ArticleTheoretical biology & medical modelling2013
An integrated multidisciplinary model describing initiation of cancer and the Warburg hypothesis.
Article in Theoretical biology & medical modelling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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.
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Who cites it
9 citing papers in PubMed.
- The role of glycolysis in tumorigenesis: From biological aspects to therapeutic opportunities.Neoplasia (New York, N.Y.) · 2024Review
- Emerging cancer therapies: targeting physiological networks and cellular bioelectrical differences with non-thermal systemic electromagnetic fields in the human body - a comprehensive review.Frontiers in network physiology · 2024Review
- Agent-based models for detecting the driving forces of biomolecular interactions.Scientific reports · 2022Article
- Review
- Symmetry and symmetry breaking in cancer: a foundational approach to the cancer problem.Oncotarget · 2018Article
- Cell cycle progression is regulated by intertwined redox oscillators.Theoretical biology & medical modelling · 2015Article
- Article
- Cariporide and other new and powerful NHE1 inhibitors as potentially selective anticancer drugs--an integral molecular/biochemical/metabolic/clinical approach after one hundred years of cancer research.Journal of translational medicine · 2013Review
- Theoretical Biology and Medical Modelling: ensuring continued growth and future leadership.Theoretical biology & medical modelling · 2013Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundIn this paper we propose a chemical physics mechanism for the initiation of the glycolytic switch commonly known as the Warburg hypothesis, whereby glycolytic activity terminating in lactate continues even in well-oxygenated cells. We show that this may result in cancer via mitotic failure, recasting the current conception of the Warburg effect as a metabolic dysregulation consequent to cancer, to a biophysical defect that may contribute to cancer initiation. MODEL: Our model is based on analogs of thermodynamic concepts that tie non-equilibrium fluid dynamics ultimately to metabolic imbalance, disrupted microtubule dynamics, and finally, genomic instability, from which cancers can arise. Specifically, we discuss how an analog of non-equilibrium Rayleigh-Benard convection can result in glycolytic oscillations and cause a cell to become locked into a higher-entropy state characteristic of cancer.
conclusionsA quantitative model is presented that attributes the well-known Warburg effect to a biophysical mechanism driven by a convective disturbance in the cell. Contrary to current understanding, this effect may precipitate cancer development, rather than follow from it, providing new insights into carcinogenesis, cancer treatment, and prevention.
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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.