Pub Date : 2018-07-01DOI: 10.1158/1538-7755.disp17-ia17
Lourdes A
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Pub Date : 2018-07-01DOI: 10.1158/1538-7755.DISP17-IA16
R. Fry
Epidemiologic evidence links chronic exposure to inorganic arsenic (iAs) to a host of adverse health effects, including cancer of the bladder. This study aimed to identify DNA methylation patterns associated with arsenic and its metabolites in exfoliated urothelial cells (EUCs) that originate primarily from the urinary bladder, one of the targets of arsenic-induced carcinogenesis. EUCs from 46 residents of Chihuahua, Mexico were analyzed for genome-wide, gene-specific promoter DNA methylation levels. These were analyzed in relation to intracellular concentrations of total arsenic and arsenic species. A set of 49 differentially methylated genes was identified with increased promoter methylation associated with EUC tAs, iAs, and/or monomethylated As (MMAs) enriched for their roles in metabolic disease and cancer. Notably, no genes had differential methylation associated with EUC dimethylated As (DMAs), suggesting that DMAs may influence DNA methylation-mediated urothelial cell responses to a lesser extent than iAs or MMAs. Further analysis showed that 22 of the 49 arsenic-associated genes (45%) are also differentially methylated in bladder cancer tissue identified using The Cancer Genome Atlas (TCGA) repository. Both the arsenic- and cancer-associated genes were enriched for the binding sites of common transcription factors known to play roles in carcinogenesis, demonstrating a novel potential mechanistic link between iAs exposure and bladder cancer. Citation Format: Rebecca C. Fry, Rebecca C. Fry. Identifying an epigenetic basis for arsenic-associated bladder cancer in a population in Chihuahua Mexico [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr IA16.
流行病学证据表明，长期接触无机砷与包括膀胱癌在内的一系列不利健康影响有关。本研究旨在鉴定主要源自膀胱的脱落尿路上皮细胞(EUCs)中与砷及其代谢物相关的DNA甲基化模式，膀胱是砷诱导癌变的靶点之一。对来自墨西哥奇瓦瓦州46名居民的EUCs进行了全基因组、基因特异性启动子DNA甲基化水平的分析。分析了这些与细胞内总砷浓度和砷种类的关系。一组49个差异甲基化基因被鉴定出与EUC tAs、iAs和/或单甲基化As (MMAs)相关的启动子甲基化增加，这些基因在代谢性疾病和癌症中发挥着丰富的作用。值得注意的是，没有基因存在与EUC二甲基化As (DMAs)相关的差异甲基化，这表明DMAs对DNA甲基化介导的尿路上皮细胞反应的影响程度可能低于iAs或MMAs。进一步的分析表明，49个砷相关基因中有22个(45%)在膀胱癌组织中也存在差异甲基化，这些基因是通过癌症基因组图谱(TCGA)库确定的。砷和癌症相关基因都富集了已知在致癌过程中起作用的常见转录因子的结合位点，这表明砷暴露与膀胱癌之间存在一种新的潜在机制联系。引文格式:Rebecca C. Fry, Rebecca C. Fry。确定墨西哥奇瓦瓦州人群中砷相关膀胱癌的表观遗传基础[摘要]。见:第十届AACR会议论文集:种族/少数民族和医疗服务不足人群的癌症健康差异科学;2017年9月25-28日;亚特兰大,乔治亚州。费城(PA): AACR;癌症流行病学杂志，2018;27(7增刊):摘要11 - 16。
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Pub Date : 2018-07-01DOI: 10.1158/1538-7755.disp17-ia18
K. McGlynn
Liver cancer incidence, the dominant histology of which is hepatocellular carcinoma (HCC), has been increasing in the U.S. for more than three decades. In comparison with non-Hispanic whites, all other racial/ethnic groups have notably higher incidence rates. For many years, the highest HCC rates occurred among Asians/Pacific Islanders. Recently, however, rates among Asians/Pacific Islanders have declined while rates among all other racial/ethnic groups have increased. As a consequence of the divergent trends, Hispanics are poised to become the group with the highest liver-cancer incidence in the U.S. The group that has seen the greatest increase in rates in the past twenty years, however, is non-Hispanic blacks. By 2030, forecasting models suggest that Hispanics and non-Hispanic blacks will have the highest rates and Asians/Pacific Islanders will have the lowest rates. Among all racial/ethnic groups in the U.S., males have higher rates of liver cancer than females. The male:female ratio varies from a low of 2.5:1 among American Indians/Alaska Natives to a high of 4.1:1 among non-Hispanic blacks. Males also are diagnosed at a younger average age than females, with the least discrepancy in age occurring among non-Hispanic blacks (2.7 years) and the greatest discrepancy in age occurring among Asians/Pacific Islanders (5.9 years). A likely explanation for declining HCC rates among Asian/Pacific Islanders is a declining prevalence of hepatitis B virus (HBV) infection in the population. Likely explanations for the increasing HCC rates in other racial/groups are the high rate of hepatitis C virus (HCV) infection in prior years and the increased prevalence of obesity/diabetes in the population. An analysis of population-attributable risk among persons of ages 65 and older, however, found differences in attributable risk by racial ethnic group. Among non-Hispanic whites and Hispanics, the dominant risk factor was obesity/diabetes. In contrast, HCV infection was the dominant risk factor among non-Hispanic blacks and Asians/Pacific Islanders. These differences in key factors suggest that cancer prevention strategies should be tailored to each specific racial/ethnic group. Citation Format: Katherine A. McGlynn. Liver cancer among minority populations in the United States [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr IA18.
肝癌的发病率，主要是肝细胞癌(HCC)，在美国已经增加了超过三十年。与非西班牙裔白人相比，所有其他种族/族裔群体的发病率明显更高。多年来，HCC发病率最高的人群是亚洲/太平洋岛民。然而，最近亚洲/太平洋岛民的发病率有所下降，而所有其他种族/族裔群体的发病率都有所上升。由于不同趋势的结果，西班牙裔美国人将成为美国肝癌发病率最高的群体。然而，在过去20年里，发病率增长最快的群体是非西班牙裔黑人。预测模型显示，到2030年，拉美裔和非拉美裔黑人的自杀率将最高，亚洲/太平洋岛民的自杀率将最低。在美国所有种族/民族群体中，男性患肝癌的比例高于女性。男女比例从美国印第安人/阿拉斯加原住民的2.5:1到非西班牙裔黑人的4.1:1不等。男性被诊断的平均年龄也比女性年轻，非西班牙裔黑人的年龄差异最小(2.7岁)，亚洲/太平洋岛民的年龄差异最大(5.9岁)。亚洲/太平洋岛民中HCC发病率下降的一个可能解释是乙肝病毒(HBV)感染率在人群中下降。其他种族/群体HCC发病率上升的可能解释是，前几年丙型肝炎病毒(HCV)感染率高，人群中肥胖/糖尿病患病率增加。然而，对65岁及以上人群的人口归因风险的分析发现，种族和民族群体的归因风险存在差异。在非西班牙裔白人和西班牙裔人中，主要的危险因素是肥胖/糖尿病。相比之下，丙型肝炎病毒感染是非西班牙裔黑人和亚洲/太平洋岛民的主要危险因素。这些关键因素的差异表明癌症预防策略应该针对每个特定的种族/民族群体。引用格式:Katherine A. McGlynn。美国少数民族人群的肝癌[摘要]。见:第十届AACR会议论文集:种族/少数民族和医疗服务不足人群的癌症健康差异科学;2017年9月25-28日;亚特兰大,乔治亚州。费城(PA): AACR;癌症流行病学杂志，2018;27(7增刊):摘要11 - 18。
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