The level of soluble programmed death ligand-1 in lung cancer: An exploratory biomarker study.

249 Background: A new approach to immunotherapy based on programmed death 1 (PD-1) and programmed death ligand-1 (PD-L1) pathway represents a remarkable innovation in lung cancer treatment. There is growing evidence that lung cancer cells exploit the PD-L1 to cause local immune-suppression. The aim of this prospective study was to investigate the prevalence and prognostic roles of soluble PD-L1 (sPD-L1) protein in the blood of patients with lung cancer.

METHODS: A total of 159 patients with lung cancer who were diagnosed by histopathology or cytopathology between July 2013 and October 2015 were enrolled. Blood samples plasma were collected at the time of diagnosis. 85 samples of healthy subjects matching in sex and age from the Health care Center of the hospital were also studied as control. The level of sPD-L1 protein in the blood was measured using an enzyme-linked immunosorbent assay (ELISA). 64 cases of patients with lung cancer who were treated with platinum based chemotherapy for 4-6 cycles were followed up. The median follow-up duration since the time of diagnosis was 18.6 months (range, 4-26.6 months). The associations between the level of sPD-L1 expression and clinicopathologic features and prognosis were statistically analyzed.

RESULTS: Expression of sPD-L1 in patients with lung cancer was significantly up-regulated compared with health people (P < 0.001). A cut-off value of 2.37ng/ml was distinguished in patients according to Receiver operating characteristic curve (ROC). The expression of sPD-L1 was associated with abdominal organ metastasis (P = 0.015). A high sPD-L1 expression had a worse prognosis than a low expression in patients (13.4 months vs 19.8 months, P = 0.001).

CONCLUSIONS: Our results indicated that plasma sPD-L1 protein was elevated in patients with lung cancer and was associated with a poor prognosis. Plasma sPD-L1 protein is a potent predicting biomarker in lung cancer and may play a pivotal role in tumor immune evasion.