Reversibility of atrophic gastritis and intestinal metaplasia after <i>Helicobacter pylori</i> eradication ‐ a prospective study for up to 10 years

Hwang, Young Jin; Kim, Na Young; Lee, H. S.; Lee, J. B.; Choi, Yoon Jin; Yoon, Hyuk; Shin, Cheol Min; Park, Y. S.; Lee, D. H.

doi:10.1111/apt.14424

Cited by 156 publications

(135 citation statements)

References 71 publications

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“…Along with greater extent and higher degree of gastric mucosal atrophy, and also with the variation in biological characteristics, the risk of developing stomach cancer will increase gradually. Recently several studies have showed premalignant conditions including AG and IM may be regressed by appropriate interventional treatment before it reaches “point of no return”,35, 36 which can reduce the incidence of GC. Therefore, precise evaluation focusing on severity and biological behaviors and proper intervention of high‐risk AG patients is of great significance for the prevention of gastric cancer.…”

Section: Discussionmentioning

confidence: 99%

Correlation between negative expression of pepsinogen C and a series of phenotypic markers of gastric cancer in different gastric diseases

et al. 2018

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Gastric tumorigenesis is a multistep process initiated by chronic superficial gastritis (SG), followed by atrophic gastritis (AG), then intestinal metaplasia (IM), and finally by dysplasia and adenocarcinoma according to the Correa model. Pepsinogen C (PGC) decreases gradually during progression of cancer, which makes PGC an ideal negative marker for GC. To explore the correlation between PGC and other positive tumor markers in different gastric diseases, we observed the expression of PGC, MG7‐Ag, MMP9, NM23, Ki‐67, and E‐cadherin by immunohistochemistry, quantitative RT‐PCR, and immunoblot analysis. Our results showed that in SG, PGC was highly expressed while malignant phenotype markers were rarely expressed. In contrast with SG, malignant phenotype markers were highly expressed while the positive rate of PGC reached only 1.44% in GC. So there was no coexpression of PGC and malignant phenotype markers in SG or GC tissues. Only in the AG group, which is well‐known to be gastric precancerous disease, coexpression of PGC and malignant phenotype markers was detected. Our results suggested that the expression of PGC in AG was negatively correlated with that of MG7‐Ag and MMP9. Of all AG, those with low expression of PGC and high expression of MG7‐Ag and MMP9 may possess a greater potential of malignant transformation. Combined detection of negative marker PGC and positive markers MG7‐Ag and MMP9 could be used as a potential follow‐up panel for monitoring dynamical progression of AG and improving the detection efficiency of high‐risk individuals of gastric cancer, and then taking necessary interventions on the target population.

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Section: Discussionmentioning

confidence: 99%

Correlation between negative expression of pepsinogen C and a series of phenotypic markers of gastric cancer in different gastric diseases

et al. 2018

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“…26 Six biopsy specimens were obtained from the lesser curvature, and four specimens were obtained from the greater curvature, evenly from the mid antrum and mid corpus, regardless of cancer status ( Figure S1). At each EGD, the biopsy specimens were taken to confirm diagnosis of GC and up to ten biopsy specimens were additionally obtained for H. pylori testing and histological examination.…”

Section: Esophagogastroduodenoscopy Helicobacter Pylori Tests Andmentioning

confidence: 99%

Usefulness of OLGA and OLGIM system not only for intestinal type but also for diffuse type of gastric cancer, and no interaction among the gastric cancer risk factors

et al. 2018

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Background The operative link on gastric atrophy (OLGA) and operative link on gastric intestinal metaplasia (OLGIM) stages have been suggested for risk estimation of gastric cancer (GC). However, usefulness of OLGA/OLGIM systems in diffuse type of GC was not investigated so far. The aims of this study were to evaluate the OLGA/OLGIM systems in estimating the GC risk according to Lauren's classification and to investigate the interaction among the risk factors. Materials and methods The OLGA/OLGIM stages were evaluated in 1398 (765 control and 633 GC patients) who were prospectively enrolled in the Seoul National University Bundang Hospital. Synergistic interaction among the risk factors for GC was calculated using an additive model. Results Among 387 intestinal‐type GC patients, 71 (18.3%) were high‐risk OLGA stages (III, IV) and 113 (29.2%) were high‐risk OLGIM stages (III, IV). Of the 246 patients with diffuse‐type GC, 36 (14.6%) were high‐risk OLGA stages and 39 (15.9%) were high‐risk OLGIM stages. Multivariable analysis revealed family history of GC, Helicobacter pylori infection, high‐risk OLGA stages, and high‐risk OLGIM stages as independent risk factors for GC regardless of histologic type (odds ratios [ORs] 1.78, 1.94, 2.63, and 3.18, respectively). There was no significant risk modification among the H. pylori infection, family history of GC, and high‐risk OLGA/OLGIM stages. Conclusion High‐risk OLGA/OLGIM stages are important prediction markers for GC regardless of H. pylori infection or family history of GC not only for the intestinal type but also for diffuse‐type GC.

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“…Grades of IM did not improve after ≥ 3 years of eradication in comparison with grades of IM of the HP‐negative group (Fig. b) . However, AG in both the antrum and corpus improved more quickly up to grade 0 than IM in both antrum and corpus in the present study (Fig.…”

Section: Introductionmentioning

confidence: 43%

“…pylori ‐eradicated [ n = 442]) with long‐term follow‐up for up to 10 years, we showed that AG and IM in both the antrum and the corpus continuously improved after HP eradication until reaching a point that they were not significantly different compared with those in the HP‐negative group (Fig. ) . The speed or degree of reversibility was found to be different between AG and IM (Fig.…”

Section: Introductionmentioning

confidence: 86%

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Chemoprevention of gastric cancer by Helicobacter pylori eradication and its underlying mechanism

Kim

2019

J of Gastro and Hepatol

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The cascade of gastric cancer, a leading cause of cancer incidence and mortality, is multifactorial. Helicobacter pylori (HP) infection plays a major role in gastric cancer (GC), and there has been an accumulation of data regarding the chemopreventive effect of HP eradication. However, it remains unclear how HP infection causes GC and how HP eradication prevents GC. To clarify this issue, the following approaches were performed in this review article. First, how HP‐induced atrophic gastritis (AG) and intestinal metaplasia (IM) provoke the development of GC is shown, followed by how long HP eradication takes to induce a reversible change in AG and IM. Second, epigenetic studies of PTPN6, MOS, DCC, CRK, and VAV1 were performed in noncancerous gastric specimens in terms of HP status. Among these genes, MOS was found to be a possible surrogate marker for GC development. HP eradication decreased aberrant DNA methylation in a gene‐specific manner, and MOS played a role in metachronous gastric neoplasms. Third, transforming growth factor‐β1 (TGF‐β1) and TGF‐β1‐induced epithelial‐mesenchymal transition (EMT) markers were investigated in gastric mucosa. HP infection triggered the TGF‐β1‐induced EMT pathway and caused the emergence of GC stem cells, such as CD44v8‐10. When HP was eradicated, these two pathways were inhibited. Finally, a 2222 cohort study showed that HP eradication significantly decreased the risk of noncardiac GC. Taken together, HP eradication is effective as a primary GC prevention method, and its underlying mechanism includes reversibility of AG and IM, methylation, EMT, and stem cells.

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Reversibility of atrophic gastritis and intestinal metaplasia after Helicobacter pylori eradication ‐ a prospective study for up to 10 years

Abstract: H. pylori eradication may be a preventative strategy for intestinal-type gastric cancer by regression of atrophic gastritis and intestinal metaplasia.

Cited by 156 publications

References 71 publications

Correlation between negative expression of pepsinogen C and a series of phenotypic markers of gastric cancer in different gastric diseases

Correlation between negative expression of pepsinogen C and a series of phenotypic markers of gastric cancer in different gastric diseases

Usefulness of OLGA and OLGIM system not only for intestinal type but also for diffuse type of gastric cancer, and no interaction among the gastric cancer risk factors

Chemoprevention of gastric cancer by Helicobacter pylori eradication and its underlying mechanism

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