Cellular senescence and cancer treatment

• Published in: Biochimica et biophysica acta Vol. 1775; no. 1; pp. 5 - 20
• Main Author: Schmitt, Clemens A.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 2007
• Subjects: Animals; Anticancer therapy; Antineoplastic Agents - pharmacology; Apoptosis; beta-Galactosidase - metabolism; Cell Cycle - drug effects; Cell Line, Tumor; cellular senescence; Cellular Senescence - drug effects; Cellular Senescence - physiology; DNA Damage; Drug Resistance, Neoplasm; Humans; mouse model; Neoplasms - physiopathology; Neoplasms - therapy; oncogene; Oncogenes - physiology; apoptosis; cellular senescence; mouse model; Anticancer therapy; oncogene; DNA damage
• ISSN: 0304-419X; 0006-3002; 1879-2561; 1878-2434
• DOI: 10.1016/j.bbcan.2006.08.005

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.