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[Cancer Research 57, 3325-3330, August 15, 1997]
© 1997 American Association for Cancer Research
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Characterization of Prostatic Epithelial Cell Lines Derived from Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) Model1

Barbara A. Foster, Jeffrey R. Gingrich, Eugene D. Kwon, Christopher Madias and Norman M. Greenberg2

Departments of Cell Biology [B. A. F., N. M. G.] and Urology [J. R. G.], Baylor College of Medicine, Houston, Texas 77030, and Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland 20892-0951 [E. D. K., C. M.]

To develop a syngeneic transplantable system to study immunotherapeutic approaches for the treatment of prostate cancer, three cell lines were established from a heterogeneous 32 week tumor of the transgenic adenocarcinoma mouse prostate (TRAMP) model. TRAMP is a transgenic line of C57BL/6 mice harboring a construct comprised of the minimal -426/+28 rat probasin promoter driving prostate-specific epithelial expression of the SV40 large T antigen. TRAMP males develop histological prostatic intraepithelial neoplasia by 8–12 weeks of age that progress to adenocarcinoma with distant metastases by 24–30 weeks of age. The three cell lines (TRAMP-C1, TRAMP-C2, and TRAMP-C3) express cytokeratin, E-cadherin, and androgen receptor by immunohistochemical analysis and do not appear to have a mutated p53. Although TRAMP-C1 and TRAMP-C2 are tumorigenic when grafted into syngeneic C57BL/6 hosts, TRAMP-C3 grows readily in vitro but does not form tumors. The T antigen oncoprotein is not expressed by the cell lines in vitro or in vivo. The rationale for establishing multiple cell lines was to isolate cells representing various stages of cellular transformation and progression to androgen-independent metastatic disease that could be manipulated in vitro and, in combination with the TRAMP model, provide a system to investigate therapeutic interventions, such as immunotherapy prior to clinical trials.

1 This work was supported by NIH Prostate Cancer Specialized Program of Research Excellence Grant CA58204 (to N. M. G.), National Cancer Institute Grant CA64851 (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 5/20/97. Accepted 6/26/97.




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