Supplemental Methods, Fig S1, Fig S2, Fig S3, Fig S4, Fig S5, Fig S6, Fig S7, Fig S8, Fig S9, Fig S10, Fig S11, Fig S12. from Reactive Oxygen Species Drive Proliferation in Acute Myeloid Leukemia via the Glycolytic Regulator PFKFB3

<p>This file contains Supplemental Methods, Supplemental Table S1 showing Comparison of gene changes in human hematopoietic cord blood (CD34+) mixed progenitor cells transduced with N-RASG12D or control (expressing GFP alone); Supplemental Fig. S1. Infection of human hematopoietic stem progenitor cells with mutant N-RASG12D; Supplemental Fig. S2. Over expression of NOX2 mRNA in AML; Supplemental Fig. S3. Glucose uptake in HSPC expressing mutant RAS; Supplemental Fig. S4. Validation of ROS production in AML patient blasts for the analysis of global biochemicals using ultra-high performance liquid chromatography-tandem MS (UPLC-MS/MS) and GC-MS; Supplemental Fig. S5. Random Forest analysis of AML ROShigh compared to AML ROSLow; Supplemental Fig. S6. Treatment of the Mv4;11 AML cell line with H2O2 increases biochemical levels within the pentose phosphate pathway; Supplemental Fig. S7. N-RASG12D and ROS dependent changes in protein expression of glycolytic enzymes; Supplemental Fig. S8. Validation of THP-1 AML cell line in which ROS production is ablated following NOX2 Knock down.; Supplemental Fig. S9. Hydrogen peroxide (GOX) induces proliferation in Mv4;11 leukemia cells. Supplemental Fig. S10. Effect of PFKFB3 overexpression and PFKFB3 knockdown on cell cycle distribution; Supplemental Fig. S11. ROS induced changes in p-AMPK / mTORC1 pathway; Supplemental Fig. S12. Determination of EC50 of 3PO and PFK158 on AML cell lines.</p>