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@ARTICLE{Zuckermann:127884,
      author       = {M. Zuckermann$^*$ and V. Hovestadt$^*$ and C. B.
                      Knobbe-Thomsen and M. Zapatka$^*$ and P. A. Northcott$^*$
                      and K. Schramm$^*$ and J. Belic$^*$ and D. Jones$^*$ and B.
                      Tschida and B. Moriarity and D. Largaespada and M. F.
                      Roussel and A. Korshunov$^*$ and G. Reifenberger$^*$ and S.
                      Pfister$^*$ and P. Lichter$^*$ and D. Kawauchi$^*$ and J.
                      Gronych$^*$},
      title        = {{S}omatic {CRISPR}/{C}as9-mediated tumour suppressor
                      disruption enables versatile brain tumour modelling.},
      journal      = {Nature Communications},
      volume       = {6},
      issn         = {2041-1723},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-03906},
      pages        = {7391},
      year         = {2015},
      abstract     = {In vivo functional investigation of oncogenes using somatic
                      gene transfer has been successfully exploited to validate
                      their role in tumorigenesis. For tumour suppressor genes
                      this has proven more challenging due to technical aspects.
                      To provide a flexible and effective method for investigating
                      somatic loss-of-function alterations and their influence on
                      tumorigenesis, we have established CRISPR/Cas9-mediated
                      somatic gene disruption, allowing for in vivo targeting of
                      TSGs. Here we demonstrate the utility of this approach by
                      deleting single (Ptch1) or multiple genes (Trp53, Pten, Nf1)
                      in the mouse brain, resulting in the development of
                      medulloblastoma and glioblastoma, respectively. Using
                      whole-genome sequencing (WGS) we characterized the
                      medulloblastoma-driving Ptch1 deletions in detail and show
                      that no off-targets were detected in these tumours. This
                      method provides a fast and convenient system for validating
                      the emerging wealth of novel candidate tumour suppressor
                      genes and the generation of faithful animal models of human
                      cancer.},
      keywords     = {Neurofibromin 1 (NLM Chemicals) / PTCH protein, human (NLM
                      Chemicals) / Patched Receptors (NLM Chemicals) / Patched-1
                      Receptor (NLM Chemicals) / Ptch1 protein, mouse (NLM
                      Chemicals) / Receptors, Cell Surface (NLM Chemicals) / Tumor
                      Suppressor Protein p53 (NLM Chemicals) / PTEN
                      Phosphohydrolase (NLM Chemicals) / Pten protein, mouse (NLM
                      Chemicals)},
      cin          = {B060 / L401 / B062 / G380 / L101},
      ddc          = {500},
      cid          = {I:(DE-He78)B060-20160331 / I:(DE-He78)L401-20160331 /
                      I:(DE-He78)B062-20160331 / I:(DE-He78)G380-20160331 /
                      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:26067104},
      pmc          = {pmc:PMC4467376},
      doi          = {10.1038/ncomms8391},
      url          = {https://inrepo02.dkfz.de/record/127884},
}