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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Midostaurin is an experimental drug that inhibits many enzymes, including mutant FLT3.
In nonstudy patients with CN-AML, testing for mutations in the NPM1, CEBPA, or FLT3 genes is not currently considered mandatory, but it is recommended.
Nucleophosmin mutation in Southeast Asian acute myeloid leukemia: eight novel variants, FLT3 coexistence and prognostic impact of NPM1/FLT3 mutations.
Based on results, the company that makes the drug, Ambit Biosciences, is planning larger Phase III trials, in which patients who have the FLT3 mutation will receive either quizartinib or chemotherapy after random grouping.
There has been great interest in using FLT3 drugs to treat AML, but their effectiveness has been limited because leukaemia cells gain new mistakes in the FLT3 gene, causing resistance," said Dr Spiros Linardopoulos, researcher at the ICR, in a statement.
We analyzed DNA from peripheral blood of 21 healthy subjects with this technique and did not detect any additional FLT3 signals.
FLT3 internal tandem duplication (ITD) mutations were more frequent in patients with APL than in other AML subtypes (17.
The traditional approach for diagnostic screening of Flt3 in AML patients involves PCR followed by gel electrophoresis (8, 9).
In two studies in the June Cancer Cell, Kelly and her colleagues report that drugs called PKC412 and CT53518 lock onto FLT3 in lab tests and mouse experiments.
Additionally, AML is associated with molecular gene mutations that are distinct from chromosomal structural abnormalities; of these, the best-studied is the FLT3 mutation (NCI, 2013).
A newly formed entity established by the existing shareholders of Flexus will retain, from and after the closing, all non-IDO/TDO assets of Flexus also to include those related to Flexus Phase 1 FLT3 and CDK4/6 inhibitor, its earlier stage small-molecule Treg cancer immunotherapy programs, and its current personnel and facilities.