• Korean Journal of Bronchoesophagology
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• v.17 no.1
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• pp.23-28
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• 2011

Diagnosis of early esophageal cancer has become more frequent as a result of improved endoscopic technology, surveillance programmes, and increasing experience and awareness on the part of endoscopists. In early esophageal cancer, squamous cell carcinoma and early adenocarcinoma must be managed differently because they have different origins, pathogenesis. and clinical characteristics. The current treatment options vary widely, from extended resection with lymphadenectomy to endoscopic mucosal resection (EMR) or ablation. None of these treatment options can be recommended universally. Instead, an individualized strategy should be based on the depth of tumor infiltration into the mucosa or submucosa, the presence or absence of lymph node metastases, the multicentricity of tumor growth, the length of the segment of intestinal metaplasia, and comorbidities of the patient. EMR has become increasingly important, both as a diagnostic tool for the staging of esophageal carcinomas and as a method of carrying out definitive treatment when the cancer meets certain criteria in which the risk of lymph-node metastasis is negligible. EMR may be sufficient in a subset of patients who have m1 or m2 squamous cell carcinoma and in patients who have isolated foci of high-grade intraepithelial neoplasia or mucosal cancer.

• The Korean journal of helicobacter and upper gastrointestinal research
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• v.18 no.4
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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.

• 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.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.6
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• pp.3931-3936
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• 2013

Background: Iran is a country with very high incidences of stomach cancer, especially in Northern parts. Here we assessed prognostic value of serum screening biomarkers among people >50 years old for early detection of precancerous lesions in a hot spot for gastric carcinoma in Guilan Province, North Iran. Methods: A cross-sectional population-based survey was conducted on 1,390 residents of Lashtenasha city with the mean age (SD) of 61.8 (9.02) years old (50.8% females) to assess the association of gastrin and the pepsinogen (PG) I/II ratio with premalignant gastric lesions. Blood samples were taken for CBC, blood group, and serologic exams (PGI, PGII, and gastrin 17) from each subject. Expert gastroenterologists performed upper GI endoscopy and ROC curves were generated to determine appropriate cutoff points. Results: Mean values of PGI, PGII, PGI/PGII and gastrin were significantly different between patients with and without atrophy or metaplasia (P<0.05). To diagnose atrophy and intestinal metaplasia, a significantly higher AUC was observed for the PGI/PGII ratio (70 and 72%, respectively) compared to the PGI (56, 55%), PGII (63, 64%) and gastrin (59, 61%) (all p<0.001). Conclusions: Biomarker tests such as the PGI/II ratio can be used in the screening and diagnosis of subjects at high gastric cancer risk in our region.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.5
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• pp.2555-2558
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• 2016

Background: Gastric cancer is the second most common gastrointestinal cancer and is still associated with significant morbidity and mortality due to late presentation and diagnosis at advanced stages. Studies have reported that a variable proportion of gastric cancer is positive for the human epidermal growth factor receptor 2 (HER2) and patients with HER2 positive (HER2 +ve) lesions can benefit from targeted therapy. This study was conducted to assess the prevalence of HER2 +ve gastric cancers in Brunei Darussalam, a developing Southeast Asian nation. Materials and Methods: Patients were identified from the Department of Pathology registry and retrospectively reviewed. HER2 expression was assessed by immunohistochemistry and only those staining 3+were considered positive. Results: Our study included 103 cases (66 males and 37 females) with a mean age of $65.1{\pm}14.8$ years old. There were 14 cases positive for HER2 (10 males and 4 females) giving a prevalence of 13.6%. The HER2 +ve cases were significantly older ($70.6{\pm}19.3$ years old) than the negative cases ($64.2{\pm}13.8$, p=0.041) and had significantly more advanced disease (stages 3 and 4, p=0.026). There were no significant differences in gender distribution, presence of intestinal metaplasia, EBV status, Helicobacter pylori status, tumor location (proximal vs. distal) and degree of tumor differentiation (all p values >0.05). Conclusions: Our study showed that 13.6% of our gastric cancers are positive for HER2, the affected patients being older and having more advanced disease at diagnosis.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.4
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• pp.987-992
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• 2008

This study was carried out to understand the macroscopic aspects of the digestive system symptoms occurring after taking oriental herb complex decoction as observing morphological changes in esophagus, stomach and duodenal bulb by endoscopy of upper gastrointestinal tract when these symptoms developed. The subjects of this study were 46 patients (male 22, female 24, mean age : $54.72{\pm}14.26$ years) who were chosen among ones who took oriental herb complex decoction for medical care and developed symptoms related to the gastrointestinal tract while taking an oriental herb decoction, which were assumed that the digestive symptoms were newly developed because of administration. The subjects were given morphological examination by endoscopy of the upper gastrointestinal tract. As a result of the endoscopy operated due to the digestive symptoms developed during the administration of oriental herb decoction, there were 2 cases of esophagitis, 5 cases of acute gastritis, 1 case of chronic gastritis A type, 15 cases of chronic gastritis B type, 1 case of duodenitis, 1 case of gastric ulcer, 1 case of gastric polyp, 2 cases of intestinal metaplasia, 1 case of gastric ptosis and 17 cases of normal findings which didn't have any abnormality macroscopically with endoscopy. With regards to the patients who complained of the digestive symptoms after taking oriental herb decoction, it has been found that the symptoms occurred as the oriental herbal medicine taken by the patients who had the digestive symptoms at ordinary times influenced on the gastrointestinal tract. Especially, many of them were had chronic gastritis and functional dyspepsia in the past. The disease accompanying macroscopic lesions at endoscopy which occurred due to the oriental herb decoction as direct cause, was acute gastritis, and it was the prescription to cure the pains and inflammations of skeletomuscular disease.

• 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.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.11 no.sup1
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• pp.83-92
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• 2008

Helicobacter pylori is the causative agent of chronic gastritis and has a role in the pathogenesis of peptic ulcer diseases, and gastric cancer. There have been reports suggesting a close link between these gastroduodenal disorders and a state of vitamin C deficiency. In this paper, the past, present and future perspectives on H. pylori infection and vitamin C will be discussed under the following view points. Since the ecological niche of H. pylori is the mucus layer and intercellular junctions of the gastric epithelium, the various kinds of host inflammatory cells motivated by the local and systemic immune responses cannot eliminate the microorganisms. When the invading foreign body is not removed, despite full activation of defense mechanisms, adverse consequences of the immune responses develop on the host gastric mucosa. The reasons for the body vitamin C depletion could be explained as follows; 1) the increased vitamin C consumption by increased oxygen free radical production through the prolonged hypersensitivity reactions in the gastric mucosa, 2) the increased vitamin C oxidation by the nitrite which is formed from nitrate reduction by the intragastric bacteria proliferated in the hypochlorhydric gastric cavity, 3) the strong ${\gamma}$-glutamyltranspeptidase activity of H. pylori which depletes the glutathiones in gastric mucosa. Depletion of glutathiones in the stomach favors irreversible oxidative destruction of ascorbic acid. Both persistent inflammatory burdens in the stomach by H. pylori and resultant vitamin C depletions synergistically and uninhibitedly might aggravate the hypothetical sequence of gastric carcinogenesis: atrophic gastritis${\rightarrow}$intestinal metaplasia${\rightarrow}$dysplasia${\rightarrow}$gastric adenocarcinoma. High intake of vitamin C could reverse the hypothetical sequence of the gastric carcinogenesis via direct and indirect effects on H. pylori and host-parasite relationships.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.3
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• pp.917-921
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• 2016

However, the incidence of gastric cancer (GC) has been decreased in past decades; GC is the second cause of cancer related death in the world. Evidence has illustrated that several factors including Helicobacter pylori (H. pylori) infection, host genetics, and environmental factors (smoking and particularly diet) may play a crucial role in gastric carcinogenesis. It has been demonstrated that high consumption of fresh fruits, vegetables, high level of selenium and zinc in drinking water, sufficient iron, and cholesterol protect against GC, while; smoked, pickled, and preserved foods in salt, and nitrites increase the risk of GC. Epidemiological studies have also proved that H. pylori infection and a high salt diet could independently induce atrophic gastritis and intestinal metaplasia. Recently, studies have been demonstrated that dietary factors directly influence H. pylori virulence. The use of appropriate diet could reduce levels of H. pylori colonization or virulence and prevent or delay development of peptic ulcers or gastric carcinoma. This is attractive from a number of perspectives including those of cost, treatment tolerability, and cultural acceptability. This review will describe new insights into the pathogenesis of H. pylori in relation to environmental factors, especially dietary, not only to find the developed means for preventing and treating GC, but also for understanding the role of chronic inflammation in the development of other malignancies.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6011-6016
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• 2012

Introduction: Epidemiological studies suggest a protective role for ${\beta}$-carotene with several malignancies. Esophageal adenocarcinoma frequently arises from Barrett's esophagus (BE). We postulated that ${\beta}$-carotene therapy maybe protective in BE. Materials and Method: We conducted a prospective study in which 25 mg of ${\beta}$-carotene was administered daily for six-months to six patients. Each patient underwent upper endoscopy before and after therapy and multiple mucosal biopsies were obtained. Additionally, patients completed a gastroesophageal reflux disease (GERD) symptoms questionnaire before and after therapy and severity score was calculated. To study the effect of ${\beta}$-carotene at molecular level, tissue extracts of the esophageal mucosal biopsy were subjected to assessment of heat-shock protein 70 (HSP70). Results: A significant (p<0.05) reduction in mean GERD symptoms severity score from $7.0{\pm}2.4$ to $2.7{\pm}1.7$ following ${\beta}$-carotene therapy was noted. Measurement of Barrett's segment also revealed a significant reduction in mean length after therapy. In fact, two patients had complete disappearance of intestinal metaplasia. Furthermore, marked enhancement of HSP70 expression was demonstrated in biopsy specimens from Barrett's epithelium in four cases that were tested. Conclusions: Long-term ${\beta}$-carotene therapy realizes amelioration of GERD symptoms along with restitution of the histological and molecular changes in esophageal mucosa of patients with BE, associated with concurrent increase in mucosal HSP70 expression.