1. ¹Shien-Lab, National Cancer Center Hospital, Tsukiji 5-1, Chuo-ku, Tokyo, Japan
2. ²Respiratory Medicine, Kanazawa University Hospital, Takara-machi13-1, Kanazawa, Ishikawa, Japan
3. ³Medical Oncology, National Cancer Center Hospital, Tsukiji 5-1, Chuo-ku, Tokyo, Japan
4. ⁴Pharmacology Division, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, Japan
5. ⁵Center for Medical Genomics, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, Japan

Correspondence: Dr K Nishio, Shien-Lab, National Cancer Center Hospital, Tsukiji 5-1, Chuo-ku, Tokyo, Japan. E-mail: knishio@gan2.res.ncc.go.jp

⁶These authors contributed equally to this work

Received 13 June 2006; Revised 14 September 2006; Accepted 15 September 2006; Published online 24 October 2006.

Abstract

Epidermal growth factor receptor (EGFR) mutations are strong determinants of tumour response to EGFR tyrosine kinase inhibitors in non-small-cell lung cancer (NSCLC). Pleural effusion is a common complication of lung cancer. In this study, we assessed the feasibility of detection of EGFR mutations in samples of pleural effusion fluid. We obtained 43 samples, which was the cell-free supernatant of pleural fluid, from Japanese NSCLC patients, and examined them for EGFR mutations. The epidermal growth factor receptor mutation status was determined by a direct sequencing method (exons 18–21 in EGFR). EGFR mutations were detected in 11 cases (E746_A750del in seven cases, E746_T751del insA in one case, L747_T751del in one case, and L858R in two cases). The EGFR mutations were observed more frequently in women and non-smokers. A comparison between the EGFR mutant status and the response to gefitinib in the 27 patients who received gefitinib revealed that all seven patients with partial response and one of the seven patients with stable disease had an EGFR mutation. No EGFR mutations were detected in the patients with progressive disease. The results suggest that DNA in pleural effusion fluid can be used to detect EGFR mutations and that the EGFR mutation status may be useful as a predictor of the response to gefitinib.