ArticleCancer drug resistance (Alhambra, Calif.)2019
Entrapment of DNA topoisomerase-DNA complexes by nucleotide/nucleoside analogs.
Article in Cancer drug resistance (Alhambra, Calif.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 19 citations in OpenAlex.
- The fluoropyrimidine polymer CF10 synergizes with 5-ethynyl-2'-deoxyuridine by promoting telomere attrition and mitotic catastrophe.NAR molecular medicine · 2026Article
- CF10 Displayed Improved Activity Relative to 5-FU in a Mouse CRLM Model Under Conditions of Physiological Folate.Cancers · 2025Article
- Cytotoxic mechanisms of pemetrexed and HDAC inhibition in non-small cell lung cancer cells involving ribonucleotides in DNA.Scientific reports · 2025Article
- The polymeric fluoropyrimidine CF10 overcomes limitations of 5-FU in pancreatic ductal adenocarcinoma cells through increased replication stress.Cancer biology & therapy · 2024Article
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- Transcriptomic Analysis of CRISPR/Cas9-Mediated PARP1-Knockout Cells under the Influence of Topotecan and TDP1 Inhibitor.International journal of molecular sciences · 2023Article
- Review of 5-FU resistance mechanisms in colorectal cancer: clinical significance of attenuated on-target effects.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- Oligonucleotides Carrying Nucleoside Antimetabolites as Potential Prodrugs.Current medicinal chemistry · 2023Review
- Therapy resistance: opportunities created by adaptive responses to targeted therapies in cancer.Nature reviews. Cancer · 2022Review
- Evaluation of Floxuridine Oligonucleotide Conjugates Carrying Potential Enhancers of Cellular Uptake.International journal of molecular sciences · 2021Article
- Parallel G-quadruplex Structures Increase Cellular Uptake and Cytotoxicity of 5-Fluoro-2'-deoxyuridine Oligomers in 5-Fluorouracil Resistant Cells.Molecules (Basel, Switzerland) · 2021Article
- Improved Antitumor Activity of the Fluoropyrimidine Polymer CF10 in Preclinical Colorectal Cancer Models through Distinct Mechanistic and Pharmacologic Properties.Molecular cancer therapeutics · 2021Article
- Targeting DNA topoisomerases: past & future.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- Chemistry of Fluorinated Pyrimidines in the Era of Personalized Medicine.Molecules (Basel, Switzerland) · 2020Review
- Fluoropyrimidine Modulation of the Anti-Tumor Immune Response-Prospects for Improved Colorectal Cancer Treatment.Cancers · 2020Review
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Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Topoisomerases are well-validated targets for cancer chemotherapy and DNA topoisomerase 1 (Top1) is the sole target of the camptothecin (CPT) class of anticancer drugs. Over the last 20 years, multiple studies have shown Top1 activity is modulated by non-native DNA structures and this can lead to trapping of Top1 cleavage complexes (Top1cc) and conversion to DNA double strand breaks. Among the perturbations to DNA structure that generate Top1cc are nucleoside analogs that are incorporated into genomic DNA during replication including cytarabine, gemcitabine, and 5-fluoro-2'-deoxyuridine (FdU). We review the literature summarizing the role of Top1cc in mediating the DNA damaging and cytotoxic activities of nucleoside analogs. We also summarize studies demonstrating distinct differences between Top1cc induced by nucleoside analogs and CPTs, particularly with regard to DNA repair. Collectively, these studies demonstrate that, while Top1 is a common target for both Top1 poisons such as CPT and nucleoside analogs such as FdU, these agents are not redundant. In recent years, studies have shown that Top1 poisons and nucleoside analogs together with other anti-cancer drugs such as cisplatin cause replication stress and the DNA repair pathways that modulate the cytotoxic activities of these compounds are being elucidated. We present an overview of this evolving literature, which has implications for how targeting of Top1 with nucleoside analogs can be used more effectively for cancer treatment.
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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.