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About the Authors:
Joydeep Mukherjee
Affiliations Department of Neurological Surgery, University of California San Francisco, San Francisco, California, United States of America, The Brain Tumor Research Center, University of California San Francisco, San Francisco, California, United States of America
Joanna J. Phillips
Affiliations Department of Neurological Surgery, University of California San Francisco, San Francisco, California, United States of America, Department of Pathology, University of California San Francisco, San Francisco, California, United States of America, The Brain Tumor Research Center, University of California San Francisco, San Francisco, California, United States of America
Shichun Zheng
Affiliations Department of Neurological Surgery, University of California San Francisco, San Francisco, California, United States of America, The Brain Tumor Research Center, University of California San Francisco, San Francisco, California, United States of America
John Wiencke
Affiliations Department of Neurological Surgery, University of California San Francisco, San Francisco, California, United States of America, The Brain Tumor Research Center, University of California San Francisco, San Francisco, California, United States of America
Sabrina M. Ronen
Affiliations Department of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, California, United States of America, The Brain Tumor Research Center, University of California San Francisco, San Francisco, California, United States of America
Russell O. Pieper
* E-mail: [email protected]
Affiliations Department of Neurological Surgery, University of California San Francisco, San Francisco, California, United States of America, The Brain Tumor Research Center, University of California San Francisco, San Francisco, California, United States of America
Introduction
Tumor cell metabolism differs from normal cell metabolism in ways that have broad consequences for our understanding of the tumorigenic process. Normal non-proliferative cells under oxygenated conditions convert glucose to pyruvate, then move pyruvate into the mitochondria where processing in the citric acid cycle generates the reducing equivalents necessary for oxidative phosphorylation and ATP generation [1], [2]. Under hypoxic conditions, normal cells shunt pyruvate away from the mitochondria and converted it to lactate. This anaerobic glycolysis supports energy production but at a much lower level than under oxygenated conditions [3]. Proliferating tumor cells most resemble hypoxic cells in that they favor conversion of pyruvate to lactate. Tumor cells, however, convert pyruvate to lactate even under oxygenated conditions in a process referred to as aerobic glycolysis [4], [5]. This so-called “Warburg effect” limits...