Virus Oncogenesis and Tumor Immunogenicity in the Mouse Mammary Tumor System1
[CANCER RESEARCH 34, 1319 1324, June 1974] Virus Oncogenesis and Tumor Immunogenicity in the Mouse Mammary Tumor System1 Jan Vaage and Daniel Medina Department of Cancer Therapy Development, Pondville Hospital, Walpole, Massachusetts 02081 [J. K.J, and Department oj Cell Biology, Baylor College of Medicine, Houston. Texas 77025 [D. M.\ SUMMARY INTRODUCTION Mammary tumorigenesis and mammary tumor trans Several factors are known to be involved in the etiology of plantation immunogenicity were examined in breeding fe spontaneous mammary tumors in mice; most important males of 2 syngeneic sublines of the C3H strain: in among them are viral (2, 5, 15, 16), hormonal (16), and mammary tumor virus (MTV) plus nodule-inducing virus- genetic (8, 15) factors. In the C3H strain, 2 mammary infected C3H/Sed mice; and in MTV-free, nodule-inducing tumor viruses have been recognized: the MTV3 of high and virus-infected C3Hf/Sed mice. early oncogenic activity; and the NIV, of high but late Ninety-seven % of the C3H mice (29 of 30) developed oncogenic activity (11). The oncogenic effect of the in mammary tumors at an average age of 280 days. Of 43 M/ero-transmitted NIV is distinguishable in the C3Hf different C3H tumors tested for transplantation immunoge mouse, which was established as a syngeneic subline of C3H nicity in the C3H strain of origin, 13 (30%) had non-MTV- by foster nursing to exclude the milk-transmitted MTV, and associated tumor-specific transplantation antigens (TSTA). the high but late mammary tumor incidence in C3Hf mice Of 5 primary C3H hosts that developed multiple mammary becomes apparent in animals with a very long normal tumors, 4 animals developed both TSTA-positive and life-span in the infection-free conditions of a hygienic and TSTA-negative tumors.
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