ENDOTHELIAL-CELL PROLIFERATION ACTIVITY IN BENIGN PROSTATIC HYPERPLASIA AND PROSTATE-CANCER - AN IN-VITRO MODEL FOR ASSESSMENT

Citation
K. Weingartner et al., ENDOTHELIAL-CELL PROLIFERATION ACTIVITY IN BENIGN PROSTATIC HYPERPLASIA AND PROSTATE-CANCER - AN IN-VITRO MODEL FOR ASSESSMENT, The Journal of urology, 159(2), 1998, pp. 465-470
Citations number
33
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00225347
Volume
159
Issue
2
Year of publication
1998
Pages
465 - 470
Database
ISI
SICI code
0022-5347(1998)159:2<465:EPAIBP>2.0.ZU;2-D
Abstract
Purpose: Urinary excretion of several pro-angiogenic and antiangiogeni c substances has been correlated with malignant tumor growth. The aim of this study was to assay angiogenic activity in urine from patients with cancer of the prostate and benign prostatic hyperplasia (BPH). Ma terials and Methods: Urine specimens from 22 healthy male volunteers ( control), 33 patients with BPH and 29 with organ confined prostate can cer were analyzed for angiogenic activity in a bovine capillary endoth elial cell proliferation assay. In parallel the concentration of basic fibroblast growth factor and vascular endothelial growth factor was d etermined by enzyme immunoassay in the corresponding urine specimens. Results: Urine samples from patients with BPH and prostate cancer incr eased bovine capillary endothelial cell proliferation by 13.1% and 15. 1%, respectively, whereas urine from the control group showed a signif icantly lower angiogenic activity, increasing endothelial cell prolife ration by only 0.7% (p = 0.001). Urinary basic fibroblast growth facto r and vascular endothelial growth factor were highest in patients with BPH and lowest in the group with prostate cancer (p = 0.0001). Conclu sions: Urine from patients with BPH and prostate cancer stimulates end othelial cell proliferative activity. The degree of endothelial cell s timulation does not correlate with the concentration of basic fibrobla st growth factor or vascular endothelial growth factor. Whether the ob served pro-angiogenic activity is due to an increased production or re lease of (an) other angiogenic factor(s) and/or loss of (an) angiogene sis inhibitor(s), deserves further investigation.