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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 ) -AL K 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 - AL K 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-AL K fusion gene may become a potential target for anti-tumor therapy.   Electronic supplementary material  The online version of this article (doi:10.1186/s13045-016-0296-8) contains supplementary material, which is available to authorized users.

journal of hematology and oncology

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