ArticleJournal of drug metabolism & toxicology2015
IS METABOLIC ACTIVATION OF TOPOISOMERASE II POISONS IMPORTANT IN THE MECHANISM OF CYTOTOXICITY?
Article in Journal of drug metabolism & toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
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
6 citing papers in PubMed, 21 citations in OpenAlex.
- Spontaneous Non-Catalyzed Molecular Reactions and Interactions in the Human Body: Biomedical Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Quetiapine Moderates Doxorubicin-Induced Cognitive Deficits: Influence of Oxidative Stress, Neuroinflammation, and Cellular Apoptosis.International journal of molecular sciences · 2023Article
- Controlled masking and targeted release of redox-cycling ortho-quinones via a C-C bond-cleaving 1,6-elimination.Nature chemistry · 2022Article
- Neuroprotective Potential of Berberine Against Doxorubicin-Induced Toxicity in Rat's Brain.Neurochemical research · 2021Article
- Nitric oxide reverses drug resistance by inhibiting ATPase activity of p-glycoprotein in human multi-drug resistant cancer cells.Biochimica et biophysica acta. General subjects · 2018Article
- Nitric oxide inhibits topoisomerase II activity and induces resistance to topoisomerase II-poisons in human tumor cells.Biochimica et biophysica acta · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The antitumor drugs doxorubicin and etoposide, a phodophyllotoxin derivative, are clinically active for the treatment of human malignancies. Because of their extreme effectiveness in the clinic, their modes of actions have been the subject of intense research for over several decades both in the laboratory and in the clinic. It has been found that both doxorubicin and etoposide (VP-16) act on topoisomerase II, induce DNA cleavage, and form double-strand breaks, causing tumor cell death. However, both of these drugs also undergo extensive metabolism in tumor cells and
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Registered trials
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