Taken together, these cross-species results further support Smad4 as potential target of chr 18 loss in the adenoma to colorectal carcinoma transition and highlight how synteny must be considered in cross-species analyses of aneuploidy, given the differing genomic arrangement of two of the most frequently altered TSGs (Apc and Smad4) in human colorectal carcinoma. This evidence concerns the gene SMAD4 and adenoma.