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目的 :探讨人乙肝病毒 (HBV)和黄曲霉毒素 B1 (AFB1 )致肝细胞癌 (HCC)及协同致 HCC作用的机制。方法 :将树鼠句分为 4组 :A组 :感染 HBV加摄入 AFB1 ;B组 :只感染 HBV;C组 :只摄入 AFB1 ;D组 :作空白对照。然后定期行肝活检 ,用免疫组化、分子生物学等技术动态观察一些癌基因 (蛋白 )和抑癌基因的表达。结果 :1A组谷胱苷肽转移酶(GGT)阳性灶个数及面积明显多于、大于 B、C组 ;2 A组 P2 1蛋白检出率明显高于 B和 C组 ,A组 6只 P2 1蛋白阳性的树鼠句到 12 0周时全部发生了 HCC;3实验后期 ,A组 HBx Ag检出率及 HBV DNA整合率明显高于 B组 ;4在诱癌过程中 ,IGF- 表达率呈波动形 ,带癌肝的表达率显著高于无癌肝 ;5 10 5周时 ,A、B、C组 P5 3蛋白表达率显著高于 D组 ;在 A,C组检出 p5 3异常带 ;6第 45及 10 5周时 ,A组 c- fos表达率分别为 2 3.1%和 2 0 % ;C组为 38.5 %和 15 .4% ,B,D两组均未检出 ;7H- c- myc基因 :直到 12 0周 ,无癌肝组织均未见异常 ;在肝癌组织中 ,A组有 4例扩增 ,C组无异常 ;8CDK4基因 :只有 A组在第 75周有 1例扩增 ,该树鼠句在第 10 6周时发生了 HCC。在 HCC中 ,A组有 2 5 %出现 CDK4扩增 ,C组未见异常。结论 :再次证实 HBV和 AFB1 有协同致 HCC作用 ;AFB1 有利于 HBx Ag的表达和 HB
Objective: To investigate the mechanism of human hepatic carcinoma (HCC) induced by hepatitis B virus (HBV) and aflatoxin B1 (AFB1) and the synergistic effect of HCC. Methods: The rats and mice were divided into 4 groups: A group: infected HBV plus AFB1; B: only infected HBV; C: only AFB1 intake; D: blank control. Liver biopsies are then routinely performed to dynamically observe the expression of some oncogenes and tumor suppressor genes using techniques such as immunohistochemistry and molecular biology. RESULTS: The number and area of positive glutathione transferase (GGT) positive cells in group A were significantly greater than or greater than those in group B and C. The detection rate of P2 protein in group 2A was significantly higher than that in group B and C, and that in group A was only 6. The H2CC was detected in the P2 1 protein-positive tree mouse at the 12th week; 3 The HBx Ag detection rate and the HBV DNA integration rate in the A group were significantly higher than those in the B group at the late stage of the experiment; 4 The IGF-expression during the process of carcinogenesis The rate was fluctuating and the expression rate of cancerous liver was significantly higher than that of non-cancerous liver. The expression of P53 protein in group A, B and C was significantly higher than that in group D at 5-10 weeks; p53 was detected in group A and group C. Abnormal zone; 6 At the 45th and 10th weeks, the expression rate of c-fos in group A was 2 3.1% and 20%, respectively; in group C, 38.5% and 15.4%, neither group B nor D was detected. 7H-c-myc gene: No abnormalities were observed in the non-cancerous liver tissue up to 12 weeks; in the liver cancer tissue, 4 cases were amplified in group A, and there was no abnormality in group C; 8 CDK4 gene: only group A had at week 75 In 1 case, HCC occurred at the 10th week of the tree mouse sentence. In HCC, CDK4 amplification occurred in 25% of the A group, and no abnormality was seen in the C group. Conclusion : It is confirmed once again that HBV and AFB1 have a synergistic effect on HCC; AFB1 is beneficial to the expression of HBx Ag and HB