Treatment data for patients having epidermal growth factor receptor (EGFR)-mutated non–small-cell lung cancer (NSCLC) handled with EGFR tyrosine kinase inhibitors vary greatly (EGFR-TKIs). The primary focus of the research was to identify genetic biomarkers that predict EGFR-TKI primary opposition in NSCLC patients. To use an upcoming sequencing panel, 168 cancer-related genes, plasma samples, and paired tumor biopsy from NSCLC patients were analyzed before diagnosis. Imaging examinations were performed on patients who were taking EGFR-TKIs. The relationship between co-alternative genes and progression-free survival (PFS) was investigated.

Further than the EGFR mutation, 46 (95.83%) of the 48 patients receiving EGFR-TKIs had to have at least one genetic co-variant. Multivariate analysis revealed that co-alterations in the PIK3CA, RB1,  and ERBB2 genes, instead of the number of co-alternative genes, have been autonomously linked to poor PFS. The best probability ratio χ2, Akaike information criterion, and Harrell concordance index were found when patients were grouped by particular gene condition.

The average PFS for sick people in team A (less genetic co-variations and wild genetic basis), team B (more genetic co-variations and wild specific genes), team C (less genetic co-variations and modified specific genes), and team D (more genetic co-variations and altered specific genes) have been 10.4, 9.13 (vs. team A; P = .3112), 6.33 (vs. team B; P = .0465), and 3.90 (vs. team C; P = .0309) months, respectively.

Patients with EGFR-mutated NSCLC had a significant rate of concurrent genetic changes. Specific gene variants were found to be more important than the number of changed genes in predicting poor PFS, which could help doctors identify patients who need new treatments.