Abstract
Many hormones exert their effects through specific nuclear receptors which belong to a superfamily of ligand-activated transcription factors. These receptors control target gene expression through the recruitment of different cofactors acting as transcription activation or repression mediators, generally as parts of multiprotein complexes. The importance and the role in physiopathology of these different cofactors only begin to be defined. Different types of alterations affecting genes coding nuclear receptor transcription cofactors have indeed been described in cancer. The most important examples are gene amplification that leads to overexpression and gene mutations or translocations introducing qualitative modifications. This paper aims at bringing together the corresponding literature and focuses on gene alterations observed in solid tumors.
MeSH terms
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Breast Neoplasms / drug therapy
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Breast Neoplasms / genetics
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Chromosomal Proteins, Non-Histone
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Chromosome Aberrations*
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DNA Helicases
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DNA-Binding Proteins / genetics
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Drug Resistance, Neoplasm / genetics
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Estrogen Antagonists / therapeutic use
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Gene Amplification
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Genes, BRCA1
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Humans
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Neoplasms / genetics*
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Neoplasms / metabolism
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Nuclear Proteins / genetics
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Nuclear Receptor Coactivator 3
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Receptors, Cytoplasmic and Nuclear / genetics*
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SMARCB1 Protein
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Terminology as Topic
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Trans-Activators / genetics
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Transcription Factors / genetics*
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Transcription, Genetic*
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Transcriptional Activation
Substances
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Chromosomal Proteins, Non-Histone
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DNA-Binding Proteins
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Estrogen Antagonists
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Nuclear Proteins
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Receptors, Cytoplasmic and Nuclear
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SMARCB1 Protein
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SMARCB1 protein, human
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Trans-Activators
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Transcription Factors
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Nuclear Receptor Coactivator 3
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SMARCA4 protein, human
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DNA Helicases