Intrinsic tumour suppression
Scott W. Lowe (),
Enrique Cepero and
Gerard Evan
Additional contact information
Scott W. Lowe: Cold Spring Harbor Laboratory
Enrique Cepero: Cold Spring Harbor Laboratory
Gerard Evan: Cancer Research Institute, University of California at San Francisco
Nature, 2004, vol. 432, issue 7015, 307-315
Abstract:
Abstract Mutations that drive uncontrolled cell-cycle progression are requisite events in tumorigenesis. But evolution has installed in the proliferative programmes of mammalian cells a variety of innate tumour-suppressive mechanisms that trigger apoptosis or senescence, should proliferation become aberrant. These contingent processes rely on a series of sensors and transducers that act in a coordinated network to target the machinery responsible for apoptosis and cell-cycle arrest at different points. Although oncogenic mutations that disable such networks can have profound and varied effects on tumour evolution, they may leave intact latent tumour-suppressive potential that can be harnessed therapeutically.
Date: 2004
References: Add references at CitEc
Citations:
Downloads: (external link)
https://www.nature.com/articles/nature03098 Abstract (text/html)
Access to the full text of the articles in this series is restricted.
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:432:y:2004:i:7015:d:10.1038_nature03098
Ordering information: This journal article can be ordered from
https://www.nature.com/
DOI: 10.1038/nature03098
Access Statistics for this article
Nature is currently edited by Magdalena Skipper
More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().