Gastrointestinal stem cells are considered pivotal in colonic carcinogenesi
s. There is evidence to suggest that early microadenomas in the colon are p
olyclonal in origin. Adenomas, once initiated, enlarge by the process of cr
ypt fission. It is also the main mechanism by which neoplastic clones sprea
d through the colorectal epithelium. Both concepts are important for our un
derstanding of the early events in colonic carcinogenesis.