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@ARTICLE{Gartlgruber:166292,
      author       = {M. Gartlgruber$^*$ and A. K. Sharma$^*$ and A. Quintero$^*$
                      and D. Dreidax$^*$ and S. Jansky$^*$ and Y.-G. Park$^*$ and
                      S. Kreth$^*$ and J. Meder and D. Doncevic$^*$ and P. Saary
                      and U. H. Toprak$^*$ and N. Ishaque and E. Afanasyeva$^*$
                      and E. Wecht$^*$ and J. Koster and R. Versteeg and T.
                      Grünewald$^*$ and D. T. W. Jones$^*$ and S. M. Pfister$^*$
                      and K.-O. Henrich$^*$ and J. van Nes and C. Herrmann and F.
                      Westermann$^*$},
      title        = {{S}uper enhancers define regulatory subtypes and cell
                      identity in neuroblastoma},
      journal      = {Nature cancer},
      volume       = {2},
      issn         = {2662-1347},
      address      = {London},
      publisher    = {Nature Research},
      reportid     = {DKFZ-2020-02785},
      pages        = {114–128},
      year         = {2021},
      note         = {#EA:B087#LA:B087# VOL 2 | JANUARy 2021 | 114–128},
      abstract     = {Half of the children diagnosed with neuroblastoma (NB) have
                      high-risk disease, disproportionately contributing to
                      overall childhood cancer-related deaths. In addition to
                      recurrent gene mutations, there is increasing evidence
                      supporting the role of epigenetic deregulation in disease
                      pathogenesis. Yet, comprehensive cis-regulatory network
                      descriptions from NB are lacking. Here, using genome-wide
                      H3K27ac profiles across 60 NBs, covering the different
                      clinical and molecular subtypes, we identified four major
                      super-enhancer-driven epigenetic subtypes and their
                      underlying master regulatory networks. Three of these
                      subtypes recapitulated known clinical groups; namely,
                      MYCN-amplified, MYCN non-amplified high-risk and MYCN
                      non-amplified low-risk NBs. The fourth subtype, exhibiting
                      mesenchymal characteristics, shared cellular identity with
                      multipotent Schwann cell precursors, was induced by RAS
                      activation and was enriched in relapsed disease. Notably,
                      CCND1, an essential gene in NB, was regulated by both
                      mesenchymal and adrenergic regulatory networks converging on
                      distinct super-enhancer modules. Overall, this study reveals
                      subtype-specific super-enhancer regulation in NBs.},
      cin          = {B087 / B410 / HD01 / B360 / B062},
      ddc          = {610},
      cid          = {I:(DE-He78)B087-20160331 / I:(DE-He78)B410-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)B360-20160331 /
                      I:(DE-He78)B062-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1038/s43018-020-00145-w},
      url          = {https://inrepo02.dkfz.de/record/166292},
}