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@ARTICLE{Herrlinger:128762,
      author       = {U. Herrlinger and D. Jones$^*$ and M. Glas and E. Hattingen
                      and D. Gramatzki and M. Stuplich and J. Felsberg and O.
                      Bähr and G. H. Gielen and M. Simon and D. Wiewrodt and M.
                      Schabet and V. Hovestadt$^*$ and D. Capper$^*$ and J. P.
                      Steinbach and A. von Deimling$^*$ and P. Lichter$^*$ and S.
                      Pfister$^*$ and M. Weller and G. Reifenberger$^*$},
      title        = {{G}liomatosis cerebri: no evidence for a separate brain
                      tumor entity.},
      journal      = {Acta neuropathologica},
      volume       = {131},
      number       = {2},
      issn         = {1432-0533},
      address      = {Berlin},
      publisher    = {Springer},
      reportid     = {DKFZ-2017-04777},
      pages        = {309 - 319},
      year         = {2016},
      abstract     = {Gliomatosis cerebri (GC) is presently considered a distinct
                      astrocytic glioma entity according to the WHO classification
                      for CNS tumors. It is characterized by widespread, typically
                      bilateral infiltration of the brain involving three or more
                      lobes. Genetic studies of GC have to date been restricted to
                      the analysis of individual glioma-associated genes, which
                      revealed mutations in the isocitrate dehydrogenase 1 (IDH1)
                      and tumor protein p53 (TP53) genes in subsets of patients.
                      Here, we report on a genome-wide analysis of DNA methylation
                      and copy number aberrations in 25 GC patients. Results were
                      compared with those obtained for 105 patients with various
                      types of conventional, i.e., non-GC gliomas including
                      diffuse astrocytic gliomas, oligodendrogliomas and
                      glioblastomas. In addition, we assessed the prognostic role
                      of methylation profiles and recurrent DNA copy number
                      aberrations in GC patients. Our data reveal that the
                      methylation profiles in 23 of the 25 GC tumors corresponded
                      to either IDH mutant astrocytoma (n = 6), IDH mutant and
                      1p/19q codeleted oligodendroglioma (n = 5), or IDH
                      wild-type glioblastoma including various molecular
                      subgroups, i.e., H3F3A-G34 mutant (n = 1), receptor
                      tyrosine kinase 1 (RTK1, n = 4), receptor tyrosine kinase
                      2 (classic) (RTK2, n = 2) or mesenchymal (n = 5)
                      glioblastoma groups. Two tumors showed methylation profiles
                      of normal brain tissue due to low tumor cell content. While
                      histological grading (WHO grade IV vs. WHO grade II and III)
                      was not prognostic, the molecular classification as
                      classic/RTK2 or mesenchymal glioblastoma was associated with
                      worse overall survival. Multivariate Cox regression analysis
                      revealed MGMT promoter methylation as a positive prognostic
                      factor. Taken together, DNA-based large-scale molecular
                      profiling indicates that GC comprises a genetically and
                      epigenetically heterogeneous group of diffuse gliomas that
                      carry DNA methylation and copy number profiles closely
                      matching the common molecularly defined glioma entities.
                      These data support the removal of GC as a distinct glioma
                      entity in the upcoming revision of the WHO classification.},
      keywords     = {Tumor Suppressor Proteins (NLM Chemicals) / Isocitrate
                      Dehydrogenase (NLM Chemicals) / IDH1 protein, human (NLM
                      Chemicals) / DNA Modification Methylases (NLM Chemicals) /
                      MGMT protein, human (NLM Chemicals) / DNA Repair Enzymes
                      (NLM Chemicals)},
      cin          = {L401 / L101 / L501 / B062 / B060 / G380},
      ddc          = {610},
      cid          = {I:(DE-He78)L401-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)L501-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)B060-20160331 / I:(DE-He78)G380-20160331},
      pnm          = {319H - Addenda (POF3-319H)},
      pid          = {G:(DE-HGF)POF3-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26493382},
      doi          = {10.1007/s00401-015-1495-z},
      url          = {https://inrepo02.dkfz.de/record/128762},
}