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Advances in Brief |
Center for Advanced Biotechnology and Medicine [C. A-S., W. A. B-P., X. S., K. D. E., N. D., M. M. S.], Departments of Medicine [C. A-S., W. A. B-P., X. S., K. D. E.], Neuroscience and Cell Biology [C. A-S., W. A. B-P., X. S., K. D. E.], and Pediatrics [N. D., M. M. S.], and The Cancer Institute of New Jersey [C. A-S., M. M. S.], University of Medicine and Dentistry, New Jersey-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, and Department of Medical Pathology and Center for Comparative Medicine, University of California, Davis, California [J. P. G., A. D. B., R. D. C.]
Recent studies have shown that several loss-of-function mouse models of prostate carcinogenesis can develop a spectrum of precancerous lesions that resemble human prostatic intraepithelial neoplasia (PIN). Here, we have investigated the malignant potential of the high-grade PIN lesions that form in Nkx3.1+/-; Pten+/- compound mutant mice and demonstrate their neoplastic progression in a serial transplantation/tissue recombination assay. Furthermore, we find that a majority of Nkx3.1+/-; Pten+/- mice greater than 1 year of age develop invasive adenocarcinoma, which is frequently accompanied by metastases to lymph nodes. Finally, we observe androgen independence of high-grade PIN lesions after androgen ablation of Nkx3.1+/-; Pten+/- mice. We conclude that Nkx3.1+/-; Pten+/- mice recapitulate key features of advanced prostate cancer and represent a useful model for investigating associated molecular mechanisms and for evaluating therapeutic approaches.
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