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Breast cancer type 2 susceptibility protein (BRCA2) is a tumor suppressor protein encoded by the *BRCA2* gene. It plays a critical role in the repair of double-stranded DNA breaks via homologous recombination, ensuring genomic stability and proper cell cycle progression[1][3][5][7]. Inactivation or mutation of BRCA2 leads to impaired DNA repair, resulting in genome instability and an increased risk for several malignancies, most notably hereditary breast and ovarian cancers, as well as prostate and pancreatic cancers[1][3][5][7]. BRCA2 dysfunction is also associated with Fanconi anemia when both gene copies are defective[5]. Clinically, individuals with BRCA2 mutations are eligible for targeted therapies such as PARP inhibitors, exploiting the concept of synthetic lethality in tumor cells deficient in homologous recombination repair[7]. BRCA2 status serves as an important biomarker for patient risk assessment, treatment selection, and prognostic evaluation in oncology[1][7].
Synthetic lethality via PARP inhibition in BRCA2-deficient cells, DNA damage repair interference
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