ENDOTHELIAL CELL PROLIFERATION ACTIVITY IN BENIGN PROSTATIC HYPERPLASIA AND PROSTATE CANCER: AN IN VITRO MODEL FOR ASSESSMENT |
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Authors: | Karl Weingartner Shmuel A. Ben-Sasson Robert Stewart J.P. Richie Hubertus Riedmiller Judah Folkman |
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Affiliation: | Department of Urology, Julius-Maximilians University Wurzburg, Wurzburg, German, and Departments of Surgery, Children's Hospital and Harvard Medical School, Department of Surgery, Division of Urology, Brigham and Women's Hospital, Boston, Massachusetts. |
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Abstract: | PurposeUrinary excretion of several pro-angiogenic and antiangiogenic 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).Materials and MethodsUrine specimens from 22 healthy male volunteers (control), 33 patients with BPH and 29 with organ confined prostate cancer were analyzed for angiogenic activity in a bovine capillary endothelial cell proliferation assay. In parallel the concentration of basic fibroblast growth factor and vascular endothelial growth factor was determined by enzyme immunoassay in the corresponding urine specimens.ResultsUrine samples from patients with BPH and prostate cancer increased bovine capillary endothelial cell proliferation by 13.1% and 15.1%, respectively, whereas urine from the control group showed a significantly lower angiogenic activity, increasing endothelial cell proliferation by only 0.7% (p = 0.001). Urinary basic fibroblast growth factor and vascular endothelial growth factor were highest in patients with BPH and lowest in the group with prostate cancer (p = 0.0001).ConclusionsUrine from patients with BPH and prostate cancer stimulates endothelial cell proliferation activity. The degree of endothelial cell stimulation does not correlate with the concentration of basic fibroblast growth factor or vascular endothelial growth factor. Whether the observed pro-angiogenic activity is due to an increased production or release of (an) other angiogenic factor(s) and/or loss of (an) angiogenesis inhibitor(s), deserves further investigation. |
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