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Une re-vue de la sénescence cellulaire : Ami ou ennemi de la promotion tumorale ?

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.
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https://hal-pasteur.archives-ouvertes.fr/pasteur-03236210
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Oliver Bischof, Anne Dejean, Pascal Pineau. Une re-vue de la sénescence cellulaire : Ami ou ennemi de la promotion tumorale ?. médecine/sciences, EDP Sciences, 2009, 25 (2), pp.153-160. ⟨10.1051/medsci/2009252153⟩. ⟨pasteur-03236210⟩

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