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@ARTICLE{Giachino:126585,
      author       = {C. Giachino and J.-L. Boulay and R. Ivanek and A. Alvarado
                      and C. Tostado and S. Lugert and J. Tchorz and M. Coban and
                      L. Mariani and B. Bettler and J. Lathia and S. Frank and S.
                      Pfister$^*$ and M. Kool$^*$ and V. Taylor},
      title        = {{A} {T}umor {S}uppressor {F}unction for {N}otch {S}ignaling
                      in {F}orebrain {T}umor {S}ubtypes.},
      journal      = {Cancer cell},
      volume       = {28},
      number       = {6},
      issn         = {1535-6108},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2017-02613},
      pages        = {730 - 742},
      year         = {2015},
      abstract     = {In the brain, Notch signaling maintains normal neural stem
                      cells, but also brain cancer stem cells, indicating an
                      oncogenic role. Here, we identify an unexpected tumor
                      suppressor function for Notch in forebrain tumor subtypes.
                      Genetic inactivation of RBP-Jκ, a key Notch mediator, or
                      Notch1 and Notch2 receptors accelerates PDGF-driven glioma
                      growth in mice. Conversely, genetic activation of the Notch
                      pathway reduces glioma growth and increases survival. In
                      humans, high Notch activity strongly correlates with
                      distinct glioma subtypes, increased patient survival, and
                      lower tumor grade. Additionally, simultaneous inactivation
                      of RBP-Jκ and p53 induces primitive neuroectodermal-like
                      tumors in mice. Hence, Notch signaling cooperates with p53
                      to restrict cell proliferation and tumor growth in mouse
                      models of human brain tumors.},
      keywords     = {Basic Helix-Loop-Helix Transcription Factors (NLM
                      Chemicals) / Hes5 protein, mouse (NLM Chemicals) /
                      Immunoglobulin J Recombination Signal Sequence-Binding
                      Protein (NLM Chemicals) / Notch1 protein, mouse (NLM
                      Chemicals) / Notch2 protein, mouse (NLM Chemicals) /
                      Platelet-Derived Growth Factor (NLM Chemicals) /
                      Proto-Oncogene Proteins c-sis (NLM Chemicals) / Rbpj
                      protein, mouse (NLM Chemicals) / Receptor, Notch1 (NLM
                      Chemicals) / Receptor, Notch2 (NLM Chemicals) / Receptors,
                      Notch (NLM Chemicals) / Recombinant Proteins (NLM Chemicals)
                      / Repressor Proteins (NLM Chemicals) / Tumor Suppressor
                      Protein p53 (NLM Chemicals) / Tumor Suppressor Proteins (NLM
                      Chemicals) / platelet-derived growth factor A (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:26669487},
      doi          = {10.1016/j.ccell.2015.10.008},
      url          = {https://inrepo02.dkfz.de/record/126585},
}