DNA REPAIR MECHANISMS IN BREAST CANCER: MOLECULAR AND GENOMIC PERSPECTIVES

Breast cancer remains one of the best-researched malignancies, not only due to its current prevalence but also its complex interdependence with the integrity of DNA repair processes. The disease is intimately associated with the breakdowns in the DNA repair systems, allowing the genome to endure daily harm. Homologous recombination is interrupted by defects in key genes, including BRCA1, BRCA2, and PALB2, and new data also point to the role of abnormalities in RAD51 activity, replication-fork stability, and chromatin remodelling in tumorigenesis. Such vulnerabilities in the molecules make the tumor vulnerable to therapeutic agents such as PARP inhibitors; however, resistance is often acquired through reversion mutations or by using other repair pathways. Studies in 2023 and 2024 emphasize the growing relevance of precision diagnostics, which include liquid biopsy and functional tests, to select patients who have the highest chance of responding to DNA-repair-targeted treatments. At the same time, new types of drug approaches are expanding the therapeutic horizon, including PARP1-selective inhibitors and ATR inhibitors. All these developments underscore the importance of DNA repair in determining the biology and clinical treatment of breast cancer, hence the possibility of directing repair pathways to provide highly specific and long-lasting treatments in the near future