Figure 3. Loss of EphA2 results in decreased tumor burden and increased survival in a TKI resistant EGFR^L858R+T790M transgenic model.

(A) Lungs of EGFR^L858R+T790M mice from wild-type (EphA2^+/+) or EphA2 knockout (EphA2^−/−) were collected, and total lung wet weight was measured at 10 and 15 weeks of age to assess the additional mass contributed to the lungs by the tumor burden. Average lung weight ± SEM is shown (n = 10 per time point per genotype). **p≤0.005; two way ANOVA with Bonferroni post hoc analysis. n.s. not significant (B) Wild-type and EphA2 deficient mice were subjected to MRI analysis at 15 and 20 weeks of age. T2-weighted MRI images were taken in the axial plane with slice thickness of 1mm. Representative images at 15 and 20 weeks are shown. White arrows indicate tumor tissue. H, heart; S, spine. (C) Tumor volumes were quantified as a composite of 10 serial MRI slices of the lung per mouse using the Matlab software and were graphed as an average tumor volume (mm³) ± SEM (n ≥ at least 5 mice per genotype). (D) Kaplan-Meier survival curves for EGFR^L858R+T790M mice with or without EphA2. Mutant EGFR gene expression was induced by doxycycline (DOX) at 3 weeks of age. *p < 0.005.