Met and c-Src cooperate to compensate for loss of epidermal growth factor receptor kinase activity in breast cancer cells.

@article{Mueller2008MetAC,
  title={Met and c-Src cooperate to compensate for loss of epidermal growth factor receptor kinase activity in breast cancer cells.},
  author={Kelly L. Mueller and Lauren A Hunter and Stephen P Ethier and Julie L. Boerner},
  journal={Cancer research},
  year={2008},
  volume={68 9},
  pages={3314-22}
}
Breast cancers are not responsive to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI), although 30% of breast cancers overexpress EGFR. The mechanism of intrinsic resistance to EGFR TKIs in breast cancer is the focus of current studies. Here, we observed that EGFR remains tyrosine phosphorylated in breast cancer cells that proliferate in the presence of EGFR TKIs. In one such cell line, SUM229, inhibiting c-Src kinase activity with either a dominant-negative c-Src or a c… CONTINUE READING

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