ArticlePloS one2020
Influence of EGFR-activating mutations on sensitivity to tyrosine kinase inhibitors in a KRAS mutant non-small cell lung cancer cell line.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Article
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- A competing TMPO-AS1-let-7b-5p-kinesin superfamily RNA network predicts poor lung cancer patient survival.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2026Article
- Pulmonary Adenocarcinoma In Situ and Minimally Invasive Adenocarcinomas in European Patients Have LessInternational journal of molecular sciences · 2024Article
- Modern therapies of nonsmall cell lung cancer.Journal of applied genetics · 2023Review
- Pathologic complete response to neoadjuvant imatinib of a gastric stromal tumor with concomitant mutations inClinical case reports · 2023Article
- Identification of the effects of COVID-19 on patients with pulmonary fibrosis and lung cancer: a bioinformatics analysis and literature review.Scientific reports · 2022Review
- CRISPR and KRAS: a match yet to be made.Journal of biomedical science · 2021Review
- LncRNA SOX2-OT regulates AKT/ERK and SOX2/GLI-1 expression, hinders therapy, and worsens clinical prognosis in malignant lung diseases.Molecular oncology · 2021Article
- Mutation Spectrum ofPathology oncology research : POR · 2021Article
- Status of 10 targeted genes of non-small cell lung cancer in eastern China: A study of 884 patients based on NGS in a single institution.Thoracic cancer · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In non-small cell lung cancer (NSCLC), oncogenic driver mutations including those in KRAS and EGFR are typically mutually exclusive. However, recent reports indicate that multiple driver mutations are found in a certain percentage of cancers, and that the therapeutic responses of such cases with co-mutations of driver genes are largely unclear. Here, using CRISPR-Cas9-mediated genome editing, we generated isogenic cell lines harboring one or two copies of an EGFR-activating mutation from the human NSCLC cell line A549, which is known to harbor a homozygous KRAS gene mutation. In comparison with parent cells with KRAS mutation alone, cells with concomitant EGFR mutation exhibited higher sensitivity to EGFR-tyrosine kinase inhibitors (TKIs) but not to conventional anti-cancer drugs. In particular, cells with two copies of EGFR mutation were markedly more sensitive to EGFR-TKIs compared with parent cells. Thus, the presence of concomitant EGFR mutation can affect the TKI response of KRAS-mutated cells, implying that EGFR-TKI may represent an effective treatment option against NSCLC with EGFR/KRAS co-mutation.
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