Role of 18F-Fluorodeoxyglucose Positron-Emission Tomography (FDG-PET) in the Management of Pancreatic Cancer

A hallmark of cancer cells is the deregulated uptake of glucose in an effort to sustain the biosynthetic demands of rapid cellular proliferation. This metabolic process was first described by German physiologist Otto Warburg in the 1920s. In the seminal study, Warburg et al. observed a significant increase in glucose consumption and lactic acid production by cancer cells as compared to normal (non-cancerous) cells, despite aerobic conditions, suggesting an anomalous energy metabolism. Subsequent investigators have corroborated this clinical observation and concluded that cancer cells have the ability to reprogram their energy metabolism such that they rely primarily on glucose catabolism for cellular energy production. In contrast, the energy pathway favored by normal tissue cells under aerobic conditions is the coupling of glycolysis with mitochondrial oxidative phosphorylation, as it yields an approximately 18-fold increase in energy production in comparison to glycolysis alone. However, cancer cells are able to compensate by upregulating glucose transporters (GLUT) on the cell membrane, namely, GLUT1, resulting in an increased uptake of glucose into cells.