[Senescence and cellular immortality].
Senescence was originally described from the observation of the limited ability of normal cells to grow in culture, and may be generated by telomere erosion, accumulation of DNA damages, oxidative stress and modulation of oncogenes or tumor suppressor genes. Senescence corresponds to a cellular response aiming to control tumor progression by limiting cell proliferation and thus constitutes an anticancer barrier. Senescence is observed in pre-malignant tumor stages and disappears from malignant tumors. Agents used in standard chemotherapy also have the potential to induce senescence, which may partly explain their therapeutic activities. It is possible to restore senescence in tumors using targeted therapies that triggers telomere dysfunction or reactivates suppressor genes functions, which are essential for the onset of senescence.
Structure des acides nucléiques, télomères et évolution, Muséum national d'histoire naturelle, Inserm U565, CNRS UMR 7196, 75005 Paris, France.
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D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D049109:Cell Proliferation; D002470:Cell Survival / Q000235:genetics / Q000502:physiology*; D016922:Cellular Senescence / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D004249:DNA Damage; D004261:DNA Replication / Q000502:physiology; D016147:Genes, Tumor Suppressor / Q000502:physiology; D006801:Humans; D051379:Mice; D009369:Neoplasms / Q000188:drug therapy / Q000235:genetics; D009857:Oncogenes; D018384:Oxidative Stress / Q000502:physiology; D019098:Telomerase / Q000502:physiology*; D016615:Telomere / Q000235:genetics / Q000502:physiology*
D000970:Antineoplastic Agents; C509186:TERT protein, human; D019098:Telomerase