A continuum model for tumour suppression

被引：349

作者：

Berger, Alice H. ^{[1
,2
]}

Knudson, Alfred G. ^{[3
]}

Pandolfi, Pier Paolo ^{[1
,2
]}

机构：

[1] Harvard Univ, Sch Med, Dept Med, Canc Genet Program,Beth Israel Deaconess Canc Ctr, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Pathol, Canc Genet Program,Beth Israel Deaconess Canc Ctr, Boston, MA 02115 USA

[3] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA

来源：

NATURE | 2011年 / 476卷 / 7359期

关键词：

HEMATOPOIETIC STEM-CELLS; EMBRYONIC-DEVELOPMENT; EPITHELIAL-CELLS; CONDITIONAL LOSS; GENE-MUTATIONS; CANCER GENES; PTEN; RETINOBLASTOMA; IDENTIFICATION; P53;

D O I：

10.1038/nature10275

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页码：163 / 169

页数：7

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