Effect of Helicobacter pylori eradication on malignant transformation of gastric adenoma

Saitô, Kenichi; Arai, Kozo; Mori, Masataka; Kobayashi, Ryouta; Ohki, Ichiro

doi:10.1067/mge.2000.106112

Cited by 65 publications

(33 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Recently, we and others have found that eradication of H. pylori in the stomach can reduce the risk of gastric cancer (Uemura et al, 1997;Saito et al, 2000;Sung et al, 2000). The current study may provide clue to the underlying mechanism that H. pylori-mediated cytokine expression-enhanced tumour progression in a subset of gastric cancer where SOCS-1 was hypermethylated.…”

Section: Discussionsupporting

confidence: 52%

Constitutional activation of IL-6-mediated JAK/STAT pathway through hypermethylation of SOCS-1 in human gastric cancer cell line

Chan

Leung

et al. 2004

Br J Cancer

View full text Add to dashboard Cite

The interleukin-mediated Janus kinase (JAK)/STAT pathway plays a crucial role in carcinogenesis. Recently, increased STAT3 activity was found in hepatocellular carcinoma and multiple myeloma in which there was silencing of SOCS-1 (suppressor of cytokine signalling-1) by gene promoter hypermethylation. We investigated the expression level of interleukin-6 (IL-6) and SOCS-1 in gastric cancer cell lines. Expression of SOCS-1 correlated with IL-6 level in most of the cell lines, except for AGS cells in which SOCS-1 was absent despite a high level of IL-6 production. Methylation analysis by methylation-specific polymerase chain reaction and bisulphite sequencing revealed that CpG island of SOCS-1 was densely methylated in AGS cells. Demethylation treatment by 5 0 azadeoxycytidine restored SOCS-1 expression and also suppressed constitutive STAT3 phosphorylation in AGS cells. Moreover, methylation of SOCS-1 was detected in 27.5% (11 of 40) of primary gastric tumours samples, 10% (one of 10) of adjacent noncancer tissues but not in any (zero of nine) normal gastric mucosa. Methylation of SOCS-1 also correlated with the loss of mRNA expression in some primary gastric cancers. In conclusion, this is the first report to demonstrate that hypermethylation of SOCS-1 led to gene silencing in gastric cancer cell line and primary tumour samples. Downregulation of SOCS-1 cooperates with IL-6 in the activation of JAK/STAT pathway in gastric cancer.

show abstract

Section: Discussionsupporting

confidence: 52%

Constitutional activation of IL-6-mediated JAK/STAT pathway through hypermethylation of SOCS-1 in human gastric cancer cell line

Chan

Leung

et al. 2004

Br J Cancer

View full text Add to dashboard Cite

show abstract

“…There are some data showing that H. pylori eradication is associated with a decrease in the recurrence rate in patients with early gastric cancer that is resected endoscopically (39,44) Some reports emphasize the importance of H. pylori treatment at a young age. These studies conclude that H. pylori eradication is also useful for the prevention of new cancer development from high-risk mucosa for gastric cancer (3,21,40) .…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Helicobacter pylori infection in advanced gastric carcinoma

Araújo‐Filho

Brandão-Neto

Pinheiro

et al. 2006

Arq. Gastroenterol.

View full text Add to dashboard Cite

show abstract

“…The same group of investigators found that eradication of H pylori was able to prevent relapse after endoscopic resection of early stage gastric cancer [73] . Another study by Saito et al [74] showed that H pylori eradication had a favorable impact on gastric cancer development in patients with gastric adenoma. More recently, Take et al [75] published the results from a large prospective Japanese intervention trial.…”

Section: Clinical Studiesmentioning

confidence: 99%

Eradication of H pylori for the prevention of gastric cancer

Trautmann¹,

Stolte²,

Miehlke³

2006

WJG

View full text Add to dashboard Cite

Infection with H pylori is the most important known etiological factor associated with gastric cancer. While colonization of the gastric mucosa with H pylori results in active and chronic gastritis in virtually all individuals infected, the likelihood of developing gastric cancer depends on environmental, bacterial virulence and host specific factors. The majority of all gastric cancer cases are attributable to H pylori infection and therefore theoretically preventable. There is evidence from animal models that eradication of H pylori at an early time point can prevent gastric cancer development. However, randomized clinical trials exploring the prophylactic effect of H pylori eradication on the incidence of gastric cancer in humans remain sparse and have yielded conflicting results. Better markers for the identification of patients at risk for H pylori induced gastric malignancy are needed to allow the development of a more efficient public eradication strategy. Meanwhile, screening and treatment of H pylori in first-degree relatives of gastric cancer patients as well as certain high-risk populations might be beneficial.

show abstract

Effect of Helicobacter pylori eradication on malignant transformation of gastric adenoma

Cited by 65 publications

References 31 publications

Constitutional activation of IL-6-mediated JAK/STAT pathway through hypermethylation of SOCS-1 in human gastric cancer cell line

Constitutional activation of IL-6-mediated JAK/STAT pathway through hypermethylation of SOCS-1 in human gastric cancer cell line

Prevalence of Helicobacter pylori infection in advanced gastric carcinoma

Eradication of H pylori for the prevention of gastric cancer

Contact Info

Product

Resources

About