Mishra N K, Pant K J, Thomas F O, Price P J
Int J Cancer. 1976 Dec 15;18(6):852-8. doi: 10.1002/ijc.2910180618.
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.
通过使用溴化乙锭（EtBr）作为病毒互补DNA（cDNA）整合到宿主基因组中的抑制剂，研究了劳舍尔白血病病毒（RLV）增殖在病毒 - 化学协同致癌作用中的重要作用。当RLV接种时存在EtBr可抑制协同致癌转化，但添加到预先感染的细胞中则无效。蛋白质合成抑制剂嘌呤霉素和环己酰亚胺也抑制慢性感染细胞的协同致癌转化。以抑制85%RLV产生的浓度使用的纯化大鼠干扰素并未改变协同致癌转化的进程。讨论了这些观察结果对病毒特异性蛋白质在协同致癌过程中可能作用的影响。
