Retrospective real-world associations between EGFR alterations and furmonertinib outcomes in advanced non-small cell lung cancer
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Published on: June 26, 2019
Yameng Cui1, Shaozhang Zhou2, Zheng Liu3
1Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Background:
Furmonertinib, a third-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI), has shown promising efficacy in EGFR-mutant non-small cell lung cancer (NSCLC). This real-world study aimed to explore efficacy differences among EGFR mutation subtypes and the influence of concomitant genetic alterations on furmonertinib.
Methods:
This retrospective multicenter real-world study enrolled patients with unresectable stage IIIB/C-IV EGFR-mutant NSCLC who received furmonertinib (80 milligrams per day). Main eligibility criteria included advanced EGFR-mutant NSCLC, measurable lesions, and available next-generation sequencing (NGS) molecular data. Patients were recruited from five Chinese medical centers. Progression-free survival (PFS) was defined as time from furmonertinib initiation to disease progression or any-cause death; overall survival (OS) was defined as time from furmonertinib initiation to any-cause death or last follow-up. Baseline clinical and NGS-detected molecular data were collected. Survival endpoints included objective response rate (ORR), disease control rates (DCRs), PFS and OS. Kaplan-Meier and Cox proportional-hazards models were applied to evaluate prognostic associations, reporting hazard ratios (HR) with 95% confidence intervals (CIs) alongside exact P values.
Results:
A total of 139 patients were included, among whom 64 harbored EGFR exon 19 deletion and 74 harbored L858R mutation. TP53 mutations were detected in 64.4% (58/90) of the tested patients. There were 136 patients profiled for additional concurrent driver alterations. Among 131 evaluable patients, ORR was 69.5% and the DCR was 97.7%. Median PFS of the entire cohort was 623 days (approximately 20.8 months); median OS was not reached. Compared with L858R, EGFR exon19 deletion was associated with longer PFS (adjusted HR =1.77, 95% CI: 1.09-2.87, P=0.02). After adjusting for age, disease stage, and EGFR mutation subtype, multiple gene mutations were associated with poorer PFS (HR =4.03, 95% CI: 1.98-8.19, P<0.001) and OS (HR =3.25, 95% CI: 1.07-9.86, P=0.04). No significant prognostic association was observed for TP53 co-mutation.
Conclusions:
This retrospective real-world cohort suggests that EGFR subtypes and multiple concurrent genomic alterations are associated with survival outcomes under furmonertinib treatment.
