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神经内分泌细胞,尤其是D细胞,在残胃癌的发生发展中起作用吗?

Do neuroendocrine cells, particularly the D-cell, play a role in the development of gastric stump cancer?

作者信息

Waldum H L, Haugen O A, Brenna E

机构信息

Department of Medicine, University Hospital, Trondheim, Norway.

出版信息

Cancer Detect Prev. 1994;18(6):431-6.

PMID:7867015
Abstract

Previously, we have shown that a significant proportion of human gastric carcinomas of the diffuse type may be neuroendocrine tumors derived from the enterochromaffinlike (ECL) cell. The growth of the ECL cell is specifically regulated by gastrin, suggesting an important role of gastrin in human gastric carcinogenesis. However, patients with antral-resected stomachs have reduced plasma gastrin and despite that an increased risk of gastric cancer. Recently, it has been shown that gastrin has a negative trophic effect on the oxyntic D-cell of the rat. The present study evaluates whether gastric stump carcinomas are D-cell derived. Twenty gastric stump carcinomas that had developed from 20 to 53 years after antral resection were examined for neuroendocrine differentiation by neuron-specific enolase immunohistochemistry and for D-cell origin by somatostatin immunohistochemistry. Half the tumors were classified as gastric carcinomas of the intestinal type, while the other half initially was classified as gastric carcinomas of the diffuse type. One of these latter tumors could, however, be reclassified as carcinoid tumor by appearance in hematoxylin erythrosin saffron-stained sections as well as by neuron-specific enolase positivity. Interestingly, this tumor was also positive for somatostatin, suggesting D-cell origin. Three other tumors were positive for neuron-specific enolase, but they were negative for somatostatin. Nevertheless, this study suggests that some gastric stump carcinomas may be malignant neuroendocrine tumors derived from neuroendocrine cells and possibly from D-cells. Furthermore, this study may indicate an important role for hormones and neuroendocrine cells in human gastric carcinogenesis.

摘要

此前,我们已经表明,相当一部分弥漫型人类胃癌可能是源自肠嗜铬样(ECL)细胞的神经内分泌肿瘤。ECL细胞的生长受到胃泌素的特异性调节,这表明胃泌素在人类胃癌发生过程中发挥着重要作用。然而,胃窦切除患者的血浆胃泌素水平降低,尽管如此,其患胃癌的风险却增加。最近,研究表明胃泌素对大鼠胃壁细胞D细胞具有负性营养作用。本研究评估胃残端癌是否源自D细胞。对20例在胃窦切除术后20至53年发生的胃残端癌进行了检查,通过神经元特异性烯醇化酶免疫组织化学检测神经内分泌分化情况,通过生长抑素免疫组织化学检测D细胞起源。一半的肿瘤被归类为肠型胃癌,而另一半最初被归类为弥漫型胃癌。然而,其中一个后者肿瘤在苏木精伊红藏红染色切片中的外观以及神经元特异性烯醇化酶阳性情况可重新归类为类癌肿瘤。有趣的是,该肿瘤生长抑素也呈阳性,提示其起源于D细胞。另外三个肿瘤神经元特异性烯醇化酶呈阳性,但生长抑素呈阴性。尽管如此,本研究表明一些胃残端癌可能是源自神经内分泌细胞且可能源自D细胞的恶性神经内分泌肿瘤。此外,本研究可能表明激素和神经内分泌细胞在人类胃癌发生过程中发挥重要作用。

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