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@ARTICLE{Erkek:142866,
      author       = {S. Erkek$^*$ and P. Johann$^*$ and M. A. Finetti and Y.
                      Drosos and H.-C. Chou and M. Zapatka$^*$ and D. Sturm$^*$
                      and D. Jones$^*$ and A. Korshunov$^*$ and M. Rhyzova and S.
                      Wolf$^*$ and J.-P. Mallm$^*$ and K. Beck$^*$ and O. Witt$^*$
                      and A. E. Kulozik and M. C. Frühwald and P. A. Northcott
                      and J. O. Korbel and P. Lichter$^*$ and R. Eils$^*$ and A.
                      Gajjar and C. W. M. Roberts and D. Williamson and M.
                      Hasselblatt and L. Chavez$^*$ and S. Pfister$^*$ and M.
                      Kool$^*$},
      title        = {{C}omprehensive {A}nalysis of {C}hromatin {S}tates in
                      {A}typical {T}eratoid/{R}habdoid {T}umor {I}dentifies
                      {D}iverging {R}oles for {SWI}/{SNF} and {P}olycomb in {G}ene
                      {R}egulation.},
      journal      = {Cancer cell},
      volume       = {35},
      number       = {1},
      issn         = {1535-6108},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2019-00496},
      pages        = {95 - 110.e8},
      year         = {2019},
      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.},
      cin          = {B062 / B060 / B360 / B300 / W190 / B310 / B080 / B066 /
                      L101},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)B060-20160331 /
                      I:(DE-He78)B360-20160331 / I:(DE-He78)B300-20160331 /
                      I:(DE-He78)W190-20160331 / I:(DE-He78)B310-20160331 /
                      I:(DE-He78)B080-20160331 / I:(DE-He78)B066-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30595504},
      pmc          = {pmc:PMC6341227},
      doi          = {10.1016/j.ccell.2018.11.014},
      url          = {https://inrepo02.dkfz.de/record/142866},
}