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At least 19 recordsLinked to original sources
PubMed1988

Cooperation between the polyomavirus middle-T-antigen gene and the human c-myc oncogene in a rat thyroid epithelial differentiated cell line: model of in vitro progression.

Two rat thyroid epithelial differentiated cell lines, PC Cl 3 and PC myc, were infected with the polyoma murine leukemia virus (PyMLV) carrying the Middle-T-antigen gene of polyomavirus. After infection, both cell lines acquired the typical markers of neoplastic transformation; however, the PC myc cells showed a greater malignant phenotype. Furthermore, the thyroid differentiated functions were completely suppressed in PC myc cells transformed by PyMLV, whereas they were, at least partially, retained in PC Cl 3 cells transformed by PyMLV, and in particular, thyroglobulin synthesis and secretion were not affected at all. Since no differences in the expression of the middle-T-antigen gene were observed in the two PyMLV-transformed cell lines, the different properties shown by these two infected cell lines must be ascribed to the expression of the c-myc oncogene.

Animals↗
PubMed1979

Isolation of polyomavirus-induced surface antigens of mouse cells: affinity chromatography and biologic activities.

Tumor-specific transplantation antigen (TSTA) and polyomavirus-induced tumor-associated surface antigen (TASA) were isolated from polyomavirus-transformed BALB/c mouse cells with the use of 3-M KCl solubilization and affinity chromatography on antibody-coated Sepharose 4B. Particular conditions were chosen for removal of the nonspecifically bound proteins from the gel. Under these conditions, the ratio between the amounts of crude extract and specifically bound proteins giving the same TASA activity was about 5,000. Mice inoculated with this material were protected against tumor challenge. We therefore assume that TSTA is a part of TASA. Furthermore, these antigens can be dissociated from the major histocompatibility antigens.

Animals↗
PubMed1977

Multiple free viral DNA copies in polyoma virus-transformed mouse cells surviving productive infection.

Mouse 3T6 cells were infected with polyoma virus at high multiplicity, and survivors were isolated. Clones from single cells were then established and were found to be resistant to a second infection. However, in some clones viral functions could at least be partially expressed during reinfection, as judged from a stimulation of nuclear tumor antigen expression. One such clone was studied in detail. These cells were transformed and produced low amounts of virus (less than 1 PFU per cell per generation). The persistent infection did not seem to be a carrier-state phenomenon, since infectious-center assays showed that most cells produced virus. The resistance of the cells to reinfection can be explained by interference from viral DNA present in the cells, averaging about 1,500 "free" copies per cell. This DNA had the normal physical characteristics of polyoma DNA. However, it had a slightly larger size than authentic polyoma DNA. Mapping with restriction endonucleases showed that the addition to the DNA was about 5% of the wild-type genome and was located close to the origin of DNA replication. This DNA was infectious, although it had a 10-fold lower infectivity than wild-type polyoma DNA. Both virus and DNA from the polyoma-resistant cells had a small-plaque morphology, as opposed to the large-plaque morphology of the virus used for the initial selection of cells.

Antigens, Viral↗
PubMed1976

Limitations and utility of a cytolytic assay for measuring simian virus 40-induced cell surface antigens.

Antisera were produced against an SV40-transformed cell line in the syngeneic AL/N mouse. With a microcytolytic assay, the specificity of antisera produced by various immunization schedules and their ability to lyse numerous SV40-transformed cell lines were determined. Various AL/N mouse cell lines, newly transformed by SV40 and cloned, were found to be lysed by the antisera. When tumors were induced by SV40-transformed cells in the syngeneic mouse and cell lines were reestablished from tumors and such procedures were repeated, the susceptibility to serum-mediated cytolysis of the sublines was the same as that of the original SV40-transformed cell line, in spite of differences in tumorigenicity. Polyoma virus-transformed AL/N cell lines were also lysed while AL/N embryo cells, untransformed by SV40 or by polyoma, were not. SV40-transformed T-antigen-positive BALB/c mouse or hamster cell lines or a T-antigen-positive tissue cultured human cell were also resistant to lysis. A competition type of microassay demonstrated specific inhibition of the serum-mediated cytolysis by all of the SV40 T-antigen-positive cell lines tested. Thus, the lack of lysis of cells did not necessarily indicate the absence of SV40-induced surface antigens. The polyoma-transformed AL/N cell line also inhibited the antisera, but to a lesser extent, suggesting the possibility that SV40 and polyoma virus transformation may result in the appearance of partially common cell surface antigens.

Animals↗
PubMed1978

Neoplastic transformation of hamster brain cells in vitro by polyoma virus.

The transformation of cultivated hamster brain cells by polyoma virus is reported. The transformed cell line contained polyoma virus-specific nuclear, surface and transplantation antigens. Subcutaneous and intracranial inoculations revealed high tumorigenicity of the cells. Brain-specific S 100 protein was found in these tumors with immuno-peroxidase staining, suggesting that they were of a nervous nature. Both in vivo and in vitro, the cells had glial features as studied by phase contrast, light and electron microscopy. Type-H virus-like particles were found in the tumor cells and might have played a role in the viral transformation.

Animals↗
PubMed1977

[Transformation, in vitro, of cerebral hamster cells by polyoma virus].

A cell line called HCxPy was obtained in vitro by transformation of dissociated hamster brain cell cultures by polyoma virus. The first foci of transformed cells became evident 90 to 120 days after viral infection. This cell line is now at the 46th passage. The cells appear tumorigenic for hamsters after subcutaneous and intracerebral injection. They carry the polyoma virus T and cell surface antigens. Good evidence for astrocytic differentiation can be found by morphological examination of the tumours and of the cultured cells.

Animals↗
PubMed1976

Regulation of viral transciption and tumor antigen expression in cells transformed by simian virus 40.

We have studied the expression of simian virus 40 (SV40) specific tumor antigen (T-antigen) and viral RNA in SV40-transformed mouse 3T3 cells that are temperature-sensitive for the expression of the transformed phenotype (ts SV3T3). Although transformed by wild-type SV40, ts SV3T3 cells at 32 degrees behave like standard transformants, while at 39 degrees they became arrested in G1 after reaching saturation density or under conditions of serum starvation. ts SV3T3 cells at 32 degrees or exponentially growing at 39 degrees are uniformly T-antigen positive. However, after G1 arrest at 39 degrees the majority of the cells becomes T-antigen negative. Induction of proliferation in the resting cultures results in the reappearance of T-antigen in most of the cells, concomitant with the induction of DNA synthesis. The reason for the disappearance of T-antigen from ts SV3T3 cells arrested in G1 seems to reside in a transcriptional control operating on the integrated viral DNA, since these cells contain no appreciable amounts of SV40 specific RNA. Viral RNA can be easily detected in cells growint at 32 degrees or at 39 degrees. The results suggest that transcription of the viral genome in SV40-transformed cells is cell-cycle-dependent.

Antigens, Viral↗
PubMed1977

Characterization of polyoma virus T antigen.

High-titer antiserum raised in rats against the tumor (T) antigen of polyoma virus was used to purify the T antigen by the Staphylococcus protein A antibody adsorbent technique. Sodium dodecyl sulfate/polyacrylamide gel electrophoresis allowed the identification of a protein with an apparent molecular weight of 100,000-108,000 as a major component induced in lytically infected mouse cells. In cells infected by ts A mutants this component was temperature sensitive. Several minor components were also observed. In pulse and chase experiments there was a slight decrease in electrophoretic mobility of T antigen during the chase period at the permissive temperature, suggesting that the T antigen is a modified protein. In two lines of transformed cells, the amount of T antigen seemed to be considerably less than in lytically infected cells, but the size of the antigen appeared to be equal.

Antibody Specificity↗
PubMed1979

Construction and analysis of viable deletion mutants of polyoma virus.

Viable mutants of polyoma with small deletions ranging in size from 2 to 75 base pairs were obtained by infecting 3T3 cells with polyoma DNA that had been cleaved once with HaeII endonuclease or with DNase-Mn2+ digestion. The HaeII endonuclease-cleaved DNA yielded mutants with deletions at map position 72--73, whereas the mutants generated by DNase I-Mn2+ digestion had deletions either at map position 72--73 or within the map coordinates 92 and 99. Both groups of mutants appeared to grow as well as wild-type virus in 3T3 cells. The deletions at map position 72--73 did not alter the virus's ability to transform rat cells. Hence, the region just to the early side of the origin of DNA replication is not essential for vegetative growth or transformation. But the mutants with deletions in the region between map coordinates 92 and 99, a segment thought to code for polyoma large and middle T antigens (Hutchinson et al., Cell 15:65--77, 1978; Smart and Ito, Cell 15:1427--1437, 1978; Soeda et al., Cell 17:357--370, 1979), transformed rat cells at 0.2 to 0.05 the efficiency of wild-type virus.

Animals↗
PubMed1978

Polyoma virus, as a model for viral skin carcinogenesis.

Polyoma virus is presented as the simplest model of transformation by a DNA virus. The three possible ways of virus/cell interaction are recalled: lytic infection, abortive infection and malignant transformation. Nuclear and surface antigenic modifications are also recalled as well as their possible correlation with the transformation mechanism. Lastly, in "in vivo" systems, we have tried to schematize the interactions of host and virus-induced tumour.

Animals↗