American Journal of BioMedicine Volume 2, Issue 8, pages 992-1009, September 2014
Bill A. Lynch; Suzan M. Lyman; Jan H. Kasper
Abstract
The FMS-like tyrosine kinase 3 (FLT3-ITD) acute myeloid leukemia (AML) often present with more aggressive disease and have a significantly higher marrow blast percentage, higher likelihood of relapse, and shorter survival. Activating mutations of the kinase occur in about one third of patients with AML. The therapeutic approach for these patients has traditionally included intensive induction chemotherapy, followed by consolidative chemotherapy or hematopoietic cell transplantation (HCT). A number of small-molecule kinase inhibitors such as lestaurtinib (CEP-701), midostaurin (PKC412), and tandutinib (MLN518) block the autophosphorylation of FLT3 and lead to inhibition of cell proliferation and induction of apoptosis; they have demonstrated clinical activity in patients with AML, in particular those with mutations. This review summarizes what is known regarding the FLT3-ITD targeting therapy.
Keywords: Acute myeloid leukemia; FLT3-ITD; Chemotherapy; Targeting therapy
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