Infrequent somatic mutations of the ICAT gene in various human cancers with frequent 1p-LOH and/or abnormal nuclear accumulation of β-catenin

Mitsuho Imai, Tsutomu Nakamura, Tetsu Akiyama, Akira Horii

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Abnormal nuclear accumulation of β-catenin (CTNNB1) plays one of the key roles in the upregulation of the Wnt signalling pathway that can cause acceleration of cell proliferation. ICAT, inhibitor of β-catenin and TCF4/β-catenin-interacting protein, was isolated and mapped to 1p36, a frequent target for LOH in many human cancers. We have previously observed that a number of tumors showing abnormal accumulation of the CTNNB1 protein do not harbor a mutation of the CTNNB1 gene. We studied the precise localization and genomic structure of the ICAT gene and analyzed its mutations in 178 human tumors developed in organs with frequent nuclear accumulation of the CTNNB1 protein and/or frequent LOHs of 1p36, but no genetic alterations were observed. Our results imply that i) genetic alteration of the ICAT gene does not play an important role in abnormal accumulation of CTNNB1 that would cause up-regulation of the Wnt signalling pathway, ii) mechanisms other than genetic alteration may have inactivated ICAT function, or iii) gene(s) on 1p36 other than ICAT may be the responsible tumor suppressor gene for tumors that show frequent 1p36-LOH.

Original languageEnglish
Pages (from-to)1099-1103
Number of pages5
JournalOncology reports
Volume12
Issue number5
DOIs
Publication statusPublished - 2004 Nov

Keywords

  • 1p36
  • ICAT
  • Wnt signalling
  • β-catenin

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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