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| Molecular Changes Of Epidermal Growth Factor Receptor And Its Impact On The Clinical Outcomes In Surgically Resected Adenocarcinoma Of The Lung | ||||||||||||||||||||||||||||||||||||||||||||||||
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Back to 86th Annual Meeting Back to Program Outline Objective: Recent studies reported that clinical response to epidermal growth factor receptor (EGFR) inhibitors was associated with somatic changes of EGFR in the advanced stage of the lung cancer. However, there is no clear data demonstrating whether such molecular changes of EGFR per se can affect the clinical outcome of early stage cancer after surgical resection. Methods: DNA mutations of EGFR and KRAS were investigated in 71 adenocarcinoma patients who received surgical resection. Fluorescence in situ hybridization (FISH) of EGFR gene amplification was performed in 48 samples. Results: We detected EGFR mutations in 25 patients (35.2%). EGFR mutation was more frequently found in cases with bronchioloalveolar features (13/22 (59.1%) : 13/49 (26.5%); p=0.008) and in never smokers (7/30 (46.3%) : 19/41 (23.3%); p=0.047). However, the EGFR mutation was not associated with age, gender, or clinical stage. Only the mutation of EGFR in exon 21 was associated with depletion of EGFR copy in FISH result (p=0.003). The amplification of EGFR copy was frequently observed in the female gender (12/29 (41.4%) : 3/19 (15.8%); p=0.061) and in the advanced stage (>=Stage IIIA, 9/19 (47.4%) : 6/29 (20.7%); p=0.051). KRAS mutations were present in 5 patients (7.0%) and none of them showed EGFR mutation. KRAS mutations (p=0.000), male gender (p=0.001), absence of bronchioloalveolar feature (p=0.003), advanced stage (p=0.039), and smoking history (p=0.030) were poor prognostic factors for overall survival, whereas either EGFR mutation (p=0.184) or amplification (p=0.756) was not. Conclusions: Molecular changes of EGFR did not affect the clinical outcome of early lung cancer after surgical resection. This result provides an important message for protocol design of future trials of EGFR inhibitor in early lung cancer. As the KRAS mutation was a poor prognostic factor and it presents reciprocally with EGFR mutation, the KRAS mutation should be investigated in such trials.
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