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

被引:271
作者
Feagins, Linda A. [1 ,2 ]
Souza, Rhonda F. [2 ]
Spechler, Stuart J. [2 ]
机构
[1] Dallas Vet Affairs Med Ctr, Div Gastroenterol 111B1, Dallas, TX 75216 USA
[2] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA
关键词
INFLAMMATORY-BOWEL-DISEASE; GROWTH-FACTOR RECEPTOR; CHRONIC ULCERATIVE-COLITIS; STEM-CELL PROPERTIES; KI-RAS MUTATIONS; DNA ANEUPLOIDY; RISK-FACTOR; CYCLOOXYGENASE-2; INHIBITOR; CHROMOSOMAL ALTERATIONS; SCLEROSING CHOLANGITIS;
D O I
10.1038/nrgastro.2009.44
中图分类号
R57 [消化系及腹部疾病];
学科分类号
100201 [内科学];
摘要
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.
引用
收藏
页码:297 / 305
页数:9
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