There is ongoing debate about the optimal choice of TKI for the rare EGFR mutations, but earlier reports indicate that these mutations may respond more favorably to second-generation TKIs compared to first-generation. This report underscores the significance of thorough molecular profiling in NSCLC.
P2, N=35, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2027
29 days ago
Trial completion date • Trial primary completion date
In participants with atypical EGFR-mutated advanced NSCLC, amivantamab-lazertinib demonstrated clinically meaningful antitumor activity with no new safety signals.
This study represents the largest cohort of NSCLC patients with EGFR G719X + S768I co-mutations treated with first-line afatinib. Our findings confirmed the effectiveness and safety of afatinib in this patient population. Furthermore, the presence of the G719X + S768I co-mutations serves as an independent predictor of favorable PFS for NSCLC patients. This study will provide new clinical evidence supporting afatinib therapy for patients with EGFR G719X + S768I co-mutations, both in China and globally. This study fills an important gap in the existing literature by providing robust, large-scale clinical data, offering new insights for the treatment of NSCLC patients with these uncommon mutations.
Furthermore, patients with EGFR-mutant lung adenocarcinoma undergoing treatment with EGFR tyrosine kinase inhibitors exhibited a significantly extended survival rate compared with those with wild-type EGFR receiving chemotherapy. In conclusion, the present study demonstrated that immunohistochemistry with pleural effusion cell blocks can aid in clarifying the histological subtype of lung cancer, and enable EGFR mutation detection, which can effectively guide molecular targeted therapy.
First-line osimertinib may provide real-world clinical benefits for patients with advanced NSCLC with atypical EGFR mutations, with results suggesting greater benefit in those harboring compound EGFR mutations.
RICTOR mutations in lung adenocarcinoma define a molecularly distinct subgroup characterized by preferential co-occurrence with EGFR, KRAS, and TP53, as well as a broader spectrum of genomic alterations. These findings support the view that RICTOR functions within complex oncogenic contexts and warrant further investigation in larger, multi-institutional cohorts.