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肿瘤抑制的连续统模型。

A continuum model for tumour suppression.

机构信息

Cancer Genetics Program, Beth Israel Deaconess Cancer Center, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Nature. 2011 Aug 10;476(7359):163-9. doi: 10.1038/nature10275.

Abstract

This year, 2011, marks the forty-year anniversary of the statistical analysis of retinoblastoma that provided the first evidence that tumorigenesis can be initiated by as few as two mutations. This work provided the foundation for the two-hit hypothesis that explained the role of recessive tumour suppressor genes (TSGs) in dominantly inherited cancer susceptibility syndromes. However, four decades later, it is now known that even partial inactivation of tumour suppressors can critically contribute to tumorigenesis. Here we analyse this evidence and propose a continuum model of TSG function to explain the full range of TSG mutations found in cancer.

摘要

今年,2011 年,标志着对视网膜母细胞瘤进行统计学分析的四十周年,这为肿瘤发生可以由少至两次突变引发提供了首个证据。这项工作为双打击假说奠定了基础,该假说解释了隐性肿瘤抑制基因 (TSG) 在显性遗传性癌症易感性综合征中的作用。然而,四十年后,现在已知即使是肿瘤抑制剂的部分失活也会对肿瘤发生产生重大影响。在这里,我们分析了这些证据,并提出了 TSG 功能的连续模型,以解释在癌症中发现的 TSG 突变的全部范围。

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