| Abstract: |
Exposure of mouse lymphocytic LI 210 cells to 0.02–0.5 Mg/ml of camptothecin (CAM) causes a slowdown in the rate of cell progression through S and G2 phases of the cell cycle; the “terminal” point of CAM action is about 1 h prior to mitosis. Some cells also enter higher DNA ploidy and progress through the cycle at that ploidy. CAM exerts similar effects (S- and G2-phase arrest, entrance to higher DNA ploidy, low initial cytotoxicity) on human lymphocytic MOLT-4 leukemia cells. In contrast, treatment of human promyelocyte HL-60 cells with CAM results in the immediate (occurring as early as 2 h after treatment) death of S- and G2+M-phase cells; the dead cells exhibit decreased DNA stainability with intercalating dyes, suggestive of DNA degradation. Although CAM is less cytotoxic to another human myelogenous leukemic cell line, KG1, the latter cells also respond like HL-60, namely by selective death in S and G2. The data indicate that there may be a tissue (leukemia type) specificity in the response of cells to camptothecin and suggest that myelogenous leukemias, especially those characterized by high proliferation rates, may be especially sensitive to the cytotoxic action of this and perhaps other topoisomerase I inhibitors. © 1990, American Association for Cancer Research. All rights reserved. |
| Keywords: |
human cell; nonhuman; animal cell; mouse; animal; mice; camptothecin; tumor cells, cultured; cell culture; leukemia cell; leukemia, myeloid; dna, neoplasm; lymphatic leukemia; cell cycle phase; dna topoisomerase; dna topoisomerases, type i; growth inhibition; myeloid leukemia; interphase; leukemia l1210; leukemia, lymphocytic; human; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.
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