原发性肝癌和癌旁组织中TTVDNA的原位杂交研究

DETECTION OF TTVDNA IN THE TISSUES OF HEPATOCELLULAR CARCINOMA AND BESIDE THE TUMORS WITH HYBRIDIZATION IN SITU

目的:通过对肝癌组织、癌旁组织和肝炎组织中TTVDNA的分布情况分析,探讨TTV感染与原发性肝癌的发病关系。方法:选择符合全国诊断标准并感染乙型肝炎病毒的原发性肝癌病人的肝癌组织及癌旁组织和乙型肝炎肝组织切片各为87、87和39份。以地高辛标记物制备TTVDNA探针,原位杂交法检测组织切片中TTVDNA。结果:肝癌组织中浆型阳性率明显高于癌旁组织(P<0·05),但两者核型阳性率差异无统计学意义(P>0·05);肝炎组织中浆型和核型阳性率与癌旁组织比较差异无统计学意义(P>0·05,)。肝癌组织中浆型阳性率明显高于肝炎组织(P<0·01),相反,肝炎组织中核型阳性率明显高于肝癌组织(P<0·01);癌旁组织中浆型+核型阳性率与肝炎组织比较差异无统计学意义(P>0·05);肝癌组织和癌旁组织浆型+核型阳性率明显高于肝炎组织(P<0·01)。结论:有3种可能:①TTV感染与原发性肝癌发生存在一定关系,TTV感染肝细胞后在肝炎期主要分布于肝细胞核内,当肝细胞发生癌变后,TTV主要分布向肝细胞浆内转移;②浆型TTV感染可能与乙型肝炎病毒协同而易发生癌变;③TTV亦仅仅是乙型肝炎病毒的伴随病毒。

Objective：To probe the relationship between transfusion transmitted virus （TTV） infection and hepatocellular carcinoma （HCC） by detecting the tissues of HCC and beside the tumors with hybridization in situ. Methods：87, 87 and 38 pieces of slices of tissues from HCC beside the tumor and hepatic tissue with hepatitis B were investigated respectively. TTVDNA in the tissues was tested by hybridization in situ. Result：The positive rate of TTVDNA in cytoplasm of hepatocytes （cytoplasm type） was significantly higher than that of the tissues beside carcinoma （ P 〈0.05, X^2 =6.04） ; but no obviously differences were seen in the TTVDNA positive rate in the nuclei of hepatocytes （nuclei type ） between the tissues of HCC and those beside the tumors （ P 〈0.05, X^2=0.25）. The positive rate of cytoplasm and nuclei types in hepatitis B tissues was almost the same as the tissues beside tumor （ P 〈0.05, X^2=3.28）. The positive rate of cytoplasm type in tumor tissues was significantly higher than that of the tissues in hepatitis B （ P 〈0.01, X^2 =10.6）. But the opposite results was seen in the positive rate of nuclei type （ P 〈0.01, X^2 =4.45） ; no significant difference was found between the positive rate of cytoplasm and nuclei types in the tissues beside tumor and in the tissues of hepatitis B （ P〈0.05,X^2 =3.18 and 2.38 respectively）. The positive rate of cytoplasm and nuclei types of tumor and the tissues beside tumors was significantly higher than that of the hepatitis B tissues （ P〈0.01, X^2= 13.4）. Conclusion： There might be three possibilities for explaining the results above：①there might be a relationship between TTV infection and HCC, TTV situates in bepatocyte nuclei in the hepatitis B phase, which may emigrate to hepatocytic cytoplasm after deterioration of hepatoytes;②TTV infection in hepatocytic cytoplasm may be in coordination with HBV in the etiology of HCC occurrence.③TTV may be only a company virus with HBV infection, but not a pathogenic factor.