Haematologica, Vol 92, Issue 11, 1557-1560 doi:10.3324/haematol.11201
Copyright © 2007 by Ferrata Storti Foundation
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Juvenile Myelomonocytic Leukemia

Role of mutation independent constitutive activation of FLT3 in juvenile myelomonocytic leukemia

Andrica C.H. de Vries, Ronald W. Stam, Pauline Schneider, Charlotte M. Niemeyer, Elisabeth R. van Wering, Oskar A. Haas, Christian P. Kratz, Monique L. den Boer, Rob Pieters, Marry M. van den Heuvel-Eibrink

From the Erasmus MC-Sophia Children’s Hospital, Pediatric Oncology/Hematology, Rotterdam, The Netherlands (ACHdV, RWS, RP, MLdB, RB, MMvdH-E); Department of Pediatrics and Adolescent Medicine, Division of Pediatric Hematology and Oncology, University of Freiburg, Germany (CMN, CPK); Dutch Childhood Oncology Group, The Hague, The Netherlands (ERvW, MMvdH-E); Children’s Cancer Research Institute, Vienna, Austria (OAH)

Correspondence: Marry M. van den Heuvel-Eibrink, MD, PhD, ErasmusMC-Sophia Children’s Hospital, Dept. of Pediatric Hematology/Oncology, Room Sp 2568, Dr. Molewaterplein 60, 3015 GJ, Rotterdam, The Netherlands. E-mail: m.vandenheuvel{at}eras-musmc.nl

FLT3 gene mutations have been identified as prognostic factors in myeloid malignancies. Furthermore, FLT3 can be activated by wild type overexpression or ligand-dependent in leukemic cells co-expressing FLT3 ligand (FLT3L). So far no data are available on FLT3/FLT3L expression and activation in JMML. In 51 clinical JMML samples, activating mutations were screened, FLT3 and FLT3L mRNA levels were assessed and the sensitivity of JMML cells to the FLT3 inhibitor PKC412 was tested by MTT assays. No evidence for constitutively activation of FLT3/FLT3L was found in JMML, indicating that FLT3 inhibitors are unlikely to be effective in JMML.

Key words: FLT3, JMML, PKC412.


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A. C.H. de Vries, C. M. Zwaan, and M. M. van den Heuvel-Eibrink
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