Effect of loss of thymidine kinase activity on the tumorigenicity of clones of SV40-transformed hamster cells.
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.
D000818:Animals; D001345:Autoradiography; D002460:Cell Line; D002471:Cell Transformation, Neoplastic; D002999:Clone Cells / Q000201:enzymology*; D006224:Cricetinae; D003470:Culture Media; D003582:Cytogenetics; D004247:DNA / Q000096:biosynthesis; D007668:Kidney / Q000201:enzymology; D009368:Neoplasm Transplantation; D013539:Simian virus 40; D013937:Thymidine Kinase / Q000032:analysis / Q000378:metabolism*; D014316:Tritium
D003470:Culture Media; D014316:Tritium; D004247:DNA; D013937:Thymidine Kinase