ReviewF1000Research2018
Variation in RAD51 details a hub of functions: opportunities to advance cancer diagnosis and therapy.
Review in F1000Research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Selective killing of ALT-cancer cells by Withaferin-A involves destabilization of Rad51 and disruption of DNA repair.Cell death & disease · 2026Article
- Nucleolar origins: challenging perspectives on evolution and function.Open biology · 2025Review
- RAD51 protein is a predictor of chemosensitivity and survival prognosis in patients with advanced high-grade serous ovarian cancer undergoing neoadjuvant chemotherapy.Frontiers in oncology · 2025Article
- Decline of DNA damage response along with myogenic differentiation.Life science alliance · 2024Article
- DNA damage response proteins in canine cancer as potential research targets in comparative oncology.Veterinary and comparative oncology · 2022Review
- miR-125a attenuates the malignant biological behaviors of cervical squamous cell carcinoma cells through Rad51.Bioengineered · 2022Article
- Targeting RAD51-Mediated Homologous Recombination as a Treatment for Advanced Solid and Hematologic Malignancies: Opportunities and Challenges Ahead.OncoTargets and therapy · 2022Review
- Review
- Emerging functions and clinical applications of exosomes in human oral diseases.Cell & bioscience · 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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of genome stability is one of the hallmarks of the enabling characteristics of cancer development. Homologous recombination is a DNA repair process that often breaks down as a prelude to developing cancer. Conversely, homologous recombination can be the Achilles' heel in common anti-cancer therapies, which are effective by inducing irreparable DNA damage. Here, we review recent structural and functional studies of RAD51, the protein that catalyzes the defining step of homologous recombination: homology recognition and DNA strand exchange. Specific mutations can be linked to structural changes and known essential functions. Additional RAD51 interactions and functions may be revealed. The identification of viable mutations in this essential protein may help define the range of activity and interactions needed. All of this information provides opportunities to fine-tune existing therapies based on homologous recombination status, guide diagnosis, and hopefully develop new clinical tools.
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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.