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@ARTICLE{Patnana:277439,
      author       = {P. K. Patnana and L. Liu and D. Frank and S. C. Nimmagadda
                      and M. Behrens and H. Ahmed and X. Xie and M. Liebmann and
                      L. Wei and A. Gerdemann and A. Thivakaran and H.-U. Humpf
                      and L. Klotz and M. Dugas and J. Varghese and M.
                      Trajkovic-Arsic$^*$ and J. Siveke$^*$ and H. Hanenberg and
                      B. Opalka and U. Dührsen and H. C. Reinhardt and U.
                      Guenther and N. von Bubnoff and C. Khandanpour},
      title        = {{D}ose-dependent expression of {GFI}1 alters metabolism in
                      the haematopoietic progenitors and {MLL}::{AF}9-induced
                      leukaemic cells.},
      journal      = {British journal of haematology},
      volume       = {202},
      number       = {5},
      issn         = {0007-1048},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {DKFZ-2023-01376},
      pages        = {1033-1048},
      year         = {2023},
      note         = {2023 Sep;202(5):1033-1048},
      abstract     = {Growth factor independence 1 (GFI1) is a transcriptional
                      repressor protein that plays an essential role in the
                      differentiation of myeloid and lymphoid progenitors. We and
                      other groups have shown that GFI1 has a dose-dependent role
                      in the initiation, progression, and prognosis of acute
                      myeloid leukaemia (AML) patients by inducing epigenetic
                      changes. We now demonstrate a novel role for dose-dependent
                      GFI1 expression in regulating metabolism in haematopoietic
                      progenitor and leukaemic cells. Using in-vitro and ex-vivo
                      murine models of MLL::AF9-induced human AML and
                      extra-cellular flux assays, we now demonstrate that a lower
                      GFI1 expression enhances oxidative phosphorylation rate via
                      upregulation of the FOXO1- MYC axis. Our findings underscore
                      the significance of therapeutic exploitation in
                      GFI1-low-expressing leukaemia cells by targeting oxidative
                      phosphorylation and glutamine metabolism.},
      keywords     = {AML (Other) / GFI1 (Other) / metabolism (Other)},
      cin          = {ED01},
      ddc          = {610},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37423893},
      doi          = {10.1111/bjh.18939},
      url          = {https://inrepo02.dkfz.de/record/277439},
}