% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Orth:186218,
      author       = {M. F. Orth and D. Surdez and T. Faehling$^*$ and A.
                      Ehlers$^*$ and A. Marchetto and S. Grossetête and R.
                      Volckmann and D. A. Zwijnenburg and J. S. Gerke and S. Zaidi
                      and J. Alonso and A. Sastre and S. Baulande and M. Sill$^*$
                      and F. Cidre-Aranaz$^*$ and S. Ohmura$^*$ and T.
                      Kirchner$^*$ and S. M. Hauck and E. Reischl and M. Gymrek
                      and S. Pfister$^*$ and K. Strauch and J. Koster and O.
                      Delattre and T. Grünewald$^*$},
      title        = {{S}ystematic multi-omics cell line profiling uncovers
                      principles of {E}wing sarcoma fusion oncogene-mediated gene
                      regulation.},
      journal      = {Cell reports},
      volume       = {41},
      number       = {10},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2022-03015},
      pages        = {111761},
      year         = {2022},
      note         = {#LA:B410#},
      abstract     = {Ewing sarcoma (EwS) is characterized by EWSR1-ETS fusion
                      transcription factors converting polymorphic GGAA
                      microsatellites (mSats) into potent neo-enhancers. Although
                      the paucity of additional mutations makes EwS a genuine
                      model to study principles of cooperation between dominant
                      fusion oncogenes and neo-enhancers, this is impeded by the
                      limited number of well-characterized models. Here we present
                      the Ewing Sarcoma Cell Line Atlas (ESCLA), comprising
                      whole-genome, DNA methylation, transcriptome, proteome, and
                      chromatin immunoprecipitation sequencing (ChIP-seq) data of
                      18 cell lines with inducible EWSR1-ETS knockdown. The ESCLA
                      shows hundreds of EWSR1-ETS-targets, the nature of
                      EWSR1-ETS-preferred GGAA mSats, and putative indirect modes
                      of EWSR1-ETS-mediated gene regulation, converging in the
                      duality of a specific but plastic EwS signature. We identify
                      heterogeneously regulated EWSR1-ETS-targets as potential
                      prognostic EwS biomarkers. Our freely available ESCLA
                      (http://r2platform.com/escla/) is a rich resource for EwS
                      research and highlights the power of comprehensive datasets
                      to unravel principles of heterogeneous gene regulation by
                      chimeric transcription factors.},
      keywords     = {CP: Cancer (Other) / ChiP-seq (Other) / EWSR1-ERG (Other) /
                      EWSR1-ETS (Other) / EWSR1-FLI1 (Other) / Ewing sarcoma
                      (Other) / enhancer (Other) / microsatellites (Other) /
                      multi-omics (Other) / pediatric sarcoma (Other) / tumor
                      heterogeneity (Other)},
      cin          = {B410 / HD01 / B062 / MU01},
      ddc          = {610},
      cid          = {I:(DE-He78)B410-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)B062-20160331 / I:(DE-He78)MU01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36476851},
      doi          = {10.1016/j.celrep.2022.111761},
      url          = {https://inrepo02.dkfz.de/record/186218},
}