This thesis describes the characterization and further application of a model system for
prostate cancer, the human prostatic adenocarcinoma PC-82 which is transplantable in
athymic nude mice.
The mortality rate of patients suffering from prostatic carcinoma is high, in spite of the
high response rates which are initially achieved with hormonal treatment ofthese patients.
Growth and function of the prostate are primarily dependent on androgenic stimuli.
Hormonal treatment of prostatic carcinoma is based upon the suppression of the testicular
production of androgens. This can be achieved directly by surgical removal of the testes or
indirectly by inhibiting the hypophyseal gonadotropin release through treatment with
estrogens or analogues of luteinizing hormone-releasing hormone (LHRH). However, in
the majority of patients relapse of the tumor occurs following a favorable response to
androgen-ablation therapy. Progression is caused mainly by a loss of androgen-sensitivity of
the tumor.
Since many investigations relevant to prostate cancer cannot be performed in patients,
there is a great need for well-characterized model systems which reflect the properties of
clinical prostate cancer. Relevant aspects of the prostate in general and of prostatic
carcinoma in particular are described in chapter 1, which also contains a summary of the
current knowledge of androgen action in the prostate and information on the available
model systems for prostatic cancer