FLT3 is a member of the platelet-derived growth factor receptor subfamily, with 2 types of mutations having prognostic significance in AML. FLT3 Internal Tandem Duplications (ITD) result in an in-frame duplication of a region of the juxtamembrane domain, allowing ligand-independent dimerisation of the receptor to occur, leading to activation of the kinase and the downstream signalling pathways. The second type of variants observed in FLT3 are in the tyrosine kinase domain (TKD), with the most common variants affecting p.Asp835/p.Ile836 resulting in amino acid substitution/deletion. Variants affecting these amino acids again lead to ligand-independent dimerisation of the receptor and therefore activation of the kinase and the downstream signalling pathways.
In this programme, participants are provided with lyophilised cell-lines or patient derived material for FLT3 mutation status analysis. Participants are asked to submit a qualitative result as well as the size of the ITD if applicable, together with details of the methodology.
In addition to the two trial samples issued for FLT3-ITD analysis, one educational sample per trial distribution will be issued for FLT3 tyrosine kinase domain (TKD) (p.Asp835/p.Ile836) analysis from 2022/23.
Instructions for storage, reconstitution and use of the lyophilised samples are included with the samples. Three send-outs are issued per annum, with each send-out consisting of two samples. Periodically, additional educational samples may be dispatched alongside scored trial samples. FLT3 mutations, if present, should be expected at 'diagnostic' levels.
No activities in relation to this EQA programme are subcontracted.
To register for this programme, please click here.