論文

査読有り
2004年11月

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

ONCOLOGY REPORTS
  • M Imai
  • ,
  • T Nakamura
  • ,
  • T Akiyama
  • ,
  • A Horii

12
5
開始ページ
1099
終了ページ
1103
記述言語
英語
掲載種別
研究論文(学術雑誌)
出版者・発行元
PROFESSOR D A SPANDIDOS

Abnormal nuclear accumulation of beta-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 beta-catenin and TCF4/beta-catenin-interacting protein, was isolated and mapped to lp36, a frequent target for LOH in many human cancers. We have previously observed that a number of turnors 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 upregulation 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 lp36-LOH.

Web of Science ® 被引用回数 : 13

リンク情報
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000224717900022&DestApp=WOS_CPL

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