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@ARTICLE{Schmitt:278355,
      author       = {A. Schmitt and M. Grimm and N. Kreienkamp and H. Junge and
                      J. Labisch and L. Schuhknecht and C. Schönfeld and E. S.
                      Görsch and A. Tibello and K. Menck and A. Bleckmann and C.
                      Lengerke and F. Rosenbauer and M. Grau and M. Zampieri and
                      K. Schulze Osthoff$^*$ and P. Klener and A. Dolnikova and G.
                      Lenz and S. Hailfinger},
      title        = {{BRD}4 inhibition sensitizes diffuse large {B}-cell
                      lymphoma cells to ferroptosis},
      journal      = {Blood},
      volume       = {12},
      number       = {10},
      issn         = {0006-4971},
      address      = {Washington, DC},
      publisher    = {American Society of Hematology},
      reportid     = {DKFZ-2023-01609},
      pages        = {e12363},
      year         = {2023},
      note         = {2023 Oct;12(10):e12363},
      abstract     = {Diffuse large B-cell lymphoma (DLBCL), the most common form
                      of non-Hodgkin lymphoma, is characterized by an aggressive
                      clinical course. In approximately one-third of DLBCL
                      patients, first-line multi-agent immunochemotherapy fails to
                      produce a durable response. Molecular heterogeneity and
                      apoptosis resistance pose major therapeutic challenges in
                      DLBCL treatment. To circumvent apoptosis resistance, the
                      induction of ferroptosis might represent a promising
                      strategy for lymphoma therapy. Here, a compound library
                      targeting epigenetic modulators was screened to identify
                      ferroptosis-sensitizing drugs. Strikingly, bromodomain and
                      extra-terminal domain (BET) inhibitors sensitized cells of
                      the germinal center B cell-like (GCB) subtype of DLBCL to
                      ferroptosis induction and the combination of BET inhibitors
                      with ferroptosis inducers, such as dimethyl fumarate (DMF)
                      or RSL3, synergized in the killing of DLBCL cells in vitro
                      and in vivo. On the molecular level, the BET protein BRD4
                      was found to be an essential regulator of ferroptosis
                      suppressor protein 1 (FSP1) expression and to thus protect
                      GCB-DLBCL cells from ferroptosis. Collectively, we
                      identified and characterized BRD4 as an important player in
                      ferroptosis suppression in GCB-DLBCL and provide a rationale
                      for the combination of BET inhibitors with
                      ferroptosis-inducing agents as a novel therapeutic approach
                      for DLBCL treatment.},
      cin          = {TU01},
      ddc          = {610},
      cid          = {I:(DE-He78)TU01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37294920},
      doi          = {10.1182/blood.2022019274},
      url          = {https://inrepo02.dkfz.de/record/278355},
}