Unfortunately, in the field of BC, HDAC inhibitors have shown limited effect as single agents. The acetylation of histone proteins provokes the transcription of genes involved in cell growth, and the expression of histone deacetylases (HDACs) is frequently up-regulated in many malignancies. Given the fact that epigenetic processes control both the initiation and progression of TNBC, there is an increasing interest in the mechanisms, molecules and signaling pathways that participate at the epigenetic modulation of genes expressed in carcinogenesis. It is essential to find new therapies against TNBC, in order to surpass the resistance and the invasiveness of already existing therapies. Unfortunately, TNBC’s treatment continues to be a clinical problem because of its relatively poor prognosis, its aggressiveness and the lack of targeted therapies, leaving chemotherapy as the mainstay of treatment. It comprises approximately 15-20% of breast cancers (BCs). Triple-negative breast cancer (TNBC) lacks expression of estrogen receptor (ER), progesterone receptor (PR) and HER2 gene.
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