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17 results on '"Barnett, Matt P."'

9. Large-scale association analysis identifies new lung cancer susceptibility loci and heterogeneity in genetic susceptibility across histological subtypes

Author

McKay, James D, Hung, Rayjean J, Han, Younghun, Zong, Xuchen, Carreras-Torres, Robert, Christiani, David Christopher, Caporaso, Neil E, Johansson, Mattias, Xiao, Xiangjun, Li, Yafang, Byun, Jinyoung, Dunning, Alison, Pooley, Karen A, Qian, David C, Ji, Xuemei, Liu, Geoffrey, Timofeeva, Maria N, Bojesen, Stig E, Wu, Xifeng, Le Marchand, Loic, Albanes, Demetrios, Bickeböller, Heike, Aldrich, Melinda C, Bush, William S, Tardon, Adonina, Rennert, Gad, Teare, M Dawn, Field, John K, Kiemeney, Lambertus A, Lazarus, Philip, Haugen, Aage, Lam, Stephen, Schabath, Matthew B, Andrew, Angeline S, Shen, Hongbing, Hong, Yun-Chul, Yuan, Jian-Min, Bertazzi, Pier Alberto, Pesatori, Angela C, Ye, Yuanqing, Diao, Nancy, Su, Li, Zhang, Ruyang, Brhane, Yonathan, Leighl, Natasha, Johansen, Jakob S, Mellemgaard, Anders, Saliba, Walid, Haiman, Christopher A, Wilkens, Lynne R, Fernandez-Somoano, Ana, Fernandez-Tardon, Guillermo, van der Heijden, Henricus F M, Kim, Jin Hee, Dai, Juncheng, Hu, Zhibin, Davies, Michael P A, Marcus, Michael W, Brunnström, Hans, Manjer, Jonas, Melander, Olle, Muller, David C, Overvad, Kim, Trichopoulou, Antonia, Tumino, Rosario, Doherty, Jennifer A, Barnett, Matt P, Chen, Chu, Goodman, Gary E, Cox, Angela, Taylor, Fiona, Woll, Penella, Brüske, Irene, Wichmann, H-Erich, Manz, Judith, Muley, Thomas R, Risch, Angela, Rosenberger, Albert, Grankvist, Kjell, Johansson, Mikael, Shepherd, Frances A, Tsao, Ming-Sound, Arnold, Susanne M, Haura, Eric B, Bolca, Ciprian, Holcatova, Ivana, Janout, Vladimir, Kontic, Milica, Lissowska, Jolanta, Mukeria, Anush, Ognjanovic, Simona, Orlowski, Tadeusz M, Scelo, Ghislaine, Swiatkowska, Beata, Zaridze, David, Bakke, Per, Skaug, Vidar, Zienolddiny, Shanbeh, Duell, Eric J, Butler, Lesley M, Koh, Woon-Puay, Gao, Yu-Tang, Houlston, Richard S, McLaughlin, John, Stevens, Victoria L, Joubert, Philippe, Lamontagne, Maxime, Nickle, David C, Obeidat, Ma, Timens, Wim, Zhu, Bin, Song, Lei, Kachuri, Linda, Artigas, María Soler, Tobin, Martin D, Wain, Louise V, Rafnar, Thorunn, Thorgeirsson, Thorgeir E, Reginsson, Gunnar W, Stefansson, Kari, Hancock, Dana B, Bierut, Laura J, Spitz, Margaret R, Gaddis, Nathan C, Lutz, Sharon M, Gu, Fangyi, Johnson, Eric O, Kamal, Ahsan, Pikielny, Claudio, Zhu, Dakai, Lindströem, Sara, Jiang, Xia, Tyndale, Rachel F, Chenevix-Trench, Georgia, Beesley, Jonathan, Bossé, Yohan, Chanock, Stephen, Brennan, Paul, Landi, Maria Teresa, and Amos, Christopher I

Published
2017
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10. Selenium and Prostate Cancer: Analysis of Individual Participant Data From Fifteen Prospective Studies

Author

Allen, Naomi E., Travis, Ruth C., Appleby, Paul N., Albanes, Demetrius, Barnett, Matt J., Black, Amanda, Bueno-de-Mesquita, H. Bas, Deschasaux, Mélanie, Galan, Pilar, Goodman, Gary E., Goodman, Phyllis J., Gunter, Marc J., Heliövaara, Markku, Helzlsouer, Kathy J., Henderson, Brian E., Hercberg, Serge, Knekt, Paul, Kolonel, Laurence N., Lasheras, Christina, Linseisen, Jakob, Metter, E. Jeffrey, Neuhouser, Marian L., Olsen, Anja, Pala, Valeria, Platz, Elizabeth A., Rissanen, Harri, Reid, Mary E., Schenk, Jeannette M., Stampfer, Meir J., Stattin, Pär, Tangen, Catherine M., Touvier, Mathilde, Trichopoulou, Antonia, van den Brandt, Piet A., and Key, Timothy J.

Abstract

Background: Some observational studies suggest that a higher selenium status is associated with a lower risk of prostate cancer but have been generally too small to provide precise estimates of associations, particularly by disease stage and grade. Methods: Collaborating investigators from 15 prospective studies provided individual-participant records (from predominantly men of white European ancestry) on blood or toenail selenium concentrations and prostate cancer risk. Odds ratios of prostate cancer by selenium concentration were estimated using multivariable-adjusted conditional logistic regression. All statistical tests were two-sided. Results: Blood selenium was not associated with the risk of total prostate cancer (multivariable-adjusted odds ratio [OR] per 80 percentile increase = 1.01, 95% confidence interval [CI] = 0.83 to 1.23, based on 4527 case patients and 6021 control subjects). However, there was heterogeneity by disease aggressiveness (ie, advanced stage and/or prostate cancer death, Pheterogeneity = .01), with high blood selenium associated with a lower risk of aggressive disease (OR = 0.43, 95% CI = 0.21 to 0.87) but not with nonaggressive disease. Nail selenium was inversely associated with total prostate cancer (OR = 0.29, 95% CI = 0.22 to 0.40, Ptrend < .001, based on 1970 case patients and 2086 control subjects), including both nonaggressive (OR = 0.33, 95% CI = 0.22 to 0.50) and aggressive disease (OR = 0.18, 95% CI = 0.11 to 0.31, Pheterogeneity = .08). Conclusions: Nail, but not blood, selenium concentration is inversely associated with risk of total prostate cancer, possibly because nails are a more reliable marker of long-term selenium exposure. Both blood and nail selenium concentrations are associated with a reduced risk of aggressive disease, which warrants further investigation.

Published
2016
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12. Dietary Supplement Use and Prostate Cancer Risk in the Carotene and Retinol Efficacy Trial.

Author

Neuhouser, Marian L., Barnett, Matt J., Kristal, Alan R., Ambrosone, Christine B., King, Irena B., Thomquist, Mark, and Goodman, Gary G.

Abstract

The article presents a study on the Carotene and Retinol Placebo Efficacy Trial (CARET) associated with dietary supplement use and prostate cancer risk. The method of the study includes the placebo intervention among 18,314 individuals by which their dietary supplements, health history, and lifestyle habits were assessed. Using the Cox proportion, men in the placebo intervention arm associated with additional supplement consumption manifest relative risk for aggressive prostate cancer.

Published
2009
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13. V89L Polymorphism of the 5α-Reductase Type II Gene (SRD5A2), Endogenous Sex Hormones, and Prostate Cancer Risk.

Author

Boger-Megiddo, Inbal, Weiss, Noel S., Barnett, Matt J., Goodman, Gary E., and Chu Chen

Abstract

The article focuses on the results of a study which examined the combined effect of circulating sex hormones and SRD5A2 V89L polymorphism on prostate cancer risk. It notes that prostate cancer is the most common cancer and is the second most common cause of cancer mortality in men in the U.S. It associates above-median serum levels of dehydroepiandrosterone sulfate (DHEAS) and 3α-diol with the risk of aggressive prostate cancer.

Published
2008
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14. Polymorphisms in Oxidative Stress-Related Genes Are Not Associated with Prostate Cancer Risk in Heavy Smokers.

Author

Ji-Yeob Choi, Marian L., Neuhouser, Barnett, Matt, Hudson, Matthew, Kristal, Alan R., Thornquist, Mark, King, Irena B., Goodman, Gary E., and Ambrosone, Christine B.

Abstract

The article provides information on a study that evaluated potential associations between gene variants that result in reduced neutralization of reactive oxygen species and prostate cancer risk among men with incident prostate cancer. It concludes that genetic polymorphisms in genes relevant to oxidative stress may not play an important role in the development of prostate cancer, particularly among heavy smokers and men with occupational exposure to asbestos.

Published
2007
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15. Associated Links Among Smoking, Chronic Obstructive Pulmonary Disease, and Small Cell Lung Cancer: A Pooled Analysis in the International Lung Cancer Consortium

Author

Huang, Ruyi, Wei, Yongyue, Hung, Rayjean J., Liu, Geoffrey, Su, Li, Zhang, Ruyang, Zong, Xuchen, Zhang, Zuo-Feng, Morgenstern, Hal, Brüske, Irene, Heinrich, Joachim, Hong, Yun-Chul, Kim, Jin Hee, Cote, Michele, Wenzlaff, Angela, Schwartz, Ann G., Stucker, Isabelle, Mclaughlin, John, Marcus, Michael W., Davies, Michael P.A., Liloglou, Triantafillos, Field, John K., Matsuo, Keitaro, Barnett, Matt, Thornquist, Mark, Goodman, Gary, Wang, Yi, Chen, Size, Yang, Ping, Duell, Eric J., Andrew, Angeline S., Lazarus, Philip, Muscat, Joshua, Woll, Penella, Horsman, Janet, Dawn Teare, M., Flugelman, Anath, Rennert, Gad, Zhang, Yan, Brenner, Hermann, Stegmaier, Christa, van der Heijden, Erik H.F.M., Aben, Katja, Kiemeney, Lambertus, Barros-Dios, Juan, Pérez-Ríos, Monica, Ruano-Ravina, Alberto, Caporaso, Neil E., Bertazzi, Pier Alberto, Landi, Maria Teresa, Dai, Juncheng, Shen, Hongbing, Fernandez-Tardon, Guillermo, Rodriguez-Suarez, Marta, Tardon, Adonina, and Christiani, David C.

Subjects
COPD, chronic obstructive pulmonary disease, CPG, cigarettes per day, ILCCO, International Lung Cancer Consortium, MeSH, medical subject headings, NSCLC, non-small cell lung cancer, OR, odds ratio, SCLC, small cell lung cancer, Smoking behaviors, Chronic obstructive pulmonary disease, Small cell lung cancer risk, Multicenter pooling, Causal mediation analysis
Published
2015
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16. Circulating Fatty Acids and Prostate Cancer Risk: Individual Participant Meta-Analysis of Prospective Studies

Author

Crowe, Francesca L., Appleby, Paul N., Travis, Ruth C., Barnett, Matt, Brasky, Theodore M., Bueno-de-Mesquita, H. Bas, Chajes, Veronique, Chavarro, Jorge E., Chirlaque, Maria-Dolores, English, Dallas R., Gibson, Robert A., Giles, Graham G., Goodman, Gary E., Henning, Susanne M., Kaaks, Rudolf, King, Irena B., Kolonel, Lawrence N., Kristal, Alan R., Neuhouser, Marian L., Park, Song-Yi, Severi, Gianluca, Siddiq, Afshan, Stampfer, Meir J., Stattin, Pär, Tangen, Catherine M., Tjønneland, Anne, Trichopoulos, Dimitrios, Tumino, Rosario, Wilkens, Lynne R., Key, Timothy J., and Allen, Naomi E.

Abstract

Background: Individual studies have suggested that some circulating fatty acids are associated with prostate cancer risk, but have not been large enough to provide precise estimates of associations, particularly by stage and grade of disease. Methods: Principal investigators of prospective studies on circulating fatty acids and prostate cancer were invited to collaborate. Investigators provided individual participant data on circulating fatty acids (weight percent) and other characteristics of prostate cancer cases and controls. Prostate cancer risk by study-specific fifths of 14 fatty acids was estimated using multivariable-adjusted conditional logistic regression. All statistical tests were two-sided. Results: Five thousand and ninety-eight case patients and 6649 control patients from seven studies with an average follow-up of 5.1 (SD = 3.3) years were included. Stearic acid (18:0) was inversely associated with total prostate cancer (odds ratio [OR] Q5 vs Q1 = 0.88, 95% confidence interval [CI] = 0.78 to 1.00, P trend = .043). Prostate cancer risk was, respectively, 14% and 16% greater in the highest fifth of eicosapentaenoic acid (20:5n-3) (OR = 1.14, 95% CI = 1.01 to 1.29, P trend = .001) and docosapentaenoic acid (22:5n-3) (OR = 1.16, 95% CI = 1.02 to 1.33, P trend = .003), but in each case there was heterogeneity between studies (P = .022 and P < .001, respectively). There was heterogeneity in the association between docosapentaenoic acid and prostate cancer by grade of disease (P = .006); the association was statistically significant for low-grade disease but not high-grade disease. The remaining 11 fatty acids were not statistically associated with total prostate cancer risk. Conclusion: There was no strong evidence that circulating fatty acids are important predictors of prostate cancer risk. It is not clear whether the modest associations of stearic, eicosapentaenoic, and docosapentaenoic acid are causal.

Published
2014
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17. A Mouse to Human Search for Plasma Proteome Changes Associated with Pancreatic Tumor Development

Author

Faca, Vitor M, Song, Kenneth S, Krasnoselsky, Alexei L, Newcomb, Lisa F, Plentz, Ruben R, Redston, Mark S, Pitteri, Sharon J, Pereira-Faca, Sandra R, Ireton, Renee C, Katayama, Hiroyuki, Glukhova, Veronika, Phanstiel, Douglas, Brenner, Dean E, Anderson, Michelle A, Misek, David, Scholler, Nathalie, Urban, Nicole D, Barnett, Matt J, Edelstein, Cim, Goodman, Gary E, Thornquist, Mark D, McIntosh, Martin W, Bardeesy, Nabeel, Hanash, Samir M, Wang, Hong, Zhang, Qing, Gurumurthy, Sushma, and DePinho, Ronald A.

Abstract

Background: The complexity and heterogeneity of the human plasma proteome have presented significant challenges in the identification of protein changes associated with tumor development. Refined genetically engineered mouse (GEM) models of human cancer have been shown to faithfully recapitulate the molecular, biological, and clinical features of human disease. Here, we sought to exploit the merits of a well-characterized GEM model of pancreatic cancer to determine whether proteomics technologies allow identification of protein changes associated with tumor development and whether such changes are relevant to human pancreatic cancer. Methods and Findings: Plasma was sampled from mice at early and advanced stages of tumor development and from matched controls. Using a proteomic approach based on extensive protein fractionation, we confidently identified 1,442 proteins that were distributed across seven orders of magnitude of abundance in plasma. Analysis of proteins chosen on the basis of increased levels in plasma from tumor-bearing mice and corroborating protein or RNA expression in tissue documented concordance in the blood from 30 newly diagnosed patients with pancreatic cancer relative to 30 control specimens. A panel of five proteins selected on the basis of their increased level at an early stage of tumor development in the mouse was tested in a blinded study in 26 humans from the CARET (Carotene and Retinol Efficacy Trial) cohort. The panel discriminated pancreatic cancer cases from matched controls in blood specimens obtained between 7 and 13 mo prior to the development of symptoms and clinical diagnosis of pancreatic cancer. Conclusions: Our findings indicate that GEM models of cancer, in combination with in-depth proteomic analysis, provide a useful strategy to identify candidate markers applicable to human cancer with potential utility for early detection.

Published
2008
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