Chief cell proliferation of the gastric mucosa mimicking early gastric cancer: an unusual variant of fundic gland polyp

Abstract Background and study aims Magnifying endoscopy with narrow band imaging (M-NBI) has made a huge contribution to endoscopic diagnosis of early gastric cancer (EGC). However, we sometimes encountered false-negative cases with M-NBI diagnosis (i. e., M-NBI diagnostic limitation lesion: M-NBI-DLL). However, clinicopathological features of M-NBI-DLLs have not been well elucidated. We aimed to clarify the clinicopathological features and histological reasons of M-NBI-DLLs. Patients and methods In this single-center retrospective study, M-NBI-DLLs were extracted from 456 EGCs resected endoscopically at our hospital. We defined histological types of M-NBI-DLLs and analyzed clinicopathologically to clarify histological reasons of M-NBI-DLLs. Results Of 456 EGCs, 48 lesions (10.5 %) of M-NBI-DLLs were enrolled. M-NBI-DLLs was classified into four histological types as follows: gastric adenocarcinoma of fundic-gland type (GA-FG, n = 25), gastric adenocarcinoma of fundic-gland mucosal type (GA-FGM, n = 1), differentiated adenocarcinoma (n = 14), and undifferentiated adenocarcinoma (n = 8). Thirty-nine lesions of M-NBI-DLLs were H. pylori-negative gastric cancers (39/47, 82.9 %). Histological reasons for M-NBI-DLLs were as follows: 1) completely covered with non-neoplastic mucosa (25/25 GA-FG, 8/8 undifferentiated adenocarcinoma); 2) well-differentiated adenocarcinoma with low-grade atypia (1/1 GA-FGM, 14/14 differentiated adenocarcinoma); 3) similarity of surface structure (10/14 differentiated adenocarcinoma); and 4) partially covered and/or mixed with a non-neoplastic mucosa (1/1 GA-FGM, 6/14 differentiated adenocarcinoma). Conclusions Diagnostic limitations of M-NBI depend on four distinct histological characteristics. For accurate diagnosis of M-NBI-DLLs, it may be necessary to fully understand endoscopic features of these lesions using white light imaging and M-NBI based on these histological characteristics and to take a precise biopsy.

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SPORADIC FUNDIC GLAND POLYP-RELATED ADENOMAS OCCURRED IN NON-ATROPHIC GASTRIC MUCOSA WITHOUT HELICOBACTER PYLORI INFECTION

Digestive Endoscopy ◽

10.1111/j.1443-1661.2010.01082.x ◽

2011 ◽

Vol 23 (2) ◽

pp. 182-186 ◽

Cited By ~ 3

Author(s):

Shuhei Tazaki ◽

Fumihiko Nozu ◽

Nozomi Yosikawa ◽

Michio Imawari ◽

Naoto Suzuki ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Helicobacter Pylori Infection ◽

Fundic Gland ◽

Fundic Gland Polyp

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ATP4B suppresses cell proliferation and migration via mitochondrial/p53/NF-κB pathway in gastric cancer

10.21203/rs.3.rs-15787/v1 ◽

2020 ◽

Author(s):

Yuanming Pan ◽

Yuqi He ◽

Shuye Lin ◽

Min Zhu ◽

Yangjie Li ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Proliferation ◽

Gastric Mucosa ◽

Tumor Model ◽

Suppressor Gene ◽

Mitochondrial Pathway ◽

Loss Of Function ◽

Normal Tissues ◽

And Migration ◽

Induced Apoptosis

Abstract Background: Hydrogen/Potassium ATPase β (ATP4B) is a key protein in gastric mucosa barrier acting an essential role in gastric acid secretion. However, the exact role and precise mechanism of ATP4B in gastric cancer (GC) remain obscure. This study aimed to investigate the clinical significance of ATP4B in GC and its biological role in tumor progression.Methods: We evaluated ATP4B expression in GC cell lines and patient specimens via qPCR and Immunofluorescence. The correlations between ATP4B expression level and clinicopathologic parameters, as well as the relevance of ATP4B expression with overall survival were assessed. The functional roles of ATP4B in GC were verified by gain- and loss-of-function cell models and xenograft tumor model. The possible downstream effects of ATP4B were analyzed by iTRAQ‑based quantitative proteomics analysis.Results: A dramatic decrease of ATP4B expression in GC cells and tissues compared with the adjacent normal tissues was observed; Downexpression of ATP4B was associated with the malignant transformation in gastric mucosa lesions and correlated with poor prognosis, high grade of TNM stage, and vessel carcinoma embolus in GC patients. Restoration of ATP4B expression in GC cells significantly inhibited cell proliferation, cell viability, migration, invasion, tumorigenicity and induced apoptosis, whereas ATP4B silencing exerted the opposite effects. Mechanistically, we found a constitutive activation of p53 and inactivation of NF-κB signaling correlated with the mitochondrial pathway in ATP4B-overexpressing GC cells.Conclusion: Our data suggest that ATP4B perform the promising tumor suppressor gene by regulating p53/NF-κB/mitochondrial pathway in GC.

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