ReviewCancer research2022
BRCA1-Dependent and Independent Recruitment of PALB2-BRCA2-RAD51 in the DNA Damage Response and Cancer.
Review in Cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Meta-analysis of the association between overexpression of RAD51 family genes and prognosis and clinical features in breast cancer.Scientific reports · 2025Pooled it
- CXorf67 in malignancies: Deciphering epigenetic landscapes and clinical implications for precision oncology.Genes & diseases · 2026Review
- Multidimensional molecular mechanisms of drug resistance in breast cancer: Implications for clinical decision‑making and treatment strategies (Review).Oncology reports · 2026Review
- Molecular cartography of breast cancer: decoding genomes, heterogeneity and the tumor microenvironment for personalized targeted therapeutics.Molecular biology reports · 2026Review
- GNL3 SUMOylation is essential for DNA double-strand break repair by homologous recombination.Nature communications · 2026Article
- Functional profiling of ovarian cancer models reveals Bcl-xL/NOTCH targeting to overcome resistance.NPJ precision oncology · 2026Article
- A radiotherapy resistance-related prognostic signature predicts survival and the immune landscape in rectal cancer.Translational cancer research · 2026Article
- PARP Inhibitor Sensitivity in Tumors Harboring Non-BRCA Homologous Recombination Gene Alterations: Current Evidence Across Ovarian, Breast, Prostate, and Pancreatic Cancers.International journal of molecular sciences · 2026Review
- T Cell-Independent Role of PD-L1 in Kidney Repair: Mitigation of Tubular DNA Damage via PD-L1/BRCA1 Interaction Following AKI.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanisms of resistance in small cell lung cancer.Chinese medical journal · 2026Review
- Long-Term PET-Nanoplastic Exposure Alters DNA Damage Response Capacity in BEAS-2B Human Bronchial Epithelial Cells.International journal of molecular sciences · 2026Article
- Replication origin flexibility: a tool to mitigate the hazards of excess replication.Trends in genetics : TIG · 2026Review
- Decoding the Transcriptional Complexity of the Human BRCA2 DNA Repair Gene Using Hybrid-seq.Biochemical genetics · 2026Article
- Review
- Article
- Interplay Between Poly(ADP-ribosyl)ation and Specific Inner Cellular Events That Suggest Combination Strategies for Overcoming PARP Inhibitor Resistance.Pharmaceutics · 2026Review
- Functional Germline DNA Repair Mutations as Predictors of Acute Radiodermatitis in Breast Cancer.Diagnostics (Basel, Switzerland) · 2026Article
- Pathogenic Germline PALB2 and RAD50 Variants in Patients With Relapsed Ewing Sarcoma.Pediatric blood & cancer · 2026Article
- BRCA1-Associated Protein 1 (BAP1) in Human Cancer and its Emerging Role as a Novel Potential Therapeutic Target.Current oncology reports · 2026Review
- Predicting interaction-specific protein-protein interaction perturbations by missense variants with MutPred-PPI.bioRxiv : the preprint server for biology · 2026Article
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
Abstract
The BRCA1-PALB2-BRCA2 axis plays essential roles in the cellular response to DNA double-strand breaks (DSB), maintenance of genome integrity, and suppression of cancer development. Upon DNA damage, BRCA1 is recruited to DSBs, where it facilitates end resection and recruits PALB2 and its associated BRCA2 to load the central recombination enzyme RAD51 to initiate homologous recombination (HR) repair. In recent years, several BRCA1-independent mechanisms of PALB2 recruitment have also been reported. Collectively, these available data illustrate a series of hierarchical, context-dependent, and cooperating mechanisms of PALB2 recruitment that is critical for HR and therapy response either in the presence or absence of BRCA1. Here, we review these BRCA1-dependent and independent mechanisms and their importance in DSB repair, cancer development, and therapy. As BRCA1-mutant cancer cells regain HR function, for which PALB2 is generally required, and become resistant to targeted therapies, such as PARP inhibitors, targeting BRCA1-independent mechanisms of PALB2 recruitment represents a potential new avenue to improve treatment of BRCA1-mutant tumors.
Indexed as
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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.