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News and Views
Nature Medicine 11, 920 - 922 (2005)
doi:10.1038/nm0905-920
Senescence comes of age
Masashi Narita1 & Scott W Lowe1
- The authors are at the Cold Spring Harbor Laboratory and Scott W. Lowe is also at the Howard Hughes Medical Institute, Cold Spring Harbor, New York 11724, USA. e-mail: lowe@cshl.edu
Abstract
Normal cells can respond to expression of activated oncogenes by initiating cellular senescence, a permanent state of proliferative arrest. But whether this process reflects a relevant anticancer mechanism has been debated. Several studies now show that oncogene-induced senescence can occur in vivo and provides a bona fide barrier to tumorigenesis.
More than 40 years ago, Hayflick observed that cells can lose the ability to divide after a limited number of cell divisions, and enter a state of proliferative arrest1. This state of cellular senescence, we now know, is similar to apoptosis—involving a gene-directed program that irrevocably arrests cell division by blocking normal responses to growth factors2.
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