Helicobacter pylori infection in relation to gastric cancer progression

Ananthapur, Venkateshwari; Krishnaveni, Devulapalli; Venugopal, Sangeetha; Shashikumar, Pratibha; Vidyasagar, A.; Jyothy, A.

doi:10.4103/0019-509x.75840

Cited by 16 publications

(9 citation statements)

References 24 publications

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“…Hence, it could be deduced that H. pylori is present in the asymptomatic subjects but the virulent factors are expressed in a fraction of them. However, virulent strains may give rise to a plethora of gastric diseases when the suitable pathobiological conditions culminate in the gastric environment of the patients [27][28][29][30][31][32][33][34][35][36][37] .…”

Section: Discussionmentioning

confidence: 99%

Association of smoking, alcohol and NSAIDs use with expression of cag A and cag T genes of Helicobacter pylori in salivary samples of asymptomatic subjects

Ghosh

Bodhankar

2012

Asian Pacific Journal of Tropical Biomedicine

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Section: Discussionmentioning

confidence: 99%

Association of smoking, alcohol and NSAIDs use with expression of cag A and cag T genes of Helicobacter pylori in salivary samples of asymptomatic subjects

Ghosh

Bodhankar

2012

Asian Pacific Journal of Tropical Biomedicine

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“…Even to the cases of non-gastrointestinal diseases, such as chronic cardiovascular disease, liver and biliary tract diseases and colorectal cancer, H. pylori also has a synergistic contribution[2]. In 1994 H. pylori was labeled as one of the first class cancer causing factors by the International Institute for Cancer Research[3]. Over half of the world’s population are infected with H. pylori during their lifetime.…”

Section: Introductionmentioning

confidence: 99%

Gene polymorphisms of pathogenic Helicobacter pylori in patients with different types of gastrointestinal diseases

Chen¹,

Mo²,

Huang³

et al. 2016

WJG

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Helicobacter pylori (H. pylori) is a kind of chronic infectious pathogen which can cause chronic gastritis, peptic ulcer, gastric cancer and other diseases. The genetic structure of the pathogenic genes of H. pylori varies largely, which contributes to the differences in virulence among various strains, and in clinical symptoms. Virulence genes of H. pylori can be categorized into three main classes: those related to adhesion and colonization, those related to gastric mucosal injury, and others. This review focuses on the relationship between genetic polymorphisms of the three classes of virulence genes of H. pylori and diseases. Most of the genetic polymorphisms of the main virulence factors of H. pylori are summarized in this paper.

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“…Helicobacter pylori infection, the preneoplastic lesion chronic atrophic gastritis, intestinal metaplasia, free radicals, and familial GC predisposition have been identified as risk factors for GC. [6][7][8][9][10][11] Recently, studies have demonstrated that H. pylori infection may double the risk of stomach cancer. Infection with a particular type of H. pylori called cytoxin-associated antigen A (cagA)-positive H. pylori can increase the risk even more.…”

Section: Introductionmentioning

confidence: 99%

Stepwise cumulation of RUNX3 methylation mediated by Helicobacter pylori infection contributes to gastric carcinoma progression

Liu

et al. 2012

Cancer

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BACKGROUND: Helicobacter pylori has been recognized as a definite carcinogen for gastric cancer (GC); however, the pathogenesis of H. pylori infection remains unclear. Runt-related transcription factor 3 (RUNX3) is a candidate tumor suppressor gene whose deficiency is causally related to GC. However, in H. pylori infection-associated GC, the role of RUNX3 has not been studied. METHODS: The authors used real-time methylation-specific polymerase chain reaction analysis to determine methylation status of the RUNX3 promoter in a spectrum of gastric lesions, including 220 samples of chronic atrophic gastritis, 196 samples of intestinal metaplasia, 134 samples of gastric adenoma, 102 samples of dysplasia, and 202 samples of GC with paired noncancerous mucosa tissues and corresponding blood specimens. The association of abnormal methylation with precancerous gastric lesions was evaluated along with the association between RUNX3 methylation and H. pylori infection, and the concordance of methylation levels was investigated between serum and tissues. RESULTS: The results indicated that increasing RUNX3 promoter methylation was correlated with distinct stages of GC progression. GC tissues had the highest methylation proportion (75.2%) compared with precancerous gastric lesions, including chronic atrophic gastritis (15.9%), intestinal metaplasia (36.7%), gastric adenoma (41.8%), and dysplasia (54.9%). H. pylori infection, a major risk factor for GC, contributed to the inactivation of RUNX3 in gastric epithelial cells through promoter hypermethylation. The levels of RUNX3 methylation in serum were in significant concordance with the methylation levels observed in GC tissues (P ¼ .887). CONCLUSIONS: The current findings supported RUNX3 methylation as a risk factors for the carcinogenesis of chronic atrophic gastritis with H. pylori infection and indicated that circulating RUNX3 methylation is a valuable biomarker for the detection of early GC.

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Helicobacter pylori infection in relation to gastric cancer progression

Cited by 16 publications

References 24 publications

Association of smoking, alcohol and NSAIDs use with expression of cag A and cag T genes of Helicobacter pylori in salivary samples of asymptomatic subjects

Association of smoking, alcohol and NSAIDs use with expression of cag A and cag T genes of Helicobacter pylori in salivary samples of asymptomatic subjects

Gene polymorphisms of pathogenic Helicobacter pylori in patients with different types of gastrointestinal diseases

Stepwise cumulation of RUNX3 methylation mediated by Helicobacter pylori infection contributes to gastric carcinoma progression

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