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Activation mechanisms of STAT5 by oncogenic Flt3-ITD.
Mutations in the receptor tyrosine kinase Flt3 represent a very common genetic lesion in acute myeloid leukemia (AML). Internal tandem duplication (ITD) mutations clustered in the juxtamembraneExpand
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Suppression of myeloid transcription factors and induction of STAT response genes by AML-specific Flt3 mutations.
The receptor tyrosine kinase Flt3 is expressed and functionally important in early myeloid progenitor cells and in the majority of acute myeloid leukemia (AML) blasts. Internal tandem duplicationsExpand
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