Targeting DNA damage response kinases in cancer therapy

Abstract

Cancer cells die when their decimated DNA damage response (DDR) unsuccessfully handles DNA damage. This notion has been successfully exploited when targeting PARP (poly ADP-ribose polymerase) in homologous recombination-deficient cells. With the greater understanding of DDR achieved in the last decade, new cancer therapy targets within the DDR network have been identified. Intriguingly, many of the molecules that have advanced into clinical trials are inhibitors of DDR kinases. This special issue is devoted to discussing the mechanism of cell killing and the level of success that such inhibitors have reached in pre-clinical and clinical settings.