Cancer cells not only exhibit the well known “hallmarks” that Hanahan and Weinberg enumerated in 2000 but also several other molecular alterations, notably a profound metabolic rewiring. This often, but not always, entails the Warburg effect, i.e., tumor cells maintain high rates of glycolysis even in the ...
Cancer cells not only exhibit the well known “hallmarks” that Hanahan and Weinberg enumerated in 2000 but also several other molecular alterations, notably a profound metabolic rewiring. This often, but not always, entails the Warburg effect, i.e., tumor cells maintain high rates of glycolysis even in the presence of a normoxic environment (aerobic glycolysis). Metabolic defects have long been viewed as a mere epiphenomenon of cancer and not as an active contributor to tumorigenesis. The discovery that that germline mutations in two enzymes of the Krebs cycle, namely fumarate hydratase (FH) and succinate dehydrogenase (SDH), are associated with an increased risk of tumorigenesis founded the notion of “oncometabolites” and paved the way for the study of metabolism as an oncogenic factor. In this Research Topic, we accept review articles, perspectives, research articles dealing with the oncogenic (and oncosuppressive) roles of intermediate and respiratory metabolism.
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