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FLT3 tyrosine kinase domain (TKD) mutation

Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.

IDBIO-FLT3-D835
TypeBiomarker
Aliases
FLT3 D835FLT3 I836FLT3-TKDFLT3-TKD (D835 / I836)Мутація тірозінкіназного домену FLT3 (TKD)
Statusreviewed 2026-04-27 | pending_clinical_signoff
DiseasesNone declared
SourcesSRC-ELN-AML-2022 SRC-NCCN-AML-2025 SRC-RATIFY-STONE-2017

Biomarker Facts

Biomarker typegene_mutation
Mutation details{"exon": "20 (activation loop)", "functional_impact": "Constitutive FLT3 kinase activation via activation-loop conformational change", "gene": "FLT3", "gene_hugo_id": "HGNC:3765", "hotspots": ["D835Y", "D835V", "D835H", "D835E", "I836 deletion / substitution"], "variant_type": "missense"}
Measurement
MethodPCR + EcoRV restriction digest (classical) OR NGS panel
Unitscategorical (positive/negative); VAF reported
Sensitivity requirementRapid TAT preferred at AML diagnosis; type-II FLT3 inhibitors (quizartinib) less active against TKD vs type-I (gilteritinib, midostaurin)
Actionability lookup{"gene": "FLT3", "variant": "D835Y"}
Related biomarkersBIO-FLT3-ITD BIO-NPM1

Notes

~7–10% of AML; can co-occur with FLT3-ITD. Type-I FLT3 inhibitors (midostaurin, gilteritinib, crenolanib) inhibit both ITD and TKD; type-II (quizartinib, sorafenib) bind only inactive conformation and are less effective against D835. FLT3-TKD also acts as a resistance mechanism to type-II inhibitors during therapy. ELN-2022 classifies FLT3-TKD without ITD as intermediate-risk (revised down from adverse).

Used By

Actionability

Biomarker