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Your search keyword '"Antitumor, Drug Synergism, Etoposide"' showing total 2 results
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2 results on '"Antitumor, Drug Synergism, Etoposide"'

1. Potentiation of tumour necrosis factor-mediated cell killing by VP16 on human ovarian cancer cell lines. In vitro results and clinical implications

Author

M. Venturini, Gabriella Mariani, M Valenti, P. Russo, Pierfranco Conte, Silvio Parodi, and Guido Cimoli

Subjects
Cancer Research, Necrosis, Cell Survival, medicine.medical_treatment, Uterine Cervical Neoplasms, Biology, Drug Screening Assays, Dose-Response Relationship, chemistry.chemical_compound, Tumor Cells, Cultured, medicine, Humans, Cytotoxicity, Tumor Stem Cell Assay, Etoposide, Ovarian Neoplasms, therapy, drug effects, Dose-Response Relationship, Drug, Drug Screening Assays, Antitumor, Drug Synergism, Etoposide, therapeutic use, Female, Humans, Ovarian Neoplasms, therapy, Tumor Cells, Cultured, drug effects, Tumor Necrosis Factor-alpha, therapeutic use, Tumor Stem Cell Assay, Uterine Cervical Neoplasms, drug therapy, Dose-Response Relationship, Drug, Tumor Necrosis Factor-alpha, Drug Synergism, Antitumor, Immunotherapy, medicine.disease, Tumor Cells, Cell killing, Oncology, chemistry, Cell culture, drug effects, therapeutic use, Immunology, Cancer research, Female, Tumor necrosis factor alpha, Drug, Drug Screening Assays, Antitumor, medicine.symptom, Growth inhibition, Ovarian cancer
Abstract

Synergism between recombinant human tumour necrosis factor (rHuTNF) and DNA topoisomerase II inhibitor VP16 during the killing of cells has been studied in six human ovarian cancer cell lines (A2774, A2780, SW626, IGROV-1, SKOV3, Pa1) and a cervical carcinoma cell line (Me180). Studies were performed using an assay of colony formation inhibition (drug treatment for 1 h) and a growth inhibition assay (continuous exposure for 20 h). Concomitant treatment of cells with VP16+rHuTNF enhanced cell killing in all the cell lines tested—an effect observed in both short- and long-term cytotoxicity assays. This study suggests that the activity of VP16 in ovarian cancer cell lines might be enhanced by rHuTNF in in vitro models.

Published
1993

2. Reversal of 'atypical'-multidrug resistance by recombinant human tumor necrosis factor in the human ovarian cancer cell line A2780-DX3

Author

Cimoli, G., Valenti, M., Parodi, S., Mazzoni, A., Sessa, F., Conte, P., and patrizia russo

Subjects
drug therapy/metabolism, Drug Resistance, DNA, Single-Stranded, Antineoplastic Agents, Drug Screening Assays, administration /&/ dosage/pharmacokinetics/pharmacology, Antineoplastic Combined Chemotherapy Protocols, pharmacokinetics/pharmacology, DNA Damage, DNA, Neoplasm, drug effects/metabolism, DNA, Single-Stranded, drug effects/metabolism, Doxorubicin, administration /&/ dosage/pharmacokinetics/pharmacology, Drug Resistance, Drug Screening Assays, Antitumor, Drug Synergism, Etoposide, administration /&/ dosage/pharmacokinetics/pharmacology, Female, Humans, Mitoxantrone, administration /&/ dosage/pharmacokinetics/pharmacology, Ovarian Neoplasms, drug therapy/metabolism, Recombinant Proteins, pharmacology, Topoisomerase II Inhibitors, Tumor Cells, Cultured, drug effects, Tumor Necrosis Factor-alpha, administration /&/ dosage/pharmacology, Antineoplastic Combined Chemotherapy Protocols, Tumor Cells, Cultured, Humans, Topoisomerase II Inhibitors, Etoposide, Ovarian Neoplasms, administration /&/ dosage/pharmacokinetics/pharmacology, Tumor Necrosis Factor-alpha, pharmacokinetics/pharmacology, Drug Synergism, DNA, Neoplasm, DNA, Antitumor, Recombinant Proteins, Tumor Cells, Doxorubicin, drug effects, Female, Drug Screening Assays, Antitumor, Mitoxantrone, pharmacology, drug effects/metabolism, DNA Damage
Abstract

A2780 human ovarian cancer cell line and its multidrug resistant counterpart A2780-DX3 were utilized for this in vitro study. A2780-DX3 is resistant in various degrees to several topoisomerase II inhibitors but sensitive to vinca alkaloids. Simultaneous treatment of the A2780-DX3 line with 1000 U/mL rHuTNF largely reverses resistance to most topoisomerase II inhibitors. By itself, 1000 U/mL rHuTNF is not toxic to the resistant line. Uptake and retention of [3H]-Mitoxantrone are not modified by rHuTNF, whereas rHuTNF is very active in potentiating the effects of Mitoxantrone. After treatment with topoisomerase II inhibitors, Doxorubicin, Mitoxantrone, or VP16, rHuTNF restores DNA-SSB and DNA-protein cross-links in the resistant line to the level of the wild type. The cleavage activity of topoisomerase II in the resistant line is about 40% of the level present in the parental line. Five minutes after the addition of 1000 U/mL of rHuTNF, the cleavage activity in the resistant line is about 85% of the level present in the parental line. The catalytic activity of topoisomerase II is only 15% lower in the resistant line, but it is increased by about 50% 5 min after the addition of rHuTNF to the resistant line. These effects are transient and cannot be observed after 30 min. These transient direct effects of rHuTNF on topoisomerase II could be associated with its ability to restore sensitivity to inhibitors of topoisomerase II in the A2780-DX3 line.

Published
1993

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