ArticleBlood2013
Inhibiting glutamine uptake represents an attractive new strategy for treating acute myeloid leukemia.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 191 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Pegcrisantaspase in Combination With Venetoclax for Treatment of Relapsed or Refractory Acute Myeloid Leukemia
2157GCCC: a Phase I Trial of Calaspargase Pegol-mknl in Combination with High Dose Cytarabine and Idarubicin in Adult Patients with Newly Diagnosed Acute Myeloid Leukemia
Who cites it
191 citing papers in PubMed, 280 citations in OpenAlex.
- Proteomic profiling of breast cancer metabolism identifies SHMT2 and ASCT2 as prognostic factors.Breast cancer research : BCR · 2017Trial
- Application of Glutamine-enriched nutrition therapy in childhood acute lymphoblastic leukemia.Nutrition journal · 2016Trial
- Glutamine Metabolism in Health and Diseases.MedComm · 2026Review
- Plumbagin Is a PKM2 Activator That Modulates Glutamine Metabolism and Dependency in Leukemia.Metabolites · 2026Article
- Article
- Clinico-Metabolic Profiling Unraveled Key Metabolic Alterations Underlying the Pathophysiology of Chronic Myeloid Leukemia.ACS omega · 2026Article
- Function and regulatory mechanism of RNA-binding protein IGF2BP2 in obesity and cancers.Molecular biology reports · 2026Review
- Article
- Targeting the Glutamine Transporter SLC1A5 Enhances Sensitivity of Acute Myeloid Leukemia to MLN4924.Biomedicines · 2026Article
- Fueling the Fire: How Glutamine Metabolism Sustains Leukemia Growth and Resistance.BioMed (Basel, Switzerland) · 2026Article
- Glutamine metabolism drives tumor aggressiveness but not chemoresistance in ovarian carcinoma cell lines.Translational cancer research · 2025Article
- Repurposing Asparaginase Therapy to Target Cisplatin-Resistant Cancer Cells.Fundamental & clinical pharmacology · 2025Article
- Metabolic Signature ofJournal of personalized medicine · 2025Review
- Metabolomic Profiling and Bioanalysis of Chronic Myeloid Leukemia: Identifying Biomarkers for Treatment Response and Disease Monitoring.Metabolites · 2025Article
- The Critical Role of Adipocytes in Leukemia.Biology · 2025Review
- WNK1 signalling regulates amino acid transport and mTORC1 activity to sustain acute myeloid leukaemia growth.Nature communications · 2025Article
- Review
- Understanding and Targeting Metabolic Vulnerabilities in Acute Myeloid Leukemia: An Updated Comprehensive Review.Cancers · 2025Review
- Article
- Article
131 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 9 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells require nutrients and energy to adapt to increased biosynthetic activity, and protein synthesis inhibition downstream of mammalian target of rapamycin complex 1 (mTORC1) has shown promise as a possible therapy for acute myeloid leukemia (AML). Glutamine contributes to leucine import into cells, which controls the amino acid/Rag/mTORC1 signaling pathway. We show in our current study that glutamine removal inhibits mTORC1 and induces apoptosis in AML cells. The knockdown of the SLC1A5 high-affinity transporter for glutamine induces apoptosis and inhibits tumor formation in a mouse AML xenotransplantation model. l-asparaginase (l-ase) is an anticancer agent also harboring glutaminase activity. We show that l-ases from both Escherichia coli and Erwinia chrysanthemi profoundly inhibit mTORC1 and protein synthesis and that this inhibition correlates with their glutaminase activity levels and produces a strong apoptotic response in primary AML cells. We further show that l-ases upregulate glutamine synthase (GS) expression in leukemic cells and that a GS knockdown enhances l-ase-induced apoptosis in some AML cells. Finally, we observe a strong autophagic process upon l-ase treatment. These results suggest that l-ase anticancer activity and glutamine uptake inhibition are promising new therapeutic strategies for AML.
Indexed as
Identifiers
What OpenQuestion holds
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.