A continuum model for tumour suppression.

A continuum model for tumour suppression.
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DOI:
10.1038/nature10275
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发表时间:
2011-08-10
期刊:
影响因子:
64.8
通讯作者:
Pandolfi, Pier Paolo
Pandolfi, Pier Paolo
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Berger, Alice H.;Knudson, Alfred G.;Pandolfi, Pier Paolo

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2011年是视网膜母细胞瘤统计分析40周年,该分析首次提供了肿瘤发生可以由两个突变引发的证据。这项工作为解释隐性肿瘤抑制基因(TSGs)在显性遗传癌症易感性综合征中的作用的两次打击假说提供了基础。然而,四十年后,现在人们知道,即使是肿瘤抑制因子的部分失活也会对肿瘤发生产生重要影响。在这里,我们分析了这些证据,并提出了TSG功能的连续模型来解释癌症中发现的TSG突变的全部范围。
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.
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