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Abstract #1162

The Effect of Altered Glucose Utilization on Dynamic GlucoCEST in a Preclinical Model of Glioblastoma

Xiang Xu1,2, Jing Liu1,3,4, Jiadi Xu1,2, Linda Knutsson1,5, Huanling Liu1,6, Yuguo Li1,2, Bachchu Lal7, John Laterra7, Peter C.M. van Zijl1,2, and Kannie Chan1,8

1Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University, Baltimore, MD, United States, 2F. M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Research Institute, Baltimore, MD, United States, 3Radiology College, Guizhou Medical University, Guiyang, China, 4Department of Radiology, Guangdong Academy of Medical Sciences/Guangdong General Hospital, Guangzhou, China, 5Department of Medical Radiation Physics, Lund University, Lund, Sweden, 6Department of Ultrasound, Guangzhou Panyu Central Hospital, Guangdong, China, 7Division of Cancer Imaging Research, Johns Hopkins University School of Medicine, Baltimore, MD, United States, 8Department of Mechanical and Biomedical Engineering, City University of Hong Kong, Hong Kong, Hong Kong

To investigate the origin of glucoCEST contrast, we altered glucose utilization using an mTOR inhibitor (rapamycin) and studied dynamic glucoCEST signals in a human glioblastoma mouse model. By inhibiting glucose transport, cellular uptake and metabolism are suppressed and the perfusion of vessels and leakage into extravascular extracellular space highlighted. A great increase in glucoCEST contrast was seen in tumors in mice with the inhibitor compared to without. This provides evidence of a large extracellular glucose contribution to glucoCEST, and suggests that we can use glucoCEST to monitor the efficacy of rapamicin with respect to its inhibitory effect.

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