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目的 :探讨乙肝病毒 (HBV)和黄曲霉毒素B1(AFB1)在肝癌形成中的作用及机理。方法 :用免疫组化、原位杂文及印迹杂交检测树鼠句肝和肿瘤组织。结果 :两次实验中 ,感染HBV又摄入AFB1的A组树鼠句肝细胞癌(HCC)发生率分别为 5 2 94%和 6 6 7% ;单纯感染HBV的B组分别为 11 1%和 0 ;只摄入AFB1的C组分别为 12 5 %和 30 % ;空白对照组D均无HCC发生。A组HCC的发生率均显著高于各组 (P <0 0 5 )。癌前病变r GT灶的个数及面积也如此。IGF Ⅱ的过表达与HCC发生密切有关 ;HBV和AFB1可协同激活ras基因 ;c myc主要参与HCC的演进 ,CDK4参与了HCC的发生和演进过程。这两种基因的改变与HBV感染有关。结论 :HBV能诱发肝癌前病变和肝癌 ,并与AFB1有协同致肝癌作用。在树鼠句肝癌形成过程有多种基因的改变
Objective: To investigate the role and mechanism of hepatitis B virus (HBV) and aflatoxin B1 (AFB1) in hepatocarcinogenesis. METHODS: The liver and tumor tissues of tree and mouse were detected by immunohistochemistry, in situ essay and blot hybridization. RESULTS: In the two experiments, the incidence of hepatocellular carcinoma (HCC) in group A mice infected with HBV and AFB1 was 492% and 666%, respectively; the group B infected with HBV alone was 11%. And 0; only intake of AFB1 in the C group were 125% and 30%; blank control group D no HCC occurred. The incidence of HCC in group A was significantly higher than that in each group (P < 0 05). The number and area of precancerous lesions are also the same. Overexpression of IGF II is closely related to the occurrence of HCC; HBV and AFB1 can synergistically activate ras genes; c myc is mainly involved in the evolution of HCC, and CDK4 is involved in the occurrence and evolution of HCC. Changes in these two genes are associated with HBV infection. Conclusion: HBV can induce precancerous lesions of liver cancer and liver cancer, and cooperate with AFB1 to induce liver cancer. There are many kinds of genetic changes in the process of hepatocarcinogenesis in tree mouse sentences