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[Cancer Research 61, 8298-8305, November 15, 2001]
© 2001 American Association for Cancer Research

Tumor Biology

Transgenic Polyoma Middle-T Mice Model Premalignant Mammary Disease1

Jeannie E. Maglione2, Drew Moghanaki2, Lawrence J. T. Young2, Cathyryne K. Manner, Lesley G. Ellies, Sasha O. Joseph, Benjamin Nicholson, Robert D. Cardiff2,,3 and Carol L. MacLeod2,,3

Department of Medicine, Cancer Center, School of Medicine, University of California, San Diego, La Jolla, California 92093 [J. E. M., D. M., C. K M., L. G. E., S. O. J., B. N., C. L. M.], and Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine and the Department of Pathology, University of California, Davis, Davis, California 95616 [L. J. T. Y., R. D. C.]

Mice transgenic for the Polyomavirus middle T (PyV-mT) gene have been widely used to study mammary tumorigenesis and metastasis. Although numerous molecular insights were gained from the analysis of these transgenic malignant tumors, the early events leading to malignant transformation have not been systematically investigated nor has the biological potential of hyperplastic lesions been documented. This paper presents the first comprehensive histopathological characterization of transgenic PyV-mT hyperplasias together with classical transplantation experiments designed to test the growth potential of these lesions. Moreover, stable hyperplastic outgrowth lines were established as a tool to study premalignant PyV-mT-induced hyperplasias in detail. Each line has a different tumor latency, indicating that PyV-mT-induced hyperplasias, like early proliferative lesions seen in the human breast, are heterogeneous with respect to their malignant potential. Our results settle a controversy; they establish that PyV-mT gene expression alone is insufficient to induce tumors and that additional events are required for tumorigenesis and metastasis. These results support the use of PyV-mT transgenic mice as a model for investigating the multistep progression of malignant mammary tumorigenesis and metastasis.




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