Taken together, through profiling with a first-generation mouse CGP panel and incorporation of synteny, our results support AK and AKP as high-fidelity models of the neoplastic progression of human colorectal carcinoma through biallelic Apc and Trp53 loss, shared loss of Smad4 during the transition from adenoma to adenocarcinoma, and conserved (syntenic) aneuploidy-based CN profiles. This evidence concerns the gene SMAD4 and adenocarcinoma.