AML-associated Flt3 kinase domain mutations show signal transduction differences compared with Flt3 ITD mutations.

@article{Choudhary2005AMLassociatedFK,
  title={AML-associated Flt3 kinase domain mutations show signal transduction differences compared with Flt3 ITD mutations.},
  author={C. Choudhary and J. Schwaeble and C. Brandts and L. Tickenbrock and B. Sargin and T. Kindler and T. Fischer and W. E. Berdel and C. M{\"u}ller-Tidow and H. Serve},
  journal={Blood},
  year={2005},
  volume={106 1},
  pages={
          265-73
        }
}
  • C. Choudhary, J. Schwaeble, +7 authors H. Serve
  • Published 2005
  • Medicine, Biology
  • Blood
  • Activating mutations of Flt3 are found in approximately one third of patients with acute myeloid leukemia (AML) and are an attractive drug target. Two classes of Flt3 mutations occur: internal tandem duplications (ITDs) in the juxtamembrane and point mutations in the tyrosine kinase domain (TKD). We and others have shown that Flt3-ITD induced aberrant signaling including strong activation of signal transducer and activator of transcription 5 (STAT5) and repression of CCAAT/estradiol-binding… CONTINUE READING
    217 Citations
    SRC is a signaling mediator in FLT3-ITD- but not in FLT3-TKD-positive AML.
    • 58
    • PDF
    Activation mechanisms of STAT5 by oncogenic Flt3-ITD.
    • 183
    • PDF
    FLT3 activating mutations display differential sensitivity to multiple tyrosine kinase inhibitors
    • 19
    • PDF

    References

    SHOWING 1-10 OF 53 REFERENCES
    Overexpression and constitutive activation of FLT3 induces STAT5 activation in primary acute myeloid leukemia blast cells.
    • 174
    • PDF
    Flt3 receptor tyrosine kinase as a drug target in leukemia.
    • 68