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Dual drive coexistence of ALK rearrangement and KRAS mutation advanced lung adenocarcinoma and response to crizotinib

Chromosomal translocation resulting in the fusion between the echinoderm microtubule-associated protein-like 4 (EML4) gene and the anaplastic lymphoma kinase (ALK) gene has been considered as a novel oncogenic fusion in a subset of non-small cell lung cancer (NSCLC), mostly in non-smokers with adeno...

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Detalles Bibliográficos
Autores principales: Zhu, You-Cai, Wan, Bing, Wu, Li-Xin, Li, Xing-Liang, Wang, Wen-Xian, Xu, Chun-Wei, Zhuang, Wu, Wei, Jian-Guo, Du, Kai-Qi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8798733/
https://www.ncbi.nlm.nih.gov/pubmed/35116907
http://dx.doi.org/10.21037/tcr.2019.06.23
Descripción
Sumario:Chromosomal translocation resulting in the fusion between the echinoderm microtubule-associated protein-like 4 (EML4) gene and the anaplastic lymphoma kinase (ALK) gene has been considered as a novel oncogenic fusion in a subset of non-small cell lung cancer (NSCLC), mostly in non-smokers with adenocarcinoma. EML4-ALK translocations are commonly reported to be mutually exclusive with epidermal growth factor receptor (EGFR) or KRAS mutations. Herein, we reported a rare case of 47-year-old female was diagnosed with lung adenocarcinoma and treated with three cycles of chemotherapy. A biopsy acquired after disease progression revealed concurrent KRAS mutation and ALK translocation by an next-generation sequencing (NGS) assay. The patient had a favorable tumor response to crizotinib, a tyrosine kinase inhibitor (TKI). A further understanding of the molecular biology with multiple oncogenic drivers will promote the optimal treatment for NSCLC.