ArticleScientific reports2017
CRISPR/Cas9-derived models of ovarian high grade serous carcinoma targeting Brca1, Pten and Nf1, and correlation with platinum sensitivity.
Article in Scientific reports, 2017. 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 64 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
64 citing papers in PubMed, 120 citations in OpenAlex.
- CDK12/13 inhibition overcomes platinum resistance by impairing RNA metabolism.Signal transduction and targeted therapy · 2026Article
- Article
- Phenotypic and genotypic characterization of single circulating tumor cells in the follow-up of high-grade serous ovarian cancer.Molecular oncology · 2026Article
- CRISPR technology in ovarian cancer research: advances from gene editing to precision diagnosis and therapy.Translational cancer research · 2026Review
- Models of high-grade serous carcinoma of tubo-ovarian origin.Oncology reviews · 2026Review
- EPI-SauriCas9-based mouse ovarian cancer models recapitulating pten deletion in patients.Communications biology · 2025Article
- RAS/PI3K pathway mutations sensitise epithelial ovarian cancer cells to a PARP/NAMPT inhibitor combination.Communications biology · 2025Article
- Immunocompetent C57BL/6 syngeneic mouse ovarian cancer models with defined genetic alterations.Scientific reports · 2025Article
- Specific Genetic Mutations Impact Chemotherapy Resistance and Therapeutic Efficacy of Oncolytic Viruses in Ovarian Cancer.Molecular cancer therapeutics · 2025Article
- Loss ofOncotarget · 2025Article
- Unmatched Cell Line Collections Are Not Optimal for Identification of PARP Inhibitor Response and Drug Synergies.Journal of cellular and molecular medicine · 2025Article
- Myeloid cell networks govern re-establishment of original immune landscapes in recurrent ovarian cancer.Cancer cell · 2025Article
- Autocrine interferon poisoning mediates ADAR1-dependent synthetic lethality in BRCA1/2-mutant cancers.Nature communications · 2025Article
- Murine cell lines with defined mutations model different histological subtypes of epithelial ovarian cancer.Disease models & mechanisms · 2025Article
- CXCL10-induced regulatory T cells and adenosine signaling promote immunosuppression and progression of epithelial ovarian cancer.Scientific reports · 2025Article
- Aggressive Serous Carcinomas of the Female Reproductive Tract: Cancer-Prone Cell States and Genetic Drivers.Cancers · 2025Review
- Therapeutic Targeting in Ovarian Cancer: Nano-Enhanced CRISPR/Cas9 Gene Editing and Drug Combination Therapy.International journal of nanomedicine · 2025Review
- Transglutaminase 2 regulates ovarian cancer metastasis by modulating the immune microenvironment.Frontiers in immunology · 2025Article
- Epigenetic editing ofEpigenetics · 2024Article
- PTEN Loss Shapes Macrophage Dynamics in High-Grade Serous Ovarian Carcinoma.Cancer research · 2024Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Transplantable murine models of ovarian high grade serous carcinoma (HGSC) remain an important research tool. We previously showed that ID8, a widely-used syngeneic model of ovarian cancer, lacked any of the frequent mutations in HGSC, and used CRISPR/Cas9 gene editing to generate derivatives with deletions in Trp53 and Brca2. Here we have used one ID8 Trp53
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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.