| Literature DB >> 15494708 |
Shigeki Sekine1, Tadakazu Shimoda, Satoshi Nimura, Yukihiro Nakanishi, Takayuki Akasu, Hitoshi Katai, Takuji Gotoda, Tatsuhiro Shibata, Michiie Sakamoto, Setsuo Hirohashi.
Abstract
We report a patient with familial adenomatous polyposis who developed high-grade dysplasia against a background of fundic gland polyposis. Two large high-grade dysplasia lesions were found in the gastric body, where numerous fundic gland polyps were present. In both lesions, the dysplastic epithelium covered non-neoplastic oxyntic glands that occasionally exhibit cystic changes. A genetic analysis for APC (adenomatous polyposis coli) revealed a somatic 50-bp deletion involving codons 1502-1517 and 2-bp deletion at codon 1465 in each lesion of high-grade dysplasia. In contrast, six of the 18 fundic gland polyps were found to harbor an identical mutation: 1-bp insertion at codon 1556. Both lesions of high-grade dysplasia and the fundic gland polyps were similarly located in the fundic gland area and were caused by the inactivation of APC; however, their mutation profiles of APC were different. These results imply that fundic gland polyps and high-grade dysplasia of the stomach have distinct preferences for APC genotypes in their development.Entities:
Mesh:
Year: 2004 PMID: 15494708 DOI: 10.1038/modpathol.3800178
Source DB: PubMed Journal: Mod Pathol ISSN: 0893-3952 Impact factor: 7.842