Enterochromaffin‐like Cell Pathobiology of Mastomys
Enterochromaffin‐like Cell Pathobiology of Mastomys
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乳鼠肠嗜铬样细胞病理学
DOI：
10.1111/j.1749-6632.1994.tb17287.x
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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
直到最近，胃肿瘤仍被认为主要是起源于腺癌。未知恶性潜能的间质瘤被认为是有趣的，但很少见。最近，人们的注意力集中在胃底神经内分泌肿瘤的发展上。这些病变主要是肠嗜铬细胞或肠嗜铬样细胞起源的。特别令人感兴趣的是，有报道称肠嗜铬样（ECL继承性肿瘤细胞）可能存在于 40% 的弥漫型胃癌中。2 一般而言，低酸状态或高胃泌素血症与胃底 ECLomas 的发生之间似乎存在显着关系。% 参与肿瘤的细胞的特征和病变本身的病理生理学尚未明确描述。肠嗜铬样细胞类型及其肿瘤的起源，我们研究了来自撒哈拉以南沙漠地区的啮齿类动物，最初用于鼠疫媒介的流行病学研究，在这些研究中，很明显，很大一部分动物死于胃肿瘤，后来被定性为胃类癌。’~~更详细的研究表明，该肿瘤是 ECL 细胞的肿瘤。^ 病变产生组胺和组织胺。在之前的研究中，我们已经证明，任何能够产生长期和持续的酸抑制的药物治疗剂都会导致乳腺胃底 ECL 细胞的一系列增生、发育不良和肿瘤形成。 在我们的饲养品系中，未经治疗的动物中，15-30% 在持续酸抑制治疗的情况下，高达 80% 的动物会自发产生胃类癌。动物将在四个月内患上胃类癌。为了研究导致这种肿瘤现象发生的调节机制，我们评估了多种药物诱导 ECL 细胞肿瘤形成的能力。我们使用不可逆组胺 H 受体拮抗剂（H，RA）洛西替丁来产生持续的低酸状态，因为很明显女性在肿瘤形成过程中发病率占主导地位，因此我们进一步研究了这种肿瘤形成的机制。
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
大鼠肠嗜铬样细胞分泌组胺。
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
通过转化生长因子 α 抑制壁细胞 H 分泌：一种可能的自分泌调节机制。
影响因子：
3.8
作者：
Lewis,JJ;Goldenring,JR;Modlin,IM;Coffey,RJ
通讯作者：
Coffey,RJ