Hypersensitivity of thymidine kinase-deficient Friend leukaemia cells to the induction of cytogenetic aberrations by mitomycin C.
Clone 707 of the Friend leukaemia cell line was compared with the hypermutable thymidine kinase deficient subclone 707 BUF for sensitivity to the induction of cytogenetic aberrations by mitomycin C (MMC). Two 16-h doses of MMC were utilized, namely 0.1 and 0.15 microgram ml-1. Following removal of MMC from the cultures, metaphase spreads were prepared after 15, 29 and 43 h growth in non-selective medium. Thirteen types of aberrations were scored. The thymidine kinase deficient subclone showed considerably increased sensitivity to the induction of aberrations, with the aberrations also persisting longer. In light of these and earlier reported results, the significance of thymidine kinase for accurate DNA repair is discussed.
D000818:Animals; D002869:Chromosome Aberrations / Q000187:drug effects*; D002999:Clone Cells; D007942:Leukemia, Experimental / Q000235:genetics*; D051379:Mice; D016685:Mitomycin; D008937:Mitomycins / Q000494:pharmacology*; D014411:Neoplastic Stem Cells / Q000187:drug effects / Q000201:enzymology*; D013234:Stem Cells / Q000201:enzymology*; D013937:Thymidine Kinase / Q000378:metabolism; D013997:Time Factors
D008937:Mitomycins; D016685:Mitomycin; D013937:Thymidine Kinase