Article Abstract

Rational for targeting the hedgehog signalling pathway in acute myeloid leukemia with FLT3 mutation

Authors: Didier Bouscary

Abstract

The FLT3 gene is frequently altered in acute myeloid leukemia (AML) and represents a hallmark of adverse prognosis (1). FLT3-ITD mutation induces constitutive tyrosine kinase activity of the receptor which is located in the endoplasmic reticulum (ER) where it activates STAT5. Clinical trials using FLT3 tyrosine kinase inhibitors (TKI) as monotherapy in AML patients with FLT3 mutation show clinical activity but failed to demonstrate long lasting remissions.

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