Abstract

Ovarian cancer, a leading cause of gynecologic cancer mortality, is characterized by DNA repair deficiencies in up to 50% of cases, particularly in BRCA-mutated and homologous recombination-deficient (HRD) tumors. Poly (ADPribose) polymerase (PARP) inhibitors, such as olaparib, niraparib, and rucaparib, exploit these vulnerabilities, offering significant therapeutic advances. This article reviews the mechanisms, clinical trial outcomes, and challenges of PARP inhibitors in ovarian cancer treatment. Results demonstrate prolonged progression-free survival (PFS) in maintenance and recurrent settings, though resistance remains a hurdle. Future directions include combination therapies and biomarker development to optimize patient selection.