ArticleCell reports2018
BRCA1 Mutation-Specific Responses to 53BP1 Loss-Induced Homologous Recombination and PARP Inhibitor Resistance.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 58 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
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- Pooled it
- Decoding PARP roles in breast cancer therapy resistance.Molecular biology reports · 2026Review
- Cryptic redundancy between PAR1b and PAR1a, two members of the PAR1 kinase family, in the survival of PAR1b-knockout mice.Scientific reports · 2026Article
- Article
- New twist on BRCA1-mediated DNA recombination repair and tumor suppression.Trends in cell biology · 2026Review
- RAD51 is chromatin enriched and targetable in BRCA1-deficient cells.Molecular cell · 2025Article
- PALB2 and 53BP1 govern post-resection homologous recombination DNA repair.Molecular cell · 2025Article
- Exploring the Ligandability of 53BP1 through Fragment-Based Approaches.ACS medicinal chemistry letters · 2025Article
- Characterization of TNG348: A Selective, Allosteric USP1 Inhibitor That Synergizes with PARP Inhibitors in Tumors with Homologous Recombination Deficiency.Molecular cancer therapeutics · 2025Article
- Targeting BRCA1-deficient PARP inhibitor-resistant cells with nickases reveals nick resection as a cancer vulnerability.Nature cancer · 2025Article
- Shieldin and CST co-orchestrate DNA polymerase-dependent tailed-end joining reactions independently of 53BP1-governed repair pathway choice.Nature structural & molecular biology · 2025Article
- STK39-mediated amplification of γ-H2A.X promotes homologous recombination and contributes to PARP inhibitor resistance.Nucleic acids research · 2024Article
- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).Nature communications · 2024Article
- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).bioRxiv : the preprint server for biology · 2024Article
- Nucleolytic processing of abasic sites underlies PARP inhibitor hypersensitivity in ALC1-deficient BRCA mutant cancer cells.Nature communications · 2024Article
- H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours.Nature communications · 2024Article
- Discovery of a small-molecule inhibitor that traps Polθ on DNA and synergizes with PARP inhibitors.Nature communications · 2024Article
- Unveiling the relationship between WWOX and BRCA1 in mammary tumorigenicity and in DNA repair pathway selection.Cell death discovery · 2024Article
- Protein-folding chaperones predict structure-function relationships and cancer risk in BRCA1 mutation carriers.Cell reports · 2024Article
- BRCA1/2 alterations and reversion mutations in the area of PARP inhibitors in high grade ovarian cancer: state of the art and forthcoming challenges.Frontiers in oncology · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
20 authors at 3 institutions in 1 country.
Funding
Abstract
BRCA1 functions in homologous recombination (HR) both up- and downstream of DNA end resection. However, in cells with 53BP1 gene knockout (KO), BRCA1 is dispensable for the initiation of resection, but whether BRCA1 activity is entirely redundant after end resection is unclear. Here, we found that 53bp1 KO rescued the embryonic viability of a Brca1
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.