Intrinsic tumour suppression
Intrinsic tumour suppression
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DOI：
10.1038/nature03098
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发表时间：
2004-11-18
期刊：
影响因子：
64.8
通讯作者：
Evan, G
中科院分区：
文献类型：
--
作者：
Lowe, SW;Cepero, E;Evan, G
驱动不受控制的细胞周期进展的突变是肿瘤发生的必要事件。但是，在哺乳动物细胞的增殖计划中，进化已经安装在各种触发凋亡或衰老的先天性肿瘤抑制机制中，应该变得异常。这些偶然过程依赖于在协调网络中起作用的一系列传感器和传感器，以针对负责在不同点上凋亡和细胞周期停滞的机械。尽管禁用此类网络的致癌突变可能会对肿瘤的进化产生深远而多样化的影响，但它们可能会留下可以在治疗上利用的完整潜在潜在抑制潜力。
Mutations that drive uncontrolled cell-cycle progression are requisite events in tumorigenesis. But evolution has installed in the proliferative programmes of mammalian cells a variety of innate tumour-suppressive mechanisms that trigger apoptosis or senescence, should proliferation become aberrant. These contingent processes rely on a series of sensors and transducers that act in a coordinated network to target the machinery responsible for apoptosis and cell-cycle arrest at different points. Although oncogenic mutations that disable such networks can have profound and varied effects on tumour evolution, they may leave intact latent tumour-suppressive potential that can be harnessed therapeutically.