Objective:Epidermal growth factor receptor (EGFR) mutations are strong determinants of tumor response to EGFR tyrosine kinase inhibitors in non-small-cell lung cancer (NSCLC) patients. The aim of this study was to evaluate the correspondence between EGFR mutations in non-small-cell lung cancer tissues and in circulating DNA. Methods:The research was conducted in 50 non-small-cell lung cancer patients who had undergone curative surgery,and in whom both serum and neoplastic tissues were available. Meanwhile sera of 33 cases of advanced NSCLC patients were also analyzed. DNA were extracted from each sample. Mutations of EGFR in exon18-21 were examined by PCR amplification method and direct sequencing. Results:EGFR mutations were detected in 15 (30%) of 50 neoplastic tissue samples,6 cases were in-frame deletion del E746-A750 in exon19,9 cases were substitution in exon 21 (all were L858R except one was L861Q),but no mutated DNA resulted in paired serum circulating DNA samples of 50 resectable patients. As the 33 advanced NSCLC patients,EGFR mutations were detected in only 2 serum circulating DNA samples,all were L858R mutation in exon 21. Conclusion:These data indicated that it was difficult to identify EGFR mutations in circulating DNA of NSCLC patients. The use of EGFR mutation in serum as a clinical method for decision making of TKI therapy is unsatisfactory. Objective: This study was to evaluate the correspondence between EGFR mutations in non-small-cell lung cancer (NSCLC) patients. Small-cell lung cancer tissues and in circulating DNA. Methods: The research was conducted in 50 non-small-cell lung cancer patients who had undergone curative surgery, and in both serum and neoplastic tissues were available. Meanwhile sera of 33 cases of Mutations of EGFR in exon 18-21 were examined by PCR amplification method and direct sequencing. Results: EGFR mutations were detected in 15 (30%) of 50 neoplastic tissue samples, 6 Cases were in-frame deletion del E746-A750 in exon19,9 cases were substitution in exon 21 (all were L858R except one was L861Q), but no mutated DNA resulted in paired serum circulating DNA samples of 50 resecta ble patients. As the 33 advanced NSCLC patients, EGFR mutations were detected in only 2 serum circulating DNA samples, all were L858R mutation in exon 21. Conclusion: These data showed that it was difficult to identify EGFR mutations in circulating DNA of NSCLC patients. The use of EGFR mutation in serum as a clinical method for decision making of TKI therapy is unsatisfactory.