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@ARTICLE{Reuss:127371,
      author       = {D. E. Reuss$^*$ and A. Kratz$^*$ and F. Sahm$^*$ and D.
                      Capper$^*$ and D. Schrimpf$^*$ and C. Koelsche$^*$ and V.
                      Hovestadt$^*$ and M. Bewerunge-Hudler$^*$ and D. Jones$^*$
                      and J. Schittenhelm and M. Mittelbronn$^*$ and E. Rushing
                      and M. Simon and M. Westphal and A. Unterberg and M.
                      Platten$^*$ and W. Paulus and G. Reifenberger$^*$ and J.-C.
                      Tonn and K. Aldape and S. Pfister$^*$ and A. Korshunov$^*$
                      and M. Weller and C. Herold-Mende and W. Wick$^*$ and S.
                      Brandner and A. von Deimling$^*$},
      title        = {{A}dult {IDH} wild type astrocytomas biologically and
                      clinically resolve into other tumor entities.},
      journal      = {Acta neuropathologica},
      volume       = {130},
      number       = {3},
      issn         = {1432-0533},
      address      = {Berlin},
      publisher    = {Springer},
      reportid     = {DKFZ-2017-03396},
      pages        = {407 - 417},
      year         = {2015},
      abstract     = {IDH wild type (IDHwt) anaplastic astrocytomas WHO grade III
                      (AA III) are associated with poor outcome. To address the
                      possibilities of molecular subsets among astrocytoma or of
                      diagnostic reclassification, we analyzed a series of 160
                      adult IDHwt tumors comprising 120 AA III and 40 diffuse
                      astrocytomas WHO grade II (A II) for molecular hallmark
                      alterations and established methylation and copy number
                      profiles. Based on molecular profiles and hallmark
                      alterations the tumors could be grouped into four major
                      sets. 124/160 $(78 \%)$ tumors were diagnosed as the
                      molecular equivalent of conventional glioblastoma (GBM), and
                      15/160 $(9 \%)$ as GBM-H3F3A mutated (GBM-H3). 13/160
                      $(8 \%)$ exhibited a distinct methylation profile that was
                      most similar to GBM-H3-K27, however, lacked the H3F3A
                      mutation. This group was enriched for tumors of
                      infratentorial and midline localization and showed a trend
                      towards a more favorable prognosis. All but one of the 120
                      IDHwt AA III could be assigned to these three groups. 7
                      tumors recruited from the 40 A II, comprised a variety of
                      molecular signatures and all but one were reclassified into
                      distinct WHO entities of lower grades. Interestingly, TERT
                      mutations were exclusively restricted to the molecular GBM
                      $(78 \%)$ and associated with poor clinical outcome.
                      However, the GBM-H3 group lacking TERT mutations appeared to
                      fare even worse. Our data demonstrate that most of the
                      tumors diagnosed as IDHwt astrocytomas can be allocated to
                      other tumor entities on a molecular basis. The diagnosis of
                      IDHwt diffuse astrocytoma or anaplastic astrocytoma should
                      be used with caution.},
      keywords     = {Biomarkers, Tumor (NLM Chemicals) / Isocitrate
                      Dehydrogenase (NLM Chemicals) / isocitrate dehydrogenase 2,
                      human (NLM Chemicals) / IDH1 protein, human (NLM Chemicals)
                      / TERT protein, human (NLM Chemicals) / Telomerase (NLM
                      Chemicals)},
      cin          = {G380 / B060 / W110 / B062 / G160 / G370 / L101 / L401 /
                      L701 / L501 / L801},
      ddc          = {610},
      cid          = {I:(DE-He78)G380-20160331 / I:(DE-He78)B060-20160331 /
                      I:(DE-He78)W110-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)G160-20160331 / I:(DE-He78)G370-20160331 /
                      I:(DE-He78)L101-20160331 / I:(DE-He78)L401-20160331 /
                      I:(DE-He78)L701-20160331 / I:(DE-He78)L501-20160331 /
                      I:(DE-He78)L801-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26087904},
      doi          = {10.1007/s00401-015-1454-8},
      url          = {https://inrepo02.dkfz.de/record/127371},
}