Editorial: Molecular studies and therapeutic approaches on BRCA-associated cancers

mutations. Both BRCA1 and BRCA2 genes are key players in maintaining genomic stability 1. When mutated, cells lose the ability to repair DNA damage, leading to the accumulation of mutations and an increased risk of developing cancers, particularly those of the breast and ovaries 2. Studies have unraveled a complex network of molecular pathways disrupted in BRCA-deficient cells, importantly cell cycle regulation and apoptotic pathways 3,4. The BRCA1/2 mutations, though relatively rare in the general population, account for a significant proportion of breast, ovarian, and other cancers, and their implications for both patients and healthcare systems are profound 5. The past decade has seen remarkable progress in therapies specifically targeting BRCA-mutated tumors, most notably PARP inhibitors (PARPi), although resistance remains a growing concern 6,7. BRCA-mutated tumors also exhibit higher levels of genomic instability, generating tumor-specific neoantigens that enhance immune visibility and spurring interest in combining immune checkpoint inhibitors with DNAtargeted therapies such as PARPi. Another promising therapeutic frontier is synthetic lethality, targeting genes or pathways that, when inhibited in conjunction with BRCA mutations, lead to cancer cell death 8. In this special issue, we bring together the latest molecular studies and therapeutic approaches to BRCA-associated cancers, shedding light on emerging insights and potential avenues for future treatments.