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Oncology-Basic Science: Basic ScienceCorrelative Studies |
1 Clinical Cooperation Unit Nuclear Medicine, German Cancer Research Center, Heidelberg, Germany; 2 Surgical Clinic, Klinikum Ludwigshafen, Ludwigshafen, Germany; 3 Institute of Immunology, University of Rostock, Rostock, Germany
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Objectives: Transport and phosphorylation of F-18-Deoxyglucose (FDG) in tumor cells determine primarily the FDG kinetics. Other biological processes like proliferation may have an impact on the FDG uptake.
Methods: The evaluation is based on dynamic PET FDG studies in 25 patients with colorectal tumors. Volumes-of-Interest were used to obtain tracer concentrations from the tumor and a reference area. A two-tissue-compartment model was fitted and the constants k1-k4 as well as the fractional blood volume (VB) were calculated using the software PMOD (PMOD Technologies Ltd., Adliswil, Switzerland). Tumor specimen and specimen from a reference area were obtained by surgery and quantitative gene expression data were obtained by gene array analysis (U133A gene chip, Affymetrix Inc., Santa Clara,CA,USA). PET and gene array data were evaluated with the GenePET module of PMOD.
Results: A quantitative data evaluation was performed in 25 patients (32 specimen of tumors and normal colon tissue). The median SUV was 7.30 for the tumors and 1.72 for the reference tissue. The evaluation of gene expression data was focussed on cyclines, which are controlling the cell cycle. We noted significant correlations for the SUV and the cyclin-dependent kinase 6 (0.4796), cyclin D2 (0.4134), and cyclin G1 (0.4024). K1 was correlated with the cyclin-dependent kinase 2 (0.5073) and k3 with p15 (-0.4493). The SUV was significantly correlated with cyclin G1. The impact of the cyclines on the variance of the FDG uptake was less than 30 %.
Conclusions: The cell cycle associated genes have a moderate impact on the FDG kinetics and contribute to about 20-30 % of the total variation in FDG uptake.
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