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• W2042902581 abstract "EML 4‐ ALK lung cancer accounts for approximately 3–7% of non‐small‐cell lung cancer cases. To investigate the molecular mechanism underlying tumor progression and targeted drug sensitivity/resistance in EML 4‐ ALK lung cancer, clinically relevant animal models are indispensable. In this study, we found that the lung adenocarcinoma cell line A925L expresses an EML 4‐ ALK gene fusion (variant 5a, E2:A20) and is sensitive to the ALK inhibitors crizotinib and alectinib. We further established highly tumorigenic A925 LPE 3 cells, which also have the EML 4‐ ALK gene fusion (variant 5a) and are sensitive to ALK inhibitors. By using A925 LPE 3 cells with luciferase gene transfection, we established in vivo imaging models for pleural carcinomatosis, bone metastasis, and brain metastasis, all of which are significant clinical concerns of advanced EML 4‐ ALK lung cancer. Interestingly, crizotinib caused tumors to shrink in the pleural carcinomatosis model, but not in bone and brain metastasis models, whereas alectinib showed remarkable efficacy in all three models, indicative of the clinical efficacy of these ALK inhibitors. Our in vivo imaging models of multiple organ sites may provide useful resources to analyze further the pathogenesis of EML 4‐ ALK lung cancer and its response and resistance to ALK inhibitors in various organ microenvironments." @default.
• W2042902581 created "2016-06-24" @default.
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• W2042902581 date "2015-02-17" @default.
• W2042902581 modified "2023-10-13" @default.
• W2042902581 title "<i>In vivo</i> imaging models of bone and brain metastases and pleural carcinomatosis with a novel human <i> <scp>EML</scp> 4‐ <scp>ALK</scp> </i> lung cancer cell line" @default.
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• W2042902581 doi "https://doi.org/10.1111/cas.12600" @default.
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