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. Author manuscript; available in PMC: 2017 Apr 26.
Published in final edited form as: Cell Rep. 2017 Feb 21;18(8):1958–1969. doi: 10.1016/j.celrep.2017.01.069

Figure 1.

Figure 1

MAPK signal amplification promotes early and widespread lung tumor growth in KrasLSL-G12D/+;p53flox/flox mice. (a) KrasLSL-G12D/+;p53flox/flox mice were infected with Ad:CMVCre by forced inhalation to initiate lung tumors. One week post Cre, treatment with control or PLX4720-containing diet was initiated and maintained for the indicated durations. (b) Kaplan-Meier survival analysis of Ad:CMVCre infected mice that were maintained on control or PLX4720 containing diets, p<0.0001, log-rank (Mantel–Cox) test. (c) H&E images of lung tumors and hyperplasias from mice at the survival endpoint. (d) Tumor grades in treated with control or PLX4720 for survival analysis, (contingency χ2 test for trend, p<0.0001, Student’s t-test of mean number of AAH per mouse, p=0.08).(e) Immunohistochemistry for pMek and pErk five weeks post Ad:CMVCre. (f-g) KrasLSL-G12D/+;p53flox/flox mice were infected with 5×107 or 5×106 pfu of Ad:CMVCre as indicated. (f) Percent lung tumor burden after five weeks after Ad:CMVCre infection, p<0.0001. (g) Tumor number in lungs of mice five weeks after Ad:CMVCre infection, p=0.0001. (h) Whole lung lobes (upper panel) and lung sections (middle and lower panels) analyzed by fluorescence microscopy from KrasLSL-G12D/+; p53flox/flox; Rosa26Motley/+ mice five weeks after Ad:CMV-Cre infection. Scale bars are 25 microns. Error bars represent SEM from average. Also see Figures S1 and S2.