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Abstract #0398

Differentiation of IDH1 mutant and wild-type gliomas based on metabolic signatures obtained from pH- and oxygen-sensitive molecular MRI

Jingwen Yao1,2,3, Ararat Chakhoyan1,3, Catalina Raymond1,3, Noriko Salamon3, Linda Liau4,5, William Yong6,7, Phioanh Nghiemphu8, Albert Lai5,8, Whitney Pope3, Timothy Cloughesy8, and Benjamin Ellingson1,2,3,5,9,10

1Brain Tumor Imaging Laboratory (BTIL), Center of Computer Vision and Imaging Biomarker, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States, 2Department of Bioengineering, Henry Samueli School of Engineering and Applied Science, University of California, Los Angeles, Los Angeles, CA, United States, 3Department of Radiological Sciences, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States, 4Department of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States, 5UCLA Brain Research Institute (BRI), David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States, 6Brain Tissue Translational Resource (BTTR), David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States, 7Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States, 8Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States, 9Physics and Biology in Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States, 10Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States

In the current study, we have demonstrated that pH- and oxygen-sensitive amine CEST-SAGE-EPI (chemical exchange saturation transfer spin-and-gradient-echo echoplanar imaging) is a clinically feasible, powerful imaging technique for distinguishing between IDH1-mutant and wild-type gliomas. Results suggest that IDH1 mutation is associated with lower MTRasym at 3.0ppm and lower R2’, implying lower acidity and vascular hypoxia. We hypothesize that 2-HG produced by IDH1-mutant activates PHD and the degradation of HIF1α, subsequently preventing a metabolic shift from oxidative phosphorylation to glycolysis. This is supported by our histological findings of loss of correlation between levels of hypoxia and HIF1α tissue expression in IDH1 mutants.

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