肝细胞癌
HBx公司
乙型肝炎病毒
突变
病毒学
基因
基础(医学)
病毒
发起人
基因突变
生物
医学
癌症研究
内科学
遗传学
基因表达
胰岛素
作者
Xiaokui Guo,Jing Yan,Qian Gao,Hong Tu
标识
DOI:10.1016/j.jhep.2008.06.026
摘要
Background/Aims To investigate the mutations in hepatitis B virus (HBV) that might be related to hepatocellular carcinoma (HCC) in the high-risk area Qidong, China. Methods DNA sequences of HBV basal core promoter (BCP) and the overlapping X gene were determined in 58 HCC and 71 chronic hepatitis (CH) patients. In addition, a consecutive series of plasma samples from 15 HCC cases were employed to compare the CP/X sequences before and after the occurrence of HCC. Results T1762/A1764 double mutation was frequently found in Qidong patients, regardless of clinical status (65.5% in HCC and 73.2% in CH, P > 0.05). Unexpectedly, the adjacent T1766/A1768 mutation significantly increased the risk of HCC (P < 0.05). Moreover, the prevalence of triple mutations in BCP was significantly higher in patients with HCC than those with CH (P < 0.05). The longitudinal study demonstrated that the mutations in BCP were gradually accumulated during the development of HCC. Colony formation assay showed while A1764 mutation alone did not alter the colony-inhibitory activity of HBx, double or triple mutations largely abrogated this effect. Conclusions The complex mutation involving T1766/A1768 was closely related to HCC. The enhanced risk of HCC caused by BCP variants could be attributable partially to the aberrant activity of HBx. To investigate the mutations in hepatitis B virus (HBV) that might be related to hepatocellular carcinoma (HCC) in the high-risk area Qidong, China. DNA sequences of HBV basal core promoter (BCP) and the overlapping X gene were determined in 58 HCC and 71 chronic hepatitis (CH) patients. In addition, a consecutive series of plasma samples from 15 HCC cases were employed to compare the CP/X sequences before and after the occurrence of HCC. T1762/A1764 double mutation was frequently found in Qidong patients, regardless of clinical status (65.5% in HCC and 73.2% in CH, P > 0.05). Unexpectedly, the adjacent T1766/A1768 mutation significantly increased the risk of HCC (P < 0.05). Moreover, the prevalence of triple mutations in BCP was significantly higher in patients with HCC than those with CH (P < 0.05). The longitudinal study demonstrated that the mutations in BCP were gradually accumulated during the development of HCC. Colony formation assay showed while A1764 mutation alone did not alter the colony-inhibitory activity of HBx, double or triple mutations largely abrogated this effect. The complex mutation involving T1766/A1768 was closely related to HCC. The enhanced risk of HCC caused by BCP variants could be attributable partially to the aberrant activity of HBx.
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