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乙肝病毒(HBV)致肝细胞癌(HCC)过程中,免疫/炎症分子遗传易感性与HBV交互作用维持了乙肝慢性化。HBV蛋白如大S抗原和HBx通过抑制免疫维持了非可控性炎症。促炎细胞因子反式激活核酸编辑酶如胞苷脱氨酶的表达,促进病毒和宿主基因组变异。绝大部分变异细胞在生存竞争中被淘汰,只有极其少数细胞通过改变细胞生存依赖的信号通路,具备了上皮细胞向间质细胞转化等逆向分化的潜能,获得了克服衰老、掠夺营养、无限增值和化疗抵抗等“干性”特征而被选择出来,成为癌症起始细胞。这类细胞逐渐适应了促癌炎症微环境,演绎了“变异—选择—适应”的进化过程。癌症进化发育学理论可能为癌症监测、预防和预后预测提供可靠生物标志和靶向治疗有效靶标。
In the process of hepatocellular carcinoma (HCC) caused by hepatitis B virus (HBV), the interaction between immune / inflammatory molecular genetic susceptibility and HBV maintains the chronicity of hepatitis B. HBV proteins such as large S antigens and HBx maintain non-controllable inflammation by inhibiting immunity. Pro-inflammatory cytokine transactivation nucleic acid editing enzymes such as cytidine deaminase expression, promote virus and host genome variation. Most of the mutant cells are eliminated in the competition of survival. Only a very few cells have the potential to reverse the differentiation of epithelial cells into stromal cells by changing the signal pathways of cell survival dependence, and have obtained the potential to overcome aging, plundering nutrition, And chemotherapy resistance “” dry “feature was chosen to become cancer initiating cells. These cells gradually adapt to the cancer-promoting microenvironment, deducing the evolution of ”mutation-selection-adaptation". Theories of cancer evolutionary development may provide reliable biomarkers of cancer monitoring, prevention and prediction of prognosis as well as effective targets for targeted therapies.