Enterochromaffin‐like Cell Pathobiology of Mastomys
Enterochromaffin‐like Cell Pathobiology of Mastomys
复制标题
乳鼠肠嗜铬样细胞病理学
DOI:
10.1111/j.1749-6632.1994.tb17287.x
复制
发表时间:
1994
影响因子:
5.2
通讯作者:
C. Soroka
中科院分区:
文献类型:
--
作者:
I. Modlin;Laura H. Tang;G. Lawton;UMER M. Darr;Zhao;C. Soroka
Until recently, gastric neoplasia was regarded as predominantly adenocarcinoma in origin. Stromal tumors of unknown malignant potential were considered of interest, but rare. More recently, attention has been focused upon the development of neuroendocrine neoplasia of the gastric fundus.’ These lesions are predominantly of enterochromaffin cell, or enterochromaffin-like cell origin. Of particular interest are reports that enterochromaffin-like (ECLHerived tumor cells may be present in 40% of gastric carcinomas of the diffuse type.2 In general, it appears that there is a significant relationship between either low acid states or hypergastrinemia, and the genesis of fundic ECLomas.% The characterization of the cells involved in the neoplasm and the pathophysiology of the lesion itself are not yet clearly delineated. In order to investigate the biology of the enterochromaffin-like cell type, and the genesis of its neoplasia, we have studied the rodent species mastomys. This animal derives from the sub-Saharan desert areas and was initially used in the epidemiologic study of plague vectors. During these studies, it became apparent that a large percentage of the animals died from gastric neoplasia, which was later characterized as gastric carcinoid.’~~ More detailed studies revealed the tumor to be of ECL cell rig in.^ The lesion produces histamine and can be generated in association with hypergastrinemia related to a sustained low acid state. In previous studies, we have demonstrated that any pharmacotherapeutic agent capable of producing prolonged and sustained acid inhibition generates a sequence of hyperplasia, dysplasia, and neoplasia of the fundic ECL cells of mastornys.’&l2 In untreated animals of our breeding strain, 15-30% spontaneously develop gastric carcinoids within two years. Under circumstances of sustained acid inhibitory therapy, up to 80% of animals will develop gastric carcinoids within four months.’OIn order to investigate the regulatory mechanisms responsible for the development of this neoplastic phenomenon, we evaluated a number of agents with respect to their ability to induce ECL cell neoplasia. We used the irreversible histamine-H, receptor antagonist (H,RA), loxtidine, to generate a sustained low acid state. Because it was apparent that there was a predominant female incidence in the development of the neoplasia, we further
影响因子:
29.4
作者:
Prinz,C;Kajimura,M;Scott,DR;Mercier,F;Helander,HF;Sachs,G
通讯作者:
Sachs,G
影响因子:
3.8
作者:
Lewis,JJ;Goldenring,JR;Modlin,IM;Coffey,RJ
通讯作者:
Coffey,RJ