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The chemoprevention of colorectal carcinoma
Author(s) -
Gasche C.
Publication year - 2004
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.2004.02045.x
Subject(s) - colorectal cancer , microsatellite instability , medicine , mesalazine , familial adenomatous polyposis , mouse model of colorectal and intestinal cancer , cancer , inflammatory bowel disease , cancer prevention , aspirin , chromosome instability , cancer research , bioinformatics , oncology , disease , microsatellite , genetics , gene , biology , allele , chromosome
Summary This review aims to provide an insight into some of the common pathways involved in the development of colorectal cancer — so‐called chromosomal instability and microsatellite instability. There is both clinical and molecular evidence to show that colorectal cancer development occurs over an extended period of time. Together with a knowledge of the molecular pathogenesis of colorectal cancer, this time window allows physicians to counteract cancer development, a strategy known as chemoprevention. In familial and sporadic colorectal cancer, aspirin, other nonsteroidal anti‐inflammatory drugs and cyclo‐oxygenase‐2 inhibitors have been tested for their ability to reduce polyp and cancer development in clinical studies. In inflammatory bowel disease‐related colorectal cancer, evidence from retrospective case–control studies shows that mesalazine (mesalamine) can reduce the development of dysplastic lesions or cancer. Although the mechanisms behind this are incompletely understood, general anti‐inflammatory, oxygen scavenger and some pro‐apoptotic and cyclo‐oxygenase inhibitory activities of mesalazine are thought to be involved. New molecular evidence points to a direct DNA stabilizing effect of mesalazine, resulting in a significant reduction of spontaneous microsatellite mutations.