Truncation mutations in the adenomatous polyposis coli (APC) gene are responsible for familial and sporadic colorectal cancer.APC is a multifunctional protein involved in cell migration,proliferation and differentiation.The APC protein forms specific clusters in the cell periphery that correlate with sites of active cell migration.Little is known about the molecular mechanisms that govern these clusters.Here,we identify a novel interaction of an N-terminal region of APC with the extreme C-terminal 300 amino acids of APC and also with itself.