Neuroendocrine proliferation in the gastric mucosa: biological behaviour and management.

: Neuroendocrine proliferation of gastric mucosa is commonly encontered in routine gastric biopsies and is an indirect effect of modern drugs suppressing acid secretion. The process is virtually circumscribed to the ECL cell, the most common endocrine cell of the oxyntic mucosa, and is dependent on the trophic effect of the concomitant hypergastrinemia in most cases. It starts in the form of hyperplastic lesions that in some cases evolves into dysplasia and neoplasia. Gastrin has promoting but not transforming properties for such ECL cell tumour induction. Proven or potential transforming factors include the allelic loss of the MEN-1 suppressor gene at 11q13, the still unknown factor(s) associated with atrophic corporal gastritis in which overexpression of BCL-2 likely plays a favouring role by prolonging ECL exposure to mitogens, and agents with still unclarified role, such as basic fibroblast growth factor, human chorionic gonadotropin-alpha and transforming growth factor-alpha. Gastric neuroendocrine tumours independent of the trophic effect of gastrin are less frequent but more malignant. Their pathogenesis and precursor lesions are ignored.