Genomic profiles reveal the mechanism of PD-L1-induced resistance to EGFR-TKIs in lung adenocarcinoma

Concurrent presence of PD-L1-positive and activating epidermal growth factor receptor (EGFR) mutations in advanced Non-Small Cell Lung Cancer (NSCLC) typically results in restricted effectiveness of EGFR-tyrosine kinase inhibitors (EGFR-TKIs), and the underlying mechanism remains unidentified. We enrolled 103 EGFR-mutant LUAD patients, evaluating PD-L1 expression and conducting Next-generation sequencing (NGS) for gene mutation analysis. This study elucidates the molecular mechanism of PD-L1-induced primary resistance to EGFR-TKI. Nevertheless, for patients with concurrent mutations in EGFR and PD-L1 expression, a first-line treatment strategy that combines EGFR-TKI with chemotherapy may provide a more potent alternative.