Apc mutant (Apc Min ) mice develop multiple adenomas in their intestines and are widely used to study colorectal carcinogenesis and chemopreventive approaches. Molecular imaging of intestinal adenomas could potentially provide noninvasive longitudinal evaluation of these lesions in living mice. Therefore, the aim of this study was to investigate the role of 18 F-FDG PET in the Apc Min mouse model. Methods: Apc Min mice (n 5 8) fed a purified diet were imaged serially after injection of 18 F-FDG at age 9 and 12 wk using a small-animal PET scanner. Abdominal uptake of the tracer was quantified. After dissection, intestines were imaged separately, and intestinal tracer uptake was quantified. Tracer distribution was compared with results from microscopic examination regarding adenoma number and size. Thereafter, findings were validated serially in 20 Apc Min mice aged 6, 8, 10, and 12 wk that received standard chow to increase adenoma numbers. In vivo abdominal 18 F-FDG uptake was correlated with microscopy results. Results: Microscopic examination showed that the mice developed 25-35 intestinal adenomas at age 12 wk. Ex vivo 18 F-FDG PET of the dissected intestines visualized all large adenomas and most small adenomas. Ex vivo total intestinal 18 F-FDG uptake correlated with in vivo total abdominal uptake and with the number of large adenomas at age 9 and 12 wk. At 12 wk, there was a clear correlation between in vivo abdominal tracer uptake and the number of large adenomas but not the total number of lesions. Conclusion: Intestinal adenomas in Apc Min mice are metabolically active lesions that take up 18 F-FDG. Abdominal 18 F-FDG uptake at age 12 wk serves as a readout modality for large intestinal adenomas.