Lung adenocarcinoma harboring concomitant SPTBN1-ALK fusion, c-Met overexpression, and HER-2 amplification with inherent resistance to crizotinib, chemotherapy, and radiotherapy

作者：Gu, Fei-fei; Zhang, Yong; Liu, Yang-yang; Hong, Xiao-hua; Liang, Jin-yan; Tong, Fan; Yang, Jing-song; Liu, Li^*

来源：Journal of Hematology & Oncology, 2016, 9(1): 66.

DOI：10.1186/s13045-016-0296-8

• NSCLC
• Lung adenocarcinoma
• Oncogenic drivers
• SPTBN1-ALK
• c-Met
• HER-2
• Crizotinib
• Chemotherapy
• Radiotherapy

Crizotinib is a multi-targeted tyrosine kinase inhibitor (TKI) with activity against mesenchymal-epithelial transition factor (MET) and anaplastic lymphoma kinase (ALK). However, the concomitant oncogenic drivers may affect the sensitivity of crizotinib. Herein, we present a 69-year-old never-smoker Chinese male with advanced lung adenocarcinoma harboring concomitant spectrin beta non-erythrocytic 1 (SPTBN1)-ALK fusion, c-Met overexpression, and human epidermal growth factor receptor-2 (HER-2) amplification with inherent resistance to crizotinib, chemotherapy, and radiotherapy. Although the patient received timely and comprehensive treatment, the overall survival was only 8 months. Therefore, c-Met overexpression, HER-2 gene amplification, and SPTBN1-ALK gene fusion can coexist in lung adenocarcinoma and may become a potential biomarker of cancer refractory to crizotinib, chemotherapy, and radiotherapy as well as of a relatively poor prognosis. In addition, the novel SPTBN1-ALK fusion gene may become a potential target for anti-tumor therapy.

• 出版日期2016-8-5
• 单位华中科技大学; 湖北省肿瘤医院; 武汉大学