Morphologic and antigenic properties of mouse mammary tumor virus produced in a hormone-responsive fashion by C57Bl/10 mammary tumors of non-viral origin.

Bl-MaTU/A1 mouse mammary tumor cells, derived from a C57B1/10 mammary adenocarcinoma induced by dimethylbenzanthracene and mammotropic hormones, express virus particles and proteins related to mouse mammary tumor virus (MMTV). Immunocytochemical analysis by means of monospecific and monoclonal anti-gp52 sera revealed a different localization of the main structural proteins of MMTV in Bl-MaTU/A1 and GR cells (the latter used as a positive virus-producing control). Immunoelectron microscopy of B-type particles budding from the microvilli of dexamethasone-stimulated Bl-MaTU/A1 cells showed remarkably weak reactivity of the viral envelope with anti-gp52-protein A-gold complexes as compared with that of dexamethasone-stimulated GR cells. Since Bl-MaTU/A1-associated MMTV originates from the amplified unit II of endogenous MMTV, which is altered probably within the env gene, the observed antigenic difference in the Bl-MaTU/A1-associated MMTV may be due to altered synthesis of gp52 glycoprotein in these cells.

Hormone-responsive genes of the mouse mammary tumor virus.

By optimal hormonal treatment the production of exogenously transmitted MMTV can be stimulated in vitro to different degrees, depending on cultivation conditions and origin of tumor cells. Moreover, after appropriate hormonal treatment, endogenous MMTV-Y can be rescued from primary cell cultures derived from dimethyl benzanthracene- and hormone-induced C57BL/10 mouse mammary adenocarcinoma, as determined by reverse transcriptase assay, distribution of 3H-uridine-labelled viral particles, immunofluorescence, and electron microscopy. On the contrary, all attempts to rescue MMTV-Y from cultures derived from urethane-induced C57BL/10 tumors failed. These data indicate that upon syncarcinogenic action of non-viral carcinogenes, estrogen and prolactin, the MMTV-Y genome can be expressed in mammary gland parenchymatous cells, which in turn may result in cell transformation. The full MMTV-Y gene expression occur after appropriate hormonal stimulation of the C57BL/10 mammary cancer cells in vitro.

Pathogenicity for rats of a strain of chicken sarcoma virus.

The RBI rat tumor, induced with cell suspensions from chicken sarcoma B77, is pathogenic for chicks as well as for rats. Cell suspensions from RBI tumors induced sarcomas in 100 percent of inoculated chicks. Cell suspensions of this chicken sarcoma induced early RBA sarcomas in 50 percent of 171 rats. Most of these rats died within 4 weeks after inoculation. The early tumors regressed in 15 of the 85 tumor-bearing rats, and the animals died of cystic hemorrhagic disease. The sarcoma was induced in 9 animals within 50 to 70 days after inoculation, and cystic hemorrhagic disease developed in 117. None of the 171 rats remained free from either tumor or cyst and only 12 survived for 3 months or longer. The tumors induced in rats were transplantable into rats and after transplantation of early-appearing tumors, tumors and cysts developed. Virus strongly infective in chicks was demonstrated by cell-free filtrates and virus preparations from RBI and RBA rat sarcomas induced by chicken sarcoma cells. Cell suspensions from the wall of small cysts induced tumors in chicks and cystic hemorrhagic disease and tumors in rats.