VHL Gene Mutation In HCC And Its Relations With VEGF,MVD And Its Clinic-Pathological Features

[Introduction]von Hippel-Lindau(VHL) disease is an autosomal dorminant .inherited cancer syndrome that is characterized by extensively vascularized tumors, such as hemangioblastomas of the retina and central nervous system,renal cellcarcinomas(RCCs),and pheochromocytomas.The VHL tumor suppressor gene was cloned in 1993 by Latif and was identified in on chromosome 3p25-3p26.According to the two-hit hypothesis for tumor suppressor genes, inactivation of both alleles of the VHLgene leads to tumor formation. As a typical tumor suppressor gene, VHL gene inhibitor carcinogenesis by its encoding protein pVHL which preventing EloginABC complex formation on transcription level. Complex formation between elongin B,elongin C,CUL2 and pVHL is required for the von Hippel-Lindau protein to to destabilize hypoxia-inducible mRNAs under normoxic conditions.Loss of pVHL leads to an accumulation of hypoxia-inducible mRNAs,such as the VEGF mRNAs.Other suggested functions of pVHL include downregulation of transcriptional elongation,cell-cycle control and fibronectin metabolism. VHL gene has close relation with von Hippel-Lindau tomor which is characterized by extensively vascularization, the same as HCC.So we have sufficient reasons to think HCC has also close relation with VHL gene but little was reported about this topic.This tset was designed to explored the VHL gene mutation in HCC and its relations with VEGF , MVD and its clinic- pathological features. [Objective]To explored the VHL gene mutation in HCC and its relations with VEGF , MVD and its clinic-pathological features. [Materias and Methods]...