Evidence map›Paper›PMID 28575452›Full record

ArticleNucleic acids research2017

Selective disruption of an oncogenic mutant allele by CRISPR/Cas9 induces efficient tumor regression.

Taeyoung Koo, A-Rum Yoon, Hee-Yeon Cho, Sangsu Bae, Chae-Ok Yun, Jin-Soo Kim

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 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 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
4.4field-weighted citation impact, top 5% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

81 citing papers in PubMed, 124 citations in OpenAlex.

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  7. The Role of CRISPR and Its Therapeutic Applications in Glioblastoma.International journal of molecular sciences · 2026
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  9. Designing nucleic acid-based therapeutics for cancer treatment: Updates on the state of the art.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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21 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Taeyoung KooCenter for Genome Engineering, Institute for Basic Science (IBS), Seoul 08826, Korea.
A-Rum YoonDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul 04763, Korea.
Hee-Yeon ChoCenter for Genome Engineering, Institute for Basic Science (IBS), Seoul 08826, Korea.
Sangsu BaeDepartment of Chemistry, Hanyang University, Seoul 04763, Korea.
Chae-Ok YunDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul 04763, Korea.
Jin-Soo KimCenter for Genome Engineering, Institute for Basic Science (IBS), Seoul 08826, Korea.
Hanyang University · KRKorea University of Science and Technology · KRInstitute for Basic Science · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Approximately 15% of non-small cell lung cancer cases are associated with a mutation in the epidermal growth factor receptor (EGFR) gene, which plays a critical role in tumor progression. With the goal of treating mutated EGFR-mediated lung cancer, we demonstrate the use of clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR associated protein 9 (Cas9) system to discriminate between the oncogenic mutant and wild-type EGFR alleles and eliminate the carcinogenic mutant EGFR allele with high accuracy. We targeted an EGFR oncogene harboring a single-nucleotide missense mutation (CTG > CGG) that generates a protospacer-adjacent motif sequence recognized by the CRISPR/Cas9 derived from Streptococcus pyogenes. Co-delivery of Cas9 and an EGFR mutation-specific single-guide RNA via adenovirus resulted in precise disruption at the oncogenic mutation site with high specificity. Furthermore, this CRISPR/Cas9-mediated mutant allele disruption led to significantly enhanced cancer cell killing and reduced tumor size in a xenograft mouse model of human lung cancer. Taken together, these results indicate that targeting an oncogenic mutation using CRISPR/Cas9 offers a powerful surgical strategy to disrupt oncogenic mutations to treat cancers; similar strategies could be used to treat other mutation-associated diseases.

Indexed as

Genes, erbB-1Mutation, MissenseA549 CellsAllelesAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCRISPR-Cas SystemsErbB ReceptorsGene TargetingHumansLung NeoplasmsMaleMiceMice, NudeOncogenesEGFR protein, humanErbB Receptors

Identifiers

PMID28575452
PMCPMC5570104
OpenAlexW2618393503

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.