ArticleBlood cells, molecules & diseases2015
Targeting glutamine metabolism in myeloproliferative neoplasms.
Article in Blood cells, molecules & diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Metabolic pathways fuelling devil facial tumour diseases.The FEBS journal · 2026Article
- Metabolomic Profiling Reveals Distinct Signatures in Primary and Secondary Polycythemia.Metabolites · 2025Article
- A glutamine tug-of-war between cancer and immune cells: recent advances in unraveling the ongoing battle.Journal of experimental & clinical cancer research : CR · 2024Review
- Multiomic profiling reveals metabolic alterations mediating aberrant platelet activity and inflammation in myeloproliferative neoplasms.The Journal of clinical investigation · 2024Article
- Metabolomics: A Tool to Envisage Biomarkers in Clinical Interpretation of Cancer.Current drug research reviews · 2024Review
- Deepening Our Understanding of the Factors Affecting Landscape of Myeloproliferative Neoplasms: What Do We Know about Them?Cancers · 2023Review
- Rethinking glutamine metabolism and the regulation of glutamine addiction by oncogenes in cancer.Frontiers in oncology · 2023Review
- Article
- Circulating Biomarkers for Therapeutic Monitoring of Anti-cancer Agents.The oncologist · 2022Review
- Amino acid depletion triggered by ʟ-asparaginase sensitizes MM cells to carfilzomib by inducing mitochondria ROS-mediated cell death.Blood advances · 2020Article
- Metabolic Vulnerabilities and Epigenetic Dysregulation in Myeloproliferative Neoplasms.Frontiers in immunology · 2020Review
- Article
- Apatinib induces 3-hydroxybutyric acid production in the liver of mice by peroxisome proliferator-activated receptor α activation to aid its antitumor effect.Cancer science · 2019Article
- Review
- The elevated glutaminolysis of bladder cancer and T cells in a simulated tumor microenvironment contributes to the up-regulation of PD-L1 expression by interferon-γ.OncoTargets and therapy · 2018Article
- Metabolomics Applications in Precision Medicine: An Oncological Perspective.Current topics in medicinal chemistry · 2017Review
- From Krebs to clinic: glutamine metabolism to cancer therapy.Nature reviews. Cancer · 2016Review
- Emerging applications of metabolomics in drug discovery and precision medicine.Nature reviews. Drug discovery · 2016Review
- Evolving Therapeutic Strategies for the Classic Philadelphia-Negative Myeloproliferative Neoplasms.EBioMedicine · 2016Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
JAK2(V617F) mutation can be detected in the majority of myeloproliferative neoplasm (MPN) patients. The JAK2 inhibitor Ruxolitinib is the first FDA-approved treatment for MPNs. However, its use is limited by various dose related toxicities. Here, we studied the metabolic state and glutamine metabolism of BaF3-hEPOR-JAK2V617F and BaF3-hEPOR-JAK2WT cells. We found that the JAK2(V617F)-mutant cells were associated with increased oxygen consumption rate and extracellular acidification rate than the JAK2(WT) cells and there was an increased glutamine metabolism in JAK2(V617F)-mutant cells compared to wild-type cells. Glutaminase (GLS), the key enzyme in glutamine metabolism, was upregulated in the JAK2(V617F)-mutant BaF3 cells compared to the JAK2(WT) BaF3 cells. In MPN patient peripheral blood CD34+ cells, GLS expression was increased in JAK2(V617F)-mutant progenitor cells compared to JAK2 wild-type progenitor cells from the same patients and GLS levels were increased at the time of disease progression compared to at earlier time points. Moreover, GLS inhibitor increased the growth inhibitory effect of Ruxolitinib in both JAK2(V617F)-mutant cell lines and peripheral blood CD34+ cells from MPN patients. Therefore, GLS inhibitor should be further explored to enhance the therapeutic effectiveness of JAK2 inhibitor and allow the administration of lower doses of the drug to avoid its toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.