Targeted inhibition of the molecular chaperone Hsp90 overcomes ALK inhibitor resistance in non-small cell lung cancer.

@article{Sang2013TargetedIO,
  title={Targeted inhibition of the molecular chaperone Hsp90 overcomes ALK inhibitor resistance in non-small cell lung cancer.},
  author={Jim Sang and Jaime Acquaviva and Julie C. Friedland and Donald L. Smith and Manuel Sequeira and Chaohua Zhang and Qin Jiang and Liquan Xue and Christine M Lovly and John-Paul Jimenez and Alice Tsang Shaw and Robert C Doebele and Suqin He and Richard C. Bates and David Ross Camidge and Stephan W. Morris and Iman A. El-Hariry and David A. Proia},
  journal={Cancer discovery},
  year={2013},
  volume={3 4},
  pages={430-43}
}
UNLABELLED EML4-ALK gene rearrangements define a unique subset of patients with non-small cell lung carcinoma (NSCLC), and the clinical success of the anaplastic lymphoma kinase (ALK) inhibitor crizotinib in this population has become a paradigm for molecularly targeted therapy. Here, we show that the Hsp90 inhibitor ganetespib induced loss of EML4-ALK expression and depletion of multiple oncogenic signaling proteins in ALK-driven NSCLC cells, leading to greater in vitro potency, superior… CONTINUE READING
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