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6. Alcohol consumption and prostate cancer incidence and progression: A Mendelian randomisation study

Author

Brunner, Clair, Davies, Neil M., Martin, Richard M., Eeles, Rosalind, Easton, Doug, Kote‐Jarai, Zsofia, Al Olama, Ali Amin, Benlloch, Sara, Muir, Kenneth, Giles, Graham, Wiklund, Fredrik, Gronberg, Henrik, Haiman, Christopher A., Schleutker, Johanna, Nordestgaard, Børge G., Travis, Ruth C., Neal, David, Donovan, Jenny, Hamdy, Freddie C., Pashayan, Nora, Khaw, Kay‐Tee, Stanford, Janet L., Blot, William J., Thibodeau, Stephen, Maier, Christiane, Kibel, Adam S., Cybulski, Cezary, Cannon‐Albright, Lisa, Brenner, Hermann, Park, Jong, Kaneva, Radka, Batra, Jyotsna, Teixeira, Manuel R., Pandha, Hardev, and Zuccolo, Luisa

Subjects
Aged, 80 and over, Male, Alcohol Drinking, alcohol, Aldehyde Dehydrogenase, Mitochondrial, Incidence, Prostatic Neoplasms, Retinal Dehydrogenase, Aldehyde Dehydrogenase, Middle Aged, prostate cancer, Polymorphism, Single Nucleotide, Survival Analysis, Aldehyde Dehydrogenase 1 Family, Linkage Disequilibrium, Case-Control Studies, Disease Progression, Humans, Regression Analysis, alcohol metabolising genes, Neoplasm Grading, Mendelian randomisation, Cancer Epidemiology, Aged
Abstract

Prostate cancer is the most common cancer in men in developed countries, and is a target for risk reduction strategies. The effects of alcohol consumption on prostate cancer incidence and survival remain unclear, potentially due to methodological limitations of observational studies. In this study, we investigated the associations of genetic variants in alcohol‐metabolising genes with prostate cancer incidence and survival. We analysed data from 23,868 men with prostate cancer and 23,051 controls from 25 studies within the international PRACTICAL Consortium. Study‐specific associations of 68 single nucleotide polymorphisms (SNPs) in 8 alcohol‐metabolising genes (Alcohol Dehydrogenases (ADHs) and Aldehyde Dehydrogenases (ALDHs)) with prostate cancer diagnosis and prostate cancer‐specific mortality, by grade, were assessed using logistic and Cox regression models, respectively. The data across the 25 studies were meta‐analysed using fixed‐effect and random‐effects models. We found little evidence that variants in alcohol metabolising genes were associated with prostate cancer diagnosis. Four variants in two genes exceeded the multiple testing threshold for associations with prostate cancer mortality in fixed‐effect meta‐analyses. SNPs within ALDH1A2 associated with prostate cancer mortality were rs1441817 (fixed effects hazard ratio, HRfixed = 0.78; 95% confidence interval (95%CI):0.66,0.91; p values = 0.002); rs12910509, HRfixed = 0.76; 95%CI:0.64,0.91; p values = 0.003); and rs8041922 (HRfixed = 0.76; 95%CI:0.64,0.91; p values = 0.002). These SNPs were in linkage disequilibrium with each other. In ALDH1B1, rs10973794 (HRfixed = 1.43; 95%CI:1.14,1.79; p values = 0.002) was associated with prostate cancer mortality in men with low‐grade prostate cancer. These results suggest that alcohol consumption is unlikely to affect prostate cancer incidence, but it may influence disease progression., What's new? Alcohol may spur prostate cancer progression, though it does not appear to affect incidence, according to new analysis. Variation in genes involved in alcohol metabolism affect how much the body is exposed to carcinogenic metabolites. These authors examined 68 genetic variants in alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) genes, seeking a link with prostate cancer risk. While they found no evidence that these variants alter prostate cancer incidence, they did show that SNPs in the ALDH1A2 gene affect prostate cancer mortality. From a public health standpoint, these results suggest reducing alcohol consumption could slow prostate cancer disease progression.

Published
2017

7. Investigating the possible causal role of coffee consumption with prostate cancer risk and progression using Mendelian randomization analysis

Author

Taylor, Amy E, Martin, Richard M, Geybels, Milan S, Stanford, Janet L, Shui, Irene, Eeles, Rosalind, Easton, Doug, Kote-Jarai, Zsofia, Amin Al Olama, Ali, Benlloch, Sara, Muir, Kenneth, Giles, Graham G, Wiklund, Fredrik, Gronberg, Henrik, Haiman, Christopher A, Schleutker, Johanna, Nordestgaard, Børge G, Travis, Ruth C, Neal, David, Pashayan, Nora, Khaw, Kay-Tee, Blot, William, Thibodeau, Stephen, Maier, Christiane, Kibel, Adam S, Cybulski, Cezary, Cannon-Albright, Lisa, Brenner, Hermann, Park, Jong, Kaneva, Radka, Batra, Jyotsna, Teixeira, Manuel R, Pandha, Hardev, PRACTICAL Consortium, Donovan, Jenny, Munafò, Marcus R, Easton, Douglas [0000-0003-2444-3247], Amin Al Olama, Ali [0000-0002-7178-3431], Khaw, Kay-Tee [0000-0002-8802-2903], and Apollo - University of Cambridge Repository

Subjects
Male, Prostate cancer, Tobacco and Alcohol, coffee, Genetic Variation, Prostatic Neoplasms, Mendelian Randomization Analysis, Middle Aged, Brain and Behaviour, prostate cancer, Centre for Surgical Research, Mendelian Randomization, Risk Factors, Mendelian randomization, Disease Progression, Humans, ICEP, Alleles, Aged
Abstract

Coffee consumption has been shown in some studies to be associated with lower risk of prostate cancer. However, it is unclear if this association is causal or due to confounding or reverse causality. We conducted a Mendelian randomisation analysis to investigate the causal effects of coffee consumption on prostate cancer risk and progression. We used two genetic variants robustly associated with caffeine intake (rs4410790 and rs2472297) as proxies for coffee consumption in a sample of 46,687 men of European ancestry from 25 studies in the PRACTICAL consortium. Associations between genetic variants and prostate cancer case status, stage and grade were assessed by logistic regression and with all-cause and prostate cancer-specific mortality using Cox proportional hazards regression. There was no clear evidence that a genetic risk score combining rs4410790 and rs2472297 was associated with prostate cancer risk (OR per additional coffee increasing allele: 1.01, 95% CI: 0.98,1.03) or having high-grade compared to low-grade disease (OR: 1.01, 95% CI: 0.97,1.04). There was some evidence that the genetic risk score was associated with higher odds of having nonlocalised compared to localised stage disease (OR: 1.03, 95% CI: 1.01, 1.06). Amongst men with prostate cancer, there was no clear association between the genetic risk score and all-cause mortality (HR: 1.00, 95% CI: 0.97,1.04) or prostate cancer-specific mortality (HR: 1.03, 95% CI: 0.98,1.08). These results, which should have less bias from confounding than observational estimates, are not consistent with a substantial effect of coffee consumption on reducing prostate cancer incidence or progression.

Published
2017

8. Assessing the role of insulin-like growth factors and binding proteins in prostate cancer using Mendelian randomization: Genetic variants as instruments for circulating levels

Author

Bonilla, Carolina, Lewis, Sarah J, Rowlands, Mari-Anne, Gaunt, Tom R, Davey Smith, George, Gunnell, David, Palmer, Tom, Donovan, Jenny L, Hamdy, Freddie C, Neal, David E, Eeles, Rosalind, Easton, Doug, Kote-Jarai, Zsofia, Al Olama, Ali Amin, Benlloch, Sara, Muir, Kenneth, Giles, Graham G, Wiklund, Fredrik, Grönberg, Henrik, Haiman, Christopher A, Schleutker, Johanna, Nordestgaard, Børge G, Travis, Ruth C, Pashayan, Nora, Khaw, Kay-Tee, Stanford, Janet L, Blot, William J, Thibodeau, Stephen, Maier, Christiane, Kibel, Adam S, Cybulski, Cezary, Cannon-Albright, Lisa, Brenner, Hermann, Park, Jong, Kaneva, Radka, Batra, Jyotsna, Teixeira, Manuel R, Pandha, Hardev, PRACTICAL consortium, Lathrop, Mark, Martin, Richard M, Holly, Jeff MP, Easton, Douglas [0000-0003-2444-3247], Khaw, Kay-Tee [0000-0002-8802-2903], and Apollo - University of Cambridge Repository

Subjects
Male, Prostatic Neoplasms, ALSPAC, Mendelian Randomization Analysis, Middle Aged, prostate cancer, insulin-like growth factor-binding proteins, Polymorphism, Single Nucleotide, PRACTICAL, United Kingdom, UKHLS, Insulin-Like Growth Factor Binding Proteins, single nucleotide polymorphisms, IGFBP3, Somatomedins, insulin-like growth factors, Case-Control Studies, Mendelian randomization, Humans, ProtecT, Longitudinal Studies, Neoplasm Grading, Aged, Genome-Wide Association Study, Neoplasm Staging
Abstract

Circulating insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) are associated with prostate cancer. Using genetic variants as instruments for IGF peptides, we investigated whether these associations are likely to be causal. We identified from the literature 56 single nucleotide polymorphisms (SNPs) in the IGF axis previously associated with biomarker levels (8 from a genome-wide association study [GWAS] and 48 in reported candidate genes). In ∼700 men without prostate cancer and two replication cohorts (N ∼ 900 and ∼9,000), we examined the properties of these SNPS as instrumental variables (IVs) for IGF-I, IGF-II, IGFBP-2 and IGFBP-3. Those confirmed as strong IVs were tested for association with prostate cancer risk, low (< 7) vs. high (≥ 7) Gleason grade, localised vs. advanced stage, and mortality, in 22,936 controls and 22,992 cases. IV analysis was used in an attempt to estimate the causal effect of circulating IGF peptides on prostate cancer. Published SNPs in the IGFBP1/IGFBP3 gene region, particularly rs11977526, were strong instruments for IGF-II and IGFBP-3, less so for IGF-I. Rs11977526 was associated with high (vs. low) Gleason grade (OR per IGF-II/IGFBP-3 level-raising allele 1.05; 95% CI: 1.00, 1.10). Using rs11977526 as an IV we estimated the causal effect of a one SD increase in IGF-II (∼265 ng/mL) on risk of high vs. low grade disease as 1.14 (95% CI: 1.00, 1.31). Because of the potential for pleiotropy of the genetic instruments, these findings can only causally implicate the IGF pathway in general, not any one specific biomarker.

Published
2016

9. Alcohol consumption and prostate cancer incidence and progression: A Mendelian randomisation study

Author

Brunner, Clair, Davies, Neil M, Martin, Richard M, Eeles, Rosalind, Easton, Doug, Kote-Jarai, Zsofia, Al Olama, Ali Amin, Benlloch, Sara, Muir, Kenneth, Giles, Graham, Wiklund, Fredrik, Gronberg, Henrik, Haiman, Christopher A, Schleutker, Johanna, Nordestgaard, Børge G, Travis, Ruth C, Neal, David, Donovan, Jenny, Hamdy, Freddie C, Pashayan, Nora, Khaw, Kay-Tee, Stanford, Janet L, Blot, William J, Thibodeau, Stephen, Maier, Christiane, Kibel, Adam S, Cybulski, Cezary, Cannon-Albright, Lisa, Brenner, Hermann, Park, Jong, Kaneva, Radka, Batra, Jyotsna, Teixeira, Manuel R, Pandha, Hardev, PRACTICAL Consortium, Zuccolo, Luisa, Easton, Douglas [0000-0003-2444-3247], Khaw, Kay-Tee [0000-0002-8802-2903], and Apollo - University of Cambridge Repository

Subjects
Aged, 80 and over, Male, Alcohol Drinking, alcohol, Aldehyde Dehydrogenase, Mitochondrial, Incidence, Prostatic Neoplasms, Retinal Dehydrogenase, Aldehyde Dehydrogenase, Middle Aged, prostate cancer, Polymorphism, Single Nucleotide, Survival Analysis, Aldehyde Dehydrogenase 1 Family, Linkage Disequilibrium, Case-Control Studies, Disease Progression, Humans, Regression Analysis, alcohol metabolising genes, Neoplasm Grading, Mendelian randomisation, Aged
Abstract

Prostate cancer is the most common cancer in men in developed countries, and is a target for risk reduction strategies. The effects of alcohol consumption on prostate cancer incidence and survival remain unclear, potentially due to methodological limitations of observational studies. In this study, we investigated the associations of genetic variants in alcohol-metabolising genes with prostate cancer incidence and survival. We analysed data from 23,868 men with prostate cancer and 23,051 controls from 25 studies within the international PRACTICAL Consortium. Study-specific associations of 68 single nucleotide polymorphisms (SNPs) in 8 alcohol-metabolising genes (Alcohol Dehydrogenases (ADHs) and Aldehyde Dehydrogenases (ALDHs)) with prostate cancer diagnosis and prostate cancer-specific mortality, by grade, were assessed using logistic and Cox regression models, respectively. The data across the 25 studies were meta-analysed using fixed-effect and random-effects models. We found little evidence that variants in alcohol metabolising genes were associated with prostate cancer diagnosis. Four variants in two genes exceeded the multiple testing threshold for associations with prostate cancer mortality in fixed-effect meta-analyses. SNPs within ALDH1A2 associated with prostate cancer mortality were rs1441817 (fixed effects hazard ratio, HRfixed = 0.78; 95% confidence interval (95%CI):0.66,0.91; p values = 0.002); rs12910509, HRfixed = 0.76; 95%CI:0.64,0.91; p values = 0.003); and rs8041922 (HRfixed = 0.76; 95%CI:0.64,0.91; p values = 0.002). These SNPs were in linkage disequilibrium with each other. In ALDH1B1, rs10973794 (HRfixed = 1.43; 95%CI:1.14,1.79; p values = 0.002) was associated with prostate cancer mortality in men with low-grade prostate cancer. These results suggest that alcohol consumption is unlikely to affect prostate cancer incidence, but it may influence disease progression.

Published
2016
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10. Blood lipids and prostate cancer: a Mendelian randomization analysis

Author

Bull, Caroline J, Bonilla, Carolina, Holly, Jeff MP, Perks, Claire M, Davies, Neil, Haycock, Philip, Yu, Oriana Hoi Yun, Richards, J Brent, Eeles, Rosalind, Easton, Doug, Kote-Jarai, Zsofia, Amin Al Olama, Ali, Benlloch, Sara, Muir, Kenneth, Giles, Graham G, MacInnis, Robert J, Wiklund, Fredrik, Gronberg, Henrik, Haiman, Christopher A, Schleutker, Johanna, Nordestgaard, Børge G, Travis, Ruth C, Neal, David, Pashayan, Nora, Khaw, Kay-Tee, Stanford, Janet L, Blot, William J, Thibodeau, Stephen, Maier, Christiane, Kibel, Adam S, Cybulski, Cezary, Cannon-Albright, Lisa, Brenner, Hermann, Park, Jong, Kaneva, Radka, Batra, Jyotsna, Teixeira, Manuel R, Micheal, Agnieszka, Pandha, Hardev, Smith, George Davey, Lewis, Sarah J, Martin, Richard M, PRACTICAL Consortium, Easton, Douglas [0000-0003-2444-3247], Amin Al Olama, Ali [0000-0002-7178-3431], Khaw, Kay-Tee [0000-0002-8802-2903], and Apollo - University of Cambridge Repository

Subjects
Male, Genetic Variation, Prostatic Neoplasms, Mendelian Randomization Analysis, prostate cancer, Lipids, Polymorphism, Single Nucleotide, statins, Cholesterol, Quantitative Trait, Heritable, Meta-Analysis as Topic, Case-Control Studies, Population Surveillance, Mendelian randomization, Odds Ratio, Humans, lipids (amino acids, peptides, and proteins), Genetic Predisposition to Disease, Neoplasm Grading, Genetic Association Studies, Genome-Wide Association Study, Neoplasm Staging
Abstract

Genetic risk scores were used as unconfounded instruments for specific lipid traits (Mendelian randomization) to assess whether circulating lipids causally influence prostate cancer risk. Data from 22,249 prostate cancer cases and 22,133 controls from 22 studies within the international PRACTICAL consortium were analyzed. Allele scores based on single nucleotide polymorphisms (SNPs) previously reported to be uniquely associated with each of low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglyceride (TG) levels, were first validated in an independent dataset, and then entered into logistic regression models to estimate the presence (and direction) of any causal effect of each lipid trait on prostate cancer risk. There was weak evidence for an association between the LDL genetic score and cancer grade: the odds ratio (OR) per genetically instrumented standard deviation (SD) in LDL, comparing high- (≥7 Gleason score) versus low-grade (

Published
2016
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12. gsSKAT: Rapid gene set analysis and multiple testing correction for rare‐variant association studies using weighted linear kernels

Author

Larson, Nicholas B., primary, McDonnell, Shannon, additional, Cannon Albright, Lisa, additional, Teerlink, Craig, additional, Stanford, Janet, additional, Ostrander, Elaine A., additional, Isaacs, William B., additional, Xu, Jianfeng, additional, Cooney, Kathleen A., additional, Lange, Ethan, additional, Schleutker, Johanna, additional, Carpten, John D., additional, Powell, Isaac, additional, Bailey‐Wilson, Joan E., additional, Cussenot, Olivier, additional, Cancel‐Tassin, Geraldine, additional, Giles, Graham G., additional, MacInnis, Robert J., additional, Maier, Christiane, additional, Whittemore, Alice S., additional, Hsieh, Chih‐Lin, additional, Wiklund, Fredrik, additional, Catolona, William J., additional, Foulkes, William, additional, Mandal, Diptasri, additional, Eeles, Rosalind, additional, Kote‐Jarai, Zsofia, additional, Ackerman, Michael J., additional, Olson, Timothy M., additional, Klein, Christopher J., additional, Thibodeau, Stephen N., additional, and Schaid, Daniel J., additional

Published
2017
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13. Post hoc Analysis for Detecting Individual Rare Variant Risk Associations Using Probit Regression Bayesian Variable Selection Methods in Case-Control Sequencing Studies

Author

Larson, Nicholas B., primary, McDonnell, Shannon, additional, Albright, Lisa Cannon, additional, Teerlink, Craig, additional, Stanford, Janet, additional, Ostrander, Elaine A., additional, Isaacs, William B., additional, Xu, Jianfeng, additional, Cooney, Kathleen A., additional, Lange, Ethan, additional, Schleutker, Johanna, additional, Carpten, John D., additional, Powell, Isaac, additional, Bailey-Wilson, Joan, additional, Cussenot, Olivier, additional, Cancel-Tassin, Geraldine, additional, Giles, Graham, additional, MacInnis, Robert, additional, Maier, Christiane, additional, Whittemore, Alice S., additional, Hsieh, Chih-Lin, additional, Wiklund, Fredrik, additional, Catolona, William J., additional, Foulkes, William, additional, Mandal, Diptasri, additional, Eeles, Rosalind, additional, Kote-Jarai, Zsofia, additional, Ackerman, Michael J., additional, Olson, Timothy M., additional, Klein, Christopher J., additional, Thibodeau, Stephen N., additional, and Schaid, Daniel J., additional

Published
2016
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15. Prediction of individual genetic risk to prostate cancer using a polygenic score

Author

Szulkin, Robert, primary, Whitington, Thomas, additional, Eklund, Martin, additional, Aly, Markus, additional, Eeles, Rosalind A., additional, Easton, Douglas, additional, Kote-Jarai, ZSofia, additional, Amin Al Olama, Ali, additional, Benlloch, Sara, additional, Muir, Kenneth, additional, Giles, Graham G., additional, Southey, Melissa C., additional, Fitzgerald, Liesel M., additional, Henderson, Brian E., additional, Schumacher, Fredrick, additional, Haiman, Christopher A., additional, Schleutker, Johanna, additional, Wahlfors, Tiina, additional, Tammela, Teuvo LJ, additional, Nordestgaard, Børge G., additional, Key, Tim J., additional, Travis, Ruth C., additional, Neal, David E., additional, Donovan, Jenny L., additional, Hamdy, Freddie C., additional, Pharoah, Paul, additional, Pashayan, Nora, additional, Khaw, Kay-Tee, additional, Stanford, Janet L., additional, Thibodeau, Stephen N., additional, McDonnell, Shannon K., additional, Schaid, Daniel J., additional, Maier, Christiane, additional, Vogel, Walther, additional, Luedeke, Manuel, additional, Herkommer, Kathleen, additional, Kibel, Adam S., additional, Cybulski, Cezary, additional, Lubiński, Jan, additional, Kluźniak, Wojciech, additional, Cannon-Albright, Lisa, additional, Brenner, Hermann, additional, Butterbach, Katja, additional, Stegmaier, Christa, additional, Park, Jong Y., additional, Sellers, Thomas, additional, Lim, Hui-Yi, additional, Slavov, Chavdar, additional, Kaneva, Radka, additional, Mitev, Vanio, additional, Batra, Jyotsna, additional, Clements, Judith A., additional, BioResource, The Australian Prostate Cancer, additional, Spurdle, Amanda, additional, Teixeira, Manuel R., additional, Paulo, Paula, additional, Maia, Sofia, additional, Pandha, Hardev, additional, Michael, Agnieszka, additional, Kierzek, Andrzej, additional, consortium, the PRACTICAL, additional, Gronberg, Henrik, additional, and Wiklund, Fredrik, additional

Published
2015
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20. Macrophage inhibitory cytokine-1 (MIC-1/GDF15): a new marker of all-cause mortality

Author

Wiklund, Fredrik E., primary, Bennet, Anna M., additional, Magnusson, Patrik K. E., additional, Eriksson, Ulrika K., additional, Lindmark, Fredrik, additional, Wu, Liyun, additional, Yaghoutyfam, Nasreen, additional, Marquis, Christopher P., additional, Stattin, Pär, additional, Pedersen, Nancy L., additional, Adami, Hans-Olov, additional, Grönberg, Henrik, additional, Breit, Samuel N., additional, and Brown, David A., additional

Published
2010
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21. Inherited genetic markers discovered to date are able to identify a significant number of men at considerably elevated risk for prostate cancer

Author

Sun, Jielin, primary, Kader, A. Karim, additional, Hsu, Fang-Chi, additional, Kim, Seong-Tae, additional, Zhu, Yi, additional, Turner, Aubrey R., additional, Jin, Tao, additional, Zhang, Zheng, additional, Adolfsson, Jan, additional, Wiklund, Fredrik, additional, Zheng, S. Lilly, additional, Isaacs, William B., additional, Grönberg, Henrik, additional, and Xu, Jianfeng, additional

Published
2010
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22. Genome-wide linkage analysis of 1,233 prostate cancer pedigrees from the International Consortium for prostate cancer Genetics using novel sumLINK and sumLOD analyses

Author

Christensen, G. Bryce, primary, Baffoe‐Bonnie, Agnes B., additional, George, Asha, additional, Powell, Isaac, additional, Bailey‐Wilson, Joan E., additional, Carpten, John D., additional, Giles, Graham G., additional, Hopper, John L., additional, Severi, Gianluca, additional, English, Dallas R., additional, Foulkes, William D., additional, Maehle, Lovise, additional, Moller, Pal, additional, Eeles, Ros, additional, Easton, Douglas, additional, Badzioch, Michael D., additional, Whittemore, Alice S., additional, Oakley‐Girvan, Ingrid, additional, Hsieh, Chih‐Lin, additional, Dimitrov, Latchezar, additional, Xu, Jianfeng, additional, Stanford, Janet L., additional, Johanneson, Bo, additional, Deutsch, Kerry, additional, McIntosh, Laura, additional, Ostrander, Elaine A., additional, Wiley, Kathleen E., additional, Isaacs, Sarah D., additional, Walsh, Patrick C., additional, Isaacs, William B., additional, Thibodeau, Stephen N., additional, McDonnell, Shannon K., additional, Hebbring, Scott, additional, Schaid, Daniel J., additional, Lange, Ethan M., additional, Cooney, Kathleen A., additional, Tammela, Teuvo L.J., additional, Schleutker, Johanna, additional, Paiss, Thomas, additional, Maier, Christiane, additional, Grönberg, Henrik, additional, Wiklund, Fredrik, additional, Emanuelsson, Monica, additional, Farnham, James M., additional, Cannon‐Albright, Lisa A., additional, and Camp, Nicola J., additional

Published
2010
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23. Estimation of absolute risk for prostate cancer using genetic markers and family history

Author

Xu, Jianfeng, primary, Sun, Jielin, additional, Kader, A. Karim, additional, Lindström, Sara, additional, Wiklund, Fredrik, additional, Hsu, Fang-Chi, additional, Johansson, Jan-Erik, additional, Zheng, S. Lilly, additional, Thomas, Gilles, additional, Hayes, Richard B., additional, Kraft, Peter, additional, Hunter, David J., additional, Chanock, Stephen J., additional, Isaacs, William B., additional, and Grönberg, Henrik, additional

Published
2009
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25. Association of reported prostate cancer risk alleles with PSA levels among men without a diagnosis of prostate cancer

Author

Wiklund, Fredrik, primary, Zheng, S. Lilly, additional, Sun, Jielin, additional, Adami, Hans‐Olov, additional, Lilja, Hans, additional, Hsu, Fang‐Chi, additional, Stattin, Pär, additional, Adolfsson, Jan, additional, Cramer, Scott D., additional, Duggan, David, additional, Carpten, John D., additional, Chang, Bao‐Li, additional, Isaacs, William B., additional, Grönberg, Henrik, additional, and Xu, Jianfeng, additional

Published
2008
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26. Cumulative effect of five genetic variants on prostate cancer risk in multiple study populations

Author

Sun, Jielin, primary, Chang, Bao-Li, additional, Isaacs, Sarah D., additional, Wiley, Kathleen E., additional, Wiklund, Fredrik, additional, Stattin, Pär, additional, Duggan, David, additional, Carpten, John D., additional, Trock, Bruce J., additional, Partin, Alan W., additional, Walsh, Patrick C., additional, Grönberg, Henrik, additional, Xu, Jianfeng, additional, Isaacs, William B., additional, and Zheng, S. Lilly, additional

Published
2008
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29. A comprehensive association study for genes in inflammation pathway provides support for their roles in prostate cancer risk in the CAPS study

Author

Zheng, S. Lilly, primary, Liu, Wennuan, additional, Wiklund, Fredrik, additional, Dimitrov, Latchezar, additional, Bälter, Katarina, additional, Sun, Jielin, additional, Adami, Hans-Olov, additional, Johansson, Jan-Erik, additional, Sun, Jishan, additional, Chang, Baoli, additional, Loza, Matthew, additional, Turner, Aubrey R., additional, Bleecker, Eugene R., additional, Meyers, Deborah A., additional, Carpten, John D., additional, Duggan, David, additional, Isaacs, William B., additional, Xu, Jianfeng, additional, and Grönberg, Henrik, additional

Published
2006
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31. Systematic replication study of reported genetic associations in prostate cancer: Strong support for genetic variation in the androgen pathway

Author

Lindström, Sara, primary, Zheng, S. Lilly, additional, Wiklund, Fredrik, additional, Jonsson, Björn-Anders, additional, Adami, Hans-Olov, additional, Bälter, Katarina Augustsson, additional, Brookes, Anthony J., additional, Sun, Jielin, additional, Chang, Bao-Li, additional, Liu, Wennuan, additional, Li, Ge, additional, Isaacs, William B., additional, Adolfsson, Jan, additional, Grönberg, Henrik, additional, and Xu, Jianfeng, additional

Published
2006
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34. Genome‐wide scan of Swedish families with hereditary prostate cancer: Suggestive evidence of linkage at 5q11.2 and 19p13.3

Author

Wiklund, Fredrik, primary, Gillanders, Elizabeth M., additional, Albertus, Julie A., additional, Bergh, Anders, additional, Damber, Jan‐Erik, additional, Emanuelsson, Monica, additional, Freas‐Lutz, Diana L., additional, Gildea, Derek E., additional, Göransson, Ingela, additional, Jones, MaryPat S., additional, Jonsson, Björn‐Anders, additional, Lindmark, Fredrik, additional, Markey, Carol J., additional, Riedesel, Erica L., additional, Stenman, Elisabeth, additional, Trent, Jeffry M., additional, and Grönberg, Henrik, additional

Published
2003
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35. A population-based prospective study ofChlamydia trachomatisinfection and cervical carcinoma

Author

Wallin, Keng-Ling, primary, Wiklund, Fredrik, additional, Luostarinen, Tapio, additional, Ångström, Tord, additional, Anttila, Tarja, additional, Bergman, Frank, additional, Hallmans, Göran, additional, Ikäheimo, Irma, additional, Koskela, Pentti, additional, Lehtinen, Matti, additional, Stendahl, Ulf, additional, Paavonen, Jorma, additional, and Dillner, Joakim, additional

Published
2002
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40. A prospective study on the risk of cervical intra-epithelial neoplasia among healthy subjects with serum antibodies to HPV compared with HPV DNA in cervical smears

Author

Chua, Keng-Ling, primary, Wiklund, Fredrik, additional, Lenner, Per, additional, Ångström, Tord, additional, Hallmans, Göran, additional, Bergman, Frank, additional, Sapp, Martin, additional, Schiller, John, additional, Wadell, Göran, additional, Hjerpe, Anders, additional, and Dillner, Joakim, additional

Published
1996
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