原发性肝癌患者及慢性乙肝病毒携带者肝组织中乙型肝炎病毒X基因的变异
Variation of hepatitis B virus X gene in liver tissues of hepatocellular carcinoma patient and chronic asymptomatic carrier
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摘要: 目的:探讨乙型肝炎病毒(hepatitis B virus,HBV)X基因及其变异与原发性肝细胞癌(hepatocellular carcinoma,HCC)发生、发展的关系。方法:采用聚合酶链反应(polymerase chain reaction,PCR)方法,检测22例乙型肝炎表面抗原(hepatitis Bsurface antigen,HBsAg)阳性的HCC患者及15例慢性乙肝病毒携带者(chronic asymptomatic carrier,CAC)患者肝组织中HBVX基因,并对PCR产物进行基因测序,同时检测5例无HBV携带者正常肝脏组织中HBV X基因。结果:22例HCC患者癌组织及15例CAC患者肝组织中HBVX基因检出率分别为68.18%和46.67%,5例正常肝脏组织中均未检测到HBVX基因,差异有统计学意义(P<0.05)。肝癌组织及HBV携带者肝组织中HBV X基因检出率差异无统计学意义(P>0.05)。肝癌组织及携带者肝组织中HBV X基因发生1 762T/1 764A双突变率分别为93.33%和2/7,肝癌组织中双突变率高于携带者肝组织(P=0.004 3),未发现1 762T及1 764A单独发生突变。结论:HCC患者肝组织中HBV X基因检出率高,肝癌组织中发生1762T/1764A双突变的频率高,HBV X基因及1762T/1764A双突变与HCC的发生可能有重要关系。Abstract: Objective: To study the association of hepatitis B virus (HBV)X gene and its mutation with hepatocellular carcinogenesis (HCC).Methods: HBV X gene in the liver tissues of 22 HCC patients whose hepatitis B surface antigen (HBsAg)was positive and 15 chronic asymptomatic carriers (CAC)patients were detected wih polymerase chain reaction (PCR);the PCR product was sequenced and analyzed;5 normal liver tissues with negative HBsAg acted as control.Results: The detection rate of HBV X gene in the carcinoma tissues of 22 HCC patients and 15 CAC patients was 68.18% and 46.67%,respectively.HBV X gene was not detected in the 5 normal liver tissues.The difference was significant between them (P<0.05).The detection rate of HBV X gene in carcinoma tissues and CAC liver tissues had no statistical difference (P>0.05).The double mutation rate of 1 762T/1 764A in carcinoma tissues and CAC liver tissues was 93.33% and 2/7,respectively.And the former was higher than the latter (P=0.004 3).There was no detection of mutation of 1 762T or 1 764A alone.Conclusions: There is a high detection rate of HBV X gene and a high double mutation rate of 1762T/1764A in the carcinoma tissues of HCC patients.HBV X gene and double mutations may play an important role in the carcinogenesis of HCC.