Gastric dysplasia causing gastric outlet obstruction

Gastric dysplasia signifies the presence of atypical cells in the gastric mucosa, which have not invaded beyond the lamina propria, and it rarely leads to tissue growth large enough to cause gastric outlet obstruction (GOO) to the gastric contents. However, GOO is commonly observed as a first clinical manifestation of advanced invasive gastric cancer in developing countries where patients seek medical care late. The present case highlights the treatment journey of a young woman who presented to us with features of GOO. Her endoscopic and radiological findings revealed a nodular gastric antral thickening causing GOO. An endoscopic biopsy showed features of dysplasia. She underwent distal gastrectomy following discussion in a multidisciplinary tumour board. Histopathological examination of the gastrectomy specimen confirmed dysplasia without any invasion beyond lamina. To the best of our knowledge, this is perhaps the first report of dysplasia of the stomach presenting as GOO.

Effects of orally administered Euglena gracilis and its reserve polysaccharide, paramylon, on gastric dysplasia in A4gnt knockout mice

Euglena gracilis is widely utilized as food or supplement to promote human and animal health, as it contains rich nutrients. In this study, we administered spray-dried powder of E. gracilis and paramylon, β-glucan stored in E. gracilis cells, to A4gnt knockout (KO) mice. A4gnt KO mice are a mutant mouse model that spontaneously develops gastric cancer through hyperplasia-dysplasia-adenocarcinoma sequence in the antrum of the stomach, and we observed the effects of E. gracilis and paramylon on the early involvements of A4gnt KO mice. Male and female 10-week-old A4gnt KO mice and their age-matched wildtype C57BL/6J mice were orally administered with 50 mg of E. gracilis or paramylon suspended in saline or saline as a control. After 3-week administration, animals were euthanatized and the stomach was examined histopathologically and immunohistochemically. Gene expression patterns of the stomach, which have been reported to be altered with A4gnt KO, and IgA concentration in small intestine were also analyzed with real-time PCR and ELISA, respectively. Administration of Euglena significantly reduced the number of stimulated CD3-positive T-lymphocytes in pyloric mucosa of A4gnt KO mice and tend to reduce polymorphonuclear leukocytes infiltration. Euglena administration further downregulated the expression of Il11 and Cxcl1 of A4gnt KO mice. Euglena administration also affected IgA concentration in small intestinal contents of A4gnt KO mice. Paramylon administration reduced the number of CD3-positive lymphocytes in pyloric mucosa of A4gnt KO mice, and downregulated the expressions of Il11 and Ccl2 of A4gnt KO mice. Although we found no significant effects on gross and microscopic signs of gastric dysplasia and cell proliferation, the present study suggests that the administration of Euglena and paramylon may ameliorate the early involvements of A4gnt mice through the effects on inflammatory reactions in the gastric mucosa. The cancer-preventing effects should be studied with long-term experiments until actual gastric cancer formation.

Molecular Alterations in Gastric Preneoplastic Lesions and Early Gastric Cancer

Prognosis of gastric cancer is dramatically improved by early diagnosis. Correa’s cascade correlates the expression of some molecular markers with the progression of preneoplastic lesions toward carcinoma. This article reviews the diagnostic and prognostic values of molecular markers in complete (MUC2) and incomplete (MUC2, MUC5AC, and MUC6) intestinal metaplasia, gastric dysplasia/intra-epithelial neoplasia, and early gastric cancer. In particular, considering preinvasive neoplasia and early gastric cancer, some studies have demonstrated a correlation between molecular alterations and prognosis, for example, mucins phenotype in gastric dysplasia, and GATA6, TP53 mutation/LOH and MUC6 in early gastric cancer. Moreover, this review considers novelties from the literature regarding the (immuno)histochemical characterization of diffuse-type/signet ring cell gastric cancer, with particular attention to clinical outcomes of patients. The aim of this review is the evaluation of the state of the art regarding suitable biomarkers used in the pre-surgical phase, which can distinguish patients with different prognoses and help decide the best therapeutic strategy.

Hsp60 Quantification in Human Gastric Mucosa Shows Differences between Pathologies with Various Degrees of Proliferation and Malignancy Grade

Background: Stomach diseases are an important sector of gastroenterology, including proliferative benign; premalignant; and malignant pathologies of the gastric mucosa, such as gastritis, hyperplastic polyps, metaplasia, dysplasia, and adenocarcinoma. There are data showing quantitative changes in chaperone system (CS) components in inflammatory pathologies and tumorigenesis, but their roles are poorly understood, and information pertaining to the stomach is scarce. Here, we report our findings on one CS component, the chaperone Hsp60, which we studied first considering its essential functions inside and outside mitochondria. Methods: We performed immunohistochemical experiments for Hsp60 in different samples of gastric mucosa. Results: The data obtained by quantitative analysis showed that the average percentages of Hsp60 were of 32.8 in normal mucosa; 33.5 in mild-to-moderate gastritis; 51.8 in severe gastritis; 58.5 in hyperplastic polyps; 67.0 in intestinal metaplasia; 89.4 in gastric dysplasia; and 92.5 in adenocarcinomas. Noteworthy were: (i) the difference between dysplasia and adenocarcinoma with the other pathologies; (ii) the progressive increase in Hsp60 from gastritis to hyperplastic polyp, gastric dysplasia, and gastric carcinoma; and (iii) the correlation of Hsp60 levels with histological patterns of cell proliferation and, especially, with tissue malignancy grades. Conclusions: This trend likely reflects the mounting need for cells for Hsp60 as they progress toward malignancy and is a useful indicator in differential diagnosis, as well as the call for research on the mechanisms underpinning the increase in Hsp60 and its possible roles in carcinogenesis.