Abstract
SWI/SNF chromatin remodelling complexes use the energy of ATP hydrolysis to remodel nucleosomes and to modulate transcription. Growing evidence indicates that these complexes have a widespread role in tumour suppression, as inactivating mutations in several SWI/SNF subunits have recently been identified at a high frequency in a variety of cancers. However, the mechanisms by which mutations in these complexes drive tumorigenesis are unclear. In this Review we discuss the contributions of SWI/SNF mutations to cancer formation, examine their normal functions and discuss opportunities for novel therapeutic interventions for SWI/SNF-mutant cancers.
MeSH terms
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Animals
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Chromatin Assembly and Disassembly*
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Chromosomal Proteins, Non-Histone / genetics
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Chromosomal Proteins, Non-Histone / physiology
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DNA Helicases / genetics
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DNA Helicases / physiology
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / physiology
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Humans
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Mutation
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Neoplasms / etiology*
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Neoplasms / genetics
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Nuclear Proteins / genetics
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Nuclear Proteins / physiology
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Nucleosomes / physiology*
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SMARCB1 Protein
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Transcription Factors / genetics
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Transcription Factors / physiology*
Substances
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ARID1A protein, human
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Chromosomal Proteins, Non-Histone
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DNA-Binding Proteins
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Nuclear Proteins
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Nucleosomes
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PBRM1 protein, human
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SMARCB1 Protein
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SMARCB1 protein, human
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Transcription Factors
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SMARCA4 protein, human
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DNA Helicases