ReviewNature reviews. Cancer2015
Therapeutic opportunities within the DNA damage response.
Review in Nature reviews. Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 314 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
314 citing papers in PubMed.
- Chronic Cigarette Smoke Extract Exposure Promotes Genomic and Phenotypic Reprogramming in Lung Cancer Cells.Thoracic cancer · 2026Article
- The ribonuclease ZC3H12A stabilizes BRCA1 mRNA in DNA damage response.Redox biology · 2026Article
- Docking-Based Virtual Screening Identifies a Small-Molecule Inhibitor of the Translesion Synthesis REV7/REV3 Protein-Protein Interaction.ChemMedChem · 2026Article
- Chalcones as multitarget modulators in non-small cell lung cancer: mechanistic insights and therapeutic perspectives.Archives of toxicology · 2026Review
- Complete and Persistent Response to Immunotherapy in Highly Pretreated MSS TMB-High Pancreatic Adenocarcinoma: A Case Report and Literature Review.International journal of molecular sciences · 2026Review
- Unsupervised Deep Representation Learning and Probabilistic Clustering for the Systems-Level Discovery of Germline Mutation Signatures in Pediatric Cancers.Biomedicines · 2026Article
- B.R.E.A.S.T. Breast canceR Enhanced AI-Supported Therapy: A New Interpretable Proteomics-Driven Machine Learning Framework for Therapy Response Prediction in Breast Cancer.International journal of molecular sciences · 2026Article
- A small molecule disrupts G4-STAT1 interaction and synergizes with olaparib to drive cancer cell death.Nucleic acids research · 2026Article
- Association of homologous recombination repair gene mutation with clinical prognosis in histological subtypes of epithelial ovarian cancer patients.Journal of gynecologic oncology · 2026Article
- Nanotechnology-driven STING regulation for on-demand therapy.Acta pharmaceutica Sinica. B · 2026Review
- Targeted CRISPR knockout screening identifies known and novel chemogenomic interactions between DNA damaging agents and DNA repair genes.NAR cancer · 2026Article
- Article
- Design and synthesis of 2-amino-4-(trifluoromethyl)pyrimidine derivatives as potential Werner-dependent antiproliferative agents.Molecular diversity · 2026Article
- DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026Review
- MOKCa-3D database: functional and structural analysis of missense mutations in cancer.Database : the journal of biological databases and curation · 2026Article
- Accurate prediction of candidate lncRNAs associated with DNA damage response based on gene expression patterns from graph neural networks.Bioinformatics advances · 2026Article
- Efficacy and safety of PARP inhibitors in metastatic breast cancer patients with homologous recombination repair pathway gene mutations: a retrospective multicenter real-world study.Therapeutic advances in medical oncology · 2026Article
- Mutation patterns and prognostic potentiality of homologous recombination repair genes in gliomas.BMC cancer · 2025Article
- TRIM37-PARP1-TET1 axis maintains stemness and prevents osteoporosis by inhibiting DNMT1 alternative splicing via 5hmC regulation.Nature communications · 2025Article
- Aurora kinase B phosphorylates ZBP1 to drive PANoptosis following treatment with PARP and ATR inhibitors combination.Nature communications · 2025Article
254 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
5 authors.
Funding
Abstract
The DNA damage response (DDR) is essential for maintaining the genomic integrity of the cell, and its disruption is one of the hallmarks of cancer. Classically, defects in the DDR have been exploited therapeutically in the treatment of cancer with radiation therapies or genotoxic chemotherapies. More recently, protein components of the DDR systems have been identified as promising avenues for targeted cancer therapeutics. Here, we present an in-depth analysis of the function, role in cancer and therapeutic potential of 450 expert-curated human DDR genes. We discuss the DDR drugs that have been approved by the US Food and Drug Administration (FDA) or that are under clinical investigation. We examine large-scale genomic and expression data for 15 cancers to identify deregulated components of the DDR, and we apply systematic computational analysis to identify DDR proteins that are amenable to modulation by small molecules, highlighting potential novel therapeutic targets.
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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.