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━━ Background. The transformation of lung adenocarcinoma by an epidermal growth factor receptor (EGFR)-activating mutation to small-cell lung cancer (SCLC) is one of the resistance mechanisms for EGFRtyrosine kinase inhibitor (TKI) therapy. Standard chemotherapy for SCLC may prove effective in such cases. Case. A 47-year-old woman, who had never smoked, was admitted to our hospital because of an abnormal shadow observed in a chest X-ray that was taken in 2010. A left upper lobectomy and lymph node dissection were performed in April 2010, and the postoperative definitive diagnosis was of lung adenocarcinoma (pT2aN2M0, stage IIIA). Since the tumor on the left pleura had increased in size by 2012, gefitinib therapy was initiated. Gefitinib was initially effective, however, the volume of the pleural effusion and the size of the left pleural mass rapidly increased, and the tumor marker level of neuron-specific enolase (NSE) was found to be elevated in 2013. The cytological diagnosis of SCLC was confirmed from the pleural effusion specimens. Chemotherapy with carboplatin+ etoposide (CBDCA+ETP) was effective, however, after 6 cycles, the mass on the left pleura continued to increase in size, and the tumor marker level of carcinoembryonic antigen (CEA) became elevated. A re-challenge with gefitinib was effective, however, the mass on the pleura became enlarged after 6 months. The mass on the left pleura was diagnosed as SCLC with an EGFR-activating mutation by CT-guided needle biopsy. Conclusion. Physicians should consider the possible transformation of non-small-cell lung cancer to SCLC after patients acquire resistance to EGFR-TKI therapy. (JJLC. 2015;55:155-160)

A Case of Lung Adenocarcinoma with an EGFR-activating Mutation That Transformed to Small-cell Lung Cancer