| Literature DB >> 23377182 |
Miriam J Smith1, James O'Sullivan, Sanjeev S Bhaskar, Kristen D Hadfield, Gemma Poke, John Caird, Saba Sharif, Diana Eccles, David Fitzpatrick, Daniel Rawluk, Daniel du Plessis, William G Newman, D Gareth Evans.
Abstract
One-third of all primary central nervous system tumors in adults are meningiomas. Rarely, meningiomas occur at multiple sites, usually occurring in individuals with type 2 neurofibromatosis (NF2). We sequenced the exomes of three unrelated individuals with familial multiple spinal meningiomas without NF2 mutations. We identified two individuals with heterozygous loss-of-function mutations in the SWI/SNF chromatin-remodeling complex subunit gene SMARCE1. Sequencing of SMARCE1 in six further individuals with spinal meningiomas identified two additional heterozygous loss-of-function mutations. Tumors from individuals with SMARCE1 mutations were of clear-cell histological subtype, and all had loss of SMARCE1 protein, consistent with a tumor suppressor mechanism. Our findings identify multiple-spinal-meningioma disease as a new discrete entity and establish a key role for the SWI/SNF complex in the pathogenesis of both meningiomas and tumors with clear-cell histology.Entities:
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Year: 2013 PMID: 23377182 DOI: 10.1038/ng.2552
Source DB: PubMed Journal: Nat Genet ISSN: 1061-4036 Impact factor: 38.330