( 11 C)acetate in an androgen-sensitive and androgen-independent prostate cancer xenograft model

Background: Androgen deprivation (AD) is generally used as a first-line palliative treatment in prostate cancer (PCa) patients with rising prostate-specific antigen (PSA) after primary therapy. To acquire an accurate detection of tumour viability following AD with positron emission tomography (PET), an androgen-independent uptake of tracers would be advantageous. Several metabolic PET tracers are employed for detecting recurrent PCa. We evaluated the effect of AD on the uptake of 2-deoxy-2-[ 18 F]fluoro-D-glucose ([ 18 F]FDG), [ 11 C]choline and [ 11 C]acetate in vivo. Methods: An [ 18 F]FDG, [ 11 C]choline and [ 11 C]acetate baseline micro(μ)PET/μ computed tomography (CT) scan was subsequently performed in xenografts of androgen-sensitive (LAPC-4) and androgen-independent (22Rv1) tumours in nude mice. An untreated control group was compared to a surgical castration group, i.e. androgen-deprived group. μPET/μCT imaging with the above-mentioned tracers was repeated 5 days after the start of treatment. The percentage change of SUVmax and SUVmeanTH in the tumours was calculated. Results: AD did not significantly affect the uptake of [ 18 F]FDG and [ 11 C]choline in LAPC-4 tumours as compared with the uptake of both tracers in untreated tumours. In control 22Rv1 tumours, [ 11 C]choline and [ 18 F]FDG uptake increased over time. However, compared with the uptake in control tumours, AD significantly decreased the uptake of [ 11 C] choline and tended to decrease [ 18 F]FDG uptake. [ 11 C]acetate uptake remained unaffected by AD in both PCa xenograft models. Conclusions: [ 18 F]FDG and especially [ 11 C]choline PET, which is currently used for the detection of recurrent PCa, could miss or underestimate the presence of local recurrent PCa following AD therapy. [ 11 C]acetate uptake occurs