Relationships between cagA, vacA, and iceA genotypes of Helicobacter pylori and DNA damage in the gastric mucosa
Helicobacter pylori (H. pylori) is believed to predispose carriers to gastric cancer by inducing chronic inflammation. The inflammatory processes may result in the generation of reactive oxygen and nitrogen species that damage DNA. In this study, we investigated the relationships between DNA damage...
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Published in: | Environmental and molecular mutagenesis Vol. 44; no. 2; pp. 91 - 98 |
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Main Authors: | , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
2004
Wiley-Liss |
Subjects: | |
Online Access: | Get full text |
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Summary: | Helicobacter pylori (H. pylori) is believed to predispose carriers to gastric cancer by inducing chronic inflammation. The inflammatory processes may result in the generation of reactive oxygen and nitrogen species that damage DNA. In this study, we investigated the relationships between DNA damage in the gastric mucosa and cagA, vacA, and iceA genotypes of H. pylori. The study was conducted with biopsies from the gastric antrum and corpus of 98 H. pylori‐infected and 26 uninfected control patients. H. pylori genotypes were determined by PCR and DNA damage was measured in gastric mucosal cells by the Comet assay (single cell gel electrophoresis). All patients were nonsmokers, not abusing alcohol, and not using prescription or recreational drugs. Levels of DNA damage were significantly higher (P < 0.0001) in the H. pylori‐infected patients than in uninfected patients. In comparison with the level of DNA damage in the uninfected controls, the extent of DNA damage in both the antrum (OR = 8.45; 95% CI = 2.33–37.72) and the corpus (OR = 6.55; 95% CI = 2.52–17.72) was related to infection by cagA+/vacAs1m1 and iceA1 strains. The results indicate that the genotype of H. pylori is related to the amount of DNA damage in the gastric mucosa. These genotypes could serve as biomarkers for the risk of extensive DNA damage and possibly gastric cancer. Environ. Mol. Mutagen. 44:91–98, 2004. © 2004 Wiley‐Liss, Inc. |
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Bibliography: | Fundação de Amparo à Pesquisa do Estado de São Paulo - No. 97/05026-3; No. 03/09217-0; No. 97/11839-7; No. 03/05043-5 istex:6CF4B5BD7EF373EE6BBC61023D9CC5AD29B8C823 ArticleID:EM20045 ark:/67375/WNG-H23X0308-N ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
ISSN: | 0893-6692 1098-2280 |
DOI: | 10.1002/em.20045 |