TY - JOUR T1 - Effectors and potential targets selectively upregulated in human <em>KRAS</em>-mutant lung adenocarcinomas JF - bioRxiv DO - 10.1101/041137 SP - 041137 AU - Jinyu Li AU - Raffaella Sordella AU - Scott Powers Y1 - 2016/01/01 UR - http://biorxiv.org/content/early/2016/02/29/041137.abstract N2 - Genetic and proteomic analysis of human tumor samples can provide an important compliment to information obtained from model systems. Here we examined protein and gene expression from the Cancer Genome and Proteome Atlases (TCGA and TCPA) to characterize proteins and protein-coding genes that are selectively upregulated in KRAS-mutant lung adenocarcinomas. Phosphoprotein activation of several Raf/MAPK signaling components was considerably stronger in KRAS-mutants than any other group of tumors. However, both KRAS-mutants and tumors with other activating mutations in the Raf/MAPK pathway showed comparable activation of mTOR. Co-occurring mutations in KRAS-mutants were associated with differential activation of PDK1 and PKC-alpha. Genes showing strong activation in RNA-seq data included negative regulators of Raf/MAPK signaling along with potential oncogenic effectors including activators of Rac and Rho proteins and the receptor protein-tyrosine phosphatase gene PTPRE. These results corroborate Raf/MAPK signaling as an important therapeutic target in KRAS-mutant lung adenocarcinomas and pinpoint new potential targets. ER -