VASCULAR ENDOTHELIAL GROWTH-FACTOR (VEGF) EXPRESSION IN PROSTATE-CANCER AND BENIGN PROSTATIC HYPERPLASIA

Citation
Mw. Jackson et al., VASCULAR ENDOTHELIAL GROWTH-FACTOR (VEGF) EXPRESSION IN PROSTATE-CANCER AND BENIGN PROSTATIC HYPERPLASIA, The Journal of urology, 157(6), 1997, pp. 2323-2328
Citations number
52
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00225347
Volume
157
Issue
6
Year of publication
1997
Pages
2323 - 2328
Database
ISI
SICI code
0022-5347(1997)157:6<2323:VEG(EI>2.0.ZU;2-Z
Abstract
Purpose: Vascular endothelial growth factor (VEGF) is a potent inducer of endothelial cell growth and is expressed at elevated levels in sev eral tumor types. In this study immunohistochemical localization and d istribution of isoforms of VEGF were examined in malignant and non-mal ignant human prostatic tissues. Materials and Methods: Immunohistochem ical localization of VEGF was performed on thirty well, moderately and poorly differentiated stage D-2 prostate cancer specimens and twenty benign prostatic hyperplasia (BPH) specimens. VEGF mRNA was determined by polymerase chain reaction and VEGF protein isoforms were detected by Western blotting of prostate cancer and BPH specimens. Results: Cyt oplasmic immunoreactivity for VEGF was detected in tumor cells and per itumoral stromal cells of prostate cancer specimens and in non-maligna nt glandular epithelial cells and interglandular stromal cells in BPH specimens. Staining was focal with areas of strongly to weakly stained cells adjacent to negatively staining areas. mRNA's for VEGF(121), VE GF(165) and VEGF(189) were present in all benign and malignant prostat e specimens. VEGF protein isoforms of molecular sizes corresponding to VEGF(165) and VEGF(189) were detected in cytosolic extracts of prosta te cancers and BPH specimens by Western blotting. In addition, two nov el higher molecular weight immunoreactive bands were detected in the p rostate specimens. Conclusions: Widespread distribution of VEGF in pro state cancers and BPH specimens suggest that the VEGF(165), VEGF(189) isoforms and novel 90 and 110 kD forms detected may contribute to the establishment or progression of these conditions.