Molecular genetics of dysplasia in ulcerative colitis

doi:10.1016/0959-8049(95)00142-6

European Journal of Cancer

Volume 31, Issues 7–8, July–August 1995, Pages 1171-1173

https://doi.org/10.1016/0959-8049(95)00142-6 Get rights and content

Abstract

Numerous molecular genetic events occurring in the development of sporadic colorectal neoplasia have been previously denned. The most frequent genetic alterations are mutations of the APC, KRAS, and TP53 genes, as well as loss of the DCC gene and of the second TP53 allele. The data from several groups indicate that these genes play an important role in ulcerative colitis-associated dysplasias and cancer, as they do in sporadic colorectal adenomas and carcinomas. KRAS and TP53 mutations were detected in dysplasia, but also in villous regeneration and active colitis, and affect a subpopulation of the cells composing these lesions. We conclude that in histologically denned dysplasia, clones can be found that genetically represent precancerous lesions in ulcerative colitis. Seen in this way, part of the active colitis and villous regeneration lesions might be considered as preneoplastic. When present, KRAS mutation is an excellent genetic marker to map populations of preneoplastic cells.

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Citation Excerpt :
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Molecular genetics of dysplasia in ulcerative colitis

Abstract

Cell

Gaslroenterology

Gastroenterohgy

Gastroenterotogy

Gastroenterology

Gastroenterology

Eur J Cancer