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R J Huebner

Publications and source records attributed to R J Huebner.

At least 55 records · Page 3Linked to original sources
PubMed1976

An approach to C-type virus immunoprevention of spontaneously occurring tumors in laboratory mice.

A review of our current progress in C-type virus vaccine research is presented. This includes the findings of C-type virus or its antigen expressions in every naturally occurring tumor of two strains of "low-incidence" laboratory mice, the BALB/cCr mouse and the NIH Swiss mouse. Vaccine preparation methods are described including the inactivation of C-type virus infectivity with optimal maintenance of the antigen titers of at least two of the polypeptides of the C-type virus, gp69/71 and p30. The cell-mediated immune response of the mouse to C-type virus vaccines, as measured by a footpad assay for delayed-type hypersensitivity and an in vitro lymphocyte transformation assay, is described. Studies with two murine C-type viruses (Rauscher leukemia and Gross leukemia) a simian C-type virus, and an avian C-type virus (avian myeloblastosis virus) showed that the cell-mediated immune response of the animal includes type-specific, group-specific, and interspecies-specific reactivity. The mouse gave a cell-mediated immune response to at least one of the polypeptides of the C-type virus, the gp69/71, whether this polypeptide was presented to the immune system of the mouse as whole virus, Tween-ether-treated virus, or a purified polypeptide. One measure of the effectiveness of the C-type virus vaccines was provided by immunization of the mouse with Rauscher leukemia virus preparation that induced resistance to challenge with both live Rauscher leukemia virus and a naturally occurring BALB/c leukemia virus. Evidence is presented that the C-type virus can act as an effective transplantation antigen in syngeneic tumor cell lines resulting in the immunogenicity and loss of tumorigenicity of these cell lines. An approach to the viral immunoprevention of spontaneously occurring tumors is discussed.

Animals↗
PubMed1975

Characterization of non-producer human cells induced by Kirsten sarcoma virus.

Non-producer (NP) human cells induced by the Kirsten sarcoma virus were characterized. These morphologically altered NP cells produced neither infectious virus nor complement-fixing antigens of the murine sarcoma-leukemia virus complex. The NP cells did not release RNA-dependent DNA polymerase and type-C virus particles with a density of approximately 1.15 g/ml in sucrose gradients by 3H-uridine labelling. The NP cells produced tumors when transplanted subcutaneously into athymic nude mice. The tumor cells re-established in culture resembled the orginal NP cells, were confirmed as human cells by karyological analysis and were also found to be "non-producer". The sarcoma virus genome in NP cells could be rescued not only by co-cultivation with "helper virus"-releasing cells but also by superinfection with helper type-C viruses. Murine (Rauscher, Ki-MuLV, AT-124 and two other xenotropic viruses), feline, RD-114 and Simian (woolly monkey and baboon) type-C viruses possessed the ability to rescue the sarcoma genome from NP cells but not AKR leukemia virus. In addition, the feline leukemia virus titer obtained by the rescuing technique in NP cells was the same as those obtained in feline embryo and NP cells by CF induction assay.

Animals↗
PubMed1975

Transforming potential of the anticancer drug adriamycin.

A Fischer rat embryo cell system in vitro, which had been shown to be highly accurate in identifying chemical carcinogens and to have application in the study of chemicals having anticancer properties, was used to study the anticancer drug adriamycin. At a nontoxic dose adriamycin not only did not protect the cells from transformation by the carcinogen 3-methylcholanthrene, but was found in two separate experiments to act on its own as a transforming agent.

Animals↗
PubMed1975

Transformation of horse skin cells by type-C sarcoma viruses.

A horse skin cell line (E. Derm, NBL-6, CCL-57) was susceptible to focus formation by the Kirsten mouse sarcoma virus, feline sarcoma virus (ST stain) and the MSV pseudotypes with woolly monkey, gibbon monkey, RD-114, AT-124, baboon placenta and murine xenotropic (BALB/c 3T3 and C57L/JD) type-C viruses. Foci were detected within 5 days after infection and the transformed cells continued to produce infectious virus and group-specific antigen of their respective type-C leukemia viruses. The transformation efficiency of various type-C sarcoma viruses in horse cells was also very high.

Animals↗
PubMed1975

Non-producer human cells induced by murine sarcoma virus.

Non-produces (NP) human cells were isolated from transformed foci induced by the Kirsten mouse sarcoma virus. These morphologically altered NP cells produced neither infectious virus nor complement-fixing antigens of the murine sarcoma-leukemia virus complex. However, the sarcoma virus genome could be rescued from these NF cells by co-cultivation with cells carrying "helper" Kirsten mouse leukemia virus or Woolly Monkey leukemia virus. The possible usefulness of these cells in efforts designed to detect covert or repressed RNA tumor viruses in various animal and human tissues is discussed.

Animals↗
PubMed1975

Type-C virus-specific nucleic acid sequences in cultured rat cells.

Single-stranded DNA transcripts of rat type-C viruses prepared in the presence of actinomycin D, hybridized specifically to DNA of several rat cell cultures with no obvious qualitative or quantitative differences. Similar products prepared from a pseudo-type sarcoma virus with contributions from rat and mouse type-C viruses hybridized to both rat and mouse cellular DNA, while mouse viral transcripts did not hybridize to rat cell DNA. Viral RNA was detected in all rat cells by means of the rat viral DNA transcripts, with some differences between untreated low-passage cells and sister cultures treated with bromodeoxyuridine or bromodeoxyuridine and methylcholanthrene. Cells treated with both compounds were previously shown to be transformed and turorigenic, and these were distinguishable by kinetic analysis from the control cells.

Amino Acid Sequence↗
PubMed1975

Type-C RNA viruses of the NIH nude mouse.

Several types of tumors from various species were propagated in NIH athymic nude mice. Subsequently, cell lines were established from the tumors and examined for evidence of type-C virus activity. Hybrid mice (NIH Swiss and BALB/c) harbored murine type-C viruses of three categories: N-tropic, B-tropic and X-tropic.

Animals↗
PubMed1975

Transformation of human osteosarcoma cells by a chemical carcinogen.

A human osteosarcoma clonal cell line (TE-85, clone F-5) was treated in vitro with various levels of 7,12-dimethylbenz[a]anthracene or dimethyl sulfoxide (control). Cells treated only with the carcinogen underwent morphologic alteration in vitro, and one of these altered cell lines produced tumors subcutaneously and intracerebrally when injected into NIH nude mice.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1975

Cordycepin inhibition of 3-methylcholanthrene-induced transformation in vitro.

Cordycepin (3-deoxyadenosine), an inhibitor of poly (a) synthesis, was found to inhibit the induction of the endogenous type "C" RNA virus by 5-iodo-2'-deoxyuridine in a line of Fisher rat embryo cells (H43) grown in vitro, and when continuously incorporated into the medium at those same concentrations, it was found to protect the cells from transformation by the chemical carcinogen 3-methylcholanthrene.

Cell Line↗
PubMed1975

Studies of FBJ osteosarcoma virus in tissue culture. II. Autoinhibition of focus formation.

A high-titered non-focus-forming virus, FBJ-MuLV (murine leukemia virus), present in FBJ tumor preparations, inhibited significantly the expression and production of FBJ-MuSV (murine sarcoma virus) in tissue culture. This "autoinhibition" was comparable to that observed when a 3- to 4-log excess of infectious MuLV was added to standard MuSV. The degree of inhibition was influenced by the tropism of the MuLV (or the ease of spread and propagation of MuLV in certain cells), multiplicity of infection by MuLV, amount of excess MuLV, and ability of the MuSV-transformed cells to replicate independently. The FBJ MuLV-MuSV complex may be a model system for the detection of sarcoma viruses in spontaneous tumors in various animals where inhibition by excess nontransforming virus could be an important biologic phenomenon.

Animals↗