title: Telomeres, senescence and cellular radiation response.
abstract: Telomeres shield the ends of chromosomes from degradation and end-to-end fusions. They shorten at each cell division and when they reach a critically short length, cells arrest in the G1 phase of the cell cycle and undergo senescence. This effectively limits the proliferative potential of cells. Senescence functions as a tumour suppressor mechanism and appears to contribute to the process of ageing. If senescence is circumvented by tumour viruses, proliferation is re-initiated until cells enter crisis. Activation of telomerase prevents telomere attrition and cells become immortal. Cellular response to ionizing radiation involves induction of cell cycle checkpoint arrests and programmed cell death. Because radiation produces double strand breaks in DNA, which cause telomere-less chromosome ends, radiation response appears to be the result of inappropriate induction of cellular senescence mechanisms.
authors.affiliation: Institute of Medical Radiobiology, Villigen-PSI, Switzerland. crompton@psi.ch
authors.forename: N E
authors.initials: NE
authors.lastname: Crompton
mesh_terms: D000818:Animals; D017209:Apoptosis; D002453:Cell Cycle / Q000528:radiation effects; D002471:Cell Transformation, Neoplastic; D016922:Cellular Senescence; D004249:DNA Damage; D004261:DNA Replication; D004789:Enzyme Activation; D009858:Oncogenic Viruses / Q000502:physiology; D011839:Radiation, Ionizing; D015398:Signal Transduction; D019098:Telomerase / Q000378:metabolism; D016615:Telomere / Q000502:physiology* / Q000528:radiation effects*
chemical_list: D019098:Telomerase