• Journal of Digestive Cancer Reports
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• 제7권2호
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• pp.31-39
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• 2019

The early detection of early gastric cancer (EGC) is important. However, the sensitivity of conventional white light imaging (WLI) in detecting EGC had been reported to range only from 77% to 84%. Although the resolution of endoscopes has been remarkably developed, precancerous lesions such as adenomas and microscopic early cancers are difficult to diagnose with general endoscopy. Linked Color Imaging (LCI) magnifies the differences in color for easy detection. Therefore, it produces a bright image from a distance and is performed for screening endoscopy. The 410 nm wavelength of BLI (Blue Light Imaging) helps to detect cancer by showing microstructure and microvessels in the mucosal superficial layer. This review will focus on the utility of Image enhanced endoscopy (IEE) techniques in diagnosis of gastrointestinal cancer.

• Journal of Gastric Cancer
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• 제1권3호
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• pp.129-135
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• 2001

Purpose: Dysplasia or flat adenoma of the stomach is regarded as a precancerous lesion. However, the frequency and the evolutionary process of malignant transformation of gastric dysplasia are still debated. In order to see whether the lesion was a monoclonal or a polyclonal proliferation, clonality was assayed by X-linked HUMARA polymorphism. Materials and Methods: DNA was extracted from the paraffin-embedded tissue of 16 consecutive cases of endoscopic biopsy, eight of which supplied both dysplastic and nondysplastic tissue for comparison. HUMARA was amplified by PCR with or without pretreatment with methylationsensitive restriction enzyme, HpaII. The amplification products were electrophoresed on polyacrylamide gel and silver-stained. Results: Among the 16 cases, 13 cases were informative and 3 cases noninformative. Of the 13 cases, one case showed skewed lyonization, rendering 12 cases to be analyzed further. A monoclonal band pattern was noted in 2 cases, and a polyclonal band pattern in 10 cases. A review of the histopathologies of the monoclonal and the polyclonal cases did not reveal features discriminating the two groups. Conclusion: These results suggest that gastric dysplasia is a disease entity heterogeneous in the genetic level, and many cases may be non-neoplastic.

• Asian Pacific Journal of Cancer Prevention
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• 제13권4호
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• pp.1407-1412
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• 2012

Background & Objectives: Gastric cancer is a leading cause of cancer-related deaths in both sexes in Iran. This study was designed to assess upper GI endoscopic findings among people > 50 years targeted in a mass screening program in a hot-point region. Methods: Based on the pilot results in Guilan Cancer Registry study (GCRS), one of the high point regions for GC-Lashtenesha- was selected. The target population was called mainly using two methods: in rural regions, by house-house direct referral and in urban areas using public media. Upper GI endoscopy was performed by trained endoscopists. All participants underwent biopsies for rapid urea test (RUT) from the antrum and also further biopsies from five defined points of stomach for detection of precancerous lesions. In cases of visible gross lesions, more diagnostic biopsies were taken and submitted for histopathologic evaluation. Results: Of 1,394 initial participants, finally 1,382 persons (702 women, 680 men) with a mean age of $61.7{\pm}9.0$ years (range: 50-87 years) underwent upper GI endoscopy. H. pylori infection based on the RUT was positive in 66.6%. Gastric adenocarcinoma and squamous cell carcinoma of esophagus were detected in seven (0.5%) and one (0.07%) persons, respectively. A remarkable proportion of studied participants were found to have esophageal hiatal hernia (38.4%). Asymptomatic gastric masses found in 1.1% (15) of cases which were mostly located in antrum (33.3%), cardia (20.0%) and prepyloric area (20.0%). Gastric and duodenal ulcers were found in 5.9% (82) and 6.9% (96) of the screened population. Conclusion: Upper endoscopy screening is an effective technique for early detection of GC especially in high risk populations. Further studies are required to evaluate cost effectiveness, cost benefit and mortality and morbidity of this method among high and moderate risk population before recommending this method for the GC surveillance program at the national level.

• BMB Reports
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• 제36권1호
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• pp.82-94
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• 2003

Although debates still exist whether Helicobacter pylori infection is really class I carcinogen or not, H. pylori has been known to provoke precancerous lesions like gastric adenoma and chronic atrophic gastritis with intestinal metaplasia as well as gastric cancer. Chronic persistent, uncontrolled gastric inflammations are possible basis for ensuing gastric carcinogenesis and H. pylori infection increased COX-2 expressions, which might be the one of the mechanisms leading to gastric cancer. To know the implication of long-term treatment of antiinflammatory drugs, rebamipide or nimesulide, on H. pylori-associated gastric carcinogenesis, we infected C57BL/6 mice with H. pylori, especially after MNU administration to promote carcinogenesis and the effects of the long-term administration of rebamipide or nimesulide were evaluated. C57BL/6 mice were sacrificed 50 weeks after H. pylori infection. Colonization rates of H. pylori, degree of gastric inflammation and other pathological changes including atrophic gastritis and metaplasia, serum levels and mRNA transcripts of various mouse cytokines and chemokines, and NF-${\kappa}B$ binding activities, and finally the presence of gastric adenocarcinoma were compared between H. pylori infected group (HP), and H. pylori infected group administered with long-term rebamipide containing pellet diets (HPR) or nimesulide mixed pellets (HPN). Gastric mucosal expressions of ICAM-1, HCAM, MMP, and transcriptional regulations of NF-${\kappa}B$ binding were all significantly decreased in HPR group than in HP group. Multi-probe RNase protection assay showed the significantly decreased mRNA levels of apoptosis related genes and various cytokines genes like IFN-$\gamma$, RANTES, TNF-$\alpha$, TNFR p75, IL-$1{\beta}$ in HPR group. In the experiment designed to provoke gastric cancer through MNU treatment with H. pylori infection, the incidence of gastric carcinoma was not changed between HP and HPR group, but significantly decreased in HPN group, suggesting the chemoprevention of H. pylori-associated gastric carcinogenesis by COX-2 inhibition. Long-term administration of antiinflammatory drugs should be considered in the treatment of H. pylori since they showed the molecular and biologic advantages with possible chemopreventive effect against H. pylori-associated gastric carcinogenesis. If the final concrete proof showing the causal relationship between H. pylori infection and gastric carcinogenesis could be obtained, that will shed new light on chemoprevention of gastric cancer, that is, that gastric/cancer could be prevented through either the eradication of H. pylori or lessening the inflammation provoked by H. pylori infection in high risk group.

• 한국식생활문화학회지
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• 제5권1호
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• pp.169-180
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• 1990

MNNG 투여에 의한 백서 위십이지장암 발생에 있어서 우유의 영향을 조사하고 그 원인을 분석키 위해 조직학적 및 혈청학적 분석을 시도하였다. 실험군은 생후 8주 전후의 Sprague-Dawley 백서 136마리로서 일반사료만 준 대조군 20마리(제 1군)와 6% 우유사료만 준 군 20마리(제 2군), MNNG$(100\;{\mu}g/ml)$ 투여군 24마리(제 3군), MNNG 및 6% 우유사료군 24마리(제 4군), MNNG 및 13% 우유사료군 24마리(제 5군), MNNG 및 26% 우유사료군 24마리(제 6군)로 분류한 후 군별에 따라 28주간 발암제 및 우유사료를 투여하고 실험시작 40주째 생존한 109마리에 대해 다음과 같은 결과를 얻었다. 1. MNNG 단독 투여로 실험시작 12주 이후의 성장에 영향을 주었으나(p<0.01) 가역적이었고 생존에 미치는 영향은 없었다. 2. 위암발생은 대조군, 우유사료군에서 없었고 제 3군 25%, 제 4군 36.8%, 제 5군 27.8%, 제 6군 14.3%로 우유사료군에서 우유농도 증가에 따라 위암발생의 감소가 관찰되었고 제 6군에서는 제 3군보다 암발생이 억제되었다. 그러나 제 4군에서는 제 3군보다 상회하는 발암율을 보였다. 3. 위의 양성병변은 재생성 과증식, 선종성 과증식, 섬유 증식증 등이었고 MNNG 투여 각 우유사료군간의 분포는 우유농도 증가에 따라 위 양성병변이 증가하였으며 특히 암 수반율이 작은 재생성 과증식 발생군에서 뚜렷하였다. 재생성 과증식군에서의 암 수반율은 22.2%, 선종성 과증식군에서는 57.9%로 유의한 차이를 보였다(p<0.05). 4. 소장암 발생은 위암에서와 같이 십이지장의 선암이 주이었고 종양 발생 빈도는 3군에서 5%, 4군에서 21.1%, 5군에서 22.2%, 6군에서 9.5%이었으나 발생예수가 작아 각 군간의 통계적 유의성은 없었다. 5. 혈중가스트린치는 암발생이 많았던 제 4군에서 증가되었고(p<0.01), 양성 위 병변과 관련된 혈중 가스트린치도 제 4군에서 증가하였으며, 특히 재생성 과증식 수반동물군에서의 가스트린 증가는 유의하였으며(p<0.05), 위암발생군에서도 가스트린이 유의한 증가를 보였다(p<0.05). 이상의 성적을 바탕으로 위암발생은 우유농도 증가에 따라 감소되며 고농도의 우유사료군에서 발생이 억제되고 있음은 전암성 병변으로부터의 암발생을 억제하려는 우유의 암 발생 지연효과인 것 같다. 저농도 우유사료군에서의 암발생율의 증가는 혈중 가스트린치의 증가가 그 한 요인으로 해석되며 암발생군에서의 가스트린치의 증가와 더불어(p<0.05) 전암성 병변인 재생성 과증식군에서의 가스트린 증가가(p<0.05) 이를 뒷받침하고 있다.