Cellular senescence is a condition of long-lasting 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 up-regulation of their receptors are discussed in this review.