AFFILIATIONS – underline presenting author

BACKGROUND/AIMS: Acute myeloid leukemia (AML) is a clinically challenging disease with high interpatient variability in response to chemotherapy. Despite continuing advances in treatment options, current 5-year survival rates for pediatric AML are suboptimal at ~60%. Variability in treatment response and survival outcomes are due in part to the heterogeneous nature of AML, with many genetic lesions and cytogenetic features contributing to disease progression. One of the most well known genetic lesions associated with AML involves Fms-Like Tyrosine Kinase-3 (FLT3), a receptor tyrosine kinase expressed in hematopoietic stem cells. Internal tandem duplication of the juxtamembrane domain coding sequence of FLT3 (FLT3/ITD) causes autonomous cellular proliferations leading to disease progression. Previous metabolomics studies have successfully identified significant metabolic alterations in hematological malignancies. However, no metabolomics studies on pediatric AML have been reported at this time. In this study, we propose to use global and targeted metabolomics to identify differential metabolite abundance, metabolic profile, and pathway activity associated with FLT3-ITD status in pediatric AML patients treated in the St Jude AML02 clinical trial.