ArticlePloS one2015
Eltrombopag modulates reactive oxygen species and decreases acute myeloid leukemia cell survival.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 36 citations in OpenAlex.
- An unconquered challenge in MDS: review of pathophysiology, clinical manifestations, and management options of MDS with thrombocytopenia.Annals of hematology · 2025Review
- Emerging Roles of the Iron Chelators in Inflammation.International journal of molecular sciences · 2022Review
- Exploring the Potential of Eltrombopag: Room for More?Frontiers in pharmacology · 2022Article
- Osteosarcoma in Children: Not Only Chemotherapy.Pharmaceuticals (Basel, Switzerland) · 2021Review
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- Anticancer Activity of the Acetylenic Derivative of Betulin Phosphate Involves Induction of Necrotic-Like Death in Breast Cancer Cells In Vitro.Molecules (Basel, Switzerland) · 2021Article
- Current evidence and the emerging role of eltrombopag in severe aplastic anemia.Therapeutic advances in hematology · 2021Review
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- Switching thrombopoietin receptor agonist treatments in patients with primary immune thrombocytopenia.Therapeutic advances in hematology · 2019Review
- The synergistic antileukemic effects of eltrombopag and decitabine in myeloid leukemia cells.Cancer management and research · 2019Article
- Thrombopoietin receptor-independent stimulation of hematopoietic stem cells by eltrombopag.Science translational medicine · 2018Article
- Protein Kinase C Epsilon Is a Key Regulator of Mitochondrial Redox Homeostasis in Acute Myeloid Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- c-MPL provides tumor-targeted T-cell receptor-transgenic T cells with costimulation and cytokine signals.Blood · 2017Article
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- From chronic immune thrombocytopenia to severe aplastic anemia: recent insights into the evolution of eltrombopag.Therapeutic advances in hematology · 2017Review
- Revealing eltrombopag's promotion of human megakaryopoiesis through AKT/ERK-dependent pathway activation.Haematologica · 2016Article
- Thrombocytopenia in MDS: epidemiology, mechanisms, clinical consequences and novel therapeutic strategies.Leukemia · 2016Review
- Myelodysplastic Syndromes in the Elderly: Treatment Options and Personalized Management.Drugs & aging · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have demonstrated that the small molecule thrombopoietin (TPO) mimetic, eltrombopag (E), induces apoptosis in acute myeloid leukemia (AML) cells. Here, we sought to define the mechanism of the anti-leukemic effect of eltrombopag. Our studies demonstrate that, at a concentration of 5 μM E in 2% serum, E induces apoptosis in leukemia cells by triggering PARP cleavage and activation of caspase cascades within 2-6 hours. The induction of apoptotic enzymes is critically dependent on drug concentration and the concentration of serum. This effect is not associated with an alteration in mitochondrial potential but is associated with a rapid decrease in a reactive oxygen species (ROS) in particular hydrogen peroxide (H2O2). Interestingly, E also decreases mitochondrial maximal and spare respiratory capacities suggesting an induced mitochondrial dysfunction that may not be readily apparent under basal conditions but becomes manifest only under stress. Co-treatment of MOLM14 AML cells with E plus Tempol or H2O2 provides a partial rescue of cell toxicity. Ferric ammonioum citrate (FAC) also antagonized the E induced toxicity, by inducing notable increase in ROS level. Overall, we propose that E dramatically decreases ROS levels leading to a disruption of AML intracellular metabolism and rapid cell death.
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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.