Augmentation of antineoplastic effects by the combination of recombinant human tumor necrosis factor and mitoxantrone on primary culture of human ovarian cancer cells

G. Cimoli, M. Valenti, M. Venturini, P. Conte, P. Russo

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Recombinant human tumor Necrosis Factor (rHuTNF) produced dose-dependent cytoxicity against human ovarian cancer cells, OSC and OMC, obtained from fresh ascites. A combination of rHuTNF and the topoisomerase II inhibitor, Mitoxantrone, produced dose-dependent synergistic cytotocixity on OSC and OMC cells. When OMC cells were incubated simultaneously for one hour with rHuTNF and Mitoxantrone, increased numbers of DNA single-strands breaks were produced. rHuTNF alone did not induce DNA single-strands breaks. These data are consistent with a role for topoisomerase-linked DNA lesions in the rHuTNF mediated potentiation of killing cells by Mitoxantrone.

Original languageEnglish
Pages (from-to)1411-1414
Number of pages4
JournalAnticancer Research
Volume12
Issue number5
Publication statusPublished - 1992

Fingerprint

Mitoxantrone
Antineoplastic Agents
Ovarian Neoplasms
Single-Stranded DNA Breaks
Topoisomerase II Inhibitors
Type I DNA Topoisomerase
Ascites
human TNF protein

Keywords

  • DNA-damage
  • Mitoxantrone-cytotoxicity
  • rHuTNF

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

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T1 - Augmentation of antineoplastic effects by the combination of recombinant human tumor necrosis factor and mitoxantrone on primary culture of human ovarian cancer cells

AU - Cimoli, G.

AU - Valenti, M.

AU - Venturini, M.

AU - Conte, P.

AU - Russo, P.

PY - 1992

Y1 - 1992

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AB - Recombinant human tumor Necrosis Factor (rHuTNF) produced dose-dependent cytoxicity against human ovarian cancer cells, OSC and OMC, obtained from fresh ascites. A combination of rHuTNF and the topoisomerase II inhibitor, Mitoxantrone, produced dose-dependent synergistic cytotocixity on OSC and OMC cells. When OMC cells were incubated simultaneously for one hour with rHuTNF and Mitoxantrone, increased numbers of DNA single-strands breaks were produced. rHuTNF alone did not induce DNA single-strands breaks. These data are consistent with a role for topoisomerase-linked DNA lesions in the rHuTNF mediated potentiation of killing cells by Mitoxantrone.

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