Author: Thomas N Seyfried 1 and Laura M Shelton 1
Affiliation: 1Biology Department, Boston College, Chestnut Hill, MA 02467, USA Corresponding author. Thomas N Seyfried: thomas.seyfried@bc.edu; Laura M Shelton: sheltola@bc.edu
Conference/Journal: Nutr Metab (Lond).
Date published: 2010 Jan 27
Other:
Special Notes: doi: 10.1186/1743-7075-7-7 , Word Count: 108
Emerging evidence indicates that impaired cellular energy metabolism is the defining characteristic of nearly all cancers regardless of cellular or tissue origin. In contrast to normal cells, which derive most of their usable energy from oxidative phosphorylation, most cancer cells become heavily dependent on substrate level phosphorylation to meet energy demands. Evidence is reviewed supporting a general hypothesis that genomic instability and essentially all hallmarks of cancer, including aerobic glycolysis (Warburg effect), can be linked to impaired mitochondrial function and energy metabolism. A view of cancer as primarily a metabolic disease will impact approaches to cancer management and prevention.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845135/