FLT3


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FLT3

A gene on chromosome 13q12 that encodes a class-III receptor tyrosine kinase, which regulates haematopoiesis. FLT3 is activated by binding the fms-related tyrosine kinase 3 ligand to the extracellular domain, which induces homodimer formation in the plasma membrane leading to autophosphorylation of the receptor. The activated receptor kinase in turn phosphorylates and activates multiple cytoplasmic effectors involved in apoptosis, proliferation and differentiation of haematopoietic cells in bone marrow.

Molecular pathology
FLT3 mutations that activate the receptor are thought to induce acute (myeloid or lymphocytic) leukaemia.
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Flt3 protein is expressed on immature hematopoietic and lymphoid progenitors, and seems to play an important role in early stem cell survival and myeloid differentiation (6), (7).
FLT3 is fused to ETV6 in a myeloproliferative disorder with hypereosinophilia and a t(12; 13)(p13; q12) translocation.
FLT3-ITD mutations are generally associated with significant leukocytosis and poor response to chemotherapy; although both ITD and TKD mutations can activate the FLT3 receptor causing an uncontrolled proliferation of leukemic blasts, they result in distinct gene expression profiles as well as signal transduction patterns.
In contrast, some mutations, such as DNMT3A, NPM1, and FLT3, exhibit a strong tendency to co-occur.
An oral therapy, RYDAPT (midostaurin) is administered twice daily for adults with FLT3 mutation-positive AML.
56,67,95) Although many of the same mutations are found in MDS and de novo AML, mutations in TP53, NF1, U2AF1, SF3B1, EZH2, and BCOR appear more common in MDS, while mutations in FLT3, NPM1, DNMT3A, IDH1, and IDH2 are more common in AML.
CD117 expression is a sensitive but nonspecific predictor of FLT3 mutation in Tacute lymphoblastic leukemia and T/ myeloid acute leukemia.
In normal karyotype AML, overexpression of WT1 at diagnosis has been associated with decreased CR, DFS and OS in both Flt3 negative and Flt3 positive AML patients.
Eight cytokines in the plasma were quantitatively measured by Luminex assays, including Flt3 ligand (Flt3L), interferon (IFN)-a2, IFN-a, interleukin (IL)-10, IL-17A, IL-6, transforming growth factor (TGF) -[sz]1, and TGF-[sz]2.
If the FLT3 mutation is detected in blood or bone marrow samples using the LeukoStrat CDx FLT3 Mutation Assay, the patient may be eligible for treatment with Rydapt in combination with chemotherapy.
Detection of NPM1 exon 12 mutations and FLT3 - internal tandem duplications by high resolution melting analysis in normal karyotype acute myeloid leukemia.