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[Cancer Research 61, 2736-2743, March 15, 2001]
© 2001 American Association for Cancer Research

Tumor Biology

Angiogenesis and Prostate Cancer: Identification of A Molecular Progression Switch1

Wendy J. Huss, Colleen F. Hanrahan, Roberto J. Barrios, Jonathan W. Simons and Norman M. Greenberg2

Department of Molecular and Cellular Biology [W. J. H., N. M. G.], Scott Department of Urology [N. M. G.], and Department of Pathology [R. J. B.], Baylor College of Medicine, Houston, Texas 77030; The Johns Hopkins Oncology Center, Brady Urological Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287 [C. F. H.]; and Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia 30321 [J. W. S.]

To elucidate the sequence of molecular events intricate with angiogenesis and the initiation and progression prostate cancer, the temporal and spatial expression patterns of platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31), hypoxia-induced factor-1 {alpha} (HIF-1{alpha}), vascular endothelial growth factor (VEGF), and the cognate receptors VEGFR1 and VEGFR2 were characterized. Immunohistochemical and in situ analyses of prostate tissue specimens derived from the spontaneous autochthonous transgenic adenocarcinoma of the mouse prostate (TRAMP) model identified a distinct early angiogenic switch consistent with the expression of PECAM-1, HIF-1{alpha}, and VEGFR1 and the recruitment of new vasculature to lesions representative of high-grade prostatic epithelial neoplasia (PIN). During progression of prostate cancer, the intraductal microvessel density (IMVD) was also observed to increase as a function of tumor grade. Immunoblot and in situ analyses further demonstrated a distinct late angiogenic switch consistent with decreased expression of VEGFR1, increased expression of VEGFR2, and the transition from a differentiated adenocarcinoma to a more poorly differentiated state. Analysis of clinical prostate cancer specimens validated the predictions of the TRAMP model. This resolution of prostate cancer-associated angiogenesis into distinct early and late molecular events establishes the basis for a "progression-switch" model to explain how the targets of antiangiogenic therapy might change as a function of tumor progression.




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