PMID: 9189100Jun 1, 1997Paper

p53 and K-ras status in duodenal adenomas in familial adenomatous polyposis

The British Journal of Surgery
H KashiwagiR K Phillips

Abstract

The genetic alterations in patients with familial adenomatous polyposis (FAP) and duodenal adenomas are poorly characterized when compared with data relating to colorectal tumorigenesis in the same patients. Point mutation of the K-ras oncogene and point mutation and overexpression of the TP53 tumour suppressor gene were investigated in 32 duodenal polyps (seven without mucosal pathology, 23 with mildly dysplastic adenomas and two with moderately dysplastic adenomas) from 21 patients with FAP. K-ras mutation, TP53 mutation or positive p53 staining were not found in duodenal polyps without histological abnormality. Of 25 duodenal adenomas, K-ras mutation was found in three (two mildly dysplastic, one moderately dysplastic), 20 showed positive p53 immunostaining, and mutation of the TP53 gene was found in one moderately dysplastic adenoma. p53 protein overexpression in duodenal adenomas was significantly more frequent than mutation of either K-ras or TP53 (P < 0.01). p53 dysfunction is a hallmark of duodenal adenomas in patients with FAP. Overexpression may indicate DNA damage and thus an early step in tumorigenesis.

References

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Citations

Aug 24, 2000·Surgery Today·H Kashiwagi, A D Spigelman
Sep 26, 2006·Familial Cancer·Michelle C GallagherSteffen Bulow
Jul 17, 1998·The British Journal of Surgery·M H Wallace, R K Phillips
Mar 14, 2009·Clinical Gastroenterology and Hepatology : the Official Clinical Practice Journal of the American Gastroenterological Association·Andrew R LatchfordSusan K Clark

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