Suppression of myeloid transcription factors and induction of STAT response genes by AML-specific Flt3 mutations.

@article{Mizuki2003SuppressionOM,
  title={Suppression of myeloid transcription factors and induction of STAT response genes by AML-specific Flt3 mutations.},
  author={M. Mizuki and Joachim Schwable and C. Steur and C. Choudhary and Shuchi Agrawal and B. Sargin and B. Steffen and I. Matsumura and Y. Kanakura and F. B{\"o}hmer and C. M{\"u}ller-Tidow and W. Berdel and H. Serve},
  journal={Blood},
  year={2003},
  volume={101 8},
  pages={
          3164-73
        }
}
  • M. Mizuki, Joachim Schwable, +10 authors H. Serve
  • Published 2003
  • Biology, Medicine
  • Blood
  • 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 duplications (ITDs) in the juxtamembrane domain of the receptor occur in 25% of AML cases. Previously, we have shown that these mutations activate the receptor and induce leukemic transformation. In this study, we performed genome-wide parallel expression analyses of 32Dcl3 cells stably transfected with either… CONTINUE READING
    310 Citations
    Signal Transduction of Oncogenic Flt3
    • 92
    Activation mechanisms of STAT5 by oncogenic Flt3-ITD.
    • 183
    • PDF
    Mutant FLT3 signaling contributes to a block in myeloid differentiation
    • 32

    References

    SHOWING 1-10 OF 57 REFERENCES
    Constitutive activation of FLT3 in acute myeloid leukaemia and its consequences for growth of 32D cells
    • 169
    Essential Role of Signal Transducer and Activator of Transcription (Stat)5a but Not Stat5b for Flt3-Dependent Signaling
    • 208
    • PDF