Objective:To investigate the driver gene mutation status and prognostic influencing factors in patients with operable lung adenosquamous carcinoma (LASC).Methods:A retrospective case series study was conducted. Clinical and pathologic data were retrospectively collected from patients with LASC who underwent surgical treatment at the Second Affiliated Hospital of Air Force Military Medical University from January 2008 to December 2018, and the patients' surgically resected specimens were sequenced for epidermal growth factor receptor (EGFR) and Kirsten rat sarcoma (KRAS) genes. The distribution of driver gene EGFR and KRAS mutations in patients was analyzed, and the differences in the distribution of mutations among patients stratified by clinical factors were compared; disease-free survival (DFS) of patients stratified by clinical factors was analyzed by the Kaplan-Meier method, and the comparison between groups was performed by the log-rank test.Results:A total of 106 patients were included, including 64 (60.4%) males and 42 (39.6%) females, aged (58±10) years old. Patients with EGFR and KRAS gene mutations accounted for 38.7% (41/106), of which 33.0% (35/106) were patients with EGFR mutations and 5.7% (6/106) were patients with KRAS mutations. The EGFR mutation loci included 19del, L858R, L861Q and 20in, and the KRAS mutation loci included G12A, G12D, G12C and G12V. Patients aged ≤65 years old, female, with lesions in the lower lobe of the left lung, non-squamous cell carcinoma as the main pathological component, and with a smoking index of <400 were more likely to have EGFR and KRAS gene mutations, but the differences were not statistically significant (all P>0.05), and there was no statistically significant difference in the proportions of patients with EGFR and KRAS gene mutations among patients with different TNM stages, T stages and N stages (all P > 0.05). The median follow-up time was 51 months (range: 14-96 months). The difference in DFS among patients with different N stages was statistically significant ( P= 0.002), and the DFS of N 0 stage was better than that of N 1, N 2 and N 3 stages, and the differences were statistically significant (all P < 0.05). The median DFS time of N 0, N 1 and N 2 stages was 44.4, 17.5 and 23.9 months, respectively, and the median DFS time of N 3 stage (1 case) was 8.7 months. Patients with different TNM stages had a tendency to have differences in DFS, but the difference was not statistically significant ( P = 0.060); the difference in DFS between patients with different pathological components was not statistically significant ( P = 0.177); patients without pleural invasion had a tendency to have better DFS than patients with pleural invasion, but the difference was not statistically significant ( P = 0.252). The difference in DFS between patients with and without driver gene EGFR and KRAS mutations was not statistically significant ( P = 0.809), and further subgroup analysis showed that the difference in DFS among mutated patients with different TNM stages was not statistically significant ( P = 0.684). Conclusions:The driver gene EGFR and KRAS mutations are more common in patients with early LASC; DFS may be related to TNM stage and N stage, but may not be related to the mutation status of EGFR and KRAS genes, the type of pathology, or whether or not the pleura is invaded.Objective To investigate the driver gene mutation status and prognostic influencing factors in patients with operable lung adenosquamous carcinoma (LASC). Methods A retrospective case series study was conducted. Clinical and pathologic data were retrospectively collected from patients with LASC who underwent surgical treatment at the Second Affiliated Hospital of Air Force Military Medical University from January 2008 to December 2018, and the patients' surgically resected specimens were sequenced for epidermal growth factor receptor (EGFR) and Kirsten rat sarcoma (KRAS) genes. The distribution of driver gene EGFR and KRAS mutations in patients was analyzed, and the differences in the distribution of mutations among patients stratified by clinical factors were compared; disease-free survival (DFS) of patients stratified by clinical factors was analyzed by the Kaplan-Meier method, and the comparison between groups was performed by the log-rank test. Results A total of 106 patients were included, including 64 (60.4%) males and 42 (39.6%) females, aged (58±10) years old. Patients with EGFR and KRAS gene mutations accounted for 38.7% (41/106), of which 33.0% (35/106) were patients with EGFR mutations and 5.7% (6/106) were patients with KRAS mutations. The EGFR mutation loci included 19del, L858R, L861Q and 20in, and the KRAS mutation loci included G12A, G12D, G12C and G12V. Patients aged ≤65 years old, female, with lesions in the lower lobe of the left lung, non-squamous cell carcinoma as the main pathological component, and with a smoking index of <400 were more likely to have EGFR and KRAS gene mutations, but the differences were not statistically significant (all P>0.05), and there was no statistically significant difference in the proportions of patients with EGFR and KRAS gene mutations among patients with different TNM stages, T stages and N stages (all P > 0.05). The median follow-up time was 51 months (range: 14-96 months). The difference in DFS among patients with different N stages was statistically significant ( P= 0.002), and the DFS of N 0 stage was better than that of N 1, N 2 and N 3 stages, and the differences were statistically significant (all P < 0.05). The median DFS time of N 0, N 1 and N 2 stages was 44.4, 17.5 and 23.9 months, respectively, and the median DFS time of N 3 stage (1 case) was 8.7 months. Patients with different TNM stages had a tendency to have differences in DFS, but the difference was not statistically significant ( P = 0.060); the difference in DFS between patients with different pathological components was not statistically significant ( P = 0.177); patients without pleural invasion had a tendency to have better DFS than patients with pleural invasion, but the difference was not statistically significant ( P = 0.252). The difference in DFS between patients with and without driver gene EGFR and KRAS mutations was not statistically significant ( P = 0.809), and further subgroup analysis showed that the difference in DFS among mutated patients with different TNM stages was not statistically significant ( P = 0.684). Conclusions The driver gene EGFR and KRAS mutations are more common in patients with early LASC; DFS may be related to TNM stage and N stage, but may not be related to the mutation status of EGFR and KRAS genes, the type of pathology, or whether or not the pleura is invaded.

Objective    To investigate the expression and biological function of centromere protein F (CENPF) in non-small cell lung cancer (NSCLC) and the association with prognosis. Methods    Through retrieving and analyzing the bioinformatics data such as Oncomine database, Human Protein Atlas (HPA), Kaplan-Meier Plotter, STRING and DAVID database, the expression of CENPF in both normal tissues and cancer tissues of lung cancer patients was identified, and the protein interaction network analysis, functional annotation and pathway analysis of CENPF with its associated genes were carried out. Results    CENPF was overexpressed in lung adenocarcinoma tissues, but not in normal tissues. The median overall survival (OS) of NSCLC patients with low expression of CENPF was significantly longer than that of patients with high expression of CENPF. Further sub-analysis showed that low expression group from lung adenocarcinoma patients had longer median disease-free survival and OS compared with high expression group patients. CENPF and its associated hub genes mainly affected the protein K11-linked ubiquitination in biological process, anaphase-promoting complex (APC) in cell composition, ATP binding in molecular function, and cell cycle in KEGG pathway. Conclusion    CENPF is regulated in tumorigenesis and progression of NSCLC, and its protein expression level has the value of early diagnosis and prognosis evaluation in lung adenocarcinoma. It is suggested that CENPF gene can be a potential target for molecular targeted therapy of NSCLC.