarajan, K
   Kumar, MNS
   Wadhwani, A
AF Tummala, Shashank
   Gowthamarajan, K.
   Kumar, M. N. Satish
   Wadhwani, Ashish
TI Oxaliplatin immuno hybrid nanoparticles for active targeting: an
   approach for enhanced apoptotic activity and drug delivery to colorectal
   tumors
SO DRUG DELIVERY
LA English
DT Article
DE Colorectal cancer; immuno nanoparticles; oxaliplatin; specificity; TRAIL
ID IN-VIVO; CANCER; CHEMOTHERAPY; COLON; PERSPECTIVES; THERAPIES; SYSTEM;
   CELLS; SIRNA
AB Tumor necrosis factor related apoptosis inducing ligand (TRAIL) proved to be a promising new target for colorectal cancer treatment. Elevated expression of TRAIL protein in tumor cells distinguishes it from healthy cells, thereby delivering the drug at the specific site. Here, we formulated oxaliplatin immunohybrid nanoparticles (OIHNPs) to deliver oxaliplatin and anti-TRAIL for colorectal cancer treatment in xenograft tumor models. The polymeric chitosan layer binds to the lipid film with the mixture of phospholipids by an ultra sound method followed by conjugating with thiolated antibody using DSPE-PEG-mal3400, resulting in the formation of OIHNPs. The polymer layer helps in more encapsulation of the drug (71 +/- 0.09%) with appreciable particle size (95 +/- 0.01 nm), and lipid layer prevents degradation of the drug in serum by preventing nanoparticle aggregation. OIHNPs have shown a 4-fold decrease in the IC50 value compared to oxaliplatin in HT-29 cells by the MTT assay. These immuno-nanoparticles represent the successful uptake and internalization of oxaliplatin in HT-29 cells rather than in MCF-7 cells determined by triple fluorescence method. Apoptotic activity in vitro of OIHNPs was determined by the change in the mitochondria membrane potential that further elevates its anti-tumor property. Furthermore, the conjugated nanoparticles can effectively deliver the drug to the tumor sites, which can be attributed to its ability in reducing tumor mass and tumor volume in xenograft tumor models in vivo along with sustaining its release in vitro. These findings indicated that the oxaliplatin immuno-hybrid nanoparticles would be a promising nano-sized active targeted formulation for colorectal-tumor targeted therapy.
C1 [Tummala, Shashank; Gowthamarajan, K.] JSS Univ, JSS Coll Pharm Off Campus, Dept Pharmaceut, Mysore, Karnataka, India.
   [Kumar, M. N. Satish] JSS Univ, JSS Coll Pharm Off Campus, Dept Pharmacol, Mysore, Karnataka, India.
   [Wadhwani, Ashish] JSS Univ, JSS Coll Pharm Off Campus, Dept Biotechnol, Mysore, Karnataka, India.
C3 JSS Academy of Higher Education & Research; JSS Academy of Higher
   Education & Research; JSS Academy of Higher Education & Research
RP Tummala, S; Gowthamarajan, K (corresponding author), JSS Coll Pharm, Dept Pharmaceut, Ootacamund, Tamilnadu, India.
EM tummala.shashank@outlook.com; gowthamsang@gmail.com
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NR 35
TC 43
Z9 43
U1 1
U2 33
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1071-7544
EI 1521-0464
J9 DRUG DELIV
JI Drug Deliv.
PY 2016
VL 23
IS 5
SI SI
BP 1773
EP 1787
DI 10.3109/10717544.2015.1084400
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DV5EM
UT WOS:000382949300028
PM 26377238
OA Bronze
DA 2025-01-04
ER

PT J
AU Scavo, MP
   Fucci, L
   Caldarola, L
   Mangia, A
   Azzariti, A
   Simone, G
   Gasparini, G
   Krol, S
AF Scavo, Maria Principia
   Fucci, Livia
   Caldarola, Lucia
   Mangia, Anita
   Azzariti, Amalia
   Simone, Giovanni
   Gasparini, Giampietro
   Krol, Silke
TI Frizzled-10 and cancer progression: Is it a new prognostic marker?
SO ONCOTARGET
LA English
DT Article
DE colon cancer; melanoma; gastric cancer; frizzled-10; prognostic marker
ID BETA-CATENIN; SIGNALING PATHWAY; PROTEIN; FAMILY; FZD10; EXPRESSION;
   RECEPTORS; MELANOMA
AB Frizzled (FZD) proteins, a family of Wnt receptors, are involved in carcinogenesis in different organs. One interesting FZD protein is FZD-10 highly expressed in embryogenesis but completely absent in the membrane or cytosol of healthy proliferated cells. We studied in detail the expression level and the location of Frizzled-10 protein in different cancerous tissues, such as colon, melanoma and gastric cancer and in function of different staging of the tumor and in metastases. We observed a correlation between cancer evolution and FZD-10 expression, and localization of protein during carcinogenesis. In colon, we have an increase of cytoplasmic FZD-10 expression from hyperplastic mucosa to metastatic tissues, while the amount in the nucleus decreases significantly in T3 and T4 staging tumors as well as in metastases. In melanoma and gastric cancer, we observed the opposite trend of FZD-10 protein in the cytosol but both show a decrease in the T3 and T4 stage of the tumor and in metastases. However, the decrease is less prominent in gastric cancer.
   Our findings indicate an important role of FZD-10 in tumor progression especially in the later stages of tumor. The nuclear expression of FZD-10 or its absence can give a new tool for tumor staging to pathologists. For target therapy, at least for colon cancer, the high presence of FZD-10 in the later stages of tumor progression and the absence in healthy tissue present a promising new approach.
C1 [Scavo, Maria Principia; Krol, Silke] IRCCS, Ist Tumori Giovanni Paolo II, Translat Nanotechnol Lab, I-70124 Bari, Italy.
   [Fucci, Livia; Caldarola, Lucia; Simone, Giovanni] IRCCS, Ist Tumori Giovanni Paolo II, Pathol Lab, I-70124 Bari, Italy.
   [Mangia, Anita] IRCCS, Ist Tumori Giovanni Paolo II, Funct Biomorphol Lab, I-70124 Bari, Italy.
   [Azzariti, Amalia] IRCCS, Ist Tumori Giovanni Paolo II, Expt Pharmacol Lab, I-70124 Bari, Italy.
   [Gasparini, Giampietro] IRCCS, Ist Tumori Giovanni Paolo II, Direz Sci, I-70124 Bari, Italy.
   [Krol, Silke] Fdn IRCCS, Ist Neurol Carlo Besta, I-20133 Milan, Italy.
C3 IRCCS Istituto Tumori Bari Giovanni Paolo II; IRCCS Istituto Tumori Bari
   Giovanni Paolo II; IRCCS Istituto Tumori Bari Giovanni Paolo II; IRCCS
   Istituto Tumori Bari Giovanni Paolo II; IRCCS Istituto Tumori Bari
   Giovanni Paolo II; Fondazione IRCCS Istituto Neurologico Carlo Besta
RP Scavo, MP; Krol, S (corresponding author), IRCCS, Ist Tumori Giovanni Paolo II, Translat Nanotechnol Lab, I-70124 Bari, Italy.; Krol, S (corresponding author), Fdn IRCCS, Ist Neurol Carlo Besta, I-20133 Milan, Italy.
EM mariapiascavo9@gmail.com; silke.krol@ifom.eu
RI caldarola, lucia/AAJ-7348-2020; Fucci, Livia/AAH-2509-2020; Krol,
   Silke/F-2599-2014; Scavo, Maria/AAR-6713-2020; Azzariti,
   Amalia/K-4498-2016; Mangia, Anita/K-3662-2018
OI Azzariti, Amalia/0000-0002-6149-5049; Mangia, Anita/0000-0003-4729-0888;
   scavo, maria principia/0000-0002-0812-4441; Krol,
   Silke/0000-0003-3108-9821
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NR 17
TC 17
Z9 19
U1 0
U2 5
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD JAN 2
PY 2018
VL 9
IS 1
BP 824
EP 830
DI 10.18632/oncotarget.23159
PG 7
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FS2NN
UT WOS:000419615500068
PM 29416658
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Lai, E
   Pretta, A
   Impera, V
   Mariani, S
   Giampieri, R
   Casula, L
   Pusceddu, V
   Coni, P
   Fanni, D
   Puzzoni, M
   Demurtas, L
   Ziranu, P
   Faa, G
   Scartozzi, M
AF Lai, Eleonora
   Pretta, Andrea
   Impera, Valentino
   Mariani, Stefano
   Giampieri, Riccardo
   Casula, Laura
   Pusceddu, Valeria
   Coni, Pierpaolo
   Fanni, Daniela
   Puzzoni, Marco
   Demurtas, Laura
   Ziranu, Pina
   Faa, Gavino
   Scartozzi, Mario
TI BRAF-mutant colorectal cancer, a different breed evolving
SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS
LA English
DT Review
DE BRAF; colorectal cancer; prognostic value; predictive value; BRAF
   inhibitors
ID FOLFIRI PLUS CETUXIMAB; III COLON-CANCER; GENE MUTATION STATUS;
   ANTI-EGFR TREATMENT; KRAS WILD-TYPE; MICROSATELLITE INSTABILITY;
   1ST-LINE TREATMENT; MISMATCH REPAIR; V600E MUTATION; STAGE-II
AB Introduction: BRAF mutant colorectal cancer (BRAF MT CRC) is a unique category of colorectal tumour with peculiar molecular, pathological and clinical features and poor prognosis; despite recent research, BRAF mutation predictive value and standard treatment of BRAF MT CRC still have to be defined. In this review, we focused on this challenging topic.Areas covered: The potential use of BRAF mutational status among recent additional prognostic and predictive indicators and current treatment strategy in use in these patients is discussed. Moreover, implications and characteristics of new BRAF mutations other than BRAFV600E are analyzed. An in-deep outlook on the immediate future for clinical and translational research in this subgroup of patients is also presented, such as combination therapy with agents targeting the RAS/RAF/MEK/ERK pathway and standard chemotherapy in order to overcome resistance. We performed a research on Pubmed typing BRAF mutation', colorectal cancer', predictive and prognostic value', targeted therapy', BRAF inhibition'.Expert commentary: BRAFV600E mutation represents a strong, independent negative prognostic factor in II-III stage MSS CRC and mCRC. The best treatment still has to be identified; currently, in good performance status patients, an intensive-chemotherapy-combination remains the standard of care. Further investigations are warranted to explore new horizons to change BRAF MT mCRC outcomes.
C1 [Lai, Eleonora; Pretta, Andrea; Impera, Valentino] Sapienza Univ Rome, Med Oncol, Rome, Italy.
   [Lai, Eleonora; Pretta, Andrea; Impera, Valentino; Mariani, Stefano; Casula, Laura; Pusceddu, Valeria; Puzzoni, Marco; Demurtas, Laura; Ziranu, Pina; Scartozzi, Mario] Univ Hosp, Med Oncol Unit, Cagliari, Italy.
   [Lai, Eleonora; Pretta, Andrea; Impera, Valentino; Mariani, Stefano; Casula, Laura; Pusceddu, Valeria; Puzzoni, Marco; Demurtas, Laura; Ziranu, Pina; Scartozzi, Mario] Univ Cagliari, Cagliari, Italy.
   [Giampieri, Riccardo] Univ Hosp, Med Oncol Unit, Ancona, Italy.
   [Giampieri, Riccardo] Univ Politecn Marche, Ancona, Italy.
   [Coni, Pierpaolo; Fanni, Daniela; Faa, Gavino] Univ Cagliari, Div Pathol, Dept Surg Sci, Ancona, Italy.
C3 Sapienza University Rome; University of Cagliari; Azienda
   Ospedaliero-Universitaria di Cagliari; University of Cagliari; Marche
   Polytechnic University; University of Cagliari
RP Scartozzi, M (corresponding author), Univ Hosp, Med Oncol Unit, Cagliari, Italy.; Scartozzi, M (corresponding author), Univ Cagliari, Cagliari, Italy.
EM marioscartozzi@gmail.com
RI Fanni, Daniela/ABD-9643-2020; pusceddu, valeria/GZM-3173-2022; Ziranu,
   Pina/JVO-2087-2024; PUZZONI, MARCO/T-5453-2019; Lai,
   Eleonora/LPQ-8961-2024
OI SCARTOZZI, MARIO/0000-0001-5977-5546; Lai, Eleonora/0000-0002-0275-8187;
   puzzoni, marco/0000-0001-5880-4309; Ziranu, Pina/0000-0002-5659-7366;
   Pretta, Andrea/0000-0002-0262-9270
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NR 108
TC 20
Z9 23
U1 0
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1473-7159
EI 1744-8352
J9 EXPERT REV MOL DIAGN
JI Expert Rev. Mol. Diagn.
PY 2018
VL 18
IS 6
BP 499
EP 512
DI 10.1080/14737159.2018.1470928
PG 14
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA GJ1IN
UT WOS:000435008800004
PM 29708446
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Li, ZW
   Duan, DY
   Li, L
   Peng, D
   Ming, Y
   Ni, R
   Liu, Y
AF Li, Ziwei
   Duan, Dongyu
   Li, Li
   Peng, Dan
   Ming, Yue
   Ni, Rui
   Liu, Yao
TI Tumor-associated macrophages in anti-PD-1/PD-L1 immunotherapy for
   hepatocellular carcinoma: recent research progress
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE tumor-associated macrophages (TAMs); hepatocellular carcinoma (HCC);
   PD-1/PD-L1; T cell; immunotherapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; APOPTOSIS-INDUCING LIGAND; ANTITUMOR
   IMMUNE-RESPONSE; T-CELL-ACTIVATION; CANCER-CELLS; B7-H1 EXPRESSION;
   UP-REGULATION; COLON-CANCER; LIVER; GROWTH
AB Hepatocellular carcinoma (HCC) is one of the cancers that seriously threaten human health. Immunotherapy serves as the mainstay of treatment for HCC patients by targeting the programmed cell death protein 1/programmed cell death 1 ligand 1 (PD-1/PD-L1) axis. However, the effectiveness of anti-PD-1/PD-L1 treatment is limited when HCC becomes drug-resistant. Tumor-associated macrophages (TAMs) are an important factor in the negative regulation of PD-1 antibody targeted therapy in the tumor microenvironment (TME). Therefore, as an emerging direction in cancer immunotherapy research for the treatment of HCC, it is crucial to elucidate the correlations and mechanisms between TAMs and PD-1/PD-L1-mediated immune tolerance. This paper summarizes the effects of TAMs on the pathogenesis and progression of HCC and their impact on HCC anti-PD-1/PD-L1 immunotherapy, and further explores current potential therapeutic strategies that target TAMs in HCC, including eliminating TAMs in the TME, inhibiting TAMs recruitment to tumors and functionally repolarizing M2-TAMs (tumor-supportive) to M1-TAMs (antitumor type).
C1 [Li, Ziwei; Duan, Dongyu; Li, Li; Peng, Dan; Ming, Yue; Ni, Rui; Liu, Yao] Army Med Univ, Daping Hosp, Dept Pharm, Chongqing, Peoples R China.
C3 Army Medical University
RP Ni, R; Liu, Y (corresponding author), Army Med Univ, Daping Hosp, Dept Pharm, Chongqing, Peoples R China.
EM 853359565@qq.com; swhliuyao@163.com
RI Yue, Ming/KXR-9199-2024
FU Traditional Chinese Medicine Key Project of Chongqing Science and Health
   Joint [2023ZDXM032]; Chongqing Clinical Pharmacy Key Specialties
   Construction Project; National Health Commission of the People's
   Republic of China [WKZX2023CX210006]; Innovative ability enhancement
   program for medical staff of the Army Medical Center [130333]; The
   general program of Development Center for Medical Science and Technology
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This work was funded by
   the Traditional Chinese Medicine Key Project of Chongqing Science and
   Health Joint (Grant No. 2023ZDXM032), the Innovative ability enhancement
   program for medical staff of the Army Medical Center (Grant No. 130333),
   Chongqing Clinical Pharmacy Key Specialties Construction Project, and
   the general program of Development Center for Medical Science and
   Technology, National Health Commission of the People's Republic of China
   (Grant No. WKZX2023CX210006).
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NR 213
TC 4
Z9 4
U1 4
U2 4
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 18
PY 2024
VL 15
AR 1382256
DI 10.3389/fphar.2024.1382256
PG 20
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA XB0S6
UT WOS:001259112000001
PM 38957393
OA gold
DA 2025-01-04
ER

PT J
AU Geva, R
   Sarid, N
   Shacham-Shmueli, E
AF Geva, Ravit
   Sarid, Nadav
   Shacham-Shmueli, Einat
TI Retrospective analysis of efficacy and safety of third-line chemotherapy
   for metastatic colorectal cancer among elderly patients receiving
   targeted therapy in early lines
SO JOURNAL OF CLINICAL GERONTOLOGY & GERIATRICS
LA English
DT Article
DE elderly patients; metastatic colorectal cancer; third-line chemotherapy
ID III COLON-CANCER; ADJUVANT CHEMOTHERAPY; POOLED ANALYSIS; OXALIPLATIN;
   SURVIVAL; FLUOROURACIL; LEUCOVORIN; IRINOTECAN
AB Background/Purpose: About one-half of metastatic colorectal cancer (MCRC) patients are >= 70 years of age. There is uncertainty regarding the benefit patients derive from advanced chemotherapy lines. In this study, we aim to evaluate the efficacy and safety of third-line chemotherapy treatments among MCRC patients.
   Methods: Consecutive patients 70 years or older at the time of diagnosis of metastatic disease who received third-line chemotherapy at the Tel-Aviv Sourasky Medical Center between the years 2000-2009 were collected. Data on demographics, stage of disease, treatment lines and oncological outcomes were extracted from their medical files.
   Results: Only 34 out of 63 patients (54%) available patients received third-line treatments. The (median) age of all patients, third-line patients and the remaining patients, were similar (74.5, 74 and 75.3 years, respectively, P = NS). Following third-line treatments, only 9% had a partial response, and the disease was stable in 29% of patients seen. Thirteen weeks is the median duration of third-line treatments. Only three patients had symptomatic relief. Importantly, 15 patients (44%) required dose reduction or treatment delay due to toxicity (neutropenia or thrombocytopenia). The median survival (mOS) is 9 months for patients with first-line treatment, 19 months for second-line treatment and 37 months for third-line treatment (Log Rank < 0.0001). There was a significant association between the number of lines of treatment and the mOS ( P = 0.0001).
   Conclusion: Third-line chemotherapy treatment of elderly MCRC patients was associated with a minor clinical response, a considerable number of side effects, but a longer survival rate. Third-line chemotherapy in fit elderly patients should be pursued, however, protocols must be adjusted before third-line treatment is implemented. Copyright (C) 2015, Asia Pacific League of Clinical Gerontology & Geriatrics. Published by Elsevier Taiwan LLC.
C1 [Geva, Ravit] Tel Aviv Univ, Sackler Fac Med, Tel Aviv Sourasky Med Ctr, Gastrointestinal Tract Malignancies Ctr,Dept Onco, Tel Aviv, Israel.
   [Sarid, Nadav] Tel Aviv Univ, Dept Hematol, Tel Aviv Sourasky Med Ctr, Sackler Fac Med, Tel Aviv, Israel.
   [Shacham-Shmueli, Einat] Sheba Med Ctr, Ctr Canc, Dept Gastrointestinal Oncol, Tel Hashomer, Israel.
C3 Tel Aviv University; Tel Aviv Sourasky Medical Center; Tel Aviv
   University; Tel Aviv Sourasky Medical Center; Chaim Sheba Medical Center
RP Geva, R (corresponding author), Tel Aviv Sourasky Med Ctr, Gastrointestinal Tract Malignancies Ctr, Dept Oncol, 6 Weizman St, IL-6423906 Tel Aviv, Israel.
EM ravitg@tlvmc.gov.il
RI Shacham-Shmueli, Einat/AAO-5068-2021
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NR 14
TC 3
Z9 3
U1 0
U2 0
PU ASIA PACIFIC LEAGUE CLINICAL GERONTOLOGY & GERIATRICS
PI TAIPEI
PA ASIA PACIFIC LEAGUE CLINICAL GERONTOLOGY & GERIATRICS, TAIPEI, 00000,
   TAIWAN
SN 2210-8335
EI 2210-8343
J9 J CLIN GERONTOL GERI
JI J. Clin. Gerontol. Geriatr.
PD SEP
PY 2015
VL 6
IS 3
BP 95
EP 99
DI 10.1016/j.jcgg.2015.02.006
PG 5
WC Geriatrics & Gerontology
WE Emerging Sources Citation Index (ESCI)
SC Geriatrics & Gerontology
GA V34VU
UT WOS:000215861300005
OA hybrid
DA 2025-01-04
ER

PT J
AU Anim, MT
   Tuffour, I
   Willis, R
   Schell, M
   Ostlund, T
   Mahnashi, MH
   Halaweish, F
   Willand-Charnley, R
AF Anim, Mathias T.
   Tuffour, Isaac
   Willis, Rylan
   Schell, Matthew
   Ostlund, Trevor
   Mahnashi, Mater H.
   Halaweish, Fathi
   Willand-Charnley, Rachel
TI Deacetylated Sialic Acid Sensitizes Lung and Colon Cancers to Novel
   Cucurbitacin-Inspired Estrone Epidermal Growth Factor Receptor (EGFR)
   Inhibitor Analogs
SO MOLECULES
LA English
DT Article
DE sialic acid; CASD1; apoptosis; estrone analogs; Epidermal Growth Factor
   Receptor (EGFR)
ID MULTIDRUG-RESISTANCE; TARGETED THERAPY; IN-VITRO; PHOSPHATIDYLSERINE;
   APOPTOSIS; DEATH; CELLS; PHOSPHORYLATION; RECOGNITION; SIALYLATION
AB Cancers utilize sugar residues such as sialic acids (Sia) to improve their ability to survive. Sia presents a variety of functional group alterations, including O-acetylation on the C6 hydroxylated tail. Previously, sialylation has been reported to suppress EGFR activation and increase cancer cell sensitivity to Tyrosine Kinase Inhibitors (TKIs). In this study, we report on the effect of deacetylated Sia on the activity of three novel EGFR-targeting Cucurbitacin-inspired estrone analogs (CIEAs), MMA 294, MMA 321, and MMA 320, in lung and colon cancer cells. Acetylation was modulated by the removal of Sialate O-Acetyltransferase, also known as CAS1 Domain-containing protein (CASD1) gene via CRISPR-Cas9 gene editing. Using a variety of cell-based approaches including MTT cell viability assay, flow cytometry, immunofluorescence assay and in-cell ELISA we observed that deacetylated Sia-expressing knockout cells (1.24-6.49 & mu;M) were highly sensitive to all CIEAs compared with the control cells (8.82-20.97 & mu;M). Apoptosis and varied stage cell cycle arrest (G0/G1 and G2/M) were elucidated as mechanistic modes of action of the CIEAs. Further studies implicated overexpression of CIEAs' cognate protein target, phosphorylated EGFR, in the chemosensitivity of the deacetylated Sia-expressing knockout cells. This observation correlated with significantly decreased levels of key downstream proteins (phosphorylated ERK and mTOR) of the EGFR pathway in knockout cells compared with controls when treated with CIEAs. Collectively, our findings indicate that Sia deacetylation renders lung and colon cancer cells susceptible to EGFR therapeutics and provide insights for future therapeutic interventions.
C1 [Anim, Mathias T.; Tuffour, Isaac; Willis, Rylan; Schell, Matthew; Ostlund, Trevor; Halaweish, Fathi; Willand-Charnley, Rachel] South Dakota State Univ, Dept Chem & Biochem, Brookings, SD 57007 USA.
   [Mahnashi, Mater H.] Najran Univ, Dept Pharmaceut Chem, POB 1988, Najran, Saudi Arabia.
C3 South Dakota State University; Najran University
RP Willand-Charnley, R (corresponding author), South Dakota State Univ, Dept Chem & Biochem, Brookings, SD 57007 USA.
EM aytiem@gmail.com; isaac.tuffour@jacks.sdstate.edu;
   rylan.willis@jacks.sdstate.edu; matthew.schell@jacks.sdstate.edu;
   ostlu104@umn.edu; fathi.halaweish@sdstate.edu; mhmahneshi@nu.edu.sa;
   rachel.willand@sdstate.edu
RI Mahnashi, Mater/GRJ-8274-2022
OI Ostlund, Trevor/0000-0002-1181-3088; Willand-Charnley,
   Rachel/0000-0003-2721-6955
FU We thank Michael Bassik for providing us with the CRISPR-Cas9 stably
   expressing cells and the third-generation lentiviral system. Special
   thanks also go to Colin Parish for generously providing CASD1 and SIAE
   knockout A549 cell lines. We also thank Fathi H
FX We thank Michael Bassik for providing us with the CRISPR-Cas9 stably
   expressing cells and the third-generation lentiviral system. Special
   thanks also go to Colin Parish for generously providing CASD1 and SIAE
   knockout A549 cell lines. We also thank Fathi Halaweish for supplying
   the estrone analogs (CIEAs) used for this study.
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NR 56
TC 0
Z9 1
U1 2
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD SEP
PY 2023
VL 28
IS 17
AR 6257
DI 10.3390/molecules28176257
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA R1CL5
UT WOS:001061788200001
PM 37687086
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Nindra, U
   Shahnam, A
   Mahon, KL
AF Nindra, Udit
   Shahnam, Adel
   Mahon, Kate L.
TI Review of systemic chemotherapy in unresectable colorectal peritoneal
   carcinomatosis
SO ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Review
DE 5&#8208; fluorouracil; bevacizumab; cetuximab; panitumumab; targeted
   therapy
ID SEVERITY SCORE PSDSS; CANCER PATIENTS; BEVACIZUMAB; METASTASES;
   SURVIVAL; MALIGNANCIES; TRIALS; ORIGIN; INDEX; RISK
AB Colorectal cancer remains the third most common malignancy in Australia with the peritoneum being the second most common metastatic site. Colorectal peritoneal carcinomatosis (CPC) can be treated with cytoreductive surgery and hyperthermic intraperitoneal chemotherapy but this is only limited to a small subset of patients. Those with inoperable disease have a particularly poor prognosis. While the ideal systemic regimen has not been defined, 5-fluorouracil-based chemotherapy regimens appear to provide overall and progression free survival benefits. The role of targeted agents such as bevacizumab (vascular endothelial growth factor inhibitor) or cetuximab (epidermal growth factor inhibitor) in the setting of CPC is still evolving. Currently, retrospective analyses have shown promising results for the use of bevacizumab in addition to systemic chemotherapy but similar results have not been seen with cetuximab or panitumumab. However, there is significant heterogeneity in the trial data, lack of prospective randomized controlled trials and demonstrated treatment variability based on age and tumour characteristics. This review summarises the current literature in regard to treatment in the unresectable CPC setting as well as discussing issues with the current data and highlighting the need for further trials.
C1 [Nindra, Udit; Shahnam, Adel] Royal Prince Alfred Hosp, Sydney, NSW, Australia.
   [Nindra, Udit; Shahnam, Adel; Mahon, Kate L.] Chris OBrien Lifehouse, Sydney, NSW, Australia.
   [Nindra, Udit; Mahon, Kate L.] Garvan Inst Med Res, Sydney, NSW, Australia.
   [Mahon, Kate L.] Univ NSW, Sydney, NSW, Australia.
   [Mahon, Kate L.] Univ Sydney, Sydney, NSW, Australia.
C3 NSW Health; Royal Prince Alfred Hospital; University of Sydney; Chris
   O'Brien Lifehouse; Garvan Institute of Medical Research; University of
   New South Wales Sydney; University of Sydney
RP Nindra, U (corresponding author), Royal Prince Alfred Hosp, Sydney, NSW, Australia.
EM uditnindra@gmail.com
OI Nindra, Udit/0000-0002-2612-9502; Shahnam, Adel/0000-0002-0043-8374;
   Mahon, Kate/0000-0002-6801-0841
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NR 41
TC 5
Z9 6
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-7555
EI 1743-7563
J9 ASIA-PAC J CLIN ONCO
JI Asia-Pac. J. Clin. Oncol.
PD FEB
PY 2022
VL 18
IS 1
BP 7
EP 12
DI 10.1111/ajco.13552
EA FEB 2021
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YV2BG
UT WOS:000619626900001
PM 33609014
OA Bronze
DA 2025-01-04
ER

PT J
AU Takemura, N
   Saiura, A
AF Takemura, Nobuyuki
   Saiura, Akio
TI Role of surgical resection for non-colorectal non-neuroendocrine liver
   metastases
SO WORLD JOURNAL OF HEPATOLOGY
LA English
DT Review
DE Non-colorectal non-neuroendocrine liver metastasis; Metastatic liver
   tumor; Hepatectomy; Gastric cancer liver metastasis; Gastrointestinal
   stromal tumor liver metastasis; Breast cancer liver metastasis; Melanoma
   liver metastasis; Sarcoma liver metastasis; Renal cell carcinoma liver
   metastasis; Ovarian cancer liver metastasis
ID GASTROINTESTINAL STROMAL TUMORS; SINGLE-CENTER EXPERIENCE; CURATIVE
   INTENT SURGERY; LONG-TERM SURVIVAL; HEPATIC RESECTION; GASTRIC-CANCER;
   BREAST-CANCER; NONCOLORECTAL PRIMARY; DIRECTED SURGERY; TARGETED THERAPY
AB It is widely accepted that the indications for hepatectomy in colorectal cancer liver metastases and liver metastases of neuro-endocrine tumors result in relatively better prognoses, whereas, the indications and prognoses of hepatectomy for non-colorectal non-neuroendocrine liver metastases (NCNNLM) remain controversial owing to the limited number of cases and the heterogeneity of the primary diseases. There have been many publications on NCNNLM; however, its background heterogeneity makes it difficult to reach a specific conclusion. This heterogeneous disease group should be discussed in the order from its general to specific aspect. The present review paper describes the general prognosis and risk factors associated with NCNNLM while specifically focusing on the liver metastases of each primary disease. A multidisciplinary approach that takes into consideration appropriate timing for hepatectomy combined with chemotherapy may prolong survival and/or contribute to the improvement of the quality of life while giving respite from systemic chemotherapy.
C1 [Takemura, Nobuyuki; Saiura, Akio] JR Tokyo Gen Hosp, Dept Surg Gastroenterol, Tokyo 1518528, Japan.
RP Takemura, N (corresponding author), JR Tokyo Gen Hosp, Dept Surg Gastroenterol, Shibuya Ku, 2-1-3 Yoyogi, Tokyo 1518528, Japan.
EM takemuranobu-tky@umin.ac.jp
RI Nobuyuki, Takemura/GLT-3305-2022; Saiura, Akio/AAH-5008-2020
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NR 63
TC 28
Z9 30
U1 2
U2 9
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5182
J9 WORLD J HEPATOL
JI World J. Hepatol.
PD FEB 18
PY 2017
VL 9
IS 5
BP 242
EP 251
DI 10.4254/wjh.v9.i5.242
PG 10
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA EY3RU
UT WOS:000403892000002
PM 28261381
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Polivka, J
   Pesta, M
   Janku, F
AF Polivka, Jiri, Jr.
   Pesta, Martin
   Janku, Filip
TI Testing for oncogenic molecular aberrations in cell-free DNA-based
   liquid biopsies in the clinic: are we there yet?
SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS
LA English
DT Review
DE Liquid biopsy; cell-free DNA; advanced cancer; targeted therapy;
   personalized medicine
ID CIRCULATING TUMOR DNA; FREE NUCLEIC-ACIDS; COLORECTAL-CANCER PATIENTS;
   LUNG-CANCER; PLASMA DNA; ACQUIRED-RESISTANCE; PROGNOSTIC VALUE;
   FOLLOW-UP; K-RAS; PROMOTER HYPERMETHYLATION
AB The optimal choice of cancer therapy depends upon analysis of the tumor genome for druggable molecular alterations. The spatial and temporal intratumor heterogeneity of cancers creates substantial challenges, as molecular profile depends on time and site of tumor tissue collection. To capture the entire molecular profile, multiple biopsies from primary and metastatic sites at different time points would be required, which is not feasible for ethical or economic reasons.Molecular analysis of circulating cell-free DNA offers a novel, minimally invasive method that can be performed at multiple time-points and plausibly better represents the prevailing molecular profile of the cancer. Molecular analysis of this cell-free DNA offers multiple clinically useful applications, such as identification of molecular targets for cancer therapy, monitoring of tumor molecular profile in real time, detection of emerging molecular aberrations associated with resistance to particular therapy, determination of cancer prognosis and diagnosis of cancer recurrence or progression.
C1 [Polivka, Jiri, Jr.] Charles Univ Prague, Dept Histol & Embryol, Fac Med Plzen, Plzen, Czech Republic.
   [Polivka, Jiri, Jr.] Charles Univ Prague, Biomed Ctr, Fac Med Plzen, Plzen, Czech Republic.
   [Polivka, Jiri, Jr.] Fac Hosp Plzen, Dept Neurol, Plzen, Czech Republic.
   [Pesta, Martin] Charles Univ Prague, Fac Med Plzen, Dept Biol, Plzen, Czech Republic.
C3 Charles University Prague; Charles University Prague; Charles University
   Prague
RP Janku, F (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, Phase Clin Trials Program 1, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM fjanku@mdanderson.org
RI Janku, Filip/ABB-9136-2020
FU MH CZ - DRO (Faculty Hospital Plzen - FNPl) [00669806]; National
   Sustainability Program I (NPU I) by the Ministry of Education Youth and
   Sports of the Czech Republic [LO1503]; Elsa U. Pardee Foundation; Sidney
   Kimmel Foundation for Cancer Research; Sheikh Khalifa Al Nahyan Ben
   Zayed Institute for Personalized Cancer Therapy; U.S. National Center
   for Advancing Translational Sciences [UL1 TR000371]; U.S. National
   Institutes of Health through MD Anderson's Cancer Center Support Grant
   [P30 CA016672]; Biocartis (Mechelen, Belgium); Trovagene (San Diego, CA,
   USA); Illumina (San Diego)
FX The authors were supported by MH CZ - DRO (Faculty Hospital Plzen -
   FNPl, 00669806) and by the National Sustainability Program I (NPU I) Nr.
   LO1503 provided by the Ministry of Education Youth and Sports of the
   Czech Republic, the Elsa U. Pardee Foundation, the Sidney Kimmel
   Foundation for Cancer Research, the Sheikh Khalifa Al Nahyan Ben Zayed
   Institute for Personalized Cancer Therapy, the U.S. National Center for
   Advancing Translational Sciences (grant no. UL1 TR000371), and the U.S.
   National Institutes of Health through MD Anderson's Cancer Center
   Support Grant (P30 CA016672). F Janku received research support from
   Biocartis (Mechelen, Belgium), Trovagene (San Diego, CA, USA) and
   Illumina (San Diego) and is on the Scientific Advisory Board of
   Trovagene. 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 120
TC 49
Z9 49
U1 0
U2 20
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 DEC 2
PY 2015
VL 15
IS 12
BP 1631
EP 1644
DI 10.1586/14737159.2015.1110021
PG 14
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA CY1XS
UT WOS:000366202200001
PM 26559503
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Morley-Bunker, A
   Walker, LC
   Currie, MJ
   Pearson, J
   Eglinton, T
AF Morley-Bunker, A.
   Walker, L. C.
   Currie, M. J.
   Pearson, J.
   Eglinton, T.
TI Translating colorectal cancer genetics into clinically useful biomarkers
SO COLORECTAL DISEASE
LA English
DT Article
ID CIRCULATING TUMOR-CELLS; MICROSATELLITE-INSTABILITY; COLON-CANCER;
   MOLECULAR-GENETICS; DNA METHYLATION; EXPRESSION; SUBTYPES;
   CLASSIFICATION; MUTATIONS; MARKERS
AB Colorectal cancer (CRC) is a major health problem worldwide accounting for over a million deaths annually. While many patients with Stage II and III CRC can be cured with combinations of surgery, radiotherapy and chemotherapy, this is morbid costly treatment and a significant proportion will suffer recurrence and eventually die of CRC. Increased understanding of the molecular pathogenesis of CRC has the potential to identify high risk patients and target therapy more appropriately. Despite increased understanding of the molecular events underlying CRC development, established molecular techniques have only produced a limited number of biomarkers suitable for use in routine clinical practice to predict risk, prognosis and response to treatment. Recent rapid technological developments, however, have made genomic sequencing of CRC more economical and efficient, creating potential for the discovery of genetic biomarkers that have greater diagnostic, prognostic and therapeutic capabilities for the management of CRC. This paper reviews the current understanding of the molecular pathogenesis of CRC, and summarizes molecular biomarkers that surgeons will encounter in current clinical use as well as those under development in clinical and preclinical trials. New molecular technologies are reviewed together with their potential impact on the understanding of the molecular pathogenesis of CRC and their potential clinical utility in classification, diagnosis, prognosis and targeting of therapy.
C1 [Morley-Bunker, A.; Walker, L. C.; Currie, M. J.] Univ Otago, Mackenzie Canc Res Grp, Dept Pathol, Christchurch, New Zealand.
   [Pearson, J.] Univ Otago, Biostat & Computat Biol Unit, Christchurch, New Zealand.
   [Eglinton, T.] Univ Otago, Dept Surg, Christchurch, New Zealand.
C3 University of Otago; University of Otago; University of Otago
RP Eglinton, T (corresponding author), Univ Otago, Dept Surg, Christchurch, New Zealand.
EM Tim.eglinton@cdhb.health.nz
RI Eglinton, Tim/H-8606-2019; Pearson, John/D-7428-2012; Currie,
   Margaret/I-6223-2015
OI Walker, Logan/0000-0003-0018-3719; Currie, Margaret/0000-0002-9788-8098
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NR 81
TC 3
Z9 4
U1 0
U2 11
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 AUG
PY 2016
VL 18
IS 8
BP 749
EP 762
DI 10.1111/codi.13334
PG 14
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA DS6OQ
UT WOS:000380901900010
PM 26990814
DA 2025-01-04
ER

PT J
AU Wu, CC
   Hsu, CW
   Hsieh, MC
   Wang, JH
   Chang, MC
   Yang, CS
   Su, YC
AF Wu, Chih-Chien
   Hsu, Chao-Wen
   Hsieh, Meng-Che
   Wang, Jui-Ho
   Chang, Min-Chi
   Yang, Ching-Shiang
   Su, Yi-Chia
TI Optimal Sequence and Second-Line Systemic Treatment of Patients with
   <i>RAS</i> Wild-Type Metastatic Colorectal Cancer: A Meta-Analysis
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE sequential therapy; patient management; RAS-WT mCRC; targeted therapy;
   metastatic cancer treatment
ID 1ST PROGRESSION; RANDOMIZED PHASE-3; PLUS CETUXIMAB; ANTI-EGFR;
   BEVACIZUMAB; THERAPY; TRIAL; EFFICACY; FOLFIRI; IMPACT
AB Although several sequential therapy options are available for treating patients with RAS wild-type (WT) metastatic colorectal cancer (mCRC), the optimal sequence of these therapies is not well established. A systematic review and meta-analysis of 13 randomized controlled trials and 4 observational studies were performed, resulting from a search of the Cochrane Library, PubMed, and Embase databases. Overall survival (OS) did not differ significantly in patients with RAS-WT failure who were administered a second-line regimen of changed chemotherapy (CT) plus anti-epidermal growth factor receptor (EGFR) versus only changed CT, changed CT plus bevacizumab versus changed CT plus anti-EGFR, or changed CT versus maintaining CT plus anti-EGFR after first-line therapy with CT, plus bevacizumab. However, OS was significantly different with a second-line regimen that included changed CT plus bevacizumab, versus only changing CT. Analysis of first-line therapy with CT plus anti-EGFR for treatment of RAS-WT mCRC indicated that second-line therapy of changed CT plus an anti-EGFR agent resulted in better outcomes than changing CT without targeted agents. The pooled data study demonstrated that the optimal choice of second-line treatment for improved OS was an altered CT regimen with retention of bevacizumab after first-line bevacizumab failure. The best sequence for first-to-second-line therapy of patients with RAS-WT mCRC was cetuximab-based therapy, followed by a bevacizumab-based regimen.
C1 [Wu, Chih-Chien; Hsu, Chao-Wen; Wang, Jui-Ho; Chang, Min-Chi] Kaohsiung Vet Gen Hosp, Div Colorectal Surg, Dept Surg, Kaohsiung 813, Taiwan.
   [Wu, Chih-Chien; Hsu, Chao-Wen] Natl Yang Ming Chiao Tung Univ, Dept Surg, Coll Med, Taipei 112, Taiwan.
   [Hsieh, Meng-Che] E Da Canc Hosp, Dept Hematol & Oncol, Kaohsiung 824, Taiwan.
   [Hsieh, Meng-Che] I Shou Univ, Coll Med, Kaohsiung 824, Taiwan.
   [Chang, Min-Chi] Meiho Univ, Dept Hlth Business Adm, Pingtung 912, Taiwan.
   [Yang, Ching-Shiang; Su, Yi-Chia] Kaohsiung Vet Gen Hosp, Dept Pharm, Kaohsiung 813, Taiwan.
   [Su, Yi-Chia] Natl Cheng Kung Univ, Inst Clin Pharm & Pharmaceut Sci, Coll Med, Tainan 701, Taiwan.
   [Su, Yi-Chia] Shu Zen Jr Coll Med & Management, Dept Nursing, Kaohsiung 821, Taiwan.
C3 Kaohsiung Veterans General Hospital; National Yang Ming Chiao Tung
   University; E-Da Hospital; I Shou University; Kaohsiung Veterans General
   Hospital; National Cheng Kung University
RP Su, YC (corresponding author), Kaohsiung Vet Gen Hosp, Dept Pharm, Kaohsiung 813, Taiwan.; Su, YC (corresponding author), Natl Cheng Kung Univ, Inst Clin Pharm & Pharmaceut Sci, Coll Med, Tainan 701, Taiwan.; Su, YC (corresponding author), Shu Zen Jr Coll Med & Management, Dept Nursing, Kaohsiung 821, Taiwan.
EM pauleoswu@gmail.com; cwhsu@vghks.gov.tw; philips115@gmail.com;
   wang@vghks.gov.tw; mcchang100@vghks.gov.tw; csyang429@vghks.gov.tw;
   s19101080@gm.ym.edu.tw
RI Su, Yichia/HJI-3668-2023
OI Wu, Chih-Chien/0000-0001-5791-4047; Su, Yi-Chia/0000-0002-9544-1153
FU Kaohsiung Veterans General Hospital [KSVGH110-054, KSVGH110-018]
FX FundingThis work was supported by Kaohsiung Veterans General Hospital
   [grant number: KSVGH110-054 and KSVGH110-018].
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NR 32
TC 3
Z9 3
U1 1
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD NOV
PY 2021
VL 10
IS 21
AR 5166
DI 10.3390/jcm10215166
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA XJ2KU
UT WOS:000726624400001
PM 34768686
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yin, FX
   Zhao, R
   Gorja, DR
   Fu, XR
   Lu, N
   Huang, H
   Xu, BB
   Chen, HY
   Shim, JH
   Liu, KD
   Li, Z
   Laster, KV
   Dong, ZG
   Lee, MH
AF Yin, Fanxiang
   Zhao, Ran
   Gorja, Dhilli Rao
   Fu, Xiaorong
   Lu, Ning
   Huang, Hai
   Xu, Beibei
   Chen, Hanyong
   Shim, Jung-Hyun
   Liu, Kangdong
   Li, Zhi
   Laster, Kyle Vaughn
   Dong, Zigang
   Lee, Mee-Hyun
TI Novel dual inhibitor for targeting PIM1 and FGFR1 kinases inhibits
   colorectal cancer growth<i> in</i><i> vitro</i> and patient-derived
   xenografts<i> in</i><i> vivo</i>
SO ACTA PHARMACEUTICA SINICA B
LA English
DT Article
DE PIM1; FGFR1; Colorectal cancer; HCI-48; Targeted therapy; Small molecule
   compound of chalcone; Patient-derived xenograft&nbsp; model; Kinase
   activity
ID CELL-CYCLE PROGRESSION; COLON-CANCER; CHALCONE; PROLIFERATION;
   CARCINOMA; SURVIVAL; PATHWAY; RISK; METASTASIS; ACTIVATION
AB Colorectal cancer (CRC) is the second most common cause of cancer-related death in the world. The pro-viral integration site for Moloney murine leukemia virus 1 (PIM1) is a proto-oncogene and belongs to the serine/threonine kinase family, which are involved in cell proliferation, migration, and apoptosis. Fibroblast growth factor receptor 1 (FGFR1) is a tyrosine kinase that has been implicated in cell proliferation, differentiation and migration. Small molecule HCI-48 is a derivative of chalcone, a class of compounds known to possess anti-tumor, anti-inflammatory and antibacterial effects. However, the underlying mechanism of chalcones against colorectal cancer remains unclear. This study reports that HCI-48 mainly targets PIM1 and FGFR1 kinases, thereby eliciting antitumor effects on colorectal cancer growth in vitro and in vivo. HCI-48 inhibited the activity of both PIM1 and FGFR1 kinases in an ATP -dependent manner, as revealed by computational docking models. Cell-based assays showed that HCI-48 inhibited cell proliferation in CRC cells (HCT-15, DLD1, HCT-116 and SW620), and induced cell cycle arrest in the G2/M phase through modulation of cyclin A2. HCI-48 also induced cellular apoptosis, as evidenced by an increase in the expression of apoptosis biomarkers such as cleaved PARP, cleaved cas-pase 3 and cleaved caspase 7. Moreover, HCI-48 attenuated the activation of downstream components of the PIM1 and FGFR1 signaling pathways. Using patient-derived xenograft (PDX) murine tumor models, we found that treatment with HCI-48 diminished the PDX tumor growth of implanted CRC tissue expressing high protein levels of PIM1 and FGFR1. This study suggests that the inhibitory effect of HCI-48 on colorectal tumor growth is mainly mediated through the dual-targeting of PIM1 and FGFR1 kinases. This work provides a theoretical basis for the future application of HCI-48 in the treatment of clinical CRC. 2022 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting 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 [Yin, Fanxiang; Zhao, Ran; Fu, Xiaorong; Lu, Ning; Xu, Beibei; Liu, Kangdong; Dong, Zigang; Lee, Mee-Hyun] Zhengzhou Univ, Sch Basic Med Sci, Dept Pathophysiol, Zhengzhou 450001, Peoples R China.
   [Yin, Fanxiang; Zhao, Ran; Gorja, Dhilli Rao; Fu, Xiaorong; Lu, Ning; Huang, Hai; Xu, Beibei; Liu, Kangdong; Laster, Kyle Vaughn; Dong, Zigang; Lee, Mee-Hyun] China US Henan Hormel Canc Inst, Zhengzhou 450008, Peoples R China.
   [Yin, Fanxiang] Zhengzhou Univ, Affiliated Hosp 1, Translat Med Ctr, Zhengzhou 450052, Peoples R China.
   [Chen, Hanyong; Dong, Zigang] Univ Minnesota, Hormel Inst, Austin, MN 55912 USA.
   [Shim, Jung-Hyun] Mokpo Natl Univ, Coll Pharm, Dept Biomed Hlth & Life Convergencen Sci, BK21 Four, Jeonnam 58554, South Korea.
   [Liu, Kangdong] Collaborat Innovat Ctr Henan Prov Canc Chemopreven, Zhengzhou 450001, Peoples R China.
   [Li, Zhi] Zhengzhou Univ, Affiliated Tumor Hosp, Dept Gen Surg, Zhengzhou 450008, Peoples R China.
   [Lee, Mee-Hyun] Dongshin Univ, Coll Korean Med, Naju 58245, South Korea.
C3 Zhengzhou University; Zhengzhou University; University of Minnesota
   System; Mokpo National University; Zhengzhou University; Dongshin
   University
RP Dong, ZG; Lee, MH (corresponding author), Zhengzhou Univ, Sch Basic Med Sci, Dept Pathophysiol, Zhengzhou 450001, Peoples R China.; Dong, ZG; Lee, MH (corresponding author), China US Henan Hormel Canc Inst, Zhengzhou 450008, Peoples R China.; Dong, ZG (corresponding author), Univ Minnesota, Hormel Inst, Austin, MN 55912 USA.; Lee, MH (corresponding author), Dongshin Univ, Coll Korean Med, Naju 58245, South Korea.
EM zgdong@hci-cn.org; mhyun_lee@hanmail.net
RI wang, wei/JYP-7819-2024; Huang, Qiuju/HGV-0866-2022; chen,
   huan/GXZ-8858-2022; Xu, Beibei/IQT-2456-2023
FU National Natural Science Foundation of China [81972839, 82002620,
   82073075]; Scientific and Technological Project in Henan Province and
   Henan Provincial Government (China) [212102310882, 222102310104]
FX This work was supported by grant funding from the National Natural
   Science Foundation of China (81972839, 82002620 and 82073075), and the
   Scientific and Technological Project in Henan Province and Henan
   Provincial Government (Nos. 212102310882, and 222102310104, China). We
   wish to thank Dr. Xiang Li, Ran Yang, Sen Yang, and Fangfang Liu in the
   China-US (Henan) Hormel Cancer Institute, Zhengzhou, China for
   supporting materials and experiments, and Dr. Jaeki Min in Induced
   Proximity Platform (IPP) Amgen, USA for discussing the HCI-48 compound.
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NR 65
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Z9 13
U1 0
U2 23
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 NOV
PY 2022
VL 12
IS 11
BP 4122
EP 4137
DI 10.1016/j.apsb.2022.07.005
EA NOV 2022
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 6D0ST
UT WOS:000882412500006
PM 36386480
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhao, W
   Jin, LJ
   Chen, P
   Li, DC
   Gao, WX
   Dong, GL
AF Zhao, Wen
   Jin, Lujia
   Chen, Peng
   Li, Dingchang
   Gao, Wenxing
   Dong, Guanglong
TI Colorectal cancer immunotherapy-Recent progress and future directions
SO CANCER LETTERS
LA English
DT Article
DE Colorectalcarcinoma; Immunotherapy; Immunecheckpointblockade
ID REGULATORY T-CELLS; TUMOR-INFILTRATING LYMPHOCYTES; WNT/BETA-CATENIN
   PATHWAY; MICROSATELLITE INSTABILITY; IMMUNE-RESPONSES; PD-1 BLOCKADE;
   PLUS CHEMOTHERAPY; SUPPRESSOR-CELLS; RANDOMIZED-TRIAL; OPEN-LABEL
AB Compared with conventional chemotherapy and targeted therapy, immunotherapy has changed the treatment prospects of various solid tumors and has recently become the main treatment method for metastatic or recurrent solid tumors, including malignant melanoma, non-small-cell lung cancer, and renal cell carcinoma. The appli-cation of immune checkpoint inhibitor (ICI)-based immunotherapy in patients with colorectal cancer (CRC) has yielded satisfactory results in terms of safety and efficacy, and several immunotherapeutic agents, including pembrolizumab, nivolumab, and ipilimumab, have been approved for the treatment of advanced CRC. The advent of other immunotherapies, such as chimeric antigen receptor-modified T (CAR-T) cells or cancer vaccines, have also contributed to the development of immunotherapy for CRC. Here, we summarize the findings of recent clinical trials on the efficacy of immunotherapy in CRC and briefly describe the mechanisms associated with tumor-intrinsic resistance to ICIs. We then discuss potential biomarkers for predicting the efficacy of immunotherapy.
C1 [Zhao, Wen; Dong, Guanglong] Nankai Univ, Sch Med, Tianjin 300071, Peoples R China.
   [Zhao, Wen; Jin, Lujia; Chen, Peng; Li, Dingchang; Gao, Wenxing; Dong, Guanglong] Chinese Peoples Liberat Army Gen Hosp, Dept Gen Surg, Beijing 100853, Peoples R China.
C3 Nankai University; Chinese People's Liberation Army General Hospital
RP Dong, GL (corresponding author), Chinese Peoples Liberat Army Gen Hosp, Dept Gen Surg, Beijing 100853, Peoples R China.
EM dongguanglong@301hospital.com.cn
RI Lujia, Jin/KGK-4981-2024; Zhao, Wen/AEF-4469-2022; G, wx/KCY-8947-2024
FU National Natural Science Foundation of China [81773247]
FX Acknowledgments The research work was supported by the National Natural
   Science Foundation of China (Grant Nos. 81773247) .
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NR 139
TC 57
Z9 59
U1 1
U2 42
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 OCT 1
PY 2022
VL 545
AR 215816
DI 10.1016/j.canlet.2022.215816
EA JUL 2022
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3G5YY
UT WOS:000831431000005
PM 35810989
DA 2025-01-04
ER

PT J
AU Gaggianesi, M
   Mangiapane, LR
   Modica, C
   Pantina, VD
   Porcelli, G
   Di Franco, S
   Lo Iacono, M
   D'Accardo, C
   Verona, F
   Pillitteri, I
   Turdo, A
   Veschi, V
   Brancato, OR
   Muratore, G
   Pistone, G
   Bongiorno, MR
   Todaro, M
   De Maria, R
   Stassi, G
AF Gaggianesi, Miriam
   Mangiapane, Laura Rosa
   Modica, Chiara
   Pantina, Vincenzo Davide
   Porcelli, Gaetana
   Di Franco, Simone
   Lo Iacono, Melania
   D'Accardo, Caterina
   Verona, Francesco
   Pillitteri, Irene
   Turdo, Alice
   Veschi, Veronica
   Brancato, Ornella Roberta
   Muratore, Giampaolo
   Pistone, Giuseppe
   Bongiorno, Maria Rita
   Todaro, Matilde
   De Maria, Ruggero
   Stassi, Giorgio
TI Dual Inhibition of Myc Transcription and PI3K Activity Effectively
   Targets Colorectal Cancer Stem Cells
SO CANCERS
LA English
DT Article
DE anti-tumor drug resistance; colorectal cancer; combination therapies;
   cancer stem cells
ID COLON-CANCER; RAS MUTATIONS; RESISTANCE; BRAF
AB Simple Summary Compelling evidence has shown that cancer stem cells (CSCs) are responsible for high resistance to conventional anti-cancer therapies. Here, we demonstrate that the tumor microenvironment protects CR-CSCs from EGFR/HER2, BRAF and PI3K targeting, promoting CD44v6 and Myc expression. Alternatively, as a substitution for HER2 and BRAF, the Myc transcription inhibitor can overcome the protective effects of microenvironmental cytokines, impairing the survival of CR-CSCs. These data highlight the targeting of Myc and PI3K activity as a novel therapeutic strategy against advanced colorectal cancer. Despite advances in the curative approach, the survival rate of advanced colorectal cancer (CRC) patients is still poor, which is likely due to the emergence of cancer cell clones resistant to the available therapeutic options. We have already shown that CD44v6-positive CRC stem cells (CR-CSCs) are refractory toward standard anti-tumor therapeutic agents due to the activation of the PI3K pathway together with high HER2 expression levels. Tumor microenvironmental cytokines confer resistance to CR-CSCs against HER2/PI3K targeting by enhancing activation of the MAPK pathway. Here, we show that the CSC compartment, spared by BRAF inhibitor-based targeted therapy, is associated with increased expression levels of CD44v6 and Myc and retains boosted clonogenic activity along with residual tumorigenic potential. Inhibition of Myc transcription, downstream of the MAPK cascade components, and PI3K pathway activity was able to overcome the protective effects of microenvironmental cytokines, affecting the survival and the clonogenic activity of CR-CSCs, regardless of their mutational background. Likewise, the double targeting induced stabilization of mouse tumor avatars. Altogether, these data outline the rationale for dual kinase targeting of CR-CSCs to prevent their adaptive response, which would lead to disease progression.
C1 [Gaggianesi, Miriam; Modica, Chiara; Pantina, Vincenzo Davide; Di Franco, Simone; Lo Iacono, Melania; Pillitteri, Irene; Veschi, Veronica; Brancato, Ornella Roberta; Muratore, Giampaolo; Stassi, Giorgio] Univ Palermo, Dept Surg Oncol & Stomatol Sci DICHIRONS, I-90127 Palermo, Italy.
   [Mangiapane, Laura Rosa; Porcelli, Gaetana; D'Accardo, Caterina; Verona, Francesco; Turdo, Alice; Pistone, Giuseppe; Bongiorno, Maria Rita; Todaro, Matilde] Univ Palermo, Dept Hlth Promot Sci Internal Med & Med Specialti, I-90127 Palermo, Italy.
   [De Maria, Ruggero] Univ Cattolica Sacro Cuore, Fac Med & Chirurg, Dipartimento Med & Chirurg Traslaz, I-00168 Rome, Italy.
   [De Maria, Ruggero] Fdn Policlin A Gemelli IRCCS, I-00168 Rome, Italy.
C3 University of Palermo; University of Palermo; Catholic University of the
   Sacred Heart; IRCCS Policlinico Gemelli; Catholic University of the
   Sacred Heart; IRCCS Policlinico Gemelli
RP Stassi, G (corresponding author), Univ Palermo, Dept Surg Oncol & Stomatol Sci DICHIRONS, I-90127 Palermo, Italy.; De Maria, R (corresponding author), Univ Cattolica Sacro Cuore, Fac Med & Chirurg, Dipartimento Med & Chirurg Traslaz, I-00168 Rome, Italy.; De Maria, R (corresponding author), Fdn Policlin A Gemelli IRCCS, I-00168 Rome, Italy.
EM miriam.gaggianesi@unipa.it; laurarosa.mangiapane@unipa.it;
   chiara.modica@unipa.it; vincenzodavide.pantina@unipa.it;
   gaetana.porcelli@unipa.it; simone.difranco@unipa.it;
   melania.loiacono@unipa.it; caterina.daccardo@unipa.it;
   francesco.verona@unipa.it; irene.pillitteri@policlinico.pa.it;
   alice.turdo@unipa.it; veronica.veschi@unipa.it;
   ornellaroberta.brancato@community.unipa.it; giampaolo.muratore@unipa.it;
   giuseppe.pistone@unipa.it; mariarita.bongiorno@unipa.it;
   matilde.todaro@unipa.it; ruggero.demaria@unicatt.it;
   giorgio.stassi@unipa.it
RI D Accardo, Caterina/IAQ-6545-2023; Mangiapane, Laura'Rosa/LQL-1966-2024;
   Stassi, Giorgio/JAZ-0703-2023; Veschi, Veronica/K-4143-2018; De Maria,
   Ruggero/S-6385-2019; Iacono, Melania/A-2882-2014; Turdo,
   Alice/ABB-8063-2022; GAGGIANESI, Miriam/IAQ-6692-2023; Porcelli,
   Gaetana/IAQ-6506-2023; di franco, simone/M-3714-2019
OI Turdo, Alice/0000-0002-6152-4903; Stassi, Giorgio/0000-0002-1016-9059;
   modica, chiara/0000-0002-7000-5216; Bongiorno, Maria
   Rita/0000-0002-6355-2588; Pantina, Vincenzo Davide/0000-0003-1144-0434;
   Muratore, Giampaolo/0000-0002-5447-3992; Veschi,
   Veronica/0000-0002-6379-7366; GAGGIANESI, Miriam/0000-0002-7810-856X;
   Brancato, Ornella Roberta/0000-0002-2783-0720; Porcelli,
   Gaetana/0000-0002-7991-407X; di franco, simone/0000-0002-6217-2161;
   Mangiapane, Laura Rosa/0000-0003-4186-0157; Verona,
   Francesco/0000-0001-6226-4624; todaro, matilde/0000-0001-8686-8043
FU AIRC IG [21492, RF2018-12367044, 21445]; PRIN [2017WNKSLR]
FX This work was supported by the following grants: AIRC IG (21492) to
   M.T., RF2018-12367044 to M.T. and R.D.M. and PRIN (Prot. No. 2017WNKSLR)
   and AIRC IG (21445) to G.S.
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NR 55
TC 4
Z9 4
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 FEB
PY 2022
VL 14
IS 3
AR 673
DI 10.3390/cancers14030673
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZA6MU
UT WOS:000756276400001
PM 35158939
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Feng, YM
   Hu, TT
   Fang, P
   Zhou, LL
   Li, WM
   Fang, Q
   Fang, J
AF Feng, Yiming
   Hu, Tingting
   Fang, Pan
   Zhou, Linlin
   Li, Wanming
   Fang, Qun
   Fang, Jin
TI Consecutive and automatic detection of multi-gene mutations from
   colorectal cancer samples by coupling droplet array-based capillary
   electrophoresis and PCR-RFLP
SO ANALYTICAL AND BIOANALYTICAL CHEMISTRY
LA English
DT Article
DE Capillary electrophoresis; Droplets; Multi-gene detection; Gene
   mutation; PCR-RFLP
ID RESISTANCE; THERAPY; BENEFIT; KRAS; CHEMOTHERAPY; SEPARATION; INJECTION;
   SYSTEM; PTEN; GENE
AB The efficacy of targeted therapy is associated with multi-gene mutation status. Carrying out effective multi-genotyping analysis in combination has been a challenge in clinical settings. We therefore developed a droplet-based capillary electrophoresis (CE) system coupled with PCR-restriction fragment length polymorphism (PCR-RFLP) technology to detect multi-gene mutations from a small volume of samples. A 16 x 16 200-nL droplet array for sample encapsulation was constructed on a glass chip. The electrophoresis system consisted of a tapered vertical capillary filled with polyvinylpyrrolidone, a laser-induced fluorescence detector, and a high voltage power supply. Notably, a droplet-based electrokinetic sample introduction method and a "boolean AND" shape capillary were developed to facilitate consecutive droplet sampling using a home-made automatic control module. The DL2000 DNA marker was consecutively separated, achieving high migration time and plate number reproducibility. The system was further applied to detect PCR-RFLP products. For colorectal cancer (CRC) cell lines, KRAS, BRAF, and PIK3CA were genotyped with a sensitivity of 0.25%. For CRC patient specimens, 30 samples were consecutively and automatically multi-genotyped without inter-sample contamination, with a lowest mutation frequency of 0.37%. For the first time, we developed a droplet-based CE system for consecutive DNA analysis with low sample consumption. This automated CE system could be further developed to integrate the full process of gene mutation detection, serving as a more effective platform for individualised therapy.
C1 [Feng, Yiming; Hu, Tingting; Zhou, Linlin; Li, Wanming; Fang, Jin] China Med Univ, Dept Cell Biol, Key Lab Cell Biol, Minist Publ Hlth, 77 Puhe Rd, Shenyang 110122, Liaoning, Peoples R China.
   [Feng, Yiming; Hu, Tingting; Zhou, Linlin; Li, Wanming; Fang, Jin] China Med Univ, Key Lab Med Cell Biol, Minist Educ, 77 Puhe Rd, Shenyang 110122, Liaoning, Peoples R China.
   [Fang, Pan; Fang, Qun] Zhejiang Univ, Inst Microanalyt Syst, Dept Chem, Chem Expt Bldg, Hangzhou 310058, Zhejiang, Peoples R China.
C3 China Medical University; China Medical University; Zhejiang University
RP Fang, J (corresponding author), China Med Univ, Dept Cell Biol, Key Lab Cell Biol, Minist Publ Hlth, 77 Puhe Rd, Shenyang 110122, Liaoning, Peoples R China.; Fang, J (corresponding author), China Med Univ, Key Lab Med Cell Biol, Minist Educ, 77 Puhe Rd, Shenyang 110122, Liaoning, Peoples R China.; Fang, Q (corresponding author), Zhejiang Univ, Inst Microanalyt Syst, Dept Chem, Chem Expt Bldg, Hangzhou 310058, Zhejiang, Peoples R China.
EM fangqun@zju.edu.cn; jfang@cmu.edu.cn
RI Feng, Yiming/KZV-0094-2024; tingting, hu/AGX-8728-2022; Fang,
   Jin/HKF-5214-2023; Fang, Qun/C-8216-2011
OI Fang, Jin/0000-0001-5188-5206
FU National Natural Science Foundation of China [81672920, 21375149]
FX This research work was financially supported by the National Natural
   Science Foundation of China (Grant number 81672920 and 21375149).
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NR 45
TC 2
Z9 2
U1 2
U2 30
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1618-2642
EI 1618-2650
J9 ANAL BIOANAL CHEM
JI Anal. Bioanal. Chem.
PD MAY
PY 2020
VL 412
IS 13
SI SI
BP 3037
EP 3049
DI 10.1007/s00216-020-02567-y
EA APR 2020
PG 13
WC Biochemical Research Methods; Chemistry, Analytical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA LK1MK
UT WOS:000524155900002
PM 32249344
DA 2025-01-04
ER

PT J
AU Rogers, JE
AF Rogers, Jane E.
TI Patient considerations in metastatic colorectal cancer - role of
   panitumumab
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE receptor; epidermal growth factor; antineoplastic agent; antibodies;
   monoclonal; colorectal neoplasms
ID QUALITY-OF-LIFE; FACTOR RECEPTOR INHIBITORS; PHASE-III TRIAL; WILD-TYPE
   KRAS; OPEN-LABEL; SKIN TOXICITY; 1ST-LINE TREATMENT; INFUSION REACTIONS;
   PATIENTS PTS; CETUXIMAB
AB Epidermal growth factor receptor (EGFR) is overexpressed in many malignancies, including colorectal cancer (CRC), making EGFR an attractive treatment option. Panitumumab and cetuximab, monoclonal antibodies (mAbs) directed at EGFR, are both currently utilized in the management of metastatic CRC (mCRC). Through the development of these agents in mCRC, key issues surrounding each mAbs use have been revealed. These key issues include negative patient outcome avoidance when determining use, the economic burden with high-cost medication, predictive biomarkers, tumor location, patient geographic location, patient quality of life, and the prevention of debilitating adverse effects. CRC remains a common malignancy, with many of these patients expected to receive targeted therapy, including EGFR mAb therapy. Oncologists must recognize these EGFR mAb factors in order to improve outcomes. This review aims to provide a chronological timeline on the development of panitumumab, clinical pearls, and guidance on the current use of panitumumab in mCRC.
C1 [Rogers, Jane E.] Univ Texas MD Anderson Canc Ctr, Pharm Clin Programs, 1515 Holcombe Blvd, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center
RP Rogers, JE (corresponding author), Univ Texas MD Anderson Canc Ctr, Pharm Clin Programs, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM jerogers@mdanderson.org
OI Rogers, Jane/0000-0002-7275-7008
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NR 58
TC 9
Z9 9
U1 1
U2 1
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 2033
EP 2044
DI 10.2147/OTT.S115430
PG 12
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA ER1SH
UT WOS:000398572800001
PM 28435294
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, YH
   Oliver, PG
   Lu, WY
   Pathak, V
   Sridharan, S
   Augelli-Szafran, CE
   Buchsbaum, DJ
   Suto, MJ
AF Li, Yonghe
   Oliver, Patsy G.
   Lu, Wenyan
   Pathak, Vibha
   Sridharan, Sivaram
   Augelli-Szafran, Corinne E.
   Buchsbaum, Donald J.
   Suto, Mark J.
TI RETRACTED: SRI36160 is a specific inhibitor of Wnt/β-catenin signaling
   in human pancreatic and colorectal cancer cells (Retracted article. See
   vol. 422, pg. 131, 2018)
SO CANCER LETTERS
LA English
DT Article; Retracted Publication
DE Wnt signaling; Benzimidazole; Niclosamide; Targeted therapy; Drug
   discovery
ID BETA-CATENIN; COLON-CANCER; WNT PATHWAY; R-SPONDIN; DUCTAL
   ADENOCARCINOMA; DRUG DESIGN; STEM-CELLS; NICLOSAMIDE; ACTIVATION;
   EXPRESSION
AB Activation of Wnt/beta-catenin signaling is associated with pancreatic and colorectal cancer, among others. To-date, there are no FDA-approved small molecule Wnt/beta-catenin inhibitors and many past efforts resulted in compounds with undesirable off-target effects. We recently identified a series of benzimidazole analogs as potent inhibitors of Wnt/beta-catenin signaling. Here, we show that the lead compound SRI36160 displayed selective Wnt inhibition and potent antiproliferative activity in pancreatic and colorectal cancer cells. Moreover, SRI36160 had no effect on, STAT3 and mTORC1 signaling in pancreatic and colorectal cancer cells, and was not effective in inhibiting proliferation of non-cancerous cells. Our findings suggest that this series of benzimidazole analogs presents a novel approach for the treatment of Wnt-dependent cancers such as colorectal and pancreatic cancer. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
C1 [Li, Yonghe; Lu, Wenyan; Pathak, Vibha; Augelli-Szafran, Corinne E.; Suto, Mark J.] Drug Discovery Div, Southern Res, 2000 Ninth Ave South, Birmingham, AL 35255 USA.
   [Oliver, Patsy G.; Sridharan, Sivaram; Buchsbaum, Donald J.] Univ Alabama Birmingham, Dept Radiat Oncol, Birmingham, AL USA.
C3 University of Alabama System; University of Alabama Birmingham
RP Li, YH (corresponding author), Drug Discovery Div, Southern Res, 2000 Ninth Ave South, Birmingham, AL 35255 USA.
EM yli@southernresearch.org
RI Sridharan, Sivaram/AAU-6840-2021
OI Buchsbaum, Donald/0000-0003-2797-5847
FU National Institutes of Health [R01CA124531, R21CA182056, P50CA101955];
   Alabama Innovation Fund; UAB Comprehensive Cancer Center; UAB School of
   Medicine
FX We thank Janet A. Houghton and Ruowen Zhang for helpful discussion and
   support during the course of this study, and Lynae Hanks for critical
   reading of the manuscript. This work was partially supported by grants
   from the National Institutes of Health R01CA124531, R21CA182056 and
   P50CA101955, the Alabama Innovation Fund, the UAB Comprehensive Cancer
   Center, and the UAB School of Medicine.
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NR 54
TC 8
Z9 10
U1 0
U2 19
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 MAR 28
PY 2017
VL 389
BP 41
EP 48
DI 10.1016/j.canlet.2016.12.030
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EN2NB
UT WOS:000395846100005
PM 28043913
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Wu, KL
   Kuo, CM
   Huang, EY
   Pan, HM
   Huang, CC
   Chen, YF
   Hsiao, CC
   Yang, KD
AF Wu, Keng-Liang
   Kuo, Chung-Mou
   Huang, Eng-Yen
   Pan, Hui-Mei
   Huang, Chao-Cheng
   Chen, Yi-Fan
   Hsiao, Chang-Chun
   Yang, Kuender D.
TI Extracellular galectin-3 facilitates colon cancer cell migration and is
   related to the epidermal growth factor receptor
SO AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH
LA English
DT Article
DE Colorectal carcinoma; galectin-3; EGFR; cell migration
ID DIFFERENTIAL EXPRESSION; COLORECTAL-CANCER; THYROID-CARCINOMA; EGFR;
   INDUCTION; PATHWAY; ENDOTHELIUM; PROGRESSION; METASTASIS; ACTIVATION
AB We previously found that galectin-3 enhanced DLD-1 cell migration through the K-Ras-Raf-Erk1/2 pathway, but the effect of extracellular galectin-3 on cancer cell migration and its interaction with the epidermal growth factor receptor (EGFR) remained unknown. We aimed to determine the effect of extracellular galectin-3 on colon cancer cell migration and its correlation with the EGFR expression. Western blotting was performed to analyze galectin-3 secretion, shRNA was used to stably knock down galectin-3 expression and a migration assay was performed to evaluate colon cancer cell migration. Tissues from eighty patients with four different stages of colon cancer were obtained and compared to normal colon tissue. The galectin-3 knockdown colon cancer cells exhibited decreased migration, which was restored by recombinant galectin-3. An EGFR blocking antibody decreased colon cancer cell migration. The addition of recombinant galectin-3 increased phosphorylated EGFR expression within minutes and enhanced the internalization of the EGFR from the cell membrane to the cytoplasm, particularly upon EGF stimulation. Extracellular galectin-3 increased colon cancer cell migration, which correlated with the EGFR. Targeting galectin-3 may have a synergistic effect on EGFR-targeted therapy.
C1 [Wu, Keng-Liang; Kuo, Chung-Mou; Pan, Hui-Mei] Kaohsiung Chang Gung Mem Hosp, Dept Internal Med, Div Hepatogastroenterol, 123 Ta Pei Rd, Kaohsiung 83301, Taiwan.
   [Huang, Eng-Yen; Chen, Yi-Fan] Kaohsiung Chang Gung Mem Hosp, Dept Radiat Oncol, 123 Ta Pei Rd, Kaohsiung 83301, Taiwan.
   [Huang, Chao-Cheng] Kaohsiung Chang Gung Mem Hosp, Dept Pathol, 123 Ta Pei Rd, Kaohsiung 83301, Taiwan.
   [Wu, Keng-Liang; Huang, Eng-Yen; Hsiao, Chang-Chun; Yang, Kuender D.] Chang Gung Univ, Grad Inst Clin Med Sci, Coll Med, 123 Ta Pei Rd, Kaohsiung 83301, Taiwan.
   [Hsiao, Chang-Chun] Kaohsiung Chang Gung Mem Hosp, Ctr Shockwave Med & Tissue Engn, 123 Ta Pei Rd, Kaohsiung 83301, Taiwan.
   [Yang, Kuender D.] Natl Yang Ming Univ, Inst Clin Med, 155,Sec 2,Linong St, Taipei 112, Taiwan.
   [Yang, Kuender D.] Mackay Mem Hosp, Mackay Med Sch, Inst Biomed Sci, Dept Med Res, 46,Sec 3,Zhongzheng Rd, New Taipei 252, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung Memorial Hospital; Chang Gung
   Memorial Hospital; Chang Gung University; Chang Gung Memorial Hospital;
   National Yang Ming Chiao Tung University; Mackay Memorial Hospital
RP Hsiao, CC; Yang, KD (corresponding author), Chang Gung Univ, Grad Inst Clin Med Sci, Coll Med, 123 Ta Pei Rd, Kaohsiung 83301, Taiwan.; Yang, KD (corresponding author), Mackay Mem Hosp, Mackay Med Sch, Inst Biomed Sci, Dept Med Res, 92,Sec 2,Zhongshan North Rd, Taipei 104, Taiwan.
EM cchsiao@mail.cgu.edu.tw; yangkd.yeh@hotmail.com
RI Hung, Chun-Hsiung/D-5521-2009; Huang, Chao/L-1445-2019
OI Hsiao, Chang-Chun/0000-0002-7275-4675; Chen, Yi Fan/0000-0003-2080-843X
FU Chang Gung Memorial Hospital, Taiwan [CMRPG-970204, CMRPG8C0911,
   CMRPG8C0912, CMRPG8D0991]; National Science Council, Taiwan, R.O.C.
   [MOST103-2325-B-758-001]; Tissue Bank of Kaohsiung Chang Gung Memorial
   Hospital [CLRPG8B0033]
FX This study was supported by grants CMRPG-970204, CMRPG8C0911,
   CMRPG8C0912 and CMRPG8D0991 from Chang Gung Memorial Hospital, Taiwan to
   Dr. KL Wu and another grant, MOST103-2325-B-758-001, to Dr. KD Yang from
   the National Science Council, Taiwan, R.O.C. The authors thank the
   Tissue Bank of Kaohsiung Chang Gung Memorial Hospital (CLRPG8B0033) for
   providing the decoded materials for this study. We appreciated the
   Biostatistics Center, Kaohsiung Chang Gung Memorial Hospital for
   statistics work.
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NR 27
TC 16
Z9 17
U1 0
U2 2
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1943-8141
J9 AM J TRANSL RES
JI Am. J. Transl. Res.
PY 2018
VL 10
IS 8
BP 2402
EP 2412
PG 11
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA GS5QU
UT WOS:000443724100014
PM 30210679
DA 2025-01-04
ER

PT J
AU Zhang, TH
   Xu, J
   Shen, HC
   Dong, W
   Ni, Y
   Du, JJ
AF Zhang, Tiehong
   Xu, Jun
   Shen, Hongchang
   Dong, Wei
   Ni, Yang
   Du, Jiajun
TI Tumor-stroma ratio is an independent predictor for survival in NSCLC
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE TSR; non-small cell lung cancer; prognosis; targeted therapy
ID CELL LUNG-CANCER; PROGNOSTIC-FACTOR; COLON-CANCER; CARCINOMA;
   FIBROBLASTS; STATISTICS; HISTOLOGY; STAGE
AB Tumor-stroma ratio (TSR) has been identified as a new and practicable prognostic factor in some solid tumors. The aim of the study is to evaluate the prognostic value of TSR in non-small cell lung cancer (NSCLC). A total of 404 patients who underwent surgery resection for NSCLC were included in this study. TSR was assessed visually on the hematoxylin-stained tissue sections of surgical specimens. Patients with more than 50% intratumor stroma were quantified as the stroma-rich group and those with less than 50% as the stroma-poor group. In 404 cases of tissue samples, 302 cases were included in the stroma-poor group, while 102 cases in stroma-rich group. The different expression of TSR in NSCLC tissue was not correlated with gender, age, smoking history, tumor diameter, histology, differentiation grade and pTNM staging. In the Cox univariate and multivariate analyses of the 5-year OS, the HRs of the TSR were 1.818 (95% CI; 1.323-2.497; P<0.001) and 1.748 (95% CI; 1.262-2.422; P<0.05), respectively. As for DFS, the HRs were 1.715 (95% CI; 1.249-2.354; P<0.001) and 1.570 (95% CI; 1.135-2.172; P<0.05). Stroma-rich tumors were associated with poor prognosis and an increased risk of relapse, which may serve as a new prognostic histological characteristic in NSCLC.
C1 [Zhang, Tiehong; Xu, Jun; Du, Jiajun] Shandong Univ, Shandong Prov Hosp, Inst Oncol, Jinan 250100, Peoples R China.
   [Dong, Wei; Du, Jiajun] Shandong Univ, Shandong Prov Hosp, Dept Thorac Surg, Jinan 250021, Peoples R China.
   [Shen, Hongchang; Ni, Yang] Shandong Univ, Shandong Prov Hosp, Dept Oncol, Jinan 250021, Peoples R China.
C3 Shandong First Medical University & Shandong Academy of Medical
   Sciences; Shandong University; Shandong First Medical University &
   Shandong Academy of Medical Sciences; Shandong University; Shandong
   First Medical University & Shandong Academy of Medical Sciences;
   Shandong University
RP Du, JJ (corresponding author), Shandong Univ, Shandong Prov Hosp, Dept Thorac Surg, 324 Jingwu Rd, Jinan 250021, Peoples R China.
EM dujiajun@sdu.edu.cn
RI shen, hong/HTQ-6147-2023
FU Provincial Natural Science Foundation of Shandong [ZR2013HZ-001];
   National Natural Science Foundation of China [81301728]
FX The work was supported by Provincial Natural Science Foundation of
   Shandong (ZR2013HZ-001) and the National Natural Science Foundation of
   China (project 81301728).
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NR 20
TC 45
Z9 48
U1 0
U2 5
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1936-2625
J9 INT J CLIN EXP PATHO
JI Int. J. Clin. Exp. Pathol.
PY 2015
VL 8
IS 9
BP 11348
EP 11355
PG 8
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA DA4ZX
UT WOS:000367812800176
PM 26617859
DA 2025-01-04
ER

PT J
AU Li, H
   Zhong, YF
   Wang, SM
   Zha, ML
   Gu, WX
   Liu, GY
   Wang, BH
   Yu, ZD
   Wang, Y
   Li, K
   Yin, YX
   Mu, J
   Chen, XY
AF Li, Hui
   Zhong, Yanfeng
   Wang, Shumin
   Zha, Menglei
   Gu, Wenxing
   Liu, Guoyong
   Wang, Bohan
   Yu, Zhendong
   Wang, Yu
   Li, Kai
   Yin, Yuxin
   Mu, Jing
   Chen, Xiaoyuan
TI <i>In vivo</i> bioorthogonal labeling of rare-earth doped nanoparticles
   for improved NIR-II tumor imaging by extracellular vesicle mediated
   targeting
SO NANO RESEARCH
LA English
DT Article
DE NIR-II; rare earth-doped nanoparticles; bioorthogonal labeling;
   extracellular vesicles; tumor imaging
ID NEAR-INFRARED WINDOW; CARBON NANOTUBES; QUANTUM DOTS; EXOSOMES; DELIVERY
AB The development of efficient contrast agents for tumor-targeted imaging remains a critical challenge in the clinic, Herein, we proposed a tumor-derived extracellular vesicle (EV)-mediated targeting approach to improve in vivo tumor imaging using ternary downconversion nanoparticles (DCNPs) with strong near infrared II (NIR-11) luminescence at 1,525 nm. The EVs were metabolically engineered with azide group, followed by in vivo labeling of DCNPs through copper-free click chemistry. By taking advantage of the homologous targeting property of tumor derived EVs, remarkable improvement in the tumor accumulation (6.5% injection dose (ID)/g) was achieved in the subcutaneous colorectal cancer model when compared to that of individual DCNPs via passive targeting (1.1% ID/g). Importantly, such bioorthogonal labeling significantly increased NIR-II luminescence signals and prolonged the retention at tumor sites. Our work demonstrates the great potential of EVs-mediated bioorthogonal approach for in vivo labeling of NIR-Il optical probes, which provides a robust tool for tumor-specific imaging and targeted therapy.
C1 [Li, Hui; Wang, Shumin; Gu, Wenxing; Liu, Guoyong; Yin, Yuxin; Mu, Jing] Peking Univ, Shenzhen Peking Univ Hong Kong Univ Sci & Tech Me, Inst Precis Med, Shenzhen Hosp, Shenzhen 518036, Peoples R China.
   [Li, Hui; Chen, Xiaoyuan] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Diagnost Radiol, Singapore 119074, Singapore.
   [Li, Hui; Chen, Xiaoyuan] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Surg, Singapore 119074, Singapore.
   [Li, Hui; Chen, Xiaoyuan] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Chem & Biomol Engn, Singapore 119074, Singapore.
   [Li, Hui; Chen, Xiaoyuan] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Biomed Engn, Singapore 119074, Singapore.
   [Li, Hui; Chen, Xiaoyuan] Natl Univ Singapore, Coll Design & Engn, Singapore 119074, Singapore.
   [Zhong, Yanfeng; Yu, Zhendong] Peking Univ, Cent Lab, Shenzhen Hosp, Shenzhen 518036, Peoples R China.
   [Zha, Menglei; Li, Kai] Southern Univ Sci & Tech SUSTech, Dept Biomed Engn, Shenzhen 518055, Peoples R China.
   [Wang, Bohan; Wang, Yu] Shenzhen Univ, Inst Microscale Optoelect, Shenzhen 518060, Peoples R China.
   [Chen, Xiaoyuan] ASTAR, Inst Mol & Cell Biol, 61 Biopolis Dr, Singapore 138673, Singapore.
C3 Peking University; National University of Singapore; National University
   of Singapore; National University of Singapore; National University of
   Singapore; National University of Singapore; Peking University; Shenzhen
   University; Agency for Science Technology & Research (A*STAR); A*STAR -
   Institute of Molecular & Cell Biology (IMCB)
RP Mu, J (corresponding author), Peking Univ, Shenzhen Peking Univ Hong Kong Univ Sci & Tech Me, Inst Precis Med, Shenzhen Hosp, Shenzhen 518036, Peoples R China.; Chen, XY (corresponding author), Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Diagnost Radiol, Singapore 119074, Singapore.; Chen, XY (corresponding author), Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Surg, Singapore 119074, Singapore.; Chen, XY (corresponding author), Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Chem & Biomol Engn, Singapore 119074, Singapore.; Chen, XY (corresponding author), Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Biomed Engn, Singapore 119074, Singapore.; Chen, XY (corresponding author), Natl Univ Singapore, Coll Design & Engn, Singapore 119074, Singapore.; Yu, ZD (corresponding author), Peking Univ, Cent Lab, Shenzhen Hosp, Shenzhen 518036, Peoples R China.; Chen, XY (corresponding author), ASTAR, Inst Mol & Cell Biol, 61 Biopolis Dr, Singapore 138673, Singapore.
EM dongboyaa@163.com; mujing1921@gmail.com; chen.shawn@nus.edu.sg
RI ZHA, Menglei/KXR-9954-2024; Chen, Xiao Yuan/K-3324-2016; Wang,
   Yu/ITT-1027-2023; Mu, Jing/GLT-2155-2022; Wang, Yu/N-4119-2018
OI Wang, Yu/0000-0001-5971-6597
FU China Postdoctoral Science Foundation [2022M712157]; China National
   Postdoctoral Program for Innovative Talents [BX20220215]; China
   Scientific Research Foundation of Peking University Shenzhen Hospital
   [KYQD202100X]; National Natural Science Foundation of China [32101074];
   Shenzhen Science and Technology Innovation Committee Discipline Layout
   Project [JCYJ20170816105345191]; National University of Singapore
   Start-up Grant [NUHSRO/2020/133/Startup/08]; NUS School of Medicine
   Nanomedicine Translational Research Programme
   [NULISR0/2021/034/TRP/09/Nanomedicine]; National Medical Research
   Council (NMRC) Centre Grant Programme [CG21APR1005]
FX This work was financially supported by the China Postdoctoral Science
   Foundation (No. 2022M712157), China National Postdoctoral Program for
   Innovative Talents (No. BX20220215), China Scientific Research
   Foundation of Peking University Shenzhen Hospital (No. KYQD202100X), the
   National Natural Science Foundation of China (No. 32101074), Shenzhen
   Science and Technology Innovation Committee Discipline Layout Project
   (No. JCYJ20170816105345191), National University of Singapore Start-up
   Grant (No. NUHSRO/2020/133/Startup/08), NUS School of Medicine
   Nanomedicine Translational Research Programme (No.
   NULISR0/2021/034/TRP/09/Nanomedicine), and the National Medical Research
   Council (NMRC) Centre Grant Programme (No. CG21APR1005).
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NR 60
TC 11
Z9 11
U1 15
U2 31
PU TSINGHUA UNIV PRESS
PI BEIJING
PA B605D, XUE YAN BUILDING, BEIJING, 100084, PEOPLES R CHINA
SN 1998-0124
EI 1998-0000
J9 NANO RES
JI Nano Res.
PD FEB
PY 2023
VL 16
IS 2
BP 2895
EP 2904
DI 10.1007/s12274-022-5033-8
EA NOV 2022
PG 10
WC Chemistry, Physical; Nanoscience & Nanotechnology; Materials Science,
   Multidisciplinary; Physics, Applied
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science;
   Physics
GA R0LC9
UT WOS:000886901900001
DA 2025-01-04
ER

PT J
AU Mancarella, C
   Scotlandi, K
AF Mancarella, Caterina
   Scotlandi, Katia
TI IGF system in sarcomas: a crucial pathway with many unknowns to exploit
   for therapy
SO JOURNAL OF MOLECULAR ENDOCRINOLOGY
LA English
DT Review
DE sarcomas; IGF system; targeted therapy; clinical trials
ID GROWTH-FACTOR-I; ADVANCED SOLID TUMORS; RNA-BINDING-PROTEIN;
   GASTROINTESTINAL STROMAL TUMORS; SOFT-TISSUE SARCOMA; METASTATIC
   COLORECTAL-CANCER; REFRACTORY EWING SARCOMA; OSTEOSARCOMA CELL-LINES;
   FACTOR-RECEPTOR IGF-1R; PHASE-I
AB The insulin-like growth factor (IGF) system has gained substantial interest due to its involvement in regulating cell proliferation, differentiation and survival during anoikis and after conventional and targeted therapies. However, results from clinical trials have been largely disappointing, with only a few but notable exceptions, such as trials targeting sarcomas, especially Ewing sarcoma. This review highlights key studies focusing on IGF signaling in sarcomas, specifically studies underscoring the properties that make this system an attractive therapeutic target and identifies new relationships that may be exploited. This review discusses the potential roles of IGF2 mRNA-binding proteins (IGF2BPs), discoidin domain receptors (DDRs) and metalloproteinase pregnancy-associated plasma protein-A (PAPP-A) in regulating the IGF system. Deeper investigation of these novel regulators of the IGF system may help us to further elucidate the spatial and temporal control of the IGF axis, as understanding the control of this axis is essential for future clinical studies.
C1 [Mancarella, Caterina; Scotlandi, Katia] Orthopaed Rizzoli Inst, CRS Dev Biomol Therapies, Expt Oncol Lab, Bologna, Italy.
RP Scotlandi, K (corresponding author), Orthopaed Rizzoli Inst, CRS Dev Biomol Therapies, Expt Oncol Lab, Bologna, Italy.
EM katia.scotlandi@ior.it
RI Mancarella, Caterina/C-7463-2019; scotlandi, katia/J-9009-2016
OI Mancarella, Caterina/0000-0002-5778-4251; scotlandi,
   katia/0000-0001-6114-9499
FU Italian Association for Cancer Research [IG2016_18451]; Istituto
   Ortopedico Rizzoli (5xmille contributions to the Rizzoli Institute);
   Fondazione Italiana per la Ricerca sul Cancro-FIRC (FIRC project)
   [17984]; Guido Berlucchi Foundation
FX This work was supported by the Italian Association for Cancer Research
   (IG2016_18451 to K S) and by the Istituto Ortopedico Rizzoli (5xmille
   contributions to the Rizzoli Institute). Caterina Mancarella was awarded
   the 'Guglielmina Lucatello e Gino Mazzega' fellowship granted by
   Fondazione Italiana per la Ricerca sul Cancro-FIRC (FIRC project code:
   17984), and she was partially supported by the Guido Berlucchi
   Foundation.
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NR 152
TC 20
Z9 21
U1 0
U2 3
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
   ENGLAND
SN 0952-5041
EI 1479-6813
J9 J MOL ENDOCRINOL
JI J. Mol. Endocrinol.
PD JUL
PY 2018
VL 61
IS 1
BP T45
EP T60
DI 10.1530/JME-17-0250
PG 16
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA GN5NV
UT WOS:000439108000011
PM 29273680
OA Bronze
DA 2025-01-04
ER

PT J
AU Tao, T
   Yang, X
   Zheng, J
   Feng, D
   Qin, Q
   Shi, X
   Wang, Q
   Zhao, C
   Peng, Z
   Liu, H
   Jiang, WG
   He, J
AF Tao, T.
   Yang, X.
   Zheng, J.
   Feng, D.
   Qin, Q.
   Shi, X.
   Wang, Q.
   Zhao, C.
   Peng, Z.
   Liu, H.
   Jiang, W. G.
   He, J.
TI PDZK1 inhibits the development and progression of renal cell carcinoma
   by suppression of SHP-1 phosphorylation
SO ONCOGENE
LA English
DT Article
ID TYROSINE-PHOSPHATASE SHP-1; BREAST-CANCER; CLEAR-CELL;
   COLORECTAL-CANCER; TARGETED THERAPY; PROTEIN; EXPRESSION; GROWTH;
   TUMORIGENESIS; SURVIVAL
AB Renal cell carcinoma (RCC) is one of the most aggressive urologic cancers, however, the mechanism on supporting RCC carcinogenesis is still not clear. By using gene expression profile analysis and functional clustering, PDZ domain-containing 1 (PDZK1) was revealed to be downregulated in human clear cell renal cell carcinoma (ccRCC) samples, which was also verified in several independent public ccRCC data sets. Using PDZK1 overexpression and knockdown models in ccRCC cell lines, we demonstrated that PDZK1 inhibited cell proliferation, cell cycle G1/S phase transition, cell migration and invasion, indicating a tumor-suppressor role in the development and progression of ccRCC. Our study further demonstrated that PDZK1 inhibited cell proliferation and migration of ccRCC via targeting SHP-1. PDZK1 was further identified to suppress cell proliferation by blocking SHP-1 phosphorylation at Tyr536 via inhibition of the association between SHP-1 and PLC beta 3, and then retarding Akt phosphorylation and promoting STAT5 phosphorylation in ccRCC cells. Moreover, the inhibitive effects of PDZK1 on SHP-1 phosphorylation and the tumor growth were verified in vivo by xenograft tumor studies. Accordingly, PDZK1 expression was negatively correlated with SHP-1 activation and phosphorylation, advanced pathologic stage, tumor weight and size, and prognosis of ccRCC patients. These findings have provided first lines of evidences that PDZK1 expression is negatively correlated with SHP-1 activation and poor clinical outcomes in ccRCC. PDZK1 was identified as a novel tumor suppressor in ccRCC by negating SHP-1 activity.
C1 [Tao, T.; Yang, X.; Zheng, J.; Qin, Q.; Shi, X.; Wang, Q.; Zhao, C.; Peng, Z.; Liu, H.; He, J.] Capital Med Univ, Dept Biochem & Mol Biol, 10 Xitoutiao, Beijing 100069, Peoples R China.
   [Yang, X.; Zheng, J.; Qin, Q.; Liu, H.; He, J.] Capital Med Univ, Beijing Int Cooperat Base Sci & Technol China UK, Beijing Key Lab Canc Invas & Metastasis Res, Beijing, Peoples R China.
   [Feng, D.] Shanxi Med Univ, Hosp 1, Dept Intervent Radiol, Taiyuan, Shanxi, Peoples R China.
   [Jiang, W. G.] Cardiff Univ, Cardiff China Med Res Collaborat, Sch Med, Heath Pk, Cardiff, S Glam, Wales.
C3 Capital Medical University; Capital Medical University; Shanxi Medical
   University; Cardiff University
RP Liu, H; He, J (corresponding author), Capital Med Univ, Dept Biochem & Mol Biol, 10 Xitoutiao, Beijing 100069, Peoples R China.
EM hualh08@ccmu.edu.cn; jq_he@ccmu.edu.cn
RI Jiang, Wen/AAF-1876-2020; Jiang, Wen G./B-1293-2010
OI Jiang, Wen G./0000-0002-3283-1111
FU National Natural Science Foundation of the People's Republic of China
   [81472409, 81572333]; Beijing Natural Science Foundation Program;
   Beijing Municipal Commission of Education [KZ201710025015]; Project of
   High-level Teachers in Beijing Municipal Universities [IDHT20170516];
   Beijing BaiQianWan Talents Program
FX This work was supported by the National Natural Science Foundation of
   the People's Republic of China (No. 81472409, 81572333); Beijing Natural
   Science Foundation Program and Scientific Research Key Program of
   Beijing Municipal Commission of Education (KZ201710025015); Support
   Project of High-level Teachers in Beijing Municipal Universities in the
   Period of 13th Five-year Plan (IDHT20170516); Beijing BaiQianWan Talents
   Program (2017-2018).
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NR 36
TC 31
Z9 32
U1 0
U2 19
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD NOV 2
PY 2017
VL 36
IS 44
BP 6119
EP 6131
DI 10.1038/onc.2017.199
PG 13
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA FL5CU
UT WOS:000414249800006
PM 28692056
DA 2025-01-04
ER

PT J
AU Rathore, M
   Zhang, W
   Wright, M
   Bhattacharya, R
   Fan, F
   Vaziri-Gohar, A
   Winter, J
   Wang, ZH
   Markowitz, SD
   Willis, J
   Ellis, LM
   Wang, R
AF Rathore, Moeez
   Zhang, Wei
   Wright, Michel'le
   Bhattacharya, Rajat
   Fan, Fan
   Vaziri-Gohar, Ali
   Winter, Jordan
   Wang, Zhenghe
   Markowitz, Sanford D.
   Willis, Joseph
   Ellis, Lee M.
   Wang, Rui
TI Liver Endothelium Promotes HER3-Mediated Cell Survival in Colorectal
   Cancer with Wild-Type and Mutant <i>KRAS</i>
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
AB We previously identified that human epidermal growth factor receptor 3 (HER3, also known as ERBB3) is a key mediator in liver endothelial cell (EC) promoting colorectal cancer growth and chemoresistance, and suggested HER3-targeted therapy as a strategy for treating patients with metastatic colorectal cancer in the liver. Meanwhile, KRAS mutations occur in 40%-50% of metastatic colorectal cancer and render colorectal cancer resistant to therapies targeting the other HER family protein epidermal growth factor receptor (EGFR). It is necessary to elucidate the roles of KRAS mutation status in HER3-mediated cell survival and colorectal cancer response to HER3 inhibition. In the present study, we used primary ECs isolated from non-neoplastic liver tissues to recapitulate the liver EC microenvironment. We demonstrated that liver EC-secreted factors activated colorectal cancer-associated HER3, and increased colorectal cancer cell survival in vitro and promoted colorectal cancer patient-derived xenograft tumor growth in vivo. Moreover, we determined that blocking HER3, either by siRNA knockdown or the humanized antibody seribantumab, blocked EC-induced colorectal cancer survival in vitro in both KRAS wild-type and mutant colorectal cancer cells, and the HER3 antibody seribantumab significantly decreased colorectal cancer tumor growth and sensitized tumors to chemotherapy in an orthotopic xenograft model with colorectal cancer tumors developed in the liver. In summary, our findings demonstrated that blocking HER3 had significant effects on attenuating liver EC-induced colorectal cancer cell survival independent of the KRAS mutation status. Implications: This body of work highlighted a potential strategy of using HER3 antibodies in combination with standard chemotherapy agents for treating patients with either KRAS wild-type or KRAS mutant metastatic colorectal cancer.
C1 [Rathore, Moeez; Zhang, Wei; Wright, Michel'le; Vaziri-Gohar, Ali; Winter, Jordan; Wang, Rui] Case Western Reserve Univ, Dept Surg, Cleveland, OH 44106 USA.
   [Rathore, Moeez; Zhang, Wei; Wright, Michel'le; Vaziri-Gohar, Ali; Winter, Jordan; Wang, Zhenghe; Markowitz, Sanford D.; Willis, Joseph; Wang, Rui] Case Western Reserve Univ, Case Comprehens Canc Ctr, Cleveland, OH 44106 USA.
   [Bhattacharya, Rajat; Fan, Fan; Ellis, Lee M.] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX USA.
   [Winter, Jordan; Wang, Rui] Univ Hosp Cleveland, Med Ctr, Dept Surg, Div Surg Oncol, Cleveland, OH USA.
   [Wang, Zhenghe] Case Western Reserve Univ, Dept Genet & Genome Sci, Cleveland, OH 44106 USA.
   [Markowitz, Sanford D.] Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA.
   [Willis, Joseph] Case Western Reserve Univ, Univ Hosp, Cleveland, OH 44106 USA.
   [Willis, Joseph] Univ Hosp Cleveland, Med Ctr, Cleveland, OH USA.
   [Ellis, Lee M.] Univ Texas MD Anderson Canc Ctr, Dept Mol Oncol, Houston, TX USA.
   [Ellis, Lee M.] Univ Texas MD Anderson Canc Ctr, Dept Mol Oncol, Houston, TX USA.
C3 University System of Ohio; Case Western Reserve University; University
   System of Ohio; Case Western Reserve University; University of Texas
   System; UTMD Anderson Cancer Center; University System of Ohio; Case
   Western Reserve University; Case Western Reserve University Hospital;
   University Hospitals of Cleveland; University System of Ohio; Case
   Western Reserve University; University System of Ohio; Case Western
   Reserve University; University Hospitals of Cleveland; University System
   of Ohio; Case Western Reserve University; University Hospitals of
   Cleveland; University System of Ohio; Case Western Reserve University;
   Case Western Reserve University Hospital; University of Texas System;
   UTMD Anderson Cancer Center; University of Texas System; UTMD Anderson
   Cancer Center
RP Wang, R (corresponding author), Case Western Reserve Univ, Univ Hosp Cleveland, Med Ctr, Dept Surg, 10900 Euclid Ave Wolstein Res Bldg Room 2127, Cleveland, OH 44106 USA.
EM Rui.Wang17@case.edu
RI wang, zhenghe/KXQ-5620-2024; Wang, Rui/JFJ-5076-2023
OI Bhattacharya, Rajat/0000-0001-5693-6754; Wang, Rui/0000-0001-5794-7201;
   Wang, Zhenghe/0000-0003-1546-1080; Vaziri-Gohar, Ali/0000-0002-6924-8691
FU NIH [R00CA225756, P30CA016672, P30CA043703, 5P50CA150964-08]; DOD
   [CA171038]
FX This project was supported by the NIH grant R00CA225756 (R. Wang), the
   NIH GI SPORE grant 5P50CA150964-08 (R. Wang), the DOD grant CA171038
   (L.M. Ellis), and the NIH institutional grants P30CA016672 (MDACC CCSG),
   and P30CA043703 (CWRU CCSG).
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NR 50
TC 3
Z9 3
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
EI 1557-3125
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD JUN 3
PY 2022
VL 20
IS 6
BP 996
EP 1008
DI 10.1158/1541-7786.MCR-21-0633
PG 13
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA VO0QB
UT WOS:001285555600011
PM 35276002
OA Green Accepted, Bronze, Green Submitted
DA 2025-01-04
ER

PT J
AU Pung, HS
   Tye, GJ
   Leow, CH
   Ng, WK
   Lai, NS
AF Pung, Hai Shin
   Tye, Gee Jun
   Leow, Chiuan Herng
   Ng, Woei Kean
   Lai, Ngit Shin
TI Generation of peptides using phage display technology for cancer
   diagnosis and molecular imaging
SO MOLECULAR BIOLOGY REPORTS
LA English
DT Review
DE Phage display; Peptide-based phage display library; Cancer diagnosis;
   Molecular imaging; Nanoparticle conjugation
ID IN-VIVO; DRUG-DELIVERY; LUNG-CANCER; COLORECTAL-CANCER; QUANTUM DOTS;
   IDENTIFICATION; BINDING; NANOPARTICLES; FIBRONECTIN; METASTASIS
AB Cancer is one of the leading causes of mortality worldwide; nearly 10 million people died from it in 2020. The high mortality rate results from the lack of effective screening approaches where early detection cannot be achieved, reducing the chance of early intervention to prevent cancer development. Non-invasive and deep-tissue imaging is useful in cancer diagnosis, contributing to a visual presentation of anatomy and physiology in a rapid and safe manner. Its sensitivity and specificity can be enhanced with the application of targeting ligands with the conjugation of imaging probes. Phage display is a powerful technology to identify antibody- or peptide-based ligands with effective binding specificity against their target receptor. Tumour-targeting peptides exhibit promising results in molecular imaging, but the application is limited to animals only. Modern nanotechnology facilitates the combination of peptides with various nanoparticles due to their superior characteristics, rendering novel strategies in designing more potent imaging probes for cancer diagnosis and targeting therapy. In the end, a myriad of peptide candidates that aimed for different cancers diagnosis and imaging in various forms of research were reviewed.
C1 [Pung, Hai Shin; Tye, Gee Jun; Leow, Chiuan Herng; Lai, Ngit Shin] Univ Sains Malaysia, Inst Res Mol Med INFORMM, George Town, Malaysia.
   [Ng, Woei Kean] AIMST Univ, Fac Med, Bedong 08100, Kedah, Malaysia.
C3 Universiti Sains Malaysia; AIMST University
RP Lai, NS (corresponding author), Univ Sains Malaysia, Inst Res Mol Med INFORMM, George Town, Malaysia.
EM laingitshin@usm.my
RI ng, woei/AAO-8342-2020; TYE, GEE/F-4559-2014; Leow, Chiuan/F-8877-2014
FU Institute for Research in Molecular Medicine (INFORMM), Universiti Sains
   Malaysia
FX The authors express gratitude to the Institute for Research in Molecular
   Medicine (INFORMM), Universiti Sains Malaysia for their support. We
   would also like to thank Gan Shin Yi for her kind guidance.
CR Abraham R, 2005, J BIOL CHEM, V280, P34123, DOI 10.1074/jbc.M508155200
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NR 87
TC 10
Z9 11
U1 12
U2 27
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0301-4851
EI 1573-4978
J9 MOL BIOL REP
JI Mol. Biol. Rep.
PD MAY
PY 2023
VL 50
IS 5
BP 4653
EP 4664
DI 10.1007/s11033-023-08380-x
EA APR 2023
PG 12
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA E3OQ2
UT WOS:000964421400001
PM 37014570
OA Bronze, Green Published
DA 2025-01-04
ER

PT J
AU Shao, YF
   Jia, HT
   Huang, L
   Li, SC
   Wang, CX
   Aikemu, B
   Yang, G
   Hong, HJ
   Yang, X
   Zhang, S
   Sun, J
   Zheng, MH
AF Shao, Yanfei
   Jia, Hongtao
   Huang, Ling
   Li, Shuchun
   Wang, Chenxing
   Aikemu, Batuer
   Yang, Guang
   Hong, Hiju
   Yang, Xiao
   Zhang, Sen
   Sun, Jing
   Zheng, Minhua
TI An Original Ferroptosis-Related Gene Signature Effectively Predicts the
   Prognosis and Clinical Status for Colorectal Cancer Patients
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; ferroptosis; gene signature; prognostic model; drug
   sensitivity
ID CELL-DEATH; METABOLISM; MECHANISMS; TARGET; NRF2
AB Background Colorectal cancer (CRC) is one of the most common malignant tumors in the world. Ferroptosis is a newly defined form of cell death, distinguished by different morphology, biochemistry, and genetics, and involved in CRC progression and treatment. This study aims to establish a predictive model to elucidate the relationship between ferroptosis and prognosis of CRC patients, to explore the potential value of ferroptosis in therapeutic options. Methods The ferroptosis-related genes were obtained from the GeneCards and FerrDb websites. The limma R package was used to screen the differential ferroptosis-related genes (DEGs) in CRC from The Cancer Genome Atlas (TCGA) dataset. The least absolute shrinkage and selection operator (LASSO) and multivariate Cox regressions were to establish the 10-gene prognostic signature. The survival and receiver operating characteristic (ROC) curves were illustrated to evaluate the predictive effect of the signature. Besides, independent prognostic factors, downstream functional enrichment, drug sensitivity, somatic mutation status, and immune feature were analyzed. Moreover, all these conclusions were verified by using multiple datasets in International Cancer Genome Consortium (ICGC) and Gene Expression Omnibus (GEO). Results Ten ferroptosis-related gene signature (TFAP2C, SLC39A8, NOS2, HAMP, GDF15, FDFT1, CDKN2A, ALOX12, AKR1C1, ATP6V1G2) was established to predict the prognosis of CRC patients by Lasso cox analysis, demonstrating a good performance on Receiver operating characteristic (ROC) and Kaplan-Meier (K-M) analyses. The CRC patients in the high- or low-risk group showed significantly different fractions of immune cells, such as macrophage cells and CD8+ T cells. Drug sensitivity and somatic mutation status like TP53 were also closely associated with the risk scores. Conclusions In this study, we identified a novel ferroptosis-related 10-gene signature, which could effectively predict the prognosis and survival time of CRC patients, and provide meaningful clinical implications for targeted therapy or immunotherapy. Targeting ferroptosis is a good therapeutic option for CRC patients. Further studies are needed to reveal the underlying mechanisms of ferroptosis in CRC.
C1 [Shao, Yanfei; Jia, Hongtao; Huang, Ling; Li, Shuchun; Wang, Chenxing; Aikemu, Batuer; Yang, Guang; Hong, Hiju; Yang, Xiao; Zhang, Sen; Sun, Jing; Zheng, Minhua] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Gen Surg, Shanghai, Peoples R China.
   [Shao, Yanfei; Jia, Hongtao; Huang, Ling; Li, Shuchun; Wang, Chenxing; Aikemu, Batuer; Yang, Guang; Hong, Hiju; Yang, Xiao; Zhang, Sen; Sun, Jing; Zheng, Minhua] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Shanghai Minimally Invas Surg, Shanghai, Peoples R China.
   [Shao, Yanfei; Jia, Hongtao; Huang, Ling; Zhang, Sen] 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; Shanghai
   Jiao Tong University
RP Zhang, S; Sun, J (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Gen Surg, Shanghai, Peoples R China.; Zhang, S; Sun, J (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Shanghai Minimally Invas Surg, Shanghai, Peoples R China.; Zhang, S (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Shanghai Inst Digest Surg, Shanghai, Peoples R China.
EM zhangsen6886@163.com; sj11788@rjh.com.cn
RI huang, ling/KLC-7916-2024; zhang, sen/GXH-3513-2022; yang,
   guang/AAV-2451-2021
OI Yang, Guang/0000-0001-6079-5093
FU Youth Cultivation Project of Ruijin Hospital [KY2021611]; National
   Nature Science Foundation of China (NSFC) [81871984]
FX This research was funded by Youth Cultivation Project of Ruijin Hospital
   (Grant No. KY2021611) and the National Nature Science Foundation of
   China (NSFC) (Grant No. 81871984).
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NR 69
TC 63
Z9 63
U1 0
U2 43
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JUN 24
PY 2021
VL 11
AR 711776
DI 10.3389/fonc.2021.711776
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TF2YD
UT WOS:000670576900001
PM 34249766
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Li, ZS
   Wang, SQ
   Guo, T
   Yan, XY
   Chen, CQ
   Zhang, WJ
   Zhao, JY
   Zhang, JR
   Zhao, SL
   Wang, Y
   Qi, YF
   Gu, CD
AF Li, Zhuoshi
   Wang, Shiqing
   Guo, Tao
   Yan, Xinyi
   Chen, Chaoqun
   Zhang, Wenjing
   Zhao, Jinyao
   Zhang, Jinrui
   Zhao, Shilei
   Wang, Yang
   Qi, Yangfan
   Gu, Chundong
TI MACC1 ablation suppresses the dedifferentiation process of non-CSCs in
   lung cancer through stabilizing KLF4
SO CELL DEATH DISCOVERY
LA English
DT Article
ID CELL-LIKE PROPERTIES; STEM-CELLS; ADENOCARCINOMA; PROGRESSION;
   EXPRESSION; PLASTICITY; APOPTOSIS; MIGRATION; INVASION; MARKERS
AB Metastasis-associated in colon cancer-1 (MACC1) was identified as a new player in lung cancer development, and some stemness-related genes can be novel transcriptional targets of MACC1. Cancer stem cells (CSCs) are responsible for sustaining tumorigenesis and plasticity. Both CSCs and non-CSCs are plastic and capable of undergoing phenotypic transition, especially the dedifferentiation of non-CSCs switch to CSC-like cells. However, the precise role of MACC1 during this process is largely unknown. Here, we showed that MACC1 promoted the transition from non-CSC to CSC in lung cancer. We found MACC1 was overexpressed in stemness enriched cells, enhancing the transition from no-CSCs to CSCs, while short-hairpin RNA-mediated Knockdown of MACC1 impaired this process. High-throughput sequencing and tumor specimen analysis revealed that MACC1 was negative correlated with Kr & uuml;ppel-like factor 4 (KLF4) expression level, which acts as a negative stemness regulator in lung cancer. Mechanistically, MACC1 delays the degradation of KLF4 mRNA by repressing the expression of microRNA-25, thereby promoting the KLF4 mRNA stabilization at the post-transcriptional level. Collectively, our findings may facilitate efforts to promote the development of precision targeted therapy for cancer stem cells in lung cancer.
C1 [Li, Zhuoshi; Wang, Shiqing; Guo, Tao; Zhao, Shilei; Gu, Chundong] Dalian Med Univ, Dept Thorac Surg, Affiliated Hosp 1, Dalian 116044, Peoples R China.
   [Li, Zhuoshi; Wang, Shiqing; Guo, Tao; Zhao, Shilei; Gu, Chundong] Dalian Med Univ, Affiliated Hosp 1, Lung Canc Diag & Treatment Ctr Dalian, Dalian 116011, Liaoning, Peoples R China.
   [Yan, Xinyi] Dalian Univ Technol, Dept Nephrol, Dalian Municipal Cent Hosp, Dalian 116033, Peoples R China.
   [Chen, Chaoqun; Zhang, Wenjing; Zhao, Jinyao; Zhang, Jinrui; Wang, Yang; Qi, Yangfan] Dalian Med Univ, Inst Canc Stem Cell, Dalian 116044, Peoples R China.
RP Gu, CD (corresponding author), Dalian Med Univ, Dept Thorac Surg, Affiliated Hosp 1, Dalian 116044, Peoples R China.; Gu, CD (corresponding author), Dalian Med Univ, Affiliated Hosp 1, Lung Canc Diag & Treatment Ctr Dalian, Dalian 116011, Liaoning, Peoples R China.; Qi, YF (corresponding author), Dalian Med Univ, Inst Canc Stem Cell, Dalian 116044, Peoples R China.
EM yangfanshy@163.com; guchundong@dmu.edu.cn
RI 陈, 超群/HOF-7394-2023; Wang, Shiqing/IWM-0467-2023
FU National Natural Science Foundation of China (National Science
   Foundation of China)
FX We acknowledge Prof. Chuanchun Han for his generously sharing the
   vectors of KLF4. We acknowledge Prof. Guangzhe Li for his contribution
   on language polishing.
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NR 56
TC 0
Z9 0
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2058-7716
J9 CELL DEATH DISCOV
JI Cell Death Discov.
PD DEC 18
PY 2024
VL 10
IS 1
AR 494
DI 10.1038/s41420-024-02256-0
PG 14
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA P8B2J
UT WOS:001380088800015
PM 39695175
DA 2025-01-04
ER

PT J
AU Xu, DH
   Luo, YH
   Wang, P
   Li, JX
   Ma, LR
   Huang, J
   Zhang, H
   Yang, XM
   Li, LQ
   Zheng, YH
   Fang, G
   Yan, PY
AF Xu, Donghan
   Luo, Yehao
   Wang, Peng
   Li, Jiaxin
   Ma, Linrui
   Huang, Jie
   Zhang, Hao
   Yang, Xiaoman
   Li, Liqi
   Zheng, Yuhong
   Fang, Gang
   Yan, Peiyu
TI Clinical progress of anti-angiogenic targeted therapy and combination
   therapy for gastric cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE gastric cancer; anti-angiogenic; tyrosine kinase inhibitor; response
   biomarker; clinical progress
ID ENDOTHELIAL GROWTH-FACTOR; MULTICENTER PHASE-II; METASTATIC
   COLORECTAL-CANCER; RAMUCIRUMAB PLUS PACLITAXEL; NONSMALL CELL LUNG;
   GASTROESOPHAGEAL JUNCTION; TUMOR ANGIOGENESIS; DOUBLE-BLIND; 2ND-LINE
   TREATMENT; REAL-WORLD
AB The incidence of gastric cancer is increasing year by year. Most gastric cancers are already in the advanced stage with poor prognosis when diagnosed, which means the current treatment is not satisfactory. Angiogenesis is an important link in the occurrence and development of tumors, and there are multiple anti-angiogenesis targeted therapies. To comprehensively evaluate the efficacy and safety of anti-angiogenic targeted drugs alone and in combination against gastric cancer, we systematically searched and sorted out relevant literature. In this review, we summarized the efficacy and safety of Ramucirumab, Bevacizumab, Apatinib, Fruquintinib, Sorafenib, Sunitinib, Pazopanib on gastric cancer when used alone or in combination based on prospective clinical trials reported in the literature, and sorted response biomarkers. We also summarized the challenges faced by anti-angiogenesis therapy for gastric cancer and available solutions. Finally, the characteristics of the current clinical research are summarized and suggestions and prospects are raised. This review will serve as a good reference for the clinical research of anti-angiogenic targeted drugs in the treatment of gastric cancer.
C1 [Xu, Donghan; Wang, Peng; Li, Jiaxin; Ma, Linrui; Huang, Jie; Zhang, Hao; Yang, Xiaoman; Li, Liqi; Zheng, Yuhong; Yan, Peiyu] Macau Univ Sci & Technol, Fac Chinese Med, Macau, Macao, Peoples R China.
   [Luo, Yehao] Guangzhou Univ Chinese Med, Sch Clin Med 2, Guangzhou, Peoples R China.
   [Fang, Gang] Guangxi Univ Chinese Med, Guangxi Key Lab Appl Fundamental Res Zhuang Med, Nanning, Peoples R China.
   [Yan, Peiyu] Macau Univ Sci & Technol, Zhuhai MUST Sci & Technol Res Inst, State Key Lab Qual Res Chinese Med, Macau, Macao, Peoples R China.
C3 Macau University of Science & Technology; Guangzhou University of
   Chinese Medicine; Guangxi University of Chinese Medicine; Macau
   University of Science & Technology
RP Yan, PY (corresponding author), Macau Univ Sci & Technol, Fac Chinese Med, Macau, Macao, Peoples R China.; Fang, G (corresponding author), Guangxi Univ Chinese Med, Guangxi Key Lab Appl Fundamental Res Zhuang Med, Nanning, Peoples R China.; Yan, PY (corresponding author), Macau Univ Sci & Technol, Zhuhai MUST Sci & Technol Res Inst, State Key Lab Qual Res Chinese Med, Macau, Macao, Peoples R China.
EM fglzyznn@gxtcmu.edu.cn; pyyan@must.edu.mo
RI Li, Jiaxin/GOV-4862-2022; Zhang, Wenbin/JXX-8070-2024
OI Li, Jiaxin/0000-0002-7489-8840
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NR 194
TC 3
Z9 5
U1 2
U2 14
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 12
PY 2023
VL 13
AR 1148131
DI 10.3389/fonc.2023.1148131
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA K0CC1
UT WOS:001013203000001
PM 37384288
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Choi, Y
   Park, NJY
   Le, TM
   Lee, E
   Lee, D
   Nguyen, HDT
   Cho, J
   Park, JY
   Han, HS
   Chong, GO
AF Choi, Yeseul
   Park, Nora Jee-Young
   Le, Tan Minh
   Lee, Eunmi
   Lee, Donghyeon
   Nguyen, Hong Duc Thi
   Cho, Junghwan
   Park, Ji-Young
   Han, Hyung Soo
   Chong, Gun Oh
TI Immune Pathway and Gene Database (IMPAGT) Revealed the Immune
   Dysregulation Dynamics and Overactivation of the PI3K/Akt Pathway in
   Tumor Buddings of Cervical Cancer
SO CURRENT ISSUES IN MOLECULAR BIOLOGY
LA English
DT Article
DE tumor budding; cervical cancer; RNA sequencing; differentially expressed
   genes; Gene Ontology; tumor immune microenvironment; immune profiling;
   immune database; PI3K; Akt signaling pathway
ID EPITHELIAL-MESENCHYMAL TRANSITION; SIGNALING PATHWAY; COLORECTAL-CANCER;
   GASTRIC-CANCER; PROGRESSION; DEGRADATION; INHIBITION; APOPTOSIS; GROWTH;
   EMT
AB Tumor budding (TB) is a small cluster of malignant cells at the invasive front of a tumor. Despite being an adverse prognosis marker, little research has been conducted on the tumor immune microenvironment of tumor buddings, especially in cervical cancer. Therefore, RNA sequencing was performed using 21 formalin-fixed, paraffin-embedded slides of cervical tissues, and differentially expressed genes (DEGs) were analyzed. Immune Pathway and Gene Database (IMPAGT) was generated for immune profiling. "Pathway in Cancer" was identified as the most enriched pathway for both up- and downregulated DEGs. Kyoto Encyclopedia of Genes and Genomes Mapper and Gene Ontology further revealed the activation of the PI3K/Akt signaling pathway. An IMPAGT analysis revealed immune dysregulation even at the tumor budding stage, especially in the PI3K/Akt/mTOR axis, with a high efficiency and integrity. These findings emphasized the clinical significance of tumor buddings and the necessity of blocking the overactivation of the PI3K/Akt/mTOR pathway to improve targeted therapy in cervical cancer.
C1 [Choi, Yeseul; Le, Tan Minh; Lee, Eunmi; Lee, Donghyeon; Nguyen, Hong Duc Thi; Han, Hyung Soo] Kyungpook Natl Univ, Grad Sch, Dept Biomed Sci, Daegu 41944, South Korea.
   [Choi, Yeseul; Le, Tan Minh; Lee, Eunmi; Lee, Donghyeon; Nguyen, Hong Duc Thi; Han, Hyung Soo] Kyungpook Natl Univ, Sch Med, BK21 Four Program, Daegu 41944, South Korea.
   [Park, Nora Jee-Young; Park, Ji-Young] Kyungpook Natl Univ, Sch Med, Dept Pathol, Daegu 41944, South Korea.
   [Park, Nora Jee-Young; Park, Ji-Young] Kyungpook Natl Univ, Dept Pathol, Chilgok Hosp, Daegu 41404, South Korea.
   [Park, Nora Jee-Young; Cho, Junghwan; Han, Hyung Soo; Chong, Gun Oh] Kyungpook Natl Univ, Clin Omics Inst, Daegu 41405, South Korea.
   [Han, Hyung Soo] Kyungpook Natl Univ, Sch Med, Dept Physiol, Daegu 41944, South Korea.
   [Chong, Gun Oh] Kyungpook Natl Univ, Sch Med, Dept Obstet & Gynecol, Daegu 41944, South Korea.
   [Chong, Gun Oh] Kyungpook Natl Univ, Dept Obstet & Gynecol, Chilgok Hosp, Daegu 41404, South Korea.
C3 Kyungpook National University (KNU); Kyungpook National University
   (KNU); Kyungpook National University (KNU); Kyungpook National
   University (KNU); Kyungpook National University (KNU); Kyungpook
   National University (KNU); Kyungpook National University (KNU);
   Kyungpook National University (KNU)
RP Han, HS (corresponding author), Kyungpook Natl Univ, Grad Sch, Dept Biomed Sci, Daegu 41944, South Korea.; Han, HS (corresponding author), Kyungpook Natl Univ, Sch Med, BK21 Four Program, Daegu 41944, South Korea.; Han, HS; Chong, GO (corresponding author), Kyungpook Natl Univ, Clin Omics Inst, Daegu 41405, South Korea.; Han, HS (corresponding author), Kyungpook Natl Univ, Sch Med, Dept Physiol, Daegu 41944, South Korea.; Chong, GO (corresponding author), Kyungpook Natl Univ, Sch Med, Dept Obstet & Gynecol, Daegu 41944, South Korea.; Chong, GO (corresponding author), Kyungpook Natl Univ, Dept Obstet & Gynecol, Chilgok Hosp, Daegu 41404, South Korea.
EM hshan@knu.ac.kr; gochong@knu.ac.kr
RI Cho, Junghwan/AAK-4752-2020; Nguyen, Minh-Hoang/GQO-9183-2022; Le,
   Tan/ITT-2150-2023
OI Nguyen, Hong Duc/0000-0003-0649-9175; Chong, Gun Oh/0000-0003-4887-4017;
   Lee, Olive/0000-0002-4150-2491; Le, Tan/0000-0002-9621-8877
FU National Research Foundation of Korea (NRF) - Korea government (MSIT)
   [NRF-2020R1F1A1076816, NRF-2022R1F1A1061498]; Brain Pool Program through
   the NRF - Ministry of Science and ICT [NRF-2020H1D3A2A02102040]
FX This research was supported by the National Research Foundation of Korea
   (NRF) grant funded by the Korea government (MSIT) (Nos.
   NRF-2020R1F1A1076816 and NRF-2022R1F1A1061498) and a grant of the Brain
   Pool Program through the NRF funded by the Ministry of Science and ICT
   (No. NRF-2020H1D3A2A02102040).
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NR 72
TC 6
Z9 7
U1 1
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1467-3037
EI 1467-3045
J9 CURR ISSUES MOL BIOL
JI Curr. Issues Mol. Biol.
PD NOV
PY 2022
VL 44
IS 11
BP 5139
EP 5152
DI 10.3390/cimb44110350
PG 14
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 6A8MV
UT WOS:000880903600001
PM 36354662
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Pachmayr, E
   Treese, C
   Stein, U
AF Pachmayr, Eva
   Treese, Christoph
   Stein, Ulrike
TI Underlying Mechanisms for Distant Metastasis - Molecular Biology
SO VISCERAL MEDICINE
LA English
DT Review
DE Metastasis; Molecular mechanism; Cancer therapy
ID COLORECTAL-CANCER; GASTRIC-CANCER; BETA-CATENIN; CELL MOTILITY;
   DOUBLE-BLIND; E-CADHERIN; TUMOR MICROENVIRONMENT; 1ST-LINE TREATMENT;
   PROGNOSTIC VALUE; SOLID TUMORS
AB Background: The formation of distant metastases constitutes a complex process with a variety of different genes and pathways involved. To improve patient survival, it is necessary to understand the underlying mechanisms of metastasis to allow for targeted intervention. Methods: This review provides an overview of the general concepts of metastasis, focusing on the most important genes and pathways involved and on interventional strategies. Results: Cancer cells undergo different steps to form metastasis: most prominently, local invasion, intravasation, survival in the circulation, arrest at a distant organ site and extravasation, micrometastasis formation, and metastatic colonization. In order to pass these steps, different molecular pathways are of major importance: EGF/RAS/RAF/MEK/ERK, PI3K/Akt/mTOR, HGF/Met, Wnt/beta-catenin, and VEGF signaling. The HGF/Met regulator MACC1 and the Wnt signaling target S100A4 have been shown to play a major role in the metastatic process. Each gene and pathway provides an opportunity for therapeutic intervention. Conclusion: Since metastasis represents a highly limiting factor in cancer therapy causing 90% of cancer deaths, it is imperative to reveal the underlying mechanisms. This is fundamental for uncovering prognostic markers and new targeted therapy options. (C) 2017 S. Karger GmbH, Freiburg
C1 [Pachmayr, Eva; Treese, Christoph; Stein, Ulrike] Charite Univ Med Berlin, Expt & Clin Res Ctr, Berlin, Germany.
   [Pachmayr, Eva; Treese, Christoph; Stein, Ulrike] Max Delbruck Ctr Mol Med, Robert Rossle Str 10, D-13125 Berlin, Germany.
   [Treese, Christoph] Charite Univ Med Berlin, Dept Gastroenterol, Infect Dis, Rheumatol,Campus Benjamin Franklin, Berlin, Germany.
   [Treese, Christoph] BIH, Berlin, Germany.
   [Stein, Ulrike] German Canc Consortium DKTK, 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;
   Helmholtz Association; German Cancer Research Center (DKFZ)
RP Stein, U (corresponding author), Max Delbruck Ctr Mol Med, Robert Rossle Str 10, D-13125 Berlin, Germany.
EM ustein@mdc-berlin.de
OI Treese, Christoph/0000-0001-9120-6773; Stein, Ulrike/0000-0001-7006-282X
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NR 112
TC 89
Z9 102
U1 0
U2 11
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 2297-4725
EI 2297-475X
J9 VISC MED
JI Visc. Med.
PY 2017
VL 33
IS 1
BP 11
EP 20
DI 10.1159/000454696
PG 10
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA EP0FW
UT WOS:000397063600003
PM 28785563
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Elhamamsy, AR
   Metge, BJ
   Alsheikh, HA
   Shevde, LA
   Samant, RS
AF Elhamamsy, Amr R.
   Metge, Brandon J.
   Alsheikh, Heba A.
   Shevde, Lalita A.
   Samant, Rajeev S.
TI Ribosome Biogenesis: A Central Player in Cancer Metastasis and
   Therapeutic Resistance
SO CANCER RESEARCH
LA English
DT Review
ID RNA-POLYMERASE I; PERINUCLEOLAR COMPARTMENT PREVALENCE; TRANSLATIONAL
   CONTROL; NONCODING RNAS; MULTIDRUG-RESISTANCE; COLORECTAL-CANCER;
   PROTEIN; CELLS; LEUKEMIA; GROWTH
AB Ribosomes are a complex ensemble of rRNA and ribosomal proteins that function as mRNA translation machines. Ribosome biogenesis is a multistep process that begins in the nucleolus and concludes in the cytoplasm. The process is tightly controlled by multiple checkpoint and surveillance pathways. Perturbations in these checkpoints and pathways can lead to hyperactivation of ribosome biogenesis. Emerging evidence suggests that cancer cells harbor a specialized class of ribosomes (onco-ribosomes) that facilitates the oncogenic translation program, modulates cellular functions, and promotes metabolic rewiring. Mutations in ribo-somal proteins, rRNA processing, and ribosome assembly factors result in ribosomopathies that are associated with an increased risk of developing malignancies. Recent studies have linked mutations in ribosomal proteins and aberrant ribosomes with poor prognosis, highlighting ribosome-targeted therapy as a promising approach for treating patients with cancer. Here, we summarize various aspects of dysregulation of ribosome biogenesis and the impact of resultant onco-ribosomes on malignant tumor behavior, therapeu-tic resistance, and clinical outcome. Ribosome biogenesis is a promising therapeutic target, and understanding the important determinants of this process will allow for improved and perhaps selective therapeutic strategies to target ribosome biosynthesis.
C1 [Elhamamsy, Amr R.; Metge, Brandon J.; Alsheikh, Heba A.; Shevde, Lalita A.; Samant, Rajeev S.] Univ Alabama Birmingham, Dept Pathol, Birmingham, AL USA.
   [Shevde, Lalita A.; Samant, Rajeev S.] Univ Alabama Birmingham, ONeal Comprehens Canc Ctr, Birmingham, AL USA.
   [Samant, Rajeev S.] Birmingham VA Med Ctr, Birmingham, AL USA.
   [Samant, Rajeev S.] Univ Alabama Birmingham, WTI 320E,1824 6th Ave South, Birmingham, AL 35233 USA.
C3 University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham; US
   Department of Veterans Affairs; Veterans Health Administration (VHA);
   Veterans Affairs Medical Center - Birmingham; University of Alabama
   System; University of Alabama Birmingham
RP Samant, RS (corresponding author), Univ Alabama Birmingham, WTI 320E,1824 6th Ave South, Birmingham, AL 35233 USA.
EM rsamant@uab.edu
OI Elhamamsy, Amr/0000-0001-8579-0184; Metge, Brandon/0000-0001-8615-2934;
   Samant, Rajeev/0000-0001-5681-4976; Alsheikh,
   HebaAllah/0000-0002-7006-5294
FU O?Neal Invests Award [W81XWH-18-1-0036, W81XWH-10-1-0755]; NCI/NIH
   [W81XWH-18-1-0036, W81XWH-10-1-0755]; O'Neal Invests Award; Department
   of Defense [I01 BX003374, CA194048]
FX The work is supported in part by I01 BX003374 (VA), CA194048 (NCI/NIH),
   and O'Neal Invests Award (to R.S. Samant); Department of Defense
   (W81XWH-18-1-0036 and W81XWH-10-1-0755) and O'Neal Invests Award (to
   L.A. Shevde).
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NR 141
TC 116
Z9 120
U1 16
U2 52
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 JUL 1
PY 2022
VL 82
IS 13
BP 2344
EP 2353
DI 10.1158/0008-5472.CAN-21-4087
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3G2OH
UT WOS:000831194700001
PM 35303060
OA hybrid, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Liu, J
   Huang, BJ
   Ding, FF
   Li, YM
AF Liu, Jie
   Huang, Binjie
   Ding, Feifei
   Li, Yumin
TI Environment factors, DNA methylation, and cancer
SO ENVIRONMENTAL GEOCHEMISTRY AND HEALTH
LA English
DT Review
DE DNA methylation; Environment; Cancer; Epigenetics; Prevention
ID TUMOR-SUPPRESSOR GENES; POLYCYCLIC AROMATIC-HYDROCARBONS; CPG ISLAND
   METHYLATION; ONE-CARBON METABOLISM; UMBILICAL-CORD BLOOD;
   COLORECTAL-CANCER; PROMOTER METHYLATION; HELICOBACTER-PYLORI;
   GASTRIC-CANCER; ALCOHOL-CONSUMPTION
AB Today, the rapid development of science and technology and the rapid change in economy and society are changing the way of life of human beings and affecting the natural, living, working, and internal environment on which human beings depend. At the same time, the global incidence of cancer has increased significantly yearly, and cancer has become the number one killer that threatens human health. Studies have shown that diet, living habits, residential environment, mental and psychological factors, intestinal flora, genetics, social factors, and viral and non-viral infections are closely related to human cancer. However, the molecular mechanisms of the environment and cancer development remain to be further explored. In recent years, DNA methylation has become a key hub and bridge for environmental and cancer research. Some environmental factors can alter the hyper/hypomethylation of human cancer suppressor gene promoters, proto-oncogene promoters, and the whole genome, causing low/high expression or gene mutation of related genes, thereby exerting oncogenic or anticancer effects. It is expected to develop early warning markers of cancer environment based on DNA methylation, thereby providing new methods for early detection of cancers, diagnosis, and targeted therapy. This review systematically expounds on the internal mechanism of environmental factors affecting cancer by changing DNA methylation, aiming to help establish the concept of cancer prevention and improve people's health.
C1 [Liu, Jie; Huang, Binjie; Ding, Feifei; Li, Yumin] Lanzhou Univ, Dept Gen Surg, Hosp 2, Lan Zhou, Peoples R China.
   [Liu, Jie; Huang, Binjie; Ding, Feifei; Li, Yumin] Lanzhou Univ, Key Lab Digest Syst Tumors Gansu Prov, Hosp 2, Lan Zhou, Peoples R China.
C3 Lanzhou University; Lanzhou University
RP Li, YM (corresponding author), Lanzhou Univ, Dept Gen Surg, Hosp 2, Lan Zhou, Peoples R China.
EM liym@lzu.edu.cn
RI DING, FEI/KLD-8925-2024
FU Fundamental Research Funds for the Central Universities
   [lzujbky2022-sp08]; Project of Gansu Provincial Department of Education
   [2021jyjbgs-02]; Project of Gansu Provincial Development and Reform
   Commission [2020-2022]; Major Science and Technology Project of Gansu
   Province [20zd7fa003]; Medical Innovation and Development Project of
   Lanzhou University [lzuyxcx-2022-154, lzuyxcx-2022-141]
FX This work was supported by the Fundamental Research Funds for the
   Central Universities [lzujbky-2022-sp08]; Project of Gansu Provincial
   Department of Education [2021jyjbgs-02]; Project of Gansu Provincial
   Development and Reform Commission [2020-2022]; Major Science and
   Technology Project of Gansu Province [20zd7fa003]; Medical Innovation
   and Development Project of Lanzhou University [lzuyxcx-2022-154,
   lzuyxcx-2022-141].
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NR 192
TC 13
Z9 13
U1 4
U2 24
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0269-4042
EI 1573-2983
J9 ENVIRON GEOCHEM HLTH
JI Environ. Geochem. Health
PD NOV
PY 2023
VL 45
IS 11
BP 7543
EP 7568
DI 10.1007/s10653-023-01749-8
EA SEP 2023
PG 26
WC Engineering, Environmental; Environmental Sciences; Public,
   Environmental & Occupational Health; Water Resources
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Environmental Sciences & Ecology; Public, Environmental &
   Occupational Health; Water Resources
GA W9YA7
UT WOS:001067812300002
PM 37715840
DA 2025-01-04
ER

PT J
AU Dobre, M
   Boscencu, R
   Neagoe, IV
   Surcel, M
   Milanesi, E
   Manda, G
AF Dobre, Maria
   Boscencu, Rica
   Neagoe, Ionela Victoria
   Surcel, Mihaela
   Milanesi, Elena
   Manda, Gina
TI Insight into the Web of Stress Responses Triggered at Gene Expression
   Level by Porphyrin-PDT in HT29 Human Colon Carcinoma Cells
SO PHARMACEUTICS
LA English
DT Article
DE photodynamic therapy; colon carcinoma cells; stress responses
ID PHOTODYNAMIC THERAPY; COLORECTAL-CANCER; INDUCED APOPTOSIS; HYPOXIA;
   PROTEIN; DEATH; SURVIVAL; P53; TRANSCRIPTION; COMBINATION
AB Photodynamic therapy (PDT), a highly targeted therapy with acceptable side effects, has emerged as a promising therapeutic option in oncologic pathology. One of the issues that needs to be addressed is related to the complex network of cellular responses developed by tumor cells in response to PDT. In this context, this study aims to characterize in vitro the stressors and the corresponding cellular responses triggered by PDT in the human colon carcinoma HT29 cell line, using a new asymmetric porphyrin derivative (P2.2) as a photosensitizer. Besides investigating the ability of P2.2-PDT to reduce the number of viable tumor cells at various P2.2 concentrations and fluences of the activating light, we assessed, using qRT-PCR, the expression levels of 84 genes critically involved in the stress response of PDT-treated cells. Results showed a fluence-dependent decrease of viable tumor cells at 24 h post-PDT, with few cells that seem to escape from PDT. We highlighted following P2.2-PDT the concomitant activation of particular cellular responses to oxidative stress, hypoxia, DNA damage and unfolded protein responses and inflammation. A web of inter-connected stressors was induced by P2.2-PDT, which underlies cell death but also elicits protective mechanisms that may delay tumor cell death or even defend these cells against the deleterious effects of PDT.
C1 [Dobre, Maria; Neagoe, Ionela Victoria; Surcel, Mihaela; Milanesi, Elena; Manda, Gina] Victor Babes Natl Inst Pathol, Radiobiol Dept, 99-101 Splaiul Independentei, Bucharest 050096, Romania.
   [Boscencu, Rica] Carol Davila Univ Med & Pharm, Fac Pharm, 6 Traian Vuia St, Bucharest 020956, Romania.
C3 Victor Babes National Institute of Pathology; Carol Davila University of
   Medicine & Pharmacy
RP Manda, G (corresponding author), Victor Babes Natl Inst Pathol, Radiobiol Dept, 99-101 Splaiul Independentei, Bucharest 050096, Romania.
EM maria_dobre70@yahoo.com; rboscencu@yahoo.com; neagoevictoria@gmail.com;
   msurcel2002@yahoo.com; elena.k.milanesi@gmail.com; gina.manda@gmail.com
RI Victoria, Neagoe/AAT-1827-2021; Dobre, Maria/AAT-1781-2021; Milanesi,
   Elena/J-9489-2014; Surcel, Mihaela/AFS-0892-2022; Manda,
   Gina/B-7205-2011
OI Surcel, Mihaela/0000-0001-5163-4378; Dobre, Maria/0000-0002-1376-4021;
   Manda, Gina/0000-0002-9706-1883; Milanesi, Elena/0000-0003-2753-3395
FU Romanian Ministry of Research, Innovation and Digitization [PCCDI
   64/2018, PN 19.29.02.02]; European Regional Development Fund,
   Competitiveness Operational Program 2014-2020 [P_37_732/2016 REDBRAIN]
FX This research was funded by the Romanian Ministry of Research,
   Innovation and Digitization, grant number PCCDI 64/2018. Publication
   charges were funded by the Romanian Ministry of Research, Innovation and
   Digitization, grant PN 19.29.02.02 (Nucleu Programme). EM is recipient
   of a post-doctoral contract of the European Regional Development Fund,
   Competitiveness Operational Program 2014-2020, through the grant
   P_37_732/2016 REDBRAIN.
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NR 98
TC 7
Z9 8
U1 0
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD JUL
PY 2021
VL 13
IS 7
AR 1032
DI 10.3390/pharmaceutics13071032
PG 25
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA TO2DA
UT WOS:000676728100001
PM 34371724
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Singh, G
   Kutcher, D
   Lally, R
   Rai, V
AF Singh, Gurkaranjot
   Kutcher, Drew
   Lally, Rajeshwar
   Rai, Vikrant
TI Targeting Neoantigens in Pancreatic Ductal Adenocarcinoma
SO CANCERS
LA English
DT Review
DE pancreatic ductal adenocarcinoma; chemotherapy; immunotherapy; treatment
   resistance; neoantigens; targeted therapy; personalized therapy
ID GEMCITABINE RESISTANCE; ABC TRANSPORTERS; DRUG-RESISTANCE; CANCER;
   IMMUNOTHERAPY; VACCINE; GENE; MUTATIONS; CELLS; ZEB1
AB Simple Summary Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer deaths in the United States due to its late-stage diagnosis. Currently, there are no early diagnostic tests. The best treatment for PDAC is surgery, but by then, the cancer has already spread, making it difficult to perform. This study aims to address the potential of targeting neoantigens, unique cancer-specific proteins that trigger an immune response, as potential immunotherapy targets. However, PDAC develops characteristics such as immune cell avoidance, creating an environment suppressing immune cells, and converting cells to become unstable. Targeting neoantigens could revolutionize PDAC therapy, offering better survival rates. Though trials are still in the early stages, they do offer a greater understanding and potential for fighting cancer. This article hopes to shed light and pave the way for innovative treatments to improve the prognosis of PDAC patients.Abstract Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer and is currently the third leading cause of cancer-related death in the United States after lung and colon cancer. PDAC is estimated to be the second leading cause of cancer-related death by 2030. The diagnosis at a late stage is the underlying cause for higher mortality and poor prognosis after surgery. Treatment resistance to chemotherapy and immunotherapy results in recurrence after surgery and poor prognosis. Neoantigen burden and CD8+ T-cell infiltration are associated with clinical outcomes in PDAC and paucity of neoantigen-reactive tumor-infiltrating lymphocytes may be the underlying cause for treatment resistance for immunotherapy. This suggests a need to identify additional neoantigens and therapies targeting these neoantigens to improve clinical outcomes in PDAC. In this review, we focus on describing the pathophysiology, current treatment strategies, and treatment resistance in PDAC followed by the need to target neoantigens in PDAC.
C1 [Singh, Gurkaranjot; Kutcher, Drew; Lally, Rajeshwar; Rai, Vikrant] Western Univ Hlth Sci, Coll Osteopath Med Pacific, Dept Translat Res, Pomona, CA 91766 USA.
C3 Western University of Health Sciences
RP Rai, V (corresponding author), Western Univ Hlth Sci, Coll Osteopath Med Pacific, Dept Translat Res, Pomona, CA 91766 USA.
EM gurkaranjot.singh@westernu.edu; drew.kutcher@westernu.edu;
   rajeshwar.lally@westernu.edu; vrai@westernu.edu
RI Rai, Vikrant/J-3680-2019
OI Rai, Vikrant/0000-0001-6286-2341
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NR 105
TC 4
Z9 4
U1 1
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUN
PY 2024
VL 16
IS 11
AR 2101
DI 10.3390/cancers16112101
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UA9O5
UT WOS:001245461200001
PM 38893220
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wu, ML
   Huang, QR
   Xie, Y
   Wu, XY
   Ma, HB
   Zhang, YW
   Xia, Y
AF Wu, Mengling
   Huang, Qianrui
   Xie, Yao
   Wu, Xuyi
   Ma, Hongbo
   Zhang, Yiwen
   Xia, Yong
TI Improvement of the anticancer efficacy of PD-1/PD-L1 blockade via
   combination therapy and PD-L1 regulation
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Review
DE Immunotherapy; PD-1; PD-L1; Combination therapy; PD-L1 regulation
ID CELL LUNG-CANCER; IMMUNE-CHECKPOINT BLOCKADE; TUMOR-INFILTRATING
   LYMPHOCYTES; PROMOTES ANTITUMOR IMMUNITY; T-CELLS; UP-REGULATION;
   OPEN-LABEL; PROGRAMMED DEATH-1; ANTI-PD-1 ANTIBODY; COLON-CANCER
AB Immune checkpoint molecules are promising anticancer targets, among which therapeutic antibodies targeting the PD-1/PD-L1 pathway have been widely applied to cancer treatment in clinical practice and have great potential. However, this treatment is greatly limited by its low response rates in certain cancers, lack of known biomarkers, immune-related toxicity, innate and acquired drug resistance, etc. Overcoming these limitations would significantly expand the anticancer applications of PD-1/PD-L1 blockade and improve the response rate and survival time of cancer patients. In the present review, we first illustrate the biological mechanisms of the PD-1/PD-L1 immune checkpoints and their role in the healthy immune system as well as in the tumor microenvironment (TME). The PD-1/PD-L1 pathway inhibits the anticancer effect of T cells in the TME, which in turn regulates the expression levels of PD-1 and PD-L1 through multiple mechanisms. Several strategies have been proposed to solve the limitations of anti-PD-1/PD-L1 treatment, including combination therapy with other standard treatments, such as chemotherapy, radiotherapy, targeted therapy, anti-angiogenic therapy, other immunotherapies and even diet control. Downregulation of PD-L1 expression in the TME via pharmacological or gene regulation methods improves the efficacy of anti-PD-1/PD-L1 treatment. Surprisingly, recent preclinical studies have shown that upregulation of PD-L1 in the TME also improves the response and efficacy of immune checkpoint blockade. Immunotherapy is a promising anticancer strategy that provides novel insight into clinical applications. This review aims to guide the development of more effective and less toxic anti-PD-1/PD-L1 immunotherapies.
C1 [Wu, Mengling; Huang, Qianrui; Wu, Xuyi; Ma, Hongbo; Zhang, Yiwen; Xia, Yong] Sichuan Univ, Dept Rehabil Med, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.
   [Wu, Mengling; Huang, Qianrui; Wu, Xuyi; Ma, Hongbo; Zhang, Yiwen; Xia, Yong] Sichuan Univ, Ctr Canc, Natl Clin Res Ctr Geriatr, West China Hosp, Chengdu 610041, Peoples R China.
   [Xie, Yao] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Dept Obstet & Gynaecol, Chengdu 610072, Peoples R China.
   [Xie, Yao] Chinese Acad Sci Sichuan Translat Med Res Hosp, Chengdu 610072, Peoples R China.
   [Wu, Xuyi; Xia, Yong] Rehabil Med Res Inst, Key Lab Rehabil Med Sichuan Prov, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan Provincial People's
   Hospital; University of Electronic Science & Technology of China
RP Zhang, YW; Xia, Y (corresponding author), Sichuan Univ, Dept Rehabil Med, State Key Lab Biotherapy, Chengdu 610041, Peoples R China.; Zhang, YW; Xia, Y (corresponding author), Sichuan Univ, Ctr Canc, Natl Clin Res Ctr Geriatr, West China Hosp, Chengdu 610041, Peoples R China.
EM yiwenzhang@scu.edu.cn; yxia4@scu.edu.cn
RI Xia, Yong/E-8689-2013; ZHANG, YIWEN/JYP-9193-2024
FU National Natural Science Foundation of China [82173280]; Chengdu Science
   and Technology Bureau International Cooperation Project
   [2019-GH02-00036-HZ]; Department of Science and Technology of Sichuan
   Province [2021YJ0450]
FX This work was supported by the National Natural Science Foundation of
   China (Grant No. 82173280), the Chengdu Science and Technology Bureau
   International Cooperation Project (Grant Number: 2019-GH02-00036-HZ) and
   the Department of Science and Technology of Sichuan Province (Grant
   Number: 2021YJ0450).
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NR 316
TC 222
Z9 242
U1 35
U2 338
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 MAR 12
PY 2022
VL 15
IS 1
AR 24
DI 10.1186/s13045-022-01242-2
PG 58
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA ZR7BT
UT WOS:000767934400001
PM 35279217
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Aznab, M
   Roozbahani, NE
   Moazen, H
AF Aznab, Mozaffar
   Roozbahani, Narges Eskandari
   Moazen, Homa
TI Clinical Characteristics and Risk Factors of COVID-19 in 60 Adult Cancer
   Patients
SO CLINICAL MEDICINE INSIGHTS-ONCOLOGY
LA English
DT Article
DE Risk factor; hematologic neoplasms; COVID-19; malignant neoplasms;
   mortality
AB BACKGROUND: During the pandemic of COVID-19, cancer patients have been considered as one high-risk group in the morbidity and mortality of COVID-19. This study aimed to describe the clinical symptoms and risk factors of COVID-19 in cancer patients.
   METHOD: In a prospective cross-sectional study, during a year, all cancer patients who underwent chemotherapy and/or targeted therapy in our clinic (Kermanshah, Iran) were followed up in terms of getting COVID-19. We analyzed the effect of tumor features and demographic information on clinical manifestations, survival status, therapeutic outcomes, and severity of the disease COVID-19 in 2 categories of cancer (hematologic and solid cancers).
   RESULTS: Most of the patients (68%) were in the solid tumor category, including breast cancer (24.4%), colon cancer (22%), and gastric cancer (9.8%). There was a statistically significant difference between 2 categories of cancer in the clinical manifestations: the stage of cancer and survival status (P < .05). Logistic regression analysis showed that the risk of death in cancer patients with COVID-19 along with symptoms of diarrhea (odds ratio [OR] = 12.8, P = .004), the difficulty of breath (OR = 10.73, P = .034), drop of SO2 (OR = 1.334, P = .003), thrombocytopenia (OR = 1.022, P = .02), anemia (OR = 2.72, P = .011), requiring mechanical ventilation (OR = 9.24, P = .004), pleural infusion (OR = 10.28, P = .02), and intensive care unit (ICU) admission (OR = 7.389, P = .009) increases independent of other variables. The COVID-19 mortality rate in our cancer patients was 23%.
   CONCLUSIONS: Thrombocytopenia, anemia, and diarrhea are symptoms that, along with common symptoms such as lung involvement, difficulty breathing, and the need for a ventilator, increase the risk of death in cancer patients with COVID-19.
C1 [Aznab, Mozaffar] Kermanshah Univ Med Sci, Internal Med Dept, Kermanshah, Iran.
   [Roozbahani, Narges Eskandari] Kermanshah Univ Med Sci, Imam Reza Hosp, Clin Res Dev Ctr, Kermanshah, Iran.
   [Moazen, Homa] Shahid Sadoughi Univ Med Sci, Dept Biostat & Epidemiol, Yazd, Iran.
C3 Kermanshah University of Medical Sciences; Kermanshah University of
   Medical Sciences
RP Roozbahani, NE (corresponding author), Kermanshah Univ Med Sci, Imam Reza Hosp, Clin Res Dev Ctr, Kermanshah, Iran.
EM neskandari32@gmail.com
RI Eskandari-Roozbahani, Narges/AFJ-4946-2022; Aznab, Mozaffar/B-5648-2018
OI Eskandari Roozbahani, Narges/0000-0003-2509-9177
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NR 40
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
EI 1179-5549
J9 CLIN MED INSIGHTS-ON
JI Clin. Med. Insights-Oncol.
PD JAN
PY 2022
VL 16
AR 11795549221074168
DI 10.1177/11795549221074168
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YU0LA
UT WOS:000751741600001
PM 35110966
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Liu, X
   Zhang, YQ
   Wu, XY
   Xu, FY
   Ma, HB
   Wu, ML
   Xia, Y
AF Liu, Xuan
   Zhang, Yiqian
   Wu, Xuyi
   Xu, Fuyan
   Ma, Hongbo
   Wu, Mengling
   Xia, Yong
TI Targeting Ferroptosis Pathway to Combat Therapy Resistance and
   Metastasis of Cancer
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE ferroptosis; drug resistance; cancer; metastasis; peroxidation
ID CELL LUNG-CANCER; OVERCOMING RADIATION-RESISTANCE; MEDIATES CONTACT
   INHIBITION; HIPPO SIGNALING-PATHWAY; GEMCITABINE RESISTANCE; CISPLATIN
   RESISTANCE; COLORECTAL-CANCER; TUMOR-SUPPRESSOR; BREAST-CANCER;
   NASOPHARYNGEAL CARCINOMA
AB Ferroptosis is an iron-dependent regulated form of cell death caused by excessive lipid peroxidation. This form of cell death differed from known forms of cell death in morphological and biochemical features such as apoptosis, necrosis, and autophagy. Cancer cells require higher levels of iron to survive, which makes them highly susceptible to ferroptosis. Therefore, it was found to be closely related to the progression, treatment response, and metastasis of various cancer types. Numerous studies have found that the ferroptosis pathway is closely related to drug resistance and metastasis of cancer. Some cancer cells reduce their susceptibility to ferroptosis by downregulating the ferroptosis pathway, resulting in resistance to anticancer therapy. Induction of ferroptosis restores the sensitivity of drug-resistant cancer cells to standard treatments. Cancer cells that are resistant to conventional therapies or have a high propensity to metastasize might be particularly susceptible to ferroptosis. Some biological processes and cellular components, such as epithelial-mesenchymal transition (EMT) and noncoding RNAs, can influence cancer metastasis by regulating ferroptosis. Therefore, targeting ferroptosis may help suppress cancer metastasis. Those progresses revealed the importance of ferroptosis in cancer, In order to provide the detailed molecular mechanisms of ferroptosis in regulating therapy resistance and metastasis and strategies to overcome these barriers are not fully understood, we described the key molecular mechanisms of ferroptosis and its interaction with signaling pathways related to therapy resistance and metastasis. Furthermore, we summarized strategies for reversing resistance to targeted therapy, chemotherapy, radiotherapy, and immunotherapy and inhibiting cancer metastasis by modulating ferroptosis. Understanding the comprehensive regulatory mechanisms and signaling pathways of ferroptosis in cancer can provide new insights to enhance the efficacy of anticancer drugs, overcome drug resistance, and inhibit cancer metastasis.
C1 [Liu, Xuan; Zhang, Yiqian; Wu, Xuyi; Xu, Fuyan; Wu, Mengling; Xia, Yong] Sichuan Univ, West China Hosp, Dept Rehabil Med, Chengdu, Peoples R China.
   [Liu, Xuan; Zhang, Yiqian; Ma, Hongbo] Sichuan Univ, West China Sch Pharm, Chengdu, Peoples R China.
   [Wu, Xuyi; Xia, Yong] Rehabil Med Res Inst, Key Lab Rehabil Med Sichuan Prov, Chengdu, Peoples R China.
C3 Sichuan University; Sichuan University
RP Xia, Y (corresponding author), Sichuan Univ, West China Hosp, Dept Rehabil Med, Chengdu, Peoples R China.; Xia, Y (corresponding author), Rehabil Med Res Inst, Key Lab Rehabil Med Sichuan Prov, Chengdu, Peoples R China.
EM yxia4@scu.edu.cn
RI Xia, Yong/E-8689-2013
FU National Natural Science Foundation of China [82173280]; Department of
   Science and Technology of Sichuan Province [2021YJ0450]; West China
   Hospital, Sichuan University [2019HXBH017]
FX Funding This work was supported by the National Natural Science
   Foundation of China (Grant No. 82173280), the Department of Science and
   Technology of Sichuan Province (grant number: 2021YJ0450), and the
   Post-Doctor Research Project, West China Hospital, Sichuan University
   (Grant No. 2019HXBH017).
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NR 236
TC 39
Z9 40
U1 1
U2 68
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 30
PY 2022
VL 13
AR 909821
DI 10.3389/fphar.2022.909821
PG 27
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 2Z6YU
UT WOS:000826721500001
PM 35847022
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wei, SC
   Zhang, JX
   Wu, XH
   Chen, ML
   Huang, HC
   Zeng, SQ
   Xiang, ZX
   Li, XY
   Dong, WG
AF Wei, Shuchun
   Zhang, Jixiang
   Wu, Xiaohan
   Chen, Meilin
   Huang, Hancheng
   Zeng, Suqi
   Xiang, Zixuan
   Li, Xiangyun
   Dong, Weiguo
TI Fusobacterium nucleatum Extracellular Vesicles Promote Experimental
   Colitis by Modulating Autophagy via the miR-574-5p/CARD3 Axis
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Article
DE Fusobacterium nucleatum; extracellular vesicles; ulcerative colitis;
   miR-574-5p; CARD3; autophagy
ID COLORECTAL-CANCER; ULCERATIVE-COLITIS; MEMBRANE-VESICLES; MICROBIOTA;
   INFLAMMATION
AB Background Ulcerative colitis (UC) may be exacerbated by Fusobacterium nucleatum (Fn) infection. However, the mechanism underlying Fn-mediated progression of UC has yet to be established. Here, we aimed to establish whether and how Fn-derived extracellular vesicles (Fn-EVs) participate in the development of experimental colitis through microRNAs (miRNAs). Methods EVs were isolated and purified by ultracentrifugation from Fn and Escherichia coli culture supernatants. Differentially expressed miRNAs in control intestinal epithelial cells (IECs) and Fn-EV-treated IECs were identified by miRNA sequencing. EVs were cocultured with IECs or administered to CARD3(wt)/CARD3(-/-) mice by gavage to assess inflammatory responses to and the mechanism of action of Fn-EVs. Results Fn-EVs promoted upregulation of proinflammatory cytokines (interleukin [IL]-1 beta, IL-6, tumor necrosis factor alpha), downregulation of anti-inflammatory IL-10 and intercellular tight junction proteins ZO-1 and occludin, and epithelial barrier dysfunction in IECs. Fn-EVs significantly aggravated experimental colitis in mice associated with Fn-EV-mediated downregulation of miR-574-5p expression and autophagy activation. Blockade of autophagy using chloroquine alleviates barrier damage exacerbated by Fn-EVs in vitro and in vivo. Inhibition of the miR-574-5p/CARD3 axis reduced the severity of colitis, epithelial barrier damage, and autophagy activation induced by Fn-EVs. Conclusions Here, we describe a new mechanism by which Fn-EVs mediate experimental colitis severity through miR-574-5p/CARD3-dependent autophagy activation, providing a novel target for UC monitoring and targeted therapy.
   Lay Summary Fusobacterium nucleatum-derived extracellular vesicles (Fn-EVs) alter the microRNA profile of intestinal epithelial cells and colitis tissues, especially the expression of miR-574-5p. Fn-EVs mediate experimental colitis severity through miR-574-5p/CARD3-dependent autophagy activation. Hence, inhibiting Fn-EV-activated autophagy or targeting the miR-574-5p/CARD3 axis may be potential new therapeutic strategies in ulcerative colitis.
C1 [Wei, Shuchun; Zhang, Jixiang; Wu, Xiaohan; Chen, Meilin; Huang, Hancheng; Zeng, Suqi; Xiang, Zixuan; Li, Xiangyun; Dong, Weiguo] Wuhan Univ, Renmin Hosp, Dept Gastroenterol, Jiefang Rd 238, Wuhan 430060, Peoples R China.
   [Wei, Shuchun; Wu, Xiaohan; Chen, Meilin; Huang, Hancheng; Zeng, Suqi; Xiang, Zixuan; Li, Xiangyun] Hubei Key Lab Digest Syst Dis, Wuhan, Peoples R China.
C3 Wuhan University
RP Dong, WG (corresponding author), Wuhan Univ, Renmin Hosp, Dept Gastroenterol, Jiefang Rd 238, Wuhan 430060, Peoples R China.
EM dongweiguo@whu.edu.cn
RI li, xiangyun/AAE-2888-2020; wu, xiaohan/JLL-8682-2023
OI Dong, Weiguo/0000-0002-4228-6508
FU National Natural Science Foundation of China [82170549, 81870392,
   82000521]
FX This work was supported by the National Natural Science Foundation of
   China (Nos. 82170549, 81870392, and 82000521).
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NR 47
TC 18
Z9 20
U1 1
U2 40
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1078-0998
EI 1536-4844
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD JAN
PY 2023
VL 29
IS 1
BP 9
EP 26
DI 10.1093/ibd/izac177
EA AUG 2022
PG 18
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 8R5MD
UT WOS:000843211300001
PM 35998069
DA 2025-01-04
ER

PT J
AU Zheng, Y
   Fu, Y
   Wang, PP
   Ding, ZY
AF Zheng, Yue
   Fu, Yang
   Wang, Pei-Pei
   Ding, Zhen-Yu
TI Neoantigen: A Promising Target for the Immunotherapy of Colorectal
   Cancer
SO DISEASE MARKERS
LA English
DT Review
ID MISMATCH REPAIR-DEFICIENT; MICROSATELLITE INSTABILITY; SOMATIC
   MUTATIONS; MASS-SPECTROMETRY; FRAMESHIFT-MUTATION; IMMUNE-RESPONSES;
   PD-1 BLOCKADE; PREDICTION; PEPTIDES; EPITOPES
AB At present, there are various treatment strategies for colorectal cancer, including surgery, chemotherapy, radiotherapy, and targeted therapy. In recent years, with the continuous development of immunotherapy, immune checkpoint inhibitors (ICIs) can significantly improve the treatment of advanced colorectal cancer patients with high levels of microsatellite instability. In addition to ICIs, neoantigens, as a class of tumor-specific antigens (TSA), are regarded as new immunotherapy targets for many cancer species and are being explored for antitumor therapy. Immunotherapy strategies based on neoantigens include tumor vaccines and adoptive cell therapy (ACT). These methods aim to eliminate tumor cells by enhancing the immune response of host T-cells to neoantigens. In addition, for MSS colorectal cancer, such "cold tumors" with low mutation rates and stable microsatellites are not sensitive to ICIs, whereas neoantigens could provide a promising immunotherapeutic avenue. In this review, we summarized the current status of colorectal cancer neoantigen prediction and current clinical trials of neoantigens and discussed the difficulties and limitations of neoantigens-based therapies for the treatment of CRC.
C1 [Zheng, Yue; Fu, Yang; Wang, Pei-Pei; Ding, Zhen-Yu] Sichuan Univ, West China Hosp, Canc Ctr, West China Med Sch,Dept Biotherapy, Chengdu, Peoples R China.
C3 Sichuan University
RP Ding, ZY (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, West China Med Sch,Dept Biotherapy, Chengdu, Peoples R China.
EM elenazhengy8396@163.com; fuyang1208@163.com; wpp7349@163.com;
   dingzhenyu@scu.edu.cn
RI Wang, Peipei/JVP-1674-2024
OI Wang, Peipei/0000-0001-7201-4928
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NR 93
TC 24
Z9 25
U1 2
U2 21
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 0278-0240
EI 1875-8630
J9 DIS MARKERS
JI Dis. Markers
PD FEB 15
PY 2022
VL 2022
AR 8270305
DI 10.1155/2022/8270305
PG 11
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
   Research & Experimental; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
   Experimental Medicine; Pathology
GA ZY2QY
UT WOS:000772435000001
PM 35211210
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ioannou, M
   Papamichali, R
   Samara, M
   Paraskeva, E
   Papacharalambous, C
   Baxevanidou, K
   Koukoulis, G
AF Ioannou, Maria
   Papamichali, Roidoula
   Samara, Maria
   Paraskeva, Efrosini
   Papacharalambous, Constantina
   Baxevanidou, Korina
   Koukoulis, George
TI Diagnostic value of immunohistochemistry for the detection of the
   <i>BRAF</i> V600E mutation in colorectal carcinoma
SO JOURNAL OF BUON
LA English
DT Article
DE BRAF V600E mutation; colorectal carcinoma; DNA sequence analysis;
   immunohistochemistry
ID ISLAND METHYLATOR PHENOTYPE; MONOCLONAL-ANTIBODY; MUTANT PROTEIN; POOR
   SURVIVAL; CANCER; COLON; ADENOCARCINOMA; PATHWAY; KRAS; VE1
AB Purpose: V600E is the most common activating BRAF mutation in colorectal carcinomas (CRCs). It is a crucial biomarker for patient selection and response to targeted therapy with BRAF V600E inhibitors. Previous studies using immunohistochemistry (IHC) have shown different results. In this study, we evaluated the IHC expression of the mutated BRAF protein in archival material from CRC specimens and correlated it with DNA sequence analysis.
   Methods: 51 cases of primary colon adenocarcinoma were stained with BRAF V600E-specific clone VE1 antibody against mutated BRAF protein. DNA sequence analysis was performed and the results were compared.
   Results: BRAF V600E protein was detected in the cytoplasm of neoplastic cells in 15 of the 51 examined cases (29.4%). The correlation between IHC staining and DNA sequence analysis showed 93.75% sensitivity and 100% specificity.
   Conclusions: Our data show that IHC could be used in routine clinical practice as a screening method for BRAF V600E mutant protein detection in CRC patients.
C1 [Ioannou, Maria; Papamichali, Roidoula; Samara, Maria; Papacharalambous, Constantina; Baxevanidou, Korina; Koukoulis, George] Univ Thessaly, Fac Med, Dept Pathol, Biopolis 41110, Larissa, Greece.
   [Paraskeva, Efrosini] Univ Thessaly, Fac Med, Dept Physiol, Biopolis 41110, Larissa, Greece.
C3 University of Thessaly; University of Thessaly
RP Ioannou, M (corresponding author), Univ Thessaly, Fac Med, Dept Pathol, Biopolis 41110, Larissa, Greece.
EM mioan@med.uth.gr
RI SAMARA, MARIA/IAN-4481-2023; Paraskeva, Efrosyni/E-6449-2015
OI SAMARA, MARIA/0000-0003-0433-6436; Paraskeva,
   Efrosyni/0000-0002-1312-0322
CR Adackapara CA, 2013, HISTOPATHOLOGY, V63, P187, DOI 10.1111/his.12154
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NR 33
TC 4
Z9 4
U1 0
U2 0
PU IMPRIMATUR PUBLICATIONS
PI ATHENS
PA 30 DEM POLIORKETES ST, ATHENS, 136 76, GREECE
SN 1107-0625
EI 2241-6293
J9 J BUON
JI J. BUON
PD MAY-JUN
PY 2016
VL 21
IS 3
BP 618
EP 625
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DQ1RU
UT WOS:000378978900014
PM 27569082
DA 2025-01-04
ER

PT J
AU Nikas, I
   Giaginis, C
   Petrouska, K
   Alexandrou, P
   Michail, A
   Sarantis, P
   Tsourouflis, G
   Danas, E
   Pergaris, A
   Politis, PK
   Nakopoulou, L
   Theocharis, S
AF Nikas, Ilias
   Giaginis, Constantinos
   Petrouska, Kalliopi
   Alexandrou, Paraskevi
   Michail, Artemis
   Sarantis, Panagiotis
   Tsourouflis, Gerasimos
   Danas, Eugene
   Pergaris, Alexandros
   Politis, Panagiotis K.
   Nakopoulou, Lydia
   Theocharis, Stamatios
TI EPHA2, EPHA4, and EPHA7 Expression in Triple-Negative Breast Cancer
SO DIAGNOSTICS
LA English
DT Article
DE biomarker; basal-like breast cancer; EPH; ephrin; targeted therapy
ID INTERNATIONAL EXPERT CONSENSUS; SQUAMOUS-CELL CARCINOMA; TYROSINE
   KINASE; METASTATIC PROGRESSION; HISTOLOGICAL GRADE; COLORECTAL-CANCER;
   PRIMARY THERAPY; RECEPTOR; EPHRINS; OVEREXPRESSION
AB Ongoing research continues to elucidate the complex role of ephrin receptors (EPHs) and their ligands (ephrins) in breast cancer pathogenesis, with their varying expression patterns implied to have an important impact on patients' outcome. The current study aims to investigate the clinical significance of EPHA2, EPHA4, and EPHA7 expression in triple-negative breast cancer (TNBC) cases. EPHA2, EPHA4, and EPHA7 protein expression was assessed immunohistochemically on formalin-fixed and paraffin-embedded (FFPE) TNBC tissue sections from 52 TNBC patients and correlated with key clinicopathologic parameters and patients' survival data (overall survival (OS); disease-free survival (DFS)). EPHA2, EPHA4, and EPHA7 expression was further examined in TNBC cell lines. EPHA2 overexpression was observed in 26 (50%) of the TNBC cases, who exhibited a shorter OS and DFS than their low-expression counterparts, with EPHA2 representing an independent prognostic factor for OS and DFS (p = 0.0041 and p = 0.0232, respectively). EPHA4 overexpression was associated with lymph node metastasis in TNBC patients (p = 0.0546). Alterations in EPHA2, EPHA4, and EPHA7 expression levels were also noted in the examined TNBC cell lines. Our study stresses that EPHA2 expression constitutes a potential prognostic factor for TNBC patients. Given the limited treatment options and poorer outcome that accompany the TNBC subtype, EPHA2 could also pose as a target for novel, more personalized, and effective therapeutic approaches for those patients.
C1 [Nikas, Ilias; Petrouska, Kalliopi; Alexandrou, Paraskevi; Sarantis, Panagiotis; Danas, Eugene; Pergaris, Alexandros; Nakopoulou, Lydia; Theocharis, Stamatios] Natl & Kapodistrian Univ Athens, Med Sch, Dept Pathol 1, Athens 11527, Greece.
   [Nikas, Ilias] European Univ Cyprus, Sch Med, CY-2404 Nicosia, Cyprus.
   [Giaginis, Constantinos] Univ Aegean, Sch Environm, Dept Food Sci & Nutr, Myrina 81100, Lemnos, Greece.
   [Michail, Artemis; Politis, Panagiotis K.] Acad Athens, Biomed Res Fdn, Ctr Basic Res, 4 Soranou Efesiou Str, Athens 11527, Greece.
   [Tsourouflis, Gerasimos] Natl & Kapodistrian Univ Athens, Med Sch, Laikon Hosp, Dept Propedeut Surg 2, Athens 11527, Greece.
C3 National & Kapodistrian University of Athens; European University
   Cyprus; Academy of Athens; National & Kapodistrian University of Athens;
   Laiko General Hospital
RP Theocharis, S (corresponding author), Natl & Kapodistrian Univ Athens, Med Sch, Dept Pathol 1, Athens 11527, Greece.
EM I.nikas@euc.accy; cgiaginis@aegean.gr; ppetrouska@hotmail.com;
   parialexandro@yahoo.com; artemisbio@gmail.com; psarantis@med.uoa.gr;
   gtsourouflis@med.uoa.gr; eugenedanas@gmail.com; alexperg@yahoo.com;
   lnako@med.uoa.gr; lnako@med.uoa.gr; tamtheo@med.uoa.gr
RI Politis, Panagiotis/AAO-2423-2020; Sarantis, Panagiotis/AAF-4774-2021;
   Theocharis, Serafeim/ABC-9663-2021; Giaginis, Constantinos/JMQ-9552-2023
OI Pergaris, Alexandros/0000-0002-4960-672X; Sarantis,
   Panagiotis/0000-0001-5848-7905; Nikas, Ilias/0000-0001-8625-2556; Danas,
   Eougken-Eugene/0000-0002-2865-3893; Giaginis,
   Constantinos/0000-0003-2878-4831
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NR 68
TC 19
Z9 19
U1 0
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD FEB
PY 2022
VL 12
IS 2
AR 366
DI 10.3390/diagnostics12020366
PG 15
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA ZL9IR
UT WOS:000763983400001
PM 35204461
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU El Guerrab, A
   Bamdad, M
   Bignon, YJ
   Penault-Llorca, F
   Aubel, C
AF El Guerrab, Abderrahim
   Bamdad, Mahchid
   Bignon, Yves-Jean
   Penault-Llorca, Frederique
   Aubel, Corinne
TI Anti-EGFR monoclonal antibodies enhance sensitivity to DNA-damaging
   agents in <i>BRCA1</i>-mutated and <i>PTEN</i>-wild-type triple-negative
   breast cancer cells
SO MOLECULAR CARCINOGENESIS
LA English
DT Article
DE epidermal growth factor receptor; Anti-EGFR targeted therapy;
   chemotherapeutic agents; cytotoxicity
ID GROWTH-FACTOR RECEPTOR; METASTATIC COLORECTAL-CANCER; ACTIVATED
   PROTEIN-KINASE; RANDOMIZED PHASE-II; GENE COPY NUMBER; BRCA1 MUTATIONS;
   CETUXIMAB; PATHWAY; EXPRESSION; CHEMOTHERAPY
AB Increased epidermal growth factor receptor (EGFR) expression in triple-negative breast cancer (TNBC) is recognized as a promising therapeutic target, specifically through the use of selective EGFR inhibitors combined with chemotherapies. TNBC is characterized by genetic instability that leads to increased sensitivity to cytotoxic agents. We analyzed the effect of anti-EGFR monoclonal antibodies (mAbs; cetuximab and panitumumab) in combination with chemotherapeutic agents (docetaxel, cisplatin, and epirubicin) on EGFR-expressing TNBC cell lines that have different mutation statuses for one oncogene (KRAS) and two tumor suppressor genes (PTEN and BRCA1). Both mAbs failed to improve the cytotoxic effect of chemotherapies in the KRAS mutant cell line (MDA-MB-231) and PTEN-null cell lines (HCC-1937 and MDA-MB-468). In contrast, mAbs combined with DNA-damaging agents (cisplatin or epirubicin) had a synergistic effect in the BRCA1-mutant cell line SUM-1315 (wild-type KRAS and PTEN). The reintroduction of wild-type BRCA1 into SUM-1315 cells abolished this synergism. The improved effect of combination therapy was associated with cell cycle arrest at G1 phase and inhibition of the phosphorylation of EGFR and ERK1/2 proteins. These results suggest that patients with BRCA1-associated TNBC without genetic alterations in the PTEN and KRAS genes may have improved therapeutic responses to anti-EGFR mAbs combined with DNA-damaging agents. (C) 2017 Wiley Periodicals, Inc.
C1 [El Guerrab, Abderrahim; Bignon, Yves-Jean; Penault-Llorca, Frederique; Aubel, Corinne] Ctr Jean Perrin, ERTICa, EA4677, 58 Rue Montalembert,BP392, F-63011 Clermont Ferrand, France.
   [El Guerrab, Abderrahim; Bamdad, Mahchid; Bignon, Yves-Jean; Penault-Llorca, Frederique; Aubel, Corinne] Univ Auvergne, Clermont Univ, ERTICa, Fac Med,EA4677, Clermont Ferrand, France.
   [Bamdad, Mahchid] Ensemble Univ Cezeaux, Clermont Univ, ERTICa, Univ Auvergne,Inst Univ Technol,Dept Genie Biol,E, Clermont Ferrand, France.
C3 UNICANCER; Centre Jean Perrin; Universite Clermont Auvergne (UCA);
   Universite Clermont Auvergne (UCA)
RP Bignon, YJ; Aubel, C (corresponding author), Ctr Jean Perrin, ERTICa, EA4677, 58 Rue Montalembert,BP392, F-63011 Clermont Ferrand, France.
EM yves-jean.bignon@cjp.fr; corinne.aubel@udamail.fr
RI aubel, corinne/Y-7143-2019; Bamdad, Mahchid/Y-1363-2019
OI Bamdad, Mahchid/0000-0002-2474-6910; Aubel, Corinne/0000-0003-4500-6505
FU French Ligue Nationale Contre le Cancer
FX Grant sponsor: French Ligue Nationale Contre le Cancer
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NR 55
TC 13
Z9 14
U1 0
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0899-1987
EI 1098-2744
J9 MOL CARCINOGEN
JI Mol. Carcinog.
PD MAY
PY 2017
VL 56
IS 5
BP 1383
EP 1394
DI 10.1002/mc.22596
PG 12
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA ES5PB
UT WOS:000399592100001
PM 27864890
DA 2025-01-04
ER

PT J
AU Van Leeuwen, MT
   Luu, S
   Gurney, H
   Brown, MR
   Pearson, SA
   Webber, K
   Hunt, L
   Hong, S
   Delaney, GP
   Vajdic, CM
AF Van Leeuwen, Marina T.
   Luu, Steven
   Gurney, Howard
   Brown, Martin R.
   Pearson, Sallie-Anne
   Webber, Kate
   Hunt, Lee
   Hong, Soojung
   Delaney, Geoffrey P.
   Vajdic, Claire M.
TI Cardiovascular Toxicity of Targeted Therapies for Cancer: An Overview of
   Systematic Reviews
SO JNCI CANCER SPECTRUM
LA English
DT Review
ID ENDOTHELIAL GROWTH-FACTOR; CELL LUNG-CANCER; METASTATIC
   COLORECTAL-CANCER; TYROSINE KINASE INHIBITORS; CONGESTIVE-HEART-FAILURE;
   ARTERIAL THROMBOEMBOLIC EVENTS; ANDROGEN-DEPRIVATION THERAPY; RESISTANT
   PROSTATE-CANCER; FATAL ADVERSE EVENTS; ADVANCED HEPATOCELLULAR-CARCINOMA
AB Background: Several targeted therapies for cancer have been associated with cardiovascular toxicity. The evidence for this association has not been synthesized systematically nor has the quality of evidence been considered. We synthesized systematic review evidence of cardiovascular toxicity of individual targeted agents. Methods: We searched MEDLINE, Embase, and the Cochrane Database of Systematic Reviews for systematic reviews with meta-analyses of cardiovascular outcomes for individual agents published to May 2020. We selected reviews according to prespecified eligibility criteria (International Prospective Register of Systematic Reviews CRD42017080014). We classified evidence of cardiovascular toxicity as sufficient, probable, possible, or indeterminate for specific cardiovascular outcomes based on statistical significance, study quality, and size. Results: From 113 systematic reviews, we found at least probable systematic review evidence of cardiovascular toxicity for 18 agents, including high- and all-grade hypertension for bevacizumab, ramucirumab, axitinib, cediranib, pazopanib, sorafenib, sunitinib, vandetanib, aflibercept, abiraterone, and enzalutamide, and all-grade hypertension for nintedanib; high- and all-grade arterial thromboembolism (includes cardiac and/or cerebral events) for bevacizumab and abiraterone, high-grade arterial thromboembolism for trastuzumab, and all-grade arterial thromboembolism for sorafenib and tamoxifen; high- and all-grade venous thromboembolism (VTE) for lenalidomide and thalidomide, high-grade VTE for cetuximab and panitumumab, and all-grade VTE for bevacizumab; high- and all-grade left ventricular ejection fraction decline or congestive heart failure for bevacizumab and trastuzumab, and all-grade left ventricular ejection fraction decline/congestive heart failure for pazopanib and sunitinib; and all-grade corrected QT interval prolongation for vandetanib. Conclusions: Our review provides an accessible summary of the cardiovascular toxicity of targeted therapy to assist clinicians and patients when managing cardiovascular health.
C1 [Van Leeuwen, Marina T.; Luu, Steven; Pearson, Sallie-Anne; Hong, Soojung; Vajdic, Claire M.] Univ New South Wales, Ctr Big Data Res Hlth, Sydney, NSW 2052, Australia.
   [Gurney, Howard; Brown, Martin R.] Macquarie Univ, Fac Med & Hlth Sci, Sydney, NSW, Australia.
   [Webber, Kate] Monash Hlth, Dept Oncol, Clayton, Vic, Australia.
   [Webber, Kate] Monash Univ, Sch Clin Sci, Clayton, Vic, Australia.
   [Hunt, Lee] Canc Voices NSW, Milsons Point, NSW, Australia.
   [Hong, Soojung] Natl Hlth Insurance Serv Ilsan Hosp, Dept Internal Med, Div Oncol Haematol, Goyang, South Korea.
   [Delaney, Geoffrey P.] Liverpool Canc Therapy Ctr, Liverpool, NSW, Australia.
   [Delaney, Geoffrey P.] Ingham Inst Appl Med Res, Collaborat Canc Outcomes Res & Evaluat, Liverpool, NSW, Australia.
   [Delaney, Geoffrey P.] Univ New South Wales, South Western Sydney Clin Sch, Liverpool, NSW, Australia.
C3 University of New South Wales Sydney; Macquarie University; Monash
   Health; Monash University; National Health Insurance Service; Ingham
   Institute for Applied Medical Research; University of New South Wales
   Sydney
RP Van Leeuwen, MT (corresponding author), Univ New South Wales, Ctr Big Data Res Hlth, Sydney, NSW 2052, Australia.
EM m.vanleeuwen@unsw.edu.au
RI Gurney, Howard/ABF-6924-2020; Vajdic, Claire/AAP-5940-2020; Webber,
   Kate/L-8659-2019; brown, martin/H-4106-2011; van Leeuwen,
   Marina/AAQ-5339-2021
OI brown, martin/0000-0001-6230-4286; Webber, Kate/0000-0003-4350-0884;
   Hong, Soojung/0000-0002-4350-2794; Delaney, Geoff/0000-0002-1829-396X;
   van Leeuwen, Marina/0000-0002-1570-2852; Gurney,
   Howard/0000-0003-0217-5261; Pearson, Sallie-Anne/0000-0001-7137-6855;
   Vajdic, Claire/0000-0002-3612-8298
FU National Health and Medical Research Council [1012141]; University of
   New South Wales
FX MTvL receives a postdoctoral fellowship from the National Health and
   Medical Research Council (ID 1012141); HG reports personal fees from,
   and is on the Advisory Board for BMS, Pfizer, MSD, Ipsen, Roche,
   AstraZeneca, Astellas, outside the submitted work. CMV is supported by a
   Scientia Fellowship from the University of New South Wales. SL, MRB, KW,
   S-AP, LH, SH, and GPD have nothing to disclose.
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NR 208
TC 25
Z9 25
U1 2
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
EI 2515-5091
J9 JNCI CANCER SPECT
JI JNCI Cancer Spectr.
PD DEC
PY 2020
VL 4
IS 6
AR pkaa076
DI 10.1093/jncics/pkaa076
PG 15
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA PY7NB
UT WOS:000612227700012
PM 33392444
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Shafei, A
   El-Bakly, W
   Sobhy, A
   Wagdy, O
   Reda, A
   Aboelenin, O
   Marzouk, A
   Habak, K
   Mostafa, R
   Ali, MA
   Ellithy, M
AF Shafei, Ayman
   El-Bakly, Wesam
   Sobhy, Ahmed
   Wagdy, Omar
   Reda, Ahmed
   Aboelenin, Omar
   Marzouk, Amr
   El Habak, Khalil
   Mostafa, Randa
   Ali, Mahmoud A.
   Ellithy, Mahmoud
TI A review on the efficacy and toxicity of different doxorubicin
   nanoparticles for targeted therapy in metastatic breast cancer
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
ID PEGYLATED LIPOSOMAL DOXORUBICIN; PHASE-III TRIAL; PALMAR-PLANTAR
   ERYTHRODYSESTHESIA; OVERCOMING MULTIDRUG-RESISTANCE; CONVENTIONAL
   DOXORUBICIN; PRETREATED PATIENTS; ENCAPSULATED DOXORUBICIN; REDUCED
   CARDIOTOXICITY; MAGNETIC NANOPARTICLES; COLORECTAL-CANCER
AB In metastatic breast cancer (MBC), the conventional doxorubicin (DOX) has various problems due to lack of selectivity with subsequent therapeutic failure and adverse effects. DOX-induced cardiotoxicity is a major problem that necessitates the presence of new forms to decrease the risk of associated morbidity.
   Nanoparticles (NPs) are considered an important approach to selectively increase drug accumulation inside tumor cells and thus decreasing the associated side effects. Tumor cells develop resistance to chemotherapeutic agents through multiple mechanisms, one of which is over expression of efflux transporters. Various NPs have been investigated to overcome efflux mediated resistance.
   To date, only liposomal doxorubicin (LD) and pegylated liposomal doxorubicin (PLD) have entered phase II and III clinical trials and FDA-approved for clinical use in MBC. This review addresses the effects of LD and PLD on the hematological and palmar-plantar erythrodysesthesia (PPE) in anthracycline naive and pretreated MBC patients. For evidence, studies to be included in this review were identified through PubMed, Cochrane and Google scholar databases. The results derived from: four phase III clinical trials that compared LD with the conventional DOX in naive MBC patients, and ten non-comparative clinical trials investigated LD and PLD as monotherapy or combination in pretreated MBC. This work confirmed the cardiac tolerability profile of LD and PLD versus DOX, while hematological and skin toxicities were more common.
   Other DOX-NPs in preclinical trials were discussed in a chronological order. Finally, the modern preclinical development framework for DOX includes exosomal DOX (exo-DOX). Exosomal NPs are non-toxic, non-immunogenic, and can be engineered to have high cargo loading capacity and targeting specificity. These NPs have not been investigated clinically. Our study shows that the full clinical potentiality of DOX-NPs remains to be addressed to move the field forward.
C1 [Shafei, Ayman; Mostafa, Randa; Ali, Mahmoud A.] Armed Forces Coll Med, Biomed Res Dept, Cairo, Egypt.
   [El-Bakly, Wesam] Ain Shams Univ, Fac Med, Dept Pharmacol, Cairo, Egypt.
   [Sobhy, Ahmed; Wagdy, Omar; Reda, Ahmed; Aboelenin, Omar; Marzouk, Amr; El Habak, Khalil] Armed Forces Coll Med, Cairo, Egypt.
   [Ellithy, Mahmoud] Ain Shams Univ, Fac Med, Dept Clin Oncol, Cairo, Egypt.
C3 Armed Forces College of Medicine (AFCM); Egyptian Knowledge Bank (EKB);
   Ain Shams University; Armed Forces College of Medicine (AFCM); Egyptian
   Knowledge Bank (EKB); Ain Shams University
RP El-Bakly, W (corresponding author), Ain Shams Univ, Fac Med, Dept Pharmacol, Cairo, Egypt.
EM w_bakly@yahoo.com
RI Bakly, wesam/Q-1398-2015; M.Mostafa, Randa/F-1258-2019; Shafei,
   Ayman/ABG-6116-2021
OI Wagdy, Omar/0000-0002-2013-8985
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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 2017
VL 95
BP 1209
EP 1218
DI 10.1016/j.biopha.2017.09.059
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA FP6OC
UT WOS:000417744400139
PM 28931213
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Ferrari, SM
   La Motta, C
   Sartini, S
   Baldini, E
   Materazzi, G
   Politti, U
   Ruffilli, I
   Ulisse, S
   Miccoli, P
   Antonelli, A
   Fallahi, P
AF Ferrari, Silvia Martina
   La Motta, Concettina
   Sartini, Stefania
   Baldini, Enke
   Materazzi, Gabriele
   Politti, Ugo
   Ruffilli, Ilaria
   Ulisse, Salvatore
   Miccoli, Paolo
   Antonelli, Alessandro
   Fallahi, Poupak
TI Pyrazolopyrimidine Derivatives as Antineoplastic Agents: with a Special
   Focus on Thyroid Cancer
SO MINI-REVIEWS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE Antiangiogenic inhibitors; CLM29; CLM3; PP1; PP2;
   pyrazolo[3,4-d]pyrimidine; RET inhibitors; tyrosine kinase inhibitors
ID TYROSINE-KINASE INHIBITORS; STRUCTURE-BASED OPTIMIZATION;
   ALPHA-CHEMOKINE CXCL10; IN-VITRO; TARGETED THERAPY; GROWTH-FACTOR;
   ANTIANGIOGENIC PROPERTIES; COLORECTAL-CANCER; ENDOCRINE TUMORS;
   PHOSPHOLIPASE-D
AB Tyrosine kinase inhibitors (TKIs) are molecules that compete with ATP on tyrosine kinase receptors (TKRs), blocking tyrosine kinase (TK) activation and then oncogenic pathways; they have been studied, and some of them are right approved for the treatment of many types of cancer. Among TKIs, one of the most explored chemical template is the pyrazolo[3,4-d]pyrimidine (PP) heterocyclic core, which proved to be a useful scaffold for the obtainment of effective compounds. Actually, derivatives belonging to this structural class show a large spectrum of activity, thus standing out as multi-target agents. Different PP compounds have been shown to act as: a) ABL inhibitors and antiproliferative agents against human leukemia cell lines; b) Src kinase inhibitors in neuroblastoma, medulloblastoma and osteosarcoma; c) Phospholipase D inhibitors in different neoplasias; d) Urokinase plasminogen activator inhibitors, in breast cancer. In thyroid cancer (TC), PP1 and PP2 (inhibitors of RET, Hck, lck, and fynT kinases, and a good inhibitor of c-Src and platelet-derived growth factor receptor) showed antineoplastic actvity in human papillary TC cell lines that carry spontaneous RET/PTC1 rearrangements. More recently, new derivatives, (R)-1-phenethyl-N-(1-phenylethyl)-1H-pyrazolo[3,4-d]pyrimidin-4-amine, namely, CLM3 and CLM29, have been demonstrated to exert a multiple signal transduction inhibition (including the RET-TK, BRAF, EGFR, and with antiangiogenic activity), showing antineoplastic activity, in vitro and in vivo, in papillary dedifferentiated, medullary and anaplastic TC. These data have shown the antineoplastic activity of PP in different neoplasias, opening the way to a future clinical evaluation in human cancers.
C1 [Ferrari, Silvia Martina; Politti, Ugo; Ruffilli, Ilaria; Antonelli, Alessandro; Fallahi, Poupak] Univ Pisa, Dept Clin & Expt Med, I-56126 Pisa, Italy.
   [La Motta, Concettina; Sartini, Stefania] Univ Pisa, Dept Pharm, I-56126 Pisa, Italy.
   [Baldini, Enke; Ulisse, Salvatore] Univ Roma La Sapienza, Dept Expt Med, I-00185 Rome, Italy.
   [Materazzi, Gabriele; Miccoli, Paolo] Univ Pisa, Dept Surg Med Mol Pathol & Crit Area, I-56126 Pisa, Italy.
C3 University of Pisa; University of Pisa; Sapienza University Rome;
   University of Pisa
RP Antonelli, A (corresponding author), Univ Pisa, Dept Clin & Expt Med, Via Savi 10, I-56126 Pisa, Italy.
EM alessandro.antonelli@med.unipi.it
RI Ulisse, Salvatore/H-5362-2019; Antonelli, Alessandro/AAU-2291-2020;
   Fallahi, Poupak/AAC-6041-2022; LA MOTTA, Concettina/M-3821-2015
OI Ulisse, Salvatore/0000-0002-7573-0759; LA MOTTA,
   Concettina/0000-0002-0194-5431
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NR 99
TC 15
Z9 17
U1 0
U2 28
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1389-5575
EI 1875-5607
J9 MINI-REV MED CHEM
JI Mini-Rev. Med. Chem.
PY 2016
VL 16
IS 2
BP 86
EP 93
DI 10.2174/1389557515666151016124208
PG 8
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CX1PO
UT WOS:000365468300002
PM 26471970
OA Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Lin, W
   Dai, SH
   Chen, T
   Kawai, N
   Miyake, K
   Okada, M
   Haba, R
   Yamaoto, Y
   Tamiya, T
   Fei, Z
AF Lin, Wei
   Dai, Shu-hui
   Chen, Tao
   Kawai, Nobuyuki
   Miyake, Keisuke
   Okada, Masaki
   Haba, Reiji
   Yamaoto, Yuka
   Tamiya, Takashi
   Fei, Zhou
TI Expression of 58-kD Microspherule Protein (MSP58) is Highly Correlated
   with PET Imaging of Tumor Malignancy and Cell Proliferation in Glioma
   Patients
SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
LA English
DT Article
DE Fluorothymidine (FLT); Glioma; MSP58; Positron emission tomography
   (PET); Proliferation
ID POSITRON-EMISSION-TOMOGRAPHY; HUMAN COLORECTAL-CANCER; NEWLY-DIAGNOSED
   GLIOMA; THYMIDINE ANALOGS; DOWN-REGULATION; BRAIN-TUMORS; IN-VIVO;
   F-18-FLT; LINES; FLT
AB Background/Aims: The nucleolar 58-kDa microspherule protein (MSP58) has important transcriptional regulation functions and plays a crucial role in the tumorigenesis and progression of cancers. 3'-deoxy-3'-[F-18] fluorothymidine (FLT) has emerged as a promising positron emission tomography (PET) tracer for evaluating tumor malignancy and cell proliferation. Methods: In the present study, the expression of MSP58 was evaluated by immunohistochemistry and the corresponding PET image was examined using FLT-PET in 55 patients with various grades of gliomas. Results: The immunoreactivity score (IRS) of MSP58 increased with tumor grade with grade IV gliomas exhibiting the highest expression and showed a highly significant positive correlation with the Ki-67 index (r = 0.65, P < 0.001). The IRS of MSP58 in the tumor showed a highly significant positive correlation with corresponding FLT uptake value (r = 0.61, P < 0.001). The correlation between MSP58 expression and glioma malignancy was also confirmed by immunofluorescence, RT-PCR and western blot analysis. FLT uptake value also exhibited a highly significant positive correlation with the Ki-67 index (r = 0.59, P < 0.001). Kaplan-Meier analysis revealed that MSP58 expression has a significant prognostic ability for the overall survival time similar to that found in the uptake value of FLT-PET. Conclusion: These results indicate that MSP58 plays an important role in cell proliferation and will be one of the potential candidates of molecular therapy targeting proliferation. FLT-PET might be used as an early measure of treatment response in the proliferation-targeted therapy. (C) 2016 The Author(s) Published by S. Karger AG, Basel
C1 [Lin, Wei; Dai, Shu-hui; Chen, Tao; Fei, Zhou] Fourth Mil Med Univ, Xijing Hosp, Dept Neurosurg, 127 ChangLe West Rd, Xian 710032, Shaanxi Provinc, Peoples R China.
   [Lin, Wei; Kawai, Nobuyuki; Miyake, Keisuke; Okada, Masaki; Tamiya, Takashi] Kagawa Univ, Fac Med, Dept Neurol Surg, Takamatsu, Kagawa 760, Japan.
   [Haba, Reiji] Kagawa Univ, Fac Med, Dept Diagnost Pathol, Takamatsu, Kagawa 760, Japan.
   [Yamaoto, Yuka] Kagawa Univ, Fac Med, Dept Radiol, Takamatsu, Kagawa 760, Japan.
   [Chen, Tao] PLA, Hosp 123, Dept Neurosurg, Bengbu, Peoples R China.
C3 Air Force Military Medical University; Kagawa University; Kagawa
   University; Kagawa University
RP Fei, Z (corresponding author), Fourth Mil Med Univ, Xijing Hosp, Dept Neurosurg, 127 ChangLe West Rd, Xian 710032, Shaanxi Provinc, Peoples R China.; Tamiya, T (corresponding author), Kagawa Univ, Fac Med, Dept Neurol Surg, Takamatsu, Kagawa 760, Japan.
EM Tamiya_kagawa@163.com; fmmuzhoufei@163.com
RI Kawai, Nobuyuki/M-4902-2014; tang, cheng/KLD-8823-2024
FU Ministry of Education, Science and Culture of Japan [26293324]; Grant of
   China (National Nature Science Foundation of China) [81001123,
   81572469]; Grants-in-Aid for Scientific Research [26293324] Funding
   Source: KAKEN
FX We gratefully acknowledge the excellent technical support of PET
   radiological technologist at our institution. This study was supported
   by a Grant-in-Aid for Scientific Research (B) (26293324) from the
   Ministry of Education, Science and Culture of Japan. Lin Wei is a
   research doctor from the Department of Neurosurgery, Xijing Hospital,
   Fourth Military Medical University, China. This study was also supported
   by a Grant of China (National Nature Science Foundation of China, No:
   81001123 and No:81572469).
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U1 0
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PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1015-8987
EI 1421-9778
J9 CELL PHYSIOL BIOCHEM
JI Cell. Physiol. Biochem.
PY 2016
VL 38
IS 2
BP 635
EP 645
DI 10.1159/000438656
PG 11
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA DF1ER
UT WOS:000371082300016
PM 26849376
OA gold
DA 2025-01-04
ER

PT J
AU Sticz, T
   Molnár, A
   Dankó, T
   Hujber, Z
   Petovári, G
   Nagy, N
   Végso, G
   Kopper, L
   Sebestyén, A
AF Sticz, Tamas
   Molnar, Anna
   Danko, Titanilla
   Hujber, Zoltan
   Petovari, Gabor
   Nagy, Noemi
   Vegso, Gyula
   Kopper, Laszlo
   Sebestyen, Anna
TI The Effects of Different mTOR Inhibitors in EGFR Inhibitor Resistant
   Colon Carcinoma Cells
SO PATHOLOGY & ONCOLOGY RESEARCH
LA English
DT Article
DE Colon carcinoma; EGFR inhibitor; mTOR inhibitor; Resistance
ID TARGETED THERAPY; COLORECTAL-CANCER; IN-VITRO; PHASE-I; CISPLATIN;
   EFFICACY; TEMSIROLIMUS; COMBINATION; STRATEGIES; IRINOTECAN
AB Several monoclonal antibodies and inhibitors targeting signalling pathways are being used in personalised medicine. Anti-EGFR antibodies seem to be effective, however, therapy resistance often occurs in colon carcinoma cases. mTOR inhibitors (mTORIs) could have a potential role in the breakthrough of therapy resistance. The mTOR activity related protein expression patterns and the in vitro effects of EGFR inhibitors (EGFRIs), mTORIs and their combinations were studied in different colon carcinoma cell lines (with different genetic backgrounds). Alamar Blue test and flow cytometry were used to analyse the in vitro proliferation and apoptotic effects of cetuximab, gefitinib, cisplatin, rapamycin, PP242 and NVP-BEZ235. The expressions of mTOR activity related proteins (p-70S6K, p-S6, Rictor, p-mTOR, Raptor) were studied by Western blot, immunocytochemistry and Duolink staining. The EGFRI resistance of the studied colon carcinoma cell lines related to their known mutations were confirmed, neither gefitinib nor cetuximab inhibited the proliferation or induced apoptosis in vitro. Individual differences in Rictor and Raptor expressions were detected by Western blot and immunocytochemistry beside elevated mTOR activity of these different colon carcinoma cell lines. These expression patterns correlated to the mTORIs sensitivity differences, moreover, mTORIs could enhance the effects of EGFRIs and other in vitro treatments. Our results suggest that mTORI combinations could be helpful in both EGFRI and platinum-based therapy of colon carcinomas. Moreover, we suggest determining both mTOR complex activity and mutations in Akt/mTOR signalling pathways for selecting the appropriate mTORIs and patients in potential future combination treatments.
C1 [Sticz, Tamas; Molnar, Anna; Danko, Titanilla; Hujber, Zoltan; Petovari, Gabor; Nagy, Noemi; Kopper, Laszlo; Sebestyen, Anna] Semmelweis Univ, Dept Pathol & Expt Canc Res 1, Ulloi Ut 26, H-1085 Budapest, Hungary.
   [Vegso, Gyula] Semmelweis Univ, Dept Transplantat & Surg, Ulloi Ut 26, H-1085 Budapest, Hungary.
   [Sebestyen, Anna] Hungarian Acad Sci, Joint Res Org, Tumour Progress Res Grp, Ulloi Ut 26, H-1085 Budapest, Hungary.
   [Sebestyen, Anna] Semmelweis Univ, Ulloi Ut 26, H-1085 Budapest, Hungary.
C3 Semmelweis University; Semmelweis University; Hungarian Academy of
   Sciences; Semmelweis University
RP Sebestyén, A (corresponding author), Semmelweis Univ, Dept Pathol & Expt Canc Res 1, Ulloi Ut 26, H-1085 Budapest, Hungary.; Sebestyén, A (corresponding author), Hungarian Acad Sci, Joint Res Org, Tumour Progress Res Grp, Ulloi Ut 26, H-1085 Budapest, Hungary.; Sebestyén, A (corresponding author), Semmelweis Univ, Ulloi Ut 26, H-1085 Budapest, Hungary.
EM hsebanna@gmail.com
RI Kopper, Laszlo/F-2594-2013
OI Gabor, Petovari/0000-0002-1957-2864
FU OTKA project [K84262]; Semmelweis University Scientific and Innovation
   Founds [STIA-KF-17]; Bolyai fellowship [590/2015]; New National
   Excellence Programs [UNKP-17-3, UNKP-17-2]
FX The project was supported by OTKA project (K84262) and Semmelweis
   University Scientific and Innovation Founds (STIA-KF-17); and by Bolyai
   fellowship (590/2015 Hungarian Academy of Sciences) of the corresponding
   author (A. Sebestyen). The related research works of Z.Hujber and T.
   Danko were also supported by New National Excellence Programs
   (UNKP-17-3; UNKP-17-2).
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NR 36
TC 5
Z9 5
U1 0
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1219-4956
EI 1532-2807
J9 PATHOL ONCOL RES
JI Pathol. Oncol. Res.
PD OCT
PY 2019
VL 25
IS 4
BP 1379
EP 1386
DI 10.1007/s12253-018-0434-4
PG 8
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA JH3JE
UT WOS:000492663100014
PM 29882195
DA 2025-01-04
ER

PT J
AU Makowiec, F
   Bronsert, P
   Klock, A
   Hopt, UT
   Neeff, HP
AF Makowiec, Frank
   Bronsert, Peter
   Klock, Andrea
   Hopt, Ulrich T.
   Neeff, Hannes P.
TI Prognostic influence of hepatic margin after resection of colorectal
   liver metastasis: role of modern preoperative chemotherapy
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Article
DE Colorectal liver metastasis; Neoadjuvant chemotherapy; Hepatic
   resection; Resection margin; Survival
ID SURGICAL MARGIN; NEOADJUVANT CHEMOTHERAPY; R1 RESECTION; SURVIVAL;
   CANCER; SURGERY; ERA; DETERMINANT; RECURRENCE; THERAPY
AB Modern chemotherapy (CTX) increases survival in stage IV colorectal cancer. In colorectal liver metastases (CLM), neoadjuvant (neo) CTX may increase resectability and improve survival. Due to widespread use of CTX in CLM, recent studies assessed the role of the hepatic margin after CTX, with conflicting results. We evaluated the outcome after resection of CLM in relation to CTX and hepatic resection status.
   Since 2000, 334 patients with first hepatic resection for isolated CLM were analyzed. Thirty-two percent had neoadjuvant chemotherapy (targeted therapy in 42%). Sixty-eight percent never had CTX before hepatectomy or longer than 6 months before resection. The results were gained by analysis of our prospective database.
   Positive hepatic margins occurred in 8% (independent of neoCTx). Patients after neoCTX had higher numbers of CLM (p < 0.01) and a longer duration of surgery (p < 0.03). After hepatectomy, 5-year survival was 45% and correlated strongly with the margin status (47% in R-0 and 21% in R-1; p < 0.001). Survival also correlated with margin status in the subgroups with neoCTX (p < 0.01) or without neoCTx (p < 0.01). In multivariate analysis of the entire group, hepatic margin status (RR 3.2; p < 0.001) and age > 65 years (RR 1.6; p < 0.01) were associated with poorer survival. In the subgroup of patients after neoCTX (n = 106), only the resection margin was an independent predictor of survival (p < 0.001).
   In patients with isolated colorectal liver metastases undergoing resection, the hepatic margin status was the strongest independent prognostic factor. This effect was also present after neoadjuvant chemotherapy for CLM.
C1 [Makowiec, Frank; Klock, Andrea; Hopt, Ulrich T.; Neeff, Hannes P.] Univ Freiburg, Dept Surg, Hugstetter Str 55, D-79106 Freiburg, Germany.
   [Makowiec, Frank; Bronsert, Peter; Neeff, Hannes P.] Univ Freiburg, Ctr Comprehens Canc, Hugstetter Str 55, D-79106 Freiburg, Germany.
   [Bronsert, Peter] Univ Freiburg, Inst Pathol, Hugstetter Str 55, D-79106 Freiburg, Germany.
C3 University of Freiburg; University of Freiburg; University of Freiburg
RP Makowiec, F (corresponding author), Univ Freiburg, Dept Surg, Hugstetter Str 55, D-79106 Freiburg, Germany.; Makowiec, F (corresponding author), Univ Freiburg, Ctr Comprehens Canc, Hugstetter Str 55, D-79106 Freiburg, Germany.
EM frank.makowiec@uniklinik-freiburg.de
RI Neeff, Hannes/V-4968-2019
OI Klock, Andrea/0000-0002-0295-0574
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NR 25
TC 18
Z9 20
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0179-1958
EI 1432-1262
J9 INT J COLORECTAL DIS
JI Int. J. Colorectal Dis.
PD JAN
PY 2018
VL 33
IS 1
BP 71
EP 78
DI 10.1007/s00384-017-2916-3
PG 8
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA FR5WV
UT WOS:000419138200011
PM 29098384
DA 2025-01-04
ER

PT J
AU Park, S
   Park, S
   Lee, SH
   Suh, B
   Ock, CY
   Keam, B
   Kim, TM
   Kim, DW
   Kim, YW
   Heo, DS
AF Park, Sehhoon
   Park, Seongyeol
   Lee, Se-Hoon
   Suh, Beomseok
   Ock, Chan-Young
   Keam, Bhumsuk
   Kim, Tae Min
   Kim, Dong-Wan
   Kim, Young Whan
   Heo, Dae Seog
TI Pretreatment albumin-to-globulin ratio as a predictive marker for
   tyrosine kinase inhibitor in non-small cell lung cancer
SO CANCER BIOMARKERS
LA English
DT Article
DE Albumins; globulins; non-small-cell lung carcinoma; tyrosine kinases
   inhibitor; epidermal growth factor receptor; disease-free survival
ID LONG-TERM MORTALITY; COLORECTAL-CANCER; EGFR-TKI; 1ST-LINE TREATMENT;
   PROGNOSTIC VALUE; TUMOR NECROSIS; OPEN-LABEL; INFLAMMATION; ERLOTINIB;
   CHEMOTHERAPY
AB BACKGROUND: A low albumin-to-globulin ratio (AGR) has been known as a prognostic factor for cancer-related mortality. However, no study has elucidated its usefulness as a predictive factor in the era of targeted therapy, and so, we evaluated this in the present study.
   METHODS: We retrospectively analyzed 2012 non-small cell lung cancer (NSCLC) patients treated with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs). Among these patients, 645 patients who had EGFR mutation and suitable pretreatment laboratory values were included. AGR was calculated 2 months before treatment and 4 months after treatment in each patient. The optimal cutoff value of AGR, and progression free survival (PFS) were also determined.
   RESULTS: The optimal cutoff value of AGR was 1.17, which yielded a highest HR of 1.89 (P < 0.001) for poor PFS. The median PFS was 9.5 months (95% confidential interval [CI] 7.0-10.4) in patients with pretreatment AGR < 1.17 and 13.5 months (95% CI 11.9-14.7) in those with pretreatment AGR >= 1.17. Pretreatment AGR showed an independent predictive value (adjusted HR 1.80, P < 0.001) when age, performance status, and pre-TKI systemic treatment was adjusted for.
   CONCLUSIONS: We suggest that patients with NSCLC with EGFR mutations who have AGR values lower than 1.17 at the beginning of EGFR TKI treatment should be considered to have a high risk of early EGFR TKI failure.
C1 [Park, Sehhoon; Park, Seongyeol; Lee, Se-Hoon; Ock, Chan-Young; Keam, Bhumsuk; Kim, Tae Min; Kim, Dong-Wan; Kim, Young Whan; Heo, Dae Seog] Seoul Natl Univ Hosp, Dept Internal Med, Seoul 110744, South Korea.
   [Suh, Beomseok] Seoul Natl Univ Hosp, Dept Family Med, Seoul 110744, South Korea.
   [Suh, Beomseok] Seoul Natl Univ Hosp, Hlth Promot Ctr, Seoul 110744, South Korea.
   [Lee, Se-Hoon] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Med,Div Hematol Oncol, 81 Irwon Ro, Seoul 06351, South Korea.
C3 Seoul National University (SNU); Seoul National University Hospital;
   Seoul National University (SNU); Seoul National University Hospital;
   Seoul National University (SNU); Seoul National University Hospital;
   Sungkyunkwan University (SKKU); Samsung Medical Center
RP Lee, SH (corresponding author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Med,Div Hematol Oncol, 81 Irwon Ro, Seoul 06351, South Korea.
EM sehoon.lee119@gmail.com
RI Heo, Dae/J-2184-2012; Kim, Sang/AAI-5704-2020; Kim, Il
   Young/LLK-4732-2024; Kim, Dong-Wan/J-5391-2012
FU Innovative Research Institute for Cell Therapy, Republic of Korea
   [A062260]
FX This study was supported by a grant from the Innovative Research
   Institute for Cell Therapy, Republic of Korea (A062260).
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NR 28
TC 20
Z9 20
U1 0
U2 0
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 1574-0153
EI 1875-8592
J9 CANCER BIOMARK
JI Cancer Biomark.
PY 2016
VL 16
IS 3
BP 425
EP 433
DI 10.3233/CBM-160581
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DJ4NG
UT WOS:000374182100015
PM 27062699
DA 2025-01-04
ER

PT J
AU Tobin, NP
   Foukakis, T
   De Petris, L
   Bergh, J
AF Tobin, N. P.
   Foukakis, T.
   De Petris, L.
   Bergh, J.
TI The importance of molecular markers for diagnosis and selection of
   targeted treatments in patients with cancer
SO JOURNAL OF INTERNAL MEDICINE
LA English
DT Review
DE Breast; colon; lung; immunohistochemistry; gene expression; next
   generation sequencing
ID CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER; EARLY BREAST-CANCER;
   PHASE-III TRIAL; OXALIPLATIN-BASED CHEMOTHERAPY; CLINICAL-PRACTICE
   GUIDELINES; PLUS ADJUVANT CHEMOTHERAPY; GENE-EXPRESSION SIGNATURES;
   OPEN-LABEL; 1ST-LINE TREATMENT
AB The past 30 years have seen the introduction of a number of cancer therapies with the aim of restricting the growth and spread of primary and metastatic tumours. A shared commonality among these therapies is their targeting of various aspects of the cancer hallmarks, that is traits that are essential to successful tumour propagation and dissemination. The evolution of molecular-scale technology has been central to the identification of new cancer targets, and it is not a coincidence that improved therapies have emerged at the same time as gene expression arrays and DNA sequencing have enhanced our understanding of cancer genetics. Modern tumour pathology is now viewed at the molecular level ranging from IHC biomarkers, to gene signature classifiers and gene mutations, all of which provide crucial information about which patients will respond to targeted therapy regimens. In this review, we briefly discuss the general types of targeted therapies used in a clinical setting and provide a short background on immunohistochemical, gene expression and DNA sequencing technologies, before focusing on three tumour types: breast, lung and colorectal cancers. For each of these cancer types, we provide a background to the disease along with an overview of the current standard therapies and then focus on the relevant targeted therapies and the pathways they inhibit. Finally, we highlight several strategies that are pivotal to the successful development of targeted anti-cancer drugs.
C1 Karolinska Inst, Dept Pathol & Oncol, Stockholm, Sweden.
   Univ Hosp, Stockholm, Sweden.
C3 Karolinska Institutet
RP Tobin, NP (corresponding author), Karolinska Univ Hosp, CCK, R 8-3, SE-17176 Stockholm, Sweden.
EM nick.tobin@ki.se
RI Foukakis, Theodoros/KJL-9701-2024; Tobin, Nicholas/AAE-9806-2019
OI Bergh, Jonas/0000-0001-5526-1847; Tobin, Nicholas/0000-0003-2343-9772;
   Foukakis, Theodoros/0000-0001-8952-9987
FU Swedish Cancer Society; Stockholm Cancer Society; BRECT (Karolinska
   Institutet); BRECT (Stockholm County Council); Knut and Alice Wallenberg
   Foundation; King Gustav V Jubilee Foundation; ALF Foundation; Linne
   Foundation; Swedish Research Council; Merck; Amgen; Roche;
   Sanofi-Aventis; Bayer, through Karolinska University Hospital
FX Jonas Bergh's research group is supported by grants from the Swedish
   Cancer Society, the Stockholm Cancer Society, BRECT (Karolinska
   Institutet and Stockholm County Council), Knut and Alice Wallenberg
   Foundation, the King Gustav V Jubilee Foundation, the ALF Foundation,
   the Linne Foundation and the Swedish Research Council. JB receives
   research funding from Merck, Amgen, Roche, Sanofi-Aventis and Bayer,
   through Karolinska University Hospital.
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NR 176
TC 40
Z9 46
U1 0
U2 17
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0954-6820
EI 1365-2796
J9 J INTERN MED
JI J. Intern. Med.
PD DEC
PY 2015
VL 278
IS 6
BP 545
EP 570
DI 10.1111/joim.12429
PG 26
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA CY7RE
UT WOS:000366605600001
PM 26373821
OA Bronze
DA 2025-01-04
ER

PT J
AU Hsu, JC
   Chang, SM
   Lu, CY
AF Hsu, Jason C.
   Chang, Sheng-Mao
   Lu, Christine Y.
TI Geographic Variations and Time Trends in Cancer Treatments in Taiwan
SO BMC PUBLIC HEALTH
LA English
DT Article
DE Cancer; Targeted Therapy; Geographic regions; Taiwan
ID CELL LUNG-CANCER; BREAST-CANCER; UNITED-STATES; COLORECTAL-CANCER;
   RISK-FACTORS; HIGH COST; HEPATOCELLULAR-CARCINOMA; NECK-CANCER; THERAPY;
   DRUGS
AB Background: Targeted therapies have become important treatment options for cancer care in many countries. This study aimed to examine recent trends in utilization of antineoplastic drugs, particularly the use of targeted therapies for treatment of cancer, by geographic region in Taiwan (northern, midwestern, southern, and eastern regions and the outer islands).
   Methods: This was a retrospective observational study of antineoplastic agents using 2009-2012 quarterly claims data from Taiwan's National Health Insurance Research Database. Yearly market shares by prescription volume and costs for targeted therapies among total antineoplastic agents by region were estimated. We used multivariate regression model and ANOVA to examine variations in utilization of targeted therapies between geographic regions and used ARIMA models to estimate longitudinal trends.
   Results: Population-adjusted use and costs of antineoplastic drugs (including targeted therapies) were highest in the southern region of Taiwan and lowest in the outer islands. We found a 4-fold difference in use of antineoplastic drugs and a 49-fold difference in use of targeted therapies between regions if the outer islands were included. There were minimal differences in use of antineoplastic drugs between other regions with about a 2-fold difference in use of targeted therapies. Without considering the outer islands, the market share by prescription volume and costs of targeted therapies increased almost 2-fold (1.84-1.90) and 1.5-fold (1.26-1.61) respectively between 2009 and 2012. Furthermore, region was not significantly associated with use of antineoplastic agents or use of targeted therapies after adjusting for confounders. Region was associated with costs of antineoplastic agents but it was not associated with costs of targeted therapies after confounding adjustments.
   Conclusions: Use of antineoplastic drugs overall and use of targeted therapies for treatment of cancer varied somewhat between regions in Taiwan; use was notably low in the outer islands. Strategies might be needed to ensure access to cancer care in each region as economic burden of cancer care increase due to growing use of targeted therapies.
C1 [Hsu, Jason C.] Natl Cheng Kung Univ, Coll Med, Sch Pharm, 1 Daxue Rd, Tainan 70101, Taiwan.
   [Hsu, Jason C.] Natl Cheng Kung Univ, Coll Med, Inst Clin Pharm & Pharmaceut Sci, 1 Daxue Rd, Tainan 70101, Taiwan.
   [Chang, Sheng-Mao] Natl Cheng Kung Univ, Dept Stat, Coll Management, Tainan, Taiwan.
   [Lu, Christine Y.] Harvard Med Sch, Dept Populat Med, Boston, MA USA.
   [Lu, Christine Y.] Harvard Pilgrim Hlth Care Inst, Boston, MA USA.
C3 National Cheng Kung University; National Cheng Kung University; National
   Cheng Kung University; Harvard University; Harvard Medical School;
   Harvard Pilgrim Health Care
RP Hsu, JC (corresponding author), Natl Cheng Kung Univ, Coll Med, Sch Pharm, 1 Daxue Rd, Tainan 70101, Taiwan.; Hsu, JC (corresponding author), Natl Cheng Kung Univ, Coll Med, Inst Clin Pharm & Pharmaceut Sci, 1 Daxue Rd, Tainan 70101, Taiwan.
EM jasonhsuharvard@gmail.com
OI Lu, Christine Y./0000-0002-7550-6837; Chang,
   Sheng-Mao/0000-0003-2785-0155
FU Taiwan Ministry of Science and Technology grants [MOST
   104-2320-B-006-005, MOST 105-2314-B-006-021]
FX Dr. Hsu was supported by Taiwan Ministry of Science and Technology
   grants (Grant ID: MOST 104-2320-B-006-005, MOST 105-2314-B-006-021). 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 49
TC 5
Z9 6
U1 1
U2 9
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2458
J9 BMC PUBLIC HEALTH
JI BMC Public Health
PD AUG 2
PY 2017
VL 18
AR 89
DI 10.1186/s12889-017-4615-y
PG 11
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Public, Environmental & Occupational Health
GA FC3QO
UT WOS:000406754200004
PM 28768504
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yadav, P
   Vengoji, R
   Jain, M
   Batra, SK
   Shonka, N
AF Yadav, Poonam
   Vengoji, Raghupathy
   Jain, Maneesh
   Batra, Surinder K.
   Shonka, Nicole
TI Pathophysiological role of histamine signaling and its implications in
   glioblastoma
SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
LA English
DT Review
DE Glioblastoma; Histamine; Antihistamine
ID ENDOTHELIAL GROWTH-FACTOR; MAST-CELLS; MESENCHYMAL TRANSITION;
   EXTRACELLULAR-MATRIX; INTERNATIONAL UNION; COLORECTAL-CANCER;
   TUMOR-GROWTH; EXPRESSION; RECEPTOR; GLIOMA
AB Glioblastoma (GBM), an extremely aggressive and prevalent malignant brain tumor, remains a challenge to treat. Despite a multimodality treatment approach, GBM recurrence remains inevitable, particularly with the emergence of temozolomide (TMZ) resistance and limited treatment options. Surprisingly, previous studies show that a history of allergies, atopy, or asthma is inversely associated with GBM risk. Further, the electronic medical record at the University Hospital of Lausanne showed that the GBM patients taking antihistamine during treatment had better survival. Histamine is an essential neurotransmitter in the brain and plays a significant role in regulating sleep, hormonal balance, and cognitive functions. Elevated levels of histamine and increased histamine receptor expression have been found in different tumors and their microenvironments, including GBM. High histamine 1 receptor (HRH1) expression is inversely related to overall and progression-free survival in GBM patients, further emphasizing the role of histamine in disease progression. This review aims to provide insights into the challenges of GBM treatment, the role of histamine in GBM progression, and the rationale for considering antihistamines as targeted therapy. The review concludes by encouraging further investigation into antihistamine mechanisms and their impact on the tumor microenvironment.
C1 [Yadav, Poonam; Vengoji, Raghupathy; Jain, Maneesh; Batra, Surinder K.] Univ Nebraska Med Ctr, Dept Biochem & Mol Biol, Omaha, NE 68198 USA.
   [Jain, Maneesh; Batra, Surinder K.; Shonka, Nicole] Univ Nebraska Med Ctr, Fred & Pamela Buffett Canc Ctr, Omaha, NE 68198 USA.
   [Jain, Maneesh; Batra, Surinder K.] Univ Nebraska Med Ctr, Eppley Inst Res Canc & Allied Dis, Omaha, NE 68198 USA.
   [Shonka, Nicole] Univ Nebraska Med Ctr, Dept Internal Med, 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
RP Batra, SK; Shonka, N (corresponding author), Univ Nebraska Med Ctr, Fred & Pamela Buffett Canc Ctr, Omaha, NE 68198 USA.
EM sbatra@unmc.edu; nshonka@unmc.edu
FU Institutes of Health (NIH) [R01CA273319, R01CA273349, P01CA217798,
   U01CA200466]
FX The authors are partly supported by grants from the National Institutes
   of Health (NIH) R01CA273319, R01CA273349, P01CA217798, and U01CA200466.r
   Institutes of Health (NIH) R01CA273319, R01CA273349, P01CA217798, and
   U01CA200466.
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NR 128
TC 1
Z9 1
U1 3
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0304-419X
EI 1879-2561
J9 BBA-REV CANCER
JI Biochim. Biophys. Acta-Rev. Cancer
PD SEP
PY 2024
VL 1879
IS 5
AR 189146
DI 10.1016/j.bbcan.2024.189146
EA JUL 2024
PG 13
WC Biochemistry & Molecular Biology; Biophysics; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Oncology
GA YW0W8
UT WOS:001271413900001
PM 38955315
DA 2025-01-04
ER

PT J
AU Chen, JF
   Yu, BX
   Yu, R
   Ma, L
   Lv, XY
   Cheng, Y
   Ma, Q
AF Chen, Jun-Feng
   Yu, Bi-Xia
   Yu, Rui
   Ma, Liang
   Lv, Xiu-Yi
   Cheng, Yue
   Ma, Qi
TI Monoclonal antibody Zt/g4 targeting RON receptor tyrosine kinase
   enhances chemosensitivity of bladder cancer cells to Epirubicin by
   promoting G1/S arrest and apoptosis
SO ONCOLOGY REPORTS
LA English
DT Article
DE RON; non-muscle invasive bladder tumors; epirubicin; chemosensitivity;
   cell cycle; cell apoptosis; proliferation and invasion
ID INVASIVE UROTHELIAL CARCINOMA; CYCLIN-DEPENDENT KINASES;
   COLORECTAL-CANCER; TUMORIGENIC ACTIVITIES; THERAPEUTIC TARGET; TUMOR
   PROGRESSION; EAU GUIDELINES; CROSS-TALK; EXPRESSION; GROWTH
AB Epirubicin (EPI) is one of the most used intravesical chemotherapy agents after transurethral resection to non muscle invasive bladder tumors (NMIBC) to prevent cancer recurrence and progression. However, even after resection of bladder tumors and intravesical chemotherapy, half of them will recur and progress. RON is a membrane tyrosine kinase receptor usually overexpressed in bladder cancer cells and associated with poor pathological features. This study aims to investigate the effects of anti-RON monoclonal antibody Zt/g4 on the chemosensitivity of bladder cells to EPI. After Zt/g4 treatment, cell cytotoxicity was significantly increased and cell invasion was markedly suppressed in EPI-treated bladder cancer cells. Further investigation indicated that combing Zt/g4 with EPI promoted cell G1/S-phase arrest and apoptosis, which are the potential mechanisms that RON signaling inhibition enhances chemosensitivity of EPI. Thus, combing antibody-based RON targeted therapy enhances the therapeutic effects of intravesical chemotherapy, which provides new strategy for further improvement of NMIBC patient outcomes.
C1 [Chen, Jun-Feng; Yu, Bi-Xia; Ma, Liang; Lv, Xiu-Yi; Cheng, Yue; Ma, Qi] Ningbo Univ, Affiliated Hosp, Ningbo Hosp 1, Translat Res Lab Urol, Ningbo 315010, Zhejiang, Peoples R China.
   [Cheng, Yue; Ma, Qi] Ningbo Univ, Affiliated Hosp, Ningbo Hosp 1, Dept Urol, Ningbo 315010, Zhejiang, Peoples R China.
   [Yu, Rui] Ningbo Univ, Sch Med, Zhejiang Key Lab Pathophysiol, Dept Biochem & Mol Biol, Ningbo 315212, Zhejiang, Peoples R China.
C3 Ningbo University; Ningbo University; Ningbo University
RP Cheng, Y; Ma, Q (corresponding author), Ningbo Univ, Affiliated Hosp, Ningbo Hosp 1, Translat Res Lab Urol, Ningbo 315010, Zhejiang, Peoples R China.; Cheng, Y; Ma, Q (corresponding author), Ningbo Univ, Affiliated Hosp, Ningbo Hosp 1, Dept Urol, Ningbo 315010, Zhejiang, Peoples R China.
EM yue.cheng@eyou.com; qi.ma@eyou.com
RI Ma, Liang/L-1363-2016; Chen, Junfeng/M-2765-2014; Cheng,
   Yue/Z-4456-2019; ma, qi/AGL-6070-2022
OI Ma, Qi/0000-0002-5350-0362
FU National Natural Science Foundation of China [81272828, 31501113];
   Zhejiang Provincial Foundation for Medical and Health Sciences
   [2016KYB263, 2014KYB355]; Ningbo Natural Science Foundation
   [2015A610224, 2015A610177]
FX This study was supported by the National Natural Science Foundation of
   China (grant no. 81272828 to Q.M., and no. 31501113 to R.Y.), Zhejiang
   Provincial Foundation for Medical and Health Sciences (grant no.
   2016KYB263 and 2014KYB355 to Q.M.), and Ningbo Natural Science
   Foundation (grant no. 2015A610224 to J.-F.C. and no. 2015A610177 to
   R.Y.).
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NR 46
TC 9
Z9 11
U1 0
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD FEB
PY 2017
VL 37
IS 2
BP 721
EP 728
DI 10.3892/or.2017.5356
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EJ3BU
UT WOS:000393086900008
PM 28075465
OA Green Submitted, hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Zhao, ZL
   Wang, XX
   Ding, Y
   Cao, XF
   Zhang, XY
AF Zhao, Zonglei
   Wang, Xixiu
   Ding, Yan
   Cao, Xuefeng
   Zhang, Xingyuan
TI SMC4, a novel tumor prognostic marker and potential tumor therapeutic
   target
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE SMC4; tumor; prognosis; biomarker; targeted therapy; overall survival
ID STRUCTURAL MAINTENANCE; COLORECTAL-CANCER; BREAST-CANCER; CHROMOSOMES 4;
   CONDENSIN; CELLS
AB The structural maintenance of chromosome 4 (SMC4) is a member of the ATPase family of chromosomes. The most widely reported function of SMC4, as well as the remaining subunits of whole condensin complexes, is compression and dissociation of sister chromatids, DNA damage repair, DNA recombination, and pervasive transcription of the genome. Studies have also shown that SMC4 plays an exceedingly essential role in the division cycle of embryonic cells, such as RNA splicing, DNA metabolic process, cell adhesion, and extracellular matrix. On the other hand, SMC4 is also a positive regulator of the inflammatory innate immune response, while excessive innate immune responses not only disrupt immune homeostasis and may lead to autoimmune diseases, but even cancer. To further understand the expression and prognostic value of SMC4 in tumors, we provide an in-depth review of the literature and several bioinformatic databases, for example, The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), Clinical Proteomic Tumor Analysis Consortium (CPTAC), The Human Protein Atlas and Kaplan Meier plotter tools, illustrating that SMC4 plays a vital role in the occurrence and development of tumors, and high expression of SMC4 seems to consistently predict worse overall survival. In conclusion, we present this review which introduces the structure, biological function of SMC4, and its correlation with the tumor in detail; it might provide new insight into a novel tumor prognostic marker and potential tumor therapeutic target.
C1 [Zhao, Zonglei; Ding, Yan; Cao, Xuefeng; Zhang, Xingyuan] Binzhou Med Univ Hosp, Dept Hepatobiliary Surg, Binzhou, Shandong, Peoples R China.
   [Wang, Xixiu] Binzhou Med Univ Hosp, Dept Cardiovasc Dis, Binzhou, Shandong, Peoples R China.
C3 Binzhou Medical University; Binzhou Medical University
RP Cao, XF (corresponding author), Binzhou Med Univ Hosp, Dept Hepatobiliary Surg, Binzhou, Shandong, Peoples R China.
EM byfygdwk_cxf@163.com
RI Cao, Xuefeng/HHD-0152-2022
OI Zhao, Zonglei/0000-0002-5752-0491
FU Project of Medical and Health Technology Development Program in Shandong
   Province [202104081018]
FX Funding This research was supported by the Project of Medical and Health
   Technology Development Program in Shandong Province (No. 202104081018).
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Z9 4
U1 1
U2 7
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD MAR 17
PY 2023
VL 13
AR 1117642
DI 10.3389/fonc.2023.1117642
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C3XV7
UT WOS:000961292900001
PM 37007153
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Stein, MK
   Oluoha, O
   Patel, K
   VanderWalde, A
AF Stein, Matthew K.
   Oluoha, Oluchukwu
   Patel, Kruti
   VanderWalde, Ari
TI Precision Medicine in Oncology: A Review of Multi-Tumor Actionable
   Molecular Targets with an Emphasis on Non-Small Cell Lung Cancer
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Review
DE cancer; next-generation sequencing; targeted therapy; precision
   oncology; tumor-agnostic indications; solid tumors; tumor markers;
   FDA-approved therapeutics
ID METASTATIC BREAST-CANCER; DABRAFENIB PLUS TRAMETINIB; UNCOMMON EGFR
   MUTATIONS; TYROSINE KINASE INHIBITORS; POSITIVE SOLID TUMORS;
   BRAF-MUTANT MELANOMA; I/II ARROW TRIAL; PHASE-II TRIAL; OPEN-LABEL; FDA
   APPROVAL
AB Precision medicine is essential for the modern care of a patient with cancer. Comprehensive molecular profiling of the tumor itself is necessary to determine the presence or absence of certain targetable abnormalities or biomarkers. In particular, lung cancer is a disease for which targetable genomic alterations will soon guide therapy in the majority of cases. In this comprehensive review of solid tumor-based biomarkers, we describe the genomic alterations for which targeted agents have been approved by the United States Food and Drug Administration (FDA). While focusing on alterations leading to approvals in a tumor-agnostic fashion (MSI-h, TMB-h, NTRK) and on those alterations with approvals in multiple malignancies (BRAF, ERBB2, RET, BRCA, PD-L1), we also describe several biomarkers or indications that are likely to lead to an approved drug in the near future (e.g., KRAS G12C, PD-L1 amplification, HER2 overexpression in colon cancer, HER2 mutations in lung cancer). Finally, we detail the current landscape of additional actionable alterations (EGFR, ALK, ROS1, MET) in lung cancer, a biomarker-rich malignancy that has greatly benefitted from the precision oncology revolution.
C1 [Stein, Matthew K.] Missouri Baptist Med Ctr, Heartland Canc Res, NCI Community Oncol Res Program, St Louis, MO 63131 USA.
   [Oluoha, Oluchukwu; Patel, Kruti] Univ Tennessee, Hlth Sci Ctr, Div Hematol & Oncol, Memphis, TN 38103 USA.
   [VanderWalde, Ari] West Canc Ctr & Res Inst, Germantown, TN 38138 USA.
C3 University of Tennessee System; University of Tennessee Health Science
   Center
RP VanderWalde, A (corresponding author), West Canc Ctr & Res Inst, Germantown, TN 38138 USA.
EM Matthew.stein@bjc.org; ooluoha@westclinic.com; kpatel@westclinic.com;
   avanderwalde@westclinic.com
RI VanderWalde, Ari/HLQ-7510-2023; Patel, Kruti/IAO-8038-2023
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NR 228
TC 13
Z9 13
U1 0
U2 9
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 JUN
PY 2021
VL 11
IS 6
AR 518
DI 10.3390/jpm11060518
PG 33
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA SY6RA
UT WOS:000666011500001
PM 34198738
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Noeparast, A
   Teugels, E
   Giron, P
   Verschelden, G
   De Brakeleer, S
   Decoster, L
   De Grève, J
AF Noeparast, Amir
   Teugels, Erik
   Giron, Philippe
   Verschelden, Gil
   De Brakeleer, Sylvia
   Decoster, Lore
   De Greve, Jacques
TI Non-V600 BRAF mutations recurrently found in lung cancer predict
   sensitivity to the combination of Trametinib and Dabrafenib
SO ONCOTARGET
LA English
DT Article
DE non-V600 BRAF; lung cancer; impaired; kinase; Trametinib; Dabrafenib
ID ACQUIRED-RESISTANCE; COLORECTAL-CANCER; RAF INHIBITORS; METASTATIC
   MELANOMA; PRECLINICAL MODELS; TUMOR PROGRESSION; MEK INHIBITION; CRAF;
   ACTIVATION; MECHANISM
AB Approximately half of BRAF-mutated Non-small cell lung cancers (NSCLCs) harbor a non-V600 BRAF mutation, accounting for similar to 40,000 annual deaths worldwide. Recent studies have revealed the benefits of combined targeted therapy with a RAF-inhibitor (Dabrafenib) and a MEK-inhibitor (Trametinib) in treating V600 BRAF mutant cancers, including NSCLC. In contrast, sensitivity of non-V600 BRAF mutations to these inhibitors is not documented. Non-V600 mutations can either increase or impair BRAF kinase activity. However, impaired BRAF kinases can still activate the ERK pathway in a CRAF-dependent manner. Herein, beyond describing a cohort of BRAF mutant NSCLC patients and functionally analyzing 13 tumor-derived BRAF mutations, we demonstrate that both types of non-V600 BRAF mutations can be sensitive to clinically relevant doses of Dabrafenib and Trametinib in HEK293T cells, in lung epithelial cellular model (BEAS-2B) and in human cancer cell lines harboring non-V600 BRAF mutations. ERK activity induced by both types of these mutations is further reduced by combinatorial drug treatment. Moreover, the combination leads to more prolonged ERK inhibition and has anti-proliferative and pro-apoptotic effects in cells harboring both types of non-V600 BRAF mutations. This study provides a basis for the clinical exploration of non-V600 BRAF mutant lung cancers upon treatment with Trametinib and Dabrafenib.
C1 [Noeparast, Amir; Teugels, Erik; Giron, Philippe; Verschelden, Gil; De Brakeleer, Sylvia; Decoster, Lore; De Greve, Jacques] Vrije Univ Brussel, Oncol Centrum, UZ Brussel, Lab Mol Oncol, Brussels, Belgium.
   [Noeparast, Amir; Teugels, Erik; Giron, Philippe; Verschelden, Gil; De Brakeleer, Sylvia; Decoster, Lore; De Greve, Jacques] Vrije Univ Brussel, Oncol Centrum, UZ Brussel, Dept Med Oncol, Brussels, Belgium.
C3 Vrije Universiteit Brussel; University Hospital Brussels; Vrije
   Universiteit Brussel; University Hospital Brussels
RP De Grève, J (corresponding author), Vrije Univ Brussel, Oncol Centrum, UZ Brussel, Lab Mol Oncol, Brussels, Belgium.; De Grève, J (corresponding author), Vrije Univ Brussel, Oncol Centrum, UZ Brussel, Dept Med Oncol, Brussels, Belgium.
EM jacques.degreve@uzbrussel.be
RI Decoster, Lore/JZT-9347-2024; Giron, Philippe/ACK-1563-2022; De Greve,
   Jacques/J-4939-2012
OI Noeparast, Maxim/0000-0002-3216-5630; Giron,
   Philippe/0000-0002-1331-1890
FU Cancer Plan Belgium [29-39]; Wetenschappelijk Fonds Willy Gepts of the
   UZ Brussel, Vrije Universiteit Brussel
FX The work was funded by the Cancer Plan 29-39 Belgium and by the
   Wetenschappelijk Fonds Willy Gepts of the UZ Brussel, Vrije Universiteit
   Brussel.
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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 1
PY 2017
VL 8
IS 36
BP 60094
EP 60108
DI 10.18632/oncotarget.11635
PG 15
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FF4RQ
UT WOS:000408944300007
PM 28947956
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Ahronian, LG
   Corcoran, RB
AF Ahronian, Leanne G.
   Corcoran, Ryan B.
TI Strategies for monitoring and combating resistance to combination kinase
   inhibitors for cancer therapy
SO GENOME MEDICINE
LA English
DT Review
ID MUTANT LUNG-CANCER; METASTATIC BREAST-CANCER; CIRCULATING TUMOR DNA;
   ACQUIRED-RESISTANCE; COLORECTAL-CANCER; BRAF-MUTANT; TARGETED THERAPY;
   INTRATUMOR HETEROGENEITY; MEK INHIBITION; RAF INHIBITORS
AB Targeted therapies such as kinase inhibitors and monoclonal antibodies have dramatically altered cancer care in recent decades. Although these targeted therapies have improved patient outcomes in several cancer types, resistance ultimately develops to these agents. One potential strategy proposed to overcome acquired resistance involves taking repeat tumor biopsies at the time of disease progression, to identify the specific molecular mechanism driving resistance in an individual patient and to select a new agent or combination of agents capable of surmounting that specific resistance mechanism. However, recent studies sampling multiple metastatic lesions upon acquired resistance, or employing " liquid biopsy" analyses of circulating tumor DNA, have revealed that multiple, heterogeneous resistance mechanisms can emerge in distinct tumor subclones in the same patient. This heterogeneity represents a major clinical challenge for devising therapeutic strategies to overcome resistance. In many cancers, multiple drug resistance mechanisms often converge to reactivate the original pathway targeted by the drug. This convergent evolution creates an opportunity to target a common signaling node to overcome resistance. Furthermore, integration of liquid biopsy approaches into clinical practice may allow real-time monitoring of emerging resistance alterations, allowing intervention prior to standard detection of radiographic progression. In this review, we discuss recent advances in understanding tumor heterogeneity and resistance to targeted therapies, focusing on combination kinase inhibitors, and we discuss approaches to address these issues in the clinic.
C1 [Ahronian, Leanne G.; Corcoran, Ryan B.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02129 USA.
   [Ahronian, Leanne G.; Corcoran, Ryan B.] Harvard Med Sch, Dept Med, Boston, MA 02115 USA.
C3 Harvard University; Massachusetts General Hospital; Harvard University;
   Harvard Medical School
RP Corcoran, RB (corresponding author), Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02129 USA.; Corcoran, RB (corresponding author), Harvard Med Sch, Dept Med, Boston, MA 02115 USA.
EM rbcorcoran@partners.org
FU NIH/NCI Gastrointestinal Cancer [SPORE P50 CA127003]; Damon Runyon
   Clinical Investigator Award, NIH/NCI [1K08CA166510, 1R01CA208437]; Stand
   Up to Cancer Colorectal Cancer Dream Team Grant
FX RBC acknowledges support from the NIH/NCI Gastrointestinal CancerSPORE
   P50 CA127003, a Damon Runyon Clinical Investigator Award, NIH/NCI
   1K08CA166510, 1R01CA208437, and a Stand Up to Cancer Colorectal Cancer
   Dream Team Grant.
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NR 89
TC 46
Z9 53
U1 0
U2 17
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1756-994X
J9 GENOME MED
JI Genome Med.
PD APR 21
PY 2017
VL 9
AR 37
DI 10.1186/s13073-017-0431-3
PG 12
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA ES8WL
UT WOS:000399837500001
PM 28431544
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, HZ
   Zhou, LH
   Zhou, J
   Li, Q
   Ji, Q
AF Li, Haoze
   Zhou, Lihong
   Zhou, Jing
   Li, Qi
   Ji, Qing
TI Underlying mechanisms and drug intervention strategies for the tumour
   microenvironment
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Review
DE TME; Cancer development; Molecular targets; Drug intervention strategies
ID CANCER-ASSOCIATED FIBROBLASTS; PLACEBO-CONTROLLED TRIAL; CELL
   LUNG-CANCER; BREAST-CANCER; HEPATOCELLULAR-CARCINOMA; SUPPRESSOR-CELLS;
   PD-L1 EXPRESSION; COLON-CANCER; MOLECULAR-MECHANISMS; PANCREATIC-CANCER
AB Cancer occurs in a complex tissue environment, and its progression depends largely on the tumour microenvironment (TME). The TME has a highly complex and comprehensive system accompanied by dynamic changes and special biological characteristics, such as hypoxia, nutrient deficiency, inflammation, immunosuppression and cytokine production. In addition, a large number of cancer-associated biomolecules and signalling pathways are involved in the above bioprocesses. This paper reviews our understanding of the TME and describes its biological and molecular characterization in different stages of cancer development. Furthermore, we discuss in detail the intervention strategies for the critical points of the TME, including chemotherapy, targeted therapy, immunotherapy, natural products from traditional Chinese medicine, combined drug therapy, etc., providing a scientific basis for cancer therapy from the perspective of key molecular targets in the TME.
C1 [Li, Haoze; Zhou, Lihong; Zhou, Jing; Li, Qi; Ji, Qing] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Med Oncol, Shanghai 201203, Peoples R China.
   [Li, Haoze; Zhou, Lihong; Zhou, Jing; Li, Qi; Ji, Qing] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Canc Inst, Shanghai 201203, Peoples R China.
   [Li, Haoze; Zhou, Lihong; Zhou, Jing; Li, Qi; Ji, Qing] Shanghai Univ Tradit Chinese Med, Acad Integrat Med, Shanghai 201203, 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; Ji, Q (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Med Oncol, Shanghai 201203, Peoples R China.; Li, Q; Ji, Q (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Canc Inst, Shanghai 201203, Peoples R China.
EM qili@shutcm.edu.cn; ttt99118@hotmail.com
FU National Science Foundation of China [82030118, 81830120, 81520108031,
   82074225, 81973651]; 3 year plan of action for innovation of traditional
   Chinese medicine in Shanghai [ZY2020-CCCX-2003-03]; Key project of
   Shanghai Municipal Science and Technology Commission [16401970500]
FX This work was supported by National Science Foundation of China
   (82030118, 81830120, 81520108031 to Q.L.; 82074225 to Q.J.; 81973651 to
   L.Z.), 3 year plan of action for innovation of traditional Chinese
   medicine in Shanghai (ZY2020-CCCX-2003-03 to Q.L.), Key project of
   Shanghai Municipal Science and Technology Commission (16401970500 to
   Q.L.).
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NR 167
TC 31
Z9 34
U1 4
U2 37
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 MAR 15
PY 2021
VL 40
IS 1
AR 97
DI 10.1186/s13046-021-01893-y
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QX8AM
UT WOS:000629565400002
PM 33722297
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Gao, XH
   Li, J
   Liu, LJ
   Zheng, NX
   Zheng, K
   Mei, ZB
   Bai, CG
   Zhang, W
AF Gao, Xian Hua
   Li, Juan
   Liu, Lian Jie
   Zheng, Nan Xin
   Zheng, Kuo
   Mei, Zubing
   Bai, Chen Guang
   Zhang, Wei
TI Trends, clinicopathological features, surgical treatment patterns and
   prognoses of early-onset versus late-onset colorectal cancer: A
   retrospective cohort study on 34067 patients managed from 2000 to 2021
   in a Chinese tertiary center
SO INTERNATIONAL JOURNAL OF SURGERY
LA English
DT Article
DE Early-onset colorectal cancer; Late-onset colorectal cancer; Trends;
   Clinicopathological features; Prognosis; Comparative study
ID MOLECULAR-FEATURES; YOUNG-ONSET; SURVIVAL; COLON; AGE; ADENOCARCINOMA;
   GUIDELINES; OUTCOMES
AB Background: In recent decades, the incidence of early-onset colorectal cancer (EOCRC) has reportedly increased in several developed countries, whereas that of late-onset colorectal cancer (LOCRC) has decreased continuously. The trends, clinicopathological features, surgical treatment patterns, and prognoses of EOCRC and LOCRC in China remain unclear. Materials and methods: This retrospective cohort study was performed in China using data from our pathology registry collected in 2000-2021. Pathologically confirmed cases of colorectal cancer (CRC) were analyzed. The average annual percentage change (AAPC) was estimated to quantify the secular trends. Clinicopathological features, surgical treatment patterns, and prognoses were compared between the two groups. Multivariate Cox regression analyses were performed for disease-free survival and overall survival. Results: A total of 34,067 cases of CRC were included, with 6,369 cases of EOCRC and 27,698 cases of LOCRC. Overall, the numbers of EOCRC (AAPC = 8.4%), LOCRC (AAPC = 11.6%), and CRC (AAPC = 11.0%) cases increased significantly from 2000 to 2021. Compared to the LOCRC group, the EOCRC group had fewer men, comorbidities, concomitant cancers, polyps, and KRAS mutations; more symptoms, rectal cancers, multiple primary CRCs, deficient mismatch repair tumors, poorly differentiated, mucinous adenocarcinoma or signet ring cell carcinoma, advanced TNM stage, vascular invasion, perineural invasion; less laparoscopic surgery and sphincter-preserving surgery; more extended radical resection, perioperative chemoradiotherapy and targeted therapy; and similar disease-free and overall survival rates. Conclusion: The numbers of EOCRC and LOCRC cases have continuously increased over the last two decades. The EOCRC group has more aggressive features, advanced TNM stage, intensified surgical treatment and perioper-ative treatment than the LOCRC group, but similar disease-free and overall survival rates. More CRC screening programs are recommended for younger adults to combat the rapidly increasing trend of EOCRC.
C1 [Gao, Xian Hua; Liu, Lian Jie; Zheng, Nan Xin; Zheng, Kuo; Zhang, Wei] Naval Med Univ, Changhai Hosp, Dept Colorectal Surg, Shanghai, Peoples R China.
   [Gao, Xian Hua; Liu, Lian Jie; Zheng, Nan Xin; Zheng, Kuo; Zhang, Wei] Changhai Hosp, Hereditary Colorectal Canc Ctr, Shanghai, Peoples R China.
   [Gao, Xian Hua; Liu, Lian Jie; Zheng, Nan Xin; Zheng, Kuo; Mei, Zubing] Changhai Hosp, Genet Block Ctr Familial Canc, Shanghai, Peoples R China.
   [Li, Juan] Naval Med Univ, Changhai Hosp, Dept Nephrol, Shanghai, Peoples R China.
   [Mei, Zubing] Shanghai Univ Tradit Chinese Med, Dept Anorectal Surg, Shuguang Hosp, Shanghai, Peoples R China.
   [Mei, Zubing] Shuguang Hosp, Anorectal Dis Inst, Zhangheng Rd, Shanghai 202103, Peoples R China.
   [Bai, Chen Guang] Naval Med Univ, Changhai Hosp, Dept Pathol, Shanghai, Peoples R China.
   [Zhang, Wei] Changhai Hosp, Dept Colorectal Surg, 168 Changhai Rd, Shanghai 200433, Peoples R China.
C3 Naval Medical University; Naval Medical University; Naval Medical
   University; Naval Medical University; Shanghai University of Traditional
   Chinese Medicine; Naval Medical University; Naval Medical University
RP Mei, ZB (corresponding author), Shanghai Univ Tradit Chinese Med, Dept Anorectal Surg, Shuguang Hosp, Shanghai, Peoples R China.; Bai, CG (corresponding author), Naval Med Univ, Changhai Hosp, Dept Pathol, Shanghai, Peoples R China.; Zhang, W (corresponding author), Changhai Hosp, Dept Colorectal Surg, 168 Changhai Rd, Shanghai 200433, Peoples R China.
EM herrmayor@126.com; bcg709@126.com; weizhang2000cn@163.com
RI Mei, Zubing/H-7879-2019; Gao, Xian Hua/HJA-0052-2022
OI Mei, Zubing/0000-0001-6823-7205
FU Shanghai Pujiang Program [2019PJD052]; 234 Subject Climbing Plan of
   Changhai Hospital [2020YXK022]; National Natural Science Foundation of
   China [81572332, 82072750]; Natural Science Fund of Shanghai
   [20ZR1457200]; Medical innovation research project of Shanghai
   scientific and technological innovation action plan [21Y11912900]
FX This work was supported by the Shanghai Pujiang Program (#2019PJD052),
   234 Subject Climbing Plan of Changhai Hospital (#2020YXK022), National
   Natural Science Foundation of China (#81572332, #82072750), Natural
   Science Fund of Shanghai (20ZR1457200) and Medical innovation research
   project of Shanghai scientific and technological innovation action plan
   (21Y11912900).
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NR 37
TC 30
Z9 33
U1 2
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1743-9191
EI 1743-9159
J9 INT J SURG
JI Int. J. Surg.
PD AUG
PY 2022
VL 104
AR 106780
DI 10.1016/j.ijsu.2022.106780
EA JUL 2022
PG 10
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA 3M6LL
UT WOS:000835570900009
PM 35850466
DA 2025-01-04
ER

PT J
AU Alam, M
   Ahmed, S
   Elasbali, AM
   Adnan, M
   Alam, S
   Hassan, MI
   Pasupuleti, VR
AF Alam, Manzar
   Ahmed, Sarfraz
   Elasbali, Abdelbaset Mohamed
   Adnan, Mohd
   Alam, Shoaib
   Hassan, Imtaiyaz
   Pasupuleti, Visweswara Rao
TI Therapeutic Implications of Caffeic Acid in Cancer and Neurological
   Diseases
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE caffeic acid; clinical trials; diabetic neuropathy; inflammatory
   diseases; inhibitors; targeted therapy
ID NF-KAPPA-B; SQUAMOUS-CELL CARCINOMA; PHENETHYL ESTER; OXIDATIVE STRESS;
   CHLOROGENIC ACID; IN-VITRO; ANTIOXIDANT ACTIVITY; ALZHEIMERS-DISEASE;
   MOLECULAR TARGETS; COLORECTAL-CANCER
AB Caffeic acid (CA) is found abundantly in fruits, vegetables, tea, coffee, oils, and more. CA and its derivatives have been used for many centuries due to their natural healing and medicinal properties. CA possesses various biological and pharmacological activities, including antioxidant, anti-inflammatory, anticancer, and neuroprotective effects. The potential therapeutic effects of CA are mediated via repression and inhibition of transcription and growth factors. CA possesses potential anticancer and neuroprotective effects in human cell cultures and animal models. However, the biomolecular interactions and pathways of CA have been described highlighting the target binding proteins and signaling molecules. The current review focuses on CA's chemical, physical, and pharmacological properties, including antioxidant, anti-inflammatory, anticancer, and neuroprotective effects. We further described CA's characteristics and therapeutic potential and its future directions.
C1 [Alam, Manzar; Hassan, Imtaiyaz] Jamia Millia Islamia, Ctr Interdisciplinary Res Basic Sci, New Delhi, India.
   [Ahmed, Sarfraz] Jamia Millia Islamia, Dept Biosci, New Delhi, India.
   [Elasbali, Abdelbaset Mohamed] Jouf Univ, Coll Appl Sci Qurayyat, Dept Clin Lab Sci, Sakakah, Saudi Arabia.
   [Adnan, Mohd] Univ Hail, Coll Sci, Dept Biol, Hail, Saudi Arabia.
   [Alam, Shoaib] Jamia Millia Islamia, Dept Biotechnol, New Delhi, India.
   [Pasupuleti, Visweswara Rao] Univ Malaysia Sabah, Fac Med & Hlth Sci, Dept Biomed Sci & Therapeut, Kota Kinabalu, Malaysia.
   [Pasupuleti, Visweswara Rao] Abdurrab Univ, Fac Med & Hlth Sci, Dept Biochem, Pekanbaru, Indonesia.
   [Pasupuleti, Visweswara Rao] Reva Univ, Ctr Int Collaborat & Res, Rukmini Knowledge Pk,Kattigenahalli, Bangalore, India.
C3 Jamia Millia Islamia; Jamia Millia Islamia; Al Jouf University;
   University Ha'il; Jamia Millia Islamia; Universiti Malaysia Sabah; REVA
   University
RP Elasbali, AM (corresponding author), Jouf Univ, Coll Appl Sci Qurayyat, Dept Clin Lab Sci, Sakakah, Saudi Arabia.; Pasupuleti, VR (corresponding author), Univ Malaysia Sabah, Fac Med & Hlth Sci, Dept Biomed Sci & Therapeut, Kota Kinabalu, Malaysia.; Pasupuleti, VR (corresponding author), Abdurrab Univ, Fac Med & Hlth Sci, Dept Biochem, Pekanbaru, Indonesia.; Pasupuleti, VR (corresponding author), Reva Univ, Ctr Int Collaborat & Res, Rukmini Knowledge Pk,Kattigenahalli, Bangalore, India.
EM aeelasbali@ju.edu.sa; pvrao@ums.edu.my
RI Elasbali, abdelbaset/AEY-0035-2022; PASUPULETI, VISWESWARA
   RAO/A-7429-2013; Hassan, Md. Imtaiyaz/G-7072-2017; Adnan,
   Mohd/N-9207-2015
OI PASUPULETI, VISWESWARA RAO/0000-0002-4454-3408; Hassan, Md.
   Imtaiyaz/0000-0002-3663-4940; Alam, Manzar/0000-0002-8024-1191;
   Elasbali, Abdelbaset Mohamed/0000-0002-7003-9846; Adnan,
   Mohd/0000-0002-7080-6822
FU Indian Council of Medical Research [45/6/2020-DDI/BMS]; 
   [DSR-2021-01-0368];  [SR/FST/LSII/2020/782]
FX This work is supported and funded through the Indian Council of Medical
   Research (Grant No. 45/6/2020-DDI/BMS).
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NR 255
TC 111
Z9 112
U1 14
U2 57
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 10
PY 2022
VL 12
AR 860508
DI 10.3389/fonc.2022.860508
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0G9FE
UT WOS:000778342900001
PM 35359383
OA Green Published, gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Hosseinzadeh, E
   Mansoori, B
   Mohammadi, A
   Khaze, V
   Rezazadeh, M
   Baradaran, B
AF Hosseinzadeh, Elham
   Mansoori, Behzad
   Mohammadi, Ali
   Khaze, Vahid
   Rezazadeh, Maryam
   Baradaran, Behzad
TI The Inhibitory Effect of Hsa-miR-330 Replacement on the Proliferation
   and Migration of Breast Cancer MCF-7 Cells
SO INTERNATIONAL JOURNAL OF WOMENS HEALTH AND REPRODUCTION SCIENCES
LA English
DT Article
DE Breast cancer; E2F1; Hsa-miR-330; Cancer therapy
ID COLORECTAL-CANCER; MICRO-RNAS; GROWTH; E2F1; PROGRESSION; EXPRESSION;
   BIOMARKERS; APOPTOSIS; DIAGNOSIS; TARGETS
AB Objectives: miRNAs comprise a group of master gene expression regulators, exerting their effects after transcription through targeting specific mRNAs, hence, influencing cellular processes. A considerable number of miRNAs are known to affect cell proliferation and migration in breast cancer, one of which is hsa-miR-330, a key player in various types of cancers. The purpose of this study was to evaluate the anti-proliferative and anti-migrative effects of hsa-miR-330 on MCF-7 cell line.
   Materials and Methods: MCF-7 cells were transfected with pCMV-miR-330 vector and cell selection was performed in media containing Geneticin (G418). Subsequently, MTT assay was performed to evaluate the effect of hsa-miR-330 on proliferation and scratch wound healing assay was employed to evaluate cellular migration. Finally, using real-time PCR, the expression of hsamiR-330 as well as the repressive impact on the expression of E2F was investigated.
   Results: Upon confirmation of hsa-miR-330 induction in MCF-7 cells via GFP channel imaging system, miR-330 expression was demonstrated to be increased 10 folds in stable cells. The results of MTT and wound-healing assays demonstrated an inhibitory role for hsa-miR-330 in proliferation and migration of stable hsa-miR-330-transfected MCF-7 cancer cells compared to controls. In addition, after transfecting cells with hsa-miR-330, E2F1 was down-regulated in comparison with controls.
   Conclusions: Based on the results of the current study, we suggest a potential inhibitory role for hsa-miRNA-330 in cell proliferation as well as cell migration in breast cancer by targeting E2F1 mRNA. Additionally, a therapeutic role can be suggested for hsa-miR-330 in terms of target therapy for breast cancer.
C1 [Hosseinzadeh, Elham; Mansoori, Behzad; Mohammadi, Ali; Khaze, Vahid; Baradaran, Behzad] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
   [Hosseinzadeh, Elham; Rezazadeh, Maryam] Tabriz Univ Med Sci, Fac Med, Dept Med Genet, Tabriz, Iran.
   [Mansoori, Behzad] Tabriz Univ Med Sci, Student Res Comm, Tabriz, Iran.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science; Tabriz University of Medical Science
RP Baradaran, B (corresponding author), Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.; Rezazadeh, M (corresponding author), Tabriz Univ Med Sci, Fac Med, Dept Med Genet, Tabriz, Iran.
EM rezazadeh.mary@gmail.com; Behzad_im@yahoo.com
RI Khaze, Vahid/S-9805-2019; Baradaran, Behzad/AAQ-5177-2020; Mansoori,
   Behzad/T-2720-2017
OI Khaze, Vahid/0000-0001-6160-5925; Mansoori, Behzad/0000-0001-9444-7134;
   baradaran, behzad/0000-0002-8642-6795
FU Vice Chancellor for Research of Tabriz University of Medical Sciences
FX This work was supported by the Vice Chancellor for Research of Tabriz
   University of Medical Sciences.
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NR 32
TC 1
Z9 1
U1 0
U2 1
PU ARAS PART MEDICAL INT PRESS
PI TABRIZ
PA NO 1, S SHAREATI ST, 5138815941, TABRIZ, 00000, IRAN
SN 2330-4456
J9 INT J WOMEN HEAL REP
JI Int. J. Womens Health Reprod. Sci.
PD JUL
PY 2019
VL 7
IS 3
BP 360
EP 365
DI 10.15296/ijwhr.2019.59
PG 6
WC Reproductive Biology
WE Emerging Sources Citation Index (ESCI)
SC Reproductive Biology
GA IK5QQ
UT WOS:000476640100020
OA gold
DA 2025-01-04
ER

PT J
AU Labots, M
   van der Mijn, JC
   Beekhof, R
   Piersma, SR
   de Goeij-de Haas, RR
   Pham, TV
   Knol, JC
   Dekker, H
   van Grieken, NCT
   Verheul, HMW
   Jiménez, CR
AF Labots, Mariette
   van der Mijn, Johannes C.
   Beekhof, Robin
   Piersma, Sander R.
   de Goeij-de Haas, Richard R.
   Pham, Thang V.
   Knol, Jaco C.
   Dekker, Henk
   van Grieken, Nicole C. T.
   Verheul, Henk M. W.
   Jimenez, Connie R.
TI Phosphotyrosine-based-phosphoproteomics scaled-down to biopsy level for
   analysis of individual tumor biology and treatment selection
SO JOURNAL OF PROTEOMICS
LA English
DT Article
DE Phosphoproteomics; Cancer; MS/MS; Phosphotyrosine signaling; Treatment
   selection; Targeted therapy; Personalized medicine
ID PERSONALIZED CANCER-THERAPIES; LUNG-CANCER; SIGNALING NETWORKS; IN-VIVO;
   PROTEIN; PHOSPHORYLATION; CHALLENGES; PROTEOMICS; MUTATIONS; DISCOVERY
AB Mass spectrometry-based phosphoproteomics of cancer cell and tissue lysates provides insight in aberrantly activated signaling pathways and potential drug targets. For improved understanding of individual patient's tumor biology and to allow selection of tyrosine kinase inhibitors in individual patients, phosphoproteomics of small clinical samples should be feasible and reproducible. We aimed to scale down a pTyr-phosphopeptide enrichment protocol to biopsy-level protein input and assess reproducibility and applicability to tumor needle biopsies. To this end, phosphopeptide immunoprecipitation using anti-phosphotyrosine beads was performed using 10, 5 and 1 mg protein input from lysates of colorectal cancer (CRC) cell line HCT116. Multiple needle biopsies from 7 human CRC resection specimens were analyzed at the 1 mg-level. The total number of phosphopeptides captured and detected by LC-MS/MS ranged from 681 at 10 mg input to 471 at 1 mg HCT116 protein. ID-reproducibility ranged from 60.5% at 10 mg to 43.9% at 1 mg. Per 1 mg-level biopsy sample, >200 phosphopeptides were identified with 57% ID-reproducibility between paired tumor biopsies. Unsupervised analysis clustered biopsies from individual patients together and revealed known and potential therapeutic targets.
   Significance: This study demonstrates the feasibility of label-free pTyr-phosphoproteomics at the tumor biopsy level based on reproducible analyses using 1 mg of protein input. The considerable number of identified phosphopeptides at this level is attributed to an effective down-scaled immuno-affinity protocol as well as to the application of ID propagation in the data processing and analysis steps. Unsupervised cluster analysis reveals patient-specific profiles. Together, these findings pave the way for clinical trials in which pTyr-phosphoproteomics will be performed on pre- and on-treatment biopsies. Such studies will improve our understanding of individual tumor biology and may enable future pTyr-phosphoproteomics-based personalized medicine. (C) 2017 Published by Elsevier B.V.
C1 [Labots, Mariette; van der Mijn, Johannes C.; Beekhof, Robin; Piersma, Sander R.; de Goeij-de Haas, Richard R.; Pham, Thang V.; Knol, Jaco C.; Dekker, Henk; Verheul, Henk M. W.; Jimenez, Connie R.] Vrije Univ Amsterdam, Med Ctr, Dept Med Oncol, De Boelelaan 1117, NL-1081 HV Amsterdam, Netherlands.
   [van Grieken, Nicole C. T.] Vrije Univ Amsterdam, Med Ctr, Dept Pathol, De Boelelaan 1117, NL-1081 HV Amsterdam, Netherlands.
C3 Vrije Universiteit Amsterdam; Vrije Universiteit Amsterdam
RP Jiménez, CR (corresponding author), Vrije Univ Amsterdam, Med Ctr, Dept Med Oncol, Room CCA 1-160,De Boelelaan 1117, NL-1081 HV Amsterdam, Netherlands.; Verheul, HMW (corresponding author), Vrije Univ Amsterdam, Med Ctr, Dept Med Oncol, Room 3A46,De Boelelaan 1117, NL-1081 HV Amsterdam, Netherlands.
EM h.verheul@vumc.nl; c.jimenez@vumc.nl
RI Verheul, Henk/V-6462-2019; Labots, Mariette/J-9731-2013; Jimenez,
   Connie/AAI-3763-2020
OI van Grieken, Nicole/0000-0001-9992-0760; Dekker,
   Henk/0000-0001-6228-8319; Labots, Mariette/0000-0002-7095-1771; Jimenez,
   Connie R/0000-0002-3103-4508; Verheul, Henk/0000-0001-5981-922X;
   Beekhof, Robin/0000-0002-9500-528X
FU Vitromics Healthcare Services, The Netherlands; Department of Medical
   Oncology; AEGON International Scholarship in Oncology
FX This work was financially supported by a research grant from Vitromics
   Healthcare Services, The Netherlands to VUmc, Department of Medical
   Oncology and the AEGON International Scholarship in Oncology (M.
   Labots). These funding sources were not involved in the collection,
   analysis and interpretation of data; in the writing of the report; nor
   in the decision to submit the article for publication.
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NR 38
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Z9 27
U1 1
U2 21
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1874-3919
EI 1876-7737
J9 J PROTEOMICS
JI J. Proteomics
PD JUN 6
PY 2017
VL 162
BP 99
EP 107
DI 10.1016/j.jprot.2017.04.014
PG 9
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA EY9KW
UT WOS:000404318500010
PM 28442448
DA 2025-01-04
ER

PT J
AU Roy, A
   Datta, S
   Bhatia, KS
   Bhumika
   Jha, P
   Prasad, R
AF Roy, Arpita
   Datta, Shreeja
   Bhatia, Karanpreet Singh
   Bhumika
   Jha, Priyanka
   Prasad, Ram
TI Role of plant derived bioactive compounds against cancer
SO SOUTH AFRICAN JOURNAL OF BOTANY
LA English
DT Review
DE Natural products; cancer; conventional therapies; plant metabolites
ID METASTATIC COLORECTAL-CANCER; BREAST-CANCER; IN-VITRO; TOPOISOMERASE-I;
   ELLAGIC ACID; CUCURBITACIN B; KAPPA-B; SYNERGISTIC INTERACTIONS;
   INHIBITS PROLIFERATION; ANTICANCER ACTIVITY
AB Cancer is an uncontrolled division of cells that has been attributed to various factors due to the advancement in cell biology and widespread genomic studies. Traditional chemotherapy in which a single cause is targeted is not a viable option for cancer treatment as multiple factors like various genes or epigenetic factors are found to be responsible for cancer phenotype. Formation of tumor is due to the somatic mutations in genome, same phenotypic expression of various cancer types. Many times, chemotherapy drugs given in two different patients of similar types of cancer do not produce the same effect in both the patients due to differ-ent somatic mutations or different genes involved in the same cancer phenotype. Thus, mono-target therapy usually encounters more failures than successes. In the past decades, research has begun to understand the various genetic mutations involved in a variety of cancers and this knowledge could be used to guide a new generation of medicinal chemists to design and discover novel drug moieties which would be able to influ-ence multiple targets involved in tumor expression. Combinatorial formulations (synthetic as well as natural) could be beneficial in such a scenario. In this review, mechanisms of cancer, conventional methods to treat cancer and various plant secondary metabolites for effective treatment of cancer have been discussed.(c) 2021 SAAB. Published by Elsevier B.V. All rights reserved.
C1 [Roy, Arpita] Sharda Univ, Sch Engn & Technol, Dept Biotechnol, Greater Noida, India.
   [Datta, Shreeja; Bhumika] Delhi Technol Univ, Dept Biotechnol, Delhi, India.
   [Bhatia, Karanpreet Singh] Natl Univ Singapore, 21 Lower Kent Ridge Rd, Singapore 119077, Singapore.
   [Jha, Priyanka] Amity Univ, Amity Inst Biotechnol, Kolkata 700156, West Bengal, India.
   [Prasad, Ram] Mahatma Gandhi Cent Univ, Dept Bot, Motihari 845401, Bihar, India.
C3 Sharda University; Delhi Technological University; National University
   of Singapore
RP Roy, A (corresponding author), Sharda Univ, Sch Engn & Technol, Dept Biotechnol, Greater Noida, India.; Prasad, R (corresponding author), Mahatma Gandhi Cent Univ, Dept Bot, Motihari 845401, Bihar, India.
EM arbt2014@gmail.com; rpjnu2001@gmail.com
RI Roy, Arpita/AAC-1536-2020; Prasad, Ram/Q-8875-2018
OI Jha, Priyanka/0000-0002-2313-4517; Prasad, Ram/0000-0002-3670-0450; roy,
   arpita/0000-0002-1928-3093
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NR 151
TC 22
Z9 22
U1 1
U2 12
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0254-6299
EI 1727-9321
J9 S AFR J BOT
JI S. Afr. J. Bot.
PD SEP
PY 2022
VL 149
BP 1017
EP 1028
DI 10.1016/j.sajb.2021.10.015
EA SEP 2022
PG 12
WC Plant Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences
GA 4Q4EP
UT WOS:000856036500004
OA hybrid
DA 2025-01-04
ER

PT J
AU Sepulveda, AR
   Hamilton, SR
   Allegra, CJ
   Grody, W
   Cushman-Vokoun, AM
   Funkhouser, WK
   Kopetz, SE
   Lieu, C
   Lindor, NM
   Minsky, BD
   Monzon, FA
   Sargent, DJ
   Singh, VM
   Willis, J
   Clark, J
   Colasacco, C
   Rumble, RB
   Temple-Smolkin, R
   Ventura, CB
   Nowak, JA
AF Sepulveda, Antonia R.
   Hamilton, Stanley R.
   Allegra, Carmen J.
   Grody, Wayne
   Cushman-Vokoun, Allison M.
   Funkhouser, William K.
   Kopetz, Scott E.
   Lieu, Christopher
   Lindor, Noralane M.
   Minsky, Bruce D.
   Monzon, Federico A.
   Sargent, Daniel J.
   Singh, Veena M.
   Willis, Joseph
   Clark, Jennifer
   Colasacco, Carol
   Rumble, R. Bryan
   Temple-Smolkin, Robyn
   Ventura, Christina B.
   Nowak, Jan A.
TI Molecular Biomarkers for the Evaluation of Colorectal Cancer
   <i>Guideline From the American Society for Clinical Pathology, College
   of American Pathologists, Association for Molecular Pathology, and
   American Society of Clinical Oncology</i>
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Article
DE Molecular diagnostics; Gastrointestinal; Histology; Genetics; Oncology
ID RECEPTOR MONOCLONAL-ANTIBODIES; KRAS MUTATION DETECTION; ANTI-EGFR
   THERAPY; III COLON-CANCER; K-RAS MUTATIONS; MICROSATELLITE-INSTABILITY;
   PIK3CA MUTATION; ADJUVANT CHEMOTHERAPY; 1ST-LINE TREATMENT; PTEN
   EXPRESSION
AB Objectives: To develop evidence-based guideline recommendations through a systematic review of the Literature to establish standard molecular biomarker testing of colorectal cancer (CRC) tissues to guide epidermal growth factor receptor (EGFR) therapies and conventional chemotherapy regimens.
   Methods: The American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology, and American Society of Clinical Oncology convened an expert panel to develop an evidence-based guideline to establish standard molecular biomarker testing and guide therapies for patients with CRC. A comprehensive Literature search that included more than 4,000 articles was conducted.
   Results: Twenty-one guideline statements were established.
   Conclusions: Evidence supports mutational testing for EGFR signaling pathway genes, since they provide clinically actionable information as negative predictors of benefit to anti-EGFR monoclonal antibody therapies for targeted therapy of CRC. Mutations in several of the biomarkers have clear prognostic value. Laboratory approaches to operationalize CRC molecular testing are presented.
C1 [Sepulveda, Antonia R.] Columbia Univ, Dept Pathol & Cell Biol, 630 W 168th St VC 14-212, New York, NY 10032 USA.
   [Hamilton, Stanley R.] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
   [Kopetz, Scott E.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal GI Med Oncol, Houston, TX 77030 USA.
   [Minsky, Bruce D.] Univ Texas MD Anderson Canc Ctr, Dept Radiat Oncol, Houston, TX 77030 USA.
   [Allegra, Carmen J.] Univ Florida, Med Ctr, Div Hematol & Oncol, Gainesville, FL USA.
   [Grody, Wayne] Univ Calif Los Angeles, Med Ctr, Dept Pathol & Lab Med, Los Angeles, CA 90024 USA.
   [Grody, Wayne] Univ Calif Los Angeles, Med Ctr, Dept Pediat, Los Angeles, CA 90024 USA.
   [Grody, Wayne] Univ Calif Los Angeles, Med Ctr, Dept Human Genet, Los Angeles, CA 90024 USA.
   [Cushman-Vokoun, Allison M.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
   [Funkhouser, William K.] Univ N Carolina, Sch Med, Dept Pathol & Lab Med, Chapel Hill, NC USA.
   [Lieu, Christopher] Univ Colorado, Sch Med, Div Med Oncol, Denver, CO USA.
   [Lindor, Noralane M.] Mayo Clin, Dept Med Genet, Scottsdale, AZ USA.
   [Monzon, Federico A.] Castle Biosci, Friendswood, TX USA.
   [Sargent, Daniel J.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
   [Singh, Veena M.] Biocept, San Diego, CA USA.
   [Willis, Joseph] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA.
   [Clark, Jennifer] Amer Soc Clin Pathologists, ASCP Inst Sci Technol & Policy, Washington, DC USA.
   [Colasacco, Carol] Coll Amer Pathologists, Lab & Pathol Qual Ctr, Northfield, IL USA.
   [Rumble, R. Bryan] Amer Soc Clin Oncol, Alexandria, VA USA.
   [Temple-Smolkin, Robyn] Assoc Mol Pathol, Bethesda, MD USA.
   [Nowak, Jan A.] Roswell Pk Canc Inst, Dept Pathol & Lab Med, Buffalo, NY 14263 USA.
C3 Columbia University; University of Texas System; UTMD Anderson Cancer
   Center; University of Texas System; UTMD Anderson Cancer Center;
   University of Texas System; UTMD Anderson Cancer Center; State
   University System of Florida; University of Florida; University of
   California System; University of California Los Angeles; University of
   California Los Angeles Medical Center; University of California System;
   University of California Los Angeles; University of California Los
   Angeles Medical Center; University of California System; University of
   California Los Angeles; University of California Los Angeles Medical
   Center; University of Nebraska System; University of Nebraska Medical
   Center; University of North Carolina; University of North Carolina
   Chapel Hill; University of North Carolina School of Medicine; University
   of Colorado System; University of Colorado Anschutz Medical Campus;
   University of Colorado Denver; Mayo Clinic; Mayo Clinic Phoenix; Mayo
   Clinic; University System of Ohio; Case Western Reserve University;
   College of American Pathologists; American Society of Clinical Oncology;
   Roswell Park Comprehensive Cancer Center
RP Sepulveda, AR (corresponding author), Columbia Univ, Dept Pathol & Cell Biol, 630 W 168th St VC 14-212, New York, NY 10032 USA.
EM as4400@cumc.columbia.edu
RI Kopetz, Scott/AAC-1387-2019; Colasacco, Carol/AAA-2736-2022
OI Temple-Smolkin, Robyn/0000-0002-5728-5436; Monzon,
   Federico/0000-0002-6890-9793; Kopetz, Scott/0000-0001-9647-3416;
   Colasacco, Carol/0000-0001-7856-7531
FU NCATS NIH HHS [UL1 TR000371] Funding Source: Medline
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NR 148
TC 99
Z9 106
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD MAR
PY 2017
VL 19
IS 2
BP 187
EP 225
DI 10.1016/j.jmoldx.2016.11.001
PG 39
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA EL9DS
UT WOS:000394920200002
PM 28185757
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Ambrogi, V
   Tamburrini, A
   Tajé, R
AF Ambrogi, Vincenzo
   Tamburrini, Alessandro
   Taje, Riccardo
TI Results of redo pulmonary metastasectomy
SO JOURNAL OF THORACIC DISEASE
LA English
DT Review
DE Pulmonary metastasectomy; redo metastasectomy; target therapy; immune
   therapy
ID LONG-TERM SURVIVAL; ASSISTED THORACIC-SURGERY; COLORECTAL-CANCER; LUNG
   METASTASES; SURGICAL RESECTION; REPEAT RESECTION; COMPLETION
   PNEUMONECTOMY; SARCOMATOUS METASTASES; THORACOSCOPIC SURGERY;
   PROGNOSTIC-FACTORS
AB Repeat surgical resection (redo) for pulmonary metastases is a questionable, albeit intriguing topic. We performed an extensive review of the literature, to specifically analyze results of redo pulmonary metastasectomies. We reviewed a total of 3,523 papers. Among these, 2,019 were excluded for redundancy and 1,105 because they were not completely retrievable. Out of 399 eligible papers, 183 had missing information or missing abstract, while 96 lacked data on survival. A total of 120 papers dated from 1991 onwards were finally included. Data regarding mortality, major morbidity, prognostic factors and long-term survivals of the first redo pulmonary metastasectomies were retrieved and analyzed. Homogeneity of data was affected by the lack of guidelines for redo pulmonary metastasectomy and the risks of bias when comparing different studies has to be considered. According to the histology sub-types, redo metastasectomies papers were grouped as: colorectal (n=42), sarcomas (n=36), others (n=20) and all histologies (n=22); the total number of patients was 3,015. Data about chemotherapy were reported in half of the papers, whereas targeted or immunotherapy in 9. None of these associated therapies, except chemotherapy in two records, did significantly modify outcomes. Disease-free interval before the redo procedure was the prevailing prognostic factor and nearly all papers showed a significant correlation between patients' comorbidities and prognosis. No perioperative mortality was reported, while perioperative major morbidity was overall quite low. Where available, overall survival after the first redo metastasectomy ranged from 10 to 72 months, with a 5-years survival of approximately 50%. The site of first recurrence after the redo procedure was mainly lung. Despite the data retrievable from literature are heterogeneous and confounding, we can state that redo lung metastasectomy is worthwhile when the lesions are resectable and the perioperative risk is low. At present, there are no "non-surgical" therapeutic options to replace redo pulmonary metastasectomies.
C1 [Ambrogi, Vincenzo] Tor Vergata Univ Polyclin, Thorac Surg Unit, Rome, Italy.
   [Tamburrini, Alessandro] Southampton Univ Hosp, Thorac Surg Unit, Southampton, Hants, England.
   [Taje, Riccardo] Tor Vergata Univ, Sch Med, Rome, Italy.
C3 University of Southampton; University of Rome Tor Vergata
RP Ambrogi, V (corresponding author), Policlin Univ Roma Tor Vergata, UOC Chirurg Torac, Viale Oxford 81, I-00133 Rome, Italy.
EM ambrogi@med.uniroma2.it
OI Ambrogi, Vincenzo/0000-0002-8947-3175; Taje,
   Riccardo/0009-0008-3120-3886
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NR 155
TC 7
Z9 7
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 2072-1439
EI 2077-6624
J9 J THORAC DIS
JI J. Thorac. Dis.
PD APR
PY 2021
VL 13
IS 4
BP 2669
EP 2685
DI 10.21037/jtd-19-4064
PG 17
WC Respiratory System
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Respiratory System
GA TA8LO
UT WOS:000667497200029
PM 34012616
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Che, YJ
   Wu, HW
   Hung, LY
   Liu, CA
   Chang, HY
   Wang, K
   Lee, GB
AF Che, Yu-Jui
   Wu, Huei-Wen
   Hung, Lien-Yu
   Liu, Ching-Ann
   Chang, Hwan-You
   Wang, Kuan
   Lee, Gwo-Bin
TI An integrated microfluidic system for screening of phage-displayed
   peptides specific to colon cancer cells and colon cancer stem cells
SO BIOMICROFLUIDICS
LA English
DT Article
AB Affinity reagents recognizing biomarkers specifically are essential components of clinical diagnostics and target therapeutics. However, conventional methods for screening of these reagents often have drawbacks such as large reagent consumption, the labor-intensive or time-consuming procedures, and the involvement of bulky or expensive equipment. Alternatively, microfluidic platforms could potentially automate the screening process within a shorter period of time and reduce reagent and sample consumption dramatically. It has been demonstrated recently that a subpopulation of tumor cells known as cancer stem cells possess high drug resistance and proliferation potential and are regarded as the main cause of metastasis. Therefore, a peptide that recognizes cancer stem cells and differentiates them from other cancer cells will be extremely useful in early diagnosis and target therapy. This study utilized M13 phage display technology to identify peptides that bind, respectively, to colon cancer cells and colon cancer stem cells using an integrated microfluidic system. In addition to positive selection, a negative selection process was integrated on the chip to achieve the selection of peptides of high affinity and specificity. We successfully screened three peptides specific to colon cancer cells and colon cancer stem cells, namely, HOLC-1, HOLC-2, and COLC-1, respectively, and their specificity was measured by the capture rate between target, control, and other cell lines. The capture rates are 43.4067.23%, 45.1667.12%, and 49.7965.34% for colon cancer cells and colon cancer stem cells, respectively, showing a higher specificity on target cells than on control and other cell lines. The developed technique may be promising for early diagnosis of cancer cells and target therapeutics. (C) 2015 AIP Publishing LLC.
C1 [Che, Yu-Jui; Wu, Huei-Wen; Hung, Lien-Yu; Lee, Gwo-Bin] Natl Tsing Hua Univ, Dept Power Mech Engn, Hsinchu 30013, Taiwan.
   [Liu, Ching-Ann; Wang, Kuan] Acad Sinica, Nanomed Program, Taipei 11529, Taiwan.
   [Liu, Ching-Ann; Wang, Kuan] Acad Sinica, Inst Biol Chem, Taipei 11529, Taiwan.
   [Chang, Hwan-You] Natl Tsing Hua Univ, Inst Mol Med, Hsinchu 30013, Taiwan.
   [Lee, Gwo-Bin] Natl Tsing Hua Univ, Inst NanoEngn & Microsyst, Hsinchu 30013, Taiwan.
   [Lee, Gwo-Bin] Natl Tsing Hua Univ, Inst Biomed Engn, Hsinchu 30013, Taiwan.
C3 National Tsing Hua University; Academia Sinica - Taiwan; Academia Sinica
   - Taiwan; National Tsing Hua University; National Tsing Hua University;
   National Tsing Hua University
RP Lee, GB (corresponding author), Natl Tsing Hua Univ, Dept Power Mech Engn, Hsinchu 30013, Taiwan.
RI Lee, G. B./D-3032-2012
OI Lee, G. B./0000-0001-6910-9133
FU National Science Council of Taiwan [NSC 102-2221-E-007-054-MY3];
   National Health Research Institutes; "Innovative Research Grant" (IRG)
   [NHRI-EX104-10428EI]; Towards A World-class University Project;
   Nanomedicine Program, Academia Sinica
FX The authors would like to thank the National Science Council of Taiwan
   for financial support (NSC 102-2221-E-007-054-MY3). Partial financial
   support from National Health Research Institutes, the "Innovative
   Research Grant" (IRG, NHRI-EX104-10428EI), the "Towards A World-class
   University Project," and Nanomedicine Program, Academia Sinica is also
   greatly appreciated.
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NR 28
TC 25
Z9 26
U1 0
U2 34
PU AMER INST PHYSICS
PI MELVILLE
PA 1305 WALT WHITMAN RD, STE 300, MELVILLE, NY 11747-4501 USA
SN 1932-1058
J9 BIOMICROFLUIDICS
JI Biomicrofluidics
PD SEP
PY 2015
VL 9
IS 5
AR 054121
DI 10.1063/1.4933067
PG 14
WC Biochemical Research Methods; Biophysics; Nanoscience & Nanotechnology;
   Physics, Fluids & Plasmas
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Science & Technology -
   Other Topics; Physics
GA CV6US
UT WOS:000364407300033
PM 26543513
OA Green Published
DA 2025-01-04
ER

PT J
AU Lavudi, K
   Nuguri, SM
   Pandey, P
   Kokkanti, RR
   Wang, QE
AF Lavudi, Kousalya
   Nuguri, Shreya Madhav
   Pandey, Prashant
   Kokkanti, Rekha Rani
   Wang, Qi-En
TI ALDH and cancer stem cells: Pathways, challenges, and future directions
   in targeted therapy
SO LIFE SCIENCES
LA English
DT Article
DE Cancer stem cells; Aldehyde dehydrogenase; ALDH inhibitors; Drug
   resistance; Immunotherapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; ALDEHYDE DEHYDROGENASE 1;
   BREAST-CANCER; OVARIAN-CANCER; COLORECTAL-CANCER; INITIATING CELLS;
   TUMOR MICROENVIRONMENT; CISPLATIN RESISTANCE; PANCREATIC-CANCER;
   SELF-RENEWAL
AB Human ALDH comprise 19 subfamilies in which ALDH1A1, ALDH1A3, ALDH3A1, ALDH5A1, ALDH7A1, and ALDH18A1 are implicated in CSC. Studies have shown that ALDH can also be involved in drug resistance and standard chemotherapy regimens are ineffective in treating patients at the stage of disease recurrence. Existing chemotherapeutic drugs eliminate the bulk of tumors but are usually not effective against CSC which express ALDH+ population. Henceforth, targeting ALDH is convincing to treat the patient's post-relapse. Combination therapies that interlink signaling mechanisms seem promising to increase the overall disease-free survival rate. Therefore, targeting ALDH through ALDH inhibitors along with immunotherapies may create a novel platform for translational research. This review aims to fill in the gap between ALDH1 family members in relation to its cell signaling mechanisms, highlighting their potential as molecular targets to sensitize recurrent tumors and bring forward the future development concerning the current progress and draw backs. This review summarizes the role of cancer stem cells and their upregulation by maintaining the tumor microenvironment in which ALDH is specifically highlighted. It discusses the regulation of ALDH family proteins and the crosstalk between ALDH and CSC in relation to cancer metabolism. Furthermore, it establishes the correlation between ALDH involved signaling mechanisms and their specific targeted inhibitors, as well as their functional modularity, bioavailability, and mechanistic role in various cancers.
C1 [Lavudi, Kousalya; Wang, Qi-En] Ohio State Univ, Coll Med, Dept Radiat Oncol, Columbus, OH 43210 USA.
   [Lavudi, Kousalya; Wang, Qi-En] Ohio State Univ, Comprehens Canc Ctr, 490 TMRF,410 12th Ave, Columbus, OH 43210 USA.
   [Nuguri, Shreya Madhav] Ohio State Univ, Dept Food Sci & Technol, Columbus, OH USA.
   [Pandey, Prashant] Babasaheb Bhimrao Ambedkar Univ, Dept Pharmaceut Sci, Lucknow 226025, Uttar Pradesh, India.
   [Pandey, Prashant] Univ Alberta, Fac Pharm & Pharmaceut Sci, Edmonton, AB T6G 2E1, Canada.
   [Kokkanti, Rekha Rani] KIIT Deemed be Univ, Sch Biotechnol, Bhubaneswar, India.
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; Babasaheb
   Bhimrao Ambedkar University; University of Alberta; Kalinga Institute of
   Industrial Technology (KIIT)
RP Wang, QE (corresponding author), Ohio State Univ, Coll Med, Dept Radiat Oncol, Columbus, OH 43210 USA.; Wang, QE (corresponding author), Ohio State Univ, Comprehens Canc Ctr, 490 TMRF,410 12th Ave, Columbus, OH 43210 USA.
EM Qi-En.Wang@osumc.edu
RI Lavudi, Kousalya/GXG-0083-2022; PANDEY, PRASHANT/AFF-8342-2022
OI PANDEY, PRASHANT/0000-0003-0700-914X
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NR 253
TC 8
Z9 8
U1 10
U2 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD NOV 1
PY 2024
VL 356
AR 123033
DI 10.1016/j.lfs.2024.123033
EA SEP 2024
PG 19
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA G5R4N
UT WOS:001317204400001
PM 39222837
DA 2025-01-04
ER

PT J
AU Mortezaee, K
   Najafi, M
   Farhood, B
   Ahmadi, A
   Shabeeb, D
   Musa, AE
AF Mortezaee, Keywan
   Najafi, Masoud
   Farhood, Bagher
   Ahmadi, Amirhossein
   Shabeeb, Dheyauldeen
   Musa, Ahmed E.
TI NF-κB targeting for overcoming tumor resistance and normal tissues
   toxicity
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Review
DE chemotherapy; nuclear factor kappa B (NF-kappa B); normal tissue
   toxicity; radiotherapy; tumor resistance
ID CANCER CHEMOPREVENTIVE ACTIVITY; SUPEROXIDE-DISMUTASE GENE;
   NECROSIS-FACTOR-ALPHA; STRAND BREAK REPAIR; CHRONIC OXIDATIVE STRESS;
   HUMAN COLORECTAL-CANCER; INDUCED APOPTOSIS; DNA-DAMAGE; SIGNALING
   PATHWAYS; NITRIC-OXIDE
AB Radiotherapy andchemotherapy are two famous modalities in tumor-targeted therapy that lead to systemic and local toxicities for normal tissues. Moreover, several studies have confirmed that exposure of the tumor to radiation or chemotherapy drugs stimulate some signaling pathways in the tumor microenvironment (TME), leading to resistance of cancer cells to apoptosis, as well as promoting angiogenesis and tumor growth. Nuclear factor kappa B (NF-kappa B) plays a central role in the regulation of inflammatory responses in both normal tissues and tumors via the release of several cytokines, regulation of prostaglandins, reduction/oxidation (redox) reactions, angiogenesis, and cell death. Upregulation of NF-kappa B in normal tissues causes an appearance of inflammatory reactions and oxidative stress, whereas it regulates angiogenesis and suppresses apoptosis, leading to resistance to subsequent doses of radiation or chemotherapy. Selective inhibition of NF-kappa B in experimental studies has shown promising results for tumor sensitization via apoptosis induction, inhibition of angiogenesis, and increasing delay of tumor growth. The use of some agents for NF-kappa B inhibition has been shown to alleviate radiation/chemotherapy toxicities in normal cells/ tissues. In this current review, we explained the pivotal role of NF-kappa B in both normal tissue toxicity and tumor resistance. We also discussed the promising strategies for overcoming these problems with regard to chemotherapy and radiotherapy.
C1 [Mortezaee, Keywan] Kurdistan Univ Med Sci, Sch Med, Dept Anat, Sanandaj, Iran.
   [Najafi, Masoud] Kermanshah Univ Med Sci, Sch Paramed Sci, Radiol & Nucl Med Dept, Kermanshah, Iran.
   [Farhood, Bagher] Kashan Univ Med Sci, Fac Paramed Sci, Dept Med Phys, Kashan, Iran.
   [Farhood, Bagher] Kashan Univ Med Sci, Fac Paramed Sci, Dept Radiol, Kashan, Iran.
   [Ahmadi, Amirhossein] Mazandaran Univ Med Sci, Fac Pharm, Pharmaceut Sci Res Ctr, Sari 48175861, Iran.
   [Shabeeb, Dheyauldeen] Univ Misan, Coll Med, Dept Physiol, Misan, Iraq.
   [Musa, Ahmed E.] Univ Tehran Med Sci, Dept Med Phys, Int Campus, Tehran, Iran.
C3 Kurdistan University of Medical Sciences; Kermanshah University of
   Medical Sciences; Mazandaran University of Medical Sciences; Tehran
   University of Medical Sciences; Misan University; Tehran University of
   Medical Sciences
RP Najafi, M (corresponding author), Kermanshah Univ Med Sci, Sch Paramed Sci, Radiol & Nucl Med Dept, Kermanshah, Iran.; Farhood, B (corresponding author), Kashan Univ Med Sci, Fac Paramed Sci, Dept Med Phys, Kashan, Iran.; Farhood, B (corresponding author), Kashan Univ Med Sci, Fac Paramed Sci, Dept Radiol, Kashan, Iran.; Ahmadi, A (corresponding author), Mazandaran Univ Med Sci, Fac Pharm, Pharmaceut Sci Res Ctr, Sari 48175861, Iran.
EM najafi_ma@yahoo.com; bffarhood@gmail.com; amirhossein_pharma@yahoo.com
RI Najafi, Masoud/L-8434-2019; Musa, Ahmed/E-6018-2019; Shabeeb,
   Dheyauldeen/AAP-4178-2020; Farhood, Bagher/W-3234-2018; Ahmadi,
   Amirhossein/H-2136-2011
OI Farhood, Bagher/0000-0003-2290-7220; najafi, masoud/0000-0002-6341-9007;
   Ahmadi, Amirhossein/0000-0002-9737-3633
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PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD OCT
PY 2019
VL 234
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BP 17187
EP 17204
DI 10.1002/jcp.28504
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WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA IH7ML
UT WOS:000474688200038
PM 30912132
DA 2025-01-04
ER

PT J
AU Lasinska, I
   Mackiewicz, J
AF Lasinska, Izabela
   Mackiewicz, Jacek
TI Integrins as A New Target for Cancer Treatment
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE Integrins; targeted therapy; cancer treatment; monoclonal antibodies;
   transmembrane glycoproteins; signal transduction
ID SQUAMOUS-CELL CARCINOMA; EPIDERMOLYSIS-BULLOSA; MONOCLONAL-ANTIBODY;
   PHASE-II; ALPHA(V)BETA(3) ANTAGONISTS; ALPHA-V-BETA-6 INTEGRIN;
   PROGNOSTIC INDICATOR; ADHESION MOLECULE-1; 1ST-LINE TREATMENT;
   LIGAND-BINDING
AB Despite the great progress in the development of targeted therapies for different types of cancer utilizing monoclonal antibodies (e.g., cetuximab for colorectal cancer and head and neck cancer therapy), kinase inhibitors (e.g., sorafenib for kidney cancer and gastrointestinal stromal tumours therapy), and immunomodulatory treatments (e.g., aivolumab and pembrolizumab for melanoma therapy and lung cancer therapy), there is still a need to search for new, more effective treatments.
   Integrins are responsible for intercellular adhesion and interaction with the cellular matrix. The function of integrins is related to the transduction of intracellular signals associated with adhesion, migration, cell proliferation, differentiation, and apoptosis. Molecules targeting integrins that lead to cancer cell death have been developed. The most advanced molecules studied in clinical trials are abituzumab, intetumumab and cilengitide. There are different groups of anti-integrin drugs: monoclonal antibodies (e.g., abituzumab) and other such as cilengitide, E7820 and MK-0429. These drugs have been evaluated in various cancer types. However, they have shown modest efficacy, and none of them have yet been approved for cancer treatment. Studies have shown that patient selection using biomarkers might improve the efficacy of anti-integrin cancer treatment. Many preclinical models have demonstrated promising results using integrin visualization for cancer detection and treatment efficacy monitoring; however, these strategies require further evaluation in humans.
C1 [Lasinska, Izabela; Mackiewicz, Jacek] Poznan Univ Med Sci, Heliodor Swiecicki Univ Hosp, Dept Med & Expt Oncol, Poznan, Poland.
   [Mackiewicz, Jacek] Univ Med Sci, Dept Biol & Environm Studies, Poznan, Poland.
   [Mackiewicz, Jacek] Greater Poland Canc Ctr, Dept Diagnost & Canc Immunol, Poznan, Poland.
C3 Poznan University of Medical Sciences; Wielkopolskie Centrum Onkologii
RP Lasinska, I (corresponding author), Univ Med Sci, Heliodor Swiecicki Univ Hosp, Dept Med & Expt Oncol, Grunwaldzka 16-18, Poznan, Poland.
EM lasinska.izabela@spsk2.pl
RI Łasińska, Izabela/M-6061-2019
OI Lasinska, Izabela/0000-0001-5426-2725
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NR 82
TC 24
Z9 26
U1 1
U2 24
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1871-5206
EI 1875-5992
J9 ANTI-CANCER AGENT ME
JI Anti-Cancer Agents Med. Chem.
PY 2019
VL 19
IS 5
BP 580
EP 586
DI 10.2174/1871520618666181119103413
PG 7
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA IF5DF
UT WOS:000473100800001
PM 30451118
DA 2025-01-04
ER

PT J
AU Wang, S
   Chen, J
   Guo, XZ
AF Wang, Shuo
   Chen, Jiang
   Guo, Xiao-Zhong
TI <i>KAI1</i>/<i>CD82</i> gene and autotaxin-lysophosphatidic acid axis in
   gastrointestinal cancers
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE KAI1/CD82; Autotaxin; Lysophosphatidic acid; Pancreatic cancer; Liver
   cancer
ID METASTASIS SUPPRESSOR GENE; LIPID PHOSPHATE PHOSPHATASE-1; FOCAL
   ADHESION KINASE; RECEPTOR 6 LPAR6; PANCREATIC-CANCER; COLON-CANCER;
   CELL-PROLIFERATION; GASTRIC-CANCER; KAI1 EXPRESSION; IN-VITRO
AB The KAI1/CD82 gene inhibits the metastasis of most tumors and is remarkably correlated with tumor invasion and prognosis. Cell metabolism dysregulation is an important cause of tumor occurrence, development, and metastasis. As one of the important characteristics of tumors, cell metabolism dysregulation is attracting increasing research attention. Phospholipids are an indispensable substance in the metabolism in various tumor cells. Phospholipid metabolites have become important cell signaling molecules. The pathological role of lysophosphatidic acid (LPA) in tumors was identified in the early 1990s. Currently, LPA inhibitors have entered clinical trials but are not yet used in clinical treatment. Autotaxin (ATX) has lysophospholipase D (lysoPLD) activity and can regulate LPA levels in vivo. The LPA receptor family and ATX/lysoPLD are abnormally expressed in various gastrointestinal tumors. According to our recent pre-experimental results, KAI1/CD82 might inhibit the migration and metastasis of cancer cells by regulating the ATX-LPA axis. However, no relevant research has been reported. Clarifying the mechanism of ATX-LPA in the inhibition of cancer metastasis by KAI1/CD82 will provide an important theoretical basis for targeted cancer therapy. In this paper, the molecular compositions of the KAI1/CD82 gene and the ATX-LPA axis, their physiological functions in tumors, and their roles in gastrointestinal cancers and target therapy are reviewed.
C1 [Wang, Shuo; Chen, Jiang; Guo, Xiao-Zhong] Gen Hosp Northern Theater Command, Dept Gastroenterol, Shenyang, Liaoning, Peoples R China.
   [Wang, Shuo] Gen Hosp Northern Theater Command, Dept Gastroenterol, 83 Wenhua Rd, Shenyang 110840, Liaoning, Peoples R China.
RP Wang, S (corresponding author), Gen Hosp Northern Theater Command, Dept Gastroenterol, 83 Wenhua Rd, Shenyang 110840, Liaoning, Peoples R China.
EM guoxiaozhong1962@126.com
RI Guo, Xiaozhong/AAX-5269-2020
OI Guo, Xiaozhong/0000-0002-6397-0501
FU National Natural Science Foundation of China [81672465]; Science and
   Technology Program of Liaoning Province [2019JH8/10300080]
FX Supported by the National Natural Science Foundation of China, No.
   81672465; and the Science and Technology Program of Liaoning Province,
   No. 2019JH8/10300080.
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NR 202
TC 1
Z9 1
U1 2
U2 12
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD AUG 15
PY 2022
VL 14
IS 8
BP 1388
EP 1405
DI 10.4251/wjgo.v14.i8.1388
PG 18
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA 4F2XL
UT WOS:000848378700002
PM 36160748
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhao, PY
   Jiao, YN
   Ma, ZF
   Yan, Y
   Li, YX
   Hu, SD
   Li, SY
   Du, XH
AF Zhao, Peng-yue
   Jiao, Ya-nan
   Ma, Zhao-fu
   Yan, Yang
   Li, Yu-xuan
   Hu, Shi-dong
   Li, Song-yan
   Du, Xiao-hui
TI Publication trends and hotspots of drug resistance in colorectal cancer
   during 2002-2021: A bibliometric and visualized analysis
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE drug resistance; colorectal cancer; bibliometric analysis; microRNA; EMT
ID ACQUIRED-RESISTANCE; OXALIPLATIN RESISTANCE; EGFR THERAPY;
   CHEMORESISTANCE; DETERMINANTS; METASTASIS; EVOLUTION; GROWTH; CELLS
AB BackgroundChemotherapy, radiotherapy, targeted therapy and immunotherapy have demonstrated expected clinical efficacy, while drug resistance remains the predominant limiting factor to therapeutic failure in patients with colorectal cancer (CRC). Although there have been numerous basic and clinical studies on CRC resistance in recent years, few publications utilized the bibliometric method to evaluate this field. The objective of current study was to provide a comprehensive analysis of the current state and changing trends of drug resistance in CRC over the past 20 years. MethodsThe Web of Science Core Collection (WOSCC) was utilized to extracted all studies regarding drug resistance in CRC during 2002-2021. CiteSpace and online platform of bibliometrics were used to evaluate the contributions of various countries/regions, institutions, authors and journals in this field. Moreover, the recent research hotspots and promising future trends were identified through keywords analysis by CiteSpace and VOSviewer. Results1451 related publications from 2002 to 2021 in total were identified and collected. The number of global publications in this field has increased annually. China and the USA occupied the top two places with respect to the number of publications, contributing more than 60% of global publications. Sun Yat-sen University and Oncotarget were the institution and journal which published the most papers, respectively. Bardelli A from Italy was the most prolific writer and had the highest H-index. Keywords burst analysis identified that "Growth factor receptor", "induced apoptosis" and "panitumumab" were the ones with higher burst strength in the early stage of this field. Analysis of keyword emergence time showed that "oxaliplatin resistance", "MicroRNA" and "epithelial mesenchymal transition (EMT)" were the keywords with later average appearing year (AAY). ConclusionsThe number of publications and research interest on drug resistance in CRC have been increasing annually. The USA and China were the main driver and professor Bardelli A was the most outstanding researcher in this field. Previous studies have mainly concentrated on growth factor receptor and induced apoptosis. Oxaliplatin resistance, microRNA and EMT as recently appeared frontiers of research that should be closely tracked in the future.
C1 [Zhao, Peng-yue; Jiao, Ya-nan; Ma, Zhao-fu; Yan, Yang; Li, Yu-xuan; Hu, Shi-dong; Li, Song-yan; Du, Xiao-hui] Peoples Liberat Army PLA Gen Hosp, Med Ctr Chinese 1, Dept Gen Surg, Beijing, Peoples R China.
RP Zhao, PY; Du, XH (corresponding author), Peoples Liberat Army PLA Gen Hosp, Med Ctr Chinese 1, Dept Gen Surg, Beijing, Peoples R China.
EM 15010112665@163.com; duxiaohui301@sina.com
RI Li, Yuxuan/GWC-8159-2022; Zhao, Peng-yue/AAL-7965-2021
OI Zhao, Peng-yue/0000-0002-7813-1604
FU National Natural Science Foundation of China; Key Project of Military
   Medical Innovation Program;  [81871317];  [18CXZ025]
FX Funding This work was supported by grants from the National Natural
   Science Foundation of China (No. 81871317) and the Key Project of
   Military Medical Innovation Program (No. 18CXZ025).
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NR 45
TC 7
Z9 7
U1 0
U2 22
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 AUG 30
PY 2022
VL 12
AR 947658
DI 10.3389/fonc.2022.947658
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5N0WA
UT WOS:000871510300001
PM 36110958
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Oliveira, LFS
   Predes, D
   Borges, HL
   Abreu, JG
AF Oliveira, Luiz F. S.
   Predes, Danilo
   Borges, Helena L.
   Abreu, Jose G.
TI Therapeutic Potential of Naturally Occurring Small Molecules to Target
   the Wnt/β-Catenin Signaling Pathway in Colorectal Cancer
SO CANCERS
LA English
DT Review
DE small molecules; anticancer drugs; target therapy; natural compounds
ID HUMAN-DEVELOPMENT INDEX; POLYPOSIS-COLI APC; BETA-CATENIN; STEM-CELLS;
   ANTITUMOR-ACTIVITY; WNT PROTEINS; TUMOR-GROWTH; OPEN SURGERY; IN-VITRO;
   PROLIFERATION
AB Simple Summary Colorectal cancer (CRC) is an emerging public health problem and the second leading cause of death worldwide, with a significant socioeconomic impact in several countries. The 5-year survival rate is only 12% due to the lack of early diagnosis and resistance to available treatments, and the canonical Wnt signaling pathway is involved in this process. This review underlines the importance of understanding the fundamental roles of this pathway in physiological and pathological contexts and analyzes the use of naturally occurring small molecules that inhibits the Wnt/beta-catenin pathway in experimental models of CRC. We also discuss the progress and challenges of moving these small molecules off the laboratory bench into the clinical platform. Colorectal cancer (CRC) ranks second in the number of cancer deaths worldwide, mainly due to late diagnoses, which restrict treatment in the potentially curable stages and decrease patient survival. The treatment of CRC involves surgery to remove the tumor tissue, in addition to radiotherapy and systemic chemotherapy sessions. However, almost half of patients are resistant to these treatments, especially in metastatic cases, where the 5-year survival rate is only 12%. This factor may be related to the intratumoral heterogeneity, tumor microenvironment (TME), and the presence of cancer stem cells (CSCs), which is impossible to resolve with the standard approaches currently available in clinical practice. CSCs are APC-deficient, and the search for alternative therapeutic agents such as small molecules from natural sources is a promising strategy, as these substances have several antitumor properties. Many of those interfere with the regulation of signaling pathways at the central core of CRC development, such as the Wnt/beta-catenin, which plays a crucial role in the cell proliferation and stemness in the tumor. This review will discuss the use of naturally occurring small molecules inhibiting the Wnt/beta-catenin pathway in experimental CRC models over the past decade, highlighting the molecular targets in the Wnt/beta-catenin pathway and the mechanisms through which these molecules perform their antitumor activities.
C1 [Oliveira, Luiz F. S.; Predes, Danilo; Borges, Helena L.; Abreu, Jose G.] Univ Fed Rio Janeiro, Programa Biol Celular & Desenvolvimento, Inst Ciencias Biomed, BR-21941902 Rio De Janeiro, Brazil.
RP Oliveira, LFS; Abreu, JG (corresponding author), Univ Fed Rio Janeiro, Programa Biol Celular & Desenvolvimento, Inst Ciencias Biomed, BR-21941902 Rio De Janeiro, Brazil.
EM oliveira.lfs@ufrj.br; danilopredes@gmail.com; hborges@icb.ufrj.br;
   garciajr@icb.ufrj.br
RI Borges, Helena/E-5044-2013; Predes, Danilo/J-7558-2015; Silva Oliveira,
   Luiz Fernando/ABF-7815-2021; Abreu, Jose/G-6159-2010
OI Abreu Jr, Jose Garcia Ribeiro/0000-0002-1363-1755
FU Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
   [433522/2018-6-18/02/2019, 430847/2018-1, 313023/2020-4]; Fundacao
   Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro
   (FAPERJ) [E-26/203.009/2018, E-26/210.307/2019]; Coordenacao de
   Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
FX This research was funded by Conselho Nacional de Desenvolvimento
   Cientifico e Tecnologico (CNPq) grant number 433522/2018-6-18/02/2019,
   430847/2018-1 and 313023/2020-4; by the Fundacao Carlos Chagas Filho de
   Amparo a Pesquisa do Estado do Rio de Janeiro (FAPERJ), grant number
   E-26/203.009/2018 and E-26/210.307/2019, and by the Coordenacao de
   Aperfeicoamento de Pessoal de Nivel Superior (CAPES).
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NR 185
TC 22
Z9 22
U1 1
U2 17
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2022
VL 14
IS 2
AR 403
DI 10.3390/cancers14020403
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YO1UZ
UT WOS:000747733100001
PM 35053565
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Jian, M
   Ren, L
   He, GD
   Lin, Q
   Tang, WT
   Chen, YJ
   Chen, JW
   Liu, TY
   Ji, ML
   Wei, Y
   Chang, WJ
   Xu, JM
AF Jian, Mi
   Ren, Li
   He, Guodong
   Lin, Qi
   Tang, Wentao
   Chen, Yijiao
   Chen, Jingwen
   Liu, Tianyu
   Ji, Meiling
   Wei, Ye
   Chang, Wenju
   Xu, Jianmin
TI A novel patient-derived organoids-based xenografts model for preclinical
   drug response testing in patients with colorectal liver metastases
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Colorectal cancer; Liver metastases; Animal model; Organoids
ID COLON-CANCER; POOR-PROGNOSIS; DISCOVERY; DNA; ADENOCARCINOMA; MUTATIONS;
   CELLS; MICE
AB Backgrounds Cancer-related mortality in patients with colorectal cancer (CRC) is predominantly caused by development of colorectal liver metastases (CLMs). How to screen the sensitive chemotherapy and targeted therapy is the key element to improve the prognosis of CLMs patients. The study aims to develop patient-derived organoids-based xenografted liver metastases (PDOX-LM) model of CRC, to recapitulate the clinical drug response. Methods We transplanted human CRC primary tumor derived organoids in murine spleen to obtain xenografted liver metastases in murine liver. Immunohistochemistry (IHC) staining, whole-exome and RNA sequencing, and drug response testing were utilized to identify the homogeneity in biological and genetic characteristics, and drug response between the PDOX-LM models and donor liver metastases. Results We successfully established PDOX-LM models from patients with CLMs. IHC staining showed that positive expression of CEA, Ki67, VEGF, FGFR2 in donor liver metastases were also well preserved in matched xenografted liver metastases. Whole-exon sequencing and transcriptome analysis showed that both xenografted and donor liver metastases were highly concordant in somatic variants (>= 0.90 frequency of concordance) and co-expression of driver genes (Pearson's correlation coefficient reach up to 0.99,P = 0.001). Furthermore, drug response testing showed that the PDOX-LM models can closely recapitulated the clinical response to mFOLFOX6 regiments. Conclusions This PDOX-LM model provides a more convenient and informative platform for preclinical testing of individual tumors by retaining the histologic and genetic features of donor liver metastases. This technology holds great promise to predict treatment sensitivity for patients with CLMs undergoing chemotherapy.
C1 [Jian, Mi; Ren, Li; He, Guodong; Lin, Qi; Tang, Wentao; Chen, Yijiao; Chen, Jingwen; Liu, Tianyu; Ji, Meiling; Wei, Ye; Chang, Wenju; Xu, Jianmin] Fudan Univ, Zhongshan Hosp, Dept Gen Surg, 180 Fenglin Rd, Shanghai 200030, Peoples R China.
   [Ren, Li; He, Guodong; Lin, Qi; Tang, Wentao; Chen, Jingwen; Ji, Meiling; Wei, Ye; Chang, Wenju; Xu, Jianmin] Shanghai Engn Res Ctr Colorectal Canc Minimally I, Shanghai 200030, Peoples R China.
C3 Fudan University
RP Chang, WJ; Xu, JM (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Gen Surg, 180 Fenglin Rd, Shanghai 200030, Peoples R China.
EM chang_erich@hotmail.com; xujmin@aliyun.com
RI Chen, Jinyan/JJF-7875-2023; Chen, Hao/P-1633-2016
FU National Natural Science Foundation of China [81602035, 81272390];
   Shanghai Engineering Research Center of Colorectal Cancer Minimally
   Invasive [17DZ2250600]; Shanghai Municipal Health Commission: Shanghai
   Outstanding Youth Specialist Training Program [Q2017-059]; Clinical
   Science and Technology Innovation Project of Shanghai [SHDC12016104];
   Shanghai Science and Technology Committee Project [17411951300,
   S2019-069]
FX This study was supported by Grants from the National Natural Science
   Foundation of China (81602035, 81272390), the Shanghai Engineering
   Research Center of Colorectal Cancer Minimally Invasive (17DZ2250600)
   and the Shanghai Municipal Health Commission: Shanghai Outstanding Youth
   Specialist Training Program (Q2017-059), Clinical Science and Technology
   Innovation Project of Shanghai (SHDC12016104), and Shanghai Science and
   Technology Committee Project (17411951300, S2019-069).
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NR 50
TC 16
Z9 16
U1 1
U2 14
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 JUN 12
PY 2020
VL 18
IS 1
AR 234
DI 10.1186/s12967-020-02407-8
PG 17
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA MB5EC
UT WOS:000542624700001
PM 32532289
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, JZ
   Ren, GH
   Huang, T
   Sang, YM
   Zhong, Y
   Yi, YX
AF Zhang, Jizong
   Ren, Guanghui
   Huang, Tao
   Sang, Yiming
   Zhong, Yan
   Yi, Yongxiang
TI miRNA-363-3p Hinders Proliferation, Migration, Invasion and Autophagy of
   Thyroid Cancer Cells by Controlling SYT1 Transcription to affect NF-κB
SO ENDOCRINE METABOLIC & IMMUNE DISORDERS-DRUG TARGETS
LA English
DT Article
DE Thyroid cancer; miRNA-363-3p; SYT1; malignant progression; cancer cells;
   NF-& kappa;B pathway
ID PROMOTES PROLIFERATION; COLORECTAL-CANCER; SUPPRESSES; CARCINOMA;
   PROGRESSION; METASTASIS; APOPTOSIS; GROWTH; EXPRESSION; TARGETS
AB Background Thyroid cancer (TC) is a frequent endocrine malignant tumor with various pathologic types. miRNA-363-3p plays a pivotal part in the occurrence, development, prognosis, and treatment of cancer.Objective To explore the mechanism of miRNA-363-3p in TC and provide a new idea for targeted therapy of TC.Methods Differential miRNAs and downstream target mRNAs in TC tissues were predicted with bioinformatics analysis. Expression levels of miRNA-363-3p and Synaptotagmin I (SYT1) in TC cells were ascertained by qRT-PCR. Cell migration, invasion, and proliferation were detected by wound healing assay, transwell assay, colony formation assay, CCK-8, and BrdU fluorescence experiment, respectively. Flow cytometry was utilized to detect the levels of apoptosis and necrosis. Immunofluorescence assay was used for detecting autophagosome formation in cells, and the expression levels of autophagy-related proteins, as well as NF-?B related proteins, were measured by western blot. Dual-luciferase reporter gene assay was applied for detecting the interaction between miRNA-363-3p and SYT1.Results miRNA-363-3p was prominently down-regulated in TC cells. miRNA-363-3p overexpression suppressed migration, invasion, and proliferation, promoting apoptosis and necrosis of TC cells. As the downstream target of miRNA-363-3p, SYT1 was up-regulated in TC cells. SYT1 overexpression reversed the inhibition of TC cell proliferation, invasion, migration, and autophagy mediated by miRNA-363-3p overexpression. In addition, miRNA-363-3p overexpression inhibited the activation of the NF-?B pathway in cells, while further overexpression of SYT1 weakened the inhibition of miRNA-363-3p overexpression on the NF-?B pathway.Conclusion miRNA-363-3p affected the NF-?B signaling pathway by down-regulating SYT1 expression to inhibit the malignant progression of TC cells, providing theoretical support for the treatment of TC.
C1 [Zhang, Jizong; Ren, Guanghui; Huang, Tao; Sang, Yiming; Zhong, Yan; Yi, Yongxiang] Nanjing Univ Chinese Med, Hosp Nanjing 2, Dept Gen Surg, 1-1 Zhongfu Rd, Nanjing 210009, Jiangsu, Peoples R China.
C3 Nanjing University of Chinese Medicine
RP Zhong, Y; Yi, YX (corresponding author), Nanjing Univ Chinese Med, Hosp Nanjing 2, Dept Gen Surg, 1-1 Zhongfu Rd, Nanjing 210009, Jiangsu, Peoples R China.
EM yiyxyiyiyi@163.com; delsonstank@163.com
RI Wang, Yifeng/AAC-2564-2019; Huang, Tao/GPK-7568-2022
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NR 31
TC 5
Z9 5
U1 1
U2 7
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1871-5303
EI 2212-3873
J9 ENDOCR METAB IMMUNE
JI Endocr. Metab. Immune Disord.-Drug Targets
PY 2024
VL 24
IS 1
BP 153
EP 162
DI 10.2174/1871530323666230504112553
EA JUL 2023
PG 10
WC Endocrinology & Metabolism; Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Immunology; Pharmacology & Pharmacy
GA GS9S2
UT WOS:001043621600001
PM 37150983
DA 2025-01-04
ER

PT J
AU Zenbout, I
   Bouramoul, A
   Meshoul, S
   Amrane, M
AF Zenbout, Imene
   Bouramoul, Abdelkrim
   Meshoul, Souham
   Amrane, Mounira
TI Efficient Bioinspired Feature Selection and Machine Learning Based
   Framework Using Omics Data and Biological Knowledge Data Bases in Cancer
   Clinical Endpoint Prediction
SO IEEE ACCESS
LA English
DT Article
DE Biomarker discovery; Integrative omics; cancer classification; deep
   canonical correlation analysis; enrichment analysis; feature selection;
   grey wolf optimization; machine learning
ID FUNCTIONAL PROTEOMICS; BIOMARKER DISCOVERY; EXPRESSION; DIAGNOSIS;
   PATHWAY
AB Cancer Research has advanced during the past few years. Using high throughput technology and advances in artificial intelligence, it is now possible to improve cancer diagnosis and targeted therapy, by integrating the investigation and analysis of clinical and omics profiles. The high dimensionality and class imbalance of the majority of available data sets represent a serious challenge to the development of computational methods and tools for cancer diagnosis and biomarker discovery. Taking into account multi-omics data further complicates the undertaking. In this paper, we describe a five-step integrative architecture for dealing with the three aforementioned problems by incorporating proteomics data, protein-protein interaction networks, and signaling pathways in order to identify protein biomarkers with a direct association to cancerous patients' overall survival (OS) and progression free interval (PFI). The core parts of this architecture are a cluster based grey wolf optimization algorithm (CB-GWO) for feature selection and a deep stacked canonical correlation autoencoder (DSCC-AE) for clinical endpoint prediction. A thorough experimental study was carried out to evaluate the performance of the proposed optimization algorithm for feature selection, as well as the performance of the deep learning model in terms of Mathew coefficient correlation (MCC) and Area under the curve (AUC) on breast, lung, colon, and rectum cancers. The results were compared to other methods in the literature. The results are very promising and show the effectiveness of the proposed framework and its ability to outperform the other algorithms and models in terms of AUC (0.91) and MCC (0.64). In addition, hub marker genes with the potential occurence of alterations in colorectal cancer, breast cancer, and lung cancer have been identified.
C1 [Zenbout, Imene] Constantine 2 Univ Abdelhamid Mehri, Dept Fundamental Informat & Its Applicat, MISC Lab, Constantine, Algeria.
   [Zenbout, Imene] Natl Biotechnol Res Ctr CRBT, Constantine 25000, Algeria.
   [Meshoul, Souham] Princess Nourah bint Abdulrahman Univ, Coll Comp & Informat Sci, Dept Informat Technol, Riyadh, Saudi Arabia.
   [Amrane, Mounira] Univ Ferhat Abbas Set 1, Set Univ Hosp, Biochem Dept, Setif, Algeria.
C3 Princess Nourah bint Abdulrahman University
RP Zenbout, I (corresponding author), Constantine 2 Univ Abdelhamid Mehri, Dept Fundamental Informat & Its Applicat, MISC Lab, Constantine, Algeria.; Zenbout, I (corresponding author), Natl Biotechnol Res Ctr CRBT, Constantine 25000, Algeria.; Meshoul, S (corresponding author), Princess Nourah bint Abdulrahman Univ, Coll Comp & Informat Sci, Dept Informat Technol, Riyadh, Saudi Arabia.
EM imene.zenbout@univ-constantine2.dz; sbmeshoul@pnu.edu.sa
RI BOURAMOUL, Abdelkrim/AAG-5658-2019
OI Bouramoul, Abdelkrim/0000-0002-8628-6817; Zenbout,
   Imene/0000-0002-5168-2449
FU Princess Nourah Bint Abdulrahman University, Riyadh, Saudi Arabia
   [PNURSP2023R196]
FX This work was supported by the Princess Nourah Bint Abdulrahman
   University Researchers Supporting Project through Princess Nourah Bint
   Abdulrahman University, Riyadh, Saudi Arabia, under Grant
   PNURSP2023R196.
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NR 101
TC 5
Z9 5
U1 4
U2 17
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 2169-3536
J9 IEEE ACCESS
JI IEEE Access
PY 2023
VL 11
BP 2674
EP 2699
DI 10.1109/ACCESS.2023.3234294
PG 26
WC Computer Science, Information Systems; Engineering, Electrical &
   Electronic; Telecommunications
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Computer Science; Engineering; Telecommunications
GA 7U7PR
UT WOS:000912321700001
OA gold
DA 2025-01-04
ER

PT J
AU Smith, CIE
AF Smith, C. I. Edvard
TI Enigmas in tumor resistance to kinase inhibitors and calculation of the
   drug resistance index for cancer (DRIC)
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Review
DE Acalabrutinib; Alectinib; Brigatinib; Ceritinib; Crizotinib; Dabrafenib;
   Dasatinib; Erlotinib; Gefitinib; Ibrutinib; Imatinib; Lorlatinib;
   Nilotinib; Osimertinib; Rociletinib; Trametinib; Vemurafenib
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; CELL LUNG-CANCER; CHRONIC
   MYELOID-LEUKEMIA; ANAPLASTIC LYMPHOMA KINASE; MUTANT COLORECTAL-CANCER;
   BRUTONS TYROSINE KINASE; NON-ONCOGENE ADDICTION; ACQUIRED-RESISTANCE;
   TARGETED THERAPY; BCR-ABL
AB Darwinian selection is also applicable when antibiotics, the immune system or other host factors shape the repertoire of microorganisms, and similarly, clonal selection is the hallmark of tumor evolution. The ongoing revolution in new anti-cancer treatment modalities, combined with an unprecedented precision in characterizing malignant clones at the level below one percent, profoundly improves the understanding of repertoire-tuning mechanisms. There is no fundamental difference between selection of the tumor cells in the presence, or absence, of therapy. However, under treatment the influence of a single agent can be measured, simplifying the analysis. Because of their beneficial and selective therapeutic effect, the focus in this review is set on protein kinase inhibitors (PKIs), predominantly tyrosine kinase inhibitors (TKIs). This is one of the most rapidly growing families of novel cancer medicines. In order to limit the number of drugs, the following representative target kinases are included: ALK, BCR-ABL, BRAF, BTK, and EGFR.
   A key therapeutic challenge is how to reduce tumor growth after treatment, since this is rate-limiting for the generation and expansion of more malignant escape mutants. Thus, upon efficient treatment, tumor cell loss often enables a profoundly increased growth rate among resistant cells. Strategies to reduce this risk, such as concomitant, competitive outgrowth of non-transformed cells, are described.
   Seven parameters: 1. Drug type, 2. tumor type, 3. presence of metastases or phenotypic change, 4. tumor cell number, 5. net growth rate (proliferation minus cell death), 6. inherited genetic- and 7. epigenetic variations are crucial for drug responses. It is envisaged that it might become possible to calculate a clinically relevant Drug Resistance Index for Cancer (DRIC) for each patient. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Smith, C. I. Edvard] Karolinska Univ Hosp Huddinge, Karolinska Inst, Dept Lab Med, Clin Res Ctr, SE-14186 Huddinge, Sweden.
C3 Karolinska Institutet; Karolinska University Hospital
RP Smith, CIE (corresponding author), Karolinska Univ Hosp Huddinge, Karolinska Inst, Dept Lab Med, Clin Res Ctr, SE-14186 Huddinge, Sweden.
EM edvard.smith@ki.se
OI SMITH, C. I. Edvard/0000-0003-1907-3392
FU Swedish Cancer Society [CAN2013/389]; Swedish Medical Research Council
   [K2015-68X-11247-21-3]; Swedish County Council (ALF) [2012006]
FX This work was supported by the Swedish Cancer Society (CAN2013/389), the
   Swedish Medical Research Council (K2015-68X-11247-21-3) and the Swedish
   County Council (ALF-project 2012006). I would especially like to thank
   Anna Berglof for making the graphical presentions and for her invaluable
   help with the manuscript. Birger Christensson, Gosta Gahrton, Moustapha
   Hassan, Robert Mansson, Klas Wiman and Rula Zain, are gratefully
   acknowledged for valuable comments on the manuscript.
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NR 155
TC 8
Z9 9
U1 0
U2 13
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
EI 1096-3650
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD AUG
PY 2017
VL 45
BP 36
EP 49
DI 10.1016/j.semcancer.2016.11.008
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FF3GB
UT WOS:000408782400005
PM 27865897
DA 2025-01-04
ER

PT S
AU Lopez, NE
   Yeh, JJ
AF Lopez, Nicole E.
   Yeh, Jen Jen
BE Bentrem, D
   Benson, A
TI Gastrointestinal Malignancy: Genetic Implications to Clinical
   Applications
SO GASTROINTESTINAL MALIGNANCIES
SE Cancer Treatment and Research
LA English
DT Article; Book Chapter
DE Targeted therapy; Molecular medicine; Personalized medicine
ID METASTATIC COLORECTAL-CANCER; ISLAND METHYLATOR PHENOTYPE; FAMILIAL
   ADENOMATOUS POLYPOSIS; GROWTH-FACTOR RECEPTOR; PHASE-III TRIAL; STROMAL
   TUMORS GIST; PEUTZ-JEGHERS-SYNDROME; V600E BRAF MUTATIONS;
   SUCCINATE-DEHYDROGENASE SUBUNIT; OXALIPLATIN-BASED CHEMOTHERAPY
AB Alterations in the DNA sequences of genes, or mutations, have traditionally been viewed as the primary factors driving tumor progression, however, epigenetic evidence would suggest that some heritable traits are mediated by changes in DNA expression that are not dependent upon alterations in the primary DNA sequence. Advances in the genetic understanding of cancer have, in some instances, allowed for more precise administration of anti-neoplastic therapy. Targeted therapies, the aim of which are to target specific cellular proteins or processes used by the cancer cells, have been advocated to avoid the adverse side effects attributable to a lack of cell specificity associated with traditional chemotherapy. Here we aim to describe the current state of understanding regarding the genetic related causes of cancers, the targeted therapies aimed at killing them and the inter-relationship between these two.
C1 [Lopez, Nicole E.; Yeh, Jen Jen] Univ N Carolina, Div Surg Oncol, 170 Manning Dr,CB 7213,1150 Phys Off Bldg, Chapel Hill, NC 27599 USA.
C3 University of North Carolina; University of North Carolina Chapel Hill
RP Yeh, JJ (corresponding author), Univ N Carolina, Div Surg Oncol, 170 Manning Dr,CB 7213,1150 Phys Off Bldg, Chapel Hill, NC 27599 USA.
EM jen_jen_yeh@med.unc.edu
RI Lopez, Nicole/GZL-3059-2022
OI Lopez, Nicole/0000-0002-4807-7360
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NR 481
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 0927-3042
BN 978-3-319-34244-3; 978-3-319-34242-9
J9 CANCER TREAT RES
JI Canc. Treat. Res.
PY 2016
VL 168
BP 393
EP 479
DI 10.1007/978-3-319-34244-3_19
D2 10.1007/978-3-319-34244-3
PG 87
WC Oncology; Gastroenterology & Hepatology
WE Book Citation Index – Science (BKCI-S)
SC Oncology; Gastroenterology & Hepatology
GA BH1KN
UT WOS:000398098200019
PM 29206386
DA 2025-01-04
ER

PT J
AU Song, QY
   Zheng, YF
   Zhong, GQ
   Wang, SP
   He, CC
   Li, MS
AF Song, Qiuyu
   Zheng, Yifeng
   Zhong, Guoqiang
   Wang, Shanping
   He, Chengcheng
   Li, Mingsong
TI Application of Nanoparticles in the Diagnosis and Treatment of
   Colorectal Cancer
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE Colorectal cancer; nanoparticles; nanomedicine; application; diagnosis;
   treatment
ID IN-VIVO; SILVER NANOPARTICLES; TARGETED NANOPARTICLES; PHOTODYNAMIC
   THERAPY; DRUG-DELIVERY; CARBON NANOTUBES; SIRNA DELIVERY; E-SELECTIN;
   CELLS; CHEMOTHERAPY
AB Colorectal cancer is a common malignant tumor with high morbidity and mortality rates, imposing a huge burden on both patients and the healthcare system. Traditional treatments such as surgery, chemotherapy and radiotherapy have limitations, so finding more effective diagnostic and therapeutic tools is critical to improving the survival and quality of life of colorectal cancer patients. While current tumor targeting research mainly focuses on exploring the function and mechanism of molecular targets and screening for excellent drug targets, it is crucial to test the efficacy and mechanism of tumor cell therapy that targets these molecular targets. Selecting the appropriate drug carrier is a key step in effectively targeting tumor cells. In recent years, nanoparticles have gained significant interest as gene carriers in the field of colorectal cancer diagnosis and treatment due to their low toxicity and high protective properties. Nanoparticles, synthesized from natural or polymeric materials, are NM-sized particles that offer advantages such as low toxicity, slow release, and protection of target genes during delivery. By modifying nanoparticles, they can be targeted towards specific cells for efficient and safe targeting of tumor cells. Numerous studies have demonstrated the safety, efficiency, and specificity of nanoparticles in targeting tumor cells, making them a promising gene carrier for experimental and clinical studies. This paper aims to review the current application of nanoparticles in colorectal cancer diagnosis and treatment to provide insights for targeted therapy for colorectal cancer while also highlighting future prospects for nanoparticle development.
C1 [Song, Qiuyu; Zheng, Yifeng; Zhong, Guoqiang; Wang, Shanping; He, Chengcheng; Li, Mingsong] Guangzhou Med Univ, Guangdong Prov Clin Res Ctr Obstet & Gynecol, Guangdong Prov Key Lab Major Obstet Dis, Dept Gastroenterol,Affiliated Hosp 3, Guangzhou, Peoples R China.
C3 Guangzhou Medical University
RP He, CC (corresponding author), Guangzhou Med Univ, Guangdong Prov Clin Res Ctr Obstet & Gynecol, Guangdong Prov Key Lab Major Obstet Dis, Dept Gastroenterol,Affiliated Hosp 3, Guangzhou, Peoples R China.
EM cbslhy@163.com
RI He, Chengcheng/KVY-9707-2024; Zheng, Yifeng/LUZ-6052-2024
OI li, Mingsong/0000-0003-2115-5928; He, Chengcheng/0000-0001-8176-8588;
   Zhong, Guoqiang/0009-0005-8196-3013; Wang, Shanping/0000-0003-1313-369X;
   Zheng, Yifeng/0009-0006-8031-9063
FU National Natural Science Funds of China [82303391]; Guangdong Basic and
   Applied Basic Research Fund [2022A1515111193]; Guangzhou Science and
   Technology Plan Project [2023A04J0581]
FX This work was supported by the National Natural Science Funds of China
   (82303391), the Guangdong Basic and Applied Basic Research Fund
   (2022A1515111193), the Guangzhou Science and Technology Plan Project
   (2023A04J0581)
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PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1871-5206
EI 1875-5992
J9 ANTI-CANCER AGENT ME
JI Anti-Cancer Agents Med. Chem.
PY 2024
VL 24
IS 18
BP 1305
EP 1326
DI 10.2174/0118715206323900240807110122
EA AUG 2024
PG 22
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA I7F4H
UT WOS:001298831600001
PM 39129164
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Cortés-Guiral, D
   Pastor-Iodate, C
   del Arco, CD
   del Puerto-Nevado, L
   Fernández-Aceñero, MJ
AF Cortes-Guiral, D.
   Pastor-Iodate, C.
   Diaz del Arco, C.
   del Puerto-Nevado, L.
   Fernandez-Acenero, M. J.
TI CPEB4 immunohistochemical expression is associated to prognosis in stage
   IV colorectal carcinoma
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Article
DE Hepatic metastasis; Colorectal carcinoma; Prognosis; CPEB4 expression
ID HEPATIC RESECTION; LIVER METASTASES; CANCER; CHEMOTHERAPY; RECURRENCE;
   SURVIVAL; GLIOMA; SCORE
AB The cytoplasmic polyadenylation element binding protein 4 (CPEB4) is a RNA binding protein and translational regulator. It has been associated with tumor growth, vascularization and invasion and with tumor progression in breast, pancreas and lung carcinomas. To the best of our knowledge only one previous report has analyzed the prognostic value of CPEB4 in an experimental model of colorectal carcinoma. We have reviewed the files of patients with stage IV colorectal carcinoma metastatic to the liver. All the patients had received chemotherapy followed by hepatic metastasis resection and subsequent resection of the colon (liver-first approach). We have gathered demographic, analytical and morphological data of the primary tumors. We have performed immunohistochemical analysis of CPEB4 expression in these tumors and analyzed the potential prognostic value of this protein. 50 patients fulfilled inclusion criteria for the present study. All of them received preoperative chemotherapy based on platinum and also postoperative chemotherapy, with or without targeted drugs (18% received anti-epidermal growth factor receptor (EGFR) drugs and 24% anti-vascular endothelial growth factor receptor (VEGFR) drugs. 66% of the primaries were of sigmoid-rectal origin. CPEB4 expression was mainly cytoplasmic and it was scored as intense in 46% of the patients. Survival analysis revealed a significant association between progression free survival (PFS) and overall survival (OS) and CPEB4 immunohistochemical expression, which was independent in the multivariate analysis.
   CPEB4 behaves as a significant predictor of prognosis in stage IV colorectal carcinoma. The existence of CPEB4 specific inhibitors can open a new way for targeted therapy. Larger prospective studies are needed to confirm our promising results. (C) 2017 Elsevier GmbH. All rights reserved.
C1 [Cortes-Guiral, D.; Pastor-Iodate, C.; Fernandez-Acenero, M. J.] Fdn Jimenez Diaz, Dept Surg, Madrid, Spain.
   [Diaz del Arco, C.; Fernandez-Acenero, M. J.] Hosp Clin San Carlos, Surg Pathol, Madrid, Spain.
   [del Puerto-Nevado, L.] Fdn Jimenez Diaz, Traslat Oncol Unit, Madrid, Spain.
C3 Hospital Clinico San Carlos
RP Fernández-Aceñero, MJ (corresponding author), Hosp Clin San Carlos, Dept Surg Pathol, Avda Prof Martin Lagos S-N, Madrid 28040, Spain.
EM mgg10167@gmail.com
RI Cortés-Guiral, Delia/AAJ-3762-2020; Aceñero, Mª/ABC-5904-2020; Diaz del
   Arco, Cristina/ABC-8808-2020; del Puerto Nevado, Laura/LMO-1460-2024
OI Fernandez-Acenero/0000-0002-2439-3553; Diaz del Arco,
   Cristina/0000-0002-6100-4967; del Puerto Nevado,
   Laura/0000-0003-0594-9656
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NR 16
TC 6
Z9 7
U1 0
U2 5
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0344-0338
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PY 2017
VL 213
IS 6
BP 639
EP 642
DI 10.1016/j.prp.2017.04.020
PG 4
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA EY9KV
UT WOS:000404318400008
PM 28551384
DA 2025-01-04
ER

PT J
AU Guglielmo, A
   Staropoli, N
   Giancotti, M
   Mauro, M
AF Guglielmo, Annamaria
   Staropoli, Nicoletta
   Giancotti, Monica
   Mauro, Marianna
TI Personalized medicine in colorectal cancer diagnosis and treatment: a
   systematic review of health economic evaluations
SO COST EFFECTIVENESS AND RESOURCE ALLOCATION
LA English
DT Review
DE Personalized medicine; Economic evaluation; Cost-effectiveness analysis;
   Colorectal cancer; CRC
ID COST-EFFECTIVENESS ANALYSIS; LYNCH SYNDROME; STRATEGIES; KRAS;
   PHARMACOGENOMICS; TRANSFERABILITY; IDENTIFY
AB Background: Due to its epidemiological relevance, several studies have been performed to assess the cost-effectiveness of diagnostic tests and treatments in colorectal cancer (CRC) patients.
   Objective: We reviewed economic evaluations on diagnosis of inherited CRC-syndromes and genetic tests for the detection of mutations associated with response to therapeutics.
   Methods: A systematic literature review was performed by searching the main literature databases for relevant papers on the field, published in the last 5 years.
   Results: 20 studies were included in the final analysis: 14 investigating the cost-effectiveness of hereditary-CRC screening; 5 evaluating the cost-effectiveness of KRAS mutation assessment before treatment; and 1 study analysing the cost-effectiveness of genetic tests for early-stage CRC patients prognosis. Overall, we found that: (a) screening strategies among CRC patients were more effective than no screening; (b) all the evaluated interventions were cost-saving for certain willingness-to-pay (WTP) threshold; and (c) all new CRC patients diagnosed at age 70 or below should be screened. Regarding patients treatment, we found that KRAS testing is economically sustainable only if anticipated in patients with non-metastatic CRC (mCRC), while becoming unsustainable, due to an incremental cost-effectiveness ratio (ICER) beyond the levels of WTP-threshold, in all others evaluated scenarios.
   Conclusions: The poor evidence in the field, combined to the number of assumptions done to perform the models, lead us to a high level of uncertainty on the cost-effectiveness of genetic evaluations in CRC, suggesting that major research is required in order to assess the best combination among detection tests, type of genetic test screening and targeted-therapy.
C1 [Guglielmo, Annamaria; Staropoli, Nicoletta; Giancotti, Monica; Mauro, Marianna] Magna Graecia Univ Catanzaro, Dept Clin & Expt Med, Viale Europa, I-88100 Catanzaro, Italy.
C3 Magna Graecia University of Catanzaro
RP Guglielmo, A (corresponding author), Magna Graecia Univ Catanzaro, Dept Clin & Expt Med, Viale Europa, I-88100 Catanzaro, Italy.
EM guglielmo@unicz.it
RI GIANCOTTI, MONICA/C-7340-2018; Guglielmo, Annamaria/A-1445-2014;
   Staropoli, Nicoletta/GZM-5038-2022; Mauro, Marianna/AAK-4645-2020
OI Staropoli, Nicoletta/0000-0001-9579-3960
CR Alberts SR, 2014, PHARMACOECONOMICS, V32, P1231, DOI 10.1007/s40273-014-0207-1
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NR 37
TC 25
Z9 27
U1 0
U2 14
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1478-7547
J9 COST EFFECT RESOUR A
JI Cost Effect. Resour Alloc.
PD JAN 22
PY 2018
VL 16
AR 2
DI 10.1186/s12962-018-0085-z
PG 14
WC Health Policy & Services
WE Social Science Citation Index (SSCI)
SC Health Care Sciences & Services
GA FT4MR
UT WOS:000423129700001
PM 29386984
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kono, H
   Goi, T
   Matsunaka, T
   Koneri, K
AF Kono, Hiroko
   Goi, Takanori
   Matsunaka, Takayuki
   Koneri, Kenji
TI Anti-Prokineticin1 Suppresses Liver Metastatic Tumors in a Mouse Model
   of Colorectal Cancer with Liver Metastasis
SO CURRENT ISSUES IN MOLECULAR BIOLOGY
LA English
DT Article
DE prokineticin1; colorectal cancer; proliferation; liver metastasis;
   targeted therapy; antibody
ID ENDOTHELIAL GROWTH-FACTOR; ANGIOGENESIS; THERAPY; MECHANISMS; EXPRESSION
AB Multidisciplinary treatment for colorectal cancer (CRC) has undergone significant advances, and molecularly targeted drugs have substantially improved patient prognosis. However, one problem with current molecularly targeted therapeutics is that they must be used in combination with anticancer agents. New molecular targeted therapies that can be used alone are needed. We have previously identified prokineticin1 (PROK1) factor as a therapeutic potential target for CRC. PROK1 factor is involved in the angiogenesis of tissues surrounding CRC tumors. Additionally, PROK1 receptors 1 and 2 are expressed in CRC cell lines, playing roles in cell proliferation via an autocrine mechanism and in the signaling system. In this study, a liver metastasis mouse model was developed using human colorectal cancer cell lines, and mice were divided into anti-PROK1 antibody administration and control groups. Mice were treated intraperitoneally with antibodies or phosphate-buffered saline (control) every three days. The number, size, and cell proliferation ability of metastatic lesions were analyzed. Our results suggested that the number, size, and cancer cell proliferation ability of metastatic lesions decreased, and the survival time significantly increased in the antibody-treated group compared to those in the control group. Thus, the anti-PROK1 antibody therapy suppressed the cell proliferation ability of liver metastatic lesions in a CRC mouse model, suggesting its potential as a novel treatment strategy.
C1 [Kono, Hiroko; Goi, Takanori; Matsunaka, Takayuki; Koneri, Kenji] Univ Fukui, Dept Surg 1, 23-3 Eiheiji Cho, Eiheiji, Fukui 9101193, Japan.
C3 University of Fukui
RP Goi, T (corresponding author), Univ Fukui, Dept Surg 1, 23-3 Eiheiji Cho, Eiheiji, Fukui 9101193, Japan.
EM hyrk@u-fukui.ac.jp; tgoi@u-fukui.ac.jp; tak.681220@gmail.com;
   koneri@hotmail.co.jp
OI Goi, Takanori/0000-0001-7671-0648
FU Grant-in-Aid for Scientific Research (C) from the Japan Society for the
   Promotion of Science
FX The technical assistance of Saitoh M. in this study is appreciated.
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NR 21
TC 1
Z9 1
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1467-3037
EI 1467-3045
J9 CURR ISSUES MOL BIOL
JI Curr. Issues Mol. Biol.
PD JAN
PY 2024
VL 46
IS 1
BP 44
EP 52
DI 10.3390/cimb46010004
PG 9
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA FY3K2
UT WOS:001149371400001
PM 38275664
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Tantoy, IY
   Cataldo, JK
   Aouizerat, BE
   Dhruva, A
   Miaskowski, C
AF Tantoy, Ilufredo Y.
   Cataldo, Janine K.
   Aouizerat, Bradley E.
   Dhruva, Anand
   Miaskowski, Christine
TI A Review of the Literature on Multiple Co-occurring Symptoms in Patients
   With Colorectal Cancer Who Received Chemotherapy Alone or Chemotherapy
   With Targeted Therapies
SO CANCER NURSING
LA English
DT Review
DE Chemotherapy; Colorectal cancer; Quality of life; Symptoms; Targeted
   therapy
ID ONCOLOGY OUTPATIENTS; LIFE; PREVALENCE; DISTRESS; LUNG; EXPERIENCE;
   FATIGUE; TRAJECTORIES; PROFILES; CLUSTERS
AB Background: Patients with colorectal cancer (CRC) rarely experience a single symptom associated with their disease and its treatment. Objective: Purpose of this literature review was to summarize the current state of knowledge of multiple co-occurring symptoms in CRC patients who received chemotherapy (CTX) alone or CTX with targeted therapies. Methods: Comprehensive literature search was conducted from 1990 to 2014. These studies were evaluated in terms of the occurrence of multiple co-occurring symptoms in CRC patients who received CTX alone or CTX with targeted therapies; the most common symptom assessment and quality of life (QOL) instruments used; and the associations identified between select demographic and treatment characteristics, QOL, and multiple co-occurring symptoms. Results: Only 5 studies met this review's inclusion criteria. Two studies compared symptoms in patients who received CTX alone or CTX with targeted therapies, and only 1 study reported on symptom occurrence. Of the 5 studies identified, only 2 used the same instrument to assess symptoms, and only 2 studies evaluated for associations between demographic and treatment characteristics and symptom burden, as well as QOL outcomes. Conclusions: Given the larger number of patients with CRC, as well as the increased number of CRC patients who will receive targeted therapies with or without CTX, future studies need to describe the occurrence, severity, and distress of multiple co-occurring symptoms and their impact on CRC patients' QOL. Implications for Practice: To deliver effective symptom management interventions, the most common, severe, and distressing symptoms that CRC patients experience need to be identified.
C1 [Tantoy, Ilufredo Y.; Cataldo, Janine K.; Aouizerat, Bradley E.; Miaskowski, Christine] Univ Calif San Francisco, Sch Nursing, Dept Physiol Nursing, San Francisco, CA 94143 USA.
   [Dhruva, Anand] Univ Calif San Francisco, Sch Med, San Francisco, CA USA.
   [Aouizerat, Bradley E.] Univ Calif San Francisco, Inst Human Genet, San Francisco, CA 94143 USA.
C3 University of California System; University of California San Francisco;
   University of California System; University of California San Francisco;
   University of California System; University of California San Francisco
RP Tantoy, IY (corresponding author), Univ Calif San Francisco, Dept Physiol Nursing, 2 Koret Way,N631Y, San Francisco, CA 94143 USA.
EM Ilufredo.tantoy@ucsf.edu
OI Tantoy, Ilufredo/0000-0002-0193-0280
FU National Cancer Institute (NCI) [CA134900]; NCI [CA168960]; National
   Institute of Health [T32NR007088]
FX This study was funded by a grant from the National Cancer Institute
   (NCI, CA134900). C.M. is an American Cancer Society Clinical Research
   professor and is funded by a K07 award from the NCI (CA168960). I.Y.T.
   is funded by a National Institute of Health T32 grant (T32NR007088).
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NR 43
TC 23
Z9 25
U1 7
U2 18
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0162-220X
EI 1538-9804
J9 CANCER NURS
JI Cancer Nurs.
PD NOV-DEC
PY 2016
VL 39
IS 6
BP 437
EP 445
DI 10.1097/NCC.0000000000000343
PG 9
WC Oncology; Nursing
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Oncology; Nursing
GA EB1LS
UT WOS:000387114100009
PM 26895413
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Suzuki, K
   Tahara, S
   Hattori, Y
   Teramoto, S
   Ishisaka, E
   Inomoto, C
   Osamura, RY
   Morita, A
   Murai, Y
AF Suzuki, Koji
   Tahara, Shigeyuki
   Hattori, Yujiro
   Teramoto, Shinichiro
   Ishisaka, Eitaro
   Inomoto, Chie
   Osamura, Robert Yoshiyuki
   Morita, Akio
   Murai, Yasuo
TI Lung adenocarcinoma metastasis within a pituitary neuroendocrine tumor:
   a case report with review of literature
SO ENDOCRINE JOURNAL
LA English
DT Review
DE Collision tumor; Metastasis; Pituitary neuroendocrine tumor; Lung
   adenocarcinoma; Molecular-targeted therapy
ID RENAL-CELL CARCINOMA; ADENOMA CASE-REPORT; CANCER; GROWTH; PROLACTINOMA
AB Collision tumors involving the metastasis of malignant neoplasms to pituitary neuroendocrine tumors (PitNETs) are extremely rare. We herein report a case involving a patient with lung adenocarcinoma metastasis within a PitNET who exhibited relatively rapid progression of neurological symptoms. A 75-year-old man who underwent tumor resection 36 and 18 years prior to presentation for bladder and colon cancer, respectively, without recurrence presented with bitemporal hemianopsia, ptosis, and diplopia of the right eye. Subsequent magnetic resonance imaging (MRI) revealed a tumor 3.2 cm in diameter that extended from the anterior pituitary gland to the suprasellar region. Gadolinium-enhanced MRI of the tumor showed heterogeneous contrast enhancement. Considering the relatively rapid progression of neurological symptoms, semi emergency endoscopic endonasal transsphenoidal surgery was performed. Histopathological examination revealed a group of thyroid transcription factor -1-and napsin A-positive papillary proliferating cells intermingled with alpha-subunit-and steroidogenic factor-1-positive PitNET cells. Thus, the patient was diagnosed with lung adenocarcinoma metastasis within a gonadotroph PitNET. Genetic testing revealed the presence of an EGFR (Ex-19del) mutation, after which chemotherapy was initiated. Additional stereotactic radiotherapy was performed for the residual tumor in the sella turcica. With continued chemotherapy, good control of both the primary and metastatic tumors was noted after 24 months after surgery. Cases of malignant neoplasm metastasis within a PitNET are difficult to diagnose. In the case of a sella turcica tumor with relatively rapid progression of neurological symptoms, early surgical intervention is recommended given the possibility of a highly proliferative tumor and the need to obtain pathologic specimens.
C1 [Suzuki, Koji; Hattori, Yujiro; Morita, Akio; Murai, Yasuo] Nippon Med Sch, Dept Neurol Surg, Tokyo 1138603, Japan.
   [Tahara, Shigeyuki; Ishisaka, Eitaro] Musashikosugi Hosp, Dept Neurol Surg, Nippon Med Sch, Kawasaki, Kanagawa 2118233, Japan.
   [Hattori, Yujiro] Nippon Med Sch, Grad Sch Med, Dept Anat & Neurobiol, Tokyo 1138602, Japan.
   [Teramoto, Shinichiro] Juntendo Univ, Dept Neurosurg, Sch Med, Tokyo 1138431, Japan.
   [Inomoto, Chie] Tokai Univ, Sch Med, Dept Pathol, Kanagawa 2591143, Japan.
   [Osamura, Robert Yoshiyuki] Nippon Koukan Hosp, Dept Pathol, Kawasaki, Kanagawa 2100852, Japan.
   [Tahara, Shigeyuki] Musashikosugi Hosp, Dept Neurol Surg, Nippon Med Sch, 1-383 Kosugi Cho,Nakahara Ku, Kawasaki, Kanagawa 2118233, Japan.
C3 Nippon Medical School; Nippon Medical School; Nippon Medical School;
   Juntendo University; Tokai University; Nippon Medical School
RP Tahara, S (corresponding author), Musashikosugi Hosp, Dept Neurol Surg, Nippon Med Sch, 1-383 Kosugi Cho,Nakahara Ku, Kawasaki, Kanagawa 2118233, Japan.
EM tabara@nms.ac.jp
RI Hattori, Yujiro/AAR-9559-2020
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NR 36
TC 1
Z9 1
U1 2
U2 3
PU JAPAN ENDOCRINE SOC
PI KYOTO
PA 75  YANAGINOBANBA NISHIIRU-MASUYA-CHO, SANJOU-DORI, NAKAGYOU-KU, KYOTO,
   604-8111, JAPAN
SN 0918-8959
EI 1348-4540
J9 ENDOCR J
JI Endocr. J.
PY 2024
VL 71
IS 3
BP 295
EP 303
DI 10.1507/endocrj.EJ23-0372
EA DEC 2023
PG 9
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA MP2J4
UT WOS:001136656600001
PM 38171721
OA gold
DA 2025-01-04
ER

PT J
AU González-Urías, A
   Manzanares-Guevara, LA
   Licea-Claveríe, A
   Ochoa-Terán, A
   Licea-Navarro, AF
   Bernaldez-Sarabia, J
   Zapata-González, I
AF Gonzalez-Urias, Alejandra
   Manzanares-Guevara, Lizbeth A.
   Licea-Claverie, Angel
   Ochoa-Teran, Adrian
   Licea-Navarro, Alexei F.
   Bernaldez-Sarabia, Johanna
   Zapata-Gonzalez, Ivan
TI Stimuli responsive nanogels with intrinsic fluorescence: Promising
   nanovehicles for controlled drug delivery and cell internalization
   detection in diverse cancer cell lines
SO EUROPEAN POLYMER JOURNAL
LA English
DT Article
DE Nanogels; Fluorescent probes; Cancer cells; Responsive polymers
ID IMMUNOGLOBULIN-E RESPONSE; CATIONIC NANOGELS; CONTROLLED-RELEASE;
   IMMUNE-RESPONSES; TARGETED THERAPY; MIXED MICELLES; CISPLATIN;
   NANOPARTICLES; TEMPERATURE; NANOHYDROGELS
AB Nanogels are an important class of nanomaterials with a wide field of potential applications in nanomedicine. Fluorescent nanogels have the great advantage of the application in theranostics. In this study, intrinsic fluorescent nanogels, crosslinked with fluorescein O,O'-diacrylate (FDA), were synthetized and studied for first time, via a robust methodology of one-pot, resulting in yields in scale of grams. This new type of nanovehicles avoid the susceptibility to leaching, inhomogeneity, or degradation of the fluorescent moieties, observed in others approaches using encapsulation or conjugation of fluorescent molecules, additionally they show multi-stimuli response to temperature and pH. Both anionic (AFN) and cationic fluorescent nanogels (CFN) were successfully produced, which showed strong fluorescence intensity at neutral pH, the fluorescence was quenched at pH 5. Cisplatin (CDDP) and 5-fluorouracil (5-FU) were loaded into the nanogels, leading to partially quenching of the fluorescence. The kinetics of drug release and cell-viability studies are also reported. Cell-internalization studies were performed by fluorescence microscopy in non-small lung adenocarcinoma cell line NCI-H1437 and human colorectal cancer cell line HCT-116; demonstrating that the AFN were not internalized and CFN were easily internalized at concentrations of 100 mu g/mL in 5 min, irrespective of the molecular weight of the Poly (ethylenglycol)-chains. The developed method can be expanded to the preparation of other fluorescent nanogel types; whereas the prepared AFN and CFN could be studied as nanocarriers to be internalized in diverse celllines.
C1 [Gonzalez-Urias, Alejandra; Manzanares-Guevara, Lizbeth A.; Licea-Claverie, Angel; Ochoa-Teran, Adrian] Tecnol Nacl Mexico, IT Tijuana, Ctr Grad & Invest Quim, AP 1166, Tijuana 22430, BC, Mexico.
   [Licea-Navarro, Alexei F.; Bernaldez-Sarabia, Johanna] Ctr Invest Cient & Educ Super Ensenada CICESE, Dept Innovac Biomed, Ensenada 22860, Baja California, Mexico.
   [Zapata-Gonzalez, Ivan] Catedras CONACYT Tecnol Nacl Mexico, IT Tijuana, Ctr Grad & Invest Quim, AP 1166, Tijuana 22430, BC, Mexico.
C3 CICESE - Centro de Investigacion Cientifica y de Educacion Superior de
   Ensenada
RP Licea-Claveríe, A; Zapata-González, I (corresponding author), Tecnol Nacl Mexico, Inst Tecnol Tijuana, Ctr Grad & Invest Quim, Blvd Alberto Limon Padilla & Ave ITT Tijuana S-N, Tijuana 22430, BC, Mexico.
EM aliceac@tectijuana.mx; ivan.zapata@tectijuana.edu.mx
RI Licea-Claverie, Angel/LRB-9519-2024; Zapata-Gonzalez, Ivan/H-7587-2017;
   Licea, Alexei/B-4106-2016; Bernaldez Sarabia, Johanna/F-1981-2019
OI OCHOA-TERAN, ADRIAN/0000-0002-3746-3960; Licea,
   Alexei/0000-0003-4022-7405; Zapata-Gonzalez, Ivan/0000-0002-0912-3627;
   Gonzalez Urias, Maria Alejandra/0000-0002-9244-8966; Bernaldez Sarabia,
   Johanna/0000-0003-4894-5604
FU National Council of Science and Technology of Mexico (CONACYT)
   [Catedras-CONACYT-707-2015, INFR2016-269007,
   SEP-CONACYT-2018-A1-S-54944, CB2016-285419]
FX National Council of Science and Technology of Mexico (CONACYT) through
   grants: Catedras-CONACYT-707-2015, INFR2016-269007,
   SEP-CONACYT-2018-A1-S-54944 and CB2016-285419.
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NR 76
TC 16
Z9 16
U1 0
U2 31
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0014-3057
EI 1873-1945
J9 EUR POLYM J
JI Eur. Polym. J.
PD FEB 5
PY 2021
VL 144
AR 110200
DI 10.1016/j.eurpolymj.2020.110200
EA JAN 2021
PG 19
WC Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Polymer Science
GA PT7QD
UT WOS:000608805400003
DA 2025-01-04
ER

PT J
AU Noguchi, R
   Yamaguchi, K
   Ikenoue, T
   Terakado, Y
   Ohta, Y
   Yamashita, N
   Kainuma, O
   Yokoi, S
   Maru, Y
   Nagase, H
   Furukawa, Y
AF Noguchi, Rei
   Yamaguchi, Kiyoshi
   Ikenoue, Tsuneo
   Terakado, Yumi
   Ohta, Yasunori
   Yamashita, Naohide
   Kainuma, Osamu
   Yokoi, Sana
   Maru, Yoshiaki
   Nagase, Hiroki
   Furukawa, Yoichi
TI Genetic alterations in Japanese extrahepatic biliary tract cancer
SO ONCOLOGY LETTERS
LA English
DT Article
DE biliary tract cancer; extrahepatic bile duct carcinoma; gallbladder
   carcinoma; ampulla of Vater carcinoma; somatic mutation; next generation
   sequencing
ID K-RAS MUTATION; RENAL-CELL CARCINOMA; TUMOR-SUPPRESSOR; INTRAHEPATIC
   CHOLANGIOCARCINOMAS; GALLBLADDER CARCINOMA; COLORECTAL-CANCER; TARGETED
   THERAPY; SMAD4 MUTATIONS; UNITED-STATES; RISK-FACTORS
AB Biliary tract cancer (BTC) is one of the most devastating types of malignant neoplasms worldwide. However, the mechanisms underlying the development and progression of BTC remain unresolved. BTC includes extrahepatic bile duct carcinoma (EBDC), gallbladder carcinoma (GBC) and ampulla of Vater carcinoma (AVC), named according to the location of the tumor. Although genetic alterations of intrahepatic cholangiocarcinoma have been investigated, those of EBDC, GBC and AVC have not yet been fully understood. The present study analyzed somatic mutations of 50 cancer-associated genes in 27 Japanese BTC cells, including: 11 EBDC, 14 GBC and 2 AVC. Next-generation sequencing using an Ion AmpliSeq Cancer Panel identified a total of 44 somatic mutations across 14 cancer-associated genes. Among the 11 mutations, 42 were judged as pathological mutations. Frequent mutations were identified in tumor protein 53 (TP53) (14/27), SMAD family member 4 (SMAD4) (6/27), phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit a (PIK3CA) (6/27), and Kirsten rat sarcoma (KRAS) (6/27); no significant differences were identified between EBDC and GBC tissues. Notably, the frequency of the PIK3CA mutation was higher when compared with previous reports. This result may suggest that the activation of the PIK3CA-protein kinase B signaling pathway, in addition to the abrogation of p53, SMAD4 and RAS mitogen-activated protein kinase may have a crucial role in the carcinogenesis of Japanese BTC. These findings may be useful for the development of personalized therapies for BTC.
C1 [Noguchi, Rei; Yamaguchi, Kiyoshi; Ikenoue, Tsuneo; Terakado, Yumi; Furukawa, Yoichi] Univ Tokyo, Inst Med Sci, Div Clin Genome Res, Tokyo 1088639, Japan.
   [Ohta, Yasunori] Univ Tokyo, Inst Med Sci, Dept Pathol, Tokyo 1088639, Japan.
   [Yamashita, Naohide] Univ Tokyo, Inst Med Sci, Dept Adv Med Sci, Tokyo 1088639, Japan.
   [Kainuma, Osamu] Chiba Canc Ctr Hosp, Dept Gastroenterol Surg, Chiba 2608718, Japan.
   [Yokoi, Sana] Chiba Canc Ctr, Res Inst, Div Translat Genet, Chiba 2608718, Japan.
   [Maru, Yoshiaki; Nagase, Hiroki] Chiba Canc Ctr, Res Inst, Div Canc Genet, Chiba 2608718, Japan.
C3 University of Tokyo; University of Tokyo; University of Tokyo; Chiba
   Cancer Center; Chiba Cancer Center; Chiba Cancer Center
RP Furukawa, Y (corresponding author), Univ Tokyo, Inst Med Sci, Div Clin Genome Res, Minato Ku, 4-6-1 Shirokanedai, Tokyo 1088639, Japan.
EM furukawa@ims.u-tokyo.ac.jp
OI NOGUCHI, REI/0000-0003-1180-2394
FU Japan Society for the Promotion of Science [25280105]; Grants-in-Aid for
   Scientific Research [17K09369, 25280105] Funding Source: KAKEN
FX The authors thank Ms. Seira Hatakeyama, Mrs. Yuko Yamaguchi and Mrs.
   Nozomi Yusa for their excellent technical assistance. This study was
   supported by the Grant-in-Aid (grant no. 25280105) from the Japan
   Society for the Promotion of Science.
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NR 56
TC 14
Z9 16
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 JUL
PY 2017
VL 14
IS 1
BP 877
EP 884
DI 10.3892/ol.2017.6224
PN B
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FA7RY
UT WOS:000405645800051
PM 28693246
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Han, C
   Seebacher, NA
   Hornicek, FJ
   Kan, QC
   Duan, ZF
AF Han, Chao
   Seebacher, Nicole A.
   Hornicek, Francis J.
   Kan, Quancheng
   Duan, Zhenfeng
TI Regulation of microRNAs function by circular RNAs in human cancer
SO ONCOTARGET
LA English
DT Review
DE circRNA; miRNA; cancer; gene regulatory mechanisms; target therapy
ID SQUAMOUS-CELL CARCINOMA; COLORECTAL-CANCER; BREAST-CANCER; IN-SITU;
   EXPRESSION; REVEALS; BIOGENESIS; PROLIFERATION; INVASION; MIGRATION
AB Circular RNAs (circRNAs) are a newly validated class of endogenous non-coding RNA, generated from the ligation of exons, introns, or both, which arise via a diverse number of cellular mechanisms. Due to rapid advances in the development of combined high-throughput sequencing and bioinformatics analyzing tools, many circRNAs have recently been discovered, revealing an expansive number of ubiquitously expressed mammalian circRNAs. Interestingly, it has recently been confirmed that circRNAs bind to microRNAs (miRs), as miR "sponges", acting to suppress miR function. As miRs are known to alter the development and progression of cancer, circRNAs may offer a novel diagnostic and prognostic biomarker for cancer. Indeed, recent evidence has shown that circRNAs are associated with many human cancers. Herein, we review the molecular characteristics and biogenesis of circRNAs, with a focus on newly identified circRNAs that may play an important role in human cancer, through their regulation of miR expression.
C1 [Han, Chao; Kan, Quancheng; Duan, Zhenfeng] Zhengzhou Univ, Dept Pharm, Affiliated Hosp 1, Zhengzhou, Henan, Peoples R China.
   [Han, Chao; Seebacher, Nicole A.; Hornicek, Francis J.; Duan, Zhenfeng] Massachusetts Gen Hosp, Ctr Sarcoma & Connect Tissue Oncol, Sarcoma Biol Lab, Boston, MA 02114 USA.
   [Han, Chao; Seebacher, Nicole A.; Hornicek, Francis J.; Duan, Zhenfeng] Harvard Med Sch, Boston, MA 02115 USA.
C3 Zhengzhou University; Harvard University; Massachusetts General
   Hospital; Harvard University; Harvard Medical School
RP Kan, QC; Duan, ZF (corresponding author), Zhengzhou Univ, Dept Pharm, Affiliated Hosp 1, Zhengzhou, Henan, Peoples R China.; Duan, ZF (corresponding author), Massachusetts Gen Hosp, Ctr Sarcoma & Connect Tissue Oncol, Sarcoma Biol Lab, Boston, MA 02114 USA.; Duan, ZF (corresponding author), Harvard Med Sch, Boston, MA 02115 USA.
EM quanchengkan@yeah.net; zduan@mgh.harvard.edu
OI Hornicek, Francis/0000-0002-6916-8042; Seebacher,
   Nicole/0000-0002-8616-8407
FU Joint Research Fund devoted to clinical pharmacy and precision medicine;
   National Natural Science Foundation of China [81402266, 81372875];
   Gattegno fund; Wechsler fund; Henan Scholarship Council
FX This work was supported by a Joint Research Fund devoted to clinical
   pharmacy and precision medicine (Z.D. and Q.K.). Support has also been
   provided by the National Natural Science Foundation of China (No.:
   81402266 and 81372875), the Gattegno and Wechsler funds. Dr. Han is
   supported by a scholarship from the Henan Scholarship Council.
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NR 109
TC 44
Z9 52
U1 0
U2 21
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 8
PY 2017
VL 8
IS 38
BP 64622
EP 64637
DI 10.18632/oncotarget.19930
PG 16
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FG4XE
UT WOS:000410284800150
PM 28969099
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Sepulveda, AR
   Hamilton, SR
   Allegra, CJ
   Grody, W
   Cushman-Vokoun, AM
   Funkhouser, WK
   Kopetz, SE
   Lieu, C
   Lindor, NM
   Minsky, BD
   Monzon, FA
   Sargent, DJ
   Singh, VM
   Willis, J
   Clark, J
   Colasacco, C
   Rumble, RB
   Temple-Smolkin, R
   Ventura, CB
   Nowak, JA
AF Sepulveda, Antonia R.
   Hamilton, Stanley R.
   Allegra, Carmen J.
   Grody, Wayne
   Cushman-Vokoun, Allison M.
   Funkhouser, William K.
   Kopetz, Scott E.
   Lieu, Christopher
   Lindor, Noralane M.
   Minsky, Bruce D.
   Monzon, Federico A.
   Sargent, Daniel J.
   Singh, Veena M.
   Willis, Joseph
   Clark, Jennifer
   Colasacco, Carol
   Rumble, R. Bryan
   Temple-Smolkin, Robyn
   Ventura, Christina B.
   Nowak, Jan A.
TI Molecular Biomarkers for the Evaluation of Colorectal Cancer Guideline
   From the American Society for Clinical Pathology, College of American
   Pathologists, Association for Molecular Pathology, and American Society
   of Clinical Oncology
SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
ID RECEPTOR MONOCLONAL-ANTIBODIES; KRAS MUTATION DETECTION; ANTI-EGFR
   THERAPY; III COLON-CANCER; K-RAS MUTATIONS; MICROSATELLITE-INSTABILITY;
   PIK3CA MUTATION; ADJUVANT CHEMOTHERAPY; 1ST-LINE TREATMENT; PTEN
   EXPRESSION
AB Objectives.-To develop evidence-based guideline recommendations through a systematic review of the literature to establish standard molecular biomarker testing of colorectal cancer (CRC) tissues to guide epidermal growth factor receptor (EGFR) therapies and conventional chemotherapy regimens.
   Methods.-The American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology, and American Society of Clinical Oncology convened an expert panel to develop an evidence-based guideline to establish standard molecular biomarker testing and guide therapies for patients with CRC. A comprehensive literature search that included more than 4,000 articles was conducted.
   Results.-Twenty-one guideline statements were established.
   Conclusions.-Evidence supports mutational testing for EGFR signaling pathway genes, since they provide clinically actionable information as negative predictors of benefit to anti-EGFR monoclonal antibody therapies for targeted therapy of CRC. Mutations in several of the biomarkers have clear prognostic value. Laboratory approaches to operationalize CRC molecular testing are presented.
C1 [Sepulveda, Antonia R.] Columbia Univ, Dept Pathol & Cell Biol, New York, NY USA.
   [Hamilton, Stanley R.] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
   [Kopetz, Scott E.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal GI Med Oncol, Houston, TX 77030 USA.
   [Minsky, Bruce D.] Univ Texas MD Anderson Canc Ctr, Dept Radiat Oncol, Houston, TX 77030 USA.
   [Allegra, Carmen J.] Univ Florida, Med Ctr, Div Hematol & Oncol, Gainesville, FL USA.
   [Grody, Wayne] Univ Calif Los Angeles, Med Ctr, Dept Pathol & Lab Med, Los Angeles, CA 90024 USA.
   [Grody, Wayne] Univ Calif Los Angeles, Med Ctr, Dept Pediat, Los Angeles, CA 90024 USA.
   [Grody, Wayne] Univ Calif Los Angeles, Med Ctr, Dept Human Genet, Los Angeles, CA 90024 USA.
   [Cushman-Vokoun, Allison M.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
   [Funkhouser, William K.] Univ N Carolina, Dept Pathol & Lab Med, Sch Med, Chapel Hill, NC USA.
   [Lieu, Christopher] Univ Colorado, Denver Sch Med, Div Med Oncol, Denver, CO 80202 USA.
   [Lindor, Noralane M.] Mayo Clin, Dept Med Genet, Scottsdale, AZ USA.
   [Monzon, Federico A.] Castle Biosci, Friendswood, TX USA.
   [Sargent, Daniel J.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
   [Singh, Veena M.] Biocept, San Diego, CA USA.
   [Willis, Joseph] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA.
   [Clark, Jennifer] Amer Soc Clin Pathologists, ASCP Inst Sci Technol & Policy, Washington, DC USA.
   [Colasacco, Carol; Ventura, Christina B.] Coll Amer Pathologists, Lab & Pathol Qual Ctr, Northfield, IL USA.
   [Rumble, R. Bryan] Amer Soc Clin Oncol, Alexandria, VA USA.
   [Temple-Smolkin, Robyn] Assoc Mol Pathol, Bethesda, MD USA.
   [Nowak, Jan A.] Roswell Pk Canc Inst, Dept Pathol & Lab Med, Buffalo, NY 14263 USA.
C3 Columbia University; University of Texas System; UTMD Anderson Cancer
   Center; University of Texas System; UTMD Anderson Cancer Center;
   University of Texas System; UTMD Anderson Cancer Center; State
   University System of Florida; University of Florida; University of
   California System; University of California Los Angeles; University of
   California Los Angeles Medical Center; University of California System;
   University of California Los Angeles; University of California Los
   Angeles Medical Center; University of California System; University of
   California Los Angeles; University of California Los Angeles Medical
   Center; University of Nebraska System; University of Nebraska Medical
   Center; University of North Carolina; University of North Carolina
   Chapel Hill; University of North Carolina School of Medicine; University
   of Colorado System; University of Colorado Denver; University of
   Colorado Anschutz Medical Campus; Mayo Clinic; Mayo Clinic Phoenix; Mayo
   Clinic; University System of Ohio; Case Western Reserve University;
   College of American Pathologists; American Society of Clinical Oncology;
   Roswell Park Comprehensive Cancer Center
RP Sepulveda, AR (corresponding author), Columbia Univ, Med Ctr, Dept Pathol & Cell Biol, 630 W 168th St,VC 14 RM 212, New York, NY 10032 USA.
EM as4400@cumc.columbia.edu
RI Colasacco, Carol/AAA-2736-2022; Kopetz, Scott/AAC-1387-2019
OI Temple-Smolkin, Robyn/0000-0002-5728-5436; Monzon,
   Federico/0000-0002-6890-9793; Kopetz, Scott/0000-0001-9647-3416;
   Colasacco, Carol/0000-0001-7856-7531
FU ASCP; CAP; AMP; ASCO
FX The ASCP, CAP, AMP, and ASCO provided funding for the administration of
   the project; no industry funds were used in the development of the
   guideline. All panel members volunteered their time and were not
   compensated for their involvement, except for the contracted
   methodologist. Please see the Supplemental Digital Content (SDC) at
   www.archivesofpathology.org in the May 2017 table of contents for full
   details on the COI policy.
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NR 149
TC 48
Z9 49
U1 0
U2 7
PU COLL AMER PATHOLOGISTS
PI NORTHFIELD
PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA
SN 0003-9985
EI 1543-2165
J9 ARCH PATHOL LAB MED
JI Arch. Pathol. Lab. Med.
PD MAY
PY 2017
VL 141
IS 5
BP 625
EP 657
DI 10.5858/arpa.2016-0554-CP
PG 33
WC Medical Laboratory Technology; Medicine, Research & Experimental;
   Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology; Research & Experimental Medicine;
   Pathology
GA EW0IM
UT WOS:000402173100004
PM 28165284
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Khan, SA
   Sharma, R
AF Khan, Sameea Ahmed
   Sharma, Rajesh
TI Super Para-Magnetic Iron Oxide Nanoparticles (SPIONs) in the Treatment
   of Cancer: Challenges, Approaches, and its Pivotal Role in Pancreatic,
   Colon, and Prostate Cancer
SO CURRENT DRUG DELIVERY
LA English
DT Review
DE Nanoparticles; SPIONs; targeted therapy; tumor treatment; pancreatic
   cancer; colon cancer; and prostate cancer
ID RECEPTOR-MEDIATED ENDOCYTOSIS; TARGETED DRUG-DELIVERY;
   THERMAL-DECOMPOSITION; MEMBRANE ANTIGEN; IN-VIVO; SURFACE; GEMCITABINE;
   STRATEGIES; THERAPY; AGENTS
AB Super Para-magnetic Iron Oxide Nanoparticles (SPIONs) have been manifested for their broad spectrum of applications ranging from biomedical imaging to the treatment of many diseases. Many experiments are being conducted across the globe to especially investigate their potential in the field of targeted treatment for malignant tissues. However, challenges pertaining to the desired delivery of anticancer drugs in the body remain unresolved or unattended. The bare iron oxide nanoparticles are liable to form agglomerates or get easily oxidized in the air which can lead to loss of their magnetism and viability. Moreover, in several reactions, these magnetic nanoparticles leach into the solution/ suspension, making it kinetically unstable. The nanoparticles, further readily metabolize in the stomach pH or are phagocytosed by macrophages. In this article, we address these issues by shedding light on the impact of controlling parameters like size, synthesis method, and surface engineering. After studying the existing literature, it is noted that currently, these magnetically guided delivery systems are being rigorously tested in areas like pancreatic cancer, colon cancer, and prostate cancer, which will be discussed in this review. The fact that the major issue in the conventional treatment of these cancers is intrinsic and acquired drug resistance is a key issue. In this context, the potential of SPIONs as efficient nanotherapeutics is presented. The article provides a deeper insight into the research conducted on these focused areas in cancer. This review also discusses, in brief, the consolidation of artificial intelligence in cancer nanomedicine assuring a better treatment outcome in near future.
C1 [Khan, Sameea Ahmed; Sharma, Rajesh] Devi Ahilya Vishwavidyalaya, Sch Pharm, Takshashila Campus,Khandwa Rd Ring Road, Indore 452001, Madhya Pradesh, India.
C3 Devi Ahilya University
RP Sharma, R (corresponding author), Devi Ahilya Vishwavidyalaya, Sch Pharm, Takshashila Campus,Khandwa Rd Ring Road, Indore 452001, Madhya Pradesh, India.
EM rbsm73@yahoo.co.in
RI ; SHARMA, RAJESH/V-1698-2018
OI , Sameea Ahmed/0000-0002-2132-8844; SHARMA, RAJESH/0000-0003-4054-1840
FU School of Pharmacy
FX Authors are grateful to Head, School of Pharmacy, Devi Ahilya
   Vishwavidyalaya, Indore, for providing facilities for this work.
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NR 112
TC 3
Z9 3
U1 3
U2 17
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1567-2018
EI 1875-5704
J9 CURR DRUG DELIV
JI Curr. Drug Deliv.
PY 2023
VL 20
IS 6
BP 643
EP 655
DI 10.2174/1567201819666220509164611
PG 13
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA H9VE7
UT WOS:000999347700001
PM 35579147
DA 2025-01-04
ER

PT J
AU Li, Z
   She, TS
   Yang, H
   Su, T
   Shi, QX
   Tao, Z
   Feng, YR
   Yang, F
   Cheng, JQ
   Lu, XF
AF Li, Zhao
   She, Tianshan
   Yang, Hao
   Su, Tao
   Shi, Qiuxiao
   Tao, Ze
   Feng, Yanru
   Yang, Fen
   Cheng, Jingqiu
   Lu, Xiaofeng
TI A novel tumor-homing TRAIL variant eradicates tumor xenografts of
   refractory colorectal cancer cells in combination with tumor
   cell-targeted photodynamic therapy
SO DRUG DELIVERY
LA English
DT Article
DE Tumor necrosis factor-related apoptosis-inducing ligand; photodynamic
   therapy; cancer-targeted therapy; multidrug resistance; colorectal
   cancer
ID HIGH-AFFINITY; RESISTANCE; EXPRESSION; AFFIBODY; DELIVERY; DEATH
AB Multidrug resistance (MDR), which is common in colorectal cancer (CRC), induces high mortality in patients. Due to its robust and selective apoptosis induction in some CRC cells with MDR, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is attractive as a novel tool for CRC therapy. However, TRAIL is limited by its poor tumor-homing ability and inefficient apoptosis induction in CRC cells expressing low levels of death receptor (DR). Here, the tumor-homing RGR peptide (CRGRRST) was fused to TRAIL to produce RGR-TRAIL. Compared with TRAIL, RGR-TRAIL showed greater cell binding and cytotoxicity in CRC cells. In addition, RGR-TRAIL exerted significantly enhanced tumor uptake and growth suppression in mice bearing CRC tumor xenografts. Notably, RGR-TRAIL eradicated all tumor xenografts of DR-overexpressing COLO205 cells. However, TRAIL only showed mild tumor growth suppression under the same conditions, indicating that RGR fusion significantly increased the antitumor effect of TRAIL in DR-overexpressing CRC cells by improving tumor homing. Nevertheless, RGR fusion did not significantly enhance the antitumor effect of TRAIL in HT29 cells expressing low levels of DR. We found that DR expression in HT29 cells was enhanced by epidermal growth factor receptor (EGFR)-targeted photodynamic therapy (PDT). Moreover, both the in vitro and in vivo antitumor effects of RGR-TRAIL were significantly improved by combination with PDT. HT29 tumor xenografts (similar to 20%) were even eradicated by combination therapy. These results indicate that it is valuable to further evaluate the combination therapy of RGR-TRAIL and tumor-targeted PDT for clinical therapy of CRC with MDR.
C1 [Li, Zhao; She, Tianshan; Yang, Hao; Shi, Qiuxiao; Tao, Ze; Feng, Yanru; Yang, Fen; Cheng, Jingqiu; Lu, Xiaofeng] Sichuan Univ, West China Hosp, NHC Key Lab Transplant Engn & Immunol, Chengdu 610041, Peoples R China.
   [Yang, Hao; Tao, Ze; Cheng, Jingqiu; Lu, Xiaofeng] Sichuan Univ, West China Hosp, Sichuan Prov Engn Lab Pathol Clin Applicat, Chengdu, Peoples R China.
   [Yang, Hao; Tao, Ze; Cheng, Jingqiu; Lu, Xiaofeng] Sichuan Univ, West China Hosp, Frontiers Sci Ctr Dis Related Mol Network, Chengdu, Peoples R China.
   [Su, Tao; Cheng, Jingqiu] Sichuan Univ, West China Hosp, Inst Syst Genet, Lab Clin Prote & Metabol, Chengdu, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University; Sichuan
   University
RP Lu, XF (corresponding author), Sichuan Univ, West China Hosp, NHC Key Lab Transplant Engn & Immunol, Chengdu 610041, Peoples R China.
EM xiaofenglu@scu.edu.cn
RI zhang, chenhong/HCH-9822-2022; Lu, Xiaofeng/ABD-9075-2021; Feng,
   YanRu/AAA-2183-2020; li, zhao/IYS-8424-2023
OI Tao, Ze/0000-0002-0726-192X; li, zhao/0000-0003-0302-1635
FU National Natural Science Fund of China [82073362, 82173727]; 1.3.5
   Project for Disciplines of Excellence, West China Hospital, Sichuan
   University [ZYGD18014]
FX This study was funded by the National Natural Science Fund of China
   (82073362 and 82173727), and the "1.3.5 Project for Disciplines of
   Excellence, West China Hospital, Sichuan University" (ZYGD18014).
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NR 36
TC 8
Z9 8
U1 1
U2 31
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1071-7544
EI 1521-0464
J9 DRUG DELIV
JI Drug Deliv.
PD DEC 31
PY 2022
VL 29
IS 1
BP 1698
EP 1711
DI 10.1080/10717544.2022.2079766
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 1Q6EG
UT WOS:000802777400001
PM 35635308
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wang, LC
   Yu, M
   Yang, H
AF Wang, Liucan
   Yu, Min
   Yang, Hua
TI Recent Progress in the Diagnosis and Precise Nanocarrier-Mediated
   Therapy of Inflammatory Bowel Disease
SO JOURNAL OF INFLAMMATION RESEARCH
LA English
DT Article
DE inflammatory bowel disease; gastrointestinal tract microenvironment;
   drug delivery system; precise therapy; diagnose
ID MESOPOROUS SILICA NANOPARTICLES; DRUG-DELIVERY SYSTEM;
   ULCERATIVE-COLITIS; ORAL DELIVERY; COLON-CANCER; IN-VIVO; TARGETED
   NANOPARTICLES; MULTIDRUG TRANSPORTER; LIPID NANOPARTICLES; GOLD
   NANOPARTICLES
AB The effective colon drug delivery remains to be an international frontier research in inflammatory bowel disease (IBD) therapy. The exploration and research of nanocarrier-based nanomedicine with great potential brings new opportunities for IBD therapy and diagnoses. Functional nanocarriers with varying morphology and characteristics can not only effectively avoid the destruction of the complex gastrointestinal (GI) tract microenvironment but also endow drugs with target therapy and improved bioavailability, thus elevating therapeutic efficacy. In this review, we illustrated several challenges in IBD therapy, then emphasis on some latest research progress of nanoparticles based therapy of oral administration, rectal administration and parenteral administration, as well as IBD diagnoses. Finally, we described the future perspective of nanocarriers in the treatment and diagnoses of IBD.
C1 [Wang, Liucan; Yu, Min; Yang, Hua] Army Med Univ, Xinqiao Hosp, Dept Gen Surg, Chongqing, Peoples R China.
C3 Army Medical University
RP Yu, M; Yang, H (corresponding author), Army Med Univ, Xinqiao Hosp, Dept Gen Surg, Chongqing, Peoples R China.
EM yumimianbao@163.com; huayang@tmmu.edu.cn
OI Yu, Min/0000-0002-8845-8977
FU National Natural Science Foundation of China [NSFC 81873551, NSFC
   81970468]; Innovative Research Team of Ministry of Education of China
   [IRT_17R16]
FX This research was supported by grants from the National Natural Science
   Foundation of China (NSFC 81873551 to H.Y. and NSFC 81970468 to M.Y.),
   and Innovative Research Team of Ministry of Education of China
   (IRT_17R16 to H.Y.).
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NR 130
TC 13
Z9 13
U1 4
U2 73
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
EI 1178-7031
J9 J INFLAMM RES
JI J. Inflamm. Res.
PY 2021
VL 14
BP 1701
EP 1716
DI 10.2147/JIR.S304101
PG 16
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA RY3CB
UT WOS:000647792100001
PM 33953597
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zekri, ARN
   Youssef, ASE
   Lotfy, MM
   Gabr, R
   Ahmed, OS
   Nassar, A
   Hussein, N
   Omran, D
   Medhat, E
   Eid, S
   Hussein, MM
   Ismail, MY
   Alenzi, FQ
   Bahnassy, AA
AF Zekri, Abdel-Rahman N.
   Youssef, Amira Salah El-Din
   Lotfy, Mai M.
   Gabr, Reham
   Ahmed, Ola S.
   Nassar, Auhood
   Hussein, Nehal
   Omran, Dalia
   Medhat, Eman
   Eid, Salam
   Hussein, Marwa Mahmoud
   Ismail, Maha Yahia
   Alenzi, Faris Q.
   Bahnassy, Abeer A.
TI Circulating Serum miRNAs as Diagnostic Markers for Colorectal Cancer
SO PLOS ONE
LA English
DT Article
ID MICRORNAS; EXPRESSION; TUMOR; GENE; METASTASIS; STATISTICS; BIOMARKERS;
   CLUSTER; FAMILY
AB Aim
   The study was designed to assess the possibility of using circulating miRNAs (serum miR-NAs) as diagnostic biomarkers in colorectal cancer (CRC) and to identify their possibility as candidates for targeted therapy.
   Methods
   The study involved two sample sets: 1-a training set which included 90 patients with colorectal related disease (30 with CRC, 18 with inflammatory bowel disease (IBD), 18 with colonic polyps (CP) and 24 with different colonic symptoms but without any colonoscopic abnormality who were enrolled as control group) and 2-a validation set which included 100 CRC patients. Serum miRNAs were extracted from all subjects to assess the expression profiles for the following miRNAs (miR-17, miR-18a, miR-19a, miR-19b, miR-20a, miR-21, miR-146a, miR-223, miR-24, miR-454, miR-183, miR-135a, miR-135b and miR-92a) using the custom miScript miRNA PCR-based sybergreen array. The area under the receiver operating characteristic curve (AUC) was used to evaluate the diagnostic performance of the studied miRNAs for colorectal cancer diagnosis.
   Results
   Data analysis of miRNA from the training set showed that; compared to control group, only miR-19b was significantly up-regulated in patients with IBD group (fold change = 5.24, p = 0.016), whereas in patients with colonic polyps, miR-18a was significantly up-regulated (fold change = 3.49, p-value = 0.018). On the other hand, miR-17, miR-19a, miR-20a and miR-223 were significantly up-regulated (fold change = 2.35, 3.07, 2.38 and 10.35; respectively and p-value = 0.02, 0.015, 0.017 and 0.016; respectively in CRC patients. However, the validation set showed that only miR-223 was significantly up-regulated in CRC patients (fold change = 4.06, p-value = 0.04).
   Conclusion
   Aberrant miRNA expressions are highly involved in the cascade of colorectal carcinogenesis. We have found that (miR-17, miR-19a, miR-20a and miR-223) could be used as diagnostic biomarkers for CRC. On the other hand, miR-19b and miR-18a could be used as diagnostic biomarkers for CP and IBD respectively.
C1 [Zekri, Abdel-Rahman N.; Youssef, Amira Salah El-Din; Lotfy, Mai M.; Gabr, Reham; Ahmed, Ola S.; Nassar, Auhood; Hussein, Nehal] Cairo Univ, Natl Canc Inst, Dept Canc Biol, Mol Virol & Immunol Unit, Cairo, Egypt.
   [Omran, Dalia; Medhat, Eman] Cairo Univ, Kasr El Aini Hosp, Dept Trop Med, Fac Med, Cairo, Egypt.
   [Eid, Salam; Hussein, Marwa Mahmoud; Ismail, Maha Yahia] Cairo Univ, Natl Canc Inst, Dept Med Oncol, Cairo, Egypt.
   [Alenzi, Faris Q.] King Saud Univ, Coll Appl Med Sci, Dept Clin Lab Sci, Alkharaj, Saudi Arabia.
   [Bahnassy, Abeer A.] Cairo Univ, Natl Canc Inst, Dept Pathol, Cairo, Egypt.
C3 Egyptian Knowledge Bank (EKB); Cairo University; National Cancer
   Institute - Egypt; Egyptian Knowledge Bank (EKB); Cairo University;
   Egyptian Knowledge Bank (EKB); National Cancer Institute - Egypt; Cairo
   University; King Saud University; Egyptian Knowledge Bank (EKB);
   National Cancer Institute - Egypt; Cairo University
RP Zekri, ARN (corresponding author), Cairo Univ, Natl Canc Inst, Dept Canc Biol, Mol Virol & Immunol Unit, Cairo, Egypt.
EM ncizekri@yahoo.com
RI Zekri, Abdel-Rahman/A-3768-2008; Alenzi, Faris/IAO-8150-2023; Hussein,
   Marwa/I-4842-2019; Lotfy, Mai/U-3152-2019; Medhat, M.E./AAB-2042-2019
OI Omran, Dalia/0000-0002-5513-6955; Youssef, Amira/0000-0003-3091-691X;
   Lotfy, Mai/0000-0001-8282-8773; moustafa, medhat/0000-0002-7050-7910;
   Zekri, Abdel-Rahman/0000-0003-3939-0416; Eid Salem,
   Salem/0000-0002-6204-5031; Hussein, Marwa/0000-0002-7619-7087; Nassar,
   Auhood/0000-0002-5704-9281; Gabr, Reham/0000-0002-5303-6360
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NR 32
TC 65
Z9 67
U1 0
U2 16
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 MAY 2
PY 2016
VL 11
IS 5
AR e0154130
DI 10.1371/journal.pone.0154130
PG 14
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA DL5KB
UT WOS:000375674800014
PM 27135244
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yan, J
   He, WX
   Li, X
   You, WM
   Liu, XJ
   Lin, SM
   Chen, JH
   Zhao, YY
   Zhang, YM
   Ji, FP
AF Yan, Jin
   He, Wangxiao
   Li, Xiao
   You, Weiming
   Liu, Xiaojing
   Lin, Shumei
   Chen, Jianghao
   Zhao, Yunyu
   Zhang, Yanmin
   Ji, Fanpu
TI Carnosic acid-induced co-self-assembly of metal-peptide complexes into a
   nanocluster-based framework with tumor-specific accumulation for
   augmented immunotherapy
SO CHEMICAL ENGINEERING JOURNAL
LA English
DT Article
DE Co-self-assembly; Supermolecule; Peptide; Cancer immunotherapy;
   Anti-cancer therapy
ID DYNAMIC COMBINATORIAL CHEMISTRY; BIOLOGICAL BARRIERS;
   ACQUIRED-RESISTANCE; IN-VIVO; NANOPARTICLES; BLOCKADE; HYPOXIA
AB Tumor immunotherapy by PD-1/PD-L1 blockade (PPB) has emerged as a standard of care treatment and can bring long-lasting clinical benefits, yet less than one-third of patients respond to it. While combination PPB therapies have shown improved outcomes, more optimal multimodality therapies, particularly those combinations with molecularly targeted therapies, are still required to improve the therapeutic benefit of PPB. Herein, we describe a design of PPB sensitizer with supramolecular nanostructure constructed through a dynamic combinatorial chemistry (DCC)-based co-self-assembled strategy. Upon the stimulation of a ?-catenin inhibitor termed carnosic acid (CA), two competing molecular blocks three-dimensionally and orderly co-self-assembled into a nanocluster-based framework (CA-NBF) under thermo-dynamic control. With properties of tumor-specific accumulation and glutathione-triggered release, CA-NBF potently suppressed the Wnt/?-catenin signaling cascade in vitro and in vivo, while keeping a favorable safety feature. Moreover, CA-NBF potently restored the intratumoral infiltration of cytotoxic T lymphocyte cells and consequently promoted tumor response to Anti-PDL1 antibody in B16F10 melanoma model and Anti-PD1 antibody in MC38 model of colon cancer. Given these encouraging results, this work may provide a new option for promoting the response of PPB therapy, and the DCC-based co-self-assembled strategy may be a promising tool to develop a class of supramolecular nanomedicines for the molecular targeted therapy of diseases including cancer.
C1 [Yan, Jin; You, Weiming; Ji, Fanpu] Xi An Jiao Tong Univ, Affiliated Hosp 2, Natl & Local Joint Engn Res Ctr Biodiag & Biother, Xian 710004, Peoples R China.
   [Yan, Jin; You, Weiming] Western China Sci & Technol Innovat Port, Dept Tumor & Immunol Precis, Med Inst, Xian 710004, Peoples R China.
   [He, Wangxiao] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Talent Highland, Xian 710061, Peoples R China.
   [Li, Xiao] Fourth Mil Med Univ, Xijing Hosp, Dept Hepatobiliary Surg, Xian 710032, Peoples R China.
   [Liu, Xiaojing; Lin, Shumei] Xi An Jiao Tong Univ, Affiliated Hosp 1, Infect Dept, Xian 710061, Peoples R China.
   [Chen, Jianghao] Xi An Jiao Tong Univ, Sch Med, Afliated Hosp 1, Dept Stomatol, Xian, Peoples R China.
   [Zhao, Yunyu; Ji, Fanpu] Xi An Jiao Tong Univ, Affiliated Hosp 2, Dept Infect Dis, Xian 710004, Peoples R China.
   [Zhang, Yanmin] Xi An Jiao Tong Univ, Hlth Sci Ctr, Sch Pharm, Xian 710061, Peoples R China.
   [Ji, Fanpu] Xi An Jiao Tong Univ, Minist Educ China, Key Lab Environm & Genes Related Dis, Xian 710061, Peoples R China.
C3 Xi'an Jiaotong University; Xi'an Jiaotong University; Air Force Military
   Medical University; Xi'an Jiaotong University; Xi'an Jiaotong
   University; Xi'an Jiaotong University; Xi'an Jiaotong University; Xi'an
   Jiaotong University
RP Yan, J; Ji, FP (corresponding author), Xi An Jiao Tong Univ, Affiliated Hosp 2, Natl & Local Joint Engn Res Ctr Biodiag & Biother, Xian 710004, Peoples R China.; He, WX (corresponding author), Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Talent Highland, Xian 710061, Peoples R China.; Zhang, YM (corresponding author), Xi An Jiao Tong Univ, Hlth Sci Ctr, Sch Pharm, Xian 710061, Peoples R China.
EM yanjin19920602@xjtu.edu.cn; hewangxiao5366@xjtu.edu.cn;
   zhang2008@xjtu.edu.cn; infection@xjtu.edu.cn
RI liu, feng/KCL-0778-2024; He, Wangxiao/F-3296-2019
OI Zhang, Yanmin/0000-0001-7307-9408; Ji, Fanpu/0000-0002-1463-8035
FU "Young Talent Support Plan" of Xi'an Jiaotong University; Thousand
   Talents Plan of Shaanxi Province; Postdoctoral innovation talent support
   program [BX20190278]; Natural Science Basic Research Plan in Shaanxi
   Province of China [2017JM8083, 2020JQ-092]; Fundamental Research Funds
   for the Central Universities [xjh012020038, xxj022019031, xzy032020040];
   National Natural Science Foundation of China [22007076]; National Major
   Scientific and Technological Projects [2017ZX10201201]
FX This work was supported by "The Young Talent Support Plan" of Xi'an
   Jiaotong University (For W. He), Thousand Talents Plan of Shaanxi
   Province (For W. He), Postdoctoral innovation talent support program
   (No. BX20190278), The Project Supported by Natural Science Basic
   Research Plan in Shaanxi Province of China (No. 2017JM8083 and No.
   2020JQ-092), the Fundamental Research Funds for the Central Universities
   (No. xjh012020038, No. xxj022019031 and No. xzy032020040), the National
   Natural Science Foundation of China (No. 22007076) and Project supported
   by the National Major Scientific and Technological Projects (No.
   2017ZX10201201). We thank Instrument Analysis Center of Xi'an Jiaotong
   University for their assistance with TEM, HRTEM, FT-IR, UV-Vis and DLS
   analysis. We also appreciate the help of RNA-seq analysis from
   BioNovoGene (Suzhou) Co., Ltd.
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NR 45
TC 28
Z9 28
U1 8
U2 119
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 1385-8947
EI 1873-3212
J9 CHEM ENG J
JI Chem. Eng. J.
PD JUL 15
PY 2021
VL 416
AR 129141
DI 10.1016/j.cej.2021.129141
EA FEB 2021
PG 11
WC Engineering, Environmental; Engineering, Chemical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering
GA RY1NH
UT WOS:000647683000002
DA 2025-01-04
ER

PT J
AU Zou, T
   Liu, JY
   She, L
   Chen, J
   Zhu, T
   Yin, JY
   Li, X
   Li, XP
   Zhou, HH
   Liu, ZQ
AF Zou, Ting
   Liu, Junyan
   She, Li
   Chen, Juan
   Zhu, Tao
   Yin, Jiye
   Li, Xi
   Li, Xiangping
   Zhou, Honghao
   Liu, Zhaoqian
TI A perspective profile of ADCY1 in cAMP signaling with drug-resistance in
   lung cancer
SO JOURNAL OF CANCER
LA English
DT Review
DE ADCY1; cAMP; Lung cancer; Drug resistance; Signaling pathway
ID PLATINUM-BASED CHEMOTHERAPY; DNA-REPAIR PATHWAYS; PROTEIN-KINASE;
   PROTEASOMAL DEGRADATION; INCREASED EXPRESSION; DOWN-REGULATION;
   UP-REGULATION; CELLS; CISPLATIN; POLYMORPHISMS
AB Adenylate cyclase 1 (ADCY1 or AC1) is a member of ADCY superfamily and was primarily found to be expressed in the brain. ADCY1 is responsible for catalyzing ATP to cyclic AMP (cAMP). As a secondary messenger, cAMP can regulate plenty of cellular activities. cAMP can perform its regulation in cellular transport through the binding to cAMP dependent protein kinases (PKAs), cAMP-activated guanine exchange factors (EPACs) and cyclic nucleotide-gated channels functioning in transduction of sensory signals (CNGs). Lung cancer is one of the leading factors of cancer-related death worldwide. Platinum-based chemotherapy is the first-line treatment for advanced lung cancer patients. In addition, surgical treatment, radiation treatment, and molecular targeted therapy are also therapeutic options for lung cancer patients in clinical settings. However, drug resistance and toxicity are the major obstacles that affect chemotherapy outcome and prognosis of lung cancer patients. And the therapeutic efficiency and adverse effects are varying with each individual. In recent years, investigations based on genetic sequencing have revealed the emerging role of ADCY1 mutations in affecting drug efficiency in various cancers such as lung cancer, esophageal cancer and colorectal cancer. The potential function of ADCY1 in chemotherapy resistance is of great importance to be noticed and investigated.
C1 [Zou, Ting] Cent South Univ, Xiangya Hosp, Natl Inst Drug Clin Trial, Changsha, Hunan, Peoples R China.
   [Zou, Ting; Zhu, Tao; Yin, Jiye; Li, Xi; Li, Xiangping; Zhou, Honghao; Liu, Zhaoqian] Cent South Univ, Xiangya Hosp, Dept Clin Pharmacol, Changsha 410008, Hunan, Peoples R China.
   [Zou, Ting; Liu, Zhaoqian] Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha, Hunan, Peoples R China.
   [Liu, Junyan] Univ South China, Dept Orthopaed, Affiliated Hosp 1, Hengyang, Hunan, Peoples R China.
   [She, Li] Cent South Univ, Xiangya Hosp, Dept Otolaryngol Head & Neck Surg, Changsha, Hunan, Peoples R China.
   [She, Li] Otolaryngol Major Dis Res Key Lab Hunan Prov, Changsha, Hunan, Peoples R China.
   [Chen, Juan] Cent South Univ, Xiangya Hosp, Dept Pharm, Changsha, Hunan, Peoples R China.
C3 Central South University; Central South University; Central South
   University; University of South China; Central South University; Central
   South University
RP Liu, ZQ (corresponding author), Cent South Univ, Xiangya Hosp, Dept Clin Pharmacol, Changsha 410008, Hunan, Peoples R China.; Liu, ZQ (corresponding author), Cent South Univ, Inst Clin Pharmacol, Changsha, Hunan, Peoples R China.
EM zgliu@mail.csu.edu.cn
RI Zhu, Tao/JEF-1129-2023; liu, zhaoqian/A-5810-2013; Zhou,
   Honghao/JWO-4641-2024; Yin, Ji-Ye/AAE-6794-2020; liu,
   junyan/HGV-1505-2022
FU National High-tech R&D Program of China (863 Program) [2012AA02A517];
   National Natural Science Foundation of China [81373490, 81573508]; Hunan
   Provincial Science and Technology Plan of China [2015TP1043]; Hunan
   Provincial Natural Science Foundation of China [2019JJ50946]; Youth
   Science Foundation of Xiangya Hospital, Central South University
   [2018Q014]
FX This work was supported by the National High-tech R&D Program of China
   (863 Program) (2012AA02A517), National Natural Science Foundation of
   China (81373490, 81573508), Hunan Provincial Science and Technology Plan
   of China (2015TP1043), Hunan Provincial Natural Science Foundation of
   China (2019JJ50946), and Youth Science Foundation of Xiangya Hospital,
   Central South University (2018Q014).
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NR 88
TC 32
Z9 36
U1 0
U2 15
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 27
BP 6848
EP 6857
DI 10.7150/jca.36614
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KK3XM
UT WOS:000512679100009
PM 31839819
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Poloznikov, A
   Nikulin, S
   Bolotina, L
   Kachmazov, A
   Raigorodskaya, M
   Kudryavtseva, A
   Bakhtogarimov, I
   Rodin, S
   Gaisina, I
   Topchiy, M
   Asachenko, A
   Novosad, V
   Tonevitsky, A
   Alekseev, B
AF Poloznikov, Andrey
   Nikulin, Sergey
   Bolotina, Larisa
   Kachmazov, Andrei
   Raigorodskaya, Maria
   Kudryavtseva, Anna
   Bakhtogarimov, Ildar
   Rodin, Sergey
   Gaisina, Irina
   Topchiy, Maxim
   Asachenko, Andrey
   Novosad, Victor
   Tonevitsky, Alexander
   Alekseev, Boris
TI 9-ING-41, a Small Molecule Inhibitor of GSK-3β, Potentiates the Effects
   of Chemotherapy on Colorectal Cancer Cells
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE colorectal cancer; KRAS; tumor organoids; GSK-3; 9-ING-41; cell cycle
ID PANCREATIC-CANCER; KINASE-ACTIVITY; RAS MUTATIONS; KRAS; GENE; SURVIVAL;
   EXPRESSION; STK33; PROMOTES; PATHWAY
AB Colorectal cancer (CRC) is one of the most common and lethal types of cancer. Although researchers have made significant efforts to study the mechanisms underlying CRC drug resistance, our knowledge of this disease is still limited, and novel therapies are in high demand. It is urgent to find new targeted therapy considering limited chemotherapy options. KRAS mutations are the most frequent molecular alterations in CRC. However, there are no approved K-Ras targeted therapies for these tumors yet. GSK-3 beta is demonstrated to be a critically important kinase for the survival and proliferation of K-Ras-dependent pancreatic cancer cells. In this study, we tested combinations of standard-of-care therapy and 9-ING-41, a small molecule inhibitor of GSK-3 beta, in CRC cell lines and patient-derived tumor organoid models of CRC. We demonstrate that 9-ING-41 inhibits the growth of CRC cells via a distinct from chemotherapy mechanism of action. Although molecular biomarkers of 9-ING-41 efficacy are yet to be identified, the addition of 9-ING-41 to the standard-of-care drugs 5-FU and oxaliplatin could significantly enhance growth inhibition in certain CRC cells. The results of the transcriptomic analysis support our findings of cell cycle arrest and DNA repair deficiency in 9-ING-41-treated CRC cells. Notably, we find substantial similarity in the changes of the transcriptomic profile after inhibition of GSK-3 beta and suppression of STK33, another critically important kinase for K-Ras-dependent cells, which could be an interesting point for future research. Overall, the results of this study provide a rationale for the further investigation of GSK-3 inhibitors in combination with standard-of-care treatment of CRC.
C1 [Poloznikov, Andrey; Nikulin, Sergey; Tonevitsky, Alexander] Fac Biol & Biotechnol, Higher Sch Econ, Moscow, Russia.
   [Poloznikov, Andrey; Nikulin, Sergey; Bolotina, Larisa; Kachmazov, Andrei; Alekseev, Boris] Minist Hlth Russian Federat, P Hertsen Moscow Oncol Res Inst, Branch Natl Med Res Radiol Ctr, Moscow, Russia.
   [Nikulin, Sergey] Far Eastern Fed Univ, Sch Biomed, Vladivostok, Russia.
   [Raigorodskaya, Maria; Tonevitsky, Alexander] Sci Res Ctr Bioclinicum, Moscow, Russia.
   [Kudryavtseva, Anna; Bakhtogarimov, Ildar] Russian Acad Sci, Engelhardt Inst Mol Biol, Moscow, Russia.
   [Rodin, Sergey] Uppsala Univ, Dept Surg Sci, Uppsala, Sweden.
   [Gaisina, Irina] Univ Illinois, Coll Pharm, Dept Pharmaceut Sci, Chicago, IL USA.
   [Topchiy, Maxim; Asachenko, Andrey] Russian Acad Sci, AV Topchiev Inst Petrochem Synth, Moscow, Russia.
   [Novosad, Victor; Tonevitsky, Alexander] RAS, Lab Microfluid Technol Biomed, Shemyakin Ovchinnikov Inst Bioorgan Chem, Moscow, Russia.
C3 HSE University (National Research University Higher School of
   Economics); Ministry of Health of the Russian Federation; Far Eastern
   Federal University; Russian Academy of Sciences; Engelhardt Institute of
   Molecular Biology, RAS; Uppsala University; University of Illinois
   System; University of Illinois Chicago; University of Illinois Chicago
   Hospital; Russian Academy of Sciences; Topchiev Institute of
   Petrochemical Synthesis RAS; 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 Poloznikov, A (corresponding author), Fac Biol & Biotechnol, Higher Sch Econ, Moscow, Russia.; Poloznikov, A (corresponding author), Minist Hlth Russian Federat, P Hertsen Moscow Oncol Res Inst, Branch Natl Med Res Radiol Ctr, Moscow, Russia.
EM apoloznikov@hse.ru
RI Tonevitsky, Alexander/R-5596-2019; Bolotina, Larisa/U-5441-2019;
   Novosad, Victor/AAC-3105-2022; Kudryavtseva, Anna/C-9032-2014;
   Asachenko, Andrey/AAC-7862-2022; Gaisina, Irina/AAR-9546-2020; Topchiy,
   Maxim/J-9911-2019; Nikulin, Sergey/T-3068-2019; Alekseev,
   Boris/O-1008-2017
OI Rodin, Sergey/0000-0002-6954-1986; Kachmazov,
   Andrei/0000-0001-5530-3234; Asachenko, Andrey/0000-0001-8638-9261;
   Topchiy, Maxim/0000-0002-6604-7034; Nikulin, Sergey/0000-0002-7900-5810;
   , Maria/0000-0003-0527-7773; Alekseev, Boris/0000-0002-3398-4128;
   Bakhtogarimov, Ildar/0000-0003-0937-313X
FU Russian Science Foundation [19-15-00397]; HSE University Basic Research
   Program; Russian Science Foundation [19-15-00397] Funding Source:
   Russian Science Foundation
FX This work was financially supported by the Russian Science Foundation
   (Project No. 19-15-00397) and in part (bioinformatic analysis) by HSE
   University Basic Research Program.
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NR 102
TC 5
Z9 6
U1 1
U2 8
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 DEC 9
PY 2021
VL 12
AR 777114
DI 10.3389/fphar.2021.777114
PG 18
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA YA9DR
UT WOS:000738625600001
PM 34955846
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ba, L
   Wang, QR
   Wang, HH
   Zhu, LS
   Zhang, T
   Ren, JH
   Lin, ZY
AF Ba, Li
   Wang, Qingrui
   Wang, Haihong
   Zhu, Lisheng
   Zhang, Tao
   Ren, Jinghua
   Lin, Zhenyu
TI Survival analysis and prognostic factors of palliative radiotherapy in
   patients with metastatic colorectal cancer: a propensity score analysis
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Article
DE Metastatic colorectal cancer (mCRC); palliative radiotherapy; propensity
   score matching (PSM); survival analysis
ID LIVER METASTASES; RANDOMIZED-TRIAL; LOCAL RECURRENCE; LUNG METASTASES;
   RESECTION; FLUOROURACIL; LEUCOVORIN; ABLATION; TRENDS
AB Background: Radiation therapy (RT) is known to have beneficial effects on the palliative treatment of patients with advanced cancer. However, valid data on this treatment method are limited, especially for patients with metastatic colorectal cancer (mCRC). This study aimed to identify prognostic factors and investigate the outcomes of mCRC patients who received palliative RT. Methods: A total of 488 mCRC patients who underwent systemic therapy with or without palliative RT between 2014 and 2019 were included in the study. Of the 488 patients, 155 received systemic treatment combined with palliative RT (RT group), while 333 were only administered systemic treatment (non-RT group). Propensity score matching (PSM) was conducted to eliminate possible bias, and overall survival (OS) was calculated using the Kaplan-Meier (KM) method. A log-rank test was used to compare the survival outcomes of each group, and a multivariate analysis was conducted using a Cox proportional hazards model. Results: The RT group had a higher OS than that of the non-RT group (P=0.001). After PSM, the median OS of the RT group was 50.8 months, and for the non-RT group it was 32.2 months (P=0.003). Subgroup analysis revealed that RT had a better effect on the OS of patients who had synchronous metastasis, or who didn't receive targeted therapy or local treatment (including surgery, ablation, and intervention). Multivariate analysis of the whole cohort showed that palliative RT was associated with improved OS. Moreover, multivariate analysis of the RT group showed that systemic therapy before RT, and the site of RT was in the liver and lung, were independent prognostic factors affecting survival time. Conclusions: We demonstrated that systemic treatment followed by palliative RT led to a better OS for mCRC patients. This combination method can therefore be seen as a suitable treatment approach for patients with mCRC.
C1 [Ba, Li] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Ultrasound, Wuhan, Peoples R China.
   [Wang, Qingrui] Jianghan Univ, Affiliated Hosp, Hosp Wuhan 6, Dept Oncol, Wuhan, Peoples R China.
   [Wang, Haihong; Zhu, Lisheng; Zhang, Tao; Ren, Jinghua; Lin, Zhenyu] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Canc Ctr, Wuhan 430022, Peoples R China.
C3 Huazhong University of Science & Technology; Jianghan University;
   Huazhong University of Science & Technology
RP Lin, ZY (corresponding author), Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Canc Ctr, Wuhan 430022, Peoples R China.
EM whxhlzy@hust.edu.cn
RI Ren, Jinghua/IST-4349-2023
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NR 32
TC 2
Z9 4
U1 0
U2 1
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD OCT
PY 2021
VL 12
IS 5
BP 2211
EP 2222
DI 10.21037/jgo-21-540
PG 12
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA WR6KF
UT WOS:000714606000025
PM 34790386
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Qiu, GQ
   Xie, X
   Zhao, B
   Xu, LZ
   Chen, YQ
AF Qiu, G. Q.
   Xie, X.
   Zhao, B.
   Xu, L. Z.
   Chen, Y. Q.
TI Fusion protein tTF-EG3287 induces occlusion of tumor vessels and impairs
   tumor growth in human colon cancer
SO NEOPLASMA
LA English
DT Article
DE colon cancer; tTF-EG3287; targeted therapy; vascular thrombosis;
   xenografts
ID PANCREATIC DUCTAL ADENOCARCINOMA; TRUNCATED TISSUE FACTOR; NEUROPILIN-1;
   ASSOCIATION; INHIBITION; RESISTANCE; INDUCTION; TTF
AB The problems including narrow indications, low drug loading, and difficulty in intervention severely affect the clinical efficacy of anti-tumor embolization. Here, we designed a novel tTF-EG3287 protein consisting of the truncated tissue factor (tTF) fused with the bicyclic polypeptide which was encoded by exons 7 and 8 for accurate localization in the tumor vascular endothelial cells (EG3287). This study aims to explore its anti-cancer effect. Gene sequencing was used to verify the fusion gene and SDS-PAGE gel to confirm the optimal induction time and concentration of tTF-EG3287. Nickel affinity chromatography column was used to purify the fusion protein. Confocal microscopy was used to assess the target activity of tTF-EG3287 on colon cancer cells in vitro. Thrombelastography assay was used to identify the pro-coagulant activity of tTF-EG3287. In in vivo experiments, the specific localization of tTF-EG3287 in tumor tissues and the effect of tTF-EG3287 on tumor thrombosis were further detected by in vivo imaging and HE staining, respectively. The tTF-EG3287 fusion protein was efficiently purified by nickel-affinity chromatography column. Moreover, tTF-EG3287 fusion protein showed strong coagulation activity and specific binding ability to the cell surface of colon cancer. In vivo, tTF-EG3287 stably and persistently accumulated in tumor tissues, and specifically induced mixed thrombus formation in tumor vessels, and then impaired tumor growth (tumor inhibition rate-79.2%, p<0.01). Our data prove that the fusion protein tTF-EG3287 could be used as a novel and promising anti-cancer strategy and has great potential value for clinical applications.
C1 [Qiu, G. Q.; Xie, X.; Xu, L. Z.; Chen, Y. Q.] Xiamen Univ, Dept Oncol, Chenggong Hosp, Xiamen 361000, Fujian, Peoples R China.
   [Zhao, B.] Xiamen Univ, Med Coll, Xiamen 361002, Fujian, Peoples R China.
C3 Xiamen University; Xiamen University
RP Chen, YQ (corresponding author), Xiamen Univ, Dept Oncol, Chenggong Hosp, Xiamen 361000, Fujian, Peoples R China.
EM chenyq707@163.com
FU Tumor Treatment Center Special Fund; Medical Science Innovation Fund of
   the Nanjing Military Region of the People's Liberation Army [14ZD33]
FX The Tumor Treatment Center Special Fund and The Medical Science
   Innovation Fund of the Nanjing Military Region of the People's
   Liberation Army (grant no. 14ZD33).
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IS 2
BP 252
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PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HU3GN
UT WOS:000465160800011
PM 30569722
OA Bronze
DA 2025-01-04
ER

PT J
AU Xu, LW
   Su, TQ
   Xu, XY
   Zhu, LD
   Shi, L
AF Xu, Liwei
   Su, Tongqi
   Xu, Xinyue
   Zhu, Lide
   Shi, Li
TI Platelets membrane camouflaged irinotecan-loaded gelatin nanogels for
   <i>in vivo</i> colorectal carcinoma therapy
SO JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
LA English
DT Article
DE Platelets membrane; Irinotecan; Nanodrug delivery system; Targeted tumor
   therapy; Colorectal carcinoma
ID DRUG-DELIVERY; CANCER; CELL; NANOPARTICLES; TUMOR; BLOOD
AB Nanodrug delivery systems possess the potential to revolutionize cancer therapy. An ideal nanoplatform should can effectively avoid the clearance of reticuloendothelial system (RES) and targeted accumulate at tumor sites. In addition, it should be nontoxic to the organism. Herein, the authors fabricated a biomimetic nanodrug delivery system possessed with these properties for targeted colorectal carcinoma therapy. This bilayer system was composed of irinotecan (IRN)-loaded gelatin nanogels (GN) as the inner cores and platelets membranes (PTM) as the outer shells, noted as PTM/GN/IRN. The resulting core-shell nanostructure of PTM/GN/IRN could effectively prevent the premature release of the laden IRN, which was beneficial for reducing the system side effects of IRN. Meanwhile, because of the tumor targeting ability of the coated PTM, PTM/GN/IRN could effectively accumulate at tumor sites. The in vivo antitumor activity results towards the HT-29 xenografts mouse models indicated that the PTM/GN/IRN could obviously suppress the tumor cells growth through causing the necrosis and apoptosis of tumor cells. In addition, since the PTM coating could avoid the premature release of the laden IRN, PTM/GN/IRN exhibited minimal side effects. The work presented here provides a promising strategy for effective targeted therapy of colorectal carcinoma.
C1 [Xu, Liwei; Xu, Xinyue; Zhu, Lide; Shi, Li] Changchun Univ Tradit Chinese Med, Dept Hematol & Oncol, Affiliated Hosp, Changchun, Jilin, Peoples R China.
   [Su, Tongqi] Changchun Univ Tradit Chinese Med, Dept Gen Surg, Affiliated Hosp, Changchun, Jilin, Peoples R China.
C3 Changchun University of Chinese Medicine; Changchun University of
   Chinese Medicine
RP Shi, L (corresponding author), Changchun Univ Tradit Chinese Med, Dept Hematol & Oncol, Affiliated Hosp, Changchun, Jilin, Peoples R China.
EM liwei_xuan45@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 25
Z9 26
U1 1
U2 48
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1773-2247
EI 2588-8943
J9 J DRUG DELIV SCI TEC
JI J. Drug Deliv. Sci. Technol.
PD OCT
PY 2019
VL 53
AR 101190
DI 10.1016/j.jddst.2019.101190
PG 7
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA JA6PF
UT WOS:000487963600067
DA 2025-01-04
ER

PT J
AU Okoye, C
   Tran, M
   Soladoye, E
   Akahara, DE
   Emeasoba, CM
   Ojinna, BT
   Anasonye, E
   Obadare, OO
   Diala, CS
   Salaudeen, BH
   Evbayekha, EO
   Okobi, OE
AF Okoye, Chiugo
   Tran, My
   Soladoye, Elizabeth
   Akahara, Darlington E.
   Emeasoba, Chinemerem M.
   Ojinna, Blessing T.
   Anasonye, Emmanuel
   Obadare, Oyindamola O.
   Diala, Chiamaka S.
   Salaudeen, Bolanle H.
   Evbayekha, Endurance O.
   Okobi, Okelue E.
TI A Review of 10-Year Survivability of Immunotherapy in the Management of
   Colon Cancer
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Review
DE immunotherapy; progression-free rates; survival rates; colon
   adenocarcinoma; colon gist; colon lymphoma
ID LYMPHOMA; TUMORS
AB Colon cancer is one of the most common cancers in the United States of America. In addition to conventional treatment approaches such as surgery, chemotherapy, and radiation for colorectal cancer, immunotherapy has gained recognition over the past few years. However, its effectiveness in colorectal cancer treatment is controversial. Our study investigates the survival and progression-free rates of immunotherapy for different types of colorectal cancer over the last 10 years. We conducted literature reviews from various clinical trials and research studies to evaluate immunotherapy's role in colorectal cancer treatment. We also investigated how it affects clinical outcomes. We discovered a range of effective immunotherapy approaches targeting various growth factors and signaling pathways. These modalities include monoclonal antibodies aimed at growth factors such as epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), human epidermal growth factor receptor 2 (HER2), and downstream signaling pathways such as mitogen-activated protein kinase (MAPK), kirsten rat sarcoma viral oncogene (KRAS), B-raf proto-oncogene, serine/threonine kinase (BRAF), and phosphatase and tensin homolog (PTEN). Additionally, we identified immune checkpoint inhibitors, such as cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) inhibitors and programmed cell death ligand 1 (PD-L1) inhibitors, as well as target therapy and adoptive cell therapy as promising immunotherapeutic options. Nevertheless, the application of immunotherapy remains highly limited due to various factors influencing survival and progression-free rates, including tumor microenvironment, microsatellite instability, immune checkpoint expression, and gut microbiome. Additionally, its effectiveness is restricted to a small subgroup of patients, accompanied by side effects and the development of drug resistance mechanisms. To unlock its full potential, further clinical trials and research on molecular pathways in colorectal cancer are imperative. This will ultimately enhance drug discovery success and lead to more effective clinical management approaches.
C1 [Okoye, Chiugo; Ojinna, Blessing T.] Calif Inst Behav Neurosci & Psychol, Internal Med, Fairfield, CT 94534 USA.
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C3 University of Texas System; University of Texas Health Science Center
   Houston; Lagos State University; Saint Luke's Hospital - Missouri
RP Okoye, C (corresponding author), Calif Inst Behav Neurosci & Psychol, Internal Med, Fairfield, CT 94534 USA.
EM thechiokoye@gmail.com
RI Okobi, Okelue/AAZ-6709-2021
OI Okobi, Okelue/0000-0001-7709-2757
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NR 52
TC 1
Z9 1
U1 0
U2 3
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD AUG 9
PY 2023
VL 15
IS 8
AR e43189
DI 10.7759/cureus.43189
PG 15
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA IT5I2
UT WOS:001168593900011
PM 37692610
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Furuki, H
   Yamada, T
   Takahashi, G
   Iwai, T
   Koizumi, M
   Shinji, S
   Yokoyama, Y
   Takeda, K
   Taniai, N
   Uchida, E
AF Furuki, Hiroyasu
   Yamada, Takeshi
   Takahashi, Goro
   Iwai, Takuma
   Koizumi, Michihiro
   Shinji, Seiichi
   Yokoyama, Yasuyuki
   Takeda, Kohki
   Taniai, Nobuhiko
   Uchida, Eiji
TI Evaluation of liquid biopsies for detection of emerging mutated genes in
   metastatic colorectal cancer
SO EJSO
LA English
DT Article
DE Colon cancer; Gene mutation; Genomic evolution; Liquid biopsy;
   Next-generation sequencing
ID CELL-FREE DNA; PRIMARY TUMORS; BRAF MUTATIONS; KRAS; RADIOTHERAPY;
   CONCORDANCE; RESISTANCE; EVOLUTION; CETUXIMAB; THERAPY
AB Background: Detection of gene mutations is important for planning molecular targeted therapy. Although most gene mutations are concordant between primary colon cancers and their liver metastases, new mutations can emerge in metastases. The liquid biopsy is a newly developed, gene analytic method to detect mutations in metastatic tumors. In this prospective study, we evaluated the applicability of liquid biopsies in the detection of mutations in primary and metastatic tumors.
   Methods: We included 22 patients with liver metastases from colorectal cancer and extracted DNA from primary colorectal tumors, metastatic liver tumors, and peripheral blood (liquid biopsy). Next-generation sequencing (NGS) and digital PCR were performed to detect mutations in these three sample types.
   Results: We found a total of 36 different mutations in samples from primary tumors, liver metastases, and liquid biopsies using NGS. Twenty-eight of these mutations were found in all three types of samples, whereas liquid biopsy did not identify four mutations that had been found in both primary tumors and liver metastases, but did identify four mutations that were found in liver tumors but not in primary tumors. The sensitivity of liquid biopsies for detecting mutations in liver metastases was 64% (23/36) using NGS and 89% (32/36, P = 0.02) using dPCR. The specificities of NGS and dPCR were 100% (23/23) and 100% (32/32), respectively.
   Conclusions: Emerging mutations, which are not found in primary tumors, can be detected in their metastases and liquid biopsies. (C) 2018 Elsevier Ltd, BASO similar to The Association for Cancer Surgery, and the European Society of Surgical Oncology. All rights reserved.
C1 [Furuki, Hiroyasu; Yamada, Takeshi; Takahashi, Goro; Iwai, Takuma; Koizumi, Michihiro; Shinji, Seiichi; Yokoyama, Yasuyuki; Takeda, Kohki; Taniai, Nobuhiko; Uchida, Eiji] Nippon Med Sch, Dept Gastrointestinal & Hepatobiliary Pancreat Su, Tokyo, Japan.
C3 Nippon Medical School
RP Yamada, T (corresponding author), Nippon Med Sch, Dept Gastrointestinal & Hepatobiliary Pancreat Su, Bunkyo Ku, 1-1-5 Sendagi, Tokyo 1138602, Japan.
EM y-tak@nms.ac.jp
RI Takuma, Iwai/AAL-1144-2020
OI Takeda, Kohki/0000-0002-4528-0742; Yamada, Takeshi/0000-0002-1436-7482;
   Takahashi, Goro/0000-0002-8561-8349; Furuki,
   Hiroyasu/0000-0003-1351-8434; Shinji, Seiichi/0000-0002-9204-6393; Iwai,
   Takuma/0000-0002-4706-1228
FU Department of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery,
   Nippon Medical School
FX We thank Ms. Hazuki Kanno for technical support with the experiments and
   Dr. Trish Reynolds, MBBS, FRACP, from Edanz Group
   (https://www.edanzediting.com/ac) for editing a draft of this
   manuscript. We also thank Mark Abramovitz, PhD, from Edanz Group
   (www.edanzediting.com/ac) for editing a draft of this manuscript. This
   work was supported by the Department of Gastrointestinal and
   Hepato-Biliary-Pancreatic Surgery, Nippon Medical School.
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NR 31
TC 33
Z9 35
U1 0
U2 7
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0748-7983
EI 1532-2157
J9 EJSO-EUR J SURG ONC
JI EJSO
PD JUL
PY 2018
VL 44
IS 7
BP 975
EP 982
DI 10.1016/j.ejso.2018.01.224
PG 8
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA GL7OL
UT WOS:000437391100009
PM 29452859
DA 2025-01-04
ER

PT J
AU Grifantini, R
   Taranta, M
   Gherardini, L
   Naldi, I
   Parri, M
   Grandi, A
   Giannetti, A
   Tombelli, S
   Lucarini, G
   Ricotti, L
   Campagnoli, S
   De Camilli, E
   Pelosi, G
   Baldini, F
   Menciassi, A
   Viale, G
   Pileri, P
   Cinti, C
AF Grifantini, Renata
   Taranta, Monia
   Gherardini, Lisa
   Naldi, Ilaria
   Parri, Matteo
   Grandi, Alberto
   Giannetti, Ambra
   Tombelli, Sara
   Lucarini, Gioia
   Ricotti, Leonardo
   Campagnoli, Susanna
   De Camilli, Elisa
   Pelosi, Gualtiero
   Baldini, Francesco
   Menciassi, Arianna
   Viale, Giuseppe
   Pileri, Piero
   Cinti, Caterina
TI Magnetically driven drug delivery systems improving targeted
   immunotherapy for colon-rectal cancer
SO JOURNAL OF CONTROLLED RELEASE
LA English
DT Article
DE Magnetic delivery system; Monoclonal antibody; Targeting; Nanoparticles;
   Colorectal cancer
ID MONOCLONAL-ANTIBODY; NANOPARTICLES; THERAPY; FAT1
AB Colorectal cancer (CRC) is one of the major causes of cancer-associated mortality worldwide. The currently approved therapeutic agents show a rather limited efficacy. We have recently demonstrated that the atypical cadherin FAT1 is a specific marker of CRC and that the FAT1-specific monoclonal antibody mAb198.3 may offer new therapeutic opportunities for CRC, being efficiently internalized by cancer cells and reducing cancer growth in colon cancer xenograft models.
   In this study we explored the therapeutic efficacy of mAb198.3 using two drug delivery systems (DDS) for improving the targeted treatment of CRC. The mAb198.3 was either directly bound to super-paramagnetic nanoparticles (spmNPs) or embedded into human erythrocyte-based magnetized carriers, named Erythro-MagnetoHemagglutinin Virosomes (EMHVs) to produce two different novel mAb198.3 formulations. Both DDS were endowed with magnetic properties and were anchored in the target tumor site by means of an external permanent magnet. The antibody loading efficiency of these two magnetically driven drug delivery systems and the overall therapeutic efficacy of these two formulations were assessed both in vitro and in a proof-of-concept in vivo study.
   We demonstrated that mAb198.3 bound to spmNPs or embedded into EMHVs was very effective in targeting FAT1-positive colon cancer cells in vitro and accumulating in the tumor mass in vivo. Although both in vivo administered mAb198.3 formulations have approximately 200 lower antibody doses needed, these showed to achieve a relevant therapeutic effect, thus reducing cancer growth more efficiently respect to the naked antibody. These results indicate that the two proposed magnetically driven drug delivery systems have a considerable potential as platforms to improve bioavailability and pharmacodynamics of anti-FAT mAb198.3 and raise new opportunities for a targeted therapy of CRC.
C1 [Grifantini, Renata] Natl Inst Mol Genet, Milan, Italy.
   [Taranta, Monia; Gherardini, Lisa; Naldi, Ilaria; Pelosi, Gualtiero; Cinti, Caterina] Natl Res Council CNR Italy, Inst Clin Physiol, Expt Oncol Unit, Siena, Italy.
   [Grifantini, Renata; Parri, Matteo; Grandi, Alberto; Campagnoli, Susanna; Pileri, Piero] Externautics Srl, Siena, Italy.
   [Giannetti, Ambra; Tombelli, Sara; Baldini, Francesco] Natl Res Council CNR Italy, Inst Appl Phys, Florence, Italy.
   [Lucarini, Gioia; Ricotti, Leonardo; Menciassi, Arianna] Scuola Super Sant Anna, BioRobot Inst, Pisa, Italy.
   [De Camilli, Elisa; Viale, Giuseppe] European Inst Oncol, Milan, Italy.
   [Viale, Giuseppe] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
C3 Consiglio Nazionale delle Ricerche (CNR); Istituto di Genetica
   Molecolare (IGM-CNR); Consiglio Nazionale delle Ricerche (CNR); Istituto
   di Fisica Applicata "Nello Carrara" (IFAC-CNR); Istituto di Fisiologia
   Clinica (IFC-CNR); Scuola Superiore Sant'Anna; IRCCS European Institute
   of Oncology (IEO); University of Milan
RP Cinti, C (corresponding author), Natl Res Council CNR Italy, Inst Clin Physiol, Expt Oncol Unit, Siena, Italy.
EM caterina.cinti@cnr.it
RI Taranta, Monia/IUO-4735-2023; Ricotti, Leonardo/GXF-0124-2022; Viale,
   Giuseppe/AAE-8921-2019; Baldini, Francesco/C-2210-2015; Cinti,
   Caterina/HLX-2432-2023; Renata, Grifantini/AAB-9969-2022; /N-6227-2016;
   GIANNETTI, AMBRA/Q-2681-2015; Tombelli, Sara/H-6430-2013; gherardini,
   lisa/HCI-2927-2022
OI /0000-0002-2888-8748; Taranta, Monia/0009-0005-4245-2448; GIANNETTI,
   AMBRA/0000-0002-0002-2977; Baldini, Francesco/0000-0002-2689-5952;
   Tombelli, Sara/0000-0003-1660-9833; gherardini,
   lisa/0000-0002-7003-4295; Cinti, Caterina/0000-0001-8049-0369; Ricotti,
   Leonardo/0000-0001-8797-3742; Grifantini, Renata/0000-0003-0024-3355;
   Grandi, Alberto/0000-0002-3496-0187
FU Regione Toscana and European Funds [1200]; national flagship project
   NANOMAX funds; ENCODER project; CNR funds; national flagship project
   NANOMAX; Regione Toscana [POR-CREO-FESR2007/2013]; project NANOMAX; 
   [POR-CREO-FESR 2007/2013-ACTILA];  [6408.30122011.026000013]
FX This work has been supported by Regione Toscana and European Funds
   (D.G.R. N. 1200) with the POR-CREO-FESR 2007/2013-ACTILA Project (N.
   6408.30122011.026000013), the national flagship project NANOMAX funds
   with the ENCODER project and by CNR funds.S.T wishes to thank the
   national flagship project NANOMAX for the funding with the project
   ENCODER. M.T wishes to thank the Regione Toscana for funding
   POR-CREO-FESR2007/2013 ACTILA project and the national flagship project
   NANOMAX for funding with the project ENCODER.
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NR 33
TC 38
Z9 40
U1 0
U2 50
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 JUN 28
PY 2018
VL 280
BP 76
EP 86
DI 10.1016/j.jconrel.2018.04.052
PG 11
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA GI5AH
UT WOS:000434382100008
PM 29733876
DA 2025-01-04
ER

PT J
AU Huang, L
   Dai, G
AF Huang, Long
   Dai, Gang
TI RETRACTED: Long non-coding RNA DCST1-AS1/hsa-miR-582-5p/HMGB1 axis
   regulates colorectal cancer progression (Retracted Article)
SO BIOENGINEERED
LA English
DT Article; Retracted Publication
DE DCST1-AS1; CRC; hsa-miR-582-5p; HMGB1
ID GROUP BOX 1; CELL-PROLIFERATION; LNCRNA DCST1-AS1;
   HEPATOCELLULAR-CARCINOMA; POOR-PROGNOSIS; GASTRIC-CANCER; BREAST-CANCER;
   METASTASIS; MIR-582-5P; HMGB1
AB Long non-coding RNAs (lncRNAs) are related to the initiation and progression of tumor and regulate various cellular processes including growth, invasion, migration, and apoptosis. Understanding the roles and mechanisms of lncRNAs in regulating cancer progression is crucial for formulating novel therapeutic strategies. Although lncRNA DCST1-antisense RNA 1(AS1) has been implicated in several cancers, its role in the progression of colorectal cancer (CRC) remains to be explored. This study focuses on elucidating the function of lncRNA DCST1-AS1 in CRC development and its underlying mechanism. We found that the expression of lncRNA DCST1-AS1 was up-regulated in CRC tissues and cell lines, and CRC patients with high lncRNA DCST1-AS1 expression were associated with a poor prognosis. Loss-of-function and gain-of-function experiment in CRC cell lines confirmed that lncRNA DCST1-AS1 promoted the malignant phenotype of CRC cells, including cell proliferation, colony formation, migration, and invasion. In addition, we identified the binding sites between lncRNA DCST1-AS1 and hsa-miR-582-5p, and between hsa-miR-582-5p and High Mobility Group Box 1 (HMGB1) through DIANA Tools and TargetScan database, which was further confirmed by dual-luciferase reporter assay. Functional assay further confirmed the crucial role of lncRNA DCST1-AS1/hsa-miR-582-5p/HMGB1 axis in modulating the malignant phenotype of CRC cells. Collectively, our data suggest that lncRNA DCST1-AS1 regulates the aggressiveness of CRC cells through hsa-miR-582-5p/HMGB1 axis. Our study provides novel insight into the mechanism of lncRNA DCST1-AS1 in CRC cells for targeted therapy.
C1 [Huang, Long] Beibei Tradit Chinese Med Hosp, Dept Gen Surg, Chongqing, Peoples R China.
   [Dai, Gang] Fengdu Peoples Hosp, Dept Gen Surg, 251 Zhonghua Rd, Chongqing 408200, Fengdu County, Peoples R China.
RP Dai, G (corresponding author), Fengdu Peoples Hosp, Dept Gen Surg, 251 Zhonghua Rd, Chongqing 408200, Fengdu County, Peoples R China.
EM weriok123@163.com
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NR 53
TC 19
Z9 19
U1 0
U2 7
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 2165-5979
EI 2165-5987
J9 BIOENGINEERED
JI Bioengineered
PD JAN 1
PY 2022
VL 13
IS 1
BP 12
EP 26
DI 10.1080/21655979.2021.1976894
PG 15
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA XX7VS
UT WOS:000736498700001
PM 34967274
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Mizuno, T
   Yoshida, T
   Sunami, K
   Koyama, T
   Okita, N
   Kubo, T
   Sudo, K
   Shimoi, T
   Ueno, H
   Saito, E
   Katanoda, K
   Shibata, T
   Yonemori, K
   Okusaka, T
   Boku, N
   Ohe, Y
   Hiroshima, Y
   Ueno, M
   Kuboki, Y
   Doi, T
   Nakamura, K
   Kohno, T
   Yatabe, Y
   Yamamoto, N
AF Mizuno, Takaaki
   Yoshida, Tatsuya
   Sunami, Kuniko
   Koyama, Takafumi
   Okita, Natsuko
   Kubo, Takashi
   Sudo, Kazuki
   Shimoi, Tatsunori
   Ueno, Hideki
   Saito, Eiko
   Katanoda, Kota
   Shibata, Taro
   Yonemori, Kan
   Okusaka, Takuji
   Boku, Narikazu
   Ohe, Yuichiro
   Hiroshima, Yukihiko
   Ueno, Makoto
   Kuboki, Yasutoshi
   Doi, Toshihiko
   Nakamura, Kenichi
   Kohno, Takashi
   Yatabe, Yasushi
   Yamamoto, Noboru
TI Study protocol for NCCH1908 (UPFRONT-trial): a prospective clinical
   trial to evaluate the feasibility and utility of comprehensive genomic
   profiling prior to the initial systemic treatment in advanced solid
   tumour patients
SO JAPANESE JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
DE comprehensive genomic profiling; solid tumour; molecular targeted
   therapy; actionable genomic alteration; first-line treatment
AB Comprehensive genomic profiling has been approved for use in patients with advanced solid tumours; however, it is only indicated in advanced solid tumour patients without available standard chemotherapeutic treatment or those who have completed standard treatments in Japan, and there are no available data on the clinical feasibility and utility of comprehensive genomic profiling in treatment-naive patients. This multicentre, single-arm, prospective study aims to evaluate the feasibility and utility of the OncoGuide NCC Oncopanel System in treatment-naive patients with six advanced major malignancies: non-small cell lung cancer, breast cancer, gastric cancer, colon cancer, pancreatic cancer and biliary tract cancer (NCCH1908). This study (study cohort) will be compared with the other prospective observational study (control cohort), which enrols patients not receiving comprehensive genomic profiling prior to initial systemic treatment. A total of 200 patients will be enrolled in the study over 21 months.
C1 [Mizuno, Takaaki; Yoshida, Tatsuya; Koyama, Takafumi; Sudo, Kazuki; Yonemori, Kan; Yamamoto, Noboru] Natl Canc Ctr, Dept Expt Therapeut, Tokyo, Japan.
   [Mizuno, Takaaki; Yoshida, Tatsuya; Ohe, Yuichiro; Yamamoto, Noboru] Natl Canc Ctr, Dept Thorac Oncol, Tokyo, Japan.
   [Mizuno, Takaaki; Kohno, Takashi] Natl Canc Ctr, Div Genome Biol, Tokyo, Japan.
   [Sunami, Kuniko; Kubo, Takashi] Natl Canc Ctr, Dept Clin Labs, Tokyo, Japan.
   [Okita, Natsuko; Boku, Narikazu] Natl Canc Ctr, Dept Gastrointestinal Med Oncol, Tokyo, Japan.
   [Okita, Natsuko; Shibata, Taro; Nakamura, Kenichi] Natl Canc Ctr, Clin Trial Support Off, Tokyo, Japan.
   [Sudo, Kazuki; Shimoi, Tatsunori; Yonemori, Kan] Natl Canc Ctr, Dept Med Oncol, Tokyo, Japan.
   [Ueno, Hideki; Okusaka, Takuji] Natl Canc Ctr Hospitali, Dept Hepatobiliary & Pancreat Oncol, Tokyo, Japan.
   [Saito, Eiko; Katanoda, Kota] Natl Canc Ctr, Ctr Canc Control & Informat Serv, Div Canc Stat Integrat, Tokyo, Japan.
   [Shibata, Taro] Natl Canc Ctr, Ctr Res Adm & Support, Biostat Div, Tokyo, Japan.
   [Hiroshima, Yukihiko] Kanagawa Canc Ctr, Dept Canc Genom, Res Inst, Yokohama, Kanagawa, Japan.
   [Ueno, Makoto] Kanagawa Canc Ctr, Dept Gastroenterol, Hepatobiliary & Pancreat Med Oncol Div, Yokohama, Kanagawa, Japan.
   [Kuboki, Yasutoshi; Doi, Toshihiko] Natl Canc Ctr Hosp East, Dept Expt Therapeut, Chiba, Japan.
   [Yatabe, Yasushi] Natl Canc Ctr, Dept Diagnost Pathol, Tokyo, Japan.
C3 National Cancer Center - Japan; National Cancer Center - Japan; National
   Cancer Center - Japan; National Cancer Center - Japan; National Cancer
   Center - Japan; National Cancer Center - Japan; National Cancer Center -
   Japan; National Cancer Center - Japan; National Cancer Center - Japan;
   Kanagawa Prefectural Cancer Center; Kanagawa Prefectural Cancer Center;
   National Cancer Center - Japan; National Cancer Center - Japan
RP Yoshida, T (corresponding author), Natl Canc Ctr, Dept Thorac Oncol, Chuo Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
EM tatyoshi@ncc.go.jp
RI Ueno, Hideki/L-1237-2016; Katanoda, Kota/AFV-8519-2022; Kohno,
   Takashi/M-8823-2013; YATABE, Yasushi/J-6461-2014; Saito,
   Eiko/AGG-2592-2022
OI YATABE, Yasushi/0000-0003-1788-559X; Saito, Eiko/0000-0002-4550-9631
FU AMED [JP21ck0106576]; Grants-in-Aid for Scientific Research [20H03461]
   Funding Source: KAKEN
FX This research was supported by AMED under grant number JP21ck0106576.
CR Chawla A, 2018, JCO PRECIS ONCOL, V2, DOI 10.1200/PO.18.00074
   Ebi Hiromichi, 2019, JCO Precis Oncol, V3, DOI 10.1200/PO.19.00291
   Flaherty KT, 2020, J CLIN ONCOL, V38, DOI 10.1200/JCO.19.03010
   Sunami K, 2019, CANCER SCI, V110, P1480, DOI 10.1111/cas.13969
NR 4
TC 4
Z9 4
U1 0
U2 0
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 DEC
PY 2021
VL 51
IS 12
BP 1757
EP 1760
DI 10.1093/jjco/hyab159
EA OCT 2021
PG 4
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YW6BV
UT WOS:000753498500010
PM 34622931
OA Bronze
DA 2025-01-04
ER

PT J
AU Xu, JS
   Liu, YH
   Liu, S
   Ou, WQ
   White, A
   Stewart, S
   Tkaczuk, KHR
   Ellis, LM
   Wan, J
   Lu, XB
   He, XM
AF Xu, Jiangsheng
   Liu, Yunhua
   Liu, Sheng
   Ou, Wenquan
   White, Alisa
   Stewart, Samantha
   Tkaczuk, Katherine H. R.
   Ellis, Lee M.
   Wan, Jun
   Lu, Xiongbin
   He, Xiaoming
TI Metformin bicarbonate-mediated efficient RNAi for precise targeting of
   <i>TP53</i> deficiency in colon and rectal cancers
SO NANO TODAY
LA English
DT Article
DE Metformin; Targeted therapy; Gene delivery; Endosomal escape; POLR2A
ID SYSTEMICALLY ADMINISTERED SIRNA; NEGATIVE BREAST-CANCER; EXTRACELLULAR
   VESICLES; P53 PATHWAY; VULNERABILITIES; CHALLENGES; PREVENTION
AB Colon and rectal cancers are the leading causes of cancer-related deaths in the United States and effective targeted therapies are in need for treating them. Our genomic analyses show hemizygous deletion of TP53, an important tumor suppressor gene, is highly frequent in both cancers, and the 5-year survival of patients with the more prevalent colon cancer is significantly reduced in the patients with the cancer harboring such deletion, although such reduction is not observed for rectal cancer. Unfortunately, direct targeting TP53 has been unsuccessful for cancer therapy. Interestingly, POLR2A, a gene essential for cell survival and proliferation, is almost always deleted together with TP53 in colon and rectal cancers. Therefore, RNA interference (RNAi) with small interfering RNAs (siRNAs) to precisely target/inhibit POLR2A may be an effective strategy for selectively killing cancer cells with TP53 deficiency. However, the difficulty of delivering siRNAs specifically into the cytosol where they perform their function, is a major barrier for siRNA-based therapies. Here, metformin bicarbonate (MetC) is synthesized to develop pH-responsive MetC-nanoparticles with a unique "bomb" effect for effective cytosolic delivery of POLR2A siRNA, which greatly facilitates its endo/lysosomal escape into the cytosol and augments its therapeutic efficacy of cancer harboring TP53 deficiency. Moreover, the MetC-based nanoparticles without functional siRNA show notable therapeutic effect with no evident systemic toxicity or immunogenicity. (C) 2022 Elsevier Ltd. All rights reserved.
C1 [Xu, Jiangsheng; Ou, Wenquan; White, Alisa; Stewart, Samantha; He, Xiaoming] Univ Maryland, Fischell Dept Bioengn, College Pk, MD 20742 USA.
   [Liu, Yunhua] Zhejiang Univ, Affiliated Hosp 2, Dept Pathol & Pathophysiol, Sch Med, Hangzhou 310058, Peoples R China.
   [Liu, Yunhua] Zhejiang Univ, Affiliated Hosp 2, Dept Colorectal Surg & Oncol, Sch Med, Hangzhou 310058, Peoples R China.
   [Liu, Yunhua; Lu, Xiongbin] Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
   [Liu, Yunhua; Liu, Sheng; Wan, Jun; Lu, Xiongbin] Indiana Univ Sch Med, Melvin & Bren Simon Canc Ctr, Indianapolis, IN 46202 USA.
   [Tkaczuk, Katherine H. R.; He, Xiaoming] Univ Maryland, Marlene & Stewart Greenebaum Comprehens Canc Ctr, Baltimore, MD 21201 USA.
   [Ellis, Lee M.] Univ Texas MD Anderson Canc Ctr, Dept Surg Oncol, Houston, TX 77030 USA.
C3 University System of Maryland; University of Maryland College Park;
   Zhejiang University; Zhejiang University; Indiana University System;
   Indiana University Bloomington; Indiana University System; Indiana
   University Bloomington; University System of Maryland; University of
   Maryland Baltimore; University of Texas System; UTMD Anderson Cancer
   Center
RP He, XM (corresponding author), Univ Maryland, Fischell Dept Bioengn, College Pk, MD 20742 USA.; Liu, YH; Lu, XB (corresponding author), Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
EM yunhualiu@zju.edu.cn; xiolu@iu.edu; shawnhe@umd.edu
RI Lu, Xiaoyu/GOJ-7569-2022; OU, WENQUAN/GPW-8828-2022; Wan,
   Jun/AAT-8147-2020; Xu, Jiangsheng/AAD-3829-2022; He,
   Xiaoming/C-5499-2008
OI XU, JIANGSHENG/0000-0002-9595-9550; He, Xiaoming/0000-0003-0125-6086
FU NIH [R01CA206366]
FX This work was partially supported by a grant from NIH (R01CA206366).
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NR 59
TC 12
Z9 12
U1 2
U2 44
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 1748-0132
EI 1878-044X
J9 NANO TODAY
JI Nano Today
PD APR
PY 2022
VL 43
AR 101406
DI 10.1016/j.nantod.2022.101406
EA FEB 2022
PG 16
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA 2P6FV
UT WOS:000819835300001
PM 35251293
OA Green Accepted, Bronze
DA 2025-01-04
ER

PT J
AU Hao, JJ
   Huang, JS
   Hua, CY
   Zuo, Y
   Yu, WD
   Wu, XJ
   Li, LR
   Xue, GQ
   Wan, XY
   Ru, LY
   Guo, ZY
   Han, SL
   Deng, WG
   Lin, F
   Guo, W
AF Hao, Jiaojiao
   Huang, Jinsheng
   Hua, Chunyu
   Zuo, Yan
   Yu, Wendan
   Wu, Xiaojun
   Li, Liren
   Xue, Guoqing
   Wan, Xinyu
   Ru, Liyuan
   Guo, Ziyue
   Han, Shilong
   Deng, Wuguo
   Lin, Fei
   Guo, Wei
TI A novel TOX3-WDR5-ABCG2 signaling axis regulates the progression of
   colorectal cancer by accelerating stem-like traits and chemoresistance
SO PLOS BIOLOGY
LA English
DT Article
ID COLON-CANCER; CELLS; TRANSCRIPTION; CRYPT; WDR5; TOX3
AB The eradication of cancer stem cells (CSCs) with drug resistance confers the probability of local tumor control after chemotherapy or targeted therapy. As the main drug resistance marker, ABCG2 is also critical for colorectal cancer (CRC) evolution, in particular cancer stem-like traits expansion. Hitherto, the knowledge about the expression regulation of ABCG2, in particular its upstream transcriptional regulatory mechanisms, remains limited in cancer, including CRC. Here, ABCG2 was found to be markedly up-regulated in CRC CSCs (cCSCs) expansion and chemo-resistant CRC tissues and closely associated with CRC recurrence. Mechanistically, TOX3 was identified as a specific transcriptional factor to drive ABCG2 expression and subsequent cCSCs expansion and chemoresistance by binding to -261 to -141 segments of the ABCG2 promoter region. Moreover, we found that TOX3 recruited WDR5 to promote tri-methylation of H3K4 at the ABCG2 promoter in cCSCs, which further confers stem-like traits and chemoresistance to CRC by co-regulating the transcription of ABCG2. In line with this observation, TOX3, WDR5, and ABCG2 showed abnormal activation in chemo-resistant tumor tissues of in situ CRC mouse model and clinical investigation further demonstrated the comprehensive assessment of TOX3, WDR5, and ABCG2 could be a more efficient strategy for survival prediction of CRC patients with recurrence or metastasis. Thus, our study found that TOX3-WDR5/ABCG2 signaling axis plays a critical role in regulating CRC stem-like traits and chemoresistance, and a combination of chemotherapy with WDR5 inhibitors may induce synthetic lethality in ABCG2-deregulated tumors.
   This study reveals that a novel TOX3-WDR5-H3K4me3/ABCG2 signaling axis is upregulated in colorectal cancer (CRC) stem cells; these proteins show potential as biomarkers for predicting survival of CRC patients, and targeting the pathway may help overcome the challenges of drug tolerance, recurrence and metastasis.
C1 [Hao, Jiaojiao; Hua, Chunyu; Zuo, Yan; Yu, Wendan; Xue, Guoqing; Wan, Xinyu; Ru, Liyuan; Guo, Ziyue; Han, Shilong; Guo, Wei] Dalian Med Univ, Inst Canc Stem Cells, Dalian, Peoples R China.
   [Hao, Jiaojiao; Hua, Chunyu; Zuo, Yan; Yu, Wendan; Xue, Guoqing; Wan, Xinyu; Ru, Liyuan; Guo, Ziyue; Han, Shilong; Guo, Wei] Dalian Med Univ, Affiliated Hosp 1, Dalian, Peoples R China.
   [Huang, Jinsheng; Wu, Xiaojun; Li, Liren; Deng, Wuguo] Sun Yat Sen Univ, Canc Ctr, Guangzhou, Peoples R China.
   [Huang, Jinsheng; Wu, Xiaojun; Li, Liren; Deng, Wuguo] Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou, Peoples R China.
   [Lin, Fei] Jinan Univ, Guangdong Prov Hosp Integrated Tradit Chinese & We, Dept Oncol, Foshan, Peoples R China.
   [Lin, Fei] Jinan Univ, Affiliated Nanhai Hosp Tradit Chinese Med, Foshan, Peoples R China.
C3 Dalian Medical University; Dalian Medical University; Sun Yat Sen
   University; State Key Lab Oncology South China
RP Guo, W (corresponding author), Dalian Med Univ, Inst Canc Stem Cells, Dalian, Peoples R China.; Guo, W (corresponding author), Dalian Med Univ, Affiliated Hosp 1, Dalian, Peoples R China.; Deng, WG (corresponding author), Sun Yat Sen Univ, Canc Ctr, Guangzhou, Peoples R China.; Deng, WG (corresponding author), Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Guangzhou, Peoples R China.; Lin, F (corresponding author), Jinan Univ, Guangdong Prov Hosp Integrated Tradit Chinese & We, Dept Oncol, Foshan, Peoples R China.; Lin, F (corresponding author), Jinan Univ, Affiliated Nanhai Hosp Tradit Chinese Med, Foshan, Peoples R China.
EM dengwg@sysucc.org.cn; linfei@sysucc.org.cn; wei1015@dmu.edu.cn
RI xue, guoqing/AAC-7903-2021; huang, jinsheng/HPH-7961-2023
OI Hao, Jiaojiao/0000-0001-6487-6800; huang, jinsheng/0000-0002-5859-4994
FU National Natural Science Foundation of China [82072711, 82172949,
   81972569, 82100780, 82172802]; Liaoning Revitalization Talents Program
   [XLYC2007172]; Guangdong Basic and Applied Basic Research Foundation
   [2022A1515012508]
FX This study was supported by the funds from the National Natural Science
   Foundation of China [grant number: 82072711 WG, 82172949 WD, 81972569
   WD, 82100780 JH, 82172802 LL], Liaoning Revitalization Talents Program
   [grant number: XLYC2007172 WG], the Guangdong Basic and Applied Basic
   Research Foundation (2022A1515012508 WD). The funders provided research
   funds for the implementation of the experiments involved in the whole
   study, but did not participate in the design of the study, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 54
TC 6
Z9 6
U1 1
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1544-9173
EI 1545-7885
J9 PLOS BIOL
JI PLoS. Biol.
PD SEP
PY 2023
VL 21
IS 9
AR e3002256
DI 10.1371/journal.pbio.3002256
PG 29
WC Biochemistry & Molecular Biology; Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA S1WC8
UT WOS:001069134500004
PM 37708089
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Maslowska, K
   Halik, PK
   Tymecka, D
   Misicka, A
   Gniazdowska, E
AF Maslowska, Katarzyna
   Halik, Pawel Krzysztof
   Tymecka, Dagmara
   Misicka, Aleksandra
   Gniazdowska, Ewa
TI The Role of VEGF Receptors as Molecular Target in Nuclear Medicine for
   Cancer Diagnosis and Combination Therapy
SO CANCERS
LA English
DT Review
DE VEGF; VEGF receptors; radiopharmaceuticals; anti-angiogenic therapy
ID ENDOTHELIAL GROWTH-FACTOR; VASCULAR-PERMEABILITY FACTOR;
   POSITRON-EMISSION-TOMOGRAPHY; TYROSINE KINASE INHIBITOR; IN-VITRO
   EVALUATION; TUMOR ANGIOGENESIS; SIGNAL-TRANSDUCTION; BINDING-SITES;
   PRECLINICAL EVALUATION; COLORECTAL-CANCER
AB Simple Summary
   The rapid development of diagnostic and therapeutic methods of the cancer treatment causes that these diseases are becoming better known and the fight against them is more and more effective. Substantial contribution in this development has nuclear medicine that enables very early cancer diagnosis and early start of the so-called targeted therapy. This therapeutic concept compared to the currently used chemotherapy, causes much fewer undesirable side effects, due to targeting a specific lesion in the body. This review article discusses the possible applications of radionuclide-labelled tracers (peptides, antibodies or synthetic organic molecules) that can visualise cancer cells through pathological blood vessel system in close tumour microenvironment. Hence, at a very early step of oncological disease, targeted therapy can involve in tumour formation and growth.
   One approach to anticancer treatment is targeted anti-angiogenic therapy (AAT) based on prevention of blood vessel formation around the developing cancer cells. It is known that vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptors (VEGFRs) play a pivotal role in angiogenesis process; hence, application of angiogenesis inhibitors can be an effective approach in anticancer combination therapeutic strategies. Currently, several types of molecules have been utilised in targeted VEGF/VEGFR anticancer therapy, including human VEGF ligands themselves and their derivatives, anti-VEGF or anti-VEGFR monoclonal antibodies, VEGF binding peptides and small molecular inhibitors of VEGFR tyrosine kinases. These molecules labelled with diagnostic or therapeutic radionuclides can become, respectively, diagnostic or therapeutic receptor radiopharmaceuticals. In targeted anti-angiogenic therapy, diagnostic radioagents play a unique role, allowing the determination of the emerging tumour, to monitor the course of treatment, to predict the treatment outcomes and, first of all, to refer patients for AAT. This review provides an overview of design, synthesis and study of radiolabelled VEGF/VEGFR targeting and imaging agents to date. Additionally, we will briefly discuss their physicochemical properties and possible application in combination targeted radionuclide tumour therapy.
C1 [Maslowska, Katarzyna; Halik, Pawel Krzysztof; Gniazdowska, Ewa] Inst Nucl Chem & Technol, Ctr Radiochem & Nucl Chem, Dorodna 16, PL-03195 Warsaw, Poland.
   [Tymecka, Dagmara; Misicka, Aleksandra] Univ Warsaw, Fac Chem, Pasteura 1, PL-02093 Warsaw, Poland.
C3 Institute of Nuclear Chemistry Technology; University of Warsaw
RP Maslowska, K; Halik, PK (corresponding author), Inst Nucl Chem & Technol, Ctr Radiochem & Nucl Chem, Dorodna 16, PL-03195 Warsaw, Poland.
EM k.maslowska@ichtj.waw.pl; p.halik@ichtj.waw.pl; dulok@chem.uw.edu.pl;
   misicka@chem.uw.edu.pl; e.gniazdowska@ichtj.waw.pl
RI Halik, Paweł/ADH-8005-2022
OI Halik, Pawel/0000-0003-0657-3793; Maslowska,
   Katarzyna/0000-0001-9993-4804; Tymecka, Dagmara/0000-0002-8909-4087;
   Misicka, Aleksandra/0000-0001-7446-2396
FU National Science Centre (Poland) [2019/33/B/NZ7/02818]
FX This research was carried out within grant 2019/33/B/NZ7/02818,
   supported by the National Science Centre (Poland).
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NR 298
TC 29
Z9 29
U1 1
U2 32
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 1072
DI 10.3390/cancers13051072
PG 46
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QV4XB
UT WOS:000627975400001
PM 33802353
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Baba, Y
   Tamura, T
   Satoh, Y
   Gotou, M
   Sawada, H
   Ebara, S
   Shibuya, K
   Soeda, J
   Nakamura, K
AF Baba, Yuji
   Tamura, Toshiya
   Satoh, Yoshihiko
   Gotou, Masamitsu
   Sawada, Hiroshi
   Ebara, Shunsuke
   Shibuya, Kazunori
   Soeda, Jumpei
   Nakamura, Kazuhide
TI Panitumumab interaction with TAS-102 leads to combinational anticancer
   effects via blocking of EGFR-mediated tumor response to trifluridine
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE colorectal cancer; EGFR; panitumumab; phosphorylation; TAS-102;
   trifluridine
ID METASTATIC COLORECTAL-CANCER; GROWTH-FACTOR RECEPTOR; ORAL
   CHEMOTHERAPEUTIC-AGENT; THYMIDYLATE SYNTHASE; GASTROINTESTINAL
   MALIGNANCIES; ANTITUMOR-ACTIVITY; TARGETED THERAPY; CELLS; DNA;
   INHIBITION
AB Panitumumab is a monoclonal antibody developed against the human epidermal growth factor receptor (EGFR). TAS-102 is a novel chemotherapeutic agent containing trifluridine (FTD) as the active cytotoxic component. Both panitumumab and TAS-102 have been approved for the treatment of metastatic colorectal cancer. In this study, we revealed the mechanism underlying the anticancer effects of panitumumab/TAS-102 combination using preclinical models. Panitumumab/FTD cotreatment showed additive antiproliferative effects in LIM1215 and synergistic antiproliferative effects in SW48 colon cancer cells. Consistent with the in vitro effects, panitumumab/TAS-102 combination caused tumor regression in LIM1215 and COL-01-JCK colon cancer patient-derived xenograft models. In LIM1215 cells, FTD induced extracellular signal-regulated kinase (ERK)/protein kinase B (AKT)/signal transducer and activator of transcription 3 (STAT3) phosphorylation and subsequent serine/threonine phosphorylation of EGFR, while it had no effects on EGFR tyrosine phosphorylation. Panitumumab and the tyrosine kinase inhibitor erlotinib reduced the basal level of EGFR tyrosine phosphorylation and reversed FTD-induced ERK/AKT/STAT3 and EGFR serine/threonine phosphorylation. These results suggested that FTD in combination with the basal activity of EGFR tyrosine kinase induced downstream prosurvival signaling through ERK/AKT/STAT3 phosphorylation. Collectively, we propose that panitumumab interacts with FTD by targeting EGFR-mediated adaptive responses, thereby exerting anticancer effects when used in combination with TAS-102. These preclinical findings provide a compelling rationale for evaluating the combination of anti-EGFR antibodies with TAS-102 against metastatic colorectal cancer.
C1 [Baba, Yuji; Tamura, Toshiya; Satoh, Yoshihiko; Ebara, Shunsuke; Nakamura, Kazuhide] Takeda Pharmaceut Co Ltd, Div Pharmaceut Res, Oncol Drug Discovery Unit, 26-1,Muraoka Higashi 2 Chome, Fujisawa, Kanagawa 2518555, Japan.
   [Gotou, Masamitsu; Sawada, Hiroshi] Takeda Pharmaceut Co Ltd, Div Pharmaceut Res, Integrated Technol Res Labs, Fujisawa, Kanagawa, Japan.
   [Shibuya, Kazunori; Soeda, Jumpei] Takeda Pharmaceut Co Ltd, Med Affairs Dept, Tokyo, Japan.
C3 Takeda Pharmaceutical Company Ltd; Takeda Pharmaceutical Company Ltd;
   Takeda Pharmaceutical Company Ltd
RP Nakamura, K (corresponding author), Takeda Pharmaceut Co Ltd, Div Pharmaceut Res, Oncol Drug Discovery Unit, 26-1,Muraoka Higashi 2 Chome, Fujisawa, Kanagawa 2518555, Japan.; Soeda, J (corresponding author), Takeda Pharmaceut Co Ltd, Med Affairs Dept, Japan Oncol Business Unit, Tokyo, Japan.
EM jumpei.soeda@takeda.com; kazuhide.nakamura@takeda.com
RI Soeda, Jumpei/JAC-0196-2023
OI Shibuya, Kazunori/0000-0003-3606-309X; Nakamura,
   Kazuhide/0000-0002-5155-1932; Soeda, Junpei/0000-0003-3753-0999
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NR 48
TC 19
Z9 19
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1878-0261
J9 MOL ONCOL
JI Mol. Oncol.
PD AUG
PY 2017
VL 11
IS 8
BP 1065
EP 1077
DI 10.1002/1878-0261.12074
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FC1YL
UT WOS:000406633900012
PM 28486761
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lim, ZF
   Ma, PC
AF Lim, Zuan-Fu
   Ma, Patrick C.
TI Emerging insights of tumor heterogeneity and drug resistance mechanisms
   in lung cancer targeted therapy
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Review
DE Tumor heterogeneity; Acquired drug resistance; Adaptive evolution;
   Minimal residual disease
ID TYROSINE KINASE INHIBITOR; DABRAFENIB PLUS TRAMETINIB; TO-MESENCHYMAL
   TRANSITION; MINIMAL RESIDUAL DISEASE; BRAF-MUTANT MELANOMA; EGFR T790M
   MUTATION; RANDOMIZED PHASE-II; ACQUIRED-RESISTANCE; OPEN-LABEL;
   COLORECTAL-CANCER
AB The biggest hurdle to targeted cancer therapy is the inevitable emergence of drug resistance. Tumor cells employ different mechanisms to resist the targeting agent. Most commonly in EGFR-mutant non-small cell lung cancer, secondary resistance mutations on the target kinase domain emerge to diminish the binding affinity of first- and second-generation inhibitors. Other alternative resistance mechanisms include activating complementary bypass pathways and phenotypic transformation. Sequential monotherapies promise to temporarily address the problem of acquired drug resistance, but evidently are limited by the tumor cells' ability to adapt and evolve new resistance mechanisms to persist in the drug environment. Recent studies have nominated a model of drug resistance and tumor progression under targeted therapy as a result of a small subpopulation of cells being able to endure the drug (minimal residual disease cells) and eventually develop further mutations that allow them to regrow and become the dominant population in the therapy-resistant tumor. This subpopulation of cells appears to have developed through a subclonal event, resulting in driver mutations different from the driver mutation that is tumor-initiating in the most common ancestor. As such, an understanding of intratumoral heterogeneity-the driving force behind minimal residual disease-is vital for the identification of resistance drivers that results from branching evolution. Currently available methods allow for a more comprehensive and holistic analysis of tumor heterogeneity in that issues associated with spatial and temporal heterogeneity can now be properly addressed. This review provides some background regarding intratumoral heterogeneity and how it leads to incomplete molecular response to targeted therapies, and proposes the use of single-cell methods, sequential liquid biopsy, and multiregion sequencing to discover the link between intratumoral heterogeneity and early adaptive drug resistance. In summary, minimal residual disease as a result of intratumoral heterogeneity is the earliest form of acquired drug resistance. Emerging technologies such as liquid biopsy and single-cell methods allow for studying targetable drivers of minimal residual disease and contribute to preemptive combinatorial targeting of both drivers of the tumor and its minimal residual disease cells.
C1 [Lim, Zuan-Fu] West Virginia Univ, WVU Canc Inst, Morgantown, WV 26506 USA.
   [Lim, Zuan-Fu] West Virginia Univ, Robert C Byrd Hlth Sci Ctr, Canc Cell Biol Program, Morgantown, WV 26506 USA.
   [Lim, Zuan-Fu; Ma, Patrick C.] Penn State Univ, Penn State Hlth Milton S Hershey Med Ctr, Penn State Canc Inst, POB 850,Mail Code CH46,500 Univ Dr, Hershey, PA 17033 USA.
C3 West Virginia University; West Virginia University; Pennsylvania
   Commonwealth System of Higher Education (PCSHE); Pennsylvania State
   University; Penn State Health
RP Ma, PC (corresponding author), Penn State Univ, Penn State Hlth Milton S Hershey Med Ctr, Penn State Canc Inst, POB 850,Mail Code CH46,500 Univ Dr, Hershey, PA 17033 USA.
EM patrickma@pennstatehealth.psu.edu
FU WVU Cancer Institute, West Virginia University; Penn State Cancer
   Institute, Penn State Health Milton S. Hershey Medical Center, Penn
   State University
FX This work is supported by the WVU Cancer Institute, West Virginia
   University and Penn State Cancer Institute, Penn State Health Milton S.
   Hershey Medical Center, Penn State University.
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NR 169
TC 340
Z9 381
U1 14
U2 102
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 9
PY 2019
VL 12
IS 1
AR 134
DI 10.1186/s13045-019-0818-2
PG 18
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA KH8QQ
UT WOS:000510915900002
PM 31815659
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Morgenstern-Kaplan, D
   Kareff, SA
   Trabolsi, A
   Rodriguez, E
   Krause, H
   Ribeiro, JR
   Tan, H
   Antonarakis, ES
   Lou, EM
   Nagasaka, M
   Algaze, S
   Lenz, HJ
   Liu, S
   Halmos, B
   Hoon, DSB
   Seeber, A
   Ma, PC
   El-Deiry, WS
   Vanderwalde, AM
   Lopes, G
AF Morgenstern-Kaplan, Dan
   Kareff, Samuel A.
   Trabolsi, Asaad
   Rodriguez, Estelamari
   Krause, Harris
   Ribeiro, Jennifer R.
   Tan, Heng
   Antonarakis, Emmanuel S.
   Lou, Emil
   Nagasaka, Misako
   Algaze, Sandra
   Lenz, Heinz-Josef
   Liu, Stephen, V
   Halmos, Balazs
   Hoon, Dave S. B.
   Seeber, Andreas
   Ma, Patrick C.
   El-Deiry, Wafik S.
   Vanderwalde, Ari M.
   Lopes, Gilberto
TI Genomic, immunologic, and prognostic associations of TROP2 (TACSTD2)
   expression in solid tumors
SO ONCOLOGIST
LA English
DT Article
DE TROP2; precision oncology; targeted therapy; tumor genetics
ID PEMBROLIZUMAB PLUS CHEMOTHERAPY; NEGATIVE BREAST-CANCER; SACITUZUMAB
   GOVITECAN; MOLECULAR SUBTYPES; IMMUNE; ANTIBODY; THERAPY
AB Background TROP2 (TACSTD2) expression is associated with decreased overall survival (OS) in some solid tumors, and the TROP2-targeting antibody-drug conjugate (ADC) sacituzumab govitecan has been approved in breast and urothelial carcinomas. We aimed to explore the multi-omic landscape associated with TACSTD2 gene expression in various solid tumors to identify patients most likely to benefit from this approach.Methods Breast (N = 11 246), colorectal (N = 15 425), hepatocellular (N = 433), pancreatic (N = 5488), and urothelial (N = 4125) tumors were stratified into quartiles by TACSTD2 gene expression, analyzed by next-generation DNA sequencing, whole transcriptome sequencing, and immunohistochemistry at Caris Life Sciences (Phoenix, AZ). Survival data were obtained from insurance claims, and Kaplan-Meier estimates were calculated for molecularly defined cohorts.Results Several pathogenic mutations were associated with TACSTD2-high tumors, including TP53 in breast, colorectal (CRC), pancreatic, and hepatocellular cancers; KRAS in pancreatic and CRC cancers; ARID1A and FGFR3 in urothelial cancer; and CTNNB1 in hepatocellular cancer. TACSTD2-low breast tumors were enriched for copy number amplifications in CCND1 and FGF/R family member genes. TACSTD2 high was generally associated with more immune cell infiltration and greater T-cell inflammation scores. Patients with TACSTD2-high breast, CRC, and pancreatic cancers demonstrated a significantly shorter OS than TACSTD2-low tumors. This was restricted to CRC with microsatellite stable tumors and patients with pancreatic cancer with KRAS-mutant tumors. Patients with breast cancer with TACSTD2-high tumors also experienced significantly worse OS following immune checkpoint inhibitors.Conclusions TACSTD2 expression is associated with key driver alterations and a more active immune microenvironment, suggesting possible combinatorial strategies with TROP2-targeting ADCs plus immunotherapy in various solid tumors.
   The TROP2-targeting antibody-drug conjugate sacituzumab govitecan has been approved in breast and urothelial carcinomas. This study explored the multi-omic landscape associated with TACSTD2 gene expression in various solid tumors to identify patients most likely to benefit from this approach.
C1 [Morgenstern-Kaplan, Dan; Kareff, Samuel A.; Trabolsi, Asaad; Rodriguez, Estelamari; Tan, Heng; Lopes, Gilberto] Univ Miami, Jackson Mem Hosp, Dept Med, Div Med Oncol,Sylvester Comprehens Canc Ctr, Miami, FL 33131 USA.
   [Krause, Harris; Ribeiro, Jennifer R.; Vanderwalde, Ari M.] Caris Life Sci, Phoenix, AZ 85040 USA.
   [Antonarakis, Emmanuel S.; Lou, Emil] Univ Minnesota, Masonic Canc Ctr, Minneapolis, MN 55455 USA.
   [Nagasaka, Misako] Univ Calif Irvine, Sch Med, Orange, CA 92617 USA.
   [Algaze, Sandra; Lenz, Heinz-Josef] Univ Southern Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
   [Liu, Stephen, V] Georgetown Univ, Washington, DC 20007 USA.
   [Halmos, Balazs] Montefiore Einstein Comprehens Canc Ctr, Bronx, NY 10461 USA.
   [Hoon, Dave S. B.] Providence Hlth Syst, St Johns Canc Inst, Santa Monica, CA 90404 USA.
   [Seeber, Andreas] Innsbruck Med Univ, A-6020 Innsbruck, Austria.
   [Ma, Patrick C.] Penn State Canc Inst, Hershey, PA 17033 USA.
   [El-Deiry, Wafik S.] Brown Univ, Warren Alpert Med Sch, Providence, RI 02912 USA.
C3 University of Miami; University of Minnesota System; University of
   Minnesota Twin Cities; University of California System; University of
   California Irvine; University of Southern California; Georgetown
   University; Medical University of Innsbruck; Pennsylvania Commonwealth
   System of Higher Education (PCSHE); Pennsylvania State University; Penn
   State Health; Brown University
RP Lopes, G (corresponding author), Univ Miami, Sylvester Comprehens Canc Ctr, 1240 NW 14th St,Suite 650L, Miami, FL 33131 USA.
EM glopes@med.miami.edu
RI Hoon, Dave/C-7146-2018; Antonarakis, Emmanuel/E-4550-2011; Kareff,
   Samuel/GRF-1664-2022; Morgenstern-Kaplan, Dan/F-8651-2018
OI Morgenstern-Kaplan, Dan/0000-0002-9031-2256; Lou,
   Emil/0000-0002-1607-1386; Ribeiro, Jennifer/0000-0002-1685-8568; Krause,
   Harris/0000-0003-3481-8364; trabolsi, asaad/0000-0002-2479-1797;
   Antonarakis, Emmanuel Stylianos/0000-0003-3531-3851
FU NCI [P30 CA077598]
FX E.S.A. is partially funded by NCI grant (P30 CA077598).
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NR 41
TC 0
Z9 0
U1 6
U2 6
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 JUL 10
PY 2024
VL 29
IS 11
BP e1480
EP e1491
DI 10.1093/oncolo/oyae168
EA JUL 2024
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA L3X0K
UT WOS:001268437800001
PM 38986529
OA gold
DA 2025-01-04
ER

PT J
AU Sabbadini, F
   Bertolini, M
   De Matteis, S
   Mangiameli, D
   Contarelli, S
   Pietrobono, S
   Melisi, D
AF Sabbadini, Fabio
   Bertolini, Monica
   De Matteis, Serena
   Mangiameli, Domenico
   Contarelli, Serena
   Pietrobono, Silvia
   Melisi, Davide
TI The Multifaceted Role of TGF-β in Gastrointestinal Tumors
SO CANCERS
LA English
DT Review
DE TGF-beta; gastrointestinal tumors; EMT; targeted therapy; immune
   plasticity
ID GROWTH-FACTOR-BETA; REGULATORY T-CELLS; EPITHELIAL-MESENCHYMAL
   TRANSITION; LATENT TRANSFORMING GROWTH-FACTOR-BETA-1; BETA/SMAD
   SIGNALING PATHWAY; COLON-CANCER CELLS; PANCREATIC-CANCER;
   GASTRIC-CANCER; COLORECTAL-CANCER; EXTRACELLULAR-MATRIX
AB Simple Summary: The transforming growth factor beta signaling pathway elicits a broad range of physiological re-sponses, and its misregulation has been related to cancer. The secreted cytokine TGF beta exerts a tumor-suppressive effect that counteracts malignant transformation. However, once tumor has developed, TGF beta can support tumor progression regulating epithelial to mesenchymal transition, invasion and metastasis, stimulating fibrosis, angiogenesis and immune suppression. Here we review the dichotomous role of TGF-beta in the progression of gastrointestinal tumors, as well as its intricate crosstalk with other signaling pathways. We also discuss about the therapeutic strate-gies that are currently explored in clinical trials to counteract TGF-beta functions.
   Transforming growth factor-beta (TGF-beta) is a secreted cytokine that signals via serine/threonine kinase receptors and SMAD effectors. Although TGF-beta acts as a tumor suppressor during the early stages of tumorigenesis, it supports tumor progression in advanced stages. Indeed, TGF-beta can modulate the tumor microenvironment by modifying the extracellular matrix and by sustaining a paracrine interaction between neighboring cells. Due to its critical role in cancer development and progression, a wide range of molecules targeting the TGF-beta signaling pathway are currently under active clinical development in different diseases. Here, we focused on the role of TGF-beta in modulating different pathological processes with a particular emphasis on gastrointestinal tumors.
C1 [Sabbadini, Fabio; Bertolini, Monica; De Matteis, Serena; Mangiameli, Domenico; Contarelli, Serena; Pietrobono, Silvia; Melisi, Davide] Univ Verona, Dept Med, Digest Mol Clin Oncol Res Unit, I-37134 Verona, Italy.
   [De Matteis, Serena] Univ Bologna, Dept Expt Diagnost & Specialty Med, AlmaMater Studiorum, I-40126 Bologna, Italy.
   [Melisi, Davide] Azienda Osped Univ Integrata Verona, Expt Canc Med Unit, I-37134 Verona, Italy.
C3 University of Verona; University of Bologna; University of Verona;
   Azienda Ospedaliera Universitaria Integrata Verona
RP Melisi, D (corresponding author), Univ Verona, Dept Med, Digest Mol Clin Oncol Res Unit, I-37134 Verona, Italy.; Melisi, D (corresponding author), Azienda Osped Univ Integrata Verona, Expt Canc Med Unit, I-37134 Verona, Italy.
EM fabio.sabbadini@univr.it; monica.bertolini@univr.it;
   serena.dematteis2@unibo.it; domenico.mangiameli@univr.it;
   serena.contarelli@univr.it; silvia.pietrobono@ittumori.it;
   davide.melisi@univr.it
RI Mangiameli, Domenico/AAD-1216-2022; De Matteis, Serena/GRY-4379-2022;
   Melisi, Davide/K-7947-2016; Contarelli, Serena/AAC-6155-2022;
   Pietrobono, Silvia/K-3932-2016
OI Bertolini, Monica/0000-0001-9430-8871; Contarelli,
   Serena/0000-0002-7033-7923; Sabbadini, Fabio/0000-0002-1122-3125;
   Pietrobono, Silvia/0000-0002-5544-7286; Mangiameli,
   Domenico/0000-0003-2577-1277
FU Associazione Italiana per la Ricerca sul Cancro (AIRC) [19111, 23719,
   12182]; post-doctoral AIRC fellowships for Italy [23920, 21168]; Italian
   Ministry of Health [GR-2016-02361134]; "Nastro Viola" association of
   patients' donations; "Voglio il Massimo" association of patients'
   donations
FX This work was partially supported by Associazione Italiana per la
   Ricerca sul Cancro (AIRC, grant numbers 19111, 23719, and 5 x 1000 Grant
   number 12182), by Ricerca Finalizzata 2016 (Italian Ministry of Health,
   grant number GR-2016-02361134), and by "Nastro Viola" and "Voglio il
   Massimo" associations of patients' donations to D.M. (Davide Melisi),
   S.C. and S.P. were supported by post-doctoral AIRC fellowships for Italy
   (projects nr. 23920 and 21168, respectively).
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NR 228
TC 22
Z9 24
U1 0
U2 12
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD AUG
PY 2021
VL 13
IS 16
AR 3960
DI 10.3390/cancers13163960
PG 24
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UG0OE
UT WOS:000688962200001
PM 34439114
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ding, YB
   Zhou, RH
   Shi, GW
   Jiang, YK
   Li, ZF
   Xu, XL
   Ma, JB
   Huang, JN
   Fu, CJ
   Zhou, HC
   Wang, HF
   Li, JX
   Dong, ZY
   Yu, QL
   Jiang, KX
   An, YH
   Liu, YW
   Li, YL
   Yu, L
   Li, ZJ
   Zhang, XD
   Wang, JG
AF Ding, Youbin
   Zhou, Runhua
   Shi, Guangwei
   Jiang, Yuke
   Li, Zhifen
   Xu, Xiaolong
   Ma, Jingbo
   Huang, Jingnan
   Fu, Chunjin
   Zhou, Hongchao
   Wang, Huifang
   Li, Jiexuan
   Dong, Zhiyu
   Yu, Qingling
   Jiang, Kexin
   An, Yehai
   Liu, Yawei
   Li, Yilei
   Yu, Le
   Li, Zhijie
   Zhang, Xiaodong
   Wang, Jigang
TI Cadherin 17 Nanobody-Mediated Near-Infrared-II Fluorescence
   Imaging-Guided Surgery and Immunotoxin Delivery for Colorectal Cancer
SO BIOMATERIALS RESEARCH
LA English
DT Article
ID 5-FLUOROURACIL
AB Surgery and targeted therapy are of equal importance for colorectal cancer (CRC) treatment. However, complete CRC tumor resection remains challenging, and new targeted agents are also needed for efficient CRC treatment. Cadherin 17 (CDH17) is a membrane protein that is highly expressed in CRC and, therefore, is an ideal target for imaging-guided surgery and therapeutics. This study utilizes CDH17 nanobody (E8Nb) with the near-infrared (NIR) fluorescent dye IRDye800CW to construct a NIR-II fluorescent probe, E8-Nb-IR800CW, and a Pseudomonas exotoxin (PE)-based immunotoxin, E8-Nb-PE38, to evaluate their performance for CRC imaging, imaging-guided precise tumor excision, and antitumor effects. Our results show that E8-Nb-IR800CW efficiently recognizes CDH17 in CRC cells and tumor tissues, produces highquality NIR-II images for CRC tumors, and enables precise tumor removal guided by NIR-II imaging. Additionally, fluorescent imaging confirms the targeting ability and specificity of the immunotoxin toward CDH17-positive tumors, providing the direct visible evidence for immunotoxin therapy. E8-Nb-PE38 immunotoxin markedly delays the growth of CRC through the induction of apoptosis and immunogenic cell death (ICD) in multiple CRC tumor models. Furthermore, E8-Nb-PE38 combined with 5-FU exerts synergistically antitumor effects and extends survival. This study highlights CDH17 as a promising target for CRC imaging, imaging-guided surgery, and drug delivery. Nanobodies targeting CDH17 hold great potential to construct NIR-II fluorescent probes for surgery navigation, and PE-based toxins fused with CDH17 nanobodies represent a novel therapeutic strategy for CRC treatment. Further investigation is warranted to validate these findings for potential clinical translation.
C1 [Ding, Youbin; Zhang, Xiaodong; Wang, Jigang] Southern Med Univ, Dept Med Imaging, Acad Orthoped Guangdong Prov, Affiliated Hosp 3, Guangzhou 510515, Peoples R China.
   [Ding, Youbin; Shi, Guangwei; Jiang, Yuke; Xu, Xiaolong; Ma, Jingbo; Huang, Jingnan; Fu, Chunjin; Zhou, Hongchao; Wang, Huifang; Li, Jiexuan; Dong, Zhiyu; Li, Zhijie; Wang, Jigang] Shenzhen Peoples Hosp, Shenzhen Clin Res Ctr Geriatr, Dept Geriatr, Shenzhen 518020, Guangdong, Peoples R China.
   [Ding, Youbin; Zhou, Runhua; Jiang, Yuke; Li, Zhifen; Xu, Xiaolong; Ma, Jingbo; Huang, Jingnan; Fu, Chunjin; Zhou, Hongchao; Wang, Huifang; Li, Jiexuan; Dong, Zhiyu; Li, Zhijie; Wang, Jigang] Jinan Univ, Southern Univ Sci & Technol, Affiliated Hosp 1, Clin Med Coll, Shenzhen 518020, Guangdong, Peoples R China.
   [Zhou, Runhua; An, Yehai; Yu, Le; Wang, Jigang] Southern Med Univ, NMPA Key Lab Res & Evaluat Drug Metab, Guangzhou 510515, Peoples R China.
   [Zhou, Runhua; An, Yehai; Wang, Jigang] Southern Med Univ, Guangdong Prov Key Lab New Drug Screening, R China, Guangzhou 510515, Peoples R China.
   [Zhou, Runhua; An, Yehai; Wang, Jigang] Southern Med Univ, Sch Pharmaceut Sci, Guangdong Hongkong Macao Joint Lab New Drug Screen, Guangzhou 510515, Guangdong, Peoples R China.
   [Zhou, Runhua; Li, Yilei] Southern Med Univ, Nanfang Hosp, Dept Pharm, Guangzhou 510515, Peoples R China.
   [Shi, Guangwei; Liu, Yawei] Southern Med Univ, Peoples Hosp Shunde Foshan 1, Dept Neurosurg, Guangzhou 510515, Peoples R China.
   [Shi, Guangwei; Liu, Yawei] Southern Med Univ, Shunde Hosp, Peoples Hosp Shunde Foshan 1, Med Res Ctr, Guangzhou 510515, Peoples R China.
   [Li, Zhifen] Shanxi Datong Univ, Sch Chem & Chem Engn, Datong 037009, Shanxi, Peoples R China.
   [Wang, Jigang] China Acad Chinese Med Sci, Artemisinin Res Ctr, State Key Lab Qual Ensurance & Sustainable Use Dao, Beijing 100700, Peoples R China.
   [Wang, Jigang] China Acad Chinese Med Sci, Inst Chinese Mat Med, Beijing 100700, Peoples R China.
   [Wang, Jigang] Henan Univ, Sch Pharm, State Key Lab Antiviral Drugs, Kaifeng 475004, Henan, Peoples R China.
   [Wang, Jigang] Southwest Med Univ, Dept Oncol, Affiliated Hosp, Luzhou 646000, Sichuan, Peoples R China.
C3 Southern Medical University - China; Jinan University; Jinan University;
   Southern University of Science & Technology; Southern Medical University
   - China; Southern Medical University - China; Southern Medical
   University - China; Southern Medical University - China; Southern
   Medical University - China; Southern Medical University - China; Shanxi
   Datong University; China Academy of Chinese Medical Sciences; China
   Academy of Chinese Medical Sciences; Institute of Chinese Materia
   Medica, CACMS; Henan University; Southwest Medical University
RP Zhang, XD; Wang, JG (corresponding author), Southern Med Univ, Dept Med Imaging, Acad Orthoped Guangdong Prov, Affiliated Hosp 3, Guangzhou 510515, Peoples R China.; Li, ZJ; Wang, JG (corresponding author), Shenzhen Peoples Hosp, Shenzhen Clin Res Ctr Geriatr, Dept Geriatr, Shenzhen 518020, Guangdong, Peoples R China.; Yu, L; Wang, JG (corresponding author), Southern Med Univ, NMPA Key Lab Res & Evaluat Drug Metab, Guangzhou 510515, Peoples R China.; Wang, JG (corresponding author), China Acad Chinese Med Sci, Artemisinin Res Ctr, State Key Lab Qual Ensurance & Sustainable Use Dao, Beijing 100700, Peoples R China.; Wang, JG (corresponding author), China Acad Chinese Med Sci, Inst Chinese Mat Med, Beijing 100700, Peoples R China.; Wang, JG (corresponding author), Henan Univ, Sch Pharm, State Key Lab Antiviral Drugs, Kaifeng 475004, Henan, Peoples R China.; Wang, JG (corresponding author), Southwest Med Univ, Dept Oncol, Affiliated Hosp, Luzhou 646000, Sichuan, Peoples R China.
EM yule0423@gmail.com; li.zhijie@szhospital.com; ddautumn@126.com;
   jgwang@icmm.ac.cn
RI LI, ZHIJIE/HJG-6926-2022; Ding, youbin/KOD-0875-2024; wang,
   jigang/HJA-0506-2022
OI yehai, An/0009-0005-9373-0508
FU Guang Dong Basic and Applied Basic Research Foundation [2024A1515010352,
   2022A1515110745, 2021A1515012164]; President Foun-dation of the Third
   Affiliated Hospital of Southern Medical University [YM2021012]; National
   Key Research Program of China [2020YFA0908000, 2022YFC2303600]; National
   Natural Science Foundation of China [82373775, 32200540]; International
   Science and Technology Cooperation for Shenzhen Technology Innovation
   Plan [GJHZ20200731095411034]; Innovation Team and Talents Cultivation
   Program of the National Administration of Traditional Chinese Medicine
   [ZYYCXTD-C-202002]; Science and Technology Foundation of Shenzhen
   (Shenzhen Clinical Medical Research Center for Geriatric Diseases);
   Shenzhen Medical Research Fund of Shenzhen Medical Academy of Research
   and Translation [B2302051]; Shenzhen Science and Technology Innovation
   Committee (SZSTI) [RCYX20221008092950121]; CACMS Innovation Fund
   [CI2023E002, CI2021A05101, CI2021A05104]; Scientific and Technological
   Innovation Project of China Academy of Chinese Medical Sciences
   [CI2023D003, CI2023D008, CI2021B014]; National Key R&D Program of China
   [2023YFE0204500]; Fundamental Research Funds for the Central public
   welfare research institutes [ZZ16-ND-10-23, ZZ15-ND-10, ZZ14-ND-010,
   ZZ14-FL-002, ZZ14-YQ-050, ZZ14-YQ-051]; Shenzhen Fund for Guangdong
   Provincial High-level Clinical Key Specialties [SZGSP001]; Shenzhen
   Governmental Sustainable Development Fund [KCXFZ-20201221173612034];
   Shenzhen key Laboratory of Kidney Diseases [ZDSYS201504301616234];
   Natural Science Foundation of Shenzhen City, China
   [KCXFZ20201221173600001]
FX This work was supported by the Guang Dong Basic and Applied Basic
   Research Foundation (2024A1515010352, 2022A1515110745, and
   2021A1515012164) , the President Foun-dation of the Third Affiliated
   Hospital of Southern Medical University (YM2021012) , the National Key
   Research Program of China (2020YFA0908000 and 2022YFC2303600) , the
   HUILAN Public Welfare, the National Natural Science Foundation of China
   (82373775 and 32200540) , the International Science and Technology
   Cooperation for Shenzhen Technology Innovation Plan
   (GJHZ20200731095411034) , the Innovation Team and Talents Cultivation
   Program of the National Administration of Traditional Chinese Medicine
   (ZYYCXTD-C-202002) , the Science and Technology Foundation of Shenzhen
   (Shenzhen Clinical Medical Research Center for Geriatric Diseases) , the
   Shenzhen Medical Research Fund of Shenzhen Medical Academy of Research
   and Translation (B2302051) , the Shenzhen Science and Technology
   Innovation Committee (SZSTI) (RCYX20221008092950121) , the CACMS
   Innovation Fund (CI2023E002, CI2021A05101, and CI2021A05104) , the
   Scientific and Technological Innovation Project of China Academy of
   Chinese Medical Sciences (CI2023D003, CI2023D008, and CI2021B014) , the
   Key Special Project of "Strategic Science and Technology Innovation
   Cooperation" from National Key R&D Program of China (2023YFE0204500) ,
   the Fundamental Research Funds for the Central public welfare research
   institutes (ZZ16-ND-10-23, ZZ15-ND-10, ZZ14-ND-010, ZZ14-FL-002,
   ZZ14-YQ-050, and ZZ14-YQ-051) , the Shenzhen Fund for Guangdong
   Provincial High-level Clinical Key Specialties (SZGSP001) , the Shenzhen
   Governmental Sustainable Development Fund (KCXFZ-20201221173612034) ,
   the Shenzhen key Laboratory of Kidney Diseases (ZDSYS201504301616234) ,
   and the Natural Science Foundation of Shenzhen City, China
   (KCXFZ20201221173600001) .
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NR 48
TC 0
Z9 0
U1 9
U2 9
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 JUN 21
PY 2024
VL 28
AR 0041
DI 10.34133/bmr.0041
PG 18
WC Engineering, Biomedical; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Materials Science
GA WC7J4
UT WOS:001252732700001
PM 38911825
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Bakrim, S
   El Hachlafi, N
   Khalid, A
   Abdalla, AN
   El Omari, N
   Aboulaghras, S
   Sakran, AM
   Goh, KW
   Ming, LC
   Razi, P
   Bouyahya, A
AF Bakrim, Saad
   El Hachlafi, Naoufal
   Khalid, Asaad
   Abdalla, Ashraf N.
   El Omari, Nasreddine
   Aboulaghras, Sara
   Sakran, Ashraf M.
   Goh, Khang Wen
   Ming, Long Chiau
   Razi, Pakhrur
   Bouyahya, Abdelhakim
TI Recent advances and molecular mechanisms of TGF-β signaling in
   colorectal cancer, with focus on bioactive compounds targeting
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Colorectal cancer; TGF-/3 signaling; Cancer biomarker; Bioactive
   compounds; Malignancy; Targeted therapy; Human and disease
ID GROWTH-FACTOR-BETA; ULTRASOUND-ASSISTED EXTRACTION; URSOLIC ACID;
   OLEANOLIC ACID; TANSHINONE-IIA; LIQUID-CHROMATOGRAPHY;
   SALVIA-MILTIORRHIZA; RP-HPLC; MAGNOLIA-OFFICINALIS; MEDITERRANEAN DIET
AB Colorectal cancer (CRC) is one of the most significant forms of human cancer. It is characterized by its heterogeneity because several molecular factors are involved in contiguity and can link it to others without having a linear correlation. Among the factors influencing tumor transformation in CRC, transforming growth factor-beta (TGF-/3) plays a key promoter role. This factor is associated with human colorectal tumors with a very high prognosis: it increases the survival, invasion, and metastasis of CRC cells, thus functioning as an oncogene. The inhibition of this factor can constitute a major therapeutic route for CRC treatment. Various chemical drugs including synthetic molecules and biotherapies have been developed as TGF-/3 inhibitors. Moreover, the scientific community has recently shown a major interest in screening natural drugs inhibiting TGF-/3 in CRC. In this context, we carried out this review article using computerized databases, such as PubMed, Google Scholar, Springer Link, Science Direct, Cochrane Library, Embase, Web of Science, and Scopus, to highlight the molecular mechanism of TGF-/3 in CRC induction and progression and current advances in the pharmacodynamic effects of natural bioactive substances targeting TGF-/3 in CRC.
C1 [Bakrim, Saad] Ibn Zohr Univ, Polydisciplinary Fac Taroudant, Geobioenvironment Engn & Innovat Lab, Mol Engn Biotechnol & Innovat Team, Agadir, Morocco.
   [El Hachlafi, Naoufal] Sidi Mohmed Ben Abdellah Univ, Sci & Technol Fac, Microbial Biotechnol & Bioact Mol Lab, Imouzzer Rd,POB 2002, Fes, Morocco.
   [Khalid, Asaad] Jazan Univ, Hlth Res Ctr, POB 114, Jazan 45142, Saudi Arabia.
   [Abdalla, Ashraf N.] Umm Al Qura Univ, Coll Pharm, Dept Pharmacol & Toxicol, Al Abidiyya 21955, Makkah, Saudi Arabia.
   [El Omari, Nasreddine] High Inst Nursing Profess & Hlth Tech Tetouan, Tetouan, Morocco.
   [Aboulaghras, Sara; Bouyahya, Abdelhakim] Mohammed V Univ Rabat, Fac Sci, Dept Biol, Lab Human Pathol Biol, Rabat 10106, Morocco.
   [Sakran, Ashraf M.] Umm Alqura Univ, Fac Med, Dept Anat, Mecca 21955, Saudi Arabia.
   [Goh, Khang Wen] INTI Int Univ, Fac Data Sci & Informat Technol, Nilai, Malaysia.
   [Ming, Long Chiau] Sunway Univ, Sch Med & Life Sci, Sunway City, Malaysia.
   [Razi, Pakhrur] Univ Negeri Padang, Ctr Disaster Monitoring & Earth Observat, Padang, Indonesia.
C3 Ibn Zohr University of Agadir; Sidi Mohamed Ben Abdellah University of
   Fez; Jazan University; Umm Al Qura University; Mohammed V University in
   Rabat; Umm Al Qura University; INTI International University; Sunway
   University; Universitas Negeri Padang
RP Khalid, A (corresponding author), Jazan Univ, Hlth Res Ctr, POB 114, Jazan 45142, Saudi Arabia.; Ming, LC (corresponding author), Sunway Univ, Sch Med & Life Sci, Sunway City, Malaysia.; Razi, P (corresponding author), Univ Negeri Padang, Ctr Disaster Monitoring & Earth Observat, Padang, Indonesia.
EM akahmed@jazanu.edu.sa; ming.long@bath.edu; fhrrazi@fmipa.unp.ac.id
RI KHALID, ASAAD/HJH-6413-2023; Goh, Khang Wen/HCH-4693-2022; El Omari,
   Nasreddine/ABG-6138-2021; El Hachlafi, Naoufal/AAI-2021-2021; BAKRIM,
   SAAD/HPC-6347-2023; Ming, Long/JPA-6335-2023
OI Ahmed, Asaad Khalid/0000-0001-8734-2588
FU Deanship of Graduate Studies and Scientific Research, Jazan University,
   Saudi Arabia [RG24-L05]
FX This research is funded by the Deanship of Graduate Studies and
   Scientific Research, Jazan University, Saudi Arabia (Project Number:
   RG24-L05)
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NR 147
TC 1
Z9 1
U1 2
U2 2
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 2024
VL 177
AR 116886
DI 10.1016/j.biopha.2024.116886
EA JUL 2024
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA ZW2A7
UT WOS:001278246400001
PM 38945700
OA gold
DA 2025-01-04
ER

PT J
AU Kim, SY
   Oh, SO
   Kim, K
   Lee, J
   Kang, S
   Kim, KM
   Lee, W
   Kim, ST
   Nam, DN
AF Kim, Sun Young
   Oh, Seiyoon Oh
   Kim, Kyung
   Lee, Jeeyun
   Kang, SoYoung
   Kim, Kyoung-Mee
   Lee, WooYong
   Kim, Seung Tae
   Nam, Dohyun Nam
TI NCOA4-RET fusion in colorectal cancer: Therapeutic challenge using
   patient-derived tumor cell lines
SO JOURNAL OF CANCER
LA English
DT Article
DE Colorectal cancer; RET fusion; vandetanib
ID LUNG-CANCER; RET PROTOONCOGENE; PLUS IRINOTECAN; OPEN-LABEL;
   IDENTIFICATION; CABOZANTINIB; PHASE-2; TRIAL; ALK
AB The RET fusion is considered as the potential novel target in solid tumors. However, RET fusion is not well yet identified in colorectal cancer (CRC), and the effect of RET kinase inhibitor is also not evaluated in CRC with RET fusion. We established patient-derived tumor cells (PDCs) with RET fusion from recurrent brain metastatic lesion that newly appeared during the surveillance for stage III CRC patient. To investigate therapeutic options to CRC patient with a RET fusion, we performed cell viability assays using the PDCs. NCOA4-RET fusion was detected by FusionPlex using the resected brain metastatic tissue of CRC patient with solitary brain metastasis and then reconfirmed by fluorescence in situ hybridization (FISH) test. We also confirmed the RET fusions by a qPCR in matched PDCs. We tested whether the PDCs from RET fusion colon cancer were sensitive to carbozantinib, sorafenib, vandetanib, and PD0331992. Cell viability assays showed that carbozantinib, sorafenib, and PD0332991 did not suppress cell viability. Only, vandetanib revealed the significant inhibitory effect in MTT proliferation assay. Next, we analyzed regulation of targeted downstream pathways upon exposure to vandetanib by immunoblot assay. In colon cancer PDCs with NCOA4-RET fusion, vandetanib potently inhibited AKT and ERK phosphorylation. This study shows that vandetanib might be one of useful treatment strategies for CRC patient with NCOA4-RET fusion. Therefore, inhibition of the RET kinase is a promising targeted therapy for cancer patients whose tumors harbor a RET rearrangement.
C1 [Kim, Sun Young; Kim, Kyung; Lee, Jeeyun; Kim, Seung Tae] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Div Hematol Oncol,Dept Med, 81 Irwon Ro, Seoul 06351, South Korea.
   [Oh, Seiyoon Oh] Cornell Univ, Coll Human Ecol, Dept Human Biol Hlth & Soc, Ithaca, NY 14850 USA.
   [Kang, SoYoung; Kim, Kyoung-Mee] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol & Translat Genom, Seoul, South Korea.
   [Lee, WooYong] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Surg, Seoul, South Korea.
   [Nam, Dohyun Nam] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Neurosurg, 81 Irwon Ro, Seoul 06351, South Korea.
C3 Sungkyunkwan University (SKKU); Samsung Medical Center; Cornell
   University; Sungkyunkwan University (SKKU); Samsung Medical Center;
   Sungkyunkwan University (SKKU); Samsung Medical Center; Sungkyunkwan
   University (SKKU); Samsung Medical Center
RP Kim, ST (corresponding author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Div Hematol Oncol,Dept Med, 81 Irwon Ro, Seoul 06351, South Korea.; Nam, DN (corresponding author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Neurosurg, 81 Irwon Ro, Seoul 06351, South Korea.
EM seungtae1.kim@samsung.com; dhns.nam@samsung.com
RI Lee, Jee/C-9646-2011; Kim, Kihyun/D-5175-2013; kim, st/O-5928-2014; Kim,
   Sung/G-4114-2014; Kim, Sun Young/O-4847-2018
OI Kim, Sun Young/0000-0002-1180-0367
FU Korean Health Technology R&D Project, Ministry of Health & Welfare,
   Republic of Korea [HI14C3418]; Basic Science Research Program through
   the National Research Foundation of Korea(NRF) - the Ministry of
   Education [2016R1A6A3A11932444]
FX This work was supported by a grant from the Korean Health Technology R&D
   Project, Ministry of Health & Welfare, Republic of Korea (HI14C3418).
   Support was also provided by a grant from Basic Science Research Program
   through the National Research Foundation of Korea(NRF) funded by the
   Ministry of Education (2016R1A6A3A11932444)
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NR 19
TC 20
Z9 21
U1 0
U2 2
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2018
VL 9
IS 17
BP 3032
EP 3037
DI 10.7150/jca.26256
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GS9CN
UT WOS:000444013500006
PM 30210625
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Park, DY
   Choi, C
   Shin, E
   Lee, JH
   Kwon, CH
   Jo, HJ
   Kim, HR
   Kim, HS
   Oh, N
   Lee, JS
   Park, OK
   Park, E
   Park, J
   Shin, JY
   Kim, JI
   Seo, JS
   Park, HD
   Park, J
AF Park, Do Youn
   Choi, Chan
   Shin, Eunji
   Lee, Jae Hyuk
   Kwon, Chae Hwa
   Jo, Hong-Jae
   Kim, Hyeong-Rok
   Kim, Hyun Sung
   Oh, Nahmgun
   Lee, Ji Shin
   Park, Ok Ku
   Park, Eok
   Park, Jonghoon
   Shin, Jong-Yeon
   Kim, Jong-Il
   Seo, Jeong-Sun
   Park, Hee Dong
   Park, Joonghoon
TI <i>NTRK1</i> fusions for the therapeutic intervention of Korean patients
   with colon cancer
SO ONCOTARGET
LA English
DT Article
DE NTRK1 fusion; Korean colon cancer; RNA-seq; predictive biomarker;
   targeted therapy
ID METASTATIC COLORECTAL-CANCER; TYROSINE KINASE INHIBITOR; CETUXIMAB PLUS
   IRINOTECAN; CELL LUNG-CANCER; RET GENE FUSION; PHASE-III TRIAL;
   DOUBLE-BLIND; BEVACIZUMAB; OXALIPLATIN; ADENOCARCINOMA
AB The identification and clinical validation of cancer driver genes are essential to accelerate the translational transition of cancer genomics, as well as to find clinically confident targets for the therapeutic intervention of cancers. Here we identified recurrent LMNA-NTRK1 and TPM3-NTRK1 fusions in Korean patients with colon cancer (3 out of 147, 2%) through next-generation RNA sequencing (RNA-seq). NTRK1 fusions were mutually exclusive oncogenic drivers of colon cancer that were accompanied with in vitro potential of colony formation and in vivo tumorigenicity comparable to KM12, a human colon cancer cell line harboring TPM3-NTRK1 fusion. NTRK1-encoded TrkA protein was prevalent in 11 out of 216 Korean (5.1%) and 28 out of 472 Chinese patients (5.9%) from independent cohorts, respectively. The expression level of TrkA was significantly correlated with NTRK1 fusion (p = 0.0192), which was verified by a fluorescence in situ hybridization (FISH). Korean patients with TrkA-positive colon cancer had a marginal but significant shorter overall survival time than TrkA-negative colon cancer [ hazard ratio (HR) = 0.5346, 95% confidential interval (CI) = 0.2548-0.9722, p = 0.0411]. In addition, KM12 cell line was sensitive to selective TrkA inhibitors. These results demonstrate that NTRK1 fusion is granted as a clinically relevant target for therapeutic intervention of colon cancer.
C1 [Park, Do Youn; Kwon, Chae Hwa] Pusan Natl Univ, Dept Pathol, Busan, South Korea.
   [Park, Do Youn; Kwon, Chae Hwa; Jo, Hong-Jae; Kim, Hyun Sung; Oh, Nahmgun] Pusan Natl Univ, Sch Med, Busan, South Korea.
   [Park, Do Youn; Kwon, Chae Hwa; Jo, Hong-Jae; Kim, Hyun Sung; Oh, Nahmgun] Pusan Natl Univ Hosp, Biomed Res Inst, Busan, South Korea.
   [Jo, Hong-Jae; Kim, Hyun Sung; Oh, Nahmgun] Pusan Natl Univ Hosp, Dept Surg, Busan, South Korea.
   [Choi, Chan; Lee, Jae Hyuk; Lee, Ji Shin] Chonnam Natl Univ, Hwasun Hosp, Dept Pathol, Hwasun Gun, Jeollanam Do, South Korea.
   [Kim, Hyeong-Rok] Chonnam Natl Univ, Hwasun Hosp, Dept Surg, Hwasun Gun, Jeollanam Do, South Korea.
   [Shin, Jong-Yeon; Kim, Jong-Il; Seo, Jeong-Sun] Seoul Natl Univ, Med Res Ctr, GMI, Seoul, South Korea.
   [Kim, Jong-Il; Seo, Jeong-Sun] Seoul Natl Univ, Coll Med, Dept Biochem & Mol Biol, Seoul, South Korea.
   [Seo, Jeong-Sun] Macrogen Inc, Seoul, South Korea.
   [Park, Ok Ku; Park, Eok; Park, Jonghoon; Park, Hee Dong; Park, Joonghoon] LG Life Sci Ltd, R&D Pk, Daejeon, South Korea.
C3 Pusan National University; Pusan National University; Pusan National
   University; Pusan National University Hospital; Pusan National
   University; Pusan National University Hospital; Chonnam National
   University; Chonnam National University; Seoul National University
   (SNU); Seoul National University (SNU); Macrogen, Inc.; LG Life Sciences
   Ltd
RP Park, J (corresponding author), LG Life Sci Ltd, R&D Pk, Daejeon, South Korea.
EM joonghoon@lgls.com
RI Kim, Sung/G-4114-2014; Kim, Han/AAA-5787-2021; Seo,
   Jeong-Sun/J-2763-2012; KIM, JONG-IL/D-1019-2011
OI KIM, JONG-IL/0000-0002-7240-3744
FU National Research Foundation [2014R1A2A1A11052217]; Ministry of Science,
   ICT and Future Planning, Republic of Korea
FX This work has been supported in part by a grant (No.
   2014R1A2A1A11052217) from the National Research Foundation, the Ministry
   of Science, ICT and Future Planning, Republic of Korea (D.Y.P.).
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NR 38
TC 22
Z9 38
U1 0
U2 2
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD FEB 16
PY 2016
VL 7
IS 7
BP 8399
EP 8412
DI 10.18632/oncotarget.6724
PG 14
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DE0PD
UT WOS:000370325900080
PM 26716414
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Alidadi, S
   Mohammadian, M
   Zohdiaghdam, R
   Esgandari, K
   Behrouzkia, Z
AF Alidadi, Saba
   Mohammadian, Mahshid
   Zohdiaghdam, Reza
   Esgandari, Kosar
   Behrouzkia, Zhaleh
TI Evaluation of the Silver Graphene Quantum Dot Effect when Combined with
   Resveratrol and Radiation in Colorectal Cancer Cells
SO IRANIAN RED CRESCENT MEDICAL JOURNAL
LA English
DT Article
DE Apoptosis; HCT-116 cells; Radiation; Resveratrol
ID NANOPARTICLES; RADIOTHERAPY; ENHANCEMENT; RADIOSENSITIZATION;
   CYTOTOXICITY; APOPTOSIS
AB Background: Colorectal cancer (CRC) is one of the major leading causes of cancer related death throughout the world. Among various therapeutic strategies for CRC, neoadjuvant radiotherapy, targeted therapy, and chemotherapy are the main techniques to destroy cancerous cells.
   Objectives: The main purpose of this study was to evaluate the efficacy of radiotherapy in combination with silver graphene quantum dot (SQD) and Resveratrol (Res) on the HCT-116 colorectal cancer (CRC) cells.
   Methods: Minimally cytotoxic concentrations of SQD (50 mu m) with Res (0.5 xIC50 and 0.25 xIC50) and radiation (2'Gy of x-ray radiation) were selected for double and triple treatments. The Acridine Orange/Ethidium Bromide staining was used to detect apoptosis. The Caspase-3 mRNA expression level was measured by the real-time PCR method. In addition, cyclooxygenase 2 (COX-2) protein expression was studied by the western blot technique. Similarly, the superoxide dismutase (SOD), glutathione peroxidase (GPX) enzyme activities, and malondialdehyde (MDA) levels were determined in this study.
   Results: In this study, after 24 h, triple combined cases showed decreased cell viability versus double and single treatments (P<0.05). Moreover, cellular viability was decreased in the SQD-radiation treated cells, compared to the related single treatments (P<0.05). The increased apoptotic cells were observed in the triple combination group, compared to the double and single treated cases. Triple combination treatment exhibited decreased GPX activity versus single treatments (P<0.05). The triple combined case showed reduced SOD activity than the radiation and SQD single treatments. A remarkable increase in the MDA concentration was observed in the triple combination versus single treatments. According to the results, in double and triple treatments, upregulation of Caspase-3 mRNA was presented versus single treatments. There was a decreased COX-2 protein expression level in triple combinatorial cases versus double and single treated cells.
   Conclusion: These findings proposed that SQD in combination with Res and radiation showed significant anti-cancer effects on CRC in vitro.
C1 [Alidadi, Saba; Zohdiaghdam, Reza; Esgandari, Kosar; Behrouzkia, Zhaleh] Urmia Univ Med Sci, Fac Med, Med Phys Dept, Orumiyeh, Iran.
   [Mohammadian, Mahshid] Urmia Univ Med Sci, Fac Med, Dept Clin Biochem, Orumiyeh, Iran.
C3 Urmia University of Medical Sciences; Urmia University of Medical
   Sciences
RP Behrouzkia, Z (corresponding author), Urmia Univ Med Sci, Fac Med, Med Phys Dept, Orumiyeh, Iran.
EM clinicalbiochem86@gmail.com
FU Urmia University of Medical Sciences, Urmia, Iran
FX This study was supported financially by Urmia University of Medical
   Sciences, Urmia, Iran.
CR [Anonymous], 2014, JMSCR
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NR 32
TC 1
Z9 1
U1 0
U2 3
PU ZAMENSALAMATI PUBL CO
PI MASHHAD
PA KHORASAN, MASHHAD, SANABAD-EBNE SINA ST, MASHHAD, IRAN
SN 2074-1804
EI 2074-1812
J9 IRAN RED CRESCENT ME
JI Iran. Red Crescent Med. J.
PD FEB
PY 2022
VL 24
IS 2
AR e1474
DI 10.32592/ircmj.2022.24.2.1474
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 1H7RT
UT WOS:000796737500006
OA hybrid
DA 2025-01-04
ER

PT J
AU Gil, J
   Karpinski, P
   Sasiadek, MM
AF Gil, Justyna
   Karpinski, Pawel
   Sasiadek, Maria M.
TI Transcriptomic Profiling for the Autophagy Pathway in Colorectal Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE autophagy; gene expression; colorectal cancer
ID CONSENSUS MOLECULAR SUBTYPES; EXPRESSION; TUMORIGENESIS; MUTATIONS;
   UNDERLIE; PROTEINS
AB The role of autophagy in colorectal cancer (CRC) pathogenesis appears to be crucial. Autophagy acts both as a tumor suppressor, by removing redundant cellular material, and a tumor-promoting factor, by providing access to components necessary for growth, metabolism, and proliferation. To date, little is known about the expression of genes that play a basal role in the autophagy in CRC. In this study, we aimed to compare the expression levels of 46 genes involved in the autophagy pathway between tumor-adjacent and tumor tissue, employing large RNA sequencing (RNA-seq) and microarray datasets. Additionally, we verified our results using data on 38 CRC cell lines. Gene set enrichment analysis revealed a significant deregulation of autophagy-related gene sets in CRC. The unsupervised clustering of tumors using the mRNA levels of autophagy-related genes revealed the existence of two major clusters: microsatellite instability (MSI)-enriched and -depleted. In cluster 1 (MSI-depleted), ATG9B and LAMP1 genes were the most prominently expressed, whereas cluster 2 (MSI-enriched) was characterized by DRAM1 upregulation. CRC cell lines were also clustered according to MSI-enriched/-depleted subgroups. The moderate deregulation of autophagy-related genes in cancer tissue, as compared to adjacent tissue, suggests a prominent field cancerization or early disruption of autophagy. Genes differentiating these clusters are promising candidates for CRC targeting therapy worthy of further investigation.
C1 [Gil, Justyna; Karpinski, Pawel; Sasiadek, Maria M.] Wroclaw Med Univ, Dept Genet, Marcinkowskiego 1, PL-50368 Wroclaw, Poland.
   [Karpinski, Pawel] Polish Acad Sci, Inst Immunol & Expt Therapy, Lab Genom & Bioinformat, PL-53114 Wroclaw, Poland.
C3 Wroclaw Medical University; Polish Academy of Sciences; Hirszfeld
   Institute of Immunology & Experimental Therapy of the Polish Academy of
   Sciences
RP Gil, J (corresponding author), Wroclaw Med Univ, Dept Genet, Marcinkowskiego 1, PL-50368 Wroclaw, Poland.
RI Gil, Justyna/L-5618-2019; Karpinski, Pawel/LQJ-4449-2024
OI Sasiadek, Maria/0000-0002-7599-7074; Karpinski,
   Pawel/0000-0003-3885-694X; Gil, Justyna/0000-0003-0991-7686
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NR 66
TC 8
Z9 8
U1 0
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD OCT
PY 2020
VL 21
IS 19
AR 7101
DI 10.3390/ijms21197101
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA OO1QM
UT WOS:000587161100001
PM 32993062
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Randon, G
   Intini, R
   Cremolini, C
   Elez, E
   Overman, MJ
   Lee, J
   Manca, P
   Bergamo, F
   Pagani, F
   Antista, M
   Angerilli, V
   Montaña, FJR
   Lavacchi, D
   Boccaccino, A
   Fucà, G
   Brich, S
   Cattaneo, L
   Fassan, M
   Pietrantonio, F
   Lonardi, S
AF Randon, Giovanni
   Intini, Rossana
   Cremolini, Chiara
   Elez, Elena
   Overman, Michael J.
   Lee, Jeeyun
   Manca, Paolo
   Bergamo, Francesca
   Pagani, Filippo
   Antista, Maria
   Angerilli, Valentina
   Ros Montana, Francisco Javier
   Lavacchi, Daniele
   Boccaccino, Alessandra
   Fuca, Giovanni
   Brich, Silvia
   Cattaneo, Laura
   Fassan, Matteo
   Pietrantonio, Filippo
   Lonardi, Sara
TI Original Research Tumour mutational burden predicts resistance to EGFR/
   BRAF blockade in BRAF-mutated microsatellite stable metastatic
   colorectal cancer
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Metastatic colorectal cancer; BRAF mutation; <p>EGFR/BRAF inhibitor</p>;
   Primary resistance; Tumour mutational burden
ID DABRAFENIB; TRAMETINIB; EFFICACY; SUBTYPES; MEK; INHIBITION; THERAPY
AB Aim: To unveil genomic and immunohistochemical expression profiles associated with primary resistance to EGFR/BRAF targeted therapy in patients with BRAF-mutated and microsatellite stable (MSS) metastatic colorectal cancer.& nbsp;Experimental design: In this multicenter case-control study on patients treated with EGFR/ BRAF f MEK blockade, we compared a primary resistance cohort (N Z 20; RECISTv1.1PD/SD, and progression-free survival [PFS] < 16 weeks) versus a sensitive one (N = 19; RECISTv1.1 PR/CR, and PFS > 16 weeks) in terms of clinical and genomic/expression data by means of comprehensive genomic profiling, tumour mutational burden (TMB), BRAF-mutant transcriptional subtypes (BM) classification and PTEN expression.& nbsp;Results: Left-sided tumours (28% of the total) were enriched in the sensitive versus resistant cohort (53% versus 10%, P = 0.010). Genomic alterations in the PIK3CA/MTOR pathway, BM1 status and PTEN loss were similarly distributed among patients with resistant and sensitive tumours. Amplification of CCND1-3 genes were found only in patients with primary resistance (20% versus 0%, P = 0.106). TMB and prevalence of intermediate TMB (TMB-I 6-20 mutations/Mb) were higher in the resistant versus sensitive cohort (median TMB: 6 [IQR, 3-7.29] versus 3 [IQR, 1.26-3.5] ; P = 0.013; TMB-I/H: 60% versus 11%; P = 0.001). Patients with TMB-I had shorter PFS (3.3 versus 5.9 months; HR = 2.19, 95% CI, 1.07-4.47, P = 0.031) and overall survival (6.3 versus 10.5 months; HR = 2.22, 95% CI, 1.02-4.81, P = 0.044).& nbsp;Conclusion: Despite the small sample size, the association of a relatively higher TMB with limited benefit from EGFR/BRAF blockade in patients with MSS and BRAF-mutated mCRC deserves prospective validation. (C) 2021 Elsevier Ltd. All rights reserved.
C1 [Randon, Giovanni; Manca, Paolo; Pagani, Filippo; Antista, Maria; Fuca, Giovanni; Pietrantonio, Filippo] Fdn IRCCS Ist Nazl Tumouri Milano, Dept Med Oncol, Milan, Italy.
   [Intini, Rossana; Bergamo, Francesca; Fassan, Matteo; Lonardi, Sara] IRCCS, Dept Oncol, Ist Oncol Veneto, Padua, Italy.
   [Cremolini, Chiara; Boccaccino, Alessandra] Azienda Osped Univ Pisana, Unit Med Oncol 2, Pisa, Italy.
   [Cremolini, Chiara] Univ Pisa, Dept Translat Res & New Technol Med & Surg, Pisa, Italy.
   [Elez, Elena; Ros Montana, Francisco Javier] Vall DHebron Univ Hosp HUVH, Barcelona, Spain.
   [Elez, Elena; Ros Montana, Francisco Javier] Vall DHebron Inst Oncol VHIO, Barcelona, Spain.
   [Overman, Michael J.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
   [Lee, Jeeyun] Sungkyunkwan Univ, Samsung Med Ctr, Div Hematol Oncol, Dept Med,Sch Med, Seoul, South Korea.
   [Angerilli, Valentina; Fassan, Matteo] Univ Padua, Dept Med DIMED, Surg Pathol Unit, Padua, Italy.
   [Lavacchi, Daniele] Azienda Osped Univ Careggi, Med Oncol Unit, Florence, Italy.
   [Brich, Silvia; Cattaneo, Laura] Fdn IRCCS Ist Nazl Tumouri Milano, Dept Pathol & Lab Med, Milan, Italy.
C3 IRCCS Istituto Oncologico Veneto (IOV); University of Pisa; Azienda
   Ospedaliero Universitaria Pisana; University of Pisa; Hospital
   Universitari Vall d'Hebron; Vall d'Hebron Institut d'Oncologia (VHIO);
   University of Texas System; UTMD Anderson Cancer Center; Sungkyunkwan
   University (SKKU); Samsung Medical Center; University of Padua;
   University of Florence; Azienda Ospedaliero Universitaria Careggi
RP Pietrantonio, F (corresponding author), Fdn IRCCS Ist Nazl Tumouri, Med Oncol Dept, Via G Venezian 1, I-20133 Milan, Italy.
EM fillippo.pietrantorno@istitutotumori.mi.it
RI brich, silvia/K-4049-2016; Cattaneo, Laura/ABI-6609-2020; Ros,
   Javier/HKF-1171-2023; Fuca, Giovanni/AAF-2378-2019; Bergamo,
   Francesca/AAB-9010-2019; Pagani, Filippo/LSK-6113-2024; Lee,
   Jee/C-9646-2011; Intini, Rossana/F-9492-2018; Cremolini,
   Chiara/AAC-1889-2019; Lavacchi, Daniele/AAC-3109-2022; Antista,
   Maria/AAC-2415-2020; Fassan, Matteo/F-5152-2012; Lonardi,
   Sara/F-4228-2014; Pietrantonio, Filippo/C-2180-2017
OI CREMOLINI, CHIARA/0000-0002-0520-4841; , Filippo
   Pagani/0009-0007-7393-7477; Ros, Javier/0000-0002-8137-5415; Fuca,
   Giovanni/0000-0002-1560-2253; Fassan, Matteo/0000-0001-6515-5482; Manca,
   Paolo/0000-0002-3813-6339; Lonardi, Sara/0000-0002-7593-8138;
   Pietrantonio, Filippo/0000-0002-8530-8420; Cattaneo,
   Laura/0000-0001-8890-719X
CR Arai K, 2019, J THORAC ONCOL, V14, pS846, DOI 10.1016/j.jtho.2019.08.1829
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NR 30
TC 13
Z9 14
U1 0
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD JAN
PY 2022
VL 161
BP 90
EP 98
DI 10.1016/j.ejca.2021.11.018
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 1A7QF
UT WOS:000791945800010
PM 34933155
DA 2025-01-04
ER

PT J
AU Roberto, M
   Marchetti, P
   Arrivi, G
   Di Pietro, FR
   Cascinu, S
   Gelsomino, F
   Caputo, F
   Cerma, K
   Ghidini, M
   Ratti, M
   Pizzo, C
   Ficorella, C
   Parisi, A
   Cortellini, A
   Urbano, F
   Calandrella, ML
   Botticelli, A
   Dell'Aquila, E
   Minelli, A
   Fulgenzi, C
   Montori, A
   Pilozzi, E
   Mazzuca, F
AF Roberto, Michela
   Marchetti, Paolo
   Arrivi, Giulia
   Di Pietro, Francesca Romana
   Cascinu, Stefano
   Gelsomino, Fabio
   Caputo, Francesco
   Cerma, Krisida
   Ghidini, Michele
   Ratti, Margherita
   Pizzo, Claudio
   Ficorella, Corrado
   Parisi, Alessandro
   Cortellini, Alessio
   Urbano, Federica
   Calandrella, Maria Letizia
   Botticelli, Andrea
   Dell'Aquila, Emanuela
   Minelli, Alessandro
   Fulgenzi, Claudia
   Montori, Andrea
   Pilozzi, Emanuela
   Mazzuca, Federica
TI The treatment paradigm of right-sided metastatic colon cancer: harboring
   BRAF mutation makes the difference
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Article
DE Colorectal cancer; RCC; Sidedness; BRAF; Anti-EGFR
ID FOLFOXIRI PLUS BEVACIZUMAB; COLORECTAL-CANCER; MICROSATELLITE
   INSTABILITY; TUMOR LOCATION; RAS MUTATIONS; SURVIVAL; IMPACT; CETUXIMAB;
   THERAPY; BENEFIT
AB Purpose BRAF mutations represent the main negative prognostic factor for metastatic colorectal cancer and a supposed negative predictive factor of response to standard chemotherapy. We have explored survival difference in right-sided colon cancer (RCC) patients according to BRAF mutations, with the aim to identify any predictive factors of response to targeted-based therapy. Methods A retrospective study of RCC patients, with BRAF known mutation status, treated with chemotherapy (CT) from October 2008 to June 2019 in 5 Italian centers, was conducted. Results We identified 207 advanced RCC patients: 20.3% BRAF mutant and 79.7% BRAF wild type (wt). BRAF-mutant cancers were more likely to be pT4 (50.0% v 25.7%, p = 0.016), undifferentiated (71.4% v 44.0%, p = 0.004), KRAS wt (90.5% v 38.2%, p < 0.001), and MSI-H (41.7% v 16.2%, p = 0.019) tumors, with synchronous (52.4% v 31.5%, p = 0.018) and peritoneal metastases (38.1% v 22.4%, p = 0.003). Median overall survival (OS) was 16 v 27 months in BRAF mutant and BRAF wt (P = 0.020). In first-line setting, BRAF-mutant showed a 2ys OS of 80% in clinical trials, 32% in anti-VEGF, 14% in epidermial growth factor receptor (EGFR), and 0% in chemotherapy alone regimens (P = 0.009). BRAF-mutant patients demonstrated worse survival, regardless of targeted therapy administered. However, survival difference was statistically significant in the anti-EGFR-treated subgroup (16 v 28 months, P = 0.005 in BRAF mutant v BRAF wt, respectively). Conclusions Our study demonstrated that BRAF status makes the difference in treatment's outcome. Therefore, the anti-EGFR should not be excluded in all advanced RCC but considered on a case-by-case basis.
C1 [Roberto, Michela; Marchetti, Paolo; Arrivi, Giulia; Di Pietro, Francesca Romana; Botticelli, Andrea; Mazzuca, Federica] Univ Roma La Sapienza, St Andrea Hosp, Dept Clin & Mol Med, Oncol Unit, Rome, Italy.
   [Marchetti, Paolo; Urbano, Federica; Calandrella, Maria Letizia; Botticelli, Andrea] Sapienza Univ, Dept Radiol Oncol & Pathol, Policlin Umberto 1, Rome, Italy.
   [Cascinu, Stefano; Gelsomino, Fabio; Caputo, Francesco; Cerma, Krisida] Univ Hosp Modena, Dept Oncol & Hematol, Div Oncol, Modena, Italy.
   [Ghidini, Michele; Ratti, Margherita; Pizzo, Claudio] ASST Cremona, Oncol Unit, Oncol Dept, Cremona, Italy.
   [Ficorella, Corrado; Parisi, Alessandro; Cortellini, Alessio] Univ Aquila, St Salvatore Hosp, Dept Biotechnol & Appl Clin Sci, Med Oncol, Laquila, Italy.
   [Dell'Aquila, Emanuela; Minelli, Alessandro; Fulgenzi, Claudia] Policlin Univ Campus Biomed Roma, Oncol Med, Rome, Italy.
   [Montori, Andrea; Pilozzi, Emanuela] Univ Roma La Sapienza, St Andrea Hosp, Dept Clin & Mol Med, UOC Anat Patol, Rome, Italy.
C3 Sapienza University Rome; Azienda Ospedaliera Sant'Andrea; Sapienza
   University Rome; University Hospital Sapienza Rome; Universita di Modena
   e Reggio Emilia; Universita di Modena e Reggio Emilia Hospital;
   University of L'Aquila; Fondazione Policlinico Universitario Campus
   Bio-Medico; Sapienza University Rome; Azienda Ospedaliera Sant'Andrea
RP Marchetti, P (corresponding author), Univ Roma La Sapienza, St Andrea Hosp, Dept Clin & Mol Med, Oncol Unit, Rome, Italy.; Marchetti, P (corresponding author), Sapienza Univ, Dept Radiol Oncol & Pathol, Policlin Umberto 1, Rome, Italy.
EM paolo.marchetti@uniroma1.it
RI montori, andrea/IQR-8952-2023; Cortellini, Alessio/AAB-8609-2019;
   Dell'Aquila, Emanuela/HZI-5685-2023; Botticelli, Andrea/J-9926-2018;
   Mazzuca, Federica/LSK-7446-2024; Parisi, Alessandro/AAB-9728-2019;
   gelsomino, fabio/AAB-8967-2022; Roberto, Michela/AAC-2552-2022; Di
   Pietro, Francesca Romana/AAB-8300-2022; Marchetti, Paolo/K-1469-2016;
   PILOZZI, Emanuela/AAC-1854-2022; Ghidini, Michele/I-7362-2018;
   Marchetti, Paolo/J-9890-2018; Caputo, Francesco/HSF-6337-2023
OI Ghidini, Michele/0000-0001-5435-1218; MONTORI,
   ANDREA/0000-0003-1013-8460; Parisi, Alessandro/0000-0003-4629-7762;
   Fulgenzi, Claudia/0000-0002-5654-9225; Di Pietro, Francesca
   Romana/0000-0002-6779-8753; MAZZUCA, FEDERICA/0000-0002-6580-286X;
   gelsomino, fabio/0000-0001-7979-4795; Cortellini,
   Alessio/0000-0002-1209-5735; Marchetti, Paolo/0000-0002-9064-8761;
   Caputo, Francesco/0000-0003-0331-3582; Roberto,
   Michela/0000-0001-5339-8348; Dell'Aquila, Emanuela/0000-0002-7258-1364
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NR 60
TC 8
Z9 9
U1 1
U2 3
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0179-1958
EI 1432-1262
J9 INT J COLORECTAL DIS
JI Int. J. Colorectal Dis.
PD AUG
PY 2020
VL 35
IS 8
BP 1513
EP 1527
DI 10.1007/s00384-020-03589-9
EA MAY 2020
PG 15
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA MH0JI
UT WOS:000530962000002
PM 32382835
DA 2025-01-04
ER

PT J
AU Long, JT
   Xie, Y
   Yin, JM
   Lu, W
   Fang, S
AF Long, Jianting
   Xie, Ying
   Yin, Junmei
   Lu, Wei
   Fang, Shi
TI RETRACTED: SphK1 promotes tumor cell migration and invasion in
   colorectal cancer (retracted article)
SO TUMOR BIOLOGY
LA English
DT Article; Retracted Publication
DE Colorectal cancer; SphK1; Proliferation; Invasion; EMT; Targeted therapy
ID SPHINGOSINE KINASE 1; PROSTATE-CANCER; ANGIOGENESIS; SURVEILLANCE;
   METASTASIS; INHIBITION; SENSITIZES; PROGNOSIS; APOPTOSIS; CONSENSUS
AB Colorectal cancer (CRC) is one of the most common cancers worldwide. Sphingosine kinase 1 (SphKI), which phosphorylates sphingosine to sphingosine-1-phosphate (SIP), is overexpressed in various types of cancers and may act as an oncogene in tumorigenesis. However, little is known about the role of SphK1 in CRC patients. We studied the expression of SphK1 in 85 cases of CRC tissues by immunohistochemistry, qRT-PCR, and western blot. We also evaluated the effect of SphK1 on cell proliferation and invasion by MTT and transwell invasion assay. SphK1 is overexpressed in CRC tissues and cell lines, and upregulation of SphK1 correlated significantly with the following parameters: lymph node metastasis, liver metastasis, and advanced TNM stage. SphK1 knockdown results in inhibition of cancer cell proliferation. Inhibition of CRC cell migration and invasion is also evident through reversal of EMT by increases in E-cadherin expression and decreases in vimentin expression. In conclusion, SphKI is associated with the proliferation and invasiveness of CRC cells and the SphK1 gene may contribute to a novel therapeutic approach against CRC.
C1 [Long, Jianting] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Med Oncol, Guangzhou 510080, Guangdong, Peoples R China.
   [Xie, Ying; Yin, Junmei; Lu, Wei; Fang, Shi] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Clin Nutr, 58 Zhongshan 2nd Rd, Guangzhou 510080, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University
RP Fang, S (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 1, Dept Clin Nutr, 58 Zhongshan 2nd Rd, Guangzhou 510080, Guangdong, Peoples R China.
EM fangshi@mail.sysu.edu.cn
RI long, jianting/JCE-8178-2023
FU Science and Technology Planning Project of Guangdong Province
   [2013B021800284]
FX This work is supported by the Science and Technology Planning Project of
   Guangdong Province (2013B021800284)
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NR 23
TC 39
Z9 44
U1 0
U2 19
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1010-4283
EI 1423-0380
J9 TUMOR BIOL
JI Tumor Biol.
PD MAY
PY 2016
VL 37
IS 5
BP 6831
EP 6836
DI 10.1007/s13277-015-4542-4
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DM6MC
UT WOS:000376465800128
PM 26662312
DA 2025-01-04
ER

PT J
AU Trojan, J
   Klein-Scory, S
   Koch, C
   Schmiegel, W
   Baraniskin, A
AF Trojan, Joerg
   Klein-Scory, Susanne
   Koch, Christine
   Schmiegel, Wolff
   Baraniskin, Alexander
TI Clinical Application of Liquid Biopsy in Targeted Therapy of Metastatic
   Colorectal Cancer
SO CASE REPORTS IN ONCOLOGICAL MEDICINE
LA English
DT Article
ID KRAS DISCORDANCE; TUMOR
AB Background. Colorectal cancers (CRC) shed DNA into blood circulation. There is growing evidence that the analysis of circulating tumor DNA can be effectively used for monitoring of disease, to track tumor heterogeneity and to evaluate response to treatment. Case Presentation. Here, we describe two cases of patients with advanced CRC. The first case is about a patient with no available tissue for analysis of RAS mutation status. Liquid biopsy revealed RAS-wild-type and the therapy with anti-EGFR (epidermal growth factor receptor) monoclonal antibody cetuximab could be initiated. In the second case, the mutational profile of a patient with initial wild-type RAS-status was continually tracked during the course of treatment. An acquired KRAS exon 3 mutation was detected. The number of KRAS mutated fragments decreased continuously after the discontinuation of the therapy with EGFR-specific antibodies. Conclusion. Liquid biopsy provides a rapid genotype result, which accurately reproduces the current mutation status of tumor tissue. Furthermore, liquid biopsy enables close monitoring of the onset of secondary resistance to anti-EGFR therapy.
C1 [Trojan, Joerg; Koch, Christine] Goethe Univ Frankfurt, Dept Med, Gastroenterol, Frankfurt, Germany.
   [Klein-Scory, Susanne; Schmiegel, Wolff; Baraniskin, Alexander] Univ Klinikum Knappschaftskrankenhaus Bochum, IMBL Med Clin, Bochum, Germany.
   [Schmiegel, Wolff; Baraniskin, Alexander] Ruhr Univ Bochum, Dept Med Hematol & Oncol, Bochum, Germany.
C3 Goethe University Frankfurt; Ruhr University Bochum; Ruhr University
   Bochum
RP Baraniskin, A (corresponding author), Univ Klinikum Knappschaftskrankenhaus Bochum, IMBL Med Clin, Bochum, Germany.; Baraniskin, A (corresponding author), Ruhr Univ Bochum, Dept Med Hematol & Oncol, Bochum, Germany.
EM alexander.baraniskin@rub.de
RI Koch, Christine/J-8698-2019; Trojan, Jörg/C-1616-2009; Klein-Scory,
   Susanne/JMB-0127-2023
OI Klein-Scory, Susanne/0000-0003-1930-3354
FU Ministry of Science, North Rhine-Westphalia, Germany
FX This study was supported by a grant (PURE) from the Ministry of Science,
   North Rhine-Westphalia, Germany.
CR Ekinci AS, 2015, J BUON, V20, P128
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NR 11
TC 13
Z9 15
U1 0
U2 4
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2090-6706
EI 2090-6714
J9 CASE REP ONCOL MED
JI Case Rep. Oncol. Med.
PY 2017
VL 2017
AR 6139634
DI 10.1155/2017/6139634
PG 3
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA EK6FR
UT WOS:000394021000001
PM 28232873
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Xiao, Y
   Jiang, XY
   Yin, K
   Miao, TS
   Lu, HL
   Wang, WQ
   Ma, LJ
   Zhao, YH
   Liu, CY
   Qiao, Y
   Zhang, PJ
AF Xiao, Yi
   Jiang, Xiaoyu
   Yin, Ke
   Miao, Tianshu
   Lu, Hanlin
   Wang, Wenqing
   Ma, Lijuan
   Zhao, Yinghui
   Liu, Chunyan
   Qiao, Yun
   Zhang, Pengju
TI USP35 promotes cell proliferation and chemotherapeutic resistance
   through stabilizing FUCA1 in colorectal cancer
SO ONCOGENESIS
LA English
DT Article
ID ALPHA-L-FUCOSIDASE; 5-FLUOROURACIL; MECHANISMS; SURVIVAL
AB Ubiquitin-specific-processing proteases 35 (USP35) is an under-characterized deubiquitinase and its role in colorectal cancer (CRC) remains unclear. Here, we focus on delineating the impact of USP35 on CRC cell proliferation and chemo-resistance, as well as the possible regulatory mechanism. By examining the genomic database and clinical samples, we found that USP35 was overexpressed in CRC. Further functional studies showed that enhanced USP35 expression promoted CRC cell proliferation and resistance to oxaliplatin (OXA) and 5-fluorouracil (5-FU), whereas USP35 depletion impeded cell proliferation and sensitized cells to OXA and 5-FU treatments. Then, to explore the possible mechanism underlying USP35-triggered cellular responses, we performed co-immunoprecipitation (co-IP) followed by mass spectrometry (MS) analysis and identified alpha-L-fucosidase 1 (FUCA1) as a direct deubiquitiation target of USP35. Importantly, we demonstrated that FUCA1 was an essential mediator for USP35-induced cell proliferation and chemo-resistance in vitro and in vivo. Finally, we observed that nucleotide excision repair (NER) components (e.g., XPC, XPA, ERCC1) were up-regulated by USP35-FUCA1 axis, indicating a potential mechanism for USP35-FUCA1-mediated platinum resistance in CRC. Together, our results for the first time explored the role and important mechanism of USP35 in CRC cell proliferation and chemotherapeutic response, providing a rationale for USP35-FUCA1-targeted therapy in CRC.
C1 [Xiao, Yi; Jiang, Xiaoyu; Miao, Tianshu; Lu, Hanlin; Wang, Wenqing; Ma, Lijuan; Zhang, Pengju] Shandong Univ, Cheeloo Coll Med, Sch Basic Med Sci, Dept Biochem & Mol Biol,Key Lab Expt Teratol,Minis, Jinan 250012, Shandong, Peoples R China.
   [Xiao, Yi] Univ Nebraska, Med Ctr, Eppley Inst Res Canc & Allied Dis, Fred & Pamela Buffett Canc Ctr, Omaha, NE 68198 USA.
   [Yin, Ke] Shandong Univ, Shandong Prov Hosp, Dept Pathol, Jinan 250021, Shandong, Peoples R China.
   [Lu, Hanlin] Shandong Univ, Qilu Hosp, Dept Cardiol, Jinan 250012, Shandong, Peoples R China.
   [Zhao, Yinghui] Shandong Univ, Second Hosp, Dept Clin Lab, 247 Beiyuan St, Jinan 250033, Shandong, Peoples R China.
   [Liu, Chunyan] Qingdao Univ, Med Coll, Dept Integrated Tradit Chinese & Western Med, Qingdao 266071, Shandong, Peoples R China.
   [Qiao, Yun] Shandong Univ, Qilu Hosp, Dept Tradit Chinese Med, Jinan 250012, Shandong, Peoples R China.
C3 Shandong University; University of Nebraska System; University of
   Nebraska Medical Center; Shandong University; Shandong First Medical
   University & Shandong Academy of Medical Sciences; Shandong University;
   Shandong University; Qingdao University; Shandong University
RP Zhang, PJ (corresponding author), Shandong Univ, Cheeloo Coll Med, Sch Basic Med Sci, Dept Biochem & Mol Biol,Key Lab Expt Teratol,Minis, Jinan 250012, Shandong, Peoples R China.; Qiao, Y (corresponding author), Shandong Univ, Qilu Hosp, Dept Tradit Chinese Med, Jinan 250012, Shandong, Peoples R China.
EM qiaoyun@qiluhospital.com; zhpj@sdu.edu.cn
OI wang, wenqing/0000-0002-6710-4045
FU National Natural Science Foundation of China [31870781, 81672858,
   81802759]; Shandong Provincial Natural Science Foundation [ZR2021MH326];
   China Postdoctoral Science Foundation Funded Project [2019M652312]
FX his work was supported by the National Natural Science Foundation of
   China (Nos.31870781, 81672858, 81802759), Shandong Provincial Natural
   Science Foundation(ZR2021MH326), and the China Postdoctoral Science
   Foundation Funded Project(2019M652312)
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NR 55
TC 5
Z9 6
U1 3
U2 7
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2157-9024
J9 ONCOGENESIS
JI Oncogenesis
PD MAR 3
PY 2023
VL 12
IS 1
AR 12
DI 10.1038/s41389-023-00458-2
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9N2YR
UT WOS:000942783800001
PM 36864055
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Babaei, K
   Khaksar, R
   Zeinali, T
   Hemmati, H
   Bandegi, A
   Samidoust, P
   Ashoobi, MT
   Hashemian, H
   Delpasand, K
   Talebinasab, F
   Naebi, H
   Mirpour, SH
   Keymoradzadeh, A
   Norollahi, SE
AF Babaei, Kosar
   Khaksar, Roya
   Zeinali, Tahereh
   Hemmati, Hossein
   Bandegi, Ahmadreza
   Samidoust, Pirouz
   Ashoobi, Mohammad Taghi
   Hashemian, Hooman
   Delpasand, Kourosh
   Talebinasab, Fereshteh
   Naebi, Hoora
   Mirpour, Seyed Hossein
   Keymoradzadeh, Arman
   Norollahi, Seyedeh Elham
TI Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in
   carcinogenesis and tumorigenesis of colorectal cancer
SO BIOMEDICINE-TAIWAN
LA English
DT Review
DE Epigenetics; Fluctuations; Tumorigenesis; Carcinogenesis
ID TUMOR-SUPPRESSOR GENE; DNA METHYLATION; GERMLINE MUTATIONS; REPAIR
   GENES; EXPRESSION; KRUPPEL-LIKE-FACTOR-4; REGULATIONS; FLUCTUATION;
   BIOMARKERS; NUMBER
AB Colorectal cancer (CRC) is distinguished by epigenetic elements like DNA methylation, histone modification, histone acetylation and RNA remodeling which is related with genomic instability and tumor initiation. Correspondingly, as a main epigenetic regulation, DNA methylation has an impressive ability in order to be used in CRC targeted therapy. Meaningly, DNA methylation is identified as one of most important epigenetic regulators in gene expression and is considered as a notable potential driver in tumorigenesis and carcinogenesis through gene-silencing of tumor suppressors genes. Abnormal methylation situation, even in the level of promoter regions, does not essentially change the gene expression levels, particularly if the gene was become silenced, leaving the mechanisms of methylation without any response. According to the methylation situation which has a strong eagerness to be highly altered on CpG islands in carcinogenesis and tumorigenesis, considering its epigenetic fluctuations in finding new biomarkers is of great importance. Modifications in DNA methylation pattern and also enrichment of methylated histone signs in the promoter regions of some certain genes like MUTYH, KLF4/6 and WNT1 in different signaling pathways could be a notable key contributors to the upregulation of tumor initiation in CRC. These epigenetic alterations could be employed as a practical diagnostic biomarkers for colorectal cancer. In this review, we will be discuss these fluctuations of MUTYH, KLF4/6 and WNT1 genes in CRC.
C1 [Babaei, Kosar] Islamic Azad Univ, Dept Biol, Tonekabon Branch, Tonekabon, Iran.
   [Khaksar, Roya; Zeinali, Tahereh; Keymoradzadeh, Arman; Norollahi, Seyedeh Elham] Guilan Univ Med Sci, Gastrointestinal & Liver Dis Res Ctr, Rasht, Iran.
   [Hemmati, Hossein; Samidoust, Pirouz] Guilan Univ Med Sci, Razi Clin Res Dev Unit, Rasht, Iran.
   [Bandegi, Ahmadreza; Talebinasab, Fereshteh; Naebi, Hoora] Semnan Univ Med Sci, Fac Med, Dept Biochem, Semnan, Iran.
   [Ashoobi, Mohammad Taghi] Guilan Univ Med Sci, Poursina Hosp, Dept Surg, Rasht, Iran.
   [Hashemian, Hooman] Guilan Univ Med Ciences, Pediat Dis Res Ctr, Rasht, Iran.
   [Delpasand, Kourosh] Kurdistan Univ Md Ciences, Sch Med, Sanandaj, Iran.
   [Mirpour, Seyed Hossein] Guilan Univ Med Sci, Razi Hosp, Sch Med, Dept Hematol & Oncol, Rasht, Iran.
C3 Islamic Azad University; Guilan University of Medical Sciences; Guilan
   University of Medical Sciences; Semnan University of Medical Sciences;
   Guilan University of Medical Sciences; Guilan University of Medical
   Sciences
RP Norollahi, SE (corresponding author), Guilan Univ Med Sci, Razi Hosp, Gastrointestinal & Liver Dis Res Ctr, Sardar Jangal St, Rasht, Iran.
EM elnaz_Norollahi2000@yahoo.com
RI Mirpour, Seyed/AAG-4187-2021; Hemmati, Hossein/K-2440-2017; Ashoubi,
   Mohammad Taghi/P-9338-2018; Delpasand, kourosh/B-1951-2019; Bandegi,
   Ahmad Reza/ABG-3938-2021; Delpasand, kourosh/O-3681-2018
OI hemmati, hossein/0009-0006-6978-9689; Delpasand,
   kourosh/0000-0001-6842-3374
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NR 74
TC 13
Z9 15
U1 0
U2 4
PU EDP SCIENCES S A
PI LES ULIS CEDEX A
PA 17, AVE DU HOGGAR, PA COURTABOEUF, BP 112, F-91944 LES ULIS CEDEX A,
   FRANCE
SN 2211-8020
EI 2211-8039
J9 BIOMEDICINE-TAIWAN
JI BioMedicine-Taiwan
PD DEC
PY 2019
VL 9
IS 4
BP 1
EP 9
AR 22
DI 10.1051/bmdcn/2019090422
PG 9
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA KD0ZJ
UT WOS:000507600900001
PM 31724937
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Grote, S
   Traub, F
   Mittelstaet, J
   Seitz, C
   Kaiser, A
   Handgretinger, R
   Schleicher, S
AF Grote, Stefan
   Traub, Frank
   Mittelstaet, Joerg
   Seitz, Christian
   Kaiser, Andrew
   Handgretinger, Rupert
   Schleicher, Sabine
TI Adapter Chimeric Antigen Receptor (AdCAR)-Engineered NK-92 Cells for the
   Multiplex Targeting of Bone Metastases
SO CANCERS
LA English
DT Article
DE NK-92; adapter; chimeric antigen receptor; bone metastasis; solid tumors
ID NATURAL-KILLER-CELLS; CAR-T-CELLS; ADOPTIVE IMMUNOTHERAPY; HLA-E;
   CANCER; TRIAL; BLINATUMOMAB; REMISSIONS; EXPRESSION; MOLECULES
AB Simple Summary
   Metastatic disease remains one of the biggest challenges for tumor therapy. The aim of our study was the preclinical evaluation of adapter chimeric antigen receptor (AdCAR)-engineered NK-92 cell efficacy as a possible treatment strategy for various types of bone metastatic cancers. We confirmed that AdCAR NK-92 cells successfully induces tumor cell lysis in bone metastasis cell lines derived from mammary, renal cell and colorectal carcinoma as well as melanoma in a specific and controllable manner, thus, establishing a potent cellular product with universal applicability and quick clinical translation potential for the treatment of solid tumors, including metastases.
   Background: Since metastatic spreading of solid tumor cells often leads to a fatal outcome for most cancer patients, new approaches for patient-individualized, targeted immunotherapy are urgently needed. Methods: Here, we established cell lines from four bone metastases of different tumor entities. We assessed AdCAR NK-92-mediated cytotoxicity in vitro in standard cytotoxicity assays as well as 3D spheroid models Results: AdCAR-engineered NK-92 cells successfully demonstrated distinct and specific cytotoxic potential targeting different tumor antigens expressed on cell lines established from bone metastases of mammary, renal cell and colorectal carcinoma as well as melanomas. In that process AdCAR NK-92 cells produced a multitude of NK effector molecules as well as pro inflammatory cytokines. Furthermore, AdCAR NK-92 showed increased cytotoxicity in 3D spheroid models which can recapitulate in vivo architecture, thereby bridging the gap between in vitro and in vivo models. Conclusions: AdCAR NK-92 cells may provide an interesting and promising "off-the-shelf" cellular product for the targeted therapy of cancers metastasizing to the bone, while utilization of clinically approved, therapeutic antibodies, as exchangeable adapter molecules can facilitate quick clinical translation.
C1 [Grote, Stefan; Seitz, Christian; Handgretinger, Rupert; Schleicher, Sabine] Univ Hosp Tuebingen, Childrens Hosp, Dept Hematol & Oncol, D-72076 Tubingen, Germany.
   [Traub, Frank] Johannes Gutenberg Univ Mainz, Univ Med Ctr Mainz, Dept Orthoped & Traumatol, D-55131 Mainz, Germany.
   [Mittelstaet, Joerg; Kaiser, Andrew] Miltenyi Biotec GmbH, D-51429 Bergisch Gladbach, Germany.
C3 Eberhard Karls University of Tubingen; Eberhard Karls University
   Hospital; TUBINGEN UNIVERSITY CHILDRENS HOSPITAL; Johannes Gutenberg
   University of Mainz; Miltenyi Biotec
RP Grote, S (corresponding author), Univ Hosp Tuebingen, Childrens Hosp, Dept Hematol & Oncol, D-72076 Tubingen, Germany.
EM stefan.grote@med.uni-tuebingen.de; frank.traub@unimedizin-mainz.de;
   joergmi@miltenyi.com; christian.seitz@med.uni-tuebingen.de;
   andrewk@miltenyi.com; rupert.handgretinger@med.uni-tuebingen.de;
   sabine.schleicher@med.uni-tuebingen.de
RI Handgretinger, Rupert/AGW-2806-2022; Seitz, Christian/ABA-9467-2020
OI Schleicher, Sabine/0000-0002-1847-2984; Traub,
   Frank/0000-0002-6400-3257; Grote, Stefan/0000-0001-8713-6709
FU Miltenyi Biotec GmbH
FX The employing institution of S.G., C.S., R.H. and S.S. (University
   Children's Hospital Tuebingen) received research funding by Miltenyi
   Biotec GmbH on the basis of a collaboration research agreement.
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NR 46
TC 6
Z9 6
U1 0
U2 9
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 1124
DI 10.3390/cancers13051124
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QV4XL
UT WOS:000627976400001
PM 33807875
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Le, VH
   Thornblade, L
   Mph, PHGI
   Lai, LL
   Melstrom, KA
AF Le, Viet H.
   Thornblade, Lucas
   Mph, Phillip H. G. Ituarte
   Lai, Lily L.
   Melstrom, Kurt A.
TI Metachronous peritoneal metastases following curative resection for
   colon cancer: Understanding risk factors and patterns of recurrence
SO JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Article
DE colectomy isolated peritoneal recurrence; colon cancer metachronous
   recurrence; colon cancer metastases; colon cancer peritoneal metastases;
   peritoneal carcinomatosis colon resection
ID COLORECTAL-CANCER; CARCINOMATOSIS; GUIDELINES; SURGERY; SURVIVAL;
   SOCIETY
AB Background A subset of metachronous colon cancer recurrence manifests as peritoneal metastases (PM). Risk factors for metachronous PM recurrence are not well-defined in patients with stage II or III colon cancers after curative resection and standard adjuvant treatments.
   Methods Population data from the California Cancer Registry for patients with Stage II or III colon cancer were collected between 2004 and 2012. Multivariate analysis was used to identify factors associated with metachronous PM.
   Results Of the 2077 patients with stage II or III colon cancer, female patients (odds ratio [OR] = 1.84, p = 0.02), T4 primary tumor (OR = 2.36, p = 0.02), mucinous (OR = 3.97, p < 0.01) or signet-ring histology (OR = 6.01, p = 0.01), and right-sided cancer (OR = 2.2, p < 0.01) were found with increased risk of metachronous isolated PM recurrence after curative resection. Median survival after diagnosis for patients without PM recurrence was 22 months, compared with 12 months for PM recurrence (p < 0.001).
   Conclusion PM recurrence groups have a worse overall survival than patients with recurrent disease in other sites. A better understanding of the tumor biology and molecular characteristics of colon cancers likely to recur as PM is needed to explain behavior and identify potential targeted therapy.
C1 [Le, Viet H.; Thornblade, Lucas; Mph, Phillip H. G. Ituarte; Lai, Lily L.; Melstrom, Kurt A.] City Hope Natl Med Ctr, Dept Surg, 1500 East Duarte Rd, Duarte, CA 91010 USA.
C3 City of Hope
RP Melstrom, KA (corresponding author), City Hope Natl Med Ctr, Dept Surg, 1500 East Duarte Rd, Duarte, CA 91010 USA.
EM kmelstrom@coh.org
OI Melstrom, Kurt/0000-0001-8085-998X; Le, Viet/0000-0001-6599-1018;
   Thornblade, Lucas/0000-0002-9669-2472
CR [Anonymous], 2017, COLON RECTUM
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NR 28
TC 13
Z9 14
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 FEB
PY 2021
VL 123
IS 2
BP 622
EP 629
DI 10.1002/jso.26322
EA DEC 2020
PG 8
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA TR1DH
UT WOS:000594501500001
PM 33616972
DA 2025-01-04
ER

PT J
AU Du, F
   Han, Y
   Hu, X
   Xiao, YJ
   Shi, YW
   Sun, J
   Sun, ZW
   Yang, Y
   Yu, J
   Zhang, XD
   Jia, J
AF Du, Feng
   Han, Ying
   Hu, Xiao
   Xiao, Yanjie
   Shi, Youwu
   Sun, Jing
   Sun, Zhiwei
   Yang, Ying
   Yu, Jing
   Zhang, Xiaodong
   Jia, Jun
TI Large cell neuroendocrine carcinoma transformation: A novel acquired
   drug resistance mechanism in colorectal adenocarcinoma
SO CANCER INNOVATION
LA English
DT Article
DE metastatic colorectal cancer; large cell neuroendocrine carcinoma;
   histologic transformation; immunotherapy
ID CANCER
AB Acquired resistance is a major problem limiting the clinical efficacy of treatments for metastatic colorectal cancer (mCRC). Histological transformation is an important mechanism underlying the acquired resistance of non-small cell lung cancer and prostate cancer to targeted therapy. However, no report has examined the role of histological transformation in mCRC. Here, we report the first case of histologically transformed large cell neuroendocrine carcinoma from primary colon adenocarcinoma during antiangiogenesis and anti-PD-1 combination therapy. The histologic conversion was confirmed by the observation that the transformed large cell neuroendocrine carcinoma lesion retained the original mutational signature found in the primary tumor. Sequential tumor biopsy and dynamic changes in tumor markers demonstrated the transformed process. The histological transformation not only resulted in discordant responses to the same treatment but also significantly shortened overall survival. This case calls for more attention to histological transformation in mCRC. Tumor rebiopsy upon disease progression and monitoring dynamic changes in tumor markers would help to identify such cases.
   The case reported the histologic transformation from colon adenocarcinoma into large cell neuroendocrine carcinoma (LCNEC) after treatment. Notably, this case suggests that the phenotypic transformation into LCNEC might represent a novel mechanism of acquired resistance to antiangiogenesis and ICIs combination in metastatic colorectal cancer. image
C1 [Du, Feng; Xiao, Yanjie; Shi, Youwu; Sun, Jing; Sun, Zhiwei; Yang, Ying; Yu, Jing; Zhang, Xiaodong; Jia, Jun] Peking Univ, Canc Hosp & Inst, Minist Educ Beijing, VIPII Gastrointestinal Canc Div,Med Dept, 52 Fucheng Rd, Beijing 100142, Peoples R China.
   [Han, Ying] Peking Univ, Canc Hosp & Inst, Minist Educ Beijing, Key Lab Carcinogenesis & Translat Res,Dept Day Car, Beijing, Peoples R China.
   [Hu, Xiao] Peking Univ, Canc Hosp & Inst, Minist Educ Beijing, Key Lab Carcinogenesis & Translat Res,Dept Pathol, Beijing, Peoples R China.
C3 Peking University; Peking University; Peking University
RP Du, F; Jia, J (corresponding author), Peking Univ, Canc Hosp & Inst, Minist Educ Beijing, VIPII Gastrointestinal Canc Div,Med Dept, 52 Fucheng Rd, Beijing 100142, Peoples R China.
EM d609218518@126.com; vm26@netease.com
RI Jun, Jia/KHV-1561-2024
FU Beijing Excellent Talent Cultivation Subsidy Young Backbone Individual
   Project; Science Foundation of Peking University Cancer Hospital
   [A002226]
FX Beijing Excellent Talent Cultivation Subsidy Young Backbone Individual
   Project and Science Foundation of Peking University Cancer Hospital,
   Grant/Award Number: A002226
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NR 12
TC 2
Z9 2
U1 1
U2 1
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 159
EP 164
DI 10.1002/cai2.57
PG 6
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA G8M7Q
UT WOS:001319119700003
PM 38090055
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Battaglin, F
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   Millstein, J
   Yang, Y
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   Innocenti, F
   Mumenthaler, SM
   Jayachandran, P
   Kawanishi, N
   Lenz, A
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   Algaze, S
   Zhang, W
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   Seeber, A
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   Weinberg, BA
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   Marshall, JL
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   Lenz, HJ
AF Battaglin, Francesca
   Baca, Yasmine
   Millstein, Joshua
   Yang, Yan
   Xiu, Joanne
   Arai, Hiroyuki
   Wang, Jingyuan
   Ou, Fang-Shu
   Innocenti, Federico
   Mumenthaler, Shannon M.
   Jayachandran, Priya
   Kawanishi, Natsuko
   Lenz, Annika
   Soni, Shivani
   Algaze, Sandra
   Zhang, Wu
   Khoukaz, Taline
   Roussos Torres, Evanthia
   Seeber, Andreas
   Abraham, Jim P.
   Lou, Emil
   Philip, Philip A.
   Weinberg, Benjamin A.
   Shields, Anthony F.
   Goldberg, Richard M.
   Marshall, John L.
   Venook, Alan P.
   Korn, W. Michael
   Lenz, Heinz-Josef
TI <i>CCR5</i> and <i>CCL5</i> gene expression in colorectal cancer:
   comprehensive profiling and clinical value
SO JOURNAL FOR IMMUNOTHERAPY OF CANCER
LA English
DT Article
DE Immunotherapy; Gastrointestinal Neoplasms; Gene Expression Profiling;
   Molecular Targeted Therapy; Tumor Biomarkers
ID PEMBROLIZUMAB; BLOCKADE; CELLS
AB Background The C-C motif chemokine receptor 5 (CCR5)/C-C motif chemokine ligand 5 (CCL5) axis plays a major role in colorectal cancer (CRC). We aimed to characterize the molecular features associated with CCR5/CCL5 expression in CRC and to determine whether CCR5/CCL5 levels could impact treatment outcomes.Methods 7604 CRCs tested with NextGen Sequencing on DNA and RNA were analyzed. Molecular features were evaluated according to CCR5 and CCL5 tumor gene expression quartiles. The impact on treatment outcomes was assessed in two cohorts, including 6341 real-world patients and 429 patients from the Cancer and Leukemia Group B (CALGB)/SWOG 80405 trial.Results CCR5/CCL5 expression was higher in right-sided versus left-sided tumors, and positively associated with consensus molecular subtypes 1 and 4. Higher CCR5/CCL5 expression was associated with higher tumor mutational burden, deficiency in mismatch repair and programmed cell death ligand 1 (PD-L1) levels. Additionally, high CCR5/CCL5 were associated with higher immune cell infiltration in the tumor microenvironment (TME) of MMR proficient tumors. Ingenuity pathway analysis revealed upregulation of the programmed cell death protein 1 (PD-1)/PD-L1 cancer immunotherapy pathway, phosphatase and tensin homolog (PTEN) and peroxisome proliferator-activated receptors (PPAR) signaling, and cytotoxic T-lymphocyte antigen 4 (CTLA-4) signaling in cytotoxic T lymphocytes, whereas several inflammation-related pathways were downregulated. Low CCR5/CCL5 expression was associated with increased benefit from cetuximab-FOLFOX treatment in the CALGB/SWOG 80405 trial, where significant treatment interaction was observed with biologic agents and chemotherapy backbone.Conclusions Our data show a strong association between CCR5/CCL5 gene expression and distinct molecular features, gene expression profiles, TME cell infiltration, and treatment benefit in CRC. Targeting the CCR5/CCL5 axis may have clinical applications in selected CRC subgroups and may play a key role in developing and deploying strategies to modulate the immune TME for CRC treatment.
C1 [Battaglin, Francesca; Arai, Hiroyuki; Wang, Jingyuan; Mumenthaler, Shannon M.; Jayachandran, Priya; Kawanishi, Natsuko; Lenz, Annika; Soni, Shivani; Algaze, Sandra; Zhang, Wu; Khoukaz, Taline; Roussos Torres, Evanthia; Lenz, Heinz-Josef] Univ Southern Calif, Norris Comprehens Canc Ctr, Los Angeles, CA 90007 USA.
   [Baca, Yasmine; Xiu, Joanne; Abraham, Jim P.; Korn, W. Michael] Caris Life Sci, Phoenix, AZ USA.
   [Millstein, Joshua; Yang, Yan] Univ Southern Calif, Keck Sch Med, Dept Populat & Publ Hlth Sci, Los Angeles, CA USA.
   [Ou, Fang-Shu] Mayo Clin, Alliance Stat & Data Management Ctr, Rochester, MN USA.
   [Innocenti, Federico] Univ N Carolina, Chapel Hill, NC USA.
   [Mumenthaler, Shannon M.] Lawrence J Ellison Inst Transformat Med, Los Angeles, CA USA.
   [Seeber, Andreas] Innsbruck Med Univ, Comprehens Canc Ctr Innsbruck, Dept Hematol & Oncol, Innsbruck, Tirol, Austria.
   [Lou, Emil] Univ Minnesota, Div Hematol Oncol & Transplantat, Minneapolis, MN USA.
   [Philip, Philip A.] Wayne State Univ, Karmanos Canc Inst, Dept Oncol & Pharmacol, Detroit, MI USA.
   [Weinberg, Benjamin A.; Marshall, John L.] Georgetown Univ, Ruesch Ctr Cure Gastrointestinal Canc, Lombardi Comprehens Canc Ctr, Med Ctr, Washington, DC USA.
   [Shields, Anthony F.] Wayne State Univ, Karmanos Canc Inst, Dept Oncol, Detroit, MI USA.
   [Goldberg, Richard M.] West Virginia Univ, Canc Inst, Morgantown, WV USA.
   [Venook, Alan P.] Univ Calif San Francisco, San Francisco, CA USA.
C3 University of Southern California; University of Southern California;
   Mayo Clinic; University of North Carolina; University of North Carolina
   Chapel Hill; Medical University of Innsbruck; University of Minnesota
   System; University of Minnesota Twin Cities; Wayne State University;
   Barbara Ann Karmanos Cancer Institute; Georgetown University; Wayne
   State University; Barbara Ann Karmanos Cancer Institute; West Virginia
   University; University of California System; University of California
   San Francisco
RP Battaglin, F (corresponding author), Univ Southern Calif, Norris Comprehens Canc Ctr, Los Angeles, CA 90007 USA.
EM fbattagl@usc.edu
RI Millstein, Joshua/AFU-6153-2022; Mumenthaler, Shannon/AGY-8535-2022;
   Battaglin, Francesca/C-2746-2017
OI Battaglin, Francesca/0000-0002-9869-0163; Arai,
   Hiroyuki/0000-0002-1886-7070
FU National Cancer Institute of the National Institutes of Health
   [U10CA180821, UG1CA233163, UG1CA233373, UG1CA239758, P30CA014089,
   U10CA180888]; Gloria Borges WunderGlo Foundation; Dhont Family
   Foundation; Victoria and Philip Wilson Research Fund; San Pedro
   Peninsula Cancer Guild; Ming Hsieh Research; Daniel Butler Research
   Fund; Bristol -Myers Squibb; Genentech; Pfizer
FX Research reported in this publication was partly supported by the
   National Cancer Institute of the National Institutes of Health under
   Award Numbers U10CA180821 (to the Alliance for Clinical Trials in
   Oncology), UG1CA233163, UG1CA233373, UG1CA239758 (to BAW), P30CA014089
   (to H-JL), U10CA180888 (SWOG), Gloria Borges WunderGlo Foundation, Dhont
   Family Foundation, Victoria and Philip Wilson Research Fund, San Pedro
   Peninsula Cancer Guild, Ming Hsieh Research and Daniel Butler Research
   Fund. Also supported in part by funds from Bristol -Myers Squibb,
   Genentech, and Pfizer (to the Alliance for Clinical Trials in Oncology).
   The content is solely the responsibility of the authors and does not
   necessarily represent the official views of the National Institutes of
   Health. Clinical data from Cancer and Leukemia Group B 80405 were
   obtained directly from the Alliance for Clinical Trials in Oncology, a
   National Clinical Trials Network cooperative group, under Alliance study
   A152001. https://acknowledgments.alliancefound.org
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NR 25
TC 3
Z9 3
U1 1
U2 1
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 JAN
PY 2024
VL 12
IS 1
AR e007939
DI 10.1136/jitc-2023-007939
PG 15
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA FC9L6
UT WOS:001143666600002
PM 38212126
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Singh, S
   Gouri, V
   Samant, M
AF Singh, Sumeet
   Gouri, Vinita
   Samant, Mukesh
TI TGF-β in correlation with tumor progression, immunosuppression and
   targeted therapy in colorectal cancer
SO MEDICAL ONCOLOGY
LA English
DT Review
DE Colorectal cancer; TGF-beta; Immunosuppression; Immunotherapy; Natural
   compound; Therapeutic relevance
ID TRANSFORMING-GROWTH-FACTOR; EPITHELIAL-MESENCHYMAL TRANSITION;
   FLUOROURACIL PLUS CISPLATIN; COLON-CANCER; T-CELLS; DENDRITIC CELLS;
   URSOLIC ACID; PHASE-III; PHENETHYL ISOTHIOCYANATE; INFUSION FLUOROURACIL
AB Colorectal cancer (CRC) is a complex malignancy responsible for the second-highest cancer deaths worldwide. TGF-beta maintains normal cellular homeostasis by inhibiting the cell cycle and inducing apoptosis, but its elevated level is correlated with colorectal cancer progression, as TGF-beta is a master regulator of the epithelial-to-mesenchymal transition, a critical step of metastasis. Tumors, including CRC, use elevated TGF-beta levels to avoid immune surveillance by modulating immune cell differentiation, proliferation, and effector function. Presently, the treatment of advanced CRC is mainly based on chemotherapy, with multiple adverse effects. Thus, there is a need to develop alternate tactics because CRC continue to be mostly resistant to the present therapeutic regimen. TGF-beta blockade has emerged as a promising therapeutic target in cancer therapy. Blocking TGF-beta with phytochemicals and other molecules, such as antisense oligonucleotides, monoclonal antibodies, and bifunctional traps, alone or in combination, may be a safer and more effective way to treat CRC. Furthermore, combination immunotherapy comprising TGF-beta blockers and immune checkpoint inhibitors is gaining popularity because both molecules work synergistically to suppress the immune system. Here, we summarize the current understanding of TGF-beta as a therapeutic target for managing CRC and its context-dependent tumor-promoting or tumor-suppressing nature.
C1 [Singh, Sumeet; Gouri, Vinita; Samant, Mukesh] Soban Singh Jeena Univ, Dept Zool, Cell Mol Biol Lab, Almora, Uttarakhand, India.
   [Gouri, Vinita] Kumaun Univ, Dept Zool, Naini Tal, Uttaranchal, India.
C3 Kumaun University
RP Samant, M (corresponding author), Soban Singh Jeena Univ, Dept Zool, Cell Mol Biol Lab, Almora, Uttarakhand, India.
EM mukeshsamant@gmail.com
FU DST-FIST [SR/FST/LS-I/2018/131]
FX This work is supported by the DST-FIST Grant SR/FST/LS-I/2018/131 to the
   Department of Zoology, Soban Singh Jeena University.
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NR 184
TC 8
Z9 8
U1 1
U2 6
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1357-0560
EI 1559-131X
J9 MED ONCOL
JI Med. Oncol.
PD OCT 19
PY 2023
VL 40
IS 11
AR 335
DI 10.1007/s12032-023-02204-5
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA U6ML0
UT WOS:001085923200001
PM 37855975
DA 2025-01-04
ER

PT J
AU Akutagawa, T
   Aoki, S
   Yamamoto-Rikitake, M
   Iwakiri, R
   Fujimoto, K
   Toda, S
AF Akutagawa, Takashi
   Aoki, Shigehisa
   Yamamoto-Rikitake, Mihoko
   Iwakiri, Ryuichi
   Fujimoto, Kazuma
   Toda, Shuji
TI Cancer-adipose tissue interaction and fluid flow synergistically
   modulate cell kinetics, HER2 expression, and trastuzumab efficacy in
   gastric cancer
SO GASTRIC CANCER
LA English
DT Article
DE Cancer-associated adipocyte; Fluid flow; Human epidermal growth factor
   receptor 2 (HER2); Mitogen-activated protein kinase (MAPK); Trastuzumab
ID VASCULAR ENDOTHELIAL-CELLS; COLORECTAL-CANCER; SHEAR-STRESS;
   COLON-CANCER; CYTOPLASMIC OVEREXPRESSION; BOWEL MOVEMENT; STEM-CELLS;
   IN-VITRO; RISK; CONSTIPATION
AB Background Early local tumor invasion in gastric cancer results in likely encounters between cancer cells and submucosal and subserosal adipose tissue, but these interactions remain to be clarified. Microenvironmental mechanical forces, such as fluid flow, are known to modulate normal cell kinetics, but the effects of fluid flow on gastric cancer cells are poorly understood. We analyzed the cell kinetics and chemosensitivity in gastric cancer using a simple in vitro model that simultaneously replicated the cancer-adipocyte interaction and physical microenvironment.
   Methods Gastric cancer cells (MKN7 and MKN74) were seeded on rat adipose tissue fragment-embedded discs or collagen discs alone. To generate fluid flow, samples were placed on a rotatory shaker in a CO2 incubator. Proliferation, apoptosis, invasion, and motility-related molecules were analyzed by morphometry and immunostaining. Proteins were evaluated by western blot analysis. Chemosensitivity was investigated by trastuzumab treatment.
   Results Adipose tissue and fluid flow had a positive synergistic effect on the proliferative potential and invasive capacity of gastric cancer cells, and adipose tissue inhibited apoptosis in these cells. Adipose tissue upregulated ERK1/2 signaling in gastric cancer cells, but downregulated p38 signaling. Notably, adipose tissue and fluid flow promoted membranous and cytoplasmic HER2 expression and modulated chemosensitivity to trastuzumab in gastric cancer cells.
   Conclusion We have demonstrated that cancer-adipocyte interaction and physical microenvironment mutually modulate gastric cancer cell kinetics. Further elucidation of the microenvironmental regulation in gastric cancer will be very important for the development of strategies involving molecular targeted therapy.
C1 [Akutagawa, Takashi; Aoki, Shigehisa; Yamamoto-Rikitake, Mihoko; Toda, Shuji] Saga Univ, Fac Med, Dept Pathol & Microbiol, 5-1-1 Nabeshima, Saga, Saga 8498501, Japan.
   [Akutagawa, Takashi; Iwakiri, Ryuichi; Fujimoto, Kazuma] Saga Univ, Fac Med, Dept Internal Med & Gastrointestinal Endoscopy, 5-1-1 Nabeshima, Saga, Saga 8498501, Japan.
C3 Saga University; Saga University
RP Akutagawa, T; Aoki, S (corresponding author), Saga Univ, Fac Med, Dept Pathol & Microbiol, 5-1-1 Nabeshima, Saga, Saga 8498501, Japan.; Akutagawa, T (corresponding author), Saga Univ, Fac Med, Dept Internal Med & Gastrointestinal Endoscopy, 5-1-1 Nabeshima, Saga, Saga 8498501, Japan.
EM 14624001@edu.cc.saga-u.ac.jp; aokis@cc.saga-u.ac.jp
RI Aoki, Shigehisa/AFQ-9927-2022
OI Aoki, Shigehisa/0000-0002-1778-8944
FU Center for Clinical and Translational Research of Kyushu University
   Hospital; Japanese Ministry of Education, Culture, Sports, Science and
   Technology [17K09352, 16K09284]; Grants-in-Aid for Scientific Research
   [16K09284, 17K09352] Funding Source: KAKEN
FX This work was supported in part by the Center for Clinical and
   Translational Research of Kyushu University Hospital (to S.A.), and
   Grants-in-Aid from the Japanese Ministry of Education, Culture, Sports,
   Science and Technology for Scientific Research (no. 17K09352 to S.T. and
   no. 16K09284 to S.A.).
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NR 38
TC 14
Z9 15
U1 0
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1436-3291
EI 1436-3305
J9 GASTRIC CANCER
JI Gastric Cancer
PD NOV
PY 2018
VL 21
IS 6
BP 946
EP 955
DI 10.1007/s10120-018-0829-7
PG 10
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA GW8KL
UT WOS:000447226700006
PM 29696406
OA Bronze
DA 2025-01-04
ER

PT J
AU Zhang, JY
   Ali, KR
   Wang, JW
AF Zhang, Junyi
   Ali, Kamran
   Wang, Jianwei
TI Research Advances of Lipid Nanoparticles in the Treatment of Colorectal
   Cancer
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE lipid nanoparticles; colorectal cancer; tumor targeting; drug delivery;
   nanotechnology
ID DRUG-DELIVERY SYSTEMS; MESSENGER-RNA; IN-VITRO; PEGYLATED LIPOSOMES;
   ORAL DELIVERY; TARGETED NANOPARTICLES; IMMUNE-RESPONSE; PR-B; TUMOR;
   SIRNA
AB Colorectal cancer (CRC) is a common type of gastrointestinal tract (GIT) cancer and poses an enormous threat to human health. Current strategies for metastatic colorectal cancer (mCRC) therapy primarily focus on chemotherapy, targeted therapy, immunotherapy, and radiotherapy; however, their adverse reactions and drug resistance limit their clinical application. Advances in nanotechnology have rendered lipid nanoparticles (LNPs) a promising nanomaterial-based drug delivery system for CRC therapy. LNPs can adapt to the biological characteristics of CRC by modifying their formulation, enabling the selective delivery of drugs to cancer tissues. They overcome the limitations of traditional therapies, such as poor water solubility, nonspecific biodistribution, and limited bioavailability. Herein, we review the composition and targeting strategies of LNPs for CRC therapy. Subsequently, the applications of these nanoparticles in CRC treatment including drug delivery, thermal therapy, and nucleic acid-based gene therapy are summarized with examples provided. The last section provides a glimpse into the advantages, current limitations, and prospects of LNPs in the treatment of CRC.
C1 [Zhang, Junyi; Ali, Kamran; Wang, Jianwei] Zhejiang Univ, Affiliated Hosp 4, Sch Med, Yiwu, Peoples R China.
   [Zhang, Junyi; Ali, Kamran; Wang, Jianwei] Zhejiang Univ, Int Inst Med, Int Sch Med, Yiwu, Peoples R China.
   [Wang, Jianwei] Zhejiang Univ, Affiliated Hosp 2, Dept Colorectal Surg & Oncol, Key Lab Canc Prevent & Intervent,Minist Educ,Sch M, Hangzhou, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang University
RP Wang, JW (corresponding author), Zhejiang Univ, Affiliated Hosp 2, Dept Colorectal Surg & Oncol, Key Lab Canc Prevent & Intervent,Minist Educ,Sch M, Hangzhou, Peoples R China.
EM ypzju@zju.edu.cn
OI Ali, Kamran/0000-0002-0304-6130; Zhang, Junyi/0009-0006-3841-9458
FU Zhejiang Provincial Natural Science Foundation of China [LHDMZ23H160003]
FX We would like to thank the Zhejiang Provincial Natural Science
   Foundation of China for funding this research work with the project
   number "LHDMZ23H160003".
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NR 201
TC 3
Z9 3
U1 10
U2 10
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-2013
J9 INT J NANOMED
JI Int. J. Nanomed.
PY 2024
VL 19
BP 6693
EP 6715
DI 10.2147/IJN.S466490
PG 23
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA XM6B3
UT WOS:001262128700001
PM 38979534
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Chitkara, A
   Bakhtiar, M
   Sahin, IH
   Hsu, DN
   Zhang, JN
   Anamika, F
   Mahnoor, M
   Ahmed, R
   Gholami, S
   Saeed, A
AF Chitkara, Akshit
   Bakhtiar, Muhammad
   Sahin, Ibrahim Halil
   Hsu, Dennis
   Zhang, Janie
   Anamika, Fnu
   Mahnoor, Mahnoor
   Ahmed, Rabeea
   Gholami, Sepideh
   Saeed, Anwaar
TI A Meta-Analysis to Assess the Efficacy of HER2-Targeted Treatment
   Regimens in HER2-Positive Metastatic Colorectal Cancer (mCRC)
SO CURRENT ONCOLOGY
LA English
DT Review
DE trastuzumab deruxtecan; HER2-positive; tyrosine kinase inhibitors;
   metastatic colorectal cancer
ID ESMO CONSENSUS GUIDELINES; PLUS TRASTUZUMAB; OPEN-LABEL; MULTICENTER;
   STATISTICS; MANAGEMENT; LAPATINIB; COLON
AB Recent trials provide evidence that HER2 is a potential new target for patients with colorectal cancer. While HER2-positive tumors do not show a very encouraging response to anti-HER2-positive agents like trastuzumab alone, promising results have been observed when combined with other synergistically acting tyrosine kinase inhibitors (TKIs). Our meta-analysis was conducted following the Cochrane Handbook and written following the PRISMA guidelines. The protocol was registered on PROSPERO with the registration number CRD42022338935. After a comprehensive search for relevant articles, 14 CTs were identified and uploaded to Rayyan, and six trials were ultimately selected for inclusion. The meta-analysis revealed that a median of three prior lines of therapy was used before enrolling in the six trials comprising 238 patients with HER2-positive metastatic colorectal cancer (mCRC). The pooled objective response rate (ORR) and disease control rate (DCR) were 31.33% (95% confidence interval [CI] 24.27-38.39) and 74.37% (95% CI 64.57-84.17), respectively. The pooled weighted progression-free survival (PFS) was 6.2 months. The pooled ORR and DCR meta-analysis indicate a significant response to HER2-targeted therapy in this patient in HER2-positive mCRC. Additionally, a pooled PFS of 6.2 months suggests that HER2-targeted treatment regimens are associated with a meaningful improvement in survival outcomes in this population.
C1 [Chitkara, Akshit] Univ Calif Riverside, Dept Internal Med, Riverside, CA 92521 USA.
   [Bakhtiar, Muhammad; Ahmed, Rabeea] King Edward Med Univ, Mayo Hosp, Sch Med, Lahore 54000, Pakistan.
   [Sahin, Ibrahim Halil; Hsu, Dennis; Zhang, Janie; Saeed, Anwaar] Univ Pittsburgh Med Ctr UPMC, Dept Med, Div Hematol Oncol, Pittsburgh, PA 15232 USA.
   [Anamika, Fnu] Hackensack Meridian Ocean Univ, Dept Internal Med, Med Ctr, Brick, NJ 08724 USA.
   [Mahnoor, Mahnoor] Mohtarma Benazir Bhutto Shaheed Med Coll, Sch Med, Mirpur 10230, Pakistan.
   [Gholami, Sepideh] Northwell Hlth Canc Inst, Dept Hematol Oncol, New Hyde Pk, NY 11042 USA.
C3 University of California System; University of California Riverside;
   Pennsylvania Commonwealth System of Higher Education (PCSHE); University
   of Pittsburgh
RP Saeed, A (corresponding author), Univ Pittsburgh Med Ctr UPMC, Dept Med, Div Hematol Oncol, Pittsburgh, PA 15232 USA.
EM akshit.chitkara@medsch.ucr.edu; hussainbakhtiar77@gmail.com;
   sahinih@upmc.edu; hsudj@upmc.edu; zhangjy2@upmc.edu;
   fnu.anamika@hmhn.org; mahnoor2653@gmail.com; ahmedra99@gmail.com;
   sgholami@northwell.edu; saeeda3@upmc.edu
RI Sahin, Ibrahim/AAO-1035-2020; Bakhtiar, Muhammad/KEE-6933-2024;
   Chitkara, Akshit/AAY-7022-2020
OI Bakhtiar, Muhammad/0009-0002-5742-8895; Chitkara,
   Akshit/0000-0003-0198-186X
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NR 39
TC 4
Z9 4
U1 0
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1198-0052
EI 1718-7729
J9 CURR ONCOL
JI Curr. Oncol.
PD SEP
PY 2023
VL 30
IS 9
BP 8266
EP 8277
DI 10.3390/curroncol30090600
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA S8CH0
UT WOS:001073386500001
PM 37754515
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Cho, M
   Beechinor, R
   Gholami, S
   Grothey, A
AF Cho, May
   Beechinor, Ryan
   Gholami, Sepideh
   Grothey, Axel
TI Precision Medicine for the Treatment of Colorectal Cancer: the Evolution
   and Status of Molecular Profiling and Biomarkers
SO CURRENT COLORECTAL CANCER REPORTS
LA English
DT Article
DE Colorectal cancer; Targeted therapy; Molecular targets; Biomarkers;
   EGFR; BRAF; HER-2; NRTK; Microsatellite instability; Tumor mutational
   burden
ID KRAS WILD-TYPE; PHASE-III TRIAL; CETUXIMAB PLUS IRINOTECAN; TUMOR
   MUTATIONAL BURDEN; POSITIVE SOLID TUMORS; 1ST-LINE TREATMENT;
   MISMATCH-REPAIR; COLON-CANCER; POOLED ANALYSIS;
   MICROSATELLITE-INSTABILITY
AB Purpose of Review The application of advanced genomic testing to develop tumor-specific molecular profiles is essential to facilitating precision medicine pharmacotherapy. These approaches are highly relevant in colorectal cancer, where tumors frequently contain druggable molecular mutations, as well as the potential to respond to immunotherapy. Here we review the literature characterizing biomarker-driven pharmacotherapy for colorectal cancer, and highlight the pivotal ongoing trials that will help inform future treatment of this disease. Recent Findings Both prospective and retrospective studies have confirmed that the benefit from adding anti-epidermal growth factor receptor therapy is limited to patients with stage IV disease, RAS wild-type tumors, and left-sided primary tumors. Furthermore, patients with BRAF-mutated tumors derive significantly less benefit from the addition anti-epidermal growth factor receptor therapy. The use of BRAF inhibitors in the second-line setting is associated with a relatively high response rate, and regimens incorporating first-line treatment with BRAF inhibitors may soon become standard of care for patients with BRAF-mutated tumors. In the relapsed setting, the use of targeted agents and immunotherapy should be prioritized for patients with respective tumor profiles. There has been significant advancement in the understanding of how to utilize molecular profiling and tumor biomarkers to tailor pharmacotherapy in colorectal cancer. Future studies should continue to incorporate these tests at enrollment to further define patient cohorts deriving the greatest benefit from precision medicine, characterize ideal sequence of therapy, and advance understanding of drug resistance mechanisms.
C1 [Cho, May] Univ Calif Irvine, Hematol Oncol, Irvine, CA 92868 USA.
   [Beechinor, Ryan; Gholami, Sepideh] UC Davis Comprehens Canc Ctr, Sacramento, CA 95817 USA.
   [Grothey, Axel] West Canc Ctr, Med Oncol, Germantown, TN 38138 USA.
C3 University of California System; University of California Irvine
RP Grothey, A (corresponding author), West Canc Ctr, Med Oncol, Germantown, TN 38138 USA.
EM agrothey@WESTCLINIC.com
RI Beechinor, Ryan/AAU-2156-2021
OI Grothey, Axel/0000-0002-9341-6499; Beechinor, Ryan/0000-0002-2774-0899
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NR 122
TC 2
Z9 2
U1 0
U2 1
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 AUG
PY 2021
VL 17
IS 4
BP 55
EP 68
DI 10.1007/s11888-021-00466-7
EA JUL 2021
PG 14
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA TS6XP
UT WOS:000678141500001
DA 2025-01-04
ER

PT J
AU Yao, YMM
   Donoho, GP
   Iversen, PW
   Zhang, YY
   Van Horn, RD
   Forest, A
   Novosiadly, RD
   Webster, YW
   Ebert, P
   Bray, S
   Ting, JC
   Aggarwal, A
   Henry, JR
   Tiu, RV
   Plowman, GD
   Peng, SB
AF Yao, Yung-mae M.
   Donoho, Gregory P.
   Iversen, Philip W.
   Zhang, Youyan
   Van Horn, Robert D.
   Forest, Amelie
   Novosiadly, Ruslan D.
   Webster, Yue Wang
   Ebert, Philip
   Bray, Steven
   Ting, Jason C.
   Aggarwal, Amit
   Henry, James R.
   Tiu, Ramon V.
   Plowman, Gregory D.
   Peng, Sheng-Bin
TI Mouse PDX Trial Suggests Synergy of Concurrent Inhibition of RAF and
   EGFR in Colorectal Cancer with <i>BRAF</i> or <i>KRAS</i> Mutations
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; CETUXIMAB PLUS IRINOTECAN; ACQUIRED-RESISTANCE;
   TARGETED THERAPY; COLON-CANCER; PHASE-III; PANITUMUMAB; VEMURAFENIB;
   LY3009120; ANTIBODY
AB Purpose: To evaluate the antitumor efficacy of cetuximab in combination with LSN3074753, an analog of LY3009120 and pan-RAF inhibitor in 79 colorectal cancer patient-derived xenograft (PDX) models.
   Experimental Design: Seventy-nine well-characterized colorectal cancer PDX models were employed to conduct a single mouse per treatment group (n = 1) trial.
   Results: Consistent with clinical results, cetuximab was efficacious in wild-type KRAS and BRAF PDX models, with an overall response rate of 6.3% and disease control rate (DCR) of 20.3%. LSN3074753 was active in a small subset of PDX models that harbored KRAS or BRAF mutations. However, the combination treatment displayed the enhanced antitumor activity with DCR of 35.4%. Statistical analysis revealed that BRAF and KRAS mutations were the best predictors of the combinatorial activity and were significantly associated with synergistic effect with a P value of 0.01 compared with cetuximab alone. In 12 models with BRAF mutations, the combination therapy resulted in a DCR of 41.7%, whereas either monotherapy had aDCRof 8.3%. Among 44 KRAS mutation models, cetuximab or LSN3074753 monotherapy resulted in a DCR of 13.6% or 11.4%, respectively, and the combination therapy increasedDCRto 34.1%. Molecular analysis suggests that EGFR activation is a potential feedback and resistant mechanism of pan-RAF inhibition.
   Conclusions: MAPK and EGFR pathway activations are two major molecular hallmarks of colorectal cancer. This mouse PDX trial recapitulated clinical results of cetuximab. Concurrent EGFR and RAF inhibition demonstrated synergistic antitumor activity for colorectal cancer PDX models with a KRAS or BRAF mutation. (C) 2017 AACR.
C1 [Yao, Yung-mae M.; Forest, Amelie; Novosiadly, Ruslan D.; Plowman, Gregory D.] Eli Lilly & Co, Oncol Discovery Res, New York, NY USA.
   [Donoho, Gregory P.; Zhang, Youyan; Van Horn, Robert D.; Ebert, Philip; Bray, Steven; Ting, Jason C.; Aggarwal, Amit; Plowman, Gregory D.; Peng, Sheng-Bin] Eli Lilly & Co, Oncol Business Unit, Oncol Discovery Res, Indianapolis, IN 46285 USA.
   [Iversen, Philip W.] Eli Lilly & Co, Oncol Business Unit, Stat, Indianapolis, IN 46285 USA.
   [Webster, Yue Wang] Eli Lilly & Co, Oncol Business Unit, IT Bioinformat, Indianapolis, IN 46285 USA.
   [Henry, James R.] Eli Lilly & Co, Oncol Business Unit, Discovery Chem, Indianapolis, IN 46285 USA.
   [Tiu, Ramon V.] Eli Lilly & Co, Oncol Business Unit, EarlyPhase Oncol, Indianapolis, IN 46285 USA.
C3 Eli Lilly; Eli Lilly; Eli Lilly; Eli Lilly; Eli Lilly; Eli Lilly
RP Peng, SB (corresponding author), Eli Lilly & Co, Lilly Corp Ctr, Indianapolis, IN 46285 USA.
EM peng-sheng-bin@lilly.com
OI Bray, Steven/0000-0002-0854-8121; Ebert, Philip/0000-0002-8945-2948;
   Donoho, Greg/0009-0007-8865-5093
FU Eli Lilly and Company
FX LThis work was supported by Eli Lilly and Company.
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NR 49
TC 37
Z9 41
U1 2
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD SEP 15
PY 2017
VL 23
IS 18
BP 5547
EP 5560
DI 10.1158/1078-0432.CCR-16-3250
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FH2DD
UT WOS:000410948000024
PM 28611205
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Saha, S
   Ghosh, M
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   Wen, AS
   Galluzzi, L
   Martinez, LA
   Montrose, DC
AF Saha, Suchandrima
   Ghosh, Monisankar
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TI Serine Depletion Promotes Antitumor Immunity by Activating Mitochondrial
   DNA-Mediated cGAS-STING Signaling
SO CANCER RESEARCH
LA English
DT Article
ID METABOLISM; CANCER; PROGNOSIS; RELEASE; MTDNA
AB Serine is critical for supporting cancer metabolism, and depriving malignant cells of this nonessential amino acid exerts antineoplastic effects, in large part, through disrupting metabolic pathways. Given the intricate relationship between cancer metabolism and the immune system, the metabolic defects imposed by serine deprivation might impact tumor-targeting immunity. In this study, we demonstrated that restricting endogenous and exogenous sources of serine in colorectal cancer cells results in mitochondrial dysfunction, leading to mitochondrial DNA (mtDNA) accumulation in the cytosol and consequent cGAS-STING1-driven type I IFN secretion. Depleting mtDNA or blocking its release attenuated cGAS-STING1 activation during serine deprivation. In vivo studies revealed that serine deprivation limits tumor growth, accompanied by enhanced type I IFN signaling and intratumoral infiltration of immune effector cells. Notably, the tumor-suppressive and immune-enhancing effects of serine restriction were impaired by T-cell depletion and IFN receptor blockade. Moreover, disrupting cGAS-STING1 signaling in colorectal cancer cells limited the immunostimulatory and tumor-suppressive effects of serine deprivation. Lastly, serine depletion increased the sensitivity of tumors to an immune checkpoint inhibitor targeting PD-1. Taken together, these findings reveal a role for serine as a suppressor of antitumor immunity, suggesting that serine deprivation may be employed to enhance tumor immunogenicity and improve responsiveness to immune checkpoint inhibitors.
   Significance: Depriving cancer cells of serine provokes mitochondrial perturbations that induce cytosolic mitochondrial DNA accumulation and subsequent activation of cGAS-STING signaling, stimulating tumor-targeting immune responses that can be enhanced with PD-1 targeted therapy.
C1 [Saha, Suchandrima; Ghosh, Monisankar; Li, Jinyu; Wen, Asher; Martinez, Luis A.; Montrose, David C.] SUNY Stony Brook, Dept Pathol, Renaissance Sch Med, MART Bldg,9M 0816,Lauterbur Dr, Stony Brook, NY 11794 USA.
   [Galluzzi, Lorenzo] Weill Cornell Med Coll, Dept Radiat Oncol, New York, NY USA.
   [Galluzzi, Lorenzo] Sandra & Edward Meyer Canc Ctr, New York, NY USA.
   [Galluzzi, Lorenzo] Caryl & Israel Englander Inst Precis Med, New York, NY USA.
   [Martinez, Luis A.; Montrose, David C.] Stony Brook Canc Ctr, Stony Brook, NY USA.
C3 State University of New York (SUNY) System; Stony Brook University;
   Stony Brook University Hospital; Cornell University; Weill Cornell
   Medicine; State University of New York (SUNY) System; Stony Brook
   University
RP Montrose, DC (corresponding author), SUNY Stony Brook, Dept Pathol, Renaissance Sch Med, MART Bldg,9M 0816,Lauterbur Dr, Stony Brook, NY 11794 USA.
EM david.montrose@stonybrookmedicine.edu
RI jinyu, Li/JQV-7729-2023; Li, Jinyu/F-8820-2014
OI Ghosh, Monisankar/0000-0002-7393-0175; Li, Jinyu/0000-0002-7677-9992;
   Wen, Asher/0009-0008-1145-2017; Saha, Suchandrima/0009-0002-1130-1303;
   Montrose, David/0000-0002-5687-0406
FU American Cancer Society [21-143-01-IRG]; Stony Brook Cancer Center and
   Bahl Center for Metabolomics and Imaging; NIH/NCI [CA271915, CA274291];
   US DoD BCRP [W81XWH2120034]; Laura Ziskin Prize in Translational
   Research [ZP-6177]; Leukemia and Lymphoma Society; Functional Genomics
   Initiative; Pre-SPORE grant; Sandra and Edward Meyer Cancer Center;
   Department of Radiation Oncology at Weill Cornell Medicine; Lytix
   Biopharma (Oslo, Norway); Promontory (New York, NY); Onxeo (Paris,
   France);  [5R01CA166974-08]
FX This work is supported in part by Institutional Research Grant
   21-143-01-IRG from the American Cancer Society and startup funds from
   the Stony Brook Cancer Center and Bahl Center for Metabolomics and
   Imaging (D.C. Montrose) and by 5R01CA166974-08 (L.A. Martinez). L.
   Galluzzi is/has been supported (as a PI unless otherwise indicated) by
   one R01 grant from the NIH/NCI (#CA271915); by two Breakthrough Level 2
   grants from the US DoD BCRP (#BC180476P1 and #BC210945); by a grant from
   the Starr Cancer Consortium (#I16-0064); by a Transformative Breast
   Cancer Consortium Grant from the US DoD BCRP (#W81XWH2120034, PI:
   Formenti); by a U54 grant from NIH/NCI (#CA274291, PI: Deasy, Formenti,
   Weichselbaum); by the 2019 Laura Ziskin Prize in Translational Research
   (#ZP-6177, PI: Formenti) from the Stand Up to Cancer; by a Mantle Cell
   Lymphoma Research Initiative grant (PI: Chen-Kiang) from the Leukemia
   and Lymphoma Society; by a Rapid Response Grant from the Functional
   Genomics Initiative (New York, NY), by a pre-SPORE grant (PI: Demaria,
   Formenti) and a Clinical Trials Innovation Grant from the Sandra and
   Edward Meyer Cancer Center (New York, NY); by startup funds from the
   Department of Radiation Oncology at Weill Cornell Medicine (New York,
   NY); by industrial collaborations with Lytix Biopharma (Oslo, Norway),
   Promontory (New York, NY), and Onxeo (Paris, France); and by donations
   from Promontory (New York, NY), the Luke Heller TECPR2 Foundation
   (Boston, MA), Sotio a.s. (Prague, Czech Republic), Lytix Biopharma
   (Oslo, Norway), Onxeo (Paris, France), Ricerchiamo (Brescia, Italy), and
   Noxopharm (Chatswood, Australia).
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NR 50
TC 5
Z9 5
U1 7
U2 7
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 AUG 15
PY 2024
VL 84
IS 16
BP 2645
EP 2659
DI 10.1158/0008-5472.CAN-23-1788
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C8O0K
UT WOS:001291894000002
PM 38861367
DA 2025-01-04
ER

PT J
AU Hashimoto, T
   Takayanagi, D
   Yonemaru, J
   Naka, T
   Nagashima, K
   Machida, E
   Kohno, T
   Yatabe, Y
   Kanemitsu, Y
   Hamamoto, R
   Takashima, A
   Shiraishi, K
   Sekine, S
AF Hashimoto, Taiki
   Takayanagi, Daisuke
   Yonemaru, Junpei
   Naka, Tomoaki
   Nagashima, Kengo
   Machida, Erika
   Kohno, Takashi
   Yatabe, Yasushi
   Kanemitsu, Yukihide
   Hamamoto, Ryuji
   Takashima, Atsuo
   Shiraishi, Kouya
   Sekine, Shigeki
TI A comprehensive appraisal of HER2 heterogeneity in <i>HER2</i>-amplified
   and HER2-low colorectal cancer
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
ID INTRATUMORAL HETEROGENEITY; BREAST-CANCER; AMPLIFICATION
AB BackgroundThis study aimed to elucidate the clinicopathological and molecular features of HER2-amplified and HER2-low colorectal cancers (CRCs). We also characterised HER2 expression statuses in CRCs focusing on their intratumoral heterogeneity and alterations in metastatic lesions to establish practical HER2 status assessment.MethodsWe evaluated 1009 CRCs for HER2 expression and HER2 amplification by immunohistochemistry and FISH, respectively, and correlated the results to clinicopathological and molecular data. For HER2-positive tumours, HER2 expression in metastatic lesions was also assessed.ResultsTwenty-five HER2-amplified (2.5%) and 46 HER2-low tumours (4.6%) were identified. HER2-amplified tumours consistently lacked a mucinous component and HER2-low tumours tended to be in the right colon, but no other clinicopathological features were noted. KRAS, NRAS or BRAF mutations were detected in only two HER2-amplified tumours (8%), whereas 23 HER2-low tumours (50%) had one of these mutations. Most HER2-amplified and HER2-low tumours showed a homogeneous or mosaic HER2 expression pattern and a clustered heterogeneous expression pattern was rather rare. HER2 expression was maintained in most metastatic lesions in both HER2-amplified (93%) and HER2-low tumours (81%).ConclusionsThese results suggest that biopsy-based assessment of primary lesions is appropriate for the identification of CRC patients eligible for systemic HER2-targeted therapy.
C1 [Hashimoto, Taiki; Yonemaru, Junpei; Naka, Tomoaki; Yatabe, Yasushi; Sekine, Shigeki] Natl Canc Ctr, Div Diagnost Pathol, Tokyo, Japan.
   [Takayanagi, Daisuke; Machida, Erika; Kohno, Takashi; Shiraishi, Kouya] Natl Canc Ctr, Div Genome Biol, Tokyo, Japan.
   [Takayanagi, Daisuke] Showa Univ, Dept Med, Div Med Oncol, Sch Med, Tokyo, Japan.
   [Takayanagi, Daisuke] Showa Univ, Clin Res Inst Clin Pharmacol & Therapeut, Dept Clin Diagnost Oncol, Tokyo, Japan.
   [Nagashima, Kengo] Keio Univ Hosp, Clin & Translat Res Ctr, Biostat Unit, Tokyo, Japan.
   [Yatabe, Yasushi; Sekine, Shigeki] Natl Canc Ctr, Div Mol Pathol, Tokyo, Japan.
   [Kanemitsu, Yukihide] Natl Canc Ctr, Dept Colorectal Surg, Tokyo, Japan.
   [Hamamoto, Ryuji] Natl Canc Ctr, Div Med AI Res & Dev, Tokyo, Japan.
   [Takashima, Atsuo] Natl Canc Ctr, Div Gastrointestinal Med Oncol, Tokyo, Japan.
   [Shiraishi, Kouya] Natl Canc Ctr, Dept Clin Genom, Tokyo, Japan.
C3 National Cancer Center - Japan; National Cancer Center - Japan; Showa
   University; Showa University; Keio University; National Cancer Center -
   Japan; National Cancer Center - Japan; National Cancer Center - Japan;
   National Cancer Center - Japan; National Cancer Center - Japan
RP Sekine, S (corresponding author), Natl Canc Ctr, Div Diagnost Pathol, Tokyo, Japan.; Sekine, S (corresponding author), Natl Canc Ctr, Div Mol Pathol, Tokyo, Japan.
EM ssekine@ncc.go.jp
RI Hamamoto, Ryuji/AAF-9600-2019; Takayanagi, Daisuke/GQI-2016-2022; Kohno,
   Takashi/M-8823-2013; Nagashima, Kengo/I-4258-2019; Nagashima,
   Kengo/I-1726-2013; Hashimoto, Taiki/HKE-9203-2023; YATABE,
   Yasushi/J-6461-2014
OI Nagashima, Kengo/0000-0003-4529-9045; Hashimoto,
   Taiki/0000-0003-3148-9243; YATABE, Yasushi/0000-0003-1788-559X;
   Takayanagi, Daisuke/0000-0001-9644-9782
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NR 35
TC 6
Z9 6
U1 5
U2 12
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 2023
VL 129
IS 7
BP 1176
EP 1183
DI 10.1038/s41416-023-02382-z
EA AUG 2023
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA T4BJ6
UT WOS:001042773300002
PM 37543670
DA 2025-01-04
ER

PT J
AU Huang, SY
   Qing, C
   Huang, ZK
   Zhu, YF
AF Huang, Shuying
   Qing, Cheng
   Huang, Zikun
   Zhu, Yuanfang
TI The long non-coding RNA CCAT2 is up-regulated in ovarian cancer and
   associated with poor prognosis
SO DIAGNOSTIC PATHOLOGY
LA English
DT Article
DE Ovarian cancer; LncRNAs; Colon cancer associated transcript 2; Prognosis
ID GASTRIC-CANCER; EXPRESSION; PROMOTES; IDENTIFICATION; TUMORIGENESIS;
   METASTASIS; BIOMARKERS; GROWTH
AB Background: Ovarian cancer is a malignant tumor with a poor prognosis. Accumulating evidence demonstrates that long non-coding RNAs (lncRNAs) are emerging regulators in cancer biology, and can be used as potential biomarkers for cancer diagnosis, prognosis and targeted therapy. The lncRNA CCAT2 (colon cancer associated transcript 2) was recently shown to be involved in several cancers; however, its role in ovarian cancer remains unknown.
   Methods: Expression levels of the lncRNA CCAT2 in ovarian cancer tissues, adjacent normal tissues, and cell lines were assessed by quantitative real-time PCR. Then, the associations of CCAT2 expression levels with clinicopathological features and prognosis were evaluated. In addition, CCAT2 functions in tumor progression and invasion were further determined by siRNA-induced CCAT2 silencing in vitro.
   Results: Expression levels of the lncRNA CCAT2 in ovarian cancer tissues and cell lines were significantly higher compared with values obtained for adjacent non-tumor tissues and normal ovarian epithelial cells. Interestingly, higher CCAT2 expression levels were associated with a shorter overall survival (P = 0.006) and disease-free survival (P = 0.001) in ovarian cancer patients. In addition, CCAT2 expression was positively correlated with FIGO stage (P = 0.002), tumor grade (P = 0.006) and distant metastasis (P < 0.001). Moreover, CCAT2 knockdown in ovarian cancer cells markedly suppressed cell proliferation, migration, and invasion.
   Conclusions: The lncRNA CCAT2 is a novel factor involved in ovarian cancer progression, and constitutes a potential prognostic biomarker and therapeutic target for patients with ovarian cancer.
C1 [Huang, Shuying; Zhu, Yuanfang] Nanchang Univ, Affiliated Hosp 1, Dept Obstet & Gynecol, Nanchang 330006, Jiangxi, Peoples R China.
   [Qing, Cheng] Nanchang Univ, Affiliated Hosp 1, Intens Care Unit, Nanchang 330006, Jiangxi, Peoples R China.
   [Huang, Zikun] Nanchang Univ, Affiliated Hosp 1, Dept Clin Lab, Nanchang 330006, Jiangxi, Peoples R China.
   [Zhu, Yuanfang] Shenzhen Baoan Matemal & Chlid Hlth Hosp, Dept Obstet & Gynecol, Shenzhen 518133, Guangdong, Peoples R China.
C3 Nanchang University; Nanchang University; Nanchang University
RP Zhu, YF (corresponding author), Nanchang Univ, Affiliated Hosp 1, Dept Obstet & Gynecol, Nanchang 330006, Jiangxi, Peoples R China.; Zhu, YF (corresponding author), Shenzhen Baoan Matemal & Chlid Hlth Hosp, Dept Obstet & Gynecol, Shenzhen 518133, Guangdong, Peoples R China.
EM zyf20151207@163.com
FU Jiangxi Provincial Natural Science Foundation of China [20151BAB205046]
FX This study was supported by the Jiangxi Provincial Natural Science
   Foundation of China (20151BAB205046).
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NR 25
TC 81
Z9 95
U1 0
U2 15
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1746-1596
J9 DIAGN PATHOL
JI Diagn. Pathol.
PD JUN 10
PY 2016
VL 11
AR 49
DI 10.1186/s13000-016-0499-x
PG 7
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA FH7FD
UT WOS:000411348300001
PM 27283598
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Rath, T
   Kiesslich, R
   Neurath, MF
   Atreya, R
AF Rath, Timo
   Kiesslich, Ralf
   Neurath, Markus F.
   Atreya, Raja
TI Molecular imaging within the lower gastrointestinal tract: From
   feasibility to future
SO DIGESTIVE ENDOSCOPY
LA English
DT Review
DE colorectal cancer; endoscopy; inflammatory bowel diseases; molecular
   imaging
ID COLORECTAL-CANCER; ENDOSCOPY; ADENOMAS; DYSPLASIA; ANTIBODY;
   IDENTIFICATION; SURVEILLANCE; COLONOSCOPY; NEOPLASIA; PEPTIDE
AB Molecular imaging is based on the labelling of defined molecular targets through the utilization of fluorescently linked probes and their subsequent detection with high-resolution endoscopic devices, thereby enabling visualization of single molecules including receptors. Whereas early studies have used molecular imaging for improved visualization and detection of early dysplasia and cancer as well as for assessing intestinal inflammation and inflammation-associated cancer within the gastrointestinal (GI) tract, more recent studies have impressively demonstrated that molecular imaging can also be used to characterize and visualize the molecular fingerprint of cancer and inflammation in vivo and in real time. With this, molecular imaging can be used to guide expression-tailored individualized therapy. With the rapid expansion and diversification of the repertoire of biological agents utilized in inflammatory bowel disease and cancer, this approach is gaining increasing attention. Within this review, we first summarize the technical components commonly used for molecular imaging and then review preclinical and clinical studies and evolving clinical applications on molecular imaging within the lower GI tract. Molecular imaging has the potential to significantly change endoscopic diagnosis and subsequent targeted therapy of gastrointestinal cancer and chronic gastrointestinal diseases.
C1 [Rath, Timo; Neurath, Markus F.; Atreya, Raja] Univ Hosp Erlangen, Div Gastroenterol, Ludwig Demling Endoscopy Ctr Excellence, Ulmenweg 18, D-91054 Erlangen, Germany.
   [Kiesslich, Ralf] Helios Dr Horst Schmidt Kliniken, Div Gastroenterol, Dept Med, Wiesbaden, Germany.
C3 University of Erlangen Nuremberg
RP Rath, T (corresponding author), Univ Hosp Erlangen, Div Gastroenterol, Ludwig Demling Endoscopy Ctr Excellence, Ulmenweg 18, D-91054 Erlangen, Germany.
EM Timo.Rath@uk-erlangen.de
RI Ralf Kiesslich, Dr./AAK-9313-2021
OI Rath, Timo/0000-0002-7728-9338
CR [Anonymous], GUT
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NR 48
TC 5
Z9 5
U1 0
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0915-5635
EI 1443-1661
J9 DIGEST ENDOSC
JI Dig. Endosc.
PD NOV
PY 2018
VL 30
IS 6
BP 730
EP 738
DI 10.1111/den.13251
PG 9
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA GZ9OL
UT WOS:000449829700002
PM 30075487
OA Bronze
DA 2025-01-04
ER

PT J
AU Liao, PF
   Wu, TW
   Peng, TR
AF Liao, Pei-Fei
   Wu, Ta-Wei
   Peng, Tzu-Rong
TI Monoclonal Antibodies for First-Line Treatment of Metastatic Colorectal
   Cancer
SO AMERICAN JOURNAL OF THERAPEUTICS
LA English
DT Article
DE monoclonal antibodies; metastatic colorectal cancer; chemotherapy;
   progression-free survival
ID CETUXIMAB PLUS IRINOTECAN; PHASE-III; CHEMOTHERAPY; KRAS; FLUOROURACIL;
   BEVACIZUMAB; LEUCOVORIN; SURVIVAL; TRIAL; METAANALYSIS
AB Background:In addition to discontinuing treatment at disease progression, cumulative toxicity limitations and genetic mutations play important roles in chemotherapy choice in metastatic colorectal cancer (mCRC). However, in recent years, targeted therapies, such as immune checkpoint inhibitors or monoclonal antibodies (MoAbs), have been used with chemotherapy to improve clinical outcomes in patients with mCRC.Areas of Uncertainty:Approximately 15% of patients with CRC would be eligible for further targeted therapy with immune checkpoint inhibitors based on genetic testing, but most patients with CRC would not qualify, especially Kirsten rat sarcoma wild-type. Therefore, adding MoAb is only an option for most patients until disease progression or unacceptable toxicity occurs. However, the results are not consistent with the combination of MoAb and different chemotherapy bases. In addition, most results from combining MoAb with different chemotherapy bases are not consistent.Data Sources:This meta-analysis includes published of the PubMed and Embase databases, limited to English literature, and patients were treated with MoAb combination. Randomized control trials conducted published up to May 2021 were considered for inclusion.Therapeutic Advances:Fluoropyrimidine-based chemotherapy has been the backbone of palliative therapy for mCRC, with demonstrated benefits. This article will review the efficacy and safety of randomized control trials comparing different MoAb with fluoropyrimidine-based chemotherapy as first-line therapy for patients with mCRC, particularly in Kirsten rat sarcoma wild-type.Conclusion:This meta-analysis revealed that MoAb plus chemotherapy has better progression-free survival and objective response rate than chemotherapy alone. However, treatment-related serious adverse events (grade >= 3) should be considered, particularly severe rash, diarrhea, and hypertension.
C1 [Liao, Pei-Fei; Wu, Ta-Wei; Peng, Tzu-Rong] Taipei Tzu Chi Hosp, Buddhist Tzu Chi Med Fdn, Dept Pharm, 289 Jianguo Rd, New Taipei City 23142, Taiwan.
C3 Buddhist Tzu Chi General Hospital; Taipei Tzu Chi Hospital
RP Peng, TR (corresponding author), Taipei Tzu Chi Hosp, Buddhist Tzu Chi Med Fdn, Dept Pharm, 289 Jianguo Rd, New Taipei City 23142, Taiwan.
EM kuifuture@gmail.com; alwaysluckys777@yahoo.com.tw;
   tzu.rong@tzuchi.com.tw
OI peng, tzu-rong/0000-0002-0754-5682
FU Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation
   [TCRD-TPE-111-54]
FX Supported by grants from the Taipei Tzu Chi Hospital, Buddhist Tzu Chi
   Medical Foundation (TCRD-TPE-111-54).
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NR 45
TC 0
Z9 0
U1 2
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1075-2765
EI 1536-3686
J9 AM J THER
JI Am. J. Ther.
PD MAY-JUN
PY 2024
VL 31
IS 3
BP e286
EP e297
DI 10.1097/MJT.0000000000001547
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA PV3U8
UT WOS:001216827300023
PM 35972911
DA 2025-01-04
ER

PT J
AU Oh, Y
   Jung, HR
   Min, S
   Kang, J
   Jang, D
   Shin, S
   Kim, J
   Lee, SE
   Sung, CO
   Lee, WS
   Lee, C
   Jeong, EM
   Cho, SY
AF Oh, Yumi
   Jung, Hae Rim
   Min, Seoyeon
   Kang, Jinjoo
   Jang, Dongjun
   Shin, Seungjae
   Kim, Jiwon
   Lee, Sang Eun
   Sung, Chang Ohk
   Lee, Won-Suk
   Lee, Charles
   Jeong, Eui Man
   Cho, Sung-Yup
TI Targeting antioxidant enzymes enhances the therapeutic efficacy of the
   BCL-X<sub>L</sub> inhibitor ABT-263 in <i>KRAS</i>-mutant colorectal
   cancers
SO CANCER LETTERS
LA English
DT Article
DE Colorectal cancer; KRAS mutation; ABT-263; Antioxidant system;
   2-Methoxyestradiol
ID BH3 MIMETIC ABT-737; NAVITOCLAX ABT-263; 2-METHOXYESTRADIOL-INDUCED
   APOPTOSIS; HEPATOCELLULAR-CARCINOMA; IMATINIB MESYLATE; IN-VITRO;
   FAMILY; COMBINATION; CELLS; PHARMACOKINETICS
AB Cancer chemotherapeutic drugs exert cytotoxic effects by modulating intracellular reactive oxygen species (ROS) levels. However, whether ROS modulates the efficacy of targeted therapeutics remains poorly understood. Previously, we reported that upregulation of the anti-apoptotic protein, BCL-X-L, by KRAS activating mutations was a potential target for KRAS-mutant colorectal cancer (CRC) treatment. Here, we demonstrated that the BCL-X-L targeting agent, ABT-263, increased intracellular ROS levels and targeting antioxidant pathways augmented the therapeutic efficacy of this BH3 mimetic. ABT-263 induced expression of genes associated with ROS response and increased intracellular ROS levels by enhancing mitochondrial superoxide generation. The superoxide dismutase inhibitor, 2-methoxyestradiol (2-ME), exhibited synergism with ABT-263 in KRAS-mutant CRC cell lines. This synergistic effect was attributed to the inhibition of mTOR-dependent translation of the anti-apoptotic MCL1 protein via caspase 3-mediated cleavage of AKT and S6K. In addition, combination treatment of ABT-263 and 2-ME demonstrated a synergistic effect in in vivo patient-derived xenografts harboring KRAS mutations. Our data suggest a novel role for ROS in BH3 mimetic-based targeted therapy and provide a novel strategy for treatment of CRC patients with KRAS mutations.
C1 [Oh, Yumi; Jung, Hae Rim] Seoul Natl Univ, Dept Biochem & Mol Biol, Coll Med, Seoul 03080, South Korea.
   [Min, Seoyeon; Kang, Jinjoo] Ewha Womans Univ, Dept Life Sci, Seoul 03760, South Korea.
   [Jang, Dongjun; Shin, Seungjae; Kim, Jiwon; Lee, Sang Eun; Cho, Sung-Yup] Seoul Natl Univ, Dept Biomed Sci, Coll Med, Seoul 03080, South Korea.
   [Sung, Chang Ohk] Univ Ulsan, Asan Med Ctr, Dept Pathol, Coll Med, Seoul 05505, South Korea.
   [Lee, Won-Suk] Gachon Univ, Gil Med Ctr, Dept Surg, Incheon 21565, South Korea.
   [Lee, Charles] Jackson Lab Genom Med, Farmington, CT 06032 USA.
   [Jeong, Eui Man] Jeju Natl Univ, Coll Pharm, Dept Pharm, Jeju City 63243, Jeju Special Se, South Korea.
   [Jeong, Eui Man] Jeju Natl Univ, Interdisciplinary Grad Program Adv Convergence Te, Jeju City 63243, Jeju Special Se, South Korea.
   [Jeong, Eui Man] Jeju Natl Univ, Biohlth Mat Core Facil Ctr, Jeju City 63243, Jeju Special Se, South Korea.
   [Jeong, Eui Man] Jeju Natl Univ, Pract Translat Res Ctr, Jeju City 63243, Jeju Special Se, South Korea.
   [Cho, Sung-Yup] Seoul Natl Univ, Canc Res Inst, Seoul 03080, South Korea.
   [Cho, Sung-Yup] Seoul Natl Univ, Med Res Ctr, Genom Med Inst GMI, Coll Med, Seoul 03080, South Korea.
C3 Seoul National University (SNU); Ewha Womans University; Seoul National
   University (SNU); University of Ulsan; Gachon University; Jackson
   Laboratory; Jeju National University; Jeju National University; Jeju
   National University; Jeju National University; Seoul National University
   (SNU); Seoul National University (SNU)
RP Jeong, EM (corresponding author), Jeju Natl Univ, Jeju City 63243, Jeju Special Se, South Korea.; Cho, SY (corresponding author), Seoul Natl Univ, Coll Med, Seoul 03080, South Korea.
EM emjeong@jejunu.ac.kr; csybio@smu.ac.kr
RI lee, charles/AAW-6627-2021
OI Sung, Chang Ohk/0000-0002-8567-456X
FU Bio & Medical Technology Development Program of NRF - Ministry of
   Science ICT [2018M3A9F3056902, 2019M3E5D4066900]; NRF - Korea government
   (MSIT) [2017R1C1B2002183, 2020R1A2C1102124]; Korea Basic Science
   Institute (National Research Facilities and Equipment Center) - Ministry
   of Education [2020R1A6C101A188]
FX This work was supported by Bio & Medical Technology Development Program
   of NRF, funded by the Ministry of Science & ICT (grant No.
   2018M3A9F3056902 and 2019M3E5D4066900); the NRF grant funded by the
   Korea government (MSIT) (grant No. 2017R1C1B2002183 and
   2020R1A2C1102124); and Korea Basic Science Institute (National Research
   Facilities and Equipment Center) grant funded by the Ministry of
   Education (2020R1A6C101A188).
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NR 60
TC 10
Z9 11
U1 0
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 JAN 28
PY 2021
VL 497
BP 123
EP 136
DI 10.1016/j.canlet.2020.10.018
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PB4JE
UT WOS:000596288200001
PM 33068701
DA 2025-01-04
ER

PT J
AU Choudhary, S
   Pardo, A
   Rosinke, R
   Batra, JK
   Barth, S
   Verma, RS
AF Choudhary, Swati
   Pardo, Alessa
   Rosinke, Reinhard
   Batra, Janendra K.
   Barth, Stefan
   Verma, Rama S.
TI Targeting c-kit receptor in neuroblastomas and colorectal cancers using
   stem cell factor (SCF)-based recombinant bacterial toxins
SO APPLIED MICROBIOLOGY AND BIOTECHNOLOGY
LA English
DT Article
DE Protein-fusion toxins; Stem cell factor; c-kit receptor; Targeting
ID TYROSINE KINASE; CARCINOMA CELLS; CYTOTOXIC ACTIVITY; IMATINIB MESYLATE;
   EGF RECEPTOR; IN-VITRO; EXPRESSION; APOPTOSIS; PROTEINS; GROWTH
AB Autocrine activation of c-kit (KIT receptor tyrosine kinase) has been postulated to be a potent oncogenic driver in small cell lung cancer, neuroblastoma (NB), and poorly differentiated colorectal carcinoma (CRC). Although targeted therapy involving tyrosine kinase inhibitors (TKIs) such as imatinib mesylate is highly effective for gastrointestinal stromal tumor carrying V560G c-kit mutation, it does not show much potential for targeting wild-type KIT (WT-KIT). Our study demonstrates the role of stem cell factor (SCF)-based toxin conjugates for targeting WT-KIT-overexpressing malignancies such as NBs and CRCs. We constructed SCF-based recombinant bacterial toxins by genetically fusing mutated form of natural ligand SCF to receptor binding deficient forms of Diphtheria toxin (DT) or Pseudomonas exotoxin A (ETA') and evaluated their efficacy in vitro. Efficient targeting was achieved in all receptor-positive neuroblastoma (IMR-32 and SHSY5Y) and colon cancer cell lines (COLO 320DM, HCT 116, and DLD-1) but not in receptor-negative breast carcinoma cell line (MCF-7) thereby proving specificity. While dose- and time-dependent cytotoxicity was observed in both neuroblastoma cell lines, COLO 320DM and HCT 116 cells, only an anti-proliferative effect was observed in DLD-1 cells. We prove that these novel targeting agents have promising potential as KIT receptor tyrosine kinase targeting system.
C1 [Choudhary, Swati; Verma, Rama S.] Indian Inst Technol, Bhupat & Jyoti Mehta Sch Biosci, Dept Biotechnol, Madras 600036, Tamil Nadu, India.
   [Pardo, Alessa; Barth, Stefan] Univ Hosp RWTH Aachen, Inst Appl Med Engn, Dept Expt Med & Immunotherapy, D-52074 Aachen, Germany.
   [Rosinke, Reinhard; Barth, Stefan] Fraunhofer Inst Mol Biol & Appl Ecol IME, Dept Pharmaceut Prod Dev, D-52074 Aachen, Germany.
   [Batra, Janendra K.] Natl Inst Immunol, New Delhi 110067, India.
C3 Indian Institute of Technology System (IIT System); Indian Institute of
   Technology (IIT) - Madras; RWTH Aachen University; RWTH Aachen
   University Hospital; Fraunhofer Gesellschaft; Department of
   Biotechnology (DBT) India; National Institute of Immunology (NII)
RP Verma, RS (corresponding author), Indian Inst Technol, Bhupat & Jyoti Mehta Sch Biosci, Dept Biotechnol, Madras 600036, Tamil Nadu, India.
EM stefan.barth@uct.ac.za; vermars@iitm.ac.in
RI Batra, Janendra/GWQ-8031-2022; Barth, Stefan/F-7301-2012
OI Batra, Janendra/0000-0003-2206-3398; Verma, Rama/0000-0001-7287-7803;
   Barth, Stefan/0000-0001-9589-653X; Choudhary, Swati/0000-0001-5928-8529
FU DAAD; MHRD; Department of Biotechnology (DBT), Government of India
   [BT/PR13463/PID/06/488/2010]
FX We are grateful to Aslam Basha for helping with fermentation, DAAD and
   MHRD for providing fellowships to SC, and the Department of
   Biotechnology (DBT), Government of India for providing grant
   (BT/PR13463/PID/06/488/2010) to support this work.
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NR 64
TC 9
Z9 11
U1 0
U2 13
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0175-7598
EI 1432-0614
J9 APPL MICROBIOL BIOT
JI Appl. Microbiol. Biotechnol.
PD JAN
PY 2016
VL 100
IS 1
BP 263
EP 277
DI 10.1007/s00253-015-6978-2
PG 15
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA DA6LN
UT WOS:000367916200022
PM 26428235
DA 2025-01-04
ER

PT J
AU Xu, YX
   Ni, FX
   Sun, DX
   Peng, Y
   Zhao, YX
   Wu, XJ
   Li, SS
   Qi, XY
   He, XK
   Li, M
   Zhou, YZ
   Zhang, C
   Yan, M
   Yao, CF
   Zhu, SS
   Yang, Y
   An, BJ
   Yang, CH
   Zhang, GL
   Jiang, WG
   Mi, J
   Chen, XJ
   Wei, PF
   Tian, G
   Zhang, Y
AF Xu, Yuxue
   Ni, Feixue
   Sun, Daxi
   Peng, Yue
   Zhao, Yaxuan
   Wu, Xiaojun
   Li, Shasha
   Qi, Xiangyu
   He, Xinkang
   Li, Min
   Zhou, Yizi
   Zhang, Chao
   Yan, Miao
   Yao, Cuifang
   Zhu, Shuaishuai
   Yang, Yang
   An, Baijiao
   Yang, Chunhua
   Zhang, Guilong
   Jiang, Wenguo
   Mi, Jia
   Chen, Xinju
   Wei, Pengfei
   Tian, Geng
   Zhang, Yin
TI Glucagon Enhances Chemotherapy Efficacy By Inhibition of Tumor Vessels
   in Colorectal Cancer
SO ADVANCED SCIENCE
LA English
DT Article
DE chemotherapy; colorectal cancer; glucagon; tumor angiogenesis; vascular
   mimicry
ID VASCULOGENIC MIMICRY FORMATION; RECEPTOR ANTAGONIST LY2409021; 1ST-LINE
   TREATMENT; TARGETED THERAPY; BEVACIZUMAB; 5-FLUOROURACIL; FLUOROURACIL;
   LEUCOVORIN; ANGIOGENESIS; OXALIPLATIN
AB Chemotherapy is widely used to treat colorectal cancer (CRC). Despite its substantial benefits, the development of drug resistance and adverse effects remain challenging. This study aimed to elucidate a novel role of glucagon in anti-cancer therapy. In a series of in vitro experiments, glucagon inhibited cell migration and tube formation in both endothelial and tumor cells. In vivo studies demonstrated decreased tumor blood vessels and fewer pseudo-vessels in mice treated with glucagon. The combination of glucagon and chemotherapy exhibited enhanced tumor inhibition. Mechanistic studies demonstrated that glucagon increased the permeability of blood vessels, leading to a pronounced disruption of vessel morphology. Signaling pathway analysis identified a VEGF/VEGFR-dependent mechanism whereby glucagon attenuated angiogenesis through its receptor. Clinical data analysis revealed a positive correlation between elevated glucagon expression and chemotherapy response. This is the first study to reveal a role for glucagon in inhibiting angiogenesis and vascular mimicry. Additionally, the delivery of glucagon-encapsulated PEGylated liposomes to tumor-bearing mice amplified the inhibition of angiogenesis and vascular mimicry, consequently reinforcing chemotherapy efficacy. Collectively, the findings demonstrate the role of glucagon in inhibiting tumor vessel network and suggest the potential utility of glucagon as a promising predictive marker for patients with CRC receiving chemotherapy.
   Glucagon plays an essential role in metabolism, however, its involvement in tumor development is not well understood. Here, a new biological function of glucagon is uncovered in modulation of tumor vessels. Glucagon showed a pronounced inhibition in tumor angiogenesis and vascular mimicry. This discovery suggests glucagon maybe developed as an endogenous antiangiogenic inhibitor for cancer therapy.image
C1 [Xu, Yuxue; Ni, Feixue; Sun, Daxi; Peng, Yue; Zhao, Yaxuan; Wu, Xiaojun; Li, Shasha; Qi, Xiangyu; Li, Min; Zhou, Yizi; Zhang, Chao; Yan, Miao; Yao, Cuifang; Yang, Yang; An, Baijiao; Yang, Chunhua; Zhang, Guilong; Jiang, Wenguo; Mi, Jia; Wei, Pengfei; Tian, Geng; Zhang, Yin] Binzhou Med Univ, Sch Rehabil, Yantai 264003, Peoples R China.
   [Xu, Yuxue; Ni, Feixue; Sun, Daxi; Peng, Yue; Zhao, Yaxuan; Wu, Xiaojun; Li, Shasha; Qi, Xiangyu; Yan, Miao; Yao, Cuifang; Yang, Yang; An, Baijiao; Yang, Chunhua; Zhang, Guilong; Jiang, Wenguo; Mi, Jia; Wei, Pengfei; Tian, Geng; Zhang, Yin] Shandong Technol Innovat Ctr Mol Targeting & Intel, Yantai 264003, Peoples R China.
   [He, Xinkang] Zhejiang Univ, Dept Gastroenterol, Sir Run Run Shaw Hosp, Med Sch, Hangzhou 310016, Peoples R China.
   [Zhu, Shuaishuai; Chen, Xinju] Henan Univ Tradit Chinese Med, Affiliated Hosp 1, 19 Renmin Rd, Zhengzhou 450000, Henan, Peoples R China.
C3 Binzhou Medical University; Zhejiang University; Henan University of
   Traditional Chinese Medicine
RP Wei, PF; Tian, G; Zhang, Y (corresponding author), Binzhou Med Univ, Sch Rehabil, Yantai 264003, Peoples R China.; Wei, PF; Tian, G; Zhang, Y (corresponding author), Shandong Technol Innovat Ctr Mol Targeting & Intel, Yantai 264003, Peoples R China.
EM pfwei@mail.ustc.edu.cn; tiangeng@bzmc.edu.cn; yin_zhang@bzmc.edu.cn
RI An, Baijiao/X-9854-2019; Jiang, Wen/AAF-1876-2020; Zhao,
   Yang/IXD-7496-2023; li, feiyang/KHW-5210-2024; Peng, Yue/HOH-9382-2023;
   Wei, Pengfei/J-1264-2016; Li, Shasha/AAT-3255-2021; qi,
   xiangyu/IQR-4340-2023; Zhang, Yin/IQR-7670-2023
OI Zhang, Yin/0000-0002-5591-645X
FU Taishan Scholar's program; National Natural Science Foundation of China
   [31800985 XYX]; Major Basic Research Project of Shandong Provincial
   Natural Science Foundation; Shandong Province Higher Educational Youth
   Innovation Science and Technology Program [2019KJE013]; Special Project
   of Central Government for Local Science and Technology Development of
   Shandong Province [YDZX20203700001291]; Natural Science Foundation of
   Shandong Province for Excellent Youth Scholars [ZR2016JL026]; Natural
   Science Foundation of Shandong Province [ZR2021MH292]; Youth Science
   Foundation project of Shandong Province Natural Science Foundation;
   Science and Technology development plan project of Medicine and health
   care of Shandong province [2017WS694 XYX, 2019WS319]; Yantai Development
   Project of University; Development plan of Youth Innovation Team in
   Colleges and universities of Shandong Province [2021KJ052 WPF]; Key R&D
   Program of Shandong Province, China [2023CXPT012]; Yantai Science and
   Technology Innovation Development Plan Project [2023JCYJ072 XYX];
   Scientific research foundation of Binzhou Medical College [BY2017KYQD09,
   BY2018KYQD08, BY2021KYQD21]; Department of Gastric; Yantai Affiliated
   Hospital of Binzhou Medical University;  [tstp20221145]; 
   [tsqn201812100];  [tsqn202103112]
FX This study was funded by Taishan Scholar's program including TG
   (tstp20221145), ZY (tsqn201812100), and WPF (tsqn202103112), the
   National Natural Science Foundation of China (31800985 XYX, 31771284
   TG), Major Basic Research Project of Shandong Provincial Natural Science
   Foundation (ZR2019ZD27 TG), Shandong Province Higher Educational Youth
   Innovation Science and Technology Program (2019KJE013 TG), Special
   Project of Central Government for Local Science and Technology
   Development of Shandong Province (YDZX20203700001291 TG), Natural
   Science Foundation of Shandong Province for Excellent Youth Scholars
   (ZR2016JL026 TG), Natural Science Foundation of Shandong Province
   (ZR2021MH292, ZY), Youth Science Foundation project of Shandong Province
   Natural Science Foundation (ZR2020QH242 YY), Science and Technology
   development plan project of Medicine and health care of Shandong
   province (2017WS694 XYX, 2019WS319 YM), Yantai Development Project of
   University and Government Integration (2019XDRHXMPT14 TG), Development
   plan of Youth Innovation Team in Colleges and universities of Shandong
   Province (2021KJ052 WPF), Key R&D Program of Shandong Province, China
   (No. 2023CXPT012 TG), Shandong Province Higher Educational Youth
   Innovation Science and Technology Program (No. 2019KJE013), Yantai
   Science and Technology Innovation Development Plan Project (2023JCYJ072
   XYX), and Scientific research foundation of Binzhou Medical College
   (BY2017KYQD09 XYX, BY2018KYQD08 YY, BY2021KYQD21 WPF, ZR2021MH292 ZY).
   The authors acknowledge the generous support of Department of Gastric
   and Intestine, Yantai Affiliated Hospital of Binzhou Medical University.
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NR 44
TC 0
Z9 0
U1 4
U2 16
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2198-3844
J9 ADV SCI
JI Adv. Sci.
PD FEB
PY 2024
VL 11
IS 6
DI 10.1002/advs.202307271
EA DEC 2023
PG 18
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA HP4K2
UT WOS:001118475300001
PM 38072640
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Morgado, S
   Silva, M
   Fonseca, O
   Roque, F
   Morgado, M
AF Morgado, Sandra
   Silva, Mafalda
   Fonseca, Olimpia
   Roque, Fatima
   Morgado, Manuel
TI Targeted therapy for metastatic colorectal cancer: what do we currently
   have in clinical practice?
SO DRUGS & THERAPY PERSPECTIVES
LA English
DT Article
ID TYROSINE KINASE INHIBITORS; MULTICENTER ANALYSIS; RANDOMIZED PHASE-3;
   1ST-LINE TREATMENT; DOUBLE-BLIND; OPEN-LABEL; BEVACIZUMAB; PLUS;
   REGORAFENIB; FLUOROURACIL
AB Colorectal cancer (CRC) is one of the three most prevalent types of cancer (along with lung cancer and breast cancer) and the second most deadly cancer. The International Agency for Research on Cancer (IARC) estimates that in 2020, CRC was the cause of almost 1 million deaths worldwide. This work aims to review the available targeted therapeutic approaches in the treatment of metastatic CRC (mCRC), namely, monoclonal antibodies and inhibitors of protein kinases with therapeutic indication in mCRC. The databases of medicines for human use of the US Food and Drug Administration (FDA) and the European Medicines Agency (EMA) were searched to identify targeted drugs with an approved indication for the treatment of mCRC. Within the scope of targeted therapies for the treatment of mCRC, ten drugs are currently available in the pharmaceutical market: a fusion protein with a mechanism of action that has similarities with monoclonal antibodies (aflibercept), seven monoclonal antibodies (bevacizumab, cetuximab, nivolumab + ipilimumab, panitumumab, pembrolizumab and ramucirumab), and two protein kinase inhibitors (encorafenib and regorafenib). An analysis was also carried out of the antineoplastic therapeutic regimens in which each of these drugs are included and their respective therapeutic indications. The high incidence and mortality of CRC require new therapeutic approaches, with proven efficacy and high levels of safety. Detailed study of the individual behavior of the tumor allows the use of targeted therapies, optimizing therapeutic results.
C1 [Morgado, Sandra; Silva, Mafalda; Fonseca, Olimpia; Morgado, Manuel] Univ Hosp Ctr Cova da Beira, Pharmaceut Serv, Covilha, Portugal.
   [Fonseca, Olimpia; Morgado, Manuel] Univ Beira Interior FCS UBI, Hlth Sci Fac, Covilha, Portugal.
   [Roque, Fatima; Morgado, Manuel] Polytech Inst Guarda, Sch Hlth Sci, Ave Rainha D Amelia,S-N, P-6300749 Guarda, Portugal.
   [Roque, Fatima; Morgado, Manuel] Polytech Guarda UDI IPG, Res Unit Inland Dev, Guarda, Portugal.
   [Roque, Fatima; Morgado, Manuel] Univ Beira Interior CICS UBI, Hlth Sci Res Ctr, Covilha, Portugal.
C3 Instituto Politecnico da Guarda; Universidade da Beira Interior
RP Morgado, M (corresponding author), Univ Hosp Ctr Cova da Beira, Pharmaceut Serv, Covilha, Portugal.; Morgado, M (corresponding author), Univ Beira Interior FCS UBI, Hlth Sci Fac, Covilha, Portugal.; Morgado, M (corresponding author), Polytech Inst Guarda, Sch Hlth Sci, Ave Rainha D Amelia,S-N, P-6300749 Guarda, Portugal.; Morgado, M (corresponding author), Polytech Guarda UDI IPG, Res Unit Inland Dev, Guarda, Portugal.; Morgado, M (corresponding author), Univ Beira Interior CICS UBI, Hlth Sci Res Ctr, Covilha, Portugal.
EM sandracristinamorgado@gmail.com; mafaldasilva00@gmail.com;
   olimpia.fonseca@chcbeira.min-saude.pt; froque@ipg.pt;
   manuelaugustomorgado@gmail.com
RI Roque, Fatima/H-1713-2013; Morgado, Manuel/S-9303-2019
OI Morgado, Manuel/0000-0003-2112-2835
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NR 72
TC 0
Z9 0
U1 0
U2 5
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 1172-0360
EI 1179-1977
J9 DRUGS THER PERSPECT
JI Drugs. Ther. Perspect.
PD MAY
PY 2022
VL 38
IS 5
BP 222
EP 234
DI 10.1007/s40267-022-00915-9
EA JUN 2022
PG 13
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA 2H9RH
UT WOS:000804500000001
DA 2025-01-04
ER

PT J
AU van Helden, EJ
   Elias, SG
   Gerritse, SL
   van Es, SC
   Boon, E
   Huisman, MC
   van Grieken, NCT
   Dekker, H
   van Dongen, GAMS
   Vugts, DJ
   Boellaard, R
   van Herpen, CML
   de Vries, EGE
   Oyen, WJG
   Brouwers, AH
   Verheul, HMW
   Hoekstra, OS
   van Oordt, CWM
AF van Helden, E. J.
   Elias, S. G.
   Gerritse, S. L.
   van Es, S. C.
   Boon, E.
   Huisman, M. C.
   van Grieken, N. C. T.
   Dekker, H.
   van Dongen, G. A. M. S.
   Vugts, D. J.
   Boellaard, R.
   van Herpen, C. M. L.
   de Vries, E. G. E.
   Oyen, W. J. G.
   Brouwers, A. H.
   Verheul, H. M. W.
   Hoekstra, O. S.
   van Oordt, C. W. Menke-van der Houven
TI [<SUP>89</SUP>Zr]Zr-cetuximab PET/CT as biomarker for cetuximab
   monotherapy in patients with RAS wild-type advanced colorectal cancer
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Article
DE Colorectal cancer; Targeted therapy; Cetuximab; Imaging biomarker; PET;
   CT
ID GROWTH-FACTOR RECEPTOR; EGFR EXPRESSION; PHASE-I; TUMOR;
   PHARMACOKINETICS; METAANALYSIS; PROGNOSIS; SURVIVAL; BENEFIT
AB Purpose One-third of patients with RAS wild-type mCRC do not benefit from anti-EGFR monoclonal antibodies. This might be a result of variable pharmacokinetics and insufficient tumor targeting. We evaluated cetuximab tumor accumulation on [Zr-89]Zr-cetuximab PET/CT as a potential predictive biomarker and determinant for an escalating dosing strategy. Patients and methods PET/CT imaging of [Zr-89]Zr-cetuximab (37 MBq/10 mg) after a therapeutic pre-dose (500 mg/m(2) <= 2 h) cetuximab was performed at the start of treatment. Patients without visual tumor uptake underwent dose escalation and a subsequent [Zr-89]Zr-cetuximab PET/CT. Treatment benefit was defined as stable disease or response on CT scan evaluation after 8 weeks. Results Visual tumor uptake on [Zr-89]Zr-cetuximab PET/CT was observed in 66% of 35 patients. There was no relationship between PET positivity and treatment benefit (52% versus 80% for PET-negative, P = 0.16), progression-free survival (3.6 versus 5.7 months, P = 0.15), or overall survival (7.1 versus 9.4 months, P = 0.29). However, in 67% of PET-negative patients, cetuximab dose escalation (750-1250 mg/m(2)) was applied, potentially influencing outcome in this group. None of the second [Zr-89]Zr-cetuximab PET/CT was positive. Eighty percent of patients without visual tumor uptake had treatment benefit, making [Zr-89]Zr-cetuximab PET/CT unsuitable as a predictive biomarker. Tumor SUVpeak did not correlate to changes in tumor size on CT (P = 0.23), treatment benefit, nor progression-free survival. Cetuximab pharmacokinetics were not related to treatment benefit. BRAF mutations, right-sidedness, and low sEGFR were correlated with intrinsic resistance to cetuximab. Conclusion Tumor uptake on [Zr-89]Zr-cetuximab PET/CT failed to predict treatment benefit in patients with RAS wild-type mCRC receiving cetuximab monotherapy. BRAF mutations, right-sidedness, and low sEGFR correlated with intrinsic resistance to cetuximab.
C1 [van Helden, E. J.; Gerritse, S. L.; Dekker, H.; Verheul, H. M. W.; van Oordt, C. W. Menke-van der Houven] Vrije Univ Amsterdam Med Ctr, Med Oncol, Canc Ctr Amsterdam, Amsterdam UMC, Amsterdam, Netherlands.
   [Elias, S. G.] Univ Utrecht, Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
   [van Es, S. C.; de Vries, E. G. E.] Univ Groningen, Univ Med Ctr Groningen, Med Oncol, Groningen, Netherlands.
   [Boon, E.; van Herpen, C. M. L.] Radboud Univ Nijmegen, Med Oncol, Med Ctr, Nijmegen, Netherlands.
   [Huisman, M. C.; van Dongen, G. A. M. S.; Vugts, D. J.; Boellaard, R.; Hoekstra, O. S.] Vrije Univ Amsterdam Med Ctr, Radiol & Nucl Med, Canc Ctr Amsterdam, Amsterdam UMC, Amsterdam, Netherlands.
   [van Grieken, N. C. T.] Vrije Univ Amsterdam Med Ctr, Pathol, Canc Ctr Amsterdam, Amsterdam UMC, Amsterdam, Netherlands.
   [Oyen, W. J. G.] Radboud Univ Nijmegen, Radiol & Nucl Med, Med Ctr, Nijmegen, Netherlands.
   [Oyen, W. J. G.] Inst Canc Res, London, England.
   [Oyen, W. J. G.] Royal Marsden Hosp, London, England.
   [Brouwers, A. H.] Univ Groningen, Univ Med Ctr Groningen, Nucl Med & Mol Imaging, Groningen, Netherlands.
C3 University of Amsterdam; Vrije Universiteit Amsterdam; VU UNIVERSITY
   MEDICAL CENTER; Utrecht University; Utrecht University Medical Center;
   University of Groningen; Radboud University Nijmegen; University of
   Amsterdam; Vrije Universiteit Amsterdam; VU UNIVERSITY MEDICAL CENTER;
   Vrije Universiteit Amsterdam; VU UNIVERSITY MEDICAL CENTER; University
   of Amsterdam; Radboud University Nijmegen; University of London;
   Institute of Cancer Research - UK; Royal Marsden NHS Foundation Trust;
   Royal Marsden NHS Foundation Trust; University of Groningen
RP van Oordt, CWM (corresponding author), Vrije Univ Amsterdam Med Ctr, Med Oncol, Canc Ctr Amsterdam, Amsterdam UMC, Amsterdam, Netherlands.
EM c.menke@amsterdamumc.nl
RI van+der+Houven+van+Oordt, C./AAE-8064-2020; Oyen, Wim/AAD-3373-2020;
   Verheul, Henk/V-6462-2019; van Herpen, Carla/N-3576-2014; Elias,
   Sjoerd/E-6057-2011; Boon, Eline/D-1298-2015
OI de Vries, Elisabeth/0000-0002-8949-7425; Menke-van der Houven van Oordt,
   C. Willemien/0000-0002-5404-5883; van Dongen, Guus/0000-0001-5939-9851;
   Brouwers, Adrienne/0000-0003-2698-1516; Hoekstra, Otto
   S/0000-0003-0767-2734
FU Alpe d'HuZes, Dutch Cancer Society [KWF 2012-5565]
FX This study was funded by Alpe d'HuZes, Dutch Cancer Society (KWF
   2012-5565).
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NR 31
TC 24
Z9 24
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1619-7070
EI 1619-7089
J9 EUR J NUCL MED MOL I
JI Eur. J. Nucl. Med. Mol. Imaging
PD APR
PY 2020
VL 47
IS 4
BP 849
EP 859
DI 10.1007/s00259-019-04555-6
EA NOV 2019
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA KU7UX
UT WOS:000495208100001
PM 31705176
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Yamasaki, A
   Miyake, R
   Hara, Y
   Okuno, H
   Imaida, T
   Okita, K
   Okazaki, S
   Akiyama, Y
   Hirotani, K
   Endo, Y
   Masuko, K
   Masuko, T
   Tomioka, Y
AF Yamasaki, Akitaka
   Miyake, Rikuto
   Hara, Yuta
   Okuno, Hideki
   Imaida, Takuya
   Okita, Kouki
   Okazaki, Shogo
   Akiyama, Yasutoshi
   Hirotani, Kenji
   Endo, Yuichi
   Masuko, Kazue
   Masuko, Takashi
   Tomioka, Yoshihisa
TI Dual-targeting therapy against HER3/MET in human colorectal cancers
SO CANCER MEDICINE
LA English
DT Article
DE colorectal cancer; Forkhead Box protein M1; human epidermal growth
   factor receptor family; mesenchymal to epithelial transition factor
ID TYROSINE KINASE; MET; INHIBITOR; GROWTH; CELLS; HETEROGENEITY;
   RESISTANCE; ANTIBODIES; PROMOTES; SURVIVAL
AB BackgroundColorectal cancer (CRC) is the most common malignancy in the world, and novel molecular targeted therapies for CRC have been vigorously pursued. We searched for novel combination therapies based on the expression patterns of membrane proteins in CRC cell lines. ResultsA positive correlation was observed between the expression of human pidermal growth factor receptor (HER) 3 and mesenchymal-to-epithelial transition factor (MET) on the cell surface of CRC cell lines. The brief stimulation of HER3/MET-high SW1116 CRC cells with both neuregulin-1 (NRG1) and hepatocyte growth factor enhanced ERK phosphorylation and cell proliferation more than each stimulation alone. In addition, a prolonged NRG1 stimulation resulted in the tyrosine phosphorylation of MET. In this context, the Forkhead Box protein M1 (FOXM1)-regulated tyrosine phosphorylation of MET by NRG1 was demonstrated, suggesting the existence of a signaling pathway mediated by FOXM1 upon the NRG1 stimulation. Since the co-expression of HER3 and MET was also demonstrated in in vivo CRC tissues by immunohistochemistry, we investigated whether the co-inhibition of HER3 and MET could be an effective therapy for CRC. We established HER3-and/or MET-KO SW1116 cell lines, and HER3/MET-double KO resulted in the inhibition of in vitro cell proliferation and in vivo tumor growth in nude mice by SW1116 cells. Furthermore, the combination of patritumab, an anti-HER3 fully human mAb, and PHA665752, a MET inhibitor, markedly inhibited in vitro cell proliferation, 3D-colony formation, and in vivo tumor growth in nude mice by SW1116 cells ConclusionThe dual targeting of HER3/MET has potential as CRC therapy.
C1 [Yamasaki, Akitaka; Miyake, Rikuto; Hara, Yuta; Okuno, Hideki; Imaida, Takuya; Okita, Kouki; Masuko, Kazue; Masuko, Takashi] Kindai Univ, Fac Pharm, Cell Biol Lab, Osaka, Japan.
   [Yamasaki, Akitaka; Akiyama, Yasutoshi; Tomioka, Yoshihisa] Tohoku Univ, Grad Sch Pharmaceut Sci, Lab Oncol Pharm Practice & Sci, Sendai, Japan.
   [Okita, Kouki] Carna Biosci Inc, Prod & Mfg, Kobe, Japan.
   [Okazaki, Shogo] Nihon Univ, Sch Dens, Dept Microbiol, Div Immunol & Pathobiol, Tokyo, Japan.
   [Hirotani, Kenji] Daiichi Sankyo Co Ltd, R&D Div, Early Clin Dev Dept, Tokyo, Japan.
   [Endo, Yuichi; Masuko, Takashi] Kindai Univ, Fac Pharm, Nat Drug Resources, Osaka, Japan.
   [Masuko, Takashi] Kindai Univ, Fac Pharm, Nat Drug Resources, Higashiosaka, Osaka 5778502, Japan.
C3 Kindai University (Kinki University); Tohoku University; Nihon
   University; Daiichi Sankyo Company Limited; Kindai University (Kinki
   University); Kindai University (Kinki University)
RP Masuko, T (corresponding author), Kindai Univ, Fac Pharm, Nat Drug Resources, Higashiosaka, Osaka 5778502, Japan.
EM masuko@phar.kindai.ac.jp
RI Okazaki, Shogo/A-8119-2014
OI Akiyama, Yasutoshi/0000-0002-0211-7793
FU MEXT/JSPS KAKENHI [18H05463]; Grants-in-Aid for Scientific Research
   [21K06865, 22K07157] Funding Source: KAKEN
FX MEXT/JSPS KAKENHI, Grant/Award Number: 18H05463
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NR 55
TC 2
Z9 2
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD APR
PY 2023
VL 12
IS 8
BP 9684
EP 9696
DI 10.1002/cam4.5673
EA FEB 2023
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AQ9I7
UT WOS:000928922900001
PM 36751113
OA gold
DA 2025-01-04
ER

PT J
AU Senetta, R
   Duregon, E
   Sonetto, C
   Spadi, R
   Mistrangelo, M
   Racca, P
   Chiusa, L
   Munoz, FH
   Ricardi, U
   Arezzo, A
   Cassenti, A
   Castellano, I
   Papotti, M
   Morino, M
   Risio, M
   Cassoni, P
AF Senetta, Rebecca
   Duregon, Eleonora
   Sonetto, Cristina
   Spadi, Rossella
   Mistrangelo, Massimiliano
   Racca, Patrizia
   Chiusa, Luigi
   Munoz, Fernando H.
   Ricardi, Umberto
   Arezzo, Alberto
   Cassenti, Adele
   Castellano, Isabella
   Papotti, Mauro
   Morino, Mario
   Risio, Mauro
   Cassoni, Paola
TI YKL-40/c-Met Expression in Rectal Cancer Biopsies Predicts Tumor
   Regression following Neoadjuvant Chemoradiotherapy: A
   Multi-Institutional Study
SO PLOS ONE
LA English
DT Article
ID PREOPERATIVE CHEMORADIOTHERAPY; C-MET; COMPLETE RESPONSE; INVASIVE
   GROWTH; BETA-CATENIN; ADENOCARCINOMA; RADIOTHERAPY; METASTASIS;
   CARCINOMA; RADIATION
AB Background
   Neoadjuvant chemo-radiotherapy (CRT) followed by surgical resection is the standard treatment for locally advanced rectal cancer, although complete tumor pathological regression is achieved in only up to 30% of cases. A clinicopathological and molecular predictive stratification of patients with advanced rectal cancer is still lacking. Here, c-Met and YKL-40 have been studied as putative predictors of CRT response in rectal cancer, due to their reported involvement in chemoradioresistance in various solid tumors.
   Material and Methods
   A multicentric study was designed to assess the role of c-Met and YKL-40 expression in predicting chemoradioresistance and to correlate clinical and pathological features with CRT response. Immunohistochemistry and fluorescent in situ hybridization for c-Met were performed on 81 rectal cancer biopsies from patients with locally advanced rectal adenocarcinoma. All patients underwent standard (50.4 gy in 28 fractions + concurrent capecitabine 825 mg/m(2)) neoadjuvant CRT or the XELOXART protocol. CRT response was documented on surgical resection specimens and recorded as tumor regression grade (TRG) according to the Mandard criteria.
   Results
   A significant correlation between c-Met and YKL-40 expression was observed (R = 0.43). The expressions of c-Met and YKL-40 were both significantly associated with a lack of complete response (86% and 87% of c-Met and YKL-40 positive cases, p<0.01 and p = 0.006, respectively). Thirty of the 32 biopsies co-expressing both markers had partial or absent tumor response (TRG 2-5), strengthening their positive predictive value (94%). The exclusive predictive role of YKL-40 and c-Met was confirmed using a multivariate analysis (p = 0.004 and p = 0.007 for YKL-40 and c-Met, respectively). TRG was the sole morphological parameter associated with poor outcome.
   Conclusion
   c-Met and YKL-40 expression is a reliable predictor of partial/absent response to neoadjuvant CRT in rectal cancer. Targeted therapy protocols could take advantage of prior evaluations of c-MET and YKL-40 expression levels to increase therapeutic efficacy.
C1 [Senetta, Rebecca; Chiusa, Luigi; Cassenti, Adele; Castellano, Isabella; Cassoni, Paola] Univ Turin, Dept Med Sci, Turin, Italy.
   [Duregon, Eleonora; Munoz, Fernando H.; Ricardi, Umberto; Papotti, Mauro] Univ Turin, Dept Oncol, Turin, Italy.
   [Sonetto, Cristina; Spadi, Rossella; Racca, Patrizia] City Hlth & Sci Hosp Turin, SSCVD Colorectal Canc Unit, Turin, Italy.
   [Mistrangelo, Massimiliano; Arezzo, Alberto; Morino, Mario] Univ Turin, Ctr Minimal Invas Surg, Digest & Colorectal Surg, Turin, Italy.
   [Risio, Mauro] IRCCS, FPO, Candiolo Canc Inst, Turin, Italy.
C3 University of Turin; University of Turin; A.O.U. Citta della Salute e
   della Scienza di Torino; University of Turin; IRCCS Fondazione del
   Piemonte per l'Oncologia
RP Cassoni, P (corresponding author), Univ Turin, Dept Med Sci, Turin, Italy.
EM paola.cassoni@unito.it
RI Castellano, Isabella/K-1888-2018; Cassoni, Paola/I-8544-2018; Morino,
   Mario/AAI-6437-2020; Mistrangelo, Massimiliano/AAK-4428-2020; Duregon,
   Eleonora/L-9509-2019; Senetta, Rebecca/IAQ-9688-2023; Arezzo,
   Alberto/AAB-6552-2020
OI Castellano, isabella/0000-0002-9072-1615; Arezzo,
   Alberto/0000-0002-2110-4082; Morino, Mario/0000-0003-4540-1409;
   Mistrangelo, Massimiliano/0000-0001-8506-6794
FU FIRC (Fondazione Italiana per la Ricerca sul Cancro); Associazione
   Italiana per la Ricerca sul Cancro Funding Source: Custom
FX RS has received fellowships from FIRC (Fondazione Italiana per la
   Ricerca sul Cancro). The funder had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript.
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NR 63
TC 12
Z9 14
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 15
PY 2015
VL 10
IS 4
AR e0123759
DI 10.1371/journal.pone.0123759
PG 17
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CG1EL
UT WOS:000353015800114
PM 25875173
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Galbiati, S
   Damin, F
   Ferraro, L
   Soriani, N
   Burgio, V
   Ronzoni, M
   Gianni, L
   Ferrari, M
   Chiari, M
AF Galbiati, Silvia
   Damin, Francesco
   Ferraro, Lucia
   Soriani, Nadia
   Burgio, Valentina
   Ronzoni, Monica
   Gianni, Luca
   Ferrari, Maurizio
   Chiari, Marcella
TI Microarray Approach Combined with ddPCR: An Useful Pipeline for the
   Detection and Quantification of Circulating Tumour DNA Mutations
SO CELLS
LA English
DT Article
DE ctDNA; liquid biopsy; metastatic colorectal cancer; microarray; ddPCR
AB It has now been established that in biological fluids such as blood, it is possible to detect cancer causing genomic alterations by analysing circulating tumour DNA (ctDNA). Information derived from ctDNA offers a unique opportunity to enrich our understanding of cancer biology, tumour evolution and therapeutic efficacy and resistance. Here, we propose a workflow to identify targeted mutations by a customized microarray-based assay for the simultaneous detection of single point mutations in different oncogenes (KRAS, NRAS and BRAF) followed by droplet digital PCR (ddPCR) to determine the fractional abundance of the mutated allele. Genetic variants were determined in the plasma of 20 metastatic colorectal cancer (mCRC) patients previously genotyped on tissue biopsy at the diagnosis for medication planning (T0) and following the tumour genetic evolution during treatment phase (T1 and T2) with the objective of allowing therapy response prediction and monitoring. Our preliminary results show that this combined approach is suitable for routine clinical practice. The microarray platform enables for a rapid, specific and sensitive detection of the most common mutations suitable for high-throughput analysis without costly instrumentation while, the ddPCR, consents an absolute quantification of the mutated allele in a longitudinal observational study on patients undergoing targeted therapy.
C1 [Galbiati, Silvia; Soriani, Nadia; Ferrari, Maurizio] IRCCS San Raffaele Sci Inst, Div Genet & Cell Biol, Genom Unit Diag Human Pathol, I-20132 Milan, Italy.
   [Damin, Francesco; Ferraro, Lucia; Chiari, Marcella] CNR, Ist Chim Riconoscimento Mol, I-20131 Milan, Italy.
   [Burgio, Valentina; Ronzoni, Monica; Gianni, Luca] IRCCS Osped San Raffaele, Dipartimento Oncol Med, I-20132 Milan, Italy.
   [Ferrari, Maurizio] IRCCS Osped San Raffaele, Lab Clin Mol Biol, I-20132 Milan, Italy.
   [Ferrari, Maurizio] Univ Vita Salute San Raffaele, I-20132 Milan, Italy.
C3 Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
   Consiglio Nazionale delle Ricerche (CNR); Istituto di Chimica del
   Riconoscimento Molecolare (ICRM-CNR); Vita-Salute San Raffaele
   University; IRCCS Ospedale San Raffaele; Vita-Salute San Raffaele
   University; IRCCS Ospedale San Raffaele; Vita-Salute San Raffaele
   University
RP Galbiati, S (corresponding author), IRCCS San Raffaele Sci Inst, Div Genet & Cell Biol, Genom Unit Diag Human Pathol, I-20132 Milan, Italy.
EM galbiati.silvia@hsr.it
RI Burgio, Valentina/AAC-1682-2019; Galbiati, Silvia/AAC-1218-2019;
   Ferrari, Maurizio/D-9107-2013; Damin, Francesco/AAL-8998-2021
OI Galbiati, Silvia/0000-0003-1642-8506; Ferrari,
   Maurizio/0000-0002-1721-801X; Damin, Francesco/0000-0003-1780-7823
FU European Union [766466]
FX This project has received funding from the European Union's Horizon 2020
   research and innovation programme under grant agreement No 766466.
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NR 22
TC 12
Z9 13
U1 0
U2 10
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD AUG
PY 2019
VL 8
IS 8
AR 769
DI 10.3390/cells8080769
PG 14
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA IV8TI
UT WOS:000484537500002
PM 31344983
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Park, SY
   Yang, Y
   Zhou, R
   Jung, SC
   Bae, WK
   Chung, LJ
   Kim, KK
   Kim, H
AF Park, So-Yeon
   Yang, Yi
   Zhou, Rui
   Jung, Sang-Chul
   Bae, Woo Kyun
   Chung, Lk Joo
   Kim, Kyung Keun
   Kim, Hangun
TI ErbB4/KITENIN-Mediated Signaling is Activated in Cetuximab-Resistant
   Colorectal Cancer Cells
SO JOURNAL OF NANOSCIENCE AND NANOTECHNOLOGY
LA English
DT Article
DE ErbB4; KITENIN; EGFR; Cetuximab; Resistance; Colorectal Cancer
ID EGFR-TARGETED THERAPIES; LUNG-CANCER; KITENIN; ERBB4
AB ErbB4/KITENIN signaling plays a role in epidermal growth factor receptor (EGFR)-independent EGF pathways mediating the invasiveness and tumorigenesis of colorectal cancer cells. However, whether alterations in ErbB4/KITENIN signaling play a role in the resistance to anti-EGFR therapy remains unclear. Here, we established cetuximab-resistant DLD1 and HT29 cells, and analyzed changes in ErbB4/KITENIN signaling. c-Jun, a final effector in ErbB4/KITENIN-mediated signaling, was upregulated, whereas KITENIN levels remained constant in both cetuximab-resistant cell lines. The phosphorylation of EGFR and ErbB4 was increased in cetuximab-resistant cells, suggesting that ErbB4/KITENIN signaling contributed to the acquisition of cetuximab resistance in the cells. Silencing of KITENIN and/or ErbB4 increased cetuximab sensitivity in cetuximab-resistant cells. This study is the first to report the activation of ErbB4/KITENIN-mediated signaling in cetuximab-resistant colorectal cancer cells and the potential clinical application of ErbB4/KITENIN-targeting therapy for overcoming anti-EGFR resistance.
C1 [Park, So-Yeon; Yang, Yi; Zhou, Rui; Kim, Hangun] Sunchon Natl Univ, Coll Pharm, Sunchon 57922, Jeonnam, South Korea.
   [Jung, Sang-Chul] Sunchon Natl Univ, Dept Environm Engn, Sunchon 57922, Jeonnam, South Korea.
   [Bae, Woo Kyun; Chung, Lk Joo] Chonnam Natl Univ, Med Sch, Dept Hematol Oncol, Gwangju 61469, South Korea.
   [Kim, Kyung Keun] Chonnam Natl Univ, Med Sch, Med Res Ctr Gene Regulat, Gwangju 61469, South Korea.
C3 Sunchon National University; Sunchon National University; Chonnam
   National University; Chonnam National University
RP Kim, H (corresponding author), Sunchon Natl Univ, Coll Pharm, Sunchon 57922, Jeonnam, South Korea.
RI Kim, Dae/D-8864-2013; zhou, rui/KZT-9353-2024
FU National Research Foundation of Korea - Korea government (MSIP)
   [NRF-2016 R1C1B2007494, NRF-2016R1D1A1B03934637, NRF-2015R1A4A1041219,
   MRC-2011-0030132]
FX This work was supported by National Research Foundation of Korea grants
   (NRF-2016 R1C1B2007494, NRF-2016R1D1A1B03934637, NRF-2015R1A4A1041219,
   and MRC-2011-0030132) funded by the Korea government (MSIP).
CR Ahmed D, 2013, ONCOGENESIS, V2, DOI 10.1038/oncsis.2013.35
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NR 11
TC 6
Z9 6
U1 2
U2 33
PU AMER SCIENTIFIC PUBLISHERS
PI VALENCIA
PA 26650 THE OLD RD, STE 208, VALENCIA, CA 91381-0751 USA
SN 1533-4880
EI 1533-4899
J9 J NANOSCI NANOTECHNO
JI J. Nanosci. Nanotechnol.
PD FEB
PY 2019
VL 19
IS 2
BP 1166
EP 1171
DI 10.1166/jnn.2019.15899
PG 6
WC Chemistry, Multidisciplinary; 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 GX8JT
UT WOS:000448031900096
PM 30360226
DA 2025-01-04
ER

PT J
AU Rachdi, H
   Labidi, S
   Mejri, N
   El Benna, H
   Daoud, N
   Bayar, R
   Marghli, A
   Khalfallah, M
   Boussen, H
AF Rachdi, Haifa
   Labidi, Soumaya
   Mejri, Nesrine
   El Benna, Houda
   Daoud, Nouha
   Bayar, Rached
   Marghli, Adel
   Khalfallah, MedTahar
   Boussen, Hamouda
TI Local treatment of liver and lung metastases from colorectal cancer: a
   multicenter Tunisian study
SO COLORECTAL CANCER
LA English
DT Article
DE cancer; colorectal; hepatic; metastases; pulmonary; surgery; suvival
ID LONG-TERM OUTCOMES; PULMONARY METASTASES; RESECTION; CARCINOMA;
   CHEMOTHERAPY; SURVIVAL
AB Aim: Surgical treatment of hepatic or pulmonary metastases is the optimal therapeutic goal in metastatic colorectal cancer (CRC). Methods: Our retrospective study concerned 70 patients treated for CRC, collected from 2003 to 2015, presenting liver metastases (LM) in 61 cases and pulmonary metastases (PM) in nine cases, treated by surgery for their distant disease. We collected and compared their epidemiologic, anatomoclinical parameters and analyzed several prognostic factors. Results: Metastases were multiple (>= 4) in 9/61 LM and in 5/9 PM. Patients had synchronous metastases in 32 cases (30 LM/2 PM) and metachronous metastases in 33 cases (32 LM and 11 PM). Surgery for LM consisted of metastasectomy (49/61), segmentectomy (5/61) and hepatectomy for the remaining seven patients; ten patients had also subsequent liver radiofrequency. LM were treated by wedge resection in 6/9 and lobectomy in two cases, radiofrequency was performed in five cases. 56/61 (80%) patients received chemotherapy, mostly FOLFOX protocol as the first-line treatment and targeted therapy in 55% of cases. For the overall population, median OS and PFS were, respectively, 44 and 32 months. We did not observe any significant difference in terms of OS (p=0.659) and PFS (p=0.318) between resected LM or/and PM. A better survival was found when there was disease-free interval between the occurrence of the primary and the metastases exceeded 18 months and in patients with less than four metastases. Conclusion: Resection of metastatic disease mostly in liver and lungs improves survival of patients with CRC. The patients with longer disease-free interval and less than four metastases had the best outcomes.
C1 [Rachdi, Haifa; Labidi, Soumaya; Mejri, Nesrine; El Benna, Houda; Daoud, Nouha; Boussen, Hamouda] Abderrahmen Mami Hosp, Med Oncol Dept SOMA, Ariana, Tunisia.
   [Bayar, Rached; Khalfallah, MedTahar] Mongi Slim Hosp, Hepatobibary Surg Dept, La Marsa, Tunisia.
   [Marghli, Adel] Univ Hosp Abderrahmen Mami Hosp, Thorac Surg Dept, Ariana, Tunisia.
C3 Universite de Tunis-El-Manar; Hopital Abderrahmene Mami; Universite de
   Tunis-El-Manar; Hopital Mongi Slim
RP Rachdi, H (corresponding author), Abderrahmen Mami Hosp, Med Oncol Dept SOMA, Ariana, Tunisia.
EM haifa.rachdi@yahoo.fr
RI Boussen, Hamouda/AAI-2796-2020; Bayar, Rached/GLN-7721-2022
CR Adam R, 2017, EUR J CANCER, V78, P7, DOI 10.1016/j.ejca.2017.03.009
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NR 32
TC 1
Z9 1
U1 0
U2 1
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1758-194X
EI 1758-1958
J9 COLORECTAL CANCER
JI Colorectal Cancer
PD MAR
PY 2019
VL 8
IS 1
AR CRC08
DI 10.2217/crc-2018-0002
PG 10
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA IL1HV
UT WOS:000477051200003
OA gold
DA 2025-01-04
ER

PT J
AU Feliu, J
   Garcia-Carbonero, R
   Capdevila, J
   Guasch, I
   Alonso-Orduna, V
   Lopez, C
   Garcia-Alfonso, P
   Castanon, C
   Sevilla, I
   Cerezo, L
   Conill, C
   Quintana-Angel, B
   Sanchez, ME
   Ghanem, I
   Martin-Richard, M
   Lopez-Gomez, M
   Leon, A
   Caro, M
   Fernandez, T
   Maurel, J
AF Feliu, Jaime
   Garcia-Carbonero, Rocio
   Capdevila, Jaume
   Guasch, Inmaculada
   Alonso-Orduna, Vicente
   Lopez, Carlos
   Garcia-Alfonso, Pilar
   Castanon, Carmen
   Sevilla, Isabel
   Cerezo, Laura
   Conill, Carles
   Quintana-Angel, Begona
   Sanchez, Maria E.
   Ghanem, Ismael
   Martin-Richard, Marta
   Lopez-Gomez, Miriam
   Leon, Ana
   Caro, Monica
   Fernandez, Teresa
   Maurel, Joan
TI VITAL phase 2 study: Upfront 5-fluorouracil, mitomycin-C, panitumumab
   and radiotherapy treatment in nonmetastatic squamous cell carcinomas of
   the anal canal (GEMCAD 09-02)
SO CANCER MEDICINE
LA English
DT Article
DE chemotherapy; radiotherapy; rectal cancer; target therapy
ID GROWTH-FACTOR RECEPTOR; CETUXIMAB PLUS CHEMORADIOTHERAPY;
   HUMAN-PAPILLOMAVIRUS; CONVENTIONAL CHEMORADIOTHERAPY; OPEN-LABEL;
   CANCER; COMBINATION; CISPLATIN; CHEMORADIATION; TRIAL
AB Aim VITAL, a phase II single-arm study, aimed to evaluate efficacy and safety of panitumumab addition to 5-fluorouracil (5-FU), mitomycin-C (MMC) and radiotherapy (RT) in patients with localized squamous cell carcinoma of the anal canal (SCCAC). Methods Adult, treatment-naive SCCAC patients (Stage T2-T4, any N, M0) and ECOG-PS <= 2, received panitumumab (6 mg/kg, day 1 and Q2W; 8 weeks), 5-FU (1000 mg/m(2)/d, days 1-4 and 29-32), MMC (10 mg/m(2), days 1 and 29) and RT 45 Gy (1.8 Gy/fraction) to the primary tumor and mesorectal, iliac and inguinal lymph nodes, plus 10-15 Gy boost dose to the primary tumor and affected lymph nodes. The primary objective was disease free survival rate (DFS) at 3-years (expected 3-year DFS rate: 73.7 +/- 12%). Results Fifty-eight patients (31 women; median age: 59 years; ECOG-PS 0-1:98%; TNM II [29%] (T2 or T3/N0/M0)/IIIA (T1-T3/N1/M0 or T4/N0/M0) [21%]/IIIB (T4/N1/M0 or any T/N2 or N3/M0) [47%]/nonevaluable [4%]) were included. The median follow-up was 45 months. The 3-year DFS rate was 61.1% (95% CI: 47.1, 72.4). The 3-year overall survival rate was 78.4% (95% CI: 65.1, 87.1). Eighteen patients (31.0%) required a colostomy within 2 years posttreatment. Grade 3-4 toxicities were experienced by 53 (91%) patients. Most common grade 3-4 treatment-related events were radiation skin injury (40%) and neutropenia (24%). No toxic deaths occurred. Improved efficacy in colostomy-free survival and complete response rate was observed in human papilloma virus positive patients. Conclusions Panitumumab addition to MMC-5FU regimen in SCCAC patients increases toxicity and does not improve patients' outcomes. RT plus MMC-5FU remains the standard of care for localized SCCAC patients.
C1 [Feliu, Jaime; Ghanem, Ismael] Hosp Univ La Paz, Dept Med Oncol, Catedra UAM AMGEN, CIBERONC, Madrid, Spain.
   [Garcia-Carbonero, Rocio] Hosp Univ Virgen del Rocio, Dept Med Oncol, Seville, Spain.
   [Garcia-Carbonero, Rocio] Hosp Univ 12 Octubre, CNIO, UCM, CIBERONC,Dept Med Oncol,Imas12, Madrid, Spain.
   [Capdevila, Jaume] VHIO, Dept Med Oncol, Hosp Univ Vall dHebron, Barcelona, Spain.
   [Guasch, Inmaculada] Hosp Althaia Manresa, Dept Med Oncol, Manresa, Spain.
   [Alonso-Orduna, Vicente] Hosp Univ Miguel Servet, Inst Invest Sanitaria Aragon, Dept Med Oncol, Zaragoza, Spain.
   [Lopez, Carlos] Hosp Univ Marques Valdecilla, Dept Med Oncol, Santander, Spain.
   [Garcia-Alfonso, Pilar] Hosp Gen Univ Gregorio Maranon, Dept Med Oncol, Madrid, Spain.
   [Castanon, Carmen] Hosp Virgen Blanca, Dept Med Oncol, Leon, Spain.
   [Sevilla, Isabel] Hosp Univ Reg & Virgen Victoria, Inst Invest Biomed Malaga IBIMA, Invest Clin & Traslac Canc, Malaga, Spain.
   [Cerezo, Laura] Hosp Univ La Princesa, Dept Radiat Oncol, Madrid, Spain.
   [Conill, Carles] Univ Barcelona, Hosp Clin, Dept Radiat Oncol, IDIBAPS, Barcelona, Spain.
   [Quintana-Angel, Begona] Hosp Univ Virgen del Rocio, Dept Radiat Oncol, Seville, Spain.
   [Sanchez, Maria E.] Hosp Univ La Paz, Dept Oncol, Madrid, Spain.
   [Martin-Richard, Marta] Hosp Santa Creu & Sant Pau, Dept Med Oncol, Barcelona, Spain.
   [Lopez-Gomez, Miriam] Hosp Univ Infanta Sofia, Dept Med Oncol, Madrid, Spain.
   [Leon, Ana] Hosp Univ Fdn Jimenez Diaz, Dept Med Oncol, Madrid, Spain.
   [Caro, Monica] Hosp Badalona Germans Trias & Pujol, Dept Radiat Oncol, ICO Badalona, Badalona, Spain.
   [Fernandez, Teresa] Hosp Son Llatzer, Dept Med Oncol, Palma De Mallorca, Spain.
   [Maurel, Joan] Univ Barcelona, Hosp Clin, Dept Med Oncol, IDIBAPS,Translat Genom & Targeted Therapeut Solid, Barcelona, Spain.
C3 CIBER - Centro de Investigacion Biomedica en Red; CIBERONC; Hospital
   Universitario La Paz; Virgen del Rocio University Hospital; Complutense
   University of Madrid; CIBER - Centro de Investigacion Biomedica en Red;
   CIBERONC; Hospital Universitario 12 de Octubre; Centro Nacional de
   Investigaciones Oncologicas (CNIO); Vall d'Hebron Institut d'Oncologia
   (VHIO); Hospital Universitari Vall d'Hebron; Miguel Servet University
   Hospital; Hospital Universitario Marques de Valdecilla (HUMV); General
   University Gregorio Maranon Hospital; Instituto de Investigacion
   Biomedica de Malaga y Plataforma en Nanomedicina (IBIMA); Universidad de
   Malaga; University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS;
   Virgen del Rocio University Hospital; Hospital Universitario La Paz;
   Hospital of Santa Creu i Sant Pau; Hospital Universitario Infanta Sofia;
   Hospital Germans Trias i Pujol; Institut Catala d'Oncologia; Hospital
   Universitari Son Llatzer; University of Barcelona; Hospital Clinic de
   Barcelona; IDIBAPS
RP Feliu, J (corresponding author), Hosp Univ La Paz, Serv Oncol Med, Paseo Casteliana 261, Madrid 28046, Spain.
EM jaime.feliu@salud.madrid.org
RI LOPEZ, CARLOS/ABP-9145-2022; Ghanem, Ismael/HTS-9038-2023
OI Lopez Lopez, Carlos/0000-0002-8901-741X; Garcia-Carbonero,
   Rocio/0000-0002-3342-397X; Feliu, Jaime/0000-0003-4867-1420; Ghanem,
   Ismael/0000-0002-1859-0737; Maurel, Joan/0000-0002-9413-5592
FU Amgen S.A.
FX This work was supported by Amgen S.A.
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NR 42
TC 8
Z9 8
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD FEB
PY 2020
VL 9
IS 3
BP 1008
EP 1016
DI 10.1002/cam4.2722
EA DEC 2019
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KH4IZ
UT WOS:000503116400001
PM 31851776
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lv, QY
   Zou, HZ
   Xu, YY
   Shao, ZY
   Wu, RQ
   Li, KJ
   Deng, X
   Gu, DN
   Jiang, HX
   Su, M
   Zou, CL
AF Lv, Qi-yuan
   Zou, Hai-zhou
   Xu, Yu-yan
   Shao, Zhen-yong
   Wu, Ruo-qi
   Li, Ke-jie
   Deng, Xia
   Gu, Dian-na
   Jiang, Hong-xiao
   Su, Meng
   Zou, Chang-lin
TI Expression levels of chemokine (C-X-C motif) ligands CXCL1 and CXCL3 as
   prognostic biomarkers in rectal adenocarcinoma: evidence from Gene
   Expression Omnibus (GEO) analyses
SO BIOENGINEERED
LA English
DT Article
DE Rectal adenocarcinoma; bioinformatics analysis; CXCL1; CXCL2; CXCL3
ID CANCER-ASSOCIATED FIBROBLASTS; CELL-PROLIFERATION; WEB SERVER; PROMOTES;
   COLON; INVASION
AB Rectal cancer is a life-threatening disease worldwide. Chemotherapy resistance is common in rectal adenocarcinoma patients and has unfavorable survival outcomes; however, its related molecular mechanisms remain unknown. To identify genes related to the initiation and progression of rectal adenocarcinoma, three datasets were obtained from the Gene Expression Omnibus database. In total, differentially expressed genes were analyzed from 294 tumor and 277 para-carcinoma samples from patients with rectal cancer. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes functions were investigated. Cytoscape software and MicroRNA Enrichment Turned Network were applied to construct a protein-protein interaction network of the dependent hub genes and related microRNAs. The Oncomine database was used to identify hub genes. Additionally, Gene Expression Profiling Interactive Analysis was applied to determine the RNA expression level. Tumor immune infiltration was assessed using the Tumor Immune Estimation Resource database. The expression profiles of hub genes between stages, and their prognostic value, were also evaluated. During this study, data from The Cancer Genome Atlas were utilized. In rectal adenocarcinoma, four hub genes including CXCL1, CXCL2, CXCL3, and GNG4 were highly expressed at the gene and RNA levels. The expression of CXCL1, CXCL2, and CXCL3 was regulated by has-miR-1-3p and had a strong positive correlation with macrophage and neutrophil. CXCL2 and CXCL3 were differentially expressed at different tumor stages. High expression levels of CXCL1 and CXCL3 predicted poor survival. In conclusion, the CXCL1 and CXCL3 genes may have potential for prognosis and molecular targeted therapy of rectal adenocarcinoma.
C1 [Lv, Qi-yuan; Xu, Yu-yan; Shao, Zhen-yong; Wu, Ruo-qi; Li, Ke-jie; Deng, Xia; Su, Meng; Zou, Chang-lin] Wenzhou Med Univ, Dept Radiotherapy, Affiliated Hosp 1, Wenzhou, Zhejiang, Peoples R China.
   [Zou, Hai-zhou] Wenzhou Hosp Tradit Chinese Med, Dept Oncol, Wenzhou, Zhejiang, Peoples R China.
   [Gu, Dian-na] Wenzhou Med Univ, Affiliated Hosp 1, Dept Med Oncol, Wenzhou, Zhejiang, Peoples R China.
   [Jiang, Hong-xiao] Omigen Inc, Hangzhou, Peoples R China.
C3 Wenzhou Medical University; Wenzhou Medical University
RP Su, M; Zou, CL (corresponding author), Wenzhou Med Univ, Dept Radiotherapy, Affiliated Hosp 1, Wenzhou, Zhejiang, Peoples R China.
EM smeng1989@163.com; zcl19670115@163.com
RI Li, Kejie/D-3595-2013; 徐, 语言/IAM-3326-2023
FU Wenzhou Science and Technology Bureau [Y20180220]
FX This work was supported by the Wenzhou Science and Technology Bureau
   under Grant number Y20180220.
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NR 53
TC 10
Z9 10
U1 1
U2 9
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 2165-5979
EI 2165-5987
J9 BIOENGINEERED
JI Bioengineered
PD JAN 1
PY 2021
VL 12
IS 1
BP 3711
EP 3725
DI 10.1080/21655979.2021.1952772
PG 15
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA TK4NC
UT WOS:000674136000001
PM 34269159
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Boleij, A
   Tops, BBJ
   Rombout, PDM
   Dequeker, EM
   Ligtenberg, MJL
   van Krieken, JH
AF Boleij, Annemarie
   Tops, Bastiaan B. J.
   Rombout, Paul D. M.
   Dequeker, Elizabeth M.
   Ligtenberg, Marjolijn J. L.
   van Krieken, J. Han
CA Dutch RAS EQA Initiative
TI RAS testing in metastatic colorectal cancer: excellent reproducibility
   amongst 17 Dutch pathology centers
SO ONCOTARGET
LA English
DT Article
DE RAS; colorectal cancer; metastasis; quality control; next generation
   sequencing
ID EXTERNAL-QUALITY-ASSESSMENT; WILD-TYPE KRAS; PANITUMUMAB; PERCENTAGE;
   MUTATIONS; CETUXIMAB; TRIAL
AB In 2013 the European Medicine Agency (EMA) restricted the indication for anti-EGFR targeted therapy to metastatic colorectal cancer (mCRC) with a wild-type RAS gene, increasing the need for reliable RAS mutation testing. We evaluated the completeness and reproducibility of RAS-testing in the Netherlands.
   From 17 laboratories, tumor DNA of the first 10 CRC cases tested in 2014 in routine clinical practice was re-tested by a reference laboratory using a custom next generation sequencing panel. In total, 171 CRC cases were re-evaluated for hotspot mutations in KRAS, NRAS and BRAF.
   Most laboratories had introduced complete RAS-testing (65%) and BRAF-testing (71%) by January 2014. The most employed method for all hotspot regions was Sanger sequencing (range 35.7 - 49.2%). The reference laboratory detected all mutations that had been found in the participating laboratories (n = 92), plus 10 additional mutations. This concerned three RAS and seven BRAF mutations that were missed due to incomplete testing of the participating laboratory. Overall, the concordance of tests performed by both the reference and participating laboratory was 100% (163/163; kappa-static 1.0) for RAS and 100% (144/144; kappa-static 1.0) for BRAF.
   Our study shows that RAS and BRAF mutations can be reproducibly assessed using a variety of testing methods.
C1 [Boleij, Annemarie; Rombout, Paul D. M.; Ligtenberg, Marjolijn J. L.; van Krieken, J. Han] Radboud Univ Nijmegen, Med Ctr, Dept Pathol, Nijmegen, Netherlands.
   [Tops, Bastiaan B. J.; Ligtenberg, Marjolijn J. L.] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, Nijmegen, Netherlands.
   [Dequeker, Elizabeth M.] Univ Leuven, KU Leuven, Biomed Qual Assurance Res Unit, Dept Publ Hlth & Primary Care, Leuven, Belgium.
   Univ Amsterdam, Acad Med Ctr, Dept Pathol, NL-1105 AZ Amsterdam, Netherlands.
   St Antonius Hosp, Dept Pathol, Nieuwegein, Netherlands.
   Canisius Wilhelmina Ziekenhuis, Dept Pathol, Nijmegen, Netherlands.
   Diakonessen Hosp, Pathol Lab, Utrecht, Netherlands.
   Dutch Canc Inst NKI, Amsterdam, Netherlands.
   St Elizabeth Hosp, Dept Mol Pathol, Tilburg, Netherlands.
   Erasmus MC, Dept Pathol, Mol Diagnost, Rotterdam, Netherlands.
   Isala, Dept Pathol, Zwolle, Netherlands.
   Jeroen Bosch Ziekenhuis, Mol Diagnost, Shertogenbosch, Netherlands.
   Lab Pathol Oost Nederland LABPON, Hengelo, Netherlands.
   Leiden Univ, Med Ctr, Dept Pathol, Leiden, Netherlands.
   Lab Pathol & Med Microbiol PAMM, Eindhoven, Netherlands.
   Pathan BV, Mol Diagnost, Rotterdam, Netherlands.
   Rijnstate Ziekenhuis, Dept Pathol, Arnhem, Netherlands.
   Univ Med Ctr UMC Utrecht, Mol Pathol, Utrecht, Netherlands.
   [Dutch RAS EQA Initiative] Univ Groningen, Univ Med Ctr Groningen, Dept Pathol, NL-9713 AV Groningen, Netherlands.
   Vrije Univ Amsterdam, Med Ctr, Dept Pathol, Amsterdam, Netherlands.
C3 Radboud University Nijmegen; Radboud University Nijmegen; KU Leuven;
   University of Amsterdam; Academic Medical Center Amsterdam; Vrije
   Universiteit Amsterdam; St. Antonius Hospital Utrecht;
   Canisius-Wilhelmina Hospital; Diakonessenhuis; Netherlands Cancer
   Institute; Elisabeth-TweeSteden Ziekenhuis (ETZ); Erasmus University
   Rotterdam; Erasmus MC; Jeroen Bosch Ziekenhuis; Leiden University - Excl
   LUMC; Leiden University; Leiden University Medical Center (LUMC);
   Rijnstate Hospital; University of Groningen; Vrije Universiteit
   Amsterdam
RP van Krieken, JH (corresponding author), Radboud Univ Nijmegen, Med Ctr, Dept Pathol, Nijmegen, Netherlands.
EM Han.vanKrieken@radboudumc.nl
RI Ligtenberg, Marjolijn/N-9666-2013; van Krieken, Joannes/D-4138-2009;
   Boleij, Annemarie/L-3975-2013; Tops, Bastiaan/L-4697-2015
OI van Grieken, Nicole/0000-0001-9992-0760; van Krieken,
   Joannes/0000-0002-8105-0450; Boleij, Annemarie/0000-0003-4495-5880;
   tops, funnel/0000-0003-3116-4203; Tops, Bastiaan/0000-0002-1699-8210;
   Sie, Daoud/0000-0001-6762-2582; Diepstra, Arjan/0000-0001-9239-1050
FU MERCK Group KGaA
FX This study was funded by MERCK Group KGaA. The source of funding did not
   have any influence on the design and the analysis of the results.
CR Amado RG, 2008, J CLIN ONCOL, V26, P1626, DOI 10.1200/JCO.2007.14.7116
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NR 25
TC 11
Z9 12
U1 0
U2 13
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD JUN 20
PY 2015
VL 6
IS 17
BP 15681
EP 15689
DI 10.18632/oncotarget.3804
PG 9
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CO2TY
UT WOS:000359010700076
PM 25944693
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Su, YC
   Wu, CC
   Chen, YH
   Su, CC
   Chang, YC
   Hsieh, MC
   Yang, YHK
AF Su, Yi-Chia
   Wu, Chih-Chien
   Chen, Yu-Hsun
   Su, Chien-Chou
   Chang, Yu-Ching
   Hsieh, Meng-Che
   Kao Yang, Yea-Huei
TI Assessing the effectiveness of targeted agents in adjuvant therapy for
   patients with metastatic colorectal cancer undergoing surgical
   resection: a retrospective cohort study
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Article
DE adjuvant therapy; metastatic colorectal cancer; surgical resection;
   targeted agents
ID LIVER METASTASES; SYSTEMIC CHEMOTHERAPY; COMORBIDITY INDEX; PLUS
   CETUXIMAB; BEVACIZUMAB; FOLFIRI; SURGERY; TAIWAN
AB Background: Primary tumor resection and metastasectomy may be beneficial for many patients with metastatic colorectal cancer (mCRC).Objective: To assess the differences in postoperative survival outcomes between adjuvant therapy with chemotherapy alone and chemotherapy plus targeted agents (TAs).Design: Retrospective cohort study.Methods: Patients with mCRC who underwent surgical resection for primary colorectal tumor and distant metastases and received adjuvant therapy from 1 January 2010 to 31 December 2017 were enrolled in the Taiwan Cancer Registry. We analyzed the overall survival of patients with resectable or initially unresectable mCRC who received adjuvant chemotherapy alone and chemotherapy plus TAs.Results: We enrolled 1124 and 542 patients with resectable and initially unresectable mCRC, respectively. Adjuvant chemotherapy plus TAs and chemotherapy alone resulted in similar mortality rates among patients with resectable mCRC [adjusted hazard ratio (aHR) = 1.13; 95% confidence interval (CI), 0.93-1.36]; however, it marginally reduced the mortality rate among patients with initially unresectable mCRC who underwent conversion surgery after neoadjuvant therapy (aHR = 0.81; 95% CI, 0.62-1.06). The subgroup analysis of patients who received more than nine cycles of TAs preoperatively and anti-epidermal growth factor receptor agents revealed aHRs of 0.48 (95% CI, 0.27-0.87) and 0.33 (95% CI, 0.18-0.60), respectively.Conclusion: Adjuvant chemotherapy plus TAs may improve survival in patients with initially unresectable tumors who underwent conversion surgery following neoadjuvant therapy with TAs, especially in those who respond well to the targeted therapy. Our study underscores the importance of stratifying patients with mCRC based on tumor resectability when selecting the adjuvant therapy regimen.
C1 [Su, Yi-Chia; Chang, Yu-Ching; Kao Yang, Yea-Huei] Natl Cheng Kung Univ, Inst Clin Pharm & Pharmaceut Sci, Coll Med, 1,Univ Rd, Tainan 701, Taiwan.
   [Kao Yang, Yea-Huei] Natl Cheng Kung Univ, Hlth Outcome Res Ctr, Tainan, Taiwan.
   [Su, Yi-Chia] Kaohsiung Vet Gen Hosp, Dept Pharm, Kaohsiung, Taiwan.
   [Su, Yi-Chia] Chia Nan Univ Pharm & Sci, Dept Pharm, Tainan, Taiwan.
   [Su, Yi-Chia] Shu Zen Jr Coll Med & Management, Dept Nursing, Kaohsiung, Taiwan.
   [Wu, Chih-Chien; Chen, Yu-Hsun] Kaohsiung Vet Gen Hosp, Dept Surg, Div Colorectal Surg, Kaohsiung, Taiwan.
   [Wu, Chih-Chien] Natl Yang Ming Chiao Tung Univ, Sch Med, Dept Surg, Taipei, Taiwan.
   [Su, Chien-Chou] Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Clin Innovat Ctr, Tainan, Taiwan.
   [Su, Chien-Chou] Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Coll Med, Dept Pharm, Tainan, Taiwan.
   [Hsieh, Meng-Che] E Da Canc Hosp, Dept Hematol & Oncol, Kaohsiung, Taiwan.
   [Hsieh, Meng-Che] I Shou Univ, Coll Med, Kaohsiung, Taiwan.
C3 National Cheng Kung University; National Cheng Kung University;
   Kaohsiung Veterans General Hospital; Chia Nan University of Pharmacy &
   Science; 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; E-Da Hospital; I Shou University
RP Yang, YHK (corresponding author), Natl Cheng Kung Univ, Inst Clin Pharm & Pharmaceut Sci, Coll Med, 1,Univ Rd, Tainan 701, Taiwan.; Yang, YHK (corresponding author), Natl Cheng Kung Univ, Hlth Outcome Res Ctr, Tainan, Taiwan.
EM yhkao@mail.ncku.edu.tw
RI chen, yuling/JMQ-4121-2023; Su, Yichia/HJI-3668-2023
FU Higher Education Sprout Project, Ministry of Education, to the
   Headquarters of University Advancement at National Cheng Kung University
   (NCKU); National Science and Technology Council [D111-F2547,
   A1102-104B]; Kaohsiung Veterans General Hospital [KSVGH 112-137, KSVGH
   113-083]
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and/or publication of this article: This research
   was partly supported by the Higher Education Sprout Project, Ministry of
   Education, to the Headquarters of University Advancement at National
   Cheng Kung University (NCKU) and partly by the National Science and
   Technology Council [grant number D111-F2547 and A1102-104B] and
   Kaohsiung Veterans General Hospital [grant number KSVGH 112-137 and
   KSVGH 113-083].
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NR 32
TC 0
Z9 0
U1 1
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PY 2024
VL 16
AR 17588359241246427
DI 10.1177/17588359241246427
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OG6T9
UT WOS:001206164900001
PM 38655393
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Rotundo, MS
   Bagnardi, V
   Rotundo, M
   Comandè, M
   Zampino, MG
AF Rotundo, Maria Saveria
   Bagnardi, Vincenzo
   Rotundo, Miryam
   Comande, Mario
   Zampino, Maria Giulia
TI PD-1/PD-L1 blockade, a novel strategy for targeting metastatic
   colorectal cancer: A systematic review and meta-analysis of randomized
   trials
SO ONCOLOGY LETTERS
LA English
DT Review
DE colorectal cancer; immune checkpoint inhibitor; immunotherapy;
   meta-analysis; programmed cell death protein 1; programmed death ligand
   1
ID IMMUNE CHECKPOINT INHIBITORS; MICROSATELLITE INSTABILITY;
   CLINICAL-EVIDENCE; COLON-CANCER; TUMORS; CHEMOTHERAPY; COMBINATION;
   CHALLENGES; MUTATION; CRITERIA
AB Currently, standard treatment of patients with metastatic colorectal cancer (mCRC) comprises chemotherapy (CT) and/or biological therapy (BT) and/or best supportive care (BSC). The present study performed a meta-analysis on five phase II-III randomized clinical trials, which compared CT/BT/BSC as the control arm with the immune checkpoint inhibitors (ICIs) anti-programmed cell death protein 1 (PD-1) or its ligand (PD-L1) alone or in combination with cytotoxic T lymphocyte antigen 4 or mitogen activated protein kinase kinase inhibitors as the experimental arm, to evaluate whether a standard approach could be overcome using the novel target therapy strategy. Pooled hazard ratio (HR) for progression-free survival was 0.95 in favor of the experimental arm [95% confidence interval (CI), 0.74-1.22; P=0.68]. Heterogeneity was significant: Cochran's Q, 21.0; P=0.0082; I-2 index, 76%. Pooled HR for overall survival was 0.88 in favor of the experimental arm (95% CI, 0.75-1.02; P=0.08). Heterogeneity was not significant (Cochran's Q, 6.0; P=0.31; I-2 index, 16%). The present meta-analysis demonstrated a trend toward the improvement of survival by PD-1/PD-L1 blockade in mCRC. Further homogeneous studies are necessary to strengthen these results, beyond the known benefits of ICIs in deficient mismatch repair/high microsatellite instability tumors.
C1 [Rotundo, Maria Saveria; Comande, Mario] Uboldo Hosp, Complex Operat Unit Med Oncol, I-20063 Milan, Italy.
   [Bagnardi, Vincenzo] Univ Milano Bicocca, Dept Stat & Quantitat Methods, I-20126 Milan, Italy.
   [Rotundo, Miryam] Magna Graecia Univ Catanzaro, Dept Expt & Clin Med Med, Vet & Pharmaceut Biotechnol, I-88100 Catanzaro, Italy.
   [Zampino, Maria Giulia] Ist Ricovero & Cura Carattere Sci, European Inst Oncol, Div Gastrointestinal Med Oncol & Neuroendocrine T, Via Ripamonti 435, I-20141 Milan, Italy.
C3 University of Milano-Bicocca; Magna Graecia University of Catanzaro;
   IRCCS Ca Granda Ospedale Maggiore Policlinico; IRCCS European Institute
   of Oncology (IEO)
RP Zampino, MG (corresponding author), Ist Ricovero & Cura Carattere Sci, European Inst Oncol, Div Gastrointestinal Med Oncol & Neuroendocrine T, Via Ripamonti 435, I-20141 Milan, Italy.
EM maria.zampino@ieo.it
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NR 72
TC 2
Z9 2
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 2022
VL 23
IS 4
AR 134
DI 10.3892/ol.2022.13254
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZP7OY
UT WOS:000766610600001
PM 35251353
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Karasic, TB
   Rosen, MA
   O'Dwyer, PJ
AF Karasic, Thomas B.
   Rosen, Mark A.
   O'Dwyer, Peter J.
TI Antiangiogenic tyrosine kinase inhibitors in colorectal cancer: is there
   a path to making them more effective?
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Review
DE Sorafenib; Regorafenib; Antiangiogenesis; Colorectal cancer; VEGFR2
   signaling; DCE-MRI
ID RENAL-CELL CARCINOMA; ENDOTHELIAL GROWTH-FACTOR; PHASE-I TRIAL;
   OXALIPLATIN-BASED CHEMOTHERAPY; COMBINATION TARGETED THERAPY; FACTOR
   RECEPTOR INHIBITOR; REGORAFENIB BAY 73-4506; CONTRAST-ENHANCED MRI;
   DOUBLE-BLIND; 1ST-LINE TREATMENT
AB Antiangiogenic therapy has a proven survival benefit in metastatic colorectal cancer. Inhibition of the VEGF pathway using a variety of extracellular antibody approaches has clear benefit in combination with chemotherapy, while intracellular blockade using tyrosine kinase inhibitors (TKIs) such as sorafenib and regorafenib has had more limited success. Pharmacodynamic modeling using modalities such as DCE-MRI indicates potent antiangiogenic effects of these TKIs, yet numerous combination therapies, primarily with chemotherapy, have failed to demonstrate an additive benefit. The sole comparative study of a single agent TKI against placebo showed a survival benefit of regorafenib in patients with advanced, refractory disease. Preclinical data demonstrate synergy between antiantiogenic TKIs and targeted interventions including autophagy inhibition, and together with a renewed effort to define markers of susceptibility, such combinations may be a way to improve the limited efficacy of this once-promising drug class.
C1 [Karasic, Thomas B.; O'Dwyer, Peter J.] Univ Penn, Abramson Canc Ctr, 3400 Civic Ctr Blvd, Philadelphia, PA 19146 USA.
   [Rosen, Mark A.] Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
C3 University of Pennsylvania; University of Pennsylvania
RP Karasic, TB (corresponding author), Univ Penn, Abramson Canc Ctr, 3400 Civic Ctr Blvd, Philadelphia, PA 19146 USA.
EM thomas.karasic@uphs.upenn.edu
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NR 98
TC 6
Z9 7
U1 0
U2 11
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 OCT
PY 2017
VL 80
IS 4
BP 661
EP 671
DI 10.1007/s00280-017-3389-3
PG 11
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA FH9TS
UT WOS:000411555500001
PM 28721456
DA 2025-01-04
ER

PT J
AU Johnson, SP
   Ogunlade, O
   Lythgoe, MF
   Beard, P
   Pedley, RB
AF Johnson, S. Peter
   Ogunlade, Olumide
   Lythgoe, Mark F.
   Beard, Paul
   Pedley, R. Barbara
TI Longitudinal Photoacoustic Imaging of the Pharmacodynamic Effect of
   Vascular Targeted Therapy on Tumors
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID DISRUPTING AGENT OXI4503; CANCER; TOMOGRAPHY; MODEL; RADIOIMMUNOTHERAPY;
   NORMALIZATION; OXYGENATION; ULTRASOUND; PERFUSION; TISSUE
AB Purpose: Photoacoustic imaging (PAI) is a novel noninvasive and nonionizing imaging technique that allows longitudinal imaging of tumor vasculature in vivo and monitoring of response to therapy, especially for vascular targeted chemotherapy agents. In this study, we used a novel high-resolution all-optical PAI scanner to observe the pharmacodynamic response to the vascular-disrupting agent OXi4503.
   Experimental Design: Two models of colorectal carcinoma (SW1222 and LS174T) that possess differing pathophysiologic vascularization were established as subcutaneous tumors in mice. Monitoring of response was performed over a 16-day "regrowth" period following treatment at 40 mg/kg, and at day 2 for a "dose response" study at 40 mg/kg, 10 mg/kg, 1 mg/kg, and sham dose.
   Results: Qualitative and quantitative changes in PA signal are observed, with an initial decrease followed by a plateau and subsequent return of signal indicating regrowth. Both tumor types exhibited a decrease in signal; however, the more vascularized SW1222 tumors show greater response to treatment. Decreasing the dose of OXi4503 led to a decrease in PA signal intensity of 60%, 52%, and 20% in SW1222 tumors and 30%, 26%, and 4% for LS174T tumors.
   Conclusions: We have shown for the first time that PAI can observe the pharmacodynamic response of tumor vasculature to drug treatment both longitudinally and at different dose levels. Assessment of differing response to treatment based on vascular pathophysiologic differences among patients has the potential to provide personalized drug therapy; we have demonstrated that PAI, which is clinically translatable, could be a powerful tool for this purpose.
C1 [Johnson, S. Peter; Pedley, R. Barbara] UCL, UCL Canc Inst, London, England.
   [Ogunlade, Olumide; Beard, Paul] UCL, UCL Dept Med Phys & Biomed Engn, London, England.
   [Lythgoe, Mark F.] UCL, UCL Ctr Adv Biomed Imaging, Div Med, London, England.
C3 University of London; University College London; University of London;
   University College London; University of London; University College
   London
RP Johnson, SP (corresponding author), UCL, London WC1E 6DD, England.
EM peter.johnson@crick.ac.uk
OI Ogunlade, Olumide/0000-0003-0123-4397
FU King's College London; University College London Comprehensive Cancer
   Imaging Centre; Cancer Research UK; Engineering and Physical Sciences
   Research Council (EPSRC); Medical Research Council, UK [C1519/A10331];
   Department of Health, UK [C1519/A10331]; ERC [741149]; MRC [G1001497]
   Funding Source: UKRI; European Research Council (ERC) [741149] Funding
   Source: European Research Council (ERC)
FX The VDA OXi4503 (combretastatin A1-diphosphate/CA1P), currently in
   clinical trial for cancer treatment (NCT02576301), was a kind gift from
   Dr. David Chaplin (Mateon Therapeutics). This work was also supported by
   King's College London and University College London Comprehensive Cancer
   Imaging Centre, Cancer Research UK, and the Engineering and Physical
   Sciences Research Council (EPSRC), in association with the Medical
   Research Council and Department of Health, UK(C1519/A10331), and ERC
   Advanced Grant Ref: 741149.
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NR 53
TC 29
Z9 31
U1 0
U2 21
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 15
PY 2019
VL 25
IS 24
BP 7436
EP 7447
DI 10.1158/1078-0432.CCR-19-0360
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KG5JC
UT WOS:000509983400021
PM 31551349
OA Bronze, Green Submitted, Green Accepted
DA 2025-01-04
ER

PT J
AU Abumustafa, W
   Zamer, BA
   Khalil, BA
   Hamad, M
   Maghazachi, AA
   Muhammad, JS
AF Abumustafa, Wafaa
   Zamer, Batoul Abi
   Khalil, Bariaa A.
   Hamad, Mawieh
   Maghazachi, Azzam A.
   Muhammad, Jibran Sualeh
TI Protein arginine N-methyltransferase 5 in colorectal carcinoma: Insights
   into mechanisms of pathogenesis and therapeutic strategies
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE PRMT5; Colorectal cancer; Epigenetics; Histone modification;
   Theranostics
ID KAPPA-B; CANCER RISK; CELL-GROWTH; HEPATOCELLULAR-CARCINOMA;
   UP-REGULATION; IN-VITRO; PRMT5; EXPRESSION; TRAIL; METHYLATION
AB Protein arginine N-methyltransferase 5 (PRMT5) enzyme is one of the eight canonical PRMTs, classified as a type II PRMT, induces arginine monomethylation and symmetric dimethylation. PRMT5 is known to be overexpressed in multiple cancer types, including colorectal cancer (CRC), where its overexpression is associated with poor survival. Recent studies have shown that upregulation of PRMT5 induces tumor growth and metastasis in CRC. Moreover, various novel PRMT5 inhibitors tested on CRC cell lines showed promising anticancer effects. Also, it was suggested that PRMT5 could be a valid biomarker for CRC diagnosis and prognosis. Hence, a deeper understanding of PRMT5-mediated CRC carcinogenesis could provide new avenues towards developing a targeted therapy. In this study, we started with in silico analysis correlating PRMT5 expression in CRC patients as a prelude to further our investigation of its role in CRC. We then carried out a comprehensive review of the scientific literature that dealt with the role(s) of PRMT5 in CRC pathogenesis, diagnosis, and prognosis. Also, we have summarized key findings from in vitro research using various therapeutic agents and strategies directly targeting PRMT5 or disrupting its function. In conclusion, PRMT5 seems to play a significant role in the pathogenesis of CRC; therefore, its prognostic and therapeutic potential merits further investigation.
C1 [Abumustafa, Wafaa; Zamer, Batoul Abi; Muhammad, Jibran Sualeh] Univ Sharjah, Coll Med, Dept Basic Med Sci, Sharjah 27272, U Arab Emirates.
   [Abumustafa, Wafaa; Zamer, Batoul Abi; Khalil, Bariaa A.; Hamad, Mawieh; Maghazachi, Azzam A.; Muhammad, Jibran Sualeh] Univ Sharjah, Res Inst Med & Hlth Sci, Sharjah, U Arab Emirates.
   [Hamad, Mawieh] Univ Sharjah, Coll Hlth Sci, Dept Med Lab Sci, Sharjah, U Arab Emirates.
   [Maghazachi, Azzam A.] Univ Sharjah, Coll Med, Dept Clin Sci, Sharjah, U Arab Emirates.
C3 University of Sharjah; University of Sharjah; University of Sharjah;
   University of Sharjah
RP Muhammad, JS (corresponding author), Univ Sharjah, Coll Med, Dept Basic Med Sci, Sharjah 27272, U Arab Emirates.
EM dr.jibran@live.com
OI Maghazachi, Azzam/0000-0002-3310-678X; Muhammad, Jibran
   Sualeh/0000-0002-9565-1062
FU Al-Jalila Foundation, Dubai, UAE [AJF2018036]; Research Institute of
   Medical and Health Sciences, University of Sharjah (UOS) [1901090159];
   Terry Fox Foundation; Sharjah Research Academy; University of Sharjah
FX J.S.M is funded by "Al-Jalila Foundation, Dubai, UAE", grant number
   AJF2018036", "Research Institute of Medical and Health Sciences,
   Uni-versity of Sharjah (UOS) , grant number 1901090159". A.A.M. is
   sup-ported by grants from Terry Fox Foundation and from Sharjah Research
   Academy. MH is supported by research grants from the University of
   Sharjah and Sharjah Research Academy. The funders had no role in the
   study's design, in the collection, analyses, or interpretation of data,
   in the writing of the manuscript, or in the decision to publish the
   results.
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NR 134
TC 12
Z9 12
U1 5
U2 27
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 2022
VL 145
AR 112368
DI 10.1016/j.biopha.2021.112368
EA NOV 2021
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA XG8GF
UT WOS:000724985500001
PM 34794114
OA gold
DA 2025-01-04
ER

PT J
AU Chou, YT
   Jiang, JK
   Yang, MH
   Lu, JW
   Lin, HK
   Wang, HD
   Yuh, CH
AF Chou, Yu-Ting
   Jiang, Jeng-Kai
   Yang, Muh-Hwa
   Lu, Jeng-Wei
   Lin, Hua-Kuo
   Wang, Horng-Dar
   Yuh, Chiou-Hwa
TI Identification of a noncanonical function for ribose-5-phosphate
   isomerase A promotes colorectal cancer formation by stabilizing and
   activating β-catenin via a novel C-terminal domain
SO PLOS BIOLOGY
LA English
DT Article
ID ADENOMATOUS POLYPOSIS-COLI; PENTOSE-PHOSPHATE PATHWAY; TUMOR-SUPPRESSOR;
   HEPATOCELLULAR-CARCINOMA; APC MUTATIONS; ZEBRAFISH; EXPRESSION; CELLS;
   PHOSPHORYLATION; COMPLEX
AB Altered metabolism is one of the hallmarks of cancers. Deregulation of ribose-5-phosphate isomerase A (RPIA) in the pentose phosphate pathway (PPP) is known to promote tumorigenesis in liver, lung, and breast tissues. Yet, the molecular mechanism of RPIA-mediated colorectal cancer (CRC) is unknown. Our study demonstrates a noncanonical function of RPIA in CRC. Data from the mRNAs of 80 patients' CRC tissues and paired nontumor tissues and protein levels, as well as a CRC tissue array, indicate RPIA is significantly elevated in CRC. RPIA modulates cell proliferation and oncogenicity via activation of beta-catenin in colon cancer cell lines. Unlike its role in PPP in which RPIA functions within the cytosol, RPIA enters the nucleus to form a complex with the adenomatous polyposis coli (APC) and beta-catenin. This association protects beta-catenin by preventing its phosphorylation, ubiquitination, and subsequent degradation. The C-terminus of RPIA (amino acids 290 to 311), a region distinct from its enzymatic domain, is necessary for RPIA-mediated tumorigenesis. Consistent with results in vitro, RPIA increases the expression of beta-catenin and its target genes, and induces tumorigenesis in gut-specific promotor-carrying RPIA transgenic zebrafish. Together, we demonstrate a novel function of RPIA in CRC formation in which RPIA enters the nucleus and stabilizes beta-catenin activity and suggests that RPIA might be a biomarker for targeted therapy and prognosis.
C1 [Chou, Yu-Ting; Lu, Jeng-Wei; Lin, Hua-Kuo; Yuh, Chiou-Hwa] Natl Hlth Res Inst, Inst Mol & Genom Med, Miaoli, Taiwan.
   [Chou, Yu-Ting; Wang, Horng-Dar] Natl Tsing Hua Univ, Inst Biotechnol, Hsinchu, Taiwan.
   [Jiang, Jeng-Kai] Taipei Vet Gen Hosp, Dept Surg, Div Colon & Rectal Surg, Taipei, Taiwan.
   [Yang, Muh-Hwa] Natl Yang Ming Univ, Inst Clin Med, Taipei, Taiwan.
   [Lu, Jeng-Wei] Natl Cent Univ, Dept Life Sci, Taoyuan, Taiwan.
   [Yuh, Chiou-Hwa] Natl Tsing Hua Univ, Inst Bioinformat & Struct Biol, Hsinchu, Taiwan.
   [Yuh, Chiou-Hwa] Natl Chiao Tung Univ, Dept Biol Sci & Technol, Hsinchu, Taiwan.
C3 National Health Research Institutes - Taiwan; National Tsing Hua
   University; Taipei Veterans General Hospital; National Yang Ming Chiao
   Tung University; National Central University; National Tsing Hua
   University; National Yang Ming Chiao Tung University
RP Yuh, CH (corresponding author), Natl Hlth Res Inst, Inst Mol & Genom Med, Miaoli, Taiwan.; Wang, HD (corresponding author), Natl Tsing Hua Univ, Inst Biotechnol, Hsinchu, Taiwan.; Yuh, CH (corresponding author), Natl Tsing Hua Univ, Inst Bioinformat & Struct Biol, Hsinchu, Taiwan.; Yuh, CH (corresponding author), Natl Chiao Tung Univ, Dept Biol Sci & Technol, Hsinchu, Taiwan.
EM hdwang@life.nthu.edu.tw; chyuh@nhri.org.tw
RI Chou, Yu-Ting/IYT-3589-2023; Yuh, Chiou-Hwa/AAL-3531-2020; Wang,
   Hong-Gang/A-3018-2015
OI Wang, Horng-Dar/0000-0001-9570-3611; Chou, Yu-Ting/0000-0001-8524-4220;
   Yuh, Chiou-Hwa/0000-0002-2356-1551; Lu, Jeng-Wei/0000-0003-2128-2046
FU Ministry of Health and Welfare, Taiwan (Advance Medical Plan)
   [106-0324-01-10-07]; Ministry of Science and Technology, Taiwan
   [105-2319-B-400-001]; National Health Research Institutes, Taiwan
   [MG-105-PP-06]; Ministry of Science and Technology, ROC
   [105-2314-B-400-031-MY2, 102-2311-B-007-008-MY3]; Veterans General
   Hospitals University System of Taiwan [VGHUST 104-G6-1-1]
FX The Ministry of Health and Welfare, Taiwan (Advance Medical Plan)
   http://www.mohw.gov.tw/mp-2.html (grant number 106-0324-01-10-07)
   received by CHY. The funder had no role in study design, data collection
   and analysis, decision to publish, or preparation of the manuscript.
   Ministry of Science and Technology, Taiwan
   https://www.most.gov.tw/en/public (grant number 105-2319-B-400-001)
   received by CHY. The funder had no role in study design, data collection
   and analysis, decision to publish, or preparation of the manuscript.
   National Health Research Institutes, Taiwan
   http://english.nhri.org.tw/NHRI_WEB/nhriw001Action.do (grant number
   MG-105-PP-06) received by CHY. The funder had no role in study design,
   data collection and analysis, decision to publish, or preparation of the
   manuscript. Ministry of Science and Technology, ROC
   https://www.most.gov.tw/en/public (grant number 105-2314-B-400-031-MY2)
   received by CHY. The funder had no role in study design, data collection
   and analysis, decision to publish, or preparation of the manuscript.
   Ministry of Science and Technology, ROC
   littps://www.most.gov:.tw/en/public (grant number
   102-2311-B-007-008-MY3) received by HDW. The funder had no role in study
   design, data collection and analysis, decision to publish, or
   preparation of the manuscript. Veterans General Hospitals University
   System of Taiwan http://ust.edu.tw/new/english/f01_1.htm (grant number
   VGHUST 104-G6-1-1) received by HDW. The funder had no role in study
   design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
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NR 50
TC 28
Z9 28
U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1545-7885
J9 PLOS BIOL
JI PLoS. Biol.
PD JAN
PY 2018
VL 16
IS 1
AR e2003714
DI 10.1371/journal.pbio.2003714
PG 23
WC Biochemistry & Molecular Biology; Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA FU4NR
UT WOS:000423830300011
PM 29337987
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Kobayashi, Y
   Shida, D
   Boku, N
   Yasui, K
   Nakamura, Y
   Kudose, Y
   Imaizumi, J
   Kanemitsu, Y
AF Kobayashi, Yasunobu
   Shida, Dai
   Boku, Narikazu
   Yasui, Kohei
   Nakamura, Yuya
   Kudose, Yozo
   Imaizumi, Jun
   Kanemitsu, Yukihide
TI Prognostic Factors of Bone Metastases From Colorectal Cancer in the Era
   of Targeted Therapy
SO DISEASES OF THE COLON & RECTUM
LA English
DT Article
DE Bone metastases; Colorectal cancer; Prognostic factors
ID SCORING SYSTEM; SURVIVAL; PREDICTION; RESECTION; RISK
AB BACKGROUND: Various prognostic factors have been reported for bone metastases from different primary tumor sites. However, bone metastases from colorectal cancer are very rare, and the prognostic factors have not been investigated in detail.OBJECTIVE: This study aimed to identify prognostic factors of bone metastases from colorectal cancer.DESIGN: This is a retrospective cohort study using data from a prospectively collected database.SETTINGS: This study was conducted at a single tertiary care cancer center in Japan.PATIENTS: Patients who developed bone metastases from colorectal cancer during the study period among all patients who received initial treatment for colorectal cancer at our hospital between 2005 and 2016 (n = 4538) were included.MAIN OUTCOME MEASURES: Overall survival after diagnosis of bone metastases from colorectal cancer was the main outcome measure.RESULTS: Ninety-four patients developed bone metastases during the study period. The 5-year overall survival rate was 11.0%. Multivariable analysis identified the following independent risk factors associated with poor prognosis: & GE;70 years of age at diagnosis of bone metastases (HR, 2.48; 95% CI, 1.24-4.95; p < 0.01), curative surgery not performed as initial treatment (HR, 2.54; 95% CI, 1.24-5.19; p = 0.01), multiple bone metastases (HR, 2.44; 95% CI, 1.30-4.57; p < 0.01), albumin level < 3.7 g/dL (HR, 3.80; 95% CI, 1.95-7.39; p < 0.01), CEA & GE;30 ng/mL (HR, 1.94; 95% CI, 1.09-3.46; p = 0.02), and less than 3 chemotherapy options remaining at diagnosis of bone metastases (HR, 2.83; 95% CI, 1.51-5.30; p < 0.01). The median survival times for patients with 0-2, 3, and 4-6 risk factors were 25.0, 8.8, and 4.3 months, respectively.LIMITATIONS: The main limitation is the single-center, retrospective design of this study.CONCLUSIONS: Our results may facilitate multidisciplinary decision-making in patients with bone metastases from colorectal cancer.
C1 [Kobayashi, Yasunobu; Shida, Dai; Yasui, Kohei; Nakamura, Yuya; Kudose, Yozo; Imaizumi, Jun; Kanemitsu, Yukihide] Natl Canc Ctr, Dept Colorectal Surg, Chuo Ku, Tokyo, Japan.
   [Shida, Dai] Univ Tokyo, Inst Med Sci, Div Frontier Surg, Minato Ku, Tokyo, Japan.
   [Boku, Narikazu] Natl Canc Ctr, Dept Gastrointestinal Med Oncol, Chuo Ku, Tokyo, Japan.
   [Shida, Dai] Univ Tokyo, Inst Med Sci, Div Frontier Surg, 4-6-1 Shirokanedai,Minato Ku, Tokyo 1088639, Japan.
C3 National Cancer Center - Japan; University of Tokyo; National Cancer
   Center - Japan; University of Tokyo
RP Shida, D (corresponding author), Univ Tokyo, Inst Med Sci, Div Frontier Surg, 4-6-1 Shirokanedai,Minato Ku, Tokyo 1088639, Japan.
RI Nakamura, Yuya/GLR-3870-2022
OI Nakamura, Yuya/0000-0003-4516-0561
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NR 32
TC 2
Z9 2
U1 0
U2 2
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 MAR
PY 2023
VL 66
IS 3
BP 401
EP 409
DI 10.1097/DCR.0000000000002270
PG 9
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA I0IY2
UT WOS:000999709500020
PM 35239524
DA 2025-01-04
ER

PT J
AU Zheng, G
   Tseng, LH
   Haley, L
   Ibrahim, J
   Bynum, J
   Xian, R
   Gocke, CD
   Eshleman, JR
   Lin, MT
AF Zheng, Gang
   Tseng, Li-Hui
   Haley, Lisa
   Ibrahim, Junaid
   Bynum, Jennifer
   Xian, Rena
   Gocke, Christopher D.
   Eshleman, James R.
   Lin, Ming-Tseh
TI Clinical validation of coexisting driver mutations in colorectal cancers
SO HUMAN PATHOLOGY
LA English
DT Article
DE Coexisting mutation; BRAF; KRAS; NRAS; PIK3CA; Colorectal cancer
ID BRAF MUTATION; ONCOGENIC MUTATIONS; AMERICAN SOCIETY; LUNG-CANCER; KRAS;
   METASTASES; CARCINOMA; BIOMARKERS; CETUXIMAB; GENE
AB Mutational profiling is recommended for selecting targeted therapy and predicting prognosis of metastatic colorectal cancer (CRC). Detection of coexisting mutations within the same pathway, which are usually mutually exclusive, raises the concern for potential laboratory errors. In this retrospective study for quality assessment of a next-generation sequencing assay, we examined BRAF, KRAS, and NRAS genes within the mitogen-activated protein kinase (MAPK) pathway and the PIK3CA gene within the phosphatidylinositol 3-kinase (mTOR) pathway in 744 CRC specimens submitted to our clinical diagnostics laboratory. Although coexistence of mutations between the MAPK and mTOR pathways was observed, it rarely occurred within the MAPK pathway. Retrospective quality assessments identified false detection of coexisting activating KRAS and NRAS mutations in 1 specimen and confirmed 2 activating KRAS mutations in 2 specimens and coexisting activating KRAS and NRAS mutations in 2 specimens, but no coexisting activating RAS and BRAF mutations. There were 15 CRCs with a kinase-impaired BRAF mutation, including 3 with a coexisting activating KRAS mutation, which may have therapeutic implications. Multiregional analysis based on different histologic features demonstrated that coexisting KRAS and NRAS mutations may be present in the same or different tumor populations and showed that invasion of adenomas by synchronous adenocarcinomas of different clonal origin may result in detection of coexisting mutations within the MAPK pathway. In this study, we proposed an operating procedure for clinical validation of unexpected coexisting mutations. Further studies are warranted to elucidate the biological significance and clinical implications of coexisting mutations within the MAPK pathway. (C) 2018 Elsevier Inc. All rights reserved.
C1 [Zheng, Gang; Tseng, Li-Hui; Haley, Lisa; Ibrahim, Junaid; Bynum, Jennifer; Xian, Rena; Gocke, Christopher D.; Eshleman, James R.; Lin, Ming-Tseh] Johns Hopkins Univ, Sch Med, Dept Pathol, 1812 Ashland Ave,Suite 200, Baltimore, MD 21205 USA.
   [Tseng, Li-Hui] Natl Taiwan Univ Hosp, Dept Med Genet, Taipei 100, Taiwan.
   [Xian, Rena; Gocke, Christopher D.; Eshleman, James R.] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
C3 Johns Hopkins University; National Taiwan University; National Taiwan
   University Hospital; Johns Hopkins University
RP Zheng, G (corresponding author), Johns Hopkins Univ, Sch Med, Dept Pathol, 1812 Ashland Ave,Suite 200, Baltimore, MD 21205 USA.
EM gzheng5@jhmi.edu
RI zheng, gang/KMX-5568-2024
OI Zheng, Gang/0000-0003-0276-9430
FU National Institutes of Health-National Cancer Institute of the United
   States [1UM1CA186691-01]
FX This retrospective analysis for quality improvement was supported by
   1UM1CA186691-01 from the National Institutes of Health-National Cancer
   Institute of the United States.
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NR 38
TC 13
Z9 13
U1 1
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0046-8177
EI 1532-8392
J9 HUM PATHOL
JI Hum. Pathol.
PD APR
PY 2019
VL 86
BP 12
EP 20
DI 10.1016/j.humpath.2018.11.014
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA HV8VA
UT WOS:000466261000002
PM 30481508
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Patras, L
   Sylvester, B
   Luput, L
   Sesarman, A
   Licarete, E
   Porfire, A
   Muntean, D
   Drotar, DM
   Rusu, AD
   Nagy, AL
   Catoi, C
   Tomuta, I
   Vlase, L
   Banciu, M
   Achim, M
AF Patras, Laura
   Sylvester, Bianca
   Luput, Lavinia
   Sesarman, Alina
   Licarete, Emilia
   Porfire, Alina
   Muntean, Dana
   Drotar, Denise Minerva
   Rusu, Alexandra Doina
   Nagy, Andras-Laszlo
   Catoi, Cornel
   Tomuta, Ioan
   Vlase, Laurian
   Banciu, Manuela
   Achim, Marcela
TI Liposomal prednisolone phosphate potentiates the antitumor activity of
   liposomal 5-fluorouracil in C26 murine colon carcinoma <i>in vivo</i>
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE Colon carcinoma; combination therapy; liposomes; prednisolone;
   5-fluorouracil; angiogenesis; inflammation
ID TUMOR-ASSOCIATED MACROPHAGES; ENDOTHELIAL GROWTH-FACTOR; OXIDATIVE
   STRESS; COLORECTAL-CANCER; KAPPA-B; EXPRESSION; SIMVASTATIN; ACTIVATION;
   MECHANISMS; STAGE
AB The antitumor efficacy of 5-fluorouracil (5-FU) in advanced colorectal cancer (CRC) is hindered not only by the low therapeutic index, but also by tumor cell resistance to this cytotoxic drug. Therefore, to enhance the 5-FU antitumor activity, the present research used a novel tumor-targeted therapy based on the co-administration of 5-FU encapsulated in long-circulating liposomes (LCL-5-FU) together with liposomal prednisolone phosphate (LCL-PLP), a formulation with known anti-angiogenic actions on C26 murine colon carcinoma cells. Thus, we assessed the in vivo effects of the combined liposomal drug therapy on C26 carcinoma growth as well as on the production of molecular markers with key roles in tumor development such as angiogenic, inflammatory, and oxidative stress molecules. To get further insight into the polarization state of tumor microenvironment after the treatment, we determined the IL-10/IL-12p70 ratio in tumors. Our results showed that combined liposomal drug therapy inhibited almost totally tumor growth and was superior as antitumor activity to both single liposomal drug therapies tested. The antitumor efficacy of the combined therapy was mainly related to the anti-angiogenic and anti-inflammatory actions on C26 carcinoma milieu, being favored by its controlling effect on intratumor oxidative stress and the skewing of polarization of tumor microenvironmental cells toward their antineoplastic phenotypes. Thus, our study unveils a promising treatment strategy for CRC that should be furthermore considered.
C1 [Patras, Laura; Luput, Lavinia; Sesarman, Alina; Licarete, Emilia; Drotar, Denise Minerva; Rusu, Alexandra Doina; Banciu, Manuela] Babes Bolyai Univ, Fac Biol & Geol, Dept Mol Biol & Biotechnol, Cluj Napoca, Romania.
   [Patras, Laura; Luput, Lavinia; Sesarman, Alina; Licarete, Emilia; Drotar, Denise Minerva; Rusu, Alexandra Doina; Banciu, Manuela] Babes Bolyai Univ, Inst Interdisciplinary Res Bionanosci, Mol Biol Ctr, Cluj Napoca, Romania.
   [Sylvester, Bianca; Porfire, Alina; Muntean, Dana; Tomuta, Ioan; Vlase, Laurian; Achim, Marcela] Iuliu Hatieganu Univ Med & Pharm, Fac Pharm, Dept Pharmaceut Technol & Biopharmaceut, Cluj Napoca, Romania.
   [Nagy, Andras-Laszlo; Catoi, Cornel] Univ Agr Sci & Vet Med, Dept Vet Toxicol, Cluj Napoca, Romania.
C3 Babes Bolyai University from Cluj; Babes Bolyai University from Cluj;
   Iuliu Hatieganu University of Medicine & Pharmacy; University of
   Agricultural Sciences & Veterinary Medicine Cluj Napoca
RP Banciu, M (corresponding author), Fac Biol & Geol, Dept Mol Biol & Biotechnol, 5-7 Clinicilor St, Cluj Napoca 400006, Romania.
EM manuela.banciu@ubbcluj.ro
RI LUPUT, LAVINIA/C-4464-2017; Sesarman, Alina/F-6841-2011; Cornel,
   Catoi/KLC-4257-2024; Banciu, Manuela/D-6425-2011; Andras,
   Nagy/AAH-8789-2019; Muntean, Dana/C-4220-2011; Vlase,
   Laurian/B-6311-2011; TOMUTA, Ioan/B-8433-2011; Porfire,
   Alina/IWD-5346-2023; Patras, Laura/C-4477-2017; Licarete,
   Emilia/O-7030-2014
OI Muntean, Dana/0000-0002-3914-0110; Banciu, Manuela/0000-0003-2556-4008;
   Vlase, Laurian/0000-0002-0664-3387; Boitor,
   Alexandra/0000-0001-6362-015X; TOMUTA, Ioan/0000-0002-5094-008X;
   Porfire, Alina/0000-0001-8475-2792; Patras, Laura/0000-0002-6981-3881;
   Nagy, Andras-Laszlo/0000-0002-9596-2899; Sesarman,
   Alina/0000-0002-7491-9955; Licarete, Emilia/0000-0003-1190-6003
FU UEFISCDI (Romanian Ministry of Education, Research and Innovation)
   [PN-II-PTPCCA-2011-3-2-1060, 95/2012, PN-II-RU-TE-2014-4-1191,
   235/01.10.2015]
FX This work was supported by the UEFISCDI (Romanian Ministry of Education,
   Research and Innovation) under Grant PN-II-PTPCCA-2011-3-2-1060 (No.
   95/2012) and Grant PN-II-RU-TE-2014-4-1191 (No. 235/01.10.2015).
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NR 58
TC 10
Z9 11
U1 2
U2 12
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.
PY 2017
VL 18
IS 8
BP 616
EP 626
DI 10.1080/15384047.2017.1345392
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FN4MB
UT WOS:000415978600009
PM 28696813
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Alhazzani, K
   Venkatesan, T
   Natarajan, U
   Algahtani, M
   Alaseem, A
   Alobid, S
   Rathinavelu, A
AF Alhazzani, Khalid
   Venkatesan, Thiagarajan
   Natarajan, Umamaheswari
   Algahtani, Mohammad
   Alaseem, Ali
   Alobid, Saad
   Rathinavelu, Appu
TI Evaluation of antitumor effects of VEGFR-2 inhibitor F16 in a colorectal
   xenograft model
SO BIOTECHNOLOGY LETTERS
LA English
DT Article
DE F16; VEGF; VEGFR-2; Angiogenesis; Apoptosis; Colorectal cancer; HUVEC
   cells; Xenograft
ID ENDOTHELIAL-GROWTH-FACTOR; TUMOR-NECROSIS-FACTOR; INTERFERON-ALPHA;
   TNF-ALPHA; IN-VIVO; ANGIOGENESIS; EXPRESSION; CANCER; HYPOXIA;
   HIF-1-ALPHA
AB Objectives Colorectal cancer (CRC) is the third most prevalent type of cancer in the United States. The treatment options for cancer include surgery, chemotherapy, radiation, and/or targeted therapy, which show significant improvement in overall survival. Among the various available treatments, antagonizing VEGF/VEGFR-2 pathways have shown effectiveness in limiting colorectal cancer growth and improving clinical outcomes. In this regard, we hypothesized that F16, a novel VEGFR-2 inhibitor, would control colorectal cancer growth by blocking the VEGFR-2 singling pathway in both in vitro and in vivo conditions. Therefore, the current study was aimed to analyze the efficacy of F16 on the growth of Colo 320DM cells under in vitro and in vivo conditions. Results Human RT2 profiler PCR array analysis results clearly showed that angiogenesis and anti-apoptosis-related gene expressions were significantly reduced in HUVEC cells after F16 (5 mu M) treatment. In addition, Western blot results revealed that F16 attenuated the downstream signaling of the VEGFR-2 pathway in HUVEC cells by up-regulating the p53 and p21 levels and down-regulating the p-AKT and p-FAK levels. Accordingly, F16 confirmed potent cytotoxic effects against the cell viability of Colo 320DM tumors, with an IC50 value of 9.52 +/- 1.49 mu M. Furthermore, treatment of mice implanted with Colo 320DM xenograft tumors showed a significant reduction in tumor growth and increases in survival rate compared to controls. Immunohistochemistry analysis of tumor tissues showed a reduction in CD31 levels also in F16 treated groups. Conclusions These results justify further evaluation of F16 as a potential new therapeutic agent for treating colorectal cancers.
C1 [Alhazzani, Khalid; Algahtani, Mohammad; Alobid, Saad] King Saud Univ, Coll Pharm, Pharmacol & Toxicol Dept, Riyadh 12371, Saudi Arabia.
   [Venkatesan, Thiagarajan; Natarajan, Umamaheswari; Rathinavelu, Appu] Nova Southeastern Univ, Rumbaugh Goodwin Inst Canc Res, 3321 Coll Ave, Ft Lauderdale, FL 33314 USA.
   [Alaseem, Ali] Al Imam Mohammad Ibn Saud Islamic Univ, Coll Med, Riyadh 13317, Saudi Arabia.
   [Rathinavelu, Appu] Nova Southeastern Univ, Coll Pharm, Ft Lauderdale, FL 33314 USA.
C3 King Saud University; Nova Southeastern University; Imam Mohammad Ibn
   Saud Islamic University (IMSIU); Nova Southeastern University
RP Rathinavelu, A (corresponding author), Nova Southeastern Univ, Rumbaugh Goodwin Inst Canc Res, 3321 Coll Ave, Ft Lauderdale, FL 33314 USA.
EM appu@nova.edu
RI Alaseem, Ali/HJA-5083-2022; Algahtani, Mohammad/ABD-2520-2020;
   Alhazzani, Khalid/ABD-2607-2020; Alobid, Saad/JZE-2700-2024
OI , Umamaheswari/0000-0001-8791-5032; Alhazzani,
   Khalid/0000-0002-1890-1291; Alobid, Saad/0000-0002-0157-9240; Algahtani,
   Mohammad/0000-0002-0398-6712
FU Royal Dames of Cancer Research Inc., Ft. Lauderdale, Florida
FX The funding for this project was provided by the Royal Dames of Cancer
   Research Inc., Ft. Lauderdale, Florida.
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NR 44
TC 3
Z9 3
U1 1
U2 3
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 2022
VL 44
IS 5-6
BP 787
EP 801
DI 10.1007/s10529-022-03243-0
EA APR 2022
PG 15
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA 1N3RU
UT WOS:000789708900001
PM 35501620
DA 2025-01-04
ER

PT J
AU Murakami, T
   Kiyuna, T
   Kawaguchi, K
   Igarashi, K
   Singh, AS
   Hiroshima, Y
   Zhang, Y
   Zhao, M
   Miyake, K
   Nelson, SD
   Dry, SM
   Li, YF
   DeLong, JC
   Lwin, TM
   Chishima, T
   Tanaka, K
   Bouvet, M
   Endo, I
   Eilber, FC
   Hoffman, RM
AF Murakami, Takashi
   Kiyuna, Tasuku
   Kawaguchi, Kei
   Igarashi, Kentaro
   Singh, Arun S.
   Hiroshima, Yukihiko
   Zhang, Yong
   Zhao, Ming
   Miyake, Kentaro
   Nelson, Scott D.
   Dry, Sarah M.
   Li, Yunfeng
   DeLong, Jonathan C.
   Lwin, Thinzar M.
   Chishima, Takashi
   Tanaka, Kuniya
   Bouvet, Michael
   Endo, Itaru
   Eilber, Fritz C.
   Hoffman, Robert M.
TI The irony of highly-effective bacterial therapy of a patient-derived
   orthotopic xenograft (PDOX) model of Ewing's sarcoma, which was blocked
   by Ewing himself 80years ago
SO CELL CYCLE
LA English
DT Article
DE bacterial therapy of cancer; Ewing's sarcoma; patient-derived orthotopic
   xenograft; PDOX; Salmonella typhimurium A1-R
ID SALMONELLA-TYPHIMURIUM A1-R; NUDE-MOUSE MODEL; HUMAN PANCREATIC-CANCER;
   SOFT-TISSUE SARCOMA; HUMAN OVARIAN-CANCER; HUMAN COLON-CANCER; ANTI-CEA
   ANTIBODY; BREAST-CANCER; TARGETED THERAPY; LUNG METASTASIS
AB William B. Coley developed bacterial therapy of cancer more than 100years ago and had clinical success. James Ewing, a very famous cancer pathologist for whom the Ewing sarcoma is named, was Coley's boss at Memorial Hospital in New York and terminated Coley's bacterial therapy of cancer. A tumor from a patient with soft-tissue Ewing's sarcoma, who failed doxorubicin (DOX) therapy, was previously implanted in nude mice to establish a patient-derived orthotopic xenograft (PDOX) model. In the present study, the Ewing's sarcoma PDOX was treated with tumor-targeting S. typhimurium A1-R expressing green fluorescent (GFP), alone and in combination with DOX. S. typhimurium A1-R-GFP was detected in the tumors after intratumor (i.t.) or intravenous (i.v.) injection. The combination of S. typhimurium A1-R and DOX significantly reduced tumor weight (37.8 +/- 15.6 mg) compared to the untreated control (73.8 +/- 10.1mg, P < 0.01). S. typhimurium A1-R monotherapy-treated tumors tended to be smaller (50.9 +/- 17.8mg, P = 0.051). DOX monotherapy did not show efficacy (66.3 +/- 26.4mg, P = 0.82), as was the case with the patient. The PDOX model faithfully replicated the DOX resistance the Ewing's sarcoma had in the patient. S. typhimurium A1-R converted the Ewing's sarcoma from DOX resistant to sensitive. One can only wonder how bacterial therapy and immunotherapy of cancer would have developed over the past 80years if Ewing did not stop Coley.
C1 [Murakami, Takashi; Kiyuna, Tasuku; Kawaguchi, Kei; Igarashi, Kentaro; Zhang, Yong; Zhao, Ming; Miyake, Kentaro; Hoffman, Robert M.] AntiCancer Inc, 7917 Ostrow St, San Diego, CA 92111 USA.
   [Murakami, Takashi; Miyake, Kentaro; DeLong, Jonathan C.; Lwin, Thinzar M.; Bouvet, Michael; Hoffman, Robert M.] Univ Calif San Diego, Dept Surg, San Diego, CA 92103 USA.
   [Murakami, Takashi; Hiroshima, Yukihiko; Miyake, Kentaro; Chishima, Takashi; Tanaka, Kuniya; Endo, Itaru] Yokohama City Univ, Grad Sch Med, Dept Surg Gastroenterol, Yokohama, Kanagawa, Japan.
   [Singh, Arun S.] Univ Calif Los Angeles, Div Hematol Oncol, Los Angeles, CA USA.
   [Nelson, Scott D.; Dry, Sarah M.; Li, Yunfeng] Univ Calif Los Angeles, Dept Pathol, Los Angeles, CA 90024 USA.
   [Eilber, Fritz C.] Univ Calif Los Angeles, Div Surg Oncol, Los Angeles, CA USA.
C3 AntiCancer, Inc.; University of California System; University of
   California San Diego; Yokohama City University; University of California
   System; University of California Los Angeles; University of California
   System; University of California Los Angeles; University of California
   System; University of California Los Angeles
RP Hoffman, RM (corresponding author), AntiCancer Inc, 7917 Ostrow St, San Diego, CA 92111 USA.; Eilber, FC (corresponding author), Univ Calif Los Angeles, Div Surg Oncol, Surg, 10833 LeConte Ave,Rm 54-140 CHS, Los Angeles, CA 90095 USA.; Eilber, FC (corresponding author), Univ Calif Los Angeles, Div Surg Oncol, Mol & Med Pharmacol, 10833 LeConte Ave,Rm 54-140 CHS, Los Angeles, CA 90095 USA.
EM fceilber@mednet.ucla.edu; all@anticancer.com
RI Miyake, Kentaro/A-2996-2019; Li, Tengfei/AAI-5043-2020
OI Murakami, Takashi/0000-0002-9429-5705; Igarashi,
   Kentaro/0000-0003-2278-1736
FU National Cancer Institute [CA213649]; JSPS [26830081, 26462070,
   24592009]; Grants-in-Aid for Scientific Research [26830081, 24592009,
   26462070] Funding Source: KAKEN
FX This study was supported by National Cancer Institute grant number
   CA213649 and JSPS KAKENHI grant numbers 26830081 to YH, 26462070 to IE
   and 24592009 to KT.
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U2 5
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1538-4101
EI 1551-4005
J9 CELL CYCLE
JI Cell Cycle
PY 2017
VL 16
IS 11
BP 1046
EP 1052
DI 10.1080/15384101.2017.1304340
PG 7
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA EY4HO
UT WOS:000403938500007
PM 28296559
OA Green Published, Bronze
DA 2025-01-04
ER

PT J
AU Wei, YL
   Li, Y
   Chen, YA
   Liu, P
   Huang, S
   Zhang, YP
   Sun, YL
   Wu, Z
   Hu, MC
   Wu, Q
   Wu, HN
   Liu, FX
   She, TH
   Ning, ZF
AF Wei, Yaolu
   Li, Yan
   Chen, Yenan
   Liu, Pei
   Huang, Sheng
   Zhang, Yuping
   Sun, Yanling
   Wu, Zhe
   Hu, Meichun
   Wu, Qian
   Wu, Hongnian
   Liu, Fuxing
   She, Tonghui
   Ning, Zhifeng
TI ALDH1: A potential therapeutic target for cancer stem cells in solid
   tumors
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE ALDH1; stem cell markers; solid tumors; targeted therapy; cancer
   resistance
ID DEHYDROGENASE 1A1 ALDH1A1; ALDEHYDE DEHYDROGENASE; POOR-PROGNOSIS;
   ESOPHAGEAL CANCER; OVARIAN-CANCER; MARKERS ALDH1; DNA-DAMAGE;
   EXPRESSION; CARCINOMA; METASTASIS
AB Solid tumors can be divided into benign solid tumors and solid malignant tumors in the academic community, among which malignant solid tumors are called cancers. Cancer is the second leading cause of death in the world, and the global incidence of cancer is increasing yearly New cancer patients in China are always the first. After the concept of stem cells was introduced in the tumor community, the CSC markers represented by ALDH1 have been widely studied due to their strong CSC cell characteristics and potential to be the driving force of tumor metastasis. In the research results in the past five years, it has been found that ALDH1 is highly expressed in various solid cancers such as breast cancer, lung cancer, colorectal cancer, liver cancer, gastric cancer, cervical cancer, esophageal cancer, ovarian cancer, head,and neck cancer. ALDH1 can activate and transform various pathways (such as the USP28/MYC signaling pathway, ALDH1A1/HIF-1 alpha/VEGF axis, wnt/beta-catenin signaling pathway), as well as change the intracellular pH value to promote formation and maintenance, resulting in drug resistance in tumors. By targeting and inhibiting ALDH1 in tumor stem cells, it can enhance the sensitivity of drugs and inhibit the proliferation, differentiation, and metastasis of solid tumor stem cells to some extent. This review discusses the relationship and pathway of ALDH1 with various solid tumors. It proposes that ALDH1 may serve as a diagnosis and therapeutic target for CSC, providing new insights and new strategies for reliable tumor treatment.
C1 [Wei, Yaolu; Li, Yan; Zhang, Yuping; Sun, Yanling; Wu, Zhe; Hu, Meichun; Wu, Qian; Wu, Hongnian; Liu, Fuxing; She, Tonghui; Ning, Zhifeng] Hubei Univ Sci & Technol, Xianning Med Coll, Sch Basic Med Sci, Xianning, Peoples R China.
   [Chen, Yenan; Liu, Pei; Huang, Sheng] Hubei Univ Sci & Technol, Xianning Med Coll, Xianning, Peoples R China.
C3 Hubei University of Science & Technology; Hubei University of Science &
   Technology
RP Liu, FX; She, TH; Ning, ZF (corresponding author), Hubei Univ Sci & Technol, Xianning Med Coll, Sch Basic Med Sci, Xianning, Peoples R China.
EM Liufx6505@126.com; xnsth@hbust.edu.cn; ningzhifeng1976@163.com
RI SUN, YANLING/JTT-9082-2023; Yuanlei, Zhang/AGW-9772-2022; Hu,
   Meichun/JAX-1849-2023
OI Hu, Meichun/0009-0007-9752-8977
FU Hubei Department of Education Science Research project [Q20192802];
   National Natural Science Foundation of China Youth Science Foundation
   project [81902937]
FX This study was supported by the following grants: Hubei Department of
   Education Science Research project (grant no. Q20192802) for QW,
   National Natural Science Foundation of China Youth Science Foundation
   project (grant no. 81902937) for YS.
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NR 228
TC 39
Z9 42
U1 2
U2 29
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 28
PY 2022
VL 12
AR 1026278
DI 10.3389/fonc.2022.1026278
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 6F1ML
UT WOS:000883834100001
PM 36387165
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Tao, YF
   Lin, F
   Li, RD
   Shen, J
   Wang, ZX
AF Tao, Yifeng
   Lin, Feng
   Li, Ruidong
   Shen, Jie
   Wang, Zhengxin
TI Prolyl hydroxylase-2 inhibits liver tumor cell proliferation and cyclin
   D1 expression in a hydroxylase-dependent manner
SO INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
LA English
DT Article
DE PHD2; Cyclin D1; Tumor suppressor; Liver cancer; Doxycycline
ID COLORECTAL-CANCER CELLS; HIF-ALPHA; OVER-EXPRESSION; TGF-BETA; KAPPA-B;
   HYPOXIA; GROWTH; PROTEIN; PROLYL-4-HYDROXYLASE; OVEREXPRESSION
AB Prolyl hydroxylase 2 is a key regulator of hypoxia-inducible factor 1 alpha protein, and has previously been implicated as a tumor suppressor in various cancers. However, the function of prolyl hydroxylase 2 in liver cancer has yet to be elucidated. Characterization of prolyl hydroxylase 2 function and related mechanisms in liver cancer may enable the development of targeted therapy. Here we found that prolyl hydroxylase 2 overexpression in human hepatocellular carcinoma cancer cell lines inhibited cell proliferation, while prolyl hydroxylase 2 knockdown enhanced cell proliferation. Further analyses revealed that the prolyl hydroxylase 2-mediated inhibition of cell proliferation was due to a cell cycle arrest at the G1/S transition. Moreover, the block in cell cycle was facilitated by negative regulation of cyclin D1, a process dependent on the hydroxylase activity of prolyl hydroxylase 2. Using an in vivo xenograft mouse model, we found that the overexpression of prolyl hydroxylase 2 led to a reduction in tumor size. Evaluation of paired human liver cancer patient samples revealed that prolyl hydroxylase 2 protein levels were significantly reduced in 6 of the 10 cancer tissues as compared to their respective normal tissue controls. Furthermore, elevated expression of prolyl hydroxylase 2 was associated with significantly prolonged survival in patients with liver cancer. These results suggest that prolyl hydroxylase 2 plays an important tumor suppressive role in liver cancer and may prove to be of prognostic and therapeutic value. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Tao, Yifeng; Li, Ruidong; Wang, Zhengxin] Fudan Univ, Dept Gen Surg, Huashan Hosp, Shanghai 200040, Peoples R China.
   [Lin, Feng; Shen, Jie] Taizhou First Peoples Hosp, Dept Gen Surg, Taizhou 318020, Zhejiang, Peoples R China.
C3 Fudan University
RP Wang, ZX (corresponding author), 12 Middle Wulumuqi Rd, Shanghai 200040, Peoples R China.; Shen, J (corresponding author), 218 Hengjie Rd, Taizhou 318020, Zhejiang, Peoples R China.
EM shenjietzh@126.com; wangzhengxinhsh@163.com
FU National Natural Science Foundation of China [81270551, 81001327]
FX This work was supported by the National Natural Science Foundation of
   China (grant 81001327 and 81270551)
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Z9 10
U1 0
U2 13
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1357-2725
EI 1878-5875
J9 INT J BIOCHEM CELL B
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PY 2016
VL 77
BP 129
EP 140
DI 10.1016/j.biocel.2016.05.022
PN A
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA DT7EL
UT WOS:000381649800016
PM 27307407
DA 2025-01-04
ER

EF