Carcinogenesis in IBD: Potential targets for the prevention of colorectal cancer

Research output: Contribution to journalArticle

168 Citations (Scopus)

Abstract

In patients with IBD, chronic colonic inflammation increases the risk of colorectal cancer, perhaps because inflammation predisposes these tissues to genomic instability. Carcinogenesis in the inflamed colon seems to follow a different sequence of genetic alterations than that observed in sporadic cancers in the uninflamed colon. In this Review, we focus on the genetic alterations in colitis-associated colorectal cancer that contribute to the acquisition of the essential hallmarks of cancer, and on how those alterations differ from sporadic colorectal cancers. Our intent is to provide a conceptual basis for categorizing carcinogenetic molecular abnormalities in IBD, and for understanding how cancer-preventive therapies might target reversal of acquired abnormalities in specific biochemical pathways.

Original languageEnglish (US)
Pages (from-to)297-305
Number of pages9
JournalNature Reviews Gastroenterology and Hepatology
Volume6
Issue number5
DOIs
StatePublished - 2009

Fingerprint

Colorectal Neoplasms
Carcinogenesis
Colon
Inflammation
Neoplasms
Genomic Instability
Colitis
Therapeutics

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology
  • Medicine(all)

Cite this

@article{3860feee22d041dfbb2720c16f42302e,
title = "Carcinogenesis in IBD: Potential targets for the prevention of colorectal cancer",
abstract = "In patients with IBD, chronic colonic inflammation increases the risk of colorectal cancer, perhaps because inflammation predisposes these tissues to genomic instability. Carcinogenesis in the inflamed colon seems to follow a different sequence of genetic alterations than that observed in sporadic cancers in the uninflamed colon. In this Review, we focus on the genetic alterations in colitis-associated colorectal cancer that contribute to the acquisition of the essential hallmarks of cancer, and on how those alterations differ from sporadic colorectal cancers. Our intent is to provide a conceptual basis for categorizing carcinogenetic molecular abnormalities in IBD, and for understanding how cancer-preventive therapies might target reversal of acquired abnormalities in specific biochemical pathways.",
author = "Feagins, {Linda A.} and Souza, {Rhonda F.} and Spechler, {Stuart J.}",
year = "2009",
doi = "10.1038/nrgastro.2009.44",
language = "English (US)",
volume = "6",
pages = "297--305",
journal = "Nature Reviews Gastroenterology and Hepatology",
issn = "1759-5045",
publisher = "Nature Publishing Group",
number = "5",

}

TY - JOUR

T1 - Carcinogenesis in IBD

T2 - Potential targets for the prevention of colorectal cancer

AU - Feagins, Linda A.

AU - Souza, Rhonda F.

AU - Spechler, Stuart J.

PY - 2009

Y1 - 2009

N2 - In patients with IBD, chronic colonic inflammation increases the risk of colorectal cancer, perhaps because inflammation predisposes these tissues to genomic instability. Carcinogenesis in the inflamed colon seems to follow a different sequence of genetic alterations than that observed in sporadic cancers in the uninflamed colon. In this Review, we focus on the genetic alterations in colitis-associated colorectal cancer that contribute to the acquisition of the essential hallmarks of cancer, and on how those alterations differ from sporadic colorectal cancers. Our intent is to provide a conceptual basis for categorizing carcinogenetic molecular abnormalities in IBD, and for understanding how cancer-preventive therapies might target reversal of acquired abnormalities in specific biochemical pathways.

AB - In patients with IBD, chronic colonic inflammation increases the risk of colorectal cancer, perhaps because inflammation predisposes these tissues to genomic instability. Carcinogenesis in the inflamed colon seems to follow a different sequence of genetic alterations than that observed in sporadic cancers in the uninflamed colon. In this Review, we focus on the genetic alterations in colitis-associated colorectal cancer that contribute to the acquisition of the essential hallmarks of cancer, and on how those alterations differ from sporadic colorectal cancers. Our intent is to provide a conceptual basis for categorizing carcinogenetic molecular abnormalities in IBD, and for understanding how cancer-preventive therapies might target reversal of acquired abnormalities in specific biochemical pathways.

UR - http://www.scopus.com/inward/record.url?scp=67650330166&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67650330166&partnerID=8YFLogxK

U2 - 10.1038/nrgastro.2009.44

DO - 10.1038/nrgastro.2009.44

M3 - Article

C2 - 19404270

AN - SCOPUS:67650330166

VL - 6

SP - 297

EP - 305

JO - Nature Reviews Gastroenterology and Hepatology

JF - Nature Reviews Gastroenterology and Hepatology

SN - 1759-5045

IS - 5

ER -