BACKGROUND/AIM: Mutations of the adenomatous polyposis coli (APC) tumor suppressor gene have been described in a subset of pancreatic carcinomas. The APC gene modulates the beta-catenin-Tcf pathway. The major player in this pathway is the beta-catenin protein encoded by the beta-catenin gene. A variety of different tumors, including colon, prostate, endometrial, and hepatocellular carcinomas, carry mutations in exon 3 of the beta-catenin gene. The aim of this study was to determine the role of the beta-catenin gene in the genesis of exocrine and endocrine tumors of the pancreas. METHODS: 78 ductal pancreatic adenocarcinomas, 14 ductal pancreatic cancer cell lines, and 33 endocrine pancreatic tumors were evaluated for mutations in exon 3 of the beta-catenin gene by single-strand conformation polymorphism analysis and direct DNA sequencing. In addition, 40 ductal pancreatic adenocarcinomas were analyzed for intracellular beta-catenin accumulation by immunohistochemistry, indicating alterations of the beta-catenin gene. RESULTS: Neither the 111 exocrine and endocrine pancreatic tumors nor the 14 pancreatic cancer cell lines carried mutations in exon 3 of the beta-catenin gene. Intracellular beta-catenin accumulation was not identified in any of the 40 pancreatic adenocarcinomas. CONCLUSION: These data suggest that the beta-catenin gene as the major player of the beta-catenin-Tcf pathway does not play an important role in the genesis of pancreatic tumors.
BACKGROUND/AIM: Mutations of the adenomatous polyposis coli (APC) tumor suppressor gene have been described in a subset of pancreatic carcinomas. The APC gene modulates the beta-catenin-Tcf pathway. The major player in this pathway is the beta-catenin protein encoded by the beta-catenin gene. A variety of different tumors, including colon, prostate, endometrial, and hepatocellular carcinomas, carry mutations in exon 3 of the beta-catenin gene. The aim of this study was to determine the role of the beta-catenin gene in the genesis of exocrine and endocrine tumors of the pancreas. METHODS: 78 ductal pancreatic adenocarcinomas, 14 ductal pancreatic cancer cell lines, and 33 endocrine pancreatic tumors were evaluated for mutations in exon 3 of the beta-catenin gene by single-strand conformation polymorphism analysis and direct DNA sequencing. In addition, 40 ductal pancreatic adenocarcinomas were analyzed for intracellular beta-catenin accumulation by immunohistochemistry, indicating alterations of the beta-catenin gene. RESULTS: Neither the 111 exocrine and endocrine pancreatic tumors nor the 14 pancreatic cancer cell lines carried mutations in exon 3 of the beta-catenin gene. Intracellular beta-catenin accumulation was not identified in any of the 40 pancreatic adenocarcinomas. CONCLUSION: These data suggest that the beta-catenin gene as the major player of the beta-catenin-Tcf pathway does not play an important role in the genesis of pancreatic tumors.
Authors: Richard L Watson; Aaron C Spalding; Steven P Zielske; Meredith Morgan; Alex C Kim; Guido T Bommer; Hagit Eldar-Finkelman; Thomas Giordano; Eric R Fearon; Gary D Hammer; Theodore S Lawrence; Edgar Ben-Josef Journal: Neoplasia Date: 2010-05 Impact factor: 5.715
Authors: V Hervieu; F Lepinasse; G Gouysse; O Guillaud; C Barel; M-L Chambonniere; P-P Bringuier; G Poncet; C Lombard-Bohas; C Partensky; J-A Chayvialle; J-Y Scoazec Journal: J Clin Pathol Date: 2006-05-26 Impact factor: 3.411
Authors: Edgar Ben-Josef; Asha George; William F Regine; Ross Abrams; Meredith Morgan; Dafydd Thomas; Paul L Schaefer; Thomas A DiPetrillo; Mitchel Fromm; William Small; Samir Narayan; Kathryn Winter; Kent A Griffith; Chandan Guha; Terence M Williams Journal: Clin Cancer Res Date: 2015-08-03 Impact factor: 12.531