Tcf-3 expression and β-catenin mediated transcriptional activation in aggressive fibromatosis (desmoid tumour)

被引：29

作者：

Tejpar, S

Li, C

Yu, C

Poon, R

Denys, H

Sciot, R

Van Cutsem, E

Cassiman, JJ

Alman, BA

机构：

[1] Hosp Sick Children, Program Dev Biol, Toronto, ON M5G 1X8, Canada

[2] Univ Toronto, Toronto, ON M5G 1X8, Canada

[3] Katholieke Univ Leuven, Ctr Human Genet, B-3000 Louvain, Belgium

[4] Katholieke Univ Leuven, Dept Pathol, B-3000 Louvain, Belgium

[5] Katholieke Univ Leuven, Dept Gastroenterol, B-3000 Louvain, Belgium

[6] Hosp Sick Children, Dept Surg, Toronto, ON M5G 1X8, Canada

[7] Hosp Sick Children, Div Orthopaed Surg, Toronto, ON M5G 1X8, Canada

来源：

BRITISH JOURNAL OF CANCER | 2001年 / 85卷 / 01期

基金：

英国医学研究理事会;

关键词：

beta-catenin; tcf/lef transcription factors; aggressive fibromatosis; APC;

D O I：

10.1054/bjoc.2001.1857

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Aggressive fibromatosis harbours mutations resulting in beta -catenin protein stabilization. Primary cell cultures demonstrate constitutive tcf activation in aggressive fibromatosis. Expression and co-immunoprecipitation studies suggest that beta -catenin binds and activates tcf-3 in this tumour. This is the first demonstration of tcf-3 activation by beta -catenin stabilization in a human neoplastic process. (C) 2001 Cancer Research Campaign http://www.bjcancer.com.

引用

页码：98 / 101

页数：4

共 20 条

[1]

Alman BA, 1997, AM J PATHOL, V151, P329

[2] Aggressive fibromatosis (desmoid tumor) is a monoclonal disorder [J].