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Metastatic Prostate Cancer in a Transgenic Mouse¹

Department of Cell Biology [F. J. D., J. M. R., N. M. G.], Scott Department of Urology [J. R. G., R. A. M., N. M. G.], and Department of Pathology [R. J. B.], Baylor College of Medicine, Houston, Texas 77030; Department of Pathology, Texas Children's Hospital, Houston Texas 77030 [M. J. F.]; Department of Pathology, University of Texas Health Sciences, San Antonio, Texas 78284 [B. F. B.]; and University of Athens Medical School, 11627 Athens, Greece [R. A.]

We have previously reported the development of a transgenic mouse model for prostate cancer derived from PB-Tag transgenic line 8247, henceforth designated the TRAMP (transgenic adenocarcinoma mouse prostate) model. We now describe the temporal and spatial consequences of transgene expression and report the identification and characterization of metastatic disease in the TRAMP model. TRAMP mice characteristically express the T antigen oncoprotein by 8 weeks of age and develop distinct pathology in the epithelium of the dorsolateral prostate by 10 weeks of age. Distant site metastases can be detected as early as 12 weeks of age. The common sites of metastases are the periaortic lymph nodes and lungs, with occasional metastases to the kidney, adrenal gland, and bone. By 28 weeks of age, 100% harbor metastatic prostate cancer in the lymph nodes or lungs. We have also demonstrated the loss of normal E-cadherin expression, as observed in human prostate cancer, as primary tumors become less differentiated and metastasize. The TRAMP model provides a consistent source of primary and metastatic tumors for histopathobiological and molecular analysis to further define the earliest molecular events involved in the genesis, progression, and metastasis of prostate cancer.

¹ This work was supported in part by NIH Prostate Cancer Specialized Program of Research Excellence Grant CA58204 (to N. M. G.) and Grant CA40035 (to B. F. B.), 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 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 6/20/96. Accepted 7/31/96.

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				J. A. Nemeth, J. F. Harb, U. Barroso Jr., Z. He, D. J. Grignon, and M. L. Cher Severe Combined Immunodeficient-hu Model of Human Prostate Cancer Metastasis to Human Bone Cancer Res., April 1, 1999; 59(8): 1987 - 1993. [Abstract] [Full Text] [PDF]

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				P. J. Russell, S. Bennett, and P. Stricker Growth factor involvement in progression of prostate cancer Clin. Chem., April 1, 1998; 44(4): 705 - 723. [Abstract] [Full Text] [PDF]

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				K. B. J .M. Cleutjens, H. A. G. M. van der Korput, C. C. Ehren-van Eekelen, R. A. Sikes, C. Fasciana, L. W. Chung, and J. Trapman A 6-kb Promoter Fragment Mimics in Transgenic Mice the Prostate-Specific and Androgen-Regulated Expression of the Endogenous Prostate-Specific Antigen Gene in Humans Mol. Endocrinol., August 1, 1997; 11(9): 1256 - 1265. [Abstract] [Full Text]

				G. Han, B. A. Foster, S. Mistry, G. Buchanan, J. M. Harris, W. D. Tilley, and N. M. Greenberg Hormone Status Selects for Spontaneous Somatic Androgen Receptor Variants That Demonstrate Specific Ligand and Cofactor Dependent Activities in Autochthonous Prostate Cancer J. Biol. Chem., March 30, 2001; 276(14): 11204 - 11213. [Abstract] [Full Text] [PDF]

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				B. Kwabi-Addo, D. Giri, K. Schmidt, K. Podsypanina, R. Parsons, N. Greenberg, and M. Ittmann Haploinsufficiency of the Pten tumor suppressor gene promotes prostate cancer progression PNAS, September 25, 2001; 98(20): 11563 - 11568. [Abstract] [Full Text] [PDF]