Oncogenic RAS pathway activation promotes resistance to anti-VEGF therapy through G-CSF-induced neutrophil recruitment.

@article{Phan2013OncogenicRP,
  title={Oncogenic RAS pathway activation promotes resistance to anti-VEGF therapy through G-CSF-induced neutrophil recruitment.},
  author={Vernon T. Phan and Xiumin Wu and J. H. Cheng and Rebecca X Sheng and Alicia S. Chung and Guanglei Zhuang and Christopher N.-Q. Tran and Qinghua Song and Marcin Kowanetz and Amy Sambrone and Martha Tan and Y. Gloria Meng and Erica L. Jackson and Franklin V. Peale and Melissa R Junttila and Napoleone M. A. Ferrara},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2013},
  volume={110 15},
  pages={6079-84}
}
Granulocyte-colony stimulating factor (G-CSF) promotes mobilization of CD11b(+)Gr1(+) myeloid cells and has been implicated in resistance to anti-VEGF therapy in mouse models. High G-CSF production has been associated with a poor prognosis in cancer patients. Here we show that activation of the RAS/MEK/ERK pathway regulates G-CSF expression through the Ets transcription factor. Several growth factors induced G-CSF expression by a MEK-dependent mechanism. Inhibition of G-CSF release with a MEK… CONTINUE READING
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