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Cellular senescence in cancer treatment: friend or foe?
Pascal Kahlem, … , Bernd Dörken, Clemens A. Schmitt
Pascal Kahlem, … , Bernd Dörken, Clemens A. Schmitt
Published January 15, 2004
Citation Information: J Clin Invest. 2004;113(2):169-174. https://doi.org/10.1172/JCI20784.
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Cellular senescence in cancer treatment: friend or foe?

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Abstract

Damage to DNA, the prime target of anticancer therapy, triggers programmed cellular responses. In addition to apoptosis, therapy-mediated premature senescence has been identified as another drug-responsive program that impacts the outcome of cancer therapy. Here, we discuss whether induction of senescence is a beneficial or, rather, a detrimental consequence of the therapeutic intervention.

Authors

Pascal Kahlem, Bernd Dörken, Clemens A. Schmitt

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Drug-inducible senescence: friend or foe? In response to DNA-damaging ag...
Drug-inducible senescence: friend or foe? In response to DNA-damaging agents, cancer cells can rapidly undergo apoptosis or may enter premature senescence as a potential back-up mechanism. Whether cells re-enter the cycle or execute apoptosis out of drug-mediated senescence remains unclear. A terminal arrest of the entire cancer cell population, possibly augmented through increased immunogenicity of senescent cells, is beneficial for the host. In contrast, feeder-like growth that reflects paracrine activity of senescent cells on their non-senescent neighbors, or escape from senescence based on acquired or preexisting mutations, is considered a detrimental outcome.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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