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Unformatted text preview: DOI: 10.1126/science.1160809 , 1029 (2009); 324 Science et al. Matthew G. Vander Heiden, Requirements of Cell Proliferation Understanding the Warburg Effect: The Metabolic www.sciencemag.org (this information is current as of November 10, 2009 ): The following resources related to this article are available online at http://www.sciencemag.org/cgi/content/full/324/5930/1029 version of this article at: including high-resolution figures, can be found in the online Updated information and services, http://www.sciencemag.org/cgi/content/full/324/5930/1029#otherarticles , 16 of which can be accessed for free: cites 45 articles This article http://www.sciencemag.org/cgi/content/full/324/5930/1029#otherarticles 3 articles hosted by HighWire Press; see: cited by This article has been http://www.sciencemag.org/cgi/collection/medicine Medicine, Diseases : subject collections This article appears in the following http://www.sciencemag.org/about/permissions.dtl in whole or in part can be found at: this article permission to reproduce of this article or about obtaining reprints Information about obtaining registered trademark of AAAS. is a Science 2009 by the American Association for the Advancement of Science; all rights reserved. The title Copyright American Association for the Advancement of Science, 1200 New York Avenue NW, Washington, DC 20005. (print ISSN 0036-8075; online ISSN 1095-9203) is published weekly, except the last week in December, by the Science on November 10, 2009 www.sciencemag.org Downloaded from Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation Matthew G. Vander Heiden, 1,2 Lewis C. Cantley, 2 * Craig B. Thompson 3 * In contrast to normal differentiated cells, which rely primarily on mitochondrial oxidative phosphorylation to generate the energy needed for cellular processes, most cancer cells instead rely on aerobic glycolysis, a phenomenon termed “ the Warburg effect. ” Aerobic glycolysis is an inefficient way to generate adenosine 5´-triphosphate (ATP), however, and the advantage it confers to cancer cells has been unclear. Here we propose that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass (e.g., nucleotides, amino acids, and lipids) needed to produce a new cell. Supporting this idea are recent studies showing that (i) several signaling pathways implicated in cell proliferation also regulate metabolic pathways that incorporate nutrients into biomass; and that (ii) certain cancer-associated mutations enable cancer cells to acquire and metabolize nutrients in a manner conducive to proliferation rather than efficient ATP production. A better understanding of the mechanistic links between cellular metabolism and growth control may ultimately lead to better treatments for human cancer....
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This note was uploaded on 01/23/2011 for the course BCHS 4361 taught by Professor Echberg during the Spring '09 term at University of Houston.
- Spring '09