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Journal articles on the topic 'Warburg hypothesis'

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Published: 3 June 2025

Last updated: 31 July 2025

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1

Liboff, Abraham R. "The Warburg hypothesis and weak ELF biointeractions." Electromagnetic Biology and Medicine 39, no. 2 (2020): 45–48. http://dx.doi.org/10.1080/15368378.2020.1737810.

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Kaczanowski, Szymon, Joanna Klim, and Urszula Zielenkiewicz. "An Apoptotic and Endosymbiotic Explanation of the Warburg and the Inverse Warburg Hypotheses." International Journal of Molecular Sciences 19, no. 10 (2018): 3100. http://dx.doi.org/10.3390/ijms19103100.

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Otto Warburg, a Nobel prize winner, observed that cancer cells typically “switch” from aerobic to anaerobic respiration. He hypothesized that mitochondrial damage induces neoplastic transformation. In contrast, pathological aging is observed mainly in neuron cells in neurodegenerative diseases. Oxidative respiration is particularly active in neurons. There is inverse comorbidity between cancer and neurodegenerative diseases. This led to the creation of the “inverse Warburg hypothesis”, according to which excessive mitochondrial activity induces pathological aging. The findings of our studies s

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Gonzalez, Claudio D., Silvia Alvarez, Alejandro Ropolo, Carla Rosenzvit, Maria F. Gonzalez Bagnes, and Maria I. Vaccaro. "Autophagy, Warburg, and Warburg Reverse Effects in Human Cancer." BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/926729.

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Autophagy is a highly regulated-cell pathway for degrading long-lived proteins as well as for clearing cytoplasmic organelles. Autophagy is a key contributor to cellular homeostasis and metabolism. Warburg hypothesized that cancer growth is frequently associated with a deviation of a set of energy generation mechanisms to a nonoxidative breakdown of glucose. This cellular phenomenon seems to rely on a respiratory impairment, linked to mitochondrial dysfunction. This mitochondrial dysfunction results in a switch to anaerobic glycolysis. It has been recently suggested that epithelial cancer cell

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Ganapathy, Vadivel, Muthusamy Thangaraju, and Puttur D. Prasad. "Nutrient transporters in cancer: Relevance to Warburg hypothesis and beyond." Pharmacology & Therapeutics 121, no. 1 (2009): 29–40. http://dx.doi.org/10.1016/j.pharmthera.2008.09.005.

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SHIOTA, G. "The hypothesis of Warburg revisited: A metabolic switch in carcinogenesis." Hepatology Research 36, no. 3 (2006): 156–57. http://dx.doi.org/10.1016/j.hepres.2006.08.012.

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Haowen, Jiang, Rachel L. Greathouse, Bo He, et al. "Abstract 2180: Deciphering the Warburg effect: Redox is the key to tumor differentiation." Cancer Research 82, no. 12_Supplement (2022): 2180. http://dx.doi.org/10.1158/1538-7445.am2022-2180.

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Abstract It was proposed by Warburg that the cause and consequence of the Warburg effect were the injury of respiration and cell dedifferentiation, respectively. However, the underlying mechanism was unclear due to limited understanding of metabolic control of epigenetics. Inhibition of mitochondrial electron transport chain (ETC) causes reduction of NAD+/NADH ratio. Recently it was discovered that this redox stress not only drives lactate production from pyruvate to enhance the Warburg effect, but also promotes the conversion of α-ketoglutarate (αKG) to 2-hydroxyglutarate (2HG), turning the s

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Schuster, Stefan, Daniel Boley, Philip Möller, Heiko Stark, and Christoph Kaleta. "Mathematical models for explaining the Warburg effect: a review focussed on ATP and biomass production." Biochemical Society Transactions 43, no. 6 (2015): 1187–94. http://dx.doi.org/10.1042/bst20150153.

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For producing ATP, tumour cells rely on glycolysis leading to lactate to about the same extent as on respiration. Thus, the ATP synthesis flux from glycolysis is considerably higher than in the corresponding healthy cells. This is known as the Warburg effect (named after German biochemist Otto H. Warburg) and also applies to striated muscle cells, activated lymphocytes, microglia, endothelial cells and several other cell types. For similar phenomena in several yeasts and many bacteria, the terms Crabtree effect and overflow metabolism respectively, are used. The Warburg effect is paradoxical a

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Alberghina, Lilia. "The Warburg Effect Explained: Integration of Enhanced Glycolysis with Heterogeneous Mitochondria to Promote Cancer Cell Proliferation." International Journal of Molecular Sciences 24, no. 21 (2023): 15787. http://dx.doi.org/10.3390/ijms242115787.

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The Warburg effect is the long-standing riddle of cancer biology. How does aerobic glycolysis, inefficient in producing ATP, confer a growth advantage to cancer cells? A new evaluation of a large set of literature findings covering the Warburg effect and its yeast counterpart, the Crabtree effect, led to an innovative working hypothesis presented here. It holds that enhanced glycolysis partially inactivates oxidative phosphorylation to induce functional rewiring of a set of TCA cycle enzymes to generate new non-canonical metabolic pathways that sustain faster growth rates. The hypothesis has b

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Hofmann, Peter. "Cancer and Exercise: Warburg Hypothesis, Tumour Metabolism and High-Intensity Anaerobic Exercise." Sports 6, no. 1 (2018): 10. http://dx.doi.org/10.3390/sports6010010.

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Rhodes, Christopher J. "The cancer hypothesis of pulmonary arterial hypertension: are polyamines the new Warburg?" European Respiratory Journal 56, no. 5 (2020): 2002350. http://dx.doi.org/10.1183/13993003.02350-2020.

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Akl, Maher Monir. "Glucolipotoxicity: A Novel Different Perspective on the Causes of Cancer." Cell & Cellular Life Sciences Journal 9, no. 1 (2024): 1–6. http://dx.doi.org/10.23880/cclsj-16000196.

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The Warburg effect, characterized by increased glucose uptake and lactate production in cancer cells even in the presence of oxygen, has long been recognized as a hallmark of cancer metabolism. This metabolic alteration provides cancer cells with a growth advantage, facilitating their rapid proliferation. The underlying mechanisms driving the Warburg effect involve dysregulated glucose metabolism, upregulation of glucose transporters, and metabolic reprogramming favoring glycolysis. The resulting accumulation of metabolic intermediates, such as lactate, contributes to the acidic tumor microenv

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McEwan, D. ""The Enemy of Hypothesis": Fritz Saxl as Acting Director of the Bibliothek Warburg." Leo Baeck Institute Yearbook 49, no. 1 (2004): 75–86. http://dx.doi.org/10.1093/leobaeck/49.1.75.

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Nijsten, Maarten W. N., and Gooitzen M. van Dam. "Hypothesis: Using the Warburg effect against cancer by reducing glucose and providing lactate." Medical Hypotheses 73, no. 1 (2009): 48–51. http://dx.doi.org/10.1016/j.mehy.2009.01.041.

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Isidoro, Antonio, Enrique Casado, Andrés Redondo, et al. "Breast carcinomas fulfill the Warburg hypothesis and provide metabolic markers of cancer prognosis." Carcinogenesis 26, no. 12 (2005): 2095–104. http://dx.doi.org/10.1093/carcin/bgi188.

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van Beek, Johannes H. G. M. "The dynamic side of the Warburg effect: glycolytic intermediates as buffer for fluctuating glucose and O2 supply in tumor cells." F1000Research 7 (August 2, 2018): 1177. http://dx.doi.org/10.12688/f1000research.15635.1.

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Background: Tumor cells show the Warburg effect: high glucose uptake and lactate production despite sufficient oxygen supply. Otto Warburg found this effect in tissue slices and in suspensions of Ehrlich ascites tumor cells. Remarkably, these ascites tumor cells can transiently take up glucose an order of magnitude faster than the steady high rate measured by Warburg for hours. Methods: The purpose of the transiently very high glucose uptake is investigated here with a computational model of glycolysis, oxidative phosphorylation and ATP consumption which reproduces short kinetic experiments on

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Neuzil, Jiri, and Rafael Moreno-Sanchez. "Editorial (Hot Topic: The Bioenergetics of Cancer, the Warburg Hypothesis and the Mitochondrial Function)." Current Pharmaceutical Biotechnology 14, no. 3 (2013): 249–50. http://dx.doi.org/10.2174/1389201011314030001.

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Reiter, Russel J., Ramaswamy Sharma, Qiang Ma, Sergio Rorsales-Corral, and Luiz G. de Almeida Chuffa. "Melatonin inhibits Warburg-dependent cancer by redirecting glucose oxidation to the mitochondria: a mechanistic hypothesis." Cellular and Molecular Life Sciences 77, no. 13 (2020): 2527–42. http://dx.doi.org/10.1007/s00018-019-03438-1.

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Kozal, Karolina, Paweł Jóźwiak, and Anna Krześlak. "Contemporary Perspectives on the Warburg Effect Inhibition in Cancer Therapy." Cancer Control 28 (January 2021): 107327482110412. http://dx.doi.org/10.1177/10732748211041243.

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In the 1920s, Otto Warburg observed the phenomenon of altered glucose metabolism in cancer cells. Although the initial hypothesis suggested that the alteration resulted from mitochondrial damage, multiple studies of the subject revealed a precise, multistage process rather than a random pattern. The phenomenon of aerobic glycolysis emerges not only from mitochondrial abnormalities common in cancer cells, but also results from metabolic reprogramming beneficial for their sustenance. The Warburg effect enables metabolic adaptation of cancer cells to grow and proliferate, simultaneously enabling

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Halma, Matthew T. J., Jack A. Tuszynski, and Paul E. Marik. "Cancer Metabolism as a Therapeutic Target and Review of Interventions." Nutrients 15, no. 19 (2023): 4245. http://dx.doi.org/10.3390/nu15194245.

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Cancer is amenable to low-cost treatments, given that it has a significant metabolic component, which can be affected through diet and lifestyle change at minimal cost. The Warburg hypothesis states that cancer cells have an altered cell metabolism towards anaerobic glycolysis. Given this metabolic reprogramming in cancer cells, it is possible to target cancers metabolically by depriving them of glucose. In addition to dietary and lifestyle modifications which work on tumors metabolically, there are a panoply of nutritional supplements and repurposed drugs associated with cancer prevention and

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Damaghi, Mehdi, Jeffrey West, Mark Robertson-Tessi, et al. "The harsh microenvironment in early breast cancer selects for a Warburg phenotype." Proceedings of the National Academy of Sciences 118, no. 3 (2021): e2011342118. http://dx.doi.org/10.1073/pnas.2011342118.

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The harsh microenvironment of ductal carcinoma in situ (DCIS) exerts strong evolutionary selection pressures on cancer cells. We hypothesize that the poor metabolic conditions near the ductal center foment the emergence of a Warburg Effect (WE) phenotype, wherein cells rapidly ferment glucose to lactic acid, even in normoxia. To test this hypothesis, we subjected low-glycolytic breast cancer cells to different microenvironmental selection pressures using combinations of hypoxia, acidosis, low glucose, and starvation for many months and isolated single clones for metabolic and transcriptomic pr

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Schwartsburd, P. M. "Adaptive Self-Defense of Mature Cells against Damage Is Based on the Warburg Effect, De-Differentiation of Cells and Resistance to Cell Death." Biofizika 69, no. 4 (2024): 778–85. http://dx.doi.org/10.31857/s0006302924040105.

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This review analyzes the hypothesis of the preserved ability of various specialized mammalian cells to protect themselves from lethal injury by enacting a protective atavistic mechanism of cell dedifferentiation. The development of such protection is accompanied by a transition of differentiated cells from the mitochondrial oxygen-dependent type of metabolism to regenerative oxygen-independent metabolism (called the Warburg effect). This transition allows cells to increase the resistance to cell death from hypoxia, and can also induce the emergence of fetal markers characteristic of cell dedif

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Parkinson, E. Kenneth, Jerzy Adamski, Grit Zahn, et al. "Extracellular citrate and metabolic adaptations of cancer cells." Cancer and Metastasis Reviews 40, no. 4 (2021): 1073–91. http://dx.doi.org/10.1007/s10555-021-10007-1.

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Abstract It is well established that cancer cells acquire energy via the Warburg effect and oxidative phosphorylation. Citrate is considered to play a crucial role in cancer metabolism by virtue of its production in the reverse Krebs cycle from glutamine. Here, we review the evidence that extracellular citrate is one of the key metabolites of the metabolic pathways present in cancer cells. We review the different mechanisms by which pathways involved in keeping redox balance respond to the need of intracellular citrate synthesis under different extracellular metabolic conditions. In this conte

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Keri, Ben, Howard Phang, Jaclyn Bergstrom, Stephen Dozier, Lina Scandalis, and Anthony Molina. "THE RELATIONSHIP BETWEEN CELLULAR GLYCOLYSIS AND AGE IN BLOOD CELLS OF ADULTS." Innovation in Aging 8, Supplement_1 (2024): 1170–71. https://doi.org/10.1093/geroni/igae098.3751.

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Abstract Mitochondrial dysfunction is a hallmark of aging that leads to inefficient cellular energy production, causing a shift towards aerobic glycolysis termed the Warburg Effect. While most studies examined the effect of aging on oxidative phosphorylation (OXPHOS), the relationships between glycolysis and age are less understood. Blood cells are a promising avenue for establishing biomarkers for their accessibility and versatility. We hypothesized that blood cells from older participants would have higher glycolytic function compared to blood cells from younger donors. We used blood collect

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Bahrami, Hassan, and Majid Tafrihi. "Understanding the Warburg Effect Yields New Insights into the Metabolic Control of Cancer." Journal of Cancer Research Updates 12 (December 7, 2023): 44–48. http://dx.doi.org/10.30683/1929-2279.2023.12.8.

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Human cells may use either aerobic or anaerobic cellular respiration processes to produce energy, depending on cellular conditions. When there is enough oxygen, cells respire aerobically, but in case of oxygen deficiency, anaerobic cellular respiration is used, which leads to lactic acidosis and an increased risk of cancer according to Warburg's hypothesis. This paper reviews key aspects related to the historical evolutionary origins of metabolic pathways in cancer cells and compares similarities between cancer cells and ancient unicellular organisms to address the origins of metabolic c

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Samudio, Ismael J., Michael Fiegl, Marina Konopleva, et al. "Targeting Anaplerotic Pathways That Support Fatty Acid Metabolism as a Therapeutic Strategy for Hematological Malignancies: The Achilles’ Heel of the Warburg Effect." Blood 112, no. 11 (2008): 1631. http://dx.doi.org/10.1182/blood.v112.11.1631.1631.

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Abstract More than half a century ago, Otto Warburg proposed that the origin of cancer cells was closely linked to a permanent respiratory defect that bypassed the Pasteur effect, i.e. the inhibition of anaerobic fermentation by oxygen. However, permanent and transmissible defects in the respiratory capacity of cancer cells that could broadly support Warburg’s hypothesis have not been identified. Notably, we have recently demonstrated that mitochondrial uncoupling – the abrogation of ATP synthesis in response to mitochondrial membrane potential – can promote the Warburg effect in leukemia cell

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Alawfi, Jumanah, and Lamis Alghamdi. "The Effect of Carbohydrates Intake, Free Sugars, and Ketogenic Diet on Cancer Development: Critical Review of the literature." Majmaah Journal of Health Sciences 10, no. 4 (2022): 95. http://dx.doi.org/10.5455/mjhs.2022.04.009.

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In 1920, Otto Warburg established the Warburg Effect which is defined as the unusual fuel generation by the cancer cells through their dependence on glucose metabolism. The aim of the current review is to present the evidence for the association between cancer development and carbohydrate intake and the ketogenic diet usefulness for these patients. Search was conducted in PubMed, Scopes, and Wiley Online Library during 5th November 2021 to 1st December 2021 with searching terms of sugar and cancer, carbohydrates intake and cancer, the ketogenic diet and cancer. RefWorks was used for managing t

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Bahrami, Hassan, Majid Tafrihi, and Ted Greiner. "A small-scale test of whether alkalizing diets can reduce the risk of disease as predicted by the Warburg Hypothesis." World Nutrition 14, no. 4 (2023): 3–15. http://dx.doi.org/10.26596/wn.20231443-15.

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Diet and so-called dietary acid load have a significant effect on what have traditionally been called acid-base disorders and various disease states, including cancer. However, the effect has been poorly investigated, and standards of care in medical treatments for cancer patients generally do not consider monitoring acid-base disorders and resolving them using dietary interventions.This paper begins by explaining the Warburg Hypothesis, focusing on dietary interventions thought to help maintain acid-base balance and reduce inflammation at the cellular level, as reflected in certain venous blo

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Reiter, Russel J., Ramaswamy Sharma, Qiang Ma, Sergio Rosales-Corral, Dario Acuna-Castroviejo, and Germaine Escames. "Inhibition of mitochondrial pyruvate dehydrogenase kinase: a proposed mechanism by which melatonin causes cancer cells to overcome cytosolic glycolysis, reduce tumor biomass and reverse insensitivity to chemotherapy." Melatonin Research 2, no. 3 (2019): 105–19. http://dx.doi.org/10.32794/mr11250033.

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This review presents a hypothesis to explain the role of melatonin in regulating glucose metabolism in cancer cells. Many cancer cells use cytosolic glycolysis (the Warburg effect) to produce energy (ATP). Under these conditions, glucose is primarily converted to lactate which is released into the blood in large quantities. The Warburg effect gives cancer cells advantages in terms of enhanced macromolecule synthesis required for accelerated cellular proliferation, reduced cellular apoptosis which enhances tumor biomass and a greater likelihood of metastasis. Based on available data, high circu

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Di Gregorio, Emanuela Di, Gianmaria Miolo, Asia Saorin, Agostino Steffan, and Giuseppe Corona. "From Metabolism to Genetics and Vice Versa: The Rising Role of Oncometabolites in Cancer Development and Therapy." International Journal of Molecular Sciences 22, no. 11 (2021): 5574. http://dx.doi.org/10.3390/ijms22115574.

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Over the last decades, the study of cancer metabolism has returned to the forefront of cancer research and challenged the role of genetics in the understanding of cancer development. One of the major impulses of this new trend came from the discovery of oncometabolites, metabolic intermediates whose abnormal cellular accumulation triggers oncogenic signalling and tumorigenesis. These findings have led to reconsideration and support for the long-forgotten hypothesis of Warburg of altered metabolism as oncogenic driver of cancer and started a novel paradigm whereby mitochondrial metabolites play

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Ren, Zhenxing, Cynthia Rajani, and Wei Jia. "The Distinctive Serum Metabolomes of Gastric, Esophageal and Colorectal Cancers." Cancers 13, no. 4 (2021): 720. http://dx.doi.org/10.3390/cancers13040720.

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Three of the most lethal cancers in the world are the gastrointestinal cancers—gastric (GC), esophageal (EC) and colorectal cancer (CRC)—which are ranked as third, sixth and fourth in cancer deaths globally. Early detection of these cancers is difficult, and a quest is currently on to find non-invasive screening tests to detect these cancers. The reprogramming of energy metabolism is a hallmark of cancer, notably, an increased dependence on aerobic glycolysis which is often referred to as the Warburg effect. This metabolic change results in a unique metabolic profile that distinguishes cancer

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Vallée, Alexandre, Yves Lecarpentier, Rémy Guillevin, and Jean-Noël Vallée. "Aerobic glycolysis in amyotrophic lateral sclerosis and Huntington’s disease." Reviews in the Neurosciences 29, no. 5 (2018): 547–55. http://dx.doi.org/10.1515/revneuro-2017-0075.

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AbstractNeurodegenerative cells are the sites of numerous metabolic and energetic abnormalities with abnormalities in energy production. Energy is the primary determinant of neuronal viability. In neurodegenerative cells, metabolic enzymes are modified by the dysregulation of the canonical WNT/β-catenin pathway. In amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD), WNT/β-catenin pathway is upregulated. We focused this review on the hypothesis of aerobic glycolysis stimulated by the upregulation of WNT/β-catenin pathway in ALS and HD. Upregulation of WNT/β-catenin pathway induce

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Dal Bello, Simone, Francesca Valdemarin, Deborah Martinuzzi, Francesca Filippi, Gian Luigi Gigli, and Mariarosaria Valente. "Ketogenic Diet in the Treatment of Gliomas and Glioblastomas." Nutrients 14, no. 18 (2022): 3851. http://dx.doi.org/10.3390/nu14183851.

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In recent years, scientific interest in the use of the ketogenic diet (KD) as a complementary approach to the standard cancer therapy has grown, in particular against those of the central nervous system (CNS). In metabolic terms, there are the following differences between healthy and neoplastic cells: neoplastic cells divert their metabolism to anaerobic glycolysis (Warburg effect), they alter the normal mitochondrial functioning, and they use mainly certain amino acids for their own metabolic needs, to gain an advantage over healthy cells and to lead to a pro-oncogenetic effect. Several work

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Carpentieri, A., E. Cozzoli, M. Scimeca, E. Bonanno, A. M. Sardanelli, and A. Gambacurta. "Differentiation of human neuroblastoma cells toward the osteogenic lineage by mTOR inhibitor." Cell Death & Disease 6, no. 11 (2015): e1974-e1974. http://dx.doi.org/10.1038/cddis.2015.244.

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Abstract Current hypothesis suggest that tumors can originate from adult cells after a process of 'reprogramming' driven by genetic and epigenetic alterations. These cancer cells, called cancer stem cells (CSCs), are responsible for the tumor growth and metastases. To date, the research effort has been directed to the identification, isolation and manipulation of this cell population. Independently of whether tumors were triggered by a reprogramming of gene expression or seeded by stem cells, their energetic metabolism is altered compared with a normal cell, resulting in a high aerobic glycoly

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Mirza, Zeenat, and Sajjad Karim. "Unraveling the Mystery of Energy-Sensing Enzymes and Signaling Pathways in Tumorigenesis and Their Potential as Therapeutic Targets for Cancer." Cells 13, no. 17 (2024): 1474. http://dx.doi.org/10.3390/cells13171474.

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Cancer research has advanced tremendously with the identification of causative genes, proteins, and signaling pathways. Numerous antitumor drugs have been designed and screened for cancer therapeutics; however, designing target-specific drugs for malignant cells with minimal side effects is challenging. Recently, energy-sensing- and homeostasis-associated molecules and signaling pathways playing a role in proliferation, apoptosis, autophagy, and angiogenesis have received increasing attention. Energy-metabolism-based studies have shown the contribution of energetics to cancer development, wher

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Lacerda-Abreu, Marco Antonio, Claudia Fernanda Dick, and José Roberto Meyer-Fernandes. "The Role of Inorganic Phosphate Transporters in Highly Proliferative Cells: From Protozoan Parasites to Cancer Cells." Membranes 13, no. 1 (2022): 42. http://dx.doi.org/10.3390/membranes13010042.

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In addition to their standard inorganic phosphate (Pi) nutritional function, Pi transporters have additional roles in several cells, including Pi sensing (the so-called transceptor) and a crucial role in Pi metabolism, where they control several phenotypes, such as virulence in pathogens and tumour aggressiveness in cancer cells. Thus, intracellular Pi concentration should be tightly regulated by the fine control of intake and storage in organelles. Pi transporters are classified into two groups: the Pi transporter (PiT) family, also known as the Pi:Na+ symporter family; and the Pi:H+ symporte

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Dauchy, Erin M., Robert T. Dauchy, Steven M. Hill, et al. "Abstract 222: Exposure to dim light at night disrupts the nocturnal melatonin signal in male nude rats bearing tissue-isolated castration-sensitive VCaP human prostate cancer: Impact on tumor circadian dynamics of the Warburg effect, lipid signaling and proliferation." Cancer Research 82, no. 12_Supplement (2022): 222. http://dx.doi.org/10.1158/1538-7445.am2022-222.

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Abstract Over 248,000 men in the U.S. alone this year will be diagnosed with prostate cancer, and over 33,300 will die from the disease. The World Health Organization, in the case of breast cancer, has classified night-shift work involving light at night (LAN)-induced circadian disruption to be a probable carcinogen (Class 2A). Exposure to LAN suppresses nighttime pineal melatonin (MLT) production that influences normal and neoplastic tissue metabolism, physiology, and proliferation. Previously, we showed in rodent and human tumors in vivo that MLT inhibits linoleic acid (LA)-uptake and conver

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Salmaggi, Andrea, Chiara Vasco, Ambra Rizzo, et al. "EXTH-01. A SYNGENIC MOUSE MODEL TO STUDY THE EFFICACY OF KETOGENIC DIET IN HIGH GRADE GLIOMAS." Neuro-Oncology 21, Supplement_6 (2019): vi82. http://dx.doi.org/10.1093/neuonc/noz175.335.

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Abstract Glioblastoma multiforme is the most malignant subtype of brain tumor. Despite multimodal treatment (surgical resection and chemo/radiotherapy) the prognosis remains unsatisfactory. Based on the Warburg hypothesis, ketogenic diet (KD) has been suggested in the treatment of GBM. The syngenic, orthotopic GL261 mouse glioma model was used to evaluate the effects of KD on 7T magnetic resonance imaging/spectroscopy and metabolic response of the tumor to diet. Mice were injected with 10^5 GL261 cells into the caudate nucleus. Following implantation, animals were fed standard chow for five da

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IG, Telessy. "The position of low carb diet in the cancer adjuvant therapy: Clinical nutrition with low carb diet in cancer patients." Asploro Journal of Biomedical and Clinical Case Reports 2, S1 (2019): 28–33. http://dx.doi.org/10.36502/2019/asjbccr.6139.

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Low carbohydrate diet (Low Carb Diet; LCD) is known for ages and exert a positive effect on the health-related quality of life in plenty of people [1]. It is also used over 100 years as a therapeutic tool in various illnesses. In epilepsy this – and the more aggressive version, the ketogenic diet (KD) – is a well-accepted evidence-based treatment modality for patients suffering from pharmacotherapy resistant type of the illness [2]. LCD is also used as a slimming diet among others under the name “Atkins diet“, that has been introduced for public ca. 50 years ago (Atkins Nutritional Approach).

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Iacobini, Carla, Martina Vitale, Giuseppe Pugliese та Stefano Menini. "Normalizing HIF-1α Signaling Improves Cellular Glucose Metabolism and Blocks the Pathological Pathways of Hyperglycemic Damage". Biomedicines 9, № 9 (2021): 1139. http://dx.doi.org/10.3390/biomedicines9091139.

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Intracellular metabolism of excess glucose induces mitochondrial dysfunction and diversion of glycolytic intermediates into branch pathways, leading to cell injury and inflammation. Hyperglycemia-driven overproduction of mitochondrial superoxide was thought to be the initiator of these biochemical changes, but accumulating evidence indicates that mitochondrial superoxide generation is dispensable for diabetic complications development. Here we tested the hypothesis that hypoxia inducible factor (HIF)-1α and related bioenergetic changes (Warburg effect) play an initiating role in glucotoxicity.

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Csomós, Bence, Dénes Fodor, and István Vajda. "Estimation of Battery Separator Area, Cell Thickness and Diffusion Coefficient Based on Non-Ideal Liquid-Phase Diffusion Modeling." Energies 13, no. 23 (2020): 6238. http://dx.doi.org/10.3390/en13236238.

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The aim of this work is to present a fast and in situ diffusion modeling technique to extract essential electrochemical parameters from liquid-phase diffusion which can be used to implement a realistic battery in a pseudo-2D finite element modeling environment. A generalized Warburg element was used within an extended Randles equivalent circuit to obtain an appropriate fit on non-ideal diffusion impedance. Based on the calculation method presented in this paper, the values of diffusion-related parameters such as the cross-sectional area of the separator Asep, cell thickness Lcell as well as li

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Jayaswal, Parth K., Taha Muhammad, Ashley Brown, Jeffrey Norris, and Shaleen B. Korch. "Abstract 3694: Metabolic response in human cervical cancer cells to modifications in bioavailable ATP." Cancer Research 83, no. 7_Supplement (2023): 3694. http://dx.doi.org/10.1158/1538-7445.am2023-3694.

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Abstract Introduction: Cancer cells utilize a markedly reduced oxidative phosphorylation (OXPHOS) when experiencing conditions of high oxygen stress (Warburg Effect/aerobic glycolysis), a phenomenon first studied by Otto Warburg. While there have been many discoveries associated with metabolic differences across cancer cells, one of the most common alterations is the primary means of generating ATP. The importance of deciphering these cellular decisions will enable an understanding of the multifaceted role ATP has in cancer proliferation, senescence, and chemotherapeutic resistance. The use of

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Hamaguchi, Reo, Masahide Isowa, Ryoko Narui, Hiromasa Morikawa, Toshihiro Okamoto, and Hiromi Wada. "How Does Cancer Occur? How Should It Be Treated? Treatment from the Perspective of Alkalization Therapy Based on Science-Based Medicine." Biomedicines 12, no. 10 (2024): 2197. http://dx.doi.org/10.3390/biomedicines12102197.

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This review article investigates the relationship between mitochondrial dysfunction and cancer progression, emphasizing the metabolic shifts that promote tumor growth. Mitochondria are crucial for cellular energy production, but they also play a significant role in cancer progression by promoting glycolysis even under oxygen-rich conditions, a phenomenon known as the Warburg effect. This metabolic reprogramming enables cancer cells to maintain an alkaline internal pH and an acidic external environment, which are critical for their proliferation and survival in hypoxic conditions. The article a

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Ospina, Hamlet Acevedo, and Albert Descoteaux. "Leishmania donovani modulates host macrophage mitochondrial metabolism, integrity, and function." Journal of Immunology 204, no. 1_Supplement (2020): 82.26. http://dx.doi.org/10.4049/jimmunol.204.supp.82.26.

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Abstract To colonize macrophages, Leishmania promastigotes employ virulence factors, including lipophosphoglycan (LPG), to impair host cell processes. Whereas previous studies revealed that Leishmania alters signaling axes that regulate mitochondrial function, scarce attention has been paid to the characterization of host cell mitochondrial metabolism during Leishmania infection and to the effectors involved therein. In this study, we addressed the hypothesis that L. donovani modulates host cell mitochondrial metabolism and function in an LPG-dependent manner. To this end, we infected bone-mar

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Goldberg, D. M., and E. P. Diamandis. "Models of neoplasia and their diagnostic implications: a historical perspective." Clinical Chemistry 39, no. 11 (1993): 2360–74. http://dx.doi.org/10.1093/clinchem/39.11.2360.

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Abstract In comparison with normal cells, cancer cells have an enhanced ability to trap both nitrogen and energy; an enhanced operation of the glycolytic and direct oxidative pathways, leading to accumulation of lactate and increased production of NADPH; and a greater content of lysosomal hydrolases. These changes represent a reprogramming of gene expression, which, at its most specific, is accompanied by the reappearance in the cell and ultimately in the body fluids of oncodevelopmental proteins not normally found in mature adult tissues. The most florid stage of this reprogramming leads to t

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Lisk, Christina, Francesca I. Cendali, Delany Swindle, et al. "Circulating Peripheral Blood Mononuclear Cells from Adults with Sickle Cell Disease (SCD)- Associated Pulmonary Hypertension (PH) Patients Have Increased Iron Content and a Unique Multi-Omic Signature." Blood 144, Supplement 1 (2024): 1116. https://doi.org/10.1182/blood-2024-211406.

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Introduction: The prevalence of PH in the SCD adult population is 6-10%, compared to approximately 3 in one million in the general population. However, the molecular mechanisms are not clearly defined, particularly as they relate to the onset and progression of SCD-PH. Previously, we have shown an accumulation of pulmonary vascular macrophages (Mϕ), iron, and hemoglobin (Hb) in SCD-PH, suggesting that hemolysis-mediated iron-overloading is a pathological contributor to progressive pulmonary vascular disease with SCD patients. Hypothesis: Here we hypothesized that PBMCs in SCD-PH patients will

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Kelsey, Maxfield M. G. "Reconsidering LINE-1’s role in cancer: does LINE-1 function as a reporter detecting early cancer-associated epigenetic signatures?" Evolution, Medicine, and Public Health 9, no. 1 (2021): 78–82. http://dx.doi.org/10.1093/emph/eoab004.

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Abstract Long interspersed nuclear element-1 (LINE-1 or L1) is the only autonomously active retrotransposon in humans. While L1 has been implicated in several pathologies and the aging process, I present a model which challenges an understanding of L1 as predominantly antagonistic to human health. I hypothesize that L1 serves as a reporter in an early cancer alert system: a tripwire strung throughout the genome poised to trigger p53 and a type I interferon (IFN-1) response when the epigenetic landscape portends cancer. Cell proliferation and a shift to aerobic glycolysis cause dramatic changes

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Zieker, D., I. Koenigsrainer, S. Beckert, et al. "Effect of changes in the glycolytic metabolism on tumor progression and dissemination in gastric cancer." Journal of Clinical Oncology 29, no. 4_suppl (2011): 47. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.47.

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47 Background: Metastases are a frequent finding in gastric cancer patients and are associated with a poor prognosis. Recent data indicate that there might be a link between metabolic changes in the glycolytic system and dissemination in gastric cancer. The enhanced expression of the glycolytic enzyme phosphoglycerate kinase 1 (PGK1) and its signalling targets CXCR4 and CXCL12 seem to play a crucial role in enabling gastric tumours to develop dissemination. Methods: Microarray analysis was conducted investigating human specimens from consecutive gastric cancer patients with dissemination versu

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Brücher, Björn L. D. M., and Ijaz S. Jamall. "Synopsis: Special Issue on “Disruption of signaling homeostasis induced crosstalk in the carcinogenesis paradigm Epistemology of the origin of cancer”." 4open 2 (2019): 28. http://dx.doi.org/10.1051/fopen/2019023.

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It is increasingly evident that carcinogenesis, in the vast majority of cancers, cannot be explained simply through an accumulation of somatic mutations, or epigenetics, the stem cell theory, or the Warburg effect. Here, decades of thinking based on incorrect assumptions has resulted in an incorrect hypothesis on the origin of cancer. Many papers studying DNA, genetics, RNA, miRNA, proteomics, and epigenetics have increased our understanding of biology. Our paradigm, though more complex, is more reliable and plausible. It states that cancer originates from a disruption of homeostasis. This ess

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Bet-Lachin, Anna, Frank Jiang, Lingjing Chen, et al. "Metabolic Profiling of CNS Lymphoma and Its Microenvironment." Blood 118, no. 21 (2011): 588. http://dx.doi.org/10.1182/blood.v118.21.588.588.

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Abstract Abstract 588 Background: Establishing the pathologic basis of focal brain lesions caused by disease processes such as CNS lymphoma is often difficult. Results of standard MRI-based neuro-imaging are non-specific and cytological testing of cerebrospinal fluid (CSF) is highly insensitive. We tested the hypothesis that the metabolic constituents of the CSF reflect pathologic processes within the brain and thus might lead to the identification of novel diagnostic and prognostic biomarkers and provide insight into mechanisms of CNS lymphoma pathogenesis and its impact on cognitive function

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Chan, Lai N., Huimin Geng, and Markus Muschen. "Lineage-Specific Functions of LKB1 in CML and B Lymphoid Blast Crisis." Blood 120, no. 21 (2012): 34. http://dx.doi.org/10.1182/blood.v120.21.34.34.

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Abstract Abstract 34 Background: The serine-threonine liver kinase B1 (LKB1, also called STK11) acts as negative regulator of aerobic glycoloysis, a metabolic pathway that is typically used in cancer cells (commonly referred to as ‘Warburg effect’). LKB1, together with AMPKs, shifts the metabolic balance from aerobic glycolysis to oxidative phosphorylation and thereby reverses the metabolic program of cancer cells and functions as tumor suppressor. Recently, it has been shown that LKB1 plays a critical role in the maintenance of quiescence and metabolic homeostasis of hematopoietic stem cells

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