Increased Cell Proliferation in Chronic<i>Helicobacter pylori</i>Positive Gastritis and Gastric Carcinoma – Correlation between Immuno-Histochemistry and Tv Image Cytometry

Szaleczky, Erika; Pajor, László; Molnár, Béla; Berczi, Lajos; Fehér, János; Tulassay, Zsolt

doi:10.1155/2000/830906

Cited by 17 publications

(10 citation statements)

References 17 publications

(19 reference statements)

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“…In previous studies, patients with H. pylori infection and chronic gastritis exhibited significantly increased rates of epithelial cell proliferation. Cell proliferation decreases after successful H. pylori eradication [30, 31]. Although the mean Ki-67 index was decreased (decreased cell proliferation) following H. pylori eradication in our study, there was no significant difference in mean Ki-67 index between patients with IM and those without IM.…”

Section: Discussioncontrasting

confidence: 51%

“…Although the mean Ki-67 index was decreased (decreased cell proliferation) following H. pylori eradication in our study, there was no significant difference in mean Ki-67 index between patients with IM and those without IM. The condition of gastric mucosal cell proliferation might be due to the status of H. pylori infection and chronic gastritis, but not the status of IM [30, 31]. …”

Section: Discussionmentioning

confidence: 99%

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Analyzing the influence of gastric intestinal metaplasia on gastric ulcer healing in Helicobacter pylori–infected patients without atrophic gastritis

et al. 2017

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BackgroundGastric epithelial hyper-proliferation was reported in patients with Helicobacter pylori (H. pylori)–infected gastric mucosa with intestinal metaplasia (IM) changes. In patients with gastric ulcer (GU) and IM, the GU may have a different healing rate in comparison to patients without IM. This study aimed to compare the difference in GU healing between H. pylori–infected patients with IM and those without IM.MethodsWe retrospectively analyzed patients at the Keelung Chung Gung Memorial Hospital during the period from March 2005 to January 2011. The inclusion criteria were: 1) endoscopic findings of GU and biopsy histological examination plus rapid urease test indicating H. pylori infection; 2) gastric IM adjacent to a GU but with no atrophic gastritis changes; 3) patients receiving H. pylori eradication triple therapy and 8 weeks of maintenance therapy with a proton pump inhibitor; and 4) patients receiving follow-up endoscopy within the 3rd and the 4th months after treatment.ResultsIn total, 327 patients with GU and H. pylori infection (136 with IM and 191 without IM) were included. Patients with IM had a higher GU healing rate than those without IM (91.9% vs. 84.3%, P = 0.040). Multivariate logistical regression analysis revealed that failure of H. pylori eradication (Odds = 4.013, 95% CI: 1.840–8.951, P < 0.001) and gastric IM (Odds = 0.369, 95% CI: 0.168–0.812, P = 0.013) were the predictors of non-healing GU following treatment.ConclusionsPatient with gastric IM change may have a higher GU healing rate than those without gastric IM. However, successful H. pylori eradication is a more important factor for GU healing than gastric IM.

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Section: Discussioncontrasting

confidence: 51%

Section: Discussionmentioning

confidence: 99%

Analyzing the influence of gastric intestinal metaplasia on gastric ulcer healing in Helicobacter pylori–infected patients without atrophic gastritis

et al. 2017

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“…This suggests that H. pylori infection induces DNA methylation in both stem cells, which will persist, and nonstem cells, which will drop off the gastric mucosae in a few days (25). If the methylation status of stem cells is copied into the cells in the entire gland without active induction, the methylation levels in the gastric mucosae will reflect the fraction of methylated stem cells among the entire (8). Cell proliferation itself has been suggested as a promoting factor for de novo DNA methylation (21,26).…”

Section: Discussionmentioning

confidence: 99%

“…In an animal model with Mongolian gerbil chronic infection with H. pylori rarely induces gastric cancers by itself, but markedly enhances their incidences after initiation with a mutagen, such as N-methyl-N-nitrosourea (7). This promoting effect of H. pylori has been attributed to the induction of chronic inflammation and cell proliferation (8). Cell proliferation increases a chance for initiated cells to escape growth suppression and undergo further mutations.…”

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confidence: 99%

High Levels of Aberrant DNA Methylation in Helicobacter pylori–Infected Gastric Mucosae and its Possible Association with Gastric Cancer Risk

Maekita

Nakazawa

Mihara³

et al. 2006

Clinical Cancer Research

576

522

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Introduction: Risk prediction of gastric cancers is important to implement appropriate screening procedures. Although aberrant DNA methylation is deeply involved in gastric carcinogenesis, its induction by Helicobacter pylori, a strong gastric carcinogen, is unclear. Here, we analyzed the effect of H. pylori infection on the quantity of methylated DNA molecules in noncancerous gastric mucosae and examined its association with gastric cancer risk. Experimental Design: Gastric mucosae were collected from 154 healthy volunteers (56 H. pylori negative and 98 H. pylori positive) and 72 cases with differentiated-type gastric cancers (29 H. pylori negative and 43 H. pylori positive) by endoscopy. The numbers of DNA molecules methylated and unmethylated for eight regions of seven CpG islands (CGI) were quantified by quantitative PCR after bisulfite modification, and fractions of methylated molecules (methylation levels) were calculated. Results: Among healthy volunteers, methylation levels of all the eight regions were 5.4-to 303-fold higher in H. pylori positives than in H. pylori negatives (P < 0.0001). Methylation levels of the LOX, HAND1, andTHBD promoter CGIs and p41ARC exonic CGI were as high as 7.4% or more in H. pylori^positive individuals. Among H. pylori^negative individuals, methylation levels of all the eight regions were 2.2-to 32-fold higher in gastric cancer cases than in age-matched healthy volunteers (P V 0.01). Among H. pylori^positive individuals, methylation levels were highly variable, and that of only HAND1 was significantly increased in gastric cancer cases (1.4-fold, P = 0.02). Conclusions: It was indicated that H. pylori infection potently induces methylation of CGIs to various degrees. Methylation levels of specific CGIs seemed to reflect gastric cancer risk in H. pylori^negative individuals.Gastric cancer is one of the most common malignancies worldwide and remains a leading cause of cancer death in Asia and some European countries (1). To reduce its mortality, early detection by endoscopy and curative resection are important (2). However, considering the potential risk and costs of early detection by endoscopic examination, implementation reflecting an individual's risk for developing a gastric cancer would be ideal. Also, endoscopic mucosal resection, which conserves the noncancerous gastric mucosae, is becoming popular, and the problem of metachronous gastric cancer recurrence is being recognized (3). Again, if the future risk of developing metachronous cancers in a specific case can be estimated, the information will be useful in the decision on either surgical resection or endoscopic mucosal resection for the case.The major etiologic risk factor for gastric cancers is Helicobacter pylori infection, which increases gastric cancer risk 2.2-to 21-fold (4 -6). In an animal model with Mongolian gerbil chronic infection with H. pylori rarely induces gastric cancers by itself, but markedly enhances their incidences after initiation with a mutagen, such as N-methyl-N-nitrosourea (7). Thi...

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“…H. pylori promotes gastric carcinogenesis through chronic inflammation and cell proliferation [11]. Chronic inflammation may lead to DNA damage or mutation.…”

Section: Introductionmentioning

confidence: 99%

Risk Prediction of Gastric Cancer by Analysis of Aberrant DNA Methylation in Non-Neoplastic Gastric Epithelium

et al. 2007

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Background: Aberrant DNA methylation is one of the major events in carcinogenesis. Promoter DNA methylation is also present in various non-neoplastic tissues including gastric epithelium as age-related phenomenon, suggesting that it occurs early in the process of tumorigenesis. Aim: We aimed to clarify the relationship of aberrant DNA methylation in non-neoplastic gastric epithelia with the risk of gastric cancer, Helicobactor pylori infection, and the degree of H. pylori-induced gastritis. Methods: 89 patients enrolled in this study. The status of aberrant DNA methylation was compared in two groups of patients: 43 cases with gastric cancer (mean age 65.9 years [29–91], F:M = 0.30, intestinal type [n = 25], diffuse type [n = 18]) and 46 age- and sex-matched patients without gastric cancer (peptic ulcer diseases [n = 11], gastritis [n = 35]) as a control group. Genomic DNA was extracted directly from non-neoplastic epithelia of antral biopsies obtained by endoscopy. The promoter methylation status of the p14 and p21 genes was determined by methylation-specific-polymerase chain reaction (MSP). The promoter methylation status of the p16 gene was quantified by digital densitographic analysis following MSP. The degree of gastritis in the antrum was assessed according to the updated Sydney system. The PG I/II ratio was calculated based on the data of serum PG I and PG II levels measured by radioimmunoassay. Results: In all 89 subjects, CpG island methylation was found in 25.8% for p14, 52.8% for p16, 1.1% for p21. Among non-cancer patients, the methylation frequency of the p14 gene was significantly higher in H. pylori-positive than in H. pylori-negative patients (38.5 vs. 10.0%, p = 0.03). The mean (± SD) methylation levels of the p16 gene in non-neoplastic gastric epithelium was significantly higher in gastric cancer cases both in all patients and in H. pylori-positive patients (0.45 ± 0.31 vs. 0.20 ± 0.17; p = 0.019, 0.45 ± 0.31 vs. 0.20 ± 0.17; p = 0.016, respectively). The methylation level of the p16 gene was also associated with the presence of intestinal-type gastric cancer (p = 0.017). The methylation level of the p16 gene was significantly higher in patients with intestinal metaplasia (IM) than those without (p = 0.04). Furthermore, the methylation level of the p16 gene was correlated with lower PG l/ll ratio (p = 0.04). The methylation of the p21gene was found in only 1 patient with gastric cancer. Conclusions: Our data suggest that promoter of the p14 gene may be one of the specific regions whose methylation is closely associated with H. pylori infection. Methylation levels of the p16 gene seem to be accumulated in the progression of gastric mucosal atrophy and IM, and thus may be associated with the presence of gastric cancer especially for intestinal-type histopathology.

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Increased Cell Proliferation in ChronicHelicobacter pyloriPositive Gastritis and Gastric Carcinoma – Correlation between Immuno-Histochemistry and Tv Image Cytometry

Cited by 17 publications

References 17 publications

Analyzing the influence of gastric intestinal metaplasia on gastric ulcer healing in Helicobacter pylori–infected patients without atrophic gastritis

Analyzing the influence of gastric intestinal metaplasia on gastric ulcer healing in Helicobacter pylori–infected patients without atrophic gastritis

High Levels of Aberrant DNA Methylation in Helicobacter pylori–Infected Gastric Mucosae and its Possible Association with Gastric Cancer Risk

Risk Prediction of Gastric Cancer by Analysis of Aberrant DNA Methylation in Non-Neoplastic Gastric Epithelium

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