ReviewCell cycle (Georgetown, Tex.)2019
DNA double-strand break repair pathway choice - from basic biology to clinical exploitation.
Review in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 26 citations in OpenAlex.
- Acetylation-dependent regulation of FOX-Ku interaction by GCN5-SIRT1 axis controls non-homologous end-joining DNA repair.Archives of pharmacal research · 2026Article
- Pancreatic ductal adenocarcinoma: integrating molecular insights for targeted interventions.Signal transduction and targeted therapy · 2026Review
- From survival of irradiated mice to modern molecular insights: a seventy-year journey in radiobiology at the institute of biophysics, Czech academy of sciences.European biophysics journal : EBJ · 2025Review
- Phase separation in DNA repair: orchestrating the cellular response to genomic stability.PeerJ · 2025Review
- Alterations in the expression of homologous recombination repair (HRR) genes in breast cancer tissues considering germline BRCA1/2 mutation status.Breast cancer research and treatment · 2024Article
- Large-scale analysis of CDH1 mutations defines a distinctive molecular subset with treatment implications in gastric cancer.NPJ precision oncology · 2024Article
- Triple-Negative Breast Cancer and Emerging Therapeutic Strategies: ATR and CHK1/2 as Promising Targets.Cancers · 2024Review
- Trypanosoma cruzi infection induces DNA double-strand breaks and activates DNA damage response pathway in host epithelial cells.Scientific reports · 2024Article
- Review
- Conjunctive Analyses of BSA-Seq and BSR-Seq Unveil theInternational journal of molecular sciences · 2022Article
- Genome Integrity and Neurological Disease.International journal of molecular sciences · 2022Review
- Cruciform DNA Structures Act as Legible Templates for Accelerating Homologous Recombination in Transgenic Animals.International journal of molecular sciences · 2022Article
- Acquired temozolomide resistance in MGMTCell death & disease · 2022Article
- Elucidation of the Clustered Nano-Architecture of Radiation-Induced DNA Damage Sites and Surrounding Chromatin in Cancer Cells: A Single Molecule Localization Microscopy Approach.International journal of molecular sciences · 2021Article
- Origin, Regulation, and Fitness Effect of Chromosomal Rearrangements in the YeastInternational journal of molecular sciences · 2021Review
- A New Twist in Protein Kinase B/Akt Signaling: Role of Altered Cancer Cell Metabolism in Akt-Mediated Therapy Resistance.International journal of molecular sciences · 2020Review
- Targeting DNA Damage Response in Prostate and Breast Cancer.International journal of molecular sciences · 2020Review
- Review
- DNA end resection and its role in DNA replication and DSB repair choice in mammalian cells.Experimental & molecular medicine · 2020Review
- PARP Inhibitor Resistance Mechanisms and Implications for Post-Progression Combination Therapies.Cancers · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in genes encoding components of the DNA damage response (DDR) are among the most frequent aberrations in human tumors. Moreover, a large array of human syndromes is caused by mutations in genes involved in DDR pathways. Among others, homologous recombination repair (HR) of DNA double-strand breaks (DSB) is frequently affected by disabling mutations. While impaired HR is clearly promoting tumorigenesis, it is also associated with an actionable sensitivity against PARP inhibitors. PARP inhibitors have recently received FDA approval for the treatment of breast- and ovarian cancer. However, as with all molecularly targeted agents, acquired resistance limits its use. Both pharmaco-genomic approaches and the study of human genome instability syndromes have led to a profound understanding of PARP inhibitor resistance. These experiments have revealed new insights into the molecular mechanisms that drive mammalian DSB repair. Here, we review recent discoveries in the field and provide a clinical perspective.
Indexed as
Identifiers
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.