Cancer Therapy : Preclinical The mTOR Kinase Inhibitors , CC 2141 and CC 2142 , Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

Beatrice Gini,Ciro Zanca,Deliang Guo,Tomoo Matsutani,Kenta Masui,Shiro Ikegami,Huijun Yang,David Nathanson, Genaro R. Villa, David Shackelford,Shaojun Zhu,Kazuhiro Tanaka,Ivan Babic,David Akhavan, Kelly Lin, Alvaro Assuncao,Yuchao Gu,Bruno Bonetti,Deborah S. Mortensen,Shuichan Xu,Heather K. Raymon,Webster K. Cavenee,Frank B. Furnari,C. David James,Guido Kroemer,James R. Heath,Kristen Hege,Rajesh Chopra,Timothy F. Cloughesy,Paul S. Mischel

semanticscholar（2013）

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摘要

Purpose: mTOR pathway hyperactivation occurs in approximately 90% of glioblastomas, but the allosteric mTOR inhibitor rapamycin has failed in the clinic. Here, we examine the efficacy of the newly discovered ATP-competitive mTOR kinase inhibitors CC214-1 and CC214-2 in glioblastoma, identifying molecular determinants of response andmechanisms of resistance, and develop a pharmacologic strategy to

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