The well-recognised adenomacarcinoma sequence in the natural history of large bowel cancer suggests that this is a malignancy likely to be susceptible to screening. Detection and removal of precancerous adenomas and early invasive carcinomas should lead to a reduction in incidence and mortality respectively. Moreover the disease itself and the methods of testing for it fulfil many of the criteria required before implementation of a public health screening programme (Wilson & Jungner, 1968 Hardcastle, 1985).Another criterion for screening is that the natural history of the disease should be understood. This requirement is not fully met in the case of colorectal cancer or, for that matter, for any other malignant disease. Nevertheless it is known that at least some carcinomas of the large bowel develop within polypoid adenomas, and that increasing size of adenomas and a villous, as opposed to tubular, histology indicate increasing likelihood of malignancy (Morson, 1976). This implies a progression of epithelial changes of increasing severity over time. The great majority of adenomas, however, do not progress to malignancy, as shown by the prevalence of adenomas found at autopsy of people who died from other causes. One study (Vatn & Stalsberg, 1982) estimated that the autopsy prevalence of large bowel adenomas was ten times higher than the cumulative lifetime incidence of colorectal cancer. Little is known about the distribution of time from onset of adenoma to invasion in those adenomas that do progress. In a recent series of patients who developed carcinoma having previously had an untreated polyp, the cumulative risk of progression to cancer was 2.5% at 5 years, 8% at 10 years and 24% at 20 years (Stryker et al., 1987). Recent evidence on the molecular genetics of colorectal cancer also supports the adenomacarcinoma sequence, since mutation of the ras oncogene occurs in premalignant adenomas as well as colorectal carcinomas; it has been suggested that two later events in carcinogenesis, recessive changes on chromosomes 5 and 18, mark the transition from adenoma to carcinoma (Kerr, 1989).