Cell cycle effects of the novel topoisomerase I inhibitor NU/ICRF 505 in a panel of Chinese hamster ovary cell lines.

[1]  J. S. Macpherson,et al.  Development of anthracenyl-amino acid conjugates as topoisomerase I and II inhibitors that circumvent drug resistance. , 1996, Biochemical pharmacology.

[2]  J. S. Macpherson,et al.  Induction of apoptosis in human cancer cell lines by the novel anthracenyl-amino acid topoisomerase I inhibitor NU/ICRF 505. , 1996, British Journal of Cancer.

[3]  J. S. Macpherson,et al.  Cytogenetic evaluation of the mechanism of cell death induced by the novel anthracenyl-amino acid topoisomerase II catalytic inhibitor NU/ICRF 500. , 1995, Mutation research.

[4]  J. S. Macpherson,et al.  Biochemistry of topoisomerase I and II inhibition by anthracenyl-amino acid conjugates. , 1995, Biochemical pharmacology.

[5]  K W Kohn,et al.  Unscheduled activation of cyclin B1/Cdc2 kinase in human promyelocytic leukemia cell line HL60 cells undergoing apoptosis induced by DNA damage. , 1995, Cancer research.

[6]  H. Strutt,et al.  Different fates of camptothecin-induced replication fork-associated double-strand DNA breaks in mammalian cells. , 1994, Carcinogenesis.

[7]  F. Palitti,et al.  Higher G2 sensitivity to the induction of chromosomal damage in the CHO mutant EM9 than in its parental line AA8 by camptothecin, an inhibitor of DNA topoisomerase I. , 1993, Mutation research.

[8]  R. Lock,et al.  Inhibition of p34cdc2 kinase activation, p34cdc2 tyrosine dephosphorylation, and mitotic progression in Chinese hamster ovary cells exposed to etoposide. , 1992, Cancer research.

[9]  L. Liu,et al.  The involvement of active DNA synthesis in camptothecin-induced G2 arrest: altered regulation of p34cdc2/cyclin B. , 1992, Cancer research.

[10]  A. Harris,et al.  Reduced topoisomerase II and elevated alpha class glutathione S-transferase expression in a multidrug resistant CHO cell line highly cross-resistant to mitomycin C. , 1992, Biochemical pharmacology.

[11]  Z. Darżynkiewicz,et al.  The concentration-dependent diversity of effects of DNA topoisomerase I and II inhibitors on the cell cycle of HL-60 cells. , 1991, Experimental cell research.

[12]  L. Liu,et al.  Involvement of nucleic acid synthesis in cell killing mechanisms of topoisomerase poisons. , 1990, Cancer research.

[13]  Z. Darżynkiewicz,et al.  Diverse effects of camptothecin, an inhibitor of topoisomerase I, on the cell cycle of lymphocytic (L1210, MOLT-4) and myelogenous (HL-60, KG1) leukemic cells. , 1990, Cancer research.

[14]  Ian D. Hickson,et al.  Isolation and partial characterisation of a mammalian cell mutant hypersensitive to topoisomerase II inhibitors and X-rays. , 1990, Mutation research.

[15]  L. Liu,et al.  Arrest of replication forks by drug-stabilized topoisomerase I-DNA cleavable complexes as a mechanism of cell killing by camptothecin. , 1989, Cancer research.

[16]  C. Robson,et al.  Nuclear topoisomerase II levels correlate with the sensitivity of mammalian cells to intercalating agents and epipodophyllotoxins. , 1988, The Journal of biological chemistry.

[17]  A. Harris,et al.  Cross-sensitivity to topoisomerase II inhibitors in cytotoxic drug-hypersensitive Chinese hamster ovary cell lines. , 1987, Cancer research.

[18]  L. Li,et al.  Action of camptothecin on mammalian cells in culture. , 1972, Cancer research.