• Applied Microscopy
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• v.11 no.1
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• pp.21-28
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• 1981

Gastric xanthoma which is not a true neoplasm and clinically insignificant consists of the small yellowish lesion of the gastric mucosa, frequently of multiple occurrence. Histologically the lesion shows chronic superficial gastritis with intestinal metaplasia and occasional collections of foam cells within the lamina propria. Electron microscopically. the xanthoma, cells are composed of. lipid-laden histiocytes with. many autophagocytic Iysosomes surrounding the cytoplasmic lipid vacuoles. Many residual bodies are also noted. The pathogenesis of the gastric xanthoma is obscure, however it is thought that a previous focal lesion of the gastric mucosa may have been a factor. One case of gastric xanthoma is reported here and a brief review of literature is also made.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.7
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• pp.3437-3441
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• 2012

Background: Oncogenic Bmi-1 (B-lymphoma Moloney murine leukemia virus insertion region-1) belongs to the Polycomb-group (PcG) family of proteins and plays an important role in the regulation of proliferation, senescence, cell cycle and apoptosis, chromosome stability, activation of gene transcription. Methods: To clarify the roles of Bmi-1 in tumourigenesis and progression of gastric carcinomas, it was examined by immunohistochemistry (IHC) and real-time RT-PCR in gastric carcinomas, dysplasia, intestinal metaplasia (IM), and gastritis with a comparison of its expression with clinicopathological parameters of carcinomas. Results: There was gradually increased Bmi-1 protein expression from gastritis, IM, dyplasia to carcinoma (p<0.001). Bmi-1 expression was positively linked to tumor size, depth of invasion, lymph node metastasis and worse prognosis of carcinomas (p<0.001), but not to age or sex of carcinoma patients (p>0.05). There was higher Bmi-1 protein expression in intestinal-type carcinomas than diffuse-type ones (p<0.001). At mRNA level, Bmi-1 protein expression was increased from gastritis, IM, dysplasia and carcinoma (p<0.001). Bmi-1 overexpression was observed in gastric carcinoma with larger diameter, deeper invasion, lymph node metastasis, and intestinal-type carcinoma (p<0.05). Conclusion: These findings indicate that up-regulated Bmi-1 expression is positively linked to pathogenesis, growth, invasion, metastasis and differentiation of gastric carcinomas. It was considered as a promising marker to indicate the aggressive behaviors and prognosis of gastric carcinomas.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.4
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• pp.1571-1574
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• 2015

Background: Treatment of Helicobacter pylori (H. pylori) decreases the prevalence of gastric cancer, and may inhibit gastric precancerous lesions progression into gastric cancer. The aim of this study was to determine the effect of treatment on subsequent gastric precancerous lesion development. Materials and Methods: We prospectively studied 27 patients who had low grade dysplasia at the time of enrollment, in addition to dysplasia atrophic gastritis and intestinal metaplasia observed in all patients. All were prescribed quadruple therapy to treat H. Pylori infection for 10 days. Patients underwent endoscopy with biopsy at enrollment and then at follow up two years later. Biopsy samples included five biopsies from the antrum of lesser curvature, antrum of greater curvature, angularis, body of stomach and fundus. Results of these biopsies were compared before and after treatment. Results: Overall, the successful eradication rate after two years was 15/27 (55.6%). After antibiotic therapy, the number of patients with low grade dysplasia decreased significantly (p=0.03), also with reduction of the atrophic lesions (p=0.01), but not metaplasia. Conclusions: Treatment of H. pylori likely is an effective therapy in preventing the development of subsequent gastric premalignant lesions.

• Journal of Digestive Cancer Research
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• v.12 no.1
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• pp.6-14
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• 2024

Gastric cancer is the 4th leading cause of death worldwide. The primary cause of gastric cancer is known to be Helicobacter pylori (H. pylori). The advancement of molecular biology has enabled the identification of microbiomes that could not be confirmed through cultivation, and it has been revealed that the microbial communities vary among normal mucosa, atrophic gastritis, intestinal metaplasia, and gastric cancer. It has also been confirmed that the composition of the microbial community differs depending on the presence or absence of H. pylori. Whether changes in the microbiome are causative factors in the carcinogenesis process is not yet clear. Experiments using animal models and in vitro studies on the role of microbes other than H. pylori in the carcinogenic process are underway, but the data is still insufficient.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5691-5694
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• 2012

Ectopic expression of CDX2 in the stomach is closely associated with chronic Helicobacter pylori (H. pylori) infection and intestinal metaplasia. Whether CDX2 has tumor suppression or tumorigenesis potential remains to be elucidated. In this study, we investigated the association between the CDX2 G543C polymorphism (silent mutation) and the risk for H. pylori-induced gastric atrophy and cancer as well as H. pylori infection, using 454 Japanese subjects undergoing a health checkup and 202 gastric cancer patients. The frequency of the minor allele was the same as previously reported in China, but different from that reported in England. CDX2 G543C was not associated with risk of H. pylori infection, gastric atrophy, or gastric cancer, although the point estimate for non-cardiac differentiated gastric cancer as compared to controls with gastric atrophy was 2.22 (95%CI=0.17-29.4). In conclusion, our results indicate that the CDX2 G543C polymorphism is unlikely to affect the H. pylori infection-gastric atrophy-gastric cancer sequence.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.9
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• pp.5199-5205
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• 2013

Background/Aim: The Hippo signaling pathway is a newly discovered and conserved signaling cascade, which regulates organ size control by governing cell proliferation and apoptosis. This study aimed to investigate its effects in human gastric cancer. Methods: Tumor tissues (n=60), adjacent non-tumor tissues (n=60) and normal tissues (n=60) were obtained from the same patients with primary gastric cancer (GC). In addition, 70 samples of chronic atrophic gastritis (CAG) tissues were obtained from patients with intestinal metaplasia (IM) by endoscopic biopsy. Hippo signaling molecules, including Mst1, Lats1, YAP1, TAZ, TEAD1, Oct4 and CDX2, were determined by quantitative polymerase chain reaction (qPCR). Protein expression of Mst1, Lats1, YAP1, TEAD1 and CDX2 was assessed by immunohistochemistry and Western blotting. Results: Mst1, Lats1 and Oct4 mRNA expression showed an increasing tendency from GC tissues to normal gastric tissues, while the mRNA expression of YAP1, TAZ and TEAD1 was up-regulated (all P<0.01). Mst1 and Lats1 protein expression presented a similar trend with their mRNA expression. In addition, YAP1 and TEAD1 protein expression in GC was significantly higher than in the other groups (all P<0.01). CDX2 mRNA and protein expression in the CAG group were higher than in the other groups (all P<0.01). In GC, mRNA expression of Mst1, Lats1, Oct4, YAP1, TAZ, TEAD1 and CDX2 had a close correlation with lymphatic metastasis and tumor TNM stage (all P<0.01). Furthermore, protein expression of Mst1, Lats1, YAP1, TAZ, TEAD1 and CDX2 had a close correlation between each other (P<0.05). Conclusion: The Hippo signaling pathway is involved in the development, progression and metastasis of human gastric cancer. Therefore, manipulation of Hippo signaling molecules may be a potential therapeutic strategy for gastric cancer.

• The Journal of the Korea Contents Association
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• v.10 no.9
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• pp.251-258
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• 2010

Despite significant advance in laparoscopy, upper gastrointestinal (UGI) series is still generally carried out for preoperative localization of gastrectomy. The aim of the study was to compare the accuracy of UGI series and postoperative pathological findings in the diagnosis and localization of gastric cancer. A retrospective review was carried out for 102 patients who underwent gastrectomy between October 2007 and April 2009. Preoperative reports of UGI series were compared with postoperative pathology reports and the accuracy of the preoperative reports was calculated. Two radiographer retrospectively reviewed the analysis of UGI series. postoperative pathology reports of the surgical specimens, were compared with the preoperative reports of the location and extent of the tumor were correct in 81 case("sure", 79.4%) and incorrect in 21 case("failed, 20.6%). In 92 case UGI series revealed intestinal metaplasia (90.2%) at consensus review and these results demonstrate the limitation of the UGI series in the diagnosis of type IIb gastric cancer with size less than 1.0cm and the poor detection of gastric cancer is that the overlying mucous membrane often appears to be normal in these patients. In conclusion, UGI series is accurate the detection of the tumor localization and diagnosis of intestinal metaplasia. However, for the overcome with the limitation of UGI series should be used accurate technique for the region of the stomach. To achieve this goal, it is necessary to determine the changes of the mucus membrane of the stomach and UGI series is gaining acceptance as a standard method for preoperative gastric cancer screening.

• Journal of Gastric Cancer
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• v.1 no.1
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• pp.4-9
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• 2001

Purpose: The trefoil factor family 1 (TFF1) has a protective effect against gastric mucosal damage induced by nonsteroidal anti-inflammatory drugs or ethanol. In addition, a TFF1 knockout mouse model has exhibited circumferential adenomas with high-grade dysplasia, of which $30\%$ progressed into frankly invasive carcinomas. We tried to determine whether the expression pattern of the TFF1 could be involved in the development of sporadic gastric carcinomas. Materials and Methods: We examined TFF1 expression in a series of 43 sporadic gastric carcinomas and 18 gastric adenomas by immunohistochemistry. Results: Strong positive TFF1 staining was identified primarily in the normal gastric mucosa, mainly in the cytoplasm of the superficial and foveolar epithelium. We found TFF1 expression in $55.8\%$ (24 out of 43) of the gastric carcinomas and in $16.7\%$ (3 out of 18) of the gastric adenomas. Statistically, TFF1 immunoreactivity was significantly higher in diffuse-type ($82.4\%$) than in intestinal-type ($38.5\%$) carcinomas(p=0.0058, Fisher's exact test). Conclusion: Our findings provide sufficient evidence that the expression of TFF1 in gastric cancer may simply disclose gastric-type differentiation of neoplastic cells and provide further support for the existence of at least two pathways of malignant transformation of the gastric mucosa: one via intestinal metaplasia and adenomatous dysplasia, leading to glandular carcinomas with intestinal-type differentiation, and the other via hyperplastic changes or de novo changes, leading to diffuse carcinomas and to a subset of glandular carcinomas displaying gastric-type differentiation.

• Parasites, Hosts and Diseases
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• v.41 no.1
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• pp.63-67
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• 2003

A 69-year-old Korean man was admitted to emergency room with complaints of abdominal pain, vomiting, and diarrhea, Laboratory tests revealed eosinophilia, anemia, hypoproteinemia, and hyponatremia. The gastric mucosa showed whitish mottled and slightly elevated lesions on the body angle of antrum. Microscopically, chronic gastritis with incomplete intestinal metaplasia was observed. Many adult worms, larvae, and eggs in cross sections were located in the crypts. Furthermore, the filariform larvae of Strongyloides stercoralis with a notched tail were detected through the culture.

• Journal of Gastric Cancer
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• v.14 no.3
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• pp.147-155
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• 2014

Homeostatic imbalance between cell proliferation and death in gastric mucosal epithelia may lead to gastritis and gastric cancer. Despite abundant gastrokine 1 (GKN1) expression in the normal stomach, the loss of GKN1 expression is frequently detected in gastric mucosa infected with Helicobacter pylori, as well as in intestinal metaplasia and gastric cancer tissues, suggesting that GKN1 plays an important role in gastric mucosal defense, and the gene functions as a gastric tumor suppressor. In the stomach, GKN1 is involved in gastric mucosal inflammation by regulating cytokine production, the nuclear factor-${\kappa}B$ signaling pathway, and cyclooxygenase-2 expression. GKN1 also inhibits the carcinogenic potential of H. pylori protein CagA by binding to it, and up-regulates antioxidant enzymes. In addition, GKN1 reduces cell viability, proliferation, and colony formation by inhibiting cell cycle progression and epigenetic modification by down-regulating the expression levels of DNMT1 and EZH2, and DNMT1 activity, and inducing apoptosis through the death receptor-dependent pathway. Furthermore, GKN1 also inhibits gastric cancer cell invasion and metastasis via coordinated regulation of epithelial mesenchymal transition-related protein expression, reactive oxygen species production, and PI3K/Akt signaling pathway activation. Although the modes of action of GKN1 have not been clearly described, recent limited evidence suggests that GKN1 acts as a gastricspecific tumor suppressor. This review aims to discuss, comment, and summarize the recent progress in the understanding of the role of GKN1 in gastric cancer development and progression.