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. Author manuscript; available in PMC: 2016 May 15.
Published in final edited form as: Cancer Res. 2015 Mar 25;75(10):2109–2119. doi: 10.1158/0008-5472.CAN-14-3122

Figure 4.

Figure 4

The iEIP gliomas are sensitive to genetic suppression of EGFR* induction but are refractory to EGFR TKI treatment. A, Kaplan-Meier survival analysis of cohorts of tumor bearing iEIP transgenic mice treated with vehicle (n = 6), erlotinib (n = 4), or Dox (n = 6). Day 0 represents the day when treatment was initiated. B, EGFR* phosphorylation but not EGFR* protein was downregulated in erlotinib treated tumors. Shown are representative images of H&E and IHC staining against EGFR and phospho-EGFR (p-EGFR) on tumor sections from (A). C, Kaplan-Meier survival analysis of mouse cohorts that were orthotopically transplanted with iEIP glioma cells and treated with vehicle (n = 4), gefitinib (n = 3), erlotinib (n = 5), or Dox (n = 7) after tumors were established. Day 0 represents the day when treatment was initiated. D, shown are representative bioluminescence images of animals subjected to the indicated treatment from (C). E, EGFR* phosphorylation but not EGFR* protein levels were diminished in tumors treated with gefitinib or erlotinib. Representative tumor sections from (C) were stained with H&E, anti-EGFR, or anti-p-EGFR. Scale bars represent 50 μm.