作者: Dieter Marmé , Karin Weindel , Georg Martiny-Baron , Bernhard Barleon , Katja Mohrs
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摘要: Mutations or loss of both alleles the von Hippel-Lindau (VHL) tumor suppressor gene has been documented in sporadic renal cell carcinomas and neoplasms that arise individuals having VHL syndrome. The well-vascularized phenotype tumors form disease let us consider vascular endothelial growth factor (VEGF) as a mediator disease. Human carcinoma cells either lacked endogenous wild-type were transfected with an inactive mutant showed deregulated expression VEGF on mRNA protein level was reverted by introduction VHL. Stimulation proliferation conditioned medium expressing almost abolished neutralizing VEGF. In contrast, basic fibroblast c-myc proto-oncogene not affected Our data suggest key angiogenesis