PURPOSE: To study the contribution of immunologic background to the uptake of fluorine-18-fluorodeoxyglucose ((18)F-FDG) by the tumor tissues. METHODS: The uptakes of (18)F-FDG to the same experimental tumor model (SCCVII) xenografted into immunocompetent and immunodeficient (athymic) mice were compared. In addition, the immunomodifying effect of steroid on the uptake of (18)F-FDG by these tumors was investigated. RESULTS: The uptake of (18)F-FDG by the tumors in immunocompetent mice was significantly higher than that in immunodeficient (athymic) mice. Although steroid pretreatment had no effect on the tumor uptake in immunodeficient mice, it significantly decreased the tumor uptake in immunocompetent mice. CONCLUSION: The higher tumor uptake of (18)F-FDG observed in immunocompetent mice, modulated by steroid pretreatment, was contributed by the host immune reaction, probably cellular immunity employed by T-lymphocytes. These findings can clinically conclude that the intense accumulation of (18)F-FDG in the metastatic lymph nodes, which contain only a small number of cancer cells, was caused by the enhanced uptake of (18)F-FDG by activated T-lymphocytes due to host immunity against cancer cells present in metastatic lymph nodes.
PURPOSE: To study the contribution of immunologic background to the uptake of fluorine-18-fluorodeoxyglucose ((18)F-FDG) by the tumor tissues. METHODS: The uptakes of (18)F-FDG to the same experimental tumor model (SCCVII) xenografted into immunocompetent and immunodeficient (athymic) mice were compared. In addition, the immunomodifying effect of steroid on the uptake of (18)F-FDG by these tumors was investigated. RESULTS: The uptake of (18)F-FDG by the tumors in immunocompetent mice was significantly higher than that in immunodeficient (athymic) mice. Although steroid pretreatment had no effect on the tumor uptake in immunodeficientmice, it significantly decreased the tumor uptake in immunocompetent mice. CONCLUSION: The higher tumor uptake of (18)F-FDG observed in immunocompetent mice, modulated by steroid pretreatment, was contributed by the host immune reaction, probably cellular immunity employed by T-lymphocytes. These findings can clinically conclude that the intense accumulation of (18)F-FDG in the metastatic lymph nodes, which contain only a small number of cancer cells, was caused by the enhanced uptake of (18)F-FDG by activated T-lymphocytes due to host immunity against cancer cells present in metastatic lymph nodes.
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