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Modelling the molecular circuitry of cancer
Author(s): Hahn WC, Weinberg RA
Source: NATURE REVIEWS CANCER    Volume: 2    Issue: 5    Pages: 331-341    Published: MAY 2002  
Times Cited: 390     References: 157     
Abstract: 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.
Document Type: Review
Language: English
Reprint Address: Hahn, WC (reprint author), Whitehead Inst Biomed Res, 9 Cambridge Ctr, Cambridge, MA 02142 USA
Addresses:
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
Publisher: NATURE PUBLISHING GROUP, MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
Subject Category: Oncology
IDS Number: 636GQ
ISSN: 1474-175X
DOI: 10.1038/nrc795
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