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Investigation of galectin-3 and heparanase in endometrioid and serous carcinomas of the endometrium and correlation with known predictors of survival.

Authors :
Ege CB
Akbulut M
Zekioğlu O
Ozdemir N
Source :
Archives of gynecology and obstetrics [Arch Gynecol Obstet] 2011 Nov; Vol. 284 (5), pp. 1231-9. Date of Electronic Publication: 2010 Dec 12.
Publication Year :
2011

Abstract

Introduction: Inhibitors of tumor angiogenesis and metastasis are emerging as important new drug candidates for cancer therapy. Galectin-3 and heparanase have been shown to function in tumor progression and metastatic spread. Both of them exert pleiotropic effects; proliferation, cell migration, differentiation and tissue remodeling. The aim of this study was to investigate heparanase and galectin-3 expression in endometrioid and serous carcinomas of the endometrium and their relation with well-known prognostic factors, in addition to estrogen, progesterone, C-erbB-2, Ki-67 and p53.<br />Materials and Methods: Sixty-four endometrial cancers, which include 24 serous types, were obtained from previously untreated patients. Immunohistochemical analysis of 64 carcinomas, 20 endometrial hyperplasia (ten of simple hyperplasia and ten of complex atypic hyperplasia) and 20 normal endometrium (ten of proliferative and ten of secretory) was performed.<br />Conclusion: This investigation suggests that the decreased expression of galectin-3 may be involved in the pathogenesis of endometrial carcinomas from normal endometrium to carcinoma. Also down-regulated stromal expression of galectin-3 in endometrial carcinoma may be involved in lymph node metastasis. Further studies on a larger advanced stage (FIGO stage 3-4) endometrial carcinoma group may determine the value of heparanase in the endometrial carcinoma.

Details

Language :
English
ISSN :
1432-0711
Volume :
284
Issue :
5
Database :
MEDLINE
Journal :
Archives of gynecology and obstetrics
Publication Type :
Academic Journal
Accession number :
21153652
Full Text :
https://doi.org/10.1007/s00404-010-1766-9