Many chemotherapeutic drugs can influence, directly or indirectly, the signaling pathways, glucose transporters, and metabolic enzymes controlling aerobic glycolysis. In vitro, cytotoxic drugs such as topotecan, paclitaxel, cisplatin and etoposide can block glycolysis by decreasing HIF-1 levels and/or down-regulating hexokinases and glucose transporters. Drugs designed to target cell surface receptors, receptor tyrosine kinases, the estrogen receptor, and other signaling molecules (e.g., Ras, mTOR) also suppress glycolysis, and this suppression has, in some cases, correlated with clinical efficacy. Increased glycolysis is a hallmark of cancer; the accumulating evidence that diverse classes of chemotherapeutic drugs can modulate glycolosis supports the utility of FDG-PET for monitoring chemotherapy. For further details, please see Kelloff et al. on page 2785 in this issue.

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