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Article

Pediatric AML primary samples with FLT3/ITD mutations are preferentially killed by FLT3 inhibition.

Blood - 15 Sept 2004

Brown Patrick, Meshinchi Soheil, Levis Mark, Alonzo Todd A, Gerbing Robert, Lange Beverly, Arceci Robert, Small Donald

Abstract excerpt

Pediatric acute myelogenous leukemia (AML) has a poor prognosis, and novel therapies are needed. The FLT3 tyrosine kinase represents a promising target in pediatric AML. FLT3 is constitutively activated either by an internal tandem duplication (ITD) or by a point mutation (PM) in 17% to 24% of pediatric AML cases. Autocrine stimulation of wild-type (WT) FLT3 by coexpressed FLT3 ligand (FL) occurs in many other...

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Source

Identifiers

PMID: 15166029
DOI: 10.1182/blood-2004-03-1034

Genes

FLT3

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Pediatric AML primary samples with FLT3/ITD mutations are preferentially killed by FLT3 inhibition.PMID 15166029Read ↗

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