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2. Fine-mapping analysis including over 254,000 East Asian and European descendants identifies 136 putative colorectal cancer susceptibility genes

Author

Chen, Zhishan, Guo, Xingyi, Tao, Ran, Huyghe, Jeroen R., Law, Philip J., Fernandez-Rozadilla, Ceres, Ping, Jie, Jia, Guochong, Long, Jirong, Li, Chao, Shen, Quanhu, Xie, Yuhan, Timofeeva, Maria N., Thomas, Minta, Schmit, Stephanie L., Díez-Obrero, Virginia, Devall, Matthew, Moratalla-Navarro, Ferran, Fernandez-Tajes, Juan, Palles, Claire, Sherwood, Kitty, Briggs, Sarah E. W., Svinti, Victoria, Donnelly, Kevin, Farrington, Susan M., Blackmur, James, Vaughan-Shaw, Peter G., Shu, Xiao-Ou, Lu, Yingchang, Broderick, Peter, Studd, James, Harrison, Tabitha A., Conti, David V., Schumacher, Fredrick R., Melas, Marilena, Rennert, Gad, Obón-Santacana, Mireia, Martín-Sánchez, Vicente, Oh, Jae Hwan, Kim, Jeongseon, Jee, Sun Ha, Jung, Keum Ji, Kweon, Sun-Seog, Shin, Min-Ho, Shin, Aesun, Ahn, Yoon-Ok, Kim, Dong-Hyun, Oze, Isao, Wen, Wanqing, Matsuo, Keitaro, Matsuda, Koichi, Tanikawa, Chizu, Ren, Zefang, Gao, Yu-Tang, Jia, Wei-Hua, Hopper, John L., Jenkins, Mark A., Win, Aung Ko, Pai, Rish K., Figueiredo, Jane C., Haile, Robert W., Gallinger, Steven, Woods, Michael O., Newcomb, Polly A., Duggan, David, Cheadle, Jeremy P., Kaplan, Richard, Kerr, Rachel, Kerr, David, Kirac, Iva, Böhm, Jan, Mecklin, Jukka-Pekka, Jousilahti, Pekka, Knekt, Paul, Aaltonen, Lauri A., Rissanen, Harri, Pukkala, Eero, Eriksson, Johan G., Cajuso, Tatiana, Hänninen, Ulrika, Kondelin, Johanna, Palin, Kimmo, Tanskanen, Tomas, Renkonen-Sinisalo, Laura, Männistö, Satu, Albanes, Demetrius, Weinstein, Stephanie J., Ruiz-Narvaez, Edward, Palmer, Julie R., Buchanan, Daniel D., Platz, Elizabeth A., Visvanathan, Kala, Ulrich, Cornelia M., Siegel, Erin, Brezina, Stefanie, Gsur, Andrea, Campbell, Peter T., Chang-Claude, Jenny, Hoffmeister, Michael, Brenner, Hermann, Slattery, Martha L., Potter, John D., Tsilidis, Kostas K., Schulze, Matthias B., Gunter, Marc J., Murphy, Neil, Castells, Antoni, Castellví-Bel, Sergi, Moreira, Leticia, Arndt, Volker, Shcherbina, Anna, Bishop, D. Timothy, Giles, Graham G., Southey, Melissa C., Idos, Gregory E., McDonnell, Kevin J., Abu-Ful, Zomoroda, Greenson, Joel K., Shulman, Katerina, Lejbkowicz, Flavio, Offit, Kenneth, Su, Yu-Ru, Steinfelder, Robert, Keku, Temitope O., van Guelpen, Bethany, Hudson, Thomas J., Hampel, Heather, Pearlman, Rachel, Berndt, Sonja I., Hayes, Richard B., Martinez, Marie Elena, Thomas, Sushma S., Pharoah, Paul D. P., Larsson, Susanna C., Yen, Yun, Lenz, Heinz-Josef, White, Emily, Li, Li, Doheny, Kimberly F., Pugh, Elizabeth, Shelford, Tameka, Chan, Andrew T., Cruz-Correa, Marcia, Lindblom, Annika, Hunter, David J., Joshi, Amit D., Schafmayer, Clemens, Scacheri, Peter C., Kundaje, Anshul, Schoen, Robert E., Hampe, Jochen, Stadler, Zsofia K., Vodicka, Pavel, Vodickova, Ludmila, Vymetalkova, Veronika, Edlund, Christopher K., Gauderman, W. James, Shibata, David, Toland, Amanda, Markowitz, Sanford, Kim, Andre, Chanock, Stephen J., van Duijnhoven, Franzel, Feskens, Edith J. M., Sakoda, Lori C., Gago-Dominguez, Manuela, Wolk, Alicja, Pardini, Barbara, FitzGerald, Liesel M., Lee, Soo Chin, Ogino, Shuji, Bien, Stephanie A., Kooperberg, Charles, Li, Christopher I., Lin, Yi, Prentice, Ross, Qu, Conghui, Bézieau, Stéphane, Yamaji, Taiki, Sawada, Norie, Iwasaki, Motoki, Le Marchand, Loic, Wu, Anna H., Qu, Chenxu, McNeil, Caroline E., Coetzee, Gerhard, Hayward, Caroline, Deary, Ian J., Harris, Sarah E., Theodoratou, Evropi, Reid, Stuart, Walker, Marion, Ooi, Li Yin, Lau, Ken S., Zhao, Hongyu, Hsu, Li, Cai, Qiuyin, Dunlop, Malcolm G., Gruber, Stephen B., Houlston, Richard S., Moreno, Victor, Casey, Graham, Peters, Ulrike, Tomlinson, Ian, and Zheng, Wei

Published
2024
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4. Combining Asian and European genome-wide association studies of colorectal cancer improves risk prediction across racial and ethnic populations

Author

Thomas, Minta, Su, Yu-Ru, Rosenthal, Elisabeth A., Sakoda, Lori C., Schmit, Stephanie L., Timofeeva, Maria N., Chen, Zhishan, Fernandez-Rozadilla, Ceres, Law, Philip J., Murphy, Neil, Carreras-Torres, Robert, Diez-Obrero, Virginia, van Duijnhoven, Franzel J. B., Jiang, Shangqing, Shin, Aesun, Wolk, Alicja, Phipps, Amanda I., Burnett-Hartman, Andrea, Gsur, Andrea, Chan, Andrew T., Zauber, Ann G., Wu, Anna H., Lindblom, Annika, Um, Caroline Y., Tangen, Catherine M., Gignoux, Chris, Newton, Christina, Haiman, Christopher A., Qu, Conghui, Bishop, D. Timothy, Buchanan, Daniel D., Crosslin, David R., Conti, David V., Kim, Dong-Hyun, Hauser, Elizabeth, White, Emily, Siegel, Erin, Schumacher, Fredrick R., Rennert, Gad, Giles, Graham G., Hampel, Heather, Brenner, Hermann, Oze, Isao, Oh, Jae Hwan, Lee, Jeffrey K., Schneider, Jennifer L., Chang-Claude, Jenny, Kim, Jeongseon, Huyghe, Jeroen R., Zheng, Jiayin, Hampe, Jochen, Greenson, Joel, Hopper, John L., Palmer, Julie R., Visvanathan, Kala, Matsuo, Keitaro, Matsuda, Koichi, Jung, Keum Ji, Li, Li, Le Marchand, Loic, Vodickova, Ludmila, Bujanda, Luis, Gunter, Marc J., Matejcic, Marco, Jenkins, Mark A., Slattery, Martha L., D’Amato, Mauro, Wang, Meilin, Hoffmeister, Michael, Woods, Michael O., Kim, Michelle, Song, Mingyang, Iwasaki, Motoki, Du, Mulong, Udaltsova, Natalia, Sawada, Norie, Vodicka, Pavel, Campbell, Peter T., Newcomb, Polly A., Cai, Qiuyin, Pearlman, Rachel, Pai, Rish K., Schoen, Robert E., Steinfelder, Robert S., Haile, Robert W., Vandenputtelaar, Rosita, Prentice, Ross L., Küry, Sébastien, Castellví-Bel, Sergi, Tsugane, Shoichiro, Berndt, Sonja I., Lee, Soo Chin, Brezina, Stefanie, Weinstein, Stephanie J., Chanock, Stephen J., Jee, Sun Ha, Kweon, Sun-Seog, Vadaparampil, Susan, Harrison, Tabitha A., Yamaji, Taiki, Keku, Temitope O., Vymetalkova, Veronika, Arndt, Volker, Jia, Wei-Hua, Shu, Xiao-Ou, Lin, Yi, Ahn, Yoon-Ok, Stadler, Zsofia K., Van Guelpen, Bethany, Ulrich, Cornelia M., Platz, Elizabeth A., Potter, John D., Li, Christopher I., Meester, Reinier, Moreno, Victor, Figueiredo, Jane C., Casey, Graham, Lansdorp Vogelaar, Iris, Dunlop, Malcolm G., Gruber, Stephen B., Hayes, Richard B., Pharoah, Paul D. P., Houlston, Richard S., Jarvik, Gail P., Tomlinson, Ian P., Zheng, Wei, Corley, Douglas A., Peters, Ulrike, and Hsu, Li

Published
2023
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10. Alcohol drinking and head and neck cancer risk: the joint effect of intensity and duration

Author

Di Credico, Gioia, Polesel, Jerry, Dal Maso, Luigino, Pauli, Francesco, Torelli, Nicola, Luce, Daniele, Radoï, Loredana, Matsuo, Keitaro, Serraino, Diego, Brennan, Paul, Holcatova, Ivana, Ahrens, Wolfgang, Lagiou, Pagona, Canova, Cristina, Richiardi, Lorenzo, Healy, Claire M, Kjaerheim, Kristina, Conway, David I, Macfarlane, Gary J, Thomson, Peter, Agudo, Antonio, Znaor, Ariana, Franceschi, Silvia, Herrero, Rolando, Toporcov, Tatiana N, Moyses, Raquel A, Muscat, Joshua, Negri, Eva, Vilensky, Marta, Fernandez, Leticia, Curado, Maria Paula, Menezes, Ana, Daudt, Alexander W, Koifman, Rosalina, Wunsch-Filho, Victor, Olshan, Andrew F, Zevallos, Jose P, Sturgis, Erich M, Li, Guojun, Levi, Fabio, Zhang, Zuo-Feng, Morgenstern, Hal, Smith, Elaine, Lazarus, Philip, La Vecchia, Carlo, Garavello, Werner, Chen, Chu, Schwartz, Stephen M, Zheng, Tongzhang, Vaughan, Thomas L, Kelsey, Karl, McClean, Michael, Benhamou, Simone, Hayes, Richard B, Purdue, Mark P, Gillison, Maura, Schantz, Stimson, Yu, Guo-Pei, Chuang, Shu-Chun, Boffetta, Paolo, Hashibe, Mia, Yuan-Chin, Amy Lee, and Edefonti, Valeria

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Dental/Oral and Craniofacial Disease, Alcoholism, Alcohol Use and Health, Digestive Diseases, Cancer, Prevention, Rare Diseases, Tobacco, Substance Misuse, Tobacco Smoke and Health, 2.2 Factors relating to the physical environment, Aetiology, Good Health and Well Being, Adolescent, Adult, Aged, Aged, 80 and over, Alcohol Drinking, Case-Control Studies, Female, Head and Neck Neoplasms, Humans, Laryngeal Neoplasms, Male, Middle Aged, Mouth Neoplasms, Oropharyngeal Neoplasms, Risk Factors, Severity of Illness Index, Smoking, Time Factors, Young Adult, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundAlcohol is a well-established risk factor for head and neck cancer (HNC). This study aims to explore the effect of alcohol intensity and duration, as joint continuous exposures, on HNC risk.MethodsData from 26 case-control studies in the INHANCE Consortium were used, including never and current drinkers who drunk ≤10 drinks/day for ≤54 years (24234 controls, 4085 oral cavity, 3359 oropharyngeal, 983 hypopharyngeal and 3340 laryngeal cancers). The dose-response relationship between the risk and the joint exposure to drinking intensity and duration was investigated through bivariate regression spline models, adjusting for potential confounders, including tobacco smoking.ResultsFor all subsites, cancer risk steeply increased with increasing drinks/day, with no appreciable threshold effect at lower intensities. For each intensity level, the risk of oral cavity, hypopharyngeal and laryngeal cancers did not vary according to years of drinking, suggesting no effect of duration. For oropharyngeal cancer, the risk increased with durations up to 28 years, flattening thereafter. The risk peaked at the higher levels of intensity and duration for all subsites (odds ratio = 7.95 for oral cavity, 12.86 for oropharynx, 24.96 for hypopharynx and 6.60 for larynx).ConclusionsPresent results further encourage the reduction of alcohol intensity to mitigate HNC risk.

Published
2020

12. 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, Brain Disorders, Cardiovascular, Heart Disease, Aging, Prevention, Climate-Related Exposures and Conditions, 2.2 Factors relating to the physical environment, Aetiology, 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

13. Age at start of using tobacco on the risk of head and neck cancer: Pooled analysis in the International Head and Neck Cancer Epidemiology Consortium (INHANCE)

Author

Chang, Chun-Pin, Chang, Shen-Chih, Chuang, Shu-Chun, Berthiller, Julien, Ferro, Gilles, Matsuo, Keitaro, Wünsch-Filho, Victor, Toporcov, Tatiana N, de Carvalho, Marcos Brasilino, La Vecchia, Carlo, Olshan, Andrew F, Zevallos, Jose P, Serraino, Diego, Muscat, Joshua, Sturgis, Erich M, Li, Guojun, Morgenstern, Hal, Levi, Fabio, Dal Maso, Luigino, Smith, Elaine, Kelsey, Karl, McClean, Michael, Vaughan, Thomas L, Lazarus, Philip, Ramroth, Heribert, Chen, Chu, Schwartz, Stephen M, Winn, Deborah M, Bosetti, Cristina, Edefonti, Valeria, Garavello, Werner, Negri, Eva, Hayes, Richard B, Purdue, Mark P, Boccia, Stefania, Cadoni, Gabriella, Shangina, Oxana, Koifman, Rosalina, Curado, Maria Paula, Vilensky, Marta, Swiatkowska, Beata, Herrero, Rolando, Franceschi, Silvia, Benhamou, Simone, Fernandez, Leticia, Menezes, Ana MB, Daudt, Alexander W, Mates, Dana, Schantz, Stimson, Yu, Guo-Pei, Lissowska, Jolanta, Brenner, Hermann, Fabianova, Eleonora, Rudnai, Peter, Brennan, Paul, Boffetta, Paolo, Zhang, Zuo-Feng, Hashibe, Mia, and Lee, Yuan-Chin Amy

Subjects
Biomedical and Clinical Sciences, Epidemiology, Health Services and Systems, Health Sciences, Public Health, Oncology and Carcinogenesis, Prevention, Rare Diseases, Cancer, Tobacco Smoke and Health, Dental/Oral and Craniofacial Disease, Substance Misuse, Tobacco, Aetiology, 2.2 Factors relating to the physical environment, Good Health and Well Being, Adult, Age Factors, Aged, Case-Control Studies, Female, Head and Neck Neoplasms, Humans, Male, Middle Aged, Risk Factors, Nicotiana, Age at start of tobacco use, Head and neck cancer, Oral cancer, Oropharyngeal cancer, Hypopharyngeal cancer, Laryngeal cancer, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundTobacco use is a well-established risk factor for head and neck cancer (HNC). However, less is known about the potential impact of exposure to tobacco at an early age on HNC risk.MethodsWe analyzed individual-level data on ever tobacco smokers from 27 case-control studies (17,146 HNC cases and 17,449 controls) in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using random-effects logistic regression models.ResultsWithout adjusting for tobacco packyears, we observed that younger age at starting tobacco use was associated with an increased HNC risk for ever smokers (OR

Published
2019

14. Joint effects of intensity and duration of cigarette smoking on the risk of head and neck cancer: A bivariate spline model approach

Author

Di Credico, Gioia, Edefonti, Valeria, Polesel, Jerry, Pauli, Francesco, Torelli, Nicola, Serraino, Diego, Negri, Eva, Luce, Daniele, Stucker, Isabelle, Matsuo, Keitaro, Brennan, Paul, Vilensky, Marta, Fernandez, Leticia, Curado, Maria Paula, Menezes, Ana, Daudt, Alexander W, Koifman, Rosalina, Wunsch-Filho, Victor, Holcatova, Ivana, Ahrens, Wolfgang, Lagiou, Pagona, Simonato, Lorenzo, Richiardi, Lorenzo, Healy, Claire, Kjaerheim, Kristina, Conway, David I, Macfarlane, Tatiana V, Thomson, Peter, Agudo, Antonio, Znaor, Ariana, Rios, Leonardo F Boaventura, Toporcov, Tatiana N, Franceschi, Silvia, Herrero, Rolando, Muscat, Joshua, Olshan, Andrew F, Zevallos, Jose P, La Vecchia, Carlo, Winn, Deborah M, Sturgis, Erich M, Li, Guojun, Fabianova, Eleonora, Lissowska, Jolanda, Mates, Dana, Rudnai, Peter, Shangina, Oxana, Swiatkowska, Beata, Moysich, Kirsten, Zhang, Zuo-Feng, Morgenstern, Hal, Levi, Fabio, Smith, Elaine, Lazarus, Philip, Bosetti, Cristina, Garavello, Werner, Kelsey, Karl, McClean, Michael, Ramroth, Heribert, Chen, Chu, Schwartz, Stephen M, Vaughan, Thomas L, Zheng, Tongzhang, Menvielle, Gwenn, Boccia, Stefania, Cadoni, Gabriella, Hayes, Richard B, Purdue, Mark, Gillison, Maura, Schantz, Stimson, Yu, Guo-Pei, Brenner, Hermann, D'Souza, Gypsyamber, Gross, Neil D, Chuang, Shu-Chun, Boffetta, Paolo, Hashibe, Mia, Lee, Yuan-Chin Amy, and Dal Maso, Luigino

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Prevention, Tobacco Smoke and Health, Substance Misuse, Tobacco, Dental/Oral and Craniofacial Disease, Rare Diseases, Cancer, 2.2 Factors relating to the physical environment, Good Health and Well Being, Adult, Aged, Aged, 80 and over, Case-Control Studies, Cigarette Smoking, Female, Head and Neck Neoplasms, Humans, Male, Middle Aged, Risk Factors, Bivariate spline models, Cigarette smoking duration, Cigarette smoking intensity, Head and neck cancer, INHANCE, Laryngeal cancer, Oral cavity and pharyngeal cancers, Dentistry, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

ObjectivesThis study aimed at re-evaluating the strength and shape of the dose-response relationship between the combined (or joint) effect of intensity and duration of cigarette smoking and the risk of head and neck cancer (HNC). We explored this issue considering bivariate spline models, where smoking intensity and duration were treated as interacting continuous exposures.Materials and methodsWe pooled individual-level data from 33 case-control studies (18,260 HNC cases and 29,844 controls) participating in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. In bivariate regression spline models, exposures to cigarette smoking intensity and duration (compared with never smokers) were modeled as a linear piecewise function within a logistic regression also including potential confounders. We jointly estimated the optimal knot locations and regression parameters within the Bayesian framework.ResultsFor oral-cavity/pharyngeal (OCP) cancers, an odds ratio (OR) >5 was reached after 30 years in current smokers of ∼20 or more cigarettes/day. Patterns of OCP cancer risk in current smokers differed across strata of alcohol intensity. For laryngeal cancer, ORs >20 were found for current smokers of ≥20 cigarettes/day for ≥30  years. In former smokers who quit ≥10  years ago, the ORs were approximately halved for OCP cancers, and ∼1/3 for laryngeal cancer, as compared to the same levels of intensity and duration in current smokers.ConclusionReferring to bivariate spline models, this study better quantified the joint effect of intensity and duration of cigarette smoking on HNC risk, further stressing the need of smoking cessation policies.

Published
2019

15. Novel Common Genetic Susceptibility Loci for Colorectal Cancer

Author

Schmit, Stephanie L, Edlund, Christopher K, Schumacher, Fredrick R, Gong, Jian, Harrison, Tabitha A, Huyghe, Jeroen R, Qu, Chenxu, Melas, Marilena, Van Den Berg, David J, Wang, Hansong, Tring, Stephanie, Plummer, Sarah J, Albanes, Demetrius, Alonso, M Henar, Amos, Christopher I, Anton, Kristen, Aragaki, Aaron K, Arndt, Volker, Barry, Elizabeth L, Berndt, Sonja I, Bezieau, Stéphane, Bien, Stephanie, Bloomer, Amanda, Boehm, Juergen, Boutron-Ruault, Marie-Christine, Brenner, Hermann, Brezina, Stefanie, Buchanan, Daniel D, Butterbach, Katja, Caan, Bette J, Campbell, Peter T, Carlson, Christopher S, Castelao, Jose E, Chan, Andrew T, Chang-Claude, Jenny, Chanock, Stephen J, Cheng, Iona, Cheng, Ya-Wen, Chin, Lee Soo, Church, James M, Church, Timothy, Coetzee, Gerhard A, Cotterchio, Michelle, Correa, Marcia Cruz, Curtis, Keith R, Duggan, David, Easton, Douglas F, English, Dallas, Feskens, Edith JM, Fischer, Rocky, FitzGerald, Liesel M, Fortini, Barbara K, Fritsche, Lars G, Fuchs, Charles S, Gago-Dominguez, Manuela, Gala, Manish, Gallinger, Steven J, Gauderman, W James, Giles, Graham G, Giovannucci, Edward L, Gogarten, Stephanie M, Gonzalez-Villalpando, Clicerio, Gonzalez-Villalpando, Elena M, Grady, William M, Greenson, Joel K, Gsur, Andrea, Gunter, Marc, Haiman, Christopher A, Hampe, Jochen, Harlid, Sophia, Harju, John F, Hayes, Richard B, Hofer, Philipp, Hoffmeister, Michael, Hopper, John L, Huang, Shu-Chen, Huerta, Jose Maria, Hudson, Thomas J, Hunter, David J, Idos, Gregory E, Iwasaki, Motoki, Jackson, Rebecca D, Jacobs, Eric J, Jee, Sun Ha, Jenkins, Mark A, Jia, Wei-Hua, Jiao, Shuo, Joshi, Amit D, Kolonel, Laurence N, Kono, Suminori, Kooperberg, Charles, Krogh, Vittorio, Kuehn, Tilman, Küry, Sébastien, LaCroix, Andrea, Laurie, Cecelia A, Lejbkowicz, Flavio, Lemire, Mathieu, Lenz, Heinz-Josef, and Levine, David

Subjects
Prevention, Cancer, Digestive Diseases, Human Genome, Genetics, Clinical Research, Colo-Rectal Cancer, Aetiology, 2.1 Biological and endogenous factors, Case-Control Studies, Colorectal Neoplasms, Ethnicity, Follow-Up Studies, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Polymorphism, Single Nucleotide, Prognosis, United States, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

BackgroundPrevious genome-wide association studies (GWAS) have identified 42 loci (P < 5 × 10-8) associated with risk of colorectal cancer (CRC). Expanded consortium efforts facilitating the discovery of additional susceptibility loci may capture unexplained familial risk.MethodsWe conducted a GWAS in European descent CRC cases and control subjects using a discovery-replication design, followed by examination of novel findings in a multiethnic sample (cumulative n = 163 315). In the discovery stage (36 948 case subjects/30 864 control subjects), we identified genetic variants with a minor allele frequency of 1% or greater associated with risk of CRC using logistic regression followed by a fixed-effects inverse variance weighted meta-analysis. All novel independent variants reaching genome-wide statistical significance (two-sided P < 5 × 10-8) were tested for replication in separate European ancestry samples (12 952 case subjects/48 383 control subjects). Next, we examined the generalizability of discovered variants in East Asians, African Americans, and Hispanics (12 085 case subjects/22 083 control subjects). Finally, we examined the contributions of novel risk variants to familial relative risk and examined the prediction capabilities of a polygenic risk score. All statistical tests were two-sided.ResultsThe discovery GWAS identified 11 variants associated with CRC at P < 5 × 10-8, of which nine (at 4q22.2/5p15.33/5p13.1/6p21.31/6p12.1/10q11.23/12q24.21/16q24.1/20q13.13) independently replicated at a P value of less than .05. Multiethnic follow-up supported the generalizability of discovery findings. These results demonstrated a 14.7% increase in familial relative risk explained by common risk alleles from 10.3% (95% confidence interval [CI] = 7.9% to 13.7%; known variants) to 11.9% (95% CI = 9.2% to 15.5%; known and novel variants). A polygenic risk score identified 4.3% of the population at an odds ratio for developing CRC of at least 2.0.ConclusionsThis study provides insight into the architecture of common genetic variation contributing to CRC etiology and improves risk prediction for individualized screening.

Published
2019

16. Interactions between folate intake and genetic predictors of gene expression levels associated with colorectal cancer risk

Author

Haas, Cameron B., Su, Yu-Ru, Petersen, Paneen, Wang, Xiaoliang, Bien, Stephanie A., Lin, Yi, Albanes, Demetrius, Weinstein, Stephanie J., Jenkins, Mark A., Figueiredo, Jane C., Newcomb, Polly A., Casey, Graham, Le Marchand, Loic, Campbell, Peter T., Moreno, Victor, Potter, John D., Sakoda, Lori C., Slattery, Martha L., Chan, Andrew T., Li, Li, Giles, Graham G., Milne, Roger L., Gruber, Stephen B., Rennert, Gad, Woods, Michael O., Gallinger, Steven J., Berndt, Sonja, Hayes, Richard B., Huang, Wen-Yi, Wolk, Alicja, White, Emily, Nan, Hongmei, Nassir, Rami, Lindor, Noralane M., Lewinger, Juan P., Kim, Andre E., Conti, David, Gauderman, W. James, Buchanan, Daniel D., Peters, Ulrike, and Hsu, Li

Published
2022
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19. Global estimates of mortality associated with long-term exposure to outdoor fine particulate matter.

Author

Burnett, Richard, Chen, Hong, Szyszkowicz, Mieczysław, Fann, Neal, Hubbell, Bryan, Pope, C Arden, Apte, Joshua S, Brauer, Michael, Cohen, Aaron, Weichenthal, Scott, Coggins, Jay, Di, Qian, Brunekreef, Bert, Frostad, Joseph, Lim, Stephen S, Kan, Haidong, Walker, Katherine D, Thurston, George D, Hayes, Richard B, Lim, Chris C, Turner, Michelle C, Jerrett, Michael, Krewski, Daniel, Gapstur, Susan M, Diver, W Ryan, Ostro, Bart, Goldberg, Debbie, Crouse, Daniel L, Martin, Randall V, Peters, Paul, Pinault, Lauren, Tjepkema, Michael, van Donkelaar, Aaron, Villeneuve, Paul J, Miller, Anthony B, Yin, Peng, Zhou, Maigeng, Wang, Lijun, Janssen, Nicole AH, Marra, Marten, Atkinson, Richard W, Tsang, Hilda, Quoc Thach, Thuan, Cannon, John B, Allen, Ryan T, Hart, Jaime E, Laden, Francine, Cesaroni, Giulia, Forastiere, Francesco, Weinmayr, Gudrun, Jaensch, Andrea, Nagel, Gabriele, Concin, Hans, and Spadaro, Joseph V

Subjects
Humans, Air Pollutants, Proportional Hazards Models, Bayes Theorem, Risk Assessment, Cohort Studies, Air Pollution, Environmental Exposure, Time Factors, Particulate Matter, Global Health, Global Burden of Disease, Noncommunicable Diseases, concentration, exposure, fine particulate matter, mortality, risk
Abstract

Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries-the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5-10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9-8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3-4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.

Published
2018

20. Identifying Novel Susceptibility Genes for Colorectal Cancer Risk From a Transcriptome-Wide Association Study of 125,478 Subjects

Author

Guo, Xingyi, Lin, Weiqiang, Wen, Wanqing, Huyghe, Jeroen, Bien, Stephanie, Cai, Qiuyin, Harrison, Tabitha, Chen, Zhishan, Qu, Conghui, Bao, Jiandong, Long, Jirong, Yuan, Yuan, Wang, Fangqin, Bai, Mengqiu, Abecasis, Goncalo R., Albanes, Demetrius, Berndt, Sonja I., Bézieau, Stéphane, Bishop, D. Timothy, Brenner, Hermann, Buch, Stephan, Burnett-Hartman, Andrea, Campbell, Peter T., Castellví-Bel, Sergi, Chan, Andrew T., Chang-Claude, Jenny, Chanock, Stephen J., Cho, Sang Hee, Conti, David V., Chapelle, Albert de la, Feskens, Edith J.M., Gallinger, Steven J., Giles, Graham G., Goodman, Phyllis J., Gsur, Andrea, Guinter, Mark, Gunter, Marc J., Hampe, Jochen, Hampel, Heather, Hayes, Richard B., Hoffmeister, Michael, Kampman, Ellen, Kang, Hyun Min, Keku, Temitope O., Kim, Hyeong Rok, Le Marchand, Loic, Lee, Soo Chin, Li, Christopher I., Li, Li, Lindblom, Annika, Lindor, Noralane, Milne, Roger L., Moreno, Victor, Murphy, Neil, Newcomb, Polly A., Nickerson, Deborah A., Offit, Kenneth, Pearlman, Rachel, Pharoah, Paul D.P., Platz, Elizabeth A., Potter, John D., Rennert, Gad, Sakoda, Lori C., Schafmayer, Clemens, Schmit, Stephanie L., Schoen, Robert E., Schumacher, Fredrick R., Slattery, Martha L., Su, Yu-Ru, Tangen, Catherine M., Ulrich, Cornelia M., van Duijnhoven, Franzel J.B., Van Guelpen, Bethany, Visvanathan, Kala, Vodicka, Pavel, Vodickova, Ludmila, Vymetalkova, Veronika, Wang, Xiaoliang, White, Emily, Wolk, Alicja, Woods, Michael O., Casey, Graham, Hsu, Li, Jenkins, Mark A., Gruber, Stephen B., Peters, Ulrike, and Zheng, Wei

Published
2021
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21. Genomewide meta‐analysis identifies loci associated with IGF‐I and IGFBP‐3 levels with impact on age‐related traits

Author

Teumer, Alexander, Qi, Qibin, Nethander, Maria, Aschard, Hugues, Bandinelli, Stefania, Beekman, Marian, Berndt, Sonja I, Bidlingmaier, Martin, Broer, Linda, Group, CHARGE Longevity Working, Cappola, Anne, Ceda, Gian Paolo, Chanock, Stephen, Chen, Ming‐Huei, Chen, Tai C, Chen, Yii‐Der Ida, Chung, Jonathan, Del Greco Miglianico, Fabiola, Eriksson, Joel, Ferrucci, Luigi, Friedrich, Nele, Gnewuch, Carsten, Goodarzi, Mark O, Grarup, Niels, Guo, Tingwei, Hammer, Elke, Hayes, Richard B, Hicks, Andrew A, Hofman, Albert, Houwing‐Duistermaat, Jeanine J, Hu, Frank, Hunter, David J, Husemoen, Lise L, Isaacs, Aaron, Jacobs, Kevin B, Janssen, Joop AMJL, Jansson, John‐Olov, Jehmlich, Nico, Johnson, Simon, Juul, Anders, Karlsson, Magnus, Kilpelainen, Tuomas O, Kovacs, Peter, Kraft, Peter, Li, Chao, Linneberg, Allan, Liu, Yongmei, Loos, Ruth JF, Consortium, Body Composition Genetics, Lorentzon, Mattias, Lu, Yingchang, Maggio, Marcello, Magi, Reedik, Meigs, James, Mellström, Dan, Nauck, Matthias, Newman, Anne B, Pollak, Michael N, Pramstaller, Peter P, Prokopenko, Inga, Psaty, Bruce M, Reincke, Martin, Rimm, Eric B, Rotter, Jerome I, Pierre, Aude Saint, Schurmann, Claudia, Seshadri, Sudha, Sjögren, Klara, Slagboom, P Eline, Strickler, Howard D, Stumvoll, Michael, Suh, Yousin, Sun, Qi, Zhang, Cuilin, Svensson, Johan, Tanaka, Toshiko, Tare, Archana, Tönjes, Anke, Uh, Hae‐Won, van Duijn, Cornelia M, van Heemst, Diana, Vandenput, Liesbeth, Vasan, Ramachandran S, Völker, Uwe, Willems, Sara M, Ohlsson, Claes, Wallaschofski, Henri, and Kaplan, Robert C

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Clinical Research, Aging, 2.1 Biological and endogenous factors, Aetiology, Metabolic and endocrine, Cardiovascular, Adult, Female, Gene Expression Regulation, Genome-Wide Association Study, Humans, Insulin-Like Growth Factor Binding Protein 3, Insulin-Like Growth Factor I, Male, Metabolome, Quantitative Trait Loci, Quantitative Trait, Heritable, Regulatory Sequences, Nucleic Acid, aging, genomewide association study, growth hormone axis, IGF-I, IGFBP-3, longevity, CHARGE Longevity Working Group, Body Composition Genetics Consortium, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

The growth hormone/insulin-like growth factor (IGF) axis can be manipulated in animal models to promote longevity, and IGF-related proteins including IGF-I and IGF-binding protein-3 (IGFBP-3) have also been implicated in risk of human diseases including cardiovascular diseases, diabetes, and cancer. Through genomewide association study of up to 30 884 adults of European ancestry from 21 studies, we confirmed and extended the list of previously identified loci associated with circulating IGF-I and IGFBP-3 concentrations (IGF1, IGFBP3, GCKR, TNS3, GHSR, FOXO3, ASXL2, NUBP2/IGFALS, SORCS2, and CELSR2). Significant sex interactions, which were characterized by different genotype-phenotype associations between men and women, were found only for associations of IGFBP-3 concentrations with SNPs at the loci IGFBP3 and SORCS2. Analyses of SNPs, gene expression, and protein levels suggested that interplay between IGFBP3 and genes within the NUBP2 locus (IGFALS and HAGH) may affect circulating IGF-I and IGFBP-3 concentrations. The IGF-I-decreasing allele of SNP rs934073, which is an eQTL of ASXL2, was associated with lower adiposity and higher likelihood of survival beyond 90 years. The known longevity-associated variant rs2153960 (FOXO3) was observed to be a genomewide significant SNP for IGF-I concentrations. Bioinformatics analysis suggested enrichment of putative regulatory elements among these IGF-I- and IGFBP-3-associated loci, particularly of rs646776 at CELSR2. In conclusion, this study identified several loci associated with circulating IGF-I and IGFBP-3 concentrations and provides clues to the potential role of the IGF axis in mediating effects of known (FOXO3) and novel (ASXL2) longevity-associated loci.

Published
2016

23. Relationship of prediagnostic body mass index with survival after colorectal cancer: Stage‐specific associations

Author

Kocarnik, Jonathan M, Chan, Andrew T, Slattery, Martha L, Potter, John D, Meyerhardt, Jeffrey, Phipps, Amanda, Nan, Hongmei, Harrison, Tabitha, Rohan, Thomas E, Qi, Lihong, Hou, Lifang, Caan, Bette, Kroenke, Candyce H, Strickler, Howard, Hayes, Richard B, Schoen, Robert E, Chong, Dawn Q, White, Emily, Berndt, Sonja I, Peters, Ulrike, and Newcomb, Polly A

Subjects
Colo-Rectal Cancer, Nutrition, Digestive Diseases, Cancer, Prevention, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Good Health and Well Being, Aged, Aged, 80 and over, Body Mass Index, Colorectal Neoplasms, Female, Humans, Male, Middle Aged, Neoplasm Staging, Obesity, Overweight, Population Surveillance, Proportional Hazards Models, Risk Factors, Survival Rate, body mass index, cancer stage, colorectal cancer, mortality, survival, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Higher body mass index (BMI) is a well-established risk factor for colorectal cancer (CRC), but is inconsistently associated with CRC survival. In 6 prospective studies participating in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), 2,249 non-Hispanic white CRC cases were followed for a median 4.5 years after diagnosis, during which 777 died, 554 from CRC-related causes. Associations between prediagnosis BMI and survival (overall and CRC-specific) were evaluated using Cox regression models adjusted for age at diagnosis, sex, study and smoking status (current/former/never). The association between BMI category and CRC survival varied by cancer stage at diagnosis (I-IV) for both all-cause (p-interaction = 0.03) and CRC-specific mortality (p-interaction = 0.04). Compared to normal BMI (18.5-24.9 kg/m(2) ), overweight (BMI 25.0-29.9) was associated with increased mortality among those with Stage I disease, and decreased mortality among those with Stages II-IV disease. Similarly, obesity (BMI ≥30) was associated with increased mortality among those with Stages I-II disease, and decreased mortality among those with Stages III-IV disease. These results suggest the relationship between BMI and survival after CRC diagnosis differs by stage at diagnosis, and may emphasize the importance of adequate metabolic reserves for colorectal cancer survival in patients with late-stage disease.

Published
2016

24. Mouthwash use and cancer of the head and neck

Author

Boffetta, Paolo, Hayes, Richard B, Sartori, Samantha, Lee, Yuan-Chin A, Muscat, Joshua, Olshan, Andrew, Winn, Deborah M, Castellsagué, Xavier, Zhang, Zuo-Feng, Morgenstern, Hal, Chen, Chu, Schwartz, Stephen M, Vaughan, Thomas L, Wunsch-Filho, Victor, Purdue, Mark, Koifman, Sergio, Curado, Maria P, Vilensky, Marta, Gillison, Maura, Fernandez, Leticia, Menezes, Ana, Daudt, Alexander W, Schantz, Stimson, Yu, Guopei, D’Souza, Gypsyamber, Haddad, Robert I, La Vecchia, Carlo, and Hashibe, Mia

Subjects
Health Services and Systems, Biomedical and Clinical Sciences, Health Sciences, Tobacco, Digestive Diseases, Prevention, Tobacco Smoke and Health, Cancer, Dental/Oral and Craniofacial Disease, Substance Misuse, Oral and gastrointestinal, Good Health and Well Being, Adult, Case-Control Studies, Female, Follow-Up Studies, Head and Neck Neoplasms, Humans, International Agencies, Male, Meta-Analysis as Topic, Mouthwashes, Prevalence, Prognosis, Retrospective Studies, Risk Factors, alcohol, head and neck cancer, laryngeal cancer, mouthwash, oral cancer, pharyngeal cancer, Oncology and Carcinogenesis, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis, Public health
Abstract

Most mouthwashes contain alcohol, a known cause of head and neck cancer (oral cavity, pharynx, larynx), likely through the carcinogenic activity of acetaldehyde, formed in the oral cavity from alcohol. We carried out a pooled analysis of 8981 cases of head and neck cancer and 10 090 controls from 12 case-control studies with comparable information on mouthwash use in the International Head and Neck Cancer Epidemiology Consortium. Logistic regression was used to assess the association of mouthwash use with cancers of the oral cavity, oropharynx, hypopharynx, and larynx, adjusting for study, age, sex, pack-years of tobacco smoking, number of alcoholic drinks/day, and education. Compared with never users of mouthwash, the odds ratio (OR) of all head and neck cancers was 1.01 [95% confidence interval (CI): 0.94-1.08] for ever users, based on 12 studies. The corresponding ORs of cancer of the oral cavity and oropharynx were 1.11 (95% CI: 1.00-1.23) and 1.28 (95% CI: 1.06-1.56), respectively. OR for all head and neck cancer was 1.15 (95% CI: 1.01-1.30) for use for more than 35 years, based on seven studies (P for linear trend=0.01), and OR 1.31 (95% CI: 1.09-1.58) for use more than one per day, based on five studies (P for linear trend

Published
2016

25. Comparison of hematological alterations and markers of B-cell activation in workers exposed to benzene, formaldehyde and trichloroethylene

Author

Bassig, Bryan A, Zhang, Luoping, Vermeulen, Roel, Tang, Xiaojiang, Li, Guilan, Hu, Wei, Guo, Weihong, Purdue, Mark P, Yin, Songnian, Rappaport, Stephen M, Shen, Min, Ji, Zhiying, Qiu, Chuangyi, Ge, Yichen, Hosgood, H Dean, Reiss, Boris, Wu, Banghua, Xie, Yuxuan, Li, Laiyu, Yue, Fei, Freeman, Laura E Beane, Blair, Aaron, Hayes, Richard B, Huang, Hanlin, Smith, Martyn T, Rothman, Nathaniel, and Lan, Qing

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Stem Cell Research, Rare Diseases, Cancer, Prevention, Lymphoma, Hematology, Adult, B-Lymphocytes, Benzene, Biomarkers, Tumor, China, Female, Formaldehyde, Hemolytic Agents, Humans, Leukemia, Lymphocyte Activation, Lymphoma, Non-Hodgkin, Male, Myeloid Progenitor Cells, Occupational Exposure, Trichloroethylene, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

Benzene, formaldehyde (FA) and trichloroethylene (TCE) are ubiquitous chemicals in workplaces and the general environment. Benzene is an established myeloid leukemogen and probable lymphomagen. FA is classified as a myeloid leukemogen but has not been associated with non-Hodgkin lymphoma (NHL), whereas TCE has been associated with NHL but not myeloid leukemia. Epidemiologic associations between FA and myeloid leukemia, and between benzene, TCE and NHL are, however, still debated. Previously, we showed that these chemicals are associated with hematotoxicity in cross-sectional studies of factory workers in China, which included extensive personal monitoring and biological sample collection. Here, we compare and contrast patterns of hematotoxicity, monosomy 7 in myeloid progenitor cells (MPCs), and B-cell activation biomarkers across these studies to further evaluate possible mechanisms of action and consistency of effects with observed hematologic cancer risks. Workers exposed to benzene or FA, but not TCE, showed declines in cell types derived from MPCs, including granulocytes and platelets. Alterations in lymphoid cell types, including B cells and CD4+ T cells, and B-cell activation markers were apparent in workers exposed to benzene or TCE. Given that alterations in myeloid and lymphoid cell types are associated with hematological malignancies, our data provide biologic insight into the epidemiological evidence linking benzene and FA exposure with myeloid leukemia risk, and TCE and benzene exposure with NHL risk.

Published
2016

26. Low frequency of cigarette smoking and the risk of head and neck cancer in the INHANCE consortium pooled analysis

Author

Berthiller, Julien, Straif, Kurt, Agudo, Antonio, Ahrens, Wolfgang, dos Santos, Alexandre Bezerra, Boccia, Stefania, Cadoni, Gabriella, Canova, Cristina, Castellsague, Xavier, Chen, Chu, Conway, David, Curado, Maria Paula, Dal Maso, Luigino, Daudt, Alexander W, Fabianova, Eleonora, Fernandez, Leticia, Franceschi, Silvia, Fukuyama, Erica E, Hayes, Richard B, Healy, Claire, Herrero, Rolando, Holcatova, Ivana, Kelsey, Karl, Kjaerheim, Kristina, Koifman, Sergio, Lagiou, Pagona, La Vecchia, Carlo, Lazarus, Philip, Levi, Fabio, Lissowska, Jolanta, Macfarlane, Tatiana, Mates, Dana, McClean, Michael, Menezes, Ana, Merletti, Franco, Morgenstern, Hal, Muscat, Joshua, Olshan, Andrew F, Purdue, Mark, Ramroth, Heribert, Rudnai, Peter, Schwartz, Stephen M, Serraino, Diego, Shangina, Oxana, Smith, Elaine, Sturgis, Erich M, Szeszenia-Dabrowska, Neonila, Thomson, Peter, Vaughan, Thomas L, Vilensky, Marta, Wei, Qingyi, Winn, Deborah M, Wünsch-Filho, Victor, Zhang, Zuo-Feng, Znaor, Ariana, Ferro, Gilles, Brennan, Paul, Boffetta, Paolo, Hashibe, Mia, and Lee, Yuan-Chin Amy

Subjects
Cancer, Prevention, Dental/Oral and Craniofacial Disease, Tobacco Smoke and Health, Substance Misuse, Clinical Research, Rare Diseases, Tobacco, Respiratory, Good Health and Well Being, Adult, Aged, Alcohol Drinking, Case-Control Studies, Cigarette Smoking, Female, Head and Neck Neoplasms, Humans, Logistic Models, Male, Middle Aged, Odds Ratio, Public Health, Risk Factors, Head and neck cancer, low frequency cigarette smoking, risk factors, pooled analysis, Statistics, Public Health and Health Services, Epidemiology
Abstract

BackgroundCigarette smoking is a major risk factor for head and neck cancer (HNC). To our knowledge, low cigarette smoking (0-3, >3-5, >5-10 cigarettes per day.ResultsSmoking >0-3 cigarettes per day was associated with a 50% increased risk of HNC in the study population [odds ratio (OR) = 1.52, 95% confidence interval (CI): (1.21, 1.90). Smoking >3-5 cigarettes per day was associated in each subgroup from OR = 2.01 (95% CI: 1.22, 3.31) among never alcohol drinkers to OR = 2.74 (95% CI: 2.01, 3.74) among women and in each cancer site, particularly laryngeal cancer (OR = 3.48, 95% CI: 2.40, 5.05). However, the observed increased risk of HNC for low smoking frequency was not found among smokers with smoking duration shorter than 20 years.ConclusionOur results suggest a public health message that low frequency of cigarette consumption contributes to the development of HNC. However, smoking duration seems to play at least an equal or a stronger role in the development of HNC.

Published
2016

27. Ambient Particulate Matter Air Pollution Exposure and Mortality in the NIH-AARP Diet and Health Cohort

Author

Thurston, George D, Ahn, Jiyoung, Cromar, Kevin R, Shao, Yongzhao, Reynolds, Harmony R, Jerrett, Michael, Lim, Chris C, Shanley, Ryan, Park, Yikyung, and Hayes, Richard B

Subjects
Cardiovascular, Heart Disease, Prevention, Climate-Related Exposures and Conditions, Aging, Clinical Research, Aetiology, 2.2 Factors relating to the physical environment, Good Health and Well Being, Aged, Air Pollutants, Air Pollution, Cardiovascular Diseases, Cohort Studies, Female, Humans, Male, Middle Aged, Mortality, Ozone, Particulate Matter, Prospective Studies, Respiratory Tract Diseases, Smoking, United States, Environmental Sciences, Medical and Health Sciences, Toxicology
Abstract

BackgroundOutdoor fine particulate matter (≤ 2.5 μm; PM2.5) has been identified as a global health threat, but the number of large U.S. prospective cohort studies with individual participant data remains limited, especially at lower recent exposures.ObjectivesWe aimed to test the relationship between long-term exposure PM2.5 and death risk from all nonaccidental causes, cardiovascular (CVD), and respiratory diseases in 517,041 men and women enrolled in the National Institutes of Health-AARP cohort.MethodsIndividual participant data were linked with residence PM2.5 exposure estimates across the continental United States for a 2000-2009 follow-up period when matching census tract-level PM2.5 exposure data were available. Participants enrolled ranged from 50 to 71 years of age, residing in six U.S. states and two cities. Cox proportional hazard models yielded hazard ratio (HR) estimates per 10 μg/m3 of PM2.5 exposure.ResultsPM2.5 exposure was significantly associated with total mortality (HR = 1.03; 95% CI: 1.00, 1.05) and CVD mortality (HR = 1.10; 95% CI: 1.05, 1.15), but the association with respiratory mortality was not statistically significant (HR = 1.05; 95% CI: 0.98, 1.13). A significant association was found with respiratory mortality only among never smokers (HR = 1.27; 95% CI: 1.03, 1.56). Associations with 10-μg/m3 PM2.5 exposures in yearly participant residential annual mean, or in metropolitan area-wide mean, were consistent with baseline exposure model results. Associations with PM2.5 were similar when adjusted for ozone exposures. Analyses of California residents alone also yielded statistically significant PM2.5 mortality HRs for total and CVD mortality.ConclusionsLong-term exposure to PM2.5 air pollution was associated with an increased risk of total and CVD mortality, providing an independent test of the PM2.5-mortality relationship in a new large U.S. prospective cohort experiencing lower post-2000 PM2.5 exposure levels.CitationThurston GD, Ahn J, Cromar KR, Shao Y, Reynolds HR, Jerrett M, Lim CC, Shanley R, Park Y, Hayes RB. 2016. Ambient particulate matter air pollution exposure and mortality in the NIH-AARP Diet and Health cohort. Environ Health Perspect 124:484-490; http://dx.doi.org/10.1289/ehp.1509676.

Published
2016

28. Corrigendum: genome-wide association study of colorectal cancer identifies six new susceptibility loci.

Author

Schumacher, Fredrick R, Schmit, Stephanie L, Jiao, Shuo, Edlund, Christopher K, Wang, Hansong, Zhang, Ben, Hsu, Li, Huang, Shu-Chen, Fischer, Christopher P, Harju, John F, Idos, Gregory E, Lejbkowicz, Flavio, Manion, Frank J, McDonnell, Kevin, McNeil, Caroline E, Melas, Marilena, Rennert, Hedy S, Shi, Wei, Thomas, Duncan C, Van Den Berg, David J, Hutter, Carolyn M, Aragaki, Aaron K, Butterbach, Katja, Caan, Bette J, Carlson, Christopher S, Chanock, Stephen J, Curtis, Keith R, Fuchs, Charles S, Gala, Manish, Giovannucci, Edward L, Gogarten, Stephanie M, Hayes, Richard B, Henderson, Brian, Hunter, David J, Jackson, Rebecca D, Kolonel, Laurence N, Kooperberg, Charles, Küry, Sébastien, LaCroix, Andrea, Laurie, Cathy C, Laurie, Cecelia A, Lemire, Mathieu, Levine, David, Ma, Jing, Makar, Karen W, Qu, Conghui, Taverna, Darin, Ulrich, Cornelia M, Wu, Kana, Kono, Suminori, West, Dee W, Berndt, Sonja I, Bezieau, Stephane, Brenner, Hermann, Campbell, Peter T, Chan, Andrew T, Chang-Claude, Jenny, Coetzee, Gerhard A, Conti, David V, Duggan, David, Figueiredo, Jane C, Fortini, Barbara K, Gallinger, Steven J, Gauderman, W James, Giles, Graham, Green, Roger, Haile, Robert, Harrison, Tabitha A, Hoffmeister, Michael, Hopper, John L, Hudson, Thomas J, Jacobs, Eric, Iwasaki, Motoki, Jee, Sun Ha, Jenkins, Mark, Jia, Wei-Hua, Joshi, Amit, Li, Li, Lindor, Noralene M, Matsuo, Keitaro, Moreno, Victor, Mukherjee, Bhramar, Newcomb, Polly A, Potter, John D, Raskin, Leon, Rennert, Gad, Rosse, Stephanie, Severi, Gianluca, Schoen, Robert E, Seminara, Daniela, Shu, Xiao-Ou, Slattery, Martha L, Tsugane, Shoichiro, White, Emily, Xiang, Yong-Bing, Zanke, Brent W, Zheng, Wei, Le Marchand, Loic, Casey, Graham, and Gruber, Stephen B

Subjects
MD Multidisciplinary
Published
2015

29. Erratum: Corrigendum: Genome-wide association study of colorectal cancer identifies six new susceptibility loci

Author

Schumacher, Fredrick R, Schmit, Stephanie L, Jiao, Shuo, Edlund, Christopher K, Wang, Hansong, Zhang, Ben, Hsu, Li, Huang, Shu-Chen, Fischer, Christopher P, Harju, John F, Idos, Gregory E, Lejbkowicz, Flavio, Manion, Frank J, McDonnell, Kevin, McNeil, Caroline E, Melas, Marilena, Rennert, Hedy S, Shi, Wei, Thomas, Duncan C, Van Den Berg, David J, Hutter, Carolyn M, Aragaki, Aaron K, Butterbach, Katja, Caan, Bette J, Carlson, Christopher S, Chanock, Stephen J, Curtis, Keith R, Fuchs, Charles S, Gala, Manish, Giovannucci, Edward L, Gogarten, Stephanie M, Hayes, Richard B, Henderson, Brian, Hunter, David J, Jackson, Rebecca D, Kolonel, Laurence N, Kooperberg, Charles, Küry, Sébastien, LaCroix, Andrea, Laurie, Cathy C, Laurie, Cecelia A, Lemire, Mathieu, Levine, David, Ma, Jing, Makar, Karen W, Qu, Conghui, Taverna, Darin, Ulrich, Cornelia M, Wu, Kana, Kono, Suminori, West, Dee W, Berndt, Sonja I, Bezieau, Stephane, Brenner, Hermann, Campbell, Peter T, Chan, Andrew T, Chang-Claude, Jenny, Coetzee, Gerhard A, Conti, David V, Duggan, David, Figueiredo, Jane C, Fortini, Barbara K, Gallinger, Steven J, Gauderman, W James, Giles, Graham, Green, Roger, Haile, Robert, Harrison, Tabitha A, Hoffmeister, Michael, Hopper, John L, Hudson, Thomas J, Jacobs, Eric, Iwasaki, Motoki, Jee, Sun Ha, Jenkins, Mark, Jia, Wei-Hua, Joshi, Amit, Li, Li, Lindor, Noralene M, Matsuo, Keitaro, Moreno, Victor, Mukherjee, Bhramar, Newcomb, Polly A, Potter, John D, Raskin, Leon, Rennert, Gad, Rosse, Stephanie, Severi, Gianluca, Schoen, Robert E, Seminara, Daniela, Shu, Xiao-Ou, Slattery, Martha L, Tsugane, Shoichiro, White, Emily, Xiang, Yong-Bing, Zanke, Brent W, Zheng, Wei, Le Marchand, Loic, Casey, Graham, and Gruber, Stephen B

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Digestive Diseases, Cancer, Colo-Rectal Cancer
Published
2015

32. Relation of allium vegetables intake with head and neck cancers: Evidence from the INHANCE consortium

Author

Galeone, Carlotta, Turati, Federica, Zhang, Zuo-Feng, Guercio, Valentina, Tavani, Alessandra, Serraino, Diego, Brennan, Paul, Fabianova, Eleonora, Lissowska, Jola, Mates, Dana, Rudnai, Peter, Shangina, Oxana, Szeszenia-Dabrowska, Neonila, Vaughan, Thomas L, Kelsey, Karl, McClean, Michael, Levi, Fabio, Hayes, Richard B, Purdue, Mark P, Bosetti, Cristina, Brenner, Hermann, Pelucchi, Claudio, Lee, Yuan-Chin Amy, Hashibe, Mia, Boffetta, Paolo, and La Vecchia, Carlo

Subjects
Biomedical and Clinical Sciences, Nutrition and Dietetics, Rare Diseases, Dental/Oral and Craniofacial Disease, Cancer, Allium, Case-Control Studies, Diet, Head and Neck Neoplasms, Humans, Logistic Models, Risk Factors, Vegetables, Allium vegetables, Garlic, Onion, Food Sciences, Public Health and Health Services, Food Science, Nutrition & Dietetics, Food sciences, Nutrition and dietetics
Abstract

ScopeOnly a few studies analyzed the role of allium vegetables with reference to head and neck cancers (HNC), with mixed results. We investigated the potential favorable role of garlic and onion within the International Head and Neck Cancer Epidemiology (INHANCE) Consortium.Methods and resultsWe analyzed pooled individual-level data from eight case-control studies, including 4590 cases and 7082 controls. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) for associations between garlic and onion intakes and HNC risk. Compared with no or low garlic use, the ORs of HNC were 0.95 (95% CI 0.71-1.27) for intermediate and 0.74 (95% CI 0.55-0.99) for high garlic use (p for trend = 0.02). The ORs of HNC for increasing categories of onion intake were 0.91 (95% CI 0.68-1.21) for >1 to ≤3 portions per week, and 0.83 (95% CI 0.60-1.13) for >3 portions per week (p for trend = 0.02), as compared to

Published
2015

33. Genome-wide association study of colorectal cancer identifies six new susceptibility loci.

Author

Schumacher, Fredrick R, Schmit, Stephanie L, Jiao, Shuo, Edlund, Christopher K, Wang, Hansong, Zhang, Ben, Hsu, Li, Huang, Shu-Chen, Fischer, Christopher P, Harju, John F, Idos, Gregory E, Lejbkowicz, Flavio, Manion, Frank J, McDonnell, Kevin, McNeil, Caroline E, Melas, Marilena, Rennert, Hedy S, Shi, Wei, Thomas, Duncan C, Van Den Berg, David J, Hutter, Carolyn M, Aragaki, Aaron K, Butterbach, Katja, Caan, Bette J, Carlson, Christopher S, Chanock, Stephen J, Curtis, Keith R, Fuchs, Charles S, Gala, Manish, Giovannucci, Edward L, Gogarten, Stephanie M, Hayes, Richard B, Henderson, Brian, Hunter, David J, Jackson, Rebecca D, Kolonel, Laurence N, Kooperberg, Charles, Küry, Sébastien, LaCroix, Andrea, Laurie, Cathy C, Laurie, Cecelia A, Lemire, Mathieu, Levine, David, Ma, Jing, Makar, Karen W, Qu, Conghui, Taverna, Darin, Ulrich, Cornelia M, Wu, Kana, Kono, Suminori, West, Dee W, Berndt, Sonja I, Bezieau, Stéphane, Brenner, Hermann, Campbell, Peter T, Chan, Andrew T, Chang-Claude, Jenny, Coetzee, Gerhard A, Conti, David V, Duggan, David, Figueiredo, Jane C, Fortini, Barbara K, Gallinger, Steven J, Gauderman, W James, Giles, Graham, Green, Roger, Haile, Robert, Harrison, Tabitha A, Hoffmeister, Michael, Hopper, John L, Hudson, Thomas J, Jacobs, Eric, Iwasaki, Motoki, Jee, Sun Ha, Jenkins, Mark, Jia, Wei-Hua, Joshi, Amit, Li, Li, Lindor, Noralene M, Matsuo, Keitaro, Moreno, Victor, Mukherjee, Bhramar, Newcomb, Polly A, Potter, John D, Raskin, Leon, Rennert, Gad, Rosse, Stephanie, Severi, Gianluca, Schoen, Robert E, Seminara, Daniela, Shu, Xiao-Ou, Slattery, Martha L, Tsugane, Shoichiro, White, Emily, Xiang, Yong-Bing, Zanke, Brent W, and Zheng, Wei

Subjects
Humans, Colorectal Neoplasms, Genetic Predisposition to Disease, Odds Ratio, Case-Control Studies, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Genetics, Digestive Diseases, Prevention, Cancer, Human Genome, Colo-Rectal Cancer, 2.1 Biological and endogenous factors, MD Multidisciplinary
Abstract

Genetic susceptibility to colorectal cancer is caused by rare pathogenic mutations and common genetic variants that contribute to familial risk. Here we report the results of a two-stage association study with 18,299 cases of colorectal cancer and 19,656 controls, with follow-up of the most statistically significant genetic loci in 4,725 cases and 9,969 controls from two Asian consortia. We describe six new susceptibility loci reaching a genome-wide threshold of P

Published
2015

34. Estimating and explaining the effect of education and income on head and neck cancer risk: INHANCE consortium pooled analysis of 31 case‐control studies from 27 countries

Author

Conway, David I, Brenner, Darren R, McMahon, Alex D, Macpherson, Lorna MD, Agudo, Antonio, Ahrens, Wolfgang, Bosetti, Cristina, Brenner, Hermann, Castellsague, Xavier, Chen, Chu, Curado, Maria Paula, Curioni, Otávio A, Dal Maso, Luigino, Daudt, Alexander W, de Gois Filho, José F, D'Souza, Gypsyamber, Edefonti, Valeria, Fabianova, Eleonora, Fernandez, Leticia, Franceschi, Silvia, Gillison, Maura, Hayes, Richard B, Healy, Claire M, Herrero, Rolando, Holcatova, Ivana, Jayaprakash, Vijayvel, Kelsey, Karl, Kjaerheim, Kristina, Koifman, Sergio, La Vecchia, Carlo, Lagiou, Pagona, Lazarus, Philip, Levi, Fabio, Lissowska, Jolanta, Luce, Daniele, Macfarlane, Tatiana V, Mates, Dana, Matos, Elena, McClean, Michael, Menezes, Ana M, Menvielle, Gwenn, Merletti, Franco, Morgenstern, Hal, Moysich, Kirsten, Müller, Heiko, Muscat, Joshua, Olshan, Andrew F, Purdue, Mark P, Ramroth, Heribert, Richiardi, Lorenzo, Rudnai, Peter, Schantz, Stimson, Schwartz, Stephen M, Shangina, Oxana, Simonato, Lorenzo, Smith, Elaine, Stucker, Isabelle, Sturgis, Erich M, Szeszenia‐Dabrowska, Neonila, Talamini, Renato, Thomson, Peter, Vaughan, Thomas L, Wei, Qingyi, Winn, Deborah M, Wunsch‐Filho, Victor, Yu, Guo‐Pei, Zhang, Zuo‐Feng, Zheng, Tongzhang, Znaor, Ariana, Boffetta, Paolo, Chuang, Shu‐Chun, Ghodrat, Marianoosh, Lee, Yuan‐Chin Amy, Hashibe, Mia, and Brennan, Paul

Subjects
Behavioral and Social Science, Tobacco, Dental/Oral and Craniofacial Disease, Tobacco Smoke and Health, Cancer, Prevention, Substance Misuse, Basic Behavioral and Social Science, Reduced Inequalities, Good Health and Well Being, Alcohol Drinking, Case-Control Studies, Education, Female, Follow-Up Studies, Global Health, Head and Neck Neoplasms, Humans, Income, Male, Meta-Analysis as Topic, Middle Aged, Prognosis, Risk Factors, Smoking, Socioeconomic Factors, head and neck cancer, socioeconomic inequalities, epidemiology, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Low socioeconomic status has been reported to be associated with head and neck cancer risk. However, previous studies have been too small to examine the associations by cancer subsite, age, sex, global region and calendar time and to explain the association in terms of behavioral risk factors. Individual participant data of 23,964 cases with head and neck cancer and 31,954 controls from 31 studies in 27 countries pooled with random effects models. Overall, low education was associated with an increased risk of head and neck cancer (OR = 2.50; 95% CI = 2.02 - 3.09). Overall one-third of the increased risk was not explained by differences in the distribution of cigarette smoking and alcohol behaviors; and it remained elevated among never users of tobacco and nondrinkers (OR = 1.61; 95% CI = 1.13 - 2.31). More of the estimated education effect was not explained by cigarette smoking and alcohol behaviors: in women than in men, in older than younger groups, in the oropharynx than in other sites, in South/Central America than in Europe/North America and was strongest in countries with greater income inequality. Similar findings were observed for the estimated effect of low versus high household income. The lowest levels of income and educational attainment were associated with more than 2-fold increased risk of head and neck cancer, which is not entirely explained by differences in the distributions of behavioral risk factors for these cancers and which varies across cancer sites, sexes, countries and country income inequality levels.

Published
2015

35. Risk factors for head and neck cancer in young adults: a pooled analysis in the INHANCE consortium

Author

Toporcov, Tatiana Natasha, Znaor, Ariana, Zhang, Zuo-Feng, Yu, Guo-Pei, Winn, Deborah M, Wei, Qingyi, Vilensky, Marta, Vaughan, Thomas, Thomson, Peter, Talamini, Renato, Szeszenia-Dabrowska, Neonila, Sturgis, Erich M, Smith, Elaine, Shangina, Oxana, Schwartz, Stephen M, Schantz, Stimson, Rudnai, Peter, Richiardi, Lorenzo, Ramroth, Heribert, Purdue, Mark P, Olshan, Andrew F, Eluf-Neto, José, Muscat, Joshua, Moyses, Raquel Ajub, Morgenstern, Hal, Menezes, Ana, McClean, Michael, Matsuo, Keitaro, Mates, Dana, Macfarlane, Tatiana V, Lissowska, Jolanta, Levi, Fabio, Lazarus, Philip, La Vecchia, Carlo, Lagiou, Pagona, Koifman, Sergio, Kjaerheim, Kristina, Kelsey, Karl, Holcatova, Ivana, Herrero, Rolando, Healy, Claire, Hayes, Richard B, Franceschi, Silvia, Fernandez, Leticia, Fabianova, Eleonora, Daudt, Alexander W, Curioni, Otávio Alberto, Maso, Luigino Dal, Curado, Maria Paula, Conway, David I, Chen, Chu, Castellsague, Xavier, Canova, Cristina, Cadoni, Gabriella, Brennan, Paul, Boccia, Stefania, Antunes, José Leopoldo Ferreira, Ahrens, Wolfgang, Agudo, Antonio, Boffetta, Paolo, Hashibe, Mia, Lee, Yuan-Chin Amy, and Filho, Victor Wünsch

Subjects
Prevention, Cancer, Clinical Research, Tobacco, Tobacco Smoke and Health, Dental/Oral and Craniofacial Disease, Rare Diseases, Digestive Diseases, Aging, Good Health and Well Being, Adult, Age Factors, Alcohol Drinking, Case-Control Studies, Female, Genetic Predisposition to Disease, Head and Neck Neoplasms, Humans, Incidence, Male, Middle Aged, Odds Ratio, Registries, Risk Factors, Sex Factors, Smoking, Head and neck neoplasms, adult, smoking, alcohol drinking, diet, Statistics, Public Health and Health Services, Epidemiology
Abstract

BackgroundIncreasing incidence of head and neck cancer (HNC) in young adults has been reported. We aimed to compare the role of major risk factors and family history of cancer in HNC in young adults and older patients.MethodsWe pooled data from 25 case-control studies and conducted separate analyses for adults ≤ 45 years old ('young adults', 2010 cases and 4042 controls) and >45 years old ('older adults', 17700 cases and 22 704 controls). Using logistic regression with studies treated as random effects, we estimated adjusted odds ratios (ORs) and 95% confidence intervals (CIs).ResultsThe young group of cases had a higher proportion of oral tongue cancer (16.0% in women; 11.0% in men) and unspecified oral cavity / oropharynx cancer (16.2%; 11.1%) and a lower proportion of larynx cancer (12.1%; 16.6%) than older adult cases. The proportions of never smokers or never drinkers among female cases were higher than among male cases in both age groups. Positive associations with HNC and duration or pack-years of smoking and drinking were similar across age groups. However, the attributable fractions (AFs) for smoking and drinking were lower in young when compared with older adults (AFs for smoking in young women, older women, young men and older men, respectively, = 19.9% (95% CI=9.8%, 27.9%), 48.9% (46.6%, 50.8%), 46.2% (38.5%, 52.5%), 64.3% (62.2%, 66.4%); AFs for drinking=5.3% (-11.2%, 18.0%), 20.0% (14.5%, 25.0%), 21.5% (5.0%, 34.9%) and 50.4% (46.1%, 54.3%). A family history of early-onset cancer was associated with HNC risk in the young [OR=2.27 (95% CI=1.26, 4.10)], but not in the older adults [OR=1.10 (0.91, 1.31)]. The attributable fraction for family history of early-onset cancer was 23.2% (8.60% to 31.4%) in young compared with 2.20% (-2.41%, 5.80%) in older adults.ConclusionsDifferences in HNC aetiology according to age group may exist. The lower AF of cigarette smoking and alcohol drinking in young adults may be due to the reduced length of exposure due to the lower age. Other characteristics, such as those that are inherited, may play a more important role in HNC in young adults compared with older adults.

Published
2015

36. Association Between Intake of Red and Processed Meat and Survival in Patients With Colorectal Cancer in a Pooled Analysis

Author

Carr, Prudence R., Banbury, Barbara L., Berndt, Sonja I., Campbell, Peter T., Chang-Claude, Jenny, Hayes, Richard B., Howard, Barbara V., Jansen, Lina, Jacobs, Eric J., Lane, Dorothy S., Nishihara, Reiko, Ogino, Shuji, Phipps, Amanda I., Slattery, Martha L., Stefanick, Marcia L., Wallace, Robert, Walter, Viola, White, Emily, Wu, Kana, Peters, Ulrike, Chan, Andrew T., Newcomb, Polly A., Brenner, Hermann, and Hoffmeister, Michael

Published
2019
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38. Adult height and head and neck cancer: a pooled analysis within the INHANCE Consortium

Author

Leoncini, Emanuele, Ricciardi, Walter, Cadoni, Gabriella, Arzani, Dario, Petrelli, Livia, Paludetti, Gaetano, Brennan, Paul, Luce, Daniele, Stucker, Isabelle, Matsuo, Keitaro, Talamini, Renato, La Vecchia, Carlo, Olshan, Andrew F, Winn, Deborah M, Herrero, Rolando, Franceschi, Silvia, Castellsague, Xavier, Muscat, Joshua, Morgenstern, Hal, Zhang, Zuo-Feng, Levi, Fabio, Dal Maso, Luigino, Kelsey, Karl, McClean, Michael, Vaughan, Thomas L, Lazarus, Philip, Purdue, Mark P, Hayes, Richard B, Chen, Chu, Schwartz, Stephen M, Shangina, Oxana, Koifman, Sergio, Ahrens, Wolfgang, Matos, Elena, Lagiou, Pagona, Lissowska, Jolanta, Szeszenia-Dabrowska, Neonila, Fernandez, Leticia, Menezes, Ana, Agudo, Antonio, Daudt, Alexander W, Richiardi, Lorenzo, Kjaerheim, Kristina, Mates, Dana, Betka, Jaroslav, Yu, Guo-Pei, Schantz, Stimson, Simonato, Lorenzo, Brenner, Hermann, Conway, David I, Macfarlane, Tatiana V, Thomson, Peter, Fabianova, Eleonora, Znaor, Ariana, Rudnai, Peter, Healy, Claire, Boffetta, Paolo, Chuang, Shu-Chun, Lee, Yuan-Chin Amy, Hashibe, Mia, and Boccia, Stefania

Subjects
Tobacco Smoke and Health, Clinical Research, Prevention, Tobacco, Cancer, Rare Diseases, Dental/Oral and Craniofacial Disease, Good Health and Well Being, Adult, Aged, Alcohol Drinking, Body Height, Case-Control Studies, Educational Status, Female, Head and Neck Neoplasms, Humans, Incidence, Interviews as Topic, Logistic Models, Male, Middle Aged, Odds Ratio, Overweight, Risk Factors, Smoking, Height, Consortium, Head and neck neoplasms, Public Health and Health Services, Epidemiology
Abstract

Several epidemiological studies have shown a positive association between adult height and cancer incidence. The only study conducted among women on mouth and pharynx cancer risk, however, reported an inverse association. This study aims to investigate the association between height and the risk of head and neck cancer (HNC) within a large international consortium of HNC. We analyzed pooled individual-level data from 24 case-control studies participating in the International Head and Neck Cancer Epidemiology Consortium. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated separately for men and women for associations between height and HNC risk. Educational level, tobacco smoking, and alcohol consumption were included in all regression models. Stratified analyses by HNC subsites were performed. This project included 17,666 cases and 28,198 controls. We found an inverse association between height and HNC (adjusted OR per 10 cm height = 0.91, 95% CI 0.86-0.95 for men; adjusted OR = 0.86, 95% CI 0.79-0.93 for women). In men, the estimated OR did vary by educational level, smoking status, geographic area, and control source. No differences by subsites were detected. Adult height is inversely associated with HNC risk. As height can be considered a marker of childhood illness and low energy intake, the inverse association is consistent with prior studies showing that HNC occur more frequently among deprived individuals. Further studies designed to elucidate the mechanism of such association would be warranted.

Published
2014

39. 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

40. Determining Risk of Colorectal Cancer and Starting Age of Screening Based on Lifestyle, Environmental, and Genetic Factors

Author

Jeon, Jihyoun, Du, Mengmeng, Schoen, Robert E., Hoffmeister, Michael, Newcomb, Polly A., Berndt, Sonja I., Caan, Bette, Campbell, Peter T., Chan, Andrew T., Chang-Claude, Jenny, Giles, Graham G., Gong, Jian, Harrison, Tabitha A., Huyghe, Jeroen R., Jacobs, Eric J., Li, Li, Lin, Yi, Le Marchand, Loïc, Potter, John D., Qu, Conghui, Bien, Stephanie A., Zubair, Niha, Macinnis, Robert J., Buchanan, Daniel D., Hopper, John L., Cao, Yin, Nishihara, Reiko, Rennert, Gad, Slattery, Martha L., Thomas, Duncan C., Woods, Michael O., Prentice, Ross L., Gruber, Stephen B., Zheng, Yingye, Brenner, Hermann, Hayes, Richard B., White, Emily, Peters, Ulrike, and Hsu, Li

Published
2018
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41. Identification of Genetic Susceptibility Loci for Colorectal Tumors in a Genome-Wide Meta-analysis

Author

Peters, Ulrike, Jiao, Shuo, Schumacher, Fredrick R, Hutter, Carolyn M, Aragaki, Aaron K, Baron, John A, Berndt, Sonja I, Bézieau, Stéphane, Brenner, Hermann, Butterbach, Katja, Caan, Bette J, Campbell, Peter T, Carlson, Christopher S, Casey, Graham, Chan, Andrew T, Chang–Claude, Jenny, Chanock, Stephen J, Chen, Lin S, Coetzee, Gerhard A, Coetzee, Simon G, Conti, David V, Curtis, Keith R, Duggan, David, Edwards, Todd, Fuchs, Charles S, Gallinger, Steven, Giovannucci, Edward L, Gogarten, Stephanie M, Gruber, Stephen B, Haile, Robert W, Harrison, Tabitha A, Hayes, Richard B, Henderson, Brian E, Hoffmeister, Michael, Hopper, John L, Hudson, Thomas J, Hunter, David J, Jackson, Rebecca D, Jee, Sun Ha, Jenkins, Mark A, Jia, Wei–Hua, Kolonel, Laurence N, Kooperberg, Charles, Küry, Sébastien, LaCroix, Andrea Z, Laurie, Cathy C, Laurie, Cecelia A, Le Marchand, Loic, Lemire, Mathieu, Levine, David, Lindor, Noralane M, Liu, Yan, Ma, Jing, Makar, Karen W, Matsuo, Keitaro, Newcomb, Polly A, Potter, John D, Prentice, Ross L, Qu, Conghui, Rohan, Thomas, Rosse, Stephanie A, Schoen, Robert E, Seminara, Daniela, Shrubsole, Martha, Shu, Xiao–Ou, Slattery, Martha L, Taverna, Darin, Thibodeau, Stephen N, Ulrich, Cornelia M, White, Emily, Xiang, Yongbing, Zanke, Brent W, Zeng, Yi–Xin, Zhang, Ben, Zheng, Wei, Hsu, Li, and Registry, Genetics and Epidemiology of Colorectal Cancer Consortium Colon Cancer Family

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Nutrition and Dietetics, Digestive Diseases, Prevention, Genetics, Cancer, Colo-Rectal Cancer, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Age Distribution, Aged, Aged, 80 and over, Colorectal Neoplasms, Cyclin D2, DNA-Binding Proteins, Female, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Incidence, Laminin, Male, Middle Aged, Polymorphism, Single Nucleotide, Prognosis, Risk Assessment, Sex Distribution, T-Box Domain Proteins, Colon Cancer Family Registry and the Genetics and Epidemiology of Colorectal Cancer Consortium, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology, Clinical sciences, Nutrition and dietetics
Abstract

Background & aimsHeritable factors contribute to the development of colorectal cancer. Identifying the genetic loci associated with colorectal tumor formation could elucidate the mechanisms of pathogenesis.MethodsWe conducted a genome-wide association study that included 14 studies, 12,696 cases of colorectal tumors (11,870 cancer, 826 adenoma), and 15,113 controls of European descent. The 10 most statistically significant, previously unreported findings were followed up in 6 studies; these included 3056 colorectal tumor cases (2098 cancer, 958 adenoma) and 6658 controls of European and Asian descent.ResultsBased on the combined analysis, we identified a locus that reached the conventional genome-wide significance level at less than 5.0 × 10(-8): an intergenic region on chromosome 2q32.3, close to nucleic acid binding protein 1 (most significant single nucleotide polymorphism: rs11903757; odds ratio [OR], 1.15 per risk allele; P = 3.7 × 10(-8)). We also found evidence for 3 additional loci with P values less than 5.0 × 10(-7): a locus within the laminin gamma 1 gene on chromosome 1q25.3 (rs10911251; OR, 1.10 per risk allele; P = 9.5 × 10(-8)), a locus within the cyclin D2 gene on chromosome 12p13.32 (rs3217810 per risk allele; OR, 0.84; P = 5.9 × 10(-8)), and a locus in the T-box 3 gene on chromosome 12q24.21 (rs59336; OR, 0.91 per risk allele; P = 3.7 × 10(-7)).ConclusionsIn a large genome-wide association study, we associated polymorphisms close to nucleic acid binding protein 1 (which encodes a DNA-binding protein involved in DNA repair) with colorectal tumor risk. We also provided evidence for an association between colorectal tumor risk and polymorphisms in laminin gamma 1 (this is the second gene in the laminin family to be associated with colorectal cancers), cyclin D2 (which encodes for cyclin D2), and T-box 3 (which encodes a T-box transcription factor and is a target of Wnt signaling to β-catenin). The roles of these genes and their products in cancer pathogenesis warrant further investigation.

Published
2013

42. Discovery of common and rare genetic risk variants for colorectal cancer

Author

Huyghe, Jeroen R., Bien, Stephanie A., Harrison, Tabitha A., Kang, Hyun Min, Chen, Sai, Schmit, Stephanie L., Conti, David V., Qu, Conghui, Jeon, Jihyoun, Edlund, Christopher K., Greenside, Peyton, Wainberg, Michael, Schumacher, Fredrick R., Smith, Joshua D., Levine, David M., Nelson, Sarah C., Sinnott-Armstrong, Nasa A., Albanes, Demetrius, Alonso, M. Henar, Anderson, Kristin, Arnau-Collell, Coral, Arndt, Volker, Bamia, Christina, Banbury, Barbara L., Baron, John A., Berndt, Sonja I., Bézieau, Stéphane, Bishop, D. Timothy, Boehm, Juergen, Boeing, Heiner, Brenner, Hermann, Brezina, Stefanie, Buch, Stephan, Buchanan, Daniel D., Burnett-Hartman, Andrea, Butterbach, Katja, Caan, Bette J., Campbell, Peter T., Carlson, Christopher S., Castellví-Bel, Sergi, Chan, Andrew T., Chang-Claude, Jenny, Chanock, Stephen J., Chirlaque, Maria-Dolores, Cho, Sang Hee, Connolly, Charles M., Cross, Amanda J., Cuk, Katarina, Curtis, Keith R., de la Chapelle, Albert, Doheny, Kimberly F., Duggan, David, Easton, Douglas F., Elias, Sjoerd G., Elliott, Faye, English, Dallas R., Feskens, Edith J. M., Figueiredo, Jane C., Fischer, Rocky, FitzGerald, Liesel M., Forman, David, Gala, Manish, Gallinger, Steven, Gauderman, W. James, Giles, Graham G., Gillanders, Elizabeth, Gong, Jian, Goodman, Phyllis J., Grady, William M., Grove, John S., Gsur, Andrea, Gunter, Marc J., Haile, Robert W., Hampe, Jochen, Hampel, Heather, Harlid, Sophia, Hayes, Richard B., Hofer, Philipp, Hoffmeister, Michael, Hopper, John L., Hsu, Wan-Ling, Huang, Wen-Yi, Hudson, Thomas J., Hunter, David J., Ibañez-Sanz, Gemma, Idos, Gregory E., Ingersoll, Roxann, Jackson, Rebecca D., Jacobs, Eric J., Jenkins, Mark A., Joshi, Amit D., Joshu, Corinne E., Keku, Temitope O., Key, Timothy J., Kim, Hyeong Rok, Kobayashi, Emiko, Kolonel, Laurence N., Kooperberg, Charles, Kühn, Tilman, Küry, Sébastien, Kweon, Sun-Seog, Larsson, Susanna C., Laurie, Cecelia A., Le Marchand, Loic, Leal, Suzanne M., Lee, Soo Chin, Lejbkowicz, Flavio, Lemire, Mathieu, Li, Christopher I., Li, Li, Lieb, Wolfgang, Lin, Yi, Lindblom, Annika, Lindor, Noralane M., Ling, Hua, Louie, Tin L., Männistö, Satu, Markowitz, Sanford D., Martín, Vicente, Masala, Giovanna, McNeil, Caroline E., Melas, Marilena, Milne, Roger L., Moreno, Lorena, Murphy, Neil, Myte, Robin, Naccarati, Alessio, Newcomb, Polly A., Offit, Kenneth, Ogino, Shuji, Onland-Moret, N. Charlotte, Pardini, Barbara, Parfrey, Patrick S., Pearlman, Rachel, Perduca, Vittorio, Pharoah, Paul D. P., Pinchev, Mila, Platz, Elizabeth A., Prentice, Ross L., Pugh, Elizabeth, Raskin, Leon, Rennert, Gad, Rennert, Hedy S., Riboli, Elio, Rodríguez-Barranco, Miguel, Romm, Jane, Sakoda, Lori C., Schafmayer, Clemens, Schoen, Robert E., Seminara, Daniela, Shah, Mitul, Shelford, Tameka, Shin, Min-Ho, Shulman, Katerina, Sieri, Sabina, Slattery, Martha L., Southey, Melissa C., Stadler, Zsofia K., Stegmaier, Christa, Su, Yu-Ru, Tangen, Catherine M., Thibodeau, Stephen N., Thomas, Duncan C., Thomas, Sushma S., Toland, Amanda E., Trichopoulou, Antonia, Ulrich, Cornelia M., Van Den Berg, David J., van Duijnhoven, Franzel J. B., Van Guelpen, Bethany, van Kranen, Henk, Vijai, Joseph, Visvanathan, Kala, Vodicka, Pavel, Vodickova, Ludmila, Vymetalkova, Veronika, Weigl, Korbinian, Weinstein, Stephanie J., White, Emily, Win, Aung Ko, Wolf, C. Roland, Wolk, Alicja, Woods, Michael O., Wu, Anna H., Zaidi, Syed H., Zanke, Brent W., Zhang, Qing, Zheng, Wei, Scacheri, Peter C., Potter, John D., Bassik, Michael C., Kundaje, Anshul, Casey, Graham, Moreno, Victor, Abecasis, Goncalo R., Nickerson, Deborah A., Gruber, Stephen B., Hsu, Li, and Peters, Ulrike

Published
2019
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43. Characterization of Gene–Environment Interactions for Colorectal Cancer Susceptibility Loci

Author

Hutter, Carolyn M, Chang-Claude, Jenny, Slattery, Martha L, Pflugeisen, Bethann M, Lin, Yi, Duggan, David, Nan, Hongmei, Lemire, Mathieu, Rangrej, Jagadish, Figueiredo, Jane C, Jiao, Shuo, Harrison, Tabitha A, Liu, Yan, Chen, Lin S, Stelling, Deanna L, Warnick, Greg S, Hoffmeister, Michael, Küry, Sébastien, Fuchs, Charles S, Giovannucci, Edward, Hazra, Aditi, Kraft, Peter, Hunter, David J, Gallinger, Steven, Zanke, Brent W, Brenner, Hermann, Frank, Bernd, Ma, Jing, Ulrich, Cornelia M, White, Emily, Newcomb, Polly A, Kooperberg, Charles, LaCroix, Andrea Z, Prentice, Ross L, Jackson, Rebecca D, Schoen, Robert E, Chanock, Stephen J, Berndt, Sonja I, Hayes, Richard B, Caan, Bette J, Potter, John D, Hsu, Li, Bézieau, Stéphane, Chan, Andrew T, Hudson, Thomas J, and Peters, Ulrike

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Digestive Diseases, Nutrition, Prevention, Cancer, Colo-Rectal Cancer, Human Genome, Colorectal Neoplasms, Diet, Gene-Environment Interaction, Genetic Predisposition to Disease, Genotype, Humans, Polymorphism, Single Nucleotide, Oncology and Carcinogenesis, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Genome-wide association studies (GWAS) have identified more than a dozen loci associated with colorectal cancer (CRC) risk. Here, we examined potential effect-modification between single-nucleotide polymorphisms (SNP) at 10 of these loci and probable or established environmental risk factors for CRC in 7,016 CRC cases and 9,723 controls from nine cohort and case-control studies. We used meta-analysis of an efficient empirical-Bayes estimator to detect potential multiplicative interactions between each of the SNPs [rs16892766 at 8q23.3 (EIF3H/UTP23), rs6983267 at 8q24 (MYC), rs10795668 at 10p14 (FLJ3802842), rs3802842 at 11q23 (LOC120376), rs4444235 at 14q22.2 (BMP4), rs4779584 at 15q13 (GREM1), rs9929218 at 16q22.1 (CDH1), rs4939827 at 18q21 (SMAD7), rs10411210 at 19q13.1 (RHPN2), and rs961253 at 20p12.3 (BMP2)] and select major CRC risk factors (sex, body mass index, height, smoking status, aspirin/nonsteroidal anti-inflammatory drug use, alcohol use, and dietary intake of calcium, folate, red meat, processed meat, vegetables, fruit, and fiber). The strongest statistical evidence for a gene-environment interaction across studies was for vegetable consumption and rs16892766, located on chromosome 8q23.3, near the EIF3H and UTP23 genes (nominal P(interaction) = 1.3 × 10(-4); adjusted P = 0.02). The magnitude of the main effect of the SNP increased with increasing levels of vegetable consumption. No other interactions were statistically significant after adjusting for multiple comparisons. Overall, the association of most CRC susceptibility loci identified in initial GWAS seems to be invariant to the other risk factors considered; however, our results suggest potential modification of the rs16892766 effect by vegetable consumption.

Published
2012

44. Meta-analysis of new genome-wide association studies of colorectal cancer risk

Author

Peters, Ulrike, Hutter, Carolyn M, Hsu, Li, Schumacher, Fredrick R, Conti, David V, Carlson, Christopher S, Edlund, Christopher K, Haile, Robert W, Gallinger, Steven, Zanke, Brent W, Lemire, Mathieu, Rangrej, Jagadish, Vijayaraghavan, Raakhee, Chan, Andrew T, Hazra, Aditi, Hunter, David J, Ma, Jing, Fuchs, Charles S, Giovannucci, Edward L, Kraft, Peter, Liu, Yan, Chen, Lin, Jiao, Shuo, Makar, Karen W, Taverna, Darin, Gruber, Stephen B, Rennert, Gad, Moreno, Victor, Ulrich, Cornelia M, Woods, Michael O, Green, Roger C, Parfrey, Patrick S, Prentice, Ross L, Kooperberg, Charles, Jackson, Rebecca D, LaCroix, Andrea Z, Caan, Bette J, Hayes, Richard B, Berndt, Sonja I, Chanock, Stephen J, Schoen, Robert E, Chang-Claude, Jenny, Hoffmeister, Michael, Brenner, Hermann, Frank, Bernd, Bézieau, Stéphane, Küry, Sébastien, Slattery, Martha L, Hopper, John L, Jenkins, Mark A, Le Marchand, Loic, Lindor, Noralane M, Newcomb, Polly A, Seminara, Daniela, Hudson, Thomas J, Duggan, David J, Potter, John D, and Casey, Graham

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Genetics, Colo-Rectal Cancer, Aging, Human Genome, Cancer, Prevention, Digestive Diseases, 2.1 Biological and endogenous factors, Aetiology, Colorectal Neoplasms, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Odds Ratio, Polymorphism, Single Nucleotide, Risk Factors, Complementary and Alternative Medicine, Paediatrics and Reproductive Medicine, Genetics & Heredity, Reproductive medicine
Abstract

Colorectal cancer is the second leading cause of cancer death in developed countries. Genome-wide association studies (GWAS) have successfully identified novel susceptibility loci for colorectal cancer. To follow up on these findings, and try to identify novel colorectal cancer susceptibility loci, we present results for GWAS of colorectal cancer (2,906 cases, 3,416 controls) that have not previously published main associations. Specifically, we calculated odds ratios and 95% confidence intervals using log-additive models for each study. In order to improve our power to detect novel colorectal cancer susceptibility loci, we performed a meta-analysis combining the results across studies. We selected the most statistically significant single nucleotide polymorphisms (SNPs) for replication using ten independent studies (8,161 cases and 9,101 controls). We again used a meta-analysis to summarize results for the replication studies alone, and for a combined analysis of GWAS and replication studies. We measured ten SNPs previously identified in colorectal cancer susceptibility loci and found eight to be associated with colorectal cancer (p value range 0.02 to 1.8 × 10(-8)). When we excluded studies that have previously published on these SNPs, five SNPs remained significant at p

Published
2012

45. Diet and the risk of head and neck cancer: a pooled analysis in the INHANCE consortium

Author

Chuang, Shu-Chun, Jenab, Mazda, Heck, Julia E, Bosetti, Cristina, Talamini, Renato, Matsuo, Keitaro, Castellsague, Xavier, Franceschi, Silvia, Herrero, Rolando, Winn, Deborah M, Vecchia, Carlo La, Morgenstern, Hal, Zhang, Zuo-Feng, Levi, Fabio, Maso, Luigino Dal, Kelsey, Karl, McClean, Michael D, Vaughan, Thomas, Lazarus, Philip, Muscat, Joshua, Ramroth, Heribert, Chen, Chu, Schwartz, Stephen M, Eluf-Neto, Jose, Hayes, Richard B, Purdue, Mark, Boccia, Stefania, Cadoni, Gabriella, Zaridze, David, Koifman, Sergio, Curado, Maria Paula, Ahrens, Wolfgang, Benhamou, Simone, Matos, Elena, Lagiou, Pagona, Szeszenia-Dabrowska, Neonilla, Olshan, Andrew F, Fernandez, Leticia, Menezes, Ana, Agudo, Antonio, Daudt, Alexander W, Merletti, Franco, Macfarlane, Gary J, Kjaerheim, Kristina, Mates, Dana, Holcatova, Ivana, Schantz, Stimson, Yu, Guo-Pei, Simonato, Lorenzo, Brenner, Hermann, Mueller, Heiko, Conway, David I, Thomson, Peter, Fabianova, Eleonora, Znaor, Ariana, Rudnai, Peter, Healy, Claire M, Ferro, Gilles, Brennan, Paul, Boffetta, Paolo, and Hashibe, Mia

Subjects
Nutrition, Cancer, Prevention, Clinical Research, Dental/Oral and Craniofacial Disease, Adult, Aged, Case-Control Studies, Diet, Female, Head and Neck Neoplasms, Humans, Male, Middle Aged, Risk Factors, Head and neck cancer, Fruit and vegetable, Red meat, Processed meat, Oncology and Carcinogenesis, Public Health and Health Services, Epidemiology
Abstract

We investigated the association between diet and head and neck cancer (HNC) risk using data from the International Head and Neck Cancer Epidemiology (INHANCE) consortium. The INHANCE pooled data included 22 case-control studies with 14,520 cases and 22,737 controls. Center-specific quartiles among the controls were used for food groups, and frequencies per week were used for single food items. A dietary pattern score combining high fruit and vegetable intake and low red meat intake was created. Odds ratios (OR) and 95% confidence intervals (CI) for the dietary items on the risk of HNC were estimated with a two-stage random-effects logistic regression model. An inverse association was observed for higher-frequency intake of fruit (4th vs. 1st quartile OR = 0.52, 95% CI = 0.43-0.62, p (trend) < 0.01) and vegetables (OR = 0.66, 95% CI = 0.49-0.90, p (trend) = 0.01). Intake of red meat (OR = 1.40, 95% CI = 1.13-1.74, p (trend) = 0.13) and processed meat (OR = 1.37, 95% CI = 1.14-1.65, p (trend) < 0.01) was positively associated with HNC risk. Higher dietary pattern scores, reflecting high fruit/vegetable and low red meat intake, were associated with reduced HNC risk (per score increment OR = 0.90, 95% CI = 0.84-0.97).

Published
2012

46. Genome-wide association study of prostate cancer in men of African ancestry identifies a susceptibility locus at 17q21

Author

Haiman, Christopher A, Chen, Gary K, Blot, William J, Strom, Sara S, Berndt, Sonja I, Kittles, Rick A, Rybicki, Benjamin A, Isaacs, William B, Ingles, Sue A, Stanford, Janet L, Diver, W Ryan, Witte, John S, Hsing, Ann W, Nemesure, Barbara, Rebbeck, Timothy R, Cooney, Kathleen A, Xu, Jianfeng, Kibel, Adam S, Hu, Jennifer J, John, Esther M, Gueye, Serigne M, Watya, Stephen, Signorello, Lisa B, Hayes, Richard B, Wang, Zhaoming, Yeboah, Edward, Tettey, Yao, Cai, Qiuyin, Kolb, Suzanne, Ostrander, Elaine A, Zeigler-Johnson, Charnita, Yamamura, Yuko, Neslund-Dudas, Christine, Haslag-Minoff, Jennifer, Wu, William, Thomas, Venetta, Allen, Glenn O, Murphy, Adam, Chang, Bao-Li, Zheng, S Lilly, Leske, M Cristina, Wu, Suh-Yuh, Ray, Anna M, Hennis, Anselm JM, Thun, Michael J, Carpten, John, Casey, Graham, Carter, Erin N, Duarte, Edder R, Xia, Lucy Y, Sheng, Xin, Wan, Peggy, Pooler, Loreall C, Cheng, Iona, Monroe, Kristine R, Schumacher, Fredrick, Le Marchand, Loic, Kolonel, Laurence N, Chanock, Stephen J, Berg, David Van Den, Stram, Daniel O, and Henderson, Brian E

Subjects
Biological Sciences, Genetics, Human Genome, Aging, Urologic Diseases, Prevention, Prostate Cancer, Cancer, 2.1 Biological and endogenous factors, Aetiology, Black or African American, Chromosomes, Human, Pair 17, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Polymorphism, Single Nucleotide, Prostatic Neoplasms, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

In search of common risk alleles for prostate cancer that could contribute to high rates of the disease in men of African ancestry, we conducted a genome-wide association study, with 1,047,986 SNP markers examined in 3,425 African-Americans with prostate cancer (cases) and 3,290 African-American male controls. We followed up the most significant 17 new associations from stage 1 in 1,844 cases and 3,269 controls of African ancestry. We identified a new risk variant on chromosome 17q21 (rs7210100, odds ratio per allele = 1.51, P = 3.4 × 10(-13)). The frequency of the risk allele is ∼5% in men of African descent, whereas it is rare in other populations (

Published
2011

47. Sexual behaviours and the risk of head and neck cancers: a pooled analysis in the International Head and Neck Cancer Epidemiology (INHANCE) consortium

Author

Heck, Julia E, Berthiller, Julien, Vaccarella, Salvatore, Winn, Deborah M, Smith, Elaine M, Shan'gina, Oxana, Schwartz, Stephen M, Purdue, Mark P, Pilarska, Agnieszka, Eluf-Neto, Jose, Menezes, Ana, McClean, Michael D, Matos, Elena, Koifman, Sergio, Kelsey, Karl T, Herrero, Rolando, Hayes, Richard B, Franceschi, Silvia, Wünsch-Filho, Victor, Fernández, Leticia, Daudt, Alexander W, Curado, Maria Paula, Chen, Chu, Castellsagué, Xavier, Ferro, Gilles, Brennan, Paul, Boffetta, Paolo, and Hashibe, Mia

Subjects
Health Services and Systems, Health Sciences, Cancer, Dental/Oral and Craniofacial Disease, Sexually Transmitted Infections, Infectious Diseases, Adult, Age Factors, Aged, Case-Control Studies, Confounding Factors, Epidemiologic, Female, Head and Neck Neoplasms, Health Behavior, Humans, Male, Middle Aged, Odds Ratio, Papillomavirus Infections, Sexual Behavior, Socioeconomic Factors, Sexual practices, head and neck cancer, oropharyngeal neoplasms, homosexual, gay men, risk factors, pooled analyses, Statistics, Public Health and Health Services, Epidemiology, Public health
Abstract

BackgroundSexual contact may be the means by which head and neck cancer patients are exposed to human papillomavirus (HPV).MethodsWe undertook a pooled analysis of four population-based and four hospital-based case-control studies from the International Head and Neck Cancer Epidemiology (INHANCE) consortium, with participants from Argentina, Australia, Brazil, Canada, Cuba, India, Italy, Spain, Poland, Puerto Rico, Russia and the USA. The study included 5642 head and neck cancer cases and 6069 controls. We calculated odds ratios (ORs) of associations between cancer and specific sexual behaviours, including practice of oral sex, number of lifetime sexual partners and oral sex partners, age at sexual debut, a history of same-sex contact and a history of oral-anal contact. Findings were stratified by sex and disease subsite.ResultsCancer of the oropharynx was associated with having a history of six or more lifetime sexual partners [OR = 1.25, 95% confidence interval (CI) 1.01, 1.54] and four or more lifetime oral sex partners (OR = 2.25, 95% CI 1.42, 3.58). Cancer of the tonsil was associated with four or more lifetime oral sex partners (OR = 3.36, 95 % CI 1.32, 8.53), and, among men, with ever having oral sex (OR = 1.59, 95% CI 1.09, 2.33) and with an earlier age at sexual debut (OR = 2.36, 95% CI 1.37, 5.05). Cancer of the base of the tongue was associated with ever having oral sex among women (OR = 4.32, 95% CI 1.06, 17.6), having two sexual partners in comparison with only one (OR = 2.02, 95% CI 1.19, 3.46) and, among men, with a history of same-sex sexual contact (OR = 8.89, 95% CI 2.14, 36.8).ConclusionsSexual behaviours are associated with cancer risk at the head and neck cancer subsites that have previously been associated with HPV infection.

Published
2010

49. Evidence that humans metabolize benzene via two pathways.

Author

Rappaport, Stephen M, Kim, Sungkyoon, Lan, Qing, Vermeulen, Roel, Waidyanatha, Suramya, Zhang, Luoping, Li, Guilan, Yin, Songnian, Hayes, Richard B, Rothman, Nathaniel, and Smith, Martyn T

Subjects
Humans, Benzene, Air Pollutants, Signal Transduction, Models, Theoretical, Adolescent, Adult, Middle Aged, Female, Gas Chromatography-Mass Spectrometry, Young Adult, benzene, biomonitoring, cancer risk, cytochrome P450, metabolism, Models, Theoretical, Environmental Sciences, Medical and Health Sciences, Toxicology
Abstract

BackgroundRecent evidence has shown that humans metabolize benzene more efficiently at environmental air concentrations than at concentrations > 1 ppm. This led us to speculate that an unidentified metabolic pathway was mainly responsible for benzene metabolism at ambient levels.ObjectiveWe statistically tested whether human metabolism of benzene is better fitted by a kinetic model having two pathways rather than one.MethodsWe fit Michaelis-Menten-like models to levels of urinary benzene metabolites and the corresponding air concentrations for 263 nonsmoking Chinese females. Estimated benzene concentrations ranged from less than 0.001 ppm to 299 ppm, with 10th and 90th percentile values of 0.002 ppm and 8.97 ppm, respectively.ResultsUsing values of Akaike's information criterion obtained under the two models, we found strong statistical evidence favoring two metabolic pathways, with respective affinities (benzene air concentrations analogous to K(m) values) of 301 ppm for the low-affinity pathway (probably dominated by cytochrome P450 enzyme 2E1) and 0.594 ppm for the high-affinity pathway (unknown). The exposure-specific metabolite level predicted by our two-pathway model at nonsaturating concentrations was 184 muM/ppm of benzene, a value close to an independent estimate of 194 muM/ppm for a typical nonsmoking Chinese female. Our results indicate that a nonsmoking woman would metabolize about three times more benzene from the ambient environment under the two-pathway model (184 muM/ppm) than under the one-pathway model (68.6 muM/ppm). In fact, 73% of the ambient benzene dose would be metabolized via the unidentified high-affinity pathway.ConclusionBecause regulatory risk assessments have assumed nonsaturating metabolism of benzene in persons exposed to air concentrations well above 10 ppm, our findings suggest that the true leukemia risks could be substantially greater than currently thought at ambient levels of exposure-about 3-fold higher among nonsmoking females in the general population.

Published
2009

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