Oesophageal adenocarcinoma (OAC) is a devastating disease with an average 5-year survival of around 15%.1 Moreover, rates of OAC have increased substantially in recent decades, adding greatly to the clinical and economic burden of this disease.2

OAC arises out of a metaplastic precursor in which the normal squamous lining of the oesophagus is replaced with columnar, mucin-secreting cells. This is termed Barrett’s oesophagus (BO) and is thought to form as a protective mechanism in response to gastro-oesophageal reflux disease (GORD).

The cells that make up this oesophageal metaplasia can take several forms, roughly being broken down into gastric-type (GM) and intestinal-type (IM) metaplasias and are often composed of a mixture of differentiation cell types. GM should not be confused with IM of the stomach, which largely phenocopies oesophageal IM and also carries a risk of progression to adenocarcinoma. It has been suggested that in the majority of patients, BO develops from cells within the gastric cardia. This raises the possibility that GM may be the earliest metaplasia to form in the lower oesophagus.3 However, the exact relationship between GM and IM as well as the risk of progression in GM remains controversial. UK guidelines include GM in the definition of BO, whereas other countries require the presence of goblet cells (intestinal differentiation or IM) to meet the definition of BO. As IM can be highly patchy …