
Among the mechanisms of tumor growth in prostate cancer that are under investigation, VEGF and its role in tumor neovascularization continue to receive significant attention. Several angiogenesis factors including VEGF, platelet-derived growth factor (PDGF) and transforming growth factor (TGF) are expressed to a greater degree in malignant than in nonmalignant prostate tissue; among these, the VEGF ligand has been identified as the predominant regulator of angiogenesis.1
The importance of angiogenic activity in prostate cancer is highlighted by the correlation between tumor growth and microvessel density. Evidence of angiogenesis can be detected through an evaluation of microvessel density, which is higher in primary prostate cancer tissue than in adjacent nonmalignant hyperplastic tissue or normal prostate tissue.1
Another important consideration in the link between angiogenesis and tumor growth is the evident VEGF production of tumors themselves. Tumors can stimulate production of VEGF through several pathways via mechanisms including1:
Just as microvessel density correlates with metastasis in breast and lung cancer, microvessel density may also correlate with metastasis in prostate cancer. In one study, Weidner and colleagues evaluated tumor specimens from 74 patients with invasive prostate cancer (29 with metastasis, 45 without). The specimens were stained for factor VIII-related antigen (F8-RA) to show microvessel densities. The investigators found that microvessel counts increased significantly with a greater histologic grade (P<0.0001).9
