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Background  Programmed cell death 1 (PD-1) inhibitors act as immune checkpoint inhibitors and are more effective for improving survival time with less toxicity as compared with conventional chemotherapies. In anti PD-1 therapy, it is important to evaluate metabolism in the cancer microenvironment, as this helps to clarify the pathological conditions. Herein, we investigate the early effects of PD-1 therapy on 2-deoxy-2-[ 18 F]fluoro- d -glucose ([ 18 F]FDG) uptake in vivo, focusing on cell distribution and glycolysis in both cancer and immune cells.    Results  In a B16F10 melanoma model, [ 18 F]FDG-positron emission tomography (PET) was performed before treatment and 7 days after the start of treatment. Values were calculated as the percentage-injected activity per gram of tissue (%IA/g). Flow-cytometry was then performed to assess immune cell populations and glucose metabolism. There was a negligible difference in [ 18 F]FDG uptake between tumors in the treatment group and non-treatment group before the treatment. In contrast, mean [ 18 F]FDG uptake in the treatment group tumors was significantly higher (8.06 ± 0.48 %IA/g;  P  = 0.0074) than that in the non-treatment group (4.02 ± 1.03 %IA/g) after anti PD-1 treatment. Assessment of tumor immune cell populations showed that treatment slightly enriched CD8 +  T cells and CD4 +  T cells; however, infiltration of immune cells was negligible, and thus, immune cells were not responsible for the increase in [ 18 F]FDG uptake. On the other hand, anti PD-1 treatment significantly increased glucose transporter 1 (GLUT1) and hexokinase II expression in CD45 −  cancer cells, indicating that anti PD-1 treatment increased glucose metabolism in cancer cells.    Conclusion  The present study shows that anti PD-1 therapy increases glucose metabolism in cancer cells.    Electronic supplementary material  The online version of this article (10.1186/s13550-018-0433-1) contains supplementary material, which is available to authorized users.

Anti PD-1 treatment increases [18F]FDG uptake by cancer cells in a mouse B16F10 melanoma model