ReviewFrontiers in oncology2014
Chemotherapeutic compounds targeting the DNA double-strand break repair pathways: the good, the bad, and the promising.
Review in Frontiers in oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 120 citations in OpenAlex.
- Spatiotemporal regulation of DNA repair proteins between Golgi and nucleus maintains genome stability.The Journal of cell biology · 2026Article
- Regulation of Cell Cycle-Related Damage/Repair Mechanism and Oxidative Stress Status by Oroxylin A in Hepatocellular Carcinoma Cells.International journal of molecular sciences · 2025Article
- Epigenetic drugs in cancer therapy.Cancer metastasis reviews · 2025Review
- Article
- Cocaine-induced DNA-PK relieves RNAP II pausing by promoting TRIM28 phosphorylation.bioRxiv : the preprint server for biology · 2024Article
- Identification and Validation of New DNA-PKcs Inhibitors through High-Throughput Virtual Screening and Experimental Verification.International journal of molecular sciences · 2024Article
- Whole-genome mapping of APOBEC mutagenesis in metastatic urothelial carcinoma identifies driver hotspot mutations and a novel mutational signature.Cell genomics · 2024Article
- Phase I study of peposertib and avelumab with or without palliative radiotherapy in patients with advanced solid tumors.ESMO open · 2024Article
- 6-Methoxydihydrosanguinarine exhibits cytotoxicity and sensitizes TRAIL-induced apoptosis of hepatocellular carcinoma cells through ROS-mediated upregulation of DR5.Medical oncology (Northwood, London, England) · 2023Article
- Identification of collateral sensitivity and evolutionary landscape of chemotherapy-induced drug resistance using cellular barcoding technology.Frontiers in pharmacology · 2023Article
- Feline XRCC4 undergoes rapid Ku-dependent recruitment to DNA damage sites.FEBS open bio · 2022Article
- A clinically relevant heterozygous ATR mutation sensitizes colorectal cancer cells to replication stress.Scientific reports · 2022Article
- Recent Advances in the Development of Non-PIKKs Targeting Small Molecule Inhibitors of DNA Double-Strand Break Repair.Frontiers in oncology · 2022Review
- Editorial: Cancer Therapeutics: Targeting DNA Repair Pathways.Frontiers in molecular biosciences · 2022Article
- Radiotherapy in Medulloblastoma-Evolution of Treatment, Current Concepts and Future Perspectives.Cancers · 2021Review
- Comprehensive molecular characterization of pediatric radiation-induced high-grade glioma.Nature communications · 2021Article
- Structural and mechanistic insights into the Artemis endonuclease and strategies for its inhibition.Nucleic acids research · 2021Article
- SCR7, a potent cancer therapeutic agent and a biochemical inhibitor of nonhomologous DNA end-joining.Cancer reports (Hoboken, N.J.) · 2021Review
- COMMD1, from the Repair of DNA Double Strand Breaks, to a Novel Anti-Cancer Therapeutic Target.Cancers · 2021Article
- Epigenetic Mechanisms in DNA Double Strand Break Repair: A Clinical Review.Frontiers in molecular biosciences · 2021Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The repair of DNA double-strand breaks (DSBs) is a critical cellular mechanism that exists to ensure genomic stability. DNA DSBs are the most deleterious type of insult to a cell's genetic material and can lead to genomic instability, apoptosis, or senescence. Incorrectly repaired DNA DSBs have the potential to produce chromosomal translocations and genomic instability, potentially leading to cancer. The prevalence of DNA DSBs in cancer due to unregulated growth and errors in repair opens up a potential therapeutic window in the treatment of cancers. The cellular response to DNA DSBs is comprised of two pathways to ensure DNA breaks are repaired: homologous recombination and non-homologous end joining. Identifying chemotherapeutic compounds targeting proteins involved in these DNA repair pathways has shown promise as a cancer therapy for patients, either as a monotherapy or in combination with genotoxic drugs. From the beginning, there have been a number of chemotherapeutic compounds that have yielded successful responses in the clinic, a number that have failed (CGK-733 and iniparib), and a number of promising targets for future studies identified. This review looks in detail at how the cell responds to these DNA DSBs and investigates the chemotherapeutic avenues that have been and are currently being explored to target this repair process.
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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.