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




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Journal of Hematology and Oncology

, 9:66

First Online: 05 August 2016Received: 24 July 2016Accepted: 02 August 2016DOI: 10.1186-s13045-016-0296-8

Cite this article as: Gu, F., Zhang, Y., Liu, Y. et al. J Hematol Oncol 2016 9: 66. doi:10.1186-s13045-016-0296-8

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 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.

KeywordsNSCLC Lung adenocarcinoma Oncogenic drivers SPTBN1-ALK c-Met HER-2 Crizotinib Chemotherapy Radiotherapy Fei-fei Gu and Yong Zhang are co-first authors.

Electronic supplementary materialThe online version of this article doi:10.1186-s13045-016-0296-8 contains supplementary material, which is available to authorized users.

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Autor: Fei-fei Gu - Yong Zhang - Yang-yang Liu - Xiao-hua Hong - Jin-yan Liang - Fan Tong - Jing-song Yang - Li Liu

Fuente: https://link.springer.com/







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