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• W2059177512 endingPage "3454" @default.
• W2059177512 startingPage "3450" @default.
• W2059177512 abstract "Cultured rat embryo cells are resistant to neoplastic transformation by chemical carcinogens unless they are extensively subcultured or infected with a murine leukemia virus (MuLV) first. We found that, in normal cultured cells, MuLV activates expression of rat genes that are the progenitors of sarcoma virus genes, but not those of endogenous leukemia virus. Elevated levels of sarcoma virus-related RNA in normal cells infected with MuLV were indistinguishable from the levels in cells transformed spontaneously or by a carcinogen or a sarcoma virus. Because of previous reports that some carcinomas in rats also contain elevated levels of sarcoma virus-related RNA, we believe these events can be explained by a molecular genetic model which may be generally valid for initiation of carcinogenesis. The basic elements of the model are: transcriptional activation of all the multiple copies of normal rat progenitors of sarcoma virus genes is required before cellular transformation can be initiated, and initiation occurs when a spontaneous or induced mutation in any one active copy of these same genes generates a dominant transforming function." @default.
• W2059177512 created "2016-06-24" @default.
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• W2059177512 date "1980-06-01" @default.
• W2059177512 modified "2023-09-25" @default.
• W2059177512 title "Toward a model for the molecular genetics of carcinogenesis in rats." @default.
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• W2059177512 doi "https://doi.org/10.1073/pnas.77.6.3450" @default.
• W2059177512 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/349634" @default.
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