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Evaluation of androgen-induced effects on the uptake of [18F]FDG, [11C]choline and [11C]acetate in an androgen-sensitive and androgen-independent prostate cancer xenograft model

Kimy M Emonds1, Johannes V Swinnen2, Evelyne Lerut3, Michel Koole1, Luc Mortelmans1 and Felix M Mottaghy145*

Author Affiliations

1 Department of Nuclear Medicine, University Hospitals Leuven, Leuven 3000, Belgium

2 Laboratory of Lipid Metabolism and Cancer, Department of Oncology, KU Leuven, Leuven 3000, Belgium

3 Department of Morphology and Molecular Pathology, University Hospitals Leuven, Leuven 3000, Belgium

4 Department of Nuclear Medicine, University Hospital of Aachen, Aachen 52057, Germany

5 Department of Nuclear Medicine, Maastricht University Medical Center, Maastricht, 6202, the Netherlands

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EJNMMI Research 2013, 3:31  doi:10.1186/2191-219X-3-31

Published: 24 April 2013



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-[18F]fluoro-D-glucose ([18F]FDG), [11C]choline and [11C]acetate in vivo.


An [18F]FDG, [11C]choline and [11C]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.


AD did not significantly affect the uptake of [18F]FDG and [11C]choline in LAPC-4 tumours as compared with the uptake of both tracers in untreated tumours. In control 22Rv1 tumours, [11C]choline and [18F]FDG uptake increased over time. However, compared with the uptake in control tumours, AD significantly decreased the uptake of [11C]choline and tended to decrease [18F]FDG uptake. [11C]acetate uptake remained unaffected by AD in both PCa xenograft models.


[18F]FDG and especially [11C]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. [11C]acetate uptake occurs independently of androgens and thus may be more favourable for detecting tumour viability during or following AD.

Prostate cancer; Androgen deprivation; PET; [18F]FDG; [11C]choline; [11C]acetate