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探讨癌基因ras和抑癌基因P5 3蛋白在实验性肝癌发生中的表达与内在联系。方法 应用原位杂交和免疫组织化学 (SABC)法 ,在 38例化学致癌剂二乙基亚硝胺 (DENA)诱发大鼠原发性肝细胞癌及癌前增殖结节中 ,观察P5 3蛋白和ras家族基因 (N ras,H ras,Ki ras)蛋白表达。结果 化学诱癌生成为 6 8.42 % (2 6 / 38) ,癌前增生性病例为 31.5 8% (12 / 38)。在癌与增生性病变中ras基因蛋白高表达分别为 88.46 % (2 3/ 2 6 )和 75 % (9/ 12 ) ,两组无显著差异(P >0 .0 5 ) ,但与癌的恶性分化程度密切相关 (P <0 .0 1)。在增生性病灶中未检出P5 3蛋白的表达 ,在癌中P5 3蛋白表达阳性率为 46 .15 % (12 / 2 6 ) ,但与ras蛋白表达无显著相关性 (P >0 .0 5 )。结论 ras基因是肝癌转化较早的分子改变 ;癌前嗜碱性增生性结节和不典型增生性腺瘤结节具有较高的恶化潜能 ;ras和P5 3在癌变形成中作用点不同
To investigate the expression and intrinsic relationship between oncogene ras and tumor suppressor gene P53 protein in the occurrence of experimental liver cancer. Methods In situ hybridization and immunohistochemistry (SABC) were used to observe P53 protein in 38 primary hepatocellular carcinoma and precancerous nodules induced by diethylnitrosamine (DENA). And ras family gene (N ras, H ras, Ki ras) protein expression. RESULTS: Chemically induced carcinogenesis was found to be 6.42% (26/38) and precancerous hyperplasia was 31.58% (12/38). The high expression of ras gene protein in cancerous and proliferative lesions were 88.46% (23/26) and 75% (9/12), respectively, with no significant difference between the two groups (P > 0.05), but with cancer The degree of malignant differentiation was closely related (P < 0.01). No expression of P53 protein was detected in proliferative lesions. The positive rate of P53 protein expression in cancer was 46.15% (12/26), but there was no significant correlation with ras protein expression (P > 0.05). 5). Conclusion The ras gene is an early molecular alteration in the transformation of hepatocellular carcinoma; pre-cancer basophilic proliferative nodule and atypical hyperplasia adenoma nodule have higher aggravation potential; ras and P5 3 have different roles in carcinogenesis