Open AccessSignificance of CXCR3 expression in gastric low‐grade B‐cell lymphoma of mucosa‐associated lymphoid tissue type for predicting responsiveness to Helicobacter pylori eradication
Author(s) -
Yamamoto Hideko,
Nakamura Tsuneya,
Matsuo Keitaro,
Tajika Masahiro,
Kawai Hiroki,
Ohmiya Naoki,
Niwa Yasumasa,
Goto Hidemi,
Nakamura Shigeo
Publication year - 2008
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2008.00883.x
Subject(s) - helicobacter pylori , cxcr3 , medicine , malt lymphoma , lymphoma , mucosa associated lymphoid tissue , gastric mucosa , gastroenterology , odds ratio , immunology , stomach , chemokine , chemokine receptor , inflammation
Gastric mucosa‐associated lymphoid tissue (MALT) lymphoma is a distinct low‐grade lymphoma that often regresses upon Helicobacter pylori eradication. It was reported that the chemokine receptor CXCR3 is expressed not only on activated T cells, but also on MALT lymphoma cells, and that CXCR3‐positive B lymphocytes migrate or home to the MALT of MALT lymphoma. In the present study, we aimed to elucidate the correlation between CXCR3 expression and the clinicopathological features of gastric MALT lymphoma, and to determine whether CXCR3 expression was predictive of responsiveness to H. pylori eradication. Sixty‐seven patients with gastric MALT lymphoma in a single‐center study were treated with H. pylori eradication therapy. We evaluated the correlation of CXCR3 expression with response to H. pylori eradication therapy by logistic regression stratified according to potential confounders. Immunohistochemical analysis revealed that 28 of 67 cases (42%) were positive for CXCR3 expression. CXCR3 expression was significantly more prevalent in those without H. pylori infection, advanced‐stage disease, and in those with API2–MALT1 fusion. In overall analysis, those with CXCR3 expression showed a significantly increased risk of non‐responsiveness to H. pylori eradication therapy (odds ratio = 28.6; 95% confidence interval 5.70–143.4) compared to those without CXCR3 expression. This higher risk was observed consistently regardless of sex, API2–MALT1 fusion, H. pylori infection, or clinical stage. We showed that CXCR3 expression was an independent predictive factor for non‐responsiveness to H. pylori eradication therapy in patients with gastric MALT lymphoma. ( Cancer Sci 2008; 99: 1769–1773)