It has been known for decades that cancer cells have altered metabolism relative to normal cells. In the 1920s, Warburg first described the fact that cancer cells take up large amounts of glucose, performing glycoly-sis at an elevated rate even in the presence of oxygen.12 Warburg hypothesized that this high rate of aerobic glycolysis was a result of dysfunctional mitochondrial electron transport, decreased production of ATP via oxidative metabolism, and a compensatory increase in ATP production by glycolysis. Others have proposed that the increased glucose uptake and glycolysis seen in cancer cells may be a primary effect, with subsequent suppression of oxidative phosphorylation. Whatever the mechanism, many cancer cells, including most lymphomas, take up excess amounts of glucose. It is this increased glucose uptake that targets FDG to cancer cells and is the basis of FDG-PET imaging of cancer.
18-Fluoro-2-deoxyglucose is a labeled glucose analog that is taken up by cells in a manner and at a rate similar to glucose. Upon entry into the cell, the molecule is phosphorylated by hexokinase, therefore trapping it inside the cell. While glucose is subsequently metabolized via glycolysis, the 2-deoxyglucose analog cannot be further metabolized, resulting in accumulation of the labeled, phosphorylated molecule within highly metabolic tissues. The label can then be detected by PET.
While FDG-PET is increasingly used in the care of patients with cancer, the optimal role for this imaging modality is still under investigation. The following sections review the status of FDG-PET imaging in detection and initial staging, response assessment, and follow-up of patients with lymphoma.
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