Abstract
Ataxia-telangiectasia mutated (ATM) kinase is a central DNA damage response (DDR) component signalling the presence of DNA double strand breaks (DSBs) to DNA repair, checkpoint and survival pathways. Clinical doses of fractionated radiotherapy directed at tumours kill cells by inducing single strand breaks and DSBs, the latter being particularly lethal to all cells if not repaired. Poor survival rates of glioblastoma multiforme (GBM) patients is attributed to an inability to excise all invasive tumor tissue (if operable) and an intrinsic tumour chemoradioresistance, which has been linked to elevated ATM activity in glioma stem cells.