Mapping intratumoral heterogeneity in adolescent CNS tumors using simultaneous amide proton transfer-weighted signal and 18F-choline PET: A feasibility study.
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BACKGROUND: Pediatric and adolescent gliomas and glioneuronal tumors remain challenging to assess noninvasively. Amide proton transfer (APT) chemical exchange saturation transfer (CEST) MRI has shown promise in adult gliomas but has not been well studied in younger patients. We conducted a feasibility study to assess whether APT-weighted signal can act as a noninvasive surrogate of tumor proliferation in adolescent central nervous system (CNS) tumors by correlating it with 18F-choline PET uptake (standardized uptake value [SUV]) as a proxy for membrane synthesis/proliferative activity. METHODS: Ten adolescent patients (14-19 years), seven with histologically confirmed and three with radiologically suspected CNS tumors, underwent simultaneous APT-CEST and 18F-choline PET-MRI. Regions of interest (ROIs) corresponding to nonenhancing, enhancing, necrotic tumor, and contralateral white matter were delineated. Mean APT-weighted signal intensity and PET SUV were extracted per ROI. Nonparametric statistics and Spearman's correlation analyses were performed. RESULTS: APT-weighted signal was significantly elevated in enhancing, nonenhancing, and necrotic tumor ROIs compared to normal white matter (P < .001). 18F-choline SUV was elevated in enhancing and necrotic ROIs vs white matter, but not significantly so for nonenhancing tumor (P = .02). A correlation between enhancing and whole-tumor APT-weighted signal and 18F-choline SUV was seen (P < .001). CONCLUSION: This pilot feasibility study demonstrates that APT-CEST MRI is technically feasible in adolescents with CNS tumors and that APT-weighted signal may reflect tumor metabolic activity. The findings are hypothesis-generating and require validation in larger, histologically homogeneous cohorts. The detection of elevated APT-weighted signal even in nonenhancing tumor regions suggests potential utility in monitoring noncontrast-enhancing disease. Larger cohorts and multimodal correlation (eg Ki-67, amino acid PET) are warranted to confirm and extend these findings.