Rugal hyperplastic gastritis increases the risk of gastric carcinoma, especially diffuse and p53-independent subtypes

Akihiko Oguri, Naoki Omiya, Ayumu Taguchi, Akihiro Itoh, Yoshiki Hirooka, Yasumasa Niwa, Osamu Maeda, Takafumi Ando, Hidemi Goto

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

OBJECTIVES: Infection with Helicobacter pylori has been linked to chronic gastritis with atrophy or hyperrugosity. The development of noncardia gastric carcinoma, especially the intestinal type in Lauren's classification, has been associated with severe atrophic gastritis and p53 mutations. The objective of this study was to determine the association between hyperrugosity and gastric carcinogenesis, including p53 mutations. PARTICIPANTS AND METHODS: Barium meal roentgenograms were performed in 395 control participants and 132 gastric carcinoma patients. The fold width was measured at the greater curvature of the middle portion of the gastric body. Serum pepsinogens I and II were determined along with gastrin levels. Complete coding sequences and splice junctions for exons 5-8 of p53 gene were screened for mutations by polymerase chain reaction-based single-strand conformational polymorphism analysis. RESULTS: Rugal hyperplastic gastritis (gastric body fold width ≥ 5 mm) increased the risk of gastric carcinoma [odds ratio, 2.60; 95% confidence interval, 1.69-4.01] as compared with the control group, especially diffuse-type gastric carcinoma (odds ratio, 4.13; 95% confidence interval, 2.36-7.24). The p53 mutational rate was significantly lower in gastric carcinoma patients with rugal hyperplastic gastritis. In intestinal-type gastric carcinoma with hyperrugosity, the incidence of p53 gene mutations decreased, but no association was found in diffuse-type gastric carcinoma between p53 mutations and rugal hyperplastic gastritis. CONCLUSIONS: Rugal hyperplastic gastritis was associated with an elevated risk of gastric carcinoma, especially diffuse-type, and a lower frequency of p53 mutations.

Original languageEnglish
Pages (from-to)561-566
Number of pages6
JournalEuropean Journal of Gastroenterology and Hepatology
Volume19
Issue number7
DOIs
Publication statusPublished - 01-07-2007
Externally publishedYes

Fingerprint

Gastritis
Stomach
Carcinoma
Mutation
p53 Genes
Pepsinogen C
Odds Ratio
Confidence Intervals
Pepsinogen A
Atrophic Gastritis
Gastrins
Mutation Rate
Barium
Helicobacter pylori
Atrophy
Meals
Exons
Carcinogenesis
Polymerase Chain Reaction
Control Groups

All Science Journal Classification (ASJC) codes

  • Gastroenterology

Cite this

Oguri, Akihiko ; Omiya, Naoki ; Taguchi, Ayumu ; Itoh, Akihiro ; Hirooka, Yoshiki ; Niwa, Yasumasa ; Maeda, Osamu ; Ando, Takafumi ; Goto, Hidemi. / Rugal hyperplastic gastritis increases the risk of gastric carcinoma, especially diffuse and p53-independent subtypes. In: European Journal of Gastroenterology and Hepatology. 2007 ; Vol. 19, No. 7. pp. 561-566.
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abstract = "OBJECTIVES: Infection with Helicobacter pylori has been linked to chronic gastritis with atrophy or hyperrugosity. The development of noncardia gastric carcinoma, especially the intestinal type in Lauren's classification, has been associated with severe atrophic gastritis and p53 mutations. The objective of this study was to determine the association between hyperrugosity and gastric carcinogenesis, including p53 mutations. PARTICIPANTS AND METHODS: Barium meal roentgenograms were performed in 395 control participants and 132 gastric carcinoma patients. The fold width was measured at the greater curvature of the middle portion of the gastric body. Serum pepsinogens I and II were determined along with gastrin levels. Complete coding sequences and splice junctions for exons 5-8 of p53 gene were screened for mutations by polymerase chain reaction-based single-strand conformational polymorphism analysis. RESULTS: Rugal hyperplastic gastritis (gastric body fold width ≥ 5 mm) increased the risk of gastric carcinoma [odds ratio, 2.60; 95{\%} confidence interval, 1.69-4.01] as compared with the control group, especially diffuse-type gastric carcinoma (odds ratio, 4.13; 95{\%} confidence interval, 2.36-7.24). The p53 mutational rate was significantly lower in gastric carcinoma patients with rugal hyperplastic gastritis. In intestinal-type gastric carcinoma with hyperrugosity, the incidence of p53 gene mutations decreased, but no association was found in diffuse-type gastric carcinoma between p53 mutations and rugal hyperplastic gastritis. CONCLUSIONS: Rugal hyperplastic gastritis was associated with an elevated risk of gastric carcinoma, especially diffuse-type, and a lower frequency of p53 mutations.",
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Rugal hyperplastic gastritis increases the risk of gastric carcinoma, especially diffuse and p53-independent subtypes. / Oguri, Akihiko; Omiya, Naoki; Taguchi, Ayumu; Itoh, Akihiro; Hirooka, Yoshiki; Niwa, Yasumasa; Maeda, Osamu; Ando, Takafumi; Goto, Hidemi.

In: European Journal of Gastroenterology and Hepatology, Vol. 19, No. 7, 01.07.2007, p. 561-566.

Research output: Contribution to journalArticle

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T1 - Rugal hyperplastic gastritis increases the risk of gastric carcinoma, especially diffuse and p53-independent subtypes

AU - Oguri, Akihiko

AU - Omiya, Naoki

AU - Taguchi, Ayumu

AU - Itoh, Akihiro

AU - Hirooka, Yoshiki

AU - Niwa, Yasumasa

AU - Maeda, Osamu

AU - Ando, Takafumi

AU - Goto, Hidemi

PY - 2007/7/1

Y1 - 2007/7/1

N2 - OBJECTIVES: Infection with Helicobacter pylori has been linked to chronic gastritis with atrophy or hyperrugosity. The development of noncardia gastric carcinoma, especially the intestinal type in Lauren's classification, has been associated with severe atrophic gastritis and p53 mutations. The objective of this study was to determine the association between hyperrugosity and gastric carcinogenesis, including p53 mutations. PARTICIPANTS AND METHODS: Barium meal roentgenograms were performed in 395 control participants and 132 gastric carcinoma patients. The fold width was measured at the greater curvature of the middle portion of the gastric body. Serum pepsinogens I and II were determined along with gastrin levels. Complete coding sequences and splice junctions for exons 5-8 of p53 gene were screened for mutations by polymerase chain reaction-based single-strand conformational polymorphism analysis. RESULTS: Rugal hyperplastic gastritis (gastric body fold width ≥ 5 mm) increased the risk of gastric carcinoma [odds ratio, 2.60; 95% confidence interval, 1.69-4.01] as compared with the control group, especially diffuse-type gastric carcinoma (odds ratio, 4.13; 95% confidence interval, 2.36-7.24). The p53 mutational rate was significantly lower in gastric carcinoma patients with rugal hyperplastic gastritis. In intestinal-type gastric carcinoma with hyperrugosity, the incidence of p53 gene mutations decreased, but no association was found in diffuse-type gastric carcinoma between p53 mutations and rugal hyperplastic gastritis. CONCLUSIONS: Rugal hyperplastic gastritis was associated with an elevated risk of gastric carcinoma, especially diffuse-type, and a lower frequency of p53 mutations.

AB - OBJECTIVES: Infection with Helicobacter pylori has been linked to chronic gastritis with atrophy or hyperrugosity. The development of noncardia gastric carcinoma, especially the intestinal type in Lauren's classification, has been associated with severe atrophic gastritis and p53 mutations. The objective of this study was to determine the association between hyperrugosity and gastric carcinogenesis, including p53 mutations. PARTICIPANTS AND METHODS: Barium meal roentgenograms were performed in 395 control participants and 132 gastric carcinoma patients. The fold width was measured at the greater curvature of the middle portion of the gastric body. Serum pepsinogens I and II were determined along with gastrin levels. Complete coding sequences and splice junctions for exons 5-8 of p53 gene were screened for mutations by polymerase chain reaction-based single-strand conformational polymorphism analysis. RESULTS: Rugal hyperplastic gastritis (gastric body fold width ≥ 5 mm) increased the risk of gastric carcinoma [odds ratio, 2.60; 95% confidence interval, 1.69-4.01] as compared with the control group, especially diffuse-type gastric carcinoma (odds ratio, 4.13; 95% confidence interval, 2.36-7.24). The p53 mutational rate was significantly lower in gastric carcinoma patients with rugal hyperplastic gastritis. In intestinal-type gastric carcinoma with hyperrugosity, the incidence of p53 gene mutations decreased, but no association was found in diffuse-type gastric carcinoma between p53 mutations and rugal hyperplastic gastritis. CONCLUSIONS: Rugal hyperplastic gastritis was associated with an elevated risk of gastric carcinoma, especially diffuse-type, and a lower frequency of p53 mutations.

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