The correlation between programmed death-ligand 1 expression and driver gene mutations in NSCLC

// Haitao Yang 1, * , Huijuan Chen 1, * , Shuimei Luo 1 , Lina Li 1 , Sijing Zhou 1 , Ruifen Shen 1 , Heng Lin 1, 2 , Xianhe Xie 1 1 Department of Chemotherapy, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350005, China 2 Department of Oncology, Fuzhou Pulmonary Hospital, Fuzhou, Fujian 350008, China * These authors are contributed equally to this work Correspondence to: Xianhe Xie, email: xiexianhe@yahoo.com Keywords: PD-L1, EGFR, ALK, KRAS, NSCLC Received: November 15, 2016      Accepted: February 13, 2017      Published: February 22, 2017 ABSTRACT Objectives: This study aimed to evaluate the correlation between positive PD-L1 expression and driver gene mutations in NSCLC and to seek preliminary evidence in favor of the strategy of PD-L1 inhibitors plus targeted agents. Results: The overall analyses revealed that positive PD-L1 expression had a significant relationship with KRAS status (RR = 1.26; 95% CI, 1.06−1.50, P = 0.010), but no correlation with clinical characteristics (gender, smoking status, histological types), driver gene status (EGFR, ALK) and overall survival (OS): male versus female (RR = 1.16; 95% CI, 0.95−1.42; P = 0.15), never smoking versus former/current smoking (RR = 0.79; 95% CI, 0.56−1.11; P = 0.17), adenocarcinoma versus non-adenocarcinoma (RR = 0.94; 95% CI, 0.63−1.41; P = 0.77), EGFR mutation versus EGFR wild type (RR = 0.74; 95% CI, 0.52−1.06; P = 0.10), ALK positive versus ALK negative (RR = 1.02; 95% CI, 0.75−1.38; P = 0.91), OS of positive PD-L1 expression versus that of negative PD-L1 expression (HR = 1.31, 95% CI, 0.90−1.90; P = 0.15), respectively. Noteworthily, subgroup analyses exhibited that in Chinese cohort studies, positive PD-L1 expression was significantly correlated with OS (HR = 1.75, 95% CI, 1.36−2.24, P < 0.0001); and in the studies using PD-L1 monoclonal antibodies (McAbs), positive PD-L1 expression was significantly correlated with KRAS mutation (RR = 1.32, 95% CI, 1.06−1.65, P = 0.01) and EGFR mutation (RR = 0.51, 95% CI, 0.28−0.93, P = 0.03). Materials and Methods: After thoroughly searching PubMed, EMBASE and Cochrane Library databases, 11 relevant studies incorporating 3128 cases were identified. The pooled data were analyzed via Review manager 5.3 software. Conclusions: PD-L1 inhibitors probably was a potential promising option to manage advanced NSCLC harboring KRAS mutation.