Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Immunohistological analysis of E-cadherin, alpha-, beta- and gamma-catenin expression in colorectal cancer: Implications for cell adhesion and signaling

Item Type:Article
Title:Immunohistological analysis of E-cadherin, alpha-, beta- and gamma-catenin expression in colorectal cancer: Implications for cell adhesion and signaling
Creators Name:Ghadimi, B.M. and Behrens, J. and Hoffmann, I. and Haensch, W. and Birchmeier, W. and Schlag, P.M.
Abstract:Intercellular adhesion mediated by the E-cadherin/catenin complex is a prerequisite for epithelial integrity and differentiation. In carcinomas, E-cadherin function is frequently disturbed, and has been suggested to increase invasion and metastasis of tumour cells. beta-catenin has also been implicated in signaling pathways essential for tumour formation. We analysed the E-cadherin/catenin adhesion system of colorectal tumours at different clinical stages. In primary carcinomas (n = 91), there was a frequent reduction in E-cadherin (44%) and alpha-catenin expression (36%). In contrast, beta-catenin and gamma-catenin expression were seldom reduced (4% and 15%, respectively). Similar expression patterns were observed in liver metastases from unrelated colorectal tumours (n = 27). There was a significant relationship between loss of E-cadherin and alpha-catenin expression and poorly differentiated (G3-4) tumours. Our results suggest that reduction of E-cadherin/alpha-catenin expression is a frequent event in primary and metastatic colorectal carcinomas. Furthermore, beta-catenin expression remains normal in colorectal cancer, suggesting the essential role of beta-catenin in signaling pathways.
Keywords:E-Cadherin, Catenins, Colorectal Cancer, Metastasis
Source:European Journal of Cancer
ISSN:0959-8049
Publisher:Pergamon Press (U.K.)
Volume:35
Number:1
Page Range:60-65
Date:January 1999
Official Publication:https://doi.org/10.1016/S0959-8049(98)00344-X
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library