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@ARTICLE{Faria:126496,
      author       = {C. C. Faria and B. J. Golbourn and A. M. Dubuc and M. Remke
                      and R. J. Diaz and S. Agnihotri and A. Luck and N. Sabha and
                      S. Olsen and X. Wu and L. Garzia and V. Ramaswamy$^*$ and S.
                      C. Mack and X. Wang and M. Leadley and D. Reynaud and L.
                      Ermini and M. Post and P. A. Northcott$^*$ and S.
                      Pfister$^*$ and S. E. Croul and M. Kool$^*$ and A.
                      Korshunov$^*$ and C. A. Smith and M. D. Taylor and J. T.
                      Rutka},
      title        = {{F}oretinib is effective therapy for metastatic sonic
                      hedgehog medulloblastoma.},
      journal      = {Cancer research},
      volume       = {75},
      number       = {1},
      issn         = {1538-7445},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2017-02525},
      pages        = {134 - 146},
      year         = {2015},
      abstract     = {Medulloblastoma is the most common malignant pediatric
                      brain tumor, with metastases present at diagnosis conferring
                      a poor prognosis. Mechanisms of dissemination are poorly
                      understood and metastatic lesions are genetically divergent
                      from the matched primary tumor. Effective and less toxic
                      therapies that target both compartments have yet to be
                      identified. Here, we report that the analysis of several
                      large nonoverlapping cohorts of patients with
                      medulloblastoma reveals MET kinase as a marker of sonic
                      hedgehog (SHH)-driven medulloblastoma. Immunohistochemical
                      analysis of phosphorylated, active MET kinase in an
                      independent patient cohort confirmed its correlation with
                      increased tumor relapse and poor survival, suggesting that
                      patients with SHH medulloblastoma may benefit from
                      MET-targeted therapy. In support of this hypothesis, we
                      found that the approved MET inhibitor foretinib could
                      suppress MET activation, decrease tumor cell proliferation,
                      and induce apoptosis in SHH medulloblastomas in vitro and in
                      vivo. Foretinib penetrated the blood-brain barrier and was
                      effective in both the primary and metastatic tumor
                      compartments. In established mouse xenograft or transgenic
                      models of metastatic SHH medulloblastoma, foretinib
                      administration reduced the growth of the primary tumor,
                      decreased the incidence of metastases, and increased host
                      survival. Taken together, our results provide a strong
                      rationale to clinically evaluate foretinib as an effective
                      therapy for patients with SHH-driven medulloblastoma.},
      keywords     = {Anilides (NLM Chemicals) / GSK 1363089 (NLM Chemicals) /
                      Hedgehog Proteins (NLM Chemicals) / Quinolines (NLM
                      Chemicals) / SHH protein, human (NLM Chemicals) /
                      Proto-Oncogene Proteins c-met (NLM Chemicals) / Receptor,
                      Platelet-Derived Growth Factor beta (NLM Chemicals)},
      cin          = {B062 / G380},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)G380-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25391241},
      doi          = {10.1158/0008-5472.CAN-13-3629},
      url          = {https://inrepo02.dkfz.de/record/126496},
}