ReviewMedComm2023
Double-strand DNA break repair: molecular mechanisms and therapeutic targets.
Review in MedComm, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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
53 citing papers in PubMed, 65 citations in OpenAlex.
- Advanced gene editing technologies for oncology mechanisms, applications, and clinical implementation.Cancer gene therapy · 2026Review
- Triptonide enhances DNA damage by inhibiting TRIP13‑mediated DNA repair and synergizes with bortezomib to suppress multiple myeloma.International journal of oncology · 2026Article
- Structural and Functional Characteristics of the Liver After Fractionated Local Electron Irradiation and Against the Background of Ascorbic Acid Administration.Journal of personalized medicine · 2026Review
- Review
- Homologous recombination is essential for DNA damage-induced regeneration of Drosophila testis germline stem cells.Development (Cambridge, England) · 2026Article
- Lysine l-Lactylation: Bridging Metabolism, Chromatin and Disease.Cell proliferation · 2026Review
- DNA repair pathways in Mycobacterium leprae: insights from reductive genome evolution and therapeutic opportunities.Archives of microbiology · 2026Review
- Targeting E3 ubiquitin ligases: Mechanistic breakthroughs and novel clinical translation pathways for tumor radioimmunotherapy.Molecular cancer · 2026Review
- SNORA23-KDM5C epigenetic axis mediates dual DNA repair pathways to drive radioresistance in esophageal squamous cell carcinoma.Cell death and differentiation · 2026Article
- R-loops and D-loops: a delicate balance in genomic stability and instability.Cell communication and signaling : CCS · 2026Review
- The microbiota-lymphocyte protective axis (MLPA): a novel paradigm for overcoming radiation-induced lymphopenia (RIL) and potentiating the efficacy of tumor immuno-combination therapy.Cancer immunology, immunotherapy : CII · 2026Review
- Comprehensive Review of the Interplay of MicroRNA and Epithelial-Mesenchymal Transition in Radiation Resistance of Cancer.International journal of molecular sciences · 2026Review
- EFHD2 drives lactate-mediated DNA damage repair and immunosuppression via HMGB1 and HIF-1α to confer radioresistance in colorectal cancer.Cell death & disease · 2026Article
- Phosphorylation of RBM39 by CDK13 stabilizes RAD50 mRNA to drive cisplatin resistance in endometrial cancer.The Journal of biological chemistry · 2026Article
- Exosome-loaded nanoradiosensitizers in radiotherapy for preventing post-irradiation tumor recurrence: mechanisms, preclinical evidence, and translational challenges.Discover nano · 2026Review
- Dysfunctional DNA Mismatch Repair Drives the Evolution of Gene Amplification in MTX-Resistant Human Colorectal Cancer Cells.International journal of molecular sciences · 2026Article
- Non-coding RNA regulation of the radiation-induced DNA damage response and its translational relevance.Discover oncology · 2026Review
- Laminaria japonica Polysaccharide Alleviates Radiation-Induced Salivary Gland Injury by Promoting DNA Damage Repair.International dental journal · 2026Article
- DNA end configurations dictate synaptic complex formation during NHEJ-mediated end bridging.Nature communications · 2026Article
- Kinesin Family Member 26A Disrupts DNA-Dependent Protein Kinase Complex Formation to Enhance Chemoradiotherapy Sensitivity in Colorectal Cancer.International journal of biological sciences · 2026Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Double-strand break (DSB), a significant DNA damage brought on by ionizing radiation, acts as an initiating signal in tumor radiotherapy, causing cancer cells death. The two primary pathways for DNA DSB repair in mammalian cells are nonhomologous end joining (NHEJ) and homologous recombination (HR), which cooperate and compete with one another to achieve effective repair. The DSB repair mechanism depends on numerous regulatory variables. DSB recognition and the recruitment of DNA repair components, for instance, depend on the MRE11-RAD50-NBS1 (MRN) complex and the Ku70/80 heterodimer/DNA-PKcs (DNA-PK) complex, whose control is crucial in determining the DSB repair pathway choice and efficiency of HR and NHEJ. In-depth elucidation on the DSB repair pathway's molecular mechanisms has greatly facilitated for creation of repair proteins or pathways-specific inhibitors to advance precise cancer therapy and boost the effectiveness of cancer radiotherapy. The architectures, roles, molecular processes, and inhibitors of significant target proteins in the DSB repair pathways are reviewed in this article. The strategy and application in cancer therapy are also discussed based on the advancement of inhibitors targeted DSB damage response and repair proteins.
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What OpenQuestion holds
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.