Zhen Zhang1, Shengyu Zhou2. 1. Department of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin's Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer Tianjin, China. 2. Department of Medical Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College Beijing, China.
Abstract
Objective: To detect the serum epithelial growth factor receptor (EGFR) gene mutation status in patients with lung cancer via second-generation sequencing and to analyze its correlations with the clinical features of patients and its therapeutic effects. Methods: A total of 110 patients with non-small cell lung cancer (NSCLC) treated in our hospital were recruited as subjects of our study. The distribution of the EGFR gene mutation in patients was detected via second-generation sequencing and then patients were divided into mutant-type EGFR group (n=37) and wild-type EGFR group (n=73). The clinical features and therapeutic effects were compared between the two groups of patients. Results: A total of 5 kinds of EGFR gene mutation [19del (45.95%), L858R (43.24%), L861Q (5.41%), S768I (2.70%), and G719X (2.70%)] were detected via second-generation sequencing. In the mutant-type EGFR group, the proportions of female patients, patients with adenocarcinoma, and those with no history of smoking were high, and the differences were statistically significant (P<0.05). Moreover, there were statistically significant differences in gender, type of cancer, tumor-node-metastasis (TNM) staging, and smoking history between the mutant-type EGFR group and the wild-type EGFR group (P<0.05). Results of a multivariate logistic regression analysis showed that the EGFR gene mutation status was significantly associated with the type of cancer, gender, TNM staging, and smoking history of patients with NSCLC (P<0.05). The clinical effective rate of patients in the mutant-type EGFR group was significantly higher than that in the wild-type EGFR group (54.05% vs. 19.18%) while progression-free survival (PFS) was significantly longer than that in the wild-type EGFR group [(9.75±1.64) months vs. (5.51±0.40) months] (P<0.05). The expression level of carcinoembryonic antigen (CEA) in patients in the mutant-type EGFR group was apparently higher than that in the wild-type EGFR group, but the levels of carbohydrate antigen 125 (CA125), CY21-1 and squamous cell carcinoma-related antigen (SCC-Ag) were apparently lower than those in the wild-type EGFR group. There were statistically significant differences in the expression levels of serum tumor markers between the two groups (P<0.05). Conclusion: EGFR mutation status is closely related to the clinical features of NSCLC patients, such as gender, type of cancer, tumor staging, smoking history, and clinical effect. The second-generation sequencing is an important detection method to identify EGFR gene mutation status, which provides an applicable scaffold for the clinical treatment of patients. IJCEP
Objective: To detect the serum epithelial growth factor receptor (EGFR) gene mutation status in patients with lung cancer via second-generation sequencing and to analyze its correlations with the clinical features of patients and its therapeutic effects. Methods: A total of 110 patients with non-small cell lung cancer (NSCLC) treated in our hospital were recruited as subjects of our study. The distribution of the EGFR gene mutation in patients was detected via second-generation sequencing and then patients were divided into mutant-type EGFR group (n=37) and wild-type EGFR group (n=73). The clinical features and therapeutic effects were compared between the two groups of patients. Results: A total of 5 kinds of EGFR gene mutation [19del (45.95%), L858R (43.24%), L861Q (5.41%), S768I (2.70%), and G719X (2.70%)] were detected via second-generation sequencing. In the mutant-type EGFR group, the proportions of female patients, patients with adenocarcinoma, and those with no history of smoking were high, and the differences were statistically significant (P<0.05). Moreover, there were statistically significant differences in gender, type of cancer, tumor-node-metastasis (TNM) staging, and smoking history between the mutant-type EGFR group and the wild-type EGFR group (P<0.05). Results of a multivariate logistic regression analysis showed that the EGFR gene mutation status was significantly associated with the type of cancer, gender, TNM staging, and smoking history of patients with NSCLC (P<0.05). The clinical effective rate of patients in the mutant-type EGFR group was significantly higher than that in the wild-type EGFR group (54.05% vs. 19.18%) while progression-free survival (PFS) was significantly longer than that in the wild-type EGFR group [(9.75±1.64) months vs. (5.51±0.40) months] (P<0.05). The expression level of carcinoembryonic antigen (CEA) in patients in the mutant-type EGFR group was apparently higher than that in the wild-type EGFR group, but the levels of carbohydrate antigen 125 (CA125), CY21-1 and squamous cell carcinoma-related antigen (SCC-Ag) were apparently lower than those in the wild-type EGFR group. There were statistically significant differences in the expression levels of serum tumor markers between the two groups (P<0.05). Conclusion:EGFR mutation status is closely related to the clinical features of NSCLCpatients, such as gender, type of cancer, tumor staging, smoking history, and clinical effect. The second-generation sequencing is an important detection method to identify EGFR gene mutation status, which provides an applicable scaffold for the clinical treatment of patients. IJCEP
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