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Pathogenesis of ECL cell tumors in humans Bordi C; D'Adda T; Azzoni C; Ferraro GYale J Biol Med 1998[May]; 71 (3-4): 273-84In ECL cell tumors developed in the setting of hypergastrinemic conditions (ECL cell carcinoids type 1 and 2), hypergastrinemia is the dominant agent acting as a promoter in all steps (hyperplasia-dysplasia-neoplasia) of the tumorigenic sequence. In contrast, it apparently lacks transforming properties as shown by the absence of ECL cell carcinoids in patients exposed to hypergastrinemia alone, i.e., those with sporadic Zollinger-Ellison syndrome. The potential transforming factors include: the allelic loss of the MEN-1 suppressor gene in the genetically predisposed MEN-1 patients, an alteration that may induce ECL cell tumors even in the absence of hypergastrinemia; the still unknown factor(s) associated with atrophic corporal gastritis; agents whose role in the induction of human ECL cell tumors is still unclarified, such as basic Fibroblast Growth Factor, human Chorionic Gonadotropin-alpha and Transforming Growth Factor-alpha; and agents having a favoring role on the ECL exposure to mitogens such as BCL-2. No information is currently available on the pathogenesis of gastrin-independent, sporadic ECL cell carcinoids (type 3) or of gastric neuroendocrine carcinomas.|Animals[MESH]|Carcinoid Tumor/epidemiology/*pathology[MESH]|Enterochromaffin-like Cells/*metabolism/*pathology[MESH]|Female[MESH]|Fibroblast Growth Factor 2[MESH]|Gastrins/metabolism[MESH]|Gastritis, Atrophic/pathology[MESH]|Glycoprotein Hormones, alpha Subunit/analysis/metabolism[MESH]|Humans[MESH]|Male[MESH]|Multiple Endocrine Neoplasia Type 1/genetics/pathology[MESH]|Proto-Oncogene Proteins c-bcl-2/metabolism[MESH]|Sex Characteristics[MESH]|Stomach Neoplasms/epidemiology/*pathology[MESH] |
