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@ARTICLE{Wiese:130935,
      author       = {M. Wiese and F. Schill and D. Sturm$^*$ and S. Pfister$^*$
                      and E. Hulleman and S. A. Johnsen and C. M. Kramm},
      title        = {{N}o {S}ignificant {C}ytotoxic {E}ffect of the {EZH}2
                      {I}nhibitor {T}azemetostat ({EPZ}-6438) on {P}ediatric
                      {G}lioma {C}ells with {W}ildtype {H}istone 3 or {M}utated
                      {H}istone 3.3.},
      journal      = {Klinische Pädiatrie},
      volume       = {228},
      number       = {3},
      issn         = {1439-3824},
      address      = {Stuttgart},
      publisher    = {Thieme},
      reportid     = {DKFZ-2017-06011},
      pages        = {113 - 117},
      year         = {2016},
      abstract     = {Glioblastoma multiforme (GBM) and diffuse intrinsic pontine
                      glioma (DIPG) belong to the most aggressive cancers in
                      children with poor prognosis and limited therapeutic
                      options. Therapeutic targeting of epigenetic proteins may
                      offer new treatment options. Preclinical studies identified
                      Enhancer of Zeste Homolog 2 (EZH2) within polycomb repressor
                      complex 2 (PRC2) as a potential epigenetic anti-tumor target
                      in adult GBM cells but similar inhibition studies in
                      pediatric GBM/DIPG were still missing. Moreover,
                      approximately $30\%$ of pediatric high grade gliomas
                      (pedHGG) including GBM and DIPG harbor a lysine 27 mutation
                      (K27M) in histone 3.3 (H3.3) which is correlated with poor
                      outcome and was shown to influence EZH2 function.The present
                      study investigated the correlation of expression of EZH2 and
                      other PRC2 genes (EZH1, SUZ12, EED) with overall survival of
                      pediatric GBM patients and the cytotoxic impact of EZH2
                      inhibition by the novel agent Tazemetostat in pediatric
                      GBM/DIPG cells harboring either a H3.3 mutation or a H3
                      wildtype.EZH2 gene expression does not correlate with
                      survival of pedHGG patients, and EZH2 inhibition does not
                      induce significant cytotoxicity in pedHGG cells
                      independently of H3.3 mutations.We suggest that EZH2
                      inhibition might not offer an effective single agent
                      treatment option for paedHGG patients. However, the
                      therapeutic efficacy in combination with cytotoxic and/or
                      other epigenetically active agents still has to be
                      elucidated.},
      keywords     = {Benzamides (NLM Chemicals) / EPZ-6438 (NLM Chemicals) /
                      Histones (NLM Chemicals) / Pyridones (NLM Chemicals) / EZH2
                      protein, human (NLM Chemicals) / Enhancer of Zeste Homolog 2
                      Protein (NLM Chemicals)},
      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:27135271},
      doi          = {10.1055/s-0042-105292},
      url          = {https://inrepo02.dkfz.de/record/130935},
}