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Oncogene-Induced Senescence: Putting the Brakes on Tumor Development

¹ Department of Hematology/Oncology, Charité-Universitätsmedizin Berlin and ² Max-Delbrück-Center for Molecular Medicine, Berlin, Germany

Requests for reprints: Clemens Schmitt, Department of Hematology, Oncology, and Tumor Immunology, Charité-Universitätsmedizin Berlin (CVK), Augustenburger Platz 1, 13353 Berlin, Germany. Phone: 49-30-450-553-687; Fax: 49-30-450-553-986; E-mail: clemens.schmitt{at}charite.de.

Cellular senescence, a permanent cell cycle arrest, is considered a safeguard mechanism that may prevent aged or abnormal cells from further expansion. Although the term "replicative senescence" stands for the widely accepted model of a terminal growth arrest due to telomere attrition, the significance of "oncogene-inducible senescence" remained an issue of debate over the years. A number of recent studies now show the effect of this acute and telomere-independent form of senescence as a tumor-protective, fail-safe mechanism in vivo that shares conceptual and possibly therapeutic similarities with the genetically encoded apoptosis machinery. (Cancer Res 2006; 66(6): 2881-4)

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