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 Blood, 21 May 2009, Vol. 113, No. 21, pp. 5250-5253.
Prepublished online as a Blood First Edition Paper on March 11, 2009; DOI 10.1182/blood-2008-09-172668.

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Submitted September 8, 2008
Accepted February 17, 2009

NPM1, but not FLT3-ITD mutations predict early blast cell clearance and CR rate in patients with normal karyotype AML (NK-AML) or high risk myelodysplastic syndrome (MDS)

Friederike Schneider, Eva Hoster, Michael Unterhalt, Stephanie Schneider, Annika Dufour, Tobias Benthaus, Gudrun Mellert, Evelin Zellmeier, Stefan K. Bohlander, Michaela Feuring-Buske, Christian Buske, Jan Braess, Susanne Fritsch, Achim Heinecke, Maria C. Sauerland, Wolfgang E. Berdel, Thomas Buechner, Bernhard J. Woermann, Wolfgang Hiddemann, and Karsten Spiekermann*

Laboratory for Leukemia Diagnostics, Department of Internal Medicine III, University Hospital Munich, Munich, Germany
Clinical Cooperative Group Acute Leukemias, Helmholtz Center, Munich, Germany
Department of Medical Informatics and Biomathematics, University of Muenster, Muenster, Germany
Department of Medicine, Hematology and Oncology, University of Muenster, Muenster, Germany
Klinikum Braunschweig, Braunschweig, Germany

* Corresponding author; email: karsten.spiekermann{at}med.uni-muenchen.de.

Mutations in the NPM1 gene represent the most frequent genetic alterations in patients with acute myeloid leukemia (AML) and are associated with a favorable outcome. In 690 normal karyotype (NK) AML patients the complete remission rates (CR) and the percentage of patients with adequate in vivo blast cell reduction one week after the end of the first induction cycle were significantly higher in NPM1+ (75% and 80%, respectively) than in NPM1- (57% and 57%, respectively) patients, but were unaffected by the FLT3-ITD status. Multivariate analyses revealed the presence of a NPM1 mutation as an independent positive prognostic factor for the achievement of an adequate d16 blast clearance and a CR. In conclusion, NPM1+ blast cells show a high in vivo sensitivity towards induction chemotherapy irrespective of the FLT3-ITD mutation status. These findings provide insight into the pathophysiology and help to understand the favorable clinical outcome of NPM1+ AML.


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