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

Abstract
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 oncog enic drivers may affect the sensitivity of crizotinib. Herein, we present a 69-year-old neve r-smoker Chinese male with advance d lung adenocarcinoma harbor ing concomitant spect rin beta non-eryt hrocytic 1 ( SPTBN1 )-AL K fusion, c-Met overexpression,and human epidermal growth factor receptor-2 ( HER-2 ) amplificatio n with inherent resistance to crizotinib,chemotherapy, and rad iotherapy. Although the patien t received timely and comp rehensive treatment, the overall survival was only 8 months. Theref ore, c-Met overexpression , HER-2 gene amp lification, and SPTBN1 - ALK gen e fusion can coexist in lung adenocarcinoma and may become a potential biomarker of can cer refractory to crizo tinib,chemotherapy, and rad iotherapy as well as of a relatively poo r prognos is. In addition, the nove l SPTBN1 -AL K fusion gene may become a potential target for anti-tumor therapy.
Keywords: NSCLC, Lung adenocarcin oma, Oncog enic drivers, SPTBN1-ALK , c-Met, HER- 2 , Crizotinib, Chemotherap y,Radiotherap

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