论文部分内容阅读
AIM:To analyze the genetic and epigenetic alterations ofRUNX3 gene,a potential putative tumor suppressor gene,in hepatocellular carcinoma (HCC).METHODS:PCR-based loss of heterozygosity (LOH)detection,analysis of mutation with PCR-single strandconformational polymorphism (SSCP) and sequencing,andmethylation study with methylation specific PCR (MSP) wereperformed on RUNX3 gene in a series of 62 HCCs alongwith their matched normal tissues.RESULTS:Mutation of RUNX3 gene was not found,butone single nucleotide polymorphism with T to A transversionat the second nucleotide of the 18th condon was found.Nine of 26 informative cases (34.6%) showed allelic losson the polymorphic site and 30 cases (48.4%) revealedhypermethylation of RUNX3 gene in promoter CpG islands.Furthermore,of the 9 cases with LOH,8 (88.9%) also hadhypermethylation.CONCLUSION:Our findings indicate that inactivation ofRUNX3 gene through allelic loss and promoter hypermethylationmight be one of the major mechanisms in hepatocellualrcarcinogenesis.
AIM: To analyze the genetic and epigenetic alterations of ROXX gene, a potential putative tumor suppressor gene, in hepatocellular carcinoma (HCC). METHODS: PCR-based loss of heterozygosity (LOH) detection, analysis of mutation with PCR- single strand conformational polymorphism ) and sequencing, and methylation study with methylation specific PCR (MSP) were performed on RUNX3 gene in a series of 62 HCCs along with their matched normal tissues .RESULTS: Mutation of RUNX3 gene was not found, butone single nucleotide polymorphism with T to A transversionat the second nucleotide of the 18th condon was found. Nine of 26 informative cases (34.6%) showed allelic loss of the polymorphic site and 30 cases (48.4%) revealedhypermethylation of RUNX3 gene in promoter CpG islands. Further edited, of the 9 cases with LOH, 8 ( 88.9%) also hadhypermethylation.CONCLUSION: Our findings indicate that inactivation of RUNX3 gene through allelic loss and promoter hypermethylationmight be one of the major mechanisms in hepatocell ualrcarcinogenesis.