| 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 |
| DOI: |
10.1158/1078-0432.22471412.v1 |
| 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 |
| Externí odkaz: |
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