Introducing a G12V activating mutation overcomes the inability of KRAS^C118S to promote HRAS^G12V-driven tumor growth.

<p>(<b>A</b>) RT-PCR amplification of <i>Flag-KRAS</i>, <i>Flag-HRAS</i>, <i>p110CAAX</i> and <i>GAPDH</i> mRNA (note that this is the same gel as in <b><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0123918#pone.0123918.g001" target="_blank">Fig 1A</a></b>, except with the addition of analysis for Flag-KRAS^G12V,C118S, one of two replicate experiments), (<b>B</b>) mean ± SEM tumor volume over time, (<b>C</b>) photographs of excised tumors at end point and (<b>D</b>) mean ± SEM tumor weight at end point of tumors developing in immunocompromised mice (n = 5) injected with Flag-HRAS^G12V-transformed HEK-TtH cells infected with retroviruses encoding p110CAAX and <i>KRAS</i> shRNA alone (pink circles) or with wild-type (WT, orange squares), C118S-mutant (light green triangles) or G12V,C118S-mutant (dark green reverse triangles) Flag-tagged and shRNA-resistant KRAS. ns: non-significant, *: <i>P</i><0.05, **: <i>P</i><0.01 and ***: <i>P</i><0.001, as determined by one-way ANOVA plus post-hoc Bonferroni’s multiple comparison test using GraphPad Prism 5 Software. The full-length gel is shown in <b><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0123918#pone.0123918.s001" target="_blank">S1A Fig</a>.</b>