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突变的癌基因和肿瘤抑制基因是如何引发癌症的?

How do mutated oncogenes and tumor suppressor genes cause cancer?

作者信息

Grandér D

机构信息

Research Laboratory of Radiumhemmet, Karolinska Hospital, Stockholm, Sweden.

出版信息

Med Oncol. 1998 Apr;15(1):20-6. doi: 10.1007/BF02787340.

Abstract

In recent decades we have been given insight into the process that transforms a normal cell into a malignant cancer cell. It has been recognised that malignant transformation occurs through successive mutations in specific cellular genes, leading to the activation of oncogenes and inactivation of tumor suppressor genes. The further study of these genes has generated much of its excitement from the convergence of experiments addressing the genetic basis of cancer, together with cellular pathways that normally control important cellular regulatory programmes. In the present review the context in which oncogenes and tumor suppressor genes normally function as key regulators of physiological processes such as proliferation, cell death/apoptosis, differentiation and senescence will be described, as well as how these cellular programmes become deregulated in cancer due to mutations.

摘要

近几十年来,我们对将正常细胞转变为恶性癌细胞的过程有了深入了解。人们已经认识到,恶性转化是通过特定细胞基因的连续突变发生的,导致癌基因激活和肿瘤抑制基因失活。对这些基因的进一步研究产生了许多令人兴奋的成果,这些成果来自于针对癌症遗传基础的实验与通常控制重要细胞调节程序的细胞途径的融合。在本综述中,将描述癌基因和肿瘤抑制基因通常作为增殖、细胞死亡/凋亡、分化和衰老等生理过程的关键调节因子发挥作用的背景,以及这些细胞程序在癌症中如何因突变而失调。

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