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Carcinogenesis Advance Access originally published online on January 7, 2006
Carcinogenesis 2006 27(7):1391-1397; doi:10.1093/carcin/bgi334
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

A past history of gastric ulcers and Helicobacter pylori infection increase the risk of gastric malignant lymphoma

Takeshi Suzuki 1, 3, Keitaro Matsuo 1, *, Hidemi Ito 1, Kaoru Hirose 1, Kenji Wakai 1, Toshiko Saito 1, Shigeki Sato 3, Yasuo Morishima 2, Shigeo Nakamura 4, Ryuzo Ueda 3 and Kazuo Tajima 1

1 Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan, 2 Department of Hematology and Cell Therapy, Aichi Cancer Center Hospital, Nagoya, Japan, 3 Department of Internal Medicine and Molecular Science, Nagoya City University Graduate School of Medical Science, Nagoya, Japan and 4 Department of Clinical Pathophysiology, Nagoya University Graduate School of Medicine, Nagoya, Japan

* To whom correspondence should be addressed. Tel: +81 52 762 6111; Fax: +81 52 763 5233; Email: kmatsuo{at}aichi-cc.jp

Helicobacter pylori (H. pylori) is a causative agent for peptic ulcers as well as some types of gastric lymphoma; however, the relationship between a peptic ulcer history in combination with H. pylori infection and the risk of gastric lymphoma has not been fully evaluated. To examine this point, we conducted a case-control study with 645 patients histologically diagnosed as having malignant lymphomas and 3225 non-cancer controls. Plasma H. pylori IgG status was assessed for subgroups for which blood samples were available (116 cases and 114 controls). An association with a history of gastric, but not duodenal ulcers was found for gastric lymphoma [odds ratio (OR) = 5.41, 95% confidence interval (CI): 3.12–9.39]. In the examination according to histological subtype, the OR was high for both gastric mucous-associated lymphoid tissue (MALT) lymphoma (OR = 5.54, 95% CI: 2.56–12.01) and diffuse large B-cell lymphoma (DLBCL) (OR = 7.23, 95% CI: 2.62–19.90). In the analysis of H. pylori antibody, the risk of total gastric lymphoma was associated with H. pylori infection (OR = 5.34, 95% CI: 1.42–20.05). A high prevalence of H. pylori infection was also found for both gastric MALT lymphoma (8 out of 10: 80.0%) and DLBCL (8 out of 9: 88.9%). Further, in subgroup analysis of subjects with H. pylori infection, gastric ulcer history, but not duodenal ulcer history was associated with the risk of gastric lymphoma (OR = 4.15, 95% CI: 1.02–16.89). In conclusion, we found a positive association with a past history of gastric ulcer and H. pylori infection for gastric lymphoma, while duodenal ulcer history was no association. These results suggested the risk of gastric lymphoma increased by interaction between H. pylori infection and gastric ulcer history. Further studies are warranted.


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