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@ARTICLE{Kawauchi:128633,
      author       = {D. Kawauchi$^*$ and R. J. Ogg and L. Liu and D. J. H. Shih
                      and D. Finkelstein and B. L. Murphy and J. E. Rehg and A.
                      Korshunov$^*$ and C. Calabrese and F. Zindy and T. Phoenix
                      and Y. Kawaguchi and J. Gronych$^*$ and R. J. Gilbertson and
                      P. Lichter$^*$ and A. Gajjar and M. Kool$^*$ and P. A.
                      Northcott and S. Pfister$^*$ and M. F. Roussel},
      title        = {{N}ovel {MYC}-driven medulloblastoma models from multiple
                      embryonic cerebellar cells.},
      journal      = {Oncogene},
      volume       = {36},
      number       = {37},
      issn         = {1476-5594},
      address      = {Basingstoke},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2017-04649},
      pages        = {5231 - 5242},
      year         = {2017},
      abstract     = {Group3 medulloblastoma (MBG3) that predominantly occur in
                      young children are usually associated with MYC amplification
                      and/or overexpression, frequent metastasis and a dismal
                      prognosis. Physiologically relevant MBG3 models are
                      currently lacking, making inferences related to their
                      cellular origin thus far limited. Using in utero
                      electroporation, we here report that MBG3 mouse models can
                      be developed in situ from different multipotent embryonic
                      cerebellar progenitor cells via conditional expression of
                      Myc and loss of Trp53 function in several Cre driver mouse
                      lines. The Blbp-Cre driver that targets embryonic neural
                      progenitors induced tumors exhibiting a
                      large-cell/anaplastic histopathology adjacent to the fourth
                      ventricle, recapitulating human MBG3. Enforced co-expression
                      of luciferase together with Myc and a dominant-negative form
                      of Trp53 revealed that GABAergic neuronal progenitors as
                      well as cerebellar granule cells give rise to MBG3 with
                      their distinct growth kinetics. Cross-species gene
                      expression analysis revealed that these novel MBG3 models
                      shared molecular characteristics with human MBG3,
                      irrespective of their cellular origin. We here developed
                      MBG3 mouse models in their physiological environment and we
                      show that oncogenic insults drive this MB subgroup in
                      different cerebellar lineages rather than in a specific cell
                      of origin.},
      keywords     = {MYC protein, human (NLM Chemicals) / Myc protein, mouse
                      (NLM Chemicals) / Proto-Oncogene Proteins c-myc (NLM
                      Chemicals)},
      cin          = {B062 / G380 / B060},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)G380-20160331 /
                      I:(DE-He78)B060-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28504719},
      pmc          = {pmc:PMC5605674},
      doi          = {10.1038/onc.2017.110},
      url          = {https://inrepo02.dkfz.de/record/128633},
}