ReviewFrontiers in oncology2019
Harnessing DNA Double-Strand Break Repair for Cancer Treatment.
Review in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
130 citing papers in PubMed, 1 synthesis or guideline pooled it.
- DNA Repair Genes as Drug Candidates for Early Breast Cancer Onset in Latin America: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Breaking the Balance: Baseline Oxidative Stress and DNA Repair Capacity in Multiple Myeloma Therapy.Cancers · 2026Article
- DNA-PKcs promotes therapy resistance and metastatic recurrence in neuroblastoma.Cancer letters · 2026Article
- ZNF184 negatively regulates HR repair and predicts poor prognosis in acute lymphoblastic leukemia.Nucleic acids research · 2026Article
- Simultaneous CRISPR/Cas9-induced double-strand breaks are lethal in models of pancreatic cancer.The Journal of clinical investigation · 2026Article
- Pathway for the Development of ATR Inhibitors in Pediatric Malignancies: An ACCELERATE Multistakeholder Analysis.JCO precision oncology · 2026Review
- Delineation of molecular subtypes based on pathway activation signatures reveals intrinsic tumor heterogeneity and pan-cancer shared features.Frontiers in oncology · 2026Article
- The breakome of BRCA1 and BRCA2 pathway mutation carriers reveals early processes in breast oncogenesis.Cell death & disease · 2025Article
- Emerging insights into alternative end‑joining: Mechanisms, genome instability and therapeutic opportunities in cancer (Review).International journal of oncology · 2025Review
- 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
- Update on R-loops in genomic integrity: Formation, functions, and implications for human diseases.Genes & diseases · 2025Review
- Elevated nonhomologous end-joining by AATF enables efficient DNA damage repair and therapeutic resistance in glioblastoma.Nature communications · 2025Article
- Cancer Vulnerabilities Through Targeting the ATR/Chk1 and ATM/Chk2 Axes in the Context of DNA Damage.Cells · 2025Review
- Alpha-synuclein regulates nucleolar DNA double-strand break repair in melanoma.Science advances · 2025Article
- Radiosensitization Induced by Magnetic Hyperthermia of PEGylated Nickel Ferrite Nanoparticles on Breast Cancer Cells.International journal of molecular sciences · 2025Article
- γ-tubulin mediates DNA double-strand break repair.Journal of cell science · 2025Article
- ISGylation: is our genome yearning for such a modification?Acta biochimica et biophysica Sinica · 2025Review
- Crotonylation of MCM6 enhances chemotherapeutics sensitivity of breast cancer via inducing DNA replication stress.Cell proliferation · 2025Article
- Targeting Ataxia Telangiectasia-Mutated and Rad3-Related for Anaplastic Thyroid Cancer.Cancers · 2025Article
- Synergistic effects of retinol and retinyl palmitate in alleviating UVB-induced DNA damage and promoting the homologous recombination repair in keratinocytes.Frontiers in pharmacology · 2025Article
70 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double-strand breaks (DSBs) are highly deleterious, with a single unrepaired DSB being sufficient to trigger cell death. Compared to healthy cells, cancer cells have a higher DSB burden due to oncogene-induced replication stress and acquired defects in DNA damage response (DDR) mechanisms. Consequently, hyperproliferating cancer cells rely on efficient DSB repair for their survival. Moreover, augmented DSB repair capacity is a major cause of radio- and chemoresistance and, ultimately, cancer recurrence. Although inherited DDR defects can predispose individuals to develop certain cancers, the very same vulnerability may be therapeutically exploited to preferentially kill tumor cells. A paradigm for DNA repair targeted therapy has emerged in cancers that exhibit mutations in
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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.