Summary of metabolic vulnerabilities reported in hematological malignancies
| Metabolic pathways/targets . | Examples in hematological malignancies . | References . |
|---|---|---|
| Glycolysis | PFKFB3 was found to be upregulated in TKI-resistant CML | 52,92,117 |
| GLUT5 inhibition synergized with standard chemotherapy to eradicate AML cells | ||
| Glycolytic signatures upregulated in B-ALL | ||
| TCA cycle | Inhibition of OXPHOS/ETC tested in CML and AML | 64,80,81,83,125 |
| Upregulation of OXPHOS confers resistance to B-ALL | ||
| Fatty acid metabolism | Increased uptake of fatty acids confers chemoresistance in AML | 96,131 |
| Upregulation of fatty acid synthesis in the central nervous system ALL | ||
| Amino acids and their transporters | Depletion of exogenous arginine studied in AML and ALL | 66,77,82,87,88,133,134,137,141,148 |
| Inhibition of glutamine anaplerosis sensitizes AML cells to TKI therapy | ||
| Asparaginase used in the treatment of ALL | ||
| Targeting of the serine-glycine regulatory enzyme PRMT7 results in the reduction of CML LSCs | ||
| BCAA metabolism drives epigenetic rewiring in CML and AML | ||
| Increased expression of amino acid transporter LAT1 in AML and ALL |
| Metabolic pathways/targets . | Examples in hematological malignancies . | References . |
|---|---|---|
| Glycolysis | PFKFB3 was found to be upregulated in TKI-resistant CML | 52,92,117 |
| GLUT5 inhibition synergized with standard chemotherapy to eradicate AML cells | ||
| Glycolytic signatures upregulated in B-ALL | ||
| TCA cycle | Inhibition of OXPHOS/ETC tested in CML and AML | 64,80,81,83,125 |
| Upregulation of OXPHOS confers resistance to B-ALL | ||
| Fatty acid metabolism | Increased uptake of fatty acids confers chemoresistance in AML | 96,131 |
| Upregulation of fatty acid synthesis in the central nervous system ALL | ||
| Amino acids and their transporters | Depletion of exogenous arginine studied in AML and ALL | 66,77,82,87,88,133,134,137,141,148 |
| Inhibition of glutamine anaplerosis sensitizes AML cells to TKI therapy | ||
| Asparaginase used in the treatment of ALL | ||
| Targeting of the serine-glycine regulatory enzyme PRMT7 results in the reduction of CML LSCs | ||
| BCAA metabolism drives epigenetic rewiring in CML and AML | ||
| Increased expression of amino acid transporter LAT1 in AML and ALL |