Detection of an increased incidence of early gastric cancer in patients with intestinal metaplasia type III who are closely followed up.

Rokkas, Theodoros; Filipe, M. I.; Sladen, G E

doi:10.1136/gut.32.10.1110

Cited by 231 publications

(147 citation statements)

References 17 publications

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“…74 Some patients with incomplete metaplasia have shown progression to dysplasia and early gastric cancer. 74,75 The larger proportion of sulfated mucins we observed in Barrett's esophagus compared to gastric intestinal metaplasia, taken together with the morphologic characteristics, support previous evidence that Barrett's esophagus essentially represents the incomplete type of intestinal metaplasia. 17,76 However, in all cases, cells other than goblet cells were found: Alcian blue-positive columnar cells accumulating acid mucins which might represent a 'pregoblet' intestinal phenotype, as well as periodic acid-Schiff-positive cells which might represent a 'normal' gastric phenotype.…”

Section: Discussionsupporting

confidence: 86%

Phenotypic differences between esophageal and gastric intestinal metaplasia

et al. 2004

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Intestinal metaplasia is a cancer precursor in the esophagus and the stomach. Marked differences exist between the carcinogenic processes in the two locations in terms of natural history and clinical significance. We investigated biopsies from 52 patients with Barrett's esophagus and from 50 patients with gastric intestinal metaplasia in an attempt to throw light on their pathogenic processes. Morphologic characteristics, presence of Helicobacter pylori (H. pylori), and markers of differentiation, inflammation, and proliferation were evaluated by histochemical and immunohistochemical techniques. The area covered by incomplete type of intestinal metaplasia and the proportion of sulfomucins were significantly higher in the esophagus than in the stomach. Immunoreactivity with MUC1, MUC2, MUC5AC, Das-1, cytokeratins 7 and 20, inducible nitric oxide synthase and cyclooxygenase-2 antibodies was also significantly greater in Barrett's esophagus than in gastric intestinal metaplasia. In gastric intestinal metaplasia, the presence of MUC1, MUC5AC, Das-1 and cytokeratin 7 was restricted to areas with the incomplete type of metaplasia. Cell proliferation (Ki-67) was significantly higher in Barrett's esophagus than in gastric intestinal metaplasia. H. pylori was absent in all of the patients with Barrett's esophagus, while it was present in 70% of the patients with gastric intestinal metaplasia. Our observations made clear that Barrett's esophagus shares some phenotypic characteristics with gastric intestinal metaplasia, leading us to suggest that both could arise in response to injuries with eventual carcinogenic potential. However, the progression to more advanced lesions could be modulated by the nature of the carcinogenic insult.

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Section: Discussionsupporting

confidence: 86%

Phenotypic differences between esophageal and gastric intestinal metaplasia

et al. 2004

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“…Type I corresponds to the complete type, while type II and type III were classified from the incomplete type according to the mucins secreted by the columnar cells: sialomucins in type II and sulphomucins in type III. Several studies claimed that only type III of IM is associated with an increased risk of gastric cancer, [9][10][11] but other reports cast doubt on it. [12][13][14] Different subtypes of IM may coexist in the same foci, and this mosaic pattern complicates efforts at subtyping.…”

mentioning

confidence: 99%

CDX2 expression is progressively decreased in human gastric intestinal metaplasia, dysplasia and cancer

et al. 2007

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Intestinal metaplasia is a key event in multistep gastric carcinogenesis. CDX2, a master regulator of intestinal phenotype, was shown to play a tumor-suppressive role in colon cancer. However, it was reported to be expressed in nearly all gastric intestinal metaplasia and many gastric cancers. As CDX2 is differentially expressed in normal stomach and intestine, we sought to relate the CDX2 expression to gastrointestinal differentiation along gastric carcinogenesis. The expression of CDX2 protein in gastric intestinal metaplasia, dysplasia and cancer was examined and related to their gastrointestinal differentiation. CDX2 expression was significantly decreased in incomplete intestinal metaplasia, which expresses both gastric mucins (MUC5AC and MUC6) and intestinal mucin (MUC2), compared with complete intestinal metaplasia, which expresses intestinal mucin (MUC2) only. Although incomplete intestinal metaplasia morphologically resembles colon, its CDX2 expression was apparently lower than that in the normal colon. Moreover, CDX2 expression was progressively reduced in gastric dysplasia and cancer. The CDX2 expression in gastric cancer was also inversely correlated with the expression of gastric mucins. As incomplete intestinal metaplasia is associated with higher risk of gastric cancer, its lower CDX2 expression compared with that in complete intestinal metaplasia and normal colon epithelium resolved the current contradiction between the tumor-suppressive role of CDX2 in the colon and the high prevalence of CDX2 in intestinal metaplasia. Further decrease of CDX2 expression in gastric dysplasia and cancer suggests that CDX2 plays a similar anticarcinogenic role in intestinal metaplasia as it does in colon. Intestinal metaplasia or dysplasia with low expression of CDX2 may serve as predictive markers for gastric cancer.

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“…Surveillance EDITORIAL with endoscopy and biopsy sampling is important in patients with premalignant lesions and may lead to the early detection of cancer [6] . Gastric intraepithelial dysplasia/adenomas are considered to be precancerous lesions with a variable clinical course [7,8] . The term intraepithelial dysplasia/adenoma, however, is complex and confusing because of the lack of a uniform classification regarding the features that differentiate between dysplasia/adenoma and EGC.…”

Section: Introductionmentioning

confidence: 99%

Treatment strategy for gastric non-invasive intraepithelial neoplasia diagnosed by endoscopic biopsy

Nishida¹

2011

WJGP

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Treatment strategies, whether as follow-up or "total incisional biopsy" for gastric noninvasive intraepithelial neoplasia diagnosed by examination of an endoscopic forceps biopsy specimen, are controversial due to problems associated with the diagnostic accuracy of endoscopic forceps biopsy and questions about the safety and efficacy of endoscopic treatment. Based on the histological findings of the biopsy specimen, it is difficult to differentiate between reactive or regenerative changes, inflammation and neoplastic changes, intraepithelial and invasive tumors. Therefore, gastric neoplasia diagnosed as noninvasive intraepithelial often develop into invasive carcinoma during follow-up. Recent advances in endoscopic modalities and treatment devices, such as image-enhanced endoscopy and highfrequency generators, may make endoscopic treatment, such as endoscopic submucosal dissection (ESD), a therapeutic option for gastric intraepithelial neoplasia, including low-grade neoplasms. Future studies are required to evaluate whether ESD is a valid strategy for gastric intraepithelial neoplasm with regard to safety and cost effectiveness.

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Detection of an increased incidence of early gastric cancer in patients with intestinal metaplasia type III who are closely followed up.

Cited by 231 publications

References 17 publications

Phenotypic differences between esophageal and gastric intestinal metaplasia

Phenotypic differences between esophageal and gastric intestinal metaplasia

CDX2 expression is progressively decreased in human gastric intestinal metaplasia, dysplasia and cancer

Treatment strategy for gastric non-invasive intraepithelial neoplasia diagnosed by endoscopic biopsy

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