Role of BRCA1 and BRCA2 Mutations in the Molecular Genetic Mechanisms of Ovarian Cancer

Ovarian cancer is one of the most lethal oncological diseases among women, and hereditary factors play a crucial role in its pathogenesis. In this regard, the BRCA1 and BRCA2 genes are of particular importance as key tumor suppressor genes involved in the repair of DNA double-strand breaks through homologous recombination. Pathogenic mutations in these genes lead to disruptions in genome stability, the accumulation of DNA damage, and uncontrolled cell proliferation. As a result, the risk of developing ovarian cancer increases significantly. BRCA1 and BRCA2 gene mutations can be both hereditary (germinal) and somatic, and the spectrum of these mutations encompasses point mutations, insertion-deletion changes, and loss of large genomic segments. At the molecular-genetic level, these changes weaken DNA repair mechanisms and activate alternative, error-prone repair pathways. Recent studies have shown that ovarian cancer in BRCA mutation carriers has a different biological behavior and response to treatment; in particular, there is a high sensitivity to PARP inhibitors. For this reason, studying the molecular-genetic roles and mutation mechanisms of the BRCA1 and BRCA2 genes is of significant scientific and clinical importance for personalized diagnostics, risk assessment, and the development of targeted therapies.