|1.||Okamoto, Isamu: 2 articles (11/2012 - 04/2011)|
|2.||Takezawa, Ken: 2 articles (11/2012 - 04/2011)|
|3.||Nishio, Kazuto: 2 articles (11/2012 - 04/2011)|
|4.||Nakagawa, Kazuhiko: 2 articles (11/2012 - 04/2011)|
|5.||Jänne, Pasi A: 2 articles (04/2011 - 12/2010)|
|6.||Gray, Nathanael S: 2 articles (12/2010 - 01/2007)|
|7.||Qiang, Jiankun: 1 article (10/2014)|
|8.||Han, Siqi: 1 article (10/2014)|
|9.||Li, Guangchao: 1 article (10/2014)|
|10.||Yang, Lin: 1 article (10/2014)|
05/03/2011 - "Although crizotinib was ineffectual against EML4-ALK harboring the gatekeeper mutation, we observed that two structurally different ALK inhibitors, NVP-TAE684 and AP26113, were highly active against the resistant cancer cells in vitro and in vivo. "
01/01/2011 - "We also compared the effect of TAE684 with PF2341066, a c-Met and ALK small molecule inhibitor currently in clinical trial in cancers harboring ALK fusions, and demonstrated that TAE684 is a much more potent inhibitor of EML4-ALK. "
01/01/2011 - "We show here that TAE684 inhibits proliferation and induces cell cycle arrest, apoptosis, and tumor regression in two NSCLC models that harbor EML4-ALK fusions. "
12/01/2010 - "18F-FDG-PET-CT scans revealed almost complete inhibition of tumor metabolic activity within 24 hours of TAE684 exposure. "
08/01/2011 - "Treatment of two different ALK inhibitors, WHI-P154 and NVP-TAE684, resulted in the down-regulation of aberrant ALK signaling, shrinkage of tumor, and suppression of metastasis and significantly improved survival of ALK mutant-bearing mice. "
|2.||Neoplasm Metastasis (Metastasis)
|3.||Lung Neoplasms (Lung Cancer)
10/01/2014 - "Combined TAE684 with PI3K inhibitor synergistically inhibited the proliferation of EML4-ALK-positive cells in vitro and significantly suppressed the growth of H2228 xenografts in vivo, suggesting the potential clinical application of such combinatorial therapy regimens in patients with EML4-ALK positive lung cancer."
11/15/2012 - "We established lines of EML4-ALK-positive H3122 lung cancer cells that are resistant to the ALK inhibitor TAE684 (H3122/TR cells) and investigated their resistance mechanism with the use of immunoblot analysis, ELISA, reverse transcription and real-time PCR analysis, and an annexin V binding assay. "
07/01/2012 - "Endothelial cells and fibroblasts, which produce the EGFR ligands and HGF, respectively, decreased the sensitivity of EML4-ALK lung cancer cells to crizotinib and TAE684, respectively. "
07/01/2012 - "We tested the effects of ligands produced by endothelial cells and fibroblasts, and the cells themselves, on the susceptibility of EML4-ALK lung cancer cell lines to crizotinib and TAE684, a selective ALK inhibitor active against cells with ALK amplification and gatekeeper mutations, both in vitro and in vivo. "
04/15/2011 - "The specific ALK inhibitor TAE684 induced apoptosis that was accompanied both by upregulation of BIM, a proapoptotic member of the Bcl-2 family, and by downregulation of survivin, a member of the inhibitor of apoptosis protein (IAP) family, in EML4-ALK-expressing NIH 3T3 cells as well as in H3122 human lung cancer cells harboring endogenous EML4-ALK. "
12/15/2011 - "Activating ALK mutations found in neuroblastoma are inhibited by Crizotinib and NVP-TAE684."
12/01/2011 - "An independent resistance screen in ALK-mutant neuroblastoma cells yielded the same L1198P resistance mutation but defined two additional mutations conferring resistance to TAE684 but not to PF02341066. "
|5.||Inhibitor of Apoptosis Proteins
|1.||Heterologous Transplantation (Xenotransplantation)