Comparing mRNA expression between carrier treated and sorafenib treated Myc/NrasG12V liver tumors

To profile determinants of sensitivity and resistance towards the multikinase inhibitor sorafenib in liver cancer (HCC), we generated HCCs with elevated MYC expression and activated Raf-MEK-ERK signaling. To trigger tumor development, we co-delivered transposable elements encoding for Myc and oncogenic NrasG12V via hydrodynamic injection into the hepatocytes of C57BL/6 wildtype mice. To characterize the response of Myc/NrasG12V HCCs towards sorafenib, we analyzed their transcriptomes after three weeks of sorafenib or carrier treatment. Overall design: mRNA expression of carrier treated and sorafenib treated Myc/NrasG12V liver tumors was compared via mRNAseq analysis