Gastric cancer remains one of the most common malignancies in the world.¹ The great majority of cases are fatal because the tumour has usually reached an incurable stage by the time of diagnosis.² The early potentially curable stage of the disease is usually asymptomatic and consequently patients mainly present when they have developed symptoms of advanced or complicated disease.^2,3 There is considerable interest in a means of detecting this common cancer at an early and curable stage.

In the Western world, the incidence of gastric cancer distal to the cardia has fallen over recent decades whereas that at the cardia and gastro-oesophageal junction has increased markedly.⁴ However, at a global level, non-cardia gastric cancer remains the predominant type and it is this which we are discussing.¹

Major advances have been made in our understanding of the aetiology and pathogenesis of non-cardia gastric cancer and of the precancerous changes which occur in the gastric mucosa. Helicobacter pylori infection is now accepted as an essential cofactor in the majority of cases of non-cardia gastric cancer.⁵ However, detecting the presence of the infection is, in itself, of limited value in predicting cancer occurrence; more than 50% of the world’s population have the infection and the lifetime risk of an infected individual developing the cancer is less than 2%.

Recent studies have indicated that the risk of a person with H pylori infection developing non-cardia gastric cancer is highly dependent on the pattern of gastritis and altered physiology which the infection induces in their stomach.⁶ In some patients, the infection induces an antral predominant non-atrophic gastritis associated with normal or high acid …