@article{oai:kanazawa-u.repo.nii.ac.jp:00027527,
 author = {谷本, 梓 and 山田, 忠明 and 南條, 成輝 and 竹内, 伸司 and 衣斐, 寛倫 and 北, 賢二 and 松本, 邦夫 and 矢野, 聖二 and Tanimoto, Azusa and Yamada, Tadaaki and Nanjo, Shigeki and Takeuchi, Shinji and Ebi, Hiromichi and Kita, Kenji and Matsumoto, Kunio and Yano, Seiji},
 issue = {13},
 journal = {Oncotarget},
 month = {Jan},
 note = {Alectinib is a new generation ALK inhibitor with activity against the gatekeeper L1196M mutation that showed remarkable activity in a phase I/II study with echinoderm microtubule associated protein-like 4 (EML4) - anaplastic lymphoma kinase (ALK) non-small cell lung cancer (NSCLC) patients. However, alectinib resistance may eventually develop. Here, we found that EGFR ligands and HGF, a ligand of the MET receptor, activate EGFR and MET, respectively, as alternative pathways, and thereby induce resistance to alectinib. Additionally, the heat shock protein 90 (Hsp90) inhibitor suppressed protein expression of ALK, MET, EGFR, and AKT, and thereby induced apoptosis in EML4-ALK NSCLC cells, even in the presence of EGFR ligands or HGF. These results suggest that Hsp90 inhibitors may overcome ligand-triggered resistance to new generation ALK inhibitors and may result in more successful treatment of NSCLC patients with EML4-ALK., 金沢大学がん進展制御研究所},
 pages = {4920--4928},
 title = {Receptor ligand-triggered resistance to alectinib and its circumvention by Hsp90 inhibition in EML4-ALK lung cancer cells},
 volume = {5},
 year = {2014}
}