Next, to visualize the changes of higher-order heterochromatin structure in carcinogenesis, we used a well-established mouse model of intestinal tumorigenesis—ApcMin/+ mice where a mutation in adenomatous polyposis coli (Apc) causes spontaneous development of multiple intestinal neoplasia (Min) and closely mimics familial adenomatous polyposis in human colorectal neoplasia24. This evidence concerns the gene APC and Familial adenomatous polyposis.