EXPRESSION OF TRANSFORMING-GROWTH-FACTOR-BETA RECEPTORS IN NORMAL HUMAN COLON AND SPORADIC ADENOCARCINOMAS

Citation
R. Eskinazi et al., EXPRESSION OF TRANSFORMING-GROWTH-FACTOR-BETA RECEPTORS IN NORMAL HUMAN COLON AND SPORADIC ADENOCARCINOMAS, Gastroenterology, 114(6), 1998, pp. 1211-1220
Citations number
49
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
00165085
Volume
114
Issue
6
Year of publication
1998
Pages
1211 - 1220
Database
ISI
SICI code
0016-5085(1998)114:6<1211:EOTRIN>2.0.ZU;2-I
Abstract
Background & Aims: An absence or a presence of mutated transforming gr owth factor (TGF)-beta receptors is a possible hypothesis explaining t he resistance of cancer cells to the growth-inhibitory effect of TGF-b eta, Mutations involving microsatellite-like regions of the type II TG F-beta receptor have been described in subgroups of colorectal cancers . The aim of this study was to investigate the expression and distribu tion of TGF-beta receptors in sporadic colorectal cancers and normal t issues. Methods: Thirty-three sporadic colorectal cancers and 20 norma l colonic tissues were explored by immunohistochemistry for the expres sion of type I and type II TGF-beta receptors, Eighteen tumor and 20 n ormal samples were used for radioactive thermocycling and sequencing o f the two microsatellite-like regions of the type II receptor, Results : Both receptors were overexpressed in tumors compared with normal sam ples. There was a relationship between the abundance of type II recept or expression and the degree of differentiation of the tumors but not the Dukes' staging or the localization of the neoplasias. No mutation was observed in the microsatellite-like regions of receptor II in any of the samples. Conclusions: Sporadic colorectal cancers do not show a n absence or a presence of mutated TGF-beta receptors that could expla in a resistance to TGF-beta-mediated growth inhibition. The pathways t o tumorigenesis of sporadic colorectal cancers may be different from t hose of some hereditary ones.