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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Aged, Carcinoma, Renal Cell, CpG Islands, DNA Methylation, Disease Progression, Female, Humans, Hypoxia, Immunohistochemistry, Kidney Neoplasms, Male, Mutation, Promoter Regions, Genetic, Treatment Outcome, Von Hippel-Lindau Tumor Suppressor Protein.
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Is different angiogenic potential in low and high grade sporadic clear cell renal cell carcinoma related to alterations in the von Hippel-Lindau gene? Context: von Hippel-Lindau (VHL) inactivation is common in sporadic clear cell renal cell carcinomas (ccRCC). pVHL is part of the ubiquitin ligase complex that targets the alpha subunits of hypoxia-inducible transcription factor (HIF) for degradation under well-oxygenated conditions. In the absence of wild-type pVHL, as observed in VHL patients and most sporadic ccRCCs, constitutive upregulation of HIF results in transcriptional activation of angiogenesis-related genes, such as VEGF. Differences in angiogenic activity within the group of ccRCCs were reported and strong genotype-phenotype correlations were found in patients with VHL disease, raising a question about the importance of VHL inactivation status in angiogenic behaviour and tumour progression. To address this question, we investigated the influence of VHL mutation (direct sequencing)/hypermethylation (methylation-specific PCR) on angiogenesis/tumour parameters (immunohistochemistry) in 150 patients with sporadic ccRCC. We found no significant association between VHL mutation or methylation and angiogenesis/tumour parameters.
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These data indicate that tumour progression and angiogenesis are not directly influenced by VHL alterations and that additional genetic/epigenetic events should be considered to explain the diverse angiogenic and proliferative behaviour during tumour progression. Final Decision: no