ArticleCells2020
Targeting Cellular Metabolism in Acute Myeloid Leukemia and The Role of Patient Heterogeneity.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Glycolysis and glycolytic enzymes in acute myeloid leukemia: Warburg and beyond.Frontiers in pharmacology · 2026Review
- Targeting aerobic glycolysis by quercetin inhibits acute monocytic leukemia SHI-1 cells.Annals of medicine and surgery (2012) · 2025Article
- The effect of 2-Deoxy-D-glucose on glycolytic metabolism in acute myeloblastic leukemic ML-1 cells.Scientific reports · 2025Article
- Article
- Review
- Metabolic Function and Therapeutic Potential of CD147 for Hematological Malignancies: An Overview.International journal of molecular sciences · 2024Review
- Leukemic Stem Cells and Hematological Malignancies.International journal of molecular sciences · 2024Review
- Metformin: A potential adjunct for treatment of systemic mastocytosis.The journal of allergy and clinical immunology. Global · 2024Article
- Combined GLUT1 and OXPHOS inhibition eliminates acute myeloid leukemia cells by restraining their metabolic plasticity.Blood advances · 2023Article
- Molecular Insight into Iron Homeostasis of Acute Myeloid Leukemia Blasts.International journal of molecular sciences · 2023Article
- Targeting Glutamine Metabolism as an Attractive Therapeutic Strategy for Acute Myeloid Leukemia.Current treatment options in oncology · 2023Review
- Review
- Advancements in Oncoproteomics Technologies: Treading toward Translation into Clinical Practice.Proteomes · 2023Review
- Heterogeneity of Patient-Derived Acute Myeloid Leukemia Cells Subjected to SYK In Vitro Inhibition.International journal of molecular sciences · 2022Article
- A statistical network pre-processing method to improve relevance and significance of gene lists in microarray gene expression studies.BMC bioinformatics · 2022Article
- Metabolic Reprogramming in Hematologic Malignancies: Advances and Clinical Perspectives.Cancer research · 2022Review
- Review
- High Metabolic Dependence on Oxidative Phosphorylation Drives Sensitivity to Metformin Treatment inCancers · 2022Article
- Metformin and Thymoquinone Synergistically Inhibit Proliferation of Imatinib-Resistant Human Leukemic Cells.Frontiers in pharmacology · 2022Article
- Exploring the Metabolic Landscape of AML: From Haematopoietic Stem Cells to Myeloblasts and Leukaemic Stem Cells.Frontiers in oncology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is an aggressive blood cancer resulting in accumulation of immature, dysfunctional blood cells in the bone marrow. Changes in cell metabolism are features of many cancers, including AML and this may be exploited as a therapeutic target. In this study we investigated the in vitro antileukemic effects of seven metabolic inhibitors that target different metabolic pathways. The metabolic inhibitors were tested on AML cells derived from 81 patients using proliferation and viability assays; we also compared global gene expression and proteomic profiles for various patient subsets. Metformin, 2DG, 6AN, BPTES and ST1326 had strong antiproliferative and proapoptotic effects for most patients, whereas lonidamine and AZD3965 had an effect only for a minority. Antiproliferative effects on AML cells were additive when combined with the chemotherapeutic agent AraC. Using unsupervised hierarchical clustering, we identified a strong antiproliferative effect on AML cells after treatment with metabolic inhibitors for a subset of 29 patients. Gene expression and proteomic studies suggested that this subset was characterized by altered metabolic and transcriptional regulation. In addition, the Bcl-2 inhibitor venetoclax, in combination with 2DG or 6AN, increased the antiproliferative effects of these metabolic inhibitors on AML cells. Therapeutic targeting of cellular metabolism may have potential in AML, but the optimal strategy will likely differ between patients.
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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.