Antitumor activity of the sorafenib in parental and TKI-resistant HCT116 xenografts.

<p>A, Parental (WT) HCT116 cancer cells; B, GEF-R HCT116 cancer cells; C, VAN-R HCT116 cancer cells; D, HCT116 cancer cells. Athymic nude mice were injected subcutaneously into the dorsal flank with 10⁷ cancer cells. After 7 to 10 days (average tumor size, 75 mm³), mice were treated as indicated in Materials and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0028841#s4" target="_blank">Methods</a> for 5 weeks. Each treatment group consisted of 8 mice. Data represent the average (±SD). Student's <i>t</i> test was used to compare tumor sizes among different treatment groups at day 35 following the start of treatment. A, HCT116 WT: sorafenib versus control (two-sided p<0.001); B, HCT116: sorafenib versus control (two-sided p<0.001). C, HCT116 VAN-R: sorafenib versus control (two-sided p<0.001); D, HCT116 ERL-R: sorafenib versus control (two-sided p<0.001).