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Angiogenesis is a major driving factor in the pathogenesis of renal cell carcinoma (RCC). The angiogenic phenotype occurs as a result of the high incidence of von Hippel-Lindau tumor suppressor gene (VHL) loss, which leads to hypoxia-inducible factor (HIF) dysregulation and a subsequent increase in proangiogenic factors.2,4 Thus, it would be expected that vascular endothelial growth factor (VEGF) overexpression would be evident in RCC. Indeed, several investigators have confirmed this hypothesis by measuring VEGF expression either through mRNA or protein levels. VEGF expression was observed in the vast majority of RCCs, and several reports noted increased VEGF expression in tumor tissue compared with normal renal tissue.11-16 Together, these data demonstrate that VEGF is a key mediator of angiogenesis in RCC.
A number of investigators have examined RCCs to see whether VEGF is overexpressed. Their methods include the measurement of VEGF mRNA expression, as well as the measurement of VEGF protein levels. The results of 6 clinical studies show that the vast majority of RCCs overexpress VEGF, underscoring the critical role of VEGF and angiogenesis in RCC.11-16
