Triple-negative breast cancer (TNBC) cells frequently harbor defects in the homologous recombination pathway,
1 which plays a prime role in DNA double-strand breaks repair. In a context of homologous recombination deficiency, use of poly(adenosine diphosphate ribose) polymerase (PARP) inhibitors indirectly increases the frequency of unrepaired double-strand break by affecting the base excision repair pathway after DNA-damaging stresses,
2 such as chemotherapy or radiotherapy. Preclinical studies have confirmed the radiosensitizing properties of PARP inhibitors in breast cancer murine models.
3