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Although somatic mutation burden in acute myeloid leukemia (AML) is low compared with other tumor types, there are certain genetic and epigenetic dysregulations typical for the disease. Examples of functional classes often disrupted by mutations in AML are: signalling and kinase pathways, nucleophosmin (NPM1) functions, transcription factors, tumor suppressors, spliceosome complexes, cohesin complexes and epigenetic modifiers (DNA methylation and chromatin modification).1 Cytogenetic information is used at diagnosis to stratify adult patients with AML into risk categories (favorable, intermediate, unfavorable)2, 3, however, pediatric AML is different to adult AML, both in terms of genomic alterations and therapeutic response.
Daelynn R Buelow, Division of Pharmaceutics and Pharmaceutical Chemistry, Ohio State University, US, and colleagues4 conducted a study to define and understand mutations that occur alongside the common Fms-like tyrosine kinase 3 (FLT3 ) -internal tandem duplication (ITD) mutation in pediatric AML.3 They used RNA sequencing and an analysis of known AML associated gene mutations (MLL-PTD, DNMT3A, U2AF1, FLT3 -ITD, and IDH2) to identify co-occurring mutations and analyse changes in clonal heterogeneity between diagnosis and relapse (by the assessment of variant allele frequency; VAF) in a cohort of 37 cytogenetically normal FLT3-ITD–positive pediatric patients with AML.
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