Cancer Cell Glucose Metabolism Version 1.1

Deeper understanding of cell metabolism in cancer can result in innovation frequency strategies for eliminating altered cells. Frequency data are provided to Frequency Foundation subscribers in a private blog that regularly updates frequency sets for researchers. The cancer cell metabolism program is a good indicator of abnormal cells. A positive muscle test when running this program indicates premalignant or malignant cells.

Altered metabolism in cancer
Jason W Locasale and Lewis C Cantley

Locasale and Cantley BMC Biology 2010, 8:88
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Cancer cells have different metabolic requirements from their normal counterparts. Understanding the consequences of this differential metabolism requires a detailed understanding of glucose metabolism and its relation to energy production in cancer cells. A recent study in BMC Systems Biology by Vasquez et al. developed a mathematical model to assess some features of this altered metabolism. Here, we take a broader look at the regulation of energy metabolism in cancer cells, considering their anabolic as well as catabolic needs.

Cancer is a disease of uncontrolled cell growth in which cells acquire genetic alterations that allow them to proliferate outside the context of normal tissue development. In the evolution of this transformation, cells acquire mutations that confer selective advantages for the growth of the tumor. Genetic alterations in many of the known oncogenes are selected to adapt cellular metabolism to meet the requirements of rapid cell proliferation as well as autonomous growth and survival in an environment absent of contact with extracellular matrix. Accumulating evidence indicates that almost every known oncogene regulates downstream targets that are directly connected to metabolic regulation. A detailed biochemical and systems-level understanding of precisely how oncogenes rewire metabolism is essential to understand tumor biology, but concomitantly requires an assessment of the metabolic adaptations required to support the proliferation of cancer cells. Understanding the consequences of this differential metabolism requires a thorough analysis of glucose metabolism and its relation to energy production in cancer cells.

In a majority of tumor types, an enhanced rate of glucose uptake is observed and serves as a reasonable starting point for understanding differential metabolism in tumors. Otto Warburg’s initial observation that tumors often metabolize relatively large quantities of glucose predominantly through a fermentative-like metabolism, resulting in lactate production in aerobic conditions (termed aerobic glycolysis), provided the phenomenological foundation for studying altered metabolism in cancer [2]. Rapid progress is being made towards a molecular understanding of why lactate production from glucose gives cancer cells a growth advantage. Paradoxically, cells that achieve high rates of aerobic glycolysis often show relatively small changes in the rate of oxygen consumption in response to changes in glucose uptake; that is, oxidative catabolic flux through the Krebs cycle leading to mitochondrial ATP generation is somewhat independent of glucose metabolism.

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