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Night-shift work, circadian and melatonin pathway related genes and their interaction on breast cancer risk: evidence from a case-control study in Korean women

机译:夜班工作,昼夜思想和褪黑激素途径相关基因及其对乳腺癌风险的互动:韩国女性案例对照研究的证据

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Our purpose is to investigate the impact of circadian and melatonin pathway genes as well as their interactions with night-shift work (NSW) on breast cancer risk in Korean women. Information about NSW and other covariates was collected using a structured questionnaire and twenty-two polymorphisms in 11 genes were analyzed in a hospital-based case-control study with 941 cases of breast cancer and 959 controls. In analysis of the main effects of each single nucleotide polymorphisms(SNPs), variants in CLOCK rs11133373 was associated with breast cancer risk even after false discovery rate (FDR) correction (Odd Ratios (OR)?=?1.38 (95% Confident Interval (CI) 1.14-1.69) in CG and CC compared to GG genotype. Analysis of MTNR1A rs2119882 demonstrated a decreased risk of breast cancer in CC compared to TT (p-FDR?=?0.043). A correlation between NSW and breast cancer interaction was found in two loci. NSW increased risk of breast cancer in women who carried the heterozygote genotype of CRY2 rs2292912 (OR?=?1.98, 95% CI?=?1.14-3.44) or carried at least one minor allele of RORA rs1482057 (OR?=?2.20, 95% CI?=?1.10-4.37). Our study results support a putative role for several loci of circadian genes and genes of melatonin biosynthesis and their interaction, and the gene interactions with NSW in the development of breast cancer.
机译:我们的目的是调查昼夜派发和褪黑激素途径基因的影响以及韩国女性乳腺癌风险对夜班工作(NSW)的影响。有关NSW和其他协变量的信息使用结构化问卷收集,并在3个基于医院的病例对照研究中分析了11种基因中的22种多态性,其乳腺癌和959例对照组。在分析每种单一核苷酸多态性(SNP)的主要效果中,即使在虚假发现率(FDR)校正(奇数比率(或)?=?1.38(95%自信间隔(95%)(95%)(95%自信)校正后,时钟RS11133373中的变体与乳腺癌风险有关。 CI)1.14-1.69)在CG和CC与GG基因型相比。MTNR1A RS2119882的分析表明,与TT(P-FDR?= 0.043)相比,CC中乳腺癌风险降低。NSW与乳腺癌相互作用之间的相关性在两个基因座中发现。南威尔士核武器南威尔士州纳维乳腺癌患者患有Cry2 Rs2292912的杂合子基因型的乳腺癌风险(或?=?1.98,95%CI?=?1.14-3.44)或者携带至少一个RORA RS1482057(或?=?2.20,95%ci?=?1.10-4.37)。我们的研究结果支持焦炭生物合成的几个基因和它们的相互作用的几个基因和基因的调整作用,以及与新乳腺癌发育中的基因相互作用。

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