ArticleFrontiers in oncology2013
Mitochondrial uncoupling and the reprograming of intermediary metabolism in leukemia cells.
Article in Frontiers in oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 43 citations in OpenAlex.
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- A clinical pharmacokinetic drug-drug interaction study between dextromethorphan and emvododstat, a potent anti-SARS-CoV-2 dihydroorotate dehydrogenase inhibitor.European journal of clinical pharmacology · 2023Article
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- RETRACTED:Metabolites · 2022Article
- Novel Triterpenic Acid-Benzotriazole Esters Act as Pro-Apoptotic Antimelanoma Agents.International journal of molecular sciences · 2022Article
- Article
- UCP2 silencing restrains leukemia cell proliferation through glutamine metabolic remodeling.Frontiers in immunology · 2022Article
- Metabolic management of microenvironment acidity in glioblastoma.Frontiers in oncology · 2022Review
- Oxidative Stress and X-ray Exposure Levels-Dependent Survival and Metabolic Changes in Murine HSPCs.Antioxidants (Basel, Switzerland) · 2021Article
- Glutamine Homeostasis and Its Role in the Adaptive Strategies of the Blind Mole Rat, Spalax.Metabolites · 2021Article
- DHODH inhibition modulates glucose metabolism and circulating GDF15, and improves metabolic balance.iScience · 2021Article
- DHODH and cancer: promising prospects to be explored.Cancer & metabolism · 2021Review
- Mitochondrial metabolism as a target for acute myeloid leukemia treatment.Cancer & metabolism · 2021Review
- New strategies to treat AML: novel insights into AML survival pathways and combination therapies.Leukemia · 2021Review
- Bioenergetic Profiling of the Differentiating Human MDS Myeloid Lineage with Low and High Bone Marrow Blast Counts.Cancers · 2020Article
- On the Origin of ATP Synthesis in Cancer.iScience · 2020Review
- Long noncoding RNA PVT1 promotes tumor cell proliferation, invasion, migration and inhibits apoptosis in oral squamous cell carcinoma by regulating miR‑150‑5p/GLUT‑1.Oncology reports · 2020Article
- Fatty Acid Metabolism, Bone Marrow Adipocytes, and AML.Frontiers in oncology · 2020Review
- A mechanism for increased sensitivity of acute myeloid leukemia to mitotoxic drugs.Cell death & disease · 2019Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
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Abstract
Nearly 60 years ago Otto Warburg proposed, in a seminal publication, that an irreparable defect in the oxidative capacity of normal cells supported the switch to glycolysis for energy generation and the appearance of the malignant phenotype (Warburg, 1956). Curiously, this phenotype was also observed by Warburg in embryonic tissues, and recent research demonstrated that normal stem cells may indeed rely on aerobic glycolysis - fermenting pyruvate to lactate in the presence of ample oxygen - rather than on the complete oxidation of pyruvate in the Krebs cycle - to generate cellular energy (Folmes et al., 2012). However, it remains to be determined whether this phenotype is causative for neoplastic development, or rather the result of malignant transformation. In addition, in light of mounting evidence demonstrating that cancer cells can carry out electron transport and oxidative phosphorylation, although in some cases predominantly using electrons from non-glucose carbon sources (Bloch-Frankenthal et al., 1965), Warburg's hypothesis needs to be revisited. Lastly, recent evidence suggests that the leukemia bone marrow microenvironment promotes the Warburg phenotype adding another layer of complexity to the study of metabolism in hematological malignancies. In this review we will discuss some of the evidence for alterations in the intermediary metabolism of leukemia cells and present evidence for a concept put forth decades ago by lipid biochemist Feodor Lynen, and acknowledged by Warburg himself, that cancer cell mitochondria uncouple ATP synthesis from electron transport and therefore depend on glycolysis to meet their energy demands (Lynen, 1951; Warburg, 1956).
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