Supplementary Data from Targeting Glutamine Metabolism and Redox State for Leukemia Therapy

Autor: James DeGregori, Angelo D’Alessandro, Kirk C. Hansen, Craig T. Jordan, Biniam Adane, Sarah Gehrke, Vadym Zaberezhnyy, Hae J. Park, Travis Nemkov, Mark A. Gregory
Rok vydání: 2023
Popis: Figure S1. The glutaminase inhibitor CB-839 impairs glutathione metabolism in FLT3WT AML cells. Figure S2. The glutaminase inhibitor CB-839 decreases glutathione levels, but does not increase total cellular ROS levels in AML cells. Figure S3. Antioxidant vitamin E suppresses mitoROS and apoptosis induced by CB-839/pro-oxidant combination therapies. Figure S4. CB-839 cooperates with the pro-oxidant drug ATO in inducing apoptosis, mitoROS and AML cell death. Figure S5. CB-839/HHT therapy induces total cellular ROS. AML cells that survive therapy are metabolically similar to drug naive cells and are not resistant to subsequent therapy. Figure S6. CB-839/ATO and CB-839/HHT combination therapies do not exhibit toxicity in vivo in mice or toward normal human CD34+ cells. Figure S7. CB-839 cooperates with HHT in inducing mitoROS and apoptosis in primary human AML cells and cell death/apoptosis in ALL cells. Table S1. Combination index (CI values) for drug combinations tested in cell viability assays. Table S2. The clinical characteristics of the AML cohort studied are summarized.
Databáze: OpenAIRE