Abstract
Simple SummaryBreast cancer is a genetically heterogeneous disease with different molecular biological and clinical characteristics. The available knowledge about the genetic heterogeneity of the most aggressive molecular subtype of breast cancer—triple-negative—has led to discoveries in drug treatment. Identification of the molecular-genetic phenotype of breast cancer is an important prognostic factor of the disease and allows personalization of the patient’s treatment.Understanding of the genetic mechanisms and identification of the biological markers of tumor progression that form the individual molecular phenotype of transformed cells can characterize the degree of tumor malignancy, the ability to metastasize, the hormonal sensitivity, and the effectiveness of chemotherapy, etc. Breast cancer (BC) is a genetically heterogeneous disease with different molecular biological and clinical characteristics. The available knowledge about the genetic heterogeneity of the most aggressive molecular subtype of breast cancer—triple-negative (TN)—has led to discoveries in drug treatment, including the use of DNA damaging agents (platinum and PARP inhibitors) for these tumors, as well as the use of immunotherapy. Most importantly, the ability to prescribe optimal drug treatment regimens for patients with TNBC based on knowledge of the molecular-genetic characteristics of this subtype of BC will allow the achievement of high rates of overall and disease-free survival. Thus, identification of the molecular-genetic phenotype of breast cancer is an important prognostic factor of the disease and allows personalization of the patient’s treatment.
Highlights
Breast cancer (BC) is a heterogeneous, solid, malignant neoplasm and an extremely heterogeneous disease in terms of prognosis and sensitivity to antitumor therapy, which is related primarily to a variety of molecular-genetic changes leading to its development and progression
There were four different molecular subtypes of BC: two subgroups with positive expression of estrogen and/or progesterone receptors (ER+/PR+)—luminal A and B, which account for approximately 70% of all breast cancer cases; one subgroup with overexpression/amplification of the HER/2-neu gene and negative expression of hormonal receptors (HER/2 positive subgroup); and triple-negative breast cancer (TNBC), with no expression of steroid hormone receptors and HER2
When correlating the literature data on the cell-signaling pathways and pathways characteristic of TNBC, determined by genes whose mutations occur in TNBC and not in non-TNBC according to TCGA database, the intersection of three cellular pathways was revealed—DNA repair pathways, focal adhesion: PI3K-Akt-mTOR-signaling pathway, and PI3K-Akt signaling pathway (Figure 2)
Summary
Breast cancer (BC) is a heterogeneous, solid, malignant neoplasm and an extremely heterogeneous disease in terms of prognosis and sensitivity to antitumor therapy, which is related primarily to a variety of molecular-genetic changes leading to its development and progression. If a complete pathological response is not achieved, the best result of preoperative treatment is combined with a worse prognosis in the postoperative period, lower rates of relapse-free and overall survival (p < 0.0001), and a higher probability of disease relapse. This phenomenon is called the triple-negative breast cancer paradox [6,7]. Gallen-2015 and ESMO-2015, patients with this molecular subtype are subject to chemotherapy with taxanes and anthracyclines, and in the presence of a BRCA mutation, it is possible to use platinum drugs [19] The reasons for this TNBC paradox are still unclear. The presented review is devoted to the analysis of the most relevant data of the molecular-genetic parameters of TN breast cancer from the point of view of their possible use as targets for therapy
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