Mutations in β-Catenin and APC Genes are Uncommon in Esophageal and Esophagogastric Junction Adenocarcinomas

摘要: Beta-catenin plays important roles in both intercellular adhesion and signal transduction. Mutations the beta-catenin or adenomatous polyposis coli (APC) gene can alter degradation of cause aberrant accumulation result increased transcription target genes. The dysregulated APC/beta-catenin pathway has been recently discovered as an mechanism tumorigenesis various cancers, but its role esophageal adenocarcinomas is not clear. Therefore, we studied mutation, allelic loss chromosome 5q, APC mutation esophagogastric junction adenocarcinomas. Two (2%) somatic mutations exon 3 gene, encompassing region for glycogen synthase kinase-3beta phosphorylation, were detected from 109 Chromosomal on 5q was frequent 45.3% (44/97) tumors. Only one missense cluster 38 with loss. Our results based partial screening mutational analyses indicate that pathway, unlike colorectal carcinoma, involve only a small subset adenocarcinoma.