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Original article Dietary mercury intake, the IL23R rs10889677 polymorphism, and the risk of gastric cancer: a hospital-based case-control study
Ji Hyun Kim1orcid , Madhawa Gunathilake1orcid , Jeonghee Lee2orcid , Il Ju Choi3orcid , Young-Il Kim3orcid , Jeongseon Kim1orcid
Epidemiol Health 2024;e2024051
DOI: https://doi.org/10.4178/epih.e2024051 [Accepted]
Published online: May 21, 2024
1National Cancer Center Graduate School of Cancer Science and Policy, Goyang-si, Korea
2National Cancer Center Graduate School of Cancer Science and Policy, Goyang-si, Korea
3Center for Gastric Cancer, National Cancer Center Hospital, National Cancer Center, Goyang-si, Korea
Corresponding author:  Jeongseon Kim,
Email: jskim@ncc.re.kr
Received: 30 January 2024   • Revised: 1 April 2024   • Accepted: 10 April 2024
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Abstract

OBJECTIVES
Mercury can stimulate immune responses through T helper 17 (Th17). The gene IL23R is a key factor in Th17 function, which may also contribute to digestive tract diseases. The aim of this study was to observe the associations between dietary mercury and gastric cancer (GC) and to investigate whether the IL23R rs10889677 polymorphism modifies those associations.
METHODS
This case-control study included 377 patients with GC and 756 healthy controls. Dietary mercury intake (total mercury and methylmercury) was assessed using a dietary heavy metal database incorporated into the food frequency questionnaire. IL23R genetic polymorphism rs10889677 (A>C) was genotyped. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression models with adjustments for potential confounders.
RESULTS
A higher dietary methylmercury intake was associated with an elevated risk of GC (OR for the highest versus lowest tertile [T3 vs. T1]=2.02; 95% CI, 1.41–2.91; p for trend <0.001). The IL23R rs10889677 reduced the risk of GC in individuals who carried at least 1 minor allele (OR=0.62; 95% CI, 0.46–0.83; p=0.001; AC/CC vs. AA). Individuals with a C allele exhibited a lower susceptibility to GC through methylmercury intake than those with the AA genotype (OR for the T3 of methylmercury and AA carriers=2.93; 95% CI, 1.77–4.87; and OR for the T3 of methylmercury and AC/CC genotype=1.30; 95% CI, 0.76–2.21; p-interaction=0.013).
CONCLUSIONS
Our findings suggest that a genetic polymorphism, rs10889677 in IL23R, plays a role in modifying the association between dietary methylmercury intake and the risk of GC.

Epidemiol Health : Epidemiology and Health
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