Transcription profiling of mouse Apc1638N intestinal tumors vs WT intestinal mucosa

The majority of sporadic colorectal cancer cases are initiated by mutations in the APC tumor suppressor gene leading to constitutive activation of the Wnt/b-catenin signaling pathway and adenoma formation. Several pre-clinical models carrying germline mutations in the endogenous mouse Apc tumor supressor gene have been generated and their phenotype characterized. The predisposition of these mouse models to multiple intestinal adenomas closely resembles the FAP phenotype at the molecular, cellular and phenotypic level and may prove valuable to elucidate the molecular and cellular mechanisms underlying colorectal tumorigenesis. The goal of this study is to establish an expression signature characteristic of intestinal tumors characterized by the inactivation of Apc. Experiment Overall Design: We have compared 3 intestinal tumor samples collected from the mouse model Apc1638N against 2 normal intestinal samples collected from wild type C57Bl6/J animals. In both cases only epithelial cells were used for the signature since we have collected our samples were laser capture microdissected.