E-GEOD-13298 - Transcription profiling of mouse Rb1 deficient Apc1638N cecal tumors vs duodenal tumors
Submitted on 21 October 2008, released on 13 November 2008, last updated on 27 March 2012
To examine the role of Rb1 in gastrointestinal (GI) tumors we generated mice with an Apc1638N allele, Rbtm2brn floxed alleles, and a villlin-cre transgene (RBVCA). These mice had reduced median survival due to an increase in tumor incidence and multiplicity in the cecum and the proximal colon; they differed from murine intestinal tumors of the Apc1638N type which normally arise solely in the small intestine. We have examined by micro-array analysis three cecal tumors from these mice (probable adenomas), and compared them to three duodenal tumors (probable adenocarcinomas). Expression profiles of duodenal and cecal tumors relative to each other show unique gene subsets up and down regulated. The two tumor types were subsequently shown to differentially regulate distinct sets of genes over expressed in a majority of human colorectal carcinomas. Experiment Overall Design: We have compared 3 cecal tumors with 3 duodenal tumors from Rb1 deficient Apc1638N mice.
transcription profiling by array, unknown experiment type
Loss of Rb1 in the gastrointestinal tract of Apc1638N mice promotes tumors of the cecum and proximal colon. Melanie H Kucherlapati, Kan Yang, Kunhua Fan, Mari Kuraguchi, Dmitriy Sonkin, Andrew Rosulek, Martin Lipkin, Roderick T Bronson, Bruce J Aronow, Raju Kucherlapati.