Differentially expressed genes in iKRAS tumor treated with Trametinib or Kras extinction

To identify the differentially expressed gene in ikras tumors treated with Trametinib or Kras extinction. Overall design: Despite the essential role of MAPK pathway in PDAC maintenance, blocking MAPK signaling with MEK inhibitors has been shown to exert marginal impact on tumor growth or overall survival in both preclinical models and PDAC patients. In an effort to further explore potential MAPK co-inhibition targets, we leveraged the unique ability of the iKras model to genetically extinct oncogenic Kras in advanced tumors and conducted global transcriptomic analysis to identify KRAS downstream effector pathways/activities that are not affected by MAPK inhibition. Specifically, RNAseq analysis was performed in orthotopic xenograft tumors established with primary tumor lines from the iKras/p53 model to compare the transcriptomic profiles following KRAS extinction or Trametinib treatment for 1 or 3 days.