PCR technique was used to detect HBV DNA in liver tissue samples for study of the prevalence of HBV DNA in tumorous and nearby nontumorous liver tissues from 16 hepatocellular carcinoma(HCC) patients.Three primer pair...PCR technique was used to detect HBV DNA in liver tissue samples for study of the prevalence of HBV DNA in tumorous and nearby nontumorous liver tissues from 16 hepatocellular carcinoma(HCC) patients.Three primer pairs, Sl/S2, C1/C2 and X1/X2, used in this study were selected from S region, pre C and C region,and X region of HBV DNA, respectively. The detecting with agarose gel electrophoresis and ethidium bromide staining(PCR-EB) was 10-2 pg, and that with Southern blot hybridization was 10-6 pg. The positive rates in amplification of HBV DNA by S, C and X region primer pairs in liver samples were 43.8%(14/32), 71.9%(23/32)and 71.9%(23/32), respectively. There was significant difference between the positive rates in amplification with S primer and with C Primer(P<0.05), but no significant difference between the C primer and the X primer(P<0.05), and between the S primer and the X primer(0.10>P>0.05). HBV DNA fragments were detected in the livers from all 16 cases. The results indicated that X gene integration inducing hepatocellular carcinogenesis and arrest of C gene expression causing escape from host immune surveillance are the possible mechanisms of HCC development in patients with perisistent HBV infection.展开更多
文摘PCR technique was used to detect HBV DNA in liver tissue samples for study of the prevalence of HBV DNA in tumorous and nearby nontumorous liver tissues from 16 hepatocellular carcinoma(HCC) patients.Three primer pairs, Sl/S2, C1/C2 and X1/X2, used in this study were selected from S region, pre C and C region,and X region of HBV DNA, respectively. The detecting with agarose gel electrophoresis and ethidium bromide staining(PCR-EB) was 10-2 pg, and that with Southern blot hybridization was 10-6 pg. The positive rates in amplification of HBV DNA by S, C and X region primer pairs in liver samples were 43.8%(14/32), 71.9%(23/32)and 71.9%(23/32), respectively. There was significant difference between the positive rates in amplification with S primer and with C Primer(P<0.05), but no significant difference between the C primer and the X primer(P<0.05), and between the S primer and the X primer(0.10>P>0.05). HBV DNA fragments were detected in the livers from all 16 cases. The results indicated that X gene integration inducing hepatocellular carcinogenesis and arrest of C gene expression causing escape from host immune surveillance are the possible mechanisms of HCC development in patients with perisistent HBV infection.
