Abstract Lifetime exposure to ambient air pollution and methylation of tumor suppressor genes in breast tumors
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Lifetime exposure to ambient air pollution and methylation of tumor suppressor genes in breast tumors

机译：终生暴露于环境空气污染和乳腺癌中抑癌基因的甲基化

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AbstractBackgroundWe previously reported increased risk of breast cancer associated with early life exposure to two measures of air pollution exposure, total suspended particulates (TSP) and traffic emissions (TE), possible proxies for exposure to polycyclic aromatic hydrocarbons (PAHs). Exposure to PAHs has been shown to be associated with aberrant patterns of DNA methylation in peripheral blood of healthy individuals. Exposure to PAHs and methylation in breast tumor tissue has received little attention. We examined the association of early life exposure to TSP and TE with patterns of DNA methylation in breast tumors.MethodsWe conducted a study of women enrolled in the Western New York Exposures and Breast Cancer (WEB) Study. Methylation of nine genes (SFN, SCGB3A1, RARB, GSTP1, CDKN2A CCND2, BRCA1, FHIT,andSYK)was assessed using bisulfite-based pyrosequencing. TSP exposure at each woman's home address at birth, menarche, and when she had her first child was estimated. TE exposure was modeled for each woman's residence at menarche, her first birth, and twenty and ten years prior to diagnosis. Unconditional logistic regression was employed to estimate odds ratios (OR) of having methylation greater than the median value, adjusting for age, secondhand smoke exposure before age 20, current smoking status, and estrogen receptor status.ResultsExposure to higher TSP at a woman's first birth was associated with lower methylation ofSCGB3A1(OR = 0.48, 95% CI: 0.23–0.99) and higher methylation ofSYK(OR = 1.86, 95% CI: 1.03–3.35). TE at menarche was associated with increased methylation ofSYK(OR = 2.37, 95% CI: 1.05–5.33). TE at first birth and ten years prior to diagnosis was associated with decreased methylation ofCCND2(OR ten years prior to diagnosis=0.48, 95% CI: 0.26–0.89). Although these associations were nominally significant, none were significant after adjustment for multiple comparisons (p < 0.01).ConclusionsWe observed suggestive evidence that exposure to ambient air pollution throughout life, measured as TSP and TE, may be associated with DNA methylation of some tumor suppressor genes in breast tumor tissue. Future studies with a larger sample size that assess methylation of more sites are warranted.Highlights•DNA was extracted from breast tumor tissue and methylation of nine genes was measured.•Total suspended particulates and traffic exposures throughout life were considered.•Exposure to TSP of a woman's first birth was associated with higher methylation ofSYKand lower methylation ofSCGB3A1.•Traffic exposure was associated with methylation of certain genes.•Our observed associations were not statistically significant after adjustment for multiple comparisons.
机译： 摘要 背景 我们之前报道了与乳腺癌相关的风险增加在早期生活中要接触两种空气污染指标，即总悬浮颗粒物（TSP）和交通排放量（TE），以及可能接触多环芳烃（PAHs）的指标。研究表明，暴露于PAHs与健康个体外周血中DNA甲基化的异常模式有关。暴露于乳腺肿瘤组织中的PAHs和甲基化反应很少受到关注。我们检查了乳腺癌中TSP和TE的早期暴露与DNA甲基化模式的关系。 方法 我们对参与纽约西部暴露和乳腺癌（WEB）研究的妇女进行了一项研究。使用亚硫酸氢盐评估了9个基因（ SFN，SCGB3A1，RARB，GSTP1，CDKN2A CCND2，BRCA1，FHIT，和 SYK）的甲基化基于焦磷酸测序。估计每个妇女在出生，初潮和生下第一个孩子时的家庭住所中的TSP暴露量。针对每个妇女在月经初潮时的住所，她的第一胎以及诊断前的二十十年建模了TE暴露。使用无条件逻辑回归来估计甲基化大于中值的比值比（OR），并调整年龄，20岁之前的二手烟暴露量，当前吸烟状况和雌激素受体状况。 < / ce：abstract-sec> 结果 妇女首次生育时暴露于较高的TSP与 SCGB3A1 的甲基化程度较低有关（OR = 0.48、95 ％CI：0.23–0.99）和更高的 SYK 甲基化（OR = 1.86，95％CI：1.03-3.35）。月经初潮时的TE与 SYK 的甲基化增加有关（OR = 2.37，95％CI：1.05-5.33）。第一胎和诊断前十年的TE与 CCND2 的甲基化降低有关（或诊断前十年= 0.48，95％CI：0.26-0.89）。尽管这些关联在名义上是显着的，但是在进行多次比较调整后，所有关联均不显着（p <0.01）。 结论 我们观察到提示性有证据表明，一生中暴露于环境空气污染（以TSP和TE衡量）可能与乳腺肿瘤组织中某些抑癌基因的DNA甲基化有关。有必要进行更大样本量的评估，以评估更多位点的甲基化。 突出显示 • DNA从乳腺肿瘤组织中提取并测量了9个基因的甲基化。 • 已考虑到整个生命中的总悬浮颗粒物和交通暴露。 • 妇女首次生育TSP暴露与甲基化程度较高有关 SYK 和 SCGB3A1 的较低甲基化。 • 交通暴露与某些基因的甲基化有关。 • 我们观察到的关联在统计后不具有统计学意义调整多个比较。

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  • 来源
    《Environmental research》 |2018年第2期|418-424|共7页
  • 作者

    Catherine L. Callahan; Matthew R. Bonner; Jing Nie; Daikwon Han; Youjin Wang; Meng-Hua Tao; Peter G. Shields; Catalin Marian; Kevin H. Eng; Maurizio Trevisan; Jan Beyea; Jo L. Freudenheim;

  • 作者单位

    Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo;

    Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo;

    Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo;

    Department of Epidemiology and Biostatistics, Texas A&M Texas A&M University;

    Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo;

    Department of Biostatistics and Epidemiology, University of North Texas Health Science Center;

    Division of Cancer Prevention and Control, College of Medicine and The Ohio State University Comprehensive Cancer Center;

    Division of Cancer Prevention and Control, College of Medicine and The Ohio State University Comprehensive Cancer Center,Department of Biochemistry and Pharmacology, University of Medicine an Pharmacy Timisoara;

    Department of Biostatistics and Bioinformatics, Roswell Park Cancer Institute;

    City College of New York;

    Consulting in the Public Interest, Lambertville;

    Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo;

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