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@ARTICLE{Lin:129056,
      author       = {C. Y. Lin and S. Erkek$^*$ and Y. Tong$^*$ and L. Yin and
                      A. J. Federation and M. Zapatka$^*$ and P. Haldipur and D.
                      Kawauchi$^*$ and T. Risch and H.-J. Warnatz and B. Worst$^*$
                      and B. Ju and B. A. Orr and R. Zeid and D. R. Polaski and M.
                      Segura-Wang and S. M. Waszak and D. Jones$^*$ and M.
                      Kool$^*$ and V. Hovestadt$^*$ and I. Buchhalter$^*$ and L.
                      Sieber$^*$ and P. Johann$^*$ and L. Chavez$^*$ and S.
                      Gröschel$^*$ and M. Ryzhova and A. Korshunov$^*$ and W.
                      Chen and V. V. Chizhikov and K. J. Millen and V.
                      Amstislavskiy and H. Lehrach and M.-L. Yaspo and R. Eils$^*$
                      and P. Lichter$^*$ and J. O. Korbel and S. Pfister$^*$ and
                      J. E. Bradner and P. A. Northcott$^*$},
      title        = {{A}ctive medulloblastoma enhancers reveal subgroup-specific
                      cellular origins.},
      journal      = {Nature},
      volume       = {530},
      number       = {7588},
      issn         = {1476-4687},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2017-05061},
      pages        = {57 - 62},
      year         = {2016},
      abstract     = {Medulloblastoma is a highly malignant paediatric brain
                      tumour, often inflicting devastating consequences on the
                      developing child. Genomic studies have revealed four
                      distinct molecular subgroups with divergent biology and
                      clinical behaviour. An understanding of the regulatory
                      circuitry governing the transcriptional landscapes of
                      medulloblastoma subgroups, and how this relates to their
                      respective developmental origins, is lacking. Here, using
                      H3K27ac and BRD4 chromatin immunoprecipitation followed by
                      sequencing (ChIP-seq) coupled with tissue-matched DNA
                      methylation and transcriptome data, we describe the active
                      cis-regulatory landscape across 28 primary medulloblastoma
                      specimens. Analysis of differentially regulated enhancers
                      and super-enhancers reinforced inter-subgroup heterogeneity
                      and revealed novel, clinically relevant insights into
                      medulloblastoma biology. Computational reconstruction of
                      core regulatory circuitry identified a master set of
                      transcription factors, validated by ChIP-seq, that is
                      responsible for subgroup divergence, and implicates
                      candidate cells of origin for Group 4. Our integrated
                      analysis of enhancer elements in a large series of primary
                      tumour samples reveals insights into cis-regulatory
                      architecture, unrecognized dependencies, and cellular
                      origins.},
      keywords     = {Transcription Factors (NLM Chemicals)},
      cin          = {B062 / B060 / L101 / B080 / G100 / G240 / G380},
      ddc          = {070},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)B060-20160331 /
                      I:(DE-He78)L101-20160331 / I:(DE-He78)B080-20160331 /
                      I:(DE-He78)G100-20160331 / I:(DE-He78)G240-20160331 /
                      I:(DE-He78)G380-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26814967},
      pmc          = {pmc:PMC5168934},
      doi          = {10.1038/nature16546},
      url          = {https://inrepo02.dkfz.de/record/129056},
}