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@ARTICLE{Huang:144001,
      author       = {M. Huang and J. Tailor and Q. Zhen and A. H. Gillmor and M.
                      L. Miller and H. Weishaupt and J. Chen and T. Zheng and E.
                      K. Nash and L. K. McHenry and Z. An and F. Ye and Y.
                      Takashima and J. Clarke and H. Ayetey and F. M. G. Cavalli
                      and B. Luu and B. S. Moriarity and S. Ilkhanizadeh and L.
                      Chavez$^*$ and C. Yu and K. M. Kurian and T. Magnaldo and N.
                      Sevenet and P. Koch$^*$ and S. M. Pollard and P. Dirks and
                      M. P. Snyder and D. A. Largaespada and Y. J. Cho and J. J.
                      Phillips and F. J. Swartling and A. S. Morrissy and M.
                      Kool$^*$ and S. M. Pfister$^*$ and M. D. Taylor and A. Smith
                      and W. A. Weiss},
      title        = {{E}ngineering {G}enetic {P}redisposition in {H}uman
                      {N}euroepithelial {S}tem {C}ells {R}ecapitulates
                      {M}edulloblastoma {T}umorigenesis.},
      journal      = {Cell stem cell},
      volume       = {25},
      number       = {3},
      issn         = {1934-5909},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2019-01552},
      pages        = {433-446.e7},
      year         = {2019},
      abstract     = {Human neural stem cell cultures provide progenitor cells
                      that are potential cells of origin for brain cancers.
                      However, the extent to which genetic predisposition to tumor
                      formation can be faithfully captured in stem cell lines is
                      uncertain. Here, we evaluated neuroepithelial stem (NES)
                      cells, representative of cerebellar progenitors. We
                      transduced NES cells with MYCN, observing medulloblastoma
                      upon orthotopic implantation in mice. Significantly,
                      transcriptomes and patterns of DNA methylation from
                      xenograft tumors were globally more representative of human
                      medulloblastoma compared to a MYCN-driven genetically
                      engineered mouse model. Orthotopic transplantation of NES
                      cells generated from Gorlin syndrome patients, who are
                      predisposed to medulloblastoma due to germline-mutated
                      PTCH1, also generated medulloblastoma. We engineered
                      candidate cooperating mutations in Gorlin NES cells, with
                      mutation of DDX3X or loss of GSE1 both accelerating
                      tumorigenesis. These findings demonstrate that human NES
                      cells provide a potent experimental resource for dissecting
                      genetic causation in medulloblastoma.},
      cin          = {B062},
      ddc          = {570},
      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:31204176},
      doi          = {10.1016/j.stem.2019.05.013},
      url          = {https://inrepo02.dkfz.de/record/144001},
}