ArticleCancer chemotherapy and pharmacology1994
Reduced levels of topoisomerase II alpha and II beta in a multidrug-resistant lung-cancer cell line.
Article in Cancer chemotherapy and pharmacology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 25 citations in OpenAlex.
- Naturally mutagenic sequence diversity in a human type II topoisomerase.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Tumor and host factors that may limit efficacy of chemotherapy in non-small cell and small cell lung cancer.Critical reviews in oncology/hematology · 2010Review
- Topoisomerase II alpha mRNA and tumour cell proliferation in non-Hodgkin's lymphoma.Journal of clinical pathology · 1997Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously shown that the doxorubicin-selected multidrug-resistant small-cell lung-cancer cell line H69AR is resistant to VP-16-induced single-strand DNA breaks as compared with its parental H69 cell line. Levels of immunoreactive topoisomerase II alpha are also reduced in H69AR cells. In the present study, we found that cleaved complex formation in the presence of VP-16 was decreased in H69AR cells as compared with H69 cells. In addition, the resistant cells contained lower levels of both topoisomerase II alpha and topoisomerase II beta protein and mRNA. However, these changes were not accompanied by a decrease in the P4-unknotting (strand-passing) activity of 0.67 M NaCl nuclear extracts of H69AR cells, nor was there any difference in VP-16 inhibition of unknotting activity in the H69 and H69AR nuclear extracts. These data suggest that reduced levels of topoisomerase II alpha and II beta may contribute to the resistance of H69AR cells to VP-16 and other drugs that target these isoenzymes.
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