Transformation to Small Cell Lung Cancer of Pulmonary Adenocarcinoma: Clinicopathologic Analysis of Six Cases.
- Author:
Soomin AHN
1
;
Soo Hyun HWANG
;
Joungho HAN
;
Yoon La CHOI
;
Se Hoon LEE
;
Jin Seok AHN
;
Keunchil PARK
;
Myung Ju AHN
;
Woong Yang PARK
Author Information
- Publication Type:Original Article
- Keywords: Lung neoplasms; Receptor, epidermal growth factor; Tyrosine kinase inhibitor; Small cell lung carcinoma; Adenocarcinoma
- MeSH: Adenocarcinoma*; Biopsy; Carcinoma, Non-Small-Cell Lung; Female; Humans; Lung; Lung Neoplasms; Phenotype; Protein-Tyrosine Kinases; Receptor, Epidermal Growth Factor; Small Cell Lung Carcinoma*
- From:Journal of Pathology and Translational Medicine 2016;50(4):258-263
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: NSCLC can acquire a neuroendocrine phenotype with or without EGFR TKI treatment.
