[Brainlife] Bui Thi et al (2006) - Cancer's sweet tooth

Etiology and Pathogenesis > Tumor Biology

Cancer Cell, Vol 9, 419-420, 13 June 2006. DOI: 10.1016/j.ccr.2006.05.012. Available online 12 June 2006

Comment
	Cancer's sweet tooth Thi Bui¹ and Craig B. Thompson^1,* ¹The Abramson Family Cancer Research Institute and the Departments of Medicine and Cancer Biology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104. *Corresponding author

	Even in the presence of an adequate oxygen supply, many tumors metabolize the majority of the glucose they take up through glycolysis. It has been a long-held belief that this glycolytic phenotype is due to cancer-specific defects in mitochondrial oxidative phosphorylation. In this issue of Cancer Cell, Fantin et al. now report that most tumor cells have a substantial reserve capacity to produce ATP by oxidative phosphorylation when glycolysis is suppressed. These new data add to mounting evidence that the high rate of glycolysis exhibited by most tumors is required to support cell growth rather than to compensate for defect(s) in mitochondrial function.

	Copyright © 2006 Elsevier B.V.
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