BACKGROUND: Abnormalities in coagulation/platelet activation and angiogenesis are present in all common human cancers. We hypothesized that surgical treatment of prostate cancer would modulate these abnormalities. METHODS: Forty-two men with biopsy-proven prostate cancer were recruited of whom 24 had radical prostatectomy (RP), 12 other treatments and 6 had no treatment. RP patients were followed up from baseline, and samples were collected at 3- and 12-month intervals to assess the effects of the surgery. Plasma was obtained for the measurement of markers of vascular/coagulation/platelet activation (von Willebrand factor (vWf), soluble P selectin (sPsel) (all ELISA), fibrinogen and D-dimer (both nephelometry)) and angiogenesis (vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2) and their receptors s-Flt-1 and s-Tie-2). We also measured the angiogenesis markers VEGF and angiopoietin-1 within platelets (all ELISA). RESULTS: In those undergoing RP, there were changes in plasma VEGF (to 48% of pre-surgery levels at 1 year follow up), Ang-1 (to 82%), Ang-2 (to 27%), sPsel (78%), and fibrinogen (to 91%) at 3 months and/or 12 months (p<0.03). The relative falls in Ang-2, Ang-1 and VEGF were not significant (p=0.448). CONCLUSIONS: RP is associated with a lowering of markers of angiogenesis and platelet activation. This suggests that these pathological processes are driven to a large extent by the tumour and/or tumour-secreted factors, and that removal of the primary growth results in a gradual normalisation of measured indices.
BACKGROUND:Abnormalities in coagulation/platelet activation and angiogenesis are present in all common humancancers. We hypothesized that surgical treatment of prostate cancer would modulate these abnormalities. METHODS: Forty-two men with biopsy-proven prostate cancer were recruited of whom 24 had radical prostatectomy (RP), 12 other treatments and 6 had no treatment. RP patients were followed up from baseline, and samples were collected at 3- and 12-month intervals to assess the effects of the surgery. Plasma was obtained for the measurement of markers of vascular/coagulation/platelet activation (von Willebrand factor (vWf), soluble P selectin (sPsel) (all ELISA), fibrinogen and D-dimer (both nephelometry)) and angiogenesis (vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2) and their receptors s-Flt-1 and s-Tie-2). We also measured the angiogenesis markers VEGF and angiopoietin-1 within platelets (all ELISA). RESULTS: In those undergoing RP, there were changes in plasma VEGF (to 48% of pre-surgery levels at 1 year follow up), Ang-1 (to 82%), Ang-2 (to 27%), sPsel (78%), and fibrinogen (to 91%) at 3 months and/or 12 months (p<0.03). The relative falls in Ang-2, Ang-1 and VEGF were not significant (p=0.448). CONCLUSIONS: RP is associated with a lowering of markers of angiogenesis and platelet activation. This suggests that these pathological processes are driven to a large extent by the tumour and/or tumour-secreted factors, and that removal of the primary growth results in a gradual normalisation of measured indices.