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Scott Department of Urology [J. R. G., M. W. K., N. M. G.], Department of Pathology [R. J. B.], Information Technology Program [M. W. K.], and Department of Pathology [M. J. F.], Texas Children's Hospital, and Department of Cell Biology, Baylor College of Medicine [H. S. N., N. M. G.], Houston, Texas 77030
We previously established the autochthonous transgenic adenocarcinoma mouse prostate (TRAMP) model to facilitate characterization of molecular mechanisms involved in the initiation and progression of prostate cancer. TRAMP mice display high grade prostatic intraepithelial neoplasia or well-differentiated prostate cancer by 10–12 weeks of age. To test the hypothesis that molecular events leading to androgen independence and metastasis can occur early in the natural history of prostate cancer yet remain silent until selective pressures such as androgen deprivation are applied, we have examined the consequences of castration on the initiation and progression to metastatic prostate cancer in TRAMP mice. Cohorts were castrated at 12 weeks of age and sacrificed at 18 (T12/18) or 24 (T12/24) weeks of age, and the development of primary cancer and metastatic disease was compared to noncastrated (T18 and T24) controls. Median T12/18 and T12/24 genitourinary (GU) weight was significantly less than T18 and T24, respectively. In addition, T12/24 GU weight was significantly greater than T12/18. Histological prostate tumors developed in 3 of 7 T12/18 and 8 of 10 T12/24 mice. All tumors that developed in castrated mice were poorly differentiated in contrast to 27% in noncastrated controls. Although castration significantly decreased GU tumor burden, overall progression to poorly differentiated and metastatic disease was not ultimately delayed. These results demonstrate that prostate cancer in the TRAMP model is heterogeneous with respect to androgen dependence as early as 12 weeks of age; therefore, early androgen ablation may have a variable impact on progression in an individual mouse. Further analysis of this prostate cancer model to identify specific molecular mechanisms that determine androgen sensitivity may facilitate future initiation of appropriate individualized hormonal therapy for the management of human prostate cancer.
1 This work was supported in part by NIH Prostate Cancer Specialized Program of Research Excellence Grant CA58204 (to N. M. G.), National Cancer Institute Grant CA64851 (to N. M. G.), an award from CaP CURE (to N. M. G.), and American Cancer Society Grant PRTA-21 (to J. R. G.).
2 Present address: Department of Urology, University of Tennessee at Memphis, 956 Court Avenue, H220, Memphis, TN 38163.
3 To whom requests for reprints should be addressed, at Department of Cell Biology, Baylor College of Medicine, One Baylor Plaza M626, Houston, TX 77030.
Received 7/ 9/97. Accepted 9/22/97.
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