Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K.

@article{Villanueva2010AcquiredRT,
  title={Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K.},
  author={Jessie Villanueva and A Vultur and John T. Lee and Rajasekharan Somasundaram and Mizuho Fukunaga-Kalabis and Angela K Cipolla and Bradley Wubbenhorst and Xiaowei Xu and Phyllis A. Gimotty and Damien Kee and Ademi E Santiago-Walker and Richard Letrero and Kurt D'Andrea and Anitha Pushparajan and James E. Hayden and Kimberly Dahlman Brown and Sylvie Laquerre and Grant Mcarthur and Jeffrey A. Sosman and Katherine L Nathanson and Meenhard Herlyn},
  journal={Cancer cell},
  year={2010},
  volume={18 6},
  pages={683-95}
}
BRAF is an attractive target for melanoma drug development. However, resistance to BRAF inhibitors is a significant clinical challenge. We describe a model of resistance to BRAF inhibitors developed by chronic treatment of BRAF(V)⁶⁰⁰(E) melanoma cells with the BRAF inhibitor SB-590885; these cells are cross-resistant to other BRAF-selective inhibitors. Resistance involves flexible switching among the three RAF isoforms, underscoring the ability of melanoma cells to adapt to pharmacological… CONTINUE READING
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