Figure 4
Metabolic flux analysis reveals NPM-ALK–driven shift toward biomass production. (A) Quantitation of lactate levels by metabolomic analysis. Representative spectra for DMSO- (blue) and CEP- (red) treated cells. The quantitation of lactate based on 4 replicates is shown in the inset. (B) Metabolic flux analysis of lactate in SU-DHL-1 cell following 300 nM CEP treatment. All species of labeled lactate are shown. m, mass. (C) Flux analysis for fully labeled glucose 6-phosphate/fructose 6-phosphate (G6P/F6P), fructose bisphosphate (FBP), and ribose 5-phosphate/xylose 5-phosphate (R5P/X5P) are shown in the presence of DMSO or ALK inhibitor. (D) Total pool abundance (all labeled and unlabeled species combined) for ADP and ATP in the presence of DMSO or ALK inhibitor. (E) Biochemical assays for lactate and ATP after 300 nM CEP for 6 hours. Data are normalized by cell number. Mean ± SD; *P < .05, **P < .01.

Metabolic flux analysis reveals NPM-ALK–driven shift toward biomass production. (A) Quantitation of lactate levels by metabolomic analysis. Representative spectra for DMSO- (blue) and CEP- (red) treated cells. The quantitation of lactate based on 4 replicates is shown in the inset. (B) Metabolic flux analysis of lactate in SU-DHL-1 cell following 300 nM CEP treatment. All species of labeled lactate are shown. m, mass. (C) Flux analysis for fully labeled glucose 6-phosphate/fructose 6-phosphate (G6P/F6P), fructose bisphosphate (FBP), and ribose 5-phosphate/xylose 5-phosphate (R5P/X5P) are shown in the presence of DMSO or ALK inhibitor. (D) Total pool abundance (all labeled and unlabeled species combined) for ADP and ATP in the presence of DMSO or ALK inhibitor. (E) Biochemical assays for lactate and ATP after 300 nM CEP for 6 hours. Data are normalized by cell number. Mean ± SD; *P < .05, **P < .01.

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