AI Article Synopsis
- Cancer genome sequencing has uncovered that chromatin modifiers, especially SWI/SNF (BAF) complexes, are often mutated in many cancer types, affecting about 20% of human cancers.
- These mutations are mostly loss-of-function, which makes them hard to target directly in treatment, prompting researchers to explore the mechanisms behind these mutations and their effects.
- New findings suggest that these mutations create abnormal SWI/SNF complexes, presenting potential vulnerabilities that could be used for developing targeted therapies in cancers with these specific mutations.
Article 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.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159614 | PMC |
| http://dx.doi.org/10.1016/j.ccr.2014.07.018 | DOI Listing |
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