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@ARTICLE{Lee:142895,
      author       = {C. Lee and V. A. Rudneva and S. Erkek$^*$ and M.
                      Zapatka$^*$ and L. Q. Chau and S. K. Tacheva-Grigorova and
                      A. Garancher and J. M. Rusert and O. Aksoy and R. Lea and H.
                      P. Mohammad and J. Wang and W. A. Weiss and H. L. Grimes and
                      S. M. Pfister and P. A. Northcott and R. J. Wechsler-Reya},
      title        = {{L}sd1 as a therapeutic target in {G}fi1-activated
                      medulloblastoma.},
      journal      = {Nature Communications},
      volume       = {10},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2019-00525},
      pages        = {332},
      year         = {2019},
      abstract     = {Drugs that modify the epigenome are powerful tools for
                      treating cancer, but these drugs often have pleiotropic
                      effects, and identifying patients who will benefit from them
                      remains a major clinical challenge. Here we show that
                      medulloblastomas driven by the transcription factor Gfi1 are
                      exquisitely dependent on the enzyme lysine demethylase 1
                      (Kdm1a/Lsd1). We demonstrate that Lsd1 physically associates
                      with Gfi1, and that these proteins cooperate to inhibit
                      genes involved in neuronal commitment and differentiation.
                      We also show that Lsd1 is essential for Gfi1-mediated
                      transformation: Gfi1 proteins that cannot recruit Lsd1 are
                      unable to drive tumorigenesis, and genetic ablation of Lsd1
                      markedly impairs tumor growth in vivo. Finally,
                      pharmacological inhibitors of Lsd1 potently inhibit growth
                      of Gfi1-driven tumors. These studies provide important
                      insight into the mechanisms by which Gfi1 contributes to
                      tumorigenesis, and identify Lsd1 inhibitors as promising
                      therapeutic agents for Gfi1-driven medulloblastoma.},
      keywords     = {Antibiotics, Antineoplastic (NLM Chemicals) / DNA-Binding
                      Proteins (NLM Chemicals) / GFI1 protein, human (NLM
                      Chemicals) / Transcription Factors (NLM Chemicals) /
                      Doxorubicin (NLM Chemicals) / Aof2 protein, mouse (NLM
                      Chemicals) / Histone Demethylases (NLM Chemicals)},
      cin          = {B062 / B060 / L101},
      ddc          = {500},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)B060-20160331 /
                      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:30659187},
      pmc          = {pmc:PMC6338772},
      doi          = {10.1038/s41467-018-08269-5},
      url          = {https://inrepo02.dkfz.de/record/142895},
}