| Objective: Primary hepatic carcinoma (PHC) can be divided into three kinds in histology: hepatocellular carcinoma (HCC, 91.5%), cholangiocellular carcinoma (CCC, 5.5%), mixed hepatocellular and cholangiocarcinoma (3%). PHC is one of the most frequent carcinoma in human. The sufferers get poor prognosis. So the etiology research is very important for the prevention and control of PHC. The importance of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection in the development of PHC has been well established by epidemiological and molecular studies. Epstein-Barr virus (EBV) has been associated with several human malignancies. In recent years, some investigations suggest that EBV may play a role in HCC carcinogenesis, while some viewpoints are contrary. The aim of this study was to find out the infection state of EBV in PHC patients, and discuss whether EBV act as a helper virus and cooperate with hepatitis viruses hi PHC carcinogenesis.Methods: Polymerase chain reaction (PCR) method was processed to detect EBV EamH I W DNA, EBV LMP1 DNA, HBV X DNA, and HBV S DNA in formalin-fixed, paraffin-embedded liver tissue specimens from hepatocellular carcinoma (HCC, 67 cases) and cholangiocellular carcinoma (CCC, 14 cases) patients. 26 non-tumorous liver specimens served as normal controls. The positive ratios were compared between HCC (or CCC) group and normal control group by means of the chi-square test, P<0.05 was considered a significant difference. Reversetranscription PCR (RT-PCR) method was processed to detect HCV RNA and HDV RNA in tumor specimen of 18 patients with HCC. At last immunohistochemistry method was used to identify the character and location of gene expression in 13 cases those EBV DNA were positive.Result: The positive ratio of HBV DNA (X gene and/or S gene) is 73.1% in HCC group (49 of 67), 78.6% in CCC group (11 of 14), and 26.9% in normal control group (7 of 26). The positive rate of EBV DNA (BamHI W and/or LMP1) is 35.8% in HCC group (24 of 67), 14.3% in CCC group (2 of 14), and 7.7% in normal control group (2 of 26). The positive rate of HCV RNA is 5.6% in HCC group (1 of 18). HDV RNA was negative in HCC group. HBV and EBV were more frequently detected in HCC group than the normal control group (P<0.05), so we suggest that the existence of HBV and EBV may promote the development of HCC to some extent. HBV was more frequently detected in CCC group than the normal control group (P<0.05), so we suggest that the existence of HBV may promote the development of HCC. But the differences of positive rate of EBV gene between CCC group and normal control group have no sense in statistics. The existence of EBV and HBV in HCC group and CCC group has no obvious correlation, so we suggest that they cannot cooperate with each other during the course of development of HPC. The result of immunology histochemical detection showed that LMP1 located at the nucleus and cytoplasm of carcinoma cell and lymphocyte in stroma. HCV located at nucleus of carcinoma cell. Its positive ratio was 69.3% (9 of 13 ) .Conclusion: Through retrospective molecular epidemiology method, we investigated the paraffin specimens of PHC that were kept in archives. At first, we affirmed the existence of EBV infection in HCC and CCC tissues, and suggest that EBV may have some relations with HCC. Thedetection ratio of EBV between CCC group and normal control group has no statistic difference. We should increase the amount of specimens to go on our research. Second, the EBV and HBV have no obvious correlation in the development of hepatic carcinoma. Whether EBV DNA detected by PCR method is from carcinoma cell or stroma lymphocyte? We must do more experiments. The beforehand experiments show that perhaps there is correlation between EBV and HCV in the development of HCC, the research of this correlation will be the focus of our next phase. We find that there is no direct role for HDV in HCC carcinogenesis. If the hypothesis of the relation of EBV and HCC come into existence, to increase the research and spread of...
|
PDF Full Text Request