Assessment of gastric carcinoma risk associated with Helicobacter pylori may vary depending on the antigen used

Maeda, Shin; Yoshida, Haruhiko; Ogura, Keiji; Yamaji, Yutaka; Ikenoue, Tsuneo; Mitsushima, Toru; Tagawa, Hiroyuki; Kawaguchi, Ryuji; Mori, Kiyoshi; Mafune, Ken–ichi; Kawabe, Takao; Shiratori, Yasushi; Omata, Masao

doi:10.1002/(sici)1097-0142(20000401)88:7<1530::aid-cncr5>3.3.co;2-w

Cited by 10 publications

(9 citation statements)

References 13 publications

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“…We and other researchers in the United States, Germany, Sweden, and Japan noted that cagA ϩ H. pylori strains increase the risk of gastric cancer beyond that associated with other H. pylori strains [16][17][18][19][20][21]. However, this finding was not universal; some investigators in Asia reported either no accentuation of the risk associated with cagA ϩ strains or no relationship between the presence of cagA ϩ strains and an increased risk for gastric carcinoma [22][23][24].…”

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confidence: 99%

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Helicobacter pyloriCagA Seropositivity and Gastric Carcinoma Risk in a Japanese American Population

et al. 2002

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Helicobacter pylori colonization is associated with gastric cancer, but whether and to what extent the risk is greater for strains with the cagA gene than for those without needs to be determined. Between 1967 and 1977, 9963 Japanese American men were recruited and examined. By 1996, incident cases of gastric carcinoma of the distal stomach had been diagnosed in 261 men. Stored serum samples from these case patients and 261 age-matched control subjects were tested for immunoglobulin G antibodies to H. pylori and to the CagA product of H. pylori, using antibody-specific enzyme-linked immunosorbent assays. Compared with H. pylori-negative, CagA-negative men, H. pylori-positive, CagA-negative men had an odds ratio (OR) of 2.7 (95% confidence interval [CI], 1.3-5.6) for intestinal gastric carcinoma. Men seropositive for both H. pylori and CagA had an OR of 4.1 (95% CI, 2.2-7.7). This suggests that colonization by an H. pylori strain with the cagA gene is associated with a greater risk of intestinal gastric carcinoma.

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confidence: 99%

“…Furthermore, only 2 [16,17] of the 9 investigations used serum samples obtained many years before the diagnosis of gastric cancer. The other studies [18][19][20][21][22][23][24], which were crosssectional in design, tested serum samples collected at the time of diagnosis. This could have affected the results of the investigation.…”

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confidence: 99%

Helicobacter pyloriCagA Seropositivity and Gastric Carcinoma Risk in a Japanese American Population

et al. 2002

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“…Therefore, (112) the higher relative risk associated with CagA seropositivity observed in some studies may, in fact, reflect a better ability to classify correctly the true status of the past exposure. Discrepant findings may also result from the analysis of different populations, and the use of distinct methods of assays and/ or antigens to detect anti-CagA antibodies (70). In this regard, limitations in test reproducibility have already been reported (113).…”

Section: Discussionmentioning

confidence: 99%

Clinical Usefulness of Virulence Factors of Helicobacter pylori as Predictors of the Outcomes of Infection. What is the Evidence?

González

Peña

Capellà

2003

Scandinavian Journal of Gastroenterology

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“…H.pylori has been acknowledged as a possible carcinogen [3][4][5][6][7][8][9][10][11][12][13][14][15][16] . Genome integration is the most important carcinogenic mechanism in some microorganisms [19][20][21] .…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have showed that H.pylori infection is closely related with gastritis, peptic ulcer and gastric cancer, and may play a causative role at the early phases of this chain [3][4][5][6][7][8][9][10][11][12][13][14][15][16] . H.pylori was classified as a class I carcinogen by the International Agency for Research on Cancer in 1994.…”

Section: Introductionmentioning

confidence: 99%

Detection ofH. pyloriDNA in gastric epithelial cells byin situhybridization

Lu¹,

Qian²,

Tang³

et al. 2002

WJG

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AIM: To investigate the presence of H.pylori DNA within gastric epithelial cells in patients with H.pylori infection and its possible carcinogenic mechanism. METHODS:Total 112 patients, with pathologically confirmed chronic superficial gastritis, chronic atrophic gastritis, intestinal metaplasia, atypical hyperplasia or gastric cancer were studied. Among them, 28 were H.pylori negative and 84 H.pylori positive. H.pylori DNA in gastric epithelial cells was detected by GenPoint catalyzed signal amplification system for in situ hybridization. RESULTS:In the H.pylori positive group, zero out of 24 chronic superficial gastritis (0.0%), four out of 25 precancerous changes (16.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the nucleus of gastric epithelial cells, the positive rates of H.pylori DNA in the nucleus of gastric epithelial cells were progressively increased in chronic superficial gastritis, precancerous changes and gastric cancer groups (χ χ χ χ χ 2 =12.56, P=0.002); One out of 24 chronic superficial gastritis (4.2%), eleven out of 25 precancerous changes (44.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the cytoplasm of gastric epithelial cells (χ χ χ χ χ 2

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Assessment of gastric carcinoma risk associated with Helicobacter pylori may vary depending on the antigen used

Cited by 10 publications

References 13 publications

Helicobacter pyloriCagA Seropositivity and Gastric Carcinoma Risk in a Japanese American Population

Helicobacter pyloriCagA Seropositivity and Gastric Carcinoma Risk in a Japanese American Population

Clinical Usefulness of Virulence Factors of Helicobacter pylori as Predictors of the Outcomes of Infection. What is the Evidence?

Detection ofH. pyloriDNA in gastric epithelial cells byin situhybridization

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