ReviewCell cycle (Georgetown, Tex.)2015
Molding BRCA2 function through its interacting partners.
Review in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- The impact of pathogenicSAGE open medicine · 2024Article
- Identification of a large intra-exonic deletion inTherapeutic advances in medical oncology · 2023Article
- Assessing the Variations in Breast/Ovarian Cancer Risk for ChineseJournal of oncology · 2022Article
- Guardians of the Genome: BRCA2 and Its Partners.Genes · 2021Review
- BRCA2 binding through a cryptic repeated motif to HSF2BP oligomers does not impact meiotic recombination.Nature communications · 2021Article
- FEN1 Blockade for Platinum Chemo-Sensitization and Synthetic Lethality in Epithelial Ovarian Cancers.Cancers · 2021Article
- Attenuation of SRC Kinase Activity Augments PARP Inhibitor-mediated Synthetic Lethality inClinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- K3326X and Other C-Terminal BRCA2 Variants Implicated in Hereditary Cancer Syndromes: A Review.Cancers · 2021Review
- A new interaction between BRCA2 and DDX5 promotes the repair of DNA breaks at transcribed chromatin.Molecular & cellular oncology · 2021Article
- BRCA1/2 Variants and Metabolic Factors: Results From a Cohort of Italian Female Carriers.Cancers · 2020Article
- Calibration of Pathogenicity Due to Variant-Induced Leaky Splicing Defects by UsingCancer research · 2020Article
- Review
- Double Trouble: ConcomitantClinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Non-Coding Variants inCancers · 2018Review
- Interaction with PALB2 Is Essential for Maintenance of Genomic Integrity by BRCA2.PLoS genetics · 2016Article
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of the tumor suppressor BRCA2 has been shaped over 2 decades thanks to the discovery of its protein and nucleic acid partners, biochemical and structural studies of the protein, and the functional evaluation of germline variants identified in breast cancer patients. Yet, the pathogenic and functional effect of many germline mutations in BRCA2 remains undetermined, and the heterogeneity of BRCA2-associated tumors challenges the identification of causative variants that drive tumorigenesis. In this review, we propose an overview of the established and emerging interacting partners and functional pathways attributed to BRCA2, and we speculate on how variants altering these functions may contribute to cancer susceptibility.
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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.