30 results on '"Goodman P.J."'
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2. The age-dependent association of risk factors with pancreatic cancer
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Yuan, C., primary, Kim, J., additional, Wang, Q.L., additional, Lee, A.A., additional, Babic, A., additional, Amundadottir, L.T., additional, Klein, A.P., additional, Li, D., additional, McCullough, M.L., additional, Petersen, G.M., additional, Risch, H.A., additional, Stolzenberg-Solomon, R.Z., additional, Perez, K., additional, Ng, K., additional, Giovannucci, E.L., additional, Stampfer, M.J., additional, Kraft, P., additional, Wolpin, B.M., additional, Ardanaz, E., additional, Arslan, A.A., additional, Beane-Freeman, L.E., additional, Bracci, P.M., additional, Bueno-de-Mesquita, B., additional, Du, M., additional, Gallinger, S., additional, Giles, G.G., additional, Goodman, P.J., additional, Katzke, V.A., additional, Kooperberg, C., additional, Malats, N., additional, Marchand, L.L., additional, Milne, R.L., additional, Neoptolemos, J.P., additional, Perdomo, S., additional, Shu, X.O., additional, Van Den Eeden, S.K., additional, Visvanathan, K., additional, White, E., additional, and Zheng, W., additional
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- 2022
- Full Text
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3. Corrigendum to ‘Measures of body fatness and height in early and mid-to-late adulthood and prostate cancer: risk and mortality in The Pooling Project of Prospective Studies of Diet and Cancer’
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Genkinger, J.M., primary, Wu, K., additional, Wang, M., additional, Albanes, D., additional, Black, A., additional, van den Brandt, P.A., additional, Burke, K.A., additional, Cook, M.B., additional, Gapstur, S.M., additional, Giles, G.G., additional, Giovannucci, E., additional, Goodman, G.G., additional, Goodman, P.J., additional, Håkansson, N., additional, Key, T.J., additional, Männistö, S., additional, Le Marchand, L., additional, Liao, L.M., additional, MacInnis, R.J., additional, Neuhouser, M.L., additional, Platz, E.A., additional, Sawada, N., additional, Schenk, J.M., additional, Stevens, V.L., additional, Travis, R.C., additional, Tsugane, S., additional, Visvanathan, K., additional, Wilkens, L.R., additional, Wolk, A., additional, and Smith-Warner, S.A., additional
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- 2021
- Full Text
- View/download PDF
4. Mendelian randomization analysis of n-6 polyunsaturated fatty acid levels and pancreatic cancer risk.
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Ghoneim D.H., Zhu J., Zheng W., Long J., Murff H.J., Ye F., Setiawan V.W., Wilkens L.R., Khankari N.K., Haycock P., Antwi S.O., Yang Y., Arslan A.A., Freeman L.E.B., Bracci P.M., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Scelo G., Visvanathan K., White E., Albane D., Amiano P., Andreott G., Babic A., Bamlet W.R., Berndt S.I., Brais L.K., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Rabe K.G., Chanock S.J., Duggal P., Fuchs C.S., Gaziano J.M., Goggins M.G., Hackert T., Hassan M.M., Helzlsouer K.J., Holly E.A., Hoover R.N., Katske V., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Oberg A.L., Porta M., Rothman N., Sesso H.D., Silverman D.T., Ian T., Wactawski-Wende J., Wang X., Wentzensen N., Yu H., Zeleniuch-Jacquotte A., Yu K., Wolpin B.M., Jacobs E.J., Duell E.J., Risch H.A., Petersen G.M., Amundadottir L.T., Kraft P., Klein A.P., Stolzenberg-Solomon R.Z., Shu X.-O., Wu L., Ghoneim D.H., Zhu J., Zheng W., Long J., Murff H.J., Ye F., Setiawan V.W., Wilkens L.R., Khankari N.K., Haycock P., Antwi S.O., Yang Y., Arslan A.A., Freeman L.E.B., Bracci P.M., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Scelo G., Visvanathan K., White E., Albane D., Amiano P., Andreott G., Babic A., Bamlet W.R., Berndt S.I., Brais L.K., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Rabe K.G., Chanock S.J., Duggal P., Fuchs C.S., Gaziano J.M., Goggins M.G., Hackert T., Hassan M.M., Helzlsouer K.J., Holly E.A., Hoover R.N., Katske V., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Oberg A.L., Porta M., Rothman N., Sesso H.D., Silverman D.T., Ian T., Wactawski-Wende J., Wang X., Wentzensen N., Yu H., Zeleniuch-Jacquotte A., Yu K., Wolpin B.M., Jacobs E.J., Duell E.J., Risch H.A., Petersen G.M., Amundadottir L.T., Kraft P., Klein A.P., Stolzenberg-Solomon R.Z., Shu X.-O., and Wu L.
- Abstract
Background: Whether circulating polyunsaturated fatty acid (PUFA) levels are associated with pancreatic cancer risk is uncertain. Mendelian randomization (MR) represents a study design using genetic instruments to better characterize the relationship between exposure and outcome. Method(s): We utilized data from genome-wide association studies within the Pancreatic Cancer Cohort Consortium and Pancreatic Cancer Case-Control Consortium, involving approximately 9,269 cases and 12,530 controls of European descent, to evaluate associations between pancreatic cancer risk and genetically predicted plasma n-6 PUFA levels. Conventional MR analyses were performed using individual-level and summary-level data. Result(s): Using genetic instruments, we did not find evidence of associations between genetically predicted plasma n-6 PUFA levels and pancreatic cancer risk [estimates per one SD increase in each PUFA-specific weighted genetic score using summary statistics: Linoleic acid odds ratio (OR)1.00, 95% confidence interval (CI) 0.98-1.02; arachidonic acid OR 1.00, 95% CI 0.99-1.01; and dihomo-gamma-linolenic acid OR 0.95, 95% CI 0.87-1.02]. The OR estimates remained virtually unchanged after adjustment for covariates, using individual-level data or summary statistics, or stratification by age and sex. Conclusion(s): Our results suggest that variations of genetically determined plasma n-6 PUFA levels are not associated with pancreatic cancer risk. Impact: These results suggest that modifying n-6 PUFA levels through food sources or supplementation may not influence risk of pancreatic cancer.Copyright © 2020 American Association for Cancer Research Inc.. All rights reserved.
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- 2021
5. Publisher Correction: Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction (Nature Genetics, (2021), 53, 1, (65-75), 10.1038/s41588-020-00748-0).
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Lessel D., Townsend P.A., Aukim-Hastie C., Bush W.S., Aldrich M.C., Crawford D.C., Srivastava S., Cullen J.C., Petrovics G., Casey G., Roobol M.J., Jenster G., van Schaik R.H.N., Hu J.J., Sanderson M., Varma R., McKean-Cowdin R., Torres M., Mancuso N., Berndt S.I., Van Den Eeden S.K., Easton D.F., Chanock S.J., Cook M.B., Wiklund F., Nakagawa H., Witte J.S., Eeles R.A., Kote-Jarai Z., Haiman C.A., Conti D.V., Darst B.F., Moss L.C., Saunders E.J., Sheng X., Chou A., Schumacher F.R., Olama A.A.A., Benlloch S., Dadaev T., Brook M.N., Sahimi A., Hoffmann T.J., Takahashi A., Matsuda K., Momozawa Y., Fujita M., Muir K., Lophatananon A., Wan P., Le Marchand L., Wilkens L.R., Stevens V.L., Gapstur S.M., Carter B.D., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Giles G.G., Southey M.C., MacInnis R.J., Cybulski C., Wokolorczyk D., Lubinski J., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Nordestgaard B.G., Nielsen S.F., Weischer M., Bojesen S.E., Roder M.A., Iversen P., Batra J., Chambers S., Moya L., Horvath L., Clements J.A., Tilley W., Risbridger G.P., Gronberg H., Aly M., Szulkin R., Eklund M., Nordstrom T., Pashayan N., Dunning A.M., Ghoussaini M., Travis R.C., Key T.J., Riboli E., Park J.Y., Sellers T.A., Lin H.-Y., Albanes D., Weinstein S.J., Mucci L.A., Giovannucci E., Lindstrom S., Kraft P., Hunter D.J., Penney K.L., Turman C., Tangen C.M., Goodman P.J., Thompson I.M., Hamilton R.J., Fleshner N.E., Finelli A., Parent M.-E., Stanford J.L., Ostrander E.A., Geybels M.S., Koutros S., Freeman L.E.B., Stampfer M., Wolk A., Hakansson N., Andriole G.L., Hoover R.N., Machiela M.J., Sorensen K.D., Borre M., Blot W.J., Zheng W., Yeboah E.D., Mensah J.E., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Wu Y., Zhao S.-C., Sun Z., Thibodeau S.N., McDonnell S.K., Schaid D.J., West C.M.L., Burnet N., Barnett G., Maier C., Schnoeller T., Luedeke M., Kibel A.S., Drake B.F., Cussenot O., Cancel-Tassin G., Menegaux F., Truong T., Koudou Y.A., John E.M., Grindedal E.M., Maehle L., Khaw K.-T., Ingles S.A., Stern M.C., Vega A., Gomez-Caamano A., Fachal L., Rosenstein B.S., Kerns S.L., Ostrer H., Teixeira M.R., Paulo P., Brandao A., Watya S., Lubwama A., Bensen J.T., Fontham E.T.H., Mohler J., Taylor J.A., Kogevinas M., Llorca J., Castano-Vinyals G., Cannon-Albright L., Teerlink C.C., Huff C.D., Strom S.S., Multigner L., Blanchet P., Brureau L., Kaneva R., Slavov C., Mitev V., Leach R.J., Weaver B., Brenner H., Cuk K., Holleczek B., Saum K.-U., Klein E.A., Hsing A.W., Kittles R.A., Murphy A.B., Logothetis C.J., Kim J., Neuhausen S.L., Steele L., Ding Y.C., Isaacs W.B., Nemesure B., Hennis A.J.M., Carpten J., Pandha H., Michael A., De Ruyck K., De Meerleer G., Ost P., Xu J., Razack A., Lim J., Teo S.-H., Newcomb L.F., Lin D.W., Fowke J.H., Neslund-Dudas C., Rybicki B.A., Gamulin M., Kulis T., Usmani N., Singhal S., Parliament M., Claessens F., Joniau S., Van den Broeck T., Gago-Dominguez M., Castelao J.E., Martinez M.E., Larkin S., Lessel D., Townsend P.A., Aukim-Hastie C., Bush W.S., Aldrich M.C., Crawford D.C., Srivastava S., Cullen J.C., Petrovics G., Casey G., Roobol M.J., Jenster G., van Schaik R.H.N., Hu J.J., Sanderson M., Varma R., McKean-Cowdin R., Torres M., Mancuso N., Berndt S.I., Van Den Eeden S.K., Easton D.F., Chanock S.J., Cook M.B., Wiklund F., Nakagawa H., Witte J.S., Eeles R.A., Kote-Jarai Z., Haiman C.A., Conti D.V., Darst B.F., Moss L.C., Saunders E.J., Sheng X., Chou A., Schumacher F.R., Olama A.A.A., Benlloch S., Dadaev T., Brook M.N., Sahimi A., Hoffmann T.J., Takahashi A., Matsuda K., Momozawa Y., Fujita M., Muir K., Lophatananon A., Wan P., Le Marchand L., Wilkens L.R., Stevens V.L., Gapstur S.M., Carter B.D., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Giles G.G., Southey M.C., MacInnis R.J., Cybulski C., Wokolorczyk D., Lubinski J., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Nordestgaard B.G., Nielsen S.F., Weischer M., Bojesen S.E., Roder M.A., Iversen P., Batra J., Chambers S., Moya L., Horvath L., Clements J.A., Tilley W., Risbridger G.P., Gronberg H., Aly M., Szulkin R., Eklund M., Nordstrom T., Pashayan N., Dunning A.M., Ghoussaini M., Travis R.C., Key T.J., Riboli E., Park J.Y., Sellers T.A., Lin H.-Y., Albanes D., Weinstein S.J., Mucci L.A., Giovannucci E., Lindstrom S., Kraft P., Hunter D.J., Penney K.L., Turman C., Tangen C.M., Goodman P.J., Thompson I.M., Hamilton R.J., Fleshner N.E., Finelli A., Parent M.-E., Stanford J.L., Ostrander E.A., Geybels M.S., Koutros S., Freeman L.E.B., Stampfer M., Wolk A., Hakansson N., Andriole G.L., Hoover R.N., Machiela M.J., Sorensen K.D., Borre M., Blot W.J., Zheng W., Yeboah E.D., Mensah J.E., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Wu Y., Zhao S.-C., Sun Z., Thibodeau S.N., McDonnell S.K., Schaid D.J., West C.M.L., Burnet N., Barnett G., Maier C., Schnoeller T., Luedeke M., Kibel A.S., Drake B.F., Cussenot O., Cancel-Tassin G., Menegaux F., Truong T., Koudou Y.A., John E.M., Grindedal E.M., Maehle L., Khaw K.-T., Ingles S.A., Stern M.C., Vega A., Gomez-Caamano A., Fachal L., Rosenstein B.S., Kerns S.L., Ostrer H., Teixeira M.R., Paulo P., Brandao A., Watya S., Lubwama A., Bensen J.T., Fontham E.T.H., Mohler J., Taylor J.A., Kogevinas M., Llorca J., Castano-Vinyals G., Cannon-Albright L., Teerlink C.C., Huff C.D., Strom S.S., Multigner L., Blanchet P., Brureau L., Kaneva R., Slavov C., Mitev V., Leach R.J., Weaver B., Brenner H., Cuk K., Holleczek B., Saum K.-U., Klein E.A., Hsing A.W., Kittles R.A., Murphy A.B., Logothetis C.J., Kim J., Neuhausen S.L., Steele L., Ding Y.C., Isaacs W.B., Nemesure B., Hennis A.J.M., Carpten J., Pandha H., Michael A., De Ruyck K., De Meerleer G., Ost P., Xu J., Razack A., Lim J., Teo S.-H., Newcomb L.F., Lin D.W., Fowke J.H., Neslund-Dudas C., Rybicki B.A., Gamulin M., Kulis T., Usmani N., Singhal S., Parliament M., Claessens F., Joniau S., Van den Broeck T., Gago-Dominguez M., Castelao J.E., Martinez M.E., and Larkin S.
- Abstract
In the version of this article originally published, the names of the equally contributing authors and jointly supervising authors were switched. The correct affiliations are: "These authors contributed equally: David V. Conti, Burcu F. Darst. These authors jointly supervised this work: David V. Conti, Rosalind A. Eeles, Zsofia Kote-Jarai, Christopher A. Haiman." The error has been corrected in the HTML and PDF versions of the article.Copyright © 2021, The Author(s), under exclusive licence to Springer Nature America, Inc.
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- 2021
6. Genome-wide genediabetes and geneobesity interaction scan in 8,255 cases and 11,900 controls from panscan and PanC4 consortia.
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Campa D., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A., Bueno-De-Mesquita B., Buring J.E., Chanock S.J., Childs E., Duell E.J., Fuchs C., Michael Gaziano J., Goggins M., Hartge P., Hassam M.H., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Orlow I., Peters U., Porta M., Rabe K.G., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Thompson I.M., Tjonneland A., Trichopoulou A., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Amundadottir L.T., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Chatterjee N., Klein A.P., Li D., Kraft P., Wei P., Tang H., Jiang L., Stolzenberg-Solomon R.Z., Arslan A.A., Beane Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., Giles G.G., Campa D., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A., Bueno-De-Mesquita B., Buring J.E., Chanock S.J., Childs E., Duell E.J., Fuchs C., Michael Gaziano J., Goggins M., Hartge P., Hassam M.H., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Orlow I., Peters U., Porta M., Rabe K.G., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Thompson I.M., Tjonneland A., Trichopoulou A., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Amundadottir L.T., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Chatterjee N., Klein A.P., Li D., Kraft P., Wei P., Tang H., Jiang L., Stolzenberg-Solomon R.Z., Arslan A.A., Beane Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., and Giles G.G.
- Abstract
Background: Obesity and diabetes are major modifiable risk factors for pancreatic cancer. Interactions between genetic variants and diabetes/obesity have not previously been comprehensively investigated in pancreatic cancer at the genome-wide level. Method(s): We conducted a gene-environment interaction (GxE) analysis including 8,255 cases and 11,900 controls from four pancreatic cancer genome-wide association study (GWAS) datasets (Pancreatic Cancer Cohort Consortium I-III and Pancreatic Cancer Case Control Consortium). Obesity (body mass index >=30 kg/m2) and diabetes (duration >=3 years) were the environmental variables of interest. Approximately 870,000 SNPs (minor allele frequency >=0.005, genotyped in at least one dataset) were analyzed. Case-control (CC), case-only (CO), and joint-effect test methods were used for SNP-level GxE analysis. As a complementary approach, gene-based GxE analysis was also performed. Age, sex, study site, and principal components accounting for population substructure were included as covariates. Meta-analysis was applied to combine individual GWAS summary statistics. Result(s): No genome-wide significant interactions (departures from a log-additive odds model) with diabetes or obesity were detected at the SNP level by the CC or CO approaches. The joint-effect test detected numerous genome-wide significant GxE signals in the GWAS main effects top hit regions, but the significance diminished after adjusting for the GWAS top hits. In the gene-based analysis, a significant interaction of diabetes with variants in the FAM63A (family with sequence similarity 63 member A) gene (significance threshold P < 1.25 106) was observed in the meta-analysis (PGxE 1/4 1.2 106, PJoint 1/4 4.2 107). Conclusion(s): This analysis did not find significant GxE interactions at the SNP level but found one significant interaction with diabetes at the gene level. A larger sample size might unveil additional genetic factors via GxE scans. Impact: This study may
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- 2021
7. Smoking modifies pancreatic cancer risk loci on 2q21.3.
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Mocci E., Kundu P., Wheeler W., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A.L., Bueno-De-Mesquita B., Buring J.E., Campa D., Chanock S.J., Childs E.J., Duell E.J., Fuchs C.S., Gaziano J.M., Giovannucci E.L., Goggins M.G., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Panico S., Peters U., Porta M., Rabe K.G., Riboli E., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Stevens V.L., Strobel O., Thompson I.M., Tjonneland A., Trichopoulou A., van Den Eeden S.K., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Yuan F., Zeleniuch-Jacquotte A., Amundadottir L.T., Li D., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Kraft P., Chatterjee N., Klein A.P., Stolzenberg-Solomon R., Mocci E., Kundu P., Wheeler W., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A.L., Bueno-De-Mesquita B., Buring J.E., Campa D., Chanock S.J., Childs E.J., Duell E.J., Fuchs C.S., Gaziano J.M., Giovannucci E.L., Goggins M.G., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Panico S., Peters U., Porta M., Rabe K.G., Riboli E., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Stevens V.L., Strobel O., Thompson I.M., Tjonneland A., Trichopoulou A., van Den Eeden S.K., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Yuan F., Zeleniuch-Jacquotte A., Amundadottir L.T., Li D., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Kraft P., Chatterjee N., Klein A.P., and Stolzenberg-Solomon R.
- Abstract
Germline variation and smoking are independently associated with pancreatic ductal adenocarcinoma (PDAC). We conducted genome-wide smoking interaction analysis of PDAC using genotype data from four previous genome-wide association studies in individuals of European ancestry (7,937 cases and 11,774 controls). Examination of expression quantitative trait loci data from the Genotype-Tissue Expression Project followed by colocalization analysis was conducted to determine whether there was support for common SNP(s) underlying the observed associations. Statistical tests were two sided and P < 5 10-8 was considered statistically significant. Genome-wide significant evidence of qualitative interaction was identified on chr2q21.3 in intron 5 of the transmembrane protein 163 (TMEM163) and upstream of the cyclin T2 (CCNT2). The most significant SNP using the Empirical Bayes method, in this region that included 45 significantly associated SNPs, was rs1818613 [per allele OR in never smokers 0.87, 95% confidence interval (CI), 0.82-0.93; former smokers 1.00, 95% CI, 0.91-1.07; current smokers 1.25, 95% CI 1.12-1.40, Pinteraction 1/4 3.08 10-9). Examination of the Genotype-Tissue Expression Project data demonstrated an expression quantitative trait locus in this region for TMEM163 and CCNT2 in several tissue types. Colocalization analysis supported a shared SNP, rs842357, in high linkage disequilibrium with rs1818613 (r2 1/4 0. 94) driving both the observed interaction and the expression quantitative trait loci signals. Future studies are needed to confirm and understand the differential biologic mechanisms by smoking status that contribute to our PDAC findings.Copyright © 2021 American Association for Cancer Research.
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- 2021
8. Hepcidin-regulating iron metabolism genes and pancreatic ductal adenocarcinoma: a pathway analysis of genome-wide association studies.
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Julian-Serrano S., Yuan F., Wheeler W., Benyamin B., Machiela M.J., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Duell E.J., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Shu X.-O., Van Den Eeden S.K., Visvanathan K., Zheng W., Albanes D., Andreotti G., Ardanaz E., Babic A., Berndt S.I., Brais L.K., Brennan P., Bueno-de-Mesquita B., Buring J.E., Chanock S.J., Childs E.J., Chung C.C., Fabianova E., Foretova L., Fuchs C.S., Gaziano J.M., Gentiluomo M., Giovannucci E.L., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holcatova I., Holly E.A., Hung R.I., Janout V., Kurtz R.C., Lee I.-M., Malats N., McKean D., Milne R.L., Newton C.C., Oberg A.L., Perdomo S., Peters U., Porta M., Rothman N., Schulze M.B., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., Weiderpass E., Wenstzensen N., White E., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Zhong J., Kraft P., Li D., Campbell P.T., Petersen G.M., Wolpin B.M., Risch H.A., Amundadottir L.T., Klein A.P., Yu K., Stolzenberg-Solomon R.Z., Julian-Serrano S., Yuan F., Wheeler W., Benyamin B., Machiela M.J., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Duell E.J., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Shu X.-O., Van Den Eeden S.K., Visvanathan K., Zheng W., Albanes D., Andreotti G., Ardanaz E., Babic A., Berndt S.I., Brais L.K., Brennan P., Bueno-de-Mesquita B., Buring J.E., Chanock S.J., Childs E.J., Chung C.C., Fabianova E., Foretova L., Fuchs C.S., Gaziano J.M., Gentiluomo M., Giovannucci E.L., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holcatova I., Holly E.A., Hung R.I., Janout V., Kurtz R.C., Lee I.-M., Malats N., McKean D., Milne R.L., Newton C.C., Oberg A.L., Perdomo S., Peters U., Porta M., Rothman N., Schulze M.B., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., Weiderpass E., Wenstzensen N., White E., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Zhong J., Kraft P., Li D., Campbell P.T., Petersen G.M., Wolpin B.M., Risch H.A., Amundadottir L.T., Klein A.P., Yu K., and Stolzenberg-Solomon R.Z.
- Abstract
BACKGROUND: Epidemiological studies have suggested positive associations for iron and red meat intake with risk of pancreatic ductal adenocarcinoma (PDAC). Inherited pathogenic variants in genes involved in the hepcidin-regulating iron metabolism pathway are known to cause iron overload and hemochromatosis. OBJECTIVE(S): The objective of this study was to determine whether common genetic variation in the hepcidin-regulating iron metabolism pathway is associated with PDAC. METHOD(S): We conducted a pathway analysis of the hepcidin-regulating genes using single nucleotide polymorphism (SNP) summary statistics generated from 4 genome-wide association studies in 2 large consortium studies using the summary data-based adaptive rank truncated product method. Our population consisted of 9253 PDAC cases and 12,525 controls of European descent. Our analysis included 11 hepcidin-regulating genes [bone morphogenetic protein 2 (BMP2), bone morphogenetic protein 6 (BMP6), ferritin heavy chain 1 (FTH1), ferritin light chain (FTL), hepcidin (HAMP), homeostatic iron regulator (HFE), hemojuvelin (HJV), nuclear factor erythroid 2-related factor 2 (NRF2), ferroportin 1 (SLC40A1), transferrin receptor 1 (TFR1), and transferrin receptor 2 (TFR2)] and their surrounding genomic regions (+/-20 kb) for a total of 412 SNPs. RESULT(S): The hepcidin-regulating gene pathway was significantly associated with PDAC (P = 0.002), with the HJV, TFR2, TFR1, BMP6, and HAMP genes contributing the most to the association. CONCLUSION(S): Our results support that genetic susceptibility related to the hepcidin-regulating gene pathway is associated with PDAC risk and suggest a potential role of iron metabolism in pancreatic carcinogenesis. Further studies are needed to evaluate effect modification by intake of iron-rich foods on this association.Copyright Published by Oxford University Press on behalf of the American Society for Nutrition 2021.
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- 2021
9. Genome-wide association study data reveal genetic susceptibility to chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma risk.
- Author
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Wang X., Yuan F., Hung R.J., Walsh N., Zhang H., Platz E.A., Wheeler W., Song L., Arslan A.A., Beane Freeman L.E., Bracci P., Canzian F., Du M., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Shi J., Duell E.J., Amundadottir L.T., Li D., Petersen G.M., Wolpin B.M., Risch H.A., Yu K., Klein A.P., Stolzenberg-Solomon R., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Rosendahl J., Scelo G., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Amiano P., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Chanock S.J., Fuchs C.S., Michael Gaziano J., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Katzke V., Kirsten H., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Ng K., Oberg A.L., Porta M., Rabe K.G., Real F.X., Rothman N., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., Wentzensen N., Wang X., Yuan F., Hung R.J., Walsh N., Zhang H., Platz E.A., Wheeler W., Song L., Arslan A.A., Beane Freeman L.E., Bracci P., Canzian F., Du M., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Shi J., Duell E.J., Amundadottir L.T., Li D., Petersen G.M., Wolpin B.M., Risch H.A., Yu K., Klein A.P., Stolzenberg-Solomon R., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Rosendahl J., Scelo G., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Amiano P., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Chanock S.J., Fuchs C.S., Michael Gaziano J., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Katzke V., Kirsten H., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Ng K., Oberg A.L., Porta M., Rabe K.G., Real F.X., Rothman N., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., and Wentzensen N.
- Abstract
Registry-based epidemiologic studies suggest associations between chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma (PDAC). As genetic susceptibility contributes to a large proportion of chronic inflammatory intestinal diseases, we hypothesize that the genomic regions surrounding established genome-wide associated variants for these chronic inflammatory diseases are associated with PDAC. We examined the association between PDAC and genomic regions (+500 kb) surrounding established common susceptibility variants for ulcerative colitis, Crohn's disease, inflammatory bowel disease, celiac disease, chronic pancreatitis, and primary sclerosing cholangitis. We analyzed summary statistics from genome-wide association studies data for 8,384 cases and 11,955 controls of European descent from two large consortium studies using the summary data-based adaptive rank truncated product method to examine the overall association of combined genomic regions for each inflammatory disease group. Combined genomic susceptibility regions for ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis were associated with PDAC at P values < 0.05 (0.0040, 0.0057, 0.011, and 3.4 x 10-6, respectively). After excluding the 20 PDAC susceptibility regions (+500 kb) previously identified by GWAS, the genomic regions for ulcerative colitis, Crohn disease, and inflammatory bowel disease remained associated with PDAC (P 1/4 0.0029, 0.0057, and 0.0098, respectively). Genomic regions for celiac disease (P 1/4 0.22) and primary sclerosing cholangitis (P 1/4 0.078) were not associated with PDAC. Our results support the hypothesis that genomic regions surrounding variants associated with inflammatory intestinal diseases, particularly, ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis are associated with PDAC.Copyright © 2020 American Association for Cancer Research.
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- 2021
10. Genetically predicted circulating concentrations of micronutrients and risk of colorectal cancer among individuals of European descent: a Mendelian randomization study.
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Hampe J., Zuber V., Cross A.J., Perez-Cornago A., Hunter D.J., van Duijnhoven F.J.B., Albanes D., Arndt V., Berndt S.I., Bezieau S., Bishop D.T., Boehm J., Brenner H., Burnett-Hartman A., Campbell P.T., Casey G., Castellvi-Bel S., Chan A.T., Chang-Claude J., de la Chapelle A., Figueiredo J.C., Gallinger S.J., Giles G.G., Goodman P.J., Gsur A., Markozannes G., Hampel H., Hoffmeister M., Jenkins M.A., Keku T.O., Kweon S.-S., Larsson S.C., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., Milne R.L., Moreno V., Nan H., Nassir R., Newcomb P.A., Offit K., Pharoah P.D.P., Platz E.A., Potter J.D., Qi L., Rennert G., Sakoda L.C., Schafmayer C., Slattery M.L., Snetselaar L., Schenk J., Thibodeau S.N., Ulrich C.M., Van Guelpen B., Harlid S., Visvanathan K., Vodickova L., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Zheng W., Bueno-de-Mesquita B., Boutron-Ruault M.-C., Hughes D.J., Jakszyn P., Kuhn T., Palli D., Riboli E., Giovannucci E.L., Banbury B.L., Gruber S.B., Peters U., Gunter M.J., Tsilidis K.K., Papadimitriou N., Dimou N., Gill D., Lewis S.J., Martin R.M., Murphy N., Burrows K., Lopez D.S., Key T.J., Travis R.C., Hampe J., Zuber V., Cross A.J., Perez-Cornago A., Hunter D.J., van Duijnhoven F.J.B., Albanes D., Arndt V., Berndt S.I., Bezieau S., Bishop D.T., Boehm J., Brenner H., Burnett-Hartman A., Campbell P.T., Casey G., Castellvi-Bel S., Chan A.T., Chang-Claude J., de la Chapelle A., Figueiredo J.C., Gallinger S.J., Giles G.G., Goodman P.J., Gsur A., Markozannes G., Hampel H., Hoffmeister M., Jenkins M.A., Keku T.O., Kweon S.-S., Larsson S.C., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., Milne R.L., Moreno V., Nan H., Nassir R., Newcomb P.A., Offit K., Pharoah P.D.P., Platz E.A., Potter J.D., Qi L., Rennert G., Sakoda L.C., Schafmayer C., Slattery M.L., Snetselaar L., Schenk J., Thibodeau S.N., Ulrich C.M., Van Guelpen B., Harlid S., Visvanathan K., Vodickova L., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Zheng W., Bueno-de-Mesquita B., Boutron-Ruault M.-C., Hughes D.J., Jakszyn P., Kuhn T., Palli D., Riboli E., Giovannucci E.L., Banbury B.L., Gruber S.B., Peters U., Gunter M.J., Tsilidis K.K., Papadimitriou N., Dimou N., Gill D., Lewis S.J., Martin R.M., Murphy N., Burrows K., Lopez D.S., Key T.J., and Travis R.C.
- Abstract
BACKGROUND: The literature on associations of circulating concentrations of minerals and vitamins with risk of colorectal cancer is limited and inconsistent. Evidence from randomized controlled trials (RCTs) to support the efficacy of dietary modification or nutrient supplementation for colorectal cancer prevention is also limited. OBJECTIVE(S): To complement observational and RCT findings, we investigated associations of genetically predicted concentrations of 11 micronutrients (beta-carotene, calcium, copper, folate, iron, magnesium, phosphorus, selenium, vitamin B-6, vitamin B-12, and zinc) with colorectal cancer risk using Mendelian randomization (MR). METHOD(S): Two-sample MR was conducted using 58,221 individuals with colorectal cancer and 67,694 controls from the Genetics and Epidemiology of Colorectal Cancer Consortium, Colorectal Cancer Transdisciplinary Study, and Colon Cancer Family Registry. Inverse variance-weighted MR analyses were performed with sensitivity analyses to assess the impact of potential violations of MR assumptions. RESULT(S): Nominally significant associations were noted for genetically predicted iron concentration and higher risk of colon cancer [ORs per SD (ORSD): 1.08; 95% CI: 1.00, 1.17; P value=0.05] and similarly for proximal colon cancer, and for vitamin B-12 concentration and higher risk of colorectal cancer (ORSD: 1.12; 95% CI: 1.03, 1.21; P value=0.01) and similarly for colon cancer. A nominally significant association was also noted for genetically predicted selenium concentration and lower risk of colon cancer (ORSD: 0.98; 95% CI: 0.96, 1.00; P value=0.05) and similarly for distal colon cancer. These associations were robust to sensitivity analyses. Nominally significant inverse associations were observed for zinc and risk of colorectal and distal colon cancers, but sensitivity analyses could not be performed. None of these findings survived correction for multiple testing. Genetically predicted concentrations of beta-caroten
- Published
- 2021
11. Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction.
- Author
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Thompson I.M., Muir K., Lophatananon A., Wan P., Stern M.C., Vega A., Gomez-Caamano A., Fachal L., Rosenstein B.S., Kerns S.L., Ostrer H., Teixeira M.R., Paulo P., Brandao A., Watya S., Lubwama A., Bensen J.T., Fontham E.T.H., Mohler J., Taylor J.A., Kogevinas M., Llorca J., Castano-Vinyals G., Cannon-Albright L., Teerlink C.C., Huff C.D., Strom S.S., Multigner L., Blanchet P., Brureau L., Kaneva R., Slavov C., Mitev V., Leach R.J., Weaver B., Brenner H., Cuk K., Holleczek B., Saum K.-U., Klein E.A., Hsing A.W., Kittles R.A., Murphy A.B., Logothetis C.J., Kim J., Neuhausen S.L., Steele L., Ding Y.C., Isaacs W.B., Nemesure B., Hennis A.J.M., Carpten J., Pandha H., Michael A., De Ruyck K., De Meerleer G., Ost P., Xu J., Razack A., Lim J., Teo S.-H., Newcomb L.F., Lin D.W., Fowke J.H., Neslund-Dudas C., Rybicki B.A., Gamulin M., Lessel D., Kulis T., Usmani N., Singhal S., Parliament M., Claessens F., Joniau S., Van den Broeck T., Gago-Dominguez M., Castelao J.E., Martinez M.E., Larkin S., Townsend P.A., Aukim-Hastie C., Bush W.S., Aldrich M.C., Crawford D.C., Srivastava S., Cullen J.C., Petrovics G., Casey G., Roobol M.J., Jenster G., van Schaik R.H.N., Hu J.J., Sanderson M., Varma R., McKean-Cowdin R., Torres M., Mancuso N., Berndt S.I., Van Den Eeden S.K., Easton D.F., Chanock S.J., Cook M.B., Wiklund F., Nakagawa H., Witte J.S., Eeles R.A., Kote-Jarai Z., Haiman C.A., Conti D.V., Darst B.F., Moss L.C., Saunders E.J., Sheng X., Chou A., Schumacher F.R., Olama A.A.A., Benlloch S., Dadaev T., Brook M.N., Sahimi A., Hoffmann T.J., Takahashi A., Matsuda K., Momozawa Y., Le Marchand L., Wilkens L.R., Stevens V.L., Gapstur S.M., Carter B.D., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Giles G.G., Southey M.C., MacInnis R.J., Cybulski C., Wokolorczyk D., Lubinski J., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Nordestgaard B.G., Nielsen S.F., Weischer M., Bojesen S.E., Roder M.A., Iversen P., Batra J., Chambers S., Moya L., Horvath L., Clements J.A., Tilley W., Risbridger G.P., Gronberg H., Aly M., Szulkin R., Eklund M., Nordstrom T., Pashayan N., Dunning A.M., Ghoussaini M., Travis R.C., Key T.J., Riboli E., Park J.Y., Sellers T.A., Lin H.-Y., Albanes D., Weinstein S.J., Mucci L.A., Giovannucci E., Lindstrom S., Kraft P., Hunter D.J., Penney K.L., Turman C., Tangen C.M., Goodman P.J., Fujita M., Hamilton R.J., Fleshner N.E., Finelli A., Parent M.-E., Stanford J.L., Ostrander E.A., Geybels M.S., Koutros S., Freeman L.E.B., Stampfer M., Wolk A., Hakansson N., Andriole G.L., Hoover R.N., Machiela M.J., Sorensen K.D., Borre M., Blot W.J., Zheng W., Yeboah E.D., Mensah J.E., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Wu Y., Zhao S.-C., Sun Z., Thibodeau S.N., McDonnell S.K., Schaid D.J., West C.M.L., Burnet N., Barnett G., Maier C., Schnoeller T., Luedeke M., Kibel A.S., Drake B.F., Cussenot O., Cancel-Tassin G., Menegaux F., Truong T., Koudou Y.A., John E.M., Grindedal E.M., Maehle L., Khaw K.-T., Ingles S.A., Thompson I.M., Muir K., Lophatananon A., Wan P., Stern M.C., Vega A., Gomez-Caamano A., Fachal L., Rosenstein B.S., Kerns S.L., Ostrer H., Teixeira M.R., Paulo P., Brandao A., Watya S., Lubwama A., Bensen J.T., Fontham E.T.H., Mohler J., Taylor J.A., Kogevinas M., Llorca J., Castano-Vinyals G., Cannon-Albright L., Teerlink C.C., Huff C.D., Strom S.S., Multigner L., Blanchet P., Brureau L., Kaneva R., Slavov C., Mitev V., Leach R.J., Weaver B., Brenner H., Cuk K., Holleczek B., Saum K.-U., Klein E.A., Hsing A.W., Kittles R.A., Murphy A.B., Logothetis C.J., Kim J., Neuhausen S.L., Steele L., Ding Y.C., Isaacs W.B., Nemesure B., Hennis A.J.M., Carpten J., Pandha H., Michael A., De Ruyck K., De Meerleer G., Ost P., Xu J., Razack A., Lim J., Teo S.-H., Newcomb L.F., Lin D.W., Fowke J.H., Neslund-Dudas C., Rybicki B.A., Gamulin M., Lessel D., Kulis T., Usmani N., Singhal S., Parliament M., Claessens F., Joniau S., Van den Broeck T., Gago-Dominguez M., Castelao J.E., Martinez M.E., Larkin S., Townsend P.A., Aukim-Hastie C., Bush W.S., Aldrich M.C., Crawford D.C., Srivastava S., Cullen J.C., Petrovics G., Casey G., Roobol M.J., Jenster G., van Schaik R.H.N., Hu J.J., Sanderson M., Varma R., McKean-Cowdin R., Torres M., Mancuso N., Berndt S.I., Van Den Eeden S.K., Easton D.F., Chanock S.J., Cook M.B., Wiklund F., Nakagawa H., Witte J.S., Eeles R.A., Kote-Jarai Z., Haiman C.A., Conti D.V., Darst B.F., Moss L.C., Saunders E.J., Sheng X., Chou A., Schumacher F.R., Olama A.A.A., Benlloch S., Dadaev T., Brook M.N., Sahimi A., Hoffmann T.J., Takahashi A., Matsuda K., Momozawa Y., Le Marchand L., Wilkens L.R., Stevens V.L., Gapstur S.M., Carter B.D., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Giles G.G., Southey M.C., MacInnis R.J., Cybulski C., Wokolorczyk D., Lubinski J., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Nordestgaard B.G., Nielsen S.F., Weischer M., Bojesen S.E., Roder M.A., Iversen P., Batra J., Chambers S., Moya L., Horvath L., Clements J.A., Tilley W., Risbridger G.P., Gronberg H., Aly M., Szulkin R., Eklund M., Nordstrom T., Pashayan N., Dunning A.M., Ghoussaini M., Travis R.C., Key T.J., Riboli E., Park J.Y., Sellers T.A., Lin H.-Y., Albanes D., Weinstein S.J., Mucci L.A., Giovannucci E., Lindstrom S., Kraft P., Hunter D.J., Penney K.L., Turman C., Tangen C.M., Goodman P.J., Fujita M., Hamilton R.J., Fleshner N.E., Finelli A., Parent M.-E., Stanford J.L., Ostrander E.A., Geybels M.S., Koutros S., Freeman L.E.B., Stampfer M., Wolk A., Hakansson N., Andriole G.L., Hoover R.N., Machiela M.J., Sorensen K.D., Borre M., Blot W.J., Zheng W., Yeboah E.D., Mensah J.E., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Wu Y., Zhao S.-C., Sun Z., Thibodeau S.N., McDonnell S.K., Schaid D.J., West C.M.L., Burnet N., Barnett G., Maier C., Schnoeller T., Luedeke M., Kibel A.S., Drake B.F., Cussenot O., Cancel-Tassin G., Menegaux F., Truong T., Koudou Y.A., John E.M., Grindedal E.M., Maehle L., Khaw K.-T., and Ingles S.A.
- Abstract
Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 (95% confidence interval (CI), 4.84-5.29) for men of European ancestry to 3.74 (95% CI, 3.36-4.17) for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher (95% CI, 2.14-2.22), and men of East Asian ancestry 0.73-times lower (95% CI, 0.71-0.76), than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction.Copyright © 2021, The Author(s), under exclusive licence to Springer Nature America, Inc.
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- 2021
12. Genetically predicted circulating concentrations of micronutrients and risk of colorectal cancer among individuals of European descent: A Mendelian randomization study.
- Author
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Tsilidis K.K., Papadimitriou N., Dimou N., Gill D., Lewis S.J., Martin R.M., Murphy N., Markozannes G., Zuber V., Cross A.J., Burrows K., Lopez D.S., Key T.J., Travis R.C., Perez-Cornago A., Hunter D.J., Van Duijnhoven F.J.B., Albanes D., Arndt V., Berndt S.I., Bezieau S., Bishop D.T., Boehm J., Brenner H., Burnett-Hartman A., Campbell P.T., Casey G., Castellvi-Bel S., Chan A.T., Chang-Claude J., De La Chapelle A., Figueiredo J.C., Gallinger S.J., Giles G.G., Goodman P.J., Gsur A., Hampe J., Hampel H., Hoffmeister M., Jenkins M.A., Keku T.O., Kweon S.-S., Larsson S.C., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., Milne R.L., Moreno V., Nan H., Nassir R., Newcomb P.A., Offit K., Pharoah P.D.P., Platz E.A., Potter J.D., Qi L., Rennert G., Sakoda L.C., Schafmayer C., Slattery M.L., Snetselaar L., Schenk J., Thibodeau S.N., Ulrich C.M., Van Guelpen B., Harlid S., Visvanathan K., Vodickova L., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Zheng W., Bueno-De-Mesquita B., Boutron-Ruault M.-C., Hughes D.J., Jakszyn P., Kuhn T., Palli D., Riboli E., Giovannucci E.L., Banbury B.L., Gruber S.B., Peters U., Gunter M.J., Tsilidis K.K., Papadimitriou N., Dimou N., Gill D., Lewis S.J., Martin R.M., Murphy N., Markozannes G., Zuber V., Cross A.J., Burrows K., Lopez D.S., Key T.J., Travis R.C., Perez-Cornago A., Hunter D.J., Van Duijnhoven F.J.B., Albanes D., Arndt V., Berndt S.I., Bezieau S., Bishop D.T., Boehm J., Brenner H., Burnett-Hartman A., Campbell P.T., Casey G., Castellvi-Bel S., Chan A.T., Chang-Claude J., De La Chapelle A., Figueiredo J.C., Gallinger S.J., Giles G.G., Goodman P.J., Gsur A., Hampe J., Hampel H., Hoffmeister M., Jenkins M.A., Keku T.O., Kweon S.-S., Larsson S.C., Le Marchand L., Li C.I., Li L., Lindblom A., Martin V., Milne R.L., Moreno V., Nan H., Nassir R., Newcomb P.A., Offit K., Pharoah P.D.P., Platz E.A., Potter J.D., Qi L., Rennert G., Sakoda L.C., Schafmayer C., Slattery M.L., Snetselaar L., Schenk J., Thibodeau S.N., Ulrich C.M., Van Guelpen B., Harlid S., Visvanathan K., Vodickova L., Wang H., White E., Wolk A., Woods M.O., Wu A.H., Zheng W., Bueno-De-Mesquita B., Boutron-Ruault M.-C., Hughes D.J., Jakszyn P., Kuhn T., Palli D., Riboli E., Giovannucci E.L., Banbury B.L., Gruber S.B., Peters U., and Gunter M.J.
- Abstract
Background: The literature on associations of circulating concentrations of minerals and vitamins with risk of colorectal cancer is limited and inconsistent. Evidence from randomized controlled trials (RCTs) to support the efficacy of dietary modification or nutrient supplementation for colorectal cancer prevention is also limited. Objective(s): To complement observational and RCT findings, we investigated associations of genetically predicted concentrations of 11 micronutrients (beta-carotene, calcium, copper, folate, iron, magnesium, phosphorus, selenium, vitamin B-6, vitamin B-12, and zinc) with colorectal cancer risk using Mendelian randomization (MR). Method(s): Two-sample MR was conducted using 58,221 individuals with colorectal cancer and 67,694 controls from the Genetics and Epidemiology of Colorectal Cancer Consortium, Colorectal Cancer Transdisciplinary Study, and Colon Cancer Family Registry. Inverse variance-weighted MR analyses were performed with sensitivity analyses to assess the impact of potential violations of MR assumptions. Result(s): Nominally significant associations were noted for genetically predicted iron concentration and higher risk of colon cancer [ORs per SD (ORSD): 1.08 95% CI: 1.00, 1.17 P value = 0.05] and similarly for proximal colon cancer, and for vitamin B-12 concentration and higher risk of colorectal cancer (ORSD: 1.12 95% CI: 1.03, 1.21 P value = 0.01) and similarly for colon cancer. A nominally significant association was also noted for genetically predicted selenium concentration and lower risk of colon cancer (ORSD: 0.98 95% CI: 0.96, 1.00 P value = 0.05) and similarly for distal colon cancer. These associations were robust to sensitivity analyses. Nominally significant inverse associations were observed for zinc and risk of colorectal and distal colon cancers, but sensitivity analyses could not be performed. None of these findings survived correction for multiple testing. Genetically predicted concentrations of beta-caroten
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- 2021
13. A transcriptome-wide association study identifies novel candidate susceptibility genes for pancreatic cancer.
- Author
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Hasan M., Zhang T., Xiao W., Albanes D., Andreotti G., Arslan A.A., Babic A., Bamlet W.R., Beane-Freeman L., Berndt S., Borgida A., Bracci P.M., Brais L., Brennan P., Bueno-De-Mesquita B., Buring J., Canzian F., Childs E.J., Cotterchio M., Du M., Duell E.J., Fuchs C., Gallinger S., Michael Gaziano J., Giles G.G., Giovannucci E., Goggins M., Goodman G.E., Goodman P.J., Haiman C., Hartge P., Helzlsouer K.J., Holly E.A., Klein E.A., Kogevinas M., Kurtz R.J., LeMarchand L., Malats N., Mannisto S., Milne R., Neale R.E., Ng K., Obazee O., Oberg A.L., Orlow I., Patel A.V., Peters U., Porta M., Rothman N., Scelo G., Sesso H.D., Severi G., Sieri S., Silverman D., Sund M., Tjonneland A., Thornquist M.D., Tobias G.S., Trichopoulou A., van Den Eeden S.K., Visvanathan K., Wactawski-Wende J., Wentzensen N., White E., Yu H., Yuan C., Zeleniuch-Jacquotte A., Hoover R., Brown K., Kooperberg C., Risch H.A., Jacobs E.J., Li D., Yu K., Shu X.-O., Chanock S.J., Wolpin B.M., Stolzenberg-Solomon R.Z., Chatterjee N., Klein A.P., Smith J.P., Kraft P., Shi J., Petersen G.M., Zheng W., Amundadottir L.T., Zhong J., Jermusyk A., Wu L., Hoskins J.W., Collins I., Mocci E., Zhang M., Song L., Chung C.C., Hasan M., Zhang T., Xiao W., Albanes D., Andreotti G., Arslan A.A., Babic A., Bamlet W.R., Beane-Freeman L., Berndt S., Borgida A., Bracci P.M., Brais L., Brennan P., Bueno-De-Mesquita B., Buring J., Canzian F., Childs E.J., Cotterchio M., Du M., Duell E.J., Fuchs C., Gallinger S., Michael Gaziano J., Giles G.G., Giovannucci E., Goggins M., Goodman G.E., Goodman P.J., Haiman C., Hartge P., Helzlsouer K.J., Holly E.A., Klein E.A., Kogevinas M., Kurtz R.J., LeMarchand L., Malats N., Mannisto S., Milne R., Neale R.E., Ng K., Obazee O., Oberg A.L., Orlow I., Patel A.V., Peters U., Porta M., Rothman N., Scelo G., Sesso H.D., Severi G., Sieri S., Silverman D., Sund M., Tjonneland A., Thornquist M.D., Tobias G.S., Trichopoulou A., van Den Eeden S.K., Visvanathan K., Wactawski-Wende J., Wentzensen N., White E., Yu H., Yuan C., Zeleniuch-Jacquotte A., Hoover R., Brown K., Kooperberg C., Risch H.A., Jacobs E.J., Li D., Yu K., Shu X.-O., Chanock S.J., Wolpin B.M., Stolzenberg-Solomon R.Z., Chatterjee N., Klein A.P., Smith J.P., Kraft P., Shi J., Petersen G.M., Zheng W., Amundadottir L.T., Zhong J., Jermusyk A., Wu L., Hoskins J.W., Collins I., Mocci E., Zhang M., Song L., and Chung C.C.
- Abstract
Background: Although 20 pancreatic cancer susceptibility loci have been identified through genome-wide association studies in individuals of European ancestry, much of its heritability remains unexplained and the genes responsible largely unknown. Method(s): To discover novel pancreatic cancer risk loci and possible causal genes, we performed a pancreatic cancer transcriptome-wide association study in Europeans using three approaches: FUSION, MetaXcan, and Summary-MulTiXcan. We integrated genome-wide association studies summary statistics from 9040 pancreatic cancer cases and 12 496 controls, with gene expression prediction models built using transcriptome data from histologically normal pancreatic tissue samples (NCI Laboratory of Translational Genomics [n = 95] and Genotype-Tissue Expression v7 [n = 174] datasets) and data from 48 different tissues (Genotype-Tissue Expression v7, n = 74-421 samples). Result(s): We identified 25 genes whose genetically predicted expression was statistically significantly associated with pancreatic cancer risk (false discovery rate <.05), including 14 candidate genes at 11 novel loci (1p36.12: CELA3B; 9q31.1: SMC2, SMC2-AS1; 10q23.31: RP11-80H5.9; 12q13.13: SMUG1; 14q32.33: BTBD6; 15q23: HEXA; 15q26.1: RCCD1; 17q12: PNMT, CDK12, PGAP3; 17q22: SUPT4H1; 18q11.22:RP11-888D10.3; and 19p13.11: PGPEP1) and 11 at six known risk loci (5p15.33: TERT, CLPTM1L, ZDHHC11B; 7p14.1: INHBA; 9q34.2: ABO; 13q12.2: PDX1; 13q22.1: KLF5; and 16q23.1: WDR59, CFDP1, BCAR1, TMEM170A). The association for 12 of these genes (CELA3B, SMC2, and PNMT at novel risk loci and TERT, CLPTM1L, INHBA, ABO, PDX1, KLF5, WDR59, CFDP1, and BCAR1 at known loci) remained statistically significant after Bonferroni correction. Conclusion(s): By integrating gene expression and genotype data, we identified novel pancreatic cancer risk loci and candidate functional genes that warrant further investigation.Copyright © 2020 Oxford University Press. All rights reserved.
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- 2021
14. Associations between genetically predicted blood protein biomarkers and pancreatic cancer risk.
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Haiman C.A., Bracci P., Katzke V., Neale R.E., Gallinger S., van Den Eeden S.K., Arslan A.A., Canzian F., Kooperberg C., Beane Freeman L.E., Scelo G., Visvanathan K., Li D., Le Marchand L., Yu H., Petersen G.M., Stolzenberg-Solomon R., Klein A.P., Cai Q., Long J., Shu X.-O., Zheng W., Wu L., Shu X., Guo X., Liu D., Bao J., Milne R.L., Giles G.G., Wu C., Du M., White E., Risch H.A., Malats N., Duell E.J., Goodman P.J., Zhu J., Haiman C.A., Bracci P., Katzke V., Neale R.E., Gallinger S., van Den Eeden S.K., Arslan A.A., Canzian F., Kooperberg C., Beane Freeman L.E., Scelo G., Visvanathan K., Li D., Le Marchand L., Yu H., Petersen G.M., Stolzenberg-Solomon R., Klein A.P., Cai Q., Long J., Shu X.-O., Zheng W., Wu L., Shu X., Guo X., Liu D., Bao J., Milne R.L., Giles G.G., Wu C., Du M., White E., Risch H.A., Malats N., Duell E.J., Goodman P.J., and Zhu J.
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Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, with few known risk factors and biomarkers. Several blood protein biomarkers have been linked to PDAC in previous studies, but these studies have assessed only a limited number of biomarkers, usually in small samples. In this study, we evaluated associations of circulating protein levels and PDAC risk using genetic instruments. Method(s): To identify novel circulating protein biomarkers of PDAC, we studied 8,280 cases and 6,728 controls of European descent from the Pancreatic Cancer Cohort Consortium and the Pancreatic Cancer Case-Control Consortium, using genetic instruments of protein quantitative trait loci. Result(s): We observed associations between predicted concentrations of 38 proteins and PDAC risk at an FDR of < 0.05, including 23 of those proteins that showed an association even after Bonferroni correction. These include the protein encoded by ABO, which has been implicated as a potential target gene of PDAC risk variant. Eight of the identified proteins (LMA2L, TM11D, IP-10, ADH1B, STOM, TENC1, DOCK9, and CRBB2) were associated with PDAC risk after adjusting for previously reported PDAC risk variants (OR ranged from 0.79 to 1.52). Pathway enrichment analysis showed that the encoding genes for implicated proteins were significantly enriched in cancer-related pathways, such as STAT3 and IL15 production. Conclusion(s): We identified 38 candidates of protein biomarkers for PDAC risk. Impact: This study identifies novel protein biomarker candidates for PDAC, which if validated by additional studies, may contribute to the etiologic understanding of PDAC development.Copyright © 2020 American Association for Cancer Research.
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- 2021
15. Genome-wide gene⇓diabetes and gene⇓obesity interaction scan in 8,255 cases and 11,900 controls from panscan and PanC4 consortia
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Tang, H. Jiang, L. Stolzenberg-Solomon, R.Z. Arslan, A.A. Beane Freeman, L.E. Bracci, P.M. Brennan, P. Canzian, F. Du, M. Gallinger, S. Giles, G.G. Goodman, P.J. Kooperberg, C. Le Marchand, L. Neale, R.E. Shu, X.-O. Visvanathan, K. White, E. Zheng, W. Albanes, D. Andreotti, G. Babic, A. Bamlet, W.R. Berndt, S.I. Blackford, A. Bueno-De-Mesquita, B. Buring, J.E. Campa, D. Chanock, S.J. Childs, E. Duell, E.J. Fuchs, C. Michael Gaziano, J. Goggins, M. Hartge, P. Hassam, M.H. Holly, E.A. Hoover, R.N. Hung, R.J. Kurtz, R.C. Lee, I.-M. Malats, N. Milne, R.L. Ng, K. Oberg, A.L. Orlow, I. Peters, U. Porta, M. Rabe, K.G. Rothman, N. Scelo, G. Sesso, H.D. Silverman, D.T. Thompson, I.M. Tjønneland, A. Trichopoulou, A. Wactawski-Wende, J. Wentzensen, N. Wilkens, L.R. Yu, H. Zeleniuch-Jacquotte, A. Amundadottir, L.T. Jacobs, E.J. Petersen, G.M. Wolpin, B.M. Risch, H.A. Chatterjee, N. Klein, A.P. Li, D. Kraft, P. Wei, P.
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Background: Obesity and diabetes are major modifiable risk factors for pancreatic cancer. Interactions between genetic variants and diabetes/obesity have not previously been comprehensively investigated in pancreatic cancer at the genome-wide level. Methods: We conducted a gene–environment interaction (GxE) analysis including 8,255 cases and 11,900 controls from four pancreatic cancer genome-wide association study (GWAS) datasets (Pancreatic Cancer Cohort Consortium I–III and Pancreatic Cancer Case Control Consortium). Obesity (body mass index ≥30 kg/m2) and diabetes (duration ≥3 years) were the environmental variables of interest. Approximately 870,000 SNPs (minor allele frequency ≥0.005, genotyped in at least one dataset) were analyzed. Case–control (CC), case-only (CO), and joint-effect test methods were used for SNP-level GxE analysis. As a complementary approach, gene-based GxE analysis was also performed. Age, sex, study site, and principal components accounting for population substructure were included as covariates. Meta-analysis was applied to combine individual GWAS summary statistics. Results: No genome-wide significant interactions (departures from a log-additive odds model) with diabetes or obesity were detected at the SNP level by the CC or CO approaches. The joint-effect test detected numerous genome-wide significant GxE signals in the GWAS main effects top hit regions, but the significance diminished after adjusting for the GWAS top hits. In the gene-based analysis, a significant interaction of diabetes with variants in the FAM63A (family with sequence similarity 63 member A) gene (significance threshold P < 1.25 106) was observed in the meta-analysis (PGxE ¼ 1.2 106, PJoint ¼ 4.2 107). Conclusions: This analysis did not find significant GxE interactions at the SNP level but found one significant interaction with diabetes at the gene level. A larger sample size might unveil additional genetic factors via GxE scans. Impact: This study may contribute to discovering the mechanism of diabetes-associated pancreatic cancer. © 2020 American Association for Cancer Research.
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- 2020
16. Measures of body fatness and height in early and mid-to-late adulthood and prostate cancer: risk and mortality in The Pooling Project of Prospective Studies of Diet and Cancer
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Genkinger, J.M., primary, Wu, K., additional, Wang, M., additional, Albanes, D., additional, Black, A., additional, van den Brandt, P.A., additional, Burke, K.A., additional, Cook, M.B., additional, Gapstur, S.M., additional, Giles, G.G., additional, Giovannucci, E., additional, Goodman, G.G., additional, Goodman, P.J., additional, Håkansson, N., additional, Key, T.J., additional, Männistö, S., additional, Le Marchand, L., additional, Liao, L.M., additional, MacInnis, R.J., additional, Neuhouser, M.L., additional, Platz, E.A., additional, Sawada, N., additional, Schenk, J.M., additional, Stevens, V.L., additional, Travis, R.C., additional, Tsugane, S., additional, Visvanathan, K., additional, Wilkens, L.R., additional, Wolk, A., additional, and Smith-Warner, S.A., additional
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- 2020
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17. Discovery of common and rare genetic risk variants for colorectal cancer
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Huyghe, J.R. Bien, S.A. Harrison, T.A. Kang, H.M. Chen, S. Schmit, S.L. Conti, D.V. Qu, C. Jeon, J. Edlund, C.K. Greenside, P. Wainberg, M. Schumacher, F.R. Smith, J.D. Levine, D.M. Nelson, S.C. Sinnott-Armstrong, N.A. Albanes, D. Alonso, M.H. Anderson, K. Arnau-Collell, C. Arndt, V. Bamia, C. Banbury, B.L. Baron, J.A. Berndt, S.I. Bézieau, S. Bishop, D.T. Boehm, J. Boeing, H. Brenner, H. Brezina, S. Buch, S. Buchanan, D.D. Burnett-Hartman, A. Butterbach, K. Caan, B.J. Campbell, P.T. Carlson, C.S. Castellví-Bel, S. Chan, A.T. Chang-Claude, J. Chanock, S.J. Chirlaque, M.-D. Cho, S.H. Connolly, C.M. Cross, A.J. Cuk, K. Curtis, K.R. de la Chapelle, A. Doheny, K.F. Duggan, D. Easton, D.F. Elias, S.G. Elliott, F. English, D.R. Feskens, E.J.M. Figueiredo, J.C. Fischer, R. FitzGerald, L.M. Forman, D. Gala, M. Gallinger, S. Gauderman, W.J. Giles, G.G. Gillanders, E. Gong, J. Goodman, P.J. Grady, W.M. Grove, J.S. Gsur, A. Gunter, M.J. Haile, R.W. Hampe, J. Hampel, H. Harlid, S. Hayes, R.B. Hofer, P. Hoffmeister, M. Hopper, J.L. Hsu, W.-L. Huang, W.-Y. Hudson, T.J. Hunter, D.J. Ibañez-Sanz, G. Idos, G.E. Ingersoll, R. Jackson, R.D. Jacobs, E.J. Jenkins, M.A. Joshi, A.D. Joshu, C.E. Keku, T.O. Key, T.J. Kim, H.R. Kobayashi, E. Kolonel, L.N. Kooperberg, C. Kühn, T. Küry, S. Kweon, S.-S. Larsson, S.C. Laurie, C.A. Le Marchand, L. Leal, S.M. Lee, S.C. Lejbkowicz, F. Lemire, M. Li, C.I. Li, L. Lieb, W. Lin, Y. Lindblom, A. Lindor, N.M. Ling, H. Louie, T.L. Männistö, S. Markowitz, S.D. Martín, V. Masala, G. McNeil, C.E. Melas, M. Milne, R.L. Moreno, L. Murphy, N. Myte, R. Naccarati, A. Newcomb, P.A. Offit, K. Ogino, S. Onland-Moret, N.C. Pardini, B. Parfrey, P.S. Pearlman, R. Perduca, V. Pharoah, P.D.P. Pinchev, M. Platz, E.A. Prentice, R.L. Pugh, E. Raskin, L. Rennert, G. Rennert, H.S. Riboli, E. Rodríguez-Barranco, M. Romm, J. Sakoda, L.C. Schafmayer, C. Schoen, R.E. Seminara, D. Shah, M. Shelford, T. Shin, M.-H. Shulman, K. Sieri, S. Slattery, M.L. Southey, M.C. Stadler, Z.K. Stegmaier, C. Su, Y.-R. Tangen, C.M. Thibodeau, S.N. Thomas, D.C. Thomas, S.S. Toland, A.E. Trichopoulou, A. Ulrich, C.M. Van Den Berg, D.J. van Duijnhoven, F.J.B. Van Guelpen, B. van Kranen, H. Vijai, J. Visvanathan, K. Vodicka, P. Vodickova, L. Vymetalkova, V. Weigl, K. Weinstein, S.J. White, E. Win, A.K. Wolf, C.R. Wolk, A. Woods, M.O. Wu, A.H. Zaidi, S.H. Zanke, B.W. Zhang, Q. Zheng, W. Scacheri, P.C. Potter, J.D. Bassik, M.C. Kundaje, A. Casey, G. Moreno, V. Abecasis, G.R. Nickerson, D.A. Gruber, S.B. Hsu, L. Peters, U.
- Abstract
To further dissect the genetic architecture of colorectal cancer (CRC), we performed whole-genome sequencing of 1,439 cases and 720 controls, imputed discovered sequence variants and Haplotype Reference Consortium panel variants into genome-wide association study data, and tested for association in 34,869 cases and 29,051 controls. Findings were followed up in an additional 23,262 cases and 38,296 controls. We discovered a strongly protective 0.3% frequency variant signal at CHD1. In a combined meta-analysis of 125,478 individuals, we identified 40 new independent signals at P < 5 × 10 −8 , bringing the number of known independent signals for CRC to ~100. New signals implicate lower-frequency variants, Krüppel-like factors, Hedgehog signaling, Hippo-YAP signaling, long noncoding RNAs and somatic drivers, and support a role for immune function. Heritability analyses suggest that CRC risk is highly polygenic, and larger, more comprehensive studies enabling rare variant analysis will improve understanding of biology underlying this risk and influence personalized screening strategies and drug development. © 2018, This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply.
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- 2019
18. Correction to: Association analyses of more than 140,000 men identify 63 new prostate cancer susceptibility loci (Nature Genetics, (2018), 50, 7, (928-936), 10.1038/s41588-018-0142-8).
- Author
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Xu J., Tyrer J., Truong T., Koudou Y.A., Khaw K.-T., Cannon-Albright L., Pandha H., Michael A., Thibodeau S.N., McDonnell S.K., Schaid D.J., Lindstrom S., Turman C., Ma J., Hunter D.J., Riboli E., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Hoover R.N., Machiela M.J., Cui Z., Kraft P., Amos C.I., Conti D.V., Easton D.F., Wiklund F., Chanock S.J., Henderson B.E., Kote-Jarai Z., Haiman C.A., Eeles R.A., Schumacher F.R., Olama A.A.A., Berndt S.I., Benlloch S., Ahmed M., Saunders E.J., Dadaev T., Leongamornlert D., Anokian E., Cieza-Borrella C., Goh C., Brook M.N., Sheng X., Fachal L., Dennis J., Muir K., Lophatananon A., Stevens V.L., Gapstur S.M., Carter B.D., Tangen C.M., Goodman P.J., Thompson I.M., Batra J., Chambers S., Moya L., Clements J., Horvath L., Tilley W., Risbridger G.P., Gronberg H., Aly M., Nordstrom T., Pharoah P., Pashayan N., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Albanes D., Weinstein S., Wolk A., Hakansson N., West C.M.L., Dunning A.M., Burnet N., Mucci L.A., Giovannucci E., Andriole G.L., Cussenot O., Cancel-Tassin G., Koutros S., Beane Freeman L.E., Sorensen K.D., Orntoft T.F., Borre M., Maehle L., Grindedal E.M., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Travis R.C., Key T.J., Hamilton R.J., Fleshner N.E., Finelli A., Ingles S.A., Stern M.C., Rosenstein B.S., Kerns S.L., Ostrer H., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Guo X., Wang G., Sun Z., Giles G.G., Southey M.C., MacInnis R.J., FitzGerald L.M., Kibel A.S., Drake B.F., Vega A., Gomez-Caamano A., Szulkin R., Eklund M., Kogevinas M., Llorca J., Castano-Vinyals G., Penney K.L., Stampfer M., Park J.Y., Sellers T.A., Lin H.-Y., Stanford J.L., Cybulski C., Wokolorczyk D., Lubinski J., Ostrander E.A., Geybels M.S., Nordestgaard B.G., Nielsen S.F., Weischer M., Bisbjerg R., Roder M.A., Iversen P., Brenner H., Cuk K., Holleczek B., Maier C., Luedeke M., Schnoeller T., Kim J., Logothetis C.J., John E.M., Teixeira M.R., Paulo P., Cardoso M., Neuhausen S.L., Steele L., Ding Y.C., De Ruyck K., De Meerleer G., Ost P., Razack A., Lim J., Teo S.-H., Lin D.W., Newcomb L.F., Lessel D., Gamulin M., Kulis T., Kaneva R., Usmani N., Singhal S., Slavov C., Mitev V., Parliament M., Claessens F., Joniau S., Van den Broeck T., Larkin S., Townsend P.A., Aukim-Hastie C., Gago-Dominguez M., Castelao J.E., Martinez M.E., Roobol M.J., Jenster G., van Schaik R.H.N., Menegaux F., Xu J., Tyrer J., Truong T., Koudou Y.A., Khaw K.-T., Cannon-Albright L., Pandha H., Michael A., Thibodeau S.N., McDonnell S.K., Schaid D.J., Lindstrom S., Turman C., Ma J., Hunter D.J., Riboli E., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Hoover R.N., Machiela M.J., Cui Z., Kraft P., Amos C.I., Conti D.V., Easton D.F., Wiklund F., Chanock S.J., Henderson B.E., Kote-Jarai Z., Haiman C.A., Eeles R.A., Schumacher F.R., Olama A.A.A., Berndt S.I., Benlloch S., Ahmed M., Saunders E.J., Dadaev T., Leongamornlert D., Anokian E., Cieza-Borrella C., Goh C., Brook M.N., Sheng X., Fachal L., Dennis J., Muir K., Lophatananon A., Stevens V.L., Gapstur S.M., Carter B.D., Tangen C.M., Goodman P.J., Thompson I.M., Batra J., Chambers S., Moya L., Clements J., Horvath L., Tilley W., Risbridger G.P., Gronberg H., Aly M., Nordstrom T., Pharoah P., Pashayan N., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Albanes D., Weinstein S., Wolk A., Hakansson N., West C.M.L., Dunning A.M., Burnet N., Mucci L.A., Giovannucci E., Andriole G.L., Cussenot O., Cancel-Tassin G., Koutros S., Beane Freeman L.E., Sorensen K.D., Orntoft T.F., Borre M., Maehle L., Grindedal E.M., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Travis R.C., Key T.J., Hamilton R.J., Fleshner N.E., Finelli A., Ingles S.A., Stern M.C., Rosenstein B.S., Kerns S.L., Ostrer H., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Guo X., Wang G., Sun Z., Giles G.G., Southey M.C., MacInnis R.J., FitzGerald L.M., Kibel A.S., Drake B.F., Vega A., Gomez-Caamano A., Szulkin R., Eklund M., Kogevinas M., Llorca J., Castano-Vinyals G., Penney K.L., Stampfer M., Park J.Y., Sellers T.A., Lin H.-Y., Stanford J.L., Cybulski C., Wokolorczyk D., Lubinski J., Ostrander E.A., Geybels M.S., Nordestgaard B.G., Nielsen S.F., Weischer M., Bisbjerg R., Roder M.A., Iversen P., Brenner H., Cuk K., Holleczek B., Maier C., Luedeke M., Schnoeller T., Kim J., Logothetis C.J., John E.M., Teixeira M.R., Paulo P., Cardoso M., Neuhausen S.L., Steele L., Ding Y.C., De Ruyck K., De Meerleer G., Ost P., Razack A., Lim J., Teo S.-H., Lin D.W., Newcomb L.F., Lessel D., Gamulin M., Kulis T., Kaneva R., Usmani N., Singhal S., Slavov C., Mitev V., Parliament M., Claessens F., Joniau S., Van den Broeck T., Larkin S., Townsend P.A., Aukim-Hastie C., Gago-Dominguez M., Castelao J.E., Martinez M.E., Roobol M.J., Jenster G., van Schaik R.H.N., and Menegaux F.
- Abstract
In the version of this article initially published, the name of author Manuela Gago-Dominguez was misspelled as Manuela Gago Dominguez. The error has been corrected in the HTML and PDF version of the article.Copyright © 2018, The Author(s), under exclusive licence to Springer Nature America, Inc.
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- 2019
19. Author Correction: Association analyses of more than 140,000 men identify 63 new prostate cancer susceptibility loci (Nature Genetics, (2018), 50, 7, (928-936), 10.1038/s41588-018-0142-8).
- Author
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Truong T., Khaw K.-T., Cannon-Albright L., Pandha H., Michael A., Thibodeau S.N., McDonnell S.K., Schaid D.J., Lindstrom S., Turman C., Ma J., Hunter D.J., Riboli E., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Hoover R.N., Machiela M.J., Cui Z., Kraft P., Amos C.I., Conti D.V., Easton D.F., Wiklund F., Chanock S.J., Henderson B.E., Kote-Jarai Z., Haiman C.A., Eeles R.A., Schumacher F.R., Olama A.A.A., Berndt S.I., Benlloch S., Ahmed M., Saunders E.J., Dadaev T., Leongamornlert D., Anokian E., Cieza-Borrella C., Goh C., Brook M.N., Sheng X., Fachal L., Dennis J., Tyrer J., Muir K., Lophatananon A., Stevens V.L., Gapstur S.M., Carter B.D., Tangen C.M., Goodman P.J., Thompson I.M., Batra J., Chambers S., Moya L., Clements J., Horvath L., Tilley W., Risbridger G.P., Gronberg H., Aly M., Nordstrom T., Pharoah P., Pashayan N., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Albanes D., Weinstein S., Wolk A., Hakansson N., West C.M.L., Dunning A.M., Burnet N., Mucci L.A., Giovannucci E., Andriole G.L., Cussenot O., Cancel-Tassin G., Koutros S., Beane Freeman L.E., Sorensen K.D., Orntoft T.F., Borre M., Maehle L., Grindedal E.M., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Travis R.C., Key T.J., Hamilton R.J., Fleshner N.E., Finelli A., Ingles S.A., Stern M.C., Rosenstein B.S., Kerns S.L., Ostrer H., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Guo X., Wang G., Sun Z., Giles G.G., Southey M.C., MacInnis R.J., FitzGerald L.M., Kibel A.S., Drake B.F., Vega A., Gomez-Caamano A., Szulkin R., Eklund M., Kogevinas M., Llorca J., Castano-Vinyals G., Penney K.L., Stampfer M., Park J.Y., Sellers T.A., Lin H.-Y., Stanford J.L., Cybulski C., Wokolorczyk D., Lubinski J., Ostrander E.A., Geybels M.S., Nordestgaard B.G., Nielsen S.F., Weischer M., Bisbjerg R., Roder M.A., Iversen P., Brenner H., Cuk K., Holleczek B., Maier C., Luedeke M., Schnoeller T., Kim J., Logothetis C.J., John E.M., Teixeira M.R., Paulo P., Cardoso M., Neuhausen S.L., Steele L., Ding Y.C., De Ruyck K., De Meerleer G., Ost P., Razack A., Lim J., Teo S.-H., Lin D.W., Newcomb L.F., Lessel D., Gamulin M., Kulis T., Kaneva R., Usmani N., Singhal S., Slavov C., Mitev V., Parliament M., Claessens F., Joniau S., Van den Broeck T., Larkin S., Townsend P.A., Aukim-Hastie C., Gago-Dominguez M., Castelao J.E., Martinez M.E., Roobol M.J., Jenster G., van Schaik R.H.N., Menegaux F., Koudou Y.A., Xu J., Truong T., Khaw K.-T., Cannon-Albright L., Pandha H., Michael A., Thibodeau S.N., McDonnell S.K., Schaid D.J., Lindstrom S., Turman C., Ma J., Hunter D.J., Riboli E., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Hoover R.N., Machiela M.J., Cui Z., Kraft P., Amos C.I., Conti D.V., Easton D.F., Wiklund F., Chanock S.J., Henderson B.E., Kote-Jarai Z., Haiman C.A., Eeles R.A., Schumacher F.R., Olama A.A.A., Berndt S.I., Benlloch S., Ahmed M., Saunders E.J., Dadaev T., Leongamornlert D., Anokian E., Cieza-Borrella C., Goh C., Brook M.N., Sheng X., Fachal L., Dennis J., Tyrer J., Muir K., Lophatananon A., Stevens V.L., Gapstur S.M., Carter B.D., Tangen C.M., Goodman P.J., Thompson I.M., Batra J., Chambers S., Moya L., Clements J., Horvath L., Tilley W., Risbridger G.P., Gronberg H., Aly M., Nordstrom T., Pharoah P., Pashayan N., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Albanes D., Weinstein S., Wolk A., Hakansson N., West C.M.L., Dunning A.M., Burnet N., Mucci L.A., Giovannucci E., Andriole G.L., Cussenot O., Cancel-Tassin G., Koutros S., Beane Freeman L.E., Sorensen K.D., Orntoft T.F., Borre M., Maehle L., Grindedal E.M., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Travis R.C., Key T.J., Hamilton R.J., Fleshner N.E., Finelli A., Ingles S.A., Stern M.C., Rosenstein B.S., Kerns S.L., Ostrer H., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Guo X., Wang G., Sun Z., Giles G.G., Southey M.C., MacInnis R.J., FitzGerald L.M., Kibel A.S., Drake B.F., Vega A., Gomez-Caamano A., Szulkin R., Eklund M., Kogevinas M., Llorca J., Castano-Vinyals G., Penney K.L., Stampfer M., Park J.Y., Sellers T.A., Lin H.-Y., Stanford J.L., Cybulski C., Wokolorczyk D., Lubinski J., Ostrander E.A., Geybels M.S., Nordestgaard B.G., Nielsen S.F., Weischer M., Bisbjerg R., Roder M.A., Iversen P., Brenner H., Cuk K., Holleczek B., Maier C., Luedeke M., Schnoeller T., Kim J., Logothetis C.J., John E.M., Teixeira M.R., Paulo P., Cardoso M., Neuhausen S.L., Steele L., Ding Y.C., De Ruyck K., De Meerleer G., Ost P., Razack A., Lim J., Teo S.-H., Lin D.W., Newcomb L.F., Lessel D., Gamulin M., Kulis T., Kaneva R., Usmani N., Singhal S., Slavov C., Mitev V., Parliament M., Claessens F., Joniau S., Van den Broeck T., Larkin S., Townsend P.A., Aukim-Hastie C., Gago-Dominguez M., Castelao J.E., Martinez M.E., Roobol M.J., Jenster G., van Schaik R.H.N., Menegaux F., Koudou Y.A., and Xu J.
- Abstract
In the version of this article initially published, the name of author Manuela Gago-Dominguez was misspelled as Manuela Gago Dominguez. The error has been corrected in the HTML and PDF version of the article.Copyright © 2018, The Author(s), under exclusive licence to Springer Nature America, Inc.
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- 2019
20. Genome-wide meta-analysis identifies five new susceptibility loci for pancreatic cancer
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Klein, A.P. Wolpin, B.M. Risch, H.A. Stolzenberg-Solomon, R.Z. Mocci, E. Zhang, M. Canzian, F. Childs, E.J. Hoskins, J.W. Jermusyk, A. Zhong, J. Chen, F. Albanes, D. Andreotti, G. Arslan, A.A. Babic, A. Bamlet, W.R. Beane-Freeman, L. Berndt, S.I. Blackford, A. Borges, M. Borgida, A. Bracci, P.M. Brais, L. Brennan, P. Brenner, H. Bueno-De-Mesquita, B. Buring, J. Campa, D. Capurso, G. Cavestro, G.M. Chaffee, K.G. Chung, C.C. Cleary, S. Cotterchio, M. Dijk, F. Duell, E.J. Foretova, L. Fuchs, C. Funel, N. Gallinger, S. Gaziano, J.M.M. Gazouli, M. Giles, G.G. Giovannucci, E. Goggins, M. Goodman, G.E. Goodman, P.J. Hackert, T. Haiman, C. Hartge, P. Hasan, M. Hegyi, P. Helzlsouer, K.J. Herman, J. Holcatova, I. Holly, E.A. Hoover, R. Hung, R.J. Jacobs, E.J. Jamroziak, K. Janout, V. Kaaks, R. Khaw, K.-T. Klein, E.A. Kogevinas, M. Kooperberg, C. Kulke, M.H. Kupcinskas, J. Kurtz, R.J. Laheru, D. Landi, S. Lawlor, R.T. Lee, I.-M. Lemarchand, L. Lu, L. Malats, N. Mambrini, A. Mannisto, S. Milne, R.L. Mohelníková-Duchoňová, B. Neale, R.E. Neoptolemos, J.P. Oberg, A.L. Olson, S.H. Orlow, I. Pasquali, C. Patel, A.V. Peters, U. Pezzilli, R. Porta, M. Real, F.X. Rothman, N. Scelo, G. Sesso, H.D. Severi, G. Shu, X.-O. Silverman, D. Smith, J.P. Soucek, P. Sund, M. Talar-Wojnarowska, R. Tavano, F. Thornquist, M.D. Tobias, G.S. Van Den Eeden, S.K. Vashist, Y. Visvanathan, K. Vodicka, P. Wactawski-Wende, J. Wang, Z. Wentzensen, N. White, E. Yu, H. Yu, K. Zeleniuch-Jacquotte, A. Zheng, W. Kraft, P. Li, D. Chanock, S. Obazee, O. Petersen, G.M. Amundadottir, L.T.
- Abstract
In 2020, 146,063 deaths due to pancreatic cancer are estimated to occur in Europe and the United States combined. To identify common susceptibility alleles, we performed the largest pancreatic cancer GWAS to date, including 9040 patients and 12,496 controls of European ancestry from the Pancreatic Cancer Cohort Consortium (PanScan) and the Pancreatic Cancer Case-Control Consortium (PanC4). Here, we find significant evidence of a novel association at rs78417682 (7p12/TNS3, P = 4.35 × 10-8). Replication of 10 promising signals in up to 2737 patients and 4752 controls from the PANcreatic Disease ReseArch (PANDoRA) consortium yields new genome-wide significant loci: Rs13303010 at 1p36.33 (NOC2L, P = 8.36 × 10-14), rs2941471 at 8q21.11 (HNF4G, P = 6.60 × 10-10), rs4795218 at 17q12 (HNF1B, P = 1.32 × 10-8), and rs1517037 at 18q21.32 (GRP, P = 3.28 × 10-8). rs78417682 is not statistically significantly associated with pancreatic cancer in PANDoRA. Expression quantitative trait locus analysis in three independent pancreatic data sets provides molecular support of NOC2L as a pancreatic cancer susceptibility gene. © 2018 The Author(s).
- Published
- 2018
21. Association analyses of more than 140,000 men identify 63 new prostate cancer susceptibility loci.
- Author
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Grindedal E.M., Maier C., Luedeke M., Schnoeller T., Kim J., Logothetis C.J., John E.M., Teixeira M.R., Paulo P., Cardoso M., Neuhausen S.L., Steele L., Ding Y.C., De Ruyck K., De Meerleer G., Ost P., Razack A., Lim J., Teo S.-H., Lin D.W., Newcomb L.F., Lessel D., Gamulin M., Kulis T., Kaneva R., Usmani N., Singhal S., Slavov C., Mitev V., Parliament M., Claessens F., Joniau S., Van Den Broeck T., Larkin S., Townsend P.A., Aukim-Hastie C., Dominguez M.G., Castelao J.E., Martinez M.E., Roobol M.J., Jenster G., Van Schaik R.H.N., Menegaux F., Truong T., Koudou Y.A., Xu J., Khaw K.-T., Cannon-Albright L., Pandha H., Michael A., Thibodeau S.N., McDonnell S.K., Schaid D.J., Lindstrom S., Turman C., Ma J., Hunter D.J., Riboli E., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Hoover R.N., Machiela M.J., Cui Z., Kraft P., Amos C.I., Conti D.V., Easton D.F., Wiklund F., Chanock S.J., Henderson B.E., Kote-Jarai Z., Haiman C.A., Eeles R.A., Schumacher F.R., Al Olama A.A., Berndt S.I., Benlloch S., Ahmed M., Saunders E.J., Dadaev T., Leongamornlert D., Anokian E., Cieza-Borrella C., Goh C., Brook M.N., Sheng X., Fachal L., Dennis J., Tyrer J., Muir K., Lophatananon A., Stevens V.L., Gapstur S.M., Carter B.D., Tangen C.M., Goodman P.J., Thompson I.M., Batra J., Chambers S., Moya L., Clements J., Horvath L., Tilley W., Risbridger G.P., Gronberg H., Aly M., Nordstrom T., Pharoah P., Pashayan N., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Albanes D., Weinstein S., Wolk A., Hakansson N., West C.M.L., Dunning A.M., Burnet N., Mucci L.A., Giovannucci E., Andriole G.L., Cussenot O., Cancel-Tassin G., Koutros S., Beane Freeman L.E., Sorensen K.D., Orntoft T.F., Borre M., Maehle L., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Travis R.C., Key T.J., Hamilton R.J., Fleshner N.E., Finelli A., Ingles S.A., Stern M.C., Rosenstein B.S., Kerns S.L., Ostrer H., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Guo X., Wang G., Sun Z., Giles G.G., Southey M.C., MacInnis R.J., Fitzgerald L.M., Kibel A.S., Drake B.F., Vega A., Gomez-Caamano A., Szulkin R., Eklund M., Kogevinas M., Llorca J., Castano-Vinyals G., Penney K.L., Stampfer M., Park J.Y., Sellers T.A., Lin H.-Y., Stanford J.L., Cybulski C., Wokolorczyk D., Lubinski J., Ostrander E.A., Geybels M.S., Nordestgaard Bo.G., Nielsen S.F., Weischer M., Bisbjerg R., Roder M.A., Iversen P., Brenner H., Cuk K., Holleczek B., Grindedal E.M., Maier C., Luedeke M., Schnoeller T., Kim J., Logothetis C.J., John E.M., Teixeira M.R., Paulo P., Cardoso M., Neuhausen S.L., Steele L., Ding Y.C., De Ruyck K., De Meerleer G., Ost P., Razack A., Lim J., Teo S.-H., Lin D.W., Newcomb L.F., Lessel D., Gamulin M., Kulis T., Kaneva R., Usmani N., Singhal S., Slavov C., Mitev V., Parliament M., Claessens F., Joniau S., Van Den Broeck T., Larkin S., Townsend P.A., Aukim-Hastie C., Dominguez M.G., Castelao J.E., Martinez M.E., Roobol M.J., Jenster G., Van Schaik R.H.N., Menegaux F., Truong T., Koudou Y.A., Xu J., Khaw K.-T., Cannon-Albright L., Pandha H., Michael A., Thibodeau S.N., McDonnell S.K., Schaid D.J., Lindstrom S., Turman C., Ma J., Hunter D.J., Riboli E., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Hoover R.N., Machiela M.J., Cui Z., Kraft P., Amos C.I., Conti D.V., Easton D.F., Wiklund F., Chanock S.J., Henderson B.E., Kote-Jarai Z., Haiman C.A., Eeles R.A., Schumacher F.R., Al Olama A.A., Berndt S.I., Benlloch S., Ahmed M., Saunders E.J., Dadaev T., Leongamornlert D., Anokian E., Cieza-Borrella C., Goh C., Brook M.N., Sheng X., Fachal L., Dennis J., Tyrer J., Muir K., Lophatananon A., Stevens V.L., Gapstur S.M., Carter B.D., Tangen C.M., Goodman P.J., Thompson I.M., Batra J., Chambers S., Moya L., Clements J., Horvath L., Tilley W., Risbridger G.P., Gronberg H., Aly M., Nordstrom T., Pharoah P., Pashayan N., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Albanes D., Weinstein S., Wolk A., Hakansson N., West C.M.L., Dunning A.M., Burnet N., Mucci L.A., Giovannucci E., Andriole G.L., Cussenot O., Cancel-Tassin G., Koutros S., Beane Freeman L.E., Sorensen K.D., Orntoft T.F., Borre M., Maehle L., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Travis R.C., Key T.J., Hamilton R.J., Fleshner N.E., Finelli A., Ingles S.A., Stern M.C., Rosenstein B.S., Kerns S.L., Ostrer H., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Guo X., Wang G., Sun Z., Giles G.G., Southey M.C., MacInnis R.J., Fitzgerald L.M., Kibel A.S., Drake B.F., Vega A., Gomez-Caamano A., Szulkin R., Eklund M., Kogevinas M., Llorca J., Castano-Vinyals G., Penney K.L., Stampfer M., Park J.Y., Sellers T.A., Lin H.-Y., Stanford J.L., Cybulski C., Wokolorczyk D., Lubinski J., Ostrander E.A., Geybels M.S., Nordestgaard Bo.G., Nielsen S.F., Weischer M., Bisbjerg R., Roder M.A., Iversen P., Brenner H., Cuk K., and Holleczek B.
- Abstract
Genome-wide association studies (GWAS) and fine-mapping efforts to date have identified more than 100 prostate cancer (PrCa)-susceptibility loci. We meta-analyzed genotype data from a custom high-density array of 46,939 PrCa cases and 27,910 controls of European ancestry with previously genotyped data of 32,255 PrCa cases and 33,202 controls of European ancestry. Our analysis identified 62 novel loci associated (P < 5.0 x 10-8) with PrCa and one locus significantly associated with early-onset PrCa (<=55 years). Our findings include missense variants rs1800057 (odds ratio (OR) = 1.16; P = 8.2 x 10-9; G>C, p.Pro1054Arg) in ATM and rs2066827 (OR = 1.06; P = 2.3 x 10-9; T>G, p.Val109Gly) in CDKN1B. The combination of all loci captured 28.4% of the PrCa familial relative risk, and a polygenic risk score conferred an elevated PrCa risk for men in the ninetieth to ninety-ninth percentiles (relative risk = 2.69; 95% confidence interval (CI): 2.55-2.82) and first percentile (relative risk = 5.71; 95% CI: 5.04-6.48) risk stratum compared with the population average. These findings improve risk prediction, enhance fine-mapping, and provide insight into the underlying biology of PrCa 1 .Copyright © 2018 The Author(s).
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- 2018
22. Circulating sex hormones in relation to anthropometric, sociodemographic and behavioural factors in an international dataset of 12,300 men
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Watts, E.L. Appleby, P.N. Albanes, D. Black, A. Chan, J.M. Chen, C. Cirillo, P.M. Cohn, B.A. Cook, M.B. Donovan, J.L. Ferrucci, L. Garland, C.F. Giles, G.G. Goodman, P.J. Habel, L.A. Haiman, C.A. Holly, J.M.P. Hoover, R.N. Kaaks, R. Knekt, P. Kolonel, L.N. Kubo, T. Le Marchand, L. Luostarinen, T. MacInnis, R.J. Mäenpää, H.O. Männistö, S. Metter, E.J. Milne, R.L. Nomura, A.M.Y. Oliver, S.E. Parsons, J.K. Peeters, P.H. Platz, E.A. Riboli, E. Ricceri, F. Rinaldi, S. Rissanen, H. Sawada, N. Schaefer, C.A. Schenk, J.M. Stanczyk, F.Z. Stampfer, M. Stattin, P. Stenman, U.-H. Tjønneland, A. Trichopoulou, A. Thompson, I.M. Tsugane, S. Vatten, L. Whittemore, A.S. Ziegler, R.G. Allen, N.E. Key, T.J. Travis, R.C.
- Abstract
Introduction Sex hormones have been implicated in the etiology of a number of diseases. To better understand disease etiology and the mechanisms of disease-risk factor associations, this analysis aimed to investigate the associations of anthropometric, sociodemographic and behavioural factors with a range of circulating sex hormones and sex hormone-binding globulin. Methods Statistical analyses of individual participant data from 12,330 male controls aged 25–85 years from 25 studies involved in the Endogenous Hormones Nutritional Biomarkers and Prostate Cancer Collaborative Group. Analysis of variance was used to estimate geometric means adjusted for study and relevant covariates. Results Older age was associated with higher concentrations of sex hormone-binding globulin and dihydrotestosterone and lower concentrations of dehydroepiandrosterone sulfate, free testosterone, androstenedione, androstanediol glucuronide and free estradiol. Higher body mass index was associated with higher concentrations of free estradiol, androstanediol glucuronide, estradiol and estrone and lower concentrations of dihydrotestosterone, testosterone, sex hormone-binding globulin, free testosterone, androstenedione and dehydroepiandrosterone sulfate. Taller height was associated with lower concentrations of androstenedione, testosterone, free testosterone and sex hormone-binding globulin and higher concentrations of androstanediol glucuronide. Current smoking was associated with higher concentrations of androstenedione, sex hormone-binding globulin and testosterone. Alcohol consumption was associated with higher concentrations of dehydroepiandrosterone sulfate, androstenedione and androstanediol glucuronide. East Asians had lower concentrations of androstanediol glucuronide and African Americans had higher concentrations of estrogens. Education and marital status were modestly associated with a small number of hormones. Conclusion Circulating sex hormones in men are strongly associated with age and body mass index, and to a lesser extent with smoking status and alcohol consumption. This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.
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- 2017
23. A microcomputer method for continuous measurement, recording and control of ion activity during nitrate uptake by Lolium perenne
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GOODMAN, P.J., WILLIAMS, JANET, and WILLIAMS, T.E.
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- 1987
24. Three new pancreatic cancer susceptibility signals identified on chromosomes 1q32.1, 5p15.33 and 8q24.21
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Zhang, M. Wang, Z. Obazee, O. Jia, J. Childs, E.J. Hoskins, J. Figlioli, G. Mocci, E. Collins, I. Chung, C.C. Hautman, C. Arslan, A.A. Beane-Freeman, L. Bracci, P.M. Buring, J. Duell, E.J. Gallinger, S. Giles, G.G. Goodman, G.E. Goodman, P.J. Kamineni, A. Kolonel, L.N. Kulke, M.H. Malats, N. Olson, S.H. Sesso, H.D. Visvanathan, K. White, E. Zheng, W. Abnet, C.C. Albanes, D. Andreotti, G. Brais, L. Bas Bueno-de-Mesquita, H. Basso, D. Berndt, S.I. Boutron-Ruault, M.-C. Bijlsma, M.F. Brenner, H. Burdette, L. Campa, D. Caporaso, N.E. Capurso, G. Cavestro, G.M. Cotterchio, M. Costello, E. Elena, J. Boggi, U. Michael Gaziano, J. Gazouli, M. Giovannucci, E.L. Goggins, M. Gross, M. Haiman, C.A. Hassan, M. Helzlsouer, K.J. Hu, N. Hunter, D.J. Iskierka-Jazdzewska, E. Jenab, M. Kaaks, R. Key, T.J. Khaw, K.-T. Klein, E.A. Kogevinas, M. Krogh, V. Kupcinskas, J. Kurtz, R.C. Landi, M.T. Landi, S. Marchand, L.L. Mambrini, A. Mannisto, S. Milne, R.L. Neale, R.E. Oberg, A.L. Panico, S. Patel, A.V. Peeters, P.H.M. Peters, U. Pezzilli, R. Porta, M. Purdue, M. Ramón Quiros, J. Riboli, E. Rothman, N. Scarpa, A. Scelo, G. Shu, X.-O. Silverman, D.T. Soucek, P. Strobel, O. Sund, M. Malecka-Panas, E. Taylor, P.R. Tavano, F. Travis, R.C. Thornquist, M. Tjønneland, A. Tobias, G.S. Trichopoulos, D. Vashist, Y. Vodicka, P. Wactawski-Wende, J. Wentzensen, N. Yu, H. Yu, K. Zeleniuch-Jacquotte, A. Kooperberg, C. Risch, H.A. Jacobs, E.J. Li, D. Fuchs, C. Hoover, R. Hartge, P. Chanock, S.J. Petersen, G.M. Stolzenberg-Solomon, R.S. Wolpin, B.M. Kraft, P. Klein, A.P. Canzian, F. Amundadottir, L.T.
- Abstract
Genome-wide association studies (GWAS) have identified common pancreatic cancer susceptibility variants at 13 chromosomal loci in individuals of European descent. To identify new susceptibility variants, we performed imputation based on 1000 Genomes (1000G) Project data and association analysis using 5,107 case and 8,845 control subjects from 27 cohort and case-control studies that participated in the PanScan I-III GWAS. This analysis, in combination with a two-staged replication in an additional 6,076 case and 7,555 control subjects from the PANcreatic Disease ReseArch (PANDoRA) and Pancreatic Cancer Case-Control (PanC4) Consortia uncovered 3 new pancreatic cancer risk signals marked by single nucleotide polymorphisms (SNPs) rs2816938 at chromosome 1q32.1 (per allele odds ratio (OR) = 1.20, P = 4.88x10-15), rs10094872 at 8q24.21 (OR = 1.15, P = 3.22x10-9) and rs35226131 at 5p15.33 (OR = 0.71, P = 1.70x10-8). These SNPs represent independent risk variants at previously identified pancreatic cancer risk loci on chr1q32.1 (NR5A2), chr8q24.21 (MYC) and chr5p15.33 (CLPTM1L-TERT) as per analyses conditioned on previously reported susceptibility variants. We assessed expression of candidate genes at the three risk loci in histologically normal (n = 10) and tumor (n = 8) derived pancreatic tissue samples and observed a marked reduction of NR5A2 expression (chr1q32.1) in the tumors (fold change -7.6, P = 5.7x10-8). This finding was validated in a second set of paired (n = 20) histologically normal and tumor derived pancreatic tissue samples (average fold change for three NR5A2 isoforms -31.3 to -95.7, P = 7.5x10-4-2.0x10-3). Our study has identified new susceptibility variants independently conferring pancreatic cancer risk that merit functional follow-up to identify target genes and explain the underlying biology.
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- 2016
25. A randomized controlled Alzheimer's disease prevention trial's evolution into an exposure trial: The preadvise trial
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Kryscio, R.J., primary, Abner, E.L., additional, Schmitt, F.A., additional, Goodman, P.J., additional, Mendiondo, M., additional, Caban-Holt, A., additional, Dennis, B.C., additional, Mathews, M., additional, Klein, E.A., additional, and Crowley, J.J., additional
- Published
- 2013
- Full Text
- View/download PDF
26. 1217 THE PROSTATE CANCER PREVENTION TRIAL (PCPT) RISK CALCULATOR AND THE RELATIONSHIP BETWEEN PSA AND BIOPSY OUTCOME
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Vickers, A.J., primary, Sjoberg, D., additional, Ankerst, D.P., additional, Tangen, C.M., additional, Goodman, P.J., additional, and Thompson, I.M., additional
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- 2012
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- View/download PDF
27. Operating Characteristics of Prostate-Specific Antigen in Men With an Initial PSA Level of 3.0 Ng/Ml or Lower
- Author
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Thompson, I.M., primary, Ankerst, D.P., additional, Chi, C., additional, Lucia, M.S., additional, Goodman, P.J., additional, Crowley, J.J., additional, Parnes, H.L., additional, and Coltman, C.A., additional
- Published
- 2006
- Full Text
- View/download PDF
28. Computer based project tools.
- Author
-
Bowness M.J., Mine to mill 1998 Brisbane, Queensland 11-Oct-9814-Oct-98, Goodman P.J., Leaning R.W., Lidgate P.N., Bowness M.J., Mine to mill 1998 Brisbane, Queensland 11-Oct-9814-Oct-98, Goodman P.J., Leaning R.W., and Lidgate P.N.
- Abstract
A guide is presented for the selection of the optimum type of software package for overall system simulation, discrete unit optimisation and drafting and design. Discussion is illustrated by case studies: Fluor Daniel Australia's dynamic simulation model for BHP's Port Hedland and Finucane Island iron ore shipping facilities in Western Australia; the use of JKSimMet to design a crushing plant; and the use of photogrammetry in the retrofitting of existing plant., A guide is presented for the selection of the optimum type of software package for overall system simulation, discrete unit optimisation and drafting and design. Discussion is illustrated by case studies: Fluor Daniel Australia's dynamic simulation model for BHP's Port Hedland and Finucane Island iron ore shipping facilities in Western Australia; the use of JKSimMet to design a crushing plant; and the use of photogrammetry in the retrofitting of existing plant.
- Published
- 1998
29. PHYSIOLOGICAL ANALYSIS OF THE EFFECTS OF DIFFERENT SOILS ON SUGAR BEET CROPS IN DIFFERENT YEARS.
- Author
-
Goodman, P.J.
- Subjects
- *
SUGAR beets , *SOILS , *NITROGEN fertilizers - Abstract
Studies the physiological analysis of the effects of different soils on sugar beet crops in years 1960, 1961 and 1962. Effect of leaf area index on yield of beet crops; Influence of nitrogen fertilizers on yields of roots, tops and sugar beet crops; Implication of early sowing for yield in 1961 and 1962; Relationship between leaf area index and leaf area duration; Dependence of crop growth rate on leaf area index.
- Published
- 1968
- Full Text
- View/download PDF
30. The possible role of pathogenic fungi in die-back of Spartina townsendii agg.
- Author
-
Goodman, P.J., primary
- Published
- 1959
- Full Text
- View/download PDF
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