The treatment of disseminated prostate cancer remains a great challenge in 
current oncology practice. The proliferation of prostate cancer cells is 
testosterone-driven, but clonal selection during androgen deprivation therapy 
promotes the development of androgen-independent (hormone-refractory) cells, 
which become phenotypically dominant. Human epidermal growth factor receptor 
type 2 (HER2) is capable of activating the androgen receptor pathway, even in 
the absence of the ligand. The detection of phenotypic changes associated with 
the development of androgen independence may influence patient management, 
suggesting the initiation of a second-line therapy. This study aimed to 
establish the level of HER2 expression in a number of prostate cancer cell lines 
(LNCaP, PC3 and DU145) in order that they be used as models in further studies, 
and to evaluate the binding and cellular processing of [(111)In]-labeled 
trastuzumab and the anti-HER2 synthetic Affibody molecule ABY-025 in these cell 
lines. The expression of HER2 was demonstrated and quantified in all three 
tested prostate cancer cell-lines. Studies on cellular processing demonstrated 
that internalization of both conjugates increased continuously during the whole 
incubation. The internalization rate was approximately equal for both monoclonal 
antibodies and Affibody molecules. In both cases, internalization was moderately 
rapid. Such features would definitely favor the use of radiometal labels for 
trastuzumab and, most likely, for affibody molecules. The level of HER2 
expression in these cell lines is sufficient for in vivo molecular imaging.