BET inhibitors as novel therapeutic agents in breast cancer

Alberto Ocaña _, Cristina Nieto-Jiménez and Atanasio Pandiella

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Oncotarget. 2017; 8:71285-71291. https://doi.org/10.18632/oncotarget.19744

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Alberto Ocaña1, Cristina Nieto-Jiménez1 and Atanasio Pandiella2

1Unidad de Investigación Traslacional, Hospital Universitario de Albacete, Universidad de Castilla La Mancha, Albacete, Spain

2Instituto de Biología Molecular y Celular del Cáncer and CIBERONC, CSIC-Universidad de Salamanca, Salamanca, Spain

Correspondence to:

Alberto Ocaña, email: [email protected]

Keywords: breast cancer, BET inhibitors, novel targets

Received: May 16, 2017     Accepted: June 28, 2017     Published: August 01, 2017


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.

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