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@ARTICLE{Eckardt:284759,
      author       = {J.-N. Eckardt and S. Stasik and C. Röllig and A. Petzold
                      and T. Sauer$^*$ and S. Scholl and A. Hochhaus and M.
                      Crysandt and T. H. Brümmendorf and R. Naumann and B.
                      Steffen and V. Kunzmann and H. Einsele and M. Schaich and A.
                      Burchert and A. Neubauer and K. Schäfer-Eckart and C.
                      Schliemann and S. W. Krause and R. Herbst and M. Hänel and
                      M. Hanoun and U. Kaiser and M. Kaufmann and Z. Rácil and J.
                      Mayer and U. Oelschlägel and W. E. Berdel and G. Ehninger
                      and H. Serve and C. Müller-Tidow$^*$ and U. Platzbecker and
                      C. D. Baldus and A. Dahl and J. Schetelig and M.
                      Bornhäuser$^*$ and J. M. Middeke and C. Thiede},
      title        = {{M}utated {IKZF}1 is an independent marker of adverse risk
                      in acute myeloid leukemia.},
      journal      = {Leukemia},
      volume       = {37},
      number       = {12},
      issn         = {0887-6924},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2023-02070},
      pages        = {2395-2403},
      year         = {2023},
      note         = {2023 Dec;37(12):2395-2403},
      abstract     = {Genetic lesions of IKZF1 are frequent events and
                      well-established markers of adverse risk in acute
                      lymphoblastic leukemia. However, their function in the
                      pathophysiology and impact on patient outcome in acute
                      myeloid leukemia (AML) remains elusive. In a multicenter
                      cohort of 1606 newly diagnosed and intensively treated adult
                      AML patients, we found IKZF1 alterations in 45 cases with a
                      mutational hotspot at N159S. AML with mutated IKZF1 was
                      associated with alterations in RUNX1, GATA2, KRAS, KIT,
                      SF3B1, and ETV6, while alterations of NPM1, TET2, FLT3-ITD,
                      and normal karyotypes were less frequent. The clinical
                      phenotype of IKZF1-mutated AML was dominated by anemia and
                      thrombocytopenia. In both univariable and multivariable
                      analyses adjusting for age, de novo and secondary AML, and
                      ELN2022 risk categories, we found mutated IKZF1 to be an
                      independent marker of adverse risk regarding complete
                      remission rate, event-free, relapse-free, and overall
                      survival. The deleterious effects of mutated IKZF1 also
                      prevailed in patients who underwent allogeneic hematopoietic
                      stem cell transplantation (n = 519) in both univariable and
                      multivariable models. These dismal outcomes are only
                      partially explained by the hotspot mutation N159S. Our
                      findings suggest a role for IKZF1 mutation status in AML
                      risk modeling.},
      cin          = {A360 / A350 / DD01},
      ddc          = {610},
      cid          = {I:(DE-He78)A360-20160331 / I:(DE-He78)A350-20160331 /
                      I:(DE-He78)DD01-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37833543},
      doi          = {10.1038/s41375-023-02061-1},
      url          = {https://inrepo02.dkfz.de/record/284759},
}