Differential response of sister chromatid exchange and chromosome aberrations to mitomycin C of normal and abnormal human lymphocytic cell lines.
Mitomycin C (MMC) induced chromosome aberrations and an increased sister chromatid exchange (SCE) incidence in a cell line derived from normal lymphocytes, whereas in lines originating from cells of chronic lymphocytic leukemia (lines SN1029 and SN1033) and Burkitt lymphoma (lines B35 M and HR1K) MMC caused a striking increase in SCE, but not in the frequency of chromosome abnormalities. The latter may be due to the failure of the cells with chromosome aberrations to survive, possibly related to their high sensitivity to MMC. The increased rate of SCE with MMC treatment was more marked in the neoplastic lymphocytic cells than in the normal ones; the sensitivity of SN1029 and SN1033 cells was 10 times higher and that of B35M and HR1K cells about 5 times higher than that of the normal cells. These observations suggest that the MMC-induced high rate of SCE in the neoplastic cells may in some aspects differ from the mechanism(s) leading to chromosome aberrations; and that SCE is a much more sensitive indicator of MMC effects than chromosome aberrations.
D000818:Animals; D002051:Burkitt Lymphoma / Q000235:genetics*; D002460:Cell Line; D002869:Chromosome Aberrations; D003434:Crossing Over, Genetic / Q000187:drug effects*; D006801:Humans; D007942:Leukemia, Experimental / Q000235:genetics; D007945:Leukemia, Lymphoid / Q000235:genetics*; D008214:Lymphocytes / Q000187:drug effects*; D008937:Mitomycins / Q000494:pharmacology*; D009374:Neoplasms, Experimental / Q000235:genetics
D008937:Mitomycins