Cancer as a metabolic disease

Abstract

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.

Journal

Journal ID (nlm-ta): Nutr Metab (Lond)

Title: Nutrition & Metabolism

Publisher: BioMed Central

ISSN (Electronic): 1743-7075

Publication date Collection: 2010

Publication date (Electronic): 27 January 2010

Volume: 7

Page: 7

Affiliations

[1 ]Biology Department, Boston College, Chestnut Hill, MA 02467, USA

Article

Publisher ID: 1743-7075-7-7

DOI: 10.1186/1743-7075-7-7

PMC ID: 2845135

PubMed ID: 20181022

SO-VID: bd26387b-8487-4dda-8b8c-925276ce9d78

Copyright statement: Copyright ©2010 Seyfried and Shelton; licensee BioMed Central Ltd.

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Product

Self URI: http://www.nutritionandmetabolism.com/content/7/1/7

Categories

Subject: Review