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Mammary Tumorigenesis in 7,12-Dimethybenzanthracene-treated C57BL x DBA/2f F₁ Mice¹

Departments of Cell Biology [D. M., S. H. S., F. L. M.] and Virology [J. S. B.], Baylor College of Medicine, Houston, Texas 77030

Mammary tumors induced by 7,12-dimethylbenzanthracene (DMBA) in female C57BL/6 x DBA/2f F₁ mice were characterized by their histopathology, ovarian dependence, and expression of mouse mammary tumor virus (MuMTV) RNA and antigens. DMBA induced a high incidence of mammary tumors in virgin (69%) and hormone-stimulated mice (81%). Approximately 70% of the mammary tumors in both groups were adenocarcinomas, and the remaining 30% were adenoacanthomas. The distribution of the adenoacanthomas, but not of the adenocarcinomas, was nonrandom since 13 of 14 developed by 30 weeks of host age. Of the tumors examined, almost one-half exhibited a significant degree of ovary responsiveness. These ovary-responsive tumors fell into two categories: ovary dependent (tumors that grew better in the presence of the ovary); and ovary sensitive (tumors that grew better in the absence of the ovary). These results together with previous ones indicate that C57BL/6 x DBA/2f F₁ mice are particularly apt to develop ovary-responsive tumors after chemical carcinogen treatment.

A significant level of MuMTV RNA was detected by molecular hybridization in the mammary glands of untreated control mice and in DMBA-induced tumors (at 0.01% of total RNA). These results support the hypothesis that enhanced expression of the MuMTV genome is not necessary for maintenance of the tumor phenotype in DMBA-induced mammary tumors. Interestingly, few of the C57BL/6 x DBA/2f F₁ tumors (2 of 14) reacted with antiserum directed against C3H MuMTV glycoprotein with a molecular weight of 52,000, although a majority (13 of 14) reacted with anti-MuMTV serum. The possible significance of these results is discussed.

¹ This research was supported in part by NIH Grant CA-11944 and by Contract NO1-CP-81006 within the Virus Cancer Program of the National Cancer Institute.

Received 8/ 2/79. Accepted 11/ 1/79.

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