ArticleLeukemia2015
Pathological glycogenesis through glycogen synthase 1 and suppression of excessive AMP kinase activity in myeloid leukemia cells.
Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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Who cites it
33 citing papers in PubMed, 70 citations in OpenAlex.
- A novel combination approach targeting P300 and DNA-PK exploits epigenetic dependencies in acute myeloid leukemia.Molecular therapy. Oncology · 2026Article
- Linolamide in apoptotic bodies: a key factor in mesenchymal stem cell immunotherapy for two abortion models.Stem cell research & therapy · 2025Article
- Discrimination of superficial lymph nodes using ultrasonography and tissue metabolomics coupled with machine learning.Frontiers in oncology · 2025Article
- Article
- Gluconeogenesis and glycogenolysis required in metastatic breast cancer cells.Frontiers in oncology · 2024Article
- Glycogen synthase 1 targeting reveals a metabolic vulnerability in triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2023Article
- Metabolic targeting of malignant tumors: a need for systemic approach.Journal of cancer research and clinical oncology · 2023Review
- GBE1 Promotes Glioma Progression by Enhancing Aerobic Glycolysis through Inhibition of FBP1.Cancers · 2023Article
- Adenosine Monophosphate Activated Protein Kinase (AMPK) enhances chemotherapy response in Acute Myeloid Leukemia (AML).Cancer letters · 2022Article
- Pitavastatin Is Anti-Leukemic in a Bone Marrow Microenvironment Model of B-Lineage Acute Lymphoblastic Leukemia.Cancers · 2022Article
- Revealing the Mysteries of Acute Myeloid Leukemia: From Quantitative PCR through Next-Generation Sequencing and Systemic Metabolomic Profiling.Journal of clinical medicine · 2022Review
- Integrated genomic-metabolic classification of acute myeloid leukemia defines a subgroup with NPM1 and cohesin/DNA damage mutations.Leukemia · 2021Article
- Article
- Aurora Kinase B Expression, Its Regulation and Therapeutic Targeting in Human Retinoblastoma.Investigative ophthalmology & visual science · 2021Article
- Mitochondrial Effects on Seeds of Cancer Survival in Leukemia.Frontiers in oncology · 2021Review
- Cellular Metabolomics Profiles Associated With Drug Chemosensitivity in AML.Frontiers in oncology · 2021Article
- GBE1 Is an Independent Prognostic Marker and Associated With CD163Frontiers in oncology · 2021Article
- Functional proteomic analysis reveals roles for PKCδ in regulation of cell survival and cell death: Implications for cancer pathogenesis and therapy.Advances in biological regulation · 2020Article
- Hypoxia-induced GBE1 expression promotes tumor progression through metabolic reprogramming in lung adenocarcinoma.Signal transduction and targeted therapy · 2020Article
- The differential activation of metabolic pathways in leukemic cells depending on their genotype and micro-environmental stress.Metabolomics : Official journal of the Metabolomic Society · 2020Article
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 5 countries.
Funding
Abstract
The rapid proliferation of myeloid leukemia cells is highly dependent on increased glucose metabolism. Through an unbiased metabolomics analysis of leukemia cells, we found that the glycogenic precursor UDP-D-glucose is pervasively upregulated, despite low glycogen levels. Targeting the rate-limiting glycogen synthase 1 (GYS1) not only decreased glycolytic flux but also increased activation of the glycogen-responsive AMP kinase (AMPK), leading to significant growth suppression. Further, genetic and pharmacological hyper-activation of AMPK was sufficient to induce the changes observed with GYS1 targeting. Cancer genomics data also indicate that elevated levels of the glycogenic enzymes GYS1/2 or GBE1 (glycogen branching enzyme 1) are associated with poor survival in AML. These results suggest a novel mechanism whereby leukemic cells sustain aberrant proliferation by suppressing excess AMPK activity through elevated glycogenic flux and provide a therapeutic entry point for targeting leukemia cell metabolism.
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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.