ArticleTherapeutic advances in medical oncology2025
Potential biomarkers of primary resistance to first- and second-generation EGFR-TKIs in non-small-cell lung cancer: a real-world study.
Article in Therapeutic advances in medical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Advances in Computational Drug Repurposing, Driver Genes, and Therapeutics in Lung Adenocarcinoma.Biomolecules · 2025Review
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12 authors.
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Abstract
Background: Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) significantly improve the prognosis of EGFR-sensitive mutant non-small-cell lung cancer (NSCLC). However, the mechanisms underlying primary resistance to EGFR-TKIs remain unclear. Objective: This study aimed to explore the biomarkers associated with primary resistance to first- and second-generation EGFR-TKIs. Primary resistance to EGFR-TKIs was defined as disease progression within 90 days (3 months) of treatment in patients with EGFR-sensitive mutant adenocarcinoma without any evidence of objective response. Design: Retrospective, single-center study. Methods: This study retrospectively screened patients with NSCLC who received EGFR-TKIs at Hunan Cancer Hospital from January 2018 to December 2022. According to pre-determined clinical outcomes, we divided the patients into primary resistance and sensitivity groups. Only patients with sufficient samples that passed quality control were included in this study. Tumor tissue and paired peripheral blood samples collected from patients before treatment were subjected to next-generation sequencing using an 825-gene panel. In addition, tumor tissue samples were analyzed for programmed cell death ligand 1 (PD-L1) expression. Results: A total of 70 patients were enrolled in this study, with 35 in each of the primary resistant and sensitive groups. Patients with exon 4 mutations in the Conclusion: The potential mechanisms of primary resistance to EGFR-TKIs are highly heterogeneous. Combining some somatic variants affecting tumor function and high PD-L1 expression may contribute to this resistance.
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