ArticleCommunications biology2019
Genome-scale CRISPR knockout screen identifies
Article in Communications biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 45 citations in OpenAlex.
- Genome-wide CRISPR-Cas9 screening identifies CLK1 inhibition as a strategy to restore PARP inhibitor sensitivity via ERCC1 isoform switching.Protein & cell · 2026Article
- HMBOX1 plays a critical role in plumbagin-induced growth inhibition of hepatocellular carcinoma cells.Scientific reports · 2025Article
- Revealing genetic drivers of ovarian cancer and chemoresistance: insights from whole-genome CRISPR-knockout library screens.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Methylstat sensitizes ovarian cancer cells to PARP-inhibition by targeting the histone demethylases JMJD1B/C.Cancer gene therapy · 2025Article
- In vivo Therapeutic Inhibition of the Tp53-Induced Glycolysis and Apoptosis Regulator (TIGAR) by Intravenous Administration of an Anti-Oncological siRNA-Biopolymer, TI6752 (Tituxistatin), in a Preclinical Xenograft Model of Colorectal Cancer.Journal of experimental pharmacology · 2025Article
- Critical Differential Expression Assessment for Individual Bulk RNA-Seq Projects.bioRxiv : the preprint server for biology · 2024Article
- Revolutionizing DNA repair research and cancer therapy with CRISPR-Cas screens.Nature reviews. Molecular cell biology · 2023Review
- Amplified therapeutic targets in high-grade serous ovarian carcinoma - a review of the literature with quantitative appraisal.Cancer gene therapy · 2023Review
- Genome-wide CRISPR/Cas9 screening for drug resistance in tumors.Frontiers in pharmacology · 2023Review
- The genomic landscape of sensitivity to arsenic trioxide uncovered by genome-wide CRISPR-Cas9 screening.Frontiers in oncology · 2023Article
- CRISPR screens guide the way for PARP and ATR inhibitor biomarker discovery.The FEBS journal · 2022Review
- A CRISPR Path to Finding Vulnerabilities and Solving Drug Resistance: Targeting the Diverse Cancer Landscape and Its Ecosystem.Advanced genetics (Hoboken, N.J.) · 2022Review
- Review
- CRISPR/Cas9‑induced saturated mutagenesis identifiesMolecular medicine reports · 2022Article
- Nuclear TIGAR mediates an epigenetic and metabolic autoregulatory loopActa pharmaceutica Sinica. B · 2022Article
- Evolution of Molecular Targeted Cancer Therapy: Mechanisms of Drug Resistance and Novel Opportunities Identified by CRISPR-Cas9 Screening.Frontiers in oncology · 2022Review
- 3D CRISPR screen in prostate cancer cells reveals PARP inhibitor sensitization through TBL1XR1-SMC3 interaction.Frontiers in oncology · 2022Article
- Structure, regulation, and biological functions of TIGAR and its role in diseases.Acta pharmacologica Sinica · 2021Review
- Effect of the p53 P72R Polymorphism on Mutant TP53 Allele Selection in Human Cancer.Journal of the National Cancer Institute · 2021Article
- Metabolic landscapes in sarcomas.Journal of hematology & oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Treatment of cancer with poly (ADP-ribose) polymerase (PARP) inhibitors is currently limited to cells defective in the homologous recombination (HR) pathway. Identification of genetic targets that induce or mimic HR deficiencies will extend the clinical utility of PARP inhibitors. Here we perform a CRISPR/Cas9-based genome-scale loss-of-function screen, using the sensitivity of PARP inhibitor olaparib as a surrogate. We identify
Indexed as
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.