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大量文献报道,在急、慢性乙型肝炎以及肝硬变和肝细胞癌患者的肝组织中,存在有整合的乙型肝炎病毒(HBV)DNA。但是,这些研究都未能在分子水平上清楚地揭示HBV的致癌作用。本文以宿主细胞基因组中整合的HBVDNA为标志物,研究转移性肝细胞癌(HCC)病人肿瘤细胞的起源问题。作者对一位有病毒性肝炎史的转移性HCC患者的肝和肺受损害部分进行了DNA限制性内切酶消化和Southern印迹分析。结果发现,由右叶肝癌组织中提取的DNA,未经内切酶消化时,在20kb左右有一弥散性杂交信号带,经不同内切酶消化后,在大于3.2kb的位置得到一些确定的杂交信号带;用内切酶HindⅢ和PuvⅡ充分消化,则产生一条杂交信号带。以
A large body of literature reports the existence of integrated hepatitis B virus (HBV) DNA in the liver tissues of acute and chronic hepatitis B patients and patients with cirrhosis and hepatocellular carcinoma. However, none of these studies clearly revealed the oncogenic role of HBV at the molecular level. In this paper, the integration of host cells in the genome of HBV DNA markers for the study of metastatic hepatocellular carcinoma (HCC) patients with the origin of tumor cells. The authors performed DNA restriction endonuclease digestion and Southern blot analysis of damaged parts of the liver and lung in a metastatic HCC patient with a history of viral hepatitis. The results showed that DNA extracted from the right lobe liver cancer tissue without digestion by endonuclease had a diffusible hybridization signal band of about 20 kb and after digestion with different endonucleases, some definite hybridization was obtained at a position larger than 3.2 kb Signal band; digested with restriction enzymes Hind III and Puv II to produce a hybridization signal band. To