Modelling the molecular circuitry of cancer

被引：724

作者：

Hahn, WC

Weinberg, RA

机构：

[1] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA

[2] Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Adult Oncol, Dept Med, Boston, MA 02115 USA

[3] MIT, Dept Biol, Cambridge, MA 02139 USA

来源：

NATURE REVIEWS CANCER | 2002年 / 2卷 / 05期

关键词：

D O I：

10.1038/nrc795

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Cancer arises from a stepwise accumulation of genetic changes that liberates neoplastic cells from the homeostatic mechanisms that govern normal cell proliferation. In humans, at least four to six mutations are required to reach this state, but fewer seem to be required in mice. By rationalizing the shared and unique elements of human and mouse models of cancer, we should be able to identify the molecular circuits that function differently in humans and mice, and use this knowledge to improve existing models of cancer.

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收藏

页码：331 / 341

页数：11

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