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TFF2-CXCR4 Axis Is Associated with BRAF V600E Colon Cancer

Oncogene-induced senescence (OIS), a tumor-suppressive mechanism that is induced by the replicative and metabolic stress of oncogene activation, is a key barrier in the development of BRAF V600E colon cancer. Inhibition of this mechanism has been observed through epigenetic changes observed in spora... Full description

Journal Title: Cancer prevention research (Philadelphia Pa.), July 2015, Vol.8(7), pp.614-9
Main Author: Gala, Manish K
Other Authors: Austin, Thomas , Ogino, Shuji , Chan, Andrew T
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1940-6215 ; PMID: 25899003 Version:1 ; DOI: 10.1158/1940-6207.CAPR-14-0444
Link: http://pubmed.gov/25899003
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recordid: medline25899003
title: TFF2-CXCR4 Axis Is Associated with BRAF V600E Colon Cancer
format: Article
creator:
  • Gala, Manish K
  • Austin, Thomas
  • Ogino, Shuji
  • Chan, Andrew T
subjects:
  • Colonic Neoplasms -- Genetics
  • Peptides -- Metabolism
  • Proto-Oncogene Proteins B-Raf -- Genetics
  • Receptors, Cxcr4 -- Metabolism
ispartof: Cancer prevention research (Philadelphia, Pa.), July 2015, Vol.8(7), pp.614-9
description: Oncogene-induced senescence (OIS), a tumor-suppressive mechanism that is induced by the replicative and metabolic stress of oncogene activation, is a key barrier in the development of BRAF V600E colon cancer. Inhibition of this mechanism has been observed through epigenetic changes observed in sporadic serrated polyps, as well as through the germline mutations associated with those who develop serrated polyposis. We hypothesize that upregulated autocrine factors exist that are specific to the serrated pathway and also promote bypass of oncogene-induced senescence. To identify such autocrine factors, we integrate analyses of microarrays of sessile serrated polyps and two large colon cancer cohorts, the Cancer Genome Atlas (TCGA; n = 153), and French national Cartes d'Identité des Tumeurs (CIT) program (n = 462), with enhanced gene annotation through natural language processing techniques of the existing medical corpus. We reproducibly associate higher expression of the ligand-receptor axis...
language: eng
source:
identifier: E-ISSN: 1940-6215 ; PMID: 25899003 Version:1 ; DOI: 10.1158/1940-6207.CAPR-14-0444
fulltext: fulltext
issn:
  • 19406215
  • 1940-6215
url: Link


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titleTFF2-CXCR4 Axis Is Associated with BRAF V600E Colon Cancer
creatorGala, Manish K ; Austin, Thomas ; Ogino, Shuji ; Chan, Andrew T
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subjectColonic Neoplasms -- Genetics ; Peptides -- Metabolism ; Proto-Oncogene Proteins B-Raf -- Genetics ; Receptors, Cxcr4 -- Metabolism
descriptionOncogene-induced senescence (OIS), a tumor-suppressive mechanism that is induced by the replicative and metabolic stress of oncogene activation, is a key barrier in the development of BRAF V600E colon cancer. Inhibition of this mechanism has been observed through epigenetic changes observed in sporadic serrated polyps, as well as through the germline mutations associated with those who develop serrated polyposis. We hypothesize that upregulated autocrine factors exist that are specific to the serrated pathway and also promote bypass of oncogene-induced senescence. To identify such autocrine factors, we integrate analyses of microarrays of sessile serrated polyps and two large colon cancer cohorts, the Cancer Genome Atlas (TCGA; n = 153), and French national Cartes d'Identité des Tumeurs (CIT) program (n = 462), with enhanced gene annotation through natural language processing techniques of the existing medical corpus. We reproducibly associate higher expression of the ligand-receptor axis...
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descriptionOncogene-induced senescence (OIS), a tumor-suppressive mechanism that is induced by the replicative and metabolic stress of oncogene activation, is a key barrier in the development of BRAF V600E colon cancer. Inhibition of this mechanism has been observed through epigenetic changes observed in sporadic serrated polyps, as well as through the germline mutations associated with those who develop serrated polyposis. We hypothesize that upregulated autocrine factors exist that are specific to the serrated pathway and also promote bypass of oncogene-induced senescence. To identify such autocrine factors, we integrate analyses of microarrays of sessile serrated polyps and two large colon cancer cohorts, the Cancer Genome Atlas (TCGA; n = 153), and French national Cartes d'Identité des Tumeurs (CIT) program (n = 462), with enhanced gene annotation through natural language processing techniques of the existing medical corpus. We reproducibly associate higher expression of the ligand-receptor axis...
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abstractOncogene-induced senescence (OIS), a tumor-suppressive mechanism that is induced by the replicative and metabolic stress of oncogene activation, is a key barrier in the development of BRAF V600E colon cancer. Inhibition of this mechanism has been observed through epigenetic changes observed in sporadic serrated polyps, as well as through the germline mutations associated with those who develop serrated polyposis. We hypothesize that upregulated autocrine factors exist that are specific to the serrated pathway and also promote bypass of oncogene-induced senescence. To identify such autocrine factors, we integrate analyses of microarrays of sessile serrated polyps and two large colon cancer cohorts, the Cancer Genome Atlas (TCGA; n = 153), and French national Cartes d'Identité des Tumeurs (CIT) program (n = 462), with enhanced gene annotation through natural language processing techniques of the existing medical corpus. We reproducibly associate higher expression of the ligand-receptor axis...
doi10.1158/1940-6207.CAPR-14-0444
pmid25899003
date2015-07