ArticleHeliyon2018
Competitive evolution of NSCLC tumor clones and the drug resistance mechanism of first-generation EGFR-TKIs in Chinese NSCLC patients.
Article in Heliyon, 2018. 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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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.
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Who cites it
11 citing papers in PubMed, 41 citations in OpenAlex.
- Osimertinib Versus Comparator EGFR TKI as First-Line Treatment for EGFR-Mutated Advanced NSCLC: FLAURA China, A Randomized Study.Targeted oncology · 2021Trial
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- Network Pharmacology Approach and Experimental Verification to Explore the Anti-NSCLC Mechanism of Grifolic Acid.International journal of molecular sciences · 2025Article
- STAT3-specific nanocarrier for shRNA/drug dual delivery and tumor synergistic therapy.Bioactive materials · 2024Article
- Can Liquid Biopsy Based on ctDNA/cfDNA Replace Tissue Biopsy for the Precision Treatment of EGFR-Mutated NSCLC?Journal of clinical medicine · 2023Review
- Applications of Liquid Biopsies in Non-Small-Cell Lung Cancer.Diagnostics (Basel, Switzerland) · 2022Review
- Prevalence of targeted therapy-related genetic variations in NSCLC and their relationship with clinicopathological characteristics.PloS one · 2022Article
- Discovery of a novel third-generation EGFR inhibitor and identification of a potential combination strategy to overcome resistance.Molecular cancer · 2020Article
- Review
- A novel virtual barcode strategy for accurate panel-wide variant calling in circulating tumor DNA.BMC bioinformatics · 2020Article
- Integration of Random Forest Classifiers and Deep Convolutional Neural Networks for Classification and Biomolecular Modeling of Cancer Driver Mutations.Frontiers in molecular biosciences · 2019Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAlthough many studies have reported on the resistance mechanism of first-generation EGFR TKIs (1 EXPERIMENTAL
designA prospective study was conducted in patients with advanced NSCLC with acquired resistance to erlotinib, gefitinib or icotinib. By liquid biopsy, we detected mutations in 124 tumor-associated genes in the context of drug resistance. These 124 genes covered all tumor therapeutic targets and related biological pathways. During the entire course of treatment, the interval between two liquid biopsies was two months.
resultsUnlike the common mutations tested in tissue samples, our data showed a higher coverage of tumor heterogeneity (32.65%), more complex patterns of resistance and some new resistance mutation sites, such as EGFR p.V769M and KRAS p.A11V. The major resistance-associated mutations detected were still EGFR p.T790M (45.28%), other point mutations in
conclusionsThe constitution and competitive evolution of the tumor clones have a decisive influence on treatment and can be regulated by targeted drugs and chemotherapy. Additionally, EGFR p.T790M spatial and temporal diversity during treatment warrants more attention, and this spatial and temporal diversity may be useful for the choice of treatment strategies for certain NSCLC patients. Through longitudinal cfDNA sample analysis, the resistance mechanism and dynamic clinical features of Chinese NSCLC patients are systematically established as reliable and meaningful to understand acquired resistance and make further personalized treatment decisions dynamically. Two new potential drug resistance-associated mutations in
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