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. Author manuscript; available in PMC: 2014 Jan 15.
Published in final edited form as: Clin Cancer Res. 2012 Dec 4;19(2):380–392. doi: 10.1158/1078-0432.CCR-12-1555

Figure 2.

Figure 2

Figure 2

Figure 2

c-Src activation contributes to erlotinib resistance but not cetuximab resistance in vivo. (A) VC-2 and DA-Src-5 HNSCC cells were inoculated into the flanks of nude mice. Mice were treated 5 days per week with either vehicle control (20% trappsol) or 40mg/kg erlotinib by oral gavage for 4 weeks. Treatment began 5 days after tumor implantation. Results represent the mean tumor volumes ± S.E. of 14 tumors per treatment group. Unpaired Student’s t-test, *P<0.05. (B) Representative images and quantitative results of immunohistochemical staining of cell proliferating cells by Ki67 and apoptotic cells by Tunel assay. The results are presented as the mean number of apoptotic cells or Ki67 positive cells per area ± S.E. Unpaired Student’s t test, P<0.05*, P<0.0005***. Scale bar= 50μm. (C) 1 × 106 DA-Src-5 HNSCC cells were inoculated into the flanks of nude mice. Mice were treated 2 days per week with either vehicle control (saline) or 0.03mg cetuximab i.p. for 13 days. Treatment began 15 days after tumor implantation. Results represent the mean tumor volumes ± S.E. of 7 tumors per treatment group. Unpaired Student’s t-test, *P<0.05.