Stephan K. Metzelder

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AML patients with internal tandem duplication (ITD) mutations in the Fms-like tyrosine-3 (Flt3) gene have a dismal prognosis. Here we report compassionate-use results with the multi-kinase-, and Flt3-ITD-inhibitor sorafenib for the treatment of relapsed or refractory Flt3-ITD-positive AML. Sorafenib induced clinically meaningful and very rapid responses in(More)
Gain-of-function mutations in the RAS and FLT3 genes are frequently found in cells of acute myeloid leukemia (AML), leading to constitutive activation of signaling pathways that regulate fundamental cellular processes, and are therefore attractive targets for AML therapy. The multi-targeted kinase inhibitor sorafenib is efficacious in AML with FLT3-internal(More)
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