Abstract
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Objectives To evaluate the ability of FDG and three 18F-labeled amino acids targeting different transport systems to distinguish mouse DBT gliomas from radiation necrosis using microPET.
Methods Radiation necrosis was induced in the brains of BALB/c mice (n=4) with a single 60 Gy fraction using a gamma knife system. Approximately 6 weeks after irradiation, the mice underwent MRI for lesion confirmation followed by dynamic microPET using the 18F-labeled tracers (R)-MeFAMP (system A substrate), FET (system L substrate), (S)-AFETP (cationic amino acid transport substrate), and FDG. These tracers were also evaluated in a separate group of mice implanted with intracranial DBT gliomas (n=3 or 4). The percent change in SUV between early (7.5-12.5 min) and late (47.5-60 min) time points was compared using 2-tailed t-tests.
Results For each tracer, the average SUVs were similar in the DBT tumors and radiation necrosis lesions, possibly due to the relatively short time interval between irradiation and imaging. The percentage of activity present at the late time point relative to the early time point was significantly different for radiation necrosis versus DBT tumors with FDG and MeFAMP but not with AFETP or FET. In the case of FDG, uptake was decreased at the late time point in radiation necrosis (83±11% of early value) but was increased at the late time point in the DBT tumors (131±30% of early value, p = 0.04). In the case of MeFAMP, uptake was also decreased at the late time point in radiation necrosis (44±4% of early value) but was relatively constant at the late time point in DBT tumors (94±17% of early value, p = 0.03).
Conclusions The kinetics, but not the absolute amount of uptake, of FDG and MeFAMP appear to distinguish radiation necrosis from DBT tumors in this model. This relatively simple PET imaging paradigm could be adapted for evaluating patients with brain tumors after radiation therapy.
Research Support NIH/NCI P50CA094056 (Washington University Molecular Imaging Center) K08CA15479