This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Magnusson, P. K. E. Articles by Gyllensten, U. B. Search for Related Content PubMed PubMed Citation Articles by Magnusson, P. K. E. Articles by Gyllensten, U. B.

Gastric Cancer and Human Leukocyte Antigen

Distinct DQ and DR Alleles Are Associated with Development of Gastric Cancer and Infection by Helicobacter pylori¹

Department of Genetics and Pathology, Section of Medical Genetics, Rudbeck Laboratory, SE-751 85 Uppsala [P. K. E. M., I. E., U. B. G.]; Department of Medical Epidemiology, Karolinska Institutet, SE-171 77, Stockholm [H. E., M. H., O. N., L. E., L-E. H.]; and Smittskyddsinstitutet, SE-105 21 Stockholm [L. E.], Sweden

DNA and sera from 130 cases of gastric cancer and 263 population-based controls were analyzed to study the association of HLA class II DR-DQ alleles with Helicobacter pylori (Hp) infection and the risk for gastric cancer. Presence of the DQA1*0102 allele was inversely and significantly associated with Hp seropositivity (P = 2 x 10^-5), which is an independent replication of previous findings. However, this inverse relationship with Hp did not correspond with a reduced risk of gastric cancer. At the DRB1 locus, the *1601 allele was significantly associated with an increased gastric cancer risk with an odds ratio (95% confidence interval) of 8.7 (range, 2.7–28.0). The effect of *1601 was more pronounced among Hp-negative subjects, and the association was stronger with the diffuse, rather than with the intestinal, histological type of gastric cancer. Because none of the HLA alleles were associated with both Hp infection and gastric cancer, the HLA DR-DQ alleles are linked with gastric cancer risk through other mechanisms than an increased susceptibility to Hp infection.

This article has been cited by other articles:

				Q. Huang and L. H. Zhang The Histopathologic Spectrum of Carcinomas Involving the Gastroesophageal Junction in the Chinese International Journal of Surgical Pathology, January 1, 2007; 15(1): 38 - 52. [Abstract] [PDF]

				M.-S. Wu, C.-J. Chen, and J.-T. Lin Host-Environment Interactions: Their Impact on Progression from Gastric Inflammation to Carcinogenesis and on Development of New Approaches to Prevent and Treat Gastric Cancer Cancer Epidemiol. Biomarkers Prev., August 1, 2005; 14(8): 1878 - 1882. [Abstract] [Full Text] [PDF]

				D. Veneri, M. Gottardi, E. Guizzardi, C. Zanuso, M. Krampera, M. Franchini, G. Emilia, M. Luppi, M. Morselli, G. Longo, et al. Idiopathic thrombocytopenic purpura, Helicobacter pylori infection, and HLA class II alleles Blood, August 13, 2002; 100(5): 1925 - 1927. [Full Text] [PDF]