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10.1016/j.gde.2017.02.004

http://scihub22266oqcxt.onion/10.1016/j.gde.2017.02.004
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pmid28391084
      Curr+Opin+Genet+Dev 2017 ; 42 (ä): 56-67
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  • Mammalian SWI/SNF complexes in cancer: emerging therapeutic opportunities #MMPMID28391084
  • St Pierre R ; Kadoch C
  • Curr Opin Genet Dev 2017[Feb]; 42 (ä): 56-67 PMID28391084 show ga
  • 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.
  • |Animals [MESH]
  • |Chromosomal Proteins, Non-Histone/antagonists & inhibitors/*genetics [MESH]
  • |Humans [MESH]
  • |Mammals [MESH]
  • |Mutation [MESH]
  • |Neoplasms/*genetics/therapy [MESH]


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