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@ARTICLE{Jeibmann:126065,
      author       = {A. Jeibmann and K. Eikmeier and A. Linge and M. Kool$^*$
                      and B. Koos and J. Schulz and S. Albrecht and K. Bartelheim
                      and M. C. Frühwald and S. Pfister$^*$ and W. Paulus and M.
                      Hasselblatt},
      title        = {{I}dentification of genes involved in the biology of
                      atypical teratoid/rhabdoid tumours using {D}rosophila
                      melanogaster.},
      journal      = {Nature Communications},
      volume       = {5},
      issn         = {2041-1723},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-02180},
      pages        = {4005},
      year         = {2014},
      abstract     = {Atypical teratoid/rhabdoid tumours (AT/RT) are malignant
                      brain tumours. Unlike most other human brain tumours, AT/RT
                      are characterized by inactivation of one single gene,
                      SMARCB1. SMARCB1 is a member of the evolutionarily conserved
                      SWI/SNF chromatin remodelling complex, which has an
                      important role in the control of cell differentiation and
                      proliferation. Little is known, however, about the pathways
                      involved in the oncogenic effects of SMARCB1 inactivation,
                      which might also represent targets for treatment. Here we
                      report a comprehensive genetic screen in the fruit fly that
                      revealed several genes not yet associated with loss of snr1,
                      the Drosophila homologue of SMARCB1. We confirm the
                      functional role of identified genes (including merlin, kibra
                      and expanded, known to regulate hippo signalling pathway
                      activity) in human rhabdoid tumour cell lines and AT/RT
                      tumour samples. These results demonstrate that fly models
                      can be employed for the identification of clinically
                      relevant pathways in human cancer.},
      keywords     = {Chromosomal Proteins, Non-Histone (NLM Chemicals) /
                      DNA-Binding Proteins (NLM Chemicals) / Drosophila Proteins
                      (NLM Chemicals) / Intracellular Signaling Peptides and
                      Proteins (NLM Chemicals) / Membrane Proteins (NLM Chemicals)
                      / Neurofibromin 2 (NLM Chemicals) / SMARCB1 Protein (NLM
                      Chemicals) / SMARCB1 protein, human (NLM Chemicals) / Snr1
                      protein, Drosophila (NLM Chemicals) / Transcription Factors
                      (NLM Chemicals) / Tumor Suppressor Proteins (NLM Chemicals)
                      / expanded protein, Drosophila (NLM Chemicals) / kibra
                      protein, Drosophila (NLM Chemicals) / merlin, Drosophila
                      (NLM Chemicals) / Protein-Serine-Threonine Kinases (NLM
                      Chemicals) / hpo protein, Drosophila (NLM Chemicals)},
      cin          = {B062},
      ddc          = {500},
      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:24892285},
      doi          = {10.1038/ncomms5005},
      url          = {https://inrepo02.dkfz.de/record/126065},
}