6544 Background: Pediatric trisomy 21 was present in 90% of patients by CNV detection. Fusions were only found in 5% of infant AML (p=0.02) vs. 29.2% - 34.5% in other groups. FLT3 variants were lower in infant (10%) and childhood AML (13.7%) vs. adolescent (25.5%) EZH2 CNV loss (7q36) were more prevalent in YA & childhood AML (4.7% & 3.4% vs. 0%). Upon aggregating genes by their molecular function, infant AML had a lower prevalence of variants in epigenetic genes (6.7% vs. 15.57-24.8%, p=0.02), RAS (10% vs. 23.2%-25.5%), & signaling genes (16.7% vs. 27.5% – 41.2%). Variants in DNA repair genes were more frequent in adolescent AML (13.7% vs. 3.9% - 6.7%, p=0.01). Conclusions: Infant, childhood, adolescent, & YA AML harbor unique genetic profiles that distinguish themselves from each other and reflect divergent and evolutionarily favored mechanisms behind leukemogenesis. Understanding these genetic profiles can help predict prognosis & help tailor more effective treatments.
Scarpa et al. (Wed,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: