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@ARTICLE{Gallo:126558,
      author       = {M. Gallo and F. J. Coutinho and R. J. Vanner and T. Gayden
                      and S. C. Mack and A. Murison and M. Remke and R. Li and N.
                      Takayama and K. Desai and L. Lee and X. Lan and N. I. Park
                      and D. Barsyte-Lovejoy and D. Smil and D. Sturm$^*$ and M.
                      M. Kushida and R. Head and M. D. Cusimano and M. Bernstein
                      and I. D. Clarke and J. E. Dick and S. Pfister$^*$ and J. N.
                      Rich and C. H. Arrowsmith and M. D. Taylor and N. Jabado and
                      D. P. Bazett-Jones and M. Lupien and P. B. Dirks},
      title        = {{MLL}5 {O}rchestrates a {C}ancer {S}elf-{R}enewal {S}tate
                      by {R}epressing the {H}istone {V}ariant {H}3.3 and
                      {G}lobally {R}eorganizing {C}hromatin.},
      journal      = {Cancer cell},
      volume       = {28},
      number       = {6},
      issn         = {1535-6108},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2017-02586},
      pages        = {715 - 729},
      year         = {2015},
      abstract     = {Mutations in the histone 3 variant H3.3 have been
                      identified in one-third of pediatric glioblastomas (GBMs),
                      but not in adult tumors. Here we show that H3.3 is a dynamic
                      determinant of functional properties in adult GBM. H3.3 is
                      repressed by mixed lineage leukemia 5 (MLL5) in
                      self-renewing GBM cells. MLL5 is a global epigenetic
                      repressor that orchestrates reorganization of chromatin
                      structure by punctuating chromosomes with foci of compacted
                      chromatin, favoring tumorigenic and self-renewing
                      properties. Conversely, H3.3 antagonizes self-renewal and
                      promotes differentiation. We exploited these epigenetic
                      states to rationally identify two small molecules that
                      effectively curb cancer stem cell properties in a
                      preclinical model. Our work uncovers a role for MLL5 and
                      H3.3 in maintaining self-renewal hierarchies in adult GBM.},
      keywords     = {Antineoplastic Agents (NLM Chemicals) / DNA-Binding
                      Proteins (NLM Chemicals) / Histones (NLM Chemicals) / MLL5
                      protein, human (NLM Chemicals)},
      cin          = {B062},
      ddc          = {610},
      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:26626085},
      doi          = {10.1016/j.ccell.2015.10.005},
      url          = {https://inrepo02.dkfz.de/record/126558},
}