Chemical-viral co-carcinogenesis: requirement for leukemia virus expression in accelerated transformation.
The essential role of Rauscher leukemia virus (RLV) multiplication in viral-chemical co-carcinogenesis was investigated by the use of ethidium bromide (EtBr) as an inhibitor of viral complementary DNA (cDNA) integration in the host genome. EtBr inhibited co-carcinogenic transformation when present at the time of RLV inoculation but was ineffective when added to preinfected cells. Inhibitors of protein synthesis, puromycin and cyclohexamide also inhibited co-carcinogenic transformation of chronically infected cells. Purified rat interferon used at a concentration which inhibited 85% of RLV production did not modify the course of co-carcinogenic transformation. The implications of these observations in terms of the possible role of the virus-specific protein (s) in the co-carcinogenic process are discussed.
D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D002471:Cell Transformation, Neoplastic / Q000187:drug effects; D002999:Clone Cells; D003043:Cocarcinogenesis; D004261:DNA Replication / Q000187:drug effects; D004279:DNA, Viral / Q000378:metabolism; D004259:DNA-Directed DNA Polymerase / Q000378:metabolism; D004996:Ethidium / Q000494:pharmacology; D007372:Interferons / Q000494:pharmacology; D051381:Rats; D011925:Rauscher Virus; D014779:Virus Replication / Q000187:drug effects
D000900:Anti-Bacterial Agents; D004279:DNA, Viral; D007372:Interferons; D004259:DNA-Directed DNA Polymerase; D004996:Ethidium