Intestinal-type gastric adenocarcinoma evolves in a field of pre-existing metaplasia. Over the past 20 years, a number of murine models have been developed to address aspects of the physiology and pathophysiology of metaplasia induction. Although none of these models has achieved true recapitulation of the induction of adenocarcinoma, they have led to important insights into the factors that influence the induction and progression of metaplasia. Here, we review the pathologic definitions relevant to alterations in gastric corpus lineages and classification of metaplasia by specific lineage markers. In addition, we review present murine models of the induction and progression of spasmolytic polypeptide (TFF2)-expressing metaplasia, the predominant metaplastic lineage observed in murine models. These models provide a basis for the development of a broader understanding of the physiological and pathophysiological roles of metaplasia in the stomach.
Keywords: ATPase, adenosine triphosphatase; BMP, bone morphogenic protein; Chief Cell; EGF, epidermal growth factor; EGFR, epidermal growth factor receptor; Gastric Cancer; Hip1r, Huntington interacting protein 1 related; Hyperplasia; IFN, interferon; Intestinal Metaplasia; MUC, mucin; SDF1, stromal-derived factor 1; SPEM; SPEM, spasmolytic polypeptide–expressing metaplasia; TFF, trefoil factor; TFF2; TGF, transforming growth factor; Tg, transgene; Th, T-helper.