Cancer as a metabolic disease

被引:429
作者
Seyfried, Thomas N. [1 ]
Shelton, Laura M. [1 ]
机构
[1] Boston Coll, Dept Biol, Chestnut Hill, MA 02467 USA
关键词
DIETARY ENERGY RESTRICTION; ENDOTHELIAL GROWTH-FACTOR; GENE-EXPRESSION PROFILE; SOMATIC MUTATION THEORY; A TRANSFERASE-ACTIVITY; MARROW-DERIVED CELLS; CALORIC RESTRICTION; MITOCHONDRIAL DYSFUNCTION; KETOGENIC DIET; TUMOR PROGRESSION;
D O I
10.1186/1743-7075-7-7
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
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.
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页数:22
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