Effect of <i>Helicobacter pylori</i> Eradication on Incidence of Gastric Cancer in Human and Animal Models: Underlying Biochemical and Molecular Events

Kabir, Shahjahan

doi:10.1111/j.1523-5378.2009.00677.x

Cited by 51 publications

(41 citation statements)

References 147 publications

(175 reference statements)

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“…In the case of gastric cancers, eradication of H. pylori is the primary strategy for prevention (47), but the incidence of gastric cancers remains high, even after H. pylori eradication, especially in persons with intestinal metaplasia and gastric atrophy (48). Notably, aberrant methylation in gastric mucosae decreases by H. pylori eradication, but it does not disappear completely (14,49).…”

Section: Discussionmentioning

confidence: 99%

Prevention of Helicobacter pylori–Induced Gastric Cancers in Gerbils by a DNA Demethylating Agent

Niwa

Toyoda

Tsukamoto

et al. 2013

Cancer Prevention Research

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Suppression of aberrant DNA methylation is a novel approach to cancer prevention, but, so far, the efficacy of the strategy has not been evaluated in cancers associated with chronic inflammation. Gastric cancers induced by Helicobacter pylori infection are known to involve aberrant DNA methylation and associated with severe chronic inflammation in their early stages. Here, we aimed to clarify whether suppression of aberrant DNA methylation can prevent H. pylori-induced gastric cancers using a Mongolian gerbil model. Administration of a DNA demethylating agent, 5-aza-2 0 -deoxycytidine (5-aza-dC), to gerbils (0.125 mg/kg for 50-55 weeks) decreased the incidence of gastric cancers induced by H. pylori infection and N-methyl-N-nitrosourea (MNU) treatment from 55.2% to 23.3% (P < 0.05). In gastric epithelial cells, DNA methylation levels of six CpG islands (HE6, HG2, SB1, SB5, SF12, and SH6) decreased to 46% to 68% (P < 0.05) of gerbils without 5-aza-dC treatment. Also, the global DNA methylation level decreased from 83.0% AE 4.5% to 80.3% AE 4.4% (mean AE SD) by 5-aza-dC treatment (P < 0.05). By 5-aza-dC treatment, Il1b and Nos2 were downregulated (42% and 58% of gerbils without, respectively) but Tnf was upregulated (187%), suggesting that 5-aza-dC treatment induced dysregulation of inflammatory responses.No obvious adverse effect of 5-aza-dC treatment was observed, besides testicular atrophy. These results showed that 5-aza-dC treatment can prevent H. pylori-induced gastric cancers and suggested that removal of induced DNA methylation and/or suppression of DNA methylation induction can become a target for prevention of chronic inflammation-associated cancers. Cancer Prev Res; 6(4); 263-70. Ó2013 AACR.

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Section: Discussionmentioning

confidence: 99%

Prevention of Helicobacter pylori–Induced Gastric Cancers in Gerbils by a DNA Demethylating Agent

Niwa

Toyoda

Tsukamoto

et al. 2013

Cancer Prevention Research

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“…Lymphocyte count was higher and the granulocyte count was lower in H.Pylori infected individuals comparing to healthy individuals. Other hematological parameters showed no significant difference between the H.Pylori positive subjects and the control subjects.The classical sign of vitamin B 12 deficiency is megaloblastic anemia which, however, occurs in only 50 % of vitamin B 12 -deficient subjects [13] . No evidence of megaloblastic anaemia was determined among the study group, according to the haematological values, this may be due to the infection period orto the severity of the infection.…”

Section: Discussionmentioning

confidence: 99%

“…Gastric parietal cells are responsible for production of both hydrochloric acid and IF. Absorbed vB 12 is then stored in the liver, Some H. pylori patients develop auto antibodies directed against gastric parietal H+/K+-ATPase cells (APCAs), resulting in achlorhydria and increased infection with H. pylori, which in turn contributes to gastric damage and atrophy of the corpus [13].…”

Section: Introductionmentioning

confidence: 99%

Association of helicobacter Pylori Infection and Vitamin B12 Level among Sudanese Patients

Humeida¹

2017

IOSR JDMS

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“…Although the pathogenic roles of H. pylori are not fully elucidated, H. pylori eradication leads to histological resolution of CAG, probably prevents progression of CAG and may reduce the incidence of gastric cancer (Kabir, 2009). However, bacterial eradication in all H. pylori-infected patients remains difficult because of potential side effects, bacterial resistance to antibiotics and cost.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effects of Japanese apricot (Prunus mume Siebold et Zucc.; Ume) on Helicobacter pylori-related chronic gastritis

et al. 2010

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Objectives: We investigated the correlation between Japanese apricot (JA) intake and Helicobacter pylori-related chronic atrophic gastritis (CAG). Methods: A questionnaire was administered and serum anti-H. pylori IgG antibodies measured in 1358 asymptomatic adults. The subjects were divided into high-intake and low-intake groups. Histological and serological evaluation of H. pylori-related CAG was performed in 68 non-elderly volunteers. Results: The H. pylori-negative rate did not differ significantly between the high-intake and low-intake groups. Mean antibody titers were lower in the high-intake group, but the difference was not significant. There was no significant difference in the rate of H. pylori infection on the basis of JA intake when subjects were stratified by age. Among H. pylori-positive non-elderly subjects, antibody titers were significantly lower in the high-intake group (P ¼ 0.041). Endoscopic tissue biopsy from the 68 volunteers showed less H. pylori bacterial load and mononuclear infiltration irrespective of gastric site in the high-intake group. In the highintake group, antral neutrophil infiltration was significantly less pronounced and corporal atrophy was less extensive. Serological evaluation using serum PG levels also confirmed these histopathological data. Conclusions: Our findings strongly indicate a preventive effect of JA intake on CAG by inhibiting H. pylori infection and reducing active mucosal inflammation.

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Effect of Helicobacter pylori Eradication on Incidence of Gastric Cancer in Human and Animal Models: Underlying Biochemical and Molecular Events

Cited by 51 publications

References 147 publications

Prevention of Helicobacter pylori–Induced Gastric Cancers in Gerbils by a DNA Demethylating Agent

Prevention of Helicobacter pylori–Induced Gastric Cancers in Gerbils by a DNA Demethylating Agent

Association of helicobacter Pylori Infection and Vitamin B12 Level among Sudanese Patients

Inhibitory effects of Japanese apricot (Prunus mume Siebold et Zucc.; Ume) on Helicobacter pylori-related chronic gastritis

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