Tumors often have an increased uptake of glucose and can be detected by PET imaging using 18F-FDG. 18F-FDG is converted to 18F-FDG-6-phosphate (18F-FDG-6-P), and the usual assumption is that 18F-FDG-6-P is not a substrate for subsequent enzymatic reactions and that tumor hot spots reflect trapping of 18F-FDG-6-P. We recently found, however, that in the pig liver, 18F-FDG is metabolized not only to 18F-FDG-6-P but also to the subsequent oxygenation product 2-18F-fluoro-2-deoxy-6-phospho-D-glucononate (18F-FD-PG1). We therefore wished to characterize the metabolism of 18F-FDG in experimental tumors in mice.
Methods: 18F-FDG was given intravenously to mice with either SCCVII squamous cell carcinoma or C3H mammary carcinoma grown on the back. 18F-Labeled metabolites were determined by radio-high-performance liquid chromatography in tumor tissue biopsies, in a time course of 180 min (12 mice of each tumor type), and in liver tissue biopsies 80 min after tracer injection (2 mice of each type).
Results: After the tracer injection, not only 18F-FDG and 18F-FDG-6-P but also 18F-FD-PG1 and 2-18F-fluoro-2-deoxy-1,6-biphosphate were detected in both tumors, relatively more in SCCVII carcinoma than in C3H carcinoma. Both tumors accumulated radioactivity throughout the 180-min measurement period, 4-fold more in SCCVII carcinoma than in C3H carcinoma. At 80 min, the radioactivity was approximately 6 and 1.2 times higher in the respective tumors than in liver tissue.
Conclusion: Our results agree with the general finding that most malignant tumor tissues accumulate significantly more 18F-radioactivity than do normal tissues, but our results do not support the concept that this increase is caused solely by accumulation of 18F-FDG-6-P. Furthermore, the rate of 18F-FDG metabolism was higher in SCCVII carcinoma than in C3H carcinoma.