Usefulness of magnifying narrow-band imaging endoscopy for the diagnosis of gastric and colorectal lesions.

A series of studies about the potential usefulness of magnifying endoscopy with narrow-band imaging (NBI) for the diagnosis of gastric and colonic lesion is reviewed. Concerning the magnifying NBI appearances of gastric lesions, a light blue crest is a highly accurate sign of the presence of histological intestinal metaplasia. Also, the degree of irregularity of the mucosal and vascular pattern is correlated with the histological severity of Helicobacter pylori-associated chronic gastritis. According to the 'VS classification', an irregular microvascular pattern and/or an irregular microsurface pattern together with a clear demarcation line are characteristic for early gastric carcinoma, and a multicenter prospective randomized controlled trial demonstrated that magnifying endoscopy with NBI is superior to ordinary white light endoscopy for making a differential diagnosis of a small depressed lesion between carcinoma and non-carcinoma. Concerning the magnifying NBI appearances of colonic tumor, the vague or invisible microvascular pattern is mostly observed in hyperplastic polyp. The regular meshed microvascular pattern is mostly observed in adenoma. The irregular meshed microvascular pattern is mostly observed in intramucosal or shallow submucosal-invasive carcinoma. The decreased or loose microvasucular pattern is mostly observed in deep submucosal-invasive carcinoma. Thus, magnifying NBI endoscopy is useful for the differentiation of colorectal non-adenomatous lesions from adenoma, the differentiation of adenoma from carcinoma, and the assessment of invasion depth of early colorectal carcinoma. At present, several magnifying NBI classifications for the diagnosis of early colorectal neoplasia have been proposed in Japan. Recently, the NICE classification based on NBI findings with/without magnification for colorectal tumor was established by an international group.

Selenoprotein S (SEPS1) gene -105G>A promoter polymorphism influences the susceptibility to gastric cancer in the Japanese population.

BACKGROUND: Inflammation is a key factor in the process of carcinogenesis from chronic gastritis induced by Helicobacter pylori. Selenoprotein S (SEPS1) is involved in the control of the inflammatory response in the endoplasmic reticulum (ER). Recently the -105G>A polymorphism in the promoter of SEPS1 was shown to increase pro-inflammatory cytokine expression. We examined the association between this polymorphism and the risk of gastric cancer. METHODS: We took stomach biopsies during endoscopies of 268 Japanese gastric cancer patients (193 males and 75 females, average age 65.3), and 306 control patients (184 males and 122 females, average age 62.7) and extracted the DNA from the biopsy specimens. All subjects provided written informed consent. For the genotyping of the SEPS1 promoter polymorphism at position -105G>A, PCR-RFLP methods were used and the PCR products were digested with PspGI. Logistic-regression analysis was used to estimate odds ratios (OR) and 95% confidence intervals (CI), adjusting for age, sex, and H. pylori infection status. RESULTS: Among cases, the distribution of genotypes was as follows: 88.4% were GG, 11.2% were GA, and 0.4% were AA. Among controls, the distribution was as follows: 92.5% were GG, 7.2% were GA, and 0.3% were AA. Among males, carrying the A allele was associated with an increased odds of gastric cancer, compared with the GG genotype (OR: 2.0, 95% CI 1.0-4.1, p = 0.07). Compared with the GG genotype, carrying the A allele was significantly associated with increased risks of intestinal type gastric cancer (OR: 2.0, 95%CI 1.0-3.9, p < 0.05) as well as of gastric cancer located in the middle third of the stomach (OR: 2.0, 95%CI 1.0-3.9, p < 0.05). CONCLUSION: The -105G>A promoter polymorphism of SEPS1 was associated with the intestinal type of gastric cancer. This polymorphism may influence the inflammatory conditions of gastric mucosa. Larger population-based studies are needed for clarifying the relation between inflammatory responses and SEPS1 polymorphism.