胸苷激酶活性丧失对SV40转化的仓鼠细胞克隆致瘤性的影响。
Effect of loss of thymidine kinase activity on the tumorigenicity of clones of SV40-transformed hamster cells.
作者信息
Rothschild H, Black P H
出版信息
Proc Natl Acad Sci U S A. 1970 Oct;67(2):1042-9. doi: 10.1073/pnas.67.2.1042.
Abstract
Cells deficient in the enzyme thymidine kinase were derived from transplantable SV40-transformed hamster cells. The resultant cell lines were less transplantable when inoculated into hamsters. Tumors which did arise from such cells had prolonged latent periods and were found to contain a mixture of enzyme-containing and enzyme-deficient cells. Revertant cell lines obtained either spontaneously or after mutagenesis in vitro contained intermediate levels of thymidine kinase activity and displayed an oncogenic potential which was intermediate between the wild type and enzyme-deficient cells. It is postulated that salvage pathway enzymes may play a rate-limiting role in tumorigenesis.
摘要
缺乏胸苷激酶的细胞源自可移植的SV40转化仓鼠细胞。将所得细胞系接种到仓鼠体内时，其移植能力较低。由这类细胞产生的肿瘤潜伏期延长，且发现含有含酶细胞和缺酶细胞的混合物。自发获得或体外诱变后获得的回复细胞系含有中等水平的胸苷激酶活性，并表现出介于野生型细胞和缺酶细胞之间的致癌潜力。据推测，补救途径酶可能在肿瘤发生中起限速作用。
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