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Due to endogenous and exogenous factors, such as UV radiation, ionizing radiation and genotoxic chemicals, DNA in every cell of the body is at constant risk of damage [1-3]. To overcome damage to DNA, repair pathways are needed. These pathways are collectively referred to as DNA damage response (DDR) [1, 4].

Click here for more information about the DDR

PARP is involved in DDR via several mechanisms [5-7]:

  • Repair of double-strand breaks through homologous recombination repair (HRR)
  • Non-homologous end joining (NHEJ)
  • Micro-homology mediated end joining (MMEJ; also known as alt-NHEJ).
  • Repair of single strand breaks (SSB) via base excision repair (BER).

Click here to find out more on what happens at the molecular level. 

References

  1. Lord CJ, Ashworth A. The DNA damage response and cancer therapy. Nature 2012; 481: 287-294.
  2. Friedberg EC. A brief history of the DNA repair field. Cell Res 2008; 18: 3-7.
  3. Ashworth A. A synthetic lethal therapeutic approach: poly(ADP) ribose polymerase inhibitors for the treatment of cancers deficient in DNA double-strand break repair. J Clin Oncol 2008; 26: 3785-3790.
  4. Lord CJ, Ashworth A. PARP inhibitors: Synthetic lethality in the clinic. Science 2017; 355: 1152-1158.
  5. Moynahan ME, Jasin M. Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesis. Nat Rev Mol Cell Biol 2010; 11: 196-207.
  6. Murai J, Huang SY, Das BB et al. Trapping of PARP1 and PARP2 by Clinical PARP Inhibitors. Cancer Res 2012; 72: 5588-5599.
  7. Cerrato A, Morra F, Celetti A. Use of poly ADP-ribose polymerase [PARP] inhibitors in cancer cells bearing DDR defects: the rationale for their inclusion in the clinic. J Exp Clin Cancer Res 2016; 35: 179.

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