• Biology, Medicine
• Published in Oncogene 2011
• DOI:10.1038/onc.2010.408

Hyperactivation of MEK–ERK1/2 signaling and resistance to apoptosis induced by the oncogenic B-RAF inhibitor, PLX4720, in mutant N-RAS melanoma cells

@article{Kaplan2011HyperactivationOM,
  title={Hyperactivation of MEK–ERK1/2 signaling and resistance to apoptosis induced by the oncogenic B-RAF inhibitor, PLX4720, in mutant N-RAS melanoma cells},
  author={Fred M. Kaplan and Yingkuan Shao and Melanie M. Mayberry and Andrew E Aplin},
  journal={Oncogene},
  year={2011},
  volume={30},
  pages={366-371}
}

• Fred M. Kaplan, Yingkuan Shao, +1 author Andrew E Aplin

Activating mutations in B-RAF and N-RAS occur in ∼60 and ∼15% of melanomas, respectively. The most common mutation in B-RAF is V600E, which activates B-RAF and the downstream MEK–ERK1/2 pathway. Thus, B-RAFV600E is a viable therapeutic target. PLX4720 is a selective inhibitor of mutant B-RAF and its analog, PLX4032, is currently undergoing clinical trials in melanoma. However, the effects of PLX4720 across the genotypic spectrum in melanoma remain unclear. Here, we describe that PLX4720… CONTINUE READING

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