| Literature DB >> 30595504 |
Serap Erkek1, Pascal D Johann2, Martina A Finetti3, Yiannis Drosos4, Hsien-Chao Chou4, Marc Zapatka5, Dominik Sturm2, David T W Jones6, Andrey Korshunov7, Marina Rhyzova8, Stephan Wolf9, Jan-Philipp Mallm10, Katja Beck11, Olaf Witt12, Andreas E Kulozik13, Michael C Frühwald14, Paul A Northcott15, Jan O Korbel16, Peter Lichter17, Roland Eils18, Amar Gajjar4, Charles W M Roberts4, Daniel Williamson3, Martin Hasselblatt19, Lukas Chavez6, Stefan M Pfister2, Marcel Kool20.
Abstract
Biallelic inactivation of SMARCB1, encoding a member of the SWI/SNF chromatin remodeling complex, is the hallmark genetic aberration of atypical teratoid rhabdoid tumors (ATRT). Here, we report how loss of SMARCB1 affects the epigenome in these tumors. Using chromatin immunoprecipitation sequencing (ChIP-seq) on primary tumors for a series of active and repressive histone marks, we identified the chromatin states differentially represented in ATRTs compared with other brain tumors and non-neoplastic brain. Re-expression of SMARCB1 in ATRT cell lines enabled confirmation of our genome-wide findings for the chromatin states. Additional generation of ChIP-seq data for SWI/SNF and Polycomb group proteins and the transcriptional repressor protein REST determined differential dependencies of SWI/SNF and Polycomb complexes in regulation of diverse gene sets in ATRTs.Entities:
Keywords: EZH2; SMARCA4; SMARCB1; atypical teratoid rhabdoid tumor; chromatin states; pediatric brain tumor
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Year: 2018 PMID： 30595504 PMCID： PMC6341227 DOI： 10.1016/j.ccell.2018.11.014
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743