Subtypes of intestinal metaplasia and Helicobacter pylori.

Craanen, M. E.; Blok, P.; Dekker, W.; Ferwerda, J.; Tytgat, G. N. J.

doi:10.1136/gut.33.5.597

Cited by 85 publications

(56 citation statements)

References 28 publications

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“…Intestinal metaplasia has long been considered to play an important role in the development of gastric carcinoma. Type III incomplete intestinal metaplasia was found to be more common in the mucosa of gastric carcinoma than in the mucosa of chronic gastritis and greater number of genetic mutations developed in incomplete metaplasia (6)(7)(8)(9). The rate of evolution into gastric carcinoma was 4.58 times higher in type III intestinal metaplasia than in type I intestinal metaplasia (10).…”

Section: Introductionmentioning

confidence: 88%

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p53 Mutations and Microsatellite Instabilities in the Subtype of Intestinal Metaplasia of the Stomach

et al. 2002

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To investigate the potential implication of the subtype of intestinal metaplasia in the progression to the gastric carcinoma, we analyzed the mutations of the p53 gene and microsatellite instability (MSI) both in the complete type (type I) and in the sulphomucin-secreting incomplete type (type III) intestinal metaplasia located adjacent to the gastric carcinoma. p53 mutations were observed in 13.3% of type I, in 6.6% of type III intestinal metaplasia, and in 40% of gastric carcinoma. The difference between p53 mutations observed in type I and type III intestinal metaplasia was not statistically significant. No identical mutation of the p53 gene was found in the intestinal metaplasia and carcinoma specimens from the patients. There was no case of intestinal metaplasia showing MSI. In gastric carcinomas, MSI was observed in six cases (40%). The cases harboring BAT-26 instability did not have the mutation of the p53 gene. These data suggest that intestinal metaplasia adjacent to gastric carcinoma, irrespective of its subtype, do not have the genetic alterations as showing in their carcinoma tissues.

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Section: Introductionmentioning

confidence: 88%

“…Intestinal metaplasia is classified into complete (I) and incomplete (II & III) types depending on the secreted mucin and mucosal characteristics, and these subtypes may exist concomitantly in a patient (5,6). Intestinal metaplasia has long been considered to play an important role in the development of gastric carcinoma.…”

Section: Introductionmentioning

confidence: 99%

p53 Mutations and Microsatellite Instabilities in the Subtype of Intestinal Metaplasia of the Stomach

et al. 2002

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“…This is in keeping with a previous study [21] . H pylori infection associated atrophy and intestinal metaplasia progresses with age [22,23] . Thus, older patients may be more liable to have false-negative results from the commonly biopsied sites in our practice.…”

Section: Discussionmentioning

confidence: 99%

Gastric juice for the diagnosis of H pylori infection in patients on proton pump inhibitors

Yakoob¹,

Rasool²,

Abbas³

et al. 2008

WJG

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H pylori is a spiral gram negative microaerophilic bacterium that infects the human gastric mucosa and is associated with gastritis, gastroduodenal ulcer disease, gastric carcinoma and mucosal associated lymphoid tissue lymphoma [1,2] . The prevalence of H pylori is high in developing countries. A recent study revealed an early colonization/infection of infants with H pylori and a prevalence of 67% at 9 mo of age in a peri-urban community in Karachi, Pakistan [3] . H pylori serology was positive in 58% of our general population in a previous study but is likely to actually be higher [4] . Currently, several diagnostic tests of varying sensitivity and specificity are available for determining the presence of H pylori, which include rapid urease test (RUT), histology, culture, urea breath test (UBT), and serology. Isolation of H pylori from gastric biopsy specimens constitutes the most specific way to establish the diagnosis of infection and to study the genotype of the infecting strains, however, it is a time consuming process. RUT and histology are still commonly used for the diagnosis of H pylori infection in our country as other modalities of H pylori testing, such as UBT and facilities for H pylori stool antigen tests, are not widely available.In Pakistan, self-prescription is common and medications are available over the counter without prescriptions [5] . It is known that acid reducing drugs; e.g, proton pump inhibitor (PPI), histamine-2 receptor blocker (H2RB), antibiotics and bismuth compounds reduce the sensitivity and specificity of the diagnostic tests for H pylori [6,7] . In our previous studies, we demonstrated that histology is comparatively less affected by PPI than RUT [8,9] . Polymerase chain reaction (PCR) is a highly

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“…Its etiology is unknown, but strong associations exist with several dietary or environmental factors and with gastric mucosal infection by the bacterium Helicobacter pylori (Craanen et al, 1992;Parsonnet et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Hypermethylation of the hMLH1 gene promoter is associated with microsatellite instability in early human gastric neoplasia

Esteller²,

et al. 2001

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A signi®cant portion of gastric cancers exhibit defective DNA mismatch repair, manifested as microsatellite instability (MSI). High-frequency MSI (MSI-H) is associated with hypermethylation of the human mut-L homologue 1 (hMLH1) mismatch repair gene promoter and diminished hMLH1 expression in advanced gastric cancers. However, the relationship between MSI and hMLH1 hypermethylation has not been studied in early gastric neoplasms. We therefore investigated hMLH1 hypermethylation, hMLH1 expression and MSI in a group of early gastric cancers and gastric adenomas. Sixty-four early gastric neoplasms were evaluated, comprising 28 adenomas, 18 mucosal carcinomas, and 18 carcinomas with super®cial submucosal invasion but clear margins. MSI was evaluated using multiplex uorescent PCR to amplify loci D2S123, D5S346, D17S250, BAT 25 and BAT 26. Methylation-speci®c PCR was performed to determine the methylation status of hMLH1. In two hypermethylated MSI-H cancers, hMLH1 protein expression was also evaluated by immunohistochemistry. Six of sixty-four early gastric lesions were MSI-H, comprising 1 adenoma, 4 mucosal carcinomas, and 1 carcinoma with super®cial submucosal invasion. Two lesions (one adenoma and one mucosal carcinoma) demonstrated low-frequency MSI (MSI-L). The remaining 56 neoplasms were MSI-stable (MSI-S). Six of six MSI-H, one of two MSI-L, and none of thirty MSI-S lesions showed hMLH1 hypermethylation (P50.001). Diminished hMLH1 protein expression was demonstrated by immunohistochemistry in two of two MSI-H hypermethylated lesions. hMLH1 promoter hypermethylation is signi®cantly associated with MSI and diminished hMLH1 expression in early gastric neoplasms. MSI and hypermethylation-associated inactivation of hMLH1 are more prevalent in early gastric cancers than in gastric adenomas. Thus, hypermethylation-associated inactivation of the hMLH1 gene can occur early in gastric carcinogenesis. Oncogene (2001) 20, 329 ± 335.

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Subtypes of intestinal metaplasia and Helicobacter pylori.

Cited by 85 publications

References 28 publications

p53 Mutations and Microsatellite Instabilities in the Subtype of Intestinal Metaplasia of the Stomach

p53 Mutations and Microsatellite Instabilities in the Subtype of Intestinal Metaplasia of the Stomach

Gastric juice for the diagnosis of H pylori infection in patients on proton pump inhibitors

Hypermethylation of the hMLH1 gene promoter is associated with microsatellite instability in early human gastric neoplasia

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