Morphological, molecular, and prognostic aspects of gastric endocrine tumors

Microsc Res Tech. 2000 Mar 15;48(6):339-48. doi: 10.1002/(SICI)1097-0029(20000315)48:6<339::AID-JEMT4>3.0.CO;2-D.


This paper aims at describing the neuroendocrine cell growths of the gastric mucosa and their pathogenesis. In the corpus-fundus mucosa, gastric neuroendocrine nontumor growths are mostly represented by hyperplastic and, more rarely, dysplastic enterochromaffin-like (ECL) cell changes, while hyperplasia of gastrin-producing (G) cells and, rarely, of somatostatin-producing (D) cells are reported in the antral mucosa. The large majority of gastric neuroendocrine tumors is made by benign, gastrin-dependent, well-differentiated ECL cell growths arising in a background of chronic atrophic gastritis (type I) or, more rarely, associated with type I multiple endocrine neoplasia (MEN I) and Zollinger-Ellison (ZE) syndromes (type II). Rare, aggressive, frequently metastatic, well-differentiated gastric neuroendocrine tumors are gastrin-independent and arise as sporadic lesions in the absence of specific gastric pathology (type III). Poorly differentiated neuroendocrine carcinomas (PDEC) are rare, highly aggressive carcinomas. A central role for gastrin is postulated in the pathogenesis of well-differentiated type I and II ECL cell tumors with different possible genetic mechanisms. A more complex genetic background, independent of gastrin and possibly implicating altered function or mutation of p53 and other genes is highly suspected for the development of aggressive type III ECL cell carcinomas and PDECs.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Gastric Mucosa / pathology
  • Humans
  • Neuroendocrine Tumors / genetics
  • Neuroendocrine Tumors / mortality
  • Neuroendocrine Tumors / pathology*
  • Prognosis
  • Stomach Neoplasms / genetics
  • Stomach Neoplasms / mortality
  • Stomach Neoplasms / pathology*