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@ARTICLE{Batora:119621,
      author       = {N. Batora$^*$ and D. Sturm$^*$ and D. Jones$^*$ and M.
                      Kool$^*$ and S. Pfister$^*$ and P. A. Northcott$^*$},
      title        = {{T}ransitioning from genotypes to epigenotypes: why the
                      time has come for medulloblastoma epigenomics.},
      journal      = {Neuroscience},
      volume       = {264},
      issn         = {0306-4522},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DKFZ-2017-00252},
      pages        = {171 - 185},
      year         = {2014},
      abstract     = {Recent advances in genomic technologies have allowed for
                      tremendous progress in our understanding of the biology
                      underlying medulloblastoma, a malignant childhood brain
                      tumor. Consensus molecular subgroups have been put forth by
                      the pediatric neuro-oncology community and next-generation
                      genomic studies have led to an improved description of
                      driver genes and pathways somatically altered in these
                      subgroups. In contrast to the impressive pace at which
                      advances have been made at the level of the medulloblastoma
                      genome, comparable studies of the epigenome have lagged
                      behind. Complementary data yielded from genomic sequencing
                      and copy number profiling have verified frequent targeting
                      of chromatin modifiers in medulloblastoma, highly suggestive
                      of prominent epigenetic deregulation in the disease. Past
                      studies of DNA methylation-dependent gene silencing and
                      microRNA expression analyses further support the concept of
                      medulloblastoma as an epigenetic disease. In this Review, we
                      aim to summarize the key findings of past reports pertaining
                      to medulloblastoma epigenetics as well as recent and ongoing
                      genomic efforts linking somatic alterations of the genome
                      with inferred deregulation of the epigenome. In addition, we
                      predict what is on the horizon for medulloblastoma
                      epigenetics and how aberrant changes in the medulloblastoma
                      epigenome might serve as an attractive target for future
                      therapies.},
      subtyp        = {Review Article},
      cin          = {B062},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:23876321},
      doi          = {10.1016/j.neuroscience.2013.07.030},
      url          = {https://inrepo02.dkfz.de/record/119621},
}