Elevated choline phospholipid metabolism is a hallmark of cancer. Here, we show that silencing choline kinase a (CKα), the rate-limiting enzyme in choline phospholipid biosynthesis, abrogates total choline (tCho) production from [2H9]-choline in patient-derived glioma models, indicating that tCho production from [2H9]-choline predominantly reflects CKα activity. Importantly, we show that [2H9]-choline metabolism to tCho serves to delineate tumor from normal brain in mice bearing orthotopic patient-derived low-grade gliomas. Furthermore, [2H9]-choline informs on response to therapy, at early timepoints when anatomical alterations cannot be detected, pointing to the ability of [2H9]-choline to assess pseudoprogression, which is a challenge in glioma imaging.
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