Abstract

BackgroundAs we all know, patients with sensitive genes mutation could achieve better overall survival by taking targeted drugs. Many trials showed that non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EFGR) mutation responded to PD-1/PD-L1 inhibitors worse than EGFR wild-type. And subgroups of trials also reported the efficacy of PD-1/PD-L1 inhibitors in the treatment of NSCLC patients with other sensitive genes mutation. So we conducted a complementary systematic review and meta-analysis to compare efficacy of PD-1/PD-L1 inhibitors for NSCLC patients with sensitive genes mutation. MethodsPubMed, EMBASE, Web of Science and the Cochrane Central Register of Controlled Trials (Central) databases were searched for all clinical trials in NSCLC until 5th of January 2019. Eligible studies included randomized controlled trials (RCTs) comparing PD-1/PD-L1 inhibitors with chemotherapy in NSCLC patients with sensitive genes mutation. The hazard ratio (HR) and 95% confidence intervals (CIs) of overall survival (OS) or progression-free survival (PFS) were used. ResultsA total of 2419 patients from 4 RCTs (2 with PD-1 inhibitors; 2 with PD-L1 inhibitors) were included. PD-1/PD-L1 inhibitors significantly prolonged the OS (HR, 0.67; 95% CI, 0.60–0.67) and PFS (HR, 0.46; 95% CI, 0.36–0.60) in NSCLC patients with EGFR wild-type versus chemotherapy. Meanwhile, PD-1/PD-L1 inhibitors prolonged the OS (HR, 0.61; 95% CI, 0.39–0.94) in NSCLC patients with KRAS mutation versus chemotherapy. However, for NSCLC patients with EGFR mutation (the OS of HR, 1.11; 95% CI, 0.80–1.55; the PFS of HR, 0.76; 95% CI, 0.35–1.64) and KRAS wild-type (the OS of HR, 0.89; 95% CI, 0.68–1.17), there were no significant differences between PD-1/PD-L1 inhibitors and chemotherapy. ConclusionsPD-1/PD-L1 inhibitors are more efficacious in NSCLC patients with EGFR wild-type and KRAS mutation compared with chemotherapy. There was no significant difference between PD-1/PD-L1 inhibitors and chemotherapy in NSCLC patients with EGFR mutation and KRAS wild-type. Legal entity responsible for the studyThe authors. FundingNational Natural Science Foundation of China (No. 81873396). DisclosureAll authors have declared no conflicts of interest.

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