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The secondary FLT3-ITD F691L mutation induces resistance to AC220 in FLT3-ITD+ AML but retains in vitro sensitivity to PKC412 and Sunitinib

Leukemia volume 27, pages 1416–1418 (2013)Cite this article

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We report on a secondary FLT3 internal tandem duplication (FLT3-ITD) mutation in a 48-year-old female patient with FLT3-ITD+ acute myeloid leukemia (AML) mediating resistance to the FLT3 inhibitor AC220.

Initially, the patient presented with white blood cell (WBC) count of 27.03 g/l, platelets count of 101g/l, and 70% peripheral blood (PB) and 52% bone marrow (BM) blasts. Marrow cytogenetics showed a normal karyotype, and molecular analysis revealed mutation of NPM1 and an ITD mutation of 87 bp length within the juxtamembrane region of FLT3.

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Author notes

  1. H Leischner

    Present address: 4Present address: Department of Hematology, Oncology and Tumor Immunology, HELIOS Klinikum Berlin-Buch, Berlin, Germany,

  2. C Albers and H Leischner: These authors contributed equally to this work.

Authors and Affiliations

  1. Department of Internal Medicine III, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany

    C Albers, H Leischner, M Verbeek, C Yu & C Peschel

  2. Department of Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany

    A L Illert, N von Bubnoff & J Duyster

Authors
  1. C Albers
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  2. H Leischner
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  3. M Verbeek
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  4. C Yu
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  5. A L Illert
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  6. C Peschel
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  7. N von Bubnoff
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  8. J Duyster
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Corresponding author

Correspondence to J Duyster.

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Albers, C., Leischner, H., Verbeek, M. et al. The secondary FLT3-ITD F691L mutation induces resistance to AC220 in FLT3-ITD+ AML but retains in vitro sensitivity to PKC412 and Sunitinib. Leukemia 27, 1416–1418 (2013). https://doi.org/10.1038/leu.2013.14

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  • DOI: https://doi.org/10.1038/leu.2013.14

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