Imanishi Naoko
   Department   University Hospital  General Thoracic Surgery, Clinical Departments
   Position  
Article types journal article
Language English
Peer review Peer reviewed
Title Squamous cell carcinoma transformation from adenocarcinoma as an acquired resistance after the EGFR TKI therapy in (EGFR-mutated) non-small cell lung cancer.
Journal Formal name:Journal of thoracic disease
Abbreviation:J Thorac Dis
ISSN code:20721439
Domestic / ForeginForegin
Volume, Issue, Page 10(7),526-531頁
Author and coauthor Shinji Shinohara1, Yoshinobu Ichiki1, Yukiko Fukuichi1, Yohei Honda1, Masatoshi Kanayama1, Akihiro Taira1, Yusuke Nabe1, Taiji Kuwata1, Masaru Takenaka1, Soichi Oka1, Yasuhiro Chikaishi1, Ayako Hirai1, Naoko Imanishi1, Koji Kuroda1, Kazue Yoneda1, Hirotsugu Noguchi2, Fumihiro Tanaka1
Publication date 2018/11
Summary Lung cancer remains the leading cause of cancer mortality worldwide. The incidence of recurrence or distant metastasis after complete resection of primary tumors is reported to be 37%, even in patients with stage I non-small cell lung carcinoma (NSCLC) (1). Recently, the treatment for lung cancer has diversified dramatically and the indication of such treatment is determined according to pathological and cytogenetic features, the EGFR gene status, fusion genes consisting of echinoderm microtubule-associated protein-like 4 and anaplastic lymphoma kinase, and the appearance of the immune checkpoint inhibitor. The newly introduced treatment with epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) among patients with EGFR-mutated NSCLC is associated with response rates of 56–74%. Despite its high response rate, however, most patients experience tumor progression within 1 to 2 years after the treatment (1). When tumor recurrence or progression occurs, the biological and genetic changes of the tumor should be reassessed, because biological features and histological characteristics of the primary tumor are occasionally different from those of the recurrent site. Regarding the mechanisms of acquired drug resistance to EGFR-TKIs in EGFR-mutated NSCLC, some investigators have suggested an association with a secondary mutation in EGFR
T790M or other mechanisms that do not involve signaling through EGFRs, such as MET or HER2 amplification (2,3). Histological transformation from adenocarcinoma to small cell lung carcinoma (SCLC) (2,3) or squamous cell carcinoma (SCC) (4) has also been reported as a mechanism of acquired resistance. However, there are few reports on SCC transformation from adenocarcinoma in NSCLC. We herein report a case of a resected lung adenocarcinoma that showed SCC transformation of a recurrent lesion of the pleura after administration of EGFR-TKIs.
DOI 10.21037
PMID 30174925