[Antiangiogenic biotherapy and chemotherapy in breast cancer: review of literature and case report].

Breast cancer incidence is 120/100,000 women and thus, it is the most frequent malignant disease in women. Despite the ever-increasing incidence, mortality has stayed stable; this is due to screening with detection of early breast cancers, adjuvant treatment and advances in targeted therapy. Currently, we perceive breast cancer as a phenotypically different subunits, influenced by genetic and epigenetic changes. All 5 basic subgroups (luminal A, B, basal-like, HER-2 positive and claudin-low) vary significantly in their prognosis and therapeutic options. The subgroup of basal-like tumors without hormone receptors positivity and HER-2 antigen (triple-negative breast cancer) is prognostically and therapeutically a very unfavorable group. Hormonal and anti-HER-2 therapy is excluded, and the effect of chemotherapy is limited and short-lived. Research for this sub-group of breast tumors in recent years focused on the influence of angiogenesis and DNA repair systems. Therapeutic manipulation of angiogenesis is based on the concept of its influence in the development and maintenance of the malignant process. The longest used and in terms of studies and clinical practice explored treatment is the main path of angiogenesis, the vascular endothelial growth factor. In the last few years, the real effect in the metastatic breast cancer is discussed. The initial positive results of pilot clinical trials showing a significant extension of the progression free survival bring disappointment since they were not translated into prolongation of overall survival. The following case-report presents a patient with metastatic triple-negative breast cancer with combined chemobiotherapy (capecitabine + bevacizumab). In the second part of the article, we discuss possible causes of inconsistent outcomes with antiangiogenic therapy in breast cancer, new directions in scientific research and today knowledge of prediction of its therapeutic effect.