Sensitivity of glioblastomas to clinically available MEK inhibitors is defined by neurofibromin 1 deficiency.

@article{See2012SensitivityOG,
  title={Sensitivity of glioblastomas to clinically available MEK inhibitors is defined by neurofibromin 1 deficiency.},
  author={Wendy L. See and I-Li Tan and J. Mukherjee and Theodore P. Nicolaides and Russell O. Pieper},
  journal={Cancer research},
  year={2012},
  volume={72 13},
  pages={3350-9}
}
Loss of neurofibromin 1 (NF1) leads to hyperactivation of RAS, which in turn signals through the RAF/MEK/ERK and phosphoinositide 3-kinase (PI3K)/mTOR pathways to regulate cell growth and survival. Because NF1-deficient acute myeloid leukemias are sensitive to MEK inhibitors, we investigated here whether NF1-deficient glioblastoma multiforme (GBM) would respond to MEK inhibition. In 19 GBM cell lines, we found that treatment with the clinically available MEK inhibitors PD0325901 or AZD6244… CONTINUE READING
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