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Review
. 2011 Apr 1:4:13.
doi: 10.1186/1756-8722-4-13.

Downstream molecular pathways of FLT3 in the pathogenesis of acute myeloid leukemia: biology and therapeutic implications

Affiliations
Review

Downstream molecular pathways of FLT3 in the pathogenesis of acute myeloid leukemia: biology and therapeutic implications

Shinichiro Takahashi. J Hematol Oncol. .

Abstract

FLT3 is a type III receptor tyrosine kinase. Mutations of FLT3 comprise one of the most frequently identified types of genetic alterations in acute myeloid leukemia. One-third of acute myeloid leukemia patients have mutations of this gene, and the majority of these mutations involve an internal tandem duplication in the juxtamembrane region of FLT3, leading to constitutive activation of downstream signaling pathways and aberrant cell growth. This review summarizes the current understanding of the effects of the downstream molecular signaling pathways after FLT3 activation, with a particular focus on the effects on transcription factors. Moreover, this review describes novel FLT3-targeted therapies, as well as efficient combination therapies for FLT3-mutated leukemia cells.

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Figures

Figure 1
Figure 1
Schematic presentation of the FLT3 receptor.
Figure 2
Figure 2
Mechanisms of FLT3-ITD induced leukemogenesis. Depicted is an outline of known pathways downstream of FLT3-ITD.

References

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