Cell Transformation by Andrew Sivak, Alice S. Tu (auth.), J. Celis, A. Graessmann

By Andrew Sivak, Alice S. Tu (auth.), J. Celis, A. Graessmann (eds.)

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DUESBERG ET AL. In an effort to explain why mutated proto-Ha-ras transforms preneoplastic 3T3 cells, but not rat or human embryo cells, it has recently been proposed that mutated proto-Ha-ras is only one of at least two activated genes that are necessary to induce cancer (54, 55,69). This two-gene hypothesis has been tested by transfecting primary rat cells with a mixture of the mutated human proto-Ha-ras and either MC29 provirus or activated proto-myc from mouse plasmacytoma (54), or the EIA gene of adenovirus (69) as helper genes.

Such viruses have only been isolated from animals with neoplasms, while all other retroviruses and all DNA viruses with oncogenic potential are regularly isolated from animals without neoplasms. This is consistent with single gene carcinogenesis by retroviruses with ana genes and possibl e multigene carcinogenesis with all other viruses. Indeed, retroviral ana genes are the only genes known that initiate and maintain cancers per see That they are necessary for transformation has been proven genetically with temperature-sensitive (ts) mutants of Rous (RSV) (8), Kirsten (KiSV) (9), and Fujinami sarcoma viruses (10,11), with avian erythroblastosis virus (12), and with deletion mutants of these and other retroviruses (13-19).

The 51 end of the transforming gene of Fujinami sarcoma virus and of the cellular proto-fps gene are not colinear, Virology, 133, 460. , PHARES, W. H. (1983). Structural relationship between chicken DNA locus, proto-fps, and the transforming gene of Fujinami sarcoma virus (~gag-fps), Virology, 129, 79. G. P. (1982). Nucleotide sequence of the transforming gene of avian myeloblastosis virus, Science, 216, 1421. S. M. (1982). , 453. , MOSCOVICI, C. H. (1983). Tripartite structure of the avian erythroblastosis virus E26 transforming gene, Nature, 306, 391.

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