ReviewCancers2021
Regulation of RAD51 at the Transcriptional and Functional Levels: What Prospects for Cancer Therapy?
Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Research progress on the role and mechanism of DNA damage repair in germ cell development.Frontiers in endocrinology · 2023Pooled it
- Overcoming Resistance in Triple-Negative Breast Cancer: A Translational Perspective on Next-Generation DNA Damage Response Inhibitors and Synthetic Lethality.Molecules (Basel, Switzerland) · 2026Review
- Molecular convergence in gallbladder cancer: MEK-ERK signalling at the crossroads of oncogenic hubs and pathway cross-talks.Cancer cell international · 2026Review
- The Molecular and Functional Landscape of Resistance to FOLFIRI Chemotherapy in Metastatic Colorectal Cancer.Cancer discovery · 2026Article
- AQB improves carboplatin sensitivity in endometrial cancer through dual DNA repair modulation: suppression of the p21-E2F1-RAD51 and ATF3-HDAC1-BRCA1 signaling.Cell death & disease · 2025Article
- The toxicological impact of PET-MPs exposure on atherosclerosis: insights from network toxicology, molecular docking, and machine learning.Scientific reports · 2025Article
- Prognostic Significance ofBiology · 2025Article
- Homologous Recombination Deficiency in Ovarian and Breast Cancers: Biomarkers, Diagnosis, and Treatment.Current issues in molecular biology · 2025Review
- Review
- NEK kinases in cell cycle regulation, DNA damage response, and cancer progression.Tissue & cell · 2025Review
- Genetic Variants inGenes · 2025Article
- Identification of prognostic and cellular senescence gene E2F1 of papillary thyroid carcinoma through bioinformatics analyses and experimental verification.Frontiers in genetics · 2025Article
- Article
- RAD51 High-Expressed Hepatocellular Carcinomas Are Associated With High Cell Proliferation.The Journal of surgical research · 2024Article
- Review
- CircCDYL2 bolsters radiotherapy resistance in nasopharyngeal carcinoma by promoting RAD51 translation initiation for enhanced homologous recombination repair.Journal of experimental & clinical cancer research : CR · 2024Article
- Genetically Regulated Gene Expression in the Brain Associated With Chronic Pain: Relationships With Clinical Traits and Potential for Drug Repurposing.Biological psychiatry · 2024Article
- Antitumoral Activity of the Universal Methyl DonorMolecules (Basel, Switzerland) · 2024Article
- RAD51 and Infertility: A Review and Case-Control Study.Biochemical genetics · 2024Review
- Human Rad51 Protein Requires Higher Concentrations of Calcium Ions for D-Loop Formation than for Oligonucleotide Strand Exchange.International journal of molecular sciences · 2024Article
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 at 3 institutions in 1 country.
Funding
Abstract
The RAD51 recombinase is a critical effector of Homologous Recombination (HR), which is an essential DNA repair mechanism for double-strand breaks. The RAD51 protein is recruited onto the DNA break by BRCA2 and forms homopolymeric filaments that invade the homologous chromatid and use it as a template for repair. RAD51 filaments are detectable by immunofluorescence as distinct foci in the cell nucleus, and their presence is a read out of HR proficiency. RAD51 is an essential gene, protecting cells from genetic instability. Its expression is low and tightly regulated in normal cells and, contrastingly, elevated in a large fraction of cancers, where its level of expression and activity have been linked with sensitivity to genotoxic treatment. In particular, BRCA-deficient tumors show reduced or obliterated RAD51 foci formation and increased sensitivity to platinum salt or PARP inhibitors. However, resistance to treatment sets in rapidly and is frequently based on a complete or partial restoration of RAD51 foci formation. Consequently, RAD51 could be a highly valuable therapeutic target. Here, we review the multiple levels of regulation that impact the transcription of the RAD51 gene, as well as the post-translational modifications that determine its expression level, recruitment on DNA damage sites and the efficient formation of homofilaments. Some of these regulation levels may be targeted and their impact on cancer cell survival discussed.
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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.