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

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Title: Anti PD-1 treatment increases [F-18]FDG uptake by cancer cells in a mouse B16F10 melanoma model
Authors: Tomita, Mayu Browse this author
Yasui, Hironobu Browse this author
Higashikawa, Kei Browse this author
Nakajima, Kohei Browse this author
Takakura, Hideo Browse this author
Shiga, Tohru Browse this author
Kuge, Yuji Browse this author
Ogawa, Mikako Browse this author →KAKEN DB
Keywords: PD-1
Immune checkpoint inhibitor
[F-18]FDG
Tumor microenvironment
Mouse melanoma
Issue Date: 16-Aug-2018
Publisher: Springer (SpringerOpen)
Journal Title: EJNMMI research
Volume: 8
Start Page: 82
Publisher DOI: 10.1186/s13550-018-0433-1
Abstract: 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-[F-18]fluoro-D-glucose ([F-18]FDG) uptake in vivo, focusing on cell distribution and glycolysis in both cancer and immune cells. Results: In a B16F10 melanoma model, [F-18]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 [18F]FDG uptake between tumors in the treatment group and non-treatment group before the treatment. In contrast, mean [F-18]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 [F-18]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.
Rights: http://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/71528
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 小川 美香子

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