ReviewJournal of molecular cell biology2011
BRCA1, PARP, and 53BP1: conditional synthetic lethality and synthetic viability.
Review in Journal of molecular cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 107 citations in OpenAlex.
- PARP inhibitor resistance in IDH1-mutant cancers due to loss of end protection factors, 53BP1 and REV7.NAR cancer · 2025Article
- The loss of DNA polymerase epsilon accessory subunits POLE3-POLE4 leads to BRCA1-independent PARP inhibitor sensitivity.Nucleic acids research · 2024Article
- RNF126, 168 and CUL1: The Potential Utilization of Multi-Functional E3 Ubiquitin Ligases in Genome Maintenance for Cancer Therapy.Biomedicines · 2023Review
- Fatty acid oxidation facilitates DNA double-strand break repair by promoting PARP1 acetylation.Cell death & disease · 2023Article
- Article
- GA-OH enhances the cytotoxicity of photon and proton radiation in HPVFrontiers in oncology · 2023Article
- PARP inhibitors in the treatment of ARID1A mutant ovarian clear cell cancer: PI3K/Akt1-dependent mechanism of synthetic lethality.Frontiers in oncology · 2023Article
- Multivalent binding of the hub protein LC8 at a newly discovered site in 53BP1.Biophysical journal · 2022Article
- Cyclin-Dependent Kinase Synthetic Lethality Partners in DNA Damage Response.International journal of molecular sciences · 2022Review
- Drug resistance in metastatic castration-resistant prostate cancer: an update on the status quo.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Shifting landscapes of human MTHFR missense-variant effects.American journal of human genetics · 2021Article
- Review
- Targeting Non-Oncogene Addiction for Cancer Therapy.Biomolecules · 2021Review
- DNA double-strand break repair in cancer: A path to achieving precision medicine.International review of cell and molecular biology · 2021Review
- Targeted Therapy as a Potential De-Escalation Strategy in Locally Advanced HPV-Associated Oropharyngeal Cancer: A Literature Review.Frontiers in oncology · 2021Review
- Targeting UHRF1-dependent DNA repair selectively sensitizes KRAS mutant lung cancer to chemotherapy.Cancer letters · 2020Article
- Identification of synthetic chemosensitivity genes paired with BRAF for BRAF/MAPK inhibitors.Scientific reports · 2020Article
- Development of synthetic lethality in cancer: molecular and cellular classification.Signal transduction and targeted therapy · 2020Review
- A scalable CRISPR/Cas9-based fluorescent reporter assay to study DNA double-strand break repair choice.Nature communications · 2020Article
- Vitamin D in Triple-Negative and BRCA1-Deficient Breast Cancer-Implications for Pathogenesis and Therapy.International journal of molecular sciences · 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRCA1 plays a critical role in the regulation of homologous recombination (HR)-mediated DNA double-strand break repair. BRCA1-deficient cancers have evolved to tolerate loss of BRCA1 function. This renders them vulnerable to agents, such as PARP inhibitors, that are conditionally 'synthetic lethal' with their underlying repair defect. Recent studies demonstrate that BRCA1-deficient cells may acquire resistance to these agents by partially correcting their defect in HR-mediated repair, either through reversion mutations in BRCA1 or through 'synthetic viable' loss of 53BP1. These findings and their clinical implications will be reviewed in this article.
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.