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The Breast Cancer gene 1 (BRCA1) and Breast Cancer gene 2 (BRCA2) genes are pivotal human tumor suppressor genes that are essential for preserving genomic stability. Mutations in BRCA1 and BRCA2 prevent homologous recombination, which is regulated by cell cycle checkpoints, thereby hindering the repair of double-stranded DNA. The ultimate result of genomic instability is characterized by altered transcriptional control and abnormal expression of essential cell-cycle proteins. As significant genetic factors, any mutations in the BRCA1 and BRCA2 genes substantially elevated a woman's risk of getting ovarian and breast cancer, often resulting in the development of these cancers earlier in life. Treatment of breast and ovarian cancer brought on by BRCA gene mutations focuses heavily on germline BRCA-mutated (gBRCAm) testing, targeted therapies such as Poly (ADP-ribose) polymerase inhibitors (PARP inhibitors), in addition to other options such as traditional chemotherapy and immunotherapy. This systematic review examines the crucial role of BRCA1 and BRCA2 in DNA repair, as well as how their mutations contribute to the development of inherited gynecological malignancies, and potential treatments targeting BRCA-deficient tumors. Also discusses resistance mechanisms to PARP inhibitors, the potential for combination therapies (PARP inhibitors + immune checkpoint inhibitors), and Advances in nanotechnology-based drug delivery, dynamic biomarker development, and CRISPR-based gene repair for BRCA mutations as future challenges and direction for curable patient.
Georgy et al. (Tue,) studied this question.