Analysis of beta-catenin gene mutations in pancreatic tumors

Background/Aim: Mutations of the adenomatous polyposis coli (APC) tumor sup pressor gene have been described in a subset of pancreatic carcinomas. The APC gene modulates the beta-catenin-Tcf pathway. The major player in this p athway is the beta-catenin protein encoded by the beta-catenin gene. A vari ety of different tumors, including colon, prostate, endometrial, and hepato cellular carcinomas, carry mutations in exon 3 of the beta-catenin gene. Th e aim of this study was to determine the role of the beta-catenin gene in t he genesis of exocrine and endocrine tumors of the pancreas. Methods: 78 du ctal pancreatic adenocarcinomas, 14 ductal pancreatic cancer cell lines, an d 33 endocrine pancreatic tumors were evaluated for mutations in exon 3 of the beta-catenin gene by single-strand conformation polymorphism analysis a nd direct DNA sequencing. in addition, 40 ductal pancreatic adenocarcinomas were analyzed for intracellular beta-catenin accumulation by immunohistoch emistry, indicating alterations of the beta-catenin gene. Results: Neither the 111 exocrine and endocrine pancreatic tumors nor the 14 pancreatic canc er cell lines carried mutations in exon 3 of the beta-catenin gene. Intrace llular beta-catenin accumulation was not identified in any of the 40 pancre atic adenocarcinomas. Conclusion: These data suggest that the beta-catenin gene as the major player of the beta-catenin-Tcf pathway does not play an i mportant role in the genesis of pancreatic tumors.