ArticleProceedings of the National Academy of Sciences of the United States of America1999
XK469, a selective topoisomerase IIbeta poison.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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Who cites it
34 citing papers in PubMed, 96 citations in OpenAlex.
- Pharmacological correlates of topoisomerase II-directed protection against anthracycline-induced DNA damage and cardiotoxicity: a comparative evaluation of catalytic topoisomerase II inhibitors.Archives of toxicology · 2026Article
- Use of CRISPR/Cas9 with Homology-Directed Repair to Gene-Edit Topoisomerase IIThe Journal of pharmacology and experimental therapeutics · 2024Article
- Exploring the effects of topoisomerase II inhibitor XK469 on anthracycline cardiotoxicity and DNA damage.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Effects of hsa-miR-9-3p and hsa-miR-9-5p on Topoisomerase IIThe Journal of pharmacology and experimental therapeutics · 2023Article
- Synthesis of Morpholine-, Piperidine-, andACS pharmacology & translational science · 2022Article
- Article
- Chemical Inhibitors of a Selective SWI/SNF Function Synergize with ATR Inhibition in Cancer Cell Killing.ACS chemical biology · 2020Article
- Synthesis and Antimicrobial Activity of Some New Substituted Quinoxalines.Molecules (Basel, Switzerland) · 2019Article
- Smoothed Potential MD Simulations for Dissociation Kinetics of Etoposide To Unravel Isoform Specificity in Targeting Human Topoisomerase II.Journal of chemical information and modeling · 2019Article
- Molecular basis for the DNA damage induction and anticancer activity of asymmetrically substituted anthrapyridazone PDZ-7.Oncotarget · 2017Article
- Natural variation in a single amino acid substitution underlies physiological responses to topoisomerase II poisons.PLoS genetics · 2017Article
- Nitric oxide inhibits ATPase activity and induces resistance to topoisomerase II-poisons in human MCF-7 breast tumor cells.Biochemistry and biophysics reports · 2017Article
- Natural Compounds as Anticancer Agents Targeting DNA Topoisomerases.Current genomics · 2017Review
- Mining expression and prognosis of topoisomerase isoforms in non-small-cell lung cancer by using Oncomine and Kaplan-Meier plotter.PloS one · 2017Article
- A "Double-Edged" Scaffold: Antitumor Power within the Antibacterial Quinolone.Current medicinal chemistry · 2016Review
- Quinoxaline 1,4-di-N-Oxides: Biological Activities and Mechanisms of Actions.Frontiers in pharmacology · 2016Review
- Ultrasensitive isolation, identification and quantification of DNA-protein adducts by ELISA-based RADAR assay.Nucleic acids research · 2014Article
- Nicotine mediates hypochlorous acid-induced nuclear protein damage in mammalian cells.Inflammation · 2014Article
- Drugging topoisomerases: lessons and challenges.ACS chemical biology · 2013Review
- Mechanism of generation of therapy related leukemia in response to anti-topoisomerase II agents.International journal of environmental research and public health · 2012Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
XK469 (NSC 697887) is a synthetic quinoxaline phenoxypropionic acid derivative that possesses unusual solid tumor selectivity and activity against multidrug-resistant cancer cells. We report here that XK469 and its S(-) and R(+)-isomers induce reversible protein-DNA crosslinks in mammalian cells. Under protein denaturing conditions, the protein-DNA crosslinks are rendered irreversible and stable to DNA banding by CsCl gradient ultracentrifugation. Several lines of evidence indicate that the primary target of XK469 is topoisomerase IIbeta. Preferential targeting of topoisomerase IIbeta may explain the solid tumor selectivity of XK469 and its analogs because solid tumors, unlike leukemias, often have large populations of cells in the G(1)/G(0) phases of the cell cycle in which topoisomerase IIbeta is high whereas topoisomerase IIalpha, the primary target of many leukemia selective drugs, is low.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.