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[Cancer Research 44, 4333-4336, October 1, 1984]
© 1984 American Association for Cancer Research

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Development and Characterization of the BALB/cNIV Mouse Strain1

Lawrence J. T. Young, Kenneth B. DeOme, Phyllis B. Blair, Dorothy R. Pitelka and Robert D. Cardiff2

Department of Pathology, School of Medicine, University of California, Davis, California 95616 [L. J. T. Y., R. D. C.]; Cancer Research Laboratory [D. R. P., K. B. D.], and Department of Microbiology and Immunology, University of California, Berkeley, California 94720 [P. B. B.]

The strain BALB/cNIV/Crgl was developed by infecting BALB/c/Crgl mice with mouse mammary tumor virus from C3Hf mice. A BALB/c normal mammary duct was transplanted into the gland-free fat pad of a hormone-stimulated female C3Hf x BALB/c F1 mouse. A hyperplastic alveolar nodule was found in the BALB/c ductal outgrowth and was transplanted into another hybrid gland-free fat pad. The resultant hyperplastic alveolar outgrowth was finally transplanted to female BALB/c mice. The hyperplastic alveolar outgrowth contained an exogenous, infectious mouse mammary tumor virus named the nodule-inducing virus, which was thought to be derived from the endogenous low oncogenic mouse mammary tumor virus found in C3Hf mice. The hyperplastic alveolar outgrowth-bearing BALB/c mice were inbred for four generations, and one family was selected as the strain BALB/cNIV/Crgl. It was found that (a) the mouse mammary tumor virus found in the BALB/cNIV strain was milk transmitted, but not transmitted by infected males; (b) the BALB/cNIV breeding females had a low tumor incidence (40%) and a longer latent period (14 months) than did female BALB/cfC3H mice (92% at 8 months); (c) the BALB/cNIV nodule outgrowths had low tumor-producing capabilities (50%) and longer latent periods (13.4 months) than did nodule outgrowths derived from female BALB/cfC3H mice (100% at 7.7 months).

1 This research was supported by USPHS Grant CA-05388 and Contract N01 CP 0-1008 from the National Cancer Institute, NIH. Presented in part at the 71st Annual Meeting of the American Association for Cancer Research, May 28 to 31, 1980, San Diego, CA (38).

2 To whom requests for reprints should be addressed.

Received 1/ 4/82. Accepted 6/21/84.




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Acceleration of Mouse Mammary Tumor Virus-Induced Murine Mammary Tumorigenesis by a p53172H Transgene: Influence of FVB Background on Tumor Latency and Identification of Novel Sites of Proviral Insertion
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[Abstract] [Full Text] [PDF]




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Copyright © 1984 by the American Association for Cancer Research.