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[Cancer Research 62, 2999-3004, June 1, 2002]
© 2002 American Association for Cancer Research

Advances in Brief

Nkx3.1 Mutant Mice Recapitulate Early Stages of Prostate Carcinogenesis1

Minjung J. Kim, Rajula Bhatia-Gaur2, Whitney A. Banach-Petrosky, Nishita Desai, Yuzhuo Wang3, Simon W. Hayward4, Gerald R. Cunha, Robert D. Cardiff, Michael M. Shen5 and Cory Abate-Shen5

Center for Advanced Biotechnology and Medicine [M. J. K., R. B-G., W. A. B-P., N. D., M. M. S., C. A-S.], Departments of Neuroscience [M. J. K., R. B-G., W. A. B-P., C. A-S.], Medicine [C. A-S.], and Pediatrics [N. D., M. M. S.], The Cancer Institute of New Jersey [M. M. S., C. A-S.], University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854; Department of Anatomy, University of California, San Francisco, California 94143 [Y. W., S. W. H., G. R. C.]; and Center for Comparative Medicine, University of California, Davis, California 95616 [R. D. C.]

Recent studies of human cancers and mutant mouse models have implicated the Nkx3.1 homeobox gene as having a key role in prostate carcinogenesis. Consistent with such a role, here we show that Nkx3.1 displays growth-suppressing activities in cell culture, and that aged Nkx3.1 mutant mice display histopathological defects resembling prostatic intraepithelial neoplasia (PIN), the presumed precursor of human prostate cancer. Using a tissue recombination approach, we found that PIN-like lesions from Nkx3.1 mutants can undergo progressively severe histopathological alterations after serial transplantation in nude mice. Our findings indicate that Nkx3.1 loss-of-function is a critical event in prostate cancer initiation, and that Nkx3.1 mutant mice accurately model early stages of prostate carcinogenesis. More generally, our tissue recombination assay provides an empirical test to examine the relationship of PIN to prostate carcinoma.




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