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Mammary Tumorigenesis and Tumor Morphology in Four C3H Sublines with or without Exogenous Mammary Tumor Virus¹

Department of Experimental Pathology, Roswell Park Memorial Institute, Buffalo, New York, 14263 [J. V., B. B. A.], and Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20205 [G. H. S., Y. T.]

Mammary tumorigenesis was surveyed in retired breeding females in four sublines of the C3H strain: in standard milk-transmitted early oncogenic mouse mammary tumor virus (MMTV)-infected C3H/He and C3H/Ki mice; and in standard milk-transmitted early oncogenic MMTV free C3Hf/He and C3Hf/Ki mice. All of 58 C3H/Ki mice and 98% (306 of 309) of the C3H/He mice developed palpable mammary tumors at average ages of 276 and 284 days, respectively. Thirty-one % (47 of 152) of the C3Hf/Ki mice and 77% (168 of 218) of the C3Hf/He mice developed palpable mammary tumors at average ages of 798 and 757 days, respectively.

The mammary tumors removed from C3H/He and C3H/Ki mice were all adenocarcinomas of epithelial origin, and all contained MMTV. The mammary tumors removed from C3Hf/He and C3Hf/Ki mice were either adenocarcinomas or sarcomas. The carcinomas were of epithelial origin and all expressed the late oncogenic endogenous MMTV. The sarcomas were of histiocyte or fibrocyte origin and contained neither virus particles nor MMTV antigenic markers. It is concluded that exogenous standard milk-transmitted oncogenic MMTV oncogenesis in C3H mice is not modified by host genetic factors. In contrast, late oncogenic endogenous MMTV oncogenesis is influenced both by host genetic control of the expression of the late oncogenic MMTV provirus and by the location of the proviral genes in the germline DNA.

¹ This work was supported by Grants CA-29660 and CA-32937 from the National Cancer Institute.

² To whom requests for reprints should be addressed.

Received 9/ 5/85. Revised 12/ 5/85. Accepted 12/31/85.