FLT3

Overview

FLT3 is a receptor tyrosine kinase whose activating mutations drive proliferation in acute leukemias. In the corpus it is the most frequently mutated kinase in infant MLL-rearranged ALL PMID:25730765.

Alterations observed in the corpus

  • Activating mutations found in 19% of infant MLL-R ALL cases; often sub-clonal and frequently lost at relapse PMID:25730765.
  • Part of the kinase/PI3K/RAS signaling pathway mutations detected in 47% of infant MLL-R cases PMID:25730765.
  • Focal copy-number loss on chromosome 13 in anaplastic thyroid carcinoma (ATC) PMID:38412093.
  • Activating mutations (ITD and kinase domain) detected in pediatric ALL (St. Jude WGS/WES, 44 tumors); FLT3 alterations enriched in hyperdiploid B-ALL PMID:23334668
  • Mutated in 56/200 (28%) of AML cases; part of the activated-signaling category; mutually exclusive with other tyrosine kinases/RAS-family genes; co-occurs with NPM1 and DNMT3A PMID:23634996
  • FLT3 internal tandem duplications (ITDs) in AML serve as the conceptual parallel for the FGFR1 kinase-domain ITD identified in pilocytic astrocytoma PMID:23817572
  • FLT3 is listed among the genomic context genes in nasopharyngeal carcinoma (NPC) therapeutic development. PMID:24952746
  • FLT3-ITD present in 22% (341/1,540) of AML; deleterious effect strongest in NPM1+/DNMT3A+ context; FLT3-TKD is mutationally and prognostically distinct from FLT3-ITD (different co-mutation patterns, different interaction with KMT2A-PTD); FLT3 and RAS-pathway inhibitors expected to alter outcome predictions for respective subgroups PMID:27276561
  • FLT3 variant co-occurring with TET2 and KIT in an AML patient in the PIPseq pediatric cohort; KIT D816H as the primary targetable event PMID:28007021.

Cancer types (linked)

Co-occurrence and mutual exclusivity

Therapeutic relevance

  • Kinase/PI3K/RAS pathway mutations showed a trend toward poorer EFS and OS, suggesting potential utility for pathway-targeted therapy PMID:25730765.

Open questions

  • Sub-clonal FLT3 mutations are frequently lost at relapse, raising questions about their necessity for leukemic maintenance PMID:25730765.

Sources

This page was processed by entity-page-writer on 2026-05-11. - PMID:23334668

This page was processed by entity-page-writer on 2026-05-11. - PMID:23634996

This page was processed by entity-page-writer on 2026-05-11. - PMID:23817572

This page was processed by entity-page-writer on 2026-05-11. - PMID:24952746

This page was processed by entity-page-writer on 2026-05-11. - PMID:27276561

This page was processed by entity-page-writer on 2026-05-15. - PMID:28007021

This page was processed by wiki-cli on 2026-05-14.