EGFR mutation occurred frequently in the female never smoke patients with NSCLC. KRAS mutation was more common in old patients. Negative MET protein expression could be used as a negative predictive marker of MET amplification. MET protein expression was an independent prognostic factor for NSCLC.

To explore the relationship between PD-L1 expression and gene mutations and survival. PD L1, ALK and MET protein expression were detected by immunohistochemistry, and EGFR gene mutation by RT-PCR in 209 cases of NSCLC. The correlations between PD-L1 expression and gene mutations, clinicopathological features and survival was analyzed. PD-L1 was expressed in 99/209 cases (47.4%) of NSCLC, including score 1 (≥ 1% to < 5%) 23 cases (11%), score 2 (≥ 5% to < 50%) 36 cases (17.2%), and score 3 (> 50%) 40 cases (19.1%). There were 89 cases (42.6%) of EGFR mutation, 12 (5.7%) of ALK and 90 (43.1%) of MET protein positive. PD-L1 positive expression occurred more frequently in men and non-adenocarcinoma, and was negatively correlated with EGFR mutation and histological differentiation of NSCLC. PD-L1 expression was concordant in primary and metastatic cancers. There was no any effect of PD-L1 expression on overall survival of patients with NSCLC. These results suggested that PD-L1 expression is not an independent risk factor for survival of patients with NSCLC. Because of mutual complementarities of PD-L1 expression and EGFR mutation in NSCLC, both should be simultaneously detected for the patients to achieve eligible treatments.

Triple negative breast carcinoma (TNBC) is a rapid progressive tumor and has a poor overall survival. Therefore, it is crucial to find out effective molecular targets and develop optimal therapeutic strategies for TNBC. In this study, immunohistochemical staining was used to detect expressions of programmed death-ligand 1 (PD-L1) and phosphatase and tensin homolog (PTEN) in 136 breast carcinomas including 50 TNBC. The effect of PTEN on regulation of PD-L1 expression was assessed in vitro in the PTEN knockdown TNBC cells. We found that PD-L1(SP142) positive rate in TNBC (48.0%) was significantly higher than non-TNBC (23.3%). PTEN negative rate was 42% in TNBC. The inverse correlation between PTEN and PD-L1(SP142) expression in TNBC was statistically significant (P<0.05). After PTEN knockdown, PD-L1 expression in TNBC cells increased significantly, and the expression level of AKT increased simultaneously. PTEN knockdown promoted cell proliferation, viability and G1/S switch of TNBC cells. These results suggested that PTEN may involve in regulation of PD-L1 expression, because PTEN loss can upregulate PD-L1 expression in TNBC. Antitumor immunity of PD-L1 could be enhanced in TNBC when targeting PTEN at the same time.