ReviewNucleic acids research2014
A fine-scale dissection of the DNA double-strand break repair machinery and its implications for breast cancer therapy.
Review in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Pooled it
- Review
- Associations Between DNA Repair Gene Polymorphisms and Breast Cancer Histopathological Subtypes: A Preliminary Study.Journal of clinical medicine · 2025Article
- Homeodomain protein PRRX1 anchors the Ku heterodimers at DNA double-strand breaks to promote nonhomologous end-joining.Nucleic acids research · 2025Article
- Particulate hexavalent chromium inhibits global transcription of genes in DNA repair pathways, particularly targeting homologous recombination repair, base excision repair, mismatch repair and microhomology-mediated end-joining.Journal of hazardous materials · 2025Article
- Unveiling the relationship between WWOX and BRCA1 in mammary tumorigenicity and in DNA repair pathway selection.Cell death discovery · 2024Article
- TP53 and its Regulatory Genes as Prognosis of Cutaneous Melanoma.Cancer informatics · 2023Article
- Identifying collateral and synthetic lethal vulnerabilities within the DNA-damage response.BMC bioinformatics · 2021Article
- The Role ofCancers · 2021Review
- Review
- Cancer Stemness: p53 at the Wheel.Frontiers in oncology · 2020Review
- Aberrant RNA Splicing in Cancer and Drug Resistance.Cancers · 2018Review
- Comparative genome-wide survey of single nucleotide variation uncovers the genetic diversity and potential biomedical applications among six Macaca species.International journal of molecular sciences · 2018Article
- New therapeutic strategies to treat human cancers expressing mutant p53 proteins.Journal of experimental & clinical cancer research : CR · 2018Review
- Nuclear poly(A)-binding protein 1 is an ATM target and essential for DNA double-strand break repair.Nucleic acids research · 2018Article
- ELAS1 induces apoptotic death in adenocarcinoma DU145 and squamous-cell carcinoma SAS cancer cells, but not in normal KD cells.Oncotarget · 2017Article
- Challenges for Super-Resolution Localization Microscopy and Biomolecular Fluorescent Nano-Probing in Cancer Research.International journal of molecular sciences · 2017Article
- FANCJ helicase controls the balance between short- and long-tract gene conversions between sister chromatids.Nucleic acids research · 2017Article
- Mechanisms of DNA damage, repair, and mutagenesis.Environmental and molecular mutagenesis · 2017Review
- Androgen receptor inhibitor-induced "BRCAness" and PARP inhibition are synthetically lethal for castration-resistant prostate cancer.Science signaling · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
DNA-damage response machinery is crucial to maintain the genomic integrity of cells, by enabling effective repair of even highly lethal lesions such as DNA double-strand breaks (DSBs). Defects in specific genes acquired through mutations, copy-number alterations or epigenetic changes can alter the balance of these pathways, triggering cancerous potential in cells. Selective killing of cancer cells by sensitizing them to further DNA damage, especially by induction of DSBs, therefore requires careful modulation of DSB-repair pathways. Here, we review the latest knowledge on the two DSB-repair pathways, homologous recombination and non-homologous end joining in human, describing in detail the functions of their components and the key mechanisms contributing to the repair. Such an in-depth characterization of these pathways enables a more mechanistic understanding of how cells respond to therapies, and suggests molecules and processes that can be explored as potential therapeutic targets. One such avenue that has shown immense promise is via the exploitation of synthetic lethal relationships, for which the BRCA1-PARP1 relationship is particularly notable. Here, we describe how this relationship functions and the manner in which cancer cells acquire therapy resistance by restoring their DSB repair potential.
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.