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@ARTICLE{Haag:167358,
      author       = {D. Haag$^*$ and N. Mack$^*$ and P. Benites Goncalves da
                      Silva$^*$ and B. Statz$^*$ and J. Clark$^*$ and K. Tanabe
                      and T. Sharma$^*$ and N. Jäger$^*$ and D. T. W. Jones$^*$
                      and D. Kawauchi$^*$ and M. Wernig and S. Pfister$^*$},
      title        = {{H}3.3-{K}27{M} drives neural stem cell-specific
                      gliomagenesis in a human i{PSC}-derived model.},
      journal      = {Cancer cell},
      volume       = {39},
      number       = {3},
      issn         = {1535-6108},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2021-00304},
      pages        = {407-422.e13},
      year         = {2021},
      note         = {#EA:B062#LA:B062#2021 Mar 8;39(3):407-422.e13},
      abstract     = {Diffuse intrinsic pontine glioma (DIPG) is an aggressive
                      childhood tumor of the brainstem with currently no curative
                      treatment available. The vast majority of DIPGs carry a
                      histone H3 mutation leading to a lysine 27-to-methionine
                      exchange (H3K27M). We engineered human induced pluripotent
                      stem cells (iPSCs) to carry an inducible H3.3-K27M allele in
                      the endogenous locus and studied the effects of the mutation
                      in different disease-relevant neural cell types. H3.3-K27M
                      upregulated bivalent promoter-associated developmental
                      genes, producing diverse outcomes in different cell types.
                      While being fatal for iPSCs, H3.3-K27M increased
                      proliferation in neural stem cells (NSCs) and to a lesser
                      extent in oligodendrocyte progenitor cells (OPCs). Only NSCs
                      gave rise to tumors upon induction of H3.3-K27M and TP53
                      inactivation in an orthotopic xenograft model recapitulating
                      human DIPGs. In NSCs, H3.3-K27M leads to maintained
                      expression of stemness and proliferative genes and a
                      premature activation of OPC programs that together may cause
                      tumor initiation.},
      keywords     = {DIPG (Other) / H3.3-K27M (Other) / H3K27me3 (Other) /
                      H3K4me3 (Other) / NSC (Other) / OPC (Other) / bivalent
                      chromatin (Other) / glioma (Other) / iPSC (Other) /
                      orthotopic xenograft (Other)},
      cin          = {B062 / HD01 / B360},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)B360-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33545065},
      doi          = {10.1016/j.ccell.2021.01.005},
      url          = {https://inrepo02.dkfz.de/record/167358},
}