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Mammary Carcinogenesis in Foster-nursed X/Gf Mice¹

Cancer and Radiobiological Research Laboratory, New York City Department of Health and Hospitals, Delafield Hospital, and Department of Biology, New York University, New York, New York 10032

Newborn X/Gf mice were foster nursed by mothers of the DBA/212 mouse strain. [The X/Gf mice are highly resistant to spontaneous development of mammary tumors, whereas DBA/212 mice produce mammary tumors in high instances and contain an abundance of the mammary tumor virus (MMTV).] Varied numbers of F₁ to F₇ generations of foster-nursed females produced mammary tumors at ages ranging from 12 to 24 months. Sections of the tumors stained with hematoxylin and eosin and studied by light microscopy showed the characteristic appearance of mammary carcinomas, although differing in degree of differentiation. Electron microscope studies revealed the characteristic type MMTV particles in the tumors. The budding process of type B virus particle formation on cell membranes is illustrated in the electron micrographs. Morphologically, the virus particles in X/Gf mammary tumors appeared identical to those seen in spontaneous mammary tumors of the DBA/212 foster mothers. Separate biochemical studies on molecular level of growing X/Gf tumor extracts revealed viral-specific high-molecular-weight 70 S RNA and reverse transcriptase; the putative viral complex was localized in sucrose gradients at a density of 1.16 g/ml, the position characteristic of RNA MMTV. Thus, the electron microscope and biochemical data on a molecular level provide documentary evidence of the infectivity of the MMTV in the host cells.

X/Gf mice, challenged with MMTV by foster nursing, produced mammary tumors in early generations but failed to develop tumors after the seventh generation. This suggests that the X/Gf host, known to generate high levels of antibodies against MMTV, may be responsible for the cessation of mammary tumor development and not the virus. Thus, the significance of the immune competence of the host in neoplasia becomes apparent.

¹ Supported in part by grants from the Health Research Council of the City of New York #U-1354. NIH RO1-CA-12076-03, and from the Mildred Werner League for Cancer Research.

Received 1/23/74. Accepted 5/10/74.