Barrett’s oesophagus (BO) is an acquired premaligant condition that is the only known precursor to oesophageal adenocarcinoma (OA); a malignancy whose incidence has risen steadily in the Western world in the last 20–30 years.¹ The lifetime risk of developing an adenocarcinoma in the context of BO is 2–5%,² and despite recent advances in its treatment the associated morbidity and mortality remain high.³ BO advances through a series of morphological stages: from metaplasia through dysplasia of different grades and finally to adenocarcinoma—the metaplasia-dysplasia-adenocarcinoma sequence (MCS).^4,5 Although this genetic process is not as well outlined as in the colon,⁴ it is thought to be a similar multistep process consisting of genetic and epigenetic mutations, involving the same or a similar group of genes, which over many years leads to increasing genomic instability and ultimately to the formation of an autonomous clone of cells with invasive and metastatic properties.⁵

Knowledge of the natural history of the adenoma:carcinoma sequence in the colon has translated to clinical medicine, prompting the removal of adenomatous polyps at the premalignant stage, with an associated reduction in the incidence of colorectal cancer.^6,7 Regrettably, thus far, such gains have not been made in dysplasia in the context of BO, with the effectiveness of current surveillance strategies yet to be conclusively proven; a matter soon to be addressed by the BOSS (Barrett’s Oesophagus Surveillance Study), a study integrated with the AspECT (Aspirin and Esomprazole Chemoprevention Trial of Cancer in Barrett’s Oesophagus) (7500 patients in total).⁸ At present, a patient with BO can only be risk stratified on the basis of either …