Song Sang Shin, Huang ShaoKai, Park Sunmin
Obesity/Diabetes Research Center, Department of Food and Nutrition, Hoseo University, Asan 31499, Korea.
Department of Bio-Convergence System, Hoseo University, Asan 31499, Korea.
Cancers (Basel). 2021 Mar 25;13(7):1510. doi: 10.3390/cancers13071510.
The incidence of thyroid cancer continues to increase steadily, and this increasing incidence cannot be attributed solely to the overdiagnosis of microcarcinoma or technical advancements in detection methods and may also depend on environmental and genetic factors. However, the impacts and interactions of genetic and environmental factors remain controversial, and they may differ in Eastern and Western countries. The study's purpose was to identify single nucleotide polymorphisms of genes related to cell differentiation and inflammation to influence thyroid cancer incidence and determine interactions with lifestyles in a large city hospital-based cohort. Genetic variants were selected by genome-wide association study with thyroid cancer participants (case; = 495) and controls without cancers ( = 56,439). SNPs having gene-gene interactions were selected by generalized multifactor dimensionality reduction. Polygenic risk scores (PRSs) were generated by summing the number of selected SNP risk alleles. PRSs of the best model included 6 SNPs, that is, _rs6759952, _rs13059137, _rs7834206, _rs72616195, _rs1369535, and _rs11175834. Participants with a high-PRS had a higher thyroid cancer risk by 3.9-fold than those with a low-PRS. The following variables were related to an increased thyroid cancer risk; female (OR = 4.21), high white blood cell count (OR = 4.03), and high energy (OR = 7.00), low alcohol (OR = 4.11), and high seaweed (OR = 4.02) intakes. These variables also interacted with PRS to influence thyroid cancer risk. Meat/noodle diet patterns interacted with PRSs to increase thyroid cancer risk ( = 0.0023). In conclusion, women with a high-PRS associated with cell differentiation and inflammation were at an elevated thyroid cancer risk. Daily energy, seaweeds, and alcohol intake interacted with PRS for thyroid cancer risk. These results could be applied to personalized nutrition plans to reduce the risk of thyroid cancer.
甲状腺癌的发病率持续稳步上升，而这种发病率的上升不能仅仅归因于微癌的过度诊断或检测方法的技术进步，还可能取决于环境和遗传因素。然而，遗传和环境因素的影响及相互作用仍存在争议，且在东西方国家可能有所不同。该研究的目的是在一家大型城市医院的队列中，识别与细胞分化和炎症相关基因的单核苷酸多态性，以影响甲状腺癌发病率，并确定与生活方式的相互作用。通过对甲状腺癌患者（病例组；n = 495）和无癌症的对照组（n = 56,439）进行全基因组关联研究来选择基因变异。通过广义多因素降维法选择具有基因-基因相互作用的单核苷酸多态性（SNP）。通过对选定的SNP风险等位基因数量求和来生成多基因风险评分（PRS）。最佳模型的PRS包括6个SNP，即_rs6759952、_rs13059137、_rs7834206、_rs72616195、_rs1369535和_rs11175834。高PRS参与者患甲状腺癌的风险比低PRS参与者高3.9倍。以下变量与甲状腺癌风险增加相关；女性（比值比 = 4.21）、高白细胞计数（比值比 = 4.03）、高能量（比值比 = 7.00）、低酒精摄入量（比值比 = 4.11）和高海藻摄入量（比值比 = 4.02）。这些变量也与PRS相互作用以影响甲状腺癌风险。肉类/面食饮食模式与PRS相互作用以增加甲状腺癌风险（P = 0.0023）。总之，具有与细胞分化和炎症相关的高PRS的女性患甲状腺癌的风险升高。每日能量、海藻和酒精摄入量与甲状腺癌风险的PRS相互作用。这些结果可应用于个性化营养计划以降低甲状腺癌风险。
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