﻿FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Feng, YW
   Ye, ZQ
   Song, FR
   He, YF
   Liu, J
AF Feng, Yawei
   Ye, Zhiqiang
   Song, Furong
   He, Yufeng
   Liu, Jun
TI RETRACTED: The Role of TAMs in Tumor Microenvironment and New Research
   Progress (Retracted Article)
SO STEM CELLS INTERNATIONAL
LA English
DT Article; Retracted Publication
ID BREAST-CANCER; MACROPHAGE DIFFERENTIATION; COLORECTAL-CANCER; SIGNALING
   PATHWAY; CELLS; POLARIZATION; NANOPARTICLES; EXPRESSION; TISSUE;
   ACTIVATION
AB Tumor-associated macrophages (TAMs) are an important part of tumor microenvironment (TME) and play a key role in TME, participating in the process of tumor occurrence, growth, invasion, and metastasis. Among them, metastasis to tumor tissue is the key step of malignant development of tumor. In this paper, the latest progress in the role of TAMs in the formation of tumor microenvironment is summarized. It is particularly noteworthy that cell and animal experiments show that TAMs can provide a favorable microenvironment for the occurrence and development of tumors. At the same time, clinical pathological experiments show that the accumulation of TAMs in tumor is related to poor clinical efficacy. Finally, this paper discusses the feasibility of TAMs-targeted therapy as a new indirect cancer therapy. This paper provides a theoretical basis for finding a potentially effective macrophage-targeted tumor therapy.
C1 [Feng, Yawei; Song, Furong; Liu, Jun] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Anesthesiol, Guangzhou, Guangdong, Peoples R China.
   [Ye, Zhiqiang] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Emergency, Guangzhou, Guangdong, Peoples R China.
   [He, Yufeng] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Intens Care Med, Guangzhou, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University
RP Liu, J (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 3, Dept Anesthesiol, Guangzhou, Guangdong, Peoples R China.
EM fengyaw@mail.sysu.edu.cn; yezhiq@mail.sysu.edu.cn; love001j@126.com;
   heyf29@mail2.sysu.edu.cn; liujun53@mail.sysu.edu.cn
RI Ye, Zhi-Qiang/N-8513-2014
OI Liu, Jun/0000-0001-5297-143X
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NR 112
TC 40
Z9 41
U1 0
U2 13
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-966X
EI 1687-9678
J9 STEM CELLS INT
JI Stem Cells Int.
PD AUG 15
PY 2022
VL 2022
AR 5775696
DI 10.1155/2022/5775696
PG 11
WC Cell & Tissue Engineering
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 4E8GZ
UT WOS:000848059700001
PM 36004381
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Qi, X
   Gao, J
   Li, ZH
   Zhang, GX
   Li, JL
   Fu, YL
   Cai, MJ
   Wang, HD
   Tong, T
AF Qi, Xiao
   Gao, Jing
   Li, Zihao
   Zhang, Guangxin
   Li, Jialin
   Fu, Yilin
   Cai, Mingjun
   Wang, Hongda
   Tong, Ti
TI CDCP1: A promising diagnostic biomarker and therapeutic target for human
   cancer
SO LIFE SCIENCES
LA English
DT Review
DE CUB domain-containing protein 1; Cancers; Tumorigenesis; Metastases;
   Targeted therapy; Biomarker
ID DOMAIN-CONTAINING PROTEIN-1; SURFACE GLYCOPROTEIN CDCP1; CUB-DOMAIN;
   CELL-SURFACE; PKC-DELTA; TYROSINE PHOSPHORYLATION;
   PROGNOSTIC-SIGNIFICANCE; TRASTUZUMAB RESISTANCE; ANTICANCER ANTIBODIES;
   COLORECTAL-CANCER
AB CUB domain-containing protein 1 (CDCP1), as an emerging transmembrane protein, is overexpressed in a variety of malignant tumors including respiratory tumors, digestive system cancers, hematological malignancies and urogenital cancers. Several cancer-related proteins have been reported to interact with CDCP1. It acts as a crucial hub in multiple classical signaling pathways of tumorigenesis and progression. Its overexpression and activation are also associated with prognosis and drug resistance. Due to its important roles in malignant tumors, CDCP1 is expected to be a promising therapeutic target for treatment and a new biomarker for diagnosis. In this article, we review the roles of CDCP1 in diagnosis and management of malignant tumors, and also its regulation in several essential tumor-related pathways.
C1 [Qi, Xiao; Li, Zihao; Zhang, Guangxin; Tong, Ti] Second Hosp Jilin Univ, Dept thorac Surg, Changchun 130041, Jilin, Peoples R China.
   [Gao, Jing; Cai, Mingjun; Wang, Hongda] Chinese Acad Sci, Changchun Inst Appl Chem, Res Ctr Biomembran, State Key Lab Electroanalyt Chem, Changchun 130022, Jilin, Peoples R China.
   [Li, Jialin] Jilin Univ, China Japan Union Hosp, Dept Neurol, Changchun 130012, Jilin, Peoples R China.
   [Fu, Yilin] Shandong First Med Univ, Shandong Prov Hosp, Dept Thorac Surg, Jinan 250021, Shandong, Peoples R China.
   [Wang, Hongda] Univ Sci & Technol China, Hefei 230027, Anhui, Peoples R China.
   [Wang, Hongda] Qing dao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Wenhai Rd,Aoshanwei,Jimo, Qingdao 266237, Shandong, Peoples R China.
C3 Jilin University; Chinese Academy of Sciences; Changchun Institute of
   Applied Chemistry, CAS; Jilin University; Shandong First Medical
   University & Shandong Academy of Medical Sciences; Chinese Academy of
   Sciences; University of Science & Technology of China, CAS; Laoshan
   Laboratory
RP Tong, T (corresponding author), Second Hosp Jilin Univ, Dept thorac Surg, Changchun 130041, Jilin, Peoples R China.
EM qixiao20@mails.jlu.edu.cn; gaojing@ciac.ac.cn; zhl19@mails.jlu.edu.cn;
   guangxinzhang@jlu.edu.cn; fuyl18@mails.jlu.edu.cn;
   caimingjun@ciac.ac.cn; hdwang@ciac.ac.cn; tongti@jlu.edu.cn
RI L., Michael/HNP-8517-2023; qi, xiao/KHU-5513-2024; Li,
   Jialin/IYJ-1259-2023; Cai, Mingjun/JCF-0780-2023
FU Department of Finance of Jilin Province of China [2020SCZT006,
   2019SRCJ023]
FX Acknowledgments This work was supported by Department of Finance of
   Jilin Province of China [Grant number 2020SCZT006, Grant number
   2019SRCJ023] . Figures were created with Bio-Render software,
   ?biorender.com .
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NR 105
TC 6
Z9 6
U1 2
U2 41
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 JUL 15
PY 2022
VL 301
AR 120600
DI 10.1016/j.lfs.2022.120600
EA MAY 2022
PG 12
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 1S1MQ
UT WOS:000803822700003
PM 35504333
DA 2025-01-04
ER

PT J
AU Zhong, JL
   Kang, JL
   Wang, XX
   Jiang, WY
   Liao, H
   Yuan, J
AF Zhong, Jiali
   Kang, Jiali
   Wang, Xiaoxia
   Jiang, Wenyan
   Liao, Hua
   Yuan, Jin
TI TAT-OSBP-1-MKK6(E), a novel TAT-fusion protein with high selectivity for
   human ovarian cancer, exhibits anti-tumor activity
SO MEDICAL ONCOLOGY
LA English
DT Article
DE TAT-OSBP-1-MKK6(E); Ovarian cancer; Apoptosis; Target therapy
ID CELL-PENETRATING PEPTIDES; TARGETED DRUG-DELIVERY; IN-VIVO;
   HEPATOCELLULAR-CARCINOMA; LEUKEMIA-CELLS; COLON-CANCER; KINASE; GENE;
   APOPTOSIS; PATHWAY
AB To improve the selectivity of TAT-fusion proteins for targeted cancer therapy, we developed a novel TAT-based target-specific fusion protein, TAT-OSBP-1-MKK6(E), and evaluated its selectivity and anti-tumor activity in vitro and in vivo. The fusion protein containing TAT-OSBP-1-MKK6(E) has three functional domains: (1) the protein transduction domain of TAT, (2) the human ovarian cancer HO8910 cell-specific binding peptide (OSBP-1) and (3) the potential anti-tumor effector domain of MKK6(E). The transduction efficiency, selectivity, cytotoxicity and apoptotic effect of TAT-OSBP-1-MKK6(E) were examined using immunofluorescence, CCK8 assay and flow cytometry. The in vivo anti-tumor efficacy and target specificity of the fusion protein were evaluated using a nudemouse model with subcutaneous xenografts of human ovarian cancer HO8910 cells. Tumor-bearing mice were divided into three treatment groups that received tail vein injections of TAT-OSBP-1-MKK6(E), TAT-OSBP-1 or normal saline. Tumor growth inhibition was determined by tumor volume, weight and morphology. The distribution and apoptotic effect of TAT-OSBP-1-MKK6(E) were assessed by immunohistochemical staining and TUNEL assays. TAT-OSBP-1-MKK6(E) can be selectively internalized into human ovarian cancer HO8910 cells, rather than normal ovarian OSE cells. In vivo, the fusion protein was mainly expressed in the tumor xenograft, but not in ovary or liver tissues. As a result, TAT-OSBP-1-MKK6(E) significantly induced growth inhibition and apoptosis of tumor cells in vitro and in vivo, with limited effects in normal cells and tissues. TAT-OSBP-1-MKK6(E) treatment can selectively target HO8910 cells in vitro and in vivo, leading to growth inhibition and apoptosis of tumor cells. As such, TAT-OSBP-1-MKK6(E) may be a potential approach for ovarian cancer target therapy.
C1 [Zhong, Jiali; Kang, Jiali; Wang, Xiaoxia; Jiang, Wenyan; Liao, Hua; Yuan, Jin] Guangzhou Med Univ, Guangzhou Peoples Hosp 1, Dept Obstet & Gynecol, Guangzhou 510180, Guangdong, Peoples R China.
C3 Guangzhou Medical University
RP Kang, JL (corresponding author), Guangzhou Med Univ, Guangzhou Peoples Hosp 1, Dept Obstet & Gynecol, Guangzhou 510180, Guangdong, Peoples R China.
EM kangjiali1961@21cn.com
FU Natural Science Foundation of Guangdong Province, China
   [S2012010009341]; Bureau of Science and Technology of Guangzhou
   Municipality, China [11A53150713]
FX This work was supported by Natural Science Foundation of Guangdong
   Province, China (S2012010009341) and Bureau of Science and Technology of
   Guangzhou Municipality, China (11A53150713).
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Z9 9
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 APR
PY 2015
VL 32
IS 4
AR 118
DI 10.1007/s12032-015-0495-0
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CE0DG
UT WOS:000351474100032
PM 25782870
DA 2025-01-04
ER

PT J
AU Al Bitar, S
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   Doughan, S
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AF Al Bitar, Samar
   El-Sabban, Marwan
   Doughan, Samer
   Abou-Kheir, Wassim
TI Molecular mechanisms targeting drug-resistance and metastasis in
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SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Colorectal cancer; Metastatic colorectal cancer; Targeted therapy;
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ID GROWTH-FACTOR RECEPTOR; PHASE-II TRIAL; WILD-TYPE KRAS;
   TRIFLURIDINE/TIPIRACIL PLUS BEVACIZUMAB; POTENTIAL THERAPEUTIC TARGET;
   1ST-LINE TREATMENT; COLON-CANCER; OPEN-LABEL; MULTIDRUG-RESISTANCE;
   THYMIDYLATE SYNTHASE
AB Colorectal cancer (CRC) is the third most diagnosed malignancy and a major leading cause of cancer-related deaths worldwide. Despite advances in therapeutic regimens, the number of patients presenting with metastatic CRC (mCRC) is increasing due to resistance to therapy, conferred by a small population of cancer cells, known as cancer stem cells. Targeted therapies have been highly successful in prolonging the overall survival of patients with mCRC. Agents are being developed to target key molecules involved in drug-resistance and metastasis of CRC, and these include vascular endothelial growth factor, epidermal growth factor receptor, human epidermal growth factor receptor-2, mitogen-activated extracellular signal-regulated kinase, in addition to immune checkpoints. Currently, there are several ongoing clinical trials of newly developed targeted agents, which have shown considerable clinical efficacy and have improved the prognosis of patients who do not benefit from conventional chemotherapy. In this review, we highlight recent developments in the use of existing and novel targeted agents against drug-resistant CRC and mCRC. Furthermore, we discuss limitations and challenges associated with targeted therapy and strategies to combat intrinsic and acquired resistance to these therapies, in addition to the importance of implementing better preclinical models and the application of personalized therapy based on predictive biomarkers for treatment selection.
C1 [Al Bitar, Samar; El-Sabban, Marwan; Abou-Kheir, Wassim] Amer Univ Beirut, Dept Anat, Cell Biol & Physiol Sci, Beirut 11072020, Lebanon.
   [Doughan, Samer] Amer Univ Beirut, Dept Surg, Med Ctr, Beirut 11072020, Lebanon.
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C3 American University of Beirut; 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
RI Abou-Kheir, Wassim/AAP-2587-2020
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NR 239
TC 24
Z9 24
U1 2
U2 12
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAR 7
PY 2023
VL 29
IS 9
BP 1395
EP 1426
DI 10.3748/wjg.v29.i9.1395
PG 32
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA D4PD6
UT WOS:000968558600001
PM 36998426
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Benson, A
   Venook, AP
   Al-Hawary, MM
   Arain, MA
   Chen, YJ
   Ciombor, KK
   Cohen, S
   Cooper, HS
   Deming, D
   Farkas, L
   Garrido-Laguna, I
   Grem, JL
   Gunn, A
   Hecht, JR
   Hoffe, S
   Hubbard, J
   Hunt, S
   Johung, KL
   Kirilcuk, N
   Krishnamurthi, S
   Messersmith, WA
   Meyerhardt, J
   Miller, ED
   Mulcahy, MF
   Nurkin, S
   Overman, MJ
   Parikh, A
   Patel, H
   Pedersen, K
   Saltz, L
   Schneider, C
   Shibata, D
   Skibber, JM
   Sofocleous, CT
   Stoffel, EM
   Stotsky-Himelfarb, E
   Willett, CG
   Gregory, KM
   Gurski, LA
AF Benson, Al B.
   Venook, Alan P.
   Al-Hawary, Mahmoud M.
   Arain, Mustafa A.
   Chen, Yi-Jen
   Ciombor, Kristen K.
   Cohen, Stacey
   Cooper, Harry S.
   Deming, Dustin
   Farkas, Linda
   Garrido-Laguna, Ignacio
   Grem, Jean L.
   Gunn, Andrew
   Hecht, J. Randolph
   Hoffe, Sarah
   Hubbard, Joleen
   Hunt, Steven
   Johung, Kimberly L.
   Kirilcuk, Natalie
   Krishnamurthi, Smitha
   Messersmith, Wells A.
   Meyerhardt, Jeffrey
   Miller, Eric D.
   Mulcahy, Mary F.
   Nurkin, Steven
   Overman, Michael J.
   Parikh, Aparna
   Patel, Hitendra
   Pedersen, Katrina
   Saltz, Leonard
   Schneider, Charles
   Shibata, David
   Skibber, John M.
   Sofocleous, Constantinos T.
   Stoffel, Elena M.
   Stotsky-Himelfarb, Eden
   Willett, Christopher G.
   Gregory, Kristina M.
   Gurski, Lisa A.
TI Colon Cancer, Version 2.2021
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; WILD-TYPE KRAS; FOLFIRI PLUS BEVACIZUMAB;
   MONOCLONAL-ANTIBODY THERAPY; RANDOMIZED PHASE-III; OXALIPLATIN-RELATED
   NEUROTOXICITY; RESECTABLE LIVER METASTASES; GENE MUTATION STATUS; DOSE
   IPILIMUMAB IPI; DNA MISMATCH REPAIR
AB This selection from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Colon Cancer focuses on systemic therapy options for the treatment of metastatic colorectal cancer (mCRC), because important updates have recently been made to this section. These updates include recommendations for first-line use of checkpoint inhibitors for mCRC, that is deficient mismatch repair/ microsatellite instability-high, recommendations related to the use of biosimilars, and expanded recommendations for biomarker testing. The systemic therapy recommendations now include targeted therapy options for patients with mCRC that is HER2-amplified, or BRAF V600E mutation?positive. Treatment and management of nonmetastatic or resectable/ablatable metastatic disease are discussed in the complete version of the NCCN Guidelines for Colon Cancer available at NCCN.org. Additional topics covered in the complete version include risk assessment, staging, pathology, posttreatment surveillance, and survivorship.
C1 [Benson, Al B.; Mulcahy, Mary F.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
   [Venook, Alan P.; Arain, Mustafa A.] UCSF Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
   [Al-Hawary, Mahmoud M.; Stoffel, Elena M.] Univ Michigan, Rogel Canc Ctr, Ann Arbor, MI 48109 USA.
   [Chen, Yi-Jen] City Hope Natl Med Ctr, 1500 E Duarte Rd, Duarte, CA 91010 USA.
   [Ciombor, Kristen K.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
   [Cohen, Stacey] Fred Hutchinson Canc Res Ctr, Seattle Canc Care Alliance, 1124 Columbia St, Seattle, WA 98104 USA.
   [Cooper, Harry S.] Fox Chase Canc Ctr, 7701 Burholme Ave, Philadelphia, PA 19111 USA.
   [Deming, Dustin] Univ Wisconsin, Carbone Canc Ctr, Madison, WI 53706 USA.
   [Farkas, Linda] UT Southwestern Simmons Comprehens Canc Ctr, Dallas, TX USA.
   [Garrido-Laguna, Ignacio] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
   [Grem, Jean L.] Fred & Pamela Buffett Canc Ctr, Omaha, NE USA.
   [Gunn, Andrew] UAB, ONeal Comprehens Canc Ctr, Birmingham, AL USA.
   [Hecht, J. Randolph] UCLA Jonsson Comprehens Canc Ctr, Los Angeles, CA USA.
   [Hoffe, Sarah] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
   [Hubbard, Joleen] Mayo Clin, Canc Ctr, Rochester, MN USA.
   [Hunt, Steven; Pedersen, Katrina] Barnes Jewish Hosp, Siteman Canc Ctr, St Louis, MO 63110 USA.
   [Hunt, Steven; Pedersen, Katrina] Washington Univ, Sch Med, St Louis, MO USA.
   [Johung, Kimberly L.] Yale Canc Ctr, Smilow Canc Hosp, New Haven, CT USA.
   [Kirilcuk, Natalie] Stanford Canc Inst, Stanford, CA USA.
   [Krishnamurthi, Smitha] Univ Hosp Seidman Canc Ctr, Case Comprehens Canc Ctr, Cleveland, OH USA.
   [Krishnamurthi, Smitha] Cleveland Clin, Taussig Canc Inst, Cleveland, OH 44106 USA.
   [Messersmith, Wells A.] Univ Colorado, Canc Ctr, Boulder, CO 80309 USA.
   [Meyerhardt, Jeffrey] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
   [Miller, Eric D.] Ohio State Univ, Comprehens Canc Ctr, James Canc Hosp & Solove Res Inst, Columbus, OH 43210 USA.
   [Nurkin, Steven] Roswell Park Comprehens Canc Ctr, Buffalo, NY USA.
   [Overman, Michael J.; Skibber, John M.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
   [Parikh, Aparna] Massachusetts Gen Hosp, Canc Ctr, Boston, MA 02114 USA.
   [Patel, Hitendra] UC San Diego Moores Canc Ctr, San Diego, CA USA.
   [Saltz, Leonard; Sofocleous, Constantinos T.] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
   [Schneider, Charles] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
   [Shibata, David] Univ Tennessee, Hlth Sci Ctr, Knoxville, TN 37996 USA.
   [Stotsky-Himelfarb, Eden] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
   [Willett, Christopher G.] Duke Canc Inst, Durham, NC USA.
   [Gregory, Kristina M.; Gurski, Lisa A.] Natl Comprehens Canc Network, Plymouth Meeting, PA USA.
C3 Northwestern University; Ann & Robert H. Lurie Children's Hospital of
   Chicago; Robert H. Lurie Comprehensive Cancer Center; University of
   California System; University of California San Francisco; UCSF Medical
   Center; UCSF Helen Diller Family Comprehensive Cancer Center; University
   of Michigan System; University of Michigan; City of Hope; Vanderbilt
   University; Seattle Cancer Care Alliance; Fred Hutchinson Cancer Center;
   Fox Chase Cancer Center; University of Wisconsin System; University of
   Wisconsin Madison; Utah System of Higher Education; University of Utah;
   Huntsman Cancer Institute; University of Alabama System; University of
   Alabama Birmingham; UCLA Jonsson Comprehensive Cancer Center; H Lee
   Moffitt Cancer Center & Research Institute; Mayo Clinic; Barnes-Jewish
   Hospital; Siteman Cancer Center; Washington University (WUSTL);
   Washington University (WUSTL); Yale University; Stanford Cancer
   Institute; University System of Ohio; Case Western Reserve University;
   Cleveland Clinic Foundation; University of Colorado System; University
   of Colorado Anschutz Medical Campus; University of Colorado Boulder;
   Harvard University; Dana-Farber Cancer Institute; University System of
   Ohio; Ohio State University; James Cancer Hospital & Solove Research
   Institute; Roswell Park Comprehensive Cancer Center; University of Texas
   System; UTMD Anderson Cancer Center; Harvard University; Massachusetts
   General Hospital; Memorial Sloan Kettering Cancer Center; University of
   Pennsylvania; University of Tennessee System; University of Tennessee
   Health Science Center; Johns Hopkins University; Johns Hopkins Medicine;
   Duke University
RP Benson, A (corresponding author), Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
RI Krishnamurthi, Smitha/ABB-8593-2021; Meyerhardt, Jeffrey/IAP-4528-2023;
   Garrido-Laguna, Ignacio/ABD-1875-2020; chen, yuling/JMQ-4121-2023;
   Pedersen, Katrina/KBA-8737-2024
OI Pedersen, Katrina/0000-0003-2793-6901
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NR 335
TC 479
Z9 536
U1 5
U2 14
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 2021
VL 19
IS 3
BP 329
EP 359
DI 10.6004/jnccn.2021.0012
PG 31
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RB1GH
UT WOS:000631864200010
PM 33724754
OA Bronze
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Parmar, A
   Chan, KKW
   Ko, YJ
AF Parmar, A.
   Chan, K. K. W.
   Ko, Y. J.
TI Metastatic colorectal cancer: therapeutic options for treating
   refractory disease
SO CURRENT ONCOLOGY
LA English
DT Review
DE Colorectal cancer; metastatic; targeted therapy; immunotherapy;
   treatment-refractory disease
ID PHASE-III TRIAL; TRIFLURIDINE/TIPIRACIL TAS-102; ANTITUMOR-ACTIVITY;
   SUPPORTIVE CARE; ASIAN PATIENTS; DOUBLE-BLIND; REGORAFENIB; MULTICENTER;
   PLACEBO; PLUS
AB Therapeutic options for chemorefractory metastatic colorectal cancer (mcnc) have significantly expanded since 2009. The oral targeted therapies regorafenib and trifluridine/tipiracil have been established to be efficacious and safe in patients with mcnc who have progressed beyond 2 or more lines of chemotherapy. Evidence for the use of immunotherapy in a subgroup of this patient population is also encouraging, particularly in patients with mcnc that exhibits high microsatellite instability or deficient mismatch repair. Those significant advances have led to Health Canada approval of 3 novel therapeutic options for the treatment of patients with chemorefractory mcnc. However, the limited clinical efficacy of those treatments underscores the need for ongoing development of systemic therapy options for this unique cohort of patients. Here, we review the current and emerging treatment landscape for chemorefractory mcRc.
C1 [Parmar, A.; Chan, K. K. W.; Ko, Y. J.] Sunnybrook Hlth Sci Ctr, Odette Canc Ctr, 2075 Bayview Ave,Room T2-044, Toronto, ON M4N 3M5, Canada.
   [Chan, K. K. W.] Canadian Ctr Appl Res Canc Control, Toronto, ON, Canada.
C3 University of Toronto; Sunnybrook Health Science Center; Sunnybrook
   Research Institute
RP Ko, YJ (corresponding author), Sunnybrook Hlth Sci Ctr, Odette Canc Ctr, 2075 Bayview Ave,Room T2-044, Toronto, ON M4N 3M5, Canada.
EM yooj-joung.ko@sunnybrook.ca
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NR 47
TC 12
Z9 12
U1 0
U2 0
PU MULTIMED INC
PI TORONTO
PA 66 MARTIN ST, TORONTO, ON L9T 2R2, CANADA
SN 1198-0052
J9 CURR ONCOL
JI Curr. Oncol.
PD NOV
PY 2019
VL 26
SU 1
BP S24
EP S32
DI 10.3747/co.26.5575
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JP0PF
UT WOS:000497973400004
PM 31819707
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Schulte, ML
   Hight, MR
   Ayers, GD
   Liu, Q
   Shyr, Y
   Washington, MK
   Manning, HC
AF Schulte, Michael L.
   Hight, Matthew R.
   Ayers, Gregory D.
   Liu, Qi
   Shyr, Yu
   Washington, M. Kay
   Manning, H. Charles
TI Non-Invasive Glutamine PET Reflects Pharmacological Inhibition of
   BRAF<SUP>V600E</SUP> <i>In Vivo</i>
SO MOLECULAR IMAGING AND BIOLOGY
LA English
DT Article
DE Glutamine; Pet; Colon; Cancer; BRAF
ID POSITRON-EMISSION-TOMOGRAPHY; CANCER-CELL METABOLISM; C-MYC; GROWTH;
   EXPRESSION; GLUCOSE; TUMORS; ASCT2
AB This study aimed to study whether cancer cells possess distinguishing metabolic features compared with surrounding normal cells, such as increased glutamine uptake. Given this, quantitative measures of glutamine uptake may reflect critical processes in oncology. Approximately, 10 % of patients with colorectal cancer (CRC) express BRAF (V600E) , which may be actionable with selective BRAF inhibitors or in combination with inhibitors of complementary signaling axes. Non-invasive and quantitative predictive measures of response to these targeted therapies remain poorly developed in this setting. The primary objective of this study was to explore 4-[F-18]fluoroglutamine (4-[F-18]F-GLN) positron emission tomography (PET) to predict response to BRAF(V600E)-targeted therapy in preclinical models of colon cancer.
   Tumor microarrays from patients with primary human colon cancers (n = 115) and CRC liver metastases (n = 111) were used to evaluate the prevalence of ASCT2, the primary glutamine transporter in oncology, by immunohistochemistry. Subsequently, 4-[F-18]F-GLN PET was evaluated in mouse models of human BRAF (V600E) -expressing and BRAF wild-type CRC.
   Approximately 70 % of primary colon cancers and 53 % of metastases exhibited positive ASCT2 immunoreactivity, suggesting that [F-18]4-F-GLN PET could be applicable to a majority of patients with colon cancer. ASCT2 expression was not associated selectively with the expression of mutant BRAF. Decreased 4-[F-18]F-GLN predicted pharmacological response to single-agent BRAF and combination BRAF and PI3K/mTOR inhibition in BRAF (V600E) -mutant Colo-205 tumors. In contrast, a similar decrease was not observed in BRAF wild-type HCT-116 tumors, a setting where BRAF(V600E)-targeted therapies are ineffective.
   4-[F-18]F-GLN PET selectively reflected pharmacodynamic response to BRAF inhibition when compared with 2-deoxy-2[F-18]fluoro-d-glucose PET, which was decreased non-specifically for all treated cohorts, regardless of downstream pathway inhibition. These findings illustrate the utility of non-invasive PET imaging measures of glutamine uptake to selectively predict response to BRAF-targeted therapy in colon cancer and may suggest further opportunities to inform colon cancer clinical trials using targeted therapies against MAPK activation.
C1 [Schulte, Michael L.; Manning, H. Charles] Vanderbilt Univ, Med Ctr, Vanderbilt Ctr Mol Probes, Nashville, TN 37232 USA.
   [Schulte, Michael L.; Hight, Matthew R.; Manning, H. Charles] Vanderbilt Univ, Med Ctr, Inst Imaging Sci, Nashville, TN 37232 USA.
   [Schulte, Michael L.; Manning, H. Charles] Vanderbilt Univ, Med Ctr, Dept Radiol & Radiol Sci, Nashville, TN 37232 USA.
   [Ayers, Gregory D.] Vanderbilt Univ, Med Ctr, Dept Biostat, Nashville, TN 37232 USA.
   [Liu, Qi; Shyr, Yu] Vanderbilt Univ, Med Ctr, Vanderbilt Ctr Quantitat Sci, Nashville, TN USA.
   [Shyr, Yu; Washington, M. Kay; Manning, H. Charles] Vanderbilt Univ, Med Ctr, VICC, Nashville, TN 37232 USA.
   [Washington, M. Kay; Manning, H. Charles] Vanderbilt Univ, Med Ctr, Dept Pathol, Nashville, TN 37232 USA.
   [Manning, H. Charles] Vanderbilt Univ, Dept Biomed Engn, Nashville, TN 37232 USA.
   [Manning, H. Charles] Vanderbilt Univ, Med Ctr, Dept Neurosurg, Nashville, TN 37232 USA.
   [Manning, H. Charles] Vanderbilt Univ, Dept Chem, Nashville, TN 37232 USA.
C3 Vanderbilt University; Vanderbilt University; Vanderbilt University;
   Vanderbilt University; Vanderbilt University; Vanderbilt University;
   Vanderbilt University; Vanderbilt University; Vanderbilt University;
   Vanderbilt University
RP Manning, HC (corresponding author), Vanderbilt Univ, Med Ctr, Vanderbilt Ctr Mol Probes, Nashville, TN 37232 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Med Ctr, Inst Imaging Sci, Nashville, TN 37232 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Med Ctr, Dept Radiol & Radiol Sci, Nashville, TN 37232 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Med Ctr, VICC, Nashville, TN 37232 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Med Ctr, Dept Pathol, Nashville, TN 37232 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Dept Biomed Engn, Nashville, TN 37232 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Med Ctr, Dept Neurosurg, Nashville, TN 37232 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Dept Chem, Nashville, TN 37232 USA.
EM henry.c.manning@vanderbilt.edu
RI Shyr, Yu/KSM-5348-2024; Liu, Qi/KLZ-9389-2024
OI Shyr, Yu/0000-0003-2086-9670
FU National Institutes of Health [R01-CA140628, P50-CA95103, 5P30-DK058404,
   P30-CA068485]; Kleberg Foundation; Vanderbilt Center for Molecular
   Probes
FX These studies were supported by grants from the National Institutes of
   Health (R01-CA140628, P50-CA95103, 5P30-DK058404, P30-CA068485), the
   Kleberg Foundation, and the Vanderbilt Center for Molecular Probes. The
   authors wish to thank Ping Zhao for her assistance with the animal
   experiments, Md. Noor Tantaway for his assistance with the small animal
   PET acquisition, and Michael Nickels for his assistance with radio
   tracer production.
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NR 40
TC 17
Z9 18
U1 0
U2 16
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1536-1632
EI 1860-2002
J9 MOL IMAGING BIOL
JI Mol. Imaging. Biol.
PD JUN
PY 2017
VL 19
IS 3
BP 421
EP 428
DI 10.1007/s11307-016-1008-z
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA ET4UD
UT WOS:000400279600016
PM 27770401
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Wang, YZ
   An, Y
   Ma, Y
   Guo, JC
AF Wang, Yizhi
   An, Yang
   Ma, Yi
   Guo, Junchao
TI F-box/WD-40 repeat-containing protein 7: A potential target in the
   progression and treatment of gastrointestinal malignancy
SO ONCOLOGY LETTERS
LA English
DT Review
DE F-box and WD-40 repeat-containing protein 7; gastrointestinal
   malignancy; targeted therapy; tumor progression; chemoresistance
ID HUMAN GASTRIC-CANCER; TUMOR-SUPPRESSOR; COLORECTAL-CANCER;
   PANCREATIC-CANCER; FBXW7 EXPRESSION; CELL-CYCLE;
   HEPATOCELLULAR-CARCINOMA; POOR-PROGNOSIS; F-BOX; DEPENDENT DEGRADATION
AB Cancer is a principal cause of human morbidity and mortality, with gastrointestinal malignancies, in particular, resulting in a marked number of tumor-associated mortalities. The progression of gastrointestinal malignancy is regulated by a variety of aberrantly expressed proteins, a number of which facilitate tumor progression, whereas, others function as tumor suppressors. The detection of such proteins not only contributes to the early diagnosis of cancer, they may additionally serve as potential therapeutic targets. In normal tissues, numerous proteins encoded by proto-oncoproteins are degraded by ubiquitylation enzymes, consisting of F-box/WD-40 repeat-containing protein 7 (Fbw7) and other proteins, thus avoiding tumorigenesis and maintaining homeostasis. In tumor tissues, the downregulation of Fbw7, caused by various factors, leads to disorders in ubiquitinase synthesis, which may induce tumor progression and chemoresistance, particularly in gastrointestinal malignancy. Therefore, an in-depth study of the regulatory mechanisms involved in disorders of Fbw7 expression and the role of Fbw7 in chemoresistance of gastrointestinal tumors may suggest improvements for early diagnostic screening and targeted therapy.
C1 [Wang, Yizhi; Guo, Junchao] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Gen Surg, 1 Shuaifuyuan Rd, Beijing 100730, Peoples R China.
   [Wang, Yizhi; Guo, Junchao] Peking Union Med Coll, 1 Shuaifuyuan Rd, Beijing 100730, Peoples R China.
   [An, Yang] China Med Univ, Hosp 1, Dept Anesthesia, Shenyang 110001, Liaoning, Peoples R China.
   [Ma, Yi] China Med Univ, Hosp 1, Dept Thorac Surg, Shenyang 110001, Liaoning, 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;
   China Medical University; China Medical University
RP Guo, JC (corresponding author), Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Gen Surg, 1 Shuaifuyuan Rd, Beijing 100730, Peoples R China.; Guo, JC (corresponding author), Peking Union Med Coll, 1 Shuaifuyuan Rd, Beijing 100730, Peoples R China.
EM gjcpumch@163.com
OI Guo, Junchao/0000-0002-1174-924X; Ma, Yi/0000-0002-1068-6486; Guo,
   Junchao/0000-0002-7878-8315
FU China Academy of Medical Sciences Innovation Fund for Medical Sciences
   [2016-I2M-3-019]; non-profit Central Research Institute Fund of Chinese
   of Academy of Medical Sciences [2018PT32014]
FX The present study was supported by The China Academy of Medical Sciences
   Innovation Fund for Medical Sciences (grant no. 2016-I2M-3-019) and the
   non-profit Central Research Institute Fund of Chinese of Academy of
   Medical Sciences (grant no. 2018PT32014).
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NR 90
TC 2
Z9 2
U1 0
U2 19
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD APR
PY 2019
VL 17
IS 4
BP 3625
EP 3634
DI 10.3892/ol.2019.10036
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HQ8AB
UT WOS:000462644700001
PM 30881487
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Xiao, M
   Benoit, A
   Hasmim, M
   Duhem, C
   Vogin, G
   Berchem, G
   Noman, MZ
   Janji, B
AF Xiao, Malina
   Benoit, Alice
   Hasmim, Meriem
   Duhem, Caroline
   Vogin, Guillaume
   Berchem, Guy
   Noman, Muhammad Zaeem
   Janji, Bassam
TI Targeting Cytoprotective Autophagy to Enhance Anticancer Therapies
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE autophagy; cancer resistance; chemotherapy; radiotherapy; targeted
   therapy; immunotherapy
ID CANCER-CELLS; COLORECTAL-CANCER; INHIBITING AUTOPHAGY; CHLOROQUINE;
   RESISTANCE; PROMOTES; RADIOSENSITIVITY; ANGIOGENESIS; SIMVASTATIN;
   INDUCTION
AB Autophagy is a highly regulated multi-step process that occurs at the basal level in almost all cells. Although the deregulation of the autophagy process has been described in several pathologies, the role of autophagy in cancer as a cytoprotective mechanism is currently well established and supported by experimental and clinical evidence. Our understanding of the molecular mechanism of the autophagy process has largely contributed to defining how we can harness this process to improve the benefit of cancer therapies. While the role of autophagy in tumor resistance to chemotherapy is extensively documented, emerging data point toward autophagy as a mechanism of cancer resistance to radiotherapy, targeted therapy, and immunotherapy. Therefore, manipulating autophagy has emerged as a promising strategy to overcome tumor resistance to various anti-cancer therapies, and autophagy modulators are currently evaluated in combination therapies in several clinical trials. In this review, we will summarize our current knowledge of the impact of genetically and pharmacologically modulating autophagy genes and proteins, involved in the different steps of the autophagy process, on the therapeutic benefit of various cancer therapies. We will also briefly discuss the challenges and limitations to developing potent and selective autophagy inhibitors that could be used in ongoing clinical trials.
C1 [Xiao, Malina; Benoit, Alice; Hasmim, Meriem; Berchem, Guy; Noman, Muhammad Zaeem; Janji, Bassam] Luxembourg Inst Hlth, Dept Oncol, Tumor Immunotherapy & Microenvironrnent TIME Grp, Luxembourg, Luxembourg.
   [Duhem, Caroline; Berchem, Guy] Ctr Hosp Luxembourg, Dept Hematooncol, Luxembourg, Luxembourg.
   [Vogin, Guillaume] Univ Lorraine, UMR 7365, Ingn Mol & Physiopathol Articulaire IMoPA, Vandoeuvre Les Nancy, France.
   [Vogin, Guillaume] Ctr Francois Baolesse, Esch Sur Alzette, Luxembourg.
C3 Luxembourg Institute of Health; Luxembourg Hospital Center; Universite
   de Lorraine; Centre National de la Recherche Scientifique (CNRS); CNRS -
   Institute for Engineering & Systems Sciences (INSIS)
RP Janji, B (corresponding author), Luxembourg Inst Hlth, Dept Oncol, Tumor Immunotherapy & Microenvironrnent TIME Grp, Luxembourg, Luxembourg.
EM bassam.janji@lih.lu
RI NOMAN, Muhammmad/AAJ-1466-2021; Benoit, Alice/JOJ-6071-2023; Berchem,
   Guy/C-9364-2014
OI NOMAN, Muhammad Zaeem/0000-0002-1837-3097; Vogin,
   Guillaume/0000-0002-8114-5900; JANJI, Bassam/0000-0002-9763-0943;
   Berchem, Guy/0000-0003-0157-2257; Hasmim, Meriem/0000-0002-7920-2443
FU Luxembourg Institute of Health; Luxembourg National Research Fund
   [PRIDE15/10675146/CANBIO, C18/BM/12670304/COMBATIC]; FNRS Televie
   [7.4606.18, 7.4579.20]; Fondation Cancer, Luxembourg [FC/2018/06];
   Kriibskrank Kanner Foundation, Luxembourg; RCMS foundation; Action LIONS
   Vaincre le Cancer Luxembourg; Janssen Cilag Pharma; Roche Pharma
FX This work was supported by Luxembourg Institute of Health and grants
   from the Luxembourg National Research Fund (PRIDE15/10675146/CANBIO and
   C18/BM/12670304/COMBATIC); FNRS Televie (grants 7.4606.18 and
   7.4579.20); Fondation Cancer, Luxembourg (FC/2018/06); Kriibskrank
   Kanner Foundation, Luxembourg (2019); RCMS foundation, and Action LIONS
   Vaincre le Cancer Luxembourg. The authors also declare that this study
   received funding from Janssen Cilag Pharma and Roche Pharma. These
   funders were not involved in the study design, collection, analysis,
   interpretation of data, the writing of this article or the decision to
   submit it for publication.
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NR 146
TC 22
Z9 23
U1 0
U2 26
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD FEB 25
PY 2021
VL 11
AR 626309
DI 10.3389/fonc.2021.626309
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QU7IC
UT WOS:000627451800001
PM 33718194
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Sharma, A
   Jadhav, HR
   Rai, A
   Lakkaniga, NR
   Chandramoorthy, HC
   Kamli, HM
   Alshahrani, MY
   Rajagopalan, P
AF Sharma, Amit
   Jadhav, Hemant R.
   Rai, Anubhav
   Lakkaniga, Naga Rajiv
   Chandramoorthy, Harish C.
   Kamli, Hossam Mohammed
   Alshahrani, Mohammad Y.
   Rajagopalan, Prasanna
TI A Comprehensive Review of Systemic Targeted Therapies in Cancer
   Treatment
SO CURRENT CANCER THERAPY REVIEWS
LA English
DT Review
DE Anti-cancer therapeutics; targeted therapy; kinase inhibitors;
   monoclonal antibodies; oncology; cancer treatment
ID TYROSINE KINASE INHIBITOR; SMALL-MOLECULE INHIBITORS; METASTATIC
   BREAST-CANCER; MONOCLONAL-ANTIBODIES; 1ST-LINE TREATMENT;
   COLORECTAL-CANCER; RADIATION-THERAPY; CHEMOTHERAPY; EFFICACY; GROWTH
AB Cancer is one of the significant healthcare challenges in today's world, even afteradvancements in modern science, including oncology. The complex nature of the disease, whichinvolves multiple proteins and pathways, poses a substantial challenge in drug discovery. Several therapeutic options have emerged in the last decade. Systemic cancer therapies began with theadvent of chemotherapy and were revolutionized with the development of targeted therapies.The present review is a definite overview of the advances in various therapeutic optionsfor cancer, with a particular emphasis on targeted therapy using small molecules and biologicals.
C1 [Sharma, Amit; Jadhav, Hemant R.] Birla Inst Technol & Sci, Dept Pharm, Lab Pharmaceut Chem, Pilani, India.
   [Rai, Anubhav; Lakkaniga, Naga Rajiv] Indian Inst Technol, Indian Sch Mines, Dept Chem & Chem Biol, Dhanbad, India.
   [Chandramoorthy, Harish C.] King Khalid Univ, Coll Med, Stem Cells & Regenerat Med Unit, Abha, Saudi Arabia.
   [Chandramoorthy, Harish C.] King Khalid Univ, Coll Med, Dept Microbiol & Clin Parasitol, Abha, Asir, Saudi Arabia.
   [Kamli, Hossam Mohammed; Alshahrani, Mohammad Y.; Rajagopalan, Prasanna] King Khalid Univ, Coll Appl Med Sci, Dept Clin Lab Sci, Abha, Asir, Saudi Arabia.
   [Rajagopalan, Prasanna] King Khalid Univ, Coll Appl Med Sci, Cent Res Lab, Abha, Asir, Saudi Arabia.
C3 Birla Institute of Technology & Science Pilani (BITS Pilani); Indian
   Institute of Technology System (IIT System); Indian Institute of
   Technology (Indian School of Mines) Dhanbad; King Khalid University;
   King Khalid University; King Khalid University; King Khalid University
RP Jadhav, HR (corresponding author), Birla Inst Technol & Sci, Dept Pharm, Lab Pharmaceut Chem, Pilani, India.
EM hemantrj@pilani.bits-pilani.ac.in
RI Lakkaniga, Naga/ABC-4847-2020; KAMLI, HOSSAM/ABC-9461-2021; Sharma,
   Amit/W-4209-2019
OI , Amit Sharma/0009-0003-2377-4172
FU Deanship of Scientific Research, King Khalid University [G.R.P 2/27/40]
FX This work was supported by a grant from the Deanship of Scientific
   Research, King Khalid University via Grant number G.R.P 2/27/40 to Dr.
   Harish C. Chandramoorthy.
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NR 155
TC 0
Z9 0
U1 3
U2 3
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1573-3947
EI 1875-6301
J9 CURR CANCER THER REV
JI Curr. Cancer Ther. Rev.
PY 2024
VL 20
IS 5
BP 461
EP 480
DI 10.2174/0115733947261058231017170056
PG 20
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA YE7Z7
UT WOS:001266887800005
DA 2025-01-04
ER

PT J
AU Zhang, XF
   Zhang, WJ
   Cao, PA
AF Zhang, Xiaofei
   Zhang, Wenjun
   Cao, Pingan
TI Advances in CpG Island Methylator Phenotype Colorectal Cancer Therapies
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE colorectal cancer; CpG island methylator phenotype; chemotherapy;
   targeted therapy; DNA methylation inhibitor
ID DNA METHYLATION; MOLECULAR-FEATURES; SURVIVAL BENEFIT; CIMP;
   5-FLUOROURACIL; TEMOZOLOMIDE; ASSOCIATION; COMBINATION; BIOMARKER;
   MUTATION
AB With the aging of the population, the incidence of colorectal cancer in China is increasing. One of the epigenetic alterations: CpG island methylator phenotype (CIMP) plays an important role in the incidence of colorectal cancer. Recent studies have shown that CIMP is closely related to some specific clinicopathological phenotypes and multiple molecular phenotypes in colorectal cancer. In this paper, the newest progress of CIMP colorectal cancer in chemotherapeutic drugs, targeted agents and small molecular methylation inhibitors are going to be introduced. We hope to provide potential clinical treatment strategies for personalized and precise treatment of colorectal cancer patients.
C1 [Zhang, Xiaofei; Cao, Pingan] Dalian Univ, Xinhua Hosp, Dept Med Oncol, Dalian, Peoples R China.
   [Zhang, Wenjun] Dalian Univ, Xinhua Hosp, Dept Colorectal Surg, Dalian, Peoples R China.
C3 Dalian University; Dalian University
RP Zhang, XF (corresponding author), Dalian Univ, Xinhua Hosp, Dept Med Oncol, Dalian, Peoples R China.
EM zhangxiaofei@hotmail.co.jp
RI 张, 肖飞/IYI-9416-2023
FU Guidance Plan of Natural Science Foundation of Liaoning Province
   [2019-ZD-0302]; Dalian Youth Science and Technology Star Plan
   [2019RQ096]; Clinical plus Excellence Project [2020ZYA003]; Shanghai
   Nucleic Acid Chemistry and Nanomedicine Key Laboratory
FX This work was financially supported by the Guidance Plan of Natural
   Science Foundation of Liaoning Province (2019-ZD-0302), Dalian Youth
   Science and Technology Star Plan (2019RQ096), and Clinical plus
   Excellence Project (2020ZYA003) from Shanghai Nucleic Acid Chemistry and
   Nanomedicine Key Laboratory.
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NR 56
TC 18
Z9 18
U1 3
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 FEB 26
PY 2021
VL 11
AR 629390
DI 10.3389/fonc.2021.629390
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QV1YP
UT WOS:000627774100001
PM 33718206
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Sari, IN
   Phi, LTH
   Jun, NY
   Wijaya, YT
   Lee, S
   Kwon, HY
AF Sari, Ita Novita
   Lan Thi Hanh Phi
   Jun, Nayoung
   Wijaya, Yoseph Toni
   Lee, Sanghyun
   Kwon, Hyog Young
TI Hedgehog Signaling in Cancer: A Prospective Therapeutic Target for
   Eradicating Cancer Stem Cells
SO CELLS
LA English
DT Review
DE Hedgehog signaling pathway; cancer therapy; cancer stem cells
ID TUMOR-SUPPRESSOR GENE; PROTEIN-KINASE-A; SONIC-HEDGEHOG; INDIAN
   HEDGEHOG; PATHWAY INHIBITOR; HUMAN HOMOLOG; SELF-RENEWAL;
   COLORECTAL-CANCER; COLON-CANCER; GLI PROTEINS
AB The Hedgehog (Hh) pathway is a signaling cascade that plays a crucial role in many fundamental processes, including embryonic development and tissue homeostasis. Moreover, emerging evidence has suggested that aberrant activation of Hh is associated with neoplastic transformations, malignant tumors, and drug resistance of a multitude of cancers. At the molecular level, it has been shown that Hh signaling drives the progression of cancers by regulating cancer cell proliferation, malignancy, metastasis, and the expansion of cancer stem cells (CSCs). Thus, a comprehensive understanding of Hh signaling during tumorigenesis and development of chemoresistance is necessary in order to identify potential therapeutic strategies to target various human cancers and their relapse. In this review, we discuss the molecular basis of the Hh signaling pathway and its abnormal activation in several types of human cancers. We also highlight the clinical development of Hh signaling inhibitors for cancer therapy as well as CSC-targeted therapy.
C1 [Sari, Ita Novita; Lan Thi Hanh Phi; Jun, Nayoung; Wijaya, Yoseph Toni; Lee, Sanghyun; Kwon, Hyog Young] Soonchunhyang Univ, Soonchunhyang Inst Medi Bio Sci, Cheonan 31151, South Korea.
C3 Soonchunhyang University
RP Kwon, HY (corresponding author), Soonchunhyang Univ, Soonchunhyang Inst Medi Bio Sci, Cheonan 31151, South Korea.
EM itanov07@gmail.com; hanhlan.11@gmail.com; jny0407@naver.com;
   yoseph.toni@gmail.com; october-92@daum.net; hykwon@sch.ac.kr
RI Phi, Lan/GPS-4933-2022; Kwon, Hyog/T-7915-2019
OI Wijaya, Yoseph Toni/0000-0003-3002-8592; Sari, Ita
   Novita/0000-0001-9475-7992; Phi, Lan/0000-0003-3967-2747
FU Soonchunhyang University Research Fund; Basic Science Research Program
   through the National Research Foundation of Korea [NRF-2017R1A2B4001996]
FX This work was supported by the Soonchunhyang University Research Fund
   and Basic Science Research Program through the National Research
   Foundation of Korea (NRF-2017R1A2B4001996).
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NR 249
TC 138
Z9 147
U1 2
U2 17
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD NOV
PY 2018
VL 7
IS 11
AR 208
DI 10.3390/cells7110208
PG 33
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA HB8BD
UT WOS:000451308000027
PM 30423843
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Papadopoulou, E
   Metaxa-Mariatou, V
   Tsaousis, G
   Tsoulos, N
   Tsirigoti, A
   Efstathiadou, C
   Apessos, A
   Agiannitopoulos, K
   Pepe, G
   Bourkoula, E
   Nasioulas, G
AF Papadopoulou, Eirini
   Metaxa-Mariatou, Vasiliki
   Tsaousis, Georgios
   Tsoulos, Nikolaos
   Tsirigoti, Angeliki
   Efstathiadou, Chrisoula
   Apessos, Angela
   Agiannitopoulos, Konstantinos
   Pepe, Georgia
   Bourkoula, Eugenia
   Nasioulas, George
TI Molecular predictive markers in tumors of the gastrointestinal tract
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Predictive biomarkers; Targeted therapy; Next generation sequencing;
   Gastrointestinal tract; Somatic mutations; Liquid biopsy
ID METASTATIC COLORECTAL-CANCER; II COLON-CANCER; SQUAMOUS-CELL CARCINOMA;
   ANTI-EGFR TREATMENT; GASTRIC-CANCER; MICROSATELLITE INSTABILITY;
   STAGE-II; GENOMIC ALTERATIONS; TARGETED THERAPIES; ESOPHAGEAL CANCER
AB Gastrointestinal malignancies are among the leading causes of cancer-related deaths worldwide. Like all human malignancies they are characterized by accumulation of mutations which lead to inactivation of tumor suppressor genes or activation of oncogenes. Advances in Molecular Biology techniques have allowed for more accurate analysis of tumors' genetic profiling using new breakthrough technologies such as next generation sequencing (NGS), leading to the development of targeted therapeutical approaches based upon biomarker-selection. During the last 10 years tremendous advances in the development of targeted therapies for patients with advanced cancer have been made, thus various targeted agents, associated with predictive biomarkers, have been developed or are in development for the treatment of patients with gastrointestinal cancer patients. This review summarizes the advances in the field of molecular biomarkers in tumors of the gastrointestinal tract, with focus on the available NGS platforms that enable comprehensive tumor molecular profile analysis.
C1 [Papadopoulou, Eirini; Metaxa-Mariatou, Vasiliki; Tsaousis, Georgios; Tsoulos, Nikolaos; Tsirigoti, Angeliki; Efstathiadou, Chrisoula; Apessos, Angela; Agiannitopoulos, Konstantinos; Pepe, Georgia; Bourkoula, Eugenia; Nasioulas, George] GeneKor Med SA, Dept Mol Biol, 52 Spaton Ave, Gerakas 15344, Greece.
RP Nasioulas, G (corresponding author), GeneKor Med SA, Dept Mol Biol, 52 Spaton Ave, Gerakas 15344, Greece.
EM gnasioulas@genekor.com
RI Tsaousis, Georgios/L-5504-2013
OI Tsaousis, Georgios/0000-0002-8975-8779; NASIOULAS,
   GEORGE/0009-0002-9891-1883; PAPADOPOULOU, EIRINI/0000-0001-5519-5325;
   AGIANNITOPOULOS, KONSTANTINOS/0000-0003-0432-3256
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NR 115
TC 5
Z9 5
U1 1
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD NOV 15
PY 2016
VL 8
IS 11
BP 772
EP 785
DI 10.4251/wjgo.v8.i11.772
PG 14
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA FE9TR
UT WOS:000408546600002
PM 27895815
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Shao, XY
   Sun, YB
   Zhong, KQ
   Gu, JR
   Yu, Y
   Hu, T
   Kuai, XY
   Xing, YC
AF Shao, Xinyu
   Sun, Yibin
   Zhong, Kaiqiang
   Gu, Jinrong
   Yu, Yang
   Hu, Tong
   Kuai, Xiaoyi
   Xing, Yechen
TI TYRO3 promotes tumorigenesis and drug resistance in colorectal cancer by
   enhancing the epithelial-mesenchymal transition process
SO AGING-US
LA English
DT Article
DE TYRO3; colorectal cancer; drug -resistance; ENO1; EMT
ID RECEPTOR TYROSINE KINASES; THERAPEUTIC TARGET; SIGNALING PATHWAY;
   PHOSPHATIDYLSERINE; ACTIVATION; GROWTH; ENO1; EGFR
AB Colorectal cancer (CRC) is a leading cause of cancer mortality worldwide. Although considerable advances in CRC treatment have been achieved, effective treatment improvement has hit a bottleneck. This study demonstrated that TYRO3 expression was aberrantly increased in CRC tissues with prognosis association. The prediction model of prognosis for CRC patients was constructed based on TYRO3 expression. The model suggested that the TYRO3 level is crucial to the final prediction results. We observed that knockdown TYRO3 expression could inhibit the proliferation and migration ability and reverse the drug resistance by constructing drug-resistant CRC cell lines. In vivo experiments also confirmed this conclusion. Thus, targeting TYRO3 combined with 5-Fu treatment could provide a better therapeutic effect. Additionally, TYRO3 could inhibit the EMT process by down-regulating ENO1, which may be achieved by interfering with energy metabolism in cancer cells. Therefore, the current study provides a theoretical basis for TYRO3 in drug-resistance of CRC cells and highlights a new strategy for CRC-targeted therapy.
C1 [Shao, Xinyu; Sun, Yibin; Yu, Yang; Hu, Tong; Kuai, Xiaoyi; Xing, Yechen] Nanjing Med Univ, Suzhou Municipal Hosp, Affiliated Suzhou Hosp, Dept Gastroenterol,Gusu Sch, Suzhou 215000, Jiangsu, Peoples R China.
   [Zhong, Kaiqiang; Gu, Jinrong] Soochow Univ, Affiliated Hosp 1, Dept Gen Surg, Suzhou 215000, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Soochow University - China
RP Kuai, XY; Xing, YC (corresponding author), Nanjing Med Univ, Suzhou Municipal Hosp, Affiliated Suzhou Hosp, Dept Gastroenterol,Gusu Sch, Suzhou 215000, Jiangsu, Peoples R China.
EM zoekxy@126.com; xingyechennjmu@163.com
RI yang, yu/JAC-9403-2023
FU Suzhou Special Project of Diagnosis and Treatment for Key Clinical
   Disease [LCZX201814]; Project of Youth Foundation in Science and
   Education of Department of Public Health of Suzhou [KJXW2021038]; Suzhou
   Science and Technology Development Project [SYSD2018144]
FX This study was supported by the Suzhou Special Project of Diagnosis and
   Treatment for Key Clinical Disease (LCZX201814) , the Project of Youth
   Foundation in Science and Education of Department of Public Health of
   Suzhou (KJXW2021038) , and Suzhou Science and Technology Development
   Project (SYSD2018144) .
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NR 41
TC 3
Z9 3
U1 2
U2 6
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
SN 1945-4589
J9 AGING-US
JI Aging-US
PD APR 30
PY 2023
VL 15
IS 8
BP 3035
EP 3051
PG 17
WC Cell Biology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Geriatrics & Gerontology
GA H0EF7
UT WOS:000992775400016
PM 37116196
OA gold, Green Published
DA 2025-01-04
ER

PT B
AU Everett, JN
   Raymond, VM
AF Everett, Jessica N.
   Raymond, Victoria M.
BE Roychowdhury, S
   VanAllen, EM
TI Managing Germline Findings from Molecular Testing in Precision Oncology
SO PRECISION CANCER MEDICINE: Challenges and Opportunities
LA English
DT Article; Book Chapter
DE Precision oncology; Genetic counseling; Germline variants; NGS testing;
   Clinical genomics; Targeted therapy
ID CANCER PREDISPOSITION GENES; INTEGRATIVE CLINICAL GENOMICS;
   CONTRALATERAL BREAST-CANCER; BRCA2 MUTATION CARRIERS; RISK ASSESSMENT
   BREAST; INCIDENTAL FINDINGS; COLORECTAL-CANCER; AMERICAN SOCIETY;
   PANCREATIC-CANCER; MEDICAL GENETICS
AB Molecular genetic testing of the germline for hereditary cancer risk and molecular testing of tumor tissue for therapeutic decision making are no longer clearly distinct. Here we review how changes in sequencing technology have impacted use of germline and tumor molecular testing, implications for identifying incidental pathogenic germline variants through tumor testing, relevance of pathogenic germline variants in cancer care and prevention, and emerging research guiding clinical practice in this area.
C1 [Everett, Jessica N.; Raymond, Victoria M.] NYU, New York, NY 10016 USA.
C3 New York University
RP Everett, JN (corresponding author), NYU, New York, NY 10016 USA.
EM jessica.everett@nyulangone.org
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NR 76
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER NATURE SWITZERLAND AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, CH-4052, SWITZERLAND
BN 978-3-030-23637-3; 978-3-030-23636-6
PY 2019
BP 111
EP 128
DI 10.1007/978-3-030-23637-3_8
D2 10.1007/978-3-030-23637-3
PG 18
WC Oncology; Medicine, General & Internal
WE Book Citation Index – Science (BKCI-S)
SC Oncology; General & Internal Medicine
GA BR2XW
UT WOS:000642277700008
DA 2025-01-04
ER

PT J
AU Wang, JT
   Ma, X
   Si, H
   Ma, ZJ
   Ma, Y
   Wang, J
   Cao, BW
AF Wang, Jingting
   Ma, Xiao
   Si, Hai
   Ma, Zhongjun
   Ma, Yan
   Wang, Jing
   Cao, Bangwei
TI Role of long non-coding RNA H19 in therapy resistance of digestive
   system cancers
SO MOLECULAR MEDICINE
LA English
DT Review
DE LncRNA-H19; Digestive system cancer; Chemoresistant; Radioresistant
ID EPITHELIAL-MESENCHYMAL TRANSITION; COLORECTAL-CANCER; DRUG-RESISTANCE;
   ESOPHAGEAL CANCER; TARGETED THERAPY; DIPHTHERIA-TOXIN; DOWN-REGULATION;
   POOR-PROGNOSIS; CHEMORESISTANCE; EMT
AB Digestive system cancers are associated with high morbidity and mortality. Chemotherapy and radiotherapy are the main treatment modalities for these cancers. However, the development of therapy resistance leads to high rates of tumor recurrence and metastasis, resulting in dismal prognosis. Long non-coding RNA (LncRNA) H19, one of the most intriguing non-coding RNAs, has been shown to play a key role in the development and therapy resistance of various digestive system cancers (including hepatocellular carcinoma, colorectal cancer, pancreatic ductal adenocarcinoma, esophageal carcinoma, gastric cancer, and biliary system cancer) by regulating the abnormal expression of genes. In this review, we discuss the potential mechanisms of LncRNA H19 related therapy resistance in the context of digestive system cancers. LncRNA H19 is a potential novel therapeutic target for amelioration of cancer therapy resistance.
C1 [Wang, Jingting; Ma, Xiao; Si, Hai; Ma, Zhongjun; Wang, Jing; Cao, Bangwei] Capital Med Univ, Beijing Friendship Hosp, Dept Oncol, 95 Yong An Rd, Beijing 100050, Peoples R China.
   [Ma, Yan] Beijing Shijingshan Hosp, Dept Comprehens Med, 24 Shijingshan Rd, Beijing 100043, Peoples R China.
   [Wang, Jing] Yale Sch Med, New Haven, CT 06510 USA.
C3 Capital Medical University; Yale University
RP Wang, J (corresponding author), Capital Med Univ, Beijing Friendship Hosp, Dept Oncol, 95 Yong An Rd, Beijing 100050, Peoples R China.; Wang, J (corresponding author), Yale Sch Med, New Haven, CT 06510 USA.
EM wangjing1981@ccmu.edu.cn
FU Digestive Medical Coordinated Development Center of Beijing Hospitals
   Authority [XXT01]; Beijing key clinical specialty (2018-2020); pilot
   project of clinical collaboration with traditional Chinese medicine and
   western medicine in major refractory disease-Esophageal cancer
   [2019-ZX-005]
FX This study was supported by the Digestive Medical Coordinated
   Development Center of Beijing Hospitals Authority. No: XXT01; Beijing
   key clinical specialty (2018-2020); The pilot project of clinical
   collaboration with traditional Chinese medicine and western medicine in
   major refractory disease-Esophageal cancer (2019-ZX-005).
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NR 58
TC 21
Z9 23
U1 2
U2 38
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1076-1551
EI 1528-3658
J9 MOL MED
JI Mol. Med.
PD JAN
PY 2021
VL 27
IS 1
AR 1
DI 10.1186/s10020-020-00255-2
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA PO5LV
UT WOS:000605211500001
PM 33402118
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Chrysostomou, A
   Furlan, C
   Saccenti, E
AF Chrysostomou, Andreas
   Furlan, Cristina
   Saccenti, Edoardo
TI Machine learning based analysis of single-cell data reveals evidence of
   subject-specific single-cell gene expression profiles in acute myeloid
   leukaemia patients and healthy controls
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS
LA English
DT Article
DE Genomics; Classification; Personalized medicine; Gene regulation
ID COLON-CANCER; STEM; TRYPTASE; SELECTION; COEFFICIENT; ASSOCIATION;
   DEPENDENCY; PHENOTYPES; POWERFUL; COMPLEX
AB Acute Myeloid Leukaemia (AML) is characterized by uncontrolled growth of immature myeloid cells, disrupting normal blood production. Treatment typically involves chemotherapy, targeted therapy, and stem cell transplantation but many patients develop chemoresistance, leading to poor outcomes due to the disease's high heterogeneity. In this study, we used publicly available single-cell RNA sequencing data and machine learning to classify AML patients and healthy, monocytes, dendritic and progenitor cells population. We found that gene expression profiles of AML patients and healthy controls can be classified at the individual level with high accuracy (>70 %) when using progenitor cells, suggesting the existence of subject-specific single cell transcriptomics profiles. The analysis also revealed molecular determinants of patient heterogeneity (e.g. TPSD1, CT45A1, and GABRA4) which could support new strategies for patient stratification and personalized treatment in leukaemia.
C1 [Chrysostomou, Andreas; Furlan, Cristina; Saccenti, Edoardo] Wageningen Univ & Res, Lab Syst & Synthet Biol, Stippeneng 4, NL-6708 WE Wageningen, Netherlands.
   [Chrysostomou, Andreas] Univ Amsterdam, Dept Med Microbiol & Infect Prevent, Lab Expt Virol, Med Ctr, Amsterdam, Netherlands.
C3 Wageningen University & Research; University of Amsterdam
RP Furlan, C; Saccenti, E (corresponding author), Wageningen Univ & Res, Lab Syst & Synthet Biol, Stippeneng 4, NL-6708 WE Wageningen, Netherlands.
EM cristina.furlan@wur.nl; edoardo.saccenti@wur.nl
OI Saccenti, Edoardo/0000-0001-8284-4829
FU Netherlands Organisation for Health Research and Development (ZonMW)
   through the PERMIT project [456008002]
FX E.S. acknowledge the funding from the Netherlands Organisation for
   Health Research and Development (ZonMW) through the PERMIT project
   (Personalized Medicine in Infections: from Systems Biomedicine and
   Immunometabolism to Precision Diagnosis and Stratification Permitting
   Individualized Therapies, project number 456008002) under the PerMed
   Joint Transnational call JTC 2018 (Research projects on personalised
   medicine-smart combination of pre-clinical and clinical research with
   data and ICT solutions) .
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NR 137
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1874-9399
EI 1876-4320
J9 BBA-GENE REGUL MECH
JI Biochim. Biophys. Acta-Gene Regul. Mech.
PD DEC
PY 2024
VL 1867
IS 4
AR 195062
DI 10.1016/j.bbagrm.2024.195062
EA OCT 2024
PG 14
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA J1K8N
UT WOS:001334738400001
PM 39366464
OA hybrid
DA 2025-01-04
ER

PT J
AU Martín, AJM
   Ramírez, SP
   Morán, LO
   Zamorano, MR
   Benéitez, MCV
   Salcedo, IA
   Escobar, IG
   Fernández, JMS
AF Munoz Martin, Andres J.
   Perez Ramirez, Sara
   Ortega Moran, Laura
   Ruiz Zamorano, Magdalena
   Vinuela Beneitez, Maria Carmen
   Aparicio Salcedo, Inmaculada
   Garcia Escobar, Ignacio
   Soria Fernandez, Jose Manuel
TI Pharmacological cancer treatment and venous thromboembolism risk
SO EUROPEAN HEART JOURNAL SUPPLEMENTS
LA English
DT Article
DE Venous thromboembolism; Arterial thromboembolism; Cancer; Chemotherapy;
   Targeted therapy; Hormonotherapy; Immunotherapy; Supportive care
ID CELL LUNG-CANCER; ANGIOGENESIS INHIBITOR BEVACIZUMAB; METASTATIC
   COLORECTAL-CANCER; TYROSINE KINASE INHIBITORS; PLACEBO-CONTROLLED
   TRIALS; ADVANCED BREAST-CANCER; PROSTATE-CANCER; DOUBLE-BLIND;
   PHASE-III; INCREASED SURVIVAL
AB Risk factors for cancer-associated thrombosis are commonly divided into three categories: patient-, cancer-, and treatment-related factors. Currently, different types of drugs are used in cancer treatment. Chemotherapy has been identified as an independent risk factor for venous thromboembolism (VTE). However, it should be noted, that the risk of VTE is not consistent among all cytotoxic agents. In addition, different supportive care drugs, such as erythropoiesis stimulating agents or granulocyte colony stimulating factors, and hormonotherapy have been associated to an increased risk of VTE. Immunotherapy and molecular-targeted therapies have significantly changed the treatment of cancer over the past decade. The main subtypes include tyrosine-kinase inhibitors, monoclonal antibodies, small molecules, and immunomodulatory agents. The relationship between VTE and targeted therapies remains largely unknown.
C1 [Munoz Martin, Andres J.; Perez Ramirez, Sara; Ortega Moran, Laura; Aparicio Salcedo, Inmaculada] Hosp Gen Univ Gregorio Maranon, Med Oncol Dept, Calle Doctor Esquerdo 46, Madrid 28007, Spain.
   [Ruiz Zamorano, Magdalena; Vinuela Beneitez, Maria Carmen] Univ Complutense, Fac Med, Dept Med, Av Seneca 2, Madrid 28040, Spain.
   [Garcia Escobar, Ignacio] Hosp Gen Univ Ciudad Real, Med Oncol Dept, Calle Obispo Rafael Torija S-N, Ciudad Real 130050, Spain.
   [Soria Fernandez, Jose Manuel] Inst Invest St Pau IIB St PAU, Genom Complex Dis Unit, Joan Alcover 7-2 2a, Barcelona 08031, Spain.
C3 General University Gregorio Maranon Hospital; Complutense University of
   Madrid
RP Martín, AJM (corresponding author), Hosp Gen Univ Gregorio Maranon, Med Oncol Dept, Calle Doctor Esquerdo 46, Madrid 28007, Spain.
EM andresmunmar@hotmail.com
RI Soria Fernández, José/AAD-6761-2019
OI Soria Fernandez, Jose Manuel/0000-0002-6226-4293; Ruiz Zamorano,
   Magdalena C./0000-0002-8853-4984
FU Boehringer Ingelheim
FX This paper was published as part of a supplement supported by an
   educational grant from Boehringer Ingelheim.
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NR 111
TC 12
Z9 14
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1520-765X
EI 1554-2815
J9 EUR HEART J SUPPL
JI Eur. Heart J. Suppl.
PD APR
PY 2020
VL 22
IS C
BP C2
EP C14
DI 10.1093/eurheartj/suaa004
PG 13
WC Cardiac & Cardiovascular Systems
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA MR0WG
UT WOS:000553313300005
PM 32368194
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Zhu, QR
   Zhang, RN
   Gu, XQ
   Zhao, ZM
   Gao, Q
   Chen, M
   Wu, QB
   Xie, T
   Sui, XB
AF Zhu, Qianru
   Zhang, Ruonan
   Gu, Xiaoqing
   Zhao, Ziming
   Gao, Quan
   Chen, Min
   Wu, Qibiao
   Xie, Tian
   Sui, Xinbing
TI Honokiol enhances the sensitivity of cetuximab in KRASG13D mutant
   colorectal cancer through destroying SNX3-retromer complex
SO THERANOSTICS
LA English
DT Article
DE colorectal cancer; honokiol; cetuximab; KRAS; SNX3
ID MALIGNANT GLIOMA; EGFR THERAPY; RESISTANCE; RETROMER; MUTATIONS
AB Rationale: : the proto-oncogene KRAS is frequently mutated in colorectal cancer (CRC), leading to inherent resistance against monoclonal antibodies targeting the epidermal growth factor receptor (EGFR), such as cetuximab. Therefore, addressing the primary resistance and expanding the indications for target therapy have become critical challenges. Methods: : the screening of a natural product library against KRAS mutant CRC cells was conducted, leading to the discovery of a small molecule compound that sensitive to the KRASG13D G13D mutation site. The anti-tumor activity of this small molecule compound in combination with cetuximab was evaluated using the KRASG13D G13D mutant CRC models both in vivo and in vitro. . This evaluation includes an examination of its effects on cell proliferation, viability, apoptosis, cell cycle progression, and tumor growth. Furthermore, RNA sequencing, western blot analysis, immunofluorescence, real-time quantitative PCR, and pull-down assays were employed to explore the molecular mechanisms underlying the synergistic anti-tumor effect of this small molecule compound in combination with cetuximab. Results: : our study screened 882 compounds in KRAS mutant CRC cells and identified honokiol, a small molecule compound that exhibits specific sensitivity to KRASG13D G13D mutant CRC cells. Furthermore, we revealed that the synergistic augmentation of cetuximab's sensitivity in vivo and in vitro models of KRASG13D G13D mutant CRC in combination with honokiol. Mechanistically, honokiol suppresses SNX3-retromer mediated trafficking, thereby impeding lysosomal proteolytic capacity and inhibiting autophagy and macropinocytosis fluxes. Moreover, honokiol inhibits the conversion of RAS GDP to RAS GTP, heightening the susceptibility of KRASG13D G13D CRC mutant cells to cetuximab. Conclusions: : honokiol enhances the sensitivity of cetuximab by destroying SNX3 retromer in KRASG13D G13D mutant CRC preclinical model. These findings present a promising strategy for expanding the indications of target therapy in KRAS mutant colorectal cancer patients.
C1 [Zhu, Qianru; Zhang, Ruonan; Gu, Xiaoqing; Gao, Quan; Xie, Tian; Sui, Xinbing] Hangzhou Normal Univ, Sch Pharm, Hangzhou 311121, Zhejiang, Peoples R China.
   [Zhu, Qianru; Zhao, Ziming; Gao, Quan; Chen, Min; Wu, Qibiao; Xie, Tian; Sui, Xinbing] Macau Univ Sci & Technol, Fac Chinese Med, State Key Lab Qual Res Chinese Med, Macau, Peoples R China.
   [Sui, Xinbing] Hangzhou Normal Univ, Affiliated Hosp, Dept Med Oncol, Hangzhou 311121, Zhejiang, Peoples R China.
C3 Hangzhou Normal University; Macau University of Science & Technology;
   Hangzhou Normal University
RP Xie, T; Sui, XB (corresponding author), Hangzhou Normal Univ, Sch Pharm, Hangzhou 311121, Zhejiang, Peoples R China.; Wu, QB; Xie, T; Sui, XB (corresponding author), Macau Univ Sci & Technol, Fac Chinese Med, State Key Lab Qual Res Chinese Med, Macau, Peoples R China.; Sui, XB (corresponding author), Hangzhou Normal Univ, Affiliated Hosp, Dept Med Oncol, Hangzhou 311121, Zhejiang, Peoples R China.
EM qbwu@must.edu.mo; xbs@hznu.edu.cn; hzzju@hznu.edu.cn
RI Xie, Tian/LUA-1225-2024; Sui, Xinbing/ADE-9174-2022; Gu,
   Xiaoqing/GPP-6913-2022
OI Wu, Qibiao/0000-0002-1670-1050
FU National Natural Science Foundation of China [U23A20518]; Science and
   Technology Development Fund, Macau SAR [0098/2021/A2, 0048/2023/AFJ];
   China Postdoctoral Science Foundation [2024M753701]; Zhejiang Province
   Medicine and Health Project [2021KY248, 2023KY962]
FX This study is supported in part by the National Natural Science
   Foundation of China (grant No. U23A20518) , the Science and Technology
   Development Fund, Macau SAR (0098/2021/A2 and 0048/2023/AFJ) , the China
   Postdoctoral Science Foundation (No. 2024M753701) , and the Zhejiang
   Province Medicine and Health Project (2021KY248 and 2023KY962) .
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NR 52
TC 0
Z9 0
U1 19
U2 19
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 14
BP 5443
EP 5460
DI 10.7150/thno.97180
PG 18
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA F9I0Z
UT WOS:001312857600006
PM 39310106
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Khalid, S
   Khalid, A
   Clark, BA
   Haddad, A
   Spiro, TP
   Daw, H
AF Khalid, Sidra
   Khalid, Aariez
   Clark, Bernadette A.
   Haddad, Abdo
   Spiro, Timothy Pp.
   Daw, Hamed
TI Dosage Adjustments for Chemotherapy and Targeted Therapies in Colorectal
   and Pancreatic Cancer Patients with Hepatic Impairment
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Review
DE hepatic impairment; colon cancer; rectal cancer; pancreatic cancer;
   chemotherapy; targeted therapy
ID PHASE-I; PHARMACOKINETICS; GEMCITABINE; CAPECITABINE; REGORAFENIB;
   MULTICENTER; DYSFUNCTION; EVEROLIMUS; TRIAL
AB There are many novel chemotherapeutic options and targeted therapies available for the treatment of colorectal and pancreatic cancer. Patients with these cancers often have hepatic impairment either from the metastasis to the liver or from the chemotherapy or targeted therapies used to treat the disease. It is important to describe the effects of these agents in patients with hepatic impairment. This article will review the dosage recommendations for the chemotherapy regimens and targeted therapies in colorectal and pancreatic cancer patients in the setting of hepatic impairment.
C1 [Khalid, Sidra] Cleveland Clin, Fairview Hosp, Cleveland, OH 44106 USA.
   [Khalid, Aariez] Univ Guelph, Sci Biomed Sci, Binbrook, ON, Canada.
   [Clark, Bernadette A.] Cleveland Clin, Fairview Hosp, Oncol, Cleveland, OH 44106 USA.
   [Haddad, Abdo; Spiro, Timothy Pp.; Daw, Hamed] Cleveland Clin, Fairview Hosp, Dept Hematol & Oncol, Cleveland, OH 44106 USA.
C3 Cleveland Clinic Foundation; University of Guelph; Cleveland Clinic
   Foundation; Cleveland Clinic Foundation
RP Khalid, S (corresponding author), Cleveland Clin, Fairview Hosp, Cleveland, OH 44106 USA.
EM drsidrakhalid@hotmail.com
RI ahmed, haddad/AAD-7743-2019; khalid, sidra/KOD-4672-2024
CR [Anonymous], 2018, SUNITINIB EVEROLIMUS
   [Anonymous], 2016, ERLOTINIB DOSAGE
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NR 32
TC 4
Z9 4
U1 0
U2 4
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 JUN
PY 2018
VL 10
IS 6
AR e2798
DI 10.7759/cureus.2798
PG 9
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA HB3HK
UT WOS:000450941500075
PM 30116677
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Bilgin, B
   Kuralay, Y
   Yucel, S
AF Bilgin, Burak
   Kuralay, Yunus
   Yucel, Sebnem
TI Prognostic importance of prognostic nutritional index and modified
   Glasgow prognostic score in advanced lung cancer with targetable
   mutation
SO JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
LA English
DT Article
DE Nutrition; Inflammation; EGFR; ALK; Lung cancer
ID COLORECTAL-CANCER; LYMPHOCYTE RATIO; NEUTROPHIL; SURVIVAL
AB Background Inflammation and nutrition are important parameters that significantly affect survival in various malignancies. Prognostic nutritional index (PNI) and modified Glasgow prognostic score (mGPS) can reflect both inflammatory and nutritional conditions. Therefore, we aimed to evaluate the prognostic value of PNI and mGPS in patients who had the targetable mutation and also received targeted therapy. Materials and Methods Advanced lung cancer patients with EGFR mutation (mut) and ALK rearrangement were enrolled to study, retrospectively. PNI has with the following formula: 10 x serum albumin (g/dl) + 0.005 x peripheral lymphocyte count (per mm(3)) and threshold value was accepted as 50. Modified GPS was also calculated using albumin and CRP level and patients were scored as range 0 to 2. Results A total of 182 patients enrolled in the study. 132 and 50 of 182 patients had EGFR mut and ALK rearrangement, respectively. PFS was significantly longer in high PNI group in both the EGFR and ALK rearrangement-positive subgroups (P = 0.004 for EGFR mut-positive group; P = 0.017 for ALK rearrangement-positive group). Additionally, PFS was significantly shortened from mGPS 0 to 2 (P = < 0.001 for EGFR mut-positive group; P = 0.016 for ALK rearrangement-positive group). Conclusion Both PNI and mGPS can be used as a reliable, inexpensive, and easily applicable prognostic index in the advanced lung cancer patients who had the targetable mutation and also received targeted therapy.
C1 [Bilgin, Burak; Yucel, Sebnem] Ankara Yildirim Beyazit Univ, Ankara Bilkent City Hosp, Dept Med Oncol, TR-06800 Ankara, Turkiye.
   [Kuralay, Yunus] Erzurum Reg Educ & Res Hosp, Dept Internal Med, Erzurum, Turkiye.
C3 Ankara Yildirim Beyazit University; Erzurum Bolge Training & Research
   Hospital; Ataturk University
RP Bilgin, B (corresponding author), Ankara Yildirim Beyazit Univ, Ankara Bilkent City Hosp, Dept Med Oncol, TR-06800 Ankara, Turkiye.
EM drbbilgin@hotmail.com
OI BILGIN, BURAK/0000-0003-1717-8246
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NR 19
TC 1
Z9 1
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 26
PY 2024
VL 150
IS 4
AR 215
DI 10.1007/s00432-023-05529-w
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OY0D4
UT WOS:001210710900003
PM 38668879
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Colombo, A
   Cordio, S
   Porretto, CM
AF Colombo, Alfredo
   Cordio, Stefano
   Porretto, Concetta Maria
TI Immune check point inhibitors in BRAF mutated metastatic colorectal
   cancer: A review
SO INTERNATIONAL JOURNAL OF GASTROINTESTINAL INTERVENTION
LA English
DT Review
DE Colon; Immunotherapy; Mutation; Neoplasms; Proto-oncogene proteins B-raf
ID MISMATCH REPAIR-DEFICIENT; CONSENSUS MOLECULAR SUBTYPES; MICROSATELLITE
   INSTABILITY; OPEN-LABEL; 1ST-LINE TREATMENT; SUBGROUP ANALYSES; PD-L1
   EXPRESSION; PLUS CETUXIMAB; PEMBROLIZUMAB; BLOCKADE
AB Metastatic colorectal cancers with BRAF mutation are a class of tumors that have a poor prognosis compared to wild type patients. Even if this group has found some hope in targeted therapy with multi-targeted blockade of the mitogen-activated protein kinase (MAPK) signalling pathway, more work must be done to increase treatment efficacy, particularly for the microsatellite stability/DNA proficient mismatch repair (MSS/pMMR) subtype. Patients with BRAF mutant colorectal cancer and high microsatellite instability/DNA deficient mismatch repair (MSI-H/dMMR) are considered to have a high tumor mutation load and a lot of neoantigen, which makes immunotherapy likely to be effective. It is generally accepted that MSS/pMMR colorectal cancer is an immunologically "cold" tumor that is resistant to immunotherapy. Then, patients with BRAF mutant colorectal cancer appear to find hope with targeted therapy paired with immune checkpoint blockade therapy. The clinical effectiveness and developing new approaches of immune checkpoint blockade therapy for MSI-H/dMMR and MSS/pMMR BRAF mutant metastatic colorectal cancer are reviewed in this paper. We also address possible biomarkers in the tumor immune microenvironment for predicting immunotherapeutic response in BRAF mutant colorectal cancer.
C1 [Colombo, Alfredo; Porretto, Concetta Maria] Casa Cura Macchiarella SpA, Oncol Unit, Viale Regina Margherita 25, I-90138 Palermo, Italy.
   [Cordio, Stefano] Osped Maria Paterno Arezzo Ragusa, Dept Oncol, Ragusa, Italy.
RP Colombo, A (corresponding author), Casa Cura Macchiarella SpA, Oncol Unit, Viale Regina Margherita 25, I-90138 Palermo, Italy.
EM alfredocolombo63@gmail.com
RI Colombo, Alfredo/KOD-1042-2024
OI Colombo, Alfredo/0000-0001-6902-5028
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NR 106
TC 0
Z9 0
U1 1
U2 1
PU SOC GASTROINTESTINAL INTERVENTION
PI SEOUL
PA 12, HAKDONG-RO 31, GANGNAM-GU, SEOUL, 00000, SOUTH KOREA
SN 2636-0004
EI 2636-0012
J9 INT J GASTROINT INT
JI Int. J. Gastrointest. Interv.
PD JUL
PY 2024
VL 13
IS 3
BP 74
EP 81
DI 10.18528/ijgii240030
PG 8
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA A6O8D
UT WOS:001283717500002
OA gold
DA 2025-01-04
ER

PT J
AU Parikh, A
   Atreya, C
   Korn, WM
   Venook, AP
AF Parikh, Aparna
   Atreya, Chloe
   Korn, W. Michael
   Venook, Alan P.
TI Prolonged Response to HER2-Directed Therapy in a Patient With
   HER2-Amplified, Rapidly Progressive Metastatic Colorectal Cancer
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID TARGETED THERAPY; TRASTUZUMAB; OVEREXPRESSION
AB HER2 gene amplifications and activating mutations in the HER2 receptor tyrosine kinase are present in 4% of metastatic colorectal cancers (mCRCs). HER2-targeted therapy is not standard of care, although preclinical and clinical data suggest that patients with HER2 amplifications and/or HER2-activating mutations may benefit from HER2-directed therapy. HER2 amplifications and activating mutations have also been implicated in resistance to anti-epidermal growth factor receptor based therapy. This report describes a patient with KRAS, NRAS, and BRAF wild-type mCRC who experienced disease progression on first-line treatment with FOLFIRI and cetuximab after only 5 months, and subsequently experienced progression on second-line treatment with capecitabine and oxaliplatin plus bevacizumab after 2 months with significant functional decline. Next-generation sequencing of the primary tumor identified HER2 amplification, and we were able to obtain trastuzumab-DM1 for off-label use. The patient had symptomatic clinical benefit from trastuzumab-DM1 and had radiographic disease control for 7 months. On progression, therapy was changed to trastuzumab and pertuzumab, but the patient's disease progressed 3 months later. Treatment with the trastuzumab-DM1 resulted in a sustained response that was longer than his prior responses in the first and second lines of treatment, with a dramatic improvement in the patient's functional status. This case represents the first report, to our knowledge, of successful single-agent treatment of HER2-amplifed CRC with trastuzumab-DM1. Clinical trials targeting patients with HER2-mutated and -amplified metastatic colon cancer are currently underway. Molecular insights from investigating HER2 activation and the impact of HER2-directed therapies in a wide variety of solid tumors will create the needed evidence base to more broadly inform patient care.
C1 [Parikh, Aparna; Atreya, Chloe; Korn, W. Michael; Venook, Alan P.] Univ Calif San Francisco, Hellen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
C3 University of California System; University of California San Francisco;
   UCSF Medical Center; UCSF Helen Diller Family Comprehensive Cancer
   Center
RP Parikh, A (corresponding author), Massachusetts Gen Hosp, 55 Fruit St, Boston, MA 02114 USA.
EM aparna.parikh@mgh.harvard.edu
FU Genentech; GlaskoSmithKline; Novartis; Merck; Genentech/Roche; Bayer;
   Bristol-Myers Squibb; Lily; Onyx
FX Dr. Parikh has disclosed receiving salary from Genentech. Dr. Atreya has
   disclosed receiving research support from GlaskoSmithKline, Novartis,
   and Merck, and has disclosed serving in a consulting/advisory role for
   Genentech, and Bayer Diagnostics. Dr. Korn has disclosed serving in a
   consulting/advisory role for Merrimack and Foundation Medicine; having a
   patent from Exelexis; and receiving travel expenses from Merrimack. Dr.
   Venook has disclosed serving in a consulting/advisory role for
   Genentech/Roche, and receiving research support from Genentech/Roche,
   Bayer, Bristol-Myers Squibb, GlaskoSmithKline, Lily, and Onyx.
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NR 26
TC 26
Z9 26
U1 0
U2 7
PU HARBORSIDE PRESS
PI COLD SPRING HARBOR
PA 37 MAIN ST, COLD SPRING HARBOR, NY 11724 USA
SN 1540-1405
EI 1540-1413
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD JAN
PY 2017
VL 15
IS 1
BP 3
EP 8
DI 10.6004/jnccn.2017.0002
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EH8TT
UT WOS:000392045900002
PM 28040715
OA Green Submitted, Green Accepted, Bronze
DA 2025-01-04
ER

PT J
AU Wu, YC
   Liu, FQ
   Cai, GX
   Wang, MH
   Zheng, HT
   Wang, L
   Li, XX
   Cai, SJ
   Xu, Y
AF Wu, Yuchen
   Liu, Fangqi
   Cai, Guoxiang
   Wang, Minghe
   Zheng, Hongtu
   Wang, Lu
   Li, Xinxiang
   Cai, Sanjun
   Xu, Ye
TI Surgical management of colorectal cancer: the Fudan University Shanghai
   Cancer Center experience
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Review
DE Colorectal cancer (CRC); surgical management; Fudan University Cancer
   Center
ID LIVER METASTASES; NEOADJUVANT CHEMOTHERAPY; COLON-CANCER; STATISTICS;
   RESECTION; SURGERY
AB The incidence and mortality of colorectal cancer (CRC) are increasing in China. Although surgery is the initially preferred intervention, systematic and individualized treatment has become far more important, on account of the considerable developments in radiotherapy and chemotherapy. Nowadays, treatment decisions are usually made following multidisciplinary team (MDT) meetings, especially in Fudan University Shanghai Cancer Center (FUSCC). With precise and specific imaging examinations, effective preoperative staging and restaging after neoadjuvant therapy have been the routine, resulting in individualized treatments guided by MDT. These advantages also result in less invasive and function-preserving surgery. Based on clinical evidence of targeted therapy compared with traditional chemotherapy, effective treatment of CRC with metastasis, especially liver and peritoneal metastasis (PM), became more effective. Screening of patients with hereditary CRC, special consultant for surgical procedure and surveillance of hereditary CRC families are routinely performed.
C1 [Wu, Yuchen; Liu, Fangqi; Cai, Guoxiang; Wang, Minghe; Zheng, Hongtu; Wang, Lu; Li, Xinxiang; Cai, Sanjun; Xu, Ye] Fudan Univ, Dept Colorectal Surg, Shanghai Canc Ctr, Shanghai 200032, Peoples R China.
C3 Fudan University
RP Xu, Y (corresponding author), Fudan Univ, Shanghai Canc Ctr, Shanghai 200032, Peoples R China.
EM xu_shirley021@163.com
RI Cai, Jun/GLS-4538-2022; xu, ye/GQO-8972-2022; CAI,
   GUOXIANG/LKK-9614-2024
OI Cai, Guoxiang/0000-0002-7772-7078
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NR 21
TC 2
Z9 2
U1 0
U2 11
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2218-676X
EI 2219-6803
J9 TRANSL CANCER RES
JI Transl. Cancer Res.
PD DEC
PY 2017
VL 6
IS 6
BP 1351
EP 1357
DI 10.21037/tcr.2017.09.30
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FR2EW
UT WOS:000418881000038
DA 2025-01-04
ER

PT J
AU Yang, J
   Yang, X
   Gao, L
   Zhang, J
   Yi, C
   Huang, Y
AF Yang, Ju
   Yang, Xi
   Gao, Ling
   Zhang, Jie
   Yi, Cheng
   Huang, Ying
TI The role of the renin-angiotensin system inhibitors in malignancy: a
   review
SO COGENT SOCIAL SCIENCES
LA English
DT Review
DE RASi; ARB; AECI; cancer treatment
ID II TYPE-1 RECEPTOR; BREAST-CANCER RECURRENCE; CONVERTING
   ENZYME-INHIBITORS; RENAL-CELL CARCINOMA; COLORECTAL-CANCER;
   PANCREATIC-CANCER; ACE-INHIBITORS; GLIOBLASTOMA PATIENTS; ANGIOGENIC
   INHIBITOR; TUMOR ANGIOGENESIS
AB Hypertension is one of the most prevalent diseases in cardiology. The angiotensin receptor blockers (ARBs)/angiotensin converting enzyme inhibitors (ACEIs) are widely used drugs to stabilize the blood pressure via inhibition of the renin-angiotensin system (RAS). Studies have found that the exposure to RAS inhibitors (RASi) can suppress the development of cancers via multimodal mechanisms and has attracted increased attentions in the recent past. Owing the potential of RASi to inhibit tumor growth, proliferation and metastasis, they are considered as the potential and exciting candidates to enhance the effect of chemo-radiotherapy and targeted therapy efficacy. However, there are conflicting reports as to the use of ARB/ACEI in all facets of tumor growth. In this study, we comprehensively summarize and review the potential mechanisms of RASi in cancer treatment, like inhibition of tumor angiogenesis, reduction of cancer-associated fibroblasts (CAFs) and extracellular matrix (ECM), regulation of immune cells and improvement of hypoxia. Additionally, based on the basic and clinical experiments, we analyze the views and results regarding the role of RASi plays in tumor from genesis to recurrence, and certainly cancer treatment (chemo-radiotherapy and targeted therapy). In the last, not only do we discuss the prospects of using RASi to enhance cancer treatment efficacy but also point out the conflicting situation with the intention to give some directions and inspiration on this topic.
C1 [Yang, Ju; Huang, Ying] Sichuan Univ, West China Sch Basic Med Sci & Forens Med, 17,Sect 3,People South Rd, Chengdu 610041, Sichuan, Peoples R China.
   [Yang, Xi; Gao, Ling; Yi, Cheng] Sichuan Univ, West China Hosp, Canc Ctr, Dept Med Oncol, 37 Guoxue Lane, Chengdu 610041, Sichuan, Peoples R China.
   [Zhang, Jie] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Lab Expt Oncol, Chengdu 610041, Peoples R China.
   [Zhang, Jie] Sichuan Univ, West China Hosp, Canc Ctr, Chengdu 610041, Peoples R China.
   [Zhang, Jie] Collaborat Innovat Ctr, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University; Sichuan
   University
RP Huang, Y (corresponding author), Sichuan Univ, West China Sch Basic Med Sci & Forens Med, 17,Sect 3,People South Rd, Chengdu 610041, Sichuan, Peoples R China.; Yi, C (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, Dept Med Oncol, 37 Guoxue Lane, Chengdu 610041, Sichuan, Peoples R China.
EM yicheng6834@126.com; huangying68@163.com
RI yi, cheng/KHC-5004-2024
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NR 105
TC 0
Z9 0
U1 0
U2 3
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 2331-1886
J9 COGENT SOC SCI
JI Cogent Soc. Sci.
PD JAN 1
PY 2021
VL 7
IS 1
BP 884
EP 897
PG 14
WC Social Sciences, Interdisciplinary
WE Emerging Sources Citation Index (ESCI)
SC Social Sciences - Other Topics
GA RM0EN
UT WOS:000639335700021
DA 2025-01-04
ER

PT J
AU Chen, BQ
   Dragomir, MP
   Yang, C
   Li, QQ
   Horst, D
   Calin, GA
AF Chen, BaoQing
   Dragomir, Mihnea P.
   Yang, Chen
   Li, Qiaoqiao
   Horst, David
   Calin, George A.
TI Targeting non-coding RNAs to overcome cancer therapy resistance
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID BREAST-CANCER; COLORECTAL-CANCER; DRUG-RESISTANCE; CHROMOSOMAL
   INSTABILITY; CLINICAL-IMPLICATIONS; MOLECULAR-MECHANISMS;
   BLADDER-CANCER; CELL CARCINOMA; MICRORNA; EXPRESSION
AB It is now well known that non-coding RNAs (ncRNAs), rather than protein-coding transcripts, are the preponderant RNA transcripts. NcRNAs, particularly microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), are widely appreciated as pervasive regulators of multiple cancer hallmarks such as proliferation, apoptosis, invasion, metastasis, and genomic instability. Despite recent discoveries in cancer therapy, resistance to chemotherapy, radiotherapy, targeted therapy, and immunotherapy continue to be a major setback. Recent studies have shown that ncRNAs also play a major role in resistance to different cancer therapies by rewiring essential signaling pathways. In this review, we present the intricate mechanisms through which dysregulated ncRNAs control resistance to the four major types of cancer therapies. We will focus on the current clinical implications of ncRNAs as biomarkers to predict treatment response (intrinsic resistance) and to detect resistance to therapy after the start of treatment (acquired resistance). Furthermore, we will present the potential of targeting ncRNA to overcome cancer treatment resistance, and we will discuss the challenges of ncRNA-targeted therapy-especially the development of delivery systems.
C1 [Chen, BaoQing; Yang, Chen; Li, Qiaoqiao] Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Dept Radiat Oncol,Canc Ctr, Guangzhou 510060, Guangdong, Peoples R China.
   [Dragomir, Mihnea P.; Horst, David] Charite Univ Med Berlin, Inst Pathol, D-10117 Berlin, Germany.
   [Dragomir, Mihnea P.; Horst, David] Free Univ Berlin, D-10117 Berlin, Germany.
   [Dragomir, Mihnea P.; Horst, David] Humboldt Univ, D-10117 Berlin, Germany.
   [Dragomir, Mihnea P.; Horst, David] Berlin Inst Hlth, D-10117 Berlin, Germany.
   [Dragomir, Mihnea P.] Berlin Inst Hlth, Anna Louisa Karsch Str 2, D-10178 Berlin, Germany.
   [Dragomir, Mihnea P.; Horst, David] German Canc Res Ctr, German Canc Consortium DKTK, Partner Site Berlin, D-69210 Heidelberg, Germany.
   [Calin, George A.] Univ Texas MD Anderson Canc Ctr, Dept Translat Mol Pathol, Houston, TX 77030 USA.
   [Calin, George A.] Univ Texas MD Anderson Canc Ctr, Ctr RNA Interference & Noncoding RNAs, Houston, TX 77030 USA.
C3 Sun Yat Sen University; State Key Lab Oncology South China; Berlin
   Institute of Health; Free University of Berlin; Humboldt University of
   Berlin; Charite Universitatsmedizin Berlin; Free University of Berlin;
   Humboldt University of Berlin; Berlin Institute of Health; Berlin
   Institute of Health; Helmholtz Association; German Cancer Research
   Center (DKFZ); University of Texas System; UTMD Anderson Cancer Center;
   University of Texas System; UTMD Anderson Cancer Center
RP Chen, BQ (corresponding author), Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Dept Radiat Oncol,Canc Ctr, Guangzhou 510060, Guangdong, Peoples R China.; Dragomir, MP (corresponding author), Charite Univ Med Berlin, Inst Pathol, D-10117 Berlin, Germany.; Dragomir, MP (corresponding author), Free Univ Berlin, D-10117 Berlin, Germany.; Dragomir, MP (corresponding author), Humboldt Univ, D-10117 Berlin, Germany.; Dragomir, MP (corresponding author), Berlin Inst Hlth, D-10117 Berlin, Germany.; Dragomir, MP (corresponding author), Berlin Inst Hlth, Anna Louisa Karsch Str 2, D-10178 Berlin, Germany.; Dragomir, MP (corresponding author), German Canc Res Ctr, German Canc Consortium DKTK, Partner Site Berlin, D-69210 Heidelberg, Germany.; Calin, GA (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Translat Mol Pathol, Houston, TX 77030 USA.; Calin, GA (corresponding author), Univ Texas MD Anderson Canc Ctr, Ctr RNA Interference & Noncoding RNAs, Houston, TX 77030 USA.
EM chenbq@sysucc.org.cn; mihnea.dragomir@charite.de; gcalin@mdanderson.org
RI Dragomir, Mihnea/ABB-8207-2020
OI Calin, George/0000-0002-7427-0578; Horst, David/0000-0003-4755-5743;
   Dragomir, Mihnea P./0000-0002-5550-3516; Yang, Chen/0000-0002-7593-5316
FU National Natural Science Foundation of China [81902462]; Charite -
   Universitatsmedizin Berlin; Berlin Institute of Health; NCI [1R01
   CA182905-01, 1R01CA222007-01A1]; NIGMS [1R01GM122775-01]; DoD Idea Award
   [W81XWH2110030]; Team DOD grant in Gastric Cancer, a Chronic Lymphocytic
   Leukemia Moonshot Flagship project; CLL Global Research Foundation; G.
   Harold & Leila Y. Mathers Foundation; Torrey Coast Foundation;
   Institutional Research Grant and Development Grant [2P50CA127001];
   National Cancer Institute [R01CA222007] Funding Source: NIH RePORTER
FX We thank Bryan Tutt, Scientific Editor, Research Medical Library, MDACC
   for editorial support. The work of B.C. is supported by National Natural
   Science Foundation of China (No. 81902462). M.P.D. is a participant in
   the BIH-Charite Junior Clinical Scientist Program funded by the Charite
   - Universitatsmedizin Berlin and the Berlin Institute of Health. G.A.C.
   is the Felix L. Haas Endowed Professor in Basic Science. Work in
   G.A.C.'s laboratory is supported by NCI grants 1R01 CA182905-01 and
   1R01CA222007-01A1, NIGMS grant 1R01GM122775-01, DoD Idea Award
   W81XWH2110030, a Team DOD grant in Gastric Cancer, a Chronic Lymphocytic
   Leukemia Moonshot Flagship project, a CLL Global Research Foundation
   2019 grant, a CLL Global Research Foundation 2020 grant, The G. Harold &
   Leila Y. Mathers Foundation, a grant from Torrey Coast Foundation, and
   an Institutional Research Grant and Development Grant associated with
   the Brain SPORE 2P50CA127001.
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NR 176
TC 186
Z9 197
U1 15
U2 81
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD APR 13
PY 2022
VL 7
IS 1
AR 121
DI 10.1038/s41392-022-00975-3
PG 20
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 0M9AU
UT WOS:000782440400002
PM 35418578
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Zhu, KR
   Yang, XY
   Tai, HB
   Zhong, XR
   Luo, T
   Zheng, H
AF Zhu, Kunrui
   Yang, Xinyi
   Tai, Hebei
   Zhong, Xiaorong
   Luo, Ting
   Zheng, Hong
TI HER2-targeted therapies in cancer: a systematic review
SO BIOMARKER RESEARCH
LA English
DT Review
DE HER2; Targeted therapy; Antibody-drug conjugates
ID GROWTH-FACTOR-RECEPTOR; TRASTUZUMAB-EMTANSINE T-DM1; IN-SITU
   HYBRIDIZATION; DERUXTECAN T-DXD; PHASE-II TRIAL; HER2-AMPLIFIED
   BREAST-CANCER; METASTATIC COLORECTAL-CANCER; HER2-MUTANT LUNG CANCERS;
   ANTIBODY-DRUG CONJUGATE; OPEN-LABEL
AB Abnormal alterations in human epidermal growth factor receptor 2 (HER2, neu, and erbB2) are associated with the development of many tumors. It is currently a crucial treatment for multiple cancers. Advanced in molecular biology and further exploration of the HER2-mediated pathway have promoted the development of medicine design and combination drug regimens. An increasing number of HER2-targeted drugs including specific monoclonal antibodies, tyrosine kinase inhibitors (TKIs), and antibody-drug conjugates (ADCs) have been approved by the U.S. Food and Drug Administration. The emergence of ADCs, has significantly transformed the treatment landscape for various tumors, such as breast, gastric, and bladder cancer. Classic monoclonal antibodies and novel TKIs have not only demonstrated remarkable efficacy, but also expanded their indications, with ADCs in particular exhibiting profound clinical applications. Moreover the concept of low HER2 expression signifies a breakthrough in HER2-targeted therapy, indicating that an increasing number of tumors and patients will benefit from this approach. This article, provides a comprehensive review of the underlying mechanism of action, representative drugs, corresponding clinical trials, recent advancements, and future research directions pertaining to HER2-targeted therapy.
C1 [Zhu, Kunrui; Zhong, Xiaorong; Luo, Ting; Zheng, Hong] Sichuan Univ, West China Hosp, Inst Breast Hlth Med, Canc Ctr,Breast Ctr, Chengdu 610041, Sichuan, Peoples R China.
   [Yang, Xinyi; Tai, Hebei] Guizhou Med Univ, Coll Clin Med, Guiyang 550000, Guizhou, Peoples R China.
C3 Sichuan University; Guizhou Medical University
RP Luo, T; Zheng, H (corresponding author), Sichuan Univ, West China Hosp, Inst Breast Hlth Med, Canc Ctr,Breast Ctr, Chengdu 610041, Sichuan, Peoples R China.
EM luoting@wchscu.cn; hzheng@scu.edu.cn
RI Yang, Xinyi/IVH-6916-2023
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NR 191
TC 13
Z9 14
U1 16
U2 29
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2050-7771
J9 BIOMARK RES
JI Biomark. Res.
PD FEB 2
PY 2024
VL 12
IS 1
AR 16
DI 10.1186/s40364-024-00565-1
PG 17
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA GU8J6
UT WOS:001155274600002
PM 38308374
OA Green Published, gold
HC Y
HP N
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
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Review
DE Molecular diagnostics; Gastrointestinal; Histology; Genetics; Oncology
ID RECEPTOR MONOCLONAL-ANTIBODIES; KRAS MUTATION DETECTION; ANTI-EGFR
   THERAPY; K-RAS MUTATIONS; MICROSATELLITE-INSTABILITY; ADJUVANT
   CHEMOTHERAPY; PIK3CA MUTATION; 1ST-LINE TREATMENT; QUALITY ASSESSMENT;
   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 Denver, 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; 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 School of Medicine; University of
   North Carolina; University of North Carolina Chapel Hill; University of
   Colorado System; University of Colorado Denver; University of Colorado
   Anschutz Medical Campus; Children's Hospital Colorado; 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 Colasacco, Carol/0000-0001-7856-7531; Temple-Smolkin,
   Robyn/0000-0002-5728-5436; Kopetz, Scott/0000-0001-9647-3416; Monzon,
   Federico/0000-0002-6890-9793
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NR 149
TC 26
Z9 27
U1 0
U2 7
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9173
EI 1943-7722
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD MAR
PY 2017
VL 147
IS 3
BP 221
EP 260
DI 10.1093/ajcp/aqw209
PG 40
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA EP0XE
UT WOS:000397109200001
PM 28165529
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Scotti, GB
   Sapienza, P
   Lapolla, P
   Crocetti, D
   Tarallo, M
   Brachini, G
   Mingoli, A
   Fiori, E
AF Scotti, Giorgia Burrelli
   Sapienza, Paolo
   Lapolla, Pierfrancesco
   Crocetti, Daniele
   Tarallo, Mariarita
   Brachini, Gioia
   Mingoli, Andrea
   Fiori, Enrico
TI Endoscopic Stenting and Palliative Chemotherapy in Advanced Colorectal
   Cancer: Friends or Foes? An Analysis of the Current Literature
SO IN VIVO
LA English
DT Review
DE Endoscopic stenting; colorectal cancer; palliative chemotherapy; review
ID SURGERY; PERFORATION; BEVACIZUMAB; OBSTRUCTION; OUTCOMES
AB Background/Aim: Chemotherapy offers a clear benefit in terms of survival rates of stage IV metastatic colorectal cancer (CRC) patients, but this advantage might be mitigated by the theoretical risks of short- and mid-term complications in the cases of contextual self-expandable metal stent (SEMS) positioning, which might also affect survival rates. Materials and Methods: We reviewed all available literature from Medline and Scopus databases to study the role of chemotherapy with or without the simultaneous administration of targeted therapy in increasing the risk of the complications after SEMS positioning and, eventually, in affecting the survival rates. Results: Thirteen retrospective studies and 1 randomized controlled trial (RCT) were eligible for the present analysis. The study group consisted of a total of 682 patients. A total of 305 patients were treated with conventional chemotherapy, 212 with conventional chemotherapy also containing targeted therapy, and 165 with no chemotherapy administration. Chemotherapy administration did not increase the rate of SEMS-related complications and these complications did not affect the overall survival rates. Conclusion: Chemotherapy administration is not associated with a higher risk of SEMS-related complications and a reduction in the survival rates.
C1 [Scotti, Giorgia Burrelli; Sapienza, Paolo; Lapolla, Pierfrancesco; Crocetti, Daniele; Tarallo, Mariarita; Brachini, Gioia; Mingoli, Andrea; Fiori, Enrico] Sapienza Univ Rome, Dept Surg Pietro Valdoni, Viale Policlin 155, I-00161 Rome, Italy.
C3 Sapienza University Rome
RP Crocetti, D (corresponding author), Sapienza Univ Rome, Dept Surg Pietro Valdoni, Viale Policlin 155, I-00161 Rome, Italy.
EM daniele.crocetti@uniroma1.it
RI MORELLI, ANDREA/D-1515-2018; Crocetti, Daniele/G-8694-2014; Burrelli
   Scotti, Giorgia/JFS-8843-2023; Sapienza, Paolo/AAL-7381-2020; Lapolla,
   Pierfrancesco/AAT-8407-2021
OI Crocetti, Daniele/0000-0001-9950-3553; Lapolla,
   Pierfrancesco/0000-0002-3088-5263
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NR 30
TC 2
Z9 2
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 0258-851X
EI 1791-7549
J9 IN VIVO
JI In Vivo
PD MAY-JUN
PY 2022
VL 36
IS 3
BP 1053
EP 1058
DI 10.21873/invivo.12802
PG 6
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 1C6DU
UT WOS:000793208100001
PM 35478131
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU McFall, T
   Stites, EC
AF McFall, Thomas
   Stites, Edward Cooper
TI A mechanism for the response of KRAS<SUP>G13D</SUP> expressing
   colorectal cancers to EGFR inhibitors
SO MOLECULAR & CELLULAR ONCOLOGY
LA English
DT Article
DE KRAS; personalized medicine; targeted therapy; systems biology;
   mathematical models; oncogene; GTPase; EGFR
ID KRAS; CHEMOTHERAPY; ASSOCIATION; ACTIVATION
AB Previous analysis of Phase 3 clinical trial data for colorectal cancer patients treated with cetuximab revealed that patients harboring a KRAS mutation did not benefit from treatment. This finding set the stage for one of the first examples of cancer personalized medicine. Confusingly, patients with a Glycine to Aspartic Acid mutation at amino acid 13 of KRAS (KRAS(G13D)) appeared to respond positively to cetuximab, suggesting this mutation is an exception to the rule that KRAS mutations confer resistance to Epidermal Growth Factor Receptor (EGFR) inhibitors. Oncologists have stated that the mechanism that explains why the KRAS(G13D) mutation is an exception should be identified before KRAS(G13D) colorectal cancer patients should be treated differently. We have recently elucidated this mechanism using mathematical modeling of the KRAS biochemical system coupled with experimental biology. The mechanism we revealed involves a cetuximab-mediated reduction in HRAS and NRAS signaling within KRAS(G13D) cancer cells, owing to impaired binding of KRAS(G13D) to the tumor suppressor, Neurofibromin (NF1).
C1 [McFall, Thomas; Stites, Edward Cooper] Salk Inst Biol Studies, Integrat Biol Lab, 10010 N Torrey Pines Rd, La Jolla, CA 92037 USA.
C3 Salk Institute
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 NIH [K22CA216318, T32CA009370, P30CA014195]
FX This project was supported NIH K22CA216318, NIH T32CA009370 and NIH
   P30CA014195.
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U2 2
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PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
EI 2372-3556
J9 MOL CELL ONCOL
JI MOL. CELL ONCOL.
PD MAR 3
PY 2020
VL 7
IS 2
AR 1701914
DI 10.1080/23723556.2019.1701914
EA JAN 2020
PG 3
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA KS9WU
UT WOS:000507472400001
PM 32158916
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Peng, F
   Fan, HL
   Li, S
   Peng, C
   Pan, XQ
AF Peng, Fu
   Fan, Huali
   Li, Sui
   Peng, Cheng
   Pan, Xiaoqi
TI MicroRNAs in Epithelial-Mesenchymal Transition Process of Cancer:
   Potential Targets for Chemotherapy
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE miRNA; cancer; epithelial-mesenchymal transition; drug candidates
ID NEGATIVE BREAST-CANCER; GASTRIC-CANCER; INHIBITS PROLIFERATION;
   COLORECTAL-CANCER; TUMOR-SUPPRESSOR; E-CADHERIN; EMT; CELLS; INVASION;
   METASTASIS
AB In the last decades, a kind of small non-coding RNA molecules, called as microRNAs, has been applied as negative regulators in various types of cancer treatment through down-regulation of their targets. More recent studies exert that microRNAs play a critical role in the EMT process of cancer, promoting or inhibiting EMT progression. Interestingly, accumulating evidence suggests that pure compounds from natural plants could modulate deregulated microRNAs to inhibit EMT, resulting in the inhibition of cancer development. This small essay is on the purpose of demonstrating the significance and function of microRNAs in the EMT process as oncogenes and tumor suppressor genes according to studies mainly conducted in the last four years, providing evidence of efficient target therapy. The review also summarizes the drug candidates with the ability to restrain EMT in cancer through microRNA regulation.
C1 [Peng, Fu; Fan, Huali; Li, Sui] Sichuan Univ, West China Sch Pharm, Dept Pharmacol,Sichuan Engn Lab Plant Sourced Dru, Key Lab Drug Targeting & Drug Delivery Syst,Educ, Chengdu 610041, Peoples R China.
   [Peng, Fu; Fan, Huali; Li, Sui] Sichuan Univ, West China Sch Pharm, Sichuan Res Ctr Drug Precis Ind Technol, Chengdu 610041, Peoples R China.
   [Peng, Cheng; Pan, Xiaoqi] Chengdu Univ Tradit Chinese Med, State Key Lab Southwestern Chinese Med Resources, Chengdu 611137, Peoples R China.
C3 Sichuan University; Sichuan University; Chengdu University of
   Traditional Chinese Medicine
RP Peng, C; Pan, XQ (corresponding author), Chengdu Univ Tradit Chinese Med, State Key Lab Southwestern Chinese Med Resources, Chengdu 611137, Peoples R China.
EM fujing126@yeah.net; hwari_f@163.com; lisui98@163.com;
   pengchengchengdu@126.com; panxiaoqi1104@cdutcm.edu.cn
RI CHENG, PENG/HNP-4206-2023; PENG, Fu/KRQ-8632-2024
OI Peng, Cheng/0000-0003-3303-906X; PENG, Fu/0000-0003-0289-4426
FU National Natural Science Foundation of China [82003879, 82004056]; Youth
   Talent Promotion Project of China Association for Science and Technology
   [CACM2020-QNRC1-01]; Key Project of Science and Technology Department of
   Sichuan Province [20ZDYF3092]; Open Research Fund of Chengdu University
   of Traditional Chinese Medicine Key Laboratory of Systematic Research of
   Distinctive Chinese Medicine Resources in Southwest China
FX This research was funded by the National Natural Science Foundation of
   China (82003879; 82004056), Youth Talent Promotion Project of China
   Association for Science and Technology (CACM2020-QNRC1-01), the Key
   Project of Science and Technology Department of Sichuan Province (No.
   20ZDYF3092), and the Open Research Fund of Chengdu University of
   Traditional Chinese Medicine Key Laboratory of Systematic Research of
   Distinctive Chinese Medicine Resources in Southwest China.
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NR 133
TC 14
Z9 15
U1 2
U2 18
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 JUL
PY 2021
VL 22
IS 14
AR 7526
DI 10.3390/ijms22147526
PG 19
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA TO4BH
UT WOS:000676858800001
PM 34299149
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Xiao, A
   Fakih, M
AF Xiao, Annie
   Fakih, Marwan
TI KRAS G12C Inhibitors in the Treatment of Metastatic Colorectal Cancer
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE Combination therapies; KRAS G12C inhibitor resistance mechanisms; RAS
   inhibitors; Targeted therapy
ID SOLID TUMORS; CODON 12; SOTORASIB; COMBINATION; DABRAFENIB; TRAMETINIB;
   BIOMARKERS; EFFICACY; MUTATION; FOLFIRI
AB KRAS mutations contribute substantially to the overall colorectal cancer burden and have long been a focus of drug development efforts. After a lengthy preclinical road, KRAS inhibition via the G12C allele has finally become a therapeutic reality. Unlike in NSCLC, early studies of KRAS inhibitors in CRC struggled to demonstrate single agent activity. Investigation into these tissue-specific treatment differences has led to a deeper understanding of the complexities of MAPK signaling and the diverse adaptive feedback responses to KRAS inhibition. EGFR reactivation has emerged as a principal resistance mechanism to KRAS inhibitor monotherapy. Thus, the field has pivoted to dual EGFR/KRAS blockade with promising efficacy. Despite significant strides in the treatment of KRAS G12C mutated CRC, new challenges are on the horizon. Alternative RTK reactivation and countless acquired molecular resistance mechanisms have shifted the treatment goalpost. This review focuses on the historical and contemporary clinical strategies of targeting KRAS G12C alterations in CRC and highlights future directions to overcome treatment challenges.
C1 [Xiao, Annie; Fakih, Marwan] City Hope Comprehens Canc Ctr, Dept Med Oncol & Therapeut Res, Pavil,Room 3208,1500 E Duarte Rd, Duarte, CA 91010 USA.
C3 City of Hope
RP Fakih, M (corresponding author), City Hope Comprehens Canc Ctr, Dept Med Oncol & Therapeut Res, Pavil,Room 3208,1500 E Duarte Rd, Duarte, CA 91010 USA.
EM mfakih@coh.org
OI Fakih, Marwan/0000-0002-6554-5488
FX MF reports research funding from AgenusBio (institution) , Bristol-Myers
   Squibb (institution) , Genentech (institution) , and Verastem
   (institution) ; consulting/advisory relationships with AbbVie,
   AstraZeneca, Bristol-Myers Squibb, Incyte Corporation, Janssen, Pfizer,
   and Taiho Oncology; and scientific advisory board for Bayer Corporation,
   Eisai, Entos, Inc., GlaxoSmithKline, Merck, Mirati Therapeutics, Inc.,
   Nouscom, and Roche/Genentech. The other authors have no conflicts of
   interest to report.
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NR 51
TC 1
Z9 1
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 199
EP 206
DI 10.1016/j.clcc.2024.05.004
EA AUG 2024
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA G4V3T
UT WOS:001316629800001
PM 38825433
DA 2025-01-04
ER

PT J
AU Ren, XX
   Chen, WK
   Yang, QX
   Li, XX
   Xu, LX
AF Ren, Xiaoxue
   Chen, Weikang
   Yang, Qingxia
   Li, Xiaoxing
   Xu, Lixia
TI Patient-derived cancer organoids for drug screening: Basic technology
   and clinical application
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Review
DE cancer organoids; drug screening; precision medicine
ID MODELING COLORECTAL-CANCER; IN-VITRO EXPANSION; ON-A-CHIP; STEM-CELL;
   LONG-TERM; HUMAN COLON; LIVER; DISEASE; CULTURES; BIOBANK
AB Cancer organoids, a three-dimensional (3D) culture system of cancer cells derived from tumor tissues, recapitulate physiological structure of the parental tumor. Different tumor organoids have been established for a variety of tumor types, such as colorectal, liver, stomach, pancreatic and brain tumors. Some tumor organoid biobanks are built to screen and discover novel antitumor drug targets. Moreover, patients-derived tumor organoids (PDOs) could predict treatment response to chemoradiotherapy, targeted therapy and immunotherapy to provide guidance for personalized cancer therapy. In this review, we provide an updated overview of tumor organoid development, summarize general approach to establish tumor organoids, and discuss the application of anti-cancer drug screening based on tumor organoid and its application in personalized therapy. We also outline the opportunities and challenges for organoids to guide precision medicine.
C1 [Ren, Xiaoxue; Yang, Qingxia; Xu, Lixia] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Oncol, Guangzhou 510080, Guangdong, Peoples R China.
   [Ren, Xiaoxue; Chen, Weikang; Yang, Qingxia; Li, Xiaoxing; Xu, Lixia] Sun Yat Sen Univ, Affiliated Hosp 1, Inst Precis Med, Guangzhou, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University
RP Xu, LX (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 1, Dept Oncol, Guangzhou 510080, Guangdong, Peoples R China.
EM xulixia@mail.sysu.edu.cn
RI yang, qingxia/IRZ-2603-2023; Li, Xiaoxing/B-9114-2008
OI Li, Xiaoxing/0000-0001-8791-7505
FU National Natural Science Foundation of China [82173191]; Guangdong Basic
   and Applied Basic Research Foundation [2019B151502009]
FX The project was supported by the National Natural Science Foundation of
   China (82173191) and Guangdong Basic and Applied Basic Research
   Foundation (2019B151502009).
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NR 112
TC 29
Z9 31
U1 4
U2 43
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD AUG
PY 2022
VL 37
IS 8
SI SI
BP 1446
EP 1454
DI 10.1111/jgh.15930
EA JUL 2022
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 3M4QE
UT WOS:000821392000001
PM 35771719
DA 2025-01-04
ER

PT J
AU Zhao, YY
   Xu, JJ
   Le, VM
   Gong, QY
   Li, SY
   Gao, F
   Ni, L
   Liu, JW
   Liang, X
AF Zhao, Yuyu
   Xu, Jiajun
   Van Minh Le
   Gong, Qianyi
   Li, Shaoyu
   Gao, Feng
   Ni, Lei
   Liu, Jianwen
   Liang, Xin
TI EpCAM Aptamer-Functionalized Cationic Liposome-Based Nanoparticles
   Loaded with miR-139-5p for Targeted Therapy in Colorectal Cancer
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE nanoparticle; CRC; targeted therapy; miR-139-5p
ID III COLON-CANCER; DSPE-PEG; STAGE-II; CARCINOMA; SURVIVAL; DELIVERY
AB Colorectal cancer (CRC) is one of the most common cancers worldwide. MicroRNAs (miRNAs) play a vital role in a variety of biology processes. Our previous work identified miR-139-5p as a tumor suppressor gene overexpressed in CRC that assisted in inhibiting progression of cancer. The main challenge of miRNAs as therapeutic agents is their rapid degradation in plasma, poor uptake, and off-target effects. Therefore, the development of miRNA-based therapies is necessary. In this study, we developed a cationic liposome-based nanoparticle loaded with miR-139-5p (miR-139-5p-HSPC/DOTAP/Chol/DSPE-PEG2000-COOH nanoparticles, MNPs) and surface-decorated with epithelial cell adhesion molecule (EpCAM) aptamer (Apt) (miR-139-5p-EpCAM Apt-HSPC/DOTAP/Chol/DSPE-PEG2000-COOH nanoparticles, MANPs) for the targeted treatment of CRC. The size of MANPs was 150.3 +/- 8.8 nm, which had a round-shaped appearance and functional dispersion capabilities. It also showed negligible hemolysis in the blood. MANPs markedly inhibited the proliferation, migration, and invasion of one or more CRC cell lines in vitro. Furthermore, we demonstrated the uptake and targeting ability of MANPs in vivo and in vitro. MANPs inhibit the growth of HCT8 cells in vitro and have a significant tumor suppressive effect on subcutaneous HCT8 colorectal tumor mice. Our results demonstrated that MANPs were an effective carrier approach to deliver therapeutic miRNAs to CRC.
C1 [Zhao, Yuyu; Gong, Qianyi; Liu, Jianwen; Liang, Xin] East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Sch Pharm, Shanghai, Peoples R China.
   [Zhao, Yuyu; Gong, Qianyi; Liu, Jianwen; Liang, Xin] East China Univ Sci & Technol, Shanghai Key Lab New Drug Design, Shanghai, Peoples R China.
   [Xu, Jiajun; Gao, Feng] East China Univ Sci & Technol, Sch Pharm, Dept Pharmaceut, Shanghai 200237, Peoples R China.
   [Van Minh Le] Natl Inst Med Mat, Res Ctr Ginseng & Med Mat, Ho Chi Minh City, Vietnam.
   [Li, Shaoyu] Xinjiang Med Univ, Affiliated Hosp 3, Dept Clin Lab, Urumqi, Xinjiang, Peoples R China.
   [Gao, Feng] East China Univ Sci & Technol, Shanghai Key Lab Funct Mat Chem, Shanghai 200237, Peoples R China.
   [Gao, Feng] East China Univ Sci & Technol, Shanghai Key Lab New Drug Design, Shanghai, Peoples R China.
   [Ni, Lei] Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, Dept Respirat, 197 Ruijin Rd 2, Shanghai 200025, Peoples R China.
C3 East China University of Science & Technology; East China University of
   Science & Technology; East China University of Science & Technology;
   Xinjiang Medical University; East China University of Science &
   Technology; East China University of Science & Technology; Shanghai Jiao
   Tong University
RP Liu, JW; Liang, X (corresponding author), East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Sch Pharm, Shanghai, Peoples R China.; Liu, JW; Liang, X (corresponding author), East China Univ Sci & Technol, Shanghai Key Lab New Drug Design, Shanghai, Peoples R China.; Ni, L (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, Dept Respirat, 197 Ruijin Rd 2, Shanghai 200025, Peoples R China.
EM nilei625@yahoo.com; liujian@ecust.edu.cn; xin.liang@ecust.edu.cn
RI li, shaoyu/ITT-9848-2023; XU, Jiajun/IQU-6535-2023; Van Minh,
   Le/JAN-6420-2023
OI Liu, Jianwen/0000-0003-4149-4257; Le, Van Minh/0000-0003-4541-2319
FU Science and Technology Commission of Shanghai Municipality
   [17430741600]; National Natural Science Foundation of China [81860378,
   81873050]
FX This work was financially supported by the Science and Technology
   Commission of Shanghai Municipality (no. 17430741600) and the National
   Natural Science Foundation of China (no. 81860378, 81873050).
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NR 39
TC 62
Z9 65
U1 5
U2 97
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1543-8384
EI 1543-8392
J9 MOL PHARMACEUT
JI Mol. Pharm.
PD NOV
PY 2019
VL 16
IS 11
BP 4696
EP 4710
DI 10.1021/acs.molpharmaceut.9b00867
PG 15
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA JK5PC
UT WOS:000494894300025
PM 31589818
DA 2025-01-04
ER

PT J
AU Tantoy, IY
   Cooper, BA
   Dhruva, A
   Cataldo, J
   Paul, SM
   Conley, YP
   Hammer, M
   Wright, F
   Dunn, LB
   Levine, JD
   Miaskowski, C
AF Tantoy, Ilufredo Y.
   Cooper, Bruce A.
   Dhruva, Anand
   Cataldo, Janine
   Paul, Steven M.
   Conley, Yvette P.
   Hammer, Marilyn
   Wright, Fay
   Dunn, Laura B.
   Levine, Jon D.
   Miaskowski, Christine
TI Changes in the Occurrence, Severity, and Distress of Symptoms in
   Patients With Gastrointestinal Cancers Receiving Chemotherapy
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Gastrointestinal cancer; chemotherapy; targeted therapy; severity;
   distress; pain; fatigue; sleep disturbance; taste changes; feeling
   drowsy
ID QUALITY-OF-LIFE; INDUCED PERIPHERAL NEUROPATHY; COLORECTAL-CANCER;
   INDUCED NAUSEA; BREAST-CANCER; PSYCHOLOGICAL DISTRESS; PERFORMANCE
   STATUS; TASTE ALTERATIONS; ASSESSMENT SCALE; RESPONSE SHIFT
AB Context. Studies on multiple dimensions of the symptom experience of patients with gastrointestinal cancers are extremely limited.
   Objective. Purpose was to evaluate for changes over time in the occurrence, severity, and distress of seven common symptoms in these patients.
   Methods. Patients completed Memorial Symptom Assessment Scale, six times over two cycles of chemotherapy (CTX). Changes over time in occurrence, severity, and distress of pain, lack of energy, nausea, feeling drowsy, difficulty sleeping, and change in the way food tastes were evaluated using multilevel regression analyses. In the conditional models, effects of treatment group (i.e., with or without targeted therapy), age, number of metastatic sites, time from cancer diagnosis, number of prior cancer treatments, cancer diagnosis, and CTX regimen on enrollment levels, as well as the trajectories of symptom occurrence, severity, and distress were evaluated.
   Results. Although the occurrence rates for pain, lack of energy, feeling drowsy, difficulty sleeping, and change in the way food tastes declined over the two cycles of CTX, nausea and numbness/tingling in hands/feet had more complex patterns of occurrence. Severity and distress ratings for the seven symptoms varied across the two cycles of CTX.
   Conclusions. Demographic and clinical characteristics associated with differences in enrollment levels as well as changes over time in occurrence, severity, and distress of these seven common symptoms were highly variable. These findings can be used to identify patients who are at higher risk for more severe and distressing symptoms during CTX and to enable the initiation of preemptive symptom management interventions. (C) 2017 American Academy of Hospice and Palliative Medicine. Published by Elsevier Inc. All rights reserved.
C1 [Tantoy, Ilufredo Y.; Cooper, Bruce A.; Cataldo, Janine; Paul, Steven M.; Miaskowski, Christine] Univ Calif San Francisco, Sch Nursing, San Francisco, CA 94143 USA.
   [Dhruva, Anand; Levine, Jon D.] Univ Calif San Francisco, Sch Med, San Francisco, CA USA.
   [Conley, Yvette P.] Univ Pittsburgh, Sch Nursing, Pittsburgh, PA 15261 USA.
   [Hammer, Marilyn] Mt Sinai Med Ctr, Dept Nursing, New York, NY 10029 USA.
   [Wright, Fay] Yale Univ, Sch Nursing, New Haven, CT 06536 USA.
   [Dunn, Laura B.] Stanford Univ, Sch Med, Palo Alto, CA USA.
C3 University of California System; University of California San Francisco;
   University of California System; University of California San Francisco;
   Pennsylvania Commonwealth System of Higher Education (PCSHE); University
   of Pittsburgh; Icahn School of Medicine at Mount Sinai; Yale University;
   Stanford University
RP Miaskowski, C (corresponding author), Univ Calif San Francisco, Dept Physiol Nursing, 2 Koret Way N631F, San Francisco, CA 94143 USA.
EM chris.miaskowski@ucsf.edu
RI Wright, Fay/AAH-9449-2020; Paul, Steve/ABE-5400-2020
OI Wright, Fay/0000-0001-9636-0411; Tantoy, Ilufredo/0000-0002-0193-0280;
   Conley, Yvette/0000-0002-1784-6067; Levine, Jon/0000-0003-0681-5545
FU National Cancer Institute (NCI) [CA134900]; K05 award from the NCI
   [CA168960]; National Institutes of Health (NIH) T32 grant [NR007088];
   T32 postdoctoral fellowship [NR008346]
FX This study was funded by a grant from the National Cancer Institute
   (NCI, CA134900). Dr. Christine Miaskowski is an American Cancer Society
   Clinical Research professor and is funded by a K05 award from the NCI
   (CA168960). Mr. Tantoy was funded by a National Institutes of Health
   (NIH) T32 grant (NR007088). Dr. Wright was funded by a T32 postdoctoral
   fellowship (NR008346).
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NR 72
TC 21
Z9 22
U1 0
U2 13
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0885-3924
EI 1873-6513
J9 J PAIN SYMPTOM MANAG
JI J. Pain Symptom Manage.
PD MAR
PY 2018
VL 55
IS 3
BP 808
EP 834
DI 10.1016/j.jpainsymman.2017.10.004
PG 27
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
   Neurology
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Health Care Sciences & Services; General & Internal Medicine;
   Neurosciences & Neurology
GA FX9UL
UT WOS:000426453500018
PM 29051114
OA Green Accepted, Green Published
DA 2025-01-04
ER

PT J
AU Küçükköse, E
   Wensink, GE
   Roelse, CM
   van Schelven, SJ
   Raats, DAE
   Boj, SF
   Koopman, M
   Laoukili, J
   Roodhart, JML
   Kranenburg, O
AF Kucukkose, Emre
   Wensink, G. Emerens
   Roelse, Celine M.
   van Schelven, Susanne J.
   Raats, Danielle A. E.
   Boj, Sylvia F.
   Koopman, Miriam
   Laoukili, Jamila
   Roodhart, Jeanine M. L.
   Kranenburg, Onno
TI Mismatch Repair Status in Patient-Derived Colorectal Cancer Organoids
   Does Not Affect Intrinsic Tumor Cell Sensitivity to Systemic Therapy
SO CANCERS
LA English
DT Article
DE organoids; colorectal cancer; deficient mismatch repair; mutation; drug
   screens
ID MICROSATELLITE-INSTABILITY; BRAF MUTATION; COLON; CHEMOTHERAPY;
   CETUXIMAB; EFFICACY; BENEFIT
AB Simple Summary: The large majority of patients with metastatic colorectal cancer (mCRC) receive chemotherapy with or without targeted therapy. Tumors with a deficient DNA mismatch repair (dMMR) system respond poorly to systemic therapy and are associated with poor prognosis. However, it is unclear whether dMMR causes therapy resistance in a tumor cell-intrinsic manner, or whether other mechanisms underlie this association. We address this issue by exposing a panel of MMR-deficient and -proficient Patient-Derived Organoids (PDOs) to a series of clinically relevant drugs. We show that MMR status did not correlate with the response of PDOs to any of the drugs tested. By contrast, the presence of activating mutations in the KRAS and BRAF oncogenes was significantly associated with resistance to chemotherapy and sensitivity to drugs targeting oncogene-activated pathways. We conclude that tumor cell-intrinsic signals link oncogene status, but not MMR status, to variation in therapy response in CRC.DNA mismatch repair deficiency (dMMR) in metastatic colorectal cancer (mCRC) is associated with poor survival and a poor response to systemic treatment. However, it is unclear whether dMMR results in a tumor cell-intrinsic state of treatment resistance, or whether alternative mechanisms play a role. To address this, we generated a cohort of MMR-proficient and -deficient Patient-Derived Organoids (PDOs) and tested their response to commonly used drugs in the treatment of mCRC, including 5-fluorouracil (5-FU), oxaliplatin, SN-38, binimetinib, encorafenib, and cetuximab. MMR status did not correlate with the response of PDOs to any of the drugs tested. In contrast, the presence of activating mutations in the KRAS and BRAF oncogenes was significantly associated with resistance to chemotherapy and sensitivity to drugs targeting oncogene-activated pathways. We conclude that mutant KRAS and BRAF impact the intrinsic sensitivity of tumor cells to chemotherapy and targeted therapy. By contrast, tumor cell-extrinsic mechanisms-for instance signals derived from the microenvironment-must underlie the association of MMR status with therapy response. Future drug screens on rationally chosen cohorts of PDOs have great potential in developing tailored therapies for specific CRC subtypes including, but not restricted to, those defined by BRAF/KRAS and MMR status.
C1 [Kucukkose, Emre; Roelse, Celine M.; van Schelven, Susanne J.; Raats, Danielle A. E.; Laoukili, Jamila; Roodhart, Jeanine M. L.; Kranenburg, Onno] Univ Med Ctr Utrecht, Div Imaging & Canc, Lab Translat Oncol, NL-3584 CX Utrecht, Netherlands.
   [Wensink, G. Emerens; Koopman, Miriam; Roodhart, Jeanine M. L.] Univ Med Ctr Utrecht, Dept Med Oncol, Div Imaging & Canc, NL-3584 CX Utrecht, Netherlands.
   [Boj, Sylvia F.] Fdn Hubrecht Organoid Technol, NL-3584 CM Utrecht, Netherlands.
   [Kranenburg, Onno] Univ Utrecht, Utrecht Platform Organoid Technol, NL-3584 CX Utrecht, Netherlands.
C3 Utrecht University; Utrecht University Medical Center; Utrecht
   University; Utrecht University Medical Center; Utrecht University
RP Roodhart, JML; Kranenburg, O (corresponding author), Univ Med Ctr Utrecht, Div Imaging & Canc, Lab Translat Oncol, NL-3584 CX Utrecht, Netherlands.; Roodhart, JML (corresponding author), Univ Med Ctr Utrecht, Dept Med Oncol, Div Imaging & Canc, NL-3584 CX Utrecht, Netherlands.; Kranenburg, O (corresponding author), Univ Utrecht, Utrecht Platform Organoid Technol, NL-3584 CX Utrecht, Netherlands.
EM e.kucukkose@umcutrecht.nl; g.e.wensink@umcutrecht.nl;
   c.roelse@umcutrecht.nl; s.j.vanschelven@umcutrecht.nl;
   d.a.e.raats@umcutrecht.nl; s.boj@hub4organoids.nl;
   m.koopman-6@umcutrecht.nl; j.laoukili@umcutrecht.nl;
   j.roodhart@umcutrecht.nl; o.kranenburg@umcutrecht.nl
RI Kucukkose, Emre/HMD-6982-2023
OI Roelse, Celine M./0000-0002-9652-4794; Kucukkose,
   Emre/0000-0002-8983-9464; Wensink, Emerens/0000-0002-4103-5811
FU Dutch Cancer Society (KWF/Alpe d'HuZes) [UU-10660]
FX This research was funded by the Dutch Cancer Society (KWF/Alpe d'HuZes),
   grant number #UU-10660.
CR Aasebo KO, 2019, CANCER MED-US, V8, P3623, DOI 10.1002/cam4.2205
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NR 32
TC 4
Z9 4
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD NOV
PY 2021
VL 13
IS 21
AR 5434
DI 10.3390/cancers13215434
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WY3EZ
UT WOS:000719165000001
PM 34771595
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Shimada, Y
   Yagi, R
   Kameyama, H
   Nagahashi, M
   Ichikawa, H
   Tajima, Y
   Okamura, T
   Nakano, M
   Nakano, M
   Sato, Y
   Matsuzawa, T
   Sakata, J
   Kobayashi, T
   Nogami, H
   Maruyama, S
   Takii, Y
   Kawasaki, T
   Homma, K
   Izutsu, H
   Kodama, K
   Ring, JE
   Protopopov, A
   Lyle, S
   Okuda, S
   Akazawa, K
   Wakai, T
AF Shimada, Yoshifumi
   Yagi, Ryoma
   Kameyama, Hitoshi
   Nagahashi, Masayuki
   Ichikawa, Hiroshi
   Tajima, Yosuke
   Okamura, Takuma
   Nakano, Mae
   Nakano, Masato
   Sato, Yo
   Matsuzawa, Takeaki
   Sakata, Jun
   Kobayashi, Takashi
   Nogami, Hitoshi
   Maruyama, Satoshi
   Takii, Yasumasa
   Kawasaki, Takashi
   Homma, Kei-ichi
   Izutsu, Hiroshi
   Kodama, Keisuke
   Ring, Jennifer E.
   Protopopov, Alexei
   Lyle, Stephen
   Okuda, Shujiro
   Akazawa, Kohei
   Wakai, Toshifumi
TI Utility of comprehensive genomic sequencing for detecting HER2-positive
   colorectal cancer
SO HUMAN PATHOLOGY
LA English
DT Article
DE HER2; Colorectal cancer; Next-generation sequencing; Comprehensive
   genomic sequencing; Immunohistochemistry; Fluorescence in situ
   hybridization
ID IN-SITU HYBRIDIZATION; BREAST-CANCER; CLINICAL-IMPLICATIONS; HER2;
   AMPLIFICATION; OVEREXPRESSION; TRASTUZUMAB; EXPRESSION; RESISTANCE;
   CARCINOMA
AB HER2-targeted therapy is considered effective for KRAS codon 12/13 wild-type, HER2-positive metastatic colorectal cancer (CRC). In general, HER2 status is determined by the use of immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH). Comprehensive genomic sequencing (CGS) enables the detection of gene mutations and copy number alterations including KRAS mutation and HER2 amplification; however, little is known about the utility of CGS for detecting HER2-positive CRC. To assess its utility, we retrospectively investigated 201 patients with stage I-IV CRC. The HER2 status of the primary site was assessed using IHC and FISH, and HER2 amplification of the primary site was also assessed using CGS, and the findings of these approaches were compared in each patient. CGS successfully detected alterations in 415 genes including KRAS codon 12/13 mutation and HER2 amplification. Fifty-nine (29%) patients had a KRAS codon 12/13 mutation. Ten (5%) patients were diagnosed as HER2 positive because of HER2 MC 3+, and the same 10 (5%) patients had HER2 amplification evaluated using CGS. The results of HER2 status and HER2 amplification were completely identical in all 201 patients (P < .001). Nine of the 10 HER2-positive patients were KRAS 12/13 wild-type and were considered possible candidates for HER2-targeted therapy. CGS has the same utility as IHC and FISH for detecting HER2-positive patients who are candidates for HER2-targeted therapy, and facilitates precision medicine and tailor-made treatment. (C) 2017 The Authors. Published by Elsevier Inc.
C1 [Shimada, Yoshifumi; Yagi, Ryoma; Kameyama, Hitoshi; Nagahashi, Masayuki; Ichikawa, Hiroshi; Tajima, Yosuke; Okamura, Takuma; Nakano, Mae; Nakano, Masato; Sakata, Jun; Kobayashi, Takashi; Wakai, Toshifumi] Niigata Univ, Div Digest & Gen Surg, Grad Sch Med & Dent Sci, Niigata 9518510, Japan.
   [Sato, Yo; Matsuzawa, Takeaki] Niigata Univ Med & Dent Hosp, Uonuma Inst Community Med, Dept Digest & Gen Surg, Niigata 9497302, Japan.
   [Nogami, Hitoshi; Maruyama, Satoshi; Takii, Yasumasa] Niigata Canc Ctr Hosp, Dept Surg, Niigata 9518566, Japan.
   [Kawasaki, Takashi; Homma, Kei-ichi] Niigata Canc Ctr Hosp, Dept Pathol, Niigata 9518566, Japan.
   [Izutsu, Hiroshi; Kodama, Keisuke] Denka Co Ltd, Denka Innovat Ctr, Life Innovat Res Inst, Diagnost Res Dept, Tokyo 1948560, Japan.
   [Ring, Jennifer E.; Protopopov, Alexei; Lyle, Stephen] KEW Inc, Cambridge, MA 02139 USA.
   [Lyle, Stephen] Univ Massachusetts, Sch Med, Worcester, MA 01655 USA.
   [Okuda, Shujiro] Niigata Univ, Div Bioinformat, Grad Sch Med & Dent Sci, Niigata 9518510, Japan.
   [Akazawa, Kohei] Niigata Univ, Dept Med Informat, Grad Sch Med & Dent Sci, Niigata 9518510, Japan.
C3 Niigata University; Niigata University; Denka Company Limited;
   University of Massachusetts System; University of Massachusetts
   Worcester; Niigata University; Niigata University
RP Shimada, Y (corresponding author), Niigata Univ, Div Digest & Gen Surg, Grad Sch Med & Dent Sci, Niigata 9518510, Japan.
EM shimaday@med.niigata-u.ac.jp
RI Tajima, Yosuke/HDN-8985-2022; Okuda, Shujiro/D-1700-2016; Ichikawa,
   Hiroshi/AER-0034-2022; Nagahashi, Masayuki/AAB-4202-2020
FU Denka Co, Ltd, Tokyo, Japan; Ministry of Education, Culture, Sports,
   Science, and Technology of Japan [15K10130]; Grants-in-Aid for
   Scientific Research [15K10130] Funding Source: KAKEN
FX This project was supported by funding from Denka Co, Ltd, Tokyo, Japan.
   Y. Shimada is supported in part by a Grant-in-Aid for Scientific
   Research, no. 15K10130 (Y.S.), from the Ministry of Education, Culture,
   Sports, Science, and Technology of Japan.
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NR 34
TC 29
Z9 31
U1 0
U2 3
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 AUG
PY 2017
VL 66
BP 1
EP 9
DI 10.1016/j.humpath.2017.02.004
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA FI4AF
UT WOS:000411911000001
PM 28235632
OA Green Submitted, hybrid
DA 2025-01-04
ER

PT J
AU Zhou, CF
   Zhang, J
AF Zhou, Chenfei
   Zhang, Jun
TI Immunotherapy-based combination strategies for treatment of
   gastrointestinal cancers: current status and future prospects
SO FRONTIERS OF MEDICINE
LA English
DT Review
DE gastrointestinal cancer; immune checkpoint inhibitor; combination
   therapy
ID ENDOTHELIAL GROWTH-FACTOR; METASTATIC COLORECTAL-CANCER; MISMATCH REPAIR
   DEFICIENCY; DENDRITIC CELLS; IMMUNE CHECKPOINTS; 1ST-LINE TREATMENT;
   GASTRIC-CANCER; DOUBLE-BLIND; TUMOR-CELLS; OPEN-LABEL
AB Strategies in comprehensive therapy for gastrointestinal (GI) cancer have been optimized in the last decades to improve patients' outcomes. However, treatment options remain limited for late-stage or refractory diseases. The efficacy of immune checkpoint inhibitors (ICIs) for treatment of refractory GI cancer has been confirmed by randomized clinical trials. In 2017, pembrolizumab was approved by the US Food and Drug Administration as the first agent for treatment of metastatic solid tumors with mismatch repair deficiency, especially for colorectal cancer. Given the different mechanisms, oncologists have focused on determining whether ICIs-based combination strategies could achieve higher efficacy than conventional therapy alone in late-stage or even front-line treatment of GI cancer. This review discusses the current status of combining immune checkpoint inhibitors with molecular targeted therapy, chemotherapy, or radiotherapy in GI cancer in terms of mechanisms, safety, and efficacy to provide basis for future research.
C1 [Zhou, Chenfei; Zhang, Jun] Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Oncol, Sch Med, Shanghai 200025, Peoples R China.
C3 Shanghai Jiao Tong University
RP Zhang, J (corresponding author), Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Oncol, Sch Med, Shanghai 200025, Peoples R China.
EM junzhang@188.com
RI ZHANG, JU/JLL-0250-2023
OI Zhang, Jun/0000-0002-7973-8416
FU National Natural Science Foundation of China [81672327, 81802319];
   Program of Shanghai Academic/Technology Research Leader [17XD1402600];
   Program for Outstanding Medical Academic Leader; Shanghai Municipal
   Education Commission-Gaofeng Clinical Medicine Grant Support [20161410];
   Development Grant for Clinical Trial [SHDC12017X06]
FX The study was supported by National Natural Science Foundation of China
   (Nos. 81672327 and 81802319) and Program of Shanghai Academic/Technology
   Research Leader (No. 17XD1402600) and Program for Outstanding Medical
   Academic Leader and Shanghai Municipal Education Commission-Gaofeng
   Clinical Medicine Grant Support (No. 20161410) and Development Grant for
   Clinical Trial (No. SHDC12017X06).
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NR 91
TC 14
Z9 15
U1 3
U2 15
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2095-0217
EI 2095-0225
J9 FRONT MED-PRC
JI Front. Med.
PD FEB
PY 2019
VL 13
IS 1
BP 12
EP 23
DI 10.1007/s11684-019-0685-9
PG 12
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA HP0CZ
UT WOS:000461334300003
PM 30796606
OA hybrid
DA 2025-01-04
ER

PT J
AU Wang, SL
   Yuan, LW
AF Wang, Shalong
   Yuan, Lianwen
TI Predictive biomarkers for targeted and cytotoxic agents in gastric
   cancer for personalized medicine
SO BIOSCIENCE TRENDS
LA English
DT Review
DE Gastric cancer; biomarkers; chemotherapy; targeted therapy; personalized
   medicine; predictive marker
ID CIRCULATING TUMOR-CELLS; MODULATES MULTIDRUG-RESISTANCE; CONFERS
   CISPLATIN RESISTANCE; HER2 GENE AMPLIFICATION; FACTOR RECEPTOR EGFR;
   PHASE-II; GASTROESOPHAGEAL JUNCTION; PROGNOSTIC-SIGNIFICANCE; 1ST-LINE
   TREATMENT; COLORECTAL-CANCER
AB Gastric cancer (GC) is the fourth most common cancer and the second leading cause of cancer. The treatment of GC remains challenging as the outcomes achieved with surgery alone or adjuvant or neoadjuvant chemotherapy and radiotherapy are relatively poor. New treatment strategies are emerging and are being tested in solid tumors including GC. Over the past few years, the treatment of metastatic colorectal cancer (CRC) has made great advances, but strategies to manage GC have improved little. Multiple drug resistance is common in GC chemotherapy and targeted therapy; some patients appear to receive treatment that is suboptimal or even inefficacious. Unfortunately, there are few validated predictive biomarkers to guide the tailored treatment of GC. ToGA and AVAGAST are two phase III trials that tested the efficacy and safety of targeted agents in advanced gastric cancer (AGC), and results clearly indicated that patients need to be selected and that targeted agents are the best hope for better results. This review aims to provide an overview of potential predictive biomarkers for cytotoxic and targeted agents in GC.
C1 [Wang, Shalong; Yuan, Lianwen] Cent S Univ, Xiangya Hosp Affiliated 2, Geriatr Surg Dept, 139 Renming Rd, Changsha 410011, Hunan, Peoples R China.
C3 Central South University
RP Yuan, LW (corresponding author), Cent S Univ, Xiangya Hosp Affiliated 2, Geriatr Surg Dept, 139 Renming Rd, Changsha 410011, Hunan, Peoples R China.
EM yuanlianwen1971@aliyun.com
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NR 92
TC 8
Z9 10
U1 0
U2 12
PU IRCA-BSSA
PI TOKYO
PA PEARL CITY KOISHIKAWA 603, 2-4-5 KASUGA, BUNKYO-KU, TOKYO, 112-0003,
   JAPAN
SN 1881-7815
EI 1881-7823
J9 BIOSCI TRENDS
JI BioSci. Trends
PD JUN
PY 2016
VL 10
IS 3
BP 171
EP 180
DI 10.5582/bst.2016.01078
PG 10
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA DQ5OC
UT WOS:000379253700002
PM 27251446
OA Bronze
DA 2025-01-04
ER

PT J
AU Chen, YX
   Chen, M
   Deng, K
AF Chen, Yuxiang
   Chen, Mo
   Deng, Kai
TI Blocking the Wnt/β-catenin signaling pathway to treat colorectal cancer:
   Strategies to improve current therapies (Review)
SO INTERNATIONAL JOURNAL OF ONCOLOGY
LA English
DT Review
DE colorectal cancer; Wnt; beta-catenin signaling pathway; occurrence;
   recurrence; inhibitors; targeted therapy
ID BETA-CATENIN; STEM-CELLS; TANKYRASE INHIBITION; VITAMIN-D; IN-VIVO; WNT;
   GROWTH; EXPRESSION; METASTASIS; RESISTANCE
AB Colorectal cancer (CRC) is one of the most common malignant tumor types occurring in the digestive system. The incidence of CRC has exhibits yearly increases and the mortality rate among patients with CRC is high. The Wnt/beta-catenin signaling pathway, which is associated with carcinogenesis, is abnormally activated in CRC. Most patients with CRC have adenomatous polyposis coli mutations, while half of the remaining patients have beta-catenin gene mutations. Therefore, targeting the Wnt/beta-catenin signaling pathway for the treatment of CRC is of clinical value. In recent years, with in-depth research on the Wnt/beta-catenin signaling pathway, inhibitors have been developed that are able to suppress or hinder the development and progression of CRC. In the present review, the role of the Wnt/beta-catenin signaling pathway in CRC is summarized, the research status on Wnt/beta-catenin pathway inhibitors is outlined and potential targets for inhibition of this pathway are presented.
C1 [Chen, Yuxiang; Deng, Kai] Sichuan Univ, Dept Gastroenterol & Hepatol, Chengdu 610041, Sichuan, Peoples R China.
   [Chen, Yuxiang; Deng, Kai] Sichuan Univ, Lab Sichuan Univ, Oxford Univ Huaxi Gastrointestinal Canc Ctr, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.
   [Chen, Mo] Sichuan Univ, Tibetan Chengdu Branch Hosp West China Hosp, Dept Gerontol, Chengdu 610041, Sichuan, Peoples R China.
   [Chen, Mo] Hosp Chengdu Off Peoples Govt Tibetan Autonomous R, Dept Gerontol, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University
RP Deng, K (corresponding author), Sichuan Univ, Dept Gastroenterol & Hepatol, Chengdu 610041, Sichuan, Peoples R China.; Deng, K (corresponding author), Sichuan Univ, Lab Sichuan Univ, Oxford Univ Huaxi Gastrointestinal Canc Ctr, West China Hosp, Chengdu 610041, Sichuan, Peoples R China.; Chen, M (corresponding author), Sichuan Univ, Tibetan Chengdu Branch Hosp West China Hosp, Dept Gerontol, Chengdu 610041, Sichuan, Peoples R China.; Chen, M (corresponding author), Hosp Chengdu Off Peoples Govt Tibetan Autonomous R, Dept Gerontol, Chengdu 610041, Sichuan, Peoples R China.
EM chenmo_1986@qq.com; dengkai@wchscu.cn
RI Wang, Zixuan/HZJ-2348-2023; Deng, Kai/JRY-2663-2023
OI Deng, Kai/0000-0002-0096-5211
FU National Natural Science Foundation of China [81600511]; Science
   Foundation of Sichuan Health and Family Planning Commission
   [20PJYY0314]; Sichuan Science and Technology Program [22ZDYF1618,
   2021YFH0005]; 1.3.5 Project for Disciplines of Excellence, West China
   Hospital, Sichuan University [2019-051, 2021-150]; Operation Funding of
   Sichuan University-University of Oxford Huaxi Joint Centre for
   Gastrointestinal Cancer [161200021]
FX The corresponding author (KD) was supported by the National Natural
   Science Foundation of China (grant no. 81600511), Science Foundation of
   Sichuan Health and Family Planning Commission (grant no. 20PJYY0314),
   Sichuan Science and Technology Program (grant nos. 22ZDYF1618 and
   2021YFH0005), 1.3.5 Project for Disciplines of Excellence, West China
   Hospital, Sichuan University (grant nos. 2019-051 and 2021-150) and
   Operation Funding of Sichuan University-University of Oxford Huaxi Joint
   Centre for Gastrointestinal Cancer (grant no. 161200021).
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NR 222
TC 20
Z9 20
U1 5
U2 29
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 FEB
PY 2023
VL 62
IS 2
AR 24
DI 10.3892/ijo.2022.5472
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 8J4FW
UT WOS:000922374300001
PM 36579676
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Aldoughaim, M
   AlSuhebany, N
   AlZahrani, M
   AlQahtani, T
   AlGhamdi, S
   Badreldin, H
   Al Alshaykh, H
AF AlDoughaim, Maha
   AlSuhebany, Nada
   AlZahrani, Mohammed
   AlQahtani, Tariq
   AlGhamdi, Sahar
   Badreldin, Hisham
   Al Alshaykh, Hana
TI Cancer Biomarkers and Precision Oncology: A Review of Recent Trends and
   Innovations
SO CLINICAL MEDICINE INSIGHTS-ONCOLOGY
LA English
DT Review
DE Cancer biomarkers; precision medicine; targeted therapy; artificial
   intelligence; pharmacogenomics
ID METASTATIC COLORECTAL-CANCER; ACUTE MYELOID-LEUKEMIA; BREAST-CANCER;
   ARTIFICIAL-INTELLIGENCE; 1ST-LINE TREATMENT; DOUBLE-BLIND; RESISTANCE;
   DRUG; THERAPY; DISCOVERY
AB The discovery of cancer-specific biomarkers has resulted in major advancements in the field of cancer diagnostics and therapeutics, therefore significantly lowering cancer-related morbidity and mortality. Cancer biomarkers can be generally classified as prognostic biomarkers that predict specific disease outcomes and predictive biomarkers that predict disease response to targeted therapeutic interventions. As research in the area of predictive biomarkers continues to grow, precision medicine becomes far more integrated in cancer treatment. This article presents a general overview on the most recent advancements in the area of cancer biomarkers, immunotherapy, artificial intelligence, and pharmacogenomics of the Middle East.
C1 [AlDoughaim, Maha; AlSuhebany, Nada; AlZahrani, Mohammed; AlQahtani, Tariq; AlGhamdi, Sahar; Badreldin, Hisham] King Saud Bin Abdul Aziz Univ Hlth Sci KSAU HS, Coll Pharm, King Abdullah Int Med Res Ctr KAIMRC, Prince Mutib Ibn Abdullah Ibn Abdulaziz Rd, Riyadh 11481, Saudi Arabia.
   [Al Alshaykh, Hana] King Faisal Specialist Hosp & Res Ctr KFSHRC, Pharmaceut Care Devis, Riyadh, Saudi Arabia.
C3 King Saud Bin Abdulaziz University for Health Sciences; King Abdullah
   International Medical Research Center (KAIMRC)
RP Aldoughaim, M (corresponding author), King Saud Bin Abdul Aziz Univ Hlth Sci KSAU HS, Coll Pharm, King Abdullah Int Med Res Ctr KAIMRC, Prince Mutib Ibn Abdullah Ibn Abdulaziz Rd, Riyadh 11481, Saudi Arabia.
EM doughaimm@ksau-hs.edu.sa
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NR 164
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
EI 1179-5549
J9 CLIN MED INSIGHTS-ON
JI Clin. Med. Insights-Oncol.
PY 2024
VL 18
AR 11795549241298541
DI 10.1177/11795549241298541
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA M3C5N
UT WOS:001356355600001
PM 39559827
OA gold
DA 2025-01-04
ER

PT J
AU Li, XL
   Zhou, JB
   Chan, ZL
   Chooi, JY
   Chen, ZR
   Chng, WJ
AF Li, Xiao-Lan
   Zhou, Jianbiao
   Chan, Zit-Liang
   Chooi, Jing-Yuan
   Chen, Zhi-Rong
   Chng, Wee-Joo
TI PRIMA-1<SUP>met</SUP> (APR-246) inhibits growth of colorectal cancer
   cells with different p53 status through distinct mechanisms
SO ONCOTARGET
LA English
DT Article
DE colorectal cancer (CRC); p53; tumor suppressor gene (TSG); PRIMA-(1met);
   targeted therapy
ID MUTANT P53; PHARMACOLOGICAL REACTIVATION; MYELOID-LEUKEMIA; CARRYING
   MUTANT; SMALL MOLECULES; TARGETING P53; MALIGNANCIES; METASTASIS;
   COMPOUND; PATHWAYS
AB PRIMA-1(met) (APR-246) is a methylated derivative and structural analog of PRIMA-1 (p53 re-activation and induction of massive apoptosis). PRIMA-1met has been reported to restore both the wild type (wt) structure and function of mutant p53. Here, we show that PRIMA-1(met) is highly effective at limiting the growth of CRC cells regardless of p53 status. However, PRIMA-1(met) induces robust apoptosis only in CRC cells with mutant p53. Upregulation of Noxa, a proapoptotic molecule, is crucial for PRIMA-1(met) mediated activity. In human xenograft model of disease, PRIMA-1(met) effectively suppresses CRC tumor growth. Our results uncover distinct mechanisms of PRIMA-1(met) in CRC with different p53 status, thus providing a mechanistic rationale to evaluate the clinical efficacy of PRIMA-1(met) in CRC patients with different p53 status.
C1 [Li, Xiao-Lan; Zhou, Jianbiao; Chan, Zit-Liang; Chooi, Jing-Yuan; Chng, Wee-Joo] Natl Univ Singapore, Canc Sci Inst Singapore, Ctr Translat Med, Singapore 117599, Singapore.
   [Li, Xiao-Lan; Chen, Zhi-Rong] Suzhou Municipal Hosp Eastern, Dept Gastroenterol, Suzhou 215001, Jiangsu, Peoples R China.
   [Chng, Wee-Joo] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Med, Singapore 119074, Singapore.
   [Chng, Wee-Joo] Natl Univ Singapore Hosp, Dept Hematol Oncol, Singapore 119228, Singapore.
C3 National University of Singapore; National University of Singapore;
   National University of Singapore
RP Chng, WJ (corresponding author), Natl Univ Singapore, Canc Sci Inst Singapore, Ctr Translat Med, Singapore 117599, Singapore.
EM czr88188@163.com; mdccwj@nus.edu.sg
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NR 33
TC 40
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 NOV 3
PY 2015
VL 6
IS 34
BP 36689
EP 36699
DI 10.18632/oncotarget.5385
PG 11
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CY0QZ
UT WOS:000366111900123
PM 26452133
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Eefsen, RL
   Simonsen, KS
   Grundtvig, P
   Klarskov, L
   Chen, IM
   Hogdall, D
   Jensen, B
   Lorentzen, T
   Poulsen, TS
   Theile, S
   Nielsen, D
   Hogdall, E
AF Eefsen, R. L.
   Simonsen, K. S.
   Grundtvig, P.
   Klarskov, L.
   Chen, I. M.
   Hogdall, D.
   Jensen, B., V
   Lorentzen, T.
   Poulsen, T. S.
   Theile, S.
   Nielsen, D.
   Hogdall, E.
TI Genomic landscape of treatment refractory metastatic colorectal cancer
SO ACTA ONCOLOGICA
LA English
DT Article
DE Gene sequencing; next-generation sequencing; colorectal cancer; targeted
   therapy; cancer driver mutation
ID 1ST-LINE TREATMENT; OPEN-LABEL; BEVACIZUMAB; THERAPY; TUMORS;
   HETEROGENEITY; MULTICENTER; COMBINATION; MONOTHERAPY; VALIDATION
AB Background Metastatic colorectal cancer (mCRC) is a complex and heterogeneous disease with few standard and targeted treatment options. Next-generation sequencing of tumor tissue was performed to identify cancer driver mutations to discover possible personalized treatment options, as targeted treatment possibilities are limited for this patient population. Results of genomic sequencing in patients with treatment-refractory mCRC are described in this retrospective analysis. Material and methods Clinico-pathological characteristics and genomic sequence results of consecutive patients with refractory mCRC, referred to the Experimental Cancer Therapy Unit (ECTU) at Department of Oncology, Herlev & Gentofte Hospital in the period from 1 October 2015 to 14 December 2018 were reviewed in this retrospective analysis. Tumor tissue from the patients was analyzed by next-generation sequencing using the Oncomine Comprehensive primer panel to detect actionable variants of cancer driver mutations and microsatellite instability status. From August 2018 tumor mutational burden was also analyzed. Results A total of 80 patients with treatment-refractory mCRC and in a fairly good performance were referred to the ECTU during this period. Genomic sequencing of tumor tissue was performed for all 80 patients and a cancer driver mutation was identified in 90% (n = 72) of the patients. A total of 31.3% (n = 25) of the patients received therapy either as targetable therapy outside an available trial (n = 2), FDA approved therapy (n = 2), or treatment in phase 1 or 2 trials, independent of the genomic signature 26.3% (n = 21). Conclusion Most mCRC patients refractory to standard anti-neoplastic therapies, presented with a cancer driver mutation, however, only a few of these mutations gave rise to matched therapies as only 2.5% of the patients from this period received targeted therapy.
C1 [Eefsen, R. L.; Simonsen, K. S.; Grundtvig, P.; Chen, I. M.; Hogdall, D.; Jensen, B., V; Theile, S.; Nielsen, D.] Herlev Gentofte Hosp, Dept Oncol, Herlev, Denmark.
   [Klarskov, L.; Poulsen, T. S.; Hogdall, E.] Herlev Gentofte Hosp, Dept Pathol, Herlev, Denmark.
   [Lorentzen, T.] Herlev Gentofte Hosp, Dept Surg, Herlev, Denmark.
RP Eefsen, RL (corresponding author), Herlev Gentofte Hosp, Dept Oncol, Expt Canc Therapy Unit, Borgmester Ib Juuls Vej 9, DK-2730 Herlev, Denmark.
EM rikke.helene.loevendahl.eefsen@regionh.dk
RI Chen, Inna/AAB-2134-2020; Eefsen, Rikke/GZK-4168-2022; Hogdall,
   Dan/D-2269-2018
OI Hogdall, Dan/0000-0003-3832-2737; Nielsen, Dorte
   Lisbet/0000-0002-8766-8729; Chen, Inna/0000-0003-2891-0762; Eefsen,
   Rikke/0000-0003-1421-1792
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NR 58
TC 2
Z9 2
U1 0
U2 1
PU Medical Journal Sweden AB
PI Uppsala
PA Kungsngsvgen 27St, Uppsala, SWEDEN
SN 0284-186X
EI 1651-226X
J9 ACTA ONCOL
JI Acta Oncol.
PD DEC 2
PY 2021
VL 60
IS 12
BP 1621
EP 1628
DI 10.1080/0284186X.2021.1984575
EA OCT 2021
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XL3OV
UT WOS:000703413600001
PM 34606390
OA Bronze
DA 2025-01-04
ER

PT J
AU Tavberidze, N
   Zhang, W
AF Tavberidze, Nika
   Zhang, Wei
TI HER2 (ERBB2) alterations in colorectal cancers
SO HUMAN PATHOLOGY REPORTS
LA English
DT Review
DE Colorectal cancer; HER2; IHC; Scoring; MyPathway
ID BREAST-CANCER; TRASTUZUMAB
AB Human epidermal growth factor receptor 2 / HER2 (erb-b2 receptor tyrosine kinase 2 / ERBB2) alterations are present in approximately 2-5% of metastatic colorectal cancers. Although, the full significance of the HER2 status in colorectal cancers is yet to be determined, the ongoing research revealed promising results by incorporating of HER2 targeted therapy in the management of the advanced disease. Based on these findings, the most recent National Comprehensive Cancer Network Colon cancer guidelines recommends HER2 testing in metastatic colorectal cancer, which can be conducted by immunohistochemistry, in situ hybridization, or next generation sequencing. While there are no universal criteria for interpreting HER2 alterations, many specialists refer to HERACLES and MyPathway basket clinical trial criteria for the determination of HER2 status.
C1 [Tavberidze, Nika; Zhang, Wei] Univ Wisconsin, Dept Pathol & Lab Med, 600 Highland Ave,L5-131 CSC, Madison, WI 53792 USA.
RP Zhang, W (corresponding author), Univ Wisconsin, Dept Pathol & Lab Med, 600 Highland Ave,L5-131 CSC, Madison, WI 53792 USA.
EM wzhang566@wisc.edu
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NR 22
TC 4
Z9 4
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2772-736X
J9 HUM PATHOL REP
JI Hum. Pathol. Rep.
PD JUN
PY 2022
VL 28
AR 300628
DI 10.1016/j.hpr.2022.300628
PG 3
WC Pathology
WE Emerging Sources Citation Index (ESCI)
SC Pathology
GA P7P7O
UT WOS:001379788100001
OA gold
DA 2025-01-04
ER

PT J
AU Karri, S
   Aviel-Ronen, S
   Firer, MA
AF Karri, Sirish
   Aviel-Ronen, Sarit
   Firer, Michael A.
TI Fractal and textural imaging identify new subgroups of patients with
   colorectal cancer based on biophysical properties of the cancer cells
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Article
DE Colorectal cancer; Digital image analysis; Fractal dimension; Texture
   analysis
ID DIMENSION; TISSUE
AB Colorectal cancer (CRC) can been sub-divided, based on the generation of tertiary lymphoid structures (TLS), into CRC with a Crohn's like lymphoid reaction (CLR) representing de novo formation of TLSs or CRC lacking TLSs that show Diffuse Inflammatory infiltration (DII). The association between TLS, early treatment initiation and longer survival highlights the need for deeper patient stratification that could lead to more targeted therapies. We hypothesized that such stratification might be achieved by using digital image analyses. Here we retro-spectively analyzed 35 CRC patient samples classified as CLR or DII by digital analysis, focusing on the pa-rameters Fractal dimension, Lacunarity and the textural features Angular second momentum, Correlation, Inverse difference momentum and Entropy. Significant differences in the grades of these parameters between the two patient groups provided preliminary data that additional biophysical information can divide CRC into at least 3 subgroups which encompass CLR and DII. Additional studies are needed to test if this sub-classification aids in the selection of targeted therapy for patients with CRC.
C1 [Karri, Sirish; Firer, Michael A.] Ariel Univ, Dept Chem Engn, IL-40700 Ariel, Israel.
   [Aviel-Ronen, Sarit; Firer, Michael A.] Ariel Univ, Adelson Sch Med, IL-40700 Ariel, Israel.
   [Firer, Michael A.] Ariel Univ, Ariel Ctr Appl Canc Res, IL-40700 Ariel, Israel.
C3 Ariel University; Ariel University; Ariel University
RP Firer, MA (corresponding author), Ariel Univ, Dept Chem Engn, IL-40700 Ariel, Israel.; Firer, MA (corresponding author), Ariel Univ, Adelson Sch Med, IL-40700 Ariel, Israel.
EM firer@ariel.ac.il
RI Firer, Michael/H-4467-2019
OI Karri, Sirish/0000-0002-1674-4149
FU Ariel University Research Authority; School of Advanced Studies, Ariel
   University
FX This work was supported in part by a supportive grant from the Ariel
   University Research Authority. SK is the recipient of a graduate
   fellowship from the School of Advanced Studies, Ariel University.
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NR 35
TC 2
Z9 2
U1 2
U2 4
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
EI 1618-0631
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD OCT
PY 2022
VL 238
AR 154040
DI 10.1016/j.prp.2022.154040
EA AUG 2022
PG 7
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 4V4WI
UT WOS:000859478400004
PM 36057191
DA 2025-01-04
ER

PT J
AU Osei-Bordom, DC
   Kamarajah, S
   Christou, N
AF Osei-Bordom, Daniel-Clement
   Kamarajah, Sivesh
   Christou, Niki
TI Colorectal Cancer, Liver Metastases and Biotherapies
SO BIOMEDICINES
LA English
DT Review
DE colorectal cancer; liver metastases; immunotherapy; chemotherapy and
   biological agents
ID 1ST-LINE TREATMENT; TUMOR MICROENVIRONMENT; TARGETED THERAPY; MISMATCH
   REPAIR; CHEMOTHERAPY; CETUXIMAB; FUTURE; CHALLENGES; MANAGEMENT;
   RESISTANCE
AB (1) Background: colorectal cancer (CRC) is one of the deadliest causes of death by cancer worldwide. Its first main metastatic diffusion spreads to the liver. Different mechanisms such as the epithelial-mesenchymal transition and angiogenesis are the characteristics of this invasion. At this stage, different options are possible and still in debate, especially regarding the use of targeted therapeutics and biotherapies. (2) Methods: A review of the literature has been done focusing on the clinical management of liver metastasis of colorectal cancer and the contribution of biotherapies in this field. (3) Results: In a clinical setting, surgeons and oncologists consider liver metastasis in CRC into two groups to launch adapted therapeutics: resectable and non-resectable. Around these two entities, the combination of targeted therapies and biotherapies are of high interest and are currently tested to know in which molecular and clinical conditions they have to be applied to impact positively both on survival and quality of life of patients.
C1 [Osei-Bordom, Daniel-Clement; Kamarajah, Sivesh; Christou, Niki] Univ Hosp Birmingham, Queen Elizabeth Hosp, Dept Gen Surg, Birmingham B15 2TH, W Midlands, England.
   [Osei-Bordom, Daniel-Clement] Univ Birmingham, Inst Immunol & Immunotherapy, Birmingham B15 2TT, W Midlands, England.
   [Osei-Bordom, Daniel-Clement] Univ Birmingham, NIHR Birmingham Biomed Res Ctr, Ctr Liver & Gastroenterol Res, Birmingham B15 2TT, W Midlands, England.
   [Christou, Niki] Univ Hosp Limoges, Dept Gen Surg, F-87000 Limoges, France.
   [Christou, Niki] Fac Med, EA3842 CAPTuR Lab Cell Activat Control Tumor Prog, 2 Rue Docteur Marcland, F-87025 Limoges, France.
C3 University of Birmingham; University of Birmingham; University of
   Birmingham; CHU Limoges
RP Christou, N (corresponding author), Univ Hosp Birmingham, Queen Elizabeth Hosp, Dept Gen Surg, Birmingham B15 2TH, W Midlands, England.; Christou, N (corresponding author), Univ Hosp Limoges, Dept Gen Surg, F-87000 Limoges, France.; Christou, N (corresponding author), Fac Med, EA3842 CAPTuR Lab Cell Activat Control Tumor Prog, 2 Rue Docteur Marcland, F-87025 Limoges, France.
EM danieloseibordom@gmail.com; sivesh.kamarajah@uhb.nhs.uk;
   christou.niki19@gmail.com
RI Kamarajah, Sivesh/N-6062-2019; CHRISTOU, Niki/O-3785-2019
OI CHRISTOU, Niki/0000-0003-2125-0503; Kamarajah, Sivesh
   K/0000-0002-2748-0011
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NR 126
TC 5
Z9 6
U1 1
U2 21
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD AUG
PY 2021
VL 9
IS 8
AR 894
DI 10.3390/biomedicines9080894
PG 18
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 UF8VT
UT WOS:000688846700001
PM 34440099
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kandagatla, P
   Maguire, LH
   Hardiman, KM
AF Kandagatla, Pridvi
   Maguire, Lilias H.
   Hardiman, Karin M.
TI Biology of Nodal Spread in Colon Cancer: Insights from Molecular and
   Genetic Studies
SO EUROPEAN SURGICAL RESEARCH
LA English
DT Article
DE Colorectal cancer; Cancer genetics; Lymph node metastasis; Intratumor
   heterogeneity
ID COLORECTAL-CANCER; LYMPH-NODE; INTRATUMOR HETEROGENEITY; METASTASIS;
   EVOLUTION; EXPRESSION; KRAS; PROGRESSION; MUTATIONS; THERAPY
AB Colorectal cancer (CRC) lymph node metastases are common but their genetics and the mechanism whereby these metastases occur are not well understood. Here we present recent data regarding genetic heterogeneity in primary CRCs and their metastasis. In addition, we explain the different potential models describing the mechanisms of metastasis and the data supporting them. Multiple studies have also revealed a variety of prognostic molecular markers that are associated with lymph node metastasis in CRC. A better understanding of genetic heterogeneity and the mechanisms of metastasis is critical to predicting clinical response and resistance to targeted therapy. (c) 2018 S. Karger AG, Basel
C1 [Kandagatla, Pridvi] Wayne State Univ, Dept Surg, Henry Ford Hlth Syst, Detroit, MI USA.
   [Maguire, Lilias H.; Hardiman, Karin M.] Univ Michigan, Dept Surg, Div Colorectal Surg, Ann Arbor, MI 48109 USA.
C3 Wayne State University; Henry Ford Health System; Henry Ford Hospital;
   University of Michigan System; University of Michigan
RP Hardiman, KM (corresponding author), Dept Surg, 2922-F Taubman Ctr,1500 E Med Ctr Dr,SPC 5343, Ann Arbor, MI 48109 USA.
EM kmha@med.umich.edu
RI Kandagatla, Pridvi/CAH-5703-2022
FU American Surgical Association Foundation Fellowships [5P50CA130810];
   John S. and Suzanne C. Munn Cancer Research Fund [5P30A046592]; National
   Cancer Institute [K08CA190645]; National Cancer Institute [T32CA009672,
   P30CA046592] Funding Source: NIH RePORTER
FX K.M. Hardiman is funded by an American Surgical Association Foundation
   Fellowships (5P50CA130810), the John S. and Suzanne C. Munn Cancer
   Research Fund (5P30A046592), and the National Cancer Institute
   (K08CA190645).
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NR 34
TC 5
Z9 6
U1 0
U2 4
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0014-312X
EI 1421-9921
J9 EUR SURG RES
JI Eur. Surg. Res.
PY 2018
VL 59
IS 5-6
BP 361
EP 370
DI 10.1159/000494832
PG 10
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA HI7FC
UT WOS:000456620100006
PM 30537705
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Ramaswamy, A
   Babu, V
   Kothari, R
   Abhinav, R
   Desouza, A
   Ventrapati, P
   Kumar, A
   Kapoor, A
   Das, S
   Engineer, R
   Saklani, A
   Ostwal, V
AF Ramaswamy, Anant
   Babu, Vasu
   Kothari, Rushabh
   Abhinav, Ram
   Desouza, Ashwin
   Ventrapati, Pradeep
   Kumar, Amit
   Kapoor, Akhil
   Das, Shasanka
   Engineer, Reena
   Saklani, Avanish
   Ostwal, Vikas
TI Treatment of Metastatic Colorectal Cancers in Resource-Constrained Low-
   and Middle-Income Countries (LMICS) Scenario-Outcomes, Practice
   Patterns, and Commentary on Treatment Costs
SO SOUTH ASIAN JOURNAL OF CANCER
LA English
DT Article
DE targeted therapy; India; low- and middle-income countries; metastatic
   colorectal cancer; overall survival; resource constrained
ID BEVACIZUMAB; CETUXIMAB; FOLFIRI
AB Introduction The overall survival (OS) of metastatic colorectal cancers (mCRCs) in clinical practice and resource-constrained low- and middle-income countries (LMICS) like India is not known. Materials and Methods Data of patients with mCRC treated between January 2013 and August 2017 were accessed from a prospectively maintained database. Demographics, disease characteristics, chemotherapeutic regimens, use of monoclonal antibodies, and survival outcomes in treated patients were collected and analyzed. Costs of treatment options as off 2017 were also interpreted.
   Results The data of 403 patients satisfied prespecified inclusion criteria and were included for analysis. The median age of the cohort was 48 years (range: 17-86) with a predominance of rectal cancers (63.3%), liver alone metastases (47.1%), and resected primary (69.7%). Signet ring histology was present in 82 patients (20.3%). The most commonly used first-line regimen (CT1) was modified capecitabine-oxaliplatin (53.3%). Two hundred and nineteen patients (54.3%) received second-line systemic therapy (CT2). Patients received a median of two lines of therapy (range: 1-6). MoAbs were used by 48 patients (13.4%) with CT1 and 34 patients (15.5%) with CT2. Median OS of the entire cohort was 17.61 months (95% confidence interval: 15.48-19.74), which was within the predicted range, as per investigator hypothesis. The presence of signet ring histology ( p <0.001), raised carcinoembryonic antigen at baseline ( p =0.017), and the absence of a resected primary ( p <0.001) predicted inferior median OS.
   Conclusions Survival of patients with mCRC in a resource-constrained LMIC scenario like India is approximately 12 to 15 months lower than published trial data. Limited access to targeted therapy and newer expensive treatment options due to financial constraints may contribute to this disparity.
C1 [Ramaswamy, Anant; Babu, Vasu; Kothari, Rushabh; Abhinav, Ram; Ventrapati, Pradeep; Kumar, Amit; Kapoor, Akhil; Das, Shasanka; Ostwal, Vikas] HBNI, Tata Mem Hosp, Dept Med Oncol, Dr E Borges Rd, Mumbai 400012, Maharashtra, India.
   [Desouza, Ashwin; Saklani, Avanish] HBNI, Tata Mem Hosp, Dept Surg Oncol, Dr E Borges Rd, Mumbai, Maharashtra, India.
   [Engineer, Reena] HBNI, Tata Mem Hosp, Dept Radiat Oncol, Dr E Borges Rd, Mumbai, Maharashtra, India.
C3 Tata Memorial Centre (TMC); Tata Memorial Hospital; Homi Bhabha National
   Institute; Tata Memorial Centre (TMC); Tata Memorial Hospital; Homi
   Bhabha National Institute; Tata Memorial Centre (TMC); Tata Memorial
   Hospital; Homi Bhabha National Institute
RP Ostwal, V (corresponding author), HBNI, Tata Mem Hosp, Dept Med Oncol, Dr E Borges Rd, Mumbai 400012, Maharashtra, India.
EM dr.vikas.ostwal@gmail.com
OI Kapoor, Akhil/0000-0001-6006-2631
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NR 10
TC 0
Z9 0
U1 0
U2 0
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 2278-330X
EI 2278-4306
J9 SOUTH ASIAN J CANCER
JI South Asian J. Cancer
PD OCT
PY 2022
VL 11
IS 04
BP 293
EP 298
DI 10.1055/s-0041-1736203
EA SEP 2022
PG 6
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA 8Q2GX
UT WOS:000849033300004
PM 36756109
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Sadoughi, F
   Dana, PM
   Asemi, Z
   Yousefi, B
AF Sadoughi, Fatemeh
   Dana, Parisa Maleki
   Asemi, Zatollah
   Yousefi, Bahman
TI Targeting microRNAs by curcumin: implication for cancer therapy
SO CRITICAL REVIEWS IN FOOD SCIENCE AND NUTRITION
LA English
DT Review
DE Curcumin; microRNA; microRNA-21 (miR-21); curcumin-resistance; cancer;
   colorectal cancer; breast cancer; lung cancer
ID CELL-CYCLE ARREST; DNA-DAMAGE RESPONSE; EPITHELIAL-MESENCHYMAL
   TRANSITION; MIR-21 EXPRESSION; UP-REGULATION; CISPLATIN RESISTANCE;
   PROMOTES APOPTOSIS; MIRNA BIOGENESIS; BINDING PROTEIN; INVASION
AB In spite of all the investigations in the past 20 years that established a great body of knowledge in cancer therapy, utilizing some elderly methods such as plant compound administration might still be useful. Curcumin is a bioactive polyphenol, which has many anticancer properties but its capability in modulating miRNA expression has opened new doors in the field of cancer-targeted therapy. MiRNAs are a class of small noncoding RNAs that are able to regulate gene expression and signaling. In addition, some other effects of these RNAs such as modulating cell differentiation and regulation of cell cycle have made miRNAs great candidates for personalized cancer treatment. In this review, we try to find some answers to the questions on how curcumin exerts its impacts on cancer hallmarks through miRNAs and whether chemotherapy can be replaced by this beneficial plant compound.
C1 [Sadoughi, Fatemeh; Dana, Parisa Maleki; Asemi, Zatollah] Kashan Univ Med Sci, Res Ctr Biochem & Nutr Metab Dis, Inst Basic Sci, Kashan, Iran.
   [Yousefi, Bahman] Tabriz Univ Med Sci, Mol Med Res Ctr, Tabriz, Iran.
   [Yousefi, Bahman] Tabriz Univ Med Sci, Fac Med, Dept Biochem, Tabriz, Iran.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science
RP Asemi, Z (corresponding author), Kashan Univ Med Sci, Res Ctr Biochem & Nutr Metab Dis, Inst Basic Sci, Kashan, Iran.; Yousefi, B (corresponding author), Tabriz Univ Med Sci, Mol Med Res Ctr, Tabriz, Iran.
EM asemi_r@yahoo.com; bahmanusefi@gmail.com
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OI Maleki Dana, Parisa/0000-0003-2544-548X
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NR 115
TC 9
Z9 10
U1 2
U2 14
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1040-8398
EI 1549-7852
J9 CRIT REV FOOD SCI
JI Crit. Rev. Food Sci. Nutr.
PD OCT 3
PY 2022
VL 62
IS 28
BP 7718
EP 7729
DI 10.1080/10408398.2021.1916876
PG 12
WC Food Science & Technology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology; Nutrition & Dietetics
GA 5X5JO
UT WOS:000878636000001
PM 33905266
DA 2025-01-04
ER

PT J
AU Kamashev, D
   Sorokin, M
   Kochergina, I
   Drobyshev, A
   Vladimirova, U
   Zolotovskaia, M
   Vorotnikov, I
   Shaban, N
   Raevskiy, M
   Kuzmin, D
   Buzdin, A
AF Kamashev, Dmitry
   Sorokin, Maksim
   Kochergina, Irina
   Drobyshev, Aleksey
   Vladimirova, Uliana
   Zolotovskaia, Marianna
   Vorotnikov, Igor
   Shaban, Nina
   Raevskiy, Mikhail
   Kuzmin, Denis
   Buzdin, Anton
TI Human blood serum can donor-specifically antagonize effects of
   EGFR-targeted drugs on squamous carcinoma cell growth
SO HELIYON
LA English
DT Article
DE Lung cancer; Colorectal cancer; EGFR; HER-targeted therapy; Human blood
   serum; Cetuximab; Erlotinib; Trastuzumab; EGF; Neuregulin; NRG;
   TGF-alpha; Squamous cell carcinoma; A431; Drug resistance
ID TYROSINE KINASE INHIBITORS; FACTOR RECEPTOR; LUNG-CANCER; CETUXIMAB
   RESISTANCE; SIGNAL-TRANSDUCTION; ERBB RECEPTORS; BREAST-CANCER;
   ERLOTINIB; PHARMACOKINETICS; STABILITY
AB Many patients fail to respond to EGFR-targeted therapeutics, and personalized diagnostics is needed to identify putative responders. We investigated 1630 colorectal and lung squamous carcinomas and 1357 normal lung and colon samples and observed huge variation in EGFR pathway activation in both cancerous and healthy tissues, irrespectively on EGFR gene mutation status. We investigated whether human blood serum can affect squamous carcinoma cell growth and EGFR drug response. We demonstrate that human serum antagonizes the effects of EGFR-targeted drugs erlotinib and cetuximab on A431 squamous carcinoma cells by increasing IC50 by about 2-and 20-fold, respectively. The effects on clonogenicity varied significantly across the individual serum samples in every experiment, with up to 100% differences. EGF concentration could explain many effects of blood serum samples, and EGFR ligands-depleted serum showed lesser effect on drug sensitivity.
C1 [Kamashev, Dmitry; Sorokin, Maksim; Kochergina, Irina; Drobyshev, Aleksey; Vladimirova, Uliana; Shaban, Nina; Buzdin, Anton] Russian Acad Sci, Shemyakin Ovchinnikov Inst Bioorgan Chem, 16-10 Miklukho Maklaya St, Moscow 117997, Russia.
   [Kamashev, Dmitry; Sorokin, Maksim; Drobyshev, Aleksey; Vladimirova, Uliana; Buzdin, Anton] Sechenov First Moscow State Med Univ, World Class Res Ctr Digital Biodesign & Personali, 8-2 Trubetskaya St, Moscow 119992, Russia.
   [Sorokin, Maksim; Drobyshev, Aleksey; Zolotovskaia, Marianna; Shaban, Nina; Raevskiy, Mikhail; Kuzmin, Denis; Buzdin, Anton] Natl Res Univ, Moscow Inst Phys & Technol, Dolgoprudnyi 141700, Moscow Region, Russia.
   [Vorotnikov, Igor] Minist Hlth Russia, Blokhin Natl Med Res Ctr Oncol, Moscow, Russia.
   [Raevskiy, Mikhail] OmicsWay Corp, Walnut, CA USA.
C3 Russian Academy of Sciences; Pushchino Scientific Center for Biological
   Research (PSCBI) of the Russian Academy of Sciences; Institute of
   Bioorganic Chemistry of the Russian Academy of Sciences; Sechenov First
   Moscow State Medical University; Moscow Institute of Physics &
   Technology; Ministry of Health of the Russian Federation
RP Kamashev, D (corresponding author), Russian Acad Sci, Shemyakin Ovchinnikov Inst Bioorgan Chem, 16-10 Miklukho Maklaya St, Moscow 117997, Russia.; Kamashev, D (corresponding author), Sechenov First Moscow State Med Univ, World Class Res Ctr Digital Biodesign & Personali, 8-2 Trubetskaya St, Moscow 119992, Russia.
EM dkamashev@gmail.com
RI Zolotovskaia, Marianna/AAE-2724-2019; Raevskiy, Mikhail/AAU-1032-2021;
   Vladimirova, Uliana/KUD-1531-2024; Sorokin, Maksim/P-1459-2017;
   Kamashev, Dmitri/K-6560-2017; Kuzmin, Denis/AAT-4851-2020; Shaban,
   Nina/ABB-6531-2021
OI Raevskiy, Mikhail/0000-0002-6218-5480; Shaban, Nina/0000-0002-7632-4883;
   Vladimirova, Uliana/0000-0002-7520-3019
FU Russian Science Foundation [18-15-00061]; Russian Science Foundation
   [18-15-00061, 21-15-28010] Funding Source: Russian Science Foundation
FX This study was supported by the Russian Science Foundation grant
   (18-15-00061).
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NR 70
TC 10
Z9 11
U1 0
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
EI 2405-8440
J9 HELIYON
JI Heliyon
PD MAR
PY 2021
VL 7
IS 3
AR e06394
DI 10.1016/j.heliyon.2021.e06394
EA MAR 2021
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA RI9FT
UT WOS:000637211500018
PM 33748471
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Aalijahan, H
   Ghorbian, S
AF Aalijahan, Hamid
   Ghorbian, Saeid
TI Long non-coding RNAs and cervical cancer
SO EXPERIMENTAL AND MOLECULAR PATHOLOGY
LA English
DT Review
DE LncRNAs; Cervical cancer; Prognosis; Biomarker; HOTAIR
ID PROMOTES CELL-PROLIFERATION; EPITHELIAL-MESENCHYMAL TRANSITION;
   POOR-PROGNOSIS; HEPATOCELLULAR-CARCINOMA; COLORECTAL-CANCER;
   BREAST-CANCER; UP-REGULATION; LUNG ADENOCARCINOMA; TUMOR-METASTASIS;
   DOWN-REGULATION
AB Cervical cancer is determined as the second highest number of deaths factor in female cancers. Here is a need to find new biomarkers for detection and preliminary prognosis, metastasis. To find new treatment to enhance the survival of cervical cancer patients, pivotal actions are necessitated to be implemented. Long non-coding RNAs (lncRNAs) appear to be the crucial modulators in various processes and critically influence the oncogenesis. The commencement and general review actions of the following lncRNAs HOTAIR, H19, XIST, CCHE1, EBIC, MALATI, ANRIL, LET, NEAT1, BLACATI, UFC1, SNHG16 and SNHG20 are focused in this review article. Roles of the lncRNAs in cervical cancer in terms of prognosis and tumor progression, invasion and metastasis, apoptosis, and radio-resistance are pointed out. In this review the utilization of lncRNAs as biomarkers in cervical cancer prognosis for metastasis is discussed. An overview of this review will be useful for selection of biomarkers in diagnosis, prognosis, and targeted therapy of cervical cancer in the future.
C1 [Aalijahan, Hamid; Ghorbian, Saeid] Islamic Azad Univ, Ahar Branch, Dept Mol Genet, Ahar, Iran.
C3 Islamic Azad University
RP Ghorbian, S (corresponding author), Islamic Azad Univ, Ahar Branch, Dept Mol Genet, Ahar, Iran.
EM ghorbian20@yahoo.com
RI ghorbian, saeid/AAN-6554-2021
CR [Anonymous], FEBS LETT
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NR 136
TC 136
Z9 142
U1 1
U2 66
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4800
EI 1096-0945
J9 EXP MOL PATHOL
JI Exp. Mol. Pathol.
PD FEB
PY 2019
VL 106
BP 7
EP 16
DI 10.1016/j.yexmp.2018.11.010
PG 10
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA HM8RW
UT WOS:000459749600002
PM 30471246
DA 2025-01-04
ER

PT J
AU Limami, Y
   Pinon, A
   Riaz, A
   Simon, A
AF Limami, Y.
   Pinon, A.
   Riaz, A.
   Simon, A.
TI TRAIL and targeting cancer cells: between promises and obstacles
SO CELLULAR AND MOLECULAR BIOLOGY
LA English
DT Article
DE Cancer; TRAIL; Targeted therapy; Apoptosis; TRAIL resistance; Clinical
   Trials
ID TUMOR-NECROSIS-FACTOR; APOPTOSIS-INDUCING LIGAND; MIXED LINEAGE KINASE;
   DOMAIN-LIKE PROTEIN; X-LINKED INHIBITOR; DEATH RECEPTORS 4;
   MONOCLONAL-ANTIBODY; COLORECTAL-CANCER; DECOY RECEPTORS; CARCINOMA-CELLS
AB Targeting cancer cells is one of the challenges of current treatment strategies. TRAIL represents a promising therapeutic approach and over the past decades there was an increased interest in targeting TRAIL signaling to treat cancer. Indeed, TRAIL can specifically target cancer cells and exhibits very low cytotoxicity towards normal cells. However, rapidly accumulating experimental evidence has started to shed light on multiple factors which induce resistance against TRAIL in cancer cells. This resistance consists of various mechanisms including downregulation of death receptors and caspase-8 and overexpression of decoy receptors as well as antiapoptotic factors such as members of Bcl-2 family. Even if several studies focused on elucidating those resistance mechanisms, there still remain gray areas that need to be fully elucidated. Thus, therapeutic approaches could consist of targeting both resistance signaling pathways and TRAIL signaling to enhance TRAIL therapy efficiency.
C1 [Limami, Y.; Pinon, A.; Simon, A.] Fac Pharm, EA 1069, Lab Chim Subst Nat, Limoges, France.
   [Riaz, A.] FC Coll, Lahore, Pakistan.
RP Limami, Y (corresponding author), Fac Pharm, EA 1069, Lab Chim Subst Nat, Limoges, France.
EM limami@hotmail.com
RI Limami, Youness/AAE-9695-2021
OI Limami, Youness/0000-0002-8816-3001
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NR 84
TC 19
Z9 20
U1 0
U2 6
PU C M B  ASSOC
PI POITIERS
PA 34 BOULEVARD SOLFERINO, 86000 POITIERS, FRANCE
SN 0145-5680
EI 1165-158X
J9 CELL MOL BIOL
JI Cell. Mol. Biol.
PY 2015
VL 61
IS 6
BP 33
EP 38
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA DB4AF
UT WOS:000368454400006
PM 26518894
DA 2025-01-04
ER

PT J
AU Civit, L
   Theodorou, I
   Frey, F
   Weber, H
   Lingnau, A
   Gröber, C
   Blank, M
   Dambrune, C
   Stunden, J
   Beyer, M
   Schultze, J
   Latz, E
   Duconge, F
   Kubbutat, MHG
   Mayer, G
AF Civit, Laia
   Theodorou, Ioanna
   Frey, Franziska
   Weber, Holger
   Lingnau, Andreas
   Groeber, Carsten
   Blank, Michael
   Dambrune, Chloe
   Stunden, James
   Beyer, Marc
   Schultze, Joachim
   Latz, Eicke
   Duconge, Frederic
   Kubbutat, Michael H. G.
   Mayer, Guenter
TI Targeting hormone refractory prostate cancer by <i>in vivo</i> selected
   DNA libraries in an orthotopic xenograft mouse model
SO SCIENTIFIC REPORTS
LA English
DT Article
ID RNA APTAMER; COLORECTAL-CANCER; HIGH-AFFINITY; TUMOR-GROWTH; INHIBITION;
   CELLS; GENERATION; DELIVERY; BIND; IDENTIFICATION
AB The targeting of specific tissue is a major challenge for the effective use of therapeutics and agents mediating this targeting are strongly demanded. We report here on an in vivo selection technology that enables the de novo identification of pegylated DNA aptamers pursuing tissue sites harbouring a hormone refractory prostate tumour. To this end, two libraries, one of which bearing an 11 kDa polyethylene glycol (PEG) modification, were used in an orthotopic xenograft prostate tumour mouse model for the selection process. Next-generation sequencing revealed an in vivo enriched pegylated but not a naive DNA aptamer recognising prostate cancer tissue implanted either subcutaneous or orthotopically in mice. This aptamer represents a valuable and cost-effective tool for the development of targeted therapies for prostate cancer. The described selection strategy and its analysis is not limited to prostate cancer but will be adaptable to various tissues, tumours, and metastases. This opens the path towards DNA aptamers being experimentally and clinically engaged as molecules for developing targeted therapy strategies.
C1 [Civit, Laia; Frey, Franziska; Mayer, Guenter] Univ Bonn, Life & Med Sci LIMES Inst, Chem Biol & Chem Genet, Gerhard Domagk Str 1, D-53121 Bonn, Germany.
   [Theodorou, Ioanna; Dambrune, Chloe; Duconge, Frederic] CEA, Inst Biol Francois Jacob, Mol Imaging Res Ctr MIRCen, DRT,CNRS,UMR 9199, 18 Route Panorama, F-92260 Roses, France.
   [Weber, Holger; Lingnau, Andreas; Kubbutat, Michael H. G.] KTB Tumorforsch Gesell mbH, Res Div ProQinase, Breisacher Str 117, D-79106 Freiburg, Germany.
   [Groeber, Carsten; Blank, Michael] AptaIT GmbH, Klopferspitz 19a, D-82152 Martinsried, Germany.
   [Stunden, James; Latz, Eicke] Univ Hosp Bonn, Inst Innate Immun, Sigmund Freud Str 25, D-53127 Bonn, Germany.
   [Beyer, Marc; Schultze, Joachim] Univ Bonn, Life & Med Sci LIMES Inst, Genom & Immunoregulat, Carl Troll Str 31, D-53115 Bonn, Germany.
   [Beyer, Marc; Schultze, Joachim] DZNE, Platform Single Cell Genom & Epigenom, Sigmund Freud Str 27, D-53127 Bonn, Germany.
   [Beyer, Marc; Schultze, Joachim] Univ Bonn, Sigmund Freud Str 27, D-53127 Bonn, Germany.
   [Beyer, Marc] German Ctr Neurodegenerat Dis DZNE, Mol Immunol Neurodegenerat, Sigmund Freud Str 27, D-53127 Bonn, Germany.
   [Mayer, Guenter] Univ Bonn, CARD, Gerhard Domagk Str 1, D-53121 Bonn, Germany.
   [Weber, Holger; Kubbutat, Michael H. G.] ProQinase GmbH, Breisacher Str 117, D-79106 Freiburg, Germany.
   [Lingnau, Andreas] Genmab BV, Yalelaan 60, NL-3584 CM Utrecht, Netherlands.
C3 University of Bonn; Centre National de la Recherche Scientifique (CNRS);
   CEA; University of Bonn; University of Bonn; Helmholtz Association;
   German Center for Neurodegenerative Diseases (DZNE); University of Bonn;
   Helmholtz Association; German Center for Neurodegenerative Diseases
   (DZNE); University of Bonn; ProQinase; Genmab
RP Mayer, G (corresponding author), Univ Bonn, Life & Med Sci LIMES Inst, Chem Biol & Chem Genet, Gerhard Domagk Str 1, D-53121 Bonn, Germany.; Mayer, G (corresponding author), Univ Bonn, CARD, Gerhard Domagk Str 1, D-53121 Bonn, Germany.
EM gmayer@uni-bonn.de
RI Mayer, Günter/F-2937-2010; Duconge, Frederic/C-6729-2012; Beyer,
   Marc/ABE-1408-2021; Latz, Eicke/H-3951-2014
OI Latz, Eicke/0000-0003-1488-5666; Mayer, Gunter/0000-0003-3010-4049;
   Civit Pitarch, Laia/0009-0007-0062-8438; Theodorou,
   Ioanna/0000-0001-8591-0924; Beyer, Marc D./0000-0001-9704-148X
FU ERA-NET 'Euronanomed' [13N12249]; European Commission; BMBF [13N12247];
   DFG [SFB704]
FX This work has been made possible by funds from ERA-NET 'Euronanomed' to
   M.K., F.D. and G.M. (Grant acronym: META, Grant number: 13N12249). The
   authors also thank the European Commission for a Marie Curie Intra
   European fellowship to L.C. and BMBF (13N12247), J.L.S. and M.B. are
   members of the Excellence Cluster ImmunoSensation. J.L.S. was funded by
   the DFG (SFB704). We thank Silvana Hassel for critical reading the
   manuscript.
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NR 78
TC 9
Z9 12
U1 0
U2 15
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD MAR 21
PY 2019
VL 9
AR 4976
DI 10.1038/s41598-019-41460-2
PG 16
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA HP7RH
UT WOS:000461885900016
PM 30899039
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Loh, KP
   Mondo, E
   Hansen, EA
   Sievert, L
   Fung, C
   Sahasrabudhe, DM
   Guancial, E
AF Loh, Kah Poh
   Mondo, Esther
   Hansen, Elizabeth A.
   Sievert, Lynn
   Fung, Chunkit
   Sahasrabudhe, Deepak M.
   Guancial, Elizabeth
TI Targeted Therapy Based on Tumor Genomic Analyses in Metastatic Urachal
   Carcinoma
SO CLINICAL GENITOURINARY CANCER
LA English
DT Review
DE Chemotherapy; Genomic alterations; Metastases; Next generation
   sequencing; Urachal cancer
ID ACUTE MYELOID-LEUKEMIA; CELL LUNG-CANCER; ACTIVATING FLT3 MUTATIONS;
   KRAS MUTATIONS; MICROSATELLITE INSTABILITY; COLORECTAL-CANCER;
   ADENOCARCINOMA; CHEMOTHERAPY; MELANOMA; SURVIVAL
AB Urachal cancer is rare and has a prevalence of approximately 0.2%.
   In the setting of metastatic disease, chemotherapy has been used with some success. However, there is no standard chemotherapy regimen. Once chemotherapy fails, treatment options are limited.
   To date, there are a limited number of case reports regarding the use of targeted agents empirically, none of which were based on actionable mutations identified through tumor genomic profiling.
   In this case series, we report 2 patients with metastatic urachal cancer who were treated with targeted agents (sorafenib, sunitinib, and trametinib) based on actionable mutations found from their tumors, resulting in clinical response for 1 of the patients. The second discontinued therapy owing to adverse effects from the agent before disease response could be assessed.
   We propose that, for patients in whom standard of care chemotherapy have failed, genomic testing for actionable mutations should be considered to guide subsequent therapy selection. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Loh, Kah Poh; Mondo, Esther; Sievert, Lynn; Fung, Chunkit; Sahasrabudhe, Deepak M.; Guancial, Elizabeth] Univ Rochester, Strong Mem Hosp, James P Wilmot Canc Inst, Div Hematol Oncol, Rochester, NY 14642 USA.
   [Hansen, Elizabeth A.] Univ Rochester, Strong Mem Hosp, Dept Pharm, Rochester, NY 14642 USA.
C3 University of Rochester; University of Rochester
RP Loh, KP (corresponding author), Univ Rochester, Strong Mem Hosp, Med Ctr, James P Wilmot Canc Inst, 601 Elmwood Ave,Box 704, Rochester, NY 14642 USA.
EM Melissalkp@gmail.com
RI Loh, Kah/U-7243-2019
OI Loh, Kah Poh/0000-0002-6978-0418
CR [Anonymous], 2009, NIH Publ, P0
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NR 43
TC 21
Z9 21
U1 0
U2 1
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1558-7673
EI 1938-0682
J9 CLIN GENITOURIN CANC
JI Clin. Genitourin. Cancer
PD AUG
PY 2016
VL 14
IS 4
BP E449
EP E452
DI 10.1016/j.clgc.2016.03.013
PG 4
WC Oncology; Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Urology & Nephrology
GA DS4ON
UT WOS:000380760500042
PM 27102403
DA 2025-01-04
ER

PT J
AU Pan, QQ
   Fan, X
   Xie, L
   Wu, D
   Liu, R
   Gao, WX
   Luo, K
   He, B
   Pu, YJ
AF Pan, Qingqing
   Fan, Xi
   Xie, Li
   Wu, Di
   Liu, Rong
   Gao, Wenxia
   Luo, Kui
   He, Bin
   Pu, Yuji
TI Nano-enabled colorectal cancer therapy
SO JOURNAL OF CONTROLLED RELEASE
LA English
DT Review
DE Colorectal cancer; Nanoscale drug delivery systems; Immunotherapy; Gut
   microbiota; Therapy resistance
ID IMMUNOGENIC CELL-DEATH; TUMOR-GROWTH; APOPTOSIS-FERROPTOSIS;
   DELIVERY-SYSTEM; LOCAL TREATMENT; COLON-CANCER; CO-DELIVERY;
   NANOPARTICLES; METASTASIS; 5-FLUOROURACIL
AB Colorectal cancer (CRC), one of the most common and deadliest diseases worldwide, poses a great health threat and social burden. The clinical treatments of CRC encompassing surgery, chemotherapy, and radiotherapy are challenged with toxicity, therapy resistance, and recurrence. In the past two decades, targeted therapy and immunotherapy have greatly improved the therapeutic benefits of CRC patients but they still suffer from drug resistance and low response rates. Very recently, gut microbiota regulation has exhibited a great potential in preventing and treating CRC, as well as in modulating the efficacy and toxicity of chemotherapy and immunotherapy. In this review, we provide a cutting-edge summary of nanomedicine-based treatment in colorectal cancer, highlighting the recent progress of oral and systemic tumor-targeting and/or tumor-activatable drug delivery systems as well as novel therapeutic strategies against CRC, including nano-sensitizing immunotherapy, anti-inflammation, gut microbiota modulation therapy, etc. Finally, the recent endeavors to address therapy resistance, metastasis, and recurrence in CRC were discussed. We hope this review could offer insight into the design and development of nanomedicines for CRC and beyond.
C1 [Pan, Qingqing; Xie, Li; Liu, Rong] Chengdu Univ, Sch Preclin Med, Chengdu 610106, Peoples R China.
   [Fan, Xi; He, Bin; Pu, Yuji] Sichuan Univ, Coll Biomed Engn, Natl Engn Res Ctr Biomat, Chengdu 610064, Peoples R China.
   [Wu, Di] Chengdu Univ, Sch Food & Biol Engn, Meat Proc Key Lab Sichuan Prov, Chengdu 610106, Peoples R China.
   [Gao, Wenxia] Wenzhou Univ, Coll Chem & Mat Engn, Wenzhou 325027, Peoples R China.
   [Luo, Kui] Sichuan Univ, West China Hosp, Funct & Mol Imaging Key Lab Sichuan Prov, Dept Radiol,Huaxi MR Res Ctr HMRRC, Chengdu 610041, Peoples R China.
C3 Chengdu University; Sichuan University; Chengdu University; Wenzhou
   University; Sichuan University
RP Liu, R (corresponding author), Chengdu Univ, Sch Preclin Med, Chengdu 610106, Peoples R China.; Pu, YJ (corresponding author), Sichuan Univ, Coll Biomed Engn, Natl Engn Res Ctr Biomat, Chengdu 610064, Peoples R China.
EM liurongscu@126.com; yjpu@scu.edu.cn
RI Pu, Yuji/J-3168-2019
OI Pu, Yuji/0000-0002-4465-0262
FU National Natural Science Foundation of China [52073216, 51903172];
   Opening Project of Key Laboratory of Coarse Cereal Processing, Ministry
   of Agriculture and Rural Affairs [2020CC015]; Sichuan's Education
   Department [JG2021-1107]
FX We would like to thank the financial support by National Natural Science
   Foundation of China (52073216 and 51903172) , the Opening Project of Key
   Laboratory of Coarse Cereal Processing, Ministry of Agriculture and
   Rural Affairs (No. 2020CC015) , and the project of Sichuan's Education
   Department (No: JG2021-1107) .
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NR 145
TC 18
Z9 18
U1 20
U2 71
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0168-3659
EI 1873-4995
J9 J CONTROL RELEASE
JI J. Control. Release
PD OCT
PY 2023
VL 362
BP 548
EP 564
DI 10.1016/j.jconrel.2023.09.014
EA SEP 2023
PG 17
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA T5BB6
UT WOS:001078126700001
PM 37683732
DA 2025-01-04
ER

PT J
AU Zhai, ML
   Zhang, ZX
   Wang, HH
   Ren, JH
   Zhang, S
   Li, MJ
   Liu, LC
   Li, LS
   Zhang, L
   Li, X
   Zhang, T
   Lin, ZY
AF Zhai, Menglan
   Zhang, Zixuan
   Wang, Haihong
   Ren, Jinghua
   Zhang, Sheng
   Li, Mingjie
   Liu, Lichao
   Li, Lisha
   Zhang, Lan
   Li, Xin
   Zhang, Tao
   Lin, Zhenyu
TI Efficacy and safety of radiotherapy combined with anti-angiogenic
   therapy and immune checkpoint inhibitors in MSS/pMMR metastatic
   colorectal cancer
SO CANCER MEDICINE
LA English
DT Article
DE immunotherapy; metastatic colorectal cancer; microsatellite stable;
   radiotherapy; targeted therapy
AB Purpose: Several studies have demonstrated the effectiveness of anti-angiogenic drugs in combination with immune checkpoint inhibitors (ICIs) in patients with microsatellite stable (MSS) or mismatch repair proficient (pMMR) metastatic colorectal cancer (mCRC). However, whether combination radiotherapy (RT) can further improve the prognosis of mCRC patients after second-line treatment remains to be explored.Methods: Retrospective analysis of data from mCRC patients who received anti-angiogenic targeted therapy (TT) and immunotherapy (IT) with or without RT after the failure of standard therapy. Progression-free survival (PFS), overall survival (OS), objective response rate (ORR), disease control rate (DCR), and safety were evaluated.Results: A total of 82 patients who received TT + IT were analyzed. For RT group (n = 42) versus NRT group (n = 40), ORR was 21.4% (9/42) versus 5.0% (2/40); DCR was 83.8% (35/42) versus 65.0% (26/40). Compared with NRT group, RT improved PFS (median: 5.0 vs. 3.6 months; p = 0.04) and OS (median: 15.2 vs. 7.2 months; p = 0.01). In addition, in the population receiving RT, the PFS of RT sequential/simultaneous TT + IT was superior to TT + IT sequential RT (median: 7.1 vs. 6.2 vs. 3.5 months, p = 0.004). Multivariate analysis suggested RT was an independent prognostic factor for PFS and OS. No treatment-related deaths were reported.Conclusions: Compared with TT + IT, RT combined with TT + IT improved survival outcomes in MSS/pMMR mCRC patients, with manageable toxicity. RT sequential/simultaneous TT + IT treatment is expected to be the optimal strategy for MSS/PMMR mCRC.
C1 [Zhai, Menglan; Wang, Haihong; Ren, Jinghua; Zhang, Sheng; Li, Mingjie; Liu, Lichao; Li, Lisha; Zhang, Tao; Lin, Zhenyu] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Canc Ctr, Wuhan 430022, Peoples R China.
   [Zhang, Zixuan] Nanchang Univ, Med Dept, Queen Mary Sch, Nanchang, Jiangxi, Peoples R China.
   [Ren, Jinghua; Zhang, Sheng; Zhang, Tao; Lin, Zhenyu] Hubei Key Lab Precis Radiat Oncol, Wuhan, Peoples R China.
   [Zhang, Lan; Li, Xin] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Radiol, Wuhan, Peoples R China.
   [Zhang, Tao; Lin, Zhenyu] Huazhong Univ Sci & Technol, Union Hosp, Inst Radiat Oncol, Tongji Med Coll, Wuhan, Peoples R China.
C3 Huazhong University of Science & Technology; Nanchang University;
   Huazhong University of Science & Technology; Huazhong University of
   Science & Technology
RP Zhang, T; Lin, ZY (corresponding author), Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Canc Ctr, Wuhan 430022, Peoples R China.
EM taozhangxh@hust.edu.cn; whxhlzy@hust.edu.cn
RI Li, Mingjie/ADR-4291-2022; Ren, Jinghua/IST-4349-2023
FU Chinese Society of Clinical Oncology (CSCO)-Tongshu Oncology Research
   Fund
FX The authors have nothing to report.
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NR 14
TC 0
Z9 0
U1 2
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 JAN
PY 2024
VL 13
IS 1
DI 10.1002/cam4.6820
EA DEC 2023
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JM2V4
UT WOS:001127541300001
PM 38112050
OA Green Published
DA 2025-01-04
ER

PT J
AU Far, NP
   Varnousafaderani, MH
   Faghihkhorasani, F
   Etemad, S
   Abdulwahid, ARR
   Bakhtiarinia, N
   Mousaei, A
   Dortaj, E
   Karimi, S
   Ebrahimi, N
   Aref, AR
AF Far, Nazanin Pazhouhesh
   Varnousafaderani, Mahsa Hajiheidari
   Faghihkhorasani, Ferdos
   Etemad, Sareh
   Abdulwahid, Al-Hasnawi Rasool Riyadh
   Bakhtiarinia, Negar
   Mousaei, Afsaneh
   Dortaj, Elahe
   Karimi, Soroush
   Ebrahimi, Nasim
   Aref, Amir Reza
TI Breaking the barriers: Overcoming cancer resistance by targeting the
   NLRP3 inflammasome
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Review
DE cancer-targeted therapy; CRISPR/Cas9; immune checkpoint inhibitors;
   pyroptosis; tumour microenvironment (TME)
ID NF-KAPPA-B; CONCISE GUIDE; LUNG-CANCER; SIGNAL-TRANSDUCTION; IMMUNE
   SUPPRESSION; P2X7 RECEPTOR; GASDERMIN D; ACTIVATION; INHIBITION; CELLS
AB Inflammation has a pivotal role in the initiation and progression of various cancers, contributing to crucial processes such as metastasis, angiogenesis, cell proliferation and invasion. Moreover, the release of cytokines mediated by inflammation within the tumour microenvironment (TME) has a crucial role in orchestrating these events. The activation of inflammatory caspases, facilitated by the recruitment of caspase-1, is initiated by the activation of pattern recognition receptors on the immune cell membrane. This activation results in the production of proinflammatory cytokines, including IL-1 beta and IL-18, and participates in diverse biological processes with significant implications. The NOD-Like Receptor Protein 3 (NLRP3) inflammasome holds a central role in innate immunity and regulates inflammation through releasing IL-1 beta and IL-18. Moreover, it interacts with various cellular compartments. Recently, the mechanisms underlying NLRP3 inflammasome activation have garnered considerable attention. Disruption in NLRP3 inflammasome activation has been associated with a spectrum of inflammatory diseases, encompassing diabetes, enteritis, neurodegenerative diseases, obesity and tumours. The NLRP3 impact on tumorigenesis varies across different cancer types, with contrasting roles observed. For example, colorectal cancer associated with colitis can be suppressed by NLRP3, whereas gastric and skin cancers may be promoted by its activity. This review provides comprehensive insights into the structure, biological characteristics and mechanisms of the NLRP3 inflammasome, with a specific focus on the relationship between NLRP3 and tumour-related immune responses, and TME. Furthermore, the review explores potential strategies for targeting cancers via NLRP3 inflammasome modulation. This encompasses innovative approaches, including NLRP3-based nanoparticles, gene-targeted therapy and immune checkpoint inhibitors.
   There are two pivotal mechanisms to surmount cancer cell resistance to immunotherapy: First, the utilization of immune checkpoint inhibitors to block PD-1 on T cells, thereby preventing its interaction with PD-L1 on tumour cells and consequently augmenting T cell-mediated anti-tumour responses. Second, targeting of the NLRP3 inflammasome within tumour cells, which serves to modulate the inflammatory milieu of the tumour microenvironment. The synergistic application of these two approaches is hypothesized to effectively overcome the resistance of cancer cells to immunotherapeutic interventions, as visually represented by the green arrow on the right side of the diagram. This innovative combinatorial strategy holds promise for enhancing the efficacy of cancer immunotherapy and potentially improving patient outcomes.image
C1 [Far, Nazanin Pazhouhesh] Islamic Azad Univ, Fac Adv Sci & Technol, Dept Microbiol, Tehran Med Sci, Tehran, Iran.
   [Varnousafaderani, Mahsa Hajiheidari] Univ Debrecen, Fac Med, Debrecen, Hungary.
   [Faghihkhorasani, Ferdos; Abdulwahid, Al-Hasnawi Rasool Riyadh; Bakhtiarinia, Negar] Xi An Jiao Tong Univ, Med Campus, Xian, Peoples R China.
   [Etemad, Sareh] Univ Med Mashhad, Dept Pathol, Ghaem Hosp, Mashhad, Iran.
   [Mousaei, Afsaneh] Islamic Azad Univ, Coll Sci, Dept Biol, Qaemshahr Branch, Qaem Shahr, Iran.
   [Dortaj, Elahe] Shiraz Univ Med Sci, Sch Hlth, Dept Ergon, Shiraz, Iran.
   [Karimi, Soroush] Kermanshah Univ Med Sci, Hlth Technol Inst, Nano Drug Delivery Res Ctr, Kermanshah, Iran.
   [Ebrahimi, Nasim] Univ Isfahan, Fac Sci & Technol, Dept Cell & Mol Biol & Microbiol, Genet Div, Esfahan, Iran.
   [Aref, Amir Reza] Harvard Med Sch, Massachusetts Gen Hosp, Mass Gen Canc Ctr, Dept Surg, Boston, MA 02115 USA.
   [Aref, Amir Reza] Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.
C3 Islamic Azad University; University of Debrecen; Xi'an Jiaotong
   University; Islamic Azad University; Shiraz University of Medical
   Science; Kermanshah University of Medical Sciences; University of
   Isfahan; Harvard University; Massachusetts General Hospital; Harvard
   Medical School; Harvard University; Massachusetts Institute of
   Technology (MIT); Broad Institute
RP Ebrahimi, N (corresponding author), Univ Isfahan, Fac Sci & Technol, Dept Cell & Mol Biol & Microbiol, Genet Div, Esfahan, Iran.; Aref, AR (corresponding author), Harvard Med Sch, Massachusetts Gen Hosp, Mass Gen Canc Ctr, Dept Surg, Boston, MA 02115 USA.; Aref, AR (corresponding author), Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.
EM pazhouheshfar.nazi99@gmail.com; nasimeb69@gmail.com;
   aaref@mgh.harvard.edu
RI Dortaj, Elahe/AAB-8995-2019
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NR 185
TC 0
Z9 0
U1 3
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1188
EI 1476-5381
J9 BRIT J PHARMACOL
JI Br. J. Pharmacol.
PD JAN
PY 2025
VL 182
IS 1
BP 3
EP 25
DI 10.1111/bph.17352
EA OCT 2024
PG 23
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA O2B7W
UT WOS:001330092900001
PM 39394867
OA Bronze
DA 2025-01-04
ER

PT J
AU Zmuc, J
   Heil, J
   Herfarth, C
   Bechstein, WO
   Koch, C
   Trojan, J
   Schnitzbauer, AA
AF Zmuc, Jan
   Heil, Jan
   Herfarth, Caroline
   Bechstein, Wolf O.
   Koch, Christine
   Trojan, Joerg
   Schnitzbauer, Andreas A.
TI Chemotherapy and Targeted Therapy Strategies in Patients with
   Unresectable or Borderline Resectable Metastatic Colorectal Cancer:
   Evidence for a Lack of Focus on Resection Rates
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Review
ID FOLFIRI PLUS BEVACIZUMAB; RANDOMIZED PHASE-III; 1ST-LINE TREATMENT;
   LIVER METASTASES; OPEN-LABEL; TRIAL; FOLFOXIRI; CETUXIMAB; SURVIVAL;
   PANITUMUMAB
AB Background and aims. Chemotherapy (CTx) with targeted therapy (TT) have increased the overall response rate (ORR) and improved survival in unresectable or borderline resectable metastatic colorectal cancer (mCRC). However, the resection rate is an endpoint with often suboptimal expert involvement. The aim was to investigate whether the improvements in ORR have translated to improved resection rates (RR).
   Study design. A systematic literature search was performed using the PICO process.
   Statistical analysis. Odds ratios, and 95% confidence intervals (OR, 95% CI) were analyzed for ORR and RR using dichotomous values with the Mantel-Haenszel method. Progression-free survival (PFS) and overall survival (OS) were analyzed using the inverse-variance method and displayed as hazard ratios and 95% confidence intervals (HR, 95% CI).
   Results. The literature search returned 469 records. Sixteen articles with 5724 patients were selected for analysis. The qualitative analysis revealed low and moderate risk of bias endpoints. Higher ORR was observed with CTx + TT versus CTx only (OR: 0.62 [95% CI 0.45; 0.82], p = 0.002) and with triplet CTx + TT versus doublet CTx + TT (OR: 0.61 [95% CI 0.46; 0.81], p < 0.001). PFS and OS were improved by use of TT (HR: 0.68-0.84; p < 0.001 to 0.04). The overall RR was low (< 15%) and did not improve in the same way as the other endpoints.
   Conclusion. The ORR and survival rates in unresectable and borderline resectable mCRC were improved by modern CTx and TT that did not translate into higher RR, mostly due to the lack of expert involvement.
C1 [Zmuc, Jan] Inst Oncol Ljubljana, Dept Surg Oncol, Ljubljana, Slovenia.
   [Heil, Jan; Herfarth, Caroline; Bechstein, Wolf O.; Schnitzbauer, Andreas A.] Goethe Univ, Frankfurt Univ Hosp, Dept Gen Visceral & Transplant Surg, Frankfurt, Germany.
   [Koch, Christine; Trojan, Joerg] Goethe Univ, Frankfurt Univ Hosp, Dept Med 1, Frankfurt, Germany.
C3 Institute of Oncology - Slovenia; Goethe University Frankfurt; Goethe
   University Frankfurt Hospital; Goethe University Frankfurt; Goethe
   University Frankfurt Hospital
RP Schnitzbauer, AA (corresponding author), Goethe Univ, Frankfurt Univ Hosp, Dept Gen Visceral & Transplant Surg, Frankfurt, Germany.
EM andreas.schnitzbauer@kgu.de
RI Heil, Jan/HLP-6202-2023; Trojan, Jörg/C-1616-2009; Žmuc,
   Jan/AEU-0625-2022
OI Schnitzbauer, Andreas/0000-0003-1527-1877
FU Projekt DEAL; Astellas GmbH; Aventis; MCI Deutschland; Medupdate GmbH;
   Servier; Roche; Amgen
FX Open Access funding enabled and organized by Projekt DEAL. WOB reported
   funding received from Astellas GmbH, Aventis, MCI Deutschland, and
   Medupdate GmbH; JT reported advisory funding received from Servier,
   Roche, and Amgen
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NR 34
TC 1
Z9 1
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD NOV
PY 2023
VL 30
IS 12
BP 7624
EP 7632
DI 10.1245/s10434-023-14049-3
EA AUG 2023
PG 9
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA X1AD5
UT WOS:001064801900001
PM 37644249
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Pagani, F
   Randon, G
   Guarini, V
   Raimondi, A
   Prisciandaro, M
   Lobefaro, R
   Di Bartolomeo, M
   Sozzi, G
   de Braud, F
   Gasparini, P
   Pietrantonio, F
AF Pagani, Filippo
   Randon, Giovanni
   Guarini, Vincenzo
   Raimondi, Alessandra
   Prisciandaro, Michele
   Lobefaro, Riccardo
   Di Bartolomeo, Maria
   Sozzi, Gabriella
   de Braud, Filippo
   Gasparini, Patrizia
   Pietrantonio, Filippo
TI The Landscape of Actionable Gene Fusions in Colorectal Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE gene fusions; colorectal cancer; translocation; biomarker
ID OPEN-LABEL; SOLID TUMORS; PHASE-III; PAN-TRK; THYROID-CANCER;
   CELL-CARCINOMA; HIGH-FREQUENCY; ALK INHIBITOR; DOUBLE-BLIND; ROS1
AB The treatment scenario of metastatic colorectal cancer (mCRC) has been rapidly enriched with new chemotherapy combinations and biological agents that lead to a remarkable improvement in patients' outcome. Kinase gene fusions account for less than 1% of mCRC overall but are enriched in patients with high microsatellite instability, RAS/BRAF wild-type colorectal cancer. mCRC patients harboring such alterations show a poor prognosis with standard treatments that could be reversed by adopting novel therapeutic strategies. Moving forward to a positive selection of mCRC patients suitable for targeted therapy in the era of personalized medicine, actionable gene fusions, although rare, represent a peculiar opportunity to disrupt a tumor alteration to achieve therapeutic goal. Here we summarize the current knowledge on potentially actionable gene fusions in colorectal cancer available from retrospective experiences and promising preliminary results of new basket trials.
C1 [Pagani, Filippo; Randon, Giovanni; Guarini, Vincenzo; Raimondi, Alessandra; Prisciandaro, Michele; Lobefaro, Riccardo; Di Bartolomeo, Maria; de Braud, Filippo; Pietrantonio, Filippo] Fdn IRCCS Ist Nazl Tumori, Med Oncol Dept, I-20133 Milan, Italy.
   [Sozzi, Gabriella; Gasparini, Patrizia] Fdn IRCCS Ist Nazl Tumori, Unit Mol Cytogenet, I-20133 Milan, Italy.
   [de Braud, Filippo; Pietrantonio, Filippo] Univ Milan, Dept Oncol & Hematooncol, I-20122 Milan, Italy.
C3 Fondazione IRCCS Istituto Nazionale Tumori Milan; Fondazione IRCCS
   Istituto Nazionale Tumori Milan; University of Milan
RP Pietrantonio, F (corresponding author), Fdn IRCCS Ist Nazl Tumori, Med Oncol Dept, I-20133 Milan, Italy.; Pietrantonio, F (corresponding author), Univ Milan, Dept Oncol & Hematooncol, I-20122 Milan, Italy.
EM filippo.pagani@istitutotumori.mi.it;
   giovanni.randon@istitutotumori.mi.it;
   vincenzo.guarini@istitutotumori.mi.it;
   alessandra.raimondi@istitutotumori.mi.it;
   michele.prisciandaro@istitutotumori.mi.it;
   riccardo.lobefaro@istitutotumori.mi.it;
   maria.dibartolomeo@istitutotumori.mi.it;
   gabriella.sozzi@istitutotumori.mi.it;
   filippo.debraud@istitutotumori.mi.it;
   patrizia.gasparini@istitutotumori.mi.it;
   filippo.pietrantonio@istitutotumori.mi.it
RI Raimondi, Alessandra/AAC-1873-2022; Pagani, Filippo/LSK-6113-2024;
   Gasparini, Patrizia/Q-7626-2016; de Braud, Filippo Guglielmo
   Maria/B-9997-2017; Pietrantonio, Filippo/C-2180-2017; Di Bartolomeo,
   Maria/D-1655-2017
OI Gasparini, Patrizia/0000-0002-9548-3724; , Filippo
   Pagani/0009-0007-7393-7477; Prisciandaro, Michele/0000-0001-5596-469X;
   Lobefaro, Riccardo/0000-0003-3484-9718; de Braud, Filippo Guglielmo
   Maria/0000-0003-0103-730X; Pietrantonio, Filippo/0000-0002-8530-8420; Di
   Bartolomeo, Maria/0000-0002-7954-6609
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NR 112
TC 30
Z9 31
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 NOV
PY 2019
VL 20
IS 21
AR 5319
DI 10.3390/ijms20215319
PG 18
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA JQ4VU
UT WOS:000498946100077
PM 31731495
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Jung, E
   Choi, J
   Kim, JS
   Han, TS
AF Jung, Eunsun
   Choi, Jinhyeon
   Kim, Jang-Seong
   Han, Tae-Su
TI MicroRNA-Based Therapeutics for Drug-Resistant Colorectal Cancer
SO PHARMACEUTICALS
LA English
DT Review
DE microRNA; chemoresistance; targeted therapy; immunotherapy; anti-cancer
   drug resistance; colorectal cancer
ID 5-FLUOROURACIL-BASED CHEMOTHERAPY; CLINICAL CHARACTERISTICS; BEVACIZUMAB
   RESISTANCE; OXALIPLATIN RESISTANCE; CETUXIMAB RESISTANCE; CELL
   SENSITIVITY; SMALL MOLECULES; PHASE-II; EXPRESSION; METASTASIS
AB Although therapeutic approaches for patients with colorectal cancer (CRC) have improved in the past decades, the problem of drug resistance still persists and acts as a major obstacle for effective therapy. Many studies have shown that drug resistance is related to reduced drug uptake, modification of drug targets, and/or transformation of cell cycle checkpoints. A growing body of evidence indicates that several microRNAs (miRNAs) may contribute to the drug resistance to chemotherapy, targeted therapy, and immunotherapy by regulating the drug resistance-related target genes in CRC. These drug resistance-related miRNAs may be used as promising biomarkers for predicting drug response or as potential therapeutic targets for treating patients with CRC. In this review, we summarized the recent discoveries regarding anti-cancer drug-related miRNAs and their molecular mechanisms in CRC. Furthermore, we discussed the challenges associated with the clinical application of miRNAs as biomarkers for the diagnosis of drug-resistant patients and as therapeutic targets for CRC treatment.
C1 [Jung, Eunsun; Choi, Jinhyeon; Kim, Jang-Seong; Han, Tae-Su] Korea Res Inst Biosci & Biotechnol KRIBB, Daejeon 34141, South Korea.
C3 Korea Research Institute of Bioscience & Biotechnology (KRIBB)
RP Kim, JS; Han, TS (corresponding author), Korea Res Inst Biosci & Biotechnol KRIBB, Daejeon 34141, South Korea.
EM silverline09@kribb.re.kr; cluke@kribb.re.kr; jskim@kribb.re.kr;
   tshan@kribb.re.kr
OI Jung, Eunsun/0000-0002-5900-6138
FU National Research Foundation of Korea (NRF) - Ministry of Science and
   ICT [NRF-2020R1C1C1007431]; KRIBB Research Initiative Program
FX This study was supported by grants from the National Research Foundation
   of Korea (NRF) funded by the Ministry of Science and ICT
   (NRF-2020R1C1C1007431) and the KRIBB Research Initiative Program.
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NR 143
TC 17
Z9 17
U1 1
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1424-8247
J9 PHARMACEUTICALS-BASE
JI Pharmaceuticals
PD FEB
PY 2021
VL 14
IS 2
AR 136
DI 10.3390/ph14020136
PG 17
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA QO1BA
UT WOS:000622881000001
PM 33567635
OA Green Published
DA 2025-01-04
ER

PT J
AU Bartos, A
   Bartos, D
   Szabo, B
   Breazu, C
   Opincariu, I
   Mironiuc, A
   Iancu, C
AF Bartos, Adrian
   Bartos, Dana
   Szabo, Bianca
   Breazu, Caius
   Opincariu, Iulian
   Mironiuc, Aurel
   Iancu, Cornel
TI Recent achievements in colorectal cancer diagnostic and therapy by the
   use of nanoparticles
SO DRUG METABOLISM REVIEWS
LA English
DT Review
DE Colorectal cancer; chemotherapy; drug resistance; nanotechnology;
   targeted therapy
ID MESOPOROUS SILICA NANOPARTICLES; PEGYLATED LIPOSOMAL DOXORUBICIN;
   ENHANCED RAMAN-SCATTERING; ANTICANCER DRUG-DELIVERY; METASTATIC
   COLON-CANCER; HUMAN PANCREATIC-CANCER; GOLD NANOPARTICLES; CARBON
   NANOTUBES; IN-VITRO; OXIDATIVE STRESS
AB Colorectal cancer is a major public health issue, being the third most common cancer in men and the second in women. It is one of the leading causes of cancer deaths. Nanomedicine is an emerging field of interest, many of its aspects being linked to cancer research. Chemotherapy has a well-established role in colorectal cancer management, unfortunately being limited by inability to have a selective distribution, by multidrug resistance and adverse effects. Researches carried out in recent years about nanotechnologies aimed, among others, to resolve the issues mentioned above. Targeted and localized delivery of the chemotherapeutic drugs, using nanoparticles, with selective destruction of cancerous cells would minimize the toxicity on healthy tissues. Also, the use of nanomaterials as contrast agent could improve sensitivity and specificity of diagnosis. The purpose of this review is to highlight the recent achievements of cancer research by use of nanomaterials, in the idea of finding the ideal composite, capable to simultaneous diagnostic and treat cancer.
C1 [Bartos, Adrian] Prof Dr Octavian Fodor Reg Inst Gastroenterol & H, Dept Surg, Cluj Napoca, Romania.
   [Bartos, Dana] UMF Iuliu Hatieganu, Dept Surg, Prof Dr Octavian Fodor Reg Inst Gastroenterol & H, Cluj Napoca, Romania.
   [Bartos, Dana; Szabo, Bianca; Opincariu, Iulian] UMF Iuliu Hatieganu, Dept Anat & Embryol, Cluj Napoca, Romania.
   [Szabo, Bianca] UMF Iuliu Hatieganu, Dept Ophthalmol, Clin Emergency Hosp Cluj, Cluj Napoca, Romania.
   [Breazu, Caius] UMF Iuliu Hatieganu, Dept Anesthesiol & Intens Care, Prof Dr Octavian Fodor Reg Inst Gastroenterol & H, Cluj Napoca, Romania.
   [Mironiuc, Aurel] UMF Iuliu Hatieganu, Dept Surg, Clin Emergency Hosp, Cluj Napoca, Romania.
   [Mironiuc, Aurel] UMF Iuliu Hatieganu, Dept Surg 2, Cluj Napoca, Romania.
   [Iancu, Cornel] UMF Iuliu Hatieganu, Dept Surg, Prof Dr Octavian Fodor Reg Inst Gastroenterol & H, Dept Surg 3, Cluj Napoca, Romania.
C3 Regional Institute of Gastroenterology & Hepatology; Regional Institute
   of Gastroenterology & Hepatology; Iuliu Hatieganu University of Medicine
   & Pharmacy; Iuliu Hatieganu University of Medicine & Pharmacy; Iuliu
   Hatieganu University of Medicine & Pharmacy; Regional Institute of
   Gastroenterology & Hepatology; Iuliu Hatieganu University of Medicine &
   Pharmacy; Iuliu Hatieganu University of Medicine & Pharmacy; Iuliu
   Hatieganu University of Medicine & Pharmacy; Regional Institute of
   Gastroenterology & Hepatology; Iuliu Hatieganu University of Medicine &
   Pharmacy
RP Bartos, D (corresponding author), UMF Iuliu Hatieganu, Dept Surg, Prof Dr Octavian Fodor Reg Inst Gastroenterol & H, Cluj Napoca, Romania.; Bartos, D (corresponding author), UMF Iuliu Hatieganu, Dept Anat & Embryol, Cluj Napoca, Romania.
EM bartosdanamonica@gmail.com
RI IANCU, CORNEL/AAJ-5315-2021; IANCU, DANA/AAA-4558-2019; SZABO,
   BIANCA/I-7698-2019; Breazu, Caius/AAU-1940-2020
OI Iancu, Dana/0000-0002-7523-4747; Szabo, Bianca/0000-0002-2605-8513;
   IANCU, CORNEL/0000-0001-7100-8729; BARTOS, ADRIAN/0000-0003-3177-9232
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NR 201
TC 11
Z9 12
U1 2
U2 35
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0360-2532
EI 1097-9883
J9 DRUG METAB REV
JI Drug Metab. Rev.
PD JAN 2
PY 2016
VL 48
IS 1
BP 27
EP 46
DI 10.3109/03602532.2015.1130052
PG 20
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA DG5DM
UT WOS:000372094300002
PM 26828283
DA 2025-01-04
ER

PT J
AU Schneider, B
   Glass, Ä
   Jagdmann, S
   Hühns, M
   Claus, J
   Zettl, H
   Dräger, DL
   Maruschke, M
   Hakenberg, OW
   Erbersdobler, A
   Zimpfer, A
AF Schneider, Bjoern
   Glass, Anne
   Jagdmann, Sandra
   Huehns, Maja
   Claus, Jessica
   Zettl, Heike
   Draeger, Desiree-Louise
   Maruschke, Matthias
   Hakenberg, Oliver W.
   Erbersdobler, Andreas
   Zimpfer, Annette
TI Loss of Mismatch-repair Protein Expression and Microsatellite
   Instability in Upper Tract Urothelial Carcinoma and Clinicopathologic
   Implications
SO CLINICAL GENITOURINARY CANCER
LA English
DT Article
DE Immunohistochemistry; Lynch syndrome; Microsatellite instablility;
   Mismatch repair protein deficiency; Tissue microarray
ID UPPER URINARY-TRACT; LYNCH-SYNDROME; CELL-CARCINOMA; EUROPEAN
   ASSOCIATION; UROLOGY GUIDELINES; COLORECTAL-CANCER; TUMORS; MUTATION;
   BLADDER; NEPHROURETERECTOMY
AB Upper tract urothelial carcinoma (UTUC) is often diagnosed at advanced stage and requires additional therapy. Currently, targeted therapy with programmed death-ligand 1 inhibitors is available for solid tumors with microsatellite instability (MSI). Therefore, we investigated the prevalence of MSI in 128 patients with UTUC. A total of 28.1% of patients with UTUC harbored MSI. MSI analysis in UTUC is highly recommended as a guide for therapy decisions in advanced UTUC.
   Background: Upper tract urothelial carcinoma (UTUC) may arise in the setting of hereditary non-polyposis colorectal cancer (Lynch syndrome [LS]) or sporadically. Variable frequencies of microsatellite instability (MSI) were found in UTUC. For advanced solid MSI tumors, targeted therapy with programmed death-ligand 1 inhibitors is available. Therefore, we aimed to determine the prevalence of mismatch repair (MMR) protein loss and MSI in UTUC using a tissue microarray approach and further molecular and correlation analysis. Materials and Methods: We studied the immunohistochemical expression of MLH1, MSH2, MSH6, and PMS2 on tissue microarrays containing formalin-fixed, paraffin-embedded samples of 128 patients with UTUC. MSI analysis was performed in 79 cases with deficient MMR protein expression, and/or in patients aged 60 years and below, and/or other tumors possibly related to LS. Results: Loss of MMR protein expression was seen in 24 (18.8%) of 128 cases. MSI analysis revealed MSI-high in 29, MSI-low in 7 cases. The Fisher exact test demonstrated significant differences between MSI and loss of MMR protein expression, clinically possible LS, tumor growth pattern, inverted growth pattern, and death (P < .001, P < .001, P = .002, P = .003, and P - .033, respectively). MSI does not appear to influence survival (overall and progressionfree), but there was a significant shorter progression-free survival in MSI-high versus MSS patients who had received chemotherapy. Conclusion: The frequency of MSI in UTUC was 36 (28.1%) of 128 patients with a good accuracy of immunohistochemistry. In daily practice, MSI screening especially is recommended in patients with advanced UTUC and inverted papillary tumor growth pattern with the aim of screening patients for possible targeted therapy. (C) 2020 Elsevier Inc. All rights reserved.
C1 [Schneider, Bjoern; Huehns, Maja; Claus, Jessica; Erbersdobler, Andreas; Zimpfer, Annette] Univ Med Rostock, Inst Pathol, Strempelstr 14, D-18057 Rostock, Germany.
   [Glass, Anne] Univ Med Rostock, Inst Biostat & Informat Med, Rostock, Germany.
   [Jagdmann, Sandra] Charite, Inst Med Immunol, Berlin, Germany.
   [Zettl, Heike] Univ Med Rostock, Rostock Canc Registry, Rostock, Germany.
   [Draeger, Desiree-Louise; Maruschke, Matthias; Hakenberg, Oliver W.] Univ Med Rostock, Dept Urol, Rostock, Germany.
   [Maruschke, Matthias; Hakenberg, Oliver W.] HELIOS Hanseklinikum Stralsund, Dept Urol, Stralsund, Germany.
C3 University of Rostock; University of Rostock; Berlin Institute of
   Health; Free University of Berlin; Humboldt University of Berlin;
   Charite Universitatsmedizin Berlin; University of Rostock; University of
   Rostock
RP Schneider, B (corresponding author), Univ Med Rostock, Inst Pathol, Strempelstr 14, D-18057 Rostock, Germany.
EM bjoern.schneider@med.uni-rostock.de
RI Zimpfer, Annette/AAQ-4994-2020
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NR 48
TC 17
Z9 18
U1 1
U2 4
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1558-7673
EI 1938-0682
J9 CLIN GENITOURIN CANC
JI Clin. Genitourin. Cancer
PD OCT
PY 2020
VL 18
IS 5
BP E563
EP E572
DI 10.1016/j.clgc.2020.03.006
PG 10
WC Oncology; Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Urology & Nephrology
GA OH2JR
UT WOS:000582396100008
PM 32340874
DA 2025-01-04
ER

PT J
AU Liu, WZ
   Liu, LL
   Wang, RY
   Gong, GY
   Ding, XJ
   Yang, B
   Bao, Y
   Wang, ZQ
   Zhang, B
   Zhao, DW
   Wu, F
   Ding, Y
AF Liu, Wenzhi
   Liu, Lili
   Wang, Ruoyu
   Gong, Guanyu
   Ding, Xinjia
   Yang, Bin
   Bao, Yun
   Wang, Zhiqiang
   Zhang, Bo
   Zhao, Dewei
   Wu, Fei
   Ding, Yan
TI Bevacizumab Combined With Oxaliplatin/Capecitabine in Patient With
   Refractory and Recurrent Mucinous Adenocarcinoma of the Appendix: A Case
   Report
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE appendiceal adenocarcinoma; peritoneal carcinomatosis; next generation
   sequencing; bevacizumab; targeted therapy
ID METASTATIC COLORECTAL-CANCER; CHEMOTHERAPY; THERAPY
AB Primary appendiceal adenocarcinoma with peritoneal pseudomyxoma (PPM) has a high recurrence rate and refractory to medical interventions such as repetitive debulking surgery and systemic chemotherapy. Genome-based targeted therapy for such cases has not been well-documented. Here we present a 63-years-old women, who was diagnosed with recurrent mucinous adenocarcinoma of the appendix with local invasions and peritoneal carcinomatosis, was refractory to systemic chemotherapy after surgery. We used a regime developed using whole exome sequencing. Somatic mutations in the genes encoding VEGFR2, FGFR1, FGFR2, FGFR3, and KRAS were identified in the patient's tumor tissue. The patient was then treated with bevacizumab plus oxaliplatin. After 4 months of treatment, pelvic CT showed dramatic reduction of pseudomyoma and a decline of CA199 level from 5436.7 to 1121.4 U/ml. Continual treatment with bevacizumab-capecitabine remained effective and the patient's CA199 level further decreased to 401.26 U/ml according to the follow-up examination on Aug 15th, 2018. Results from this study show the evidence of gene mutations involving VEGF signal activation in the recurrence of appendiceal adenocarcinoma. Our results also suggest the association of these mutations with the effectiveness of anti-VEGF treatment using bevacizumab. Therefore, the screening of gene mutations involved in VEGF signaling and targeted therapy with anti-VEGF drugs may provide a new option to manage refractory/recurrent advanced-stage appendiceal adenocarcinoma.
C1 [Liu, Wenzhi; Wang, Ruoyu; Gong, Guanyu; Bao, Yun; Wang, Zhiqiang; Zhao, Dewei; Wu, Fei; Ding, Yan] Dalian Univ, Affiliated Zhongshan Hosp, Inst Translat Med, Dalian, Peoples R China.
   [Liu, Lili] Dalian Med Univ, Affiliated Hosp 2, Dept Oncol, Dalian, Peoples R China.
   [Gong, Guanyu; Yang, Bin] Genom Future Inc, Lexington, MA USA.
   [Ding, Xinjia; Zhang, Bo] Dalian Med Univ, Affiliated Hosp 2, Dept Neurosurg, Dalian, Peoples R China.
   [Yang, Bin; Ding, Yan] Harvard Med Sch, Dept Pediat, Childrens Hosp Boston, Boston, MA 02115 USA.
C3 Dalian University; Dalian Medical University; Dalian Medical University;
   Harvard University; Harvard Medical School; Boston Children's Hospital
RP Wu, F; Ding, Y (corresponding author), Dalian Univ, Affiliated Zhongshan Hosp, Inst Translat Med, Dalian, Peoples R China.; Ding, Y (corresponding author), Harvard Med Sch, Dept Pediat, Childrens Hosp Boston, Boston, MA 02115 USA.
EM wufei0348@126.com; yan.ding@childrens.harvard.edu
RI Gong, Guanyu/ABA-1935-2021; Wang, Ruoyu/ISU-3815-2023; Zhao,
   Dewei/G-8369-2016; YANG, BIN/ABF-3840-2020
OI Gong, Guanyu/0000-0002-5791-0916
CR [Anonymous], 2011, ISRN ONCOL
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NR 13
TC 7
Z9 7
U1 1
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 FEB 7
PY 2019
VL 9
AR 55
DI 10.3389/fonc.2019.00055
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HK5VS
UT WOS:000458037200001
PM 30792968
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Triest, L
   Debeuckelaere, C
   Vandamme, T
   Van Den Heuvel, B
   Van Den Brande, J
   Papadimitriou, K
   Rasschaert, M
   Prenen, H
   Peeters, M
AF Triest, Lars
   Debeuckelaere, C.
   Vandamme, T.
   Van Den Heuvel, B.
   Van Den Brande, J.
   Papadimitriou, K.
   Rasschaert, M.
   Prenen, H.
   Peeters, M.
TI Should Anti-EGFR Agents Be Used in Right-Sided RAS Wild-type Advanced
   Colorectal Cancer?
SO CURRENT COLORECTAL CANCER REPORTS
LA English
DT Article
DE Metastatic colorectal cancer (mCRC); Targeted therapies; EGFR (epidermal
   growth factor receptor); Anti-EGFR mAb; Panitumumab; Cetuximab;
   Bevacizumab; Chemotherapy; Left-sided; Right-sided; Sidedness; RAS
   wild-type; Primary tumor location (PTL); Prognostic; Predictive;
   First-line; Overall survival (OS); Progression-free survival (PFS);
   Objective response rate (ORR); BRAF mutation; Microsatellite instability
   (MSI)
ID PRIMARY TUMOR; COLON-CANCER; 1ST-LINE TREATMENT; SURVIVAL; LOCATION;
   CETUXIMAB; BENEFIT; DISTAL; METAANALYSIS; ANTIBODIES
AB Purpose of ReviewColorectal cancer is the third most common cancer worldwide with a high mortality rate at the advanced stages of the disease. Treatment options are dependent on the stage of the disease, patients' performance status, and the specific molecular makeup of the tumor. Adding an anti-epidermal growth factor receptor monoclonal antibody (anti-EGFR mAb) to conventional chemotherapy in molecularly selected patients (i.e., RAS wild-type) leads to a survival advantage. We aim to review the latest evidence on the influence of primary tumor location (PTL) on treatment response to chemotherapy combined with an anti-EGFR in patients with metastatic colorectal cancer (mCRC).Recent FindingsColon cancer arising on the left side versus the right side of the colon portrays different outcomes, emerging PTL as an important characteristic in understanding the outcomes for patients with colorectal cancer. Patients with right-sided tumors have a worse prognosis than those with left-sided tumors. Primary tumor location may also be predictive of treatment benefit from targeted therapy with an anti-EGFR or anti-VEGF in the treatment of RAS wild-type mCRC. Although no benefit in overall survival (OS) has been demonstrated, available data up to now can endorse the use of an anti-EGFR in right-sided RAS wild-type advanced colorectal cancer if the therapy goal is tumor shrinkage (given the higher objective response rate). However, the majority of data on PTL has been obtained through retrospective analysis of clinical trials where PTL was neither part of the stratification nor pre-planned subgroup analysis, rendering it susceptible to recall bias.SummaryThere is a great necessity to improve our understanding of the molecular and histological variability in left versus right-sided colon cancer and its impact on future targeted therapy.
C1 [Triest, Lars; Debeuckelaere, C.; Vandamme, T.; Van Den Heuvel, B.; Van Den Brande, J.; Papadimitriou, K.; Rasschaert, M.; Prenen, H.; Peeters, M.] Antwerp Univ Hosp, Dept Oncol, Wilrijkstr 10, B-2650 Edegem, Belgium.
C3 University of Antwerp
RP Triest, L (corresponding author), Antwerp Univ Hosp, Dept Oncol, Wilrijkstr 10, B-2650 Edegem, Belgium.
EM lars.triest@uza.be
RI van den Heuvel, Bas/LPQ-3713-2024; Vandamme, Timon/C-4961-2013
OI Prenen, Hans/0000-0001-8802-7352; Vandamme, Timon/0000-0003-3701-5305
CR [Anonymous], 2014, J CLIN ONCOL, DOI DOI 10.1200/JCO.2014.32.15_SUPPL.3511
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NR 26
TC 3
Z9 3
U1 0
U2 3
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 2019
VL 15
IS 4
BP 130
EP 134
DI 10.1007/s11888-019-00439-x
PG 5
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA IL8ZP
UT WOS:000477575300004
DA 2025-01-04
ER

PT J
AU Wu, TM
   Liu, JB
   Liu, Y
   Shi, Y
   Li, W
   Wang, GR
   Ma, YS
   Fu, D
AF Wu, Ting-Miao
   Liu, Ji-Bin
   Liu, Yu
   Shi, Yi
   Li, Wen
   Wang, Gao-Ren
   Ma, Yu-Shui
   Fu, Da
TI Power and Promise of Next-Generation Sequencing in Liquid Biopsies and
   Cancer Control
SO CANCER CONTROL
LA English
DT Article
DE cancer; NGS; cfDNA; targeted therapy; immunotherapy
ID CIRCULATING TUMOR-CELLS; COLORECTAL-CANCER; ONCOLYTIC ADENOVIRUS;
   STEM-CELLS; EXPRESSION; DELIVERY; GENE; METASTASIS; BIOMARKERS;
   STERNNESS
AB Traditional methods of cancer treatment are usually based on the morphological and histological diagnosis of tumors, and they are not optimized according to the specific situation. Precision medicine adjusts the existing treatment regimen based on the patient's genomic information to make it most suitable for patients. Detection of genetic mutations in tumors is the basis of precise cancer medicine. Through the analysis of genetic mutations in patients with cancer, we can tailor the treatment plan for each patient with cancer to maximize the curative effect, minimize damage to healthy tissues, and optimize resources. In recent years, next-generation sequencing technology has developed rapidly and has become the core technology of precise targeted therapy and immunotherapy for cancer. From early cancer screening to treatment guidance for patients with advanced cancer, liquid biopsy is increasingly used in cancer management. This is as a result of the development of better noninvasive, repeatable, sensitive, and accurate tools used in early screening, diagnosis, evaluation, and monitoring of patients. Cell-free DNA, which is a new noninvasive molecular pathological detection method, often carries tumor-specific gene changes. It plays an important role in optimizing treatment and evaluating the efficacy of different treatment options in clinical trials, and it has broad clinical applications.
C1 [Wu, Ting-Miao; Fu, Da] Anhui Med Univ, Dept Radiol, Affiliated Hosp 4, Hefei, Peoples R China.
   [Liu, Ji-Bin; Wang, Gao-Ren; Ma, Yu-Shui] Nantong Tumor Hosp, Canc Inst, Nantong, Peoples R China.
   [Liu, Yu; Shi, Yi; Li, Wen] Cent South Univ Forestry & Technol, Coll Food Sci & Engn, Natl Engn Lab Rice & By Prod Deep Proc, Chaha, Peoples R China.
   [Ma, Yu-Shui; Fu, Da] Tongji Univ, Shanghai Peoples Hosp 10, Cent Lab Med Res, Sch Med, Shanghai, Peoples R China.
C3 Anhui Medical University; Central South University of Forestry &
   Technology; Tongji University
RP Fu, D (corresponding author), Anhui Med Univ, Dept Radiol, Affiliated Hosp 4, Hefei, Peoples R China.; Ma, YS (corresponding author), Nantong Tumor Hosp, Canc Inst, Nantong, Peoples R China.; Ma, YS; Fu, D (corresponding author), Tongji Univ, Shanghai Peoples Hosp 10, Cent Lab Med Res, Sch Med, Shanghai, Peoples R China.
EM mayushui2006@126.com; fu800da900@126.com
RI ma, yushui/HGC-6206-2022; bai, yanpeng/HHZ-3923-2022; Fu,
   Da/GXF-2656-2022; liu, James/E-9699-2014; Liu, Yue/HHM-8584-2022
OI Ma, Yu-Shui/0000-0002-5728-7458
FU National Natural Science Foundation of China [81972214, 81772932,
   81472202, 81201535, 81302065, 81671716, 81301993, 81372175, 81472209];
   Fundamental Research Funds for the Central Universities [22120170212,
   22120170117]; Scientific Research Fund Project of Anhui Medical
   University [2018xkj058]; Shanghai Natural Science Foundation
   [12ZR1436000]; Shanghai Municipal Commission of Health and Family
   Planning [201540228]; Special Funding Fund for Clinical Research of Wu
   Jieping Medical Foundation [320.6750.14326]; Nantong Science and
   Technology Project [YYZ15026]; Peak of Six personnel Foundation in
   Jiangsu Province [WSW-009]; Fifth Phase of 333 Talents Engineering
   Science and Technology Project of Jiangsu Province [2017205]; Jiangsu
   Province Science Foundation for Youths [BK2012101]
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: This study
   was supported partly by grants from the National Natural Science
   Foundation of China (81972214, 81772932, 81472202, 81201535, 81302065,
   81671716, 81301993, 81372175 and 81472209), The Fundamental Research
   Funds for the Central Universities (22120170212 and 22120170117), The
   Scientific Research Fund Project of Anhui Medical University
   (2018xkj058), Shanghai Natural Science Foundation (12ZR1436000),
   Shanghai Municipal Commission of Health and Family Planning (201540228),
   Special Funding Fund for Clinical Research of Wu Jieping Medical
   Foundation (320.6750.14326), Nantong Science and Technology Project
   (YYZ15026), The Peak of Six personnel Foundation in Jiangsu Province
   (WSW-009), The Fifth Phase of 333 Talents Engineering Science and
   Technology Project of Jiangsu Province (2017205), and Jiangsu Province
   Science Foundation for Youths (BK2012101).
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NR 143
TC 10
Z9 10
U1 4
U2 14
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1073-2748
J9 CANCER CONTROL
JI Cancer Control
PD JUL
PY 2020
VL 27
IS 3
AR 1073274820934805
DI 10.1177/1073274820934805
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NF3RW
UT WOS:000563216600001
PM 32806937
OA Green Published
DA 2025-01-04
ER

PT J
AU Trevino, ENG
   Reyes, AGQ
   Murillo, JAR
   Kalife, DAD
   Gonzalez, PD
   Islas, JF
   Rodriguez, AEE
   Villarreal, CAG
AF Garza Trevino, Elsa N.
   Quiroz Reyes, Adriana G.
   Rojas Murillo, Juan Antonio
   de la Garza Kalife, David A.
   Delgado Gonzalez, Paulina
   Islas, Jose F.
   Estrada Rodriguez, Ana Esther
   Gonzalez Villarreal, Carlos A.
TI Cell Therapy as Target Therapy against Colon Cancer Stem Cells
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE cancer; cancer stem cells; colon cancer; cell therapy; T cells
ID TUMOR-INFILTRATING LYMPHOCYTES; COLORECTAL-CANCER; T-CELLS;
   CERVICAL-CANCER; GASTRIC-CANCER; KILLER-CELLS; IN-VITRO; EXPRESSION;
   TRAIL; IMMUNOTHERAPY
AB Cancer stem cells (CSCs) are a small subpopulation of cells within tumors with properties, such as self-renewal, differentiation, and tumorigenicity. CSCs have been proposed as a plausible therapeutic target as they are responsible for tumor recurrence, metastasis, and conventional therapy resistance. Selectively targeting CSCs is a promising strategy to eliminate the propagation of tumor cells and impair overall tumor development. Recent research shows that several immune cells play a crucial role in regulating tumor cell proliferation by regulating different CSC maintenance or proliferation pathways. There have been great advances in cellular immunotherapy using T cells, natural killer (NK) cells, macrophages, or stem cells for the selective targeting of tumor cells or CSCs in colorectal cancer (CRC). This review summarizes the CRC molecular profiles that may benefit from said therapy and the main vehicles used in cell therapy against CSCs. We also discuss the challenges, limitations, and advantages of combining conventional and/or current targeted treatments in the late stages of CRC.
C1 [Garza Trevino, Elsa N.; Quiroz Reyes, Adriana G.; Rojas Murillo, Juan Antonio; de la Garza Kalife, David A.; Delgado Gonzalez, Paulina; Islas, Jose F.] Univ Autonoma Nuevo Leon, Fac Med, Dept Bioquim & Med Mol, Lab Terapia Celular, Av Dr Jose Eleuterio Gonzalez 235, Monterrey 64460, Nuevo Leon, Mexico.
   [Estrada Rodriguez, Ana Esther; Gonzalez Villarreal, Carlos A.] Univ Monterrey, Dept Ciencias Basics, Vicerrectoria Ciencias Salud, Ignacio Morones Prieto 4500 Jesus M Garza, San Pedro Garza Garcia 66238, Nuevo Leon, Mexico.
C3 Universidad Autonoma de Nuevo Leon; Universidad de Monterrey;
   Tecnologico de Monterrey
RP Villarreal, CAG (corresponding author), Univ Monterrey, Dept Ciencias Basics, Vicerrectoria Ciencias Salud, Ignacio Morones Prieto 4500 Jesus M Garza, San Pedro Garza Garcia 66238, Nuevo Leon, Mexico.
EM elsa.garzatr@uanl.edu.mx; guadalupe.quirozrys@uanl.edu.mx;
   juan.rojasmrll@uanl.edu.mx; david.delagarzaka@uanl.edu.mx;
   paulina.delgadogn@uanl.edu.mx; jislas.me0117@uanl.edu.mx;
   ana.estradar@udem.edu; carlosalberto.gonzalezv@udem.edu
RI Reyes, Adriana/JGL-7369-2023; Islas, Jose Francisco/K-2728-2018
OI de la Garza, David Andres/0009-0002-9307-8482; Islas, Jose
   Francisco/0000-0002-0337-9912; Estrada, Ana/0000-0002-0301-9394; Quiroz
   Reyes, Adriana G./0000-0002-9405-7483; Rojas Murillo, Juan
   Antonio/0000-0002-0240-8486
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NR 139
TC 6
Z9 6
U1 4
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 MAY 3
PY 2023
VL 24
IS 9
AR 8163
DI 10.3390/ijms24098163
PG 21
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA G2OZ5
UT WOS:000987626400001
PM 37175871
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Nkune, NW
   Kruger, CA
   Abrahamse, H
AF Nkune, Nkune W.
   Kruger, Cherie A.
   Abrahamse, Heidi
TI Possible Enhancement of Photodynamic Therapy (PDT) Colorectal Cancer
   Treatment when Combined with Cannabidiol
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE Colorectal Cancer (CRC); combinative treatment; Cannabis sativa;
   Cannabidiol (CBD); Photodynamic Therapy (PDT); targeted therapy
ID COLON-CANCER; INDUCED APOPTOSIS; DRUG-DELIVERY; ZINC PHTHALOCYANINE;
   RADIATION-THERAPY; TARGETED THERAPY; RECTAL-CANCER; STAGE-II;
   NANOPARTICLES; AUTOPHAGY
AB Colorectal Cancer (CRC) has a high mortality rate and is one of the most difficult diseases to manage due to tumour resistance and metastasis. The treatment of choice for CRC is reliant on the phase and time of diagnosis. Despite several conventional treatments available to treat CRC (surgical excision, chemo-, radiation and immune-therapy), resistance is a major challenge, especially if it has metastasized. Additionally, these treatments often cause unwanted adverse side effects and so it remains imperative to investigate alternative combination therapies.
   Photodynamic Therapy (PDT) is a promising treatment modality for the primary treatment of CRC, since it is non-invasive, has few side effects and selectively damages only cancerous tissues, leaving adjacent healthy structures intact. PDT involves three fundamentals: a Photosensitizer (PS) drug localized in tumour tissues, oxygen, and light. Upon PS excitation using a specific wavelength of light, an energy transfer cascade occurs, that ultimately yields cytotoxic species, which in turn induces cell death. Cannabidiol (CBD) is a cannabinoid compound derived from the Cannabis sativa plant, which has shown to exert anticancer effects on CRC through different pathways, inducing apoptosis and so inhibiting tumour metastasis and secondary spread.
   This review paper highlights current conventional treatment modalities for CRC and their limitations, as well as discusses the necessitation for further investigation into unconventional active nanoparticle targeting PDT treatments for enhanced primary CRC treatment. This can be administered in combination with CBD, to prevent CRC secondary spread and enhance the synergistic efficacy of CRC treatment outcomes, with less side effects.
C1 [Nkune, Nkune W.; Kruger, Cherie A.; Abrahamse, Heidi] Univ Johannesburg, Fac Hlth Sci, Laser Res Ctr, Johannesburg, South Africa.
C3 University of Johannesburg
RP Kruger, CA (corresponding author), Univ Johannesburg, Fac Hlth Sci, Dept Laser Res Ctr, POB 17011, Johannesburg, South Africa.
EM cherier@uj.ac.za
RI Nkune, Nkune/AAK-1713-2021; Kruger, Cherie Ann/H-2004-2016; Abrahamse,
   Heidi/U-7763-2019
OI Kruger, Cherie Ann/0000-0002-4556-9132; Nkune, Nkune
   Williams/0000-0003-3746-707X; Abrahamse, Heidi/0000-0001-5002-827X
FU South African Research Chairs Initiative of the Department of Science
   and Technology; South African Research Chairs Initiative of the National
   Research Foundation of South Africa [98337]; National Research
   Foundation Thuthuka Fund [TTK180409318735]; Cancer Association of South
   Africa (CANSA) Research Funding Grant; University of Johannesburg;
   National Laser Centre; National Research Foundation of South Africa
   (CSIR-DST); CSIR-DST InterBursary Programme
FX This work is based on the research supported by the South African
   Research Chairs Initiative of the Department of Science and Technology
   and National Research Foundation of South Africa (Grant No 98337),
   National Research Foundation Thuthuka Fund (Grant No TTK180409318735)
   and Cancer Association of South Africa (CANSA) Research Funding Grant.
   The authors sincerely thank the University of Johannesburg, the National
   Laser Centre and the National Research Foundation of South Africa
   (CSIR-DST) for their financial grant support, as well as the CSIR-DST
   InterBursary Programme for postgraduate student monetary support.
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NR 111
TC 25
Z9 27
U1 4
U2 45
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1871-5206
EI 1875-5992
J9 ANTI-CANCER AGENT ME
JI Anti-Cancer Agents Med. Chem.
PY 2021
VL 21
IS 2
BP 137
EP 148
DI 10.2174/1871520620666200415102321
PG 12
WC Oncology; Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA QK4KN
UT WOS:000620356100003
PM 32294046
OA hybrid
DA 2025-01-04
ER

PT J
AU Janssen, JBE
   Medema, JP
   Gootjes, EC
   Tauriello, DVF
   Verheul, HMW
AF Janssen, Jorien B. E.
   Medema, Jan Paul
   Gootjes, Elske C.
   Tauriello, Daniele V. F.
   Verheul, Henk M. W.
TI Mutant RAS and the tumor microenvironment as dual therapeutic targets
   for advanced colorectal cancer
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE Colorectal cancer; Tumor microenvironment; RAS mutations; Immunotherapy;
   Targeted therapy
ID CONSENSUS MOLECULAR SUBTYPES; BRAF INHIBITION; COLON-CANCER; K-RAS;
   N-RAS; KRAS; CELLS; MUTATIONS; EXPRESSION; CETUXIMAB
AB RAS genes are the most frequently mutated oncogenes in cancer. These mutations occur in roughly half of the patients with colorectal cancer (CRC). RAS mutant tumors are resistant to therapy with anti-EGFR monoclonal antibodies. Therefore, patients with RAS mutant CRC currently have few effective therapy options. RAS mutations lead to constitutively active RAS GTPases, involved in multiple downstream signaling pathways. These alterations are associated with a tumor microenvironment (TME) that drives immune evasion and disease progression by mechanisms that remain incompletely understood. In this review, we focus on the available evidence in the literature explaining the potential effects of RAS mutations on the CRC microenvironment. Ongoing efforts to influence the TME by targeting mutant RAS and thereby sensitizing these tumors to immunotherapy will be discussed as well.
C1 [Janssen, Jorien B. E.; Gootjes, Elske C.; Verheul, Henk M. W.] Radboud Univ Nijmegen, Radboud Inst Hlth Sci, Dept Med Oncol, Med Ctr, Nijmegen, Netherlands.
   [Tauriello, Daniele V. F.] Radboud Univ Nijmegen, Radboud Inst Mol Life Sci, Dept Cell Biol, Med Ctr, Nijmegen, Netherlands.
   [Medema, Jan Paul] Univ Amsterdam, Ctr Expt Mol Med, Canc Ctr Amsterdam, Lab Expt Oncol & Radiobiol,Amsterdam UMC, Amsterdam, Netherlands.
   [Tauriello, Daniele V. F.; Verheul, Henk M. W.] Radboud Univ Nijmegen Med Ctr, Radboud Inst Hlth Sci, Dept Med Oncol, Geert Grootepl Zuid 8, NL-6525 GA Nijmegen, Netherlands.
C3 Radboud University Nijmegen; Radboud University Nijmegen; University of
   Amsterdam; Vrije Universiteit Amsterdam; Radboud University Nijmegen
RP Tauriello, DVF; Verheul, HMW (corresponding author), Radboud Univ Nijmegen Med Ctr, Radboud Inst Hlth Sci, Dept Med Oncol, Geert Grootepl Zuid 8, NL-6525 GA Nijmegen, Netherlands.
EM Jorien.janssen@radboudumc.nl; j.p.medema@amsterdamumc.nl;
   elske.gootjes@radboudumc.nl; Daniele.Tauriello@radboudumc.nl;
   henk.verheul@radboudumc.nl
RI Janssen, Jorien/AAD-6330-2020; Tauriello, Daniele V. F./H-4644-2018
OI Tauriello, Daniele V. F./0000-0003-1522-3496; Janssen,
   Jorien/0000-0001-9190-9911
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NR 127
TC 22
Z9 22
U1 0
U2 11
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0305-7372
EI 1532-1967
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD SEP
PY 2022
VL 109
AR 102433
DI 10.1016/j.ctrv.2022.102433
EA JUL 2022
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3Y1ZB
UT WOS:000843526900001
PM 35905558
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Chen, YF
   Luh, F
   Ho, YS
   Yen, Y
AF Chen, Yi-Fan
   Luh, Frank
   Ho, Yuan-Soon
   Yen, Yun
TI Exosomes: a review of biologic function, diagnostic and targeted therapy
   applications, and clinical trials
SO JOURNAL OF BIOMEDICAL SCIENCE
LA English
DT Review
DE Exosome; siRNA; Cancer diagnosis; Cancer therapy
ID HUMAN RIBONUCLEOTIDE REDUCTASE; SIZE-EXCLUSION CHROMATOGRAPHY;
   CANCER-THERAPY; EXTRACELLULAR VESICLES; COLORECTAL-CANCER; SYSTEMIC
   DELIVERY; IN-VITRO; SIRNA; NANOPARTICLES; CELLS
AB Exosomes are extracellular vesicles generated by all cells and they carry nucleic acids, proteins, lipids, and metabolites. They mediate the exchange of substances between cells,thereby affecting biological properties and activities of recipient cells. In this review, we briefly discuss the composition of exocomes and exosome isolation. We also review the clinical applications of exosomes in cancer biology as well as strategies in exosome-mediated targeted drug delivery systems. Finally, the application of exosomes in the context of cancer therapeutics both in practice and literature are discussed.
C1 [Chen, Yi-Fan] Taipei Med Univ, Coll Med Sci & Technol, Int Master Program Translat Sci, New Taipei City 23564, Taiwan.
   [Chen, Yi-Fan] Taipei Med Univ, Coll Med Sci & Technol, Ph D Program Translat Med, New Taipei City 23564, Taiwan.
   [Chen, Yi-Fan; Yen, Yun] Taipei Med Univ, TMU Res Ctr Canc Translat Med, Taipei 11031, Taiwan.
   [Chen, Yi-Fan] Taipei Med Univ, Coll Med Sci & Technol, Int PhD Program Translat Sci, New Taipei City 23564, Taiwan.
   [Chen, Yi-Fan] Taipei Med Univ, Sch Pharm, Master Program Clin Genom & Prote, Taipei 11031, Taiwan.
   [Luh, Frank] Sino Amer Canc Fdn, Covina, CA 91722 USA.
   [Ho, Yuan-Soon; Yen, Yun] China Med Univ, Inst Biochem & Mol Biol, Coll Life Sci, Taichung 406040, Taiwan.
   [Yen, Yun] Taipei Med Univ, Coll Med Sci & Technol, PhD Program Canc Mol Biol & Drug Discovery, Taipei 110301, Taiwan.
   [Yen, Yun] Taipei Med Univ, Grad Inst Canc Biol & Drug Discovery, Coll Med Sci & Technol, Taipei 110301, Taiwan.
   [Yen, Yun] Taipei Municipal WanFang Hosp, Canc Ctr, Taipei 11696, Taiwan.
   [Yen, Yun] Tzu Chi Univ, Ctr Canc Translat Res, Hualien 970374, Taiwan.
C3 Taipei Medical University; Taipei Medical University; China Medical
   University Taiwan; Taipei Municipal WanFang Hospital; Tzu Chi University
RP Yen, Y (corresponding author), Taipei Med Univ, TMU Res Ctr Canc Translat Med, Taipei 11031, Taiwan.; Ho, YS; Yen, Y (corresponding author), China Med Univ, Inst Biochem & Mol Biol, Coll Life Sci, Taichung 406040, Taiwan.; Yen, Y (corresponding author), Taipei Med Univ, Coll Med Sci & Technol, PhD Program Canc Mol Biol & Drug Discovery, Taipei 110301, Taiwan.; Yen, Y (corresponding author), Taipei Med Univ, Grad Inst Canc Biol & Drug Discovery, Coll Med Sci & Technol, Taipei 110301, Taiwan.; Yen, Y (corresponding author), Taipei Municipal WanFang Hosp, Canc Ctr, Taipei 11696, Taiwan.; Yen, Y (corresponding author), Tzu Chi Univ, Ctr Canc Translat Res, Hualien 970374, Taiwan.
EM hoyuansn@mail.cmu.edu.tw; yyen@tmu.edu.tw
RI Chen, Yi-Fan/AAP-1427-2020
OI Yen, Yun/0000-0003-0815-412X
FU Ministry of Science and Technology
FX No Statement Available
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NR 117
TC 8
Z9 8
U1 14
U2 14
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1021-7770
EI 1423-0127
J9 J BIOMED SCI
JI J. Biomed. Sci.
PD JUL 11
PY 2024
VL 31
IS 1
AR 67
DI 10.1186/s12929-024-01055-0
PG 16
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA YS5Y5
UT WOS:001270498000001
PM 38992695
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Garajová, I
   Ferracin, M
   Porcellini, E
   Palloni, A
   Abbati, F
   Biasco, G
   Brandi, G
AF Garajova, Ingrid
   Ferracin, Manuela
   Porcellini, Elisa
   Palloni, Andrea
   Abbati, Francesca
   Biasco, Guido
   Brandi, Giovanni
TI Non-Coding RNAs as Predictive Biomarkers to Current Treatment in
   Metastatic Colorectal Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colorectal cancer; non-coding RNA; microRNA; predictive biomarker
ID BRAF-MUTATION; CELLS; CHEMORADIOTHERAPY; OVEREXPRESSION; 5-FLUOROURACIL;
   EXPRESSION; RESISTANCE; MICRORNAS; IMMUNOTHERAPY; ANGIOGENESIS
AB The onset and selection of resistant clones during cancer treatment with chemotherapy or targeted therapy is a major issue in the clinical management of metastatic colorectal cancer patients. It is possible that a more personalized treatment selection, using reliable response-to-therapy predictive biomarkers, could lead to an improvement in the success rate of the proposed therapies. Although the process of biomarker selection and validation could be a long one, requiring solid statistics, large cohorts and multicentric validations, non-coding RNAs (ncRNAs) and in particular microRNAs, proved to be extremely promising in this field. Here we summarize some of the main studies correlating specific ncRNAs with sensitivity/resistance to chemotherapy, anti-VEGF therapy, anti-EGFR therapy and immunotherapy in colorectal cancer (CRC).
C1 [Garajova, Ingrid; Ferracin, Manuela; Porcellini, Elisa; Palloni, Andrea; Abbati, Francesca; Biasco, Guido; Brandi, Giovanni] Univ Bologna, Dept Expt Diagnost & Specialty Med DIMES, St Orsola Malpighi Hosp, I-40138 Bologna, Italy.
   [Garajova, Ingrid; Biasco, Guido] Univ Bologna, Interdept Ctr Canc Res Giorgio Prodi, I-40138 Bologna, Italy.
C3 IRCCS Azienda Ospedaliero-Universitaria di Bologna; University of
   Bologna; University of Bologna
RP Garajová, I (corresponding author), Univ Bologna, Dept Expt Diagnost & Specialty Med DIMES, St Orsola Malpighi Hosp, I-40138 Bologna, Italy.; Garajová, I (corresponding author), Univ Bologna, Interdept Ctr Canc Res Giorgio Prodi, I-40138 Bologna, Italy.
EM ingegarajova@gmail.com; manuela.ferracin@unibo.it;
   elisa.porcellini3@unibo.it; andrepalloni@gmail.com;
   francesca.abbati1989@gmail.com; guido.biasco@unibo.it;
   giovanni.brandi@unibo.it
RI Palloni, Andrea/AAB-9872-2022; Garajova, Ingrid/AFY-8069-2022; Brandi,
   Giovanni/AAD-6327-2021; Porcellini, Elisa/K-5346-2016; Ferracin,
   Manuela/K-2097-2016
OI Palloni, Andrea/0000-0003-1260-2765; Porcellini,
   Elisa/0000-0003-3991-5294; Garajova', Ingrid/0000-0002-9302-6896;
   Ferracin, Manuela/0000-0002-1595-6887
FU Italian Association for Cancer Research (AIRC) [18464]
FX The work was supported by funding from the Italian Association for
   Cancer Research (AIRC) to MF (IG 18464). We thank Miriam Ferracin for
   her assistance in the graphical abstract preparation.
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TC 21
Z9 21
U1 2
U2 5
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 JUL
PY 2017
VL 18
IS 7
AR 1547
DI 10.3390/ijms18071547
PG 10
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA FF2SJ
UT WOS:000408746800214
PM 28714940
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Bronte, G
   Silvestris, N
   Castiglia, M
   Galvano, A
   Passiglia, F
   Sortino, G
   Cicero, G
   Rolfo, C
   Peeters, M
   Bazan, V
   Fanale, D
   Giordano, A
   Russo, A
AF Bronte, Giuseppe
   Silvestris, Nicola
   Castiglia, Marta
   Galvano, Antonio
   Passiglia, Francesco
   Sortino, Giovanni
   Cicero, Giuseppe
   Rolfo, Christian
   Peeters, Marc
   Bazan, Viviana
   Fanale, Daniele
   Giordano, Antonio
   Russo, Antonio
TI New findings on primary and acquired resistance to anti-EGFR therapy in
   metastatic colorectal cancer: do all roads lead to RAS?
SO ONCOTARGET
LA English
DT Article
DE RAS; colorectal cancer; epidermal growth factor receptor; cetuximab;
   panitumumab
ID GROWTH-FACTOR RECEPTOR; KRAS WILD-TYPE; CETUXIMAB PLUS IRINOTECAN;
   DRUG-ADMINISTRATION APPROVAL; MULTICENTER PHASE-II; CELL-FREE DNA;
   1ST-LINE TREATMENT; MONOCLONAL-ANTIBODIES; TARGETED THERAPY; BRAF
   MUTATION
AB Anti-epidermal growth factor receptor therapy with the monoclonal antibodies cetuximab and panitumumab is the main targeted treatment to combine with standard chemotherapy for metastatic colorectal cancer. Many clinical studies have shown the benefit of the addition of these agents for patients without mutations in the EGFR pathway. Many biomarkers, including KRAS and NRAS mutations, BRAF mutations, PIK3CA mutations, PTEN loss, AREG and EREG expression, and HER-2 amplification have already been identified to select responders to anti-EGFR agents. Among these alterations KRAS and NRAS mutations are currently recognized as the best predictive factors for primary resistance. Liquid biopsy, which helps to isolate circulating tumor DNA, is an innovative method to study both primary and acquired resistance to anti-EGFR monoclonal antibodies. However, high-sensitivity techniques should be used to enable the identification of a wide set of gene mutations related to resistance.
C1 [Bronte, Giuseppe; Castiglia, Marta; Galvano, Antonio; Passiglia, Francesco; Sortino, Giovanni; Cicero, Giuseppe; Bazan, Viviana; Fanale, Daniele; Russo, Antonio] Univ Palermo, Dept Surg Oncol & Oral Sci, Palermo, Italy.
   [Silvestris, Nicola] Natl Canc Inst Giovanni Paolo II, Med Oncol Unit, Bari, Italy.
   [Rolfo, Christian; Peeters, Marc] Univ Antwerp Hosp, Dept Oncol, Edegem, Belgium.
   [Giordano, Antonio] Temple Univ, Sbarro Inst Canc Res & Mol Med, Philadelphia, PA 19122 USA.
   [Giordano, Antonio] Univ Siena, Dept Med Surg & Neurosci, I-53100 Siena, Italy.
C3 University of Palermo; IRCCS Istituto Tumori Bari Giovanni Paolo II;
   University of Antwerp; Pennsylvania Commonwealth System of Higher
   Education (PCSHE); Temple University; University of Siena
RP Russo, A (corresponding author), Univ Palermo, Dept Surg Oncol & Oral Sci, Palermo, Italy.
EM antonio.russo@usa.net
RI Galvano, Antonio/K-7810-2016; Castiglia, Marta/K-6569-2016; Fanale,
   Daniele/K-8630-2016; Rolfo, Christian/AAW-5173-2021; Passiglia,
   Francesco/AAC-7794-2022; Silvestris, Nicola/K-5889-2012; Peeters,
   Marc/C-5525-2013; Giordano, Antonio/F-1927-2010
OI Castiglia, Marta/0000-0002-6299-7235; Giordano,
   Antonio/0000-0002-5959-016X; Galvano, Antonio/0000-0003-4365-5683;
   Bronte, Giuseppe/0000-0002-2306-2445; Rolfo,
   Christian/0000-0002-7860-8417; Passiglia, Francesco/0000-0002-0244-5738
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NR 122
TC 72
Z9 75
U1 0
U2 17
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 22
PY 2015
VL 6
IS 28
BP 24780
EP 24796
DI 10.18632/oncotarget.4959
PG 17
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CT9TS
UT WOS:000363160100023
PM 26318427
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Fu, YH
   Sun, H
AF Fu, Yihan
   Sun, Hong
TI Biogenesis, cellular effects, and biomarker value of circHIPK3
SO CANCER CELL INTERNATIONAL
LA English
DT Review
DE CircHIPK3; MiRNAs sponge; Biomarker; Cancer
ID CIRCULAR RNA CIRCHIPK3; TO-MYOFIBROBLAST TRANSITION; PROSTATE-CANCER
   CELLS; COLORECTAL-CANCER; MYOCARDIAL-INFARCTION; INDUCED CYTOTOXICITY;
   REGULATORY NETWORK; EPITHELIAL-CELLS; GASTRIC-CANCER; PROMOTES
AB Competing endogenous RNAs (ceRNAs) can indirectly regulate gene expression by competitively binding to microRNA(miRNA) through miRNA response elements (MREs) to affect miRNA-induced gene regulation, which is of great biological significance. Among them, circular RNA (circRNA) has become a hotspot due to its highest binding capacity. A specific circRNA discussed in this review, circHIPK3, has been studied for its biological characteristics, function, cellular effects and its relationship with tumors and various diseases. Here, we review the recent researches about circHIPK3 in detail and aim to elucidate accurate conclusions from them. These circHIPK3-miRNAs-mRNA pathways will further advance the application of circHIPK3 in diseases development, early diagnosis and gene targeting therapy.
C1 [Fu, Yihan; Sun, Hong] Fudan Univ, Obstet & Gynecol Hosp, Shanghai, Peoples R China.
C3 Fudan University
RP Sun, H (corresponding author), Fudan Univ, Obstet & Gynecol Hosp, Shanghai, Peoples R China.
EM hongsun57@hotmail.com
FU Shanghai Science and Technology Department Funds
FX Shanghai Science and Technology Department Funds
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NR 102
TC 16
Z9 18
U1 0
U2 16
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 MAY 11
PY 2021
VL 21
IS 1
AR 256
DI 10.1186/s12935-021-01956-2
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SA5RH
UT WOS:000649360200001
PM 33975598
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yang, ML
   Davis, TB
   Pflieger, L
   Nebozhyn, MV
   Loboda, A
   Wang, HM
   Schell, MJ
   Thota, R
   Pledger, WJ
   Yeatman, TJ
AF Yang, Mingli
   Davis, Thomas B.
   Pflieger, Lance
   Nebozhyn, Michael, V
   Loboda, Andrey
   Wang, Heiman
   Schell, Michael J.
   Thota, Ramya
   Pledger, W. Jack
   Yeatman, Timothy J.
TI An integrative gene expression signature analysis identifies CMS4
   <i>KRAS</i>-mutated colorectal cancers sensitive to combined MEK and SRC
   targeted therapy
SO BMC CANCER
LA English
DT Article
DE Colorectal cancer; MEK inhibitor; Targeted therapy; SRC; EMT; Cancer
   stem cell; CMS; Gene expression signature
ID C-SRC; COLON-CANCER; TYROSINE KINASES; PROTEIN-KINASE; STEM-CELLS;
   INHIBITION; MUTANT; ACTIVATION; RESISTANCE; PP60C-SRC
AB Background Over half of colorectal cancers (CRCs) are hard-wired to RAS/RAF/MEK/ERK pathway oncogenic signaling. However, the promise of targeted therapeutic inhibitors, has been tempered by disappointing clinical activity, likely due to complex resistance mechanisms that are not well understood. This study aims to investigate MEK inhibitor-associated resistance signaling and identify subpopulation(s) of CRC patients who may be sensitive to biomarker-driven drug combination(s). Methods We classified 2250 primary and metastatic human CRC tumors by consensus molecular subtypes (CMS). For each tumor, we generated multiple gene expression signature scores measuring MEK pathway activation, MEKi "bypass" resistance, SRC activation, dasatinib sensitivity, EMT, PC1, Hu-Lgr5-ISC, Hu-EphB2-ISC, Hu-Late TA, Hu-Proliferation, and WNT activity. We carried out correlation, survival and other bioinformatic analyses. Validation analyses were performed in two independent publicly available CRC tumor datasets (n = 585 and n = 677) and a CRC cell line dataset (n = 154). Results Here we report a central role of SRC in mediating "bypass"-resistance to MEK inhibition (MEKi), primarily in cancer stem cells (CSCs). Our integrated and comprehensive gene expression signature analyses in 2250 CRC tumors reveal that MEKi-resistance is strikingly-correlated with SRC activation (Spearman P < 10(-320)), which is similarly associated with EMT (epithelial to mesenchymal transition), regional metastasis and disease recurrence with poor prognosis. Deeper analysis shows that both MEKi-resistance and SRC activation are preferentially associated with a mesenchymal CSC phenotype. This association is validated in additional independent CRC tumor and cell lines datasets. The CMS classification analysis demonstrates the strikingly-distinct associations of CMS1-4 subtypes with the MEKi-resistance and SRC activation. Importantly, MEKi + SRCi sensitivities are predicted to occur predominantly in the KRAS mutant, mesenchymal CSC-like CMS4 CRCs. Conclusions Large human tumor gene expression datasets representing CRC heterogeneity can provide deep biological insights heretofore not possible with cell line models, suggesting novel repurposed drug combinations. We identified SRC as a common targetable node--an Achilles' heel--in MEKi-targeted therapy-associated resistance in mesenchymal stem-like CRCs, which may help development of a biomarker-driven drug combination (MEKi + SRCi) to treat problematic subpopulations of CRC.
C1 [Yang, Mingli; Davis, Thomas B.; Wang, Heiman; Pledger, W. Jack; Yeatman, Timothy J.] Univ S Florida, Tampa Gen Hosp Canc Inst, Dept Surg & Mol Med, 560 Channelside Dr, Tampa, FL 33602 USA.
   [Pflieger, Lance] Intermt Healthcare, Precis Genom Translat Sci Ctr, 5026 South State St, Murray, UT 84107 USA.
   [Nebozhyn, Michael, V; Loboda, Andrey] Sharp & Dohme, 770 Sumneytown Pike,Bldg 53,West Point,POB 4, Merck, PA 19486 USA.
   [Schell, Michael J.] H Lee Moffitt Canc Ctr & Res Inst, Dept Biostat & Bioinformat, 12902 Magnolia Dr, Tampa, FL USA.
   [Schell, Michael J.] Res Inst, 12902 Magnolia Dr, Tampa, FL 33612 USA.
   [Thota, Ramya] Intermt Healthcare, Oncol Clin Program, 5026 South State St, Murray, UT 84107 USA.
   [Pledger, W. Jack; Yeatman, Timothy J.] Univ Utah, Huntsman Canc Inst, 2000 Cir Hope Dr, Salt Lake City, UT 84112 USA.
C3 State University System of Florida; University of South Florida;
   Intermountain Healthcare; Intermountain Medical Center; H Lee Moffitt
   Cancer Center & Research Institute; Intermountain Healthcare;
   Intermountain Medical Center; Utah System of Higher Education;
   University of Utah; Huntsman Cancer Institute
RP Yeatman, TJ (corresponding author), Univ S Florida, Tampa Gen Hosp Canc Inst, Dept Surg & Mol Med, 560 Channelside Dr, Tampa, FL 33602 USA.; Yeatman, TJ (corresponding author), Univ Utah, Huntsman Canc Inst, 2000 Cir Hope Dr, Salt Lake City, UT 84112 USA.
EM yeatman7383@gmail.com
RI Yeatman, Timothy/LJK-6730-2024
OI Yang, Mingli/0000-0002-4781-690X
FU National Institutes of Health [UH2CA227955, UH3CA227955, R21CA252436,
   R21CA255312, R21 CA256372]; Intermountain Healthcare; National Cancer
   Institute [UH3CA227955] Funding Source: NIH RePORTER
FX This work is supported by National Institutes of Health grants
   UH2CA227955 (TJY) and UH3CA227955 (TJY) as well as R21CA252436 (TJY),
   R21CA255312 (TJY) and R21 CA256372 (TJY); This work is also supported by
   the fund from Intermountain Healthcare.
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NR 57
TC 8
Z9 8
U1 0
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD MAR 10
PY 2022
VL 22
IS 1
AR 256
DI 10.1186/s12885-022-09344-3
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZQ6PM
UT WOS:000767224600002
PM 35272617
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Gerger, A
   Eisterer, W
   Fuxius, S
   Bastian, S
   Koeberle, D
   Welslau, M
   Sanoyan, DA
   Maas, C
   Uhlig, J
   Fenchel, K
   Greil, R
   von der Heyde, E
   Agocs, GR
   Weide, R
   Schwager, M
   Reichenbach, F
   Modest, DP
   Fritsch, R
AF Gerger, Armin
   Eisterer, Wolfang
   Fuxius, Stefan
   Bastian, Sara
   Koeberle, Dieter
   Welslau, Manfred
   Sanoyan, Dilara Akhoundova
   Maas, Christian
   Uhlig, Jens
   Fenchel, Klaus
   Greil, Richard
   von der Heyde, Eyck
   Agocs, Gaelle Rhyner
   Weide, Rudolf
   Schwager, Monika
   Reichenbach, Frank
   Modest, Dominik Paul
   Fritsch, Ralph
TI Retrospective Analysis of Treatment Pathways in Patients With
   BRAFV600E-mutant Metastatic Colorectal Carcinoma - MORSECRC
SO ANTICANCER RESEARCH
LA English
DT Article
DE Chemotherapy; targeted therapy; Germany; Austria; Switzerland; treatment
   reality; disease characteristics
ID CETUXIMAB PLUS IRINOTECAN; PHASE-III TRIAL; 1ST-LINE TREATMENT; RAS
   MUTATIONS; BRAF MUTATION; WILD-TYPE; MICROSATELLITE INSTABILITY; CANCER;
   FLUOROURACIL; LEUCOVORIN
AB Background/Aim: Metastatic colorectal cancer (mCRC) is a heterogeneous disease with distinct molecular subtypes. The BRAFV600E-mutation found in approximately 8-12% of mCRC patients is associated with poor prognosis. Guideline recommendations for this population are mostly based on small cohorts due to lack of clinical data. This retrospective analysis was designed to evaluate (approved) therapeutic approaches and algorithms in BRAFV600E-mutant mCRC prior to approval of the targeted combination encorafenib plus cetuximab in Germany, Austria, and Switzerland. Patients and Methods: Anonymized data from BRAFV600E-mutant mCRC patients were analyzed retrospectively regarding 1st-, 2nd- and 3rd-line treatment using descriptive statistics. Results: Forty-two patients were eligible for analysis (mean age 62.1 years, 47.6% female). At initial diagnosis, 20 patients (47.6%) were documented with right -sided tumors. Most patients (81.0%) were tested for BRAF before 1st-line. Four patients (9.5%) showed high microsatellite instability (MSI-H). Based on 94 treatment lines, chemotherapy combined with targeted therapy (TT) was used mostly (61.7%), followed by chemotherapy alone (19.1%). Backbone therapies were most frequently FOLFOXIRI (27.7%), FOLFOX/CAPOX (22.3%), or FOLFIRI (20.2%). Anti-VEGF/VEGFR and anti-EGFR-treatments were used in 45.7% and 23.4% of patients, respectively. Across all treatment lines and types, the predominantly documented reason for discontinuation was lack of efficacy. Conclusion: Combined chemotherapy+TT (anti-VEGF/VEGFR and anti-EGFR) played a predominant role in BRAFV600E-mutated mCRC treatment prior to approval of the targeted combination encorafenib plus cetuximab. Since lack of efficacy was the major reason for treatment discontinuation, newly approved therapies including encorafenib plus cetuximab and - for MSI-H tumors - pembrolizumab represent urgently needed options for future mCRC patients.
C1 [Gerger, Armin] Med Univ Graz, Div Clin Oncol, Graz, Austria.
   [Eisterer, Wolfang] Klagenfurt Hosp, Dept Internal Med Hematol & Oncol, Klagenfurt, Austria.
   [Fuxius, Stefan] Practice Oncol, Heidelberg, Germany.
   [Fuxius, Stefan; Bastian, Sara] Canton Hosp Graubunden, Dept Internal Med Med Oncol & Hematol, Chur, Switzerland.
   [Koeberle, Dieter] Univ Bern, Canc Ctr St Claraspital, Basel, Bern, Switzerland.
   [Welslau, Manfred] Hematol & Internal Oncol, Aschaffenburg, Germany.
   [Sanoyan, Dilara Akhoundova; Fritsch, Ralph] Univ Hosp Zurich, Dept Med Oncol & Haematol, Zurich, Switzerland.
   [Maas, Christian] Med Practice Hemato Oncol, Halberstadt, Germany.
   [Uhlig, Jens] Practice Internal Med, Hematol & Oncol, Naunhof, Germany.
   [Fenchel, Klaus] Med Practice Internal Oncol & Hematol, Saalfeld, Germany.
   [Greil, Richard] Paracelsus Med Univ, Salzburg Canc Res Inst, Ctr Clin Canc & Immunol Trials, Canc Cluster Salzburg, Salzburg, Austria.
   [von der Heyde, Eyck] Oncol Study Ctr Raschplatz, Hannover, Germany.
   [Agocs, Gaelle Rhyner] HFR Canton Hosp Fribourg, Dept Med Oncol, Fribourg, Switzerland.
   [Weide, Rudolf] Inst Hlth Serv Res Oncol, Koblenz, Germany.
   [Schwager, Monika] Winicker Norimed GmbH Clin Res, Berlin, Germany.
   [Reichenbach, Frank] Pierre Fabre Pharm GmbH, Freiburg, Germany.
   [Modest, Dominik Paul] Charite Univme Berlin, Dept Hematol Oncol & Canc Immunol, CVK, Berlin, Germany.
   [Gerger, Armin] Med Univ Graz, Div Clin Oncol, Auenbruggerplatz 15, A-8036 Graz, Austria.
C3 Medical University of Graz; University of Bern; University of Zurich;
   University Zurich Hospital; Paracelsus Private Medical University;
   Berlin Institute of Health; Free University of Berlin; Humboldt
   University of Berlin; Charite Universitatsmedizin Berlin; Medical
   University of Graz
RP Gerger, A (corresponding author), Med Univ Graz, Div Clin Oncol, Auenbruggerplatz 15, A-8036 Graz, Austria.
EM armin.gerger@medunigraz.att
RI Modest, Dominik Paul/AAW-9756-2021; Fritsch, Ralph/KPB-7703-2024; Greil,
   Richard/C-7673-2017
OI Akhoundova, Dilara/0000-0003-1639-3059; Fritsch,
   Ralph/0000-0001-9639-3213
FU Pierre Fabre GmbH
FX The Authors wish to thank all the patients, family members and staff
   from all the study centers that participated in the study. The Authors
   would like to acknowledge editorial support provided by Andreas
   Zaehringer, Freiburg. The Authors would also like to express their
   gratitude to Monika Schwager (Winicker Norimed GmbH, Nuremberg, Germany)
   for providing the statistical support in this project. Support for this
   assistance was funded by Pierre Fabre GmbH (Freiburg, Germany; Wels,
   Austria; Allschwil, Switzerland).
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NR 55
TC 2
Z9 2
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 OCT
PY 2022
VL 42
IS 10
BP 4773
EP 4785
DI 10.21873/anticanres.15982
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5T3LS
UT WOS:000875773200003
PM 36191968
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Bi, B
   Qiu, MJ
   Liu, P
   Wang, Q
   Wen, YF
   Li, Y
   Li, BB
   Li, YS
   He, YL
   Zhao, J
AF Bi, Bo
   Qiu, Miaojuan
   Liu, Peng
   Wang, Qiang
   Wen, Yingfei
   Li, You
   Li, Binbin
   Li, Yongshu
   He, Yulong
   Zhao, Jing
TI Protein post-translational modifications: A key factor in colorectal
   cancer resistance mechanisms
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS
LA English
DT Review
DE Post-translational modifications; PTMs; Colorectal cancer; Drug
   resistance; Protein enrichment
ID AFFINITY-CHROMATOGRAPHY; OXALIPLATIN-RESISTANCE; TARGETED THERAPY;
   CETUXIMAB; PHOSPHORYLATION; IDENTIFICATION; METHYLATION; INHIBITION;
   PATHWAY; CELLS
AB Colorectal cancer (CRC) is one of the leading causes of cancer-related death. Despite advances in treatment, drug resistance remains a critical impediment. Post-translational modifications (PTMs) regulate protein stability, localization, and activity, impacting vital cellular processes. Recent research has highlighted the essential role of PTMs in the development of CRC resistance. This review summarizes recent advancements in understanding PTMs' roles in CRC resistance, focusing on the latest discoveries. We discuss the functional impact of PTMs on signaling pathways and molecules involved in CRC resistance, progress in drug development, and potential therapeutic targets. We also summarize the primary enrichment methods for PTMs. Finally, we discuss current challenges and future directions, including the need for more comprehensive PTM analysis methods and PTMtargeted therapies. This review identifies potential therapeutic interventions for addressing medication resistance in CRC, proposes prospective therapeutic options, and gives an overview of the function of PTMs in CRC resistance.
C1 [Bi, Bo; Qiu, Miaojuan; Liu, Peng; Wang, Qiang; Li, Binbin; He, Yulong; Zhao, Jing] Sun Yat Sen Univ, Affiliated Hosp 7, Digest Dis Ctr, Shenzhen, Guangdong, Peoples R China.
   [Bi, Bo; Qiu, Miaojuan; Liu, Peng; Wang, Qiang; Li, Binbin; He, Yulong] Sun Yat Sen Univ, Affiliated Hosp 7, Guangdong Prov Key Lab Digest Canc Res, Shenzhen, Guangdong, Peoples R China.
   [Qiu, Miaojuan; Wen, Yingfei; Li, You; Li, Binbin] Sun Yat Sen Univ, Affiliated Hosp 7, Sci Res Ctr, Shenzhen, Guangdong, Peoples R China.
   [Li, Yongshu] Hubei Normal Univ, Coll Life Sci Huangshi, Huangshi, Hubei, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University;
   Hubei Normal University
RP He, YL; Zhao, J (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 7, Digest Dis Ctr, Shenzhen, Guangdong, Peoples R China.; He, YL (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 7, Guangdong Prov Key Lab Digest Canc Res, Shenzhen, Guangdong, Peoples R China.; Li, YS (corresponding author), Hubei Normal Univ, Coll Life Sci Huangshi, Huangshi, Hubei, Peoples R China.
EM 1155127933@link.cuhk.edu.hk; heyulong@mail.sysu.edu.cn;
   zhaoj265@mail.sysu.edu.cn
RI li, yongshu/JDW-0080-2023; Liu, Peng/ABI-1773-2020; Li,
   Binbin/AAO-5959-2020
FU Science and Technology Planning Project of Shenzhen Municipality Grant
   [JCYJ20210324122612032, JCYJ20220530144613030]; National Natural Science
   Foundation of China [81902426]; Sanming Project of Medicine in Shenzhen
   [SZSM201911010]; Guangdong Provincial Key Laboratory of Digestive Cancer
   Research Grant [2021B1212040006]; Shenzhen Key Laboratory of Chinese
   Medicine Active substance screening and Translational Research Grant
   [ZDSYS20220606100801003]
FX The study was supported by as follows: Science and Technology Planning
   Project of Shenzhen Municipality Grant JCYJ20210324122612032 and
   JCYJ20220530144613030. National Natural Science Foundation of China
   Grant 81902426. Sanming Project of Medicine in Shenzhen Grant
   SZSM201911010. Guangdong Provincial Key Laboratory of Digestive Cancer
   Research Grant 2021B1212040006. Shenzhen Key Laboratory of Chinese
   Medicine Active substance screening and Translational Research Grant
   ZDSYS20220606100801003.
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NR 123
TC 6
Z9 6
U1 2
U2 14
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1874-9399
EI 1876-4320
J9 BBA-GENE REGUL MECH
JI Biochim. Biophys. Acta-Gene Regul. Mech.
PD DEC
PY 2023
VL 1866
IS 4
AR 194977
DI 10.1016/j.bbagrm.2023.194977
EA AUG 2023
PG 13
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA S6FO8
UT WOS:001072103000001
PM 37625568
OA hybrid
DA 2025-01-04
ER

PT J
AU Gallo, G
   Vescio, G
   De Paola, G
   Sammarco, G
AF Gallo, Gaetano
   Vescio, Giuseppina
   De Paola, Gilda
   Sammarco, Giuseppe
TI Therapeutic Targets and Tumor Microenvironment in Colorectal Cancer
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE tumor microenvironment; colorectal cancer; targeted therapy;
   angiogenesis; tumor-associated macrophages; regulatory T cells;
   cancer-associated fibroblasts
ID ENDOTHELIAL GROWTH-FACTOR; MYELOID SUPPRESSOR-CELLS;
   EPITHELIAL-MESENCHYMAL TRANSITION; T-REGULATORY CELLS; TGF-BETA PATHWAY;
   MAST-CELLS; MATRIX METALLOPROTEINASES; COLON-CANCER;
   PROGNOSTIC-SIGNIFICANCE; MACROPHAGE ACTIVATION
AB Colorectal cancer (CRC) is a genetically, anatomically, and transcriptionally heterogeneous disease. The prognosis for a CRC patient depends on the stage of the tumor at diagnosis and widely differs accordingly. The tumor microenvironment (TME) in CRC is an important factor affecting targeted cancer therapy. The TME has a dynamic composition including various cell types, such as cancer-associated fibroblasts, tumor-associated macrophages, regulatory T cells, and myeloid-derived suppressor cells, as well as extracellular factors that surround cancer cells and have functional and structural roles under physiological and pathological conditions. Moreover, the TME can limit the efficacy of therapeutic agents through high interstitial pressure, fibrosis, and the degradation of the therapeutic agents by enzymatic activity. For this reason, the TME is a fertile ground for the discovery of new drugs. The aim of this narrative review is to present current knowledge and future perspectives regarding the TME composition based on strategies for patients with CRC.
C1 [Gallo, Gaetano; Vescio, Giuseppina; De Paola, Gilda] Univ Catanzaro, Dept Med & Surg Sci, Viale Europa, I-88100 Catanzaro, Italy.
   [Sammarco, Giuseppe] Univ Catanzaro, Dept Hlth Sci, Viale Europa, I-88100 Catanzaro, Italy.
C3 Magna Graecia University of Catanzaro; Magna Graecia University of
   Catanzaro
RP Gallo, G (corresponding author), Univ Catanzaro, Dept Med & Surg Sci, Viale Europa, I-88100 Catanzaro, Italy.
EM gallog@unicz.it; vescio@unicz.it; gilda_depaola@libero.it;
   sammarco@unicz.it
RI Gallo, Gaetano/I-6917-2019
OI De Paola, Gilda/0000-0003-0470-4729; Gallo, Gaetano/0000-0003-1066-4671
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NR 137
TC 34
Z9 34
U1 2
U2 20
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 JUN
PY 2021
VL 10
IS 11
AR 2295
DI 10.3390/jcm10112295
PG 18
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA SQ2JJ
UT WOS:000660183700001
PM 34070480
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Huang, LL
   Jiang, SY
   Shi, YK
AF Huang, Liling
   Jiang, Shiyu
   Shi, Yuankai
TI Tyrosine kinase inhibitors for solid tumors in the past 20 years
   (2001-2020)
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Review
DE Tyrosine kinase inhibitors; Solid tumors; Targeted therapy
ID CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER; LAPATINIB PLUS
   CAPECITABINE; UNRESECTABLE HEPATOCELLULAR-CARCINOMA; OPEN-LABEL;
   DOUBLE-BLIND; 1ST-LINE TREATMENT; BREAST-CANCER; PHASE-II;
   ACQUIRED-RESISTANCE
AB Tyrosine kinases are implicated in tumorigenesis and progression, and have emerged as major targets for drug discovery. Tyrosine kinase inhibitors (TKIs) inhibit corresponding kinases from phosphorylating tyrosine residues of their substrates and then block the activation of downstream signaling pathways. Over the past 20 years, multiple robust and well-tolerated TKIs with single or multiple targets including EGFR, ALK, ROS1, HER2, NTRK, VEGFR, RET, MET, MEK, FGFR, PDGFR, and KIT have been developed, contributing to the realization of precision cancer medicine based on individual patient's genetic alteration features. TKIs have dramatically improved patients' survival and quality of life, and shifted treatment paradigm of various solid tumors. In this article, we summarized the developing history of TKIs for treatment of solid tumors, aiming to provide up-to-date evidence for clinical decision-making and insight for future studies.
C1 [Huang, Liling; Jiang, Shiyu; Shi, Yuankai] Chinese Acad Med Sci & Peking Union Med Coll, Beijing Key Lab Clin Study Anticanc Mol Targeted, Natl Clin Res Ctr Canc, Dept Med Oncol,Natl Canc Ctr,Canc Hosp, 17 Panjiayuan Nanli, Beijing 100021, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College; Cancer Institute & Hospital - CAMS
RP Shi, YK (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Beijing Key Lab Clin Study Anticanc Mol Targeted, Natl Clin Res Ctr Canc, Dept Med Oncol,Natl Canc Ctr,Canc Hosp, 17 Panjiayuan Nanli, Beijing 100021, Peoples R China.
EM syuankai@cicams.ac.cn
RI xi, li/JZC-6279-2024
FU China National Major Project for New Drug Innovation [2017ZX09304015];
   Chinese Academy of Medical Sciences (CAMS) Innovation Fund for Medical
   Sciences (CIFMS) [2016-I2M-1-001]
FX This work was supported by China National Major Project for New Drug
   Innovation (Grant No. 2017ZX09304015) and Chinese Academy of Medical
   Sciences (CAMS) Innovation Fund for Medical Sciences (CIFMS) (Grant No.
   2016-I2M-1-001).
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NR 227
TC 259
Z9 281
U1 4
U2 84
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 OCT 27
PY 2020
VL 13
IS 1
AR 143
DI 10.1186/s13045-020-00977-0
PG 23
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA OP8AX
UT WOS:000588312200001
PM 33109256
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Wang, ML
   Sun, X
   Wang, H
   Xin, YL
   Jiao, WJ
AF Wang, Maolong
   Sun, Xiao
   Wang, Hao
   Xin, Yanlu
   Jiao, Wenjie
TI Long non-coding RNAs in non-small cell lung cancer: functions and
   distinctions from other malignancies
SO TRANSLATIONAL CANCER RESEARCH
LA English
DT Review
DE Lung cancer; long non-coding RNAs (lncRNAs); biomarkers targeted therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; POOR-PROGNOSIS; C-MYC; UP-REGULATION;
   COLORECTAL-CANCER; CIGARETTE-SMOKE; DOWN-REGULATION;
   HEPATOCELLULAR-CARCINOMA; PROMOTES TUMORIGENESIS; ENHANCED EXPRESSION
AB Lung cancer leads to the most cancer-related death in the world. It was shown from the increasing evidences that long non-coding RNAs (lncRNAs) are emerging as molecules for diagnosis, prognosis and even therapy of lung cancer and other malignancies. The biological functions or involved signaling pathways of lncRNAs are always found to be inconsistent among different types of malignancies. However, no available literature has systemically summarized differences in the functions and underlying molecular mechanisms of lncRNAs between lung cancer and other cancers. in this review, the biological functions and molecular mechanisms of lncRNAs in lung cancer were introduced. Furthermore, their functional differences between lung cancer and other malignancies were discussed. Finally, their potential clinical applications in future lung cancer therapy were focused on.
C1 [Wang, Maolong; Sun, Xiao; Wang, Hao; Xin, Yanlu; Jiao, Wenjie] Qingdao Univ, Affiliated Hosp, Dept Thorac Surg, Qingdao 266003, Shandong, Peoples R China.
C3 Qingdao University
RP Jiao, WJ (corresponding author), Qingdao Univ, Affiliated Hosp, Dept Thorac Surg, Qingdao 266003, Shandong, Peoples R China.
EM jiaowj@qduhospital.cn
FU Key R&D programs in Shandong Province [2018GSF118119]
FX This study was funded by Key R&D programs in Shandong Province (grant
   number: 2018GSF118119).
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NR 174
TC 14
Z9 15
U1 0
U2 5
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2218-676X
EI 2219-6803
J9 TRANSL CANCER RES
JI Transl. Cancer Res.
PD NOV
PY 2019
VL 8
IS 7
BP 2636
EP 2653
DI 10.21037/tcr.2019.10.22
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JR5MM
UT WOS:000499669000017
PM 35117021
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Jhaveri, KD
   Wanchoo, R
   Sakhiya, V
   Ross, DW
   Fishbane, S
AF Jhaveri, Kenar D.
   Wanchoo, Rimda
   Sakhiya, Vipulbhai
   Ross, Daniel W.
   Fishbane, Steven
TI Adverse Renal Effects of Novel Molecular Oncologic Targeted Therapies: A
   Narrative Review
SO KIDNEY INTERNATIONAL REPORTS
LA English
DT Review
DE AKI; chemotherapy; hypokalemia; hyponatremia; nephrotoxicity;
   onconephrology; renal failure; targeted therapy
ID CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER; OF-THE-LITERATURE;
   PHASE-III TRIAL; TYROSINE KINASE INHIBITORS; GLOMERULAR-FILTRATION-RATE;
   IMATINIB MESYLATE TREATMENT; CHRONIC MYELOID-LEUKEMIA; CHRONIC
   KIDNEY-DISEASE; BREAST-CANCER
AB Novel targeted anti-cancer therapies have resulted in improvement in patient survival compared to standard chemotherapy. Renal toxicities of targeted agents are increasingly being recognized. The incidence, severity, and pattern of renal toxicities may vary according to the respective target of the drug. Here we review the adverse renal effects associated with a selection of currently approved targeted cancer therapies, directed to EGFR, HER2, BRAF, MEK, ALK, PD1/PDL1, CTLA-4, and novel agents targeted to VEGF/R and TKIs. In summary, electrolyte disorders, renal impairment and hypertension are the most commonly reported events. Of the novel targeted agents, ipilumumab and cetuximab have the most nephrotoxic events reported. The early diagnosis and prompt recognition of these renal adverse events are essential for the general nephrologist taking care of these patients.
C1 [Jhaveri, Kenar D.; Wanchoo, Rimda; Sakhiya, Vipulbhai; Ross, Daniel W.; Fishbane, Steven] Northwell Hlth, Hofstra Northwell Sch Med, Div Kidney Dis & Hypertens, Dept Internal Med, Great Neck, NY 11021 USA.
C3 Northwell Health
RP Jhaveri, KD (corresponding author), Northwell Hlth, Hofstra Northwell Sch Med, Div Kidney Dis & Hypertens, Med, 100 Community Dr, Great Neck, NY 11021 USA.
EM kjhaveri@northwell.edu
RI Jhaveri, Kenar/X-4851-2019
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NR 130
TC 60
Z9 65
U1 0
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 2468-0249
J9 KIDNEY INT REP
JI Kidney Int. Rep.
PD JAN
PY 2017
VL 2
IS 1
BP 108
EP 123
DI 10.1016/j.ekir.2016.09.055
PG 16
WC Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Urology & Nephrology
GA FB2FF
UT WOS:000405958900016
PM 29318210
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, YN
   Xing, JQ
   Sun, YB
   Han, T
   Zhang, H
   An, FF
AF Li, Yanan
   Xing, Jingqi
   Sun, Yongbing
   Han, Tao
   Zhang, Hui
   An, Feifei
TI Magnetic resonance imaging-guided and targeted theranostics of
   colorectal cancer
SO CANCER BIOLOGY & MEDICINE
LA English
DT Review
DE Carcinogenesis; colorectal cancer; magnetic resonance imaging;
   multimodal diagnosis; targeted theranostics
ID IRON-OXIDE NANOPARTICLES; RANDOMIZED PHASE-III; COLON-CANCER; ADJUVANT
   TREATMENT; DRUG-DELIVERY; PHOTOTHERMAL ABLATION; CT COLONOGRAPHY;
   RECTAL-CANCER; THERAPY; MRI
AB Colorectal cancer (CRC) is the most common gastrointestinal tract cancer worldwide and is associated with high morbidity and mortality. The development of nanosized drug delivery systems has provided a new direction in CRC treatment. Among these systems, magnetic nanoparticle (MNP)-based multifunctional platforms provide a novel strategy for magnetic resonance imaging (MRI)-related cancer theranostics. At the beginning of this original review, the carcinogenesis and treatment status of CRC are summarized. Then, diversified preparation and functionalization methods of MNPs are systematically analyzed, followed by MRIinvolved theranostic strategies. The latest progress in MRI-mediated multimode diagnosis and image-guided targeted therapy in CRC management is the main focus. Finally, the major challenges in promoting MRI-induced precise theranostics of CRC in clinical practice are discussed.
C1 [Li, Yanan; Zhang, Hui] Shanxi Med Univ, Dept Radiol, Hosp 1, Taiyuan 030001, Peoples R China.
   [Xing, Jingqi; An, Feifei] Xi An Jiao Tong Univ, Hlth Sci Ctr, Sch Basic Med Sci, Inst Med Engn,Dept Biophys, Xian 710061, Peoples R China.
   [Sun, Yongbing] Jiangxi Univ Tradit Chinese Med, Natl Pharmaceut Engn Ctr Solid Preparat Chinese H, Div Pharmaceut, Nanchang 330006, Jiangxi, Peoples R China.
   [Han, Tao] Chengdu Normal Univ, Coll Chem & Life Sci, Inst Funct Mol, Chengdu 611130, Peoples R China.
C3 Shanxi Medical University; Xi'an Jiaotong University; Jiangxi University
   of Traditional Chinese Medicine; Chengdu Normal University
RP An, FF (corresponding author), Xi An Jiao Tong Univ, Hlth Sci Ctr, Sch Basic Med Sci, Inst Med Engn,Dept Biophys, Xian 710061, Peoples R China.; Sun, YB (corresponding author), Jiangxi Univ Tradit Chinese Med, Natl Pharmaceut Engn Ctr Solid Preparat Chinese H, Div Pharmaceut, Nanchang 330006, Jiangxi, Peoples R China.
EM yongbing_sun@hotmail.com; anfeifei@xjtu.edu.cn
RI An, Feifei/J-6079-2017
FU National Natural Science Foundation of China [81903662, 81860630,
   81560577]; China Postdoctoral Science Foundation [2019M661057]; Applied
   Basic Research Programs of Shanxi Province [201901D211347]; Scientific
   and Technological Innovation Programs of Higher Education Institutions
   in Shanxi [2019L0428]; Startup Foundation for Doctors of Shanxi Province
   [SD1827]; Startup Foundation for Doctors of Shanxi Medical University
   [XD1824]
FX This work was supported by the National Natural Science Foundation of
   China (Grant Nos. 81903662, 81860630, and 81560577), China Postdoctoral
   Science Foundation Grant (Grant No. 2019M661057), the Applied Basic
   Research Programs of Shanxi Province (Grant No. 201901D211347), the
   Scientific and Technological Innovation Programs of Higher Education
   Institutions in Shanxi (Grant No. 2019L0428), the Startup Foundation for
   Doctors of Shanxi Province (Grant No. SD1827), and the Startup
   Foundation for Doctors of Shanxi Medical University (Grant No. XD1824).
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NR 153
TC 19
Z9 20
U1 1
U2 59
PU CHINA ANTI-CANCER ASSOC
PI TIANJIN
PA TIANJIN MEDICAL UNIV, CANCER INST & HOSPITAL  TI-YUAN-BEI, HUANHU XI LU,
   HEXIQU, TIANJIN, 300060, PEOPLES R CHINA
SN 2095-3941
J9 CANCER BIOL MED
JI Cancer Biol. Med.
PD MAY
PY 2020
VL 17
IS 2
BP 307
EP 327
DI 10.20892/j.issn.2095-3941.2020.0072
PG 21
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA LZ9TH
UT WOS:000541560900005
PM 32587771
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Dadgar, N
   Sherry, C
   Zimmerman, J
   Park, H
   Lewis, C
   Donnenberg, A
   Zaidi, AH
   Fan, Y
   Xiao, KH
   Bartlett, D
   Donnenberg, V
   Wagner, PL
AF Dadgar, Neda
   Sherry, Christopher
   Zimmerman, Jenna
   Park, Hyun
   Lewis, Catherine
   Donnenberg, Albert
   Zaidi, Ali H.
   Fan, Yong
   Xiao, Kunhong
   Bartlett, David
   Donnenberg, Vera
   Wagner, Patrick L.
TI Targeting interleukin-6 as a treatment approach for peritoneal
   carcinomatosis
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE IL-6; Peritoneal carcinomatosis; Targeted therapy; Tumor immune
   microenvironment
ID RECEPTOR MONOCLONAL-ANTIBODY; CANCER-ASSOCIATED FIBROBLASTS; SOLUBLE
   IL-6 RECEPTOR; PANCREATIC-CANCER; COLORECTAL-CANCER; INFLAMMATORY
   RESPONSES; RHEUMATOID-ARTHRITIS; THERAPEUTIC TARGET; GASTRIC-CANCER;
   DOUBLE-BLIND
AB Peritoneal carcinomatosis (PC) is a complex manifestation of abdominal cancers, with a poor prognosis and limited treatment options. Recent work identifying high concentrations of the cytokine interleukin-6 (IL-6) and its soluble receptor (sIL-6-R alpha) in the peritoneal cavity of patients with PC has highlighted this pathway as an emerging potential therapeutic target. This review article provides a comprehensive overview of the current understanding of the potential role of IL-6 in the development and progression of PC. We discuss mechansims by which the IL-6 pathway may contribute to peritoneal tumor dissemination, mesothelial adhesion and invasion, stromal invasion and proliferation, and immune response modulation. Finally, we review the prospects for targeting the IL-6 pathway in the treatment of PC, focusing on common sites of origin, including ovarian, gastric, pancreatic, colorectal and appendiceal cancer, and mesothelioma.
C1 [Dadgar, Neda] Cleveland Clin, Enterprise Canc Inst, Translat Hematol & Oncol Res, Cleveland, OH 44106 USA.
   [Sherry, Christopher; Zimmerman, Jenna; Park, Hyun; Lewis, Catherine; Donnenberg, Albert; Zaidi, Ali H.; Fan, Yong; Bartlett, David; Wagner, Patrick L.] Allegheny Hlth Network Canc Inst, 314 E North Ave, Pittsburgh, PA 15212 USA.
   [Xiao, Kunhong] Allegheny Hlth Network Canc Inst, Ctr Prote & Artificial Intelligence, Ctr Clin Mass Spectrometry, Pittsburgh, PA 15224 USA.
   [Donnenberg, Vera] Univ Pittsburgh, UPMC Hillman Canc Ctr Wagner Patrick, Sch Med, Dept Cardiothorac Surg, Pittsburgh, PA USA.
   [Donnenberg, Vera] Allegheny Hlth Network Canc Inst, Pittsburgh, PA USA.
C3 Cleveland Clinic Foundation; Pennsylvania Commonwealth System of Higher
   Education (PCSHE); University of Pittsburgh
RP Wagner, PL (corresponding author), Allegheny Hlth Network Canc Inst, 314 E North Ave, Pittsburgh, PA 15212 USA.
EM patrick.wagner@ahn.org
RI Dadgar, Neda/AAQ-4926-2021
FU Department of Defense CDMRP [BC210533/ W81XWH2210009, BC211396
   W81XWH-22-1069]; NCI [R37CA232209, R01CA114246]; NHLBI [T32
   HL160526-01]; Glimmer of Hope Foundation; Pittsburgh Foundation;
   Appendix Cancer Pseudomyxoma Peritonei Research Foundation
FX VSD received funding from the Department of Defense CDMRP AWARD NUMBER:
   BC210533/ W81XWH2210009 and AWARD NUMBER: BC211396 W81XWH-22-1069. VSD
   also received funding from the NCI R37CA232209, NCI R01CA114246, and the
   NHLBI T32 HL160526-01. PW and VSD received funding from and the Glimmer
   of Hope Foundation, the Pittsburgh Foundation, and the Appendix Cancer
   Pseudomyxoma Peritonei Research Foundation.
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NR 274
TC 3
Z9 4
U1 2
U2 2
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 APR 30
PY 2024
VL 22
IS 1
AR 402
DI 10.1186/s12967-024-05205-8
PG 18
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA WP4N9
UT WOS:001256066400003
PM 38689325
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Khaliq, M
   Fallahi-Sichani, M
AF Khaliq, Mehwish
   Fallahi-Sichani, Mohammad
TI Epigenetic Mechanisms of Escape from BRAF Oncogene Dependency
SO CANCERS
LA English
DT Review
DE oncogene addiction; BRAF-mutant tumors; BRAF and MEK-targeted therapies;
   phenotype switching; tumor heterogeneity; epigenetic regulation;
   adaptive drug resistance; histone-modifying enzymes; chromatin
   regulation; DNA methylation
ID ACQUIRED-RESISTANCE; DNA METHYLATION; RAF INHIBITORS; MAPK PATHWAY;
   B-RAF; COLORECTAL-CANCER; MEK INHIBITION; CPG ISLANDS; METASTATIC
   MELANOMA; CUTANEOUS MELANOMA
AB About eight percent of all human tumors (including 50% of melanomas) carry gain-of-function mutations in the BRAF oncogene. Mutated BRAF and subsequent hyperactivation of the MAPK signaling pathway has motivated the use of MAPK-targeted therapies for these tumors. Despite great promise, however, MAPK-targeted therapies in BRAF-mutant tumors are limited by the emergence of drug resistance. Mechanisms of resistance include genetic, non-genetic and epigenetic alterations. Epigenetic plasticity, often modulated by histone-modifying enzymes and gene regulation, can influence a tumor cell's BRAF dependency and therefore, response to therapy. In this review, focusing primarily on class 1 BRAF-mutant cells, we will highlight recent work on the contribution of epigenetic mechanisms to inter- and intratumor cell heterogeneity in MAPK-targeted therapy response.
C1 [Khaliq, Mehwish; Fallahi-Sichani, Mohammad] Univ Michigan, Dept Biomed Engn, Med Sch, Ann Arbor, MI 48109 USA.
   [Khaliq, Mehwish; Fallahi-Sichani, Mohammad] Univ Michigan, Program Canc Biol, Med Sch, Ann Arbor, MI 48109 USA.
   [Fallahi-Sichani, Mohammad] Univ Michigan, Dept Dermatol, Med Sch, Ann Arbor, MI 48109 USA.
C3 University of Michigan System; University of Michigan; University of
   Michigan System; University of Michigan; University of Michigan System;
   University of Michigan
RP Fallahi-Sichani, M (corresponding author), Univ Michigan, Dept Biomed Engn, Med Sch, Ann Arbor, MI 48109 USA.; Fallahi-Sichani, M (corresponding author), Univ Michigan, Program Canc Biol, Med Sch, Ann Arbor, MI 48109 USA.; Fallahi-Sichani, M (corresponding author), Univ Michigan, Dept Dermatol, Med Sch, Ann Arbor, MI 48109 USA.
EM mehwishk@umich.edu; fallahi@umich.edu
OI Fallahi-Sichani, Mohammad/0000-0003-0917-3525
FU NCI [T32-CA009676, R00-CA194163]; Elsa Pardee Foundation; V Scholar
   Grant Award from V Foundation for Cancer Research [V2017-011];
   Department of Defense PRCRP Career Development Award [W81XWH1810427];
   U.S. Department of Defense (DOD) [W81XWH1810427] Funding Source: U.S.
   Department of Defense (DOD); National Cancer Institute [T32CA009676]
   Funding Source: NIH RePORTER
FX M.K. was supported by NCI Training Grant T32-CA009676. M.F.-S. was
   supported by NCI grant R00-CA194163, Elsa Pardee Foundation, V Scholar
   Grant Award from The V Foundation for Cancer Research (V2017-011), and
   Department of Defense PRCRP Career Development Award (W81XWH1810427).
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NR 169
TC 23
Z9 24
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 OCT
PY 2019
VL 11
IS 10
AR 1480
DI 10.3390/cancers11101480
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JQ3CF
UT WOS:000498826000077
PM 31581557
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Cuyle, PJ
   Prenen, H
AF Cuyle, Pieter-Jan
   Prenen, Hans
TI Current and future biomarkers in the treatment of colorectal cancer
SO ACTA CLINICA BELGICA
LA English
DT Article
DE Colorectal cancer; Predictive markers; Prognostic markers; Molecular
   subtypes; RAS; BRAF; MSI; DNA mismatch repair; HER2; EGFR; VEGF; CDX2;
   Targeted therapy; Personalized medicine; Liquid biopsy
ID III COLON-CANCER; ISLAND METHYLATOR PHENOTYPE; CETUXIMAB PLUS
   IRINOTECAN; DNA MISMATCH REPAIR; MICROSATELLITE-INSTABILITY STATUS;
   12-GENE RECURRENCE SCORE; DISEASE-FREE SURVIVAL; RANDOMIZED PHASE-III;
   WILD-TYPE KRAS; STAGE-II
AB Colorectal cancer (CRC) is a leading cause of cancer deaths worldwide. CRC develops as a consequence of genomic instability, characterized by various genetic and epigenetic alterations. Its molecular heterogeneity explains the large variability in patient prognosis and treatment response, emphasizing the need for development of accurate prognostic and predictive biomarkers. This article delineates the different pathways of colorectal carcinogenesis and its molecular subtype classification. With this review, we aim to provide a comprehensive overview of the current and future biomarkers guiding clinical decision-making and CRC treatment.
C1 [Cuyle, Pieter-Jan] Imelda Gen Hosp, Dept Gastroenterol Digest Oncol, Bonheiden, Belgium.
   [Cuyle, Pieter-Jan; Prenen, Hans] Univ Hosp Gasthuisberg Leuven, Dept Gastroenterol Digest Oncol, Leuven, Belgium.
C3 Imeldaziekenhuis; KU Leuven; University Hospital Leuven
RP Cuyle, PJ (corresponding author), Imeldaziekenhuis Bonheiden, Imeldalaan 9, B-2820 Bonheiden, Belgium.
EM pieter-jan.cuyle@imelda.be
OI Prenen, Hans/0000-0001-8802-7352
FU Belgian Foundation against Cancer
FX Hans Prenen is supported by Belgian Foundation against Cancer. The
   authors have not received funding from any source for the conduct of
   this review paper.
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NR 169
TC 31
Z9 34
U1 1
U2 22
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1784-3286
EI 2295-3337
J9 ACTA CLIN BELG
JI Acta Clin. Belg.
PY 2017
VL 72
IS 2
BP 103
EP 115
DI 10.1080/17843286.2016.1262996
PG 13
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA EQ5HJ
UT WOS:000398113200005
PM 27917697
DA 2025-01-04
ER

PT J
AU Foth, M
   McMahon, M
AF Foth, Mona
   McMahon, Martin
TI Autophagy Inhibition in BRAF-Driven Cancers
SO CANCERS
LA English
DT Review
DE BRAF; MEK1; 2; autophagy; targeted therapy; drug resistance; metabolism
ID ENDOPLASMIC-RETICULUM STRESS; MUTANT COLORECTAL-CANCER; ADVANCED SOLID
   TUMORS; PHASE-I TRIAL; ACQUIRED-RESISTANCE; MELANOMA-CELLS; ONCOGENIC
   KRAS; MAPK PATHWAY; RAG GTPASES; BRAF(V600E) INHIBITION
AB Simple Summary BRAF is a protein kinase that is frequently mutationally activated in cancer. Mutant BRAF can be pharmacologically inhibited, which in combination with blockade of its direct effector, MEK1/2, is an FDA-approved therapeutic strategy for several BRAF-mutated cancer patients, such as melanoma, non-small-cell lung carcinoma, and thyroid cancer. However, therapy resistance is a major clinical challenge, highlighting the need for comprehensive investigations on the biological causes of such resistance, as well as to develop novel therapeutic strategies to improve patient survival. Autophagy is a cellular recycling process, which has been shown to allow cancer cells to escape from BRAF inhibition. Combined blockade of autophagy and BRAF signaling is a novel therapeutic strategy that is currently being tested in clinical trials. This review describes the relationship between BRAF-targeted therapy and autophagy regulation and discusses possible future treatment strategies. Several BRAF-driven cancers, including advanced BRAF(V600E/K)-driven melanoma, non-small-cell lung carcinoma, and thyroid cancer, are currently treated using first-line inhibitor combinations of BRAF(V600E) plus MEK1/2. However, despite the success of this vertical inhibition strategy, the durability of patient response is often limited by the phenomenon of primary or acquired drug resistance. It has recently been shown that autophagy, a conserved cellular recycling process, is increased in BRAF-driven melanoma upon inhibition of BRAF(V600E) signaling. Autophagy is believed to promote tumor progression of established tumors and also to protect cancer cells from the cytotoxic effects of chemotherapy. To this end, BRAF inhibitor (BRAFi)-resistant cells often display increased autophagy compared to responsive lines. Several mechanisms have been proposed for BRAFi-induced autophagy, such as activation of the endoplasmic reticulum (ER) stress gatekeeper GRP78, AMP-activated protein kinase, and transcriptional regulation of the autophagy regulating transcription factors TFEB and TFE3 via ERK1/2 or mTOR inhibition. This review describes the relationship between BRAF-targeted therapy and autophagy regulation, and discusses possible future treatment strategies of combined inhibition of oncogenic signaling plus autophagy for BRAF-driven cancers.
C1 [Foth, Mona; McMahon, Martin] Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
   [McMahon, Martin] Univ Utah, Dept Dermatol, Salt Lake City, UT 84112 USA.
C3 Utah System of Higher Education; University of Utah; Huntsman Cancer
   Institute; Utah System of Higher Education; University of Utah
RP McMahon, M (corresponding author), Huntsman Canc Inst, Salt Lake City, UT 84112 USA.; McMahon, M (corresponding author), Univ Utah, Dept Dermatol, Salt Lake City, UT 84112 USA.
EM mona.foth@hci.utah.edu; martin.mcmahon@hci.utah.edu
RI Foth, Mona/AAU-5336-2021
OI Foth, Mona/0000-0001-6507-8114
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NR 197
TC 14
Z9 16
U1 0
U2 10
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JUL
PY 2021
VL 13
IS 14
AR 3498
DI 10.3390/cancers13143498
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TO3EW
UT WOS:000676800500001
PM 34298710
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Madan, B
   Ke, Z
   Harmston, N
   Ho, SY
   Frois, AO
   Alam, J
   Jeyaraj, DA
   Pendharkar, V
   Ghosh, K
   Virshup, IH
   Manoharan, V
   Ong, EHQ
   Sangthongpitag, K
   Hill, J
   Petretto, E
   Keller, TH
   Lee, MA
   Matter, A
   Virshup, DM
AF Madan, B.
   Ke, Z.
   Harmston, N.
   Ho, S. Y.
   Frois, A. O.
   Alam, J.
   Jeyaraj, D. A.
   Pendharkar, V.
   Ghosh, K.
   Virshup, I. H.
   Manoharan, V.
   Ong, E. H. Q.
   Sangthongpitag, K.
   Hill, J.
   Petretto, E.
   Keller, T. H.
   Lee, M. A.
   Matter, A.
   Virshup, D. M.
TI Wnt addiction of genetically defined cancers reversed by PORCN
   inhibition
SO ONCOGENE
LA English
DT Article
ID SMALL-MOLECULE INHIBITOR; COLON-CANCER; STEM-CELLS; EXPRESSION;
   PORCUPINE; PATHWAY; GROWTH; RNF43; TRANSCRIPTION; GENE
AB Enhanced sensitivity to Wnts is an emerging hallmark of a subset of cancers, defined in part by mutations regulating the abundance of their receptors. Whether these mutations identify a clinical opportunity is an important question. Inhibition of Wnt secretion by blocking an essential post-translational modification, palmitoleation, provides a useful therapeutic intervention. We developed a novel potent, orally available PORCN inhibitor, ETC-1922159 (henceforth called ETC-159) that blocks the secretion and activity of all Wnts. ETC-159 is remarkably effective in treating RSPO-translocation bearing colorectal cancer (CRC) patient-derived xenografts. This is the first example of effective targeted therapy for this subset of CRC. Consistent with a central role of Wnt signaling in regulation of gene expression, inhibition of PORCN in RSPO3-translocated cancers causes a marked remodeling of the transcriptome, with loss of cell cycle, stem cell and proliferation genes, and an increase in differentiation markers. Inhibition of Wnt signaling by PORCN inhibition holds promise as differentiation therapy in genetically defined human cancers.
C1 [Madan, B.; Frois, A. O.; Ghosh, K.; Virshup, I. H.; Virshup, D. M.] Duke NUS Grad Med Sch, Program Canc & Stem Cell Biol, Singapore, Singapore.
   [Ke, Z.; Ho, S. Y.; Alam, J.; Jeyaraj, D. A.; Pendharkar, V.; Manoharan, V.; Ong, E. H. Q.; Sangthongpitag, K.; Hill, J.; Keller, T. H.; Lee, M. A.; Matter, A.] ASTAR, Ctr Expt Therapeut, Biopolis, Singapore, Singapore.
   [Harmston, N.; Petretto, E.] Duke NUS Grad Med Sch, Program Cardiovasc & Metab Dis, Singapore, Singapore.
   [Virshup, D. M.] Duke Univ, Dept Pediat, Durham, NC 27706 USA.
C3 National University of Singapore; Agency for Science Technology &
   Research (A*STAR); A*STAR - Experimental Drug Development Centre (EDDC);
   Experimental Therapeutics Centre; National University of Singapore; Duke
   University
RP Madan, B; Virshup, DM (corresponding author), Duke NUS, Grad Sch Med, Program Canc & Stem Cell Biol, 07-20,8 Coll Rd, Singapore 169857, Singapore.
EM Babita.Madan@duke-nus.edu.sg; David.Virshup@duke-nus.edu.sg
RI Virshup, David/C-1449-2009
OI Virshup, David M/0000-0001-6976-850X; Virshup,
   Isaac/0000-0002-1710-8945; Keller, Thomas/0000-0002-7553-6235; Ho, Soo
   Yei/0000-0001-8535-389X; HARMSTON, NATHAN/0000-0002-8589-2938; Madan,
   Babita/0000-0003-1065-8589; Petretto, Enrico/0000-0003-2163-5921
FU National Research Foundation Singapore; Agency for Science, Technology
   and Research (A*STAR), Singapore; MRC Clinical Sciences Centre, Imperial
   College, London; MRC [MC_U120097112] Funding Source: UKRI
FX We acknowledge the assistance of members of the Virshup lab including
   Jamal Aliyev, Naushad Moti and Edison and members of Experimental
   Therapeutics Centre including Shermaine Q Y Lim, Sifang Wang, Yu Wang,
   Vivien Wei Wen Cheong, and Grace Ruiting Lin. We acknowledge Ivana
   Mihalek for help with the alignment of PORCN sequences and Ralph Bunte,
   DVM, for his expert advice with histological analysis. We also
   acknowledge the assistance of the vivarium staff including Hock Lee.
   This research is supported in part by the National Research Foundation
   Singapore and administered by the Singapore Ministry of Health's
   National Medical Research Council under the STAR Award Program to DMV.
   The research in Experimental Therapeutics Centre is supported by the
   Agency for Science, Technology and Research (A*STAR), Singapore. EP and
   NH acknowledge the support of the MRC Clinical Sciences Centre, Imperial
   College, London.
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NR 49
TC 242
Z9 276
U1 0
U2 27
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 APR 28
PY 2016
VL 35
IS 17
BP 2197
EP 2207
DI 10.1038/onc.2015.280
PG 11
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 DK5UK
UT WOS:000374986000006
PM 26257057
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Lafitte, M
   Sirvent, A
   Roche, S
AF Lafitte, Marie
   Sirvent, Audrey
   Roche, Serge
TI Collagen Kinase Receptors as Potential Therapeutic Targets in Metastatic
   Colon Cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE collagen; extracellular matrix; tumor microenvironment; receptor;
   tyrosine kinase; colorectal cancer; metastasis; targeted therapy
ID DISCOIDIN DOMAIN RECEPTOR-2; COLORECTAL-CANCER; TYROSINE KINASE;
   CHEMICAL PROTEOMICS; DDR1; INHIBITION; EXPRESSION; IMATINIB; BCR;
   COLONIZATION
AB Colorectal cancer (CRC) is one of the leading causes of tumor-related death worldwide. While surgery can cure patients with early stage CRC, the 5-year survival rate is only 10% for patients with metastatic disease. Therefore, new anti-metastatic therapies are needed for this cancer. Metastatic spread defines the dissemination of cancer cells with tumor-initiating capacities from the primary tumor and their colonization of distinct organs, mainly the liver, for secondary tumor formation. Although the underlying mechanisms are not fully understood, components of the tumor microenvironment have gained strong interest. Among the known metastatic-promoting factors, collagens are extracellular matrix components that are deposited within the tumor, the tumor microenvironment, and at metastatic site(s), and are recognized to play essential roles during metastasis development. Here, we review recent findings on the metastatic role of the collagen receptors Discoidin Domain Receptors 1 and 2 (DDR1 and DDR2) in CRC and discuss the therapeutic value of targeting these receptor tyrosine kinases in this cancer.
C1 [Lafitte, Marie; Sirvent, Audrey; Roche, Serge] Univ Montpellier, CNRS, CRBM, Montpellier, France.
C3 Universite de Montpellier; Centre National de la Recherche Scientifique
   (CNRS)
RP Sirvent, A; Roche, S (corresponding author), Univ Montpellier, CNRS, CRBM, Montpellier, France.
EM audrey.sirvent@crbm.cnrs.fr; serge.roche@crbm.cnrs.fr
OI roche, serge/0000-0003-3413-3859
FU Association pour la Recherche contre le Cancer ARC; Montpellier SIRIC
   Grant [INCa-DGOSInserm 6045]; CNRS; University of Montpellier; Fondation
   pour la Recherche Medicale (FRM); Fondation de France
FX This work was supported by the Association pour la Recherche contre le
   Cancer ARC, Montpellier SIRIC Grant "INCa-DGOSInserm 6045", CNRS, and
   the University of Montpellier. ML was supported by the Fondation pour la
   Recherche Medicale (FRM) and the Fondation de France. SR is an INSERM
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NR 77
TC 42
Z9 45
U1 3
U2 13
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD FEB 12
PY 2020
VL 10
AR 125
DI 10.3389/fonc.2020.00125
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KS0ZC
UT WOS:000518039400001
PM 32117772
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Liang, H
   He, X
   Tong, YT
   Bai, NN
   Pu, YS
   Han, K
   Wang, Y
AF Liang, Hong
   He, Xia
   Tong, Yitong
   Bai, Niuniu
   Pu, Yushu
   Han, Ke
   Wang, Yi
TI Ferroptosis open a new door for colorectal cancer treatment
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE ferroptosis; colorectal cancer; molecular mechanism; inducer;
   nanomedicine 1
ID LIPID-PEROXIDATION; SIGNALING PATHWAY; IN-VITRO; CELLS; FERRITINOPHAGY;
   MUTATIONS; CETUXIMAB; ACSL4
AB Colorectal cancer (CRC) is the third highest incidence and the second highest mortality malignant tumor in the world. The etiology and pathogenesis of CRC are complex. Due to the long course of the disease and no obvious early symptoms, most patients are diagnosed as middle and late stages. CRC is prone to metastasis, most commonly liver metastasis, which is one of the leading causes of death in CRC patients. Ferroptosis is a newly discovered cell death form with iron dependence, which is driven by excessive lipid peroxides on the cell membrane. It is different from other form of programmed cell death in morphology and mechanism, such as apoptosis, pyroptosis and necroptosis. Numerous studies have shown that ferroptosis may play an important role in the development of CRC. For advanced or metastatic CRC, ferroptosis promises to open a new door in the setting of poor response to chemotherapy and targeted therapy. This mini review focuses on the pathogenesis of CRC, the mechanism of ferroptosis and the research status of ferroptosis in CRC treatment. The potential association between ferroptosis and CRC and some challenges are discussed.
C1 [Liang, Hong; He, Xia; Bai, Niuniu; Han, Ke] Univ Elect Sci & Technol China, Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Sch Med, Dept Pharm, Chengdu, Peoples R China.
   [Liang, Hong; He, Xia] Univ Elect Sci & Technol China, Sch Med, Personalized Drug Therapy Key Lab Sichuan Prov, Chengdu, Peoples R China.
   [Tong, Yitong] Chengdu Second Peoples Hosp, Party Comm Off, Chengdu, Peoples R China.
   [Bai, Niuniu] Shanxi Med Univ, Sch Pharm, Taiyuan, Peoples R China.
   [Pu, Yushu] Nanchang Univ, Queen Mary Sch, Nanchang, Peoples R China.
   [Han, Ke] First Peoples Hosp Chengdu, Dept Pharm, Chengdu, Peoples R China.
   [Wang, Yi] Univ Elect Sci & Technol China, Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Dept Crit Care Med, Chengdu, Sicuhan, Peoples R China.
C3 Sichuan Provincial People's Hospital; University of Electronic Science &
   Technology of China; University of Electronic Science & Technology of
   China; Shanxi Medical University; Nanchang University; University of
   Electronic Science & Technology of China; Sichuan Provincial People's
   Hospital
RP Wang, Y (corresponding author), Univ Elect Sci & Technol China, Sichuan Acad Med Sci & Sichuan Prov Peoples Hosp, Dept Crit Care Med, Chengdu, Sicuhan, Peoples R China.
EM w_yi2022@163.com
RI Wang, Yi/GSD-4852-2022
FU Natural Science Foundation of China [81802504, 72174038]; National key
   R&D Program of China [2020YFC2005500]; Research Programs of Science and
   Technology Department of Sichuan Province [2022YFS0272, 2022YFH0005,
   2023YFH0010]; Personalized Drug Therapy Key Laboratory of Sichuan
   Province [2021ZD02, 2022YB02]; Sichuan Medical Association [S16068,
   Q19037]; Postdoctoral Science Foundation of Sichuan Province
   [TB2022047]; Postdoctoral Science Foundation of Sichuan Academy of
   Medical Sciences & Sichuan Provincial People's Hospital [2022BH04,
   2020LY06]
FX This study was supported by Natural Science Foundation of China
   (81802504 and 72174038), National key R&D Program of China
   (2020YFC2005500). It is also supported by Research Programs of Science
   and Technology Department of Sichuan Province (2022YFS0272, 2022YFH0005,
   2023YFH0010), Personalized Drug Therapy Key Laboratory of Sichuan
   Province (2021ZD02, 2022YB02), Sichuan Medical Association (S16068 and
   Q19037), Postdoctoral Science Foundation of Sichuan Province
   (TB2022047), and Postdoctoral Science Foundation of Sichuan Academy of
   Medical Sciences & Sichuan Provincial People's Hospital (2022BH04,
   2020LY06).
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NR 129
TC 12
Z9 12
U1 2
U2 23
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 16
PY 2023
VL 13
AR 1059520
DI 10.3389/fonc.2023.1059520
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C4IF5
UT WOS:000961562800001
PM 37007121
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Giulia, M
   Teresa, T
   Claudia, C
   Paolo, VP
   Davide, C
   Floriana, M
   Fortunato, C
   Erika, M
AF Giulia, Martini
   Teresa, Troiani
   Claudia, Cardone
   Paolo, Vitiello Pietro
   Davide, Ciardiello
   Floriana, Morgillo
   Fortunato, Ciardiello
   Erika, Martinelli
TI Anti-angiogenic Treatment in Metastatic Colorectal Cancer: Current
   Issues and Future Aims
SO CURRENT CANCER THERAPY REVIEWS
LA English
DT Review
DE Colorectal cancer; angiogenesis; resistance; VEGF; biomarkers; targeted
   therapy
ID ENDOTHELIAL GROWTH-FACTOR; PHASE-III; VESSEL NORMALIZATION; TUMOR
   ANGIOGENESIS; 1ST-LINE TREATMENT; PLACEBO PLUS; DOUBLE-BLIND;
   OPEN-LABEL; BEVACIZUMAB; FLUOROURACIL
AB Blocking angiogenesis represents a fundamental process in Colorectal Cancer (CRC) treatment. VEGF (vascular endothelial growth factor) pathway is implicated in various processes that regulate tumor vascularization and proliferation. In the last years, great efforts have been made thanks to the discovery of targeted drugs that block VEGF and its receptors conferring a benefit in a variety of tumors, including CRC. To date, four drugs have been approved for the treatment of metastatic CRC (mCRC): bevacizumab, aflibercept, ramucirumab and regorafcnib. Unfortunately, patients relapse due to the appearance of resistance. The VEGF family, its role in the angiogencsis and complex heterogeneity of mechanisms that escape tumor blockade arc not completely understood and there is a lack of biomarkers of response to anti-angiogenic drugs. We describe the principal mechanisms of resistance to anti-VEGF therapy and discuss potential biomarkers to be investigated in the near future.
C1 [Giulia, Martini; Teresa, Troiani; Claudia, Cardone; Paolo, Vitiello Pietro; Davide, Ciardiello; Floriana, Morgillo; Fortunato, Ciardiello; Erika, Martinelli] Univ Campania L Vanvitelli, Med Oncol, Dept Clin & Expt Med F Magrassi, Naples, Italy.
C3 Universita della Campania Vanvitelli
RP Erika, M (corresponding author), Univ Campania L Vanvitelli, Med Oncol, Dept Precis Med, Via Pansini 5, I-80131 Naples, Italy.
EM erika.martinelli@unicampania.it
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NR 78
TC 0
Z9 0
U1 1
U2 6
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1573-3947
EI 1875-6301
J9 CURR CANCER THER REV
JI Curr. Cancer Ther. Rev.
PY 2019
VL 15
IS 3
BP 184
EP 191
DI 10.2174/1573394714666181119145327
PG 8
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA JO5ZO
UT WOS:000497656700002
DA 2025-01-04
ER

PT J
AU Graham, DM
   Coyle, VM
   Kennedy, RD
   Wilson, RH
AF Graham, Donna M.
   Coyle, Vicky M.
   Kennedy, Richard D.
   Wilson, Richard H.
TI Molecular Subtypes and Personalized Therapy in Metastatic Colorectal
   Cancer
SO CURRENT COLORECTAL CANCER REPORTS
LA English
DT Article
DE Colorectal cancer; Biomarker stratification; Targeted therapy; Pathways;
   Molecular subtypes; Personalized medicine trials; Microsatellite
   instability; RAS; BRAF; EGFR; c-MET; HER2
ID GENE-EXPRESSION PATTERNS; DNA MISMATCH REPAIR; III COLON-CANCER;
   MICROSATELLITE INSTABILITY; 1ST-LINE TREATMENT; PROGNOSTIC IMPACT;
   MUTATION STATUS; P53 EXPRESSION; BRAF MUTATIONS; KRAS
AB Development of colorectal cancer occurs via a number of key pathways, with the clinicopathological features of specific subgroups being driven by underlying molecular changes. Mutations in key genes within the network of signalling pathways have been identified; however, therapeutic strategies to target these aberrations remain limited. As understanding of the biology of colorectal cancer has improved, this has led to a move toward broader genomic testing, collaborative research and innovative, adaptive clinical trial design. Recent developments in therapy include the routine adoption of wider mutational spectrum testing prior to use of targeted therapies and the first promise of effective immunotherapy for colorectal cancer patients. This review details current biomarkers in colorectal cancer for molecular stratification and for treatment allocation purposes, including open and planned precision medicine trials. Advances in our understanding, therapeutic strategy and technology will also be outlined.
C1 [Graham, Donna M.; Coyle, Vicky M.; Kennedy, Richard D.; Wilson, Richard H.] Queens Univ Belfast, Ctr Canc Res & Cell Biol, 97 Lisburn Rd, Belfast BT9 7AE, Antrim, North Ireland.
C3 Queens University Belfast
RP Wilson, RH (corresponding author), Queens Univ Belfast, Ctr Canc Res & Cell Biol, 97 Lisburn Rd, Belfast BT9 7AE, Antrim, North Ireland.
EM dgraham06@qub.ac.uk; v.coyle@qub.ac.uk; r.kennedy@qub.ac.uk;
   r.wilson@qub.ac.uk
OI Wilson, Richard/0000-0001-8018-7730
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NR 83
TC 32
Z9 38
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1556-3790
EI 1556-3804
J9 CURR COLORECT CANC R
JI Curr. Colorectal Cancer Rep.
PD JUN
PY 2016
VL 12
IS 3
BP 141
EP 150
DI 10.1007/s11888-016-0312-y
PG 10
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA DV1HY
UT WOS:000382673100004
PM 27340376
OA Green Published, Green Accepted, hybrid
DA 2025-01-04
ER

PT J
AU Shen, TL
   Chen, ZX
   Qiao, J
   Sun, XJ
   Xiao, Q
AF Shen, Tianli
   Chen, Zhengxi
   Qiao, Ju
   Sun, Xuejun
   Xiao, Qian
TI Neutralizing monoclonal antibody against Dickkopf2 impairs lung cancer
   progression <i>via</i> activating NK cells
SO CELL DEATH DISCOVERY
LA English
DT Article
ID CLINICAL-PRACTICE GUIDELINES; APC GENE; SOMATIC MUTATIONS; DKK2;
   PATHWAY; COMPONENTS; BLOCKADE; FAMILY; ROLES
AB Adenomatous polyposis coli (APC) and KRAS proto-oncogene (KRAS) mutations frequently co-occur in non-small cell lung cancer. Inactivating APC mutations in colorectal carcinoma has been well characterized, leading to the approaches targeting on dysregulated APC pathway. However, it remains undetermined whether such approaches are also applicable to non-small cell lung cancer patients harboring similar mutations of APC. Dickkopf-related protein 2 (DKK2) is a Wnt antagonist. Our previous study has proved that anti-DKK2 antibody 5F8 suppressed the growth of colorectal carcinoma with APC mutations, illustrating a new target agent of APC-mutated tumors. This study aimed to investigate the potential of applying anti-DKK2 antibody to non-small cell lung cancer with APC mutations. We found significant upregulation of Dkk2 expression in APC-mutated lung cancers. Administration of DKK2 antibody inhibited cancer growth via modulating tumor immune microenvironment in lung cancer mouse models. Our study provided strong evidence supporting APC mutations-directed applications of anti-DKK2 targeted therapy in a wide range of cancer types, including lung cancer.
C1 [Shen, Tianli; Sun, Xuejun] Xi An Jiao Tong Univ, Dept Gen Surg, Affiliated Hosp 1, Xian, Shaanxi, Peoples R China.
   [Shen, Tianli; Chen, Zhengxi; Xiao, Qian] Yale Univ, Sch Med, Dept Pharmacol, 10 Amistad St, New Haven, CT 06510 USA.
   [Chen, Zhengxi] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Orthodont, Sch Stomatol,Shanghai Key Lab Stomatol, Shanghai, Peoples R China.
   [Qiao, Ju] Northeastern Univ, Dept Mech & Ind Engn, Boston, MA 02115 USA.
C3 Xi'an Jiaotong University; Yale University; Shanghai Jiao Tong
   University; Northeastern University
RP Sun, XJ (corresponding author), Xi An Jiao Tong Univ, Dept Gen Surg, Affiliated Hosp 1, Xian, Shaanxi, Peoples R China.; Xiao, Q (corresponding author), Yale Univ, Sch Med, Dept Pharmacol, 10 Amistad St, New Haven, CT 06510 USA.
EM sunxy@mail.xjtu.edu.cn; qian.xiao@yale.edu
RI Xiao, Qian/ABC-6551-2021; sun, xuejun/G-5212-2011
OI Chen, Zhengxi/0000-0002-3941-111X; Xiao, Qian/0000-0002-2103-4854
FU National Cancer Institute [1R13CA236284-01]; National Natural Science
   Foundation of China [81770521]
FX This work was supported by the National Cancer Institute, Grant
   #1R13CA236284-01, and the National Natural Science Foundation of China,
   Grant #81770521.
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NR 52
TC 11
Z9 11
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.
PD JUL 31
PY 2019
VL 5
AR 123
DI 10.1038/s41420-019-0204-4
PG 12
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA JI2HV
UT WOS:000493285600002
PM 31372243
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yang, KQ
   Yi, T
AF Yang, Kangqi
   Yi, Tuo
TI Tumor cell stemness in gastrointestinal cancer: regulation and targeted
   therapy
SO FRONTIERS IN MOLECULAR BIOSCIENCES
LA English
DT Review
DE gastrointestinal tumor; cancer stem cell; tumor heterogeneity; tumor
   microenvironment; epithelial-to-mesenchymal transition;
   cancer-associated fibroblast
ID EPITHELIAL-MESENCHYMAL TRANSITION; COLORECTAL-CANCER; GASTRIC-CANCER;
   PANCREATIC-CANCER; TGF-BETA; INITIATING CELLS; GROWTH-FACTOR;
   SELF-RENEWAL; HEPATOCELLULAR-CARCINOMA; T-CELLS
AB The cancer stem cells are a rare group of self-renewable cancer cells capable of the initiation, progression, metastasis and recurrence of tumors, and also a key contributor to the therapeutic resistance. Thus, understanding the molecular mechanism of tumor stemness regulation, especially in the gastrointestinal (GI) cancers, is of great importance for targeting CSC and designing novel therapeutic strategies. This review aims to elucidate current advancements in the understanding of CSC regulation, including CSC biomarkers, signaling pathways, and non-coding RNAs. We will also provide a comprehensive view on how the tumor microenvironment (TME) display an overall tumor-promoting effect, including the recruitment and impact of cancer-associated fibroblasts (CAFs), the establishment of an immunosuppressive milieu, and the induction of angiogenesis and hypoxia. Lastly, this review consolidates mainstream novel therapeutic interventions targeting CSC stemness regulation.
C1 [Yang, Kangqi] Fudan Univ, Sch Basic Med Sci, Shanghai, Peoples R China.
   [Yi, Tuo] Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Shanghai, Peoples R China.
C3 Fudan University; Fudan University
RP Yi, T (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Shanghai, Peoples R China.
EM yi.tuo@zs-hospital.sh.cn
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NR 302
TC 0
Z9 0
U1 3
U2 5
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 FEB 22
PY 2024
VL 10
AR 1297611
DI 10.3389/fmolb.2023.1297611
PG 21
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA JZ1P9
UT WOS:001176892700001
PM 38455361
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Oliveres, H
   Pesántez, D
   Maurel, J
AF Oliveres, Helena
   Pesantez, David
   Maurel, Joan
TI Lessons to Learn for Adequate Targeted Therapy Development in Metastatic
   Colorectal Cancer Patients
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE insulin-like growth factor receptor; metastatic colorectal cancer
ID FACTOR-I RECEPTOR; EPITHELIAL-MESENCHYMAL TRANSITION; IGF-BINDING
   PROTEIN-3; GROWTH-FACTOR IGF; WILD-TYPE; PHASE-II; PATIENTS PTS; ERBB2
   AMPLIFICATION; CETUXIMAB TREATMENT; MOLECULAR SUBTYPES
AB Insulin-like growth factor 1 receptor (IGF1R) is a receptor tyrosine kinase that regulates cell growth and proliferation. Upregulation of the IGF1R pathway constitutes a common paradigm shared with other receptor tyrosine kinases such as EGFR, HER2, and MET in different cancer types, including colon cancer. The main IGF1R signaling pathways are PI3K-AKT and MAPK-MEK. However, different processes, such as post-translational modification (SUMOylation), epithelial-to-mesenchymal transition (EMT), and microenvironment complexity, can also contribute to intrinsic and acquired resistance. Here, we discuss new strategies for adequate drug development in metastatic colorectal cancer patients.
C1 [Oliveres, Helena; Pesantez, David; Maurel, Joan] Univ Barcelona, Translat Genom & Targeted Therapeut Solid Tumors, Med Oncol Dept, IDIBAPS,Hosp Clin Barcelona, Barcelona 08036, Spain.
   [Maurel, Joan] Univ Barcelona, Hosp Clin, Gastrointestinal & Pancreat Oncol Grp, IDIBAPS,CIBERehd, Barcelona 08036, Spain.
C3 University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS;
   University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS; CIBER -
   Centro de Investigacion Biomedica en Red; CIBEREHD
RP Oliveres, H; Pesántez, D; Maurel, J (corresponding author), Univ Barcelona, Translat Genom & Targeted Therapeut Solid Tumors, Med Oncol Dept, IDIBAPS,Hosp Clin Barcelona, Barcelona 08036, Spain.; Maurel, J (corresponding author), Univ Barcelona, Hosp Clin, Gastrointestinal & Pancreat Oncol Grp, IDIBAPS,CIBERehd, Barcelona 08036, Spain.
EM oliveres@clinic.cat; Pesantez@clinic.cat; jmaurel@clinic.cat
OI Maurel, Joan/0000-0002-9413-5592
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NR 115
TC 6
Z9 6
U1 5
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD MAY
PY 2021
VL 22
IS 9
AR 5019
DI 10.3390/ijms22095019
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA SC0HE
UT WOS:000650363200001
PM 34065119
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ren, CF
   Zhang, ZM
   Wang, SH
   Zhu, WT
   Zheng, PG
   Wang, WH
AF Ren, Chunfeng
   Zhang, Zhenmin
   Wang, Shunhua
   Zhu, Weitao
   Zheng, Peiguo
   Wang, Wanhai
TI Circular RNA hsa_circ_0001178 facilitates the invasion and metastasis of
   colorectal cancer through upregulating ZEB1 via sponging multiple miRNAs
SO BIOLOGICAL CHEMISTRY
LA English
DT Article
DE circular RNA; competing endogenous RNA; colorectal cancer; metastasis
ID EXPRESSION; CIRCHIPK3; ABUNDANT; ROLES
AB Metastasis is the main cause of increasing cancer morbidity and mortality. However, the underlying mechanism of cancer metastasis remains largely unknown. In the present study, we identified one circular RNA (circRNA) closely related to the metastasis of colorectal cancer (CRC), namely hsa_circ_0001178. CRC patients with high hsa_ circ_0001178 were more prone to have metastatic clinical features, advanced NM stage and adverse prognosis. Stable knockdown of hsa_circ_0001178 significantly weakened CRC cell migratory and invasive capabilities in vitro as well as lung and liver metastases in vivo. Mechanistic study revealed that hsa_circ_0001178 acted as a competing endogenous RNA (ceRNA) for miR-382/587/616 to upregulate ZEB1 (a key trigger of epithelial-to-mesenchymal transition), thereby promoting CRC metastatic dissemination. Of note, ZEB1 could also increase hsa_circ_0001178 expression via physically binding to hsa_circ_0001178 promoter region. Collectively, our data uncover the crucial role of hsa_circ_0001178 in CRC metastasis, and targeted therapy based on this positive feedback ceRNA axis may be a promising treatment for metastatic CRC patients.
C1 [Ren, Chunfeng; Zhang, Zhenmin; Wang, Shunhua; Zhu, Weitao; Zheng, Peiguo; Wang, Wanhai] Zhengzhou Univ, Clin Lab, Affiliated Hosp 1, 1 Jianshe Dong Rd, Zhengzhou 450003, Peoples R China.
C3 Zhengzhou University
RP Ren, CF (corresponding author), Zhengzhou Univ, Clin Lab, Affiliated Hosp 1, 1 Jianshe Dong Rd, Zhengzhou 450003, Peoples R China.
EM rencf896@yeah.net
RI Wang, Hui-Tian/P-7171-2019
FU Key -Project of Medical Science and Technology of Henan -Province
   [201503008]
FX This work was funded by the Key -Project of Medical Science and
   Technology of Henan -Province (No. 201503008).
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NR 30
TC 43
Z9 46
U1 1
U2 15
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1431-6730
EI 1437-4315
J9 BIOL CHEM
JI Biol. Chem.
PD APR
PY 2020
VL 401
IS 4
BP 487
EP 496
DI 10.1515/hsz-2019-0350
PG 10
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA KT6KH
UT WOS:000519122800006
PM 31747371
DA 2025-01-04
ER

PT J
AU Yoon, YS
   Kim, CW
   Roh, SA
   Cho, DH
   Kim, TW
   Kim, MB
   Kim, JC
AF Yoon, Yong Sik
   Kim, Chan Wook
   Roh, Seon Ae
   Cho, Dong Hyung
   Kim, Tae Won
   Kim, Moon Bo
   Kim, Jin Cheon
TI Development and Applicability of Integrative Tumor Response Assays for
   Metastatic Colorectal Cancer
SO ANTICANCER RESEARCH
LA English
DT Article
DE Colorectal adenocarcinoma; chemotherapy; histoculture drug-response
   assay; molecular targeted therapy; treatment outcome
ID HISTONE DEACETYLASE INHIBITORS; NECK-CANCER; CHEMOTHERAPY; CETUXIMAB;
   FLUOROURACIL; LEUCOVORIN; RESISTANCE; CISPLATIN; THERAPY; AGENTS
AB Aim: The present study investigated how well the results of integrative tumor-response assay (ITRA) compared to those of clinical response to chemotherapy in patients with metastatic colorectal cancer (CRC). Patients and Methods: A total of 129 patients with metastatic CRC were prospectively enrolled. ITRA consisted of two sequential histoculture drug-response assays (HDRAs). First-stage HDRAs were performed using 5-fluorouracil with leucovorin and oxaliplatin (FX), or with irinotecan (FR). Second-stage HDRAs (ITRA) were performed for cells surviving after the first-stage HDRA, using FX, FR, and their combinations with bevacizumab and cetuximab. Results: Among 129 patients, 42 (32.6%) completed second-line chemotherapy, results that correlated with those of ITRA. The accuracy of ITRA for predicting response to second-line chemotherapy was 61.9% (26/42), with a sensitivity of 44.4% (8/18) and a specificity of 75% (18/24). Conclusion: Despite its relatively low accuracy, ITRA might be a useful technique for predicting therapeutic efficacy and selecting for appropriate first- line and second-line anticancer regimens for patients.
C1 [Yoon, Yong Sik; Kim, Chan Wook; Kim, Jin Cheon] Univ Ulsan, Coll Med, Dept Surg, 88 Olymp Ro,43 Gil, Seoul 05505, South Korea.
   [Kim, Tae Won] Univ Ulsan, Coll Med, Dept Internal Med, Seoul, South Korea.
   [Yoon, Yong Sik; Kim, Chan Wook; Roh, Seon Ae; Cho, Dong Hyung; Kim, Tae Won; Kim, Moon Bo; Kim, Jin Cheon] Asan Med Ctr, Inst Innovat Canc Res, Seoul, South Korea.
   [Cho, Dong Hyung] Kyung Hee Univ, Grad Sch East West Med Sci, Gyeonggi Do, South Korea.
C3 University of Ulsan; University of Ulsan; University of Ulsan; Asan
   Medical Center; Kyung Hee University
RP Kim, JC (corresponding author), Univ Ulsan, Coll Med, Dept Surg, 88 Olymp Ro,43 Gil, Seoul 05505, South Korea.
EM jckim@amc.seoul.kr
RI Bin Kim, Hong/J-5452-2012; Kim, Tae Won/GRX-7323-2022; Choi, Hye
   Rin/JDV-9065-2023
FU Asan Institute for Life Sciences [2014-596]; Korea Research Foundation
   [2013R1A2A1A03070986]; Ministry of Science, ICT, and Future Planning,
   the Korea Health 21 RD Project [HI06C0868, HI13C1750]; Center for
   Development and Commercialization of Anti-Cancer Therapeutics [A102059];
   Ministry of Health and Welfare, Republic of Korea
FX This study was supported by grants from the Asan Institute for Life
   Sciences (2014-596), the Korea Research Foundation
   (2013R1A2A1A03070986), Ministry of Science, ICT, and Future Planning,
   the Korea Health 21 R&D Project (HI06C0868 and HI13C1750), and the
   Center for Development and Commercialization of Anti-Cancer Therapeutics
   (A102059), Ministry of Health and Welfare, Republic of Korea. Seoul,
   Korea. The Authors would like to thank Enago (http://www.enago.co.kr)
   for English language review.
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BP 1297
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PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EP1FA
UT WOS:000397129600044
PM 28314295
OA Bronze
DA 2025-01-04
ER

PT J
AU Bhardwaj, B
   Revannasiddaiah, S
   Bhardwaj, H
   Sree Balusu
   Shwaiki, A
AF Bhardwaj, Bhaskar
   Revannasiddaiah, Swaroop
   Bhardwaj, Himanshu
   Sree Balusu
   Shwaiki, Ali
TI Molecular targeted therapy to improve radiotherapeutic outcomes for
   non-small cell lung carcinoma
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE Targeted therapy; monoclonal antibodies; tyrosine kinase inhibitors;
   radio-sensitizer; gefitinib with radiotherapy; erlotinib with
   radiotherapy; cetuximab with radiotherapy
ID GROWTH-FACTOR-RECEPTOR; CONCURRENT THORACIC RADIOTHERAPY; PHASE-III
   TRIAL; INDUCTION CHEMOTHERAPY; EGFR MUTATION; OPEN-LABEL; MAINTENANCE
   GEFITINIB; 1ST-LINE TREATMENT; COLORECTAL-CANCER; DRIVER MUTATIONS
AB Effective treatments for non-small cell lung carcinoma (NSCLC) remain elusive. The use of concurrent chemotherapy with radiotherapy (RT) has improved outcomes, but a significant proportion of NSCLC patients are too frail to be able to tolerate an intense course of concurrent chemoradiotherapy. The development of targeted therapies ignited new hope in enhancing radiotherapeutic outcomes. The use of targeted therapies against the epidermal growth factor receptor (EGFR) has offered slight but significant benefits in concurrent use with RT for certain patients in certain situations. However, despite theoretical promise, the use of anti-angiogenics, such as bevacizumab and endostatin, has not proven clinically safe or useful in combination with RT. However, many new targeted agents against new targets are being experimented for combined use with RT. It is hoped that these agents may provide a significant breakthrough in the radiotherapeutic management of NSCLC. The current review provides a brief discussion about the targets, the targeted therapies, the rationale for the use of targeted therapies in combination with RT, and a brief review of the existing data on the subject.
C1 [Bhardwaj, Bhaskar; Sree Balusu] Univ Missouri, Dept Internal Med, Kansas City, MO 64110 USA.
   [Revannasiddaiah, Swaroop] Govt Med Coll, Dept Radiat Oncol, Haldwani, Nanital, India.
   [Bhardwaj, Himanshu] Univ Oklahoma, Dept Pulm Med & Crit Care, Norman, OK 73019 USA.
   [Shwaiki, Ali] St Lukes Hosp, Dept Hematol & Oncol, Kansas City, MO USA.
C3 University of Missouri System; University of Missouri Kansas City;
   University of Oklahoma System; University of Oklahoma - Norman; Saint
   Luke's Hospital - Missouri
RP Revannasiddaiah, S (corresponding author), Govt Med Coll, Swami Rama Canc Hosp & Res Inst, Dept Radiat Oncol, Naini Tal 263139, Uttarakhand, India.
EM swarooptheone@gmail.com
RI Bhardwaj, Bhaskar/AAP-5071-2020
OI Bhardwaj, Bhaskar/0000-0002-4963-5459; Revannasiddaiah,
   Swaroop/0000-0001-6985-9874
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NR 79
TC 14
Z9 18
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 2305-5839
EI 2305-5847
J9 ANN TRANSL MED
JI ANN. TRANSL. MED.
PD FEB
PY 2016
VL 4
IS 3
AR 50
DI 10.3978/j.issn.2305-5839.2015.10.35
PG 10
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA DY0MW
UT WOS:000384791900009
PM 26904572
DA 2025-01-04
ER

PT J
AU Muta, Y
   Linares, JF
   Martinez-Ordoñez, A
   Duran, A
   Cid-Diaz, T
   Kinoshita, H
   Zhang, X
   Han, QX
   Nakanishi, Y
   Nakanishi, N
   Cordes, T
   Arora, GK
   Ruiz-Martinez, M
   Reina-Campos, M
   Kasashima, H
   Yashiro, M
   Maeda, K
   Albaladejo-Gonzalez, A
   Torres-Moreno, D
   García-Solano, J
   Conesa-Zamora, P
   Inghirami, G
   Metallo, CM
   Osborne, TF
   Diaz-Meco, MT
   Moscat, J
AF Muta, Yu
   Linares, Juan F.
   Martinez-Ordonez, Anxo
   Duran, Angeles
   Cid-Diaz, Tania
   Kinoshita, Hiroto
   Zhang, Xiao
   Han, Qixiu
   Nakanishi, Yuki
   Nakanishi, Naoko
   Cordes, Thekla
   Arora, Gurpreet K.
   Ruiz-Martinez, Marc
   Reina-Campos, Miguel
   Kasashima, Hiroaki
   Yashiro, Masakazu
   Maeda, Kiyoshi
   Albaladejo-Gonzalez, Ana
   Torres-Moreno, Daniel
   Garcia-Solano, Jose
   Conesa-Zamora, Pablo
   Inghirami, Giorgio
   Metallo, Christian M.
   Osborne, Timothy F.
   Diaz-Meco, Maria T.
   Moscat, Jorge
TI Enhanced SREBP2-driven cholesterol biosynthesis by PKCλ/ι deficiency in
   intestinal epithelial cells promotes aggressive serrated tumorigenesis
SO NATURE COMMUNICATIONS
LA English
DT Article
ID COLORECTAL-CANCER; COLON-CANCER; MEVALONATE PATHWAY; LIPID-METABOLISM;
   STATIN USE; EXPRESSION; SURVIVAL; MICROENVIRONMENT; PERSPECTIVES;
   PROGRESSION
AB The metabolic and signaling pathways regulating aggressive mesenchymal colorectal cancer (CRC) initiation and progression through the serrated route are largely unknown. Although relatively well characterized as BRAF mutant cancers, their poor response to current targeted therapy, difficult preneoplastic detection, and challenging endoscopic resection make the identification of their metabolic requirements a priority. Here, we demonstrate that the phosphorylation of SCAP by the atypical PKC (aPKC), PKC lambda/iota promotes its degradation and inhibits the processing and activation of SREBP2, the master regulator of cholesterol biosynthesis. We show that the upregulation of SREBP2 and cholesterol by reduced aPKC levels is essential for controlling metaplasia and generating the most aggressive cell subpopulation in serrated tumors in mice and humans. Since these alterations are also detected prior to neoplastic transformation, together with the sensitivity of these tumors to cholesterol metabolism inhibitors, our data indicate that targeting cholesterol biosynthesis is a potential mechanism for serrated chemoprevention.
   The underlying mechanisms driving colorectal cancer (CRC) through the serrated route are largely unknown. Here, the authors show that reduced aPKC levels increase cholesterol biosynthesis to promote aggressiveness in serrated tumours and targeting this pathway reduces tumourigenesis in preclinical models of serrated CRC.
C1 [Muta, Yu; Linares, Juan F.; Martinez-Ordonez, Anxo; Duran, Angeles; Cid-Diaz, Tania; Kinoshita, Hiroto; Zhang, Xiao; Han, Qixiu; Ruiz-Martinez, Marc; Inghirami, Giorgio; Diaz-Meco, Maria T.; Moscat, Jorge] Weill Cornell Med, Dept Pathol & Lab Med, New York, NY 10065 USA.
   [Muta, Yu; Linares, Juan F.; Martinez-Ordonez, Anxo; Duran, Angeles; Cid-Diaz, Tania; Kinoshita, Hiroto; Zhang, Xiao; Han, Qixiu; Ruiz-Martinez, Marc; Inghirami, Giorgio; Diaz-Meco, Maria T.; Moscat, Jorge] Weill Cornell Med, Sandra & Edward Meyer Canc Ctr, New York, NY 10065 USA.
   [Muta, Yu; Nakanishi, Yuki] Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Kyoto, Japan.
   [Muta, Yu] Kobe Univ, Grad Sch Med, Dept Internal Med, Div Gastroenterol, Kobe, Japan.
   [Nakanishi, Naoko] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Endocrinol & Metab, Kyoto, Japan.
   [Cordes, Thekla; Metallo, Christian M.] Salk Inst Biol Studies, Mol & Cell Biol Lab, La Jolla, CA 92037 USA.
   [Cordes, Thekla] Tech Univ Braunschweig, Braunschweig Integrated Ctr Syst Biol BRICS, Dept Bioinformat & Biochem, Braunschweig, Germany.
   [Arora, Gurpreet K.] Sanford Burnham Prebys, Cell & Mol Biol Canc Program, La Jolla, CA 92037 USA.
   [Reina-Campos, Miguel] Univ Calif San Diego, Sch Biol Sci, Dept Mol Biol, San Diego, CA 92182 USA.
   [Kasashima, Hiroaki; Yashiro, Masakazu; Maeda, Kiyoshi] Osaka Metropolitan Univ, Grad Sch Med, Dept Gastroenterol, 1-4-3 Asahimachi,Abeno Ku, Osaka 5458585, Japan.
   [Albaladejo-Gonzalez, Ana; Torres-Moreno, Daniel; Garcia-Solano, Jose; Conesa-Zamora, Pablo] Univ Catolica Murcia UCAM, Fac Life Sci, Dept Histol & Pathol, Murcia 30107, Spain.
   [Albaladejo-Gonzalez, Ana; Garcia-Solano, Jose] Santa Lucia Gen Univ Hosp HGUSL, Dept Pathol, Calle Mezquita Sn, Cartagena 30202, Spain.
   [Torres-Moreno, Daniel; Conesa-Zamora, Pablo] Santa Lucia Gen Univ Hosp HGUSL, Dept Clin Anal, Calle Mezquita Sn, Cartagena 30202, Spain.
   [Osborne, Timothy F.] Johns Hopkins Univ, Johns Hopkins All Childrens Hosp, Inst Fundamental Biomed Res, Div Endocrinol Diabet & Metab,Sch Med, Petersburg, FL USA.
C3 Cornell University; Weill Cornell Medicine; Cornell University; Weill
   Cornell Medicine; Kyoto University; Kobe University; Kyoto Prefectural
   University of Medicine; Salk Institute; Braunschweig University of
   Technology; University of California System; University of California
   San Diego; Universidad Catolica de Murcia; Johns Hopkins University;
   Johns Hopkins Medicine
RP Diaz-Meco, MT; Moscat, J (corresponding author), Weill Cornell Med, Dept Pathol & Lab Med, New York, NY 10065 USA.; Diaz-Meco, MT; Moscat, J (corresponding author), Weill Cornell Med, Sandra & Edward Meyer Canc Ctr, New York, NY 10065 USA.
EM mtd4001@med.cornell.edu; jom4010@med.cornell.edu
RI KASASHIMA, HIROAKI/HNP-0833-2023; Reina-Campos, Miguel/AAG-3644-2019;
   Ordóñez, Anxo/L-1196-2014; Cordes, Thekla/AAQ-4465-2020; ç¥è²´,
   ä¸­è¥¿/KJD-4998-2024; Chen, Mingming/AAD-6803-2021; Metallo,
   Christian/HCH-3476-2022; Kao, Shuh-Ji/F-8418-2015
OI Martinez-Ordonez, Anxo/0000-0001-9649-2967
FU Foundation for the National Institutes of Health (Foundation for the
   National Institutes of Health, Inc.) [R01CA265892, R01CA250025,
   R01CA275846, R01CA246765, R50CA265332, R50CA252146, R01CA234245];
   National Cancer Institute of the National Institutes of Health
   [GA848098]; European Union; Japan Society for the Promotion of Science
   Cross-border Postdoctoral Fellowship
FX Research was supported by grants by the National Cancer Institute of the
   National Institutes of Health under awards numbers: R01CA265892,
   R01CA250025, and R01CA275846 to J.M.; R01CA246765 to M.T.D.-M;
   R50CA265332 to A.D; R50CA252146 to T.C.; R01CA234245 to C.M.M. Project
   support for this research was provided in part by the European Union
   Horizon's 2020 Grant (REVERT project GA848098), and the Center for
   Translational Pathology in the Department of Pathology and Laboratory
   Medicine, Weill Cornell Medicine. Y.M. was supported by the Japan
   Society for the Promotion of Science Cross-border Postdoctoral
   Fellowship. We thank Tavonna Bryant and Tararin Nikomborirak, the
   personnel of the Optical Microscopy Core at Weill Cornell Medicine, and
   Eric Rosiek of the Molecular Cytology Core at Memorial Sloan Kettering
   Cancer Center for technical assistance. J.M. and M.T.D.-M. are Homer T.
   Hirst III Professors of Oncology in Pathology.
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U1 1
U2 12
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
EI 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC 13
PY 2023
VL 14
IS 1
AR 8075
DI 10.1038/s41467-023-43690-5
PG 20
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CL3G8
UT WOS:001125362100002
PM 38092754
OA gold
DA 2025-01-04
ER

PT J
AU Picco, G
   Petti, C
   Centonze, A
   Torchiaro, E
   Crisafulli, G
   Novara, L
   Acquaviva, A
   Bardelli, A
   Medico, E
AF Picco, Gabriele
   Petti, Consalvo
   Centonze, Alessia
   Torchiaro, Erica
   Crisafulli, Giovanni
   Novara, Luca
   Acquaviva, Andrea
   Bardelli, Alberto
   Medico, Enzo
TI Loss of AXIN1 drives acquired resistance to WNT pathway blockade in
   colorectal cancer cells carrying RSPO3 fusions
SO EMBO MOLECULAR MEDICINE
LA English
DT Article
DE colorectal cancer; gene fusion; R-spondin; targeted therapy; WNT pathway
ID INTESTINAL STEM-CELLS; BETA-CATENIN; COLON-CANCER; HEPATOCELLULAR
   CARCINOMAS; NEGATIVE REGULATOR; SIGNALING PATHWAY; IN-VITRO; MUTATIONS;
   LINES; MECHANISMS
AB In colorectal cancer (CRC), WNT pathway activation by genetic rearrangements of RSPO3 is emerging as a promising target. However, its low prevalence severely limits availability of preclinical models for in-depth characterization. Using a pipeline designed to suppress stroma-derived signal, we find that RSPO3 "outlier" expression in CRC samples highlights translocation and fusion transcript expression. Outlier search in 151 CRC cell lines identified VACO6 and SNU1411 cells as carriers of, respectively, a canonical PTPRK(e1)-RSPO3(e2) fusion and a novel PTPRK(e13)-RSPO3(e2) fusion. Both lines displayed marked in vitro and in vivo sensitivity to WNT blockade by the porcupine inhibitor LGK974, associated with transcriptional and morphological evidence of WNT pathway suppression. Long-term treatment of VACO6 cells with LGK974 led to the emergence of a resistant population carrying two frameshift deletions of the WNT pathway inhibitor AXIN1, with consequent protein loss. Suppression of AXIN1 in parental VACO6 cells by RNA interference conferred marked resistance to LGK974. These results provide the first mechanism of secondary resistance to WNT pathway inhibition.
C1 [Picco, Gabriele; Petti, Consalvo; Torchiaro, Erica; Crisafulli, Giovanni; Novara, Luca; Bardelli, Alberto; Medico, Enzo] IRCCS, Candiolo Canc Inst FPO, Turin, Italy.
   [Picco, Gabriele; Petti, Consalvo; Centonze, Alessia; Bardelli, Alberto; Medico, Enzo] Univ Turin, Dept Oncol, Turin, Italy.
   [Torchiaro, Erica] Consorzio Interuniv, Ist Nazl Biostrutture & Biosistemi, Rome, Italy.
   [Acquaviva, Andrea] Politecn Torino, Dept Comp & Control Engn, Turin, Italy.
C3 IRCCS Fondazione del Piemonte per l'Oncologia; University of Turin;
   Polytechnic University of Turin
RP Medico, E (corresponding author), IRCCS, Candiolo Canc Inst FPO, Turin, Italy.; Medico, E (corresponding author), Univ Turin, Dept Oncol, Turin, Italy.
EM enzo.medico@unito.it
RI Torchiaro, Erica/AAW-3628-2020; Medico, Enzo/AAC-3185-2021; BARDELLI,
   Alberto/J-9721-2018; Petti, Consalvo/K-9367-2016; Medico,
   Enzo/K-8497-2018; Crisafulli, Giovanni/AAB-6256-2019
OI BARDELLI, Alberto/0000-0003-1647-5070; Petti,
   Consalvo/0000-0002-3509-3142; Torchiaro, Erica/0000-0002-8984-882X;
   Medico, Enzo/0000-0002-3917-2438; Crisafulli,
   Giovanni/0000-0002-5511-1555; picco, gabriele/0000-0001-8568-2781;
   Centonze, Alessia/0000-0002-4269-1933
FU AIRC [IG 16819, IG 16788, 9970-2010]; Fondazione Piemontese per la
   Ricerca sul Cancro; European Community [602901 MErCuRIC]; IMI [115749
   CANCER-ID, 635342-2]; QNRF [4-967-3-262]
FX We thank Carlotta Cancelliere, Roberta Porporato, Barbara Martinoglio,
   Daniela Cantarella, Michela Buscarino, Alice Bartolini, and Stefania
   Giove for technical assistance; Claudio Isella, Sara Erika Bellomo,
   Federica Invrea, Barbara Lupo, and Simona Lamba for help and advice; and
   Simona Destefanis for secretarial assistance. AIRC investigator grants
   (IG 16819 to E. Medico and IG 16788 to A. Bardelli), AIRC 9970-2010
   Special Program Molecular Clinical Oncology 5x1000 to E. Medico and A.
   Bardelli; Fondazione Piemontese per la Ricerca sul Cancro 5x1000
   Ministero della Salute 2010 and 2011 to E. Medico and A. Bardelli;
   European Community's Seventh Framework Programme under grant agreement
   no. 602901 MErCuRIC (A. Bardelli); IMI contract n. 115749 CANCER-ID (A.
   Bardelli); H2020 n. 635342-2 MoTriColor (A. Bardelli); QNRF National
   Priority Research Program n. 4-967-3-262 (E. Medico).
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NR 54
TC 51
Z9 56
U1 1
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1757-4676
EI 1757-4684
J9 EMBO MOL MED
JI EMBO Mol. Med.
PD MAR
PY 2017
VL 9
IS 3
BP 293
EP 303
DI 10.15252/emmm.201606773
PG 11
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA EP3QE
UT WOS:000397296000004
PM 28100566
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Awah, CU
   Glemaud, Y
   Levine, F
   Yang, KS
   Ansary, A
   Dong, F
   Ash, L
   Zhang, JF
   Ogunwobi, OO
AF Awah, Chidiebere U.
   Glemaud, Yana
   Levine, Fayola
   Yang, Kiseok
   Ansary, Afrin
   Dong, Fu
   Ash, Leonard
   Zhang, Junfei
   Ogunwobi, Olorunseun O.
TI Destabilized 3'UTR elements therapeutically degrade ERBB2 mRNA in
   drug-resistant ERBB2+cancer models
SO FRONTIERS IN GENETICS
LA English
DT Article
DE ERBB2 (HER2/neu); 3'UTR elements; cancer; drug resistance; cancer
   treatment; mRNA stabilizing; mRNA overwriting
ID BREAST-CANCER; MONOCLONAL-ANTIBODY; OSIMERTINIB; DECAY; HER2;
   ACTIVATION; MUTATIONS; HERCEPTIN; PROTEINS; SURVIVAL
AB Breast, lung, and colorectal cancer resistance to molecular targeted therapy is a major challenge that unfavorably impacts clinical outcomes leading to hundreds of thousands of deaths annually. In ERBB2+ cancers regardless of the tissue of origin, many ERBB2+ cancers are resistant to ERBB2-targeted therapy. We discovered that ERBB2+ cancer cells are enriched with poly U sequences on their 3'UTR which are mRNA-stabilizing sequences. We developed a novel technology, in which we engineered these ERBB2 mRNA-stabilizing sequences to unstable forms that successfully overwrote and outcompeted the endogenous ERBB2 mRNA-encoded message and degraded ERBB2 transcripts which led to the loss of the protein across multiple cancer cell types both in the wildtype and drug-resistance settings in vitro and in vivo, offering a unique safe novel modality to control ERBB2 mRNA and other pervasive oncogenic signals where current targeted therapies fail.
C1 [Awah, Chidiebere U.; Glemaud, Yana; Levine, Fayola; Yang, Kiseok; Ansary, Afrin; Dong, Fu; Ash, Leonard; Ogunwobi, Olorunseun O.] CUNY, Hunter Coll, Dept Biol Sci, New York, NY 10065 USA.
   [Awah, Chidiebere U.; Levine, Fayola; Ogunwobi, Olorunseun O.] Cornell Univ, Joan & Sanford I Weill Dept Med, Weill Cornell Med, New York, NY 10044 USA.
   [Zhang, Junfei] Columbia Univ, Med Ctr, Dept Pathol & Cell Biol, Dept Syst Biol, New York, NY USA.
C3 City University of New York (CUNY) System; Hunter College (CUNY);
   Cornell University; Weill Cornell Medicine; Columbia University
RP Awah, CU; Ogunwobi, OO (corresponding author), CUNY, Hunter Coll, Dept Biol Sci, New York, NY 10065 USA.; Awah, CU; Ogunwobi, OO (corresponding author), Cornell Univ, Joan & Sanford I Weill Dept Med, Weill Cornell Med, New York, NY 10044 USA.
EM cha4010@med.cornell.edu; oo158@hunter.cuny.edu
RI Zhang, Junfei/LFU-3432-2024; Ogunwobi, Olorunseun/F-3172-2010
OI Awah, Chidiebere/0000-0002-3719-8626
FU National Cancer Institute [U54CA221704]
FX OO was supported by funds from the National Cancer Institute (grant
   #U54CA221704).
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NR 42
TC 2
Z9 2
U1 0
U2 4
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 JUN 9
PY 2023
VL 14
AR 1184600
DI 10.3389/fgene.2023.1184600
PG 22
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA K6YT8
UT WOS:001017886400001
PM 37359373
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Krasteva, N
   Georgieva, M
AF Krasteva, Natalia
   Georgieva, Milena
TI Promising Therapeutic Strategies for Colorectal Cancer Treatment Based
   on Nanomaterials
SO PHARMACEUTICS
LA English
DT Review
DE colorectal cancer (CRC); nanomaterials; nanocarriers; nanoparticles;
   cancer therapy; targeted therapy; graphene; graphene oxide
ID MESOPOROUS SILICA NANOPARTICLES; DRUG-DELIVERY SYSTEMS; GRAPHENE-BASED
   NANOMATERIALS; POLYMERIC MICELLES; TARGETED DELIVERY; CARBON NANOTUBES;
   IN-VITRO; CHROMOSOMAL INSTABILITY; NANOCOMPOSITE HYDROGEL; EFFICIENT
   DELIVERY
AB Colorectal cancer (CRC) is a global health problem responsible for 10% of all cancer incidences and 9.4% of all cancer deaths worldwide. The number of new cases increases per annum, whereas the lack of effective therapies highlights the need for novel therapeutic approaches. Conventional treatment methods, such as surgery, chemotherapy and radiotherapy, are widely applied in oncology practice. Their therapeutic success is little, and therefore, the search for novel technologies is ongoing. Many efforts have focused recently on the development of safe and efficient cancer nanomedicines. Nanoparticles are among them. They are uniquewith their properties on a nanoscale and hold the potential to exploit intrinsic metabolic differences between cancer and healthy cells. This feature allows them to induce high levels of toxicity in cancer cells with little damage to the surrounding healthy tissues. Graphene oxide is a promising 2D material found to play an important role in cancer treatments through several strategies: direct killing and chemosensitization, drug and gene delivery, and phototherapy. Several new treatment approaches based on nanoparticles, particularly graphene oxide, are currently under research in clinical trials, and some have already been approved. Here, we provide an update on the recent advances in nanomaterials-based CRC-targeted therapy, with special attention to graphene oxide nanomaterials. We summarise the epidemiology, carcinogenesis, stages of the CRCs, and current nanomaterials-based therapeutic approaches for its treatment.
C1 [Krasteva, Natalia] Bulgarian Acad Sci, Inst Biophys & Biomed Engn, Acad Georgi Bonchev Str,Bl 21, Sofia 1113, Bulgaria.
   [Georgieva, Milena] Bulgarian Acad Sci, Inst Mol Biol Acad R Tsanev, Acad Georgi Bonchev Str,Bl 21, Sofia 1113, Bulgaria.
C3 Bulgarian Academy of Sciences; Bulgarian Academy of Sciences
RP Krasteva, N (corresponding author), Bulgarian Acad Sci, Inst Biophys & Biomed Engn, Acad Georgi Bonchev Str,Bl 21, Sofia 1113, Bulgaria.; Georgieva, M (corresponding author), Bulgarian Acad Sci, Inst Mol Biol Acad R Tsanev, Acad Georgi Bonchev Str,Bl 21, Sofia 1113, Bulgaria.
EM nataly@bio21.bas.bg; milenageorgy@gmail.com
RI ; Georgieva, Milena/K-8427-2016
OI Krasteva, Natalia/0000-0001-7423-7412; Georgieva,
   Milena/0000-0002-2371-7544
FU Bulgarian Science Fund [KP-06 N31/15/2019, KP-06 H31/15/2019]
FX This research was funded by the Bulgarian Science Fund, grant number
   KP-06 N31/15/2019 (KP-06 H31/15/2019).
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NR 250
TC 59
Z9 60
U1 3
U2 23
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD JUN
PY 2022
VL 14
IS 6
AR 1213
DI 10.3390/pharmaceutics14061213
PG 38
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 2K6KP
UT WOS:000816442500001
PM 35745786
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ntomi, V
   Foukas, P
   Papaconstantinou, D
   Antonopoulou, I
   Pikoulis, A
   Panagiotides, I
   Pikoulis, E
   Syrigos, K
AF Ntomi, Vasileia
   Foukas, Periklis
   Papaconstantinou, Dimitrios
   Antonopoulou, Ioanna
   Pikoulis, Andreas
   Panagiotides, Ioannis
   Pikoulis, Emmanouil
   Syrigos, Konstantinos
TI The clinical significance of PD-L1 in colorectal cancer
SO ONCOLOGY REPORTS
LA English
DT Review
DE colorectal cancer; programmed death ligand-1; immunotherapy; targeted
   therapy; programmed death receptor-1
ID LIGAND 1 EXPRESSION; PROGRAMMED DEATH LIGAND-1; TUMOR-INFILTRATING
   LYMPHOCYTES; MICROSATELLITE INSTABILITY; COLON-CANCER; OPEN-LABEL;
   PROGNOSTIC-SIGNIFICANCE; ANTI-PD-1 ANTIBODY; HODGKIN LYMPHOMA; IMMUNE
   CELLS
AB Colorectal cancer (CRC) is one of the most frequently encountered neoplasms and has a high rate of morbidity and mortality. Recent findings showing that tumor immune evasion is an important mechanism underlying propagation of a cancer have changed the landscape of medical oncology through identification of Programmed-Death receptor 1 and its ligand (PD-1 and PD-L1) as novel targets for oncological immune therapies. PD-1 is primarily expressed on peritumoral lymphocytes and when activated, it suppresses its immune functions. Conversely, PD-L1 is primarily expressed on the tumor infiltrating front with the purpose of deregulating physiological cytotoxic immune responses. Numerous studies have linked PD-L1 overexpression to specific adverse clinicopathological features, such as poor differentiation, lymphovascular invasion and worse overall survival in CRC patients. Nevertheless, there is no concrete evidence showing which patients may exhibit the maximal beneficial effects of PD-1/PD-L1 blockade therapy, and how these novel molecular targets may be optimally integrated into therapeutic regimens for management of CRC patients with resectable and generalized disease.
C1 [Ntomi, Vasileia; Papaconstantinou, Dimitrios; Antonopoulou, Ioanna; Pikoulis, Andreas; Pikoulis, Emmanouil] Natl & Kapodistrian Univ Athens, Med Sch, Attikon Univ Hosp, Dept Surg 3, Athens 12462, Greece.
   [Foukas, Periklis; Panagiotides, Ioannis] Natl & Kapodistrian Univ Athens, Med Sch, Attikon Univ Hosp, Dept Pathol 2, Athens 12462, Greece.
   [Syrigos, Konstantinos] Natl & Kapodistrian Univ Athens, Med Sch, Sotiria Gen Hosp, Dept Med 3, Athens 12462, Greece.
C3 National & Kapodistrian University of Athens; University Hospital
   Attikon; University Hospital Attikon; National & Kapodistrian University
   of Athens; National & Kapodistrian University of Athens
RP Ntomi, V (corresponding author), Attikon Univ Hosp, Dept Surg 3, 1 Rimini, Athens 12462, Greece.
EM bessydomi@hotmail.com
RI Papaconstantinou, Dimitrios/ABA-5378-2021
OI Papakonstantinou, Dimitrios/0000-0002-2319-4923
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NR 109
TC 4
Z9 4
U1 0
U2 21
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD JUN
PY 2021
VL 45
IS 6
AR 92
DI 10.3892/or.2021.8043
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RM8AW
UT WOS:000639880700001
PM 33846789
OA Bronze
DA 2025-01-04
ER

PT S
AU Morris, VK
   Strickler, JH
AF Morris, Van K.
   Strickler, John H.
BE Klotman, ME
TI Use of Circulating Cell-Free DNA to Guide Precision Medicine in Patients
   with Colorectal Cancer
SO ANNUAL REVIEW OF MEDICINE, VOL 72, 2021
SE Annual Review of Medicine
LA English
DT Review; Book Chapter
DE colorectal cancer; circulating tumor DNA; ctDNA; cell-free DNA; cfDNA;
   minimal residual disease; treatment response monitoring; EGFR
   rechallenge
ID EGFR MONOCLONAL-ANTIBODIES; PLUS CETUXIMAB TREATMENT; TUMOR DNA;
   ACQUIRED-RESISTANCE; RAS MUTATIONS; MICROSATELLITE INSTABILITY; GENOMIC
   LANDSCAPE; TARGETED THERAPY; LIQUID BIOPSIES; KRAS MUTATIONS
AB Patient-specific biomarkers form the foundation of precision medicine strategies. To realize the promise of precision medicine in patients with colorectal cancer (CRC), access to cost-effective, convenient, and safe assays is critical. Improvements in diagnostic technology have enabled ultrasensitive and specific assays to identify cell-free DNA (cfDNA) from a routine blood draw. Clinicians are already employing these minimally invasive assays to identify drivers of therapeutic resistance and measure genomic heterogeneity, particularly when tumor tissue is difficult to access or serial sampling is necessary. As cfDNA diagnostic technology continues to improve, more innovative applications are anticipated. In this review, we focus on four clinical applications for cfDNA analysis in the management of CRC: detecting minimal residual disease, monitoring treatment response in the metastatic setting, identifying drivers of treatment sensitivity and resistance, and guiding therapeutic strategies to overcome resistance.
C1 [Morris, Van K.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
   [Strickler, John H.] Duke Univ, Med Ctr, Div Med Oncol, Durham, NC 27710 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; Duke University
RP Strickler, JH (corresponding author), Duke Univ, Med Ctr, Div Med Oncol, Durham, NC 27710 USA.
EM john.strickler@duke.edu
RI Morris, Van/KIE-0809-2024
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NR 96
TC 10
Z9 11
U1 0
U2 14
PU ANNUAL REVIEWS
PI PALO ALTO
PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0897 USA
SN 0066-4219
EI 1545-326X
BN 978-0-8243-0572-7
J9 ANNU REV MED
JI Annu. Rev. Med.
PY 2021
VL 72
BP 399
EP 413
DI 10.1146/annurev-med-070119-120448
PG 15
WC Medicine, Research & Experimental
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA BQ7DY
UT WOS:000614647500025
PM 33502901
OA Bronze
DA 2025-01-04
ER

PT J
AU Kiyuna, T
   Murakami, T
   Tome, Y
   Igarashi, K
   Kawaguchi, K
   Miyake, K
   Miyake, M
   Li, Y
   Nelson, SD
   Dry, SM
   Singh, AS
   Russell, TA
   Singh, SR
   Kanaya, F
   Eilber, FC
   Hoffman, RM
AF Kiyuna, Tasuku
   Murakami, Takashi
   Tome, Yasunori
   Igarashi, Kentaro
   Kawaguchi, Kei
   Miyake, Kentaro
   Miyake, Masuyo
   Li, Yunfeng
   Nelson, Scott D.
   Dry, Sarah M.
   Singh, Arun S.
   Russell, Tara A.
   Singh, Shree Ram
   Kanaya, Fuminori
   Eilber, Fritz C.
   Hoffman, Robert M.
TI Doxorubicin-resistant pleomorphic liposarcoma with PDGFRA gene
   amplification is targeted and regressed by pazopanib in a
   patient-derived orthotopic xenograft mouse model
SO TISSUE & CELL
LA English
DT Article
DE Plemorphic liposarcoma; PDOX; Pazopanib; PDGFRA; Targeted therapy;
   Temozolomide
ID SOFT-TISSUE SARCOMA; SALMONELLA-TYPHIMURIUM A1-R; MULTIKINASE
   ANGIOGENESIS INHIBITOR; TYROSINE KINASE INHIBITOR; HUMAN COLON-CANCER;
   ANTI-CEA ANTIBODY; NUDE-MICE; EWINGS-SARCOMA; PHASE-II; PDOX
AB Pleomorphic liposarcoma (PLPS) is a heterogeneous resistant group of tumors. Complete surgical resection is the only known way to treat PLPS. PLPS is reristant to both radiation and chemotherapy. Therefore, precise individualized therapy is needed to improve outcome of advanced PLPS patients. In this study, a patient-derived orthotopic xenograft (PDOX) model of a PDGFRA-amplified PLPS was established in the biceps femoris of nude mice by surgical orthotopic implantation (SOI) in order to match the patient. The PLPS PDOX was treated with pazopanib (PAZ) which targets PDGFRA, as well as with temozolomide (TEM) and first-line therapy doxorubicin (DOX). The PLPS PDOX was resistant to DOX and responded very well to PAZ as well as TEM. The tumor volume on treatment day-14 relative to day-1 was as follows: DOX (4.50 +/- 2.6, p = 0.8087); PAZ (1.29 +/- 0.9, p = 0.0008 compared to the control, p = 0.0167 compared to DOX); TEM (1.07 +/- 0.8, p = 0.0079 compared to the control, p = 0.0079 compared to DOX). There was no significant difference in body weight between any treated group or control. The PAZ- and TEM-treated tumors showed extensive necrosis compared to the DOX-treated and untreated PDOX tumors. The present study showed that PDGFRA amplification could be effectively targeted by PAZ. The PLPS PDOX model also identified the efficacy of TEM which does not target PDGFRA, indicating that the PDOX model can identify effective targeted therapy as well as standard therapy and at the same time, identify ineffective drugs, even if they are first-line.
C1 [Kiyuna, Tasuku; Murakami, Takashi; Igarashi, Kentaro; Kawaguchi, Kei; Miyake, Kentaro; Miyake, Masuyo; Hoffman, Robert M.] AntiCancer Inc, San Diego, CA 92111 USA.
   [Kiyuna, Tasuku; Murakami, Takashi; Igarashi, Kentaro; Kawaguchi, Kei; Miyake, Kentaro; Miyake, Masuyo; Hoffman, Robert M.] Univ Calif San Diego, Dept Surg, San Diego, CA 92103 USA.
   [Kiyuna, Tasuku; Tome, Yasunori; Kanaya, Fuminori] Univ Ryukyus, Dept Orthoped Surg, Grad Sch Med, Nishihara, Okinawa, Japan.
   [Li, Yunfeng; Nelson, Scott D.; Dry, Sarah M.] Univ Calif Los Angeles, Dept Pathol, Los Angeles, CA 90024 USA.
   [Singh, Arun S.] Univ Calif Los Angeles, Div Hematol Oncol, Los Angeles, CA USA.
   [Russell, Tara A.; Eilber, Fritz C.] Univ Calif Los Angeles, Div Surg Oncol, Los Angeles, CA 90095 USA.
   [Singh, Shree Ram] NCI, Basic Res Lab, Frederick, MD 21701 USA.
C3 AntiCancer, Inc.; University of California System; University of
   California San Diego; University of the Ryukyus; 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; National
   Institutes of Health (NIH) - USA; NIH National Cancer Institute (NCI)
RP Hoffman, RM (corresponding author), AntiCancer Inc, San Diego, CA 92111 USA.; Eilber, FC (corresponding author), Univ Calif Los Angeles, Div Surg Oncol, Los Angeles, CA 90095 USA.; Singh, SR (corresponding author), NCI, Basic Res Lab, Frederick, MD 21701 USA.
EM singhshr@mail.nih.gov; fceilber@mednet.ucla.edu; all@anticancer.com
RI TOME, YASUNORI/K-4319-2019; Miyake, Kentaro/A-2996-2019; Singh,
   Akanksha/AAF-6177-2021; Singh, Shree Ram/B-7614-2008
OI Singh, Shree Ram/0000-0001-6545-583X; Igarashi,
   Kentaro/0000-0003-2278-1736; Murakami, Takashi/0000-0002-9429-5705;
   TOME, YASUNORI/0000-0002-3716-1866
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NR 66
TC 16
Z9 16
U1 0
U2 5
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
   LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0040-8166
J9 TISSUE CELL
JI Tissue Cell
PD AUG
PY 2018
VL 53
BP 30
EP 36
DI 10.1016/j.tice.2018.05.010
PG 7
WC Anatomy & Morphology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anatomy & Morphology; Cell Biology
GA GO6QL
UT WOS:000440173900005
PM 30060824
DA 2025-01-04
ER

PT J
AU Bergsland, EK
AF Bergsland, Emily K.
TI Is More Not Better? Combination Therapies in Colorectal Cancer Treatment
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Combination chemotherapy; Adjuvant therapy; Targeted therapy; First-line
   therapy; Metastatic colorectal cancer; Systemic therapy; Optimal
   sequence
ID PHASE-III TRIAL; ADVANCED RECTAL-CANCER; FLUOROURACIL PLUS LEUCOVORIN;
   OXALIPLATIN-BASED CHEMOTHERAPY; RANDOMIZED CONTROLLED-TRIAL; HIGH-DOSE
   LEUCOVORIN; 1ST-LINE TREATMENT; COLON-CANCER; ADJUVANT TREATMENT;
   STAGE-II
AB The treatment of colorectal cancer has evolved dramatically in recent years with the availability of new chemotherapeutic agents and inhibitors of the vascular endothelial growth factor- and epidermal growth factor-signaling pathways. The incremental benefit of each individual line of therapy for advanced disease is relatively small. Advances in our ability to select patients should improve the cost-effectiveness of our treatment strategies (avoiding unnecessary toxicity in the patients who are unlikely to benefit and accepting the potential for adverse events in the patients who stand to benefit the most from a given regimen).
C1 UCSF Helen Diller Family Comprehens Canc Ctr, Div Hematol & Oncol, Dept Med, San Francisco, CA 94115 USA.
C3 University of California System; University of California San Francisco;
   UCSF Medical Center; UCSF Helen Diller Family Comprehensive Cancer
   Center
RP Bergsland, EK (corresponding author), UCSF Helen Diller Family Comprehens Canc Ctr, Div Hematol & Oncol, Dept Med, 1600 Divisadro St,A727, San Francisco, CA 94115 USA.
EM emilyb@medicine.ucsf.edu
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NR 126
TC 3
Z9 3
U1 0
U2 12
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8588
EI 1558-1977
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD FEB
PY 2015
VL 29
IS 1
BP 85
EP 116
DI 10.1016/j.hoc.2014.09.002
PG 32
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA AX5FD
UT WOS:000346951300006
PM 25475574
DA 2025-01-04
ER

PT J
AU Jeon, H
   Sterpi, M
   Mo, CSA
   Bteich, F
AF Jeon, Hyein
   Sterpi, Michelle
   Mo, Christiana
   Bteich, Fernand
TI Claudins: from gatekeepers of epithelial integrity to potential targets
   in hepato-pancreato-biliary cancers
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE claudins; hepatocellular carcinoma; gallbladder cancer; bile duct
   cancer; pancreatic cancer; cancer therapeutics; targeted therapy
ID HEPATOCELLULAR-CARCINOMA; MESENCHYMAL TRANSITION; CELL-PROLIFERATION;
   COLORECTAL-CANCER; EXPRESSION; INVASION; ANTIBODY; TROGLITAZONE;
   INHIBITION; MARKER
AB Claudins, a family of tetraspan transmembrane proteins, are critical to the integrity of tight junctions in epithelia and endothelia, influencing cellular processes such as development, differentiation, and apoptosis. Abnormal claudin expression is associated with various malignancies, particularly affecting tissue architecture and potentially facilitating tumor invasion and metastasis. In this comprehensive review, we explore the multifaceted functions of claudins: their expression, specific roles in cancer with a focus on hepato-pancreato-biliary malignancies and highlight their potential as therapeutic targets. We discuss current claudin-targeted therapies, including monoclonal antibodies, antibody-drug conjugates, bispecific T-cell engager and chimeric antigen receptor T-cell therapies. These approaches show promise in pre-clinical and clinical studies, particularly in hepato-pancreato-biliary cancers with large unmet needs. Despite these early signs of efficacy, challenges remain in effectively targeting these proteins due to their structural resemblance and overlapping functions.
C1 [Jeon, Hyein; Sterpi, Michelle; Mo, Christiana; Bteich, Fernand] Albert Einstein Coll Med, Dept Med Oncol, Bronx, NY 10461 USA.
   [Jeon, Hyein; Sterpi, Michelle; Mo, Christiana; Bteich, Fernand] Montefiore Med Ctr, Dept Med Oncol, Bronx, NY 10461 USA.
C3 Montefiore Medical Center; Albert Einstein College of Medicine; Yeshiva
   University; Montefiore Medical Center; Albert Einstein College of
   Medicine
RP Bteich, F (corresponding author), Albert Einstein Coll Med, Dept Med Oncol, Bronx, NY 10461 USA.; Bteich, F (corresponding author), Montefiore Med Ctr, Dept Med Oncol, Bronx, NY 10461 USA.
EM fbteich@montefiore.org
OI Jeon, Hyein/0000-0002-5221-2844
FX The author(s) declare that no financial support was received for the
   research, authorship, and/or publication of this article.
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NR 146
TC 0
Z9 0
U1 0
U2 0
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD SEP 26
PY 2024
VL 14
AR 1454882
DI 10.3389/fonc.2024.1454882
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA I2Z5B
UT WOS:001328989900001
PM 39391254
OA gold
DA 2025-01-04
ER

PT J
AU Shan, KS
   Rehman, TU
   Ivanov, S
   Domingo, G
   Raez, LE
AF Shan, Khine S.
   Rehman, Tauseef U.
   Ivanov, Stan
   Domingo, Gelenis
   Raez, Luis E.
TI Molecular Targeting of the BRAF Proto-Oncogene/Mitogen-Activated Protein
   Kinase (MAPK) Pathway across Cancers
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE BRAF; MEK; ERK; MAPK; molecular profiling; targeted therapy; tumor
   agnostic; personalized medicine
ID DABRAFENIB PLUS TRAMETINIB; LANGERHANS CELL HISTIOCYTOSIS; OPEN-LABEL;
   SINGLE-ARM; METASTATIC MELANOMA; RADIOACTIVE IODINE; IMPROVED SURVIVAL;
   MEK INHIBITION; DOUBLE-BLIND; LUNG-CANCER
AB The mitogen-activated protein kinase (MAPK) pathway is essential for cellular proliferation, growth, and survival. Constitutive activation of this pathway by BRAF mutations can cause downstream activation of kinases, leading to uncontrolled cellular growth and carcinogenesis. Therefore, inhibition of BRAF and the downstream substrate MEK has been shown to be effective in controlling tumor growth and proliferation. Over the last decade, several BRAF and MEK inhibitors have been investigated, ranging from primarily melanoma to various cancer types with BRAF alterations. This subsequently led to several Food and Drug Administration (FDA) approvals for BRAF/MEK inhibitors for melanoma, non-small cell lung cancer, anaplastic thyroid cancer, colorectal cancer, histiocytosis neoplasms, and finally, tumor-agnostic indications. Here, this comprehensive review will cover the developments of BRAF and MEK inhibitors from melanomas to tumor-agnostic indications, novel drugs, challenges, future directions, and the importance of those drugs in personalized medicine.
C1 [Shan, Khine S.; Rehman, Tauseef U.; Ivanov, Stan; Domingo, Gelenis] Mem Canc Inst, Div Hematol Oncol, Pembroke Pines, FL 33028 USA.
   [Raez, Luis E.] Thorac Oncol Program, Mem Hlth Care, Pembroke Pines, FL 33328 USA.
RP Shan, KS (corresponding author), Mem Canc Inst, Div Hematol Oncol, Pembroke Pines, FL 33028 USA.
EM kshan@mhs.net; trehman@mhs.net; sianov@mhs.net; gdomingo@mhs.net;
   lraez@mhs.net
RI Raez, Luis/AAL-8829-2020
OI Shan, Khine/0000-0001-8035-0024; raez, luis/0000-0003-2669-5771
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NR 123
TC 6
Z9 6
U1 2
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JAN
PY 2024
VL 25
IS 1
AR 624
DI 10.3390/ijms25010624
PG 25
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA ER3A0
UT WOS:001140598500001
PM 38203795
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zheng, HL
   Wang, Y
   Tang, CN
   Jones, L
   Ye, H
   Zhang, GC
   Cao, WH
   Li, JW
   Liu, LF
   Liu, ZC
   Zhang, C
   Lou, F
   Liu, ZY
   Li, YY
   Shi, ZF
   Zhang, JB
   Zhang, DD
   Sun, H
   Dong, HC
   Dong, ZS
   Guo, BS
   Yan, H
   Lu, QY
   Huang, X
   Chen, SY
AF Zheng, Huili
   Wang, Yan
   Tang, Chuanning
   Jones, Lindsey
   Ye, Hua
   Zhang, Guangchun
   Cao, Weihai
   Li, Jingwen
   Liu, Lifeng
   Liu, Zhencong
   Zhang, Chao
   Lou, Feng
   Liu, Zhiyuan
   Li, Yangyang
   Shi, Zhenfen
   Zhang, Jingbo
   Zhang, Dandan
   Sun, Hong
   Dong, Haichao
   Dong, Zhishou
   Guo, Baishuai
   Yan, He
   Lu, Qingyu
   Huang, Xue
   Chen, Si-Yi
TI <i>TP53</i>, <i>PIK3CA</i>, <i>FBXW7</i> and <i>KRAS</i> Mutations in
   Esophageal Cancer Identified by Targeted Sequencing
SO CANCER GENOMICS & PROTEOMICS
LA English
DT Article
DE Esophageal cancer; next-generation sequencing; Ion PGM; genetic
   mutations; targeted therapy; personalized medicine
ID SQUAMOUS-CELL CARCINOMA; METASTATIC COLORECTAL-CANCER; ZINC-BINDING
   DOMAINS; TUMOR-SUPPRESSOR; UBIQUITIN LIGASE; POOR SURVIVAL; P53 PROTEIN;
   PROGNOSIS; THERAPY; ADENOCARCINOMA
AB Background/Aim: Esophageal cancer (EC) is a common malignancy with significant morbidity and mortality. As individual cancers exhibit unique mutation patterns, identifying and characterizing gene mutations in EC that may serve as biomarkers might help predict patient outcome and guide treatment. Traditionally, personalized cancer DNA sequencing was impractical and expensive. Recent technological advancements have made targeted DNA sequencing more cost-and time-effective with reliable results. This technology may be useful for clinicians to direct patient treatment. Materials and Methods: The Ion PGM and AmpliSeq Cancer Panel was used to identify mutations at 737 hotspot loci of 45 cancer-related genes in 64 EC samples from Chinese patients. Results: Frequent mutations were found in TP53 and less frequent mutations in PIK3CA, FBXW7 and KRAS. Conclusion: These results demonstrate that targeted sequencing can reliably identify mutations in individual tumors that make this technology a possibility for clinical use.
C1 [Zheng, Huili; Wang, Yan; Cao, Weihai; Li, Jingwen; Liu, Lifeng; Liu, Zhencong; Zhang, Chao] First Hosp Qiqihar, Qiqihar 161005, Peoples R China.
   [Tang, Chuanning; Ye, Hua; Zhang, Guangchun; Lou, Feng; Liu, Zhiyuan; Li, Yangyang; Shi, Zhenfen; Zhang, Jingbo; Zhang, Dandan; Sun, Hong; Dong, Haichao; Dong, Zhishou; Guo, Baishuai; Yan, He; Lu, Qingyu] San Valley Biotechnol Inc, Beijing, Peoples R China.
   [Jones, Lindsey; Huang, Xue; Chen, Si-Yi] Univ So Calif, Keck Sch Med, Kenneth Norris Jr Comprehens Canc Ctr, Dept Mol Microbiol & Immunol, Los Angeles, CA 90033 USA.
C3 University of Southern California
RP Wang, Y (corresponding author), First Hosp Qiqihar, Qiqihar 161005, Peoples R China.; Chen, SY (corresponding author), Univ So Calif, Keck Sch Med, Kenneth Norris Jr Comprehens Canc Ctr, Dept Mol Microbiol & Immunol, Los Angeles, CA 90033 USA.
EM wy2459691@163.com; siyichen@usc.edu
RI chen, siyi/KXR-2904-2024; zhang, dan-dan/AAR-5085-2020; Li,
   Yuechong/HJY-7807-2023; Li, Yuting/IVH-4108-2023; Zhang,
   Guangchun/LNQ-3061-2024
FU Wu Jieping Medical Foundation; National Institutes of Health [R01
   CA90427, R01 AI084811]
FX The Authors would like to thank Rong Shi at the Wu Jieping Foundation,
   Haibo Wang, Ying Li and other members of San Valley Biotechnology Inc.
   Beijing, for their assistance in sample and data collection. We would
   also like to thank the staff at the First Hospital of Qiqihar and
   Beijing Military Hospital for their generous support for DNA sequencing
   and data collection. This research was supported by an institutional
   grant and grants from the Wu Jieping Medical Foundation and the National
   Institutes of Health (R01 CA90427 & R01 AI084811 to SYC).
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U1 0
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PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
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EI 1790-6245
J9 CANCER GENOM PROTEOM
JI Cancer Genomics Proteomics
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VL 13
IS 3
BP 231
EP 238
PG 8
WC Oncology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Genetics & Heredity
GA DL0NI
UT WOS:000375329300006
PM 27107065
DA 2025-01-04
ER

PT J
AU Morse, MA
AF Morse, Michael A.
TI The Outlook for Immune Checkpoint Targeting Strategies in Colorectal
   Cancer
SO CURRENT COLORECTAL CANCER REPORTS
LA English
DT Article
DE Colorectal cancer; Immune checkpoint; CTLA-4; PD-1; PD-L1; mCRC;
   Immunomodulation; Vaccine; Colon cancer; Ipilimumab; Tremelimumab;
   Nivolumab; Pembrolizumab
ID TUMOR-INFILTRATING LYMPHOCYTES; SYSTEM INHIBITORY CHECKPOINTS; ANTITUMOR
   IMMUNITY; MICROSATELLITE INSTABILITY; FUSOBACTERIUM-NUCLEATUM; CTLA-4
   BLOCKADE; T-LYMPHOCYTES; COLON-CANCER; CELLS; ANTIBODY
AB Encouraging clinical activity for checkpoint blockade in melanoma, lung cancer, and a growing list of other malignancies has supported enthusiasm for testing this strategy in colorectal cancer. Although frequent observations of T cell infiltration into colorectal cancer and a well-established list of target antigens suggest colorectal cancer should be amenable to this approach, there was limited clinical evidence until recent demonstration of substantial activity for anti-PD1 antibody therapy in microsatellite instability high colorectal cancers. Addition of other therapeutic modalities such as targeted therapy, other checkpoint molecules, or other immunotherapies to anti-PD-1 antibodies is currently under evaluation with the hope that it will expand the possible spectrum of colorectal cancers treatable with checkpoint blockade.
C1 [Morse, Michael A.] Duke Univ, Med Ctr, Dept Med, Div Med Oncol, Box 3233, Durham, NC 27710 USA.
C3 Duke University
RP Morse, MA (corresponding author), Duke Univ, Med Ctr, Dept Med, Div Med Oncol, Box 3233, Durham, NC 27710 USA.
EM michael.morse@duke.edu
CR [Anonymous], J CLIN ONCOL
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NR 51
TC 0
Z9 0
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1556-3790
EI 1556-3804
J9 CURR COLORECT CANC R
JI Curr. Colorectal Cancer Rep.
PD FEB
PY 2016
VL 12
IS 1
BP 51
EP 56
DI 10.1007/s11888-016-0309-6
PG 6
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA DV1HR
UT WOS:000382672300007
DA 2025-01-04
ER

PT J
AU Li, WL
   Lee, MR
   Cho, MY
AF Li, Wan Lu
   Lee, Mi-Ra
   Cho, Mee-Yon
TI The small molecule survivin inhibitor YM155 may be an effective
   treatment modality for colon cancer through increasing apoptosis
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Colon cancer; Apoptosis; CD133 protein; Survivin; YM155
ID ENDOTHELIAL GROWTH-FACTOR; COLORECTAL-CANCER; STEM-CELLS; EXPRESSION;
   PROTEIN; CHEMORESISTANCE; TARGET; SERUM
AB Survivin has a known beneficial role in the survival of both cancer cells and normal cells. Therapies targeting survivin have been proposed as an alternative treatment modality for various tumors; however, finding the proper indication for this toxic therapy is critical for reducing unavoidable side effects. We recently observed that high survivin expression in CD133(+) cells is related to chemoresistance in Caco-2 colon cancer cells. However, the effect of survivin-targeted therapy on CD133(+) colon cancer is unknown. In this study, we investigated the roles of CD133 and survivin expression in colon cancer biology in vitro and comparatively analyzed the anticancer effects of survivin inhibitor on CD133(+) cells (ctrl-siRNA group) and small interfering RNA (siRNA)-induced CD133(-) cells (CD133-siRNA group) obtained from a single colon cancer cell line. CD133 knockdown via siRNA transfection did not change the tumorigenicity of cells, although in vitro survivin expression levels in CD133(+) cells were higher than those in siRNA-induced CD133(-) cells. The transfection procedure seemed to induce survivin expression. Notably, a significant number of CD133(-) cells (33.8%) was found in the cell colonies of the CD133-siRNA group. In the cell proliferation assay after treatment, YM155 and a combination of YM155 and 5-fluorouracil (5-FU) proved to be far more effective than 5-FU alone. A significantly increased level of apoptosis was observed with increasing doses of YM155 in all groups. However, significant differences in therapeutic effect and apoptosis among the mock, ctrl-siRNA, and CD133-siRNA groups were not detected. Survivin inhibitor is an effective treatment modality for colon cancer; however, the role of CD133 and the use of survivin expression as a biomarker for this targeted therapy must be verified. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Li, Wan Lu; Lee, Mi-Ra; Cho, Mee-Yon] Yonsei Univ, Wonju Coll Med, Dept Pathol, 20 Ilsan Ro, Wonju 220701, Gangwon Do, South Korea.
   [Cho, Mee-Yon] Yonsei Univ, Wonju Coll Med, Inst Genom Cohort, Wonju 220701, Gangwon Do, South Korea.
C3 Yonsei University; Yonsei University
RP Cho, MY (corresponding author), Yonsei Univ, Wonju Coll Med, Dept Pathol, 20 Ilsan Ro, Wonju 220701, Gangwon Do, South Korea.
EM lvvlchina@msn.cn; mira1125@yonsei.ac.kr; meeyon@yonsei.ac.kr
RI Li, Wanlu/AAO-5769-2021
OI Cho, Mee Yon/0000-0002-7955-4211
FU Korea Science and Engineering Foundation (KOSEF) - Korean government
   (Ministry of Education, Science and Technology [2014-51-0390]
FX This study was supported by a research grant from the Korea Science and
   Engineering Foundation (KOSEF) funded by the Korean government (Ministry
   of Education, Science and Technology; grant code: 2014-51-0390).
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NR 33
TC 17
Z9 17
U1 0
U2 19
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 MAR 4
PY 2016
VL 471
IS 2
BP 309
EP 314
DI 10.1016/j.bbrc.2016.02.009
PG 6
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA DG4MG
UT WOS:000372045700007
PM 26855135
DA 2025-01-04
ER

PT J
AU Ang, C
   Stollman, A
   Zhu, HF
   Sarpel, U
   Scarborough, B
   Sahni, G
   Millis, SZ
AF Ang, Celina
   Stollman, Aryeh
   Zhu, Hongfa
   Sarpel, Umut
   Scarborough, Bethann
   Sahni, Gagan
   Millis, Sherri Z.
TI Clinical Benefit from Trametinib in a Patient with Appendiceal
   Adenocarcinoma with a <i>GNAS R201H</i> Mutation
SO CASE REPORTS IN ONCOLOGY
LA English
DT Article
DE Appendiceal adenocarcinoma; Targeted therapy; GNAS mutation; Trametinib
ID MUCINOUS NEOPLASMS; LOW-GRADE; PSEUDOMYXOMA PERITONEI;
   COLORECTAL-CANCER; MEK INHIBITOR; GNAS; TUMORS; CARCINOMATOSIS;
   MELANOMA; SURVIVAL
AB We report the case of a patient with appendiceal adenocarcinoma with mucinous peritoneal carcinomatosis who was treated with trametinib upon identification of a GNAS R201H mutation by comprehensive genomic profiling. The molecular pathology of appendiceal neoplasms is reviewed, and the mechanistic basis underlying the clinical benefit as well as the subsequent course on trametinib that were observed in this patient are discussed. (C) 2017 The Author(s) Published by S. Karger AG, Basel
C1 [Ang, Celina] Icahn Sch Med Mt Sinai, Div Hematol Oncol, New York, NY 10029 USA.
   [Stollman, Aryeh] Icahn Sch Med Mt Sinai, Dept Radiol, New York, NY 10029 USA.
   [Zhu, Hongfa] Icahn Sch Med Mt Sinai, Dept Anat Pathol, New York, NY 10029 USA.
   [Sarpel, Umut] Icahn Sch Med Mt Sinai, Div Surg Oncol, Dept Surg, New York, NY 10029 USA.
   [Scarborough, Bethann] Icahn Sch Med Mt Sinai, Brookdale Dept Geriatr & Palliat Med, New York, NY 10029 USA.
   [Sahni, Gagan] Icahn Sch Med Mt Sinai, Div Cardiol, New York, NY 10029 USA.
   [Millis, Sherri Z.] Fdn Med Inc, Cambridge, MA USA.
C3 Icahn School of Medicine at Mount Sinai; Icahn School of Medicine at
   Mount Sinai; Icahn School of Medicine at Mount Sinai; Icahn School of
   Medicine at Mount Sinai; Icahn School of Medicine at Mount Sinai; Icahn
   School of Medicine at Mount Sinai; Foundation Medicine
RP Ang, C (corresponding author), Icahn Sch Med Mt Sinai, Div Hematol Oncol, Med, One Gustave L Levy Pl,Box 1079, New York, NY 10029 USA.
EM celina.ang@mssm.edu
RI Sarpel, Umut/KBA-0247-2024
OI SAHNI, GAGAN/0000-0002-3503-6041; Sarpel, Umut/0000-0002-4346-3641
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NR 17
TC 10
Z9 12
U1 0
U2 2
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1662-6575
J9 CASE REP ONCOL
JI Case Rep. Oncol.
PY 2017
VL 10
IS 2
BP 548
EP 552
DI 10.1159/000477562
PG 5
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA FG3NG
UT WOS:000410072000025
PM 28868010
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Adamiec-Organisciok, M
   Wegrzyn, M
   Cienciala, L
   Magate, N
   Skonieczna, M
   Nackiewicz, J
AF Adamiec-Organisciok, Malgorzata
   Wegrzyn, Magdalena
   Cienciala, Lukasz
   Magate, Ngoni
   Skonieczna, Magdalena
   Nackiewicz, Joanna
TI Resistance to death pathway induction as a potential targeted therapy in
   CRISPR/Cas-9 knock-out colorectal cancer cell lines
SO GASTROENTEROLOGY REVIEW-PRZEGLAD GASTROENTEROLOGICZNY
LA English
DT Review
DE regulated cell death; ferroptosis; glutathione peroxidase GPX4;
   antioxidant defence mechanisms; CRISPR/Cas-9 genome editing
ID MECHANISMS
AB Regulated cell death is a fundamental biological process that plays a crucial role in maintaining tissue homeostasis and eliminating damaged or unnecessary cells. Ferroptosis is an iron -dependent process, characterized by the accumulation of oxidized and damaged lipids, which leads to programmed cell death. Among the ferroptotic pathway genes regulating this process, GPX4, TFRC, ACSL4, FSP1, SLC7A11, and PROM2 could be considered. There are many well-known ferroptotic pathway regulators, which are discussed in this compact review. Cells with tissues of different origin display sensitive or resistant phenotypes to such regulators. In some cases, unexpected changes during cell treatment occurred, suggesting the possibility of regulating the death pathway. We assumed that possible changing of ferro-sensitivity to ferro-resistance in cells, especially in colorectal cancer cell lines, is responded for induced chemoresistance. Using novel techniques, such as CRISPR/Cas-9 genome editing, an induced phenotype "switching" is possible.
C1 [Adamiec-Organisciok, Malgorzata; Wegrzyn, Magdalena; Cienciala, Lukasz; Magate, Ngoni; Skonieczna, Magdalena] Silesian Tech Univ, Fac Automat Control Elect & Comp Sci, Dept Syst Engn & Biol, 16 Akad St, PL-44100 Gliwice, Poland.
   [Nackiewicz, Joanna] Univ Opole, Fac Chem, Opole, Poland.
C3 Silesian University of Technology; University of Opole
RP Skonieczna, M (corresponding author), Silesian Tech Univ, Fac Automat Control Elect & Comp Sci, Dept Syst Engn & Biol, 16 Akad St, PL-44100 Gliwice, Poland.
EM magdalena.skonieczna@polsl.pl
RI Skonieczna, Magdalena/IAO-0379-2023; Adamiec-Organiściok,
   Małgorzata/AAO-5063-2020
OI Cienciala, Lukasz/0009-0008-1413-0988; Nackiewicz,
   Joanna/0000-0002-3424-1908; Adamiec-Organisciok,
   Malgorzata/0000-0003-2403-0485
FU Silesian University of Technology [02/040/BK_23/1035,
   02/040/BKM23/1041]; European Union from the European Social Fund
   [POWR.03.05.00-00-Z098/17]
FX This work was supported by Silesian University of Technology grant's No
   02/040/BK_23/1035 (M.S.) , 02/040/BKM23/1041 (M.A.O.) . Students (M.W.;
   L.C. and N.M.) . were financed in scope of 9 th funding competition for
   Project -Based Learning - PBL (The Excellence Initiative - Research
   University program) , in accordance with Regulation No. 54/2020 of the
   Rector of the Silesian University of Technology dated March 13, 2020,
   and research subsidy for students from the European Union from the
   European Social Fund in the framework of the project "Silesian
   University of Technology as a Centre of Modern Education based on
   research and innovation" POWR.03.05.00-00-Z098/17.
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NR 30
TC 2
Z9 2
U1 4
U2 4
PU TERMEDIA PUBLISHING HOUSE LTD
PI POZNAN
PA KLEEBERGA 2, POZNAN, 61-615, POLAND
SN 1895-5770
EI 1897-4317
J9 GASTROENTEROL REV
JI Gastroenterol. Rev.
PY 2024
VL 19
IS 2
BP 112
EP 120
DI 10.5114/pg.2024.134872
PG 9
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA TQ0R7
UT WOS:001242612700002
PM 38939059
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhou, HB
   Yang, L
   Liu, SF
   Xu, XH
   Chen, Z
   Li, YX
   Yuan, JH
   Wei, YC
AF Zhou, Hai-Bo
   Yang, Li
   Liu, Shi-Fang
   Xu, Xin-Hua
   Chen, Zhuo
   LI, Yun-Xiao
   Yuan, Jin-Hua
   Wei, Yong-Chang
TI CDC Like Kinase 2 plays an oncogenic role in colorectal cancer via
   modulating the Wnt/β-catenin signaling
SO NEOPLASMA
LA English
DT Article
DE CLK2; Wnt; beta-catenin; prognosis; colorectal cancer
ID BETA-CATENIN; CLK2; EXPRESSION; INHIBITOR; PROTEINS
AB Colorectal cancer (CRC) is a common malignant tumor with high morbidity and mortality, and significant heterogeneity among patients. In this study, we aimed to explore the role and mechanism of CLK2 in CRC, a kinase that phosphorylates SR proteins involved in splicing. Based on the analysis from The Cancer Genome Atlas (TCGA) dataset and tissue microarray, we found that CLK2 was upregulated in CRC tissues and associated with a higher tumor stage and poorer overall survival. Consistent with the bioinformatics analysis, the functional experiments validated that CLK2 acted as a tumor-promoting factor in CRC progression. CLK2 knockdown suppressed aggressive cell proliferation, migration, and invasion in vitro, as well as restrained tumor growth in vivo. In terms of mechanism, we found that the Wnt/beta-catenin signaling pathway was responsible for the CLK2-induced CRC progression, based on the results of pathway enrichment analysis and subsequent experimental validation. Thus, our study, for the first time, identified the role of CLK2 in CRC development and provided a compelling biomarker for targeted therapy in CRC treatment.
C1 [Zhou, Hai-Bo; Wei, Yong-Chang] Wuhan Univ, Zhongnan Hosp, Dept Radiat & Med Oncol, Wuhan, Peoples R China.
   [Zhou, Hai-Bo; Liu, Shi-Fang; Xu, Xin-Hua; Chen, Zhuo; LI, Yun-Xiao; Yuan, Jin-Hua] China Three Gorges Univ, Yichang Cent Peoples Hosp, Dept Oncol, Yichang, Peoples R China.
   [Yang, Li] China Three Gorges Univ, Yichang Cent Peoples Hosp, Dept Thyroid & Breast, Yichang, Peoples R China.
C3 Wuhan University; China Three Gorges University; China Three Gorges
   University
RP Wei, YC (corresponding author), Wuhan Univ, Zhongnan Hosp, Dept Radiat & Med Oncol, Wuhan, Peoples R China.; Yuan, JH (corresponding author), China Three Gorges Univ, Yichang Cent Peoples Hosp, Dept Oncol, Yichang, Peoples R China.
EM xhua1129@126.com; weiyongchang@whu.edu.cn
RI Zhou, Haibo/ABE-8194-2020
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NR 32
TC 8
Z9 8
U1 0
U2 10
PU AEPRESS SRO
PI BRATISLAVA
PA BAJZOVA 7, BRATISLAVA, 821 08, SLOVAKIA
SN 0028-2685
EI 1338-4317
J9 NEOPLASMA
JI Neoplasma
PY 2022
VL 69
IS 3
BP 657
EP +
DI 10.4149/neo_2022_220206N138
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2Z1EC
UT WOS:000826327800007
PM 35293765
OA Bronze
DA 2025-01-04
ER

PT J
AU Giopanou, I
   Pintzas, A
AF Giopanou, Ioanna
   Pintzas, Alexandros
TI RAS and BRAF in the foreground for non-small cell lung cancer and
   colorectal cancer: Similarities and main differences for prognosis and
   therapies
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE RAS; BRAF; Lung cancer; Colorectal cancer; Inhibitors; Therapy
ID SELUMETINIB PLUS DOCETAXEL; GROWTH-FACTOR RECEPTOR; ORAL MEK INHIBITOR;
   KRAS MUTATIONS; PHASE-II; 1ST-LINE TREATMENT; OPEN-LABEL;
   ANTITUMOR-ACTIVITY; TARGETED THERAPY; COLON CANCERS
AB Lung and colorectal cancer are included in the most tremendously threatening diseases in terms of incidence and death. Although they are located in completely different organs and differ in various characteristics they do share some common features, especially regarding their molecular mutational profile. Among several commonly mutated genes KRAS and BRAF are spotted to be highly associated with patient's poor disease outcome and resistance to targeted therapies mostly in liaison with other mutant activated genes. Many studies have shed light in these mechanisms for disease progression and numerous preclinical models, clinical trials and meta-analysis reports investigate the impact of specific treatments or combination of therapies. The present review is an effort to compare the mutational imprint of these genes between the two diseases and their impact in prognosis, current therapy, mechanisms of therapy resistance and future therapeutic plans and provide a spherical perspective regarding the systemic molecular profile of cancer.
C1 [Giopanou, Ioanna; Pintzas, Alexandros] Natl Hellen Res Fdn, Inst Chem Biol, Athens 11635, Greece.
C3 National Hellenic Research Foundation
RP Giopanou, I; Pintzas, A (corresponding author), Natl Hellen Res Fdn, Inst Chem Biol, Athens 11635, Greece.
EM giopanou@eie.gr; apint@eie.gr
OI Giopanou, Ioanna/0000-0003-4393-7517
FU General Secretariat of Research and Technology, through an action for
   the "Hellenic Network on Precision Medicine in Oncology"
FX This work was supported by the General Secretariat of Research and
   Technology, through an action for the "Hellenic Network on Precision
   Medicine in Oncology".
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NR 110
TC 10
Z9 12
U1 1
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD FEB
PY 2020
VL 146
AR 102859
DI 10.1016/j.critrevonc.2019.102859
PG 9
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA KW4ET
UT WOS:000521119200006
PM 31927392
DA 2025-01-04
ER

PT J
AU Shen, ZL
   Wang, B
   Luo, JY
   Jiang, KW
   Zhang, H
   Mustonen, H
   Puolakkainen, P
   Zhu, J
   Ye, YJ
   Wang, S
AF Shen, Zhanlong
   Wang, Bo
   Luo, Jianyuan
   Jiang, Kewei
   Zhang, Hui
   Mustonen, Harri
   Puolakkainen, Pauli
   Zhu, Jun
   Ye, Yingjiang
   Wang, Shan
TI Global-scale profiling of differential expressed lysine acetylated
   proteins in colorectal cancer tumors and paired liver metastases
SO JOURNAL OF PROTEOMICS
LA English
DT Article
DE Lysine acetylation; PTMs; Colorectal cancer; Liver metastasis
ID HISTONE DEACETYLASES; COLON-CANCER; E-CADHERIN; BEVACIZUMAB; CELLS;
   COMPLEXES; PANITUMUMAB; ACTIVATION; PROTEOMICS; THERAPIES
AB Lysine acetylated modification was indicated to impact colorectal cancer (CRC)'s distant metastasis. However, the global acetylated proteins in CRC and the differential expressed acetylated proteins and acetylated sites between CRC primary and distant metastatic tumor remains unclear. Our aim was to construct a complete atlas of acetylome in CRC and paired liver metastases. Combining high affinity enrichment of acetylated peptides with high sensitive mass spectrometry, we identified 603 acetylation sites from 316 proteins, among which 462 acetylation sites corresponding to 243 proteins were quantified. We further classified them into groups according to cell component, molecular function and biological process and analyzed the metabolic pathways, domain structures and protein interaction networks. Finally, we evaluated the differentially expressed lysine acetylation sites and revealed that 31 acetylated sites of 22 proteins were downregulated in CRC liver metastases compared to that in primary CRC while 40 acetylated sites of 32 proteins were upregulated, of which HIST2H3AK19Ac and H2BLK121Ac were the acetylated histones most changed, while TPM2 K152Ac and ADH1B K331Ac were the acetylated non-histones most altered. These results provide an expanded understanding of acetylome in CRC and its distant metastasis, and might prove applicable in the molecular targeted therapy of metastatic CRC.
   Biological significance: This study described provides, for the first time, that full-scale profiling of lysine acetylated proteins were identified and quantified in colorectal cancer (CRC) and paired liver metastases. The novelty of the study is that we constructed a complete atlas of acetylome in CRC and paired liver metastases. Moreover, we analyzed these differentially expressed acetylated proteins in cell component, molecular function and biological process. In addition, metabolic pathways, domain structures and protein interaction networks of acetylated proteins were also investigated. Our approaches shows that of the differentially expressed proteins, HIST2H3AK19Ac and H2BLK121Ac were the acetylated histones most changed, while TPM2 K152Ac and ADH1B K331Ac were the acetylated non-histones most altered. Our findings provide an expanded understanding of acetylome in CRC and its distant metastasis, and might prove applicable in the molecular targeted therapy of metastatic CRC. (C) 2016 Elsevier B.V. All rights reserved.
C1 [Shen, Zhanlong; Wang, Bo; Jiang, Kewei; Zhang, Hui; Ye, Yingjiang; Wang, Shan] Peking Univ, Dept Surg Gastroenterol, Peoples Hosp, Beijing 100044, Peoples R China.
   [Luo, Jianyuan] Peking Univ, Dept Med Genet, Hlth Sci Ctr, Beijing 100191, Peoples R China.
   [Mustonen, Harri; Puolakkainen, Pauli] Univ Helsinki, Dept Surg, Cent Hosp, Helsinki 00290, Finland.
   [Mustonen, Harri; Puolakkainen, Pauli] Univ Helsinki, Helsinki 00290, Finland.
   [Zhu, Jun] Jingjie PEW Biolab Hangzhou Co Ltd, Hangzhou 310018, Zhejiang, Peoples R China.
C3 Peking University; Peking University; University of Helsinki; Helsinki
   University Central Hospital; University of Helsinki
RP Ye, YJ; Wang, S (corresponding author), Peking Univ, Dept Surg Gastroenterol, Peoples Hosp, Beijing 100044, Peoples R China.
EM yeyingjiang@pkuph.edu.cn; shanwang60@sina.com
RI Wang, Jianye/KFA-4087-2024; Luo, Jianyuan/ABI-7585-2020
OI Mustonen, Harri Kalevi/0000-0001-5632-6796
FU National Natural Science Foundation of China [81372290, 81372291];
   Peking University People's Hospital Funds (RDB)
FX This study was supported by grants from the National Natural Science
   Foundation of China (81372290, 81372291) and the Peking University
   People's Hospital Funds (RDB 2013-15).
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NR 38
TC 33
Z9 35
U1 0
U2 26
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 16
PY 2016
VL 142
BP 24
EP 32
DI 10.1016/j.jprot.2016.05.002
PG 9
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA DP4MB
UT WOS:000378468900003
PM 27178108
DA 2025-01-04
ER

PT J
AU Alrahawy, M
   Javed, S
   Atif, H
   Elsanhoury, K
   Mekhaeil, K
   Eskandar, G
AF Alrahawy, Mahmoud
   Javed, Saryia
   Atif, Haitham
   Elsanhoury, Kareem
   Mekhaeil, Kamel
   Eskandar, George
TI Microbiome and Colorectal Cancer Management
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Review
DE colorectal cancer; target therapy; diagnosis; biomarker; crc; cancer;
   colorectal; microbiome
ID HUMAN GUT MICROBIOME; INFLAMMATION; DISEASE; METAANALYSIS; DYSBIOSIS;
   IMMUNITY
AB Globally, colorectal cancer (CRC) is one of the most typical lethal cancers. One of the main factors for better outcomes in CRC management is the early detection of the disease. As an integral component of human metabolism and homeostasis, gut microbiome has recently been a subject of extensive research for its role in the pathogenesis, diagnosis, and treatment of CRC.
   Microbial dysbiosis (the decrease in beneficial gut flora and the increase of detrimental populations) leads to chronic inflammation and genetic alteration in the host cells, triggering and promoting CRC carcinogenesis. Identifying these microbial changes in depth would potentially isolate the pathogenic microbiota species and establish biomarker models for early detection of CRC. On the other hand, modifying these microbial changes would help formulate preventative and therapeutic strategies for CRC, developing a more precise CRC management plan according to each patient's microbial print. This essay explains gut microbiome composition, microbial changes (dysbiosis) in CRC carcinogenesis, the probability of creating microbiome-based CRC biomarkers, and potential microbiome-targeted treatment options.
C1 [Alrahawy, Mahmoud; Atif, Haitham] Menoufia Univ, Gen Surg, Menoufia, Egypt.
   [Javed, Saryia] Queen Elizabeth Univ Hosp, Gen Surg, Glasgow, Lanark, Scotland.
   [Elsanhoury, Kareem; Mekhaeil, Kamel] James Cook Univ Hosp, Vasc Surg, Middlesbrough, Cleveland, England.
   [Eskandar, George] James Cook Univ Hosp, Surg, Middlesbrough, Cleveland, England.
C3 Egyptian Knowledge Bank (EKB); Menofia University; Queen Elizabeth
   University Hospital (QEUH); James Cook University Hospital; James Cook
   University Hospital
RP Alrahawy, M (corresponding author), Menoufia Univ, Gen Surg, Menoufia, Egypt.
EM mahmoudrahawy@gmail.com
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NR 98
TC 3
Z9 4
U1 2
U2 11
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 OCT 26
PY 2022
VL 14
IS 10
AR e30720
DI 10.7759/cureus.30720
PG 9
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA E9GN4
UT WOS:000978541800031
PM 36457613
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Huang, MY
   Tsai, HL
   Huang, JJ
   Wang, JY
AF Huang, Ming-Yii
   Tsai, Hsiang-Lin
   Huang, Joh-Jong
   Wang, Jaw-Yuan
TI Clinical Implications and Future Perspectives of Circulating Tumor Cells
   and Biomarkers in Clinical Outcomes of Colorectal Cancer
SO TRANSLATIONAL ONCOLOGY
LA English
DT Review
ID SERUM CARCINOEMBRYONIC ANTIGEN; III COLON-CANCER; MULTIPLE MOLECULAR
   MARKERS; POLYMERASE-CHAIN-REACTION; POOR PROGNOSTIC-FACTOR;
   GROWTH-FACTOR RECEPTOR; PERIPHERAL-BLOOD; MICROSATELLITE INSTABILITY;
   CURATIVE RESECTION; RT-PCR
AB Colorectal cancer (CRC) is a major public health problem. Early CRC detection, pretherapeutic responsiveness prediction, and postoperative micrometastasis monitoring are the hallmarks for successful CRC treatment. Here, the methodologies used for detecting circulating tumor cells (CTCs) from CRC are reviewed. In addition to the traditional CRC biomarkers, the persistent presence of posttherapeutic CTCs indicates resistance to adjuvant chemotherapy and/or radiotherapy; hence, CTCs also play a decisive role in the subsequent relapse of CRC. Moreover, the genetic and phenotypic profiling of CTCs often differs from that of the primary tumor; this difference can be used to select the most effective targeted therapy. Consequently, studying CTCs can potentially individualize treatment strategies for patients with CRC. Therefore, CTC detection and characterization may be valuable tools for refining prognosis, and CTCs can be used in a real-time tumor biopsy for designing individually tailored therapy against CRC.
C1 [Huang, Ming-Yii] Kaohsiung Med Univ Hosp, Dept Radiat Oncol, Ctr Canc, Kaohsiung 807, Taiwan.
   [Huang, Ming-Yii] Kaohsiung Med Univ, Dept Radiat Oncol, Coll Med, Fac Med, Kaohsiung 807, Taiwan.
   [Huang, Ming-Yii; Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Med, Ctr Biomarkers & Biotech Drugs, Kaohsiung 807, Taiwan.
   [Tsai, Hsiang-Lin] Kaohsiung Med Univ, Dept Surg, Div Gen Surg Med, Kaohsiung Med Univ Hosp, Kaohsiung 807, Taiwan.
   [Tsai, Hsiang-Lin; Wang, Jaw-Yuan] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Div Gastroenterol & Gen Surg, Dept Surg, Kaohsiung 807, Taiwan.
   [Wang, Jaw-Yuan] Kaohsiung Med Univ, Grad Inst Clin Med, Dept Surg, Kaohsiung 807, Taiwan.
   [Huang, Joh-Jong] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Family Med, Kaohsiung 807, Taiwan.
   [Huang, Joh-Jong] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Community Med, Kaohsiung 807, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University; Kaohsiung Medical University; Kaohsiung
   Medical University; Kaohsiung Medical University Hospital; Kaohsiung
   Medical University; Kaohsiung Medical University Hospital; Kaohsiung
   Medical University; Kaohsiung Medical University; Kaohsiung Medical
   University Hospital; Kaohsiung Medical University; Kaohsiung Medical
   University Hospital
RP Wang, JY (corresponding author), Kaohsiung Med Univ, Grad Inst Clin Med, Dept Surg, Kaohsiung 807, Taiwan.; Huang, JJ (corresponding author), Kaohsiung Med Univ Hosp, Dept Family Med, Kaohsiung 807, Taiwan.; Huang, JJ (corresponding author), Kaohsiung Med Univ Hosp, Dept Community Med, Kaohsiung 807, Taiwan.
EM jjhua511227@gmail.com
RI Huang, Ming-Yii/AAS-8132-2021; Jaw-Yuan, Wang/AFS-8845-2022
OI Wang, Jaw-Yuan/0000-0002-7705-2621
FU Ministry of Science and Technology [MOST103-2325-B-037-005, MOST
   103-2314-B-037-010-MY3]; Kaohsiung Medical University Hospital
   [KMUH103-3M58, KMUH104-4M46, KMUH104-4M51]; Center for Biomarkers and
   Biotech Drugs; Kaohsiung Medical University; Aim for the Top
   Universities Grant [KMU-TP104C00, KMU-TP104C01, KMU-TP104C02]; Grant of
   Biosignature in Colorectal Cancers, Academia Sinica, Taiwan; Excellence
   for Cancer Research Center Grant; Ministry of Health and Welfare
   [MOHW105-TDU-B-212-134007]; Health and welfare surcharge of tobacco
   products, Taiwan, Republic of China
FX The work was supported by the Ministry of Science and Technology
   (MOST103-2325-B-037-005, MOST 103-2314-B-037-010-MY3); Kaohsiung Medical
   University Hospital (KMUH103-3M58, KMUH104-4M46, KMUH104-4M51); Center
   for Biomarkers and Biotech Drugs, Kaohsiung Medical University, Aim for
   the Top Universities Grant (KMU-TP104C00, KMU-TP104C01, KMU-TP104C02);
   the Grant of Biosignature in Colorectal Cancers, Academia Sinica,
   Taiwan; Excellence for Cancer Research Center Grant, funded by the
   Ministry of Health and Welfare (MOHW105-TDU-B-212-134007), Health and
   welfare surcharge of tobacco products, Taiwan, Republic of China.
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NR 82
TC 34
Z9 38
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1936-5233
J9 TRANSL ONCOL
JI Transl. Oncol.
PD AUG
PY 2016
VL 9
IS 4
BP 340
EP 347
DI 10.1016/j.tranon.2016.06.006
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EA6XI
UT WOS:000386772100011
PM 27567958
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Brun, VH
   Knutsen, E
   Stenvold, H
   Halvorsen, H
AF Brun, Vegard Heimly
   Knutsen, Erik
   Stenvold, Helge
   Halvorsen, Hanne
TI Severe hypercalcemia caused by parathyroid hormone in a rectal cancer
   metastasis: a case report
SO BMC ENDOCRINE DISORDERS
LA English
DT Article
DE Parathyroid hormone; Hypercalcemia; Colorectal cancer; Metastasis; Case
   report
AB BackgroundHypercalcemia of malignancy is relatively common in several cancers. However, in colorectal cancer, paraneoplastic phenomena that cause hypercalcemia is uncommon. In the few cases that are reported, secretion of parathyroid hormone-related peptide mediates the effect. We describe the first case of severe hypercalcemia mediated by intact parathyroid hormone secretion from a bone metastasis of colorectal origin. This was a diagnostic and therapeutic challenge.Case presentationA 68-year-old male treated for rectal adenocarcinoma 10years earlier developed a bone metastasis. After initial treatment of the metastasis with surgery and irradiation, he developed a relapse with severe hypercalcemia and corresponding elevated parathyroid hormone levels. The workup showed no signs of parathyroid adenomas, but the metastasis produced intact parathyroid hormone. The hypercalcemia was successfully treated by irradiation and osteoclast inhibitor, and the patient received chemotherapy. Survival was 24months from the onset of hypercalcemia.ConclusionsProper diagnosis of the uncommon endocrine disturbance allowed targeted therapy and avoidance of neck exploration for wrongly suspecting primary hyperparathyroidism. Intact parathyroid hormone should be measured in cases of malignant hypercalcemia.
C1 [Brun, Vegard Heimly] Univ Hosp North Norway, Dept Breast & Endocrine Surg, Sykehusvegen 38, N-9019 Tromso, Norway.
   [Brun, Vegard Heimly; Knutsen, Erik] UiT Arctic Univ Norway, Fac Hlth Sci, Hansine Hansens Veg 18, N-9019 Tromso, Norway.
   [Stenvold, Helge] Univ Hosp North Norway, Dept Oncol, Sykehusvegen 38, N-9019 Tromso, Norway.
   [Halvorsen, Hanne] Univ Hosp North Norway, Dept Clin Pathol, Sykehusvegen 38, N-9019 Tromso, Norway.
C3 UiT The Arctic University of Tromso; University Hospital of North
   Norway; UiT The Arctic University of Tromso; UiT The Arctic University
   of Tromso; University Hospital of North Norway; UiT The Arctic
   University of Tromso; University Hospital of North Norway
RP Brun, VH (corresponding author), Univ Hosp North Norway, Dept Breast & Endocrine Surg, Sykehusvegen 38, N-9019 Tromso, Norway.; Brun, VH (corresponding author), UiT Arctic Univ Norway, Fac Hlth Sci, Hansine Hansens Veg 18, N-9019 Tromso, Norway.
EM vegardbrun@gmail.com
RI Brun, Vegard/ADZ-5405-2022; Knutsen, Erik/ABH-6287-2020
OI Brun, Vegard/0000-0002-4136-3073; Knutsen, Erik/0000-0002-4903-0150
FU UiT The Arctic University of Norway
FX This research did not receive any specific grant from any funding agency
   in the public, commercial or not-for-profit sector. The publication
   charges for this article have been funded by a grant from the
   publication fund of UiT The Arctic University of Norway.
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NR 10
TC 1
Z9 2
U1 0
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1472-6823
J9 BMC ENDOCR DISORD
JI BMC Endocr. Disord.
PD JAN 7
PY 2021
VL 21
IS 1
AR 4
DI 10.1186/s12902-020-00664-8
PG 6
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA PS9WG
UT WOS:000608273400002
PM 33413267
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Mondaca, S
   Yaeger, R
AF Mondaca, Sebastian
   Yaeger, Rona
TI Genetics of rectal cancer and novel therapies: primer for radiologists
SO ABDOMINAL RADIOLOGY
LA English
DT Article
DE Rectal cancer; Next-generation sequencing; Targeted therapy; Genomics
ID MICROSATELLITE INSTABILITY; PREOPERATIVE CHEMORADIATION; MUTATION
   STATUS; RAS MUTATIONS; COLON-CANCER; OPEN-LABEL; CETUXIMAB; KRAS;
   RADIOTHERAPY; CAPECITABINE
AB Rectal cancer accounts for one-third of newly diagnosed colorectal cancer cases. Given its anatomical location and risk for local recurrence, a multidisciplinary treatment program including surgery, radiation therapy, and chemotherapy has demonstrated improved outcomes in localized disease. Genetic analysis has become part of the standard approach for management of advanced disease and new trials are considering tailored therapies for locally advanced disease. This review describes molecular subsets of colorectal cancer; implications for clinical management, including patterns of metastatic spread and response to therapies; and emerging matched therapies. During the last decade, significant biological differences have been noted based on colorectal cancer primary location and here we focus on rectal cancers and relevant markers for this disease. As more treatment for localized rectal cancer is shifted to the neoadjuvant setting and more targeted regimens are developed for metastatic disease, radiologists will increasingly see patients defined by molecular subsets and their awareness of the genetics of rectal cancer will help further refine our understanding of this disease.
C1 [Mondaca, Sebastian; Yaeger, Rona] Mem Sloan Kettering Canc Ctr, Dept Med, 300 E 66th St,10th Floor, New York, NY 10065 USA.
C3 Memorial Sloan Kettering Cancer Center
RP Yaeger, R (corresponding author), Mem Sloan Kettering Canc Ctr, Dept Med, 300 E 66th St,10th Floor, New York, NY 10065 USA.
EM yaegerr@mskcc.org
FU National Institutes of Health Memorial Sloan Kettering Cancer Center
   Core Grant [P30 CA 008748]
FX Supported by the National Institutes of Health Memorial Sloan Kettering
   Cancer Center Core Grant (P30 CA 008748).
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NR 61
TC 9
Z9 9
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2366-004X
EI 2366-0058
J9 ABDOM RADIOL
JI Abdom. Radiol.
PD NOV
PY 2019
VL 44
IS 11
SI SI
BP 3743
EP 3750
DI 10.1007/s00261-019-02051-x
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA JS8KO
UT WOS:000500551000024
PM 31073721
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Wang, H
   Li, ZW
   Ou, QX
   Wu, X
   Nagasaka, M
   Shao, Y
   Ou, SHI
   Yang, Y
AF Wang, Hui
   Li, Zhi-Wei
   Ou, Qiuxiang
   Wu, Xue
   Nagasaka, Misako
   Shao, Yang
   Ou, Sai-Hong Ignatius
   Yang, Yu
TI <i>NTRK</i> fusion positive colorectal cancer is a unique subset of CRC
   with high TMB and microsatellite instability
SO CANCER MEDICINE
LA English
DT Article
DE colorectal cancer; gene fusions; microsatellite instability; NTRK; POLE;
   POLD1; tumor mutation burden
ID TRK; DISCOVERY
AB TRK fusions are rare but targetable mutations which occur across a wide variety of cancer types. We report the prevalence of approximately 0.7% for NTRK-positive colorectal cancer (CRC) by genetically profiling 2519 colonic and rectal tumors. The aberrations of APC and TP53 frequently co-occurred with NTRK gene fusions, whereas RAS/BRAF oncogenic alterations and NTRK fusions were almost always mutually exclusive. NTRK-driven colorectal cancer patients demonstrated increased TMB (median = 53 mut/MB, 95% CI: 36.8-68.0 mut/MB), high microsatellite instability, and an enrichment for POLE/POLD1 mutations when compared to molecularly unstratified colorectal cancer population. These data shed light on possible future approach of multimodality treatment regimen including TRK-targeted therapy and immune checkpoint inhibitor therapy in NTRK-positive CRCs.
C1 [Wang, Hui] Chinese Acad Med Sci, Beijing Hosp, Natl Ctr Gerontol, Inst Geriatr Med,Dept Med Oncol, Beijing, Peoples R China.
   [Li, Zhi-Wei] Harbin Med Univ, Canc Hosp, Dept Internal Med, Harbin, Peoples R China.
   [Ou, Qiuxiang; Wu, Xue; Shao, Yang] Nanjing Geneseeq Technol Inc, Geneseeq Res Inst, Nanjing, Jiangsu, Peoples R China.
   [Nagasaka, Misako] Wayne State Univ, Karmanos Canc Inst, Detroit, MI USA.
   [Shao, Yang] Nanjing Med Univ, Sch Publ Hlth, Nanjing, Jiangsu, Peoples R China.
   [Ou, Sai-Hong Ignatius] Univ Calif Irvine, Chao Family Comprehens Canc Ctr, Sch Med, 101 City Dr,Bldg 56,RT81,Rm241, Orange, CA 92668 USA.
   [Yang, Yu] Harbin Med Univ, Affiliated Hosp 2, Dept Oncol, Harbin 150086, Peoples R China.
C3 Beijing Hospital; Chinese Academy of Medical Sciences - Peking Union
   Medical College; Harbin Medical University; Geneseeq Technology Inc.;
   Wayne State University; Barbara Ann Karmanos Cancer Institute; Nanjing
   Medical University; University of California System; University of
   California Irvine; Harbin Medical University
RP Ou, SHI (corresponding author), Univ Calif Irvine, Chao Family Comprehens Canc Ctr, Sch Med, 101 City Dr,Bldg 56,RT81,Rm241, Orange, CA 92668 USA.; Yang, Y (corresponding author), Harbin Med Univ, Affiliated Hosp 2, Dept Oncol, Harbin 150086, Peoples R China.
EM siou@uci.edu; h02758@hrbmu.edu.cn
RI wu, xue/JTS-4312-2023
OI Ou, Qiuxiang/0000-0002-2961-2057; Ou, Sai-Hong/0000-0002-1764-4975
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NR 23
TC 29
Z9 30
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD JUL
PY 2022
VL 11
IS 13
BP 2541
EP 2549
DI 10.1002/cam4.4561
EA MAY 2022
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2P8SV
UT WOS:000790293500001
PM 35506567
OA Green Published
DA 2025-01-04
ER

PT J
AU Xin, L
   Gao, JF
   Zheng, ZL
   Chen, YY
   Lv, SX
   Zhao, ZK
   Yu, CH
   Yang, XT
   Zhang, RP
AF Xin, Lei
   Gao, Jinfang
   Zheng, Ziliang
   Chen, Yiyou
   Lv, Shuxin
   Zhao, Zhikai
   Yu, Chunhai
   Yang, Xiaotang
   Zhang, Ruiping
TI Fibroblast Activation Protein-α as a Target in the Bench-to-Bedside
   Diagnosis and Treatment of Tumors: A Narrative Review
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE cancer-associated fibroblast; FAP substrates; immunosuppressive;
   targeted therapy; nanomaterials; fibroblast activation protein-alpha
ID DIPEPTIDYL-PEPTIDASE-IV; CANCER-ASSOCIATED FIBROBLASTS;
   MONOCLONAL-ANTIBODY F-19; MEMBRANE-BOUND PROTEASE; SERINE-PROTEASE;
   ENHANCED PERMEABILITY; STROMAL CELLS; COLON-CANCER; FAP-ALPHA;
   POPULATION PHARMACOKINETICS
AB Fibroblast activation protein-alpha (FAP) is a type II integral serine protease that is specifically expressed by activated fibroblasts. Cancer-associated fibroblasts (CAFs) in the tumor stroma have an abundant and stable expression of FAP, which plays an important role in promoting tumor growth, invasion, metastasis, and immunosuppression. For example, in females with a high incidence of breast cancer, CAFs account for 50-70% of the cells in the tumor's microenvironment. CAF overexpression of FAP promotes tumor development and metastasis by influencing extracellular matrix remodeling, intracellular signaling, angiogenesis, epithelial-to-mesenchymal transition, and immunosuppression. This review discusses the basic biological characteristics of FAP and its applications in the diagnosis and treatment of various cancers. We review the emerging basic and clinical research data regarding the use of nanomaterials that target FAP.
C1 [Xin, Lei; Chen, Yiyou; Zhao, Zhikai; Yu, Chunhai; Yang, Xiaotang; Zhang, Ruiping] Shanxi Med Univ, Affiliated Tumor Hosp, Dept Radiol, Taiyuan, Peoples R China.
   [Gao, Jinfang; Lv, Shuxin] Shanxi Med Univ, Shanxi Bethune Hosp, Shanxi Acad Med Sci, Hosp 3, Taiyuan, Peoples R China.
   [Zheng, Ziliang] Shanxi Med Univ, Dept Biochem & Mol Biol, Taiyuan, Peoples R China.
C3 Shanxi Medical University; Shanxi Medical University; Shanxi Medical
   University
RP Yang, XT; Zhang, RP (corresponding author), Shanxi Med Univ, Affiliated Tumor Hosp, Dept Radiol, Taiyuan, Peoples R China.
EM yxtbean@126.com; zrp_7142@sxmu.edu.cn
RI Zheng, Ziliang/KIJ-6987-2024
OI Lyu, Shuxin/0009-0005-9716-8954
FU National Natural Science Foundation of China [82071987, 81771907];
   Science and technology innovation team project of Shanxi Province
   [201705D131026]; Engineering Technology Research Center of Shanxi
   Province [201805D121008]; Scientific and Technological Achievements
   Transformation Project of Shanxi Province [201704D131006]; Projects for
   Local Science and Technology Development Guided by the Central Committee
   [YDZX20191400002537]; Shanxi Scholarship Council of China [2020-177];
   Fund Program for the Scientific Activities of Selected Returned Overseas
   Professionals in Shanxi Province [20200006]; applied basic research
   project of Shanxi Science and Technology Department [201901D111416];
   Laboratory Construction Project of Shanxi Province [YDZX20191400002537]
FX This work has been financially supported by the National Natural Science
   Foundation of China [Nos. 82071987, 81771907]; Science and technology
   innovation team project of Shanxi Province [No. 201705D131026];
   Engineering Technology Research Center of Shanxi Province [No.
   201805D121008]; Scientific and Technological Achievements Transformation
   Project of Shanxi Province [No. 201704D131006]; Laboratory Construction
   Project of Shanxi Province, and the Projects for Local Science and
   Technology Development Guided by the Central Committee [No.
   YDZX20191400002537]; Research Project Supported by Shanxi Scholarship
   Council of China [No. 2020-177]; Fund Program for the Scientific
   Activities of Selected Returned Overseas Professionals in Shanxi
   Province [NO: 20200006]; and the applied basic research project of
   Shanxi Science and Technology Department under Grant [No.
   201901D111416].
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NR 138
TC 88
Z9 93
U1 2
U2 74
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 19
PY 2021
VL 11
AR 648187
DI 10.3389/fonc.2021.648187
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UL8CM
UT WOS:000692872700001
PM 34490078
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Mu, JF
   Sun, PF
   Ma, ZM
   Sun, PD
AF Mu, Jianfeng
   Sun, Pengfei
   Ma, Zhiming
   Sun, Pengda
TI BRD4 promotes tumor progression and NF-κB/CCL2-dependent
   tumor-associated macrophage recruitment in GIST
SO CELL DEATH & DISEASE
LA English
DT Article
ID B SIGNALING PATHWAY; COLORECTAL-CANCER; IMATINIB MESYLATE; TARGETED
   THERAPY; RESISTANCE; EFFICACY; SAFETY; CELLS
AB The most commonly occurring sarcoma of the soft tissue is gastrointestinal stromal tumor (GIST). Treatment and prevention of the disease necessitate an understanding of the molecular mechanisms involved. However, the role of BRD4 in the progression of GIST is still unclear. While it is known there are abundant infiltrating tumor-associated macrophages (TAMs) in the tumor microenvironment, the exact role of these cells has yet to be studied. This work showed an upregulation of BRD4 in GIST that was associated with GIST prognosis. Through gain and loss of function studies, it was found that BRD4 promotes GIST growth and angiogenesis in vitro and in vivo. Mechanistically, BRD4 enhances CCL2 expression by activating the NE-kappa B signaling pathway. Furthermore, this CCL2 upregulation causes recruitment of macrophages into the tumor leading to tumor growth. A likely mechanism for interactions in the GIST microenvironment has been outlined by this work to show the role and potential use of BRD4 as a treatment target in GIST.
C1 [Mu, Jianfeng] First Hosp Jilin Univ, Dept Gastr & Colorectal Surg, Changchun, Jilin, Peoples R China.
   [Sun, Pengfei] Changchun Railway Med Insurance Management Off, Changchun, Jilin, Peoples R China.
   [Ma, Zhiming; Sun, Pengda] Second Hosp Jilin Univ, Dept Gastrointestinal Nutr & Hernia Surg, Changchun, Jilin, Peoples R China.
C3 Jilin University; Jilin University
RP Sun, PD (corresponding author), Second Hosp Jilin Univ, Dept Gastrointestinal Nutr & Hernia Surg, Changchun, Jilin, Peoples R China.
EM sunpd@jlu.edu.cn
RI Chen, Shanshan/M-5985-2013
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NR 50
TC 32
Z9 35
U1 2
U2 18
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 DEC 9
PY 2019
VL 10
AR 935
DI 10.1038/s41419-019-2170-4
PG 11
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA JW3SM
UT WOS:000502975000002
PM 31819043
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xiao, Y
   Cheng, HJ
   Wang, L
   Luo, SX
AF Xiao, Y.
   Cheng, H. J.
   Wang, L.
   Luo, S. X.
TI Short-term curative effect and safety of bevacizumab combined with
   chemotherapy for treating recurrent and metastatic cervical cancer
SO EUROPEAN JOURNAL OF GYNAECOLOGICAL ONCOLOGY
LA English
DT Article
DE Cervical neoplasms; Bevacizumab; Drug therapy; Targeted therapy; Drug
   toxicity
ID PHASE-II TRIAL; COLORECTAL-CANCER; THERAPY; COMBINATION
AB Objective: To observe bevacizumab plus chemotherapy curative effect and safety for recurrent and metastatic cervical cancer. Materials and Methods: Retrospective analysis of 30 recurrent and metastatic cervical cancer cases. The experimental group received bevacizumab plus paclitaxel-, docetaxel-, and platinum-based chemotherapy. The control group received only chemotherapy. Curative effects were recorded after at least two treatment cycles; adverse reactions were recorded with every cycle. Results: Experimental group patients were treated for an average 2.6 cycles. Compared to the control group, the experimental group effective rate (26.7%) was similar, disease control rate (73.7%) was significantly higher, and median survival time was three months longer. Bevacizumab-associated adverse reactions were bleeding, hypertension, and thrombosis/ embolism; most were level 1 and 2 reactions. Adverse reactions in the two groups were not statistically different. Conclusions: The bevacizumab plus chemotherapy disease control rate for recurrent and metastatic cervical cancer is comparatively high, prolonging median survival; bevacizumab-associated adverse reactions are mild and tolerable.
C1 [Xiao, Y.; Cheng, H. J.; Wang, L.; Luo, S. X.] Zhengzhou Univ, Canc Hosp, Dept Gynecol Oncol, Henan Tumor Hosp, Zhengzhou, Peoples R China.
C3 Zhengzhou University
RP Wang, L (corresponding author), Zhengzhou Univ, Henan Canc Hosp, Affiliated Canc Hosp, Dongming Rd 127, Zhengzhou 450008, Peoples R China.
EM hnlyxy@sina.com
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NR 14
TC 2
Z9 2
U1 0
U2 3
PU MRE PRESS
PI SINGAPORE
PA 14 ROBINSON RD #08-01A FAR EAST FINANCE, SINGAPORE, SINGAPORE
SN 0392-2936
EI 2709-0086
J9 EUR J GYNAECOL ONCOL
JI Eur. J. Gynaecol. Oncol.
PY 2017
VL 38
IS 1
BP 76
EP 79
DI 10.12892/ejgo3322.2017
PG 4
WC Oncology; Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Obstetrics & Gynecology
GA EO4ER
UT WOS:000396648700014
PM 29767869
DA 2025-01-04
ER

PT J
AU Reinwald, M
   Boch, T
   Hofmann, WK
   Buchheidt, D
AF Reinwald, Mark
   Boch, Tobias
   Hofmann, Wolf-Karsten
   Buchheidt, Dieter
TI Risk of Infectious Complications in Hemato-Oncological Patients Treated
   with Kinase Inhibitors
SO BIOMARKER INSIGHTS
LA English
DT Article
DE TKI; kinase inhibitors; infections; infectious complications; targeted
   therapy; EGFR; BCR-ABL; BRAF; VEGF; BCR signaling; mTOR; JAK
ID CHRONIC MYELOID-LEUKEMIA; CELL LUNG-CANCER; ACUTE
   LYMPHOBLASTIC-LEUKEMIA; GASTROINTESTINAL STROMAL TUMORS; METASTATIC
   COLORECTAL-CANCER; TUBEROUS SCLEROSIS COMPLEX; PLACEBO-CONTROLLED TRIAL;
   GROWTH-FACTOR RECEPTOR; SOFT-TISSUE SARCOMA; FUNCTION IN-VITRO
AB Infectious complications are a major cause of morbidity and mortality in patients with hemato-oncological diseases. Although disease-related immunosuppression represents one factor, aggressive treatment regimens, such as chemotherapy, stem cell transplantation, or antibody treatment, account for a large proportion of infectious side effects. With the advent of targeted therapies affecting specific kinases in malignant diseases, the outcome of patients has further improved. Nonetheless, dependent on the specific pathway targeted or off-target activity of the kinase inhibitor, therapy-associated infectious complications may occur. We review the most common and approved kinase inhibitors targeting a variety of hemato-oncological malignancies for their immunosuppressive potential and evaluate their risk of infectious side effects based on preclinical evidence and clinical data in order to raise awareness of the potential risks involved.
C1 [Reinwald, Mark; Boch, Tobias; Hofmann, Wolf-Karsten; Buchheidt, Dieter] Heidelberg Univ, Mannheim Univ Hosp, Dept Hematol & Oncol, Mannheim, Germany.
C3 Ruprecht Karls University Heidelberg
RP Reinwald, M (corresponding author), Heidelberg Univ, Mannheim Univ Hosp, Dept Hematol & Oncol, Mannheim, Germany.
EM mark.reinwald@medma.uni-heidelberg.de
OI Buchheidt, Dieter/0000-0002-4425-6134
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NR 180
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U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1177-2719
J9 BIOMARK INSIGHTS
JI Biomark. Insights
PY 2015
VL 10
SU 3
BP 55
EP 68
DI 10.4137/BMI.S22430
PG 14
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA VK4SA
UT WOS:000703354800002
PM 27127405
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Azadi, A
   Golchini, A
   Delazar, S
   Kahaki, FA
   Dehnavi, SM
   Payandeh, Z
   Eyvazi, S
AF Azadi, Ali
   Golchini, Alireza
   Delazar, Sina
   Abarghooi Kahaki, Fatemeh
   Dehnavi, Seyed Mohsen
   Payandeh, Zahra
   Eyvazi, Shirin
TI Recent Advances on Immune Targeted Therapy of Colorectal Cancer Using
   bi-Specific Antibodies and Therapeutic Vaccines
SO BIOLOGICAL PROCEDURES ONLINE
LA English
DT Review
DE Colorectal cancer; Cancer vaccines; Bi-specific antibody; mRNA vaccines;
   Nanobodies; MGD007
ID GROWTH-FACTOR RECEPTOR; T-CELL RESPONSES; CARCINOEMBRYONIC ANTIGEN;
   MONOCLONAL-ANTIBODY; DENDRITIC CELLS; PHASE-I; PROGNOSTIC-FACTOR;
   MOLECULAR-BASIS; CLINICAL-TRIAL; NANOPARTICLES
AB Colorectal cancer (CRC) is a universal heterogeneous disease that is characterized by genetic and epigenetic alterations. Immunotherapy using monoclonal antibodies (mAb) and cancer vaccines are substitute strategies for CRC treatment. When cancer immunotherapy is combined with chemotherapy, surgery, and radiotherapy, the CRC treatment would become excessively efficient. One of the compelling immunotherapy approaches to increase the efficiency of CRC therapy is the deployment of therapeutic mAbs, nanobodies, bi-specific antibodies and cancer vaccines, which improve clinical outcomes in patients. Also, among the possible therapeutic approaches for CRC patients, gene vaccines in combination with antibodies are recently introduced as a new perspective. Here, we aimed to present the current progress in CRC immunotherapy, especially using Bi-specific antibodies and dendritic cells mRNA vaccines. For this aim, all data were extracted from Google Scholar, PubMed, Scopus, and Elsevier, using keywords cancer vaccines; CRC immunotherapy and CRC mRNA vaccines. About 97 articles were selected and investigated completely based on the latest developments and novelties on bi-specific antibodies, mRNA vaccines, nanobodies, and MGD007.
C1 [Azadi, Ali] De La Salle Hlth Sci Inst, Dept Med, Dasmarinas, Philippines.
   [Golchini, Alireza] Shiraz Univ Med Sci, Canc Surg Dept, Shiraz Med Sch, Shiraz, Iran.
   [Delazar, Sina] Univ Tehran Med Sci, Dept Radiol, Tehran, Iran.
   [Abarghooi Kahaki, Fatemeh] Shahid Beheshti Univ Med Sci, Dept Biotechnol, Sch Adv Technol Med, Tehran, Iran.
   [Dehnavi, Seyed Mohsen] Shahid Beheshti Univ, Fac Life Sci & Biotechnol, Tehran, Iran.
   [Payandeh, Zahra] Tabriz Univ Med Sci, Biomed Inst, Immunol Res Ctr, Tabriz, Iran.
   [Eyvazi, Shirin] Islamic Azad Univ, Tabriz Branch, Dept Biol, Tabriz, Iran.
   [Eyvazi, Shirin] Islamic Azad Univ, Tabriz Branch, Biotechnol Res Ctr, Tabriz, Iran.
C3 De La Salle University; De La Salle University Dasmarinas; Shiraz
   University of Medical Science; Tehran University of Medical Sciences;
   Shahid Beheshti University Medical Sciences; Shahid Beheshti University;
   Tabriz University of Medical Science; Islamic Azad University; Islamic
   Azad University
RP Payandeh, Z (corresponding author), Tabriz Univ Med Sci, Biomed Inst, Immunol Res Ctr, Tabriz, Iran.; Eyvazi, S (corresponding author), Islamic Azad Univ, Tabriz Branch, Biotechnol Res Ctr, Tabriz, Iran.
EM Zpayandeh58@yahoo.com; shirin_biotech@yahoo.com
RI Eyvazi, Shirin/AAO-3828-2021; payandeh, zahra/CAF-0179-2022; Dehnavi,
   Seyed Mohsen/GRJ-8899-2022; delazar, sina/HKM-8452-2023
OI Dehnavi, Seyed Mohsen/0000-0001-9314-6698
FU Tabriz University of medical science, Tabriz, Iran
FX The authors like to thank the Tabriz University of medical science,
   Tabriz, Iran, for supporting this study.
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PU BMC
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PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
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PY 2021
VL 23
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DI 10.1186/s12575-021-00147-7
PG 13
WC Biochemical Research Methods
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA TC3LG
UT WOS:000668540700001
PM 34193050
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Musa, M
   Ali, A
AF Musa, Marahaini
   Ali, Adli
TI Cancer-associated fibroblasts of colorectal cancer and their markers:
   updates, challenges and translational outlook
SO FUTURE ONCOLOGY
LA English
DT Review
DE colon; marker; neoplasm; tumor heterogeneity; tumor microenvironment
ID MOLECULAR SUBTYPES; ACTIVATION PROTEIN; MYOFIBROBLASTS; CARCINOMA;
   CELLS; HETEROGENEITY; EXPRESSION; MIGRATION; GENETICS; STEMNESS
AB Accumulation of cancer-associated fibroblasts (CAFs) in the tumor microenvironment is associated with poor prognosis and recurrence of colorectal cancer (CRC). Despite their prominent roles in colorectal carcinogenesis, there is a lack of robust and specific markers to classify the heterogeneous and highly complex CAF populations. This has resulted in confusing and misleading definitions of CAFs in cancer niche. Advancements in molecular biology approaches have open doors to reliable CAF marker detection methods in various solid tumors. These discoveries would contribute to more efficient screening, monitoring and targeted therapy of CRC thus potentially will reduce cancer morbidity and mortality rates. This review highlights current scenarios, dilemma, translational potentials of CAF biomarker and future therapeutic applications involving CAF marker identification in CRC.
C1 [Musa, Marahaini] Univ Sains Malaysia, Sch Med Sci, Human Genome Ctr, Hlth Campus, Kubang Kerian 16150, Kelantan, Malaysia.
   [Ali, Adli] Univ Kebangsaan Malaysia, Med Ctr, Dept Paediat, Jalan Yaacob Latif, Kuala Lumpur 56000, Malaysia.
   [Ali, Adli] Univ Oxford, Childrens Hosp, John Radcliffe Hosp, Dept Paediat, Level 2, Oxford OX3 9DU, England.
C3 Universiti Sains Malaysia; Universiti Kebangsaan Malaysia; University of
   Oxford
RP Musa, M (corresponding author), Univ Sains Malaysia, Sch Med Sci, Human Genome Ctr, Hlth Campus, Kubang Kerian 16150, Kelantan, Malaysia.
EM marahaini.musa@usm.my
RI Ali, Adli/AAD-5529-2021; Musa, Marahaini/E-9987-2019
OI Musa, Marahaini/0000-0002-0165-5741; Ali, Adli/0000-0001-5615-5966
FU Short Term Research Grant, Universiti Sains Malaysia (USM)
   [304/PPSP/6315409]
FX This work was supported by Short Term Research Grant, Universiti Sains
   Malaysia (USM) (grant number: 304/PPSP/6315409). 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 98
TC 16
Z9 16
U1 1
U2 23
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PD OCT
PY 2020
VL 16
IS 29
BP 2329
EP 2344
DI 10.2217/fon-2020-0384
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PA7MJ
UT WOS:000595814500001
PM 32687721
DA 2025-01-04
ER

PT J
AU Nguyen, HV
   Phung, DT
   Nguyen, TT
   Tran, BT
   Mai, KNT
   Trinh, HL
AF Nguyen, Hung Van
   Phung, Duong Thuy
   Nguyen, Trung Thanh
   Tran, Bach Trung
   Mai, Kim Ngan Thi
   Trinh, Huy Le
TI Management of brain metastasis from rectal cancer using whole-brain
   radiation therapy followed by bevacizumab and chemotherapy: A case
   report
SO ONCOLOGY LETTERS
LA English
DT Article
DE case report; brain metastasis; rectal cancer; bevacizumab; whole-brain
   radiation therapy
ID COLORECTAL-CANCER; 1ST-LINE TREATMENT; TRIAL
AB Brain metastases in colorectal cancer are uncommon, which has resulted in a shortage of data concerning their screening and management. Multiple therapeutic modalities with chemotherapy, chemoradiation and targeted therapy, including bevacizumab and cetuximab regimens, have shown promising results. The present study describes the case of a 47-year-old male, diagnosed with T4N2M1 rectal cancer who underwent systemic therapy with modified FOLFOXIRI and cetuximab. The patient achieved a complete clinical response after 12 cycles. Following the discontinuation of cetuximab, the patient was given capecitabine as a maintenance therapy and subsequently developed brain metastasis. The patient received whole-brain radiation therapy (WBRT) followed by a bevacizumab plus FOLFIRI regimen. The patient showed a good response as revealed by cranial magnetic resonance imaging, with a reduction in lesion size and no sign of cerebral edema. In addition, the patient maintained a stable neurological condition for >10 months. These findings suggest that the early detection of brain metastases requires the close monitoring of neurological symptoms. In addition, WBRT followed by bevacizumab and chemotherapy is a potential management plan for brain metastasis from rectal cancer.
C1 [Nguyen, Hung Van; Mai, Kim Ngan Thi; Trinh, Huy Le] Hanoi Med Univ Hosp, Dept Oncol & Palliat Care, Hanoi 100000, Vietnam.
   [Nguyen, Hung Van; Phung, Duong Thuy; Nguyen, Trung Thanh; Tran, Bach Trung; Mai, Kim Ngan Thi; Trinh, Huy Le] Hanoi Med Univ, Dept Oncol, 1 Ton That Tung St, Hanoi 100000, Vietnam.
C3 Hanoi Medical University; Hanoi Medical University
RP Phung, DT (corresponding author), Hanoi Med Univ, Dept Oncol, 1 Ton That Tung St, Hanoi 100000, Vietnam.
EM duongphung.hmu@gmail.com
RI Nguyen, Thuong/AAF-5848-2019; Nguyen, Van Hung/IWL-8020-2023
OI Nguyen, Hung/0000-0002-8240-3641; Phung, Duong/0009-0002-5698-1269
FU Not applicable.
FX Not applicable.
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NR 22
TC 0
Z9 0
U1 0
U2 1
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD OCT
PY 2023
VL 26
IS 4
AR 446
DI 10.3892/ol.2023.14033
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA S6GM9
UT WOS:001072127100001
PM 37720667
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhang, WM
   Song, GX
   Han, X
   Li, X
   Luo, D
AF Zhang, Weiming
   Song, Guoxin
   Han, Xue
   Li, Xiao
   Luo, Dan
TI A validation study for the use VE1 immunohistochemical staining in
   screening for <i>BRAF</i> mutation in cutaneous malignant melanoma
SO BIOMEDICAL RESEARCH-INDIA
LA English
DT Article
DE Braf; Mutation; Melanoma immunohistochemistry; ARMS
ID V600E MUTATION; COLORECTAL-CARCINOMA; BRAF(V600E) MUTATION;
   MONOCLONAL-ANTIBODY; EXPRESSION
AB BRAF V600E mutation analysis has been an important companion diagnostic assay to evaluate prognosis of malignant melanoma and to guide target therapy with BRAF inhibitor. The aim of this study was to assess the sensitivity and specificity of Immunohistochemistry (IHC) using VE1 mutation specific antibody on screening for BRAF V600E mutation patients with cutaneous malignant melanoma. We detected BRAF V600E mutation on a total of 90 formalin-fixed paraffin-embedded melanoma tissue samples by ARMS-PCR and immunohistochemistry simultaneously. The results obtained from ARMS were set as a diagnostic gold standard; IHC staining with BRAF V600E mutation-specific antibody displayed 100% sensitivity and 96.8% specificity. Further statistical analysis showed that results from the two methods were consistent (kappa=0.948 p<0.001), Positive Predictive Value (PPV) and Negative Predictive Value (NPV) were 93.1% and 100%. Therefore, as a simple, fast and low cost method, IHC can be used as a routine screening method for BRAF V600E mutation analysis in cutaneous malignant melanoma.
C1 [Zhang, Weiming; Song, Guoxin; Han, Xue; Li, Xiao] Nanjing Med Univ, Dept Pathol, Affiliated Hosp 1, Nanjing, Jiangsu, Peoples R China.
   [Luo, Dan] Nanjing Med Univ, Dept Dermatol, Affiliated Hosp 1, Nanjing, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University
RP Luo, D (corresponding author), Nanjing Med Univ, Dept Dermatol, Affiliated Hosp 1, Nanjing, Jiangsu, Peoples R China.
RI Luo, Dan/HZM-2412-2023; Zhang, Wei-Ming/L-5761-2017
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NR 29
TC 1
Z9 1
U1 0
U2 0
PU ALLIED ACAD
PI LONDON
PA 40 BLOOMSBURY WAY, LOWER GROUND FLR, LONDON, WC1A 2SE, ENGLAND
SN 0970-938X
EI 0976-1683
J9 BIOMED RES-INDIA
JI Biomed. Res.-India
PY 2017
VL 28
IS 11
BP 4886
EP 4890
PG 5
WC Engineering, Biomedical; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Engineering; Research & Experimental Medicine
GA FD1VG
UT WOS:000407324200030
DA 2025-01-04
ER

PT J
AU Rizzo, A
   Frega, G
   Ricci, AD
   Palloni, A
   Abbati, F
   De Lorenzo, S
   Deserti, M
   Tavolari, S
   Brandi, G
AF Rizzo, Alessandro
   Frega, Giorgio
   Ricci, Angela Dalia
   Palloni, Andrea
   Abbati, Francesca
   De Lorenzo, Stefania
   Deserti, Marzia
   Tavolari, Simona
   Brandi, Giovanni
TI Anti-EGFR Monoclonal Antibodies in Advanced Biliary Tract Cancer: A
   Systematic Review and Meta-analysis
SO IN VIVO
LA English
DT Review
DE Biliary tract cancer; BTC; anti-EGFR; cetuximab; panitumumab; KRAS;
   meta-analysis; review
ID METASTATIC COLORECTAL-CANCER; GALL-BLADDER CANCER; PHASE-II TRIAL;
   INTRAHEPATIC CHOLANGIOCARCINOMA; TARGETED THERAPY; OPEN-LABEL;
   LONG-TERM; SKIN RASH; GEMCITABINE; OXALIPLATIN
AB Background: Despite several clinical trials and advances in understanding the genetic basis of biliary tract cancer (BTC), the addition of epidermal growth factor receptor (EGFR) targeted therapy does not seem to enhance the activity of first-line chemotherapy (CHT). Materials and Methods: We carried out a meta-analysis of available randomized clinical trials to assess the efficacy and safety of gemcitabine-based first-line CHT plus monoclonal antibodies against EGFR (EGFR-mAbs) in advanced or metastatic BTC. Results: In the overall population, the pooled hazard ratio for overall (OS) and progression-free (PFS) survival were 0.82 (95% confidence interval=0.64-1.06) and 0.88 (95% confidence intervaI=0.73-1.08), respectively. No differences were detected in objective response rate between the two groups. Patients treated with gemcitabine-based CHT plus EGFR-mAbs showed a statistically significant increased risk of grade 3-4 neutropenia, grade 3-4 thrombocytopenia and especially grade 3-4 skin rash. Conclusion: The addition of EGFR-mAbs to gemcitabine-based first-line CHT does not significantly improve overall and progression-free survival, nor the objective response rate in patients with advanced BTC and increases the risk of hematological and cutaneous adverse drug events.
C1 [Rizzo, Alessandro; Frega, Giorgio; Ricci, Angela Dalia; Palloni, Andrea; Abbati, Francesca; De Lorenzo, Stefania; Deserti, Marzia; Tavolari, Simona; Brandi, Giovanni] S Orsola Malpighi Univ Hosp, Dept Expt Diagnost & Specialty Med, Bologna, Italy.
C3 IRCCS Azienda Ospedaliero-Universitaria di Bologna
RP Rizzo, A (corresponding author), S Orsola Malpighi Univ Hosp, Dept Expt Diagnost & Specialty Med, Bologna, Italy.
EM rizzo.alessandro179@gmail.com
RI Palloni, Andrea/AAB-9872-2022; Rizzo, Alessandro/AAD-8360-2022;
   Tavolari, Simona/KUC-8713-2024; Ricci, Angela Dalia/ABF-7971-2021;
   Brandi, Giovanni/AAD-6327-2021; Frega, Giorgio/W-8099-2019; Tavolari,
   Simona/K-3540-2018
OI Frega, Giorgio/0000-0001-9153-0557; Ricci, Angela
   Dalia/0000-0002-0701-6764; DESERTI, MARZIA/0000-0001-7608-638X;
   Tavolari, Simona/0000-0002-2410-9698; Achilonu,
   Conrad/0000-0002-3016-5004; Palloni, Andrea/0000-0003-1260-2765
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NR 48
TC 62
Z9 63
U1 1
U2 15
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0258-851X
EI 1791-7549
J9 IN VIVO
JI In Vivo
PD MAR-APR
PY 2020
VL 34
IS 2
BP 479
EP 488
DI 10.21873/invivo.11798
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA KS2ML
UT WOS:000518144400001
PM 32111744
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ren, SN
   Zhang, ZY
   Guo, RJ
   Wang, DR
   Chen, FF
   Chen, XB
   Fang, XD
AF Ren, Sheng-Nan
   Zhang, Zhan-Yi
   Guo, Rui-Jie
   Wang, Da-Ren
   Chen, Fang-Fang
   Chen, Xue-Bo
   Fang, Xue-Dong
TI Application of nanotechnology in reversing therapeutic resistance and
   controlling metastasis of colorectal cancer
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Colorectal cancer; Therapeutic resistance; Nanotechnology; Drug delivery
   system; Combined treatment
ID NEUTROPHIL EXTRACELLULAR TRAPS; BLEBBISHIELD EMERGENCY PROGRAM;
   CETUXIMAB PLUS IRINOTECAN; STEM-CELLS; TUMOR MICROENVIRONMENT; GOLD
   NANOPARTICLES; GROWTH-FACTOR; UP-REGULATION; TGF-BETA; DIHYDROPYRIMIDINE
   DEHYDROGENASE
AB Colorectal cancer (CRC) is the most common digestive malignancy across the world. Its first-line treatments applied in the routine clinical setting include surgery, chemotherapy, radiotherapy, targeted therapy, and immunotherapy. However, resistance to therapy has been identified as the major clinical challenge that fails the treatment method, leading to recurrence and distant metastasis. An increasing number of studies have been attempting to explore the underlying mechanisms of the resistance of CRC cells to different therapies, which can be summarized into two aspects: (1) The intrinsic characters and adapted alterations of CRC cells before and during treatment that regulate the drug metabolism, drug transport, drug target, and the activation of signaling pathways; and (2) the suppressive features of the tumor microenvironment (TME). To combat the issue of therapeutic resistance, effective strategies are warranted with a focus on the restoration of CRC cells' sensitivity to specific treatments as well as reprogramming impressive TME into stimulatory conditions. To date, nanotechnology seems promising with scope for improvement of drug mobility, treatment efficacy, and reduction of systemic toxicity. The instinctive advantages offered by nanomaterials enable the diversity of loading cargoes to increase drug concentration and targeting specificity, as well as offer a platform for trying the combination of different treatments to eventually prevent tumor recurrence, metastasis, and reversion of therapy resistance. The present review intends to summarize the known mechanisms of CRC resistance to chemotherapy, radiotherapy, immunotherapy, and targeted therapy, as well as the process of metastasis. We have also emphasized the recent application of nanomaterials in combating therapeutic resistance and preventing metastasis either by combining with other treatment approaches or alone. In summary, nanomedicine is an emerging technology with potential for CRC treatment; hence, efforts should be devoted to targeting cancer cells for the restoration of therapeutic sensitivity as well as reprogramming the TME. It is believed that the combined strategy will be beneficial to achieve synergistic outcomes contributing to control and management of CRC in the future.
C1 [Ren, Sheng-Nan; Chen, Fang-Fang] Jilin Univ, China Japan Union Hosp, Nanomed & Translat Res Ctr, Changchun 130033, Jilin, Peoples R China.
   [Zhang, Zhan-Yi; Guo, Rui-Jie; Wang, Da-Ren] Jilin Univ, Bethune Clin Med Coll 3, Changchun 130021, Jilin, Peoples R China.
   [Chen, Xue-Bo; Fang, Xue-Dong] Jilin Univ, Dept Gastrointestinal Colorectal & Anal Surg, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China.
   [Chen, Xue-Bo] Jilin Univ, Dept Gastrointestinal Colorectal & Anal Surg, China Japan Union Hosp, 126 Xiantai St, Changchun 130033, Jilin, Peoples R China.
C3 Jilin University; Jilin University; Jilin University; Jilin University
RP Chen, XB (corresponding author), Jilin Univ, Dept Gastrointestinal Colorectal & Anal Surg, China Japan Union Hosp, 126 Xiantai St, Changchun 130033, Jilin, Peoples R China.
EM chenxb@jlu.edu.cn
RI Cheng, Shuqun/HTS-9930-2023
OI Chen, Fangfang/0000-0002-3284-3331
FU Natural Science Foundation of Jilin Province [20210101433JC]
FX Supported by the Natural Science Foundation of Jilin Province, No.
   20210101433JC.
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NR 297
TC 2
Z9 2
U1 1
U2 7
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD APR 7
PY 2023
VL 29
IS 13
BP 1911
EP 1941
DI 10.3748/wjg.v29.i13.1911
PG 31
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA E9OS4
UT WOS:000978755100001
PM 37155531
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Dankner, M
AF Dankner, Matthew
TI Targeted Therapy for Colorectal Cancers With Non-V600 BRAF Mutations:
   Perspectives for Precision Oncology
SO JCO PRECISION ONCOLOGY
LA English
DT Review
ID DNA MISMATCH REPAIR; CELL LUNG-CANCER; OPEN-LABEL; RAS MUTATIONS;
   COLON-CANCER; MICROSATELLITE INSTABILITY; ACQUIRED-RESISTANCE; GENOMIC
   LANDSCAPE; IMPROVED SURVIVAL; PLUS BEVACIZUMAB
AB BRAF mutations are found in up to 10% of colorectal cancers (CRC). Whereas the majority of BRAF mutant CRCs harbor V600 mutations, up to 25% express non-V600 BRAF mutations. It has been established that BRAF V600E mutations in CRC predict unresponsiveness to epidermal growth factor receptor (EGFR) inhibition-cetuximab and/or panitumumab-as a result of the constitutive activation of the mitogen-activated protein kinase pathway downstream of EGFR signaling. As more centers begin using next-generation sequencing assays to detect BRAF mutations, oncologists are more frequently confronted with treating patients with non-V600 BRAF mutations. In many instances, clinicians may be hesitant to use EGFR inhibitors for these patients, as it is largely assumed that tumors with non-V600 BRAF mutations activate the mitogen-activated protein kinase pathway in a similar manner to RAS or BRAF V600E mutations and would therefore be equally refractory to EGFR inhibition; however, the evidence that currently exists to substantiate this claim is mixed and incomplete. Recent data demonstrate that non-V600 BRAF mutant CRC is a distinct clinical entity with a favorable prognosis compared with CRC with V600E mutations. Preclinical data and several case reports suggest that a subset of BRAF non-V600 mutations that impair the protein's kinase activity may in fact confer heightened sensitivity to EGFR inhibition because of dependency on upstream receptor tyrosine kinase signaling. This review summarizes the clinical characteristics and targeted therapy approaches for non-V600 BRAF mutant CRCs, speculates on the value of non-V600 BRAF mutations as predictive biomarkers of responsiveness to EGFR inhibitors, and highlights outstanding questions in this emerging area of precision oncology. (C) 2018 by American Society of Clinical Oncology
C1 [Dankner, Matthew] McGill Univ, Montreal, PQ, Canada.
C3 McGill University
RP Dankner, M (corresponding author), McGill Univ, Goodman Canc Res Ctr, 1160 Pine Ave West, Montreal, PQ H3A 1A3, Canada.
EM matthew.dankmer@mail.mcgill.ca
OI Dankner, Matthew/0000-0003-4869-5895
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NR 75
TC 18
Z9 19
U1 0
U2 7
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 NOV 8
PY 2018
VL 2
DI 10.1200/PO.18.00195
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HQ1WY
UT WOS:000462191400001
PM 35135170
OA Bronze
DA 2025-01-04
ER

PT J
AU Zhang, CX
   Fei, YX
   Wang, H
   Hu, S
   Liu, C
   Hu, R
   Du, QM
AF Zhang, Chunxue
   Fei, Yuxiang
   Wang, Hui
   Hu, Sheng
   Liu, Chao
   Hu, Rong
   Du, Qianming
TI CAFs orchestrates tumor immune microenvironment-A new target in cancer
   therapy?
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE tumor microenvironment; cancer-associated fibroblasts; immune cells;
   CAF-targeted therapy; cancer
ID CARCINOMA-ASSOCIATED FIBROBLASTS; MESENCHYMAL STEM-CELLS; REGULATORY
   T-CELLS; PANCREATIC-CANCER; DENDRITIC CELLS; BREAST-CANCER; CLINICAL
   DEVELOPMENT; SUPPRESSOR-CELLS; GROWTH-FACTOR; COLON-CANCER
AB Cancer immunotherapy has opened a new landscape in cancer treatment, however, the poor specificity and resistance of most targeted therapeutics have limited their therapeutic efficacy. In recent years, the role of CAFs in immune regulation has been increasingly noted as more evidence has been uncovered regarding the link between cancer-associated fibroblasts (CAFs) and the evolutionary process of tumor progression. CAFs interact with immune cells to shape the tumor immune microenvironment (TIME) that favors malignant tumor progression, a crosstalk process that leads to the failure of cancer immunotherapies. In this review, we outline recent advances in the immunosuppressive function of CAFs, highlight the mechanisms of CAFs-immune cell interactions, and discuss current CAF-targeted therapeutic strategies for future study.
C1 [Zhang, Chunxue; Wang, Hui] China Pharmaceut Univ, Sch Basic Med & Clin Pharm, Nanjing, Peoples R China.
   [Fei, Yuxiang; Liu, Chao] Nanjing Med Univ, Nanjing Hosp 1, Dept Pharm, Nanjing, Peoples R China.
   [Hu, Sheng] Xinjiang Med Univ, Coll Pharm, Urumqi, Peoples R China.
   [Hu, Rong] China Pharmaceut Univ, Dept Physiol, State Key Lab Nat Med, Nanjing, Jiangsu, Peoples R China.
   [Du, Qianming] Nanjing Med Univ, Nanjing Hosp 1, Gen Clin Res Ctr, Nanjing, Peoples R China.
C3 China Pharmaceutical University; Nanjing Medical University; Xinjiang
   Medical University; China Pharmaceutical University; Nanjing Medical
   University
RP Liu, C (corresponding author), Nanjing Med Univ, Nanjing Hosp 1, Dept Pharm, Nanjing, Peoples R China.; Hu, R (corresponding author), China Pharmaceut Univ, Dept Physiol, State Key Lab Nat Med, Nanjing, Jiangsu, Peoples R China.; Du, QM (corresponding author), Nanjing Med Univ, Nanjing Hosp 1, Gen Clin Res Ctr, Nanjing, Peoples R China.
EM liuchaogermany@sina.cn; ronghu@cpu.edu.cn; duqianming@njmu.edu.cn
RI wang, wei/JBS-7400-2023; WANG, HUI/JFA-9683-2023; hu,
   shengquan/S-8266-2019
FU Natural Science Foundation of China [82172558, 82273971, 82204394];
   Distinguished Young Scholars of Nanjing [JQX20008]
FX This work was supported by the Natural Science Foundation of China (No.
   82172558, 82273971, 82204394), the Distinguished Young Scholars of
   Nanjing (JQX20008).
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NR 191
TC 30
Z9 30
U1 4
U2 16
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 MAR 14
PY 2023
VL 14
AR 1113378
DI 10.3389/fphar.2023.1113378
PG 18
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA C5DV9
UT WOS:000962127500001
PM 37007004
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Quiroz-Reyes, AG
   Islas, JF
   Delgado-Gonzalez, P
   Franco-Villarreal, H
   Garza-Treviño, EN
AF Quiroz-Reyes, Adriana G.
   Islas, Jose F.
   Delgado-Gonzalez, Paulina
   Franco-Villarreal, Hector
   Garza-Trevino, Elsa N.
TI Therapeutic Approaches for Metastases from Colorectal Cancer and
   Pancreatic Ductal Carcinoma
SO PHARMACEUTICS
LA English
DT Review
DE lung metastasis; liver metastasis; cancer stem cells; cancer treatments
   and progression biomarkers
AB Metastasis is the process of dissemination of a tumor, whereby cells from the primary site dislodge and find their way to other tissues where secondary tumors establish. Metastasis is the primary cause of death related to cancer. This process warrants changes in original tumoral cells and their microenvironment to establish a metastatic niche. Traditionally, cancer therapy has focused on metastasis prevention by systematic treatments or direct surgical re-sectioning. However, metastasis can still occur. More recently, new therapies direct their attention to targeting cancer stem cells. As they propose, these cells could be the orchestrators of the metastatic niche. In this review, we describe conventional and novel developments in cancer therapeutics for liver and lung metastasis. We further discuss the resistance mechanisms of targeted therapy, the advantages, and disadvantages of diverse treatment approaches, and future novel strategies to enhance cancer prognosis.
C1 [Quiroz-Reyes, Adriana G.; Islas, Jose F.; Delgado-Gonzalez, Paulina; Garza-Trevino, Elsa N.] Univ Autonoma Nuevo Leon, Sch Med, Biochem & Mol Med Dept, Monterrey 64460, Mexico.
   [Franco-Villarreal, Hector] Althian Clin Res, Monterrey 64000, Mexico.
C3 Universidad Autonoma de Nuevo Leon
RP Garza-Treviño, EN (corresponding author), Univ Autonoma Nuevo Leon, Sch Med, Biochem & Mol Med Dept, Monterrey 64460, Mexico.
EM he.franco@althian.com; jose.islasc@uanl.mx;
   paulina.delgadogn@uanl.edu.mx; dr.hectorfranco@gmail.com;
   elsa.garzatr@uanl.edu.mx
RI Reyes, Adriana/JGL-7369-2023; Islas, Jose Francisco/K-2728-2018
OI Quiroz Reyes, Adriana G./0000-0002-9405-7483; Islas, Jose
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NR 148
TC 9
Z9 10
U1 1
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1999-4923
J9 PHARMACEUTICS
JI Pharmaceutics
PD JAN
PY 2021
VL 13
IS 1
AR 103
DI 10.3390/pharmaceutics13010103
PG 24
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA PW5JU
UT WOS:000610705800001
PM 33466892
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Viswanath, B
   Kim, S
   Lee, K
AF Viswanath, Buddolla
   Kim, Sanghyo
   Lee, Kiyoung
TI Recent insights into nanotechnology development for detection and
   treatment of colorectal cancer
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Review
DE colorectal cancer; nanotechnology; detection; treatment; targeted
   therapy
ID CIRCULATING TUMOR-CELLS; GROWTH-FACTOR RECEPTOR; COLON-CANCER; CHITOSAN
   NANOPARTICLES; PLGA NANOPARTICLES; PERIPHERAL-BLOOD; DRUG-DELIVERY;
   QUANTUM DOTS; CURCUMIN; DENDRIMERS
AB The global incidence of colorectal cancer (CRC) is 1.3 million cases. It is the third most frequent cancer in males and females. Most CRCs are adenocarcinomas and often begin as a polyp on the inner wall of the rectum or colon. Some of these polyps become malignant, eventually. Detecting and removing these polyps in time can prevent CRC. Therefore, early diagnosis of CRC is advantageous for preventive and instant action interventions to decrease the mortality rates. Nanotechnology has been enhancing different methods for the detection and treatment of CRCs, and the research has provided hope within the scientific community for the development of new therapeutic strategies. This review presents the recent development of nanotechnology for the detection and treatment of CRC.
C1 [Viswanath, Buddolla; Kim, Sanghyo] Gachon Univ, Dept Bionanotechnol, San 65, Songnam 461701, Gyeonggi Do, South Korea.
   [Lee, Kiyoung] Gachon Univ, Gil Hosp, Div Endocrinol & Metab, Inchon 405760, South Korea.
C3 Gachon University; Gachon University
RP Kim, S (corresponding author), Gachon Univ, Dept Bionanotechnol, San 65, Songnam 461701, Gyeonggi Do, South Korea.; Lee, K (corresponding author), Gachon Univ, Gil Hosp, Div Endocrinol & Metab, Inchon 405760, South Korea.
EM samkim@gachon.ac.kr; kylee@gilhospital.com
FU R&D Program for Society of the National Research Foundation - Ministry
   of Science, ICT & Future Planning [2013M3C8A3078806, 2015M3A9E2031372]
FX This research was supported by the R&D Program for Society of the
   National Research Foundation funded by the Ministry of Science, ICT &
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NR 70
TC 43
Z9 50
U1 2
U2 23
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 2016
VL 11
BP 2491
EP 2504
DI 10.2147/IJN.S108715
PG 14
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA DN5DL
UT WOS:000377086400001
PM 27330292
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU [Anonymous]
AF [Anonymous]
TI Targeting KRAS<SUP>G12C</SUP>-Mutated Advanced Colorectal Cancer:
   Research and Clinical Developments
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE KRAS(G12C); sotorasib; adagrasib; colorectal cancer; targeted therapy
ID CELL LUNG-CANCER; DABRAFENIB PLUS TRAMETINIB; AMG 510; RAS MUTATIONS;
   OPEN-LABEL; KRAS G12C; INHIBITOR; VEMURAFENIB; CETUXIMAB; EFFICACY
AB Identifying mutations in the KRAS gene has become increasingly important in the treatment of colorectal cancer with many prognostic and therapeutic implications. However, efforts to develop drugs that target KRAS mutations have not been successful until more recently with the introduction of the KRAS(G12C) inhibitors, sotorasib (AMG510) and adagrasib (MRTX849). Both agents have demonstrated safety and promising efficacy in preclinical studies and early phase trials, but it appears that not all tumor types harboring the KRAS(G12C) mutation are sensitive to monotherapy approaches. In particular, patients with colorectal cancer (CRC) derive less benefit compared to those with non-small cell lung cancer (NSCLC), likely due to rapid treatment-induced resistance through increased epidermal growth factor receptor (EGFR) signaling. As a result, combination therapy trials with EGFR inhibitors are currently underway. Here, we will review the available clinical trial data on KRAS(G12C) inhibitors in KRAS(G12C)-mutated CRC, possible mechanisms of resistance to monotherapy, the research studying why available agents are proving to be less efficacious in CRC compared to NSCLC, and future directions for these promising new drugs.
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NR 72
TC 22
Z9 24
U1 1
U2 12
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 2022
VL 15
BP 747
EP 756
DI 10.2147/OTT.S340392
PG 10
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA 2Z1LV
UT WOS:000826348300001
PM 35837349
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Bui, QL
   Mas, L
   Hollebecque, A
   Tougeron, D
   de la Fouchardiere, C
   Pudlarz, T
   Alouani, E
   Guimbaud, R
   Taieb, J
   Andre, T
   Colle, R
   Cohen, R
AF Bui, Quang Loc
   Mas, Leo
   Hollebecque, Antoine
   Tougeron, David
   de la Fouchardiere, Christelle
   Pudlarz, Thomas
   Alouani, Emily
   Guimbaud, Rosine
   Taieb, Julien
   Andre, Thierry
   Colle, Raphael
   Cohen, Romain
TI Treatments after Immune Checkpoint Inhibitors in Patients with dMMR/MSI
   Metastatic Colorectal Cancer
SO CANCERS
LA English
DT Article
DE metastatic colorectal cancer; microsatellite instability; mismatch
   repair deficiency; chemotherapy after immunotherapy
ID MISMATCH REPAIR-DEFICIENT; COLON-CANCER; POOLED ANALYSIS; OPEN-LABEL;
   IMMUNOTHERAPY; CHEMOTHERAPY; PEMBROLIZUMAB; MULTICENTER; EFFICACY;
   THERAPY
AB Simple Summary Several studies suggested an enhanced efficacy of conventional treatments (CT, i.e., chemotherapy +/- targeted therapy) administered after immune checkpoint inhibitors (ICI) in certain tumor types, but no data are available concerning metastatic colorectal cancer (mCRC) patients harboring mismatch repair deficiency/microsatellite instability (dMMR/MSI). The aim of our study was to assess the outcomes of dMMR/MSI mCRC patients receiving CT after ICI failure. We retrospectively collected clinical data from a multicentric cohort of 31 patients. Although limited by the small number of patients, our results did not suggest improved outcomes with CT in our population, and no significant association with previous ICI efficacy or with anti-VEGF agents was evidenced. However, prolonged disease control was observed in several cases, suggesting that some patients might derive an unexpected benefit from post-ICI treatments. With ICI becoming the standard of care in patients newly diagnosed with dMMR/MSI mCRC, these results might help to inform clinical decision-making and to guide future therapeutic strategies for these patients. Background: Several studies reported improved outcomes with conventional treatments (CT, i.e., chemotherapy +/- targeted therapy) administered after immune checkpoints inhibitors (ICI) in certain tumor types. No data are available concerning patients (pts) with metastatic colorectal cancer (mCRC) harboring mismatch repair deficiency/microsatellite instability (dMMR/MSI). We aimed to assess the outcomes of dMMR/MSI mCRC pts receiving CT after ICI failure. Methods: We conducted a retrospective multicenter study investigating the outcomes of all dMMR/MSI mCRC pts who received post-ICI CT between 2015 and 2020. Results: 31 pts (male 61%, median age 56 years) were included. ICI was an anti-PD(L)1 monotherapy in 71% of pts, and 61% received >2 lines before post-ICI CT. The overall response rate and disease control rate were 13% and 45%, with a median progression-free survival (PFS) and overall survival of 2.9 and 7.4 months, respectively. No association of the outcomes with either ICI efficacy or anti-angiogenic agents was observed. Prolonged PFS (range 16.1-21.3 months) was observed in 4 pts (13%). Conclusions: Although conducted on a limited number of patients, our results do not support an association of previous ICI treatment with an enhanced efficacy of CT in dMMR/MSI mCRC. However, prolonged disease control was observed in several cases, suggesting that some pts might derive an unexpected benefit from post-ICI treatments.
C1 [Bui, Quang Loc; Mas, Leo; Pudlarz, Thomas; Andre, Thierry; Colle, Raphael; Cohen, Romain] Sorbonne Univ, Hop Saint Antoine, Assistance Publ Hopitaux Paris AP HP, Dept Med Oncol, F-75012 Paris, France.
   [Bui, Quang Loc] Bach Mai Hosp, Nucl Med & Oncol Ctr, Hanoi 116300, Vietnam.
   [Bui, Quang Loc] Vietnam Natl Univ, Sch Med & Pharm, Hanoi 123105, Vietnam.
   [Hollebecque, Antoine] Saclay Univ Paris, Gustave Roussy, Drug Dev Dept DITEP, F-94800 Villejuif, France.
   [Tougeron, David] Univ Poitiers Hosp, Dept Gastroenterol, F-86000 Poitiers, France.
   [de la Fouchardiere, Christelle] Lyon 1 Univ, Ctr Leon Berard, Med Oncol Dept, F-69008 Lyon, France.
   [Alouani, Emily; Guimbaud, Rosine] CHU Toulouse, IUCT Rangueil Larrey, Digest Med Oncol, F-31059 Toulouse, France.
   [Taieb, Julien] Paris Descartes Univ, Georges Pompidou European Hosp, Dept Digest Oncol, Sorbonne Paris Cite, F-75004 Paris, France.
   [Andre, Thierry; Cohen, Romain] Sorbonne Univ, INSERM, Ctr Rech Saint Antoine,Equipe Labellisee Ligue Na, Equipe Instabilite Microsatellites & Canc,Unite M, F-75012 Paris, France.
C3 Assistance Publique Hopitaux Paris (APHP); Sorbonne Universite; Hopital
   Universitaire Saint-Antoine - APHP; UNICANCER; Gustave Roussy;
   Universite de Poitiers; CHU Poitiers; Universite Claude Bernard Lyon 1;
   UNICANCER; Centre Leon Berard; Universite de Toulouse; Universite
   Toulouse III - Paul Sabatier; CHU de Toulouse; Assistance Publique
   Hopitaux Paris (APHP); Universite Paris Cite; Hopital Universitaire
   Europeen Georges-Pompidou - APHP; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Sorbonne Universite
RP Cohen, R (corresponding author), Sorbonne Univ, Hop Saint Antoine, Assistance Publ Hopitaux Paris AP HP, Dept Med Oncol, F-75012 Paris, France.; Cohen, R (corresponding author), Sorbonne Univ, INSERM, Ctr Rech Saint Antoine,Equipe Labellisee Ligue Na, Equipe Instabilite Microsatellites & Canc,Unite M, F-75012 Paris, France.
EM quangloc.bui.md@gmail.com; leo.mas@aphp.fr;
   antoine.hollebecque@gustaveroussy.fr; david.tougeron@chu-poitiers.fr;
   christelle.delafouchardiere@lyon.unicancer.fr; thomas.pudlarz@aphp.fr;
   emilyalouani@yahoo.fr; guimbaud.r@chu-toulouse.fr; julien.taieb@aphp.fr;
   thierry.andre@aphp.fr; raphael.colle@aphp.fr; romain.cohen@aphp.fr
RI de la Fouchardiere, Christelle/AAW-7887-2021; André,
   Thierry/N-8830-2017; tougeron, david/ABF-3217-2020; Cohen,
   Romain/AAC-9089-2019; Hollebecque, Antoine/M-2695-2013
OI , Emily/0000-0002-2303-118X; Cohen, Romain/0000-0001-9602-5162; DE LA
   FOUCHARDIERE, CHRISTELLE/0000-0003-2291-5693; taieb,
   julien/0000-0002-9955-4753; Hollebecque, Antoine/0000-0003-2869-7551;
   BUI, Quang Loc/0000-0001-5876-5872; tougeron, david/0000-0002-8065-9635;
   Andre, Thierry/0000-0002-5103-7095
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NR 31
TC 10
Z9 10
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 JAN
PY 2022
VL 14
IS 2
AR 406
DI 10.3390/cancers14020406
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZB7JX
UT WOS:000757015200001
PM 35053568
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sharifi-Azad, M
   Fathi, M
   Cho, WC
   Barzegari, A
   Dadashi, H
   Dadashpour, M
   Jahanban-Esfahlan, R
AF Sharifi-Azad, Masoumeh
   Fathi, Marziyeh
   Cho, William C.
   Barzegari, Abolfazl
   Dadashi, Hamed
   Dadashpour, Mehdi
   Jahanban-Esfahlan, Rana
TI Recent advances in targeted drug delivery systems for resistant
   colorectal cancer
SO CANCER CELL INTERNATIONAL
LA English
DT Review
DE Colorectal cancer; Drug delivery; Single cell approaches; Artificial
   intelligence; Exosome; Circulating tumor cells; Cancer stem cells
ID PI3K/AKT SIGNALING PATHWAY; CHROMOSOMAL INSTABILITY;
   CLINICAL-IMPLICATIONS; CELL-MEMBRANES; STEM-CELLS; DOXORUBICIN;
   EXOSOMES; ENHANCE; ACID
AB Colorectal cancer (CRC) is one of the deadliest cancers in the world, the incidences and morality rate are rising and poses an important threat to the public health. It is known that multiple drug resistance (MDR) is one of the major obstacles in CRC treatment. Tumor microenvironment plus genomic instability, tumor derived exosomes (TDE), cancer stem cells (CSCs), circulating tumor cells (CTCs), cell-free DNA (cfDNA), as well as cellular signaling pathways are important issues regarding resistance. Since non-targeted therapy causes toxicity, diverse side effects, and undesired efficacy, targeted therapy with contribution of various carriers has been developed to address the mentioned shortcomings. In this paper the underlying causes of MDR and then various targeting strategies including exosomes, liposomes, hydrogels, cell-based carriers and theranostics which are utilized to overcome therapeutic resistance will be described. We also discuss implication of emerging approaches involving single cell approaches and computer-aided drug delivery with high potential for meeting CRC medical needs.
C1 [Sharifi-Azad, Masoumeh; Dadashi, Hamed; Jahanban-Esfahlan, Rana] Tabriz Univ Med Sci, Fac Adv Med Sci, Dept Med Biotechnol, Tabriz, Iran.
   [Fathi, Marziyeh; Barzegari, Abolfazl] Tabriz Univ Med Sci, Biomed Inst, Res Ctr Pharmaceut Nanotechnol, Tabriz, Iran.
   [Cho, William C.] Queen Elizabeth Hosp, Dept Clin Oncol, Hong Kong, Peoples R China.
   [Dadashpour, Mehdi] Semnan Univ Med Sci, Dept Med Biotechnol, Fac Med, Semnan, Iran.
   [Dadashpour, Mehdi] Semnan Univ Med Sci, Canc Res Ctr, Semnan, Iran.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science; Semnan University of Medical Sciences; Semnan University of
   Medical Sciences
RP Jahanban-Esfahlan, R (corresponding author), Tabriz Univ Med Sci, Fac Adv Med Sci, Dept Med Biotechnol, Tabriz, Iran.; Dadashpour, M (corresponding author), Semnan Univ Med Sci, Dept Med Biotechnol, Fac Med, Semnan, Iran.
EM dadashpourm@semums.ac.ir; jahanbanr@tbzmed.ac.ir
RI Jahanban-Esfahlan, Rana/Y-4861-2018; Dadashpour/O-8273-2019; Dadashi,
   Hamed/AAU-8806-2021; Cho, William/H-7429-2019
OI Dadashi, Hamed/0000-0001-6739-740X; Barzegari,
   Abolfazl/0000-0002-8429-3618
FU Tabriz University of Medical Sciences [68972]
FX RJE is funded by Tabriz University of Medical Sciences, grant number
   68972.
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NR 165
TC 22
Z9 22
U1 1
U2 27
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 MAY 19
PY 2022
VL 22
IS 1
AR 196
DI 10.1186/s12935-022-02605-y
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 1J5RI
UT WOS:000797975600003
PM 35590367
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yang, MH
   Baek, SH
   Ha, IJ
   Um, JY
   Ahn, KS
AF Yang, Min Hee
   Baek, Seung Ho
   Ha, In Jin
   Um, Jae-Young
   Ahn, Kwang Seok
TI Brassinin enhances the anticancer actions of paclitaxel by targeting
   multiple signaling pathways in colorectal cancer cells
SO PHYTOTHERAPY RESEARCH
LA English
DT Article
DE brassinin; colorectal cancer cells; JAKs; STAT3; PI3K; Akt; mTOR
ID TUMOR-GROWTH; INDUCED APOPTOSIS; POTENTIAL ROLE; STAT3; INHIBITION;
   PROLIFERATION; SURVIVAL; TRANSDUCER; ACTIVATION; INDUCTION
AB Brassinin (BSN), a precursor of phytoalexins, extracted from Chinese cabbage has been reported to act as a promising anti-neoplastic agent. However, the effects of BSN on colon cancer cells and its underlying mechanisms have not been fully elucidated. This study aimed at investigating the anti-neoplastic impact of BSN and its possible synergistic effect with paclitaxel on colon cancer cells. The effect of BSN on Janus-activated kinases (JAKs)/signal transducer and activator of transcription 3 (STAT3) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathways and its downstream functions was deciphered using diverse assays in colon carcinoma cells. We found that BSN displayed significant cytotoxic effect and suppressed cell proliferation on colon carcinoma cells. Additionally, it was noted that BSN modulated oncogenic gene expression and induced apoptosis through down regulating multiple oncogenic signaling cascades such as JAKs/STAT3 and PI3K/Akt/mTOR simultaneously. Besides, BSN-paclitaxel combination significantly increased cytotoxicity and induced apoptosis synergistically as compared with individual treatment of both the agents. Overall, our findings indicate that BSN may be a novel candidate for anti-colon cancer targeted therapy.
C1 [Yang, Min Hee; Ahn, Kwang Seok] Kyung Hee Univ, KHU KIST Dept Converging Sci & Technol, Seoul, South Korea.
   [Yang, Min Hee; Um, Jae-Young; Ahn, Kwang Seok] Kyung Hee Univ, Dept Sci Korean Med, Seoul, South Korea.
   [Baek, Seung Ho] Dongguk Univ, Coll Korean Med, Goyang Si, South Korea.
   [Ha, In Jin] Kyung Hee Univ, Korean Med Hosp, Korean Med Clin Trial Ctr K CTC, Seoul, South Korea.
C3 Kyung Hee University; Kyung Hee University; Dongguk University; Kyung
   Hee University; Kyung Hee University Hospital
RP Ahn, KS (corresponding author), Kyung Hee Univ, Dept Korean Pathol, Coll Korean Med, 24 Kyungheedae Ro, Seoul 02447, South Korea.
EM ksahn@khu.ac.kr
OI Ha, In Jin/0000-0002-9210-1401
FU Korean government (MSIP); National Research Foundation of Korea (NRF)
   [2018R1D1A1B07042969, NRF-2017M3A9E4065333]
FX Korean government (MSIP); National Research Foundation of Korea (NRF),
   Grant/Award Numbers: 2018R1D1A1B07042969, NRF-2017M3A9E4065333
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NR 55
TC 16
Z9 19
U1 0
U2 1
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 JUL
PY 2021
VL 35
IS 7
BP 3875
EP 3885
DI 10.1002/ptr.7095
EA APR 2021
PG 11
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA TS8TH
UT WOS:000635639500001
PM 33792984
DA 2025-01-04
ER

PT J
AU Kasperska, A
   Borowczak, J
   Szczerbowski, K
   Stec, E
   Ahmadi, N
   Szylberg, L
AF Kasperska, Anna
   Borowczak, Jedrzej
   Szczerbowski, Krzysztof
   Stec, Ewa
   Ahmadi, Navid
   Szylberg, Lukasz
TI Current Challenges in Targeting Tumor Desmoplasia to Improve the
   Effi-cacy of Immunotherapy
SO CURRENT CANCER DRUG TARGETS
LA English
DT Review
DE Cancer; immunotherapy; desmoplasia; immunoresistance; CXCR-4; PD-L1
ID FIBROBLAST ACTIVATION PROTEIN; CARCINOMA-ASSOCIATED-FIBROBLASTS;
   EPITHELIAL-MESENCHYMAL TRANSITION; BREAST-CANCER CELLS;
   CLINICAL-IMPLICATIONS; STROMAL FIBROBLASTS; COLORECTAL-CANCER;
   PROGNOSTIC ROLE; T-LYMPHOCYTES; THERAPEUTIC TARGET
AB Desmoplasia is crucial for the development, progression and treatment of immune -resistant malignancies. Targeting desmoplasia-related metabolic pathways appears to be an interesting approach to expand our stock of disposable anti-tumor agents. CXCL12/CXCR4 axis inhibition reduces fibrosis, alleviates immunosuppression and significantly enhances the efficacy of PD-1 immunotherapy. CD40L substitute therapy may increase the activity of T-cells, downregulate CD40+, prolong patients' survival and prevent cancer progression. Although FAP alpha antagonists used in preclinical models did not lead to permanent cure, an alleviation of immune-resistance, modification of desmoplasia and a decrease in angiogenesis were observed. Targeting DDR2 may enhance the effect of anti-PD-1 treatment in multiple neoplasm cell lines and has the ability to overcome the adaptation to BRAF-targeted therapy in melanoma. Reprogramming desmoplasia could potentially cooperate not only with present treatment, but also other potential therapeutic targets. We present the most promising metabolic pathways related to desmoplasia and discuss the emerging strategies to improve the efficacy of immunotherapy.
C1 [Kasperska, Anna; Borowczak, Jedrzej; Szczerbowski, Krzysztof; Stec, Ewa; Szylberg, Lukasz] Nicolaus Copernicus Univ, Coll Med Bydgoszcz, Dept Clin Pathomorphol, Torun, Poland.
   [Ahmadi, Navid] Royal Papworth Hosp, Dept Cardiothorac Surg, Cambridge, England.
   [Szylberg, Lukasz] Prof Franciszek Lukaszczyk Mem Hosp, Oncol Ctr, Dept Tumor Pathol & Pathomorphol, Bydgoszcz, Poland.
C3 Nicolaus Copernicus University; Papworth Hospital
RP Szczerbowski, K (corresponding author), Nicolaus Copernicus Univ, Coll Med Bydgoszcz, Dept Clin Pathomorphol, Torun, Poland.
EM szczerbowskikm@gmail.com
RI Borowczak, Jędrzej/ABF-3767-2020; Szylberg, Lukasz/H-1854-2014
OI Ahmadi, Navid/0000-0002-0425-2606; Szczerbowski,
   Krzysztof/0000-0003-0722-7139; Kasperska, Anna/0000-0003-0632-3268;
   Borowczak, Jedrzej/0000-0001-9873-3285; Stec, Ewa/0000-0003-2923-0259;
   Szylberg, Lukasz/0000-0003-1349-5906
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NR 148
TC 0
Z9 0
U1 2
U2 5
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1568-0096
EI 1873-5576
J9 CURR CANCER DRUG TAR
JI Curr. Cancer Drug Targets
PY 2021
VL 21
IS 11
BP 919
EP 931
DI 10.2174/1568009621666210825101456
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YC7DK
UT WOS:000739847800003
PM 34525931
DA 2025-01-04
ER

PT J
AU Koo, S
   Lee, MG
   Sharma, A
   Li, ML
   Zhang, XC
   Pu, KY
   Chi, SG
   Kim, JS
AF Koo, Seyoung
   Lee, Min-Goo
   Sharma, Amit
   Li, Mingle
   Zhang, Xingcai
   Pu, Kanyi
   Chi, Sung-Gil
   Kim, Jong Seung
TI Harnessing GLUT1-Targeted Pro-oxidant Ascorbate for Synergistic
   Phototherapeutics
SO ANGEWANDTE CHEMIE-INTERNATIONAL EDITION
LA English
DT Article
DE Ascorbate; GLUT1; Phototherapeutics; Pro-Oxidant; Targeted Therapy
ID PHOTODYNAMIC THERAPY; VITAMIN-C; DEHYDROASCORBIC ACID; CANCER-CELLS;
   NANOPARTICLES; TRANSPORT; ANTIOXIDANT; OXIDATION; EMISSION
AB Despite extensive efforts to realize effective photodynamic therapy (PDT), there is still a lack of therapeutic approaches concisely structured to mitigate the major obstacles of PDT in clinical applications. Herein, we report a molecular strategy exploiting ascorbate chemistry to enhance the efficacy of PDT in cancer cells overexpressing glucose transporter 1 (GLUT1). AA-EtNBS, a 5-O-substituted ascorbate-photosensitizer (PS) conjugate, undergoes a reversible structural conversion of the ascorbate moiety in the presence of reactive oxygen species (ROS) and glutathione (GSH), thereby promoting its uptake in GLUT1-overexpressed KM12C colon cancer cells and perturbing tumor redox homeostasis, respectively. Due to the unique pro-oxidant role of ascorbate in tumor environments, AA-EtNBS effectively sensitized KM12C cancer cells prior to PS-mediated generation of superoxide radicals under near-infrared (NIR) illumination. AA-EtNBS successfully exhibited GLUT1-targeted synergistic therapeutic efficacy during PDT both in vitro and in vivo. Therefore, this study outlines a promising strategy employing ascorbate both as a targeting unit for GLUT1-overexpressed cancer cells and redox homeostasis destruction agent, thereby enhancing therapeutic responses towards anticancer treatment when used in conjunction with conventional PDT.
C1 [Koo, Seyoung; Li, Mingle; Kim, Jong Seung] Korea Univ, Dept Chem, Seoul 02841, South Korea.
   [Lee, Min-Goo; Chi, Sung-Gil] Korea Univ, Dept Life Sci, Seoul 02841, South Korea.
   [Sharma, Amit] CSIR, Cent Sci Instruments Org, Sect 30C, Chandigarh 160030, India.
   [Zhang, Xingcai] Harvard Univ, John A Paulson Sch Engn & Appl Sci, Cambridge, MA 02138 USA.
   [Zhang, Xingcai] MIT, Sch Engn, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
   [Pu, Kanyi] Nanyang Technol Univ, Sch Chem & Biomed Engn, 70 Nanyang Dr, Singapore 637457, Singapore.
C3 Korea University; Korea University; Council of Scientific & Industrial
   Research (CSIR) - India; CSIR - Central Scientific Instruments
   Organisation (CSIO); Harvard University; Massachusetts Institute of
   Technology (MIT); Nanyang Technological University
RP Kim, JS (corresponding author), Korea Univ, Dept Chem, Seoul 02841, South Korea.; Chi, SG (corresponding author), Korea Univ, Dept Life Sci, Seoul 02841, South Korea.; Pu, KY (corresponding author), Nanyang Technol Univ, Sch Chem & Biomed Engn, 70 Nanyang Dr, Singapore 637457, Singapore.
EM kypu@ntu.edu.sg; chi6302@korea.ac.kr; jongskim@korea.ac.kr
RI Lee, Min/AAS-4636-2020; Kim, Jong Seung/N-4504-2015; zhang,
   xingcai/AAK-8496-2021; Koo, Seyoung/HPC-8129-2023; Li,
   Mingle/AAZ-6369-2020; zhang, xingcai/L-9533-2017; Sharma,
   Amit/F-7316-2018; Pu, Kanyi/F-2957-2010
OI zhang, xingcai/0000-0001-7114-1095; Li, Mingle/0000-0002-0384-9128;
   Sharma, Amit/0000-0003-2815-8208; Pu, Kanyi/0000-0002-8064-6009
FU National Research Foundation of Korea [2018R1A3B1052702,
   NRF-2021R1A2B03002487, NRF-2018R1D1A1B07041512, 2020H1D3A1A02080172];
   Basic Science Research Program [2020R1A6A3A01100558]; 2018 Korea
   University Research Fellow Grant; Department of Biotechnology, New Delhi
   [BT/RLF/Re-entry/59/2018]
FX This work was supported by the National Research Foundation of Korea
   (CRI project no. 2018R1A3B1052702, J.S.K. and NRF-2021R1A2B03002487,
   S.-G.C. and NRF-2018R1D1A1B07041512, M.-G. L and KRF Grant No.
   2020H1D3A1A02080172, M.L.), Basic Science Research Program
   (2020R1A6A3A01100558, S.K.), 2018 Korea University Research Fellow Grant
   (M.-G.L). We are also thankful for the Department of Biotechnology, New
   Delhi (Ramalingaswami Fellowship 2019, Grant No.
   BT/RLF/Re-entry/59/2018, A.S.).
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NR 47
TC 27
Z9 29
U1 10
U2 116
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA POSTFACH 101161, 69451 WEINHEIM, GERMANY
SN 1433-7851
EI 1521-3773
J9 ANGEW CHEM INT EDIT
JI Angew. Chem.-Int. Edit.
PD APR 19
PY 2022
VL 61
IS 17
AR e202110832
DI 10.1002/anie.202110832
EA MAR 2022
PG 9
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA 2T4YO
UT WOS:000763535100001
PM 35142018
DA 2025-01-04
ER

PT J
AU Yin, XJ
   He, ZQ
   Ge, WY
   Zhao, ZH
AF Yin, Xiujuan
   He, Zhenqiang
   Ge, Weiying
   Zhao, Zhenhua
TI Application of aptamer functionalized nanomaterials in targeting
   therapeutics of typical tumors
SO FRONTIERS IN BIOENGINEERING AND BIOTECHNOLOGY
LA English
DT Review
DE aptamer; nanomaterials; targeting therapeutics; tumours; drug delivery
ID GROWTH-FACTOR RECEPTOR; MESOPOROUS SILICA NANOPARTICLES; ADENOCARCINOMA
   IN-VITRO; DRUG-DELIVERY-SYSTEMS; HEPATOCELLULAR-CARCINOMA; COLON-CANCER;
   CO-DELIVERY; PHOTOTHERMAL THERAPY; PANCREATIC-CANCER; DNA APTAMER
AB Cancer is a major cause of human death all over the world. Traditional cancer treatments include surgery, radiotherapy, chemotherapy, immunotherapy, and hormone therapy. Although these conventional treatment methods improve the overall survival rate, there are some problems, such as easy recurrence, poor treatment, and great side effects. Targeted therapy of tumors is a hot research topic at present. Nanomaterials are essential carriers of targeted drug delivery, and nucleic acid aptamers have become one of the most important targets for targeted tumor therapy because of their high stability, high affinity, and high selectivity. At present, aptamer-functionalized nanomaterials (AFNs), which combine the unique selective recognition characteristics of aptamers with the high-loading performance of nanomaterials, have been widely studied in the field of targeted tumor therapy. Based on the reported application of AFNs in the biomedical field, we introduce the characteristics of aptamer and nanomaterials, and the advantages of AFNs first. Then introduce the conventional treatment methods for glioma, oral cancer, lung cancer, breast cancer, liver cancer, colon cancer, pancreatic cancer, ovarian cancer, and prostate cancer, and the application of AFNs in targeted therapy of these tumors. Finally, we discuss the progress and challenges of AFNs in this field.
C1 [Yin, Xiujuan; Zhao, Zhenhua] Shaoxing Peoples Hosp, Dept Radiol, Shaoxing, Peoples R China.
   [Yin, Xiujuan; Zhao, Zhenhua] Key Lab Funct Mol Imaging Tumor & Intervent Diag &, Shaoxing, Peoples R China.
   [He, Zhenqiang] Hebei Univ, Clin Med Coll, Baoding, Peoples R China.
   [He, Zhenqiang; Ge, Weiying] Hebei Univ, Dept Radiol, Affiliated Hosp, Baoding, Peoples R China.
   [Zhao, Zhenhua] Zhejiang Univ, Med Coll, Hangzhou, Peoples R China.
C3 Hebei University; Hebei University; Zhejiang University
RP Zhao, ZH (corresponding author), Shaoxing Peoples Hosp, Dept Radiol, Shaoxing, Peoples R China.; Zhao, ZH (corresponding author), Key Lab Funct Mol Imaging Tumor & Intervent Diag &, Shaoxing, Peoples R China.; Zhao, ZH (corresponding author), Zhejiang Univ, Med Coll, Hangzhou, Peoples R China.
EM zhao2075@163.com
FU Zhejiang Province Public Welfare Technology Application Social
   Development Field Project [LGF20H180008]; Zhejiang Provincial Natural
   Science Foundation General Project [LY16H180006]; Zhejiang Provincial
   Medical and Health Science and Technology Program-Platform Program
   [2019ZD022, 2018KY170]; Zhejiang Health and Health Science and
   Technology Program [2022KY1304]
FX The work was supported by the Zhejiang Province Public Welfare
   Technology Application Social Development Field Project (LGF20H180008),
   Zhejiang Provincial Natural Science Foundation General Project
   (LY16H180006), Zhejiang Provincial Medical and Health Science and
   Technology Program-Platform Program (2019ZD022 and 2018KY170), and the
   Zhejiang Health and Health Science and Technology Program (2022KY1304).
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NR 184
TC 5
Z9 5
U1 17
U2 66
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-4185
J9 FRONT BIOENG BIOTECH
JI Front. Bioeng. Biotechnol.
PD FEB 16
PY 2023
VL 11
AR 1092901
DI 10.3389/fbioe.2023.1092901
PG 24
WC Biotechnology & Applied Microbiology; Engineering, Biomedical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Engineering
GA 9M8BZ
UT WOS:000942449400001
PM 36873354
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Negri, F
   Bottarelli, L
   de'Angelis, GL
   Gnetti, L
AF Negri, Francesca
   Bottarelli, Lorena
   de'Angelis, Gian Luigi
   Gnetti, Letizia
TI KRAS: A Druggable Target in Colon Cancer Patients
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE KRAS oncogene; RAS pathway; colon cancer; targeted therapy; sotorasib;
   adagrasib
ID METASTATIC COLORECTAL-CANCER; CELL LUNG-CANCER; PROTEIN TRANSFERASE
   INHIBITOR; K-RAS MUTATIONS; MUTANT KRAS; ADAGRASIB MRTX849; PHASE IB;
   STAGE-II; MICROSATELLITE INSTABILITY; MONOCLONAL-ANTIBODY
AB Mutations in KRAS are among the most frequent aberrations in cancer, including colon cancer. KRAS direct targeting is daunting due to KRAS protein resistance to small molecule inhibition. Moreover, its elevated affinity to cellular guanosine triphosphate (GTP) has made the design of specific drugs challenging. Indeed, KRAS was considered 'undruggable'. KRASG12C is the most commonly mutated variant of KRAS in non-small cell lung cancer. Currently, the achievements obtained with covalent inhibitors of this variant have given the possibility to assess the best therapeutic approach to KRAS-driven tumors. Mutation-related biochemical assets and the tissue of origin are expected to influence responses to treatment. Further attempts to obtain mutant-specific KRAS (KRASG12C) switch-II covalent inhibitors are ongoing and the results are promising. Drugs targeted to block KRAS effector pathways could be combined with direct KRAS inhibitors, immunotherapy or T cell-targeting approaches in KRAS-mutant tumors. The development of valuable combination regimens will be essential against potential mechanisms of resistance that may arise during treatment.
C1 [Negri, Francesca; de'Angelis, Gian Luigi] Azienda Osped Univ Parma, Gastroenterol & Endoscopy Unit, I-43126 Parma, Italy.
   [Bottarelli, Lorena] Univ Parma, Dept Med & Surg, I-43126 Parma, Italy.
   [Gnetti, Letizia] Azienda Osped Univ Parma, Pathol Unit, I-43126 Parma, Italy.
C3 University of Parma; University Hospital of Parma; University of Parma;
   University of Parma; University Hospital of Parma
RP Negri, F (corresponding author), Azienda Osped Univ Parma, Gastroenterol & Endoscopy Unit, I-43126 Parma, Italy.
EM fnegri@ao.pr.it; lorena.bottarelli@unipr.it;
   gianluigi.deangelis@unipr.it; lgnetti@ao.pr.it
OI Negri, Francesca/0000-0002-5847-3623
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NR 137
TC 22
Z9 22
U1 4
U2 26
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 2022
VL 23
IS 8
AR 4120
DI 10.3390/ijms23084120
PG 21
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 0U9FE
UT WOS:000787950900001
PM 35456940
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Eser, PÖ
   Jänne, PA
AF Eser, Pinar O.
   Janne, Pasi A.
TI TGFβ pathway inhibition in the treatment of non-small cell lung cancer
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE NSCLC; TGF beta; Chemotherapy; Targeted therapy; Immune checkpoint
   blockade; Drug resistance
ID GROWTH-FACTOR-BETA; EPITHELIAL-MESENCHYMAL TRANSITION;
   CARCINOMA-ASSOCIATED-FIBROBLASTS; TUMOR-ASSOCIATED MACROPHAGES; FINGER
   TRANSCRIPTION FACTOR; I KINASE INHIBITOR; DRUG-RESISTANCE; STEM-CELLS;
   CHECKPOINT BLOCKADE; COLORECTAL-CANCER
AB Advanced non-small cell lung cancer (NSCLC) continues to be an incurable family of thoracic malignancies that is chronically managed with chemotherapy, targeted therapy, and immunotherapy. While the discovery of driver oncogenes and the advent of targeted and immunotherapies in the last decade have vastly improved clinical disease management for patients harboring druggable mutations, the mainstay treatment for the majority of NSCLC patients remains cytotoxic chemotherapy. The clinical efficacy of targeted, immune, and cytotoxic therapies is limited by the development of drug resistance. Transforming growth factor beta (TGF beta) signaling, a crucial mediator of embryonic development and peripheral immune tolerance, may be dysregulated in some malignant contexts, including lung cancer, and has been correlated with poor prognosis in advanced cancers. Aberrant upregulation of TGF beta expression In the tumor microenvironment has also been implicated in promoting NSCLC progression and metastasis, as well as driving the development of resistance to cytotoxic, targeted, and immunomodulatory therapeutic interventions. Here, we examine the mechanisms underlying TGF beta-mediated drug resistance in NSCLC, and consider TGF beta as a combinatorial therapeutic intervention to circumvent or delay the development of NSCLC treatment resistance.
C1 [Eser, Pinar O.; Janne, Pasi A.] Dana Farber Canc Inst, Lowe Ctr Thorac Oncol, Boston, MA 02215 USA.
   [Eser, Pinar O.; Janne, Pasi A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
   [Eser, Pinar O.; Janne, Pasi A.] Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 USA.
   [Eser, Pinar O.; Janne, Pasi A.] Harvard Med Sch, Boston, MA USA.
   [Eser, Pinar O.] Harvard Med Sch, Program Biol & Biomed Sci, Boston, MA USA.
   [Janne, Pasi A.] Dana Farber Canc Inst, Belfer Ctr Appl Canc Sci, Boston, MA 02215 USA.
C3 Harvard University; Dana-Farber Cancer Institute; Harvard University;
   Dana-Farber Cancer Institute; Harvard University; Brigham & Women's
   Hospital; Harvard University; Harvard Medical School; Harvard
   University; Harvard Medical School; Harvard University; Dana-Farber
   Cancer Institute
RP Jänne, PA (corresponding author), Dana Farber Canc Inst, 450 Brookline Ave,LC4114, Boston, MA 02215 USA.
EM Pasi_Janne@dfci.harvard.edu
FU Astellas Pharma; AstraZeneca; Daiichi Sankyo; Eli Lilly; Puma
   Biotechnology
FX P.O. Eser has no conflicts of interest to report. P.A. Janne is a
   shareholder of Gatekeeper Pharmaceuticals and LOXO Oncology; reports
   receiving commercial research funding from Astellas Pharma, AstraZeneca,
   Daiichi Sankyo, Eli Lilly, and Puma Biotechnology; is a
   consultant/advisory board member for ACEA Biosciences, Araxes
   Pharmaceuticals, ARIAD Pharmaceuticals, AstraZeneca, Boehringer
   Ingelheim, Chugai Pharmaceuticals, Eli Lilly, Ignyta, LOXO Oncology,
   Merrimack Pharmaceuticals, Pfizer, and Roche/Genentech; and receives
   postmarkeing royalties from a Dana-Farber Cancer Institute owned patent
   on EGFR mutations licensed to Lab Corp.
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NR 258
TC 84
Z9 89
U1 2
U2 52
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 APR
PY 2018
VL 184
BP 112
EP 130
DI 10.1016/j.pharmthera.2017.11.004
PG 19
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA GC0YR
UT WOS:000429504300007
PM 29129643
DA 2025-01-04
ER

PT J
AU Fassan, M
   Scarpa, A
   Remo, A
   De Maglio, G
   Troncone, G
   Marchetti, A
   Doglioni, C
   Ingravallo, G
   Perrone, G
   Parente, P
   Luchini, C
   Mastracci, L
AF Fassan, Matteo
   Scarpa, Aldo
   Remo, Andrea
   De Maglio, Giovanna
   Troncone, Giancarlo
   Marchetti, Antonio
   Doglioni, Claudio
   Ingravallo, Giuseppe
   Perrone, Giuseppe
   Parente, Paola
   Luchini, Claudio
   Mastracci, Luca
TI Current prognostic and predictive biomarkers for gastrointestinal tumors
   in clinical practice
SO PATHOLOGICA
LA English
DT Review
DE prognostic markers; predictive markers; targeted therapy; molecular
   pathology; immunohistochemistry
ID METASTATIC COLORECTAL-CANCER; MISMATCH REPAIR DEFICIENCY;
   EPSTEIN-BARR-VIRUS; OF-AMERICAN-PATHOLOGISTS; HER2 SCORING SYSTEM;
   MICROSATELLITE INSTABILITY; GASTRIC-CANCER; LYNCH-SYNDROME; BRAF
   MUTATION; MOLECULAR CHARACTERIZATION
AB The pathologist emerged in the personalized medicine era as a central actor in the definition of the most adequate diagnostic and therapeutic algorithms. In the last decade, gastrointestinal oncology has seen a significantly increased clinical request for the integration of novel prognostic and predictive biomarkers in histopathological reports. This request couples with the significant contraction of invasive sampling of the disease, thus conferring to the pathologist the role of governor for both proper pathologic characterization and customized processing of the biospecimens. This overview will focus on the most commonly adopted immunohistochemical and molecular biomarkers in the routine clinical characterization of gastrointestinal neoplasms referring to the most recent published recommendations, guidelines and expert opinions.
C1 [Fassan, Matteo] Univ Padua, Dept Med DIMED, Surg Pathol Unit, Padua, Italy.
   [Scarpa, Aldo] Univ Verona, ARC NET Res Ctr, Verona, Italy.
   [Scarpa, Aldo; Luchini, Claudio] Univ & Hosp Trust Verona, Dept Diagnost & Publ Hlth, Sect Pathol, Piazzale LA Scuro 10, I-37134 Verona, VR, Italy.
   [Remo, Andrea] ULSS9 Scaligera, Pathol Unit, Serv Dept, Verona, Italy.
   [De Maglio, Giovanna] Univ Hosp Udine, Dept Pathol, Udine, Italy.
   [Troncone, Giancarlo] Federico II Univ Med Sch Naples, Dept Publ Hlth, Naples, Italy.
   [Marchetti, Antonio] Univ G dAnnunzio, Ctr Predict Mol Med, Ctr Excellence Aging & Translat Med, Chieti, Italy.
   [Doglioni, Claudio] Vita & Salute Univ, Milan, Italy.
   [Doglioni, Claudio] IRCCS, Pancreas Translat & Clin Res Ctr, Pathol Unit, San Raffaele Sci Inst, Milan, Italy.
   [Ingravallo, Giuseppe] Univ Bari Aldo Moro, Dept Emergency & Organ Transplantat, Sect Pathol Anat, Bari, Italy.
   [Perrone, Giuseppe] Campus Biomed Univ, Dept Pathol, Rome, Italy.
   [Parente, Paola] Fdn IRCCS Osped Casa Sollievo Sofferenza, Pathol Unit, San Giovanni Rotondo, FG, Italy.
   [Mastracci, Luca] San Martino IRCCS Hosp, Anat Pathol, Genoa, Italy.
   [Mastracci, Luca] Univ Genoa, Dept Surg Sci & Integrated Diagnost DISC, Anat Pathol, Genoa, Italy.
C3 University of Padua; University of Verona; University of Verona; Azienda
   Ospedaliera Universitaria Integrata Verona; University of Udine;
   University Hospital of Udine; University of Naples Federico II; G
   d'Annunzio University of Chieti-Pescara; Vita-Salute San Raffaele
   University; Vita-Salute San Raffaele University; IRCCS Ospedale San
   Raffaele; Universita degli Studi di Bari Aldo Moro; University Campus
   Bio-Medico - Rome Italy; University of Genoa
RP Luchini, C (corresponding author), Univ & Hosp Trust Verona, Dept Diagnost & Publ Hlth, Sect Pathol, Piazzale LA Scuro 10, I-37134 Verona, VR, Italy.
EM claudio.luchini@univr.it
RI Remo, Andrea/Q-7746-2016; Luchini, Claudio/Q-4922-2016; INGRAVALLO,
   Giuseppe/N-2466-2019; Perrone, Giuseppe/GLR-7098-2022; Mastracci,
   Luca/AAA-6411-2020; Fassan, Matteo/F-5152-2012; Parente,
   Paola/AAY-6963-2020; Scarpa, Aldo/K-6832-2016
OI Fassan, Matteo/0000-0001-6515-5482; Parente, Paola/0000-0003-0591-6723;
   Scarpa, Aldo/0000-0003-1678-739X
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NR 112
TC 39
Z9 39
U1 1
U2 5
PU PACINI EDITORE
PI PISA
PA VIA DELLA GHERARDESCA-ZONA INDUSTRIALE OSPEDALETTO, 56121 PISA, ITALY
SN 0031-2983
EI 1591-951X
J9 PATHOLOGICA
JI Pathologica
PD SEP
PY 2020
VL 112
IS 3
BP 248
EP 259
DI 10.32074/1591-951X-158
PG 12
WC Pathology
WE Emerging Sources Citation Index (ESCI)
SC Pathology
GA PP3EA
UT WOS:000605748200011
PM 33179625
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Reece, M
   Saluja, H
   Hollington, P
   Karapetis, CS
   Vatandoust, S
   Young, GP
   Symonds, EL
AF Reece, Mifanwy
   Saluja, Hariti
   Hollington, Paul
   Karapetis, Christos S.
   Vatandoust, Sina
   Young, Graeme P.
   Symonds, Erin L.
TI The Use of Circulating Tumor DNA to Monitor and Predict Response to
   Treatment in Colorectal Cancer
SO FRONTIERS IN GENETICS
LA English
DT Review
DE circulating tumor DNA (ctDNA); colorectal cancer (CRC); mutation;
   methylation; surgery; chemotherapy
ID CELL-FREE DNA; PHASE-II TRIAL; LIQUID BIOPSY; ACQUIRED-RESISTANCE;
   MUTATION DETECTION; COLON-CANCER; PLASMA DNA; FOLLOW-UP; PIK3CA
   MUTATIONS; KRAS MUTATIONS
AB Background: Colorectal cancer is one of the most common cancers worldwide and has a high mortality rate following disease recurrence. Treatment efficacy is maximized by providing tailored cancer treatment, ideally involving surgical resection and personalized neoadjuvant and adjuvant therapies, including chemotherapy, radiotherapy and increasingly, targeted therapy. Early detection of recurrence or disease progression results in more treatable disease and is essential to improving survival outcomes. Recent advances in the understanding of tumor genetics have resulted in the discovery of circulating tumor DNA (ctDNA). A growing body of evidence supports the use of these sensitive biomarkers in detecting residual disease and diagnosing recurrence as well as enabling targeted and tumor-specific adjuvant therapies. Methods: A literature search in Pubmed was performed to identify all original articles preceding April 2019 that utilize ctDNA for the purpose of monitoring response to colorectal cancer treatment. Results: Ninety-two clinical studies were included. These studies demonstrate that ctDNA is a reliable measure of tumor burden. Studies show the utility of ctDNA in assessing the adequacy of surgical tumor clearance and changes in ctDNA levels reflect response to systemic treatments. ctDNA can be used in the selection of targeted treatments. The reappearance or increase in ctDNA, as well as the emergence of new mutations, correlates with disease recurrence, progression, and resistance to therapy, with ctDNA measurement allowing more sensitive monitoring than currently used clinical tools. Conclusions: ctDNA shows enormous promise as a sensitive biomarker for monitoring response to many treatment modalities and for targeting therapy. Thus, it is emerging as a new way for guiding treatment decisions-initiating, altering, and ceasing treatments, or prompting investigation into the potential for residual disease. However, many potentially useful ctDNA markers are available and more work is needed to determine which are best suited for specific purposes and for improving specific outcomes.
C1 [Reece, Mifanwy; Hollington, Paul] Flinders Med Ctr, Div Surg & Perioperat Med, Colorectal Surg, Bedford Pk, SA, Australia.
   [Saluja, Hariti] Flinders Univ S Australia, Coll Med & Publ Hlth, Dept Med, Bedford Pk, SA, Australia.
   [Saluja, Hariti; Karapetis, Christos S.; Young, Graeme P.; Symonds, Erin L.] Flinders Univ S Australia, Flinders Ctr Innovat Canc, Coll Med & Publ Hlth, Bedford Pk, SA, Australia.
   [Karapetis, Christos S.; Vatandoust, Sina] Flinders Med Ctr, Dept Med Oncol, Bedford Pk, SA, Australia.
   [Symonds, Erin L.] Flinders Med Ctr, Bowel Hlth Serv, Bedford Pk, SA, Australia.
C3 Flinders Medical Centre; Flinders University South Australia; Flinders
   University South Australia; Flinders Medical Centre; Flinders Medical
   Centre
RP Symonds, EL (corresponding author), Flinders Univ S Australia, Flinders Ctr Innovat Canc, Coll Med & Publ Hlth, Bedford Pk, SA, Australia.; Symonds, EL (corresponding author), Flinders Med Ctr, Bowel Hlth Serv, Bedford Pk, SA, Australia.
EM Erin.Symonds@sa.gov.au
OI Young, Graeme/0000-0001-9458-8383; Karapetis,
   Christos/0000-0003-1741-996X; Symonds, Erin/0000-0003-2451-0358;
   Vatandoust, Sina/0000-0002-4815-0994; Hollington,
   Paul/0000-0002-6622-0060
FU Cancer Council SA's Beat Cancer Project; State Government of South
   Australia through the Department of Health; Flinders Medical Centre
   Foundation
FX GY, CK, and ES are recipients of a grant funded by the financial support
   of Cancer Council SA's Beat Cancer Project on behalf of its donors and
   the State Government of South Australia through the Department of Health
   together with the support of the Flinders Medical Centre Foundation, its
   donors and partners.
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NR 132
TC 58
Z9 63
U1 0
U2 18
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD NOV 21
PY 2019
VL 10
AR 1118
DI 10.3389/fgene.2019.01118
PG 25
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA JT8XM
UT WOS:000501266300001
PM 31824558
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xu, T
   Wang, XC
   Wang, ZH
   Deng, T
   Qi, CS
   Liu, D
   Li, YY
   Ji, CC
   Li, J
   Shen, L
AF Xu, Ting
   Wang, Xicheng
   Wang, Zhenghang
   Deng, Ting
   Qi, Changsong
   Liu, Dan
   Li, Yanyan
   Ji, Congcong
   Li, Jian
   Shen, Lin
TI Molecular mechanisms underlying the resistance of BRAF V600E-mutant
   metastatic colorectal cancer to EGFR/BRAF inhibitors
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Article
DE BRAF mutation; colorectal cancer; drug resistance; predictive biomarker;
   targeted therapy
ID ACQUIRED-RESISTANCE; EGFR; MET; RAF; AMPLIFICATION; THERAPY;
   COMBINATIONS; ENCORAFENIB; DABRAFENIB; TRAMETINIB
AB Background: Combinatorial inhibition of epidermal growth factor receptor (EGFR) and BRAF shows remarkable clinical benefits in patients with BRAF V600E-mutant metastatic colorectal cancer (mCRC). However, the tumor may inevitably develop resistance to the targeted therapy, thereby limiting the response rate and durability. This study aimed to determine the genetic alterations associated with intrinsic and acquired resistance to EGFR/BRAF inhibitors in BRAF V600E-mutant mCRC. Methods: Targeted sequencing of 520 cancer-related genes was performed in tumor tissues and in plasma samples collected from patients with BRAF V600E-mutant mCRC, who were treated with EGFR/BRAFx2004;+/- MEK inhibitors, before and after the targeted treatment. Clinical benefit was defined as an objective response or a stable disease lasting longer than the median progression-free survival (PFS). Results: In all, 25 patients with BRAF V600E-mutant mCRC were included in this study. Those with RNF43 mutations (n = 8) were more likely to achieve clinical benefit from EGFR/BRAF inhibitors than those with wild-type RNF43 (87.5% versus 37.5%, p = 0.034). Genetic alterations in receptor tyrosine kinase genes (n = 6) were associated with worse PFS (p = 0.005). Among the 23 patients whose disease progressed after the EGFR/BRAF-targeted therapy, at least one acquired resistance-related mutation was detected in 12 patients. Acquired mutations were most frequently observed in the mitogen-activated protein kinase pathway-related genes (n = 9), including KRAS (G12D and Q61H/R), NRAS (Q61L/R/K and amplification), BRAF (amplification), and MEK1 (K57T). MET amplification and PIK3R1 Q579fs mutation emerged in three patients and one patient, respectively, after disease progression. Conclusion: Multiple genetic alterations are associated with clinical benefits and resistance to EGFR/BRAF inhibitors in BRAF V600E-mutant mCRC. Our findings provide novel insights into strategies for overcoming resistance to EGFR/BRAF inhibitors in patients with BRAF V600E-mutant mCRC.
C1 [Xu, Ting; Wang, Xicheng; Wang, Zhenghang; Qi, Changsong; Liu, Dan; Li, Yanyan; Ji, Congcong; Li, Jian; Shen, Lin] Peking Univ, Canc Hosp & Inst, Key Lab Carcinogenesis & Translat Res, Dept Gastrointestinal Oncol,Minist Educ, 52 Fucheng Rd, Beijing 100142, Peoples R China.
   [Deng, Ting] Tianjin Med Univ Canc Inst & Hosp, Key Lab Canc Prevent & Therapy, Tianjins Clin Res Ctr Canc, Natl Clin Res Ctr Canc, Tianjin, Peoples R China.
C3 Peking University; Tianjin Medical University
RP Li, J; Shen, L (corresponding author), Peking Univ, Canc Hosp & Inst, Key Lab Carcinogenesis & Translat Res, Dept Gastrointestinal Oncol,Minist Educ, 52 Fucheng Rd, Beijing 100142, Peoples R China.
EM oncogene@163.com; linshenpku@163.com
RI Wang, Xicheng/A-3329-2009; 齐, 长松/KHV-6581-2024; wang,
   zongren/AAO-6888-2021; Shen, Lin/JPX-7656-2023; Xu, Ting/AAW-7829-2021;
   Ding, Suling/GZL-5430-2022; Li, YanY/ABC-3649-2020
FU Beijing Xisike Clinical Oncology Research Foundation [Y-Young2020-0516]
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and/or publication of this article: This project
   was supported by Beijing Xisike Clinical Oncology Research Foundation
   [grant number Y-Young2020-0516].
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NR 37
TC 14
Z9 14
U1 0
U2 7
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PD JUN
PY 2022
VL 14
AR 17588359221105022
DI 10.1177/17588359221105022
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2H0PN
UT WOS:000814001300001
PM 35747165
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU He, Y
   Kan, WQ
   Li, YQ
   Hao, Y
   Huang, AL
   Gu, HJ
   Wang, MN
   Wang, QQ
   Chen, JL
   Sun, ZL
   Liu, MY
   Chen, YH
   Yi, ZF
AF He, Yuan
   Kan, Weiqiong
   Li, Yunqi
   Hao, Yun
   Huang, Anling
   Gu, Haijun
   Wang, Minna
   Wang, Qingqing
   Chen, Jinlian
   Sun, Zhenliang
   Liu, Mingyao
   Chen, Yihua
   Yi, Zhengfang
TI A potent and selective small molecule inhibitor of myoferlin attenuates
   colorectal cancer progression
SO CLINICAL AND TRANSLATIONAL MEDICINE
LA English
DT Article
DE colorectal cancer; myoferlin; rab; small molecule inhibitor
ID LOCALIZATION
AB As a pivotal vesicular trafficking protein, Myoferlin (MYOF) has become an attractive target for cancer therapy. However, the roles of MYOF in colorectal cancer invasion remain enigmatic, and MYOF-targeted therapy in this malignancy has not been explored. In the present study, we provided the first functional evidence that MYOF promoted the cell invasion of colorectal cancer. Furthermore, we identified a novel small molecule inhibitor of MYOF (named YQ456) that showed high binding affinity to MYOF (K-D = 37 nM) and excellent anti-invasion capability (IC50 = 110 nM). YQ456 was reported for the first time to interfere with the interactions between MYOF and Ras-associated binding (Rab) proteins at low nanomolar levels. This interference disrupted several vesicle trafficking processes, including lysosomal degradation, exosome secretion, and mitochondrial dynamics. Further, YQ456 exhibited excellent inhibitory effects on the growth and invasiveness of colorectal cancer. As the first attempt, the anticancer efficacy of YQ456 in the patient-derived xenograft (PDX) mouse model indicated that targeting MYOF may serve as a novel and practical therapeutic approach for colorectal cancer.
C1 [He, Yuan; Kan, Weiqiong; Li, Yunqi; Hao, Yun; Huang, Anling; Gu, Haijun; Wang, Minna; Liu, Mingyao; Chen, Yihua; Yi, Zhengfang] East China Normal Univ, Shanghai 200241, Peoples R China.
   [He, Yuan; Kan, Weiqiong; Li, Yunqi; Hao, Yun; Huang, Anling; Gu, Haijun; Wang, Minna; Liu, Mingyao; Chen, Yihua; Yi, Zhengfang] East China Normal Univ, Shanghai Fengxian Dist Cent Hosp, Joint Ctr Translat Med, Shanghai Key Lab Regulatory Biol,Inst Biomed Sci, Shanghai 200241, Peoples R China.
   [He, Yuan; Kan, Weiqiong; Li, Yunqi; Hao, Yun; Huang, Anling; Gu, Haijun; Wang, Minna; Liu, Mingyao; Chen, Yihua; Yi, Zhengfang] East China Normal Univ, Sch Life Sci, 500 Dongchuan Rd, Shanghai 200241, Peoples R China.
   [He, Yuan; Wang, Qingqing; Chen, Jinlian; Sun, Zhenliang; Yi, Zhengfang] Southern Med Univ, Affiliated Fengxian Hosp, Joint Ctr Translat Med, Shanghai 201499, Peoples R China.
C3 East China Normal University; East China Normal University; East China
   Normal University; Southern Medical University - China
RP Liu, MY; Chen, YH; Yi, ZF (corresponding author), East China Normal Univ, Sch Life Sci, 500 Dongchuan Rd, Shanghai 200241, Peoples R China.; Liu, MY; Chen, YH; Yi, ZF (corresponding author), East China Normal Univ, Inst Biomed Sci, 500 Dongchuan Rd, Shanghai 200241, Peoples R China.
EM myliu@bio.ecnu.edu.cn; yhchen@bio.ecnu.edu.cn; zfyi@bio.ecnu.edu.cn
RI Wang, Qingqing/KPA-9705-2024; Chen, Yihua/A-4323-2013
OI Chen, Yihua/0000-0003-1733-7980
FU National Key R&D Program of China [2018YFA0507001, 2015CB910400];
   National Natural Science Foundation of China [82073310, 81773204,
   81973160, 81830083, 81673304, 81872418, 81903098]; China Postdoctoral
   Science Foundation [2018M630417]; Innovation Program of Shanghai
   Municipal Education Commission [2017-01-07-00-05-E00011]; Shenzhen
   Municipal Government of China [KQTD20170810160226082]; Shanghai Natural
   Science Foundation [18ZR1431700]; Outstanding Young Talents in Medical
   and Health Sciences in Shanghai [2017YQ048]; Science and Technology
   Commission of Shanghai Municipality [2017YQ048, 20JC1417900,
   11DZ2260300]; ECNU Construction Fund of Innovation and Entrepreneurship
   Laboratory [4440020201-532300/021]; ECNU Multifunctional Platform for
   innovation [011]
FX National Key R&D Program of China, Grant/Award Numbers: 2018YFA0507001,
   2015CB910400; National Natural Science Foundation of China, Grant/Award
   Numbers: 82073310, 81773204, 81973160, 81830083, 81673304, 81872418,
   81903098; China Postdoctoral Science Foundation, Grant/Award Number:
   2018M630417; Innovation Programof Shanghai Municipal Education
   Commission, Grant/Award Number: 2017-01-07-00-05-E00011; Shenzhen
   MunicipalGovernment of China, Grant/Award Number: KQTD20170810160226082;
   ShanghaiNatural Science Foundation, Grant/Award Number: 18ZR1431700;
   Outstanding YoungTalents in Medical and Health Sciences in Shanghai,
   Grant/AwardNumber: 2017YQ048; Science andTechnology Commission of
   ShanghaiMunicipality, Grant/Award Numbers: 20JC1417900, 11DZ2260300;
   ECNUConstruction Fund of Innovation and Entrepreneurship Laboratory,
   Grant/Award Number: 4440020201-532300/021; ECNU Multifunctional Platform
   for innovation, Grant/Award Number: 011
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NR 42
TC 15
Z9 15
U1 2
U2 25
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 2001-1326
J9 CLIN TRANSL MED
JI Clin. Transl. Med.
PD FEB
PY 2021
VL 11
IS 2
AR e289
DI 10.1002/ctm2.289
PG 21
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA QQ4BW
UT WOS:000624468800006
PM 33634965
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Qin, SK
   Li, J
   Bai, YX
   Deng, YH
   Yang, L
   Xu, RH
   Zhong, HJ
   Chen, ZD
   Pan, HM
   Guo, WJ
   Shu, YQ
   Xu, JM
   Peng, CK
   Chen, Y
   Li, HY
   Wang, N
   Guo, XJ
   Peng, MY
   Fan, SH
   Shen, L
AF Qin, Shukui
   Li, Jin
   Bai, Yuxian
   Deng, Yanhong
   Yang, Lei
   Xu, Rui-Hua
   Zhong, Haijun
   Chen, Zhendong
   Pan, Hongming
   Guo, Weijian
   Shu, Yongqian
   Xu, Jianming
   Peng, Cike
   Chen, Yun
   Li, Hongyan
   Wang, Ning
   Guo, Xiaojun
   Peng, Mengye
   Fan, Songhua
   Shen, Lin
TI Quality-adjusted survival in patients with metastatic colorectal cancer
   treated with fruquintinib in FRESCO trial
SO FUTURE ONCOLOGY
LA English
DT Article
DE fruquintinib; metastatic colorectal cancer; Q-TWiST; quality-adjusted
   life years; VEGF-inhibitor
ID Q-TWIST ANALYSIS; SUPPORTIVE CARE; ADJUVANT THERAPY; PLACEBO PLUS;
   DOUBLE-BLIND; REGORAFENIB
AB Lay abstract
   The objective of the study was to assess the benefit of fruqintinib, a chemotherapy drug for patients with metastatic colorectal cancer (mCRC) who do not respond well to previous chemotherapy. The study considered both the time of survival and the quality of life after patients received fruqintinib. In measuring patients' quality of life, the study assessed the time that was free from cancer symptoms and any severe side effects from treatment. The study used data obtained from a Phase III clinical trial, FRESCO, which included 416 mCRC patients receiving fruqintinib or placebo. The results showed that fruqintinib significantly extended patients' symptom-free and side effects-free survival time by approximately 2 months and 5 days. Fruqintinib was 16.7-39.9% more effective than placebo in extending mCRC patients' high-quality life, regardless of prior targeted therapy.
   Aim: To assess whether the survival benefit of fruquintinib is quality-adjusted. Materials & methods: Data of 416 metastatic colorectal cancer patients from the Phase III FRESCO trial were used. The Quality-adjusted Time Without Symptoms or Toxicity (Q-TWiST) analysis assessed the quality-adjusted survival benefit of fruquintinib versus placebo, accounting for freedom from symptomatic disease and from severe side effects of treatment. Results: Fruquintinib significantly improved patients' Q-TWiST (difference: 2.23 [1.41, 3.04] months) versus placebo. The Q-TWiST gain was 28.3% in the base case and ranged from 16.7 to 39.9% in the threshold analysis, favoring fruquintinib. The Q-TWiST benefit was observed in fruquintinib-treated patients regardless of prior targeted therapy. Conclusion: Fruquintinib provides a clinically meaningful quality-adjusted survival benefit versus placebo as a third-line treatment for metastatic colorectal cancer patients.
C1 [Qin, Shukui] Jinling Hosp, Dept Med Oncol, Ctr Canc, Nanjing 210029, Peoples R China.
   [Li, Jin] Tongji Univ, Dept Med Oncol, East Hosp, Shanghai 200120, Peoples R China.
   [Bai, Yuxian] Harbin Med Univ, Dept Med Oncol, Canc Hosp, Harbin 120081, Peoples R China.
   [Deng, Yanhong] Sun Yat Sen Univ, Hosp 6, Dept Med Oncol, Guangzhou 510655, Peoples R China.
   [Yang, Lei] Nantong Tumor Hosp, Dept Med Oncol, Nantong 226361, Peoples R China.
   [Xu, Rui-Hua] Sun Yat Sen Univ, Dept Med Oncol, Guangzhou 510080, Peoples R China.
   [Zhong, Haijun] Zhejiang Canc Hosp, Dept Med Oncol, Hangzhou 310022, Peoples R China.
   [Chen, Zhendong] Anhui Med Univ, Dept Med Oncol, Hosp 2, Hefei 230601, Peoples R China.
   [Pan, Hongming] Sir Run Run Shaw Hosp, Dept Med Oncol, Hangzhou 310020, Peoples R China.
   [Guo, Weijian] Fudan Univ, Shanghai Canc Ctr, Shanghai Med Coll, Dept Med Oncol, Shanghai 200032, Peoples R China.
   [Shu, Yongqian] Jiangsu Prov Hosp, Dept Med Oncol, Nanjing 210029, Peoples R China.
   [Xu, Jianming] 307th Hosp Chinese PLA, Affiliated Hosp Mil Med Sci, Dept Med Oncol, Beijing 100071, Peoples R China.
   [Peng, Cike; Chen, Yun; Li, Hongyan; Wang, Ning] Eli Lilly & Co China Affiliate, Lilly China Drug Dev & Med Affairs Ctr, Shanghai 200041, Peoples R China.
   [Guo, Xiaojun; Peng, Mengye; Fan, Songhua] Hutchison MediPharma Ltd, Shanghai 201203, Peoples R China.
   [Shen, Lin] Peking Univ, Dept Gastrointestinal Oncol, Key Lab Carcinogenesis & Translat Res, Minist Educ,Canc Hosp & Inst, Beijing 100048, Peoples R China.
C3 Tongji University; Harbin Medical University; Sun Yat Sen University;
   Sun Yat Sen University; Zhejiang Cancer Hospital; Anhui Medical
   University; Zhejiang University; Fudan University; Nanjing Medical
   University; Peking University
RP Shen, L (corresponding author), Peking Univ, Dept Gastrointestinal Oncol, Key Lab Carcinogenesis & Translat Res, Minist Educ,Canc Hosp & Inst, Beijing 100048, Peoples R China.
EM linshenpku@163.com
RI Liu, Wen-Yang/GZM-3215-2022; Shen, Lin/JPX-7656-2023; Peng,
   Cike/JOJ-9513-2023; Xu, Jianming/KWU-3367-2024; Shu,
   Yongqian/ABD-5698-2021; Li, Jinluan/HTO-3028-2023; Xu,
   Rui-Hua/AAW-4766-2021
OI Xu, Rui-Hua/0000-0001-9771-8534; Peng, Cike/0000-0002-1904-8077
FU Eli Lilly and Company China Affiliate; Lilly China Drug Development and
   Medical Affairs Center; Lilly China Drug Development; Medical Affairs
   Center
FX The study was funded by Eli Lilly and Company China Affiliate, Lilly
   China Drug Development and Medical Affairs Center. C.P., Y.C., H.L, and
   N.W. were employees of Eli Lilly and Company China Affiliate, Lilly
   China Drug Development and Medical Affairs Center at the time of the
   study; X.G., M.P., and S.F. were employees of Hutchison MediPharma Ltd.
   at the time of the study; other authors declared no potential conflict
   of interest. 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 24
TC 3
Z9 4
U1 0
U2 11
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 MAY
PY 2021
VL 17
IS 15
BP 1923
EP 1931
DI 10.2217/fon-2020-1215
EA FEB 2021
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RN9IH
UT WOS:000616539800001
PM 33563040
DA 2025-01-04
ER

PT J
AU Gomes, SE
   Pereira, DM
   Roma-Rodrigues, C
   Fernandes, AR
   Borralho, PM
   Rodrigues, CMP
AF Gomes, Sofia E.
   Pereira, Diane M.
   Roma-Rodrigues, Catarina
   Fernandes, Alexandra R.
   Borralho, Pedro M.
   Rodrigues, Cecilia M. P.
TI Convergence of miR-143 overexpression, oxidative stress and cell death
   in HCT116 human colon cancer cells
SO PLOS ONE
LA English
DT Article
ID COLORECTAL-CANCER; SUPEROXIDE-DISMUTASE-1 SOD1; DOWN-REGULATION;
   TUMOR-GROWTH; MICRORNAS; DYSREGULATION; ANGIOGENESIS; TARGETS; RNA;
   TUMORIGENESIS
AB MicroRNAs (miRNAs) regulate a wide variety of biological processes, including tumourigenesis. Altered miRNA expression is associated with deregulation of signalling pathways, which in turn cause abnormal cell growth and de-differentiation, contributing to cancer. miR-143 and miR-145 are anti-tumourigenic and influence the sensitivity of tumour cells to chemotherapy and targeted therapy. Comparative proteomic analysis was performed in HCT116 human colon cancer cells stably transduced with miR-143 or miR-145 compared to Empty control cells. Further, Gene Ontology and pathway enrichment analysis indicated that proteins involved in specific cell signalling pathways such as cell death, response to oxidative stress, and protein folding might be modulated by these miRNAs. In particular, antioxidant enzyme superoxide dismutase 1 (SOD1) was downregulated by stable expression of either miR-143 or miR-145. Further, SOD1 gain-of-function experiments rescued cells from miR-143-induced oxidative stress. Moreover, miR-143 overexpression increased oxaliplatin-induced apoptosis associated with reactive oxygen species generation, which was abrogated by genetic and pharmacological inhibition of oxidative stress. Overall, miR-143 might circumvent resistance of colon cancer cells to oxaliplatin via increased oxidative stress in HCT116 human colon cancer cells.
C1 [Gomes, Sofia E.; Pereira, Diane M.; Borralho, Pedro M.; Rodrigues, Cecilia M. P.] Univ Lisbon, Fac Pharm, Res Inst Med iMed ULisboa, Lisbon, Portugal.
   [Roma-Rodrigues, Catarina; Fernandes, Alexandra R.] Univ Nova Lisboa, Fac Sci & Technol, Dept Ciencias Vida, UCIBIO, Caparica, Portugal.
C3 Universidade de Lisboa; Universidade Nova de Lisboa
RP Rodrigues, CMP (corresponding author), Univ Lisbon, Fac Pharm, Res Inst Med iMed ULisboa, Lisbon, Portugal.; Fernandes, AR (corresponding author), Univ Nova Lisboa, Fac Sci & Technol, Dept Ciencias Vida, UCIBIO, Caparica, Portugal.
EM ma.fernandes@fct.unl.pt; cmprodrigues@ff.ulisboa.pt
RI Borralho, Pedro/AAJ-2829-2021; gomes, sofia/I-9436-2016; Fernandes,
   Alexandra/C-7465-2011; Pereira Rodrigues, Cecilia Maria/M-3572-2013;
   Roma-Rodrigues, Catarina/S-6144-2016; Pereira, Diane/L-5220-2013;
   Borralho, Pedro/C-2727-2011
OI Fernandes, Alexandra/0000-0003-2054-4438; Pereira Rodrigues, Cecilia
   Maria/0000-0002-4829-754X; Roma-Rodrigues, Catarina/0000-0002-8676-6562;
   Pereira, Diane/0000-0002-4151-4775; Borralho, Pedro/0000-0003-4488-7240
FU European Structural and Investment Funds through the COMPETE Programme
   [SAICTPAC/0019/2015]; National Funds through Fundacao para a Ciencia e a
   Tecnologia (FCT); FEDER [POCI-01-0145-FEDER-007728]; FCT
   [UID/DTP/04138/2013, UID/Multi/04378/2013, SFRH/BD/88619/2012,
   SFRH/BD/96517/2013]; Fundação para a Ciência e a Tecnologia
   [SFRH/BD/96517/2013, SFRH/BD/88619/2012] Funding Source: FCT
FX This work was supported by Programme grant SAICTPAC/0019/2015 funded by
   European Structural and Investment Funds through the COMPETE Programme
   and by National Funds through Fundacao para a Ciencia e a Tecnologia
   (FCT, http://www.fct.pt) (CMPR), iMed.ULisboa funded by FCT
   (UID/DTP/04138/2013) (CR), UCIBIO funded by FCT (UID/Multi/04378/2013)
   (ARF) and co-funded by FEDER under PT2020 Partnership Agreement
   POCI-01-0145-FEDER-007728, and fellowships SFRH/BD/88619/2012 (SEG) and
   SFRH/BD/96517/2013 (DMP) from FCT. 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 54
TC 35
Z9 42
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 JAN 23
PY 2018
VL 13
IS 1
AR e0191607
DI 10.1371/journal.pone.0191607
PG 19
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA FT4YS
UT WOS:000423161800040
PM 29360852
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Fischer, S
   Gillessen, S
   Rothermundt, C
AF Fischer, Stefanie
   Gillessen, Silke
   Rothermundt, Christian
TI 3 Sequence of treatment in locally advanced and metastatic renal cell
   carcinoma
SO TRANSLATIONAL ANDROLOGY AND UROLOGY
LA English
DT Review
DE Algorithms; carcinoma; renal cell; molecular targeted therapy
ID ADVANCED COLORECTAL-CANCER; TYROSINE KINASE INHIBITORS; PROGRESSION-FREE
   SURVIVAL; HIGH-DOSE INTERLEUKIN-2; CHOI RESPONSE CRITERIA; BLIND
   PHASE-III; INTERFERON-ALPHA; TARGETED THERAPY; PROSTATE-CANCER;
   COMBINATION CHEMOTHERAPY
AB The spectrum of drugs that have shown activity in advanced or metastatic renal cell carcinoma (RCC) has led to a debate on the optimal sequence of treatments. There is agreement on recommending targeted agents as the standard of care in this disease. Uncertainty, however, remains on the best first-line drug choice. Physicians and patients may select sunitinib, bevacizumab in combination with interferon-alpha (IFN-alpha), pazopanib, or-in poor risk patients-temsirolimus. There are also a variety of therapies with proven efficacy on hand in the second-line setting: sorafenib, pazopanib, axitinib, and everolimus. While most randomized RCC trials assessed progression free survival (PFS) as primary endpoint, some agents were shown to improve median overall survival (OS), and given in sequence they have extended the life expectancy of RCC patients from 13 months in the cytokine era to over 30 months. Despite the progress made, there are sobering aspects to the oncologic success story in RCC, as the new treatments do not obtain an objective response or disease stabilization (SD) in all patients. There are also as yet no predictors to select patients who might benefit and those who are primary resistant to specific drugs, and ultimately almost all patients will experience disease progression. Bearing inevitable treatment failure in mind, availability of further drugs and switching therapy while the patient is in a condition to continue pharmacotherapy is essential. Of note, depending on the setting, only 33-59% of patients receive second-line treatment. In this review we present data on first-, second-, and third-line treatment in RCC, and discuss the difficulties in their interpretation in the context of treatment sequence. We summarize biological aspects and discuss mechanisms of resistance to anti-angiogenic therapy and their implications for treatment selection.
C1 [Fischer, Stefanie; Gillessen, Silke; Rothermundt, Christian] Kantonsspital St Gallen, Div Oncol Haematol, Rorschacherstrasse 95,9007 St, St Gallen, Switzerland.
C3 Kantonsspital St. Gallen
RP Rothermundt, C (corresponding author), Kantonsspital St Gallen, Div Oncol Haematol, Rorschacherstrasse 95,9007 St, St Gallen, Switzerland.
EM christian.rothermundt@kssg.ch
RI ; Gillessen, Silke/C-6093-2019
OI Rothermundt, Christian/0000-0002-2104-7794; Gillessen,
   Silke/0000-0001-5746-6555
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NR 126
TC 19
Z9 20
U1 0
U2 2
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2223-4683
EI 2223-4691
J9 TRANSL ANDROL UROL
JI Transl. Androl. Urol.
PD JUN
PY 2015
VL 4
IS 3
BP 310
EP 325
DI 10.3978/j.issn.2223-4683.2015.04.07
PG 16
WC Andrology; Urology & Nephrology
WE Emerging Sources Citation Index (ESCI)
SC Endocrinology & Metabolism; Urology & Nephrology
GA V5R7B
UT WOS:000219877800009
PM 26816832
DA 2025-01-04
ER

PT J
AU Aziz, MA
   Yousef, Z
   Saleh, AM
   Mohammad, S
   Al Knawy, B
AF Aziz, Mohammad Azhar
   Yousef, Zeyad
   Saleh, Ayman M.
   Mohammad, Sameer
   Al Knawy, Bandar
TI Towards personalized medicine of colorectal cancer
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Colorectal cancer; Personalized medicine; Genomics; Transcriptomics;
   Proteomics; Metabolomics
ID SURGICAL ADJUVANT BREAST; III COLON-CANCER; MICROSATELLITE INSTABILITY;
   MOLECULAR SUBTYPES; PIK3CA MUTATIONS; TARGETED THERAPY; STAGE-II; RISK;
   FLUOROURACIL; KRAS
AB Efforts in colorectal cancer (CRC) research aim to improve early detection and treatment for metastatic stages which could translate into better prognosis of this disease. One of the major challenges that hinder these efforts is the heterogeneous nature of CRC and involvement of diverse molecular pathways. New large-scale 'omics' technologies are making it possible to generate, analyze and interpret biological data from molecular determinants of CRC. The developments of sophisticated computational analyses would allow information from different omics platforms to be integrated, thus providing new insights into the biology of CRC. Together, these technological advances and an improved mechanistic understanding might allow CRC to be clinically managed at the level of the individual patient. This review provides an account of the current challenges in CRC management and an insight into how new technologies could allow the development of personalized medicine for CRC.
C1 [Aziz, Mohammad Azhar] King Saud Bin Abdulaziz Univ Hlth Sci, KAIMRC, Colorectal Canc Res Program, Natl Guard Hlth Affairs, POB 22490, Riyadh 11426, Saudi Arabia.
   [Yousef, Zeyad] King Saud Bin Abdulaziz Univ Hlth Sci, KAIMRC, Dept Surg, Natl Guard Hlth Affairs, POB 22490, Riyadh 11426, Saudi Arabia.
   [Saleh, Ayman M.] King Saud Bin Abdulaziz Univ Hlth Sci, Dept Clin Lab Sci, Coll Appl Med Sci, King Abdulaziz Med City,Natl Guard Hlth Affairs, Mail Code 6610,POB 9515, Jeddah 21423, Saudi Arabia.
   [Saleh, Ayman M.] KAIMRC, King Abdulaziz Med City, Natl Guard Hlth Affairs, POB 9515, Jeddah 21423, Saudi Arabia.
   [Mohammad, Sameer] King Saud Bin Abdulaziz Univ Hlth Sci, KAIMRC, Dept Expt Med, Natl Guard Hlth Affairs, POB 22490, Riyadh 11426, Saudi Arabia.
   [Al Knawy, Bandar] King Saud Bin Abdulaziz Univ Hlth Sci, KAIMRC, Off Chief Execut Officer, Natl Guard Hlth Affairs, POB 22490, Riyadh 11426, Saudi Arabia.
C3 King Saud Bin Abdulaziz University for Health Sciences; King Abdullah
   International Medical Research Center (KAIMRC); Ministry of National
   Guard - Health Affairs; King Saud Bin Abdulaziz University for Health
   Sciences; Ministry of National Guard - Health Affairs; King Abdullah
   International Medical Research Center (KAIMRC); King Saud Bin Abdulaziz
   University for Health Sciences; Ministry of National Guard - Health
   Affairs; King Saud Bin Abdulaziz University for Health Sciences; King
   Abdullah International Medical Research Center (KAIMRC); Ministry of
   National Guard - Health Affairs; King Saud Bin Abdulaziz University for
   Health Sciences; Ministry of National Guard - Health Affairs; King
   Abdullah International Medical Research Center (KAIMRC); King Saud Bin
   Abdulaziz University for Health Sciences; Ministry of National Guard -
   Health Affairs; King Abdullah International Medical Research Center
   (KAIMRC)
RP Aziz, MA (corresponding author), King Saud Bin Abdulaziz Univ Hlth Sci, KAIMRC, King Abdulaziz Med City, Minist Natl Guard Hlth Affairs, POB 22490, Riyadh 11426, Saudi Arabia.
EM azizmo@ngha.med.sa; yousefz@ngha.med.sa; salehay@ngha.med.sa;
   mohammadsa1@ngha.med.sa; knawyb@ngha.med.sa
RI Aziz, Mohammad/F-7486-2013; Alwasel, Saleh/AAD-4023-2019; Mohammad,
   Sameer/GWV-2875-2022
OI Saleh, Ayman M/0000-0003-1126-6018; AZIZ, MOHAMMAD/0000-0002-0798-5063;
   Mohammad, Sameer/0000-0002-1129-7685; Alknawy,
   Bandar/0000-0002-4552-9683
FU King Abdullah International Medical Research Center [KAIMRC] [RC10/083];
   King Abdul Aziz City for Science and Technology [KACST] in Riyadh, Saudi
   Arabia [M-S-20-36]
FX This project is supported by a research grant awarded to MAA [Grant
   number RC10/083] by King Abdullah International Medical Research Center
   [KAIMRC] and [M-S-20-36] by King Abdul Aziz City for Science and
   Technology [KACST] in Riyadh, Saudi Arabia.
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NR 116
TC 33
Z9 34
U1 0
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD OCT
PY 2017
VL 118
BP 70
EP 78
DI 10.1016/j.critrevonc.2017.08.007
PG 9
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA FJ3HD
UT WOS:000412620400008
PM 28917272
DA 2025-01-04
ER

PT J
AU Beckman, RA
   Loeb, LA
AF Beckman, Robert A.
   Loeb, Lawrence A.
TI Evolutionary dynamics and significance of multiple subclonal mutations
   in cancer
SO DNA REPAIR
LA English
DT Review
DE Cancer; Mutator hypothesis; DNA replication; DNA repair; Carcinogenesis;
   Evolutionary dynamics; Duplex sequencing; Mathematical models
ID GENETIC INSTABILITY; SOMATIC MUTATIONS; MUTATOR PHENOTYPE;
   DNA-REPLICATION; COLON-CANCER; REPAIR; MODEL; 8-HYDROXYGUANINE;
   CARCINOGENESIS; IDENTIFICATION
AB For the last 40 years the authors have collaborated on trying to understand the complexities of human cancer by formulating testable mathematical models that are based on mutation accumulation in human malignancies. We summarize the concepts encompassed by multiple mutations in human cancers in the context of source, accumulation during carcinogenesis and tumor progression, and therapeutic consequences. We conclude that the efficacious treatment of human cancer by targeted therapy will involve individualized, uniquely directed specific agents singly and in simultaneous combinations, and take into account the importance of targeting resistant subclonal mutations, particularly those subclones with alterations in DNA repair genes, DNA polymerase, and other genes required to maintain genetic stability.
C1 [Beckman, Robert A.] Georgetown Univ, Med Ctr, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC 20007 USA.
   [Beckman, Robert A.] Georgetown Univ, Med Ctr, Lombardi Comprehens Canc Ctr, Dept Biostat Bioinfonnat & Biomath, Washington, DC 20007 USA.
   [Loeb, Lawrence A.] Georgetown Univ, Med Ctr, Innovat Ctr Biomed Informat, Washington, DC 20007 USA.
   [Loeb, Lawrence A.] Univ Washington, Sch Med, Joseph Gottstein Mem Canc Res Lab, Dept Pathol, Seattle, WA 98195 USA.
   [Loeb, Lawrence A.] Univ Washington, Sch Med, Joseph Gottstein Mem Canc Res Lab, Dept Biochem, Seattle, WA 98195 USA.
C3 Georgetown University; Georgetown University; Georgetown University;
   University of Washington; University of Washington Seattle; University
   of Washington; University of Washington Seattle
RP Loeb, LA (corresponding author), Georgetown Univ, Med Ctr, Innovat Ctr Biomed Informat, Washington, DC 20007 USA.; Loeb, LA (corresponding author), Univ Washington, Sch Med, Joseph Gottstein Mem Canc Res Lab, Dept Pathol, Seattle, WA 98195 USA.; Loeb, LA (corresponding author), Univ Washington, Sch Med, Joseph Gottstein Mem Canc Res Lab, Dept Biochem, Seattle, WA 98195 USA.
EM laaloeb@gmail.com
FU National Institute of Health [NCI P01-CA77852, NCI R01-CA160674, NCI
   R01-CA102029]
FX Supported by the National Institute of Health under award numbers NCI
   P01-CA77852, NCI R01-CA160674 and NCI R01-CA102029 (to L.A.L.). We thank
   J. Shen, A. Kamath-Loeb and M. Blair for comments and editing.
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NR 79
TC 12
Z9 15
U1 0
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
EI 1568-7856
J9 DNA REPAIR
JI DNA Repair
PD AUG
PY 2017
VL 56
SI SI
BP 7
EP 15
DI 10.1016/j.dnarep.2017.06.002
PG 9
WC Genetics & Heredity; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Toxicology
GA FD6TX
UT WOS:000407661900002
PM 28652129
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Li, JX
   Cai, Y
   Deng, YH
AF Li, Jianxia
   Cai, Yue
   Deng, Yanhong
TI Selection of Oral Therapeutics in China for the Treatment of Colorectal
   Cancer
SO CURRENT TREATMENT OPTIONS IN ONCOLOGY
LA English
DT Review
DE Colorectal cancer; Oral therapy; Antiangiogenetic tyrosine kinase
   inhibitor; Epidermal growth factor receptor tyrosine kinase inhibitor;
   BRAF inhibitor; MEK inhibitor; Modified fluoropyrimidine
ID PHASE-II TRIAL; FLUOROURACIL PLUS LEUCOVORIN; OPEN-LABEL; DOUBLE-BLIND;
   1ST-LINE TREATMENT; NON-INFERIORITY; COMBINED BRAF; TAS-102 MONOTHERAPY;
   RANDOMIZED-TRIAL; TUMOR LOCATION
AB Opinion statement Intravenous administration of fluoropyrimidine-based chemotherapy has been the backbone of treatment in colorectal cancer (CRC) for decades. The availability of oral capecitabine has improved the tolerability and simplified combination schedules. In addition to capecitabine, several other oral drugs have proven efficacy, particularly in palliative treatment lines. Clinical guidelines describe several available third-line treatment options for metastatic CRC (mCRC), but few insights are provided to guide the selection and sequence. In this review, we describe the available evidence and most recent data concerning oral drugs with proven efficacy in CRC, including antiangiogenetic tyrosine kinase inhibitors (VEGFR TKIs), inhibitors blocking EGFR/Raf/MEK/ERK signaling pathway and modified fluoropyrimidine, and share recommendations and insights on selecting third-line oral therapies for mCRC in China. In general, third-line treatment options for mCRC are mainly regorafenib, fruquintinib, and chemo/targeted therapy reintroduction, while FTD/TPI was rarely used in China probably due to poor accessibility. Fruquintinib is preferred in patients with poor performance status (PS), elder age, and severe organ dysfunction, compared to regorafenib. New drugs of clinical trials were more recommended for the patients with BRAF mutant tumor, and those with good previous treatment efficacy tended to be recommended for chemo/targeted therapy reintroduction. The management of mCRC is evolving, and it must be emphasized that the consideration and recommendations presented here reflect current treatment practices in China and thus might change according to new clinical data as well as the availability of new oral drugs.
C1 [Li, Jianxia; Cai, Yue; Deng, Yanhong] Sun Yat Sen Univ, Dept Med Oncol, Affiliated Hosp 6, Guangdong Prov Key Lab Colorectal & Pelv Floor Di, Guangzhou 510655, Guangdong, Peoples R China.
C3 Sun Yat Sen University
RP Deng, YH (corresponding author), Sun Yat Sen Univ, Dept Med Oncol, Affiliated Hosp 6, Guangdong Prov Key Lab Colorectal & Pelv Floor Di, Guangzhou 510655, Guangdong, Peoples R China.
EM dengyanh@mail.sysu.edu.cn
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NR 100
TC 7
Z9 7
U1 0
U2 11
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1527-2729
EI 1534-6277
J9 CURR TREAT OPTION ON
JI Curr. Treat. Options Oncol.
PD JUL
PY 2021
VL 22
IS 7
AR 55
DI 10.1007/s11864-021-00852-1
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA SO1OY
UT WOS:000658750100003
PM 34097129
DA 2025-01-04
ER

PT J
AU Levati, L
   Bassi, C
   Mastroeni, S
   Lupini, L
   Cappellini, GCA
   Bonmassar, L
   Alvino, E
   Caporali, S
   Lacal, PM
   Narducci, MG
   Molineris, I
   De Galitiis, F
   Negrini, M
   Russo, G
   D'Atri, S
AF Levati, Lauretta
   Bassi, Cristian
   Mastroeni, Simona
   Lupini, Laura
   Cappellini, Gian Carlo Antonini
   Bonmassar, Laura
   Alvino, Ester
   Caporali, Simona
   Lacal, Pedro Miguel
   Narducci, Maria Grazia
   Molineris, Ivan
   De Galitiis, Federica
   Negrini, Massimo
   Russo, Giandomenico
   D'Atri, Stefania
TI Circulating miR-1246 and miR-485-3p as Promising Biomarkers of Clinical
   Response and Outcome in Melanoma Patients Treated with Targeted Therapy
SO CANCERS
LA English
DT Article
DE circulating miRNAs; melanoma; BRAF inhibitors; MEK inhibitors;
   resistance
ID OPERATING CHARACTERISTIC ANALYSIS; TO-MESENCHYMAL TRANSITION;
   CELL-PROLIFERATION; MICRORNA EXPRESSION; COLORECTAL-CANCER; RESISTANCE;
   PROGRESSION; METASTASIS; MIGRATION; INVASION
AB Simple Summary Several therapeutic options exist for patients with advanced BRAF-mutant melanoma. Biomarkers able to identify patients with refractory disease or with poor progression-free survival (PFS) and overall survival (OS) expectancy with respect to specific treatments might allow a more personalized therapeutic approach. Here, we profiled plasma miRNAs at baseline and at progression in patients treated with BRAF inhibitors (BRAFi) or BRAFi + MEKi. Selected miRNAs associated with response to therapy were subjected to validation by real-time quantitative RT-PCR. Receiver Operating Characteristics (ROC), Kaplan-Meier and univariate and multivariate Cox regression analyses were performed on miR-1246 and miR-485-3p baseline levels to assess their ability to discriminate between responding and non-responding patients and to determine their prognostic value for PFS and OS. Globally, our results suggest that circulating miR-1246 and miR-485-3p could be valuable biomarkers for identifying patients most likely to be resistant to targeted therapy or with a poor expectancy of PFS and OS. Prospective studies in a larger cohort of patients are warranted. Despite the significant improvements in advanced melanoma therapy, there is still a pressing need for biomarkers that can predict patient response and prognosis, and therefore support rational treatment decisions. Here, we investigated whether circulating miRNAs could be biomarkers of clinical outcomes in patients treated with targeted therapy. Using next-generation sequencing, we profiled plasma miRNAs at baseline and at progression in patients treated with BRAF inhibitors (BRAFi) or BRAFi + MEKi. Selected miRNAs associated with response to therapy were subjected to validation by real-time quantitative RT-PCR. Receiver Operating Characteristics (ROC), Kaplan-Meier and univariate and multivariate Cox regression analyses were performed on the validated miR-1246 and miR-485-3p baseline levels. The median baseline levels of miR-1246 and miR-485-3p were significantly higher and lower, respectively, in the group of patients not responding to therapy (NRs) as compared with the group of responding patients (Rs). In Rs, a trend toward an increase in miR-1246 and a decrease in miR-485-3p was observed at progression. Baseline miR-1246 level and the miR-1246/miR-485-3p ratio showed a good ability to discriminate between Rs and NRs. Poorer PFS and OS were observed in patients with unfavorable levels of at least one miRNA. In multivariate analysis, a low level of miR-485-3p and a high miR-1246/miR-485-3p ratio remained independent negative prognostic factors for PFS, while a high miR-1246/miR-485-3p ratio was associated with an increased risk of mortality, although statistical significance was not reached. Evaluation of miR-1246 and miR-485-3p baseline plasma levels might help clinicians to identify melanoma patients most likely to be unresponsive to targeted therapy or at higher risk for short-term PFS and mortality, thus improving their management.
C1 [Levati, Lauretta; Bonmassar, Laura; Caporali, Simona; Lacal, Pedro Miguel; Narducci, Maria Grazia; Russo, Giandomenico; D'Atri, Stefania] IDI IRCCS, Lab Mol Oncol, Via Monti Creta 104, I-00167 Rome, Italy.
   [Bassi, Cristian; Lupini, Laura; Negrini, Massimo] Univ Ferrara, Dept Translat Med, Via Fossato Mortara 70, I-44121 Ferrara, Italy.
   [Bassi, Cristian; Negrini, Massimo] Univ Ferrara, LTTA Ctr, Via Fossato Mortara 70, I-44121 Ferrara, Italy.
   [Mastroeni, Simona] IDI IRCCS, Clin Epidemiol Unit, Via Monti Creta 104, I-00167 Rome, Italy.
   [Cappellini, Gian Carlo Antonini; De Galitiis, Federica] IDI IRCCS, Dept Oncol & Dermatol Oncol, Via Monti Creta 104, I-00167 Rome, Italy.
   [Alvino, Ester] Natl Council Res, Inst Translat Pharmacol, Via Fosso Cavaliere 100, I-00133 Rome, Italy.
   [Molineris, Ivan] Univ Turin, Dept Life Sci & Syst Biol, Via Accademia Albertina 13, I-10123 Turin, Italy.
   [Cappellini, Gian Carlo Antonini] Interpresidio ASL RM2, UOC Oncol, Via Monti Tiburtini 387, I-00157 Rome, Italy.
   [Caporali, Simona] San Camillo Hosp, Reg Transplant Ctr Lazio CRTL, Circonvallaz Gianicolense 87, I-00152 Rome, Italy.
C3 IRCCS Istituto Dermopatico dell'Immacolata (IDI); University of Ferrara;
   University of Ferrara; IRCCS Istituto Dermopatico dell'Immacolata (IDI);
   IRCCS Istituto Dermopatico dell'Immacolata (IDI); Consiglio Nazionale
   delle Ricerche (CNR); Istituto di Farmacologia Traslazionale (IFT-CNR);
   University of Turin
RP D'Atri, S (corresponding author), IDI IRCCS, Lab Mol Oncol, Via Monti Creta 104, I-00167 Rome, Italy.
EM s.datri@idi.it
RI D'Atri, Stefania/K-6039-2016; Narducci, Maria/L-3093-2018; Lupini,
   Laura/K-6736-2016; Levati, Lauretta/ABC-5572-2020; Lacal,
   Pedro/JAC-9700-2023; Molineris, Ivan/H-5071-2019; Bassi,
   Cristian/K-2356-2018
OI D'Atri, Stefania/0000-0001-9852-7377; Bassi,
   Cristian/0000-0002-5823-709X
FU Italian Association for Cancer Research (AIRC) [IG 17585]; Italian
   Ministry of Health [PE-2016-02364102]
FX This research was funded by the Italian Association for Cancer Research
   (AIRC, grant IG 17585 to S.D.), and by the Italian Ministry of Health
   (grant PE-2016-02364102 to G.R.).
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NR 98
TC 6
Z9 6
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 AUG
PY 2022
VL 14
IS 15
AR 3706
DI 10.3390/cancers14153706
PG 25
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3T3ML
UT WOS:000840182700001
PM 35954369
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Gupta, S
   Johnson, SH
   Vasmatzis, G
   Porath, B
   Rustin, JG
   Rao, P
   Costello, BA
   Leibovich, BC
   Thompson, RH
   Cheville, JC
   Sukov, WR
AF Gupta, Sounak
   Johnson, Sarah H.
   Vasmatzis, George
   Porath, Binu
   Rustin, Jeannette G.
   Rao, Priya
   Costello, Brian A.
   Leibovich, Bradley C.
   Thompson, R. Houston
   Cheville, John C.
   Sukov, William R.
TI <i>TFEB</i>-<i>VEGFA</i> (6p21.1) co-amplified renal cell carcinoma: a
   distinct entity with potential implications for clinical management
SO MODERN PATHOLOGY
LA English
DT Article
ID BREAST-CANCER; DEK OVEREXPRESSION; HUMAN OSTEOSARCOMA;
   COLORECTAL-CANCER; EXPRESSED GENES; POOR-PROGNOSIS; FUSION GENES;
   TUMOR-GROWTH; ONCOPROTEIN; IDENTIFICATION
AB A subset of renal cell carcinomas shows TFEB overexpression secondary to MALAT1-TFEB gene fusion. As alternate mechanisms of TFEB overexpression are likely to have the same effect, we sought to determine the frequency of amplification of TFEB and the adjacent VEGFA gene at 6p21.1. As patients with metastatic renal cell carcinomas are managed with anti-VEGF therapies, we retrospectively assessed therapeutic response in patients with amplified tumors. Amplification status was analyzed for 875 renal cell carcinomas from our institution, a consultative case and 794 cases from The Cancer Genome Atlas. Cases were classified as having low level (5-10 copies), and high-level amplification (410 copies), and were further analyzed for adjacent oncogene copy number status (n=6; 3 single-nucleotide polymorphism genomic microarray, 3 The Cancer Genome Atlas) and structural rearrangements (n=1; mate-pair sequencing). These were then reviewed for histopathology, immunophenotype, and response to VEGF-targeted therapy on follow-up. In all, 10/875 (1.1%) institutional cases, 1 consultative case, and 3/794 (0.4%) of The Cancer Genome Atlas cases showed TFEB highlevel amplification, while 14/875 (1.6%) cases showed TFEB low-level amplification. All cases had associated VEGFA amplification. This was confirmed with evaluation for copy number changes (n=6). The 6p21.1 high and low-level amplified tumors occurred in adults (mean age: 66), with over half being >= pT3 (13/25, 52%), and most showed oncocytic, tubulopapillary features and high grade (>= grade 3: 20/22, 91%). These were aggressive tumors with metastasis and death from renal cell carcinoma in 11 (of 24, 46%) cases. Four patients received targeted therapy and had a mean survival of 31 months (range: 17-50) post nephrectomy. In summary, a group of aggressive renal cell carcinomas show genomic amplification of the 6p21.1 region including TFEB and VEGFA genes and share morphologic features. Additional studies are warranted to determine whether these patients respond to anti-VEGF therapy.
C1 [Gupta, Sounak; Porath, Binu; Rustin, Jeannette G.; Cheville, John C.; Sukov, William R.] Mayo Clin, Dept Lab Med & Pathol, Hilton 9,200 First St Southwest, Rochester, MN 55905 USA.
   [Johnson, Sarah H.] Mayo Clin, Ctr Individualized Med, Rochester, MN USA.
   [Vasmatzis, George] Mayo Clin, Dept Mol Med, Rochester, MN USA.
   [Rao, Priya] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
   [Costello, Brian A.] Mayo Clin, Div Med Oncol, Rochester, MN USA.
   [Leibovich, Bradley C.; Thompson, R. Houston] Mayo Clin, Dept Urol, Rochester, MN USA.
C3 Mayo Clinic; Mayo Clinic; Mayo Clinic; University of Texas System; UTMD
   Anderson Cancer Center; Mayo Clinic; Mayo Clinic
RP Sukov, WR (corresponding author), Mayo Clin, Dept Lab Med & Pathol, Hilton 9,200 First St Southwest, Rochester, MN 55905 USA.
EM Sukov.william@mayo.edu
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NR 50
TC 70
Z9 74
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
EI 1530-0285
J9 MODERN PATHOL
JI Mod. Pathol.
PD JUL
PY 2017
VL 30
IS 7
BP 998
EP 1012
DI 10.1038/modpathol.2017.24
PG 15
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA EZ4YJ
UT WOS:000404718100009
PM 28338654
OA Bronze
DA 2025-01-04
ER

PT J
AU Gazzaniga, P
   Raimondi, C
   Nicolazzo, C
   Carletti, R
   di Gioia, C
   Gradilone, A
   Cortesi, E
AF Gazzaniga, Paola
   Raimondi, Cristina
   Nicolazzo, Chiara
   Carletti, Raffaella
   di Gioia, Cira
   Gradilone, Angela
   Cortesi, Enrico
TI The rationale for liquid biopsy in colorectal cancer: a focus on
   circulating tumor cells
SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS
LA English
DT Review
DE cancer stem cells; circulating tumor cells; colorectal cancer;
   epithelial-mesenchymal transition; liquid biopsy; targeted therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; STEM-CELLS; BREAST-CANCER;
   HETEROGENEITY; DEVICE; EXPRESSION; METASTASIS; PLASTICITY; ENRICHMENT;
   RESISTANCE
AB Capturing circulating tumor cells (CTCs) and/or circulating tumor DNA from blood, which represents a precious source of biological material derived from both primary and metastatic tumors, has been named a liquid biopsy'. While the circulating tumor DNA might be more representative of the bulk of the metastatic tumor, CTCs are thought to reflect more of the metastases-initiating cells. Consequently, a liquid biopsy made of tumor cells and tumor DNA that is able to track cancer evolution, as a fingerprint of the patient's individual tumor, and is easy to perform at every stage of the disease course, sounds attractive. This article mainly focuses on the applications of CTCs to track tumor dynamics in real time using colorectal cancer as a model system. The analysis of viable CTCs at DNA, RNA and protein levels, as well as their expansion in vitro, may allow deep investigation of the features of metastases-initiating cells.
C1 [Gazzaniga, Paola; Raimondi, Cristina; Nicolazzo, Chiara; Gradilone, Angela] Sapienza Univ Roma, Dipartimento Med Mol, Rome, Italy.
   [Carletti, Raffaella; di Gioia, Cira; Cortesi, Enrico] Sapienza Univ Roma, Dipartimento Sci Radiol Oncol & Anatomopatol, Rome, Italy.
C3 Sapienza University Rome; Sapienza University Rome
RP Gazzaniga, P (corresponding author), Sapienza Univ Roma, Dipartimento Med Mol, Rome, Italy.
EM paola.gazzaniga@uniroma1.it
RI Cortesi, Enrico/AAA-2983-2019; gazzaniga, paola/AAA-2250-2019;
   Nicolazzo, Chiara/AAG-2625-2019
OI di Gioia, Cira/0000-0003-4696-0560
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NR 44
TC 16
Z9 17
U1 0
U2 14
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 JUL
PY 2015
VL 15
IS 7
BP 925
EP 932
DI 10.1586/14737159.2015.1045491
PG 8
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA CL4OS
UT WOS:000356933200008
PM 25959553
DA 2025-01-04
ER

PT J
AU Wu, YH
   Wei, W
   Jing, Z
   Qing, Z
   Yani, Z
   Wang, YYQ
   Han, SW
AF Yinhang, Wu
   Wei, Wu
   Jing, Zhuang
   Qing, Zhou
   Yani, Zhou
   Yangyanqiu, Wang
   Shuwen, Han
TI Biological roles of toll-like receptors and gut microbiota in colorectal
   cancer
SO FUTURE MICROBIOLOGY
LA English
DT Review
DE colorectal cancer; gut micro-organisms; immune cell; intestinal
   inflammation; intestinal microecology; microbial-associated molecular
   patterns; pattern recognition receptors; probiotics; toll-like receptors
ID ENTEROTOXIGENIC BACTEROIDES-FRAGILIS; POTENTIATES INTESTINAL
   TUMORIGENESIS; HELICOBACTER-PYLORI INFECTION; FUSOBACTERIUM-NUCLEATUM;
   ESCHERICHIA-COLI; HUMAN COMMENSAL; CLOSTRIDIUM-SEPTICUM;
   ULCERATIVE-COLITIS; INNATE IMMUNITY; EMERGING ROLES
AB Colorectal cancer (CRC) is one of the most considerably common malignancies of the alimentary system, with high mortality and incidence rates. The present study suggested that the occurrence of CRC is closely related to bacteria, as the large intestine is a gathering place for human micro-organisms. However, the nosogenesis of bacteria leading to tumorigenesis is still obscure. Recently, many studies have reported that toll-like receptors and their related molecular pathways are involved in the process of gut micro-organisms generating CRC. Gut micro-organisms can promote or inhibit the development of CRC via binding to special toll-like receptors. In this paper, the authors review the relationship among toll-like receptors, gut micro-organisms and CRC in order to provide a reference for future tumor immunotherapy and targeted therapy.
C1 [Yinhang, Wu; Wei, Wu; Jing, Zhuang; Qing, Zhou; Yani, Zhou; Yangyanqiu, Wang; Shuwen, Han] Huzhou Univ, Huzhou Cent Hosp, Affiliated Cent Hosp, 1558 Sanhuan North Rd, Huzhou 313000, Zhejiang, Peoples R China.
   [Yinhang, Wu] Zhejiang Chinese Med Univ, Sch Clin Med 2, 548 Binwen Rd, Hangzhou 310053, Zhejiang, Peoples R China.
   [Yinhang, Wu; Wei, Wu; Jing, Zhuang; Qing, Zhou; Shuwen, Han] Key Lab Multi Res & Clin Transformat Digest Canc, 1558 Sanhuan North Rd, Huzhou 313000, Zhejiang, Peoples R China.
   [Yani, Zhou; Yangyanqiu, Wang] Zhejiang Univ, Grad Sch, Med Fac, 866 Yuhangtang Rd, Hangzhou 310058, Zhejiang, Peoples R China.
C3 Huzhou University; Zhejiang Chinese Medical University; Zhejiang
   University
RP Han, SW (corresponding author), Huzhou Univ, Huzhou Cent Hosp, Affiliated Cent Hosp, 1558 Sanhuan North Rd, Huzhou 313000, Zhejiang, Peoples R China.; Han, SW (corresponding author), Key Lab Multi Res & Clin Transformat Digest Canc, 1558 Sanhuan North Rd, Huzhou 313000, Zhejiang, Peoples R China.
EM shuwenhan985@163.com
RI Han, Shuwen/ADV-3790-2022
OI Han, Shuwen/0000-0001-6180-9565; Wu, Wei/0000-0002-4894-7178; Wu,
   Yinhang/0000-0001-5227-7413
FU Advanced Soldier Program of Science and Technology Department of
   Zhejiang Province [2022C03026]; Major Science and Technology Projects of
   Zhejiang Provincial Health Commission [WKJ-ZJ-2013]
FX This work was supported by the Advanced Soldier Program of Science and
   Technology Department of Zhejiang Province (2022C03026) and Major
   Science and Technology Projects of Zhejiang Provincial Health Commission
   (no. WKJ-ZJ-2013). 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.Editage language
   editing services were paid for by the corresponding author, H Shuwen.
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NR 198
TC 6
Z9 6
U1 1
U2 19
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1746-0913
EI 1746-0921
J9 FUTURE MICROBIOL
JI Future Microbiol.
PD SEP
PY 2022
VL 17
IS 13
BP 1071
EP 1089
DI 10.2217/fmb-2021-0072
EA AUG 2022
PG 19
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA 3S5GV
UT WOS:000834798500001
PM 35916158
DA 2025-01-04
ER

PT J
AU Schulc, K
   Nagy, ZT
   Kamp, S
   Molnár, J
   Veres, DV
   Csermely, P
   Kovács, BM
AF Schulc, Klara
   Nagy, Zsolt T.
   Kamp, Sebestyen
   Molnar, Janos
   Veres, Daniel V.
   Csermely, Peter
   Kovacs, Borbala M.
TI Modular Reorganization of Signaling Networks during the Development of
   Colon Adenoma and Carcinoma
SO JOURNAL OF PHYSICAL CHEMISTRY B
LA English
DT Article
ID PROTEIN-INTERACTION NETWORKS; COLORECTAL-CANCER; GROWTH-FACTOR;
   SURVIVAL; CETUXIMAB
AB Network science is an emerging tool in systems biology and oncology, providing novel, system-level insight into the development of cancer. The aim of this project was to study the signaling networks in the process of oncogenesis to explore the adaptive mechanisms taking part in the cancerous transformation of healthy cells. For this purpose, colon cancer proved to be an excellent candidate as the preliminary phase, and adenoma has a long evolution time. In our work, transcriptomic data have been collected from normal colon, colon adenoma, and colon cancer samples to calculating link (i.e., network edge) weights as approximative proxies for protein abundances, and link weights were included in the Human Cancer Signaling Network. Here we show that the adenoma phase clearly differs from the normal and cancer states in terms of a more scattered link weight distribution and enlarged network diameter. Modular analysis shows the rearrangement of the apoptosis- and the cell-cycle-related modules, whose pathway enrichment analysis supports the relevance of targeted therapy. Our work enriches the system-wide assessment of cancer development, showing specific changes for the adenoma state.
C1 [Schulc, Klara; Nagy, Zsolt T.; Veres, Daniel V.; Csermely, Peter; Kovacs, Borbala M.] Semmelweis Univ, Dept Mol Biol, H-1085 Budapest, Hungary.
   [Kamp, Sebestyen; Molnar, Janos; Veres, Daniel V.] Turbine Ltd, Budapest, Hungary.
C3 Semmelweis University
RP Csermely, P (corresponding author), Semmelweis Univ, Dept Mol Biol, H-1085 Budapest, Hungary.
EM csermely.peter@med.semmelweis-univ.hu
RI Veres, Daniel/GNH-2578-2022; Csermely, Peter/J-2067-2017; Veres,
   Daniel/J-3564-2015
OI Csermely, Peter/0000-0001-9234-0659; Veres, Daniel/0000-0002-2968-0666
FU Hungarian National Research, Development and Innovation Office
   [K131458]; Higher Education Institutional Excellence Programme of the
   Ministry of Human Capacities in Hungary within Semmelweis University;
   Thematic Excellence Programme (Temateruleti Kivalosagi Program) of the
   Ministry for Innovation and Technology in Hungary within Semmelweis
   University [2020-4.1.1.-TKP2020]; New National Excellence Program of the
   Ministry of Human Capacities [UNKP-19-2-I-SE-54]
FX We thank the anonymous referee of this article for excellent suggestions
   to better our manuscript. This work was supported by the Hungarian
   National Research, Development and Innovation Office (K131458), the
   Higher Education Institutional Excellence Programme of the Ministry of
   Human Capacities in Hungary within the framework of the molecular
   biology thematic programmes of Semmelweis University, the Thematic
   Excellence Programme (Temateruleti Kivalosagi Program,
   2020-4.1.1.-TKP2020) of the Ministry for Innovation and Technology in
   Hungary within the framework of the molecular biology thematic programme
   of the Semmelweis University, and the UNKP-19-2-I-SE-54 New National
   Excellence Program of the Ministry of Human Capacities. The LINK network
   science group (http://linkgroup.hu) where this work was also born
   gratefully acknowledges the guidance and support of Prof. Ruth Nussinov,
   both scientifically and personally, for the last 10 years.
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NR 58
TC 1
Z9 2
U1 0
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1520-6106
EI 1520-5207
J9 J PHYS CHEM B
JI J. Phys. Chem. B
PD FEB 25
PY 2021
VL 125
IS 7
BP 1716
EP 1726
DI 10.1021/acs.jpcb.0c09307
EA FEB 2021
PG 11
WC Chemistry, Physical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA QQ2WZ
UT WOS:000624387300002
PM 33562960
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Hu, QL
   Chen, LJ
   Li, KR
   Liu, RT
   Sun, L
   Han, T
AF Hu, Qilin
   Chen, Lujun
   Li, Kerui
   Liu, Ruotong
   Sun, Lei
   Han, Tao
TI Circulating tumor DNA: current implementation issues and future
   challenges for clinical utility
SO CLINICAL CHEMISTRY AND LABORATORY MEDICINE
LA English
DT Review
DE ctDNA; early detection; MRD; targeted therapy; immunotherapy
ID CELL LUNG-CANCER; OPEN-LABEL; PHASE-III; ACQUIRED-RESISTANCE; 1ST-LINE
   ERLOTINIB; COLORECTAL-CANCER; OSIMERTINIB; MUTATION; PLASMA;
   HETEROGENEITY
AB Over the past decades, liquid biopsy, especially circulating tumor DNA (ctDNA), has received tremendous attention as a noninvasive detection approach for clinical applications, including early diagnosis of cancer and relapse, real-time therapeutic efficacy monitoring, potential target selection and investigation of drug resistance mechanisms. In recent years, the application of next-generation sequencing technology combined with AI technology has significantly improved the accuracy and sensitivity of liquid biopsy, enhancing its potential in solid tumors. However, the increasing integration of such promising tests to improve therapy decision making by oncologists still has complexities and challenges. Here, we propose a conceptual framework of ctDNA technologies and clinical utilities based on bibliometrics and highlight current challenges and future directions, especially in clinical applications such as early detection, minimal residual disease detection, targeted therapy, and immunotherapy. We also discuss the necessities of developing a dynamic field of translational cancer research and rigorous clinical studies that may support therapeutic strategy decision making in the near future.
C1 [Han, Tao] China Med Univ, Hosp 1, Dept Med Oncol, 155 Nanjingbei Rd, Shenyang 110001, Liaoning, Peoples R China.
   [Chen, Lujun] China Med Univ, Gen Hosp Northern Theater Command Training Base Gr, Shenyang, Peoples R China.
   [Liu, Ruotong] Shenyang Med Coll, Clin Med, Shenyang, Peoples R China.
   [Sun, Lei] China Med Univ, Hosp 1, Dept Thorac Surg, 155 Nanjingbei Rd, Shenyang 110001, Liaoning, Peoples R China.
   [Hu, Qilin; Li, Kerui] China Med Univ, Hosp 1, Dept Med Oncol, Shenyang, Peoples R China.
C3 China Medical University; China Medical University; Shenyang Medical
   College; China Medical University; China Medical University
RP Han, T (corresponding author), China Med Univ, Hosp 1, Dept Med Oncol, 155 Nanjingbei Rd, Shenyang 110001, Liaoning, Peoples R China.; Sun, L (corresponding author), China Med Univ, Hosp 1, Dept Thorac Surg, 155 Nanjingbei Rd, Shenyang 110001, Liaoning, Peoples R China.
EM 15998850222@163.com; than1984@sina.com
RI Li, Kerui/U-4005-2019; liu, ruotong/JFA-0473-2023
OI Han, Tao/0000-0003-3814-8492; Hu, Qilin/0009-0002-5372-286X
FU Educational funding of Liaoning Province
FX No Statement Available
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NR 91
TC 2
Z9 2
U1 2
U2 7
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1434-6621
EI 1437-4331
J9 CLIN CHEM LAB MED
JI Clin. Chem. Lab. Med.
PD OCT 28
PY 2024
VL 62
IS 11
BP 2094
EP 2110
DI 10.1515/cclm-2023-1157
EA DEC 2023
PG 17
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA H2P7E
UT WOS:001127124700001
PM 38109307
DA 2025-01-04
ER

PT S
AU Polzer, B
   Klein, CA
AF Polzer, Bernhard
   Klein, Christoph A.
BE Cote, RJ
   Datar, RH
TI Evolution of Metastatic Disease: The Need for Monitoring and Emerging
   Therapeutic Opportunities
SO CIRCULATING TUMOR CELLS: ADVANCES IN BASIC SCIENCE AND CLINICAL
   APPLICATIONS
SE Current Cancer Research
LA English
DT Article; Book Chapter
DE Tumor cell heterogeneity; Parallel progression model; HER2; Disseminated
   cancer cells; Targeted therapy; Therapy resistance; Single cell analysis
ID DISSEMINATED TUMOR-CELLS; BREAST-CANCER PATIENTS; WHOLE GENOME
   AMPLIFICATION; SINGLE-CELL; BONE-MARROW; ADJUVANT TRASTUZUMAB; CLONAL
   EVOLUTION; COLORECTAL-CANCER; GENETIC-ANALYSIS; DNA-POLYMERASE
AB During the last few years tailored therapies have improved overall survival of patients with metastatic disease. However, iatrogenic selection pressure continues to drive the evolution of systemically spread cancer cells, resulting in the generation of aggressive and therapy-resistant tumor cells. The outcome is cancer relapse and death in the majority of patients. In early disease stages, (neo) adjuvant targeted therapies often fail for unknown reasons. Therefore, diagnostic and therapeutic strategies have to be reevaluated on the basis of an evolutionary concept of disease. This obviously implies the ability to monitor the molecular evolution of the disease. To this end, a novel diagnostic pathology for systemic cancer has to be developed that will enable precision medicine for cancer patients.
C1 [Polzer, Bernhard; Klein, Christoph A.] Univ Regensburg, Expt Med & Therapy Res, Franz Josef Str Allee 11, D-93053 Regensburg, Germany.
   [Klein, Christoph A.] Fraunhofer Project Grp Personalized Tumor ITEM, Josef Engert Str 9, D-93053 Regensburg, Germany.
C3 University of Regensburg
RP Klein, CA (corresponding author), Univ Regensburg, Expt Med & Therapy Res, Franz Josef Str Allee 11, D-93053 Regensburg, Germany.; Klein, CA (corresponding author), Fraunhofer Project Grp Personalized Tumor ITEM, Josef Engert Str 9, D-93053 Regensburg, Germany.
EM christoph.klein@ukr.de
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NR 100
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES
SN 2199-2584
EI 2199-2592
BN 978-1-4939-3363-1; 978-1-4939-3361-7
J9 CURR CANCER RES
PY 2016
BP 271
EP 292
DI 10.1007/978-1-4939-3363-1_14
D2 10.1007/978-1-4939-3363-1
PG 22
WC Oncology
WE Book Citation Index – Science (BKCI-S)
SC Oncology
GA BE3WW
UT WOS:000371329000016
DA 2025-01-04
ER

PT J
AU Abosalem, H
   Mahgoub, S
   Emara, M
   Kotb, N
   Soror, S
AF Abosalem, Hadeer
   Mahgoub, Shahenda
   Emara, Mohamed
   Kotb, Nahla
   Soror, Sameh
TI Interrupted Crosstalk between Natural Killer Cells and Anti-epidermal
   Growth Factor Receptor: A Possible Role in Hepatocellular Carcinoma
   Treatment Failure
SO CURRENT CANCER DRUG TARGETS
LA English
DT Review
DE HCC immunotherapy; molecular target therapy; tumor microenvironment; NK;
   anti-EGFR mAb; ADCC
ID CANCER-ASSOCIATED FIBROBLASTS; METASTATIC COLORECTAL-CANCER;
   COLON-CANCER; NK CELLS; T-CELLS; EGFR; EXPRESSION; LIVER; CETUXIMAB;
   CYTOTOXICITY
AB Hepatocellular carcinoma (HCC) is a major health problem worldwide. Most patients are diagnosed for the first time at late stages, which leads to very poor prognosis. It is challenging to discover strategies for treatment at these advanced stages. Recently, monoclonl antibodies (mAbs) targeting specific cellular signaling pathways in HCC have been developed. Unfortunately, they still have a low survival rate, and some of them failed clinically to produce effective responses even if they showed very good results against HCC in preclinical studies. This review focuses on and discusses the possible causes for the failure of mAbs, precisely anti-Epidermal Growth Factor Receptor (EGFR) mAb and the crosstalk between this mAb and patients' NK cells.
C1 [Abosalem, Hadeer] Egyptian Drug Author EDA, Biotechnol Unit, Giza 12654, Egypt.
   [Mahgoub, Shahenda; Soror, Sameh] Helwan Univ, Fac Pharm, Dept Biochem & Mol Biol, Cairo 11795, Egypt.
   [Emara, Mohamed] Helwan Univ, Fac Pharm, Dept Microbiol & Immunol, Cairo 11795, Egypt.
   [Kotb, Nahla] Egyptian Drug Author EDA, Blood Derivat Unit, Giza 12654, Egypt.
C3 Egyptian Knowledge Bank (EKB); Helwan University; Egyptian Knowledge
   Bank (EKB); Helwan University
RP Mahgoub, S (corresponding author), Helwan Univ, Fac Pharm, Dept Biochem & Mol Biol, Cairo 11795, Egypt.
EM Shahenda.mahgoub@pharm.helwan.edu.eg
RI Emara, Mohamed/GPK-2394-2022; Soror, Sameh/G-5228-2019; mahgoub,
   shahenda/D-6395-2019
OI Soror, Sameh/0000-0001-6474-8884; mahgoub, shahenda/0000-0002-6095-1081;
   Emara, Mohamed/0000-0001-7708-9435
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NR 62
TC 0
Z9 0
U1 0
U2 9
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1568-0096
EI 1873-5576
J9 CURR CANCER DRUG TAR
JI Curr. Cancer Drug Targets
PY 2021
VL 21
IS 7
BP 601
EP 607
DI 10.2174/1568009621666210519105203
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UY1GI
UT WOS:000701279400004
PM 34011259
DA 2025-01-04
ER

PT J
AU Simard, J
   Kamath, S
   Kircher, S
AF Simard, Jillian
   Kamath, Suneel
   Kircher, Sheetal
TI Survivorship Guidance for Patients with Colorectal Cancer
SO CURRENT TREATMENT OPTIONS IN ONCOLOGY
LA English
DT Review
DE Colorectal neoplasms; Survivorship; Neoplasms; Cancer; Diet; Exercise;
   Recurrence; Genetics
ID QUALITY-OF-LIFE; BODY-MASS INDEX; LONG-TERM SURVIVORS; III COLON-CANCER;
   PHYSICAL-ACTIVITY; PRACTICE GUIDELINE; FINANCIAL BURDEN; ADJUVANT
   CHEMOTHERAPY; SECONDARY PREVENTION; AMERICAN SOCIETY
AB Opinion statementEffective therapy for treatment of colorectal cancer includes comprehensive and evidence-based therapies that may include a combination of surgery, chemotherapy, targeted therapy, and/or radiation. However, in order to provide patients with the highest quality of care, providers must consider all aspects of survivorship care including: surveillance for recurrence/second primaries, genetic counseling, psychosocial/physical late effects of cancer and its therapies, and preventative lifestyle strategies. Health systems, providers, and researchers need to identify systematic methods of addressing the unique needs of the survivorship population that include multidisciplinary teams including supportive oncology (i.e., psychologists, social workers), specialties (i.e., cardiology), and primary care physicians.
C1 [Simard, Jillian] Univ Calif San Francisco, 505 Parnassus Ave, San Francisco, CA 94143 USA.
   [Kamath, Suneel; Kircher, Sheetal] Northwestern Univ, Feinberg Sch Med, 676 N St Clair,Suite 850, Chicago, IL 60611 USA.
C3 University of California System; University of California San Francisco;
   Northwestern University; Feinberg School of Medicine
RP Kircher, S (corresponding author), Northwestern Univ, Feinberg Sch Med, 676 N St Clair,Suite 850, Chicago, IL 60611 USA.
EM jillian.simard@gmail.com; s-kircher@northwestern.edu
RI Kamath, Suneel/AAW-8168-2020
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NR 88
TC 30
Z9 30
U1 2
U2 19
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 MAY
PY 2019
VL 20
IS 5
AR 38
DI 10.1007/s11864-019-0635-4
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HR3ZN
UT WOS:000463082600004
PM 30937550
DA 2025-01-04
ER

PT J
AU Fong, WN
   To, KKW
AF Fong, Winnie
   To, Kenneth K. W.
TI Drug repurposing to overcome resistance to various therapies for
   colorectal cancer
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Review
DE Cetuximab; 5-Fluorouracil; Immunotherapy; Irinotecan; Molecular targeted
   chemotherapy; Pembrolizumab
ID GROWTH-FACTOR RECEPTOR; CLINICAL-PRACTICE GUIDELINES; KAPPA-B ACTIVITY;
   COLON-CANCER; MULTIDRUG-RESISTANCE; CETUXIMAB RESISTANCE;
   ACQUIRED-RESISTANCE; PIK3CA MUTATION; ASPIRIN USE; DOWN-REGULATION
AB Emergence of novel treatment modalities provides effective therapeutic options, apart from conventional cytotoxic chemotherapy, to fight against colorectal cancer. Unfortunately, drug resistance remains a huge challenge in clinics, leading to invariable occurrence of disease progression after treatment initiation. While novel drug development is unfavorable in terms of time frame and costs, drug repurposing is one of the promising strategies to combat resistance. This approach refers to the application of clinically available drugs to treat a different disease. With the well-established safety profile and optimal dosing of these approved drugs, their combination with current cancer therapy is suggested to provide an economical, safe and efficacious approach to overcome drug resistance and prolong patient survival. Here, we review both preclinical and clinical efficacy, as well as cellular mechanisms, of some extensively studied repurposed drugs, including non-steroidal anti-inflammatory drugs, statins, metformin, chloroquine, disulfiram, niclosamide, zoledronic acid and angiotensin receptor blockers. The three major treatment modalities in the management of colorectal cancer, namely classical cytotoxic chemotherapy, molecular targeted therapy and immunotherapy, are covered in this review.
C1 [Fong, Winnie; To, Kenneth K. W.] Chinese Univ Hong Kong, Fac Med, Sch Pharm, Shatin, Room 801N, Hong Kong, Peoples R China.
C3 Chinese University of Hong Kong
RP To, KKW (corresponding author), Chinese Univ Hong Kong, Fac Med, Sch Pharm, Shatin, Room 801N, Hong Kong, Peoples R China.
EM kennethto@cuhk.edu.hk
RI To, Kenneth/M-4500-2013
OI To, Kenneth/0000-0003-2755-0283
FU Health and Medical Research Fund [Food and Health Bureau, Hong Kong SAR]
   [03140276]; Medicine Panel of the Chinese University of Hong Kong
   [4054371]
FX The authors' team was supported by the Health and Medical Research Fund
   [Food and Health Bureau, Hong Kong SAR, grant number 03140276] and a
   research grant from the Medicine Panel of the Chinese University of Hong
   Kong [Direct Grant for Research 4054371].
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NR 134
TC 57
Z9 60
U1 0
U2 46
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1420-682X
EI 1420-9071
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD SEP
PY 2019
VL 76
IS 17
BP 3383
EP 3406
DI 10.1007/s00018-019-03134-0
PG 24
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA IR9YR
UT WOS:000481803500008
PM 31087119
OA Green Published
DA 2025-01-04
ER

PT J
AU Ma, J
   Zhu, J
   Ding, TY
   Cai, LB
   Zhou, CP
   Zhang, YM
AF Ma, Jun
   Zhu, Juan
   Ding, Tengyun
   Cai, Libin
   Zhou, Chaoping
   Zhang, Yaming
TI Thrombus formation in the suprahepatic inferior vena cava after
   microwave ablation in patients with hepatic metastasis: a case report
SO THROMBOSIS JOURNAL
LA English
DT Article
DE Rectal cancer; Hepatic metastasis; Thrombus; Microwave ablation
ID PERCUTANEOUS RADIOFREQUENCY ABLATION; HEPATOCELLULAR-CARCINOMA;
   COLORECTAL-CANCER; THERMAL ABLATION; PORTAL-VEIN; COMPLICATIONS; TUMORS
AB BackgroundMicrowave ablation (MWA) via ultrasound guidance is an important tool in the treatment of liver metastases. The most common postoperative complications are abdominal hemorrhage and bile leakage, whereas thrombosis in the suprahepatic inferior vena cava (IVC) is very rare, and clinical management is very difficult when the head end of the thrombus reaches the right atrium.Case presentationThis is a case report of a 52-year-old man with hepatic metastasis 21 months after radical resection of rectal cancer. After chemotherapy combined with targeted therapy, metastasis in segment IV (S4) of the liver was treated with microwave ablation. Two months after treatment, the hepatic metastasis in S4 showed a microwave ablation zone on MRI.Enhanced MRI showed venous thrombosis located in the left hepatic vein and IVC, and the head of the thrombus reached the right atrium. After two weeks of anticoagulation and thrombolytic treatment, the follow-up MRI showed that the venous thrombus had nearly disappeared.ConclusionWhen liver metastases are close to the hepatic vein, clinicians should pay attention to the occurrence of hepatic vein and IVC thrombosis following MWA; through early diagnosis and anticoagulation, pulmonary thromboembolism (PTE) can be minimized.
C1 [Ma, Jun; Zhou, Chaoping; Zhang, Yaming] Anqing Municipal Hosp, Dept Gen Surg, 352 Ren Ming Rd, Anqing 24600, Anhui, Peoples R China.
   [Zhu, Juan; Cai, Libin] Anqing Municipal Hosp, Dept Imaging, Anqing 246000, Peoples R China.
   [Ding, Tengyun] Anqing Municipal Hosp, Dept Ultrasound, Anqing 246000, Peoples R China.
RP Zhang, YM (corresponding author), Anqing Municipal Hosp, Dept Gen Surg, 352 Ren Ming Rd, Anqing 24600, Anhui, Peoples R China.
EM zhangyaming2014@163.com
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NR 30
TC 1
Z9 1
U1 3
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1477-9560
J9 THROMB J
JI Thromb. J.
PD APR 4
PY 2023
VL 21
IS 1
AR 36
DI 10.1186/s12959-023-00481-8
PG 8
WC Hematology; Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology; Cardiovascular System & Cardiology
GA C6OF5
UT WOS:000963080600001
PM 37016383
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Mo, C
   Chadha, B
   Kuang, CY
AF Mo, Christiana
   Chadha, Bhawneet
   Kuang, Chaoyuan
TI An Evolving Landscape: New Therapies for Metastatic Colorectal Cancer
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE Immunotherapy; Targeted therapy; Colorectal cancer; Chemotherapy;
   Clinical trials
ID CETUXIMAB PLUS IRINOTECAN; OPEN-LABEL; 1ST-LINE TREATMENT; SUBGROUP
   ANALYSES; DOUBLE-BLIND; SINGLE-ARM; PHASE-II; MULTICENTER; SURVIVAL;
   PLACEBO
AB Substantial progress is being made in the development of novel therapies directed against colorectal cancer. The discovery of various molecular markers and advances in tumor profiling have facilitated the development of new targeted agents and immunotherapy. Not only have these drugs improved progression-free survival and even overall survival in some cases, but their related outcomes have also raised questions as to how to best combine or sequence therapies for even greater efficacy. Furthermore, we are beginning to understand how these combination therapies may yield for greater therapeutic response for patients with microsatellite stable colorectal cancer for which there is much need for improvement. In this article, we review recent trial data and explore the outcomes of various targeted therapies and immunotherapies for patient with advanced colorectal cancer.
C1 [Mo, Christiana; Chadha, Bhawneet; Kuang, Chaoyuan] Montefiore Einstein, Dept Oncol, Bronx, NY USA.
   [Mo, Christiana; Chadha, Bhawneet] Montefiore Einstein Comprehens Canc Ctr, Bronx, NY USA.
   [Kuang, Chaoyuan] Montefiore Einstein, Dept Mol Pharmacol, Bronx, NY USA.
RP Kuang, CY (corresponding author), Montefiore Einstein Comprehens Canc Ctr, Montefiore Einstein, Dept Oncol, Chanin Bldg,Room 628,1300 Morris Pk Ave, Bronx, NY 10461 USA.
EM Chaoyuan.kuang@einsteinmed.edu
OI Kuang, Chaoyuan/0000-0002-8984-3906
FU Montefiore Einstein Comprehensive Cancer Center Support Grant
   [5P30CA013330]
FX Figure was created using BioRender.com . This work was supported by the
   Montefiore Einstein Comprehensive Cancer Center Support Grant
   (5P30CA013330) .
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NR 69
TC 0
Z9 0
U1 4
U2 4
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD DEC
PY 2024
VL 23
IS 4
BP 337
EP 345
DI 10.1016/j.clcc.2024.08.003
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA O2U1Y
UT WOS:001369734800001
PM 39332920
DA 2025-01-04
ER

PT J
AU Aparicio, T
   Pamoukdjian, F
   Quero, L
   Manfredi, S
   Wind, P
   Paillaud, E
AF Aparicio, Thomas
   Pamoukdjian, Frederic
   Quero, Laurent
   Manfredi, Sylvain
   Wind, Philippe
   Paillaud, Elena
TI Colorectal cancer care in elderly patients: Unsolved issues
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Review
DE Adjuvant therapy; Chemotherapy; Geriatric oncology; Radiotherapy;
   Targeted therapy
ID COMPREHENSIVE GERIATRIC ASSESSMENT; RANDOMIZED CONTROLLED-TRIAL;
   CETUXIMAB PLUS IRINOTECAN; MISMATCH REPAIR PHENOTYPE; COLON-CANCER;
   RECTAL-CANCER; ADJUVANT-CHEMOTHERAPY; OLDER PATIENTS; POOLED ANALYSIS;
   1ST-LINE CHEMOTHERAPY
AB Colorectal cancers are common in elderly patients. However, cancer screening is poorly used after 75. Elderly patients form a heterogeneous population with specific characteristics. Standards of care cannot therefore be transposed from young to elderly patients. Tumour resection is frequently performed but adjuvant chemotherapy is rarely prescribed as there are no clearly established standards of care. In a metastatic setting, recent phase III studies have demonstrated that doublet front-line chemotherapy provided no survival benefit. Moreover, several studies have established the benefit of bevacizumab in association with chemotherapy. There is a lack of evidence for the efficacy of anti-epidermal growth factor antibodies in elderly patients. Geriatric assessments could help to select the adequate treatment strategy for individual patients. Geriatric oncology is now the challenge we have to face, and more specific trials are needed. (C) 2016 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Aparicio, Thomas] CHU Avicenne, APHP, Gastroenterol & Digest Oncol Dept, Bobigny, France.
   [Pamoukdjian, Frederic] CHU Avicenne, APHP, Dept Geriatr, Bobigny, France.
   [Quero, Laurent] CHU St Louis, APHP, Dept Radiotherapy, Paris, France.
   [Manfredi, Sylvain] CHU Dijon, INSERM U866, Hepatogastroenterol & Oncol Dept, Dijon, France.
   [Wind, Philippe] CHU Avicenne, APHP, Dept Surg, Bobigny, France.
   [Paillaud, Elena] CHU Henri Mondor, APHP, Dept Geriatr, Creteil, France.
C3 Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
   Ambroise-Pare - APHP; Hopital Universitaire Avicenne - APHP; Assistance
   Publique Hopitaux Paris (APHP); Hopital Universitaire Avicenne - APHP;
   Hopital Universitaire Ambroise-Pare - APHP; Assistance Publique Hopitaux
   Paris (APHP); Hopital Universitaire Ambroise-Pare - APHP; Universite
   Paris Cite; Hopital Universitaire Saint-Louis - APHP; Hopital
   Universitaire Hotel-Dieu - APHP; Institut Agro; AgroSup Dijon; Institut
   National de la Sante et de la Recherche Medicale (Inserm); CHU Dijon
   Bourgogne; Universite de Bourgogne; Assistance Publique Hopitaux Paris
   (APHP); Hopital Universitaire Avicenne - APHP; Hopital Universitaire
   Ambroise-Pare - APHP; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris-Est-Creteil-Val-de-Marne (UPEC); Hopital Universitaire
   Henri-Mondor - APHP; Hopital Universitaire Ambroise-Pare - APHP
RP Aparicio, T (corresponding author), Hop Avicenne, HUPSSD, Serv Gastroenterol & Cancerol Digest, 125 Rue Stalingrad, F-93000 Bobigny, France.
EM thomas.aparicio@aphp.fr
RI Pamoukdjian, Frédéric/Z-5051-2019; Quero, Laurent/K-6089-2019; Paillaud,
   Elena/K-5616-2017
OI Quero, Laurent/0000-0002-8781-2540; Paillaud, Elena/0000-0002-5579-9927
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NR 84
TC 32
Z9 32
U1 0
U2 6
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 OCT
PY 2016
VL 48
IS 10
BP 1112
EP 1118
DI 10.1016/j.dld.2016.05.011
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DW9YD
UT WOS:000384017800002
PM 27260332
DA 2025-01-04
ER

PT J
AU Soler, A
   Cayrefourcq, L
   Mazard, T
   Babayan, A
   Lamy, PJ
   Assou, S
   Assenat, E
   Pantel, K
   Alix-Panabières, C
AF Soler, Alexandra
   Cayrefourcq, Laure
   Mazard, Thibault
   Babayan, Anna
   Lamy, Pierre-Jean
   Assou, Said
   Assenat, Eric
   Pantel, Klaus
   Alix-Panabieres, Catherine
TI Autologous cell lines from circulating colon cancer cells captured from
   sequential liquid biopsies as model to study therapy-driven tumor
   changes
SO SCIENTIFIC REPORTS
LA English
DT Article
ID BREAST-CANCER; COLORECTAL-CANCER; EXPRESSION; METASTASIS; SURVIVAL;
   METAANALYSIS; PROGRESSION; PD-L1
AB Circulating tumor cells (CTCs) are important clinical indicators for prognosis and treatment efficacy. However, CTC investigation is hampered by their low number, making the establishment of permanent CTC lines very challenging. We derived and characterized nine CTC lines using blood samples from a patient with metastatic colorectal cancer collected before and after chemotherapy and targeted therapy, and during cancer progression. These cell lines displayed an intermediate epithelial/ mesenchymal phenotype, stem-cell like characteristics, angiogenesis potential, an osteomimetic signature and the capacity to escape from the immune system. Moreover, they showed changes in mRNA and protein expression (e.g., DEFA6, ABCB1 and GAL), whereas analysis of chromosomal copy number aberrations revealed no significant variation overtime. These data indicate that although CTC lines derived from sequential blood samples during therapy have common traits, treatment-resistant CTC clones with distinct phenotypic characteristics are selected over time.
C1 [Soler, Alexandra; Cayrefourcq, Laure; Alix-Panabieres, Catherine] Univ Med Ctr Montpellier, Lab Rare Human Circulating Cells, EA2415, Montpellier, France.
   [Mazard, Thibault] Canc Inst Montpellier, Dept Med Oncol, Montpellier, France.
   [Babayan, Anna; Pantel, Klaus] Univ Med Ctr Hamburg Eppendorf, Dept Tumor Biol, Hamburg, Germany.
   [Lamy, Pierre-Jean] Labosud, Imagenome, Montpellier, France.
   [Assou, Said] Montpellier Univ, Univ Med Ctr Montpellier, IRMB, INSERM,U1183, Montpellier, France.
   [Assenat, Eric] Univ Med Ctr Montpellier, Dept Med Oncol, Montpellier, France.
C3 Universite de Montpellier; CHU de Montpellier; Universite de
   Montpellier; University of Hamburg; University Medical Center
   Hamburg-Eppendorf; Institut National de la Sante et de la Recherche
   Medicale (Inserm); Universite de Montpellier; CHU de Montpellier;
   Universite de Montpellier; CHU de Montpellier
RP Alix-Panabières, C (corresponding author), Univ Med Ctr Montpellier, Lab Rare Human Circulating Cells, EA2415, Montpellier, France.
RI MAZARD, Thibault/ABH-6334-2020; Lamy, Pierre-Jean/AAZ-1696-2020;
   ALIX-PANABIERES, Catherine/AAC-1773-2019; Lamy, Pierre-Jean/I-6077-2015
OI Cayrefourcq, Laure/0000-0002-6124-7029; assou, said/0000-0001-6448-7995;
   Lamy, Pierre-Jean/0000-0002-5750-159X
FU DGOS; National Institute of Cancer (INCA - National COLOSPOT project);
   Region Languedoc-Roussillon (GEPETOS project); CANCER-ID, an Innovative
   Medicines Initiative Joint Undertaking from the European Union's Seventh
   Framework Program (FP7/2007-2013) [115749]; EFPIA; FEDER
FX The authors received support from DGOS, the National Institute of Cancer
   (INCA - National COLOSPOT project), FEDER and the Region
   Languedoc-Roussillon (GEPETOS project). This work was also supported by
   CANCER-ID, an Innovative Medicines Initiative Joint Undertaking under
   grant agreement no. 115749, based on financial contributions from the
   European Union's Seventh Framework Program (FP7/2007-2013), and EFPIA
   companies' in-kind contribution.
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NR 40
TC 61
Z9 65
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 OCT 29
PY 2018
VL 8
AR 15931
DI 10.1038/s41598-018-34365-z
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GY5CZ
UT WOS:000448589200007
PM 30374140
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU OuYang, CH
   Xie, Y
   Fu, QB
   Xu, GF
AF OuYang, Canhui
   Xie, Yun
   Fu, Qubo
   Xu, Guofeng
TI SYNPO2 suppresses hypoxia-induced proliferation and migration of
   colorectal cancer cells by regulating YAP-KLF5 axis
SO TISSUE & CELL
LA English
DT Article
DE Colorectal cancer (CRC); Synapsopoprotein 2 (SYNPO2); YAP; Kruppel like
   factor 5 (KLF5); Epithelial-mesenchymal transformation (EMT)
ID BLADDER-CANCER; ANGIOGENESIS; EXPRESSION; CARCINOMA; GROWTH
AB Colorectal cancer (CRC) is one of the most common tumors that has a high incidence worldwide. Targeted therapy for CRC has received much attention recently. It is still necessary to develop novel and promising therapeutic targets to improve the prognosis. SYNPO2, also known as synapsopoprotein 2 or myopod, encodes actin binding proteins and has been characterized as a tumor suppressor for aggressive cancers. SYNPO2 has been reported to inhibit the activity of YAP/TAZ. However, whether SYNPO2 could regulate the progression of CRC through the YAP/YAZ signaling pathway remains unclear. Herein, it was found that the expression of SYNPO2 was low in hypoxia-exposed CRC cells, consistent with the data from TCGA database. SYNPO2 inhibited the growth of CRC cells upon hypoxia treatment and promoted the cell apoptosis. Additionally, SYNPO2 inhibited the migration and epithelial-mesenchymal transformation (EMT) CRC cell upon hypoxia treatment. Mechanically, the results demonstrated that SYNPO2 suppressed hypoxia-induced progression of CRC by regulating YAP-Kruppel like factor 5 (KLF5) axis. Therefore, SYNPO2 can serve as a promising therapeutic target for CRC treatment.
C1 [OuYang, Canhui; Xie, Yun; Fu, Qubo; Xu, Guofeng] Gannan Med Univ, Dept Gastroenterol, Affiliated Hosp 1, 128 Jinling Rd, Ganzhou City 341000, Jiangxi, Peoples R China.
C3 Gannan Medical University
RP Xu, GF (corresponding author), Gannan Med Univ, Dept Gastroenterol, Affiliated Hosp 1, 128 Jinling Rd, Ganzhou City 341000, Jiangxi, Peoples R China.
EM xugf2019@gmail.com
RI Xu, Guofeng/I-3063-2016
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NR 31
TC 12
Z9 12
U1 0
U2 9
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
   LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0040-8166
J9 TISSUE CELL
JI Tissue Cell
PD DEC
PY 2021
VL 73
AR 101598
DI 10.1016/j.tice.2021.101598
EA JUL 2021
PG 7
WC Anatomy & Morphology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anatomy & Morphology; Cell Biology
GA YJ0XW
UT WOS:000744263300007
PM 34333382
DA 2025-01-04
ER

PT J
AU Szalai, F
   Sztankovics, D
   Krencz, I
   Moldvai, D
   Pápay, J
   Sebestyén, A
   Khoor, A
AF Szalai, Fatime
   Sztankovics, Daniel
   Krencz, Ildiko
   Moldvai, Dorottya
   Papay, Judit
   Sebestyen, Anna
   Khoor, Andras
TI Rictor-A Mediator of Progression and Metastasis in Lung Cancer
SO CANCERS
LA English
DT Review
DE lung cancer; mTOR pathway; mTORC2; RICTOR amplification; Rictor
   overexpression
ID EPITHELIAL-MESENCHYMAL TRANSITION; RAPAMYCIN AY-22,989;
   COLORECTAL-CANCER; COMPONENT RICTOR; MTOR; COMPLEX; PATHWAY; KINASE;
   PHOSPHORYLATION; EXPRESSION
AB Simple Summary Despite recent advances in targeted therapy and immunotherapy, the treatment of lung cancer remains challenging due to its high metastatic potential, which adversely affects both the prognosis and the quality of life of these patients. Rictor, the scaffold protein of the mTORC2 complex, plays an important role in regulating essential cellular functions and promoting metastases through epithelial-mesenchymal transition. Amplification of the RICTOR gene and subsequent overexpression of the Rictor protein can activate mTORC2 and promote cell survival and migration. Recent studies suggest that RICTOR amplification and Rictor overexpression may serve as markers of mTORC2 activation. Potentially, they can also provide druggable targets for advanced therapy. Although these drugs are still in a preclinical phase, selective mTORC2 inhibitors are a promising approach to inhibit tumor cell migration and metastasis formation. This review highlights the importance of Rictor and mTORC2 as predictive markers and promising therapeutic targets in the treatment of lung cancer.Abstract Lung carcinoma is one of the most common cancer types for both men and women. Despite recent breakthroughs in targeted therapy and immunotherapy, it is characterized by a high metastatic rate, which can significantly affect quality of life and prognosis. Rictor (encoded by the RICTOR gene) is known as a scaffold protein for the multiprotein complex mTORC2. Among its diverse roles in regulating essential cellular functions, mTORC2 also facilitates epithelial-mesenchymal transition and metastasis formation. Amplification of the RICTOR gene and subsequent overexpression of the Rictor protein can result in the activation of mTORC2, which promotes cell survival and migration. Based on recent studies, RICTOR amplification or Rictor overexpression can serve as a marker for mTORC2 activation, which in turn provides a promising druggable target. Although selective inhibitors of Rictor and the Rictor-mTOR association are only in a preclinical phase, they seem to be potent novel approaches to reduce tumor cell migration and metastasis formation. Here, we summarize recent advances that support an important role for Rictor and mTORC2 as potential therapeutic targets in the treatment of lung cancer. This is a traditional (narrative) review based on Pubmed and Google Scholar searches for the following keywords: Rictor, RICTOR amplification, mTORC2, Rictor complexes, lung cancer, metastasis, progression, mTOR inhibitors.
C1 [Szalai, Fatime; Sztankovics, Daniel; Krencz, Ildiko; Moldvai, Dorottya; Papay, Judit; Sebestyen, Anna] Semmelweis Univ, Dept Pathol & Expt Canc Res, Ullo Ut 26, H-1085 Budapest, Hungary.
   [Khoor, Andras] Mayo Clin, Dept Lab Med & Pathol, 4500 San Pablo Rd, Jacksonville, FL 32224 USA.
C3 Semmelweis University; Mayo Clinic
RP Khoor, A (corresponding author), Mayo Clin, Dept Lab Med & Pathol, 4500 San Pablo Rd, Jacksonville, FL 32224 USA.
EM fatie.salay@gmail.com; sztankovics.daniel@gmail.com;
   krencz.ildiko@gmail.com; moldvai.dorottya@gmail.com;
   papayjudith@gmail.com; hsebanna@gmail.com; khoor.andras@mayo.edu
RI Krencz, Ildiko/O-6434-2015
OI Sebestyen, Anna/0000-0001-8814-4794; dr. Moldvai,
   Dorottya/0009-0004-7831-6176; Sztankovics, Daniel/0009-0007-3168-1151;
   Szalai, Fatime/0009-0002-6129-6143
FU Hungarian National Research, Development and Innovation Office;
   Department of Pathology and Experimental Cancer Research, Semmelweis
   University institutional license
FX Figures were prepared using BioRender (https://biorender.com, accessed
   on 20 January 2024). Full access was covered by the Department of
   Pathology and Experimental Cancer Research, Semmelweis University
   institutional license.
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NR 100
TC 2
Z9 2
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 FEB
PY 2024
VL 16
IS 3
AR 543
DI 10.3390/cancers16030543
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HO7A6
UT WOS:001160499900001
PM 38339294
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lundy, J
   Harris, M
   Zalcberg, J
   Zimet, A
   Goldstein, D
   Gebski, V
   Borsaru, A
   Desmond, C
   Swan, M
   Jenkins, BJ
   Croagh, D
AF Lundy, Joanne
   Harris, Marion
   Zalcberg, John
   Zimet, Allan
   Goldstein, David
   Gebski, Val
   Borsaru, Adina
   Desmond, Christopher
   Swan, Michael
   Jenkins, Brendan J.
   Croagh, Daniel
TI EUS-FNA Biopsies to Guide Precision Medicine in Pancreatic Cancer:
   Results of a Pilot Study to Identify <i>KRAS</i> Wild-Type Tumours for
   Targeted Therapy
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE pancreatic cancer; endoscopic ultrasound; KRAS; molecular analysis;
   precision medicine
ID METASTATIC COLORECTAL-CANCER; FINE-NEEDLE-ASPIRATION; PHASE-III TRIAL;
   CLINICAL-TRIALS; K-RAS; SIGNALING PATHWAYS; 1ST-LINE TREATMENT; PLUS
   GEMCITABINE; CORE BIOPSY; ERLOTINIB
AB BackgroundPancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer death and lacks effective treatment options. Diagnostic endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) biopsies represent an appealing source of material for molecular analysis to inform targeted therapy, as they are often the only available tissue for patients presenting with PDAC irrespective of disease stage. However, EUS-FNA biopsies are typically not used to screen for precision medicine studies due to concerns about low tissue yield and quality. Epidermal growth factor receptor (EGFR) inhibition has shown promise in clinical trials of unselected patients with advanced pancreatic cancer, but has not been prospectively tested in KRAS wild-type patients. Here, we examine the clinical utility of EUS-FNA biopsies for molecular screening of KRAS wild-type PDAC patients for targeted anti-EGFR therapy to assess the feasibility of this approach. Patients and MethodsFresh frozen EUS-FNA or surgical biopsies from PDAC patient tumours were used to screen for KRAS mutations. Eligible patients with recurrent, locally advanced, or metastatic KRAS wild-type status who had received at least one prior line of chemotherapy were enrolled in a pilot study (ACTRN12617000540314) and treated with panitumumab at 6mg/kg intravenously every 2 weeks until progression or unacceptable toxicity. The primary endpoint was 4-month progression-free survival (PFS). Results275 patient biopsies were screened for KRAS mutations, which were detected in 88.3% of patient samples. 8 eligible KRAS wild-type patients were enrolled onto the interventional study between November 2017 and December 2020 and treated with panitumumab. 4-month PFS was 14.3% with no objective tumour responses observed. The only grade 3/4 treatment related toxicity observed was hypomagnesaemia. ConclusionsThis study demonstrates proof-of-principle feasibility to molecularly screen patients with pancreatic cancer for targeted therapies, and confirms diagnostic EUS-FNA biopsies as a reliable source of tumour material for molecular analysis. Single agent panitumumab was safe and tolerable but led to no objective tumour responses in this population.
C1 [Lundy, Joanne; Jenkins, Brendan J.; Croagh, Daniel] Hudson Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic, Australia.
   [Lundy, Joanne; Jenkins, Brendan J.] Monash Univ, Fac Med Nursing & Hlth Sci, Dept Mol & Translat Sci, Clayton, Vic, Australia.
   [Lundy, Joanne; Croagh, Daniel] Monash Univ, Fac Med Nursing & Hlth Sci, Dept Surg, Clayton, Vic, Australia.
   [Harris, Marion] Monash Univ, Fac Med Nursing & Hlth Sci, Dept Oncol, Clayton, Vic, Australia.
   [Harris, Marion] Monash Univ, Sch Clin Sci, Clayton, Vic, Australia.
   [Zalcberg, John] Alfred Hlth, Dept Med Oncol, Melbourne, Vic, Australia.
   [Zalcberg, John] Monash Univ, Publ Hlth & Preventat Med, Melbourne, Vic, Australia.
   [Zimet, Allan] Epworth Med Fdn, Dept Med Oncol, Melbourne, Vic, Australia.
   [Goldstein, David] Univ New South Wales, Prince Wales Clin Sch, Sydney, NSW, Australia.
   [Goldstein, David] Prince Wales Hosp, Dept Med Oncol, Randwick, NSW, Australia.
   [Gebski, Val] Univ Sydney, Clin Trials Ctr, Natl Hlth & Med Res Council, Camperdown, NSW, Australia.
   [Borsaru, Adina] Monash Hlth, Diagnost Imaging, Melbourne, Vic, Australia.
   [Desmond, Christopher; Swan, Michael] Monash Hlth, Dept Gastroenterol, Melbourne, Vic, Australia.
   [Croagh, Daniel] Epworth Healthcare, Dept Surg, Melbourne, Vic, Australia.
C3 Hudson Institute of Medical Research; Monash University; Monash
   University; Monash University; Monash University; Monash University;
   Epworth Medical Foundation; University of New South Wales Sydney;
   University of New South Wales Sydney; Prince of Wales Hospital (POWH);
   University of Sydney; Monash Health; Monash Health
RP Croagh, D (corresponding author), Hudson Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic, Australia.; Croagh, D (corresponding author), Monash Univ, Fac Med Nursing & Hlth Sci, Dept Surg, Clayton, Vic, Australia.; Croagh, D (corresponding author), Epworth Healthcare, Dept Surg, Melbourne, Vic, Australia.
EM Daniel.Croagh@monashhealth.org
RI goldstein, david/J-6711-2012; jenkins, brendan/J-7854-2012; Gebski,
   Val/HNJ-2164-2023
OI Zalcberg, John/0000-0002-6624-0782; Gebski, Val/0000-0001-8748-1844;
   Lundy, Joanne/0000-0003-0210-4930
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NR 73
TC 6
Z9 6
U1 0
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD DEC 9
PY 2021
VL 11
AR 770022
DI 10.3389/fonc.2021.770022
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YA4QR
UT WOS:000738320200001
PM 34956889
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Gao, X
   Xu, WH
   Lu, TX
   Zhou, JL
   Ge, XS
   Hua, D
AF Gao, Xiang
   Xu, Wenhuan
   Lu, Tingxun
   Zhou, Jialiang
   Ge, Xiaosong
   Hua, Dong
TI MicroRNA-142-3p Promotes Cellular Invasion of Colorectal Cancer Cells by
   Activation of RAC1
SO TECHNOLOGY IN CANCER RESEARCH & TREATMENT
LA English
DT Article
DE microRNA-142-3p; invasion; colorectal cancer; RAC1
ID BIOGENESIS; MIR-142-3P; CARCINOMA; PATHWAYS
AB Background: Colorectal cancer has been proved more difficult to treat owing to potently malignant metastasis. The present study was aimed to explore the functional role of miR-142-3p in cell migration and invasion of colorectal cancer cells, as well as its underlying mechanism. Materials and Methods: Expressions of miR-142-3p were analyzed in colorectal cancer tissues and cell lines. Ras-related C3 botulinum toxin substrate 1 (RAC1) was predicted as a target of miR-142-3p using software and network resources. SW480 cells were transfected with miR-142-3p expression plasmid and miR-142-3p silencer plasmid, and the expression of RAC1 and the cellular invasion were measured. Results: In colorectal cancer cells transfected with miR-142-3p expression plasmid, RAC1 was specifically upregulated and invasiveness of cells was downregulated. Moreover, RAC1 was significantly associated with tumor stage (P = .029) and tumor metastasis (P = .012). Conclusion: miR-142-3p promotes cellular invasion in colorectal cancer cells by activating RAC1. Thereby, miR-142-3p is a potential candidate for molecular targeted therapy of colorectal cancer.
C1 [Gao, Xiang; Xu, Wenhuan; Lu, Tingxun; Zhou, Jialiang; Ge, Xiaosong; Hua, Dong] Jiangnan Univ, Affiliated Hosp, Dept Med Oncol, Wuxi, Peoples R China.
C3 Jiangnan University
RP Ge, XS; Hua, D (corresponding author), Jiangnan Univ, Wuxi Canc Inst, Affiliated Hosp, Dept Med Oncol, 200 Huihe Rd, Wuxi 214062, Jiangsu, Peoples R China.
EM gexiaosong@qq.com; wx89211@163.com
RI LU, TINGXUN/JXX-4050-2024; Zhou, Jialiang/HCH-1210-2022
FU National Natural Science Foundation of China [81372375, 81502042,
   81402487]; Natural Science Foundation for Young Scholars of Jiangsu
   Province, China [BK20140171]
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: This study
   was supported by the National Natural Science Foundation of China (Grant
   No. 81372375 and 81502042, 81402487), Natural Science Foundation for
   Young Scholars of Jiangsu Province, China (Grant No. BK20140171).
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NR 17
TC 27
Z9 27
U1 0
U2 5
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.
PD JUL 31
PY 2018
VL 17
DI 10.1177/1533033818790508
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GW7EM
UT WOS:000447129700001
PM 30064309
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lv, Y
   Zheng, P
   Mao, YH
   Xu, YQ
   Chang, WJ
   Lin, Q
   Ji, ML
   Ye, LC
   Tang, WT
   Xu, JM
AF Lv, Yang
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   Mao, Yihao
   Xu, Yuqiu
   Chang, Wenju
   Lin, Qi
   Ji, Meiling
   Ye, Lechi
   Tang, Wentao
   Xu, Jianmin
TI Intratumor APOL3 delineates a distinctive immunogenic ferroptosis subset
   with prognosis prediction in colorectal cancer
SO CANCER SCIENCE
LA English
DT Article
DE apolipoprotein L3; colorectal cancer; immunogenic ferroptosis;
   prognosis; tumor microenvironment
ID INFILTRATING IMMUNE; TISSUE; CELLS; STATISTICS; EXPRESSION; DISEASE
AB With the essential role of lipid transporting signaling in cancer-related immunity, apolipoprotein L3 (APOL3), a member of the apolipoprotein L gene family, demonstrated significant modulation ability in immunity. However, the expression profile and critical role of APOL3 in colorectal cancer (CRC) remain unclear. This study aimed to investigate the prognostic significance of APOL3 expression and its biological predictive value in CRC. The study enrolled multiple cohorts, consisting of 911 tumor microarray specimens of CRC patients from Zhongshan Hospital, 412 transcriptional data from The Cancer Genome Atlas, and 30 single-cell RNA sequencing (scRNA-seq) from internal and external CRC patients. APOL3 mRNA expression was directly acquired from public datasets, and APOL3 protein expression was detected using immunohistochemistry. Finally, the associations of APOL3 expression with clinical outcomes, immune context, and genomic and ferroptotic features were analyzed. Low APOL3 expression predicted poor prognosis and inferior responsiveness to 5-fluorouracil-based adjuvant chemotherapy (ACT) and targeted therapy. APOL3 fosters an immune-active microenvironment characterized by the promotion of ferroptosis, downregulation of macrophages, and upregulation of CD8+ T cell infiltration. Moreover, the expression of APOL3 in CD8+ T cells is intrinsically linked to ferroptosis and immune activation in CRC. In summary, APOL3 serves as an independent prognosticator and predictive biomarker for immunogenic ferroptosis, ACT, and targeted therapy in CRC. Furthermore, the APOL3 signaling activator could be a novel agent alone or in combination with current therapeutic strategies for CRC.
C1 [Lv, Yang; Zheng, Peng; Mao, Yihao; Xu, Yuqiu; Chang, Wenju; Lin, Qi; Ji, Meiling; Ye, Lechi; Tang, Wentao; Xu, Jianmin] Fudan Univ, Zhongshan Hosp, Dept Colorectal Surg, Shanghai, Peoples R China.
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   [Zheng, Peng; Mao, Yihao; Xu, Yuqiu; Chang, Wenju; Lin, Qi; Ji, Meiling; Tang, Wentao; Xu, Jianmin] Shanghai Engn Res Ctr Colorectal Canc Minimally In, Shanghai, Peoples R China.
   [Ye, Lechi; Tang, Wentao; Xu, Jianmin] 180 Fenglin Rd, Shanghai 200032, Peoples R China.
C3 Fudan University; Fudan University
RP Ye, LC; Tang, WT; Xu, JM (corresponding author), 180 Fenglin Rd, Shanghai 200032, Peoples R China.
EM yljwenzhou@126.com; tangwt1988@163.com; xujmin@aliyun.com
FU This manuscript has not been submitted to any other journal and is not
   currently being considered for publication by another journal. We Thank
   the doctors and nurses who performed the treatment.
FX This manuscript has not been submitted to any other journal and is not
   currently being considered for publication by another journal. We Thank
   the doctors and nurses who performed the treatment.
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NR 53
TC 3
Z9 3
U1 2
U2 11
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1347-9032
EI 1349-7006
J9 CANCER SCI
JI Cancer Sci.
PD JAN
PY 2024
VL 115
IS 1
BP 257
EP 269
DI 10.1111/cas.16009
EA NOV 2023
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GO1T7
UT WOS:001107594400001
PM 37986654
OA gold
DA 2025-01-04
ER

PT J
AU Meng, B
   Zhao, X
   Jiang, SC
   Xu, ZJ
   Li, SJ
   Wang, X
   Ma, W
   Li, LT
   Liu, D
   Zheng, JN
   Peng, H
   Shi, M
AF Meng, Bi
   Zhao, Xuan
   Jiang, Shuchang
   Xu, Zijian
   Li, Sijin
   Wang, Xu
   Ma, Wen
   Li, Liantao
   Liu, Dan
   Zheng, Junnian
   Peng, Hui
   Shi, Ming
TI AURKA inhibitor-induced PD-L1 upregulation impairs antitumor immune
   responses
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE targeted drugs; MLN8237; AURKA inhibitor; PD-L1; p-STAT3; tumor
   immunotherapy
ID CANCER; CELLS; EXPRESSION; BLOCKADE; EFFICACY; PATHWAY; KINASE; AURORA;
   STAT3
AB IntroductionTumor immunotherapy targeting PD-L1 has emerged as one of the powerful tools for tumor therapy. Numerous studies indicate that tumor-targeted drugs critically have an influence on the interaction between the immune system and tumors by changing the expression of PD-L1, which is beneficial for immunotherapy. Our study provided novel evidence for improving the drug regimen in tumor targeted therapy and immunotherapy.MethodsThe expression of PD-L1 on SKBR3, MDA-MB-231, MCF7, 4T1, MC38 and B16 cells was evaluated by flow cytometry after treatment with six preclinical targeted drugs (ARN-509, AZD3514, Galeterone, Neratinib, MLN8237 and LGK974). AURKA was knockdowned by using the specific siRNA or CRISPR-Cas9 technology. In the 4T1-breast tumor and colorectal cancer xenograft tumor models, we determined the number of infiltrated CD3+ and CD8+ T cells in tumor tissues by IHC.ResultsWe found that AURKA inhibitor MLN8237 promoted the expression of PD-L1 in a time- and concentration-dependent manner while exerted its antitumor effect. Knockdown of AURKA could induce the upregulation of PD-L1 on SKBR3 cells. MLN8237-induced PD-L1 upregulation was mainly associated with the phosphorylation of STAT3. In the 4T1-breast tumor xenograft model, the infiltrated CD3+ and CD8+ T cells decreased after treatment with MLN8237. When treated with MLN8237 in combination with anti-PD-L1 antibody, the volumes of tumor were significantly reduced and accompanied by increasing the infiltration of CD3+ and CD8+ T cells in colorectal cancer xenograft tumor model.DiscussionOur data demonstrated that MLN8237 improved the effect of immunology-related therapy on tumor cells by interacting with anti-PD-L1 antibody, which contributed to producing creative sparks for exploring the possible solutions to overcoming drug resistance to tumor targeted therapy.
C1 [Meng, Bi; Zhao, Xuan; Xu, Zijian; Li, Sijin; Wang, Xu; Ma, Wen; Liu, Dan; Shi, Ming] Xuzhou Med Univ, Canc Inst, Xuzhou, Jiangsu, Peoples R China.
   [Meng, Bi; Zhao, Xuan; Xu, Zijian; Li, Sijin; Wang, Xu; Ma, Wen; Li, Liantao; Liu, Dan; Zheng, Junnian; Shi, Ming] Xuzhou Med Univ, Affiliated Hosp, Ctr Clin Oncol, Xuzhou, Jiangsu, Peoples R China.
   [Meng, Bi; Zhao, Xuan; Xu, Zijian; Li, Sijin; Wang, Xu; Ma, Wen; Li, Liantao; Liu, Dan; Zheng, Junnian; Shi, Ming] Xuzhou Med Univ, Jiangsu Ctr Collaborat & Innovat Canc Biotherapy, Xuzhou, Jiangsu, Peoples R China.
   [Jiang, Shuchang; Peng, Hui] Tianjin Inst Environm & Operat Med, Dept Operat Med, Tianjin, Peoples R China.
C3 Xuzhou Medical University; Xuzhou Medical University; Xuzhou Medical
   University
RP Shi, M (corresponding author), Xuzhou Med Univ, Canc Inst, Xuzhou, Jiangsu, Peoples R China.; Zheng, JN; Shi, M (corresponding author), Xuzhou Med Univ, Affiliated Hosp, Ctr Clin Oncol, Xuzhou, Jiangsu, Peoples R China.; Zheng, JN; Shi, M (corresponding author), Xuzhou Med Univ, Jiangsu Ctr Collaborat & Innovat Canc Biotherapy, Xuzhou, Jiangsu, Peoples R China.; Peng, H (corresponding author), Tianjin Inst Environm & Operat Med, Dept Operat Med, Tianjin, Peoples R China.
EM jnzheng@xzhmu.edu.cn; p_h2002@hotmail.com; sm200@sohu.com
RI Xu, Zijian/HHZ-7926-2022; li, sijin/T-2280-2018
OI Shi, Ming/0000-0001-9263-6468
FU This work was supported by National Natural Science Foundation of China
   (81972719, 82003164, 82273207), Jiangsu Province Natural Science
   Foundation (No. BK20201012), Science and Technology Project of Xuzhou
   (No. KC20126), National science research in Unive [81972719, 82003164,
   82273207]; National Natural Science Foundation of China [BK20201012];
   Jiangsu Province Natural Science Foundation [KC20126]; Science and
   Technology Project of Xuzhou [20KJB320032, 21KJA320008]; National
   science research in Universities of Jiangsu Province [2022M722680];
   China Postdoctoral Science Foundation [D2019050]; Scientific Research
   Foundation of Xuzhou Medical University [KYCX20_2459]; Jiangsu Research
   Innovation Program for College Graduates
FX This work was supported by National Natural Science Foundation of China
   (81972719, 82003164, 82273207), Jiangsu Province Natural Science
   Foundation (No. BK20201012), Science and Technology Project of Xuzhou
   (No. KC20126), National science research in Universities of Jiangsu
   Province (No. 20KJB320032, No. 21KJA320008), China Postdoctoral Science
   Foundation funded project (No. 2022M722680), Scientific Research
   Foundation of Xuzhou Medical University (No. D2019050), Jiangsu Research
   Innovation Program for College Graduates (No. KYCX20_2459).
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NR 42
TC 3
Z9 3
U1 3
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 SEP 12
PY 2023
VL 14
AR 1182601
DI 10.3389/fimmu.2023.1182601
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA S3WY9
UT WOS:001070519200001
PM 37781397
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xie, YH
   Chen, YX
   Fang, JY
AF Xie, Yuan-Hong
   Chen, Ying-Xuan
   Fang, Jing-Yuan
TI Comprehensive review of targeted therapy for colorectal cancer
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; PHASE-III TRIAL; WILD-TYPE
   KRAS; TIVANTINIB ARQ 197; CONSENSUS MOLECULAR SUBTYPES; CETUXIMAB PLUS
   IRINOTECAN; PHOSPHOLIPASE-C-GAMMA; GENE COPY NUMBER; OXALIPLATIN-BASED
   CHEMOTHERAPY
AB Colorectal cancer (CRC) is among the most lethal and prevalent malignancies in the world and was responsible for nearly 881,000 cancer-related deaths in 2018. Surgery and chemotherapy have long been the first choices for cancer patients. However, the prognosis of CRC has never been satisfying, especially for patients with metastatic lesions. Targeted therapy is a new optional approach that has successfully prolonged overall survival for CRC patients. Following successes with the anti-EGFR (epidermal growth factor receptor) agent cetuximab and the anti-angiogenesis agent bevacizumab, new agents blocking different critical pathways as well as immune checkpoints are emerging at an unprecedented rate. Guidelines worldwide are currently updating the recommended targeted drugs on the basis of the increasing number of high-quality clinical trials. This review provides an overview of existing CRC-targeted agents and their underlying mechanisms, as well as a discussion of their limitations and future trends.
C1 [Xie, Yuan-Hong; Chen, Ying-Xuan; Fang, Jing-Yuan] Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes, Shanghai Inst Digest Dis,Minist Hlth,Key Lab Gast, Renji Hosp,Sch Med,Div Gastroenterol & Hepatol, 145 Middle Shandong Rd, Shanghai 200001, Peoples R China.
C3 Shanghai Jiao Tong University
RP Chen, YX; Fang, JY (corresponding author), Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes, Shanghai Inst Digest Dis,Minist Hlth,Key Lab Gast, Renji Hosp,Sch Med,Div Gastroenterol & Hepatol, 145 Middle Shandong Rd, Shanghai 200001, Peoples R China.
EM yingxuanchen71@126.com; jingyuanfang@sjtu.edu.cn
RI FANG, Jing-Yuan/JOZ-1388-2023
OI fang, jingyuan/0000-0003-2282-0248
FU National Natural Science Foundation of China [81421001, 81530072,
   81830081, 81772506]
FX This work was supported by grants from the National Natural Science
   Foundation of China (81421001, 81530072, 81830081 and 81772506). We
   thank Dr. Yao Zhang for her verification of all table data.
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NR 507
TC 986
Z9 1038
U1 19
U2 213
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 MAR 20
PY 2020
VL 5
IS 1
AR 22
DI 10.1038/s41392-020-0116-z
PG 30
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA KW0HB
UT WOS:000520853100001
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Yan, CR
   Wang, JR
   Yang, YY
   Ma, WB
   Chen, XL
AF Yan, Chengrui
   Wang, Jiaru
   Yang, Yuyan
   Ma, Wenbin
   Chen, Xiaolin
TI Molecular biomarker-guided anti-angiogenic targeted therapy for
   malignant glioma
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Review
DE anti-angiogenic; biomarkers; glioma; molecular; therapy
ID NEWLY-DIAGNOSED GLIOBLASTOMA; STANDARD TREATMENT; OPEN-LABEL;
   BEVACIZUMAB; TEMOZOLOMIDE; CANCER; TRIAL; RADIOTHERAPY; ENZASTAURIN;
   CILENGITIDE
AB Despite aggressive multimodality treatment, the prognosis of glioma, especially malignant glioma, remains very poor. After decades of effort, anti-angiogenic therapy has become an important method of cancer treatment in addition to surgery, radiotherapy and chemotherapy. Although the performance of anti-angiogenic therapy in colorectal cancer is good, its performance in malignant glioma remains unsatisfactory. Several phase III clinical trials showed no overall survival benefits. To solve this problem, the division of patients into groups based on their molecular biomarkers is an important step. This paper provides current insights into anti-angiogenic drugs undergoing clinical trials and discusses the potential of molecular biomarkers to guide glioma diagnosis.
C1 [Yan, Chengrui] Peking Univ, Int Hosp, Dept Neurosurg, Beijing, Peoples R China.
   [Yan, Chengrui; Wang, Jiaru; Yang, Yuyan; Ma, Wenbin] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Neurosurg, Beijing, Peoples R China.
   [Chen, Xiaolin] Capital Med Univ, Beijing Tiantan Hosp, Dept Neurosurg, Beijing, Peoples R China.
C3 Peking University; Chinese Academy of Medical Sciences - Peking Union
   Medical College; Peking Union Medical College Hospital; Capital Medical
   University
RP Ma, WB (corresponding author), Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Neurosurg, Beijing, Peoples R China.; Chen, XL (corresponding author), Capital Med Univ, Beijing Tiantan Hosp, Dept Neurosurg, Beijing, Peoples R China.
EM mawb2001@hotmail.com; xiaolinchen488@hotmail.com
OI Yang, Yuyan/0000-0002-0698-4093
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NR 48
TC 13
Z9 13
U1 2
U2 15
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 AUG
PY 2019
VL 23
IS 8
BP 4876
EP 4882
DI 10.1111/jcmm.14417
PG 7
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA IR6EN
UT WOS:000481532600003
PM 31210419
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhang, YY
   Luo, JY
   Yang, WK
   Ye, WC
AF Zhang, Yuying
   Luo, Jingyan
   Yang, Weikang
   Ye, Wen-Chu
TI CircRNAs in colorectal cancer: potential biomarkers and therapeutic
   targets
SO CELL DEATH & DISEASE
LA English
DT Review
ID CIRCULAR RNA; PROMOTES METASTASIS; BIOGENESIS; TRANSLATION; PROGRESSION;
   EXPRESSION; BINDING; VACCINES; ABUNDANT
AB Globally, colorectal cancer (CRC) is the third most prevalent cancer and the second leading cause of cancer-related deaths. Circular RNAs (circRNAs) are single-stranded RNA with covalently closed-loop structures and are highly stable, conserved, and abundantly expressed in various organs and tissues. Recent research found abnormal circRNA expression in CRC patients' blood/serum, cells, CRC tissues, and exosomes. Furthermore, mounting data demonstrated that circRNAs are crucial to the development of CRC. CircRNAs have been shown to exert biological functions by acting as microRNA sponges, RNA-binding protein sponges, regulators of gene splicing and transcription, and protein/peptide translators. These characteristics make circRNAs potential markers for CRC diagnosis and prognosis, potential therapeutic targets, and circRNA-based therapies. However, further studies are still necessary to improve the understanding of the roles and biological mechanisms of circRNAs in the development of CRC. In this review, up-to-date research on the role of circRNAs in CRC was examined, focusing on their potential application in CRC diagnosis and targeted therapy, which would advance the knowledge of the functions of circRNAs in the development and progression of CRC.
C1 [Zhang, Yuying] Shenzhen Longhua Matern & Child Healthcare Hosp, Cent Lab, Shenzhen 518109, Peoples R China.
   [Luo, Jingyan] Guangzhou Int Biotech Isl, Forevergen Biosci Ctr, Guangzhou 510300, Peoples R China.
   [Yang, Weikang] Shenzhen Longhua Matern & Child Healthcare Hosp, Dept Prevent & Healthcare, Shenzhen 518109, Peoples R China.
   [Ye, Wen-Chu] Chinese Univ Hong Kong, Shenzhen Res Inst, Shenzhen, Peoples R China.
C3 The Chinese University of Hong Kong, Shenzhen; CUHK Shenzhen Research
   Institute
RP Ye, WC (corresponding author), Chinese Univ Hong Kong, Shenzhen Res Inst, Shenzhen, Peoples R China.
EM wenchu_ye@163.com
RI Yang, Wei-Kang/ABE-6938-2021; Ye, Wen-Chu/AEA-6605-2022
FU National Natural Science Foundation of China [82000407, 81802551];
   Shenzhen Science and Technology Program [JCYJ20220531091200001]; Natural
   Science Foundation of Guangdong Province [2023A1515010425]
FX This work was supported by the grants from National Natural Science
   Foundation of China (No. 82000407 and 81802551), Shenzhen Science and
   Technology Program(No. JCYJ20220531091200001) and Natural Science
   Foundation of Guangdong Province (2023A1515010425).
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NR 157
TC 45
Z9 45
U1 6
U2 24
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 JUN 9
PY 2023
VL 14
IS 6
AR 353
DI 10.1038/s41419-023-05881-2
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA I6QV3
UT WOS:001004018900004
PM 37296107
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Dastjerdi, S
   Valizadeh, M
   Nemati, R
   Honardoost, MA
   Dolatabadi, NF
   Zamani, A
   Tabatabaeian, H
AF Dastjerdi, Shaghayegh
   Valizadeh, Mehdi
   Nemati, Rasoul
   Honardoost, Mohammad Amin
   Dolatabadi, Nasrin Fattahi
   Zamani, Atefeh
   Tabatabaeian, Hossein
TI Highly expressed TLX1NB and NPSR1-AS1 lncRNAs could serve as diagnostic
   tools in colorectal cancer
SO HUMAN CELL
LA English
DT Article
DE TLX1NB; NPSR1-AS1; Long non-coding RNA; Colorectal cancer; Diagnosis
ID RNA INTERACTION NETWORKS; LONG NONCODING RNAS
AB Colorectal cancer is the main cause of human death due to cancer. This fact could be due to the insufficiency of early diagnosis or poor therapeutic strategies. Various molecular tools have been utilized in studies to assess their potentials as diagnostic biomarkers or determining factors in precision medicine. Among these molecules, long non-coding RNAs (lncRNA) have been emerging as accurate and potent transcripts to improve the detection of cancer. The overexpressed lncRNAs could also be deeply studied as the molecules for the targeted therapy in different malignancies, in particular colorectal cancer. Thus, we utilized an unbiased approach to select the up-regulated lncRNAs in colon adenocarcinoma via analyzing the TCGA dataset. Then, we validated the overexpression of two first-ranked lncRNAs, i.e., NPSR1-AS1 and TLX1NB, in our in-house colorectal cancer samples as compared to the paired adjacent normal tissues. The analyses revealed that these lncRNAs could significantly distinguish the tumor against the normal samples. The results may have implications in the early diagnosis and targeted therapy of colorectal cancer.
C1 [Dastjerdi, Shaghayegh; Dolatabadi, Nasrin Fattahi; Zamani, Atefeh] Genet & Biotechnol Acad, Gene Raz Bu Ali, Esfahan, Iran.
   [Dastjerdi, Shaghayegh] Islamic Azad Univ, Dept Cellular & Mol Sci, Fac Adv Sci & Technol, Tehran Med Sci, Tehran, Iran.
   [Valizadeh, Mehdi] Ardabil Univ Med Sci, Digest Dis Res Ctr, Unit Genom Res, Ardebil, Iran.
   [Nemati, Rasoul] Ardabil Univ Med Sci, Digest Dis Res Ctr, Sch Med & Allied Med Sci, Dept Internal Med, Ardebil, Iran.
   [Honardoost, Mohammad Amin; Tabatabaeian, Hossein] Univ Isfahan, Fac Biol Sci & Technol, Dept Cell & Mol Biol & Microbiol, Esfahan, Iran.
   [Tabatabaeian, Hossein] Isfahan Healthcare City, Anahid Canc Clin, Esfahan, Iran.
C3 Islamic Azad University; Ardabil University of Medical Sciences; Ardabil
   University of Medical Sciences; University of Isfahan
RP Tabatabaeian, H (corresponding author), Univ Isfahan, Fac Biol Sci & Technol, Dept Cell & Mol Biol & Microbiol, Esfahan, Iran.; Tabatabaeian, H (corresponding author), Isfahan Healthcare City, Anahid Canc Clin, Esfahan, Iran.
EM csiht@nus.edu.sg
RI Tabatabaeian, Hossein/I-2235-2019
OI fattahi, nasrin/0000-0003-4705-6223; Tabatabaeian,
   Hossein/0000-0001-9757-6150
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NR 22
TC 7
Z9 7
U1 1
U2 4
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 0914-7470
EI 1749-0774
J9 HUM CELL
JI Hum. Cell
PD NOV
PY 2021
VL 34
IS 6
BP 1765
EP 1774
DI 10.1007/s13577-021-00597-x
EA AUG 2021
PG 10
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA WB4ZR
UT WOS:000686052400001
PM 34406628
DA 2025-01-04
ER

PT J
AU Kazazian, K
   Brashavitskaya, O
   Zih, FSW
   Berger-Richardson, D
   Xu, RSZ
   Pacholczyk, K
   Macmillan, J
   Swallow, CJ
AF Kazazian, Karineh
   Brashavitskaya, Olga
   Zih, Francis S. W.
   Berger-Richardson, David
   Xu, Roland S. Z.
   Pacholczyk, Karina
   Macmillan, Jennifer
   Swallow, Carol J.
TI Polo-Like Kinases in Colorectal Cancer: Potential for Targeted Therapy
SO CURRENT COLORECTAL CANCER REPORTS
LA English
DT Article
DE Colorectal cancer; Personalized cancermedicine; Polo-like kinase family;
   Plk1; Plk2; Plk3; Plk4; Plk5; Carcinogenesis; Tumor progression; Cell
   cycle regulator; Targeted therapy; Centrosome
ID INHIBITS TUMOR-GROWTH; ACUTE MYELOID-LEUKEMIA; VOLASERTIB BI 6727;
   CELL-CYCLE ARREST; PHASE-II TRIAL; CENTRIOLE DUPLICATION; BREAST-CANCER;
   OPEN-LABEL; CENTROSOME AMPLIFICATION; PROGNOSTIC-SIGNIFICANCE
AB The five individual members of the mammalian polo-like kinase family play non-redundant roles in centriole replication and maturation, mitotic progression, cytokinesis, and the DNA damage response. In human colorectal cancer, Plk1 and Plk4 are expressed at higher levels in tumor than adjacent normal mucosa, and the degree of overexpression correlates with adverse prognosis. In colorectal cancer cell lines, suppression of Plk1 activity leads to mitotic arrest and apoptosis, while inhibition of Plk4 activity reduces tumor growth and invasion. Inhibition of Plk1 or Plk4 in mice using orally bioavailable agents reduces the growth of human colorectal cancer xenografts. On the basis of these preclinical studies, clinical trials of several different targeted anti-Plk1 agents have been undertaken in patients with advanced solid tumors, and a phase I trial of the anti-Plk4 inhibitor CFI-400945 is currently accruing. Here, we review the rationale, results, and potential limitations of Plks as therapeutic targets. Evidence from genetic mouse models suggests that Plk1, Plk2, Plk3, and Plk4 may all possess tumor suppressive activity, particularly with aging. Thus, enthusiasm for the use of targeted Plk inhibitors in cancer therapy must be tempered somewhat by the potential for development of second primary tumors in the long term.
C1 [Kazazian, Karineh; Brashavitskaya, Olga; Zih, Francis S. W.; Berger-Richardson, David; Xu, Roland S. Z.; Pacholczyk, Karina; Swallow, Carol J.] Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, 600 Univ Ave, Toronto, ON M5G 1X5, Canada.
   [Kazazian, Karineh; Zih, Francis S. W.; Berger-Richardson, David; Macmillan, Jennifer; Swallow, Carol J.] Univ Toronto, Dept Surg, Toronto, ON, Canada.
   [Kazazian, Karineh; Zih, Francis S. W.; Berger-Richardson, David; Swallow, Carol J.] Univ Toronto, Inst Med Sci, Toronto, ON, Canada.
   [Brashavitskaya, Olga; Swallow, Carol J.] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada.
C3 University of Toronto; Sinai Health System Toronto; Lunenfeld Tanenbaum
   Research Institute; University of Toronto; University of Toronto;
   University of Toronto
RP Swallow, CJ (corresponding author), Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, 600 Univ Ave, Toronto, ON M5G 1X5, Canada.
EM kkazazian@gmail.com; olga@lunenfeld.ca; francis.zih@gmail.com;
   david.berger.richardson@mail.utoronto.ca;
   shuzhengrong.xu@mail.utoronto.ca; karina@lunenfeld.ca;
   jcmacmd@gmail.com; cswallow@mtsinai.on.ca
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NR 159
TC 3
Z9 6
U1 0
U2 4
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 2015
VL 11
IS 4
BP 187
EP 199
DI 10.1007/s11888-015-0275-4
PG 13
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA V2G8T
UT WOS:000217568200005
DA 2025-01-04
ER

PT J
AU Li, WM
   Bing, T
   Wang, R
   Jin, SH
   Shangguan, DH
   Chen, H
AF Li, Wanming
   Bing, Tao
   Wang, Rui
   Jin, Sihan
   Shangguan, Dihua
   Chen, Hang
TI Cell-SELEX-based selection of ssDNA aptamers for specifically targeting
   <i>BRAF</i> V600E-mutated melanoma
SO ANALYST
LA English
DT Article
ID IN-VITRO SELECTION; COLORECTAL-CANCER; DNA APTAMERS; VEMURAFENIB;
   MUTATION; PHASE-3
AB Malignant melanoma is regarded as the most aggressive form of skin cancer, and is responsible for most death caused by skin cancer. BRAF mutations occur in approximately 40-50% of melanomas, with V600E being the most common mutation. Testing for BRAF mutations and targeted therapy have markedly improved long-term survival for patients with BRAF-mutated melanoma. Here, we report two aptamers, CH1 and CH5 generated by Cell-SELEX, against BRAF V600E-mutated human melanoma cells A375. The two aptamers exhibited high affinity to target cells with low dissociation constants (K-d) in the nanomolar range. Furthermore, the binding of two aptamers to target cells was independent of incubation temperature, and their molecular targets were demonstrated to be membrane proteins on the cell surface. We also demonstrated that aptamer CH1 was able to bind to metastatic colorectal cancer cells harboring BRAF V600E mutation, indicating a relationship between aptamer CH1 and BRAF V600E-related metastatic cancer. Owing to the structure stability and high selectivity to BRAF V600E-mutated targeting cells, aptamer CH1 holds great potential as a molecular probe for the detection of BRAF V600E-mutated metastatic melanoma.
C1 [Li, Wanming; Jin, Sihan] China Med Univ, Dept Cell Biol, Key Lab Cell Biol, Minist Publ Hlth,Minist Educ, Shenyang 110122, Liaoning, Peoples R China.
   [Li, Wanming; Jin, Sihan] China Med Univ, Key Lab Med Cell Biol, Minist Educ, Shenyang 110122, Liaoning, Peoples R China.
   [Bing, Tao; Shangguan, Dihua] Chinese Acad Sci, Beijing Natl Lab Mol Sci, Key Lab Analyt Chem Living Biosyst, CAS Res Educ Ctr Excellence Mol Sci,Inst Chem, Beijing 100190, Peoples R China.
   [Wang, Rui] China Med Univ, Dept Stem Cells & Regenerat Med, Key Lab Cell Biol, Minist Publ Hlth China,Minist Educ China, Shenyang 110122, Liaoning, Peoples R China.
   [Wang, Rui] China Med Univ, Key Lab Med Cell Biol, Minist Educ China, Shenyang 110122, Liaoning, Peoples R China.
   [Chen, Hang] China Med Univ, Coll Basic Med, Expt Teaching Ctr Funct Subjects, 77 Puhe Rd, Shenyang 110122, Liaoning, Peoples R China.
C3 China Medical University; China Medical University; Chinese Academy of
   Sciences; Institute of Chemistry, CAS; China Medical University; China
   Medical University; China Medical University
RP Shangguan, DH (corresponding author), Chinese Acad Sci, Beijing Natl Lab Mol Sci, Key Lab Analyt Chem Living Biosyst, CAS Res Educ Ctr Excellence Mol Sci,Inst Chem, Beijing 100190, Peoples R China.; Chen, H (corresponding author), China Med Univ, Coll Basic Med, Expt Teaching Ctr Funct Subjects, 77 Puhe Rd, Shenyang 110122, Liaoning, Peoples R China.
EM sgdh@iccas.ac.cn; lnfsch@hotmail.com
RI Jin, Si/KGK-5977-2024; Bing, Tao/F-3476-2017; Shangguan,
   Dihua/G-4530-2011
OI chen, hang/0000-0001-5081-4414; Bing, Tao/0000-0002-5121-053X;
   Shangguan, Dihua/0000-0002-5746-803X
FU Natural Science Foundation of Liaoning Province, China [2020-MS-174,
   2020-MS-164]; Shengyang Youth Science and Technology Project [RC190261]
FX This research work was financially supported by the Natural Science
   Foundation of Liaoning Province, China (No. 2020-MS-174 and 2020-MS-164)
   and the Shengyang Youth Science and Technology Project (No. RC190261).
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NR 37
TC 5
Z9 5
U1 1
U2 20
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 0003-2654
EI 1364-5528
J9 ANALYST
JI Analyst
PD DEC 20
PY 2021
VL 147
IS 1
BP 187
EP 195
DI 10.1039/d1an01579f
EA NOV 2021
PG 9
WC Chemistry, Analytical
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA XR1PI
UT WOS:000727426400001
PM 34874026
DA 2025-01-04
ER

PT J
AU Hu, LM
   Dong, HY
   He, LY
   Shi, MC
   Xiang, NL
   Su, YX
   Wang, C
   Tian, Y
   Hu, YJ
   Wang, HH
   Liu, HL
   Wen, CY
   Yang, XL
AF Hu, Limei
   Dong, Haiyan
   He, Lingyuan
   Shi, Mengchen
   Xiang, Nanlin
   Su, Yixi
   Wang, Chen
   Tian, Yu
   Hu, Yijia
   Wang, Huihui
   Liu, Huanliang
   Wen, Chuangyu
   Yang, Xiangling
TI Evacetrapib Elicits Antitumor Effects on Colorectal Cancer by Inhibiting
   the Wnt/β-Catenin Signaling Pathway and Activating the JNK Signaling
   Pathway
SO BIOLOGICAL & PHARMACEUTICAL BULLETIN
LA English
DT Article
DE Evacetrapib; colorectal cancer; Wnt; beta-catenin; c-Jun NH2-terminal
   kinase; cholesteryl ester transfer protein
ID ESTER TRANSFER PROTEIN; CELLS; CHOLESTEROL; METABOLISM; APOPTOSIS;
   OUTCOMES
AB Despite advances in colorectal cancer (CRC) treatment, most advanced CRC patients who experience disease progression after chemotherapy, targeted therapy, and immunotherapy face a situation in which there is no available medicine. Thus, new therapeutic drugs for CRC are urgently needed. Studies have shown that cholesteryl ester transfer protein (CETP) has a vital role in tumor development and is a possible target for CRC therapy. We found that Evacetrapib, a CETP inhibitor, suppressed CRC cell growth by inhibiting the Wnt/beta-catenin signaling pathway and activating the c-Jun NH2-terminal kinase (JNK) signaling pathway in CRC. Therefore, Evacetrapib displays an anti-cancer effect and is a possible option for treating CRC.
C1 [Hu, Limei; Dong, Haiyan; He, Lingyuan; Shi, Mengchen; Su, Yixi; Wang, Chen; Tian, Yu; Hu, Yijia; Wang, Huihui; Liu, Huanliang; Yang, Xiangling] Sun Yat Sen Univ, Affiliated Hosp 6, Dept Clin Lab, Guangzhou 510655, Guangdong, Peoples R China.
   [Hu, Limei; Dong, Haiyan; He, Lingyuan; Shi, Mengchen; Xiang, Nanlin; Su, Yixi; Wang, Chen; Tian, Yu; Hu, Yijia; Wang, Huihui; Liu, Huanliang; Wen, Chuangyu; Yang, Xiangling] Sun Yat Sen Univ, Affiliated Hosp 6, Guangdong Inst Gastroenterol, Guangdong Prov Key Lab Colorectal & Pelv Floor Dis, Guangzhou 510655, Guangdong, Peoples R China.
   [Wen, Chuangyu] Southern Med Univ, Affiliated Dongguan Hosp, Dept Obstet & Gynecol, Dongguan 542800, Guangdong, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Southern Medical
   University - China
RP Yang, XL (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 6, Dept Clin Lab, Guangzhou 510655, Guangdong, Peoples R China.; Wen, CY; Yang, XL (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 6, Guangdong Inst Gastroenterol, Guangdong Prov Key Lab Colorectal & Pelv Floor Dis, Guangzhou 510655, Guangdong, Peoples R China.; Wen, CY (corresponding author), Southern Med Univ, Affiliated Dongguan Hosp, Dept Obstet & Gynecol, Dongguan 542800, Guangdong, Peoples R China.
EM wenchyu@mail3.sysu.edu.cn; yangxl28@mail.sysu.edu.cn
RI Su, Yixi/K-9119-2013; Li, Huang/IZE-8023-2023; Dong, Haiyan/Z-1782-2019
FU Project to Attract High Level Foreign Experts [G20200019016]; China
   Postdoctoral Scientific Foundation [2020M683114]; Dongguan Science and
   Technology of Social Development Program [202050715001215]; Project of
   Administration of Traditional Chinese Medicine of Guangdong Province of
   China [20211405]
FX This work was supported by Project to Attract High Level Foreign Experts
   (G20200019016) ; China Postdoctoral Scientific Foundation (2020M683114)
   ; Dongguan Science and Technology of Social Development Program
   (202050715001215) ; Project of Administration of Traditional Chinese
   Medicine of Guangdong Province of China (20211405) .
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NR 36
TC 2
Z9 2
U1 2
U2 5
PU PHARMACEUTICAL SOC JAPAN
PI TOKYO
PA 2-12-15 SHIBUYA, SHIBUYA-KU, TOKYO, 150-0002, JAPAN
SN 0918-6158
EI 1347-5215
J9 BIOL PHARM BULL
JI Biol. Pharm. Bull.
PD SEP
PY 2022
VL 45
IS 9
BP 1238
EP 1245
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 5C2DD
UT WOS:000864075300004
PM 36047191
OA gold
DA 2025-01-04
ER

PT J
AU Eke, I
   Makinde, AY
   Aryankalayil, MJ
   Ahmed, MM
   Coleman, CN
AF Eke, Iris
   Makinde, Adeola Y.
   Aryankalayil, Molykutty J.
   Ahmed, Mansoor M.
   Coleman, C. Norman
TI Comprehensive molecular tumor profiling in radiation oncology: How it
   could be used for precision medicine
SO CANCER LETTERS
LA English
DT Review
DE Molecular profiling; Precision medicine; Radiation oncology; Targeted
   therapy
ID CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER; ISOCITRATE DEHYDROGENASE
   MUTATIONS; RESISTANT PROSTATE-CANCER; ACUTE MYELOID-LEUKEMIA; ADVANCED
   RECTAL-CANCER; PHASE-III; PHOSPHOPROTEOMIC ANALYSIS;
   GLIOBLASTOMA-MULTIFORME; PROMOTER METHYLATION
AB New technologies enabling the analysis of various molecules, including DNA, RNA, proteins and small metabolites, can aid in understanding the complex molecular processes in cancer cells. In particular, for the use of novel targeted therapeutics, elucidation of the mechanisms leading to cell death or survival is crucial to eliminate tumor resistance and optimize therapeutic efficacy. While some techniques, such as genomic analysis for identifying specific gene mutations or epigenetic testing of promoter methylation, are already in clinical use, other "omics-based" assays are still evolving. Here, we provide an overview of the current status of molecular profiling methods, including promising research strategies, as well as possible challenges, and their emerging role in radiation oncology. Published by Elsevier Ireland Ltd.
C1 [Eke, Iris; Makinde, Adeola Y.; Aryankalayil, Molykutty J.; Coleman, C. Norman] NCI, Radiat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
   [Ahmed, Mansoor M.; Coleman, C. Norman] NCI, Radiat Res Program, NIH, Rockville, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); National Institutes of Health (NIH) - USA; NIH National Cancer
   Institute (NCI)
RP Eke, I (corresponding author), NCI, Radiat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM iris.eke@nih.gov
RI Ahmed, Mansoor/AAK-5988-2020; Eke, Iris/B-9251-2016
OI Eke, Iris/0000-0002-3591-019X
FU NIH Intramural Research Program, National Cancer Institute, Center for
   Cancer Research
FX This study was supported by the NIH Intramural Research Program,
   National Cancer Institute, Center for Cancer Research. The authors thank
   the NIH Fellows Editorial Board for editorial assistance and Katherine
   Wilsdon (NCI, NIH) for critical reading and discussion of the
   manuscript.
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NR 127
TC 15
Z9 15
U1 0
U2 10
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
EI 1872-7980
J9 CANCER LETT
JI Cancer Lett.
PD NOV 1
PY 2016
VL 382
IS 1
BP 118
EP 126
DI 10.1016/j.canlet.2016.01.041
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EA9SU
UT WOS:000386985800013
PM 26828133
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Hasanzad, M
   Sarhangi, N
   Meybodi, HRA
   Nikfar, S
   Khatami, F
   Larijani, B
AF Hasanzad, Mandana
   Sarhangi, Negar
   Meybodi, Hamid Reza Aghaei
   Nikfar, Shekoufeh
   Khatami, Fatemeh
   Larijani, Bagher
TI Precision Medicine in Non Communicable Diseases
SO INTERNATIONAL JOURNAL OF MOLECULAR AND CELLULAR MEDICINE
LA English
DT Review
DE Precision medicine; non-communicable diseases; canliovascular diseases;
   type 2 diabetes; chronic obstructive pulmonary disease; cancer
ID CELL LUNG-CANCER; GENOME-WIDE ASSOCIATION; CIRCULATING TUMOR-CELLS;
   PERSONALIZED MEDICINE; COLORECTAL-CANCER; BREAST-CANCER; MOLECULAR
   CHARACTERIZATION; DIFFERENTIATED CARCINOMAS; BIOMARKER DEVELOPMENT;
   CLINICAL-SIGNIFICANCE
AB Non-conununicable diseases (NCDs) are the leading cause of death and disease burden globally, cardiovascular diseases (CVDs) account for the major part of death related to NCDs followed by different types of cancer. chronic obstructive pulmonary disease (COPD), and diabetes. As the World Health Organization (WHO) and the United Nations have announced a 25% reduction in mortality of NCDs by 2025, different communities need to adopt preventive strategies for achieving this goal. Personalized medicine approach as a predictive and preventive strategy aims for a better therapeutic goal to the patients to maximize benefits and reduce harms. The clinical benefits of this approach are already realized in cancer targeted therapy, and its impact on other conditions needs more studies in different societies. In this review, we essentially describe the concept of personalized (or precision) medicine in association with NCDs and the future of precision medicine in prediction, prevention, and personalized treatment.
C1 [Hasanzad, Mandana] Islamic Azad Univ, Med Genom Res Ctr, Tehran Med Sci, Tehran, Iran.
   [Hasanzad, Mandana; Sarhangi, Negar; Meybodi, Hamid Reza Aghaei; Nikfar, Shekoufeh; Larijani, Bagher] Univ Tehran Med Sci, Personalized Med Res Ctr, Endocrinol & Metab Clin Sci Inst, Tehran, Iran.
   [Nikfar, Shekoufeh] Univ Tehran Med Sci, Fac Pharm, Dept Pharmacoecon & Pharmaceut Adm, Tehran, Iran.
   [Khatami, Fatemeh] Univ Tehran Med Sci, Chron Dis Res Ctr, Endocrinol & Metab Populat Sci Inst, Tehran, Iran.
   [Larijani, Bagher] Univ Tehran Med Sci, Endocrinol & Metab Res Ctr, Endocrinol & Metab Clin Sci Inst, Tehran, Iran.
C3 Islamic Azad University; Tehran University of Medical Sciences; Tehran
   University of Medical Sciences; Tehran University of Medical Sciences;
   Tehran University of Medical Sciences
RP Larijani, B (corresponding author), Univ Tehran Med Sci, Personalized Med Res Ctr, Endocrinol & Metab Clin Sci Inst, Tehran, Iran.
EM larijanib1340@gmail.com
RI Sarhangi, Negar/AAK-1682-2020; Khatami, Fatemeh/AAQ-3091-2021; Hasanzad,
   Mandana/AAG-4122-2021; Aghaei Meybodi, Hamid Reza/AAY-7383-2021;
   larijani, Bagher/ABE-3315-2020
OI Larijani, Bagher/0000-0001-5386-7597
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NR 132
TC 13
Z9 14
U1 1
U2 3
PU CELLULAR & MOLECULAR BIOLOGY RESEARCH CENTER
PI BABOL
PA BABOL UNIV MEDICAL SCIENCES, GANJAFROUZ AVE, BABOL, 4717647745, IRAN
SN 2251-9637
EI 2251-9645
J9 INT J MOL CELL MED
JI Int. J. Mol. Cell. Med.
PD WIN
PY 2019
VL 8
SU 1
BP 1
EP 18
DI 10.22088/IJMCM.BUMS.8.2.1
PG 18
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA KE5FI
UT WOS:000508580900001
PM 32351905
DA 2025-01-04
ER

PT J
AU Raval, SH
   Singh, RD
   Joshi, DV
   Patel, HB
   Mody, SK
AF Raval, Samir H.
   Singh, Ratn D.
   Joshi, Dilip V.
   Patel, Hitesh B.
   Mody, Shailesh K.
TI Recent developments in receptor tyrosine kinases targeted anticancer
   therapy
SO VETERINARY WORLD
LA English
DT Review
DE cancer; monoclonal antibodies; small molecule drugs; receptor tyrosine
   kinases; targeted therapy
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER;
   PHASE-III TRIAL; BREAST-CANCER; PROTEIN EXPRESSION; ACTIVATING
   MUTATIONS; ANTITUMOR-ACTIVITY; MOUSE DEVELOPMENT; MULTIPLE-MYELOMA
AB Novel concepts and understanding of receptors lead to discoveries and optimization of many small molecules and antibodies as anti-cancerous drugs. Receptor tyrosine kinases (RTKs) are such a promising class of receptors under the investigation in past three decades. RTKs are one of the essential mediators of cell signaling mechanism for various cellular processes. Transformations such as overexpression, dysregulation, or mutations of RTKs may result into malignancy, and thus are an important target for anticancer therapy. Numerous subfamilies of RTKs, such as epidermal growth factor receptor, vascular endothelial growth factor receptor, fibroblast growth factor receptors, insulin-like growth factor receptor, and hepatocyte growth factor receptor, have been being investigated in recent years as target for anticancer therapy. The present review focuses several small molecules drugs as well as monoclonal antibodies targeting aforesaid subfamilies either approved or under investigation to treat the various cancers.
C1 [Raval, Samir H.; Joshi, Dilip V.] Sardarkrushinagar Dantiwada Agr Univ, Dept Vet Pathol, Coll Vet Sci & Anim Husb, Banaskantha 385506, Gujarat, India.
   [Singh, Ratn D.; Patel, Hitesh B.; Mody, Shailesh K.] Sardarkrushinagar Dantiwada Agr Univ, Dept Pharmacol & Toxicol, Coll Vet Sci & Anim Husb, Banaskantha 385506, Gujarat, India.
RP Raval, SH (corresponding author), Sardarkrushinagar Dantiwada Agr Univ, Dept Vet Pathol, Coll Vet Sci & Anim Husb, Banaskantha 385506, Gujarat, India.
EM samirraval81@gmail.com; ratn1709@yahoo.com; drdvjoshi@rediffmail.com;
   drhitesh2002@rediffmail.com; skm12_ad1@yahoo.com
RI ; SINGH, RATN DEEP/I-8521-2016
OI Joshi, D.V./0000-0002-7236-7958; HB, Patel/0000-0001-8218-2570; SINGH,
   RATN DEEP/0000-0003-1725-6128; S.K., Mody/0000-0001-7480-7745
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NR 139
TC 14
Z9 18
U1 0
U2 9
PU VETERINARY WORLD
PI GUJARAT
PA STAR, GULSHAN PARK, NH-8A, CHANDRAPUR RD, WANKANER, GUJARAT, 363 621,
   INDIA
SN 0972-8988
EI 2231-0916
J9 VET WORLD
JI Vet. World
PD JAN
PY 2016
VL 9
IS 1
BP 80
EP 90
DI 10.14202/vetworld.2016.80-90
PG 11
WC Agriculture, Dairy & Animal Science; Veterinary Sciences
WE Emerging Sources Citation Index (ESCI)
SC Agriculture; Veterinary Sciences
GA DU1AY
UT WOS:000381939000015
PM 27051190
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Perincheri, S
   Hui, P
AF Perincheri, Sudhir
   Hui, Pei
TI KRAS mutation testing in clinical practice
SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS
LA English
DT Review
DE clinical oncology; KRAS; mutation testing
ID METASTATIC COLORECTAL-CANCER; K-RAS MUTATIONS; CELL LUNG-CANCER;
   COLON-CANCER; DUCTAL ADENOCARCINOMA; CYTOLOGY SPECIMENS; 1ST-LINE
   TREATMENT; DIGITAL PCR; CETUXIMAB; GENES
AB Activating mutation of KRAS plays a significant role in the pathogenesis of common human malignancies and molecular testing of KRAS mutation has emerged as an essential biomarker in the current practice of clinical oncology. The presence of KRAS mutation is generally associated with clinical aggressiveness of the cancer and reduced survival of the patient. Therapeutically, KRAS mutation testing has maximum utility in stratifying metastatic colorectal carcinoma and lung cancer patients for treatment with targeted therapy. Diagnostically, KRAS mutation testing is useful in the workup of pancreaticobiliary and thyroid cancers, particularly using cytological specimens. In the era of precision medicine, the role of KRAS mutation testing is poised to expand, likely in a setting of combinatorial therapeutic strategy and requiring additional mutation testing of its upstream and/or downstream effectors.
C1 [Perincheri, Sudhir; Hui, Pei] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA.
C3 Yale University
RP Hui, P (corresponding author), Yale Univ, Sch Med, Dept Pathol, 333 Cedar St, New Haven, CT 06520 USA.
EM pei.hui@yale.edu
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NR 93
TC 10
Z9 13
U1 2
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 MAR
PY 2015
VL 15
IS 3
BP 375
EP 384
DI 10.1586/14737159.2015.986102
PG 10
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA CC2BB
UT WOS:000350148500011
PM 25487540
DA 2025-01-04
ER

PT S
AU Thall, PF
AF Thall, Peter F.
BE Reid, N
TI Adaptive Enrichment Designs in Clinical Trials
SO ANNUAL REVIEW OF STATISTICS AND ITS APPLICATION, VOL 8, 2021
SE Annual Review of Statistics and Its Application
LA English
DT Article; Book Chapter
DE adaptive signature design; Bayesian design; biomarker; clinical trial;
   group sequential design; precision medicine; subset selection; targeted
   therapy; variable selection
ID SUBGROUP IDENTIFICATION; COLORECTAL-CANCER; PROSTATE-CANCER;
   RANDOMIZATION; SELECTION; HETEROGENEITY; MULTIARM; THERAPY; MUTATIONS;
   INFERENCE
AB Adaptive enrichment designs for clinical trials may include rules that use interim data to identify treatment-sensitive patient subgroups, select or compare treatments, or change entry criteria. A common setting is a trial to compare a new biologically targeted agent to standard therapy. An enrichment design's structure depends on its goals, how it accounts for patient heterogeneity and treatment effects, and practical constraints. This article first covers basic concepts, including treatment-biomarker interaction, precision medicine, selection bias, and sequentially adaptive decision making, and briefly describes some different types of enrichment. Numerical illustrations are provided for qualitatively different cases involving treatment-biomarker interactions. Reviews are given of adaptive signature designs; a Bayesian design that uses a random partition to identify treatment-sensitive biomarker subgroups and assign treatments; and designs that enrich superior treatment sample sizes overall or within subgroups, make subgroup-specific decisions, or include outcome-adaptive randomization.
C1 [Thall, Peter F.] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center
RP Thall, PF (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
EM rex@mdanderson.org
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NR 61
TC 14
Z9 16
U1 0
U2 20
PU ANNUAL REVIEWS
PI PALO ALTO
PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0897 USA
SN 2326-8298
EI 2326-831X
J9 ANNU REV STAT APPL
PY 2021
VL 8
BP 393
EP 411
DI 10.1146/annurev-statistics-040720-032818
PG 19
WC Mathematics, Interdisciplinary Applications; Statistics & Probability
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Mathematics
GA BR0BI
UT WOS:000627718500018
PM 36212769
OA Bronze, Green Accepted
DA 2025-01-04
ER

PT J
AU Schulte, ML
   Fu, A
   Zhao, P
   Li, J
   Geng, L
   Smith, ST
   Kondo, J
   Coffey, RJ
   Johnson, MO
   Rathmell, JC
   Sharick, JT
   Skala, MC
   Smith, JA
   Berlin, J
   Washington, MK
   Nickels, ML
   Manning, HC
AF Schulte, Michael L.
   Fu, Allie
   Zhao, Ping
   Li, Jun
   Geng, Ling
   Smith, Shannon T.
   Kondo, Jumpei
   Coffey, Robert J.
   Johnson, Marc O.
   Rathmell, Jeffrey C.
   Sharick, Joe T.
   Skala, Melissa C.
   Smith, Jarrod A.
   Berlin, Jordan
   Washington, M. Kay
   Nickels, Michael L.
   Manning, H. Charles
TI Pharmacological blockade of ASCT2-dependent glutamine transport leads to
   antitumor efficacy in preclinical models
SO NATURE MEDICINE
LA English
DT Article
ID BREAST-CANCER; SIGNALING PATHWAYS; COLORECTAL-CANCER; LUNG-CANCER;
   CELL-GROWTH; IN-VIVO; METABOLISM; INHIBITION; EXPRESSION; AUTOPHAGY
AB The unique metabolic demands of cancer cells underscore potentially fruitful opportunities for drug discovery in the era of precision medicine. However, therapeutic targeting of cancer metabolism has led to surprisingly few new drugs to date. The neutral amino acid glutamine serves as a key intermediate in numerous metabolic processes leveraged by cancer cells, including biosynthesis, cell signaling, and oxidative protection. Herein we report the preclinical development of V-9302, a competitive small molecule antagonist of transmembrane glutamine flux that selectively and potently targets the amino acid transporter ASCT2. Pharmacological blockade of ASCT2 with V-9302 resulted in attenuated cancer cell growth and proliferation, increased cell death, and increased oxidative stress, which collectively contributed to antitumor responses in vitro and in vivo. This is the first study, to our knowledge, to demonstrate the utility of a pharmacological inhibitor of glutamine transport in oncology, representing a new class of targeted therapy and laying a framework for paradigm-shifting therapies targeting cancer cell metabolism.
C1 [Schulte, Michael L.; Fu, Allie; Zhao, Ping; Li, Jun; Geng, Ling; Smith, Shannon T.; Nickels, Michael L.; Manning, H. Charles] Vanderbilt Univ, Med Ctr, Vanderbilt Ctr Mol Probes, Nashville, TN 37235 USA.
   [Schulte, Michael L.; Nickels, Michael L.; Manning, H. Charles] Vanderbilt Univ, Med Ctr, Inst Imaging Sci, Nashville, TN 37235 USA.
   [Schulte, Michael L.; Nickels, Michael L.; Manning, H. Charles] Vanderbilt Univ, Med Ctr, Dept Radiol & Radiol Sci, Nashville, TN 37232 USA.
   [Kondo, Jumpei; Coffey, Robert J.] Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN USA.
   [Coffey, Robert J.; Berlin, Jordan; Washington, M. Kay; Manning, H. Charles] Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Nashville, TN 37235 USA.
   [Coffey, Robert J.] Tennessee Valley Healthcare Syst, Vet Hlth Adm, Nashville, TN USA.
   [Johnson, Marc O.; Rathmell, Jeffrey C.; Washington, M. Kay] Vanderbilt Univ, Med Ctr, Dept Pathol Microbiol & Immunol, Nashville, TN 37235 USA.
   [Sharick, Joe T.; Skala, Melissa C.; Manning, H. Charles] Vanderbilt Univ, Dept Biomed Engn, Nashville, TN 37235 USA.
   [Smith, Jarrod A.] Vanderbilt Univ, Vanderbilt Ctr Struct Biol, 221 Kirkland Hall, Nashville, TN 37235 USA.
   [Smith, Jarrod A.] Vanderbilt Univ, Dept Biochem, Nashville, TN 37232 USA.
   [Manning, H. Charles] Vanderbilt Univ, Med Ctr, Dept Neurosurg, Nashville, TN 37235 USA.
   [Manning, H. Charles] Vanderbilt Univ, Dept Chem, Nashville, TN 37235 USA.
   [Skala, Melissa C.] Univ Wisconsin, Dept Biomed Engn, Morgridge Inst Res, Madison, WI USA.
C3 Vanderbilt University; Vanderbilt University; Vanderbilt University;
   Vanderbilt University; Vanderbilt University; US Department of Veterans
   Affairs; Veterans Health Administration (VHA); VA Tennessee Valley
   Healthcare System; Vanderbilt University; Vanderbilt University;
   Vanderbilt University; Vanderbilt University; Vanderbilt University;
   Vanderbilt University; University of Wisconsin System; University of
   Wisconsin Madison; The Morgridge Institute for Research, Inc.
RP Manning, HC (corresponding author), Vanderbilt Univ, Med Ctr, Vanderbilt Ctr Mol Probes, Nashville, TN 37235 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Med Ctr, Inst Imaging Sci, Nashville, TN 37235 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Med Ctr, Dept Radiol & Radiol Sci, Nashville, TN 37232 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Nashville, TN 37235 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Dept Biomed Engn, Nashville, TN 37235 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Med Ctr, Dept Neurosurg, Nashville, TN 37235 USA.; Manning, HC (corresponding author), Vanderbilt Univ, Dept Chem, Nashville, TN 37235 USA.
EM henry.c.manning@vanderbilt.edu
RI Skala, Melissa/A-1253-2009; Kondo, Jumpei/AAC-4336-2020; Rathmell,
   Jeffrey/HCH-2318-2022
OI Kondo, Jumpei/0000-0002-1350-0480; Coffey, Robert/0000-0002-2180-3844;
   Rathmell, Jeffrey/0000-0002-4106-3396
FU Vanderbilt Ingram Cancer Center (National Institutes of Health (NIH)
   National Cancer Institute (NCI)) [P30CA068485]; Center for Small Animal
   Imaging; Kleberg Foundation; Vanderbilt Trans-Institutional Program
   (TIPS) Award; Vanderbilt Specialized Program of Research Excellence
   (SPORE) in Gastrointestinal Cancer [NIH NCI P50CA095103]; NCI
   [R35CA197570]; Vanderbilt Digestive Disease Research Center (NIH
   National Institute of Diabetes and Digestive and Kidney Diseases
   (NIDDK)) [P30DK058404]
FX The authors acknowledge M. Tantawy for assistance with PET imaging, F.
   Revetta for histology expertise, and A. Rosenberg and A. Cohen for
   helpful discussions and editorial assistance. The authors wish to
   acknowledge research support from the Vanderbilt Ingram Cancer Center
   Support Grant (National Institutes of Health (NIH) National Cancer
   Institute (NCI) P30CA068485, H.C.M.), which supports the
   Vanderbilt-Ingram Cancer Center (VICC) Chemical Synthesis Core,
   Vanderbilt University Medical Center (VUMC) Radiochemistry Core, and
   Center for Small Animal Imaging; the Kleberg Foundation (H.C.M.); a
   Vanderbilt Trans-Institutional Program (TIPS) Award to the Vanderbilt
   Center for Molecular Probes (H.C.M.); the Vanderbilt Specialized Program
   of Research Excellence (SPORE) in Gastrointestinal Cancer (NIH NCI
   P50CA095103, R.J.C. and H.C.M.); an Outstanding Investigator Award from
   the NCI (R35CA197570, R.J.C.); and the Vanderbilt Digestive Disease
   Research Center (NIH National Institute of Diabetes and Digestive and
   Kidney Diseases (NIDDK) P30DK058404, H.C.M.).
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NR 42
TC 332
Z9 363
U1 8
U2 157
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD FEB
PY 2018
VL 24
IS 2
BP 194
EP +
DI 10.1038/nm.4464
PG 13
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 FV1MQ
UT WOS:000424327200016
PM 29334372
OA Green Accepted
DA 2025-01-04
ER

PT S
AU Khotskaya, YB
   Mills, GB
   Shaw, KRM
AF Khotskaya, Yekaterina B.
   Mills, Gordon B.
   Shaw, Kenna R. Mills
BE Caskey, CT
TI Next-Generation Sequencing and Result Interpretation in Clinical
   Oncology: Challenges of Personalized Cancer Therapy
SO ANNUAL REVIEW OF MEDICINE, VOL 68
SE Annual Review of Medicine
LA English
DT Review; Book Chapter
DE driver mutations; passenger mutations; decision support; variant
   actionability
ID MUTATION CARRIERS; OVARIAN-CANCER; BREAST-CANCER; GYNECOLOGIC CANCERS;
   PRECISION MEDICINE; COLORECTAL-CANCER; TARGETED THERAPY;
   DECISION-SUPPORT; PROSTATE-CANCER; LYNCH-SYNDROME
AB The tools of next-generation sequencing (NGS) technology, such as targeted sequencing of candidate cancer genes and whole-exome and -genome sequencing, coupled with encouraging clinical results based on the use of targeted therapeutics and biomarker-guided clinical trials, are fueling further technological advancements of NGS technology. However, NGS data interpretation is associated with challenges that must be overcome to promote the techniques' effective integration into clinical oncology practice. Specifically, sequencing of a patient's tumor often yields 30-65 somatic variants, but most of these variants are "passenger" mutations that are phenotypically neutral and thus not targetable. Therefore, NGS data must be interpreted by multidisciplinary decision-support teams to determine mutation actionability and identify potential "drivers," so that the treating physician can prioritize what clinical decisions can be pursued in order to provide cancer therapy that is personalized to the patient and his or her unique genome.
C1 [Khotskaya, Yekaterina B.; Mills, Gordon B.; Shaw, Kenna R. Mills] Univ Texas MD Anderson Canc Ctr, Sheikh Khalifa Bin Zayed Nahyan Inst Personalized, Houston, TX 77030 USA.
   [Mills, Gordon B.] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center
RP Mills, GB (corresponding author), Univ Texas MD Anderson Canc Ctr, Sheikh Khalifa Bin Zayed Nahyan Inst Personalized, Houston, TX 77030 USA.; Mills, GB (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77030 USA.
EM gmills@mdanderson.org
RI Mills, Gordon/L-5416-2014
OI Mills, Gordon/0000-0002-0144-9614
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NR 71
TC 30
Z9 34
U1 0
U2 20
PU ANNUAL REVIEWS
PI PALO ALTO
PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0897 USA
SN 0066-4219
BN 978-0-8243-0568-0
J9 ANNU REV MED
JI Annu. Rev. Med.
PY 2017
VL 68
BP 113
EP 125
DI 10.1146/annurev-med-102115-021556
PG 13
WC Medicine, Research & Experimental
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA BH1NW
UT WOS:000398282900009
PM 27813876
OA Bronze
DA 2025-01-04
ER

PT J
AU Dantu, S
   Khan, A
   Dhir, M
AF Dantu, Siva
   Khan, Asama
   Dhir, Mashaal
TI Role of dual anti-HER2 therapy before liver resection for rectal
   metastases
SO JOURNAL OF SURGICAL CASE REPORTS
LA English
DT Article
ID COLORECTAL-CANCER; PHASE-III; FLUOROURACIL; MULTICENTER; LEUCOVORIN
AB This case presents a patient with a diagnosis of metastatic colon cancer on second-line chemotherapy. He demonstrated increased HER2 expression and was placed on dual HER2 antagonists. The patient had excellent repose and was ultimately able to undergo definitive liver resection for cure. We highlight the evolving use targeted therapy in metastatic colorectal cancer to not only extend progression-free survival, but act as a bridge to surgery.
C1 [Dantu, Siva; Khan, Asama; Dhir, Mashaal] SUNY Upstate Med Univ, Dept Surg, Syracuse, NY 13210 USA.
C3 State University of New York (SUNY) System; State University of New York
   (SUNY) Upstate Medical Center
RP Dhir, M (corresponding author), SUNY Upstate Med Univ, Dept Surg, Div Surg Oncol, 750 East Adams St, Syracuse, NY 13210 USA.
EM dhirm@upstate.edu
CR Bertotti A, 2011, CANCER DISCOV, V1, P508, DOI 10.1158/2159-8290.CD-11-0109
   Biller LH, 2021, JAMA-J AM MED ASSOC, V325, P669, DOI 10.1001/jama.2021.0106
   Grothey A, 2013, LANCET, V381, P303, DOI 10.1016/S0140-6736(12)61900-X
   Meric-Bemstam F, 2019, LANCET ONCOL, V20, P518, DOI 10.1016/S1470-2045(18)30904-5
   Peeters M, 2010, J CLIN ONCOL, V28, P4706, DOI 10.1200/JCO.2009.27.6055
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   Van Cutsem E, 2011, J CLIN ONCOL, V29, P2004, DOI 10.1200/JCO.2010.29.5436
NR 11
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 2042-8812
J9 J SURG CASE REP
JI J. Surg. Case Rep.
PD SEP 1
PY 2022
VL 2022
IS 9
DI 10.1093/jscr/rjac420
PG 3
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA 4N3NU
UT WOS:000853926500003
PM 36118993
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, C
   Cao, J
   Zhang, N
   Tu, MQ
   Xu, FW
   Wei, S
   Chen, XJ
   Xu, YH
AF Li, Chong
   Cao, Jing
   Zhang, Ning
   Tu, Meiqing
   Xu, Fengwei
   Wei, Shuang
   Chen, Xiaojing
   Xu, Yuhong
TI Identification of RSPO2 Fusion Mutations and Target Therapy Using a
   Porcupine Inhibitor
SO SCIENTIFIC REPORTS
LA English
DT Article
ID COLORECTAL-CANCER; CATENIN PATHWAY; WNT PATHWAY; RECEPTORS; PROMOTES;
   TUMOR; MECHANISMS; LRP6; LGR5
AB Cancers are driven by a variety of somatic gene mutations and identifying these mutations enables the development of novel target drugs. We have sought to identify abnormalities in Wnt pathway-related genes that are sensitive to Wnt inhibitor treatment. We examined Patient Derived Xenograft (PDX) RNA samples and found new R-Spondin 2 (RSPO2) transcript fusions with the EMC2, PVT1 or HNF4G genes. These fusion events were identified in about 1.4% of the digestive system cancer samples. We then examined the oncogenic effects of the RSPO2-EMC2 fusion gene and confirmed that it can drive oncogenesis, sustain tumor growth and promote metastasis. Finally, we used a Wnt pathway Porcupine inhibitor CGX1321 to treat PDX mouse models containing RSPO2 fusion genes. All the RSPO2 fusion tumors responded to the treatment and stopped progression. Our data show that Wnt pathway inhibition could provide an effective treatment for cancers containing RSPO2 fusion. The RSPO2 fusion will serve as a good biomarker for screening patients to support clinical treatment of digestive system cancers using Wnt pathway inhibitors.
C1 [Li, Chong; Cao, Jing; Zhang, Ning; Tu, Meiqing; Xu, Fengwei; Wei, Shuang; Chen, Xiaojing; Xu, Yuhong] Shanghai Jiao Tong Univ, Sch Pharm, Shanghai 200240, Peoples R China.
C3 Shanghai Jiao Tong University
RP Xu, YH (corresponding author), Shanghai Jiao Tong Univ, Sch Pharm, Shanghai 200240, Peoples R China.
EM yhxu@sjtu.edu.cn
RI ZHANG, NING/C-8105-2015
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NR 42
TC 33
Z9 35
U1 0
U2 9
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD SEP 24
PY 2018
VL 8
AR 14244
DI 10.1038/s41598-018-32652-3
PG 9
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GU5OL
UT WOS:000445336600012
PM 30250044
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sacdalan, DB
   Mendoza, MJ
   Vergara, JP
   Catedral, LI
   Ting, FI
   Leones, LM
   Berba, CM
   Sacdalan, DL
AF Sacdalan, Danielle Benedict
   Mendoza, Marvin Jonne
   Vergara, John Paulo
   Catedral, Lance Isidore
   Ting, Frederic Ivan
   Leones, Louis Mervyn
   Berba, Carlo Miguel
   Sacdalan, Dennis L.
TI Beyond bevacizumab: a review of targeted agents in metastatic small
   bowel adenocarcinoma
SO MEDICAL ONCOLOGY
LA English
DT Review
DE Small bowel adenocarcinoma; Targeted therapy; EGFR; HER2; NTRK;
   Immunotherapy; Immune checkpoint inhibitors
ID COMPREHENSIVE MOLECULAR CHARACTERIZATION; IMMUNE CHECKPOINT INHIBITORS;
   POSITIVE SOLID TUMORS; MICROSATELLITE INSTABILITY; HUMAN CANCER; PD-1
   BLOCKADE; COLON-CANCER; PEMBROLIZUMAB; CHEMOTHERAPY; EXPRESSION
AB Small bowel cancers are rare tumors with an incidence 50-100-fold less than colorectal cancer. These tumors carry a poor prognosis. Owing to its rarity, treatment of this disease, particularly in its advanced stages, has not been optimized and is derived mainly from treatment regimens for colorectal cancer. Based on recent studies bevacizumab, an antibody directed against vascular endothelial growth factor and used in the management of metastatic CRC, has been added to treatment guidelines for metastatic small bowel adenocarcinoma. We investigate in this review the evidence behind other targeted treatments that may be beneficial in the treatment of metastatic small bowel adenocarcinoma. These are agents against EGFR, VEGFR-2, HER2, and NTRK as well as immune checkpoint inhibitors. The last class of drugs appears to hold the greatest promise based on the preponderance of evidence supporting its use. However, overall data remains sparse. Results of studies currently underway will be valuable in shedding more light on the management of this aggressive cancer.
C1 [Sacdalan, Danielle Benedict] Univ Philippines Manila, Coll Med, Dept Pharmacol & Toxicol, Pedro Gil St, Manila 1000, Philippines.
   [Sacdalan, Danielle Benedict; Mendoza, Marvin Jonne; Vergara, John Paulo; Catedral, Lance Isidore; Ting, Frederic Ivan; Leones, Louis Mervyn; Berba, Carlo Miguel; Sacdalan, Dennis L.] Philippine Gen Hosp, Dept Med, Div Med Oncol, Taft Ave, Manila 1000, Philippines.
   [Sacdalan, Danielle Benedict; Mendoza, Marvin Jonne; Vergara, John Paulo; Catedral, Lance Isidore; Ting, Frederic Ivan; Leones, Louis Mervyn; Berba, Carlo Miguel; Sacdalan, Dennis L.] Univ Philippines Manila, Taft Ave, Manila 1000, Philippines.
C3 University of the Philippines System; University of the Philippines
   Manila; University of the Philippines System; University of the
   Philippines Manila; University of the Philippines System; University of
   the Philippines Manila
RP Sacdalan, DB (corresponding author), Univ Philippines Manila, Coll Med, Dept Pharmacol & Toxicol, Pedro Gil St, Manila 1000, Philippines.; Sacdalan, DB (corresponding author), Philippine Gen Hosp, Dept Med, Div Med Oncol, Taft Ave, Manila 1000, Philippines.; Sacdalan, DB (corresponding author), Univ Philippines Manila, Taft Ave, Manila 1000, Philippines.
EM dlsacdalan@up.edu.ph
RI Catedral, Lance/ABH-1382-2020; Sacdalan, Danielle Benedict/L-2863-2019
OI Sacdalan, Danielle Benedict/0000-0002-7400-8078; Sacdalan,
   Dennis/0000-0001-6617-9363; Leones, Louis Mervyn/0000-0002-7927-2441;
   Berba, Carlo Miguel/0000-0002-0664-4304; Vergara, John
   Paulo/0000-0002-4041-5038; Mendoza, Marvin Jonne/0000-0002-0191-4766;
   Catedral, Lance Isidore/0000-0001-8182-0227; Ting, Frederic
   Ivan/0000-0002-9161-4918
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NR 88
TC 4
Z9 4
U1 0
U2 10
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 NOV 1
PY 2020
VL 37
IS 11
AR 106
DI 10.1007/s12032-020-01432-3
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA OJ0YS
UT WOS:000583695100001
PM 33135102
DA 2025-01-04
ER

PT J
AU Liu, GY
   Xiao, X
   Xia, YJ
   Huang, WB
   Chen, W
   Xu, JN
   Chen, SY
   Wang, HJ
   Wei, JT
   Li, H
   Shu, M
   Lu, XF
   Zhang, CH
   He, YL
AF Liu, Guangyao
   Xiao, Xing
   Xia, Yujian
   Huang, Weibing
   Chen, Wei
   Xu, Jiannan
   Chen, Songyao
   Wang, Huijin
   Wei, Jitao
   Li, Huan
   Shu, Man
   Lu, Xiaofang
   Zhang, Changhua
   He, Yulong
TI Organoids From Mucinous Appendiceal Adenocarcinomas as High-Fidelity
   Models for Individual Therapy
SO FRONTIERS IN MEDICINE
LA English
DT Article
DE mucinous appendiceal adenocarcinoma; organoid culture; individualized
   therapy; drug sensitivity test; chemotherapy
ID PATIENT-DERIVED MODELS; SYSTEMIC CHEMOTHERAPY; COLORECTAL-CANCER;
   NEOPLASMS; EXPRESSION; PERITONEI; SURVIVAL; TUMORS
AB BackgroundMucinous appendiceal adenocarcinoma (MAA) is a rare, heterogeneous disease. Patients with unrespectable mucinous appendiceal adenocarcinoma presenting with peritoneal spread are treated by intraperitoneal chemotherapy, hyperthermic intraperitoneal chemotherapy, systemic chemotherapy, or targeted therapy. However, there are no guidelines for efficacious drugs against mucinous appendiceal adenocarcinoma. Therefore, relevant high-fidelity models should be investigated to identify effective drugs for individual therapy. MethodsSurgical tumor specimens were obtained from a mucinous appendiceal adenocarcinoma patient. The tissue was digested and organoid culture was established. H&E and immunohistochemistry staining as well as DNA sequencing was performed on tissue and organoid. The pathological characteristics and gene mutations of the organoid were compared to those of the original tumor. Drug sensitivity tests were performed on organoid and the patient clinical responds to chemotherapy and targeted therapy was compared. ResultsOrganoids were successfully established and stably passaged. Pathological characteristics of organoids including H&E staining and expression of protein markers (CK20, CDX-2, STAB2, CD7, PAX8) were consistent to those of the original tumor. Moreover, the organoids carried the same gene mutations as the primary tumor. Sensitivity of the organoids to chemotherapeutic drugs and tyrosine kinase inhibitors included: 5-FU (IC50 43.95 mu M), Oxaliplatin (IC50 23.49 mu M), SN38 (IC50 1.02 mu M), Apatinib (IC50 0.10 mu M), Dasatinib (IC50 2.27 mu M), Docetaxel (IC50 5.26 mu M), Regorafenib (IC50 18.90 mu M), and Everolimus (IC50 9.20 mu M). The sensitivities of organoid to these drugs were comparable to those of the patient's clinical responses. ConclusionThe mucinous appendiceal adenocarcinoma organoid model which retained the characteristics of the primary tumor was successfully established. Combined organoid-based drug screening and high throughput sequencing provided a promising way for mucinous appendiceal adenocarcinoma treatment.
C1 [Liu, Guangyao; Xiao, Xing; Huang, Weibing; Chen, Wei; Xu, Jiannan; Chen, Songyao; Wang, Huijin; Wei, Jitao; Li, Huan; Zhang, Changhua; He, Yulong] Sun Yat sen Univ, Affiliated Hosp 7, Digest Dis Ctr, Shenzhen, Peoples R China.
   [Xia, Yujian] Northern Jiangsu Peoples Hosp, Dept Gastrointestinal Surg, Yangzhou, Peoples R China.
   [Shu, Man] Sun Yat sen Univ, Affiliated Hosp 1, Dept Pathol, Guangzhou, Peoples R China.
   [Lu, Xiaofang] Sun Yat sen Univ, Affiliated Hosp 7, Dept Pathol, Shenzhen, Peoples R China.
   [He, Yulong] Sun Yat sen Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Guangzhou, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University;
   Sun Yat Sen University
RP Zhang, CH; He, YL (corresponding author), Sun Yat sen Univ, Affiliated Hosp 7, Digest Dis Ctr, Shenzhen, Peoples R China.; He, YL (corresponding author), Sun Yat sen Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Guangzhou, Peoples R China.
EM zhchangh@mail.sysu.edu.cn; heyulong@mail.sysu.edu.cn
RI lu, xiaofang/HZJ-9581-2023; Shu, Man/JFA-3305-2023
OI Huang, Weibin/0000-0003-0159-435X; Xiao, Xing/0000-0001-5771-0677
FU Sanming Project of Medicine in Shenzhen [SZSM201911010]; Shenzhen Key
   Medical Discipline Construction Fund [SZXK016]; Shenzhen Sustainable
   Project [KCXFZ202002011010593]; Guangdong Provincial Key Laboratory of
   Digestive Cancer Research [2021B1212040006]; Shenzhen Fundamental
   Research Program [JCYJ20200109142605909, ZSQYJZPI202001]
FX Funding This study was supported by Sanming Project of Medicine in
   Shenzhen (SZSM201911010), Shenzhen Key Medical Discipline Construction
   Fund (SZXK016), Shenzhen Sustainable Project (KCXFZ202002011010593),
   Guangdong Provincial Key Laboratory of Digestive Cancer Research (No.
   2021B1212040006), and Shenzhen Fundamental Research Program
   (JCYJ20200109142605909). Research start-up fund of part-time PI, SAHSYSU
   (ZSQYJZPI202001).
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NR 30
TC 3
Z9 4
U1 2
U2 13
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 JUN 2
PY 2022
VL 9
AR 829033
DI 10.3389/fmed.2022.829033
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 2D9TK
UT WOS:000811879900001
PM 35721089
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ohnishi, Y
   Yasui, H
   Nozaki, M
   Nakajima, M
AF Ohnishi, Yuichi
   Yasui, Hiroki
   Nozaki, Masami
   Nakajima, Masahiro
TI Molecularly-targeted therapy for the oral cancer stem cells
SO JAPANESE DENTAL SCIENCE REVIEW
LA English
DT Review
DE Cancer stem cells; Cetuximab; Lapatinib; Epidermal growth factor
   receptor; Oral squamous cell carcinoma; Molecularly-targeted therapy;
   Sphere formation
ID GROWTH-FACTOR RECEPTOR; METASTATIC COLORECTAL-CANCER; INTESTINAL
   EPITHELIAL-CELLS; CHEMOTHERAPY PLUS CETUXIMAB; PLATINUM-BASED
   CHEMOTHERAPY; TYROSINE-KINASE-INHIBITOR; PHASE-II MULTICENTER;
   CARCINOMA-CELLS; IN-VITRO; MONOCLONAL-ANTIBODY
AB Human cancer tissues are heterogeneous in nature and become differentiated during expansion of cancer stem cells (CSCs). CSCs initiate tumorigenesis, and are involved in tumor recurrence and metastasis. Furthermore, data show that CSCs are highly resistant to anticancer drugs. Cetuximab, a specific anti-epidermal growth factor receptor (EGFR) monoclonal antibody, is used in cancer treatment. Although development of resistance to cetuximab is well recognized, the underlying mechanisms remain unclear. Lapatinib, a dual inhibitor of epidermal growth factor receptor (EGFR)/ErbB2, has antiproliferative effects and is used to treat patients with ErbB2-positive metastatic breast cancer. In this review, cetuximab and lapatinib-resistant oral squamous cell carcinoma (OSCC) cells proliferation and migration signal transduction passway is discussed by introducing our research. (C) 2017 The Authors. Published by Elsevier Ltd.
C1 [Ohnishi, Yuichi; Yasui, Hiroki; Nakajima, Masahiro] Osaka Dent Univ, Dept Oral & Maxillofacial Surg 2, Hirakata, Osaka 5731121, Japan.
   [Ohnishi, Yuichi; Nozaki, Masami] Osaka Univ, Res Inst Microbial Dis, Dept Cell Biol, Suita, Osaka 5650871, Japan.
C3 Osaka University
RP Ohnishi, Y (corresponding author), Osaka Dent Univ, Dept Oral & Maxillofacial Surg 2, Chuo Ku, 1-5-17 Otemae, Osaka 5400008, Japan.
EM onishi_yu_ku@msn.com
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NR 59
TC 15
Z9 15
U1 0
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1882-7616
EI 2213-6851
J9 JPN DENT SCI REV
JI Jpn. Dent. Sci. Rev.
PD MAY
PY 2018
VL 54
IS 2
BP 88
EP 103
DI 10.1016/j.jdsr.2017.11.001
PG 16
WC Dentistry, Oral Surgery & Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dentistry, Oral Surgery & Medicine
GA GG1YI
UT WOS:000432484800006
PM 29755619
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yang, Z
   Liu, SW
   Zhu, MG
   Zhang, H
   Wang, J
   Xu, Q
   Lin, KS
   Zhou, XM
   Tao, M
   Li, C
   Zhu, H
AF Yang, Zhao
   Liu, Shengwu
   Zhu, Mingao
   Zhang, Hong
   Wang, Ji
   Xu, Qian
   Lin, Kaisu
   Zhou, Xiumin
   Tao, Min
   Li, Chong
   Zhu, Hong
TI PS341 inhibits hepatocellular and colorectal cancer cells through the
   FOXO3/CTNNB1 signaling pathway
SO SCIENTIFIC REPORTS
LA English
DT Article
ID PHASE-II TRIAL; MESENCHYMAL TRANSITION; TUMOR-SUPPRESSOR; PROTEASOME;
   BORTEZOMIB; BETA; EXPRESSION; SORAFENIB; UBIQUITIN; METASTASIS
AB Hepatocellular carcinoma (HCC) and colorectal cancer (CRC) are among the most common cancers across the world. Particularly, a large number of patients with CRC also have liver metastasis. Currently, there are just a few targeted drugs against these two kinds of tumors which can only benefit a very small population of patients. Therefore, the need of more effective therapeutic drugs or strategies for these two types of cancers is urgent. PS341 (Bortezomib) is the first proteasome inhibitor drug which has been approved in clinical treatment for multiple myeloma. Here we demonstrated that PS341 negatively regulated HCC and CRC both in vitro and in vivo, including the inhibition of cell proliferation, epithelial-mesenchymal transition (EMT), the expression of stemness-related genes, cell migration and invasiveness. Mechanically, PS341 upregulated the expression of FOXO3, which inhibited the transcriptional activation of CTNNB1. The downregualtion of CTNNB1 led to apoptosis, cell cycle arrest, and the inhibition of migration, invasion, self-renewal and tumor formation of these two cancer types. In sum, our findings shed light on the PS341 mediated targeted therapy against both HCC and CRC in the future.
C1 [Yang, Zhao; Zhou, Xiumin; Tao, Min; Li, Chong; Zhu, Hong] Suzhou Univ, Affiliated Hosp 1, Dept Oncol, Suzhou 215006, Peoples R China.
   [Yang, Zhao] Chinese Acad Sci, CAS Key Lab Pathogen Microbiol & Immunol, Inst Microbiol, Beijing 100101, Peoples R China.
   [Liu, Shengwu] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
   [Liu, Shengwu] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
   [Zhu, Mingao; Zhang, Hong; Wang, Ji; Xu, Qian; Lin, Kaisu] Soochow Univ, Affiliated Hosp 2, Dept Oncol, Suzhou 215000, Peoples R China.
   [Li, Chong] Chinese Acad Sci, Lab Anim Ctr, Inst Biophys, Beijing 100101, Peoples R China.
   [Yang, Zhao] Chinese Acad Sci, Inst Biophys, CAS Key Lab Infect & Immun, Beijing 100101, Peoples R China.
C3 Chinese Academy of Sciences; Institute of Microbiology, CAS; Harvard
   University; Harvard Medical School; Harvard University; Dana-Farber
   Cancer Institute; Soochow University - China; Chinese Academy of
   Sciences; Institute of Biophysics, CAS; Chinese Academy of Sciences;
   Institute of Biophysics, CAS
RP Li, C; Zhu, H (corresponding author), Suzhou Univ, Affiliated Hosp 1, Dept Oncol, Suzhou 215006, Peoples R China.; Li, C (corresponding author), Chinese Acad Sci, Lab Anim Ctr, Inst Biophys, Beijing 100101, Peoples R China.
EM lichong@moon.ibp.ac.cn; zhuhong_jasmine@suda.edu.cn
RI Zhu, Hong/HKM-4120-2023; Zhou, Xiumin/AAN-4380-2020
FU National Natural Science Foundation of China [81472413, 81000944,
   81572345, 81572992]; Shenzhen Science and Technology development Funds
   Program [CXZZ20130516153248144]; Shenzhen Strategic Emerging Industry
   Development Special Funds Program [JSGG20130411091246833]; Natural
   Science Foundation of the Jiangsu Higher Education Institutions of China
   [10KJB320020]; Tianqing Liver Disease Research Foundation [20120024];
   Priority Academic Program Development of Jiangsu Higher Education
   Institutions
FX The authors thank all the faculties and staffs of Institute of
   Microbiology, Harvard Medical School, the First Affiliated Hospital of
   Soochow University, the Second Affiliated Hospital of Soochow University
   and Institute of Biophysics whose names were not included in the author
   list, but who contributed to this work. This work was supported by the
   National Natural Science Foundation of China (81472413, 81000944,
   81572345, 81572992), Shenzhen Science and Technology development Funds
   Program CXZZ20130516153248144), Shenzhen Strategic Emerging Industry
   Development Special Funds Program (JSGG20130411091246833), Natural
   Science Foundation of the Jiangsu Higher Education Institutions of China
   (No. 10KJB320020), Tianqing Liver Disease Research Foundation (No.
   20120024) and Priority Academic Program Development of Jiangsu Higher
   Education Institutions.
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NR 48
TC 37
Z9 41
U1 0
U2 19
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD FEB 26
PY 2016
VL 6
AR 22090
DI 10.1038/srep22090
PG 15
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA DE8ZV
UT WOS:000370926100001
PM 26915315
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Bellier, J
   Nokin, MJ
   Caprasse, M
   Tiamiou, A
   Blomme, A
   Scheijen, JL
   Koopmansch, B
   MacKay, GM
   Chiavarina, B
   Costanza, B
   Rademaker, G
   Durieux, F
   Agirman, F
   Maloujahmoum, N
   Cusumano, PG
   Lovinfosse, P
   Leung, HY
   Lambert, F
   Bours, V
   Schalkwijk, CG
   Hustinx, R
   Peulen, O
   Castronovo, V
   Bellahcène, A
AF Bellier, Justine
   Nokin, Marie-Julie
   Caprasse, Maurine
   Tiamiou, Assia
   Blomme, Arnaud
   Scheijen, Jean L.
   Koopmansch, Benjamin
   MacKay, Gillian M.
   Chiavarina, Barbara
   Costanza, Brunella
   Rademaker, Gilles
   Durieux, Florence
   Agirman, Ferman
   Maloujahmoum, Naima
   Cusumano, Pino G.
   Lovinfosse, Pierre
   Leung, Hing Y.
   Lambert, Frederic
   Bours, Vincent
   Schalkwijk, Casper G.
   Hustinx, Roland
   Peulen, Olivier
   Castronovo, Vincent
   Bellahcene, Akeila
TI Methylglyoxal Scavengers Resensitize KRAS-Mutated Colorectal Tumors to
   Cetuximab
SO CELL REPORTS
LA English
DT Article
ID HEAT-SHOCK-PROTEIN; TARGETED THERAPIES; CANCER CELLS; RESISTANCE;
   GROWTH; HSP27; RAS; AKT; HEAT-SHOCK-PROTEIN-27; METABOLISM
AB The use of cetuximab anti-epidermal growth factor receptor (anti-EGFR) antibodies has opened the era of targeted and personalized therapy in colorectal cancer (CRC). Poor response rates have been unequivocally shown in mutant KRAS and are even observed in a majority of wild-type KRAS tumors. Therefore, patient selection based on mutational profiling remains problematic. We previously identified methylglyoxal (MGO), a by-product of glycolysis, as a metabolite promoting tumor growth and metastasis. Mutant KRAS cells under MGO stress show AKT-dependent survival when compared with wild-type KRAS isogenic CRC cells. MGO induces AKT activation through phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin 2 (mTORC2) and Hsp27 regulation. Importantly, the sole induction of MGO stress in sensitive wild-type KRAS cells renders them resistant to cetuximab. MGO scavengers inhibit AKT and resensitize KRAS-mutated CRC cells to cetuximab in vivo. This study establishes a link between MGO and AKT activation and pinpoints this oncometabolite as a potential target to tackle EGFR-targeted therapy resistance in CRC.
C1 [Bellier, Justine; Nokin, Marie-Julie; Caprasse, Maurine; Tiamiou, Assia; Chiavarina, Barbara; Costanza, Brunella; Rademaker, Gilles; Durieux, Florence; Agirman, Ferman; Maloujahmoum, Naima; Peulen, Olivier; Castronovo, Vincent; Bellahcene, Akeila] Univ Liege, Metastasis Res Lab, GIGA Canc, Liege, Belgium.
   [Blomme, Arnaud; MacKay, Gillian M.; Leung, Hing Y.] Canc Res UK Beatson Inst, Glasgow, Lanark, Scotland.
   [Scheijen, Jean L.; Schalkwijk, Casper G.] Maastricht Univ, Dept Internal Med, Lab Metab & Vasc Med, Maastricht, Netherlands.
   [Koopmansch, Benjamin; Lambert, Frederic; Bours, Vincent] Liege Univ Hosp, Dept Human Genet, Liege, Belgium.
   [Cusumano, Pino G.] Univ Liege, Liege Univ Hosp, Dept Senol, Liege, Belgium.
   [Lovinfosse, Pierre; Hustinx, Roland] Univ Liege, Liege Univ Hosp, Oncol Imaging Div, Liege, Belgium.
   [Leung, Hing Y.] Univ Glasgow, Inst Canc Sci, Glasgow, Lanark, Scotland.
C3 University of Liege; Beatson Institute; Maastricht University;
   University of Liege; University of Liege; University of Liege;
   University of Glasgow
RP Bellahcène, A (corresponding author), Univ Liege, Metastasis Res Lab, GIGA Canc, Liege, Belgium.
EM a.bellahcene@uliege.be
RI Costanza, Brunella/AAB-6354-2022; Scheijen, Jean/AAY-3799-2020;
   Rademaker, Gilles/X-1386-2019; Blomme, Arnaud/AAM-1440-2020; Peulen,
   Olivier/C-1250-2018
OI Peulen, Olivier/0000-0002-6933-0134; Rademaker,
   Gilles/0000-0003-0170-781X; Costanza, Brunella/0000-0001-8279-805X;
   Schalkwijk, Casper G/0000-0003-0190-2690; Blomme,
   Arnaud/0000-0003-4183-8726
FU Televie-FNRS [J.0007.19]; FNRS; University of Liege; Fondation Leon
   Fredericq; Cancer Research UK Beatson Institute [C596/A17196]; CRUK
   [A22904]
FX J.B. is a Televie PhD research fellow and A. Bellahcene. is a research
   director at the National Fund for Scientific Research (FNRS), Belgium.
   The authors are thankful to S. Nuchtern and V. Hennequiere for expert
   technical assistance. We thank Dr. K. Uchida (University of Tokyo,
   Japan) and Dr. D. Spiegel (Yale University, USA) for kindly providing
   anti-argpyrimidine antibody and MBo probe, respectively. The authors are
   thankful to Dr. S. Gofflot (CHU/ULiege Biobank) and Pr. A-F. Donneau
   (Department of Public Health, University of Liege). The authors
   acknowledge the scientific and technical support provided at the animal,
   imaging and flow cytometry, genomics, viral vectors, and immunohistology
   technology platforms of the GIGA-Research Institute (University of
   Liege, Belgium). This work was supported by a grant from Televie-FNRS
   (J.0007.19) awarded to A. Bellahcene. We thank the FNRS, University of
   Liege, and Fondation Leon Fredericq for support. A. Blomme, G.M. MacKay,
   and H.Y. Leung were supported by Cancer Research UK Beatson Institute
   core funding (C596/A17196) and CRUK core group awarded to H.Y.L
   (A22904).
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NR 82
TC 27
Z9 29
U1 0
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD FEB 4
PY 2020
VL 30
IS 5
BP 1400
EP +
DI 10.1016/j.celrep.2020.01.012
PG 23
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA KI4BU
UT WOS:000511294400012
PM 32023458
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, HG
   Xu, XW
   Shi, XP
   Han, BW
   Li, ZH
   Ren, WH
   Chen, PJ
   Lou, YF
   Li, B
   Luo, XY
AF Zhang, H. G.
   Xu, X. W.
   Shi, X. P.
   Han, B. W.
   Li, Z. H.
   Ren, W. H.
   Chen, P. J.
   Lou, Y. F.
   Li, B.
   Luo, X. Y.
TI Overexpression of forkhead box protein M1 (FOXM1) plays a critical role
   in colorectal cancer
SO CLINICAL & TRANSLATIONAL ONCOLOGY
LA English
DT Article
DE Colorectal cancer; Forkhead box protein M1; Small interfering RNA;
   Targeted therapy
ID TRANSCRIPTION FACTOR; ANGIOGENESIS; PROGRESSION; TUMOR
AB The forkhead box M1 (FOXM1), an important regulator of cell differentiation and proliferation, is overexpressed in a number of aggressive human carcinomas. However, the clinical significance of FOXM1 signaling in human colorectal cancer (CRC) pathogenesis remains unknown. The aim of this study was to evaluate the role of FOXM1 in CRC tumorigenesis.
   We investigated FOXM1 expression in 103 cases of primary CRC and matched normal tissue specimens and explored the underlying mechanisms of altered FOXM1 expression and the impact of this altered expression on CRC proliferation and metastasis using in vitro models of CRC.
   The results showed that high expression of FOXM1 staining was 85.44 % (88/103) in 103 cases of CRC and 20.39 % (21/103) in 103 cases of adjacent non-cancerous tissue samples; the difference of FOXM1 expression between two groups was statistically significant (P < 0.001). Silencing of FOXM1 inhibited the proliferation of CRC cells, and the invasion and migration of CRC cells were distinctly suppressed. Furthermore, FOXM1 knockdown led to substantial reductions in VEGF-A levels in CRC cell lines.
   Our data suggest that the pathogenesis of CRC maybe mediated by FOXM1, and FOXM1 could represent selective targets for the molecularly targeted treatments of CRC.
C1 [Zhang, H. G.; Shi, X. P.; Ren, W. H.; Chen, P. J.; Lou, Y. F.; Li, B.; Luo, X. Y.] Zhengzhou Univ, Affiliated Luoyang Cent Hosp, Dept Oncol, 288 Zhongzhou Rd, Luoyang 471000, Peoples R China.
   [Xu, X. W.; Han, B. W.; Li, Z. H.] Zhengzhou Univ, Affiliated Luoyang Cent Hosp, Dept Surg, Luoyang 471000, Peoples R China.
C3 Zhengzhou University; Zhengzhou University
RP Luo, XY (corresponding author), Zhengzhou Univ, Affiliated Luoyang Cent Hosp, Dept Oncol, 288 Zhongzhou Rd, Luoyang 471000, Peoples R China.
EM drliug6@163.com
FU Bureau of Luoyang City Science and Technology
FX This work is supported by the Bureau of Luoyang City Science and
   Technology 2015 Key Project Fund.
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NR 17
TC 16
Z9 17
U1 0
U2 9
PU SPRINGER INTERNATIONAL PUBLISHING 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 MAY
PY 2016
VL 18
IS 5
BP 527
EP 532
DI 10.1007/s12094-015-1400-1
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DI6WC
UT WOS:000373639900013
PM 26370421
DA 2025-01-04
ER

PT J
AU Jin, Y
   Zhang, ZL
   Huang, Y
   Zhang, KN
   Xiong, B
AF Jin, Y.
   Zhang, Z-L
   Huang, Y.
   Zhang, K-N
   Xiong, B.
TI MiR-182-5p inhibited proliferation and metastasis of colorectal cancer
   by targeting MTDH
SO EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES
LA English
DT Article
DE MicroRNA-182-5p (MIR-182-5p); Colorectal cancer (CRC); Metadherin
   (MTDH); Epithelial-mesenchymal transition (EMT)
ID POOR-PROGNOSIS; DOWN-REGULATION; EXPRESSION; MTDH/AEG-1; ACTIVATION;
   CARCINOMA; APOPTOSIS; PHENOTYPE; FEATURES
AB OBJECTIVE: To investigate the role and molecular mechanism of miR-182-5p in the development of colorectal cancer (CRC), thereby providing a theoretical basis for new CRC therapeutic targets.
   PATIENTS AND METHODS: The expression of miR-182-5p in CRC clinical cases and biological cell lines was detected. On-line target gene prediction and Luciferase reporter gene assay were performed to screen and verify the target of miR-182-5p, respectively. The role of miR-182-5p in CRC cell function was further analyzed.
   RESULTS: MiR-182-5p expression was significantly decreased in both CRC tissues and cell lines. Metadherin (MTDH) was screened and verified as a functional target of miR-182-5p. The cell proliferation, invasion and migration ability of CRC cells were significantly inhibited after the up-regulation of miR-182-5p. However, MTDH limited the anti-cancer effects of miR-182-5p in CRC cells.
   CONCLUSIONS: Our research demonstrated the inhibitory function of miR-182-5p in CRC. Therefore, the miR-182-5p/MTDH axis was expected to be one of the targets of CRC targeted therapy.
C1 [Jin, Y.; Xiong, B.] Wuhan Univ, Dept Gastrointestinal Surg, Zhongnan Hosp, Wuhan, Hubei, Peoples R China.
   [Zhang, Z-L; Huang, Y.; Zhang, K-N] Huazhong Univ Sci & Technol, Jingzhou Hosp, Tongji Med Coll, Dept Gastrointestinal Surg, Jingzhou, Peoples R China.
C3 Wuhan University; Huazhong University of Science & Technology
RP Xiong, B (corresponding author), Wuhan Univ, Dept Gastrointestinal Surg, Zhongnan Hosp, Wuhan, Hubei, Peoples R China.
EM binxiong1961@163.com
RI Zhang, Jiawei/ABE-8432-2020
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Z9 45
U1 0
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PU VERDUCI PUBLISHER
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PA VIA GREGORIO VII, ROME, 186-00165, ITALY
SN 1128-3602
J9 EUR REV MED PHARMACO
JI Eur. Rev. Med. Pharmacol. Sci.
PD FEB
PY 2019
VL 23
IS 4
BP 1494
EP 1501
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA HO1GJ
UT WOS:000460653200017
PM 30840271
DA 2025-01-04
ER

PT J
AU Hou, HL
   Sun, DT
   Zhang, XC
AF Hou, Helei
   Sun, Dantong
   Zhang, Xiaochun
TI The role of <i>MDM2</i> amplification and overexpression in therapeutic
   resistance of malignant tumors
SO CANCER CELL INTERNATIONAL
LA English
DT Review
DE MDM2; p53; Therapeutic resistance; Molecular mechanism
ID ACQUIRED-RESISTANCE; PROSTATE-CANCER; P53 GENE; INHIBITOR; GROWTH;
   EXPRESSION; APOPTOSIS; PROTEIN; ANGIOGENESIS; CISPLATIN
AB The MDM2 protein encoded by the mouse double minute 2 (MDM2) gene is the primary negative regulatory factor of the p53 protein. MDM2 can ligate the p53 protein via its E3 ubiquitin ligase, and the ubiquitinated p53 can be transferred to the cytoplasm and degraded by proteasomes. Therefore, MDM2 can maintain the stability of p53 signaling pathway. MDM2 amplification has been detected in many human malignancies, including lung cancer, colon cancer and other malignancies. MDM2 overexpression is associated with chemotherapeutic resistance in human malignancies. The mechanisms of chemotherapeutic resistance by MDM2 overexpression mainly include the p53-MDM2 loop-dependent and p53-MDM2 loop-independent pathways. But the role of MDM2 overexpression in tyrosine kinase inhibitors resistance remains to be further study. This paper reviews the possible mechanisms of therapeutic resistance of malignancies induced by MDM2 amplification and overexpression, including chemotherapy, radiotherapy, targeted agents and hyperprogressive disease of immunotherapy. Besides, MDM2-targeted therapy may be a potential new strategy for treating advanced malignancies.
C1 [Hou, Helei; Sun, Dantong; Zhang, Xiaochun] Qingdao Univ, Dept Med Oncol, Affiliated Hosp, 16 Jiangsu Rd, Qingdao 266005, Shandong, Peoples R China.
C3 Qingdao University
RP Zhang, XC (corresponding author), Qingdao Univ, Dept Med Oncol, Affiliated Hosp, 16 Jiangsu Rd, Qingdao 266005, Shandong, Peoples R China.
EM houheleiqdmh@163.com; zxc9670@qdu.edu.cn
RI xiang, li/JDN-4098-2023; Sun, Dantong/GWR-0984-2022
FU Taishan Scholar Foundation of Shandong Province; Qingdao People's
   Livelihood Science and Technology Program [16-6-2-3-nsh]; Chinese
   Postdoctoral Science Foundation [2017M622143]
FX This work was supported by the Taishan Scholar Foundation of Shandong
   Province (No. tshw201502061 to Xiaochun Zhang), the Qingdao People's
   Livelihood Science and Technology Program (16-6-2-3-nsh to Xiaochun
   Zhang) and Chinese Postdoctoral Science Foundation (2017M622143 to Helei
   Hou).
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TC 152
Z9 168
U1 2
U2 36
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 AUG 22
PY 2019
VL 19
IS 1
AR 216
DI 10.1186/s12935-019-0937-4
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IT7KC
UT WOS:000483053100002
PM 31440117
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Pavase, LS
   Mane, DV
AF Pavase, Laxmikant S.
   Mane, Dhananjay V.
TI Synthesis and anticancer activities of novel (tetrahydrobenzo [4,5]
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SO MEDICINAL CHEMISTRY RESEARCH
LA English
DT Article
DE Thieno pyrimidine; Proline; Gewald reaction; MCF-7; HCT-15; Antitumor
   activities
ID LUNG-CANCER; AGENTS
AB Cancer chemotherapy has been one of the major medical advances in the last few decades. The medications involved in treatment have a narrow therapeutic index, and often the responses produced are only just palliative as well as unpredictable. In contrast, targeted therapy such as Tyrosine kinases inhibitors, that has been introduced in recent years is directed against cancer-specific molecules and signaling pathways with some side effects Therefore, we studied these class of molecules to obtain new candidates of remarkable activities and minimal side effects. We herein reported SAR driven synthesis of 16 novel molecules and their anticancer profiles in specifically targeted human Breast cell line MCF-7 and Human Colon Cancer Cell Line HCT-15. Compounds 7e and 8f showed descent antitumor activities when compared to Doxorubicine (GI(50) < 0.1) for human Breast cell line MCF-7. The synthesized analogs were ensured by spectral and elemental analysis.
C1 [Pavase, Laxmikant S.; Mane, Dhananjay V.] Dr Babasaheb Ambedkar Marathwada Univ, Dept Chem, Aurangabad 431004, Maharashtra, India.
C3 Dr. Babasaheb Ambedkar Marathwada University (BAMU)
RP Pavase, LS (corresponding author), Dr Babasaheb Ambedkar Marathwada Univ, Dept Chem, Aurangabad 431004, Maharashtra, India.
EM laxmikantpavase@rediffmail.com
OI Mane, Dhananjay/0000-0003-3078-8284
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NR 19
TC 13
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U1 0
U2 9
PU SPRINGER BIRKHAUSER
PI NEW YORK
PA 233 SPRING STREET, 6TH FLOOR, NEW YORK, NY 10013 USA
SN 1054-2523
EI 1554-8120
J9 MED CHEM RES
JI Med. Chem. Res.
PD OCT
PY 2016
VL 25
IS 10
BP 2380
EP 2391
DI 10.1007/s00044-016-1692-x
PG 12
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EA5WZ
UT WOS:000386697200027
DA 2025-01-04
ER

PT J
AU Yi, Q
   Cui, HW
   Liao, Y
   Xiong, JY
   Ye, XF
   Sun, WC
AF Yi, Qian
   Cui, Hanwei
   Liao, Yi
   Xiong, Jianyi
   Ye, Xiufeng
   Sun, Weichao
TI A minor review of microRNA-338 exploring the insights of its function in
   tumorigenesis
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE MicroRNA-338; Proliferation; Migration; Apoptosis; Tumor suppressor
ID GASTRIC-CANCER CELLS; SUPPRESSES TUMOR-GROWTH; HEPATOCELLULAR-CARCINOMA;
   DOWN-REGULATION; LUNG-CANCER; BREAST-CANCER; INHIBITS PROLIFERATION;
   CISPLATIN RESISTANCE; TARGETING MIR-338-3P; COLORECTAL-CARCINOMA
AB MicroRNAs(miRNAs) are small non-coding RNAs which have a critical role in various biological processes via direct binding and post-transcriptionally regulating targeted genes expression. More than one-half of human genes were regulated by miRNAs and their aberrant expression was detected in various human diseases, including cancers. miRNA-338 is a new identified miRNA and increasing evidence show that miRNA-338 participates in the progression of lots of cancers, such as lung cancer, hepatocellular cancer, breast cancer, glioma, and so on. Although a range of targets and signaling pathways such as MACC1 and Wnt/beta-catenin signaling pathway were illustrated to be regulated by miRNA-338, which functions in tumor progression are still ambiguous and the underlying molecular mechanisms are also unclear. Herein, we reviewed the latest studies in miRNA-338 and summarized its roles in different type of human tumors, which might provide us new idea for further investigations and potential targeted therapy.
C1 [Yi, Qian; Xiong, Jianyi; Sun, Weichao] Shenzhen Univ, Affiliated Hosp 1, Shenzhen Key Lab Tissue Engn, Dept Orthoped,Shenzhen Peoples Hosp 2, Shenzhen 518035, Guangdong, Peoples R China.
   [Cui, Hanwei; Liao, Yi; Ye, Xiufeng] Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Cent Lab, Shenzhen 518035, Guangdong, Peoples R China.
   [Cui, Hanwei; Liao, Yi; Ye, Xiufeng] Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Med Genet & Mol Diagnost Ctr, Shenzhen 518035, Guangdong, Peoples R China.
   [Yi, Qian] Southwest Med Univ, Sch Basic Med Sci, Dept Physiol, Luzhou 646000, Sichuan, Peoples R China.
C3 Shenzhen University; Shenzhen University; Shenzhen University; Southwest
   Medical University
RP Xiong, JY; Sun, WC (corresponding author), Shenzhen Univ, Affiliated Hosp 1, Shenzhen Key Lab Tissue Engn, Dept Orthoped,Shenzhen Peoples Hosp 2, Shenzhen 518035, Guangdong, Peoples R China.; Ye, XF (corresponding author), Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Cent Lab, Shenzhen 518035, Guangdong, Peoples R China.; Ye, XF (corresponding author), Shenzhen Univ, Affiliated Hosp 1, Shenzhen Peoples Hosp 2, Med Genet & Mol Diagnost Ctr, Shenzhen 518035, Guangdong, Peoples R China.
EM jianyixiong@126.com; szrosexiu@126.com; weichaosunshine@163.com
RI yi, qian/HIR-8841-2022; Sun, Weichao/KXR-1734-2024; Liao,
   Yi/JVM-9413-2024
OI Sun, Weichao/0000-0003-1646-8524
FU National Natural Science Foundation of China [82003126]; China
   Postdoctoral Science Foundation [2019M663105, 2019M663106, 2019M663107,
   2020M672835]; Scientific Research Foundation of Southwest Medical
   University [2017-ZRZD-021]; Shenzhen Science and Technology Projects
   [JCYJ20170817172241688, JCYJ20170817172150505]
FX This research was supported by the National Natural Science Foundation
   of China (No. 82003126); the China Postdoctoral Science Foundation (No.
   2019M663105; 2019M663106; 2019M663107; 2020M672835); The Scientific
   Research Foundation of Southwest Medical University (2017-ZRZD-021);
   Shenzhen Science and Technology Projects (No. JCYJ20170817172241688; No.
   JCYJ20170817172150505).
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NR 135
TC 4
Z9 4
U1 1
U2 12
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD JUL
PY 2021
VL 139
AR 111720
DI 10.1016/j.biopha.2021.111720
EA MAY 2021
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA SV2VK
UT WOS:000663682000006
PM 34243620
OA gold
DA 2025-01-04
ER

PT J
AU Xiu, MX
   Wang, YB
   Li, BL
   Wang, XF
   Xiao, F
   Chen, SL
   Zhang, LL
   Zhou, B
   Hua, FZ
AF Xiu, Mengxi
   Wang, Yongbo
   Li, Baoli
   Wang, Xifeng
   Xiao, Fan
   Chen, Shoulin
   Zhang, Lieliang
   Zhou, Bin
   Hua, Fuzhou
TI The Role of Notch3 Signaling in Cancer Stemness and Chemoresistance:
   Molecular Mechanisms and Targeting Strategies
SO FRONTIERS IN MOLECULAR BIOSCIENCES
LA English
DT Review
DE cancer; Notch3; mechanism; targeted therapy; cancer biology
ID EPITHELIAL-MESENCHYMAL TRANSITION; GAMMA-SECRETASE INHIBITORS;
   NF-KAPPA-B; BREAST-CANCER; OVARIAN-CANCER; COLORECTAL-CANCER;
   UP-REGULATION; SELF-RENEWAL; TAREXTUMAB OMP-59R5; TUMOR ANGIOGENESIS
AB Aberrant Notch signaling profoundly affects cancer progression. Especially the Notch3 receptor was found to be dysregulated in cancer, where its expression is correlated with worse clinicopathological features and poor prognosis. The activation of Notch3 signaling is closely related to the activation of cancer stem cells (CSCs), a small subpopulation in cancer that is responsible for cancer progression. In addition, Notch3 signaling also contributes to tumor chemoresistance against several drugs, including doxorubicin, platinum, taxane, epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) and gemcitabine, through complex mechanisms. In this review, we mainly focus on discussing the molecular mechanisms by which Notch3 modulates cancer stemness and chemoresistance, as well as other cancer behaviors including metastasis and angiogenesis. What's more, we propose potential treatment strategies to block Notch3 signaling, such as non-coding RNAs, antibodies and antibody-drug conjugates, providing a comprehensive reference for research on precise targeted cancer therapy.
C1 [Xiu, Mengxi; Wang, Yongbo; Li, Baoli; Xiao, Fan; Chen, Shoulin; Zhang, Lieliang; Zhou, Bin; Hua, Fuzhou] Nanchang Univ, Affiliated Hosp 2, Dept Anesthesiol, Nanchang, Jiangxi, Peoples R China.
   [Xiu, Mengxi; Wang, Yongbo; Li, Baoli; Xiao, Fan; Chen, Shoulin; Zhang, Lieliang; Zhou, Bin; Hua, Fuzhou] Key Lab Anesthesiol Jiangxi Prov, Nanchang, Jiangxi, Peoples R China.
   [Wang, Xifeng] Nanchang Univ, Affiliated Hosp 1, Dept Gastroenterol, Nanchang, Jiangxi, Peoples R China.
C3 Nanchang University; Nanchang University
RP Hua, FZ (corresponding author), Nanchang Univ, Affiliated Hosp 2, Dept Anesthesiol, Nanchang, Jiangxi, Peoples R China.; Hua, FZ (corresponding author), Key Lab Anesthesiol Jiangxi Prov, Nanchang, Jiangxi, Peoples R China.
EM huafuzhou@126.com
RI Hua, Fuzhou/ABB-5380-2021
OI Hua, Fuzhou/0000-0002-6718-6490; Chen, Shoulin/0000-0002-3167-8477
FU National Natural Science Foundation of China [81860259]; Provincal
   Science foudation of Jiangxi [20202BABL206016]; Youth Team Project of
   the Second Affiliated Hospital of Nanchang University [2019YNTD12003]
FX This work was supported by grants from the National Natural Science
   Foundation of China (81860259); Provincal Science foudation of Jiangxi
   (20202BABL206016); Youth Team Project of the Second Affiliated Hospital
   of Nanchang University (2019YNTD12003).
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NR 142
TC 33
Z9 34
U1 0
U2 11
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 JUN 14
PY 2021
VL 8
AR 694141
DI 10.3389/fmolb.2021.694141
PG 17
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA TA5GK
UT WOS:000667277100001
PM 34195229
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Caiazza, F
   Ryan, EJ
   Doherty, G
   Winter, DC
   Sheahan, K
AF Caiazza, Francesco
   Ryan, Elizabeth J.
   Doherty, Glen
   Winter, Desmond C.
   Sheahan, Kieran
TI Estrogen receptors and their implications in colorectal carcinogenesis
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE estrogen; estrogen receptor; colorectal cancer; tumor immunology; tumor
   microenvironment
ID POSTMENOPAUSAL HORMONE-THERAPY; DENDRITIC CELL-DIFFERENTIATION; SIDED
   COLON-CANCER; ER-BETA; MICROSATELLITE INSTABILITY; INTESTINAL
   TUMORIGENESIS; MOLECULAR PATHWAYS; PLUS PROGESTIN; BREAST-CANCER;
   EXPRESSION
AB Upon binding their cognate receptors, ER alpha (ESR1) and ER beta (ESR2), estrogens activate intracellular signaling cascades that have important consequences for cellular behavior. Historically linked to carcinogenesis in reproductive organs, estrogens have also been implicated in the pathogenesis of different cancer types of non-reproductive tissues including the colon. ER beta is the predominant estrogen receptor expressed in both normal and malignant colonic epithelium. However, during colon cancer progression, ER beta expression is lost, suggesting that estrogen signaling may play a role in disease progression. Estrogens may in fact exert an anti-tumor effect through selective activation of pro-apoptotic signaling mediated by ER beta, inhibition of inflammatory signals and modulation of the tumor microenvironment. In this review, we analyze the estrogen pathway as a possible therapeutic avenue in colorectal cancer, we report the most recent experimental evidence to explain the cellular and molecular mechanisms of estrogen-mediated protection against colorectal tumorigenesis, and we discuss future challenges and potential avenues for targeted therapy.
C1 [Caiazza, Francesco; Ryan, Elizabeth J.; Doherty, Glen; Winter, Desmond C.; Sheahan, Kieran] St Vincents Univ Hosp, Ctr Colorectal Dis, Dublin 4, Ireland.
   [Caiazza, Francesco; Ryan, Elizabeth J.; Doherty, Glen; Sheahan, Kieran] Univ Coll Dublin, Sch Med & Med Sci, Dublin 2, Ireland.
   [Winter, Desmond C.] St Vincents Univ Hosp, Dept Surg, Dublin 4, Ireland.
   [Sheahan, Kieran] St Vincents Univ Hosp, Dept Pathol, Dublin 4, Ireland.
C3 University College Dublin; Saint Vincent's University Hospital;
   University College Dublin; University College Dublin; Saint Vincent's
   University Hospital; University College Dublin; Saint Vincent's
   University Hospital
RP Caiazza, F (corresponding author), St Vincents Univ Hosp, Dept Histopathol, Elm Pk, Dublin 4, Ireland.
EM francesco.caiazza@gmail.com; k.sheahan@st-vincents.ie
RI Caiazza, Francesco/H-9477-2019; Ryan, Elizabeth/H-9758-2019
OI Ryan, Elizabeth/0000-0002-5137-1253; Doherty, Glen/0000-0003-4384-5049;
   Caiazza, Francesco/0000-0003-4228-1130
FU UCD Foundation; Merck Serono
FX Francesco Caiazza is supported by a Newman Fellowship awarded by the UCD
   Foundation and funded by a donation from Merck Serono. 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.
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NR 112
TC 148
Z9 166
U1 2
U2 17
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD FEB 2
PY 2015
VL 5
AR 19
DI 10.3389/fonc.2015.00019
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CO3QF
UT WOS:000359072900002
PM 25699240
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Giannini, V
   Rosati, S
   Defeudis, A
   Balestra, G
   Vassallo, L
   Cappello, G
   Mazzetti, S
   De Mattia, C
   Rizzetto, F
   Torresin, A
   Sartore-Bianchi, A
   Siena, S
   Vanzulli, A
   Leone, F
   Zagonel, V
   Marsoni, S
   Regge, D
AF Giannini, Valentina
   Rosati, Samanta
   Defeudis, Arianna
   Balestra, Gabriella
   Vassallo, Lorenzo
   Cappello, Giovanni
   Mazzetti, Simone
   De Mattia, Cristina
   Rizzetto, Francesco
   Torresin, Alberto
   Sartore-Bianchi, Andrea
   Siena, Salvatore
   Vanzulli, Angelo
   Leone, Francesco
   Zagonel, Vittorina
   Marsoni, Silvia
   Regge, Daniele
TI Radiomics predicts response of individualHER2-amplified colorectal
   cancer liver metastases in patients treated withHER2-targeted therapy
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE CT liver metastases; genetic algorithms; machine learning; prediction of
   response to therapy; radiomics
ID TUMOR HETEROGENEITY; TEXTURE; INHIBITION; EMERGENCE; BLOCKADE; FEATURES;
   EGFR; MET
AB The aim of our study was to develop and validate a machine learning algorithm to predict response of individual HER2-amplified colorectal cancer liver metastases (lmCRC) undergoing dual HER2-targeted therapy. Twenty-four radiomics features were extracted after 3D manual segmentation of 141 lmCRC on pretreatment portal CT scans of a cohort including 38 HER2-amplified patients; feature selection was then performed using genetic algorithms. lmCRC were classified as nonresponders (R-), if their largest diameter increased more than 10% at a CT scan performed after 3 months of treatment, responders (R+) otherwise. Sensitivity, specificity, negative (NPV) and positive (PPV) predictive values in correctly classifying individual lesion and overall patient response were assessed on a training dataset and then validated on a second dataset using a Gaussian naive Bayesian classifier. Per-lesion sensitivity, specificity, NPV and PPV were 89%, 85%, 93%, 78% and 90%, 42%, 73%, 71% respectively in the testing and validation datasets. Per-patient sensitivity and specificity were 92% and 86%. Heterogeneous response was observed in 9 of 38 patients (24%). Five of nine patients were carriers of nonresponder lesions correctly classified as such by our radiomics signature, including four of seven harboring only one nonresponder lesion. The developed method has been proven effective in predicting behavior of individual metastases to targeted treatment in a cohort of HER2 amplified patients. The model accurately detects responder lesions and identifies nonresponder lesions in patients with heterogeneous response, potentially paving the way to multimodal treatment in selected patients. Further validation will be needed to confirm our findings.
C1 [Giannini, Valentina; Defeudis, Arianna; Cappello, Giovanni; Mazzetti, Simone; Regge, Daniele] FPO IRCCS, Candiolo Canc Inst, Radiol Unit, Candiolo, Italy.
   [Giannini, Valentina; Defeudis, Arianna; Mazzetti, Simone; Regge, Daniele] Univ Turin, Dept Surg Sci, Turin, Italy.
   [Rosati, Samanta; Balestra, Gabriella] Politecn Torino, Dept Elect & Telecommun, Turin, Italy.
   [Vassallo, Lorenzo] SS Annunziata Savigliano Hosp, Radiol Unit, Cuneo, Italy.
   [De Mattia, Cristina; Torresin, Alberto] ASST Grande Osped Metropolitano Niguarda, Dept Med Phys, Milan, Italy.
   [Rizzetto, Francesco; Vanzulli, Angelo] ASST Grande Osped Metropolitano Niguarda, Dept Radiol, Milan, Italy.
   [Torresin, Alberto] Univ Milan, Dept Phys, Milan, Italy.
   [Sartore-Bianchi, Andrea; Siena, Salvatore; Vanzulli, Angelo] Univ Milan, Dept Oncol & Hematooncol, Milan, Italy.
   [Sartore-Bianchi, Andrea; Siena, Salvatore] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Leone, Francesco] ASL Biella, Med Oncol, Biella, Italy.
   [Leone, Francesco] Univ Turin, Dept Oncol, Turin, Italy.
   [Zagonel, Vittorina] Ist Oncol Veneto IRCCS, Med Oncol Unit 1, Padua, Italy.
   [Marsoni, Silvia] IFOM FIRC Inst Mol Oncol, Precis Oncol, Milan, Italy.
C3 IRCCS Fondazione del Piemonte per l'Oncologia; University of Turin;
   Polytechnic University of Turin; University of Milan; University of
   Milan; University of Turin; IRCCS Istituto Oncologico Veneto (IOV); IFOM
   - FIRC Institute of Molecular Oncology
RP Giannini, V (corresponding author), FPO IRCCS, Candiolo Canc Inst, Dept Radiol, Str Prov 142 Km 3,95, I-10060 Turin, Italy.
EM valentina.giannini@ircc.it
RI Balestra, Gabriella/AAA-9068-2020; Vanzulli, Angelo/X-4175-2019; Siena,
   Salvatore/ACK-2413-2022; Rizzetto, Francesco/AAH-1067-2019; Regge,
   Daniele/AAC-6816-2022; Defeudis, Arianna/AAC-7329-2022; Sartore-Bianchi,
   Andrea/AAB-9848-2019; Cappello, Giovanni/JJD-7653-2023; zagonel,
   vittorina/F-4226-2014; Giannini, Valentina/M-8365-2019; Rosati,
   Samanta/L-7463-2017
OI Defeudis, Arianna/0000-0002-1745-3044; Sartore-Bianchi,
   Andrea/0000-0003-0780-0409; zagonel, vittorina/0000-0002-0829-2525;
   Rizzetto, Francesco/0000-0003-3451-9874; Giannini,
   Valentina/0000-0001-5052-8231; Balestra, Gabriella/0000-0003-2717-648X;
   Marsoni, Silvia/0000-0002-5361-7122; Rosati,
   Samanta/0000-0003-0620-594X; Regge, Daniele/0000-0001-8267-5279
FU FONDAZIONE AIRC [21091]
FX FONDAZIONE AIRC, Grant/Award Number: 21091
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NR 35
TC 25
Z9 26
U1 3
U2 11
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD DEC 1
PY 2020
VL 147
IS 11
BP 3215
EP 3223
DI 10.1002/ijc.33271
EA SEP 2020
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NY2JJ
UT WOS:000569230800001
PM 32875550
OA Green Published
DA 2025-01-04
ER

PT J
AU Larki, P
   Gharib, E
   Taleghani, MY
   Khorshidi, F
   Nazemalhosseini-Mojarad, E
   Aghdaei, HA
AF Larki, Pegah
   Gharib, Ehsan
   Taleghani, Mohammad Yaghoob
   Khorshidi, Fatemeh
   Nazemalhosseini-Mojarad, Ehsan
   Aghdaei, Hamid Asadzadeh
TI Coexistence of <i>KRAS</i> and <i>BRAF</i> Mutations in Colorectal
   Cancer: A Case Report Supporting The Concept of Tumoral Heterogeneity
SO CELL JOURNAL
LA English
DT Article
DE BRAF; CRC; EGFR; KRAS
ID KI-RAS; CETUXIMAB; ONCOGENE; TUMORIGENESIS; CHEMOTHERAPY; PANITUMUMAB;
   CARCINOMAS; EXPRESSION; METASTASES; THERAPY
AB The detection of KRAS and BRAF mutations is a crucial step for the correct therapeutic approach and predicting the epidermal growth factor receptor (EGFR)-targeted therapy resistance of colorectal carcinomas. The concomitant KRAS and BRAF mutations occur rarely in the colorectal cancers (CRCs) with the prevalence of less than 0.001% of the cases. In patients with KRAS-mutant tumors, BRAF mutations should not regularly be tested unless the patient is participating in a clinical trial enriching for the presence of KRAS or BRAF-mutated tumor. The current report demonstrates a case with advanced adenocarcinoma of the colon showing the coexistence of KRAS and BRAF mutations and may have profound clinical implications for disease progression and therapeutic responses.
C1 [Larki, Pegah; Gharib, Ehsan; Taleghani, Mohammad Yaghoob; Khorshidi, Fatemeh; Aghdaei, Hamid Asadzadeh] Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Basic & Mol Epidemiol Gastrointestinal Disorders, Tehran, Iran.
   [Nazemalhosseini-Mojarad, Ehsan] Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Gastroenterol & Liver Dis Res Ctr, Yeman St, Tehran, Iran.
C3 Shahid Beheshti University Medical Sciences; Shahid Beheshti University
   Medical Sciences
RP Nazemalhosseini-Mojarad, E (corresponding author), Shahid Beheshti Univ Med Sci, Res Inst Gastroenterol & Liver Dis, Gastroenterol & Liver Dis Res Ctr, Yeman St, Tehran, Iran.
EM Nazemalhosseini@sbmu.ac.ir
RI Gharib, Ehsan/JGD-9610-2023; Asadzadeh-Aghdaei, Hamid/AAD-4494-2022;
   Nazemalhosseini-Moja, ehsan/HGF-3165-2022
OI Larki, Pegah/0000-0002-3947-8162; Gharib, Ehsan/0000-0001-6271-6731;
   nazemalhosseini-mojarad, ehsan/0000-0001-8914-004X
FU Research Institute for Gastroenterology and Liver Diseases of the Shahid
   Beheshti University of Medical Sciences
FX The authors would like to thank the Research Institute for
   Gastroenterology and Liver Diseases of the Shahid Beheshti University of
   Medical Sciences for its support of this study. There is no conflict of
   interest in this study.
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NR 36
TC 26
Z9 30
U1 0
U2 4
PU ROYAN INST
PI TEHRAN
PA PO BOX 19395-4644, TEHRAN, 00000, IRAN
SN 2228-5806
EI 2228-5814
J9 CELL J
JI Cell J.
PD SPR
PY 2017
VL 19
SU 1
BP 113
EP 117
DI 10.22074/cellj.2017.5123
PG 5
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA EW4DO
UT WOS:000402452400013
PM 28580315
DA 2025-01-04
ER

PT J
AU Ren, CF
   Han, HB
   Pan, JJ
   Chang, Q
   Wang, WH
   Guo, XB
   Bian, J
AF Ren, Chunfeng
   Han, Hongbin
   Pan, Jingjing
   Chang, Qian
   Wang, Wanhai
   Guo, Xiaobing
   Bian, Jing
TI DLGAP1-AS2 promotes human colorectal cancer progression through
   trans-activation of Myc
SO MAMMALIAN GENOME
LA English
DT Article
AB Substantial evidence suggests that non-coding RNA plays a vital role in human cancer, especially long non-coding RNA (lncRNA) with a length greater than 200nt. Herein, we found a lncRNA facilitating human colorectal cancer (CRC) progression. DLGAP1-AS2 was significantly increased in CRC tissues and cell lines. Knockdown of DLGAP1-AS2 inhibited CRC cell proliferation, migration, invasion in vitro, and tumor growth in vivo. The subcellular localization of DLGAP1-AS2 was translocated from the cytoplasm of normal cells to the nucleus of CRC cells due to reduced levels of N-6-methyladenosine (m(6)A) modification. Further, through the screening of a series of signal pathways, we found that Myc pathway was involved in the effect of DLGAP1-AS2. Silencing of DLGAP1-AS2 markedly reduced Myc mRNA and protein levels. Blockade of Myc effectively abolished the enhanced aggressive behaviors of CRC cells caused by DLGAP1-AS2 overexpression. Mechanistically, DLGAP1-AS2 directly bound CTCF, a well-known transcriptional repressor of Myc, resulting in reduced binding of CTCF on Myc promoter and activating Myc transcription. The second hairpin structure of DLGAP1-AS2 was critical for the interaction between DLGAP1-AS2 and CTCF in the nucleus. Taken together, our study reveals the oncogenic regulatory axis of DLGAP1-AS2/CTCF/Myc in CRC, implying a promising targeted therapy for clinical application.
C1 [Ren, Chunfeng; Pan, Jingjing; Chang, Qian; Wang, Wanhai; Guo, Xiaobing; Bian, Jing] Zhengzhou Univ, Affiliated Hosp 1, Clin Lab, 1 Jianshe Dong Rd, Zhengzhou 450003, Peoples R China.
   [Han, Hongbin] Luoyang Cent Peoples Hosp, Dept Gen Surg, Luoyang 471000, Peoples R China.
C3 Zhengzhou University
RP Ren, CF (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Clin Lab, 1 Jianshe Dong Rd, Zhengzhou 450003, Peoples R China.
EM rencf896@yeah.net
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NR 35
TC 5
Z9 5
U1 3
U2 4
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0938-8990
EI 1432-1777
J9 MAMM GENOME
JI Mamm. Genome
PD DEC
PY 2022
VL 33
IS 4
BP 672
EP 683
DI 10.1007/s00335-022-09963-y
EA OCT 2022
PG 12
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 5U1HI
UT WOS:000866302500001
PM 36222892
DA 2025-01-04
ER

PT J
AU Sposito, M
   Scaglione, IM
   Eccher, S
   Pasqualin, L
   Avancini, A
   Colato, C
   Rosina, P
   Simbolo, M
   Caliò, A
   Scarpa, A
   Milella, M
   Pilotto, S
   Belluomini, L
AF Sposito, Marco
   Scaglione, Ilaria Mariangela
   Eccher, Serena
   Pasqualin, Luca
   Avancini, Alice
   Colato, Chiara
   Rosina, Paolo
   Simbolo, Michele
   Calio, Anna
   Scarpa, Aldo
   Milella, Michele
   Pilotto, Sara
   Belluomini, Lorenzo
TI Exceptional Response in BRAF p.V600E-Mutant Enteric-Type Adenocarcinoma
   of the Lung With Cutaneous Spread: A Case Report
SO JTO CLINICAL AND RESEARCH REPORTS
LA English
DT Article
DE Non-small cell lung cancer; BRAF p.V600E; Cutaneous metastases;
   Enteric-type lung adenocarcinoma; Dabrafenib plus trametinib; Case
   report
AB Background: Enteric-type adenocarcinoma of the lung (lung-ETAC) is a rare form of lung cancer with histologic similarities to colorectal cancer, with aggressive behavior and unfavorable prognosis.Case Presentation: An 81-year-old man presented with discolored skin lesions on the chest and abdomen. After comprehensive evaluation, including skin biopsy and molecular profiling, the patient was diagnosed with having lung-ETAC with a BRAF p.V600E mutation. Treatment with dabrafenib and trametinib initially resulted in positive results, with improvement in skin lesions and overall clinical condition. Nevertheless, approximately 6 months after, the disease had progression with new skin lesions reappearing.Conclusions: We reported a unique case of a patient with BRAF p.V600E-mutant lung-ETAC with metastatic skin lesions achieving complete cutaneous response after targeted treatment with dabrafenib and trametinib, highlighting the potential for targeted therapy in patients with lung-ETAC harboring a BRAF p.V600E mutation. (c) 2023 The Authors. Published by Elsevier Inc. on behalf of the International Association for the Study of Lung Cancer. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
C1 [Sposito, Marco; Scaglione, Ilaria Mariangela; Eccher, Serena; Pasqualin, Luca; Avancini, Alice; Milella, Michele; Pilotto, Sara; Belluomini, Lorenzo] Univ Verona, Dept Engn Innovat Med DIMI, Sect Innovat Biomed Oncol Area, Ple LA Scuro 10, I-37134 Verona, Italy.
   [Sposito, Marco; Scaglione, Ilaria Mariangela; Eccher, Serena; Pasqualin, Luca; Avancini, Alice; Milella, Michele; Pilotto, Sara; Belluomini, Lorenzo] Univ Hosp & Trust AOUI Verona, Ple LA Scuro 10, I-37134 Verona, Italy.
   [Avancini, Alice] Univ Verona, Dept Neurosci Biomed & Movement Sci, Verona, Italy.
   [Colato, Chiara; Simbolo, Michele; Calio, Anna; Scarpa, Aldo] Univ Verona, Dept Diagnost & Publ Hlth, Sect Pathol, Verona, Italy.
   [Rosina, Paolo] Univ Verona, Dept Med, Sect Dermatol & Venereol, Verona, Italy.
C3 University of Verona; University of Verona; University of Verona;
   University of Verona
RP Pilotto, S (corresponding author), Univ Verona, Dept Engn Innovat Med DIMI, Sect Innovat Biomed Oncol Area, Ple LA Scuro 10, I-37134 Verona, Italy.; Pilotto, S (corresponding author), Univ Hosp & Trust AOUI Verona, Ple LA Scuro 10, I-37134 Verona, Italy.
EM sara.pilotto@univr.it
RI Simbolo, Michele/AAB-1851-2019; Belluomini, Lorenzo/GXW-3089-2022;
   Milella, Michele/ABH-8606-2020; scarpa, aldo/K-6832-2016; Avancini,
   Alice/ABE-2707-2020; Pilotto, Sara/G-3725-2018
OI Belluomini, Lorenzo/0000-0003-1981-5499; Pilotto,
   Sara/0000-0003-2229-4874
CR Fassi E, 2023, LUNG CANCER, V179, DOI 10.1016/j.lungcan.2023.107176
   Gong JL, 2021, TRANSL ONCOL, V14, DOI 10.1016/j.tranon.2021.101123
   Kuhn E, 2018, PATHOLOGICA, V110, P5
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   Zhao L, 2017, MEDICINE, V96, DOI 10.1097/MD.0000000000008153
NR 9
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2666-3643
J9 JTO CLIN RES REP
JI JTO Clin. Res. Rep.
PD DEC
PY 2023
VL 4
IS 12
AR 100597
DI 10.1016/j.jtocrr.2023.100597
EA DEC 2023
PG 4
WC Oncology; Respiratory System
WE Emerging Sources Citation Index (ESCI)
SC Oncology; Respiratory System
GA GB1K1
UT WOS:001150104300001
PM 38124787
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Martinelli, E
   Morgillo, F
   Troiani, T
   Ciardiello, F
AF Martinelli, Erika
   Morgillo, Floriana
   Troiani, Teresa
   Ciardiello, Fortunato
TI Cancer resistance to therapies against the EGFR-RAS-RAF pathway: The
   role of MEK
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE MEK; Resistance; NSCLC; CRC
ID METASTATIC COLORECTAL-CANCER; CELL LUNG-CANCER; ACQUIRED-RESISTANCE;
   FEEDBACK ACTIVATION; 1ST-LINE TREATMENT; MAP KINASE; BRAF GENE;
   MESENCHYMAL TRANSITION; ANTITUMOR EFFICACY; TARGETED THERAPY
AB The mitogen-activated protein kinases (MAPKs) mediate intracellular signals activated by a wide variety of extracellular stimuli. The activation of the RAS-RAF-MEK-MAPK cascade culminates in the regulation of gene transcription promoting cancer cell proliferation, survival, migration and angiogenesis. MEK (mitogen-activated protein kinase kinase-MAPKK) 1/2 is a transducer of the growth factor receptor-RAS-RAF-MAPK signalling cascade and plays a relevant role in development and progression of human cancers, such as colorectal cancer (CRC), non small cell lung cancer (NSCLC). Direct inhibition of MEK is a promising strategy and several inhibitors are currently under evaluation in clinical trials showing initial clinical activity in different tumours. MEK activation, by different genetic mechanisms, has been described for both intrinsic and acquired resistance to drugs targeting the EGFR (Epidermal Growth Factor Receptor)-RAS-RAF pathway in CRC, NSCLC. Combination therapies with chemotherapy and/or with molecular targeted agents are warranted and biomarkers studies are needed to identify those tumours dependent on MEK signalling. (C) 2016 Elsevier Ltd. All rights reserved.
C1 [Martinelli, Erika; Morgillo, Floriana; Troiani, Teresa; Ciardiello, Fortunato] Univ Campania Luigi Vanvitelli, Dipartimento Internist Clin & Sperimentale F Magr, Oncol Med, Via S Pansini 5, I-80131 Naples, Italy.
C3 Universita della Campania Vanvitelli
RP Martinelli, E (corresponding author), Univ Campania Luigi Vanvitelli, Dipartimento Internist Clin & Sperimentale F Magr, Oncol Med, Via S Pansini 5, I-80131 Naples, Italy.
EM erika.martinelli@unina2.it
OI MORGILLO, Floriana/0000-0002-9167-323X
FU Associazione Italiana per la Ricerca sul Cancro (AIRC) [14800, 17778]
FX This work was supported by the Associazione Italiana per la Ricerca sul
   Cancro (AIRC) (F. Ciardiello-IG-grant number 14800 and E. Martinelli
   MFAG-grant number 17778).
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NR 80
TC 108
Z9 120
U1 1
U2 49
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0305-7372
EI 1532-1967
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD FEB
PY 2017
VL 53
BP 61
EP 69
DI 10.1016/j.ctrv.2016.12.001
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EK6ZS
UT WOS:000394075400007
PM 28073102
DA 2025-01-04
ER

PT J
AU Aminabee, S
   Rao, AL
   Alimunnisa
   Begum, S
   Vani, VBN
AF Aminabee, Shaik
   Rao, Atmakuri Lakshmana
   Alimunnisa
   Begum, Shabana
   Vani, V. Bhavya Naga
TI RECENT ADVANCES IN CANCER THERAPY
SO INTERNATIONAL JOURNAL OF LIFE SCIENCE AND PHARMA RESEARCH
LA English
DT Article
DE Cancer therapy; Chemotherapy; targeted therapy; virotherapy;
   antiangiogenics
AB As per studies in 2015, about 90.5 million people had cancer. About 14.1 million new cases occur a year (not including skin cancer other than melanoma). It caused about 8.8 million deaths (15.7% of deaths). The most common types of cancer in males are lung cancer, prostate cancer, colorectal cancer and stomach cancer. The major cancer treatments are surgery and Radiotherapy which is being replaced by the other therapies like Virotherpay, Robot assisted therapy, Cancer therapy involved targeting proteins DNA double strand break repair, Liquid biopsies, Antiangiogenics, Targeted specific alterations.
C1 [Aminabee, Shaik; Rao, Atmakuri Lakshmana; Alimunnisa; Begum, Shabana; Vani, V. Bhavya Naga] VV Inst Pharmaceut Sci, Dept Pharmacol, Gudlavalleru, India.
RP Aminabee, S (corresponding author), VV Inst Pharmaceut Sci, Dept Pharmacol, Gudlavalleru, India.
RI Atmakuri, Prof. Lakshmana Rao/K-5612-2014
CR Alavizadeh S.H., 2016, Current Pharmacology Reports, V2, P129, DOI [DOI 10.1007/S40495-016-0056-Z, 10.1007/s40495-016-0056-z]
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NR 12
TC 3
Z9 3
U1 0
U2 21
PU INT JOURNAL LIFESCIENCE & PHARMA RESEARCH
PI TAMILNADU
PA PLOT NO 10, 2 MAIN RD, RENGA NAGAR NEAR TO OLD ALPHA SCH, SATHANOOR MAIN
   RD, TIRUCHIRAPALLI, TAMILNADU, INDIA
SN 2250-0480
J9 INT J LIFE SCI PHARM
JI Int. J. Life Sci. Pharma Res.
PD JAN
PY 2020
SI 9
BP 144
EP 146
PG 3
WC Chemistry, Medicinal
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA MR4LS
UT WOS:000553561100035
DA 2025-01-04
ER

PT J
AU Xu, JA
   Tian, L
   Qi, WL
   Lv, QG
   Wang, T
AF Xu, Jianan
   Tian, Lin
   Qi, Wenlong
   Lv, Qingguo
   Wang, Tan
TI Advancements in NSCLC
SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS
LA English
DT Article
DE NSCLC; targeted therapy; molecular mechanisms; targeted drugs
ID CELL LUNG-CANCER; IMMUNE-CHECKPOINT INHIBITORS; PHASE-II BASKET;
   OPEN-LABEL; EGFR-MUTATION; 1ST-LINE TREATMENT; METASTATIC NSCLC; MET
   ALTERATIONS; COLON-CANCER; SINGLE-ARM
AB With the global incidence of non-small cell lung cancer (NSCLC) on the rise, the development of innovative treatment strategies is increasingly vital. This review underscores the pivotal role of precision medicine in transforming NSCLC management, particularly through the integration of genomic and epigenomic insights to enhance treatment outcomes for patients. We focus on the identification of key gene mutations and examine the evolution and impact of targeted therapies. These therapies have shown encouraging results in improving survival rates and quality of life. Despite numerous gene mutations being identified in association with NSCLC, targeted treatments are available for only a select few. This paper offers an exhaustive analysis of the pathogenesis of NSCLC and reviews the latest advancements in targeted therapeutic approaches. It emphasizes the ongoing necessity for research and development in this domain. In addition, we discuss the current challenges faced in the clinical application of these therapies and the potential directions for future research, including the identification of novel targets and the development of new treatment modalities.
C1 [Xu, Jianan] Changchun Univ Chinese Med, Coll Tradit Chinese Med, Changchun, Peoples R China.
   [Tian, Lin; Qi, Wenlong; Lv, Qingguo; Wang, Tan] Changchun Univ Chinese Med, Affiliated Hosp, Pulmonol Dept, Changchun, Peoples R China.
C3 Changchun University of Chinese Medicine; Changchun University of
   Chinese Medicine
RP Wang, T (corresponding author), 1478 Gongnong Rd, Changchun, Peoples R China.
EM 21102570133@stu.ccucm.edu.cn; 27425148@qq.com; qiwenlong871101@163.com;
   99153287@qq.com; wangtan0215@163.com
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NR 111
TC 3
Z9 3
U1 18
U2 18
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0277-3732
EI 1537-453X
J9 AM J CLIN ONCOL-CANC
JI Am. J. Clin. Oncol.-Cancer Clin. Trials
PD JUN
PY 2024
VL 47
IS 6
BP 291
EP 303
DI 10.1097/COC.0000000000001088
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZZ0P5
UT WOS:001278993100001
PM 38375734
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Zhai, ZH
   Yu, XH
   Yang, B
   Zhang, YJ
   Zhang, L
   Li, XL
   Sun, HZ
AF Zhai, Zhenhua
   Yu, Xiaohui
   Yang, Bin
   Zhang, Yunjing
   Zhang, Long
   Li, Xiaoli
   Sun, Hongzhi
TI Colorectal cancer heterogeneity and targeted therapy: Clinical
   implications, challenges and solutions for treatment resistance
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE Colorectal cancer; Heterogeneity; Anti-EGFR therapies; Drug resistance
ID GROWTH-FACTOR RECEPTOR; CETUXIMAB PLUS IRINOTECAN; EGFR
   MONOCLONAL-ANTIBODIES; KRAS P.G13D MUTATION; TUMOR HETEROGENEITY;
   EPIGENETIC ALTERATIONS; GENETIC-HETEROGENEITY; PREDICTIVE BIOMARKER;
   ACQUIRED-RESISTANCE; 1ST-LINE TREATMENT
AB Precision medicine is becoming considerably critical in colorectal cancer therapy. Particularly for targeted therapies, the response to anti-EGFR therapy largely varies among individual patients. The mechanisms of anti-EGFR-based regimens resistance have been revealed, for instance, mutations in KRAS, BRAF, and PIK3CA. It is well known that colorectal cancer is a heterogeneous disease, massive evidences indicate that there are intertumour and intratumour heterogeneities in colorectal cancer. Recently, the integrative factor of the genetic, epigenetic and microenvironmental alterations that attribute to CRC heterogeneity is associated with the response to targeted therapies. We review here the possible mechanisms of heterogeneity that influence the anti-EGFR therapy, and mainly focus on the enhancive biomarkers detection to predict the therapy efficiency and select appropriate patients who are most likely to benefit from special targeted therapies, and take advantage of simultaneously blocked the multiple molecules involved in activation of independent of ligands induced EGFR signaling pathway to overcome the resistance to anti-EGFR therapies. (C) 2016 Published by Elsevier Ltd.
C1 [Zhai, Zhenhua; Yu, Xiaohui; Sun, Hongzhi] Jinzhou Med Univ, Hosp Affiliated 1, Canc Ctr, Dept Oncol, Liaoning, Peoples R China.
   [Zhai, Zhenhua; Yang, Bin; Zhang, Yunjing; Zhang, Long; Li, Xiaoli] Jinzhou Med Univ, Hosp Affiliated 1, Lab Tumour Angiogenesis & Microenvironm, Liaoning, Peoples R China.
C3 Jinzhou Medical University; Jinzhou Medical University
RP Sun, HZ (corresponding author), Jinzhou Med Univ, Hosp Affiliated 1, Canc Ctr, Dept Oncol, 5-2 Renmin St, Jinzhou City, Liaoning Provin, Peoples R China.
EM cmushz@163.com
RI YANG, BIN/ABF-3840-2020; Li, Xiaoli/GYQ-7384-2022; Zhai,
   Zhen/GYA-1598-2022
FU First Hospital Affiliated to Jinzhou Medical University; National
   Natural Science Foundation of China [81472460]
FX We thank Lizhong Zhou for fruitful discussions and critically
   constructive suggestion. Research conducted in the Tumour Angiogenesis
   and Microenvirnment lab is supported by The First Hospital Affiliated to
   Jinzhou Medical University, and also sponsored by the National Natural
   Science Foundation of China (No. 81472460).
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NR 77
TC 73
Z9 77
U1 0
U2 36
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1084-9521
J9 SEMIN CELL DEV BIOL
JI Semin. Cell Dev. Biol.
PD APR
PY 2017
VL 64
BP 107
EP 115
DI 10.1016/j.semcdb.2016.08.033
PG 9
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA ER2GR
UT WOS:000398612700013
PM 27578007
DA 2025-01-04
ER

PT J
AU Singh, M
   Morris, VK
   Bandey, IN
   Hong, DS
   Kopetz, S
AF Singh, Manisha
   Morris, Van Karlyle
   Bandey, Irfan N.
   Hong, David S.
   Kopetz, Scott
TI Advancements in combining targeted therapy and immunotherapy for
   colorectal cancer
SO TRENDS IN CANCER
LA English
DT Review
ID ENDOTHELIAL GROWTH-FACTOR; CAR-T-CELLS; MISMATCH REPAIR-DEFICIENT; RAS
   WILD-TYPE; MICROSATELLITE INSTABILITY; OPEN-LABEL; ANTITUMOR-ACTIVITY;
   DENDRITIC CELLS; PD-1 BLOCKADE; CHEMOTHERAPY
AB Colorectal cancer (CRC) is a prevalent gastrointestinal cancer posing significant clinical challenges. CRC management traditionally involves surgery, often coupled with chemotherapy. However, unresectable or metastatic CRC (mCRC) presents a complex challenge necessitating innovative treatment strategies. Targeted therapies have emerged as the cornerstone of treatment in such cases, with interventions tailored to specific molecular attributes. Concurrently, immunotherapies have revolutionized cancer treatment by harnessing the immune system to combat malignant cells. This review explores the evolving landscape of CRC treatment, focusing on the synergy between immunotherapies and targeted therapies, thereby offering new avenues for enhancing the effectiveness of therapy for CRC.
C1 [Singh, Manisha; Morris, Van Karlyle; Bandey, Irfan N.; Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
   [Hong, David S.] Univ Texas MD Anderson Canc Ctr, Dept Invest Canc Therapeut, Div Canc Med, Houston, TX USA.
C3 University of Texas System; UTMD Anderson Cancer Center; University of
   Texas System; UTMD Anderson Cancer Center
RP Singh, M; Kopetz, S (corresponding author), Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
EM msingh4@mdanderson.org; SKopetz@mdanderson.org
RI Singh, Manisha/HCJ-0070-2022; Hong, David/HKW-1105-2023; bandey,
   irfan/KDN-7764-2024
OI singh, manisha/0000-0003-1983-4921
FU University Cancer Foundation via the Institutional Research Grant
   program at the University of Texas MD Anderson Cancer Center; Hirshberg
   Foundation for Pancreatic Cancer Research; Gastrointestinal Research
   Foundation (GIRF); Cancer Prevention and Research Institute of Texas
   [RP220416]
FX This work was supported by the University Cancer Foundation via the
   Institutional Research Grant program at the University of Texas MD
   Anderson Cancer Center and Hirshberg Foundation for Pancreatic Cancer
   Research (to M.S.), Gastrointestinal Research Foundation (GIRF) (to
   S.K.) and Cancer Prevention and Research Institute of Texas (RP220416)
   (to V.K.M.).
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NR 93
TC 10
Z9 10
U1 11
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 2405-8033
EI 2405-8025
J9 TRENDS CANCER
JI Trends Cancer
PD JUL
PY 2024
VL 10
IS 7
BP 598
EP 609
DI 10.1016/j.trecan.2024.05.001
EA JUL 2024
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C1U6Q
UT WOS:001287284200001
PM 38821852
DA 2025-01-04
ER

PT J
AU Tong, JS
   Tan, S
   Nikolovska-Coleska, Z
   Yu, J
   Zou, FD
   Zhang, L
AF Tong, Jingshan
   Tan, Shuai
   Nikolovska-Coleska, Zaneta
   Yu, Jian
   Zou, Fangdong
   Zhang, Lin
TI <i>FBW7</i>-Dependent Mcl-1 Degradation Mediates the Anticancer Effect
   of Hsp90 Inhibitors
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID E3 UBIQUITIN LIGASE; TUMOR SUPPRESSION; FBW7 MUTATIONS; KAPPA-B; CANCER;
   APOPTOSIS; RESISTANCE; PATHWAY; 17-ALLYLAMINO-17-DEMETHOXYGELDANAMYCIN;
   INACTIVATION
AB Heat shock protein 90 (Hsp90) is widely overexpressed in cancer cells and necessary for maintenance of malignant phenotypes. Hsp90 inhibition induces tumor cell death through degradation of its client oncoproteins and has shown promises in preclinical studies. However, the mechanism by which Hsp90 inhibitors kill tumor cells is not well-understood. Biomarkers associated with differential sensitivity and resistance to Hsp90 inhibitors remain to be identified. In this study, we found that colorectal cancer cells containing inactivating mutations of FBW7, a tumor suppressor and E3 ubiquitin ligase, are intrinsically insensitive to Hsp90 inhibitors. The insensitive colorectal cancer cells lack degradation of Mcl-1, a prosurvival Bcl-2 family protein. Hsp90 inhibition promotes GSK3 beta-dependent phosphorylation of Mcl-1, which subsequently binds to FBW7 and undergoes ubiquitination and proteasomal degradation. Specifically blocking Mcl-1 phosphorylation by genetic knock-in abrogates its degradation and renders in vitro and in vivo resistance to Hsp90 inhibitors, which can be overcame by Mcl-1-selective small-molecule inhibitors. Collectively, our findings demonstrate a key role of GSK3b/FBW7-dependent Mcl-1 degradation in killing of colorectal cancer cells by Hsp90 inhibitors and suggest FBW7 mutational status as a biomarker for Hsp90-targeted therapy. (C) 2017 AACR.
C1 [Tong, Jingshan; Tan, Shuai; Yu, Jian; Zhang, Lin] Univ Pittsburgh, Sch Med, Canc Inst, Pittsburgh, PA USA.
   [Tong, Jingshan; Tan, Shuai; Zhang, Lin] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA USA.
   [Tan, Shuai; Zou, Fangdong] Sichuan Univ, Coll Life Sci, Chengdu 610064, Sichuan, Peoples R China.
   [Nikolovska-Coleska, Zaneta] Univ Michigan, Dept Pathol, Med Sch, Ann Arbor, MI 48109 USA.
   [Yu, Jian] Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
   of Pittsburgh; Pennsylvania Commonwealth System of Higher Education
   (PCSHE); University of Pittsburgh; Sichuan University; University of
   Michigan System; University of Michigan; Pennsylvania Commonwealth
   System of Higher Education (PCSHE); University of Pittsburgh
RP Zou, FD (corresponding author), Sichuan Univ, Coll Life Sci, Chengdu 610064, Sichuan, Peoples R China.; Zhang, L (corresponding author), Hillman Canc Ctr, UPCI Res Pavil,Room 2-42a,5117 Ctr Ave, Pittsburgh, PA 15213 USA.
EM fundzou@scu.edu.cn; zhanglx@upmc.edu
RI Yu, Jian/A-8301-2009; Zhang, Lin/A-7389-2009
OI Tan, Shuai/0000-0003-4268-6429; Zou, Fangdong/0000-0002-2133-4320;
   Zhang, Lin/0000-0003-0018-3903
FU U.S. NIH [R01CA172136, R01CA203028, U01DK085570, U19AI068021,
   R01CA149442, P30CA047904]; National Natural Science Foundation of China
   [81672942]; National Cancer Institute [R01CA217141] Funding Source: NIH
   RePORTER
FX This study was supported by U.S. NIH grants R01CA172136, R01CA203028 to
   L. Zhang; U01DK085570, U19AI068021 to J. Yu; R01CA149442 to Z.
   Nikolovska-Coleska; P30CA047904 to University of Pittsburgh Cancer
   Institute; and National Natural Science Foundation of China grant
   81672942 to F. Zou.
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NR 48
TC 57
Z9 58
U1 2
U2 18
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
EI 1538-8514
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD SEP 1
PY 2017
VL 16
IS 9
BP 1979
EP 1988
DI 10.1158/1535-7163.MCT-17-0032
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FG1IZ
UT WOS:000409550300022
PM 28619760
OA Green Accepted, Bronze, Green Submitted
DA 2025-01-04
ER

PT J
AU Chen, W
   Frankel, WL
AF Chen, Wei
   Frankel, Wendy L.
TI A practical guide to biomarkers for the evaluation of colorectal cancer
SO MODERN PATHOLOGY
LA English
DT Article
ID MISMATCH REPAIR DEFICIENCY; SYNDROME-ASSOCIATED NEOPLASMS;
   MICROSATELLITE-INSTABILITY; LYNCH-SYNDROME; BRAF MUTATION; NEOADJUVANT
   THERAPY; INSTITUTE WORKSHOP; MLH1 METHYLATION; STAGE-II; DNA
AB Evaluation of microsatellite instability (MSI) of every colorectal cancer (CRC) is important for prognostic and therapeutic purposes, while molecular testing helps identify actionable targeted therapy for patients with metastatic disease. This review will discuss the biomarkers commonly encountered in the clinical evaluation of CRC, and practical issues regarding MSI screening, reporting, interpretation, molecular test indication, and specimen requirements.
C1 [Chen, Wei; Frankel, Wendy L.] Ohio State Univ, Dept Pathol, Wexner Med Ctr, Columbus, OH 43210 USA.
C3 University System of Ohio; Ohio State University
RP Frankel, WL (corresponding author), Ohio State Univ, Dept Pathol, Wexner Med Ctr, Columbus, OH 43210 USA.
EM Wendy.Frankel@osumc.edu
OI Frankel, Wendy/0000-0003-1658-1009
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NR 100
TC 50
Z9 51
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0893-3952
EI 1530-0285
J9 MODERN PATHOL
JI Mod. Pathol.
PD JAN 2
PY 2019
VL 32
SU S
DI 10.1038/s41379-018-0136-1
PG 15
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA IO1RO
UT WOS:000479159800001
PM 30600322
OA Bronze
DA 2025-01-04
ER

PT J
AU Ahn, DH
   Goldberg, RM
AF Ahn, Daniel H.
   Goldberg, Richard M.
TI Colorectal clinical trials: what is on the horizon?
SO FUTURE ONCOLOGY
LA English
DT Article
DE colorectal cancer; immunotherapy; next-generation sequencing; targeted
   therapy
ID WILD-TYPE KRAS; MICROSATELLITE INSTABILITY; BRAF MUTATION; OPEN-LABEL;
   ACQUIRED-RESISTANCE; GENE AMPLIFICATION; CANCER STATISTICS; PLUS
   IRINOTECAN; RAS MUTATIONS; SOLID TUMORS
AB Substantial progress has been made in the treatment of colorectal cancer, where more effective therapies have led to improved outcomes in patients with advanced disease. However, the 5-year overall survival rate remains poor. Genomic sequencing has allowed us to understand that colorectal cancer is a heterogeneous disease, where tumor-specific variants affect the prognosis and outcomes in patients. This has shaped the future directions of treatment and the development of clinical trials, including the incorporation of novel targeted therapies and investigations into the role of immunotherapy in colorectal cancer.
C1 [Ahn, Daniel H.; Goldberg, Richard M.] Ohio State Univ, Ctr Comprehens Canc, Dept Internal Med, Div Med Oncol, 460 W 10th Ave, Columbus, OH 43210 USA.
C3 University System of Ohio; Ohio State University; James Cancer Hospital
   & Solove Research Institute
RP Goldberg, RM (corresponding author), Ohio State Univ, Ctr Comprehens Canc, Dept Internal Med, Div Med Oncol, 460 W 10th Ave, Columbus, OH 43210 USA.
EM richard.goldberg@osumc.edu
RI Goldberg, Richard/O-1871-2017
FU Merck
FX RM Goldberg has research support to The Ohio State University to conduct
   clinical trials and serves as a paid consultant to Merck for the
   development of pembrolizumab in gastrointestinal cancers. 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 64
TC 1
Z9 1
U1 0
U2 4
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PY 2016
VL 12
IS 4
BP 525
EP 531
DI 10.2217/fon.15.327
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DC9FE
UT WOS:000369525700012
PM 26777152
OA Green Accepted, Green Published
DA 2025-01-04
ER

PT J
AU Deyati, A
   Bagewadi, S
   Senger, P
   Hofmann-Apitius, M
   Novac, N
AF Deyati, Avisek
   Bagewadi, Shweta
   Senger, Philipp
   Hofmann-Apitius, Martin
   Novac, Natalia
TI Systems approach for the selection of micro-RNAs as therapeutic
   biomarkers of anti-EGFR monoclonal antibody treatment in colorectal
   cancer
SO SCIENTIFIC REPORTS
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; ACQUIRED-RESISTANCE; TISSUE-SPECIFICITY;
   CETUXIMAB; EXPRESSION; CELLS; TARGET; NETWORK; DEREGULATION; MICRORNA-21
AB miRNA plays an important role in tumourgenesis by regulating expression of oncogenes and tumour suppressors. Thus affects cell proliferation and differentiation, apoptosis, invasion and angiogenesis. miRNAs are potential biomarkers for diagnosis, prognosis and therapies of different forms of cancer. However, relationship between response of cancer patients towards targeted therapy and the resulting modifications of the miRNA transcriptome in the context of pathway regulation is poorly understood. With ever-increasing pathways and miRNA-mRNA interaction databases, freely available mRNA and miRNA expression data in multiple cancer therapy have produced an unprecedented opportunity to decipher the role of miRNAs in early prediction of therapeutic efficacy in diseases. Efficient translation of -omics data and accumulated knowledge to clinical decision-making are of paramount scientific and public health interest. Well-structured translational algorithms are needed to bridge the gap from databases to decisions. Herein, we present a novel SMARTmiR algorithm to prospectively predict the role of miRNA as therapeutic biomarker for an anti-EGFR monoclonal antibody i.e. cetuximab treatment in colorectal cancer.
C1 [Deyati, Avisek; Bagewadi, Shweta; Senger, Philipp; Hofmann-Apitius, Martin] Fraunhofer Inst SCAI, D-53754 St Augustin, Germany.
   [Deyati, Avisek; Bagewadi, Shweta; Senger, Philipp; Hofmann-Apitius, Martin] Bonn Aachen Int Ctr Informat Technol B IT, Dept Appl Life Sci Informat, D-53113 Bonn, Germany.
   [Novac, Natalia] Merck Serono, D-64293 Darmstadt, Germany.
C3 Fraunhofer Gesellschaft; Merck KGaA; EMD Serono Inc.
RP Novac, N (corresponding author), Merck Serono, Frankfurter Str 250, D-64293 Darmstadt, Germany.
EM natalia.novac@merckgroup.com
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NR 58
TC 6
Z9 7
U1 0
U2 9
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD JAN 27
PY 2015
VL 5
AR 8013
DI 10.1038/srep08013
PG 9
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA AZ6SJ
UT WOS:000348349600001
PM 25622824
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Buettner, J
   Joehrens, K
   Klauschen, F
   Hummel, M
   Lenze, D
   Saeger, W
   Lehmann, A
AF Buettner, Juliane
   Joehrens, Korinna
   Klauschen, Frederick
   Hummel, Michael
   Lenze, Dido
   Saeger, Wolfgang
   Lehmann, Annika
TI Intratumoral morphological heterogeneity can be an indicator of genetic
   heterogeneity in colorectal cancer
SO EXPERIMENTAL AND MOLECULAR PATHOLOGY
LA English
DT Article
DE Colorectal cancer; KRAS; Heterogeneity; Morphology; Sequencing
ID INTRA-TUMORAL HETEROGENEITY; ANTI-EGFR THERAPY; SIGNET-RING CELL;
   ACQUIRED-RESISTANCE; MOLECULAR-FEATURES; KRAS MUTATIONS; TARGETED
   THERAPIES; PIK3CA MUTATIONS; DRUG-RESISTANCE; EVOLUTION
AB Anti-EGFR-targeted therapy is used to treat metastatic colorectal cancers with RAS wild-type. However, resistance to targeted therapy is often observed and can be primary or acquired. One reason for primary resistance is the presence of mutations that are undetected due to genetic heterogeneity, which can be expressed by differences present in primary tumor and distant metastasis or recurrence or by an intratumoral heterogeneity (presence of different subclones in the investigated tumor sample).
   The aim of our study was to investigate if morphological heterogeneity can be an indicator of intratumoral heterogeneity. We analysed 13 samples with homogeneous and six samples with heterogeneous morphology with NGS. We were able to demonstrate that intratumoral genetic heterogeneity is present in all studied tumor samples, independent of homogeneous or heterogeneous morphology. Moreover, one sample of our cohort with morphological and genetic heterogeneity had a genetic wild-type profile in one tumor component. Therefore, we recommend to include each morphologically identifiable tumor component in the mutational analysis to not overlook resistance-inducing or potentially targetable mutations.
C1 [Buettner, Juliane; Joehrens, Korinna; Klauschen, Frederick; Hummel, Michael; Lenze, Dido; Lehmann, Annika] Charite Univ Med Berlin, Inst Pathol, Charitepl 1, D-10117 Berlin, Germany.
   [Buettner, Juliane] Provitro AG, Berlin, Germany.
   [Saeger, Wolfgang] Univ Med Ctr Hamburg Eppendorf, Inst Neuropathol, Hamburg, Germany.
C3 Berlin Institute of Health; Free University of Berlin; Humboldt
   University of Berlin; Charite Universitatsmedizin Berlin; University of
   Hamburg; University Medical Center Hamburg-Eppendorf
RP Buettner, J (corresponding author), Charite Univ Med Berlin, Inst Pathol, Charitepl 1, D-10117 Berlin, Germany.
EM juliane.buettner-patho@charite.de
RI ; Klauschen, Frederick/C-5637-2015
OI Lehmann, Annika/0000-0001-9424-5882; Hummel,
   Michael/0000-0001-6717-605X; Klauschen, Frederick/0000-0002-9131-2389
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NR 57
TC 7
Z9 10
U1 0
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4800
EI 1096-0945
J9 EXP MOL PATHOL
JI Exp. Mol. Pathol.
PD FEB
PY 2018
VL 104
IS 1
BP 76
EP 81
DI 10.1016/j.yexmp.2018.01.007
PG 6
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA FV8SS
UT WOS:000424857700012
PM 29337243
DA 2025-01-04
ER

PT J
AU Guarini, C
   Grassi, T
   Pezzicoli, G
   Porta, C
AF Guarini, Chiara
   Grassi, Teresa
   Pezzicoli, Gaetano
   Porta, Camillo
TI Beyond RAS and BRAF: HER2, a New Actionable Oncotarget in Advanced
   Colorectal Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colorectal cancer; HER2; targeted therapy
ID EGFR MONOCLONAL-ANTIBODIES; HUMAN-BREAST-CANCER; FACTOR RECEPTOR 2;
   OPEN-LABEL; COLON-CANCER; AMERICAN-PATHOLOGISTS; 1ST-LINE TREATMENT;
   PROGNOSTIC-FACTOR; ELDERLY-PATIENTS; TUMOR LOCATION
AB The human epidermal growth factor receptor 2 (HER2) is a well-established oncogenic driver and a successful therapeutic target in several malignancies, such as breast and gastric cancers. HER2 alterations, including amplification and somatic mutations, have also been detected in a small but not negligible subset of patients affected by advanced colorectal cancer (aCRC). However, to date, there are no available oncotargets in this malignancy beyond RAS and BRAF that are available. Here we present an overview on the present predictive and prognostic role of HER2 expression in aCRC, as well as on its consequent potential therapeutic implications from preclinical investigations towards ongoing trials testing anti-HER2 agents in aCRC. While HER2 ' s role as a molecular predictive biomarker for anti-EGFR therapies in CRC is recognized, HER2 prognostic value remains controversial. Moreover, thanks to the impressive and growing body of clinical evidence, HER2 is strongly emerging as a new potential actionable oncotarget in aCRC. In conclusion, in the foreseeable future, HER2-targeted therapeutic strategies may integrate the algorithm of aCRC treatment towards an increasingly tailored therapeutic approach to this disease.
C1 [Guarini, Chiara; Pezzicoli, Gaetano] Univ Bari Aldo Moro, Postgrad Sch Specializat Med Oncol, I-70124 Bari, Italy.
   [Guarini, Chiara; Grassi, Teresa; Pezzicoli, Gaetano; Porta, Camillo] AOU Consorziale Policlin Bari, Div Med Oncol, I-70124 Bari, Italy.
   [Porta, Camillo] Univ Bari A Moro, Dept Biomed Sci & Human Oncol, Chair Oncol, I-70124 Bari, Italy.
C3 Universita degli Studi di Bari Aldo Moro; Universita degli Studi di Bari
   Aldo Moro
RP Guarini, C (corresponding author), Univ Bari Aldo Moro, Postgrad Sch Specializat Med Oncol, I-70124 Bari, Italy.; Guarini, C (corresponding author), AOU Consorziale Policlin Bari, Div Med Oncol, I-70124 Bari, Italy.
EM chiara.guarini@outlook.it; teresa.grassi@libero.it;
   pezzicoligaet@gmail.com; camillo.porta@gmail.com
RI Porta, Camillo/AAB-9482-2020; Pezzicoli, Gaetano/GZL-2623-2022
OI Pezzicoli, Gaetano/0000-0002-5491-0590; Porta,
   Camillo/0000-0003-2412-1563; Guarini, Chiara/0000-0003-2225-6093
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NR 144
TC 24
Z9 24
U1 3
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUL
PY 2021
VL 22
IS 13
AR 6813
DI 10.3390/ijms22136813
PG 22
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA TH3TO
UT WOS:000672016100001
PM 34202896
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Temraz, S
   Alameddine, R
   Shamseddine, A
AF Temraz, Sally
   Alameddine, Raafat
   Shamseddine, Ali
TI B-type proto-oncogene-mutated tumors of colon cancer: promising
   therapeutic approaches
SO CURRENT OPINION IN ONCOLOGY
LA English
DT Review
DE B-type proto-oncogene inhibitor; colorectal cancer; combined therapy
ID METASTATIC COLORECTAL-CANCER; BRAF MUTATION; PRECLINICAL MODELS; KRAS
   MUTATION; INHIBITION; VEMURAFENIB; EGFR; COMBINATION; RESISTANCE;
   CETUXIMAB
AB Purpose of review
   B-type proto-oncogene (BRAF) mutations have been observed in about 10.8% of patients with colorectal cancer (CRC). These patients do not respond to standard therapy with anti-epidermal growth factor receptor kinase (EGFR). Here we review novel BRAF inhibitors that are currently being investigated in these tumors.
   Recent findings
   Clinical experience with the BRAF inhibitor vemurafenib in CRC suggests significant differences in response compared with melanoma. Based on preclinical data, resistance to BRAF inhibitors employs alternative signaling pathways that in turn induce cell proliferation and survival. Therapeutic strategies that combine BRAF inhibitors in addition to targeted therapy with anti-EGFR monoclonal antibodies and phosphoinositide 3-kinase pathway inhibitors or standard therapy have yielded promising results in preclinical models and some reported cases.
   Summary
   Results from current clinical trials that are exploring novel BRAF inhibitors and others that employ combined therapy are eagerly awaited for the treatment of BRAF-mutated CRC.
C1 [Temraz, Sally; Alameddine, Raafat; Shamseddine, Ali] Amer Univ, Beirut Med Ctr, Dept Internal Med, Div Med Oncol, Beirut, Lebanon.
C3 American University of Beirut; Beirut Medical Center
EM as04@aub.edu.lb
OI Temraz, Sally/0000-0002-8995-7946
FU Merck; Roche; Aventis; GSK
FX S.T. received institutional grant from Merck. A.S. reports to have board
   membership at Roche, Eli Lily, and Aventis and has received
   institutional grant from Roche, Aventis, and GSK. R.A. has no conflicts
   of interest.
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NR 38
TC 1
Z9 1
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1040-8746
EI 1531-703X
J9 CURR OPIN ONCOL
JI Curr. Opin. Oncol.
PD MAY
PY 2015
VL 27
IS 3
BP 276
EP 281
DI 10.1097/CCO.0000000000000184
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CF6ES
UT WOS:000352650300017
PM 25774859
DA 2025-01-04
ER

PT J
AU Zhao, J
   Zhang, YS
   Zhao, GH
AF Zhao, Jun
   Zhang, Yisheng
   Zhao, Guohai
TI Emerging role of microRNA-21 in colorectal cancer
SO CANCER BIOMARKERS
LA English
DT Review
DE microRNA-21; colorectal cancer; biomarker
ID II COLON-CANCER; MIR-21 EXPRESSION; PDCD4 EXPRESSION; DIAGNOSTIC
   BIOMARKERS; PROGNOSTIC VALUE; SERUM MIR-21; TUMOR-GROWTH; CELLS; STAGE;
   INHIBITION
AB Colorectal cancer (CRC) is one of the most common types of cancers worldwide. In spite of much progress in surgery, chemotherapy and molecular targeted therapy, the mortality rate has only decreased slightly over the past years. MicroRNAs are 18-25 nucleotide, noncoding RNA molecules that regulate the translation of many genes. Evidence suggests that miRNAs may play an important role in a variety of cellular biological processes, such as cell growth, differentiation, metabolism, invasion, angiogenesis. Recently, miR-21 is found to be aberrantly expressed in CRC and miR-21 has been recognized to perform significantly in CRC, where miR-21 can regulate several different target genes and pathways involving tumor proliferation, invasion and metastasis. In this study, we will focus on the critical role of miR-21 in CRC. Hopefully, the information obtained may lead to a better understanding of the pathogenesis and development of novel therapeutic strategies for this disease.
C1 [Zhao, Jun; Zhang, Yisheng; Zhao, Guohai] Wannan Med Coll, Dept Gastrointestinal Surg, Yijishan Hosp, Wuhu 241001, Anhui, Peoples R China.
C3 Wannan Medical College
RP Zhao, GH (corresponding author), Wannan Med Coll, Dept Gastrointestinal Surg, Yijishan Hosp, West Zheshan Rd, Wuhu 241001, Anhui, Peoples R China.
EM zhaoguohai@vip.tom.com
RI zhang, yisheng/HDO-5690-2022
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NR 59
TC 23
Z9 24
U1 1
U2 16
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 2015
VL 15
IS 3
BP 219
EP 226
DI 10.3233/CBM-150468
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CK1GD
UT WOS:000355954400002
PM 25769454
DA 2025-01-04
ER

PT J
AU Angerilli, V
   Galuppini, F
   Businello, G
   Dal Santo, L
   Savarino, E
   Realdon, S
   Guzzardo, V
   Nicolè, L
   Lazzarin, V
   Lonardi, S
   Loupakis, F
   Fassan, M
AF Angerilli, Valentina
   Galuppini, Francesca
   Businello, Gianluca
   Dal Santo, Luca
   Savarino, Edoardo
   Realdon, Stefano
   Guzzardo, Vincenza
   Nicole, Lorenzo
   Lazzarin, Vanni
   Lonardi, Sara
   Loupakis, Fotios
   Fassan, Matteo
TI MicroRNAs as Predictive Biomarkers of Resistance to Targeted Therapies
   in Gastrointestinal Tumors
SO BIOMEDICINES
LA English
DT Review
DE microRNAs; GI cancers; targeted therapy; drug resistance
ID METASTATIC COLORECTAL-CANCER; ANTI-EGFR THERAPY;
   HEPATOCELLULAR-CARCINOMA CELLS; GROWTH-FACTOR RECEPTOR; GASTRIC-CANCER;
   DRUG-RESISTANCE; SORAFENIB RESISTANCE; TRASTUZUMAB RESISTANCE; CETUXIMAB
   RESISTANCE; IMATINIB RESISTANCE
AB The advent of precision therapies against specific gene alterations characterizing different neoplasms is revolutionizing the oncology field, opening novel treatment scenarios. However, the onset of resistance mechanisms put in place by the tumor is increasingly emerging, making the use of these drugs ineffective over time. Therefore, the search for indicators that can monitor the development of resistance mechanisms and above all ways to overcome it, is increasingly important. In this scenario, microRNAs are ideal candidate biomarkers, being crucial post-transcriptional regulators of gene expression with a well-known role in mediating mechanisms of drug resistance. Moreover, as microRNAs are stable molecules, easily detectable in tissues and biofluids, they are the ideal candidate biomarker to identify patients with primary resistance to a specific targeted therapy and those who have developed acquired resistance. The aim of this review is to summarize the major studies that have investigated the role of microRNAs as mediators of resistance to targeted therapies currently in use in gastro-intestinal neoplasms, namely anti-EGFR, anti-HER2 and anti-VEGF antibodies, small-molecule tyrosine kinase inhibitors and immune checkpoint inhibitors. For every microRNA and microRNA signature analyzed, the putative mechanisms underlying drug resistance were outlined and the potential to be translated in clinical practice was evaluated.
C1 [Angerilli, Valentina; Galuppini, Francesca; Businello, Gianluca; Dal Santo, Luca; Guzzardo, Vincenza; Nicole, Lorenzo; Lazzarin, Vanni; Fassan, Matteo] Univ Padua, Dept Med DIMED, Surg Pathol & Cytopathol Unit, I-35100 Padua, Italy.
   [Savarino, Edoardo] Univ Padua, Dept Surg Oncol & Gastroenterol Sci, Div Gastroenterol, I-35100 Padua, Italy.
   [Realdon, Stefano; Lonardi, Sara; Loupakis, Fotios; Fassan, Matteo] IRCCS, Ist Oncol Veneto IOV, I-35100 Padua, Italy.
C3 University of Padua; University of Padua; IRCCS Istituto Oncologico
   Veneto (IOV)
RP Fassan, M (corresponding author), Univ Padua, Dept Med DIMED, Surg Pathol & Cytopathol Unit, I-35100 Padua, Italy.; Fassan, M (corresponding author), IRCCS, Ist Oncol Veneto IOV, I-35100 Padua, Italy.
EM valentina.angerilli@gmail.com; francesca.galuppini@unipd.it;
   glc.businello@gmail.com; lucas1186dalsanto@gmail.com;
   edoardo.savarino@unipd.it; stefano.realdon@iov.veneto.it;
   vincenza.guzzardo@unipd.it; lorenzo.nic86@gmail.com;
   vanni.lazzarin@unipd.it; sara.lonardi@iov.veneto.it;
   fotios.loupakis@iov.veneto.it; matteo.fassan@unipd.it
RI Lonardi, Sara/F-4228-2014; Savarino, Edoardo/AAC-7510-2022; Dal Santo,
   Luca/JDW-4005-2023; Loupakis, Fotios/I-7243-2012; Realdon,
   Stefano/K-8664-2016; Galuppini, Francesca/AAC-2047-2019; Nicole,
   Lorenzo/AAB-2202-2022; Fassan, Matteo/F-5152-2012
OI Businello, Gianluca/0000-0002-0045-9140; Savarino,
   Edoardo/0000-0002-3187-2894; Nicole, Lorenzo/0000-0001-8126-9674;
   Galuppini, Francesca/0000-0002-3245-2322; Fassan,
   Matteo/0000-0001-6515-5482
FU Italian Health Ministry [NET-2016-02363853]
FX This research was partially funded by a grant from the Italian Health
   Ministry's research program NET-2016-02363853. The funding agency had no
   role in the design and performance of the study.
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NR 124
TC 8
Z9 8
U1 1
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD MAR
PY 2021
VL 9
IS 3
AR 318
DI 10.3390/biomedicines9030318
PG 19
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 RD3YN
UT WOS:000633417900001
PM 33801049
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hironaka-Mitsuhashi, A
   Sanchez Calle, A
   Ochiya, T
   Takayama, S
   Suto, A
AF Hironaka-Mitsuhashi, Ai
   Sanchez Calle, Anna
   Ochiya, Takahiro
   Takayama, Shin
   Suto, Akihiko
TI Towards Circulating-Tumor DNA-Based Precision Medicine
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE biomarker; breast cancer; circulating-tumor DNA; colorectal cancer; lung
   cancer; precision medicine; targeted therapy
ID CELL-FREE DNA; METASTATIC BREAST-CANCER; TYROSINE KINASE INHIBITORS;
   EGFR MUTATION STATUS; LUNG-CANCER; ESR1 MUTATIONS; ACQUIRED-RESISTANCE;
   ENDOCRINE THERAPY; TARGETED THERAPY; LIQUID BIOPSIES
AB In the era of precision medicine, targeted therapies have been implemented for various diseases. Genomic information guides decision-making in cancer treatment. The improvements in next-generation sequencing and polymerase chain reaction have made it possible to access the genetic information using circulating-tumor DNAs (ctDNAs). Molecular characteristics of individual tumors can be obtained by analysis of ctDNAs, thus making them excellent tools to guide decision-making during treatment. In oncology, the use of ctDNAs in clinical practice is now gaining importance. Molecular analysis of ctDNAs has potential for multiple clinical applications, including early diagnosis, prognosis of disease, prognostic and/or predictive biomarkers, and monitoring response to therapy and clonal evolution. In this paper, we highlight the applications of ctDNAs in cancer management, especially in metastatic setting, and summarize recent studies about the use of ctDNAs as predictive biomarkers for the therapeutic adaptation/response in lung cancer, breast cancer, and colorectal cancer. These studies offer the evidence to use ctDNAs as a promising approach to solve unmet clinical needs.
C1 [Hironaka-Mitsuhashi, Ai; Sanchez Calle, Anna; Ochiya, Takahiro] Natl Canc Ctr, Div Mol & Cellular Med, Chuo Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
   [Ochiya, Takahiro] Tokyo Med Univ, Inst Med Sci, Dept Mol & Cellular Med, Shinjuku Ku, 6-7-1 Nishishinjuku, Tokyo 1600023, Japan.
   [Takayama, Shin; Suto, Akihiko] Natl Canc Ctr, Dept Breast Surg, Chuo Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
C3 National Cancer Center - Japan; Tokyo Medical University; National
   Cancer Center - Japan
RP Hironaka-Mitsuhashi, A (corresponding author), Natl Canc Ctr, Div Mol & Cellular Med, Chuo Ku, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
EM ahironak@ncc.go.jp
RI Takayama, Shin/ABE-1802-2020; Ochiya, Takahiro/AAH-7585-2019
OI Suto, Akihiko/0000-0003-1458-2593
FU Project for Cancer Research and Therapeutic Evolution (P-CREATE)
   [19cm0106402h0004]
FX Project for Cancer Research and Therapeutic Evolution (P-CREATE; grant
   number: 19cm0106402h0004).
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NR 126
TC 9
Z9 9
U1 0
U2 6
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 SEP
PY 2019
VL 8
IS 9
AR 1365
DI 10.3390/jcm8091365
PG 14
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA JC3NA
UT WOS:000489184200099
PM 31480647
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Chen, Q
   Shen, MY
   Yan, M
   Han, XJ
   Mu, S
   Li, Y
   Li, L
   Wang, YM
   Li, SL
   Li, TT
   Wang, YY
   Wang, W
   Wei, ZQ
   Hu, C
   Jin, AS
AF Chen, Qian
   Shen, Meiying
   Yan, Min
   Han, Xiaojian
   Mu, Song
   Li, Ya
   Li, Luo
   Wang, Yingming
   Li, Shenglong
   Li, Tingting
   Wang, Yingying
   Wang, Wang
   Wei, Zhengqiang
   Hu, Chao
   Jin, Aishun
TI Targeting tumor-infiltrating CCR8<SUP>+</SUP> regulatory T cells induces
   antitumor immunity through functional restoration of CD4<SUP>+</SUP>
   T<sub>convs</sub> and CD8<SUP>+</SUP> T cells in colorectal cancer
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Colorectal cancer (CRC); Regulatory T cell (Treg); Chemokine (C-C motif)
   receptor 8 (CCR8)
ID REPAIR-DEFICIENT; GLUTAMIC-ACID; IMMUNOTHERAPY; COPPER(II); EXPRESSION;
   LANDSCAPE; NIVOLUMAB; LIGAND; FOXP3
AB Background Chemokine (C-C motif) receptor 8 (CCR8) is a chemokine receptor selectively expressed on tumor-infiltrating regulatory T cells (Tregs). Strong immunosuppression mediated byCCR8(+) Tregs observed in breast and lung malignancies suggest for their functional significance in cancer therapy. To date, detailed characterization of tumor-infiltrating CCR8(+) Tregs cells in colorectal cancer (CRC) is limited. Methods To study the presence and functional involvement of CCR8(+) Tregs in CRC, we analyzed the proportions of CCR8-expressing T cells in different T cell subsets in tumor and adjacent normal tissues and peripheral blood mononuclear cells (PBMCs) from CRC patients by Flow cytometry. Also, we compared the distribution of CCR8(+) T cells in malignant tissues and peripheral lymphoid organs from a subcutaneous CRC murine model. Bioinformatic analysis was performed to address the significance of CCR8 expression levels in CRC prognosis, immune regulatory gene expression profiles and potential molecular mechanisms associated with CCR8(+) Tregs in CRC tumors. Further, we administrated an anti-CCR8 monoclonal antibody to CT26 tumor-bearing mice and examined the antitumor activity of CCR8-targeted therapy both in vivo and in an ex vivo confirmative model. Results Here, we showed that Tregs was predominantly presented in the tumors of CRC patients (13.4 +/- 5.8, p < 0.0001) and the CRC subcutaneous murine model (35.0 +/- 2.6, p < 0.0001). CCR8 was found to be preferentially expressed on these tumor-infiltrating Tregs (CRC patients: 63.6 +/- 16.0, p < 0.0001; CRC murine model: 65.3 +/- 9.5, p < 0.0001), which correlated with poor survival. We found that majority of the CCR8(+) Tregs expressed activation markers and exhibited strong suppressive functions. Treatment with anti-CCR8 antibody hampered the growth of subcutaneous CRC tumor through effectively restoring the anti-tumor immunity of CD4+ conventional T cells (CD4(+) T-convs) and CD8(+) T cells, which was confirmed in the ex vivo examinations. Conclusions Collectively, these findings illustrate the importance of CCR8(+) Tregs for an immunosuppressive microenvironment in CRC tumors by functional inhibition of CD4(+) T-convs and CD8(+) T cells, and suggest for the applicable value of CCR8-targeted therapy for CRC.
C1 [Chen, Qian; Yan, Min; Han, Xiaojian; Wang, Yingming; Li, Tingting; Wang, Yingying; Wang, Wang; Hu, Chao; Jin, Aishun] Chongqing Med Univ, Sch Basic Med Sci, Dept Immunol, Chongqing 400010, Peoples R China.
   [Chen, Qian; Shen, Meiying; Yan, Min; Han, Xiaojian; Li, Luo; Wang, Yingming; Li, Tingting; Wang, Yingying; Wang, Wang; Hu, Chao; Jin, Aishun] Chongqing Med Univ, Chongqing Key Lab Tumor Immune Regulat & Immune In, Chongqing 400010, Peoples R China.
   [Chen, Qian] Chongqing Med Univ, Affiliated Hosp 1, Dept Obstet, Chongqing 400016, Peoples R China.
   [Shen, Meiying] Chongqing Med Univ, Affiliated Hosp 1, Dept Breast & Thyroid Surg, Chongqing 400016, Peoples R China.
   [Mu, Song] Guizhou Med Univ, Dept Colorectal Surg, Affiliated Hosp, Guiyang 550004, Guizhou, Peoples R China.
   [Li, Ya; Wei, Zhengqiang] Chongqing Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Chongqing 400016, Peoples R China.
   [Li, Luo] Chongqing Med Univ, Women & Childrens Hosp, Dept Clin Lab, Chongqing 400010, Peoples R China.
   [Li, Shenglong] Chongqing Med Univ, Sch Basic Med Sci, Chongqing 400010, Peoples R China.
C3 Chongqing Medical University; Chongqing Medical University; Chongqing
   Medical University; Chongqing Medical University; Guizhou Medical
   University; Chongqing Medical University; Chongqing Medical University;
   Chongqing Medical University
RP Hu, C; Jin, AS (corresponding author), Chongqing Med Univ, Sch Basic Med Sci, Dept Immunol, Chongqing 400010, Peoples R China.; Hu, C; Jin, AS (corresponding author), Chongqing Med Univ, Chongqing Key Lab Tumor Immune Regulat & Immune In, Chongqing 400010, Peoples R China.
EM huchao1510602@cqmu.edu.cn; aishunjin@cqmu.edu.cn
RI shen, meiying/IXW-8000-2023; Wang, Xinghuan/U-5388-2017; Hu,
   Chao/O-8030-2015
FU Postdoctoral Research Foundation of China
FX No Statement Available
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NR 44
TC 3
Z9 3
U1 5
U2 5
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 JUL 30
PY 2024
VL 22
IS 1
AR 709
DI 10.1186/s12967-024-05518-8
PG 13
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA A2S6U
UT WOS:001281084100007
PM 39080766
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Svec, J
   Onhajzer, J
   Korinek, V
AF Svec, Jiri
   Onhajzer, Jakub
   Korinek, Vladimir
TI Origin, development and therapy of colorectal cancer from the
   perspective of a biologist and an oncologist
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE chemotherapy; colorectal cancer; immunotherapy; intestinal epithelium;
   regeneration; signaling pathways; targeted therapy
ID POSITIVE SOLID TUMORS; ANTIBODY-DRUG CONJUGATE; III RANDOMIZED-TRIAL;
   STEM-CELLS; OPEN-LABEL; MICROSATELLITE INSTABILITY; 1ST-LINE TREATMENT;
   TRASTUZUMAB DERUXTECAN; SUBGROUP ANALYSES; PLUS CETUXIMAB
AB The intestinal epithelium, a rapidly renewing tissue, is characterized by a continuous cell turnover that occurs through a well-coordinated process of cell proliferation and differentiation. This dynamic is crucial for the longterm function of the gastrointestinal tract. Disruption of this process can lead to colorectal carcinoma, a common malignancy worldwide. The first part of the review focuses on the cellular composition of the epithelium and the molecular mechanisms that control its functions, and describes the pathways that lead to epithelial transformation and tumor progression. This forms the basis for understanding the development and progression of advanced colorectal cancer. The second part deals with current therapeutic approaches and presents the latest treatment options, ongoing clinical trials and new drugs. In addition, the biological and medical perspectives of the adverse effects of therapies and models of regeneration of the intestinal epithelium are highlighted and, finally, future treatment options are discussed.
C1 [Svec, Jiri; Onhajzer, Jakub; Korinek, Vladimir] Czech Acad Sci, Inst Mol Genet, Lab Cell & Dev Biol, Videnska 1083, Prague 14220, Czech Republic.
   [Svec, Jiri] Charles Univ Prague, Univ Hosp Kralovske Vinohrady, Fac Med 3, Dept Oncol, Prague, Czech Republic.
C3 Czech Academy of Sciences; Institute of Molecular Genetics of the Czech
   Academy of Sciences; University Hospital Vinohrady; Charles University
   Prague
RP Korinek, V (corresponding author), Czech Acad Sci, Inst Mol Genet, Lab Cell & Dev Biol, Videnska 1083, Prague 14220, Czech Republic.
EM vladimir.korinek@img.cas.cz
RI Svec, Jiri/G-6355-2014
OI Onhajzer, Jakub/0000-0001-6569-6836
FU Czech Science Foundation [20-31322S]; National Institute for Cancer
   Research - European Union-Next Generation EU [LX22NPO5102]
FX This research was funded by the Czech Science Foundation, grant no.
   20-31322S, and by project National Institute for Cancer Research
   (Program EXCELES, ID Project No. LX22NPO5102, Funded by the European
   Union-Next Generation EU) .
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NR 117
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD DEC
PY 2024
VL 204
AR 104544
DI 10.1016/j.critrevonc.2024.104544
EA OCT 2024
PG 14
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA L2O9I
UT WOS:001349176700001
PM 39490796
OA hybrid
DA 2025-01-04
ER

PT J
AU Hou, CY
   Yang, YM
   Wang, PW
   Xie, HM
   Jin, SL
   Zhao, LB
   Wu, GH
   Xing, H
   Chen, H
   Liu, BY
   Du, CY
   Sun, X
   He, LY
AF Hou, Chenying
   Yang, Yanmei
   Wang, Peiwen
   Xie, Huimin
   Jin, Shuiling
   Zhao, Liangbo
   Wu, Guanghua
   Xing, Hao
   Chen, Hong
   Liu, Benyu
   Du, Chunyan
   Sun, Xiao
   He, Luyun
TI CCDC113 promotes colorectal cancer tumorigenesis and metastasis via
   TGF-β signaling pathway
SO CELL DEATH & DISEASE
LA English
DT Article
ID COILED-COILS; CELLS; PROLIFERATION
AB Colorectal cancer (CRC) is the second leading cause of cancer-related mortality worldwide. Although CRC patients' survival is improved with surgical resection and immunotherapy, metastasis and recurrence remain major problems leading to poor prognosis. Therefore, exploring pathogenesis and identifying specific biomarkers are crucial for CRC early diagnosis and targeted therapy. CCDC113, a member of CCDC families, has been reported to play roles in ciliary assembly, ciliary activity, PSCI, asthma and early lung cancer diagnosis. However, the functions of CCDC113 in CRC still remain unclear. In this study, we find that CCDC113 is significantly highly expressed in CRC. High expression of CCDC113 is significantly correlated with CRC patients' poor prognosis. CCDC113 is required for CRC tumorigenesis and metastasis. RNA-seq and TCGA database analysis indicate that CCDC113 is positively correlated with TGF-beta signaling pathway. TGF-beta signaling pathway inhibitor galunisertib could reverse the increased proliferation and migration ability of CRC cells caused by CCDC113 overexpression in vitro and in vivo. These results indicate that CCDC113 promotes CRC tumorigenesis and metastasis via TGF-beta signaling pathway. In conclusion, it is the first time to explore the functions and mechanisms of CCDC113 in CRC tumorigenesis and metastasis. And CCDC113 may be a potential biomarker and therapeutic target for CRC intervention.
C1 [Hou, Chenying; Yang, Yanmei; Xie, Huimin; Zhao, Liangbo; Wu, Guanghua; Xing, Hao; Chen, Hong; Liu, Benyu; Sun, Xiao] Zhengzhou Univ, Acad Med Sci, Tianjian Lab Adv Biomed Sci, Zhengzhou, Peoples R China.
   [Wang, Peiwen; Jin, Shuiling] Zhengzhou Univ, Dept Oncol, Affiliated Hosp 1, Zhengzhou, Peoples R China.
   [Zhao, Liangbo] Zhengzhou Univ, Sch Life Sci, Zhengzhou, Peoples R China.
   [Du, Chunyan] Zhengzhou Univ, Lab Anim Ctr, Zhengzhou, Peoples R China.
   [He, Luyun] Zhengzhou Univ, Sch Basic Med Sci, Dept Pathophysiol, Zhengzhou, Peoples R China.
C3 Zhengzhou University; Zhengzhou University; Zhengzhou University;
   Zhengzhou University; Zhengzhou University
RP Sun, X (corresponding author), Zhengzhou Univ, Acad Med Sci, Tianjian Lab Adv Biomed Sci, Zhengzhou, Peoples R China.; Du, CY (corresponding author), Zhengzhou Univ, Lab Anim Ctr, Zhengzhou, Peoples R China.; He, LY (corresponding author), Zhengzhou Univ, Sch Basic Med Sci, Dept Pathophysiol, Zhengzhou, Peoples R China.
EM cydu@zzu.edu.cn; sx0507@zzu.edu.cn; hly2020@zzu.edu.cn
RI 赵, 良波/IXD-2995-2023; Wu, Guanghua/GWU-5194-2022
OI Yang, Yanmei/0000-0001-9881-2442
FU National Natural Science Foundation of China (National Science
   Foundation of China) [2021YFA1302000]; National Key Research and
   Development Program of China [222301420015, 222102310602]; Joint Funding
   of Henan Provincial Science and Technology RD Plan [23A310028]; Science
   Foundation of Henan Education Department [32170874, 82203490]; National
   Natural Science Foundation of China [2024ZZJCYJ051]; Zhengzhou basic
   research
FX This work was supported by National Key Research and Development Program
   of China (2021YFA1302000), Joint Funding of Henan Provincial Science and
   Technology R&D Plan (222301420015, 222102310602), Science Foundation of
   Henan Education Department (23A310028), National Natural Science
   Foundation of China (32170874, 82203490) and Zhengzhou basic research
   (2024ZZJCYJ051).
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NR 50
TC 0
Z9 0
U1 5
U2 5
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 11
PY 2024
VL 15
IS 9
AR 666
DI 10.1038/s41419-024-07036-3
PG 15
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA F5J1H
UT WOS:001310170100002
PM 39261464
OA gold
DA 2025-01-04
ER

PT J
AU Dezfuli, AAZ
   Abu-Elghait, M
   Salem, SS
AF Dezfuli, Aram Asareh Zadegan
   Abu-Elghait, Mohammed
   Salem, Salem S.
TI Recent Insights into Nanotechnology in Colorectal Cancer
SO APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY
LA English
DT Review
DE Nanotechnology; Colorectal cancer; Targeted therapy
ID GLYCOLIC ACID NANOPARTICLES; IRON-OXIDE NANOPARTICLES; GOLD
   NANOPARTICLES; STEM-CELLS; COLON; DELIVERY; MECHANISMS; DISEASE;
   ELECTROPORATION; NANOSTRUCTURES
AB Colorectal cancer (CRC) is the third cancer among the known causes of cancer that impact people. Although CRC drug options are imperfect, primary detection of CRC can play a key role in treating the disease and reducing mortality. Cancer tissues show many molecular markers that can be used as a new way to advance therapeutic methods. Nanotechnology includes a wide range of nanomaterials with high diagnostic and therapeutic power. Several nanomaterials and nanoformulations can be used to treat cancer, especially CRC. In this review, we discuss recent insights into nanotechnology in colorectal cancer.
C1 [Dezfuli, Aram Asareh Zadegan] Ahvaz Jundishapur Univ Med Sci, Fac Med, Dept Microbiol, Ahvaz, Iran.
   [Abu-Elghait, Mohammed; Salem, Salem S.] Al Azhar Univ, Fac Sci, Dept Bot & Microbiol, Cairo, Egypt.
C3 Ahvaz Jundishapur University of Medical Sciences (AJUMS); Egyptian
   Knowledge Bank (EKB); Al Azhar University
RP Dezfuli, AAZ (corresponding author), Ahvaz Jundishapur Univ Med Sci, Fac Med, Dept Microbiol, Ahvaz, Iran.; Salem, SS (corresponding author), Al Azhar Univ, Fac Sci, Dept Bot & Microbiol, Cairo, Egypt.
EM aramasareh836@yahoo.com; salemsalahsalem@azhar.edu.eg
RI Abu-Elghait, Mohammed/AAR-6947-2021; Dezfuli, Aram/AAX-1264-2020; Salem,
   Salem S/P-2281-2018
OI Salem, Salem S/0000-0003-2898-6708
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NR 132
TC 19
Z9 19
U1 7
U2 16
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0273-2289
EI 1559-0291
J9 APPL BIOCHEM BIOTECH
JI Appl. Biochem. Biotechnol.
PD JUL
PY 2024
VL 196
IS 7
BP 4457
EP 4471
DI 10.1007/s12010-023-04696-3
EA SEP 2023
PG 15
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA YS0W2
UT WOS:001072264200002
PM 37751009
DA 2025-01-04
ER

PT J
AU Liu, Y
   Niu, LL
   Li, NN
   Wang, Y
   Liu, MY
   Su, XM
   Bao, XH
   Yin, B
   Shen, S
AF Liu, Yao
   Niu, Lili
   Li, Nannan
   Wang, Yang
   Liu, Mingyang
   Su, Xiaomin
   Bao, Xuhui
   Yin, Bo
   Shen, Shun
TI Bacterial-Mediated Tumor Therapy: Old Treatment in a New Context
SO ADVANCED SCIENCE
LA English
DT Review
DE bacteria; bacterial components; engineered bacteria; immunotherapy;
   tumor microenvironment
ID ENTEROTOXIGENIC BACTEROIDES-FRAGILIS; ATTENUATED SALMONELLA-TYPHIMURIUM;
   CHLAMYDIA-TRACHOMATIS INFECTION; EXPRESSING MESOTHELIN CRS-207;
   OUTER-MEMBRANE VESICLES; FUSOBACTERIUM-NUCLEATUM;
   LISTERIA-MONOCYTOGENES; COLORECTAL-CANCER; BREAST-CANCER; COLON-CANCER
AB Targeted therapy and immunotherapy have brought hopes for precision cancer treatment. However, complex physiological barriers and tumor immunosuppression result in poor efficacy, side effects, and resistance to antitumor therapies. Bacteria-mediated antitumor therapy provides new options to address these challenges. Thanks to their special characteristics, bacteria have excellent ability to destroy tumor cells from the inside and induce innate and adaptive antitumor immune responses. Furthermore, bacterial components, including bacterial vesicles, spores, toxins, metabolites, and other active substances, similarly inherit their unique targeting properties and antitumor capabilities. Bacteria and their accessory products can even be reprogrammed to produce and deliver antitumor agents according to clinical needs. This review first discusses the role of different bacteria in the development of tumorigenesis and the latest advances in bacteria-based delivery platforms and the existing obstacles for application. Moreover, the prospect and challenges of clinical transformation of engineered bacteria are also summarized.
C1 [Liu, Yao] Tongji Univ, Tongji Hosp, Sch Med, Inst Biomed Engn & Nano Sci,Orthopaed Dept,Key Lab, Shanghai 200092, Peoples R China.
   [Liu, Yao; Shen, Shun] Fudan Univ, Shanghai Pudong Hosp, Pudong Med Ctr, Pharm Dept, Shanghai 201399, Peoples R China.
   [Liu, Yao; Shen, Shun] Fudan Univ, Pudong Med Ctr, Shanghai Pudong Hosp, Ctr Med Res & Innovat, Shanghai 201399, Peoples R China.
   [Niu, Lili; Li, Nannan; Wang, Yang; Su, Xiaomin] Dalian Med Univ, Affiliated Hosp 1, Inst Coll Integrat Med, Cent Lab, Dalian 116021, Peoples R China.
   [Liu, Mingyang] China Med Univ, Hosp 1, Dept Surg Oncol & Gen Surg, 155 North Nanjing St, Shenyang 110001, Peoples R China.
   [Bao, Xuhui; Yin, Bo] Fudan Univ, Pudong Med Ctr, Inst Therapeut Canc Vaccines, Shanghai 201399, Peoples R China.
   [Yin, Bo] Fudan Univ, Pudong Med Ctr, Dept Oncol, Shanghai 201399, Peoples R China.
C3 Tongji University; Fudan University; Fudan University; Dalian Medical
   University; China Medical University; Fudan University; Fudan University
RP Shen, S (corresponding author), Fudan Univ, Pudong Med Ctr, Shanghai Pudong Hosp, Ctr Med Res & Innovat, Shanghai 201399, Peoples R China.; Bao, XH; Yin, B (corresponding author), Fudan Univ, Pudong Med Ctr, Inst Therapeut Canc Vaccines, Shanghai 201399, Peoples R China.; Yin, B (corresponding author), Fudan Univ, Pudong Med Ctr, Dept Oncol, Shanghai 201399, Peoples R China.
EM xuhui.bao@duke.edu; yinbo@fudan.edu.cn; sshen@fudan.edu.cn
RI zhang, hao/JOJ-7093-2023; Liu, Mingyang/HGD-3102-2022; bao,
   xuhui/G-3191-2017; Niu, Lili/B-3929-2018
OI shen, shun/0000-0002-0184-6388
FU National Natural Science Foundation of China [32172894]; Academic
   Leaders Training Program of Pudong Health Committee of Shanghai
   [PWRd2022-09]; Shanghai Municipal Health and Family Planning Commission
   [201740083]; Scientific Research Project of Shanghai Pudong Hospital
   [YJYJRC202106]
FX This work was financially supported by the National Natural Science
   Foundation of China (32172894), Academic Leaders Training Program of
   Pudong Health Committee of Shanghai (Grant No. PWRd2022-09), Shanghai
   Municipal Health and Family Planning Commission (201740083), and the
   Scientific Research Project of Shanghai Pudong Hospital (YJYJRC202106).
   The table of contents was drawn by Figdraw (https://www.figdraw.com).
   The authors also thank Ren Tongyao from Shiyanjia Lab
   (https://www.shiyanjia.com) for drawing Figure 1.
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NR 320
TC 22
Z9 23
U1 26
U2 145
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2198-3844
J9 ADV SCI
JI Adv. Sci.
PD APR
PY 2023
VL 10
IS 12
DI 10.1002/advs.202205641
EA MAR 2023
PG 27
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA F0QM9
UT WOS:000946879800001
PM 36908053
OA Green Accepted, gold
DA 2025-01-04
ER

PT J
AU Guo, XH
   Chang, XY
   Wang, ZY
   Jiang, CJ
   Wei, ZG
AF Guo, Xiaohu
   Chang, Xingyu
   Wang, Zheyuan
   Jiang, Chenjun
   Wei, Zhengang
TI CircRNAs: promising factors for regulating angiogenesis in colorectal
   cancer
SO CLINICAL & TRANSLATIONAL ONCOLOGY
LA English
DT Review
DE CircRNA; Colorectal cancer; Targeted therapy; Angiogenesis
ID CIRCULAR RNAS; CELL-PROLIFERATION; HYPOXIA; TRANSLATION; NORMALIZATION;
   METASTASIS; BIOGENESIS; GROWTH
AB Colorectal cancer (CRC) is one of the most common cancers in the world. The incidence rate of cancer is high. The overall response to traditional treatment methods such as surgery, radiotherapy, and chemotherapy is not very satisfactory. Therefore, finding new therapeutic targets is very important for improving CRC treatment. In recent reports, the role of circRNAs in regulating colorectal angiogenesis has been gradually revealed. CircRNAs can indirectly act on angiogenesis pathways and regulate the expression of growth factors such as vascular endothelial growth factor (VEGF). CircRNAs are endogenous noncoding RNAs formed by pre-mRNAs through exon circular splicing. The covalent closed-loop structure makes these RNAs highly conserved and stable. CircRNAs have been found in human plasma, serum, urine, and other body fluids. Their highly conserved characteristics play important roles in many biological activities. CircRNAs can participate in the progression of many diseases by sponging miRNAs, interacting with proteins, and regulating transcription. Angiogenesis can provide nutrients and oxygen for tumour proliferation and metastasis. Angiogenesis is an important sign of the formation of the tumour microenvironment. Here, we will summarize the role of the latest circRNAs in the mechanism of angiogenesis in CRC and provide potential therapeutic targets for clinical treatment.
C1 [Guo, Xiaohu; Wang, Zheyuan; Wei, Zhengang] Lanzhou Univ, Hosp 2, Gen Surg Dept, Lanzhou 730030, Peoples R China.
   [Chang, Xingyu; Jiang, Chenjun] Lanzhou Univ, Clin Med Coll 1, Lanzhou 730000, Gansu, Peoples R China.
C3 Lanzhou University; Lanzhou University
RP Wei, ZG (corresponding author), Lanzhou Univ, Hosp 2, Gen Surg Dept, Lanzhou 730030, Peoples R China.
EM wzg911027@sina.com
RI WANG, ZHEYUAN/KMA-7475-2024; Guo, Xiaohu/N-5903-2017
FU Chinese Foundation for Hepatitis Prevention and
   Control-'Tian-qing-gan-bing' Research Fund [TQGB20190165]; College
   Students' Innovation, Entrepreneurship and Excellence Program of Lanzhou
   University in 2022 [20220060024]
FX Chinese Foundation for Hepatitis Prevention and
   Control-'Tian-qing-gan-bing' Research Fund, No. TQGB20190165; College
   Students' Innovation, Entrepreneurship and Excellence Program of Lanzhou
   University in 2022 (20220060024).
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NR 59
TC 7
Z9 7
U1 0
U2 6
PU SPRINGER INT PUBL AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1699-048X
EI 1699-3055
J9 CLIN TRANSL ONCOL
JI Clin. Transl. Oncol.
PD SEP
PY 2022
VL 24
IS 9
BP 1673
EP 1681
DI 10.1007/s12094-022-02829-4
EA APR 2022
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3I9NJ
UT WOS:000782374900001
PM 35416599
DA 2025-01-04
ER

PT J
AU Knickelbein, K
   Zhang, L
AF Knickelbein, Kyle
   Zhang, Lin
TI Mutant KRAS as a critical determinant of the therapeutic response of
   colorectal cancer
SO GENES & DISEASES
LA English
DT Review
DE Colorectal cancer; EGFR; KRAS; Synthetic lethality; Targeted therapy
ID ANTI-EGFR THERAPY; SYNTHETIC LETHAL INTERACTIONS; FACTOR RECEPTOR
   ANTIBODY; K-RAS; ONCOGENIC KRAS; MEK INHIBITION; GROWTH; CETUXIMAB;
   PANITUMUMAB; ACTIVATION
AB Mutations in the KRAS oncogene represent one of the most prevalent genetic alterations in colorectal cancer (CRC), the third leading cause of cancer-related death in the US. In addition to their well-characterized function in driving tumor progression, KRAS mutations have been recognized as a critical determinant of the therapeutic response of CRC. Recent studies demonstrate that KRAS-mutant tumors are intrinsically insensitive to clinically-used epidermal growth factor receptor (EGFR) targeting antibodies, including cetuximab and panitumumab. Acquired resistance to the anti-EGFR therapy was found to be associated with enrichment of KRAS-mutant tumor cells. However, the underlying molecular mechanism of mutant-KRAS-mediated therapeutic resistance has remained unclear. Despite intensive efforts, directly targeting mutant KRAS has been largely unsuccessful. This review summarizes the recent advances in understanding the biological function of KRAS mutations in determining the therapeutic response of CRC, highlighting several recently developed agents and strategies for targeting mutant KRAS, such as synthetic lethal interactions. Copyright (C) 2014, Chongqing Medical University. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license.
C1 Univ Pittsburgh, Sch Med, Dept Pharmacol, Inst Canc, Pittsburgh, PA 15213 USA.
   Univ Pittsburgh, Sch Med, Dept Chem Biol, Inst Canc, Pittsburgh, PA 15213 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
   of Pittsburgh; Pennsylvania Commonwealth System of Higher Education
   (PCSHE); University of Pittsburgh
RP Zhang, L (corresponding author), Univ Pittsburgh, Inst Canc, Hillman Canc Ctr, Room 2-42a, Pittsburgh, PA 15213 USA.
EM zhanglx@upmc.edu
RI Zhang, Lin/A-7389-2009
OI Zhang, Lin/0000-0003-0018-3903
FU Department of Pharmacology & Chemical Biology; National Institute of
   Health [R01CA106348, R01CA172136]
FX The authors would like to thank Dr. Jian Yu and Rochelle Fletcher for
   critical reading. K.K. is supported in part by the graduate student
   fellowship from the Department of Pharmacology & Chemical Biology.
   Research in L.Z.'s lab is supported by the National Institute of Health
   grants R01CA106348 and R01CA172136.
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NR 98
TC 97
Z9 118
U1 2
U2 11
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2352-4820
EI 2352-3042
J9 GENES DIS
JI Genes Dis.
PD MAR
PY 2015
VL 2
IS 1
BP 4
EP 12
DI 10.1016/j.gendis.2014.10.002
PG 9
WC Biochemistry & Molecular Biology; Genetics & Heredity
WE Emerging Sources Citation Index (ESCI)
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA V1P9K
UT WOS:000217127900003
PM 25815366
OA Green Accepted, gold
DA 2025-01-04
ER

PT J
AU Tian, ZC
   Niu, XH
   Yao, WT
AF Tian, Zhichao
   Niu, Xiaohui
   Yao, Weitao
TI Efficacy and Response Biomarkers of Apatinib in the Treatment of
   Malignancies in China: A Review
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE apatinib; tyrosine kinase inhibitor; efficacy; response biomarker;
   clinical trial
ID CELL LUNG-CANCER; CAMRELIZUMAB PLUS APATINIB; METASTATIC GASTRIC-CANCER;
   MULTICENTER PHASE-II; WILD-TYPE EGFR; SINGLE-ARM; OPEN-LABEL; VEGFR
   INHIBITOR; TYROSINE KINASE; BREAST-CANCER
AB Apatinib is a multitarget tyrosine kinase inhibitor marketed in China for the treatment of advanced gastric cancer (GC) and hepatocellular carcinoma (HCC). It has also been used off-label for the treatment of many other malignancies. To comprehensively evaluate the efficacy of apatinib as a targeted therapy in the treatment of malignancies, we conducted systematic online and manual searches of the literature on apatinib in the treatment of malignancies. In this review, we first summarized the efficacy of apatinib against various malignancies based on clinical trials where results have been reported. In prospectively registered trials, apatinib has been proven to be effective against GC, HCC, lung cancer, breast cancer, sarcoma, esophageal cancer, colorectal cancer, ovarian cancer, cervical cancer, cholangiocarcinoma, diffuse large B-cell lymphoma, nasopharyngeal carcinoma, and differentiated thyroid cancer. The response biomarkers for apatinib were also reviewed. This review will serve as a good reference for the application of apatinib in clinical studies and the design of clinical trials.
C1 [Tian, Zhichao; Yao, Weitao] Zhengzhou Univ, Affiliated Canc Hosp, Dept Orthoped, Zhengzhou, Peoples R China.
   [Tian, Zhichao; Yao, Weitao] Zhengzhou Univ, Henan Canc Hosp, Dept Orthoped, Zhengzhou, Peoples R China.
   [Niu, Xiaohui] Beijing Jishuitan Hosp, Dept Orthoped Oncol, Beijing, Peoples R China.
C3 Zhengzhou University; Zhengzhou University
RP Yao, WT (corresponding author), Zhengzhou Univ, Affiliated Canc Hosp, Dept Orthoped, Zhengzhou, Peoples R China.; Yao, WT (corresponding author), Zhengzhou Univ, Henan Canc Hosp, Dept Orthoped, Zhengzhou, Peoples R China.
EM ywt00001@163.com
RI Weitao, Yao/ABM-0873-2022
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NR 87
TC 21
Z9 22
U1 6
U2 36
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 5
PY 2021
VL 11
AR 749083
DI 10.3389/fonc.2021.749083
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA WK5FC
UT WOS:000709750200001
PM 34676173
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Hirata, W
   Itatani, Y
   Masui, H
   Kawada, K
   Mizuno, R
   Yamamoto, T
   Okamoto, T
   Ogawa, R
   Inamoto, S
   Maekawa, H
   Okamura, R
   Kiyasu, Y
   Hanada, K
   Okamoto, M
   Nishikawa, Y
   Sugimoto, N
   Tamura, T
   Hatano, E
   Sakai, Y
   Obama, K
AF Hirata, Wataru
   Itatani, Yoshiro
   Masui, Hideyuki
   Kawada, Kenji
   Mizuno, Rei
   Yamamoto, Takamasa
   Okamoto, Takuya
   Ogawa, Ryotaro
   Inamoto, Susumu
   Maekawa, Hisatsugu
   Okamura, Ryosuke
   Kiyasu, Yoshiyuki
   Hanada, Keita
   Okamoto, Michio
   Nishikawa, Yasuyo
   Sugimoto, Naoko
   Tamura, Takuya
   Hatano, Etsuro
   Sakai, Yoshiharu
   Obama, Kazutaka
TI Downregulation of osteoprotegerin in colorectal cancer cells promotes
   liver metastasis via activating tumor-associated macrophage
SO SCIENTIFIC REPORTS
LA English
DT Article
ID OSTEOCLAST DIFFERENTIATION; RECEPTOR ACTIVATOR; EXPRESSION; SMAD4; OPG;
   ACCUMULATION; THP-1
AB Osteoprotegerin (OPG) is a secreted cytokine that functions as a decoy receptor for receptor activator of nuclear factor kappa-B (RANK) ligand (RANKL). Anti-RANKL treatment for bone metastasis has been widely accepted for solid tumors. However, the mechanism of OPG-RANKL-RANK signaling in systemic colorectal cancer (CRC) metastasis remains unclear. In this study, we investigated the relevance and function of OPG expression in CRC liver metastasis. First, we performed in silico analysis using The Cancer Genome Atlas public database and found that lower OPG expression in CRC was associated with poor overall survival. Immunohistochemistry analyses using resected specimen from patients with CRC in our institute confirmed the result. Patient-matched primary CRC and liver metastases showed a significant downregulation of OPG expression in metastatic lesions. In CRC cell lines, OPG expression did not suppress cell proliferation and migration. However, OPG expression inhibited macrophage migration by suppressing the RANKL-RANK pathway. Moreover, in vivo mouse liver metastasis models showed that OPG expression in CRC cells suppressed liver metastases. In addition, treatment with an anti-RANKL neutralizing antibody also suppressed liver metastases. These results showed that downregulation of OPG expression in CRC cells promotes liver metastasis by activating tumor-associated macrophage, which can become a candidate for targeted therapy with anti-RANKL neutralizing antibody for CRC liver metastasis.
C1 [Hirata, Wataru; Itatani, Yoshiro; Masui, Hideyuki; Kawada, Kenji; Mizuno, Rei; Yamamoto, Takamasa; Okamoto, Takuya; Ogawa, Ryotaro; Maekawa, Hisatsugu; Okamura, Ryosuke; Kiyasu, Yoshiyuki; Hanada, Keita; Okamoto, Michio; Nishikawa, Yasuyo; Sugimoto, Naoko; Tamura, Takuya; Hatano, Etsuro; Sakai, Yoshiharu; Obama, Kazutaka] Kyoto Univ, Grad Sch Med, Dept Surg, 54 Shogoin Kawaharacho,Sakyo ku, Kyoto 6068507, Japan.
   [Kawada, Kenji] Kurashiki Cent Hosp, Dept Surg, Okayama 7108602, Japan.
   [Mizuno, Rei] NHO Kyoto Med Ctr, Dept Surg, Kyoto 6110041, Japan.
   [Inamoto, Susumu; Sakai, Yoshiharu] Japanese Red Cross Osaka Hosp, Dept Surg, Osaka 5438555, Japan.
   [Kiyasu, Yoshiyuki] Univ Michigan, Rogel Canc Ctr, Ann Arbor, MI 48109 USA.
C3 Kyoto University; Kurashiki Central Hospital; University of Michigan
   System; University of Michigan
RP Itatani, Y (corresponding author), Kyoto Univ, Grad Sch Med, Dept Surg, 54 Shogoin Kawaharacho,Sakyo ku, Kyoto 6068507, Japan.
EM itatani@kuhp.kyoto-u.ac.jp
RI OBAMA, KAZUTAKA/AAW-8263-2021; Hatano, Etsuro/AAX-2407-2020
OI Masui, Hideyuki/0000-0002-0771-540X
FU JSPS KAKENHI; Center for Anatomical, Pathological and Forensic Medical
   Research
FX We thank the Center for Anatomical, Pathological and Forensic Medical
   Research, Graduate School of Medicine, Kyoto University for preparing
   microscope slides. We also thank Naoya Fujita for providing MC38 cell
   line. We thank Editage (www.editage.com) for English language editing.
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NR 44
TC 1
Z9 1
U1 0
U2 3
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD DEC 14
PY 2023
VL 13
IS 1
AR 22217
DI 10.1038/s41598-023-49312-w
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CL2L3
UT WOS:001125340600065
PM 38097649
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Vidri, RJ
   Fitzgerald, TL
AF Vidri, Roberto J.
   Fitzgerald, Timothy L.
TI GSK-3: An important kinase in colon and pancreatic cancers
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
LA English
DT Review
DE GSK-3; beta-Catenin; Pancreas; Colon; Cancer
ID GLYCOGEN-SYNTHASE KINASE-3; NF-KAPPA-B; SIGNALING PATHWAYS;
   COLORECTAL-CANCER; CELL-SURVIVAL; PROTEIN-KINASE; BETA-CATENIN;
   INHIBITION; CHEMOTHERAPY; GEMCITABINE
AB In this review, the role of glycogen synthase kinase 3 (GSK-3) in pancreatic and colon cancers will be explored. GSK-3 plays a fundamental role in many metabolic processes, primarily as the final enzyme in glycogen synthesis. Active beta-catenin represents the final step for the transcription of Wnt target genes. Both GSK-3 and beta-catenin are key in the neoplastic transformation and tumorigenesis of human cells. Despite the advances in diagnosis and treatment of pancreatic malignancies, survival remains dismal. Continued poor outcomes are attributable to tumor cell resistance and high frequency of metastatic disease. Survival for patients diagnosed with colon cancer is often excellent, and many patients achieve long term remission. However, the incidence of colon cancers continues to increase, especially among the young. The future use of targeted therapy in pancreatic and colo-rectal cancer utilizing GSK-3 may be promising, pending a more thorough understanding of potential downstream effects. This article is part of a Special Issue entitled: GSK-3 and related kinases in cancer, neurological and other disorders edited by James McCubrey, Agnieszka Gizak and Dariusz Rakus.
C1 [Vidri, Roberto J.; Fitzgerald, Timothy L.] Tufts Univ, Div Surg Oncol, Sch Med, Maine Med Ctr, Portland, ME USA.
C3 Maine Medical Center; Tufts University
RP Fitzgerald, TL (corresponding author), 100 Campus Dr,Suite 111, Scarborough, ME 04074 USA.
EM tlfitzgera@mmc.org
RI Fitzgerald, Timothy/F-2045-2010
OI Vidri, Roberto/0000-0003-0912-5259
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NR 45
TC 22
Z9 24
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29a, 1043 NX AMSTERDAM, NETHERLANDS
SN 0167-4889
EI 1879-2596
J9 BBA-MOL CELL RES
JI Biochim. Biophys. Acta-Mol. Cell Res.
PD APR
PY 2020
VL 1867
IS 4
AR 118626
DI 10.1016/j.bbamcr.2019.118626
PG 4
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA KO3ER
UT WOS:000515431200017
PM 31987793
OA Bronze
DA 2025-01-04
ER

PT J
AU Lee, SY
   Oh, SC
AF Lee, Suk-young
   Oh, Sang Cheul
TI Advances of Targeted Therapy in Treatment of Unresectable Metastatic
   Colorectal Cancer
SO BIOMED RESEARCH INTERNATIONAL
LA English
DT Review
ID ENDOTHELIAL GROWTH-FACTOR; CETUXIMAB PLUS IRINOTECAN; PHASE-III TRIAL;
   KRAS WILD-TYPE; K-RAS MUTATIONS; FACTOR RECEPTOR; 1ST-LINE TREATMENT;
   OPEN-LABEL; RANDOMIZED PHASE-3; BRAF MUTATION
AB Despite being one of the most frequently diagnosed cancers worldwide, prognosis of metastatic colorectal cancer (CRC) was poor. Development and introduction of biologic agents in treatment of patients with metastatic CRC have brought improved outcomes. Monoclonal antibodies directing epidermal growth factor receptors and vascular endothelial growth factor are main biologic agents currently used in treatment of metastatic CRC. Encouraged by results from many clinical trials demonstrating efficacy of those monoclonal antibodies, the combination therapy with those targeted agents and conventional chemotherapeutic agents has been established as the standard therapy for patients with metastatic CRC. However, emergency of resistance to those target agents has limited the efficacy of treatment, and strategies to overcome the resistance are now being investigated by newly developed biological techniques clarifying how to acquire resistance. Here, we introduce mechanisms of action of the biologic agents currently used for treatment of metastatic CRC and several landmark historical clinical studies which have changed the main stream of treatment. The mechanism of resistance to those agents, one of serious problems in treatment metastatic CRC, and ongoing clinical trials to overcome the limitations and improve treatment outcomes will also be presented in this review.
C1 [Lee, Suk-young; Oh, Sang Cheul] Korea Univ, Coll Med, Dept Internal Med, Div Oncol Hematol, 148 Gurodong Ro, Seoul 08308, South Korea.
C3 Korea University; Korea University Medicine (KU Medicine)
RP Oh, SC (corresponding author), Korea Univ, Coll Med, Dept Internal Med, Div Oncol Hematol, 148 Gurodong Ro, Seoul 08308, South Korea.
EM sachoh@korea.ac.kr
RI Lee, Joo Yong/ADE-2110-2022
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NR 102
TC 24
Z9 26
U1 0
U2 2
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2314-6133
EI 2314-6141
J9 BIOMED RES INT
JI Biomed Res. Int.
PY 2016
VL 2016
AR 7590245
DI 10.1155/2016/7590245
PG 14
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA DJ7MC
UT WOS:000374394500001
PM 27127793
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Mehrgou, A
   Teimourian, S
AF Mehrgou, Amir
   Teimourian, Shahram
TI Update of gene expression/methylation and MiRNA profiling in colorectal
   cancer; application in diagnosis, prognosis, and targeted therapy
SO PLOS ONE
LA English
DT Article
ID DNA METHYLATION; PHOSPHOENOLPYRUVATE CARBOXYKINASE; CELL-PROLIFERATION;
   MOLECULAR-ORIGINS; DOWN-REGULATION; UP-REGULATION; R PACKAGE;
   EXPRESSION; SOSTDC1; HYPERMETHYLATION
AB BackgroundColorectal cancer is one of the most deadliest malignancies worldwide. Due to the dearth of appropriate biomarkers, the diagnosis of this mortal disease is usually deferred, in its turn, culminating in the failure of prevention. By the same token, proper biomarkers are at play in determining the quality of prognosis. In other words, the survival rate is contingent upon the regulation of such biomarkers. Materials and methodsThe information regarding expression (GSE41258, and GSE31905), methylation (GSE101764), and miRNA (dbDEMC) were downloaded. MEXPRESS and GEPIA confirmed the validated differentially expressed/methylated genes using TCGA data. Taking advantage of the correlation plots and receiver-operating-characteristic (ROC) curves, expression and methylation profiles were compared. The interactions between validated differentially expressed genes and differentially expressed miRNA were recognized and visualized by miRTarBase and Cytoscape, respectively. Then, the protein-protein interaction (PPI) network and hub genes were established via STRING and Cytohubba plugin. Utilizing R packages (DOSE, Enrichplot, and clusterProfiler) and DAVID database, the Functional Enrichment analysis and the detection of KEGG pathways were performed. Ultimately, in order to recognize the prognostic value of found biomarkers, they were evaluated through drawing survival plots for CRC patients. ResultsIn this research, we found an expression profile (with 13 novel genes), a methylation profile (with two novel genes), and a miRNA profile with diagnostic value. Concerning diagnosis, the expression profile was evaluated more powerful in comparison with the methylation profile. Furthermore, a prognosis-related expression profile was detected. ConclusionIn addition to diagnostic- and prognostic-applicability, the discerned profiles can assist in targeted therapy and current therapeutic strategies.
C1 [Mehrgou, Amir] Iran Univ Med Sci, Sch Med, Dept Med Genet & Mol Biol, Tehran, Iran.
   [Teimourian, Shahram] Iran Univ Med Sci, Sch Med, Dept Med Genet, Tehran, Iran.
C3 Iran University of Medical Sciences; Iran University of Medical Sciences
RP Teimourian, S (corresponding author), Iran Univ Med Sci, Sch Med, Dept Med Genet, Tehran, Iran.
EM teimourian.sh@iums.ac.ir
OI , SHAHRAM/0000-0002-8642-9128
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NR 88
TC 2
Z9 2
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PY 2022
VL 17
IS 3
AR e0265527
DI 10.1371/journal.pone.0265527
PG 34
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 0P6KD
UT WOS:000784335700032
PM 35333898
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhang, C
   Zeng, CL
   Xiong, SQ
   Zhao, ZW
   Wu, GY
AF Zhang, Cong
   Zeng, Cailing
   Xiong, Shaoquan
   Zhao, Zewei
   Wu, Guoyu
TI A mitophagy-related gene signature associated with prognosis and immune
   microenvironment in colorectal cancer
SO SCIENTIFIC REPORTS
LA English
DT Article
ID EXPRESSION; CELLS; IMMUNOTHERAPY; CHEMOTHERAPY; INHIBITION; NIVOLUMAB;
   IMPACT; GROWTH; TUMORS
AB Colorectal cancer (CRC) is a heterogeneous disease and one of the most prevalent malignancies worldwide. Previous research has demonstrated that mitophagy is crucial to developing colorectal cancer. This study aims to examine the association between mitophagy-related genes and the prognosis of CRC patients. Gene expression profiles and clinical information of CRC patients were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Univariate Cox regression and the least absolute shrinkage and selection operator (LASSO) regression analysis were applied to establish a prognostic signature using mitophagy related genes. Kaplan-Meier and receiver operating characteristic (ROC) curves were used to analyze patient survival and predictive accuracy. Meanwhile, we also used the Genomics of Drug Sensitivity in Cancer (GDSC) database and Tumor Immune Dysfunction and Exclusion (TIDE) algorithm to estimate the sensitivity of chemotherapy, targeted therapy and immunotherapy. ATG14 overexpression plasmid was used to regulate the ATG14 expression level in HCT116 and SW480 cell lines, and cell counting kit-8, colony formation and transwell migration assay were performed to validate the function of ATG14 in CRC cells. A total of 22 mitophagy-driven genes connected with CRC survival were identified, and then a novel prognostic signature was established based on 10 of them (AMBRA1, ATG14, MAP1LC3A, MAP1LC3B, OPTN, VDAC1, ATG5, CSNK2A2, MFN1, TOMM22). Patients were divided into high-risk and low-risk groups based on the median risk score, and the survival of patients in the high-risk group was significantly shorter in both the training cohort and two independent cohorts. ROC curve showed that the area under the curves (AUC) of 1-, 3- and 5-year survival were 0.66, 0.66 and 0.64, respectively. Multivariate Cox regression analysis confirmed the independent prognostic value of the signature. Then we constructed a Nomogram combining the risk score, age and M stage, which had a concordance index of survival prediction of 0.77 (95% CI 0.71-0.83) and more robust predictive accuracy. Results showed that CD8+ T cells, regulatory T cells and activated NK cells were significantly more enriched in the high-risk group. Furthermore, patients in the high-risk group are more sensitive to targeted therapy or chemotherapy, including bosutinib, elesclomol, lenalidomide, midostaurin, pazopanib and sunitinib, while the low-risk group is more likely to benefit from immunotherapy. Finally, in vitro study confirmed the oncogenic significance of ATG14 in both HCT116 and SW480 cells, whose overexpression increased CRC cell proliferation, colony formation, and migration. In conclusion, we developed a novel mitophagy-related gene signature that can be utilized not only as an independent predictive biomarker but also as a tool for tailoring personalizing treatment for CRC patients, and we confirmed ATG14 as a novel oncogene in CRC.
C1 [Zhang, Cong; Zeng, Cailing; Xiong, Shaoquan; Wu, Guoyu] Hosp Chengdu Univ Tradit Chinese Med, Chengdu 610072, Sichuan, Peoples R China.
   [Zhao, Zewei] Chengdu Univ Tradit Chinese Med, Chengdu 610072, Sichuan, Peoples R China.
C3 Chengdu University of Traditional Chinese Medicine; Chengdu University
   of Traditional Chinese Medicine
RP Wu, GY (corresponding author), Hosp Chengdu Univ Tradit Chinese Med, Chengdu 610072, Sichuan, Peoples R China.
EM 329869422@qq.com
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NR 66
TC 7
Z9 8
U1 1
U2 9
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD NOV 4
PY 2022
VL 12
IS 1
AR 18688
DI 10.1038/s41598-022-23463-8
PG 17
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA 5Y2HV
UT WOS:000879109400082
PM 36333388
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Chakraborty, B
   Agarwal, S
   Kori, S
   Das, R
   Kashaw, V
   Iyer, AK
   Kashaw, SK
AF Chakraborty, Biswadip
   Agarwal, Shivangi
   Kori, Shivam
   Das, Ratnesh
   Kashaw, Varsha
   Iyer, Arun K.
   Kashaw, Sushil Kumar
TI Multiple Protein Biomarkers and Different Treatment Strategies for
   Colorectal Carcinoma: A Comprehensive Prospective
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Biomarkers; pathogenesis; monoclonal antibody; vaccines;
   phytopharmaceuticals; clinical investigation; colorectal cancer
ID ISLAND METHYLATOR PHENOTYPE; P53 GENE-MUTATIONS; GROWTH-FACTOR-BETA;
   COLON-CANCER; T-CELL; MICROSATELLITE INSTABILITY; 1ST-LINE TREATMENT;
   15-HYDROXYPROSTAGLANDIN DEHYDROGENASE; ADOPTIVE IMMUNOTHERAPY;
   MOLECULAR-GENETICS
AB In this review, we emphasized important biomarkers, pathogenesis, and newly developed therapeutic approaches in the treatment of colorectal cancer (CRC). This includes a complete description of small-molecule inhibitors, phytopharmaceuticals with antiproliferative potential, monoclonal antibodies for targeted therapy, vaccinations as immunotherapeutic agents, and many innovative strategies to intervene in the interaction of oncogenic proteins. Many factors combine to determine the clinical behavior of colorectal cancer and it is still difficult to comprehend the molecular causes of a person's vulnerability to CRC. It is also challenging to identify the causes of the tumor's onset, progression, and responsiveness or resistance to antitumor treatment. Current recommendations for targeted medications are being updated by guidelines throughout the world in light of the growing number of high-quality clinical studies. So, being concerned about the aforementioned aspects, we have tried to present a summarized pathogenic view, including a brief description of biomarkers and an update of compounds with their underlying mechanisms that are currently under various stages of clinical testing. This will help to identify gaps or shortfalls that can be addressed in upcoming colorectal cancer research.
C1 [Chakraborty, Biswadip; Agarwal, Shivangi; Kori, Shivam; Kashaw, Sushil Kumar] Dr Harisingh Gour Univ Cent Univ, Dept Pharmaceut Sci, Integrated Drug Discovery Res Lab, Sagar 470003, Madya Pradesh, India.
   [Das, Ratnesh] ISF Coll Pharm, Dept Chem, Moga, Punjab, India.
   [Kashaw, Varsha] Sagar Inst Pharmaceut Sci, Sagar, MP, India.
   [Iyer, Arun K.] Wayne State Univ, Dept Pharmaceut Sci, Use Inspired Biomat & Integrated Nano Delivery U B, Detroit, MI USA.
   [Iyer, Arun K.] Karmanos Canc Inst, Mol Imaging Program, Detroit, MI USA.
C3 Dr. Hari Singh Gour University; ISF College of Pharmacy; Wayne State
   University; Barbara Ann Karmanos Cancer Institute
RP Kashaw, SK (corresponding author), Dr Harisingh Gour Univ Cent Univ, Dept Pharmaceut Sci, Integrated Drug Discovery Res Lab, Sagar 470003, Madya Pradesh, India.
EM sushilkashaw@gmail.com
RI Kori, Shivam/GXN-1763-2022
OI Kori, Shivam Kumar/0000-0002-6261-7474
FU AICTE, New Delhi [1-9337642094]
FX Mr. Biswadip Chakraborty (AICTE student id 1-9337642094) is thankful to
   AICTE, New Delhi for financial assistance.
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PT J
AU Zhang, L
   Liu, XZ
   Zuo, ZF
   Hao, CY
   Ma, YM
AF Zhang, Lan
   Liu, Xuezheng
   Zuo, Zhongfu
   Hao, Chunyan
   Ma, Yanmei
TI Sphingosine kinase 2 promotes colorectal cancer cell proliferation and
   invasion by enhancing MYC expression
SO TUMOR BIOLOGY
LA English
DT Article
DE Colorectal cancer; SphK2; Small interfering RNA; Proliferation; Targeted
   therapy
ID METASTASIS; GUIDELINES; SPHK2
AB Colorectal cancer (CRC) is one of the most commonly diagnosed cancers and causes of cancer death in developed countries. SphK2 is overexpressed in a number of aggressive human carcinomas; however, the expression profile and potential function of SphK2 in CRC are still unknown. In this study, we investigated the SphK2 expression in tumoral tissue and the matched normal mucosae using quantitative real-time PCR (qRT-PCR), Western blot, and immunohistochemistry. We also evaluated the impact of SphK2 knockdown on CRC cell proliferation and metastasis in vitro. SphK2 was significantly upregulated in CRC tissue as compared to the matched normal mucosae, and significant overexpression was found in the LoVo CRC cell line. SphK2 depletion by specific small interfering RNA (siRNA) in the CRC cell line was found to affect cell proliferation and cell migration. Our data suggest that the pathogenesis of CRC maybe mediated by SphK2, and SphK2 could represent a selective target for the molecularly targeted treatments of CRC.
C1 [Zhang, Lan] Liaoning Med Univ, Affiliated Hosp 1, Dept Thorac Surg, Jinzhou 121001, Liaoning, Peoples R China.
   [Liu, Xuezheng] Liaoning Med Univ, Jinzhou 121000, Liaoning, Peoples R China.
   [Zuo, Zhongfu] Liaoning Med Univ, Dept Anat Histol & Embryol, Jinzhou 121000, Liaoning, Peoples R China.
   [Hao, Chunyan; Ma, Yanmei] Liaoning Med Univ, Affiliated Hosp 1, Dept Nursing, 2,Sect 5,Renmin St, Jinzhou 121001, Liaoning, Peoples R China.
C3 Jinzhou Medical University; Jinzhou Medical University; Jinzhou Medical
   University; Jinzhou Medical University
RP Zhang, L (corresponding author), Liaoning Med Univ, Affiliated Hosp 1, Dept Thorac Surg, Jinzhou 121001, Liaoning, Peoples R China.
EM drdrsunling6@163.com
FU science research project foundation of Liaoning province [L2014338]
FX This work is supported by science research project foundation of
   Liaoning province (No: L2014338)
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NR 24
TC 25
Z9 30
U1 0
U2 7
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 JUN
PY 2016
VL 37
IS 6
BP 8455
EP 8460
DI 10.1007/s13277-015-4700-8
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DM6LT
UT WOS:000376464700145
PM 26733171
DA 2025-01-04
ER

PT J
AU Liu, YH
   Wu, WT
   Cai, CJ
   Zhang, H
   Shen, H
   Han, Y
AF Liu, Yihan
   Wu, Wantao
   Cai, Changjing
   Zhang, Hao
   Shen, Hong
   Han, Ying
TI Patient-derived xenograft models in cancer therapy: technologies and
   applications
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID CONSENSUS MOLECULAR SUBTYPES; COLORECTAL-CANCER; PRECLINICAL MODELS;
   MOUSE MODEL; IN-VITRO; MICROSATELLITE INSTABILITY;
   HEPATOCELLULAR-CARCINOMA; ACQUIRED-RESISTANCE; TUMOR XENOGRAFTS; DRUG
   DISCOVERY
AB Patient-derived xenograft (PDX) models, in which tumor tissues from patients are implanted into immunocompromised or humanized mice, have shown superiority in recapitulating the characteristics of cancer, such as the spatial structure of cancer and the intratumor heterogeneity of cancer. Moreover, PDX models retain the genomic features of patients across different stages, subtypes, and diversified treatment backgrounds. Optimized PDX engraftment procedures and modern technologies such as multi-omics and deep learning have enabled a more comprehensive depiction of the PDX molecular landscape and boosted the utilization of PDX models. These irreplaceable advantages make PDX models an ideal choice in cancer treatment studies, such as preclinical trials of novel drugs, validating novel drug combinations, screening drug-sensitive patients, and exploring drug resistance mechanisms. In this review, we gave an overview of the history of PDX models and the process of PDX model establishment. Subsequently, the review presents the strengths and weaknesses of PDX models and highlights the integration of novel technologies in PDX model research. Finally, we delineated the broad application of PDX models in chemotherapy, targeted therapy, immunotherapy, and other novel therapies.
C1 [Liu, Yihan; Wu, Wantao; Cai, Changjing; Shen, Hong; Han, Ying] Cent South Univ, Xiangya Hosp, Dept Oncol, Changsha 410008, Hunan, Peoples R China.
   [Liu, Yihan; Wu, Wantao; Cai, Changjing; Shen, Hong; Han, Ying] Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha 410008, Hunan, Peoples R China.
   [Zhang, Hao] Chongqing Med Univ, Affiliated Hosp 2, Dept Neurosurg, Chongqing, Peoples R China.
C3 Central South University; Central South University; Chongqing Medical
   University
RP Shen, H; Han, Y (corresponding author), Cent South Univ, Xiangya Hosp, Dept Oncol, Changsha 410008, Hunan, Peoples R China.; Shen, H; Han, Y (corresponding author), Cent South Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha 410008, Hunan, Peoples R China.
EM hongshen2000@csu.edu.cn; yinghan@csu.edu.cn
RI Shen, Hong/N-9734-2019; Cai, Changjing/ABA-4542-2021
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NR 298
TC 96
Z9 102
U1 15
U2 56
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD APR 12
PY 2023
VL 8
IS 1
AR 160
DI 10.1038/s41392-023-01419-2
PG 24
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA D3KX9
UT WOS:000967758700001
PM 37045827
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Wang, PP
   Lin, C
   Wang, J
   Margonis, GA
   Wu, B
AF Wang, Pei-Pei
   Lin, Chen
   Wang, Jane
   Margonis, Georgios Antonios
   Wu, Bin
TI <i>BRAF</i> Mutations in Colorectal Liver Metastases: Prognostic
   Implications and Potential Therapeutic Strategies
SO CANCERS
LA English
DT Review
DE colorectal cancer; liver metastases; BRAF mutation; prognosis; targeted
   therapy
ID 1ST-LINE TREATMENT; SUBGROUP ANALYSES; CANCER PATIENTS; V600E MUTATION;
   RAS MUTATIONS; GROWTH-FACTOR; OPEN-LABEL; SURVIVAL; CETUXIMAB; RESECTION
AB Simple Summary In this literature review, we investigated the relationship between BRAF mutation and prognosis in patients with colorectal cancer liver metastases. We also investigated factors affecting the prognosis of patients with BRAF mutations and summarized the latest research on targeted therapies. Surgery combined with chemotherapy and precision medicine is the only potential treatment for patients with colorectal cancer liver metastases (CRLM). The use of modern molecular biotechnology to identify suitable biomarkers is of great significance for predicting prognosis and formulating individualized treatment plans for these patients. BRAF mutations, particularly V600E, are widely believed to be associated with poor prognosis in patients with metastatic CRC (mCRC). However, it is unclear which specific factors affect the prognosis of CRLM patients with BRAF mutations. It is also unknown whether patients with resectable CRLM and BRAF mutations should undergo surgical treatment since there is an increased recurrence rate after surgery in these patients. In this review, we combined the molecular mechanism and clinical characteristics of BRAF mutations to explore the prognostic significance and potential targeted therapy strategies for patients with BRAF-mutated CRLM.
C1 [Wang, Pei-Pei] Univ Sci & Technol China, Affiliated Hosp 1, Dept Gen Surg, Div Life Sci & Med, Hefei 230001, Peoples R China.
   [Wang, Pei-Pei; Lin, Chen; Wu, Bin] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Peking Union Med Coll, Dept Gen Surg, Beijing 100730, Peoples R China.
   [Wang, Jane] Univ Calif San Francisco, Dept Surg, San Francisco, CA 94158 USA.
   [Margonis, Georgios Antonios] Mem Sloan Kettering Canc Ctr, Dept Surg, New York, NY 10065 USA.
C3 Chinese Academy of Sciences; University of Science & Technology of
   China, CAS; Chinese Academy of Medical Sciences - Peking Union Medical
   College; Peking Union Medical College Hospital; Peking Union Medical
   College; University of California System; University of California San
   Francisco; Memorial Sloan Kettering Cancer Center
RP Wu, B (corresponding author), Chinese Acad Med Sci, Peking Union Med Coll Hosp, Peking Union Med Coll, Dept Gen Surg, Beijing 100730, Peoples R China.
EM wubin@pumch.cn
RI wang, jane/JNS-9289-2023; Margonis, Georgios/K-7731-2019
OI Margonis, Georgios Antonios/0000-0003-4894-5743; Wang, Jaeyun
   Jane/0000-0003-3705-3993; Wang, Pei Pei/0000-0002-2648-5283
FU Non-profit Central Research Institute Fund of Chinese Academy of Medical
   Sciences [2021-JKCS-006]; CAMS Innovation Fund for Medical Sciences
   [2021-1-I2M-015]
FX This project was Supported by the Non-profit Central Research Institute
   Fund of Chinese Academy of Medical Sciences (2021-JKCS-006) and CAMS
   Innovation Fund for Medical Sciences (2021-1-I2M-015).
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NR 64
TC 4
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 SEP
PY 2022
VL 14
IS 17
AR 4067
DI 10.3390/cancers14174067
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4J1JS
UT WOS:000851027400001
PM 36077604
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Herzig, DO
   Tsikitis, VL
AF Herzig, Daniel O.
   Tsikitis, Vassiliki L.
TI Molecular Markers for Colon Diagnosis, Prognosis and Targeted Therapy
SO JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Review
DE MSI; KRAS; BRAF V600E; PI3K; TP53
ID COLORECTAL-CANCER PATIENTS; ISLAND METHYLATOR PHENOTYPE; GROWTH-FACTOR
   RECEPTOR; KIRSTEN RAS MUTATIONS; MICROSATELLITE INSTABILITY; ADJUVANT
   CHEMOTHERAPY; PLUS IRINOTECAN; PIK3CA MUTATION; POOR SURVIVAL; BRAF GENE
AB Colorectal adenocarcinoma (CRC), the second leading cancer-related death in the United States, remains a global public health issue. Sporadic CRC is considered the result of sequential mucosal changes from normal colonic mucosa to adenocarcinoma. Efforts in understanding the molecular pathways leading to CRC tumorigenesis may lead to identifying novel, individually tailored therapeutic targets for patients. In this review, we focus on well-published prognostic and predictive markers in CRC and examine their role in clinical practice. J. Surg. Oncol. 2015 111:96-102. (c) 2014 Wiley Periodicals, Inc.
C1 [Herzig, Daniel O.; Tsikitis, Vassiliki L.] Oregon Hlth & Sci Univ, Dept Surg, Portland, OR 97239 USA.
C3 Oregon Health & Science University
RP Tsikitis, VL (corresponding author), Oregon Hlth & Sci Univ, Dept Surg, Div Colorectal Surg, 3181 SW Sam Jackson Pk Rd,Mail Code L223A, Portland, OR 97239 USA.
EM tsikitis@ohsu.edu
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NR 84
TC 45
Z9 51
U1 0
U2 15
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 JAN 1
PY 2015
VL 111
IS 1
BP 96
EP 102
DI 10.1002/jso.23806
PG 7
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA AX5OF
UT WOS:000346975300014
PM 25297801
DA 2025-01-04
ER

PT J
AU Nascimento, AV
   Bousbaa, H
   Ferreira, D
   Sarmento, B
AF Nascimento, Ana Vanessa
   Bousbaa, Hassan
   Ferreira, Domingos
   Sarmento, Bruno
TI Non-Small Cell Lung Carcinoma: An Overview on Targeted Therapy
SO CURRENT DRUG TARGETS
LA English
DT Article
DE Angiogenesis; apoptosis; monoclonal antibody; non-small cell lung
   cancer; RNA interference; signal transduction; small molecules; targeted
   therapy
ID PHASE-II TRIAL; HISTONE DEACETYLASE INHIBITORS; SMALL-MOLECULE
   INHIBITORS; ADVANCED SOLID TUMORS; SHORT HAIRPIN RNA; K-RAS MUTATIONS;
   IN-VIVO; CHROMOSOMAL INSTABILITY; CANCER-THERAPY; COLORECTAL-CANCER
AB Non-small cell lung cancer (NSCLC) represents close to 90% of all lung cancers. When diagnosed, most cases are on an advanced and inoperable stage, with limited therapeutic options. Existing therapies have shown to be insufficient and novel strategies are urgently necessary. New advances in understanding the disease at cellular and molecular level however have helped researchers in devising novel strategies for therapy. These directed therapies limit cancer growth by targeting specific molecules related with tumor progression. Such strategies have shown to be more effective than chemotherapy and radiotherapy and can be complemented to existing therapeutic paradigm in augmenting beneficial outcome. Lung cancer could benefit from such innovative therapy. RNA interference (RNAi) is a sequence-specific gene silencing mechanism and, since its discovery widespread applications have pointed it as a powerful tool in cancer treatment. Several on-going clinical trials have been successfully demonstrating its potential as a novel therapeutic, including in the treatment of NSCLC. Here, we revise the recent findings concerning the therapeutic effects of molecular variations associated with NSCLC and where targeted therapies stand in its treatment, with special focus on RNAi-mediated gene silencing as a powerful strategy for NSCLC treatment.
C1 [Nascimento, Ana Vanessa; Bousbaa, Hassan; Sarmento, Bruno] Univ Porto, CESPU, IINFACTS, P-4150180 Oporto, Portugal.
   [Nascimento, Ana Vanessa; Ferreira, Domingos] Univ Porto, Fac Pharm, Lab Pharmaceut Technol, P-4150180 Oporto, Portugal.
   [Bousbaa, Hassan] Univ Porto CEQUIMED UP, Ctr Med Chem, Oporto, Portugal.
   [Sarmento, Bruno] INEB Inst Engn Biomed, Oporto, Portugal.
C3 Universidade do Porto; Universidade do Porto; Universidade do Porto;
   Universidade do Porto
RP Nascimento, AV (corresponding author), Univ Porto, INEB Inst Engn Biomed, Rua Campo Alegre 823, P-4150180 Oporto, Portugal.
EM anavanessa65@gmail.com; bruno.sarmento@ineb.up.pt
RI Nascimento, Ana/J-8819-2013; Ferreira, Domingos/M-7978-2017; Bousbaa,
   Hassan/K-5947-2019; Sarmento, Bruno/J-6265-2013
OI Nascimento, Ana/0000-0001-6828-1628; Ferreira,
   Domingos/0000-0001-6200-7169; Bousbaa, Hassan/0000-0002-4006-5779;
   Sarmento, Bruno/0000-0001-5763-7553
FU Fundacao para a Ciencia e a Tecnologia (FCT), Portugal
   [SFRH/BD/69271/2010]; CESPU - Cooperativa de Ensino Superior Politecnico
   e Universitario [02-GCQF-CICS-2011N]; Fundação para a Ciência e a
   Tecnologia [SFRH/BD/69271/2010] Funding Source: FCT
FX Ana Vanessa Nascimento gratefully acknowledges Fundacao para a Ciencia e
   a Tecnologia (FCT), Portugal for financial support (grant
   SFRH/BD/69271/2010). This work was supported by a grant
   (02-GCQF-CICS-2011N) from CESPU - Cooperativa de Ensino Superior
   Politecnico e Universitario to Bruno Sarmento.
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NR 181
TC 32
Z9 37
U1 0
U2 8
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1389-4501
EI 1873-5592
J9 CURR DRUG TARGETS
JI Curr. Drug Targets
PY 2015
VL 16
IS 13
BP 1448
EP 1463
DI 10.2174/1389450115666140528151649
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CV8HE
UT WOS:000364522400005
PM 24875380
DA 2025-01-04
ER

PT J
AU Jiang, YL
   Zhao, MY
   Tang, WX
   Zheng, XP
AF Jiang, Yunlin
   Zhao, Mingye
   Tang, Wenxi
   Zheng, Xueping
TI Impacts of systemic treatments on health-related quality of life for
   patients with metastatic colorectal cancer: a systematic review and
   network meta-analysis
SO BMC CANCER
LA English
DT Review
DE Metastatic colorectal cancer; Health-related quality of life; Network
   meta-analysis; Systematic review; Treatment selection
ID RANDOMIZED PHASE-II; CETUXIMAB PLUS IRINOTECAN; KRAS WILD-TYPE;
   CLINICAL-TRIALS; DOUBLE-BLIND; EUROPEAN ORGANIZATION; 1ST-LINE
   TREATMENT; OPEN-LABEL; RAS MUTATIONS; FLUOROURACIL
AB Objective There is limited evidence of comparative results among different treatments regarding impacts of Health-Related Quality of Life (HRQoL) for patients with metastatic colorectal cancer (mCRC). We aimed to compare efficacy of systemic treatments on HRQoL among patients with mCRC.
   Methods We collected randomized controlled trials (RCTs) reported in English up until July 2023, from databases including PubMed, Embase, Cochrane Library, ClinicalTrials.gov, and prominent conference databases, for this Bayesian network meta-analysis. Phase 2 or 3 trials that evaluated at least two therapeutic regimens were included. Primary outcomes were short-term and long-term mean changes in EORTC QLQ-C30 global health status/quality of life (GHS/QoL) scores. Secondary outcome was mean change in EQ-5D health utility scores. Mean differences (MDs) with 95% confidence intervals (CIs) were used as effect size. Subgroup analysis was performed based on whether patients received systemic treatments before. We conducted various sensitivity analyses, including differentiating between chemotherapy types, and analyzed patient cohorts with non-specified gene expression levels as well as those with target KRAS expression statuses. The current systematic review protocol was registered on PROSPERO (CRD42023453315 and CRD42023420498).
   Results Immunotherapy and targeted therapy significantly improved HRQoL over chemotherapy, with MDs of 9.27 (95% CI: 3.96 to 14.6) and 4.04 (95% CI: 0.11 to 7.94), respectively. Monotherapy significantly outperformed both combination therapy (MD 5.71, 95%CI 0.78 to 10.63) and no active treatment (MD 3.7, 95%CI 1.41 to 6.01) regarding GHS/QoL in the short-term. Combining targeted therapy with chemotherapy did not improve HRQoL. Focusing on HRQoL, cetuximab excelled when gene expression baselines were unspecified. Subgroup and sensitivity analyses upheld these robust findings, unaffected by model or patient baseline characteristics. Evidence from clinical trials without specific gene level data suggested that monotherapies, especially targeted therapies such as cetuximab, demonstrated superiority in HRQoL. For KRAS wild-type patients, no significant HRQoL differences emerged between chemotherapy, targeted therapy, or their combination.
   Conclusions Targeted therapies and immunotherapy demonstrate superior HRQoL benefits, monotherapy such as cetuximab is associated with significant improvements as compared to combination therapy. However, tailoring these results to individual gene expression profiles requires more evidence.
C1 [Jiang, Yunlin; Zheng, Xueping] Nanjing Univ Chinese Med, Nanjing Hosp Chinese Med, Nanjing, Peoples R China.
   [Jiang, Yunlin] Nanjing Univ Chinese Med, Nanjing, Peoples R China.
   [Zhao, Mingye; Tang, Wenxi] China Pharmaceut Univ, Sch Int Pharmaceut Business, Ctr Pharmacoecon & Outcomes Res, Nanjing, Jiangsu, Peoples R China.
   [Zhao, Mingye; Tang, Wenxi] China Pharmaceut Univ, Sch Int Pharmaceut Business, Dept Publ Affairs Management, Nanjing, Jiangsu, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University of Chinese
   Medicine; China Pharmaceutical University; China Pharmaceutical
   University
RP Zheng, XP (corresponding author), Nanjing Univ Chinese Med, Nanjing Hosp Chinese Med, Nanjing, Peoples R China.; Tang, WX (corresponding author), China Pharmaceut Univ, Sch Int Pharmaceut Business, Ctr Pharmacoecon & Outcomes Res, Nanjing, Jiangsu, Peoples R China.; Tang, WX (corresponding author), China Pharmaceut Univ, Sch Int Pharmaceut Business, Dept Publ Affairs Management, Nanjing, Jiangsu, Peoples R China.
EM tokammy@cpu.edu.cn; zhengxp@njucm.edu.cn
FU General Program of National Natural Science Foundation of China
   [72174207]
FX This work was supported by the General Program of National Natural
   Science Foundation of China (grant no. 72174207).
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NR 78
TC 5
Z9 5
U1 4
U2 8
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD FEB 9
PY 2024
VL 24
IS 1
AR 188
DI 10.1186/s12885-024-11937-z
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HQ3T2
UT WOS:001160940400003
PM 38336718
OA gold
DA 2025-01-04
ER

PT J
AU Beck, M
   Etienne-Selloum, N
AF Beck, Marine
   Etienne-Selloum, Nelly
TI Management of colorectal cancer
SO ACTUALITES PHARMACEUTIQUES
LA English
DT Article
DE colorectal cancer; cytotoxic chemotherapy; fluoropyrimidine; targeted
   therapy
AB Early management of colorectal cancer, through surgery and, if necessary, radiotherapy and/or drug treatment, guarantees a good prognosis, hence the importance of early detection. At an advanced stage, particularly metastatic, the use of a predominantly drug-based strategy is inevitable. The main anti-cancer drugs that can be used are cytotoxics, including fluoropyrimidines, and targeted therapies that mainly inhibit the EGFR/RAS/B-RAF pathway or angiogenesis. (c) 2023 Elsevier Masson SAS. All rights reserved
C1 [Beck, Marine; Etienne-Selloum, Nelly] Inst cancerol Strasbourg Europe, Serv Pharm, 17 rue Albert Calmette, F-67200 Strasbourg, France.
   [Etienne-Selloum, Nelly] Fac Pharm, UMR CNRS 7021, Lab Bioimagerie & pathol, 74 route Rhin, F-67400 Illkirch Graffenstaden, France.
C3 Universites de Strasbourg Etablissements Associes; Universite de
   Strasbourg
RP Etienne-Selloum, N (corresponding author), Inst cancerol Strasbourg Europe, Serv Pharm, 17 rue Albert Calmette, F-67200 Strasbourg, France.; Etienne-Selloum, N (corresponding author), Fac Pharm, UMR CNRS 7021, Lab Bioimagerie & pathol, 74 route Rhin, F-67400 Illkirch Graffenstaden, France.
EM nelly.etienne-selloum@unistra.fr
CR Institut national du cancer, PAN CANC FRANC ED 20
   Institut national du cancer, DEP CANC COL FORM PH
   legifrance.gouv, AV REL AV 21 CONV NA
   Societe francaise de pharmacie oncologique, ONC FICH VID AID BON
   Societe nationale francaise de gastro-enterologie, THES NAT CANC DIG TN
NR 5
TC 0
Z9 0
U1 1
U2 3
PU ELSEVIER MASSON, CORP OFF
PI PARIS
PA 65 CAMILLE DESMOULINS CS50083 ISSY-LES-MOULINEAUX, 92442 PARIS, FRANCE
SN 0515-3700
J9 ACTUAL PHARMACEUT
JI Actual. Pharm.
PD APR
PY 2023
VL 62
IS 625
BP 25
EP 29
DI 10.1016/j.actpha.2023.02.012
EA MAR 2023
PG 5
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA I9ES3
UT WOS:001005745500001
OA Bronze
DA 2025-01-04
ER

PT J
AU Hao, YB
   Shan, GY
   Nan, KJ
AF Hao, Yibin
   Shan, Guoyong
   Nan, Kejun
TI RETRACTED: Establishment of apoptotic regulatory network for genetic
   markers of colorectal cancer (Withdrawn Publication)
SO SAUDI JOURNAL OF BIOLOGICAL SCIENCES
LA English
DT Article; Retracted Publication
DE Colorectal cancer; Genetic marker; Meta analysis; GO analysis; KEGG
   analysis
ID CARCINOEMBRYONIC ANTIGEN; UP-REGULATION; WWOX GENE; EXPRESSION; P53
AB Our purpose is to screen out genetic markers applicable to early diagnosis for colorectal cancer and to establish apoptotic regulatory network model for colorectal cancer, thereby providing theoretical evidence and targeted therapy for early diagnosis of colorectal cancer. Taking databases including CNKI, VIP, Wanfang data, Pub Med, and MEDLINE as main sources of literature retrieval, literatures associated with genetic markers applied to early diagnosis of colorectal cancer were searched to perform comprehensive and quantitative analysis by Meta analysis, hence screening genetic markers used in early diagnosis of colorectal cancer. Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were employed to establish apoptotic regulatory network model based on screened genetic markers, and then verification experiment was conducted. Through Meta analysis, seven genetic markers were screened out, including WWOX, K-ras, COX-2, p53, APC, DCC and PTEN, among which DCC shows highest diagnostic efficiency. GO analysis of genetic markers found that six genetic markers played role in biological process, molecular function and cellular component. It was indicated in apoptotic regulatory network built by KEGG analysis and verification experiment that WWOX could promote tumor cell apoptotic in colorectal cancer and elevate expression level of p53. The apoptotic regulatory model of colorectal cancer established in this study provides clinically theoretical evidence and targeted therapy for early diagnosis of colorectal cancer. (C) 2017 The Authors. Production and hosting by Elsevier B.V. on behalf of King Saud University.
C1 [Hao, Yibin; Nan, Kejun] Xi An Jiao Tong Univ, Dept Oncol, Affiliated Hosp 1, Xian 710077, Peoples R China.
   [Hao, Yibin; Shan, Guoyong] Peoples Hosp Zhengzhou, Dept Oncol Radiotherapy, Zhengzhou 450003, Peoples R China.
C3 Xi'an Jiaotong University
RP Nan, KJ (corresponding author), Xi An Jiao Tong Univ, Dept Oncol, Affiliated Hosp 1, Xian 710077, Peoples R China.
EM nankejun2013@yeah.net
FU National Key Technology RD Program [2016YFC1303200]
FX The authors acknowledge the financial support from the National Key
   Technology R&D Program (Grant: 2016YFC1303200).
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NR 68
TC 2
Z9 2
U1 0
U2 5
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1319-562X
EI 2213-7106
J9 SAUDI J BIOL SCI
JI Saudi J. Biol. Sci.
PD MAR
PY 2017
VL 24
IS 3
BP 466
EP 476
DI 10.1016/j.sjbs.2017.01.014
PG 11
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA EW4MF
UT WOS:000402474900003
PM 28386169
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Goldstein, DA
   Shaib, WL
   Flowers, CR
AF Goldstein, Daniel A.
   Shaib, Walid L.
   Flowers, Christopher R.
TI Costs and Effectiveness of Genomic Testing in the Management of
   Colorectal Cancer
SO ONCOLOGY-NEW YORK
LA English
DT Article
ID DIPHOSPHATE GLUCURONOSYLTRANSFERASE 1A1; FLUOROURACIL DOSE ADJUSTMENT;
   PHASE-III TRIAL; 1ST-LINE TREATMENT; UDP-GLUCURONOSYLTRANSFERASE;
   ADJUVANT CHEMOTHERAPY; MICROSATELLITE INSTABILITY; PERSONALIZED
   MEDICINE; SEVERE NEUTROPENIA; GENETIC-VARIANTS
AB Numerous genomic tests are available for use in colorectal cancer, with a widely variable evidence base for their effectiveness and cost-effectiveness. In this review, we highlight many of these tests, with a focus on their proposed role, the evidence base to support that role, and the associated costs and risks. The tests with the strongest evidence base are KRAS genetic testing in the metastatic setting and microsatellite instability testing in selected patients and in stage II disease. There also may be a role for delineating recurrence-risk signatures for selected patients with stage II disease. The evidence to support broad utilization of uridine 5'-diphospho-glucuronosyltransferase 1A1 (UGT1A1) and dihydropyrimidine dehydrogenase (DPD) testing to guide irinotecan and fluorouracil dosing remains limited.There is much anticipation that next-generation sequencing will herald a new era of targeted therapy for patients with colorectal cancer; however, currently there are no data to support the introduction of widespread testing.
C1 [Goldstein, Daniel A.; Shaib, Walid L.; Flowers, Christopher R.] Emory Univ, Winship Canc Inst, Dept Hematol & Med Oncol, Atlanta, GA 30322 USA.
C3 Emory University
RP Goldstein, DA (corresponding author), Emory Univ, Winship Canc Inst, Dept Hematol & Med Oncol, Atlanta, GA 30322 USA.
RI Flowers, Christopher/F-1953-2010
OI Goldstein, Daniel/0000-0002-8082-9622
FU Abb Vie; Acerta; Celgene; Gilead Sciences; Infinity Pharmaceuticals;
   Janssen; Millennium/Takeda; Onyx Pharmaceuticals; Pharmacyclics;
   Spectrum
FX Dr. Flowers is an unpaid consultant for Genentech and Millennium/Takeda.
   He also consults for Celgene, Seattle Genetics, OptumRx, Prescription
   Solutions, and Clinical Care Options. He reports research support from
   Abb Vie, Acerta, Celgene, Gilead Sciences, Infinity Pharmaceuticals,
   Janssen, Millennium/Takeda, Onyx Pharmaceuticals, Pharmacyclics, and
   Spectrum. Dr. Goldstein and Dr. Shaib have no significant financial
   interest or other relationship with the manufacturers of any products or
   providers of any service mentioned in this article.
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NR 72
TC 18
Z9 18
U1 0
U2 8
PU UBM MEDICA
PI NORWALK
PA 535 CONNECTICUT AVE, STE 300, NORWALK, CT 06854 USA
SN 0890-9091
J9 ONCOLOGY-NY
JI Oncology-NY
PD MAR
PY 2015
VL 29
IS 3
BP 175
EP 183
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CE0HM
UT WOS:000351485100004
PM 25783977
DA 2025-01-04
ER

PT J
AU Zheng, Y
   Zhou, J
   Tong, Y
AF Zheng, Y.
   Zhou, J.
   Tong, Y.
TI Gene signatures of drug resistance predict patient survival in
   colorectal cancer
SO PHARMACOGENOMICS JOURNAL
LA English
DT Article
ID COLON-CANCER; BREAST-CANCER; TARGETED THERAPY; EXPRESSION; CELLS;
   CHEMOTHERAPY; STRATEGIES; PATHWAY; IDENTIFICATION; DETERMINANTS
AB Different combinations of 5-fluorouracil (5-FU), oxaliplatin, irinotecan and other newly developed agents have been used to treat colorectal cancer. Despite the advent of new treatment regimens, the 5-year survival rate for metastatic colorectal cancer remains low (similar to 10%). Knowing the drug sensitivity of a given tumor for a particular agent could significantly impact decision making and treatment planning. Biomarkers are proven to be successful in characterizing patients into different response groups. Using survival prediction analysis, we have identified three independent gene signatures, which are associated with sensitivity of colorectal cancer cells to 5-FU, oxaliplatin or irinotecan. On the basis of the three gene signatures, three score systems were developed to stratify patients from sensitive to resistance. These score systems exhibited robustness in stratify patients in two independent clinical studies. Patients with high scores in all three drugs exhibited the lowest survival.
C1 [Zheng, Y.; Tong, Y.] Univ Calif Los Angeles, Sch Med, Cedars Sinai Med Ctr, Dept Med, Los Angeles, CA 90048 USA.
   [Zheng, Y.] Sun Yat Sen Univ, Ctr Canc, State Key Lab Oncol South China, Collaborat Innovat Ctr Canc Med, Guangzhou 510275, Guangdong, Peoples R China.
   [Zhou, J.] Univ Arizona, Coll Publ Hlth, Div Epidemiol & Biostat, Tucson, AZ USA.
   [Tong, Y.] Xinxiang Med Univ, Dept Pathol, Xinxiang, Peoples R China.
C3 Cedars Sinai Medical Center; University of California System; University
   of California Los Angeles; University of California Los Angeles Medical
   Center; David Geffen School of Medicine at UCLA; Sun Yat Sen University;
   State Key Lab Oncology South China; University of Arizona; Xinxiang
   Medical University
RP Tong, Y (corresponding author), Univ Calif Los Angeles, Sch Med, Cedars Sinai Med Ctr, Dept Med, Room 3021,8700 Beverly Blvd, Los Angeles, CA 90048 USA.
EM tongy@cshs.org
OI zheng, yun/0000-0001-6717-3959
FU National Cancer Institute of the National Institutes of Health
   [R00CA138914]; National Natural Science Foundation [81372216]
FX This manuscript is supported by the National Cancer Institute of the
   National Institutes of Health under award number R00CA138914 (YT) and
   National Natural Science Foundation under grant number 81372216 (YT).
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NR 46
TC 52
Z9 54
U1 0
U2 12
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1470-269X
EI 1473-1150
J9 PHARMACOGENOMICS J
JI Pharmacogenomics J.
PD APR
PY 2015
VL 15
IS 2
BP 135
EP 143
DI 10.1038/tpj.2014.45
PG 9
WC Genetics & Heredity; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Pharmacology & Pharmacy
GA CE4DE
UT WOS:000351780200004
PM 25179828
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Kumai, T
   Oikawa, K
   Aoki, N
   Kimura, S
   Harabuchi, Y
   Kobayashi, H
AF Kumai, Takumi
   Oikawa, Kensuke
   Aoki, Naoko
   Kimura, Shoji
   Harabuchi, Yasuaki
   Kobayashi, Hiroya
TI Assessment of the change in cetuximab-induced antibody-dependent
   cellular cytotoxicity activity of natural killer cells by steroid
SO HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND
   NECK
LA English
DT Article
DE cetuximab; steroid; antibody-dependent cellular cytotoxicity (ADCC);
   natural killer (NK) cells; head and neck squamous cell carcinoma (HNSCC)
ID LUNG-CANCER; NECK-CANCER; PHASE-II; T-CELLS; HEAD; THERAPY; ACTIVATION;
   CARCINOMA; ANTIGEN; GLUCOCORTICOIDS
AB BackgroundEpidermal growth factor receptor (EGFR)-targeted therapy has been widely accepted as a promising treatment for solid tumors. Steroid treatment is used to prevent adverse effect of anti-EGFR antibody; however, influence of steroids in the antitumor activity of targeted antibody remains poorly understood. Herein, we demonstrated the impact of steroids in induced antibody-dependent cellular cytotoxicity (ADCC) activity of natural killer (NK) cells by cetuximab.
   MethodsVarious numbers of NK cells from healthy donors were co-cultured with tumor and/or cetuximab with or without dexamethasone. After incubation, NK cells, ADCC activity, survival, and activation markers expression were determined.
   ResultsClinical concentration of dexamethasone treatment clearly inhibited cetuximab-induced ADCC activity of NK cells against head and neck squamous cell carcinoma (HNSCC) and colon cancer. Dexamethasone decreased the activation marker CD69 expression on NK cells.
   ConclusionThis is the first report that shows the negative affect of steroids in cancer treatment using therapeutic antibody. Attention needs to be paid for using steroids in tumor treatment. (c) 2015 Wiley Periodicals, Inc. Head Neck 38: 410-416, 2016
C1 [Kumai, Takumi; Oikawa, Kensuke; Aoki, Naoko; Kimura, Shoji; Kobayashi, Hiroya] Asahikawa Med Univ, Dept Pathol, Midorigaoka Higashi 2-1-1-1, Asahikawa, Hokkaido 0788510, Japan.
   [Kumai, Takumi; Harabuchi, Yasuaki] Asahikawa Med Univ, Dept Otolaryngol Head & Neck Surg, Asahikawa, Hokkaido 0788510, Japan.
C3 Asahikawa Medical College; Asahikawa Medical College
RP Kumai, T (corresponding author), Asahikawa Med Univ, Dept Pathol, Midorigaoka Higashi 2-1-1-1, Asahikawa, Hokkaido 0788510, Japan.
EM t-kumai@asahikawa-med.ac.jp
RI kumai, takumi/JAX-8625-2023
FU JSPS KAKENHI [24791735]; Grants-in-Aid for Scientific Research
   [25460430, 24791735] Funding Source: KAKEN
FX Contract grant sponsor: JSPS KAKENHI; contract grant number: 24791735
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PY 2016
VL 38
IS 3
BP 410
EP 416
DI 10.1002/hed.23906
PG 7
WC Otorhinolaryngology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Otorhinolaryngology; Surgery
GA DD8OV
UT WOS:000370187400016
PM 25352398
DA 2025-01-04
ER

PT J
AU Mazumder, A
   Cerella, C
   Diederich, M
AF Mazumder, Aloran
   Cerella, Claudia
   Diederich, Marc
TI Natural scaffolds in anticancer therapy and precision medicine
SO BIOTECHNOLOGY ADVANCES
LA English
DT Review
DE Natural compounds; Chemotherapy; Targeted therapy; Precision medicine
ID NF-KAPPA-B; CELL-CYCLE ARREST; ACUTE MYELOID-LEUKEMIA; COLON-CANCER
   CELLS; INCREASES HISTONE ACETYLATION; RESISTANT PROSTATE-CANCER;
   CARCINOMA A431 CELLS; RNA HELICASE EIF4A; I CLINICAL-TRIAL; CARDIAC
   GLYCOSIDE
AB The diversity of natural compounds is essential for their mechanism of action. The source, structures and structure activity relationship of natural compounds contributed to the development of new classes of chemotherapy agents for over 40 years. The availability of combinatorial chemistry and high-throughput screening has fueled the challenge to identify novel compounds that mimic natures chemistry and to predict their macromolecular targets. Combining conventional and targeted therapies helped to successfully overcome drug resistance and prolong disease-free survival. Here, we aim to provide an overview of preclinical investigated natural compounds alone and in combination to further improve personalization of cancer treatment.
C1 [Mazumder, Aloran; Diederich, Marc] Seoul Natl Univ, Dept Pharm, Coll Pharm, Seoul 151742, South Korea.
   [Cerella, Claudia] Hop Kirchberg, Lab Biol Mol & Cellulaire Canc, 9 Rue Edward Steichen, L-2540 Luxembourg, Luxembourg.
C3 Seoul National University (SNU)
RP Diederich, M (corresponding author), Seoul Natl Univ, Dept Pharm, Coll Pharm, Seoul 08826, South Korea.
EM marcdiederich@snu.ac.kr
RI Diederich, Marc/O-7335-2015
OI Diederich, Marc/0000-0003-0115-4725
FU Brain Korea (BK21) PLUS program; Waxweiler grant for cancer prevention
   research from the Action Lions Vaincre le Cancer; BK21; National
   Research Foundation; MEST of Korea for Tumor Microenvironment Global
   Core Research Center [2011-0030001]; Creative-Pioneering Researchers
   Program through Seoul National University (SNU) [370C-20160062];
   Recherches Scientifiques Luxembourg (RSL)
FX AM was supported by the Brain Korea (BK21) PLUS program and Recherches
   Scientifiques Luxembourg (RSL). CC was supported by a Waxweiler grant
   for cancer prevention research from the Action Lions Vaincre le Cancer,
   and by BK21. MD's research at SNU is supported by the National Research
   Foundation, by the MEST of Korea for Tumor Microenvironment Global Core
   Research Center grant number 2011-0030001, by the Creative-Pioneering
   Researchers Program through Seoul National University (SNU) (Funding
   Number 370C-20160062), and by BK21. LBMCC thanks the Recherche Cancer et
   Sang foundation, the RSL association, the Een Haerz fir kriibskrank
   Kanner association, the Action LIONS Vaincre le Cancer association, and
   Televie Luxembourg.
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NR 203
TC 36
Z9 38
U1 1
U2 40
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0734-9750
EI 1873-1899
J9 BIOTECHNOL ADV
JI Biotechnol. Adv.
PD NOV 1
PY 2018
VL 36
IS 6
SI SI
BP 1563
EP 1585
DI 10.1016/j.biotechadv.2018.04.009
PG 23
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA GS4YB
UT WOS:000443662700002
PM 29729870
DA 2025-01-04
ER

PT J
AU Bteich, F
   Mohammadi, M
   Li, T
   Bhat, MA
   Sofianidi, A
   Wei, N
   Kuang, CY
AF Bteich, Fernand
   Mohammadi, Mahshid
   Li, Terence
   Bhat, Muzaffer Ahmed
   Sofianidi, Amalia
   Wei, Ning
   Kuang, Chaoyuan
TI Targeting KRAS in Colorectal Cancer: A Bench to Bedside Review
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colorectal cancer; KRAS; cancer therapeutics; targeted therapy
ID CELL LUNG-CANCER; ENHANCES ANTITUMOR EFFICACY; ONCOGENIC KRAS; PHASE-II;
   INHIBITOR TRAMETINIB; THERAPEUTIC STRATEGY; ACQUIRED-RESISTANCE;
   GENE-MUTATIONS; RAS MUTATIONS; AMG 510
AB Colorectal cancer (CRC) is a heterogeneous disease with a myriad of alterations at the cellular and molecular levels. Kristen rat sarcoma (KRAS) mutations occur in up to 40% of CRCs and serve as both a prognostic and predictive biomarker. Oncogenic mutations in the KRAS protein affect cellular proliferation and survival, leading to tumorigenesis through RAS/MAPK pathways. Until recently, only indirect targeting of the pathway had been investigated. There are now several KRAS allele-specific inhibitors in late-phase clinical trials, and many newer agents and targeting strategies undergoing preclinical and early-phase clinical testing. The adequate treatment of KRAS-mutated CRC will inevitably involve combination therapies due to the existence of robust adaptive resistance mechanisms in these tumors. In this article, we review the most recent understanding and findings related to targeting KRAS mutations in CRC, mechanisms of resistance to KRAS inhibitors, as well as evolving treatment strategies for KRAS-mutated CRC patients.
C1 [Bteich, Fernand; Kuang, Chaoyuan] Montefiore Med Ctr, Dept Med Oncol, Bronx, NY 10467 USA.
   [Bteich, Fernand; Mohammadi, Mahshid; Li, Terence; Bhat, Muzaffer Ahmed; Wei, Ning; Kuang, Chaoyuan] Albert Einstein Coll Med, Dept Med Oncol, Bronx, NY 10461 USA.
   [Mohammadi, Mahshid; Li, Terence; Bhat, Muzaffer Ahmed; Wei, Ning; Kuang, Chaoyuan] Albert Einstein Coll Med, Dept Mol Pharmacol, Bronx, NY 10461 USA.
   [Sofianidi, Amalia] Natl & Kapodistrian Univ Athens, Sotiria Gen Hosp Chest Dis, Dept Internal Med 3, Oncol Unit, Athens 11527, Greece.
C3 Montefiore Medical Center; Albert Einstein College of Medicine; Yeshiva
   University; Montefiore Medical Center; Albert Einstein College of
   Medicine; Yeshiva University; Montefiore Medical Center; Albert Einstein
   College of Medicine; National & Kapodistrian University of Athens
RP Kuang, CY (corresponding author), Montefiore Med Ctr, Dept Med Oncol, Bronx, NY 10467 USA.; Kuang, CY (corresponding author), Albert Einstein Coll Med, Dept Med Oncol, Bronx, NY 10461 USA.; Kuang, CY (corresponding author), Albert Einstein Coll Med, Dept Mol Pharmacol, Bronx, NY 10461 USA.
EM fbteich@montefiore.org; mahshid.mohammadi@einsteinmed.edu;
   terence.li@einsteinmed.edu; muzaffer.bhat@einsteinmed.edu;
   amalia.sofianidi@einsteinmed.edu; ning.wei@einsteinmed.edu;
   chaoyuan.kuang@einsteinmed.edu
RI Kuang, Chaoyuan/LTZ-6797-2024; Bteich, Fernand/JLM-1751-2023; WEI,
   NING/AAF-8368-2020
OI Kuang, Chaoyuan/0000-0002-8984-3906; Sofianidi,
   Amalia/0009-0005-9882-9478; WEI, NING/0000-0003-2723-4061
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NR 158
TC 10
Z9 10
U1 4
U2 13
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD AUG
PY 2023
VL 24
IS 15
AR 12030
DI 10.3390/ijms241512030
PG 24
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA O7LI9
UT WOS:001045577600001
PM 37569406
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Han, T
   Tong, J
   Wang, MX
   Gan, Y
   Gao, B
   Chen, JX
   Liu, YX
   Hao, Q
   Zhou, X
AF Han, Tao
   Tong, Jing
   Wang, Mengxin
   Gan, Yu
   Gao, Bo
   Chen, Jiaxiang
   Liu, Youxun
   Hao, Qian
   Zhou, Xiang
TI Olaparib Induces RPL5/RPL11-Dependent p53 Activation <i>via</i>
   Nucleolar Stress
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE p53; ribosomal protein (RP); nucleolar (ribosomal) stress; MDM2; PARP
   inhibitior
ID BRCA2 MUTATIONS; PARP INHIBITORS; DNA-REPAIR; PROTEIN; BREAST; L5
AB The poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi) Olaparib is a widely used targeted therapy for a variety of solid tumors with homologous recombination deficiency (HRD) caused by mutation of BRCA1/2 or other DNA repair genes. The anti-tumor activity of Olaparib has been largely attributed to its ability to inhibit PARP enzymes and block DNA single-strand break (SSB) repair, which eventually leads to the most detrimental DNA damage, double-strand breaks (DSB), in HRD cells. Although PARPi was found to induce p53-dependent cell death, the underlying molecular mechanism remains incompletely understood. Here, we report that Olaparib treatment leads to p53 stabilization and activation of its downstream target genes in a dose- and time-dependent manner. Mechanistically, Olaparib triggers nucleolar stress by inhibiting biosynthesis of the precursor of ribosomal RNAs (pre-rRNA), resulting in enhanced interaction between ribosomal proteins (RPs), RPL5 and RPL11, and MDM2. Consistently, knockdown of RPL5 and RPL11 prevents Olaparib-induced p53 activation. More importantly, Olaparib efficiently suppresses breast and colorectal cancer cell survival and proliferation through activation of p53. Altogether, our study demonstrates that Olaparib activates the nucleolar stress-RPs-p53 pathway, suggesting rRNA biogenesis as a novel target for PARPi.
C1 [Han, Tao; Wang, Mengxin; Liu, Youxun] Xinxiang Med Univ, Sch Basic Med Sci, Xinxiang, Peoples R China.
   [Tong, Jing; Gao, Bo; Hao, Qian; Zhou, Xiang] Fudan Univ, Shanghai Canc Ctr, Shanghai, Peoples R China.
   [Tong, Jing; Hao, Qian; Zhou, Xiang] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.
   [Gan, Yu; Chen, Jiaxiang] Nanchang Univ, Med Coll, Dept Physiol, Nanchang, Peoples R China.
   [Zhou, Xiang] Fudan Univ, Shanghai Canc Ctr, Key Lab Breast Canc Shanghai, Shanghai, Peoples R China.
   [Zhou, Xiang] Fudan Univ, Inst Biomed Sci, Shanghai Key Lab Med Epigenet, Int Colab Med Epigenet & Metab, Shanghai, Peoples R China.
C3 Xinxiang Medical University; Fudan University; Fudan University;
   Nanchang University; Fudan University; Fudan University
RP Hao, Q; Zhou, X (corresponding author), Fudan Univ, Shanghai Canc Ctr, Shanghai, Peoples R China.; Hao, Q; Zhou, X (corresponding author), Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai, Peoples R China.; Zhou, X (corresponding author), Fudan Univ, Shanghai Canc Ctr, Key Lab Breast Canc Shanghai, Shanghai, Peoples R China.; Zhou, X (corresponding author), Fudan Univ, Inst Biomed Sci, Shanghai Key Lab Med Epigenet, Int Colab Med Epigenet & Metab, Shanghai, Peoples R China.
EM haoqian@fudan.edu.cn; xiangzhou@fudan.edu.cn
RI gao, bo/HHC-7855-2022; Zhou, Xiang/J-5046-2017
OI Zhou, Xiang/0000-0002-1172-7948
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NR 51
TC 5
Z9 6
U1 1
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 JUN 3
PY 2022
VL 12
AR 821366
DI 10.3389/fonc.2022.821366
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2F2MU
UT WOS:000812748500001
PM 35719981
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Gaggianesi, M
   Di Franco, S
   Pantina, VD
   Porcelli, G
   D'Accardo, C
   Verona, F
   Veschi, V
   Colarossi, L
   Faldetta, N
   Pistone, G
   Bongiorno, MR
   Todaro, M
   Stassi, G
AF Gaggianesi, Miriam
   Di Franco, Simone
   Pantina, Vincenzo Davide
   Porcelli, Gaetana
   D'Accardo, Caterina
   Verona, Francesco
   Veschi, Veronica
   Colarossi, Lorenzo
   Faldetta, Naida
   Pistone, Giuseppe
   Bongiorno, Maria Rita
   Todaro, Matilde
   Stassi, Giorgio
TI Messing Up the Cancer Stem Cell Chemoresistance Mechanisms Supported by
   Tumor Microenvironment
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE cancer stem cells; tumor microenvironment; anticancer drugs;
   chemoresistance; targeted therapy
ID ACUTE MYELOID-LEUKEMIA; DNA-REPAIR GENES; COLORECTAL-CANCER; INITIATING
   CELLS; SELF-RENEWAL; ANTIANGIOGENIC THERAPY; MESENCHYMAL TRANSITION;
   MEDIATES RESISTANCE; INDUCED APOPTOSIS; THYROID-CANCER
AB Despite the recent advances in cancer patient management and in the development of targeted therapies, systemic chemotherapy is currently used as a first-line treatment for many cancer types. After an initial partial response, patients become refractory to standard therapy fostering rapid tumor progression. Compelling evidence highlights that the resistance to chemotherapeutic regimens is a peculiarity of a subpopulation of cancer cells within tumor mass, known as cancer stem cells (CSCs). This cellular compartment is endowed with tumor-initiating and metastasis formation capabilities. CSC chemoresistance is sustained by a plethora of grow factors and cytokines released by neighboring tumor microenvironment (TME), which is mainly composed by adipocytes, cancer-associated fibroblasts (CAFs), immune and endothelial cells. TME strengthens CSC refractoriness to standard and targeted therapies by enhancing survival signaling pathways, DNA repair machinery, expression of drug efflux transporters and antiapoptotic proteins. In the last years many efforts have been made to understand CSC-TME crosstalk and develop therapeutic strategy halting this interplay. Here, we report the combinatorial approaches, which perturb the interaction network between CSCs and the different component of TME.
C1 [Gaggianesi, Miriam; Di Franco, Simone; Pantina, Vincenzo Davide; Veschi, Veronica; Stassi, Giorgio] Univ Palermo, Dept Surg Oncol & Stomatol Sci DICHIRONS, Palermo, Italy.
   [Porcelli, Gaetana; D'Accardo, Caterina; Verona, Francesco; Pistone, Giuseppe; Bongiorno, Maria Rita; Todaro, Matilde] Univ Palermo, Dept Hlth Promot Sci Internal Med & Med Specialti, Palermo, Italy.
   [Colarossi, Lorenzo] Mediterranean Inst Oncol, Pathol Unit, Catania, Italy.
   [Faldetta, Naida] Villa Sofia Cervello Hosp, Dept Surg, Palermo, Italy.
C3 University of Palermo; University of Palermo; Mediterranean Institute of
   Oncology
RP Stassi, G (corresponding author), Univ Palermo, Dept Surg Oncol & Stomatol Sci DICHIRONS, Palermo, Italy.
EM giongio.stassi@unipa.it
RI Stassi, Giorgio/JAZ-0703-2023; Veschi, Veronica/K-4143-2018; D'Accardo,
   Caterina/IAQ-6545-2023; di franco, simone/M-3714-2019; GAGGIANESI,
   Miriam/IAQ-6692-2023; Porcelli, Gaetana/IAQ-6506-2023
OI D'Accardo, Caterina/0000-0003-1171-8678; Verona,
   Francesco/0000-0001-6226-4624; Pantina, Vincenzo
   Davide/0000-0003-1144-0434; Stassi, Giorgio/0000-0002-1016-9059; di
   franco, simone/0000-0002-6217-2161; Veschi,
   Veronica/0000-0002-6379-7366; GAGGIANESI, Miriam/0000-0002-7810-856X;
   Porcelli, Gaetana/0000-0002-7991-407X
FU AIRC [21492]; AIRC IG [21445]; PRIN [2017WNKSLR]
FX This work was supported by grants from AIRC (21492) to MT and AIRC IG
   (21445) and PRIN (2017WNKSLR) to GS.
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NR 280
TC 25
Z9 26
U1 2
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JUL 20
PY 2021
VL 11
AR 702642
DI 10.3389/fonc.2021.702642
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 6I1RY
UT WOS:000885909200001
PM 34354950
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Mancinelli, R
   Mammola, CL
   Sferra, R
   Pompili, S
   Vetuschi, A
   Pannarale, L
AF Mancinelli, Romina
   Mammola, Caterina Loredana
   Sferra, Roberta
   Pompili, Simona
   Vetuschi, Antonella
   Pannarale, Luigi
TI Role of the Angiogenic Factors in Cholangiocarcinoma
SO APPLIED SCIENCES-BASEL
LA English
DT Review
DE biliary epithelium; cholangiocarcinoma; angiogenic factors; VEGF
ID ENDOTHELIAL GROWTH-FACTOR; PRIMARY SCLEROSING CHOLANGITIS;
   COLORECTAL-CANCER; CHOLANGIOCELLULAR CARCINOMA;
   FUNCTIONAL-HETEROGENEITY; THERAPEUTIC TARGETS; PROGNOSTIC-FACTORS;
   SIGNALING PATHWAY; FACTOR EXPRESSION; CHOLESTATIC RATS
AB Angiogenesis plays a fundamental role in tumor growth and progression. It is regulated by several growth factors, including vascular endothelial growth factor protein family (VEGF) and its receptors, which are probably the most important factors responsible for the development of new vessels. The VEGF family includes several members: VEGF-A, VEGF-B, VEGF-C, VEGF-D, VEGF-E, placental growth factor (PlGF), and their receptors VEGFR-1, VEGFR-2 and VEGFR-3. Other relevant factors are represented by angiopoietins, thrombospondin-1, and endothelins. However, since the therapeutic benefit associated with VEGF-targeted therapy is really complex, a better understanding of these pathways will lead to future advances in the use of these agents for clinic management of tumors. Here we present a review regarding the role of angiogenic factors in cholangiocarcinoma, which arise from cholangiocytes, the epithelial cells of bile ducts. They are rare and aggressive neoplasms with a poor prognosis and limited treatment options, classified as intrahepatic, perihilar, and distal cholangiocarcinoma based on their anatomical location. Therefore, the identification of specific signaling pathways or new tumor biomarkers is crucial in order to develop more effective anti-angiogenic therapies.
C1 [Mancinelli, Romina; Mammola, Caterina Loredana; Pannarale, Luigi] Sapienza Univ Rome, Dept Anat Histol Forens Med & Orthoped Sci, I-00161 Rome, Italy.
   [Sferra, Roberta; Pompili, Simona; Vetuschi, Antonella] Univ Aquila, Dept Biotechnol & Appl Clin Sci, I-67100 Coppito, AQ, Italy.
C3 Sapienza University Rome; University of L'Aquila
RP Mancinelli, R (corresponding author), Sapienza Univ Rome, Dept Anat Histol Forens Med & Orthoped Sci, I-00161 Rome, Italy.
EM romina.mancinelli@uniroma1.it; caterinaloredana.mammola@uniroma1.it;
   roberta.sferra@univaq.it; pompili.simona@virgilio.it;
   antonella.vetuschi@univaq.it; luigi.pannarale@uniroma1.it
RI Pompili, Simona/AAL-2988-2021; Mancinelli, Romina/Y-4540-2018
OI Sferra, Roberta/0000-0003-3893-8320; Mancinelli,
   Romina/0000-0003-2040-0581
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NR 108
TC 8
Z9 9
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-3417
J9 APPL SCI-BASEL
JI Appl. Sci.-Basel
PD APR 1
PY 2019
VL 9
IS 7
AR 1393
DI 10.3390/app9071393
PG 17
WC Chemistry, Multidisciplinary; Engineering, Multidisciplinary; Materials
   Science, Multidisciplinary; Physics, Applied
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Engineering; Materials Science; Physics
GA HW2VN
UT WOS:000466547500128
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Uozumi, R
   Hamada, C
AF Uozumi, Ryuji
   Hamada, Chikuma
TI Interim decision-making strategies in adaptive designs for population
   selection using time-to-event endpoints
SO JOURNAL OF BIOPHARMACEUTICAL STATISTICS
LA English
DT Article
DE Adaptive design; interim decision-making; population selection;
   post-progression survival; semi-competing risks; time-to-event endpoints
ID PROGRESSION-FREE SURVIVAL; IMPROVED BONFERRONI PROCEDURE;
   CLINICAL-TRIALS; SUBGROUP SELECTION; COLORECTAL-CANCER; RISKS DATA;
   PACLITAXEL; ONCOLOGY; BENEFIT; MODEL
AB Adaptive designs in oncology clinical trials with interim analyses for population selection could be used in the development of targeted therapies if a predefined biomarker hypothesis exists. In this article, we consider an interim analysis using overall survival (OS), progression-free survival (PFS), and both OS and PFS, to determine whether the whole population or only the biomarker-positive population should continue into the subsequent stage of the trial, whereas the final decision is made based on OS data only. In order to increase the probability of selecting the most appropriate population at the interim analysis, we propose an interim decision-making strategy in adaptive designs with correlated endpoints considering the post-progression survival (PPS) magnitudes. In our approach, the interim decision is made on the basis of predictive power by incorporating information on OS as well as PFS to supplement the incomplete OS data. Simulation studies assuming a targeted therapy demonstrated that our interim decision-making procedure performs well in terms of selecting the proper population, especially under a scenario in which PPS affects the correlation between OS and PFS.
C1 [Uozumi, Ryuji] Kyoto Univ, Grad Sch Med, Dept Biomedicai Stat & Bioinformat, Kyoto, Japan.
   [Hamada, Chikuma] Tokyo Univ Sci, Grad Sch Engn, Dept Management Sci, Tokyo, Japan.
C3 Kyoto University; Tokyo University of Science
RP Uozumi, R (corresponding author), Kyoto Univ, Grad Sch Med, Dept Biomed Stat & Bioinformat, Sakyo Ku, 54 Kawahara Cho, Kyoto 6068507, Japan.
EM uozumi@kuhp.kyoto-u.ac.jp
OI Uozumi, Ryuji/0000-0002-9546-9869
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NR 34
TC 9
Z9 9
U1 0
U2 5
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1054-3406
EI 1520-5711
J9 J BIOPHARM STAT
JI J. Biopharm. Stat.
PY 2017
VL 27
IS 1
BP 84
EP 100
DI 10.1080/10543406.2016.1148714
PG 17
WC Pharmacology & Pharmacy; Statistics & Probability
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy; Mathematics
GA EO2VW
UT WOS:000396555100007
PM 26881477
DA 2025-01-04
ER

PT J
AU Giammona, A
   Mangiapane, LR
   Di Franco, S
   Benfante, A
   Todaro, M
   Stassi, G
AF Giammona, Alessandro
   Mangiapane, Laura Rosa
   Di Franco, Simone
   Benfante, Antonina
   Todaro, Matilde
   Stassi, Giorgio
TI Innovative Therapeutic Strategies Targeting Colorectal Cancer Stem Cells
SO CURRENT COLORECTAL CANCER REPORTS
LA English
DT Article
DE Cancer stem cells; EMT; Multidrug resistance; Oxidative phosphorylation;
   Target therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; TGF-BETA PATHWAY;
   ALDEHYDE-DEHYDROGENASE; DRUG-RESISTANCE; ACQUIRED-RESISTANCE; REDOX
   REGULATION; EMT; THERAPIES; CD44; EGFR
AB Colorectal cancer is the fourth most common cause of cancer-related death. Although many advances in the treatment of this disease have been made, a large number of patients develop metastasis and resistance to current therapies. The current evidence indicates that cancer stem cells (CSCs) and epithelial-to-mesenchymal transition (EMT) have crucial roles in colorectal carcinogenesis and metastasis. It is also very important to understand the mechanisms that allow the survival of CSCs, such as metabolic reprogramming, which permits them to obtain specific properties or the activation of alternative signaling pathways in response to first-line therapies. In this review, we discuss the failure of conventional therapies for colorectal cancer and provide a brief analysis of new therapeutic strategies for targeting non-responsive CSC. We highlight the use of combination therapies, such as horizontal or vertical targeting, as the most efficient strategy for eradicating these subpopulations of cancer cells.
C1 [Giammona, Alessandro; Mangiapane, Laura Rosa; Di Franco, Simone; Benfante, Antonina; Stassi, Giorgio] Univ Palermo, Dept Surg & Oncol Sci, Cellular & Mol Pathophysiol Lab, Via Vespro 131, I-90127 Palermo, Italy.
   [Todaro, Matilde] Univ Palermo, Cent Lab Adv Diag & Biomed Res CLADIBIOR, Via Vespro 131, I-90127 Palermo, Italy.
   [Todaro, Matilde] Univ Palermo, DiBiMIS, Piazza Clin 2, I-90127 Palermo, Italy.
C3 University of Palermo; University of Palermo; University of Palermo
RP Stassi, G (corresponding author), Univ Palermo, Dept Surg & Oncol Sci, Cellular & Mol Pathophysiol Lab, Via Vespro 131, I-90127 Palermo, Italy.
EM giorgio.stassi@unipa.it
RI Mangiapane, Laura'Rosa/LQL-1966-2024; Stassi, Giorgio/JAZ-0703-2023;
   todaro, matilde/K-9523-2016; Di Franco, Simone/AAD-4391-2019; di franco,
   simone/M-3714-2019
OI giammona, alessandro/0000-0002-5978-2241; Mangiapane, Laura
   Rosa/0000-0003-4186-0157; Stassi, Giorgio/0000-0002-1016-9059; di
   franco, simone/0000-0002-6217-2161
FU ssociazione Italiana per la Ricerca sul Cancro (AIRC) [AIRC IG 16746,
   MoH RF-2011-02349126, AIRC IG 14415]; AIRC fellowship; Fondazione
   Veronesi PostDoctoral fellowship
FX This work was supported by the Associazione Italiana per la Ricerca sul
   Cancro (AIRC) to G.S.(AIRC IG 16746 and MoH RF-2011-02349126) and
   M.T.(AIRC IG 14415). S.D.F.is an AIRC fellowship recipient for 2016 and
   a Fondazione Veronesi PostDoctoral fellowship recipient for 2017.
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NR 115
TC 1
Z9 1
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1556-3790
EI 1556-3804
J9 CURR COLORECT CANC R
JI Curr. Colorectal Cancer Rep.
PD APR
PY 2017
VL 13
IS 2
BP 91
EP 100
DI 10.1007/s11888-017-0353-x
PG 10
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA EY9BR
UT WOS:000404294600001
DA 2025-01-04
ER

PT J
AU Reissig, TM
   Ladigan-Badura, S
   Steinberg, A
   Maghnouj, A
   Li, T
   Verdoodt, B
   Liffers, ST
   Pohl, M
   Wolters, H
   Teschendorf, C
   Viebahn, R
   Admard, J
   Casadei, N
   Tannapfel, A
   Schmiegel, W
   Hahn, SA
   Vangala, DB
AF Reissig, Timm M.
   Ladigan-Badura, Swetlana
   Steinberg, Anja
   Maghnouj, Abdelouahid
   Li, Ting
   Verdoodt, Berlinda
   Liffers, Sven T.
   Pohl, Michael
   Wolters, Heiner
   Teschendorf, Christian
   Viebahn, Richard
   Admard, Jakob
   Casadei, Nicolas
   Tannapfel, Andrea
   Schmiegel, Wolff
   Hahn, Stephan A.
   Vangala, Deepak B.
TI Lasting response by vertical inhibition with cetuximab and trametinib in
   <i>KRAS</i>-mutated colorectal cancer patient-derived xenografts
SO MOLECULAR ONCOLOGY
LA English
DT Article
DE CRC; EGFR; MEK; PDX; resistance; targeted therapy
ID FOLFIRI PLUS BEVACIZUMAB; ACQUIRED-RESISTANCE; ANTITUMOR EFFICACY;
   GENOMIC LANDSCAPE; OPEN-LABEL; ACTIVATION; SELUMETINIB; IRINOTECAN;
   MUTATIONS; DISCOVERY
AB Although approximately half of all metastatic colorectal cancers (mCRCs) harbour mutations in KRAS or NRAS, hardly any progress has been made regarding targeted treatment for this group over the last few years. Here, we investigated the efficacy of vertical inhibition of the RAS-pathway by targeting epidermal growth factor receptor (EGFR) and mitogen-activated protein kinase kinase (MEK) in patient-derived xenograft (PDX) tumours with primary KRAS mutation. In total, 19 different PDX models comprising 127 tumours were tested. Responses were evaluated according to baseline tumour volume changes and graded as partial response (PR; <= - 30%), stable disease (SD; between -30% and +20%) or progressive disease (PD; >= + 20%). Vertical inhibition with trametinib and cetuximab induced SD or PR in 74% of analysed models, compared to 24% by monotherapy with trametinib. In cases of PR by vertical inhibition (47%), responses were lasting (as long as day 137), with a low incidence of secondary resistance (SR). Molecular analyses revealed that primary and SR was driven by transcriptional reprogramming activating the RAS pathway in a substantial fraction of tumours. Together, these preclinical data strongly support the translation of this combination therapy into clinical trials for CRC patients.
C1 [Reissig, Timm M.; Ladigan-Badura, Swetlana; Steinberg, Anja; Maghnouj, Abdelouahid; Li, Ting; Hahn, Stephan A.; Vangala, Deepak B.] Ruhr Univ Bochum, Fac Med, Dept Mol GI Oncol, Bochum, Germany.
   [Reissig, Timm M.] Univ Hosp Essen, West German Canc Ctr, Dept Med Oncol, Essen, Germany.
   [Reissig, Timm M.; Liffers, Sven T.] Univ Duisburg Essen, Univ Hosp Essen, Bridge Inst Expt Tumor Therapy, West German Canc Ctr, Duisburg, Germany.
   [Ladigan-Badura, Swetlana; Pohl, Michael; Schmiegel, Wolff; Vangala, Deepak B.] Ruhr Univ Bochum, Univ Hosp Knappschaftskrankenhaus, Ctr Hematooncol Dis, Bochum, Germany.
   [Verdoodt, Berlinda; Liffers, Sven T.; Tannapfel, Andrea] Ruhr Univ Bochum, Inst Pathol, Bochum, Germany.
   [Wolters, Heiner; Teschendorf, Christian] St Josef Hosp, Dept Visceral & Gen Surg, Dortmund, Germany.
   [Viebahn, Richard] Ruhr Univ Bochum, Univ Hosp Knappschaftskrankenhaus, Dept Visceral & Gen Surg, Bochum, Germany.
   [Admard, Jakob; Casadei, Nicolas] Univ Tubingen, Inst Med Genet & Appl Genom, Tubingen, Germany.
   [Vangala, Deepak B.] Ruhr Univ Bochum, Univ Hosp Knappschaftskrankenhaus, Dept Hematol & Oncol, D-44892 Bochum, Germany.
   [Hahn, Stephan A.] Ruhr Univ Bochum, Ctr Clin Res, Univ Str 150, D-44801 Bochum, Germany.
C3 Ruhr University Bochum; University of Duisburg Essen; University of
   Duisburg Essen; Ruhr University Bochum; Ruhr University Bochum; Ruhr
   University Bochum; Eberhard Karls University of Tubingen; Ruhr
   University Bochum; Ruhr University Bochum
RP Vangala, DB (corresponding author), Ruhr Univ Bochum, Univ Hosp Knappschaftskrankenhaus, Dept Hematol & Oncol, D-44892 Bochum, Germany.; Hahn, SA (corresponding author), Ruhr Univ Bochum, Ctr Clin Res, Univ Str 150, D-44801 Bochum, Germany.
EM stephan.hahn@rub.de; deepak.vangala@rub.de
RI Vangala, Deepak/HHS-5988-2022; Casadei, Nicolas/H-3283-2019; Hahn,
   Stephan/E-3880-2010
OI Admard, Jakob/0000-0003-0466-582X; Reissig, Timm/0000-0002-9955-5991;
   Hahn, Stephan/0000-0003-0855-9741
FU German Cancer Aid to Andrea Tannapfel; Wolff Schmiegel and Stephan A.
   Hahn [70111971]; Ministry of Science, North Rhine Westphalia, Germany
   (PURE/PRODI); Heinrich und Alma Vogelsang Stiftung; Projekt DEAL
FX We thank Silvia Lyer, Britta Redeker and Matthias Becker for excellent
   technical support. Furthermore we thank Christopher Schroeder and Huu
   Phuc Nguyen for establishing the contact to Tuebingen University. This
   work was thankfully supported by a grant from the German Cancer Aid to
   Andrea Tannapfel, Wolff Schmiegel and Stephan A. Hahn (70111971) and by
   a grant of the Ministry of Science, North Rhine Westphalia, Germany
   (PURE/PRODI) to Wolff Schmiegel. Timm M. Reissig gratefully received a
   grant by the Heinrich und Alma Vogelsang Stiftung. The graphical
   abstract was created with . Open Access funding enabled and organized by
   Projekt DEAL.
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NR 51
TC 4
Z9 4
U1 0
U2 3
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 NOV
PY 2023
VL 17
IS 11
BP 2396
EP 2414
DI 10.1002/1878-0261.13510
EA SEP 2023
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA X2KM7
UT WOS:001061094300001
PM 37604687
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Goto, N
   Ueo, T
   Fukuda, A
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   Sakai, Y
   Miyoshi, H
   Taketo, MM
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AF Goto, Norihiro
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   Fukuda, Akihisa
   Kawada, Kenji
   Sakai, Yoshiharu
   Miyoshi, Hiroyuki
   Taketo, Makoto Mark
   Chiba, Tsutomu
   Seno, Hiroshi
TI Distinct Roles of HES1 in Normal Stem Cells and Tumor Stem-like Cells of
   the Intestine
SO CANCER RESEARCH
LA English
DT Article
ID CRE-MEDIATED RECOMBINATION; MOUSE SMALL-INTESTINE; COLORECTAL-CANCER;
   COLON-CANCER; IN-VITRO; NOTCH; CRYPT; PROGENITORS; IDENTIFICATION;
   PROLIFERATION
AB Cancer stem cells (CSC) have attracted attention as therapeutic targets; however, CSC-targeting therapy may disrupt normal tissue homeostasis because many CSC molecules are also expressed by normal stem cells (NSC). Here, we demonstrate that NSC-specific and CSC-specific roles of the stem cell transcription factor Hes1 in the intestine enable the feasibility of a specific cancer therapy. Hes1 expression was upregulated in NSCs and intestinal tumors. Lineage-tracing experiments in adult mouse intestine revealed that Hes1 deletion in Lgr5(+) or Bmi1(+) NSCs resulted in loss of self-renewal but did not perturb homeostasis. Furthermore, in Lgr5(+) NSC, deletion of Hes1 and beta-catenin stabilization limited tumor formation and prolonged host survival. Notably, in Lgr5(+) or Dclk1(+) tumor stem cells derived from established intestinal tumors, Hes1 deletion triggered immediate apoptosis, reducing tumor burden. Our results show how Hes1 plays different roles in NSCs and CSCs, in which Hes1 disruption leads to tumor regression without perturbing normal stem cell homeostasis, preclinically validating Hes1 as a cancer therapeutic target. (C) 2017 AACR.
C1 [Goto, Norihiro; Ueo, Taro; Fukuda, Akihisa; Chiba, Tsutomu; Seno, Hiroshi] Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Sakyo Ku, Kyoto, Japan.
   [Kawada, Kenji; Sakai, Yoshiharu] Kyoto Univ, Grad Sch Med, Dept Surg, Sakyo Ku, Kyoto, Japan.
   [Miyoshi, Hiroyuki; Taketo, Makoto Mark] Kyoto Univ, Grad Sch Med, Dept Pharmacol, Sakyo Ku, Kyoto, Japan.
C3 Kyoto University; Kyoto University; Kyoto University
RP Seno, H (corresponding author), Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Sakyo Ku, Kyoto, Japan.; Seno, H (corresponding author), Kyoto Univ, Grad Sch Med, Sakyo Ku, 54 Kawara Cho, Kyoto 6068507, Japan.
EM seno@kuhp.kyoto-u.ac.jp
RI Goto, Norihiro/LXB-2981-2024
OI Seno, Hiroshi/0000-0002-8509-8128; Miyoshi, Hiroyuki/0000-0001-7400-0714
FU KAKENHI [25112707, 26293173, 15J03212, 16K09394, 16K15216, 16K15427];
   Project for Development of Innovative Research on Cancer Therapeutics
   (P-Direct) from the Ministry of Education, Culture, Sports, Science, and
   Technology; Japan Society for the Promotion of Science; Health Labour
   Sciences Research Grants from the Ministry of Health, Labour, and
   Welfare; Kobayashi Foundation for Cancer Research; Naito Foundation;
   Princess Takamatsu Cancer Research Fund [13-24514]; Mochida Foundation;
   Japanese Society of Gastroenterology; Grants-in-Aid for Scientific
   Research [16K15427, 15J03212, 26293173, 16K09394, 16K15216, 17H04157,
   25112707] Funding Source: KAKEN
FX This work was supported in part by Grants-in-Aid KAKENHI (25112707,
   26293173, 15J03212, 16K09394, 16K15216, and 16K15427) and a research
   program of the Project for Development of Innovative Research on Cancer
   Therapeutics (P-Direct) from the Ministry of Education, Culture, Sports,
   Science, and Technology, and the Japan Society for the Promotion of
   Science. This work was also supported by Health Labour Sciences Research
   Grants from the Ministry of Health, Labour, and Welfare (the development
   of innovative therapeutic drug for the intractable inflammatory bowel
   disease), the Kobayashi Foundation for Cancer Research, the Naito
   Foundation, Princess Takamatsu Cancer Research Fund13-24514, the Mochida
   Foundation, and the Japanese Society of Gastroenterology.
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NR 41
TC 22
Z9 24
U1 1
U2 12
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 2017
VL 77
IS 13
BP 3442
EP 3454
DI 10.1158/0008-5472.CAN-16-3192
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EZ4YM
UT WOS:000404718400007
PM 28536281
OA Bronze, Green Submitted
DA 2025-01-04
ER

PT J
AU Hanovich, E
   Asmis, T
   Ong, M
   Stewart, D
AF Hanovich, Ekaterina
   Asmis, Tim
   Ong, Michael
   Stewart, David
TI Rechallenge Strategy in Cancer Therapy
SO ONCOLOGY
LA English
DT Review
DE Resistance; Progressive disease; Retreatment; Rechallenge
ID CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER; PRETREATED ADVANCED
   MELANOMA; REFRACTORY PROSTATE-CANCER; RANDOMIZED PHASE-III;
   BREAST-CANCER; INTERMITTENT CHEMOTHERAPY; PALLIATIVE CHEMOTHERAPY;
   CLINICAL-PRACTICE; SINGLE-ARM
AB Drug resistance is one of the most important factors limiting the success of systemic anticancer therapy in achieving cure or prolonged overall survival. In clinical practice, resistant disease describes cancer that is found to have progressed since the time of treatment initiation. The term "drug resistant" is often used synonymously with "progressive disease" when referring to a treated tumour. Stopping a treatment at the time of disease progression is the current dominant approach of clinical trial conduct; therefore, available data from clinical trials are routinely not able to provide any information that could challenge this concept of permanent drug resistance. However, drug rechallenge and treatment continuation beyond progression have emerged as potential strategies in the past decade, especially for molecularly targeted agents and immunotherapy. In this review we focussed on rechallenge strategies for chemotherapy, immune therapy and targeted therapy in the main types of cancer.
C1 [Hanovich, Ekaterina; Asmis, Tim; Ong, Michael; Stewart, David] Univ Ottawa, Ottawa Hosp Canc Ctr, Dept Med, Div Med Oncol, Ottawa, ON, Canada.
C3 University of Ottawa; Ottawa Hospital Research Institute
RP Hanovich, E (corresponding author), Ottawa Hosp Canc Ctr, 501 Smyth Rd, Ottawa, ON K1H 8L6, Canada.
EM ehanovich@toh.ca
RI Ong, Michael/AAS-5790-2020
OI Ong, Michael/0000-0002-0347-5541
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NR 91
TC 12
Z9 13
U1 1
U2 18
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0030-2414
EI 1423-0232
J9 ONCOLOGY-BASEL
JI Oncology
PD OCT
PY 2020
VL 98
IS 10
BP 669
EP 679
DI 10.1159/000507816
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NX9SW
UT WOS:000576042400001
PM 32599578
DA 2025-01-04
ER

PT J
AU Wang, PY
   Chan, WK
   Wang, JM
   Yang, ZX
   Wang, YW
AF Wang, Peiying
   Chan, Wing Keung
   Wang, Jiming
   Yang, Zhouxin
   Wang, Youwei
TI Role of IL-22 in intestinal microenvironment and potential targeted
   therapy through diet
SO IMMUNOLOGIC RESEARCH
LA English
DT Review
DE Innate lymphoid cells; Cytokines; Intestinal immunity; Interleukin-22
ID INNATE LYMPHOID-CELLS; INTERLEUKIN 22; COLORECTAL-CANCER; STEM-CELLS;
   BINDING-PROTEIN; HOST-DEFENSE; LIVER-INJURY; RECEPTOR; EXPRESSION;
   PROMOTES
AB IL-22 is a type 2 receptor cytokine in IL-10 family. IL-22 is usually secreted by innate and adaptive immune cells and takes its effects on non-hematopoietic cells. Through activate STAT3 pathway, IL-22 plays an important role in infection clearance and tissue regeneration, which is critical for barrier integrate and homeostasis. Abnormal activation of IL-22 signal was observed in inflammation diseases, autoimmune diseases, and cancers. We review the recent discoveries about the mechanism and regulation of IL-22 signal pathway from the perspective of intestinal micro-environment. Diet-based IL-22 target therapeutic strategies and their potential clinical significance will also be discussed.
C1 [Wang, Peiying; Wang, Youwei] Tianjin Univ, Inst Med Engn & Translat Med, 92 Weijin Rd, Tianjin 300072, Peoples R China.
   [Chan, Wing Keung] Ohio State Univ, Dept Internal Med, Div Hematol, 400 W 12th Ave, Columbus, OH 43210 USA.
   [Wang, Jiming] Tianjin Econ Technol Dev Area TEDA Hosp, 65 3rd Ave, Tianjin 300451, Peoples R China.
   [Yang, Zhouxin] Zhejiang Hosp, Dept Crit Care Med, 1229 Gudun Rd, Hangzhou 310030, Peoples R China.
C3 Tianjin University; University System of Ohio; Ohio State University
RP Wang, YW (corresponding author), Tianjin Univ, Inst Med Engn & Translat Med, 92 Weijin Rd, Tianjin 300072, Peoples R China.; Yang, ZX (corresponding author), Zhejiang Hosp, Dept Crit Care Med, 1229 Gudun Rd, Hangzhou 310030, Peoples R China.
EM yangzhouxin@hotmail.com; youwei.wang@tju.edu.cn
RI Li, Xiaoli/JVZ-4089-2024
FU National Key Research and Development Program of China [2021YFF1200800];
   Natural Science Foundation of Tianjin [21JCZDJC00430]
FX This project was supported by grants from National Key Research and
   Development Program of China (2021YFF1200800) and Natural Science
   Foundation of Tianjin (21JCZDJC00430).
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NR 90
TC 0
Z9 0
U1 3
U2 16
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0257-277X
EI 1559-0755
J9 IMMUNOL RES
JI Immunol. Res.
PD APR
PY 2023
VL 71
IS 2
BP 121
EP 129
DI 10.1007/s12026-022-09325-5
EA SEP 2022
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA C3JE7
UT WOS:000863143500001
PM 36173554
DA 2025-01-04
ER

PT J
AU Cheng, ML
   Pectasides, E
   Hanna, GJ
   Parsons, HA
   Choudhury, AD
   Oxnard, GR
AF Cheng, Michael L.
   Pectasides, Eirini
   Hanna, Glenn J.
   Parsons, Heather A.
   Choudhury, Atish D.
   Oxnard, Geoffrey R.
TI Circulating tumor DNA in advanced solid tumors: Clinical relevance and
   future directions
SO CA-A CANCER JOURNAL FOR CLINICIANS
LA English
DT Article
DE circulating tumor DNA; genomic profiling; liquid biopsy; plasma
   cell&#8208; free DNA; precision oncology
ID CELL-FREE DNA; METASTATIC COLORECTAL-CANCER; BLOOD COLLECTION TUBES;
   ACQUIRED-RESISTANCE; CLONAL HEMATOPOIESIS; LIQUID BIOPSIES; EGFR
   BLOCKADE; MUTATION ANALYSIS; TARGETED THERAPY; KRAS MUTATIONS
AB The application of genomic profiling assays using plasma circulating tumor DNA (ctDNA) is rapidly evolving in the management of patients with advanced solid tumors. Diverse plasma ctDNA technologies in both commercial and academic laboratories are in routine or emerging use. The increasing integration of such testing to inform treatment decision making by oncology clinicians has complexities and challenges but holds significant potential to substantially improve patient outcomes. In this review, the authors discuss the current role of plasma ctDNA assays in oncology care and provide an overview of ongoing research that may inform real-world clinical applications in the near future.
C1 [Cheng, Michael L.; Pectasides, Eirini; Hanna, Glenn J.; Parsons, Heather A.; Choudhury, Atish D.; Oxnard, Geoffrey R.] Harvard Med Sch, Dept Med Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA.
C3 Harvard University; Harvard Medical School; Dana-Farber Cancer Institute
RP Cheng, ML (corresponding author), Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM michael_cheng@dfci.harvard.edu
RI Oxnard, Geoffrey R./HCH-4397-2022
OI Choudhury, Atish/0000-0001-9344-6631
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NR 150
TC 122
Z9 129
U1 4
U2 36
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-9235
EI 1542-4863
J9 CA-CANCER J CLIN
JI CA-Cancer J. Clin.
PD MAR
PY 2021
VL 71
IS 2
BP 176
EP 190
DI 10.3322/caac.21650
EA NOV 2020
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QS8QZ
UT WOS:000587549800001
PM 33165928
OA gold
DA 2025-01-04
ER

PT J
AU Kim, JH
   Kim, BJ
   Jang, HJ
   Kim, HS
AF Kim, Jung Han
   Kim, Bum Jun
   Jang, Hyun Joo
   Kim, Hyeong Su
TI Comparison of the RECIST and EORTC PET criteria in the tumor response
   assessment: a pooled analysis and review
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Review
DE RECIST; EORTC criteria; PET; Tumor response
ID POSITRON-EMISSION-TOMOGRAPHY; CELL LUNG-CANCER; MALIGNANT PLEURAL
   MESOTHELIOMA; METASTATIC COLORECTAL-CANCER; FDG-PET/CT; SOLID TUMORS;
   EARLY PREDICTION; BLADDER-CANCER; CHEMOTHERAPY; PERCIST
AB The EORTC PET criteria (EORTC criteria) are used to assess metabolic tumor response in patients with solid tumors. We conducted this pooled study to compare tumor responses according to the RECIST and EORTC criteria.
   Electronic databases were searched for eligible articles with the terms of "RECIST" or "EORTC criteria". We found seven articles with the data on the comparison of tumor responses by the RECIST and EORTC criteria.
   A total of 181 patients were recruited from the seven studies. Ninety-two patients (50.8%) received cytotoxic chemotherapy and 89 were treated with targeted agents. The agreement of tumor responses between the RECIST and EORTC criteria was moderate (k = 0.493). Of 181 patients, 66 (36.5%) showed disagreement in the tumor responses: tumor response was upgraded in 54 patients and downgraded in 12 when adopting the EORTC criteria. The estimated overall response rates were significantly different between the two criteria (52.5% by the EORTC vs. 29.8% by the RECIST, P < 0.0001). When comparing the two criteria according to the anti-cancer treatments (chemotherapy or targeted therapy), the levels of agreement in tumor responses were not excellent (k = 0.461 for chemotherapy and k = 0.524 for targeted therapy, respectively) regardless of therapeutic types.
   This pooled study indicates that the concordance of tumor responses between the RECIST and EORTC criteria is not excellent. When adopting the EORTC criteria instead of the RECIST, the overall response rate was significantly increased.
C1 [Kim, Jung Han; Kim, Hyeong Su] Hallym Univ, Div Hematooncol, Dept Internal Med, Kangnam Sacred Heart Hosp,Med Ctr,Coll Med, Seoul, South Korea.
   [Kim, Bum Jun] Koran Armed Forces Capital Hosp, Dept Internal Med, Armed Forces Med Command, Sungnam, Gyeonggi Do, South Korea.
   [Jang, Hyun Joo] Hallym Univ, Div Gastroenterol, Dept Internal Med, Dongtan Sacred Heart Hosp,Med Ctr,Coll Med, Hwasung, South Korea.
C3 Hallym University; Hallym University
RP Kim, JH (corresponding author), Hallym Univ, Div Hematooncol, Dept Internal Med, Kangnam Sacred Heart Hosp,Med Ctr,Coll Med, Seoul, South Korea.; Jang, HJ (corresponding author), Hallym Univ, Div Gastroenterol, Dept Internal Med, Dongtan Sacred Heart Hosp,Med Ctr,Coll Med, Hwasung, South Korea.
EM harricil@hotmail.com; jhj1229@hallym.or.kr
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PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
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J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD OCT
PY 2017
VL 80
IS 4
BP 729
EP 735
DI 10.1007/s00280-017-3411-9
PG 7
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA FH9TS
UT WOS:000411555500008
PM 28780726
DA 2025-01-04
ER

PT J
AU Hussen, BM
   Abdullah, SR
   Mohammed, AA
   Rasul, MF
   Hussein, AM
   Eslami, S
   Glassy, MC
   Taheri, M
AF Hussen, Bashdar Mahmud
   Abdullah, Snur Rasool
   Mohammed, Abdulqahar Azizkhan
   Rasul, Mohammed Fatih
   Hussein, Ali M.
   Eslami, Solat
   Glassy, Mark C.
   Taheri, Mohammad
TI Advanced strategies of targeting circular RNAs as therapeutic approaches
   in colorectal cancer drug resistance
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Review
DE Circular RNAs (circRNAs); Colorectal cancer (CRC); Drug resistance
ID CELL-PROLIFERATION; COLON-CANCER; SIGNALING PATHWAY; NONCODING RNAS;
   METASTASIS; BIOGENESIS; CIRCRNAS; GROWTH; SIRNA; ROLES
AB Colorectal cancer (CRC) stands second in terms of mortality and third among the highest prevalent kinds of cancer globally. CRC prevalence is rising in moderately and poorly developed regions and is greater in economically advanced regions. Despite breakthroughs in targeted therapy, resistance to chemotherapeutics remains a significant challenge in the long-term management of CRC. Circular RNAs (circRNAs) have been involved in growing cancer therapy resistance, particularly in CRC, according to an increasing number of studies in recent years. CircRNAs are one of the novel subclasses of non -coding RNAs, previously thought of as viroid. According to studies, circRNAs have been recommended as biological markers for therapeutic targets and diagnostic and prognostic purposes. That is particularly notable given that the expression of circRNAs has been linked to the hallmarks of CRC since they are responsible for drug resistance in CRC patients; thereby, circRNAs are significant for chemotherapy failure. Moreover, knowledge concerning circRNAs remains relatively unclear despite using all these advanced techniques. Here, in this study, we will go over the most recent published work to highlight the critical roles of circRNAs in CRC development and drug resistance and highlight the main strategies to overcome drug resistance to improve clinical outcomes.
C1 [Hussen, Bashdar Mahmud] Cihan Univ, Coll Sci, Dept Biomed Sci, Erbil, Kurdistan, Iraq.
   [Hussen, Bashdar Mahmud; Hussein, Ali M.] Hawler Med Univ, Coll Pharm, Dept Clin Anal, Erbil, Kurdistan, Iraq.
   [Abdullah, Snur Rasool] Lebanese French Univ, Coll Hlth Sci, Dept Med Lab Sci, Erbil, Kurdistan, Iraq.
   [Mohammed, Abdulqahar Azizkhan] Hawler Med Univ, Coll Pharm, Dept Pharmacognosy, Erbil, Kurdistan, Iraq.
   [Rasul, Mohammed Fatih] Tishk Int Univ, Fac Pharm, Dept Pharmaceut Basic Sci, Erbil, Kurdistan, Iraq.
   [Eslami, Solat] Alborz Univ Med Sci, Sch Med, Dept Med Biotechnol, Karaj, Iran.
   [Eslami, Solat] Alborz Univ Med Sci, Non Communicable Dis Res Ctr, Karaj, Iran.
   [Glassy, Mark C.] Univ Calif San Diego, San Diego UCSD Moores Canc Ctr, Translat Neurooncol Lab, San Diego, CA USA.
   [Taheri, Mohammad] Jena Univ Hosp, Inst Human Genet, Jena, Germany.
C3 Cihan University-Erbil; Hawler Medical University; Hawler Medical
   University; Tishk International University; University of California
   System; University of California San Diego; Friedrich Schiller
   University of Jena
RP Taheri, M (corresponding author), Jena Univ Hosp, Inst Human Genet, Jena, Germany.
EM Mohammad.taheri@uni-jena.de
RI Rasul, Mohammed/ABT-7199-2022; Eslami, Solat/S-3127-2017; Taheri,
   Mohammad/AAC-7307-2019
OI Abdullah, Snur Rasool/0009-0001-1182-8482; Taheri,
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NR 196
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
EI 1618-0631
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD AUG
PY 2024
VL 260
AR 155402
DI 10.1016/j.prp.2024.155402
EA JUN 2024
PG 17
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA WZ9W3
UT WOS:001258825800001
PM 38885593
OA hybrid
DA 2025-01-04
ER

PT J
AU Zhao, Y
   Sun, Y
   Zhang, HY
   Liu, X
   Du, WZ
   Li, YL
   Zhang, JH
   Chen, LC
   Jiang, CL
AF Zhao, Yan
   Sun, Ying
   Zhang, Haiyan
   Liu, Xing
   Du, Wenzong
   Li, Yongli
   Zhang, Junhe
   Chen, Lingchao
   Jiang, Chuanlu
TI HGF/MET signaling promotes glioma growth via up-regulation of Cox-2
   expression and PGE2 production
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE GBMs; Cox-2; MET; PGE2
ID MET PATHWAY INHIBITION; STEM-LIKE CELLS; COLON-CANCER; CARCINOMA-CELLS;
   CARCINOGENESIS; PROLIFERATION; ACTIVATION; SURVIVAL; INVASION;
   ANGIOGENESIS
AB Cyclooxygenase2 (Cox-2) is well known for glioma growth through up-regulation of prostaglandin E2 (PGE2) levels. MET, a hepatocyte growth factor (HGF) receptor, is also frequently high expressed in glioma, which promotes glioma growth and invasion. Here, we demonstrate that HGF/MET signaling can promote PGE2 production in glioma cells via Cox-2 up-regulation. RNA inhibition of MET suggested that MET signaling is essential for Cox-2 up-regulation. Moreover, HGF could enhance Cox-2 expression and PGE2 release. Knockdown of Cox-2 inhibited growth-promoting effects of HGF, suggesting that HGF/MET functioned via Cox-2/PGE2 pathway. Therefore, our work reveals a critical relationship of Cox-2/PGE2 and HGF/MET signaling in promoting glioma cells proliferation. Further, targeting MET and Cox-2 may represent an attractive target therapy for glioma.
C1 [Zhao, Yan; Sun, Ying; Liu, Xing; Du, Wenzong; Li, Yongli; Zhang, Junhe; Chen, Lingchao; Jiang, Chuanlu] Harbin Med Univ, Affiliated Hosp 2, Dept Neurosurg, Harbin 150086, Peoples R China.
   [Chen, Lingchao] Fudan Univ, Huashan Hosp, Dept Neurosurg, Shanghai 200040, Peoples R China.
   [Zhang, Haiyan] Shanghai Jiao Tong Univ, Dept Obstet & Gynecol, Int Peace Maternal & Childrens Hosp, Shanghai 200030, Peoples R China.
C3 Harbin Medical University; Fudan University; Shanghai Jiao Tong
   University
RP Jiang, CL (corresponding author), Harbin Med Univ, Affiliated Hosp 2, Dept Neurosurg, 246 Xuefu Rd, Harbin 150086, Peoples R China.
EM chenlingchao12@sina.com; jcl6688@163.com
RI Zhang, Junhe/HII-7839-2022
FU National Natural Science Foundation of China [81402053]; China
   Postdoctoral Science Foundation [2013-M531121]; Shanghai Postdoctoral
   Science Foundation [13R21411300]; China Postdoctoral Science special
   Foundation [2014T70390]; Heilongjiang Natural Science Foundation
   [H201417]
FX This work was supported by National Natural Science Foundation of China
   (81402053), China Postdoctoral Science Foundation (2013-M531121),
   Shanghai Postdoctoral Science Foundation (13R21411300), China
   Postdoctoral Science special Foundation funded project (2014T70390).
   Heilongjiang Natural Science Foundation (H201417).
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NR 31
TC 13
Z9 15
U1 1
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 4
BP 3719
EP 3726
PG 8
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA CM5OP
UT WOS:000357737900027
PM 26097553
DA 2025-01-04
ER

PT J
AU Ji, HX
   Wang, WZ
   Li, X
   Han, XY
   Zhang, XY
   Wang, J
   Liu, CX
   Huang, LQ
   Gao, WY
AF Ji, Haixia
   Wang, Wenzhe
   Li, Xia
   Han, Xiaoying
   Zhang, Xinyu
   Wang, Juan
   Liu, Changxiao
   Huang, Luqi
   Gao, Wenyuan
TI Natural Small Molecules Enabled Efficient Immunotherapy through
   Supramolecular Self-Assembly in P53-Mutated Colorectal Cancer
SO ACS APPLIED MATERIALS & INTERFACES
LA English
DT Article
DE natural products; self-assembly; anticancer; mutant p53; innate immune
   signaling
ID P53 PATHWAY; HONOKIOL; NANOPARTICLES; DELIVERY; INHIBITION
AB Nanomedicine, constructed from therapeutics, presents an advantage in drug delivery for cancer therapies. However, nanocarrier-based treatment systems have problems such as interbatch variability, multi-component complexity, poor drug delivery, and carrier-related toxicity. To solve these issues, the natural molecule honokiol (HK), an anticancer agent in a phase I clinical trial (CTR20170822), was used to form a self-assembly nanoparticle (SA) through hydrogen bonding and hydrophobicity. The preparation of SA needs no molecular precursors or excipients in aqueous solution, and 100% drug-loaded SA exhibited superior tumor-targeting ability due to the enhanced permeability and retention (EPR) effect. Moreover, SA significantly enhanced the antitumor immunity relative to free HK, and the mechanism has notable selectivity to the p53 pathway. Furthermore, SA exhibited excellent physiological stability and inappreciable toxicity. Taken together, this supramolecular self-assembly strategy provides a safe and "molecular economy" model for rational design of clinical therapies and is expected to promote targeted therapy of HK, especially in colorectal cancer patients with obvious p53 status.
C1 [Ji, Haixia; Wang, Wenzhe; Li, Xia; Han, Xiaoying; Zhang, Xinyu; Wang, Juan; Gao, Wenyuan] Tianjin Univ, Sch Pharmaceut Sci & Technol, Tianjin 300072, Peoples R China.
   [Liu, Changxiao] Tianjin Pharmaceut Res Inst, Tianjin 300193, Peoples R China.
   [Huang, Luqi] Chinese Acad Chinese Med Sci, Natl Resource Ctr Chinese Mat Med, Beijing 100700, Peoples R China.
C3 Tianjin University; National Resource Center for Chinese Materia Medica,
   CACMS
RP Gao, WY (corresponding author), Tianjin Univ, Sch Pharmaceut Sci & Technol, Tianjin 300072, Peoples R China.; Liu, CX (corresponding author), Tianjin Pharmaceut Res Inst, Tianjin 300193, Peoples R China.; Huang, LQ (corresponding author), Chinese Acad Chinese Med Sci, Natl Resource Ctr Chinese Mat Med, Beijing 100700, Peoples R China.
EM liuchangxiao@163.com; huangluqi01@126.com; pharmgao@tju.edu.cn
RI Wang, Wenzhe/T-1427-2017; Gao, Wenyuan/K-1740-2015; JI,
   Haixia/KXN-7508-2024; Liu, Jiaye/ABE-2282-2021
OI wang, wenzhe/0000-0003-2378-0540
FU National Natural Science Foundation of China [81673535]
FX This work was supported by research funds from the National Natural
   Science Foundation of China (No. 81673535).
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NR 42
TC 21
Z9 24
U1 20
U2 121
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 JAN 19
PY 2022
VL 14
IS 2
BP 2464
EP 2477
DI 10.1021/acsami.1c16737
EA JAN 2022
PG 14
WC Nanoscience & Nanotechnology; Materials Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Materials Science
GA ZS7CG
UT WOS:000741113200001
PM 35045602
DA 2025-01-04
ER

PT J
AU Hänninen, UA
   Wirta, EV
   Katainen, R
   Tanskanen, T
   Hamberg, J
   Taipale, M
   Böhm, J
   Renkonen-Sinisalo, L
   Lepistö, A
   Forsström, LM
   Pitkänen, E
   Palin, K
   Seppälä, TT
   Mäkinen, N
   Mecklin, JP
   Aaltonen, LA
AF Hanninen, Ulrika A.
   Wirta, Erkki-Ville
   Katainen, Riku
   Tanskanen, Tomas
   Hamberg, Jiri
   Taipale, Minna
   Bohm, Jan
   Renkonen-Sinisalo, Laura
   Lepisto, Anna
   Forsstrom, Linda M.
   Pitkanen, Esa
   Palin, Kimmo
   Seppala, Toni T.
   Makinen, Netta
   Mecklin, Jukka-Pekka
   Aaltonen, Lauri A.
TI Exome and immune cell score analyses reveal great variation within
   synchronous primary colorectal cancers
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
ID MICROSATELLITE INSTABILITY; MUTATIONAL PROCESSES; COLON; IMMUNOSCORE;
   PROGNOSIS; METHYLATION; SIGNATURES; CARCINOMA; FEATURES; KRAS
AB BACKGROUND: Approximately 4% of colorectal cancer (CRC) patients have at least two simultaneous cancers in the colon. Due to the shared environment, these synchronous CRCs (SCRCs) provide a unique setting to study colorectal carcinogenesis. Understanding whether these tumours are genetically similar or distinct is essential when designing therapeutic approaches.
   METHODS: We performed exome sequencing of 47 primary cancers and corresponding normal samples from 23 patients. Additionally, we carried out a comprehensive mutational signature analysis to assess whether tumours had undergone similar mutational processes and the first immune cell score analysis (IS) of SCRC to analyse the interplay between immune cell invasion and mutation profile in both lesions of an individual.
   RESULTS: The tumour pairs shared only few mutations, favouring different mutations in known CRC genes and signalling pathways and displayed variation in their signature content. Two tumour pairs had discordant mismatch repair statuses. In majority of the pairs, IS varied between primaries. Differences were not explained by any clinicopathological variable or mutation burden.
   CONCLUSIONS: The study shows major diversity within SCRCs. Rather than rely on data from one tumour, our study highlights the need to evaluate both tumours of a synchronous pair for optimised targeted therapy.
C1 [Hanninen, Ulrika A.; Katainen, Riku; Tanskanen, Tomas; Hamberg, Jiri; Forsstrom, Linda M.; Pitkanen, Esa; Palin, Kimmo; Makinen, Netta; Aaltonen, Lauri A.] Univ Helsinki, Appl Tumor Genom Res Program, Res Programs Unit, Helsinki, Finland.
   [Hanninen, Ulrika A.; Katainen, Riku; Tanskanen, Tomas; Hamberg, Jiri; Forsstrom, Linda M.; Pitkanen, Esa; Palin, Kimmo; Makinen, Netta; Aaltonen, Lauri A.] Univ Helsinki, Dept Med & Clin Genet, Med, Helsinki, Finland.
   [Wirta, Erkki-Ville] Tampere Univ Hosp, Dept Gastroenterol & Alimentary Tract Surg, Tampere, Finland.
   [Taipale, Minna] Karolinska Inst, Dept Med Biochem & Biophys, Stockholm, Sweden.
   [Bohm, Jan] Cent Finland Cent Hosp, Dept Pathol, Jyvaskyla, Finland.
   [Renkonen-Sinisalo, Laura; Lepisto, Anna; Seppala, Toni T.] Helsinki Univ Cent Hosp, Hosp Dist Helsinki & Uusimaa, Dept Surg, Helsinki, Finland.
   [Pitkanen, Esa] European Mol Biol Unit EMBL, Genome Biol Unit, Heidelberg, Germany.
   [Mecklin, Jukka-Pekka] Cent Finland Cent Hosp, Dept Surg, Jyvaskyla, Finland.
   [Mecklin, Jukka-Pekka] Univ Jyvaskyla, Fac Sport & Hlth Sci, Jyvaskyla, Finland.
C3 University of Helsinki; University of Helsinki; Tampere University;
   Tampere University Hospital; Karolinska Institutet; Central Finland
   Central Hospital; University of Helsinki; Helsinki University Central
   Hospital; Central Finland Central Hospital; University of Jyvaskyla
RP Aaltonen, LA (corresponding author), Univ Helsinki, Appl Tumor Genom Res Program, Res Programs Unit, Helsinki, Finland.; Aaltonen, LA (corresponding author), Univ Helsinki, Dept Med & Clin Genet, Med, Helsinki, Finland.
EM lauri.aaltonen@helsinki.fi
RI Mecklin, Jukka-Pekka/AAB-5378-2020; Katainen, Riku/GYR-0921-2022; Palin,
   Kimmo/ABG-5710-2020; Aaltonen, Lauri/A-5375-2010; Pitkanen,
   Esa/H-2435-2018; Seppala, Toni/D-4518-2015
OI Lepisto, Anna Henriikka/0000-0002-5866-4059; Hanninen,
   Ulrika/0000-0003-1558-0450; Wirta, Erkki-Ville/0000-0002-2255-6136;
   Makinen, Netta/0000-0003-0104-7794; Mecklin,
   Jukka-Pekka/0000-0003-4895-2249; Aaltonen, Lauri/0000-0001-6839-4286;
   Palin, Kimmo/0000-0002-4621-6128; Katainen, Riku/0000-0003-4575-4239;
   Pitkanen, Esa/0000-0002-9818-6370; Seppala, Toni/0000-0002-4940-3498
FU Academy of Finland (Centre of Excellence in Cancer Genetics Research
   2012-2017) [250345]; Academy of Finland (Centre of Excellence in Tumor
   Genetics Research 2018-2023) [312041]; Finnish Cancer Society; Sigrid
   Juselius Foundation; Jane and Aatos Erkko Foundation; Academy of Finland
   [295693]; Ida Montin Foundation; Juhani Aho Foundation for Medical
   Research; Biomedicum Helsinki Foundation; Finnish Medical Society
   "Duodecim"; Paivikki and Sakari Sohlberg Foundation; Einar and Karin
   Stroem Foundation; Emil Aaltonen Foundation; Oskar Oflund Foundation;
   Finnish-Norwegian Medical Foundation; Gastroenterological Research
   Foundation; Maud Kuistila Memorial Foundation; K. Albin Johansson
   Foundation; Orion-Pharmos Research Foundation; Academy of Finland (AKA)
   [295693] Funding Source: Academy of Finland (AKA)
FX We thank Alison Ollikainen, Iina Vuoristo, Inga-Lill Aberg, Heikki
   Metsola, Sini Marttinen, Marjo Rajalaakso, Sirpa Soisalo, Asal Fotouhi,
   Lijuan Hu, Maarit Ahtiainen, Tommi Liipo, Kirsi Pylvanainen, and
   Marjukka Friman for excellent technical assistance. We acknowledge the
   computational resources provided by the ELIXIR node, hosted at the
   CSC-IT Center for Science, Finland. This study was supported by the
   Academy of Finland (Centre of Excellence in Cancer Genetics Research
   2012-2017 (250345), Centre of Excellence in Tumor Genetics Research
   2018-2023 (312041)), The Finnish Cancer Society, The Sigrid Juselius
   Foundation, and The Jane and Aatos Erkko Foundation. Personal grants for
   N. M. to support this work were received from the Academy of Finland
   (295693), for R. K. from The Ida Montin Foundation and The Juhani Aho
   Foundation for Medical Research, and for U. A. H. from The Biomedicum
   Helsinki Foundation, The Finnish Medical Society "Duodecim", The
   Paivikki and Sakari Sohlberg Foundation, The Ida Montin Foundation, The
   Einar and Karin Stroem Foundation, The Emil Aaltonen Foundation, The
   Oskar Oflund Foundation, The Finnish-Norwegian Medical Foundation, The
   Gastroenterological Research Foundation, The Maud Kuistila Memorial
   Foundation, The Finnish Cancer Society, The K. Albin Johansson
   Foundation, The Orion-Pharmos Research Foundation, and The Juhani Aho
   Foundation for Medical Research.
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NR 52
TC 4
Z9 4
U1 0
U2 7
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 APR 30
PY 2019
VL 120
IS 9
BP 922
EP 930
DI 10.1038/s41416-019-0427-4
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HW0SL
UT WOS:000466391900006
PM 30894686
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Thermos, G
   Kalogirou, EM
   Tosios, KI
AF Thermos, Grigorios
   Kalogirou, Eleni-Marina
   Tosios, Konstantinos I.
TI Anti-epidermal growth factor receptor targeted therapy-associated
   ulcerations
SO ORAL ONCOLOGY
LA English
DT Article
DE Epidermal growth factor receptor inhibitor; Panitumumab; Osimertinib;
   Adverse effects; Oral ulcer; Stomatitis
ID COLORECTAL-CANCER PATIENTS; STOMATITIS; INHIBITOR
AB The well-studied role of epidermal growth factor receptor (EGFR) in metastatic colorectal cancer (mCRC) and non-small cell lung cancer (NSCLC) has enabled the development of drugs that target this molecule, including panitumumab for the former and osimertinib for the latter. Oral adverse events due to those agents are rarely described in the literature and their exact characterization is hampered by inadequate reporting and/or incorrect terminology used. We report two cases of panitumumab-and osimertinib-associated oral ulcerations with emphasis on their possible pathogenesis and optimal management.
C1 [Thermos, Grigorios] 43 L Vyrona St, Lefkada 31100, Greece.
   [Kalogirou, Eleni-Marina] Metropolitan Coll, Fac Hlth & Rehabil Sci, Athens 15125, Greece.
   [Tosios, Konstantinos I.] Oral Med, 15 Gr Lambraki St, Athens 16675, Greece.
RP Thermos, G (corresponding author), 43 L Vyrona St, Lefkada 31100, Greece.
EM gthermos@dent.uoa.gr; ekalogirou@mitropolitiko.edu.gr;
   ktosios@dent.uoa.gr
RI Thermos, Grigoris/IUQ-5144-2023; Tosios, Konstantinos/AFV-9448-2022
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TC 0
Z9 0
U1 0
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PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1368-8375
EI 1879-0593
J9 ORAL ONCOL
JI Oral Oncol.
PD JAN
PY 2024
VL 148
AR 106660
DI 10.1016/j.oraloncology.2023.106660
EA DEC 2023
PG 4
WC Oncology; Dentistry, Oral Surgery & Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Dentistry, Oral Surgery & Medicine
GA ED3B1
UT WOS:001136928300001
PM 38086198
DA 2025-01-04
ER

PT J
AU Guan, XY
   Guan, XL
   Jiao, ZY
AF Guan, Xiao-ying
   Guan, Xiao-li
   Jiao, Zuo-yi
TI Improving therapeutic resistance: beginning with targeting the tumor
   microenvironment
SO JOURNAL OF CHEMOTHERAPY
LA English
DT Review
DE Tumor microenvironment; therapeutic resistance; tumor metastasis; target
   therapy; chemotherapy; immunotherapy
ID CANCER-ASSOCIATED FIBROBLASTS; CELL LUNG-CANCER; TENASCIN-C; PHASE-I;
   GLUCOSE-METABOLISM; ANTITUMOR-ACTIVITY; PANCREATIC-CANCER;
   COLORECTAL-CANCER; OXIDATIVE STRESS; HYPOXIA
AB Cancer is a serious threat to human health and life. The tumor microenvironment (TME) not only plays a key role in the occurrence, development and metastasis of cancer, but also has a profound impact on treatment resistance. To improve and solve this problem, an increasing number of strategies targeting the TME have been proposed, and great progress has been made in recent years. This article reviews the characteristics and functions of the main matrix components of the TME and the mechanisms by which each component affects drug resistance. Furthermore, this article elaborates on targeting the TME as a strategy to treat acquired drug resistance, reduce tumor metastasis, recurrence, and improve efficacy.
C1 [Guan, Xiao-ying] Lanzhou Univ, Hosp 2, Pathol Dept, Lanzhou, Gansu, Peoples R China.
   [Guan, Xiao-li] Lanzhou Univ, Hosp 2, Gen Med Dept, Lanzhou, Gansu, Peoples R China.
   [Jiao, Zuo-yi] Lanzhou Univ, Dept Gen Surg 1, Hosp 2, 82 Cuiying Gate, Lanzhou 730030, Gansu, Peoples R China.
C3 Lanzhou University; Lanzhou University; Lanzhou University
RP Jiao, ZY (corresponding author), Lanzhou Univ, Dept Gen Surg 1, Hosp 2, 82 Cuiying Gate, Lanzhou 730030, Gansu, Peoples R China.
EM jiazy@lzu.edu.cn
FU Health Industry Scientific Research Program of Gansu Province
   [GSWSKY2020-78]; Lanzhou Science and Technology Development Guiding Plan
   Project [2019-ZD-54]; Science and Technology Plan Project of Gansu
   Province [20JR5RA323]
FX This work was supported by the Health Industry Scientific Research
   Program of Gansu Province (GSWSKY2020-78), Lanzhou Science and
   Technology Development Guiding Plan Project (2019-ZD-54), Science and
   Technology Plan Project of Gansu Province (20JR5RA323).
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NR 172
TC 3
Z9 3
U1 0
U2 23
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1120-009X
EI 1973-9478
J9 J CHEMOTHERAPY
JI J. Chemother.
PD NOV 17
PY 2022
VL 34
IS 8
BP 492
EP 516
DI 10.1080/1120009X.2021.2011661
EA NOV 2021
PG 25
WC Oncology; Infectious Diseases; Pathology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Infectious Diseases; Pathology; Pharmacology & Pharmacy
GA 6O0LP
UT WOS:000728708100001
PM 34873999
DA 2025-01-04
ER

PT J
AU Meng, QH
   Zhao, J
   Yu, YY
   Wang, K
   Ren, J
   Xu, C
   Wang, YS
   Wang, GY
AF Meng, Qianhao
   Zhao, Jian
   Yu, Yuanyuan
   Wang, Ke
   Ren, Jing
   Xu, Chang
   Wang, Yusheng
   Wang, Guangyu
TI Survival comparison of first-line treatment regimens in patients with
   braf-mutated advanced colorectal cancer: a multicenter retrospective
   study
SO BMC CANCER
LA English
DT Article
DE Advanced colorectal cancer; BRAF V600E mutation; Overall survival;
   Progression-free survival
ID FOLFOXIRI PLUS BEVACIZUMAB; MICROSATELLITE INSTABILITY; SUBGROUP
   ANALYSES; MISMATCH REPAIR; POOR SURVIVAL; OPEN-LABEL; CETUXIMAB;
   MUTATIONS; COLON; KRAS
AB BackgroundPatients with V-Raf murine sarcoma viral oncogene homolog B1 (BRAF) V600E-mutated advanced colorectal cancer (CRC) have a poor prognosis, and treatment options that can improve outcome are still under investigation. The purpose of this study was to discuss the differences of overall survival (OS) and progression-free survival (PFS) between patients with BRAF V600E-mutated advanced CRC who were treated with chemotherapy alone and chemotherapy combined with targeted therapy in advanced first-line therapy.MethodsGrouping of 61 patients according to first-line treatment regimen (chemotherapy alone/chemotherapy combined with bevacizumab). Kaplan-Meier method and log-rank test were used to compare OS and PFS. Cox proportional hazards regression model was used to measure the risk of first-line medication therapies while correcting for confounding factors that may affect PFS and OS.ResultsThere was no significant difference in OS between patients treated with chemotherapy alone and those treated with chemotherapy combined with bevacizumab (P = 0.93; HR, 1.027; 95% CI, 0.555-1.901). Likewise, there was no significant difference in PFS between the two groups (P = 0.29; HR, 0.734; 95% CI, 0.413-1.304). Subgroup analysis showed that OS and PFS of different treatment regimens were not significantly different among subgroups. Multivariate analysis suggested that surgical treatment of primary tumor (P = 0.001; HR, 0.326; 95% CI, 0.169-0.631) and presence of liver metastasis (P = 0.009; HR, 2.399; 95% CI, 1.242-4.635) may serve as independent prognostic indicators in patients with BRAF-mutated advanced CRC. Surgical treatment of the primary tumor (P = 0.041; HR, 0.523; 95% CI, 0.280-0.974) was significantly associated with PFS too.ConclusionFor patients with BRAF V600E-mutated advanced CRC, chemotherapy alone did not differ significantly in OS and PFS compared with chemotherapy + bevacizumab for advanced first-line therapy. Chemotherapy combined with targeted therapy did not render a survival benefit to these patients, demonstrating that the importance of developing new treatment options for this population.
C1 [Meng, Qianhao; Yu, Yuanyuan; Wang, Ke; Ren, Jing; Xu, Chang; Wang, Guangyu] Harbin Med Univ, Canc Hosp, Dept Gastrointestinal Med Oncol, 150 Haping Rd, Harbin 150040, Peoples R China.
   [Zhao, Jian; Wang, Yusheng] Shanxi Med Univ, Shanxi Prov Canc Hosp, Shanxi Hosp, Canc Hosp,Chinese Acad Med Sci,Dept Digest, Taiyuan 030013, Shanxi, Peoples R China.
C3 Harbin Medical University; Chinese Academy of Medical Sciences - Peking
   Union Medical College; Shanxi Medical University
RP Wang, GY (corresponding author), Harbin Med Univ, Canc Hosp, Dept Gastrointestinal Med Oncol, 150 Haping Rd, Harbin 150040, Peoples R China.; Wang, YS (corresponding author), Shanxi Med Univ, Shanxi Prov Canc Hosp, Shanxi Hosp, Canc Hosp,Chinese Acad Med Sci,Dept Digest, Taiyuan 030013, Shanxi, Peoples R China.
EM wangyusheng1972@163.com; guangyuwang@hrbmu.edu.cn
RI Wang, Yusheng/AAB-6702-2020; Yu, YY/ADO-6482-2022
OI Wang, Yusheng/0000-0002-9681-2876
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NR 43
TC 3
Z9 3
U1 0
U2 3
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD FEB 27
PY 2023
VL 23
IS 1
AR 191
DI 10.1186/s12885-023-10640-9
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9K8YK
UT WOS:000941147400002
PM 36849918
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Tan, L
   Li, QS
   Peng, D
   Cheng, Y
AF Tan, Li
   Li, Qing-Shu
   Peng, Dong
   Cheng, Yong
TI Does PD-1 blockade play a decisive role in the pathological complete
   remission of unresectable MSS, BRAF V600E-mutated metastatic colorectal
   cancer: A case report
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer (CRC); programmed death-1 inhibitor (PD-1 inhibitor);
   immunotherapy; targeted therapy; microsatellite-stable (MSS); case
   report
ID INHIBITION
AB BackgroundColorectal cancer (CRC) ranks third in highest incidence among human cancers. With the continuous development of anti-cancer drugs, CRC patients are treated more and more effectively. However, the treatment of patients with unresectable metastatic CRC (mCRC) remains a core point for surgeons worldwide, especially for those with microsatellite stability (MSS) and BRAF V600E mutation, who have been reported to have the worst prognosis. Case descriptionWe report a case of pathological complete remission in a patient with unresectable MSS, BRAF V600E-mutated metastatic rectal cancer after using Vemurafenib and Cetuximab in combination with Camrelizumab. ConclusionsThis case suggested that Vemurafenib and Cetuximab combined with Camrelizumab is effective in the treatment of MSS, BRAF V600E-mutated mCRC. To benefit more patients, further studies need to be completed.
C1 [Tan, Li; Peng, Dong; Cheng, Yong] Chongqing Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Chongqing, Peoples R China.
   [Li, Qing-Shu] Chongqing Med Univ, Sch Basic Med, Dept Pathol, Chongqing, Peoples R China.
C3 Chongqing Medical University; Chongqing Medical University
RP Peng, D; Cheng, Y (corresponding author), Chongqing Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Chongqing, Peoples R China.
EM carry_dong@126.com; chengyongcq@163.com
RI wang, yi/KBB-3614-2024
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NR 20
TC 1
Z9 1
U1 1
U2 2
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JAN 13
PY 2023
VL 12
AR 976622
DI 10.3389/fonc.2022.976622
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 8D8IP
UT WOS:000918530800001
PM 36713544
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Taira, K
   Nadatani, Y
   Hirano, S
   Maeda, K
   Fujiwara, Y
AF Taira, Koichi
   Nadatani, Yuji
   Hirano, Shinji
   Maeda, Kiyoshi
   Fujiwara, Yasuhiro
TI Large Skin Ulcer and Delayed Wound Healing around a Colostomy in a
   Patient with Metastatic Colorectal Cancer Receiving Vascular Endothelial
   Growth Factor Receptor-2 Inhibitor Therapy
SO CASE REPORTS IN ONCOLOGY
LA English
DT Article
DE Colostomy; Delay wound healing; Metastatic colorectal cancer; Skin
   ulcer; Vascular endothelial growth factor receptor-2 inhibitor
ID 1ST-LINE THERAPY; BEVACIZUMAB; RAMUCIRUMAB; OXALIPLATIN; COMBINATION;
   PACLITAXEL
AB Ramucirumab is an antiangiogenic agent targeting vascular endothelial growth factor receptor (VEGF)-2 that has been approved for second-line treatment of patients with metastatic colorectal cancer. VEGF-targeted therapy has various distinctive adverse effects owing to its antitumour effects. However, little is known with regard to its skin toxicity, such as its ability to cause skin ulcers. We report a case of large skin ulceration around a colostomy and delayed healing caused by ramucirumab. A 58-year-old patient diagnosed with rectal cancer with liver and lung metastases. He was administered folinic acid, fluorouracil (5-FU), and oxaliplatin (FOLFOX) and bevacizumab as first-line treatment. A laparoscopic colostomy was performed for suspected worsening of the bowel obstruction. He was then administered folinic acid, 5 fluorouracil, and irinotecan (FOLFIRI) and ramucirumab as second-line treatment after surgery. However, dehiscence and a small skin ulceration caused by ramucirumab developed around the colostomy which increased in size and became necrotic; therefore, he was administered only FOLFIRI, without ramucirumab. The ulcer decreased in size slightly with surgical debridement and showering. He resumed FOLFIRI and ramucirumab.
C1 [Taira, Koichi; Nadatani, Yuji; Hirano, Shinji; Fujiwara, Yasuhiro] Osaka City Univ, Grad Sch Med, Dept Gastroenterol, Osaka, Osaka, Japan.
   [Maeda, Kiyoshi] Osaka City Univ, Grad Sch Med, Dept Surg Oncol, Osaka, Osaka, Japan.
C3 Osaka Metropolitan University; Osaka Metropolitan University
RP Taira, K (corresponding author), Osaka City Univ, Grad Sch Med, Dept Gastroenterol, Abeno Ku, 1-4-3 Asahimachi, Osaka, Osaka, Japan.
EM koichit@med.osaka-cu.ac.jp
RI Fujiwara, Yasuhiro/AAM-5504-2020
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NR 11
TC 5
Z9 7
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 2019
VL 12
IS 2
BP 370
EP 375
DI 10.1159/000500412
PG 6
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA IW0QM
UT WOS:000484667600005
PM 31182953
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Song, MH
   Zeng, XR
   Wu, Q
   Huang, J
   Dong, JY
   Shao, LJ
   Sun, ZH
   Lin, YG
   Chen, SZ
AF Song, Minghan
   Zeng, Xianrong
   Wu, Qian
   Huang, Jie
   Dong, Jiayi
   Shao, Lijuan
   Sun, Zihao
   Lin, Yiguang
   Chen, Size
TI Metastatic Colorectal Cancer Patient with Microsatellite Stability and
   Germline BRAC2 Mutation Shows a Complete Response to Olaparib in
   Combination with a PD-1 Inhibitor and Bevacizumab: A Case Report and
   Review of the Literature
SO LIFE-BASEL
LA English
DT Review
DE colorectal cancer; immunotherapy; PARP inhibitor; BRCA2 mutation;
   microsatellite stability; case report
ID BREAST-CANCER; IRINOTECAN; THERAPY; PATHWAY
AB Metastatic colorectal cancer (mCRC) has a poor prognosis. Combining chemotherapy with targeted therapy constitutes a basic form of mCRC treatment. Immune checkpoint inhibitors have been recommended for microsatellite instability mCRC, while most patients harboring microsatellite stability (MSS) or proficient mismatch repair (pMMR) are less responsive to immunotherapy. Combinational targeted therapy, including poly-ADP ribose polymerase (PARP) inhibitors, has been considered a promising way to reverse immunotherapy resistance; however, there is no clear and consistent conclusions can be drawn from the current research. Here, we report the case of a 59-year-old woman diagnosed with stage IVB MSS mCRC who received three courses of capecitabine/oxaliplatin chemotherapy combined with bevacizumab as a first-line treatment, resulting in an overall evaluation of stable disease (-25.7%). However, the occurrence of adverse events of intolerable grade 3 diarrhea and vomiting forced the cessation of this therapy. A germline BRCA2 mutation was found by next-generation sequencing, and the patient further received a combination of olaparib, tislelizumab, and bevacizumab. This treatment regime resulted in a complete metabolic response and a partial response (-50.9%) after 3 months of treatment. Mild asymptomatic interstitial pneumonia and manageable hematologic toxicity were two adverse events associated with this combination therapy. This study provides new insights into the combination of PARP inhibitors and immunotherapy for MSS mCRC patients carrying germline BRCA2 mutations.
C1 [Song, Minghan; Zeng, Xianrong; Wu, Qian; Dong, Jiayi; Shao, Lijuan; Sun, Zihao; Lin, Yiguang; Chen, Size] Guangdong Pharmaceut Univ, Affiliated Hosp 1, Dept Immuno Oncol, Guangzhou 510080, Peoples R China.
   [Song, Minghan; Zeng, Xianrong; Wu, Qian; Dong, Jiayi; Shao, Lijuan; Sun, Zihao; Lin, Yiguang; Chen, Size] Guangdong Pharmaceut Univ, Guangdong Prov Engn Res Ctr Esophageal Canc Precis, Guangzhou 510080, Peoples R China.
   [Song, Minghan; Zeng, Xianrong; Wu, Qian; Dong, Jiayi; Shao, Lijuan; Sun, Zihao; Lin, Yiguang; Chen, Size] Guangdong Pharmaceut Univ, Guangdong Higher Educ Inst, Key Lab Canc Immunotherapy, Guangzhou 510080, Peoples R China.
   [Huang, Jie] Jinan Univ, Affiliated Hosp 5, Dept Oncol, Heyuan 517000, Peoples R China.
   [Lin, Yiguang] Guangzhou Anjie Biomed Technol Co Ltd, Guangzhou 510530, Peoples R China.
C3 Guangdong Pharmaceutical University; Guangdong Pharmaceutical
   University; Guangdong Pharmaceutical University
RP Lin, YG; Chen, SZ (corresponding author), Guangdong Pharmaceut Univ, Affiliated Hosp 1, Dept Immuno Oncol, Guangzhou 510080, Peoples R China.; Lin, YG; Chen, SZ (corresponding author), Guangdong Pharmaceut Univ, Guangdong Prov Engn Res Ctr Esophageal Canc Precis, Guangzhou 510080, Peoples R China.; Lin, YG; Chen, SZ (corresponding author), Guangdong Pharmaceut Univ, Guangdong Higher Educ Inst, Key Lab Canc Immunotherapy, Guangzhou 510080, Peoples R China.; Lin, YG (corresponding author), Guangzhou Anjie Biomed Technol Co Ltd, Guangzhou 510530, Peoples R China.
EM smh_1997@163.com; yiguang.lin@hotmail.com; chensize@gdpu.edu.cn
RI Lin, RIchard/HZH-3370-2023; dong, jiayi/ABG-7113-2021
OI Lin, Yiguang/0000-0002-4637-9701; Sun, Zihao/0009-0000-5915-8871
FU National Natural Science Foundation of China [32271225]
FX This work was supported by a research grant from the National Natural
   Science Foundation of China (number: 32271225).
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NR 52
TC 1
Z9 1
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-1729
J9 LIFE-BASEL
JI Life-Basel
PD MAY 15
PY 2023
VL 13
IS 5
AR 1183
DI 10.3390/life13051183
PG 10
WC Biology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Microbiology
GA H6RI3
UT WOS:000997207700001
PM 37240828
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Radhakrishnan, H
   Walther, W
   Zincke, F
   Kobelt, D
   Imbastari, F
   Erdem, M
   Kortüm, B
   Dahlmann, M
   Stein, U
AF Radhakrishnan, Harikrishnan
   Walther, Wolfgang
   Zincke, Fabian
   Kobelt, Dennis
   Imbastari, Francesca
   Erdem, Muege
   Kortuem, Benedikt
   Dahlmann, Mathias
   Stein, Ulrike
TI MACC1-the first decade of a key metastasis molecule from gene discovery
   to clinical translation
SO CANCER AND METASTASIS REVIEWS
LA English
DT Review
DE MACC1; metastasis; solid cancers; biomarker; prognosis and prediction;
   targeted therapy
ID COLON-CANCER 1; EPITHELIAL-MESENCHYMAL TRANSITION; TUMOR-CELL
   PROLIFERATION; GASTRIC-CANCER; COLORECTAL-CANCER;
   HEPATOCELLULAR-CARCINOMA; TARGETING MACC1; DOWN-REGULATION;
   POOR-PROGNOSIS; BETA-CATENIN
AB Deciphering the paths to metastasis and identifying key molecules driving this process is one important issue for understanding and treatment of cancer. Such a key driver molecule is Metastasis Associated in Colon Cancer 1 (MACC1). A decade long research on this evolutionarily conserved molecule with features of a transcription factor as well as an adapter protein for versatile protein-protein interactions has shown that it has manifold properties driving tumors to their metastatic stage. MACC1 transcriptionally regulates genes involved in epithelial-mesenchymal transition (EMT), including those which are able to directly induce metastasis like c-MET, impacts tumor cell migration and invasion, and induces metastasis in solid cancers. MACC1 has proven as a valuable biomarker for prognosis of metastasis formation linked to patient survival and gives promise to also act as a predictive marker for individualized therapies in a broad variety of cancers. This review discusses the many features of MACC1 in the context of the hallmarks of cancer and the potential of this molecule as biomarker and novel therapeutic target for restriction and prevention of metastasis.
C1 [Radhakrishnan, Harikrishnan; Walther, Wolfgang; Zincke, Fabian; Kobelt, Dennis; Imbastari, Francesca; Erdem, Muege; Kortuem, Benedikt; Dahlmann, Mathias; Stein, Ulrike] Charite Univ Med Berlin, Expt & Clin Res Ctr, Robert Rossle Str 10, D-13125 Berlin, Germany.
   [Radhakrishnan, Harikrishnan; Walther, Wolfgang; Zincke, Fabian; Kobelt, Dennis; Imbastari, Francesca; Erdem, Muege; Kortuem, Benedikt; Dahlmann, Mathias; Stein, Ulrike] Max Delbruck Ctr Mol Med, Robert Rossle Str 10, D-13125 Berlin, Germany.
   [Walther, Wolfgang; Zincke, Fabian; Kobelt, Dennis; Dahlmann, Mathias; Stein, Ulrike] German Canc Res Ctr, 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; Helmholtz
   Association; German Cancer Research Center (DKFZ)
RP Stein, U (corresponding author), Charite Univ Med Berlin, Expt & Clin Res Ctr, Robert Rossle Str 10, D-13125 Berlin, Germany.; Stein, U (corresponding author), Max Delbruck Ctr Mol Med, Robert Rossle Str 10, D-13125 Berlin, Germany.; Stein, U (corresponding author), German Canc Res Ctr, German Canc Consortium DKTK, Heidelberg, Germany.
EM ustein@mdc-berlin.de
RI Radhakrishnan, Harikrishnan/GWZ-6616-2022
OI Stein, Ulrike/0000-0001-7006-282X; Kortum, Benedikt/0000-0003-3734-6665;
   Walther, Wolfgang/0000-0003-2360-1370
FU German Cancer Consortium (DKTK)
FX Work in Prof. Ulrike Stein's lab is supported by the German Cancer
   Consortium (DKTK).
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NR 157
TC 61
Z9 65
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 DEC
PY 2018
VL 37
IS 4
SI SI
BP 805
EP 820
DI 10.1007/s10555-018-9771-8
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HJ8XF
UT WOS:000457482700018
PM 30607625
DA 2025-01-04
ER

PT J
AU Jacobson, RA
   Munding, E
   Hayden, DM
   Levy, M
   Kuzel, TM
   Pappas, SG
   Masood, A
AF Jacobson, Richard A.
   Munding, Emily
   Hayden, Dana M.
   Levy, Mia
   Kuzel, Timothy M.
   Pappas, Sam G.
   Masood, Ashiq
TI Evolving Clinical Utility of Liquid Biopsy in Gastrointestinal Cancers
SO CANCERS
LA English
DT Review
DE gastrointestinal cancer; liquid biopsy; circulating tumor cell;
   circulating tumor DNA
ID CIRCULATING TUMOR-CELLS; PANCREATIC-CANCER; PERIPHERAL-BLOOD; PROGNOSTIC
   VALUE; COLORECTAL-CANCER; GASTRIC-CANCER; COLON-CANCER; PRECISION
   MEDICINE; TARGETED THERAPY; DNA ANALYSIS
AB Room for improvement exists regarding recommendations for screening, staging, therapy selection, and frequency of surveillance of gastrointestinal cancers. Screening is costly and invasive, improved staging demands increased sensitivity and specificity to better guide therapy selection. Surveillance requires increased sensitivity for earlier detection and precise management of recurrences. Peripherally collected blood-based liquid biopsies enrich and analyze circulating tumor cells and/or somatic genomic material, including circulating tumor DNA along with various subclasses of RNA. Such assays have the potential to impact clinical practice at multiple stages of management in gastrointestinal cancers. This review summarizes current basic and clinical evidence for the utilization of liquid biopsy in cancers of the esophagus, pancreas, stomach, colon, and rectum. Technical aspects of various liquid biopsy methodologies and targets are reviewed and evidence supporting current commercially available assays is examined. Finally, current clinical applicability, potential future uses, and pitfalls of applying liquid biopsy to the screening, staging and therapeutic management of these diseases are discussed.
C1 [Jacobson, Richard A.; Munding, Emily; Hayden, Dana M.; Pappas, Sam G.] Rush Univ, Dept Surg, Med Ctr, Chicago, IL 60612 USA.
   [Levy, Mia; Kuzel, Timothy M.; Masood, Ashiq] Rush Univ, Div Hematol Oncol & Cell Therapy, Med Ctr, Chicago, IL 60612 USA.
   [Levy, Mia; Kuzel, Timothy M.; Masood, Ashiq] Rush Univ, Rush Precis Oncol Program, Med Ctr, Chicago, IL 60612 USA.
C3 Rush University; Rush University; Rush University
RP Masood, A (corresponding author), Rush Univ, Div Hematol Oncol & Cell Therapy, Med Ctr, Chicago, IL 60612 USA.; Masood, A (corresponding author), Rush Univ, Rush Precis Oncol Program, Med Ctr, Chicago, IL 60612 USA.
EM ashiq_masood@rush.edu
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NR 90
TC 10
Z9 11
U1 0
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD AUG
PY 2019
VL 11
IS 8
AR 1164
DI 10.3390/cancers11081164
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IV7HU
UT WOS:000484438000124
PM 31412682
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Zhang, W
   Wu, FH
   Wang, J
   Wei, HZ
   Wang, TW
   Zhang, YC
AF Zhang, Wei
   Wu, Fa-Hong
   Wang, Jia
   Wei, Hang-Zhi
   Wang, Tian-Wei
   Zhang, You-Cheng
TI Periostin: a predictable molecule to prognosis and chemotherapy
   responses of gastrointestinal and hepato-biliary-pancreatic malignant
   tumors?
SO NEOPLASMA
LA English
DT Review
DE periostin (POSTN); microenvironment; drug resistance; prognosis marker;
   tumor
ID EPITHELIAL-MESENCHYMAL TRANSITION; CANCER-ASSOCIATED FIBROBLASTS;
   GASTRIC-CANCER; POOR-PROGNOSIS; COLON-CANCER; ESOPHAGEAL CANCER; MATRIX
   PROTEIN; UP-REGULATION; EXPRESSION; INVASION
AB With the continuous development of medical science and technology, the medical community???s understanding of the disease is constantly updated, just as strategies for treating malignant tumors are constantly updated. New diagnoses, followup indicators, and treatment plan formulations need more evidence to be supported. To date, radical surgical resection is still the preferred treatment for advanced digestive system malignancies, and combination therapy including chemotherapy and targeted therapy before or after surgery is aimed at improving the prognosis and quality of life of patients. However, if tumor recurrence, metastasis, chemotherapy, and drug resistance to targeted agents after surgery prevent the achievement of the desired therapeutic effect, and if neoadjuvant chemotherapy and targeted therapy cannot reduce the staging of the tumor, surgery cannot be performed. These are huge problems that we face now and will continue to face for some time. Relevant scientific data and evidence have been produced to explain unsatisfactory efficacy, such as epithelial-mesenchymal transformation, the tumor microenvironment, extracellular matrix proteins, cancer-related fibroblasts, and other factors that may be related to tumor progression and poor therapeutic effects. An extracellular matrix protein, periostin (POSTN), influences the above factors and has received multidisciplinary attention. In this paper, periostin and digestive system related tumors are reviewed, and the production, mechanism of action, drug resistance correlation analysis, and coping strategies of periostin are summarized to further understand its characteristics. This work provides evidence for potential therapeutic targets for digestive system tumors in the future.
C1 [Zhang, Wei; Wu, Fa-Hong; Wang, Jia; Wei, Hang-Zhi; Wang, Tian-Wei; Zhang, You-Cheng] Second Hosp Lanzhou Univ, Hepat Biliary Pancreat Inst, Dept Gen Surg, Lanzhou, Gansu, Peoples R China.
   [Zhang, Wei] Lanzhou Hosp Tradit Chinese Med, Lanzhou, Gansu, Peoples R China.
RP Zhang, YC (corresponding author), Second Hosp Lanzhou Univ, Hepat Biliary Pancreat Inst, Dept Gen Surg, Lanzhou, Gansu, Peoples R China.
EM zhangychmd@126.com
OI Wu, Fahong/0000-0001-8332-3574
FU Science and technology projects in Cheng-guan District of Lanzhou City
   [2014-4-4]; Lanzhou city science and technology development guidance
   plan [2019-ZD-71]
FX Supported by Science and technology projects in Cheng-guan District of
   Lanzhou City (2014-4-4) and Lanzhou city science and technology
   development guidance plan (No. 2019-ZD-71).
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NR 95
TC 1
Z9 1
U1 1
U2 8
PU AEPRESS SRO
PI BRATISLAVA
PA BAJZOVA 7, BRATISLAVA, 821 08, SLOVAKIA
SN 0028-2685
EI 1338-4317
J9 NEOPLASMA
JI Neoplasma
PY 2022
VL 69
IS 3
BP 491
EP 503
DI 10.4149/neo_2021_211025N1521
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2S2GW
UT WOS:000821617200001
PM 35103480
OA Bronze
DA 2025-01-04
ER

PT J
AU Mittal, P
   Roberts, CWM
AF Mittal, Priya
   Roberts, Charles W. M.
TI The SWI/SNF complex in cancer - biology, biomarkers and therapy
SO NATURE REVIEWS CLINICAL ONCOLOGY
LA English
DT Review
ID MALIGNANT RHABDOID TUMORS; SMALL-CELL CARCINOMA; ATYPICAL
   TERATOID/RHABDOID TUMORS; CHROMATIN REMODELING FACTOR; SOMATIC
   MUTATIONS; HYPERCALCEMIC TYPE; ARID1A EXPRESSION; SMALL-MOLECULE; BAF
   COMPLEXES; COLON-CANCER
AB Cancer genome-sequencing studies have revealed a remarkably high prevalence of mutations in genes encoding subunits of the SWI/SNF chromatin-remodelling complexes, with nearly 25% of all cancers harbouring aberrations in one or more of these genes. A role for such aberrations in tumorigenesis is evidenced by cancer predisposition in both carriers of germline loss-of-function mutations and genetically engineered mouse models with inactivation of any of several SWI/SNF subunits. Whereas many of the most frequently mutated oncogenes and tumour-suppressor genes have been studied for several decades, the cancer-promoting role of mutations in SWI/SNF genes has been recognized only more recently, and thus comparatively less is known about these alterations. Consequently, increasing research interest is being focused on understanding the prognostic and, in particular, the potential therapeutic implications of mutations in genes encoding SWI/SNF subunits. Herein, we review the burgeoning data on the mechanisms by which mutations affecting SWI/SNF complexes promote cancer and describe promising emerging opportunities for targeted therapy, including immunotherapy with immune-checkpoint inhibitors, presented by these mutations. We also highlight ongoing clinical trials open specifically to patients with cancers harbouring mutations in certain SWI/SNF genes.
   Mutations in genes encoding subunits of the SWI/SNF chromatin-remodelling complexes occur in almost 25% of all cancers. Herein, Mittal and Roberts discuss the mechanisms by which these mutations might promote cancer and describe the associated vulnerabilities that provide opportunities for targeted therapy or immunotherapy with immune-checkpoint inhibitors.
C1 [Mittal, Priya; Roberts, Charles W. M.] St Jude Childrens Res Hosp, Dept Oncol, 332 N Lauderdale St, Memphis, TN 38105 USA.
C3 St Jude Children's Research Hospital
RP Roberts, CWM (corresponding author), St Jude Childrens Res Hosp, Dept Oncol, 332 N Lauderdale St, Memphis, TN 38105 USA.
EM charles.roberts@stjude.org
RI Mittal, Priya/Y-7613-2019; Roberts, Charles/N-2541-2018; Mittal,
   Priya/D-7941-2019
OI Roberts, Charles/0000-0003-1135-1896; Mittal, Priya/0000-0001-6921-3934
FU NCI NIH HHS [R01 CA113794, R01 CA172152] Funding Source: Medline
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NR 175
TC 344
Z9 396
U1 6
U2 100
PU NATURE RESEARCH
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1759-4774
EI 1759-4782
J9 NAT REV CLIN ONCOL
JI Nat. Rev. Clin. Oncol.
PD JUL
PY 2020
VL 17
IS 7
BP 435
EP 448
DI 10.1038/s41571-020-0357-3
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA MA3HB
UT WOS:000541807300007
PM 32303701
OA Green Accepted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Rodrigues, D
   Longatto, A
   Martins, SF
AF Rodrigues, Daniela
   Longatto-Filho, Adhemar
   Martins, Sandra F.
TI Predictive Biomarkers in Colorectal Cancer: From the Single Therapeutic
   Target to a Plethora of Options
SO BIOMED RESEARCH INTERNATIONAL
LA English
DT Review
ID PHASE-III TRIAL; CAPECITABINE PLUS OXALIPLATIN; ENDOTHELIAL
   GROWTH-FACTOR; MESSENGER-RNA LEVELS; THYMIDYLATE SYNTHASE; 1ST-LINE
   TREATMENT; DIHYDROPYRIMIDINE DEHYDROGENASE; COLON-CANCER; ADJUVANT
   THERAPY; MICROSATELLITE-INSTABILITY
AB Colorectal cancer (CRC) is one of the most frequent cancers and is a leading cause of cancer death worldwide. Treatments used for CRC may include some combination of surgery, radiation therapy, chemotherapy, and targeted therapy. The current standard drugs used in chemotherapy are 5-fluorouracil and leucovorin in combination with irinotecan and/or oxaliplatin. Most recently, biologic agents have been proven to have therapeutic benefits in metastatic CRC alone or in association with standard chemotherapy. However, patients present different treatment responses, in terms of efficacy and toxicity; therefore, it is important to identify biological markers that can predict the response to therapy and help select patients that would benefit from specific regimens. In this paper, authors review CRC genetic markers that could be useful in predicting the sensitivity/resistance to chemotherapy.
C1 [Rodrigues, Daniela; Longatto-Filho, Adhemar; Martins, Sandra F.] Univ Minho, Life & Hlth Sci Res Inst ICVS, Sch Hlth Sci, Campus Gualtar, P-4710057 Braga, Portugal.
   [Rodrigues, Daniela; Longatto-Filho, Adhemar; Martins, Sandra F.] ICVS 3Bs PT Govt Associate Lab, Campus Gualtar, P-4710057 Braga, Portugal.
   [Longatto-Filho, Adhemar] Univ Sao Paulo, Fac Med, Lab Med Invest LIM 14, BR-01246903 Sao Paulo, SP, Brazil.
   [Longatto-Filho, Adhemar] Mol Oncol Res Ctr, BR-14784400 Barretos, SP, Brazil.
   [Martins, Sandra F.] Hosp Ctr Tras Os Montes & Alto Douro, Unidade Hosp Chaves, Dept Surg, Ave Dr Francisco Sa Carneiro, P-5400279 Chaves, Portugal.
C3 Universidade do Minho; Universidade de Sao Paulo
RP Martins, SF (corresponding author), Univ Minho, Life & Hlth Sci Res Inst ICVS, Sch Hlth Sci, Campus Gualtar, P-4710057 Braga, Portugal.; Martins, SF (corresponding author), ICVS 3Bs PT Govt Associate Lab, Campus Gualtar, P-4710057 Braga, Portugal.; Martins, SF (corresponding author), Hosp Ctr Tras Os Montes & Alto Douro, Unidade Hosp Chaves, Dept Surg, Ave Dr Francisco Sa Carneiro, P-5400279 Chaves, Portugal.
EM sandramartins@ecsaude.uminho.pt
RI Longatto-Filho, Adhemar/N-3397-2019; Martins, Sandra F/T-6543-2018;
   longatto-filho, adhemar/D-7039-2013
OI Martins, Sandra F/0000-0002-3526-3199; longatto-filho,
   adhemar/0000-0002-5779-9752
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NR 90
TC 22
Z9 24
U1 0
U2 3
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2314-6133
EI 2314-6141
J9 BIOMED RES INT
JI Biomed Res. Int.
PY 2016
VL 2016
AR 6896024
DI 10.1155/2016/6896024
PG 12
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA DT3ZR
UT WOS:000381420200001
PM 27563673
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Guo, RB
   Luo, J
   Chang, JS
   Rekhtman, N
   Arcila, M
   Drilon, A
AF Guo, Robin
   Luo, Jia
   Chang, Jason
   Rekhtman, Natasha
   Arcila, Maria
   Drilon, Alexander
TI MET-dependent solid tumours - molecular diagnosis and targeted therapy
SO NATURE REVIEWS CLINICAL ONCOLOGY
LA English
DT Review
ID CELL LUNG-CANCER; GROWTH-FACTOR RECEPTOR; GENE COPY NUMBER; TYROSINE
   KINASE INHIBITOR; METASTATIC COLORECTAL-CANCER; DOMAIN BINDING-SITE;
   RANDOMIZED PHASE-II; EXON 14 MUTATIONS; C-MET; JUXTAMEMBRANE DOMAIN
AB Attempts to develop MET-targeted therapies have historically focused on MET-expressing cancers, with limited success. Thus, MET expression in the absence of a genomic marker of MET dependence is a poor predictor of benefit from MET-targeted therapy. However, owing to the development of more sensitive methods of detecting genomic alterations, high-level MET amplification and activating MET mutations or fusions are all now known to be drivers of oncogenesis. MET mutations include those affecting the kinase or extracellular domains and those that result in exon 14 skipping. The activity of MET tyrosine kinase inhibitors varies by MET alteration category. The likelihood of benefit from MET-targeted therapies increases with increasing levels of MET amplification, although no consensus exists on the optimal diagnostic cut-off point for MET copy number gains identified using fluorescence in situ hybridization and, in particular, next-generation sequencing. Several agents targeting exon 14 skipping alterations are currently in clinical development, with promising data available from early-phase trials. By contrast, the therapeutic implications of MET fusions remain underexplored. Here we summarize and evaluate the utility of various diagnostic techniques and the roles of different classes of MET-targeted therapies in cancers with MET amplification, mutation and fusion, and MET overexpression.
   Therapies targeting MET-overexpressing cancers have limited efficacy. However, owing to advances in detection methods, therapies targeting MET-dependent tumours harbouring MET amplifications, activating mutations or fusions are emerging. In this review, the authors describe emerging data on this new class of targeted therapies.
C1 [Guo, Robin; Luo, Jia; Drilon, Alexander] Mem Sloan Kettering Canc Ctr, Dept Med, Thorac Oncol Serv, Div Solid Tumor Oncol, 1275 York Ave, New York, NY 10021 USA.
   [Chang, Jason; Rekhtman, Natasha; Arcila, Maria] Mem Sloan Kettering Canc Ctr, Dept Pathol, 1275 York Ave, New York, NY 10021 USA.
   [Drilon, Alexander] Weill Cornell Med Coll, New York, NY 10065 USA.
C3 Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering Cancer
   Center; Cornell University; Weill Cornell Medicine
RP Drilon, A (corresponding author), Mem Sloan Kettering Canc Ctr, Dept Med, Thorac Oncol Serv, Div Solid Tumor Oncol, 1275 York Ave, New York, NY 10021 USA.; Drilon, A (corresponding author), Weill Cornell Med Coll, New York, NY 10065 USA.
EM drilona@mskcc.org
RI Arcila, Maria/ABE-2235-2021
OI Chang, Jason/0000-0002-1705-1870; Guo, Robin/0000-0003-1722-1742;
   Drilon, Alexander/0000-0001-6806-9061
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NR 234
TC 204
Z9 218
U1 8
U2 65
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 2020
VL 17
IS 9
BP 569
EP 587
DI 10.1038/s41571-020-0377-z
EA JUN 2020
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ND7YW
UT WOS:000538975000001
PM 32514147
OA Green Accepted
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Chen, JC
   Wang, JC
   Pan, YX
   Yi, MJ
   Chen, JB
   Wang, XH
   Fu, YZ
   Zhang, YJ
   Xu, L
   Chen, MS
   Zhang, RX
   Zhou, ZG
AF Chen, Jian-Cong
   Wang, Jun-Cheng
   Pan, Yang-Xun
   Yi, Min-Jiang
   Chen, Jin-Bin
   Wang, Xiao-Hui
   Fu, Yi-Zhen
   Zhang, Yao-Jun
   Xu, Li
   Chen, Min-Shan
   Zhang, Rong-Xin
   Zhou, Zhong-Guo
TI Preventive effect of celecoxib in sorafenib-related hand-foot syndrome
   in hepatocellular carcinoma patients, a single-center, open-label,
   randomized, controlled clinical phase III trial
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE Hand-foot syndrome; celecoxib; sorafenib; hepatocellular carcinoma
ID COLORECTAL-CANCER; SKIN REACTION; TARGETED THERAPY; ADVERSE EVENTS;
   DOUBLE-BLIND; CAPECITABINE; MANAGEMENT; DIAGNOSIS; RISK; REGORAFENIB
AB Skin toxicity, especially hand-foot syndrome (HFS), is one of the most common sorafenib-induced adverse events (AEs) in hepatocellular carcinoma (HCC) patients, leading to treatment interruption and failure. Mucocutaneous inflammation may cause HFS; therefore, we investigated whether celecoxib can alleviate HFS, improve patients' quality of life and increase survival when administered in conjunction with active therapy. Our randomized, open-label study prospectively enrolled 116 advanced HCC patients receiving sorafenib as targeted therapy from July 2015 to July 2016. All patients were randomly assigned (1:1) via a computer-generated sequence to receive sorafenib with or without celecoxib. Sorafenib-related AEs were recorded, Survival was compared between the two groups. Compared to the Sorafenib group, the SoraCele group had lower incidence rates of >= grade 2 and grade 3 HFS (63.8% vs 29.3%, P < 0.001; 19.0% vs 3.4%, P = 0.008, respectively), hair loss, rash and abdominal pain. Kaplan-Meier analysis revealed a lower risk of grade >= 2 HFS (HR, 0.384; P= 0.002) and a lower dose reduction/interruption rate (46.6% to 15.5%, P < 0.001) in the SoraCele group. Cox proportional hazards regression analysis demonstrated that celecoxib was the only independent predictive factor of developing >= grade 2 HFS (HR, 0.414; P = 0.004). Longer progression-free survival (PFS) was also observed in the SoraCele group (P = 0.039), although overall survival was not prolonged (P= 0.305). These results suggest that sorafenib + Celecoxib administration alleviated sorafenib-related skin toxicity. Longer PFS was achieved in clinical practice, although overall survival was not prolonged.
C1 [Chen, Jian-Cong; Wang, Jun-Cheng; Pan, Yang-Xun; Yi, Min-Jiang; Chen, Jin-Bin; Wang, Xiao-Hui; Fu, Yi-Zhen; Zhang, Yao-Jun; Xu, Li; Chen, Min-Shan; Zhou, Zhong-Guo] Sun Yat Sen Univ, Dept Liver Surg, Canc Ctr, Guangzhou, Peoples R China.
   [Chen, Jian-Cong] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Pancreatobiliary Surg, Guangzhou, Peoples R China.
   [Wang, Jun-Cheng; Pan, Yang-Xun; Yi, Min-Jiang; Wang, Xiao-Hui; Fu, Yi-Zhen; Zhang, Yao-Jun; Xu, Li; Chen, Min-Shan; Zhang, Rong-Xin; Zhou, Zhong-Guo] Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Canc Ctr, Guangzhou, Peoples R China.
   [Zhang, Rong-Xin] Sun Yat Sen Univ, Dept Colorectal Canc, Canc Ctr, Guangzhou, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University;
   State Key Lab Oncology South China; Sun Yat Sen University
RP Zhang, RX (corresponding author), Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Canc Ctr, Guangzhou, Peoples R China.; Zhou, ZG (corresponding author), Sun Yat Sen Univ, Canc Ctr, Dept Hepatobiliary Oncol, 651 Dongfeng Rd East, Guangzhou 510060, Guangdong, Peoples R China.
EM zhangrx@sysucc.org.cn; zhouzhg@sysucc.org.cn
RI Wang, Xiaohui/I-2314-2015
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NR 34
TC 16
Z9 16
U1 0
U2 5
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 2020
VL 10
IS 5
BP 1467
EP +
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LU0OS
UT WOS:000537463800014
PM 32509392
DA 2025-01-04
ER

PT J
AU Lu, S
   Duan, RF
   Cong, L
   Song, Y
AF Lu, Shan
   Duan, Ruifeng
   Cong, Liang
   Song, Ying
TI The effects of ARID1A mutation in gastric cancer and its significance
   for treatment
SO CANCER CELL INTERNATIONAL
LA English
DT Review
DE ARID1A mutation; Gastric cancer; Prognosis; Treatment; Biomarker
ID GASTROESOPHAGEAL JUNCTION CANCER; REMODELING GENE ARID1A;
   CELL-PROLIFERATION; TUMOR-SUPPRESSOR; SOMATIC MUTATIONS; SWI/SNF
   COMPLEXES; COLON-CANCER; EXPRESSION; PROTEIN; CHEMOTHERAPY
AB Gastric cancer (GC) has emerged as a significant issue in public health all worldwide as a result of its high mortality rate and dismal prognosis. AT-rich interactive domain 1 A (ARID1A) is a vital component of the switch/sucrose-non-fermentable (SWI/SNF) chromatin remodeling complex, and ARID1A mutations occur in various tumors, leading to protein loss and decreased expression; it then affects the tumor biological behavior or prognosis. More significantly, ARID1A mutations will likely be biological markers for immune checkpoint blockade (ICB) treatment and selective targeted therapy. To provide theoretical support for future research on the stratification of individuals with gastric cancer with ARID1A as a biomarker to achieve precision therapy, we have focused on the clinical significance, predictive value, underlying mechanisms, and possible treatment strategies for ARID1A mutations in gastric cancer in this review.
C1 [Lu, Shan; Duan, Ruifeng; Cong, Liang; Song, Ying] Jilin Univ, Gastroenter Med & Digest Endoscopy Ctr, Hosp 2, Changchun, Peoples R China.
C3 Jilin University
RP Song, Y (corresponding author), Jilin Univ, Gastroenter Med & Digest Endoscopy Ctr, Hosp 2, Changchun, Peoples R China.
EM songying@jlu.edu.cn
FU Jilin Provincial Education Department [JJKH20201088KJ]
FX This work was supported by the 13th Five-year Science and Technology
   Project of Jilin Provincial Education Department [NO. JJKH20201088KJ].
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NR 101
TC 4
Z9 5
U1 0
U2 8
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 NOV 26
PY 2023
VL 23
IS 1
AR 296
DI 10.1186/s12935-023-03154-8
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CB1T3
UT WOS:001122706200002
PM 38008753
OA gold
DA 2025-01-04
ER

PT J
AU Qureshi-Baig, K
   Ullmann, P
   Haan, S
   Letellier, E
AF Qureshi-Baig, Komal
   Ullmann, Pit
   Haan, Serge
   Letellier, Elisabeth
TI <i>T</i>umor-<i>I</i>nitiating <i>C</i>ells: a cri<i>TIC</i>al review of
   isolation approaches and new challenges in targeting strategies
SO MOLECULAR CANCER
LA English
DT Review
DE Colorectal cancer; Cancer stem cells; Tumor-initiating cells; Culturing
   conditions; Surface markers; Spheroid Culture Systems; Metabolic
   identity; Targeted therapy; Inter- and intra-tumor heterogeneity
ID CANCER STEM-CELLS; EPITHELIAL-MESENCHYMAL TRANSITION; ACUTE
   MYELOID-LEUKEMIA; IN-VITRO PROPAGATION; SELF-RENEWAL; SIDE POPULATION;
   TRANSCRIPTION FACTORS; MOLECULAR SUBTYPES; CD133 EXPRESSION; SPHERE
   FORMATION
AB Most cancers contain a subpopulation of highly tumorigenic cells, known as cancer stem cells (CSCs) or tumor-initiating cells (TICs). Targeting TICs may be essential to achieve cure, because of their self-renewal and tumorigenic properties as well as their resistance to conventional therapies. Despite significant advances in TIC biology, their isolation and identification remain largely disputed and incompletely established. In this review, we discuss the latest developments in isolation and culturing approaches of TICs, with focus on colorectal cancer (CRC). We feature recent findings on TIC-relevant signaling pathways and the metabolic identity of TICs, as well as their current clinical implications. Lastly, we highlight the influence of inter-and intra-tumoral heterogeneity on TIC function and targeting approaches.
C1 [Qureshi-Baig, Komal; Ullmann, Pit; Haan, Serge; Letellier, Elisabeth] Univ Luxembourg, Mol Dis Mech Grp, Life Sci Res Unit, 6 Ave Swing,Campus Belval, L-4367 Belvaux, Luxembourg.
C3 University of Luxembourg
RP Letellier, E (corresponding author), Univ Luxembourg, Mol Dis Mech Grp, Life Sci Res Unit, 6 Ave Swing,Campus Belval, L-4367 Belvaux, Luxembourg.
EM elisabeth.letellier@uni.lu
RI Letellier, Elisabeth/I-9515-2016
OI Letellier, Elisabeth/0000-0001-8242-9393
FU Fondation Cancer; Fonds National de la Recherche (FNR) Luxembourg;
   Fondation du Pelican de Mie and Pierre Hippert-Faber
FX Fondation Cancer, Fonds National de la Recherche (FNR) Luxembourg and
   the Fondation du Pelican de Mie and Pierre Hippert-Faber.
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NR 175
TC 69
Z9 82
U1 1
U2 17
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD FEB 16
PY 2017
VL 16
AR 40
DI 10.1186/s12943-017-0602-2
PG 16
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA EK7RT
UT WOS:000394123600001
PM 28209178
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Bourbonne, V
   Lévy, A
   Khalifa, J
   Antoni, D
   Blais, E
   Darréon, J
   Le Péchoux, C
   Lerouge, D
   Giraud, P
   Marguerit, A
   Pourel, N
   Riet, FG
   Thureau, S
AF Bourbonne, V.
   Levy, A.
   Khalifa, J.
   Antoni, D.
   Blais, E.
   Darreon, J.
   Le Pechoux, C.
   Lerouge, D.
   Giraud, P.
   Marguerit, A.
   Pourel, N.
   Riet, F. -g.
   Thureau, S.
TI Radiotherapy in the management of lung oligometastases
SO CANCER RADIOTHERAPIE
LA English
DT Article
DE Oligometastasis; Lung; Surgery; Stereotactic radiotherapy
ID STEREOTACTIC-BODY-RADIOTHERAPY; ABLATIVE RADIATION-THERAPY; LOCATED
   EARLY-STAGE; QUALITY-OF-LIFE; PHASE-II; COLORECTAL-CANCER; PULMONARY
   OLIGOMETASTASES; MULTICENTER PHASE-2; PROGNOSTIC-FACTORS;
   DOSE-ESCALATION
AB In recent years, the development of both medical imaging and new systemic agents (targeted therapy and immunotherapy) have revolutionized the field of oncology, leading to a new entity: oligometastatic disease. Adding local treatment of oligometastases to systemic treatment could lead to prolonged survival with no significant impact on quality of life. Given the high prevalence of lung oligometastases and the new systemic agents coming with increased pulmonary toxicity, this article provides a comprehensive review of the current state-of-art for radiotherapy of lung oligometastases. After reviewing pretreatment workup, the authors define several radiotherapy regimen based on the localization and size of the oligometastases. A comment on the synergistic combination of medical treatment and radiotherapy is also made, projecting on future steps in this specific clinical setting. (c) 2023 Socie ' te ' franc, aise de radiothe ' rapie oncologique (SFRO). Published by Elsevier Masson SAS. All rights reserved.
C1 [Bourbonne, V.] CHU Brest, Radiat Oncol Dept, Brest, France.
   [Bourbonne, V.] Univ Bretagne Occidentale, LaTim, Inserm, UMR 1101, Brest, France.
   [Levy, A.; Le Pechoux, C.] Ctr Int Canc Thorac CICT, Dept Radiat Oncol, Gustave Roussy, F-94805 Villejuif, France.
   [Levy, A.; Le Pechoux, C.] Univ Paris Saclay, Fac Med, F-94270 Le Kremlin Bicetre, France.
   [Khalifa, J.] Inst Claudius Regaud, Inst Univ Canc Toulouse Oncopole, Dept Radiat Oncol, Toulouse, France.
   [Antoni, D.] Inst Cancerol Strasbourg Europe, Inst Claudius Regaud, Toulouse, France.
   [Blais, E.] Inst Cancerol Strasbourg Europe, Dept Radiat Oncol, Strasbourg, France.
   [Darreon, J.] Polyclin Marzet, Dept Radiat Oncol, Pau, France.
   [Lerouge, D.] Ctr Francois Baclesse, Dept Radiat Oncol, Caen, France.
   [Giraud, P.] Hop Europeen Georges Pompidou, Ctr Francois Baclesse, Paris, France.
   [Giraud, P.] Univ Paris Cite, Paris, France.
   [Marguerit, A.] Inst Cancerol Montpellier, Paris, France.
   [Pourel, N.] Inst St Catherine, Dept Radiat Oncol, Avignon, France.
   [Riet, F. -g.] Ctr Hosp Pr St Gregoire, Dept Radiat Oncol, F-35760 St Gregoire, France.
   [Thureau, S.] Ctr Henri Becquerel, Radiotherapy Dept, Rouen, France.
   [Thureau, S.] Univ Rouen, QuantIF Litis EA4108, Rouen, France.
C3 CHU Brest; Universite de Bretagne Occidentale; Institut National de la
   Sante et de la Recherche Medicale (Inserm); UNICANCER; Gustave Roussy;
   Universite Paris Saclay; UNICANCER; Institut Claudius Regaud; UNICANCER;
   Institut Claudius Regaud; UNICANCER; Centre Francois Baclesse;
   Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Europeen Georges-Pompidou - APHP; UNICANCER;
   Centre Francois Baclesse; Universite Paris Cite; UNICANCER; Universite
   de Montpellier; Institut Regional du Cancer Montpellier / Val d'Aurelle
   (ICM); UNICANCER; Centre Henri Becquerel; Universite de Rouen Normandie
RP Thureau, S (corresponding author), Ctr Henri Becquerel, Radiotherapy Dept, Rouen, France.; Thureau, S (corresponding author), Univ Rouen, QuantIF Litis EA4108, Rouen, France.
EM sebastien.thureau@chb.unicancer.fr
OI Bourbonne, Vincent/0000-0002-2631-0029
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NR 187
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER
PI BRIDGEWATER
PA 685 ROUTE 202-206, BRIDGEWATER, NJ 08807 USA
SN 1278-3218
EI 1769-6658
J9 CANCER RADIOTHER
JI Cancer Radiother.
PD FEB
PY 2024
VL 28
IS 1
BP 36
EP 48
DI 10.1016/j.canrad.2023.06.030
EA JAN 2024
PG 13
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA KJ8D4
UT WOS:001179675000001
PM 38228422
DA 2025-01-04
ER

PT J
AU Reckamp, KL
   McQuerry, JA
   Mambetsariev, I
   Pharaon, R
   Yost, SE
   Fricke, J
   Mirzapoiazova, T
   Pillai, RK
   Khan, Z
   Fakih, M
   Yuan, Y
   Koczywas, M
   Massarelli, E
   Kulkarni, P
   Pal, SK
   Sattler, M
   Bild, A
   Salgia, R
AF Reckamp, Karen L.
   McQuerry, Jasmine A.
   Mambetsariev, Isa
   Pharaon, Rebecca
   Yost, Susan E.
   Fricke, Jeremy
   Mirzapoiazova, Tamara
   Pillai, Raju K.
   Khan, Ziad
   Fakih, Marwan
   Yuan, Yuan
   Koczywas, Marianna
   Massarelli, Erminia
   Kulkarni, Prakash
   Pal, Sumanta K.
   Sattler, Martin
   Bild, Andrea
   Salgia, Ravi
TI Co-stimulatory and co-inhibitory immune markers in solid tumors with
   <i>MET</i> alterations
SO FUTURE SCIENCE OA
LA English
DT Article
DE immune markers; MET; NanoString; solid tumors; targeted therapy
ID RECEPTOR TYROSINE KINASE; HEPATOCYTE GROWTH-FACTOR; CELL LUNG-CANCER;
   MUTATIONAL ANALYSIS; SOMATIC MUTATIONS; GENE-EXPRESSION; BREAST-CANCER;
   AMPLIFICATION; RESISTANCE; TARGET
AB The implication of MET alterations in solid tumors and the immune microenvironment remains elusive. Formalin-fixed, paraffin-embedded samples of 21 patients with solid tumors harboring MET alterations were used for immunohistochemical staining. Extracted RNA was analyzed with the NanoString nCounter human PanCancer immune profiling panel (NanoString Technologies, Inc., WA, USA). Patients were diagnosed with lung (n = 10), breast (n = 5), genitourinary (n = 3) or colorectal cancer (n = 3). Eleven had a MET missense mutation, four had an exon 14 splice site mutation and six had MET amplification. CD6, CCL19, CD40LG, XCR1, MAGEA1, ATM and CCL19 genes were significantly differentially expressed in MET-altered cancers. MET alterations may have a role in various solid tumors as potential therapeutic targets and combination therapy candidates with immune checkpoint inhibitors.
C1 [Reckamp, Karen L.; McQuerry, Jasmine A.; Mambetsariev, Isa; Pharaon, Rebecca; Yost, Susan E.; Fricke, Jeremy; Mirzapoiazova, Tamara; Khan, Ziad; Fakih, Marwan; Yuan, Yuan; Koczywas, Marianna; Massarelli, Erminia; Kulkarni, Prakash; Pal, Sumanta K.; Bild, Andrea; Salgia, Ravi] City Hope Natl Med Ctr, Dept Med Oncol & Therapeut Res, Duarte, CA 91010 USA.
   [Reckamp, Karen L.] Cedars Sinai Med Ctr, Div Med Oncol, Los Angeles, CA 90048 USA.
   [McQuerry, Jasmine A.] Univ Utah, Sch Med, Dept Oncol Sci, Salt Lake City, UT 84112 USA.
   [Pillai, Raju K.] City Hope Natl Med Ctr, Dept Pathol, Duarte, CA 91010 USA.
   [Sattler, Martin] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
   [Sattler, Martin] Brigham & Womens Hosp, Dept Surg, 75 Francis St, Boston, MA 02115 USA.
   [Sattler, Martin] Harvard Med Sch, Dept Med, Boston, MA 02115 USA.
C3 City of Hope; Cedars Sinai Medical Center; Utah System of Higher
   Education; University of Utah; City of Hope; Harvard University;
   Dana-Farber Cancer Institute; Harvard University; Brigham & Women's
   Hospital; Harvard University; Harvard Medical School
RP Salgia, R (corresponding author), City Hope Natl Med Ctr, Dept Med Oncol & Therapeut Res, Duarte, CA 91010 USA.
EM rsalgia@coh.org
RI Pillai, Raju/AAB-7230-2022
OI Reckamp, Karen/0000-0002-9213-0325; Arvanitis,
   Leonidas/0000-0002-4744-8350; Khan, Ziad/0000-0002-0846-2168; Fricke,
   Jeremy/0000-0003-4684-8114; Yuan, Yuan/0000-0001-7440-8939; Yost,
   Susan/0000-0002-9422-0316; Fakih, Marwan/0000-0002-6554-5488; Pillai,
   Raju/0000-0001-8553-4252; Pharaon, Rebecca/0000-0003-0618-590X
FU National Cancer Institute of the NIH [P30CA033572, U54CA209978,
   R01CA247471, R01CA218545]
FX This work was supported by the National Cancer Institute of the NIH
   under award numbers P30CA033572, U54CA209978, R01CA247471 and
   R01CA218545 and can be deposited on the NIHMS/PMC system. 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 51
TC 2
Z9 2
U1 0
U2 4
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 2056-5623
J9 FUTUR SCI OA
JI Futur. Sci. OA
PD FEB
PY 2021
VL 7
IS 2
AR FSO662
DI 10.2144/fsoa-2020-0159
EA NOV 2020
PG 12
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA PP1IW
UT WOS:000593401000001
PM 33437521
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lee, SJ
   Li, GG
   Kim, ST
   Hong, ME
   Jang, J
   Yoon, N
   Ahn, SM
   Murphy, D
   Christiansen, J
   Wei, G
   Hornby, Z
   Lee, DW
   Park, JO
   Park, YS
   Lim, HY
   Hong, SN
   Kim, SH
   Kang, WK
   Park, K
   Park, WY
   Kim, KM
   Lee, J
AF Lee, Su Jin
   Li, Gang Gary
   Kim, Seung Tae
   Hong, Min Eui
   Jang, Jiryeon
   Yoon, Nara
   Ahn, Soo Min
   Murphy, Danielle
   Christiansen, Jason
   Wei, Ge
   Hornby, Zachary
   Lee, Dong Woo
   Park, Joon Oh
   Park, Young Suk
   Lim, Ho Yeong
   Hong, Sung No
   Kim, Seok-Hyeong
   Kang, Won Ki
   Park, Keunchil
   Park, Woong Yang
   Kim, Kyoung-Mee
   Lee, Jeeyun
TI <i>NTRK1</i> rearrangement in colorectal cancer patients: evidence for
   actionable target using patient-derived tumor cell line
SO ONCOTARGET
LA English
DT Article
DE colorectal cancer; NTRK1 rearrangement; TRKA immunohistochemistry
ID ONCOGENES; THERAPY; IDENTIFICATION; LANDSCAPE; FUSION
AB Background: We have investigated the incidence of NTRK1 rearrangements in metastatic gastrointestinal cancer patients and demonstrated the potential for clinical response of these patients to targeted therapy.
   Methods: We prospectively collected tumor tissue specimens for one year and simultaneously generated patient-derived tumor cells (PDCs). Specimens were initially screened for TrkA protein expression using TrkA immunohistochemistry (IHC). In the case of TrkA IHC positive results, samples were further examined by fluorescence in situ hybridization (FISH) and next generation sequencing (NGS) to confirm the presence of NTRK1 rearrangements.
   Results: From January 2014 to December 2014, a total of 74 metastatic colorectal cancer (CRC) patients and 66 gastric cancer (GC) patients were initially screened by TrkA IHC. Two of the 74 CRC patients (2.7%) and one of the 66 GC patients (1.5%) were positive for TrkA expression by IHC. All three IHC positive cases had evidence of NTRK1 rearrangements by FISH. NGS was performed on the 3 IHC positive cases and confirmed TPM3-NTRK1 rearrangements in the two CRC cases. One GC patient with TrkA expression by IHC did not harbor an NTRK1 rearrangement. PDCs established from the NTRK1 positive CRC patients were positive for the NTRK1 rearrangement. Entrectinib, a pan-TRK inhibitor, profoundly inhibited cell proliferation of NTRK1-rearranged PDCs with such inhibition associated with inactivation of TrkA, and down-regulation of downstream signaling pathways.
   Conclusion: TrkA IHC is an effective, initial screening method for NTRK1 rearrangement detection in the clinic. Inhibition of the TrkA kinase is a promising targeted therapy for cancer patients whose tumors harbor a NTRK1 rearrangement.
C1 [Lee, Su Jin; Kim, Seung Tae; Jang, Jiryeon; Park, Joon Oh; Park, Young Suk; Lim, Ho Yeong; Kang, Won Ki; Park, Keunchil; Lee, Jeeyun] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Med,Div Hematol Oncol, Seoul, South Korea.
   [Li, Gang Gary; Murphy, Danielle; Christiansen, Jason; Wei, Ge; Hornby, Zachary] Ignyta Inc, San Diego, CA USA.
   [Hong, Min Eui; Yoon, Nara; Ahn, Soo Min; Kim, Seok-Hyeong; Kim, Kyoung-Mee] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol & Translat Genom, Seoul, South Korea.
   [Lee, Dong Woo] Samsung Elect, Seoul, South Korea.
   [Hong, Sung No] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Med,Div Gastroenterol, Seoul, South Korea.
   [Park, Woong Yang] Samsung Genome Inst, Seoul, South Korea.
   [Park, Joon Oh; Kim, Kyoung-Mee] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Innovat Canc Med Inst, Seoul, South Korea.
C3 Sungkyunkwan University (SKKU); Samsung Medical Center; Sungkyunkwan
   University (SKKU); Samsung Medical Center; Samsung Electronics; Samsung;
   Sungkyunkwan University (SKKU); Samsung Medical Center; Sungkyunkwan
   University (SKKU); Samsung Medical Center; Sungkyunkwan University
   (SKKU); Samsung Medical Center
RP Lee, J (corresponding author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Med,Div Hematol Oncol, Seoul, South Korea.
EM kkmkys@skku.edu; jyunlee@skku.edu
RI Park, Junsu/IQU-2241-2023; Lee, sujeong/KUD-4735-2024; Park,
   Jihye/AAC-1333-2022; kim, st/O-5928-2014; Lee, Su Hwan/R-6161-2019;
   Park, Keunchil/ABD-5852-2021; Lee, Jee/C-9646-2011; Kim,
   Kihyun/D-5175-2013; Kim, Kyunga/LCL-2839-2024; Lim, Ho
   Yeong/KBA-8868-2024
OI Lee, Su Jin/0000-0003-3405-9935; Park, Woong-Yang/0000-0003-4234-0380
FU Korea Health Industry Development Institute (KHIDI) - Ministry of Health
   & Welfare, Republic of Korea [HI13C2096, HI13C1951, HI14C3418]
FX This research was supported by a grant of the Korea Health Industry
   Development Institute (KHIDI), funded by the Ministry of Health &
   Welfare, Republic of Korea (grant number: HI13C2096, HI13C1951,
   HI14C3418).
CR Albert L, 2003, J CELL PHYSIOL, V195, P168, DOI 10.1002/jcp.10252
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NR 19
TC 54
Z9 55
U1 1
U2 7
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD NOV 17
PY 2015
VL 6
IS 36
BP 39028
EP 39035
DI 10.18632/oncotarget.5494
PG 8
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CY0RS
UT WOS:000366114000045
PM 26472021
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Teerapakpinyo, C
   Wanthong, P
   Aumchaaumchaya, M
   Chankate, P
   Kaikeaw, W
   Tosakorn, W
   Shaungshoti, S
AF Teerapakpinyo, Chinachote
   Wanthong, Phanni
   Aumchaaumchaya, Mathawee
   Chankate, Piyamai
   Kaikeaw, Warisa
   Tosakorn, Warunya
   Shaungshoti, Shanop
TI Pyrosequencing analysis of <i>KRAS</i> codon 61 mutations in Thai
   patients with advanced colorectal cancer
SO ASIAN BIOMEDICINE
LA English
DT Article
DE Colorectal cancer; KRAS; mutation; pyrosequencing; targeted therapy
ID CETUXIMAB PLUS IRINOTECAN; CHEMOTHERAPY; BRAF; PCR
AB Background: KRAS, coding for a small G-protein downstream of epidermal growth factor receptor (EGFR) plays an important role in the EGFR signaling network. Mutation in KRAS is associated with resistance to anti-EGFR in patients with advanced colorectal cancer (CRC). According to the American Society of Clinical Oncology (ASCO) guidelines, screening for mutations in KRAS codons 12 and 13 in tumor samples is mandatory for all CRC patients who are candidates for anti-EGFR targeted therapy. However, some patients with undetectable mutations in codons 12/13 do not benefit from anti-EGFR treatment, and this might be because of mutations in codon 61, which is not currently recommended for screening.
   Objectives: To develop an in-house pyrosequencing method to screen for KRAS codon 61 mutations, and examine the prevalence of mutations in Thai patients with advanced CRC with no detectable mutation in codons 12/13.
   Materials and Methods: DNA extracted from FFPE specimens was screened for KRAS codon 61 mutations using pyrosequencing. Our method was suitable for routine clinical samples (formalin-fixed, paraffin-embedded tissue), and was able to detect 5 common mutations in codon 61 of the KRAS gene, including c.182AT (p.Q61L), c.182AG (p.Q61R), c.182AC (p.Q61P), c.183AC (p.Q61H), and c.183AT (p.Q61H).
   Results: Of the 74 samples with undetectable codon 12/13 mutation examined, two (2.7%) were found to harbor mutation in codon 61.
   Conclusion: Despite the low prevalence of KRAS codon 61 mutation in our population with advanced CRC, adding the mutation test into the routine molecular service deserves consideration because the cost of treatment is very expensive.
C1 [Teerapakpinyo, Chinachote; Wanthong, Phanni; Aumchaaumchaya, Mathawee; Chankate, Piyamai; Kaikeaw, Warisa; Tosakorn, Warunya; Shaungshoti, Shanop] Chulalongkorn Univ, Fac Med, Chula GenePRO Ctr, Res Affairs, Bangkok 10330, Thailand.
   [Shaungshoti, Shanop] Chulalongkorn Univ, Fac Med, Dept Pathol, Bangkok 10330, Thailand.
C3 Chulalongkorn University; Chulalongkorn University
RP Teerapakpinyo, C (corresponding author), Chulalongkorn Univ, Fac Med, Chula GenePRO Ctr, Res Affairs, Bangkok 10330, Thailand.
EM chinachote.t@chula.ac.th
FU Ratchadapiseksompotch Fund, Faculty of Medicine, Chulalongkorn
   University [RA56-050]
FX This work was supported by the Ratchadapiseksompotch Fund, Faculty of
   Medicine, Chulalongkorn University (RA56-050). The authors wish to thank
   Ms. Jutamas Ngopon and Dr. Piyada Sitthideatphaiboon for helpful
   comments on the manuscript.
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NR 26
TC 1
Z9 1
U1 0
U2 3
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1905-7415
EI 1875-855X
J9 ASIAN BIOMED
JI Asian Biomed.
PD FEB
PY 2015
VL 9
IS 1
BP 61
EP 67
DI 10.5372/1905-7415.0901.369
PG 7
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA CG6WT
UT WOS:000353443800008
OA hybrid
DA 2025-01-04
ER

PT J
AU Yokoyama, M
   Ohnishi, H
   Ohtsuka, K
   Matsushima, S
   Ohkura, Y
   Furuse, J
   Watanabe, T
   Mori, T
   Sugiyama, M
AF Yokoyama, Masaaki
   Ohnishi, Hiroaki
   Ohtsuka, Kouki
   Matsushima, Satsuki
   Ohkura, Yasuo
   Furuse, Junji
   Watanabe, Takashi
   Mori, Toshiyuki
   Sugiyama, Masanori
TI <i>KRAS</i> Mutation as a Potential Prognostic Biomarker of Biliary
   Tract Cancers
SO JAPANESE CLINICAL MEDICINE
LA English
DT Article
DE biliary tract cancer; KRAS; molecular targeted therapy; biomarker
ID METASTATIC COLORECTAL-CANCER; GROWTH-FACTOR-RECEPTOR;
   HEPATOCELLULAR-CARCINOMA; GALLBLADDER ADENOMA; P53 OVEREXPRESSION;
   PIK3CA MUTATIONS; C-MET; RESISTANCE; CHOLANGIOCARCINOMA; CETUXIMAB
AB BACKGROUND: The aim of this study was to identify the unique molecular characteristics of biliary tract cancer (BTC) for the development of novel molecular-targeted therapies.
   MATERIALS AND METHODS: We performed mutational analysis of KRAS, BRAF, PIK3CA, and FBXW7 and immunohistochemical analysis of EGFR and TP53 in 63 Japanese patients with BTC and retrospectively evaluated the association between the molecular characteristics and clinicopathological features of BTC.
   RESULTS: KRAS mutations were identified in 9 (14%) of the 63 BTC patients; no mutations were detected within the analyzed regions of BRAF, PIK3CA, and FBXW7. EGFR overexpression was observed in 5 (8%) of the 63 tumors, while TP53 overexpression was observed in 48% (30/63) of the patients. Overall survival of patients with KRAS mutation was significantly shorter than that of patients with the wild-type KRAS gene (P = 0.005). By multivariate analysis incorporating molecular and clinicopathological features, KRAS mutations and lymph node metastasis were identified to be independently associated with shorter overall survival (KRAS, P = 0.004; lymph node metastasis, P = 0.015).
   CONCLUSIONS: Our data suggest that KRAS mutation is a poor prognosis predictive biomarker for the survival in BTC patients.
C1 [Yokoyama, Masaaki; Mori, Toshiyuki; Sugiyama, Masanori] Kyorin Univ, Sch Med, Dept Surg, Tokyo, Japan.
   [Ohnishi, Hiroaki; Ohtsuka, Kouki; Matsushima, Satsuki; Watanabe, Takashi] Kyorin Univ, Sch Med, Dept Lab Med, Tokyo, Japan.
   [Ohkura, Yasuo] Kyorin Univ, Sch Med, Dept Pathol, Tokyo, Japan.
   [Furuse, Junji] Kyorin Univ, Sch Med, Dept Med Oncol, Tokyo, Japan.
C3 Kyorin University; Kyorin University; Kyorin University; Kyorin
   University
RP Yokoyama, M (corresponding author), Kyorin Univ, Sch Med, Dept Surg, Tokyo, Japan.
EM m-yoko@ks.kyorin-u.ac.jp
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NR 34
TC 15
Z9 15
U1 0
U2 4
PU LIBERTAS ACAD
PI AUCKLAND
PA PO BOX 300-874, ALBANY 0752, AUCKLAND, 00000, NEW ZEALAND
SN 1179-6707
J9 JPN CLIN MED
JI Jpn. Clin. Med.
PY 2016
VL 7
DI 10.4137/JCM.S40549
PG 7
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA EF9LV
UT WOS:000390652600001
PM 28008299
OA Green Published
DA 2025-01-04
ER

PT J
AU Gu, XF
   Xu, HF
   Liu, Y
   Li, L
   Yu, YQ
   Zhang, X
   Wang, XH
   Wang, WJ
   Du, LB
   Duan, SX
   Cao, HL
   Zhao, YQ
   Liu, YY
   Huang, JX
   Cao, J
   Fan, YP
   Feng, CY
   Lian, XM
   Du, JC
   Rezhake, R
   Ma, L
   Qiao, YL
AF Gu, Xiao-Fen
   Xu, Hui-Fang
   Liu, Yin
   Li, Li
   Yu, Yan-Qin
   Zhang, Xi
   Wang, Xiao-Hui
   Wang, Wen-Jun
   Du, Ling-Bin
   Duan, Shuang-Xia
   Cao, He-Lu
   Zhao, Yu-Qian
   Liu, Yun-Yong
   Huang, Juan-Xiu
   Cao, Ji
   Fan, Yan-Ping
   Feng, Chang-Yan
   Lian, Xue-Mei
   Du, Jing-Chang
   Rezhake, Remila
   Ma, Li
   Qiao, You-Lin
CA China Working Grp Colorectal Canc
TI Involvement in treatment decision-making and self-reported efficacy
   among patients with advanced colorectal cancer: a nationwide
   multi-center cross-sectional study
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; treatment; decision making; self-reported efficacy;
   China
ID QUALITY-OF-LIFE; UNITED-STATES; OUTCOMES PROS; RISK-FACTORS; CHINA;
   PREFERENCES; STATISTICS; MORTALITY; KNOWLEDGE; COUNTRIES
AB IntroductionThis cross-sectional study evaluated the involvement of patients with advanced colorectal cancer (CRC) in treatment decision-making, assessed the treatment efficacy according to their self-reports, and investigated the influencing factors. MethodsPatients with advanced CRC were recruited from 19 hospitals from March 2020 to March 2021 by a multi-stage multi-level sampling method. A self-designed questionnaire was used to collect demographic and clinical characteristics, involvement of CRC patients in treatment decision-making, treatment methods, and self-reported efficacy. Univariate and unordered multinomial logistic regression analyses were used to evaluate the factors affecting the involvement in treatment decision-making and self-reported efficacy. ResultsWe enrolled 4533 patients with advanced CRC. The average age at diagnosis was 58.7 & PLUSMN; 11.8 years. For the treatment method, 32.4% of patients received surgery combined with chemotherapy, 13.1% of patients underwent surgery combined with chemotherapy and targeted therapy, and 9.7% of patients were treated with surgery alone. For treatment decision-making, 7.0% of patients were solely responsible for decision-making, 47.0% of patients shared treatment decision-making with family members, 19.0% of patients had family members solely responsible for treatment decision-making, and 27.0% of patients had their physicians solely responsible for treatment decision-making. Gender, age, education level, family income, marital status, treatment cost, hospital type, and treatment method were significantly associated with the involvement of patients in treatment decision-making. A total of 3824 patients submitted self-reported efficacy evaluations during treatment. The percentage of patients with good self-reported efficacy was 76.5% (for patients treated for the first time), 61.7% (for patients treated for the second time), and 43.2% (for patients treated after recurrence and metastasis), respectively. Occupation, education level, average annual family income, place of residence, time since cancer diagnosis, hospital type, clinical stage, targeted therapy, and involvement in treatment decision-making were the main influencing factors of self-reported efficacy of treatment. DiscussionConclusively, CRC patients are not highly dominant in treatment decision-making and more likely to make treatment decisions with their family and doctors. Timely and effective communication between doctors and patients can bolster patient involvement in treatment decision-making.
C1 [Gu, Xiao-Fen; Rezhake, Remila; Qiao, You-Lin] Xinjiang Med Univ, Affiliated Canc Hosp, Dept Student Affairs, Urumqi, Peoples R China.
   [Xu, Hui-Fang; Liu, Yin; Qiao, You-Lin] Zhengzhou Univ, Affiliated Canc Hosp, Dept Canc Epidemiol, Zhengzhou, Peoples R China.
   [Xu, Hui-Fang; Liu, Yin; Qiao, You-Lin] Henan Canc Hosp, Henan Engn Res Ctr Canc Prevent & Control, Henan Int Joint Lab Canc Prevent, Zhengzhou, Peoples R China.
   [Li, Li] Jinan Univ, Affiliated Hosp 1, Dept Clin Res, Guangzhou, Guangdong, Peoples R China.
   [Yu, Yan-Qin] Baotou Med Coll, Clin Epidemiol Res Ctr, Dept Publ Hlth & Prevent Med, Baotou, Peoples R China.
   [Zhang, Xi] Peking Univ, Canc Hosp & Inst, Key Lab Carcinogenesis & Translat Res, Beijing Off Canc Prevent & Control,Minist Educ Be, Beijing, Peoples R China.
   [Wang, Xiao-Hui] Gansu Prov Canc Hosp, Dept Publ Hlth, Lanzhou, Peoples R China.
   [Wang, Wen-Jun] Jining Med Univ, Sch Nursing, Jining, Peoples R China.
   [Du, Ling-Bin] Univ Chinese Acad Sci, Zhejiang Canc Hosp, Canc Hosp, Dept Canc Prevent, Hangzhou, Peoples R China.
   [Duan, Shuang-Xia; Cao, He-Lu] Xinxiang Cent Hosp, Dept Prevent Hlth, Xinxiang, Peoples R China.
   [Zhao, Yu-Qian] Univ Elect Sci & Technol China, Sichuan Canc Hosp & Inst, Ctr Canc Prevent Res, Sichuan Canc Ctr,Sch Med, Chengdu, Peoples R China.
   [Liu, Yun-Yong] China Med Univ, Liaoning Canc Hosp & Inst, Canc Hosp, Liaoning Off Canc Control & Res, Shenyang, Peoples R China.
   [Huang, Juan-Xiu] Wuzhou Red Cross Hosp, Dept Gastrodiges, Wuzhou, Peoples R China.
   [Cao, Ji] Guangxi Med Univ, Affiliated Hosp 1, Dept Canc Prevent & Control Off, Nanning, Peoples R China.
   [Fan, Yan-Ping] Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, Canc Ctr, State Key Lab Oncol South China, Guangzhou, Peoples R China.
   [Feng, Chang-Yan] Chongqing Univ, Canc Hosp, Chongqing Key Lab Translat Res Canc Metastasis &, Chongqing, Peoples R China.
   [Lian, Xue-Mei] Chongqing Med Univ, Sch Publ Hlth & Management, Chongqing, Peoples R China.
   [Du, Jing-Chang] Chengdu Med Coll, Sch Publ Hlth, Chengdu, Peoples R China.
   [Ma, Li] Dalian Med Univ, Publ Hlth Sch, Dalian, Peoples R China.
   [Qiao, You-Lin] Chinese Acad Med Sci & Peking Union Med Coll, Sch Populat Med & Publ Hlth, Beijing, Peoples R China.
C3 Xinjiang Medical University; Zhengzhou University; Zhengzhou University;
   Jinan University; Baotou Medical College; Peking University; Jining
   Medical University; Chinese Academy of Sciences; University of Chinese
   Academy of Sciences, CAS; Zhejiang Cancer Hospital; University of
   Electronic Science & Technology of China; China Medical University;
   Guangxi Medical University; Sun Yat Sen University; State Key Lab
   Oncology South China; Chongqing University; Chongqing Medical
   University; Chengdu Medical College; Dalian Medical University; Chinese
   Academy of Medical Sciences - Peking Union Medical College; Peking Union
   Medical College
RP Rezhake, R; Qiao, YL (corresponding author), Xinjiang Med Univ, Affiliated Canc Hosp, Dept Student Affairs, Urumqi, Peoples R China.; Qiao, YL (corresponding author), Zhengzhou Univ, Affiliated Canc Hosp, Dept Canc Epidemiol, Zhengzhou, Peoples R China.; Qiao, YL (corresponding author), Henan Canc Hosp, Henan Engn Res Ctr Canc Prevent & Control, Henan Int Joint Lab Canc Prevent, Zhengzhou, Peoples R China.; Ma, L (corresponding author), Dalian Med Univ, Publ Hlth Sch, Dalian, Peoples R China.; Qiao, YL (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Sch Populat Med & Publ Hlth, Beijing, Peoples R China.
EM Remila@xjmu.edu.cn; mali_lele@sina.com; qiaoy@cicams.ac.cn
RI Wang, Xiaohui/I-2314-2015; Qiao, You-Lin/B-4139-2012; Cheng,
   Lin/KFQ-3111-2024; zhao, yuqian/JED-8246-2023; Yu, Yanqin/AFX-9220-2022
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NR 60
TC 2
Z9 2
U1 1
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JUL 26
PY 2023
VL 13
AR 1168078
DI 10.3389/fonc.2023.1168078
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA O4YU4
UT WOS:001043893200001
PM 37564928
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kumar, A
   Gautam, V
   Sandhu, A
   Rawat, K
   Sharma, A
   Saha, L
AF Kumar, Anil
   Gautam, Vipasha
   Sandhu, Arushi
   Rawat, Kajal
   Sharma, Antika
   Saha, Lekha
TI Current and emerging therapeutic approaches for colorectal cancer: A
   comprehensive review
SO WORLD JOURNAL OF GASTROINTESTINAL SURGERY
LA English
DT Review
DE Colorectal cancer; Chemotherapy; Immunotherapy; RNA interference;
   Probiotics; Oncolytic viral therapy
ID INTENSITY-MODULATED RADIOTHERAPY; MISMATCH REPAIR-DEFICIENT; PHASE-III
   TRIAL; 1ST-LINE TREATMENT; RECTAL-CANCER; COLON-CANCER; OPEN-LABEL;
   NEOADJUVANT CHEMOTHERAPY; RANDOMIZED-TRIAL; TARGETED THERAPY
AB Colorectal cancer (CRC) affects 1 in 23 males and 1 in 25 females, making it the third most common cancer. With roughly 608000 deaths worldwide, CRC accounts for 8% of all cancer-related deaths, making it the second most common cause of death due to cancer. Standard and conventional CRC treatments include surgical expurgation for resectable CRC and radiotherapy, chemotherapy, immunotherapy, and their combinational regimen for non-resectable CRC. Despite these tactics, nearly half of patients develop incurable recurring CRC. Cancer cells resist the effects of chemotherapeutic drugs in a variety of ways, including drug inactivation, drug influx and efflux modifications, and ATP-binding cassette transporter overexpression. These constraints necessitate the development of new target-specific therapeutic strategies. Emerging therapeutic approaches, such as targeted immune boosting therapies, non-coding RNA-based therapies, probiotics, natural products, oncolytic viral therapies, and biomarker-driven therapies, have shown promising results in preclinical and clinical studies. We tethered the entire evolutionary trends in the development of CRC treatments in this review and discussed the potential of new therapies and how they might be used in conjunction with conventional treatments as well as their advantages and drawbacks as future medicines.
C1 [Kumar, Anil; Gautam, Vipasha; Sandhu, Arushi; Rawat, Kajal; Sharma, Antika; Saha, Lekha] Post Grad Inst Med Educ & Res, Dept Pharmacol, Chandigarh 160012, India.
   [Saha, Lekha] Post Grad Inst Med Educ & Res, Dept Pharmacol, Res Block B, Chandigarh 160012, India.
C3 Post Graduate Institute of Medical Education & Research (PGIMER),
   Chandigarh; Post Graduate Institute of Medical Education & Research
   (PGIMER), Chandigarh
RP Saha, L (corresponding author), Post Grad Inst Med Educ & Res, Dept Pharmacol, Res Block B, Chandigarh 160012, India.
EM lekhasaha@rediffmail.com
RI Rawat, Kajal/AAY-1345-2021
OI Sharma, Antika/0009-0008-0477-769X; Kumar, Anil/0000-0003-0000-6448
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NR 158
TC 51
Z9 51
U1 14
U2 23
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-9366
J9 WORLD J GASTRO SURG
JI World J. Gastrointest. Surg.
PD APR 27
PY 2023
VL 15
IS 4
BP 495
EP 519
DI 10.4240/wjgs.v15.i4.495
PG 25
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA G8MB6
UT WOS:000991622500001
PM 37206081
OA Green Published, gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Signorini, L
   Delbue, S
   Ferrante, P
   Bregni, M
AF Signorini, Lucia
   Delbue, Serena
   Ferrante, Pasquale
   Bregni, Marco
TI Review on the immunotherapy strategies against metastatic colorectal
   carcinoma
SO IMMUNOTHERAPY
LA English
DT Review
DE active immunotherapy; colon cancer; immune checkpoints inhibitors;
   passive immunotherapy
ID CYTOTOXIC T-LYMPHOCYTES; TUMOR-INFILTRATING LYMPHOCYTES; ENCODING
   CARCINOEMBRYONIC ANTIGEN; ACTIVE SPECIFIC IMMUNOTHERAPY; THERAPEUTIC
   CANCER VACCINES; DENDRITIC CELL VACCINATION; RANDOMIZED-PHASE-II;
   COLON-CANCER; AUTOLOGOUS TUMOR; ADOPTIVE IMMUNOTHERAPY
AB Colorectal cancer (CRC) is one of the most common malignancies throughout the world and the leading cause of cancer-related mortality in Western countries. Recent progress in CRC treatment options, such as surgery, chemotherapy, radiotherapy and target therapy, has improved the prognosis, but advanced disease with recurrence or distant metastasis is usually incurable and has an unfavorable prognosis. The introduction of immunotherapy-associated strategies, both active and passive, to the treatment of CRC aims to overcome the limits of classical treatments. We review the state of the art for CRC with respect to different immunotherapeutic approaches, such as the use of cancer vaccines and/or adoptive cellular therapy, their most current advances and limitations and perspectives for further improvements.
C1 [Signorini, Lucia] Univ Milan, Dept Biomed Surg & Dent Sci, Via Pascal 36, I-20123 Milan, Italy.
   [Bregni, Marco] Osped Circolo Busto Arsizio, Via A Da Brescia 1, I-21052 Busto Arsizio, VA, Italy.
C3 University of Milan
RP Bregni, M (corresponding author), Osped Circolo Busto Arsizio, Via A Da Brescia 1, I-21052 Busto Arsizio, VA, Italy.
EM mbregni@aobusto.it
RI Signorini, Lucia/ISS-0767-2023; delbue, serena/A-1145-2010
OI Signorini, Lucia/0000-0002-6691-736X
FU Programma, Alleanza Contro il Cancro (ACC) - Istituto Superiore di
   Sanita (ISS); Umberto Veronesi Foundation
FX This work was partially supported by Programma 3, Alleanza Contro il
   Cancro (ACC) - Istituto Superiore di Sanita (ISS) and by Umberto
   Veronesi Foundation to MB. The authors declare no conflict of interest.
   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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PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA DW5EA
UT WOS:000383663800011
PM 27605072
DA 2025-01-04
ER

PT J
AU Kieler, M
   Unseld, M
   Bianconi, D
   Waneck, F
   Mader, R
   Wrba, F
   Fuereder, T
   Marosi, C
   Raderer, M
   Staber, P
   Berger, W
   Sibilia, M
   Polterauer, S
   Müllauer, L
   Preusser, M
   Zielinski, CC
   Prager, GW
AF Kieler, Markus
   Unseld, Matthias
   Bianconi, Daniela
   Waneck, Fredrik
   Mader, Robert
   Wrba, Fritz
   Fuereder, Thorsten
   Marosi, Christine
   Raderer, Markus
   Staber, Philipp
   Berger, Walter
   Sibilia, Maria
   Polterauer, Stephan
   Muellauer, Leonhard
   Preusser, Matthias
   Zielinski, Christoph C.
   Prager, Gerald W.
TI Interim analysis of a real-world precision medicine platform for
   molecular profiling of metastatic or advanced cancers: MONDTI
SO ESMO OPEN
LA English
DT Article
DE precision medicine; molecular profile; targeted treatment
ID CELL LUNG-CANCER; PHASE-II TRIAL; BREAST-CANCER; TARGETED THERAPY;
   OPEN-LABEL; FEASIBILITY; MULTICENTER; VEMURAFENIB; PALBOCICLIB;
   COMBINATION
AB Background High-throughput genomic profiling of tumour specimens facilitates the identification of individual actionable mutations which could be used for individualised targeted therapy. This approach is becoming increasingly more common in the clinic; however, the interpretation of results from molecular profiling tests and efficient guiding of molecular therapies to patients with advanced cancer offer a significant challenge to the oncology community.
   Experimental design MONDTI is a precision medicine platform for molecular characterisation of metastatic solid tumours to identify actionable genomic alterations. From 2013 to 2016, comprehensive molecular profiles derived from real-time biopsy specimens and archived tumour tissue samples of 295 patients were performed. Results and treatment suggestions were discussed within multidisciplinary tumour board meetings.
   Results The mutational profile was obtained from 293 (99%) patients and a complete immunohistochemical (IHC) and cytogenetic profile was obtained in 181 (61%) and 188 (64%) patients. The most frequent cancer types were colorectal cancer (12%), non-Hodgkin's lymphomas (9.8%) and head and neck cancers (7.8%). The most commonly detected mutations were TP53 (39%), KRAS (19%) and PIK3CA (9.5%), whereas >= 1 mutation were identified in 217 (74%) samples. Regarding the results for IHC testing, samples were positive for phospho-mammalian target of rapamycin (phospho-mTOR) (71%), epidermal growth factor receptor (EGFR) (68%), mesenchymal epithelial transition (MET) (56%) and/or platelet-derived growth factor alpha (PDGFR alpha)-expression (48%). Of the 288 tumour samples with one or more genetic alteration detected, 160 (55.6%) targeted therapy recommendations through 67 multidisciplinary tumour board meetings were made; in 69 (24%) cases, an individual treatment concept was initiated.
   Conclusions The results reveal that the open concept for all solid tumours characterised for molecular profile and immunotherapy could not only match individualised treatment concepts at a high rate but also underscores the challenges encountered when offering molecularly matched therapies to a patient population with an advanced stage cancer.
C1 [Kieler, Markus; Unseld, Matthias; Bianconi, Daniela; Mader, Robert; Fuereder, Thorsten; Marosi, Christine; Raderer, Markus; Preusser, Matthias; Zielinski, Christoph C.; Prager, Gerald W.] Med Univ Vienna, Dept Med 1, Div Oncol, Vienna, Austria.
   [Waneck, Fredrik] Med Univ Vienna, Dept Biomed Imaging & Image Guided Therapy, Div Cardiovasc & Intervent Radiol, Vienna, Austria.
   [Wrba, Fritz; Muellauer, Leonhard] Med Univ Vienna, Dept Pathol, Vienna, Austria.
   [Staber, Philipp] Med Univ Vienna, Dept Med 1, Div Hematol & Hemostaseol, Vienna, Austria.
   [Berger, Walter; Sibilia, Maria] Med Univ Vienna, Comprehens Canc Ctr, Inst Canc Res, Dept Med 1, Vienna, Austria.
   [Polterauer, Stephan] Med Univ Vienna, Dept Obstet & Gynecol, Div Gen Gynecol & Gynecol Oncol, Vienna, Austria.
C3 Medical University of Vienna; Medical University of Vienna; Medical
   University of Vienna; Medical University of Vienna; Medical University
   of Vienna; Medical University of Vienna
RP Prager, GW (corresponding author), Med Univ Vienna, Dept Med 1, Div Oncol, Vienna, Austria.
EM prager@meduniwien.ac.at
RI Kieler, Markus/AAF-4612-2020; Polterauer, Stephan/AAG-1331-2021; Berger,
   Walter/AFQ-9733-2022; Prager, Gerald/AAS-8674-2021; Mullauer,
   Leonhard/GSN-9884-2022; Staber, Philipp/ADK-1536-2022; Preusser,
   Matthias/C-8530-2011
OI Mullauer, Leonhard/0000-0002-3399-078X; Mader,
   Robert/0000-0003-3017-8240; Kieler, Markus/0000-0002-4082-5731; Staber,
   Philipp/0000-0001-6729-7708; Sibilia, Maria/0000-0001-6129-5613; Prager,
   M.D., Gerald/0000-0002-7854-7781; Berger, Walter/0000-0003-0014-1658;
   Preusser, Matthias/0000-0003-3541-2315; Polterauer,
   Stephan/0000-0002-9649-4505
FU Initiative Krebsforschung [UE 71104027]
FX This work was supported by Initiative Krebsforschung (UE 71104027).
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NR 42
TC 8
Z9 8
U1 0
U2 6
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PD JUL
PY 2019
VL 4
IS 4
AR UNSP e000538
DI 10.1136/esmoopen-2019-000538
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA JC1WP
UT WOS:000489068900009
PM 31423337
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Wells, JC
   Tu, DS
   Siu, LL
   Shapiro, JD
   Jonker, DJ
   Karapetis, C
   Simes, J
   Liu, G
   Price, TJ
   Tebbutt, NC
   O'Callaghan, CJ
AF Wells, J. Connor
   Tu, Dongsheng
   Siu, Lillian L.
   Shapiro, Jeremy D.
   Jonker, Derek J.
   Karapetis, Christos
   Simes, John
   Liu, Geoffrey
   Price, Timothy J.
   Tebbutt, Niall C.
   O'Callaghan, Chris J.
TI Outcomes of Older Patients (≥ 70 Years) Treated With Targeted Therapy in
   Metastatic Chemorefractory Colorectal Cancer: Retrospective Analysis of
   NCIC CTG CO.17 and CO.20
SO CLINICAL COLORECTAL CANCER
LA English
DT Article
DE Cetuximab; Comorbidity; Elderly; Quality of life; Survival; Toxicity
ID ELDERLY-PATIENTS; PHASE-III; GERIATRIC ONCOLOGY; CLINICAL-TRIALS; RAS
   MUTATIONS; OPEN-LABEL; CETUXIMAB; CHEMOTHERAPY; COMORBIDITY; SURVIVAL
AB Clinical trial data were used to evaluate cancer outcomes between older (n = 251) and younger (n = 704) patients with metastatic colorectal cancer who were treated with cetuximab. Overall survival trended toward favoring younger adults, but in general, outcomes, including quality-of-life benefit, were similar between age groups.
   Background: The safety and efficacy of targeted therapy in older patients (>= 70 years) with metastatic colorectal cancer is not well evaluated. Patients and Methods: Outcomes of older patients (including overall survival [OS], progression-free survival [PFS], toxicity, and quality of life [QoL]) were compared to young patients using data from 2 large previously reported clinical trials, CO. 17 (cetuximab vs. best supportive care) and CO.20 (cetuximab plus placebo vs. cetuximab plus brivanib). Only patients with wild-type KRAS tumors were included. Results: A total of 251 (26.3%) of 955 patients were >= 70 years old. No significant differences in OS, PFS, or grade 3/4 adverse events were observed between older and younger patients treated with cetuximab (or cetuximab with placebo) in either trial. Younger patients trended toward superior OS in both CO. 17 (hazard ratio = 1.80; P = .16) and CO. 20 (hazard ratio = 1.34; P = .07). QoL maintenance favored younger patients in CO. 17 (3.6 vs. 5.7 months; P = .046) but no difference of QoL maintenance was observed in the larger CO. 20 trial (1.7 vs. 1.8 months; P = .64). Combination therapy of cetuximab and brivanib was significantly more toxic in older adults (87% vs. 77%; P = .03). Conclusion: OS, PFS, and toxicities were similar between older and younger patients with wild-type KRAS metastatic colorectal cancer when treated with cetuximab. Both age groups likely experience similar QoL maintenance with cetuximab. Dual targeted therapy was significantly more toxic in older patients. (C) 2018 Elsevier Inc. All rights reserved.
C1 [Wells, J. Connor] Queens Sch Med, Kingston, ON, Canada.
   [Tu, Dongsheng; O'Callaghan, Chris J.] Canadian Canc Trials Grp, Kingston, ON, Canada.
   [Siu, Lillian L.; Liu, Geoffrey] Univ Hlth Network, Princess Margaret Canc Ctr, Toronto, ON, Canada.
   [Shapiro, Jeremy D.] Cabrini Hlth, Melbourne, Vic, Australia.
   [Jonker, Derek J.] Univ Ottawa, Ottawa Hosp Res Inst, Ottawa, ON, Canada.
   [Karapetis, Christos] Flinders Med Ctr, Adelaide, SA, Australia.
   [Karapetis, Christos] Flinders Univ S Australia, Adelaide, SA, Australia.
   [Simes, John] Univ Sydney, Natl Hlth & Med Res Council, Clin Trials Ctr, Sydney, NSW, Australia.
   [Price, Timothy J.] Queen Elizabeth Hosp, Adelaide, SA, Australia.
   [Price, Timothy J.] Univ Adelaide, Adelaide, SA, Australia.
   [Tebbutt, Niall C.] Austin Hlth, Melbourne, Vic, Australia.
C3 University of Toronto; University Health Network Toronto; Princess
   Margaret Cancer Centre; Cabrini Health; University of Ottawa; Ottawa
   Hospital Research Institute; Flinders Medical Centre; Flinders
   University South Australia; University of Sydney; University of
   Adelaide; Florey Institute of Neuroscience & Mental Health; Austin
   Research Institute
RP Wells, JC (corresponding author), Queens Univ, Sch Med, 15 Arch St, Kingston, ON K7L 3N6, Canada.
EM jwells@qmed.ca
RI Simes, Robert/P-1497-2014; Price, Timothy/G-1404-2012; Liu,
   Geoffrey/N-4421-2016
OI Karapetis, Christos/0000-0003-1741-996X; Liu,
   Geoffrey/0000-0002-2603-7296; Wells, Connor/0000-0001-7655-1405
CR [Anonymous], ANN ONCOL S8
   [Anonymous], 2015, TOP NEWS ADVISORY FR
   [Anonymous], J CLIN ONCOL
   Aparicio T, 2013, J CLIN ONCOL, V31, P1464, DOI 10.1200/JCO.2012.42.9894
   Asmis TR, 2011, ANN ONCOL, V22, P118, DOI 10.1093/annonc/mdq309
   Bouchahda M, 2008, CRIT REV ONCOL HEMAT, V67, P255, DOI 10.1016/j.critrevonc.2008.02.003
   CHARLSON M, 1994, J CLIN EPIDEMIOL, V47, P1245, DOI 10.1016/0895-4356(94)90129-5
   Cunningham D, 2013, LANCET ONCOL, V14, P1077, DOI 10.1016/S1470-2045(13)70154-2
   Dotan Efrat, 2012, J Gastrointest Cancer, V43, P562
   Falchook Gerald S, 2014, Oncoscience, V1, P540
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NR 34
TC 2
Z9 2
U1 0
U2 0
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD MAR
PY 2019
VL 18
IS 1
BP E140
EP E149
DI 10.1016/j.clcc.2018.11.006
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HP9VM
UT WOS:000462041100014
PM 30595557
DA 2025-01-04
ER

PT J
AU Shaw, P
   Dwivedi, SKD
   Bhattacharya, R
   Mukherjee, P
   Rao, GT
AF Shaw, Pallab
   Dwivedi, Shailendra Kumar Dhar
   Bhattacharya, Resham
   Mukherjee, Priyabrata
   Rao, Geeta
TI VEGF signaling: Role in angiogenesis and beyond
SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
LA English
DT Article
DE Angiogenesis; VEGF-VEGFR; Tumor microenvironment; Intercellular
   crosstalk; Intra-organelle crosstalk; Anti-VEGF therapies
ID CELL LUNG-CANCER; VEGF/VEGFR-TARGETED THERAPY; BLOOD-VESSEL FORMATION;
   INTUSSUSCEPTIVE ANGIOGENESIS; TUMOR ANGIOGENESIS; ENDOTHELIAL-CELLS;
   COLORECTAL-CANCER; NITRIC-OXIDE; STEM-CELLS; GROWTH
AB Angiogenesis is a crucial process for tissue development, repair, and tumor survival. Vascular endothelial growth factor (VEGF) is a key driver secreted by cancer cells, promoting neovascularization. While VEGF's role in angiogenesis is well-documented, its influence on the other aspects in tumor microenvironemt is less discussed. This review elaborates on VEGF's impact on intercellular interactions within the tumor microenvironment, including how VEGF affects pericyte proliferation and migration and mediates interactions between tumorassociated macrophages and cancer cells, resulting in PDL-1-mediated immunosuppression and Nrf2-mediated epithelial-mesenchymal transition. The review discusses VEGF's involvement in intra-organelle crosstalk, tumor metabolism, stemness, and epithelial-mesenchymal transition. It also provides insights into current antiVEGF therapies and their limitations in cancer treatment. Overall, this review aims to provide a thorough overview of the current state of knowledge concerning VEGF signaling and its impact, not only on angiogenesis but also on various other oncogenic processes.
C1 [Shaw, Pallab; Dwivedi, Shailendra Kumar Dhar; Bhattacharya, Resham; Mukherjee, Priyabrata; Rao, Geeta] Univ Oklahoma, Peggy & Charles Stephenson Canc Ctr, Hlth Sci Ctr, Oklahoma City, OK 73104 USA.
   [Dwivedi, Shailendra Kumar Dhar; Bhattacharya, Resham] Univ Oklahoma, Dept Obstet & Gynecol, Hlth Sci Ctr, Oklahoma City, OK 73104 USA.
   [Shaw, Pallab; Mukherjee, Priyabrata; Rao, Geeta] Univ Oklahoma, Dept Pathol, Hlth Sci Ctr, Oklahoma City, OK 73104 USA.
   [Rao, Geeta] Univ Oklahoma, Peggy & Charles Stephenson Canc Ctr, Dept Pathol, Hlth Sci Ctr, 940 Stanton L Young Blvd,BMSB-464, Oklahoma City, OK 73104 USA.
C3 University of Oklahoma System; University of Oklahoma Health Sciences
   Center; University of Oklahoma System; University of Oklahoma Health
   Sciences Center; University of Oklahoma System; University of Oklahoma
   Health Sciences Center; University of Oklahoma System; University of
   Oklahoma Health Sciences Center
RP Rao, GT (corresponding author), Univ Oklahoma, Peggy & Charles Stephenson Canc Ctr, Dept Pathol, Hlth Sci Ctr, 940 Stanton L Young Blvd,BMSB-464, Oklahoma City, OK 73104 USA.
EM geeta-rao@ouhsc.edu
RI SHAW, PALLAB/GQH-6277-2022
OI SHAW, PALLAB/0000-0002-0783-9410
FU Peggy and Charles Stephenson Cancer Center at the University of Oklahoma
   Health Sciences Center; National Cancer Institute Cancer Center Support
   Grant [P30CA225520]; Oklahoma Tobacco Settlement Endowment Trust
FX We thank the Peggy and Charles Stephenson Cancer Center at the
   University of Oklahoma Health Sciences Center for startup funds to GR.
   Manuscript preparation was supported in part by the National Cancer
   Institute Cancer Center Support Grant P30CA225520 and the Oklahoma
   Tobacco Settlement Endowment Trust contract awarded to the Stephenson
   Cancer Center.
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NR 222
TC 24
Z9 24
U1 25
U2 47
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 MAR
PY 2024
VL 1879
IS 2
AR 189079
DI 10.1016/j.bbcan.2024.189079
EA JAN 2024
PG 16
WC Biochemistry & Molecular Biology; Biophysics; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics; Oncology
GA JL8D7
UT WOS:001173406300001
PM 38280470
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Gong, J
   Cho, M
   Fakih, M
AF Gong, Jun
   Cho, May
   Fakih, Marwan
TI Chemotherapy in patients with hepatobiliary cancers and abnormal hepatic
   function
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Biliary cancer; hepatocellular carcinoma; abnormal liver function;
   chemotherapy
ID ADVANCED BILIARY-TRACT; PHASE-II TRIAL; HEPATOCELLULAR-CARCINOMA; RENAL
   DYSFUNCTION; 5-FLUOROURACIL LEUCOVORIN; COLORECTAL-CANCER; GEMCITABINE;
   OXALIPLATIN; CAPECITABINE; FLUOROURACIL
AB Sorafenib and cisplatin plus gemcitabine currently represent first-line treatment standards in advanced hepatocellular carcinoma and biliary cancer, respectively. Conventional cytotoxic agents (monotherapy or combination therapy) have demonstrated activity in the second-line setting or in those in which first-line agents are contraindicated. A strategy for safe yet effective administration of such systemic therapies in patients with advanced hepatobiliary cancer and abnormal liver function needs to be strongly considered. Here, we highlight the safety and tolerability of systemic therapies routinely used for the treatment of advanced hepatobiliary cancer in patients with hepatic dysfunction. Based on data from available clinical studies, we review dosing strategies recommended for chemotherapy and targeted therapy in those with liver dysfunction. Dose modifications for many agents in this population remain empiric due to limited clinical evidence. Future dedicated phase I studies are needed to provide further dosing considerations for combination therapy in those with abnormal liver function in which data is lacking.
C1 [Gong, Jun; Cho, May] City Hope Natl Med Ctr, Dept Med Oncol, 1500 E Duarte Rd, Duarte, CA 91010 USA.
   [Fakih, Marwan] City Hope Comprehens Canc Ctr, Med Oncol & Expt Therapeut, Bldg 51,Room 127,1500 E Duarte St, Duarte, CA 91010 USA.
C3 City of Hope; City of Hope
RP Fakih, M (corresponding author), City Hope Comprehens Canc Ctr, Med Oncol & Expt Therapeut, Bldg 51,Room 127,1500 E Duarte St, Duarte, CA 91010 USA.
EM mfakih@coh.org
OI Fakih, Marwan/0000-0002-6554-5488
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NR 51
TC 8
Z9 8
U1 0
U2 1
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD APR
PY 2017
VL 8
IS 2
BP 314
EP 323
DI 10.21037/jgo.2016.09.17
PG 10
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA EU8YK
UT WOS:000401324200011
PM 28480070
OA Green Published
DA 2025-01-04
ER

PT J
AU Lei, YR
   He, XL
   Li, J
   Mo, CF
AF Lei, Ya-ruo
   He, Xian-lu
   Li, Jun
   Mo, Chun-fen
TI Drug Resistance in Hepatocellular Carcinoma: Theoretical Basis and
   Therapeutic Aspects
SO FRONTIERS IN BIOSCIENCE-LANDMARK
LA English
DT Review
DE chemotherapy; hepatocellular carcinoma; multidrug resistance; tumor
   microenvironment; targeted therapy; immunotherapy
ID CANCER STEM-CELLS; MULTIDRUG-RESISTANCE; MOLECULAR-MECHANISMS; 1ST-LINE
   TREATMENT; COLORECTAL-CANCER; GENE-EXPRESSION; DOWN-REGULATION;
   P-GLYCOPROTEIN; DNA-DAMAGE; OPEN-LABEL
AB Primary liver cancer is one of the most common malignant tumors with high mortality and increasing incidence worldwide. Currently, chemotherapy is an important comprehensive treatment for moderate or advanced liver cancer. Despite the effective therapeutic effects initially achieved by chemotherapy, the high phenotypic and molecular heterogeneity of liver cancer cells facilitates resistance to conventional chemotherapy or targeted therapy and even leads to multidrug resistance (MDR), which is one of the major obstacles for clinical chemotherapy. Drug resistance exhibits multiple and complex molecular mechanisms to antagonize therapy under pharmacological pressure, including overexpression of drug efflux transporters, downstream adaptive response (such as apoptosis, autophagy, and endoplasmic reticulum stress), dysfunction of DNA damage repair (DDR), epigenetic modification, tumor microenvironment (TME) as well as extracellular matrix (ECM). In this paper, we summarize the recent research progress and intervention strategies for drug resistance in hepatocellular carcinoma (HCC), which will provide a promising therapeutic strategy for overcoming MDR in liver cancer.
C1 [Lei, Ya-ruo; Mo, Chun-fen] Chengdu Med Coll, Sch Basic Med Sci, Dept Immunol, Chengdu 610500, Sichuan, Peoples R China.
   [He, Xian-lu; Mo, Chun-fen] Chengdu Med Coll, China Natl Nucl Corp 416 Hosp, Dept Gen Surg, Affiliated Hosp 2, Chengdu 610083, Sichuan, Peoples R China.
   [Li, Jun] Chengdu Med Coll, Affiliated Hosp 1, Dept Gastroenterol, Chengdu 610500, Sichuan, Peoples R China.
C3 Chengdu Medical College; China National Nuclear Corporation; Chengdu
   Medical College; Chengdu Medical College
RP Mo, CF (corresponding author), Chengdu Med Coll, Sch Basic Med Sci, Dept Immunol, Chengdu 610500, Sichuan, Peoples R China.; Mo, CF (corresponding author), Chengdu Med Coll, China Natl Nucl Corp 416 Hosp, Dept Gen Surg, Affiliated Hosp 2, Chengdu 610083, Sichuan, Peoples R China.; Li, J (corresponding author), Chengdu Med Coll, Affiliated Hosp 1, Dept Gastroenterol, Chengdu 610500, Sichuan, Peoples R China.
EM lijun84183967@126.com; mochunfen@cmc.edu.cn
FU National Natural Science Foundation of China [82170645]; Project of
   Chengdu Health and Family Planning Commission [2021076, 2022043];
   Department of Science and Technology of Sichuan Province (CN)
   [24NSFSC2357, 22NSFSC0766]; Disciplinary Construction Innovation Team
   Foundation of Chengdu Medical College [CMC-XK- 2103]
FX This study was supported by the National Natural Science Foundation of
   China (No. 82170645) , Project of Chengdu Health and Family Planning
   Commission (No. 2021076 and 2022043) , Department of Science and
   Technology of Sichuan Province (CN) (No. 24NSFSC2357 and 22NSFSC0766) ,
   Disciplinary Construction Innovation Team Foundation of Chengdu Medical
   College (CMC-XK- 2103) .
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NR 195
TC 7
Z9 7
U1 8
U2 18
PU IMR PRESS
PI ROBINSON
PA 112 ROBINSON RD, ROBINSON, SINGAPORE
SN 2768-6701
EI 2768-6698
J9 FRONT BIOSCI-LANDMRK
JI Front. Biosci.
PD FEB
PY 2024
VL 29
IS 2
AR 52
DI 10.31083/j.fbl2902052
PG 17
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA JU3J6
UT WOS:001175634000031
PM 38420802
OA gold
DA 2025-01-04
ER

PT J
AU Li, Y
   Duo, YH
   Bao, SY
   He, LS
   Ling, K
   Luo, JF
   Zhang, Y
   Huang, H
   Zhang, H
   Yu, XF
AF Li, Yang
   Duo, Yanhong
   Bao, Shiyun
   He, Lisheng
   Ling, Kai
   Luo, Jinfeng
   Zhang, Yue
   Huang, Hao
   Zhang, Han
   Yu, Xiaofang
TI EpCAM aptamer-functionalized polydopamine-coated mesoporous silica
   nanoparticles loaded with DM1 for targeted therapy in colorectal cancer
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE DM1; EpCAM aptamer; mesoporous silica nanoparticles; colorectal cancer
ID ADO-TRASTUZUMAB EMTANSINE; DRUG-DELIVERY; SURFACE MODIFICATION;
   PROSTATE; BIODISTRIBUTION; STATISTICS; EXPRESSION; MOLECULE; CELLS;
   COLON
AB DM1, a maytansine derivative, is a highly potential cytotoxic agent but with severe side effects; therefore, its application in clinical cancer therapy is limited. Here, in order to mitigate this intrinsic drawback of DM1, we developed mesoporous silica nanoparticles (MSNs) loaded with DM1 and surface-decorated with hydrochloride dopamine (PDA), polyethylene glycol (PEG), and epithelial cell adhesion molecule (EpCAM) aptamer (APt) for the targeted treatment of colorectal cancer (CRC). In this system, the PDA coating could be used as pH-sensitive gatekeepers to control the release of DM1 from MSNs in response to the pH stimulus and EpCAM APt-guided active targeting enables the increased delivery of DM1 to CRC as well as a reduction in toxicity and side effects by minimizing the exposure of normal tissues to DM1. Results demonstrated that DM1 inhibited the formation of microtubules and induced apoptosis in tumor cells via caspase signaling. In comparison with the control groups, the MSNs-DM1@PDA-PEG-APt bioconjugates exhibited increased binding ability and much higher cytotoxicity to the CRC SW480 cell line. Furthermore, in vivo assays confirmed the advantages of such a strategy. These findings suggested that MSNs-DM1@PDA-PEG-APt could represent a promising therapeutic platform for EpCAM-positive CRC.
C1 [Li, Yang; Bao, Shiyun; Zhang, Yue; Yu, Xiaofang] Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Dept Hepatobiliary & Pancreas Surg, 1017 Dongmen North Rd, Shenzhen 518000, Peoples R China.
   [Duo, Yanhong; Huang, Hao; Zhang, Han] Shenzhen Univ, Coll Optoelect Engn,Shenzhen Engn Lab Phosphorene, Collaborat Innovat Ctr Optoelect Sci & Technol, Key Lab Optoelect Devices & Syst,Minist Educ & Gu, 3688 Nanhai Rd, Shenzhen 518060, Peoples R China.
   [Duo, Yanhong] Lanzhou Univ, Sch Life Sci, Minist Educ, Key Lab Plant Cell Activ & Stress Adaptat, Lanzhou, Gansu, Peoples R China.
   [He, Lisheng; Luo, Jinfeng] Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Inst Resp Dis,Dept Pathol, Shenzhen, Peoples R China.
   [Ling, Kai] Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Inst Resp Dis, Shenzhen, Peoples R China.
C3 Jinan University; Shenzhen University; Lanzhou University; Jinan
   University; Jinan University
RP Yu, XF (corresponding author), Jinan Univ, Shenzhen Peoples Hosp, Clin Med Coll 2, Dept Hepatobiliary & Pancreas Surg, 1017 Dongmen North Rd, Shenzhen 518000, Peoples R China.; Zhang, H (corresponding author), Shenzhen Univ, Coll Optoelect Engn,Shenzhen Engn Lab Phosphorene, Collaborat Innovat Ctr Optoelect Sci & Technol, Key Lab Optoelect Devices & Syst,Minist Educ & Gu, 3688 Nanhai Rd, Shenzhen 518060, Peoples R China.
EM hzhang@szu.edu.cn; yuxfshui@hotmail.com
RI zhang, han/I-8297-2015; wang, rui/JAC-6240-2023; Li, Yang/AAM-5383-2020;
   Huang, H./M-1134-2014
FU Science, Technology & Innovation Commission of Shenzhen Municipality
   [JCYJ20160422170206664]; Natural Science Foundation of Guangdong
   Province, China [2014A030310481]
FX This research was supported by the Science, Technology & Innovation
   Commission of Shenzhen Municipality (No JCYJ20160422170206664) and the
   Natural Science Foundation of Guangdong Province, China
   (2014A030310481).
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NR 46
TC 53
Z9 55
U1 7
U2 86
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 2017
VL 12
BP 6239
EP 6257
DI 10.2147/IJN.S143293
PG 19
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA FE7RR
UT WOS:000408405100007
PM 28894364
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Shi, MK
   Wang, WR
   Zhang, JK
   Li, BB
   Lv, DX
   Wang, DH
   Wang, SZ
   Cheng, DZ
   Ma, TH
AF Shi, Minke
   Wang, Weiran
   Zhang, Jinku
   Li, Bobo
   Lv, Dongxiao
   Wang, Danhua
   Wang, Sizhen
   Cheng, Dezhi
   Ma, Tonghui
TI Identification of <i>RET</i> fusions in a Chinese multicancer
   retrospective analysis by next-generation sequencing
SO CANCER SCIENCE
LA English
DT Article
DE EGFR-TKI resistance; lung cancer; multicancer; NGS; RET fusion
ID PAPILLARY THYROID-CANCER; CELL LUNG-CANCER; GENE FUSIONS; TARGETED
   THERAPY; ROS1; ALK; REARRANGEMENTS; PROTOONCOGENE; ADENOCARCINOMAS;
   EXPRESSION
AB Fusion of RET with different partner genes has been detected in papillary thyroid, lung, colorectal, pancreatic, and breast cancer. Approval of selpercatinib for treatment of lung and thyroid cancer with RET gene mutations or fusions calls for studies to explore RET fusion partners and their eligibility for RET-based targeted therapy. In this study, RET fusion patterns in a large group of Chinese cancer patients covering several cancer types were identified using next-generation sequencing. A total of 44 fusion patterns were identified in the study cohort with KIF5B, CCDC6, and ERC1 being the most common RET fusion partners. Notably, 17 novel fusions were first reported in this study. Prevalence of functional RET fusions was 1.05% in lung cancer, 6.03% in thyroid cancer, 0.39% in colorectal cancer, and less than 0.1% in gastric cancer and hepatocellular carcinoma. Analysis showed a preference for fusion partners in different tumor types, with KIF5B being the common type in lung cancer, CCDC6 in thyroid cancer, and NCOA4 in colorectal cancer. Co-occurrence of EGFR mutations and RET fusions with rare partner genes (rather than KIF5B) in lung cancer patients was correlated with epidermal growth factor receptor-tyrosine kinase inhibitor resistance and could predict response to targeted therapies. Findings from this study provide a guide to clinicians in determining tumors with specific fusion patterns as candidates for RET targeted therapies.
C1 [Shi, Minke] Nanjing Univ, Dept Thorac & Cardiovasc Surg, Affiliated Drum Tower Hosp, Med Sch, Nanjing, Peoples R China.
   [Wang, Weiran; Wang, Danhua; Ma, Tonghui] Genetron Hlth Beijing Technol Co Ltd, Dept Translat Med, Bldg 11,Zone 1,8 Life Sci Pkwy, Beijing 102200, Peoples R China.
   [Zhang, Jinku] First Ctr Hosp Baoding, Dept Pathol, Key Lab Mol Pathol & Early Diag Tumor Hebei Prov, Baoding, Peoples R China.
   [Li, Bobo] Shandong Univ, Dept Thorac Surg, Shandong Canc Hosp, Jinan, Peoples R China.
   [Lv, Dongxiao] Shandong First Med Univ, Tumor Res & Therapy Ctr, Shandong Prov Hosp, Jinan, Peoples R China.
   [Wang, Sizhen] Genetron Hlth Beijing Technol Co Ltd, Beijing, Peoples R China.
   [Cheng, Dezhi] Wenzhou Med Univ, Dept Thorac Surg, Affiliated Hosp 1, Wenzhou 325000, Zhejiang, Peoples R China.
C3 Nanjing University; Shandong First Medical University & Shandong Academy
   of Medical Sciences; Shandong University; Shandong First Medical
   University & Shandong Academy of Medical Sciences; Wenzhou Medical
   University
RP Ma, TH (corresponding author), Genetron Hlth Beijing Technol Co Ltd, Dept Translat Med, Bldg 11,Zone 1,8 Life Sci Pkwy, Beijing 102200, Peoples R China.; Cheng, DZ (corresponding author), Wenzhou Med Univ, Dept Thorac Surg, Affiliated Hosp 1, Wenzhou 325000, Zhejiang, Peoples R China.
EM dezhicheng@sina.com; tonghuima@yeah.net
RI wang, weiran/HGU-3350-2022; Ma, Tonghui/AAE-1874-2022
OI Ma, Tonghui/0000-0002-5414-0522
FU Wenzhou Municipal Science and Technology Bureau of China [Y20180175]
FX The paper was supported by grants from the Wenzhou Municipal Science and
   Technology Bureau of China (No. Y20180175)
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NR 63
TC 26
Z9 27
U1 0
U2 13
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1347-9032
EI 1349-7006
J9 CANCER SCI
JI Cancer Sci.
PD JAN
PY 2022
VL 113
IS 1
BP 308
EP 318
DI 10.1111/cas.15181
EA NOV 2021
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YE0WK
UT WOS:000718760400001
PM 34710947
OA Green Published
DA 2025-01-04
ER

PT J
AU Wang, H
   Cui, GH
   Yu, B
   Sun, MY
   Yang, H
AF Wang, Hao
   Cui, Guihua
   Yu, Bo
   Sun, Meiyan
   Yang, Hong
TI Cancer Stem Cell Niche in Colorectal Cancer and Targeted Therapies
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
DE Cancer stem cells; multidrug resistance; cancer niche; targeted therapy;
   chemotherapy; tumor-initiating cells
ID TUMOR-INITIATING CELLS; ACUTE MYELOID-LEUKEMIA; PROMOTES DNA-REPAIR;
   COLON-CANCER; LUNG-CANCER; SIDE POPULATION; DRUG-RESISTANCE;
   SELF-RENEWAL; PANETH CELLS; OVARIAN-CANCER
AB Cancer stem cells (CSCs), also known as tumor-initiating cells, are a sub-population of tumor cells found in many human cancers that are endowed with self-renewal and pluripotency. CSCs may be more resistant to conventional anticancer therapies than average cancer cells, as they can easily escape the cytotoxic effects of standard chemotherapy, thereby resulting in tumor relapse. Despite significant progress in related research, effective elimination of CSCs remains an unmet clinical need. CSCs are localized in a specialized microenvironment termed the niche, which plays a pivotal role in cancer multidrug resistance. The niche components of CSCs, such as the extracellular matrix, also physically shelter CSCs from therapeutic agents. Colorectal cancer is the most common malignancy worldwide and presents a relatively transparent process of cancer initiation and development, making it an ideal model for CSC niche research. Here, we review recent advances in the field of CSCs using colorectal cancer as an example to illustrate the potential therapeutic value of targeting the CSC niche. These findings not only provide a novel theoretical basis for in-depth discussions on tumor occurrence, development, and prognosis evaluation, but also offer new strategies for the targeted treatment of cancer.
C1 [Wang, Hao; Yu, Bo; Yang, Hong] Liaoning Normal Univ, Sch Life Sci, Liaoning Prov Key Lab Biotechnol & Drug Discovery, Dalian, Peoples R China.
   [Wang, Hao; Sun, Meiyan] Jilin Med Univ, Lab Med Coll, Jilin, Jilin, Peoples R China.
   [Cui, Guihua] Jilin Med Univ, Sch Pharm, Jilin, Jilin, Peoples R China.
C3 Liaoning Normal University; Jilin Medical University; Jilin Medical
   University
RP Yang, H (corresponding author), Liaoning Normal Univ, Sch Life Sci, Liaoning Prov Key Lab Biotechnol & Drug Discovery, Dalian, Peoples R China.
EM hyanglnnu@126.com
RI sun, meiyan/AAW-4123-2020
OI Wang, Hao/0000-0002-2218-1194
FU National Natural Science Fund [81973380, 81473265]; Project of Science
   and Technology Development Plan of Jilin Province [20190201148JC]
FX The study was funded by the National Natural Science Fund (No. 81973380;
   81473265) and Project of Science and Technology Development Plan of
   Jilin Province (No. 20190201148JC), China.
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NR 180
TC 7
Z9 7
U1 0
U2 9
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 2020
VL 26
IS 17
BP 1979
EP 1993
DI 10.2174/1381612826666200408102305
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA LY0NO
UT WOS:000540221200004
PM 32268862
DA 2025-01-04
ER

PT J
AU Yang, J
   Yang, X
   Gao, L
   Zhang, J
   Yi, C
   Huang, Y
AF Yang, Ju
   Yang, Xi
   Gao, Ling
   Zhang, Jie
   Yi, Cheng
   Huang, Ying
TI The role of the renin-angiotensin system inhibitors in malignancy: a
   review
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Review
DE RASi; ARB; AECI; cancer treatment
ID II TYPE-1 RECEPTOR; CONVERTING ENZYME-INHIBITORS; BREAST-CANCER
   RECURRENCE; RENAL-CELL CARCINOMA; COLORECTAL-CANCER; PANCREATIC-CANCER;
   ANGIOGENIC INHIBITOR; TUMOR ANGIOGENESIS; ACE-INHIBITORS; BETA-BLOCKERS
AB Hypertension is one of the most prevalent diseases in cardiology. The angiotensin receptor blockers (ARBs)/angiotensin converting enzyme inhibitors (ACEIs) are widely used drugs to stabilize the blood pressure via inhibition of the renin-angiotensin system (RAS). Studies have found that the exposure to RAS inhibitors (RASi) can suppress the development of cancers via multimodal mechanisms and has attracted increased attentions in the recent past. Owing the potential of RASi to inhibit tumor growth, proliferation and metastasis, they are considered as the potential and exciting candidates to enhance the effect of chemo-radiotherapy and targeted therapy efficacy. However, there are conflicting reports as to the use of ARB/ACEI in all facets of tumor growth. In this study, we comprehensively summarize and review the potential mechanisms of RASi in cancer treatment, like inhibition of tumor angiogenesis, reduction of cancer-associated fibroblasts (CAFs) and extracellular matrix (ECM), regulation of immune cells and improvement of hypoxia. Additionally, based on the basic and clinical experiments, we analyze the views and results regarding the role of RASi plays in tumor from genesis to recurrence, and certainly cancer treatment (chemo-radiotherapy and targeted therapy). In the last, not only do we discuss the prospects of using RASi to enhance cancer treatment efficacy but also point out the conflicting situation with the intention to give some directions and inspiration on this topic.
C1 [Yang, Ju; Huang, Ying] Sichuan Univ, West China Sch Basic Med Sci & Forens Med, 17,Sect 3,People South Rd, Chengdu 610041, Sichuan, Peoples R China.
   [Yang, Xi; Gao, Ling; Yi, Cheng] Sichuan Univ, Canc Ctr, West China Hosp, Dept Med Oncol, 37 Guoxue Lane, Chengdu 610041, Sichuan, Peoples R China.
   [Zhang, Jie] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Lab Expt Oncol, Chengdu 610041, Peoples R China.
   [Zhang, Jie] Sichuan Univ, West China Hosp, Canc Ctr, Chengdu 610041, Peoples R China.
   [Zhang, Jie] Collaborat Innovat Ctr, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University; Sichuan
   University
RP Huang, Y (corresponding author), Sichuan Univ, West China Sch Basic Med Sci & Forens Med, 17,Sect 3,People South Rd, Chengdu 610041, Sichuan, Peoples R China.; Yi, C (corresponding author), Sichuan Univ, Canc Ctr, West China Hosp, Dept Med Oncol, 37 Guoxue Lane, Chengdu 610041, Sichuan, Peoples R China.
EM yicheng6834@126.com
RI yi, cheng/KHC-5004-2024
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NR 105
TC 11
Z9 11
U1 1
U2 13
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2156-6976
J9 AM J CANCER RES
JI Am. J. Cancer Res.
PY 2021
VL 11
IS 3
BP 884
EP 897
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA RL9ZJ
UT WOS:000639321600008
PM 33791161
DA 2025-01-04
ER

PT J
AU Zaiachuk, M
   Pryimak, N
   Kovalchuk, O
   Kovalchuk, I
AF Zaiachuk, Mariia
   Pryimak, Nazar
   Kovalchuk, Olga
   Kovalchuk, Igor
TI Cannabinoids, Medical Cannabis, and Colorectal Cancer Immunotherapy
SO FRONTIERS IN MEDICINE
LA English
DT Review
DE colorectal cancer; immunotherapy; cannabinoids; Cannabis sativa
   extracts; inflammation
ID COLON CARCINOGENESIS; SUPPRESSOR-CELLS; IMMUNE-SYSTEM; MAST-CELLS;
   INFLAMMATION; RECEPTOR; ANGIOGENESIS; PATHOGENESIS; EXPRESSION; RISK
AB Colorectal cancer is a major public health problem. Unfortunately, currently, no effective curative option exists for this type of malignancy. The most promising cancer treatment nowadays is immunotherapy which is also called biological or targeted therapy. This type of therapy boosts the patient's immune system ability to fight the malignant tumor. However, cancer cells may become resistant to immunotherapy and escape immune surveillance by obtaining genetic alterations. Therefore, new treatment strategies are required. In the recent decade, several reports suggest the effectiveness of cannabinoids and Cannabis sativa extracts for inhibiting cancer proliferation in vitro and in vivo, including intestinal malignancies. Cannabinoids were shown to modulate the pathways involved in cell proliferation, angiogenesis, programmed cell death and metastasis. Because of that, they are proposed as adjunct therapy for many malignancies. By far less information exists on the potential of the use of cannabis in combination with immunotherapy. Here, we explore the possibility of the use of cannabinoids for modulation of immunotherapy of colon cancer and discuss possible advantages and limitations.
C1 [Zaiachuk, Mariia; Pryimak, Nazar; Kovalchuk, Olga; Kovalchuk, Igor] Univ Lethbridge, Dept Biol Sci, Lethbridge, AB, Canada.
C3 University of Lethbridge
RP Kovalchuk, O; Kovalchuk, I (corresponding author), Univ Lethbridge, Dept Biol Sci, Lethbridge, AB, Canada.
EM olga.kovalchuk@uleth.ca; igor.kovalchuk@uleth.ca
FU MITACS grant
FX This research was funded by MITACS grant to OK, IK, and MZ.
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NR 123
TC 18
Z9 18
U1 1
U2 16
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 24
PY 2021
VL 8
AR 713153
DI 10.3389/fmed.2021.713153
PG 15
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA WE8SS
UT WOS:000705889700001
PM 34631734
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Li, JS
   Ji, YH
   Chen, N
   Dai, L
   Deng, HX
AF Li, Junshu
   Ji, Yanhong
   Chen, Na
   Dai, Lei
   Deng, Hongxin
TI Colitis-associated carcinogenesis: crosstalk between tumors, immune
   cells and gut microbiota
SO CELL AND BIOSCIENCE
LA English
DT Review
DE Colitis-associated carcinogenesis; IBD therapy; Intestinal epithelial
   cells; Intestinal mesenchymal cells; Immune cells; Gut microbiota
ID INTESTINAL EPITHELIAL-CELLS; CANCER-ASSOCIATED FIBROBLASTS;
   COLORECTAL-CANCER; DENDRITIC CELLS; ULCERATIVE-COLITIS;
   SUPPRESSOR-CELLS; COLON-CANCER; FUSOBACTERIUM-NUCLEATUM; MESENCHYMAL
   CELLS; STAT3 ACTIVATION
AB Colorectal cancer (CRC) is the third most common cancer worldwide. One of the main causes of colorectal cancer is inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn's disease (CD). Intestinal epithelial cells (IECs), intestinal mesenchymal cells (IMCs), immune cells, and gut microbiota construct the main body of the colon and maintain colon homeostasis. In the development of colitis and colitis-associated carcinogenesis, the damage, disorder or excessive recruitment of different cells such as IECs, IMCs, immune cells and intestinal microbiota play different roles during these processes. This review aims to discuss the various roles of different cells and the crosstalk of these cells in transforming intestinal inflammation to cancer, which provides new therapeutic methods for chemotherapy, targeted therapy, immunotherapy and microbial therapy.
C1 [Li, Junshu; Ji, Yanhong; Chen, Na; Dai, Lei; Deng, Hongxin] Sichuan Univ, West China Hosp, Canc Ctr, Dept Biotherapy, Ke Yuan Rd 4,1 Gao Peng St, Chengdu 610041, Peoples R China.
   [Li, Junshu; Ji, Yanhong; Chen, Na; Dai, Lei; Deng, Hongxin] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Ke Yuan Rd 4,1 Gao Peng St, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University
RP Dai, L; Deng, HX (corresponding author), Sichuan Univ, West China Hosp, Canc Ctr, Dept Biotherapy, Ke Yuan Rd 4,1 Gao Peng St, Chengdu 610041, Peoples R China.; Dai, L; Deng, HX (corresponding author), Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Ke Yuan Rd 4,1 Gao Peng St, Chengdu 610041, Peoples R China.
EM dailei2016@scu.edu.cn; denghongx@scu.edu.cn
RI jiang, lei/IWE-1124-2023
FU We thank Wencheng Zhou, Gang Shi and Lin Cheng for a critical reading of
   the manuscript.
FX We thank Wencheng Zhou, Gang Shi and Lin Cheng for a critical reading of
   the manuscript.
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NR 300
TC 6
Z9 6
U1 1
U2 19
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2045-3701
J9 CELL BIOSCI
JI Cell Biosci.
PD OCT 24
PY 2023
VL 13
IS 1
AR 194
DI 10.1186/s13578-023-01139-8
PG 19
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA W0LH3
UT WOS:001088626100002
PM 37875976
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Gotovac, JR
   Fujihara, KM
   Phillips, WA
   Clemons, NJ
AF Gotovac, Jovana Ranko
   Fujihara, Kenji Mark
   Phillips, Wayne Allen
   Clemons, Nicholas James
TI TGFβ Signaling and Its Targeted Therapy in Gastrointestinal Cancers
SO DISCOVERY MEDICINE
LA English
DT Article
ID GROWTH-FACTOR-BETA; COLON-CANCER; JUVENILE POLYPOSIS; COLORECTAL-CANCER;
   GASTRIC POLYPOSIS; JAPANESE PATIENTS; MUTANT MICE; SMAD4 GENE;
   EXPRESSION; MUTATIONS
AB The transforming growth factor beta (TGF beta) signaling pathway governs physiological homeostasis in the gastrointestinal system and its deregulation can lead to a diverse range of human pathologies including juvenile polyposis syndrome and tumor initiation, progression, and metastasis. In gastrointestinal malignancies, tumor cells evade the known tumor suppressive effects of TGF beta signaling through frequent inactivation of the pathway. Paradoxically, tumor cells utilize TGF beta-mediated regulation of epithelial-mesenchymal transition and immunomodulation to facilitate the invasive and migratory phenotype of gastrointestinal cancers and avoid immuno-surveillance. The dichotomous role of TGF beta as both a tumor suppressor and tumor promoter has highly challenged research efforts to specifically target TGF beta signaling as a cancer therapy. The current preclinical approach is to inhibit TGF beta-mediated generation of a favorable microenvironment for tumor growth, invasion, and metastasis. Here, we overview the alterations of TGF beta signaling and its fundamental biological relevance in gastrointestinal tumorigenesis. We further discuss future perspectives for efficacious molecular targeted treatment of contextual TGF beta tumor-promoting effects in gastrointestinal cancers.
C1 [Gotovac, Jovana Ranko; Fujihara, Kenji Mark; Phillips, Wayne Allen] Peter MacCallum Canc Ctr, Div Canc Res, Parkville, Vic 3010, Australia.
   [Gotovac, Jovana Ranko; Fujihara, Kenji Mark; Phillips, Wayne Allen] Univ Melbourne, Sir Peter MacCallum Dept Oncol, Parkville, Vic 3010, Australia.
   [Phillips, Wayne Allen] Univ Melbourne, St Vincents Hosp, Dept Surg, Parkville, Vic 3010, Australia.
C3 Peter Maccallum Cancer Center; Peter Maccallum Cancer Center; University
   of Melbourne; University of Melbourne; St Vincent's Health; St Vincent's
   Hospital Melbourne; NSW Health; St Vincents Hospital Sydney
EM nicholas.clemons@petermac.org
RI Clemons, Nicholas/AAN-6516-2020; Phillips, Wayne Allen/H-8070-2013
OI Phillips, Wayne Allen/0000-0002-7961-638X; Clemons,
   Nicholas/0000-0001-9283-9978
FU Department of Health and Human Services acting through the Victorian
   Cancer Agency, Victoria, Australia [MCRF16002]
FX N.J.C. is supported by a Fellowship (MCRF16002) from the Department of
   Health and Human Services acting through the Victorian Cancer Agency,
   Victoria, Australia.
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NR 79
TC 12
Z9 13
U1 0
U2 6
PU DISCOVERY MEDICINE
PI TIMONIUM
PA 10 GERARD AVE, STE 201, TIMONIUM, MD 21093 USA
SN 1539-6509
EI 1944-7930
J9 DISCOV MED
JI Discov. Med.
PD SEP
PY 2018
VL 26
IS 142
BP 103
EP 112
PG 10
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA HB9AP
UT WOS:000451384100004
PM 30399328
DA 2025-01-04
ER

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   Rosenberg, A
   Patel, S
   Raparia, K
   Choi, J
   Wainwright, DA
   Villaflor, V
   Cristofanilli, M
   Giles, F
AF Chae, Young Kwang
   Arya, Ayush
   Chiec, Lauren
   Shah, Hiral
   Rosenberg, Ari
   Patel, Sandip
   Raparia, Kirtee
   Choi, Jaehyuk
   Wainwright, Derek A.
   Villaflor, Victoria
   Cristofanilli, Massimo
   Giles, Francis
TI Challenges and future of biomarker tests in the era of precision
   oncology: Can we rely on immunohistochemistry (IHC) or fluorescence
   <i>in situ</i> hybridization (FISH) to select the optimal patients for
   matched therapy?
SO ONCOTARGET
LA English
DT Review
DE IHC; FISH; predictive; biomarker; targeted therapy
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; CHEMOTHERAPY PLUS CETUXIMAB;
   TUMOR-INFILTRATING LYMPHOCYTES; RANDOMIZED PHASE-III; GENE COPY NUMBER;
   METASTATIC COLORECTAL-CARCINOMA; DNA METHYLATION BIOMARKERS; MET
   SIGNALING PATHWAY; K-RAS MUTATIONS
AB Molecular techniques have improved our understanding of the pathogenesis of cancer development. These techniques have also fueled the rational development of targeted drugs for patient populations stratified by their genetic characteristics. These novel methods have changed the classic paradigm of diagnostic pathology; among them are IHC, FISH, polymerase chain reaction (PCR) and microarray technology. IHC and FISH detection methods for human epidermal growth factor receptor-2 (HER2), epidermal growth factor receptor (EGFR) and programmed death ligand-1 (PD-L1) were recently approved by the Food and Drug Administration (FDA) as routine clinical practice for cancer patients. Here, we discuss general challenges related to the predictive power of these molecular biomarkers for targeted therapy in cancer medicine. We will also discuss the prospects of utilizing new biomarkers for fibroblast growth factor receptor (FGFR) and hepatocyte growth factor receptor (cMET/MET) targeted therapies for developing new and robust predictive biomarkers in oncology.
C1 [Chae, Young Kwang; Shah, Hiral; Villaflor, Victoria; Cristofanilli, Massimo; Giles, Francis] Div Hematol Oncol, Dev Therapeut Program, Chicago, IL USA.
   [Chae, Young Kwang; Arya, Ayush; Chiec, Lauren; Rosenberg, Ari; Raparia, Kirtee; Choi, Jaehyuk; Wainwright, Derek A.; Villaflor, Victoria; Cristofanilli, Massimo; Giles, Francis] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
   [Chae, Young Kwang; Raparia, Kirtee; Choi, Jaehyuk; Wainwright, Derek A.; Villaflor, Victoria; Cristofanilli, Massimo; Giles, Francis] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
   [Patel, Sandip] Univ Calif San Diego, San Diego, CA 92103 USA.
C3 Northwestern University; Robert H. Lurie Comprehensive Cancer Center;
   Ann & Robert H. Lurie Children's Hospital of Chicago; Northwestern
   University; Feinberg School of Medicine; University of California
   System; University of California San Diego
RP Chae, YK (corresponding author), Div Hematol Oncol, Dev Therapeut Program, Chicago, IL USA.; Chae, YK (corresponding author), Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.; Chae, YK (corresponding author), Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
EM young.chae@northwestern.edu
RI Choi, Jaehyuk/N-6532-2019; Villaflor, Victoria/AAE-1713-2021; Patel,
   Sandip/O-9591-2015
OI Choi, Jaehyuk/0000-0003-2379-2226; Wainwright, Derek/0000-0001-7232-4264
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NR 244
TC 12
Z9 18
U1 1
U2 8
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 21
PY 2017
VL 8
IS 59
BP 100863
EP 100898
DI 10.18632/oncotarget.19809
PG 36
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FS1TR
UT WOS:000419561600143
PM 29246028
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Vaghari-Tabari, M
   Targhazeh, N
   Moein, S
   Qujeq, D
   Alemi, F
   Majidina, M
   Younesi, S
   Asemi, Z
   Yousefi, B
AF Vaghari-Tabari, Mostafa
   Targhazeh, Niloufar
   Moein, Soheila
   Qujeq, Durdi
   Alemi, Forough
   Majidina, Maryam
   Younesi, Simin
   Asemi, Zatollah
   Yousefi, Bahman
TI From inflammatory bowel disease to colorectal cancer: what's the role of
   miRNAs?
SO CANCER CELL INTERNATIONAL
LA English
DT Review
DE Inflammatory bowel disease; Colorectal carcinoma; miRNAs; Ulcerative
   colitis; Targeted therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; INDUCED CYTIDINE DEAMINASE;
   ARYL-HYDROCARBON RECEPTOR; COLITIS-ASSOCIATED CANCER; DSS-INDUCED
   COLITIS; NF-KAPPA-B; PROMOTES INTESTINAL INFLAMMATION; BETA-CATENIN
   ACTIVATION; DEXTRAN SODIUM-SULFATE; ULCERATIVE-COLITIS
AB Inflammatory Bowel Disease (IBD) is a chronic inflammatory disease with relapse and remission periods. Ulcerative colitis and Crohn's disease are two major forms of the disease. IBD imposes a lot of sufferings on the patient and has many consequences; however, the most important is the increased risk of colorectal cancer, especially in patients with Ulcerative colitis. This risk is increased with increasing the duration of disease, thus preventing the progression of IBD to cancer is very important. Therefore, it is necessary to know the details of events contributed to the progression of IBD to cancer. In recent years, the importance of miRNAs as small molecules with 20-22 nucleotides has been recognized in pathophysiology of many diseases, in which IBD and colorectal cancer have not been excluded. As a result, the effectiveness of these small molecules as therapeutic target is hopefully confirmed. This paper has reviewed the related studies and findings about the role of miRNAs in the course of events that promote the progression of IBD to colorectal carcinoma, as well as a review about the effectiveness of some of these miRNAs as therapeutic targets.
C1 [Vaghari-Tabari, Mostafa; Targhazeh, Niloufar; Alemi, Forough] Tabriz Univ Med Sci, Student Res Comm, Tabriz, Iran.
   [Vaghari-Tabari, Mostafa] Tabriz Univ Med Sci, Fac Med, Dept Clin Biochem & Lab Med, Tabriz, Iran.
   [Moein, Soheila] Shiraz Univ Med Sci, Med Plants Proc Res Ctr, Shiraz, Iran.
   [Moein, Soheila] Hormozgan Univ Med Sci, Fac Med, Dept Biochem, Bandar Abbas, Iran.
   [Qujeq, Durdi] Babol Univ Med Sci, Cellular & Mol Biol Res Ctr CMBRC, Hlth Res Inst, Babol, Iran.
   [Qujeq, Durdi] Babol Univ Med Sci, Dept Clin Biochem, Babol, Iran.
   [Majidina, Maryam] Urmia Univ Med Sci, Solid Tumor Res Ctr, Orumiyeh, Iran.
   [Younesi, Simin] RMIT Univ, Sch Hlth & Biomed Sci, Melborne, Vic, Australia.
   [Asemi, Zatollah] Kashan Univ Med Sci, Res Ctr Biochem & Nutr Metab Dis, Kashan, Iran.
   [Yousefi, Bahman] Tabriz Univ Med Sci, Mol Med Res Ctr, Tabriz, Iran.
C3 Tabriz University of Medical Science; Tabriz University of Medical
   Science; Shiraz University of Medical Science; Babol University of
   Medical Sciences; Babol University of Medical Sciences; Urmia University
   of Medical Sciences; Royal Melbourne Institute of Technology (RMIT);
   Tabriz University of Medical Science
RP Asemi, Z (corresponding author), Kashan Univ Med Sci, Res Ctr Biochem & Nutr Metab Dis, Kashan, Iran.; Yousefi, B (corresponding author), Tabriz Univ Med Sci, Mol Med Res Ctr, Tabriz, Iran.
EM asemi_r@yahoo.com; yousefib@tbzmed.ac.ir
RI yousefi, Bahman/AAI-2969-2021; asemi, zatollah/J-2677-2018; Qujeq,
   Durdi/H-2445-2019; Alemi, Forough/GPF-7945-2022; moein,
   Soheila/G-4684-2017; Yousefi, Bahman/AGY-4725-2022; Qujeq,
   Durdi/M-5787-2015
OI Yousefi, Bahman/0000-0002-4220-1527; Qujeq, Durdi/0000-0003-1344-9344
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NR 230
TC 15
Z9 15
U1 0
U2 11
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 11
PY 2022
VL 22
IS 1
AR 146
DI 10.1186/s12935-022-02557-3
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0K8TY
UT WOS:000781062800003
PM 35410210
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Grigoreva, T
   Sagaidak, A
   Novikova, D
   Tribulovich, V
AF Grigoreva, Tatyana
   Sagaidak, Aleksandra
   Novikova, Daria
   Tribulovich, Vyacheslav
TI New Insights into Chemoresistance Mediated by Mdm2 Inhibitors: The
   Benefits of Targeted Therapy over Common Cytostatics
SO BIOMEDICINES
LA English
DT Article
DE Nutlin-3a; paclitaxel; cytostatics; drug resistance; MDR;
   P-glycoprotein; BCRP
ID GLYCOPROTEIN DRUG EFFLUX; MULTIDRUG-RESISTANCE; COLON-CANCER;
   DOWN-REGULATION; ATPASE ACTIVITY; PACLITAXEL; TRANSPORTER; BCRP/ABCG2;
   MUTATIONS; GROWTH
AB The inhibition of the Mdm2-p53 protein-protein interaction is a promising strategy for anticancer therapy. However, the problem of developing secondary chemoresistance in tumors treated with such drugs has not yet been sufficiently studied. In this work, we compared the properties of a drug-resistant cell line obtained during long-term cultivation in the presence of an Mdm2 inhibitor, Nutlin-3a, with a similarly obtained line insensitive to the cytostatic drug paclitaxel. We first confirmed the higher safety levels of Mdm2 inhibitors when compared with cytostatics in terms of the development of secondary chemoresistance. We showed that Nutlin-3a affects both the targeted p53-mediated cellular machinery and the universal ABC-mediated efflux mechanism. While both targeted and general defense mechanisms are activated by the Mdm2 inhibitor, it still increases the susceptibility of tumor cells to other drugs. The results obtained indicate that the risks of developing chemoresistance under the therapy with a targeted agent are fundamentally lower than during cytotoxic therapy.
C1 [Grigoreva, Tatyana; Sagaidak, Aleksandra; Novikova, Daria; Tribulovich, Vyacheslav] St Petersburg State Inst Technol Tech Univ, Lab Mol Pharmacol, St Petersburg 190013, Russia.
C3 Saint Petersburg State Institute of Technology
RP Grigoreva, T; Tribulovich, V (corresponding author), St Petersburg State Inst Technol Tech Univ, Lab Mol Pharmacol, St Petersburg 190013, Russia.
EM rozentatiana@gmail.com; aleksandrasagaidak@yandex.ru;
   dc.novikova@gmail.com; tribulovich@gmail.com
RI Sagaidak, Aleksandra/AAE-8356-2019; Tribulovich, Vyacheslav/R-9426-2016;
   Grigoreva, Tatyana/H-5814-2016; Novikova, Daria/F-1554-2014
OI Tribulovich, Vyacheslav/0000-0001-7723-4962; Grigoreva,
   Tatyana/0000-0003-1271-0328; Novikova, Daria/0000-0002-5310-4570
FU Russian Science Foundation
FX No Statement Available
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NR 57
TC 1
Z9 1
U1 2
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD MAR
PY 2024
VL 12
IS 3
AR 547
DI 10.3390/biomedicines12030547
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 MD7D4
UT WOS:001191744400001
PM 38540160
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lou, JS
   Yao, P
   Tsim, KWK
AF Lou, Jian-Shu
   Yao, Ping
   Tsim, Karl W. K.
TI Cancer Treatment by Using Traditional Chinese Medicine Probing Active
   Compounds in Anti-multidrug Resistance During Drug Therapy
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE Traditional Chinese medicine; multi-drug resistance; phytomedicine;
   chemotherapy; natural compounds; combination
ID NUCLEOTIDE EXCISION-REPAIR; EPITHELIAL-MESENCHYMAL TRANSITION;
   P-GLYCOPROTEIN; MOLECULAR-MECHANISMS; COLORECTAL-CANCER; GROWTH-FACTOR;
   ANTITUMOR-ACTIVITY; MEDIATED APOPTOSIS; DOWN-REGULATION; CELL-ADHESION
AB The main challenge of cancer treatment is multidrug resistance during chemotherapy. Cancer cell can evade cell death during every round of orthodox chemotherapy drugs, consequently being resistant after several rounds of standard drug treatment. One of the regimens to address this multidrug resistance problem is by drug combination. However, synthetic drugs always have problems of strong side effects and toxicity. Natural compounds deriving from traditional Chinese medicine are known to have low toxicity and genuine promising effects in reversing multidrug resistance, either induced by orthodox chemotherapeutic or targeted therapy drugs. Numerous mechanisms including suppression of drug efflux, detoxifying systems, DNA repair systems, and anti-apoptosis pathways were responsible for such process. A range of natural compounds functioned on the suppression of apoptosis are widely reported, which include flavonoids, terpenoids, alkaloids, quinones, xanthones, saponins and polysaccharides. Here, this review summarized comprehensive data from in vitro and in vivo studies to elucidate the functional roles of natural compounds in reversing multidrug resistance during cancer therapy.
C1 [Lou, Jian-Shu] Hangzhou Normal Univ, Holist Integrat Pharm Inst, Key Lab Elemene Class Anticanc Chinese Med Zhejia, Hangzhou, Zhejiang, Peoples R China.
   [Lou, Jian-Shu; Yao, Ping; Tsim, Karl W. K.] Hong Kong Univ Sci & Technol, Ctr Chinese Med, Div Life Sci, Hong Kong, Peoples R China.
   [Lou, Jian-Shu; Tsim, Karl W. K.] Hong Kong Univ Sci & Technol, Shenzhen Res Inst, Shenzhen, Peoples R China.
C3 Hangzhou Normal University; Hong Kong University of Science &
   Technology; Hong Kong University of Science & Technology
RP Tsim, KWK (corresponding author), Hong Kong Univ Sci & Technol, Dept Life Sci, Ctr Chinese Med, Clear Water Bay, Hong Kong, Peoples R China.
EM botism@ust.hk
RI li, yan/GXH-7943-2022
OI Lou, Jianshu/0000-0002-1109-2161
FU Hong Kong Research Grants Council Theme-based Research Scheme
   [T13607/12R]; GRF [663012, 662713, M-HKUST604/13]; Foundation of The
   Awareness of Nature [TAON12SC01]; Key projects of National Natural
   Science Foundation of China [81730108]; Key Project of Zhejiang province
   Ministry of Science and Technology [2015C03055];  [TUYF15SC01]
FX This study was supported by Hong Kong Research Grants Council
   Theme-based Research Scheme (T13607/12R), GRF (663012, 662713,
   M-HKUST604/13), TUYF15SC01 and Foundation of The Awareness of Nature
   (TAON12SC01) to Karl Tsim, the grant from Key projects of National
   Natural Science Foundation of China(81730108), Key Project of Zhejiang
   province Ministry of Science and Technology (2015C03055) to Tian Xie.
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NR 96
TC 45
Z9 50
U1 6
U2 63
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PY 2018
VL 25
IS 38
BP 5128
EP 5141
DI 10.2174/0929867324666170920161922
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA HH8NE
UT WOS:000455988100007
PM 28933300
DA 2025-01-04
ER

PT J
AU Zirlik, K
   Duyster, J
AF Zirlik, Katja
   Duyster, Justus
TI Anti-Angiogenics: Current Situation and Future Perspectives
SO ONCOLOGY RESEARCH AND TREATMENT
LA English
DT Review
DE Anti-angiogenics; Angiogenesis; VEGF; Monoclonal antibodies; Tyrosine
   kinase inhibitors
ID METASTATIC COLORECTAL-CANCER; PHASE-III TRIAL; DOUBLE-BLIND; TUMOR
   ANGIOGENESIS; 1ST-LINE THERAPY; DENDRITIC CELLS; VEGF THERAPY;
   BEVACIZUMAB; PLACEBO; PLUS
AB Angiogenesis, the process leading to the formation of new blood vessels, is one of the hallmarks of cancer. Extensive studies established that i) vascular endothelial growth factor (VEGF) is a key driver of sprouting angiogenesis, ii) VEGF is overexpressed in most solid cancers, and iii) inhibition of VEGF can suppress tumor growth in animal models. This has led to the development of pharmacological agents for anti-angiogenesis to disrupt the vascular supply and starve the tumor of nutrients and oxygen, primarily through the blockade of VEGF/VEGF receptor signaling. This effort has resulted in 11 anti-VEGF drugs approved for certain advanced cancers, either alone or in combination with chemotherapy and other targeted therapies. However, inhibition of VEGF signaling is not effective in all cancers, and anti-angiogenics have often only limited impact on overall survival of cancer patients. This review focuses on the current status of FDA-approved anti-angiogenic antibodies and tyrosine kinase inhibitors and summarizes the progress and future directions of VEGF-targeted therapy. (c) 2018 S. Karger GmbH, Freiburg
C1 [Zirlik, Katja; Duyster, Justus] Univ Med Ctr Freiburg, Dept Med Hematol Oncol & Stem Cell Transplantat 1, Hugstetterstr 55, D-79106 Freiburg, Germany.
   [Zirlik, Katja] Tumor & Breast Ctr ZeTuP, St Gallen, Switzerland.
C3 University of Freiburg
RP Duyster, J (corresponding author), Univ Med Ctr Freiburg, Dept Med Hematol Oncol & Stem Cell Transplantat 1, Hugstetterstr 55, D-79106 Freiburg, Germany.
EM justus.duyster@uniklinik-freiburg.de
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NR 42
TC 165
Z9 181
U1 1
U2 16
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 2296-5270
EI 2296-5262
J9 ONCOL RES TREAT
JI Oncol. Res. Treat.
PY 2018
VL 41
IS 4
BP 166
EP 171
DI 10.1159/000488087
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GC9KG
UT WOS:000430115300002
PM 29562226
OA Bronze
DA 2025-01-04
ER

PT J
AU Haraldsdottir, S
   Goldberg, RM
AF Haraldsdottir, Sigurdis
   Goldberg, Richard M.
TI Conversion Therapy for Initially Borderline/Unresectable Metastases in
   Colon Cancer: What Is the Best Neoadjuvant Chemotherapy?
SO CURRENT COLORECTAL CANCER REPORTS
LA English
DT Article
DE Colon cancer; Resectable metastases; Liver metastases; Lung metastases;
   Neoadjuvant chemotherapy; Pseudoadjuvant chemotherapy
ID COLORECTAL LIVER METASTASES; OXALIPLATIN-BASED CHEMOTHERAPY; PORTAL-VEIN
   EMBOLIZATION; RANDOMIZED PHASE-III; PREOPERATIVE CHEMOTHERAPY; 1ST-LINE
   TREATMENT; HEPATIC RESECTION; PERIOPERATIVE CHEMOTHERAPY; EXTRAHEPATIC
   DISEASE; PLUS CHEMOTHERAPY
AB Purpose of Review Resection of metastatic colorectal cancer (mCRC) can dramatically improve overall survival (OS), particularly in patients with isolated colorectal liver metastases (CLMs). In this review, we summarize recent findings and studies addressing chemotherapy +/- targeted therapy before and after metastatectomies in patients with CLM.
   Recent Findings For initially unresectable CLM that could become resectable after response to medical therapy, FOLFIRINOX has the highest response and conversion rates and is safely administered with bevacizumab. In RAS wild-type, left-sided tumors, chemotherapy with Epidermal Growth Factor Receptor-targeted therapy should be strongly considered given high (similar to 70%) response rates. In patients who present with resectable CLM, there is no clear indication that neoadjuvant chemotherapy improves OS. While the New EPOC trial showed detrimental progression-free survival in the combination arm containing cetuximab in this setting, methodologic issues with that trial have raised questions about the strength of these data.
   Summary Through multidisciplinary management in patients with isolated CLM, the best course of action to effect an R0 resection of all known disease-coupling surgery with medical therapy can significantly improve patient outcomes.
C1 [Haraldsdottir, Sigurdis] Stanford Univ, Sch Med, Div Oncol, Dept Internal Med, 875 Blake Wilbur Dr, Stanford, CA 94305 USA.
   [Goldberg, Richard M.] West Virginia Univ, Inst Canc, POB 9300,1805 Hlth Sci Ctr South, Morgantown, WV 26506 USA.
   [Goldberg, Richard M.] Mary Babb Randolph Canc Ctr, POB 9300,1805 Hlth Sci Ctr South, Morgantown, WV 26506 USA.
C3 Stanford University; West Virginia University
RP Goldberg, RM (corresponding author), West Virginia Univ, Inst Canc, POB 9300,1805 Hlth Sci Ctr South, Morgantown, WV 26506 USA.; Goldberg, RM (corresponding author), Mary Babb Randolph Canc Ctr, POB 9300,1805 Hlth Sci Ctr South, Morgantown, WV 26506 USA.
EM Richard.Goldberg@hsc.wvu.edu
RI Goldberg, Richard/O-1871-2017
OI Haraldsdottir, Sigurdis/0000-0002-5050-3699
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NR 85
TC 1
Z9 1
U1 0
U2 3
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 DEC
PY 2017
VL 13
IS 6
BP 419
EP 428
DI 10.1007/s11888-017-0393-2
PG 10
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA FV0BJ
UT WOS:000424220600002
DA 2025-01-04
ER

PT J
AU Dreanic, J
   Dhooge, M
   Sion, E
   Brezault, C
   Chaussade, S
   Coriat, R
AF Dreanic, Johann
   Dhooge, Marion
   Sion, Elena
   Brezault, Catherine
   Chaussade, Stanislas
   Coriat, Romain
TI Gastric Carcinoma at the Era of Targeted Therapies
SO CURRENT DRUG TARGETS
LA English
DT Review
DE Gastric carcinoma; gastric cancer; targeted therapy; anti VEGF; anti
   EGFR; trastuzumab
ID PHASE-II TRIAL; JUNCTION ADENOCARCINOMA; ESOPHAGOGASTRIC CANCER;
   1ST-LINE TREATMENT; DOUBLE-BLIND; ESOPHAGEAL ADENOCARCINOMA; 2ND-LINE
   TREATMENT; COLORECTAL-CANCER; MODIFIED FOLFOX6; PLUS IRINOTECAN
AB Gastric and gastro-esophageal cancers (GC/GEJ) appear as the second cancer-related death worldwide. Diagnosis is made at an advanced stage offering a curative attempt in less than 50% of cases. Despite the improvements of the systemic cytotoxic chemotherapy regimens, the prognosis of patients with metastatic GC/GEJ cancer remains poor. Recent insights in biochemical pathways have permitted to identify potential targets. The extracellular domain of HER2 receptors is implicated in cells' proliferation and in the anti-apoptotic process occurring in GC/GEJ cancers. Trastuzumab, a monoclonal antibody targeting HER2, in addition to chemotherapy permitted to obtain more than one year of survival in HER2-positive advanced GC/GEJ cancers. Recently, ramucirumab, a humanized monoclonal antibody targeting VEGFR-2 receptor demonstrated its efficacy as a second line treatment for patients with advanced GC/GEJ cancer. These encouraging results have justified evaluating targeted therapies in GC/GEJ cancers. In this review, we summarize targeted therapies that might present clinical efficacy in the treatment of advanced GC/GEJ cancers.
C1 [Dreanic, Johann; Dhooge, Marion; Sion, Elena; Brezault, Catherine; Chaussade, Stanislas; Coriat, Romain] Univ Paris 05, Sorbonne Paris Cite, Hop Cochin, AP HP,Fac Med,Gastroenterol & Endoscopy Unit, Paris, France.
C3 Universite Paris Cite; Assistance Publique Hopitaux Paris (APHP);
   Hopital Universitaire Cochin - APHP
RP Dreanic, J (corresponding author), Hop Cochin, Gastroenterol & Endoscopy Unit, 27 Rue Faubourg St Jacques, F-75014 Paris, France.
EM johann.dreanic@cch.aphp.fr
RI Coriat, Romain/O-7902-2017
OI Dhooge, Marion/0000-0002-7279-5549
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NR 71
TC 4
Z9 4
U1 0
U2 5
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1389-4501
EI 1873-5592
J9 CURR DRUG TARGETS
JI Curr. Drug Targets
PY 2016
VL 17
IS 15
BP 1818
EP 1826
DI 10.2174/1389450116666150506111327
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EB1DN
UT WOS:000387087300012
PM 25944013
DA 2025-01-04
ER

PT J
AU Pfeiffer, P
   Köhne, CH
   Qvortrup, C
AF Pfeiffer, Per
   Koehne, Claus-Henning
   Qvortrup, Camilla
TI The changing face of treatment for metastatic colorectal cancer
SO EXPERT REVIEW OF ANTICANCER THERAPY
LA English
DT Review
DE Chemotherapy; colorectal cancer; targeted therapy; personalized therapy;
   review
ID RANDOMIZED PHASE-III; FOLFIRI PLUS BEVACIZUMAB; PRIMARY TUMOR RESECTION;
   WILD-TYPE KRAS; 1ST-LINE TREATMENT; ELDERLY-PATIENTS; LIVER METASTASES;
   POOLED ANALYSIS; OPEN-LABEL; RAS MUTATIONS
AB Introduction: Since late 1990's therapy of metastatic colorectal cancer (mCRC) patients has changed considerable, and the combination of doublet or triplet chemotherapy and a targeted agent are now routinely used. With the introduction of more intensified regimens, it has become even more important to identify patients that will benefit from and can tolerate therapy. Furthermore, the increasing understanding of the biology of mCRC has led to the discovery of new potential targets. Therefore, therapy of patients with mCRC has undergone considerable change from 'one strategy fits all' towards a more personalized therapy. Areas covered: We present an overview of the recent literature on approved systemic treatment of mCRC however with focus on how the treatment strategy has changed based on clinical and molecular parameters that presently are used routinely in the clinical situation. Expert commentary: The face of treatment of mCRC has changed from 'one strategy fits all' to a personalized approach in which both clinical, molecular parameters and the aim of therapy have to be taking into account when planning the optimal treatment strategy for the individual mCRC patient.
C1 [Pfeiffer, Per] Odense Univ Hosp, Dept Oncol, Sdr Blvd 29, DK-5000 Odense C, Denmark.
   [Koehne, Claus-Henning] Carl von Ossietzky Univ Oldenburg, North West German Canc Ctr, Univ Campus Klinikum Oldenburg, Oldenburg, NS, Germany.
   [Qvortrup, Camilla] Univ Copenhagen, Rigshosp, Dept Oncol, Copenhagen, Denmark.
C3 University of Southern Denmark; Odense University Hospital; Carl von
   Ossietzky Universitat Oldenburg; University of Copenhagen;
   Rigshospitalet
RP Pfeiffer, P (corresponding author), Odense Univ Hosp, Dept Oncol, Sdr Blvd 29, DK-5000 Odense C, Denmark.
EM per.pfeiffer@rsyd.dk
RI Qvortrup, Camilla/AAD-3366-2019
OI Pfeiffer, Per/0000-0002-2925-0586
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NR 91
TC 9
Z9 9
U1 0
U2 11
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 JAN 2
PY 2019
VL 19
IS 1
BP 61
EP 70
DI 10.1080/14737140.2019.1543593
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HE3EO
UT WOS:000453235100007
PM 30381969
DA 2025-01-04
ER

PT J
AU Drury, J
   Rychahou, PG
   He, DH
   Jafari, N
   Wang, C
   Lee, EY
   Weiss, HL
   Evers, BM
   Zaytseva, YY
AF Drury, James
   Rychahou, Piotr G.
   He, Daheng
   Jafari, Naser
   Wang, Chi
   Lee, Eun Y.
   Weiss, Heidi L.
   Evers, Bernard Mark
   Zaytseva, Yekaterina Y.
TI Inhibition of Fatty Acid Synthase Upregulates Expression of CD36 to
   Sustain Proliferation of Colorectal Cancer Cells
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE lipogenesis; anticancer activity; FASN-targeted therapy; fatty acid
   metabolism; TVB inhibitors
ID SIGNALING PATHWAYS; METASTASIS; METABOLISM; SURVIVIN; OBESITY; GROWTH;
   APOPTOSIS
AB Fatty acid synthase, a key enzyme ofde novolipogenesis, is an attractive therapeutic target in cancer. The novel fatty acid synthase inhibitor, TVB-3664, shows anti-cancer activity in multiple cancers including colorectal cancer; however, it is unclear whether uptake of exogeneous fatty acids can compensate for the effect of fatty acid synthase inhibition. This study demonstrates that inhibition of fatty acid synthase selectively upregulates fatty acid translocase (CD36), a fatty acid transporter, in multiple colorectal cancer models including colorectal cancer cells with shRNA mediated knockdown of fatty acid synthase and genetically modified mouse tissues with heterozygous and homozygous deletion of fatty acid synthase. Furthermore, human colorectal cancer tissues treated with TVB-3664 show a significant and selective upregulation of CD36 mRNA. shRNA-mediated knockdown of CD36 and inhibition of CD36 via sulfosuccinimidyl oleate, a chemical inhibitor of CD36, decreased cell proliferationin vitroand reduced tumor growth in subcutaneous xenograft models. Isogenic cell populations established from patient derived xenografts and expressing high levels of CD36 show a significantly increased ability to grow tumorsin vivo. The tumor-promoting effect of CD36 is associated with an increase in the levels of pAkt and survivin. Importantly, combinatorial treatment of primary and established colorectal cancer cells with TVB-3664 and sulfosuccinimidyl oleate shows a synergistic effect on cell proliferation. In summary, our study demonstrates that upregulation of CD36 expression is a potential compensatory mechanism for fatty acid synthase inhibition and that inhibition of CD36 can improve the efficacy of fatty acid synthase-targeted therapy.
C1 [Drury, James; Jafari, Naser; Zaytseva, Yekaterina Y.] Univ Kentucky, Dept Toxicol & Canc Biol, Lexington, KY 40506 USA.
   [Rychahou, Piotr G.; He, Daheng; Wang, Chi; Weiss, Heidi L.; Evers, Bernard Mark; Zaytseva, Yekaterina Y.] Univ Kentucky, Markey Canc Ctr, Lexington, KY 40506 USA.
   [Rychahou, Piotr G.; Evers, Bernard Mark] Univ Kentucky, Dept Surg, Lexington, KY USA.
   [Lee, Eun Y.] Univ Kentucky, Dept Pathol & Lab Med, Lexington, KY USA.
C3 University of Kentucky; University of Kentucky; University of Kentucky;
   University of Kentucky
RP Zaytseva, YY (corresponding author), Univ Kentucky, Dept Toxicol & Canc Biol, Lexington, KY 40506 USA.; Zaytseva, YY (corresponding author), Univ Kentucky, Markey Canc Ctr, Lexington, KY 40506 USA.
EM yyzayt2@uky.edu
RI He, Daheng/AAR-1813-2021
FU National Institutes of Health [P20 GM121327, R01 CA208343, T32 ES07266];
   Markey Cancer Center shared resource facilities; National Cancer
   Institute [P30 CA177558]
FX National Institutes of Health (P20 GM121327 to YZ, R01 CA208343 to BE,
   T32 ES07266 to JD); Markey Cancer Center shared resource facilities
   (Biospecimen Procurement and Translational Pathology SRF, Flow Cytometry
   and Immune Monitoring SRF, Biostatistics and Bioinformatics SRF) are
   partially supported by National Cancer Institute (P30 CA177558 to BE).
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NR 54
TC 63
Z9 70
U1 2
U2 24
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 31
PY 2020
VL 10
AR 1185
DI 10.3389/fonc.2020.01185
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ND0ZW
UT WOS:000561637300001
PM 32850342
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Fasano, C
   Grossi, V
   Forte, G
   Simone, C
AF Fasano, Candida
   Grossi, Valentina
   Forte, Giovanna
   Simone, Cristiano
TI Short Linear Motifs in Colorectal Cancer Interactome and Tumorigenesis
SO CELLS
LA English
DT Review
DE short linear motifs; protein-protein interactions; SLiM-based small
   molecules; colorectal cancer interactome; targeted therapy; cancer
   driver protein interactome
ID PROTEIN-PROTEIN INTERACTION; PHOSPHORYLATED BETA-CATENIN; SMALL-MOLECULE
   PROBES; RECOMBINANT PEPTIDE; SEQUENTIAL PHOSPHORYLATION; INTERACTION
   NETWORKS; SIGNALING PATHWAYS; BRCT DOMAIN; WEB SERVER; KINASE
AB Colorectal tumorigenesis is driven by alterations in genes and proteins responsible for cancer initiation, progression, and invasion. This multistage process is based on a dense network of protein-protein interactions (PPIs) that become dysregulated as a result of changes in various cell signaling effectors. PPIs in signaling and regulatory networks are known to be mediated by short linear motifs (SLiMs), which are conserved contiguous regions of 3-10 amino acids within interacting protein domains. SLiMs are the minimum sequences required for modulating cellular PPI networks. Thus, several in silico approaches have been developed to predict and analyze SLiM-mediated PPIs. In this review, we focus on emerging evidence supporting a crucial role for SLiMs in driver pathways that are disrupted in colorectal cancer (CRC) tumorigenesis and related PPI network alterations. As a result, SLiMs, along with short peptides, are attracting the interest of researchers to devise small molecules amenable to be used as novel anti-CRC targeted therapies. Overall, the characterization of SLiMs mediating crucial PPIs in CRC may foster the development of more specific combined pharmacological approaches.
C1 [Fasano, Candida; Grossi, Valentina; Forte, Giovanna; Simone, Cristiano] Natl Inst Gastroenterol IRCCS Saverio de Bellis, Med Genet, I-70013 Bari, Italy.
   [Simone, Cristiano] Univ Bari Aldo Moro, Dept Precis & Regenerat Med & Jon Area DiMePRe J, Med Genet, I-70124 Bari, Italy.
C3 IRCCS Saverio de Bellis; Universita degli Studi di Bari Aldo Moro
RP Fasano, C; Simone, C (corresponding author), Natl Inst Gastroenterol IRCCS Saverio de Bellis, Med Genet, I-70013 Bari, Italy.; Simone, C (corresponding author), Univ Bari Aldo Moro, Dept Precis & Regenerat Med & Jon Area DiMePRe J, Med Genet, I-70124 Bari, Italy.
EM candida.fasano@irccsdebellis.it; cristiano.simone@uniba.it
RI Fasano, Candida/K-3372-2018; Grossi, Valentina/K-9821-2016; SIMONE,
   Cristiano/K-3452-2018
OI Fasano, Candida/0000-0001-5878-3480; SIMONE,
   Cristiano/0000-0002-2628-7658
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NR 175
TC 4
Z9 4
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD DEC
PY 2022
VL 11
IS 23
AR 3739
DI 10.3390/cells11233739
PG 23
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 6X4BH
UT WOS:000896359800001
PM 36496998
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Qin, H
   Yuan, MQ
   Yuan, YQ
   Xia, FQ
   Yang, YH
AF Qin, Hai
   Yuan, Manqin
   Yuan, Yaqin
   Xia, Fengqiong
   Yang, Yonghong
TI NEK2 promotes colorectal cancer progression by activating the TGF-β/
   Smad2 signaling pathway
SO TRANSLATIONAL ONCOLOGY
LA English
DT Article
DE NEK2; Colorectal Cancer; TGF-beta/Smad2; Stemness; Ubiquitination
ID CELL; KINASE
AB Colorectal cancer (CRC) is a prevalent malignancy with poor patient survival, and NIMA-associated kinase 2 (NEK2) has been implicated in the pathogenesis and progression of various cancers, including CRC. This study aimed to investigate the impact of NEK2 on CRC cell functionality and its interaction with the TGF-beta/Smad signaling pathway. NEK2 expression in CRC tissues and cell lines was assessed, and its association with patient survival was analyzed. Functional assays, including NEK2 knockdown via lentiviral infection, RT-qPCR, Western blotting, CCK-8 assay, Transwell migration, invasion assays, and goblet cell formation assays, were employed to evaluate NEK2 ' s effects on CRC cell proliferation, migration, invasion, and stemness. Mechanistic studies explored the TGF-beta/Smad2 signaling pathway, utilizing co-immunoprecipitation (Co-IP) and protein interaction analyses. In vivo experiments further evaluated NEK2 ' s role in tumor initiation, metastasis, and chemoresistance. NEK2 was found to be upregulated in CRC tissues and correlated with poor survival. NEK2 knockdown inhibited CRC cell behaviors, while NEK2 activated the TGF-beta/Smad2 signaling pathway through Smad2/3 phosphorylation. Overexpression of Smad2/3 reversed NEK2 knockdown effects, confirming the importance of this pathway in CRC. In vivo, NEK2 promoted tumor initiation, metastasis, and chemoresistance, effects partially reversed by Smad2/3 overexpression. These findings reveal the critical role of NEK2 in CRC progression and underscore its potential as a therapeutic target, offering new insights into the molecular mechanisms driving CRC and informing targeted therapy development.
C1 [Qin, Hai; Xia, Fengqiong; Yang, Yonghong] Beijing Jishuitan Hosp, Dept Clin Lab, Guizhou Hosp, 206 Sixian St, Guiyang, Guizhou, Peoples R China.
   [Yuan, Manqin] Guizhou Med Univ, Dept Clin Lab Med, 9 Beijing Rd, Guiyang, Guizhou, Peoples R China.
   [Yuan, Yaqin] Guizhou Ctr Med Device Testing, Microbiol Lab, 247 South Sect Xintian Ave, Guiyang 550001, Guizhou, Peoples R China.
C3 Guizhou Medical University
RP Qin, H; Yang, YH (corresponding author), Beijing Jishuitan Hosp, Dept Clin Lab, Guizhou Hosp, 206 Sixian St, Guiyang, Guizhou, Peoples R China.
EM 18786665889@163.com; 2301444608@qq.com
FU Health Commission of Guizhou Province [gzwkj2023-455]
FX <BOLD>Funding Information</BOLD> This study received funding from the
   Health Commission of Guizhou Province (Nos. gzwkj2023-455) .
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NR 36
TC 0
Z9 0
U1 2
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1936-5233
J9 TRANSL ONCOL
JI Transl. Oncol.
PD JAN
PY 2025
VL 51
AR 102186
DI 10.1016/j.tranon.2024.102186
EA NOV 2024
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA L5U1Z
UT WOS:001351359700001
PM 39499996
DA 2025-01-04
ER

PT J
AU Koch, JP
   Aebersold, DM
   Zimmer, Y
   Medová, M
AF Koch, Jonas P.
   Aebersold, Daniel M.
   Zimmer, Yitzhak
   Medova, Michaela
TI MET targeting: time for a rematch
SO ONCOGENE
LA English
DT Review
ID HEPATOCYTE GROWTH-FACTOR; CELL LUNG-CANCER; RECEPTOR-TYROSINE KINASE;
   MODIFIED T-CELLS; DURABLE COMPLETE RESPONSE; PRIMARY COLON-CANCER; EXON
   14 MUTATIONS; C-MET; SCATTER FACTOR; ONCOGENE ADDICTION
AB MET, the receptor tyrosine kinase (RTK) for hepatocyte growth factor, is a proto-oncogene involved in embryonic development and throughout life in homeostasis and tissue regeneration. Deregulation of MET signaling has been reported in numerous malignancies, prompting great interest in MET targeting for cancer therapy. The present review offers a summary of the biology of MET and its known functions in normal physiology and carcinogenesis, followed by an overview of the most relevant MET-targeting strategies and corresponding clinical trials, highlighting both past setbacks and promising future prospects. By placing their efforts on a more precise stratification strategy through the genetic analysis of tumors, modern trials such as the NCI-MATCH trial could revive the past enthusiasm for MET-targeted therapy.
C1 [Koch, Jonas P.; Aebersold, Daniel M.; Zimmer, Yitzhak; Medova, Michaela] Bern Univ Hosp, Inselspital, Dept BioMed Res, CH-3008 Bern, Switzerland.
   [Koch, Jonas P.; Aebersold, Daniel M.; Zimmer, Yitzhak; Medova, Michaela] Univ Bern, CH-3008 Bern, Switzerland.
   [Koch, Jonas P.; Aebersold, Daniel M.; Zimmer, Yitzhak; Medova, Michaela] Bern Univ Hosp, Inselspital, Dept Radiat Oncol, CH-3010 Bern, Switzerland.
   [Koch, Jonas P.; Aebersold, Daniel M.; Zimmer, Yitzhak; Medova, Michaela] Univ Bern, CH-3010 Bern, Switzerland.
C3 University of Bern; University Hospital of Bern; University of Bern;
   University of Bern; University Hospital of Bern; University of Bern
RP Medová, M (corresponding author), Bern Univ Hosp, Inselspital, Dept BioMed Res, CH-3008 Bern, Switzerland.; Medová, M (corresponding author), Univ Bern, CH-3008 Bern, Switzerland.; Medová, M (corresponding author), Bern Univ Hosp, Inselspital, Dept Radiat Oncol, CH-3010 Bern, Switzerland.; Medová, M (corresponding author), Univ Bern, CH-3010 Bern, Switzerland.
EM michaela.medova@dbmr.unibe.ch
RI Aebersold, Daniel/C-2946-2013
OI Medova, Michaela/0000-0003-0649-469X; Koch, Jonas/0000-0003-1833-9064
FU Werner und Hedy Berger-Janser Stiftung
FX This work has been supported by the Werner und Hedy Berger-Janser
   Stiftung (grant to MM).
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NR 210
TC 47
Z9 51
U1 0
U2 14
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD APR
PY 2020
VL 39
IS 14
BP 2845
EP 2862
DI 10.1038/s41388-020-1193-8
EA FEB 2020
PG 18
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA KZ2VB
UT WOS:000511752600005
PM 32034310
DA 2025-01-04
ER

PT J
AU Okuyan, D
AF Okuyan, Derya
TI Epidermal Growth Factor Downregulates Carbon Anhydrase III (CAIII) in
   Colon Cancer
SO CURRENT ISSUES IN MOLECULAR BIOLOGY
LA English
DT Article
DE carbonic anhydrase III; CAIII; colon carcinoma; EGF; HT-29; SW480; HUVEC
ID FACTOR RECEPTOR; COLORECTAL-CANCER; DIFFERENTIAL EXPRESSION; KINASE-B;
   STAGE-II; IX; SERUM; EGF; XII; OVEREXPRESSION
AB Colorectal cancer (CRC) is the second leading cause of cancer-related death in the world. Dysregulations in the EGF signaling pathway have been associated with colon cancer. Some members of the carbonic anhydrase family serve as biomarkers in cancer. Carbonic anhydrase III (CAIII), a member of this family, shows different activities than the other members of its family and has been associated with cancer. However, there are no studies on the effective regulation of EGF. In this study, we investigated the EGF-influenced regulation of CAIII in the HT29, SW480, and HUVEC cell lines and showed that CAIII regulation decreased with the effect of EGF. We aimed to investigate the EGF-affected mRNA and protein regulation of the CAIII gene in HT29, SW480, and HUVEC cell lines. For this purpose, we determined time-dependent CAIII mRNA and protein expression by applying EGF to HT29, SW480, and HUVEC cells. Time-dependent EGF-induced mRNA and protein level regulation of the CAIII gene decreased in the HT29, SW480, and HUVEC cell lines. EGF regulates the motility, adhesion, and metastasis of cancer cells. CAIII prevents cells from metastasizing through cell acidification. Therefore, our findings explained why the EGF-effective regulation of CAIII decreased. We suggest that the CAIII gene is promising as a targeted therapy due to the decrease in EGF-effected CAIII gene regulation in colon carcinoma.
C1 [Okuyan, Derya] Bandirma Onyedi Eylul Univ, Susurluk Agr & Forestry Vocat Sch, Dept Vet Med, TR-10600 Susurluk, Balikesir, Turkiye.
EM dokuyan@bandirma.edu.tr
FU Bandirma Onyedi Eylul University Scientific Research Projects
   Coordination Unit by providing consumables [BAP-22-1003-002]
FX This study was supported by Bandirma Onyedi Eylul University Scientific
   Research Projects Coordination Unit by providing consumables. Project
   Number: BAP-22-1003-002.
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NR 53
TC 0
Z9 0
U1 1
U2 1
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1467-3037
EI 1467-3045
J9 CURR ISSUES MOL BIOL
JI Curr. Issues Mol. Biol.
PD NOV
PY 2024
VL 46
IS 11
BP 12994
EP 13002
DI 10.3390/cimb46110774
PG 9
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA N4N3C
UT WOS:001364120000001
PM 39590368
OA gold
DA 2025-01-04
ER

PT J
AU Merenda, A
   Fenderico, N
   Maurice, MM
AF Merenda, Alessandra
   Fenderico, Nicola
   Maurice, Madelon M.
TI Wnt Signaling in 3D: Recent Advances in the Applications of Intestinal
   Organoids
SO TRENDS IN CELL BIOLOGY
LA English
DT Review
ID IN-VITRO EXPANSION; STEM-CELLS; BETA-CATENIN; HUMAN COLON;
   COLORECTAL-CANCER; CANONICAL WNT; SELF-RENEWAL; SINGLE LGR5; APC;
   PROGENITORS
AB Intestinal organoids grown from adult stem cells have emerged as prototype 3D organotypic models for studying tissue renewal and homeostasis. Owing to their strict dependence on Wnt signaling, intestinal organoids offer an unprecedented opportunity to examine Wnt pathway regulation it normal physiology and cancer. We review how alterations in growth factor dependency and orga noid morphology can be exploited to identify Wnt signaling mechanisms, characterize mutated pathway components, and predict responses of patient-derived tumors to targeted therapy. We discuss current deficits in the understanding of genotype-phenotype relationships that are to be considered when interpreting mutation-induced changes in organoid morphology.
C1 [Merenda, Alessandra; Fenderico, Nicola; Maurice, Madelon M.] Univ Med Ctr Utrecht, Ctr Mol Med, Oncode Inst, NL-3584 CX Utrecht, Netherlands.
   [Merenda, Alessandra; Fenderico, Nicola; Maurice, Madelon M.] Univ Med Ctr Utrecht, Ctr Mol Med, Dept Cell Biol, NL-3584 CX Utrecht, Netherlands.
C3 Utrecht University; Utrecht University Medical Center; Utrecht
   University; Utrecht University Medical Center
RP Maurice, MM (corresponding author), Univ Med Ctr Utrecht, Ctr Mol Med, Oncode Inst, NL-3584 CX Utrecht, Netherlands.; Maurice, MM (corresponding author), Univ Med Ctr Utrecht, Ctr Mol Med, Dept Cell Biol, NL-3584 CX Utrecht, Netherlands.
EM m.m.maurice@umcutrecht.nl
OI Fenderico, Nicola/0000-0003-3599-7931
FU Dutch Cancer Society; European Research Council [242958]; EU [608180];
   Netherlands Organization for Scientific Research (NWO) VICI [91815604];
   Netherlands Organization for Scientific Research (NWO) ECHO
   [711.013.012]; Netherlands Organization for Scientific Research (NWO)
   ZonMW TOP [91218050]; European Research Council (ERC) [242958] Funding
   Source: European Research Council (ERC)
FX We thank members of the laboratory of M.M.M. for helpful discussions and
   suggestions. The Oncode Institute is partly financed by the Dutch Cancer
   Society. This work was supported by European Research Council starting
   grant 242958 (to M.M.M.), EU FP7 grant Marie Curie ITN 608180 'WntsApp'
   (to M.M.M.), and the Netherlands Organization for Scientific Research
   (NWO) VICI grant 91815604, ECHO grant 711.013.012, and ZonMW TOP grant
   91218050 (to M.M.M.).
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NR 96
TC 66
Z9 71
U1 5
U2 54
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 0962-8924
EI 1879-3088
J9 TRENDS CELL BIOL
JI Trends Cell Biol.
PD JAN
PY 2020
VL 30
IS 1
BP 60
EP 73
DI 10.1016/j.tcb.2019.10.003
PG 14
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA JX9LG
UT WOS:000504047700006
PM 31718893
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Arjaans, M
   Schröder, CP
   Oosting, SF
   Dafni, U
   Kleibeuker, JE
   de Vries, EGE
AF Arjaans, Marlous
   Schroder, Carolina P.
   Oosting, Sjoukje F.
   Dafni, Urania
   Kleibeuker, Josee E.
   de Vries, Elisabeth G. E.
TI VEGF pathway targeting agents, vessel normalization and tumor drug
   uptake: from bench to bedside
SO ONCOTARGET
LA English
DT Article
DE antiangiogenic drugs; blood vessel normalization; tumor drug delivery
ID METASTATIC COLORECTAL-CANCER; PHASE-III TRIAL; DOUBLE-BLIND;
   ANTIANGIOGENIC THERAPY; 1ST-LINE TREATMENT; BREAST-CANCER;
   GROWTH-FACTOR; VASCULAR NORMALIZATION; BLOOD-VESSELS; ANTI-VEGF
AB Vascular endothelial growth factor (VEGF) pathway targeting agents have been combined with other anticancer drugs, leading to improved efficacy in carcinoma of the cervix, stomach, lung, colon and rectum, ovary, and breast. Vessel normalization induced by VEGF pathway targeting agents influences tumor drug uptake. Following bevacizumab treatment, preclinical and clinical studies have shown a decrease in tumor delivery of radiolabeled antibodies and two chemotherapeutic drugs. The decrease in vessel pore size during vessel normalization might explain the decrease in tumor drug uptake. Moreover, the addition of bevacizumab to cetuximab, or panitumumab in colorectal cancer patients or to trastuzumab in breast cancer patients, did not improve efficacy. However, combining bevacizumab with chemotherapy did increase efficacy in some cancer types. Novel biomarkers to select patients who may benefit from combination therapies, such as the effect of an angiogenesis inhibitor on tumor perfusion, requires innovative trial designs and large clinical trials. Small imaging studies with radiolabeled drugs could be used in the interphase to gain further insight into the interplay between VEGF targeted therapy, vessel normalization and tumor drug delivery.
C1 [Arjaans, Marlous; Schroder, Carolina P.; Oosting, Sjoukje F.; de Vries, Elisabeth G. E.] Univ Groningen, Univ Med Ctr Groningen, Dept Med Oncol, Groningen, Netherlands.
   [Dafni, Urania] Univ Athens, Lab Biostat, Athens, Greece.
   [Kleibeuker, Josee E.] Univ Cambridge, Dept Mat Sci & Met, Pembroke St, Cambridge CB2 3QZ, England.
C3 University of Groningen; National & Kapodistrian University of Athens;
   University of Cambridge
RP de Vries, EGE (corresponding author), Univ Groningen, Univ Med Ctr Groningen, Dept Med Oncol, Groningen, Netherlands.
EM e.g.e.de.vries@umcg.nl
RI Schröder, Carolina/KFA-5750-2024; Dafni, Ourania/AAH-4453-2019
OI DAFNI, URANIA/0000-0003-4367-4497; de Vries,
   Elisabeth/0000-0002-8949-7425
FU advanced ERC grant OnQview; Hoffmann La Roche; Genentech; Novartis;
   Amgen; Dutch Cancer Society [RUG 2010-4739]
FX de Vries received grant support by the advanced ERC grant OnQview.
   Research grants from Hoffmann La Roche, Genentech, Novartis and Amgen
   were awarded to the UMCG. Schroder received grant RUG 2010-4739 from the
   Dutch Cancer Society.
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NR 91
TC 85
Z9 94
U1 2
U2 38
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 19
PY 2016
VL 7
IS 16
BP 21247
EP 21258
DI 10.18632/oncotarget.6918
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DO3TY
UT WOS:000377705900014
PM 26789111
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Saikia, T
   Khanam, A
   Ahmed, N
   Bharali, A
   Kalita, T
   Rajak, P
   Sahu, BP
   Patowary, L
AF Saikia, Trideep
   Khanam, Asma
   Ahmed, Nasima
   Bharali, Alakesh
   Kalita, Tutumoni
   Rajak, Prakash
   Sahu, Bhanu P.
   Patowary, Lima
TI Disrupting Tumour Niches: Advanced Strategies for Targeting the Tumour
   Microenvironment in Cancer Therapy
SO CURRENT CANCER THERAPY REVIEWS
LA English
DT Review; Early Access
DE Tumour microenvironment; cancer-associated fibroblasts; targeted
   therapy; neovascularisation; hypoxia; immune system; tumour progression;
   therapeutic resistance
ID FIBROBLAST ACTIVATION PROTEIN; PROSTATE-CANCER; BREAST-CANCER;
   COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA; ARTIFICIAL-INTELLIGENCE;
   EXTRACELLULAR-MATRIX; ANTITUMOR-ACTIVITY; CELL METABOLISM; PHASE-II
AB The review paper provides an extensive overview of strategies for targeting the tumour microenvironment (TME) to enhance cancer therapy. It begins by underscoring the importance of profiling and comprehending the TME through advanced technologies like organ chips and artificial intelligence. The paper discusses multiple approaches to modulate the pro-tumour TME, including strategies for eliminating, normalizing, and targeting tumour cells. It delves into specific aspects such as cancer-associated fibroblasts, extracellular matrix, hypoxia, acidosis, neovascularisation, tumour-infiltrating T cells, the immune system, exosomes, tumour-associated neutrophils, and tumour angiogenesis. Emphasis is placed on the necessity of a multifaceted approach to effectively target the complex and dynamic TME, which plays a crucial role in tumour progression and therapeutic resistance. The conclusion highlights the significant impact of the TME on cancer therapy and identifies promising research and clinical application avenues. The paper underscores the shift in cancer treatment paradigms, advocating for strategies that address the intricate interactions within the TME to improve therapeutic outcomes.
C1 [Saikia, Trideep; Bharali, Alakesh; Kalita, Tutumoni; Sahu, Bhanu P.; Patowary, Lima] Girijananda Chowdhury Univ, Sch Pharmaceut Sci, Gauhati 781017, India.
   [Saikia, Trideep; Khanam, Asma; Ahmed, Nasima; Bharali, Alakesh; Kalita, Tutumoni; Rajak, Prakash; Patowary, Lima] Dibrugarh Univ, Dept Pharmaceut Sci, Dibrugarh 786004, India.
C3 Dibrugarh University
RP Patowary, L (corresponding author), Girijananda Chowdhury Univ, Sch Pharmaceut Sci, Gauhati 781017, India.; Patowary, L (corresponding author), Dibrugarh Univ, Dept Pharmaceut Sci, Dibrugarh 786004, India.
EM patowarylima@gmail.com
RI Bharali, Alakesh/ABC-8036-2021
OI Saikia, Trideep/0000-0002-4656-507X
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NR 251
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 29
PY 2024
DI 10.2174/0115733947341257241018150125
EA OCT 2024
PG 25
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA K7C9F
UT WOS:001345428900001
DA 2025-01-04
ER

PT J
AU Song, J
   Ge, YX
   Sun, XY
   Guan, QT
   Gong, SQ
   Wei, MJ
   Niu, JM
   Zhao, L
AF Song, Jia
   Ge, Yuexin
   Sun, Xiaoyu
   Guan, Qiutong
   Gong, Shiqiang
   Wei, Minjie
   Niu, Jumin
   Zhao, Lin
TI Noncoding RNAs related to the hedgehog pathway in cancer: clinical
   implications and future perspectives
SO MOLECULAR CANCER
LA English
DT Review
DE NcRNAs; Hedgehog pathway; Cancer; Biomarker; Targeted therapy
ID PRIMITIVE NEUROECTODERMAL TUMORS; BASAL-CELL CARCINOMAS; SIGNALING
   PATHWAY; SONIC HEDGEHOG; HEPATOCELLULAR-CARCINOMA; NASOPHARYNGEAL
   CARCINOMA; MESENCHYMAL TRANSITION; INHIBITS PROLIFERATION; PROMOTES
   APOPTOSIS; COLORECTAL-CANCER
AB Cancer is a type of malignant affliction threatening human health worldwide; however, the molecular mechanism of cancer pathogenesis remains to be elusive. The oncogenic hedgehog (Hh) pathway is a highly evolutionarily conserved signaling pathway in which the hedgehog-Patched complex is internalized to cellular lysosomes for degradation, resulting in the release of Smoothened inhibition and producing downstream intracellular signals. Noncoding RNAs (ncRNAs) with diversified regulatory functions have the potency of controlling cellular processes. Compelling evidence reveals that Hh pathway, ncRNAs, or their crosstalk play complicated roles in the initiation, metastasis, apoptosis and drug resistance of cancer, allowing ncRNAs related to the Hh pathway to serve as clinical biomarkers for targeted cancer therapy. In this review, we attempt to depict the multiple patterns of ncRNAs in the progression of malignant tumors via interactions with the Hh crucial elements in order to better understand the complex regulatory mechanism, and focus on Hh associated ncRNA therapeutics aimed at boosting their application in the clinical setting.
C1 [Song, Jia; Ge, Yuexin; Sun, Xiaoyu; Guan, Qiutong; Gong, Shiqiang; Wei, Minjie; Zhao, Lin] China Med Univ, Sch Pharm, Dept Pharmacol, Shenyang 110122, Peoples R China.
   [Song, Jia; Ge, Yuexin; Sun, Xiaoyu; Guan, Qiutong; Gong, Shiqiang; Wei, Minjie; Zhao, Lin] China Med Univ, Liaoning Key Lab Mol Targeted Antitumor Drug Dev, Shenyang 110122, Peoples R China.
   [Wei, Minjie] Shenyang Kangwei Med Lab Anal Co Ltd, Shenyang 110000, Peoples R China.
   [Niu, Jumin] Shenyang Womens & Childrens Hosp, Dept Gynecol, Shenyang 110011, Peoples R China.
C3 China Medical University; China Medical University
RP Zhao, L (corresponding author), China Med Univ, Liaoning Key Lab Mol Targeted Antitumor Drug Dev, Shenyang 110122, Peoples R China.; Niu, JM (corresponding author), Shenyang Womens & Childrens Hosp, Dept Gynecol, Shenyang 110011, Peoples R China.
EM niujumin@163.com; lzhao@cmu.edu.cn
FU National Natural Science Foundation of China [82073281, 82073884,
   U20A20413]; Shenyang ST Projects [19-109-4-09, 20-204-4-22]
FX This work was supported by grants from National Natural Science
   Foundation of China (No. 82073281, 82073884, U20A20413), Shenyang S&T
   Projects [19-109-4-09, 20-204-4-22].
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NR 174
TC 22
Z9 23
U1 2
U2 26
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD MAY 17
PY 2022
VL 21
IS 1
AR 115
DI 10.1186/s12943-022-01591-z
PG 16
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA 1I1MB
UT WOS:000796999100001
PM 35581586
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zhang, B
   Fang, CY
   Deng, DH
   Xia, L
AF Zhang, Bo
   Fang, Chenyan
   Deng, Dehou
   Xia, Liang
TI Research progress on common adverse events caused by targeted therapy
   for colorectal cancer (Review)
SO ONCOLOGY LETTERS
LA English
DT Review
DE colorectal cancer; adverse event
ID ENDOTHELIAL GROWTH-FACTOR; CLINICAL-PRACTICE GUIDELINES; ANTI-EGFR
   THERAPY; MONOCLONAL-ANTIBODIES; 1ST-LINE TREATMENT; POOLED ANALYSIS;
   SKIN RASH; BEVACIZUMAB; RISK; CHEMOTHERAPY
AB As targeted drug therapy is increasingly applied in the treatment of colon cancer, understanding and managing the adverse reactions of patients is becoming increasingly important. The present review examines the mechanisms of and adverse reactions to the most commonly used targeted drugs for colon cancer, and discusses methods of coping with these adverse reactions. Approved targeted drugs for metastatic colon cancer include monoclonal antibodies targeting vascular endothelial growth factor (VEGF), including bevacizumab, ziv-aflibercept and regorafenib, and monoclonal antibodies targeting epithelial growth factor receptor (EGFR), including cetuximab and panitumumab. The present review assesses the major adverse effects of these drugs and methods of dealing with reactions to them. VEGF inhibitors primarily result in cardiovascular and kidney problems. Meanwhile, EGFR receptor inhibitors are frequently reported to cause rashes, diarrhea and hypertension, and are reviewed from the point of view of resulting electrolyte disturbances.
C1 [Zhang, Bo; Deng, Dehou] Zhejiang Canc Hosp, Dept Integrated Chinese & Western Med, Hangzhou 310022, Zhejiang, Peoples R China.
   [Fang, Chenyan] Zhejiang Chinese Med Univ, Clin Med Coll 2, Dept Oncol, Hangzhou 310053, Zhejiang, Peoples R China.
   [Xia, Liang] Zhejiang Canc Hosp, Dept Neurosurg, 1 Ban Shan East Rd, Hangzhou 310022, Zhejiang, Peoples R China.
C3 Zhejiang Cancer Hospital; Zhejiang Chinese Medical University; Zhejiang
   Cancer Hospital
RP Xia, L (corresponding author), Zhejiang Canc Hosp, Dept Neurosurg, 1 Ban Shan East Rd, Hangzhou 310022, Zhejiang, Peoples R China.
EM xialiang@zjcc.org.cn
FU National Natural Science Foundation of China [81502147]; Youth
   Scientific Innovation Foundation of Zhejiang Cancer Hospital [QN201402]
FX The present study was supported by the National Natural Science
   Foundation of China (grant no. 81502147) and the Youth Scientific
   Innovation Foundation of Zhejiang Cancer Hospital (grant no. QN201402).
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NR 87
TC 27
Z9 28
U1 1
U2 15
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD JUL
PY 2018
VL 16
IS 1
BP 27
EP 33
DI 10.3892/ol.2018.8651
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GL4KQ
UT WOS:000437120300004
PM 29928383
OA gold, Green Submitted, Green Published
DA 2025-01-04
ER

PT J
AU Cao, WJ
   Xing, HZ
   Li, YM
   Tian, WL
   Song, YP
   Jiang, ZX
   Yu, JF
AF Cao, Weijie
   Xing, Haizhou
   Li, Yingmei
   Tian, Wenliang
   Song, Yongping
   Jiang, Zhongxing
   Yu, Jifeng
TI Claudin18.2 is a novel molecular biomarker for tumor-targeted
   immunotherapy
SO BIOMARKER RESEARCH
LA English
DT Review
DE Claudin18; 2; Molecular biomarker; Immunotherapy; Monoclonal antibody
   (mAb); Bispecific antibody (BsAb); Chimeric antigen receptor T (CAR-T)
   cells; Antibody-drug conjugates (ADCs); Clinical trial
ID TRANSCRIPTION FACTOR; TIGHT JUNCTIONS; PHASE-I; CANCER; EXPRESSION;
   GENE; ANTIBODY; PROTEIN; THERAPY; STRANDS
AB The claudin18.2 (CLDN18.2) protein, an isoform of claudin18, a member of the tight junction protein family, is a highly selective biomarker with limited expression in normal tissues and often abnormal expression during the occurrence and development of various primary malignant tumors, such as gastric cancer/gastroesophageal junction (GC/GEJ) cancer, breast cancer, colon cancer, liver cancer, head and neck cancer, bronchial cancer and non-small-cell lung cancer. CLDN18.2 participates in the proliferation, differentiation and migration of tumor cells. Recent studies have identified CLDN18.2 expression as a potential specific marker for the diagnosis and treatment of these tumors. With its specific expression pattern, CLDN18.2 has become a unique molecule for targeted therapy in different cancers, especially in GC; for example, agents such as zolbetuximab (claudiximab, IMAB362), a monoclonal antibody (mAb) against CLDN18.2, have been developed. In this review, we outline recent advances in the development of immunotherapy strategies targeting CLDN18.2, including monoclonal antibodies (mAbs), bispecific antibodies (BsAbs), chimeric antigen receptor T (CAR-T) cells redirected to target CLDN18.2, and antibody-drug conjugates (ADCs).
C1 [Cao, Weijie; Xing, Haizhou; Li, Yingmei; Tian, Wenliang; Song, Yongping; Jiang, Zhongxing; Yu, Jifeng] Zhengzhou Univ, Affiliated Hosp 1, Dept Hematol, Zhengzhou 450052, Henan, Peoples R China.
C3 Zhengzhou University
RP Song, YP; Jiang, ZX; Yu, JF (corresponding author), Zhengzhou Univ, Affiliated Hosp 1, Dept Hematol, Zhengzhou 450052, Henan, Peoples R China.
EM Songyongping001@126.com; Jiangzx@zzu.edu.cn; yujifengzzu@163.com
RI Jiang, ZHONG-XING/AAP-5942-2020; Yu, Jifeng/AAB-8399-2020
OI Yu, Jifeng/0000-0003-1217-4385
FU Project of Henan Provincial Education Department, China [20A320062];
   Project of Science and Technology Department of Henan Province, China
   [LHGJ20190039, SBGJ20202076]; Talent Research Fund of the First
   Affiliated Hospital of Zhengzhou University, Zhengzhou, China
FX This work was supported by the Project of Henan Provincial Education
   Department, China (20A320062, recipient JY), Project of Science and
   Technology Department of Henan Province, China (LHGJ20190039, recipient
   JY), Project of Science and Technology Department of Henan Province,
   China (SBGJ20202076, recipient JY), and Talent Research Fund of the
   First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
   (recipient JY).
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NR 111
TC 82
Z9 94
U1 18
U2 94
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2050-7771
J9 BIOMARK RES
JI Biomark. Res.
PD MAY 31
PY 2022
VL 10
IS 1
AR 38
DI 10.1186/s40364-022-00385-1
PG 21
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA 1S2YC
UT WOS:000803920800002
PM 35642043
OA Green Published, gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Kawaguchi, K
   Han, QH
   Li, SK
   Tan, YY
   Igarashi, K
   Murakami, T
   Unno, M
   Hoffman, RM
AF Kawaguchi, Kei
   Han, Qinghong
   Li, Shukuan
   Tan, Yuying
   Igarashi, Kentaro
   Murakami, Takashi
   Unno, Michiaki
   Hoffman, Robert M.
TI Efficacy of Recombinant Methioninase (rMETase) on Recalcitrant Cancer
   Patient-Derived Orthotopic Xenograft (PDOX) Mouse Models: A Review
SO CELLS
LA English
DT Review
DE recombinant methioninase; methionine dependence; nude mice; orthotopic
   implantation; patient-derived tumor
ID SALMONELLA-TYPHIMURIUM A1-R; HUMAN PANCREATIC-CANCER;
   GAMMA-MERCAPTOMETHANE-LYASE; SOFT-TISSUE SARCOMA; HUMAN COLON-CANCER;
   ANTI-CEA ANTIBODY; NUDE-MICE; SELECTIVE EFFICACY; BACTERIAL THERAPY;
   TARGETED THERAPY
AB An excessive requirement for methionine (MET), termed MET dependence, appears to be a general metabolic defect in cancer and has been shown to be a very effective therapeutic target. MET restriction (MR) has inhibited the growth of all major cancer types by selectively arresting cancer cells in the late-S/G(2) phase, when they also become highly sensitive to cytotoxic agents. Recombinant methioninase (rMETase) has been developed to effect MR. The present review describes the efficacy of rMETase on patient-derived orthotopic xenograft (PDOX) models of recalcitrant cancer, including the surprising result that rMETase administrated orally can be highly effective.
C1 [Kawaguchi, Kei; Han, Qinghong; Li, Shukuan; Tan, Yuying; Igarashi, Kentaro; Murakami, Takashi; Unno, Michiaki; Hoffman, Robert M.] AntiCancer Inc, San Diego, CA 92111 USA.
   [Kawaguchi, Kei; Hoffman, Robert M.] Univ Calif San Diego, Dept Surg, La Jolla, CA 92093 USA.
   [Kawaguchi, Kei] Tohoku Univ, Grad Sch Med, Dept Surg, Sendai, Miyagi 9808575, Japan.
C3 AntiCancer, Inc.; University of California System; University of
   California San Diego; Tohoku University
RP Hoffman, RM (corresponding author), AntiCancer Inc, San Diego, CA 92111 USA.; Hoffman, RM (corresponding author), Univ Calif San Diego, Dept Surg, La Jolla, CA 92093 USA.
EM kkawaguchi@surg.med.tohoku.ac.jp; qhhan42@gmail.com; li_62@hotmail.com;
   ytan.anticancer@hotmail.com; kenken99004@yahoo.co.jp;
   impressor@hotmail.co.jp; m_unno@surg.med.tohoku.ac.jp;
   all@anticancer.com
RI Murakami, Takashi/AAS-9039-2020; Unno, Michiaki/AAX-5246-2020
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NR 81
TC 45
Z9 47
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD MAY
PY 2019
VL 8
IS 5
AR 410
DI 10.3390/cells8050410
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA IC5FZ
UT WOS:000470994400030
PM 31052611
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Kumar, A
   Owen, JR
   Sloat, NT
   Maynard, E
   Hill, VM
   Hubbard, CB
   Mckinney, MS
   Sutton, LM
   Mccall, SJ
   Datto, MB
   Moyer, AN
   Caughey, BA
   Strickler, JH
   Ramaker, RC
AF Kumar, Anivarya
   Owen, Jennifer R.
   Sloat, Nicholette T.
   Maynard, Elizabeth
   Hill, Vanessa M.
   Hubbard, Christopher B.
   Mckinney, Matthew S.
   Sutton, Linda M.
   Mccall, Shannon J.
   Datto, Michael B.
   Moyer, Ashley N.
   Caughey, Bennett A.
   Strickler, John H.
   Ramaker, Ryne C.
TI Expansion of an Academic Molecular Tumor Board to Enhance Access to
   Biomarker-Driven Trials and Therapies in the Rural Southeastern United
   States
SO CURRENT ONCOLOGY
LA English
DT Article
DE cancer disparities; targeted therapy; molecular profiling; comprehensive
   genomic profiling
ID COLORECTAL-CANCER; FEASIBILITY; ONCOLOGY; LUNG; ERA
AB Targeting tumor-specific molecular alterations has shown significant clinical benefit. Molecular tumor boards (MTBs) connect cancer patients with personalized treatments and clinical trials. However, rural cancer centers often have limited access to MTB expertise. We established an academic-community partnership expanding our academic MTB to affiliated rural community cancer centers. We developed a centralized molecular registry of tumors (MRT) to aggregate the comprehensive genomic profiling (CGP) results and facilitate multidisciplinary MTB review. Of the 151 patients included, 87 (58%) had actionable genomic biomarkers, 42 (28%) were eligible for a targeted off-label therapy, and 27 (18%) were matched to a clinical trial. Of those with a clinical trial match, only 1 of 27 (3%) was enrolled in the identified trial. One year into implementation, community oncology providers were anonymously surveyed on persistent barriers to precision treatment utilization. The primary barriers to clinical trial enrollment were the distance to the trial center (70%), lack of transportation (55%), and lack of local trials (50%). This study offers a framework to improve access to molecular expertise, but significant barriers to the equitable use of CGP and trial enrollment persist.
C1 [Kumar, Anivarya] Duke Univ, Sch Med, Durham, NC 27710 USA.
   [Owen, Jennifer R.; Maynard, Elizabeth; Hill, Vanessa M.; Sutton, Linda M.] Duke Canc Network, Durham, NC 27707 USA.
   [Sloat, Nicholette T.; Mckinney, Matthew S.; Strickler, John H.] Duke Canc Inst, Durham, NC 27710 USA.
   [Hubbard, Christopher B.; Mccall, Shannon J.; Datto, Michael B.; Moyer, Ashley N.] Duke Univ, Dept Pathol, Sch Med, Durham, NC 27710 USA.
   [Mckinney, Matthew S.] Duke Univ, Med Ctr, Dept Med, Div Hematol Malignancies & Cellular Therapy, Durham, NC 27710 USA.
   [Caughey, Bennett A.] Massachusetts Gen Hosp, Div Hematol Oncol, Boston, MA 02114 USA.
   [Strickler, John H.; Ramaker, Ryne C.] Duke Univ, Med Ctr, Dept Med, Div Med Oncol, Durham, NC 27710 USA.
C3 Duke University; Duke University; Duke University; Duke University;
   Harvard University; Massachusetts General Hospital; Duke University
RP Ramaker, RC (corresponding author), Duke Univ, Med Ctr, Dept Med, Div Med Oncol, Durham, NC 27710 USA.
EM anivarya.kumar@duke.edu; vanessa.hill@duke.edu; chris.hubbard@duke.edu;
   matthew.mckinney@dm.duke.edu; linda.sutton@duke.edu;
   shannon.mccall@duke.edu; michael.datto@duke.edu;
   ashley.n.moyer@duke.edu; bcaughey1@mgb.org; ryne.ramaker@duke.edu
RI Hill, Vanessa/HRA-5121-2023
OI Strickler, John/0000-0001-7579-1175
FU National Comprehensive Cancer Center Network (NCCN); Eli Lilly and
   Company
FX This research was funded by the National Comprehensive Cancer Center
   Network (NCCN) Oncology Research Program from general research support
   provided by Eli Lilly and Company.
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NR 46
TC 0
Z9 0
U1 0
U2 0
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 NOV
PY 2024
VL 31
IS 11
BP 7244
EP 7257
DI 10.3390/curroncol31110534
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA N4O9J
UT WOS:001364162300001
PM 39590164
OA gold
DA 2025-01-04
ER

PT J
AU Young, O
   Ngo, N
   Lin, LS
   Stanbery, L
   Creeden, JF
   Hamouda, D
   Nemunaitis, J
AF Young, Olivia
   Ngo, Nealie
   Lin, Leslie
   Stanbery, Laura
   Creeden, Justin Fortune
   Hamouda, Danae
   Nemunaitis, John
TI Folate Receptor as a Biomarker and Therapeutic Target in Solid Tumors
SO CURRENT PROBLEMS IN CANCER
LA English
DT Article
DE Folate; Folate receptor; Solid tumor; Targeted therapy; Ovarian cancer;
   Breast cancer; ADC
ID PEGYLATED LIPOSOMAL DOXORUBICIN; METASTATIC COLORECTAL-CANCER;
   PLATINUM-RESISTANT OVARIAN; ANTIBODY-DRUG CONJUGATE; MIRVETUXIMAB
   SORAVTANSINE IMGN853; TISSUE-SPECIFIC PROMOTERS; ANTITUMOR-ACTIVITY;
   PHASE-III; ALPHA EXPRESSION; BINDING-PROTEIN
AB Folate is a B vitamin necessary for basic biological functions, including rapid cell turnover occurring in cancer cell proliferation. Though the role of folate as a causative versus protective agent in carcinogenesis is debated, several studies have indicated that the folate receptor (FR), notably subtype folate receptor alpha (FR alpha), could be a viable biomarker for diagnosis, progression, and prognosis. Several cancers, including gastrointestinal, gynecological, breast, lung, and squamous cell head and neck cancers overexpress FR and are currently under investigation to correlate receptor status to disease state. Traditional chemotherapies have included antifolate medications, such as methotrexate and pemetrexed, which generate anticancer activity during the synthesis phase of the cell cycle. Increasingly, the repertoire of pharmacotherapies is expanding to include FR as a target, with a heterogenous pool of directed therapies. Here we discuss the FR, expression and effect in cancer biology, and relevant pharmacologic inhibitors.(c) 2022 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ )
C1 [Young, Olivia; Ngo, Nealie; Lin, Leslie; Hamouda, Danae] Univ Toledo, Dept Med, Coll Med & Life Sci, Toledo, OH USA.
   [Stanbery, Laura; Nemunaitis, John] Gradalis Inc, Carrollton, TX USA.
   [Creeden, Justin Fortune] Univ Toledo, Dept Canc Biol, Coll Med & Life Sci, Toledo, OH USA.
   [Nemunaitis, John] Gradalis Inc, 2545 Golden Bear,Suite 110, Carrollton, TX 75006 USA.
C3 University System of Ohio; University of Toledo; Gradalis, Inc.;
   University System of Ohio; University of Toledo; Gradalis, Inc.
RP Nemunaitis, J (corresponding author), Gradalis Inc, 2545 Golden Bear,Suite 110, Carrollton, TX 75006 USA.
EM johnnemunaitis@gmail.com
RI Creeden, Justin/JKJ-3293-2023
OI Nemunaitis, John/0000-0002-2234-2381
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NR 127
TC 31
Z9 31
U1 6
U2 29
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0147-0272
EI 1535-6345
J9 CURR PROB CANCER
JI Curr. Probl. Cancer
PD FEB
PY 2023
VL 47
IS 1
AR 100917
DI 10.1016/j.currproblcancer.2022.100917
EA DEC 2022
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA G9GM5
UT WOS:000992155000001
PM 36508886
OA hybrid
DA 2025-01-04
ER

PT J
AU Yu, YY
   Zhu, YJ
   Xiao, ZZ
   Chen, YD
   Chang, XS
   Liu, YH
   Tang, Q
   Zhang, HB
AF Yu, Ya-ya
   Zhu, Yan-juan
   Xiao, Zhen-zhen
   Chen, Ya-dong
   Chang, Xue-song
   Liu, Yi-hong
   Tang, Qing
   Zhang, Hai-bo
TI The pivotal application of patient-derived organoid biobanks for
   personalized treatment of gastrointestinal cancers
SO BIOMARKER RESEARCH
LA English
DT Review
DE Gastrointestinal cancers; Patient-derived tumor organoids; Biobanking;
   Personalized anti-cancer therapy
ID IN-VITRO EXPANSION; COLORECTAL-CANCER; PANCREATIC-CANCER; STEM-CELLS;
   EPITHELIAL ORGANOIDS; PD-1 BLOCKADE; HUMAN COLON; REVEAL; MODEL;
   CULTURES
AB Gastrointestinal cancers (GICs) occupy more than 30% of the cancer-related incidence and mortality around the world. Despite advances in the treatment strategies, the long-term overall survival has not been improved for patients with GICs. Recently, the novel patient-derived organoid (PDO) culture technology has become a powerful tool for GICs in a manner that recapitulates the morphology, pathology, genetic, phenotypic, and behavior traits of the original tumors. Excitingly, a number of evidences suggest that the versatile technology has great potential for personalized treatment, suppling the clinical application of molecularly guided personalized treatment. In the paper, we summarize the literature on the topics of establishing organoid biobanks of PDOs, and their application in the personalized treatment allowing for radiotherapy, chemotherapy, targeted therapy, and immunotherapy selection for GICs. Despite the limitations of current organoid models, high-throughput drug screening of GIC PDO combined with next-generation sequencing technology represents a novel and pivotal preclinical model for precision medicine of tumors and has a great value in promoting the transformation from basic cancer research to clinical application.
C1 [Yu, Ya-ya; Zhu, Yan-juan; Xiao, Zhen-zhen; Chen, Ya-dong; Chang, Xue-song; Liu, Yi-hong; Tang, Qing; Zhang, Hai-bo] Guangzhou Univ Chinese Med, Affiliated Hosp 2, Dept Oncol, Guangzhou, Peoples R China.
   [Yu, Ya-ya; Zhu, Yan-juan; Xiao, Zhen-zhen; Chen, Ya-dong; Chang, Xue-song; Liu, Yi-hong; Tang, Qing; Zhang, Hai-bo] Guangdong Prov Hosp Chinese Med, Dept Oncol, Guangzhou, Guangdong, Peoples R China.
   [Tang, Qing] Guangdong Prov Hosp Chinese Med, Clin & Basic Res Team TCM Prevent & Treatment, NSCLC, Guangzhou, Peoples R China.
   [Zhang, Hai-bo] Guangzhou Univ Chinese Med, Affiliated Hosp 2, State Key Lab Dampness Syndrome Chinese Med, Guangzhou, Peoples R China.
C3 Guangzhou University of Chinese Medicine; Guangzhou University of
   Chinese Medicine; Guangzhou University of Chinese Medicine; Guangzhou
   University of Chinese Medicine
RP Zhang, HB (corresponding author), Guangdong Prov Hosp Chinese Med, Dept Oncol, Guangzhou, Guangdong, Peoples R China.
EM haibozh@gzucm.edu.cn
RI Chang, Xuesong/HGB-8879-2022; Zhang, Haibo/HLP-9266-2023
FU State Key Laboratory of Dampness Syndrome of Chinese Medicine, The
   Second Affiliated Hospital of Guangzhou University of Chinese Medicine
   [SZ2020ZZ20, SZ2021ZZ0204, SZ2021ZZ40]; Foundation for Chinese Medicine
   and Technology Research of Guangdong Provincial Hospital of Chinese
   Medicine [2017KT1820, 2016KT1571]
FX This study was supported by State Key Laboratory of Dampness Syndrome of
   Chinese Medicine, The Second Affiliated Hospital of Guangzhou University
   of Chinese Medicine (SZ2020ZZ20, SZ2021ZZ0204 and SZ2021ZZ40), and the
   Foundation for Chinese Medicine and Technology Research of Guangdong
   Provincial Hospital of Chinese Medicine (2017KT1820, 2016KT1571).
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NR 135
TC 7
Z9 8
U1 3
U2 34
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2050-7771
J9 BIOMARK RES
JI Biomark. Res.
PD OCT 8
PY 2022
VL 10
IS 1
AR 73
DI 10.1186/s40364-022-00421-0
PG 25
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA 5D6LL
UT WOS:000865050500001
PM 36207749
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Patell, K
   Mears, VL
   Storandt, MH
   Mahipal, A
AF Patell, Kanchi
   Mears, Veronica Lee
   Storandt, Michael H.
   Mahipal, Amit
TI Metabolism, toxicity and management of fruquintinib: a novel drug for
   metastatic colorectal cancer
SO EXPERT OPINION ON DRUG METABOLISM & TOXICOLOGY
LA English
DT Review
DE Colon cancer; fruquintinib; metastatic cancer; rectal cancer; targeted
   therapy; vascular endothelial growth factor
ID PEPTIDE-1 RECEPTOR AGONISTS; SGLT2 INHIBITORS; OUTCOMES; TRIALS; SAFETY;
   TISSUE
AB IntroductionColorectal cancer (CRC) is the third most diagnosed cancer globally and despite therapeutic strides, the prognosis for patients with metastatic disease (mCRC) remains poor. Fruquintinib is an oral vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor (TKI) targeting VEGFR -1, -2, and -3, and has recently received approval by the U.S. Food and Drug Administration for treatment of mCRC refractory to standard chemotherapy, anti-VEGF therapy, and anti-epidermal growth factor receptor (EGFR) therapy.Areas coveredThis article provides an overview of the pre-clinical data, pharmacokinetics, clinical efficacy, and safety profile of fruquintinib, as well as the management of clinical toxicities associated with fruquintinib.Expert opinionFruquintinib is a valuable additional treatment option for patients with refractory mCRC. The pivotal role of vigilant toxicity management cannot be understated. While fruquintinib offers a convenient and overall, well-tolerated treatment option, ongoing research is essential to determine its efficacy in different patient subsets, evaluate it in combination with chemotherapy and immunotherapy, and determine its role in earlier lines of therapy.
C1 [Patell, Kanchi; Mears, Veronica Lee; Mahipal, Amit] Case Western Reserve Univ, Univ Hosp Seidman Canc Ctr, Cleveland, OH USA.
   [Storandt, Michael H.] Mayo Clin, Rochester, MN USA.
   [Mahipal, Amit] Case Western Reserve Univ, Seidman Canc Ctr, 11100 Euclid Ave, Cleveland, OH 44106 USA.
C3 University System of Ohio; Case Western Reserve University; Mayo Clinic;
   University System of Ohio; Case Western Reserve University
RP Mahipal, A (corresponding author), Case Western Reserve Univ, Seidman Canc Ctr, 11100 Euclid Ave, Cleveland, OH 44106 USA.
EM amit.mahipal@uhhospitals.org
RI Mahipal, Amit/ABD-8395-2020
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NR 38
TC 1
Z9 1
U1 4
U2 5
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 APR 2
PY 2024
VL 20
IS 4
BP 197
EP 205
DI 10.1080/17425255.2024.2332364
EA MAR 2024
PG 9
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA OP0A5
UT WOS:001189522000001
PM 38497279
DA 2025-01-04
ER

PT J
AU Fischer, J
   Walker, LC
   Robinson, BA
   Frizelle, FA
   Church, JM
   Eglinton, TW
AF Fischer, Jesse
   Walker, Logan C.
   Robinson, Bridget A.
   Frizelle, Frank A.
   Church, James M.
   Eglinton, Tim W.
TI Clinical implications of the genetics of sporadic colorectal cancer
SO ANZ JOURNAL OF SURGERY
LA English
DT Review
DE colorectal cancer; colorectal cancer guidelines; epigenetics; genetics;
   molecular testing
ID ISLAND METHYLATOR PHENOTYPE; MICROSATELLITE INSTABILITY; BRAF MUTATION;
   PATHWAY; TUMORS
AB Colorectal cancer (CRC) is common and at least 80% of cases are sporadic, without any significant family history. Prognostication and treatment have been relatively empirical for what has become increasingly identified as a genetically heterogeneous disease. There are three main genetic pathways in sporadic CRC: the chromosomal instability pathway, the microsatellite instability pathway and the CpG island methylator phenotype pathway. There is significant overlap between these complex molecular pathways and this limits the clinical application of CRC genetics. Recent Australian and New Zealand guidelines recommend routine testing of mismatch repair (MMR) status for new cases of CRC and selective KRAS and BRAF testing on the basis of diagnostic, prognostic and therapeutic implications. It is important that all clinicians treating CRC have an understanding of the importance of and basis for identifying key genetic features of CRC. It is likely that in the future better molecular characterization such as that allowed by the consensus molecular subtype classification will allow improved prognostication and targeted therapy in order to deliver more personalized treatment for CRC.
C1 [Fischer, Jesse; Frizelle, Frank A.; Eglinton, Tim W.] Univ Otago, Dept Surg, POB 4345, Christchurch 8140, New Zealand.
   [Walker, Logan C.] Univ Otago, Dept Pathol, Christchurch, New Zealand.
   [Robinson, Bridget A.] Univ Otago, Dept Med, Christchurch, New Zealand.
   [Robinson, Bridget A.] Christchurch Hosp, Oncol Serv, Christchurch, New Zealand.
   [Frizelle, Frank A.; Eglinton, Tim W.] Canterbury Dist Hlth Board, Dept Surg, Christchurch, New Zealand.
   [Church, James M.] Cleveland Clin Fdn, Dept Colorectal Surg, 9500 Euclid Ave, Cleveland, OH 44195 USA.
C3 University of Otago; University of Otago; University of Otago;
   Christchurch Hospital New Zealand; Cleveland Clinic Foundation
RP Fischer, J (corresponding author), Univ Otago, Dept Surg, POB 4345, Christchurch 8140, New Zealand.
EM jesse.fischer@postgrad.otago.ac.nz
RI Eglinton, Tim/H-8606-2019; Fischer, Jesse/ABW-0348-2022
OI Fischer, Jesse/0000-0002-3366-5629
FU Medtronic Colorectal Surgical Society of Australia and New Zealand
   (CSSANZ) Research Fellowship Funding Source: Medline
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NR 43
TC 23
Z9 25
U1 0
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1445-1433
EI 1445-2197
J9 ANZ J SURG
JI ANZ J. Surg.
PD OCT
PY 2019
VL 89
IS 10
BP 1224
EP 1229
DI 10.1111/ans.15074
PG 6
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA JE0UG
UT WOS:000490409100035
PM 30919552
DA 2025-01-04
ER

PT J
AU Benjamin, DJ
   Kalebasty, AR
AF Benjamin, David J.
   Kalebasty, Arash Rezazadeh
TI Treatment approaches for urachal cancer: Use of immunotherapy and
   targeted therapies
SO RARE TUMORS
LA English
DT Review
DE Urachal cancer; genitourinary cancer; targeted therapy; immunotherapy
ID CARCINOMA; ADENOCARCINOMA; CHEMOTHERAPY; CISPLATIN
AB Urachal cancer is a rare genitourinary malignancy that arises from the embryologic remnant of the urachus. The malignancy is considered to be aggressive, with no clear consensus on appropriate management for advanced disease. Although traditionally considered to be related to bladder cancer given its embryologic origin, several next generation sequencing studies have revealed the genomic profile of this genitourinary malignancy most closely resembles colorectal cancer. Moreover, these studies have identified potentially actionable mutations including EGFR, KRAS and MET. In addition, recent data suggests that immunotherapy may benefit some patients with advanced urachal cancer. Nonetheless, continued research is warranted to better understand how to treat this rare genitourinary cancer.
C1 [Benjamin, David J.] Hoag Family Canc Inst, Newport Beach, CA USA.
   [Kalebasty, Arash Rezazadeh] UC Irvine Med Ctr, Div Hematol Oncol, Orange, CA USA.
   [Benjamin, David J.] Hoag Family Canc Inst, 1 Hoag Dr,Bldg 41, Newport Beach, CA 92663 USA.
C3 University of California System; University of California Irvine
RP Benjamin, DJ (corresponding author), Hoag Family Canc Inst, 1 Hoag Dr,Bldg 41, Newport Beach, CA 92663 USA.
EM David.Benjamin@hoag.org
OI Benjamin, David/0000-0002-2392-886X
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NR 28
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 2036-3605
EI 2036-3613
J9 RARE TUMORS
JI Rare Tumors
PD JUL 11
PY 2023
VL 15
AR 20363613231189984
DI 10.1177/20363613231189984
PG 6
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA M2YE2
UT WOS:001028877900001
PM 37465663
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Jeitany, M
   Leroy, C
   Tosti, P
   Lafitte, M
   Le Guet, J
   Simon, V
   Bonenfant, D
   Robert, B
   Grillet, F
   Mollevi, C
   El Messaoudi, S
   Otandault, A
   Canterel-Thouennon, L
   Busson, M
   Thierry, AR
   Martineau, P
   Pannequin, J
   Roche, S
   Sirvent, A
AF Jeitany, Maya
   Leroy, Cedric
   Tosti, Priscillia
   Lafitte, Marie
   Le Guet, Jordy
   Simon, Valerie
   Bonenfant, Debora
   Robert, Bruno
   Grillet, Fanny
   Mollevi, Caroline
   El Messaoudi, Safia
   Otandault, Amaelle
   Canterel-Thouennon, Lucile
   Busson, Muriel
   Thierry, Alain R.
   Martineau, Pierre
   Pannequin, Julie
   Roche, Serge
   Sirvent, Audrey
TI Inhibition of DDR1-BCR signalling by nilotinib asanew therapeutic
   strategy for metastatic colorectal cancer
SO EMBO MOLECULAR MEDICINE
LA English
DT Article
DE collagen receptor; colorectal cancer; invasion; targeted therapy;
   tyrosine kinase
ID CONSENSUS MOLECULAR SUBTYPES; TYROSINE KINASES; BCR-ABL; MESENCHYMAL
   TRANSITION; SRC FAMILY; KRAS; SUPPRESSION; MUTATIONS; INVASION; IMATINIB
AB The clinical management of metastatic colorectal cancer (mCRC) faces major challenges. Here, we show that nilotinib, a clinically approved drug for chronic myeloid leukaemia, strongly inhibits human CRC cell invasion invitro and reduces their metastatic potential in intrasplenic tumour mouse models. Nilotinib acts by inhibiting the kinase activity of DDR1, a receptor tyrosine kinase for collagens, which we identified as a RAS-independent inducer of CRC metastasis. Using quantitative phosphoproteomics, we identified BCR as a new DDR1 substrate and demonstrated that nilotinib prevents DDR1-mediated BCR phosphorylation on Tyr177, which is important for maintaining -catenin transcriptional activity necessary for tumour cell invasion. DDR1 kinase inhibition also reduced the invasion of patient-derived metastatic and circulating CRC cell lines. Collectively, our results indicate that the targeting DDR1 kinase activity with nilotinib may be beneficial for patients with mCRC.
C1 [Jeitany, Maya; Leroy, Cedric; Tosti, Priscillia; Lafitte, Marie; Le Guet, Jordy; Simon, Valerie; Roche, Serge; Sirvent, Audrey] Univ Montpellier, CNRS, CRBM, Montpellier, France.
   [Leroy, Cedric; Bonenfant, Debora] Postfach, Novartis Inst Biomed Res, Basel, Switzerland.
   [Leroy, Cedric] Actel Pharmaceut Ltd, Allschwil, Switzerland.
   [Robert, Bruno; Mollevi, Caroline; El Messaoudi, Safia; Otandault, Amaelle; Canterel-Thouennon, Lucile; Busson, Muriel; Thierry, Alain R.; Martineau, Pierre] Univ Montpellier, INSERM, IRCM, Montpellier, France.
   [Grillet, Fanny; Pannequin, Julie] Univ Montpellier, CNRS, INSERM, IGF, Montpellier, France.
C3 Universite de Montpellier; Centre National de la Recherche Scientifique
   (CNRS); Novartis; Actelion Pharmaceuticals Ltd; Institut National de la
   Sante et de la Recherche Medicale (Inserm); Universite de Montpellier;
   UNICANCER; Institut Regional du Cancer Montpellier / Val d'Aurelle
   (ICM); Institut National de la Sante et de la Recherche Medicale
   (Inserm); Universite de Montpellier; Centre National de la Recherche
   Scientifique (CNRS)
RP Roche, S; Sirvent, A (corresponding author), Univ Montpellier, CNRS, CRBM, Montpellier, France.
EM serge.roche@crbm.cnrs.fr; audrey.sirvent@crbm.cnrs.fr
RI ROBERT, Bruno/AAB-7581-2020; thierry, alain/F-9492-2014; Mollevi,
   Caroline/AAA-6839-2019; Martineau, Pierre/N-4386-2017
OI roche, serge/0000-0003-3413-3859; ROBERT, Bruno/0000-0001-5573-6945;
   pannequin, julie/0000-0002-9956-373X; Martineau,
   Pierre/0000-0002-7993-7183
FU ARC; Montpellier SIRIC Grant [INCa-DGOS-Inserm 6045]; Ligue Nationale
   contre le Cancer; CNRS; University of Montpellier; Montpellier SIRIC;
   Fondation pour la Recherche Medicale; INSERM; Fondation de France
FX We gratefully thank C. Laschinger, N. Maurin and P. Mangeat for various
   reagents and plasmids; I. Ait Arsa and J. Vitre for technical
   assistance; and our colleagues for helpful discussions. We also thank M.
   Boyer (IGMM, Montpellier) for flow cytometry experiments, the
   Montpellier RIO Imaging and the RHEM histology platforms; P. Balaguer
   (Screening Platform in Cancer PCC, IRCM Montpellier) and M. Del Rio
   (IRCM, Montpellier) for the HCT116 LUC+ and SW620 LUC+ cell lines
   respectively, the Montpellier Genomic Collection (MGC), the Montpellier
   Platform of CRC preclinical models (MPCC), the "Centre de Ressources
   Biologiques" (ICM, Montpellier) and the Montpellier Small Animal Imaging
   Platform (IPAM) of Montpellier. This work was supported by ARC,
   Montpellier SIRIC Grant "INCa-DGOS-Inserm 6045", Ligue Nationale contre
   le Cancer, CNRS and the University of Montpellier. CL and MJ were
   supported by the Ligue Nationale contre le Cancer; PT, JLG and LCT by
   the Montpellier SIRIC; ML by the Fondation pour la Recherche Medicale;
   VS and JP by the CNRS; BM, PM, ART and SR by the INSERM; and AS by the
   Fondation de France and the CNRS.
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NR 42
TC 85
Z9 89
U1 1
U2 16
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1757-4676
EI 1757-4684
J9 EMBO MOL MED
JI EMBO Mol. Med.
PD APR
PY 2018
VL 10
IS 4
AR e2918
DI 10.15252/emmm.201707918
PG 16
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA GB8JP
UT WOS:000429322500001
PM 29438985
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Xu, JB
   Zhang, GL
   Luo, X
   Wang, D
   Zhou, W
   Zhang, Y
   Zhang, W
   Chen, JX
   Meng, Q
   Chen, EG
   Chen, H
   Song, ZF
AF Xu, Jianbin
   Zhang, Guolin
   Luo, Xin
   Wang, Di
   Zhou, Wei
   Zhang, Yan
   Zhang, Wei
   Chen, Jiaxin
   Meng, Qing
   Chen, Engeng
   Chen, Heng
   Song, Zhangfa
TI Co-delivery of 5-fluorouracil and miRNA-34a mimics by host-guest
   self-assembly nanocarriers for efficacious targeted therapy in
   colorectal cancer patient-derived tumor xenografts
SO THERANOSTICS
LA English
DT Article
DE co-delivery; PDX model; targeted therapy; synergistic therapy
ID QUANTUM DOTS; IN-VITRO; SUPRAMOLECULAR SYSTEMS; NONHUMAN-PRIMATES;
   STEM-CELLS; MIR-34A; NANOPARTICLES; METASTASIS; BIOCOMPATIBILITY;
   CYTOTOXICITY
AB Rationale: A co-delivery system that can transport chemotherapeutic drugs and nucleotide drugs to distinct targets in tumors is an attractive strategy for cancer therapy. In this study, well-defined targeted quantum dot (QD)-based multifunctional nanocarriers were developed through self-assembly driven by host-guest interactions. 5-fluorouracil (5-FU) and microRNA-34a mimics (miR-34a(m)) were co-administered to achieve synergistic effects for colorectal cancer (CRC) therapy for the first time. Furthermore, the CRC patient-derived tumor xenograft (PDX) model, which closely mimics human CRC tumor pathological properties, was used for evaluating the therapeutic effect in this research.
   Methods: Multiple beta-cyclodextrin (CD)-attached QD nanoparticles were used as host molecules. An adamantane (ADA)-modified TCP1 peptide-targeting ligand (TCP1) was used as the guest molecule. 5-FU and miR-34a(m) were loaded into TCP1-CD-QD nanocarriers, which were used to treat CRC in vitro and in vivo. In addition, the CRC PDX model was used to evaluate the treatment efficacy of this co-delivery system.
   Results: 5-FU and miR-34a(m) can be efficiently encapsulated into TCP1-CD-QD nanocarriers and delivered into CRC cells, which led to the inhibition of the proliferation and migration of CRC cells in vitro and suppression of tumor growth in a CRC cell-derived tumor xenograft model. The obtained data further suggested that co-delivery of 5-FU and miR-34a(m) could achieve synergistic effects for CRC therapy. Notably, targeted therapy via the co-delivery of 5-FU and miR-34a(m) by TCP1-CD-QD nanocarriers significantly inhibited the growth of PDX tumors.
   Conclusions: These studies strongly indicate that such a nanocarrier-based co-delivery system is a promising combined therapeutic strategy that utilizes chemotherapeutic drugs and nucleotide drugs for enhancing colorectal cancer targeting and synergistic therapy.
C1 [Xu, Jianbin; Zhang, Guolin; Luo, Xin; Wang, Di; Zhou, Wei; Zhang, Wei; Chen, Jiaxin; Meng, Qing; Chen, Engeng; Song, Zhangfa] Zhejiang Univ, Sir Run Run Shaw Hosp, Sch Med, Dept Colorectal Surg, 3 Qingchun Rd, Hangzhou 310016, Zhejiang, Peoples R China.
   [Zhang, Yan] Nankai Univ, State Key Lab Med Chem Biol, Tianjin 301150, Peoples R China.
   [Chen, Heng] Shenzhen Univ, Shenzhen Key Lab Polymer Sci & Technol, Guangdong Res Ctr Interfacial Engn Funct Mat, Coll Mat Sci & Engn, Shenzhen 518060, Peoples R China.
C3 Zhejiang University; Nankai University; Shenzhen University
RP Chen, H; Song, ZF (corresponding author), Zhejiang Univ, Sir Run Run Shaw Hosp, Sch Med, Dept Colorectal Surg, 3 Qingchun Rd, Hangzhou 310016, Zhejiang, Peoples R China.
EM polyhengchen@szu.edu.cn; songzhangfa@zju.edu.cn
RI ; Xu, Jianbin/ISB-4232-2023
OI Chen, Heng/0000-0002-1781-9050; Chen, Engeng/0000-0002-9321-2058; Zhang,
   Guolin/0000-0002-5836-4478; Xu, Jianbin/0000-0003-0505-2160
FU National Natural Science Foundation of China [32071349, 81701820,
   81771502]; Zhejiang Provincial Natural Science Foundation of China
   [LY20H180014, LH19H160001]; Department of Health of Zhejiang Province
   [2018PY025, 2018KY473]
FX The present study was supported by the National Natural Science
   Foundation of China (32071349, 81701820 and 81771502) . This research
   was supported by the Zhejiang Provincial Natural Science Foundation of
   China under Grant No. LY20H180014, LH19H160001 and the Department of
   Health of Zhejiang Province (No. 2018PY025 and 2018KY473) .
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NR 66
TC 28
Z9 31
U1 3
U2 50
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 5
BP 2475
EP 2489
DI 10.7150/thno.52076
PG 15
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA SO5SO
UT WOS:000659032100001
PM 33500737
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, QY
   Yu, QL
   Luan, WJ
   Li, TF
   Xiao, YN
   Zhang, L
   Li, Y
   Rong, R
   Ren, CG
AF Zhang, Qiu-Yan
   Yu, Qing-Long
   Luan, Wei-Jing
   Li, Tong-Fang
   Xiao, Ya-Ni
   Zhang, Li
   Li, Yi
   Rong, Rong
   Ren, Chun-Guang
TI LWJ-M30, a conjugate of DM1 and B6, for the targeted therapy of
   colorectal cancer with improved therapeutic effects
SO RSC ADVANCES
LA English
DT Article
ID PEPTIDE; NANOPARTICLES; MAYTANSINE
AB Colorectal cancer (CRC) is one of the most prevalent cancers worldwide as well as a significant cause of mortality. The conventional treatment could cause serious side effects and induce drug resistance, recurrence and metastasis of cancers. Hence, specific targeting of cancer cells without affecting the normal tissues is currently an urgent necessity in cancer therapy. The emerging of peptide-drug conjugates (PDC) is regarded as a promising approach to address malignant tumors. LWJ-M30, a conjugate of DM1 and B6 peptide, targeted transferrin receptors (TfRs) on the surface of the CRC cells, showing a powerful anti-cancer effect. LWJ-M30 significantly inhibited the HCT116 cells proliferation and migration in vitro. LWJ-M30 also dramatically decreased the level of polymeric tubulin, while the disruption of microtubules caused the cell cycle to be arrested in the G2/M phase. LWJ-M30 induced the HCT116 cells apoptosis both in vivo and in vitro. The results in vivo demonstrated that LWJ-M30 could inhibit the HCT116 growth without affecting the mouse body weight. Taking these results together, our data indicated that LWJ-M30 could improve the therapeutic effects of DM1 while reducing the systemic toxicity in normal tissues.
C1 [Zhang, Qiu-Yan; Yu, Qing-Long; Luan, Wei-Jing; Li, Tong-Fang; Xiao, Ya-Ni; Zhang, Li; Li, Yi; Rong, Rong; Ren, Chun-Guang] Yantai Inst Mat Med, Yantai Key Lab Nanomed & Adv Preparat, Yantai, Shandong, Peoples R China.
   [Ren, Chun-Guang] Yantai Univ, Coll Life Sci, Yantai 264005, Peoples R China.
C3 Yantai University
RP Li, Y; Rong, R; Ren, CG (corresponding author), Yantai Inst Mat Med, Yantai Key Lab Nanomed & Adv Preparat, Yantai, Shandong, Peoples R China.; Ren, CG (corresponding author), Yantai Univ, Coll Life Sci, Yantai 264005, Peoples R China.
EM yli@simmyt.ac.cn; rrong@yimm.ac.cn; cgren@ytu.edu.cn
RI Wang, Yibin/KEZ-9645-2024; wang, jiantao/GRS-9485-2022; wang,
   wei/JYP-7819-2024
OI Yu, Qinglong/0000-0002-9925-2130
FU Shandong Provincial Natural Science Foundation [ZR2020QH192]; Yantai
   Science and Technology Bureau [2021MSGY035]
FX All the work were financial supported by the project ZR2020QH192
   supported by Shandong Provincial Natural Science Foundation and the
   project 2021MSGY035 supported by Yantai Science and Technology Bureau.
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NR 40
TC 5
Z9 6
U1 1
U2 10
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
EI 2046-2069
J9 RSC ADV
JI RSC Adv.
PD APR 3
PY 2023
VL 13
IS 16
BP 10840
EP 10846
DI 10.1039/d2ra07758b
PG 7
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA C5ZM9
UT WOS:000962695200001
PM 37033427
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Liu, B
   Xiang, W
   Liu, JH
   Tang, J
   Wang, JR
   Liu, B
   Long, Z
   Wang, L
   Yin, GM
   Liu, JY
AF Liu, Biao
   Xiang, Wei
   Liu, Jiahao
   Tang, Jin
   Wang, Jinrong
   Liu, Bin
   Long, Zhi
   Wang, Long
   Yin, Guangming
   Liu, Jianye
TI The regulatory role of antisense lncRNAs in cancer
SO CANCER CELL INTERNATIONAL
LA English
DT Review
DE Antisense lncRNA; Cancer; Transcriptional modulation; Translational
   control; Target therapy
ID LONG NONCODING RNA; PROMOTES TUMOR-GROWTH; CELL LUNG-CANCER;
   BLADDER-CANCER; HEPATOCELLULAR-CARCINOMA; BREAST-CANCER; CISPLATIN
   RESISTANCE; COLORECTAL-CANCER; PROGNOSTIC-FACTOR; UP-REGULATION
AB Antisense long non-coding RNAs (antisense lncRNAs), transcribed from the opposite strand of genes with either protein coding or non-coding function, were reported recently to play a crucial role in the process of tumor onset and development. Functionally, antisense lncRNAs either promote or suppress cancer cell proliferation, migration, invasion, and chemoradiosensitivity. Mechanistically, they exert their regulatory functions through epigenetic, transcriptional, post-transcriptional, and translational modulations. Simultaneously, because of nucleotide sequence complementarity, antisense lncRNAs have a special role on its corresponding sense gene. We highlight the functions and molecular mechanisms of antisense lncRNAs in cancer tumorigenesis and progression. We also discuss the potential of antisense lncRNAs to become cancer diagnostic biomarkers and targets for tumor treatment.
C1 [Liu, Biao; Xiang, Wei; Liu, Jiahao; Tang, Jin; Wang, Jinrong; Liu, Bin; Long, Zhi; Wang, Long; Yin, Guangming; Liu, Jianye] Cent South Univ, Xiangya Hosp 3, Dept Urol, 138 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China.
C3 Central South University
RP Liu, JY (corresponding author), Cent South Univ, Xiangya Hosp 3, Dept Urol, 138 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China.
EM liujianye810@163.com
RI wang, long/IZE-1764-2023
FU National Natural Science Foundation of China [81802556]; Hunan Province
   Natural Science Foundation [2019JJ30039]; Huxiang Young Talents Plan
   Project of Hunan Province [2019RS2015]; New Xiangya Talent Projects of
   the Third Xiangya Hospital of Central South University [JY201615];
   Scientific Projects of Changsha Administration of Science Technology
   [kq1901129]; Scientific Projects of Health Commission of Hunan Province
   [B2017034, 20201041]
FX This work was supported by grants from the National Natural Science
   Foundation of China (81802556), the Hunan Province Natural Science
   Foundation (2019JJ30039), Huxiang Young Talents Plan Project of Hunan
   Province (2019RS2015), the New Xiangya Talent Projects of the Third
   Xiangya Hospital of Central South University (JY201615), the Scientific
   Projects of Changsha Administration of Science &Technology (kq1901129),
   and the Scientific Projects of Health Commission of Hunan Province
   (B2017034, 20201041).
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NR 156
TC 40
Z9 46
U1 2
U2 22
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 AUG 30
PY 2021
VL 21
IS 1
AR 459
DI 10.1186/s12935-021-02168-4
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UL2HG
UT WOS:000692477700002
PM 34461912
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Al-Temaimi, RA
   Tan, TZ
   Marafie, MJ
   Thiery, JP
   Quirke, P
   Al-Mulla, F
AF Al-Temaimi, Rabeah A.
   Tan, Tuan Zea
   Marafie, Makia J.
   Thiery, Jean Paul
   Quirke, Philip
   Al-Mulla, Fahd
TI Identification of 42 Genes Linked to Stage II Colorectal Cancer
   Metastatic Relapse
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE colorectal cancer; microarray; stage II; copy number aberrations;
   disease free survival; gene expression; metastasis
ID EPITHELIAL-MESENCHYMAL TRANSITION; ALPHA(1)-ADRENERGIC RECEPTOR
   SUBTYPES; CALCINEURIN-BINDING PROTEIN-1; NUCLEAR FACTOR 6; CELL-CYCLE;
   ALPHA(1A)-ADRENERGIC RECEPTOR; HEPATOCELLULAR-CARCINOMA; HOMOLOGOUS
   RECOMBINATION; DIFFERENTIAL REGULATION; INVADOPODIA FORMATION
AB Colorectal cancer (CRC) is one of the leading causes of cancer mortality. Metastasis remains the primary cause of CRC death. Predicting the possibility of metastatic relapse in early-stage CRC is of paramount importance to target therapy for patients who really need it and spare those with low-potential of metastasis. Ninety-six stage II CRC cases were stratified using high-resolution array comparative genomic hybridization (aCGH) data based on a predictive survival algorithm and supervised clustering. All genes included within the resultant copy number aberrations were each interrogated independently at mRNA level using CRC expression datasets available from public repositories, which included 1820 colon cancers, and 167 normal colon tissues. Reduced mRNA expression driven by copy number losses and increased expression driven by copy number gains revealed 42 altered transcripts (29 reduced and 13 increased transcripts) associated with metastatic relapse, short disease-free or overall survival, and/or epithelial to mesenchymal transition (EMT). Resultant genes were classified based on gene ontology (GO), which identified four functional enrichment groups involved in growth regulation, genomic integrity, metabolism, and signal transduction pathways. The identified 42 genes may be useful for predicting metastatic relapse in stage II CRC. Further studies are necessary to validate these findings.
C1 [Al-Temaimi, Rabeah A.] Kuwait Univ, Dept Pathol, Human Genet Unit, Fac Med, Kuwait 13110, Kuwait.
   [Tan, Tuan Zea] Natl Univ Singapore, Canc Sci Inst Singapore, Singapore 117599, Singapore.
   [Marafie, Makia J.] Matern Hosp, Kuwait Med Genet Ctr, Kuwait 13001, Kuwait.
   [Thiery, Jean Paul] Natl Univ Singapore, Dept Biochem, Singapore 117599, Singapore.
   [Quirke, Philip] Univ Leeds, Leeds Inst Canc & Pathol, Pathol & Tumour Biol, Leeds LS9 7TF, W Yorkshire, England.
   [Al-Mulla, Fahd] Kuwait Univ, Dept Pathol, Mol Pathol Unit, Fac Med, Kuwait 13110, Kuwait.
C3 Kuwait University; National University of Singapore; National University
   of Singapore; University of Leeds; Kuwait University
RP Al-Mulla, F (corresponding author), Kuwait Univ, Dept Pathol, Mol Pathol Unit, Fac Med, Kuwait 13110, Kuwait.
EM rabeah@hsc.edu.kw; csittz@nus.edu.sg; mj_marafie@yahoo.com;
   bchtjp@nus.edu.sg; p.quirke@leeds.ac.uk; fahd@al-mulla.org
RI Quirke, Philip/AAI-1362-2019; Thiery, Jean/M-9387-2019; Tan,
   Tuan/I-9227-2019; Al-Mulla, Fahd/E-2068-2015; Thiery, Jean
   Paul/H-1550-2011
OI Al-Mulla, Fahd/0000-0001-5409-3829; Thiery, Jean
   Paul/0000-0003-0478-5020; Quirke, Philip/0000-0002-3597-5444; Altemaimi,
   Rabeah/0000-0002-5662-7684
FU Kuwait Foundation for the Advancement of Sciences (KFAS) [2011-1302-06]
FX This work was supported by a grant from the Kuwait Foundation for the
   Advancement of Sciences (KFAS No. 2011-1302-06) given to Fahd Al-Mulla.
   We are grateful for Diana Ann Thomas for her assistance with the aCGH
   work.
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NR 92
TC 12
Z9 13
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD MAY
PY 2016
VL 17
IS 5
AR 598
DI 10.3390/ijms17050598
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA DP9BJ
UT WOS:000378791400005
PM 27136531
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Chen, TT
   Li, H
AF Chen, Tingting
   Li, Hua
TI Fatty acid metabolism and prospects for targeted therapy of cancer
SO EUROPEAN JOURNAL OF LIPID SCIENCE AND TECHNOLOGY
LA English
DT Review
DE Cancer; Enzymes; Fatty acid; Metabolomics; Synthesis and degradation
ID STEAROYL-COA DESATURASE; ATP-CITRATE-LYASE; DE-NOVO LIPOGENESIS;
   BREAST-CANCER; PROSTATE-CANCER; CELL-PROLIFERATION; COLORECTAL-CANCER;
   OVARIAN-CANCER; MESENCHYMAL TRANSITION; CHEMICAL INHIBITION
AB Fatty acids are fundamental substrates required for energy storage, synthesis of membranes, generation of signaling molecules and lipid droplet formation in cancer cells. High levels of fatty acid metabolic activity are one of the most aberrant metabolic alterations in cancer cells. The de novo fatty acid synthesis pathway is the primary source of fatty acids in cancer cells, but cancer cells can also acquire fatty acids through the lipolytic pathway, which helps cells survive and maintain their invasiveness. Key enzymes, including ATP-citrate lyase (ACLY), fatty acid synthase (FASN), acetyl-coenzyme A (CoA) carboxylase (ACC), stearoyl-CoA desaturase 1(SCD1) and monoacylglycerol lipase (MAGL), which are involved in fatty acid synthesis and degradation, are overexpressed in cancer cells. The alterations in fatty acid metabolomics in different cancers, at different stages of cancer, and in different tissues are clinically significant. This review focuses on current research into fatty acid metabolism to explore new targets against the fatty acid metabolic pathways for anticancer therapy. Practical applications: High levels of fatty acid metabolic activity are one of the most aberrant metabolic alterations in cancer cells. Reprogramming in fatty acid metabolism plays an important role in energy storage, membrane proliferation, the generation of signaling molecules and lipid droplet formation in cancer cells. Understanding the mechanism of regulated the fatty acid metabolic pathways in cancer would reveal novel targeted therapy of cancer. To maintain the balance of the free fatty acid composition and thus promote cancer cell growth, survival, and progression, the levels of de novo fatty acid synthesis and degradation are elevated. Therefore, the targeted inhibition of key enzymes involved in fatty acid metabolism, such as ACLY, ACC, FASN, MAGL, and SCD1, and the utilization of anticancer exogenous fatty acids might constitute effective cancer therapies. ATP, adenosine-triphosphate; DAG, diacylglycerol; IHBTIS, inhibitors; MUFA, monounsaturated fatty acids; MAG, monoacylglycerol; TAG triacylglycerol.
C1 [Chen, Tingting; Li, Hua] Sichuan Univ, West China Coll Basic & Forens Med, Chengdu, Sichuan, Peoples R China.
C3 Sichuan University
RP Li, H (corresponding author), 17 Peoples South Rd, Chengdu 610041, Sichuan, Peoples R China.
EM lihua_scu@scu.edu.cn
FU Sichuan provincial Science and Technology Department [2016JY143]
FX This work was supported by Sichuan provincial Science and Technology
   Department (2016JY143).
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NR 112
TC 11
Z9 15
U1 3
U2 98
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1438-7697
EI 1438-9312
J9 EUR J LIPID SCI TECH
JI Eur. J. Lipid Sci. Technol.
PD OCT
PY 2017
VL 119
IS 10
AR 1600366
DI 10.1002/ejlt.201600366
PG 11
WC Food Science & Technology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology; Nutrition & Dietetics
GA FI6QY
UT WOS:000412122500003
DA 2025-01-04
ER

PT J
AU Pawar, S
   Sharma, A
AF Pawar, Satyajit
   Sharma, Atul
TI Molecular targets in GI malignancies - A pathologist's perspective
SO INDIAN JOURNAL OF PATHOLOGY AND MICROBIOLOGY
LA English
DT Review
DE Gastrointestinal cancer; molecular targets; monoclonal antibodies;
   targeted therapy; tyrosine kinase inhibitors
ID METASTATIC COLORECTAL-CANCER; ADVANCED GASTRIC-CANCER; BILIARY-TRACT
   CANCER; 1ST-LINE THERAPY; DOUBLE-BLIND; OPEN-LABEL; PHASE-III; SIGNALING
   PATHWAYS; PLUS IRINOTECAN; PLACEBO
AB Newer molecular diagnostics and improved understanding of cancer pathogenesis have identified multiple pathways that can be potentially targeted with the use of novel therapeutics in development. These developments have ushered cancer therapeutics in newer era of personalized medicine. Same is reflected on current management strategies for advanced gastrointestinal malignancies. Molecular profiling for BRAF and RAS is standard for colorectal cancer while Her2 and PDL1 status is needed for planning therapy of advanced gastroesophageal cancers. Tissue agnostic markers like MSI, TMB and NTRK are making headways in therapeutic armamentarium. While newer targeted therapies against FGFR, EGFR, PI3K-AKT, DDR pathways are showing promising results in initial studies. Here we review traditional as well as upcoming molecular markers in field of GI malignancies, methods of testing and evidence for rational use in clinical practice.
C1 [Pawar, Satyajit; Sharma, Atul] All India Inst Med Sci, Dr BRA Inst Rotary Canc Hosp, Dept Med Oncol, New Delhi 110029, India.
C3 All India Institute of Medical Sciences (AIIMS) New Delhi; DR. B.R.A.
   Institute Rotary Cancer Hospital
RP Sharma, A (corresponding author), All India Inst Med Sci, Dr BRA Inst Rotary Canc Hosp, Dept Med Oncol, New Delhi 110029, India.
EM atul1@hotmail.com
RI Sharma, Atul/ISS-2723-2023
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NR 86
TC 1
Z9 1
U1 0
U2 3
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S  NO 1498A-2
   VILLAGE MAROL, ANDHERI EAST, MUMBAI, Maharashtra, INDIA
SN 0377-4929
EI 0974-5130
J9 INDIAN J PATHOL MICR
JI Indian J. Pathol. Microbiol.
PD JUN
PY 2021
VL 64
IS 5
SI SI
BP 43
EP 51
DI 10.4103/IJPM.IJPM_1239_20
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA SU1ZC
UT WOS:000662939600007
PM 34135137
OA gold
DA 2025-01-04
ER

PT J
AU Wang, ZR
   Wang, JJ
   Pei, J
   Pan, YB
   Ding, R
AF Wang, Zhaorui
   Wang, Jingjing
   Pei, Jing
   Pan, Yubo
   Ding, Rui
TI Sign of Neck Mass as the Chief Complaint: A Case Report and Literature
   Review About Thyroid Metastasis of Colorectal Cancer
SO CANCER MANAGEMENT AND RESEARCH
LA English
DT Article
DE colorectum cancer metastases; secondary thyroid cancer; neck mass; case
   report; therapy; prognosis
ID RECTAL-CANCER; CELL VARIANT; GLAND; CARCINOMA; PROGNOSIS
AB Background: Commonly, the thyroid gland is regarded as an organ with fewer metastatic diseases, and colorectal metastasis to the thyroid (CMT) is rarely reported, especially, with that the clinical sign of thyroid metastasis nidus is the chief complaint. The CMT occurs in advanced colorectal cancer and is associated with poor prognosis and short survival. Case Report: In this case, we reported a patient with the sign of neck mass as the first manifestation of CMT. The patient underwent a partial thyroidectomy in June 2019, immunohistochemical findings of thyroid carcinoma suggested the possibility of adenocarcinoma of gastrointestinal tract. The patient underwent a colonoscopy in July 2019 and a colonic mass was found. Pathological examination diagnosed rectal adenocarcinoma. The patient underwent neoadjuvant chemotherapy, surgical treatment, postoperative adjuvant chemotherapy and targeted therapy. The patient died in June 2022. Conclusion: The metastasis disease would not be ignored at all, when a patient complains at signs of neck mass. Further, the possibility of metastasis cancer should be considered once thyroid nodules occur in patients with colorectal cancer. Even though the biological characteristics and stage of the primary tumor have an important impact on the prognosis, positive standardized treatments can also be helpful.
C1 [Wang, Zhaorui; Wang, Jingjing; Ding, Rui] Anhui Med Univ, Luan Peoples Hosp, Luan Hosp, Dept Emergency Surg, 21 Wanxi West Rd, Luan 237000, Anhui, Peoples R China.
   [Pei, Jing; Pan, Yubo] Anhui Med Univ, Affiliated Hosp 1, Dept Gen Surg, Hefei 230022, Anhui, Peoples R China.
C3 Anhui Medical University; Anhui Medical University
RP Ding, R (corresponding author), Anhui Med Univ, Luan Peoples Hosp, Luan Hosp, Dept Emergency Surg, 21 Wanxi West Rd, Luan 237000, Anhui, Peoples R China.
EM Dr20210908@163.com
RI Wang, Jingjing/AAE-8629-2019
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NR 31
TC 0
Z9 0
U1 1
U2 1
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1179-1322
J9 CANCER MANAG RES
JI Cancer Manag. Res.
PY 2024
VL 16
BP 575
EP 583
DI 10.2147/CMAR.S470045
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TH5O4
UT WOS:001240390700001
PM 38855326
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kit, OI
   Vodolazhsky, DI
AF Kit, O. I.
   Vodolazhsky, D. I.
TI Molecular biology of colorectal cancer in clinical practice
SO MOLECULAR BIOLOGY
LA English
DT Review
DE colorectal cancer (CRC); biomarker; targeted therapy; signaling pathway;
   microRNA; EGFR; KRAS; microsatellite instability; chromosomal
   instability; CIMP; TGF-beta; WNT
ID MICROSATELLITE INSTABILITY; DOWN-REGULATION; COLON-CANCER; DNA
   METHYLATION; POOR-PROGNOSIS; MUTATIONS; KRAS; EXPRESSION; GROWTH; BRAF
AB The review summarizes current data on the molecular genetic mechanisms underlying the pathogenesis of colorectal cancer (CRC) and addresses the connections between these mechanisms and biomarkers used for predictive diagnosis, risk stratification, prognosis, and predicting response to chemotherapy and tar-geted therapy. Evidence of microRNA involvement in the regulation of major signaling pathways affected by CRC pathogenesis is discussed, and signaling pathways that can be used as targets in the therapy of colorectal cancer are examined.
C1 [Kit, O. I.; Vodolazhsky, D. I.] Minist Healthcare Russian Federat, Rostov Res Inst Oncol, Rostov Na Donu 344037, Russia.
RP Kit, OI (corresponding author), Minist Healthcare Russian Federat, Rostov Res Inst Oncol, Rostov Na Donu 344037, Russia.
EM dvodolazhsky@gmail.com
RI Vodolazhsky, Dmitriy/AAF-7800-2020; Kit, Oleg/U-2241-2017
OI Vodolazhsky, Dmitry/0000-0003-1114-8732; Kit, Oleg/0000-0003-3061-6108
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NR 59
TC 0
Z9 0
U1 1
U2 7
PU MAIK NAUKA/INTERPERIODICA/SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA
SN 0026-8933
EI 1608-3245
J9 MOL BIOL+
JI Mol. Biol.
PD JUL
PY 2015
VL 49
IS 4
BP 471
EP 479
DI 10.1134/S0026893315040081
PG 9
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA CP3UT
UT WOS:000359808800001
DA 2025-01-04
ER

PT J
AU Liu, WW
   Zhang, ZY
   Wang, F
   Wang, H
AF Liu, Wei-Wei
   Zhang, Zhong-Yuan
   Wang, Fei
   Wang, Hao
TI Emerging roles of m6A RNA modification in cancer therapeutic resistance
SO EXPERIMENTAL HEMATOLOGY & ONCOLOGY
LA English
DT Review
DE Cancer therapy; m6A; Chemoresistance; Immunotherapy
ID CELL LUNG-CANCER; DEMETHYLASE FTO INHIBITORS; ACUTE MYELOID-LEUKEMIA;
   MESSENGER-RNA; M(6)A MODIFICATION; UP-REGULATION; BREAST-CANCER;
   GEFITINIB RESISTANCE; COLORECTAL-CANCER; COLON-CANCER
AB Marvelous advancements have been made in cancer therapies to improve clinical outcomes over the years. However, therapeutic resistance has always been a major difficulty in cancer therapy, with extremely complicated mechanisms remain elusive. N6-methyladenosine (m6A) RNA modification, a hotspot in epigenetics, has gained growing attention as a potential determinant of therapeutic resistance. As the most prevalent RNA modification, m6A is involved in every links of RNA metabolism, including RNA splicing, nuclear export, translation and stability. Three kinds of regulators, "writer" (methyltransferase), "eraser" (demethylase) and "reader" (m6A binding proteins), together orchestrate the dynamic and reversible process of m6A modification. Herein, we primarily reviewed the regulatory mechanisms of m6A in therapeutic resistance, including chemotherapy, targeted therapy, radiotherapy and immunotherapy. Then we discussed the clinical potential of m6A modification to overcome resistance and optimize cancer therapy. Additionally, we proposed existing problems in current research and prospects for future research.
C1 [Liu, Wei-Wei; Wang, Hao] Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Lab Med, Div Life Sci & Med, Hefei, Peoples R China.
   [Liu, Wei-Wei] Shandong Univ, Sch Basic Med Sci, Jinan, Peoples R China.
   [Zhang, Zhong-Yuan] Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Radiol, Div Life Sci & Med, Hefei, Peoples R China.
   [Wang, Fei] Univ Sci & Technol China, Affiliated Hosp USTC 1, Neurosurg Dept, Div Life Sci & Med, Hefei, Peoples R China.
   [Wang, Hao] Natl Clin Res Ctr Lab Med, Core Unit, Hefei, Peoples R China.
C3 Chinese Academy of Sciences; University of Science & Technology of
   China, CAS; Shandong University; Chinese Academy of Sciences; University
   of Science & Technology of China, CAS; Chinese Academy of Sciences;
   University of Science & Technology of China, CAS
RP Wang, H (corresponding author), Univ Sci & Technol China, Affiliated Hosp USTC 1, Dept Lab Med, Div Life Sci & Med, Hefei, Peoples R China.; Wang, F (corresponding author), Univ Sci & Technol China, Affiliated Hosp USTC 1, Neurosurg Dept, Div Life Sci & Med, Hefei, Peoples R China.; Wang, H (corresponding author), Natl Clin Res Ctr Lab Med, Core Unit, Hefei, Peoples R China.
EM neurosurgeonwf1@ustc.edu.cn; demo@ustc.edu.cn
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NR 187
TC 13
Z9 16
U1 9
U2 33
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2162-3619
J9 EXP HEMATOL ONCOL
JI Exp. Hematol. Oncol.
PD FEB 21
PY 2023
VL 12
IS 1
AR 21
DI 10.1186/s40164-023-00386-2
PG 22
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA 9E8ES
UT WOS:000937013200001
PM 36810281
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Tan, L
   Peng, D
   Cheng, Y
AF Tan, Li
   Peng, Dong
   Cheng, Yong
TI Significant position of <i>C-myc</i> in colorectal cancer: a promising
   therapeutic target
SO CLINICAL & TRANSLATIONAL ONCOLOGY
LA English
DT Review
DE Colorectal cancer; c-myc; Mechanism; Therapy
ID CELLULAR SENESCENCE; UP-REGULATION; DNA-BINDING; EXPRESSION; CELLS;
   GENE; PROGRESSION; DEGRADATION; INHIBITION; PROGNOSIS
AB Colorectal cancer (CRC) is a malignant tumor initiating from the mucosa of the colorectum. According to the 2020 statistics from the World Health Organization, there are 10.0% CRC cases among all 19.3 million new cancers, followed by lung and breast cancer, and 9.4% CRC cases among all 9.9 million cancer deaths, ranking second. The population of CRC patients in China is large, and its incidence and mortality continue to increase each year. Despite the continuous development of surgical methods, chemotherapy, radiotherapy, targeted therapy and immunotherapy, the overall survival of CRC patients remains low. Past research has suggested that c-myc plays a pivotal role in the development of CRC. A higher expression level of c-Myc is a negative prognostic marker in CRC. However, there are few drugs targeting c-myc directly. Therefore, we focused on discovering the mechanism of c-myc in CRC to provide a reference for a better therapy choice for patients.
C1 [Tan, Li; Peng, Dong; Cheng, Yong] Chongqing Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp 1, Chongqing 400016, Peoples R China.
C3 Chongqing Medical University
RP Peng, D; Cheng, Y (corresponding author), Chongqing Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp 1, Chongqing 400016, Peoples R China.
EM carry_dong@126.com; chengyongcq@163.com
RI wang, yi/KBB-3614-2024; Peng, Dong/GQB-3192-2022
OI Tan, Li/0000-0002-4397-090X
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NR 115
TC 12
Z9 12
U1 3
U2 20
PU SPRINGER INT PUBL AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1699-048X
EI 1699-3055
J9 CLIN TRANSL ONCOL
JI Clin. Transl. Oncol.
PD DEC
PY 2022
VL 24
IS 12
BP 2295
EP 2304
DI 10.1007/s12094-022-02910-y
EA AUG 2022
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 5Q5WI
UT WOS:000841108200001
PM 35972682
DA 2025-01-04
ER

PT J
AU Zhan, DD
   Zheng, NR
   Zhao, BB
   Cheng, F
   Tang, Q
   Liu, XQ
   Wang, JF
   Wang, YS
   Liu, HB
   Li, XL
   Su, JM
   Zhong, XJ
   Bu, Q
   Cheng, YT
   Wang, Y
   Qin, J
AF Zhan, Dongdong
   Zheng, Nairen
   Zhao, Beibei
   Cheng, Fang
   Tang, Qi
   Liu, Xiangqian
   Wang, Juanfei
   Wang, Yushen
   Liu, Haibo
   Li, Xinliang
   Su, Juming
   Zhong, Xuejun
   Bu, Qing
   Cheng, Yating
   Wang, Yi
   Qin, Jun
TI Expanding individualized therapeutic options via genoproteomics
SO CANCER LETTERS
LA English
DT Article
DE Targeted therapy; Head -to -head comparison; Actionable mutation;
   Protein overexpression; Clinical drug target
ID PROTEOGENOMIC CHARACTERIZATION; LUNG-CANCER; BREAST-CANCER; HUMAN COLON;
   KRAS(G12C); MUTATIONS; MET
AB Clinical next-generation sequencing (NGS) tests have enabled treatment recommendations for cancer patients with driver gene mutations. Targeted therapy options for patients without driver gene mutations are currently unavailable. Herein, we performed NGS and proteomics tests on 169 formalin-fixed paraffin-embedded (FFPE) samples of non-small cell lung cancers (NSCLC, 65), colorectal cancers (CRC, 61), thyroid carcinomas (THCA, 14), gastric cancers (GC, 2), gastrointestinal stromal tumors (GIST, 11), and malignant melanomas (MM, 6). Of the 169 samples, NGS detected 14 actionable mutated genes in 73 samples, providing treatment options for 43% of the patients. Proteomics identified 61 actionable clinical drug targets approved by the FDA or undergoing clinical trials in 122 samples, providing treatment options for 72% of the patients. In vivo experiments demon-strated that the Mitogen-Activated Protein Kinase (MEK) inhibitor could block lung tumor growth in mice with overexpression of Map2k1 protein. Therefore, protein overexpression is a potentially feasible indicator for guiding targeted therapies. Collectively, our analysis suggests that combining NGS and proteomics (genopro-teomics) could expand the targeted treatment options to 85% of cancer patients.
C1 [Zhan, Dongdong; Zhao, Beibei; Cheng, Fang; Tang, Qi; Liu, Xiangqian; Wang, Juanfei; Liu, Haibo; Li, Xinliang; Su, Juming; Zhong, Xuejun; Cheng, Yating; Wang, Yi; Qin, Jun] Guangzhou KingMed Ctr Clin Lab Co Ltd, KingMed Pineal Joint Innovat Lab Clin Prote, Guangzhou 510009, Peoples R China.
   [Zhan, Dongdong; Cheng, Fang; Liu, Haibo; Li, Xinliang] Beijing Pineal Diagnost Co Ltd, Beijing 102206, Peoples R China.
   [Zheng, Nairen; Wang, Yushen; Wang, Yi; Qin, Jun] Beijing Inst Life, Beijing Proteome Res Ctr, Natl Ctr Prot Sci Beijing, State Key Lab Prote, Beijing 102206, Peoples R China.
   [Zhao, Beibei; Tang, Qi; Liu, Xiangqian; Wang, Juanfei; Su, Juming; Zhong, Xuejun; Cheng, Yating] Guangzhou Med Univ, KingMed Coll Lab Med, Guangzhou 510005, Peoples R China.
   [Bu, Qing] Guangxi Med Univ, Affiliated Hosp 1, Dept Med Oncol, Nanning 530021, Peoples R China.
   [Qin, Jun] Fudan Univ, Inst Biomed Sci, Sch Life Sci, State Key Lab Genet Engn, Shanghai 200433, Peoples R China.
   [Qin, Jun] Fudan Univ, Inst Biomed Sci, Collaborat Innovat Ctr Genet & Dev, Sch Life Sci, Shanghai 200433, Peoples R China.
C3 Guangzhou Medical University; Guangxi Medical University; Fudan
   University; Fudan University
RP Cheng, YT; Wang, Y; Qin, J (corresponding author), Guangzhou KingMed Ctr Clin Lab Co Ltd, KingMed Pineal Joint Innovat Lab Clin Prote, Guangzhou 510009, Peoples R China.
EM labcyt@kingmed.com.cn; wangyi@ncpsb.org.cn; qinjun@ncpsb.org.cn
RI liu, xiao/HMD-7454-2023; Zheng, Nairen/ABD-1215-2020; Li,
   Zeyu/GXM-4336-2022
OI ALMatrafi, Tahani Ahmad/0009-0009-0822-2621; Liu,
   Haibo/0000-0002-4213-2883
FU National Key Research and Devel-opment Program of China [2018YFA0507503,
   2022YFC0867400, 2017YFA0505102, 2017YFA0505103, 2017YFA0505104];
   National Natural Science Foundation of China [81874237, 32088101,
   31970725]; State Key Laboratory of Proteomics [SKLP-K202002]
FX The study was approved by the National Key Research and Devel-opment
   Program of China (2018YFA0507503, 2022YFC0867400, 2017YFA0505102,
   2017YFA0505103, 2017YFA0505104) , National Natural Science Foundation of
   China (81874237, 32088101, 31970725) , and State Key Laboratory of
   Proteomics (SKLP-K202002).
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NR 66
TC 3
Z9 4
U1 3
U2 13
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 2023
VL 560
AR 216123
DI 10.1016/j.canlet.2023.216123
EA MAR 2023
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA C8PS5
UT WOS:000964479300001
PM 36907503
OA hybrid
DA 2025-01-04
ER

PT J
AU Arai, H
   Yang, Y
   Baca, Y
   Millstein, J
   Denda, T
   Ou, FS
   Innocenti, F
   Takeda, H
   Kubota, Y
   Doi, A
   Horie, Y
   Umemoto, K
   Izawa, N
   Wang, JY
   Battaglin, F
   Jayachandran, P
   Algaze, S
   Soni, S
   Zhang, W
   Goldberg, RM
   Hall, MJ
   Scott, AJ
   Hwang, JJ
   Lou, EM
   Weinberg, BA
   Marshall, J
   Goel, S
   Xiu, JN
   Korn, WM
   Venook, AP
   Sunakawa, Y
   Lenz, HJ
AF Arai, Hiroyuki
   Yang, Yan
   Baca, Yasmine
   Millstein, Joshua
   Denda, Tadamichi
   Ou, Fang-Shu
   Innocenti, Federico
   Takeda, Hiroyuki
   Kubota, Yohei
   Doi, Ayako
   Horie, Yoshiki
   Umemoto, Kumiko
   Izawa, Naoki
   Wang, Jingyuan
   Battaglin, Francesca
   Jayachandran, Priya
   Algaze, Sandra
   Soni, Shivani
   Zhang, Wu
   Goldberg, Richard M.
   Hall, Michael J.
   Scott, Aaron James
   Hwang, Jimmy J.
   Lou, Emil
   Weinberg, Benjamin A.
   Marshall, John
   Goel, Sanjay
   Xiu, Joanne
   Korn, W. Michael
   Venook, Alan P.
   Sunakawa, Yu
   Lenz, Heinz -Josef
TI Predictive value of<i> CDC37</i> gene expression for targeted therapy in
   metastatic colorectal cancer
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE CDC37; HSP90; Chaperone; Colorectal cancer; Targeted therapy
ID PROTEIN 90 HSP90; CDC37; BLOCKADE; STRATEGY; KIT
AB Background: CDC37 is a key determinant of client kinase recruitment to the HSP90 chaperoning system. We hypothesized that kinase-specific dependency on CDC37 alters the efficacy of targeted therapies for metastatic colorectal cancer (mCRC). Material and methods: Two independent mCRC cohorts were analyzed to compare the survival outcomes between CDC37-high and CDC37-low patients (stratified by the median cutoff values): the CALGB/SWOG 80405 trial (226 and 207 patients receiving first-line bevacizumab- and cetuximab-containing chemotherapies, respectively) and Japanese retrospective (50 refractory patients receiving regorafenib) cohorts. A dataset of specimens submitted to a commercial CLIA-certified laboratory was utilized to characterize molecular profiles of CDC37-high (top quartile, N = 5055) and CDC37-low (bottom quartile, N = 5055) CRCs. Results: In the bevacizumab-treated group, CDC37-high patients showed significantly better progression -free survival (PFS) (median 13.3 vs 9.6 months, hazard ratio [HR] 0.59, 95% confidence interval [CI] 0.44-0.79, p < 0.01) than CDC37-low patients. In the cetuximab-treated group, CDC37-high and CDC37-low patients had similar outcomes. In the regorafenib-treated group, CDC37-high patients showed significantly better overall survival (median 11.3 vs 6.0 months, HR 0.24, 95% CI 0.11-0.54, p < 0.01) and PFS (median 3.5 vs 1.9 months, HR 0.51, 95% CI 0.28-0.94, p = 0.03). Comprehensive molecular profiling revealed that CDC37-high CRCs were associated with higher VEGFA, FLT1, and KDR expressions and activated hypoxia signature. Conclusions: CDC37-high mCRC patients derived more benefit from anti-VEGF therapies, including bevacizumab and regorafenib, but not from cetuximab. Molecular profiles suggested that such tumors were dependent on angiogenesis-relating pathways.
C1 [Arai, Hiroyuki; Wang, Jingyuan; Battaglin, Francesca; Jayachandran, Priya; Algaze, Sandra; Soni, Shivani; Zhang, Wu; Lenz, Heinz -Josef] Univ Southern Calif, Norris Comprehens Canc Ctr, Keck Sch Med, Div Med Oncol, Los Angeles, CA USA.
   [Arai, Hiroyuki; Horie, Yoshiki; Umemoto, Kumiko; Izawa, Naoki; Sunakawa, Yu] St Marianna Univ, Sch Med, Dept Clin Oncol, Kawasaki, Japan.
   [Yang, Yan; Millstein, Joshua] Univ Southern Calif, Norris Comprehens Canc Ctr, Keck Sch Med, Dept Populat & Publ Hlth Sci, Los Angeles, CA USA.
   [Baca, Yasmine; Xiu, Joanne; Korn, W. Michael] Clin & Translat Res, Med Affairs, Caris Life Sci, Phoenix, AZ USA.
   [Denda, Tadamichi] Chiba Canc Ctr, Dept Gastroenterol, Chiba, Japan.
   [Ou, Fang-Shu] Alliance Stat & Data Management Ctr, Mayo Clin, Rochester, MN USA.
   [Innocenti, Federico] Univ N Carolina, UNC Eshelman Sch Pharm, Chapel Hill, NC USA.
   [Goldberg, Richard M.] West Virginia Univ, Canc Inst, Morgantown, WV USA.
   [Hall, Michael J.] Fox Chase Canc Ctr, Dept Clin Genet, Philadelphia, PA USA.
   [Scott, Aaron James] Univ Arizona, Canc Ctr, Dept Med, Tucson, AZ USA.
   [Hwang, Jimmy J.] Levine Canc Inst, Dept Solid Tumor Oncol, GI Med Oncol, Charlotte, NC USA.
   [Lou, Emil] Univ Minnesota, Div Hematol Oncol & Transplantat, Minneapolis, MN USA.
   [Weinberg, Benjamin A.; Marshall, John] Georgetown Univ, Ruesch Ctr Cure Gastrointestinal Canc, Lombardi Comprehens Canc Ctr, Washington, DC USA.
   [Goel, Sanjay] Rutgers Canc Inst New Jersey, New Brunswick, NJ USA.
   [Venook, Alan P.] Univ Calif San Francisco, San Francisco, CA USA.
   [Lenz, Heinz -Josef] Univ Southern Calif, Norris Comprehens Canc Ctr, Keck Sch Med, Div Med Oncol, 1441 Ave, Los Angeles, CA 90033 USA.
C3 University of Southern California; Saint Marianna University; University
   of Southern California; Chiba Cancer Center; Mayo Clinic; University of
   North Carolina; University of North Carolina Chapel Hill; West Virginia
   University; Fox Chase Cancer Center; University of Arizona; University
   of Minnesota System; University of Minnesota Twin Cities; Georgetown
   University; Rutgers University System; Rutgers University New Brunswick;
   Rutgers University Biomedical & Health Sciences; Rutgers Cancer
   Institute of New Jersey; University of California System; University of
   California San Francisco; University of Southern California
RP Lenz, HJ (corresponding author), Univ Southern Calif, Norris Comprehens Canc Ctr, Keck Sch Med, Div Med Oncol, 1441 Ave, Los Angeles, CA 90033 USA.
EM lenz@usc.edu
RI Sunakawa, Yu/AGW-7031-2022; Kubota, Yohei/LEL-9788-2024; Marshall,
   J/LBH-2002-2024; Millstein, Joshua/AFU-6153-2022; Battaglin,
   Francesca/C-2746-2017
OI Battaglin, Francesca/0000-0002-9869-0163; Ou,
   Fang-Shu/0000-0003-1267-8735; Yang, Yan/0000-0002-7883-0798; Arai,
   Hiroyuki/0000-0002-1886-7070
FU National Cancer Institute of the National Institutes of Health
   [U10CA180821, U10CA180882, UG1CA233373, UG1CA239758, P30CA 014089,
   U10CA180888, UG1CA180830]; Gloria Borges WunderGlo Foundation; Daniel
   Butler Research Fund; Bristol-Myers Squibb; Genentech; Pfizer; Dhont
   Family Foundation; Victoria and Philip Wilson Research Fund; San Pedro
   Peninsula Cancer Guild
FX Research reported in this publication was supported by the National
   Cancer Institute of the National Institutes of Health under Award
   Numbers U10CA180821 and U10CA180882 (to the Alliance for Clinical Trials
   in Oncology) , UG1CA233373, UG1CA239758, P30CA 014089 [to H.-J.L.] ,
   U10CA180888 and UG1CA180830 (SWOG) , Gloria Borges WunderGlo Foundation,
   Dhont Family Foundation, Victoria and Philip Wilson Research Fund, San
   Pedro Peninsula Cancer Guild, and Daniel Butler Research Fund. Also
   supported in part by funds from Bristol-Myers Squibb, Genentech, and
   Pfizer. https://acknowledgments.alli-ancefound.org. The content is
   solely the responsibility of the authors and does not necessarily
   represent the official views of the National Institutes of Health.
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NR 26
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER SCI LTD
PI London
PA 125 London Wall, London, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD APR
PY 2024
VL 201
AR 113914
DI 10.1016/j.ejca.2024.113914
EA FEB 2024
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LP8Y9
UT WOS:001188109900001
PM 38359495
DA 2025-01-04
ER

PT J
AU Basilico, C
   Modica, C
   Maione, F
   Vigna, E
   Comoglio, PM
AF Basilico, Cristina
   Modica, Chiara
   Maione, Federica
   Vigna, Elisa
   Comoglio, Paolo M.
TI Targeting the <i>MET</i> oncogene by concomitant inhibition of receptor
   and ligand via an antibody-"decoy" strategy
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE MET oncogene; antibodies; decoy; MET target therapy; anti-HGF therapy
ID HEPATOCYTE GROWTH-FACTOR; SUPPRESSES TUMOR-GROWTH; CANCER STEM-CELLS;
   C-MET; INVASIVE GROWTH; SCATTER-FACTOR; LUNG-CANCER; FACTOR/SCATTER
   FACTOR; COLORECTAL-CANCER; EGFR INHIBITORS
AB MET, a master gene sustaining "invasive growth," is a relevant target for cancer precision therapy. In the vast majority of tumors, wild-type MET behaves as a "stress-response" gene and relies on the ligand (HGF) to sustain cell "scattering," invasive growth and apoptosis protection (oncogene "expedience"). In this context, concomitant targeting of MET and HGF could be crucial to reach effective inhibition. To test this hypothesis, we combined an anti-MET antibody (MvDN30) inducing "shedding" (i.e., removal of MET from the cell surface), with a "decoy" (i.e., the soluble extracellular domain of the MET receptor) endowed with HGF-sequestering ability. To avoid antibody/decoy interaction-and subsequent neutralization-we identified a single aminoacid in the extracellular domain of MET-lysine 842-that is critical for MvDN30 binding and engineered the corresponding recombinant decoyMET (K842E). DecoyMET(K842E) retains the ability to bind HGF with high affinity and inhibits HGF-induced MET phosphorylation. In HGF-dependent cellular models, MvDN30 antibody and decoyMET(K842E) used in combination cooperate in restraining invasive growth, and synergize in blocking cancer cell "scattering." The antibody and the decoy unbridle apoptosis of colon cancer stem cells grown in vitro as spheroids. In a preclinical model, built by orthotopic transplantation of a human pancreatic carcinoma in SCID mice engineered to express human HGF, concomitant treatment with antibody and decoy significantly reduces metastatic spread. The data reported indicate that vertical targeting of the MET/HGF axis results in powerful inhibition of ligand-dependent MET activation, providing proof of concept in favor of combined target therapy of MET "expedience."
C1 [Basilico, Cristina; Modica, Chiara; Maione, Federica; Vigna, Elisa; Comoglio, Paolo M.] FPO IRCCS, Candiolo Canc Inst, Turin, Italy.
   [Modica, Chiara; Vigna, Elisa] Univ Turin, Dept Oncol, Turin, Italy.
C3 IRCCS Fondazione del Piemonte per l'Oncologia; University of Turin
RP Basilico, C (corresponding author), FPO IRCCS, Candiolo Canc Inst, Lab Mol Therapeut & Exploratory Res, Str Prov 142, I-10060 Turin, Italy.
EM cristina.basilico@ircc.it
RI Comoglio, Paolo/G-6323-2011; Vigna, Elisa/JWO-5055-2024; Maione,
   Federica/K-6679-2016
OI modica, chiara/0000-0002-7000-5216; Maione,
   Federica/0000-0003-2789-799X; Vigna, Elisa/0000-0001-9787-5732;
   Comoglio, Paolo/0000-0002-7056-5328
FU AIRC IG [15572]; FPRC 5xMille Ministero della Salute 2013; FPRC 5xMille
   Ministero della Salute 2014; AIRC Special Program 5xMille 2010 MCO
   [9970]
FX AIRC IG; Grant number: 15572; Grant sponsor: FPRC 5xMille Ministero
   della Salute 2013, FPRC 5xMille Ministero della Salute 2014; Grant
   sponsor: AIRC Special Program 5xMille 2010 MCO; Grant number: 9970
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NR 52
TC 9
Z9 12
U1 0
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD OCT 1
PY 2018
VL 143
IS 7
BP 1774
EP 1785
DI 10.1002/ijc.31550
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GS2PB
UT WOS:000443392100023
PM 29693242
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Ma, XJ
   Zhuang, BX
   Li, WT
AF Ma, Xiaojun
   Zhuang, Baoxiang
   Li, Wentao
TI MicroRNA-296-5p downregulated AKT2 to inhibit hepatocellular carcinoma
   cell proliferation, migration and invasion
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article
DE miroRNA-296-5p; hepatocellular carcinoma; AKT2; target therapy
ID COLORECTAL-CANCER; TUMOR INVASION; TARGETING AKT2; METASTASIS;
   EXPRESSION; SIGNATURES; MIR-296; GROWTH; RISK
AB Hepatocellular carcinoma (HCC) is the fifth most common malignancy in men, and the seventh in women worldwide. Despite development in the therapy of HCC, the prognosis of HCC patients remains poor. Therefore, it is of great significance to explore the molecular mechanism underlying HCC progression, and investigate novel therapeutic strategies for the treatments of HCC. MicroRNAs (miRs) are known to be involved in the pathogenesis of HCC. The present study aimed to investigate the expression patterns and potential roles of miR-296-5p in HCC. Results revealed that miR-296-5p was frequently downregulated in HCC tissue samples and cell lines. Additionally, reduced miR-296-5p expression levels were correlated with tumor size, TNM stage and metastasis in HCC. Gain-of-function demonstrated that miR-296-5p inhibited HCC cell proliferation, migration and invasion in vitro. Furthermore, AKT2 was identified as a novel direct and functional target of miR-296-5p in HCC. These findings indicated that miR-296-5p/AKT2 axis serves important roles in HCC carcinogenesis and progression, and miR-296-5p/AKT2 based target therapy hampers HCC tumor growth and metastasis.
C1 [Ma, Xiaojun; Zhuang, Baoxiang; Li, Wentao] Weifang Med Univ, Clin Med Coll, Morphol Lab, 7166 Baotong,West Rd, Weifang 261053, Shandong, Peoples R China.
C3 Shandong Second Medical University
RP Zhuang, BX (corresponding author), Weifang Med Univ, Clin Med Coll, Morphol Lab, 7166 Baotong,West Rd, Weifang 261053, Shandong, Peoples R China.
EM zhuang_baoxiang@163.com
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NR 34
TC 14
Z9 14
U1 0
U2 3
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
EI 1791-3004
J9 MOL MED REP
JI Mol. Med. Rep.
PD AUG
PY 2017
VL 16
IS 2
BP 1565
EP 1572
DI 10.3892/mmr.2017.6701
PG 8
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA EZ9VX
UT WOS:000405079300078
PM 28586057
OA Bronze
DA 2025-01-04
ER

PT J
AU Shahiwala, A
   Qawoogha, SS
   Tambuwala, MM
AF Shahiwala, Aliasgar
   Qawoogha, Samar Salam
   Tambuwala, Murtaza M.
TI Oral adjuvant therapy for colorectal cancer: recent developments and
   future targets
SO THERAPEUTIC DELIVERY
LA English
DT Review
DE colorectal cancer; immunotherapy; monoclonal antibodies; nanotechnology;
   oral chemotherapy; targeted therapy; theranostic systems
ID EVERY 3 WEEKS; INTRAVENOUS FLUOROURACIL; ANTICANCER DRUGS; PHASE-I;
   DELIVERY; OXALIPLATIN; IRINOTECAN; RESISTANCE; APATINIB; COLON
AB Colorectal cancer is considered the third most frequent malignant neoplasm occurring in both men and women worldwide. Most approaches that have been used to fight and treat this type of malignancy are either invasive or nonselective. Noninvasive therapy using oral route can increase patient compliance and reduce treatment costs. Innovative measures such as use of nanotechnology and theranostic systems have been initiated in the oral therapy, which has been proven to be greatly advantageous in decreasing side effects, improving detection and diagnoses. This manuscript investigates recent innovative and novel therapeutic approaches through oral route and potential targets in the treatment of colorectal cancer.
C1 [Shahiwala, Aliasgar; Qawoogha, Samar Salam] Dubai Pharm Coll Girls, Dubai, U Arab Emirates.
   [Tambuwala, Murtaza M.] Ulster Univ, Sch Pharm & Pharmaceut Sci, Coleraine BT52 1SA, Londonderry, North Ireland.
C3 Ulster University
RP Shahiwala, A (corresponding author), Dubai Pharm Coll Girls, Dubai, U Arab Emirates.
EM alishahiwala@gmail.com
RI Shahiwala, Aliasgar/AAY-7413-2020; Tambuwala, Murtaza/HNP-0828-2023;
   Qawoogha, Samar/AAV-8786-2020
OI Tambuwala, Murtaza/0000-0001-8499-9891; Qawoogha,
   Samar/0000-0003-0171-1093; Shahiwala, Aliasgar/0000-0001-6524-7424
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NR 66
TC 4
Z9 5
U1 2
U2 24
PU Newlands Press Ltd
PI London
PA 2 Albert Pl, London, UNITED KINGDOM
SN 2041-5990
EI 2041-6008
J9 THER DELIV
JI Ther. Deliv.
PD OCT
PY 2019
VL 10
IS 10
BP 659
EP 669
DI 10.4155/tde-2019-0067
PG 11
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA KA0KF
UT WOS:000505489300004
PM 31702443
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Yu, XZ
   Zhu, LL
   Liu, JW
   Xie, M
   Chen, J
   Li, JG
AF Yu, Xianzhe
   Zhu, Lingling
   Liu, Jiewei
   Xie, Ming
   Chen, Jiang
   Li, Jianguo
TI Emerging Role of Immunotherapy for Colorectal Cancer with Liver
   Metastasis
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE immunotherapy; colorectal cancer; liver metastasis; tumor immune
   microenvironment; immune checkpoint inhibitors; deficient DNA mismatch
   repair
ID PD-L1 BLOCKADE; KUPFFER CELLS; TUMOR-GROWTH; THERAPY; MICROENVIRONMENT;
   FUTURE; CTLA-4; ANGIOGENESIS; INSTABILITY; EXPRESSION
AB Colorectal cancer (CRC) is the third most common malignant tumor in the world and the second leading cause of cancer-related deaths, with the liver as the most common site of distant metastasis. The prognosis of CRC with liver metastasis is poor, and most patients cannot undergo surgery. In addition, conventional antitumor approaches such as chemotherapy, radiotherapy, targeted therapy, and surgery result in unsatisfactory outcomes. In recent years, immunotherapy has shown good prospects in the treatment of assorted tumors by enhancing the host's antitumor immune function, and it may become a new effective treatment for liver metastasis of CRC. However, challenges remain in applying immunotherapy to CRC with liver metastasis. This review examines how the microenvironment and immunosuppressive landscape of the liver favor tumor progression. It also highlights the latest research advances in immunotherapy for colorectal liver metastasis and identifies immunotherapy as a treatment regimen with a promising future in clinical applications.
C1 [Yu, Xianzhe; Xie, Ming; Li, Jianguo] Zunyi Med Univ, Affiliated Hosp, Gastrointestinal Dept, Zunyi, Guizhou, Peoples R China.
   [Zhu, Lingling; Liu, Jiewei] Sichuan Univ, West China Hosp, Lung Canc Ctr, Chengdu, Sichuan, Peoples R China.
   [Chen, Jiang] Zhejiang Univ, Sir Run Run Shaw Hosp, Dept Gen Surg, Hangzhou 310016, Zhejiang, Peoples R China.
C3 Zunyi Medical University; Sichuan University; Zhejiang University
RP Chen, J (corresponding author), Zhejiang Univ, Sir Run Run Shaw Hosp, Dept Gen Surg, Hangzhou 310016, Zhejiang, Peoples R China.; Li, JG (corresponding author), Zunyi Med Univ, Gastrointestinal Dept, Affiliated Hosp, Huichuan Area, Dalian Rd 149, Zunyi 563000, Guizhou, Peoples R China.
EM chenjiang520@zju.edu.cn; lijianguo826@163.com
RI Zhu, Lingling/AAF-4788-2021; 刘, 洁薇/HGB-8626-2022; Chen,
   Jiang/AAO-6940-2021
FU National Natural Science Foundation of China [31301141]; Science and
   Technology Planning Fund of Guizhou Province (Guizhou Science and
   Technology Cooperation LH [2014]) [7594]
FX This work was funded by the National Natural Science Foundation of China
   (grant number 31301141) and the Science and Technology Planning Fund of
   Guizhou Province (Guizhou Science and Technology Cooperation LH [2014]
   No. 7594).
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NR 156
TC 26
Z9 29
U1 3
U2 24
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 11645
EP 11658
DI 10.2147/OTT.S271955
PG 14
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA OQ4FK
UT WOS:000588740800001
PM 33223838
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Testa, U
   Pelosi, E
   Castelli, G
AF Testa, Ugo
   Pelosi, Elvira
   Castelli, Gerrnana
TI Cancer stem cell targeted therapies
SO ANNALI DELL ISTITUTO SUPERIORE DI SANITA
LA English
DT Article
DE cancer; cancer stein cells; targeted therapy; stein cells; leukemia;
   solid tumors
ID ACUTE MYELOID-LEUKEMIA; ACUTE MYELOGENOUS LEUKEMIA; CLONAL
   HEMATOPOIESIS; INITIATING CELLS; COLORECTAL-CANCER; PROSPECTIVE
   IDENTIFICATION; MOLECULAR CLASSIFICATION; PRELEUKEMIC MUTATIONS; SOMATIC
   MUTATIONS; MELANOMA-CELLS
AB In normal dividing tissues, cell homeostasis is maintained by rare cellular elements, the stem cells, that have the unique property of self-renewal and differentiation to generate a population of functionally mature tissue elements. Recent studies carried out in the last three decades support the existence of stem cells also in tumors, the so-called cancer stem cells. Cancer stem cells have the property of initiating and maintaining tumor growth, are able to self-renew and to differentiate, are the main drivers of intra- and inter-tumoral heterogeneity and the main cellular mediators of drug resistance, leading to tumor recurrence and metastasis. Cancer stem cells can be identified in many tumors according to specific immunophenotypic features, but cancer sternness cannot be defined as a fixed property, due to cancer plasticity.
   For these properties, cancer stem cells represent attractive targets for developing new anti-cancer therapies and there is supporting evidence that the combination of conventional anticancer therapies with drugs targeting cancer stem cells could lead to cancer eradication. Ongoing studies in some tumors strongly support the clinical utility of developing efficient strategies of cancer stem cell targeting.
C1 [Testa, Ugo; Pelosi, Elvira; Castelli, Gerrnana] Ist Super Sanita, Dipartimento Oncol, Viale Regina Elena 299, I-00161 Rome, Italy.
C3 Istituto Superiore di Sanita (ISS)
RP Testa, U (corresponding author), Ist Super Sanita, Dipartimento Oncol, Viale Regina Elena 299, I-00161 Rome, Italy.
EM ugo.testa@iss.it
RI Testa, Ugo/J-6472-2016; pelosi, elvira/J-7298-2016; castelli,
   germana/J-7244-2016
OI castelli, germana/0000-0002-3593-1230
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NR 140
TC 1
Z9 1
U1 2
U2 24
PU PENSIERO SCIENTIFICO
PI ROME
PA VIA SAN GIOVANNI VALDARNO 8, ROME, 00198, ITALY
SN 0021-2571
J9 ANN I SUPER SANITA
JI Ann. Ist. Super. Sanita
PY 2020
VL 56
IS 3
BP 336
EP 350
DI 10.4415/ANN_20_03_12
PG 15
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Public, Environmental & Occupational Health
GA NO5GG
UT WOS:000569516100011
PM 32959800
DA 2025-01-04
ER

PT J
AU Zhu, F
   Li, LS
   Chen, YY
   Pan, YF
   Zhang, WJ
   Li, LH
   Cai, LL
   Zhao, XX
   Zhao, H
   Wang, SW
   Jia, LJ
AF Zhu, Feng
   Li, Liangshan
   Chen, Yuanyuan
   Pan, Yongfu
   Zhang, Wenjuan
   Li, Lihui
   Cai, Lili
   Zhao, Xiaoxue
   Zhao, Hu
   Wang, Shiwen
   Jia, Lijun
TI CRL3<SUP>Keap1</SUP> E3 ligase facilitates ubiquitin-mediated
   degradation of oncogenic SRX to suppress colorectal cancer progression
SO NATURE COMMUNICATIONS
LA English
DT Article
ID SULFIREDOXIN; KEAP1; PEROXIREDOXIN; STATISTICS; MECHANISM; PROTEIN;
   SENSOR; COLON; NRF2; AXIS
AB The antioxidant protein sulfiredoxin-1 (SRX) is an oncogenic factor that promotes tumor progression, but the regulatory mechanism underlying SRX degradation remains to be understood. Herein, we report that Keap1, the substrate-specific adapter of CRL3 complex, specifically binds and promotes the ubiquitin-mediated degradation of SRX at residue K61. Keap1 knockdown accumulates SRX, which in turn facilitates colorectal cancer (CRC) metastasis by activating the activator protein-1/matrix metalloproteinase 9 (AP-1/MMP9) pathway. CRC-associated Keap1 mutants within the BACK domain lose the capability to ubiquitinate SRX and instead promote CRC metastasis. Moreover, inactivation of Keap1 facilitates CRC tumorigenesis and metastasis in mouse models of tumor xenograft due to SRX accumulation. Clinical sample analysis reveals that Keap1 is downregulated while SRX is overexpressed in CRC, which correlates with poor prognosis. Our findings elucidate a mechanism by which CRL3Keap1 ubiquitin ligase degrades SRX to suppress CRC progression, indicating that the Keap1-SRX axis will guide the targeted therapy towards CRC.
C1 [Zhu, Feng; Li, Liangshan; Zhao, Hu; Wang, Shiwen] Fudan Univ, Huadong Hosp, Dept Lab Med, Shanghai 200040, Peoples R China.
   [Zhu, Feng; Li, Liangshan; Wang, Shiwen; Jia, Lijun] Nanjing Univ Chinese Med, Sch Integrat Med, Nanjing 210023, Peoples R China.
   [Chen, Yuanyuan; Pan, Yongfu; Li, Lihui; Cai, Lili; Zhao, Xiaoxue] Shanghai Univ Tradit Chinese Med, Longhua Hosp, Canc Inst, Shanghai 200032, Peoples R China.
   [Zhang, Wenjuan] Fudan Univ, Shanghai Canc Ctr, Dept Breast Surg, Key Lab Breast Canc Shanghai, Shanghai 200032, Peoples R China.
C3 Fudan University; Nanjing University of Chinese Medicine; Shanghai
   University of Traditional Chinese Medicine; Fudan University
RP Wang, SW (corresponding author), Fudan Univ, Huadong Hosp, Dept Lab Med, Shanghai 200040, Peoples R China.; Wang, SW; Jia, LJ (corresponding author), Nanjing Univ Chinese Med, Sch Integrat Med, Nanjing 210023, Peoples R China.
EM wangshiwen1986@aliyun.com; jialijun2002@aliyun.com
RI Cai, Lili/AAI-1606-2020; wang, shiwen/HLQ-6303-2023
FU National Natural Science Foundation of China (National Science
   Foundation of China) [2022YFC3500200, 2022YFC3500202, 2023YFC3606600];
   National Key R&D Program of China [82372984, 82272987, 82172933];
   National Natural Science Foundation of China [2021KJ03-12]; Shanghai
   Frontiers Science Center of Disease and Syndrome Biology of Inflammatory
   Cancer Transformation [21MC1930500]; Shanghai Clinical Research Center
   of Traditional Chinese Medicine Oncology, Science and Technology
   Commission of Shanghai Municipality [23QA1403000]; Science and
   Technology Commission of Shanghai Municipality Rising-Star Program
   [20244Z0018]; Shanghai Municipal Health Commission Excellent Program
FX This work was supported by the National Key R&D Program of China
   (2022YFC3500200 to L.J., 2022YFC3500202 to L.J. and 2023YFC3606600 to
   S.W.), National Natural Science Foundation of China (82372984 to L.J.,
   82272987 to S.W. and 82172933 to S.W.), Shanghai Frontiers Science
   Center of Disease and Syndrome Biology of Inflammatory Cancer
   Transformation (2021KJ03-12 to L.J.), Shanghai Clinical Research Center
   of Traditional Chinese Medicine Oncology, Science and Technology
   Commission of Shanghai Municipality (21MC1930500 to L.J.), Science and
   Technology Commission of Shanghai Municipality Rising-Star Program
   (23QA1403000 to S.W.), and Shanghai Municipal Health Commission
   Excellent Program (20244Z0018 to S.W.). We thank Ping Wang and Lan Fang
   from Tongji University Cancer Center for providing us with the His-ub
   and HA-ub plasmids.
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U2 1
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
EI 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC 3
PY 2024
VL 15
IS 1
AR 10536
DI 10.1038/s41467-024-54919-2
PG 15
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA O2V8O
UT WOS:001369778000039
PM 39627198
OA gold
DA 2025-01-04
ER

PT J
AU Cervello, M
   Augello, G
   Cocco, L
   Ratti, S
   Follo, MY
   Martelli, AM
   Cusimano, A
   Montalto, G
   McCubrey, JA
AF Cervello, Melchiorre
   Augello, Giuseppa
   Cocco, Lucio
   Ratti, Stefano
   Follo, Matilde Y.
   Martelli, Alberto M.
   Cusimano, Antonella
   Montalto, Giuseppe
   McCubrey, James A.
TI The potential of the nutraceutical berberine in the treatment of
   hepatocellular carcinoma and other liver diseases such as NAFLD and NASH
SO ADVANCES IN BIOLOGICAL REGULATION
LA English
DT Article
DE Berberine; Nutraceuticals; Hepatocellular cancer; Natural products;
   NAFLD; NASH
ID UP-REGULATION; CELL-DEATH; NONALCOHOLIC STEATOHEPATITIS; MITOCHONDRIAL
   DYSFUNCTION; MEDIATED APOPTOSIS; RHIZOMA-COPTIDIS; DOWN-REGULATION;
   HEPATOMA-CELLS; CANCER CELLS; HEPG2 CELLS
AB Hepatocellular carcinoma (HCC) is a common cancer which unfortunately has poor outcomes. Common anti-cancer treatments such as chemotherapy and targeted therapy have not increased patient survival significantly. A common treatment for HCC patients is transplantation, however, it has limitations and complications. Novel approaches are necessary to more effectively treat HCC patients. Berberine (BBR) is a nutraceutical derived from various fruits and trees, which has been used for centuries in traditional medicine to treat various diseases such as diabetes and inflammation. More recently, the anti-proliferation effects of BBR have been investigated in the treatment of patients with various cancers, especially colorectal cancer, and in non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). In this review, we will focus on studies with BBR in liver diseases.
C1 [Cervello, Melchiorre; Augello, Giuseppa; Cusimano, Antonella; Montalto, Giuseppe] Natl Res Council CNR, Inst Biomed Res & Innovat, Palermo, Italy.
   [Cocco, Lucio; Ratti, Stefano; Follo, Matilde Y.; Martelli, Alberto M.] Univ Bologna, Dipartimento Sci Biomed & Neuromotorie, Bologna, Italy.
   [Montalto, Giuseppe] Univ Palermo, Sch Med, Internal Med & Med Specialties, PROMISE,Dept Hlth Promot Sci Maternal & Infant Car, Palermo, Italy.
   [McCubrey, James A.] East Carolina Univ, Brody Sch Med, Dept Microbiol & Immunol, Greenville, NC 27858 USA.
C3 Consiglio Nazionale delle Ricerche (CNR); Istituto Ricerca l'Innovazione
   Biomedica (IRIB-CNR); University of Bologna; University of Palermo;
   University of North Carolina; East Carolina University
RP Cervello, M (corresponding author), Natl Res Council CNR, Inst Biomed Res & Innovat, Palermo, Italy.; McCubrey, JA (corresponding author), East Carolina Univ, Brody Sch Med, Dept Microbiol & Immunol, Greenville, NC 27858 USA.
EM mccubreyj@ecu.edu
RI ratti, stefano/AAC-8714-2022; Cocco, Lucio/AAI-2206-2020
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NR 134
TC 4
Z9 4
U1 3
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2212-4926
EI 2212-4934
J9 ADV BIOL REGUL
JI Adv. Biol. Regul.
PD MAY
PY 2024
VL 92
AR 101032
DI 10.1016/j.jbior.2024.101032
EA MAY 2024
PG 19
WC Biochemistry & Molecular Biology
WE Emerging Sources Citation Index (ESCI)
SC Biochemistry & Molecular Biology
GA UE6Y9
UT WOS:001246436600001
PM 38693042
DA 2025-01-04
ER

PT J
AU Das, PK
   Saha, J
   Pillai, S
   Lam, AKY
   Gopalan, V
   Islam, F
AF Das, Plabon Kumar
   Saha, Joti
   Pillai, Suja
   Lam, Alfred K-Y
   Gopalan, Vinod
   Islam, Farhadul
TI Implications of estrogen and its receptors in colorectal carcinoma
SO CANCER MEDICINE
LA English
DT Review
DE chemotherapy; targeted therapy; colorectal carcinoma; estrogen; estrogen
   receptors
ID COLON-CANCER CELL; FATTY-ACID SYNTHASE; NEGATIVE BREAST-CANCER;
   NF-KAPPA-B; ER-BETA; TGF-BETA; EXPRESSION; PROLIFERATION; ALPHA;
   ACTIVATION
AB Estrogens have been implicated in the pathogenesis of various cancer types, including colorectal carcinoma (CRC). Estrogen receptors such as ER alpha and ER beta activate intracellular signaling cascades followed by binding to estrogen, resulting in important changes in cellular behaviors. The nuclear estrogen receptors, i.e. ER beta and ER alpha are responsible for the genomic actions of estrogens, whereas the other receptor, such as G protein-coupled estrogen receptor (GPER) regulates rapid non-genomic actions, which lead to secondary gene expression changes in cells. ER beta, the predominant estrogen receptor expressed in both normal and non-malignant colonic epithelium, has protective roles in colon carcinogenesis. ER beta may exert the anti-tumor effect through selective activation of pro-apoptotic signaling, increasing DNA repair, inhibiting expression of oncogenes, regulating cell cycle progression, and also by changing the micro-RNA pool and DNA-methylation. Thus, a better understanding of the underlying mechanisms of estrogen and its receptors in CRC pathogenesis could provide a new horizon for effective therapeutic development. Furthermore, using synthetic or natural compounds as ER agonists may induce estrogen-mediated anti-cancer activities against colon cancer. In this study, we report the most recent pre-clinical and experimental evidences related to ERs in CRC development. Also, we reviewed the actions of naturally occurring and synthetic compounds, which have a protective role against CRC development by acting as ER agonist.
C1 [Das, Plabon Kumar; Islam, Farhadul] Univ Rajshahi, Dept Biochem & Mol Biol, Rajshahi 6205, Bangladesh.
   [Das, Plabon Kumar; Islam, Farhadul] Griffith Univ, Inst Glyc, Gold Coast, Qld, Australia.
   [Saha, Joti] Univ Rajshahi, Dept Appl Chem & Chem Engn, Rajshahi, Bangladesh.
   [Pillai, Suja] Univ Queensland, Fac Med, Sch Biomed Sci, Brisbane, Qld, Australia.
   [Lam, Alfred K-Y; Gopalan, Vinod] Griffith Univ, Sch Med & Dent, Gold Coast, Qld, Australia.
C3 University of Rajshahi; Griffith University; Griffith University - Gold
   Coast Campus; University of Rajshahi; University of Queensland; Griffith
   University; Griffith University - Gold Coast Campus
RP Islam, F (corresponding author), Univ Rajshahi, Dept Biochem & Mol Biol, Rajshahi 6205, Bangladesh.
EM farhad_bio83@ru.ac.bd
RI Islam, Farhadul/R-5643-2017; Gopalan, Vinod/C-4269-2016; Lam,
   Alfred/C-1652-2008
OI Islam, Farhadul/0000-0001-5262-4702; Gopalan, Vinod/0000-0003-0366-9482;
   Lam, Alfred/0000-0003-2771-564X
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NR 102
TC 19
Z9 19
U1 0
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD FEB
PY 2023
VL 12
IS 4
BP 4367
EP 4379
DI 10.1002/cam4.5242
EA OCT 2022
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9K9QR
UT WOS:000864928600001
PM 36207986
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Shailes, H
   Tse, WY
   Freitas, MO
   Silver, A
   Martin, SA
AF Shailes, Hannah
   Tse, Wai Yiu
   Freitas, Marta O.
   Silver, Andrew
   Martin, Sarah A.
TI Statin Treatment as a Targeted Therapy for APC-Mutated Colorectal Cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal (colon) cancer; APC; synthetic lethality; personalized
   medicine; statin (HMG-CoA reductase inhibitor); biomarker
ID FAMILIAL ADENOMATOUS POLYPOSIS; BETA-CATENIN; COLON-CANCER;
   DOWN-REGULATION; MOUSE MODELS; K-RAS; ACTIVATION; CELLS; SUPPRESSION;
   INHIBITION
AB BackgroundMutations in the tumor suppressor gene Adenomatous Polyposis Coli (APC) are found in 80% of sporadic colorectal cancer (CRC) tumors and are also responsible for the inherited form of CRC, Familial adenomatous polyposis (FAP). MethodsTo identify novel therapeutic strategies for the treatment of APC mutated CRC, we generated a drug screening platform that incorporates a human cellular model of APC mutant CRC using CRISPR-cas9 gene editing and performed an FDA-approved drug screen targeting over 1000 compounds. ResultsWe have identified the group of HMG-CoA Reductase (HMGCR) inhibitors known as statins, which cause a significantly greater loss in cell viability in the APC mutated cell lines and in in vivo APC mutated patient derived xenograft (PDX) models, compared to wild-type APC cells. Mechanistically, our data reveals this new synthetic lethal relationship is a consequence of decreased Wnt signalling and, ultimately, a reduction in the level of expression of the anti-apoptotic protein Survivin, upon statin treatment in the APC-mutant cells only. This mechanism acts via a Rac1 mediated control of beta-catenin. ConclusionSignificantly, we have identified a novel synthetic lethal dependence between APC mutations and statin treatment, which could potentially be exploited for the treatment of APC mutated cancers.
C1 [Shailes, Hannah; Tse, Wai Yiu; Freitas, Marta O.; Martin, Sarah A.] Queen Mary Univ London, Barts Canc Inst, Ctr Canc Cell & Mol Biol, London, England.
   [Silver, Andrew] Queen Mary Univ London, Blizard Inst, Ctr Genom & Child Hlth, Barts & London Sch Med & Dent, London, England.
C3 University of London; Queen Mary University London; University of
   London; Queen Mary University London
RP Martin, SA (corresponding author), Queen Mary Univ London, Barts Canc Inst, Ctr Canc Cell & Mol Biol, London, England.
RI Freitas, Marta/J-8699-2013
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NR 53
TC 14
Z9 14
U1 6
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 MAY 30
PY 2022
VL 12
AR 880552
DI 10.3389/fonc.2022.880552
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2D1NV
UT WOS:000811323500001
PM 35712511
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Usman, S
   Khawer, M
   Rafique, S
   Naz, Z
   Saleem, K
AF Usman, Sana
   Khawer, Maria
   Rafique, Shazia
   Naz, Zara
   Saleem, Komal
TI The current status of anti-GPCR drugs against different cancers
SO JOURNAL OF PHARMACEUTICAL ANALYSIS
LA English
DT Review
DE GPCRs; Anticancer therapy; Pancreatic cancer; Colon cancer; CLL;
   Prostate cancer; Melanoma
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; PROTEIN-COUPLED RECEPTOR; CXCR4 CHEMOKINE
   RECEPTOR; PANCREATIC-CANCER; BREAST-CANCER; IN-VITRO; PROLIFERATION;
   EXPRESSION; ACTIVATION; MIGRATION
AB G protein coupled receptors (GPCRs) have emerged as the most potential target for a number of drug discovery programs ranging from control of blood pressure, diabetes, cure for genetic diseases to treatment of cancer. A panel of different ligands including hormones, peptides, ions and small molecules is responsible for activation of these receptors. Molecular genetics has identified key GPCRs, whose mutations or altered expressions are linked with tumorgenicity. In this review, we discussed recent advances regarding the involvement of GPCRs in the development of cancers and approaches to manipulating the mechanism behind GPCRs involved tumor growth and metastasis to treat different types of human cancer. This review provides an insight into the current scenario of GPCR-targeted therapy, progress to date and the challenges in the development of anticancer drugs. (C) 2020 Xi'an Jiaotong University. Production and hosting by Elsevier B.V.
C1 [Usman, Sana; Naz, Zara; Saleem, Komal] Univ Punjab, Ctr Appl Mol Biol, 87 West Canal Bank Rd Thokar Niaz Baig, Lahore, Pakistan.
   [Khawer, Maria; Rafique, Shazia] Univ Punjab, Ctr Excellence Mol Biol, Lahore, Pakistan.
C3 University of Punjab; University of Punjab
RP Usman, S (corresponding author), Univ Punjab, Ctr Appl Mol Biol, 87 West Canal Bank Rd Thokar Niaz Baig, Lahore, Pakistan.
EM sana_usman44@yahoo.com
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NR 55
TC 35
Z9 38
U1 1
U2 26
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2095-1779
EI 2214-0883
J9 J PHARM ANAL
JI J. Pharm. Anal.
PD DEC
PY 2020
VL 10
IS 6
BP 517
EP 521
DI 10.1016/j.jpha.2020.01.001
PG 5
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA PO1VP
UT WOS:000604958600002
PM 33425448
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yaghoubi, A
   Khazaei, M
   Avan, A
   Hasanian, SM
   Soleimanpour, S
AF Yaghoubi, Atieh
   Khazaei, Majid
   Avan, Amir
   Hasanian, Seyed Mahdi
   Soleimanpour, Saman
TI The bacterial instrument as a promising therapy for colon cancer
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Review
DE Colon cancer; Bacteriotherapy; Bacteriocins; Bacterial peptide; Toxin
ID DIPHTHERIA-TOXIN; COLORECTAL-CANCER; ADP-RIBOSYLATION; LISTERIOLYSIN-O;
   PEPTIDES; TUMORS; CLAUDIN-4; OVEREXPRESSION; EPIDEMIOLOGY; ELONGATION
AB Objective Colon cancer is a great health concern worldwide, as it is the second leading cause of cancer-related death. Conventional treatment of cancer such as surgery, radiotherapy, and chemotherapy are faced with limitations and side effects. Therefore, strategies for the treatment of cancer need to be modified or new strategies replacing the old one. Aims The aim of this study is to review the role of bacteria or their products (such as peptides, bacteriocins, and toxins) as a therapeutic agent for colon cancer. Results and conclusion Recently, the therapeutic role of bacteria and their products in colon cancer treatment holds promise as emerging novel anti-cancer agents. Unlike the conventional treatments, targeted therapy based on the use of bacteria that are able to directly target tumor cells without affecting normal cells is evolving as an alternative strategy. Moreover, several bacterial species were used in live, attenuated or genetically modified that are able to multiply selectively in tumors and inhibiting their growth.
C1 [Yaghoubi, Atieh; Soleimanpour, Saman] Mashhad Univ Med Sci, Bu Ali Res Inst, Antimicrobial Resistance Res Ctr, Mashhad, Razavi Khorasan, Iran.
   [Yaghoubi, Atieh; Soleimanpour, Saman] Mashhad Univ Med Sci, Dept Microbiol & Virol, Fac Med, Mashhad, Razavi Khorasan, Iran.
   [Khazaei, Majid] Mashhad Univ Med Sci, Fac Med, Dept Physiol, Mashhad, Razavi Khorasan, Iran.
   [Avan, Amir] Mashhad Univ Med Sci, Canc Res Ctr, Mashhad, Razavi Khorasan, Iran.
   [Hasanian, Seyed Mahdi] Mashhad Univ Med, Fac Med, Dept Med Biochem, Sci, Mashhad, Razavi Khorasan, Iran.
C3 Mashhad University of Medical Sciences; Mashhad University of Medical
   Sciences; Mashhad University of Medical Sciences; Mashhad University of
   Medical Sciences; Mashhad University of Medical Sciences
RP Soleimanpour, S (corresponding author), Mashhad Univ Med Sci, Bu Ali Res Inst, Antimicrobial Resistance Res Ctr, Mashhad, Razavi Khorasan, Iran.; Soleimanpour, S (corresponding author), Mashhad Univ Med Sci, Dept Microbiol & Virol, Fac Med, Mashhad, Razavi Khorasan, Iran.
EM soleimanpours@mums.ac.ir
RI Hassanian, Seyed Mahdi/KAL-9917-2024; Soleimanpour, Saman/AFB-2972-2022;
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NR 87
TC 28
Z9 29
U1 0
U2 18
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 APR
PY 2020
VL 35
IS 4
BP 595
EP 606
DI 10.1007/s00384-020-03535-9
EA MAR 2020
PG 12
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA KV4EQ
UT WOS:000518243000001
PM 32130489
DA 2025-01-04
ER

PT J
AU Chen, Y
   Chi, P
AF Chen, Yu
   Chi, Ping
TI Basket trial of TRK inhibitors demonstrates efficacy in TRK
   fusion-positive cancers
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Article
ID PAPILLARY THYROID-CARCINOMA; ANALOG SECRETORY CARCINOMA; ETV6-NTRK3 GENE
   FUSION; KINASE INHIBITION; SOLID TUMORS; CONGENITAL FIBROSARCOMA;
   MESOBLASTIC NEPHROMA; COLORECTAL-CARCINOMA; NTRK1 REARRANGEMENTS;
   TARGETED THERAPY
AB Unlike many conventional cancers with preferential patterns of oncogenic genetic alterations, TRK fusions resulting from NTRK1/2/3 genetic alterations drive oncogenic transformations in more than 20 different malignancies over diverse tissue/cell lineages, in both children and adults. A recent "basket" study of larotrectinib, a TRK inhibitor, has demonstrated significant efficacy in TRK fusion-positive tumors of all types from infants to the elderly. Here, we discuss the larotrectinib study and perspectives and challenges in developing "tumor-agnostic" targeted therapies in rare tumors.
C1 [Chen, Yu; Chi, Ping] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10065 USA.
   [Chen, Yu; Chi, Ping] Mem Sloan Kettering Canc Ctr, Dept Med, 1275 York Ave, New York, NY 10021 USA.
   [Chen, Yu; Chi, Ping] Weill Cornell Med Coll, Dept Med, New York, NY USA.
C3 Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering Cancer
   Center; Cornell University; Weill Cornell Medicine
RP Chi, P (corresponding author), Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10065 USA.; Chi, P (corresponding author), Mem Sloan Kettering Canc Ctr, Dept Med, 1275 York Ave, New York, NY 10021 USA.; Chi, P (corresponding author), Weill Cornell Med Coll, Dept Med, New York, NY USA.
EM chip@mskcc.org
FU NIH/NCI [R01CA193837, R01CA208100, P50CA092629, U54CA224079,
   P50CA140146, DP2 CA174499, R01CA228216]; FDA/OPD [R01FD005731]; US DOD
   [W81XWH-10-1-0197]; Prostate Cancer Foundation; Bloomberg Family
   Foundation
FX This work was supported by grants from the NIH/NCI (R01CA193837, YC;
   R01CA208100, YC; P50CA092629, YC; U54CA224079, YC; P50CA140146, PC; DP2
   CA174499, PC; R01CA228216, PC), FDA/OPD (R01FD005731, PC), US DOD
   (W81XWH-10-1-0197, PC), Prostate Cancer Foundation (YC), and Bloomberg
   Family Foundation (NTAP Collins Scholar, PC).
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NR 46
TC 37
Z9 40
U1 1
U2 5
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1756-8722
J9 J HEMATOL ONCOL
JI J. Hematol. Oncol.
PD JUN 7
PY 2018
VL 11
AR 78
DI 10.1186/s13045-018-0622-4
PG 5
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA GI6CF
UT WOS:000434456300001
PM 29880008
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU See, CS
   Kitagawa, M
   Liao, PJ
   Lee, KH
   Wong, J
   Lee, SH
   Dymock, BW
AF See, Cheng Shang
   Kitagawa, Mayumi
   Liao, Pei-Ju
   Lee, Kyung Hee
   Wong, Jasmine
   Lee, Sang Hyun
   Dymock, Brian W.
TI Discovery of the cancer cell selective dual acting anti-cancer agent
   (<i>Z</i>)-2-(1<i>H</i>-indol-3-yl)-3-(isoquinolin-5-yl)acrylonitrile
   (A131)
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE Antitumor; Antimitotic; Antiproliferative; Tumor-selective
ID IN-VITRO; PAPROTRAIN; INHIBITORS; AUTOPHAGY; MODELS; VIVO; LC3
AB Selective targeting of cancer cells over normal cells is a key objective of targeted therapy. However few approaches achieve true mechanistic selectivity resulting in debilitating side effects and dose limitation. In this work we describe the discovery of A131 (4a), a new agent with an unprecedented dual mechanism of action targeting both mitosis and autophagy. Compound 4a was first identified in a phenotypic screen in which HeLa cells treated with 4a manifested mitotic arrest along with formation of multiple vesicles. Further investigations showed that 4a causes an increase in mitotic marker pH3 and autophagy marker LC3. Importantly 4a induces cell death in cancer cells while sparing normal cells which regrow after 4a is removed. Dual activities against pH3 and LC3 markers are required for cancer cell selectivity. An extensive SAR investigation confirmed 4a as the optimal dual inhibitor with potency against a panel of 30 cancer cell lines (average antiproliferative GI(50) 1.5 mu M). In a mouse model of paclitaxel-resistant colon cancer, 4a showed 74% tumor growth inhibition when administered at a dose of 20 mg/kg IP twice a day. (C) 2018 Elsevier Masson SAS. All rights reserved.
C1 [See, Cheng Shang; Dymock, Brian W.] Natl Univ Singapore, Dept Pharm, Singapore 117543, Singapore.
   [Kitagawa, Mayumi; Liao, Pei-Ju; Lee, Kyung Hee; Wong, Jasmine; Lee, Sang Hyun] Duke NUS Med Sch, Program Canc & Stem Cell Biol, Singapore 169857, Singapore.
C3 National University of Singapore; National University of Singapore
RP Dymock, BW (corresponding author), Natl Univ Singapore, Dept Pharm, Singapore 117543, Singapore.
EM bwdnus@gmail.com
RI Lee, Sang-Hyun/ABR-3363-2022
OI Dymock, Brian/0000-0002-2374-5756
FU National University of Singapore (Faculty of Science start-up grant)
   [R-148-000-169-133]; NMRC CBRG [NMRC/CBRG/0091/2015]; Duke-NUS Medical
   School [NUS/RECA(PILOT/2013/0006)];  [NRF-RF2010-02]
FX We gratefully acknowledge Dr Yang Shili and Professor Paul Ho for
   providing the RLM and rat PK data, and Ms Sheela David Packiaraj and
   Associate Professor Ho Han Kiat for providing the TAMH, AC10 and AMES
   data. This research was funded by generous grants from the National
   University of Singapore (Faculty of Science start-up grant
   R-148-000-169-133 to B.D.), the National Research Fellow (S.H.L.;
   NRF-RF2010-02) program, NMRC CBRG (S.H.L.; NMRC/CBRG/0091/2015) and the
   Duke-NUS Medical School [NUS/RECA(PILOT/2013/0006)].
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NR 24
TC 14
Z9 14
U1 0
U2 7
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0223-5234
EI 1768-3254
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD AUG 5
PY 2018
VL 156
BP 344
EP 367
DI 10.1016/j.ejmech.2018.07.011
PG 24
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED); Index Chemicus (IC)
SC Pharmacology & Pharmacy
GA GS4YG
UT WOS:000443663200027
PM 30015072
DA 2025-01-04
ER

PT J
AU Yenurkar, D
   Nayak, M
   Mukherjee, S
AF Yenurkar, Devyani
   Nayak, Malay
   Mukherjee, Sudip
TI Recent advances of nanocrystals in cancer theranostics
SO NANOSCALE ADVANCES
LA English
DT Review
ID CELLULAR UPTAKE; SURFACE-CHARGE; IN-VITRO; ORGANIC NANOCRYSTALS;
   COLORECTAL-CANCER; DRUG NANOCRYSTALS; URSOLIC-ACID; NANOPARTICLES;
   PACLITAXEL; DELIVERY
AB Emerging cancer cases across the globe and treating them with conventional therapies with multiple limitations have been challenging for decades. Novel drug delivery systems and alternative theranostics are required for efficient detection and treatment. Nanocrystals (NCs) have been established as a significant cancer diagnosis and therapeutic tool due to their ability to deliver poorly water-soluble drugs with sustained release, low toxicity, and flexibility in the route of administration, long-term sustainable drug release, and noncomplicated excretion. This review summarizes several therapies of NCs, including anticancer, immunotherapy, radiotherapy, biotheranostics, targeted therapy, photothermal, and photodynamic. Further, different imaging and diagnostics using NCs are mentioned, including imaging, diagnosis through magnetic resonance imaging (MRI), computed tomography (CT), biosensing, and luminescence. In addition, the limitations and potential solutions of NCs in the field of cancer theranostics are discussed. Preclinical and clinical data depicting the importance of NCs in the spotlight of cancer, its current status, future aspects, and challenges are covered in detail.
C1 [Yenurkar, Devyani; Nayak, Malay; Mukherjee, Sudip] BHU, Indian Inst Technol, Sch Biomed Engn, Varanasi 221005, UP, India.
C3 Banaras Hindu University (BHU); Indian Institute of Technology System
   (IIT System); Indian Institute of Technology BHU Varanasi (IIT BHU
   Varanasi)
RP Mukherjee, S (corresponding author), BHU, Indian Inst Technol, Sch Biomed Engn, Varanasi 221005, UP, India.
EM sudip.bme@iitbhu.ac.in
RI Mukherjee, Sudip/E-5405-2012
OI MUKHERJEE, SUDIP/0000-0002-3625-2272
FU MHRD; IIT (BHU); Royal Society of Chemistry, UK [R22-2922732087]
FX DY and MN thank MHRD and IIT (BHU), Varanasi for their research and
   teaching assistant fellowship. Dr Sudip Mukherjee acknowledges director
   (Prof. Pramod Kumar Jain), Indian Institute of Technology (BHU) for
   providing research infrastructure and other facilities. SM further
   acknowledged research fund support from IIT (BHU) [OH-35-Other
   Capital/Miscellaneous Grant] and Royal Society of Chemistry, UK (No.
   R22-2922732087) for providing funding support for this work.
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NR 181
TC 11
Z9 11
U1 9
U2 36
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 2516-0230
J9 NANOSCALE ADV
JI Nanoscale Adv.
PD AUG 8
PY 2023
VL 5
IS 16
BP 4018
EP 4040
DI 10.1039/d3na00397c
EA JUL 2023
PG 23
WC Chemistry, Multidisciplinary; Nanoscience & Nanotechnology; Materials
   Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA O1ZP9
UT WOS:001035585000001
PM 37560418
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, L
   Li, CX
   Su, XL
AF Zhang, Le
   Li, Cuixia
   Su, Xiulan
TI Emerging impact of the long noncoding RNA MIR22HG on proliferation and
   apoptosis in multiple human cancers
SO JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
LA English
DT Review
DE Long noncoding RNAs; MIR22HG; Tumorigenesis; Therapeutic target
ID GASTRIC-CANCER; TGF-BETA; C-MYC; MESENCHYMAL TRANSITION;
   TUMOR-SUPPRESSOR; CELL; STAT3; PROGRESSION; NOTCH; GENE
AB An increasing number of studies have shown that long noncoding RNAs (lncRNAs) play important roles in diverse cellular processes, including proliferation, apoptosis, migration, invasion, chromatin remodeling, metabolism and immune escape. Clinically, the expression of MIR22HG is increased in many human tumors (colorectal cancer, gastric cancer, hepatocellular carcinoma, lung cancer, and thyroid carcinoma), while in others (esophageal adenocarcinoma and glioblastoma), it is significantly decreased. Moreover, MIR22HG has been reported to function as a competitive endogenous RNA (ceRNA), be involved in signaling pathways, interact with proteins and interplay with miRNAs as a host gene to participate in tumorigenesis and tumor progression. In this review, we describe the biological functions of MIR22HG, reveal its underlying mechanisms for cancer regulation, and highlight the potential role of MIR22HG as a novel cancer prognostic biomarker and therapeutic target that can increase the efficacy of immunotherapy and targeted therapy for cancer treatment.
C1 [Zhang, Le; Li, Cuixia; Su, Xiulan] Inner Mongolia Med Univ, Clin Med Res Ctr, Affiliated Hosp, 1 Tong Dao St, Hohhot 010050, Inner Mongolia, Peoples R China.
C3 Inner Mongolia Medical University
RP Su, XL (corresponding author), Inner Mongolia Med Univ, Clin Med Res Ctr, Affiliated Hosp, 1 Tong Dao St, Hohhot 010050, Inner Mongolia, Peoples R China.
EM xlsu@hotmail.com
FU National Natural Science Foundation of China [81960560]; Autonomous
   Region Science and Technology Achievement Transformation Fund
   [CGZH2018149]; Natural Science Foundation of Inner Mongolia Autonomous
   Region [2020BS08002]
FX This work was supported by the National Natural Science Foundation of
   China (81960560), Autonomous Region Science and Technology Achievement
   Transformation Fund (CGZH2018149), and Natural Science Foundation of
   Inner Mongolia Autonomous Region (2020BS08002).
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NR 96
TC 61
Z9 65
U1 0
U2 18
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 3
PY 2020
VL 39
IS 1
AR 271
DI 10.1186/s13046-020-01784-8
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PA1PK
UT WOS:000595395400001
PM 33267888
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yoshikawa, A
   Nakamura, Y
AF Yoshikawa, Ayumu
   Nakamura, Yoshiaki
TI Molecular Basis of HER2-Targeted Therapy for HER2-Positive Colorectal
   Cancer
SO CANCERS
LA English
DT Review
DE colorectal cancer; ctDNA; HER2 amplification; liquid biopsy; the TRIUMPH
   study
ID GENOMIC LANDSCAPE; PROGNOSTIC VALUE; COLON-CANCER; OPEN-LABEL;
   TRASTUZUMAB; DESTINY-CRC01; AMPLIFICATION; MULTICENTER; TUCATINIB;
   PHASE-2
AB Human epidermal growth factor receptor 2 (HER2) amplification has emerged as a biomarker in colorectal cancer (CRC), occurring in 1-4% of metastatic CRC (mCRC). In addition to conventional methods, such as immunohistochemistry and fluorescence in situ hybridization, next-generation sequencing-based tissue or circulating tumor DNA analysis has recently been used to identify HER2 amplification and assess HER2 overexpression. Prospective clinical trials have demonstrated the efficacy of HER2-targeted therapies in HER2-positive mCRC. The TRIUMPH study, a phase II study of dual HER2 antibodies, i.e., pertuzumab plus trastuzumab, demonstrated promising efficacy for patients with HER2-positive mCRC confirmed by tissue-and/or blood-based techniques, which led to the regulatory approval of this combination therapy in Japan. The mechanisms associated with efficacy and resistance have also been explored in translational studies that incorporate liquid biopsy in prospective trials. In particular, HER2 copy number and co-alterations have repeatedly been reported as biomarkers related to efficacy. To improve the therapeutic efficacy of the current strategy, many clinical trials with various HER2-targeted agents are ongoing. This review discusses the molecular basis of HER2-targeted therapeutic strategies for patients with HER2-positive mCRC.
C1 [Yoshikawa, Ayumu; Nakamura, Yoshiaki] Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa 2770882, Japan.
   [Nakamura, Yoshiaki] Natl Canc Ctr Hosp East, Int Res Promot Off, Kashiwa 2770882, Japan.
   [Nakamura, Yoshiaki] Natl Canc Ctr Hosp East, Translat Res Support Sect, Kashiwa 2770882, Japan.
C3 National Cancer Center - Japan; National Cancer Center - Japan; National
   Cancer Center - Japan
RP Nakamura, Y (corresponding author), Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa 2770882, Japan.; Nakamura, Y (corresponding author), Natl Canc Ctr Hosp East, Int Res Promot Off, Kashiwa 2770882, Japan.; Nakamura, Y (corresponding author), Natl Canc Ctr Hosp East, Translat Res Support Sect, Kashiwa 2770882, Japan.
EM yoshinak@east.ncc.go.jp
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NR 46
TC 6
Z9 6
U1 2
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2023
VL 15
IS 1
AR 183
DI 10.3390/cancers15010183
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 7Q3ID
UT WOS:000909287700001
PM 36612185
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Lu, M
   Zhang, SB
   Zhou, H
   Yu, XY
   Li, JN
   Fu, BS
   Wei, MJ
   Huang, HL
   Wu, HZ
AF Lu, Min
   Zhang, Subo
   Zhou, Heng
   Yu, Xiaoyu
   Li, Jianing
   Fu, Boshi
   Wei, Minjie
   Huang, Huilin
   Wu, Huizhe
TI The interplay between non-coding RNAs and alternative splicing: from
   regulatory mechanism to therapeutic implications in cancer
SO THERANOSTICS
LA English
DT Review
DE Alternative splicing; Non-coding RNA; Cancer; Drug resistance;
   Chemotherapy; Targeted therapy; Immunotherapy
ID PRE-MESSENGER-RNA; NATURAL ANTISENSE TRANSCRIPT; SMALL NUCLEOLAR RNAS;
   HEPATOCELLULAR-CARCINOMA; COLORECTAL-CANCER; EXPRESSION PROFILE;
   DEPENDENT CONTROL; PROTEIN; LNCRNA; OLIGONUCLEOTIDES
AB Alternative splicing (AS) is a common and conserved process in eukaryotic gene regulation. It occurs in approximately 95% of multi-exon genes, greatly enriching the complexity and diversity of mRNAs and proteins. Recent studies have found that in addition to coding RNAs, non-coding RNAs (ncRNAs) are also inextricably linked with AS. Multiple different types of ncRNAs are generated by AS of precursor long non-coding (pre-lncRNAs) or precursor messenger RNAs (pre-mRNAs). Furthermore, ncRNAs, as a novel class of regulators, can participate in AS regulation by interacting with the cis-acting elements or trans-acting factors. Several studies have implicated abnormal expression of ncRNAs and ncRNA-related AS events in the initiation, progression, and therapy resistance in various types of cancers. Therefore, owing to their roles in mediating drug resistance, ncRNAs, AS-related factors and AS-related novel antigens may serve as promising therapeutic targets in cancer treatment. In this review, we summarize the interaction between ncRNAs and AS processes, emphasizing their great influences on cancer, especially on chemoresistance, and highlighting their potential values in clinical treatment.
C1 [Lu, Min; Zhou, Heng; Yu, Xiaoyu; Li, Jianing; Fu, Boshi; Wei, Minjie; Wu, Huizhe] China Med Univ, Sch Pharm, Dept Pharmacol, Shenyang 110122, Liaoning, Peoples R China.
   [Lu, Min; Zhou, Heng; Yu, Xiaoyu; Li, Jianing; Fu, Boshi; Wei, Minjie; Wu, Huizhe] China Med Univ, Liaoning Canc Immune Peptide Drug Engn Technol Res, Liaoning Key Lab Mol Targeted Antitumor Drug Dev &, Minist Educ,Key Lab Precis Diag & Treatment Gastro, Shenyang 110122, Liaoning, Peoples R China.
   [Zhang, Subo; Huang, Huilin] Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Canc Ctr, Guangzhou 510060, Guangdong, Peoples R China.
   [Zhou, Heng] China Med Univ, Surg Oncol & Gen Surg, Hosp 1, Shenyang 110001, Liaoning, Peoples R China.
   [Wei, Minjie] Shenyang Kangwei Med Lab Anal Co LTD, Shenyang, Liaoning, Peoples R China.
C3 China Medical University; China Medical University; Sun Yat Sen
   University; State Key Lab Oncology South China; China Medical University
RP Wei, MJ; Wu, HZ (corresponding author), China Med Univ, Sch Pharm, Dept Pharmacol, Shenyang 110122, Liaoning, Peoples R China.; Wei, MJ; Wu, HZ (corresponding author), China Med Univ, Liaoning Canc Immune Peptide Drug Engn Technol Res, Liaoning Key Lab Mol Targeted Antitumor Drug Dev &, Minist Educ,Key Lab Precis Diag & Treatment Gastro, Shenyang 110122, Liaoning, Peoples R China.; Huang, HL (corresponding author), Sun Yat Sen Univ, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol South China, Canc Ctr, Guangzhou 510060, Guangdong, Peoples R China.; Wei, MJ (corresponding author), Shenyang Kangwei Med Lab Anal Co LTD, Shenyang, Liaoning, Peoples R China.
EM mjwei@cmu.edu.cn; huanghl1@sysucc.org.cn; wuhz@cmu.edu.cn
RI Li, Jianing/AAE-2394-2020; Zhou, Heng/ABH-3207-2021
FU National Natural Science Foundation of China [82272915, 82073884,
   82173058, 82201377]; project of the fourth batch of science and
   technology plan of Liaoning province [2021JH210300133]; Science and
   technology innovation team project of China Medical University
   [CXTD2022007]; Guangdong Basic and Applied Basic Research Foundation
   [2021A1515010425]; Postdoctoral Innovation Fellowships Program
   [BX2021393]
FX This work was supported by grants from the National Natural Science
   Foundation of China (82272915, 82073884, 82173058 and 82201377), the
   project of the fourth batch of science and technology plan of Liaoning
   province (2021JH210300133), Science and technology innovation team
   project of China Medical University (No. CXTD2022007, China) , Guangdong
   Basic and Applied Basic Research Foundation (2021A1515010425) and
   Postdoctoral Innovation Fellowships Program (BX2021393) . We thank
   Cloudseq Biotech Inc. (Shanghai, China) for their help, and Bullet Edits
   Limited for editing and proofreading the manuscript.
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NR 133
TC 14
Z9 14
U1 1
U2 11
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2023
VL 13
IS 8
BP 2616
EP 2631
DI 10.7150/thno.83920
PG 16
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA H7OX9
UT WOS:000997824000015
PM 37215575
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU de Almeida, LC
   Calil, FA
   Machado-Neto, JA
   Costa-Lotufo, LV
AF de Almeida, Larissa Costa
   Calil, Felipe Antunes
   Machado-Neto, Joao Agostinho
   Costa-Lotufo, Leticia Veras
TI DNA damaging agents and DNA repair: From carcinogenesis to cancer
   therapy
SO CANCER GENETICS
LA English
DT Review
DE Cancer; DNA damage; DNA repair; Chemotherapy; Carcinogenesis
ID FANCONI-ANEMIA PATHWAY; NON-HODGKIN-LYMPHOMA; CROSS-LINK REPAIR;
   MISMATCH REPAIR; HEPATOCELLULAR-CARCINOMA; HOMOLOGOUS RECOMBINATION;
   COLORECTAL-CANCER; CELL CARCINOMA; MICROSATELLITE INSTABILITY;
   ATAXIA-TELANGIECTASIA
AB Cancer genome instability arises from diverse defects in DNA-repair machinery, which make cancer cells more susceptible to DNA targeting agents. The interrelation between DNA repair deficiency and the increased effect of DNA targeting agents highlights the double-strand break (DSB) repair, which comprises the homologous recombination (HR) and non-homologous end joining (NHEJ) pathways. The DNA targeting agents are classified into two major groups: non-covalent DNA binding agents and covalent DNA-reactive agents. Although these agents have well-known limitations, such as resistance and secondary carcinogenesis risk, they are extremely important in today's real-life cancer therapy in combination with targeted therapy and immunotherapy. Indeed, DNA targeting drugs are promising therapeutics with a precise application through the background of cancer-specific DNA repair failure. In the current review, the mechanisms of action of diversified DNA-targeting agents, as well as the modulation of DNA repair pathways to increase the DNA-damaging drugs efficacy are presented. Finally, DNA-targeting-based therapies are discussed considering risks, resistance and its uses in the medicine precision era. (C) 2020 Elsevier Inc. All rights reserved.
C1 [de Almeida, Larissa Costa; Machado-Neto, Joao Agostinho; Costa-Lotufo, Leticia Veras] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, Ave Prof Lineu Prestes 1524, BR-05508900 Sao Paulo, Brazil.
   [Calil, Felipe Antunes] Univ Calif San Diego, Sch Med, Ludwig Inst Canc Res, La Jolla, CA 92093 USA.
C3 Universidade de Sao Paulo; Ludwig Institute for Cancer Research;
   University of California System; University of California San Diego
RP Costa-Lotufo, LV (corresponding author), Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, Ave Prof Lineu Prestes 1524, BR-05508900 Sao Paulo, Brazil.
EM costalotufo@gmail.com
RI Costa de Almeida, Larissa/AGZ-6563-2022; Costa-Lotufo,
   Leticia/ABC-5742-2021; Machado-Neto, João/L-8975-2016; Costa-Lotufo,
   Leticia/D-4998-2014; Calil, Felipe/D-3190-2013; Fapesp,
   Biota/F-8655-2017
OI Costa-Lotufo, Leticia/0000-0003-1861-5153; Costa de Almeida,
   Larissa/0000-0001-5828-119X; Calil, Felipe/0000-0001-7503-4078; Fapesp,
   Biota/0000-0002-9887-8449
FU Sao Paulo Research Foundation (FAPESP) [2017/176 48-4, 2019/23864-7,
   2015/171776]; National Institute of Science and Technology - INCT BioNat
   (CNPQ) [465637/2014-0]; National Institute of Science and Technology -
   INCT BioNat (FAPESP, Brazil) [2014/509260]; Coordenacao de
   Aperfeicoamento de Pessoal de Nivel Superior - Brasil (CAPES) [001]
FX This study was supported by Sao Paulo Research Foundation (FAPESP)
   (grants #2017/176 48-4; #2019/23864-7; #2015/171776) and National
   Institute of Science and Technology - INCT BioNat, (CNPQ grant
   #465637/2014-0, FAPESP grant #2014/509260, Brazil). This study was
   financed in part by the Coordenacao de Aperfeicoamento de Pessoal de
   Nivel Superior - Brasil (CAPES) - Finance Code 001.
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NR 241
TC 36
Z9 37
U1 2
U2 40
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 2210-7762
EI 2210-7770
J9 CANCER GENET-NY
JI Cancer Genet.
PD APR
PY 2021
VL 252
BP 6
EP 24
DI 10.1016/j.cancergen.2020.12.002
PG 19
WC Oncology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Genetics & Heredity
GA RP8XB
UT WOS:000642005000002
PM 33340831
DA 2025-01-04
ER

PT J
AU Rigoni, A
   Colombo, MP
   Pucillo, C
AF Rigoni, A.
   Colombo, M. P.
   Pucillo, C.
TI The Role of Mast Cells in Molding the Tumor Microenvironment
SO CANCER MICROENVIRONMENT
LA English
DT Article
DE Mast cell; Cancer; Immune responses; Immunosuppression; Extracellular
   matrix
ID ARYL-HYDROCARBON RECEPTOR; T-CELL; C-KIT; POOR-PROGNOSIS;
   COLORECTAL-CANCER; TARGETED THERAPY; PROSTATE-CANCER; GROWTH-FACTOR;
   LYMPH-NODES; INFLAMMATION
AB Mast cells (MCs) are granulocytic immune cells that reside in tissues exposed to the external environment. MCs are best known for their activity in allergic reactions, but they have been involved in different physiological and pathological conditions. In particular, MCinfiltration has been shown in several types of human tumors and in animal cancer models. Nevertheless, the role of MCs in the tumor microenvironment is still debated because they have been associated either to good or poor prognosis depending on tumor type and tissue localization. This dichotomous role relies on MC capacity to secrete a broad spectrum of molecules with modulatory functions, which may condition the final tumor outcome also promoting angiogenesis and tissue remodeling. In this review, we analyze the multifaceted role of mast cell in tumor progression and inhibition considering their ability to interact with: i) immune cells, ii) tumor cells and iii) the extracellular matrix. Eventually, the current MC targeting strategies to treat cancer patients are discussed. Deciphering the actual role of MCs in tumor onset and progression is crucial to identifyMCtargeted treatments aimed at killing cancer cells or at making the tumor vulnerable to selected anti- cancer drugs.
C1 [Rigoni, A.; Colombo, M. P.] Fdn IRCCS Ist Nazl Tumori, Dept Expt Oncol & Mol Med, Mol Immunol Unit, Via Amadeo 42, I-20133 Milan, Italy.
   [Pucillo, C.] Univ Udine, Dept Med & Biol Sci, I-33100 Udine, Italy.
C3 Fondazione IRCCS Istituto Nazionale Tumori Milan; University of Udine
RP Colombo, MP (corresponding author), Fdn IRCCS Ist Nazl Tumori, Dept Expt Oncol & Mol Med, Mol Immunol Unit, Via Amadeo 42, I-20133 Milan, Italy.
EM mario.colombo@istitutotumori.mi.it
RI ; Rigoni, Alice/C-5532-2017; Pucillo, Carlo/A-5515-2008; Colombo, Mario
   Paolo/V-7166-2017
OI danilova, irina/0000-0001-9624-3389; Rigoni, Alice/0000-0002-4147-1904;
   Pucillo, Carlo/0000-0002-4872-6156; Colombo, Mario
   Paolo/0000-0003-0042-7955
FU Fondazione Cariplo [2010-0790]; Associazione Italiana per la Ricerca sul
   Cancro (AIRC) [14194]; Associazione Italiana Mastocitosi (ASIMAS);
   Fondazione Italiana per la Ricerca sul Cancro (FIRC)
FX This work was supported by grants from Fondazione Cariplo (number
   2010-0790) and Associazione Italiana per la Ricerca sul Cancro (AIRC:
   Investigator Grant number 14194 to Mario Paolo Colombo). The work of
   Carlo Pucillo is supported by a grant from Associazione Italiana
   Mastocitosi (ASIMAS). Alice Rigoni is supported by a triennial
   fellowship from Fondazione Italiana per la Ricerca sul Cancro (FIRC).
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NR 98
TC 54
Z9 56
U1 0
U2 5
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 DEC
PY 2015
VL 8
IS 3
BP 167
EP 176
DI 10.1007/s12307-014-0152-8
PG 10
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA V5D9L
UT WOS:000219520000004
PM 25194694
OA Green Published
DA 2025-01-04
ER

PT J
AU Lester-Coll, NH
   Decker, RH
AF Lester-Coll, Nataniel H.
   Decker, Roy H.
TI The role of stereotactic body radiation therapy in the management of
   oligometastatic lung cancer
SO LUNG CANCER MANAGEMENT
LA English
DT Article
DE local therapy; non-small-cell lung cancer; oligometastases;
   oligometastatic; oligoprogressive; stereotactic body radiation therapy
   (SBRT)
ID COLORECTAL-CARCINOMA METASTASES; SYNCHRONOUS BRAIN METASTASES; TYROSINE
   KINASE INHIBITORS; ADRENAL-GLAND METASTASES; DOSE-ESCALATION TRIAL;
   RENAL-CELL CARCINOMA; PHASE I/II TRIAL; RADIOFREQUENCY ABLATION;
   PROGNOSTIC-FACTORS; PULMONARY METASTASECTOMY
AB A growing body of evidence has surfaced over the past 20 years that supports the use of surgery for metastases limited in number termed oligometastases'. Local therapy for oligometases results in long progression free survival in the absence of systemic therapy, including non-small-cell lung cancer (NSCLC). Stereotactic body radiation therapy (SBRT) allows for the delivery of anatomically precise, ablative doses of radiation therapy able to achieve local control rates of approximately 80% with minimal toxicity. In NSCLC, SBRT is emerging as an effective therapy in the management of sites resistant to targeted therapy. This review summarizes the published evidence for the use of local therapy in the management of oligometsatic cancer, with a focus on SBRT and NSCLC.
C1 [Lester-Coll, Nataniel H.; Decker, Roy H.] Yale Univ, Sch Med, Dept Therapeut Radiol, New Haven, CT 06510 USA.
   [Lester-Coll, Nataniel H.] Smilow Canc Hosp, Dept Radiat Oncol, New Haven, CT 06510 USA.
C3 Yale University
RP Lester-Coll, NH (corresponding author), Yale Univ, Sch Med, Dept Therapeut Radiol, New Haven, CT 06510 USA.
EM nataniel.lester-coll@yale.edu
RI Lester-Coll, Nataniel/AAH-2292-2021
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NR 88
TC 1
Z9 1
U1 0
U2 2
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1758-1966
EI 1758-1974
J9 LUNG CANCER MANAG
JI Lung Cancer Manag.
PY 2015
VL 4
IS 3
BP 145
EP 153
DI 10.2217/lmt.15.10
PG 9
WC Respiratory System
WE Emerging Sources Citation Index (ESCI)
SC Respiratory System
GA CW3UD
UT WOS:000364916500005
DA 2025-01-04
ER

PT J
AU Sharma, RA
   Plummer, R
   Stock, JK
   Greenhalgh, TA
   Ataman, O
   Kelly, S
   Clay, R
   Adams, RA
   Baird, RD
   Billingham, L
   Brown, SR
   Buckland, S
   Bulbeck, H
   Chalmers, AJ
   Clack, G
   Cranston, AN
   Damstrup, L
   Ferraldeschi, R
   Forster, MD
   Golec, J
   Hagan, RM
   Hall, E
   Hanauske, AR
   Harrington, KJ
   Haswell, T
   Hawkins, MA
   Illidge, T
   Jones, H
   Kennedy, AS
   McDonald, F
   Melcher, T
   O'Connor, JPB
   Pollard, JR
   Saunders, MP
   Sebag-Montefiore, D
   Smitt, M
   Staffurth, J
   Stratford, IJ
   Wedge, SR
AF Sharma, Ricky A.
   Plummer, Ruth
   Stock, Julie K.
   Greenhalgh, Tessa A.
   Ataman, Ozlem
   Kelly, Stephen
   Clay, Robert
   Adams, Richard A.
   Baird, Richard D.
   Billingham, Lucinda
   Brown, Sarah R.
   Buckland, Sean
   Bulbeck, Helen
   Chalmers, Anthony J.
   Clack, Glen
   Cranston, Aaron N.
   Damstrup, Lars
   Ferraldeschi, Roberta
   Forster, Martin D.
   Golec, Julian
   Hagan, Russell M.
   Hall, Emma
   Hanauske, Axel-R.
   Harrington, Kevin J.
   Haswell, Tom
   Hawkins, Maria A.
   Illidge, Tim
   Jones, Hazel
   Kennedy, Andrew S.
   McDonald, Fiona
   Melcher, Thorsten
   O'Connor, James P. B.
   Pollard, John R.
   Saunders, Mark P.
   Sebag-Montefiore, David
   Smitt, Melanie
   Staffurth, John
   Stratford, Ian J.
   Wedge, Stephen R.
CA NCRI CTRad Acad-Pharma Joint Worki
TI Clinical development of new drug-radiotherapy combinations
SO NATURE REVIEWS CLINICAL ONCOLOGY
LA English
DT Review
ID SURROGATE END-POINTS; CELL LUNG-CANCER; POSITRON-EMISSION-TOMOGRAPHY;
   MOLECULARLY TARGETED AGENTS; ADVANCED RECTAL-CANCER; EARLY
   BREAST-CANCER; PHASE-II TRIAL; RADIATION-THERAPY; PROSTATE-CANCER;
   NORMAL-TISSUE
AB In countries with the best cancer outcomes, approximately 60% of patients receive radiotherapy as part of their treatment, which is one of the most cost-effective cancer treatments. Notably, around 40% of cancer cures include the use of radiotherapy, either as a single modality or combined with other treatments. Radiotherapy can provide enormous benefit to patients with cancer. In the past decade, significant technical advances, such as image-guided radiotherapy, intensity-modulated radiotherapy, stereotactic radiotherapy, and proton therapy enable higher doses of radiotherapy to be delivered to the tumour with significantly lower doses to normal surrounding tissues. However, apart from the combination of traditional cytotoxic chemotherapy with radiotherapy, little progress has been made in identifying and defining optimal targeted therapy and radiotherapy combinations to improve the efficacy of cancer treatment. The National Cancer Research Institute Clinical and Translational Radiotherapy Research Working Group (CTRad) formed a Joint Working Group with representatives from academia, industry, patient groups and regulatory bodies to address this lack of progress and to publish recommendations for future clinical research. Herein, we highlight the Working Group's consensus recommendations to increase the number of novel drugs being successfully registered in combination with radiotherapy to improve clinical outcomes for patients with cancer.
C1 [Sharma, Ricky A.; Forster, Martin D.] UCL, UCL Canc Inst, 72 Huntley St, London WC1E 6DD, England.
   [Sharma, Ricky A.; Forster, Martin D.] UCL, London, England.
   [Plummer, Ruth; Wedge, Stephen R.] Newcastle Univ, Newcastle Upon Tyne, Tyne & Wear, England.
   [Stock, Julie K.; Jones, Hazel] Canc Res UK, London, England.
   [Greenhalgh, Tessa A.; Hawkins, Maria A.] Univ Oxford, Oxford, England.
   [Ataman, Ozlem] Eisai, Hatfield Business Pk, Hatfield, Herts, England.
   [Kelly, Stephen] Pfizer Ltd, Tadworth, Surrey, England.
   [Clay, Robert] Kinapse Ltd, London, England.
   [Adams, Richard A.; Staffurth, John] Cardiff Univ, Cardiff, S Glam, Wales.
   [Adams, Richard A.; Staffurth, John] Velindre Canc Ctr, Cardiff, S Glam, Wales.
   [Baird, Richard D.] Univ Cambridge, Cambridge, England.
   [Billingham, Lucinda] Univ Birmingham, Birmingham, W Midlands, England.
   [Brown, Sarah R.; Sebag-Montefiore, David] Univ Leeds, Leeds, W Yorkshire, England.
   [Bulbeck, Helen; Haswell, Tom] Natl Inst Canc Res, London, England.
   [Chalmers, Anthony J.] Univ Glasgow, Glasgow, Lanark, Scotland.
   [Clack, Glen] AstraZeneca Cheshire UK, Alderley Pk, Cheshire, England.
   [Cranston, Aaron N.] MISSION Therapeut Ltd, Cambridge, England.
   [Damstrup, Lars] Merck KGaA, Darmstadt, Germany.
   [Ferraldeschi, Roberta] Astex Pharmaceut, Cambridge, England.
   [Golec, Julian; Pollard, John R.] Vertex Pharmaceut Europe Ltd, Abingdon, Oxon, England.
   [Hagan, Russell M.] BTG Int Ltd, London, England.
   [Hall, Emma; Harrington, Kevin J.; McDonald, Fiona] Royal Marsden NIHR Biomed Res Ctr, Inst Canc Res, London, England.
   [Hanauske, Axel-R.] Eli Lilly & Co, Indianapolis, IN 46285 USA.
   [Illidge, Tim; O'Connor, James P. B.; Saunders, Mark P.; Stratford, Ian J.] Univ Manchester, Manchester, Lancs, England.
   [Kennedy, Andrew S.] Sarah Cannon Res Inst, Nashville, TN USA.
   [Melcher, Thorsten] J&J Innovat, Menlo Pk, CA USA.
   [Smitt, Melanie] Genentech Inc, San Francisco, CA 94080 USA.
C3 University of London; University College London; University of London;
   University College London; Newcastle University - UK; Cancer Research
   UK; University of Oxford; Eisai Co Ltd; Pfizer; Cardiff University;
   Velindre Cancer Centre; University of Cambridge; University of
   Birmingham; University of Leeds; University of Glasgow; Merck KGaA;
   Astex Pharmaceuticals; Vertex Pharmaceuticals; Royal Marsden NHS
   Foundation Trust; University of London; Institute of Cancer Research -
   UK; Eli Lilly; University of Manchester; Sarah Cannon Research
   Institute; Roche Holding; Genentech
RP Sharma, RA (corresponding author), UCL, UCL Canc Inst, 72 Huntley St, London WC1E 6DD, England.; Sharma, RA (corresponding author), UCL, London, England.
EM ricky.sharma@oncology.ox.ac.uk
RI Sebag-Montefiore, David/LLK-0735-2024; Baird, Richard/S-4764-2019;
   Harrington, Kevin/CAH-0578-2022; Kelly, Stephen/GZH-1668-2022; Hanna,
   Gerard/AAC-6466-2020; Illidge, Tim/M-3659-2015; Greenhalgh,
   Trisha/B-1825-2015; Hawkins, Maria Andreia/A-9404-2013
OI Brown, Sarah/0000-0002-7975-7537; Forster, Martin/0000-0003-3876-7269;
   Illidge, Tim/0000-0003-3191-7324; Baird, Richard/0000-0001-7071-6483;
   Sebag-Montefiore, David/0000-0002-5978-9259; Adams,
   Richard/0000-0003-3915-7243; O'Connor, James/0000-0002-4044-8497; Hall,
   Emma/0000-0001-5999-5020; Wedge, Steve/0000-0002-3644-6157; Greenhalgh,
   Trisha/0000-0003-2369-8088; Hawkins, Maria Andreia/0000-0002-6669-0628;
   Harrington, Kevin/0000-0002-6014-348X; Billingham,
   Lucinda/0000-0001-8581-4262; stratford, ian/0000-0002-5222-4765
FU Sirtex Technology; Affidea; BTG plc; Cancer Research Technology; Sirtex
   Medical; Vertex; AstraZeneca; Medimmune; Roche; Astex Pharmaceuticals;
   MRC [G0802755, G0500366, MC_PC_12001/2] Funding Source: UKRI
FX R.A.S. has received research funding from Sirtex Technology and
   consultation fees from Affidea, BTG plc, Cancer Research Technology,
   Sirtex Medical, and Vertex. O.A. is an employee of Eisai. S. K. and S.
   B. are employees of Pfizer Ltd. L.B. has received honorarium from Eli
   Lilly, Pfizer and Roche. G.C. is an employee and shareholder of
   AstraZeneca. A.N.C. is an employee and stockholder of MISSION
   therapeutics. L.D. is an employee of Merck KGaA. R.F. is an employee of
   Astex Pharmaceuticals. J.G. is an employee of Vertex Pharmaceuticals
   (Europe) Ltd and owns shares in Vertex Pharmaceuticals Inc. R.M.H. is an
   employee of BTG International Ltd, a manufacturer of specialist
   healthcare products. A.-R.H. is an employee and stock holder of Eli
   Lilly. T.I. receives research support from AstraZeneca, Medimmune and
   Roche. T.M. is an employee of Johnson & Johnson. J.R.P. is an employee
   of, and holds stock in, Vertex Pharmaceuticals. M.S. is an employee of
   Genentech and stockholder of Roche. I.J.S. is a recipient of a research
   grant from AstraZeneca. S.R.W. receives research funding from Astex
   Pharmaceuticals and AstraZeneca. R.P., J.K.S., T.A.G., R.C., R.A.A.,
   R.D.B., S.R.B., H.B., A.J.C., M.D.F., E.H., K.J.H., T.H., M.A.H., H.J.,
   A.S.K., F.M., J.P.B.O'C., M.P.S., D.S.-M. and J.S. declare no competing
   interests.
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NR 155
TC 248
Z9 261
U1 10
U2 131
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4774
EI 1759-4782
J9 NAT REV CLIN ONCOL
JI Nat. Rev. Clin. Oncol.
PD OCT
PY 2016
VL 13
IS 10
BP 627
EP 642
DI 10.1038/nrclinonc.2016.79
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DX3CK
UT WOS:000384250300003
PM 27245279
OA hybrid
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Hu, YH
   Gao, QZ
   Ma, S
   Yu, P
   Ding, S
   Yao, XF
   Zhang, ZY
   Lu, SY
   Lu, MM
   Zhang, JH
   Wang, YL
   Qian, XL
   Zhong, JT
AF Hu, Yuhan
   Gao, Qingzu
   Ma, Shuai
   Yu, Pei
   Ding, Shuang
   Yao, Xiaofei
   Zhang, Zheying
   Lu, Shuya
   Lu, Manman
   Zhang, Jinghang
   Wang, Yanling
   Qian, Xinlai
   Zhong, Jiateng
TI FMR1 promotes the progression of colorectal cancer cell by stabilizing
   EGFR mRNA in an m<SUP>6</SUP>A-dependent manner
SO CELL DEATH & DISEASE
LA English
DT Article
ID METASTASIS; GENE; N-6-METHYLADENOSINE; EXPRESSION; CARCINOMA; PATHWAY;
   GROWTH
AB FMR1, a new m(6)A reader, is known to be involved in the regulation of cancer progression. However, its role, regulatory mechanism, and clinical significance in colorectal cancer (CRC) are elusive. Here, we showed that FMR1 was upregulated in CRC, and it promoted proliferation and metastasis of CRC cells in vitro and in vivo. Mechanically, FMR1 recognized the m(6)A-modification site in EGFR mRNA, a key molecule in cancer occurrence and targeted therapy, sustained its stability and maintained its expression in an m(6)A-dependent manner, thereby promoting the tumorigenesis and metastasis of CRC. And the effect of FMR1 knockdown in CRC cells could be abolished by METTL3. Furthermore, FMR1 shRNA plasmid carried by attenuated Salmonella has an effective anti-tumor effect in vivo. Collectively, we identified the METTL3/FMR1/EGFR axis in the progression of CRC. This novel mechanism indicated that the METTL3/FMR1/EGFR axis is a potential target for early therapeutic intervention in CRC progression.
C1 [Hu, Yuhan; Ma, Shuai; Yu, Pei; Ding, Shuang; Yao, Xiaofei; Zhang, Zheying; Lu, Shuya; Lu, Manman; Qian, Xinlai; Zhong, Jiateng] Xinxiang Med Univ, Sch Basic Med Sci, Dept Pathol, Xinxiang 453000, Henan, Peoples R China.
   [Hu, Yuhan; Gao, Qingzu; Zhang, Jinghang; Zhong, Jiateng] Xinxiang Med Univ, Affiliated Hosp 1, Dept Pathol, Xinxiang 453000, Henan, Peoples R China.
   [Hu, Yuhan] Xinxiang Med Univ, Sch Basic Med Sci, Micromorphol Lab, Xinxiang 453000, Henan, Peoples R China.
   [Wang, Yanling] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Anesthesiol, Guangzhou, Guangdong, Peoples R China.
   [Qian, Xinlai] Xinxiang Med Univ, Affiliated Hosp 3, Dept Pathol, Xinxiang 453000, Henan, Peoples R China.
C3 Xinxiang Medical University; Xinxiang Medical University; Xinxiang
   Medical University; Sun Yat Sen University; Xinxiang Medical University
RP Qian, XL; Zhong, JT (corresponding author), Xinxiang Med Univ, Sch Basic Med Sci, Dept Pathol, Xinxiang 453000, Henan, Peoples R China.; Zhong, JT (corresponding author), Xinxiang Med Univ, Affiliated Hosp 1, Dept Pathol, Xinxiang 453000, Henan, Peoples R China.; Wang, YL (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 3, Dept Anesthesiol, Guangzhou, Guangdong, Peoples R China.; Qian, XL (corresponding author), Xinxiang Med Univ, Affiliated Hosp 3, Dept Pathol, Xinxiang 453000, Henan, Peoples R China.
EM wangyl5@mail.sysu.edu.cn; gxlsfyblk@126.com; jtzhong@xxmu.edu.cn
RI Hu, Yuhan/F-1634-2016; Zhong, Jiateng/AAB-2064-2022; wang,
   wei/JBS-7400-2023
FU National Natural Science Foundation of China [81702891, U1804173,
   82072218, 82203350]; Zhongyuan Qianren Jihua of Henan Province
   [ZYQR201810153]; Joint construction project of Henan Medical Science and
   technology research plan [LHGJ20190452]; Henan province young and
   middle-aged health science and technology innovation talent project
   [YXKC2021044]; Natural Science Foundation of Henan Province
   [212300410223, 212300410381]; Science and Technology Program foundation
   of Henan Province [202102310091]; Xinxiang Medical University
   [XYBSKYZZ201820, YJSCX202038Y]; Teaching and Research Cultivation
   Project of School of Basic Medical Sciences, Xinxiang Medical College
   [JCYXYKY202021]; Open Project Program of the Third Affiliated Hospital
   of Xinxiang Medical University [KFKTYB202125]
FX This work was supported by the National Natural Science Foundation of
   China (No. 81702891, U1804173, 82072218, and 82203350), Zhongyuan
   Qianren Jihua of Henan Province (No. ZYQR201810153), Joint construction
   project of Henan Medical Science and technology research plan (No.
   LHGJ20190452), Henan province young and middle-aged health science and
   technology innovation talent project (YXKC2021044), Natural Science
   Foundation of Henan Province (No. 212300410223 and 212300410381),
   Science and Technology Program foundation of Henan Province (No.
   202102310091) and the Xinxiang Medical University (No. XYBSKYZZ201820
   and YJSCX202038Y), Teaching and Research Cultivation Project of School
   of Basic Medical Sciences, Xinxiang Medical College (No. JCYXYKY202021),
   the Open Project Program of the Third Affiliated Hospital of Xinxiang
   Medical University (No. KFKTYB202125).
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   Zhang XX, 2019, J EXP CLIN CANC RES, V38, DOI 10.1186/s13046-019-1218-8
   Zhang ZY, 2016, CANCER LETT, V376, P62, DOI 10.1016/j.canlet.2016.03.022
   Zhao BXS, 2017, NAT REV MOL CELL BIO, V18, P31, DOI 10.1038/nrm.2016.132
   Zhao TS, 2019, CELL DEATH DIS, V10, DOI 10.1038/s41419-019-1418-3
   Zhu YJ, 2019, THERANOSTICS, V9, P3526, DOI 10.7150/thno.32796
NR 46
TC 15
Z9 17
U1 0
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 NOV 8
PY 2022
VL 13
IS 11
AR 941
DI 10.1038/s41419-022-05391-7
PG 14
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 6A0PQ
UT WOS:000880365300001
PM 36347844
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Martinelli, E
   Cremolini, C
   Mazard, T
   Vidal, J
   Virchow, 
   Tougeron, D
   Cuyle, PJ
   Chibaudel, B
   Kim, S
   Ghanem, 
   Asselain, B
   Castagné, C
   Zkik, A
   Khan, S
   Arnold, D
AF Martinelli, E.
   Cremolini, C.
   Mazard, T.
   Vidal, J.
   Virchow, I
   Tougeron, D.
   Cuyle, P-J
   Chibaudel, B.
   Kim, S.
   Ghanem, I
   Asselain, B.
   Castagne, C.
   Zkik, A.
   Khan, S.
   Arnold, D.
TI Real-world first-line treatment of patients with
   BRAF<SUP>V600E</SUP>???????- mutant metastatic colorectal cancer: the
   CAPSTAN CRC study
SO ESMO OPEN
LA English
DT Article
DE metastatic colorectal cancer; observational; BRAF mutation; treatment
   practices; targeted therapy; real world
ID FOLFOXIRI PLUS BEVACIZUMAB; BRAF MUTATION; OPEN-LABEL; SUBGROUP
   ANALYSES; RAS MUTATIONS; CETUXIMAB; SURVIVAL; KRAS; FLUOROURACIL;
   MULTICENTER
AB Background: BRAF(V600E) mutations occur in 8%-12% of metastatic colorectal cancer (mCRC) cases and are associated with poor survival. European guidelines recommend combination (doublet or triplet) chemotherapy plus bevacizumab in first line. However, an unmet need remains for more effective treatments for these patients.Patients and methods: CAPSTAN CRC is a European, retrospective, multicenter, observational study evaluating real -world treatment practices for patients with BRAF(V600E)-mutant mCRC treated between 1 January 2016 and 31 January 2020. The primary objective was to describe first-line treatment patterns. Secondary objectives included describing baseline demographics, mutational testing procedures, treatment effectiveness, and safety. Results: In total, 255 patients (median age 66.0 years; 58.4% female) with BRAF(V600E)-mutant unresectable mCRC from seven countries were included. Most had right-sided tumors (52.5%) and presented with synchronous disease at diagnosis (66.4%). Chemotherapy plus targeted therapy (68.7%) was preferred at first line over chemotherapy alone (31.3%). The main first-line treatments were FOLFOX plus bevacizumab (27.1%) and FOLFOXIRI (folinic acid, 5-fluorouracil, oxaliplatin, irinotecan) with/without bevacizumab (27.1%/19.2%). Median duration of first-line treatment was 4.9 months. Overall, 52.5% received second-line treatment. Across all first-line regimens, progression -free survival (PFS) and overall survival were 6.0 [95% confidence interval (CI) 5.3-6.7] months and 12.9 (95% CI 11.6-14.1) months, respectively. Triplet plus targeted therapy was associated with more adverse events (75.0%) compared with triplet chemotherapy alone (50.0%) and doublet chemotherapy alone (36.1%). Multivariate analysis identified low body mass index and presence of three or more metastatic sites as significant prognostic factors for PFS. Conclusions: This study is, to date, the largest real-world analysis of patients with BRAF(V600E)-mutant mCRC, providing valuable insights into routine first-line treatment practices for these patients. The data highlight the intrinsic aggressiveness of this disease subgroup, confirming results from previous real-world studies and clinical trials, and stressing the urgent need for more effective treatment options in this setting.
C1 [Martinelli, E.] Univ Campania Luigi Vanvitelli, Dept Precis Med, Med Oncol, Naples, Italy.
   [Cremolini, C.] Univ Pisa, Oncol Med, Pisa, Italy.
   [Mazard, T.] Montpellier Univ, Inst Rech Cancerol Montpellier, Inst Canc Montpellier, INSERM, Montpellier, France.
   [Vidal, J.] Hosp Mar IMIM, Dept Med Oncol, CIBERONC, Barcelona, Spain.
   [Virchow, I] Univ Duisburg Essen, Univ Hosp Essen, West German Canc Ctr, Dept Med Oncol, Essen, Germany.
   [Tougeron, D.] Univ Poitiers Hosp, Dept Hepatogastroenterol, Poitiers, France.
   [Tougeron, D.] Univ Poitiers, Poitiers, France.
   [Cuyle, P-J] Imelda Gen Hosp, Gastroenterol & Digest Oncol Dept, Bonheiden, Belgium.
   [Chibaudel, B.] Hop Franco Britann Fdn Cognacq Jay, Dept Med Oncol, Levallois Perret, France.
   [Kim, S.] Ctr Hosp Reg & Univ Besancon, Dept Med Oncol, Besancon, France.
   [Ghanem, I] Hosp Univ La Paz, Dept Med Oncol, Madrid, Spain.
   [Asselain, B.] GINECO, Paris, France.
   [Castagne, C.; Zkik, A.; Khan, S.] Pierre Fabre, Boulogne, France.
   [Arnold, D.] Asklepios Tumorzentrum Hamburg AK Altona, Hamburg, Germany.
C3 Universita della Campania Vanvitelli; University of Pisa; UNICANCER;
   Universite de Montpellier; Institut Regional du Cancer Montpellier / Val
   d'Aurelle (ICM); Institut National de la Sante et de la Recherche
   Medicale (Inserm); CIBER - Centro de Investigacion Biomedica en Red;
   CIBERONC; Hospital del Mar Research Institute; University of Duisburg
   Essen; CHU Poitiers; Universite de Poitiers; Universite de Poitiers;
   Imeldaziekenhuis; Universite de Franche-Comte; CHU Besancon; Hospital
   Universitario La Paz
RP Martinelli, E (corresponding author), Univ Campania Luigi Vanvitelli, Dept Precis Med, Med Oncol, Naples, Italy.
EM erika.martinelli@unicampania.it
RI Ghanem, Ismael/HTS-9038-2023; tougeron, david/ABF-3217-2020; Cremolini,
   Chiara/AAC-1889-2019
OI Kim, Stefano/0000-0003-2851-7119; CREMOLINI, CHIARA/0000-0002-0520-4841;
   Ghanem, Ismael/0000-0002-1859-0737
FU Pierre Fabre
FX This work was supported by Pierre Fabre (no grant number). The authors
   were responsible for all content and editorial decisions and received no
   honoraria for the development of this manuscript. Editorial support was
   provided by Anna Monk of Meditech Media, funded by Pierre Fabre.
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NR 47
TC 10
Z9 10
U1 0
U2 2
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PD DEC
PY 2022
VL 7
IS 6
DI 10.1016/j.esmoop.2022.100603
EA NOV 2022
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 7I6KG
UT WOS:000903993700005
PM 36368253
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Guan, ZH
   Lan, HR
   Chen, XG
   Jiang, XX
   Li, ZQ
   Yu, XF
   Cao, J
   Jin, KT
   Teng, LS
AF Guan, Zhonghai
   Lan, Huanrong
   Chen, Xiangheng
   Jiang, Xiaoxia
   Li, Zhongqi
   Yu, Xiongfei
   Cao, Jiang
   Jin, Ketao
   Teng, Lisong
TI Synergistic effects and mechanism of Danshen injection in combination
   with chemotherapy and antiangiogenic therapy for colon cancer
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
LA English
DT Article
DE Colon carcinoma; Danshen injection; anti-VEGF therapy; chemotherapy;
   synergistic effect; anticoagulant
ID TUMOR-SUPPRESSOR GENES; INTRINSIC MARKERS; LIVER FIBROSIS;
   DRUG-DELIVERY; TANSHINONE-I; HYPOXIA; ASPIRIN; METHYLATION; PERFUSION;
   MODELS
AB Cancer-associated hypercoagulation is a negative factor for anticancer treatment. Anticoagulant therapy might reverse the treatment bottleneck. The efficacy of Danshen injection in combination with chemotherapy and anti-VEGF targeted therapy was evaluated based on a previously established colon carcinoma patient-derived xenografts (PDXs). Immunohistochemistry and pharmacological experiments were conducted to explore the mechanism underlying the synergistic effects of Danshen. Finally, Danshen injection shown significant synergistic effect in combination with bevacizumab and Eloxatin. After Danshen injection combination treatment, hypoxia markers CAIX, GLUT1 and VEGF were suppressed, immunofluorescence expressions of fibrosis markers (PDGF-beta, TGF-beta, TIMP1 and desmin) were suppressed, and tumor vasculatures (visualized by CD31 and alpha-SMA immunostaining) shown more normalization. In addition, no tumor distant metastases (such as, liver, spleen, kidney, lung and brain) were found. In conclusion, we first reported Danshen injection as a novel efficient combination therapy with chemotherapy and anti-VEGF therapy for treatment of metastatic colon carcinoma through several possible mechanisms of improving drug distribution, such as by improving tumor hypercoagulable state and blood flow, by alleviating the tumor stroma fibrosis state, and by enhancing the tumor vasculature normalization effect of anti-VEGF therapy. In addition, Danshen injection showed no side effect of tumor distant metastases.
C1 [Guan, Zhonghai; Jin, Ketao] Zhejiang Univ, Shaoxing Peoples Hosp, Shaoxing Hosp, Dept Gastrointestinal Surg, 568 Zhongxing North Rd, Shaoxing 312000, Zhejiang, Peoples R China.
   [Lan, Huanrong] Zhejiang Univ, Shaoxing Peoples Hosp, Shaoxing Hosp, Dept Breast & Thyroid Surg, Shaoxing, Zhejiang, Peoples R China.
   [Guan, Zhonghai; Jiang, Xiaoxia; Li, Zhongqi; Yu, Xiongfei; Teng, Lisong] Zhejiang Univ, Coll Med, Affiliated Hosp 1, Dept Surg Oncol, 79 Qing Chun Rd, Hangzhou 310003, Zhejiang, Peoples R China.
   [Chen, Xiangheng] Cent S Univ, Dept Minimally Invas Surg, Xiangya Hosp 2, Changsha, Hunan, Peoples R China.
   [Cao, Jiang] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Clin Res Ctr, Hangzhou, Zhejiang, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang University; Central
   South University; Zhejiang University
RP Jin, KT (corresponding author), Zhejiang Univ, Shaoxing Peoples Hosp, Shaoxing Hosp, Dept Gastrointestinal Surg, 568 Zhongxing North Rd, Shaoxing 312000, Zhejiang, Peoples R China.; Teng, LS (corresponding author), Zhejiang Univ, Coll Med, Affiliated Hosp 1, Dept Surg Oncol, 79 Qing Chun Rd, Hangzhou 310003, Zhejiang, Peoples R China.
EM jinketao2001@zju.edu.cn; lsteng@zju.edu.cn
RI Zhang, XZ/HJA-4189-2022; JIANG, xx/KHV-3752-2024
FU National Natural Science Foundation of China [81374014]; Zhejiang
   Provincial Science and Technology Projects [2015C33264, 2017C33212,
   2017C33213]; Zhejiang Provincial Medical and Healthy Science and
   Technology Projects [2013KYA228, 2016KYA180]
FX This work was supported by National Natural Science Foundation of China
   (Grant No. 81374014), Zhejiang Provincial Science and Technology
   Projects (grants no. 2015C33264, 2017C33212 and 2017C33213), and
   Zhejiang Provincial Medical and Healthy Science and Technology Projects
   (Grants No. 2013KYA228 and 2016KYA180).
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NR 34
TC 1
Z9 1
U1 0
U2 8
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1940-5901
J9 INT J CLIN EXP MED
JI Int. J. Clin. Exp. Med.
PY 2017
VL 10
IS 4
BP 6437
EP 6444
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA ET8MJ
UT WOS:000400553200059
DA 2025-01-04
ER

PT J
AU Wu, XY
   Xu, H
   Wu, ZF
   Chen, C
   Liu, JY
   Wu, GN
   Yao, XQ
   Liu, FK
   Li, G
   Shen, L
AF Wu, Xiao Yu
   Xu, Hao
   Wu, Zhen Feng
   Chen, Che
   Liu, Jia Yun
   Wu, Guan Nan
   Yao, Xue Quan
   Liu, Fu Kun
   Li, Gang
   Shen, Liang
TI Formononetin, a novel FGFR2 inhibitor, potently inhibits angiogenesis
   and tumor growth in preclinical models
SO ONCOTARGET
LA English
DT Article
DE formononetin; angiogenesis; breast cancer; FGFR2; Akt
ID COLON-CANCER CELLS; PROMOTES ANGIOGENESIS; PATHWAY; APOPTOSIS;
   TRANSCRIPTION; SUPPRESSES; ACTIVATION; INDUCTION; XENOGRAFT; RECEPTOR
AB Most anti-angiogenic therapies currently being evaluated in clinical trials target vascular endothelial growth factor (VEGF) pathway, however, the tumor vasculature can acquire resistance to VEGF-targeted therapy by shifting to other angiogenesis mechanisms. Therefore, other potential therapeutic agents that block non-VEGF angiogenic pathways need to be evaluated. Here we identified formononetin as a novel agent with potential anti-angiogenic and anti-cancer activities. Formononetin demonstrated inhibition of endothelial cell proliferation, migration, and tube formation in response to basic fibroblast growth factor 2 (FGF2). In ex vivo and in vivo angiogenesis assays, formononetin suppressed FGF2-induced microvessel sprouting of rat aortic rings and angiogenesis. To understand the underlying molecular basis, we examined the effects of formononetin on different molecular components in treated endothelial cell, and found that formononetin suppressed FGF2-triggered activation of FGFR2 and protein kinase B (Akt) signaling. Moreover, formononetin directly inhibited proliferation and blocked the oncogenic signaling pathways in breast cancer cell. In vivo, using xenograft models of breast cancer, formononetin showed growth-inhibitory activity associated with inhibition of tumor angiogenesis. Moreover, formononetin enhanced the effect of VEGFR2 inhibitor sunitinib on tumor growth inhibition. Taken together, our results indicate that formononetin targets the FGFR2-mediated Akt signaling pathway, leading to the suppression of tumor growth and angiogenesis.
C1 [Wu, Xiao Yu; Wu, Zhen Feng; Chen, Che; Liu, Jia Yun; Wu, Guan Nan; Yao, Xue Quan; Liu, Fu Kun] Nanjing Univ Tradit Chinese Med, Affiliated Hosp, Dept Surg Oncol, Nanjing, Jiangsu, Peoples R China.
   [Xu, Hao] Nanjing Med Univ, Affiliated Hosp 1, Dept Gen Surg, Div Gastrointestinal Surg, Nanjing, Jiangsu, Peoples R China.
   [Li, Gang] Nanjing Med Univ, Affiliated Canc Hosp, Jiangsu Canc Hosp, Dept Gen Surg, Nanjing, Jiangsu, Peoples R China.
   [Shen, Liang] Dezhou Univ, Coll Life Sci, Lab Biotechnol & Biol Resource Utilizat Univ Shan, Dezhou, Shandong, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing Medical University;
   Nanjing Medical University; Dezhou University
RP Li, G (corresponding author), Nanjing Med Univ, Affiliated Canc Hosp, Jiangsu Canc Hosp, Dept Gen Surg, Nanjing, Jiangsu, Peoples R China.
EM gangli20150519@sina.com
RI Liu, Shaobo/JUU-5767-2023; wu, 晓煜/HIK-3475-2022
FU National science foundation of China [81402523, 81373990, 81201797];
   Natural Science Foundation of Jiangsu Province [BK20141493(DA14),
   BK2009445]; Jiangsu Province "Six adults just" high peak [2009-D-63];
   Youth Projects of Jiangsu Provincial Health Department [H201065]
FX This project was supported by National science foundation of China
   (81402523 to WXY, 81373990 to WXY, 81201797 to LG), the Natural Science
   Foundation of Jiangsu Province(BK20141493(DA14) to XH) (Jiangsu Province
   "Six adults just" high peak(2009-D-63 to LG), Youth Projects of Jiangsu
   Provincial Health Department (H201065 to LG), the Natural Science
   Foundation of Jiangsu Province (BK2009445 to LG)
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NR 29
TC 71
Z9 73
U1 2
U2 27
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD DEC 29
PY 2015
VL 6
IS 42
BP 44563
EP 44578
DI 10.18632/oncotarget.6310
PG 16
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA DD4QX
UT WOS:000369908800038
PM 26575424
OA Green Published, gold, Green Submitted
DA 2025-01-04
ER

PT J
AU Aprile, G
   Leone, F
   Giampieri, R
   Casagrande, M
   Marino, D
   Faloppi, L
   Cascinu, S
   Fasola, G
   Scartozzi, M
AF Aprile, Giuseppe
   Leone, Francesco
   Giampieri, Riccardo
   Casagrande, Mariaelena
   Marino, Donatella
   Faloppi, Luca
   Cascinu, Stefano
   Fasola, Gianpiero
   Scartozzi, Mario
TI Tracking the 2015 Gastrointestinal Cancers Symposium: bridging cancer
   biology to clinical gastrointestinal oncology
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE colorectal cancer; gastric cancer; ramucirumab; pembrolizumab; target
   therapy; onartuzumab; AMG 337
ID PERIOPERATIVE CHEMOTHERAPY; ESOPHAGOGASTRIC ADENOCARCINOMA; MET
   AMPLIFICATION; GASTRIC-CANCER; PREDICTION; PROGNOSIS; PROGRESS; SURGERY
AB The 2015 Gastrointestinal Cancers Symposium (San Francisco, CA, USA; January 15-17) is the world-class conference co-sponsored by the American Society of Clinical Oncology, the American Society for Radiation Oncology, the American Gastroenterological Association Institute, and the Society of Surgical Oncology, in which the most innovative research results in digestive tract oncology are presented and discussed. In its twelfth edition, the meeting has provided new insights focusing on the underpinning biology and clinical management of gastrointestinal malignancies. More than 3,400 health care professionals gathered from all over the world to share their experiences on how to bridge the recent novelties in cancer biology with everyday medical practice. In this article, the authors report on the most significant advances, didactically moving on three different anatomic tracks: gastroesophageal malignancies, pancreatic and biliary cancers, and colorectal adenocarcinomas.
C1 [Aprile, Giuseppe; Casagrande, Mariaelena; Fasola, Gianpiero] Univ & Gen Hosp, Dept Oncol, I-33100 Udine, Italy.
   [Leone, Francesco; Marino, Donatella] Univ Turin, Med Oncol Dept, Turin, Italy.
   [Leone, Francesco; Marino, Donatella] Inst Canc Res & Treatment, Turin, Italy.
   [Giampieri, Riccardo; Faloppi, Luca; Cascinu, Stefano] Univ Politecn Marche, Med Oncol Unit, Azienda Osped Univ Osped Riuniti, Ancona, Italy.
   [Scartozzi, Mario] Univ Cagliari, Med Oncol Dept, Cagliari, Italy.
   [Scartozzi, Mario] Gen Hosp, Cagliari, Italy.
C3 University of Udine; University Hospital of Udine; University of Turin;
   Marche Polytechnic University; University of Cagliari
RP Aprile, G (corresponding author), Univ & Gen Hosp, Dept Oncol, Piazzale S Maria della Misericordia 15, I-33100 Udine, Italy.
EM aprile.giuseppe@aoud.sanita.fvg.it
RI Cascinu, Stefano/AAN-1923-2020; Leone, Francesco/AAB-2355-2022; Fasola,
   Gianpiero/AAC-3629-2022; LEONE, Francesco/R-3248-2016; Marino,
   Donatella/LSJ-1295-2024; Cascinu, Stefano/G-2399-2017; Faloppi,
   Luca/K-1030-2016
OI LEONE, Francesco/0000-0001-5422-9706; Marino,
   Donatella/0000-0001-6565-0870; Cascinu, Stefano/0000-0003-2215-0731;
   Fasola, Gianpiero/0000-0002-1254-4705; SCARTOZZI,
   MARIO/0000-0001-5977-5546; Faloppi, Luca/0000-0003-3689-3085
CR An X, 2014, CANCER-AM CANCER SOC, V120, P675, DOI 10.1002/cncr.28454
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NR 42
TC 7
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 1149
EP 1156
DI 10.2147/OTT.S82624
PG 8
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA CI8CM
UT WOS:000354995300001
PM 26045669
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Codony-Servat, J
   Cuatrecasas, M
   Asensio, E
   Montironi, C
   Martínez-Cardús, A
   Marín-Aguilera, M
   Horndler, C
   Martínez-Balibrea, E
   Rubini, M
   Jares, P
   Reig, O
   Victoria, I
   Gaba, L
   Martín-Richard, M
   Alonso, V
   Escudero, P
   Fernández-Martos, C
   Feliu, J
   Méndez, JC
   Méndez, M
   Gallego, J
   Salud, A
   Rojo, F
   Castells, A
   Prat, A
   Rosell, R
   García-Albéniz, X
   Camps, J
   Maurel, J
AF Codony-Servat, Jordi
   Cuatrecasas, Miriam
   Asensio, Elena
   Montironi, Carla
   Martinez-Cardus, Anna
   Marin-Aguilera, Mercedes
   Horndler, Carlos
   Martinez-Balibrea, Eva
   Rubini, Michele
   Jares, Pedro
   Reig, Oscar
   Victoria, Ivan
   Gaba, Lydia
   Martin-Richard, Marta
   Alonso, Vicente
   Escudero, Pilar
   Fernandez-Martos, Carlos
   Feliu, Jaime
   Mendez, Jose Carlos
   Mendez, Miguel
   Gallego, Javier
   Salud, Antonieta
   Rojo, Federico
   Castells, Antoni
   Prat, Aleix
   Rosell, Rafael
   Garcia-Albeniz, Xabier
   Camps, Jordi
   Maurel, Joan
TI Nuclear IGF-1R predicts chemotherapy and targeted therapy resistance in
   metastatic colorectal cancer
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE IGF-1R; nuclear internalisation; acquired resistance; colorectal cancer;
   BRAF mutation
ID I RECEPTOR; TRANSCRIPTION FACTOR; MUTATION STATUS; POOR-PROGNOSIS;
   TUMOR-CELLS; INSULIN; COMBINATION; EXPRESSION; INHIBITOR; KRAS
AB Background: Although chemotherapy is the cornerstone treatment for patients with metastatic colorectal cancer (mCRC), acquired chemoresistance is common and constitutes the main reason for treatment failure. Monoclonal antibodies against insulin-like growth factor-1 receptor (IGF-1R) have been tested in pre-treated mCRC patients, but results have been largely deceiving.
   Methods: We analysed time to progression, overall survival, and the mutational status of RAS, BRAF and nuclear p-IGF-1R expression by immunohistochemistry, in 470 metastatic CRC patients. The effect of IGF-1R activation and distribution was also assessed using cellular models of CRC and RNAi for functional validation.
   Results: Nuclear IGF-1R increased in metastatic tumours compared to paired untreated primary tumours, and significantly correlated with poor overall survival in mCRC patients. In vitro, chemo-resistant cell lines presented significantly higher levels of IGF-1R expression within the nuclear compartment, and PIAS3, a protein implicated also in the sumoylation process of intranuclear proteins, contributed to IGF-1R nuclear sequestration, highlighting the essential role of PIAS3 in this process. Intriguingly, we observed that ganitumab, an IGF-1R blocking-antibody used in several clinical trials, and dasatinib, an SRC inhibitor, increased the nuclear localisation of IGF-1R.
   Conclusions: Our study demonstrates that IGF-1R nuclear location might lead to chemotherapy and targeted agent resistance.
C1 [Codony-Servat, Jordi; Marin-Aguilera, Mercedes; Reig, Oscar; Victoria, Ivan; Gaba, Lydia; Prat, Aleix; Maurel, Joan] Univ Barcelona, Hosp Clin, Med Oncol Dept,IDIBAPS, Translat Genom & Targeted Therapeut Solid Tumors, C Villarroel 170, Barcelona 08036, Spain.
   [Codony-Servat, Jordi; Martinez-Cardus, Anna; Martinez-Balibrea, Eva; Rosell, Rafael] Hosp Badalona Germans Trias & Pujol, Inst Catala Oncol, Med Oncol Serv, Crta Canyet S-N, Badalona 08916, Spain.
   [Cuatrecasas, Miriam; Montironi, Carla; Jares, Pedro] Univ Barcelona, Pathol Dept, Hosp Clin & Tumour Bank Biobank, IDIBAPS, C Villarroel 170, Barcelona 08036, Spain.
   [Asensio, Elena; Castells, Antoni; Camps, Jordi] IDIBAPS, CIBERehd, Gastrointestinal & Pancreat Oncol Grp, C Rossello 149-153, Barcelona 08036, Spain.
   [Horndler, Carlos] Hosp Miguel Servet, Pathol Serv, Paseo Isabel Catol 1-3, Zaragoza 50009, Spain.
   [Rubini, Michele] Univ Ferrara, Dept Expt & Diagnost Med, Via Savonarola 9, I-44121 Ferrara, Italy.
   [Martin-Richard, Marta] Hosp Sant Pau, Dept Oncol, C Sant Quinti 89, Barcelona 08026, Spain.
   [Alonso, Vicente] Hosp Miguel Servet, Dept Oncol, Paseo Isabel Catol 1-3, Zaragoza 50009, Spain.
   [Escudero, Pilar] Univ Lozano Blesa, Hosp Clin, Dept Oncol, Av San Juan Bosco 15, Zaragoza 50009, Spain.
   [Fernandez-Martos, Carlos] Inst Valenciano Oncol, Dept Med Oncol, C Prof Beltran Baguena 8, Valencia 46009, Spain.
   [Feliu, Jaime] CIBERONC, Hosp La Paz, Dept Oncol, Pso Castellana 261, Madrid 28046, Spain.
   [Mendez, Jose Carlos] Ctr Oncol Galicia, Dept Oncol, C Doctor Camilo Veiras 1, La Coruna 15009, Spain.
   [Mendez, Miguel] Hosp Mostoles, Dept Oncol, Ri Jucar S-N, Mostoles 28935, Spain.
   [Gallego, Javier] Hosp Elche, Dept Oncol, C Almazara 11, Elche 03203, Spain.
   [Salud, Antonieta] Hosp Arnau Vilanova, Dept Oncol, Av Alcalde Rovira Roure 80, Lleida 25198, Spain.
   [Rojo, Federico] Fdn Jimenez Diaz Univ, Pathol Dept, Av Reyes Catol 2, Madrid 28040, Spain.
   [Garcia-Albeniz, Xabier] Harvard TH Chan Sch Publ Hlth, 677 Huntington Ave, Boston, MA 02115 USA.
   [Camps, Jordi] Univ Autonoma Barcelona, Dept Biol Cellular Fisiol & Immunol, Unitat Biol Cellular & Genet Med, E-08193 Barcelona, Spain.
C3 University of Barcelona; Hospital Clinic de Barcelona; IDIBAPS; Institut
   Catala d'Oncologia; Hospital Germans Trias i Pujol; University of
   Barcelona; Hospital Clinic de Barcelona; IDIBAPS; CIBER - Centro de
   Investigacion Biomedica en Red; CIBEREHD; University of Barcelona;
   Hospital Clinic de Barcelona; IDIBAPS; Miguel Servet University
   Hospital; University of Ferrara; Hospital of Santa Creu i Sant Pau;
   Miguel Servet University Hospital; Lozano Blesa University Clinical
   Hospital; Instituto Valenciano De Oncologia; CIBER - Centro de
   Investigacion Biomedica en Red; CIBERONC; Hospital Universitario La Paz;
   Hospital Universitario de Mostoles; University Hospital Arnau de
   Vilanova; Harvard University; Harvard T.H. Chan School of Public Health;
   Autonomous University of Barcelona
RP Maurel, J (corresponding author), Univ Barcelona, Hosp Clin, Med Oncol Dept,IDIBAPS, Translat Genom & Targeted Therapeut Solid Tumors, C Villarroel 170, Barcelona 08036, Spain.; Camps, J (corresponding author), IDIBAPS, CIBERehd, Gastrointestinal & Pancreat Oncol Grp, C Rossello 149-153, Barcelona 08036, Spain.; Camps, J (corresponding author), Univ Autonoma Barcelona, Dept Biol Cellular Fisiol & Immunol, Unitat Biol Cellular & Genet Med, E-08193 Barcelona, Spain.
EM jcamps@clinic.cat; jmaurel@clinic.cat
RI Martinez-Balibrea, Eva/HHS-5710-2022; Prat, Aleix/P-8561-2014; Rojo,
   Federico/S-6551-2016; Castells, Antoni/ABC-1002-2021; Jares,
   Pedro/T-3778-2019; Salvia, Antonieta/C-6531-2011; Mendez,
   Miguel/M-2603-2019; Camps, Jordi/AAG-3080-2020; Cuatrecasas,
   Miriam/C-9156-2019; Martinez, Anna/AAA-4939-2020; Rubini,
   Michele/AFF-8477-2022; , Mercedes/A-4426-2014; gallego,
   Javier/HKO-0600-2023
OI Rubini, Michele/0000-0003-1448-9516; Garcia-Albeniz,
   Xabier/0000-0002-9814-2343; Maurel, Joan/0000-0002-9413-5592; JARES,
   PEDRO/0000-0002-8401-579X; Reig Torras, Oscar/0000-0003-1166-6943;
   Martinez-Balibrea, Eva/0000-0002-4501-7100; Castells,
   Antoni/0000-0001-8431-2033; Montironi, Carla/0000-0002-1453-2193; Rojo,
   Federico/0000-0001-9989-0290; , Mercedes/0000-0002-2205-3459; gallego,
   Javier/0000-0002-0584-1242
FU Instituto de Salud Carlos III; European Regional Development Fund (ERDF)
   [PI13/01728, CP13/00160, PI14/00783]; Mutua Madrilena [AP75002010];
   European Comission (COLONGEVA); Asociacion Espanola Contra el Cancer;
   Agencia de Gestio d'Ajuts Universitaris i de Recerca [2014 SGR 0903,
   2014 SGR 135]; CERCA Programme/Generalitat de Catalunya; CIBERehd; Pla
   Director d'Oncologia de Catalunya
FX We thank to Drs Cristobal Mezquita, Antonio Postigo and Mayumi Ono for
   the scientific revision of the manuscript. We also thank Dr Albert Abad
   from Hospital Germans Trias i Pujol (Barcelona, Spain) for kindly
   providing cell lines and reagents. This work was supported by Instituto
   de Salud Carlos III and co-funded by the European Regional Development
   Fund (ERDF) (PI13/01728 to JM, CP13/00160 and PI14/00783 to JC), Mutua
   Madrilena (AP75002010 to JM), the European Comission (COLONGEVA to JC),
   Asociacion Espanola Contra el Cancer (to JC), the Agencia de Gestio
   d'Ajuts Universitaris i de Recerca (2014 SGR 0903 and 2014 SGR 135) and
   CERCA Programme/Generalitat de Catalunya, and CIBERehd. Technical
   support was provided by the Banc de Tumors-Biobanc Hospital
   Clinic-IDIBAPS and Xarxa de Bancs de Tumors de Catalunya (XBTC)
   sponsored by Pla Director d'Oncologia de Catalunya.
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NR 36
TC 59
Z9 62
U1 0
U2 20
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD DEC 5
PY 2017
VL 117
IS 12
BP 1777
EP 1786
DI 10.1038/bjc.2017.279
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FP1GH
UT WOS:000417359200007
PM 29123263
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Malik, P
   Phipps, C
   Edginton, A
   Blay, J
AF Malik, Paul
   Phipps, Colin
   Edginton, Andrea
   Blay, Jonathan
TI Pharmacokinetic Considerations for Antibody-Drug Conjugates against
   Cancer
SO PHARMACEUTICAL RESEARCH
LA English
DT Review
DE antibody-drug conjugate; cancer; mechanistic; pharmacokinetic; tumour
ID NEONATAL FC-RECEPTOR; TRANSCAPILLARY ESCAPE RATE; INTERSTITIAL FLUID
   PRESSURE; TRASTUZUMAB EMTANSINE T-DM1; KNOCKOUT MOUSE MODELS;
   MONOCLONAL-ANTIBODY; POPULATION PHARMACOKINETICS; VASCULAR-PERMEABILITY;
   TISSUE DISTRIBUTION; COLON-CANCER
AB Antibody-drug conjugates (ADCs) are ushering in the next era of targeted therapy against cancer. An ADC for cancer therapy consists of a potent cytotoxic payload that is attached to a tumour-targeted antibody by a chemical linker, usually with an average drug-to-antibody ratio (DAR) of 3.5-4. The theory is to deliver potent cytotoxic payloads directly to tumour cells while sparing healthy cells. However, practical application has proven to be more difficult. At present there are only two ADCs approved for clinical use. Nevertheless, in the last decade there has been an explosion of options for ADC engineering to optimize target selection, Fc receptor interactions, linker, payload and more. Evaluation of these strategies requires an understanding of the mechanistic underpinnings of ADC pharmacokinetics. Development of ADCs for use in cancer further requires an understanding of tumour properties and kinetics within the tumour environment, and how the presence of cancer as a disease will impact distribution and elimination. Key pharmacokinetic considerations for the successful design and clinical application of ADCs in oncology are explored in this review, with a focus on the mechanistic determinants of distribution and elimination.
C1 [Malik, Paul; Phipps, Colin; Edginton, Andrea; Blay, Jonathan] Univ Waterloo, Sch Pharm, 10A Victoria St South, Kitchener, ON N2G 1C5, Canada.
   [Phipps, Colin] Abbvie Inc, DMPK & Translat Modeling, N Chicago, IL 60064 USA.
C3 University of Waterloo; AbbVie
RP Edginton, A (corresponding author), Univ Waterloo, Sch Pharm, 10A Victoria St South, Kitchener, ON N2G 1C5, Canada.
EM aedginto@uwaterloo.ca
RI Blay, Jean-Yves/N-3966-2016
OI Malik, Paul/0009-0006-5687-6791
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NR 184
TC 28
Z9 36
U1 4
U2 55
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0724-8741
EI 1573-904X
J9 PHARM RES-DORDR
JI Pharm. Res.
PD DEC
PY 2017
VL 34
IS 12
BP 2579
EP 2595
DI 10.1007/s11095-017-2259-3
PG 17
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry; Pharmacology & Pharmacy
GA FQ5HR
UT WOS:000418390000012
PM 28924691
DA 2025-01-04
ER

PT J
AU Sievers, CK
   Eng, C
AF Sievers, Chelsie K.
   Eng, Cathy
TI Moving towards more personalized approaches in locally advanced and
   metastatic colorectal cancer
SO NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Article; Early Access
AB Colorectal cancer remains a challenging heterogeneous disease with substantial morbidity and mortality. However, progressive advances over the past year have led to marked improvements and overcome challenges previously considered insurmountable. Here, we review key clinical trials in colorectal cancer in 2024, leading to personalized approaches in locally advanced and metastatic disease.
   Adagrasib combined with cetuximab is the first FDA-approved G12C targeted therapy approved for mCRC based on the phase I-II KRYSTAL-1 trial1.The TransMet trial demonstrated improved overall survival and progression-free survival following liver transplant in liver-only mCRC, which might lead to long-term durable responses3.Neoadjuvant nivolumab plus ipilimumab resulted in a 95% major pathologic response rate with no disease recurrences at 26 months in mismatch repair-deficient localized colon cancer in the NICHE-2 trial5.
C1 [Sievers, Chelsie K.; Eng, Cathy] Vanderbilt Univ, Med Ctr, Div Hematol Oncol, Vanderbilt Ingram Canc Ctr, Nashville, TN 37232 USA.
C3 Vanderbilt University
RP Eng, C (corresponding author), Vanderbilt Univ, Med Ctr, Div Hematol Oncol, Vanderbilt Ingram Canc Ctr, Nashville, TN 37232 USA.
EM cathy.eng@vumc.org
OI Eng, Cathy/0000-0003-2335-0612
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   Adam R, 2024, ECLINICALMEDICINE, V72, DOI 10.1016/j.eclinm.2024.102608
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   Yaeger R, 2023, NEW ENGL J MED, V388, P44, DOI 10.1056/NEJMoa2212419
NR 6
TC 0
Z9 0
U1 1
U2 1
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1759-5045
EI 1759-5053
J9 NAT REV GASTRO HEPAT
JI Nat. Rev. Gastroenterol. Hepatol.
PD 2024 NOV 28
PY 2024
DI 10.1038/s41575-024-01025-9
EA NOV 2024
PG 2
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA N7M3K
UT WOS:001366128800001
PM 39609570
DA 2025-01-04
ER

PT J
AU Bernocchi, O
   Sirico, M
   Corona, SP
   Strina, C
   Milani, M
   Cappelletti, MR
   Ferrero, G
   Ziglioli, N
   Cervoni, V
   Macchiavelli, A
   Roviello, G
   Generali, D
AF Bernocchi, Ottavia
   Sirico, Marianna
   Corona, Silvia Paola
   Strina, Carla
   Milani, Manuela
   Cappelletti, Maria Rosa
   Ferrero, Giuseppina
   Ziglioli, Nicoletta
   Cervoni, Valeria
   Macchiavelli, Andrea
   Roviello, Giandomenico
   Generali, Daniele
TI Tumor Type Agnostic Therapy Carrying BRAF Mutation: Case Reports and
   Review of Literature
SO PHARMACEUTICALS
LA English
DT Article
DE intrahepatic cholangiocarcinoma (ICC); Bellini duct carcinoma (BDC) BRAF
   mutation; targeted therapy; next generation sequencing; vemurafenib;
   cobimetinib; dabrafenib; trametinib
ID COLLECTING DUCT CARCINOMA; METASTATIC MELANOMA; PRECISION MEDICINE;
   COLORECTAL-CANCER; PLATINUM SALT; CHOLANGIOCARCINOMA; VEMURAFENIB;
   COMBINATION; GEMCITABINE; INHIBITION
AB Background: Precision medicine is based on molecular and genotypic patient characterization to define specific target treatment. BRAF mutation is an oncogenic driver, and the Cancer Genome Atlas has identified BRAF mutations in different cancer types. Tumor type agnostic therapy is based on targeting genomic alterations, regardless of tumor origin. In this context, novel therapeutic agents including BRAF and MEK inhibitors based on the molecular landscape in solid tumors have been investigated. Case presentation, Case 1: The first case is chemotherapy-refractory, BRAF V600E mutated intrahepaticcholangiocarcinoma treated with vemurafenib and cobimetinib as third line therapy. In this setting the dual BRAF and MEK inhibition resulted in improved progression-free survival and quality of life; Case 2: The second case shows aBRAF G466A mutated Bellini duct carcinoma (BDC), treated with dabrafenib and trametinib in second line therapy. The disease remained under control for 11 months after the first relapse. Discussion: In the literature there is strong evidence that melanoma, colorectal cancer, non small cell lung cancer and anaplastic thyroid cancer with BRAF mutations are good targets for BRAF/MEK pathway inhibitors. The VE-BASKET and ROAR basket trials explored the efficacy of vemurafenib and the combination of dabrafenib/trametinib, respectively, in BRAF V600 mutation-positive cancers other than melanoma, papillary thyroid cancer, colorectal cancer and non small cell lung cancer. Within the concept of tumor type agnostic therapy, we decided to treat our BRAF-mutated tumors with the association of BRAF and MEK inhibitors. Conclusions: Our results confirm the emerging importance of molecular tumor profiling for the successful management of cancer, and the potential of BRAF-targeted therapy in the treatment of rare solid tumors with poor prognosis and no clinical benefit from systemic therapies with.
C1 [Bernocchi, Ottavia; Corona, Silvia Paola; Generali, Daniele] Univ Trieste, Dept Med Surg & Hlth Sci, Piazza Ospitale 1, I-34129 Trieste, Italy.
   [Sirico, Marianna; Strina, Carla; Milani, Manuela; Cappelletti, Maria Rosa; Ziglioli, Nicoletta; Cervoni, Valeria; Generali, Daniele] Azienda Sociosanitaria Territoriale Cremona, Breast Canc Unit, Viale Concordia 1, I-26100 Cremona, Italy.
   [Sirico, Marianna; Strina, Carla; Milani, Manuela; Cappelletti, Maria Rosa; Ziglioli, Nicoletta; Cervoni, Valeria; Generali, Daniele] Azienda Sociosanitaria Territoriale Cremona, Translat Res Unit, Viale Concordia 1, I-26100 Cremona, Italy.
   [Ferrero, Giuseppina] Azienda Sociosanitaria Territoriale Cremona, Dept Anat Pathol, Viale Concordia 1, I-26100 Cremona, Italy.
   [Macchiavelli, Andrea] Azienda Sociosanitaria Territoriale Cremona, Hosp Pharm, Viale Concordia 1, I-26100 Cremona, Italy.
   [Roviello, Giandomenico] Univ Florence, Dept Hlth Sci, Sect Clin Pharmacol & Oncol, Viale Pieraccini 6, I-50139 Florence, Italy.
C3 University of Trieste; University of Florence
RP Bernocchi, O (corresponding author), Univ Trieste, Dept Med Surg & Hlth Sci, Piazza Ospitale 1, I-34129 Trieste, Italy.
EM ottavia.b88@gmail.com; mmed.sir@gmail.com; silcorona@hotmail.it;
   carlastrina@gmail.com; manuelamilani@googlemail.com;
   mariarosacappelletti@gmail.com; g.ferrero@asst-cremona.it;
   n.ziglioli@asst-cremona.it; valeriacervoni89@gmail.com;
   a.machiavelli@asst-cremona.it; giandomenicoroviello@gmail.com;
   dgenerali@units.it
RI Roviello, Giandomenico/AAA-5310-2019; Corona, Silvia/ABD-2358-2020
OI GENERALI, DANIELE/0000-0003-2480-3855; Roviello,
   Giandomenico/0000-0001-5504-8237; generali, daniele/0000-0001-6002-1530
FU MEDnoTE srl (Spin-off-University of Trieste)
FX This work was supported by MEDnoTE srl (Spin-off-University of Trieste).
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NR 47
TC 5
Z9 7
U1 1
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1424-8247
J9 PHARMACEUTICALS-BASE
JI Pharmaceuticals
PD FEB
PY 2021
VL 14
IS 2
AR 159
DI 10.3390/ph14020159
PG 9
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA QO1MB
UT WOS:000622909800001
PM 33669326
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Tao, XF
   Wu, XT
   Huang, T
   Mu, DG
AF Tao, Xuefang
   Wu, Xiaotang
   Huang, Tao
   Mu, Deguang
TI Identification and Analysis of Dysfunctional Genes and Pathways in
   CD8<SUP>+</SUP> T Cells of Non-Small Cell Lung Cancer Based on RNA
   Sequencing
SO FRONTIERS IN GENETICS
LA English
DT Article
DE gene; CD8(+) T cell; non-small cell lung cancer; RNA sequencing; feature
   selection; dysfunctional pathways
ID TUMOR-SUPPRESSIVE FUNCTION; CARLO FEATURE-SELECTION; DIFFERENTIAL
   EXPRESSION; ANTI-PD-L1 ANTIBODY; CHEMOKINE RECEPTOR; COLORECTAL-CANCER;
   TARGETED THERAPY; SURVIVAL; INFILTRATION; CARCINOMA
AB Lung cancer, the most common of malignant tumors, is typically of the non-small cell (NSCLC) type. T-cell-based immunotherapies are a promising and powerful approach to treating NSCLCs. To characterize the CD8(+) T cells of non-small cell lung cancer, we re-analyzed the published RNA-Seq gene expression profiles of 36 CD8(+) T cell isolated from tumor (TIL) samples and 32 adjacent uninvolved lung (NTIL) samples. With an advanced Monte Carlo method of feature selection, we identified the CD8(+) TIL specific expression patterns. These patterns revealed the key dysfunctional genes and pathways in CD8(+) TIL and shed light on the molecular mechanisms of immunity and use of immunotherapy.
C1 [Tao, Xuefang] Shaoxing Univ, Affiliated Hosp, Shaoxing, Peoples R China.
   [Wu, Xiaotang] Shanghai Engn Res Ctr Pharmaceut Translat, Shanghai, Peoples R China.
   [Huang, Tao] Chinese Acad Sci, Shanghai Inst Nutr & Hlth, Shanghai Inst Biol Sci, Shanghai, Peoples R China.
   [Mu, Deguang] Hangzhou Med Coll, Peoples Hosp, Zhejiang Prov Peoples Hosp, Dept Resp Med, Hangzhou, Peoples R China.
C3 Shaoxing University; Shanghai Academy of Science & Technology; Chinese
   Academy of Sciences; Shanghai Institute of Nutrition & Health, CAS;
   Hangzhou Medical College; Zhejiang Provincial People's Hospital
RP Huang, T (corresponding author), Chinese Acad Sci, Shanghai Inst Nutr & Hlth, Shanghai Inst Biol Sci, Shanghai, Peoples R China.; Mu, DG (corresponding author), Hangzhou Med Coll, Peoples Hosp, Zhejiang Prov Peoples Hosp, Dept Resp Med, Hangzhou, Peoples R China.
EM tohuangtao@126.com; mudeguang0314@163.com
RI Mu, D/HHM-9587-2022
FU National Natural Science Foundation of China [81172221, 31701151];
   National Key R&D Program of China [2018YFC0910403]; Shanghai Municipal
   Science and Technology Major Project [2017SHZDZX01]; Shanghai Sailing
   Program [16YF1413800]; Youth Innovation Promotion Association of Chinese
   Academy of Sciences (CAS) [2016245]
FX This study was supported by the National Natural Science Foundation of
   China (Nos. 81172221, 31701151), National Key R&D Program of China
   (2018YFC0910403), Shanghai Municipal Science and Technology Major
   Project (Grant No. 2017SHZDZX01), Shanghai Sailing Program
   (16YF1413800), and The Youth Innovation Promotion Association of Chinese
   Academy of Sciences (CAS) (2016245).
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NR 101
TC 4
Z9 4
U1 0
U2 4
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 MAY 8
PY 2020
VL 11
AR 352
DI 10.3389/fgene.2020.00352
PG 9
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA LT1GT
UT WOS:000536823800001
PM 32457792
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Knickelbein, K
   Tong, JS
   Chen, DS
   Wang, YJ
   Misale, S
   Bardelli, A
   Yu, J
   Zhang, L
AF Knickelbein, Kyle
   Tong, Jingshan
   Chen, Dongshi
   Wang, Yi-Jun
   Misale, Sandra
   Bardelli, Alberto
   Yu, Jian
   Zhang, Lin
TI Restoring PUMA induction overcomes <i>KRAS</i>-mediated resistance to
   anti-EGFR antibodies in colorectal cancer
SO ONCOGENE
LA English
DT Article
ID NF-KAPPA-B; ACQUIRED-RESISTANCE; RAS ONCOGENES; APOPTOSIS; THERAPY;
   INHIBITION; MUTATIONS; CETUXIMAB; MEK; PANITUMUMAB
AB Intrinsic and acquired resistance to anti-EGFR antibody therapy, frequently mediated by a mutant or amplified KRAS oncogene, is a significant challenge in the treatment of colorectal cancer (CRC). However, the mechanism of KRAS-mediated therapeutic resistance is not well understood. In this study, we demonstrate that clinically used anti-EGFR antibodies, including cetuximab and panitumumab, induce killing of sensitive CRC cells through p73-dependent transcriptional activation of the pro-apoptotic Bcl-2 family protein PUMA. PUMA induction and p73 activation are abrogated in CRC cells with acquired resistance to anti-EGFR antibodies due to KRAS alterations. Inhibition of aurora kinases preferentially kills mutant KRAS CRC cells and overcomes KRAS-mediated resistance to anti-EGFR antibodies in vitro and in vivo by restoring PUMA induction. Our results suggest that PUMA plays a critical role in meditating the sensitivity of CRC cells to anti-EGFR antibodies, and that restoration of PUMA-mediated apoptosis is a promising approach to improve the efficacy of EGFR-targeted therapy.
C1 [Knickelbein, Kyle; Tong, Jingshan; Chen, Dongshi; Wang, Yi-Jun; Yu, Jian; Zhang, Lin] UMPC Hillman Canc Ctr, Pittsburgh, PA 15213 USA.
   [Knickelbein, Kyle; Tong, Jingshan; Chen, Dongshi; Wang, Yi-Jun; Yu, Jian; Zhang, Lin] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA 15213 USA.
   [Misale, Sandra] Mem Sloan Kettering Canc, Program Mol Pharmacol, New York, NY 10065 USA.
   [Bardelli, Alberto] IRCCS, Candiolo Canc Inst FPO, I-10060 Candiolo, TO, Italy.
   [Bardelli, Alberto] IRCCS, Dept Oncol, I-10060 Candiolo, TO, Italy.
   [Yu, Jian] Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA 15213 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); University
   of Pittsburgh; Memorial Sloan Kettering Cancer Center; IRCCS Fondazione
   del Piemonte per l'Oncologia; IRCCS Fondazione del Piemonte per
   l'Oncologia; Pennsylvania Commonwealth System of Higher Education
   (PCSHE); University of Pittsburgh
RP Zhang, L (corresponding author), UMPC Hillman Canc Ctr, Pittsburgh, PA 15213 USA.; Zhang, L (corresponding author), Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA 15213 USA.
EM zhanglx@upmc.edu
RI wang, yi/KBB-3614-2024; Chen, Dongshi/B-9843-2015; Yu, Jian/A-8301-2009;
   BARDELLI, Alberto/J-9721-2018; Zhang, Lin/A-7389-2009
OI Tong, Jingshan/0000-0003-1640-5769; Misale, Sandra/0000-0002-6031-0137;
   BARDELLI, Alberto/0000-0003-1647-5070; Zhang, Lin/0000-0003-0018-3903
FU U.S. National Institute of Health [R01CA106348, R01CA172136,
   R01CA203028, R01CA217141, U19AI068021, R01CA215481]; Cotswold
   Foundation; Department of Pharmacology & Chemical Biology, University of
   Pittsburgh School of Medicine;  [P30CA047904]; National Cancer Institute
   [R01CA217141] Funding Source: NIH RePORTER
FX The authors thank our lab members for critical reading. This work is
   supported by U.S. National Institute of Health grants (R01CA106348,
   R01CA172136, R01CA203028, and R01CA217141 to LZ; U19AI068021 and
   R01CA215481 to JY). KK was supported by a fellowship from the Cotswold
   Foundation and the Department of Pharmacology & Chemical Biology,
   University of Pittsburgh School of Medicine. This project used the UPMC
   Hillman Cancer Center shared facilities that were supported in part by
   award P30CA047904.
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NR 44
TC 31
Z9 31
U1 0
U2 10
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD AUG 16
PY 2018
VL 37
IS 33
BP 4599
EP 4610
DI 10.1038/s41388-018-0289-x
PG 12
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA GQ5OV
UT WOS:000441736700008
PM 29755130
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Van der Jeught, K
   Xu, HC
   Li, YJ
   Lu, XB
   Ji, G
AF Van der Jeught, Kevin
   Xu, Han-Chen
   Li, Yu-Jing
   Lu, Xiong-Bin
   Ji, Guang
TI Drug resistance and new therapies in colorectal cancer
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Colorectal cancer; Therapy resistance; Antibody-drug conjugates;
   alpha-amanitin; Tumor micro-environment; Immunotherapy; Checkpoint
   inhibitors; Microbiome
ID THYMIDYLATE SYNTHASE EXPRESSION; TUMOR-INFILTRATING LYMPHOCYTES;
   PHASE-III TRIAL; T-CELL SUBSETS; WILD-TYPE KRAS; MHC CLASS-I;
   MICROSATELLITE INSTABILITY; 1ST-LINE TREATMENT; THYMIDINE PHOSPHORYLASE;
   ANTITUMOR-ACTIVITY
AB Colorectal cancer (CRC) is often diagnosed at an advanced stage when tumor cell dissemination has taken place. Chemo-and targeted therapies provide only a limited increase of overall survival for these patients. The major reason for clinical outcome finds its origin in therapy resistance. Escape mechanisms to both chemo- and targeted therapy remain the main culprits. Here, we evaluate major resistant mechanisms and elaborate on potential new therapies. Amongst promising therapies is alpha-amanitin antibody-drug conjugate targeting hemizygous p53 loss. It becomes clear that a dynamic interaction with the tumor microenvironment exists and that this dictates therapeutic outcome. In addition, CRC displays a limited response to checkpoint inhibitors, as only a minority of patients with microsatellite instable high tumors is susceptible. In this review, we highlight new developments with clinical potentials to augment responses to checkpoint inhibitors.
C1 [Van der Jeught, Kevin; Xu, Han-Chen; Li, Yu-Jing; Lu, Xiong-Bin; Ji, Guang] Shanghai Univ Tradit Chinese Med, Inst Digest Dis, Longhua Hosp, 725 South Wanping Rd, Shanghai 200032, Peoples R China.
   [Van der Jeught, Kevin; Xu, Han-Chen; Li, Yu-Jing; Lu, Xiong-Bin] Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
   [Lu, Xiong-Bin] Indiana Univ Sch Med, Indiana Univ Melvin & Bren Simon Canc Ctr, Indianapolis, IN 46202 USA.
C3 Shanghai University of Traditional Chinese Medicine; Indiana University
   System; Indiana University Bloomington; Indiana University System;
   Indiana University Bloomington
RP Ji, G (corresponding author), Shanghai Univ Tradit Chinese Med, Inst Digest Dis, Longhua Hosp, 725 South Wanping Rd, Shanghai 200032, Peoples R China.
EM jiliver@vip.sina.com
RI Van der Jeught, Kevin/Y-1212-2019; Lu, Xiaoyu/GOJ-7569-2022; Li,
   Yujing/L-2221-2019
FU National Natural Science Foundation of China [81620108030]
FX Supported by the National Natural Science Foundation of China, No.
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NR 141
TC 424
Z9 445
U1 6
U2 109
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD SEP 14
PY 2018
VL 24
IS 34
BP 3834
EP 3848
DI 10.3748/wjg.v24.i34.3834
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GT5IG
UT WOS:000444540100003
PM 30228778
OA Green Submitted, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Jiang, WQ
   Liu, PX
   Zhao, ZX
   Fan, DM
   He, XL
   Jiang, YH
   Yang, T
AF Jiang, Weiqing
   Liu, Pingxian
   Zhao, Zhangxun
   Fan, Dongmei
   He, Xinlian
   Jiang, Yunhan
   Yang, Tao
TI Design, synthesis, and biological evaluation of novel
   (E)-2-cyano-3-(4,9-dioxo-4,9-dihydronaphtho[2,3-b]furan-2-yl)
   derivatives as potent STAT3-targeting anticolorectal cancer agents
SO BIOORGANIC CHEMISTRY
LA English
DT Article
DE STAT3 inhibitors; Napabucasin; Hybridization; ROS; Colorectal cancer
ID INHIBITOR; STAT3; WP1066; GROWTH; ROS
AB Dysregulation of signal transducer and activator of transcription 3 (STAT3) is implicated in the pathogenesis of various cancers, underscoring its potential as a cancer therapeutic target. In this work, we designed and synthesized a novel series of (E)-2-cyano-3-(4,9-dioxo-4,9-dihydronaphtho[2,3-b]furan-2-yl) derivatives and evaluated their anti-proliferative effects on tumour cells. Among these derivatives, NW16 exhibited remarkable antiproliferative activity against HCT116 cells, with an IC50 value of 0.28 mu M, and exhibited dose- and time- dependent inhibition of the JAK/STAT3 signalling pathway. In addition, NW16 induced reactive oxygen species (ROS) production, which subsequently suppressed the ROS-dependent PI3K/AKT pathway and enhanced its antitumour efficacy. In vivo studies confirmed significant tumour-suppressive effects upon oral administration of NW16 along with favourable tolerability in a colorectal cancer xenograft model. These results indicate that NW16 could be a promising candidate for developing targeted therapy for colorectal cancer because of its multifaceted mechanism.
C1 [Jiang, Weiqing; Liu, Pingxian; Zhao, Zhangxun; Fan, Dongmei; He, Xinlian; Jiang, Yunhan; Yang, Tao] Sichuan Univ, West China Hosp, Lab Human Dis & Immunotherapy, Chengdu 610041, Peoples R China.
   [He, Xinlian; Yang, Tao] Sichuan Univ, West China Hosp, State Key Lab Biotherapy & Canc Ctr, Chengdu 610041, Peoples R China.
   [Jiang, Yunhan; Yang, Tao] Sichuan Univ, West China Hosp, Dept Cardiovasc Surg, Chengdu 610041, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University
RP Jiang, YH; Yang, T (corresponding author), Sichuan Univ, West China Hosp, Lab Human Dis & Immunotherapy, Chengdu 610041, Peoples R China.
EM jiangyunhan@wchscu.cn; yangtao@wchscu.cn
FU National Natural Science Foundation of China [21977076]
FX This work was financially supported by grants from the National Natural
   Science Foundation of China (21977076) . We extend our grat-itude to
   Qifeng Liu and Feijing Su from the Core Facilities of West China
   Hospital for their assistance with NMR recording, and to Qianlun Pu and
   Fei Fu from the Mass Spectrometry Center of West China Hospital for
   their help with HRMS recording.
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NR 51
TC 0
Z9 0
U1 2
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0045-2068
EI 1090-2120
J9 BIOORG CHEM
JI Bioorganic Chem.
PD DEC
PY 2024
VL 153
AR 107955
DI 10.1016/j.bioorg.2024.107955
EA NOV 2024
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Organic
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA N3V9C
UT WOS:001363665300001
PM 39577151
DA 2025-01-04
ER

PT J
AU Faugeras, L
   Dili, A
   Druez, A
   Krug, B
   Decoster, C
   D'Hondt, L
AF Faugeras, L.
   Dili, A.
   Druez, A.
   Krug, B.
   Decoster, C.
   D'Hondt, L.
TI Treatment options for metastatic colorectal cancer in patients with
   liver dysfunction due to malignancy
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Hepatic dysfunction; Chemotherapy; Hyperbilirubinaemia; Monoclonal
   antibodies; Targeted therapy
ID 1ST-LINE TREATMENT; HEPATIC-DYSFUNCTION; OXALIPLATIN XELOX; PLUS
   IRINOTECAN; PHASE-I; CETUXIMAB; EFFICACY; BEVACIZUMAB; 5-FLUOROURACIL;
   SAFETY
AB Background: The survival of colorectal cancer patients is frequently determined by the extent of metastatic invasion to the liver; in cases of major involvement, therapeutic strategies are limited because the liver is necessary for drug metabolism.
   Material and methods: We have reviewed articles about the pharmacokinetic profiles of each drug used in colorectal cancer patients with hepatic dysfunction to determine which of these treatments are most feasible.
   Results: Some drugs appear to be feasible options for patients with hepatic insufficiency. Agents such as 5-fluorouracil and oxaliplatin, as well as monoclonal antibodies such as bevacizumab, cetuximab, and panitumumab, can potentially be used in these cases. On the other hand, irinotecan and regorafenib cannot be recommended because of the risk of increased toxicity.
   Conclusion: Treatment of patients with colorectal cancer and liver dysfunction represents a major challenge because the prognosis is usually very poor and alteration of liver function is normally an exclusion criterion in clinical trials. In this review, we present evidence regarding the use of each drug in patients with colorectal cancer and hepatic impairment. (C) 2017 The Author(s). Published by Elsevier Ireland Ltd.
C1 [Faugeras, L.; D'Hondt, L.] CHU Dinant Godinne UCL Namur, Oncol Dept, 1 Rue Gaston Therasse, B-5530 Yvoir, Belgium.
   [Dili, A.] CHU Dinant Godinne UCL Namur, Serv Surg, Endocrinol, Yvoir, Belgium.
   [Druez, A.] CHU Dinant Godinne UCL Namur, Serv Gastroenterol, Yvoir, Belgium.
   [Krug, B.] CHU Dinant Godinne UCL Namur, Div Nucl Med, Yvoir, Belgium.
   [Decoster, C.] CHU Dinant Godinne UCL Namur, Pharm Dept, Yvoir, Belgium.
RP Faugeras, L (corresponding author), CHU Dinant Godinne UCL Namur, Oncol Dept, 1 Rue Gaston Therasse, B-5530 Yvoir, Belgium.
EM Laurence.faugeras@uclouvain.be
RI Dili, Alexandra/IZE-6464-2023
CR [Anonymous], STIVARGA BAYER HEALT
   [Anonymous], ONCOLOGY WILLISTON P
   [Anonymous], COURS CHIMIOTHERAPIE
   [Anonymous], CLIN COLORECTAL CANC
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NR 76
TC 23
Z9 23
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD JUL
PY 2017
VL 115
BP 59
EP 66
DI 10.1016/j.critrevonc.2017.03.029
PG 8
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA EZ1XJ
UT WOS:000404503800007
PM 28602170
OA hybrid
DA 2025-01-04
ER

PT J
AU Yang, Y
   Wang, HY
   Chen, YK
   Chen, JJ
   Song, C
   Gu, J
AF Yang, Yong
   Wang, Han-Yang
   Chen, Yong-Kang
   Chen, Jia-Jia
   Song, Can
   Gu, Jin
TI Current status of surgical treatment of rectal cancer in China
SO CHINESE MEDICAL JOURNAL
LA English
DT Review
DE Rectal cancer; Incidence trend; Early screening; Surgical treatment
ID TOTAL MESORECTAL EXCISION; TRANSANAL ENDOSCOPIC MICROSURGERY; MINIMALLY
   INVASIVE SURGERY; MRC CLASICC TRIAL; COLORECTAL-CANCER; NEOADJUVANT
   CHEMORADIATION; PREOPERATIVE RADIOTHERAPY; RANDOMIZED-TRIAL;
   ABDOMINOPERINEAL RESECTION; SUBMUCOSAL DISSECTION
AB With the changing lifestyle and the acceleration of aging in the Chinese population, the incidence and mortality of colorectal cancer (CRC) have risen in the last decades. On the contrary, the incidence and mortality of CRC have continued to decline in the USA since the 1980s, which is mainly attributed to early screening and standardized diagnosis and treatment. Rectal cancer accounts for the largest proportion of CRC in China, and its treatment regimens are complex. At present, surgical treatment is still the most important treatment for rectal cancer. Since the first Chinese guideline for diagnosis and treatment of CRC was issued in 2010, the fourth version has been revised in 2020. These guidelines have greatly promoted the standardization and internationalization of CRC diagnosis and treatment in China. And with the development of comprehensive treatment methods such as neoadjuvant chemoradiotherapy, targeted therapy, and immunotherapy, the post-operative quality of life and prognosis of patients with rectal cancer have improved. We believe that the inflection point of the rising incidence and mortality of rectal cancer will appear in the near future in China. This article reviewed the current status and research progress on surgical therapy of rectal cancer in China.
C1 [Yang, Yong; Wang, Han-Yang; Chen, Yong-Kang; Chen, Jia-Jia; Gu, Jin] Peking Univ, Gastrointestinal Canc Ctr, Minist Educ, Key Lab Carcinogenesis & Translat Res,Canc Hosp, Beijing 100142, Peoples R China.
   [Song, Can] Tsinghua Univ, Sch Life Sci, Beijing 100142, Peoples R China.
   [Song, Can; Gu, Jin] Peking Univ, Int Canc Ctr, Peking Tsinghua Ctr Life Sci, Beijing 100142, Peoples R China.
   [Gu, Jin] Peking Univ, Shougang Hosp, Dept Gastrointestinal Surg, Beijing 100144, Peoples R China.
C3 Peking University; Tsinghua University; Peking University; Peking
   University
RP Gu, J (corresponding author), Peking Univ, Gastrointestinal Canc Ctr, Minist Educ, Key Lab Carcinogenesis & Translat Res,Canc Hosp, Beijing 100142, Peoples R China.; Gu, J (corresponding author), Peking Univ, Int Canc Ctr, Peking Tsinghua Ctr Life Sci, Beijing 100142, Peoples R China.; Gu, J (corresponding author), Peking Univ, Shougang Hosp, Dept Gastrointestinal Surg, Beijing 100144, Peoples R China.
EM zlgujin@126.com
FU Beijing Municipal Science AMP; Technology Commission, Clinical
   Application and Development of Capital Characteristic [Z171100001017087]
FX This work was supported by grants from the Beijing Municipal Science &
   Technology Commission, Clinical Application and Development of Capital
   Characteristic (No. Z171100001017087).
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NR 110
TC 28
Z9 33
U1 1
U2 38
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0366-6999
EI 2542-5641
J9 CHINESE MED J-PEKING
JI Chin. Med. J.
PD NOV 20
PY 2020
VL 133
IS 22
BP 2703
EP 2711
DI 10.1097/CM9.0000000000001076
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA OL6TT
UT WOS:000585470400010
PM 32889914
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Galbán, S
   Apfelbaum, AA
   Espinoza, C
   Heist, K
   Haley, H
   Bedi, K
   Ljungman, M
   Galbán, CJ
   Luker, GD
   Van Dort, M
   Ross, BD
AF Galban, Stefanie
   Apfelbaum, April A.
   Espinoza, Carlos
   Heist, Kevin
   Haley, Henry
   Bedi, Karan
   Ljungman, Mats
   Galban, Craig J.
   Luker, Gary D.
   Van Dort, Marcian
   Ross, Brian D.
TI A Bifunctional MAPK/PI3K Antagonist for Inhibition of Tumor Growth and
   Metastasis
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID MEK INHIBITOR; NEGATIVE FEEDBACK; TARGETED THERAPY; CANCER CELLS; BRAF;
   COMBINATION; ACTIVATION; TRAMETINIB; RESISTANCE; DISCOVERY
AB Responses to targeted therapies frequently are brief, with patients relapsing with drug-resistant tumors. For oncogenic MEK and BRAF inhibition, drug resistance commonly occurs through activation of PI3K/AKT/mTOR signaling and immune checkpoint modulation, providing a robust molecular target for concomitant therapy. Here, we evaluated the efficacy of a bifunctional kinase inhibitor (ST-162) that concurrently targets MAPK and PI3K signaling pathways. Treatment with ST-162 produced regression of mutant KRAS-or BRAF-addicted xenograft models of colorectal cancer and melanoma and stasis of BRAF/PTEN-mutant melanomas. Combining ST-162 with immune checkpoint blockers further increased efficacy in a syngeneic KRAS-mutant colorectal cancer model. Nascent transcriptome analysis revealed a unique gene set regulated by ST-162 related to melanoma metastasis. Subsequent mouse studies revealed ST-162 was a potent inhibitor of melanoma metastasis to the liver. These findings highlight the significant potential of a single molecule with multikinase activity to achieve tumor control, overcome resistance, and prevent metastases through modulation of interconnected cell signaling pathways. (C) 2017 AACR.
C1 [Galban, Stefanie; Apfelbaum, April A.; Espinoza, Carlos; Heist, Kevin; Haley, Henry; Galban, Craig J.; Luker, Gary D.; Van Dort, Marcian; Ross, Brian D.] Univ Michigan, Sch Med, Ctr Mol Imaging, Ann Arbor, MI 48109 USA.
   [Galban, Stefanie; Apfelbaum, April A.; Espinoza, Carlos; Heist, Kevin; Haley, Henry; Galban, Craig J.; Luker, Gary D.; Van Dort, Marcian; Ross, Brian D.] Univ Michigan, Dept Radiol, Sch Med, Ann Arbor, MI 48109 USA.
   [Bedi, Karan; Ljungman, Mats] Univ Michigan, Dept Radiat Oncol, Sch Med, Ann Arbor, MI 48109 USA.
   [Galban, Craig J.] Univ Michigan, Sch Med, Dept Biomed Engn, Ann Arbor, MI 48109 USA.
   [Luker, Gary D.] Univ Michigan, Sch Med, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA.
   [Ross, Brian D.] Univ Michigan, Sch Med, Dept Biol Chem, Ann Arbor, MI 48109 USA.
C3 University of Michigan System; University of Michigan; University of
   Michigan System; University of Michigan; University of Michigan System;
   University of Michigan; University of Michigan System; University of
   Michigan; University of Michigan System; University of Michigan;
   University of Michigan System; University of Michigan
RP Ross, BD (corresponding author), Univ Michigan, Sch Med, Ann Arbor, MI 48109 USA.
EM bdross@med.umich.edu
RI Bedi, Karan/AAA-3331-2022
OI luker, gary/0000-0001-6832-2581; Bedi, Karan/0000-0002-7843-738X; Heist,
   Kevin/0000-0001-5161-0608
FU NIH/NCI [P01CA085878, R35CA197701, R01CA170198, R01CA196018,
   R01CA195655]; National Cancer Institute [P30CA046592, R35CA197701]
   Funding Source: NIH RePORTER
FX This work was supported in part by NIH/NCI grants P01CA085878,
   R35CA197701, R01CA170198, R01CA196018, and R01CA195655.
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NR 46
TC 15
Z9 17
U1 0
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
EI 1538-8514
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD NOV
PY 2017
VL 16
IS 11
BP 2340
EP 2350
DI 10.1158/1535-7163.MCT-17-0207
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FL5CK
UT WOS:000414248500002
PM 28775144
OA Bronze, Green Submitted, Green Accepted
DA 2025-01-04
ER

PT J
AU Zhang, JP
   Zou, SM
   Fang, LK
AF Zhang, Jieping
   Zou, Shaomin
   Fang, Lekun
TI Metabolic reprogramming in colorectal cancer: regulatory networks and
   therapy
SO CELL AND BIOSCIENCE
LA English
DT Review
DE Colorectal cancer; Metabolic reprogramming; Metabolic enzymes; Signal
   transduction; Targeted therapy
ID PENTOSE-PHOSPHATE PATHWAY; FATTY-ACID SYNTHASE; PYRUVATE-KINASE M2;
   COLON-CANCER; AEROBIC GLYCOLYSIS; MALIC ENZYME; TRANSCRIPTIONAL
   REGULATION; GLUTAMINE-METABOLISM; CELL PROLIFERATION; TUMOR PROGRESSION
AB With high prevalence and mortality, together with metabolic reprogramming, colorectal cancer is a leading cause of cancer-related death. Metabolic reprogramming gives tumors the capacity for long-term cell proliferation, making it a distinguishing feature of cancer. Energy and intermediate metabolites produced by metabolic reprogramming fuel the rapid growth of cancer cells. Aberrant metabolic enzyme-mediated tumor metabolism is regulated at multiple levels. Notably, tumor metabolism is affected by nutrient levels, cell interactions, and transcriptional and posttranscriptional regulation. Understanding the crosstalk between metabolic enzymes and colorectal carcinogenesis factors is particularly important to advance research for targeted cancer therapy strategies via the investigation into the aberrant regulation of metabolic pathways. Hence, the abnormal roles and regulation of metabolic enzymes in recent years are reviewed in this paper, which provides an overview of targeted inhibitors for targeting metabolic enzymes in colorectal cancer that have been identified through tumor research or clinical trials.
C1 [Zhang, Jieping; Zou, Shaomin; Fang, Lekun] Sun Yat Sen Univ, Affiliated Hosp 6, Dept Gen Surg, Guangdong Prov Key Lab Colorectal & Pelv Floor Dis, 26 Yuanchun Er Heng Rd, Guangzhou 510655, Guangdong, Peoples R China.
   [Zhang, Jieping; Zou, Shaomin; Fang, Lekun] Guangdong Inst Gastroenterol, Guangzhou 510655, Peoples R China.
C3 Sun Yat Sen University
RP Fang, LK (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 6, Dept Gen Surg, Guangdong Prov Key Lab Colorectal & Pelv Floor Dis, 26 Yuanchun Er Heng Rd, Guangzhou 510655, Guangdong, Peoples R China.; Fang, LK (corresponding author), Guangdong Inst Gastroenterol, Guangzhou 510655, Peoples R China.
EM fanglk3@mail.sysu.edu.cn
RI Zhang, Jieping/KII-8464-2024
OI Zhang, Jieping/0000-0003-2559-4151
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NR 225
TC 16
Z9 16
U1 5
U2 30
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2045-3701
J9 CELL BIOSCI
JI Cell Biosci.
PD FEB 8
PY 2023
VL 13
IS 1
AR 25
DI 10.1186/s13578-023-00977-w
PG 21
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 8S6ZC
UT WOS:000928725900001
PM 36755301
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Bayraktar-Ekincioglu, A
   Kucuk, E
AF Bayraktar-Ekincioglu, A.
   Kucuk, E.
TI The differences in the assessments of side effects at an oncology
   outpatient clinic
SO INTERNATIONAL JOURNAL OF CLINICAL PHARMACY
LA English
DT Article
DE Assessment; Immunotherapy; Nurse; Pharmacist; Side effects; Targeted
   therapy; Turkey
ID LONG-TERM SAFETY; METASTATIC COLORECTAL-CANCER; RENAL-CELL CARCINOMA;
   ADVERSE EVENTS; ADVANCED MELANOMA; TARGETED THERAPY; CARE; PATIENT;
   CHEMOTHERAPY; PANITUMUMAB
AB Background There is a growing interest in the use of targeted and immunotherapies in oncology. However, the assessment of side effects can be different due to interpretation of patients' health status by healthcare professionals in oncology outpatient clinics. Objective To demonstrate the differences in the assessments of side effects conducted independently by a clinical pharmacist and nurses in patients who receive targeted therapies at an oncology outpatient clinic. Setting The study was conducted at the University Oncology Hospital in an outpatient clinic from October 2015 to March 2016. Method Patients receiving ipilimumab, nivolumab, pembrolizumab, bevacizumab, panitumumab or cetuximab during study period were included. The assessment of side effects was conducted by a pharmacist and nurse independently using the NCI-CTCAE version-2. Main outcome measure To compare the severity assessments of side effects between a clinical pharmacist and nurses in an outpatient clinic. Results During the study, 204 visits for 43 patients with a total of 5508 side effect assessments were recorded where 1137 (20.64%) assessments were graded differently. Out of 1137 assessments, 473 of them were graded higher by a clinical pharmacist whereas 664 were graded higher by nurses. Statistically significant differences were detected in the assessment of vomiting, taste changes, sense changes, alopecia, fatigue, mood changes, anxiety, hearing impairment, and allergic reactions. Conclusion An assessment of side effects by healthcare providers in patients with cancer may be challenging due to an increased workload in clinics and undistinguishable symptoms of side effects and cancer itself. Therefore, a new care model which increases an interprofessional communication may improve pharmaceutical care in oncology outpatient clinics.
C1 [Bayraktar-Ekincioglu, A.; Kucuk, E.] Hacettepe Univ, Dept Clin Pharm, Fac Pharm, TR-06100 Ankara, Turkey.
C3 Hacettepe University
RP Bayraktar-Ekincioglu, A (corresponding author), Hacettepe Univ, Dept Clin Pharm, Fac Pharm, TR-06100 Ankara, Turkey.
EM aygin@hacettepe.edu.tr
FU Hacettepe University Scientific Research Coordination Unit
   [TKG-2016-11039]
FX This work was funded by Hacettepe University Scientific Research
   Coordination Unit. Project Number: TKG-2016-11039.
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NR 29
TC 7
Z9 7
U1 0
U2 9
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 2210-7703
EI 2210-7711
J9 INT J CLIN PHARM-NET
JI Int. J. Clin. Phar,.
PD APR
PY 2018
VL 40
IS 2
BP 386
EP 393
DI 10.1007/s11096-018-0590-3
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA GE1QC
UT WOS:000430990800010
PM 29353396
DA 2025-01-04
ER

PT J
AU Ding, Y
   Chen, GL
AF Ding, Yi
   Chen, Guoli
TI Molecular testing panel in colorectal cancer
SO HUMAN PATHOLOGY REPORTS
LA English
DT Review
DE Colorectal cancer; Molecular genetic testing; Next generation
   sequencing; Targeted therapy and immunotherapy
ID MUTATIONS; BLOCKADE; ASSOCIATION; MULTICENTER; ANTIBODY; THERAPY;
   SAFETY; TUMORS
AB Mainly driven by the clinical need, molecular genetic testing has been integrated into the standard patient care of cancer management including colorectal cancer (CRC) for various clinical purposes. A proper selection of anticancer therapies relies on information achieved by molecular genetic analysis. Also, molecular findings are often necessary or helpful in screening, diagnosis and prognosis of CRC and related diseases/syndromes. New molecular classification may profoundly alter the current understanding and clinical management of CRC. As a powerful sequencing tool, next generation sequencing has become the main platform of conducting cancer related molecular diagnostic tests. In this review, molecular biomarkers widely used in the current practice of CRC management are briefly discussed according to their clinical significance.
C1 [Ding, Yi] Geisinger Hlth, Dept Lab Med, Danville, PA USA.
   [Chen, Guoli] Penn State Hlth, Dept Pathol & Lab Med, Hershey, PA USA.
RP Chen, GL (corresponding author), Penn State Univ, Coll Med, Penn State Hlth Hershey Med Ctr, Dept Pathol & Lab Med, 500 Univ Dr, Hershey, PA 17033 USA.
EM gchen1@pennstatehealth.psu.edu
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NR 49
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2772-736X
J9 HUM PATHOL REP
JI Hum. Pathol. Rep.
PD JUN
PY 2022
VL 28
AR 300632
DI 10.1016/j.hpr.2022.300632
PG 5
WC Pathology
WE Emerging Sources Citation Index (ESCI)
SC Pathology
GA P7P7O
UT WOS:001379788100006
OA gold
DA 2025-01-04
ER

PT J
AU Nappi, A
   Berretta, M
   Romano, C
   Tafuto, S
   Cassata, A
   Casaretti, R
   Silvestro, L
   De Divitiis, C
   Alessandrini, L
   Fiorica, F
   Ottaiano, A
   Nasti, G
AF Nappi, Anna
   Berretta, Massimiliano
   Romano, Carmela
   Tafuto, Salvatore
   Cassata, Antonino
   Casaretti, Rossana
   Silvestro, Lucrezia
   De Divitiis, Chiara
   Alessandrini, Lara
   Fiorica, Francesco
   Ottaiano, Alessandro
   Nasti, Guglielmo
TI Metastatic Colorectal Cancer: Role of Target Therapies and Future
   Perspectives
SO CURRENT CANCER DRUG TARGETS
LA English
DT Review
DE Colorectal cancer; monoclonal antibodies; target therapy; treatment;
   anti-VEGF drugs; anti-EGFR
ID ENDOTHELIAL GROWTH-FACTOR; PHASE-III TRIAL; OXALIPLATIN-BASED
   CHEMOTHERAPY; CETUXIMAB PLUS IRINOTECAN; WILD-TYPE KRAS; 1ST-LINE
   TREATMENT; PANITUMUMAB PLUS; ELDERLY-PATIENTS; OLDER PATIENTS;
   OPEN-LABEL
AB Today, we are experiencing a real cultural revolution in the therapeutic approach to cancer of the colon - rectum, that by orphan disease, it is now becoming an important paradigm of scientific innovations and concepts.
   Survival of patients with metastatic colorectal cancer (m-CRC) has been significantly improved with the introduction of the monoclonal antibodies that have as target the vascular endothelial growth factor (VEGF) and the epidermal growth factor receptor (EGFR).
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   We can say that, among the various treatment options, the challenge of the future will be a better selection of the population, to ensure the best possible benefit from treatment with anti-VEGF drugs or anti-EGFR and a careful and customized planning of the therapeutic strategy for each patient.
C1 [Nappi, Anna; Romano, Carmela; Tafuto, Salvatore; Cassata, Antonino; Casaretti, Rossana; Silvestro, Lucrezia; De Divitiis, Chiara; Ottaiano, Alessandro; Nasti, Guglielmo] Natl Canc Inst G Pascale Fdn, Abdominal Dept, Med Oncol, I-80131 Naples, Italy.
   [Berretta, Massimiliano] Natl Canc Inst Aviano, Dept Med Oncol, I-33081 Aviano, PN, Italy.
   [Berretta, Massimiliano] Grp Oncol Ricercatori Italiani, Pordenone, PN, Italy.
   [Alessandrini, Lara] Natl Canc Inst, Div Pathol, Aviano, PN, Italy.
   [Fiorica, Francesco] St Anna Hosp, Div Radiotherapy, Ferrara, Italy.
C3 IRCCS Fondazione Pascale; IRCCS Aviano (CRO); University of Ferrara;
   Arcispedale Sant'Anna
RP Nasti, G (corresponding author), Natl Canc Inst Naples, Dept Abdominal Med Oncol, Via M Semmola, I-80131 Naples, Italy.
EM guglielmo.nasti@libero.it
RI fiorica, francesco/K-8036-2016; Berretta, Massimiliano/S-5853-2019
OI Berretta, Massimiliano/0000-0002-9837-9148; Ottaiano,
   Alessandro/0000-0002-2901-3855
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NR 68
TC 48
Z9 51
U1 0
U2 11
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1568-0096
EI 1873-5576
J9 CURR CANCER DRUG TAR
JI Curr. Cancer Drug Targets
PY 2018
VL 18
IS 5
BP 421
EP 429
DI 10.2174/1568009617666170209095143
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GH0KY
UT WOS:000433092100004
PM 28183254
DA 2025-01-04
ER

PT J
AU Wu, GN
   Liu, JY
   Wu, ZF
   Wu, XY
   Yao, XQ
AF Wu, Guannan
   Liu, Jiayun
   Wu, Zhenfeng
   Wu, Xiaoyu
   Yao, Xuequan
TI MicroRNA-184 inhibits cell proliferation and metastasis in human
   colorectal cancer by directly targeting IGF-1R
SO ONCOLOGY LETTERS
LA English
DT Article
DE microRNA-184; insulin-like growth factor 1 receptor; proliferation;
   metastasis; colorectal cancer
ID MATURE MIR-184; GROWTH; INSULIN; RECEPTOR; EXPRESSION; CARCINOMA; RNAS;
   IDENTIFICATION; STATISTICS; PREVENTION
AB Colorectal cancer is currently the third most common cancer in males and the second in females worldwide. In spite of marked progress having been achieved in surgical resection, radiotherapy and chemotherapy, the prognosis for patients with colorectal cancer remains poor. Previous studies have demonstrated that the abnormal expression of microRNAs contributed to human cancer carcinogenesis and progression, suggesting miRNAs as novel therapeutic targets in colorectal cancer. The aim of the present study was to investigate the expression, functions and underlying molecular mechanisms of microRNA-184 (miR-184) in colorectal cancer. The results identified that miR-184 was significantly downregulated in colorectal cancer tissues and cell lines. In vitro functional studies demonstrated that miR-184 significantly inhibited colorectal cancer cell proliferation, migration and invasion. Notably, insulin-like growth factor 1 receptor (IGF-1R) was identified as a direct target of miR-184 in colorectal cancer. Furthermore, the functions of IGF-1R small interfering RNA were similar to those induced by miR-184 in colorectal cancer, suggesting IGF-1R as a functional target of miR-184 in colorectal cancer. The results of the present study indicated that miR-184 may be a novel therapeutic strategy regimen of targeted therapy for colorectal cancer.
C1 [Wu, Guannan; Liu, Jiayun; Wu, Zhenfeng; Wu, Xiaoyu; Yao, Xuequan] Nanjing Univ Tradit Chinese Med, Affiliated Hosp, Dept Surg Oncol, 155 Hanzhong Rd, Nanjing 210029, Jiangsu, Peoples R China.
C3 Nanjing University of Chinese Medicine
RP Yao, XQ (corresponding author), Nanjing Univ Tradit Chinese Med, Affiliated Hosp, Dept Surg Oncol, 155 Hanzhong Rd, Nanjing 210029, Jiangsu, Peoples R China.
EM doctor_xuequanyao@163.com
RI wu, 晓煜/HIK-3475-2022
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NR 46
TC 29
Z9 29
U1 0
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
EI 1792-1082
J9 ONCOL LETT
JI Oncol. Lett.
PD SEP
PY 2017
VL 14
IS 3
BP 3215
EP 3222
DI 10.3892/ol.2017.6499
PN A
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FF0NE
UT WOS:000408597600091
PM 28927068
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Smyth, E
   Khan, K
   Valeri, N
AF Smyth, Elizabeth
   Khan, Khurum
   Valeri, Nicola
TI Translational research and application of basic biology to clinical
   trial development in GI cancers
SO ANNALS OF TRANSLATIONAL MEDICINE
LA English
DT Review
DE Gastrointestinal cancer; gastric cancer; colorectal cancer (CRC);
   clinical trials; translational; next generation sequencing (NGS); ctDNA;
   liquid biopsy
ID METASTATIC COLORECTAL-CANCER; MISMATCH-REPAIR DEFICIENCY; ADVANCED
   ESOPHAGOGASTRIC CANCER; GASTRIC-CANCER; PHASE-3 TRIAL; OPEN-LABEL;
   FOLLOW-UP; MICROSATELLITE INSTABILITY; PERIOPERATIVE CHEMOTHERAPY;
   NEOADJUVANT CHEMOTHERAPY
AB Cancers of the gastrointestinal tract have limited available treatments and are often associated with a poor prognosis. Clinical trials and translational work associated with these trials provide the opportunity to increase understanding of the mechanisms of sensitivity and resistance to cytotoxic chemotherapy and targeted therapy in these diseases. In this review we discuss the rationale for intensive translational work within the context of academic clinical trials and the successes and challenges which have been associated with translational work at our institution over the past number of years. We reflect on tissue, plasma and radiological biomarker work including a novel patient derived organoid programme and discuss the iterative application of previous results to next generation trial design.
C1 [Smyth, Elizabeth; Khan, Khurum; Valeri, Nicola] Royal Marsden, Dept Gastrointestinal Canc & Lymphoma, Downs Rd, Sutton SM2 5PT, Surrey, England.
   [Valeri, Nicola] Royal Marsden, Inst Canc Res, Gastrointestinal Canc Biol & Genom Team, Sutton, Surrey, England.
C3 Royal Marsden NHS Foundation Trust; Royal Marsden NHS Foundation Trust;
   University of London; Institute of Cancer Research - UK
RP Smyth, E (corresponding author), Royal Marsden, Dept Gastrointestinal Canc & Lymphoma, Downs Rd, Sutton SM2 5PT, Surrey, England.
EM Elizabeth.smyth2@nhs.net
RI Smyth, Elizabeth/N-6541-2019
OI valeri, nicola/0000-0002-5426-5683
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NR 48
TC 6
Z9 6
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 2305-5839
EI 2305-5847
J9 ANN TRANSL MED
JI ANN. TRANSL. MED.
PD MAY
PY 2018
VL 6
IS 9
SI SI
AR 164
DI 10.21037/atm.2018.05.05
PG 10
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA GG5EO
UT WOS:000432718400007
PM 29911112
OA Green Published, hybrid
DA 2025-01-04
ER

PT J
AU Wu, J
   Lu, JH
   Chen, QY
   Chen, HJ
   Zheng, YQ
   Cheng, MG
AF Wu, Jun
   Lu, Jinghua
   Chen, Qiuyue
   Chen, Haojie
   Zheng, Yongqiang
   Cheng, Minggang
TI Pan-cancer analysis of CLDN18.2 shed new insights on the targeted
   therapy of upper gastrointestinal tract cancers
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE CLDN18.2; alternative splicing events; upper gastrointestinal tract
   cancers; prognosis; drug sensitivity
ID CLAUDIN 18.2; EXPRESSION; GENE; ANTIBODY
AB Background CLDN18.2 is a widely researched drug target. However, previous research has primarily been based on immunohistochemistry results and focused on gastric cancer.Methods To analyze the potential cancer-targeting effect of CLDN18.2 from a multi-omics perspective, this study quantified CLDN18.2 expression in The Cancer Genome Atlas (TCGA) pan-cancer cohort. Thus, the relationships between CLDN18.2 expression and genomic alterations, immune infiltration, and prognosis were analyzed. Additionally, we performed analyses of the differentially expressed genes and enriched pathways between the high- and low-CLDN18.2 expression groups, as well as the corresponding drug sensitivity analyses.Results The results indicated that CLDN18.2 was highly expressed in pancreatic adenocarcinoma (PAAD), stomach adenocarcinoma (STAD), colorectal cancer (CRC), and esophageal carcinoma (ESCA). Moreover, the high- and low-CLDN18.2 expression groups presented significant differences in terms of genomic alterations and immune infiltration, such as the levels of methylation and CD4+ T cell infiltration. Furthermore, high CLDN18.2 expression was significantly associated with poor prognosis in bladder urothelial carcinoma (BLCA), ESCA, and PAAD. In upper gastrointestinal tract cancers (STAD, ESCA, and PAAD), downregulated gene-enriched pathways were associated with cell signaling, whereas upregulated gene-enriched pathways were associated with angiogenesis. Finally, we identified drugs associated with CLDN18.2 expression to which samples with different levels of expression were differentially sensitive.Conclusion CLDN18.2 was highly expressed in upper gastrointestinal tract cancers, and its expression had a significant effect on genomic alterations and the tumor microenvironment. Additionally, low CLDN18.2 expression was linked to favorable prognosis. Our study reveals the potential value of CLDN18.2 for tumor prognosis and targeted therapy in various cancers, especially upper gastrointestinal tract cancers.
C1 [Wu, Jun; Lu, Jinghua; Chen, Qiuyue; Cheng, Minggang] Guangdong Med Univ, Shenzhen Baoan Clin Med Coll, Peoples Hosp Baoan Dist, Dept Clin Lab, Shenzhen, Peoples R China.
   [Wu, Jun; Chen, Haojie; Zheng, Yongqiang] Sun Yat sen Univ, Canc Ctr, Guangdong Prov Clin Res Ctr Canc, State Key Lab Oncol South China, Guangzhou, Peoples R China.
C3 Guangdong Medical University; State Key Lab Oncology South China; Sun
   Yat Sen University
RP Cheng, MG (corresponding author), Guangdong Med Univ, Shenzhen Baoan Clin Med Coll, Peoples Hosp Baoan Dist, Dept Clin Lab, Shenzhen, Peoples R China.; Zheng, YQ (corresponding author), Sun Yat sen Univ, Canc Ctr, Guangdong Prov Clin Res Ctr Canc, State Key Lab Oncol South China, Guangzhou, Peoples R China.
EM zhengyq@sysucc.org.cn; cmg70@163.com
RI Zheng, Yongqiang/JGE-2907-2023
FU Chih Kuang Scholarship for Outstanding Young Physician-Scientists of Sun
   Yat-sen University Cancer Center [CKS-SYSUCC-2024009]; Postdoctoral
   Fellowship Program of CPSF [GZB20240907]
FX The author(s) declare that financial support was received for the
   research, authorship, and/or publication of this article. This study was
   supported by the Chih Kuang Scholarship for Outstanding Young
   Physician-Scientists of Sun Yat-sen University Cancer Center
   (CKS-SYSUCC-2024009) and the Postdoctoral Fellowship Program of CPSF
   (GZB20240907).
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PU FRONTIERS MEDIA SA
PI LAUSANNE
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EI 1663-9812
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PD NOV 1
PY 2024
VL 15
AR 1494131
DI 10.3389/fphar.2024.1494131
PG 16
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA M3J5Z
UT WOS:001356540200001
PM 39555091
OA gold
DA 2025-01-04
ER

PT J
AU Nomiri, S
   Hoshyar, R
   Chamani, E
   Rezaei, Z
   Salmani, F
   Larki, P
   Tavakoli, T
   Gholipour, F
   Tabrizi, NJ
   Derakhshani, A
   Santarpia, M
   Franchina, T
   Brunetti, O
   Silvestris, N
   Safarpour, H
AF Nomiri, Samira
   Hoshyar, Reyhane
   Chamani, Elham
   Rezaei, Zohreh
   Salmani, Fatemeh
   Larki, Pegah
   Tavakoli, Tahmine
   Gholipour, Faranak
   Tabrizi, Neda Jalili
   Derakhshani, Afshin
   Santarpia, Mariacarmela
   Franchina, Tindara
   Brunetti, Oronzo
   Silvestris, Nicola
   Safarpour, Hossein
TI Prediction and validation of GUCA2B as the hub-gene in colorectal cancer
   based on co-expression network analysis: In-silico and in-vivo study
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Article
DE Colorectal cancer; Molecular pathogenicity; Transcriptome analysis;
   WGCNA; GUCA2B
ID NATRIURETIC PEPTIDES; COLON-CANCER; EXPRESSION; BIOMARKERS; K+;
   ACTIVATION; APOPTOSIS; PATHWAY; DNA; SHRINKAGE
AB Background: Several serious attempts to treat colorectal cancer have been made in recent decades. However, no effective treatment has yet been discovered due to the complexities of its etiology.
   Methods: we used Weighted Gene Co-expression Network Analysis (WGCNA) to identify key modules, hub-genes, and mRNA-miRNA regulatory networks associated with CRC. Next, enrichment analysis of modules has been performed using Cluepedia. Next, quantitative real-time PCR (RT-qPCR) was used to validate the expression of selected hub-genes in CRC tissues.
   Results: Based on the WGCNA results, the brown module had a significant positive correlation (r = 0.98, pvalue=9e-07) with CRC. Using the survival and DEGs analyses, 22 genes were identified as hub-genes. Next, three candidate hub-genes were selected for RT-qPCR validation, and 22 pairs of cancerous and non-cancerous tissues were collected from CRC patients referred to the Gastroenterology and Liver Clinic. The RT-qPCR results revealed that the expression of GUCA2B was significantly reduced in CRC tissues, which is consistent with the results of differential expression analysis. Finally, top miRNAs correlated with GUCA2B were identified, and ROC analyses revealed that GUCA2B has a high diagnostic performance for CRC.
   Conclusions: The current study discovered key modules and GUCA2B as a hub-gene associated with CRC, providing references to understand the pathogenesis and be considered a novel candidate to CRC target therapy.
C1 [Nomiri, Samira; Hoshyar, Reyhane; Chamani, Elham] Birjand Univ Med Sci, Fac Med, Dept Clin Biochem, Birjand, Iran.
   [Rezaei, Zohreh] Univ Sistan & Baluchestan, Fac Sci, Dept Biol, Zahedan, Iran.
   [Salmani, Fatemeh] Birjand Univ Med Sci, Fac Hlth, Social Determinants Hlth Res Ctr, Dept Epidemiol & Biostat, Birjand, Iran.
   [Larki, Pegah] Shahid Beheshti Univ Med Sci, Gastroenterol & Liver Dis Res Ctr, Res Inst Gastroenterol & Liver Dis, Tehran, Iran.
   [Tavakoli, Tahmine] Birjand Univ Med Sci, Cardiovasc Res Ctr, Birjand, Iran.
   [Gholipour, Faranak; Tabrizi, Neda Jalili] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
   [Derakhshani, Afshin] IRCCS Ist Tumori Giovanni Paolo II, Lab Expt Pharmacol, Bari, Italy.
   [Santarpia, Mariacarmela; Franchina, Tindara] Univ Messina, Dept Human Pathol G Barresi, Med Oncol Unit, Messina, Italy.
   [Brunetti, Oronzo; Silvestris, Nicola] IRCCS Ist Tumori Giovanni Paolo II Bari, Med Oncol Unit, Bari, Italy.
   [Silvestris, Nicola] Univ Bari, Dept Biomed Sci & Human Oncol DIMO, Bari, Italy.
   [Safarpour, Hossein] Birjand Univ Med Sci, Cellular & Mol Res Ctr, Birjand, Iran.
C3 University of Sistan & Baluchestan; Shahid Beheshti University Medical
   Sciences; Tabriz University of Medical Science; IRCCS Istituto Tumori
   Bari Giovanni Paolo II; University of Messina; IRCCS Istituto Tumori
   Bari Giovanni Paolo II; Universita degli Studi di Bari Aldo Moro
RP Silvestris, N (corresponding author), IRCCS Ist Tumori Giovanni Paolo II Bari, Med Oncol Unit, Bari, Italy.; Safarpour, H (corresponding author), Birjand Univ Med Sci, Cellular & Mol Res Ctr, Birjand, Iran.
EM n.silvestris@oncologico.bari.it; H.safarpour@bums.ac.ir
RI Derakhshani, Afshin/P-9085-2019; Hoshyar, Reyhane/N-3174-2017; Chamani,
   Elham/I-5179-2017; Salmani, Fatemeh/JCO-4505-2023; Brunetti,
   Oronzo/K-4788-2016
OI Nomiri, Samira/0000-0002-3569-4650; Chamani, Elham/0000-0002-4615-0034
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NR 70
TC 10
Z9 10
U1 1
U2 13
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD MAR
PY 2022
VL 147
AR 112691
DI 10.1016/j.biopha.2022.112691
EA FEB 2022
PG 13
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA ZF5VO
UT WOS:000759635600004
PM 35151227
OA gold
DA 2025-01-04
ER

PT J
AU Xie, BB
   Bai, BJ
   Xu, YZ
   Liu, YL
   Lv, YM
   Gao, X
   Wu, F
   Fang, ZP
   Lou, Y
   Pan, HM
   Han, WD
AF Xie, Binbin
   Bai, Bingjun
   Xu, Yuzi
   Liu, Yunlong
   Lv, Yiming
   Gao, Xing
   Wu, Fei
   Fang, Zhipeng
   Lou, Ying
   Pan, Hongming
   Han, Weidong
TI Tumor-suppressive function and mechanism of HOXB13 in right-sided colon
   cancer
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Article
ID ISLAND METHYLATOR PHENOTYPE; C-MYC INHIBITOR; COLORECTAL-CANCER;
   CELL-CYCLE; GENES; EXPRESSION; BRAF; MUTATIONS; 10058-F4; LOCATION
AB Right-sided colon cancer (RCC) and left-sided colon cancer (LCC) differ in their clinical and molecular features. An investigation of differentially expressed genes (DEGs) between RCC and LCC could contribute to targeted therapy for colon cancer, especially RCC, which has a poor prognosis. Here, we identified HOXB13, which was significantly less expressed in RCC than in LCC and associated with prognosis in RCC, by using 5 datasets from the Gene Expression Omnibus (GEO). Tissue sample analysis showed that HOXB13 was differentially expressed between normal and only RCC tumor tissues. HOXB13 inhibited colon cancer cell proliferation and induced apoptosis both in vitro and in vivo. Furthermore, we found that HOXB13 might be regulated by DNMT3B and suppress C-myc expression to exert antitumor effects via beta-catenin/TCF4 signals in RCC. In conclusion, the current study is the first to demonstrate that HOXB13 has a tumor-suppressive effect in RCC. High expression levels of HOXB13 are associated with prolonged overall survival in patients with RCC. The DNMT3B-HOXB13-C-myc signaling axis might be a molecular target for the treatment of RCC.
C1 [Xie, Binbin; Liu, Yunlong; Fang, Zhipeng; Lou, Ying; Pan, Hongming; Han, Weidong] Zhejiang Univ, Dept Med Oncol, Sir Run Run Shaw Hosp, Sch Med, Hangzhou 310016, Zhejiang, Peoples R China.
   [Bai, Bingjun; Lv, Yiming] Zhejiang Univ, Dept Colorectal Surg, Sir Run Run Shaw Hosp, Sch Med, Hangzhou 310016, Zhejiang, Peoples R China.
   [Xu, Yuzi] Zhejiang Univ, Dept Stomatol, Stomatol Hosp, Sch Med, Hangzhou 310000, Zhejiang, Peoples R China.
   [Gao, Xing] Suzhou Univ, Dept Med Oncol, Affiliated Hosp 2, Sch Med, Suzhou 215000, Peoples R China.
   [Wu, Fei] Anhui Univ Sci & Technol, Sch Med, Huainan 232001, Peoples R China.
C3 Zhejiang University; Zhejiang University; Zhejiang University; Anhui
   University of Science & Technology
RP Pan, HM; Han, WD (corresponding author), Zhejiang Univ, Dept Med Oncol, Sir Run Run Shaw Hosp, Sch Med, Hangzhou 310016, Zhejiang, Peoples R China.
EM panhongming@zju.edu.cn; hanwd@zju.edu.cn
RI Fang, Zhipeng/HMW-1650-2023
OI Han, Weidong/0000-0001-7227-3671; Lv, Yiming/0000-0003-4835-0336; Bai,
   Bingjun/0000-0003-3763-638X; Xu, Yuzi/0000-0003-2097-0293
FU National Natural Science Foundation of China [81972745, 81702350,
   81572361, 81572592, 81772543]; Ten Thousand Plan Youth Talent Support
   Program of Zhejiang Province [ZJWR0108009]; Zhejiang Medical Innovative
   Discipline Construction Project-2016
FX This work was supported by the National Natural Science Foundation of
   China (81972745, 81702350, 81572361, 81572592, 81772543), the Ten
   Thousand Plan Youth Talent Support Program of Zhejiang Province (No.
   ZJWR0108009) and the Zhejiang Medical Innovative Discipline Construction
   Project-2016.
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NR 43
TC 26
Z9 29
U1 2
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD NOV 29
PY 2019
VL 4
AR 51
DI 10.1038/s41392-019-0086-1
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA JW2CU
UT WOS:000502866600002
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Deng, QC
   Yang, JG
   Chen, YJ
   Chen, ZZ
   Li, JC
   Fu, ZX
AF Deng, Qican
   Yang, Jianguo
   Chen, Yajun
   Chen, Zhenzhou
   Li, Juncai
   Fu, Zhongxue
TI LncRNA HOXB-AS4 promotes proliferation and migration of colorectal
   cancer via the miR-140-5p/hdac7 axis
SO BIOTECHNOLOGY AND GENETIC ENGINEERING REVIEWS
LA English
DT Article
DE HOXB-AS4; colorectal cancer; MiR-140-5p; HDAC7
ID CLASSIFICATION; INVASION; CERNA
AB Long noncoding RNAs (lncRNA) have a critical role in colorectal cancer (CRC) development and progression. However, the role of the lncRNA HOXB-AS4 in CRC remains unclear. In this study, we found that HOXB-AS4 was markedly upregulated in tumor tissues compared to precancerous tissues. Loss-of-function assays in HT29 and SW480 cells confirmed that knockdown of HOXB-AS4 inhibited proliferation, migration, and promoted apoptosis. In addition, HOXB-AS4 was shown to regulate histone deacetylase 7 (HDAC7) expression by acting as a molecular sponge to bind to and adsorb miR-140-5p. These findings were confirmed by the dual-luciferase reporter assay. Functional recovery experiments further demonstrated the crucial role of the HOXB-AS4/miR-140-5p/HDAC7 axis in modulating the malignant phenotype of CRC cells. Collectively, our data suggested that HOXB-AS4 regulated the malignant tumor aggression of HT29 and SW480 cells through the miR-140-5p/HDAC7 axis and PI3K/AKT signaling pathway. Our study provides novel insights into the mechanism of action of HOXB-AS4 in CRC and highlights its potential use as a targeted therapy.
C1 [Deng, Qican; Yang, Jianguo; Li, Juncai; Fu, Zhongxue] Chongqing Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Chongqing, Peoples R China.
   [Chen, Yajun; Chen, Zhenzhou] Chongqing Med Univ, Affiliated Hosp 3, Dept Gen Surg, Chongqing, Peoples R China.
C3 Chongqing Medical University; Chongqing Medical University
RP Fu, ZX (corresponding author), Chongqing Med Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Chongqing, Peoples R China.
EM fzx19990521@126.com
RI Yang, Jianguo/AAI-9398-2021
FU Chongqing key disease Research and Application Demonstration Programm
   (Colorectal Cancer Prevention and Treatment Technology Research and
   Application Demonstration) [2019ZX003]
FX This work was supported by Chongqing key disease Research and
   Application Demonstration Programm (Colorectal Cancer Prevention and
   Treatment Technology Research and Application Demonstration)
   (No.2019ZX003)
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NR 31
TC 3
Z9 3
U1 0
U2 7
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0264-8725
EI 2046-5556
J9 BIOTECHNOL GENET ENG
JI Biotechnol. Genet. Eng. Rev.
PD JUL 2
PY 2024
VL 40
IS 2
BP 1262
EP 1280
DI 10.1080/02648725.2023.2193465
EA MAR 2023
PG 19
WC Biotechnology & Applied Microbiology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA G8T4Z
UT WOS:000951844900001
PM 36951606
DA 2025-01-04
ER

PT J
AU Liu, JW
   Guo, B
AF Liu, Jingwen
   Guo, Bin
TI RNA-based therapeutics for colorectal cancer: Updates and future
   directions
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE RNA-based therapeutics; Colorectal cancer; Chemical modifications; RNA
   interference; Gene delivery; Clinical trials
ID LONG NONCODING RNA; HUMAN COLON-CARCINOMA; DOUBLE-STRANDED-RNA;
   ANTISENSE OLIGONUCLEOTIDE; CARCINOEMBRYONIC ANTIGEN; GENE-EXPRESSION;
   POOR-PROGNOSIS; CELL-PROLIFERATION; DRUG-RESISTANCE; CLINICAL-TRIAL
AB Colorectal cancer (CRC) is one of the most common causes of cancer death worldwide. While standard chemotherapy and new targeted therapy have been Unproved recently, problems such as multidrug resistance (MDR) and severe side effects remain unresolved. RNAs are essential to all biological processes including cell proliferation and differentiation, cell cycle, apoptosis, activation of tumor suppressor genes, suppression of oncogenes. Therefore, there are various potential approaches to address genetic disease like CRC at the RNA level. In contrast to conventional treatments, RNA-based therapeutics such as RNA interference, antisense oligonucleotides, RNA aptamer, ribozymes, have the advantages of high specificity, high potency and low toxicity. It has gained more and more attention due to the flexibility in modulating a wide range of targets. Here, we highlight recent advances and clinical studies involving RNA-based therapeutics and CRC. We also discuss their advantages and limitations that remain to be overcome for the treatment of human CRC.
C1 [Liu, Jingwen; Guo, Bin] Univ Houston, Dept Pharmacol & Pharmaceut Sci, Coll Pharm, Houston, TX 77030 USA.
C3 University of Houston System; University of Houston
RP Liu, JW; Guo, B (corresponding author), Univ Houston, Dept Pharmacol & Pharmaceut Sci, Coll Pharm, Houston, TX 77030 USA.
EM jliu79@central.uh.edu; bguo3@uh.edu
RI Liu, Jingwen/J-5058-2019; Guo, Bin/AAA-2445-2019
OI GUO, BIN/0000-0003-3296-9177; Liu, Jingwen/0000-0002-0748-7830
FU NIH [CA186100]
FX This work was supported in part by NIH Grant CA186100.
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NR 127
TC 32
Z9 32
U1 0
U2 19
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
EI 1096-1186
J9 PHARMACOL RES
JI Pharmacol. Res.
PD FEB
PY 2020
VL 152
AR 104550
DI 10.1016/j.phrs.2019.104550
PG 9
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA KT0KU
UT WOS:000518700200004
PM 31866285
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Chen, H
   Peng, H
   Liu, WW
   Sun, YP
   Su, N
   Tang, WT
   Zhang, XL
   Wang, J
   Cui, L
   Hu, PF
   Liu, S
AF Chen, Han
   Peng, Huan
   Liu, Wenwu
   Sun, Yanping
   Su, Ning
   Tang, Wentao
   Zhang, Xiaoli
   Wang, Jian
   Cui, Long
   Hu, Pingfang
   Liu, Sheng
TI Silencing of plasminogen activator inhibitor-1 suppresses colorectal
   cancer progression and liver metastasis
SO SURGERY
LA English
DT Article
ID UROKINASE RECEPTOR; MATRIX METALLOPROTEINASES; TUMOR INVASION; PAI-1;
   ANGIOGENESIS; INFLAMMATION; BINDING; TYPE-1; UPA
AB Background. Plasminogen activator inhibitor-I (PAI-1) is reported to be expressed in many cancer cell types and regarded as one of the most informative biochemical markers for poor prognosis. However, no previous study has evaluated whether PAI-1 could serve as a target in antitumor and antimetastasis therapies of colorectal cancer (CRC).
   Methods. The plasma level of PAI-1 in CRC patients was detected and its correlation with the clinicopathologic features was evaluated. PAI-1 protein expression was assessed by Western blot assay and immunohistochemistry: The biologic consequences of PAI-1 silencing in colon cancer cell lines and CRC bearing nude mice were also investigated.
   Results. Plasma PAI-1 level was higher in CRC patients with liver metastasis and correlated with liver metastasis, tumor size, differentiation, serosa infiltration, Duke's stage, and lymphatic metastasis. PAI-1 protein expression in the CRC tissue of patients with liver metastasis was significantly greater than that in those without liver metastasis. In addition, the abilities of proliferation, invasion, and migration of CRC cells transfected with lentivirus expressing PAI-1 small interfering RNA were reduced significantly. Nude mice inoculated with PAI-1 knockdown cells also had fewer metastatic nodules in the liver and smaller tumor volumes.
   Conclusion. Plasma PAI-1 level was increased in CRC patients with liver metastasis, and PAI-1 silencing may significantly compromise the malignant behaviors of CRC cells in vitro and in vivo. These findings may provide evidence for PAI-1 targeted therapy of CRC.
C1 [Chen, Han; Liu, Sheng] Chinese Peoples Liberat Army, Dept Gen Surg, Hosp 411, Shanghai 200081, Peoples R China.
   [Peng, Huan; Tang, Wentao; Wang, Jian] Shanghai Jiao Tong Univ, Sch Med, Dept Colorectal Surg, Xinhua Hosp, Shanghai 200030, Peoples R China.
   [Liu, Wenwu] Second Mil Med Univ, Dept Diving Med, Shanghai, Peoples R China.
   [Sun, Yanping; Su, Ning] Second Mil Med Univ, Changzheng Hosp, Dept Gen Surg, Shanghai, Peoples R China.
   [Zhang, Xiaoli] Chinese Peoples Liberat Army, Dept Pathol, Hosp 411, Shanghai 200081, Peoples R China.
   [Wang, Jian; Hu, Pingfang] Second Mil Med Univ, Changzheng Hosp, Dept Gastroenterol, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University; Naval Medical University; Naval Medical
   University; Naval Medical University
RP Liu, S (corresponding author), Chinese Peoples Liberat Army, Dept Gen Surg, Hosp 411, 15 Dongjiangwan Rd, Shanghai 200081, Peoples R China.
EM liusheng196511@163.com
RI liu, wenwu/JNE-3395-2023; PENG, HUAN/AAV-7505-2021
OI Chen, Han/0000-0002-5912-3692; Liu, Wenwu/0000-0003-1530-8860
FU National Natural Science Foundation of China [81101713, 81300305]
FX This work was supported by grants from the National Natural Science
   Foundation of China (No. 81101713 and No. 81300305).
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NR 33
TC 38
Z9 43
U1 0
U2 16
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0039-6060
J9 SURGERY
JI Surgery
PD DEC
PY 2015
VL 158
IS 6
BP 1705
EP 1714
DI 10.1016/j.surg.2015.04.053
PG 10
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA CV9MV
UT WOS:000364612200030
PM 26275833
DA 2025-01-04
ER

PT J
AU Chiang, TY
   Hsu, HC
   Chern, YJ
   Liao, CK
   Hsu, YJ
   Tsai, WS
   Hsieh, PS
   Lin, YF
   Lee, HL
   You, JF
AF Chiang, Ting-Yu
   Hsu, Hung-Chih
   Chern, Yih-Jong
   Liao, Chun-Kai
   Hsu, Yu-Jen
   Tsai, Wen-Sy
   Hsieh, Pao-Shiu
   Lin, Yu-Fen
   Lee, Hsiu-Lan
   You, Jeng-Fu
TI Skin Toxicity as a Predictor of Survival in Metastatic Colorectal Cancer
   Patients Treated with Anti-EGFR: Fact or Fallacy?
SO CANCERS
LA English
DT Article
DE metastatic CRC; mCRC; skin toxicity; survival; anti-EGFR
ID QUALITY-OF-LIFE; PANITUMUMAB; MANAGEMENT; THERAPY; IMPACT; TRIAL
AB The primary treatment for metastatic colorectal cancer (mCRC) consists of targeted therapy and chemotherapy to improve survival. A molecular target drug with an anti-epidermal growth factor receptor (EGFR) antagonist is recommended when the RAS and BRAF genes are normal. About 50-70% of patients using anti-EGFR antagonists will experience skin reactions. Some studies have shown that severe skin reactions caused by anti-EGFR antagonists may be linked to overall survival (OS) and progression-free survival (PFS), but the results are still uncertain. These data of mCRC patients who underwent anti-EGFR therapy between October 2017 and October 2018 were analyzed retrospectively. A total of 111 patients were included in this study. The survival results showed that gender, age, body mass index, primary tumor site, and recurrence did not significantly affect OS and PFS. However, the first-line anti-EGFR inhibitor treatment was significantly associated with OS (p < 0.001) and PFS (p < 0.001). There was no significant difference in the incidence of acne between males and females in grades 1 and 2, while males have a greater risk in grades 3 and 4 than females (20.3 vs. 4.8%; p-value = 0.041). Skin toxicity was not a predictor of anti-EGFR treatment response in this investigation.
C1 [Chiang, Ting-Yu; Lin, Yu-Fen; Lee, Hsiu-Lan] Chang Gung Univ, Chang Gung Mem Hosp Linkou, Coll Med, Dept Nursing, Taoyuan 33305, Taiwan.
   [Hsu, Hung-Chih] Chang Gung Univ, Chang Gung Mem Hosp Linkou, Coll Med, Div Hematol Oncol, Taoyuan 33305, Taiwan.
   [Chern, Yih-Jong; Liao, Chun-Kai; Hsu, Yu-Jen; Tsai, Wen-Sy; Hsieh, Pao-Shiu; You, Jeng-Fu] Chang Gung Univ, Chang Gung Mem Hosp Linkou, Coll Med, Dept Surg,Div Colon & Rectal Surg, Taoyuan 33305, Taiwan.
C3 Chang Gung University; Chang Gung Memorial Hospital; Chang Gung
   University; Chang Gung Memorial Hospital; Chang Gung Memorial Hospital;
   Chang Gung University
RP You, JF (corresponding author), Chang Gung Univ, Chang Gung Mem Hosp Linkou, Coll Med, Dept Surg,Div Colon & Rectal Surg, Taoyuan 33305, Taiwan.
EM jenodyssey@gmail.com
RI Lin, Yu-Fen/A-2570-2016; Tsai, Wen-Sy/F-3082-2018
OI Hsu, Yu-Jen/0000-0002-3068-8999; Liao, Chunkai/0000-0002-7497-4444; Hsu,
   Hung-Chih/0000-0002-4719-4143; Tsai, Wen-Sy/0000-0001-6873-2863; You,
   Jeng-Fu/0000-0001-5748-1659
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NR 41
TC 1
Z9 1
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2023
VL 15
IS 6
AR 1663
DI 10.3390/cancers15061663
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA D4KZ3
UT WOS:000968449700001
PM 36980549
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lee, MS
   Kopetz, S
AF Lee, Michael S.
   Kopetz, Scott
TI Current and Future Approaches to Target the Epidermal Growth Factor
   Receptor and Its Downstream Signaling in Metastatic Colorectal Cancer
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE Cetuximab; HER2; MET; Panitumumab; Targeted therapy
ID PHASE-III TRIAL; CETUXIMAB PLUS IRINOTECAN; WILD-TYPE KRAS; HUMAN
   MONOCLONAL-ANTIBODY; TIVANTINIB ARQ 197; 1ST-LINE TREATMENT;
   ACQUIRED-RESISTANCE; OPEN-LABEL; MEK INHIBITION; COLON-CANCER
AB The discovery of the key role of the epidermal growth factor receptor (EGFR) and its downstream signaling effectors in the pathophysiology of colorectal cancer (CRC) has ushered in the clinical use of targeted therapies in the treatment of metastatic CRC (mCRC). The anti-EGFR monoclonal antibodies cetuximab and panitumumab improve overall survival when combined with chemotherapy in first-line treatment of Kirsten rat sarcoma viral oncogene homolog (KRAS) and neuroblastoma RAS viral oncogene homolog (NRAS) wild type mCRC and also improve progression-free survival and response rate in first-line treatment and treatment of refractory mCRC. There are ongoing efforts to discover mechanisms of innate and acquired resistance to anti-EGFR therapies in KRAS wild type mCRC patients and to take therapeutic advantage of this knowledge by using rational combinations of targeted therapies. In this review we will discuss the evidence for current use of anti-EGFR therapies and several recent and ongoing investigations to refine treatment for KRAS wild type mCRC, including more complete inhibition of the EGFR, HER2 inhibition, and MET protooncogene, receptor tyrosine kinase (MET) inhibition. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Lee, Michael S.; Kopetz, Scott] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center
RP Kopetz, S (corresponding author), 1515 Holcombe Blvd,Unit 0426, Houston, TX 77030 USA.
EM skopetz@mdanderson.org
RI Lam, Michael/KWU-4480-2024; Kopetz, Scott/AAC-1387-2019
OI Kopetz, Scott/0000-0001-9647-3416
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NR 137
TC 22
Z9 24
U1 0
U2 12
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 1533-0028
EI 1938-0674
J9 CLIN COLORECTAL CANC
JI Clin. Colorectal Canc.
PD DEC
PY 2015
VL 14
IS 4
BP 203
EP 218
DI 10.1016/j.clcc.2015.05.006
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CX3XX
UT WOS:000365633900001
PM 26077270
DA 2025-01-04
ER

PT J
AU Cheng, HJ
   Sun, X
   Li, J
   He, P
   Liu, WQ
   Meng, XW
AF Cheng, Hongjing
   Sun, Xun
   Li, Ji
   He, Ping
   Liu, Wanqi
   Meng, Xiangwei
TI Knockdown of Uba2 inhibits colorectal cancer cell invasion and migration
   through downregulation of the Wnt/-catenin signaling pathway
SO JOURNAL OF CELLULAR BIOCHEMISTRY
LA English
DT Article
DE colorectal cancer; endothelial-mesenchymal transition; knockdown; Uba2;
   Wnt; -catenin
ID EPITHELIAL-MESENCHYMAL TRANSITION; MULTIDRUG-RESISTANCE; GASTRIC-CANCER;
   SUMO; SUMOYLATION; GENE; PROLIFERATION; ACTIVATION; MECHANISMS;
   PHENOTYPE
AB Colorectal cancer is a serious threat to human health, and has a high mortality rate. There is currently no effective therapy for end-stage colorectal cancer. In recent years, molecular targeted therapy has received increasing attention for cancer treatment. In particular, the role of Uba2, a vital component of SUMO-activating enzyme, has been highlighted, which plays important roles in the progression of certain cancers; however, its role in colorectal cancer remains unclear. Accordingly, the aim of this study was to evaluate the relationship between Uba2 and colorectal cancer. Uba2 expression was knocked down in two colorectal cancer cell lines, and gene microarray analysis was conducted, followed by proliferation, migration, and invasion assays. Uba2 knockdown influenced the expression of several genes, and significantly inhibited the proliferation, migration, and invasion of cancer cells. To determine the underlying mechanism, the expression of related signaling pathways and molecules was evaluated in the knockdown cell lines. Overall, the results suggest that Uba2 participates in the progression, invasion, and metastasis of colorectal cancer, and the possible mechanism is via regulating the Wnt signaling pathway and enhancing epithelial-mesenchymal transition behaviors of colorectal cancer cells. Therefore, Uba2 is expected to be an important oncoprotein and potential therapeutic target in colorectal cancer.
C1 [Cheng, Hongjing; Li, Ji; He, Ping; Liu, Wanqi; Meng, Xiangwei] Jilin Univ, Dept Gastroenterol, Hosp 1, 71 Xinmin St, Changchun 130021, Jilin, Peoples R China.
   [Sun, Xun] Jilin Univ, Dept Pathol, Hosp 1, Changchun, Jilin, Peoples R China.
C3 Jilin University; Jilin University
RP Meng, XW (corresponding author), Jilin Univ, Dept Gastroenterol, Hosp 1, 71 Xinmin St, Changchun 130021, Jilin, Peoples R China.
EM mxwmengxiangwei@163.com
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NR 41
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Z9 24
U1 0
U2 10
PU WILEY
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PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0730-2312
EI 1097-4644
J9 J CELL BIOCHEM
JI J. Cell. Biochem.
PD AUG
PY 2018
VL 119
IS 8
BP 6914
EP 6925
DI 10.1002/jcb.26890
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA GK9EG
UT WOS:000436542900058
PM 29744931
DA 2025-01-04
ER

PT J
AU Zhang, XL
   Dong, Z
   Cui, HJ
AF Zhang, Xiaolin
   Dong, Zhen
   Cui, Hongjuan
TI Interplay between Epigenetics and Cellular Metabolism in Colorectal
   Cancer
SO BIOMOLECULES
LA English
DT Review
DE colorectal cancer; epigenetics; cellular metabolism; targeted therapy;
   tumorigenesis
ID ATP-CITRATE LYASE; COA SYNTHETASE 2; COLON-CANCER; DNA METHYLATION;
   FOLATE-DEFICIENCY; S-ADENOSYLHOMOCYSTEINE; ACETYL-COA; IN-VITRO; C-MYC;
   LACTATE-DEHYDROGENASE
AB Cellular metabolism alterations have been recognized as one of the most predominant hallmarks of colorectal cancers (CRCs). It is precisely regulated by many oncogenic signaling pathways in all kinds of regulatory levels, including transcriptional, post-transcriptional, translational and post-translational levels. Among these regulatory factors, epigenetics play an essential role in the modulation of cellular metabolism. On the one hand, epigenetics can regulate cellular metabolism via directly controlling the transcription of genes encoding metabolic enzymes of transporters. On the other hand, epigenetics can regulate major transcriptional factors and signaling pathways that control the transcription of genes encoding metabolic enzymes or transporters, or affecting the translation, activation, stabilization, or translocation of metabolic enzymes or transporters. Interestingly, epigenetics can also be controlled by cellular metabolism. Metabolites not only directly influence epigenetic processes, but also affect the activity of epigenetic enzymes. Actually, both cellular metabolism pathways and epigenetic processes are controlled by enzymes. They are highly intertwined and are essential for oncogenesis and tumor development of CRCs. Therefore, they are potential therapeutic targets for the treatment of CRCs. In recent years, both epigenetic and metabolism inhibitors are studied for clinical use to treat CRCs. In this review, we depict the interplay between epigenetics and cellular metabolism in CRCs and summarize the underlying molecular mechanisms and their potential applications for clinical therapy.
C1 [Zhang, Xiaolin; Dong, Zhen; Cui, Hongjuan] Southwest Univ, Med Res Inst, Canc Ctr, Chongqing 400716, Peoples R China.
   [Zhang, Xiaolin; Dong, Zhen; Cui, Hongjuan] Southwest Univ, Coll Sericulture & Text & Biomass Sci, Inst Sericulture & Syst Biol, State Key Lab Silkworm Genome Biol, Chongqing 400716, Peoples R China.
   [Dong, Zhen; Cui, Hongjuan] Southwest Univ, Engn Res Ctr Canc Biomed & Translat Med, Chongqing 400716, Peoples R China.
   [Dong, Zhen; Cui, Hongjuan] Southwest Univ, Chongqing Engn & Technol Res Ctr Silk Biomat & Re, Chongqing 400716, Peoples R China.
C3 Southwest University - China; Southwest University - China; Southwest
   University - China; Southwest University - China
RP Dong, Z; Cui, HJ (corresponding author), Southwest Univ, Med Res Inst, Canc Ctr, Chongqing 400716, Peoples R China.; Dong, Z; Cui, HJ (corresponding author), Southwest Univ, Coll Sericulture & Text & Biomass Sci, Inst Sericulture & Syst Biol, State Key Lab Silkworm Genome Biol, Chongqing 400716, Peoples R China.; Dong, Z; Cui, HJ (corresponding author), Southwest Univ, Engn Res Ctr Canc Biomed & Translat Med, Chongqing 400716, Peoples R China.; Dong, Z; Cui, HJ (corresponding author), Southwest Univ, Chongqing Engn & Technol Res Ctr Silk Biomat & Re, Chongqing 400716, Peoples R China.
RI Dong, Zhen/AAJ-7172-2020
OI Cui, Hongjuan/0000-0003-1178-1570
FU National Natural Science Foundation of China [81902664, 81872071];
   Fundamental Research Funds for the Central Universities [SWU120009];
   Natural Science Foundation of Chongqing [cstc2019jcyj-zdxmX0033]
FX FundingWe are grateful for funding support from the National Natural
   Science Foundation of China (Nos. 81902664 and 81872071), the
   Fundamental Research Funds for the Central Universities (SWU120009) and
   the Natural Science Foundation of Chongqing (No.
   cstc2019jcyj-zdxmX0033).
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NR 212
TC 6
Z9 6
U1 2
U2 37
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD OCT
PY 2021
VL 11
IS 10
AR 1406
DI 10.3390/biom11101406
PG 23
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA WN1JU
UT WOS:000711532900001
PM 34680038
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Valenzuela, G
   Burotto, M
   Marcelain, K
   González-Montero, J
AF Valenzuela, Guillermo
   Burotto, Mauricio
   Marcelain, Katherine
   Gonzalez-Montero, Jaime
TI Liquid biopsy to detect resistance mutations against anti-epidermal
   growth factor receptor therapy in metastatic colorectal cancer
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Colorectal neoplasms; Precision medicine; Liquid biopsy; Cetuximab;
   Panitumumab
ID CIRCULATING TUMOR DNA; ANTI-EGFR THERAPY; ACQUIRED-RESISTANCE;
   MONOCLONAL-ANTIBODIES; RAS MUTATIONS; COLON-CANCER; HETEROGENEITY;
   CETUXIMAB; EVOLUTION; PATTERNS
AB Colorectal cancer (CRC) is a major cause of mortality worldwide, associated with a steadily growing prevalence. Notably, the identification of KRAS, NRAS, and BRAF mutations has markedly improved targeted CRC therapy by affording treatments directed against the epidermal growth factor receptor (EGFR) and other anti-angiogenic therapies. However, the survival benefit conferred by these therapies remains variable and difficult to predict, owing to the high level of molecular heterogeneity among patients with CRC. Although classification into consensus molecular subtypes could optimize response prediction to targeted therapies, the acquisition of resistance mutations to targeted therapy is, in part, responsible for the lack of response in some patients. However, the acquisition of such mutations can induce challenges in clinical practice. The utility of liquid biopsy to detect resistance mutations against anti-EGFR therapy has recently been described. This approach may constitute a new standard in the decision algorithm for targeted CRC therapy.
C1 [Valenzuela, Guillermo; Marcelain, Katherine; Gonzalez-Montero, Jaime] Univ Chile, Dept Basic & Clin Oncol, Independencia 1027,Casilla 70058, Santiago 8380453, Chile.
   [Valenzuela, Guillermo] Hosp Salvador, Dept Internal Med, Santiago 7500922, Chile.
   [Burotto, Mauricio; Gonzalez-Montero, Jaime] Bradford Hill Clin Res Ctr, Dept Oncol, Santiago 8420383, Chile.
C3 Universidad de Chile; Universidad de Chile
RP González-Montero, J (corresponding author), Univ Chile, Dept Basic & Clin Oncol, Independencia 1027,Casilla 70058, Santiago 8380453, Chile.
RI Garnacho-Montero, Jose/R-9496-2019; Marcelain, Katherine/I-2791-2013
OI Gonzalez-Montero, Jaime/0000-0003-0324-2948; Marcelain,
   Katherine/0000-0003-4018-6623
FU Agencia Nacional de Investigacion y Desarrollo de Chile, Fondo Nacional
   de Investigacion en Salud (FONIS) [SA20I0059]
FX Supported by Agencia Nacional de Investigacion y Desarrollo de Chile,
   Fondo Nacional de Investigacion en Salud (FONIS), No. SA20I0059.
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NR 75
TC 2
Z9 2
U1 1
U2 5
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD SEP 15
PY 2022
VL 14
IS 9
BP 1654
EP 1664
DI 10.4251/wjgo.v14.i9.1654
PG 11
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA 4Z7MW
UT WOS:000862388900004
PM 36187383
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Kurtovic, M
   Pitesa, N
   Bartonicek, N
   Ozretic, P
   Musani, V
   Conkas, J
   Petric, T
   King, C
   Sabol, M
AF Kurtovic, Matea
   Pitesa, Nikolina
   Bartonicek, Nenad
   Ozretic, Petar
   Musani, Vesna
   Conkas, Josipa
   Petric, Tina
   King, Cecile
   Sabol, Maja
TI RNA-seq and ChIP-seq Identification of Unique and Overlapping Targets of
   GLI Transcription Factors in Melanoma Cell Lines
SO CANCERS
LA English
DT Article
DE melanoma; HH-GLI pathway; GLI targets; MAPK pathway; targeted therapy
ID COLON-CANCER CELLS; PROMOTES PROLIFERATION; TUMOR PROGRESSION;
   LUNG-CANCER; HEDGEHOG; GROWTH; PATHWAY; GENE; EXPRESSION; INHIBITOR
AB Simple Summary The majority of melanomas show hyperactivation of the MAPK signaling pathway, most often through mutations in BRAF and NRAS. Despite significant progress in therapy, targeting this signaling pathway solely has not been the solution for stopping the progression of this disease. Recently, researchers recognized the involvement of the Hedgehog-GLI (HH-GLI) signaling pathway in melanoma and its crosstalk with the MAPK pathway. In order to identify new HH-GLI-regulated targets that could be involved in the crosstalk with the MAPK pathway, we performed RNA sequencing and ChIP sequencing on three melanoma cell lines. By combining RNA-seq and ChIP-seq results, we successfully validated 15 novel targets of GLI proteins in melanoma cell lines. These findings will contribute to a better understanding of the GLI code and its role in melanoma. Background: Despite significant progress in therapy, melanoma still has a rising incidence worldwide, and novel treatment strategies are needed. Recently, researchers have recognized the involvement of the Hedgehog-GLI (HH-GLI) signaling pathway in melanoma and its consistent crosstalk with the MAPK pathway. In order to further investigate the link between the two pathways and to find new target genes that could be considered for combination therapy, we set out to find transcriptional targets of all three GLI proteins in melanoma. Methods: We performed RNA sequencing on three melanoma cell lines (CHL-1, A375, and MEL224) with overexpressed GLI1, GLI2, and GLI3 and combined them with the results of ChIP-sequencing on endogenous GLI1, GLI2, and GLI3 proteins. After combining these results, 21 targets were selected for validation by qPCR. Results: RNA-seq revealed a total of 808 differentially expressed genes (DEGs) for GLI1, 941 DEGs for GLI2, and 58 DEGs for GLI3. ChIP-seq identified 527 genes that contained GLI1 binding sites in their promoters, 1103 for GLI2 and 553 for GLI3. A total of 15 of these targets were validated in the tested cell lines, 6 of which were detected by both RNA-seq and ChIP-seq. Conclusions: Our study provides insight into the unique and overlapping transcriptional output of the GLI proteins in melanoma. We suggest that our findings could provide new potential targets to consider while designing melanoma-targeted therapy.
C1 [Kurtovic, Matea; Pitesa, Nikolina; Ozretic, Petar; Musani, Vesna; Conkas, Josipa; Petric, Tina; Sabol, Maja] Rudjer Boskovic Inst, Div Mol Med, Zagreb 10000, Croatia.
   [Bartonicek, Nenad] Garvan Inst Med Res, 384 Victoria St, Darlinghurst, NSW 2010, Australia.
   [Bartonicek, Nenad] Kinghorn Ctr Clin Genom, 370 Victoria St, Darlinghurst, NSW 2010, Australia.
   [King, Cecile] Univ New South Wales, Fac Sci, Sch Biotechnol & Biomol Sci, Sydney, NSW 2052, Australia.
C3 Rudjer Boskovic Institute; Garvan Institute of Medical Research;
   University of New South Wales Sydney
RP Sabol, M (corresponding author), Rudjer Boskovic Inst, Div Mol Med, Zagreb 10000, Croatia.
EM maja.sabol@irb.hr
RI King, Cecile/Q-9794-2019; Musani, Vesna/K-7972-2019; Bartonicek,
   Nenad/B-6675-2016; Ozretic, Petar/G-5189-2014; Sabol, Maja/G-4177-2011
OI Ozretic, Petar/0000-0001-9757-6636; Petric, Tina/0000-0002-8565-9909;
   Sabol, Maja/0000-0001-6968-2327; Conkas, Josipa/0000-0003-1473-4868;
   Musani, Vesna/0000-0001-9927-3727
FU Croatian Science Foundation [IP-2018-01-4889]; National Health and
   Medical Research Council (NHMRC) of Australia [2004306]; Australian
   Research Council (ARC) [DP210103811]; "Young Researchers' Career
   Development Project-Training of Doctoral Students" of the Croatian
   Science Foundation
FX This research was funded by the Croatian Science Foundation project
   IP-2018-01-4889 titled "Differential regulation of the GLI code in
   BRAF/NRAS driven tumors" and the Ideas grant 2004306 from the National
   Health and Medical Research Council (NHMRC) of Australia and DP210103811
   from the Australian Research Council (ARC). The work of doctoral student
   NP has been supported by the "Young Researchers' Career Development
   Project-Training of Doctoral Students" of the Croatian Science
   Foundation.
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NR 121
TC 6
Z9 7
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD SEP
PY 2022
VL 14
IS 18
AR 4540
DI 10.3390/cancers14184540
PG 20
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4U1AS
UT WOS:000858536200001
PM 36139698
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wilson, LE
   Greiner, MA
   Altomare, I
   Rotter, J
   Dinan, MA
AF Wilson, Lauren E.
   Greiner, Melissa A.
   Altomare, Ivy
   Rotter, Jason
   Dinan, Michaela A.
TI Rapid rise in the cost of targeted cancer therapies for Medicare
   patients with solid tumors from 2006 to 2015
SO JOURNAL OF GERIATRIC ONCOLOGY
LA English
DT Article
DE Molecular targeted agents; Cost trends; Lung cancer; Breast cancer;
   Colorectal cancer; Prostate cancer
ID BURDEN; CARE; ICD-9-CM; LAUNCH; PRICES; TRENDS
AB Background: Inflation-adjusted cancer costs in the United States have increased 40% in the last decade, leading to increasing financial burden on both payers and patients. Patients under 65 show substantial increases in utilization of expensive targeted therapy anticancer agents; however, patients aged 65+ account for the majority of new malignancies. Utilization and cost trends for these emerging agents have not been examined in detail in the Medicare population.
   Patients and methods: Retrospective prevalent cohort analysis of patients 65+ with any stage of invasive lung, breast, colorectal, or prostate cancer, receiving systemic therapy drawn from the United States Medicare 5% fee-for-service sample claims (2005-2015). Yearly trends in utilization and associated costs were modeled with adjustment for inflation, demographics, and comorbidities.
   Results: Among Medicare beneficiaries with fee-for-service and Part D enrollment who were receiving some type of systemic anticancer therapy, there were 9230 patients with colorectal, 32,738 patients with breast, and 16,278 patients with lung cancers identified from 2006 to 2015, and 19,295 patients with prostate cancer from 2009 to 2015. The share of cancer costs to Medicare attributable to targeted therapies, increased dramatically for prostate cancer (1.7% to 19.4%), lung cancer (6.7% to 19.4%), colorectal cancer (11.7% to 22.2%), and breast cancer (15.8% to 25.5%). Although the proportion of patients receiving targeted therapies remained stable, mean per-patient cancer costs increased dramatically from 2006 to 2015 for patients with lung or prostate cancer receiving targeted therapy and for patients with breast cancer receiving non-hormonal targeted therapies. Targeted agents for these cancers showed substantial inflation-adjusted price growth over this time period.
   (c) 2020 Elsevier Ltd. All rights reserved.
C1 [Wilson, Lauren E.; Greiner, Melissa A.; Rotter, Jason; Dinan, Michaela A.] Duke Univ, Dept Populat Hlth Sci, Sch Med, Durham, NC 27706 USA.
   [Altomare, Ivy] Duke Univ, Div Med Oncol, Sch Med, Durham, NC 27706 USA.
   [Dinan, Michaela A.] Duke Univ, Duke Canc Inst, Sch Med, Durham, NC 27706 USA.
C3 Duke University; Duke University; Duke University
RP Wilson, LE (corresponding author), Dept Populat Hlth Sci, 215 Morris St, Durham, NC 27701 USA.
EM Lauren.e.wilson@duke.edu
FU Duke Cancer Institute
FX This work was supported by internal funding provided to Dr. Dinan
   through the Duke Cancer Institute. No grant number is applicable.
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NR 28
TC 8
Z9 8
U1 0
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1879-4068
EI 1879-4076
J9 J GERIATR ONCOL
JI J. Geriatr. Oncol.
PD APR
PY 2021
VL 12
IS 3
BP 375
EP 380
DI 10.1016/j.jgo.2020.11.007
EA MAR 2021
PG 6
WC Oncology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Geriatrics & Gerontology
GA RE8IS
UT WOS:000634391900006
PM 33250425
DA 2025-01-04
ER

PT J
AU Wang, DX
   Geng, W
   Han, L
   Song, R
   Qu, QS
   Chen, XY
   Luo, X
AF Wang, Dianxiu
   Geng, Wei
   Han, Lu
   Song, Ran
   Qu, Qiusi
   Chen, Xingyuan
   Luo, Xi
TI Pro-carcinogenic actions of miR-155/FOXO3a in colorectal cancer
   development
SO CELLULAR AND MOLECULAR BIOLOGY
LA English
DT Article
DE TALNEC2; miR-19a-3p; JNK; cerebral infarction; cell viability;
   inflammation; apoptosis
ID CELL-PROLIFERATION; SUPPRESSES PROLIFERATION; EXPRESSION; TUMOR;
   MICRORNAS; APOPTOSIS; MIGRATION; METASTASIS; INVASION; FOXO3A
AB Colorectal cancer (CRC) ranks third in cancer incidence and second in cancer mortality globally. MicroRNAs (miRNAs) are promising biomarkers and therapeutic targets for CRC diagnosis and treatment. The miR155 is reported to induce radiation resistance in CRC. In this study, we aimed to further clarify the role and underlying mechanism of the miR-155 in CRC cell malignancy. We found that miR-155 was significantly up-regulated in CRC tissues. The results of loss-of-function experiments revealed that miR-155 deficiency suppressed the proliferative capacity, invasion, and migration of CRC cells. Moreover, the downstream target genes of miR-155 were screened, and miR-155 was demonstrated to directly bind to FOXO3a in CRC cells to negatively regulate FOXO3a expression. FOXO3a was downregulated in CRC tissues and the expression of FOXO3a and miR-155 was in negative correlation in CRC tissues. FOXO3a overexpression alone was revealed to inhibit CRC cell growth, migration and invasion. Additionally, rescue assays showed that FOXO3a silencing significantly reversed the inhibitory effect of miR-155 deficiency on CRC cell malignant behaviors. In conclusion, miR-155 induces malignant phenotypes of CRC cells including cell proliferation, migration and invasion by targeting FOXO3a, which might provide clues for the targeted therapy of CRC.
C1 [Wang, Dianxiu; Han, Lu; Song, Ran; Qu, Qiusi; Chen, Xingyuan] Sijing Hosp Song Jiang Dist, Dept Gen Surg, Shanghai 201601, Peoples R China.
   [Geng, Wei] Xian Int Med Ctr Hosp, VIP Hlth Management Ctr, Xian 710100, Shaanxi, Peoples R China.
   [Luo, Xi] Peoples Hosp Qijiang Dist, Dept Gastroenterol, Chongqing 401420, Peoples R China.
RP Luo, X (corresponding author), Peoples Hosp Qijiang Dist, Dept Gastroenterol, Chongqing 401420, Peoples R China.
EM luoxi202324@163.com
RI Geng, Wei/KYQ-4201-2024
FU Agricultural Biotechnology Research Institute
FX This article was achieved based on the material and equipment of the
   Agricultural Biotechnology Research Institute, Harvard University, which
   the authors thank it
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NR 43
TC 1
Z9 1
U1 2
U2 4
PU C M B  ASSOC
PI POITIERS
PA 34 BOULEVARD SOLFERINO, 86000 POITIERS, FRANCE
SN 0145-5680
EI 1165-158X
J9 CELL MOL BIOL
JI Cell. Mol. Biol.
PY 2023
VL 69
IS 10
BP 160
EP 165
DI 10.14715/cmb/2023.69.10.23
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA Y3KY6
UT WOS:001104303300040
PM 37953568
OA hybrid
DA 2025-01-04
ER

PT J
AU Yao, YZ
   Wang, XC
   Zhou, DY
   Li, H
   Qian, H
   Zhang, JW
   Jiang, LH
   Wang, B
   Lin, Q
   Zhu, XG
AF Yao, Yizhou
   Wang, Xuchao
   Zhou, Diyuan
   Li, Hao
   Qian, Huan
   Zhang, Jiawen
   Jiang, Linhua
   Wang, Bin
   Lin, Qi
   Zhu, Xinguo
TI Loss of AKR1B10 promotes colorectal cancer cells proliferation and
   migration via regulating FGF1-dependent pathway
SO AGING-US
LA English
DT Article
DE AKR1B10; colorectal cancer; FGF1; targeted therapy
ID ALDO-KETO REDUCTASES; GROWTH-FACTOR-I; CISPLATIN RESISTANCE; EXPRESSION;
   1B10; OVEREXPRESSION; ACTIVATION; MEMBER; FGF1; IDENTIFICATION
AB Colorectal cancer (CRC) is a common malignancy worldwide with poor prognosis and survival rates. The aldoketo reductase family 1 member B10 (AKR1B10) plays an important role in metabolism, cell proliferation and mobility, and is downregulated in CRC. We hypothesized that AKR1B10 would promote CRC genesis via a noncanonical oncogenic pathway and is a novel therapeutic target. In this study, AKR1B10 expression levels in 135 pairs of CRC and para-tumor tissues were examined, and its oncogenic role was determined using in vitro and in vivo functional assays following genetic manipulation of CRC cells. AKR1B10 was downregulated in CRC tissues compared to the adjacent normal colorectal tissues, and associated with the clinicopathological status of the patients. AKR1B10 depletion promoted the proliferation and migration of CRC cells in vitro, while its ectopic expression had the opposite effect. AKR1B10 was also significantly correlated with FGF1 gene and protein levels. Knockdown of AKR1B10 promoted tumor growth in vivo, and increased the expression of FGF1. Finally, AKR1B10 inhibited FGF1, and suppressed the proliferation and migration ability of CRC cells in an FGF1-dependent manner. In conclusion, AKR1B10 acts as a tumor suppressor in CRC by inactivating FGF1, and is a novel target for combination therapy of CRC.
C1 [Yao, Yizhou; Wang, Xuchao; Zhou, Diyuan; Li, Hao; Qian, Huan; Zhang, Jiawen; Jiang, Linhua; Wang, Bin; Zhu, Xinguo] Soochow Univ, Affiliated Hosp 1, Dept Gen Surg, Suzhou, Jiangsu, Peoples R China.
   [Lin, Qi] Suzhou Emergency Ctr, Suzhou, Jiangsu, Peoples R China.
C3 Soochow University - China
RP Zhu, XG (corresponding author), Soochow Univ, Affiliated Hosp 1, Dept Gen Surg, Suzhou, Jiangsu, Peoples R China.; Lin, Q (corresponding author), Suzhou Emergency Ctr, Suzhou, Jiangsu, Peoples R China.
EM linqiemer@163.com; xgzhu45@163.com
RI Zhou, Diyuan/AAX-8401-2021; yao, yizhou/ABE-8728-2020
OI Yao, Yizhou/0000-0001-7976-1133
FU Project of National Science Foundation of Jiangsu Province, China
   [BK20161225]; Nanjing Medical University Science and Technology
   Development Fund [NMUB2018231]; Suzhou Special Project of Diagnosis and
   Treatment for key Clinical Disease [LCZX201814]; Suzhou Science and
   Technology Development Project [SYSD2018144]
FX This work was supported by Project of National Science Foundation of
   Jiangsu Province, China [grant number BK20161225]. Nanjing Medical
   University Science and Technology Development Fund (NMUB2018231), Suzhou
   Special Project of Diagnosis and Treatment for key Clinical Disease
   (LCZX201814) and Suzhou Science and Technology Development Project
   (SYSD2018144).
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NR 56
TC 23
Z9 23
U1 1
U2 10
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
SN 1945-4589
J9 AGING-US
JI Aging-US
PD JUL 15
PY 2020
VL 12
IS 13
BP 13059
EP 13075
DI 10.18632/aging.103393
PG 17
WC Cell Biology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Geriatrics & Gerontology
GA MM0YN
UT WOS:000549885700004
PM 32615540
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Kim, SY
   Kim, K
   Cho, SH
   Chun, SM
   Tak, E
   Hong, YS
   Kim, JE
   Kim, TW
AF Kim, Sun Young
   Kim, Kwoneel
   Cho, Su Han
   Chun, Sung-Min
   Tak, Eunyoung
   Hong, Yong Sang
   Kim, Jeong Eun
   Kim, Tae Won
TI Longitudinal change of genetic variations in cetuximab-treated
   metastatic colorectal cancer
SO CANCER GENETICS
LA English
DT Article
DE Colorectal cancer; Cetuximab; PCBP1; TGF-beta
ID RAS MUTATIONS; PRIMARY TUMOR; RESISTANCE; THERAPY; CHEMOTHERAPY;
   LANDSCAPE; EMERGENCE; CYTOSCAPE; EVOLUTION
AB Recurrent gene mutations and copy number alterations in cancer patients are presumably associated with resistance to targeted therapy. In the present study, we assessed the gene mutations and copy number alterations that recurrently occurred in cetuximab-treated patients with metastatic colorectal cancer (mCRC). Targeted next-generation sequencing was performed in the tumor samples obtained pre-and postcetuximab treatment to assess the variations that occurred during cetuximab treatment. Moreover, we identified the emergent gene mutations (CDK6, EPHA3, ERCC2, MYC, PCMTD1, PIK3CA, PRIM2, RICTOR, and ZNRF3) and copy number alterations (ARAF, BCL2, BRCA2, EGFR, MYC, and SMAD4) that were recurrently observed only in postprogression samples and not in pretreatment or posttreatment samples from patients revealing clinical response. Furthermore, to identify the feasible candidate variations implicated in treatment resistance, we examined the variants with clonal expansion during treatment and discovered PCBP1 as a variant associated with posttreatment progression. Various recurrent mutations were enriched in the TGF-beta signaling pathway. Collectively, we identified recurrent variations in mCRC samples exhibiting post-cetuximab progression. Additionally, future studies are required to evaluate the therapeutic potential of these variations. (c) 2021 Elsevier Inc. All rights reserved.
C1 [Kim, Sun Young; Hong, Yong Sang; Kim, Jeong Eun; Kim, Tae Won] Univ Ulsan Coll Med, Asan Med Ctr, Dept Oncol, 88 Olympic Ro,43 Gil, Seoul 05505, South Korea.
   [Kim, Kwoneel] Kyung Hee Univ, Dept Biol, Seoul, South Korea.
   [Cho, Su Han] Kyung Hee Univ, Dept Life & Nanopharmaceut Sci, Seoul, South Korea.
   [Chun, Sung-Min] Univ Ulsan Coll Med, Asan Med Ctr, Dept Pathol, Seoul, South Korea.
   [Chun, Sung-Min] Univ Ulsan Coll Med, Asan Ctr Canc Genome Discovery, Seoul, South Korea.
   [Tak, Eunyoung] Univ Ulsan Coll Med, Asan Med Ctr, Dept Convergence Med, Seoul, South Korea.
C3 University of Ulsan; Kyung Hee University; Kyung Hee University;
   University of Ulsan; Asan Medical Center; University of Ulsan;
   University of Ulsan; Asan Medical Center
RP Kim, TW (corresponding author), Univ Ulsan Coll Med, Asan Med Ctr, Dept Oncol, 88 Olympic Ro,43 Gil, Seoul 05505, South Korea.
EM twkimmd@amc.seoul.kr
RI Kim, Kwoneel/AAH-9178-2020; Kim, Tae Won/GRX-7323-2022
OI Cho, Su Han/0000-0001-5220-0352; Chun, Sung-Min/0000-0002-3357-1382
FU Bio & Medical Technology Development Program of the NRF by the Ministry
   of Science and ICT [2017M3A9B6061825]; Korea Health Technology R&D
   Project through the Korea Health Industry Development Institute (KHIDI)
   - Ministry of Health & Welfare, Republic of Korea [HI18C2383]; Asan
   Institute for Life Sciences, Seoul, Republic of Korea [2016-735]
FX This work was partially supported by a grant from the Bio & Medical
   Technology Development Program of the NRF by the Ministry of Science and
   ICT (2017M3A9B6061825) , a grant of the Korea Health Technology R&D
   Project through the Korea Health In-dustry Development Institute (KHIDI)
   funded by the Ministry of Health & Welfare, Republic of Korea
   (HI18C2383) , and a grant from the Asan Institute for Life Sciences ,
   Seoul, Republic of Korea (2016- 735) . We thank Dr. Joon Seo Lim from
   the Scientific Publications Team at Asan Medical Center for his
   assistance with the scien-tific editing of the manuscript. We also would
   like to thank Editage ( www.editage.co.kr) for English language editing.
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NR 46
TC 2
Z9 2
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 2210-7762
EI 2210-7770
J9 CANCER GENET-NY
JI Cancer Genet.
PD NOV
PY 2021
VL 258
BP 27
EP 36
DI 10.1016/j.cancergen.2021.06.007
EA JUL 2021
PG 10
WC Oncology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Genetics & Heredity
GA WB6FJ
UT WOS:000703665500006
PM 34315006
DA 2025-01-04
ER

PT J
AU Atanasova, VS
   Riedl, A
   Strobl, M
   Flandorfer, J
   Unterleuthner, D
   Weindorfer, C
   Neuhold, P
   Stang, S
   Hengstschlaeger, M
   Bergmann, M
   Dolznig, H
AF Atanasova, Velina S.
   Riedl, Angelika
   Strobl, Marcus
   Flandorfer, Julia
   Unterleuthner, Daniela
   Weindorfer, Claudia
   Neuhold, Patrick
   Stang, Simone
   Hengstschlaeger, Markus
   Bergmann, Michael
   Dolznig, Helmut
TI Selective Eradication of Colon Cancer Cells Harboring PI3K and/or MAPK
   Pathway Mutations in 3D Culture by Combined PI3K/AKT/mTOR Pathway and
   MEK Inhibition
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE 3D culture; targeted therapy; colorectal cancer; organoids; precision
   medicine
ID SELUMETINIB AZD6244; DUAL INHIBITION; TUMOR; RESISTANCE; EXPANSION;
   APOPTOSIS; MODELS; KRAS; 2D
AB Colorectal cancer (CRC) is the second deadliest cancer in the world. Besides APC and p53 alterations, the PI3K/AKT/MTOR and MAPK pathway are most commonly mutated in CRC. So far, no treatment options targeting these pathways are available in routine clinics for CRC patients. We systematically analyzed the response of CRC cells to the combination of small molecular inhibitors targeting the PI3K and MAPK pathways. We used CRC cells in 2D, 3D spheroid, collagen gel cultures and freshly isolated organoids for drug response studies. Readout for drug response was spheroid or organoid growth, spheroid outgrowth, metabolic activity, Western blotting and immunofluorescence. We found profound tumor cell destruction under treatment with a combination of Torin 1 (inhibiting mTOR), MK2206 (targeting AKT) and selumetinib (inhibiting MEK) in 3D but not in 2D. Induction of cell death was due to apoptosis. Western blot analysis revealed efficient drug action. Gedatolisib, a dual PI3K/mTOR inhibitor, could replace Torin1/MK2206 with similar efficiency. The presence of PI3K and/or RAS-RAF-MAPK pathway mutations accounted for treatment responsiveness. Here, we identified a novel, efficient therapy, which induced proliferation stop and tumor cell destruction in vitro based on the genetic background. These preclinical findings show promise to further test this combi-treatment in vivo in mice and to potentially develop a mutation specific targeted therapy for CRC patients.
C1 [Atanasova, Velina S.; Riedl, Angelika; Strobl, Marcus; Flandorfer, Julia; Unterleuthner, Daniela; Weindorfer, Claudia; Neuhold, Patrick; Stang, Simone; Hengstschlaeger, Markus; Dolznig, Helmut] Med Univ Vienna, Inst Med Genet, Wahringer Str 10, A-1090 Vienna, Austria.
   [Bergmann, Michael] Med Univ Vienna, Dept Gen Surg, Div Visceral Surg, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.
   [Bergmann, Michael; Dolznig, Helmut] Med Univ Vienna, Comprehens Canc Ctr Vienna, A-1090 Vienna, Austria.
   [Riedl, Angelika] Boehringer Ingelheim RCV GmbH & Co KG, Dr Boehringer Gasse 5-11, A-1130 Vienna, Austria.
   [Strobl, Marcus] IMP Vienna, Campus Vienna Bioctr 1, A-1030 Vienna, Austria.
   [Flandorfer, Julia] Med Univ Vienna, Dept Lab Med, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.
C3 Medical University of Vienna; Medical University of Vienna; Medical
   University of Vienna; Boehringer Ingelheim; Vienna Biocenter (VBC);
   Research Institute of Molecular Pathology (IMP); Medical University of
   Vienna
RP Dolznig, H (corresponding author), Med Univ Vienna, Inst Med Genet, Wahringer Str 10, A-1090 Vienna, Austria.; Dolznig, H (corresponding author), Med Univ Vienna, Comprehens Canc Ctr Vienna, A-1090 Vienna, Austria.
EM helmut.dolznig@meduniwien.ac.at
RI Dolznig, Helmut/L-7005-2015; Bergmann, Michael/GZK-7700-2022
OI Strobl, Marcus/0009-0002-1222-9876; Bergmann,
   Michael/0000-0001-8529-1166
FU CCC research grant (Initiative Krebsforschung) of the Medical University
   of Vienna; NFB [LSC18017]; WWTF Grant [LS20-042]; Austrian Academy of
   Sciences; Niederoesterreichische Forschungs und Bildungsges.m.bH.; Inst.
   of Medical Genetics, Medical University of Vienna
FX This research was funded in part by a CCC research grant (Initiative
   Krebsforschung) of the Medical University of Vienna; (H.D.), and the
   Niederoesterreichische Forschungs und Bildungsges.m.bH.; NFB, LSC18017
   (H.D.) and internal institutional funding (Inst. of Medical Genetics,
   Medical University of Vienna). MiB was supported by the WWTF Grant
   #LS20-042 "CheckMate-CRC". A.R. was and S.S. is a recipient of a DOC
   fellowship from the Austrian Academy of Sciences.
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NR 47
TC 9
Z9 9
U1 1
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JAN
PY 2023
VL 24
IS 2
AR 1668
DI 10.3390/ijms24021668
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 8D0FO
UT WOS:000917975100001
PM 36675180
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Dekker, E
   Tanis, PJ
   Vleugels, JLA
   Kasi, PM
   Wallace, MB
AF Dekker, Evelien
   Tanis, Pieter J.
   Vleugels, Jasper L. A.
   Kasi, Pashtoon M.
   Wallace, Michael B.
TI Colorectal cancer
SO LANCET
LA English
DT Review
ID III COLON-CANCER; ENDOSCOPIC MUCOSAL RESECTION; OXALIPLATIN-BASED
   CHEMOTHERAPY; EGFR MONOCLONAL-ANTIBODIES; LONG-TERM OUTCOMES;
   RECTAL-CANCER; ADJUVANT TREATMENT; 1ST-LINE TREATMENT; MISMATCH-REPAIR;
   OPEN-LABEL
AB Several decades ago, colorectal cancer was infrequently diagnosed. Nowadays, it is the world's fourth most deadly cancer with almost 900 000 deaths annually. Besides an ageing population and dietary habits of high-income countries, unfavourable risk factors such as obesity, lack of physical exercise, and smoking increase the risk of colorectal cancer. Advancements in pathophysiological understanding have increased the array of treatment options for local and advanced disease leading to individual treatment plans. Treatments include endoscopic and surgical local excision, downstaging preoperative radiotherapy and systemic therapy, extensive surgery for locoregional and metastatic disease, local ablative therapies for metastases, and palliative chemotherapy, targeted therapy, and immunotherapy. Although these new treatment options have doubled overall survival for advanced disease to 3 years, survival is still best for those with non-metastasised disease. As the disease only becomes symptomatic at an advanced stage, worldwide organised screening programmes are being implemented, which aim to increase early detection and reduce morbidity and mortality from colorectal cancer.
C1 [Dekker, Evelien; Vleugels, Jasper L. A.] Amsterdam Univ Med Ctr, Locat Acad Med Ctr, Dept Gastroenterol & Hepatol, NL-1105 AZ Amsterdam, Netherlands.
   [Tanis, Pieter J.] Amsterdam Univ Med Ctr, Locat Acad Med Ctr, Dept Surg, Amsterdam, Netherlands.
   [Vleugels, Jasper L. A.] Amsterdam Univ Med Ctr, Locat Acad Med Ctr, Dept Internal Med, Amsterdam, Netherlands.
   [Kasi, Pashtoon M.] Univ Iowa, Dept Med Oncol, Iowa City, IA USA.
   [Wallace, Michael B.] Mayo Clin, Dept Gastroenterol & Hepatol, Jacksonville, FL 32224 USA.
C3 University of Iowa; Mayo Clinic
RP Dekker, E (corresponding author), Amsterdam Univ Med Ctr, Locat Acad Med Ctr, Dept Gastroenterol & Hepatol, NL-1105 AZ Amsterdam, Netherlands.
EM e.dekker@amsterdamumc.nl
RI Wallace, Michael/GZL-9731-2022; Vleugels, Jasper/AAX-4659-2021; Kasi,
   Pashtoon/M-2569-2019; Dekker, Evelien/HOH-9015-2023; Tanis,
   Pieter/U-2827-2019
OI Tanis, Pieter/0000-0002-3146-3310; Wallace, Michael/0000-0002-6446-5785
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NR 165
TC 2345
Z9 2400
U1 61
U2 868
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0140-6736
EI 1474-547X
J9 LANCET
JI Lancet
PD OCT 19
PY 2019
VL 394
IS 10207
BP 1467
EP 1480
DI 10.1016/S0140-6736(19)32319-0
PG 14
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA JE5IX
UT WOS:000490727200031
PM 31631858
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Zhang, J
   Jiang, W
   Liu, W
   Wu, JJ
   Song, L
   Cheng, JX
   Yao, M
   Yang, LP
   Yao, DF
AF Zhang, Jie
   Jiang, Wen
   Liu, Wei
   Wu, Juan-Juan
   Song, Lei
   Cheng, Ji-Xian
   Yao, Ming
   Yang, Li-Ping
   Yao, Deng-Fu
TI Effective targeting of colorectal cancer cells using TORC1/2 kinase
   inhibitors <i>in vitro</i> and <i>in vivo</i>
SO FUTURE ONCOLOGY
LA English
DT Article
DE colorectal cancer; mTOR signaling pathway; PP242; rapamycin
ID MAMMALIAN TARGET; MTOR; RESISTANCE; PATHWAY; RAPAMYCIN; PI3K
AB Aim: We investigated the effects of TORC1/2 kinase inhibitors on colorectal cancer (CRC) cell lines. Materials & methods: Using selective TORC1/2 inhibitors, rapamycin and PP242, we assessed their effect on the growth of CRC cells in vitro and tumor growth in vivo. Results: Rapamycin and PP242 inhibit proliferation and induce apoptosis of CRC cells. They also enhance proapoptotic effect of conventional chemo drug doxorubicin in CRC cells in vitro. When combined with doxorubicin, rapamycin and PP242 almost completely inhibit tumor growth in vivo. Rapamycin and PP242 inhibit phosphorylation of Akt, ribosomal S6 kinase, 4EBP1 and mTOR. Conclusion: Our study suggests rapamycin and PP242 may be a useful therapeutic agent and inhibiting mTOR signaling pathway represents a new targeted therapy for CRC.
C1 [Zhang, Jie; Yao, Ming; Yao, Deng-Fu] Affiliated Hosp Nantong Univ, Nantong 226001, Peoples R China.
   [Zhang, Jie; Wu, Juan-Juan; Yang, Li-Ping] Nantong Univ, Sch Med, Nantong 226019, Peoples R China.
   [Jiang, Wen] Third Peoples Hosp Nantong, Dept Internal Med, Nantong 226001, Peoples R China.
   [Liu, Wei] Nantong Univ, Affiliated Hosp 2, Dept Orthoped, Nantong 226001, Peoples R China.
   [Song, Lei] Nantong Univ, Affiliated Hosp 2, Dept Paediat, Nantong 226001, Peoples R China.
   [Cheng, Ji-Xian] Wenzhou Med Univ, Affiliated Hosp 3, Dept Surg Oncol, Wenzhou 325001, Peoples R China.
C3 Nantong University; Nantong University; Nantong University; Nantong
   University; Wenzhou Medical University
RP Yao, DF (corresponding author), Affiliated Hosp Nantong Univ, Nantong 226001, Peoples R China.
EM romly80@sohu.com; romly80@sohu.com
RI Wu, Hui/JMB-2804-2023
FU National Natural Science Foundation of China [81272378]; China
   Postdoctoral Science Foundation [2013M541707]; Jiangsu Postdoctoral
   Science Foundation; Natural Science Fund project in Zhejiang Province
   [Y2100917]; Nantong Science and Technology Project [HS149095, HS149137,
   HS2014075]
FX The study was supported by grants from National Natural Science
   Foundation of China (81272378), China Postdoctoral Science Foundation
   (2013M541707), Jiangsu Postdoctoral Science Foundation, Natural Science
   Fund project in Zhejiang Province (Y2100917) and Nantong Science and
   Technology Project (HS149095, HS149137 and HS2014075). 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 25
TC 4
Z9 5
U1 1
U2 11
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1479-6694
EI 1744-8301
J9 FUTURE ONCOL
JI Future Oncol.
PY 2016
VL 12
IS 4
BP 515
EP 524
DI 10.2217/fon.15.248
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DC9FE
UT WOS:000369525700011
PM 26776341
DA 2025-01-04
ER

PT J
AU Fang, YY
   Liu, YN
   Dong, ZL
   Zhao, XC
   Zhang, MY
   Zheng, YW
   Yang, CS
   Wang, YF
   Liu, N
   Yan, P
   Ma, Y
   Yang, F
   Zheng, Y
   Zhang, WC
   Yang, JM
   Sun, ML
AF Fang, Yuying
   Liu, Yanan
   Dong, Zhilin
   Zhao, Xinchao
   Zhang, Mingyan
   Zheng, Yawen
   Yang, Chunsheng
   Wang, Yufeng
   Liu, Ning
   Yan, Peng
   Ma, Yuan
   Yang, Fei
   Zheng, Yan
   Zhang, Wencheng
   Yang, Jianmin
   Sun, Meili
TI JAML overexpressed in colorectal cancer promotes tumour proliferation by
   activating the PI3K-AKT-mTOR signalling pathway
SO SCIENTIFIC REPORTS
LA English
DT Article
DE Junctional adhesion molecule-like protein (JAML); Colorectal cancer;
   Proliferation; Targeted therapy; T-cell infiltration
ID JUNCTIONAL ADHESION MOLECULE; OPEN-LABEL; CHEMOTHERAPY; PEMBROLIZUMAB;
   KEYNOTE-177; BEVACIZUMAB; MIGRATION; CETUXIMAB; SURVIVAL; RECEPTOR
AB The expression and biological function of junctional adhesion molecule-like protein (JAML) in colorectal cancer (CRC) remain unclear. Paraffin tissue samples from 50 cases of CRC were collected to determine the expression of JAML. JAML was overexpressed or knock-down in CRC cells to evaluated the proliferation, migration and invasion in vitro and in vivo. Western-blot and others were applied to explore the mechanisms. The study showed that JAML was highly expressed within cancer tissues in 50% (25/50) of patients with CRC, and was correlated with higher TNM stage (p < 0.05). Patients of JAML(-high) group had poorer overall survival compared to JAML(-low) group (p = 0.0362, HR = 0.4295, 95% CI of 0.1908-0.9667). The tumour infiltrating lymphocytes (TILs) was lower in the JAML(-high) group than in the JAML(-low) group (p < 0.05). Overexpression of JAML promoted the proliferation, migration, and invasion of CRC by activating the PI3K-AKT-mTOR signalling pathway both in vitro and in vivo. TILs were reduced in JAML(-high) tumour tissues by decreasing chemokines such as CCL20 and CXCL9/10/11. Our study identified JAML, a potentially ideal target that is specifically highly expressed in CRC tissues, which promoted tumour proliferation, impaired T-lymphocytes infiltration, provided a promising therapeutic strategy for patients with CRC.
C1 [Fang, Yuying; Liu, Yanan; Dong, Zhilin; Zhao, Xinchao; Zhang, Mingyan; Zheng, Yawen; Yang, Chunsheng; Liu, Ning; Yan, Peng; Sun, Meili] Shandong First Med Univ, Cent Hosp, Dept Oncol, Jinan 250013, Shandong, Peoples R China.
   [Fang, Yuying; Liu, Yanan; Wang, Yufeng; Sun, Meili] Shandong Univ, Jinan Cent Hosp, Dept Oncol, Jinan 250013, Shandong, Peoples R China.
   [Fang, Yuying; Liu, Yanan; Zhang, Mingyan; Wang, Yufeng] Shandong First Med Univ, Cent Hosp, Res Ctr Translat Med, Lab Anim Ctr, Jinan 250013, Shandong, Peoples R China.
   [Dong, Zhilin; Zhao, Xinchao] Shandong First Med Univ, Dept Clin Med, Jinan 271016, Shandong, Peoples R China.
   [Ma, Yuan; Yang, Fei] Shandong First Med Univ, Cent Hosp, Dept Pathol, Jinan 250013, Shandong, Peoples R China.
   [Zheng, Yan] Shandong First Med Univ, Cent Hosp, Res Ctr Translat Med, Jinan 250013, Shandong, Peoples R China.
   [Zhang, Wencheng; Yang, Jianmin] Shandong Univ, Natl Key Lab Innovat & Transformat Luobing Theory, Key Lab Cardiovasc Remodeling & Funct Res, Chinese Minist Educ,Chinese Natl Hlth Commiss,Qil, Jinan 250012, Peoples R China.
   [Zhang, Wencheng; Yang, Jianmin] Shandong Univ, Qilu Hosp, Chinese Acad Med Sci, Dept Cardiol, Jinan 250012, 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 First Medical University
   & Shandong Academy of Medical Sciences; Shandong First Medical
   University & Shandong Academy of Medical Sciences; Shandong First
   Medical University & Shandong Academy of Medical Sciences; Shandong
   First Medical University & Shandong Academy of Medical Sciences;
   Shandong University; Shandong University; Chinese Academy of Medical
   Sciences - Peking Union Medical College
RP Sun, ML (corresponding author), Shandong First Med Univ, Cent Hosp, Dept Oncol, Jinan 250013, Shandong, Peoples R China.; Sun, ML (corresponding author), Shandong Univ, Jinan Cent Hosp, Dept Oncol, Jinan 250013, Shandong, Peoples R China.
EM smli1980@163.com
RI Sun, Meili/HLG-5634-2023; Zhang, Wencheng/AAO-8445-2020
OI Zhang, Wencheng/0000-0002-9416-6540
FU Natural Science Foundation of Shandong Province; Beijing Science
   Development Fund [KC2021-JX-0186-68];  [ZR2022LSW006]
FX This study was supported by the Natural Science Foundation of Shandong
   Province (ZR2022LSW006) and Beijing Science Development Fund
   (KC2021-JX-0186-68).
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NR 28
TC 0
Z9 0
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PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD OCT 18
PY 2024
VL 14
IS 1
AR 24514
DI 10.1038/s41598-024-75180-z
PG 13
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA J7X5B
UT WOS:001339153400053
PM 39424882
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Huang, JY
   Liu, WT
   Kang, WY
   He, YL
   Yang, RF
   Mou, XY
   Zhao, WJ
AF Huang, Jiayuan
   Liu, Wenting
   Kang, Wanying
   He, Yulong
   Yang, Ruifu
   Mou, Xiangyu
   Zhao, Wenjing
TI Effects of microbiota on anticancer drugs: Current knowledge and
   potential applications
SO EBIOMEDICINE
LA English
DT Review
DE Anticancer drug; Microbiota; Immune checkpoint inhibitor; Fecal
   microbiota transplantation; Probiotics
ID COLORECTAL-CANCER; FECAL MICROBIOTA; GUT MICROBIOTA; EFFICACY;
   CHEMOTHERAPY; RESISTANCE; IMMUNOTHERAPY; METABOLISM; TRANSPLANT;
   TOXICITY
AB Over the last decade, mounting evidence has revealed the key roles of gut microbiota in modulating the efficacy and toxicity of anticancer drugs, via mechanisms such as immunomodulation and microbial enzymatic degradation. As such, human microbiota presents as an exciting prospect for developing biomarkers for predicting treatment outcomes and interventional approaches for improving therapeutic effects. In this review, we analyze the current knowledge of the interplays among gut microorganisms, host responses and anticancer therapies (including cytotoxic chemotherapy and targeted therapy), with an emphasis on the immunomodulation function of microbiota which facilitates the efficacy of immune checkpoint inhibitors. Moreover, we propose several microbiota-modulating strategies including fecal microbiota transplantation and probiotics, which can be pursued to optimize the use and development of anticancer treatments. We anticipate that future clinical and preclinical studies will highlight the significance of human microbiome as a promising target towards precision medicine in cancer therapies. Copyright (C) 2022 The Authors. Published by Elsevier B.V.
C1 [Huang, Jiayuan; Liu, Wenting; Kang, Wanying; He, Yulong; Mou, Xiangyu; Zhao, Wenjing] Sun Yat Sen Univ, Sch Med, Shenzhen Campus, Shenzhen 518107, Guangdong, Peoples R China.
   [He, Yulong] Sun Yat Sen Univ, Affiliated Hosp 7, Guangdong Prov Key Lab Digest Canc Res, Shenzhen 518107, Guangdong, Peoples R China.
   [Yang, Ruifu] Beijing Inst Microbiol & Epidemiol, Dept Bacteriol, State Key Lab Pathogen & Biosecur, Beijing 100071, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Beijing Institute of
   Microbiology & Epidemiology
RP Mou, XY; Zhao, WJ (corresponding author), Sun Yat Sen Univ, Sch Med, Shenzhen Campus, Shenzhen 518107, Guangdong, Peoples R China.
EM mouxy5@ms.sysu.edu.cn; zhaowj29@ms.sysu.edu.cn
RI Mou, Xiangyu/ITT-8407-2023; Zhao, Jincun/ABD-8679-2021; Huang,
   Jiayuan/GPF-6281-2022; Kang, Wanying/E-8114-2016; Yang,
   Ruifu/A-2273-2011
OI Mou, Xiangyu/0000-0002-6227-6315; Yang, Ruifu/0000-0003-3219-7269; Zhao,
   Wenjing/0000-0003-1706-6324
FU National Key Research and Development Program of China [2020YFA0907800];
   Shenzhen Science and Technology Innovation Program
   [KQTD20200820145822023]; National Natural Science Foundation of China
   [31900056, 32000096]
FX Funding National Key Research and Development Program of China
   (2020YFA0907800) , Shenzhen Science and Technology Innovation Program
   (KQTD20200820145822023) and National Natural Science Foundation of China
   (31900056 and 32000096) .
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NR 74
TC 35
Z9 39
U1 5
U2 29
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2352-3964
J9 EBIOMEDICINE
JI EBioMedicine
PD SEP
PY 2022
VL 83
AR 104197
DI 10.1016/j.ebiom.2022.104197
PG 11
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA 6S6CF
UT WOS:000893071900001
PM 35933808
OA Green Published
DA 2025-01-04
ER

PT J
AU Lv, MY
   Cai, D
   Li, CH
   Chen, JG
   Li, GM
   Hu, CL
   Gai, BW
   Lei, JX
   Lan, P
   Wu, XJ
   He, XS
   Gao, F
AF Lv, Min-Yi
   Cai, Du
   Li, Cheng-Hang
   Chen, Junguo
   Li, Guanman
   Hu, Chuling
   Gai, Baowen
   Lei, Jiaxin
   Lan, Ping
   Wu, Xiaojian
   He, Xiaosheng
   Gao, Feng
TI Senescence-based colorectal cancer subtyping reveals distinct molecular
   characteristics and therapeutic strategies
SO MEDCOMM
LA English
DT Article
DE cancer subtype; colorectal cancer; multi-omics; senescence; therapeutic
   strategy
ID CELLULAR SENESCENCE; TUMOR HETEROGENEITY; IDENTIFICATION; HALLMARKS;
   DISCOVERY; BIOMARKER; CHINA
AB Cellular senescence has been listed as a hallmark of cancer, but its role in colorectal cancer (CRC) remains unclear. We comprehensively evaluated the transcriptome, genome, digital pathology, and clinical data from multiple datasets of CRC patients and proposed a novel senescence subtype for CRC. Multi-omics data was used to analyze the biological features, tumor microenvironment, and mutation landscape of senescence subtypes, as well as drug sensitivity and immunotherapy response. The senescence score was constructed to better quantify senescence in each patient for clinical use. Unsupervised learning revealed three transcriptome-based senescence subtypes. Cluster 1, characterized by low senescence and activated proliferative pathways, was sensitive to chemotherapeutic drugs. Cluster 2, characterized by intermediate senescence and high immune infiltration, exhibited significant immunotherapeutic advantages. Cluster 3, characterized by high senescence, high immune, and stroma infiltration, had a worse prognosis and maybe benefit from targeted therapy. We further constructed a senescence scoring system based on seven senescent genes through machine learning. Lower senescence scores were highly predictive of longer disease-free survival, and patients with low senescence scores may benefit from immunotherapy. We proposed the senescence subtypes of CRC and our findings provide potential treatment interventions for each CRC senescence subtype to promote precision treatment.
C1 [Lv, Min-Yi; Cai, Du; Li, Cheng-Hang; Chen, Junguo; Li, Guanman; Hu, Chuling; Gai, Baowen; Lei, Jiaxin; Lan, Ping; Wu, Xiaojian; He, Xiaosheng; Gao, Feng] Sun Yat Sen Univ, Affiliated Hosp 6, Dept Genaral Surg Colorectal Surg, Guangzhou, Peoples R China.
   [Lv, Min-Yi; Cai, Du; Li, Cheng-Hang; Chen, Junguo; Li, Guanman; Hu, Chuling; Gai, Baowen; Lei, Jiaxin; Lan, Ping; Wu, Xiaojian; He, Xiaosheng; Gao, Feng] Sun Yat Sen Univ, Affiliated Hosp 6, Guangdong Prov Key Lab Colorectal & Pelv Floor Dis, Guangzhou, Peoples R China.
   [Lv, Min-Yi; Cai, Du; Li, Cheng-Hang; Chen, Junguo; Li, Guanman; Hu, Chuling; Gai, Baowen; Lei, Jiaxin; Lan, Ping; Wu, Xiaojian; He, Xiaosheng; Gao, Feng] Sun Yat Sen Univ, Affiliated Hosp 6, Biomed Innovat Ctr, Guangzhou, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University; Sun Yat Sen University
RP Lan, P; Wu, XJ; He, XS; Gao, F (corresponding author), Sun Yat Sen Univ, Affiliated Hosp 6, Dept Genaral Surg Colorectal Surg, Guangzhou, Peoples R China.
EM lanping@mail.sysu.edu.cn; wuxjian@mail.sysu.edu.cn;
   hexsheng@mail.sysu.edu.cn; gaof57@mail.sysu.edu.cn
RI lan, ping/T-1708-2017; lei, jiaxin/HPH-6706-2023; Hu,
   chuling/AEJ-5246-2022
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NR 66
TC 5
Z9 5
U1 5
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2688-2663
J9 MEDCOMM
JI MedComm
PD AUG
PY 2023
VL 4
IS 4
AR e333
DI 10.1002/mco2.333
PG 16
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA M9BU5
UT WOS:001033102200001
PM 37502611
OA Green Published, gold
DA 2025-01-04
ER

PT S
AU Corcoran, RB
AF Corcoran, Ryan B.
BE Jacks, T
   Sawyers, CL
TI Circulating Tumor DNA: Clinical Monitoring and Early Detection
SO ANNUAL REVIEW OF CANCER BIOLOGY, VOL 3
SE Annual Review of Cancer Biology-Series
LA English
DT Article; Book Chapter
DE cell-free DNA; circulating tumor DNA; early detection; residual disease
ID CELL-FREE DNA; LUNG-CANCER; ACQUIRED-RESISTANCE; TARGETED THERAPY;
   CLONAL HEMATOPOIESIS; PRACTICE GUIDELINES; EGFR BLOCKADE; COLON-CANCER;
   HETEROGENEITY; MUTATIONS
AB Roughly 70 years after the presence of cell-freeDNA(cfDNA) in circulating blood was discovered, cfDNA has emerged as a transformative technology in clinical oncology. The ability to assess the presence, level, and composition of tumor DNA from a routine, noninvasive blood draw has opened the door to a broad array of high-impact clinical applications. While cfDNA is rapidly gaining clinical favor as a means of tumor mutational profiling without the need for an invasive biopsy, emerging applications in the areas of clinical monitoring and early cancer detection hold tremendous promise. These developing applications of cfDNA are reviewed herein.
C1 [Corcoran, Ryan B.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
   [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 02114 USA.; Corcoran, RB (corresponding author), Harvard Med Sch, Dept Med, Boston, MA 02115 USA.
EM rbcorcoran@partners.org
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NR 66
TC 6
Z9 7
U1 0
U2 8
PU ANNUAL REVIEWS
PI PALO ALTO
PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0897 USA
SN 2472-3428
J9 ANNU REV CANC BIOL
JI Annu. Rev. Canc. Biol.
PY 2019
VL 3
BP 187
EP 201
DI 10.1146/annurev-cancerbio-030518-055719
PG 15
WC Oncology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA BM3UP
UT WOS:000462707500010
OA Bronze
DA 2025-01-04
ER

PT J
AU Jung, J
   Kim, ST
   Ko, J
   Hong, JY
   Park, JO
   Ha, SY
   Lee, J
AF Jung, Jaeyun
   Kim, Seung Tae
   Ko, Jihoon
   Hong, Jung Yong
   Park, Joon Oh
   Ha, Sang Yun
   Lee, Jeeyun
TI Clinical Implication of <i>HER2</i> Aberration in Patients With
   Metastatic Cancer Using Next-Generation Sequencing: A Pan-Tumor Analysis
SO JCO PRECISION ONCOLOGY
LA English
DT Article
ID HER2-TARGETED THERAPY; GENE AMPLIFICATION; OVEREXPRESSION; RESISTANCE
AB PURPOSE Human epidermal growth factor receptor 2 (HER2) protein expression or gene amplification is a significant predictive biomarker for identifying patients with cancer, who may benefit from HER2-targeted therapy. The aim of this study was to survey the proportion of patients who had HER2 aberration and to investigate the correlation between HER2 amplification and HER2 overexpression in immunohistochemistry (IHC) as a real-world data. METHODS We surveyed the incidence of HER2 aberration including mutation (single-nucleotide variant [SNV]), amplification (copy-number variation), and fusion by next-generation sequencing (NGS) in 2,119 patients with cancer from Samsung Medical Center in South Korea. RESULTS Of 2,119 patients with cancer, 189 patients (8.9%) had HER2 aberration in their tumor specimen. Of 189 patients, 113 (5.3%) patients had HER2 amplification, 82 (3.9%) patients had HER2 mutations, and 11 (0.5%) patients had HER2 fusion. Of note, 10 patients (0.5%) had concurrent HER2 amplification and HER2 fusion. In addition, we identified that HER2 protein overexpression was strongly related to HER2 amplification by NGS. Of 74 patients with HER2 amplification only by NGS test, 64 patients (86.5%) had HER2 overexpression by IHC. Of 10 patients with concurrent HER2 amplification and fusion, 80% patients were HER2 overexpression. Among 51 patients with only HER2 mutation (SNV), 9 patients (17.6%) were HER2 (+). Interestingly, almost all patients with colorectal cancer (11 of 12) with HER2 amplification had very strong HER2 overexpression (3+) in their tumor specimen. CONCLUSION In conclusion, we showed that when patients with metastatic cancer receive NGS test, approximately 8.9% have HER2 aberrations in their tumor specimen. Most patients have HER2 amplification, and a small percentage of patients have HER2 fusion. A great majority of patients with HER2 amplification and/or HER2 fusion had HER2 (+) tumor by IHC.
C1 [Jung, Jaeyun; Kim, Seung Tae; Ko, Jihoon; Hong, Jung Yong; Park, Joon Oh; Lee, Jeeyun] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Div Hematol Oncol,Dept Med, Seoul, South Korea.
   [Jung, Jaeyun] Expt Therapeut Dev Ctr, Samsung Med Ctr, Seoul, South Korea.
   [Ha, Sang Yun] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol & Translat Genom, Seoul, South Korea.
   [Lee, Jeeyun] Sungkyunkwan Univ, Sch Med, Dept Med, Div Hematol Oncol,Samsung Med Ctr, 81 Irwon Ro, Seoul 06351, South Korea.
C3 Sungkyunkwan University (SKKU); Samsung Medical Center; Sungkyunkwan
   University (SKKU); Samsung Medical Center; Sungkyunkwan University
   (SKKU); Samsung Medical Center; Sungkyunkwan University (SKKU); Samsung
   Medical Center
RP Lee, J (corresponding author), Sungkyunkwan Univ, Sch Med, Dept Med, Div Hematol Oncol,Samsung Med Ctr, 81 Irwon Ro, Seoul 06351, South Korea.
EM jyunlee@skku.edu
RI Ko, Jihoon/C-5258-2019; Park, Junsu/IQU-2241-2023; Jung,
   Jaeyun/HZZ-4630-2023; kim, st/O-5928-2014
OI Ko, Jihoon/0000-0002-6555-3728; Jung, Jaeyun/0000-0001-5002-9846; Hong,
   Jung Yong/0000-0003-1363-9332; Park, Joon Oh/0000-0001-6502-2612
FU Korea Health Industry Development Institute (KHIDI) - Ministry of Health
   & Welfare, Republic of Korea [HR20C0025]
FX Supported by a grant of the Korea Health Technology R&D Project through
   the Korea Health Industry Development Institute (KHIDI),funded by the
   Ministry of Health & Welfare, Republic of Korea (GrantNo.: HR20C0025)
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NR 20
TC 1
Z9 1
U1 4
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2473-4284
J9 JCO PRECIS ONCOL
JI JCO Precis. Oncol.
PY 2023
VL 7
AR e2200537
DI 10.1200/PO.22.00537
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NA3W8
UT WOS:001197689200047
PM 37499191
OA hybrid
DA 2025-01-04
ER

PT J
AU Park, WY
   Lee, HJ
   Sim, DY
   Im, E
   Park, JE
   Ahn, CH
   Shim, BS
   Kim, SH
AF Park, Woon-Yi
   Lee, Hyo-Jung
   Sim, Deok-Yong
   Im, Eunji
   Park, Ji-Eon
   Ahn, Chi-Hoon
   Shim, Bum-Sang
   Kim, Sung-Hoon
TI miR193a-5p Mediated ZNF746 and c-Myc Signaling Axis Is Critically
   Involved in Morusin Induced Apoptosis in Colorectal Cancer Cells
SO CELLS
LA English
DT Article
DE morusin; colorectal cancer; apoptosis; ZNF746; c-Myc; miR-193a-5p
ID INFLAMMATION; FLAVONOIDS
AB Novel target therapy is on the spotlight for effective cancer therapy. Hence, in the present study, the underlying apoptotic mechanism of Morusin was explored in association with miR193a-5p mediated ZNF746/c-Myc signaling axis in colorectal cancer cells (CRCs). Herein, Morusin reduced the viability and the number of colonies in HCT116 and SW480 CRCs. Additionally, Morusin increased sub-G1 population, cleavages of poly (ADP-ribose) polymerase (PARP) and caspase-3 and inhibited the expression of zinc finger protein 746 (ZNF746) and c-Myc in HCT116 and SW480 cells. Conversely, overexpression of ZNF746 suppressed the ability of Morusin to abrogate the expression of c-Myc in HCT116 cells, as ZNF746 enhanced the stability of c-Myc via their direct binding through nuclear colocalization in HCT116 cells by immunofluorescence and immunoprecipitation. Notably, Morusin upregulated miR193a-5p as a tumor suppressor, while miR193a-5p inhibitor masked the ability of Morusin to reduce the expression of ZNF746, c-Myc, and pro-PARP in HCT116 cells. To our knowledge, these findings provide the novel insight on miR193a-5p mediated inhibition of ZNF746/c-Myc signaling in Morusin induced apoptosis in CRCs.
C1 [Park, Woon-Yi; Lee, Hyo-Jung; Sim, Deok-Yong; Im, Eunji; Park, Ji-Eon; Ahn, Chi-Hoon; Shim, Bum-Sang; Kim, Sung-Hoon] Kyung Hee Univ, Coll Korean Med, Dept Korean Pathol, Seoul 02447, South Korea.
C3 Kyung Hee University
RP Shim, BS; Kim, SH (corresponding author), Kyung Hee Univ, Coll Korean Med, Dept Korean Pathol, Seoul 02447, South Korea.
EM wy1319@naver.com; hyonice77@naver.com; simdy0821@naver.com;
   ji4137@naver.com; wdnk77@naver.com; ach2565@naver.com;
   eshimbs@khu.ac.kr; sungkim7@khu.ac.kr
RI Shim, Bum-sang/AAH-9081-2020; Lee, Hyo/G-6299-2019
OI kim, sunghoon/0000-0003-2423-1973
FU Korea Science and Engineering Foundation (KOSEF) - Korea government
   (MEST) [2021R1A2C2003277]
FX This work was supported by the Korea Science and Engineering Foundation
   (KOSEF) grant funded by the Korea government (MEST)
   (No.2021R1A2C2003277).
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Z9 4
U1 1
U2 7
PU MDPI
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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 2065
DI 10.3390/cells10082065
PG 13
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA UF8VK
UT WOS:000688845800001
PM 34440834
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Baraibar, I
   Ros, J
   Mulet, N
   Salvà, F
   Argilés, G
   Martini, G
   Cuadra, JL
   Sardo, E
   Ciardiello, D
   Tabernero, J
   Élez, E
AF Baraibar, Iosune
   Ros, Javier
   Mulet, Nuria
   Salva, Francesc
   Argiles, Guillem
   Martini, Giulia
   Cuadra, Jose Luis
   Sardo, Emilia
   Ciardiello, Davide
   Tabernero, Josep
   Elez, Elena
TI Incorporating traditional and emerging biomarkers in the clinical
   management of metastatic colorectal cancer: an update
SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS
LA English
DT Review
DE Biomarker; colorectal cancer; targeted therapy; relapse; ras refractory;
   BRAF; HER2; MSI; NTRK
ID MICROSATELLITE INSTABILITY; MISMATCH-REPAIR; RAS MUTATIONS; BRAF
   MUTATION; PHASE-II; INHIBITOR ENTRECTINIB; ACQUIRED-RESISTANCE; PLUS
   IRINOTECAN; OPEN-LABEL; CETUXIMAB
AB Introduction Molecular profiling has led to significantly longer survival in metastatic colorectal cancer (mCRC) patients. Clinical guidelines recommend testing for KRAS/NRAS, BRAF and MSI status, and new biomarkers such as HER2 amplification and NTRK fusions have emerged more recently in refractory CRC, supported by overwhelming clinical relevance. These biomarkers can guide treatment management to improve clinical outcomes in these patients. Areas covered Preclinical and clinical data over the last decade were reviewed for known and novel biomarkers with clinical implications in refractory CRC. Molecular alterations are described for classic and novel biomarkers, and data for completed and ongoing studies with targeted and immunotherapies are presented. Expert opinion Use of targeted therapies based on biomarker testing in CRC has enabled impressive improvements in clinical outcomes in refractory patients. BRAF, MSI, NRAS and KRAS should be tested upfront in all patients given their indisputable therapeutic implications. Other molecular alterations such as HER2 and NTRK are emerging. Testing for these alterations may further improve outcomes for refractory CRC patients. Nonetheless, many key aspects remain to be defined including the optimal timing and technique for testing, the most adequate panel, and whether all patients should be tested for all alterations.
C1 [Baraibar, Iosune; Ros, Javier; Salva, Francesc; Argiles, Guillem; Sardo, Emilia; Tabernero, Josep; Elez, Elena] Vall Hebron Univ Hosp, Dept Med Oncol, Barcelona, Spain.
   [Baraibar, Iosune; Ros, Javier; Mulet, Nuria; Salva, Francesc; Argiles, Guillem; Martini, Giulia; Ciardiello, Davide; Tabernero, Josep; Elez, Elena] Vall Hebron Inst Oncol VHIO, Dept Med Oncol, Barcelona, Spain.
   [Mulet, Nuria] Inst Catala Oncol IDIBELL, Dept Med Oncol, Barcelona, Spain.
   [Martini, Giulia; Ciardiello, Davide] Univ Campania Luigi Vanvitelli, Dipartimento Med Precis, Naples, Italy.
   [Cuadra, Jose Luis] IOB Quiron, Barcelona, Spain.
C3 Hospital Universitari Vall d'Hebron; Vall d'Hebron Institut d'Oncologia
   (VHIO); Institut d'Investigacio Biomedica de Bellvitge (IDIBELL);
   Institut Catala d'Oncologia; Universita della Campania Vanvitelli
RP Élez, E (corresponding author), Vall Hebron Inst Oncol VHIO, Vall Hebron Univ Hosp, Dept Med Oncol, Barcelona, Spain.
RI Ros, Javier/HKF-1171-2023; Martini, Giulia/AIB-8246-2022; Baraibar,
   Iosune/GXF-7067-2022; Ciardiello, Davide/AAC-4613-2022; Cuadra-Urteaga,
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OI Cuadra-Urteaga, Jose Luis/0000-0002-9495-7318; Ros,
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   Baraibar, Iosune/0000-0002-3500-9641; Salva,
   Francesc/0000-0001-9240-4907; MARTINI, Giulia/0000-0003-4093-2681
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NR 113
TC 8
Z9 8
U1 2
U2 8
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.
PD JUL 2
PY 2020
VL 20
IS 7
BP 653
EP 663
DI 10.1080/14737159.2020.1782194
EA JUN 2020
PG 11
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA MT6SV
UT WOS:000549066000001
PM 32552041
DA 2025-01-04
ER

PT J
AU Ma, YS
   Li, W
   Liu, Y
   Shi, Y
   Lin, QL
   Fu, D
AF Ma, Yu-Shui
   Li, Wen
   Liu, Yu
   Shi, Yi
   Lin, Qin-Lu
   Fu, Da
TI Targeting Colorectal Cancer Stem Cells as an Effective Treatment for
   Colorectal Cancer
SO TECHNOLOGY IN CANCER RESEARCH & TREATMENT
LA English
DT Review
DE CRC; CSC; CCSCs; targeted therapy; drug resistance
ID COLON-CANCER; MESENCHYMAL TRANSITION; SIGNALING PATHWAY; PROGRESSION;
   ACTIVATION; PROMOTES; GENE; METASTASIS; RESISTANCE; STERNNESS
AB As one of the common cancers that threaten human life, the recurrence and metastasis of colorectal cancer seriously affect the prognosis of patients. Although new drugs and comprehensive treatments have been adopted, the current treatment effect on this tumor, especially in advanced colorectal cancer, is still not satisfactory. More and more evidence shows that tumors are likely to be a stem cell disease. In recent years, the rise of cancer stem cell theory has provided a new way for cancer treatment. Studies have found that a small number of special cells in colorectal cancer tissues that induce tumorigenesis, proliferation, and promote tumor migration and metastasis, namely, colorectal cancer stem cells. Colorectal cancer stem cells are defined with a group of cell-surface markers, such as CD44, CD133, CD24, epithelial cell adhesion factor molecule, LGR5, and acetaldehyde dehydrogenase. They are highly tumorigenic, aggressive, and chemoresistant and thus are critical in the metastasis and recurrence of colorectal cancer. Therefore, targeting colorectal cancer stem cells may become an important research direction for the future cure of colorectal cancer.
C1 [Ma, Yu-Shui; Li, Wen; Lin, Qin-Lu; Fu, Da] Cent South Univ Forestry & Technol, Coll Food Sci & Engn, Natl Engn Lab Rice & By Prod Deep Proc, Changsha, Peoples R China.
   [Ma, Yu-Shui; Liu, Yu; Shi, Yi; Fu, Da] Tongji Univ, Sch Med, Shanghai Peoples Hosp 10, Cent Lab Med Res, Shanghai 200072, Peoples R China.
C3 Central South University of Forestry & Technology; Tongji University
RP Lin, QL (corresponding author), Cent South Univ Forestry & Technol, Coll Food Sci & Engn, Natl Engn Lab Rice & By Prod Deep Proc, Changsha, Peoples R China.; Fu, D (corresponding author), Tongji Univ, Sch Med, Shanghai Peoples Hosp 10, Cent Lab Med Res, Shanghai 200072, Peoples R China.
EM linql0403@126.com; fu800da900@126.com
RI Liu, You-Nian/G-2697-2013; ma, yushui/HGC-6206-2022; Fu,
   Da/GXF-2656-2022; Lin, Qinlu/B-1732-2019
OI Lin, Qinlu/0000-0003-2043-4220; Ma, Yu-Shui/0000-0002-5728-7458
FU National Natural Science Foundation of China [81972214, 81772932,
   81472202, 81201535, 81302065, 81671716, 81301993, 81372175, 81472209];
   Fundamental Research Funds for the Central Universities [22120170212,
   22120170117]; Shanghai Natural Science Foundation [12ZR1436000];
   Shanghai Municipal Commission of Health and Family Planning [201540228]
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: This study
   was supported partly by grants from the National Natural Science
   Foundation of China (81972214, 81772932, 81472202, 81201535, 81302065,
   81671716, 81301993, 81372175, and 81472209), The Fundamental Research
   Funds for the Central Universities (22120170212 and 22120170117),
   Shanghai Natural Science Foundation (12ZR1436000), and Shanghai
   Municipal Commission of Health and Family Planning (201540228).
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NR 105
TC 35
Z9 37
U1 1
U2 19
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.
PD JUL 31
PY 2020
VL 19
AR 1533033819892261
DI 10.1177/1533033819892261
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA NA3SZ
UT WOS:000559735600001
PM 32748700
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Mao, DL
   Zhang, Z
   Zhao, X
   Dong, XQ
AF Mao, Deli
   Zhang, Zhe
   Zhao, Xin
   Dong, Xiaoqiang
TI Exosome: a new perspective in colorectal cancer therapy
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
LA English
DT Review
DE Exosomes; colorectal cancer; treatment; drug resistance; metastasis
ID EMERGING ROLE; DELIVERY; PROMOTE; CELLS; SERUM; DIFFERENTIATION;
   MICROVESICLES; PROLIFERATION; RECURRENCE; EXPRESSION
AB Exosomes refer to the mediators between tumor cells and matrix information exchange. With the transfer of proteins and RNA mediated by exosomes, the microenvironment of tumors varies. Tumor-derived exosomes (TEXs) affect the progress, the treatment and the prognosis of colorectal cancer (CRC). In the present review, the latest research results of CRC-related exosomes in recent years are summarized, covering exosome-induced epithelial-mesenchymal cell transformation of cancer cells. They can potentiate angiogenesis, tumor cell movement, metastasis and migration and suppress immune response, and cancer chemotherapy resistance. Besides, the use of exosomes as carriers in cancer targeting therapy, and the safety and reliability of developing cancer vaccines with exosomes separated from body fluids are discussed as well. Lastly, the application prospects of exosomes as biomarkers in CRC diagnosis and prognosis are prospected.
C1 [Mao, Deli; Zhang, Zhe; Zhao, Xin; Dong, Xiaoqiang] Soochow Univ, Dept Gen Surg, Affiliated Hosp 1, Suzhou, Peoples R China.
C3 Soochow University - China
RP Dong, XQ (corresponding author), Soochow Univ, Dept Gen Surg, Affiliated Hosp 1, Suzhou, Peoples R China.
EM dongxq@hotmail.com
FU National Science Foundation of China (NSFC) [31770985]; Jiangsu
   Provincial Key Research and Development Program, China [BE2019665];
   Postdoctoral Science Foundation Grant of China [2016M591913]; Jiangsu
   Provincial Medical Youth Talent, China [QNRC2016732]; Jiangsu Provincial
   "Six Peaks Talent" Program, China [2016-WSW043]; Suzhou Municipal
   Project of Gusu Health Talent, Young Top Talent, China [2018057]; Gusu
   Health Talents Cultivation Program, China [GSWS2019028]; Scientific
   Research Program of Jiangsu Provincial "333 Projects", China
   [BRA2019327]; Science and Technology Program of Suzhou City, China
   [SYS2019053, SLC201906]; Provincial Natural Science Foundation of
   Jiangsu Province, China [BK20161225]; Scientific Research Program of
   Jiangsu Provincial Commission of Health and Family Planning, China
   [H201620]
FX This study was supported by grants from the National Science Foundation
   of China (NSFC, no. 31770985). Jiangsu Provincial Key Research and
   Development Program, China (no. BE2019665). Postdoctoral Science
   Foundation Grant of China (no. 2016M591913). Jiangsu Provincial Medical
   Youth Talent, China (no. QNRC2016732). Jiangsu Provincial "Six Peaks
   Talent" Program, China (no. 2016-WSW043). Suzhou Municipal Project of
   Gusu Health Talent, Young Top Talent, China (no. 2018057). Gusu Health
   Talents Cultivation Program, China (no. GSWS2019028). Scientific
   Research Program of Jiangsu Provincial "333 Projects", China (no.
   BRA2019327). Science and Technology Program of Suzhou City, China (no.
   SYS2019053, no. SLC201906). Provincial Natural Science Foundation of
   Jiangsu Province, China (no. BK20161225). Scientific Research Program of
   Jiangsu Provincial Commission of Health and Family Planning, China (no.
   H201620).
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NR 87
TC 1
Z9 1
U1 0
U2 7
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1940-5901
J9 INT J CLIN EXP MED
JI Int. J. Clin. Exp. Med.
PY 2019
VL 12
IS 11
BP 12619
EP 12632
PG 14
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA JS4TZ
UT WOS:000500300700002
DA 2025-01-04
ER

PT J
AU Liu, JX
   Wu, YY
   Meng, S
   Xu, P
   Li, ST
   Li, Y
   Hu, XY
   Ouyang, L
   Wang, G
AF Liu, Jiaxi
   Wu, Yongya
   Meng, Sha
   Xu, Ping
   Li, Shutong
   Li, Yong
   Hu, Xiuying
   Ouyang, Liang
   Wang, Guan
TI Selective autophagy in cancer: mechanisms, therapeutic implications, and
   future perspectives
SO MOLECULAR CANCER
LA English
DT Review
DE Selective autophagy; Cancer; Molecular mechanism; Small-molecule
   compounds; Targeted therapy
ID ENDOPLASMIC-RETICULUM TURNOVER; HELICOBACTER-PYLORI CAGA;
   TUMOR-SUPPRESSOR GENE; COA RACEMASE AMACR; CELL-PROLIFERATION; PROTEIN
   EXPRESSION; PANCREATIC-CANCER; COLORECTAL-CANCER; OXIDATIVE STRESS;
   LIPID DROPLETS
AB Eukaryotic cells engage in autophagy, an internal process of self-degradation through lysosomes. Autophagy can be classified as selective or non-selective depending on the way it chooses to degrade substrates. During the process of selective autophagy, damaged and/or redundant organelles like mitochondria, peroxisomes, ribosomes, endoplasmic reticulum (ER), lysosomes, nuclei, proteasomes, and lipid droplets are selectively recycled. Specific cargo is delivered to autophagosomes by specific receptors, isolated and engulfed. Selective autophagy dysfunction is closely linked with cancers, neurodegenerative diseases, metabolic disorders, heart failure, etc. Through reviewing latest research, this review summarized molecular markers and important signaling pathways for selective autophagy, and its significant role in cancers. Moreover, we conducted a comprehensive analysis of small-molecule compounds targeting selective autophagy for their potential application in anti-tumor therapy, elucidating the underlying mechanisms involved. This review aims to supply important scientific references and development directions for the biological mechanisms and drug discovery of anti-tumor targeting selective autophagy in the future.
C1 [Liu, Jiaxi; Wu, Yongya; Meng, Sha; Li, Shutong; Li, Yong; Hu, Xiuying; Ouyang, Liang; Wang, Guan] Sichuan Univ, West China Hosp,West China Sch Nursing, Innovat Ctr Nursing Res,Natl Clin Res Ctr Geriatr, Canc Ctr,Nursing Key Lab Sichuan Prov,State Key La, Chengdu 610041, Peoples R China.
   [Xu, Ping] Zigong Fourth Peoples Hosp, Emergency Dept, Zigong 643000, Peoples R China.
C3 Sichuan University
RP Hu, XY; Ouyang, L; Wang, G (corresponding author), Sichuan Univ, West China Hosp,West China Sch Nursing, Innovat Ctr Nursing Res,Natl Clin Res Ctr Geriatr, Canc Ctr,Nursing Key Lab Sichuan Prov,State Key La, Chengdu 610041, Peoples R China.
EM huxiuying@scu.edu.cn; ouyangliang@scu.edu.cn; guan8079@163.com
RI Xu, Ping/JAD-1741-2023
FU National Natural Science Foundation of China [22177083, 82273770];
   Sichuan Science and Technology Program [2022NSFSC1290]; The 1.3.5
   project for disciplines of excellence - Clinical Research Incubation
   Project, West China Hospital, Sichuan University [ZYJC21016]; West China
   Nursing Discipline Development Special Fund Project, Sichuan University
   [HXHL21011]
FX This work was supported by the National Natural Science Foundation of
   China (Grant 22177083 and 82273770), Sichuan Science and Technology
   Program (Grant 2022NSFSC1290), 1.3.5 project for disciplines of
   excellence - Clinical Research Incubation Project, West China Hospital,
   Sichuan University (ZYJC21016), and West China Nursing Discipline
   Development Special Fund Project, Sichuan University (Grant HXHL21011).
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NR 229
TC 20
Z9 20
U1 11
U2 26
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD JAN 24
PY 2024
VL 23
IS 1
AR 22
DI 10.1186/s12943-024-01934-y
PG 30
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA FS1D1
UT WOS:001147743200001
PM 38262996
OA gold
DA 2025-01-04
ER

PT J
AU Xu, W
   Rush, J
   Rickett, K
   Coward, JIG
AF Xu, Wen
   Rush, Jack
   Rickett, Kirsty
   Coward, Jermaine I. G.
TI Mucinous ovarian cancer: A therapeutic review
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Mucinous ovarian cancer; Chemotherapy; Targeted therapy;
   Gastrointestinal cancers
ID METASTATIC COLORECTAL-CANCER; PHASE-II TRIAL; RECURRENT EPITHELIAL
   OVARIAN; HIGH-DOSE LEUCOVORIN; ADVANCED-STAGE OVARIAN; FLUOROURACIL PLUS
   LEUCOVORIN; HEAVILY PRETREATED PATIENTS; PLATINUM-RESISTANT; 1ST-LINE
   TREATMENT; PRIMARY PERITONEAL
AB Mucinous ovarian cancer represents approximately 3% of epithelial ovarian cancers (EOC). Despite this seemingly low prevalence, it remains a diagnostic and therapeutic conundrum that has resulted in numerous attempts to adopt novel strategies in managing this disease. Anecdotally, there has been a prevailing notion that established gold standard systemic regimens should be substituted for those utilised in cancers such as gastrointestinal (GI) malignancies; tumours that share more biological similarities than other EOC subtypes. This review summarises the plethora of small studies which have adopted this philosophy and influenced the design of the multinational GOG142 study, which was ultimately terminated due to poor accrual. To date, there is a paucity of evidence to support delivering 'GI style' chemotherapy for mucinous ovarian cancer over and above carboplatin-paclitaxel doublet therapy. Hence there is an urge to develop studies focused on targeted therapeutic agents driven by refined mutational analysis and conducted within the context of harmonised international collaborations. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
C1 [Xu, Wen; Coward, Jermaine I. G.] Mater Hlth Serv, Raymond Terrace, Brisbane, Qld 4101, Australia.
   [Rush, Jack; Coward, Jermaine I. G.] Univ Queensland, Sch Med, St Lucia, Qld 4072, Australia.
   [Rickett, Kirsty] Univ Queensland Lib, UQ Mater McAuley Lib, Brisbane, Qld 4101, Australia.
   [Coward, Jermaine I. G.] Princess Alexandra Hosp, Ipswich Rd, Woolloongabba, Qld 4102, Australia.
C3 Mater Health Services; University of Queensland; University of
   Queensland; Princess Alexandra Hospital
RP Coward, JIG (corresponding author), Princess Alexandra Hosp, Ipswich Rd, Brisbane, Qld 4102, Australia.
EM Jermaine.Coward@health.qld.gov.au
RI Rickett, Kirsty/B-3691-2015; Xu, Wen/JYY-4482-2024; Coward,
   Jermaine/F-2903-2016
OI Xu, Wen/0009-0007-0759-5974; Coward, Jermaine/0000-0002-2309-9379
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NR 138
TC 43
Z9 45
U1 0
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD JUN
PY 2016
VL 102
BP 26
EP 36
DI 10.1016/j.critrevonc.2016.03.015
PG 11
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA DN1NQ
UT WOS:000376833100003
PM 27083591
DA 2025-01-04
ER

PT J
AU Acharya, D
   Satapathy, S
   Thathapudi, JJ
   Somu, P
   Mishra, G
AF Acharya, Diptikanta
   Satapathy, Sagarika
   Thathapudi, Jesse Joel
   Somu, Prathap
   Mishra, Gitanjali
TI Biogenic synthesis of silver nanoparticles using marine algae
   <i>Cladophora glomerata</i> and evaluation of apoptotic effects in human
   colon cancer cells
SO MATERIALS TECHNOLOGY
LA English
DT Article
DE Green synthesis; p53-dependent apoptosis; cell cycle; colon cancer; DNA
   damage; silver nanoparticle
AB In the current study, silver nanoparticle (AgNPs) is biogenically synthesised using marine algae Cladophora glomerata extract, and anticancer activity was studied against colon cancer cells HCT-116 in-vitro. Biosynthesised silver nanoparticles characterised using TEM, UV-Spectrophotometry, XRD, and FTIR. XRD and UV-Spectrophotometry confirmed AgNPs formation with a mean size of 8-11 nm. AgNPs demonstrated specific cytotoxicity to colon cancer cells, whereas no or minimal effect was observed in human colon epithelial cell line cells. The fluorescence microscopic of AgNPs treated HCT-116 after nucleus staining confirmed the apoptosis induction in HCT-116 cells. In the immunoblotting study, the expression of proapoptotic markers like caspases, p21, BAX/BCL-XL, and NF-kB, along with a decrease of further confirmed the p53-dependent apoptosis induced by AgNPs. Hence, overall, we concluded that our biogenically synthesised AgNPs nanoparticles possess a selective apoptotic effect against colon cancer HCT-116 cells and potential to be used in targeted therapy for colon cancer.
C1 [Acharya, Diptikanta; Satapathy, Sagarika] GIET Univ, Dept Biotechnol, Gunupur 765022, Odisha, India.
   [Acharya, Diptikanta; Mishra, Gitanjali] Berhampur Univ, Dept Zool, Berhampur 760007, Orissa, India.
   [Thathapudi, Jesse Joel; Somu, Prathap] Karunya Inst Technol & Sci Deemed Univ, Dept Biotechnol, Coimbatore, Tamil Nadu, India.
C3 GIET University; Berhampur University; Karunya Institute of Technology &
   Sciences
RP Acharya, D (corresponding author), GIET Univ, Dept Biotechnol, Gunupur 765022, Odisha, India.; Mishra, G (corresponding author), Berhampur Univ, Dept Zool, Berhampur 760007, Orissa, India.
EM dacharya249@gmail.com
RI Thathapudi, Jesse Joel/AAD-3158-2019; SOMU, PRATHAP/AAC-6584-2020
OI SOMU, PRATHAP/0000-0002-3615-8200; Joel T, Jesse/0000-0003-2055-947X
FU Karunya Institute of Technology and Sciences (Deemed-to-be University)
FX The authors would like to extend their sincere appreciation to the
   Director of NRME Research Laboratory, Newredmars Education Pvt Ltd for
   allowing to carry out the research work. The authors are also thankful
   to Dr Pralay Ranjan Behera, Scientist, Marine Biodiversity Division,
   Regional Centre of ICAR - Central Marine Fisheries Research Institute,
   Visakhapatnam, Andhra Pradesh for the identification of algal species
   Cladophora glomerata for analysis. The authors sincerely thank the
   Karunya Institute of Technology and Sciences (Deemed-to-be University)
   for their support, encouragement, and extending all the necessary
   facilities in the university.
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NR 48
TC 31
Z9 31
U1 1
U2 11
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1066-7857
EI 1753-5557
J9 MATER TECHNOL
JI Mater. Technol.
PD JUL 3
PY 2022
VL 37
IS 8
BP 569
EP 580
DI 10.1080/10667857.2020.1863597
EA DEC 2020
PG 12
WC Materials Science, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Materials Science
GA 2E1XI
UT WOS:000603789300001
DA 2025-01-04
ER

PT J
AU Coccia, M
   Wang, LL
AF Coccia, Mario
   Wang, Lili
TI Path-breaking directions of nanotechnology-based chemotherapy and
   molecular cancer therapy
SO TECHNOLOGICAL FORECASTING AND SOCIAL CHANGE
LA English
DT Article
DE Nanotechnology; Nanoscience; Biomedicine; Nanomedicine; Target therapy;
   Radical innovation; Chemotherapy; Cancer; Bibliometrics; Publications;
   Technological trajectories; Technological paradigm; Mortality driven
ID RESEARCH-AND-DEVELOPMENT; TECHNOLOGICAL-CHANGE; CONTRAST AGENTS; DRIVING
   FORCES; QUANTUM DOTS; IN-VITRO; DELIVERY; DRUG; NANOPARTICLES;
   COMMERCIALIZATION
AB A fundamental question in the field of technological forecasting and foresight is how to detect likely fruitful technological trajectories in new research fields, such as nanomedicine. We confront this question by developing an approach based on trends and networks of vital variables, analyzed by bibliometrics, which endeavours to detect fruitful trajectories of nanotechnology applied to ground-breaking anti-cancer treatments. Results tend to show two main technological waves of cancer treatments by nanotechnology applications. The early technological wave in the early 2000s was embodied in some types of chemotherapy agents with a broad spectrum of application, while after 2006 the second technological wave appeared with new applications of chemotherapy agents and molecular target therapy by nanotechnology. The present study shows new directions of nanotechnology-based chemotherapy and molecular cancer therapy in new treatments for breast, lung, brain and colon cancers. A main finding of this study is the recognition that, since the late 2000s, the sharp increase of several technological trajectories of anticancer drugs applied by nanotechnology seems to be driven by high rates of mortality of some types of cancers (e.g. pancreatic and brain) in order to find more effective anticancer therapies that increase the progression-free survival of patients: the so-called technological trajectories mortality driven. The study also points out that global research leaders tend to specialize in anticancer drugs, via nanotechnology, for specific cancers (e.g. Switzerland in prostate cancer, Japan in colon cancer, China in ovarian cancer and Greece in pancreatic cancer). These ground-breaking technological trajectories are paving new directions in biomedicine and generating a revolution in clinical practice that may lead to more effective anticancer treatments in the not-too-distant future. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Coccia, Mario] CNR, Natl Res Council Italy, I-10024 Turin, Italy.
   [Coccia, Mario] RAND Corp, Washington, DC USA.
   [Wang, Lili] UNU, MERIT, Maastricht, Netherlands.
C3 Consiglio Nazionale delle Ricerche (CNR); RAND Corporation; Maastricht
   University
RP Coccia, M (corresponding author), CNR, Natl Res Council Italy, Via Real Collegio 30, I-10024 Turin, Italy.
EM m.coccia@ceris.cnr.it
RI Wang, Lili/AAG-9458-2020; Coccia, Mario/F-9793-2015
OI Wang, Lili/0000-0002-0082-8487; Coccia, Mario/0000-0003-1957-6731
FU CNR-National Research Council of Italy [0045595]
FX This research started in 2012 by authors and further developed in 2013
   while Mario Coccia was a visiting scholar at UNU-MERIT in Maastricht. We
   thank Prof. Bart Verspagen and Secondo Rolfo for the fruitful
   suggestions to this paper. Mario Coccia gratefully acknowledges the
   CNR-National Research Council of Italy for the financial support to this
   research project by the short mobility programme at UNU-MERIT (N.
   0045595 of the 25 July 2013). Preliminary results have been presented at
   the S.NET 4th Annual Meeting of the society for the study of nanoscience
   and emerging technologies (22-25 October 2012), University of Twente
   (The Netherlands). The usual disclaimer applies.
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Z9 49
U1 0
U2 73
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0040-1625
EI 1873-5509
J9 TECHNOL FORECAST SOC
JI Technol. Forecast. Soc. Chang.
PD MAY
PY 2015
VL 94
BP 155
EP 169
DI 10.1016/j.techfore.2014.09.007
PG 15
WC Business; Regional & Urban Planning
WE Social Science Citation Index (SSCI)
SC Business & Economics; Public Administration
GA CI8SP
UT WOS:000355042300009
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Lee, PY
   Syazwani, F
   Low, TY
AF Lee, Pey Yee
   Syazwani, Farina
   Low, Teck Yew
TI Biomarkers for colorectal cancer chemotherapy: Recent updates and future
   perspective
SO MALAYSIAN JOURNAL OF PATHOLOGY
LA English
DT Review
DE Biomarker; chemotherapy; colorectal cancer; prediction; treatment
   response
ID III COLON-CANCER; TUMOR-INFILTRATING LYMPHOCYTES; PHASE-III; GUT
   MICROBIOTA; MICROSATELLITE INSTABILITY; ADJUVANT CHEMOTHERAPY;
   PROGNOSTIC BIOMARKER; MOLECULAR SUBTYPES; CLINICAL-RELEVANCE; 1ST-LINE
   TREATMENT
AB During the last few decades, the treatment options available for patients with metastatic colorectal cancer (mCRC) have undergone continuous improvements, transitioning from conventional chemotherapy to targeted therapy. These therapeutic innovations have led to significant improvements in patient clinical outcomes. However, there remains a need to improve the outcome for many CRC patients. Chemotherapy remains a cornerstone of CRC treatment, but the wide variability in tumour response and adverse reactions to chemotherapy poses a challenge to cancer treatment management. As a result, there is an unmet need to identify predictive biomarkers of chemotherapeutic response to guide treatment decisions. In this review, we summarise the conventional biomarkers used to predict chemotherapy responses in CRC and provide an overview of emerging predictive biomarkers based on the current understanding of the molecular biology of treatment response. Finally, we explore the challenges and future prospects of biomarker discovery to improve the prediction of patient response and ensure optimal treatment management for patients with metastatic CRC.
C1 [Lee, Pey Yee; Syazwani, Farina; Low, Teck Yew] Univ Kebangsaan Malaysia, UKM Med Mol Biol Inst UMBI, Kuala Lumpur 56000, Malaysia.
   [Lee, Pey Yee; Low, Teck Yew] Univ Kebangsaan Malaysia UKM, UKM Med Mol Biol Inst UMBI, UKM Med Ctr, Jalan Yaacob Latiff, Kuala Lumpur 56000, Malaysia.
C3 Universiti Kebangsaan Malaysia; Universiti Kebangsaan Malaysia
RP Lee, PY; Low, TY (corresponding author), Univ Kebangsaan Malaysia UKM, UKM Med Mol Biol Inst UMBI, UKM Med Ctr, Jalan Yaacob Latiff, Kuala Lumpur 56000, Malaysia.
EM leepeyyee@ukm.edu.my; lowteckyew@ppukm.ukm.edu.my
RI Low, Teck/Q-5946-2019; Lee, Pey/Q-9961-2019
FU Higher Institution Centre of Excellence (HICoE) - Ministry of Higher
   Education (MoHE) Malaysia [JJ-2021-004]; UKM Medical Molecular Biology
   Institute (UMBI)
FX This study was supported by the Higher Institution Centre of Excellence
   (HICoE) Grant (JJ-2021-004) awarded by the Ministry of Higher Education
   (MoHE) Malaysia to T.Y. Low. The UKM Medical Molecular Biology Institute
   (UMBI) was awarded the HICoE status in 2009.
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NR 112
TC 1
Z9 1
U1 0
U2 0
PU MALAYSIAN JOURNAL PATHOLOGY
PI KUALA LUMPUR
PA UNIV MALAYSIA, FAC MEDICINE, DEPT PATHOLOGY, KUALA LUMPUR, 59100,
   MALAYSIA
SN 0126-8635
J9 MALAYS J PATHOL
JI Malay. J. Pathol.
PD DEC
PY 2023
VL 45
IS 3
BP 317
EP 331
PG 15
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA HD1R8
UT WOS:001157469500012
PM 38155375
DA 2025-01-04
ER

PT J
AU Dey, A
   Mitra, A
   Pathak, S
   Prasad, S
   Zhang, AS
   Zhang, H
   Sun, XF
   Banerjee, A
AF Dey, Amit
   Mitra, Abhijit
   Pathak, Surajit
   Prasad, Suhanya
   Zhang, Alexander Sun
   Zhang, Hong
   Sun, Xiao-Feng
   Banerjee, Antara
TI Recent Advancements, Limitations, and Future Perspectives of the use of
   Personalized Medicine in Treatment of Colon Cancer
SO TECHNOLOGY IN CANCER RESEARCH & TREATMENT
LA English
DT Review
DE colon cancer; personalized treatment; precision medicine; targeted
   therapy; immunotherapy
ID METASTATIC COLORECTAL-CANCER; COMPLETE MESOCOLIC EXCISION; DNA MISMATCH
   REPAIR; PRECISION MEDICINE; COMBINED BRAF; T-CELL; INHIBITION;
   EXPRESSION; MUTATIONS; ENCORAFENIB
AB Due to the heterogeneity of colon cancer, surgery, chemotherapy, and radiation are ineffective in all cases. The genomic profile and biomarkers associated with the process are considered in personalized medicine, along with the patient's personal history. It is based on the response of the targeted therapies to specific genetic variations. The patient's genetic transcriptomic and epigenetic features are evaluated, and the best therapeutic approach and diagnostic testing are identified through personalized medicine. This review aims to summarize all the necessary, updated information on colon cancer related to personalized medicine. Personalized medicine is gaining prominence as generalized treatments are finding it challenging to contain colon cancer cases which currently rank fourth among global cancer incidence while being the fifth largest in total death cases worldwide. In personalized therapy, patients are grouped into specific categories, and the best therapeutic approach is chosen based on evaluating their molecular features. Various personalized strategies are currently being explored in the treatment of colon cancer involving immunotherapy, phytochemicals, and other biomarker-specific targeted therapies. However, significant challenges must be overcome to integrate personalized medicine into healthcare systems completely. We look at the various signaling pathways and genetic and epigenetic alterations associated with colon cancer to understand and identify biomarkers useful in targeted therapy. The current personalized therapies available in colon cancer treatment and the strategies being explored to improve the existing methods are discussed. This review highlights the advantages and limitations of personalized medicine in colon cancer therapy. The current scenario of personalized medicine in developed countries and the challenges faced in middle- and low-income countries are also summarized. Finally, we discuss the future perspectives of personalized medicine in colon cancer and how it could be integrated into the healthcare systems.
C1 [Dey, Amit; Mitra, Abhijit; Pathak, Surajit; Banerjee, Antara] Chettinad Hosp & Res Inst, Fac Allied Hlth Sci, Chettinad Acad Res & Educ, Chennai, India.
   [Prasad, Suhanya] Med Univ Bialystok, Dept Med Microbiol & Nanobiomed Engn, Bialystok, Poland.
   [Zhang, Alexander Sun] Karolinska Inst, Dept Oncol Pathol, Solna, Sweden.
   [Zhang, Hong] Orebro Univ, Sch Med, Dept Med Sci, Orebro, Sweden.
   [Sun, Xiao-Feng] Linkoping Univ, Dept Oncol, Linkoping, Sweden.
   [Sun, Xiao-Feng] Linkoping Univ, Dept Biomed & Clin Sci, Linkoping, Sweden.
   [Sun, Xiao-Feng] Linkoping Univ, Dept Oncol, S-58183 Linkoping, Sweden.
   [Sun, Xiao-Feng] Linkoping Univ, Dept Biomed & Clin Sci, S-58183 Linkoping, Sweden.
   [Banerjee, Antara] Chettinad Hosp & Res Inst, Chettinad Acad Res & Educ, Fac Allied Hlth Sci, Dept Med Biotechnol, Chennai 603103, Tamil Nadu, India.
C3 Medical University of Bialystok; Karolinska Institutet; Orebro
   University; Linkoping University; Linkoping University; Linkoping
   University; Linkoping University
RP Sun, XF (corresponding author), Linkoping Univ, Dept Oncol, S-58183 Linkoping, Sweden.; Sun, XF (corresponding author), Linkoping Univ, Dept Biomed & Clin Sci, S-58183 Linkoping, Sweden.; Banerjee, A (corresponding author), Chettinad Hosp & Res Inst, Chettinad Acad Res & Educ, Fac Allied Hlth Sci, Dept Med Biotechnol, Chennai 603103, Tamil Nadu, India.
EM xiao-feng.sun@liu.se; antarabanerjee@care.edu.in
RI Banerjee, Antara/AAH-4044-2020; Pathak, Surajit/AAH-4022-2020; Mitra,
   Abhijit/LPP-3829-2024
OI Banerjee, Antara/0000-0002-5519-6878; Mitra, Abhijit/0000-0001-9549-2930
FU Science and Engineering Research Board [EMR/2017/001877]
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: This work
   was supported by the Science and Engineering Research Board(grant number
   EMR/2017/001877).
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NR 195
TC 29
Z9 29
U1 5
U2 6
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.
PD MAY
PY 2023
VL 22
AR 15330338231178403
DI 10.1177/15330338231178403
PG 21
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA I2FX7
UT WOS:001001004900001
PM 37248615
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yu, IS
   Aubin, F
   Goodwin, R
   Loree, JM
   Mather, C
   Sheffield, BS
   Snow, S
   Gill, S
AF Yu, Irene S.
   Aubin, Francine
   Goodwin, Rachel
   Loree, Jonathan M.
   Mather, Cheryl
   Sheffield, Brandon S.
   Snow, Stephanie
   Gill, Sharlene
TI Tumor Biomarker Testing for Metastatic Colorectal Cancer: a Canadian
   Consensus Practice Guideline
SO THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
LA English
DT Review
DE colorectal cancer; metastasis; molecular testing; predictive biomarker;
   targeted therapy
ID KRAS WILD-TYPE; OF-AMERICAN-PATHOLOGISTS; II COLON-CANCER; EGFR
   MONOCLONAL-ANTIBODIES; PLUS CETUXIMAB TREATMENT; POSITIVE SOLID TUMORS;
   RAS MUTATIONS; STAGE-II; MICROSATELLITE INSTABILITY; 1ST-LINE TREATMENT
AB The systemic therapy management of metastatic colorectal cancer (mCRC) has evolved from primarily cytotoxic chemotherapies to now include targeted agents given alone or in combination with chemotherapy, and immune checkpoint inhibitors. A better understanding of the pathogenesis and molecular drivers of colorectal cancer not only aided the development of novel targeted therapies but led to the discovery of tumor mutations which act as predictive biomarkers for therapeutic response. Mutational status of the KRAS gene became the first genomic biomarker to be established as part of standard of care molecular testing, where KRAS mutations within exons 2, 3, and 4 predict a lack of response to anti- epidermal growth factor receptor therapies. Since then, several other biomarkers have become relevant to inform mCRC treatment; however, there are no published Canadian guidelines which reflect the current standards for biomarker testing. This guideline was developed by a pan-Canadian advisory group to provide contemporary, evidence-based recommendations on the minimum acceptable standards for biomarker testing in mCRC, and to describe additional biomarkers for consideration.
C1 [Gill, Sharlene] BC Canc Agcy, Vancouver Ctr, Dept Med Oncol, 600 W 10th Ave, Vancouver, BC V5Z 4E6, Canada.
   [Yu, Irene S.] BC Canc Surrey, Dept Med Oncol, Surrey, BC, Canada.
   [Aubin, Francine] Ctr Hosp Univ Montreal, Div Hematol & Oncol, Dept Med, Montreal, PQ, Canada.
   [Goodwin, Rachel] Ottawa Hosp Canc Ctr, Div Med Oncol, Dept Med, Ottawa, ON, Canada.
   [Loree, Jonathan M.] BC Canc Agcy Vancouver Ctr, Dept Med Oncol, Vancouver, BC, Canada.
   [Mather, Cheryl] Univ Alberta, Dept Lab Med & Pathol, Edmonton, AB, Canada.
   [Sheffield, Brandon S.] William Oster Hlth Syst, Div Adv Diagnost, Brampton, ON, Canada.
   [Snow, Stephanie] Queen Elizabeth 2 Hlth Sci Ctr, Dept Med, Halifax, NS, Canada.
C3 British Columbia Cancer Agency; Universite de Montreal; University of
   Ottawa; Ottawa Hospital Research Institute; University of Alberta; Queen
   Elizabeth II Health Sciences Centre
RP Gill, S (corresponding author), BC Canc Agcy, Vancouver Ctr, Dept Med Oncol, 600 W 10th Ave, Vancouver, BC V5Z 4E6, Canada.
EM sgill@bccancer.bc.ca
RI Snow, Stephanie/AAN-4936-2020
FU Pfizer Canada; ThermoFisher
FX The authors acknowledge medical writing support, provided by Sarah
   Doucette of IMPACT Medicom Inc., which was funded through sponsorship
   from Pfizer Canada and ThermoFisher. Medical writing services included
   project management, writing of the preliminary draft, consolidation of
   author revisions, and coordination of manuscript submission.
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NR 191
TC 9
Z9 9
U1 1
U2 8
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1758-8340
EI 1758-8359
J9 THER ADV MED ONCOL
JI Ther. Adv. Med. Oncol.
PD JUL
PY 2022
VL 14
AR 17588359221111705
DI 10.1177/17588359221111705
PG 29
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 3K5WG
UT WOS:000834145600001
PM 35898967
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Pietrantonio, F
   Oddo, D
   Gloghini, A
   Valtorta, E
   Berenato, R
   Barault, L
   Caporale, M
   Busico, A
   Morano, F
   Gualeni, AV
   Alessi, A
   Siravegna, G
   Perrone, F
   Di Bartolomeo, M
   Bardelli, A
   de Braud, F
   Di Nicolantonio, F
AF Pietrantonio, Filippo
   Oddo, Daniele
   Gloghini, Annunziata
   Valtorta, Emanuele
   Berenato, Rosa
   Barault, Ludovic
   Caporale, Marta
   Busico, Adele
   Morano, Federica
   Gualeni, Ambra Vittoria
   Alessi, Alessandra
   Siravegna, Giulia
   Perrone, Federica
   Di Bartolomeo, Maria
   Bardelli, Alberto
   de Braud, Filippo
   Di Nicolantonio, Federica
TI MET-Driven Resistance to Dual EGFR and BRAF Blockade May Be Overcome by
   Switching from EGFR to MET Inhibition in BRAF-Mutated Colorectal Cancer
SO CANCER DISCOVERY
LA English
DT Article
ID ACQUIRED-RESISTANCE; TARGETED THERAPY; LUNG-CANCER; PHASE-I;
   AMPLIFICATION; HETEROGENEITY; COMBINATIONS; VEMURAFENIB; ACTIVATION;
   CRIZOTINIB
AB A patient with metastatic BRAF-mutated colorectal cancer initially responded to combined EGFR and BRAF inhibition with panitumumab plus vemurafenib. Preexisting cells with increased MET gene copy number in the archival tumor tissue likely underwent clonal expansion during treatment, leading to the emergence of MET amplification in the rebiopsy taken at progression. In BRAF - mutated colorectal cancer cells, ectopic expression of MET conferred resistance to panitumumab and vemurafenib, which was overcome by combining BRAF and MET inhibition. Based on tumor genotyping and functional in vitro data, the patient was treated with the dual ALK-MET inhibitor crizotinib plus vemurafenib, thus switching to dual MET and BRAF blockade, with rapid and marked effectiveness of such strategy. Although acquired resistance is a major limitation to the clinical efficacy of anticancer agents, the identification of molecular targets emerging during the first treatment may afford the opportunity to design the next line of targeted therapies, maximizing patient benefit.
   SIGNIFICANCE: MET amplification is here identified-clinically and preclinically-as a new mechanism of resistance to EGFR and BRAF dual/triple block combinations in BRAF - mutated colorectal cancer. Switching from EGFR to MET inhibition, while maintaining BRAF inhibition, resulted in clinical benefit after the occurrence of MET-driven acquired resistance. (C) 2016 AACR.
C1 [Pietrantonio, Filippo; Berenato, Rosa; Caporale, Marta; Morano, Federica; Di Bartolomeo, Maria; de Braud, Filippo] Fdn IRCCS Ist Nazl Tumori, Dept Med Oncol, Milan, Italy.
   [Oddo, Daniele; Siravegna, Giulia; Bardelli, Alberto; Di Nicolantonio, Federica] Univ Torino, Dept Oncol, Candiolo, TO, Italy.
   [Oddo, Daniele; Barault, Ludovic; Siravegna, Giulia; Bardelli, Alberto; Di Nicolantonio, Federica] IRCCS, Candiolo Canc Inst FPO, Candiolo, TO, Italy.
   [Gloghini, Annunziata; Busico, Adele; Gualeni, Ambra Vittoria; Perrone, Federica] Fdn IRCCS Ist Nazl Tumori, Dept Diagnost Pathol & Lab Med, Milan, Italy.
   [Valtorta, Emanuele] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Alessi, Alessandra] Fdn IRCCS Ist Nazl Tumori, Dept Nucl Med, Milan, Italy.
   [Siravegna, Giulia] FIRC Inst Mol Oncol IFOM, Milan, Italy.
   [de Braud, Filippo] Univ Milan, Dept Oncol, Milan, Italy.
C3 Fondazione IRCCS Istituto Nazionale Tumori Milan; University of Turin;
   IRCCS Fondazione del Piemonte per l'Oncologia; Fondazione IRCCS Istituto
   Nazionale Tumori Milan; Fondazione IRCCS Istituto Nazionale Tumori
   Milan; IFOM - FIRC Institute of Molecular Oncology; University of Milan
RP Pietrantonio, F (corresponding author), Fdn IRCCS Ist Nazl Tumori, Via Venezian 1, I-20133 Milan, Italy.
EM filippo.pietrantonio@istitutotumori.mi.it
RI Siravegna, Giulia/Z-2826-2019; Gualeni, Ambra/B-8603-2017; Di
   Nicolantonio, Federica/A-2503-2011; Gloghini, Annunziata/C-1992-2017;
   Perrone, Federica/S-6171-2016; BARDELLI, Alberto/J-9721-2018; alessi,
   alessandra/C-7537-2017; Morano, Federica/B-7910-2018; Pietrantonio,
   Filippo/C-2180-2017; de Braud, Filippo Guglielmo Maria/B-9997-2017;
   Busico, Adele/D-2215-2017; Barault, Ludovic/J-2472-2016; Di Bartolomeo,
   Maria/D-1655-2017
OI Di Nicolantonio, Federica/0000-0001-9618-2010; Gloghini,
   Annunziata/0000-0002-7226-1942; Perrone, Federica/0000-0003-4406-8245;
   BARDELLI, Alberto/0000-0003-1647-5070; Siravegna,
   Giulia/0000-0002-7132-6484; alessi, alessandra/0000-0003-3853-1926;
   Morano, Federica/0000-0002-5306-3596; Pietrantonio,
   Filippo/0000-0002-8530-8420; de Braud, Filippo Guglielmo
   Maria/0000-0003-0103-730X; Busico, Adele/0000-0002-5808-0387; ODDO,
   DANIELE/0000-0001-6179-1668; VALTORTA, EMANUELE/0000-0002-5087-6233;
   Barault, Ludovic/0000-0001-5227-5047; Di Bartolomeo,
   Maria/0000-0002-7954-6609
FU AIRC IG [17707]; Fondo per la Ricerca Locale; Universita di Torino;
   Fondazione Piemontese per la Ricerca sul Cancro-ONLUS 5 per mille
   Ministero della Salute; European Community [602901]; Fondazione Umberto
   Veronesi;  [9970]
FX This work was supported by grants AIRC IG n. 17707 (F. Di Nicolantonio);
   Fondo per la Ricerca Locale (ex 60%), Universita di Torino, 2014 (F. Di
   Nicolantonio). Partial support was also obtained from AIRC 2010 Special
   Program Molecular Clinical Oncology 5 per mille, Targeting resistances
   to molecular therapies in metastatic colorectal carcinomas, Project n.
   9970 (A. Bardelli); the Fondazione Piemontese per la Ricerca sul
   Cancro-ONLUS 5 per mille 2010 e 2011 Ministero della Salute (A.
   Bardelli, F. Di Nicolantonio); and from the European Community's Seventh
   Framework Programme under grant agreement no. 602901 MErCuRIC (A.
   Bardelli, F. Di Nicolantonio). L. Barault was the recipient of a
   postdoctoral fellowship from the Fondazione Umberto Veronesi in 2015 and
   of "Assegno di Ricerca" from the University of Torino in 2016.
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NR 27
TC 85
Z9 88
U1 1
U2 10
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
EI 2159-8290
J9 CANCER DISCOV
JI Cancer Discov.
PD SEP
PY 2016
VL 6
IS 9
BP 963
EP 971
DI 10.1158/2159-8290.CD-16-0297
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DW0TT
UT WOS:000383356400022
PM 27325282
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Stefani, C
   Miricescu, D
   Stanescu-Spinu, II
   Nica, RI
   Greabu, M
   Totan, AR
   Jinga, M
AF Stefani, Constantin
   Miricescu, Daniela
   Stanescu-Spinu, Iulia-Ioana
   Nica, Remus Iulian
   Greabu, Maria
   Totan, Alexandra Ripszky
   Jinga, Mariana
TI Growth Factors, PI3K/AKT/mTOR and MAPK Signaling Pathways in Colorectal
   Cancer Pathogenesis: Where Are We Now?
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE colorectal cancer; growth factors; PI3K/AKT/mTOR & nbsp;; MAPK & nbsp;;
   growth factor inhibitors
ID RECEPTOR-TARGETED THERAPY; ANTI-VEGF ANTIBODY; GENE-MUTATIONS; PHASE-I;
   EGFR THERAPY; EXPRESSION; IGF-1; CELL; INSULIN; DIET
AB Colorectal cancer (CRC) is a predominant malignancy worldwide, being the fourth most common cause of mortality and morbidity. The CRC incidence in adolescents, young adults, and adult populations is increasing every year. In the pathogenesis of CRC, various factors are involved including diet, sedentary life, smoking, excessive alcohol consumption, obesity, gut microbiota, diabetes, and genetic mutations. The CRC tumor microenvironment (TME) involves the complex cooperation between tumoral cells with stroma, immune, and endothelial cells. Cytokines and several growth factors (GFs) will sustain CRC cell proliferation, survival, motility, and invasion. Epidermal growth factor receptor (EGFR), Insulin-like growth factor -1 receptor (IGF-1R), and Vascular Endothelial Growth Factor -A (VEGF-A) are overexpressed in various human cancers including CRC. The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) and all the three major subfamilies of the mitogen-activated protein kinase (MAPK) signaling pathways may be activated by GFs and will further play key roles in CRC development. The main aim of this review is to present the CRC incidence, risk factors, pathogenesis, and the impact of GFs during its development. Moreover, the article describes the relationship between EGF, IGF, VEGF, GFs inhibitors, PI3K/AKT/mTOR-MAPK signaling pathways, and CRC.</p>
C1 [Stefani, Constantin] Dr Carol Davila Cent Mil Emergency Univ Hosp, Dept Family Med & Clin Base, Bucharest 051075, Romania.
   [Miricescu, Daniela; Stanescu-Spinu, Iulia-Ioana; Greabu, Maria; Totan, Alexandra Ripszky] Carol Davila Univ Med & Pharm, Fac Med Dent, Dept Biochem, 8 Eroii Sanitari Blvd, Bucharest 050474, Romania.
   [Nica, Remus Iulian] Dr Carol Davila Cent Mil Emergency Univ Hosp, Surg 2, Bucharest 051075, Romania.
   [Jinga, Mariana] Dr Carol Davila Cent Mil Emergency Univ Hosp, Dept Gastroenterol, Bucharest 051075, Romania.
C3 Carol Davila University of Medicine & Pharmacy
RP Miricescu, D; Greabu, M (corresponding author), Carol Davila Univ Med & Pharm, Fac Med Dent, Dept Biochem, 8 Eroii Sanitari Blvd, Bucharest 050474, Romania.
EM constantin.stefani@umfcd.ro; daniela.miricescu@umfcd.ro;
   iulia.stanescu@umfcd.ro; nica.remus@yahoo.com; mariagreabu@umfcd.ro;
   alexandra.totan@umfcd.ro; mariana.jinga@umfcd.ro
RI Nica, Remus/HGE-3025-2022; Greabu, Maria/Q-9336-2019; Daniela,
   Miricescu/G-8788-2016; Ripszky-Totan, Alexandra/JTT-4320-2023; Jinga,
   Mariana/AAA-7101-2022; Stanescu-Spinu, Iulia-Ioana/AAD-7140-2021
OI TOTAN, ALEXANDRA/0000-0002-4345-282X; Stanescu-Spinu,
   Iulia-Ioana/0000-0001-9224-6056; Jinga, Mariana/0000-0001-5826-0815
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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 OCT
PY 2021
VL 22
IS 19
AR 10260
DI 10.3390/ijms221910260
PG 24
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA WI0MH
UT WOS:000708061200001
PM 34638601
OA Green Published, gold
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Song, LL
   Li, YM
   He, BM
   Gong, Y
AF Song, Lele
   Li, Yuemin
   He, Baoming
   Gong, Yuan
TI Development of Small Molecules Targeting the Wnt Signaling Pathway in
   Cancer Stem Cells for the Treatment of Colorectal Cancer
SO CLINICAL COLORECTAL CANCER
LA English
DT Review
DE beta-catenin; Chemotherapy; CRC; CSC; Targeted therapy
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; ACTIVATED-RECEPTOR-GAMMA;
   ADENOMATOUS POLYPOSIS-COLI; ABERRANT CRYPT FOCI;
   DIFFERENTIATION-INDUCING FACTOR; CATENIN REGULATES EXPRESSION;
   DROSOPHILA DISHEVELLED GENE; ACUTE MYELOID-LEUKEMIA; NUCLEAR
   BETA-CATENIN; CYCLIN D1
AB Colorectal cancer (CRC) was ranked third in morbidity and mortality in the United States in 2013. Although substantial progress has been made in surgical techniques and postoperative chemotherapy in recent years, the prognosis for colon cancer is still not satisfactory, mainly because of cancer recurrence and metastasis. The latest studies have shown that cancer stem cells (CSCs) play important roles in cancer recurrence and metastasis. Drugs that target CSCs might therefore have great therapeutic potential in prevention of cancer recurrence and metastasis. The wingless-int (Wnt) signaling pathway in CSCs has been suggested to play crucial roles in colorectal carcinogenesis, and has become a popular target for anti-CRC therapy. Dysregulation of the Wnt signaling pathway, mostly by inactivating mutations of the adenomatous polyposis coli tumor suppressor or oncogenic mutations of beta-catenin, has been implicated as a key factor in colorectal tumorigenesis. Abnormal increases of beta-catenin levels represents a common pathway in Wnt signaling activation and is also observed in other human malignancies. These findings highlight the importance of developing small-molecule drugs that target the Wnt pathway. Herein we provide an overview on the current development of small molecules that target the Wnt pathway in colorectal CSCs and discuss future research directions. (C) 2015 Elsevier Inc. All rights reserved.
C1 [Song, Lele; Li, Yuemin] PLA 309 Hosp, Dept Radiotherapy, Beijing 100091, Peoples R China.
   [Song, Lele] BioChain Beijing Sci & Technol Inc, Beijing, Peoples R China.
   [He, Baoming] PLA 309 Hosp, Dept Nucl Med, Beijing 100091, Peoples R China.
   [Gong, Yuan] PLA 309 Hosp, Dept Gastroenterol, Beijing 100091, Peoples R China.
RP Song, LL (corresponding author), PLA 309 Hosp, Dept Radiotherapy, 17 Heishanhu Rd, Beijing 100091, Peoples R China.
EM songlele@sina.com; liyuemin224@sina.com
RI Li, Yuqing/AAR-9383-2021
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NR 199
TC 44
Z9 48
U1 0
U2 36
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 2015
VL 14
IS 3
BP 133
EP 145
DI 10.1016/j.clcc.2015.02.001
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CP4JN
UT WOS:000359847900002
PM 25799881
DA 2025-01-04
ER

PT J
AU Ridouane, Y
   Lopes, G
   Ku, G
   Masud, H
   Haaland, B
AF Ridouane, Yassine
   Lopes, Gilberto
   Ku, Geoffrey
   Masud, Hasan
   Haaland, Benjamin
TI Targeted first-line therapies for advanced colorectal cancer: a Bayesian
   meta-analysis
SO ONCOTARGET
LA English
DT Article
DE Bayesian; colorectal cancer; decision analysis; meta-analysis; targeted
   therapy
ID FOLFIRI PLUS BEVACIZUMAB; RANDOMIZED PHASE-III; GENE MUTATION STATUS;
   RAS MUTATIONS; OPEN-LABEL; CETUXIMAB TREATMENT; AGITG MAX; CHEMOTHERAPY;
   KRAS; CAPECITABINE
AB Background: Colorectal cancer is common and deadly. First-line treatments for patients with metastatic disease include FOLFIRI and FOLFOX, which have been combined with anti-EGFR or anti-VEGF antibodies to achieve benefit in selected populations. However, optimal therapy remains unclear.
   Results: Fifteen publications on 10 trials were identified. There was a lack of decisive evidence that FOLFIRI or FOLFOX impact efficacy of either anti-EGFR or anti-VEGF, across mutational status groups. On the other hand, evidence suggests both anti-EGFR and anti-VEGF may be more effective for KRAS WT than MT patients. KRAS WT results provided evidence that anti-EGFR treatments may be more effective than anti-VEGF treatments when combined with FOLFIRI or FOLFOX. Further, evidence suggests that both anti-EGFR and anti-VEGF therapies, when combined with FOLFIRI or FOLFOX, may be harmful as compared to chemotherapy for KRAS MT patients.
   Materials and Methods: Literature was searched for randomized trials comparing anti-EGFR or anti-VEGF antibodies, paired with FOLFIRI or FOLFOX, as first-line therapy for advanced colorectal cancer. Meta-estimates were generated via Bayesian hierarchical log-linear model. The primary endpoint was overall survival.
   Conclusions: Further studies examining impact of all-RAS mutation status, left or right side location of primary tumor, and combination anti-VEGF with modern bolus fluoropyrimidine are needed.
C1 [Ridouane, Yassine; Masud, Hasan; Haaland, Benjamin] Georgia Inst Technol, H Milton Stewart Sch Ind & Syst Engn, Atlanta, GA 30332 USA.
   [Lopes, Gilberto] Univ Miami Hlth Syst, Sylvester Comprehens Canc Ctr, Miami, FL USA.
   [Ku, Geoffrey] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
   [Haaland, Benjamin] Univ Utah, Populat Hlth Sci, Salt Lake City, UT 84112 USA.
   [Haaland, Benjamin] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
C3 University System of Georgia; Georgia Institute of Technology; Memorial
   Sloan Kettering Cancer Center; Utah System of Higher Education;
   University of Utah; Utah System of Higher Education; University of Utah;
   Huntsman Cancer Institute
RP Haaland, B (corresponding author), Georgia Inst Technol, H Milton Stewart Sch Ind & Syst Engn, Atlanta, GA 30332 USA.; Haaland, B (corresponding author), Univ Utah, Populat Hlth Sci, Salt Lake City, UT 84112 USA.; Haaland, B (corresponding author), Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
EM ben.haaland@hsc.utah.edu
CR [Anonymous], J CLIN ONCOL
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NR 37
TC 7
Z9 8
U1 0
U2 1
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD SEP 12
PY 2017
VL 8
IS 39
BP 66458
EP 66466
DI 10.18632/oncotarget.20185
PG 9
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA FG4YC
UT WOS:000410291200146
PM 29029527
OA gold, Green Published, Green Submitted
DA 2025-01-04
ER

PT J
AU Veenstra, CM
   Krauss, JC
AF Veenstra, Christine M.
   Krauss, John C.
TI Emerging Systemic Therapies for Colorectal Cancer
SO CLINICS IN COLON AND RECTAL SURGERY
LA English
DT Review
DE colorectal cancer; emerging therapies; targeted therapy; immunotherapy;
   clinical trials
ID MIGRATION-INHIBITORY FACTOR; III COLON-CANCER; SURGICAL ADJUVANT BREAST;
   ENGINEERED T-CELLS; OPEN-LABEL; MONOCLONAL-ANTIBODY; IMPROVED SURVIVAL;
   PLUS BEVACIZUMAB; LIVER METASTASIS; RANDOMIZED-TRIAL
AB Despite advances over the past 20 years in colorectal cancer (CRC) screening, diagnosis, and treatment, survival outcomes remain suboptimal. Five-year survival for patients with locally advanced CRC is 69%; 5-year survival drops to 12% for patients with metastatic disease. Novel, effective systemic therapies are needed to improve long-term outcomes. In this review, we describe currently available systemic therapies for the treatment of locally advanced and metastatic CRC and discuss emerging therapies, including encouraging advances in identifying novel targeted agents and exciting responses to immunotherapeutic agents.
C1 [Veenstra, Christine M.; Krauss, John C.] Univ Michigan, Dept Internal Med, Div Hematol Oncol, 300 North Ingalls,Room 3A22, Ann Arbor, MI 48109 USA.
C3 University of Michigan System; University of Michigan
RP Veenstra, CM (corresponding author), Univ Michigan, Dept Internal Med, Div Hematol Oncol, 300 North Ingalls,Room 3A22, Ann Arbor, MI 48109 USA.
EM cveenstr@med.umich.edu
OI Krauss, John/0000-0002-5197-736X
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NR 98
TC 25
Z9 29
U1 0
U2 13
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 MAY
PY 2018
VL 31
IS 3
BP 179
EP 191
DI 10.1055/s-0037-1602238
PG 13
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA GE3MJ
UT WOS:000431117100007
PM 29720904
OA Green Published
DA 2025-01-04
ER

PT J
AU Jiang, YL
   Shao, TH
   Zhao, MY
   Xue, YH
   Zheng, XP
AF Jiang, Yunlin
   Shao, Taihang
   Zhao, Mingye
   Xue, Yahong
   Zheng, Xueping
TI A network meta-analysis of efficacy and safety for first-line and
   maintenance therapies in patients with unresectable colorectal liver
   metastases
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Article
DE metastatic colorectal cancer; unresectable liver metastases; network
   meta-analysis; firstline treatment; maintenance treatment
ID FOLFIRI PLUS BEVACIZUMAB; RANDOMIZED PHASE-III; RAS WILD-TYPE;
   OPEN-LABEL; SYSTEMIC TREATMENT; NON-INFERIORITY; CANCER FIRE-3; PRIMARY
   TUMOR; CHEMOTHERAPY; OXALIPLATIN
AB Background: Evidence comparing the efficacy of different treatments for patients with unresectable colorectal liver metastases (CRLM) receiving first-line or maintenance therapy is sparse. We aimed to assess the efficacy and safety of these treatments, with a distinct focus on evaluating first-line and maintenance treatments separately.
   Methods: We conducted Bayesian network meta-analyses, sourcing English-language randomized controlled trials (RCTs) published through July 2023 from databases including PubMed, Embase, the Cochrane Library, ClinicalTrials.gov, and key conference proceedings. Phase II or III trials that assessed two or more therapeutic regimens were included. Primary outcome was overall survival (OS). Secondary outcomes included progression-free survival (PFS), objective response rate (ORR), adverse events graded as 3 or above (SAE), and R0 liver resection rate. Hazards Ratios (HRs) and 95% confidence intervals (CI) were used as effect size for OS and PFS, Odds Ratios (ORs) and 95% CI were used for ORR, SAEs and R0 resection rate. Subgroup and sensitive analyses were conducted to analysis the model uncertainty (PROSPERO: CRD42023420498).
   Results: 56 RCTs were included (50 for first-line treatment, six for maintenance therapies), with a total of 21,323 patients. Regarding first-line, for OS, the top three mechanisms were: local treatment + single-drug chemotherapy (SingleCT), Targeted therapy (TAR)+SingleCT, and TAR + multi-drug chemotherapy (MultiCT). Resection or ablation (R/A)+SingleCT, S1, and Cetuximab + intensified fluorouracil-based combination chemotherapy (ICTFU) were identified as the best treatments. For PFS, the top three mechanisms were: Immune therapy + TAR + MultiCT, multi-targeted therapy (MultiTAR), TAR + SingleCT. The top three treatments were: Atezolizumab + Bevacizumab + fluorouracil-based combination chemotherapy (CTFU), TAS-102+bevacizumab, Bevacizumab + ICTFU. Cetuximab + CTFU was the best choice for RAS/RAF wild-type patients. Regarding maintenance treatment, Bevacizumab + SingleCT and Adavosertib were the best options for OS and PFS, respectively. For safety, MultiCT was the safest, followed by local treatment + MultiCT, TAR + MultiCT caused the most SAEs. Bevacizumab plus chemotherapy was found to be the safest among all targeted combination therapies.
   Conclusion: In first-line, local treatment or targeted therapsy plus chemotherapy are the best mechanisms. R/A + SingleCT or CTFU performed the best for OS, Atezolizumab + Bevacizumab + ICTFU was the best option regarding PFS. For RAS/RAF wild-type patients, Cetuximab + CTFU was the optimal option. Monotherapy may be preferred choice for maintenance treatment. Combination therapy resulted in more SAEs when compared to standard chemotherapy.
C1 [Jiang, Yunlin; Xue, Yahong; Zheng, Xueping] Nanjing Univ Chinese Med, Nanjing Hosp Chinese Med, Nanjing, Peoples R China.
   [Jiang, Yunlin] Nanjing Univ Chinese Med, Grad Sch, Nanjing, Peoples R China.
   [Shao, Taihang; Zhao, Mingye] China Pharmaceut Univ, Sch Int Pharmaceut Business, Dept Pharmacoecon, Nanjing, Peoples R China.
C3 Nanjing University of Chinese Medicine; Nanjing University of Chinese
   Medicine; China Pharmaceutical University
RP Xue, YH; Zheng, XP (corresponding author), Nanjing Univ Chinese Med, Nanjing Hosp Chinese Med, Nanjing, Peoples R China.
EM zhengxp@njucm.edu.cn; xueyahong_1983@126.com
FU Nanjing Health and Technology Development Plan [YKK21197]
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. The work was funded by
   Nanjing Health and Technology Development Plan (No. YKK21197).
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NR 60
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 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD JUL 26
PY 2024
VL 15
AR 1374136
DI 10.3389/fphar.2024.1374136
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA C0F2P
UT WOS:001286197700001
PM 39130637
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Strickler, JH
   Wu, C
   Bekaii-Saab, T
AF Strickler, John H.
   Wu, Christina
   Bekaii-Saab, Tanios
TI Targeting BRAF in metastatic colorectal cancer: Maximizing molecular
   approaches
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE Colorectal cancer; BRAF; Targeted therapy
ID DNA MISMATCH REPAIR; ISLAND METHYLATOR PHENOTYPE; FOLFOXIRI PLUS
   BEVACIZUMAB; III COLON-CANCER; KRAS WILD-TYPE; 1ST-LINE TREATMENT;
   MICROSATELLITE INSTABILITY; PHASE-III; MEK INHIBITION; K-RAS
AB Oncogenic mutations in B-type Raf kinase (BRAF) occur in 7-10% of metastatic colorectal cancers (mCRC). Despite recent improvements in survival in the general population of patients with mCRC, patients with BRAF-mutant mCRC continue to have poor response to most systemic therapies, and prognosis remains poor. There is a substantial unmet need for novel therapeutic strategies to treat patients with BRAF-mutant mCRC. This review outlines the epidemiology, molecular pathogenesis, prognosis, and mechanisms of treatment resistance of BRAF-mutated CRC. Additionally, this review highlights novel therapeutic strategies aimed at enhancing response and improving outcomes. (c) 2017 The Author(s). Published by Elsevier Ltd.
C1 [Strickler, John H.] Duke Univ, Sch Med, 20 Duke Med Circle, Durham, NC 27710 USA.
   [Wu, Christina] Emory Univ, 1365-C Clifton Rd NE, Atlanta, GA 30322 USA.
   [Bekaii-Saab, Tanios] Mayo Clin, 5777 E Mayo Blvd, Phoenix, AZ 85054 USA.
C3 Duke University; Emory University; Mayo Clinic; Mayo Clinic Phoenix
RP Bekaii-Saab, T (corresponding author), Mayo Clin, 5777 E Mayo Blvd, Phoenix, AZ 85054 USA.
EM bekaii-saab.tanios@mayo.edu
RI Bekaii-Saab, Tanios/AGD-6851-2022
OI Bekaii-Saab, Tanios/0000-0001-7721-1699; Strickler,
   John/0000-0001-7579-1175
FU Novartis Pharmaceuticals Corporation
FX Medical writing and editorial support were provided by ArticulateScience
   LLC, Hamilton, NJ, and this support was funded by Novartis
   Pharmaceuticals Corporation. Neither Novartis Pharmaceuticals
   Corporation nor ArticulateScience LLC influenced the content of this
   manuscript, nor did the authors receive financial compensation for
   authorship.
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NR 100
TC 44
Z9 44
U1 0
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0305-7372
EI 1532-1967
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD NOV
PY 2017
VL 60
BP 109
EP 119
DI 10.1016/j.ctrv.2017.08.006
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FN7IO
UT WOS:000416192100013
PM 28946014
OA hybrid
DA 2025-01-04
ER

PT J
AU Marzi, L
   Combes, E
   Vié, N
   Ayrolles-Torro, A
   Tosi, D
   Desigaud, D
   Perez-Gracia, E
   Larbouret, C
   Montagut, C
   Iglesias, M
   Jarlier, M
   Denis, V
   Linares, LK
   Lam, EWF
   Martineau, P
   Del Rio, M
   Gongora, C
AF Marzi, L.
   Combes, E.
   Vie, N.
   Ayrolles-Torro, A.
   Tosi, D.
   Desigaud, D.
   Perez-Gracia, E.
   Larbouret, C.
   Montagut, C.
   Iglesias, M.
   Jarlier, M.
   Denis, V.
   Linares, L. K.
   Lam, E. W-F
   Martineau, P.
   Del Rio, M.
   Gongora, C.
TI FOXO3a and the MAPK p38 are activated by cetuximab to induce cell death
   and inhibit cell proliferation and their expression predicts cetuximab
   efficacy in colorectal cancer
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE cetuximab; FOXO3a; MAPK p38; colorectal cancer; signalling
ID FACTOR RECEPTOR EGFR; PROTEIN-KINASE; ANTIBODY CETUXIMAB; TARGETED
   THERAPY; TYROSINE KINASE; WILD-TYPE; IN-VITRO; GROWTH; RESISTANCE;
   APOPTOSIS
AB Background: Cetuximab, a monoclonal antibody against EGFR used for the treatment of colorectal cancer (CRC), is ineffective in many patients. The aim of this study was to identify the signalling pathways activated by cetuximab in CRC cells and define new biomarker of response.
   Methods: We used in vitro, in vivo models and clinical CRC samples to assess the role of p38 and FOXO3a in cetuximab mechanism of action.
   Results: We show that cetuximab activates the MAPK p38. Specifically, p38 inhibition reduced cetuximab efficacy on cell growth and cell death. At the molecular level, cetuximab activates the transcription factor FOXO3a and promotes its nuclear translocation via p38-mediated phosphorylation, leading to the upregulation of its target genes p27 and BIM and the subsequent induction of apoptosis and inhibition of cell proliferation. Finally, we found that high FOXO3a and p38 expression levels are associated with better response rate and improved outcome in cetuximab-treated patients with CRC harbouring WT KRAS.
   Conclusions: We identify FOXO3a as a key mediator of cetuximab mechanism of action in CRC cells and define p38 as its activator in this context. Moreover, high FOXO3a and p38 expression could predict the response to cetuximab in patients with CRC harbouring WT KRAS.
C1 [Marzi, L.; Combes, E.; Vie, N.; Ayrolles-Torro, A.; Tosi, D.; Desigaud, D.; Perez-Gracia, E.; Larbouret, C.; Jarlier, M.; Denis, V.; Linares, L. K.; Martineau, P.; Del Rio, M.; Gongora, C.] IRCM, F-34298 Montpellier, France.
   [Marzi, L.; Combes, E.; Vie, N.; Ayrolles-Torro, A.; Tosi, D.; Desigaud, D.; Perez-Gracia, E.; Larbouret, C.; Jarlier, M.; Denis, V.; Linares, L. K.; Martineau, P.; Del Rio, M.; Gongora, C.] INSERM, U1194, F-34298 Montpellier, France.
   [Marzi, L.; Combes, E.; Vie, N.; Ayrolles-Torro, A.; Tosi, D.; Desigaud, D.; Perez-Gracia, E.; Larbouret, C.; Jarlier, M.; Denis, V.; Linares, L. K.; Martineau, P.; Del Rio, M.; Gongora, C.] Univ Montpellier, F-34298 Montpellier, France.
   [Marzi, L.; Combes, E.; Vie, N.; Ayrolles-Torro, A.; Tosi, D.; Desigaud, D.; Perez-Gracia, E.; Larbouret, C.; Jarlier, M.; Denis, V.; Linares, L. K.; Martineau, P.; Del Rio, M.; Gongora, C.] Inst Reg Canc Montpellier, F-34298 Montpellier, France.
   [Montagut, C.; Iglesias, M.] Hosp del Mar, Dept Med Oncol, Barcelona 08003, Spain.
   [Lam, E. W-F] Imperial Coll London, Imperial Ctr Translat & Expt Med, Dept Surg & Canc, Hammersmith Hosp Campus, London W12 0NN, England.
C3 Universite de Montpellier; UNICANCER; Institut Regional du Cancer
   Montpellier / Val d'Aurelle (ICM); Institut National de la Sante et de
   la Recherche Medicale (Inserm); Universite de Montpellier; Institut
   National de la Sante et de la Recherche Medicale (Inserm); Universite de
   Montpellier; UNICANCER; Universite de Montpellier; Institut Regional du
   Cancer Montpellier / Val d'Aurelle (ICM); Hospital del Mar Research
   Institute; Hospital del Mar; Imperial College London
RP Gongora, C (corresponding author), IRCM, F-34298 Montpellier, France.; Gongora, C (corresponding author), INSERM, U1194, F-34298 Montpellier, France.; Gongora, C (corresponding author), Univ Montpellier, F-34298 Montpellier, France.; Gongora, C (corresponding author), Inst Reg Canc Montpellier, F-34298 Montpellier, France.
EM celine.gongora@inserm.fr
RI Linares, Laetitia/F-9901-2018; Iglesias, Mar/JMC-1014-2023; Lam,
   Eric/AAW-8566-2020; Martineau, Pierre/N-4386-2017
OI GONGORA, Celine/0000-0001-9034-4031; Martineau,
   Pierre/0000-0002-7993-7183; Linares, Laetitia
   Karine/0000-0003-1661-2119; Lam, Eric/0000-0003-1274-3576
FU INSERM; ICM Val D'Aurelle; French government; Labex MabImprove;
   MabImprove post-doctoral fellowship; French National Research Agency
   under the programme 'Investissements d'avenir' Grant [ANR-10-LABX-53];
   SIRIC [INCA-DGOS-Inserm 6045]; MRC [MR/N012097/1] Funding Source: UKRI
FX We thank the Montpellier RIO Imaging facility for flow cytometry
   experiments, in particular Nadia Vie. The Supplementary Figure 1 was
   generated using the Servier medical art (www.servier.fr). This work was
   supported by INSERM and ICM Val D'Aurelle. LM had a PhD studentship from
   the French government. EC has a PhD studentship from the Labex
   MabImprove. AT had a MabImprove post-doctoral fellowship. The research
   leading to this publication was funded by the French National Research
   Agency under the programme 'Investissements d'avenir' Grant Agreement
   LabEx MAbImprove: ANR-10-LABX-53 and SIRIC (INCA-DGOS-Inserm 6045).
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NR 43
TC 43
Z9 43
U1 0
U2 15
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD NOV 8
PY 2016
VL 115
IS 10
BP 1223
EP 1233
DI 10.1038/bjc.2016.313
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EB7HC
UT WOS:000387556500009
PM 27685445
OA hybrid, Green Published
DA 2025-01-04
ER

PT J
AU Yang, SJ
   Yang, SY
   Wang, DD
   Chen, X
   Shen, HY
   Zhang, XH
   Zhong, SL
   Tang, JH
   Zhao, JH
AF Yang, Su-Jin
   Yang, Su-Yu
   Wang, Dan-Dan
   Chen, Xiu
   Shen, Hong-Yu
   Zhang, Xiao-Hui
   Zhong, Shan-Liang
   Tang, Jin-Hai
   Zhao, Jian-Hua
TI The miR-30 family: Versatile players in breast cancer
SO TUMOR BIOLOGY
LA English
DT Review
DE MicroRNA; miR-30 family; biomarker; breast cancer
ID EPITHELIAL-MESENCHYMAL TRANSITION; CELL LUNG-CANCER; DOWN-REGULATION;
   TUMOR-SUPPRESSOR; TAMOXIFEN RESISTANCE; POOR-PROGNOSIS; THERAPEUTIC
   TARGETS; ESTROGEN-RECEPTOR; COLORECTAL-CANCER; SIGNALING PATHWAY
AB The microRNA family, miR-30, plays diverse roles in regulating key aspects of neoplastic transformation, metastasis, and clinical outcomes in different types of tumors. Accumulating evidence proves that miR-30 family is pivotal in the breast cancer development by controlling critical signaling pathways and relevant oncogenes. Here, we review the roles of miR-30 family members in the tumorigenesis, metastasis, and drug resistance of breast cancer, and their application to predict the prognosis of breast cancer patients. We think miR-30 family members would be promising biomarkers for breast cancer and may bring a novel insight in molecular targeted therapy of breast cancer.
C1 [Yang, Su-Jin; Wang, Dan-Dan; Chen, Xiu; Shen, Hong-Yu; Zhang, Xiao-Hui] Nanjing Med Univ, Clin Sch 4, Nanjing, Jiangsu, Peoples R China.
   [Yang, Su-Jin; Wang, Dan-Dan; Chen, Xiu; Shen, Hong-Yu; Tang, Jin-Hai] Nanjing Med Univ, Canc Hosp, Canc Inst Jiangsu Prov, Dept Gen Surg, Nanjing 210009, Jiangsu, Peoples R China.
   [Yang, Su-Yu] Nanjing Univ Chinese Med, Nanjing, Jiangsu, Peoples R China.
   [Zhang, Xiao-Hui; Zhong, Shan-Liang; Zhao, Jian-Hua] Nanjing Med Univ, Ctr Clin Lab, Canc Hosp, Canc Inst Jiangsu Prov, Nanjing, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University; Nanjing
   University of Chinese Medicine; Nanjing Medical University
RP Tang, JH (corresponding author), Nanjing Med Univ, Canc Hosp, Canc Inst Jiangsu Prov, Dept Gen Surg, Nanjing 210009, Jiangsu, Peoples R China.; Zhao, JH (corresponding author), Nanjing Med Univ, Ctr Clin Lab, Canc Hosp, Canc Inst Jiangsu Prov, Nanjing, Jiangsu, Peoples R China.
EM jinhaitang210009@sina.com; zhao210009@sina.com
RI Zhang, Xiaohui/AAN-2994-2020; zhong, shan/HZJ-4647-2023; yang,
   su/AGI-3961-2022
FU National Natural Science Foundation of China [81272470, 81602551];
   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]; Key Research Program for the Social Development of Jiangsu
   Province, China [BE2015718]
FX This study was funded by the National Natural Science Foundation of
   China (grant no. 81272470), the National key clinical specialist
   construction Programs of China (No. 2013[544]), Major Program of Natural
   Science Foundation of Jiangsu Province (No. BL2014090), Natural Science
   Foundation of Jiangsu Province (No. BK20151579), the Key Research
   Program for the Social Development of Jiangsu Province, China
   (BE2015718), the National Natural Science Foundation of China (grant no.
   81602551).
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NR 112
TC 65
Z9 71
U1 0
U2 7
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 692204
DI 10.1177/1010428317692204
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ET4OS
UT WOS:000400263700014
PM 28347244
OA gold
DA 2025-01-04
ER

PT J
AU Stangl, C
   Post, JB
   van Roosmalen, MJ
   Hami, N
   Verlaan-Klink, I
   Vos, HR
   van Es, RM
   Koudijs, MJ
   Voest, EE
   Snippert, HJG
   Kloosterman, WP
AF Stangl, Christina
   Post, Jasmin B.
   van Roosmalen, Markus J.
   Hami, Nizar
   Verlaan-Klink, Ingrid
   Vos, Harmjan R.
   van Es, Robert M.
   Koudijs, Marco J.
   Voest, Emile E.
   Snippert, Hugo J. G.
   Kloosterman, W. P.
TI Diverse <i>BRAF</i> Gene Fusions Confer Resistance to EGFR-Targeted
   Therapy via Differential Modulation of BRAF Activity
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID SIGNALING PATHWAYS; SOLID TUMORS; CANCER; ACTIVATION; MUTATIONS;
   KINASES; RAF
AB Fusion genes can be oncogenic drivers in a variety of cancer types and represent potential targets for targeted therapy. The BRAF gene is frequently involved in oncogenic gene fusions, with fusion frequencies of 0.2%-3% throughout different cancers. However, BRAF fusions rarely occur in the same gene configuration, potentially challenging personalized therapy design. In particular, the impact of the wide variety of fusion partners on the oncogenic role of BRAF during tumor growth and drug response is unknown. Here, we used patient-derived colorectal cancer organoids to functionally characterize and cross-compare BRAF fusions containing various partner genes (AGAP3, DLG1, and TRIM24) with respect to cellular behavior, downstream signaling activation, and response to targeted therapies. We demonstrate that 50 fusion partners mainly promote canonical oncogenic BRAF activity by replacing the auto-inhibitory N-terminal region. In addition, the 50 partner of BRAF fusions influences their subcellular localization and intracellular signaling capacity, revealing distinct subsets of affected signaling pathways and altered gene expression. Presence of the different BRAF fusions resulted in varying sensitivities to combinatorial inhibition of MEK and the EGF receptor family. However, all BRAF fusions conveyed resistance to targeted monotherapy against the EGF receptor family, suggesting that BRAF fusions should be screened alongside other MAPK pathway alterations to identify patients with metastatic colorectal cancer to exclude from anti-EGFR-targeted treatment.
C1 [Stangl, Christina; van Roosmalen, Markus J.; Koudijs, Marco J.; Kloosterman, W. P.] Univ Med Ctr Utrecht, Ctr Mol Med, Dept Genet, Utrecht, Netherlands.
   [Stangl, Christina; Post, Jasmin B.; van Roosmalen, Markus J.; Hami, Nizar; Verlaan-Klink, Ingrid; Vos, Harmjan R.; van Es, Robert M.; Koudijs, Marco J.; Snippert, Hugo J. G.; Kloosterman, W. P.] Univ Utrecht, Utrecht, Netherlands.
   [Stangl, Christina; Voest, Emile E.] Netherlands Canc Inst, Div Mol Oncol, Amsterdam, Netherlands.
   [Stangl, Christina; van Roosmalen, Markus J.; Voest, Emile E.] Oncode Inst, Amsterdam, Netherlands.
   [Post, Jasmin B.; Hami, Nizar; Verlaan-Klink, Ingrid; Vos, Harmjan R.; van Es, Robert M.; Snippert, Hugo J. G.] Univ Med Ctr Utrecht, Mol Canc Res, Ctr Mol Med, Utrecht, Netherlands.
   [Post, Jasmin B.; Hami, Nizar; Verlaan-Klink, Ingrid; Vos, Harmjan R.; van Es, Robert M.; Snippert, Hugo J. G.] Univ Med Ctr Utrecht, Oncode Inst, Utrecht, Netherlands.
   [van Roosmalen, Markus J.] Princess Maxima Ctr Pediat Oncol, Utrecht, Netherlands.
   [Koudijs, Marco J.] Univ Med Ctr Utrecht, Ctr Personalized Canc Treatment, Utrecht, Netherlands.
   [Kloosterman, W. P.] Cyclomics, Utrecht, Netherlands.
   [Kloosterman, W. P.] Frame Canc Therapeut, Amsterdam, Netherlands.
C3 Utrecht University; Utrecht University Medical Center; Utrecht
   University; Netherlands Cancer Institute; Utrecht University; Utrecht
   University Medical Center; Utrecht University; Utrecht University
   Medical Center; Utrecht University; Utrecht University Medical Center
RP Kloosterman, WP (corresponding author), Univ Weg 100, NL-3584 CG Utrecht, Netherlands.; Voest, EE (corresponding author), Netherlands Canc Inst, Plesmanlaan, Amsterdam, Netherlands.
EM e.voest@nki.nl; wigardkloosterman@gmail.com
OI Vos, Harmjan/0000-0002-4696-6068
FU Oncode Institute; Dutch Cancer Society; Dutch Cancer Society [Koningin
   Wilhelmina Fonds (KWF)] [UU 2013-6070, UU 20125710]; SU2C-DCS
   International Translational Cancer Research Dream Team Grant
   [SU2C-AACR-DT1415]; ERC; KWF; gravitation program Cancer GenomiCs.nl
   from the Netherlands Organization for Scientific Research
FX This work was funded by the Oncode Institute, which was partly financed
   by the Dutch Cancer Society, and was funded by the gravitation program
   Cancer GenomiCs.nl from the Netherlands Organization for Scientific
   Research, by grants from the Dutch Cancer Society [Koningin Wilhelmina
   Fonds (KWF), UU 2013-6070 and UU 20125710], by a SU2C-DCS International
   Translational Cancer Research Dream Team Grant (SU2C-AACR-DT1415), and
   by a ERC starting grant (to H.J.G. Snippert), and a Dutch Cancer Society
   grant. Stand Up To Cancer is a division of the Entertainment Industry
   Foundation. Research grants were administered by the American
   Association for Cancer Research, the Scientific Partner of SU2C. The
   authors thank KWF for funding this project. Furthermore, we thank all
   the members of the Kloosterman, Voest, Snippert, and Bos laboratories
   for fruitful discussions and support. We thank the Proteomics facility
   (UMCU) and Macrogen (Korea) for their help with the Phosphoproteomics
   and RNA sequencing experiments. We thank Glen Monroe and Hans Bos for
   critical reading of the article and Francis Blokzijl for providing a
   script for the RNA sequencing analysis. We thank Robert Coebergh, Jan
   Ijzermans, Anieta Sieuwerts, and John Martens for collaborations that
   led up to this work.
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NR 50
TC 14
Z9 14
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 APR
PY 2020
VL 18
IS 4
BP 537
EP 548
DI 10.1158/1541-7786.MCR-19-0529
PG 12
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA KY8PW
UT WOS:000522839400003
PM 31911540
OA Green Submitted, Bronze
DA 2025-01-04
ER

PT J
AU Zhang, YB
   Shao, F
   Yang, CG
   Yang, DG
   Du, WF
AF Zhang, Yanbo
   Shao, Feng
   Yang, Chenggang
   Yang, Daogui
   Du, Wenfeng
TI ICG001 inhibits colon cancer growth by suppressing eIF3D signaling
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
LA English
DT Article
DE ICG001; colon cancer; eIF3D; PI3K/AKT signaling pathway
ID PROLIFERATION; KNOCKDOWN
AB Recently, several clinical trials have examined the efficacy of small molecule inhibitors of eukaryotic translation initiation factor 3 subunit D (eIF3D) for the treatment of colorectal cancer (CRC). Unfortunately, none of these compounds has proven more effective than existing chemotherapeutic drugs, resulting in a significant unmet need for effective CRC therapies. Here, we examined the anticancer effects of ICG001, a novel eIF3D inhibitor, on CRC cells using both in vitro cell growth and apoptosis assays, as well as an in vivo HCT-116 xenograft mouse model. ICG001 induced the caspase-dependent apoptosis of CRC cells by downregulating the expression of Bcl-2 in combination with increased expression of Bad and Bax. Western blot analysis demonstrated that ICG001 inhibited the expression of eIF3D and its downstream targets, PI3K and AKT, in vitro. Finally, ICG001 inhibited HCT-116 xenograft growth significantly in nude mice in a dose-dependent manner. Taken together, these data suggest that ICG001 inhibited the growth of CRC cells in vitro and in vivo via the inhibition of eIF3D signaling. These results provide a basis for further clinical investigation of ICG001 as a targeted therapy for CRC. Our findings may open a new avenue for the development of novel eIF3D inhibitors in the treatment of CRC and other cancers.
C1 [Zhang, Yanbo; Shao, Feng; Yang, Chenggang; Yang, Daogui; Du, Wenfeng] Liaocheng Peoples Hosp, Dept Gastrointestinal Surg, Liaocheng 252000, Shandong, Peoples R China.
RP Yang, CG (corresponding author), Liaocheng Peoples Hosp, Dept Gastrointestinal Surg, Liaocheng 252000, Shandong, Peoples R China.
EM Bakerham123@163.com
RI Zhang, Yanbo/IQU-6845-2023
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NR 20
TC 1
Z9 1
U1 0
U2 2
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1940-5901
J9 INT J CLIN EXP MED
JI Int. J. Clin. Exp. Med.
PY 2019
VL 12
IS 4
BP 3476
EP 3483
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA HW2DW
UT WOS:000466494200042
DA 2025-01-04
ER

PT J
AU Hazar-Rethinam, M
   Kleyman, M
   Han, GC
   Liu, D
   Ahronian, LG
   Shahzade, HA
   Chen, LF
   Parikh, AR
   Allen, JN
   Clark, JW
   Kwak, EL
   Faris, JE
   Murphy, JE
   Hong, TS
   Van Seventer, EE
   Nadres, B
   Hong, CB
   Gurski, JM
   Jessop, NA
   Dias-Santagata, D
   Iafrate, AJ
   Van Allen, EM
   Corcoran, RB
AF Hazar-Rethinam, Mehlika
   Kleyman, Marianna
   Han, G. Celine
   Liu, David
   Ahronian, Leanne G.
   Shahzade, Heather A.
   Chen, Lifeng
   Parikh, Aparna R.
   Allen, Jill N.
   Clark, Jeffrey W.
   Kwak, Eunice L.
   Faris, Jason E.
   Murphy, Janet E.
   Hong, Theodore S.
   Van Seventer, Emily E.
   Nadres, Brandon
   Hong, Catriona B.
   Gurski, Joseph M., Jr.
   Jessop, Nicholas A.
   Dias-Santagata, Dora
   Iafrate, A. John
   Van Allen, Eliezer M.
   Corcoran, Ryan B.
TI Convergent Therapeutic Strategies to Overcome the Heterogeneity of
   Acquired Resistance in &ITBRAF&IT<SUP>V600E</SUP> Colorectal Cancer
SO CANCER DISCOVERY
LA English
DT Article
ID ANTI-EGFR THERAPY; CLONAL EVOLUTION; COMBINED BRAF; TARGETED THERAPY;
   MEK INHIBITORS; RAF INHIBITION; PHASE IB; VEMURAFENIB; AMPLIFICATION;
   COMBINATIONS
AB Clonal heterogeneity associated with acquired resistance presents a critical therapeutic challenge. Whole-exome sequencing of paired tumor biopsies and targeted sequencing of cell-free DNA (cfDNA) from patients with BRAF(V600E) colorectal cancer receiving BRAF inhibitor combinations identified 14 distinct alterations in MAPK pathway components driving acquired resistance, with as many as eight alterations in a single patient. We developed a pooled clone system to study clonal outgrowth during acquired resistance, in vitro and in vivo. In vitro, the dynamics of individual resistant clones could be monitored in real time in cfDNA isolated from culture media during therapy. Outgrowth of multiple resistant clones was observed during therapy with BRAF, EGFR, and MEK inhibitor combinations. However, ERK inhibition, particularly in combination with BRAF and EGFR inhibition, markedly abrogated clonal outgrowth in vitro and in vivo. Thus, convergent, up-front therapy may suppress outgrowth of heterogeneous clones harboring clinically observed resistance alterations, which may improve clinical outcome.
   SIGNIFICANCE: We observed heterogeneous, recurrent alterations in the MAPK pathway as key drivers of acquired resistance in BRAF(V600E) colorectal cancer, with multiple concurrent resistance alterations detectable in individual patients. Using a novel pooled clone system, we identify convergent up-front therapeutic strategies capable of intercepting multiple resistance mechanisms as potential approaches to suppress emergence of acquired resistance. (C) 2018 AACR.
C1 [Hazar-Rethinam, Mehlika; Kleyman, Marianna; Ahronian, Leanne G.; Shahzade, Heather A.; Chen, Lifeng; Parikh, Aparna R.; Allen, Jill N.; Clark, Jeffrey W.; Kwak, Eunice L.; Faris, Jason E.; Murphy, Janet E.; Hong, Theodore S.; Van Seventer, Emily E.; Nadres, Brandon; Hong, Catriona B.; Gurski, Joseph M., Jr.; Jessop, Nicholas A.; Dias-Santagata, Dora; Iafrate, A. John; Corcoran, Ryan B.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
   [Hazar-Rethinam, Mehlika; Kleyman, Marianna; Ahronian, Leanne G.; Shahzade, Heather A.; Chen, Lifeng; Parikh, Aparna R.; Allen, Jill N.; Clark, Jeffrey W.; Kwak, Eunice L.; Faris, Jason E.; Murphy, Janet E.; Van Seventer, Emily E.; Nadres, Brandon; Hong, Catriona B.; Gurski, Joseph M., Jr.; Corcoran, Ryan B.] Harvard Med Sch, Dept Med, Boston, MA 02129 USA.
   [Han, G. Celine; Liu, David; Van Allen, Eliezer M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
   [Han, G. Celine; Liu, David; Van Allen, Eliezer M.] Broad Inst Massachusetts Inst Technol & Harvard, Cambridge, MA USA.
   [Hong, Theodore S.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
   [Jessop, Nicholas A.; Dias-Santagata, Dora; Iafrate, A. John] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
C3 Harvard University; Massachusetts General Hospital; Harvard University;
   Harvard Medical School; Harvard University; Dana-Farber Cancer
   Institute; Harvard University; Massachusetts Institute of Technology
   (MIT); Broad Institute; Harvard University; Massachusetts General
   Hospital; Harvard University; Massachusetts General Hospital
RP Corcoran, RB (corresponding author), Harvard Med Sch, 149 13th St, Boston, MA 02129 USA.
EM rbcorcoran@partners.org
RI Chen, Lifeng/JJE-7359-2023; Liu, David/ABF-1275-2020
OI Liu, David/0000-0003-0346-5033; Han, Celine/0000-0003-2004-8186; Hong,
   Catriona/0000-0003-2088-5056
FU NIH/NCI Gastrointestinal Cancer [SPORE P50 CA127003, R01CA208437,
   K08CA166510, U54CA224068]; Damon Runyon Clinical Investigator Award;
   Stand Up To Cancer Colorectal Cancer Dream Team Translational Research
   Grant [SU2C-AACR-DT22-17]
FX The work is supported by NIH/NCI Gastrointestinal Cancer SPORE P50
   CA127003, R01CA208437, K08CA166510, U54CA224068, and a Damon Runyon
   Clinical Investigator Award. This research is supported by a Stand Up To
   Cancer Colorectal Cancer Dream Team Translational Research Grant (grant
   number: SU2C-AACR-DT22-17). Stand Up To Cancer (SU2C) is a program of
   the Entertainment Industry Foundation. Research grants are administered
   by the American Association for Cancer Research, the scientific partner
   of SU2C.
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NR 36
TC 61
Z9 67
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
EI 2159-8290
J9 CANCER DISCOV
JI Cancer Discov.
PD APR
PY 2018
VL 8
IS 4
BP 417
EP 427
DI 10.1158/2159-8290.CD-17-1227
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GB4PL
UT WOS:000429042800023
PM 29431697
OA Green Accepted, Green Submitted, Bronze
DA 2025-01-04
ER

PT J
AU Liu, XF
   Xin, ZC
   Wang, K
AF Liu, Xiaofeng
   Xin, Zechang
   Wang, Kun
TI Patient-derived xenograft model in colorectal cancer basic and
   translational research
SO ANIMAL MODELS AND EXPERIMENTAL MEDICINE
LA English
DT Review
DE colorectal cancer; drug discovery; patient-derived xenograft model;
   precision medicine; tumor microenvironment
ID CONSENSUS MOLECULAR SUBTYPES; TUMOR XENOGRAFTS; COLON-CANCER;
   THERAPEUTIC RESPONSE; PRECISION MEDICINE; DRUG RESPONSE; IN-VITRO;
   METASTASIS; NAT10; ESTABLISHMENT
AB Colorectal cancer (CRC) is one of the most popular malignancies globally, with 930 000 deaths in 2020. The evaluation of CRC-related pathogenesis and the discovery of potential therapeutic targets will be meaningful and helpful for improving CRC treatment. With huge efforts made in past decades, the systematic treatment regimens have been applied to improve the prognosis of CRC patients. However, the sensitivity of CRC to chemotherapy and targeted therapy is different from person to person, which is an important cause of treatment failure. The emergence of patient-derived xenograft (PDX) models shows great potential to alleviate the straits. PDX models possess similar genetic and pathological characteristics as the features of primary tumors. Moreover, PDX has the ability to mimic the tumor microenvironment of the original tumor. Thus, the PDX model is an important tool to screen precise drugs for individualized treatment, seek predictive biomarkers for prognosis supervision, and evaluate the unknown mechanism in basic research. This paper reviews the recent advances in constructed methods and applications of the CRC PDX model, aiming to provide new knowledge for CRC basic research and therapeutics.
C1 [Liu, Xiaofeng; Xin, Zechang; Wang, Kun] Peking Univ Canc Hosp & Inst, Hepatopancreatobiliary Surg Dept 1, Key Lab Carcinogenesis & Translat Res, Minist Educ Beijing, Beijing, Peoples R China.
   [Liu, Xiaofeng; Wang, Kun] Peking Univ Canc Hosp & Inst, Minist Educ Beijing, Hepatopancreatobiliary Surg Department1, Key Lab Carcinogenesis & Translat Res, Beijing 100142, Peoples R China.
RP Liu, XF; Wang, K (corresponding author), Peking Univ Canc Hosp & Inst, Minist Educ Beijing, Hepatopancreatobiliary Surg Department1, Key Lab Carcinogenesis & Translat Res, Beijing 100142, Peoples R China.
EM liuxiaofeng100@bjmu.edu.cn; wang-kun@vip.sina.com
RI Liu, Xiaofeng/AAR-2488-2020
OI Liu, Xiaofeng/0000-0002-3264-122X
FU National Natural Science Foundation of China;  [81802305];  [31971192]
FX ACKNOWLEDGMENT The work was supported by the National Natural Science
   Foundation of China Grant (81802305 and 31971192).
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NR 189
TC 3
Z9 3
U1 2
U2 12
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2096-5451
EI 2576-2095
J9 ANIM MODEL EXP MED
JI Anim. Model. Exp. Med.
PD FEB
PY 2023
VL 6
IS 1
BP 26
EP 40
DI 10.1002/ame2.12299
EA DEC 2022
PG 15
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA 9O9EJ
UT WOS:000899807700001
PM 36543756
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Li, SY
   Zhang, H
   Chen, KW
   Jin, MF
   Vu, SH
   Jung, S
   He, NN
   Zheng, Z
   Lee, MS
AF Li Shangyong
   Zhang Hui
   Chen Kaiwei
   Jin Mengfei
   Vu Son Hai
   Jung, Samil
   He Ningning
   Zheng Zhou
   Lee, Myeong-Sok
TI Application of chitosan/alginate nanoparticle in oral drug delivery
   systems: prospects and challenges
SO DRUG DELIVERY
LA English
DT Article
DE Oral drug delivery; chitosan; alginate nanoparticle; insulin; ulcerative
   colitis; colon cancer
ID POLYELECTROLYTE COMPLEXES; POLYMERIC NANOPARTICLES; CHITOSAN
   NANOPARTICLES; PARTICLE-SIZE; ALGINATE; MICROSPHERES; OPTIMIZATION;
   FORMULATION; EFFICIENT; CARRIERS
AB Oral drug delivery systems (ODDSs) have various advantages of simple operation and few side effects. ODDSs are highly desirable for colon-targeted therapy (e.g. ulcerative colitis and colorectal cancer), as they improve therapeutic efficiency and reduce systemic toxicity. Chitosan/alginate nanoparticles (CANPs) show strong electrostatic interaction between the carboxyl group of alginates and the amino group of chitosan which leads to shrinkage and gel formation at low pH, thereby protecting the drugs from the gastrointestinal tract (GIT) and aggressive gastric environment. Meanwhile, CANPs as biocompatible polymer, show intestinal mucosal adhesion, which could extend the retention time of drugs on inflammatory sites. Recently, CANPs have attracted increasing interest as colon-targeted oral drug delivery system for intestinal diseases. The purpose of this review is to summarize the application and treatment of CANPs in intestinal diseases and insulin delivery. And then provide a future perspective of the potential and development direction of CANPs as colon-targeted ODDSs.
C1 [Li Shangyong; Zhang Hui; Chen Kaiwei; Jin Mengfei; He Ningning] Qingdao Univ, Qingdao Med Coll, Sch Basic Med, Qingdao, Peoples R China.
   [Li Shangyong; Vu Son Hai; Jung, Samil; Lee, Myeong-Sok] Sookmyung Womens Univ, Cellular Heterogene Res Ctr, Dept Biosyst, Mol Canc Biol Lab, Seoul, South Korea.
   [Vu Son Hai] Ho Chi Minh City Univ Technol HUTECH, Inst Appl Sci, Ho Chi Minh City, Vietnam.
   [Zheng Zhou] Minist Nat Resource, Inst Oceanog 1, Key Lab Marine Ecoenvironm Sci & Technol, Qingdao, Peoples R China.
C3 Qingdao University; Sookmyung Women's University; Vietnam National
   University Hochiminh City; Ho Chi Minh City University of Technology
   (HUTECH); First Institute of Oceanography, Ministry of Natural Resources
RP Lee, MS (corresponding author), Sookmyung Womens Univ, Cellular Heterogene Res Ctr, Dept Biosyst, Mol Canc Biol Lab, Seoul, South Korea.; Zheng, Z (corresponding author), Minist Nat Resource, Inst Oceanog 1, Key Lab Marine Ecoenvironm Sci & Technol, Qingdao, Peoples R China.
EM zhengzhou@fio.org.cn; mslee@sookmyung.ac.kr
RI Zhang, Hui/ABE-4439-2020; Zheng, Zhou/JJD-0602-2023
FU Basic Science Research Program through the National Research Foundation
   of Korea (NRF) - National Research Foundation of Korea
   [NRF-2016R1A5A1011974, NRF-2020R1A2C1102100]
FX This research was supported by the Basic Science Research Program
   through the National Research Foundation of Korea (NRF) funded by the
   National Research Foundation of Korea (NRF-2016R1A5A1011974) and
   (NRF-2020R1A2C1102100).
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NR 68
TC 88
Z9 92
U1 41
U2 451
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 1142
EP 1149
DI 10.1080/10717544.2022.2058646
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 0H5KT
UT WOS:000778772100001
PM 35384787
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Nakamura, Y
   Olsen, S
   Zhang, N
   Liao, JM
   Yoshino, T
AF Nakamura, Yoshiaki
   Olsen, Steven
   Zhang, Nicole
   Liao, Jiemin
   Yoshino, Takayuki
TI Comprehensive Genomic Profiling of Circulating Tumor DNA in Patients
   with Previously Treated Metastatic Colorectal Cancer: Analysis of a
   Real-World Healthcare Claims Database
SO CURRENT ONCOLOGY
LA English
DT Article
DE actionable genomic alterations; colorectal cancer; ctDNA profiling;
   real-world; targeted therapy
ID PLUS CETUXIMAB TREATMENT; CELL-FREE DNA; RAS MUTATIONS; TRASTUZUMAB;
   LANDSCAPE; THERAPIES; MEDICINE; SURVIVAL; BENEFIT; FOLFOX4
AB We used a real-world database (GuardantINFORM (TM)) to analyze the treatment choices for patients with mCRC who underwent next-generation sequencing of circulating tumor DNA (ctDNA) using a commercially available test (Guardant360 (R)) after first- or second-line therapy. From 18,875 patients with claims for CRC, 1064 had confirmed metastatic disease and sufficient histories for analysis (median age 59 years, 44.8% female, 44.5% left-sided). ctDNA was detectable for 997/1064 (93.7%) patients. Clinically actionable molecular profiles were present for 507/1064 (47.7%) patients, including those who had not received targeted therapy in the previous line (410/926, 44.3%). Second- or third-line targeted therapies were administered to 338/1064 patients (31.8%) and were considered matched for 193/338 (57.1%) patients. Therapies administered after testing were informed by the ctDNA results in 56.7% of patients overall (603/1064). Time to treatment discontinuation was most favorable for patients with a clinically actionable ctDNA profile who received matched therapy. This analysis demonstrates the real-world clinical value of plasma-based comprehensive genomic profiling for selecting appropriate molecular-targeted therapies in mCRC patients with disease progression after first- or second-line therapy.
C1 [Nakamura, Yoshiaki; Yoshino, Takayuki] Natl Canc Ctr Hosp East, Dept Gastroenterol & Gastrointestinal Oncol, Kashiwa, Chiba 2778577, Japan.
   [Nakamura, Yoshiaki] Natl Canc Ctr Hosp East, Translat Res Support Sect, Kashiwa, Chiba 2778577, Japan.
   [Olsen, Steven] Africa Inc, Guardant Hlth Asia, Dept Med Affairs, Middle East,Minato Ku, Tokyo Port City Takeshiba Off Tower 9th Floor, Tokyo 1057590, Japan.
   [Zhang, Nicole; Liao, Jiemin] Guardant Hlth Inc, Dept Outcomes & Evidence, Redwood City, CA 94063 USA.
C3 National Cancer Center - Japan; National Cancer Center - Japan; Guardant
   Health, Inc.; Guardant Health, Inc. AMEA; Guardant Health, Inc.
RP Olsen, S (corresponding author), Africa Inc, Guardant Hlth Asia, Dept Med Affairs, Middle East,Minato Ku, Tokyo Port City Takeshiba Off Tower 9th Floor, Tokyo 1057590, Japan.
EM yoshinak@east.ncc.go.jp; solsen@guardanthealth.com;
   niczhang@guardanthealth.com; jiliao@guardanthealth.com;
   tyoshino@east.ncc.go.jp
FU Guardant Health
FX The authors thank Nicholas D. Smith (EMC K.K.) for medical writing
   support, which was funded by Guardant Health.
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NR 52
TC 4
Z9 4
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 MAY
PY 2022
VL 29
IS 5
BP 3433
EP 3448
DI 10.3390/curroncol29050277
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 1P2UJ
UT WOS:000801869900001
PM 35621667
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Yan, B
   Zhao, DJ
   Yao, YN
   Bao, Z
   Lu, GH
   Zhou, JY
AF Yan, Bing
   Zhao, Dejian
   Yao, Yinan
   Bao, Zhang
   Lu, Guohua
   Zhou, Jianying
TI Deguelin Induces the Apoptosis of Lung Squamous Cell Carcinoma Cells
   through Regulating the Expression of Galectin-1
SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
LA English
DT Article
DE Deguelin; Lung squamous cell carcinoma; Apoptosis; Galectin-1
ID COLON-CANCER CELLS; AKT INHIBITOR; OSTEOSARCOMA CELLS; TUMOR
   PROGRESSION; POOR-PROGNOSIS; UP-REGULATION; GROWTH; PROMOTES;
   SUPPRESSES; INVASION
AB Lung cancer is the leading cause of cancer mortality around the world. Despite advances in the targeted therapy, patients with lung squamous cell carcinoma(SCC) still benefit few from it, and the search for potential effective therapies is imperative. Here, we demonstrated that deguelin induced significant apoptosis of lung SCC cells in vitro. Importantly, we found deguelin down-regulated the expression of galectin-1, which was involved in a wide range of tumorous physiologic process. Thus, we both over-expressed and down-regulated galectin-1 to perform its role in deguelin-induced apoptosis. We found that increased galectin-1 attenuated apoptosis of SCC cells exposed to deguelin, while galectin-1 knockdown sensitized lung cancer cells to deguelin treatment. Additionally, we observed that down-regulation of galectin-1 resulted in suppression of Ras/Raf/ERK pathway which was involved in deguelin-induced cell apoptosis. We also found that deguelin had a significant anti-tumor ability with decline of galectin-1 in vivo. In conclusion, these findings confirm that deguelin may act as a new chemo-preventive agent through inducing apoptosis of lung SCC cells in a galectin-1 dependent manner.
C1 [Yan, Bing; Yao, Yinan; Bao, Zhang; Lu, Guohua; Zhou, Jianying] Zhejiang Univ, Sch Med, Affiliated Hosp 1, Dept Resp Dis, Qingchun Rd 79, Hangzhou 310003, Zhejiang, Peoples R China.
   [Zhao, Dejian] Zhejiang Univ, Sch Med, Affiliated Hosp 1, Dept Clin Lab, Qingchun Rd 79, Hangzhou 310003, Zhejiang, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP Zhou, JY (corresponding author), Zhejiang Univ, Sch Med, Affiliated Hosp 1, Dept Resp Dis, Qingchun Rd 79, Hangzhou 310003, Zhejiang, Peoples R China.
EM zjyhz@zju.edu.cn
RI Zhao, Dejian/C-8321-2009; BAO, Zhang/F-2989-2010
OI BAO, Zhang/0000-0002-3057-1109
FU National Natural Science Foundation of China [81472171]; Science and
   Technology Planning Project of Zhejiang Province, China [2012C13022-2]
FX This study was supported by National Natural Science Foundation of China
   (No. 81472171) and Science and Technology Planning Project of Zhejiang
   Province, China (No. 2012C13022-2).
CR [Anonymous], HEAD NECK
   [Anonymous], J CELLULAR PHYSL
   [Anonymous], GLYCOBIOLOGY
   [Anonymous], ENV TOXICOLOGY
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NR 50
TC 23
Z9 25
U1 0
U2 9
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1449-2288
J9 INT J BIOL SCI
JI Int. J. Biol. Sci.
PY 2016
VL 12
IS 7
BP 850
EP 860
DI 10.7150/ijbs.14773
PG 11
WC Biochemistry & Molecular Biology; Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA DM9AR
UT WOS:000376656400008
PM 27313498
OA Green Published, Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Sheffield, BS
   Tessier-Cloutier, B
   Li-Chang, H
   Shen, Y
   Pleasance, E
   Kasaian, K
   Li, Y
   Jones, SJM
   Lim, HJ
   Renouf, DJ
   Huntsman, DG
   Yip, S
   Laskin, J
   Marra, M
   Schaeffer, DF
AF Sheffield, B. S.
   Tessier-Cloutier, B.
   Li-Chang, H.
   Shen, Y.
   Pleasance, E.
   Kasaian, K.
   Li, Y.
   Jones, S. J. M.
   Lim, H. J.
   Renouf, D. J.
   Huntsman, D. G.
   Yip, S.
   Laskin, J.
   Marra, M.
   Schaeffer, D. F.
TI Personalized oncogenomics in the management of gastrointestinal
   carcinomas-early experiences from a pilot study
SO CURRENT ONCOLOGY
LA English
DT Article
DE Oncogenomics; genomics; cholangiocarcinoma; colonic adenocarcinoma;
   appendiceal adenocarcinoma; targeted therapy; personalized medicine;
   bevacizumab
ID CANCER; MUTATION; THERAPY; IMPACT
AB Background Gastrointestinal carcinomas are genomically complex cancers that are lethal in the metastatic setting. Whole-genome and transcriptome sequencing allow for the simultaneous characterization of multiple oncogenic pathways.
   Methods We report 3 cases of metastatic gastrointestinal carcinoma in patients enrolled in the Personalized Onco-Genomics program at the BC Cancer Agency. Real-time genomic profiling was combined with clinical expertise to diagnose a carcinoma of unknown primary, to explore treatment response to bevacizumab in a colorectal cancer, and to characterize an appendiceal adenocarcinoma.
   Results In the first case, genomic profiling revealed an IDH1 somatic mutation, supporting the diagnosis of cholangiocarcinoma in a malignancy of unknown origin, and further guided therapy by identifying epidermal growth factor receptor amplification. In the second case, a BRAF V600E mutation and wild-type KRAS profile justified the use of targeted therapies to treat a colonic adenocarcinoma. The third case was an appendiceal adenocarcinoma defined by a p53 inactivation; RAS/RAF/MEK, Akt/mTOR, Wnt, and NOTCH pathway activation; and overexpression of RET, ERBB2 (HER2), ERBB3, met, and cell cycle regulators.
   Summary We show that whole-genome and transcriptome sequencing can be achieved within clinically effective timelines, yielding clinically useful and actionable information.
C1 [Sheffield, B. S.; Tessier-Cloutier, B.; Huntsman, D. G.; Yip, S.; Schaeffer, D. F.] Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC, Canada.
   [Li-Chang, H.] Royal Victoria Reg Hlth Ctr, Dept Pathol & Lab Med, Barrie, ON, Canada.
   [Shen, Y.; Pleasance, E.; Kasaian, K.; Li, Y.; Jones, S. J. M.; Marra, M.] BC Canc Agcy, Canadas Michael Smith Genome Sci Ctr, Vancouver, BC, Canada.
   [Lim, H. J.; Renouf, D. J.; Laskin, J.] BC Canc Agcy, Div Med Oncol, Vancouver, BC, Canada.
   [Marra, M.] Univ British Columbia, Dept Med Genet, Vancouver, BC, Canada.
C3 University of British Columbia; British Columbia Cancer Agency; British
   Columbia Cancer Agency; University of British Columbia
RP Sheffield, BS (corresponding author), Abbotsford Reg Hosp & Canc Ctr, 32900 Marshall Rd, Abbotsford, BC V2S 0C2, Canada.
EM brandon.s.sheffield@gmail.com
RI Tessier-Cloutier, Basile/HTO-7213-2023; Huntsman, David/ABE-6082-2020;
   Yip, Stephen/E-9994-2012; Marra, Marco/B-5987-2008; Jones,
   Steven/C-3621-2009
OI Jones, Steven/0000-0003-3394-2208; Marra, Marco/0000-0001-7146-7175
FU BC Cancer Foundation; Canadian Institutes of Health Research
FX This work is funded by the BC Cancer Foundation. HLC and KK receive
   fellowship funding from the Canadian Institutes of Health Research.
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NR 27
TC 8
Z9 9
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1198-0052
EI 1718-7729
J9 CURR ONCOL
JI Curr. Oncol.
PD DEC
PY 2016
VL 23
IS 6
BP E571
EP E575
DI 10.3747/co.23.3165
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EH6BV
UT WOS:000391858400007
PM 28050146
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Al-Shamsi, HO
   Alhazzani, W
   Wolff, RA
AF Al-Shamsi, Humaid O.
   Alhazzani, Waleed
   Wolff, Robert A.
TI Extended <i>RAS</i> testing in metastatic colorectal cancer-Refining the
   predictive molecular biomarkers
SO JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Extended RAS analysis; metastatic colorectal cancer (CRC); monoclonal
   antibody therapy
ID GROWTH-FACTOR RECEPTOR; CETUXIMAB PLUS IRINOTECAN; RANDOMIZED PHASE-III;
   WILD-TYPE KRAS; 1ST-LINE TREATMENT; PANITUMUMAB PLUS; TARGETED THERAPY;
   OPEN-LABEL; MUTATIONS; FLUOROURACIL
AB Mutations of exon 2 of Kirsten rat sarcoma viral oncogene homologue (KRAS) (exon 2 codons 12/13) lead to constitutive activation of the EGFR (epidermal growth factor receptor) mediated signal transduction pathway and been shown to be a negative predictive biomarker for EGFR-directed monoclonal antibodies among patients with colorectal cancer (CRC). As selection of patients is very important for administration of anti-EGFR therapy, this lone biomarker has proved to be insufficient for selecting the appropriate patients as more patients lacking exon 2 KRAS mutation were resistant to anti-EGFR therapy. The results of various randomized clinical trials have confirmed the presence of other RAS mutation including additional RAS mutations (KRAS exons 3/4 and NRAS exon 1/2/3/4). Extended RAS analysis should be considered before initiating anti-EGFR therapy to patients of metastatic CRC. This can help in proper selection of patients leading to tailored individualistic treatment, decreasing cost of treatment and the adverse effects related to use of monoclonal antibody therapy. The new evidence is supporting the need to make 'Extended RAS' analysis essential before start of treatment with anti-EGFR monoclonal antibody therapy. Prior to this the Extended RAS testing should be standardized.
C1 [Al-Shamsi, Humaid O.; Wolff, Robert A.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
   [Alhazzani, Waleed] McMaster Univ, Internal Med, Dept Gastroenterol, Hamilton, ON, Canada.
C3 University of Texas System; UTMD Anderson Cancer Center; McMaster
   University
RP Al-Shamsi, HO (corresponding author), Dept Gastrointestinal Med Oncol, Unit 426 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM halshamsi@mdanderson.org
OI Alhazzani, Waleed/0000-0001-8076-9626; Al-Shamsi, Humaid
   O./0000-0003-3819-0500
CR Allegra CJ, 2009, J CLIN ONCOL, V27, P2091, DOI 10.1200/JCO.2009.21.9170
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   [Anonymous], ANAL KRAS NRAS MUTAT
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NR 47
TC 28
Z9 31
U1 0
U2 4
PU AME PUBLISHING COMPANY
PI SHATIN
PA FLAT-RM C 16F, KINGS WING PLAZA 1, NO 3 KWAN ST, SHATIN, HONG KONG
   00000, PEOPLES R CHINA
SN 2078-6891
EI 2219-679X
J9 J GASTROINTEST ONCOL
JI J. Gastrointest. Oncol.
PD JUN
PY 2015
VL 6
IS 3
BP 314
EP 321
DI 10.3978/j.issn.2078-6891.2015.016
PG 8
WC Oncology; Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Oncology; Gastroenterology & Hepatology
GA CS4YR
UT WOS:000362082800017
PM 26029459
DA 2025-01-04
ER

PT J
AU Nemati, M
   Ajami, N
   Estiar, MA
   Rezapour, S
   Gavgani, RR
   Hashemzadeh, S
   Kafil, HS
   Sakhinia, E
AF Nemati, Masoumeh
   Ajami, Naser
   Estiar, Mehrdad Asghari
   Rezapour, Saleheh
   Gavgani, Reyhaneh Ravanbakhsh
   Hashemzadeh, Shahryar
   Kafil, Hossein Samadi
   Sakhinia, Ebrahim
TI Deregulated expression of HDAC3 in colorectal cancer and its clinical
   significance
SO ADVANCES IN CLINICAL AND EXPERIMENTAL MEDICINE
LA English
DT Article
DE HDAC3; deregulation; prognosis; colorectal cancer
ID HISTONE DEACETYLASE INHIBITORS; MOLECULAR-MECHANISMS;
   CELL-PROLIFERATION; DOWN-REGULATION; OVEREXPRESSION; EPIGENOMICS;
   BIOMARKERS; PROGNOSIS; SURVIVAL; THERAPY
AB Background. To date, 4 classes of histone deacetylases (HDACs) have been identified in humans. Class I HDACs are zinc-dependent and NAD(+)-independent enzymes, and include 4 isoforms closely related to yeast RPD3: HDAC1, 2, 3, and 8.
   Objectives. The aims of the study were to quantitatively evaluate the expression of HDAC3 in colorectal cancer (CRC) and to correlate its expression levels with clinicopathological parameters.
   Material and methods. We characterized expression patterns of HDAC3 as class I HDAC isoforms in a cohort of 48 CRC patients by quantitative (real-time) reverse transcription polymerase chain reaction (RT-PCR). In addition, the potential relationship between HDAC3 expression levels and clinicopathological parameters in patients suffering from CRC was explored.
   Results. We found that HDAC3 was highly expressed in colorectal tumors compared to normal colorectal tissues (p < 0.05). Furthermore, we found significant correlations between HDAC3 expression levels and tumor differentiation grades (p < 0.05).
   Conclusions. In this prospective study we identified a pronounced HDAC3 expression pattern in CRC. Our findings support an important role of HDAC3 as a complementary molecular marker for existing histopathological diagnostic elements; it might also have applications in prognostic and targeted therapy. Furthermore, HDAC3 can be used as a biomarker to differentiate between tumor borders and margins, and it may also be useful for characterizing field cancerization in CRC.
C1 [Nemati, Masoumeh; Gavgani, Reyhaneh Ravanbakhsh] Tabriz Univ, Dept Biol, Fac Nat Sci, Tabriz, Iran.
   [Ajami, Naser] Mashhad Univ Med Sci, Dept Med Genet, Fac Med, Mashhad, Iran.
   [Estiar, Mehrdad Asghari] Univ Tehran Med Sci, Dept Med Genet, Tehran, Iran.
   [Rezapour, Saleheh; Sakhinia, Ebrahim] Tabriz Univ Med Sci, Div Med Genet, Fac Med, Tabriz, Iran.
   [Hashemzadeh, Shahryar] Tabriz Univ Med Sci, Liver & Gastrointestinal Dis Res Ctr, Tabriz, Iran.
   [Hashemzadeh, Shahryar] Tabriz Univ Med Sci, Dept Gen & Thorac Surg, Tabriz, Iran.
   [Kafil, Hossein Samadi] Tabriz Univ Med Sci, Drug Appl Res Ctr, Tabriz, Iran.
C3 University of Tabriz; Mashhad University of Medical Sciences; Tehran
   University of Medical Sciences; Tabriz University of Medical Science;
   Tabriz University of Medical Science; Tabriz University of Medical
   Science; Tabriz University of Medical Science
RP Sakhinia, E (corresponding author), Tabriz Univ Med Sci, Div Med Genet, Fac Med, Tabriz, Iran.
EM esakhinia@yahoo.co.uk
RI Gavgani, Reyhaneh/AAK-9256-2021; Samadi Kafil, Hossein/AAX-2888-2021;
   sakhinia, ebrahim/AAA-8636-2021; Samadi Kafil, Hossein/B-5855-2012
OI Ravanbakhsh Gavgani, Reyhaneh/0000-0002-9644-6204; Samadi Kafil,
   Hossein/0000-0001-6026-8795
FU Tabriz Genetic Analysis Center (TGAC) of Tabriz University of Medical
   Sciences, Iran
FX This study was supported by Tabriz Genetic Analysis Center (TGAC) of
   Tabriz University of Medical Sciences, Iran.
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NR 50
TC 33
Z9 34
U1 1
U2 6
PU WROCLAW MEDICAL UNIV
PI WROCLAW
PA Wybrzeze L Pasteura 1, WROCLAW, 50-367, POLAND
SN 1899-5276
EI 2451-2680
J9 ADV CLIN EXP MED
JI Adv. Clin. Exp. Med.
PD MAR
PY 2018
VL 27
IS 3
BP 305
EP 311
DI 10.17219/acem/66207
PG 7
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA GB6XK
UT WOS:000429218200001
PM 29558042
OA Green Submitted, gold
DA 2025-01-04
ER

PT J
AU Wang, RX
   Lai, QH
   Tang, LZ
   Tao, YR
   Yao, YQ
   Liu, Y
   Lu, Y
   Shen, CY
   Lu, R
   Fan, CW
   Zhang, RR
   Wang, YX
   Yu, L
   Yang, TH
   Wu, YP
   Peng, YJ
   Wei, X
   Fu, YY
   Lai, WR
   Gou, LT
   Yang, JL
AF Wang, Ruixue
   Lai, Qinhuai
   Tang, Liangze
   Tao, Yiran
   Yao, Yuqin
   Liu, Yu
   Lu, Ying
   Shen, Chaoyong
   Lu, Ran
   Fan, Chuanwen
   Zhang, Ruirui
   Wang, Yuxi
   Yu, Lin
   Yang, Tinghan
   Wu, Yangping
   Peng, Yujia
   Wei, Xian
   Fu, Yuyin
   Lai, Weirong
   Gou, Lantu
   Yang, Jinliang
TI A novel 5T4-targeting antibody-drug conjugate H6-DM4 exhibits potent
   therapeutic efficacy in gastrointestinal tumor xenograft models
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE 5T4; gastrointestinal cancer; antibody-drug conjugate; DM4; targeted
   therapy
ID 5T4 ONCOFETAL ANTIGEN; CANCER STEM-CELLS; GASTRIC-CANCER; COLON-CANCER;
   EXPRESSION; RESISTANCE; TARGET; CHEMORESISTANCE; MECHANISMS
AB 5T4, also named as trophoblast glycoprotein, is often upregulated in some cancer cells. Here, we demonstrated that 5T4 was highly expressed in gastric, colorectal, and pancreatic cancer, associated with significantly poor prognosis of gastrointestinal (GI) cancer patients. To search for new targeting drugs for GI cancer, we developed a novel anti-5T4 monoclonal antibody with high affinity and robust internalization ability and conjugated it to the potent microtubule inhibitor DM4 to produce conjugate H6-DM4. This antibody-drug conjugate (ADC) displayed significant cytotoxicity in a panel of GI cancer cell lines with IC50 values in the nanomolar range. H6-DM4 eradicated established GI tumor xenograft models at 2.5 mg/kg or 10 mg/kg without observable toxicity. Further, 5T4 was highly expressed in cancer initiating cells (CICs) compared with non-CICs in colorectal cancer. In vitro and in vivo, treatment with H6-DM4 exhibited a powerful efficacy on colorectal CICs. Additionally, colorectal cancer cells resistant to platinum were effectively eliminated by H6-DM4. Taken together, our results showed 5T4-positive GI cancer cells, colorectal cancer-initiating cells, and platinum-resistant colorectal cancer cells were potently eliminated by H6-DM4, indicating H6-DM4 may be a potential candidate drug for GI cancer treatment.
C1 [Wang, Ruixue; Lai, Qinhuai; Tang, Liangze; Tao, Yiran; Yao, Yuqin; Liu, Yu; Lu, Ying; Zhang, Ruirui; Wang, Yuxi; Yu, Lin; Yang, Tinghan; Wu, Yangping; Peng, Yujia; Wei, Xian; Fu, Yuyin; Lai, Weirong; Gou, Lantu; Yang, Jinliang] Sichuan Univ, State Key Lab Biotherapy, West China Hosp, 3-17 People Rd, Chengdu 610041, Sichuan, Peoples R China.
   [Wang, Ruixue; Lai, Qinhuai; Tang, Liangze; Tao, Yiran; Yao, Yuqin; Liu, Yu; Lu, Ying; Zhang, Ruirui; Wang, Yuxi; Yu, Lin; Yang, Tinghan; Wu, Yangping; Peng, Yujia; Wei, Xian; Fu, Yuyin; Lai, Weirong; Gou, Lantu; Yang, Jinliang] Sichuan Univ, Canc Ctr, West China Hosp, Collaborat Innovat Ctr Biotherapy, 3-17 People Rd, Chengdu 610041, Sichuan, Peoples R China.
   [Yao, Yuqin] Sichuan Univ, Res Ctr Publ Hlth & Prevent Med, West China Sch Publ Hlth, 4 West China Teaching Hosp, Chengdu, Sichuan, Peoples R China.
   [Yao, Yuqin] Sichuan Univ, Hlth Food Evaluat Res Ctr, 4 West China Teaching Hosp, Chengdu, Sichuan, Peoples R China.
   [Wang, Ruixue; Yao, Yuqin; Wei, Xian; Yang, Jinliang] Guangdong Zhongsheng Pharmaceut Co Ltd, Guangzhou, Guangdong, Peoples R China.
   [Shen, Chaoyong; Yang, Tinghan] Sichuan Univ, West China Hosp, Dept Gastrointestinal Surg, Chengdu, Sichuan, Peoples R China.
   [Lu, Ran] Sichuan Univ, West China Hosp, Collaborat Innovat Ctr Biotherapy, State Key Lab Biotherapy,Lab Stem Cell Biol, Chengdu, Sichuan, Peoples R China.
   [Fan, Chuanwen] Sichuan Univ, West China Hosp, Collaborat Innovat Ctr Biotherapy, State Key Lab Biotherapy,Inst Digest Surg, Chengdu, Sichuan, Peoples R China.
   [Wei, Xian] Chengdu Med Coll, Sch Basic Med Sci, Chengdu, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University; Sichuan
   University; Sichuan University; Sichuan University; Sichuan University;
   Chengdu Medical College
RP Yang, JL (corresponding author), Sichuan Univ, State Key Lab Biotherapy, West China Hosp, 3-17 People Rd, Chengdu 610041, Sichuan, Peoples R China.; Yang, JL (corresponding author), Sichuan Univ, Canc Ctr, West China Hosp, Collaborat Innovat Ctr Biotherapy, 3-17 People Rd, Chengdu 610041, Sichuan, Peoples R China.
EM jlyang01@163.com
RI Lai, weirong/HQY-7791-2023; Yao, Yuqin/AAG-3879-2020; Tao,
   Yiran/GVS-6409-2022; lu, ran/HHC-8613-2022; wu, yangping/Q-9741-2017;
   Zhang, Yanbo/N-5858-2019; Fan, Chuanwen/GLU-5994-2022; WANG,
   RUIXUE/JXN-7577-2024
FU National Major Scientific and Technological Special Project
   [2007ZX09302-010-005-003]; National Natural Science Foundation of China
   [81372822, 81501368, 81672722]
FX This work is supported by National Major Scientific and Technological
   Special Project [grant number 2007ZX09302-010-005-003] and National
   Natural Science Foundation of China [grant numbers 81372822, 81501368
   and 81672722]. The authors gratefully acknowledge Prof. Xianming Mo for
   providing colorectal CICs. The authors thank Prof. Feng Bi for providing
   SW-480-Oxaliplatin and HCT116-Oxaliplatin cell lines; Fan Yang (Jinkai
   biotechnology company) for the mass spectrometric analysis; Min Wu for
   improving this manuscript; Hao Chen, Qiang Chen, and Dan Su for their
   help in the experiments and data analysis. Finally, the authors
   acknowledge technical expertise of Yingbin Zhao for IHC.
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NR 38
TC 13
Z9 13
U1 0
U2 17
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2156-6976
J9 AM J CANCER RES
JI Am. J. Cancer Res.
PY 2018
VL 8
IS 4
BP 610
EP +
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GE5GF
UT WOS:000431247200004
PM 29736307
DA 2025-01-04
ER

PT J
AU Suman, S
   Hota, SK
   Misra, P
   Sahu, N
   Sahu, S
AF Suman, Sweta
   Hota, Subhransu Kumar
   Misra, Pranati
   Sahu, Nageswar
   Sahu, Subrat
TI Immunohistochemical Expression of the Stem Cell Marker CD133 in
   Colorectal Carcinoma
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE pathological parameters; cd133; immunohistochemistry; cancer stem cell;
   colorectal carcinoma
ID CANCER; INSTABILITY
AB Background Colorectal carcinoma (CRC) is the second-leading cause of cancer-related death. Despite the combined (surgery, chemotherapy, radiotherapy, and immunotherapy) modalities of treatment, the prognosis remains poor, mostly because of recurrence and distant metastasis. Cancer stem cells (CSC) are thought to be responsible for the development and spread of tumors. Hence, targeted therapy against these cells hopes to reduce the chance of recurrence and metastasis and improve the prognosis. Many immune markers have been identified to detect CSC in CRC. Here, we tried to assess the immunohistochemical expression of the stem cell marker CD133 in colorectal carcinoma and its correlation with various pathological parameters. Methodology A total of 51 cases of CRC were analyzed. Immunohistochemistry for CD133 was done after standardization in our laboratory. Expression status was decided based on the total score obtained by multiplying the intensity score by the percentage score. CD133 expression was correlated with the age and gender of the patient, tumor location, histological grade, extent of invasion, lymphovascular invasion (LVI), perineural invasion (PNI), and nodal status. Results High CD133 expression was seen in 21 (41.17%) cases. There was no significant association between CD133 expression and the pathological parameters except the tumor site. CD133 expression was significantly higher as we moved from the proximal colon to the rectum. Conclusions CD133 expression was significantly higher in the distal part of the large intestine as compared to the proximal part. But there was no linear correlation between CD133 expression and histological grade, extent of invasion, or nodal status.
C1 [Suman, Sweta; Misra, Pranati; Sahu, Nageswar] Kalinga Inst Med Sci, Pathol, Bhubaneswar, India.
   [Hota, Subhransu Kumar] Hitech Med Coll & Hosp, Pathol, Bhubaneswar, India.
   [Sahu, Subrat] Kalinga Inst Med Sci, Surg, Bhubaneswar, India.
C3 Kalinga Institute of Industrial Technology (KIIT); Kalinga Institute of
   Industrial Technology (KIIT)
RP Sahu, N (corresponding author), Kalinga Inst Med Sci, Pathol, Bhubaneswar, India.
EM nageswar.sahoo@kims.ac.in
RI Sahu, Nageswar/GXG-7587-2022
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NR 25
TC 2
Z9 2
U1 0
U2 0
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD JUL 1
PY 2023
VL 15
IS 7
AR e41242
DI 10.7759/cureus.41242
PG 10
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA O1DA0
UT WOS:001041281800012
PM 37529823
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Vander Linden, C
   Corbet, C
AF Vander Linden, Catherine
   Corbet, Cyril
TI Reconciling environment-mediated metabolic heterogeneity with the
   oncogene-driven cancer paradigm in precision oncology
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE Precision oncology; Metabolism; Cancer; Targeted therapy; Drug
   resistance; Oxidative phosphorylation; Organoid
ID METASTATIC COLORECTAL-CANCER; PLUS CETUXIMAB TREATMENT; LEUKEMIC
   STEM-CELLS; BREAST-CANCER; LACTATE METABOLISM; RAS MUTATIONS;
   OXIDATIVE-PHOSPHORYLATION; GENETIC INSTABILITY; HUMAN GLIOBLASTOMAS;
   TARGETED THERAPIES
AB Precision oncology is the practice of matching one therapy to one specific patient, based on particular genetic tumor alterations, in order to achieve the best clinical response. Despite an expanding arsenal of targeted therapies, many patients still have a poor outcome because tumor cells show a remarkable capacity to develop drug resistance, thereby leading to tumor relapse. Besides genotype-driven resistance mechanisms, tumor microenvironment (TME) peculiarities strongly contribute to generate an intratumoral phenotypic heterogeneity that affects disease progression and treatment outcome. In this Review, we describe how TME-mediated metabolic heterogeneities actively participate to therapeutic failure. We report how a lactate-based metabolic symbiosis acts as a mechanism of adaptive resistance to targeted therapies and we describe the role of mitochondrial metabolism, in particular oxidative phosphorylation (OXPHOS), to support the growth and survival of therapy-resistant tumor cells in a variety of cancers. Finally, we detail potential metabolism-interfering therapeutic strategies aiming to eradicate OXPHOS-dependent relapse-sustaining malignant cells and we discuss relevant (pre)clinical models that may help integrate TME-driven metabolic heterogeneity in precision oncology.
C1 [Vander Linden, Catherine; Corbet, Cyril] UCLouvain, IREC, Pole Pharmacol & Therapeut FATH, 57 Ave Hippocrate,B1-57-04, B-1200 Brussels, Belgium.
C3 Universite Catholique Louvain
RP Corbet, C (corresponding author), UCLouvain, IREC, Pole Pharmacol & Therapeut FATH, 57 Ave Hippocrate,B1-57-04, B-1200 Brussels, Belgium.
EM cyril.corbet@uclouvain.be
FU Fonds de la Recherche Scientifique (F.R.S.-FNRS); Televie
FX This work was supported by grants from the Fonds de la Recherche
   Scientifique (F.R.S.-FNRS) and the Televie. CVL is a Televie PhD fellow
   and CC is a F.R.S.-FNRS Postdoctoral Researcher.
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NR 142
TC 23
Z9 24
U1 1
U2 17
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1084-9521
EI 1096-3634
J9 SEMIN CELL DEV BIOL
JI Semin. Cell Dev. Biol.
PD FEB
PY 2020
VL 98
SI SI
BP 202
EP 210
DI 10.1016/j.semcdb.2019.05.016
PG 9
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA KD5XE
UT WOS:000507938200021
PM 31103464
DA 2025-01-04
ER

PT J
AU Bellyei, S
   Boronkai, A
   Pozsgai, E
   Fodor, D
   Mangel, L
AF Bellyei, Szabolcs
   Boronkai, Arpad
   Pozsgai, Eva
   Fodor, David
   Mangel, Laszlo
TI Effective chemotherapy and targeted therapy supplemented with
   stereotactic radiotherapy of a patient with metastatic colon cancer
   following renal transplantation: a case report
SO JOURNAL OF MEDICAL CASE REPORTS
LA English
DT Article
DE Colorectal cancer; Kidney transplantation; Stereotactic body
   irradiation; Palliative chemotherapy; Targeted treatment
ID COLORECTAL-CANCER; CETUXIMAB PLUS; IMMUNOSUPPRESSION; RISK
AB Background Previous studies have shown that patients who underwent renal transplantation were at a greater risk of developing malignancies. Due to advances in effective surgical techniques and immunosuppressive therapies, organ recipients live longer. Yet, there is insufficient information about the recommended type of therapy for colorectal cancer patients following transplantation. We describe the oncological treatment of a patient with renal transplantation, who presented with metastatic colon cancer 5 years after transplantation. Case presentation A 66-year-old Caucasian male patient, with hypertension, type 2 diabetes mellitus, paroxysmal atrial fibrillation, and renal failure underwent successful kidney transplantation in 2013. In April 2018, the adenocarcinoma of the sigmoid colon was found, and surgical resection was performed. The histological diagnosis was low-grade adenocarcinoma. Fluorodeoxyglucose positron emission tomography/computerized tomography scan showed a 2.5-cm metastasis in the VIIth segment of the liver and a metastatic paraaortical lymph node on the left. The clinical diagnosis was, therefore, metastatic (stage IV) sigmoid colon cancer (AJCC TNM system). The ongoing medications of the patient included immunosuppressive drugs and medication for his cardiovascular comorbidities. In July 2018, palliative cetuximab plus folinic acid-fluorouracil-irinotecan chemotherapeutic treatment was initiated, then cetuximab was substituted for panitumumab because of adverse events. In August 2018, the follow-up positron emission tomography/computerized tomography scan revealed stable disease. Because of side effects, the patient was unwilling to continue with the panitumumab plus folinic acid-fluorouracil-irinotecan treatment regimen. Therefore, the patient received 10x 5 Gy stereotactic body irradiation for his liver metastasis and mono-panitumumab therapy. By January 2019, the positron emission tomography/computerized tomography scan showed regression of the liver metastasis but a progression in the paraaortic lymph node. Therefore, 5x 8 Gy stereotactic irradiation was given to the paraaortic lesion. Meanwhile, the patient received altogether 16 cycles of panitumumab until June 2019, when complete remission was attained. In July 2019, the patient suffered a hemorrhagic stroke, probably due to his cardiovascular comorbidities, and died subsequently. Conclusions Since information is scarce regarding oncological treatment of patients following organ transplantation, data about their oncological treatment is essential. To our knowledge, this is the first case report to describe the successful chemotherapy and targeted therapy supplemented with stereotactic radiotherapy of a posttransplant patient with metastatic colorectal cancer.
C1 [Bellyei, Szabolcs; Boronkai, Arpad; Fodor, David; Mangel, Laszlo] Univ Pecs, Clin Ctr, Dept Oncotherapy, Edesanyak St 10, H-7624 Pecs, Hungary.
   [Pozsgai, Eva] Univ Pecs, Med Sch, Dept Publ Hlth, Szigeti St 12, H-7624 Pecs, Hungary.
   [Pozsgai, Eva] Univ Pecs, Med Sch, Inst Primary Hlth Care, Rakoczi St 2, H-7623 Pecs, Hungary.
C3 University of Pecs; University of Pecs; University of Pecs
RP Pozsgai, E (corresponding author), Univ Pecs, Med Sch, Dept Publ Hlth, Szigeti St 12, H-7624 Pecs, Hungary.; Pozsgai, E (corresponding author), Univ Pecs, Med Sch, Inst Primary Hlth Care, Rakoczi St 2, H-7623 Pecs, Hungary.
EM pozsgay83@gmail.com
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NR 18
TC 5
Z9 5
U1 0
U2 4
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1752-1947
J9 J MED CASE REP
JI J. Med. Case Rep.
PD MAR 20
PY 2021
VL 15
IS 1
AR 125
DI 10.1186/s13256-021-02702-y
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA WD2MJ
UT WOS:000704781200001
PM 33741057
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Dominguez, OH
   Yilmaz, S
   Steele, SR
AF Dominguez, Oscar Hernandez
   Yilmaz, Sumeyye
   Steele, Scott. R. R.
TI Stage IV Colorectal Cancer Management and Treatment
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE metastatic colorectal cancer; stage IV colon cancer; stage IV rectal
   cancer; treatment of stage IV colorectal cancer
ID HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY; BEVACIZUMAB PLUS
   CAPECITABINE; SYNCHRONOUS LIVER METASTASES; CLINICAL-PRACTICE
   GUIDELINES; MONOCLONAL-ANTIBODY THERAPY; COOPERATIVE-ONCOLOGY-GROUP;
   POSITIVE SOLID TUMORS; DISEASE-FREE SURVIVAL; III RANDOMIZED-TRIAL;
   CYTOREDUCTIVE SURGERY
AB (1) Background: Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer-related mortality worldwide. Up to 50% of patients with CRC develop metastatic CRC (mCRC). Surgical and systemic therapy advances can now offer significant survival advantages. Understanding the evolving treatment options is essential for decreasing mCRC mortality. We aim to summarize current evidence and guidelines regarding the management of mCRC to provide utility when making a treatment plan for the heterogenous spectrum of mCRC. (2) Methods: A comprehensive literature search of PubMed and current guidelines written by major cancer and surgical societies were reviewed. The references of the included studies were screened to identify additional studies that were incorporated as appropriate. (3) Results: The standard of care for mCRC primarily consists of surgical resection and systemic therapy. Complete resection of liver, lung, and peritoneal metastases is associated with better disease control and survival. Systemic therapy now includes chemotherapy, targeted therapy, and immunotherapy options that can be tailored by molecular profiling. Differences between colon and rectal metastasis management exist between major guidelines. (4) Conclusions: With the advances in surgical and systemic therapy, as well as a better understanding of tumor biology and the importance of molecular profiling, more patients can anticipate prolonged survival. We provide a summary of available evidence for the management of mCRC, highlighting the similarities and presenting the difference in available literature. Ultimately, a multidisciplinary evaluation of patients with mCRC is crucial to selecting the appropriate pathway.
C1 [Dominguez, Oscar Hernandez; Yilmaz, Sumeyye; Steele, Scott. R. R.] Cleveland Clin, Digest Dis & Surg Inst, Dept Colorectal Surg, Cleveland, OH 44195 USA.
C3 Cleveland Clinic Foundation
RP Steele, SR (corresponding author), Cleveland Clin, Digest Dis & Surg Inst, Dept Colorectal Surg, Cleveland, OH 44195 USA.
EM steeles3@ccf.org
RI Hernandez Dominguez, Oscar/KQU-7271-2024
OI Hernandez Dominguez, Oscar/0000-0001-9962-948X; Yilmaz,
   Sumeyye/0000-0002-2482-1570
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NR 191
TC 46
Z9 46
U1 9
U2 44
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 MAR
PY 2023
VL 12
IS 5
AR 2072
DI 10.3390/jcm12052072
PG 26
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 9T9FN
UT WOS:000947326800001
PM 36902858
OA gold, Green Published
HC Y
HP N
DA 2025-01-04
ER

PT J
AU Plano, D
   Alcolea, V
   Sanmartín, C
   Sharma, AK
AF Plano, Daniel
   Alcolea, Veronica
   Sanmartin, Carmen
   Sharma, Arun K.
TI Methods of selecting combination therapy for colorectal cancer patients:
   a patent evaluation of US20160025730A1
SO EXPERT OPINION ON THERAPEUTIC PATENTS
LA English
DT Article
DE Biomarkers; colorectal cancer; EGFR inhibitors; monoclonal antibodies;
   combination therapy
ID GROWTH-FACTOR RECEPTOR; TYROSINE KINASE INHIBITORS; CETUXIMAB PLUS
   IRINOTECAN; ANTI-EGFR THERAPY; WILD-TYPE KRAS; IRREVERSIBLE INHIBITORS;
   ANTITUMOR-ACTIVITY; BRAF MUTATION; CELL-DEATH; IN-VITRO
AB Introduction: Colorectal cancer (CRC) is the fourth most common cancer worldwide. Targeted therapy drugs (TTDs) are a valid treatment, epithelial growth factor receptor (EGFR) inhibitors being one of the most commonly used for CRC patients. However, this treatment is only useful for patients with wild-type KRAS (wtKRAS) and is effective only on about 40 to 60% of this subset due to the high plasticity of ErbB network.
   Areas covered: The invention proposes the use of ErbB protein levels and ErbB receptor dimer formation as biomarkers for selecting, predicting and monitoring CRC patients showing sensitivity to the action of EGFR inhibitors to benefit from the combination therapy of EGFR and HER2 inhibitors. The in vitro data on Lim1215 cells suggest the over-activation of HER3 signaling pathway in response to the use of EGFR inhibitors on monotherapy; the use of HER2 or HER3 or MEK inhibitors in combination with EGFR inhibitors reversed this activation.
   Expert opinion: To assess the clinical applicability of this invention, further studies are needed since the conclusions are derived solely based on the data obtained from only one CRC cell line (Lim1215). Furthermore, other biofactors/mutations should be considered to assure the potential benefits of the combination therapies proposed.
C1 [Plano, Daniel; Alcolea, Veronica; Sanmartin, Carmen] Univ Navarra, Fac Pharm & Nutr, Dept Organ & Pharmaceut Chem, Campus Univ, Pamplona, Spain.
   [Plano, Daniel; Alcolea, Veronica; Sanmartin, Carmen] Inst Invest Sanitaria Navarra, IdiSNA, Pamplona, Spain.
   [Sharma, Arun K.] Penn State Canc Inst, Dept Pharmacol, Hershey, PA USA.
C3 University of Navarra; Pennsylvania Commonwealth System of Higher
   Education (PCSHE); Pennsylvania State University; Penn State Health
RP Sharma, AK (corresponding author), Penn State Coll Med, Penn State Canc Inst, Dept Pharmacol, CH72,500 Univ Dr, Hershey, PA 17033 USA.
EM aks14@psu.edu
RI Alcolea, Veronica/L-8709-2019; Sharma, Arun/IXN-0008-2023; Sanmartin,
   Carmen/K-1188-2014; Plano, Daniel/K-3001-2014
OI Sanmartin, Carmen/0000-0003-3431-7826; Plano,
   Daniel/0000-0002-8266-0445; Alcolea, Veronica/0000-0002-1892-9139;
   Sharma, Arun/0000-0002-7679-7779
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NR 55
TC 3
Z9 3
U1 0
U2 11
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1354-3776
EI 1744-7674
J9 EXPERT OPIN THER PAT
JI Expert Opin. Ther. Patents
PD MAY
PY 2017
VL 27
IS 5
DI 10.1080/13543776.2017.1315103
PG 11
WC Chemistry, Medicinal; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA ES4YY
UT WOS:000399544000001
PM 28366103
DA 2025-01-04
ER

PT J
AU Guo, ST
   Guo, XY
   Wang, J
   Wang, CY
   Yang, RH
   Wang, FH
   Li, XY
   Hondermarck, H
   Thorne, RF
   Wang, YF
   Jin, L
   Zhang, XD
   Jiang, CC
AF Guo, S. T.
   Guo, X. Y.
   Wang, J.
   Wang, C. Y.
   Yang, R. H.
   Wang, F. H.
   Li, X. Y.
   Hondermarck, H.
   Thorne, R. F.
   Wang, Y. F.
   Jin, L.
   Zhang, X. D.
   Jiang, C. C.
TI MicroRNA-645 is an oncogenic regulator in colon cancer
SO ONCOGENESIS
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; CHROMOSOMAL INSTABILITY; GENE-EXPRESSION;
   MOUSE; CELLS; HEREDITARY; ACTIVATION; APOPTOSIS; SOX30
AB Despite advances in early diagnosis and the development of molecularly targeted therapy, curative treatment of colon cancer once it has metastasized is yet to be accomplished. This is closely associated with deregulated CRC cell proliferation and resistance to apoptosis. Here we reveal that upregulation of microRNA-645 (miR-645) through DNA copy number gain is responsible for enhanced proliferation and resistance to apoptosis in colon cancer. MiR-645 was upregulated in most colon cancer tissues related to adjacent normal mucosa. This appeared to be associated with amplification of a section of chromosome 20q13.13, where miR-645 is located. Inhibition of miR-645 reduced proliferation and enhanced sensitivity to apoptosis triggered by the chemotherapeutic drugs 5-fluorouracil and cisplatin in CRC cells, and retarded colon cancer xenograft growth. Conversely, overexpression of miR-645 in normal colon epithelial cells enhanced proliferation and triggered anchorage-independent cell growth. Although SRY-related HMG-box 30 (SOX30) was identified as a miR-645 target, its expression was only partially affected by miR-645, suggesting that miR-645 is a fine-tuning mechanism of SOX30 expression. Moreover, overexpression of SOX30 only moderately inhibited promotion of CRC cell proliferation by miR-645, indicating that miR-645 may have more targets that contribute to its pro-proliferation effect in colon cancer. Together, this study reveals that miR-645 can regulate oncogenesis in colon cancer with SOX30 being one of its targets.
C1 [Guo, S. T.; Guo, X. Y.; Wang, J.; Wang, C. Y.; Yang, R. H.; Wang, F. H.; Li, X. Y.; Zhang, X. D.] Shanxi Canc Hosp & Inst, Dept Mol Biol, Taiyuan 030013, Shanxi, Peoples R China.
   [Guo, S. T.; Wang, C. Y.; Hondermarck, H.; Jin, L.; Zhang, X. D.] Univ Newcastle, Sch Biomed Sci & Pharm, LS3-49,Life Sci Bldg, Callaghan, NSW 2308, Australia.
   [Thorne, R. F.] Univ Newcastle, Sch Environm & Life Sci, Callaghan, NSW, Australia.
   [Wang, Y. F.] Sichuan Univ, Sch Preclin & Forens Med, Dept Pathophysiol, Chengdu, Sichuan, Peoples R China.
   [Jiang, C. C.] Univ Newcastle, Sch Med & Publ Hlth, LS3-49,Life Sci Bldg, Callaghan, NSW 2308, Australia.
C3 University of Newcastle; University of Newcastle; Sichuan University;
   University of Newcastle
RP Zhang, XD (corresponding author), Shanxi Canc Hosp & Inst, Dept Mol Biol, Taiyuan 030013, Shanxi, Peoples R China.; Zhang, XD (corresponding author), Univ Newcastle, Sch Biomed Sci & Pharm, LS3-49,Life Sci Bldg, Callaghan, NSW 2308, Australia.; Jiang, CC (corresponding author), Univ Newcastle, Sch Med & Publ Hlth, LS3-49,Life Sci Bldg, Callaghan, NSW 2308, Australia.
EM Xu.Zhang@newcastle.edu.au; Chenchen.Jiang@newcastle.edu.au
RI zhang, xuyang/GQH-3712-2022; Jin, Lei/K-2315-2019; Jiang,
   Chenchen/C-2902-2014
OI Jiang, Chen Chen/0000-0001-9133-6391; Hondermarck,
   Hubert/0000-0003-3807-2985; Jin, Lei/0000-0001-7187-9671; Zhang, Xu
   Dong/0000-0001-9457-8003
FU National Health and Medical Research Council (NHMRC) [APP1026458];
   Cancer Council NSW, Australia [RG13-04, RG 13-15]; Shanxi Scholarship
   Council [2013-133]; Shanxi Natural Science Foundation, China
   [201601D202101]; Cancer Institute NSW; NHMRC
FX This work was supported by the National Health and Medical Research
   Council (NHMRC) (APP1026458), the Cancer Council NSW (RG13-04 and RG
   13-15), Australia, and the Shanxi Scholarship Council (2013-133) and
   Shanxi Natural Science Foundation (201601D202101), China. CCJ and LJ are
   recipients of Cancer Institute NSW Fellowships. XDZ is supported by a
   Senior Research Fellowship of NHMRC.
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NR 42
TC 27
Z9 27
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 2157-9024
J9 ONCOGENESIS
JI Oncogenesis
PD MAY
PY 2017
VL 6
AR e335
DI 10.1038/oncsis.2017.37
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FB3MN
UT WOS:000406046800014
PM 28504690
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Ruff, SM
   Shannon, AH
   Pawlik, TM
AF Ruff, Samantha M.
   Shannon, Alexander H.
   Pawlik, Timothy M.
TI The Role of Targeted Therapy in the Multi-Disciplinary Approach to
   Colorectal Liver Metastasis
SO CANCERS
LA English
DT Review
DE colorectal cancer; metastases; targeted therapy; liver
ID GROWTH-FACTOR RECEPTOR; CONSENSUS MOLECULAR SUBTYPES; III
   RANDOMIZED-TRIAL; OPEN-LABEL; 1ST-LINE TREATMENT; COLON-CANCER;
   DOUBLE-BLIND; PHASE-III; PLUS BEVACIZUMAB; MICROSATELLITE INSTABILITY
AB Simple Summary Colorectal cancer (CRC) is the second most common cause of cancer-related mortality in the United States. Despite best efforts, 5-year survival for unresectable metastatic CRC is only about 20%. CRC is a heterogeneous disease and the underlying genetic differences inform behavior, treatment strategy, and prognosis. Given the limitations of cytotoxic chemotherapy and the growing role of molecular profiling, research has focused on identifying and developing targeted therapies. We herein review how genetic profiling informs prognosis, crucial cell-signaling pathways that play a role in CRC carcinogenesis, and currently approved targeted therapies for metastatic CRC. Colorectal cancer (CRC) is the second most common cause of cancer-related mortality in the United States. Among newly diagnosed patients with CRC, 20% will present with metastatic disease and another 25% will develop metastases. The surgical resection of the primary tumor and metastatic disease sites confers the best chance at long-term survival. Unfortunately, many patients will recur after resection or present with unresectable disease. As such, metastatic CRC is commonly treated with a combination of surgery, systemic therapy, and/or liver-directed therapies. Despite best efforts, 5-year survival for unresectable metastatic CRC is only about 20%. CRC is a heterogeneous disease and the underlying genetic differences inform behavior, treatment strategy, and prognosis. Given the limitations of cytotoxic chemotherapy and the growing role of molecular profiling, research has focused on identifying and developing targeted therapies. We herein review how genetic profiling informs prognosis, crucial cell-signaling pathways that play a role in CRC carcinogenesis, and currently approved targeted therapies for metastatic CRC.
C1 [Pawlik, Timothy M.] Ohio State Univ, Wexner Med Ctr, Dept Surg, Div Surg Oncol, Columbus, OH 43210 USA.
   James Comprehens Canc Ctr, Columbus, OH 43210 USA.
C3 University System of Ohio; Ohio State University; James Cancer Hospital
   & Solove Research Institute; University System of Ohio; Ohio State
   University
RP Pawlik, TM (corresponding author), Ohio State Univ, Wexner Med Ctr, Dept Surg, Div Surg Oncol, Columbus, OH 43210 USA.
EM samantha.ruff@osumc.edu; alexander.shannon@osumc.edu;
   tim.pawlik@osumc.edu
RI Pawlik, Timothy/AAO-9335-2020
OI Pawlik, Timothy/0000-0002-7994-9870
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NR 126
TC 1
Z9 1
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 JUL
PY 2023
VL 15
IS 13
AR 3513
DI 10.3390/cancers15133513
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA M2FL2
UT WOS:001028390100001
PM 37444625
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Deac, AL
   Pop, RM
   Crisan, CF
   Burz, CC
   Buzoianu, AD
AF Deac, Andrada Larisa
   Pop, Raluca Maria
   Crisan, Cristina Florina
   Burz, Claudia Cristina
   Buzoianu, Anca Dana
TI Recurrent cardiotoxicity in a fluoropyrimidine treated cancer patient -
   case report and practical recommendations
SO ARCHIVE OF CLINICAL CASES
LA English
DT Article
DE DPYD; colon cancer; fluoropyrimidines; cardiotoxicity; mutation testing
ID DIHYDROPYRIMIDINE DEHYDROGENASE; TOXICITY; 5-FLUOROURACIL; CHEMOTHERAPY;
   CAPECITABINE
AB Fluoropyrimidines remain some of the most used chemotherapeutics, despite the appearance in the therapeutic arsenal of targeted therapy and immunotherapy. Fluropyrimidines related cardiotoxicity is an undesirable adverse event and affects almost 20% of patients. The mechanisms of fluoropyrimidine toxicity are closely related to deficient allelic variants of DPYD, but considering the low penetrance and interindividual variability, not all adverse reactions are explained by their presence. In this case, we report a patient with recurrent fluoropyrimidine toxicity without a deficient allelic variant and how this case was managed by the oncologist and cardiologist, considering the need to use fluoropyrimidine in the treatment.
C1 [Deac, Andrada Larisa] Cluj Cty Emergency Clin Hosp, Dept Med Oncol, Cluj Napoca, Romania.
   [Deac, Andrada Larisa; Pop, Raluca Maria; Buzoianu, Anca Dana] Iuliu Hatieganu Univ Med & Pharm, Dept Pharmacol Toxicol & Clin Pharmacol, Fac Med, Cluj Napoca, Romania.
   [Crisan, Cristina Florina] Cardiomed Med Ctr, Cluj Napoca, Romania.
   [Burz, Claudia Cristina] Iuliu Hatieganu Univ Med & Pharm, Dept Immunol & Allergol, Fac Med, Cluj Napoca, Romania.
C3 Iuliu Hatieganu University of Medicine & Pharmacy; Iuliu Hatieganu
   University of Medicine & Pharmacy
RP Deac, AL (corresponding author), Iuliu Hatieganu Univ Med & Pharm, Dept Pharmacol Toxicol & Clin Pharmacol, Fac Med, Cluj Napoca, Romania.; Deac, AL (corresponding author), Iuliu Hatieganu Univ Med & Pharm, Fac Med, Dept Pharmacol Toxicol & Clin Pharmacol, Str Marinescu,Nr 23 & 2, Cluj Napoca, Romania.
EM andrada.deac@gmail.com
RI Pop, Raluca/I-4639-2019; Deac, Andrada/AAY-8998-2021; Burz,
   Claudia/C-4840-2012; Buzoianu, Anca Dana/M-1050-2017
OI Buzoianu, Anca Dana/0000-0002-3511-2788
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NR 17
TC 0
Z9 0
U1 0
U2 0
PU GRIGORE T POPA UNIV MEDICINE AND PHARMACY IASI
PI Iasi
PA 16 Universitatii Street, Iasi, ROMANIA
EI 2360-6975
J9 ARCH CLIN CASES
JI Arch. Clin. Cases
PY 2023
VL 10
IS 2
BP 55
EP 60
DI 10.22551/2023.39.1002.10241
PG 6
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA T5MB6
UT WOS:001078415900001
PM 37215066
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Ciobanu, AE
   Pîrvu, DC
   Marginean, CM
   Dijmarescu, AL
   Muñoz-Groza, AE
   Mesina, C
   Balseanu, TA
   Baleanu, VD
   Tenea-Cojan, TS
   Ciobanu, D
AF Ciobanu, Alina Elena
   Pirvu, Daniel-Cristian
   Marginean, Cristina Maria
   Dijmarescu, Anda Lorena
   Munoz-Groza, Adriana-Estefa
   Mesina, Cristian
   Balseanu, Tudor-Adrian
   Baleanu, Vlad Dumitru
   Tenea-Cojan, Tiberiu Stefanita
   Ciobanu, Daniela
TI Molecular prognostic factors in colorectal cancer: 5-year follow-up
SO ROMANIAN JOURNAL OF MORPHOLOGY AND EMBRYOLOGY
LA English
DT Article
DE colorectal cancer; survival; Ki67; VEGF; HER2/neu; p53
ID ENDOTHELIAL GROWTH-FACTOR; RECTAL-CANCER; FACTOR EXPRESSION;
   PREDICTIVE-VALUE; COLON-CANCER; P53; STAGE; CELL; PROLIFERATION;
   SURVIVAL
AB Colorectal cancer (CRC) is a frequently diagnosed and lethal disease. The risk of developing CRC is determined by environmental and genetic factors. Surgical treatment is the main curative modality for patients with CRC up to stage III. In recent years, a special place has been given to biological agents used as targeted therapy following the genetic analysis of the tumor: Bevacizumab (Avastin), Cetuximab (Erbitux), Ziv-aflibercept (Zaltrap). We present a study based on 46 colorectal tumor resection specimens from patients operated for CRC in the Surgery Departments of the Emergency County Clinical Hospital of Craiova, Romania. Histopathological examination and immunohistochemistry staining of tissue sections were performed to determine the degree of aggressiveness. Using the Kaplan-Meier test, we calculated the correlation coefficient between survival time and immunohistochemical prognostic factors. The patients were followed for 60 months postoperatively.
C1 [Ciobanu, Alina Elena] Univ Med & Pharm Craiova, Doctoral Sch, Craiova, Romania.
   [Pirvu, Daniel-Cristian; Marginean, Cristina Maria; Ciobanu, Daniela] Univ Med & Pharm Craiova, Dept Internal Med, Craiova, Romania.
   [Dijmarescu, Anda Lorena] Univ Med & Pharm Craiova, Dept Obstet & Gynecol, Craiova, Romania.
   [Munoz-Groza, Adriana-Estefa] Filantropia Clin Hosp, Dept Oncol, Craiova, Romania.
   [Mesina, Cristian] Univ Med & Pharm Craiova, Dept Surg, Craiova, Romania.
   [Balseanu, Tudor-Adrian] Univ Med & Pharm Craiova, Res Ctr Clin & Expt Med, Craiova, Romania.
   [Baleanu, Vlad Dumitru] Emergency Univ Hosp, Dept Surg, Bucharest, Romania.
   [Tenea-Cojan, Tiberiu Stefanita] Railway Hosp, Dept Surg, Craiova, Romania.
   [Pirvu, Daniel-Cristian; Marginean, Cristina Maria] Univ Med & Pharm Craiova, Dept Internal Med, 2 Petru Rares St, Craiova 200349, Dolj County, Romania.
C3 University of Medicine & Pharmacy of Craiova; University of Medicine &
   Pharmacy of Craiova; University of Medicine & Pharmacy of Craiova;
   University of Medicine & Pharmacy of Craiova; University of Medicine &
   Pharmacy of Craiova; University of Medicine & Pharmacy of Craiova
RP Pîrvu, DC; Marginean, CM (corresponding author), Univ Med & Pharm Craiova, Dept Internal Med, 2 Petru Rares St, Craiova 200349, Dolj County, Romania.
EM marginean22@yahoo.com
RI Pirvu, Daniel-Cristian/ADQ-4702-2022; Mărginean, Cristina/GRX-4182-2022;
   dijmarescu, lorena/KIB-5337-2024; Balseanu, Tudor-Adrian/O-2289-2018
OI Balseanu, Tudor-Adrian/0000-0002-0047-3436
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NR 36
TC 6
Z9 6
U1 3
U2 4
PU EDITURA ACAD ROMANE
PI BUCURESTI
PA CALEA 13 SEPTEMBRIE NR 13, SECTOR 5, BUCURESTI 050711, ROMANIA
SN 1220-0522
EI 2066-8279
J9 ROM J MORPHOL EMBRYO
JI Rom. J. Morphol. Embryol.
PY 2023
VL 64
IS 1
BP 65
EP 71
DI 10.47162/RJME.64.1.08
PG 7
WC Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Developmental Biology
GA K2UE4
UT WOS:001015033500008
PM 37128793
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Zhang, R
   Su, C
   Jia, YL
   Xing, ML
   Jin, SL
   Zong, H
AF Zhang, Rui
   Su, Chang
   Jia, Yongliang
   Xing, Menglu
   Jin, Shuiling
   Zong, Hong
TI Molecular mechanisms of HER2-targeted therapy and strategies to overcome
   the drug resistance in colorectal cancer
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Precision medicine; Colorectal cancer; HER2; Drug resistance;
   Antibody-drug conjugates
ID TRASTUZUMAB DERUXTECAN DS-8201; PHASE-II TRIAL; 1ST-LINE TREATMENT;
   OPEN-LABEL; BISPECIFIC ANTIBODY; ANTITUMOR-ACTIVITY; BREAST; CONJUGATE;
   MULTICENTER; TUMORS
AB HER2 amplification is one of the mechanisms that induce drug resistance to anti-EGFR therapy in colorectal cancer. In recent years, data from several randomized clinical trials show that anti-HER2 therapies improved the prognosis of patients with HER2-positive colorectal cancer. These results indicate that HER2 is a promising therapeutic target in advanced colorectal cancer. Despite the anti-HER2 therapies including monoclonal antibodies, tyrosine kinase inhibitors, and antibody-drug conjugates improving the outcomes, less than 30 % of the patients achieve objective response and eventually have drug resistance. It is necessary to explore the primary and secondary mechanisms for the resistance to anti-HER2 therapies, which will pave the way to overcome the drug resistance. Several studies have reported the potential mechanisms for the resistance to anti-HER2 therapies. In this review, we present a comprehensive overview of the recent advances in clinical research, mechanisms of treatment resistance, and strategies for reversing resistance in HER2-positive colorectal cancer patients.
C1 [Zhang, Rui; Su, Chang; Xing, Menglu; Jin, Shuiling; Zong, Hong] Zhengzhou Univ, Dept Oncol, Affiliated Hosp 1, Zhengzhou 450052, Peoples R China.
   [Jia, Yongliang] Zhengzhou Univ, BGI Coll, Zhengzhou 450052, Peoples R China.
   [Jia, Yongliang] Zhengzhou Univ, Henan Inst Med & Pharmaceut Sci, Zhengzhou 450052, Peoples R China.
C3 Zhengzhou University; Zhengzhou University; Zhengzhou University
RP Jin, SL; Zong, H (corresponding author), Zhengzhou Univ, Dept Oncol, Affiliated Hosp 1, Zhengzhou 450052, Peoples R China.
EM ruizhang8801@163.com; changsu123456@outlook.com; jiayl@zzu.edu.cn;
   mengluxing2021@163.com; fccjinsl@zzu.edu.cn; fcczongh@zzu.edu.cn
FU Henan Provincial Health Commission [SBGJ202102136]; Key Project of
   Medical Science and Technology Research Program of Henan Province
   [SBGJ202102137]; Young and Middle-aged Health Science and Technology
   Innovation Talent Program of Henan Province [YXKC2021057]; Henan
   Institute of Medical and Pharmacological Sciences [2021BP0113];
   Zhengzhou University [32212456]; Henan Science and Technology Department
   [222102310721]
FX This work was supported by the Henan Provincial Health Commission (HZ,
   grant number SBGJ202102136); the Key Project of Medical Science and
   Technology Research Program of Henan Province (SLJ, grant number
   SBGJ202102137); the Young and Middle-aged Health Science and Technology
   Innovation Talent Program of Henan Province (SLJ, grant number
   YXKC2021057); the Henan Institute of Medical and Pharmacological
   Sciences (YLJ, grant number 2021BP0113); the Zhengzhou University (YLJ,
   grant number 32212456) , and the Henan Science and Technology Department
   (YLJ, grant number 222102310721).
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NR 122
TC 0
Z9 0
U1 6
U2 6
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD OCT
PY 2024
VL 179
AR 117363
DI 10.1016/j.biopha.2024.117363
EA SEP 2024
PG 12
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA F2K2K
UT WOS:001308154200001
PM 39236476
OA gold
DA 2025-01-04
ER

PT J
AU Tyrsina, EG
   Nikulitskiy, SI
   Inshakov, AN
   Ryabaya, OO
AF Tyrsina, E. G.
   Nikulitskiy, S. I.
   Inshakov, A. N.
   Ryabaya, O. O.
TI VEGF-R1 as a Potential Molecular Target for Anticancer Therapy
SO DOKLADY BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR-1; COLORECTAL-CANCER CELLS
AB The possibility of using VEGF-R1 receptor for targeted therapy in oncology was investigated. Using the approach to measuring the protein content in intact nuclei of cells, which was developed by us, we showed the presence of this receptor in the nuclei of tumor, but not normal cells. A direct correlation between the level of VEGF-R1 expression in the nucleus and the degree of malignancy of tumor cells, indicating the prognostic value of this parameter, was found. The mechanisms of the functioning of this receptor and the pathways of inhibiting its activity are discussed, and the validity of the selection of VEGF-R1 as a molecular target for anticancer therapy is conformed.
C1 [Tyrsina, E. G.; Nikulitskiy, S. I.; Inshakov, A. N.; Ryabaya, O. O.] Minist Hlth Russian Federat, Blokhin Russian Canc Res Ctr, Moscow 115478, Russia.
C3 Ministry of Health of the Russian Federation; N.N. Blokhin Russian
   Cancer Research Center
RP Tyrsina, EG (corresponding author), Minist Hlth Russian Federat, Blokhin Russian Canc Res Ctr, Moscow 115478, Russia.
EM tyrsina@yandex.ru
RI Ryabaya, Oxana/G-1529-2017; Inshakov, Andrey/D-5017-2019
OI Inshakov, Andrey/0000-0003-1280-4105
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NR 11
TC 2
Z9 2
U1 0
U2 3
PU MAIK NAUKA/INTERPERIODICA/SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA
SN 1607-6729
EI 1608-3091
J9 DOKL BIOCHEM BIOPHYS
JI Dokl. Biochem. Biophys.
PD JAN
PY 2018
VL 478
IS 1
BP 18
EP 20
DI 10.1134/S1607672918010052
PG 3
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA FZ3GW
UT WOS:000427476100005
PM 29536302
DA 2025-01-04
ER

PT J
AU Tang, DL
   Kroemer, G
   Kang, R
AF Tang, Daolin
   Kroemer, Guido
   Kang, Rui
TI Oncogenic KRAS blockade therapy: renewed enthusiasm and persistent
   challenges
SO MOLECULAR CANCER
LA English
DT Review
DE Gene mutation; Covalent inhibitor; Drug resistance; KRAS; Targeted
   therapy
ID CELL LUNG-CANCER; SYNTHETIC LETHAL INTERACTION; K-RAS ONCOGENE;
   INHIBITOR TRAMETINIB GSK1120212; PROTEIN TRANSFERASE INHIBITOR;
   METASTATIC PANCREATIC-CANCER; PHASE-III TRIAL; ACQUIRED-RESISTANCE;
   COLORECTAL-CANCER; ERK1/2 INHIBITOR
AB Across a broad range of human cancers, gain-of-function mutations in RAS genes (HRAS, NRAS, and KRAS) lead to constitutive activity of oncoproteins responsible for tumorigenesis and cancer progression. The targeting of RAS with drugs is challenging because RAS lacks classic and tractable drug binding sites. Over the past 30 years, this perception has led to the pursuit of indirect routes for targeting RAS expression, processing, upstream regulators, or downstream effectors. After the discovery that the KRAS-G12C variant contains a druggable pocket below the switch-II loop region, it has become possible to design irreversible covalent inhibitors for the variant with improved potency, selectivity and bioavailability. Two such inhibitors, sotorasib (AMG 510) and adagrasib (MRTX849), were recently evaluated in phase I-III trials for the treatment of non-small cell lung cancer with KRAS-G12C mutations, heralding a new era of precision oncology. In this review, we outline the mutations and functions of KRAS in human tumors and then analyze indirect and direct approaches to shut down the oncogenic KRAS network. Specifically, we discuss the mechanistic principles, clinical features, and strategies for overcoming primary or secondary resistance to KRAS-G12C blockade.
C1 [Tang, Daolin] Guangzhou Med Univ, Affiliated Hosp 3, Guangzhou, Peoples R China.
   [Tang, Daolin; Kang, Rui] UT Southwestern Med Ctr, Dept Surg, Dallas, TX USA.
   [Kroemer, Guido] Sorbonne Univ, Univ Paris, Equipe Labellisee Ligue Canc, INSERM,Ctr Rech Cordeliers,Inst Univ France,U1138, Paris, France.
   [Kroemer, Guido] Gustave Roussy Canc Campus, Metabol & Cell Biol Platforms, Villejuif, France.
   [Kroemer, Guido] Hop Europeen Georges Pompidou, AP HP, Pole Biol, Paris, France.
C3 Guangzhou Medical University; University of Texas System; University of
   Texas Southwestern Medical Center Dallas; Universite Paris Cite;
   Institut Universitaire de France; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Sorbonne Universite; UNICANCER; Gustave
   Roussy; Assistance Publique Hopitaux Paris (APHP); Universite Paris
   Cite; Hopital Universitaire Europeen Georges-Pompidou - APHP
RP Tang, DL; Kang, R (corresponding author), UT Southwestern Med Ctr, Dept Surg, Dallas, TX USA.; Kroemer, G (corresponding author), Sorbonne Univ, Univ Paris, Equipe Labellisee Ligue Canc, INSERM,Ctr Rech Cordeliers,Inst Univ France,U1138, Paris, France.
EM daolin.tang@utsouthwestern.edu; kroemer@orange.fr;
   rui.kang@utsouthwestern.edu
RI KROEMER, Guido/B-4263-2013; Kang, Rui/ABD-5291-2021; Tang,
   Daolin/ABD-5062-2021
OI Tang, Daolin/0000-0002-1903-6180
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NR 209
TC 49
Z9 49
U1 3
U2 21
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD OCT 4
PY 2021
VL 20
IS 1
AR 128
DI 10.1186/s12943-021-01422-7
PG 24
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA WB4GN
UT WOS:000703532300001
PM 34607583
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Zheng, QM
   Chen, XY
   Bao, QF
   Yu, J
   Chen, LH
AF Zheng, Qiao-Mei
   Chen, Xiao-Yun
   Bao, Qiu-Fang
   Yu, Jin
   Chen, Li-Hong
TI ILK enhances migration and invasion abilities of human endometrial
   stromal cells by facilitating the epithelial-mesenchymal transition
SO GYNECOLOGICAL ENDOCRINOLOGY
LA English
DT Article
DE Endometriosis; ILK; EMT; migration; invasion
ID INTEGRIN-LINKED KINASE; COLORECTAL-CANCER CELLS; OVEREXPRESSION;
   METASTASIS; PROLIFERATION; PATHOGENESIS; CYTOSKELETON; SUPPRESSES;
   EXPRESSION; CADHERIN
AB Epithelial-mesenchymal transition (EMT) plays a significant part in the pathogenesis of endometriosis by facilitating the migration and invasion abilities of cells. Integrin-linked kinase (ILK) increases the cell migration and invasion abilities by inducing the EMT. Eutopic and control endometrial stromal cells (EuSCs and CSCs) were isolated and cultured. Cell migration and invasion abilities were detected by transwell assays. Levels of proteins were detected by Western blot. EuSCs showed higher levels of ILK, N-cadherin, vimentin and stronger migration and invasion abilities. After transfection of siRNA-ILK, E-cadherin and keratin levels were increased while N-cadherin and vimentin levels were decreased in EuSCs. Besides that, the migration and invasion abilities of EuSCs were significantly decreased after transfection of siRNA-ILK. On the contrary, levels of ILK, N-cadherin and vimentin were increased while levels of E-cadherin and keratin were decreased simultaneously after transfecting CSCs with pEGFP-C1-ILK. Simultaneously, the migration and invasion abilities of CSCs were increased after transfection of pEGFP-C1-ILK. Our study verified that high expression of ILK enhanced the migration and invasion abilities of ESCs by facilitating the EMT. Given that ILK played crucial roles in the pathogenesis of endometriosis, it may be considered as a promising targeted therapy for endometriosis.
C1 [Zheng, Qiao-Mei; Chen, Xiao-Yun; Bao, Qiu-Fang; Yu, Jin; Chen, Li-Hong] Fujian Med Univ, Affiliated Hosp 1, Dept Obstet & Gynecol, 20 Chazhong Rd, Fuzhou 350001, Fujian, Peoples R China.
C3 Fujian Medical University
RP Chen, LH (corresponding author), Fujian Med Univ, Affiliated Hosp 1, Dept Obstet & Gynecol, 20 Chazhong Rd, Fuzhou 350001, Fujian, Peoples R China.
EM chenlihong_0102@126.com
RI Zheng, Qiaomei/HPI-2128-2023
FU Sailing fund of Fujian Medical University [2017XQ1056]; Natural Science
   Foundation of Fujian Province [2018J05126]
FX This work was supported by the Sailing fund of Fujian Medical University
   (grant no. 2017XQ1056) and Natural Science Foundation of Fujian Province
   (grant no. 2018J05126).
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NR 35
TC 20
Z9 22
U1 0
U2 5
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0951-3590
EI 1473-0766
J9 GYNECOL ENDOCRINOL
JI Gynecol. Endocrinol.
PD DEC 2
PY 2018
VL 34
IS 12
BP 1091
EP 1096
DI 10.1080/09513590.2018.1498477
PG 6
WC Endocrinology & Metabolism; Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Obstetrics & Gynecology
GA HE1JC
UT WOS:000453025700019
PM 30182767
DA 2025-01-04
ER

PT J
AU Shabani, M
   Hojjat-Farsangi, M
AF Shabani, Mahdi
   Hojjat-Farsangi, Mohammad
TI Targeting Receptor Tyrosine Kinases Using Monoclonal Antibodies: The
   Most Specific Tools for Targeted-Based Cancer Therapy
SO CURRENT DRUG TARGETS
LA English
DT Review
DE Cancer; monoclonal antibody; receptor tyrosine kinase; targeted therapy
ID FACTOR-I RECEPTOR; METASTATIC COLORECTAL-CANCER; CHRONIC
   LYMPHOCYTIC-LEUKEMIA; DISCOIDIN DOMAIN RECEPTOR-1; SMALL-MOLECULE
   INHIBITORS; RENAL-CELL CARCINOMA; GROWTH-FACTOR; EPH RECEPTORS;
   BREAST-CANCER; C-MET
AB Receptor tyrosine kinases (RTKs) family is comprised of different cell surface glycoproteins. These enzymes participate in and regulate vital processes such as cell proliferation, polarity, differentiation, cell to cell interactions, signaling, and cell survival. Dysregulation of RTKs contributes to the development of different types of tumors. RTKs deregulation in different types of cancer has been reported for more than 30 RTKs. Due to their critical roles, the specific targeting of RTKs in malignancies is a promising approach. Targeted cellular and molecular therapies (personalized medicine) have been known as new types of therapeutics, which prevent tumor cell proliferation and invasion by interfering with molecules essential for tumor growth and survival. Specific targeting of RTKs using monoclonal antibodies (mAbs) in malignancies as well as in autoimmune disorders is of great interest. The growing number of mAbs approved by the authorities implies on the increasing attentions and applications of these therapeutic tools. Due to the high specificity, mAbs are the most promising substances that target RTKs expressed on the tumor cell surface. In this communication, we review the recent progresses in the development of mAbs targeting oncogenic RTKs for cancer treatment.
C1 [Shabani, Mahdi] Avicenna Res Inst ACECR, Monoclonal Antibody Res Ctr, Tehran, Iran.
   [Hojjat-Farsangi, Mohammad] Karolinska Univ Hosp Solna, CCK, Dept Oncol Pathol, Immune & Gene Therapy Lab, Stockholm, Sweden.
   [Hojjat-Farsangi, Mohammad] Karolinska Inst, Stockholm, Sweden.
   [Hojjat-Farsangi, Mohammad] Bushehr Univ Med Sci, Sch Med, Dept Immunol, Bushehr, Iran.
C3 Karolinska Institutet; Karolinska University Hospital; Karolinska
   Institutet
RP Hojjat-Farsangi, M (corresponding author), Karolinska Univ Hosp, CCK, Dept Oncol Pathol, SE-17176 Stockholm, Sweden.
EM mohammad.hojat-farsangi@Ki.se
RI ; Hojat Farsangi, Mohammad/E-8171-2018
OI , Mahdi/0000-0002-7084-5709; Hojat Farsangi,
   Mohammad/0000-0002-0589-5523
FU Felix Mindus foundation; CLL Global Research Foundation, Stockholm,
   Sweden; Monoclonal Antibody Research Center, Avicenna Research
   Institute, ACECR, Tehran, Iran
FX This study was supported by grants from Felix Mindus foundation, the CLL
   Global Research Foundation, Stockholm, Sweden, and Monoclonal Antibody
   Research Center, Avicenna Research Institute, ACECR, Tehran, Iran.
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NR 220
TC 10
Z9 10
U1 2
U2 16
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 2016
VL 17
IS 14
BP 1687
EP 1703
DI 10.2174/1389450116666151001104133
PG 17
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EB1DE
UT WOS:000387086200010
PM 26424402
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Zeng, Z
   Fu, MY
   Hu, Y
   Wei, YQ
   Wei, XW
   Luo, M
AF Zeng, Zhen
   Fu, Minyang
   Hu, Yuan
   Wei, Yuquan
   Wei, Xiawei
   Luo, Min
TI Regulation and signaling pathways in cancer stem cells: implications for
   targeted therapy for cancer
SO MOLECULAR CANCER
LA English
DT Review
DE CSCs; Regulatory networks; Cancer therapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; TUMOR-INITIATING CELLS; RNA-BINDING
   PROTEINS; HUMAN HEPATOCELLULAR-CARCINOMA; GAMMA-SECRETASE INHIBITOR;
   LONG NONCODING RNA; SELF-RENEWAL; C-MYC; COLORECTAL-CANCER;
   WNT/BETA-CATENIN
AB Cancer stem cells (CSCs), initially identified in leukemia in 1994, constitute a distinct subset of tumor cells characterized by surface markers such as CD133, CD44, and ALDH. Their behavior is regulated through a complex interplay of networks, including transcriptional, post-transcriptional, epigenetic, tumor microenvironment (TME), and epithelial-mesenchymal transition (EMT) factors. Numerous signaling pathways were found to be involved in the regulatory network of CSCs. The maintenance of CSC characteristics plays a pivotal role in driving CSC-associated tumor metastasis and conferring resistance to therapy. Consequently, CSCs have emerged as promising targets in cancer treatment. To date, researchers have developed several anticancer agents tailored to specifically target CSCs, with some of these treatment strategies currently undergoing preclinical or clinical trials. In this review, we outline the origin and biological characteristics of CSCs, explore the regulatory networks governing CSCs, discuss the signaling pathways implicated in these networks, and investigate the influential factors contributing to therapy resistance in CSCs. Finally, we offer insights into preclinical and clinical agents designed to eliminate CSCs.
C1 [Zeng, Zhen; Fu, Minyang; Wei, Yuquan; Wei, Xiawei; Luo, Min] Sichuan Univ, Natl Clin Res Ctr Geriatr, Lab Aging Res & Canc Drug Target, State Key Lab Biotherapy,West China Hosp,Canc Ctr, 17,Block 3,Southern Renmin Rd, Chengdu 610041, Sichuan, Peoples R China.
   [Hu, Yuan] Sichuan Univ, West China Hosp 2, Dept Pediat Nephrol Nursing, Minist Educ,Key Lab Birth Defects & Related Dis Wo, 17,Block 3,Southern Renmin Rd, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University
RP Luo, M (corresponding author), Sichuan Univ, Natl Clin Res Ctr Geriatr, Lab Aging Res & Canc Drug Target, State Key Lab Biotherapy,West China Hosp,Canc Ctr, 17,Block 3,Southern Renmin Rd, Chengdu 610041, Sichuan, Peoples R China.
EM minluo_scu@163.com
RI Wei, Weiqi/LKK-3400-2024; LUO, MIN/AAZ-6741-2021
OI Hu, Yuan/0000-0002-8951-5881
FU Not applicable.
FX Not applicable.
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NR 387
TC 26
Z9 29
U1 8
U2 20
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD OCT 18
PY 2023
VL 22
IS 1
AR 172
DI 10.1186/s12943-023-01877-w
PG 31
WC Biochemistry & Molecular Biology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology
GA U8QK3
UT WOS:001087390700002
PM 37853437
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Joseph, L
AF Joseph, Loren
TI The clinical utility of molecular genetic cancer profiling
SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS
LA English
DT Review
DE Gene profiling; cancer; NGS; clinical utility; molecular diagnostics;
   clinical trials; liquid biopsy
ID METASTATIC COLORECTAL-CANCER; CELL LUNG-CANCER; ALLELE-SPECIFIC
   IMBALANCE; PROOF-OF-CONCEPT; TARGETED THERAPY; MEK INHIBITION;
   CONVENTIONAL THERAPY; STRUCTURAL-VARIATION; PANCREATIC-CANCER; AMERICAN
   SOCIETY
AB Introduction: Next-Generation-Sequencing (NGS) has enabled gene mutation profiling - cataloguing sequence variants and modifications in clinical assays encompassing tens to thousands of genes in tumors and in germlines. The clinical benefit of applying multi-gene NGS to diverse applications in various malignancies remains to be demonstrated.Areas covered: Applications of gene mutation profiling in oncology include screening cancer-prone families, classification of malignancies, treatment selection, and monitoring the response to treatment of solid tumors (the liquid biopsy'). Google Scholar was used to search PubMed for the period 2011-2016 using combinations of the following search terms: clinical utility', NGS, molecular diagnostics'.Expert commentary: Clinical studies are in progress pairing mutation profiling with streamlined new trial designs to speed identification of promising drug-target combinations and to see if genotype-informed treatment selection will improve outcome across a spectrum of histologies. The analytical advantages and falling cost of NGS make focused gene panels likely to become the dominant modality in molecular diagnostic testing even if trials eventually discourage use of large panels to test all malignancies.
C1 [Joseph, Loren] Harvard Med Sch, Dept Pathol, Beth Israel Deaconess Med Ctr, Mol Diagnost Lab, Room RW763,330 Brookline Ave, Boston, MA 02215 USA.
C3 Harvard University; Beth Israel Deaconess Medical Center; Harvard
   Medical School
RP Joseph, L (corresponding author), Harvard Med Sch, Dept Pathol, Beth Israel Deaconess Med Ctr, Mol Diagnost Lab, Room RW763,330 Brookline Ave, Boston, MA 02215 USA.
EM ljjoseph@bidmc.harvard.edu
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NR 95
TC 6
Z9 6
U1 0
U2 5
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 AUG
PY 2016
VL 16
IS 8
BP 827
EP 838
DI 10.1080/14737159.2016.1197120
PG 12
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA DT2HC
UT WOS:000381300400003
PM 27253039
DA 2025-01-04
ER

PT J
AU Oh, DY
   Bang, YJ
AF Oh, Do-Youn
   Bang, Yung-Jue
TI Pertuzumab in gastrointestinal cancer
SO EXPERT OPINION ON BIOLOGICAL THERAPY
LA English
DT Article
DE HER2; HER3; pertuzumab; gastrointestinal cancer; targeted therapy
ID GROWTH-FACTOR RECEPTOR; METASTATIC BREAST-CANCER; GENE AMPLIFICATION;
   GASTRIC-CANCER; PHASE-II; DIMERIZATION INHIBITOR; PANCREATIC-CANCER;
   PROGNOSTIC INDICATOR; COLORECTAL-CANCER; EXPOSURE-RESPONSE
AB Introduction: Human epidermal growth factor receptor 2 (HER2) and HER3 are altered in multiple tumor types, including gastrointestinal cancer. The HER2/HER3 dimer is crucial for HER2-mediated signaling in HER2-positive tumors. HER2-targeting agents, including trastuzumab, lapatinib, trastuzumab emtansine, and pertuzumab, have been approved for the treatment of HER2-positive breast cancer, with trastuzumab also approved for the treatment of HER2-positive gastric cancer. Pertuzumab, a recombinant humanized immunoglobulin (Ig) G1 monoclonal antibody targeting HER-2, binds to the dimerization domain (extracellular domain II) of HER2, which leads to blocking of ligand-induced HER2 heterodimerization. It is under investigation in gastrointestinal cancers, including HER2-positive gastric cancer.Area covered: In this review, the authors summarize the biology of HER2/HER3 and its alterations in gastrointestinal cancers. The authors focus specifically on the current status of development of pertuzumab in gastrointestinal cancers.Expert opinion: The HER2/HER3 alteration in gastrointestinal cancers is quite interesting. In HER2-positive gastric cancer, the dual blockade of HER2 and HER3 using trastuzumab and pertuzumab is being tested in an international phase III trial, the JACOB study. This strategy may benefit HER2-positive gastric cancer patients more as in the case of HER2-positive breast cancer. In other gastrointestinal cancers, including biliary tract cancer, esophageal cancer, pancreatic cancer, and colorectal cancer, there is huge room for the development of pertuzumab.
C1 [Oh, Do-Youn; Bang, Yung-Jue] Seoul Natl Univ Hosp, Dept Internal Med, 101 Daehak Ro, Seoul 110744, South Korea.
   [Oh, Do-Youn; Bang, Yung-Jue] Seoul Natl Univ, Coll Med, Canc Res Inst, Seoul, South Korea.
C3 Seoul National University (SNU); Seoul National University Hospital;
   Seoul National University (SNU)
RP Bang, YJ (corresponding author), Seoul Natl Univ Hosp, Dept Internal Med, 101 Daehak Ro, Seoul 110744, South Korea.
EM bangyj@snu.ac.kr
RI Bang, Yung Jue/J-2759-2012
FU Roche
FX Yung-Jue Bang had consultancies with Roche, and YJ Bang and DY Oh
   received research funding from Roche through the institution. 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. This includes employment, consultancies, honoraria, stock
   ownership or options, expert testimony, grants or patents received or
   pending, or royalties.
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NR 84
TC 11
Z9 14
U1 1
U2 12
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.
PD FEB 1
PY 2016
VL 16
IS 2
BP 243
EP 253
DI 10.1517/14712598.2016.1126578
PG 11
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA DD8DF
UT WOS:000370154300003
PM 26619359
DA 2025-01-04
ER

PT J
AU Price, TJ
   Tang, M
   Gibbs, P
   Haller, DG
   Peeters, M
   Arnold, D
   Segelov, E
   Roy, A
   Tebbutt, N
   Pavlakis, N
   Karapetis, C
   Burge, M
   Shapiro, J
AF Price, Timothy J.
   Tang, Monica
   Gibbs, Peter
   Haller, Daniel G.
   Peeters, Marc
   Arnold, Dirk
   Segelov, Eva
   Roy, Amitesh
   Tebbutt, Niall
   Pavlakis, Nick
   Karapetis, Chris
   Burge, Matthew
   Shapiro, Jeremy
TI Targeted therapy for metastatic colorectal cancer
SO EXPERT REVIEW OF ANTICANCER THERAPY
LA English
DT Review
DE Colorectal; sidedness; review; targeted; metastatic
ID KRAS WILD-TYPE; CETUXIMAB PLUS IRINOTECAN; PHASE-III TRIAL; OPEN-LABEL;
   1ST-LINE TREATMENT; RAS MUTATIONS; MICROSATELLITE INSTABILITY;
   COMBINATION CHEMOTHERAPY; RANDOMIZED-TRIAL; BRAF MUTATION
AB Introduction: Outcomes in metastatic colorectal cancer are improving, with better understanding and use of targeted therapies.Areas covered: A review of the literature and recent conference presentations was undertaken on the topic of systemic treatment of metastatic colorectal cancer. This article reviews the current evidence for targeted therapies in advanced colorectal cancer, including up-to-date data regarding anti-epidermal growth factor receptor (EGFR) and anti-vascular endothelial growth factor (VEGF) agents, the relevance of primary tumor location and novel subgroups such as BRAF mutated, HER2 amplified, and mismatch-repair-deficient cancers.Expert commentary: EGFR-targeted and VEGF-targeted antibodies are now routinely incorporated into treatment strategies for metastatic colorectal cancer (mCRC). The use of EGFR-targeted antibodies should be restricted to patients with extended RAS wild-type profiles, and there is evidence that they should be further restricted to patients with left-sided tumors. Clinically, mCRC can be divided into subgroups based on RAS, BRAF, HER2, and MMR status, each of which have distinct treatment pathways.
C1 [Price, Timothy J.] Queen Elizabeth Hosp, Med Oncol, Woodville, SA, Australia.
   [Price, Timothy J.] Univ Adelaide, Adelaide, SA, Australia.
   [Tang, Monica] Univ Sydney, NHMRC Clin Trials Ctr, Med Oncol, Sydney, NSW, Australia.
   [Gibbs, Peter] Western Hosp, Med Oncol, Melbourne, Vic, Australia.
   [Gibbs, Peter] Walter & Eliza Hall Inst Med Res, Med Oncol, Melbourne, Vic, Australia.
   [Haller, Daniel G.] Univ Penn, Med Oncol, Abrahamson Canc Ctr, Perelman Sch Med, Philadelphia, PA 19104 USA.
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   [Peeters, Marc] Asklepios Tumorzentrum Hamburg, Hamburg, Germany.
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   [Segelov, Eva] Monash Univ, Sch Clin Sci, Monash Hlth, Med Oncol,Monash Med Ctr, Clayton, Vic, Australia.
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   [Roy, Amitesh] Flinders Univ S Australia, Med Oncol, Bedford Pk, SA, Australia.
   [Tebbutt, Niall] Austin Hlth, Med Oncol, Heidelberg, Vic, Australia.
   [Pavlakis, Nick] Royal North Shore Hosp, Med Oncol, St Leonards, NSW, Australia.
   [Burge, Matthew] Royal Brisbane Hosp, Med Oncol, Brisbane, Qld, Australia.
   [Shapiro, Jeremy] Cabrini Hosp, Med Oncol, Melbourne, Vic, Australia.
   [Shapiro, Jeremy] Monash Univ, Melbourne, Vic, Australia.
C3 University of Adelaide; University of Sydney; Western Health; Western
   Hospital; University of Pennsylvania; University of Antwerp; Monash
   Health; Monash Medical Centre; Monash University; Flinders University
   South Australia; Flinders University South Australia; Florey Institute
   of Neuroscience & Mental Health; Austin Research Institute; Royal North
   Shore Hospital; Royal Brisbane & Women's Hospital; Cabrini Health;
   Monash University
RP Price, TJ (corresponding author), Univ Adelaide, Adelaide, SA, Australia.; Price, TJ (corresponding author), Queen Elizabeth Hosp, Woodville, SA, Australia.
EM Timothy.Price@sa.gov.au
RI Roy, Amitesh/AGQ-4929-2022; Peeters, Marc/C-5525-2013; Segelov,
   Eva/Q-7611-2019; Price, Timothy/G-1404-2012
OI Karapetis, Christos/0000-0003-1741-996X; Tang,
   Monica/0000-0003-0075-2176; Roy, Amitesh/0000-0002-3583-7981
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NR 130
TC 38
Z9 41
U1 3
U2 20
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
PY 2018
VL 18
IS 10
BP 991
EP 1006
DI 10.1080/14737140.2018.1502664
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GS7HB
UT WOS:000443870500006
PM 30019590
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Hermel, DJ
   Sigal, D
AF Hermel, David J.
   Sigal, Darren
TI The Emerging Role of Checkpoint Inhibition in Microsatellite Stable
   Colorectal Cancer
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Review
DE immunotherapy; microsatellite stable; colorectal cancer; immune
   checkpoint inhibitors
ID TUMOR MUTATIONAL BURDEN; COMBINATION; EXPRESSION; PROGNOSIS; BLOCKADE;
   CELL
AB Checkpoint inhibitor therapy has introduced a revolution in contemporary anticancer therapy. It has led to dramatic improvements in patient outcomes and has spawned tremendous research into novel immunomodulatory agents and combination therapy that has changed the trajectory of cancer care. However, clinical benefit in patients with colorectal cancer has been generally limited to tumors with loss of mismatch repair function and those with specific germline mutations in the DNA polymerase gene. Unfortunately, tumors with these specific mutator phenotypes are in the minority. Recent pre-clinical and clinical studies have begun to reveal encouraging results suggesting that checkpoint inhibitor therapy can be expanded to an increasing number of colorectal tumors with microsatellite stability and the absence of traditional predictive biomarkers of checkpoint inhibitor response. These studies generally rely on combinations of checkpoint inhibitors with chemotherapy, molecular targeted therapy, radiation therapy, or other novel immunomodulatory agents. This article will review the most current data in microsatellite stable colorectal cancer.
C1 [Hermel, David J.] Univ Southern Calif, Dept Med, 2020 Zonal Ave, Los Angeles, CA 90033 USA.
   [Sigal, Darren] Scripps Clin, Div Hematol Oncol, 10666 North Torrey Pines Rd, La Jolla, CA 92037 USA.
C3 University of Southern California; Scripps Research Institute
RP Sigal, D (corresponding author), Scripps Clin, Div Hematol Oncol, 10666 North Torrey Pines Rd, La Jolla, CA 92037 USA.
EM david.hermel@med.usc.edu; Sigal.Darren@scrippshealth.org
OI Sigal, Darren/0000-0001-7839-1230
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NR 50
TC 26
Z9 27
U1 0
U2 6
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 5
DI 10.3390/jpm9010005
PG 13
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA HS6SI
UT WOS:000464001200005
PM 30654522
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Pancione, M
   Giordano, G
   Parcesepe, P
   Cerulo, L
   Coppola, L
   Del Curatolo, A
   Conciatori, F
   Milella, M
   Porras, A
AF Pancione, Massimo
   Giordano, Guido
   Parcesepe, Pietro
   Cerulo, Luigi
   Coppola, Luigi
   Del Curatolo, Anais
   Conciatori, Fabiana
   Milella, Michele
   Porras, Almudena
TI Emerging Insight into MAPK Inhibitors and Immunotherapy in Colorectal
   Cancer
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE MAPKs; colorectal cancer; immune resistance; immune check point
   inhibitors; immunotherapy; ERKs; p38 MAPKs
ID ACTIVATED PROTEIN-KINASE; PATIENT-DERIVED XENOGRAFTS; COLON-CANCER;
   T-CELL; TARGETED THERAPY; MEK INHIBITION; TUMOR-GROWTH;
   ACQUIRED-RESISTANCE; TRANSENDOTHELIAL MIGRATION; REGULATED KINASE-1/2
AB Our understanding of the genetic and non-genetic molecular alterations associated with colorectal cancer (CRC) progression and therapy resistance has markedly expanded in the recent years. In addition to their effects on tumor biology, targeted therapies can have effects on host immune responses. However, the mechanisms by which immune cells organize tumor microenvironments to regulate T-cell activity need to be comprehensively defined. There is good evidence in the literature that alterations in different members of the MAPK superfamily (mainly ERKs and p38 MAPKs) modify the inflammatory response and antitumor immunity, enhancing metastatic features of the tumors. In addition, a plethora of alterations that emerge at relapse often converge on the activation of MAPKs, particularly, ERKs, which act in concert with other oncogenic signals to modulate cellular homeostasis and clonal evolution during targeted therapies. Herein, we discuss how this knowledge can be translated into drug development strategies aimed at increasing tumor antigenicity and antitumor immune responses. Insights from these studies could provide a framework for considering additional combinations of targeted therapies and immunotherapies for the treatment of CRC.
C1 [Pancione, Massimo; Cerulo, Luigi] Univ Sannio, Dept Sci & Technol, Via Port Arsa 11, I-82100 Benevento, Italy.
   [Pancione, Massimo; Porras, Almudena] Univ Complutense Madrid, Fac Pharm, Dept Biochem & Mol Biol 2, Madrid, Spain.
   [Giordano, Guido] CRO Aviano Natl Canc Ctr, Aviano, Italy.
   [Giordano, Guido; Coppola, Luigi] San Filippo Neri Hosp, Med Oncol & Anat Pathol Unit, Rome, Italy.
   [Parcesepe, Pietro] Univ & Hosp Trust Verona, Sect Pathol, Dept Diagnost & Publ Hlth, I-31134 Verona, Italy.
   [Del Curatolo, Anais; Conciatori, Fabiana; Milella, Michele] Regina Elena Inst Canc Res, Div Med Oncol A, Via Elio Chianesi 53, I-00144 Rome, Italy.
   [Conciatori, Fabiana] Univ Rome, Rome, Italy.
   [Porras, Almudena] Hosp Clin San Carlos IdISSC, Hlth Res Inst, Madrid, Spain.
C3 University of Sannio; Complutense University of Madrid; San Filippo Neri
   Hospital; University of Verona; Azienda Ospedaliera Universitaria
   Integrata Verona; IRCCS Istituti Fisioterapici Ospitalieri (IFO); IRCCS
   Regina Elena; Sapienza University Rome; Hospital Clinico San Carlos
RP Pancione, M (corresponding author), Univ Sannio, Dept Sci & Technol, Via Port Arsa 11, I-82100 Benevento, Italy.; Pancione, M; Porras, A (corresponding author), Univ Complutense Madrid, Fac Pharm, Dept Biochem & Mol Biol 2, Madrid, Spain.
EM massimo.pancione@unisannio.it; maporras@ucm.es
RI Pancione, Massimo/AAF-2109-2019; Milella, Michele/ABH-8606-2020; Porras,
   Almudena/N-2121-2015; DEL CURATOLO, ANAIS/K-1581-2016; Conciatori,
   Fabiana/AAU-2657-2020; Giordano, Guido/IQU-6240-2023
OI DEL CURATOLO, ANAIS/0000-0001-9487-8276; Conciatori,
   Fabiana/0000-0002-8579-5222; PANCIONE, Massimo/0000-0003-1728-8816;
   Giordano, Guido/0000-0002-9310-1075
FU FUR; Italian Ministry of University and Research (MiUR); Spanish
   Ministry of Economy and Competitiveness [SAF2010-20918-C02-01,
   SAF2013-48210-C2-02]; Complutense University [AE1/14-18987, UCM 920384]
FX We thank scientists who have contributed to the preliminary unpublished
   data briefly mentioned in this review. This work was supported by grants
   from the FUR and the Italian Ministry of University and Research (MiUR)
   to M.P and by grants from the Spanish Ministry of Economy and
   Competitiveness (SAF2010-20918-C02-01 and SAF2013-48210-C2-02),
   Complutense University (AE1/14-18987 and UCM 920384) to AP). We
   apologize to all the authors whose original work is not included in the
   references owing to space limitations.
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NR 137
TC 26
Z9 27
U1 0
U2 12
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PY 2017
VL 24
IS 14
BP 1383
EP 1402
DI 10.2174/0929867324666170227114356
PG 20
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA EZ4NU
UT WOS:000404690600001
PM 28245767
DA 2025-01-04
ER

PT J
AU Yu, WY
   Liu, CP
   Li, X
   Yang, FG
   Cheng, LX
   Liu, C
   Song, Y
AF Yu, Wenyang
   Liu, Cuiping
   Li, Xin
   Yang, Fuguo
   Cheng, Lixue
   Liu, Chang
   Song, Yang
TI Inositol hexaphosphate suppresses colorectal cancer cell proliferation
   via the Akt/GSK-3β/β-catenin signaling cascade in a
   1,2-dimethylhydrazine-induced rat model
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE IP6; Colorectal cancer; Proliferation; PI3K/Akt pathway; Wnt pathway
ID NUCLEAR ANTIGEN PCNA; COLON-CANCER; BREAST-CANCER; PHYTIC ACID;
   BETA-CATENIN; WNT/BETA-CATENIN; TARGETED THERAPY; PROSTATE-CANCER; CYCLE
   ARREST; C-MYC
AB Colorectal cancer (CRC) is common worldwide, and most treatments for CRC have undesirable side effects. Many researchers have demonstrated that inositol hexaphosphate (IP6) has potent anticarcinogenic activity against CRC and no apparent toxicity to normal cells. However, the underlying mechanism is still unclear. In this study, we investigated the anticancer and anti-proliferative properties of IP6 in CRC and its possible mechanisms during this chemopreventive process. We examined the expression of genes related to the PI3K/Akt and Wnt pathways at the transcriptional and translational levels in a DMH-induced rat CRC model following IP6 administration. In addition, we also conducted cell proliferation analysis. The results demonstrated that IP6 could inhibit tumors, in terms of tumor incidence, number, weight and volume in DMH-induced rats. Additionally, Akt and c-Myc mRNA levels were significantly decreased. IP6 was also shown to downregulate Akt, pAkt, pGSK-3 beta, and c-Myc protein expression and upregulate p beta-catenin protein expression. Furthermore, tumor tissues from IP6-treated rats showed decreased proliferation. In conclusion, the anti proliferative effect of IP6 may be related to crosstalk between the PI3K/Akt and Wnt pathways, revealing a potential mechanism of CRC inhibition by IP6 in our model.
C1 [Yu, Wenyang; Cheng, Lixue; Liu, Chang; Song, Yang] Qingdao Univ, Sch Publ Hlth, Med Coll, Qingdao 266021, Peoples R China.
   [Liu, Cuiping; Yang, Fuguo] Qingdao Univ, Sch Nursing, Med Coll, Qingdao 266021, Peoples R China.
   [Li, Xin] Qingdao Univ, Sch Basic Med, Med Coll, Qingdao 266021, Peoples R China.
C3 Qingdao University; Qingdao University; Qingdao University
RP Song, Y (corresponding author), Qingdao Univ, Sch Publ Hlth, Med Coll, Qingdao 266021, Peoples R China.
EM yuwenyang1989@126.com; lcping0926@126.com; lixinyiyi@126.com;
   yfuguo@163.com; cchenglixue@163.com; ayerliu@yeah.net;
   qdsongyang81@163.com
RI yang, song/GVU-7963-2022; Liu, Cuiping/AAP-5162-2020
FU National Natural Science Foundation of China [81373001]
FX This work was supported by the National Natural Science Foundation of
   China [grant numbers 81373001].
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NR 58
TC 27
Z9 28
U1 2
U2 20
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-2999
EI 1879-0712
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD JUN 15
PY 2017
VL 805
BP 67
EP 74
DI 10.1016/j.ejphar.2017.03.011
PG 8
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EV2OJ
UT WOS:000401594700008
PM 28315345
DA 2025-01-04
ER

PT J
AU Ioannou, M
   Paraskeva, E
   Baxevanidou, K
   Simos, G
   Papamichali, R
   Papacharalambous, C
   Samara, M
   Koukoulis, G
AF Ioannou, Maria
   Paraskeva, Efrosyni
   Baxevanidou, Korina
   Simos, George
   Papamichali, Roidoula
   Papacharalambous, Constantina
   Samara, Maria
   Koukoulis, George
TI HIF-1a in colorectal carcinoma: review of the literature
SO JOURNAL OF BUON
LA English
DT Review
DE angiogenesis; colorectal carcinoma; HIP-1a; immunohistochemistry;
   prognosis
ID ENDOTHELIAL-GROWTH-FACTOR; HYPOXIA-INDUCIBLE FACTOR-1-ALPHA;
   FACTOR-I-ALPHA; ADVANCED RECTAL-CANCER; COLON-CANCER;
   CLINICOPATHOLOGICAL SIGNIFICANCE; FACTOR EXPRESSION; TARGETED THERAPY;
   HIF-1-ALPHA EXPRESSION; DOWN-REGULATION
AB Colorectal cancer (CRC) is the third most common cancer worldwide and despite the abundance of molecular pathways and markers continually being reported, the mortality rates remain high. Hypoxia inducible factor 1alpha (HIF-1 alpha) plays a major role in the response of tumors to hypoxia, and contributes to tumor aggressiveness, invasiveness and resistance to radiotherapy and chemotherapy. Targeting HIF-1 alpha is an attractive strategy, with the potential for disrupting multiple pathways crucial for tumor growth.
   In the current study, HIF-1 alpha immunohistochemical expression in CRC is reviewed along with the relation to clinical outcome and prognosis. In addition, the significant correlation of HIF-1 alpha to vascular endothelial growth factor (VEGF) expression is reported, as well as the possible role of HIF-1 alpha in predicting the therapeutic response to anti-EGFR therapies.
   Herein, an overview of the HIF-1 alpha expression in CRC is presented. This review delineates the crucial role that HIF-1 alpha plays in carcinogenesis, tumor angiogenesis and cancer progression. The evaluation of HIF-1 alpha in patient biopsies could be useful as a prognostic and/or predictive biomarker in personalized cancer treatment.
C1 [Ioannou, Maria; Baxevanidou, Korina; Papamichali, Roidoula; Papacharalambous, Constantina; Samara, Maria; Koukoulis, George] Univ Thessaly, Fac Med, Dept Pathol, Larisa 41110, Greece.
   [Paraskeva, Efrosyni] Univ Thessaly, Fac Med, Dept Physiol, Larisa 41110, Greece.
   [Simos, George] Univ Thessaly, Fac Med, Biochem Lab, Larisa 41110, Greece.
C3 University of Thessaly; University of Thessaly; University of Thessaly
RP Ioannou, M (corresponding author), Univ Thessaly, Biopolis, Fac Med, Dept Pathol, Larisa 41110, Greece.
EM mioan@med.uth.gr
RI Paraskeva, Effrosyni/JXX-8578-2024; SAMARA, MARIA/IAN-4481-2023; Simos,
   George/AAH-2596-2021; Paraskeva, Efrosyni/E-6449-2015
OI Simos, George/0000-0001-5453-3185; Paraskeva,
   Efrosyni/0000-0002-1312-0322; SAMARA, MARIA/0000-0003-0433-6436
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NR 81
TC 63
Z9 69
U1 0
U2 9
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 2015
VL 20
IS 3
BP 680
EP 689
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CN4KT
UT WOS:000358399700002
PM 26214618
DA 2025-01-04
ER

PT J
AU Ghazi, B
   El Ghanmi, A
   Kandoussi, S
   Ghouzlani, A
   Badou, A
AF Ghazi, Bouchra
   El Ghanmi, Adil
   Kandoussi, Sarah
   Ghouzlani, Amina
   Badou, Abdallah
TI CAR T-cells for colorectal cancer immunotherapy: Ready to go?
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE colorectal cancer; CAR T cells; immunotherapies; tumor
   microenvironement; tumor mutational burden; clinical data
ID TARGETED THERAPY; SOLID TUMORS; EXPRESSION; RESISTANCE; BURDEN
AB Chimeric antigen receptor (CAR) T-cells represent a new genetically engineered cell-based immunotherapy tool against cancer. The use of CAR T-cells has revolutionized the therapeutic approach for hematological malignancies. Unfortunately, there is a long way to go before this treatment can be developed for solid tumors, including colorectal cancer. CAR T-cell therapy for colorectal cancer is still in its early stages, and clinical data are scarce. Major limitations of this therapy include high toxicity, relapses, and an impermeable tumor microenvironment for CAR T-cell therapy in colorectal cancer. In this review, we summarize current knowledge, highlight challenges, and discuss perspectives regarding CAR T-cell therapy in colorectal cancer.
C1 [Ghazi, Bouchra] Mohammed VI Univ Hlth Sci UM6SS, Fac Med, Casablanca, Morocco.
   [El Ghanmi, Adil] Mohammed VI Hlth Sci UM6SS 6, Mohammed VI Int Univ Hosp, Fac Med, Casablanca, Morocco.
   [Kandoussi, Sarah; Ghouzlani, Amina; Badou, Abdallah] Hassan II Univ, Fac Med & Pharm, Immunogenet & Human Pathol Lab, Casablanca, Morocco.
C3 Mohammed VI University of Sciences & Health-UM6SS; Mohammed First
   University of Oujda; Hassan II University of Casablanca; Hassan II
   University of Casablanca
RP Badou, A (corresponding author), Hassan II Univ, Fac Med & Pharm, Immunogenet & Human Pathol Lab, Casablanca, Morocco.
EM abdallah.badou@univh2c.ma
OI Ghouzlani, Amina/0000-0001-9589-2870
FU Moroccan Ministry of Higher Education, Research and innovation; Moroccan
   Ministry of Higher Education, Research and innovation; Digital
   Development Agency "ADD"
FX This work was supported by the Moroccan Ministry of Higher Education,
   Research and innovation through a "PPR1" project and by the Moroccan
   Ministry of Higher Education, Research and innovation and the Digital
   Development Agency "ADD" through an "Al-khawarizmi" project.
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NR 229
TC 21
Z9 23
U1 5
U2 38
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 NOV 15
PY 2022
VL 13
AR 978195
DI 10.3389/fimmu.2022.978195
PG 23
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 6Q8LX
UT WOS:000891862500001
PM 36458008
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Yildirim, ME
   Karadurmus, N
   Ökten, IN
   Türk, HM
   Urakçi, Z
   Arslan,Ç
   Çelik, S
   Dane, F
   Sendur, MAN
   Bilir, C
   Karabulut, B
   Cicin, I
   Çubukcu, E
   Karaca, M
   Ozcelik, M
   Artac, M
   Tanrikulu, E
   Alacacioglu, A
   Açikgöz,Ö
   Öven, B
   Geredeli,Ç
   Çil, T
   Harputluoglu, H
   Kefeli, U
   Bozkurt, O
   Tural, D
   Sakin, A
   Yalçin, S
   Gumus, M
AF Yildirim, Mahmut Emre
   Karadurmus, Nuri
   Okten, Ilker Nihat
   Turk, Haci Mehmet
   Urakci, Zuhat
   Arslan, Cagatay
   Celik, Sinemis
   Dane, Faysal
   Sendur, Mehmet Ali Nahit
   Bilir, Cemil
   Karabulut, Bulent
   Cicin, Irfan
   Cubukcu, Erdem
   Karaca, Mustafa
   Ozcelik, Melike
   Artac, Mehmet
   Tanrikulu, Eda
   Alacacioglu, Ahmet
   Acikgoz, Ozgur
   Oven, Basak
   Geredeli, Caglayan
   Cil, Timucin
   Harputluoglu, Hakan
   Kefeli, Umut
   Bozkurt, Oktay
   Tural, Deniz
   Sakin, Abdullah
   Yalcin, Suayip
   Gumus, Mahmut
TI Real-world treatment outcomes from nationwide Onco-colon Turkey registry
   in RAS wild-type patients treated with biologics second-line mCRC
SO JOURNAL OF ONCOLOGY PHARMACY PRACTICE
LA English
DT Article; Early Access
DE colon cancer; targeted therapy; Ras wild type
ID METASTATIC COLORECTAL-CANCER; CETUXIMAB PLUS IRINOTECAN; 1ST-LINE
   TREATMENT; PHASE-III; BEVACIZUMAB; FLUOROURACIL; OXALIPLATIN;
   PANITUMUMAB; LEUCOVORIN; MUTATIONS
AB Backgrounds and Objectives Colorectal cancer is one of the leading causes of mortality both globally and in our country. In Turkey, we conducted a multicenter investigation into the effectiveness of second-line treatments and real-life data for patients with RAS wild-type metastatic colorectal cancer (NCT04757311).Materials and Methods In this retrospective analysis, records from 28 centers were collected, and histopathological, molecular, and clinical characteristics were documented. Patients were categorized into groups based on their second-line biological treatments: anti-EGFR (Group A and Group B, panitumumab and cetuximab) and anti-VEGF (Group C, bevacizumab and aflibercept). They were then compared within these groups.Results A total of 588 patients with documented RAS wild-type status were evaluated. The median OS was 15.7, 14.3 and 14.7 months in Group A, Group B and Group C, respectively (p = 0.764). The median PFS of the patients in second-line setting that received panitumumab, cetuximab and bevacizumab/aflibercept were 7.8, 6.6 and 7.4 months, respectively (p = 0.848).Conclusion According to the results of our real-life data study, there is no significant difference in efficiency between the combination of biological agent and chemotherapy used in the second-line treatments.
C1 [Yildirim, Mahmut Emre] Istanbul Dr Lutfi Kirdar Kartal City Hosp, Med Oncol Dept, Istanbul, Turkiye.
   [Karadurmus, Nuri] Gulhane Training & Res Hosp, Med Oncol Dept, Ankara, Turkiye.
   [Okten, Ilker Nihat] Medeniyet Univ, Med Oncol Dept, Goztepe Training & Res Hosp, Istanbul, Turkiye.
   [Turk, Haci Mehmet] Bezmialem Vakif Univ, Fac Med, Dept Med Oncol, Istanbul, Turkiye.
   [Urakci, Zuhat] Dicle Univ, Med Fac, Dept Med Oncol, Diyarbakir, Turkiye.
   [Arslan, Cagatay] Bahcesehir Univ, Bahcesehir Universitesi, Tip Fak, Istanbul, Turkiye.
   [Celik, Sinemis] Istanbul Oncol Hosp, Med Oncol Dept, Istanbul, Turkiye.
   [Dane, Faysal] Marmara Univ, Sch Med, Dept Internal Med, Div Med Oncol, Istanbul, Turkiye.
   [Sendur, Mehmet Ali Nahit] Ankara Yildirim Beyazit Univ, Fac Med, Med Oncol, Ankara, Turkiye.
   [Bilir, Cemil] Sakarya Univ Training & Res Hosp, Med Oncol Dept, Sakarya, Turkiye.
   [Karabulut, Bulent] Ege Univ, Med Oncol, Fac Med, Ege, Turkiye.
   [Cicin, Irfan] Trakya Univ, Div Oncol, Dept Internal Med, Fac Med, Edirne, Turkiye.
   [Cubukcu, Erdem] Uludag Univ, Fac Med, Med Oncol, Bursa, Turkiye.
   [Karaca, Mustafa] Antalya Training & Res Hosp, Med Oncol Dept, Antalya, Turkiye.
   [Ozcelik, Melike] Umraniye Training & Res Hosp, Dept Oncol, Istanbul, Turkiye.
   [Artac, Mehmet] Necmettin Erbakan Univ, Med Fac, Dept Med Oncol, Konya, Turkiye.
   [Tanrikulu, Eda] Istanbul Haydarpasa Numune Training & Res Hosp, Med Oncol, Istanbul, Turkiye.
   [Alacacioglu, Ahmet] Izmir Katip Celebi Univ Ataturk Educ & Res Hosp, Med Oncol Dept, Minist Hlth, Izmir, Turkiye.
   [Acikgoz, Ozgur] Istanbul Medipol Univ, Med Fac, Istanbul, Turkiye.
   [Oven, Basak] Yeditepe Univ Hosp, Med Oncol Dept, Istanbul, Turkiye.
   [Geredeli, Caglayan] Okmeydani Training & Res Hosp, Dept Med Oncol, Istanbul, Turkiye.
   [Cil, Timucin] Univ Hlth Sci, Adana City Educ & Res Hosp, Dept Med Oncol, Adana, Turkiye.
   [Harputluoglu, Hakan] Inonu Univ, Inonu Universitesi, Malatya, Turkiye.
   [Kefeli, Umut] Kocaeli Univ, Sch Med, Med Oncol, Kocaeli, Turkiye.
   [Bozkurt, Oktay] Erciyes Univ, Erciyes Universitesi, Kayseri, Turkiye.
   [Tural, Deniz] Istanbul Bakirkoy Dr Sadi Konuk Training & Res Hos, Med Oncol, Istanbul, Turkiye.
   [Sakin, Abdullah] Yuzuncu Yil Univ, Dept Med Oncol, Van, Turkiye.
   [Yalcin, Suayip] Hacettepe Univ, Fac Med, Dept Med Oncol, Ankara, Turkiye.
   [Gumus, Mahmut] Istanbul Medeniyet Univ, Dept Med Oncol, Istanbul, Turkiye.
   [Yildirim, Mahmut Emre] Kartal Dr Lutfi Kirdar City Hosp, Kartal, Istanbul, Turkiye.
C3 Gulhane Training & Research Hospital; Istanbul Medeniyet University;
   Istanbul Goztepe Training & Research Hospital; Bezmialem Vakif
   University; Dicle University; Bahcesehir University; Marmara University;
   Ankara Yildirim Beyazit University; Sakarya University; Sakarya Training
   & Research Hospital; Ege University; Trakya University; Uludag
   University; Antalya Training & Research Hospital; Istanbul Umraniye
   Training & Research Hospital; Necmettin Erbakan University; Istanbul
   Haydarpasa Numune Training & Research Hospital; Ministry of Health -
   Turkey; Izmir Ataturk Training & Research Hospital; Istanbul Medipol
   University; Yeditepe University; Istanbul Okmeydani Training & Research
   Hospital; University of Health Sciences Turkey; Inonu University;
   Kocaeli University; Erciyes University; Yuzuncu Yil University;
   Hacettepe University; Istanbul Medeniyet University
RP Yildirim, ME (corresponding author), Kartal Dr Lutfi Kirdar City Hosp, Kartal, Istanbul, Turkiye.
EM emremahmutyildirim@gmail.com
RI Artac, Mehmet/AAF-8158-2020; Cil, Timucin/HJZ-1735-2023; Sendur,
   Mehmet/H-7555-2014; Gumus, Mahmut/HTO-4176-2023; ozcelik,
   melike/AAS-7557-2020; KEFELI, UMUT/V-6023-2017; Cicin,
   Irfan/AAQ-5575-2020
FU Oncology departments in Turkiye
FX The authors would like to acknowledge all the support they have received
   from the Oncology departments in Turkiye.
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NR 24
TC 0
Z9 0
U1 0
U2 2
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 2024 APR 13
PY 2024
DI 10.1177/10781552241241004
EA APR 2024
PG 8
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA NO7V4
UT WOS:001201466900001
PM 38613329
DA 2025-01-04
ER

PT J
AU Albadari, N
   Xie, Y
   Li, W
AF Albadari, Najah
   Xie, Yang
   Li, Wei
TI Deciphering treatment resistance in metastatic colorectal cancer: roles
   of drug transports, EGFR mutations, and HGF/c-MET signaling
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE metastatic colorectal cancer; resistance; anti-EGFR; anti-MET; ABC drug
   transporters; tyrosine kinase inhibitors
ID GROWTH-FACTOR RECEPTOR; TIVANTINIB ARQ 197; BINDING CASSETTE SUBFAMILY;
   WILD-TYPE KRAS; MULTIDRUG-RESISTANCE; COLON-CANCER; C-MET; PHASE-II;
   CETUXIMAB RESISTANCE; THYMIDYLATE SYNTHASE
AB In 2023, colorectal cancer (CRC) is the third most diagnosed malignancy and the third leading cause of cancer death worldwide. At the time of the initial visit, 20% of patients diagnosed with CRC have metastatic CRC (mCRC), and another 25% who present with localized disease will later develop metastases. Despite the improvement in response rates with various modulation strategies such as chemotherapy combined with targeted therapy, radiotherapy, and immunotherapy, the prognosis of mCRC is poor, with a 5-year survival rate of 14%, and the primary reason for treatment failure is believed to be the development of resistance to therapies. Herein, we provide an overview of the main mechanisms of resistance in mCRC and specifically highlight the role of drug transports, EGFR, and HGF/c-MET signaling pathway in mediating mCRC resistance, as well as discuss recent therapeutic approaches to reverse resistance caused by drug transports and resistance to anti-EGFR blockade caused by mutations in EGFR and alteration in HGF/c-MET signaling pathway.
C1 [Albadari, Najah; Xie, Yang; Li, Wei] Univ Tennessee, Hlth Sci Ctr, Coll Pharm, Memphis, TN USA.
C3 University of Tennessee System; University of Tennessee Health Science
   Center
RP Li, W (corresponding author), Univ Tennessee, Hlth Sci Ctr, Coll Pharm, Memphis, TN USA.
EM wli@uthsc.edu
RI Xie, Yang/JMP-5665-2023
OI Xie, Yang/0000-0003-0656-5152
FU University of Tennessee College of Pharmacy Drug Discovery Center; NIH
   [R01CA148706, R01CA240447]
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This work is supported
   by the University of Tennessee College of Pharmacy Drug Discovery
   Center, with additional partial support from NIH grants R01CA148706 and
   R01CA240447 to WL.
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NR 303
TC 5
Z9 5
U1 2
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD JAN 10
PY 2024
VL 14
AR 1340401
DI 10.3389/fphar.2023.1340401
PG 24
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA FQ0E0
UT WOS:001147186900001
PM 38269272
OA gold
DA 2025-01-04
ER

PT J
AU Xia, X
   Zhang, JW
   Zhao, B
   Zhang, M
   Chen, ZR
   Zhang, BF
   Ji, YL
   Wang, X
   Xiong, WM
   Li, JW
   Lv, QL
AF Xia, Xue
   Zhang, Jing-wen
   Zhao, Bing
   Zhang, Min
   Chen, Zhang-ren
   Zhang, Bing-feng
   Ji, Yu-long
   Wang, Xia
   Xiong, Wen-min
   Li, Jia-wei
   Lv, Qiao-li
TI Progress of engineered bacteria for tumour therapy
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Tumor; Genetically engineered bacteria; Targeted therapy; Bacteria
ID TARGETING SALMONELLA-TYPHIMURIUM; COLORECTAL-CARCINOMA CELLS; PHASE-I;
   CANCER; METASTASIS; GROWTH; A1-R; COLI; EFFICACY; DRUG
AB Finding novel therapeutic modalities, improving drug delivery efficiency and targeting, and reducing the immune escape of tumor cells are currently hot topics in the field of tumor therapy. Bacterial therapeutics have proven highly effective in preventing tumor spread and recurrence, used alone or in combination with traditional therapies. In recent years, a growing number of researchers have significantly improved the targeting and penetration of bacteria by using genetic engineering technology, which has received widespread attention in the field of tumor therapy. In this paper, we provide an overview and assessment of the advancements made in the field of tumor therapy using genetically engineered bacteria. We cover three major aspects: the development of engineered bacteria, their integration with other therapeutic techniques, and the current state of clinical trials. Lastly, we discuss the limitations and challenges that are currently being faced in the utilization of engineered bacteria for tumor therapy.
C1 [Xia, Xue; Zhang, Jing-wen; Zhao, Bing; Ji, Yu-long; Wang, Xia; Xiong, Wen-min; Lv, Qiao-li] Jiangxi Canc Hosp, Jiangxi Clin Res Ctr Canc, Jiangxi Key Lab Translat Canc Res, NHC Key Lab Personalized Diag & Treatment Nasophar, Nanchang 330029, Jiangxi, Peoples R China.
   [Xia, Xue; Zhang, Jing-wen; Zhao, Bing; Zhang, Bing-feng; Lv, Qiao-li] Yichun Univ, Coll Chem & Bioengn, Yichun 336000, Peoples R China.
   [Zhang, Min] Nanchang Inspection & Testing Ctr, Nanchang Key Lab Food Safety, Nanchang 330012, Peoples R China.
   [Chen, Zhang-ren] Nanchang Univ, Affiliated Hosp 1, Dept Pharm, Nanchang 330000, Peoples R China.
   [Li, Jia-wei] Nanchang Univ, Affiliated Hosp 1, Dept Cardiovasc, 17 Yongwai Zhengjie, Nanchang 330029, Jiangxi, Peoples R China.
   [Lv, Qiao-li] Jiangxi Canc Hosp, Jiangxi Key Lab Translat Canc Res, 519 Beijing East Rd, Nanchang 330029, Jiangxi, Peoples R China.
C3 Yichun University; Nanchang University; Nanchang University
RP Li, JW (corresponding author), Nanchang Univ, Affiliated Hosp 1, Dept Cardiovasc, 17 Yongwai Zhengjie, Nanchang 330029, Jiangxi, Peoples R China.; Lv, QL (corresponding author), Jiangxi Canc Hosp, Jiangxi Key Lab Translat Canc Res, 519 Beijing East Rd, Nanchang 330029, Jiangxi, Peoples R China.
EM lijiawei_2023@126.com; lvqiaoli2008@126.com
RI Chen, Zhang-Ren/AAF-6270-2021; Jiawei, Li/AAS-7247-2020; zhang,
   min/IYI-9869-2023; Zhang, Jingwen/AAQ-3561-2020
FU National Natural Science Foundation of China [82360736]; Distinguished
   Young Scholars program of the Natural Science Foundation of Jiangxi
   Province [20224ACB216015]; Science and Technology Plan of Health Commis-
   sion of Jiangxi Provincial [202310059]; Science and Technology Research
   Project of Jiangxi Provincial Department of Education [GJJ2203508];
   Non-profit Central Research Institute Fund of Chinese Academy of Medical
   Sciences [2020- PT320-004]; Traditional Chinese Medicine Science
   Research Fund of Jiangxi Province [2022A319]; Jiangxi Provincial
   Institute of Lung Cancer [2021LCIG02]; Distinguished Young Scholars Fund
   of Jiangxi Cancer Hospital [2021DYS01]
FX This work was supported by the National Natural Science Foundation of
   China (No. 82360736) , The Distinguished Young Scholars program of the
   Natural Science Foundation of Jiangxi Province (20224ACB216015) ,
   Science and Technology Plan of Health Commis- sion of Jiangxi Provincial
   (202310059) , Science and Technology Research Project of Jiangxi
   Provincial Department of Education (GJJ2203508) , supported by the
   Non-profit Central Research Institute Fund of Chinese Academy of Medical
   Sciences (grant number 2020- PT320-004) , Traditional Chinese Medicine
   Science Research Fund of Jiangxi Province (No. 2022A319) , Jiangxi
   Provincial Institute of Lung Cancer (2021LCIG02) , and The Distinguished
   Young Scholars Fund of Jiangxi Cancer Hospital (2021DYS01) .
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NR 86
TC 0
Z9 0
U1 20
U2 30
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD MAY 10
PY 2024
VL 132
AR 111935
DI 10.1016/j.intimp.2024.111935
EA APR 2024
PG 10
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA RN9C9
UT WOS:001228450900001
PM 38599096
DA 2025-01-04
ER

PT J
AU Zhang, TH
   Yuan, KT
   Wang, YZ
   Xu, MZ
   Cai, SR
   Chen, CQ
   Ma, JP
AF Zhang, Tianhao
   Yuan, Kaitao
   Wang, Yingzhao
   Xu, Mingze
   Cai, Shirong
   Chen, Chuangqi
   Ma, Jinping
TI Identification of Candidate Biomarkers and Prognostic Analysis in
   Colorectal Cancer Liver Metastases
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; differentially expressed genes; liver metastasis;
   biomarkers; prognostic analysis
ID GROWTH-FACTOR-II; GENE-EXPRESSION; CELL-LINES; WEB SERVER; INSULIN;
   COLON; CARCINOMA; PLATELETS; IGF; RECEPTOR
AB Background Colorectal cancer (CRC), one of the most common malignant tumors worldwide, has a high mortality rate, especially for patients with CRC liver metastasis (CLM). However, CLM pathogenesis remains unclear. Methods We integrated multiple cohort datasets and databases to clarify and verify potential key candidate biomarkers and signal transduction pathways in CLM. GEO2R, DAVID 6.8, ImageGP, STRING, UALCAN, ONCOMINE, THE HUMAN PROTEIN ATLAS, GEPIA 2.0, cBioPortal, TIMER 2.0, DRUGSURV, CRN, GSEA 4.0.3, FUNRICH 3.1.3 and R 4.0.3 were utilized in this study. Results Sixty-three pairs of matched colorectal primary cancer and liver metastatic gene expression profiles were screened from three gene expression profiles (GSE6988, GSE14297 and GSE81558). Thirty-one up-regulated genes and four down-regulated genes were identified from these three gene expression profiles and verified by another gene expression profiles (GSE 49355) and TCGA database. Two pathways (IGFBP-IGF signaling pathway and complement-coagulation cascade), eighteen key differentially expressed genes (DEGs), six hub genes (SPARCL1, CDH2, CP, HP, TF and SERPINA5) and two biomarkers (CDH2 and SPARCL1) with significantly prognostic values were screened by multi-omics data analysis and verified by Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) cohort. Conclusions In this study, we identified a robust set of potential candidate biomarkers in CLM, which would provide potential value for early diagnosis and prognosis, and would promote molecular targeting therapy for CRC and CLM.
C1 [Zhang, Tianhao; Yuan, Kaitao; Wang, Yingzhao; Xu, Mingze; Cai, Shirong; Chen, Chuangqi; Ma, Jinping] Sun Yat Sen Univ, Div Gastrointestinal Surg Ctr, Affiliated Hosp 1, Guangzhou, Peoples R China.
C3 Sun Yat Sen University
RP Ma, JP (corresponding author), Sun Yat Sen Univ, Div Gastrointestinal Surg Ctr, Affiliated Hosp 1, Guangzhou, Peoples R China.
EM majp@mail.sysu.edu.cn
RI XU, MINGZE/AAM-5942-2021; Zhang, Tianhao/JQV-6157-2023; Wang,
   Yingzhao/JZD-6845-2024
OI Wang, Yingzhao/0009-0008-9103-8501
FU Guangzhou Association for Science Technology [K2019010101042,
   K2019010201082, K2019070201006, K20200201002, K20210101013]; Guangzhou
   Municipal Science and Technology Bureau [202002020048]; Department of
   Science and Technology of Guangdong Province [2020A1414040006]
FX This work was supported by the Guangzhou Association for Science &
   Technology (grant number: K2019010101042, K2019010201082,
   K2019070201006, K20200201002 and K20210101013), Guangzhou Municipal
   Science and Technology Bureau (grant number: 202002020048) and
   Department of Science and Technology of Guangdong Province (grant
   number: 2020A1414040006).
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NR 69
TC 17
Z9 17
U1 0
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 AUG 4
PY 2021
VL 11
AR 652354
DI 10.3389/fonc.2021.652354
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA UD7GY
UT WOS:000687374800001
PM 34422629
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Tie, J
   Desai, J
AF Tie, Jeanne
   Desai, Jayesh
TI Targeting <i>BRAF</i> mutant metastatic colorectal cancer: clinical
   implications and emerging therapeutic strategies
SO TARGETED ONCOLOGY
LA English
DT Review
DE BRAF; Colorectal cancer; Biomarker; Resistance mechanism; Targeted
   therapy
ID ISLAND METHYLATOR PHENOTYPE; K-RAS MUTATIONS; WILD-TYPE; COLON-CANCER;
   MICROSATELLITE INSTABILITY; MISMATCH-REPAIR; MOLECULAR-FEATURES; DNA
   METHYLATION; V600E MUTATION; LIFE-STYLE
AB Increasing knowledge of the underlying signaling pathways and molecular defects involved in colorectal cancer growth or progression enabled the discovery of several prognostic and predictive biomarkers, leading to the development of novel molecularly targeted therapies. The mitogen-activated protein kinase (MAPK) signaling pathway plays a critical role in colorectal cancer progression. Mutations in BRAF, a principal effector of Ras in this signaling cascade, are found in 10 % of colorectal cancer and play a clear pathogenic role, particularly in patients with metastatic disease. Intense efforts have therefore focused on targeting BRAF as an oncogenic driver, with mixed early results. This article summarizes the molecular and clinical features of BRAF mutant colorectal cancer, the prognostic and predictive role of BRAFV600E mutation in colorectal cancer, initial clinical trial results in targeting BRAFV600E, and the more recent preclinical insights into potential mechanisms of resistance to BRAF inhibition that have now led to a number of rationale-driven combination therapeutic strategies.
C1 [Tie, Jeanne; Desai, Jayesh] Ludwig Inst Canc Res, Ludwig Colon Canc Initiat Lab, Parkville, Vic, Australia.
   [Tie, Jeanne; Desai, Jayesh] Univ Melbourne, Dept Surg, Fac Med Dent & Hlth Sci, Parkville, Vic 3052, Australia.
   [Tie, Jeanne; Desai, Jayesh] Royal Melbourne Hosp, Dept Med Oncol, Parkville, Vic 3050, Australia.
   [Desai, Jayesh] Peter MacCallum Canc Ctr, Dept Canc Med, East Melbourne, Vic, Australia.
C3 Ludwig Institute for Cancer Research; University of Melbourne; Melbourne
   Health; Royal Melbourne Hospital; Peter Maccallum Cancer Center
RP Desai, J (corresponding author), Peter MacCallum Canc Ctr, Dept Canc Med, East Melbourne, Vic, Australia.
EM jayesh.desai@mh.org.au
RI Desai, Jayesh/AAV-1237-2021
OI Tie, Jeanne/0000-0001-9244-2057; Desai, Jayesh/0000-0003-4246-9344
FU Victorian Government through Victorian Cancer Agency
FX JT and JD are supported by the Victorian Government through a Victorian
   Cancer Agency Clinical Researcher Fellowship.
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NR 78
TC 25
Z9 26
U1 1
U2 12
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1776-2596
EI 1776-260X
J9 TARGET ONCOL
JI Target. Oncol.
PD JUN
PY 2015
VL 10
IS 2
BP 179
EP 188
DI 10.1007/s11523-014-0330-0
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA CJ8PQ
UT WOS:000355766100001
PM 25119972
DA 2025-01-04
ER

PT J
AU Hayes, DN
   Kim, WY
AF Hayes, D. Neil
   Kim, William Y.
TI The next steps in next-gen sequencing of cancer genomes
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Review
ID ABL TYROSINE KINASE; LEUKEMIA-CELLS; COLON-CANCER; LUNG-CANCER; T-CELLS;
   INHIBITION; MUTATIONS; SAFETY; CHEMOTHERAPY; ANTIBODY
AB The necessary infrastructure to carry out genomics-driven oncology is now widely available and has resulted in the exponential increase in characterized cancer genomes. While a subset of genomic alterations is clinically actionable, the majority of somatic events remain classified as variants of unknown significance and will require functional characterization. A careful cataloging of the genomic alterations and their response to therapeutic intervention should allow the compilation of an "actionability atlas" and the creation of a genomic taxonomy stratified by tumor type and oncogenic pathway activation. The next phase of genomic medicine will therefore require talented bioinformaticians, genomic navigators, and multidisciplinary approaches to decode complex cancer genomes and guide potential therapy. Equally important will be the ethical and interpretable return of results to practicing oncologists. Finally, the integration of genomics into clinical trials is likely to speed the development of predictive biomarkers of response to targeted therapy as well as define pathways to acquired resistance.
C1 [Hayes, D. Neil; Kim, William Y.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
   [Hayes, D. Neil; Kim, William Y.] Univ N Carolina, Dept Med, Chapel Hill, NC 27599 USA.
   [Kim, William Y.] Univ N Carolina, Dept Genet, Chapel Hill, NC 27599 USA.
   [Kim, William Y.] Univ N Carolina, Dept Urol, Chapel Hill, NC 27599 USA.
C3 University of North Carolina; University of North Carolina Chapel Hill;
   University of North Carolina; University of North Carolina Chapel Hill;
   University of North Carolina; University of North Carolina Chapel Hill;
   University of North Carolina; University of North Carolina Chapel Hill
RP Hayes, DN (corresponding author), Univ N Carolina, Lineberger Comprehens Canc Ctr, CB 7295, Chapel Hill, NC 27599 USA.
EM hayes@med.unc.edu; wykim@med.unc.edu
RI Hayes, D/AIA-2263-2022
FU NIH [R01 CA142794, U24 CA143848, U24 CA143848-02S1, U10 CA181009-01];
   University Cancer Research Fund; AACR Kure It; Bladder Cancer Advocacy
   Network (BCAN) Innovation Award
FX We acknowledge Jon Serody and Ned Sharpless for useful discussions and
   the entire UNCseq team (in particular, Michele Hayward and Ashley
   Salazar) for their dedication and work. This work was supported by NIH
   grants R01 CA142794 (to W.Y. Kim), U24 CA143848 (to D.N. Hayes), U24
   CA143848-02S1 (to D.N. Hayes), and U10 CA181009-01 (to D.N. Hayes); the
   University Cancer Research Fund (to W.Y. Kim and D.N. Hayes); AACR Kure
   It (to W.Y. Kim); and the Bladder Cancer Advocacy Network (BCAN)
   Innovation Award (to W.Y. Kim). W.Y. Kim is a Damon Runyon Merck
   Clinical Investigator.
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NR 61
TC 28
Z9 30
U1 0
U2 12
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 2015 MANCHESTER RD, ANN ARBOR, MI 48104 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD FEB
PY 2015
VL 125
IS 2
BP 462
EP 468
DI 10.1172/JCI68339
PG 7
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA CA5QK
UT WOS:000348962700003
PM 25642706
OA Green Published, Bronze, Green Submitted
DA 2025-01-04
ER

PT J
AU Kwon, JH
   Jeong, BK
   Yoon, YS
   Yu, CS
   Kim, J
AF Kwon, Jeong-Hwa
   Jeong, Byung-Kwan
   Yoon, Yong Sik
   Yu, Chang Sik
   Kim, Jihun
TI Utility of BRAF VE1 Immunohistochemistry as a Screening Tool for
   Colorectal Cancer Harboring <i>BRAF</i> V600E Mutation
SO JOURNAL OF PATHOLOGY AND TRANSLATIONAL MEDICINE
LA English
DT Article
DE Colorectal neoplasms; BRAF mutation; Immunohistochemistry; DNA
   sequencing
ID MICROSATELLITE INSTABILITY; ANTIBODY; CARCINOMA; SPECIMENS; COLON; KRAS
AB Background: BRAF mutation has been recognized as an important biomarker of colorectal cancer (CRC) for targeted therapy and prognosis prediction. However, sequencing for every CRC case is not cost-effective. An antibody specific for BRAF V600E mutant protein has been introduced, and we thus examined the utility of BRAF VE1 immunohistochemistry for evaluating BRAF mutations in CRC. Methods: Fifty-one BRAF-mutated CRCs and 100 age and sex-matched BRAF wild-type CRCs between 2005 and 2015 were selected from the archives of Asan Medical Center. Tissue microarrays were constructed and stained with BRAF VE1 antibody. Results: Forty-nine of the 51 BRAF-mutant CRCs (96.1%) showed more than moderate cytoplasmic staining, except for two weakly stained cases. Six of 100 BRAF wild-type cases also stained positive with BRAF VE1 antibody; four stained weakly and two stained moderately. Normal colonic crypts showed nonspecific weak staining, and a few CRC cases exhibited moderate nuclear reactivity (3 BRAF-mutant and 10 BRAF wild-type cases). BRAF-mutated CRC patients had higher pathologic stages and worse survival than BRAF wild-type patients. Conclusions: BRAF VE1 immunohistochemistry showed high sensitivity and specificity, but occasional nonspecific staining in tumor cell nuclei and normal colonic crypts may limit their routine clinical use. Thus, BRAF VE1 immunohistochemistry may be a useful screening tool for BRAF V600E mutation in CRCs, provided that additional sequencing studies can be done to confirm the mutation in BRAF VE1 antibody-positive cases.
C1 [Kwon, Jeong-Hwa; Jeong, Byung-Kwan; Kim, Jihun] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pathol, 88 Olymp Ro 43 Gil, Seoul 05505, South Korea.
   [Yoon, Yong Sik; Yu, Chang Sik] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Surg, Seoul, South Korea.
C3 University of Ulsan; University of Ulsan; Asan Medical Center
RP Kim, J (corresponding author), Univ Ulsan, Coll Med, Asan Med Ctr, Dept Pathol, 88 Olymp Ro 43 Gil, Seoul 05505, South Korea.
EM jihunkim@amc.seoul.kr
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NR 17
TC 10
Z9 11
U1 1
U2 3
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 MAY
PY 2018
VL 52
IS 3
BP 157
EP 163
DI 10.4132/jptm.2018.03.28
PG 7
WC Pathology
WE Emerging Sources Citation Index (ESCI)
SC Pathology
GA GF6GU
UT WOS:000432065900003
PM 29590746
OA Green Submitted, Green Published, gold
DA 2025-01-04
ER

PT J
AU Banias, L
   Jung, I
   Chiciudean, R
   Gurzu, S
AF Banias, Laura
   Jung, Ioan
   Chiciudean, Rebeca
   Gurzu, Simona
TI From Dukes-MAC Staging System to Molecular Classification: Evolving
   Concepts in Colorectal Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE Dukes MAC staging; colorectal cancer; molecular classification; TNM;
   epithelial-mesenchymal transition
ID TUMOR DEPOSITS; RECTAL-CANCER; COLON; CARCINOMA; SUBTYPES; MASPIN;
   ADENOCARCINOMA; SURVIVAL; EDITION
AB This historical review aimed to summarize the main changes that colorectal carcinoma (CRC) staging systems suffered over time, starting from the creation of the classical Duke's classification, modified Astler-Coller staging, internationally used TNM (T-primary tumor, N-regional lymph nodes' status, M-distant metastases) staging system, and ending with molecular classifications and epithelial-mesenchymal transition (EMT) concept. Besides currently used staging parameters, this paper briefly presents the author's contribution in creating an immunohistochemical (IHC)-based molecular classification of CRC. It refers to the identification of three molecular groups of CRCs (epithelial, mesenchymal and hybrid) based on the IHC markers E-cadherin, beta-catenin, maspin, and vimentin. Maspin is a novel IHC antibody helpful for tumor budding assessment, which role depends on its subcellular localization (cytoplasm vs. nuclei). The long road of updating the staging criteria for CRC has not come to an end. The newest prognostic biomarkers, aimed to be included in the molecular classifications, exert predictive roles, and become more and more important for targeted therapy decisions.
C1 [Banias, Laura; Jung, Ioan; Chiciudean, Rebeca; Gurzu, Simona] George Emil Palade Univ Med, Dept Pathol, Pharm Sci & Technol, 38 Gheorghe Marinescu St, Targu Mures 540139, Romania.
   [Gurzu, Simona] George Emil Palade Univ Med, Res Ctr Oncopathol & Transdisciplinary Res CCOMT, Pharm Sci & Technol, Targu Mures 540136, 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
RP Chiciudean, R (corresponding author), George Emil Palade Univ Med, Dept Pathol, Pharm Sci & Technol, 38 Gheorghe Marinescu St, Targu Mures 540139, Romania.
EM rebeca.peica@gmail.com
RI Banias, Laura/AAB-9233-2022; Chiciudean, Rebeca/IAO-8926-2023
OI BANIAS, LAURA/0000-0002-2240-2540; gurzu, simona/0000-0003-3968-5118
FU "George Emil Palade" University of Medicine, Pharmacy, Science and
   Technologies of Targu Mures, Romania [615/5/2019]
FX This research was supported by the "George Emil Palade" University of
   Medicine, Pharmacy, Science and Technologies of Targu Mures, Romania
   (grant no. 615/5/2019).
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NR 67
TC 14
Z9 14
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD AUG
PY 2022
VL 23
IS 16
AR 9455
DI 10.3390/ijms23169455
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 4B4TT
UT WOS:000845772600001
PM 36012726
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Wang, B
   Li, H
   Wang, XC
   Zhu, XG
AF Wang, Bin
   Li, Hao
   Wang, Xuchao
   Zhu, Xinguo
TI The association of aberrant expression of NLRP3 and p-S6K1 in colorectal
   cancer
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Article
DE Colorectal carcinoma; mTOR-S6K1 pathway; NLRP3; Prognosis
ID MAPK SIGNALING PATHWAY; NF-KAPPA-B; INFLAMMASOME ACTIVATION;
   CROHNS-DISEASE; APOPTOSIS; RECEPTORS; COLON
AB Colorectal carcinoma (CRC) is one of the most common malignancies worldwide, and except for surgery, treatments effects are limited. Recently, NLRP3 has been reported as an activator in the tumorigenesis of CRC. However, the function and mechanism of NLRP3 in CRC remains elusive. In this study, we revealed that NLRP3 was elevated in CRC tissues and related to clinical factors, such as lymph node invasion and tumor-node-metastasis (TNM) stage. Moreover, NLRP3-positive patients had a poor prognosis. Furthermore, univariate and multivariate analysis revealed that NLRP3 expression was an independent prognostic factor for the survival of CRC patients. We investigated whether NLRP3 linked with the mTOR-S6K1 pathway. The expression of p-S6K1 was upregulated in CRC tissues and NLRP3 expression level was positively associated with the p-S6K1 level. Thus, targeting NLRP3 may be promising for targeted therapy of CRC, especially for mTORC1-targeted resistant patients.
C1 [Wang, Bin; Li, Hao; Wang, Xuchao; Zhu, Xinguo] Soochow Univ, Dept Gen Surg, Affiliated Hosp 1, Suzhou 215006, Jiangsu, Peoples R China.
C3 Soochow University - China
RP Zhu, XG (corresponding author), Soochow Univ, Dept Gen Surg, Affiliated Hosp 1, Suzhou 215006, Jiangsu, Peoples R China.
EM xgzhu45@163.com
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NR 37
TC 20
Z9 22
U1 0
U2 7
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
EI 1618-0631
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD JAN
PY 2020
VL 216
IS 1
AR 152737
DI 10.1016/j.prp.2019.152737
PG 7
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA KZ9RT
UT WOS:000523597200030
PM 31757663
DA 2025-01-04
ER

PT J
AU Hussein, NH
   Amin, NS
   El Tayebi, HM
AF Hussein, Nada H.
   Amin, Nada S.
   El Tayebi, Hend M.
TI GPI-AP: Unraveling a New Class of Malignancy Mediators and Potential
   Immunotherapy Targets
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE glycosylphosphatidylinositol; glycosylphosphatidylinositol-anchored
   protein; immunotherapy; cancer; immunology
ID HUMAN CARCINOEMBRYONIC ANTIGEN; DECAY-ACCELERATING FACTOR;
   COLORECTAL-CANCER; ANCHORED PROTEINS; T-CELLS; IN-VIVO;
   GLYCOSYLPHOSPHATIDYLINOSITOL ANCHOR; GLYPICAN-3 EXPRESSION; THERAPEUTIC
   TARGET; ANTITUMOR-ACTIVITY
AB With millions of cases diagnosed annually and high economic burden to cover expensive costs, cancer is one of the most difficult diseases to treat due to late diagnosis and severe adverse effects from conventional therapy. This creates an urgent need to find new targets for early diagnosis and therapy. Progress in research revealed the key steps of carcinogenesis. They are called cancer hallmarks. Zooming in, cancer hallmarks are characterized by ligands binding to their cognate receptor and so triggering signaling cascade within cell to make response for stimulus. Accordingly, understanding membrane topology is vital. In this review, we shall discuss one type of transmembrane proteins: Glycosylphosphatidylinositol-Anchored Proteins (GPI-APs), with specific emphasis on those involved in tumor cells by evading immune surveillance and future applications for diagnosis and immune targeted therapy.
C1 [Hussein, Nada H.; Amin, Nada S.; El Tayebi, Hend M.] German Univ Cairo, Fac Pharm & Biotechnol, Dept Pharmacol & Toxicol, Mol Pharmacol Res Grp, Cairo, Egypt.
C3 Egyptian Knowledge Bank (EKB); German University in Cairo
RP El Tayebi, HM (corresponding author), German Univ Cairo, Fac Pharm & Biotechnol, Dept Pharmacol & Toxicol, Mol Pharmacol Res Grp, Cairo, Egypt.
EM hend.saber@guc.edu.eg
OI Amin, Nada/0000-0002-9541-549X
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NR 128
TC 11
Z9 13
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 DEC 4
PY 2020
VL 10
AR 537311
DI 10.3389/fonc.2020.537311
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PG2LZ
UT WOS:000599573500001
PM 33344222
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Du, Y
   Zhang, Q
   Jing, LJ
   Liang, XL
   Chi, CW
   Li, YQ
   Yang, X
   Dai, ZF
   Tian, J
AF Du, Yang
   Zhang, Qian
   Jing, Lijia
   Liang, Xiaolong
   Chi, Chongwei
   Li, Yaqian
   Yang, Xin
   Dai, Zhifei
   Tian, Jie
TI GX1-conjugated poly(lactic acid) nanoparticles encapsulating Endostar
   for improved in vivo anticolorectal cancer treatment
SO INTERNATIONAL JOURNAL OF NANOMEDICINE
LA English
DT Article
DE GX1 peptide; Endostar; colorectal cancer; angiogenesis; IRDye 800CW;
   molecular imaging
ID RECOMBINANT HUMAN ENDOSTATIN; INTEGRIN ALPHA(V)BETA(3); TUMOR
   ANGIOGENESIS; GASTRIC-CANCER; VASCULATURE; ACTIVATION; RESISTANCE;
   DELIVERY; GX1
AB Tumor angiogenesis plays a key role in tumor growth and metastasis; thus, targeting tumor-associated angiogenesis is an important goal in cancer therapy. However, the efficient delivery of drugs to tumors remains a key issue in antiangiogenesis therapy. GX1, a peptide identified by phage-display technology, is a novel tumor vasculature endothelium-specific ligand and possesses great potential as a targeted vector and antiangiogenic agent in the diagnosis and treatment of human cancers. Endostar, a novel recombinant human endostatin, has been shown to inhibit tumor angiogenesis. In this study, we developed a theranostic agent composed of GX1-conjugated poly(lactic acid) nanoparticles encapsulating Endostar (GPENs) and labeled with the near-infrared dye IRDye 800CW to improve colorectal tumor targeting and treatment efficacy in vivo. The in vivo fluorescence molecular imaging data showed that GPENs (IRDye 800CW) more specifically targeted tumors than free IRDye 800CW in colorectal tumor-bearing mice. Moreover, the antitumor efficacy was evaluated by bioluminescence imaging and immunohistology, revealing that GPENs possessed improved antitumor efficacy on subcutaneous colorectal xenografts compared to other treatment groups. Thus, our study showed that GPENs, a novel GX1 peptide guided form of nanoscale Endostar, can be used as a theranostic agent to facilitate more efficient targeted therapy and enable real-time monitoring of therapeutic efficacy in vivo.
C1 [Du, Yang; Zhang, Qian; Chi, Chongwei; Li, Yaqian; Yang, Xin; Tian, Jie] Chinese Acad Sci, Inst Automat, State Key Lab Management & Control Complex, Key Lab Mol Imaging, Beijing 100190, Peoples R China.
   [Jing, Lijia; Liang, Xiaolong; Dai, Zhifei] Peking Univ, Coll Engn, Dept Biomed Engn, Beijing 100871, Peoples R China.
C3 Chinese Academy of Sciences; Institute of Automation, CAS; Peking
   University
RP Tian, J (corresponding author), Chinese Acad Sci, Inst Automat, State Key Lab Management & Control Complex, Key Lab Mol Imaging, 95 ZhongGuanCun East Rd, Beijing 100190, Peoples R China.
EM jie.tian@ia.ac.cn
RI du, yang/V-1086-2019; Tian, Jie/H-1190-2011; Liang,
   Xiaolong/M-1941-2018; Dai, Zhifei/B-1812-2012
OI RAMLI, ZARINA/0009-0007-1729-7057
FU National Basic Research Program of China (973) [2011CB707702,
   2014CB748600, 2015CB755500]; National Natural Science Foundation of
   China [81227901, 81470083]; State Key Laboratory of Management and
   Control for Complex Systems [Y3S9021F30]
FX This work was supported by the National Basic Research Program of China
   (973) (under grants 2011CB707702, 2014CB748600, and 2015CB755500) and
   the National Natural Science Foundation of China (81227901 and
   81470083). This work was supported in part by the State Key Laboratory
   of Management and Control for Complex Systems (under grant no
   Y3S9021F30).
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TC 28
Z9 33
U1 1
U2 39
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 2015
VL 10
BP 3791
EP 3802
DI 10.2147/IJN.S82029
PG 12
WC Nanoscience & Nanotechnology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Pharmacology & Pharmacy
GA CJ0OY
UT WOS:000355177500001
PM 26060399
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Sehnalova, I
   Rihova, B
   Nemecek, R
   Kintrova, K
   Demlova, R
AF Sehnalova, Irena
   Rihova, Barbora
   Nemecek, Radim
   Kintrova, Katerina
   Demlova, Regina
TI THE REAL-WORLD COST AND EFFECTIVENESS STUDY OF TREATING mCRC WITH
   BEVACIZUMAB FOLLOWED BY CETUXIMAB OR PANITUMUMAB IN WT KRAS PATIENTS
SO FARMACIA
LA English
DT Article
DE bevacizumab; cetuximab; panitumumab; colorectal cancer; cost analysis
ID METASTATIC COLORECTAL-CANCER; PHASE-III; 1ST-LINE TREATMENT; PLUS
   IRINOTECAN; FLUOROURACIL; THERAPY; LEUCOVORIN; CHEMOTHERAPY;
   COMBINATION; MONOTHERAPY
AB Targeted monoclonal antibodies bevacizumab, cetuximab and panitumumab are reimbursed in the Czech Republic in combination with chemotherapy or alone in metastatic colorectal cancer (mCRC). However, the high cost is a potentially limiting factor. The real-world costs and effectiveness of first line bevacizumab followed by cetuximab or panitumumab (EGFRi) were retrospectively assessed from the perspective of healthcare payer. Total 71 WT KRAS patients (56% men; median age 60.5 years) were evaluated between April 2007 and May 2017. During our follow-up period (30 months on average) 55% patients died. The mean cost to PD was EUR 32,107 and EUR 24,510 in bevacizumab and EGFRi treatment respectively with median PFS 9.7 and 5.0 months. The median overall survival was 27.2 months and the mean cost from sequential therapy initiation to death was EUR 63,682. The targeted therapy made up 77%, 86% and 76% of the costs in the first line, second line and from the initiation of sequential therapy to death respectively.
C1 [Sehnalova, Irena; Rihova, Barbora; Demlova, Regina] Masaryk Univ, Fac Med, Dept Pharmacol, Kamenice 5, Brno 62500, Czech Republic.
   [Nemecek, Radim; Demlova, Regina] Masaryk Mem Canc Inst, Zluty Kopec 7, Brno 65653, Czech Republic.
   [Kintrova, Katerina] Masaryk Univ, Dept Bot & Zool, Fac Sci, Kotlarska 2, Brno 61137, Czech Republic.
C3 Masaryk University Brno; Masaryk Memorial Cancer Institute; Masaryk
   University Brno
RP Rihova, B (corresponding author), Masaryk Univ, Fac Med, Dept Pharmacol, Kamenice 5, Brno 62500, Czech Republic.
EM brihova@med.muni.cz
RI Demlova, Regina/AAI-2232-2020; Rihova, Barbora/AAU-9696-2020
OI Rihova, Barbora/0000-0003-3835-9062
FU MEYS, large infrastructure project CZECRIN [LM2015090]; European
   Regional Development Fund -Project CZECRIN_4 PACIENTY
   [CZ.02.1.01/0.0/0.0/16_ 013/0001826]
FX Supported by the state budget by the MEYS, large infrastructure project
   CZECRIN (No. LM2015090) and European Regional Development Fund -Project
   CZECRIN_4 PACIENTY (No. CZ.02.1.01/0.0/0.0/16_ 013/0001826).
CR [Anonymous], CANC INC
   [Anonymous], EC INF HLTH CAR
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   Vyzula R, MODRA KNIHA
NR 28
TC 5
Z9 5
U1 12
U2 25
PU SOC STIINTE FARMACEUTICE ROMANIA
PI BUCURESTI
PA BUCURESTI, STR TRAIAN VUIA 6, SECT 1, BUCURESTI, 020956, ROMANIA
SN 0014-8237
EI 2065-0019
J9 FARMACIA
JI Farmacia
PD MAY-JUN
PY 2020
VL 68
IS 3
BP 572
EP 578
DI 10.31925/farmacia.2020.3.25
PG 7
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA MC5KV
UT WOS:000543326400025
OA gold
DA 2025-01-04
ER

PT J
AU Kumar, AR
   Devan, AR
   Nair, B
   Vinod, BS
   Nath, LR
AF Kumar, Ayana R.
   Devan, Aswathy R.
   Nair, Bhagyalakshmi
   Vinod, Balachandran S.
   Nath, Lekshmi R.
TI Harnessing the immune system against cancer: current immunotherapy
   approaches and therapeutic targets
SO MOLECULAR BIOLOGY REPORTS
LA English
DT Review
DE Cancer immunotherapy; Checkpoint inhibitor; PD-1; PD-L1; CTLA-4; CAR T
   cells; Oncolytic viruses; Monoclonal antibodies; Cancer vaccines;
   Cytokines
ID HEAT-SHOCK PROTEINS; ANTIGEN-PRESENTING CELLS; GROWTH-FACTOR RECEPTOR;
   HUMAN DENDRITIC CELLS; HLA-G EXPRESSION; MONOCLONAL-ANTIBODY; PROGRAMMED
   DEATH-1; INNATE IMMUNITY; PD-1 PATHWAY; HOST-DEFENSE
AB Cancer immunotherapy is a rapidly evolving concept that has been given the tag "fifth pillar" of cancer therapy while radiation therapy, chemotherapy, surgery and targeted therapy remain the other four pillars. This involves the stimulation of the immune system to control tumor growth and it specifically targets the neoplastic cells rather than the normal cells. Conventional chemotherapy has many limitations which include drug resistance, recurrence of cancer and severe adverse effects. Immunology has made major treatment breakthroughs for several cancers such as colorectal cancer, prostate cancer, breast cancer, lung cancer, liver cancer, kidney cancer, stomach cancer, acute lymphoblastic leukaemia etc. Currently, therapeutic strategies harnessing the immune system involve Checkpoint inhibitors, Chimeric antigen receptor T cells (CAR T cells), Monoclonal antibodies, Cancer vaccines, Cytokines, Radio-immunotherapy and Oncolytic virus therapy. The molecular characterization of several tumor antigens (TA) indicates that these TA can be utilized as promising candidates in cancer immunotherapy strategies. Here in this review, we highlight and summarize the different categories of emerging cancer immunotherapies along with the immunologically recognized tumor antigens involved in the tumor microenvironment.
C1 [Kumar, Ayana R.; Devan, Aswathy R.; Nair, Bhagyalakshmi; Nath, Lekshmi R.] Amrita Vishwa Vidyapeetham, Dept Pharmacognosy, Amrita Sch Pharm, AIMS Hlth Sci Campus,Ponekkara PO, Kochi 682041, Kerala, India.
   [Vinod, Balachandran S.] Sree Narayana Coll, Dept Biochem, Kollam 691001, Kerala, India.
C3 Amrita Vishwa Vidyapeetham; Amrita Vishwa Vidyapeetham Kochi
RP Nath, LR (corresponding author), Amrita Vishwa Vidyapeetham, Dept Pharmacognosy, Amrita Sch Pharm, AIMS Hlth Sci Campus,Ponekkara PO, Kochi 682041, Kerala, India.; Vinod, BS (corresponding author), Sree Narayana Coll, Dept Biochem, Kollam 691001, Kerala, India.
EM drvinodsnc@gmail.com; lekshmirnath@aims.amrita.edu
RI Vinod, Balachandran/HKV-9215-2023
OI BALACHANDRAN, VINOD/0000-0002-0909-8855; Nath,
   Lekshmi.R/0000-0002-7726-7219; Nair, Bhagyalakshmi/0000-0002-0364-881X;
   , Ayana R Kumar/0000-0002-5338-8497
FU Amrita Vishwa Vidyapeetham
FX We acknowledge the support from Amrita Vishwa Vidyapeetham. We express
   our sincere gratitude to Dr Shanthikumar V Nair, Dean of research, AIMS
   and Dr Sabitha M, Principal, Amrita School of Pharmacy for all the
   facilities provided.
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NR 193
TC 54
Z9 57
U1 0
U2 18
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 DEC
PY 2021
VL 48
IS 12
BP 8075
EP 8095
DI 10.1007/s11033-021-06752-9
EA OCT 2021
PG 21
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA XA5BF
UT WOS:000709275100002
PM 34671902
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Cai, YX
   Wu, K
AF Cai, Yuxuan
   Wu, Ke
TI Exploration of the Dual Role of Dectin-1 in Tumor Development and Its
   Therapeutic Potential
SO CURRENT ONCOLOGY
LA English
DT Review
DE Dectin-1; tumor immunology; tumor microenvironment; targeted therapy;
   pattern recognition receptor
ID MACROPHAGES; RECOGNITION; ACTIVATION; INTERFERONS; NIVOLUMAB; MELANOMA
AB Immunotherapy, particularly immune checkpoint inhibitors like PD-1, PD-L1, and CTLA-4, has revolutionized cancer treatment. However, the role of the innate immune system, especially pattern recognition receptors, in cancer development and immunity is gaining more and more attention. Dectin-1, a C-type lectin receptor primarily involved in antifungal immunity, has emerged as a significant player in cancer biology, exhibiting both pro-tumor and anti-tumor roles. This dual function largely depends on the tumor type and microenvironment. Dectin-1 can promote immune responses against tumors like melanoma and breast cancer by enhancing both innate and adaptive immunity. However, in tumors like pancreatic ductal adenocarcinoma and colorectal cancer, Dectin-1 activation suppresses T cell immunity, facilitating tumor progression. This review explores the complex mechanisms by which Dectin-1 modulates the tumor microenvironment and discusses its potential as a therapeutic target for cancer treatment.
C1 [Cai, Yuxuan; Wu, Ke] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Gastrointestinal Surg, Wuhan 430022, Peoples R China.
C3 Huazhong University of Science & Technology
RP Wu, K (corresponding author), Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Gastrointestinal Surg, Wuhan 430022, Peoples R China.
EM m202276039@hust.edu.cn; wuke201288@hust.edu.cn
FU National Natural Science Foundation of China; General Project of Hubei
   Natural Science Foundation [2020CFB766];  [82273302]
FX This research was funded by the National Natural Science Foundation of
   China (No. 82273302), the General Project of Hubei Natural Science
   Foundation (No. 2020CFB766).
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NR 36
TC 0
Z9 0
U1 2
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 NOV
PY 2024
VL 31
IS 11
BP 7275
EP 7286
DI 10.3390/curroncol31110536
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA N4M3Y
UT WOS:001364096200001
PM 39590166
OA gold
DA 2025-01-04
ER

PT J
AU Zheng, YW
   Li, XC
   Kuang, LR
   Wang, Y
AF Zheng, Youwei
   Li, Xinchao
   Kuang, Lirun
   Wang, Yong
TI New insights into the characteristics of DRAK2 and its role in
   apoptosis: From molecular mechanisms to clinically applied potential
SO FRONTIERS IN PHARMACOLOGY
LA English
DT Review
DE DRAK2; DAPK; STK17B; apoptosis; targeted therapy
ID PROTEIN-KINASE ACTIVITY; ACUTE MYELOID-LEUKEMIA; BETA-CELL DEATH;
   GENE-EXPRESSION; DAP-KINASE; STEM-CELLS; ACTIVATION; INHIBITORS; CANCER;
   SIGNAL
AB As a member of the death-associated protein kinase (DAPK) family, DAP kinase-associated apoptosis-inducing kinase 2 (DRAK2) performs apoptosis-related functions. Compelling evidence suggests that DRAK2 is involved in regulating the activation of T lymphocytes as well as pancreatic beta-cell apoptosis in type I diabetes. In addition, DRAK2 has been shown to be involved in the development of related tumor and non-tumor diseases through a variety of mechanisms, including exacerbation of alcoholic fatty liver disease (NAFLD) through SRSF6-associated RNA selective splicing mechanism, regulation of chronic lymphocytic leukemia and acute myeloid leukemia, and progression of colorectal cancer. This review focuses on the structure, function, and upstream pathways of DRAK2 and discusses the potential and challenges associated with the clinical application of DRAK2-based small-molecule inhibitors, with the aim of advancing DRAK2 research.
C1 [Zheng, Youwei; Li, Xinchao; Kuang, Lirun; Wang, Yong] China Med Univ, Dept Gen Surg, Affiliated Hosp 4, Shenyang, Peoples R China.
C3 China Medical University
RP Wang, Y (corresponding author), China Med Univ, Dept Gen Surg, Affiliated Hosp 4, Shenyang, Peoples R China.
EM wangyong@cmu.edu.cn
FU Shenyang Young and Middle-aged Science and Technology Innovation Talent
   Support Program; Liaoning Province Livelihood Science and Technology
   Program;  [RC200607];  [2021JH2/10300012]
FX Funding Shenyang Young and Middle-aged Science and Technology Innovation
   Talent Support Program (RC200607), Liaoning Province Livelihood Science
   and Technology Program Project Authors' contributions
   (2021JH2/10300012).
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NR 148
TC 5
Z9 5
U1 1
U2 24
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1663-9812
J9 FRONT PHARMACOL
JI Front. Pharmacol.
PD OCT 28
PY 2022
VL 13
AR 1014508
DI 10.3389/fphar.2022.1014508
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 6E9LY
UT WOS:000883695000001
PM 36386181
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Sun, XT
   Li, Q
AF Sun, Xiaoting
   Li, Qi
TI Prostaglandin EP2 receptor: Novel therapeutic target for human cancers
   (Review)
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Review
DE EP2; mechanism; cancer; invasion; inflammation
ID SIGNALING PATHWAYS; GENE-EXPRESSION; PROSTANOID RECEPTORS;
   COLORECTAL-CANCER; DENDRITIC CELLS; E-2 RECEPTORS; UP-REGULATION;
   TUMOR-GROWTH; MOUSE SKIN; G-PROTEINS
AB Prostaglandin E2 (PGE2) receptor 2 subtype (EP2), which is a metabolite of arachidonic acid that binds with and regulates cellular responses to PGE2, is associated with numerous physiological and pathological events in a wide range of tissues. As a stimulatory G protein-coupled receptor, PGE2-induced EP2 activation can activate adenylate cyclase, leading to increased cytoplasmic cAMP levels and activation of protein kinase A. The EP2 receptor can also activate the glycogen synthase kinase 3 beta and beta-catenin pathways. The present study aimed to review the roles of the EP2 receptor in tumor development, including immunity, chronic inflammation, angiogenesis, metastasis and multidrug resistance. Furthermore, the involvement of the EP2 receptor signaling pathway in cancer was discussed. Understanding the role and mechanisms of action of the EP2 receptor, and its importance in targeted therapy, may help identify novel methods to improve management of numerous types of cancer.
C1 [Li, Qi] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Med Oncol, 528 Zhangheng Rd, Shanghai 201203, Peoples R China.
   [Li, Qi] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Canc Inst Integrat Med, 528 Zhangheng Rd, Shanghai 201203, Peoples R China.
C3 Shanghai University of Traditional Chinese Medicine; Shanghai University
   of Traditional Chinese Medicine
RP Li, Q (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Med Oncol, 528 Zhangheng Rd, Shanghai 201203, Peoples R China.; Li, Q (corresponding author), Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Canc Inst Integrat Med, 528 Zhangheng Rd, Shanghai 201203, Peoples R China.
EM lzwf@hotmail.com
FU International Cooperation Key Project of the National Natural Science
   Foundation of China [81520108031]; Science Foundation of Shanghai
   Committee of Science Project [14430722900]; Program for Outstanding
   Medical Academic Leader and Shanghai Academic Research Leader
   [16XD1403600]
FX This study was supported by the International Cooperation Key Project of
   the National Natural Science Foundation of China (grant no. 81520108031
   to Q.L.), the Science Foundation of Shanghai Committee of Science
   Project (grant no. 14430722900), and the Program for Outstanding Medical
   Academic Leader and Shanghai Academic Research Leader (grant no.
   16XD1403600).
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NR 115
TC 35
Z9 38
U1 1
U2 21
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1107-3756
EI 1791-244X
J9 INT J MOL MED
JI Int. J. Mol. Med.
PD SEP
PY 2018
VL 42
IS 3
BP 1203
EP 1214
DI 10.3892/ijmm.2018.3744
PG 12
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA GW4IE
UT WOS:000446875200001
PM 29956743
OA Bronze
DA 2025-01-04
ER

PT J
AU Geng, YT
   Zheng, X
   Zhang, DC
   Wei, SS
   Feng, J
   Wang, W
   Zhang, L
   Wu, CP
   Hu, WW
AF Geng, Yiting
   Zheng, Xiao
   Zhang, Dachuan
   Wei, Shanshan
   Feng, Jun
   Wang, Wei
   Zhang, Luo
   Wu, Changping
   Hu, Wenwei
TI CircHIF1A induces cetuximab resistance in colorectal cancer by promoting
   HIF1α-mediated glycometabolism alteration
SO BIOLOGY DIRECT
LA English
DT Article
DE Colorectal cancer; Cetuximab; CircHIF1A; HIF1 alpha
ID 1ST-LINE TREATMENT; RAS MUTATIONS; HYPOXIA; CHEMOTHERAPY; BEVACIZUMAB;
   CONTRIBUTES; OXALIPLATIN; EXPRESSION; HIF-1; KRAS
AB Epidermal growth factor receptor (EGFR)-targeted therapy is an important treatment for RAS wild-type metastatic colorectal cancer (mCRC), but the resistance mechanism remains unclear. Here, the differential expression of circRNAs between Cetuximab sensitive and resistant cell lines was analyzed using whole-transcriptome sequencing. We identified that the expression of circHIF1A was significantly higher in LIM1215-R than in LIM1215. When treated with Cetuximab, downregulation of circHIF1A level weakened the proliferation and clonal formation ability of LIM1215-R, caused more cells to enter G0-G1 phase, and significantly reduced the basal respiration, ATP production, and maximal respiration, as well as the glycolytic capacity and glycolytic reserve. The response rate and prognosis of circHIF1A-positive patients were inferior to those of negative patients. Mechanistically, circHIF1A can upregulate the level of hypoxia-inducible factor 1 A (HIF1A) by competitively binding to miR-361-5p, inducing the overexpression of enzymes such as glucose transporter 1 (GLUT1) and lactate dehydrogenase A (LDHA). In a xenograft model, inhibition of circHIF1A expression increased the sensitivity to Cetuximab treatment. In conclusion, circHIF1A can promote HIF1 alpha-mediated glycometabolism alteration to induce Cetuximab resistance in CRC. It has the potential to become a screening indicator for the Cetuximab beneficial population in mCRC and a new therapeutic target for enhancing treatment efficacy.
C1 [Geng, Yiting; Wei, Shanshan; Feng, Jun; Wang, Wei; Zhang, Luo; Wu, Changping; Hu, Wenwei] Soochow Univ, Affiliated Hosp 3, Dept Oncol, Changzhou 213003, Jiangsu, Peoples R China.
   [Zheng, Xiao; Wu, Changping] Soochow Univ, Affiliated Hosp 3, Dept Tumor Biol Treatment, Changzhou 213003, Jiangsu, Peoples R China.
   [Zheng, Xiao; Hu, Wenwei] Soochow Univ, Affiliated Hosp 3, Jiangsu Engn Res Ctr Tumor Immunotherapy, Changzhou 213003, Jiangsu, Peoples R China.
   [Zhang, Dachuan] Soochow Univ, Affiliated Hosp 3, Dept Pathol, Changzhou 213003, Jiangsu, Peoples R China.
C3 Soochow University - China; Soochow University - China; Soochow
   University - China; Soochow University - China
RP Wu, CP; Hu, WW (corresponding author), Soochow Univ, Affiliated Hosp 3, Dept Oncol, Changzhou 213003, Jiangsu, Peoples R China.; Wu, CP (corresponding author), Soochow Univ, Affiliated Hosp 3, Dept Tumor Biol Treatment, Changzhou 213003, Jiangsu, Peoples R China.; Hu, WW (corresponding author), Soochow Univ, Affiliated Hosp 3, Jiangsu Engn Res Ctr Tumor Immunotherapy, Changzhou 213003, Jiangsu, Peoples R China.
EM wcpjjt@163.com; huwenwei@suda.edu.cn
RI zhang, ying/HJB-1230-2022; wei, shanshan/GSD-9000-2022
FU National Natural Science Foundation of China [82002479, 81902386];
   Natural Science Foundation of Jiangsu Province [BK20200179, BK20211065];
   Basic Research Project of Changzhou Science and Technology Bureau
   [CJ20200116]; Young Talent Development Plan of Changzhou Health
   Commission [CZQM2020006]; Young Scientific and Technological Talent
   Support Project of Changzhou [202162]; Changzhou "14th Five-Year Plan"
   High-level Health Personnel Training Project [2022260]; China
   Postdoctoral Science Foundation [2021M700547]; Academy of Finland (AKA)
   [202162] Funding Source: Academy of Finland (AKA)
FX This work was supported by National Natural Science Foundation of China
   (No. 82002479, 81902386), Natural Science Foundation of Jiangsu Province
   (No. BK20200179, BK20211065), Basic Research Project of Changzhou
   Science and Technology Bureau (No. CJ20200116), Funding from Young
   Talent Development Plan of Changzhou Health Commission (No.
   CZQM2020006), Funding from Young Scientific and Technological Talent
   Support Project of Changzhou (202162), Changzhou "14th Five-Year Plan"
   High-level Health Personnel Training Project (2022260) and China
   Postdoctoral Science Foundation (2021M700547).
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NR 49
TC 3
Z9 3
U1 0
U2 0
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1745-6150
J9 BIOL DIRECT
JI Biol. Direct
PD MAY 7
PY 2024
VL 19
IS 1
AR 36
DI 10.1186/s13062-024-00478-x
PG 15
WC Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics
GA PQ1F4
UT WOS:001215448100002
PM 38715141
OA gold
DA 2025-01-04
ER

PT J
AU Chan, WL
   Ma, T
   Cheung, KL
   Choi, H
   Wong, J
   Lam, KO
   Yuen, KK
   Luk, MY
   Kwong, D
AF Chan, Wing-Lok
   Ma, Tiffany
   Cheung, Kwok-Leung
   Choi, Horace
   Wong, Josiah
   Lam, Ka-On
   Yuen, Kwok-Keung
   Luk, Mai-Yee
   Kwong, Dora
TI The predictive value of G8 and the Cancer and aging research group
   chemotherapy toxicity tool in treatment-related toxicity in older
   Chinese patients with cancer
SO JOURNAL OF GERIATRIC ONCOLOGY
LA English
DT Article
DE Treatment; Prediction; Toxicities; Assessment; Chinese; Screening
ID CELL LUNG-CANCER; ADJUVANT CHEMOTHERAPY; GERIATRIC ASSESSMENT; DOSE
   INTENSITY; COLON-CANCER; ADULTS; REGORAFENIB; CONSENSUS; SURVIVAL;
   TRIALS
AB Introduction: Older patients experience a higher risk of treatment-related toxicity (TRT). The G8 screening tool was developed to separate cancer older patients fit to receive standard treatment from those who are frail and experiencing functional decline due to reduced organ function and multiple comorbidities. The Cancer and Aging Research Group chemotherapy toxicity tool (CARG-tt) questionnaire was developed to predict chemotherapy toxicity in geriatric patients. This prospective observational study evaluated the performance of G8 and CARG-tt in predicting severe TRT in older Chinese cancer patients.
   Methods: Chinese patients aged >= 65 with a diagnosis of solid malignancy and scheduled to receive anti-cancer treatment (chemotherapy or targeted therapy) were enrolled from March 2016 to July 2017 at the Department of Clinical Oncology at Queen Mary Hospital in Hong Kong. All patients completed the G8 and CARG-tt screening and pre-treatment assessments before starting treatment. Patients were monitored for any severe TRT, which was defined by grades 3-5 using the National Cancer Institute's Common Terminology Criteria for Adverse Events v4.03, treatment discontinuation, or unexpected hospitalization from starting to 30 days after treatment.
   Results: A total of 259 patients (male: 154, 59.5%; median age: 73.4, age range: 65-93) were enrolled in the study. Two hundred and ten (81.1%) patients received chemotherapy while the rest (n = 49, 18.9%) received targeted therapy. Overall, 146 patients (56.8%) experienced severe TRT. The mean G8 score was 12.4 (SD: 2.8). The G8 score had a significant association with unexpected admission (cutoff: 14, 41.3% vs. 26.5%, p = 0.03) but not significant in other types of TRTs. The mean CARG-tt score was 7.67 (SD: 3.7); it was not associated with severe TRTs.
   Conclusions: The G8 and CARG-tt demonstrated a weak prediction of severe TRT in older Chinese cancer patients. Future studies need to develop predictive tools for TRT in patients receiving novel antineoplastic therapies, with a focus on subgroup analysis for different populations.
   (c) 2020 Elsevier Ltd. All rights reserved.
C1 [Chan, Wing-Lok; Ma, Tiffany; Choi, Horace; Wong, Josiah; Lam, Ka-On; Kwong, Dora] Univ Hong Kong, Dept Clin Oncol, Hong Kong, Peoples R China.
   [Cheung, Kwok-Leung] Univ Nottingham, Sch Med, Nottingham, England.
   [Yuen, Kwok-Keung; Luk, Mai-Yee] Queen Mary Hosp, Dept Clin Oncol, 1-F Professorial Block,102 Pokfulam Rd, Hong Kong, Peoples R China.
C3 University of Hong Kong; University of Nottingham; University of Hong
   Kong
RP Chan, WL (corresponding author), Queen Mary Hosp, Dept Clin Oncol, 1-F Professorial Block,102 Pokfulam Rd, Hong Kong, Peoples R China.
EM winglok@hku.hk
RI Lam, Ka/D-7948-2011
OI Cheung, Kwok-Leung/0000-0003-2973-0755; Choi,
   Horace/0000-0001-8387-8780; Ma, Tiffany SW/0000-0001-5980-6293
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NR 36
TC 17
Z9 18
U1 0
U2 5
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1879-4068
EI 1879-4076
J9 J GERIATR ONCOL
JI J. Geriatr. Oncol.
PD MAY
PY 2021
VL 12
IS 4
BP 557
EP 562
DI 10.1016/j.jgo.2020.10.013
EA MAY 2021
PG 6
WC Oncology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Geriatrics & Gerontology
GA RY2LT
UT WOS:000647749600008
PM 33127385
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Dinic, J
   Stojanov, SJ
   Dragoj, M
   Grozdanic, M
   Podolski-Renic, A
   Pesic, M
AF Dinic, Jelena
   Stojanov, Sofija Jovanovic
   Dragoj, Miodrag
   Grozdanic, Marija
   Podolski-Renic, Ana
   Pesic, Milica
TI Cancer Patient-Derived Cell-Based Models: Applications and Challenges in
   Functional Precision Medicine
SO LIFE-BASEL
LA English
DT Review
DE anticancer drugs; targeted therapy; functional assays; drug resistance;
   functional precision medicine
ID UNCOMMON EGFR MUTATIONS; ON-A-CHIP; LUNG-CANCER; COLORECTAL-CANCER;
   OPEN-LABEL; PHASE-III; 1ST-LINE TREATMENT; XENOGRAFT MODELS;
   MICROSATELLITE INSTABILITY; MOLECULAR-MECHANISMS
AB The field of oncology has witnessed remarkable progress in personalized cancer therapy. Functional precision medicine has emerged as a promising avenue for achieving superior treatment outcomes by integrating omics profiling and sensitivity testing of patient-derived cancer cells. This review paper provides an in-depth analysis of the evolution of cancer-directed drugs, resistance mechanisms, and the role of functional precision medicine platforms in revolutionizing individualized treatment strategies. Using two-dimensional (2D) and three-dimensional (3D) cell cultures, patient-derived xenograft (PDX) models, and advanced functional assays has significantly improved our understanding of tumor behavior and drug response. This progress will lead to identifying more effective treatments for more patients. Considering the limited eligibility of patients based on a genome-targeted approach for receiving targeted therapy, functional precision medicine provides unprecedented opportunities for customizing medical interventions according to individual patient traits and individual drug responses. This review delineates the current landscape, explores limitations, and presents future perspectives to inspire ongoing advancements in functional precision medicine for personalized cancer therapy.
C1 [Dinic, Jelena; Stojanov, Sofija Jovanovic; Dragoj, Miodrag; Grozdanic, Marija; Podolski-Renic, Ana; Pesic, Milica] Univ Belgrade, Inst Biol Res Sinisa Stankovic, Natl Inst Republ Serbia, Dept Neurobiol, Bulevar Despota Stefana 142, Belgrade 11108, Serbia.
C3 University of Belgrade
RP Pesic, M (corresponding author), Univ Belgrade, Inst Biol Res Sinisa Stankovic, Natl Inst Republ Serbia, Dept Neurobiol, Bulevar Despota Stefana 142, Belgrade 11108, Serbia.
EM jelena.dinic@ibiss.bg.ac.rs; sofija.jovanovic@ibiss.bg.ac.rs;
   miodrag.dragoj@ibiss.bg.ac.rs; marija.grozdanic@ibiss.bg.ac.rs;
   ana.podolski@ibiss.bg.ac.rs; camala@ibiss.bg.ac.rs
RI Pešić, Milica/I-4727-2019; Dragoj, Miodrag/AEK-7485-2022; Grozdanic,
   Marija/KBD-3999-2024; Dinic, Jelena/JQV-8913-2023; Jovanovic Stojanov,
   Sofija/JRX-2548-2023; Podolski-Renic, Ana/AFT-9806-2022
OI Pesic, Milica/0000-0002-9045-8239; Dinic, Jelena/0000-0003-3371-2381;
   Jovanovic Stojanov, Sofija/0000-0003-4348-6453; Grozdanic,
   Marija/0009-0007-7425-685X; Podolski-Renic, Ana/0000-0001-7412-3685
FU Science Fund of the Republic of Serbia [7739737]
FX This research was supported by the Science Fund of the Republic of
   Serbia, #7739737, Functional diagnostics in non-small cell lung
   carcinoma-a new concept for the improvement of personalized therapy in
   Serbian patients-Targeted Response.
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NR 263
TC 0
Z9 0
U1 4
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-1729
J9 LIFE-BASEL
JI Life-Basel
PD SEP
PY 2024
VL 14
IS 9
AR 1142
DI 10.3390/life14091142
PG 33
WC Biology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Microbiology
GA H5S1I
UT WOS:001324028100001
PM 39337925
OA gold
DA 2025-01-04
ER

PT J
AU Ju, JL
   Wu, YH
   He, W
   Zhan, L
   Yin, XL
   Zhang, JF
   Zhang, YX
   Qiu, L
   Muhammad, P
   Reis, RL
   Li, CC
AF Ju, Jiale
   Wu, Yinghua
   He, Wen
   Zhan, Lin
   Yin, Xuelian
   Zhang, Junfeng
   Zhang, Yuxi
   Qiu, Li
   Muhammad, Pir
   Reis, Rui L.
   Li, Chenchen
TI Nanocarriers for Active Ingredients of Chinese Medicine (AIFCM) Used in
   Gastrointestinal Cancer Therapy
SO JOURNAL OF BIOMEDICAL NANOTECHNOLOGY
LA English
DT Review
DE Traditional Chinese Medicine; Nanocarriers; Gastrointestinal Cancer;
   Molecular Mechanism; Targeted Therapy
ID SOLID LIPID NANOPARTICLES; BOVINE SERUM-ALBUMIN; ENDOSCOPIC MUCOSAL
   RESECTION; POLYMER HYBRID NANOPARTICLES; DRUG-DELIVERY SYSTEM;
   CELL-CYCLE ARREST; COLON-CANCER; GASTRIC-CANCER; IN-VITRO; ORAL DELIVERY
AB Active ingredients of Chinese medicine (AIFCM) are pharmacological substances taken from traditional Chinese medicine that show promise in treating gastrointestinal cancer. Compared with traditional chemotherapeutic drugs, AIFCM have advantages such as multi-target and multi-level treatment of gastrointestinal cancer. Nanocarriers have the following advantages, better bioavailability, passive or active targeting of tumor sites and responsive release of drugs. The use of nanocarriers for delivery of AIFCM in treatment of gastrointestinal cancer, can overcome the disadvantages of some AIFCM, such as insolubility and low bioavailability. In this review, we first outline the background on gastrointestinal cancer, main curative factors and conventional therapeutic approaches. Then, the mechanisms for AIFCM in gastrointestinal cancer therapy are presented in the following four aspects: gene regulation, immune modulation, cellular pathway transduction, and alteration of intestinal flora. Thirdly, preparation of various nanocarriers and results when combining AIFCM in gastrointestinal cancer are presented. Fourth, application of novel targeted nanocarriers and responsive nanocarriers in gastrointestinal tumors is further introduced. Finally, the application of AIFCM in the treatment of gastrointestinal cancer is summarized and prospected, hoping to shed some light on the nanocarrier-bound AIFCM in the treatment of gastrointestinal cancer.
C1 [Ju, Jiale; Wu, Yinghua; He, Wen; Zhan, Lin; Yin, Xuelian; Zhang, Junfeng; Zhang, Yuxi; Qiu, Li; Li, Chenchen] Shanghai Univ, Sch Med, Shanghai 200444, Peoples R China.
   [Muhammad, Pir] Hainan Med Univ, Sch Pharm, Key Lab Trop Translat Med Minist Educ, Hainan Prov Key Lab Res & Dev Trop Herbs, Haikou 571199, Hainan, Peoples R China.
   [Ju, Jiale; Wu, Yinghua; He, Wen; Zhan, Lin; Yin, Xuelian; Zhang, Junfeng; Zhang, Yuxi; Qiu, Li; Li, Chenchen] Shanghai Univ, Sch Environm & Chem Engn, Inst Nanochem & Nanobiol, Shanghai 200444, Peoples R China.
   [Reis, Rui L.] Univ Minho, 3Bs Res Grp, I3Bs Res Inst Biomat Biodegradables & Biomimet, Headquarters European Inst Excellence Tissue Engn, P-4805017 Guimaraes, Portugal.
C3 Shanghai University; Hainan Medical University; Shanghai University;
   Universidade do Minho
RP Li, CC (corresponding author), Shanghai Univ, Sch Med, Shanghai 200444, Peoples R China.; Li, CC (corresponding author), Shanghai Univ, Sch Environm & Chem Engn, Inst Nanochem & Nanobiol, Shanghai 200444, Peoples R China.
EM lichenchen0128@163.com
RI Muhammad, Pir/B-3202-2019; zhang, junfeng/JHT-7871-2023; Li,
   Chenchen/JMQ-9349-2023; Reis, Rui L./A-8938-2008; Muhammad,
   Pir/Q-5275-2019
OI Li, Chenchen/0000-0002-5888-414X; Reis, Rui L./0000-0002-4295-6129;
   Muhammad, Pir/0000-0001-5960-0279
FU National Natural Science Foundation of China [11575107, 22003038,
   81922037]
FX This work has been supported by the National Natural Science Foundation
   of China (11575107, 22003038, and 81922037).
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NR 249
TC 0
Z9 0
U1 6
U2 54
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 OCT
PY 2022
VL 18
IS 10
BP 2279
EP 2314
DI 10.1166/jbn.2022.3446
PG 36
WC Nanoscience & Nanotechnology; Materials Science, Biomaterials
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics; Materials Science
GA 8R3SV
UT WOS:000927815100001
DA 2025-01-04
ER

PT J
AU Zhang, KL
   Zhu, SJ
   Liu, YW
   Dong, XQ
   Shi, ZD
   Zhang, AL
   Liu, CY
   Chen, LY
   Wei, JW
   Pu, PY
   Zhang, JN
   Jiang, T
   Han, L
   Kang, CS
AF Zhang, Kailiang
   Zhu, Shanjun
   Liu, Yanwei
   Dong, Xiaoqun
   Shi, Zhendong
   Zhang, Anling
   Liu, Chaoyong
   Chen, Luyue
   Wei, Jianwei
   Pu, Peiyu
   Zhang, Jianning
   Jiang, Tao
   Han, Lei
   Kang, Chunsheng
TI ICAT inhibits glioblastoma cell proliferation by suppressing
   Wnt/β-catenin activity
SO CANCER LETTERS
LA English
DT Article
DE ICAT; Glioma; Wnt; beta-catenin; Proliferation
ID BETA-CATENIN; INTERACTING PROTEIN; COLORECTAL-CANCER; MALIGNANT GLIOMA;
   IDH2 MUTATIONS; INVASION; OVEREXPRESSION; EGFR; EXPRESSION; SURVIVAL
AB Inhibitor of beta-catenin and T-cell factor (ICAT) is a key component of Wnt/beta-catenin signaling. ICAT blocks the formation of the beta-catenin/TCF complex and has been demonstrated to be involved in embryonic development and carcinogenesis. As an inhibitor of canonical Wnt signaling, ICAT was presumed to be a tumor-suppressor gene. However, the ICAT functions in human glioma remain unknown. In this study, we evaluated the expression of ICAT in 305 human glioma tissues and found that negative ICAT expression correlated with higher grade glioma and poor survival in patients with glioma. Then we transfected glioma cells with ICAT plasmid. Western blotting showed an increased ICAT protein expression level in glioma cells. MTT assay, flow cytometry and cell invasion assay were used to detect cell proliferation, cell cycle distribution, apoptosis and invasion. Our studies confirmed that ICAT inhibits glioma cell proliferation and invasion, and it induces cell apoptosis and cell cycle progression arrest. Besides, ICAT slowed down tumor growth in a glioblastoma xenograft model. Therefore, our study demonstrates that ICAT may serve as a tumor-suppressor in human glioma suggesting a promising direction for targeting therapy in glioma. (c) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Zhang, Kailiang; Zhu, Shanjun; Shi, Zhendong; Zhang, Anling; Chen, Luyue; Wei, Jianwei; Pu, Peiyu; Zhang, Jianning; Han, Lei; Kang, Chunsheng] Tianjin Med Univ Gen Hosp, Tianjin Neurol Inst, Dept Neurosurg,Minist Educ,Tianjin Key Lab Injuri, Lab Neurooncol,Key Lab Posttrauma Neurorepair & R, Tianjin 300052, Peoples R China.
   [Zhang, Kailiang; Zhu, Shanjun; Liu, Yanwei; Shi, Zhendong; Zhang, Anling; Chen, Luyue; Wei, Jianwei; Pu, Peiyu; Zhang, Jianning; Jiang, Tao; Han, Lei; Kang, Chunsheng] CGCG, Beijing 100050, Peoples R China.
   [Liu, Yanwei] Capital Med Univ, Beijing Neurosurg Inst, Dept Mol Neuropathol, Beijing 100050, Peoples R China.
   [Dong, Xiaoqun; Jiang, Tao] Univ Oklahoma Hlth Sci Ctr, Dept Med, Dept Surg, Oklahoma City, OK 73104 USA.
   [Liu, Chaoyong] Tianjin Univ, Sch Mat Sci & Engn, Tianjin 300072, Peoples R China.
C3 Tianjin Medical University; Beijing Neurosurgical Institute; Capital
   Medical University; University of Oklahoma System; University of
   Oklahoma Health Sciences Center; Tianjin University
RP Han, L (corresponding author), Tianjin Med Univ Gen Hosp, Tianjin Neurol Inst, Dept Neurosurg,Minist Educ,Tianjin Key Lab Injuri, Lab Neurooncol,Key Lab Posttrauma Neurorepair & R, Tianjin 300052, Peoples R China.
EM superhanlei@hotmail.com; kang97061@gmail.com
RI Liu, Chaoyong/AAW-2916-2021; Wei, Jianwei/AAH-3502-2020; Kang,
   Chunsheng/AAM-5979-2021; zhang, ying/HJB-1230-2022; Liu,
   Chaoyong/N-7975-2015
OI Kang, Chunsheng/0000-0002-3255-3369; Liu, Chaoyong/0000-0002-0914-687X
FU National High Technology Research and Development Program 863
   [2014AA021102, 2012AA02A508]; China National Natural Scientific Fund
   [81372703, 81001128, 81101916]; Natural Science Foundation of Tianjin
   Municipal Science and Technology Commission [12ZCDZSY17300]
FX This work was partially supported by the National High Technology
   Research and Development Program 863 (2014AA021102 and 2012AA02A508),
   the China National Natural Scientific Fund (81372703, 81001128 and
   81101916), the Natural Science Foundation of Tianjin Municipal Science
   and Technology Commission (12ZCDZSY17300).
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NR 28
TC 37
Z9 44
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 FEB 1
PY 2015
VL 357
IS 1
BP 404
EP 411
DI 10.1016/j.canlet.2014.11.047
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AZ2TB
UT WOS:000348084100040
PM 25434796
DA 2025-01-04
ER

PT J
AU Zheng, SQ
   Guo, YT
   Han, Q
   Peng, XQ
   Sheng, R
   Liu, SY
   Li, Z
AF Zheng, Shaoqin
   Guo, Yitong
   Han, Qing
   Peng, Xueqiang
   Sheng, Ren
   Liu, Siyu
   Li, Zhuang
TI STING agonists and PI3Kγ inhibitor co-loaded ferric ion-punicalagin
   networks for comprehensive cancer therapy
SO INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
LA English
DT Article
DE Punicalagin; Ferroptosis; Immunotherapy
ID FERROPTOSIS
AB Nanoparticles-based drug delivery system has been a promising approach for the treatment of colorectal cancer (CRC), which can be combined with chemotherapy, targeted therapy and immunotherapy to improve the treatment of CRC. 2 ' 3' cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) is an agonist of the STING signaling pathway activating antitumor immunity. IPI-549 is a small-molecule inhibitor for phosphatidylinositol 3-kinase gamma (PI3K gamma), which can induce M1 macrophages polarization to provide pro-inflammatory microenvironment to suppress tumors. Here, we developed a ferric ion-punicalagin network (Fe-PU), which can be not only used as an inducer of ferroptosis, but also serve as a carrier to load cGAMP and IPI-549 to obtain nanohybrid (Fe-PU/CD-IPI). In order to improve the delivery effect and targeted ability to CRC, a cyclic arginineglycine-aspartic acid peptide linked-bovine serum albumin were utilized to modify Fe-PU/CD-IPI to prepare nanohybrid Fe-PU/CD-IPI@cBSA. The therapeutic effect of various nanohybrids were validated in the mice with spontaneous tumor in the colorectal area and tumor-bearing mice, which lead to the increase of ferroptosis, the activation of STING signaling pathway, and the repolarization of macrophages. Collectively, the cGAMP and IPI549 co-loaded nanohybrids effectively reshaped the tumor immune microenvironment, and exhibited prominent treatment effect of anti-colorectal cancer in vitro, patient-derived organoids, and in vivo.
C1 [Zheng, Shaoqin; Guo, Yitong; Han, Qing; Sheng, Ren; Liu, Siyu] Northeastern Univ, Coll Life & Hlth Sci, Shenyang 110819, Peoples R China.
   [Peng, Xueqiang] China Med Univ, Affiliated Hosp 4, Dept Gen Surg, Shenyang 110032, Peoples R China.
   [Li, Zhuang] China Med Univ, Hosp 1, Dept Anorectal Surg, Shenyang 110001, Peoples R China.
C3 Northeastern University - China; China Medical University; China Medical
   University
RP Sheng, R; Liu, SY (corresponding author), Northeastern Univ, Coll Life & Hlth Sci, Shenyang 110819, Peoples R China.; Li, Z (corresponding author), China Med Univ, Hosp 1, Dept Anorectal Surg, Shenyang 110001, Peoples R China.
EM shengren@mail.neu.edu.cn; liusiyu@mail.neu.edu.cn; cmu1stbill@163.com
RI Liu, Siyu/AAA-5468-2021
FU National Natural Science Foundation of China [31970721, 81902830];
   Liaoning Provincial Talents Project [XLYC1807239]
FX This work was supported by National Natural Science Foundation of China
   31970721 and 81902830 (completed) , and Liaoning Provincial Talents
   Project XLYC1807239 (completed) .
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NR 37
TC 0
Z9 0
U1 4
U2 4
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0141-8130
EI 1879-0003
J9 INT J BIOL MACROMOL
JI Int. J. Biol. Macromol.
PD DEC
PY 2024
VL 282
AR 136776
DI 10.1016/j.ijbiomac.2024.136776
EA OCT 2024
PN 2
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Applied; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry; Polymer Science
GA L3D8C
UT WOS:001349566800001
PM 39454928
DA 2025-01-04
ER

PT J
AU Rovers, KP
   Simkens, GA
   Punt, CJ
   van Dieren, S
   Tanis, PJ
   de Hingh, IH
AF Rovers, Koen P.
   Simkens, Geert A.
   Punt, Cornelis J.
   van Dieren, Susan
   Tanis, Pieter J.
   de Hingh, Ignace H.
TI Perioperative systemic therapy for resectable colorectal peritoneal
   metastases: Sufficient evidence for its widespread use? A critical
   systematic review
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Colorectal cancer; Peritoneal carcinomatosis; Peritoneal metastases;
   Cytoreductive surgery; HIPEC; Chemotherapy; Targeted therapy
ID HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY; ENDOTHELIAL GROWTH-FACTOR;
   COMPLETE CYTOREDUCTIVE SURGERY; CLOSED ABDOMEN TECHNIQUE; SURFACE
   MALIGNANCIES; POSTOPERATIVE COMPLICATIONS; NEOADJUVANT CHEMOTHERAPY;
   PROGNOSTIC-FACTORS; LIVER METASTASES; CANCER-TREATMENT
AB Background/Purpose: Despite its widespread use, no randomised studies have investigated the value of perioperative systemic therapy as adjunct to cytoreduction and HIPEC for colorectal peritoneal metastases. This systematic review evaluated the available evidence, which consists of non-randomised studies only.
   Methods: A systematic search identified studies that investigated the influence of neoadjuvant, adjuvant, or perioperative systemic therapy on overall survival (OS).
   Results: The 11 included studies (n = 1708) were clinically heterogeneous and subject to selection bias. Studies on neoadjuvant systemic therapy revealed OS benefit (n = 3), no OS benefit (n = 1), and superiority of chemotherapy with bevacizumab vs. chemotherapy (n = 2). Studies on adjuvant systemic therapy showed no OS benefit (n =3). Studies on perioperative systemic therapy demonstrated OS benefit (n= 1), and superiority of modern vs. conventional systemic therapy(n = 1).
   Conclusion: Significant limitations of available evidence question the widespread use of perioperative systemic therapy in this setting, stress the need for randomised studies, and impede conclusions regarding optimal timing and regimens. Included studies may suggest a survival benefit of neoadjuvant systemic therapy. (C) 2017 Elsevier B.V. All rights reserved.
C1 [Rovers, Koen P.; Simkens, Geert A.; de Hingh, Ignace H.] Catharine Hosp, Dept Surg Oncol, POB 1350, NL-5602 ZA Eindhoven, Netherlands.
   [Punt, Cornelis J.] Acad Med Ctr, Dept Med Oncol, Amsterdam, Netherlands.
   [van Dieren, Susan; Tanis, Pieter J.] Acad Med Ctr, Dept Surg Oncol, Amsterdam, Netherlands.
C3 Catharina Hospital; University of Amsterdam; Academic Medical Center
   Amsterdam; University of Amsterdam; Academic Medical Center Amsterdam
RP de Hingh, IH (corresponding author), Catharine Hosp, Dept Surg Oncol, POB 1350, NL-5602 ZA Eindhoven, Netherlands.
EM ignace.d.hingh@catharinaziekenhuis.nl
RI Rovers, Koen/AGQ-5109-2022; Tanis, Pieter/U-2827-2019
OI Tanis, Pieter/0000-0002-3146-3310
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NR 77
TC 44
Z9 44
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD JUN
PY 2017
VL 114
BP 53
EP 62
DI 10.1016/j.critrevonc.2017.03.028
PG 10
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA EV6NA
UT WOS:000401884900006
PM 28477747
DA 2025-01-04
ER

PT J
AU Lee, SR
   Gemenetzis, G
   Cooper, M
   Javed, AA
   Cameron, JL
   Wolfgang, CL
   Eckhauser, FE
   He, J
   Weiss, MJ
AF Lee, Shin-Rong
   Gemenetzis, Georgios
   Cooper, Michol
   Javed, Ammar A.
   Cameron, John L.
   Wolfgang, Christopher L.
   Eckhauser, Frederick E.
   He, Jin
   Weiss, Matthew J.
TI Long-Term Outcomes of 98 Surgically Resected Metastatic Tumors in the
   Pancreas
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID RENAL-CELL CARCINOMA; (18)FDG PET-CT; OF-THE-LITERATURE;
   PROGNOSTIC-FACTORS; VASCULAR INVASION; TARGETED THERAPY; BREAST-CANCER;
   PULMONARY METASTASECTOMY; COLORECTAL-CANCER; SECONDARY TUMORS
AB The goal of this study was to assess the outcomes and characteristics of patients who underwent pancreatectomy for metastatic disease to the pancreas.
   Patients who underwent surgical resection of metastatic disease to the pancreas from 1988 to 2016 were identified using a prospectively maintained database. Data on clinicopathological features and outcomes of these patients were analyzed. Cox proportional hazard models were employed to identify patient-specific risk factors that influence survival.
   Ninety-seven patients underwent 98 pancreatic metastasectomies from July 1988 through March 2016 for metastatic disease from 13 different primary cancers. Pancreaticoduodenectomy, distal pancreatectomy, and total pancreatectomy were performed in 49 (50 %), 37 (38 %), and 12 (12 %) patients, respectively. Postoperative complications occurred in 55 (56 %) patients, while 3 (3 %) perioperative deaths occurred. Median follow-up was 2.0 years, with a median survival of 3.2 years. Multivariate analysis revealed that older patients [hazard ratio (HR) 1.04/year; p = 0.006], non-renal cell carcinomas (HR 5.07; p < 0.001), vascular invasion (HR 3.53; p < 0.001), and positive resection margins (HR 2.62; p = 0.008) were independently associated with an increased risk of mortality.
   Pancreatic metastasectomy is safe and feasible in well-selected patients and is associated with acceptable long-term survival.
C1 [Lee, Shin-Rong] Yale Univ, Sch Med, Dept Surg, New Haven, CT 06510 USA.
   [Gemenetzis, Georgios; Cooper, Michol; Javed, Ammar A.; Cameron, John L.; Wolfgang, Christopher L.; Eckhauser, Frederick E.; He, Jin; Weiss, Matthew J.] Johns Hopkins Univ, Sch Med, Dept Surg, Baltimore, MD 21205 USA.
C3 Yale University; Johns Hopkins University
RP Weiss, MJ (corresponding author), Johns Hopkins Univ, Sch Med, Dept Surg, Baltimore, MD 21205 USA.
EM mweiss5@jhmi.edu
RI Wolfgang, Christopher/HGD-0863-2022; Javed, Ammar/AAE-2870-2020
OI Javed, Ammar/0000-0002-5463-5250
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NR 45
TC 19
Z9 22
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD MAR
PY 2017
VL 24
IS 3
BP 801
EP 807
DI 10.1245/s10434-016-5619-z
PG 7
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA EK8MS
UT WOS:000394178600029
PM 27770346
DA 2025-01-04
ER

PT J
AU Zhang, HY
   Qu, YJ
   Duan, JJ
   Deng, T
   Liu, R
   Zhang, L
   Bai, M
   Li, JL
   Zhou, LK
   Ning, T
   Li, HL
   Ge, SH
   Li, H
   Yin, GG
   Huang, DZ
   Ba, Y
AF Zhang, Haiyang
   Qu, Yanjun
   Duan, Jingjing
   Deng, Ting
   Liu, Rui
   Zhang, Le
   Bai, Ming
   Li, Jialu
   Zhou, Likun
   Ning, Tao
   Li, Hongli
   Ge, Shaohua
   Li, Hua
   Yin, Guoguang
   Huang, Dingzhi
   Ba, Yi
TI Integrated analysis of the miRNA, gene and pathway regulatory network in
   gastric cancer
SO ONCOLOGY REPORTS
LA English
DT Article
DE miRNA; network; pathway; bioinformatic analysis; gastric cancer
ID SQUAMOUS-CELL CARCINOMA; EPITHELIAL-MESENCHYMAL TRANSITION;
   PI3K/AKT/MTOR SIGNALING PATHWAY; HUMAN PROSTATE-CANCER;
   HEPATOCELLULAR-CARCINOMA; BREAST-CANCER; DOWN-REGULATION; LUNG-CANCER;
   MDR1/P-GLYCOPROTEIN EXPRESSION; COLORECTAL-CANCER
AB Gastric cancer is one of the most common malignant tumors worldwide; however, the efficacy of clinical treatment is limited. MicroRNAs (miRNAs) are a class of small non-coding RNAs that have been reported to play a key role in the development of cancer. They also provide novel candidates for targeted therapy. To date, in-depth studies on the molecular mechanisms of gastric cancer involving miRNAs are still absent. We previously reported that 5 miRNAs were identified as being significantly increased in gastric cancer, and the role of these miRNAs was investigated in the present study. By using bioinformatics tools, we found that more than 4,000 unique genes are potential downstream targets of gastric cancer miRNAs, and these targets belong to the protein class of nucleic acid binding, transcription factor, enzyme modulator, transferase and receptor. Pathway mapping showed that the targets of gastric cancer miRNAs are involved in the MAPK signaling pathway, pathways in cancer, the PI3K-Akt signaling pathway, the HTLV-1 signaling pathway and Ras signaling pathway, thus regulating cell growth, differentiation, apoptosis and metastasis. Analysis of the pathways related to miRNAs may provides potential drug targets for future therapy of gastric cancer.
C1 [Zhang, Haiyang; Qu, Yanjun; Duan, Jingjing; Deng, Ting; Liu, Rui; Zhang, Le; Bai, Ming; Zhou, Likun; Ning, Tao; Li, Hongli; Ge, Shaohua; Li, Hua; Yin, Guoguang; Huang, Dingzhi; Ba, Yi] Tianjin Med Univ, Canc Inst & Hosp, Natl Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy, Tianjin 300060, Peoples R China.
   [Li, Jialu] Tianjin First Ctr Hosp, Dept Gastroenterol, Tianjin 300192, Peoples R China.
C3 Tianjin Medical University
RP Ba, Y (corresponding author), Tianjin Med Univ, Canc Inst & Hosp, Natl Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy, Tianjin 300060, Peoples R China.
EM dingzhih72@163.com; bayi@tjmuch.com
RI Ying, Guoguang/JTT-7661-2023
OI ying, guoguang/0000-0002-9563-991X; Duan, Jingjing/0000-0002-4008-2536
FU National Natural Science Foundation of China [81201946, 81372394];
   National Research Platform of Clinical Evaluation Technology for New
   Anticancer Drugs [2013ZX09303001]; Chinese Ministry of Education
   Research Fund for doctoral programs [2012202120013]; Tianjin City High
   School Science and Technology Fund Planning Project [20130122]; Science
   Foundation of Medical University Of Tianjin [2011KY15]
FX The present study was supported by grants from the National Natural
   Science Foundation of China (nos. 81201946 and 81372394) and the
   National Research Platform of Clinical Evaluation Technology for New
   Anticancer Drugs (no. 2013ZX09303001). This study was also supported by
   the Chinese Ministry of Education Research Fund for doctoral programs
   (no. 2012202120013), Tianjin City High School Science and Technology
   Fund Planning Project (no. 20130122) and Science Foundation of Medical
   University Of Tianjin (no. 2011KY15).
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NR 113
TC 16
Z9 18
U1 0
U2 28
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 2016
VL 35
IS 2
BP 1135
EP 1146
DI 10.3892/or.2015.4451
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DA8IZ
UT WOS:000368049600064
PM 26719093
OA Bronze
DA 2025-01-04
ER

PT J
AU Kim, M
   Seo, AN
AF Kim, Moonsik
   Seo, An Na
TI Molecular Pathology of Gastric Cancer
SO JOURNAL OF GASTRIC CANCER
LA English
DT Review
DE Gastric cancer; Human genome project; Molecular diagnostic testing;
   Diagnostic molecular pathology; Biomarker; Molecular targeted therapy
ID EPSTEIN-BARR-VIRUS; GASTROESOPHAGEAL JUNCTION CANCER; MISMATCH
   REPAIR-DEFICIENCY; EXPRESSION-BASED CLASSIFICATION; NONPOLYPOSIS
   COLORECTAL-CANCER; OF-AMERICAN-PATHOLOGISTS; MICROSATELLITE INSTABILITY;
   GENE AMPLIFICATION; DOUBLE-BLIND; OPEN-LABEL
AB Gastric cancer (GC) is one of the most common lethal malignant neoplasms worldwide, with limited treatment options for both locally advanced and/or metastatic conditions, resulting in a dismal prognosis. Although the widely used morphological classifications may be helpful for endoscopic or surgical treatment choices, they are still insufficient to guide precise and/or personalized therapy for individual patients. Recent advances in genomic technology and high-throughput analysis may improve the understanding of molecular pathways associated with GC pathogenesis and aid in the classification of GC at the molecular level. Advances in next-generation sequencing have enabled the identification of several genetic alterations through single experiments. Thus, understanding the driver alterations involved in gastric carcinogenesis has become increasingly important because it can aid in the discovery of potential biomarkers and therapeutic targets. In this article, we review the molecular classifications of GC, focusing on The Cancer Genome Atlas (TCGA) classification. We further describe the currently available biomarker-targeted therapies and potential biomarker-guided therapies. This review will help clinicians by providing an inclusive understanding of the molecular pathology of GC and may assist in selecting the best treatment approaches for patients with GC.
C1 [Kim, Moonsik; Seo, An Na] Kyungpook Natl Univ, Chilgok Hosp, Sch Med, Dept Pathol, Daegu, South Korea.
   [Seo, An Na] Kyungpook Natl Univ, Chilgok Hosp, Sch Med, Dept Pathol, 807 Hoguk Ro, Daegu, South Korea.
C3 Kyungpook National University (KNU); Kyungpook National University (KNU)
RP Seo, AN (corresponding author), Kyungpook Natl Univ, Chilgok Hosp, Sch Med, Dept Pathol, 807 Hoguk Ro, Daegu, South Korea.
EM san_0729@naver.com
OI Kim, Moonsik/0000-0002-5804-8790
FU Kyungpook National University Chilgok Hospital Molecular Pathology
   Laboratory
FX The authors express their deep gratitude to the members of the
   Gastrointestinal Pathology Study Group of the Korean Society of
   Pathologists for their efforts in revising the Standardized Pathology
   Report for Gastric Cancer, 2nd edition. The authors are grateful for the
   support provided by the Kyungpook National University Chilgok Hospital
   Molecular Pathology Laboratory.
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NR 260
TC 8
Z9 8
U1 5
U2 34
PU KOREAN GASTRIC CANCER ASSOC
PI SEOUL
PA GWANGHWAMUN OPCIA BLDG 1616, 163 SINMUN-RO 1-GA, JONGNO-GU, SEOUL,
   110-999, SOUTH KOREA
SN 2093-582X
EI 2093-5641
J9 J GASTRIC CANCER
JI J. Gasric Cancer
PD OCT
PY 2022
VL 22
IS 4
BP 264
EP 296
DI 10.5230/jgc.2022.22.e35
PG 33
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA 5Z8DW
UT WOS:000880198400002
PM 36316106
OA Green Published
DA 2025-01-04
ER

PT J
AU Ubink, I
   van Eden, WJ
   Snaebjornsson, P
   Kok, NFM
   van Kuik, J
   van Grevenstein, WMU
   Laclé, MM
   Sanders, J
   Fijneman, RJA
   Elias, SG
   Rinkes, IHMB
   Aalbers, AGJ
   Kranenburg, O
AF Ubink, I.
   van Eden, W. J.
   Snaebjornsson, P.
   Kok, N. F. M.
   van Kuik, J.
   van Grevenstein, W. M. U.
   Lacle, M. M.
   Sanders, J.
   Fijneman, R. J. A.
   Elias, S. G.
   Rinkes, I. H. M. Borel
   Aalbers, A. G. J.
   Kranenburg, O.
TI Histopathological and molecular classification of colorectal cancer and
   corresponding peritoneal metastases
SO BRITISH JOURNAL OF SURGERY
LA English
DT Article
ID COLON-CANCER; CONSENSUS CONFERENCE; GENE-EXPRESSION; MITOMYCIN-C;
   SUBTYPES; HIPEC; CARCINOMATOSIS; OXALIPLATIN; PROGNOSIS; CYTOREDUCTION
AB Background: Patients with colorectal peritoneal carcinomatosis have a very poor prognosis. The recently developed consensus molecular subtype (CMS) classification of primary colorectal cancer categorizes tumours into four robust subtypes, which could guide subtype-targeted therapy. CMS4, also known as the mesenchymal subtype, has the greatest propensity to form distant metastases. CMS4 status and histopathological features of colorectal peritoneal carcinomatosis were investigated in this study.
   Methods: Fresh-frozen tissue samples from primary colorectal cancer and paired peritoneal metastases from patients who underwent cytoreductive surgery combined with hyperthermic intraperitoneal chemotherapy were collected. Histopathological features were analysed, and a reverse transcriptase-quantitative PCR test was used to assess CMS4 status of all collected lesions.
   Results: Colorectal peritoneal carcinomatosis was associated with adverse histopathological characteristics, including a high percentage of stroma in both primary tumours and metastases, and poor differentiation grade and high-grade tumour budding in primary tumours. Furthermore, CMS4 was significantly enriched in primary tumours with peritoneal metastases, compared with unselected stage I-IV tumours (60 per cent (12 of 20) versus 23 per cent; P =0.002). The majority of peritoneal metastases (75 per cent, 21 of 28) were also classified as CMS4. Considerable intrapatient subtype heterogeneity was observed. Notably, 15 of 16 patients with paired tumours had at least one CMS4-positive tumour location.
   Conclusion: Significant enrichment for CMS4 was observed in colorectal peritoneal carcinomatosis.
C1 [Ubink, I.; van Grevenstein, W. M. U.; Rinkes, I. H. M. Borel; Kranenburg, O.] Univ Med Ctr Utrecht, Ctr Canc, Dept Surg Oncol, Utrecht, Netherlands.
   [van Kuik, J.; Lacle, M. M.] Univ Med Ctr Utrecht, Dept Pathol, Utrecht, Netherlands.
   [Elias, S. G.] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
   [Kranenburg, O.] Univ Med Ctr Utrecht, Div Biomed Genet, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands.
   [van Eden, W. J.; Kok, N. F. M.; Aalbers, A. G. J.] Netherlands Canc Inst, Dept Surg Oncol, Amsterdam, Netherlands.
   [Snaebjornsson, P.; Sanders, J.; Fijneman, R. J. A.] Netherlands Canc Inst, Dept Pathol, Amsterdam, Netherlands.
C3 Utrecht University; Utrecht University Medical Center; Utrecht
   University; Utrecht University Medical Center; Utrecht University;
   Utrecht University Medical Center; Utrecht University; Utrecht
   University Medical Center; Netherlands Cancer Institute; Netherlands
   Cancer Institute
RP Kranenburg, O (corresponding author), Univ Med Ctr Utrecht, Div Biomed Genet, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands.; Kranenburg, O (corresponding author), Univ Med Ctr Utrecht, Ctr Canc, Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands.
EM o.kranenburg@umcutrecht.nl
RI Fijneman, Remond/X-4199-2019; Kok, Niels/AFU-6897-2022; Elias,
   Sjoerd/E-6057-2011
OI Fijneman, Remond/0000-0003-2076-5521
FU Dutch Cancer Society [UU2014-6617]
FX The authors acknowledge the NKI-AVL Core Facility Molecular Pathology
   and Biobanking for supplying NKI-AVL Biobank material. I.U. is supported
   by a grant from the Dutch Cancer Society (UU2014-6617).
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NR 31
TC 58
Z9 64
U1 0
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1323
EI 1365-2168
J9 BRIT J SURG
JI Br. J. Surg.
PD JAN
PY 2018
VL 105
IS 2
SI SI
BP E204
EP E211
DI 10.1002/bjs.10788
PG 8
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA GB4AM
UT WOS:000429002100021
PM 29341165
OA Bronze
DA 2025-01-04
ER

PT J
AU Yang, JB
   Xing, PF
   Kong, YH
   Xu, ML
   Zhang, LY
AF Yang, Jiabao
   Xing, Pengfei
   Kong, Yuehong
   Xu, Meiling
   Zhang, Liyuan
TI PD-1 inhibitor combined with radiotherapy and GM-CSF in MSS/pMMR
   metastatic colon cancer: a case report
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE colorectal cancer; immunotherapy; radiotherapy; GM-CSF; MSS; pMMR; case
   report
ID RESPONSES; IMMUNITY; TUMORS
AB Patients with chemo-refractory metastatic colorectal cancer (mCRC) have poor prognoses. The application of programmed cell death protein 1 (PD-1)/programmed cell death ligand 1 (PD-L1) inhibitors encouragingly improved the survival of mCRC patients with microsatellite instability-high (MSI-H)/mismatch repair-deficient (dMMR). Unfortunately, it was ineffective for mCRC with microsatellite-stable (MSS)/proficient mismatch repair (pMMR), which accounted for 95% of mCRC. Radiotherapy can promote local control by directly killing tumor cells and inducing positive immune activities, which might help synergistically with immunotherapy. We present the report of an advanced MSS/pMMR mCRC patient who had progressive disease (PD) after first-line chemotherapy, palliative surgery and second-line chemotherapy combined with targeted therapy. Then the patient received the therapy of PD-1 inhibitor combined with radiotherapy and granulocyte-macrophage colony-stimulating factor (GM-CSF). According to Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST1.1), the patient showed a complete response (CR) after triple-combined therapy with progression-free survival (PFS) for more than 2 years so far. The patient had no other significant adverse reactions except for fatigue (Grade 1). The triple-combination therapy provided a promising strategy for metastatic chemo-refractory MSS/pMMR mCRC patients.
C1 [Yang, Jiabao; Xing, Pengfei; Kong, Yuehong; Xu, Meiling; Zhang, Liyuan] Soochow Univ, Dept Radiotherapy & Oncol, Affiliated Hosp 2, Suzhou, Peoples R China.
   [Yang, Jiabao; Xing, Pengfei; Kong, Yuehong; Xu, Meiling; Zhang, Liyuan] Soochow Univ, Inst Radiotherapy & Oncol, Suzhou, Peoples R China.
   [Yang, Jiabao; Xing, Pengfei; Kong, Yuehong; Xu, Meiling; Zhang, Liyuan] Soochow Univ, Lab Combined Radiotherapy & Immunotherapy Canc, Affiliated Hosp 2, Suzhou, Peoples R China.
C3 Soochow University - China; Soochow University - China; Soochow
   University - China
RP Zhang, LY (corresponding author), Soochow Univ, Dept Radiotherapy & Oncol, Affiliated Hosp 2, Suzhou, Peoples R China.; Zhang, LY (corresponding author), Soochow Univ, Inst Radiotherapy & Oncol, Suzhou, Peoples R China.; Zhang, LY (corresponding author), Soochow Univ, Lab Combined Radiotherapy & Immunotherapy Canc, Affiliated Hosp 2, Suzhou, Peoples R China.
EM zhangliyuan@suda.edu.cn
RI Kong, Yuehong/KFA-0361-2024
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NR 30
TC 3
Z9 3
U1 7
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 APR 28
PY 2023
VL 13
AR 1078915
DI 10.3389/fonc.2023.1078915
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA F9FL7
UT WOS:000985331700001
PM 37188188
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Dellson, P
   Nilbert, M
   Carlsson, C
AF Dellson, Pia
   Nilbert, Mef
   Carlsson, Christina
TI Patient representatives' views on patient information in clinical cancer
   trials
SO BMC HEALTH SERVICES RESEARCH
LA English
DT Article
DE Clinical trial; Patient information; Cancer; Patient preferences;
   Layout; Focus group interview
ID INFORMED-CONSENT; PARTICIPANTS; QUALITY; ILLUSTRATIONS
AB Background: Patient enrolment into clinical trials is based on oral information and informed consent, which includes an information sheet and a consent certificate. The written information should be complete, but at the same time risks being so complex that it may be questioned if a fully informed consent is possible to provide. We explored patient representatives' views and perceptions on the written trial information used in clinical cancer trials.
   Methods: Written patient information leaflets used in four clinical trials for colorectal cancer were used for the study. The trials included phase I-III trials, randomized and non-randomized trials that evaluated chemotherapy/targeted therapy in the neoadjuvant, adjuvant and palliative settings. Data were collected through focus groups and were analysed using inductive content analysis.
   Results: Two major themes emerged: emotional responses and cognitive responses. Subthemes related to the former included individual preferences and perceptions of effect, while subthemes related to the latter were comprehensibility and layout. Based on these observations the patient representatives provided suggestions for improvement, which largely included development of future simplified and more attractive informed consent forms.
   Conclusions: The emotional and cognitive responses to written patient information reported by patient representatives provides a basis for revised formats in future trials and add to the body of information that support use of plain language, structured text and illustrations to improve the informed consent process and thereby patient enrolment into clinical trials.
C1 [Dellson, Pia; Nilbert, Mef; Carlsson, Christina] Lund Univ, Inst Clin Sci, Div Oncol & Pathol, Scheelevagen 8, S-22381 Lund, Sweden.
   [Nilbert, Mef] Univ Copenhagen, Hvidovre Hosp, Clin Res Ctr, Kettegard Alle 30, DK-2650 Copenhagen, Denmark.
C3 Lund University; University of Copenhagen
RP Carlsson, C (corresponding author), Lund Univ, Inst Clin Sci, Div Oncol & Pathol, Scheelevagen 8, S-22381 Lund, Sweden.
EM Christina.carlsson@med.lu.se
OI Nilbert, Mef/0000-0003-2717-1937
FU Nilsson Cancer Fund; Region Skane Research Fund
FX We would like to thank the focus group participants for their
   contributions and the principal investigators for permission to use the
   informed consent forms. Financial support was granted by the Nilsson
   Cancer Fund and the Region Skane Research Fund.
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NR 27
TC 10
Z9 11
U1 0
U2 8
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1472-6963
J9 BMC HEALTH SERV RES
JI BMC Health Serv. Res.
PD FEB 1
PY 2016
VL 16
AR 36
DI 10.1186/s12913-016-1272-2
PG 5
WC Health Care Sciences & Services
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Health Care Sciences & Services
GA DC4HP
UT WOS:000369182000001
PM 26831330
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Tan, X
   Zhao, XY
AF Tan, Xiao
   Zhao, Xiangyu
TI B7-H3 in acute myeloid leukemia: From prognostic biomarker to
   immunotherapeutic target
SO CHINESE MEDICAL JOURNAL
LA English
DT Review
DE B7-H3 (CD276); B7 family; Acute myeloid leukemia; Immune checkpoint;
   Immunotherapy
ID B7 FAMILY-MEMBER; COLORECTAL-CANCER CELLS; T-CELLS; TUMOR PROGRESSION;
   COSTIMULATORY MOLECULES; DENDRITIC CELLS; EXPRESSION; RECEPTOR;
   PROMOTES; CD276
AB B7-H3 (CD276), an immune checkpoint protein of the B7 family, exhibits significant upregulation in solid tumors and hematologic malignancies, exerting a crucial role in their pathophysiology. The distinct differential expression of B7-H3 between tumors and normal tissues and its multifaceted involvement in tumor pathogenesis position it as a promising therapeutic target for tumors. In the context of acute myeloid leukemia (AML), B7-H3 is prominently overexpressed and closely associated with unfavorable prognoses, yet it has remained understudied. Despite various ongoing clinical trials demonstrating the potential efficacy of immunotherapies targeting B7-H3, the precise underlying mechanisms responsible for B7-H3-mediated proliferation and immune evasion in AML remain enigmatic. In view of this, we comprehensively outline the current research progress concerning B7-H3 in AML, encompassing in-depth discussions on its structural attributes, receptor interactions, expression profiles, and biological significance in normal tissues and AML. Moreover, we delve into the protumor effects of B7-H3 in AML, examine the intricate mechanisms that underlie its function, and discuss the emerging application of B7-H3-targeted therapy in AML treatment. By juxtaposing B7-H3 with other molecules within the B7 family, this review emphasizes the distinctive advantages of B7-H3, not only as a valuable prognostic biomarker but also as a highly promising immunotherapeutic target in AML.
C1 [Tan, Xiao; Zhao, Xiangyu] Peking Univ, Peoples Hosp, Inst Hematol, Natl Clin Res Ctr Hematol Dis,Beijing Key Lab Hema, Beijing 100044, Peoples R China.
C3 Peking University
RP Zhao, XY (corresponding author), Peking Univ, Peoples Hosp, Inst Hematol, Natl Clin Res Ctr Hematol Dis,Beijing Key Lab Hema, Beijing 100044, Peoples R China.
EM zhao_xy@bjmu.edu.cn
RI Zhao, Xiangyu/AAO-2203-2020
FU National Natural Science Foundation of China [82070184, 82270228];
   Beijing Nova Program [20220484235]; Peking University People's Hospital
   Research and Development Funds [RDL2021-01]
FX This study was supported by grants from the National Natural Science
   Foundation of China (Nos. 82070184 and 82270228), Beijing Nova Program
   (No. 20220484235), and Peking University People's Hospital Research and
   Development Funds (No. RDL2021-01).
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NR 100
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0366-6999
EI 2542-5641
J9 CHINESE MED J-PEKING
JI Chin. Med. J.
PD NOV 5
PY 2024
VL 137
IS 21
BP 2540
EP 2551
DI 10.1097/CM9.0000000000003099
PG 12
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA L2Z3V
UT WOS:001349449100019
PM 38595093
OA gold
DA 2025-01-04
ER

PT J
AU Ganzetti, G
   Sartini, D
   Campanati, A
   Rubini, C
   Molinelli, E
   Brisigotti, V
   Cecati, M
   Pozzi, V
   Campagna, R
   Offidani, A
   Emanuelli, M
AF Ganzetti, Giulia
   Sartini, Davide
   Campanati, Anna
   Rubini, Corrado
   Molinelli, Elisa
   Brisigotti, Valerio
   Cecati, Monia
   Pozzi, Valentina
   Campagna, Roberto
   Offidani, Annamaria
   Emanuelli, Monica
TI Nicotinamide <i>N</i>-methyltransferase: potential involvement in
   cutaneous malignant melanoma
SO MELANOMA RESEARCH
LA English
DT Article
DE diagnostic and prognostic marker; enzyme expression;
   immunohistochemistry; NNMT
ID SQUAMOUS-CELL CARCINOMA; UP-REGULATION; COLORECTAL-CANCER; WORSE
   PROGNOSIS; DIAGNOSTIC-TEST; TUMOR-MARKER; EXPRESSION; IDENTIFICATION;
   PROLIFERATION; INHIBITORS
AB Nicotinamide N-methyltransferase (NNMT) is an enzyme that catalyzes the N-methylation of nicotinamide and pyridine compounds, participating in xenobiotic and drug metabolism. Data on literature have evidenced a possible role of NNMT in many solid cancers, but no data are currently available in cutaneous melanoma. Recent important advances have been achieved in the treatment of advanced melanoma with targeted therapy and immunotherapy. However, the identification of biomarkers that can be used for the detection of early stage disease as well as for monitoring the therapeutic response during treatment is of utmost importance. The aim of this study was to study the possible role of NNMT in melanoma. In the present study, we carried out immunohistochemical analyses to evaluate the expression of the enzyme NNMT in 34 melanomas and 34 nevi. Moreover, we explored the relationship between NNMT levels and the prognostic parameters of patients with melanoma. The results obtained showed significantly (P<0.0001) higher NNMT expression in melanoma compared with that detected in nevi. In addition, a significant (P<0.05) inverse relationship was found between enzyme levels and Breslow thickness, Clark level, the presence/number of mitoses, and ulceration. Taken together, these data seem to suggest that NNMT could represent a molecular biomarker for melanoma, thus highlighting its potential for both diagnosis and prognosis of this neoplasm.
C1 [Ganzetti, Giulia; Campanati, Anna; Molinelli, Elisa; Brisigotti, Valerio; Offidani, Annamaria] Polytech Univ Marche, Dept Clin & Mol Sci, I-60126 Ancona, Italy.
   [Sartini, Davide; Cecati, Monia; Pozzi, Valentina; Campagna, Roberto; Emanuelli, Monica] Polytech Univ Marche, Dept Clin & Stomatol Sci, Ancona, Italy.
   [Rubini, Corrado] Polytech Univ Marche, Dept Biomed Sci & Publ Hlth, Ancona, Italy.
   [Pozzi, Valentina; Emanuelli, Monica] New York Marche Struct Biol Ctr NY MaSBiC, New York, NY USA.
C3 Marche Polytechnic University; Marche Polytechnic University; Marche
   Polytechnic University
RP Campanati, A (corresponding author), Polytech Univ Marche, Dept Clin & Mol Sci, I-60126 Ancona, Italy.
EM edottor@alice.it
RI MOLINELLI, ELISA/GVR-7592-2022; Campagna, Roberto/GPT-4507-2022;
   Campanati, Anna/AAD-9584-2022
OI CAMPAGNA, ROBERTO/0000-0003-2607-2734; Cecati,
   Monia/0000-0003-4947-5157; SARTINI, Davide/0000-0003-3879-8647
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0960-8931
EI 1473-5636
J9 MELANOMA RES
JI Melanoma Res.
PD APR
PY 2018
VL 28
IS 2
BP 82
EP 88
DI 10.1097/CMR.0000000000000430
PG 7
WC Oncology; Dermatology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Dermatology; Research & Experimental Medicine
GA GA2UF
UT WOS:000428180400002
PM 29420365
DA 2025-01-04
ER

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AF Schulz, Dominik
   Wirth, Markus
   Piontek, Guido
   Buchberger, Anna Maria Stefanie
   Schlegel, Juergen
   Reiter, Rudolf
   Multhoff, Gabriele
   Pickhard, Anja
TI HNSCC cells resistant to EGFR pathway inhibitors are hypermutated and
   sensitive to DNA damaging substances
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Article
DE HNSCC; resistant cells; hypermutation
ID CANCER STEM-CELLS; DRUG-RESISTANCE; ACQUIRED-RESISTANCE; LUNG-CANCER;
   NECK-CANCER; COLORECTAL-CANCER; GENE MUTATION; HEAD; LINES; CARCINOMA
AB Despite remarkable successes with targeted therapies in the treatment of cancer, resistance can occur which limits the clinical outcome. In this study, we generated and characterized resistant cell clones derived from two different head and neck squamous cell carcinoma (HNSCC) cell lines (Cal27, UD-SCC-5) by long-term exposure to five targeted-and chemotherapeutics (afatinib, MK2206, BEZ235, olaparib and cisplatin). The resistant tumor cell clones showed an increased ERK1/2 expression and an altered expression of the stem-cell markers CD44, ALDH1, Oct4, Sox2, Nanog and Bmi1. None of the single markers alone was predictive for resistance to all five targeted-and chemotherapeutics. Furthermore, long-term exposure of tumor cells to these five drugs resulted in an eightfold increase in the mutational rate compared to untreated cells. Interestingly, targeted-and chemotherapy resistant cell clones remained sensitive to irradiation. Lastly, clones that were resistant to afatinib, MK2206 or BEZ235 showed cross-resistance to further treatment with therapeutics that affect the same signaling pathway, but remained sensitive to those affecting different pathways such as cisplatin and olaparib. In contrast, cell clones which were once resistant to cisplatin or olaparib were found to be multidrug-resistant. These data might indicate that patients with HNSCC benefit more by a first line targeted therapy followed by cisplatin as a second line therapy.
C1 [Schulz, Dominik; Wirth, Markus; Piontek, Guido; Buchberger, Anna Maria Stefanie; Pickhard, Anja] Tech Univ Munich, Dept Otolaryngol Head & Neck Surg, Ismaninger Str 22, Munich, Germany.
   [Schlegel, Juergen] Tech Univ Munich, Inst Pathol, Div Neuropathol, Ismaninger Str 22, Munich, Germany.
   [Reiter, Rudolf] Univ Ulm, Sect Phoniatr & Pedaudiol, Dept Otolaryngol Head & Neck Surg, Prittwitzstr 43, Ulm, Germany.
   [Multhoff, Gabriele] Tech Univ Munich, Dept Radiotherapy, Ismaninger Str 22, Munich, Germany.
C3 Technical University of Munich; Technical University of Munich; Ulm
   University; Technical University of Munich
RP Pickhard, A (corresponding author), Tech Univ Munich, Dept Otolaryngol Head & Neck Surg, Ismaninger Str 22, Munich, Germany.
EM a.pickhard@lrz.tum.de
RI Wirth, Markus/ABW-6155-2022; Multhoff, Gabriele/AAW-9796-2021
OI Multhoff, Gabriele/0000-0002-2616-3137; Schlegel,
   Jurgen/0000-0002-5544-2717
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NR 48
TC 8
Z9 9
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 2016
VL 6
IS 9
BP 1963
EP 1975
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DX7RK
UT WOS:000384586500009
PM 27725902
DA 2025-01-04
ER

PT J
AU Shen, CQ
   Yan, TT
   Wang, ZH
   Su, HC
   Zhu, XQ
   Tian, XL
   Fang, JY
   Chen, H
   Hong, J
AF Shen, Chaoqin
   Yan, Tingting
   Wang, Zhenhua
   Su, Heng-Chuan
   Zhu, Xiaoqiang
   Tian, Xianglong
   Fang, Jing-Yuan
   Chen, Haoyan
   Hong, Jie
TI Variant of SNP rs1317082 at CCSlnc362 (RP11-362K14.5) creates a binding
   site for miR-4658 and diminishes the susceptibility to CRC
SO CELL DEATH & DISEASE
LA English
DT Article
ID LONG NONCODING RNA; COLORECTAL-CANCER; CELL-CYCLE; RISK; EXPRESSION;
   GENE; STATISTICS; PROLIFERATION; METAANALYSIS; PROGRESSION
AB Genome-wide association studies (GWAS) have identified several loci harboring variants that affected the risk of colorectal cancer; however, the specific mechanisms by which germline variation influenced the tumorigenesis of colorectal cancer (CRC) remains unrevealed. We found the T>C variant of rs1317082, locating at the exon 1 of lncRNA RP11-362K14.5 (CCSlnc362), was predicted to be a protective locus for cancer. However, the specific role of CCSlnc362 and the interaction between CCSlnc362 and rs1317082 variation in colorectal cancer and its mechanisms remain unclear. Here we explored the expression and function of CCSlnc362 in CRC cells and tissues. We found lncRNA CCSlnc362 expression was significantly increased in CRC samples. Follow-up functional experiments elucidated that downregulation of CCSlnc362 inhibited cell proliferation, arrested cell cycle, and promoted apoptosis in CRC cells. The T>C variant of rs1317082 at CCSlnc362 exon 1 created a binding site for miR-4658 to reduce the expression of CCSlnc362 and thus decreased the susceptibility to CRC. Our findings have provided supporting evidence for the protective role of rs1317082 variation and the potential oncogenic role of lncRNA CCSlnc362 in CRC. The data shed new light on the relationship between germline variation, miRNAs, and lncRNAs and opened a new avenue for targeted therapy in CRC.
C1 [Shen, Chaoqin; Yan, Tingting; Wang, Zhenhua; Zhu, Xiaoqiang; Tian, Xianglong; Fang, Jing-Yuan; Chen, Haoyan; Hong, Jie] Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes,Sch Med, Key Lab Gastroenterol & Hepatol,Minist Hlth,Shang, Div Gastroenterol & Hepatol,Renji Hosp,Shanghai C, 145 Middle Shandong Rd, Shanghai 200001, Peoples R China.
   [Su, Heng-Chuan] Fudan Univ, Dept Urol, Shanghai Canc Ctr, Shanghai, Peoples R China.
   [Su, Heng-Chuan] Fudan Univ, Dept Oncol, Shanghai Med Coll, Shanghai, Peoples R China.
C3 Shanghai Jiao Tong University; Fudan University; Fudan University
RP Fang, JY; Chen, H; Hong, J (corresponding author), Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes,Sch Med, Key Lab Gastroenterol & Hepatol,Minist Hlth,Shang, Div Gastroenterol & Hepatol,Renji Hosp,Shanghai C, 145 Middle Shandong Rd, Shanghai 200001, Peoples R China.
EM jingyuanfang@sjtu.edu.cn; jiehong97@sjtu.edu.cn; jiehong97@sjtu.edu.cn
RI FANG, Jing-Yuan/JOZ-1388-2023; yan, Tingting/HRB-2318-2023
FU National Natural Science Foundation [81522008, 81871901, 31271366,
   81790632, 81572696, 81602222]; Program for Professor of Special
   Appointment (Eastern Scholar) at Shanghai Institutions of Higher
   Learning [201268]; Shanghai Municipal Education Commission-Gaofeng
   Clinical Medicine Grant Support [20152512]
FX This work was partly supported by grants from the National Natural
   Science Foundation (Nos. 81522008, 81871901, 31271366, 81790632,
   81572696, 81602222), the Program for Professor of Special Appointment
   (Eastern Scholar No. 201268) at Shanghai Institutions of Higher
   Learning; and Shanghai Municipal Education Commission-Gaofeng Clinical
   Medicine Grant Support (No. 20152512);
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NR 43
TC 21
Z9 23
U1 0
U2 20
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 DEC 5
PY 2018
VL 9
AR 1177
DI 10.1038/s41419-018-1222-5
PG 11
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA HD2EI
UT WOS:000452323500013
PM 30518759
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Kumasaka, A
   Matsumoto, N
   Mukae, S
   Kitano, T
   Noguchi, H
   Ohki, H
   Komiyama, K
   Ando, T
AF Kumasaka, Akira
   Matsumoto, Naoyuki
   Mukae, Shotaro
   Kitano, Taiichi
   Noguchi, Hiroyasu
   Ohki, Hidero
   Komiyama, Kazuo
   Ando, Tomohiro
TI Rapid and Specific Screening Assay for <i>KRAS</i> Oncogene Mutation by
   a Novel Gene Amplification Method
SO ANTICANCER RESEARCH
LA English
DT Article
DE KRAS mutation; LAMP; molecular targeted therapy; stratification
   biomarker
ID MEDIATED ISOTHERMAL AMPLIFICATION; RECEPTOR TYROSINE KINASE; CELL
   LUNG-CANCER; K-RAS MUTATIONS; PHASE-II TRIAL; COLORECTAL-CANCER; PLUS
   CETUXIMAB; HEAD; CARCINOMA; SPUTUM
AB Background: Epidermal growth factor receptor (EGFR) is a target of molecular therapeutics for colorectal cancer. However, mutation of Kirsten rat sarcoma viral oncogene homolog (KRAS) gene at codons 12 and 13 attenuates the therapeutic effect of anti-EGFR therapies. Therefore, the detection of KRAS gene mutation is important for therapeutic decision-making. Materials and Methods: KRAS gene mutation at codons 12 (c.34G>T, c.35G>C, c.35G>A) and 13 (c.38G>A) in six cancer cell lines were investigated. A loop-mediated isothermal amplification-based procedure was developed that employed peptide nucleic acid to suppress amplification of the wild-type allele. Results: This mutation-oriented gene-amplification procedure can amplify the DNA fragment of the KRAS gene with codon 12 and codon 13 mutation within 30 min. Moreover, boiled cells can work as template resources. Conclusion: This newly developed procedure can be useful for patient stratification for anti-EGFR therapies.
C1 [Kumasaka, Akira; Ando, Tomohiro] Tokyo Womens Med Univ, Sch Med, Dept Oral & Maxillofacial Surg, Tokyo, Japan.
   [Matsumoto, Naoyuki; Mukae, Shotaro; Kitano, Taiichi; Komiyama, Kazuo] Nihon Univ, Sch Dent, Dept Pathol, Chiyoda Ku, Tokyo 1018310, Japan.
   [Noguchi, Hiroyasu; Ohki, Hidero] Nihon Univ, Sch Dent, Dept Oral & Maxillofacial Surg, Chiyoda Ku, 1-8-13 Kanda Surugadai, Tokyo 1018310, Japan.
C3 Tokyo Women's Medical University; Nihon University; Nihon University
RP Matsumoto, N (corresponding author), Nihon Univ, Sch Dent, Dept Oral & Maxillofacial Surg, Chiyoda Ku, 1-8-13 Kanda Surugadai, Tokyo 1018310, Japan.
EM matsumoto.naoyuki@nihon-u.ac.jp
FU Ministry of Education, Cultures, Sports, Science and Technology, Japan
   [24792011]; Grants-in-Aid for Scientific Research [24792011] Funding
   Source: KAKEN
FX This study was supported by Grant-in-Aid for Young Scientists (B) to
   Shotaro Mukae (No. 24792011), and Grant-in-Aid for Scientific Research
   (C) to Naoyuki Matsumoto from the Ministry of Education, Cultures,
   Sports, Science and Technology, Japan.
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NR 35
TC 4
Z9 5
U1 0
U2 11
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD APR
PY 2016
VL 36
IS 4
BP 1571
EP 1579
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DL2GD
UT WOS:000375450600014
PM 27069133
DA 2025-01-04
ER

PT J
AU Parsa, FG
   Nobili, S
   Karimpour, M
   Aghdaei, HA
   Nazemalhosseini-Mojarad, E
   Mini, E
AF Parsa, Fatemeh Ghorbani
   Nobili, Stefania
   Karimpour, Mina
   Aghdaei, Hamid Asadzadeh
   Nazemalhosseini-Mojarad, Ehsan
   Mini, Enrico
TI Fanconi Anemia Pathway in Colorectal Cancer: A Novel Opportunity for
   Diagnosis, Prognosis and Therapy
SO JOURNAL OF PERSONALIZED MEDICINE
LA English
DT Article
DE colorectal cancer; Fanconi anemia; prognostic biomarker; predictive
   biomarker; target therapy; synthetic lethality
ID SUSCEPTIBILITY GENE-MUTATIONS; ADVANCED RECTAL-CANCER; G-QUADRUPLEX DNA;
   HOMOLOGOUS RECOMBINATION; REPLICATION STRESS; MISMATCH REPAIR;
   TUMOR-CELLS; PROTEINS; BRCA2; EXPRESSION
AB Colorectal cancer (CRC) is the third most commonly diagnosed malignancy and has the second highest mortality rate globally. Thanks to the advent of next-generation sequencing technologies, several novel candidate genes have been proposed for CRC susceptibility. Germline biallelic mutations in one or more of the 22 currently recognized Fanconi anemia (FA) genes have been associated with Fanconi anemia disease, while germline monoallelic mutations, somatic mutations, or the promoter hypermethylation of some FANC genes increases the risk of cancer development, including CRC. The FA pathway is a substantial part of the DNA damage response system that participates in the repair of DNA inter-strand crosslinks through homologous recombination (HR) and protects genome stability via replication fork stabilization, respectively. Recent studies revealed associations between FA gene/protein tumor expression levels (i.e., FANC genes) and CRC progression and drug resistance. Moreover, the FA pathway represents a potential target in the CRC treatment. In fact, FANC gene characteristics may contribute to chemosensitize tumor cells to DNA crosslinking agents such as oxaliplatin and cisplatin besides exploiting the synthetic lethal approach for selective targeting of tumor cells. Hence, this review summarizes the current knowledge on the function of the FA pathway in DNA repair and genomic integrity with a focus on the FANC genes as potential predisposition factors to CRC. We then introduce recent literature that highlights the importance of FANC genes in CRC as promising prognostic and predictive biomarkers for disease management and treatment. Finally, we represent a brief overview of the current knowledge around the FANC genes as synthetic lethal therapeutic targets for precision cancer medicine.
C1 [Parsa, Fatemeh Ghorbani; Aghdaei, Hamid Asadzadeh] Shahid Beheshti Univ Med Sci, Basic & Mol Epidemiol Gastrointestinal Disorders, Res Inst Gastroenterol & Liver Dis, Tehran 1985717413, Iran.
   [Nobili, Stefania] Univ G dAnnunzio, Dept Neurosci Imaging & Clin Sci, I-66100 Chieti, Italy.
   [Nobili, Stefania] Univ G dAnnunzio, Ctr Adv Studies & Technol CAST, I-66100 Chieti, Italy.
   [Karimpour, Mina] Tarbiat Modares Univ, Fac Biol Sci, Dept Genet, Tehran 14115154, Iran.
   [Nazemalhosseini-Mojarad, Ehsan] Shahid Beheshti Univ Med Sci, Gastroenterol & Liver Dis Res Ctr, Res Inst Gastroenterol & Liver Dis, Tehran 1985717413, 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; Tarbiat
   Modares University; Shahid Beheshti University Medical Sciences;
   University of Florence; University of Florence
RP Nazemalhosseini-Mojarad, E (corresponding author), Shahid Beheshti Univ Med Sci, Gastroenterol & Liver Dis Res Ctr, Res Inst Gastroenterol & Liver Dis, Tehran 1985717413, 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 ghorbaniparsa@tabrizu.ac.ir; stefania.nobili@unich.it;
   mina.karimpour@modares.ac.ir; hamid.asadzadeh@sbmu.ac.ir;
   e.nazemalhosseini@sbmu.ac.ir; enrico.mini@unifi.it
RI Asadzadeh-Aghdaei, Hamid/AAD-4494-2022; Nazemalhosseini-Moja,
   ehsan/HGF-3165-2022; Ghorbani Parsa, Fatemeh/F-1996-2018
OI nazemalhosseini-mojarad, ehsan/0000-0001-8914-004X; Karimpour,
   Mina/0000-0002-4169-0736; Ghorbani Parsa, Fatemeh/0000-0002-2090-1186
FU Fondo Beneficenza Intesa Sanpaolo S.p.A. (Milan, Italy)
FX This research was partially supported by Fondo Beneficenza Intesa
   Sanpaolo S.p.A. (Milan, Italy) to E.M.
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NR 153
TC 12
Z9 14
U1 2
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 MAR
PY 2022
VL 12
IS 3
AR 396
DI 10.3390/jpm12030396
PG 26
WC Health Care Sciences & Services; Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Health Care Sciences & Services; General & Internal Medicine
GA 0C0LQ
UT WOS:000775015400001
PM 35330396
OA Green Published, gold
DA 2025-01-04
ER

PT J
AU Senft, D
   Leiserson, MDM
   Ruppin, E
   Ronai, ZA
AF Senft, Daniela
   Leiserson, Mark D. M.
   Ruppin, Eytan
   Ronai, Ze'ev A.
TI Precision Oncology: The Road Ahead
SO TRENDS IN MOLECULAR MEDICINE
LA English
DT Review
ID SYNTHETIC LETHAL INTERACTIONS; PATIENT-DERIVED XENOGRAFTS;
   TO-MESENCHYMAL TRANSITION; LONG-TERM EXPANSION; PAN-CANCER ANALYSIS;
   ACQUIRED-RESISTANCE; COLORECTAL-CANCER; BREAST-CANCER; SOMATIC
   MUTATIONS; TARGETED THERAPY
AB Current efforts in precision oncology largely focus on the benefit of genomics-guided therapy. Yet, advances in sequencing techniques provide an unprecedented view of the complex genetic and nongenetic heterogeneity within individual tumors. Herein, we outline the benefits of integrating genomic and transcriptomic analyses for advanced precision oncology. We summarize relevant computational approaches to detect novel drivers and genetic vulnerabilities, suitable for therapeutic exploration. Clinically relevant platforms to functionally test predicted drugs/drug combinations for individual patients are reviewed. Finally, we highlight the technological advances in single cell analysis of tumor specimens. These may ultimately lead to the development of next-generation cancer drugs, capable of tackling the hurdles imposed by genetic and phenotypic heterogeneity on current anticancer therapies.
C1 [Senft, Daniela; Ronai, Ze'ev A.] NCI, Tumor Initiat & Maintenance Program, Designated Canc Ctr, Sanford Burnham Prebys Med Discovery Inst, La Jolla, CA 92037 USA.
   [Leiserson, Mark D. M.] Microsoft Res New England, Cambridge, MA 02142 USA.
   [Ruppin, Eytan] Tel Aviv Univ, Sch Comp Sci, IL-69978 Tel Aviv, Israel.
   [Ruppin, Eytan] Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel.
   [Leiserson, Mark D. M.; Ruppin, Eytan] Univ Maryland, Ctr Bioinformat & Computat Biol, College Pk, MD 20742 USA.
   [Ronai, Ze'ev A.] Israel Inst Technol, Technion, Fac Med, Technion Integrated Canc Ctr, IL-31096 Haifa, Israel.
C3 Sanford Burnham Prebys Medical Discovery Institute; National Institutes
   of Health (NIH) - USA; NIH National Cancer Institute (NCI); Microsoft;
   Tel Aviv University; Tel Aviv University; University System of Maryland;
   University of Maryland College Park; Technion Israel Institute of
   Technology; Rappaport Faculty of Medicine
RP Ronai, ZA (corresponding author), NCI, Tumor Initiat & Maintenance Program, Designated Canc Ctr, Sanford Burnham Prebys Med Discovery Inst, La Jolla, CA 92037 USA.; Ronai, ZA (corresponding author), Israel Inst Technol, Technion, Fac Med, Technion Integrated Canc Ctr, IL-31096 Haifa, Israel.
EM zeev@ronailab.net
RI Ruppin, Eytan/R-9698-2017; Senft, Daniela/O-6265-2018
OI RONAI, ZEEV/0000-0002-3859-0400; Senft, Daniela/0000-0002-6953-8189
FU NCI grant [R35CA197465-01]; Hervey Family Non-endowment Fund at the San
   Diego Foundation
FX Support by NCI grant (R35CA197465-01), and a Hervey Family Non-endowment
   Fund at the San Diego Foundation (to Z. R.), are gratefully
   acknowledged.
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NR 231
TC 103
Z9 113
U1 0
U2 52
PU CELL PRESS
PI CAMBRIDGE
PA 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA
SN 1471-4914
EI 1471-499X
J9 TRENDS MOL MED
JI Trends Mol. Med
PD OCT
PY 2017
VL 23
IS 10
BP 874
EP 898
DI 10.1016/j.molmed.2017.08.003
PG 25
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 FI3QU
UT WOS:000411882400003
PM 28887051
OA Green Accepted
DA 2025-01-04
ER

PT J
AU Oddo, D
   Sennott, EM
   Barault, L
   Valtorta, E
   Arena, S
   Cassingena, A
   Filiciotto, G
   Marzolla, G
   Elez, E
   van Geel, RMJM
   Bartolini, A
   Crisafulli, G
   Boscaro, V
   Godfrey, JT
   Buscarino, M
   Cancelliere, C
   Linnebacher, M
   Corti, G
   Truini, M
   Siravegna, G
   Grasselli, J
   Gallicchio, M
   Bernards, R
   Schellens, JHM
   Tabernero, J
   Engelman, JA
   Sartore-Bianchi, A
   Bardelli, A
   Siena, S
   Corcoran, RB
   Di Nicolantonio, F
AF Oddo, Daniele
   Sennott, Erin M.
   Barault, Ludovic
   Valtorta, Emanuele
   Arena, Sabrina
   Cassingena, Andrea
   Filiciotto, Genny
   Marzolla, Giulia
   Elez, Elena
   van Geel, Robin M. J. M.
   Bartolini, Alice
   Crisafulli, Giovanni
   Boscaro, Valentina
   Godfrey, Jason T.
   Buscarino, Michela
   Cancelliere, Carlotta
   Linnebacher, Michael
   Corti, Giorgio
   Truini, Mauro
   Siravegna, Giulia
   Grasselli, Julieta
   Gallicchio, Margherita
   Bernards, Rene
   Schellens, Jan H. M.
   Tabernero, Josep
   Engelman, Jeffrey A.
   Sartore-Bianchi, Andrea
   Bardelli, Alberto
   Siena, Salvatore
   Corcoran, Ryan B.
   Di Nicolantonio, Federica
TI Molecular Landscape of Acquired Resistance to Targeted Therapy
   Combinations in <i>BRAF</i>-Mutant Colorectal Cancer
SO CANCER RESEARCH
LA English
DT Article
ID MUTATIONS CONFER RESISTANCE; RAF INHIBITOR RESISTANCE; MEK INHIBITORS;
   BRAF(V600E) INHIBITION; METASTATIC MELANOMA; COLON-CANCER; EGFR;
   AMPLIFICATION; VEMURAFENIB; CETUXIMAB
AB Although recent clinical trials of BRAF inhibitor combinations have demonstrated improved efficacy in BRAF-mutant colorectal cancer, emergence of acquired resistance limits clinical benefit. Here, we undertook a comprehensive effort to define mechanisms underlying drug resistance with the goal of guiding development of therapeutic strategies to overcome this limitation. We generated a broad panel of BRAF-mutant resistant cell line models across seven different clinically relevant drug combinations. Combinatorial drug treatments were able to abrogate ERK1/2 phosphorylation in parental-sensitive cells, but not in their resistant counterparts, indicating that resistant cells escaped drug treatments through one or more mechanisms leading to biochemical reactivation of the MAPK signaling pathway. Genotyping of resistant cells identified gene amplification of EGFR, KRAS, and mutant BRAF, as well as acquired mutations in KRAS, EGFR, and MAP2K1. These mechanisms were clinically relevant, as we identified emergence of a KRAS G12C mutation and increase of mutant BRAF V600E allele frequency in the circulating tumor DNA of a patient at relapse from combined treatment with BRAF and MEK inhibitors. To identify therapeutic combinations capable of overcoming drug resistance, we performed a systematic assessment of candidate therapies across the panel of resistant cell lines. Independent of the molecular alteration acquired upon drug pressure, most resistant cells retained sensitivity to vertical MAPK pathway suppression when combinations of ERK, BRAF, and EGFR inhibitors were applied. These therapeutic combinations represent promising strategies for future clinical trials in BRAF-mutant colorectal cancer. (C) 2016 AACR.
C1 [Oddo, Daniele; Barault, Ludovic; Arena, Sabrina; Filiciotto, Genny; Marzolla, Giulia; Siravegna, Giulia; Bardelli, Alberto; Di Nicolantonio, Federica] Univ Torino, Dept Oncol, Str Prov 142,Km 3-95, I-10060 Turin, Italy.
   [Oddo, Daniele; Barault, Ludovic; Arena, Sabrina; Filiciotto, Genny; Marzolla, Giulia; Bartolini, Alice; Crisafulli, Giovanni; Buscarino, Michela; Cancelliere, Carlotta; Corti, Giorgio; Siravegna, Giulia; Bardelli, Alberto; Di Nicolantonio, Federica] IRCCS, Candiolo Canc Inst FPO, Turin, Italy.
   [Sennott, Erin M.; Godfrey, Jason T.; Engelman, Jeffrey A.; Corcoran, Ryan B.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
   [Valtorta, Emanuele; Cassingena, Andrea; Truini, Mauro; Sartore-Bianchi, Andrea; Siena, Salvatore] Grande Osped Metropolitano Niguarda, Niguarda Canc Ctr, Milan, Italy.
   [Elez, Elena; Grasselli, Julieta; Tabernero, Josep] Vall dHebron Univ Hosp, Barcelona, Spain.
   [Elez, Elena; Grasselli, Julieta; Tabernero, Josep] Univ Autonoma Barcelona, Inst Oncol VHIO, Barcelona, Spain.
   [van Geel, Robin M. J. M.; Bernards, Rene; Schellens, Jan H. M.] Netherlands Canc Inst, Amsterdam, Netherlands.
   [Boscaro, Valentina; Gallicchio, Margherita] Univ Turin, Dept Drug Sci & Technol, Turin, Italy.
   [Linnebacher, Michael] Univ Rostock, Div Mol Oncol & Immunotherapy, Dept Gen Surg, Rostock, Germany.
   [Siravegna, Giulia] FIRC Inst Mol Oncol IFOM, Milan, Italy.
   [Engelman, Jeffrey A.; Corcoran, Ryan B.] Harvard Med Sch, Dept Med, Boston, MA USA.
   [Siena, Salvatore] Univ Milan, Dept Oncol, Milan, Italy.
C3 University of Turin; IRCCS Fondazione del Piemonte per l'Oncologia;
   Harvard University; Massachusetts General Hospital; Hospital
   Universitari Vall d'Hebron; Autonomous University of Barcelona; Vall
   d'Hebron Institut d'Oncologia (VHIO); Netherlands Cancer Institute;
   University of Turin; University of Rostock; IFOM - FIRC Institute of
   Molecular Oncology; Harvard University; Harvard Medical School;
   University of Milan
RP Di Nicolantonio, F (corresponding author), Univ Torino, Dept Oncol, Str Prov 142,Km 3-95, I-10060 Turin, Italy.
EM federica.dinicolantonio@unito.it
RI Siravegna, Giulia/Z-2826-2019; Cassingena, Andrea/AGD-7137-2022;
   Sartore-Bianchi, Andrea/AAB-9848-2019; van Geel, Robin/JRY-8950-2023;
   Schellens, Jan/O-8444-2016; Linnebacher, Michael/AAT-3763-2021;
   Tabernero, Josep/AAG-5026-2019; SIENA, SALVATORE/AAC-5806-2019; Élez,
   Elena/AAH-2945-2019; Arena, Sabrina/H-4985-2012; BARTOLINI,
   ALICE/K-2534-2018; Crisafulli, Giovanni/AAB-6256-2019; BARDELLI,
   Alberto/J-9721-2018; Barault, Ludovic/J-2472-2016; Di Nicolantonio,
   Federica/A-2503-2011
OI BARTOLINI, ALICE/0000-0003-3492-0772; ODDO, DANIELE/0000-0001-6179-1668;
   Tabernero, Josep/0000-0002-2495-8139; Cassingena,
   Andrea/0000-0003-4116-3992; Crisafulli, Giovanni/0000-0002-5511-1555;
   Corti, Giorgio/0000-0001-6379-4117; BARDELLI,
   Alberto/0000-0003-1647-5070; Siravegna, Giulia/0000-0002-7132-6484;
   SIENA, SALVATORE/0000-0002-2681-2846; Barault,
   Ludovic/0000-0001-5227-5047; ARENA, Sabrina/0000-0002-1318-2494; van
   geel, Robin/0000-0003-1880-8131; Elez, Elena/0000-0002-4653-6324;
   Sartore-Bianchi, Andrea/0000-0003-0780-0409; Bernards,
   Rene/0000-0001-8677-3423; VALTORTA, EMANUELE/0000-0002-5087-6233; Di
   Nicolantonio, Federica/0000-0001-9618-2010
FU NCI NIH HHS [R01 CA208437, K08 CA166510, P50 CA127003] Funding Source:
   Medline
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NR 49
TC 89
Z9 91
U1 1
U2 24
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 1
PY 2016
VL 76
IS 15
BP 4504
EP 4515
DI 10.1158/0008-5472.CAN-16-0396
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DU6AO
UT WOS:000382295300020
PM 27312529
OA Green Submitted, Bronze, Green Accepted
DA 2025-01-04
ER

PT J
AU Zhang, HH
   Sun, FL
   Jiang, SY
   Yang, FH
   Dong, XL
   Liu, GX
   Wang, MJ
   Li, Y
   Su, M
   Wen, ZY
   Yu, CJ
   Fan, CK
   Li, XX
   Zhang, Z
   Yang, LN
   Li, B
AF Zhang, Huhu
   Sun, Fulin
   Jiang, Shuyao
   Yang, Fanghao
   Dong, Xiaolei
   Liu, Guoxiang
   Wang, Mengjun
   Li, Ya
   Su, Mohan
   Wen, Ziyuan
   Yu, Chunjuan
   Fan, Chenkai
   Li, Xiaoxia
   Zhang, Zhe
   Yang, Lina
   Li, Bing
TI METTL protein family: focusing on the occurrence, progression and
   treatment of cancer
SO BIOMARKER RESEARCH
LA English
DT Review
DE METTL protein family; Cancer progression; Biomarker; Treatment;
   Inhibitor
ID MESSENGER-RNA TRANSLATION; COLORECTAL-CANCER; PROMOTES TUMORIGENESIS;
   M6A MODIFICATION; POOR-PROGNOSIS; PROLIFERATION; CELLS; METHYLATION;
   PATHWAY; EXPRESSION
AB Methyltransferase-like protein is a ubiquitous enzyme-like protein in the human body, with binding domains for nucleic acids, proteins and other small molecules, and plays an important role in a variety of biological behaviours in normal organisms and diseases, characterised by the presence of a methyltransferase-like structural domain and a structurally conserved SAM-binding domain formed by the seven-stranded beta-fold structure in the center of the protein. With the deepening of research, the METTL protein family has been found to be abnormally expressed in a variety of tumor diseases, and the clarification of its relationship with tumor diseases can be used as a molecular therapeutic target and has an important role in the prognosis of tumors. In this paper, we review the structure, biological process, immunotherapy, drug-targeted therapy, and markers of the METTL protein family to provide new ideas for the diagnosis and treatment of tumors.
C1 [Zhang, Huhu; Sun, Fulin; Jiang, Shuyao; Yang, Fanghao; Dong, Xiaolei; Wang, Mengjun; Li, Ya; Su, Mohan; Wen, Ziyuan; Yu, Chunjuan; Fan, Chenkai; Li, Xiaoxia; Zhang, Zhe; Yang, Lina; Li, Bing] Qingdao Univ, Sch Basic Med, Dept Genet & Cell Biol, Qingdao 266071, Peoples R China.
   [Sun, Fulin; Jiang, Shuyao; Fan, Chenkai] Qingdao Univ, Hlth Sci Ctr, Qingdao 266071, Peoples R China.
   [Liu, Guoxiang] Weifang Peoples Hosp, Dept Clin Lab, 151 Guangwen Streer, Weifang 261041, Peoples R China.
   [Li, Bing] Qingdao Univ, Affiliated Haici Hosp, Dept Dermatol, Qingdao 266003, Peoples R China.
C3 Qingdao University; Qingdao University; Qingdao University
RP Yang, LN; Li, B (corresponding author), Qingdao Univ, Sch Basic Med, Dept Genet & Cell Biol, Qingdao 266071, Peoples R China.; Li, B (corresponding author), Qingdao Univ, Affiliated Haici Hosp, Dept Dermatol, Qingdao 266003, Peoples R China.
EM yanglina@qdu.edu.cn; libing_516@qdu.edu.cn
RI dong, xiaolei/HPH-5298-2023; Wang, Mengjun/LQI-9131-2024; Liu,
   Guoxiang/L-7413-2019
FU National Natural Science Foundation of China
FX Figures 2-5 were drawn by Figdraw (www.figdraw.com). Structures related
   to METTL inhibitors in Supplementary material 2 were obtained from
   https://pubchem.ncbi.nlm.nih.gov/.
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NR 206
TC 2
Z9 2
U1 6
U2 6
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2050-7771
J9 BIOMARK RES
JI Biomark. Res.
PD SEP 17
PY 2024
VL 12
IS 1
AR 105
DI 10.1186/s40364-024-00652-3
PG 29
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA G2K4D
UT WOS:001314977300001
PM 39289775
OA gold
DA 2025-01-04
ER

PT J
AU Wurm, AA
   Brilloff, S
   Kolovich, S
   Schäfer, S
   Rahimian, E
   Kufrin, V
   Bill, M
   Carrero, ZI
   Drukewitz, S
   Krüger, A
   Hüther, M
   Uhrig, S
   Oster, S
   Westphal, D
   Meier, F
   Pfütze, K
   Hübschmann, D
   Horak, P
   Kreutzfeldt, S
   Richter, D
   Schröck, E
   Baretton, G
   Heining, C
   Möhrmann, L
   Fröhling, S
   Ball, CR
   Glimm, H
AF Wurm, Alexander A.
   Brilloff, Silke
   Kolovich, Sofia
   Schaefer, Silvia
   Rahimian, Elahe
   Kufrin, Vida
   Bill, Marius
   Carrero, Zunamys I.
   Drukewitz, Stephan
   Krueger, Alexander
   Huether, Melanie
   Uhrig, Sebastian
   Oster, Sandra
   Westphal, Dana
   Meier, Friedegund
   Pfutze, Katrin
   Huebschmann, Daniel
   Horak, Peter
   Kreutzfeldt, Simon
   Richter, Daniela
   Schroeck, Evelin
   Baretton, Gustavo
   Heining, Christoph
   Moehrmann, Lino
   Froehling, Stefan
   Ball, Claudia R.
   Glimm, Hanno
TI Signaling-induced systematic repression of miRNAs uncovers cancer
   vulnerabilities and targeted therapy sensitivity
SO CELL REPORTS MEDICINE
LA English
DT Article
ID HUMAN COLON; PROTEOGENOMIC CHARACTERIZATION; FEEDBACK; ENCYCLOPEDIA;
   RESISTANCE; MUTATIONS; TUMORS; GENES; PI3K
AB Targeted therapies are effective in treating cancer, but success depends on identifying cancer vulnerabilities. In our study, we utilize small RNA sequencing to examine the impact of pathway activation on microRNA (miRNA) expression patterns. Interestingly, we discover that miRNAs capable of inhibiting key members of activated pathways are frequently diminished. Building on this observation, we develop an approach that integrates a low-miRNA-expression signature to identify druggable target genes in cancer. We train and validate our approach in colorectal cancer cells and extend it to diverse cancer models using patient-derived in vitro and in vivo systems. Finally, we demonstrate its additional value to support genomic and transcrip-tomic-based drug prediction strategies in a pan-cancer patient cohort from the National Center for Tumor Diseases (NCT)/German Cancer Consortium (DKTK) Molecularly Aided Stratification for Tumor Eradication (MASTER) precision oncology trial. In conclusion, our strategy can predict cancer vulnerabilities with high sensitivity and accuracy and might be suitable for future therapy recommendations in a variety of cancer subtypes.
C1 [Wurm, Alexander A.; Brilloff, Silke; Kolovich, Sofia; Schaefer, Silvia; Rahimian, Elahe; Kufrin, Vida; Bill, Marius] Tech Univ Dresden, Mildred Scheel Early Career Ctr, Natl Ctr Tumor Dis NCT UCC Dresden, Dresden, Germany.
   [Wurm, Alexander A.; Brilloff, Silke; Kolovich, Sofia; Schaefer, Silvia; Rahimian, Elahe; Kufrin, Vida; Bill, Marius] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dresden, Germany.
   [Wurm, Alexander A.; Brilloff, Silke; Kolovich, Sofia; Schaefer, Silvia; Rahimian, Elahe; Kufrin, Vida; Bill, Marius; Carrero, Zunamys I.; Huether, Melanie; Richter, Daniela; Heining, Christoph; Moehrmann, Lino; Ball, Claudia R.; Glimm, Hanno] Natl Ctr Tumor Dis NCT UCC Dresden, Dept Translat Med Oncol, Dresden, Germany.
   [Wurm, Alexander A.; Richter, Daniela; Heining, Christoph; Moehrmann, Lino; Ball, Claudia R.; Glimm, Hanno] Tech Univ Dresden, Fac Med, Translat Med Oncol, Dresden, Germany.
   [Wurm, Alexander A.; Brilloff, Silke; Kolovich, Sofia; Schaefer, Silvia; Rahimian, Elahe; Kufrin, Vida; Bill, Marius; Carrero, Zunamys I.; Drukewitz, Stephan; Krueger, Alexander; Huether, Melanie; Oster, Sandra; Schroeck, Evelin; Baretton, Gustavo; Heining, Christoph; Moehrmann, Lino; Ball, Claudia R.; Glimm, Hanno] Helmholtz Zentrum Dresden Rossendorf HZDR, Dresden, Germany.
   [Wurm, Alexander A.; Huebschmann, Daniel; Heining, Christoph; Moehrmann, Lino; Ball, Claudia R.; Glimm, Hanno] Tech Univ Dresden, Fac Med, Translat Med Oncol, Dresden, Germany.
   [Wurm, Alexander A.; Bill, Marius; Carrero, Zunamys I.; Drukewitz, Stephan; Krueger, Alexander; Oster, Sandra; Richter, Daniela; Schroeck, Evelin; Baretton, Gustavo; Heining, Christoph; Moehrmann, Lino; Ball, Claudia R.; Glimm, Hanno] German Canc Consortium DKTK, Dresden, Germany.
   [Bill, Marius] Univ Hosp Carl Gustav Carus, Dept Internal Med 1, Dresden, Germany.
   [Drukewitz, Stephan; Krueger, Alexander; Oster, Sandra; Schroeck, Evelin; Baretton, Gustavo] Natl Ctr Tumor Dis Dresden NCT UCC, Core Unit Mol Tumor Diagnost CMTD, Dresden, Germany.
   [Drukewitz, Stephan] Univ Leipzig, Inst Human Genet, Leipzig, Germany.
   [Uhrig, Sebastian; Huebschmann, Daniel] Natl Ctr Tumor Dis NCT Heidelberg, Mol Precis Oncol Program, Computat Oncol Grp, Heidelberg, Germany.
   [Westphal, Dana; Meier, Friedegund] Tech Univ Dresden, Fac Med, Dept Dermatol, Dresden, Germany.
   [Meier, Friedegund] Univ Canc Ctr Dresden, Skin Canc Ctr, Dresden, Germany.
   [Meier, Friedegund] Natl Ctr Tumor Dis, Dresden, Germany.
   [Pfutze, Katrin; Huebschmann, Daniel; Horak, Peter; Kreutzfeldt, Simon; Froehling, Stefan] German Canc Consortium DKTK, Heidelberg, Germany.
   [Pfutze, Katrin] Univ Hosp Heidelberg, Natl Ctr Tumor Dis NCT Heidelberg, Sample Proc Lab, Heidelberg, Germany.
   [Huebschmann, Daniel] Heidelberg Inst Stem Cell Technol & Expt Med, Heidelberg, Germany.
   [Horak, Peter; Kreutzfeldt, Simon; Froehling, Stefan] Natl Ctr Tumor Dis NCT Heidelberg, Dept Translat Med Oncol, Heidelberg, Germany.
   [Schroeck, Evelin] Tech Univ Dresden, Inst Clin Genet, Univ Hosp Carl Gustav Carus, Dresden, Germany.
   [Schroeck, Evelin] Hereditary Canc Syndrome Ctr Dresden, ERN GENTURIS, Dresden, Germany.
   [Ball, Claudia R.] Tech Univ Dresden, Fac Biol, Dresden, Germany.
   [Glimm, Hanno] Natl Ctr Tumor Dis NCT Heidelberg, Translat Funct Canc Genom, Heidelberg, Germany.
   [Uhrig, Sebastian; Pfutze, Katrin; Huebschmann, Daniel; Glimm, Hanno] Univ Heidelberg Hosp, Heidelberg, Germany.
C3 Technische Universitat Dresden; Technische Universitat Dresden; Carl
   Gustav Carus University Hospital; Technische Universitat Dresden;
   Helmholtz Association; Helmholtz-Zentrum Dresden-Rossendorf (HZDR);
   Technische Universitat Dresden; Helmholtz Association; German Cancer
   Research Center (DKFZ); Technische Universitat Dresden; Carl Gustav
   Carus University Hospital; Leipzig University; Helmholtz Association;
   German Cancer Research Center (DKFZ); Ruprecht Karls University
   Heidelberg; Technische Universitat Dresden; 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; Technische Universitat Dresden; Carl Gustav
   Carus University Hospital; Technische Universitat Dresden; Helmholtz
   Association; German Cancer Research Center (DKFZ); Ruprecht Karls
   University Heidelberg; Ruprecht Karls University Heidelberg
RP Wurm, AA (corresponding author), Tech Univ Dresden, Mildred Scheel Early Career Ctr, Natl Ctr Tumor Dis NCT UCC Dresden, Dresden, Germany.; Wurm, AA (corresponding author), Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dresden, Germany.; Wurm, AA (corresponding author), Natl Ctr Tumor Dis NCT UCC Dresden, Dept Translat Med Oncol, Dresden, Germany.; Wurm, AA (corresponding author), Tech Univ Dresden, Fac Med, Translat Med Oncol, Dresden, Germany.; Wurm, AA (corresponding author), Helmholtz Zentrum Dresden Rossendorf HZDR, Dresden, Germany.; Wurm, AA (corresponding author), Tech Univ Dresden, Fac Med, Translat Med Oncol, Dresden, Germany.
EM alexander.wurm@nct-dresden.de
RI Heining, Christoph/IUO-2974-2023; Meier, Friedegund/HTN-0745-2023
OI Ball, Claudia/0000-0002-1749-3791; Mohrmann, Lino/0000-0003-4650-6827;
   Kruger, Alexander/0000-0002-9878-1137; Westphal,
   Dana/0000-0003-4340-0402; Meier, Friedegund/0000-0003-4340-9706; Kufrin,
   Vida/0009-0002-2431-7654; Horak, Peter/0000-0003-4536-9306; Carrero,
   Zunamys/0000-0001-8501-1566; Wurm, Alexander/0000-0003-0065-9481
FU DFG (German Research Foundation) [WU977/2-1]; Deutsche Krebshilfe
   [70114086]; TU Dresden (MeDDrive); NCT Molecular Precision Oncology
   Program; DKTK Joint Funding Program; TU Dresden; SLUB Dresden; DFG
FX We thank the NCT/DKFZ Sample Processing Laboratory, the Dresden -Concept
   Genome Center Core Facility, the NCT/DKTK MASTER consortium, the
   Preclinical Model Unit (PMU) at the NCT Dresden, and the Dresden OncoRay
   animal facility team. We thank Kerstin Bruechner for help with animal
   approval. We thank Liane Stolz-Kieslich and Mechthild Krause for help
   with tumor pathology. We thank Peggy Jungke, Martin Bornhaeuser, and
   Frank Buch-holz for scientific and administrative support. This work was
   supported by grants from DFG (German Research Foundation, WU977/2-1),
   Deutsche Krebshilfe (70114086 and Mildred-Scheel Program), and TU
   Dresden (MeDDrive) to A.A.W. The NCT/DKTK MASTER program was supported
   by the NCT Molecular Precision Oncology Program and the DKTK Joint
   Funding Program. The Article Processing Charges (APC) were funded by the
   joint publication funds of the TU Dresden, including Carl Gustav Carus
   Faculty of Medicine, and the SLUB Dresden as well as the Open Access
   Publication Funding of the DFG.
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NR 64
TC 3
Z9 3
U1 0
U2 5
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 101200
DI 10.1016/j.xcrm.2023.101200
EA OCT 2023
PG 24
WC Cell Biology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Research & Experimental Medicine
GA Y5HX9
UT WOS:001105577500001
PM 37734378
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Lee, SH
   Jang, HJ
AF Lee, Sung Hak
   Jang, Hyun-Jong
TI Deep learning-based prediction of molecular cancer biomarkers from
   tissue slides: A new tool for precision oncology
SO CLINICAL AND MOLECULAR HEPATOLOGY
LA English
DT Review
DE Deep learning; Pathology; Molecular tests; Precision medicine; Precision
   oncology
ID COLORECTAL-CANCER; MICROSATELLITE INSTABILITY; SUBTYPES; MODEL
AB Molecular tests are necessary to stratify cancer patients for targeted therapy. However, high cost and technical barriers limit the application of these tests, hindering optimal treatment. Recently, deep learning (DL) has been applied to predict molecular test results from digitized images of tissue slides. Furthermore, treatment response and prognosis can be predicted from tissue slides using DL. In this review, we summarized DL-based studies regarding the prediction of genetic mutation, microsatellite instability, tumor mutational burden, molecular subtypes, gene expression, treatment response, and prognosis directly from Hematoxylin and Eosin-stained tissue slides. Although performance needs to be improved, these studies clearly demonstrated the feasibility of DL- based prediction of key molecular features in cancer tissues. With the accumulation of data and technical advances, the performance of the DL system could be improved in the near future. Therefore, we expect that DL could provide cost- and time-effective alternative tools for patient stratification in the era of precision oncology.
C1 [Lee, Sung Hak] Catholic Univ Korea, Seoul St Marys Hosp, Dept Hosp Pathol, Coll Med, Seoul, South Korea.
   [Jang, Hyun-Jong] Catholic Univ Korea, Dept Physiol, Coll Med, Catholic Big Data Integrat Ctr, Seoul, South Korea.
C3 Seoul St. Mary's Hospital; Catholic University of Korea; Catholic
   University of Korea
RP Jang, HJ (corresponding author), Catholic Univ Korea, Dept Physiol, Coll Med, 222 Banpo Daero,Seocho Gu, Seoul 06591, South Korea.
EM hjjang@catholic.ac.kr
RI Lee, Seung-Hwan/AAG-1361-2019; Jang, Hyunjong/IUO-7586-2023
OI Jang, Hyun-Jong/0000-0003-4535-1560
FU National Research Foundation of Korea [NRF-2021R1A4A5028966]; Korea
   Health Technology R&D Project through the Korea Health Industry
   Development Institute (KHIDI) - Ministry of Health & Welfare, Republic
   of Korea [HI21C0940]
FX This work was supported by a grant from the National Research Foundation
   of Korea (NRF-2021R1A4A5028966) and a grant 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: HI21C0940).
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NR 86
TC 13
Z9 13
U1 2
U2 24
PU KOREAN ASSOC STUDY LIVER
PI SEOUL
PA RM A1210, 53 MAPO-DAERO, MAPOTRAPALACE, DOWHA-DONG, MAPO-GU, SEOUL,
   04158, SOUTH KOREA
SN 2287-2728
EI 2287-285X
J9 CLIN MOL HEPATOL
JI Clin. Mol. Hepatol.
PD OCT
PY 2022
VL 28
IS 4
BP 754
EP 772
DI 10.3350/cmh.2021.0394
PG 19
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 6A2KL
UT WOS:000880487800005
PM 35443570
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Kim, SH
   Ryu, HG
   Lee, J
   Shin, J
   Harikishore, A
   Jung, HY
   Kim, YS
   Lyu, HN
   Oh, E
   Baek, NI
   Choi, KY
   Yoon, HS
   Kim, KT
AF Kim, Seong-Hoon
   Ryu, Hye Guk
   Lee, Juhyun
   Shin, Joon
   Harikishore, Amaravadhi
   Jung, Hoe-Youn
   Kim, Ye Seul
   Lyu, Ha-Na
   Oh, Eunji
   Baek, Nam-In
   Choi, Kwan-Yong
   Yoon, Ho Sup
   Kim, Kyong-Tai
TI Ursolic acid exerts anti-cancer activity by suppressing vaccinia-related
   kinase 1-mediated damage repair in lung cancer cells
SO SCIENTIFIC REPORTS
LA English
DT Article
ID TO-AUTOINTEGRATION FACTOR; 1 VRK1; COLORECTAL-CANCER; IN-VITRO; DNA;
   APOPTOSIS; P53; PHOSPHORYLATION; ACTIVATION; PATHWAY
AB Many mitotic kinases have been targeted for the development of anti-cancer drugs, and inhibitors of these kinases have been expected to perform well for cancer therapy. Efforts focused on selecting good targets and finding specific drugs to target are especially needed, largely due to the increased frequency of anti-cancer drugs used in the treatment of lung cancer. Vaccinia-related kinase 1 (VRK1) is a master regulator in lung adenocarcinoma and is considered a key molecule in the adaptive pathway, which mainly controls cell survival. We found that ursolic acid (UA) inhibits the catalytic activity of VRK1 via direct binding to the catalytic domain of VRK1. UA weakens surveillance mechanisms by blocking 53BP1 foci formation induced by VRK1 in lung cancer cells, and possesses synergistic anti-cancer effects with DNA damaging drugs. Taken together, UA can be a good anticancer agent for targeted therapy or combination therapy with DNA damaging drugs for lung cancer patients.
C1 [Kim, Seong-Hoon; Ryu, Hye Guk; Kim, Ye Seul; Lyu, Ha-Na; Kim, Kyong-Tai] Pohang Univ Sci & Technol, Dept Life Sci, Pohang 790784, South Korea.
   [Lee, Juhyun; Jung, Hoe-Youn; Choi, Kwan-Yong; Kim, Kyong-Tai] Pohang Univ Sci & Technol, Div Integrat Biosci & Biotechnol, Pohang 790784, South Korea.
   [Shin, Joon; Harikishore, Amaravadhi; Yoon, Ho Sup] Nanyang Technol Univ, Sch Biol Sci, Singapore 637551, Singapore.
   [Oh, Eunji; Baek, Nam-In] Kyung Hee Univ, Grad Sch Biotechnol, Suwon 449701, South Korea.
   [Oh, Eunji; Baek, Nam-In] Kyung Hee Univ, Plant Metab Res Ctr, Suwon 449701, South Korea.
   [Yoon, Ho Sup] Kyung Hee Univ, Dept Genet Engn, Coll Life Sci, Suwon 449701, South Korea.
C3 Pohang University of Science & Technology (POSTECH); Pohang University
   of Science & Technology (POSTECH); Nanyang Technological University;
   Kyung Hee University; Kyung Hee University; Kyung Hee University
RP Kim, KT (corresponding author), Pohang Univ Sci & Technol, Dept Life Sci, Pohang 790784, South Korea.
EM ktk@postech.ac.kr
RI Park, Mi-Kyung/J-9643-2017; Amaravadhi, Harikishore/ITV-6803-2023; Baek,
   Nam-In/AAK-7447-2020; Amaravadhi, Harikishore/E-9294-2016; Yoon, Ho
   Sup/A-2193-2011
OI Amaravadhi, Harikishore/0000-0001-6552-1534; KIM,
   KYONG-TAI/0000-0001-7292-2627; Jung, Hoe-Yune/0000-0003-1802-5428; Yoon,
   Ho Sup/0000-0002-8243-3904
FU Cooperative Research Program for Agriculture Science & Technology
   Development [PJ01121602]; Rural Development Administration, Republic of
   Korea; Ministry of Education, Korea [10Z20130012243]; National Research
   Foundation of Korea (NRF) [2014054324]; Tier 2 Grant [ARC 25/12];
   Singapore Ministry of Education
FX This work was carried out with the support of "Cooperative Research
   Program for Agriculture Science & Technology Development [Project No.
   PJ01121602]" Rural Development Administration, Republic of Korea; " BK21
   Plus" funded by the Ministry of Education, Korea [10Z20130012243];
   "Basic Research Laboratory supporting project" funded by the National
   Research Foundation of Korea (NRF) [2014054324]; "Tier 2 Grant ARC 25/12
   (H.S. Yoon)" funded by Singapore Ministry of Education. 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 70
TC 27
Z9 34
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 SEP 28
PY 2015
VL 5
AR 14570
DI 10.1038/srep14570
PG 12
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA CS1FO
UT WOS:000361808500003
PM 26412148
OA Green Submitted, gold, Green Published
DA 2025-01-04
ER

PT J
AU Cherri, S
   Melocchi, L
   Gandolfi, L
   Rossi, G
   Zaniboni, A
AF Cherri, Sara
   Melocchi, Laura
   Gandolfi, Laura
   Rossi, Giulio
   Zaniboni, Alberto
TI Integrated Decision-Making in the Treatment of Colon-Rectal Cancer: The
   Case of KRAS-Mutated Tumors
SO LIFE-BASEL
LA English
DT Review
DE cancer; chemotherapy; colon cancer; KRAS; target therapy;
   multidisciplinary team
ID METASTATIC COLORECTAL-CANCER; RAS MUTATIONS; 1ST-LINE TREATMENT;
   PROGNOSTIC-FACTOR; LIVER RESECTION; PHASE I/II; CETUXIMAB; SURVIVAL;
   TRIAL; RADIOTHERAPY
AB In recent years, precision medicine has taken an increasing place in various branches of medical oncology, including colorectal cancer. Among the potentially relevant mutations for this cancer is the KRAS mutation, initially defined as "untargetable"; today, we see the birth of new molecules that target one of the variants of the KRAS mutation, KRAS G12C, having a significant impact on the therapeutic options for other malignancies, such as metastatic lung cancer. This fundamental step forward has stimulated scientific research on other potential targets of KRAS, both indirect and direct, and combination treatments aiming to overcome the mechanisms of resistance to these drugs that decrease in efficacy in colorectal cancer. What was once a negative predictive marker of response to anti-EGFR drugs today has become a potential target for targeted treatments. In turn, the prognostic role of the mutation has become extremely interesting, making it a potentially useful element in therapeutic decision-making, not only regarding oncological treatments but also in a more complex and complete manner within a global vision of the patient, involving other figures on the multidisciplinary team, such as surgeons, radiotherapists, and interventional radiologists.
C1 [Cherri, Sara; Zaniboni, Alberto] Fdn Poliambulanza, Dept Clin Oncol, I-25124 Brescia, Italy.
   [Melocchi, Laura; Gandolfi, Laura; Rossi, Giulio] Fdn Poliambulanza, Dept Anat Pathol, I-25124 Brescia, Italy.
RP Cherri, S (corresponding author), Fdn Poliambulanza, Dept Clin Oncol, I-25124 Brescia, Italy.
EM sara.cherri@poliambulanza.it
RI Rossi, Giuseppe/K-3376-2016; Rossi, Giulio/K-6217-2016
OI Melocchi, Laura/0000-0001-5161-6305; Rossi, Giulio/0000-0001-8855-1218
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NR 89
TC 2
Z9 3
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-1729
J9 LIFE-BASEL
JI Life-Basel
PD FEB
PY 2023
VL 13
IS 2
AR 395
DI 10.3390/life13020395
PG 18
WC Biology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Microbiology
GA 9J9DZ
UT WOS:000940479500001
PM 36836752
OA gold, Green Published
DA 2025-01-04
ER

PT J
AU Parry, JL
   Hall, PS
   Young, J
AF Parry, J. L.
   Hall, P. S.
   Young, J.
TI New horizons in systemic anti-cancer therapy in older people
SO AGE AND AGEING
LA English
DT Article
DE cancer; older people; chemotherapy; targeted therapy; immunotherapy;
   toxicity; trials; systemic anti cancer therapy (SACT)
ID CELL LUNG-CANCER; ELDERLY-PATIENTS; ADJUVANT CHEMOTHERAPY; COLON-CANCER;
   BREAST-CANCER; ADULTS; TOXICITY; FATIGUE; OPTIONS; HEALTH
AB Cancer is a disease associated with ageing. Increased life expectancy means that cancer in older adults is becoming an increasingly common problem. There are unique issues to consider when making decisions about cancer treatment in older populations. Unfortunately, however, this group is still under-represented in clinical trials for new cancer therapies meaning there are less evidence-based data to guide management. This article aims to look at how we can optimise the cancer treatment for older patients with a focus on systemic anti-cancer therapy and addressing particular issues around patient selection, improving treatment tolerance and use of newer agents with different toxicity profiles.
C1 [Parry, J. L.; Hall, P. S.] Univ Edinburgh, Edinburgh Canc Res Ctr, Crewe Rd South, Edinburgh EH4 2XR, Midlothian, Scotland.
   [Young, J.] Bradford Royal Infirm, Bradford Inst Hlth Res, Bradford BD9 6RJ, W Yorkshire, England.
C3 University of Edinburgh; Bradford Royal Infirmary
RP Hall, PS (corresponding author), Univ Edinburgh, Edinburgh Canc Res Ctr, Crewe Rd South, Edinburgh EH4 2XR, Midlothian, Scotland.
EM p.s.hall@ed.ac.uk
CR Aapro M, 2005, GERONTOLOGY, V51, P287, DOI 10.1159/000086364
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NR 37
TC 4
Z9 4
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0002-0729
EI 1468-2834
J9 AGE AGEING
JI Age Ageing
PD MAY
PY 2018
VL 47
IS 3
BP 340
EP 348
DI 10.1093/ageing/afy024
PG 9
WC Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Geriatrics & Gerontology
GA GF5YK
UT WOS:000432043700007
PM 29617715
OA Green Accepted, Bronze
DA 2025-01-04
ER

PT J
AU Zhou, S
   Xu, HJ
   Tang, QL
   Xia, HW
   Bi, F
AF Zhou, Sheng
   Xu, Huanji
   Tang, Qiulin
   Xia, Hongwei
   Bi, Feng
TI Dipyridamole Enhances the Cytotoxicities of Trametinib against Colon
   Cancer Cells through Combined Targeting of HMGCS1 and MEK Pathway
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID MEVALONATE PATHWAY; PHASE-II; PLUS SIMVASTATIN; HIGHLY POTENT; ERK
   PATHWAY; CHOLESTEROL; KRAS; LUNG; INHIBITORS; SYNTHASE
AB Both the MAPK pathway and mevalonate (MVA) signaling pathway play an increasingly significant role in the carcinogenesis of colorectal carcinoma, whereas the cross-talk between these two pathways and its implication in targeted therapy remains unclear in colorectal carcinoma. Here, we identified that HMGCS1 (3-hydroxy-3-methylglutaryl-CoA synthase 1), the rate-limiting enzyme of the MVA pathway, is overexpressed in colon cancer tissues and positively regulates the cell proliferation, migration, and invasion of colon cancer cells. In addition, HMGCS1 could enhance the activity of pERK independent of the MVA pathway, and the suppression of HMGCS1 could completely reduce the EGF-induced proliferation of colon cancer cells. Furthermore, we found that trametinib, a MEK inhibitor, could only partially abolish the upregulation of HMGCS1 induced by EGF treatment, while combination with HMGCS1 knockdown could completely reverse the upregulation of HMGCS1 induced by EGF treatment and increase the sensitivity of colon cancer cells to trametinib. Finally, we combined trametinib and dipyridamole, a common clinically used drug that could suppress the activity of SREBF2 (sterol regulatory element-binding transcription factor 2), a transcription factor regulating HMGCS1 expression, and identified its synergistic effect in inhibiting the proliferation and survival of colon cancer cells in vitro as well as the in vivo tumorigenic potential of colon cancer cells. Together, the current data indicated that HMGCS1 may be a novel biomarker, and the combination of targeting HMGCS1 and MEK might be a promising therapeutic strategy for patients with colon cancer.
C1 Sichuan Univ, Dept Abdominal Oncol, Ctr Canc, West China Hosp, Chengdu, Sichuan, Peoples R China.
   Sichuan Univ, Lab Mol Targeted Therapy Oncol, West China Hosp, Chengdu, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University
RP Xia, HW; Bi, F (corresponding author), Sichuan Univ, Chengdu 610041, Sichuan, Peoples R China.
EM xiahongwei1988@126.com; bifeng@scu.edu.cn
RI Xu, Huanji/HZJ-6972-2023; Bi, Feng/J-7459-2015
OI Xu, Huanji/0000-0003-0314-5646
FU National Natural Science Foundation of China [81872020]; Sichuan Science
   and Technology Program [2019YJ0056]
FX We really appreciate the technician Zhang Yi (Core Facility of West
   China Hospital) for assistance with experiments and equipment in the
   pathological analyses. This study was supported by the National Natural
   Science Foundation of China (F. Bi, grant no. 81872020), Sichuan Science
   and Technology Program(H.W. Xia, grant no. 2019YJ0056), and Sichuan
   Science and Technology Program (F. Bi, grant no. 2019YJ0056)
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NR 48
TC 28
Z9 32
U1 1
U2 20
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
EI 1538-8514
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD JAN
PY 2020
VL 19
IS 1
BP 135
EP 146
DI 10.1158/1535-7163.MCT-19-0413
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KA3AE
UT WOS:000505667900012
PM 31554653
OA Green Submitted
DA 2025-01-04
ER

PT J
AU Lindhorst, PH
   Hummon, AB
AF Lindhorst, Philip H.
   Hummon, Amanda B.
TI Proteomics of Colorectal Cancer: Tumors, Organoids, and Cell Cultures-A
   Minireview
SO FRONTIERS IN MOLECULAR BIOSCIENCES
LA English
DT Review
DE colorectal cancer; proteomics; mass spectrometry; organoids; cell
   culture; tumors; biomarkers
ID HUMAN COLON; QUANTITATIVE PROTEOMICS; IDENTIFICATION; METASTASIS;
   SPHEROIDS; BIOMARKER; PROTEINS; LINES; RESTRICTION; REVEALS
AB Proteomics, the study of the complete protein composition of a sample, is an important field for cancer research. Changes in the proteome can serve as a biomarker of cancer or lead to the development of a targeted therapy. This minireview will focus on mass spectrometry-based proteomics studies applied specifically to colorectal cancer, particularly the variety of cancer model systems used, including tumor samples, two-dimensional (2D) and three-dimensional (3D) cell cultures such as spheroids and organoids. A thorough discussion of the application of these systems will accompany the review of the literature, as each provides distinct advantages and disadvantages for colorectal cancer research. Finally, we provide conclusions and future perspectives for the application of these model systems to cancer research as a whole.
C1 [Lindhorst, Philip H.; Hummon, Amanda B.] Ohio State Univ, Dept Chem & Biochem, Columbus, OH 43210 USA.
   [Hummon, Amanda B.] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
C3 University System of Ohio; Ohio State University; James Cancer Hospital
   & Solove Research Institute; University System of Ohio; Ohio State
   University
RP Hummon, AB (corresponding author), Ohio State Univ, Dept Chem & Biochem, Columbus, OH 43210 USA.; Hummon, AB (corresponding author), Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
EM hummon.1@osu.edu
FU Ohio State University; NIH [R01-GM110406]
FX PL was supported by a University Fellowship from The Ohio State
   University. AH was supported by R01-GM110406 from the NIH.
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NR 72
TC 15
Z9 16
U1 0
U2 19
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 DEC 10
PY 2020
VL 7
AR 604492
DI 10.3389/fmolb.2020.604492
PG 8
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA PI7NA
UT WOS:000601272000001
PM 33363210
OA gold, Green Published
DA 2025-01-04
ER

EF