ArticleChemical research in toxicology2013
Improved efficacy of acylfulvene in colon cancer cells when combined with a nuclear excision repair inhibitor.
Article in Chemical research in toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Trabectedin derails transcription-coupled nucleotide excision repair to induce DNA breaks in highly transcribed genes.Nature communications · 2024Article
- A machine learning-based gene signature of response to the novel alkylating agent LP-184 distinguishes its potential tumor indications.BMC bioinformatics · 2021Article
- Mechanism of RNA polymerase II stalling by DNA alkylation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- DNA Adducts from Anticancer Drugs as Candidate Predictive Markers for Precision Medicine.Chemical research in toxicology · 2017Article
- Nucleotide excision repair in humans.DNA repair · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The efficacy of DNA-damaging anticancer drugs is highly influenced by cellular DNA repair capacity, and by inhibiting the relevant DNA repair pathway, efficacy of alkylating agents may be increased. Therefore, combining DNA repair inhibitors with anticancer agents that selectively target tumor tissue should improve cancer treatment. The objective of this study was to test the hypothesis that cotreatment of cancer cells with acylfulvene (AF, alkylating agent) and UCN-01 (DNA repair inhibitor) would improve drug efficacy and promote the persistence of DNA adducts. Previous data regarding the relative susceptibility of repair proficient versus deficient cells toward an AF analogue suggests that corresponding adducts are repaired by nuclear excision repair (NER), a cellular process that has been shown to be prevented with UCN-01. In this study, cells were cotreated with nontoxic levels of UCN-01 together with increasing doses of AF. The efficacy of AF was assessed by measuring cytotoxicity and DNA adducts. In addition, cells were cotreated with nontoxic levels of methoxyamine, a known base excision repair (BER) inhibitor, to determine if inhibiting BER also promotes cytotoxicity of AF. DNA-adducts were measured in a sensitive and precise manner by using stable isotope-labeled mass spectrometry analysis. The data obtained in this study demonstrate for the first time that pharmacological inhibition of the NER pathway of DNA repair leads to the persistence of AF-specific adducts and promotes AF cytotoxicity.
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