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@ARTICLE{Pei:130304,
      author       = {Y. Pei and K.-W. Liu and J. Wang and A. Garancher and R.
                      Tao and L. A. Esparza and D. L. Maier and Y. T. Udaka and N.
                      Murad and S. Morrissy and H. Seker-Cin$^*$ and S.
                      Brabetz$^*$ and L. Qi and M. Kogiso and S. Schubert and J.
                      M. Olson and Y.-J. Cho and X.-N. Li and J. R. Crawford and
                      M. L. Levy and M. Kool$^*$ and S. Pfister$^*$ and M. D.
                      Taylor and R. J. Wechsler-Reya},
      title        = {{HDAC} and {PI}3{K} {A}ntagonists {C}ooperate to {I}nhibit
                      {G}rowth of {MYC}-{D}riven {M}edulloblastoma.},
      journal      = {Cancer cell},
      volume       = {29},
      number       = {3},
      issn         = {1535-6108},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2017-05383},
      pages        = {311 - 323},
      year         = {2016},
      abstract     = {Medulloblastoma (MB) is a highly malignant pediatric brain
                      tumor. Despite aggressive therapy, many patients succumb to
                      the disease, and survivors experience severe side effects
                      from treatment. MYC-driven MB has a particularly poor
                      prognosis and would greatly benefit from more effective
                      therapies. We used an animal model of MYC-driven MB to
                      screen for drugs that decrease viability of tumor cells.
                      Among the most effective compounds were histone deacetylase
                      inhibitors (HDACIs). HDACIs potently inhibit survival of
                      MYC-driven MB cells in vitro, in part by inducing expression
                      of the FOXO1 tumor suppressor gene. HDACIs also synergize
                      with phosphatidylinositol 3-kinase inhibitors to inhibit
                      tumor growth in vivo. These studies identify an effective
                      combination therapy for the most aggressive form of MB.},
      keywords     = {Forkhead Transcription Factors (NLM Chemicals) / Histone
                      Deacetylase Inhibitors (NLM Chemicals) / Proto-Oncogene
                      Proteins c-myc (NLM Chemicals) / Phosphatidylinositol
                      3-Kinases (NLM Chemicals) / Histone Deacetylases (NLM
                      Chemicals)},
      cin          = {B062 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26977882},
      pmc          = {pmc:PMC4794752},
      doi          = {10.1016/j.ccell.2016.02.011},
      url          = {https://inrepo02.dkfz.de/record/130304},
}