Expression data from Sin3Bp+/-KRaspG12D and Sin3Bp-/-KRaspG12D pancreata and from cultured primary pancreatic duct epithelial cells (PDEC) of the same genotype

Pancreatic ductal adenocarcinoma (PDAC) is strikingly resistant to conventional approaches. In this study, we report that the histone deacetylase associated SIN3B protein is required for activated KRAS-induced senescence in vivo using a mouse model of pancreatic cancer. We used microarray data to determine if SIN3B regulates KRAS-induced expression of the inflammatory response. Total RNA from Sin3Bp+/-KRaspG12D and Sin3Bp-/-KRaspG12D pancreas (two pancreata for each genotype) or PDEC (one for each genotype) was extracted and hybridized on Affymtrix microarrays.