Gastric carcinogenesis involves the loss of parietal cells (oxyntic atrophy) and subsequent
replacement of the normal gastric lineages with metaplastic cells. In humans, two
metaplastic lineages develop as sequelae of chronic Helicobacter pylori infection: intestinal
metaplasia and spasmolytic polypeptide-expressing metaplasia (SPEM). Mouse models of
both chronic Helicobacter infection and acute pharmacological oxyntic atrophy have led to
the discovery that SPEM arises from transdifferentiation of mature chief cells. The presence …