Activating FLT3 mutations are one of the most frequently affected genetic abnormalities in acute myeloid leukemia (AML) and are present in about 30–40% of newly diagnosed patients . As a member of the type III receptor tyrosine kinase subfamily, including c-KIT, c-FMS and PDGFR-α/β, it is involved in proliferation and differentiation of myeloid progenitor cells . In cytogenetically normal AML, internal tandem duplications of the FLT3 gene (FLT3-ITDs) are associated with an unfavorable prognosis due to a high relapse rate, whereas the prognostic impact of point mutations within the tyrosine kinase domain (FLT3-TKDs) remains controversial . Nevertheless, FLT3-TKDs can occur after treatment with certain FLT3 tyrosine kinase inhibitors (TKIs) as a mechanism of resistance, thus implicating an adverse prognosis .
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