Genetic alterations involving exon 3 of the beta-catenin gene do not play a role in adenocarcinomas of the esophagus

beta-catenin has been identified as an oncogene. Phosphorylation of sites e ncoded by exon 3 of the beta-catenin gene facilitates degradation of this p rotein by the adenomatous polyposis coli tape) gene product. Mutations in t hese sites or inactivation of ape lead to stabilization of beta-catenin, wh ich then translocates to the nucleus where it modulates the transcription o f genes involved in tumor formation. To explore the role of beta-catenin mu tations in adenocarcinomas of the esophagus, we screened for genetic altera tions in exon 3 in 69 tumor samples. We detected no mutations in exon 3 by PCR-SSCP analysis nor did we find large interstitial deletions involving ex on 3. beta-catenin immunostaining on 54 tumors showed focal nuclear stainin g in 7 tumors and homogeneous nuclear staining in 3 tumors; in the latter; no mutations in the mutation cluster region of ope were detected. These res ults show that genetic alterations of exon 3 of the beta-catenin gene do no t occur and therefore do not contribute to the pathogenesis of esophageal a denocarcinomas. The abnormal cytoplasmic and nuclear localization of beta-c atenin indicates that other mechanisms leading to elevated free beta-cateni n in these cancers must be involved. Int. J. Cancer 86:533-537, 2000. (C) 2 000 Wiley-Liss, Inc.