title: Praomys (Mastomys) natalensis: a model for gastric carcinoid formation.
abstract: The gastric carcinoid tumors of Praomys (Mastomys) natalensis have been reviewed with respect to histogenesis, development, biochemistry, and morphological properties. Multicentric gastric carcinoids frequently develop in the oxyntic mucosa of aging Mastomys. The development of these tumors can be significantly enhanced by drug-induced hypergastrinemia, e.g., histamine2-receptor blockade. Spontaneous and drug-induced gastric carcinoids are endocrine in nature, as evidenced by their argyrophilic staining properties and chromogranin A content. They are also rich in histidine decarboxylase activity and produce large amounts of histamine, although other hormones, such as peptide YY and enteroglucagon, have also been demonstrated in these tumors. Ultrastructurally, gastric carcinoids are composed of tumor cells with typical secretory granules resembling those of enterochromaffin-like (ECL) cells. A close examination of the gastric carcinoids in Mastomys reveals striking similarities with gastric carcinoids developing in humans suffering from chronic atrophic gastritis type A or from the Zollinger-Ellison syndrome in combination with multiple endocrine neoplasia type 1 (MEN-1). Both these conditions are associated with hypergastrinemia and a higher risk for developing multi-centric gastric carcinoids of ECL-cell origin. The Mastomys tumor model therefore appears to be a significant experimental model in which induction and formation of gastric carcinoid tumors can be studied.
authors.affiliation: Department of Histology, University of Göteborg, Sweden.
authors.forename: O
authors.initials: O
authors.lastname: Nilsson
authors.forename: B
authors.initials: B
authors.lastname: Wängberg
authors.forename: L
authors.initials: L
authors.lastname: Johansson
authors.forename: I M
authors.initials: IM
authors.lastname: Modlin
authors.forename: H
authors.initials: H
authors.lastname: Ahlman
mesh_terms: D000818:Animals; D002276:Carcinoid Tumor / Q000209:etiology / Q000473:pathology*; D002471:Cell Transformation, Neoplastic / Q000473:pathology*; D004195:Disease Models, Animal; D006801:Humans; D009115:Muridae; D013274:Stomach Neoplasms / Q000209:etiology / Q000473:pathology*