Inhibition of oncogenicity of murine sarcoma virus (Harvey) in mice by interferon.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to L D Berman.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Clones were isolated from hamster cells transformed by the adenovirus 2-SV40 and adenovirus 12-SV40 transcapsidant hybrid viruses. The clones were characterized with respect to their cytomorphology, virus and antigen content, and the histomorphology of tumors induced by transplantation of the clonal sublines to hamsters. Three different cellular and colonial morphologies were observed. Clones with an SV40 morphology gave rise to tumors predominantly with an SV40 histology, whereas clones with an adenovirus morphology produced typical adenovirus tumors upon transplantation of the transformed cells. Clones which had features of both SV40 and adenovirus transformed cells gave rise to "intermediate" and adenovirus tumors. The results indicate that multiple events occur during transformation and tumorigenesis by the transcapsidant virus populations and provide an explanation for the multiplicity of findings which have been reported with these virus populations.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The existence of a virus-induced, virus-specific transplantation, antigen in adenovirus 12-induced CBA mouse tumors was demonstrated. The antigen is virus-specific, but not related to structural virion or T antigens. It is a weak antigen, and required immunization with whole, infectious adenovirus 12 to produce considerable immunity. Comparable immunity could not be achieved with homologous cellular or subcellular materials, but some indication of enhancement was produced with low tumor dose. Immunization required at least 2 wk and was mediated by immune lymphoid cells. Serum of immunized animals showed no demonstrable cytotoxicity or enhancement. Animals immunized with virus and Freund's adjuvant showed diminished transplantation immunity, although these animals were actively immunized against adenovirus type 12 structural virion antigens.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Guinea pigs intranasally dusted with ragweed pollen (RW) for one month went into anaphylaxis in ragweed extract aerosol (RWEA). Animals which received RWEA pretreatment for one month before nasal dusting with RW pollen were nonresponsive to RWEA. The purpose of this study was to define the mechanism of nonresponsiveness. The protocol for producing either sensitivity or nonresponsiveness was applicable to another antigen, bovine serum albumin (BSA). Antibody blocking passive cutaneous anaphylaxis (PCA) in passively sensitized animals was demonstrable in BSA nonresponder serum. However, the blocking antibody probably was not responsible for the nonresponsiveness because BSA nonresponder serum was also able to sensitize passively the skin and lungs of normal recipients. Also nonresponsiveness was not due to the swallowing of antigen because feeding antigen inhibited synthesis of sensitizing antibody and precipitating antibody both of which were present in high titers in nonresponders. Sensitive guinea pig lungs contained nearly twice as much histamine as normal and nonresponder lungs. However, normal and nonresponders went into anaphylaxis at the same time in an aerosol of compound 48/80. These results suggest that the mechanism of nonresponsiveness produced by pretreatment with antigen aerosols might be due to a modification in antigen reactivity of the lung mast cells rather than to alterations in the mediators of anaphylaxis.