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肿瘤作为一种多基因突变的慢性累积病,某些肿瘤的生成和发展存在着依赖于某个癌基因的现象,即癌基因成瘾或癌基因依赖现象。癌基因成瘾理论由Weinstein在2002年首先提出,癌基因成瘾的机制目前有“怪诞”网络模型、致癌性休克模型和选择淘汰模型三种假设。肿瘤发生、发展的复杂性和显著的个体差异性,使得确认所谓的依赖性癌基因变得较为困难,除了基因组分析、高通量的蛋白功能分析、基因敲除等方法外,通过RNA干扰技术来寻找依赖性癌基因日益受到关注。癌基因依赖理论能够很好地解释某些分子靶向药物良好疗效的机制,为分子靶向药物的研发增添了理论依据,具有较好的临床应用价值,但该理论同时也面临着巨大的挑战,有待于进一步深入研究并加以完善。
Tumor as a multi-gene mutation of chronic cumulative disease, some tumors are dependent on the occurrence and development of an oncogene phenomenon, that is, the phenomenon of oncogene addiction or oncogene dependence. The theory of cancer gene addiction was first proposed by Weinstein in 2002. The mechanisms of cancer gene addiction currently include three kinds of hypotheses: the “weird” network model, the carcinogenic shock model and the opt-out model. Tumorigenesis, developmental complexity and significant individual variability make it more difficult to identify so-called dependent oncogenes. In addition to methods such as genomic analysis, high-throughput protein profiling and gene knockout, RNA interference To find dependencies oncogenes are receiving increasing attention. The theory of oncogenes dependence can well explain the good curative effect of some molecular targeted drugs, which provides a theoretical basis for the development of molecular targeted drugs and has a good clinical value, but the theory also faces great challenges , To be further studied and improved.