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肝细胞癌(hepatocellar carcinoma,HCC)是世界上发病率和病死率均位于前列的恶性肿瘤,低度和高度异型增生结节或腺瘤样增生可能是其癌前病变。很多分子变异在肝硬化组织、异型增生结节以及微小HCC结节中即已出现,包括以下6个方面:乙肝病毒整合入宿主基因组引起染色体不稳定性,进而在很多位点发生杂合性缺失,或引起插入突变、激活原癌基因等;丙肝病毒编码产物NS3P表达增加引起c-erbB2的过表达和p21waf的缺失;TSG和原癌基因甲基化状态的改变;1p/q、7q、15q、16p、17q和20q等染色体臂上的DNA增益以及3p、4q、9p和11q的缺失等;1p、4q、6q和8p在癌前病变和早期体积小、分化好的HCC中出现杂合性缺失;特异性表达于异型增生结节和早期肝癌的分子标签等。这些分子变异既是诊断HCC的重要依据,也可用于筛选肿瘤易感人群,预测这些病变何时向恶性转化,并对某些异常的基因谱系采取适当的治疗策略,进而为HCC患者的早期诊断、早期治疗和改善预后提供新的思路。
Hepatocellular carcinoma (HCC) is a malignant tumor with morbidity and mortality in the world. Low or highly heterogeneous nodules or adenomatous hyperplasia may be precancerous lesions. Many molecular aberrations have emerged in cirrhotic, dysplastic nodules and tiny HCC nodules, including the following six aspects: Hepatitis B virus integration into the host genome causes chromosomal instability and further loss of heterozygosity at many loci , Or cause insertional mutation and activate proto-oncogene. The increase of c-erbB2 overexpression and p21waf deletion caused by the increase of NS3P gene expression in hepatitis C virus; the change of methylation status of TSG and proto-oncogene; 1p / q, 7q, 15q , 16p, 17q and 20q, and the deletion of 3p, 4q, 9p and 11q. 1p, 4q, 6q and 8p appeared heterozygous in precancerous lesion and early small, well differentiated HCC Missing; specific expression in dysplastic nodules and early liver cancer molecular tag. These molecular mutations not only serve as an important basis for the diagnosis of HCC, but also for the screening of cancer-susceptible populations, predict when these malignancies are transformed, and adopt appropriate treatment strategies for certain abnormal gene lines to further diagnose HCC patients. Early treatment and improve prognosis provide new ideas.