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Background: Human epidermal growth factor receptor (HER)-2 is a driver gene in non-small cell lung cancer (NSCLC). The present study evaluated the mutation rate of HER-2 within the wild-type epidermal growth factor receptor (EGFR) lung adenocarcinoma population in China. Methods: Formalin-fixed, paraffin-embedded samples from 456 patients with wild-type EGFR lung adenocarcinoma were analyzed for HER-2 mutations by amplification-refractory mutation system (ARMS), and HER-2 protein expression was evaluated by immunohistochemistry. All samples positive for HER-2 mutation underwent direct sequencing for further verification. Results: HER-2 mutation was detected in 22/456 cases (4.8 %); the rate was 6.7 % among 331 triple-negative samples (i.e., wild-type EGFR, anaplastic lymphoma kinase, and ROS proto-oncogene 1). Direct sequencing confirmed that the results were consistent with those obtained by ARMS analysis in 19 cases. The positive rate was 15.4 % by immunohistochemical analysis of HER-2 expression; this was not correlated with mutation rate. HER-2 mutation and positivity were not correlated with gender, age, smoking status, disease stage, or histological subtype. The 22 cases of HER-2 mutations occurred only in acinar (36.4 %), papillary (36.4 %), minimally invasive (13.6 %), solid (9.2 %), and invasive mucinous (4.5 %) subtypes. Disease-free and overall survival were not associated with HER-2 mutation or HER-2 protein overexpression. Conclusion: The HER-2 mutation rate was 4.8 % among EGFR wild-type lung adenocarcinoma patients in China, and 6.7 % among driver genes, triple-negative lung adenocarcinoma. The incidence of HER-2 mutation varied among different lung adenocarcinoma subtypes, occurring mainly in acinar and papillary predominant subtypes. 15.4 % of EGFR wild-type lung adenocarcinoma patients showed HER-2 protein overexpression, but this was not correlated to HER-2 mutation. Existing follow-up data did not show a correlation between HER-2 mutation with DFS or OS. [ABSTRACT FROM AUTHOR]

Background Recent studies showed that stimulation of HDACs could induce PD-1 dynamic expression on DCs, macrophages, colonic stromal cells, and cancer cells. Surprisingly, it is little is known about the specific expression of important HDAC10 in NSCLC tissue. In this study, we evaluated the expression level of HDAC10 and the correlation of HDAC10 and PD-L1 in NSCLC tissues and analyzed the predicting role of HDAC10 in cancer cells on postoperative survival in NSCLC patients receiving pulmonary lobectomy. Methods A total of 180 NSCLC patients receiving complete pulmonary resection and systematic lymph node dissection between April 2004 and August 2009 were enrolled. All the patients had integrated clinicopathological records and follow-up data. HDAC10 and PD-L1 expression on NSCLC samples were determined by using immunohistochemistry. Results Our results showed that HDAC10 expression level in cancer tissue was significantly higher than that in para-cancer tissue. HDAC10 expression level was also positively correlated with the PD-L1 expression level (r = 0.213, P < 0.05). Multivariate analysis showed that expression level of HDAC10 was an independent prognostic factor and HDAC10 overexpression indicated a poor overall survival in pulmonary carcinoma (r = 0.540, P < 0.001). Conclusions To our knowledge, this is the first time to associate HDAC10 with lung cancer patients' survival status and to explore correlation between HDAC10 and PD-L1 expression. Our findings indicated that HDAC10 could be a valuable predicting marker that might provide help for clinicians to design effective therapeutic modality against NSCLC. Treatment response might be especially prominent in patients overexpressing HDAC10 in cancer cells. Our study suggest clinical relevance for the immune effects of HDAC10 and provide a rationale for the clinical evaluation of PD-L1 blockade in combination with HDAC10 inhibition. Legal entity responsible for the study  The First Affiliated Hospital of Jinzhou Medical University. Funding This study was supported by the CSCO-HANSOH PHARMA Science Foundation of China (number Y-HS2019-29). Disclosure The author has declared no conflicts of interest. [ABSTRACT FROM AUTHOR]