Inhibition of the PD-1/PD-L1 pathway may induce anticancer immune responses in non-small cell lung cancer (NSCLC). Here, we analyzed the correlation between PD-L1 expression and clinicopathological characteristics, stromal tumor-infiltrating lymphocyts (sTILs), pulmonary major driver gene alteration in NSCLC.
PD-L1 expression characterizations by immunohistochemistry using the clone 22C3 antibody were performed on 1156 NSCLC (329 archived and 827 recently acquired tumor) and 198 small biopsy.
PD-L1 high expression was observed in 9.7%, 6.5%, and 27.4% in recently acquired NSCLC, adenocarcinoma (ADC), and squamous cell carcinoma (SqCC) cohort, respectively, which showed higher than in archive cohorts previously reported in our group (4.9%, 0.5%, and 13.9% in NSCLC, ADC, and SqCC, respectively). In subgroup analysis, PD-L1 high expression was significantly associated with male sex (p = 0.002), larger tumor size (p < 0.001), pleural invasion (p = 0.001), venous and lymphatic invasion (p < 0.001), smoking history (p < 0.001), solid predominant histology (p < 0.001), and advanced pathological stage (p < 0.001) in ADC cohort. It tended to be more common in poorer differentiation (p = 0.011) and absence pleural invasion (p = 0.001) in SqCC. In the small biopsy specimens, PD-L1 high expression was found in 29.3% cases in NSCLC. PD-L1 high expression was significantly associated with high sTILs (p = 0.029). Both PD-L1 high and low expressions were more frequent in EGFR-wild type than in mutated type (p < 0.001).
PD-L1 high expression was significantly associated with poor differentiation and ≥50% sTILs. It was more frequently observed in EGFR-wild tumors. The prevalence of PD-L1 expression in recently acquired sample was higher than in archived sample, which suggests that PD-L1 expression should be evaluated as soon as possible after operation, otherwise will be reduced.
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