Differential Effects of Tyrosine Kinase Inhibitors on Normal and Oncogenic EGFR Signaling and Downstream Effectors
作者： Youngjoo Kim , Mihaela Apetri , BeiBei Luo , Jeffrey E. Settleman , Karen S. Anderson
DOI: 10.1158/1541-7786.MCR-14-0326
关键词:
摘要: Constitutive activation of EGFR due to overexpression or mutation in tumor cells leads dysregulated downstream cellular signaling pathways. Therefore, as well its effectorshavebeenidentifiedasimportanttherapeutictargets.The FDA-approved small-molecule inhibitors EGFR, gefitinib (Iressa) and erlotinib (Tarceva), are clinically effective a subset patients with non–small cell lung cancer (NSCLC) whose tumors harbor activating mutations within the kinase domain EGFR. The current study examined effects these drugs 32D cellsexpressingnative (WT)oroncogenic (L858R) aswell lines A431 H3255. Distinct patterns for inhibition autophosphorylation at individual tyrosines were revealed wild-type (WT) L858R Phosphorylation Y845 has been shown be important Y1045phosphorylation islinkedtoCbl-mediated
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