Abstract
Activating mutations in KRAS are very frequent in Pancreatic Ductal Adenocarcinomas (PDACs), but different approaches to directly target Ras for therapy failed in clinical trials. An alternative route for blocking RAS-driven oncogenic pathways is to target downstream effectors of RAS involved in promoting the oncogenic phenotype. Long non-coding RNAs (lncRNAs) regulate gene expression thr…