1. ¹Pathology Division, National Cancer Center Research Institute, Tokyo, Japan
2. ²Clinical Laboratory Division, National Cancer Center Research Institute, Tokyo, Japan
3. ³Department of Surgery, National Cancer Center Hospital, Tokyo, Japan
4. ⁴Department of Endoscopy, National Cancer Center Hospital, Tokyo, Japan
5. ⁵Department of Pathology, Keio University School of Medicine, Tokyo, Japan

Correspondence: S Hirohashi, MD, Pathology Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan. E-mail: shirohas@ncc.go.jp

Received 7 February 2004; Revised 21 April 2004; Accepted 21 April 2004.

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.