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2. Genetic Susceptibility to Nonalcoholic Fatty Liver Disease and Risk for Pancreatic Cancer: Mendelian Randomization.

Author

Canzian, Federico, Du, Mengmeng, Gallinger, Steven, Giles, Graham, Goodman, Phyllis, Haiman, Christopher, Kogevinas, Manolis, Kooperberg, Charles, LeMarchand, Loic, Neale, Rachel, Visvanathan, Kala, White, Emily, Albanes, Demetrius, Andreotti, Gabriella, Babic, Ana, Berndt, Sonja, Brais, Lauren, Brennan, Paul, Buring, Julie, Rabe, Kari, Bamlet, William, Chanock, Stephen, Fuchs, Charles, Gaziano, J, Giovannucci, Edward, Hackert, Thilo, Hassan, Manal, Katzke, Verena, Kurtz, Robert, Lee, I-Min, Malats, Núria, Murphy, Neil, Oberg, Ann, Orlow, Irene, Porta, Miquel, Real, Francisco, Rothman, Nathaniel, Sesso, Howard, Silverman, Debra, Thompson, Ian, Wactawski-Wende, Jean, Wang, Xiaoliang, Wentzensen, Nicolas, Yu, Herbert, Zeleniuch-Jacquotte, Anne, Yu, Kai, Wolpin, Brian, Duell, Eric, Li, Donghui, Hung, Rayjean, Perdomo, Sandra, McCullough, Marjorie, Freedman, Neal, Patel, Alpa, Peters, Ulrike, Riboli, Elio, Sund, Malin, Tjønneland, Anne, Zhong, Jun, Van Den Eeden, Stephen, Kraft, Peter, Risch, Harvey, Amundadottir, Laufey, Klein, Alison, Stolzenberg-Solomon, Rachael, Antwi, Samuel, King, Sontoria, Veliginti, Swathi, Brouwers, Martijn, Ren, Zhewen, Zheng, Wei, Setiawan, Veronica, Wilkens, Lynne, Shu, Xiao-Ou, Arslan, Alan, Beane Freeman, Laura, and Bracci, Paige

Subjects
Humans, Non-alcoholic Fatty Liver Disease, Genetic Predisposition to Disease, Genome-Wide Association Study, Mendelian Randomization Analysis, Pancreatic Neoplasms, Obesity, Polymorphism, Single Nucleotide
Abstract

BACKGROUND: There are conflicting data on whether nonalcoholic fatty liver disease (NAFLD) is associated with susceptibility to pancreatic cancer. Using Mendelian randomization (MR), we investigated the relationship between genetic predisposition to NAFLD and risk for pancreatic cancer. METHODS: Data from genome-wide association studies (GWAS) within the Pancreatic Cancer Cohort Consortium (PanScan; cases n = 5,090, controls n = 8,733) and the Pancreatic Cancer Case Control Consortium (PanC4; cases n = 4,163, controls n = 3,792) were analyzed. We used data on 68 genetic variants with four different MR methods [inverse variance weighting (IVW), MR-Egger, simple median, and penalized weighted median] separately to predict genetic heritability of NAFLD. We then assessed the relationship between each of the four MR methods and pancreatic cancer risk, using logistic regression to calculate ORs and 95% confidence intervals (CI), adjusting for PC risk factors, including obesity and diabetes. RESULTS: No association was found between genetically predicted NAFLD and pancreatic cancer risk in the PanScan or PanC4 samples [e.g., PanScan, IVW OR, 1.04; 95% confidence interval (CI), 0.88-1.22; MR-Egger OR, 0.89; 95% CI, 0.65-1.21; PanC4, IVW OR, 1.07; 95% CI, 0.90-1.27; MR-Egger OR, 0.93; 95% CI, 0.67-1.28]. None of the four MR methods indicated an association between genetically predicted NAFLD and pancreatic cancer risk in either sample. CONCLUSIONS: Genetic predisposition to NAFLD is not associated with pancreatic cancer risk. IMPACT: Given the close relationship between NAFLD and metabolic conditions, it is plausible that any association between NAFLD and pancreatic cancer might reflect host metabolic perturbations (e.g., obesity, diabetes, or metabolic syndrome) and does not necessarily reflect a causal relationship between NAFLD and pancreatic cancer.

Published
2023

9. Arsenic in private well water and birth outcomes in the United States.

Author

Bulka, Catherine M, Scannell Bryan, Molly, Lombard, Melissa A, Bartell, Scott M, Jones, Daniel K, Bradley, Paul M, Vieira, Veronica M, Silverman, Debra T, Focazio, Michael, Toccalino, Patricia L, Daniel, Johnni, Backer, Lorraine C, Ayotte, Joseph D, Gribble, Matthew O, and Argos, Maria

Subjects
Humans, Birth Weight, Arsenic, Water Pollutants, Chemical, Water Supply, Pregnancy, United States, Female, Groundwater, Drinking Water, Water Wells, Birth outcomes, Epidemiology, Private wells, Water contamination, Pediatric, Preterm, Low Birth Weight and Health of the Newborn, Prevention, Foodborne Illness, Perinatal Period - Conditions Originating in Perinatal Period, Infant Mortality, Environmental Sciences
Abstract

BackgroundPrenatal exposure to drinking water with arsenic concentrations >50 μg/L is associated with adverse birth outcomes, with inconclusive evidence for concentrations ≤50 μg/L. In a collaborative effort by public health experts, hydrologists, and geologists, we used published machine learning model estimates to characterize arsenic concentrations in private wells-federally unregulated for drinking water contaminants-and evaluated associations with birth outcomes throughout the conterminous U.S.MethodsUsing several machine learning models, including boosted regression trees (BRT) and random forest classification (RFC), developed from measured groundwater arsenic concentrations of ∼20,000 private wells, we characterized the probability that arsenic concentrations occurred within specific ranges in groundwater. Probabilistic model estimates and private well usage data were linked by county to all live birth certificates from 2016 (n = 3.6 million). We evaluated associations with gestational age and term birth weight using mixed-effects models, adjusted for potential confounders and incorporated random intercepts for spatial clustering.ResultsWe generally observed inverse associations with term birth weight. For instance, when using BRT estimates, a 10-percentage point increase in the probability that private well arsenic concentrations exceeded 5 μg/L was associated with a -1.83 g (95% CI: -3.30, -0.38) lower term birth weight after adjusting for covariates. Similarly, a 10-percentage point increase in the probability that private well arsenic concentrations exceeded 10 μg/L was associated with a -2.79 g (95% CI: -4.99, -0.58) lower term birth weight. Associations with gestational age were null.ConclusionIn this largest epidemiologic study of arsenic and birth outcomes to date, we did not observe associations of modeled arsenic estimates in private wells with gestational age and found modest inverse associations with term birth weight. Study limitations may have obscured true associations, including measurement error stemming from a lack of individual-level information on primary water sources, water arsenic concentrations, and water consumption patterns.

Published
2022

13. Machine Learning Models of Arsenic in Private Wells Throughout the Conterminous United States As a Tool for Exposure Assessment in Human Health Studies.

Author

Lombard, Melissa, Bryan, Molly, Jones, Daniel, Bulka, Catherine, Bradley, Paul, Backer, Lorraine, Focazio, Michael, Silverman, Debra, Toccalino, Patricia, Argos, Maria, Ayotte, Joseph, and Gribble, Matthew

Subjects
Arsenic, Environmental Monitoring, Groundwater, Humans, Machine Learning, United States, Water Pollutants, Chemical, Water Supply, Water Wells
Abstract

Arsenic from geologic sources is widespread in groundwater within the United States (U.S.). In several areas, groundwater arsenic concentrations exceed the U.S. Environmental Protection Agency maximum contaminant level of 10 μg per liter (μg/L). However, this standard applies only to public-supply drinking water and not to private-supply, which is not federally regulated and is rarely monitored. As a result, arsenic exposure from private wells is a potentially substantial, but largely hidden, public health concern. Machine learning models using boosted regression trees (BRT) and random forest classification (RFC) techniques were developed to estimate probabilities and concentration ranges of arsenic in private wells throughout the conterminous U.S. Three BRT models were fit separately to estimate the probability of private well arsenic concentrations exceeding 1, 5, or 10 μg/L whereas the RFC model estimates the most probable category (≤5, >5 to ≤10, or >10 μg/L). Overall, the models perform best at identifying areas with low concentrations of arsenic in private wells. The BRT 10 μg/L model estimates for testing data have an overall accuracy of 91.2%, sensitivity of 33.9%, and specificity of 98.2%. Influential variables identified across all models included average annual precipitation and soil geochemistry. Models were developed in collaboration with public health experts to support U.S.-based studies focused on health effects from arsenic exposure.

Published
2021

16. Household air pollution and epigenetic aging in Xuanwei, China

Author

Blechter, Batel, Cardenas, Andres, Shi, Junming, Wong, Jason Y.Y., Hu, Wei, Rahman, Mohammad L., Breeze, Charles, Downward, George S., Portengen, Lützen, Zhang, Yongliang, Ning, Bofu, Ji, Bu-Tian, Cawthon, Richard, Li, Jihua, Yang, Kaiyun, Bozack, Anne, Dean Hosgood, H., Silverman, Debra T., Huang, Yunchao, Rothman, Nathaniel, Vermeulen, Roel, and Lan, Qing

Published
2023
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17. Genome-wide Association Study of Bladder Cancer Reveals New Biological and Translational Insights

Author

Koutros, Stella, Kiemeney, Lambertus A., Pal Choudhury, Parichoy, Milne, Roger L., Lopez de Maturana, Evangelina, Ye, Yuanqing, Joseph, Vijai, Florez-Vargas, Oscar, Dyrskjøt, Lars, Figueroa, Jonine, Dutta, Diptavo, Giles, Graham G., Hildebrandt, Michelle A.T., Offit, Kenneth, Kogevinas, Manolis, Weiderpass, Elisabete, McCullough, Marjorie L., Freedman, Neal D., Albanes, Demetrius, Kooperberg, Charles, Cortessis, Victoria K., Karagas, Margaret R., Johnson, Alison, Schwenn, Molly R., Baris, Dalsu, Furberg, Helena, Bajorin, Dean F., Cussenot, Olivier, Cancel-Tassin, Geraldine, Benhamou, Simone, Kraft, Peter, Porru, Stefano, Carta, Angela, Bishop, Timothy, Southey, Melissa C., Matullo, Giuseppe, Fletcher, Tony, Kumar, Rajiv, Taylor, Jack A., Lamy, Philippe, Prip, Frederik, Kalisz, Mark, Weinstein, Stephanie J., Hengstler, Jan G., Selinski, Silvia, Harland, Mark, Teo, Mark, Kiltie, Anne E., Tardón, Adonina, Serra, Consol, Carrato, Alfredo, García-Closas, Reina, Lloreta, Josep, Schned, Alan, Lenz, Petra, Riboli, Elio, Brennan, Paul, Tjønneland, Anne, Otto, Thomas, Ovsiannikov, Daniel, Volkert, Frank, Vermeulen, Sita H., Aben, Katja K., Galesloot, Tessel E., Turman, Constance, De Vivo, Immaculata, Giovannucci, Edward, Hunter, David J., Hohensee, Chancellor, Hunt, Rebecca, Patel, Alpa V., Huang, Wen-Yi, Thorleifsson, Gudmar, Gago-Dominguez, Manuela, Amiano, Pilar, Golka, Klaus, Stern, Mariana C., Yan, Wusheng, Liu, Jia, Li, Shengchao Alfred, Katta, Shilpa, Hutchinson, Amy, Hicks, Belynda, Wheeler, William A., Purdue, Mark P., McGlynn, Katherine A., Kitahara, Cari M., Haiman, Christopher A., Greene, Mark H., Rafnar, Thorunn, Chatterjee, Nilanjan, Chanock, Stephen J., Wu, Xifeng, Real, Francisco X., Silverman, Debra T., Garcia-Closas, Montserrat, Stefansson, Kari, Prokunina-Olsson, Ludmila, Malats, Núria, and Rothman, Nathaniel

Published
2023
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20. Methylated polycyclic aromatic hydrocarbons from household coal use across the life course and risk of lung cancer in a large cohort of 42,420 subjects in Xuanwei, China

Author

Portengen, Lützen, Downward, George, Bassig, Bryan A., Blechter, Batel, Hu, Wei, Wong, Jason Y.Y., Ning, Bofu, Rahman, Mohammad L., Ji, Bu-Tian, Li, Jihua, Yang, Kaiyun, Hosgood, H. Dean, Silverman, Debra T., Rothman, Nathaniel, Huang, Yunchao, Vermeulen, Roel, and Lan, Qing

Published
2023
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21. PM2.5 air pollution and cause-specific cardiovascular disease mortality

Author

Hayes, Richard B, Lim, Chris, Zhang, Yilong, Cromar, Kevin, Shao, Yongzhao, Reynolds, Harmony R, Silverman, Debra T, Jones, Rena R, Park, Yikyung, Jerrett, Michael, Ahn, Jiyoung, and Thurston, George D

Subjects
Epidemiology, Public Health, Health Sciences, Clinical Research, Climate-Related Exposures and Conditions, Social Determinants of Health, Cardiovascular, Heart Disease, Prevention, Aging, 2.2 Factors relating to the physical environment, Good Health and Well Being, Aged, Air Pollutants, Air Pollution, Cardiovascular Diseases, Cohort Studies, Environmental Exposure, Female, Humans, Male, Middle Aged, Particulate Matter, Proportional Hazards Models, Risk Factors, United States, Air pollution, cardiovascular disease, mortality, Statistics, Public Health and Health Services, Public health
Abstract

BackgroundAmbient air pollution is a modifiable risk factor for cardiovascular disease, yet uncertainty remains about the size of risks at lower levels of fine particulate matter (PM2.5) exposure which now occur in the USA and elsewhere.MethodsWe investigated the relationship of ambient PM2.5 exposure with cause-specific cardiovascular disease mortality in 565 477 men and women, aged 50 to 71 years, from the National Institutes of Health-AARP Diet and Health Study. During 7.5 x 106 person-years of follow up, 41 286 cardiovascular disease deaths, including 23 328 ischaemic heart disease (IHD) and 5894 stroke deaths, were ascertained using the National Death Index. PM2.5 was estimated using a hybrid land use regression (LUR) geostatistical model. Multivariate Cox regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CI).ResultsEach increase of 10  μg/m3 PM2.5 (overall range, 2.9-28.0  μg/m3) was associated, in fully adjusted models, with a 16% increase in mortality from ischaemic heart disease [hazard ratio (HR) 1.16; 95% CI 1.09-1.22] and a 14% increase in mortality from stroke (HR 1.14; CI 1.02-1.27). Compared with PM2.5 exposure

Published
2020

22. Exposure to diesel engine exhaust and alterations to the Cys34/Lys525 adductome of human serum albumin

Author

Wong, Jason Y.Y., Imani, Partow, Grigoryan, Hasmik, Bassig, Bryan A., Dai, Yufei, Hu, Wei, Blechter, Batel, Rahman, Mohammad L., Ji, Bu-Tian, Duan, Huawei, Niu, Yong, Ye, Meng, Jia, Xiaowei, Meng, Tao, Bin, Ping, Downward, George, Meliefste, Kees, Leng, Shuguang, Fu, Wei, Yang, Jufang, Ren, Dianzhi, Xu, Jun, Zhou, Baosen, Hosgood, H. Dean, Vermeulen, Roel, Zheng, Yuxin, Silverman, Debra T., Rothman, Nathaniel, Rappaport, Stephen M., and Lan, Qing

Published
2022
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24. Ischemic Heart Disease Mortality and Diesel Exhaust and Respirable Dust Exposure in the Diesel Exhaust in Miners Study.

Author

Costello, Sadie, Attfield, Michael D, Lubin, Jay H, Neophytou, Andreas M, Blair, Aaron, Brown, Daniel M, Stewart, Patricia A, Vermeulen, Roel, Eisen, Ellen A, and Silverman, Debra T

Subjects
Heart Disease, Prevention, Cardiovascular, Heart Disease - Coronary Heart Disease, Good Health and Well Being, Adult, Air Pollutants, Occupational, Carbon, Coal Mining, Cohort Studies, Dust, Environmental Monitoring, Humans, Inhalation Exposure, Male, Middle Aged, Miners, Myocardial Ischemia, Occupational Exposure, Proportional Hazards Models, Risk Factors, Socioeconomic Factors, United States, Vehicle Emissions, cohort study, diesel exhaust, ischemic heart disease, respirable dust, Mathematical Sciences, Medical and Health Sciences, Epidemiology
Abstract

Diesel exhaust is a suggested risk factor for ischemic heart disease (IHD), but evidence from cohorts using quantitative exposure metrics is limited. We examined the impact of respirable elemental carbon (REC), a key surrogate for diesel exhaust, and respirable dust (RD) on IHD mortality, using data from the Diesel Exhaust in Miners Study in the United States. Using data from a cohort of male workers followed from 1948-1968 until 1997, we fitted Cox proportional hazards models to estimate hazard ratios for IHD mortality for cumulative and average intensity of exposure to REC and RD. Segmented linear regression models allowed for nonmonotonicity. Hazard ratios for cumulative and average REC exposure declined relative to the lowest exposure category before increasing to 0.79 and 1.25, respectively, in the highest category. Relative to the category containing the segmented regression change points, hazard ratios for the highest category were 1.69 and 1.54 for cumulative and average REC exposure, respectively. Hazard ratios for RD exposure increased across the full exposure range to 1.33 and 2.69 for cumulative and average RD exposure, respectively. Tests for trend were statistically significant for cumulative REC exposure (above the change point) and for average RD exposure. Our findings suggest excess risk of IHD mortality in relation to increased exposure to REC and RD.

Published
2018

26. Hepcidin-regulating iron metabolism genes and pancreatic ductal adenocarcinoma: a pathway analysis of genome-wide association studies

Author

Julián-Serrano, Sachelly, Yuan, Fangcheng, Wheeler, William, Benyamin, Beben, Machiela, Mitchell J, Arslan, Alan A, Beane-Freeman, Laura E, Bracci, Paige M, Duell, Eric J, Du, Mengmeng, Gallinger, Steven, Giles, Graham G, Goodman, Phyllis J, Kooperberg, Charles, Marchand, Loic Le, Neale, Rachel E, Shu, Xiao-Ou, Van Den Eeden, Stephen K, Visvanathan, Kala, Zheng, Wei, Albanes, Demetrius, Andreotti, Gabriella, Ardanaz, Eva, Babic, Ana, Berndt, Sonja I, Brais, Lauren K, Brennan, Paul, Bueno-de-Mesquita, Bas, Buring, Julie E, Chanock, Stephen J, Childs, Erica J, Chung, Charles C, Fabiánová, Eleonora, Foretová, Lenka, Fuchs, Charles S, Gaziano, J Michael, Gentiluomo, Manuel, Giovannucci, Edward L, Goggins, Michael G, Hackert, Thilo, Hartge, Patricia, Hassan, Manal M, Holcátová, Ivana, Holly, Elizabeth A, Hung, Rayjean I, Janout, Vladimir, Kurtz, Robert C, Lee, I-Min, Malats, Núria, McKean, David, Milne, Roger L, Newton, Christina C, Oberg, Ann L, Perdomo, Sandra, Peters, Ulrike, Porta, Miquel, Rothman, Nathaniel, Schulze, Matthias B, Sesso, Howard D, Silverman, Debra T, Thompson, Ian M, Wactawski-Wende, Jean, Weiderpass, Elisabete, Wenstzensen, Nicolas, White, Emily, Wilkens, Lynne R, Yu, Herbert, Zeleniuch-Jacquotte, Anne, Zhong, Jun, Kraft, Peter, Li, Dounghui, Campbell, Peter T, Petersen, Gloria M, Wolpin, Brian M, Risch, Harvey A, Amundadottir, Laufey T, Klein, Alison P, Yu, Kai, and Stolzenberg-Solomon, Rachael Z

Published
2021
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31. Diesel exhaust and bladder cancer risk by pathologic stage and grade subtypes

Author

Koutros, Stella, Kogevinas, Manolis, Friesen, Melissa C., Stewart, Patricia A., Baris, Dalsu, Karagas, Margaret R., Schwenn, Molly, Johnson, Alison, Monawar Hosain, G.M., Serra, Consol, Tardon, Adonina, Carrato, Alfredo, Garcia-Closas, Reina, Moore, Lee E., Nickerson, Michael L., Hewitt, Stephen M., Lenz, Petra, Schned, Alan R., Lloreta, Josep, Allory, Yves, Zhang, Haoyu, Chatterjee, Nilanjan, Garcia-Closas, Montserrat, Rothman, Nathaniel, Malats, Núria, and Silverman, Debra T.

Published
2020
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34. Outdoor Ultrafine Particulate Matter and Risk of Lung Cancer in Southern California

Author

Planetary Health & Exposoom, Cancer, Circulatory Health, Jones, Rena R., Fisher, Jared A., Hasheminassab, Sina, Kaufman, Joel D., Freedman, Neal D., Ward, Mary H., Sioutas, Constantinos, Vermeulen, Roel, Hoek, Gerard, Silverman, Debra T., Planetary Health & Exposoom, Cancer, Circulatory Health, Jones, Rena R., Fisher, Jared A., Hasheminassab, Sina, Kaufman, Joel D., Freedman, Neal D., Ward, Mary H., Sioutas, Constantinos, Vermeulen, Roel, Hoek, Gerard, and Silverman, Debra T.

Published
2024

35. A prospective study of smoking-related white blood cell DNA methylation markers and risk of bladder cancer

Author

IRAS OH Epidemiology Chemical Agents, IRAS – One Health Chemical, Vermeulen, Roel, Bodinier, Barbara, Dagnino, Sonia, Wada, Rin, Wang, Xuting, Silverman, Debra, Albanes, Demetrius, Freedman, Neal, Rahman, Mohammad, Bell, Douglas, Chadeau-Hyam, Marc, Rothman, Nathaniel, IRAS OH Epidemiology Chemical Agents, IRAS – One Health Chemical, Vermeulen, Roel, Bodinier, Barbara, Dagnino, Sonia, Wada, Rin, Wang, Xuting, Silverman, Debra, Albanes, Demetrius, Freedman, Neal, Rahman, Mohammad, Bell, Douglas, Chadeau-Hyam, Marc, and Rothman, Nathaniel

Published
2024

36. Outdoor Ultrafine Particulate Matter and Risk of Lung Cancer in Southern California

Author

IRAS OH Epidemiology Chemical Agents, IRAS – One Health Chemical, Jones, Rena R, Fisher, Jared A, Hasheminassab, Sina, Kaufman, Joel D, Freedman, Neal D, Ward, Mary H, Sioutas, Constantinos, Vermeulen, Roel, Hoek, Gerard, Silverman, Debra T, IRAS OH Epidemiology Chemical Agents, IRAS – One Health Chemical, Jones, Rena R, Fisher, Jared A, Hasheminassab, Sina, Kaufman, Joel D, Freedman, Neal D, Ward, Mary H, Sioutas, Constantinos, Vermeulen, Roel, Hoek, Gerard, and Silverman, Debra T

Published
2024

37. Genetic variation in the TP53 pathway and bladder cancer risk. a comprehensive analysis

Author

Chenette, Emily, Pineda Sanjuan, Silvia, Milne, Roger L, Calle, M Luz, Rothman, Nathaniel, López de Maturana, Evangelina, Herranz, Jesús, Kogevinas, Manolis, J Chanock, Stephen, Tardón, Adonina, Márquez, Mirari, Guey, Lin T, García-Closas, Montserrat, Lloreta, Josep, Baum, Erin, González-Neira, Anna, Carrato, Alfredo, Navarro, Arcadi, T Silverman, Debra, X Real, Francisco, Maltas, Núria, Chenette, Emily, Pineda Sanjuan, Silvia, Milne, Roger L, Calle, M Luz, Rothman, Nathaniel, López de Maturana, Evangelina, Herranz, Jesús, Kogevinas, Manolis, J Chanock, Stephen, Tardón, Adonina, Márquez, Mirari, Guey, Lin T, García-Closas, Montserrat, Lloreta, Josep, Baum, Erin, González-Neira, Anna, Carrato, Alfredo, Navarro, Arcadi, T Silverman, Debra, X Real, Francisco, and Maltas, Núria

Abstract

Introduction: Germline variants in TP63 have been consistently associated with several tumors, including bladder cancer, indicating the importance of TP53 pathway in cancer genetic susceptibility. However, variants in other related genes, including TP53 rs1042522 (Arg72Pro), still present controversial results. We carried out an in depth assessment of associations between common germline variants in the TP53 pathway and bladder cancer risk. Material and Methods: We investigated 184 tagSNPs from 18 genes in 1,058 cases and 1,138 controls from the Spanish Bladder Cancer/EPICURO Study. Cases were newly-diagnosed bladder cancer patients during 1998–2001. Hospital controls were age-gender, and area matched to cases. SNPs were genotyped in blood DNA using Illumina Golden Gate and TaqMan assays. Cases were subphenotyped according to stage/grade and tumor p53 expression. We applied classical tests to assess individual SNP associations and the Least Absolute Shrinkage and Selection Operator (LASSO)-penalized logistic regression analysis to assess multiple SNPs simultaneously. Results: Based on classical analyses, SNPs in BAK1 (1), IGF1R (5), P53AIP1 (1), PMAIP1 (2), SERINPB5 (3), TP63 (3), and TP73 (1) showed significant associations at p-value#0.05. However, no evidence of association, either with overall risk or with specific disease subtypes, was observed after correction for multiple testing (p-value$0.8). LASSO selected the SNP rs6567355 in SERPINB5 with 83% of reproducibility. This SNP provided an OR = 1.21, 95%CI 1.05–1.38, p-value = 0.006, and a corrected p-value = 0.5 when controlling for over-estimation. Discussion: We found no strong evidence that common variants in the TP53 pathway are associated with bladder cancer susceptibility. Our study suggests that it is unlikely that TP53 Arg72Pro is implicated in the UCB in white Europeans. SERPINB5 and TP63 variation deserve further exploration in extended studies., Fondo de Investigación Sanitaria, Spain, Red Temática de Investigación Cooperativa en Cáncer. Spain, Marató TV3, European Commission, US National Institutes of Health, The Intramural Research Program of the Division of Cancer Epidemiology and Genetics, National Cancer Institute at the National Institutes of Health, USA, Consolíder ONCOBIO. Ministerio de Economía y Competitividad, Madrid, Spain, Depto. de Estadística y Ciencia de los Datos, Fac. de Estudios Estadísticos, TRUE, pub

Published
2024

38. IARC monographs: 40 years of evaluating carcinogenic hazards to humans.

Author

Pearce, Neil, Blair, Aaron, Vineis, Paolo, Ahrens, Wolfgang, Andersen, Aage, Anto, Josep M, Armstrong, Bruce K, Baccarelli, Andrea A, Beland, Frederick A, Berrington, Amy, Bertazzi, Pier Alberto, Birnbaum, Linda S, Brownson, Ross C, Bucher, John R, Cantor, Kenneth P, Cardis, Elisabeth, Cherrie, John W, Christiani, David C, Cocco, Pierluigi, Coggon, David, Comba, Pietro, Demers, Paul A, Dement, John M, Douwes, Jeroen, Eisen, Ellen A, Engel, Lawrence S, Fenske, Richard A, Fleming, Lora E, Fletcher, Tony, Fontham, Elizabeth, Forastiere, Francesco, Frentzel-Beyme, Rainer, Fritschi, Lin, Gerin, Michel, Goldberg, Marcel, Grandjean, Philippe, Grimsrud, Tom K, Gustavsson, Per, Haines, Andy, Hartge, Patricia, Hansen, Johnni, Hauptmann, Michael, Heederik, Dick, Hemminki, Kari, Hemon, Denis, Hertz-Picciotto, Irva, Hoppin, Jane A, Huff, James, Jarvholm, Bengt, Kang, Daehee, Karagas, Margaret R, Kjaerheim, Kristina, Kjuus, Helge, Kogevinas, Manolis, Kriebel, David, Kristensen, Petter, Kromhout, Hans, Laden, Francine, Lebailly, Pierre, LeMasters, Grace, Lubin, Jay H, Lynch, Charles F, Lynge, Elsebeth, 't Mannetje, Andrea, McMichael, Anthony J, McLaughlin, John R, Marrett, Loraine, Martuzzi, Marco, Merchant, James A, Merler, Enzo, Merletti, Franco, Miller, Anthony, Mirer, Franklin E, Monson, Richard, Nordby, Karl-Cristian, Olshan, Andrew F, Parent, Marie-Elise, Perera, Frederica P, Perry, Melissa J, Pesatori, Angela Cecilia, Pirastu, Roberta, Porta, Miquel, Pukkala, Eero, Rice, Carol, Richardson, David B, Ritter, Leonard, Ritz, Beate, Ronckers, Cecile M, Rushton, Lesley, Rusiecki, Jennifer A, Rusyn, Ivan, Samet, Jonathan M, Sandler, Dale P, de Sanjose, Silvia, Schernhammer, Eva, Costantini, Adele Seniori, Seixas, Noah, Shy, Carl, Siemiatycki, Jack, and Silverman, Debra T

Subjects
Humans, Neoplasms, Carcinogens, Environmental, Public Health, Biomedical Research, Publications, International Agencies, Environmental Sciences, Medical and Health Sciences, Toxicology
Abstract

BackgroundRecently, the International Agency for Research on Cancer (IARC) Programme for the Evaluation of Carcinogenic Risks to Humans has been criticized for several of its evaluations, and also for the approach used to perform these evaluations. Some critics have claimed that failures of IARC Working Groups to recognize study weaknesses and biases of Working Group members have led to inappropriate classification of a number of agents as carcinogenic to humans.ObjectivesThe authors of this Commentary are scientists from various disciplines relevant to the identification and hazard evaluation of human carcinogens. We examined criticisms of the IARC classification process to determine the validity of these concerns. Here, we present the results of that examination, review the history of IARC evaluations, and describe how the IARC evaluations are performed.DiscussionWe concluded that these recent criticisms are unconvincing. The procedures employed by IARC to assemble Working Groups of scientists from the various disciplines and the techniques followed to review the literature and perform hazard assessment of various agents provide a balanced evaluation and an appropriate indication of the weight of the evidence. Some disagreement by individual scientists to some evaluations is not evidence of process failure. The review process has been modified over time and will undoubtedly be altered in the future to improve the process. Any process can in theory be improved, and we would support continued review and improvement of the IARC processes. This does not mean, however, that the current procedures are flawed.ConclusionsThe IARC Monographs have made, and continue to make, major contributions to the scientific underpinning for societal actions to improve the public's health.

Published
2015

39. Genome-wide association study identifies multiple susceptibility loci for pancreatic cancer

Author

Wolpin, Brian M, Rizzato, Cosmeri, Kraft, Peter, Kooperberg, Charles, Petersen, Gloria M, Wang, Zhaoming, Arslan, Alan A, Beane-Freeman, Laura, Bracci, Paige M, Buring, Julie, Canzian, Federico, Duell, Eric J, Gallinger, Steven, Giles, Graham G, Goodman, Gary E, Goodman, Phyllis J, Jacobs, Eric J, Kamineni, Aruna, Klein, Alison P, Kolonel, Laurence N, Kulke, Matthew H, Li, Donghui, Malats, Núria, Olson, Sara H, Risch, Harvey A, Sesso, Howard D, Visvanathan, Kala, White, Emily, Zheng, Wei, Abnet, Christian C, Albanes, Demetrius, Andreotti, Gabriella, Austin, Melissa A, Barfield, Richard, Basso, Daniela, Berndt, Sonja I, Boutron-Ruault, Marie-Christine, Brotzman, Michelle, Büchler, Markus W, Bueno-de-Mesquita, H Bas, Bugert, Peter, Burdette, Laurie, Campa, Daniele, Caporaso, Neil E, Capurso, Gabriele, Chung, Charles, Cotterchio, Michelle, Costello, Eithne, Elena, Joanne, Funel, Niccola, Gaziano, J Michael, Giese, Nathalia A, Giovannucci, Edward L, Goggins, Michael, Gorman, Megan J, Gross, Myron, Haiman, Christopher A, Hassan, Manal, Helzlsouer, Kathy J, Henderson, Brian E, Holly, Elizabeth A, Hu, Nan, Hunter, David J, Innocenti, Federico, Jenab, Mazda, Kaaks, Rudolf, Key, Timothy J, Khaw, Kay-Tee, Klein, Eric A, Kogevinas, Manolis, Krogh, Vittorio, Kupcinskas, Juozas, Kurtz, Robert C, LaCroix, Andrea, Landi, Maria T, Landi, Stefano, Le Marchand, Loic, Mambrini, Andrea, Mannisto, Satu, Milne, Roger L, Nakamura, Yusuke, Oberg, Ann L, Owzar, Kouros, Patel, Alpa V, Peeters, Petra HM, Peters, Ulrike, Pezzilli, Raffaele, Piepoli, Ada, Porta, Miquel, Real, Francisco X, Riboli, Elio, Rothman, Nathaniel, Scarpa, Aldo, Shu, Xiao-Ou, Silverman, Debra T, Soucek, Pavel, Sund, Malin, Talar-Wojnarowska, Renata, Taylor, Philip R, and Theodoropoulos, George E

Subjects
Cancer, Aged, Case-Control Studies, Female, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Male, Middle Aged, Pancreatic Neoplasms, Polymorphism, Single Nucleotide, White People, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

We performed a multistage genome-wide association study including 7,683 individuals with pancreatic cancer and 14,397 controls of European descent. Four new loci reached genome-wide significance: rs6971499 at 7q32.3 (LINC-PINT, per-allele odds ratio (OR) = 0.79, 95% confidence interval (CI) 0.74-0.84, P = 3.0 × 10(-12)), rs7190458 at 16q23.1 (BCAR1/CTRB1/CTRB2, OR = 1.46, 95% CI 1.30-1.65, P = 1.1 × 10(-10)), rs9581943 at 13q12.2 (PDX1, OR = 1.15, 95% CI 1.10-1.20, P = 2.4 × 10(-9)) and rs16986825 at 22q12.1 (ZNRF3, OR = 1.18, 95% CI 1.12-1.25, P = 1.2 × 10(-8)). We identified an independent signal in exon 2 of TERT at the established region 5p15.33 (rs2736098, OR = 0.80, 95% CI 0.76-0.85, P = 9.8 × 10(-14)). We also identified a locus at 8q24.21 (rs1561927, P = 1.3 × 10(-7)) that approached genome-wide significance located 455 kb telomeric of PVT1. Our study identified multiple new susceptibility alleles for pancreatic cancer that are worthy of follow-up studies.

Published
2014

40. Serum Immunoglobulin E and Risk of Pancreatic Cancer in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial

Author

Olson, Sara H, Hsu, Meier, Wiemels, Joseph L, Bracci, Paige M, Zhou, Mi, Patoka, Joseph, Reisacher, William R, Wang, Julie, Kurtz, Robert C, Silverman, Debra T, and Stolzenberg-Solomon, Rachael Z

Subjects
Epidemiology, Biomedical and Clinical Sciences, Health Sciences, Oncology and Carcinogenesis, Ovarian Cancer, Prevention, Clinical Research, Rare Diseases, Pancreatic Cancer, Food Allergies, Cancer, Clinical Trials and Supportive Activities, Digestive Diseases, 2.1 Biological and endogenous factors, Aetiology, 2.2 Factors relating to the physical environment, Adenocarcinoma, Aged, Case-Control Studies, Early Detection of Cancer, Female, Humans, Hypersensitivity, Immunoglobulin E, Incidence, Male, Mass Screening, Middle Aged, Odds Ratio, Pancreatic Neoplasms, Risk Factors, Medical and Health Sciences, Biomedical and clinical sciences, Health sciences
Abstract

Epidemiologic studies have consistently found that self-reported allergies are associated with reduced risk of pancreatic cancer. Our aim was to prospectively assess the relationship between serum immunoglobulin E (IgE), a marker of allergy, and risk. This nested case-control study within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) included subjects enrolled in 1994 to 2001 and followed through 2010. There were 283 cases of pancreatic cancer and 544 controls matched on age, gender, race, and calendar date of blood draw. Using the ImmunoCAP system, we measured total IgE (normal, borderline, elevated), IgE to respiratory allergens, and IgE to food allergens (negative or positive) in serum collected at baseline. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using conditional logistic regression. We assessed interactions with age, gender, smoking, body mass index, and time between randomization and case diagnosis. Overall, there was no association between the IgE measures and risk. We found a statistically significant interaction by baseline age: in those aged ≥65 years, elevated risks were observed for borderline total IgE (OR, 1.43; 95% CI, 0.88-2.32) and elevated total IgE (OR, 1.98; 95% CI, 1.16-3.37) and positive IgE to food allergens (OR, 2.83; 95% CI, 1.29-6.20); among participants

Published
2014

42. Benzene exposure and risk of lung cancer in the Norwegian Offshore Petroleum Worker cohort: a prospective case-cohort study

Author

Babigumira, Ronnie, primary, Veierød, Marit B, additional, Hosgood, H Dean, additional, Samuelsen, Sven Ove, additional, Bråtveit, Magne, additional, Kirkeleit, Jorunn, additional, Rothman, Nathaniel, additional, Lan, Qing, additional, Silverman, Debra T, additional, Friesen, Melissa C, additional, Shala, Nita Kaupang, additional, Grimsrud, Tom K, additional, and Stenehjem, Jo Steinson, additional

Published
2023
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43. Challenge and Opportunity: The Impact of Charter Schools on School Districts. A Report of the National Study of Charter Schools.

Author

RPP International, Emeryville, CA., Ericson, John, Silverman, Debra, and Berman, Paul

Abstract

This report examines the operational and educational changes that school administrators attribute to charter schools. It is part of the U.S. Department of Education's 4-year study to document and analyze the charter-school movement. The study asked two questions: What changes have districts made in district operations and district education that can be attributed to charter schools? and Under what conditions do charter schools affect change in district operations and district education? To answer these questions, researchers conducted in-depth site visits in 14 school districts and interviewed by telephone administrators in 35 other districts. The results indicate that every district in the study reported being affected by charter schools and, accordingly, had made operational changes. Nearly half of the district leaders believed that their diminished budgets were attributable to charter schools and had begun tracking the number of students who attended these schools. Likewise, almost half of these leaders reported becoming more customer-service oriented, increasing their marketing and public-relations efforts, or heightening their frequency of communication with parents. Most districts also implemented new educational programs, made changes in educational structures in district schools, and/or created new schools with programs that were similar to those in the local charter schools. (Contains 20 references.) (RJM)

Published
2001

48. Disinfection By-Products in Drinking Water and Bladder Cancer: Evaluation of Risk Modification by Common Genetic Polymorphisms in Two Case-Control Studies

Author

Freeman, Laura E. Beane, Kogevinas, Manolis, Cantor, Kenneth P., Villanueva, Cristina M., Prokunina-Olsson, Ludmila, Florez-Vargas, Oscar, Figueroa, Jonine D., Ward, Mary H., Koutros, Stella, Baris, Dalsu, Garcia-Closas, Montserrat, Schwenn, Molly, Johnson, Allison, Serra, Consol, Tardon, Adonina, Garcia-Closas, Reina, Carrato, Alfredo, Malats, Nuria, Karagas, Margaret R., Rothman, Nathaniel, and Silverman, Debra T.

Subjects
Toxicogenomics -- Research, Drinking water -- Contamination -- Health aspects, Bladder cancer -- Risk factors -- Environmental aspects -- Genetic aspects, Single nucleotide polymorphisms -- Health aspects, Trihalomethanes -- Environmental aspects -- Health aspects, Environmental issues, Health
Abstract

Background: By-products are formed when disinfectants react with organic matter in source water. The most common class of disinfection byproducts, trihalomethanes (THMs), have been linked to bladder cancer. Several studies have shown exposure-response associations with THMs in drinking water and bladder cancer risk. Few epidemiologic studies have evaluated gene-environment interactions for total THMs (TTHMs) with known bladder cancer susceptibility variants. Objectives: In this study, we investigated the combined effect on bladder cancer risk contributed by TTHMs, bladder cancer susceptibility variants identified through genome-wide association studies, and variants in several candidate genes. Methods: We analyzed data from two large case-control studies--the New England Bladder Cancer Study (n/n = 989 cases/1,162 controls), a population-based study, and the Spanish Bladder Cancer Study (n/n = 706 cases/772 controls), a hospital-based study. Because of differences in exposure distributions and metrics, we estimated effects of THMs and genetic variants within each study separately using adjusted logistic regression models to calculate odds ratios (ORs) and 95% confidence intervals (CI) with and without interaction terms, and then combined the results using meta-analysis. Results: Of the 16 loci showing strong evidence of association with bladder cancer, rs907611 at 11p15.5 [leukocyte- specific protein 1 (LSP1 region)] showed the strongest associations in the highest exposure category in each study, with evidence of interaction in both studies and in metaanalysis. In the highest exposure category, we observed OR= 1.66 (95% CI: 1.17, 2.34, p- trend = 0.005) for those with the rs907611-GG genotype and p-interaction = 0.02. No other genetic variants tested showed consistent evidence of interaction. Discussion: We found novel suggestive evidence for a multiplicative interaction between a putative bladder carcinogen, TTHMs, and genotypes of rs907611. Given the ubiquitous exposure to THMs, further work is needed to replicate and extend this finding and to understand potential molecular mechanisms. https://doi.org/10.1289/EHP9895, Introduction Worldwide, bladder cancer ranks as the ninth most common incident cancer and the 13th in mortality, with ~400,000 cases diagnosed each year. (1) Approximately 75% of incident cases occur [...]

Published
2022
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49. Aspirin Use and Mortality in Two Contemporary US Cohorts

Author

Huang, Wen-Yi, Daugherty, Sarah E., Shiels, Meredith S., Purdue, Mark P., Freedman, Neal D., Abnet, Christian C., Hollenbeck, Albert R., Hayes, Richard B., Silverman, Debra T., and Berndt, Sonja I.

Published
2018

50. Research Recommendations for Selected IARC-Classified Agents

Author

Ward, Elizabeth M, Schulte, Paul A, Straif, Kurt, Hopf, Nancy B, Caldwell, Jane C, Carreón, Tania, DeMarini, David M, Fowler, Bruce A, Goldstein, Bernard D, Hemminki, Kari, Hines, Cynthia J, Pursiainen, Kirsti Husgafvel, Kuempel, Eileen, Lewtas, Joellen, Lunn, Ruth M, Lynge, Elsebeth, McElvenny, Damien M, Muhle, Hartwig, Nakajima, Tamie, Robertson, Larry W, Rothman, Nathaniel, Ruder, Avima M, Schubauer-Berigan, Mary K, Siemiatycki, Jack, Silverman, Debra, Smith, Martyn T, Sorahan, Tom, Steenland, Kyle, Stevens, Richard G, Vineis, Paolo, Zahm, Shelia Hoar, Zeise, Lauren, and Cogliano, Vincent J

Subjects
Biomedical and Clinical Sciences, Environmental Sciences, Oncology and Carcinogenesis, Prevention, Cancer, Animals, Carcinogenicity Tests, Evidence-Based Medicine, Humans, animal, carcinogen, carcinogenesis, epidemiology, human, IARC, mechanisms of carcinogenicity, occupational, Medical and Health Sciences, Toxicology, Biomedical and clinical sciences, Environmental sciences, Health sciences
Abstract

ObjectivesThere are some common occupational agents and exposure circumstances for which evidence of carcinogenicity is substantial but not yet conclusive for humans. Our objectives were to identify research gaps and needs for 20 agents prioritized for review based on evidence of widespread human exposures and potential carcinogenicity in animals or humans.Data sourcesFor each chemical agent (or category of agents), a systematic review was conducted of new data published since the most recent pertinent International Agency for Research on Cancer (IARC) Monograph meeting on that agent.Data extractionReviewers were charged with identifying data gaps and general and specific approaches to address them, focusing on research that would be important in resolving classification uncertainties. An expert meeting brought reviewers together to discuss each agent and the identified data gaps and approaches.Data synthesisSeveral overarching issues were identified that pertained to multiple agents; these included the importance of recognizing that carcinogenic agents can act through multiple toxicity pathways and mechanisms, including epigenetic mechanisms, oxidative stress, and immuno- and hormonal modulation.ConclusionsStudies in occupational populations provide important opportunities to understand the mechanisms through which exogenous agents cause cancer and intervene to prevent human exposure and/or prevent or detect cancer among those already exposed. Scientific developments are likely to increase the challenges and complexities of carcinogen testing and evaluation in the future, and epidemiologic studies will be particularly critical to inform carcinogen classification and risk assessment processes.

Published
2010

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