Genetic alterations involving exon 3 of the β-catenin gene do not play a role in adenocarcinomas of the esophagus

Bas P.L. Wijnhoven, Friedel Nollet, Nico J. De Both, Hugo W. Tilanus, Winand N.M. Dinjens*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

29 Citations (Scopus)

Abstract

β-catenin has been identified as an oncogene. Phosphorylation of sites encoded by exon 3 of the β-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 β-catenin, which then translocates to the nucleus where it modulates the transcription of genes involved in tumor formation. To explore the role of β-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. β-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 β-catenin gene do not occur and therefore do not contribute to the pathogenesis of esophageal adenocarcinomas. The abnormal cytoplasmic and nuclear localization of β- catenin indicates that other mechanisms leading to elevated free β-catenin in these cancers must be involved. (C) 2000 Wiley-Liss, Inc.

Original languageEnglish
Pages (from-to)533-537
Number of pages5
JournalInternational Journal of Cancer
Volume86
Issue number4
DOIs
Publication statusPublished - 15 May 2000

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