Lu Y-Thanh, Gunathilake Madhawa, Lee Jeonghee, Choi Il Ju, Kim Young-Il, Kim Jeongseon
Department of Cancer Control and Population Health, Graduate School of Cancer Science and Policy, Goyang-si, Gyeonggi-do, Republic of Korea.
Department of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, Goyang-si, Gyeonggi-do, Republic of Korea.
Br J Nutr. 2022 Apr 14;127(7):1026-1033. doi: 10.1017/S0007114521001811. Epub 2021 Jun 3.
The vitamin B group, including riboflavin, plays paramount roles in one-carbon metabolism (OCM), and disorders related to this pathway have been linked to cancer development. The variants of genes encoding OCM enzymes and the insufficiency of B vitamins could contribute to carcinogenesis. Very few observational studies have revealed a relationship between riboflavin and gastric cancer (GC), especially under conditions of modified genetic factors. We carried out a study examining the association of riboflavin intake and its interaction with MTRR (rs1532268) genetic variants with GC risk among 756 controls and 377 cases. The OR and 95 % CI were evaluated using unconditional logistic regression models. We observed protective effects of riboflavin intake against GC, particularly in the female subgroup (OR = 0·52, 95 % CI 0·28, 0·97, Ptrend = 0·031). In the MTRR (rs1532268) genotypes analysis, the dominant model showed that the effects of riboflavin differed between the CC and CT + TT genotypes. Compared with CC carriers, low riboflavin intake in T+ carriers was significantly associated with a 93 % higher GC risk (OR = 1·93, 95 % CI 1·09, 3·42, Pinteraction = 0·037). In general, higher riboflavin intake might help reduce the risk of GC in both CC and TC + TT carriers, particularly the T+ carriers, with marginal significance (OR = 0·54, 95 % CI 0·28, 1·02, Pinteraction = 0·037). Our study indicates a protective effect of riboflavin intake against GC. Those who carry at least one minor allele and have low riboflavin intake could modify this association to increase GC risk in the Korean population.
包括核黄素在内的B族维生素在一碳代谢(OCM)中起着至关重要的作用,与该途径相关的紊乱与癌症发展有关。编码OCM酶的基因变异和B族维生素的不足可能导致致癌作用。很少有观察性研究揭示核黄素与胃癌(GC)之间的关系,特别是在基因因素改变的情况下。我们进行了一项研究,在756名对照者和377例病例中检验核黄素摄入量及其与MTRR(rs1532268)基因变异的相互作用与GC风险的关联。使用无条件逻辑回归模型评估比值比(OR)和95%可信区间(CI)。我们观察到核黄素摄入对GC有保护作用,特别是在女性亚组中(OR = 0·52, 95% CI 0·28, 0·97, P趋势 = 0·031)。在MTRR(rs1532268)基因型分析中,显性模型显示核黄素的作用在CC基因型和CT + TT基因型之间有所不同。与CC携带者相比,T+携带者中低核黄素摄入与GC风险显著高出93%相关(OR = 1·93, 95% CI 1·09, 3·42, P相互作用 = 0·037)。总体而言,较高核黄素摄入量可能有助于降低CC和TC + TT携带者,特别是T+携带者的GC风险,具有边缘显著性(OR = 0·54, 95% CI 0·28, 1·02, P相互作用 = 0·037)。我们的研究表明核黄素摄入对GC有保护作用。在韩国人群中,携带至少一个次要等位基因且核黄素摄入量低的人可能会改变这种关联以增加GC风险。