ReviewTrends in cell biology2026
New twist on BRCA1-mediated DNA recombination repair and tumor suppression.
Review in Trends in cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- The BRCA1 coiled-coil domain is dispensable for suppression of tandem duplications and tolerance of FANCM loss.The EMBO journal · 2026Article
- DDX5 (p68) and UbE2T as emerging superior cancer therapeutic targets: dual molecular glue target degradation by FL118 for conquering difficult-to-treat cancers.Journal of experimental & clinical cancer research : CR · 2026Review
- Cancer metabolism in radiation sensitization - complementary roles of O-GlcNAc transferase and PARP1.Journal of cell science · 2026Article
- The mitochondrial translocation of phosphorylated EZH2 promotes PARP inhibitor resistance in BRCA1-deficient epithelial ovarian cancer.Cell discovery · 2026Article
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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
Abstract
Ever since BRCA1 germline mutations were found to confer a strong predisposition to the development of breast and ovarian cancers, there has been great interest in determining how this protein suppresses tumor formation. Through more than two decades of research, it has become clear that BRCA1 safeguards our genome mainly by promoting DNA repair through homologous recombination (HR). This opinion article outlines our evolving view of BRCA1's role in end resection, an upstream commitment step for HR, and highlights recent discoveries suggesting that the context in which DNA breaks are generated dictates whether BRCA1 is required for end resection. In addition, strong emerging evidence for the tumor-suppressive function of BRCA1 being mediated predominantly by its indispensable role in supporting RAD51-dependent recombination downstream of end resection is discussed.
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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.