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Crizotinib-induced antitumour activity in human alveolar rhabdomyosarcoma cells is not solely dependent on ALK and MET inhibition | Journal of Experimental & Clinical Cancer Research | Full Text
![PDF] Non-Small Cell Lung Cancer Cells Acquire Resistance to the ALK Inhibitor Alectinib by Activating Alternative Receptor Tyrosine Kinases. | Semantic Scholar](https://d3i71xaburhd42.cloudfront.net/30e359daeff4eb0d4476cac93e5de239e079bad1/9-Figure6-1.png "PDF] Non-Small Cell Lung Cancer Cells Acquire Resistance to the ALK Inhibitor Alectinib by Activating Alternative Receptor Tyrosine Kinases. | Semantic Scholar")
PDF] Non-Small Cell Lung Cancer Cells Acquire Resistance to the ALK Inhibitor Alectinib by Activating Alternative Receptor Tyrosine Kinases. | Semantic Scholar
Coexistent genetic alterations involving ALK, RET, ROS1 or MET in 15 cases of lung adenocarcinoma | Modern Pathology
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Crizotinib in advanced non-small-cell lung cancer with concomitant ALK rearrangement and c-Met overexpression | BMC Cancer | Full Text
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![PDF] Activated MET acts as a salvage signal after treatment with alectinib, a selective ALK inhibitor, in ALK-positive non-small cell lung cancer. | Semantic Scholar](https://d3i71xaburhd42.cloudfront.net/de898835018d97b7f4b7d4ec3dd40fc87132b214/3-Figure2-1.png "PDF] Activated MET acts as a salvage signal after treatment with alectinib, a selective ALK inhibitor, in ALK-positive non-small cell lung cancer. | Semantic Scholar")
PDF] Activated MET acts as a salvage signal after treatment with alectinib, a selective ALK inhibitor, in ALK-positive non-small cell lung cancer. | Semantic Scholar
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