Risks of interleukin-1 genetic polymorphisms and Helicobacter pylori infection in the development of gastric cancer

被引:51
作者
Chen, A
Li, CN
Hsu, PI
Lai, KH
Tseng, HH
Hsu, PN
Lo, GH
Lo, CC
Lin, CK
Hwang, IR
Yamaoka, Y
Chen, HC
机构
[1] Natl Sun Yat Sen Univ, Inst Biomed Sci, Kaohsiung 80424, Taiwan
[2] Natl Yang Ming Univ, Kaohsiung Vet Gen Hosp, Dept Internal Med, Div Gastroenterol, Kaohsiung, Taiwan
[3] Natl Yang Ming Univ, Kaohsiung Vet Gen Hosp, Dept Pathol, Kaohsiung, Taiwan
[4] Natl Taiwan Univ, Grad Inst Immunol, Taipei 10764, Taiwan
[5] Baylor Coll Med, Houston, TX 77030 USA
[6] Kaohsiung Chang Gung Mem Hosp, Dept Radiat Oncol, Kaohsiung, Taiwan
关键词
D O I
10.1111/j.1365-2036.2004.01826.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: The host genetic factors that determine the clinical outcomes of Helicobacter pylori-infected individuals remain unclear. Aims: To elucidate the risks of host interleukin-1 (IL-1) genetic polymorphisms and H. pylori infection in the development of gastric cancer. Methods: In a case-control study of 164 controls and 142 patients with gastric cancer, the IL-1B-511 biallelic polymorphisms and the IL-1RN penta-allelic variable number of tandem repeats were genotyped. Results: The carriage of IL-1RN*2, male gender, old age and H. pylori infection independently increased the risk of gastric cancer, with odds ratios of 3.3 [95% confidence interval (CI), 1.4-7.7], 2.1 (95% CI, 1.2-3.8), 5.3 (95% CI, 3.1-9.0) and 2.2 (95% CI, 1.3-3.8), respectively. H. pylori-infected individuals who were carriers of IL-1RN*2 showed increased risks of both intestinal and diffuse types of gastric cancer, with odds ratios of 11.0 and 8.7, respectively. In addition, these individuals also had a higher score of intestinal metaplasia in the corpus than did uninfected non-carriers. Conclusions: This study is the first to verify IL-1RN*2 as an independent factor governing the development of gastric cancer in Asian individuals. A combination of H. pylori testing and host genotyping may target the eradication of H. pylori to high-risk individuals.
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页码:203 / 211
页数:9
相关论文
共 46 条
[1]   Interleukin 1β and tumour necrosis factor α Inhibit acid secretion in cultured rabbit parietal cells by multiple pathways [J].
Beales, ILP ;
Calam, J .
GUT, 1998, 42 (02) :227-234
[2]  
BLASER MJ, 1995, CANCER RES, V55, P2111
[3]   Cellular responses induced after contact with Helicobacter pylori [J].
Censini, S ;
Stein, M ;
Covacci, A .
CURRENT OPINION IN MICROBIOLOGY, 2001, 4 (01) :41-46
[4]   Helicobacter pylori virulence and genetic geography [J].
Covacci, A ;
Telford, JL ;
Del Giudice, G ;
Parsonnet, J ;
Rappuoli, R .
SCIENCE, 1999, 284 (5418) :1328-1333
[5]  
DANIS VA, 1995, CLIN EXP IMMUNOL, V99, P303
[6]   Classification and grading of gastritis - The updated Sydney System [J].
Dixon, MF ;
Genta, RM ;
Yardley, JH ;
Correa, P ;
Batts, KP ;
Dahms, BB ;
Filipe, MI ;
Haggitt, RC ;
Haot, J ;
Hui, PK ;
Lechago, J ;
Lewin, K ;
Offerhaus, JA ;
Price, AB ;
Riddell, RH ;
Sipponen, P ;
Solcia, E ;
Watanabe, H .
AMERICAN JOURNAL OF SURGICAL PATHOLOGY, 1996, 20 (10) :1161-1181
[7]   Interleukin-1 polymorphisms associated with increased risk of gastric cancer [J].
El-Omar, EM ;
Carrington, M ;
Chow, WH ;
McColl, KEL ;
Bream, JH ;
Young, HA ;
Herrera, J ;
Lissowska, J ;
Yuan, CC ;
Rothman, N ;
Lanyon, G ;
Martin, M ;
Fraumeni, JF ;
Rabkin, CS .
NATURE, 2000, 404 (6776) :398-402
[8]  
El-Omar EM, 2001, GASTROENTEROLOGY, V121, P1002, DOI 10.1016/S0016-5085(01)93000-8
[9]   INVITRO PRODUCTION OF IL-1-BETA, IL-1-ALPHA, TNF AND IL-2 IN HEALTHY-SUBJECTS - DISTRIBUTION, EFFECT OF CYCLOOXYGENASE INHIBITION AND EVIDENCE OF INDEPENDENT GENE-REGULATION [J].
ENDRES, S ;
CANNON, JG ;
GHORBANI, R ;
DEMPSEY, RA ;
SISSON, SD ;
LONNEMANN, G ;
VANDERMEER, JWM ;
WOLFF, SM ;
DINARELLO, CA .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1989, 19 (12) :2327-2333
[10]  
Figueiredo C, 2002, J NATL CANCER I, V94, P1680, DOI 10.1093/jnci/94.22.1680