The transforming gene of a human lung carcinoma-derived cell line, Hs242, has been cloned in biologically active form, and identified as c-bas/has (otherwise known as c-Ha-ras). The genetic lesion responsible for the transforming activity of the Hs242 oncogene has been localized to a point mutation in the second exon which results in the substitution of leucine for glutamine as amino acid 61 of the predicted protein. No changes were observed in the first exon, the region of c-bas/has in which a point mutation is responsible for activation of the T24 and EJ bladder carcinoma oncogenes.
When inhibitors of protein synthesis are added to BALB/c mouse cells in culture, induction of naturally integrated C-type RNA virus occurs in a high percentage of cells. The action of protein synthesis inhibitors differs from that of halogenated pyrimidines, another class of virus inducers, in their effects on biologically distinguishable viruses. The use of such inhibitors to study integrated virus expression provides a means for studying gene regulation in mammalian cells.
Infection of BALB/c mouse cells with UVirradiated herpes simplex virus (HSV) types 1 and 2 resulted in activation of a xenotropic type C virus detected by infectious center formation in permissive rat cells. The levels of type C virus activated by HSV were related to the UV dose and the multiplicity of infection used. The ability of HSV to activate type C virus was eliminated by heat-inactivation and by neutralization with specific antiserum against HSV, but was not affected by purification or treatment with DNase and RNase. Maximum levels of type C virus in the cells and medium were observed within 1 day after HSV infection, and the levels returned to control cell values within 3-4 days. The possible significance of these findings with respect to the putative oncogenic potential of HSV is discussed. Cells of many, if not all, mammalian species contain repressed genomes of type C RNA viruses. Activation of these repressed genomes with resultant virus synthesis may occur spontaneously (1) or may be induced by biological (2), chemical (3-6), or physical (7) means. Evidence exists to suggest that the genomes of these vertically transmitted endogenous RNA viruses can play a role in spontaneous tumor induction (8, 9).Viruses containing DNA rather than RNA genetic material have also been implicated in the oncogenic process. Inoculation of herpesviruses into animals (10) or cells in culture (11), for example, may be followed by the appearance of tumors or cell transformants that possess malignant potential. The putative role of herpesviruses in the oncogenic process is not clearly understood, however, and one may question whether the herpesvirus genome is in itself oncogenic or whether herpesviruses serve an indirect function by affecting a cellular factor(s) which is the direct oncogen. An example consistent with an indirect role in oncogenesis would be modification of expression of endogenous type C virus information after herpesvirus infection.
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