Clinical pathological characteristics of 4 cases of gastric gland-derived tumors

Abstract

Objective: To investigate the pathological features of gastric tumor originated from the fundic gland, including oxyntic gland adenoma (OGA) and gastric adenocarcinoma of the fundic gland (GA-FG). Methods: A retrospective analysis of 2 cases of OGA and 2 cases of GA-FG admitted to our hospital from February 2019 to September 2019 was performed. The histological features were analyzed by immunohistochemical staining combined with endoscopic observation. Results: The four cases arose from the deep layer of the lamina propria mucosae and well differentiated. Two cases of OGA confined to the mucosa, including 1 case of irregular tubules showing low-degree dysplasia and another case of irregular branching and anastomosing tubules showing high-degree dysplasia. Two cases of GA-FG combined with submucosal invasion, showed irregular branching and anastomosing tubules and formed a so-called "endless glands" pattern. Atypia, helicobacter pylori (HP) infection, chronic gastritis, intestinal metaplasia, or gastric atrophy were not observed in the superficial epithelium covering the tumor extent. Two cases of OGA and 2 cases of GA-FG showed the same result of immunohistochemical staining: pepsinogen-1 was diffusely positive in the tumor tissues and indicated chief cell differentiation, while positive ATPase and PDGFRA-α indicated parietal cells differentiation. The expression of Syn were positive in all cases, while CD10, MUC2 and CD-X2 were negative. The upregulation of p53 protein or nuclear positivity of β-catenin was not observed. The Ki-67 labeling index in the hot area was approximately 1-5%. Conclusions: GA-FG is a well-differentiated, low-grade malignant novel subtype of gastric cancer. The immunohistochemical markers and narrowband imaging combined with magnifying endoscopy (NBI-ME) enhance the diagnostic sensitivity. Whether Syn positive expression can be one of the diagnostic item needs to be further investigate. The process of tumorigenesis of GA-FG might be the transition from low-grade dysplasia to high-grade dysplasia of OGA and further to submucosal infiltration. However, the mechanism of GAFG was still unclear. Disregulation of the Shh and Wnt/β-catenin signaling pathway might be associated with tumorigenesis of GA-FG. Endoscopic submucosal dissection (ESD) is often the preferred and curative treatment.