Case Reports:

Dasatinib overrides the differentiation blockage in a patient with mutant-KIT D816V positive CBFβ-MYH11 leukemia

Kerstin M. Kampa-Schittenhelm, Wichard Vogel, Irina Bonzheim, Falko Fend, Marius Horger, Lothar Kanz, Martin Soekler and Marcus M. Schittenhelm _

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Oncotarget. 2018; 9:11876-11882. https://doi.org/10.18632/oncotarget.24376

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Kerstin M. Kampa-Schittenhelm1, Wichard Vogel1, Irina Bonzheim2, Falko Fend2, Marius Horger3, Lothar Kanz1, Martin Soekler1 and Marcus M. Schittenhelm1

1Department of Oncology, Hematology, Rheumatology, Clinical Immunology and Pulmonology, University Hospital Tübingen, Tübingen, Germany

2Institute of Pathology and Neuropathology, Reference Center for Hematopathology, University Hospital Tübingen, Tübingen, Germany

3Department of Diagnostic and Interventional Radiology, University Hospital Tübingen, Tübingen, Germany

Correspondence to:

Marcus M. Schittenhelm, email: [email protected]

Keywords: CBF AML; KIT; tyrosine kinase inhibition; differentiation

Received: September 18, 2017     Accepted: January 15, 2018     Published: January 31, 2018


Activating KIT D816V mutations are frequently found in CBF AML, which predicts for an unfavorable outcome. Dasatinib is a potent inhibitor of wildtype and mutant-KIT isoforms – including D816V. We now provide proof of antileukemic efficacy in a patient with relapsing mutant-KIT D816V CBF AML. Importantly, this effect is mediated via overriding the differentiation blockage of the leukemia clone.

In addition, we show that dasatinib is capable to induce pulmonary differentiation syndrome – and therefore needs close monitoring of patients under therapy.

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