title: The importance of senescence in ionizing radiation-induced tumour suppression.
abstract: Cellular senescence is a condition of longlasting proliferation arrest, induced in cells in response to various stressors. These stressors include telomere shortening and/or dysfunction, DNA damage, and oncogene signalling. Epithelial and mesenchymal cells and also tumour cells derived from these tissues are more resistant to radiation-induced apoptosis and respond to irradiation mainly by senescence. Senescence-associated molecular mechanisms related to the activation of canonical DNA damage pathway ATM-p53 as well as mechanisms related to the extracellular signals, cytokine increase and upregulation of their receptors are discussed in this review.
authors.affiliation: Department of Radiobiology, University of Defence in Brno, Hradec Králové, Czech Republic. vavrova@pmfhk.cz
authors.forename: J
authors.initials: J
authors.lastname: Vávrová
authors.forename: M
authors.initials: M
authors.lastname: Rezáčová
mesh_terms: D000818:Animals; D001260:Ataxia Telangiectasia / Q000235:genetics / Q000378:metabolism; D016922:Cellular Senescence / Q000235:genetics*; D004249:DNA Damage; D006801:Humans; D008954:Models, Biological; D009154:Mutation; D009381:Neoplasms, Radiation-Induced / Q000235:genetics; D011839:Radiation, Ionizing; D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism
chemical_list: D016159:Tumor Suppressor Protein p53