Dataset Information

Gastric Mucosal Atrophy Impedes Housekeeping Gene Methylation in Gastric Cancer Patients.

ABSTRACT:

Purpose

Helicobacter pylori infection induces phenotype-stabilizing methylation and promotes gastric mucosal atrophy that can inhibit CpG-island methylation. Relationship between the progression of gastric mucosal atrophy and the initiation of CpG-island methylation was analyzed to delineate epigenetic period for neoplastic transformation.

Materials and methods

Normal-appearing gastric mucosa was biopsied from 110 H. pylori-positive controls, 95 H. pylori-negative controls, 99 gastric cancer patients, and 118 gastric dysplasia patients. Gastric atrophy was assessed using endoscopic-atrophic-border score. Methylation-variable sites of eight CpG-island genes adjacent to Alu (CDH1, ARRDC4, PPARG, and TRAPPC2L) or LTR (MMP2, CDKN2A, RUNX2, and RUNX3) retroelements and stomach-specific TFF3 gene were analyzed using radioisotope-labeled methylation-specific polymerase chain reaction.

Results

Mean ages of H. pylori-positive controls with mild, moderate, and severe atrophy were 51, 54, and 65 years and those of H. pylori-associated TFF3 overmethylation at the three atrophic levels (51, 58, and 63 years) tended to be periodic. Alu-adjacent overmethylation (50 years) was earlier than TFF3 overmethylation (58 years) in H. pylori-positive controls with moderate atrophy. Cancer patients with moderate atrophy showed late Alu-adjacent (58 years) overmethylation and frequent LTR-adjacent overmethylation. LTR-adjacent overmethylation was frequent in cancer (66 years) and dysplasia (68 years) patients with severe atrophy.

Conclusion

Atrophic progression is associated with gastric cancer at moderate level by impeding the initiation of Alu-adjacent methylation. LTR-adjacent methylation is increased in cancer patients and subsequently in dysplasia patients.

SUBMITTER: Oh JH

PROVIDER: S-EPMC6334004 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature

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Publications

Gastric Mucosal Atrophy Impedes Housekeeping Gene Methylation in Gastric Cancer Patients.

Oh Jung-Hwan JH Rhyu Mun-Gan MG Kim Suk-Il SI Yun Mi-Ri MR Shin Jung-Ha JH Hong Seung-Jin SJ

Cancer research and treatment 20180430 1

<h4>Purpose</h4>Helicobacter pylori infection induces phenotype-stabilizing methylation and promotes gastric mucosal atrophy that can inhibit CpG-island methylation. Relationship between the progression of gastric mucosal atrophy and the initiation of CpG-island methylation was analyzed to delineate epigenetic period for neoplastic transformation.<h4>Materials and methods</h4>Normal-appearing gastric mucosa was biopsied from 110 H. pylori-positive controls, 95 H. pylori-negative controls, 99 gas ...[more]

PMID: 29747491

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Project description:AimIntestinal metaplasia (IM) and gastric atrophy (GA) are precancerous lesions in the stomach. There is a large debate on natural course of these lesions and surveillance strategy in these patients. This meta-analysis was aimed to find the most appropriate follow up and the rate of progression from IM and GA to GC.MethodsThis meta-analysis is followed and reported according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Electronic databases including EMBASE, PubMed, Web of Science databases, Scopus, and the Cochrane Library were searched until July 2018. Cochran's Q test and I-square (I2) test were used to examine heterogeneity across included studies. We pooled data using random-effect or fixed effect models indicated as incidence rate or proportion with 95% confidence intervals (CI). The variables of study included demographic data, endoscopy interval, follow up interval and time, GA and IM type and GC stage. Moreover, incidence rate of GC and progress rate, regress and persistence proportion in both GA and IM patients were assessed.ResultsOverall, 68 original articles out of 32981 citations were included in our meta-analysis. The pooled GC incidence rate in patients with GA was 1.24 (95% CI, 0.80, 1.76; I2: 83.6%) cases per 1,000 person-years. The rates of later diagnosis of IM and gastric dysplasia in patients with GA were estimated as 41.42 (95% CI, 3.11, 64.45; I2: 95.6%) and 6.23 (95% CI, 2.34, 11.46; I2: 83.0%) cases per 1,000 person-years, respectively. The pooled regressed proportion was 32.23 (95% CI, 18.07-48.02; I2: 94.0%) and the persistence proportion was 38.83 (95% CI, 20.20-59.13; I2: 97.0%) per 100 observations in GA patients. In IM studies, the pooled incidence rate of GC was 3.38 (95% CI, 2.13, 4.85; I2: 93.4%) cases per 1,000 person-years. The progressed rate to dysplasia in IM patient was estimated to be 12.51 (95% CI, 5.45, 22.03; I2: 95.1%) cases per 1,000 person-years. The pooled regressed proportion was 31.83 (95% CI, 25.48-38.51; I2: 91.0%) and the persistence proportion was 43.46 (95% CI, 32.52-54.71; I2: 96.0%) per 100 observations in IM patients.ConclusionOverall, the incidence of GC in patients with IM and GA are low but there is heterogeneity in data with the highest rate in Asian, males with those with incomplete IM. There is probability of regression or persistence without progression in patients with IM and GA who receive appropriate management.

Dataset Information

Gastric Mucosal Atrophy Impedes Housekeeping Gene Methylation in Gastric Cancer Patients.

Purpose

Materials and methods

Results

Conclusion

Publications

Gastric Mucosal Atrophy Impedes Housekeeping Gene Methylation in Gastric Cancer Patients.

Similar Datasets

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