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BACKGROUND

Colorectal cancer, for many years a prototypic model for the genetic basis of cancer, is now increasingly cited as an exemplar of the role of epigenetic changes in tumorigenesis. In part, this is because colorectal neoplasia provides a wide range of accessible lesions, from aberrant crypt foci to carcinoma. It also serves as a poster child for epigenetic change because of the possible role that DNA methylation has in the initiation and progression of this disease. For both these reasons, it provides an excellent opportunity to understand how epigenetics and genetics collude to produce malignancy.