AI Article Synopsis
- The study investigates the frequency of Wnt pathway activation and beta-catenin mutations in gastric cancer, finding conflicting results in previous research.
- Ninety out of 311 gastric cancer samples (29%) showed nuclear beta-catenin expression, with 73 samples further analyzed for DNA mutations.
- Of these, 19 samples (26%) had mutations in exon 3 of the beta-catenin gene, which were mostly near regulatory sites, indicating that Wnt pathway activation may play a role in the development of gastric adenocarcinomas.
Article Abstract
Studies of Wnt activation in gastric cancer have yielded conflicting results. The goals of this study were to determine the frequency of Wnt pathway activation and beta-catenin mutation in these tumors. Three hundred eleven gastric cancers were examined for beta-catenin expression by immunostaining and dissected using laser capture microscopy to obtain DNA from those tumors with nuclear beta-catenin. Exon 3 of beta-catenin was amplified using PCR and sequenced. Ninety gastric cancers (29%) displayed nuclear beta-catenin. DNAs from 73 tumors were amplified and sequenced; 19 (26%) contained mutations in exon 3 of beta-catenin, whereas no mutations were detected in 19 tumors negative for beta-catenin nuclear staining (P < 0.05). Most mutations were adjacent to or abolished known regulatory phosphorylation sites. Mutations in exon 3 of beta-catenin are common in gastric cancer that display nuclear beta-catenin. These results suggest that Wnt pathway activation contributes to carcinogenesis in a subset of gastric adenocarcinomas.
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