RESEARCH ARTICLE-κ a

DNA damage is of profound biomedical interest, as this type of lesions largely contributes to cancerogenesis [1]. DNA damage is induced by environmental factors, like ionizing radiation [2], but also by intrinsic agents, like metabolically generated reactive oxygen species [3]. Damaged DNA becomes bound by so-called sensor pro-teins, like replication protein A (RPA) or a complex composed of meiotic recombination 11 (Mre11)- radi-ation 50 (Rad50)- nijmegen breakage syndrome 1 (Nbs1) (MRN). They trigger a complex network of signal transduction pathways designated as DDR [1]. The DDR causes temporal cell cycle arrest, if the level of DNA damage is low, so the cell can repair it [4]. In response to severe DNA damage, cells undergo apoptosis to avoid transformation into tumour cells [5]. Alternatively, the cells enter permanent cell cycle arrest, called senescence [6]. In presence of DNA damage, the tumour suppressor * Correspondence