Abstract：
:Cancer genome sequencing efforts have revealed the novel theme that chromatin modifiers are frequently mutated across a wide spectrum of cancers. Mutations in genes encoding subunits of SWI/SNF (BAF) chromatin remodeling complexes are particularly prevalent, occurring in 20% of all human cancers. As these are typically loss-of-function mutations and not directly therapeutically targetable, central goals have been to elucidate mechanism and identify vulnerabilities created by these mutations. Here, we discuss emerging data that these mutations lead to the formation of aberrant residual SWI/SNF complexes that constitute a specific vulnerability and discuss the potential for exploiting these dependencies in SWI/SNF mutant cancers.
journal_name
Cancer Celljournal_title
Cancer cellauthors
Helming KC,Wang X,Roberts CWMdoi
10.1016/j.ccr.2014.07.018subject
Has Abstractpub_date
2014-09-08 00:00:00pages
309-317issue
3eissn
1535-6108issn
1878-3686pii
S1535-6108(14)00307-9journal_volume
26pub_type
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