Abstract
Models for testing new drugs for the treatment of hormone-dependent prostate cancer are restricted to a few in vivo rat tumour lines; most of them originating from the Dunning R3327 adenocarcinoma. The original tumour and the R3327-H line grow rather slowly leading to a long duration of therapeutic experiments. The R3327-G subline can be transplanted as a cell suspension or tumour fragments, ...
Abstract
Models for testing new drugs for the treatment of hormone-dependent prostate cancer are restricted to a few in vivo rat tumour lines; most of them originating from the Dunning R3327 adenocarcinoma. The original tumour and the R3327-H line grow rather slowly leading to a long duration of therapeutic experiments. The R3327-G subline can be transplanted as a cell suspension or tumour fragments, which give rise to fast and rather homogeneously growing androgen-dependent tumours. Their growth is strongly inhibited by castration or administration of diethylstilbestrol. Experiments were terminated 5 weeks after transplantation. Best results were obtained when treatment was started 1 day after transplantation. Histological sections showed therapy-dependent changes in the microarchitecture of these prostate tumours. The direct inhibitory effect of antiandrogens on prostate tumours was demonstrated when castrated, testosterone-propionate-supplemented animals were used. The short duration of experiments and reproducible responses to standard therapies are the advantages of this tumour model.
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