Abstract
Epigenetic modifications such as histone acetylation play a central role in the transcriptional regulation of many oncogenic drivers. Accumulating evidence suggests that pharmacological modulation of certain key epigenetic reader proteins such as BRD2/3/4 may serve as an attractive strategy for treatment of many cancers, including tamoxifen-resistant breast cancer.
MeSH terms
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Acetylation
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Azepines / therapeutic use
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Benzodiazepines / therapeutic use
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Breast Neoplasms / drug therapy
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Breast Neoplasms / metabolism*
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Breast Neoplasms / pathology
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Cell Cycle Proteins
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Drug Resistance, Neoplasm
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Epigenesis, Genetic
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Female
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Histone-Lysine N-Methyltransferase / metabolism
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Histones / metabolism
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Humans
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Nuclear Proteins / antagonists & inhibitors
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Nuclear Proteins / metabolism
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Protein Serine-Threonine Kinases / antagonists & inhibitors
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Protein Serine-Threonine Kinases / metabolism
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RNA-Binding Proteins / antagonists & inhibitors
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RNA-Binding Proteins / metabolism
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Receptors, Estrogen / metabolism*
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Repressor Proteins / metabolism
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Tamoxifen / therapeutic use
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Transcription Factors / antagonists & inhibitors
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Transcription Factors / metabolism
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Triazoles / therapeutic use
Substances
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(+)-JQ1 compound
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Azepines
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BRD2 protein, human
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BRD3 protein, human
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BRD4 protein, human
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Cell Cycle Proteins
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Histones
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Nuclear Proteins
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RNA-Binding Proteins
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Receptors, Estrogen
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Repressor Proteins
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Transcription Factors
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Triazoles
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Tamoxifen
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Benzodiazepines
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molibresib
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Histone-Lysine N-Methyltransferase
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NSD2 protein, human
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Protein Serine-Threonine Kinases