UNLABELLED: Several growth factors have been shown to stimulate or inhibit the growth of human ovarian surface epithelial (HOSE) cells. Platelet-derived growth factor (PDGF) is likely to be released onto the ovarian surface epithelium during follicular wound repair. We undertook the evaluation of this factor and its receptor in normal and malignant ovarian cells. OBJECTIVES: The goal of this study was to evaluate the response of HOSE cells to PDGF in vitro and identify PDGF receptors on normal and malignant ovarian epithelial cells. In addition, we wanted to examine the prognostic value of the PDGF receptors in clinical specimens. METHODS: Normal HOSE cells were cultured and growth response to PDGF assayed by 3H uptake. PDGF receptor status on HOSE cells, established ovarian carcinoma cell lines, and paraffin tissue was performed by immunohistologic techniques. Data on ovarian cancer patients relapse-free survival (RFS) were abstracted from the Lankenau Hospital Tumor Registry and RFS was plotted using the Kaplan-Meier method. RESULTS: HOSE cells increased 3H uptake in a dose-dependent manner in response to PDGF. HOSE cells stain positively for both alpha and beta receptors, as does the chemotherapy naive cell line A2780. The platinum-resistant CP30 cell line loses PDGF alpha staining. Of 21 ovarian cancer specimens, only 1 retained PDGF alpha receptors while 8 retained PDGF beta receptors. Those patients positive for PDGF receptor beta had a significantly longer relapse-free survival than PDGF beta receptor-negative patients. CONCLUSIONS: PDGF enhances the growth of HOSE cells in vitro and may play a role in ovarian cancer development. Patients whose tumors retain PDGF receptor beta staining positivity have a prolonged relapse-free survival. Copyright 1998 Academic Press.
UNLABELLED: Several growth factors have been shown to stimulate or inhibit the growth of human ovarian surface epithelial (HOSE) cells. Platelet-derived growth factor (PDGF) is likely to be released onto the ovarian surface epithelium during follicular wound repair. We undertook the evaluation of this factor and its receptor in normal and malignant ovarian cells. OBJECTIVES: The goal of this study was to evaluate the response of HOSE cells to PDGF in vitro and identify PDGF receptors on normal and malignant ovarian epithelial cells. In addition, we wanted to examine the prognostic value of the PDGF receptors in clinical specimens. METHODS: Normal HOSE cells were cultured and growth response to PDGF assayed by 3H uptake. PDGF receptor status on HOSE cells, established ovarian carcinoma cell lines, and paraffin tissue was performed by immunohistologic techniques. Data on ovarian cancerpatients relapse-free survival (RFS) were abstracted from the Lankenau Hospital Tumor Registry and RFS was plotted using the Kaplan-Meier method. RESULTS: HOSE cells increased 3H uptake in a dose-dependent manner in response to PDGF. HOSE cells stain positively for both alpha and beta receptors, as does the chemotherapy naive cell line A2780. The platinum-resistant CP30 cell line loses PDGF alpha staining. Of 21 ovarian cancer specimens, only 1 retained PDGF alpha receptors while 8 retained PDGF beta receptors. Those patients positive for PDGF receptor beta had a significantly longer relapse-free survival than PDGF beta receptor-negative patients. CONCLUSIONS: PDGF enhances the growth of HOSE cells in vitro and may play a role in ovarian cancer development. Patients whose tumors retain PDGF receptor beta staining positivity have a prolonged relapse-free survival. Copyright 1998 Academic Press.
Authors: Prakash Vishnu; Gerardo Colon-Otero; Gregory T Kennedy; Laura A Marlow; William P Kennedy; Kevin J Wu; Joseph T Santoso; John A Copland Journal: Gynecol Oncol Date: 2011-11-22 Impact factor: 5.482
Authors: Samir D Undevia; Nicholas J Vogelzang; Ann M Mauer; Linda Janisch; Sridhar Mani; Mark J Ratain Journal: Invest New Drugs Date: 2004-11 Impact factor: 3.850