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Biological Aspects and Binding Strategies of Vascular Endothelial Growth Factor in Renal Cell Carcinoma

Authors' Affiliations: ¹ Department of Solid Tumor Oncology and Urology, Cleveland Clinic Taussig Cancer Center, Cleveland, Ohio and ² University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, Chapel Hill, North Carolina

Requests for reprints: Brian I. Rini, Department of Solid Tumor Oncology and Urology, Cleveland Clinic Taussig Cancer Center, 9500 Euclid Avenue/Desk R35, Cleveland, OH 44195. Phone: 216-444-9567; Fax: 216-636-0636; E-mail: rinib2{at}ccf.org or W. Kimryn Rathmell, University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, Campus Box 7295, Room 21-237, 247, Chapel Hill, NC 27599-7295. Phone: 919-966-3522; Fax: 919-843-3160; E-mail: rathmell{at}med.unc.edu.

Vascular endothelial growth factor (VEGF) is a key mediator in the pathogenesis of renal cell carcinoma (RCC). VEGF is up-regulated in clear cell RCC as a result of loss of the von Hippel-Lindau tumor suppressor gene and subsequent activation of the hypoxia response pathway. VEGF expression drives the migration and proliferation of endothelial cells to support the extensive angiogenesis in RCC. Strategies have been developed to bind and neutralize VEGF and have been investigated in RCC with promising results. Bevacizumab, a VEGF ligand-binding antibody, has shown prolonged time-to-progression versus placebo in treatment-refractory RCC patients and is being investigated currently in multiple RCC settings. VEGF-Trap is also a VEGF binding molecule with ongoing investigation in RCC.

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