Because chromosomal and segmental aneuploidy has been described in a subset of MMR deficient adenocarcinomas [37],[38],[39], we performed array comparative genomic hybridization (aCGH) analyses of GI tumor vs. E18.5 C57BL/6 embryonic control DNA from Apc, MA, and MPA mice to identify specific genetic changes that accelerate MPA GI tumor progression. Here, APC is linked to digestive system neoplasm.