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@ARTICLE{Hckendorf:306595,
      author       = {U. Höckendorf and S. Dutta and A. Kloos and M. Runtsch and
                      C. Zötsch and S. Vosberg and Y. Wang$^*$ and S. Kienreich
                      and B. Flasch and G. Malovan and V. Jäger and S. Stanzer
                      and S. Prein and T. O. Odinius and C. V. Wagner and L.
                      Buschhorn and V. Dill and B. Perfler and T. Haferlach and K.
                      Döhner and K. S. Götze$^*$ and J. Ruland$^*$ and F.
                      Bassermann$^*$ and A. Wahida and M. Heikenwälder$^*$ and C.
                      Branca and J. Schmöllerl and J. Zuber and A.-C. Burk and R.
                      Zeiser and H. Sill and A. K. Jayavelu$^*$ and A. Zebisch and
                      M. Heuser and M. A. Dengler and P. J. Jost},
      title        = {{L}ymphotoxin alpha eradicates acute myeloid leukemia and
                      simultaneously promotes healthy hematopoiesis in mice.},
      journal      = {Science translational medicine},
      volume       = {17},
      number       = {826},
      issn         = {1946-6234},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {DKFZ-2025-02634},
      pages        = {eadu3313},
      year         = {2025},
      abstract     = {Acute myeloid leukemia (AML) is characterized by frequent
                      relapse, which is driven by resistant leukemic stem or
                      progenitor cells (LSCs). Here, we reported on a
                      tumor-suppressive mechanism that can be harnessed to
                      simultaneously clear LSCs and promote healthy hematopoiesis.
                      Genetic deletion of the tumor necrosis factor (TNF)
                      superfamily member lymphotoxin alpha (Lta) blocked cell
                      death and accelerated leukemogenesis in murine AML models.
                      Accordingly, exposure of leukemic cells to exogenous
                      recombinant lymphotoxin alpha (LTα3) induced myeloid
                      differentiation and, in part, cell death in AML progenitors.
                      In syngeneic and patient-derived xenograft mouse models,
                      exposure to recombinant LTα3 resulted in deep and durable
                      remissions. LTα3 repressed leukemia by depleting tumor
                      necrosis factor receptor (TNFR)-associated factor 2 (TRAF2)
                      through activation of TNF receptors TNFR1 and TNFR2. In
                      contrast with conventional therapies, LTα3 exerted only
                      minimal toxicity on the healthy hematopoiesis but instead
                      promoted hematopoietic progenitors. Leveraging this
                      endogenous tumor-suppressive mechanism may decouple
                      treatment efficacy on malignant cells from undesired bone
                      marrow suppression.},
      keywords     = {Animals / Leukemia, Myeloid, Acute: drug therapy /
                      Leukemia, Myeloid, Acute: pathology / Lymphotoxin-alpha:
                      therapeutic use / Lymphotoxin-alpha: pharmacology /
                      Hematopoiesis: drug effects / Mice / Humans / Cell
                      Differentiation: drug effects / Receptors, Tumor Necrosis
                      Factor, Type I: metabolism / Neoplastic Stem Cells: drug
                      effects / Neoplastic Stem Cells: pathology / Neoplastic Stem
                      Cells: metabolism / Recombinant Proteins: pharmacology /
                      Recombinant Proteins: therapeutic use / Receptors, Tumor
                      Necrosis Factor, Type II: metabolism / Lymphotoxin-alpha
                      (NLM Chemicals) / Receptors, Tumor Necrosis Factor, Type I
                      (NLM Chemicals) / Recombinant Proteins (NLM Chemicals) /
                      Receptors, Tumor Necrosis Factor, Type II (NLM Chemicals)},
      cin          = {A400 / MU01 / D440},
      ddc          = {500},
      cid          = {I:(DE-He78)A400-20160331 / I:(DE-He78)MU01-20160331 /
                      I:(DE-He78)D440-20160331},
      pnm          = {319H - Addenda (POF4-319H)},
      pid          = {G:(DE-HGF)POF4-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41296826},
      doi          = {10.1126/scitranslmed.adu3313},
      url          = {https://inrepo02.dkfz.de/record/306595},
}