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@ARTICLE{Brabetz:141665,
      author       = {S. Brabetz$^*$ and S. E. S. Leary and S. Gröbner$^*$ and
                      M. W. Nakamoto and H. Şeker-Cin$^*$ and E. J. Girard and B.
                      Cole and A. D. Strand and K. L. Bloom and V. Hovestadt$^*$
                      and N. Mack$^*$ and F. Pakiam and B. Schwalm$^*$ and A.
                      Korshunov$^*$ and G. P. Balasubramanian$^*$ and P. A.
                      Northcott$^*$ and K. D. Pedro and J. Dey and S. Hansen and
                      S. Ditzler and P. Lichter$^*$ and L. Chavez$^*$ and D.
                      Jones$^*$ and J. Koster and S. Pfister$^*$ and M. Kool$^*$
                      and J. M. Olson},
      title        = {{A} biobank of patient-derived pediatric brain tumor
                      models.},
      journal      = {Nature medicine},
      volume       = {24},
      number       = {11},
      issn         = {1546-170X},
      address      = {New York, NY},
      publisher    = {Nature America Inc.},
      reportid     = {DKFZ-2018-01936},
      pages        = {1752 - 1761},
      year         = {2018},
      abstract     = {Brain tumors are the leading cause of cancer-related death
                      in children. Genomic studies have provided insights into
                      molecular subgroups and oncogenic drivers of pediatric brain
                      tumors that may lead to novel therapeutic strategies. To
                      evaluate new treatments, better preclinical models
                      adequately reflecting the biological heterogeneity are
                      needed. Through the Children's Oncology Group ACNS02B3
                      study, we have generated and comprehensively characterized
                      30 patient-derived orthotopic xenograft models and seven
                      cell lines representing 14 molecular subgroups of pediatric
                      brain tumors. Patient-derived orthotopic xenograft models
                      were found to be representative of the human tumors they
                      were derived from in terms of histology,
                      immunohistochemistry, gene expression, DNA methylation, copy
                      number, and mutational profiles. In vivo drug sensitivity of
                      targeted therapeutics was associated with distinct molecular
                      tumor subgroups and specific genetic alterations. These
                      models and their molecular characterization provide an
                      unprecedented resource for the cancer community to study key
                      oncogenic drivers and to evaluate novel treatment
                      strategies.},
      cin          = {B062 / L101 / B060 / G380},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)B060-20160331 / 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:30349086},
      doi          = {10.1038/s41591-018-0207-3},
      url          = {https://inrepo02.dkfz.de/record/141665},
}