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Biomedical subjects

R J Huebner

Publications and source records attributed to R J Huebner.

At least 127 records · Page 7Linked to original sources
PubMed1971

Wild-type Gross leukemia virus and the pathogenesis of the glomerulonephritis of New Zealand mice.

The pathogenesis of the spontaneous glomerulonephritis of NZB and (NZB x NZW) F(1) hybrid mice is related at least in part to the formation of natural antibody against antigens of the G (Gross) system, and apparently to the deposition in the glomeruli of immune complexes of G natural antibody with G soluble antigen (GSA), type-specific antigen specified by wild-type Gross leukemia virus. G natural antibody and GSA are detectable in the acid-buffer eluate of the kidneys of NZB mice during the course of the glomerulonephritis. (NZB x NZW) F(1) hybrid mice develop glomerulonephritis and produce GSA and free G natural antibody earlier in life than do NZB mice. The proteinuria manifestation of the gomerulonephritis of (NZB x NZW) F(1) hybrid mice becomes increasingly prevalent as GSA undergoes immune elimination from the circulation. Gross leukemia virus-specified antigens together with bound immunoglobulins are located in the glomerular lesions of (NZB x NZW) F(1) hybrid mice, both in the mesangium as observed in NZB mice and also in the wall of the peripheral capillary loops of the glomeruli.

AKR murine leukemia virus↗
PubMed1971

Activation and isolation of hamster-specific C-type RNA viruses from tumors induced by cell cultures transformed by chemical carcinogens.

Cell cultures of Syrian hamster embryo were treated for 7 days with selected chemicals. Certain cultures were morphologically transformed by three different chemical preparations and yielded cell lines that subsequently produced malignant tumors in hamsters. Although the cell lines were negative for infectious virus before inoculation into animals, hamster-specific C-type RNA virus was isolated from tumors or from cell lines derived from the tumors. Since infectious C-type viruses are usually not demonstrable in hamster tissues of normal or tumor origin, we conclude that the chemical treatment and activation of the viruses are related events.

Animals↗
PubMed1971

Host-gene control of C-type tumor virus-expression and tumorigenesis: relevance of studies in inbred mice to cancer in man and other species.

C-type RNA viruses are tumorigenic in mice and other species. They are widespread and transmitted in an intimate relationship with host-cell genetic material. Tumorigenesis is no doubt a complex biological phenomenon, and involves both genetic and environmental factors. Among the genetic factors, single-locus determination is probably exceptional; yet, a number of genes are known in inbred mice and other species, including man, that can exert a major influence. Clearly, studies with inbred mice apply outside the murine model and justify generalizations on the etiology of cancer. The types of cancer observed in man are similar to those of inbred strains of mice, and their stochastic and often familial occurrences suggest that genetic factors play important roles in both man and mouse. A number of heritable disorders predipsose to tumorigenesis. Investigations of the relationship between various polymorphic phenotypes and human tumors should be intensified. For instance, a study of high-risk human-tumor groups could aid considerably not only in the recognition of etiological agents but also of underlying host-gene controlled mechanisms. Indeed epidemiological studies have already led to the identification of mutant genes that influence the incidence of human cancer. Such studies may be guided by findings in inbred strains of mice. There is good evidence in inbred mice that mutations in host chromosomes determine whether or not genes coding for RNA oncogene viral "functions" become expressed as cancer. Although an etiological role of C-type RNA virus has not yet been demonstrated in human cancer, studies of the interaction of viral and host-cell genomes in mice and other species, and the visualization of C-type virus in human tumors have provided good reasons for suspecting the presence in man of oncogenic genes (oncogenes) homologous to those of the C-type viral genomes, which are well studied in mice, hamsters, cats, rats, and chickens.

Animals↗
PubMed1971

Transformation of rat and hamster embryo cells by extracts of city smog.

Extracts of particulate matter from condensates of city air were tested for their ability to transform rat or hamster cell cultures. Uninfected rat embryo cultures were not transformed, but cultures chronically infected with Rauscher leukemia virus were transformed by benzpyrene or by extracts of city smog. The smog extracts were 600 times more active than pure benzpyrene as transforming agents. Hamster embryo cultures infected with hamster leukemia virus were equally as sensitive as leukemia-infected rat cultures to the transforming effects of smog; uninfected hamster cultures were also transformed, although tenfold higher doses of smog extract were required.

Air Pollution↗
PubMed1971

Species-specific and interspecific antigenic determinants associated with the structural protein of feline C-type virus.

The group-specific protein of feline leukemia viruses has been isolated by isoelectric focusing. This protein has a molecular weight, calculated from sodium dodecyl sulfate-acrylamide gel electrophoresis, of 25,000 and forms a resolved band in such gels when disrupted virions are analyzed. This protein contains both species-specific antigenic determinants, as well as interspecific cross-reactive determinants, as an integral part of its structure.

Animals↗
PubMed1971

Production of altered cell foci by 3-methylcholanthrene in mouse cells infected with AKR leukemia virus.

This report describes altered cell foci observed 9-14 days after treatment with 3-methylcholanthrene of mouse-embryo tissue cultures that had previously been infected with wild-type AKR (RNA tumor) virus. The foci consisted of randomly oriented, piled-up, spindle-shaped cells. When heavily stained with Giemsa, the colonies of transformed cells were grossly visible and countable. Under the same experimental conditions, such changes of morphology were not detectable in the uninfected cells treated with 3-methylcholanthrene or in untreated cells infected with virus. The procedure may provide a rapid, quantitative test system for measurement of the oncogenic potential of certain carcinogens. As in similar previous studies in rat and hamster cells, the results suggest that the infectious, but nontransforming, RNA tumor viruses provided nascent oncogenic information, which when activated by 3-methylcholanthrene served as the specific genetic determinants of transformation.

Animals↗