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Work from our group and others clearly suggest the key role of altered metabolism in cancer. The goal of this review is to summarize current knowledge on cancer metabolism, draw hy-pothesis explaining metabolic alterations and associated gene changes. Most importantly, we indicate a list of possible pharmacological targets. In short, tumor metabolism displays mixed glycolysis and neogluogenesis features; most glycolitic enzymes are activate, but the pyruvate kinase and the pyruvate deshydrogenase are inhibited. This would result from an activation of their specific kinases, or from the inactivation of phosphatases, such as PP2A, regulated by me-thylation. In parallel, the phosphatase failure would enhance “tyrosine kinase receptor” signals, as occurs with oncogenes. Such signaling pathways are similar to those activated by insuline, or IGF- Growth hormone; they control mitosis, cell survival, carbohydrate metabolism. If for some reason, their regulation fails (oncogenes, PP2A methylation deficit, enhanced kinases…) a typical tumor metabolism starts the carcinogenic process. We also describe changes in the citric acid- urea cycles, polyamines, and show how body stores feed tumor metabolic pathways above and below “bottlenecks” resulting from wrongly switched enzymes. Studying the available lit-erature, we list a number of medications that target enzymes that are essential for tumor cells. Hoping to prevent, reverse or eradicate the process. Experimental data published elsewhere by our group, seem to confirm some of these assumptions.
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Author(s): Maurice Isral and Laurent Schwartz
Cancer. Oncogenes. Tyrosine kinase receptor. PP2A methylation. Pyruvate kinase M2