期刊
CANCER CELL
卷 35, 期 1, 页码 95-+出版社
CELL PRESS
DOI: 10.1016/j.ccell.2018.11.014
关键词
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资金
- Heidelberg Center for Personalized Oncology (DKFZ-HIPO) through HIPO project [H049]
- long-term Human Frontiers Science Program (HFSP) postdoctoral fellowship [LT000432/2014]
- German Cancer Aid [111537]
- DFG [HA 3060/5-1]
- IZKF Munster [Ha3/019/15]
- NCI [R01CA172152, R01CA113794, P30CA021765]
- INSTINCT network program grant
- Brain Tumour Charity
- Great Ormond Street Children's Charity
- Children with Cancer UK [16/193]
- ICGC DE-Mining grant [01KU1505G]
- NCI Comprehensive Cancer Center Support Grant [P30 CA021765]
Biallelic inactivation of SMARCB1, encoding amember 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.
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