This thesis explores the therapeutic potential of PARP inhibitors in breast and ovarian cancers with germline or somatic BRCA1/2 variants. BRCA genes play a key role in DNA repair through homologous recombination. Defects in these genes lead to homologous recombination deficiency (HRD), rendering tumor cells vulnerable to PARP inhibition. PARP inhibitors exploit this mechanism via synthetic lethality, offering a targeted treatment strategy for HRD-positive cancers.