Background/aims: Epithelial gastric dysplasia is considered the only true marker of gastric cancer. High-grade dysplasia is a surgical therapy needing lesion and low-grade dysplasia is considered a lesion with a low oncologic risk. The aim of this experience was to verify whether there are any immunohistochemical evaluations which may enable one to foresee more precisely the evolution of epithelial gastric dysplasia.
Methodology: Immunophenotypic evaluation was effected in 70 cases of low-grade dysplasia (41 males, average age: 57.4) and in 50 cases of high-grade dysplasia (31 males, average age: 58). These cases were retrospectively selected and the studied samples are represented by gastric biopsies obtained in the course of endoscopy performed for dyspepsia. Epithelial gastric dysplasia diagnosis was done according to Goldstein and Lewin and the clinical subdivision was effected using the criteria of Rugge et al. Four antigens were studied using Abs against pepsinogen C, gastric foveolar M1, intestinal CAR-5 and pancreatic DU-PAN-2 Ags.
Results: Epithelial gastric dysplasia is characterized by a progressive reduction of gastric markers with a progressive expression of enteropancreatic antigens. Low-grade dysplasia is characterized by a frequent gastro-enteropancreatic coexpression, and high-grade dysplasia by a frequent enteropancreatic coexpression or by no markers expression. Low-grade dysplasia with greater enteropancreatic markers progresses frequently towards gastric cancer; high-grade dysplasia with enteropancreatic markers only is associated/progresses to gastric cancer, while high-grade dysplasia with gastric markers or gastric-enteropancreatic markers is included in the group with persistent or regressed cases.
Conclusions: If confirmed in further studies, such results could modify the evaluation of epithelial gastric dysplasia, not only in terms of histochemical techniques, but also of immunohistochemical techniques.
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Cancer Metastasis Rev
January 2025
Wallenberg Centre for Molecular Medicine (WCMM), Linköping University, Linköping, Sweden.
FOXQ1 is a member of the large forkhead box (FOX) family of transcription factors that is involved in all aspects of mammalian development, physiology, and pathobiology. FOXQ1 has emerged as a major regulator of epithelial-to-mesenchymal transition and tumour metastasis in cancers, especially carcinomas of the digestive tract. Accordingly, FOXQ1 induction is recognised as an independent prognostic factor for worse overall survival in several types of cancer, including gastric and colorectal cancer.
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Unit of Surgical Oncology, Department of Medicine Surgery and Neuroscience, University of Siena, Viale Mario Bracci 16, 53100, Siena, Italy.
Epithelial-to-mesenchymal transition (EMT) is a biological process by which epithelial cells increase their motility and acquire invasive capacity. It represents a crucial driver of cancer metastasis and peritoneal dissemination. EMT plasticity, with cells exhibiting hybrid epithelial/mesenchymal states, and its reverse process, mesenchymal-to-epithelial transition (MET), allows them to adapt to different microenvironments and evade therapeutic intervention.
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Laboratory of Veterinary Anatomy, Tokyo University of Agriculture and Technology, Tokyo, Japan.
The red-eared sliders (Emydidae: Trachemys scripta) is characterised by a high adaptability to a variety of environment and threatens the habitat of Japanese native species. The ability to digest a variety of diets may attribute to the high adaptive capacity of this species to various environments, however, the digestive morphology remains scarcely described in red-eared sliders. In this study, we investigated the macro- and microscopic anatomy of the esophagus, stomach, small intestine, and large intestine in red-eared sliders.
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Department of Physiology, School of Medicine, Showa University, Tokyo, 142, Japan.
Microorganisms
December 2024
State Key Laboratory of Food Science and Resources, Nanchang University, No. 235 Nanjing East Road, Nanchang 330047, China.
(), one of the most prevalent pathogenic bacteria worldwide, is the leading cause of gastritis, gastric intestinal metaplasia, and gastric cancer. Antibiotics, the conventional treatment for eliminating , often lead to severe bacterial resistance, gut dysbiosis, and hepatic insufficiency and fail to address the inflammatory response or gastric mucosal damage caused by infection. In this study, based on 10-week animal experiments, two models of NCUH062003 for the prophylaxis and therapy of infection in C57BL/6 mice were established; a comprehensive comparative analysis was performed to investigate the anti- effect of probiotics, the reduction in inflammation, and repair of gastric mucosal damage.
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