• 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.

• Journal of Yeungnam Medical Science
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• 제8권2호
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• pp.76-83
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• 1991

저자들은 최근 7년 10개월 동안 영남대학교 의과대학 병리학교실에서 위선종으로 진단된 위내시경 생검조직 48예, 53병변을 병리조직학적으로 재검토하여 아래와 같은 결론을 얻었다. 1) 환자의 평균 연령은 59세였으며, 51세이상이 40예(83%), 61세이상이 27예(56%)였고, 남녀비는 2.3 : 1로서 고연령층과 남자에게서 호발하였다. 2) 위선종의 발생부위는 전정부 33예(62%), 체부 19예(36%) 그리고 분문부 1예로서 전정부에 호발하였다. 3) 육안적인 형태는 Yamada type II가 29예(55%)로 가장 많았으며, 크기는 장경이 1cm미만이 41예(80%)로 대부분을 차지하였다. 4) 세포이형도와 위선종의 크기와의 관계는 알 수 없었다. 이는 내시경 생검조직만을 대상으로 하였기 때문으로 사료되며, 절제된 위조직을 포함한 연구가 필요할 것으로 사료되었다. 5) 53병변 모두에서 정도의 차이는 있지만 장형화생을 동반하고 있어, 위선종이 장형화생을 거쳐 발생된다고 사료되었다. 6) Grade III의 세포이형도를 보이는 6예 전부에서 Grimelius 및 Fontana-Masson 염색에 음성반응을 보였다. 7) 핵분열상은 세포이형도에 관계없이 비교적 흔히 관찰되었다. 8) 위선암종을 동반하고 있는 예는 5예(9.4%)로서, 평균연령은 61.4세였으며, 남녀비는 4 : 1로서 60세이상의 남자환자에서 위선종이 발견될 경우, 위선암종을 동반할 가능성이 많아 철저한 조사가 필요하리라 사료되었다. 9) 위선종과 위선암종과의 관계에 대한 연구는 위선종의 철저한 추적조사로서 보완 되어야 하리라 사료되었다.

• Applied Microscopy
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• 제11권1호
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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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• 제13권11호
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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.

• 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.

• 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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• 제14권3호
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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.

• 한국콘텐츠학회논문지
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• 제10권9호
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• pp.251-258
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• 2010

위절제술을 시행한 위암환자를 대상으로 수술 전 위치확인을 위한 위장조영검사의 영상을 분석하여 위암묘출의 정확도 및 한계성을 알아보고, 이에 따른 대응책을 알아보고자 하였다. 2007년 10월부터 2009년 4월까지 본원에 내원하여 병리조직학적으로 위암으로 확진되어 위절제술을 시행한 조기위암 환자 88명과 조기위암과 비슷한 진행성위암 환자 14명을 대상으로 하여, 수술 전 시행했던 위장조영검사와 수술 후 병리학적 소견을 비교분석하였으며, 영상분석은 10년 이상 근무한 방사선사 2명이 분석하였다. 위암환자 102명의 위절제 후 병리학적 위암위치와 비교를 통한 위장조영검사에서 위암의 발견율은 "확실" 81 예(79.4%), "실패" 21예(20.6%)로 판정되었다. "실패"로 판정된 21예의 위암형태는 IIb+IIc형이 2예(100%), IIb형이 5예(83.3%)로 발견율이 매우 낮았다. 위암의 전구병변인 장형화생은 위장조영검사에서 92예 (90.2%)의 발견율을 보였다. 위장조영검사의 한계점은 IIb형 및 1.0cm이하 미소위암의 발견이 어려웠다. 위암과 동반된 장형화생 92예(90.2%)의 발견은 위장조영검사에서 위암의 발견에 중요한 기준으로 평가된 다. 위장조영검사의 한계점을 극복하기 위해서는 부위에 맞는 정확한 촬영법 및 풍부한 방사선학적 경험을 통한 미세한 점막의 변화를 확인하는 촬영습관이 위암을 발견하는데 기여할 것으로 사료된다.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• 제11권sup1호
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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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• 제14권6호
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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.