Plasma hormone levels and the incidence of carcinogen-induced mammary tumours in two strains of rat.

The incidence of mammary tumours developing after administration of the carcinogen DMBA (at 50 days of age) has been determined in 2 strains of Sprague-Dawley rat. Untreated animals of each strain were exsanguinated in dioestrus at a time corresponding to the early post-carcinogen stage (at 70 days of age) and the plasma concentrations of prolactin, oestradiol-17B and progesterone were measured by radioimmunoassay. In an inbred strain of rats, tumour-induction rate was 6-4% and plasma prolactin concentration was 2-5 x lower than that found in a random-bred strain with a tumour-induction rate of 41-6%. No difference was found between the 2 strains in the level of either ovarian hormone. It is concluded that the difference between these strains in mammary gland susceptibility to DMBA may be related to plasma prolactin concentration, but it is unlikely to be determined by the ovarian hormones.     

Comparative studies of purified subviral component vaccines and formalin-treated mammary tumor viruses from four inbred strains of mice

Formalin-treated virus vaccines were prepared from purified murine mammary tumor viruses (MuMTV) from 4 inbred strains of mice: RIII/Imr, GR/Imr, C3H/Imr, and A/Imr. In addition, subviral components were isolated from these 4 strains and purified to homogeneity. The inactivated viruses, their major envelope glycoproteins (gp50-gp55), and their major internal core protein (p28) were emulsified in complete Freund's adjuvant and used as vaccines for prevention of mammary tumors in mice. All 4 Formalin-treated virus vaccines reduced significantly the incidence of mammary tumors in "virus-free" C57BL and BALB/c mice when inoculated prior to challenge with live MuMTV. The RIII-, GR-, and A-MuMTV strains showed extensive heterologous cross-protection, whereas the C3H-MuMTV strain showed significant protection only against C3H- and A-MuMTV challenge. The major viral glycoproteins gp50-gp55 reduced significantly the tumor incidence when mice were challenged with isologous infectious virus after immunization, although these glycoproteins showed different degrees of cross-protection than did the same virus strains used as "intact" but Formalin-treated preparations. RIII-gp55 and GR-gp55 cross-protected against each other but not against challenge with C3H- and A-MuMTV strains; the A-gp50 protected against challenge with A- and RIII-MuMTV strains; C3H-gp55 demonstrated limited activity against C3H-MuMTV challenge only. The internal viral core proteins (p28) were ineffective in all systems studied. The same vaccines were tested in MuMTV-positive, high-tumor-incidence strains from which they were derived. At best, the appearance of spontaneous tumors was delayed in a few experimental sets; eventually, all mice developed mammary tumors. The foster-nursed C3HfC57BL strain of mice, which is not exposed to exogenous MuMTV during suckling and which develops mammary tumors after activation of the endogenous virus genome later in life, was responsive only when the heterologous GR-MuMTV Formalin-treated vaccine was used. The association between the ability of virus vaccines to protect a mouse strain and the degree of natural virus expression in that strain is discussed.