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目的 探讨端粒酶在肿瘤发生发展过程中的激活时间及它们的因果关系。方法 利用 1,2 二甲肼诱导大鼠肠癌发生的模型 ,半定量观察端粒酶活性在肠癌发生过程中动态变化情况。结果 本研究用 1,2 二甲肼成功地诱导大鼠肠癌发生的模型 ,诱癌率达 5 7 6 9%。端粒酶在肠癌诱导的第 5周明显增高 ,到 15周肠癌形成时达到最高峰 ,以后维持在高水平。炎性病灶内端粒酶活性未见增高。结论 端粒酶的激活发生在肠癌形成的早期 ,到癌形成时 ,达到最高峰 ;端粒酶的激活可能是癌前病变的一种生物学标记物 ,与细胞恶性变的发展有密切关系
Objective To investigate the activation time of telomerase in tumorigenesis and their causal relationship. Methods 1,2-dimethylhydrazine induced colorectal cancer model in rats, semi-quantitative observation of telomerase activity in the course of occurrence of colorectal cancer. Results In this study, 1,2-dimethylhydrazine successfully induced rat colorectal cancer model, the rate of cancer-inducing 57.9%. Telomerase was significantly increased in the fifth week of colorectal cancer induction, reached the peak when colorectal cancer was formed in the 15th week, and remained high afterwards. Inflammatory lesions within the telomerase activity was not increased. Conclusion The activation of telomerase occurs in the early stage of colorectal carcinogenesis and reaches the peak when it is formed. The activation of telomerase may be a biomarker of precancerous lesions and is closely related to the development of malignant transformation