Abstract
Tumors incorporate much glucose for overcoming glycolytic pyruvate-kinase and pyruvate-dehydrogenase inhibitions; they form lactate, rather than oxidative acetyl-CoA. Tumors also need to synthetize fatty acids, which automatically turns-off their mitochondrial degradation into acetyl-CoA. Thus, ketolysis becomes their major acetyl-CoA supply. Carcinogenic mutations or deficiencies of Krebs-cycle enzymes support the ketolytic dependency of tumors.
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