Morphological, molecular, and prognostic aspects of gastric endocrine tumors

This paper aims at describing the neuroendocrine cell growths of the gastri c mucosa and their pathogenesis. In the corpus-fundus mucosa, gastric neuro endocrine nontumor growths are mostly represented by hyperplastic and, more rarely, dysplastic enterochromaffin-like (ECL) cell changes, while hyperpl asia 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-differenti ated ECL cell growths arising in a background of chronic atrophic gastritis (type I) or, more rarely, associated with type I multiple endocrine neopla sia (MEN I) and Zollinger-Ellison (ZE) syndromes (type II). Rare, aggressiv e, frequently metastatic, well-differentiated gastric neuroendocrine tumors are gastrin-independent and arise as sporadic lesions in the absence of sp ecific gastric pathology (type III). Poorly differentiated neuroendocrine c arcinomas (PDEC) are rare, highly aggressive carcinomas. A central role for gastrin is postulated in the pathogenesis of well-differentiated type I an d II ECL cell tumors with different possible genetic mechanisms. A more com plex genetic background, independent of gastrin and possibly implicating al tered function or mutation of p53 and other genes is highly suspected for t he development of aggressive type III ECL cell carcinomas and PDECs. (C) 20 00 Wiley-Liss, Inc.