Barrett's adenocarcinoma (BA) has seen a rapid increase in incidence throughout the Western world. The diagnosis of BA is often at an advanced stage and is generally associated with a poor prognosis and a mean survival of less than one year. Adenocarcinomas however do not arise de novo but follow an established sequence from Barrett's metaplasia (BM) through dysplasia to neoplasia.

Efforts to intervene in the pathogenesis of oesophageal adenocarcinomas have so far been disappointing. Reduction of gastro-oesophageal reflux disease has led to minimal regression of BM and has yet to be shown to have any impact on cancer prevention. Surveillance programmes for patients with BM have had variable results and have raised important questions about their cost effectiveness and of better risk stratification of patients with BM. The prevalence of BM in the general population is approximately 1–3%, with only 0.5–1% of patients with BM converting to neoplasia each year.1 ,2 The reliable diagnoses of intestinal metaplasia and dysplasia have also been difficult to validate in each patient, mostly related to sampling errors due to the variable anatomy of the lower oesophagus and their patchy distribution within a segment of BM.

Our understanding of the molecular biology of BM has yielded many phenotypic and genetic changes …