APC and neoplasm: When mutations occur that increase levels of β-catenin in the cell and the nucleus [e.g inactivation of the negative regulator adenomatous polyposis coli (APC)], increased transcription of key tumor progression genes results, such as c-myc and cyclin D1, leading to abhorrent cell growth and ultimately tumorigenesis (Powell et al., 1992; Morin et al., 1997; He et al., 1998; Tetsu and McCormick, 1999; Henderson, 2000).