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¹⁸F-FDG Kinetics and Gene Expression in Giant Cell Tumors

¹ Clinical Cooperation Unit Nuclear Medicine, German Cancer Research Center, Heidelberg, Germany
² Institute of Immunology, University Rostock, Rostock, Germany
³ Department I, University Orthopedic Clinic, Heidelberg, Germany

¹⁸F-FDG kinetics were evaluated by use of compartment and noncompartment models of giant cell tumors. The kinetic data were compared with the gene expression data for a subgroup of patients. Methods: Nineteen patients with giant cell tumors were examined with PET and ¹⁸F-FDG, and tracer kinetics were assessed quantitatively. A 2-compartment model, including the transport constants k1–k4 as well as the vascular fraction (VB) for ¹⁸F-FDG, was used for evaluation of the data. A noncompartment model was used to calculate the fractal dimension of the ¹⁸F-FDG time–activity curve to assess the heterogeneity of the tracer kinetics. Furthermore, tumor specimens obtained from 5 patients were assessed with gene chip technology (U95A), and these data were compared with the quantitative ¹⁸F-FDG data. Results: The giant cell tumors showed generally enhanced ¹⁸F-FDG uptake 1 h after tracer application, with a mean ¹⁸F-FDG standardized uptake value (SUV) of 4.8 (range, 1.8–9.4). Quantitative evaluation of tracer kinetics showed a preferential increase for ¹⁸F-FDG transport, with a mean k1 of 0.340. The vascular fraction accounted for 35% of the tumor volume and was high compared with those for other tumors, such as soft-tissue sarcomas. ¹⁸F-FDG kinetics were heterogeneous, with a fractal dimension of 1.3. Gene chip analysis showed that the expression of 137 genes (1.1%) exceeded the median expression value of the reference gene, ß₂-microglobulin. The highest expression was observed for the gene for the small, leucine-rich proteoglycan I (biglycan), which is important for bone cell differentiation and proliferative activity. Correlation analysis revealed an association of ¹⁸F-FDG data with the expression of several genes. Mainly genes related to angiogenesis were associated with the compartment parameters. The SUV at 56–60 min was correlated with the expression of vascular endothelial growth factor A (angiogenesis) and cell division cycle 2 protein (proliferation). Conclusion: Despite their classification as benign tumors, giant cell tumors have generally enhanced ¹⁸F-FDG uptake, mainly attributable to an enhanced vascular fraction and increased ¹⁸F-FDG transport. A comparison of gene chip data and ¹⁸F-FDG kinetic data showed a close association of quantitative ¹⁸F-FDG results and the expression of genes related to angiogenesis.

Key Words: giant cell tumor • ¹⁸F-FDG • quantification • gene expression

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