Mammalian SWI/SNF complexes in cancer: emerging therapeutic opportunities

Mammalian SWI/SNF (BAF) chromatin remodeling complexes orchestrate a diverse set of chromatin alterations which impact transcriptional output. Recent whole-exome sequencing efforts have revealed that the genes encoding subunits of mSWI/SNF complexes are mutated in over 20% of cancers, spanning a wid...

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Bibliographic Details
Published in:Current opinion in genetics & development 2017-02, Vol.42, p.56-67
Main Authors: St. Pierre, Roodolph, Kadoch, Cigall
Format: Article
Language:English
Subjects:
Animals
Chromosomal Proteins, Non-Histone - antagonists & inhibitors
Chromosomal Proteins, Non-Histone - genetics
Humans
Mammals
Medical Education
Mutation
Neoplasms - genetics
Neoplasms - therapy
Transcription Factors - antagonists & inhibitors
Transcription Factors - genetics
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Summary:Mammalian SWI/SNF (BAF) chromatin remodeling complexes orchestrate a diverse set of chromatin alterations which impact transcriptional output. Recent whole-exome sequencing efforts have revealed that the genes encoding subunits of mSWI/SNF complexes are mutated in over 20% of cancers, spanning a wide range of tissue types. The majority of mutations result in loss of subunit protein expression, implicating mSWI/SNF subunits as tumor suppressors. mSWI/SNF-deficient cancers remain a therapeutic challenge, owing to a lack of potent and selective agents which target complexes or unique pathway dependencies generated by mSWI/SNF subunit perturbations. Here, we review the current landscape of mechanistic insights and emerging therapeutic opportunities for human malignancies driven by mSWI/SNF complex perturbation.
ISSN:0959-437X
1879-0380
DOI:10.1016/j.gde.2017.02.004