An integrated multidisciplinary model describing initiation of cancer and the Warburg hypothesis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-12

AUTHORS

Edward A Rietman, Douglas E Friesen, Philip Hahnfeldt, Robert Gatenby, Lynn Hlatky, Jack A Tuszynski

ABSTRACT

BACKGROUND: In 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. CONCLUSIONS: A 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. More... »

PAGES

39

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1742-4682-10-39

DOI

http://dx.doi.org/10.1186/1742-4682-10-39

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1004374945

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/23758735


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