Abstract #1162

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

Xiang Xu^1,2, Jing Liu^1,3,4, Jiadi Xu^1,2, Linda Knutsson^1,5, Huanling Liu^1,6, Yuguo Li^1,2, Bachchu Lal⁷, John Laterra⁷, Peter C.M. van Zijl^1,2, and Kannie Chan^1,8

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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