Fig. 1.

Schematic overview of DNA repair systems and emerging anticancer targets. Repairing toxic DNA lesions induced during most common cancer treatments relies on proper DNA repair response, which has the ability to dictate the cellular outcome, e.g., cell death or cell survival. Triggering of a specific repair pathway (DR, BER, NER, MMR, HR, and NHEJ pathways) depends on the nature of the DNA damage. The main components and the signaling pathways of each repair response are indicated. Yellow boxes highlight emerging anticancer targets that are discussed in this issue. The availability of other components of these pathways to serve as anticancer targets requires further testing. DR Direct reversal, BER base excision repair, NER nucleotide excision repair, GGR global genome repair, TCR transcription coupled repair, MMR mismatch repair, HR homologous recombination, MRN Mre11-Rad50-Nbs1 complex, NHEJ non-homologous end joining, O ⁶ MeG O⁶-methylguanine