Abstract
Tumoral cells not only depend on oncogenic abnormalities to maintain its malignant phenotype but on non-oncogenic vulnerabilities. Targeting epigenomics can modify specific cellular functions required for malignant transformation. The Bromodomain (BRD) family mediates their effect by recruiting proteins of the transcription machinery, recognizing acetylated-lysine residues in nucleosomal histones. Bromodomain and extra-terminal (BET) inhibitors have shown to produce growth inhibition in several tumors through the inhibition of the expression of several transcription factors. In this review we will discuss the current knowledge regarding BET inhibitors in breast cancer. Recent data demonstrates their antiproliferative effect in several cancer subtypes, including the triple negative subtype, or when combined with cell signaling inhibitors. We will also describe options for therapeutic combinations or potential mechanisms of resistance, with special emphasis on their future clinical development.
Highlights
Breast cancer is one of the most prevalent tumors and a leading cause of death in women worldwide [1]
Around 20% of tumors overexpress the transmembrane protein HER2 due to gene amplification [3, 4]. These tumors benefit from therapies against this protein, including monoclonal antibodies like trastuzumab or pertuzumab, or small tyrosine kinase inhibitors like lapatinib or neratinib [5, 6]
For a comprehensive review of Bromodomain and extra-terminal (BET) inhibitors in clinical development we suggest to read the article by Andrieu G et al [25]
Summary
Breast cancer is one of the most prevalent tumors and a leading cause of death in women worldwide [1]. Recent data demonstrates their antiproliferative effect in several cancer subtypes, including the triple negative subtype, or when combined with cell signaling inhibitors. Inhibition of these proteins has shown antitumoral efficacy in a wide range of solid tumors including breast cancer [11, 18].
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