SMK-17, a MEK1/2-specific inhibitor, selectively induces apoptosis in β-catenin-mutated tumors

Although clinical studies have evaluated several MEK1/2 inhibitors, it is unlikely that MEK1/2 inhibitors will be studied clinically. BRAF mutations have been proposed as a responder marker of MEK1/2 inhibitors in a preclinical study. However, current clinical approaches focusing on BRAF mutations h...

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Veröffentlicht in:	Scientific reports 2015-02, Vol.5 (1), p.8155, Article 8155
Hauptverfasser:	Kiga, Masaki, Nakayama, Ayako, Shikata, Yuki, Sasazawa, Yukiko, Murakami, Ryo, Nakanishi, Toshiyuki, Tashiro, Etsu, Imoto, Masaya
Format:	Artikel
Sprache:	eng
Schlagworte:	13/106 13/109 13/2 13/89 631/67/1059/99 631/80/82/23 82/80 96/95 Animals Antineoplastic Agents - pharmacology Apoptosis - drug effects beta Catenin - genetics beta Catenin - metabolism Butadienes - toxicity Cell Line, Tumor Cell Proliferation - drug effects Diphenylamine - analogs & derivatives Diphenylamine - chemistry Diphenylamine - pharmacology Diphenylamine - therapeutic use Humanities and Social Sciences Humans MAP Kinase Kinase 1 - antagonists & inhibitors MAP Kinase Kinase 2 - antagonists & inhibitors Mice Mice, Inbred NOD Mice, SCID multidisciplinary Mutation Neoplasms - drug therapy Nitriles - toxicity Protein Kinase Inhibitors - chemistry Protein Kinase Inhibitors - pharmacology Protein Kinase Inhibitors - therapeutic use Science Sulfonamides - chemistry Sulfonamides - pharmacology Sulfonamides - therapeutic use Transcription Factor 7-Like 2 Protein - genetics Transcription Factor 7-Like 2 Protein - metabolism Transcription, Genetic
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