非1/2型胃神经内分泌肿瘤（G-NETs）的发病机制尚不清楚。本研究旨在研究G-NETs的临床病理特征及相关黏膜变化。回顾电子病历中非1/2型G-NETs患者的资料。对病理特征和黏膜变化进行H&E染色片复查。t检验和Fisher精确检验用于统计学分析。共有33名患者被分配到1组（n = 23）或2组（n = 10）。组1包括有质子泵抑制剂（PPI）使用史、胃泌素水平增高或明显PPI效应（PPI / 胃泌素相关）的患者。所有其他患者分配到第2组。两组之间的年龄和性别没有显著差异。第2组肿瘤更可能更大、更深入侵和发生转移（P＜0.05）。肝硬化患者的肿瘤倾向于更大。周围肿瘤黏膜的变化包括失去泌素腺、浅表部分增生和肠化生。组1患者的背景黏膜显示出PPI效应和神经内分泌增生或异型增生。尽管PPI /胃泌素相关的非1/2型G-NETs比典型的3型 G-NETs更小、更缓慢，但肝硬化患者的肿瘤往往更大。此外，周围肿瘤黏膜的变化可能模仿慢性萎缩性胃炎。©作者（S）2023年。由牛津大学出版社代表美国临床病理学会出版。版权所有。有关权限，请发送电子邮件：journals.permissions@oup.com。

The pathogenesis for non-type 1/2 gastric neuroendocrine tumors (G-NETs) remains unclear. The aim of this study was to examine the clinicopathologic features of G-NETs and associated mucosal changes.The electronic health records of patients with non-type 1/2 G-NETs were reviewed. H&E slides were reviewed for pathologic features and mucosal changes. The t test and Fisher exact test were used for statistical analysis.In total, 33 patients were assigned to either group 1 (n = 23) or group 2 (n = 10). Group 1 included patients with a history of proton pump inhibitor (PPI) use, increased gastrin levels, or significant PPI effect (PPI/gastrin-associated). All other patients were assigned to group 2. There was no significant difference in age and sex between the 2 groups. Group 2 tumors were more likely to be larger, invade deeper, and develop metastases (P < .05). Tumors in patients with cirrhosis tended to be larger. Peritumoral mucosal changes included loss of oxyntic glands, foveolar hyperplasia, and intestinal metaplasia. Background mucosa in group 1 patients showed PPI effect and neuroendocrine hyperplasia or dysplasia.Although PPI/gastrin-associated non-type 1/2 G-NETs were smaller and more indolent than typical type 3 G-NETs, tumors in patients with cirrhosis tended to be larger. Additionally, peritumoral mucosal changes could mimic chronic atrophic gastritis.© The Author(s) 2023. Published by Oxford University Press on behalf of American Society for Clinical Pathology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.