Cellular senescence in cancer treatment: friend or foe?
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.
Kahlem
Pascal
P
Department of Hematology, Oncology, and Tumor Immunology, Humboldt University, Charité, Berlin, Germany.
Dörken
Bernd
B
Schmitt
Clemens A
CA
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis; D045744:Cell Line, Tumor; D016922:Cellular Senescence; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D004249:DNA Damage; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000473:pathology* / Q000628:therapy*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D000970:Antineoplastic Agents; D019941:Cyclin-Dependent Kinase Inhibitor p16; D016159:Tumor Suppressor Protein p53; D004247:DNA