Transformation to Small Cell Lung Cancer of Pulmonary Adenocarcinoma: Clinicopathologic Analysis of Six Cases

• Published in: Journal of pathology and translational medicine Vol. 50; no. 4; pp. 258 - 263
• Main Authors: Ahn, Soomin, Hwang, Soo Hyun, Han, Joungho, Choi, Yoon-La, Lee, Se-Hoon, Ahn, Jin Seok, Park, Keunchil, Ahn, Myung-Ju, Park, Woong-Yang
• Format: Journal Article
• Language: English
• Published: Korea (South) Korean Society of Pathologists, Korean Society for Cytopathology 01.07.2016; The Korean Society of Pathologists and the Korean Society for Cytopathology; Korean Society of Pathologists & the Korean Society for Cytopathology; 대한병리학회
• Subjects: Adenocarcinoma; Analysis; Biopsy; Cancer therapies; Case studies; Chemotherapy; Deoxyribonucleic acid; DNA; Epidermal growth factor; Genotype & phenotype; Histology; Lung cancer; Lung neoplasms; Medical records; Morphology; Mutation; Original; Patients; Polymerase chain reaction; Receptor, epidermal growth factor; Small cell lung carcinoma; Tumors; Tyrosine kinase inhibitor; 병리학; Adenocarcinoma; Small cell lung carcinoma; Receptor, epidermal growth factor; Tyrosine kinase inhibitor; Lung neoplasms
• ISSN: 2383-7837; 2383-7845
• DOI: 10.4132/jptm.2016.04.19

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are considered the first line treatment for a subset of EGFR-mutated non-small cell lung cancer (NSCLC) patients. Although transformation to small cell lung cancer (SCLC) is one of the known mechanisms of resistance to EGFR TKIs, it is not certain whether transformation to SCLC is exclusively found as a mechanism of TKI resistance in EGFR-mutant tumors. We identified six patients with primary lung adenocarcinoma that showed transformation to SCLC on second biopsy (n = 401) during a 6-year period. Clinicopathologic information was analyzed and EGFR mutation results were compared between initial and second biopsy samples. Six patients showed transformation from adenocarcinoma to SCLC, of which four were pure SCLCs and two were combined adenocarcinoma and SCLCs. Clinically, four cases were EGFR-mutant tumors from non-smoking females who underwent TKI treatment, and the EGFR mutation was retained in the transformed SCLC tumors. The remaining two adenocarcinomas were EGFR wild-type, and one of these patients received EGFR TKI treatment. NSCLC can acquire a neuroendocrine phenotype with or without EGFR TKI treatment.