Journal
CELLULAR ONCOLOGY
Volume 41, Issue 6, Pages 605-621Publisher
SPRINGER
DOI: 10.1007/s13402-018-0409-1
Keywords
Breast cancer; Targeted therapy; Small molecule inhibitors; Immunotherapy; MicroRNAs; Long noncoding RNAs; Cancer vaccines; CRISPR-Cas9 editing
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BackgroundBreast cancer (BC) is the most common cancer among women and it is responsible for more than 40,000 deaths in the United States and more than 500,000 deaths worldwide each year. In previous decades, the development of improved screening, diagnosis and treatment methods has led to decreases in BC mortality rates. More recently, novel targeted therapeutic options, such as the use of monoclonal antibodies and small molecule inhibitors that target specific cancer cell-related components, have been developed. These components include ErbB family members (HER1, HER2, HER3 and HER4), Ras/MAPK pathway components (Ras, Raf, MEK and ERK), VEGF family members (VEGFA, VEGFB, VEGFC, VEGF and PGF), apoptosis and cell cycle regulators (BAK, BAX, BCL-2, BCL-X, MCL-1 and BCL-W, p53 and PI3K/Akt/mTOR pathway components) and DNA repair pathway components such as BRCA1. In addition, long noncoding RNA inhibitor-, microRNA inhibitor/mimic- and immunotherapy-based approaches are being developed for the treatment of BC. Finally, a novel powerful technique called CRISPR-Cas9-based gene editing is emerging as a precise tool for the targeted treatment of cancer, including BC.ConclusionsPotential new strategies that are designed to specifically target BC are presented. Several clinical trials using these strategies are already in progress and have shown promising results, but inherent limitations such as off-target effects and low delivery efficiencies still have to be resolved. By improving the clinical efficacy of current therapies and exploring new ones, it is anticipated that novel ways to overcome BC may become attainable.
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