ReviewMolecules (Basel, Switzerland)2011
Exploiting the nucleotide substrate specificity of repair DNA polymerases to develop novel anticancer agents.
Review in Molecules (Basel, Switzerland), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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.
- Exploring the Anticancer Potential of Lamivudine-Loaded Polymeric Nanoparticles:ACS applied bio materials · 2025Article
- Ribonucleotide reductase regulatory subunit M2 drives glioblastoma TMZ resistance through modulation of dNTP production.Science advances · 2023Article
- Structural basis of HIV inhibition by L-nucleosides: Opportunities for drug development and repurposing.Drug discovery today · 2022Review
- Conceptual frameworks of synthetic lethality in clear cell carcinoma of the ovary.Biomedical reports · 2018Review
- Inhibiting checkpoint kinase 1 protects bone from bone resorption by mammary tumor in a mouse model.Oncotarget · 2018Article
- Effective Synthesis of Nucleosides Utilizing O-Acetyl-Glycosyl Chlorides as Glycosyl Donors in the Absence of Catalyst: Mechanism Revision and Application to Silyl-Hilbert-Johnson Reaction.Molecules (Basel, Switzerland) · 2017Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genome is constantly exposed to mutations that can originate during replication or as a result of the action of both endogenous and/or exogenous damaging agents [such as reactive oxygen species (ROS), UV light, genotoxic environmental compounds, etc.]. Cells have developed a set of specialized mechanisms to counteract this mutational burden. Many cancer cells have defects in one or more DNA repair pathways, hence they rely on a narrower set of specialized DNA repair mechanisms than normal cells. Inhibiting one of these pathways in the context of an already DNA repair-deficient genetic background, will be more toxic to cancer cells than to normal cells, a concept recently exploited in cancer chemotherapy by the synthetic lethality approach. Essential to all DNA repair pathways are the DNA pols. Thus, these enzymes are being regarded as attractive targets for the development of specific inhibitors of DNA repair in cancer cells. In this review we examine the current state-of-the-art in the development of nucleotide analogs as inhibitors of repair DNA polymerases.
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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.