Comparison of wild-type BK virus DNA and BK virion DNA rescued from virus-transformed BHK cells

Olive, D; Lampert, Martha A.; Major, Eugene O.

doi:10.1016/0042-6822(80)90121-x

Cited by 4 publications

(2 citation statements)

References 25 publications

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“…It may also be that some of the early gene products required for viral DNA replication in productive infection may not be necessary for the maintenance of the transformed state. This has already been observed in the case of large T antigen in cells established from hamster tumors induced by polyoma virus (Israel et al, 1980) or in BK virus-transformed hamster cells (Olive et al, 1980) or human fetal brain cells containing viral genomes under an episomal state (Takemoto ef af., 1479). The strongest evidence for the expression of the viral genomes in cells transformed in vivo by papillomaviruses remains the probable existence of a tumor specific transplantation antigen involved in the cell-mediated regression of papillomas and fibropapillomas, as best documented in the CRPV system (Hellstrom et al, 1964).…”

Section: Discussionmentioning

confidence: 73%

Detection and characterization of viral genomes and search for tumoral antigens in two hamster cell lines derived from tumors induced by bovine papillomavirus type 1

Breitburd

Favre

Zoorob

et al. 1981

Intl Journal of Cancer

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Two cell lines, designated HTZ and HT3, were nolated from two transplanted hamster sarcomas induced by bovine papillomavirus type I (BPV-I) and studied after 50 to 60 subcultures. Cells are tumorigenic for hamsters and showed no detectable viral capsid protein synthesis by immunofluorescence technique. Cells contained multiple copies of the entire BPV-I genome, 100 to 500 and 10 t o 100 per diploid amount of HT2 and HT3 cell DNA, respectively, as determined by blot hybridization experiments. In unrestricted cell DNA, viral genomes migrated as free single viral DNA molecules and slow migrating species. HT2 cell DNA restricted by single cut enzymes for BPV-I DNA (Eco RI and Bam HI endonucleases) yielded only one viral genome unit length DNA molecule, indicating that the slow migrating species could correspond to free oligomeric or catenated molecules. Patterns of HT3 cell DNA restricted by Eco RI or Barn HI enzymes showed the presence of additional bands, suggesting that the slow migrating species could correspond t o viral DNA sequences integrated in cell DNA. Up to five polypeptides (I90 K, 125 K, 59 K, 33 K, 30 K) were reproducibly precipitated from[3SS]-methionine-or 32P -labelled HT2 or HT3 cell extracts by sera from hamsters bearing HT2 or HT3 cellinduced tumors and by sera from pikas bearing BPV-I induced fibrosarcomas. Polypeptides with similar molecular weights were detected by HT2 sera in a SV40 tumor hamster cell line (TSV5 CI.2) and in a rat cell line transformed in vitro by SV40 DNA form I (VI I FI Cl. I).The I90 K polypeptide was also detected in a normal hamster embryo cell strain (EH). Conversely, a pool of SV40 tumor hamster sera precipitated the 59 K and the 33 K polypeptides from HTZ cells. The polypeptides thus identified are most probably transformation-related cell proteins. Whether or not their synthesis is related t o the expression of some BPV-I transforming genes remains to be established.

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Section: Discussionmentioning

confidence: 73%

Detection and characterization of viral genomes and search for tumoral antigens in two hamster cell lines derived from tumors induced by bovine papillomavirus type 1

Breitburd

Favre

Zoorob

et al. 1981

Intl Journal of Cancer

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“…In a line of BKV-transformed baby hamster kidney (BHK)-21 cells, BKV genomes persisted in an apparent integrated state (194). These genomes could be rescued by fusion with permissive human embryonic kidney cells, indicating that they were nondefective, as had been implied by restriction endonuclease analysis.…”

Section: Bk Virus (Bkv)mentioning

confidence: 90%

Papovaviral persistent infections.

Norkin¹

1982

Microbiological Reviews

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Chemical carcinogens transform BHK cells by inducing a recessive mutation.

Bouck¹,

Mayorca²

1982

Mol. Cell. Biol.

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Treatment of BHK cells with mutagenic carcinogens induced neoplastic transformation in a single step. This transformation displayed the characteristics expected for a recessive mutation. Increasing doses of carcinogens induced transformants with kinetics similar to the kinetics with which they induced 6-thioguanine-resistant or ouabain-resistant mutants in the same population of cells. Transformants with temperature-restricted phenotypes were easily induced by carcinogens which cause mutations by base changes, but when ICR frameshift mutagens were used, the proportion of temperature-limited transformants was inversely related to the frequency with which a particular mutagen induced frameshift mutations. In hybrids between pseudodiploid isogenic strains of normal and transformed BHK cells, transformation was expressed as a dominant trait when the transformed parent was induced by a papovavirus, but was suppressed as a recessive trait when the transformed parent arose spontaneously or was chemically induced. Segregation of transformation was observed upon growth of suppressed normal hybrids, and the transformed phenotype which was reexpressed was in most cases characteristic of the original transformed parent.Although there is no controversy over the fact that mutagenic carcinogens can malignantly transform mammalian cells in vitro and in vivo (8,23) or over the fact that point mutations can be shown to accompany this transformation (30), whether mutations are necessary to malignantly transform a cell with a chemical carcinogen is still widely debated (11). One reason the role of mutations has been so difficult to assess is that in almost all transformation systems studied, if the endpoint is a cell capable of malignant growth, the process of cell transformation is the result of the sum of at least two steps (4,5,19,31,43). Sorting out the contribution of each step and the mechanism underlying each is only just beginning.There is however one cell system in which transformation can be induced to occur in a single step: the baby hamster kidney cell line BHK-21 clone 13 (BHK-21/cl 13) (9, 17, 51). This permanent cell line behaves as though the process of promotion or progression has already taken place. Only one additional event, the induction of anchorage independence, is needed to change BHK cells from nontumorigenic to tumorigenic (17); therefore, this transformation can be analyzed clearly and quantitatively. In experiments in which chemical carcinogens were used on a subclone of BHK cells (9), the frequency of spontaneous transformation, induced transformation, and reversion to normal and the occurrence of temperature-restricted transformants suggest that transformation is due to a somatic mutation. This paper provides more direct evidence for this assertion by demonstrating that mutation and transformation occur with parallel kinetics in response to increasing doses of carcinogens and that the type of transformants which are induced depend upon the type of mutations which the inducing carcinogen is capable of p...

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Comparison of wild-type BK virus DNA and BK virion DNA rescued from virus-transformed BHK cells

Cited by 4 publications

References 25 publications

Detection and characterization of viral genomes and search for tumoral antigens in two hamster cell lines derived from tumors induced by bovine papillomavirus type 1

Detection and characterization of viral genomes and search for tumoral antigens in two hamster cell lines derived from tumors induced by bovine papillomavirus type 1

Papovaviral persistent infections.

Chemical carcinogens transform BHK cells by inducing a recessive mutation.

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