• Asian Pacific Journal of Cancer Prevention
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• 제17권5호
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• pp.2719-2722
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• 2016

Circulatory miR-133a is a marker shared by several types of cancer. In this study we evaluated the feasibility of using miR-133a levels in gastric juice to screen for gastric cancer. A total of 204 samples of gastric juice and mucosa from gastric cancer, atrophic gastritis, gastric ulcer, superficial gastritis and healthy cases were collected by gastroscopy. The results showed that miR-133a levels in gastric juice and carcinoma tissues of patients with gastric cancer were significantly downregulated and positively correlated. Moreover, miR-133a in gastric juice has high operability, high reliability, high sensitivity, high specificity and relative stability, fit for clinical diagnosis of gastric cancer.

• Journal of Gastric Cancer
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• 제2권2호
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• pp.73-80
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• 2002

In spite the fact that H. pylori infection might be the causative organisms of acute and chronic gastritis, peptic ulcer diseases and the definition as the class I carcinogen by WHO IARC, still debates exist about the relationship between H. pylori and gastric carcinogenesis. Epidemiological and animal studies demonstrated a link between gastric cancer and chronic infection with H, pylori, but the exact mechanism responsible for the development of gastric cancer in H. pylori-infected patients still remain obscure. In order to declare the clear association, definate evidences like that decrement in the incidence of gastric cancer after the eradication of H. pylori in designated area compared to noneradicated region or the blockade of specific mechanism acting on the carcinogenesis by H. pylori infection. The other way is to identify the upregulating oncogenes or downregulating tumor suppressor genes specifically invovled in H. pylori-associated carcinogenesis. For that, we established the animal models using C57BL/6 mice strain. Already gastric carcinogenesis was developed in Mongolian gerbils infected with H. pylori, but there has been no development of gastric cancer in mice model infected with H. pylori after long-term evaluation. Significant changes such as atrophic gastritis were observed in mice model. However, we could observe the development of mucosal carcinoma in the stomach of transgenic mice featuring the loss of TGF-beta sig naling by the expressions of dominant negative forms of type II receptor specifically in the stomach. Moreover, the incidence of gastric adenocarcinoma was significantly increased in group administered with both MNU and H. pylori infection than MNU alone, signifying that H. pylori promoted the gastric carcinogenesis and there might be host susceptibility genes in H. pylori-associated gastric carcinogenesis. Based on the assumption that chronic, uncontrolled inflammation might predispose to carcinogenesis, there have been several evidences showing chronic atrophic gastritis predisposed to gastric carcinogenesis in H. pylori infection. Although definite outcome of chemoprevention was not drawn after the longterm administration of anti-inflammatory drug in H. pylori infection, the actual incidence of atrophic gastritis and molecular evidence of chemoprevention could be obtained. Selective COX-2 inhibitor was effective in decreasing the development of gastric carcinogenesis provoked by H. pylori infection and carcinogen like in chemoprevention of colon carcinogenesis.

• Journal of Digestive Cancer Research
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• 제10권1호
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• pp.9-15
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• 2022

Proton pump inhibitors (PPIs), a potent gastric acid inhibitor, are widely used in gastric acid-related diseases such as gastroesophageal reflux disease and peptic ulcer, and are known as the most frequently used drugs worldwide. However, as the frequency of use increases, the number of cases of long-term PPI therapy without clear indications is increasing. Recently, there have been concerns about the risk of gastric cancer in patients with long-term PPI users. Potential mechanisms for the association between PPI and gastric cancer include enterochromaffin-like cell proliferation due to hypergastrinemia caused by gastric acid suppression, progression of atrophic gastritis, and corpus-predominant type through interaction with Helicobacter pylori (H. pylori) infection. Several epidemiologic studies showed controversial results on the issue, and it is difficult to prove a causal relationship between PPI and gastric cancer. Nevertheless, long-term PPI should be administered cautiously based on individual risk-benefit profile, specifically among those with history of H. pylori infection, in high-risk region of gastric cancer.

• Journal of Digestive Cancer Research
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• 제12권1호
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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.

• The Korean Journal of Nuclear Medicine
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• 제39권6호
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• pp.456-463
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• 2005

Purpose: we often find variable degrees of FDG uptake and patterns in stomach, which can make difficult to distinguish physiologic uptake from pathologic uptake on FDG PET. The purpose of this study was to find out the significant findings of stomach on FDG PET. Materials and Methods: Thirty-eight patients who underwent both FDG PET and endoscopy within one week from Jun. 2003, to Aug. 2004 were included in this study. We reviewed 38 patients (18 for medical check up, 15 for work up of other malignancies, and 5 for the evaluation of stomach lesion). Their mean age was 56 years old (range:$32{\sim}79$), men and women were 28 and 10, respectively. Two nuclear physicians evaluated five parameters on FDG PET findings of stomach with a consensus: 1) visual grades 2) maximum SUV (max.SUV) 3) focal 4) diffuse and S) asymmetric patterns. We correlated the lesions of FDG PET findings of stomach with those of endoscopy. We considered more than equivocal findings on FDG PET as positive. Results: The six of 38 patients were proven as malignant lesions by endoscopic biopsy and others were inflammatory lesions (ulcer in 3, chronic atrophic gastritis in 12, uncommon forms of gastritis in 5), non-inflammatory lesions (n=3), and normal stomach (n=9). By the visual analysis, malignant lesions had higher FDG uptake than the others. The max.SUV of malignant lesions was $7.95{\pm}4.83$ which was significantly higher than the other benign lesions ($2.9{\pm}0.69$ in ulcer, $3.08{\pm}1.2$ in chronic atrophic gastritis, $3.2{\pm}1.49$ in uncommon forms of gastritis (p=0.044)). In the appearance of stomach on FDG PET, malignant lesions were shown focal (5 of 6) and benign inflammatory lesions were shown diffuse (9 of 20) and asymmetric (14 of 20). Benign lesions and normal stomach were shown variable degrees of uptake and patterns. Some cases of benign inflammatory lesions such as ulcer and gastritis were shown focal and mimicked cancerous lesion (4 of 15). Conclusion: Gastric malignant lesions had higher FDG uptake and focal pattern. However, benign inflammatory lesions had moderate degrees of uptake and diffuse and asymmetric patterns rather than focal. It is difficult to differentiate between benign lesions including normal.

• The Korean journal of helicobacter and upper gastrointestinal research
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• 제18권4호
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• pp.247-257
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• 2018

Background/Aims: The aim of this study was to analyze the trend of the prevalences of atrophic gastritis (AG) and intestinal metaplasia (IM) from 2011 to 2016~2017 in Korea. And, the risk factors of AG and IM were compared between 2011 and 2016~2017. Materials and Methods: A total of 4,023 subjects in 2011 and 2,506 subjects in 2016~2017 were enrolled. AG and IM were diagnosed on the basis of endoscopic findings. Multivariate analysis was performed for risk factors of AG and IM. Seventeen factors were analyzed. Results: The seroprevalence of Helicobacter pylori decreased from 2011 (59.8%; 2,407/4,023) to 2016~2017 (51.6%; 1,293/2,506; P<0.001). The prevalence of AG decreased from 2011 to 2016~2017 (P=0.018), but that of IM increased (P<0.001). The risk factors of AG in 2011 were male sex, old age, H. pylori immuoglobulin G (IgG) positivity, family history of gastric cancer (GC), and high-salt diet. For IM in 2011, the risk factors were male sex, old age, H. pylori IgG positivity, and family history of GC. Risk factors of AG in 2016~2017 were old age, H. pylori IgG positivity, and country of residence. For IM in 2016~2017, the risk factors were male sex, old age, family history of GC, high fasting glucose level (${\geq}126mg/dL$), H. pylori IgG positivity, and low income level. Conclusions: The difference in prevalence trends of AG and IM between 2016~2017 and 2011 could be the result of the different risk factors of AG and IM, such as decreased prevalence of H. pylori infection.

• Asian Pacific Journal of Cancer Prevention
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• 제14권9호
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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.

• Journal of Gastric Cancer
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• 제5권3호
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• pp.158-162
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• 2005

Purpose: In order to clarify the carcinogenesis mechanism from chronic atrophic gastritis toward gastric cancer, we measured the pepsinogen I and II and compared their ratio with several clinical findings. Materials and Methods: We measured the preoperative serum pepsinogen I and II by using a radio-immunoassay and compared their ratio with several clinical findings, such as tumor size, mucinous vs non-mucinous tumor, cell differentiation, tumor location, depth of invasion, lymph-node status, Lauren's classification, and peritumoral atrophy in 103 consecutive patients with gastric adenocarcinomas who had received resections at Bundang CHA Hospital during the period from July 2003 to February 2005. Results: There were significant differences in the serum pepsinogen I/II ratio between patients with mucinous vs non-mucinous tumors (n=4 vs 9 and mean pep I/II=1.29 vs. 2.99, p=0.0288), with tumor size more than and less than $10cm^2$ (n=55 vs. 48 and mean pep I/II=2.64 vs. 3.24, p=0.0491), and with or without peritumoral atrophy (n=94 vs. 9 and mean pep I/II=2.83 vs. 3.89, p=0.0466). In patients with peritomoral atrophy, the pepsinogen I/II ratio was also lower in larger tumors (n=48 vs. 46 and mean pep I/II=2.44 vs. 3.23, p=0.0083). Well-differentiated carcinomas showed significantly lower serum pep I/II ratios than signet-ring-ceil types. There was no correlation between serum pep I/II ratio and tumor location, depth of invasion, lymph-node status, or Lauren's classification Conclusion: We proved the existence of a correlation between serum pepsinogen level and musosal atrophy, but these results are not sufficient for clinical application of serum pepsinogen level as a screening tool for gastric cancer.

• Journal of Digestive Cancer Reports
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• 제8권2호
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• pp.81-90
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• 2020

We performed a comprehensive meta-analysis on whether Helicobacter pylori (H. pylori) eradication can prevent gastric cancer in individuals with precancerous lesions (chronic atrophic gastritis, intestinal metaplasia, and dysplasia). The studies evaluating the effect of H. pylori eradication on gastric cancer were searched from PubMed, KoreaMed, EMBASE, and Cochrane Library. Subgroup analyses by precancerous lesions, regions and follow-up time were performed. Six randomized clinical trials were included. In the overall population, H. pylori eradication significantly decreased the risk of gastric cancer (risk ratio [RR]=0.56; 95% confidence interval [CI]: 0.41-0.77, p<0.01). Eradication therapy significantly reduced the risk of gastric cancer in Asian and group who followed up more than 10 years (RR=0.51; 95% CI: 0.35-0.73, p<0.01; I²=0%, p=0.46). However, subgroup analysis according to the precancerous lesions did not show any significant results (p>0.05). In the general population especially in Asian population, H. pylori eradication can reduce the risk of gastric cancer. The effect of the eradication treatment is remarkable upon the long-term follow-up. In contrast, there is insufficient evidence whether the eradication should be recommended for the individuals with precancerous lesions.

• Asian Pacific Journal of Cancer Prevention
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• 제16권4호
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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.