PARP inhibitors in cancers other than ovarian.

• A. Breast, pancreatic, and prostate cancers with BRCA/HRD
• B. Liver cancer
• C. Lung cancer
• D. Skin cancer

Answer: (A)

PARP inhibitors work best when the tumor already has a defective DNA repair pathway, specifically BRCA1/2 or other HRD defects. In those cancers, blocking PARP prevents repair of DNA damage, leading to cancer cell death through synthetic lethality. This concept translates beyond ovarian cancer to other BRCA/HRD-associated cancers, where clinical data have shown meaningful benefit. In breast, pancreatic, and prostate cancers with BRCA mutations or HRD, PARP inhibitors have demonstrated responses and have regulatory approvals in various treatment settings. By contrast, liver, lung, and skin cancers do not have this established BRCA/HRD-driven benefit profile with PARP inhibitors, so they aren’t the typical indications you’d rely on for this drug class.