Mutational analysis of the CTNNB1 (β-catenin) gene in human endometrial cancer: Frequent mutations at codon 34 that cause nuclear accumulation

Akira Horii

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)

Abstract

Recently, CTNNB1 (β-catenin) has been found to function as an oncoprotein that works in the Wnt signaling pathway, and mutation of this gene has been reported in various human cancers. In this study, we analyzed 44 endometrial cancers and found somatic missense mutations in five (11%) tumors. Interestingly, four (80%) of the five tumors with mutations would cause amino acid alterations at residues next to Ser 33, one of the targets for phosphorylation of glycogen synthase kinase (GSK)-3β. The tumors with mutations showed accumulation of the CTNNB1 protein in cytoplasm and nucleus. This is the first report of frequent somatic mutation of the CTNNB1 gene at codons adjacent to those encoding to Ser/Thr residues in endometrial cancer.

Original languageEnglish
Pages (from-to)323-326
Number of pages4
JournalOncology reports
Volume7
Issue number2
Publication statusPublished - 2000

Keywords

  • CTNNB1
  • Endometrial cancer
  • Somatic mutation
  • β-catenin

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of 'Mutational analysis of the CTNNB1 (β-catenin) gene in human endometrial cancer: Frequent mutations at codon 34 that cause nuclear accumulation'. Together they form a unique fingerprint.

Cite this