Tumor immune microenvironment and apoptotic markers in breast cancer patients carrying <I>BRCA1</I> gene mutations

Background . It is suggested that defects in BRCA1 / 2 genes contribute to a high mutational load and immunogenicity, which modulates immune microenvironment. At the same time, it was shown -associated breast cancer tumors do not belong category of immunoactive ones. These have low expression response exhibit an immunosuppressive type This indicates need antitumor modulation maintaining optimal balance tumor CD4/CD8 T-lymphocytes ratio. In addition, there evidence additional evaluation TP53 mutation these disruption cell death process, can also be factor resistance therapy, including PARP inhibitors, serve as therapeutic target. Materials methods The prospective study included 20 patients with cancer. mutations ( 185delAG, 4153delA, 5382insC, 3819delGTAAA, 3875delGTCT, 300T>G, 2080delA, BRCA2 6174delT) were detected by real-time polymerase chain reaction. Immunohistochemical performed on paraffin embedded tissue blocks automated method ThermoScentific immunohistotainer using monoclonal antibodies. markers tumor-infiltrating CD4+ CD8+ T-lymphocytes, macrophages (CD68, CD163), apoptosis (Bcl-2, p53), adhesion (E-cadherin, β-catenin) carriers assessed. Results High ratio, characterizes microenvironment, occurred 75 % cases. 5382insC associated level TILs (p˂0.05), G ratio p = 0.039) CD163 0.02, AUC 0.739); T1 correlates levels 0.038) 0.033). Ki-67 lack Bcl-2 0.04) E-cadherin 0.02). Negative p53 has been described main tumors, suggesting combination TB53 violation mechanism tumors. Conclusion Breast hereditary gene demonstrate microenvironment mechanism. directions future therapy may include modification activation mechanisms.