% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Ottema:176967,
      author       = {S. Ottema and R. Mulet-Lazaro and C. Erpelinck-Verschueren
                      and S. van Herk and M. Havermans and A. Arricibita Varea and
                      M. Vermeulen and H. B. Beverloo and S. Gröschel$^*$ and T.
                      Haferlach and C. Haferlach and B. J Wouters and E. Bindels
                      and L. Smeenk and R. Delwel},
      title        = {{T}he leukemic oncogene {EVI}1 hijacks a {MYC}
                      super-enhancer by {CTCF}-facilitated loops.},
      journal      = {Nature Communications},
      volume       = {12},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2021-02200},
      pages        = {5679},
      year         = {2021},
      abstract     = {Chromosomal rearrangements are a frequent cause of oncogene
                      deregulation in human malignancies. Overexpression of EVI1
                      is found in a subgroup of acute myeloid leukemia (AML) with
                      3q26 chromosomal rearrangements, which is often therapy
                      resistant. In AMLs harboring a t(3;8)(q26;q24), we observed
                      the translocation of a MYC super-enhancer (MYC SE) to the
                      EVI1 locus. We generated an in vitro model mimicking a
                      patient-based t(3;8)(q26;q24) using CRISPR-Cas9 technology
                      and demonstrated hyperactivation of EVI1 by the hijacked MYC
                      SE. This MYC SE contains multiple enhancer modules, of which
                      only one recruits transcription factors active in early
                      hematopoiesis. This enhancer module is critical for EVI1
                      overexpression as well as enhancer-promoter interaction.
                      Multiple CTCF binding regions in the MYC SE facilitate this
                      enhancer-promoter interaction, which also involves a CTCF
                      binding site upstream of the EVI1 promoter. We hypothesize
                      that this CTCF site acts as an enhancer-docking site in
                      t(3;8) AML. Genomic analyses of other 3q26-rearranged AML
                      patient cells point to a common mechanism by which EVI1 uses
                      this docking site to hijack enhancers active in early
                      hematopoiesis.},
      cin          = {A380},
      ddc          = {500},
      cid          = {I:(DE-He78)A380-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34584081},
      doi          = {10.1038/s41467-021-25862-3},
      url          = {https://inrepo02.dkfz.de/record/176967},
}