Targeting mitochondrial metabolism in acute myeloid leukemia
| Autor: | Martin S Ta Llman, Robert T. Williams, Kıvanç Birsoy, Maximillian Stahl, Madison Rush Rex |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Cancer Research
business.industry Venetoclax medicine.medical_treatment Myeloid leukemia Antineoplastic Agents Hematology Enasidenib Isocitrate Dehydrogenase Targeted therapy Citric acid cycle chemistry.chemical_compound Leukemia Myeloid Acute Isocitrate dehydrogenase Oncology chemistry Cancer research Medicine Humans business Mubritinib Dihydroorotate Dehydrogenase Inhibitor |
| Zdroj: | Leukemialymphoma. 63(3) |
| ISSN: | 1029-2403 |
| Popis: | Cancer cells reprogram their metabolism to maintain sustained proliferation, which creates unique metabolic dependencies between malignant and healthy cells that can be exploited for therapy. In acute myeloid leukemia (AML), mitochondrial inhibitors that block tricarboxylic acid cycle enzymes or electron transport chain complexes have recently shown clinical promise. The isocitrate dehydrogenase 1 inhibitor ivosidenib, the isocitrate dehydrogenase 2 inhibitor enasidenib, and the BH3 mimetic venetoclax received FDA approval for treatment of AML in the last few years. Other mitochondrial inhibitors including CPI-613, CB-839, dihydroorotate dehydrogenase inhibitors, IACS-010759, and mubritinib, have shown encouraging preclinical efficacy and are currently being evaluated in clinical trials. In this review, we summarize recent metabolism-based therapies and their ability to target altered cancer metabolism in AML. |
| Databáze: | OpenAIRE |
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