Gastric dysplasia: an integrated classification of surface epithelium-derived precursor lesions.

Abstract

Gastric dysplasia comprises a heterogeneous group of non-invasive epithelial neoplasms with distinct clinicopathological and biological characteristics. This review focuses on surface epithelium-derived lesions, including intestinal-type, foveolar-type, and serrated dysplasia/adenoma. Conventional low-grade intestinal-type dysplasias/adenomas arise mainly in atrophic and metaplastic mucosa associated with Helicobacter pylori infection or, much less frequently, autoimmune gastritis. Small, pale, flat-elevated lesions with orderly small-intestinal differentiation generally behave indolently, whereas large size, redness, depression, nodularity, high-grade histology, and abnormal p53 expression are associated with an increased risk of progression. Foveolar-type dysplasia/adenoma is particularly heterogeneous. Flat-elevated foveolar-type adenoma, raspberry-type adenoma, and dysplasia arising in fundic gland polyps represent distinct dysplasia subtypes with indolent behavior. In contrast, other foveolar-type lesions are biologically heterogeneous; some are associated with microsatellite instability-high or Epstein-Barr virus-associated gastric carcinoma, whereas others may represent the superficial component of poorly differentiated or deceptively well-differentiated adenocarcinoma. Gastric serrated dysplasia is rare but is frequently associated with invasive carcinoma and should be regarded as a high-risk lesion requiring complete resection. Accurate diagnosis therefore requires integration of histological findings with endoscopic appearance and the background gastric mucosa. The principal role of pathological diagnosis is to distinguish dysplastic lesions with indolent behavior from those carrying a non-negligible risk of progression to invasive carcinoma, thereby guiding optimal clinical management.