Background: Although E-cadherins have been involved in gastric carcinogenesis, their role in precancerous lesions, such as intestinal metaplasia, is still unclear. This study aimed to assess the role of both intestinal metaplasia and H. pylori infection on E-cadherin expression in gastric mucosa.
Patients And Methods: Twenty-one consecutive patients with intestinal metaplasia were enrolled to assess E-cadherin expression in metaplastic areas. Twenty further patients without intestinal metaplasia, with and without H. pylori, were enrolled to evaluate the role of the infection on E-cadherin expression. All patients underwent upper endoscopy and gastric biopsies were taken for histological and immunohistochemical assessment.
Results: A substantial reduction of E-cadherin expression in metaplastic areas was observed in 14 (67%) of the 21 patients, similarly in H. pylori-infected and uninfected patients (64% vs 71%, p=0.3). In the group without intestinal metaplasia, no reduction in E-cadherin expression was detected either in infected patients or in those without H. pylori infection.
Conclusion: The data showed that intestinal metaplasia is associated with E-cadherin down-regulation, whereas H. pylori infection does not seem to play a direct role in this process.
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Biomimetics (Basel)
December 2024
Institute of New Frontier Research, Hallym University College of Medicine, Chuncheon 24253, Republic of Korea.
Objective: We previously developed artificial intelligence (AI) diagnosis algorithms for predicting the six classes of stomach lesions. However, this required significant computational resources. The incorporation of AI into medical devices has evolved from centralized models to decentralized edge computing devices.
View Article and Find Full Text PDFAm J Clin Pathol
December 2024
Department of Pathology and Laboratory Medicine, Emory University Hospital, Atlanta, GA, US.
Objectives: Atrophic gastritis (AG) is characterized by atrophy of gastric glands-in particular, oxyntic glands-in the setting of chronic inflammation; it is often autoimmune. The diagnosis is confirmed by immunohistochemistry (IHC) for gastrin (to confirm biopsy site), and pathologists often use IHC for neuroendocrine markers to evaluate for enterochromaffin-like cell hyperplasia (ECL-H). The utility of neuroendocrine staining is unclear, and we undertook this study to determine whether ECL pattern provided any additional information in cases of Helicobacter-negative AG.
View Article and Find Full Text PDFGastroenterology
December 2024
Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Palo Alto, California.
Description: Gastric cancer (GC) is a leading cause of preventable cancer and mortality in certain US populations. The most impactful way to reduce GC mortality is via primary prevention, namely Helicobacter pylori eradication, and secondary prevention, namely endoscopic screening and surveillance of precancerous conditions, such as gastric intestinal metaplasia (GIM). An emerging body of evidence supports the possible impact of these strategies on GC incidence and mortality in identifiable high-risk populations in the United States.
View Article and Find Full Text PDFEur J Med Res
December 2024
Department of Gastrointestinal Surgery, Shandong Provincial Hospital, Shandong University, Jinan, 250021, Shandong, China.
The gut microbiota is a complex and dynamic ecosystem that plays a crucial role in human health and disease, including obesity, diabetes, cardiovascular diseases, neurodegenerative diseases, inflammatory bowel disease, and cancer. Chronic inflammation is a common feature of these diseases and is closely related to angiogenesis (the process of forming new blood vessels), which is often dysregulated in pathological conditions. Inflammation potentially acts as a central mediator.
View Article and Find Full Text PDFStem Cell Res Ther
December 2024
Department of General Surgery, Geriatric Hospital of Nanjing Medical University, Nanjing, 210000, China.
Background: Chronic atrophic gastritis (CAG) is a chronic disease of the gastric mucosa characterized by a reduction or an absolute disappearance of the original gastric glands, possibly replaced by pseudopyloric fibrosis, intestinal metaplasia, or fibrosis. CAG develops progressively into intestinal epithelial metaplasia, dysplasia, and ultimately, gastric cancer. Epidemiological statistics have revealed a positive correlation between the incidence of CAG and age.
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