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FLT3 mutations in childhood acute lymphoblastic leukemia at first relapse

Leukemia volume 19, pages 467–468 (2005)Cite this article

TO THE EDITOR

The FMS-like tyrosine kinase 3 (FLT3) plays an important role in the pathogenesis of hematopoietic malignancies.1 Constitutive activation of FLT3, resulting in cell proliferation and survival, occurs either through coexpression of FLT3 ligand and autocrine signalling or through mutations of the FLT3 gene, which lead to autophosphorylation and activation of the FLT3 receptor. FLT3 activating mutations, internal tandem duplications (ITD) and kinase domain (KD) mutations were initially discovered in acute myeloid leukemias (AML) and are associated with poor prognosis in both adult and pediatric AML.2

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Acknowledgements

This work was supported by a grant from the Deutsche José Carreras Leukämie-Stiftung (Project DJCLS-R03/16).

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Authors and Affiliations

  1. Department of Pediatric Oncology and Hematology, Charite, Medical University of Berlin, Berlin, Germany

    S Wellmann, E Moderegger, A Zelmer, M Bettkober, A von Stackelberg, G Henze & K Seeger

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  1. S Wellmann
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  2. E Moderegger
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  3. A Zelmer
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  4. M Bettkober
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  5. A von Stackelberg
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  6. G Henze
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  7. K Seeger
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Correspondence to S Wellmann.

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Wellmann, S., Moderegger, E., Zelmer, A. et al. FLT3 mutations in childhood acute lymphoblastic leukemia at first relapse. Leukemia 19, 467–468 (2005). https://doi.org/10.1038/sj.leu.2403655

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