The association between tumour necrosis factor-α gene polymorphism and the susceptibility to rugal hyperplastic gastritis and gastric carcinoma

Itaru Ohyama, Naoki Ohmiya, Yasumasa Niwa, Kennosuke Shirai, Ayumu Taguchi, Akihiro Itoh, Yoshiki Hirooka, Kenji Wakai, Nobuyuki Hamajima, Naoyoshi Mori, Hidemi Goto

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Objectives: Some subjects infected by Helicobacter pylori have enlarged folds in the gastric body, the precise mechanism of which remains obscure. The aim of this study was to clarify the association of tumour necrosis factor-α (TNFA) gene polymorphism with susceptibility to hyper-rugosity. We also examined the association of TNFA polymorphism with gastric carcinoma. Subjects and methods: Four hundred and seventy-two subjects (male/female = 351/121, aged 26-81 years) without gastric carcinoma (control group), and 300 patients (male/female = 218/82, aged 32-91 years) with gastric carcinoma. Barium meal roentgenograms were performed in 396 subjects in the control group and fold width was measured at the greater curvature of the middle portion of the gastric body. Fasting plasma anti-H. pylori IgG titres, pepsinogens (PGs) I and II were analysed, and TNFA -857 promoter polymorphism was distinguished by the 5′ nuclease polymerase chain reaction assay and polymerase chain reaction restriction fragment length polymorphism using Hincll in both groups. Results: Adjusted odds ratios of TNFA -857 T/T genotype and H. pylori seropositivity for hyper-rugosity (fold width = 6.0 mm) were 6.7 (95% confidence interval (Cl) 1.5-28, P < 0.01) and 18,2 (95% CI 4.2-78, P < 0.0001), respectively. There were no significant differences in any genotype or allele frequencies between the control and total gastric carcinoma group. In a subgroup of gastric carcinoma patients who were negative for the PG assay, however, the odds ratio of the T allele was 1.4 (95% Cl 1.0-2.0, P < 0.05). Conclusion: The TNFA -857 T/T genotype and H. pylori infection were strongly associated with rugal hyperplastic gastritis. The TNFA -857 T allele may promote gastric carcinoma without severe atrophy.

Original languageEnglish
Pages (from-to)693-700
Number of pages8
JournalEuropean Journal of Gastroenterology and Hepatology
Volume16
Issue number7
DOIs
Publication statusPublished - 01-07-2004
Externally publishedYes

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Gastritis
Stomach
Tumor Necrosis Factor-alpha
Carcinoma
Helicobacter pylori
Genes
Genotype
Pepsinogens
Pepsinogen C
Alleles
Odds Ratio
Pepsinogen A
Polymerase Chain Reaction
Control Groups
Helicobacter Infections
Barium
Gene Frequency
Restriction Fragment Length Polymorphisms
Atrophy
Meals

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Gastroenterology

Cite this

Ohyama, Itaru ; Ohmiya, Naoki ; Niwa, Yasumasa ; Shirai, Kennosuke ; Taguchi, Ayumu ; Itoh, Akihiro ; Hirooka, Yoshiki ; Wakai, Kenji ; Hamajima, Nobuyuki ; Mori, Naoyoshi ; Goto, Hidemi. / The association between tumour necrosis factor-α gene polymorphism and the susceptibility to rugal hyperplastic gastritis and gastric carcinoma. In: European Journal of Gastroenterology and Hepatology. 2004 ; Vol. 16, No. 7. pp. 693-700.
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abstract = "Objectives: Some subjects infected by Helicobacter pylori have enlarged folds in the gastric body, the precise mechanism of which remains obscure. The aim of this study was to clarify the association of tumour necrosis factor-α (TNFA) gene polymorphism with susceptibility to hyper-rugosity. We also examined the association of TNFA polymorphism with gastric carcinoma. Subjects and methods: Four hundred and seventy-two subjects (male/female = 351/121, aged 26-81 years) without gastric carcinoma (control group), and 300 patients (male/female = 218/82, aged 32-91 years) with gastric carcinoma. Barium meal roentgenograms were performed in 396 subjects in the control group and fold width was measured at the greater curvature of the middle portion of the gastric body. Fasting plasma anti-H. pylori IgG titres, pepsinogens (PGs) I and II were analysed, and TNFA -857 promoter polymorphism was distinguished by the 5′ nuclease polymerase chain reaction assay and polymerase chain reaction restriction fragment length polymorphism using Hincll in both groups. Results: Adjusted odds ratios of TNFA -857 T/T genotype and H. pylori seropositivity for hyper-rugosity (fold width = 6.0 mm) were 6.7 (95{\%} confidence interval (Cl) 1.5-28, P < 0.01) and 18,2 (95{\%} CI 4.2-78, P < 0.0001), respectively. There were no significant differences in any genotype or allele frequencies between the control and total gastric carcinoma group. In a subgroup of gastric carcinoma patients who were negative for the PG assay, however, the odds ratio of the T allele was 1.4 (95{\%} Cl 1.0-2.0, P < 0.05). Conclusion: The TNFA -857 T/T genotype and H. pylori infection were strongly associated with rugal hyperplastic gastritis. The TNFA -857 T allele may promote gastric carcinoma without severe atrophy.",
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The association between tumour necrosis factor-α gene polymorphism and the susceptibility to rugal hyperplastic gastritis and gastric carcinoma. / Ohyama, Itaru; Ohmiya, Naoki; Niwa, Yasumasa; Shirai, Kennosuke; Taguchi, Ayumu; Itoh, Akihiro; Hirooka, Yoshiki; Wakai, Kenji; Hamajima, Nobuyuki; Mori, Naoyoshi; Goto, Hidemi.

In: European Journal of Gastroenterology and Hepatology, Vol. 16, No. 7, 01.07.2004, p. 693-700.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The association between tumour necrosis factor-α gene polymorphism and the susceptibility to rugal hyperplastic gastritis and gastric carcinoma

AU - Ohyama, Itaru

AU - Ohmiya, Naoki

AU - Niwa, Yasumasa

AU - Shirai, Kennosuke

AU - Taguchi, Ayumu

AU - Itoh, Akihiro

AU - Hirooka, Yoshiki

AU - Wakai, Kenji

AU - Hamajima, Nobuyuki

AU - Mori, Naoyoshi

AU - Goto, Hidemi

PY - 2004/7/1

Y1 - 2004/7/1

N2 - Objectives: Some subjects infected by Helicobacter pylori have enlarged folds in the gastric body, the precise mechanism of which remains obscure. The aim of this study was to clarify the association of tumour necrosis factor-α (TNFA) gene polymorphism with susceptibility to hyper-rugosity. We also examined the association of TNFA polymorphism with gastric carcinoma. Subjects and methods: Four hundred and seventy-two subjects (male/female = 351/121, aged 26-81 years) without gastric carcinoma (control group), and 300 patients (male/female = 218/82, aged 32-91 years) with gastric carcinoma. Barium meal roentgenograms were performed in 396 subjects in the control group and fold width was measured at the greater curvature of the middle portion of the gastric body. Fasting plasma anti-H. pylori IgG titres, pepsinogens (PGs) I and II were analysed, and TNFA -857 promoter polymorphism was distinguished by the 5′ nuclease polymerase chain reaction assay and polymerase chain reaction restriction fragment length polymorphism using Hincll in both groups. Results: Adjusted odds ratios of TNFA -857 T/T genotype and H. pylori seropositivity for hyper-rugosity (fold width = 6.0 mm) were 6.7 (95% confidence interval (Cl) 1.5-28, P < 0.01) and 18,2 (95% CI 4.2-78, P < 0.0001), respectively. There were no significant differences in any genotype or allele frequencies between the control and total gastric carcinoma group. In a subgroup of gastric carcinoma patients who were negative for the PG assay, however, the odds ratio of the T allele was 1.4 (95% Cl 1.0-2.0, P < 0.05). Conclusion: The TNFA -857 T/T genotype and H. pylori infection were strongly associated with rugal hyperplastic gastritis. The TNFA -857 T allele may promote gastric carcinoma without severe atrophy.

AB - Objectives: Some subjects infected by Helicobacter pylori have enlarged folds in the gastric body, the precise mechanism of which remains obscure. The aim of this study was to clarify the association of tumour necrosis factor-α (TNFA) gene polymorphism with susceptibility to hyper-rugosity. We also examined the association of TNFA polymorphism with gastric carcinoma. Subjects and methods: Four hundred and seventy-two subjects (male/female = 351/121, aged 26-81 years) without gastric carcinoma (control group), and 300 patients (male/female = 218/82, aged 32-91 years) with gastric carcinoma. Barium meal roentgenograms were performed in 396 subjects in the control group and fold width was measured at the greater curvature of the middle portion of the gastric body. Fasting plasma anti-H. pylori IgG titres, pepsinogens (PGs) I and II were analysed, and TNFA -857 promoter polymorphism was distinguished by the 5′ nuclease polymerase chain reaction assay and polymerase chain reaction restriction fragment length polymorphism using Hincll in both groups. Results: Adjusted odds ratios of TNFA -857 T/T genotype and H. pylori seropositivity for hyper-rugosity (fold width = 6.0 mm) were 6.7 (95% confidence interval (Cl) 1.5-28, P < 0.01) and 18,2 (95% CI 4.2-78, P < 0.0001), respectively. There were no significant differences in any genotype or allele frequencies between the control and total gastric carcinoma group. In a subgroup of gastric carcinoma patients who were negative for the PG assay, however, the odds ratio of the T allele was 1.4 (95% Cl 1.0-2.0, P < 0.05). Conclusion: The TNFA -857 T/T genotype and H. pylori infection were strongly associated with rugal hyperplastic gastritis. The TNFA -857 T allele may promote gastric carcinoma without severe atrophy.

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