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Drug resistance is a major obstacle to cancer cure and may influence [18F]-fluorodeoxyglucose(FDG) incorporation. In this study, glucose transport, hexokinase activity and[18F]-FDG incorporation were measured in drug-resistant tumour cells generatedby exposing H630 colon and MCF7 breast cancer cells to increasing concentrationsof tomudex (raltitrexed) or 5-fluorouracil (5FU). Drug sensitivity was determinedusing the XTT assay: Tomudex-resistant (H630TDX and MCF7TDX) cells were more than40,000-fold less sensitive to tomudex than were the parental wild-type, H630WTand MCF7WT cells, respectively. 5FU-resistant (H630R10) cells were 100-fold lesssensitive than parental H630WT cells to 5FU. As previously reported for 5FU-resistantMCF7 breast cancer cells, [18F]-FDG incorporation was decreased in H630R10 coloncancer cells compared to the parental line. By contrast, both tomudex-resistantcell lines exhibited increased [18F]-FDG incorporation compared with the parentallines. H630R10 and MCF7TDX cells exhibited higher rates of glucose transport,measured as the initial rate of O-methyl-glucose (OMG) uptake, compared to wild-typecells; however, glucose transport was not significantly different between H630TDXcells and the parental cells. Hexokinase activity was lower in H630R10 and MCF7TDXcells compared with sensitive parental cells but unchanged in H630TDX cells. Inconclusion, our results show that [18F]-FDG incorporation is influenced by resistanceto antifolate and fluoropyrimidine-based anti-cancer drugs in a drug-dependentmanner and the underlying mechanisms appear to be cell- and drug-dependent. Glucosetransport may be a useful marker of resistance to 5FU.

Influence of resistance to 5-fluorouracil and tomudex on [18F]‑FDG incorporation, glucose transport and hexokinase activity