Targeting the DNA damage response represents a promising approach to improve the
efficacy of radiation therapy. One appealing target for this approach is the serine/threonine
kinase ataxia telangiectasia mutated (ATM), which is activated by DNA double strand breaks
to orchestrate the cellular response to ionizing radiation. Small-molecule inhibitors targeting
ATM have entered clinical trials testing their safety in combination with radiation therapy or
in combination with other DNA damaging agents. Here, we review biochemical, genetic, and …