Genetic alterations involving exon 3 of the β-catenin gene do not play a role in adenocarcinomas of the esophagus
✍ Scribed by Bas P.L. Wijnhoven; Friedel Nollet; Nico J. De Both; Hugo W. Tilanus; Winand N.M. Dinjens
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- French
- Weight
- 268 KB
- Volume
- 86
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
-catenin has been identified as an oncogene. Phosphorylation of sites encoded by exon 3 of the -catenin gene facilitates degradation of this protein by the adenomatous polyposis coli (apc) gene product. Mutations in these sites or inactivation of apc lead to stabilization of -catenin, which then translocates to the nucleus where it modulates the transcription of genes involved in tumor formation. To explore the role of -catenin mutations in adenocarcinomas of the esophagus, we screened for genetic alterations in exon 3 in 69 tumor samples. We detected no mutations in exon 3 by PCR-SSCP analysis nor did we find large interstitial deletions involving exon 3. -catenin immunostaining on 54 tumors showed focal nuclear staining in 7 tumors and homogeneous nuclear staining in 3 tumors; in the latter; no mutations in the mutation cluster region of apc were detected. These results show that genetic alterations of exon 3 of the -catenin gene do not occur and therefore do not contribute to the pathogenesis of esophageal adenocarcinomas. The abnormal cytoplasmic and nuclear localization of -catenin indicates that other mechanisms leading to elevated free -catenin in these cancers must be involved. Int.