| Literature DB >> 19404270 |
Linda A Feagins1, Rhonda F Souza, Stuart J Spechler.
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.Entities:
Mesh:
Year: 2009 PMID: 19404270 DOI: 10.1038/nrgastro.2009.44
Source DB: PubMed Journal: Nat Rev Gastroenterol Hepatol ISSN: 1759-5045 Impact factor: 46.802