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Germline mutations in breast cancer susceptibility gene 1 or 2 ( BRCA 1 or  BRCA 2) significantly increase cancer risk in hereditary breast and ovarian cancer syndrome ( HBOC ). Both genes function in the homologous recombination ( HR ) pathway of the  DNA  double‐strand break ( DSB ) repair process. Therefore, the  DNA ‐repair defect characteristic of cancer cells brings about a therapeutic advantage for poly( ADP ‐ribose) polymerase ( PARP ) inhibitor‐induced synthetic lethality.  PARP  inhibitor‐based therapeutics initially cause cancer lethality but acquired resistance mechanisms have been found and need to be elucidated. In particular, it is essential to understand in detail the mechanism of  DNA  damage and repair to  PARP  inhibitor treatment. Further investigations have shown the roles of  BRCA 1/2 and its associations to other molecules in the  DSB  repair system. Notably, the repair pathway chosen in  BRCA 1‐deficient cells could be entirely different from that in  BRCA 2‐deficient cells after  PARP  inhibitor treatment. The present review describes synthetic lethality and acquired resistance mechanisms to  PARP  inhibitor through the  DSB  repair pathway and subsequent repair process. In addition, recent knowledge of resistance mechanisms is discussed. Our model should contribute to the development of novel therapeutic strategies.

cancer science

Crosstalk of DNA double‐strand break repair pathways in poly(ADP‐ribose) polymerase inhibitor treatment of breast cancer susceptibility gene 1/2‐mutated cancer