<?xml version="1.0" encoding="ASCII"?>
<biogps><data><item key="owner">ArrayExpress Uploader</item><item key="pop_total">0</item><item key="species">mouse</item><item key="factors"><item><item key="GSM1309978"><item key="GENOTYPE">Sin3B-deleted</item></item></item><item><item key="GSM1309978"><item key="GENOTYPE">Sin3B-deleted</item></item></item><item><item key="GSM1309980"><item key="GENOTYPE">wt</item></item></item><item><item key="GSM1309980"><item key="GENOTYPE">wt</item></item></item><item><item key="GSM1309982"><item key="GENOTYPE">PDEC Sin3B-deleted</item></item></item><item><item key="GSM1309983"><item key="GENOTYPE">PDEC wt</item></item></item></item><item key="id">7543</item><item key="ownerprofile_id">arrayexpress_sid</item><item key="platform">6</item><item key="summary_wrapped">Pancreatic ductal adenocarcinoma (PDAC) is strikingly resistant to conventional approaches. In this study, we report that the histone...</item><item key="geo_gse_id">E-GEOD-54197</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">1</item><item key="sample_count">6</item><item key="tags"><item>adenocarcinoma</item><item>cancer</item><item>ductal adenocarcinoma</item><item>histone</item><item>pancreas</item><item>pancreatic cancer</item><item>pancreatic ductal adenocarcinoma</item><item>protein</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_gds_id"/><item key="slug">expression-data-from-sin3bp-kraspg12d-and-sin3bp-k</item><item key="geo_id_plat">E-GEOD-54197_A-AFFY-45</item><item key="name">Expression data from Sin3Bp+/-KRaspG12D and Sin3Bp-/-KRaspG12D pancreata and from cultured primary pancreatic duct epithelial cells (PDEC) of the same genotype.</item><item key="created">Nov.12, 2014</item><item key="summary">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.</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-54197</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-54197/samples/</item></data></biogps>
