Expression Data from 12 week old APCmin/+ and littermate matched Wildtype B6 mouse Terminal Ileum (TI)

APCmin/+ mice develop spontaneous gastrointestinal polyposis due to a dominantly inhereited germline loss-of-function mutation in the tumor suppressor adenomatous polyposis coli (APC). Changes in intestinal immune activity have been documented to occur prior to the development of fulminate polyposis. Such changes are thought to contribute to disease development. We used microarrays to describe the changing intestinal transcriptional landscape in APCmin/+ mice. Whole transcriptome profiling from polypotic and nonpolypotic intestinal sections of APC/min+ mice were examined in the early stages of disease, and compared to normal intestinal sections from littermate matched wildtype B6 mice. Nonpolypotic (wildtype and APCmin/+) and Polypotic (APCmin/+) sections of terminal ileum were identified by visual inspection, and subsequently selected for RNA isolation and hydridzation to Affymetrix Mouse Genome 430A 2.0 Arrays. Interference from bacterial RNA was selected against using a probeset enriched in oligos extending into 3'-poly-A tails.APCmin/+小鼠因肿瘤抑制基因腺瘤性结肠息肉病（adenomatous polyposis coli, APC）发生显性遗传的生殖系功能丧失突变，进而自发形成胃肠道息肉病。已有研究证实，肠道免疫活性改变会先于暴发性息肉病出现，且这类改变被认为参与疾病的发生发展过程。本研究利用基因芯片（microarrays）解析APCmin/+小鼠肠道内动态变化的转录组全景：我们对疾病早期阶段的APCmin/+小鼠的息肉病变肠段与非病变肠段开展全转录组分析，并与同窝匹配的野生型B6小鼠的正常肠段进行对比。通过肉眼观察鉴定回肠末端的非病变肠段（野生型与APCmin/+小鼠样本）与病变肠段（APCmin/+小鼠样本），随后提取RNA并与Affymetrix小鼠基因组430A 2.0芯片进行杂交。为排除细菌RNA的干扰，我们采用了富集于延伸至3'端多聚腺苷酸（poly-A）尾的寡核苷酸的探针组进行筛选。