Introduction: The programmed cell death-ligand 1 (PD-L1) pathway plays an important role in maintaining immune homeostasis. PD-L1 pathway may also protect tumor from attack of cytotoxic T cells. The prognostic significance of PD-L1 expression in pulmonary squamous cell carcinoma has not been well demonstrated.

Methods: A total of 98 patients with resected pulmonary squamous cell carcinoma were included in the study. PD-L1 expression was determined by immunohistochemistry in tumor specimens. Relationship between PD-L1 expression and clinicopathological variables was investigated. The prognostic value of PD-L1 expression in overall survival (OS) and probability of freedom from recurrence [FFR] was also demonstrated in the study.

Results: PD-L1 expression was identified in 72 (73.5%) of the 98 lung tumor samples. PD-L1 expression was significantly associated with advanced stage (P = 0.045). PD-L1 expression (hazard ratio, 0.347; 95% confidence interval, 0.148 to 0.814; P = 0.015) was a significant prognostic factor for better OS in multivariate analysis. For patients with stage I/II lung squamous cell carcinoma, PD-L1 expression was a significant prognostic factor for better OS (HR, 0.299; 95% CI, 0.114 to 0.786; P = 0.014) and probability of FFR (HR, 0.346; 95% CI, 0.143 to 0.836; P = 0.025) in multivariate analysis.

Conclusions: PD-L1 expression was significantly associated with advanced stage in pulmonary squamous cell carcinoma. PD-L1 expression was a significant prognostic factor for better OS in patients with pulmonary squamous cell carcinoma, and also a significant prognostic factor for better probability of FFR in those with early-stage pulmonary squamous cell carcinoma.

Citation Format: Jung-Jyh Hung, Yu-Chung Wu, Wen-Hu Hsu. The prognostic significance of programmed cell death-ligand 1 expression in pulmonary squamous cell carcinoma [abstract]. In: Proceedings of the Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; 2016 Sept 25-28; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2016;4(11 Suppl):Abstract nr A145.