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@ARTICLE{Bandopadhayay:143931,
      author       = {P. Bandopadhayay and F. Piccioni and R. O'Rourke and P. Ho
                      and E. M. Gonzalez and G. Buchan and K. Qian and G. Gionet
                      and E. Girard and M. Coxon and M. G. Rees and L. Brenan and
                      F. Dubois and O. Shapira and N. F. Greenwald and M. Pages
                      and A. Balboni Iniguez and B. R. Paolella and A. Meng and C.
                      Sinai and G. Roti and N. V. Dharia and A. Creech and B.
                      Tanenbaum and P. Khadka and A. Tracy and H. L. Tiv and A. L.
                      Hong and S. Coy and R. Rashid and J.-R. Lin and G. S. Cowley
                      and F. C. Lam and A. Goodale and Y. Lee and K. Schoolcraft
                      and F. Vazquez and W. C. Hahn and A. Tsherniak and J. E.
                      Bradner and M. B. Yaffe and T. Milde$^*$ and S. M.
                      Pfister$^*$ and J. Qi and M. Schenone and S. A. Carr and K.
                      L. Ligon and M. W. Kieran and S. Santagata and J. M. Olson
                      and P. C. Gokhale and J. D. Jaffe and D. E. Root and K.
                      Stegmaier and C. M. Johannessen and R. Beroukhim},
      title        = {{N}euronal differentiation and cell-cycle programs mediate
                      response to {BET}-bromodomain inhibition in {MYC}-driven
                      medulloblastoma.},
      journal      = {Nature Communications},
      volume       = {10},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2019-01489},
      pages        = {2400},
      year         = {2019},
      abstract     = {BET-bromodomain inhibition (BETi) has shown pre-clinical
                      promise for MYC-amplified medulloblastoma. However, the
                      mechanisms for its action, and ultimately for resistance,
                      have not been fully defined. Here, using a combination of
                      expression profiling, genome-scale CRISPR/Cas9-mediated loss
                      of function and ORF/cDNA driven rescue screens, and
                      cell-based models of spontaneous resistance, we identify
                      bHLH/homeobox transcription factors and cell-cycle
                      regulators as key genes mediating BETi's response and
                      resistance. Cells that acquire drug tolerance exhibit a more
                      neuronally differentiated cell-state and expression of
                      lineage-specific bHLH/homeobox transcription factors.
                      However, they do not terminally differentiate, maintain
                      expression of CCND2, and continue to cycle through S-phase.
                      Moreover, CDK4/CDK6 inhibition delays acquisition of
                      resistance. Therefore, our data provide insights about the
                      mechanisms underlying BETi effects and the appearance of
                      resistance and support the therapeutic use of combined
                      cell-cycle inhibitors with BETi in MYC-amplified
                      medulloblastoma.},
      cin          = {B310 / B062 / L101},
      ddc          = {500},
      cid          = {I:(DE-He78)B310-20160331 / I:(DE-He78)B062-20160331 /
                      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:31160565},
      doi          = {10.1038/s41467-019-10307-9},
      url          = {https://inrepo02.dkfz.de/record/143931},
}