Antigenic differences among virus-induced mouse mammary tumors arising spontaneously in the same C3H-Crgl host.
نویسندگان
چکیده
The immunogenicity of multiple, distinct, mammary tumor virus-induced mammary carcinomas which arose spontaneous ly in the same C3H mouse has been surveyed in MTV-infected syngeneic C3H hosts and in MTV-free syngeneic C3Hf hosts. Nineteen different tumors from 4 original hosts were tested. Whereas all tumors tested were immunogenic in C3Hf hosts, only 5 out of 19 tumors were immunogenic in C3H hosts. All tumors tested for antigenic cross-reactivity did cross-react in C3Hf hosts. Two tumors from the same original C3H donor were immunogenic in C3H hosts but did not cross-react. The results also show that one mouse may develop both immunogenic and nonimmunogenic spontaneous tumors at the same time. This excludes the possibility that minor histocompatibility differences between donor and recipient could be the cause of resistance to tumor grafts in syngeneic C3H mice and confirms a previous conclusion that virus-induced tumors may possess individually distinct tumor antigens in addition to virus-associated antigens. It is suggested that the appearance of individually distinct, nonvirus-associated antigens in virusinduced tumors may indicate a similarity in the action of viral and chemical carcinogens.
منابع مشابه
Acquisition of Heightened Resistance and Susceptibility to Spontaneous Mouse Mammary Carcinomas in the Original Host.
Experiments were designed to answer the following question: Can mice acquire heightened reactivity of an immunological nature to their own spontaneous mammary neoplasms? Twenty-five spontaneous mammary carcinomas, arising from transplanted C3H/f/ Crgl nodule outgrowth, were removed and subsequently retransplanted into their original C3H/Crgl/2 hosts. At the same time, the tumors were transplant...
متن کاملInterleukin-12 inhibits angiogenesis and growth of transplanted but not in situ mouse mammary tumor virus-induced mammary carcinomas.
We examined the ability of recombinant murine interleukin-12 (rmIL-12) to inhibit the vasculature and growth of mammary carcinomas arising in situ in mouse mammary tumor virus (MMTV)-infected female C3H/HeN mice. Although it is a potent antiangiogenic and antitumor agent in many transplanted murine tumor models, rmIL-12 failed to inhibit the vascularity, reduce the perfusion, or alter the growt...
متن کاملInfluence of dietary phenylalanine deficiency on the mammary tumor virus activity in C3H mice.
This paper reports the blood-borne mammary tumor virus activity of C3H/Crgl female virgin mice previously fed phenylalanine-deficient diets. Whole blood was removed from three groups of female virgin C3H/Crgl mice previously fed semipurified diets containing, respectively, 0.075, 0.120, and 0.300% phenylalanine for 8 months. The blood was twice diluted and 0.3 ml was injected into each C3HfBALB...
متن کاملMammary tumorigenesis and tumor morphology in four C3H sublines with or without exogenous mammary tumor virus.
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 ave...
متن کاملType-specific antigenic determinants on the major external glycoprotein of high- and low-oncogenic murine mammary tumor viruses.
We recently showed that the 52,000-dalton external glycoprotein (gp52) of the highly oncogenic mouse mammary tumor viruses (MMTVs) of RIII, GR, and C3H mice contains both type- and group-specific antigenic determinants. This was demonstrated by using a competition radioimmunoassay with 125I-externally labeled virions and antisera to the gp52 of MMTV from RIII mice (Proc. Natl. Acad. Sci. U.S.A....
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Cancer research
دوره 29 7 شماره
صفحات -
تاریخ انتشار 1969