Coexpression of granulocyte colony stimulating factor and its receptor in primary ovarian carcinomas

Citation
Tm. Savarese et al., Coexpression of granulocyte colony stimulating factor and its receptor in primary ovarian carcinomas, CANCER LETT, 162(1), 2001, pp. 105-115
Citations number
30
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
CANCER LETTERS
ISSN journal
03043835 → ACNP
Volume
162
Issue
1
Year of publication
2001
Pages
105 - 115
Database
ISI
SICI code
0304-3835(20010110)162:1<105:COGCSF>2.0.ZU;2-Q
Abstract
Immunohistochemistry was used to determine the expression of granulocyte co lony-stimulating factor (G-CSF) and its receptor (G-CSFR) in primary ovaria n carcinomas. The expression of G-CSFR was observed in the malignant cells of each of the 46 primary carcinomas examined; G-CSF was coexpressed in bot h the malignant epithelial cells and the stroma of 56.5% of the specimens. Thus the majority of ovarian carcinomas harbor both potential autocrine and paracrine G-CSF axes. In 37% of the samples, G-CSF was expressed only with in stromal cells, suggesting that only a potential paracrine system is in p lace. In a preliminary, retrospective, evaluation, the survival of patients whose tumors expressed only the apparent paracrine loop was significantly worse than patients whose tumors expressed both potential autocrine and par acrine G-CSF-based regulatory loops (14.5 vs. 42.5 months, respectively). S tudies on the potential function of G-CSF were performed using the G-CSFR-e xpressing OVCAR-3 ovarian carcinoma line. As a single agent, rhG-CSF failed to stimulate [H-3]-thymidine incorporation in these cells, but enhanced th e mitogenic action of epidermal growth factor (EGF) in a dose-dependent man ner. Thus, potential autocrine and/or paracrine loops involving G-CSF and i ts receptor occur in over 90% of primary ovarian carcinomas, and may act to modulate the action of growth factors. (C) 2001 Elsevier Science Ireland L td. All rights reserved.