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@ARTICLE{Ptasinska:147918,
      author       = {A. Ptasinska and A. Pickin and S. A. Assi and P. S. Chin
                      and L. Ames and R. Avellino and S. Gröschel$^*$ and R.
                      Delwel and P. N. Cockerill and C. S. Osborne and C. Bonifer},
      title        = {{RUNX}1-{ETO} {D}epletion in t(8;21) {AML} {L}eads to
                      {C}/{EBP}α- and {AP}-1-{M}ediated {A}lterations in
                      {E}nhancer-{P}romoter {I}nteraction.},
      journal      = {Cell reports},
      volume       = {28},
      number       = {12},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2019-02779},
      pages        = {3022 - 3031.e7},
      year         = {2019},
      abstract     = {Acute myeloid leukemia (AML) is associated with mutations
                      in transcriptional and epigenetic regulator genes impairing
                      myeloid differentiation. The t(8;21)(q22;q22) translocation
                      generates the RUNX1-ETO fusion protein, which interferes
                      with the hematopoietic master regulator RUNX1. We previously
                      showed that the maintenance of t(8;21) AML is dependent on
                      RUNX1-ETO expression. Its depletion causes extensive changes
                      in transcription factor binding, as well as gene expression,
                      and initiates myeloid differentiation. However, how these
                      processes are connected within a gene regulatory network is
                      unclear. To address this question, we performed
                      Promoter-Capture Hi-C assays, with or without RUNX1-ETO
                      depletion and assigned interacting cis-regulatory elements
                      to their respective genes. To construct a
                      RUNX1-ETO-dependent gene regulatory network maintaining AML,
                      we integrated cis-regulatory element interactions with gene
                      expression and transcription factor binding data. This
                      analysis shows that RUNX1-ETO participates
                      in cis-regulatory element interactions. However,
                      differential interactions following RUNX1-ETO depletion are
                      driven by alterations in the binding of RUNX1-ETO-regulated
                      transcription factors.},
      cin          = {A380},
      ddc          = {610},
      cid          = {I:(DE-He78)A380-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31533028},
      doi          = {10.1016/j.celrep.2019.08.040},
      url          = {https://inrepo02.dkfz.de/record/147918},
}