Abstract
BACKGROUND: It has been proven that epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), and KRAS are common driver genes in non-small cell lung cancer (NSCLC). Molecular targeted therapy increases the overall response rate and progression-free survival (PFS) of patients with EGFR-sensitive mutation or echinoderm microtubule-associated protein like 4-anaplastic lymphoma kinase (EML4-ALK) fusion. However, target and targeted drugs for lung squamous cell carcinoma to indicate clinical therapy remain to be confirmed. The aim of this study was to analyze the relationship between the status of driver genes and the clinicopathologic characteristics of NSCLC. METHODS: A total of 90 patients were recruited and tested for EGFR, ALK and KRAS mutations. The status of EGFR and KRAS was tested by amplification refractory mutation system, and the status of ALK was tested by fluorescence in situ hybridization. RESULTS: Of the 90 patients, 8 patients had EGFR mutation (8.8%), and 2 cases had KRAS mutation (2.2%). EML4-ALK fusion was found in 1 of 18 patients (5.6%). EGFR mutation occurred more frequently in females than in males (P=0.022). Significant differences were observed in pathological stage (P=0.042) and differentiation grade (P=0.003). No significant difference in PFS was observed between EGFR-TKI treatment and chemotherapy in EGFR mutation patients with squamous cell carcinoma of the lung (P=0.607). Patients with EML4-ALK fusion could benefit from targeted therapy. CONCLUSIONS: EML4-ALK fusion occurred more frequently than EGFR and KRAS mutations in patients with lung squamous cell carcinoma. Clinicopathologic characteristics were different between EGFR mutation and EGFR wild-type patients. The relationship between molecular targeted therapy and status of EGFR or ALK genes in patients with lung squamous cell carcinoma needs further investigation.