Previous studies reported that mutation of the adenomatous polyposis coli (APC) gene was not observed in the majority of gastric cancers. To evaluate the role of the APC/β-catenin/Tcf pathway, we analyzed mutations in the β-catenin gene and the accumulation of β-catenin protein in gastric carcinomas. An interstitial deletion spanning exon 3 of the β-catenin gene was observed in 1 of 13 gastric cancer cell lines. No missense mutation was found in these 13 cell lines. Nuclear and/or cytoplasmic localization of β-catenin was observed in 16 of 70 primary gastric carcinomas by immunohistochemistry, while we found no mutations in exon 3 in 35 carcinoma tissues available for PCR amplification. Our findings suggest that somatic mutations of the β-catenin gene are rare in human gastric carcinomas and that accumulation of normal β-catenin protein in a subset of gastric cancers may be due to other mechanisms of its activation.

Keywords:
β-Catenin, Gastric carcinoma, human, Immunohistochemistry, Somatic mutation
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© 2001 S. Karger AG, Basel
2000
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