ArticleFrontiers in immunology2025
Dissecting the immune evasion and therapeutic resistance mechanisms in EGFR/TP53 co-mutated non-small cell lung cancer: implications for targeted and immunotherapy strategies.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Although precision-targeted therapies and tyrosine kinase inhibitors (TKIs) have significantly improved outcomes in non-small-cell lung cancer (NSCLC), patients with EGFR-mutant NSCLC with concurrent TP53 mutations often develop drug resistance and experience poor clinical outcomes. This study aims to investigate the molecular mechanisms underlying this aggressive subtype using single-cell RNA sequencing. Methods: Formalin-fixed paraffin-embedded (FFPE) tumor samples were obtained from 40 hospitalized NSCLC patients. Somatic mutation profiles were determined using a targeted 23-gene next-generation sequencing (NGS) panel. Four samples harboring concurrent EGFR and TP53 mutations were selected for single-cell transcriptomic profiling using the 10x Genomics platform. Results: Two dominant malignant epithelial cell populations were identified: C1_EGFR Conclusion: These findings reveal a coordinated transcriptional network that promotes immune evasion and therapeutic resistance in EGFR/TP53 co-mutated NSCLC. Targeting the STAT1/ETS1 axis, in combination with EGFR-TKIs or immune checkpoint inhibitors, may provide a novel strategy to overcome resistance and improve patient outcomes. Further validation in larger patient cohorts and functional studies is warranted to confirm these observations and support clinical translation.
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