ArticleClinical cancer research : an official journal of the American Association for Cancer Research2019
Targeting Glutamine Metabolism and Redox State for Leukemia Therapy.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
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Who cites it
116 citing papers in PubMed, 162 citations in OpenAlex.
- Glutaminase inhibition in combination with azacytidine in myelodysplastic syndromes: a phase 1b/2 clinical trial and correlative analyses.Nature cancer · 2024Trial
- Glutamine metabolism in health and disease.Signal transduction and targeted therapy · 2026Review
- Glutamine Metabolism in Health and Diseases.MedComm · 2026Review
- Article
- A novel role for transcription factor NFE2 in redox regulation and chemotherapy resistance in acute myeloid leukemia.Leukemia · 2026Article
- Functional cooperation between the B-cell receptor and NOTCH1 in regulating metabolic reprogramming in chronic lymphocytic leukemia.Leukemia · 2026Article
- BMAL1 modulates glutamine supply to control haematopoietic stem and progenitor cell expansion.Development (Cambridge, England) · 2026Article
- Molecular and Mechanistic Divergence of Seizures in Pediatric Acute Lymphoblastic Leukemia: CNS Infiltration Versus Chemotherapy-Induced Neurotoxicity.International journal of molecular sciences · 2026Review
- ProteinbioRxiv : the preprint server for biology · 2026Article
- Fueling the Fire: How Glutamine Metabolism Sustains Leukemia Growth and Resistance.BioMed (Basel, Switzerland) · 2026Article
- Intrinsic and niche-dependent metabolic regulation of haematopoietic stem cells and implications for leukaemogenesis.Nature cell biology · 2026Review
- Glutaredoxin 2 is essential for AML survival through mitochondrial permeability transition pore regulation.Blood · 2026Article
- Taurine is a natural suppressor of urea cycle via targeting ASL.Cell death discovery · 2026Article
- BCLAF1 links RNA splicing to ATF4-dependent metabolic adaptation in acute myeloid leukemia.bioRxiv : the preprint server for biology · 2026Article
- The Interdependence of Carbon Substrates and Metabolic Pathways Enables the Metabolic Plasticity of Cancer Cells.Advances in experimental medicine and biology · 2026Review
- High-Throughput Metabolomics in Transfusion Medicine.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Targeting CAF-specific metabolic pathways in breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Deciphering and targeting oncogenic pathways through integrated approaches and amino acid metabolism in hematologic malignancies.Discover oncology · 2025Review
- Therapeutic innovations: targeting ROS production in AML with natural and synthetic compounds.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The Critical Role of Adipocytes in Leukemia.Biology · 2025Review
56 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
purposeAcute myeloid leukemia (AML) is a hematologic malignancy characterized by the accumulation of immature myeloid precursor cells. AML is poorly responsive to conventional chemotherapy and a diagnosis of AML is usually fatal. More effective and less toxic forms of therapy are desperately needed. AML cells are known to be highly dependent on the amino acid glutamine for their survival. These studies were directed at determining the effects of glutaminase inhibition on metabolism in AML and identifying general weaknesses that can be exploited therapeutically. EXPERIMENTAL
designAML cancer cell lines, primary AML cells, and mouse models of AML and acute lymphoblastic leukemia (ALL) were utilized.
resultsWe show that blocking glutamine metabolism through the use of a glutaminase inhibitor (CB-839) significantly impairs antioxidant glutathione production in multiple types of AML, resulting in accretion of mitochondrial reactive oxygen species (mitoROS) and apoptotic cell death. Moreover, glutaminase inhibition makes AML cells susceptible to adjuvant drugs that further perturb mitochondrial redox state, such as arsenic trioxide (ATO) and homoharringtonine (HHT). Indeed, the combination of ATO or HHT with CB-839 exacerbates mitoROS and apoptosis, and leads to more complete cell death in AML cell lines, primary AML patient samples, and
conclusionsTargeting glutamine metabolism in combination with drugs that perturb mitochondrial redox state represents an effective and potentially widely applicable therapeutic strategy for treating multiple types of leukemia.
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Registered trials
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