Fig. 6.

In vivo demonstration of EGFR TKI-induced drug persistent cells with EMT phenotype. a Mice with HCC827 (top) and HCC4006 (bottom) tumor xenografts were treated with methylcellulose (control) or erlotinib for 21 days. After the drug treatments tumors were harvested and subjected to IHC analysis for the putative stem cell marker, ALDH1A. b Mice with HCC827 tumor xenografts were treated with methylcellulose (control) or erlotinib for 21 days. Tumors were harvested and disrupted into single cell preparations, which were then subjected to ALDH assay. c–e EGFR TKI treatment increases Vimentin expression and decreases E-cadherin expression in vivo. f EGFR TKI treatment increases Notch3 expression in vivo. g EGFR TKI treatment increases the non-phospho (activated) β-catenin levels in vivo. h EGFR TKI treatment increases β-catenin levels in vivo. Error bars represent SD from techincal triplicates