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Abstract #0186

­The origins of glucoCEST signal: effect inhibiting glucose transport in brain tumors

Xiang Xu1,2, Jiadi Xu1,2, Linda Knutsson3, Yuguo Li1,2, Huanling Liu1,4, Guanshu Liu1,2, Bachchu Lal5,6, John Laterra5,6, Dmitri Artemov7,8, Michael T. McMahon1,2, Peter C.M. van Zijl1,2, and Kannie WY Chan1,2

1Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, United States, 2FM Kirby Research Center, Kennedy Krieger Institute, Baltimore, MD, United States, 3Department of Medical Radiation Physics, Lund University, Lund, Sweden, 4Department of Ultrasound, Guangzhou Panyu Central Hospital, Panyu, China, People's Republic of, 5Department of Neurology, Kennedy Krieger Institute, Baltimore, MD, United States, 6Department of Neuroscience, Kennedy Krieger Institute, Baltimore, MD, United States, 7Division of Cancer Imaging Research, Johns Hopkins University School of Medicine, Baltimore, MD, United States, 8JHU In Vivo Cellular Molecular Imaging Center, Baltimore, MD, United States

Recently D-glucose has shown potential to be used as a biodegradable contrast agent for cancer detection. However the origins of the glucoCEST signal is not yet completely understood. To identify the contributions to glucoCEST contrast, we administrated a glucose transporter inhibitor in a group of mice with implanted glioma. By inhibiting glucose transport into the cells, the effects of cellular glucose uptake and metabolism are suppressed and the perfusion properties of the extravascular extracellular space are delineated. A greater increase in glucoCEST contrast was seen in tumors in the group of mice with glucose transporter inhibitor compared to a group of mice without. This greater uptake and retention of glucose in the inhibitor group provides evidence that the intracellular glucose contribution is minimal.

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