title: [A review of cellular senescence: friend or foe of tumorigenesis?].
abstract: Cellular senescence, like apoptosis, is now widely accepted as a potent tumor suppressor mechanism operating in normal mitotic mammalian cells. Originally, it was identified as a process that limits the replicative lifespan of primary human cells in culture because of telomere attrition and was therefore termed "replicative" senescence (RS). However, previous findings have demonstrated that a phenotype indistinguishable from replicative senescence, collectively called "stress-induced premature" senescence (SIPS), can be induced without extensive cell division in normal as well as cancer cells by a variety of stresses and signaling imbalances. Recent developments have also indicated that, despite their tumor-suppressive capacity, senescent cells themselves could produce neoplastic cells under certain circumstances and promote the growth of preneoplastic cells, raising the possibility that senescence might function as a biological "Trojan" horse. Here, we take a snapshot of the progress in understanding the causes and consequences of cellular senescence in vitro and in vivo.
authors.affiliation: Unité d'Organisation Nucléaire et Oncogenèse (ONO), Inserm U579, Institut Pasteur, 28, rue du Docteur Roux, 75724 Paris Cedex 15, France. obischof@pasteur.fr
authors.forename: Oliver
authors.initials: O
authors.lastname: Bischof
authors.forename: Anne
authors.initials: A
authors.lastname: Dejean
authors.forename: Pascal
authors.initials: P
authors.lastname: Pineau
mesh_terms: D017209:Apoptosis; D016922:Cellular Senescence / Q000502:physiology*; D004249:DNA Damage; D004260:DNA Repair / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D009369:Neoplasms / Q000503:physiopathology* / Q000517:prevention & control*; D010641:Phenotype; D016615:Telomere / Q000235:genetics / Q000502:physiology