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In acute myeloid leukemia (AML), leukemia stem cells (LSCs) have self-renewal potential and are responsible for relapse. We previously showed that, in  Mll-AF9/NRAS G12Vmurine AML, CD69 expression marks an LSC-enriched subpopulation with enhanced  in vivo  self-renewal capacity. Here, we used CyTOF to define activated signaling pathways in LSC subpopulations in  Mll-AF9/NRAS G12VAML. Furthermore, we compared the signaling activation states of CD69 High  and CD36 High  subsets of primary human AML. The human CD69 High  subset expresses low levels of Ki67 and high levels of NFκB and pMAPKAPKII. Additionally, the human CD69 High  AML subset also has enhanced colony-forming capacity. We applied Bayesian network modeling to compare the global signaling network within the human AML subsets. We find that distinct signaling states, distinguished by NFκB and pMAPKAPKII levels, correlate with divergent functional subsets, defined by CD69 and CD36 expression, in human AML. Targeting NFκB with proteasome inhibition diminished colony formation.

CD69 marks a subpopulation of acute myeloid leukemia with enhanced colony forming capacity and a unique signaling activation state