876 results on '"Purdue, Mark P."'
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2. Geographic variation of mutagenic exposures in kidney cancer genomes
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Senkin, Sergey, Moody, Sarah, Díaz-Gay, Marcos, Abedi-Ardekani, Behnoush, Cattiaux, Thomas, Ferreiro-Iglesias, Aida, Wang, Jingwei, Fitzgerald, Stephen, Kazachkova, Mariya, Vangara, Raviteja, Le, Anh Phuong, Bergstrom, Erik N., Khandekar, Azhar, Otlu, Burçak, Cheema, Saamin, Latimer, Calli, Thomas, Emily, Atkins, Joshua Ronald, Smith-Byrne, Karl, Cortez Cardoso Penha, Ricardo, Carreira, Christine, Chopard, Priscilia, Gaborieau, Valérie, Keski-Rahkonen, Pekka, Jones, David, Teague, Jon W., Ferlicot, Sophie, Asgari, Mojgan, Sangkhathat, Surasak, Attawettayanon, Worapat, Świątkowska, Beata, Jarmalaite, Sonata, Sabaliauskaite, Rasa, Shibata, Tatsuhiro, Fukagawa, Akihiko, Mates, Dana, Jinga, Viorel, Rascu, Stefan, Mijuskovic, Mirjana, Savic, Slavisa, Milosavljevic, Sasa, Bartlett, John M. S., Albert, Monique, Phouthavongsy, Larry, Ashton-Prolla, Patricia, Botton, Mariana R., Silva Neto, Brasil, Bezerra, Stephania Martins, Curado, Maria Paula, Zequi, Stênio de Cássio, Reis, Rui Manuel, Faria, Eliney Ferreira, de Menezes, Nei Soares, Ferrari, Renata Spagnoli, Banks, Rosamonde E., Vasudev, Naveen S., Zaridze, David, Mukeriya, Anush, Shangina, Oxana, Matveev, Vsevolod, Foretova, Lenka, Navratilova, Marie, Holcatova, Ivana, Hornakova, Anna, Janout, Vladimir, Purdue, Mark P., Rothman, Nathaniel, Chanock, Stephen J., Ueland, Per Magne, Johansson, Mattias, McKay, James, Scelo, Ghislaine, Chanudet, Estelle, Humphreys, Laura, de Carvalho, Ana Carolina, Perdomo, Sandra, Alexandrov, Ludmil B., Stratton, Michael R., and Brennan, Paul
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- 2024
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3. Multi-ancestry genome-wide association study of kidney cancer identifies 63 susceptibility regions
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Purdue, Mark P., Dutta, Diptavo, Machiela, Mitchell J., Gorman, Bryan R., Winter, Timothy, Okuhara, Dayne, Cleland, Sara, Ferreiro-Iglesias, Aida, Scheet, Paul, Liu, Aoxing, Wu, Chao, Antwi, Samuel O., Larkin, James, Zequi, Stênio C., Sun, Maxine, Hikino, Keiko, Hajiran, Ali, Lawson, Keith A., Cárcano, Flavio, Blanchet, Odile, Shuch, Brian, Nepple, Kenneth G., Margue, Gaëlle, Sundi, Debasish, Diver, W. Ryan, Folgueira, Maria A. A. K., van Bokhoven, Adrie, Neffa, Florencia, Brown, Kevin M., Hofmann, Jonathan N., Rhee, Jongeun, Yeager, Meredith, Cole, Nathan R., Hicks, Belynda D., Manning, Michelle R., Hutchinson, Amy A., Rothman, Nathaniel, Huang, Wen-Yi, Linehan, W. Marston, Lori, Adriana, Ferragu, Matthieu, Zidane-Marinnes, Merzouka, Serrano, Sérgio V., Magnabosco, Wesley J., Vilas, Ana, Decia, Ricardo, Carusso, Florencia, Graham, Laura S., Anderson, Kyra, Bilen, Mehmet A., Arciero, Cletus, Pellegrin, Isabelle, Ricard, Solène, Scelo, Ghislaine, Banks, Rosamonde E., Vasudev, Naveen S., Soomro, Naeem, Stewart, Grant D., Adeyoju, Adebanji, Bromage, Stephen, Hrouda, David, Gibbons, Norma, Patel, Poulam, Sullivan, Mark, Protheroe, Andrew, Nugent, Francesca I., Fournier, Michelle J., Zhang, Xiaoyu, Martin, Lisa J., Komisarenko, Maria, Eisen, Timothy, Cunningham, Sonia A., Connolly, Denise C., Uzzo, Robert G., Zaridze, David, Mukeria, Anush, Holcatova, Ivana, Hornakova, Anna, Foretova, Lenka, Janout, Vladimir, Mates, Dana, Jinga, Viorel, Rascu, Stefan, Mijuskovic, Mirjana, Savic, Slavisa, Milosavljevic, Sasa, Gaborieau, Valérie, Abedi-Ardekani, Behnoush, McKay, James, Johansson, Mattias, Phouthavongsy, Larry, Hayman, Lindsay, Li, Jason, Lungu, Ilinca, Bezerra, Stephania M., Souza, Aline G., Sares, Claudia T. G., Reis, Rodolfo B., Gallucci, Fabio P., Cordeiro, Mauricio D., Pomerantz, Mark, Lee, Gwo-Shu M., Freedman, Matthew L., Jeong, Anhyo, Greenberg, Samantha E., Sanchez, Alejandro, Thompson, R. Houston, Sharma, Vidit, Thiel, David D., Ball, Colleen T., Abreu, Diego, Lam, Elaine T., Nahas, William C., Master, Viraj A., Patel, Alpa V., Bernhard, Jean-Christophe, Freedman, Neal D., Bigot, Pierre, Reis, Rui M., Colli, Leandro M., Finelli, Antonio, Manley, Brandon J., Terao, Chikashi, Choueiri, Toni K., Carraro, Dirce M., Houlston, Richard, Eckel-Passow, Jeanette E., Abbosh, Philip H., Ganna, Andrea, Brennan, Paul, Gu, Jian, and Chanock, Stephen J.
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- 2024
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4. Genome-wide analyses characterize shared heritability among cancers and identify novel cancer susceptibility regions
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Lindström, Sara, Wang, Lu, Feng, Helian, Majumdar, Arunabha, Huo, Sijia, Macdonald, James, Harrison, Tabitha, Turman, Constance, Chen, Hongjie, Mancuso, Nicholas, Bammler, Theo, Consortium, Breast Cancer Association, Gallinger, Steve, Gruber, Stephen B, Gunter, Marc J, Le Marchand, Loic, Moreno, Victor, Offit, Kenneth, Study, Genetics And Epidemiology Of Colorectal Cancer Consortium Colorectal Transdisciplinary Study Colon Cancer Family Registry, De Vivo, Immaculata, O’Mara, Tracy A, Spurdle, Amanda B, Tomlinson, Ian, Consortium, Endometrial Cancer Association, Fitzgerald, Rebecca, Gharahkhani, Puya, Gockel, Ines, Jankowski, Janusz, Macgregor, Stuart, Schumacher, Johannes, Barnholtz-Sloan, Jill, Bondy, Melissa L, Houlston, Richard S, Jenkins, Robert B, Melin, Beatrice, Wrensch, Margaret, Brennan, Paul, Christiani, David C, Johansson, Mattias, Mckay, James, Aldrich, Melinda C, Amos, Christopher I, Landi, Maria Teresa, Tardon, Adonina, Consortium, International Lung Cancer, Bishop, D Timothy, Demenais, Florence, Goldstein, Alisa M, Iles, Mark M, Kanetsky, Peter A, Law, Matthew H, Consortium, Ovarian Cancer Association, Amundadottir, Laufey T, Stolzenberg-Solomon, Rachael, Wolpin, Brian M, Consortium, Pancreatic Cancer Cohort, Klein, Alison, Petersen, Gloria, Risch, Harvey, Consortium, The PRACTICAL Consortium Pancreatic Cancer Case-Control, Chanock, Stephen J, Purdue, Mark P, Scelo, Ghislaine, Pharoah, Paul, Kar, Siddhartha, Hung, Rayjean J, Pasaniuc, Bogdan, and Kraft, Peter
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Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Human Genome ,Genetics ,Digestive Diseases ,Prevention ,Clinical Research ,Urologic Diseases ,Cancer ,Rare Diseases ,Aetiology ,2.1 Biological and endogenous factors ,Male ,Humans ,Genome-Wide Association Study ,Genetic Predisposition to Disease ,Neoplasms ,Risk Factors ,Transcriptome ,Polymorphism ,Single Nucleotide ,Breast Cancer Association Consortium ,Colorectal Transdisciplinary Study (CORECT) ,Colon Cancer Family Registry Study (CCFR) ,Genetics And Epidemiology Of Colorectal Cancer Consortium ,Endometrial Cancer Association Consortium ,International Lung Cancer Consortium ,Ovarian Cancer Association Consortium ,Pancreatic Cancer Cohort Consortium ,Pancreatic Cancer Case-Control Consortium (Panc4) ,The PRACTICAL Consortium ,Oncology & Carcinogenesis ,Oncology and carcinogenesis - Abstract
BackgroundThe shared inherited genetic contribution to risk of different cancers is not fully known. In this study, we leverage results from 12 cancer genome-wide association studies (GWAS) to quantify pairwise genome-wide genetic correlations across cancers and identify novel cancer susceptibility loci.MethodsWe collected GWAS summary statistics for 12 solid cancers based on 376 759 participants with cancer and 532 864 participants without cancer of European ancestry. The included cancer types were breast, colorectal, endometrial, esophageal, glioma, head and neck, lung, melanoma, ovarian, pancreatic, prostate, and renal cancers. We conducted cross-cancer GWAS and transcriptome-wide association studies to discover novel cancer susceptibility loci. Finally, we assessed the extent of variant-specific pleiotropy among cancers at known and newly identified cancer susceptibility loci.ResultsWe observed widespread but modest genome-wide genetic correlations across cancers. In cross-cancer GWAS and transcriptome-wide association studies, we identified 15 novel cancer susceptibility loci. Additionally, we identified multiple variants at 77 distinct loci with strong evidence of being associated with at least 2 cancer types by testing for pleiotropy at known cancer susceptibility loci.ConclusionsOverall, these results suggest that some genetic risk variants are shared among cancers, though much of cancer heritability is cancer-specific and thus tissue-specific. The increase in statistical power associated with larger sample sizes in cross-disease analysis allows for the identification of novel susceptibility regions. Future studies incorporating data on multiple cancer types are likely to identify additional regions associated with the risk of multiple cancer types.
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- 2023
5. Circulating immune markers and risks of non-Hodgkin lymphoma subtypes: A pooled analysis.
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Rhee, Jongeun, Birmann, Brenda, De Roos, Anneclaire, Epstein, Mara, Martinez-Maza, Otoniel, Breen, Elizabeth, Magpantay, Larry, Levin, Lynn, Visvanathan, Kala, Hosgood, H, Rohan, Thomas, Smoller, Sylvia, Bassig, Bryan, Qi, Lihong, Shu, Xiao-Ou, Koh, Woon-Puay, Zheng, Wei, Yuan, Jian-Min, Weinstein, Stephanie, Albanes, Demetrius, Lan, Qing, Rothman, Nathaniel, and Purdue, Mark
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CXCL13 ,immune markers ,non-Hodgkin lymphoma ,sCD27 ,sCD30 ,Adult ,Humans ,Leukemia ,Lymphocytic ,Chronic ,B-Cell ,Lymphoma ,Non-Hodgkin ,Lymphoma ,Follicular ,Biomarkers ,Lymphoma ,Large B-Cell ,Diffuse ,Case-Control Studies ,Lymphoma ,Mantle-Cell - Abstract
Although prediagnostic circulating concentrations of the immune activation markers soluble CD27 (sCD27), sCD30 and chemokine ligand-13 (CXCL13) have been associated with non-Hodgkin lymphoma (NHL) risk, studies have been limited by sample size in associations with NHL subtypes. We pooled data from eight nested case-control studies to investigate subtype-specific relationships for these analytes. Using polytomous regression, we calculated odds ratios (ORs) with 95% confidence intervals (CIs) relating study-specific analyte tertiles to selected subtypes vs controls (n = 3310): chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL; n = 623), diffuse large B cell lymphoma (DLBCL; n = 621), follicular lymphoma (FL; n = 398), marginal zone lymphoma (MZL; n = 138), mantle cell lymphoma (MCL; n = 82) and T cell lymphoma (TCL; n = 92). We observed associations with DLBCL for elevated sCD27 [OR for third vs first tertile (ORT3 ) = 2.2, 95% CI = 1.6-3.1], sCD30 (ORT3 = 2.0, 95% CI = 1.6-2.5) and CXCL13 (ORT3 = 2.3, 95% CI = 1.8-3.0). We also observed associations with sCD27 for CLL/SLL (ORT3 = 3.3, 95% CI = 2.4-4.6), MZL (ORT3 = 7.7, 95% CI = 3.0-20.1) and TCL (ORT3 = 3.4, 95% CI = 1.5-7.7), and between sCD30 and FL (ORT3 = 2.7, 95% CI = 2.0-3.5). In analyses stratified by time from phlebotomy to case diagnosis, the sCD27-TCL and all three DLBCL associations were equivalent across both follow-up periods (
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- 2023
6. Observational and genetic associations between cardiorespiratory fitness and cancer: a UK Biobank and international consortia study
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Watts, Eleanor L., Gonzales, Tomas I., Strain, Tessa, Saint-Maurice, Pedro F., Bishop, D. Timothy, Chanock, Stephen J., Johansson, Mattias, Keku, Temitope O., Le Marchand, Loic, Moreno, Victor, Newcomb, Polly A., Newton, Christina C., Pai, Rish K., Purdue, Mark P., Ulrich, Cornelia M., Smith-Byrne, Karl, Van Guelpen, Bethany, Day, Felix R., Wijndaele, Katrien, Wareham, Nicholas J., Matthews, Charles E., Moore, Steven C., and Brage, Soren
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- 2024
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7. Serum concentrations of per- and polyfluorinated substances and risk of B-cell non-Hodgkin lymphoma
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Rhee, Jongeun, Koponen, Jani, Sampson, Joshua N., Keil, Alexander P., Ward, Mary H., Hofmann, Jonathan N., Huang, Wen-Yi, Silverman, Debra T., Rantakokko, Panu, and Purdue, Mark P.
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- 2024
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8. Transcriptome- and proteome-wide association studies identify genes associated with renal cell carcinoma
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Purdue, Mark P., Dutta, Diptavo, Machiela, Mitchell J., Gorman, Bryan R., Winter, Timothy, Okuhara, Dayne, Cleland, Sara, Ferreiro-Iglesias, Aida, Scheet, Paul, Liu, Aoxing, Wu, Chao, Antwi, Samuel O., Larkin, James, Zequi, Stênio C., Sun, Maxine, Hikino, Keiko, Hajiran, Ali, Lawson, Keith A., Cárcano, Flavio, Blanchet, Odile, Shuch, Brian, Nepple, Kenneth G., Margue, Gaëlle, Sundi, Debasish, Diver, W. Ryan, Folgueira, Maria A.A.K., van Bokhoven, Adrie, Neffa, Florencia, Brown, Kevin M., Hofmann, Jonathan N., Rhee, Jongeun, Yeager, Meredith, Cole, Nathan R., Hicks, Belynda D., Manning, Michelle R., Hutchinson, Amy A., Rothman, Nathaniel, Huang, Wen-Yi, Linehan, W. Marston, Lori, Adriana, Ferragu, Matthieu, Zidane-Marinnes, Merzouka, Serrano, Sérgio, Magnabosco, Wesley J., BioBank Japan Project Consortium, Vilas, Ana, Decia, Ricardo, Carusso, Florencia, Graham, Laura S., Anderson, Kyra, Bilen, Mehmet A., Arciero, Cletus, Pellegrin, Isabelle, Ricard, Solène, FinnGen, Scelo, Ghislaine, Banks, Rosamonde E., Vasudev, Naveen S., Soomro, Naeem, Stewart, Grant D., Adeyoju, Adebanji, Bromage, Stephen, Hrouda, David, Gibbons, Norma, Patel, Poulam, Sullivan, Mark, Protheroe, Andrew, Nugent, Francesca I., Fournier, Michelle J., Zhang, Xiaoyu, Martin, Lisa J., Komisarenko, Maria, Eisen, Timothy, Cunningham, Sonia A., Connolly, Denise C., Uzzo, Robert G., Zaridze, David, Mukeria, Anush, Holcatova, Ivana, Hornakova, Anna, Foretova, Lenka, Janout, Vladimir, Mates, Dana, Jinga, Viorel, Rascu, Stefan, Mijuskovic, Mirjana, Savic, Slavisa, Milosavljevic, Sasa, Gaborieau, Valérie, Abedi-Ardekani, Behnoush, McKay, James, Johansson, Mattias, Phouthavongsy, Larry, Hayman, Lindsay, Li, Jason, Lungu, Ilinca, Bezerra, Stephania M., de Souza, Aline G., Sares, Claudia T.G., Reis, Rodolfo B., Gallucci, Fabio P., Cordeiro, Mauricio D., Pomerantz, Mark, Lee, Gwo-Shu M., Freedman, Matthew L., Jeong, Anhyo, Greenberg, Samantha E., Sanchez, Alejandro, Thompson, R. Houston, Sharma, Vidit, Thiel, David D., Ball, Colleen T., Abreu, Diego, Lam, Elaine T., Nahas, William C., Master, Viraj A., Patel, Alpa V., Bernhard, Jean-Christophe, Freedman, Neal D., Bigot, Pierre, Reis, Rui M., Colli, Leandro M., Finelli, Antonio, Manley, Brandon J., Terao, Chikashi, Choueiri, Toni K., Carraro, Dirce M., Houlston, Richard, Eckel-Passow, Jeanette E., Abbosh, Philip H., Ganna, Andrea, Brennan, Paul, Gu, Jian, Chanock, Stephen J., Guo, Xinyu, Winter, Timothy D., Jahagirdar, Om, Ha, Eunji, and Susztak, Katalin
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- 2024
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9. The Mutographs biorepository: A unique genomic resource to study cancer around the world
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Perdomo, Sandra, Abedi-Ardekani, Behnoush, de Carvalho, Ana Carolina, Ferreiro-Iglesias, Aida, Gaborieau, Valérie, Cattiaux, Thomas, Renard, Hélène, Chopard, Priscilia, Carreira, Christine, Spanu, Andreea, Nikmanesh, Arash, Cardoso Penha, Ricardo Cortez, Antwi, Samuel O., Ashton-Prolla, Patricia, Canova, Cristina, Chitapanarux, Taned, Cox, Riley, Curado, Maria Paula, de Oliveira, José Carlos, Dzamalala, Charles, Fabianova, Elenora, Ferri, Lorenzo, Fitzgerald, Rebecca, Foretova, Lenka, Gallinger, Steven, Goldstein, Alisa M., Holcatova, Ivana, Huertas, Antonio, Janout, Vladimir, Jarmalaite, Sonata, Kaneva, Radka, Kowalski, Luiz Paulo, Kulis, Tomislav, Lagiou, Pagona, Lissowska, Jolanta, Malekzadeh, Reza, Mates, Dana, McCorrmack, Valerie, Menya, Diana, Mhatre, Sharayu, Mmbaga, Blandina Theophil, de Moricz, André, Nyirády, Péter, Ognjanovic, Miodrag, Papadopoulou, Kyriaki, Polesel, Jerry, Purdue, Mark P., Rascu, Stefan, Rebolho Batista, Lidia Maria, Reis, Rui Manuel, Ribeiro Pinto, Luis Felipe, Rodríguez-Urrego, Paula A., Sangkhathat, Surasak, Sangrajrang, Suleeporn, Shibata, Tatsuhiro, Stakhovsky, Eduard, Świątkowska, Beata, Vaccaro, Carlos, Vasconcelos de Podesta, Jose Roberto, Vasudev, Naveen S., Vilensky, Marta, Yeung, Jonathan, Zaridze, David, Zendehdel, Kazem, Scelo, Ghislaine, Chanudet, Estelle, Wang, Jingwei, Fitzgerald, Stephen, Latimer, Calli, Moody, Sarah, Humphreys, Laura, Alexandrov, Ludmil B., Stratton, Michael R., and Brennan, Paul
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- 2024
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10. Association between circulating inflammatory markers and adult cancer risk: a Mendelian randomization analysis
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Landi, Maria Teresa, Stevens, Victoria, Wang, Ying, Albanes, Demetrios, Caporaso, Neil, Brennan, Paul, Amos, Christopher I., Shete, Sanjay, Hung, Rayjean J., Bickeböller, Heike, Risch, Angela, Houlston, Richard, Lam, Stephen, Tardon, Adonina, Chen, Chu, Bojesen, Stig E., Johansson, Mattias, Wichmann, H-Erich, Christiani, David, Rennert, Gadi, Arnold, Susanne, Field, John K., Le Marchand, Loic, Melander, Olle, Brunnström, Hans, Liu, Geoffrey, Andrew, Angeline, Kiemeney, Lambertus A., Shen, Hongbing, Zienolddiny, Shan, Grankvist, Kjell, Johansson, Mikael, Teare, M. Dawn, Hong, Yun-Chul, Yuan, Jian-Min, Lazarus, Philip, Schabath, Matthew B., Aldrich, Melinda C., Eeles, Rosalind A., Haiman, Christopher A., Kote-Jarai, Zsofia, Schumacher, Fredrick R., Benlloch, Sara, Al Olama, Ali Amin, Muir, Kenneth R., Berndt, Sonja I., Conti, David V., Wiklund, Fredrik, Chanock, Stephen, Tangen, Catherine M., Batra, Jyotsna, Clements, Judith A., Grönberg, Henrik, Pashayan, Nora, Schleutker, Johanna, Albanes, Demetrius, Weinstein, Stephanie J., Wolk, Alicja, West, Catharine M.L., Mucci, Lorelei A., Cancel-Tassin, Géraldine, Koutros, Stella, Sørensen, Karina Dalsgaard, Grindedal, Eli Marie, Neal, David E., Hamdy, Freddie C., Donovan, Jenny L., Travis, Ruth C., Hamilton, Robert J., Ingles, Sue Ann, Rosenstein, Barry S., Lu, Yong-Jie, Giles, Graham G., MacInnis, Robert J., Kibel, Adam S., Vega, Ana, Kogevinas, Manolis, Penney, Kathryn L., Park, Jong Y., Stanfrod, Janet L., Cybulski, Cezary, Nordestgaard, Børge G., Nielsen, Sune F., Brenner, Hermann, Maier, Christiane, Logothetis, Christopher J., John, Esther M., Teixeira, Manuel R., Neuhausen, Susan L., De Ruyck, Kim, Razack, Azad, Newcomb, Lisa F., Lessel, Davor, Kaneva, Radka, Usmani, Nawaid, Claessens, Frank, Townsend, Paul A., Castelao, Jose Esteban, Roobol, Monique J., Menegaux, Florence, Khaw, Kay-Tee, Cannon-Albright, Lisa, Pandha, Hardev, Thibodeau, Stephen N., Hunter, David J., Kraft, Peter, Blot, William J., Riboli, Elio, Yarmolinsky, James, Robinson, Jamie W., Mariosa, Daniela, Karhunen, Ville, Huang, Jian, Dimou, Niki, Murphy, Neil, Burrows, Kimberley, Bouras, Emmanouil, Smith-Byrne, Karl, Lewis, Sarah J., Galesloot, Tessel E., Vermeulen, Sita, Martin, Paul, Hou, Lifang, Newcomb, Polly A., White, Emily, Wu, Anna H., Le Marchand, Loïc, Phipps, Amanda I., Buchanan, Daniel D., Zhao, Sizheng Steven, Gill, Dipender, Chanock, Stephen J., Purdue, Mark P., Davey Smith, George, Herzig, Karl-Heinz, Järvelin, Marjo-Riitta, Amos, Chris I., Dehghan, Abbas, Gunter, Marc J., Tsilidis, Kostas K., and Martin, Richard M.
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- 2024
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11. A metabolomic investigation of serum perfluorooctane sulfonate and perfluorooctanoate
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Rhee, Jongeun, Loftfield, Erikka, Albanes, Demetrius, Layne, Tracy M., Stolzenberg-Solomon, Rachael, Liao, Linda M., Playdon, Mary C., Berndt, Sonja I., Sampson, Joshua N., Freedman, Neal D., Moore, Steven C., and Purdue, Mark P.
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- 2023
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12. Serum concentrations of per- and polyfluoroalkyl substances and risk of renal cell carcinoma in the Multiethnic Cohort Study
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Rhee, Jongeun, Chang, Vicky C., Cheng, Iona, Calafat, Antonia M., Botelho, Julianne Cook, Shearer, Joseph J., Sampson, Joshua N., Setiawan, Veronica Wendy, Wilkens, Lynne R., Silverman, Debra T., Purdue, Mark P., and Hofmann, Jonathan N.
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- 2023
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13. Distinct germline genetic susceptibility profiles identified for common non-Hodgkin lymphoma subtypes
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Berndt, Sonja I., Vijai, Joseph, Benavente, Yolanda, Camp, Nicola J., Nieters, Alexandra, Wang, Zhaoming, Smedby, Karin E., Kleinstern, Geffen, Hjalgrim, Henrik, Besson, Caroline, Skibola, Christine F., Morton, Lindsay M., Brooks-Wilson, Angela R., Teras, Lauren R., Breeze, Charles, Arias, Joshua, Adami, Hans-Olov, Albanes, Demetrius, Anderson, Kenneth C., Ansell, Stephen M., Bassig, Bryan, Becker, Nikolaus, Bhatti, Parveen, Birmann, Brenda M., Boffetta, Paolo, Bracci, Paige M., Brennan, Paul, Brown, Elizabeth E., Burdett, Laurie, Cannon-Albright, Lisa A., Chang, Ellen T., Chiu, Brian C. H., Chung, Charles C., Clavel, Jacqueline, Cocco, Pierluigi, Colditz, Graham, Conde, Lucia, Conti, David V., Cox, David G., Curtin, Karen, Casabonne, Delphine, De Vivo, Immaculata, Diepstra, Arjan, Diver, W. Ryan, Dogan, Ahmet, Edlund, Christopher K., Foretova, Lenka, Fraumeni, Jr, Joseph F., Gabbas, Attilio, Ghesquières, Hervé, Giles, Graham G., Glaser, Sally, Glenn, Martha, Glimelius, Bengt, Gu, Jian, Habermann, Thomas M., Haiman, Christopher A., Haioun, Corinne, Hofmann, Jonathan N., Holford, Theodore R., Holly, Elizabeth A., Hutchinson, Amy, Izhar, Aalin, Jackson, Rebecca D., Jarrett, Ruth F., Kaaks, Rudolph, Kane, Eleanor, Kolonel, Laurence N., Kong, Yinfei, Kraft, Peter, Kricker, Anne, Lake, Annette, Lan, Qing, Lawrence, Charles, Li, Dalin, Liebow, Mark, Link, Brian K., Magnani, Corrado, Maynadie, Marc, McKay, James, Melbye, Mads, Miligi, Lucia, Milne, Roger L., Molina, Thierry J., Monnereau, Alain, Montalvan, Rebecca, North, Kari E., Novak, Anne J., Onel, Kenan, Purdue, Mark P., Rand, Kristin A., Riboli, Elio, Riby, Jacques, Roman, Eve, Salles, Gilles, Sborov, Douglas W., Severson, Richard K., Shanafelt, Tait D., Smith, Martyn T., Smith, Alexandra, Song, Kevin W., Song, Lei, Southey, Melissa C., Spinelli, John J., Staines, Anthony, Stephens, Deborah, Sutherland, Heather J., Tkachuk, Kaitlyn, Thompson, Carrie A., Tilly, Hervé, Tinker, Lesley F., Travis, Ruth C., Turner, Jenny, Vachon, Celine M., Vajdic, Claire M., Van Den Berg, Anke, Van Den Berg, David J., Vermeulen, Roel C. H., Vineis, Paolo, Wang, Sophia S., Weiderpass, Elisabete, Weiner, George J., Weinstein, Stephanie, Doo, Nicole Wong, Ye, Yuanqing, Yeager, Meredith, Yu, Kai, Zeleniuch-Jacquotte, Anne, Zhang, Yawei, Zheng, Tongzhang, Ziv, Elad, Sampson, Joshua, Chatterjee, Nilanjan, Offit, Kenneth, Cozen, Wendy, Wu, Xifeng, Cerhan, James R., Chanock, Stephen J., Slager, Susan L., and Rothman, Nathaniel
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- 2022
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14. A prospective nested case-control study of serum concentrations of per- and polyfluoroalkyl substances and aggressive prostate cancer risk
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Rhee, Jongeun, Barry, Kathryn H., Huang, Wen-Yi, Sampson, Joshua N., Hofmann, Jonathan N., Silverman, Debra T., Calafat, Antonia M., Botelho, Julianne Cook, Kato, Kayoko, Purdue, Mark P., and Berndt, Sonja I.
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- 2023
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15. Endogenous sex steroid hormones and risk of liver cancer among US men: Results from the Liver Cancer Pooling Project
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Wu, Zeni, Petrick, Jessica L., Florio, Andrea A., Guillemette, Chantal, Beane Freeman, Laura E., Buring, Julie E., Bradwin, Gary, Caron, Patrick, Chen, Yu, Eliassen, A. Heather, Engel, Lawrence S., Freedman, Neal D., Gaziano, J. Michael, Giovannuci, Edward L., Hofmann, Jonathan N., Huang, Wen-Yi, Kirsh, Victoria A., Kitahara, Cari M., Koshiol, Jill, Lee, I-Min, Liao, Linda M., Newton, Christina C., Palmer, Julie R., Purdue, Mark P., Rohan, Thomas E., Rosenberg, Lynn, Sesso, Howard D., Sinha, Rashmi, Stampfer, Meir J., Um, Caroline Y., Van Den Eeden, Stephen K., Visvanathan, Kala, Wactawski-Wende, Jean, Zeleniuch-Jacquotte, Anne, Zhang, Xuehong, Graubard, Barry I., Campbell, Peter T., and McGlynn, Katherine A.
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- 2023
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16. Genome-wide Association Study of Bladder Cancer Reveals New Biological and Translational Insights
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Koutros, Stella, Kiemeney, Lambertus A., Pal Choudhury, Parichoy, Milne, Roger L., Lopez de Maturana, Evangelina, Ye, Yuanqing, Joseph, Vijai, Florez-Vargas, Oscar, Dyrskjøt, Lars, Figueroa, Jonine, Dutta, Diptavo, Giles, Graham G., Hildebrandt, Michelle A.T., Offit, Kenneth, Kogevinas, Manolis, Weiderpass, Elisabete, McCullough, Marjorie L., Freedman, Neal D., Albanes, Demetrius, Kooperberg, Charles, Cortessis, Victoria K., Karagas, Margaret R., Johnson, Alison, Schwenn, Molly R., Baris, Dalsu, Furberg, Helena, Bajorin, Dean F., Cussenot, Olivier, Cancel-Tassin, Geraldine, Benhamou, Simone, Kraft, Peter, Porru, Stefano, Carta, Angela, Bishop, Timothy, Southey, Melissa C., Matullo, Giuseppe, Fletcher, Tony, Kumar, Rajiv, Taylor, Jack A., Lamy, Philippe, Prip, Frederik, Kalisz, Mark, Weinstein, Stephanie J., Hengstler, Jan G., Selinski, Silvia, Harland, Mark, Teo, Mark, Kiltie, Anne E., Tardón, Adonina, Serra, Consol, Carrato, Alfredo, García-Closas, Reina, Lloreta, Josep, Schned, Alan, Lenz, Petra, Riboli, Elio, Brennan, Paul, Tjønneland, Anne, Otto, Thomas, Ovsiannikov, Daniel, Volkert, Frank, Vermeulen, Sita H., Aben, Katja K., Galesloot, Tessel E., Turman, Constance, De Vivo, Immaculata, Giovannucci, Edward, Hunter, David J., Hohensee, Chancellor, Hunt, Rebecca, Patel, Alpa V., Huang, Wen-Yi, Thorleifsson, Gudmar, Gago-Dominguez, Manuela, Amiano, Pilar, Golka, Klaus, Stern, Mariana C., Yan, Wusheng, Liu, Jia, Li, Shengchao Alfred, Katta, Shilpa, Hutchinson, Amy, Hicks, Belynda, Wheeler, William A., Purdue, Mark P., McGlynn, Katherine A., Kitahara, Cari M., Haiman, Christopher A., Greene, Mark H., Rafnar, Thorunn, Chatterjee, Nilanjan, Chanock, Stephen J., Wu, Xifeng, Real, Francisco X., Silverman, Debra T., Garcia-Closas, Montserrat, Stefansson, Kari, Prokunina-Olsson, Ludmila, Malats, Núria, and Rothman, Nathaniel
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- 2023
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17. Alcohol drinking and head and neck cancer risk: the joint effect of intensity and duration
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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
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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.
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- 2020
18. Associations between reproductive factors and biliary tract cancers in women from the Biliary Tract Cancers Pooling Project
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Jackson, Sarah S, Adami, Hans-Olov, Andreotti, Gabriella, Beane-Freeman, Laura E, de González, Amy Berrington, Buring, Julie E, Fraser, Gary E, Freedman, Neal D, Gapstur, Susan M, Gierach, Gretchen, Giles, Graham G, Grodstein, Francine, Hartge, Patricia, Jenab, Mazda, Kirsh, Victoria, Knutsen, Synnove F, Lan, Qing, Larsson, Susanna C, Lee, I-Min, Lee, Mei-Hsuan, Liao, Linda M, Milne, Roger L, Monroe, Kristine R, Neuhouser, Marian L, O'Brien, Katie M, Petrick, Jessica L, Purdue, Mark P, Rohan, Thomas E, Sandin, Sven, Sandler, Dale P, Sawada, Norie, Shadyab, Aladdin H, Simon, Tracey G, Sinha, Rashmi, Stolzenberg-Solomon, Rachael, Tsugane, Shoichiro, Weiderpass, Elisabete, Wolk, Alicja, Yang, Hwai-I, Zheng, Wei, McGlynn, Katherine A, Campbell, Peter T, and Koshiol, Jill
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Biomedical and Clinical Sciences ,Clinical Sciences ,Aging ,Prevention ,Clinical Research ,Contraception/Reproduction ,Digestive Diseases ,Cancer ,2.1 Biological and endogenous factors ,Aetiology ,Reproductive health and childbirth ,Adult ,Aged ,Biliary Tract Neoplasms ,Female ,Follow-Up Studies ,Global Health ,Humans ,Incidence ,Middle Aged ,Prospective Studies ,Registries ,Reproduction ,Risk Assessment ,Risk Factors ,Sex Factors ,Survival Rate ,Time Factors ,Young Adult ,Reproductive factors ,Parity ,Biliary tract cancer ,Gallbladder cancer ,Public Health and Health Services ,Gastroenterology & Hepatology ,Clinical sciences - Abstract
Background & aimsGallbladder cancer (GBC) is known to have a female predominance while other biliary tract cancers (BTCs) have a male predominance. However, the role of female reproductive factors in BTC etiology remains unclear.MethodsWe pooled data from 19 studies of >1.5 million women participating in the Biliary Tract Cancers Pooling Project to examine the associations of parity, age at menarche, reproductive years, and age at menopause with BTC. Associations for age at menarche and reproductive years with BTC were analyzed separately for Asian and non-Asian women. Hazard ratios (HRs) and 95% CIs were estimated using Cox proportional hazards models, stratified by study.ResultsDuring 21,681,798 person-years of follow-up, 875 cases of GBC, 379 of intrahepatic bile duct cancer (IHBDC), 450 of extrahepatic bile duct cancer (EHBDC), and 261 of ampulla of Vater cancer (AVC) occurred. High parity was associated with risk of GBC (HR ≥5 vs. 0 births 1.72; 95% CI 1.25-2.38). Age at menarche (HR per year increase 1.15; 95% CI 1.06-1.24) was associated with GBC risk in Asian women while reproductive years were associated with GBC risk (HR per 5 years 1.13; 95% CI 1.04-1.22) in non-Asian women. Later age at menarche was associated with IHBDC (HR 1.19; 95% CI 1.09-1.31) and EHBDC (HR 1.11; 95% CI 1.01-1.22) in Asian women only.ConclusionWe observed an increased risk of GBC with increasing parity. Among Asian women, older age at menarche was associated with increased risk for GBC, IHBDC, and EHBDC, while increasing reproductive years was associated with GBC in non-Asian women. These results suggest that sex hormones have distinct effects on cancers across the biliary tract that vary by geography.Lay summaryOur findings show that the risk of gallbladder cancer is increased among women who have given birth (especially women with 5 or more children). In women from Asian countries, later age at menarche increases the risk of gallbladder cancer, intrahepatic bile duct cancer and extrahepatic bile duct cancer. We did not see this same association in women from Western countries. Age at menopause was not associated with the risk of any biliary tract cancers.
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- 2020
19. Pathway Analysis of Renal Cell Carcinoma Genome-Wide Association Studies Identifies Novel Associations
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Purdue, Mark P, Song, Lei, Scélo, Ghislaine, Houlston, Richard S, Wu, Xifeng, Sakoda, Lori C, Thai, Khanh, Graff, Rebecca E, Rothman, Nathaniel, Brennan, Paul, Chanock, Stephen J, and Yu, Kai
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Epidemiology ,Health Sciences ,Human Genome ,Genetics ,Rare Diseases ,Biotechnology ,Aetiology ,2.1 Biological and endogenous factors ,Good Health and Well Being ,Carcinoma ,Renal Cell ,Genome-Wide Association Study ,Humans ,Medical and Health Sciences ,Biomedical and clinical sciences ,Health sciences - Abstract
BackgroundMuch of the heritable risk of renal cell carcinoma (RCC) associated with common genetic variation is unexplained. New analytic approaches have been developed to increase the discovery of risk variants in genome-wide association studies (GWAS), including multi-locus testing through pathway analysis.MethodsWe conducted a pathway analysis using GWAS summary data from six previous scans (10,784 cases and 20,406 controls) and evaluated 3,678 pathways and gene sets drawn from the Molecular Signatures Database. To replicate findings, we analyzed GWAS summary data from the UK Biobank (903 cases and 451,361 controls) and the Genetic Epidemiology Research on Adult Health and Aging cohort (317 cases and 50,511 controls).ResultsWe identified 14 pathways/gene sets associated with RCC in both the discovery (P < 1.36 × 10-5, the Bonferroni correction threshold) and replication (P < 0.05) sets, 10 of which include components of the PI3K/AKT pathway. In tests across 2,035 genes in these pathways, associations (Bonferroni corrected P < 2.46 × 10-5 in discovery and replication sets combined) were observed for CASP9, TIPIN, and CDKN2C. The strongest SNP signal was for rs12124078 (P Discovery = 2.6 × 10-5; P Replication = 1.5 × 10-4; P Combined = 6.9 × 10-8), a CASP9 expression quantitative trait locus.ConclusionsOur pathway analysis implicates genetic variation within the PI3K/AKT pathway as a source of RCC heritability and identifies several promising novel susceptibility genes, including CASP9, which warrant further investigation.ImpactOur findings illustrate the value of pathway analysis as a complementary approach to analyzing GWAS data.
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- 2020
20. Abdominal and gluteofemoral size and risk of liver cancer: The liver cancer pooling project
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Florio, Andrea A, Campbell, Peter T, Zhang, Xuehong, Zeleniuch‐Jacquotte, Anne, Wactawski‐Wende, Jean, Smith‐Warner, Stephanie A, Sinha, Rashmi, Simon, Tracey G, Sesso, Howard D, Schairer, Catherine, Rosenberg, Lynn, Rohan, Thomas E, Robien, Kim, Renehan, Andrew G, Purdue, Mark P, Poynter, Jenny N, Palmer, Julie R, Newton, Christina C, Lu, Yunxia, Linet, Martha S, Liao, Linda M, Lee, I‐Min, Koshiol, Jill, Kitahara, Cari M, Kirsh, Victoria A, Hofmann, Jonathan N, Graubard, Barry I, Giovannucci, Edward, Gaziano, John M, Gapstur, Susan M, Freedman, Neal D, Demuth, Jane, Chong, Dawn Q, Chan, Andrew T, Buring, Julie E, Bradshaw, Patrick T, Freeman, Laura E Beane, McGlynn, Katherine A, and Petrick, Jessica L
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Obesity ,Rare Diseases ,Cancer ,Liver Disease ,Digestive Diseases ,Clinical Research ,Liver Cancer ,Prevention ,Adiposity ,Adult ,Aged ,Bile Duct Neoplasms ,Body Mass Index ,Carcinoma ,Hepatocellular ,Cholangiocarcinoma ,Female ,Humans ,Liver Neoplasms ,Male ,Middle Aged ,Prospective Studies ,Waist Circumference ,Waist-Hip Ratio ,hepatocellular carcinoma ,intrahepatic cholangiocarcinoma ,abdominal obesity ,gluteofemoral obesity ,epidemiology ,Oncology and Carcinogenesis ,Oncology & Carcinogenesis - Abstract
Obesity is known to be associated with primary liver cancer (PLC), but the separate effects of excess abdominal and gluteofemoral size are unclear. Thus, we examined the association between waist and hip circumference with risk of PLC overall and by histologic type-hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC). The Liver Cancer Pooling Project is a consortium of prospective cohort studies that include data from 1,167,244 individuals (PLC n = 2,208, HCC n = 1,154, ICC n = 335). Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CI) were estimated using proportional hazards regression. Waist circumference, per 5 cm increase, was associated with an 11% increased PLC risk (HR = 1.11, 95%CI: 1.09-1.14), including when adjusted for hip circumference (HR = 1.12, 95%CI: 1.08-1.17) and also when restricted to individuals in a normal body mass index (BMI) range (18.5 to
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- 2020
21. Exogenous hormone use, reproductive factors and risk of intrahepatic cholangiocarcinoma among women: results from cohort studies in the Liver Cancer Pooling Project and the UK Biobank
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Petrick, Jessica L, McMenamin, Úna C, Zhang, Xuehong, Zeleniuch-Jacquotte, Anne, Wactawski-Wende, Jean, Simon, Tracey G, Sinha, Rashmi, Sesso, Howard D, Schairer, Catherine, Rosenberg, Lynn, Rohan, Thomas E, Robien, Kim, Purdue, Mark P, Poynter, Jenny N, Palmer, Julie R, Lu, Yunxia, Linet, Martha S, Liao, Linda M, Lee, I-Min, Koshiol, Jill, Kitahara, Cari M, Kirsh, Victoria A, Hofmann, Jonathan N, Graubard, Barry I, Giovannucci, Edward, Gaziano, J Michael, Gapstur, Susan M, Freedman, Neal D, Florio, Andrea A, Chong, Dawn Q, Chen, Yu, Chan, Andrew T, Buring, Julie E, Freeman, Laura E Beane, Bea, Jennifer W, Cardwell, Christopher R, Campbell, Peter T, and McGlynn, Katherine A
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Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Liver Disease ,Cancer ,Digestive Diseases ,Contraception/Reproduction ,Clinical Research ,Digestive Diseases - (Gallbladder) ,Liver Cancer ,Prevention ,Rare Diseases ,Aetiology ,2.1 Biological and endogenous factors ,Reproductive health and childbirth ,Good Health and Well Being ,Aged ,Bile Ducts ,Bile Ducts ,Intrahepatic ,Biological Specimen Banks ,Cholangiocarcinoma ,Cohort Studies ,Contraceptives ,Oral ,Hormonal ,Estrogen Receptor alpha ,Estrogen Receptor beta ,Female ,Gene Expression Regulation ,Neoplastic ,Hormones ,Humans ,Hysterectomy ,Liver Neoplasms ,Menopause ,Middle Aged ,Proportional Hazards Models ,Risk Factors ,United Kingdom ,Public Health and Health Services ,Oncology & Carcinogenesis ,Oncology and carcinogenesis - Abstract
BackgroundIntrahepatic cholangiocarcinoma (ICC) arises from cholangiocytes in the intrahepatic bile duct and is the second most common type of liver cancer. Cholangiocytes express both oestrogen receptor-α and -β, and oestrogens positively modulate cholangiocyte proliferation. Studies in women and men have reported higher circulating oestradiol is associated with increased ICC risk, further supporting a hormonal aetiology. However, no observational studies have examined the associations between exogenous hormone use and reproductive factors, as proxies of endogenous hormone levels, and risk of ICC.MethodsWe harmonised data from 1,107,498 women who enroled in 12 North American-based cohort studies (in the Liver Cancer Pooling Project, LCPP) and the UK Biobank between 1980-1998 and 2006-2010, respectively. Cox proportional hazards regression models were used to generate hazard ratios (HR) and 95% confidence internals (CI). Then, meta-analytic techniques were used to combine the estimates from the LCPP (n = 180 cases) and the UK Biobank (n = 57 cases).ResultsHysterectomy was associated with a doubling of ICC risk (HR = 1.98, 95% CI: 1.27-3.09), compared to women aged 50-54 at natural menopause. Long-term oral contraceptive use (9+ years) was associated with a 62% increased ICC risk (HR = 1.62, 95% CI: 1.03-2.55). There was no association between ICC risk and other exogenous hormone use or reproductive factors.ConclusionsThis study suggests that hysterectomy and long-term oral contraceptive use may be associated with an increased ICC risk.
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- 2020
22. Assessment of polygenic architecture and risk prediction based on common variants across fourteen cancers.
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Zhang, Yan Dora, Hurson, Amber N, Zhang, Haoyu, Choudhury, Parichoy Pal, Easton, Douglas F, Milne, Roger L, Simard, Jacques, Hall, Per, Michailidou, Kyriaki, Dennis, Joe, Schmidt, Marjanka K, Chang-Claude, Jenny, Gharahkhani, Puya, Whiteman, David, Campbell, Peter T, Hoffmeister, Michael, Jenkins, Mark, Peters, Ulrike, Hsu, Li, Gruber, Stephen B, Casey, Graham, Schmit, Stephanie L, O'Mara, Tracy A, Spurdle, Amanda B, Thompson, Deborah J, Tomlinson, Ian, De Vivo, Immaculata, Landi, Maria Teresa, Law, Matthew H, Iles, Mark M, Demenais, Florence, Kumar, Rajiv, MacGregor, Stuart, Bishop, D Timothy, Ward, Sarah V, Bondy, Melissa L, Houlston, Richard, Wiencke, John K, Melin, Beatrice, Barnholtz-Sloan, Jill, Kinnersley, Ben, Wrensch, Margaret R, Amos, Christopher I, Hung, Rayjean J, Brennan, Paul, McKay, James, Caporaso, Neil E, Berndt, Sonja I, Birmann, Brenda M, Camp, Nicola J, Kraft, Peter, Rothman, Nathaniel, Slager, Susan L, Berchuck, Andrew, Pharoah, Paul DP, Sellers, Thomas A, Gayther, Simon A, Pearce, Celeste L, Goode, Ellen L, Schildkraut, Joellen M, Moysich, Kirsten B, Amundadottir, Laufey T, Jacobs, Eric J, Klein, Alison P, Petersen, Gloria M, Risch, Harvey A, Stolzenberg-Solomon, Rachel Z, Wolpin, Brian M, Li, Donghui, Eeles, Rosalind A, Haiman, Christopher A, Kote-Jarai, Zsofia, Schumacher, Fredrick R, Al Olama, Ali Amin, Purdue, Mark P, Scelo, Ghislaine, Dalgaard, Marlene D, Greene, Mark H, Grotmol, Tom, Kanetsky, Peter A, McGlynn, Katherine A, Nathanson, Katherine L, Turnbull, Clare, Wiklund, Fredrik, Breast Cancer Association Consortium (BCAC), Barrett’s and Esophageal Adenocarcinoma Consortium (BEACON), Colon Cancer Family Registry (CCFR), Transdisciplinary Studies of Genetic Variation in Colorectal Cancer (CORECT), Endometrial Cancer Association Consortium (ECAC), Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), Melanoma Genetics Consortium (GenoMEL), Glioma International Case-Control Study (GICC), International Lung Cancer Consortium (ILCCO), Integrative Analysis of Lung Cancer Etiology and Risk (INTEGRAL) Consortium, International Consortium of Investigators Working on Non-Hodgkin’s Lymphoma Epidemiologic Studies (InterLymph), Ovarian Cancer Association Consortium (OCAC), Oral Cancer GWAS, Pancreatic Cancer Case-Control Consortium (PanC4), Pancreatic Cancer Cohort Consortium (PanScan), and Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL)
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Breast Cancer Association Consortium ,Barrett’s and Esophageal Adenocarcinoma Consortium ,Colon Cancer Family Registry ,Transdisciplinary Studies of Genetic Variation in Colorectal Cancer ,Endometrial Cancer Association Consortium ,Genetics and Epidemiology of Colorectal Cancer Consortium ,Melanoma Genetics Consortium ,Glioma International Case-Control Study ,International Lung Cancer Consortium ,Integrative Analysis of Lung Cancer Etiology and Risk (INTEGRAL) Consortium ,International Consortium of Investigators Working on Non-Hodgkin’s Lymphoma Epidemiologic Studies ,Ovarian Cancer Association Consortium ,Oral Cancer GWAS ,Pancreatic Cancer Case-Control Consortium ,Pancreatic Cancer Cohort Consortium ,Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome ,Renal Cancer GWAS ,Testicular Cancer Consortium ,Animals ,Humans ,Neoplasms ,Genetic Predisposition to Disease ,Incidence ,Risk Assessment ,Risk Factors ,Multifactorial Inheritance ,Polymorphism ,Single Nucleotide ,Models ,Genetic ,Female ,Male ,Genome-Wide Association Study ,Human Genome ,Prevention ,Cancer ,Prostate Cancer ,Genetics ,Urologic Diseases ,2.1 Biological and endogenous factors - Abstract
Genome-wide association studies (GWAS) have led to the identification of hundreds of susceptibility loci across cancers, but the impact of further studies remains uncertain. Here we analyse summary-level data from GWAS of European ancestry across fourteen cancer sites to estimate the number of common susceptibility variants (polygenicity) and underlying effect-size distribution. All cancers show a high degree of polygenicity, involving at a minimum of thousands of loci. We project that sample sizes required to explain 80% of GWAS heritability vary from 60,000 cases for testicular to over 1,000,000 cases for lung cancer. The maximum relative risk achievable for subjects at the 99th risk percentile of underlying polygenic risk scores (PRS), compared to average risk, ranges from 12 for testicular to 2.5 for ovarian cancer. We show that PRS have potential for risk stratification for cancers of breast, colon and prostate, but less so for others because of modest heritability and lower incidence.
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- 2020
23. 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)
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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
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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
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- 2019
24. The association between genetically elevated polyunsaturated fatty acids and risk of cancer
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Tintle, Nathan, Rice, Terri, Cheng, Iona, Jenkins, Mark, Gallinger, Steve, Cornish, Alex J., Sud, Amit, Vijayakrishnan, Jayaram, Wrensch, Margaret, Johansson, Mattias, Norman, Aaron D., Klein, Alison, Clay-Gilmour, Alyssa, Franke, Andre, Ardisson Korat, Andres V., Wheeler, Bill, Nilsson, Björn, Smith, Caren, Heng, Chew-Kiat, Song, Ci, Riadi, David, Claus, Elizabeth B., Ellinghaus, Eva, Ostroumova, Evgenia, Hosnijeh, de Vathaire, Florent, Cugliari, Giovanni, Matullo, Giuseppe, Oi-Lin Ng, Irene, Passow, Jeanette E., Foo, Jia Nee, Han, Jiali, Liu, Jianjun, Barnholtz-Sloan, Jill, Schildkraut, Joellen M., Maris, John, Wiemels, Joseph L., Hemminki, Kari, Yang, Keming, Kiemeney, Lambertus A., Wu, Lang, Amundadottir, Laufey, Stern, Marc-Henri, Boutron, Marie-Christine, Iles, Mark Martin, Purdue, Mark P., Stanulla, Martin, Bondy, Melissa, Gaudet, Mia, Mobuchon, Lenha, Camp, Nicola J., Sham, Pak Chung, Guénel, Pascal, Brennan, Paul, Taylor, Philip R., Ostrom, Quinn, Stolzenberg-Solomon, Rachael, Dorajoo, Rajkumar, Houlston, Richard, Jenkins, Robert B., Diskin, Sharon, Berndt, Sonja I., Tsavachidis, Spiridon, Channock, Stephen J., Harrison, Tabitha, Galesloot, Tessel, Gyllensten, Ulf, Joseph, Vijai, Shi, Y., Yang, Wenjian, Lin, Yi, Van Den Eeden, Stephen K., Haycock, Philip C., Borges, Maria Carolina, Burrows, Kimberley, Lemaitre, Rozenn N., Burgess, Stephen, Khankari, Nikhil K., Tsilidis, Konstantinos K., Gaunt, Tom R., Hemani, Gibran, Zheng, Jie, Truong, Therese, Birmann, Brenda M., OMara, Tracy, Spurdle, Amanda B., Iles, Mark M., Law, Matthew H., Slager, Susan L., Saberi Hosnijeh, Fatemeh, Mariosa, Daniela, Cotterchio, Michelle, Cerhan, James R., Peters, Ulrike, Enroth, Stefan, Gharahkhani, Puya, Le Marchand, Loic, Williams, Ann C., Block, Robert C., Amos, Christopher I., Hung, Rayjean J., Zheng, Wei, Gunter, Marc J., Smith, George Davey, Relton, Caroline, and Martin, Richard M.
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- 2023
- Full Text
- View/download PDF
25. Correction: Distinct germline genetic susceptibility profiles identified for common non-Hodgkin lymphoma subtypes
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Berndt, Sonja I., Vijai, Joseph, Benavente, Yolanda, Camp, Nicola J., Nieters, Alexandra, Wang, Zhaoming, Smedby, Karin E., Kleinstern, Geffen, Hjalgrim, Henrik, Besson, Caroline, Skibola, Christine F., Morton, Lindsay M., Brooks-Wilson, Angela R., Teras, Lauren R., Breeze, Charles, Arias, Joshua, Adami, Hans-Olov, Albanes, Demetrius, Anderson, Kenneth C., Ansell, Stephen M., Bassig, Bryan, Becker, Nikolaus, Bhatti, Parveen, Birmann, Brenda M., Boffetta, Paolo, Bracci, Paige M., Brennan, Paul, Brown, Elizabeth E., Burdett, Laurie, Cannon-Albright, Lisa A., Chang, Ellen T., Chiu, Brian C. H., Chung, Charles C., Clavel, Jacqueline, Cocco, Pierluigi, Colditz, Graham, Conde, Lucia, Conti, David V., Cox, David G., Curtin, Karen, Casabonne, Delphine, De Vivo, Immaculata, Diepstra, Arjan, Diver, W. Ryan, Dogan, Ahmet, Edlund, Christopher K., Foretova, Lenka, Fraumeni, Jr, Joseph F., Gabbas, Attilio, Ghesquières, Hervé, Giles, Graham G., Glaser, Sally, Glenn, Martha, Glimelius, Bengt, Gu, Jian, Habermann, Thomas M., Haiman, Christopher A., Haioun, Corinne, Hofmann, Jonathan N., Holford, Theodore R., Holly, Elizabeth A., Hutchinson, Amy, Izhar, Aalin, Jackson, Rebecca D., Jarrett, Ruth F., Kaaks, Rudolph, Kane, Eleanor, Kolonel, Laurence N., Kong, Yinfei, Kraft, Peter, Kricker, Anne, Lake, Annette, Lan, Qing, Lawrence, Charles, Li, Dalin, Liebow, Mark, Link, Brian K., Magnani, Corrado, Maynadie, Marc, McKay, James, Melbye, Mads, Miligi, Lucia, Milne, Roger L., Molina, Thierry J., Monnereau, Alain, Montalvan, Rebecca, North, Kari E., Novak, Anne J., Onel, Kenan, Purdue, Mark P., Rand, Kristin A., Riboli, Elio, Riby, Jacques, Roman, Eve, Salles, Gilles, Sborov, Douglas W., Severson, Richard K., Shanafelt, Tait D., Smith, Martyn T., Smith, Alexandra, Song, Kevin W., Song, Lei, Southey, Melissa C., Spinelli, John J., Staines, Anthony, Stephens, Deborah, Sutherland, Heather J., Tkachuk, Kaitlyn, Thompson, Carrie A., Tilly, Hervé, Tinker, Lesley F., Travis, Ruth C., Turner, Jenny, Vachon, Celine M., Vajdic, Claire M., Van Den Berg, Anke, Van Den Berg, David J., Vermeulen, Roel C. H., Vineis, Paolo, Wang, Sophia S., Weiderpass, Elisabete, Weiner, George J., Weinstein, Stephanie, Doo, Nicole Wong, Ye, Yuanqing, Yeager, Meredith, Yu, Kai, Zeleniuch-Jacquotte, Anne, Zhang, Yawei, Zheng, Tongzhang, Ziv, Elad, Sampson, Joshua, Chatterjee, Nilanjan, Offit, Kenneth, Cozen, Wendy, Wu, Xifeng, Cerhan, James R., Chanock, Stephen J., Slager, Susan L., and Rothman, Nathaniel
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- 2023
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26. The renal lineage factor PAX8 controls oncogenic signalling in kidney cancer
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Patel, Saroor A., Hirosue, Shoko, Rodrigues, Paulo, Vojtasova, Erika, Richardson, Emma K., Ge, Jianfeng, Syafruddin, Saiful E., Speed, Alyson, Papachristou, Evangelia K., Baker, David, Clarke, David, Purvis, Stephenie, Wesolowski, Ludovic, Dyas, Anna, Castillon, Leticia, Caraffini, Veronica, Bihary, Dóra, Yong, Cissy, Harrison, David J., Stewart, Grant D., Machiela, Mitchell J., Purdue, Mark P., Chanock, Stephen J., Warren, Anne Y., Samarajiwa, Shamith A., Carroll, Jason S., and Vanharanta, Sakari
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- 2022
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27. Human exposure to trichloroethylene is associated with increased variability of blood DNA methylation that is enriched in genes and pathways related to autoimmune disease and cancer
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Phillips, Rachael V, Rieswijk, Linda, Hubbard, Alan E, Vermeulen, Roel, Zhang, Jinming, Hu, Wei, Li, Laiyu, Bassig, Bryan A, Wong, Jason YY, Reiss, Boris, Huang, Yongshun, Wen, Cuiju, Purdue, Mark, Tang, Xiaojiang, Zhang, Luoping, Smith, Martyn T, Rothman, Nathaniel, and Lan, Qing
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Biological Sciences ,Genetics ,Rare Diseases ,Cancer ,Prevention ,Biotechnology ,Human Genome ,2.1 Biological and endogenous factors ,Aetiology ,Adult ,Autoantigens ,Autoimmune Diseases ,CpG Islands ,DNA Methylation ,Female ,Genetic Loci ,Genetic Predisposition to Disease ,Genetic Variation ,Humans ,Male ,Neoplasms ,Trichloroethylene ,Tripartite Motif Proteins ,Ubiquitin-Protein Ligases ,TCE ,DNA methylation ,epigenome-wide association study ,epigenetics ,occupational exposure ,epigenetic variability ,autoimmune disease ,Biochemistry and Cell Biology ,Medical Biochemistry and Metabolomics ,Developmental Biology ,Biochemistry and cell biology - Abstract
Human exposure to trichloroethylene (TCE) is linked to kidney cancer, autoimmune diseases, and probably non-Hodgkin lymphoma. Additionally, TCE exposed mice and cell cultures show altered DNA methylation. To evaluate associations between TCE exposure and DNA methylation in humans, we conducted an epigenome-wide association study (EWAS) in TCE exposed workers using the HumanMethylation450 BeadChip. Across individual CpG probes, genomic regions, and globally (i.e., the 450K methylome), we investigated differences in mean DNA methylation and differences in variability of DNA methylation between 73 control (< 0.005 ppm TCE), 30 lower exposed (< 10 ppm TCE), and 37 higher exposed ( ≥ 10 ppm TCE) subjects' white blood cells. We found that TCE exposure increased methylation variation globally (Kruskal-Wallis p-value = 3.75e-3) and in 25 CpG sites at a genome-wide significance level (Bonferroni p-value < 0.05). We identified a 609 basepair region in the TRIM68 gene promoter that exhibited hypomethylation with increased exposure to TCE (FWER = 1.20e-2). Also, genes that matched to differentially variable CpGs were enriched in the 'focal adhesion' biological pathway (p-value = 2.80e-2). All in all, human exposure to TCE was associated with epigenetic alterations in genes involved in cell-matrix adhesions and interferon subtype expression, which are important in the development of autoimmune diseases; and in genes related to cancer development. These results suggest that DNA methylation may play a role in the pathogenesis of TCE exposure-related diseases and that TCE exposure may contribute to epigenetic drift.
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- 2019
28. Genetic overlap between autoimmune diseases and non‐Hodgkin lymphoma subtypes
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Din, Lennox, Sheikh, Mohammad, Kosaraju, Nikitha, Smedby, Karin Ekstrom, Bernatsky, Sasha, Berndt, Sonja I, Skibola, Christine F, Nieters, Alexandra, Wang, Sophia, McKay, James D, Cocco, Pierluigi, Maynadié, Marc, Foretová, Lenka, Staines, Anthony, Mack, Thomas M, de Sanjosé, Silvia, Vyse, Timothy J, Padyukov, Leonid, Monnereau, Alain, Arslan, Alan A, Moore, Amy, Brooks‐Wilson, Angela R, Novak, Anne J, Glimelius, Bengt, Birmann, Brenda M, Link, Brian K, Stewart, Carolyn, Vajdic, Claire M, Haioun, Corinne, Magnani, Corrado, Conti, David V, Cox, David G, Casabonne, Delphine, Albanes, Demetrius, Kane, Eleanor, Roman, Eve, Muzi, Giacomo, Salles, Gilles, Giles, Graham G, Adami, Hans‐Olov, Ghesquières, Hervé, De Vivo, Immaculata, Clavel, Jacqueline, Cerhan, James R, Spinelli, John J, Hofmann, Jonathan, Vijai, Joseph, Curtin, Karen, Costenbader, Karen H, Onel, Kenan, Offit, Kenneth, Teras, Lauren R, Morton, Lindsay, Conde, Lucia, Miligi, Lucia, Melbye, Mads, Ennas, Maria Grazia, Liebow, Mark, Purdue, Mark P, Glenn, Martha, Southey, Melissa C, Din, Morris, Rothman, Nathaniel, Camp, Nicola J, Doo, Nicole Wong, Becker, Nikolaus, Pradhan, Nisha, Bracci, Paige M, Boffetta, Paolo, Vineis, Paolo, Brennan, Paul, Kraft, Peter, Lan, Qing, Severson, Richard K, Vermeulen, Roel CH, Milne, Roger L, Kaaks, Rudolph, Travis, Ruth C, Weinstein, Stephanie J, Chanock, Stephen J, Ansell, Stephen M, Slager, Susan L, Zheng, Tongzhang, Zhang, Yawei, Benavente, Yolanda, Taub, Zachary, Madireddy, Lohith, Gourraud, Pierre‐Antoine, Oksenberg, Jorge R, Cozen, Wendy, Hjalgrim, Henrik, and Khankhanian, Pouya
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Biological Sciences ,Genetics ,Lymphoma ,Arthritis ,Neurodegenerative ,Brain Disorders ,Autoimmune Disease ,Cancer ,Human Genome ,Rare Diseases ,Hematology ,Aetiology ,2.1 Biological and endogenous factors ,Inflammatory and immune system ,Alleles ,Autoimmune Diseases ,Female ,Genetic Predisposition to Disease ,HLA Antigens ,Humans ,Lymphoma ,Non-Hodgkin ,Male ,Middle Aged ,Multifactorial Inheritance ,Polymorphism ,Single Nucleotide ,Risk Factors ,autoimmune disease ,genome-wide association study ,meta-analysis ,non-Hodgkin lymphoma ,Public Health and Health Services ,Epidemiology - Abstract
Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional genetic of overlap, (b) polygenic risk score (PRS), (c)"diseasome", (d)meta-analysis. Descriptive analysis revealed few shared genetic factors between each AD and each NHL subtype. The PRS of ADs were not increased in NHL patients (nor vice versa). In the diseasome, NHLs shared more genetic etiology with ADs than solid cancers (p = .0041). A meta-analysis (combing AD with NHL) implicated genes of apoptosis and telomere length. This GWAS-based analysis four NHL subtypes and three ADs revealed few weakly-associated shared loci, explaining little total risk. This suggests common genetic variation, as assessed by GWAS in these sample sizes, may not be the primary explanation for the link between these ADs and NHLs.
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- 2019
29. Joint effects of intensity and duration of cigarette smoking on the risk of head and neck cancer: A bivariate spline model approach
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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
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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.
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- 2019
30. MC1R variants in childhood and adolescent melanoma: a retrospective pooled analysis of a multicentre cohort
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Pellegrini, Cristina, Botta, Francesca, Massi, Daniela, Martorelli, Claudia, Facchetti, Fabio, Gandini, Sara, Maisonneuve, Patrick, Avril, Marie-Françoise, Demenais, Florence, Paillerets, Brigitte Bressac-de, Hoiom, Veronica, Cust, Anne E, Anton-Culver, Hoda, Gruber, Stephen B, Gallagher, Richard P, Marrett, Loraine, Zanetti, Roberto, Dwyer, Terence, Thomas, Nancy E, Begg, Colin B, Berwick, Marianne, Puig, Susana, Potrony, Miriam, Nagore, Eduardo, Ghiorzo, Paola, Menin, Chiara, Manganoni, Ausilia Maria, Rodolfo, Monica, Brugnara, Sonia, Passoni, Emanuela, Sekulovic, Lidija Kandolf, Baldini, Federica, Guida, Gabriella, Stratigos, Alexandros, Ozdemir, Fezal, Ayala, Fabrizio, Fernandez-de-Misa, Ricardo, Quaglino, Pietro, Ribas, Gloria, Romanini, Antonella, Migliano, Emilia, Stanganelli, Ignazio, Kanetsky, Peter A, Pizzichetta, Maria Antonietta, García-Borrón, Jose Carlos, Nan, Hongmei, Landi, Maria Teresa, Little, Julian, Newton-Bishop, Julia, Sera, Francesco, Fargnoli, Maria Concetta, Raimondi, Sara, Group, IMI Study, Alaibac, Mauro, Ferrari, Andrea, Valeri, Barbara, Sicher, Mariacristina, Mangiola, Daniela, Nazzaro, Gianluca, Tosti, Giulio, Mazzarol, Giovanni, Giudice, Giuseppe, Ribero, Simone, Astrua, Chiara, Mazzoni, Laura, Group, GEM Study, Orlow, Irene, Mujumdar, Urvi, Hummer, Amanda, Busam, Klaus, Roy, Pampa, Canchola, Rebecca, Clas, Brian, Cotignola, Javiar, Monroe, Yvette, Armstrong, Bruce, Kricker, Anne, Litchfield, Melisa, Tucker, Paul, Stephens, Nicola, Switzer, Teresa, Theis, Beth, From, Lynn, Chowdhury, Noori, Vanasse, Louise, Purdue, Mark, Northrup, David, Rosso, Stefano, Sacerdote, Carlotta, Leighton, Nancy, Gildea, Maureen, Bonner, Joe, Jeter, Joanne, Klotz, Judith, Wilcox, Homer, Weiss, Helen, Millikan, Robert, Mattingly, Dianne, and Player, Jon
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Clinical Research ,Pediatric ,Genetics ,Prevention ,Cancer ,Adolescent ,Adult ,Aged ,Biomarkers ,Tumor ,Case-Control Studies ,Child ,Female ,Genetic Predisposition to Disease ,Germ-Line Mutation ,Humans ,Logistic Models ,Male ,Melanoma ,Middle Aged ,Odds Ratio ,Polymorphism ,Genetic ,Receptor ,Melanocortin ,Type 1 ,Retrospective Studies ,Skin Neoplasms ,IMI Study Group ,GEM Study Group ,M-SKIP Study Group - Abstract
BackgroundGermline variants in the melanocortin 1 receptor gene (MC1R) might increase the risk of childhood and adolescent melanoma, but a clear conclusion is challenging because of the low number of studies and cases. We assessed the association of MC1R variants with childhood and adolescent melanoma in a large study comparing the prevalence of MC1R variants in child or adolescent patients with melanoma to that in adult patients with melanoma and in healthy adult controls.MethodsIn this retrospective pooled analysis, we used the M-SKIP Project, the Italian Melanoma Intergroup, and other European groups (with participants from Australia, Canada, France, Greece, Italy, the Netherlands, Serbia, Spain, Sweden, Turkey, and the USA) to assemble an international multicentre cohort. We gathered phenotypic and genetic data from children or adolescents diagnosed with sporadic single-primary cutaneous melanoma at age 20 years or younger, adult patients with sporadic single-primary cutaneous melanoma diagnosed at age 35 years or older, and healthy adult individuals as controls. We calculated odds ratios (ORs) for childhood and adolescent melanoma associated with MC1R variants by multivariable logistic regression. Subgroup analysis was done for children aged 18 or younger and 14 years or younger.FindingsWe analysed data from 233 young patients, 932 adult patients, and 932 healthy adult controls. Children and adolescents had higher odds of carrying MC1R r variants than did adult patients (OR 1·54, 95% CI 1·02-2·33), including when analysis was restricted to patients aged 18 years or younger (1·80, 1·06-3·07). All investigated variants, except Arg160Trp, tended, to varying degrees, to have higher frequencies in young patients than in adult patients, with significantly higher frequencies found for Val60Leu (OR 1·60, 95% CI 1·05-2·44; p=0·04) and Asp294His (2·15, 1·05-4·40; p=0·04). Compared with those of healthy controls, young patients with melanoma had significantly higher frequencies of any MC1R variants.InterpretationOur pooled analysis of MC1R genetic data of young patients with melanoma showed that MC1R r variants were more prevalent in childhood and adolescent melanoma than in adult melanoma, especially in patients aged 18 years or younger. Our findings support the role of MC1R in childhood and adolescent melanoma susceptibility, with a potential clinical relevance for developing early melanoma detection and preventive strategies.FundingSPD-Pilot/Project-Award-2015; AIRC-MFAG-11831.
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- 2019
31. Inflammatory markers in women with reported benign gynecologic pathology: an analysis of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial
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King, Lauren A., Wentzensen, Nicolas, Purdue, Mark P., Katki, Hormuzd A., Pinto, Ligia A., and Trabert, Britton
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- 2022
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32. Coffee consumption and risk of renal cancer: a meta-analysis of cohort evidence
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Rhee, Jongeun, Lim, Rachel K., and Purdue, Mark P.
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- 2022
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33. Understanding racial disparities in renal cell carcinoma incidence : estimates of population attributable risk in two US populations
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Callahan, Catherine L., Schwartz, Kendra, Corley, Douglas A., Ruterbusch, Julie J., Zhao, Wei K., Shuch, Brian, Graubard, Barry I., Rothman, Nathaniel, Chow, Wong-Ho, Silverman, Debra T., Purdue, Mark P., and Hofmann, Jonathan N.
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- 2020
34. Occupational exposure to benzene and risk of non‐Hodgkin lymphoma in an extended follow‐up of two population‐based prospective cohorts of Chinese men and women.
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Bassig, Bryan A., Shu, Xiao‐Ou, Friesen, Melissa C., Vermeulen, Roel, Purdue, Mark P., Ji, Bu‐Tian, Yang, Gong, Wong, Jason Y. Y., Appel, Nathan, Hu, Wei, Gao, Yu‐Tang, Zheng, Wei, Rothman, Nathaniel, and Lan, Qing
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PROPORTIONAL hazards models ,CHRONIC lymphocytic leukemia ,OCCUPATIONAL exposure ,CHINESE people ,HOCKEY - Abstract
The carcinogenicity of benzene was reevaluated by the International Agency for Research on Cancer in 2017, with the Working Group reaffirming positive yet inconclusive associations with non‐Hodgkin lymphoma (NHL). To extend our previous observation of a significant exposure‐response for cumulative occupational benzene exposure and NHL risk among Chinese women in a population‐based cohort in Shanghai, we extended follow‐up of this cohort and pooled the data with a similarly designed population‐based cohort of men in Shanghai. Cumulative exposure estimates were derived for 134,449 participants in the pooled analysis by combining ordinal job‐exposure matrix intensity ratings with quantitative benzene measurements from an inspection database of Shanghai factories. Associations between benzene exposure metrics and NHL (n = 363 cases including multiple myeloma [MM]) were assessed using Cox proportional hazard models. Ever occupational exposure to benzene in the pooled population was associated with NHL risk (HR = 1.5, 95% CI = 1.2–2.0), and exposure‐response relationships were observed for increasing duration (ptrend =.003) and cumulative exposure (ptrend =.003). Associations with ever exposure, duration, and cumulative exposure were similar for NHL with and without MM in the case definition, including lifetime cumulative exposures in the highest quartile (HR = 1.6, 95% CI = 1.1–2.4 with MM included; HR = 1.7, 95% CI = 1.1–2.7 with MM excluded). An elevated risk of the chronic lymphocytic leukemia subtype was suggested in the pooled analyses (HR for ever vs. never exposure = 2.3, 95% CI = 0.9–5.6). These observations provide additional support for a plausible association between occupational benzene exposure and risk of NHL. [ABSTRACT FROM AUTHOR]
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- 2024
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35. Body mass index and risk of progression from monoclonal gammopathy of undetermined significance to multiple myeloma: Results from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial
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Chang, Vicky C., Khan, Ali A., Huang, Wen-Yi, Katki, Hormuzd A., Purdue, Mark P., Landgren, Ola, and Hofmann, Jonathan N.
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- 2022
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36. Mouthwash use and cancer of the head and neck
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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
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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
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- 2016
37. Comparison of hematological alterations and markers of B-cell activation in workers exposed to benzene, formaldehyde and trichloroethylene
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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
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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.
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- 2016
38. Low frequency of cigarette smoking and the risk of head and neck cancer in the INHANCE consortium pooled analysis
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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
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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.
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- 2016
39. Genetically predicted longer telomere length is associated with increased risk of B-cell lymphoma subtypes
- Author
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Machiela, Mitchell J, Lan, Qing, Slager, Susan L, Vermeulen, Roel CH, Teras, Lauren R, Camp, Nicola J, Cerhan, James R, Spinelli, John J, Wang, Sophia S, Nieters, Alexandra, Vijai, Joseph, Yeager, Meredith, Wang, Zhaoming, Ghesquières, Hervé, McKay, James, Conde, Lucia, de Bakker, Paul IW, Cox, David G, Burdett, Laurie, Monnereau, Alain, Flowers, Christopher R, De Roos, Anneclaire J, Brooks-Wilson, Angela R, Giles, Graham G, Melbye, Mads, Gu, Jian, Jackson, Rebecca D, Kane, Eleanor, Purdue, Mark P, Vajdic, Claire M, Albanes, Demetrius, Kelly, Rachel S, Zucca, Mariagrazia, Bertrand, Kimberly A, Zeleniuch-Jacquotte, Anne, Lawrence, Charles, Hutchinson, Amy, Zhi, Degui, Habermann, Thomas M, Link, Brian K, Novak, Anne J, Dogan, Ahmet, Asmann, Yan W, Liebow, Mark, Thompson, Carrie A, Ansell, Stephen M, Witzig, Thomas E, Tilly, Hervé, Haioun, Corinne, Molina, Thierry J, Hjalgrim, Henrik, Glimelius, Bengt, Adami, Hans-Olov, Roos, Göran, Bracci, Paige M, Riby, Jacques, Smith, Martyn T, Holly, Elizabeth A, Cozen, Wendy, Hartge, Patricia, Morton, Lindsay M, Severson, Richard K, Tinker, Lesley F, North, Kari E, Becker, Nikolaus, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, Staines, Anthony, Lightfoot, Tracy, Crouch, Simon, Smith, Alex, Roman, Eve, Diver, W Ryan, Offit, Kenneth, Zelenetz, Andrew, Klein, Robert J, Villano, Danylo J, Zheng, Tongzhang, Zhang, Yawei, Holford, Theodore R, Turner, Jenny, Southey, Melissa C, Clavel, Jacqueline, Virtamo, Jarmo, Weinstein, Stephanie, Riboli, Elio, Vineis, Paolo, Kaaks, Rudolph, Boeing, Heiner, Tjønneland, Anne, Angelucci, Emanuele, Di Lollo, Simonetta, Rais, Marco, De Vivo, Immaculata, Giovannucci, Edward, Kraft, Peter, and Huang, Jinyan
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Clinical Research ,Rare Diseases ,Genetics ,Cancer ,Hematology ,Lymphoma ,Adolescent ,Adult ,Age Factors ,Aged ,Aged ,80 and over ,Female ,Genetic Association Studies ,Genetic Predisposition to Disease ,Humans ,Lymphoma ,B-Cell ,Male ,Middle Aged ,Prospective Studies ,Telomere ,Biological Sciences ,Medical and Health Sciences ,Genetics & Heredity - Abstract
Evidence from a small number of studies suggests that longer telomere length measured in peripheral leukocytes is associated with an increased risk of non-Hodgkin lymphoma (NHL). However, these studies may be biased by reverse causation, confounded by unmeasured environmental exposures and might miss time points for which prospective telomere measurement would best reveal a relationship between telomere length and NHL risk. We performed an analysis of genetically inferred telomere length and NHL risk in a study of 10 102 NHL cases of the four most common B-cell histologic types and 9562 controls using a genetic risk score (GRS) comprising nine telomere length-associated single-nucleotide polymorphisms. This approach uses existing genotype data and estimates telomere length by weighing the number of telomere length-associated variant alleles an individual carries with the published change in kb of telomere length. The analysis of the telomere length GRS resulted in an association between longer telomere length and increased NHL risk [four B-cell histologic types combined; odds ratio (OR) = 1.49, 95% CI 1.22-1.82,P-value = 8.5 × 10(-5)]. Subtype-specific analyses indicated that chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL/SLL) was the principal NHL subtype contributing to this association (OR = 2.60, 95% CI 1.93-3.51,P-value = 4.0 × 10(-10)). Significant interactions were observed across strata of sex for CLL/SLL and marginal zone lymphoma subtypes as well as age for the follicular lymphoma subtype. Our results indicate that a genetic background that favors longer telomere length may increase NHL risk, particularly risk of CLL/SLL, and are consistent with earlier studies relating longer telomere length with increased NHL risk.
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- 2016
40. Identification of a novel susceptibility locus at 13q34 and refinement of the 20p12.2 region as a multi-signal locus associated with bladder cancer risk in individuals of European ancestry
- Author
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Figueroa, Jonine D, Middlebrooks, Candace D, Banday, A Rouf, Ye, Yuanqing, Garcia-Closas, Montserrat, Chatterjee, Nilanjan, Koutros, Stella, Kiemeney, Lambertus A, Rafnar, Thorunn, Bishop, Timothy, Furberg, Helena, Matullo, Giuseppe, Golka, Klaus, Gago-Dominguez, Manuela, Taylor, Jack A, Fletcher, Tony, Siddiq, Afshan, Cortessis, Victoria K, Kooperberg, Charles, Cussenot, Olivier, Benhamou, Simone, Prescott, Jennifer, Porru, Stefano, Dinney, Colin P, Malats, Núria, Baris, Dalsu, Purdue, Mark P, Jacobs, Eric J, Albanes, Demetrius, Wang, Zhaoming, Chung, Charles C, Vermeulen, Sita H, Aben, Katja K, Galesloot, Tessel E, Thorleifsson, Gudmar, Sulem, Patrick, Stefansson, Kari, Kiltie, Anne E, Harland, Mark, Teo, Mark, Offit, Kenneth, Vijai, Joseph, Bajorin, Dean, Kopp, Ryan, Fiorito, Giovanni, Guarrera, Simonetta, Sacerdote, Carlotta, Selinski, Silvia, Hengstler, Jan G, Gerullis, Holger, Ovsiannikov, Daniel, Blaszkewicz, Meinolf, Castelao, Jose Esteban, Calaza, Manuel, Martinez, Maria Elena, Cordeiro, Patricia, Xu, Zongli, Panduri, Vijayalakshmi, Kumar, Rajiv, Gurzau, Eugene, Koppova, Kvetoslava, Bueno-De-Mesquita, H Bas, Ljungberg, Börje, Clavel-Chapelon, Françoise, Weiderpass, Elisabete, Krogh, Vittorio, Dorronsoro, Miren, Travis, Ruth C, Tjønneland, Anne, Brennan, Paul, Chang-Claude, Jenny, Riboli, Elio, Conti, David, Stern, Marianna C, Pike, Malcolm C, Van Den Berg, David, Yuan, Jian-Min, Hohensee, Chancellor, Jeppson, Rebecca P, Cancel-Tassin, Geraldine, Roupret, Morgan, Comperat, Eva, Turman, Constance, De Vivo, Immaculata, Giovannucci, Edward, Hunter, David J, Kraft, Peter, Lindstrom, Sara, Carta, Angela, Pavanello, Sofia, Arici, Cecilia, Mastrangelo, Giuseppe, Kamat, Ashish M, Zhang, Liren, Gong, Yilei, Pu, Xia, Hutchinson, Amy, Burdett, Laurie, Wheeler, William A, and Karagas, Margaret R
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Cancer ,Prevention ,Human Genome ,Genetics ,Biotechnology ,Urologic Diseases ,Aetiology ,2.1 Biological and endogenous factors ,Biomarkers ,Tumor ,Case-Control Studies ,Chromosomes ,Human ,Pair 13 ,Chromosomes ,Human ,Pair 20 ,Female ,Genetic Association Studies ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Humans ,Linkage Disequilibrium ,Male ,Polymorphism ,Single Nucleotide ,Risk Factors ,Urinary Bladder Neoplasms ,White People ,Biological Sciences ,Medical and Health Sciences ,Genetics & Heredity - Abstract
Candidate gene and genome-wide association studies (GWAS) have identified 15 independent genomic regions associated with bladder cancer risk. In search for additional susceptibility variants, we followed up on four promising single-nucleotide polymorphisms (SNPs) that had not achieved genome-wide significance in 6911 cases and 11 814 controls (rs6104690, rs4510656, rs5003154 and rs4907479, P < 1 × 10(-6)), using additional data from existing GWAS datasets and targeted genotyping for studies that did not have GWAS data. In a combined analysis, which included data on up to 15 058 cases and 286 270 controls, two SNPs achieved genome-wide statistical significance: rs6104690 in a gene desert at 20p12.2 (P = 2.19 × 10(-11)) and rs4907479 within the MCF2L gene at 13q34 (P = 3.3 × 10(-10)). Imputation and fine-mapping analyses were performed in these two regions for a subset of 5551 bladder cancer cases and 10 242 controls. Analyses at the 13q34 region suggest a single signal marked by rs4907479. In contrast, we detected two signals in the 20p12.2 region-the first signal is marked by rs6104690, and the second signal is marked by two moderately correlated SNPs (r(2) = 0.53), rs6108803 and the previously reported rs62185668. The second 20p12.2 signal is more strongly associated with the risk of muscle-invasive (T2-T4 stage) compared with non-muscle-invasive (Ta, T1 stage) bladder cancer (case-case P ≤ 0.02 for both rs62185668 and rs6108803). Functional analyses are needed to explore the biological mechanisms underlying these novel genetic associations with risk for bladder cancer.
- Published
- 2016
41. Validity of retrospective occupational exposure estimates of lead and manganese in a case–control study
- Author
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Sauvé, Jean-François, Ramsay, Joemy M, Locke, Sarah J, Dopart, Pamela J, Josse, Pabitra R, Zaebst, Dennis D, Albert, Paul S, Cantor, Kenneth P, Baris, Dalsu, Jackson, Brian P, Karagas, Margaret R, Hosain, GM Monawar, Schwenn, Molly, Johnson, Alison, Purdue, Mark P, Koutros, Stella, Silverman, Debra T, and Friesen, Melissa C
- Published
- 2019
42. Case-control investigation of occupational lead exposure and kidney cancer
- Author
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Callahan, Catherine L, Friesen, Melissa C, Locke, Sarah J, Dopart, Pamela J, Stewart, Patricia A, Schwartz, Kendra, Ruterbusch, Julie J, Graubard, Barry I, Chow, Wong-Ho, Rothman, Nathaniel, Hofmann, Jonathan N, and Purdue, Mark P
- Published
- 2019
43. Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
- Author
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Sampson, Joshua N, Wheeler, William A, Yeager, Meredith, Panagiotou, Orestis, Wang, Zhaoming, Berndt, Sonja I, Lan, Qing, Abnet, Christian C, Amundadottir, Laufey T, Figueroa, Jonine D, Landi, Maria Teresa, Mirabello, Lisa, Savage, Sharon A, Taylor, Philip R, De Vivo, Immaculata, McGlynn, Katherine A, Purdue, Mark P, Rajaraman, Preetha, Adami, Hans-Olov, Ahlbom, Anders, Albanes, Demetrius, Amary, Maria Fernanda, An, She-Juan, Andersson, Ulrika, Andriole, Gerald, Andrulis, Irene L, Angelucci, Emanuele, Ansell, Stephen M, Arici, Cecilia, Armstrong, Bruce K, Arslan, Alan A, Austin, Melissa A, Baris, Dalsu, Barkauskas, Donald A, Bassig, Bryan A, Becker, Nikolaus, Benavente, Yolanda, Benhamou, Simone, Berg, Christine, Van Den Berg, David, Bernstein, Leslie, Bertrand, Kimberly A, Birmann, Brenda M, Black, Amanda, Boeing, Heiner, Boffetta, Paolo, Boutron-Ruault, Marie-Christine, Bracci, Paige M, Brinton, Louise, Brooks-Wilson, Angela R, Bueno-de-Mesquita, H Bas, Burdett, Laurie, Buring, Julie, Butler, Mary Ann, Cai, Qiuyin, Cancel-Tassin, Geraldine, Canzian, Federico, Carrato, Alfredo, Carreon, Tania, Carta, Angela, Chan, John KC, Chang, Ellen T, Chang, Gee-Chen, Chang, I-Shou, Chang, Jiang, Chang-Claude, Jenny, Chen, Chien-Jen, Chen, Chih-Yi, Chen, Chu, Chen, Chung-Hsing, Chen, Constance, Chen, Hongyan, Chen, Kexin, Chen, Kuan-Yu, Chen, Kun-Chieh, Chen, Ying, Chen, Ying-Hsiang, Chen, Yi-Song, Chen, Yuh-Min, Chien, Li-Hsin, Chirlaque, María-Dolores, Choi, Jin Eun, Choi, Yi Young, Chow, Wong-Ho, Chung, Charles C, Clavel, Jacqueline, Clavel-Chapelon, Françoise, Cocco, Pierluigi, Colt, Joanne S, Comperat, Eva, Conde, Lucia, Connors, Joseph M, Conti, David, Cortessis, Victoria K, Cotterchio, Michelle, Cozen, Wendy, Crouch, Simon, Crous-Bou, Marta, Cussenot, Olivier, and Davis, Faith G
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Tobacco ,Clinical Research ,Urologic Diseases ,Lung ,Genetics ,Rare Diseases ,Lung Cancer ,Human Genome ,Hematology ,Cancer ,Tobacco Smoke and Health ,Prevention ,Lymphoma ,Adult ,Aged ,Asian People ,Bone Neoplasms ,Female ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Humans ,Kidney Neoplasms ,Leukemia ,Lymphocytic ,Chronic ,B-Cell ,Lung Neoplasms ,Lymphoma ,Large B-Cell ,Diffuse ,Male ,Middle Aged ,Neoplasms ,Osteosarcoma ,Polymorphism ,Single Nucleotide ,Smoking ,Testicular Neoplasms ,Tissue Array Analysis ,Urinary Bladder Neoplasms ,White People ,Oncology and Carcinogenesis ,Oncology & Carcinogenesis - Abstract
BackgroundStudies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.MethodsBetween 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.ResultsGWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl (2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.ConclusionOur results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
- Published
- 2015
44. Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for Thirteen Cancer Types.
- Author
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Sampson, Joshua N, Wheeler, William A, Yeager, Meredith, Panagiotou, Orestis, Wang, Zhaoming, Berndt, Sonja I, Lan, Qing, Abnet, Christian C, Amundadottir, Laufey T, Figueroa, Jonine D, Landi, Maria Teresa, Mirabello, Lisa, Savage, Sharon A, Taylor, Philip R, De Vivo, Immaculata, McGlynn, Katherine A, Purdue, Mark P, Rajaraman, Preetha, Adami, Hans-Olov, Ahlbom, Anders, Albanes, Demetrius, Amary, Maria Fernanda, An, She-Juan, Andersson, Ulrika, Andriole, Gerald, Andrulis, Irene L, Angelucci, Emanuele, Ansell, Stephen M, Arici, Cecilia, Armstrong, Bruce K, Arslan, Alan A, Austin, Melissa A, Baris, Dalsu, Barkauskas, Donald A, Bassig, Bryan A, Becker, Nikolaus, Benavente, Yolanda, Benhamou, Simone, Berg, Christine, Van Den Berg, David, Bernstein, Leslie, Bertrand, Kimberly A, Birmann, Brenda M, Black, Amanda, Boeing, Heiner, Boffetta, Paolo, Boutron-Ruault, Marie-Christine, Bracci, Paige M, Brinton, Louise, Brooks-Wilson, Angela R, Bueno-de-Mesquita, H Bas, Burdett, Laurie, Buring, Julie, Butler, Mary Ann, Cai, Qiuyin, Cancel-Tassin, Geraldine, Canzian, Federico, Carrato, Alfredo, Carreon, Tania, Carta, Angela, Chan, John KC, Chang, Ellen T, Chang, Gee-Chen, Chang, I-Shou, Chang, Jiang, Chang-Claude, Jenny, Chen, Chien-Jen, Chen, Chih-Yi, Chen, Chu, Chen, Chung-Hsing, Chen, Constance, Chen, Hongyan, Chen, Kexin, Chen, Kuan-Yu, Chen, Kun-Chieh, Chen, Ying, Chen, Ying-Hsiang, Chen, Yi-Song, Chen, Yuh-Min, Chien, Li-Hsin, Chirlaque, María-Dolores, Choi, Jin Eun, Choi, Yi Young, Chow, Wong-Ho, Chung, Charles C, Clavel, Jacqueline, Clavel-Chapelon, Françoise, Cocco, Pierluigi, Colt, Joanne S, Comperat, Eva, Conde, Lucia, Connors, Joseph M, Conti, David, Cortessis, Victoria K, Cotterchio, Michelle, Cozen, Wendy, Crouch, Simon, Crous-Bou, Marta, Cussenot, Olivier, and Davis, Faith G
- Subjects
Humans ,Neoplasms ,Osteosarcoma ,Bone Neoplasms ,Testicular Neoplasms ,Lung Neoplasms ,Kidney Neoplasms ,Genetic Predisposition to Disease ,Tissue Array Analysis ,Smoking ,Polymorphism ,Single Nucleotide ,Adult ,Aged ,Middle Aged ,Asian Continental Ancestry Group ,European Continental Ancestry Group ,Female ,Male ,Urinary Bladder Neoplasms ,Leukemia ,Lymphocytic ,Chronic ,B-Cell ,Lymphoma ,Large B-Cell ,Diffuse ,Genome-Wide Association Study ,Polymorphism ,Single Nucleotide ,Leukemia ,Lymphocytic ,Chronic ,B-Cell ,Lymphoma ,Large B-Cell ,Diffuse ,Oncology And Carcinogenesis ,Oncology & Carcinogenesis ,Oncology and Carcinogenesis - Abstract
BackgroundStudies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.MethodsBetween 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.ResultsGWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl (2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.ConclusionOur results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
- Published
- 2015
45. Relation of allium vegetables intake with head and neck cancers: Evidence from the INHANCE consortium
- Author
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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
46. 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
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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.
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- 2015
47. Risk factors for head and neck cancer in young adults: a pooled analysis in the INHANCE consortium
- Author
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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
48. A genome-wide association study of marginal zone lymphoma shows association to the HLA region.
- Author
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Vijai, Joseph, Wang, Zhaoming, Berndt, Sonja I, Skibola, Christine F, Slager, Susan L, de Sanjose, Silvia, Melbye, Mads, Glimelius, Bengt, Bracci, Paige M, Conde, Lucia, Birmann, Brenda M, Wang, Sophia S, Brooks-Wilson, Angela R, Lan, Qing, de Bakker, Paul IW, Vermeulen, Roel CH, Portlock, Carol, Ansell, Stephen M, Link, Brian K, Riby, Jacques, North, Kari E, Gu, Jian, Hjalgrim, Henrik, Cozen, Wendy, Becker, Nikolaus, Teras, Lauren R, Spinelli, John J, Turner, Jenny, Zhang, Yawei, Purdue, Mark P, Giles, Graham G, Kelly, Rachel S, Zeleniuch-Jacquotte, Anne, Ennas, Maria Grazia, Monnereau, Alain, Bertrand, Kimberly A, Albanes, Demetrius, Lightfoot, Tracy, Yeager, Meredith, Chung, Charles C, Burdett, Laurie, Hutchinson, Amy, Lawrence, Charles, Montalvan, Rebecca, Liang, Liming, Huang, Jinyan, Ma, Baoshan, Villano, Danylo J, Maria, Ann, Corines, Marina, Thomas, Tinu, Novak, Anne J, Dogan, Ahmet, Liebow, Mark, Thompson, Carrie A, Witzig, Thomas E, Habermann, Thomas M, Weiner, George J, Smith, Martyn T, Holly, Elizabeth A, Jackson, Rebecca D, Tinker, Lesley F, Ye, Yuanqing, Adami, Hans-Olov, Smedby, Karin E, De Roos, Anneclaire J, Hartge, Patricia, Morton, Lindsay M, Severson, Richard K, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, McKay, James, Staines, Anthony, Diver, W Ryan, Vajdic, Claire M, Armstrong, Bruce K, Kricker, Anne, Zheng, Tongzhang, Holford, Theodore R, Severi, Gianluca, Vineis, Paolo, Ferri, Giovanni M, Ricco, Rosalia, Miligi, Lucia, Clavel, Jacqueline, Giovannucci, Edward, Kraft, Peter, Virtamo, Jarmo, Smith, Alex, Kane, Eleanor, Roman, Eve, Chiu, Brian CH, Fraumeni, Joseph F, Wu, Xifeng, Cerhan, James R, Offit, Kenneth, and Chanock, Stephen J
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Humans ,Membrane Glycoproteins ,Computational Biology ,Major Histocompatibility Complex ,Genotype ,Polymorphism ,Single Nucleotide ,European Continental Ancestry Group ,Lymphoma ,B-Cell ,Marginal Zone ,Genome-Wide Association Study ,Butyrophilins ,Polymorphism ,Single Nucleotide ,Lymphoma ,B-Cell ,Marginal Zone - Abstract
Marginal zone lymphoma (MZL) is the third most common subtype of B-cell non-Hodgkin lymphoma. Here we perform a two-stage GWAS of 1,281 MZL cases and 7,127 controls of European ancestry and identify two independent loci near BTNL2 (rs9461741, P=3.95 × 10(-15)) and HLA-B (rs2922994, P=2.43 × 10(-9)) in the HLA region significantly associated with MZL risk. This is the first evidence that genetic variation in the major histocompatibility complex influences MZL susceptibility.
- Published
- 2015
49. How well does a single blood sample represent long-term exposure for epidemiological studies of PFOA among men in the general population?
- Author
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Bartell, Scott M., Purdue, Mark P., Rhee, Jongeun, Nøst, Therese H., Rusiecki, Jennifer, and Steenland, Kyle
- Published
- 2024
- Full Text
- View/download PDF
50. Genome-wide association study identifies multiple susceptibility loci for diffuse large B cell lymphoma
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Cerhan, James R, Berndt, Sonja I, Vijai, Joseph, Ghesquières, Hervé, McKay, James, Wang, Sophia S, Wang, Zhaoming, Yeager, Meredith, Conde, Lucia, de Bakker, Paul IW, Nieters, Alexandra, Cox, David, Burdett, Laurie, Monnereau, Alain, Flowers, Christopher R, De Roos, Anneclaire J, Brooks-Wilson, Angela R, Lan, Qing, Severi, Gianluca, Melbye, Mads, Gu, Jian, Jackson, Rebecca D, Kane, Eleanor, Teras, Lauren R, Purdue, Mark P, Vajdic, Claire M, Spinelli, John J, Giles, Graham G, Albanes, Demetrius, Kelly, Rachel S, Zucca, Mariagrazia, Bertrand, Kimberly A, Zeleniuch-Jacquotte, Anne, Lawrence, Charles, Hutchinson, Amy, Zhi, Degui, Habermann, Thomas M, Link, Brian K, Novak, Anne J, Dogan, Ahmet, Asmann, Yan W, Liebow, Mark, Thompson, Carrie A, Ansell, Stephen M, Witzig, Thomas E, Weiner, George J, Veron, Amelie S, Zelenika, Diana, Tilly, Hervé, Haioun, Corinne, Molina, Thierry Jo, Hjalgrim, Henrik, Glimelius, Bengt, Adami, Hans-Olov, Bracci, Paige M, Riby, Jacques, Smith, Martyn T, Holly, Elizabeth A, Cozen, Wendy, Hartge, Patricia, Morton, Lindsay M, Severson, Richard K, Tinker, Lesley F, North, Kari E, Becker, Nikolaus, Benavente, Yolanda, Boffetta, Paolo, Brennan, Paul, Foretova, Lenka, Maynadie, Marc, Staines, Anthony, Lightfoot, Tracy, Crouch, Simon, Smith, Alex, Roman, Eve, Diver, W Ryan, Offit, Kenneth, Zelenetz, Andrew, Klein, Robert J, Villano, Danylo J, Zheng, Tongzhang, Zhang, Yawei, Holford, Theodore R, Kricker, Anne, Turner, Jenny, Southey, Melissa C, Clavel, Jacqueline, Virtamo, Jarmo, Weinstein, Stephanie, Riboli, Elio, Vineis, Paolo, Kaaks, Rudolph, Trichopoulos, Dimitrios, Vermeulen, Roel CH, Boeing, Heiner, Tjonneland, Anne, Angelucci, Emanuele, Di Lollo, Simonetta, Rais, Marco, and Birmann, Brenda M
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Human Genome ,Rare Diseases ,Genetics ,Cancer ,Hematology ,Lymphoma ,Aetiology ,2.1 Biological and endogenous factors ,Chromosome Mapping ,Computational Biology ,Genetic Loci ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,Genotype ,Humans ,Likelihood Functions ,Lymphoma ,Large B-Cell ,Diffuse ,Polymorphism ,Single Nucleotide ,Quantitative Trait Loci ,White People ,Biological Sciences ,Medical and Health Sciences ,Developmental Biology - Abstract
Diffuse large B cell lymphoma (DLBCL) is the most common lymphoma subtype and is clinically aggressive. To identify genetic susceptibility loci for DLBCL, we conducted a meta-analysis of 3 new genome-wide association studies (GWAS) and 1 previous scan, totaling 3,857 cases and 7,666 controls of European ancestry, with additional genotyping of 9 promising SNPs in 1,359 cases and 4,557 controls. In our multi-stage analysis, five independent SNPs in four loci achieved genome-wide significance marked by rs116446171 at 6p25.3 (EXOC2; P = 2.33 × 10(-21)), rs2523607 at 6p21.33 (HLA-B; P = 2.40 × 10(-10)), rs79480871 at 2p23.3 (NCOA1; P = 4.23 × 10(-8)) and two independent SNPs, rs13255292 and rs4733601, at 8q24.21 (PVT1; P = 9.98 × 10(-13) and 3.63 × 10(-11), respectively). These data provide substantial new evidence for genetic susceptibility to this B cell malignancy and point to pathways involved in immune recognition and immune function in the pathogenesis of DLBCL.
- Published
- 2014
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