The potential role of HGF-MET signaling and autophagy in the war of Alectinib versus Crizotinib against ALK-positive NSCLC
Author:
Funder
National Natural Science Foundation of China
China Postdoctoral Science Foundation
Publisher
Springer Science and Business Media LLC
Subject
Cancer Research,Oncology
Link
http://link.springer.com/content/pdf/10.1186/s13046-018-0707-5.pdf
Reference10 articles.
1. Peters S, Camidge DR, Shaw AT, Gadgeel S, Ahn JS, Kim DW, Ou SI, Perol M, Dziadziuszko R, Rosell R, et al. Alectinib versus Crizotinib in untreated ALK-positive non-small-cell lung cancer. N Engl J Med. 2017;377(9):829–38.
2. Hida T, Nokihara H, Kondo M, Kim YH, Azuma K, Seto T, Takiguchi Y, Nishio M, Yoshioka H, Imamura F, et al. Alectinib versus crizotinib in patients with ALK-positive non-small-cell lung cancer (J-ALEX): an open-label, randomised phase 3 trial. Lancet. 2017;390(10089):29–39.
3. Furlan A, Kherrouche Z, Montagne R, Copin MC, Tulasne D. Thirty years of research on met receptor to move a biomarker from bench to bedside. Cancer Res. 2014;74(23):6737–44.
4. Finisguerra V, Di Conza G, Di Matteo M, Serneels J, Costa S, Thompson AA, Wauters E, Walmsley S, Prenen H, Granot Z, et al. MET is required for the recruitment of anti-tumoural neutrophils. Nature. 2015;522(7556):349–53.
5. You L, Shou J, Deng D, Jiang L, Jing Z, Yao J, Li H, Xie J, Wang Z, Pan Q, et al. Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines. Oncotarget. 2015;6(37):40268–82.
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