GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE295nnn/GSE295683/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE295683GEOGSEfalseRNA-seq Analysis of KRAS Mutant HPNE Pancreatic Ductal Epithelial CellsKRAS mutations drive pancreatic cancer initiation by reprogramming cellular signaling and the tumor microenvironment. Here, we investigate the early transcriptional impact of distinct KRAS mutants in a non-cancerous pancreatic epithelial context. Using RNA-seq, we profiled HPNE cells engineered with inducible KRAS variants (G12D, G12V, G12R, Q61H, Q61K, Q61R) compared to wild-type KRAS (WT) following 24-hour induction. This comparative analysis reveals that KRAS mutations differentially regulate immune and extracellular matrix remodeling pathways, with G12D and Q61R/H mutants driving pro-inflammatory signaling, while G12R and Q61k exhibits distinct transcriptional suppression. These findings highlight the mutation-specific transcriptional landscapes of KRAS in pancreatic epithelial cells and provide insight into the early events shaping the pancreatic tumor microenvironment.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 sapiens[41892368]