title: [Targeting telomeres to enforce cancer cells to senesce].
abstract: The telomeres protect the end of chromosomes from being recognized and processed as an accidental double stranded break. In human somatic cells, telomeres shorten progressively with every round of DNA replication, leading to dysfunctional telomeres that trigger cellular senescence or apoptosis depending on the cell type. This telomere erosion appears to play a role in cell renewal, ageing and cancer. Two recent studies demonstrated in mouse that eroded telomeres in cancer cells blocked for apoptosis limit cancer formation by triggering senescence. These results suggest that provoking senescence may provide a way to cure cancer and point to new therapeutical strategies targeting specific telomeric functions. Nevertheless, an important question remains unanswered: does replicative senescence limit tumor formation in human?
authors.affiliation: Laboratoire Télomères et Cancer, UMR7147, Institut Curie-CNRS-UPMC, 26, rue d'Ulm, 75248 Paris, France.
authors.forename: Arturo
authors.initials: A
authors.lastname: Londoño-Vallejo
authors.forename: Christelle
authors.initials: C
authors.lastname: Lenain
authors.forename: Eric
authors.initials: E
authors.lastname: Gilson
mesh_terms: D016922:Cellular Senescence; D006706:Homeostasis; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000235:genetics / Q000473:pathology / Q000503:physiopathology* / Q000517:prevention & control; D016615:Telomere / Q000235:genetics / Q000502:physiology*