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      SMARCA4 and SMARCA2 deficiency in non–small cell lung cancer: immunohistochemical survey of 316 consecutive specimens

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          The Spectrum of SWI/SNF Mutations, Ubiquitous in Human Cancers

          A Shain, Jonathan R. Pollack (2013)
          SWI/SNF is a multi-subunit chromatin remodeling complex that uses the energy of ATP hydrolysis to reposition nucleosomes, thereby modulating gene expression. Accumulating evidence suggests that SWI/SNF functions as a tumor suppressor in some cancers. However, the spectrum of SWI/SNF mutations across human cancers has not been systematically investigated. Here, we mined whole-exome sequencing data from 24 published studies representing 669 cases from 18 neoplastic diagnoses. SWI/SNF mutations were widespread across diverse human cancers, with an excess of deleterious mutations, and an overall frequency approaching TP53 mutation. Mutations occurred most commonly in the SMARCA4 enzymatic subunit, and in subunits thought to confer functional specificity (ARID1A, ARID1B, PBRM1, and ARID2). SWI/SNF mutations were not mutually-exclusive of other mutated cancer genes, including TP53 and EZH2 (both previously linked to SWI/SNF). Our findings implicate SWI/SNF as an important but under-recognized tumor suppressor in diverse human cancers, and provide a key resource to guide future investigations.
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            Recurrent SMARCA4 mutations in small cell carcinoma of the ovary.

            Petar Jelinic, Jennifer J Mueller, Narciso Olvera … (2014)
            Small cell carcinoma of the ovary, hypercalcemic type (SCCOHT) is a rare, highly aggressive form of ovarian cancer primarily diagnosed in young women. We identified inactivating biallelic SMARCA4 mutations in 100% of the 12 SCCOHT tumors examined. Protein studies confirmed loss of SMARCA4 expression, suggesting a key role for the SWI/SNF chromatin-remodeling complex in SCCOHT.
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              Molecular pathways: SWI/SNF (BAF) complexes are frequently mutated in cancer--mechanisms and potential therapeutic insights.

              Xiaofeng Wang, Jeffrey R Haswell, Charles Roberts (2014)
              SWI/SNF chromatin remodeling complexes are pleomorphic multisubunit cellular machines that utilize the energy of ATP hydrolysis to modulate chromatin structure. The complexes interact with transcription factors at promoters and enhancers to modulate gene expression and contribute to lineage specification, differentiation, and development. Initial clues to a role in tumor suppression for SWI/SNF complexes came over a decade ago when the gene encoding the SMARCB1/SNF5 core subunit was found specifically inactivated in nearly all pediatric rhabdoid tumors. In the last three years, cancer-genome sequencing efforts have revealed an unexpectedly high mutation rate of SWI/SNF subunit genes, which are collectively mutated in 20% of all human cancers and approach the frequency of p53 mutations. Here, we provide a background on these newly recognized tumor suppressor complexes, discuss mechanisms implicated in the tumor suppressor activity, and highlight findings that may lead to potential therapeutic targets for SWI/SNF-mutant cancers.
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                Author and article information

                Journal
                Title: Annals of Diagnostic Pathology
                Abbreviated Title: Annals of Diagnostic Pathology
                Publisher: Elsevier BV
                ISSN (Print): 10929134
                Publication date Created: February 2017
                Publication date (Print): February 2017
                Volume: 26
                Issue:
                Pages: 47-51
                Article
                DOI: 10.1016/j.anndiagpath.2016.10.006
                PubMed ID: 28038711
                SO-VID: 880b552d-755b-4155-b86b-ed5139e14dba
                Copyright © © 2017
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