title: Analysis of beta-catenin gene mutations in pancreatic tumors.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.affiliation: Department of General Surgery, Philipps University, Marburg, Germany. Gerdes@mailer.uni-marburg.de
authors.forename: B
authors.initials: B
authors.lastname: Gerdes
authors.forename: A
authors.initials: A
authors.lastname: Ramaswamy
authors.forename: B
authors.initials: B
authors.lastname: Simon
authors.forename: T
authors.initials: T
authors.lastname: Pietsch
authors.forename: D
authors.initials: D
authors.lastname: Bastian
authors.forename: M
authors.initials: M
authors.lastname: Kersting
authors.forename: R
authors.initials: R
authors.lastname: Moll
authors.forename: D
authors.initials: D
authors.lastname: Bartsch
mesh_terms: D000230:Adenocarcinoma / Q000737:chemistry / Q000235:genetics* / Q000473:pathology; D014408:Biomarkers, Tumor / Q000235:genetics; D015820:Cadherins / Q000032:analysis / Q000235:genetics*; D003598:Cytoskeletal Proteins / Q000032:analysis / Q000235:genetics*; D004252:DNA Mutational Analysis; D004273:DNA, Neoplasm / Q000032:analysis; D005091:Exons; D006801:Humans; D007124:Immunoenzyme Techniques; D009154:Mutation; D010190:Pancreatic Neoplasms / Q000737:chemistry / Q000235:genetics* / Q000473:pathology; D016133:Polymerase Chain Reaction; D018807:Polymorphism, Single-Stranded Conformational; D015534:Trans-Activators; D014407:Tumor Cells, Cultured; D051176:beta Catenin
chemical_list: D014408:Biomarkers, Tumor; C495270:CTNNB1 protein, human; D015820:Cadherins; D003598:Cytoskeletal Proteins; D004273:DNA, Neoplasm; D015534:Trans-Activators; D051176:beta Catenin