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. Author manuscript; available in PMC: 2013 Feb 1.
Published in final edited form as: Nat Genet. 2012 Jul 1;44(8):852–860. doi: 10.1038/ng.2330

Figure 2. AXL overexpression is necessary for acquired resistance to erlotinib treatment in EGFR-mutant NSCLC tumors in vivo.

Figure 2

a, AXL and pAXL protein levels are increased in the absence of pEGFR and increased pMET in HCC827 tumors from each erlotinib treatment cohort compared with vehicle treated tumors. Tumors were harvested for analysis at the completion of the study for each treatment group (Vehicle: Day 45; 6.25 Erl: Day 60; 12.5 Erl: Day 110; 25 Erl: Day 110; 50 Erl: Day 100) b, Acute and transient treatment of HCC827 tumors with erlotinib (12.5 mg/kg/day) decreases pAKT, pERK, pRELa and increases the levels of cleaved Parp. c, Response of parental HCC827 xenograft tumors or HCC827 ER xenograft tumors (n= 10 tumors/group) transduced with a non-target shRNA or an shRNA targeting AXL to treatment with either vehicle or erlotinib (12.5 mg/kg/day). Tumor volumes are expressed as mean ± SEM. d, Validation of AXL knockdown and the effects of erlotinib treatment on pEGFR in representative tumor xenografts (c) by western blot analysis.