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Biochim Biophys Acta. 2007 Jan;1775(1):5-20. Epub 2006 Aug 25.

Cellular senescence and cancer treatment.

Author information

1
Department of Internal Medicine/Hematology and Oncology, Charité-Universitätsmedizin Berlin (CVK), Augustenburger Platz 1, Berlin, Germany. clemens.schmitt@charite.de

Abstract

Cellular senescence, an irreversible cell-cycle arrest, reflects a safeguard program that limits the proliferative capacity of the cell exposed to endogenous or exogenous stress signals. A number of recent studies have clarified that an acutely inducible form of cellular senescence may act in response to oncogenic activation as a natural barrier to interrupt tumorigenesis at a premalignant level. Paralleling the increasing insights into premature senescence as a tumor suppressor mechanism, a growing line of evidence identifies cellular senescence as a critical effector program in response to DNA damaging chemotherapeutic agents. This review discusses molecular pathways to stress-induced senescence, the interference of a terminal arrest condition with clinical outcome, and the critical overlap between premature senescence and apoptosis as both tumor suppressive and drug-responsive cellular programs.

PMID:
17027159
DOI:
10.1016/j.bbcan.2006.08.005
[Indexed for MEDLINE]
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