ArticleBMC genomics2016
Identification of oncogenic driver mutations by genome-wide CRISPR-Cas9 dropout screening.
Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- State of the art CRISPR-based strategies for cancer diagnostics and treatment.Biomarker research · 2024Review
- In silico RNA isoform screening to identify potential cancer driver exons with therapeutic applications.Nature communications · 2024Article
- Comprehensive review of CRISPR-based gene editing: mechanisms, challenges, and applications in cancer therapy.Molecular cancer · 2024Review
- TBK1 is paradoxical in tumor development: a focus on the pathway mediating IFN-I expression.Frontiers in immunology · 2024Review
- Advances in synthetic lethality modalities for glioblastoma multiforme.Open medicine (Warsaw, Poland) · 2024Review
- Article
- Evolution of Molecular Targeted Cancer Therapy: Mechanisms of Drug Resistance and Novel Opportunities Identified by CRISPR-Cas9 Screening.Frontiers in oncology · 2022Review
- CRISPR-Cas deployment in non-small cell lung cancer for target screening, validations, and discoveries.Cancer gene therapy · 2021Review
- Developing Drugs for Tissue-Agnostic Indications: A Paradigm Shift in Leveraging Cancer Biology for Precision Medicine.Clinical pharmacology and therapeutics · 2021Review
- VRK1 Depletion Facilitates the Synthetic Lethality of Temozolomide and Olaparib in Glioblastoma Cells.Frontiers in cell and developmental biology · 2021Article
- Untangling a complex web: Computational analyses of tumor molecular profiles to decode driver mechanisms.Journal of genetics and genomics = Yi chuan xue bao · 2020Review
- Olaparib and ionizing radiation trigger a cooperative DNA-damage repair response that is impaired by depletion of the VRK1 chromatin kinase.Journal of experimental & clinical cancer research : CR · 2019Article
- CX Chemokine Receptor 7 Contributes to Survival ofCancers · 2019Article
- CRISPR Technology for Breast Cancer: Diagnostics, Modeling, and Therapy.Advanced biosystems · 2018Article
- Explaining cancer type specific mutations with transcriptomic and epigenomic features in normal tissues.Scientific reports · 2018Article
- Implication of the VRK1 chromatin kinase in the signaling responses to DNA damage: a therapeutic target?Cellular and molecular life sciences : CMLS · 2018Review
- Correction of copy number induced false positives in CRISPR screens.PLoS computational biology · 2018Article
- The Atypical Kinase RIOK1 Promotes Tumor Growth and Invasive Behavior.EBioMedicine · 2017Article
- Creating a RAW264.7 CRISPR-Cas9 Genome Wide Library.Bio-protocol · 2017Article
- Functional interrogation of non-coding DNA through CRISPR genome editing.Methods (San Diego, Calif.) · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGenome-wide CRISPR-Cas9 dropout screens can identify genes whose knockout affects cell viability. Recent CRISPR screens detected thousands of essential genes required for cellular survival and key cellular processes; however discovering novel lineage-specific genetic dependencies from the many hits still remains a challenge.
resultsTo assess whether CRISPR-Cas9 dropout screens can help identify cancer dependencies, we screened two human cancer cell lines carrying known and distinct oncogenic mutations using a genome-wide sgRNA library. We found that the gRNA targeting the driver mutation EGFR was one of the highest-ranking candidates in the EGFR-mutant HCC-827 lung adenocarcinoma cell line. Likewise, sgRNAs for NRAS and MAP2K1 (MEK1), a downstream kinase of mutant NRAS, were identified among the top hits in the NRAS-mutant neuroblastoma cell line CHP-212. Depletion of these genes targeted by the sgRNAs strongly correlated with the sensitivity to specific kinase inhibitors of the EGFR or RAS pathway in cell viability assays. In addition, we describe other dependencies such as TBK1 in HCC-827 cells and TRIB2 in CHP-212 cells which merit further investigation.
conclusionsWe show that genome-wide CRISPR dropout screens are suitable for the identification of oncogenic drivers and other essential genes.
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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.