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R J Huebner

Publications and source records attributed to R J Huebner.

At least 73 records · Page 4Linked to original sources

Sensitive in vivo assay for detection of murine leukemia viruses.

A test is reported for the in vivo detection of the replicative ability of murine leukemia viruses (MLV) in the BALB/c mouse strain. Growth in the spleen was assayed by the complement-fixation assay for MLV group-specific antigen after injection of newborn mice. Low doses of laboratory-derived and wild-type MLV from cell-culture and animal-grown sources were detected as early as 7 to 14 days postinoculation. The sensitivity of this in vivo test compared favorably with in vitro assays for MLV. In vivo detection of MLV replication was correlated with long-term oncogenicity.

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Murine C-type RNA virus from spontaneous neoplasms: in vitro host range and oncogenic potential.

Strain BALB/c mice harbor at least two host range variants of marine leukemia virus. One variant, which is host-cell tropic, is the predominant isolate from neoplastic tissues and produced lymphoreticular neoplasms when injected into BALB/c newborn mice. A second variant, whicht is isolated throughout life, grows poorly in host embryonic cells in culture and was not associated with lymphoreticular neoplasm induction when injected into newborn BALB/c mice.

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A type-C virus in human rhabdomyosarcoma cells after inoculation into NIH Swiss mice treated with antithymocyte serum.

A type-C RNA virus has been isolated that replicates readily in human and other primate cells. It was obtained from a human rhabdomyosarcoma cell (RD) that had been serially transplanted in immunosuppressed NIH Swiss mice, a strain of mouse from which infectious type-C virus has not been isolated. Various other human tumor cells, similarly transplanted, remained free of overt type-C virus expression. The virus growing in the RD cells, AT-124, has a group-specific antigen and an RNA-dependent DNA polymerase immunologically related to murine type-C viruses, but a host range similar to that of the RD-114 virus. The new isolate is either a previously undescribed, endogenous type-C virus from NIH Swiss mice or a recombinant with both mouse and human type-C genetic information.

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5-Bromo-2'-deoxyuridine potentiation of transformation of rat-embryo cells induced in vitro by 3-methylcholanthrene: induction of rat leukemia virus gs antigen in transformed cells.

Low-passage rat-embryo cells were not transformed by 3-methylcholanthrene or by 5-bromo-2' deoxyuridine. However, prior treatment with bromodeoxyuridine, followed by treatment with methylcholanthrene, resulted in cell transformation about three subpassages after removal of the carcinogen. RNA-directed DNA polymerase activity could not be detected in either normal or transformed cells. However, gs-1 antigen specific for rat C-type RNA virus was detected in cultures derived from bromodeoxyuridine-treated cells. No gs-1 antigen for the C-type RNA virus was detected in cultures that had not been treated with bromodeoxyuridine during the 25 subpassages of these experiments.High-passage rat-embryo cells, derived from a different cell pool, were transformed by either methylcholanthrene or dimethylbenzanthracene without prior infection with an exogenous virus, and without prior treatment with bromodeoxyuridine, gs-1 antigen for C-type RNA virus was also detected in 4 of 4 randomly selected transformed cell lines; the gs-1 antigen was not detected in any of 4 nontransformed control cultures. Considering these and previously published findings, we conclude that the lowpassage cells cannot be transformed by methylcholanthrene because of powerful cellular controls over the endogenous virus. Bromodeoxyuridine triggers some expressions of the endogenous virus; thus, the bromodeoxyuridine-treated cells are more susceptible to the transforming effects of methylcholanthrene. High-passage rat cells do not maintain perfect control over expression of their endogenous virus; the cell cultures are susceptible to the transforming effects of chemical carcinogens.

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