© 1992 Oxford University Press
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Somatic mutation of the APC gene in gastric cancer: frequent mutations in very well differentiated adenocarcinoma and signet-ring cell carcinoma
1Departments of Biochemistry, Cancer Institute 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170 2Departments of Pathology, Cancer Institute 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170 3First Department of Pathology, Hiroshima University School of Medicine 1-2-3, Kasumi, Minami-ku, Hiroshima 734 4Sanko Junyaku Co., Ltd. 1-10-6 Iwamoto-cho, Chiyoda-ku, Tokyo 101, Japan
*To whom correspondence should be addressed
Received September 18, 1992; Revised October 5, 1992; Accepted October 5, 1992
We searched for somatic mutations of the adenomatous polyposis coli (APC) gene in DNA samples isolated from 57 sporadic gastric cancers, by means of a ribonuclease (RNase) protection analysis coupled with DNA amplification by the polymerase chain reaction (PCR). Examining 30% of the APC coding region, including a region where somatic mutations in colorectal tumors are known to be clustered, we detected somatic mutations in 12 tumors; seven in 17 very well differentiated adenocarcinomas, two in 19 well or moderately differentiated adenocarcinomas, and three in ten signet-ring cell carcinomas. So far, no somatic mutations have been identified in 11 poorly differentiated adenocarcinomas. Eight of the 17 somatic mutations found in 12 tumors caused truncation of the gene product due to a nonsense mutation and a 1-, 2- or 5-bp deletion; nine others were point mutations that altered amino acids. Our results suggest that inactivation of APC plays a role in development of some gastric cancers, particularly very well differentiated adenocarcinomas and signet-ring cell carcinomas.
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