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@ARTICLE{Tausch:300264,
      author       = {S. Tausch and C. Villinger and G. Alexe and D. J. Urban and
                      M. Shen and D. Jahn$^*$ and J. Vischedyk and S. Scheich$^*$
                      and H. Serve$^*$ and M. D. Hall and K. Stegmaier and T.
                      Oellerich$^*$ and A. Cremer$^*$},
      title        = {{I}nflammatory signaling pathways play a role in {SYK}
                      inhibitor resistant {AML}.},
      journal      = {Scientific reports},
      volume       = {15},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-00717},
      pages        = {11673},
      year         = {2025},
      abstract     = {Trials have shown promising clinical activity of the
                      selective SYK inhibitor entospletinib in patients with high
                      expressing HOXA9/MEIS1 acute leukemias. As the development
                      of resistance mechanisms is a common problem in the use of
                      targeted drugs, we performed a chemical library screen to
                      identify drug sensitivities in SYK inhibitor resistant AML
                      cells. We identified that SYK inhibitor resistant cells
                      displayed an increased sensitivity to glucocorticoids.
                      Glucocorticoids are potent immunosuppressants which work in
                      part by inhibiting the transcription of cytokine genes. RNA
                      sequencing of entospletinib resistant cells revealed a
                      strong enrichment of inflammatory response and TNFα
                      signaling via NF-κB gene sets in comparison to naive cells.
                      Naive AML cells treated with entospletinib showed a strong
                      downregulation of the same gene sets which were upregulated
                      in the resistant state. Our data suggest that inflammatory
                      signaling pathways play a role in entospletinib resistant
                      AML cells.},
      keywords     = {Humans / Syk Kinase: antagonists $\&$ inhibitors / Syk
                      Kinase: metabolism / Leukemia, Myeloid, Acute: drug therapy
                      / Leukemia, Myeloid, Acute: metabolism / Leukemia, Myeloid,
                      Acute: genetics / Leukemia, Myeloid, Acute: pathology /
                      Signal Transduction: drug effects / Drug Resistance,
                      Neoplasm: drug effects / Protein Kinase Inhibitors:
                      pharmacology / Cell Line, Tumor / Inflammation: metabolism /
                      NF-kappa B: metabolism / Acute myeloid leukemia cells
                      (Other) / Glucocorticoids (Other) / Inflammatory pathways
                      (Other) / Resistance (Other) / Syk Kinase (NLM Chemicals) /
                      SYK protein, human (NLM Chemicals) / Protein Kinase
                      Inhibitors (NLM Chemicals) / NF-kappa B (NLM Chemicals)},
      cin          = {FM01},
      ddc          = {600},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40188268},
      doi          = {10.1038/s41598-025-96660-w},
      url          = {https://inrepo02.dkfz.de/record/300264},
}