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447 results on '"Painter, Jodie"'

101. Genetic overlap between endometriosis and endometrial cancer: Evidence from cross-disease genetic correlation and GWAS meta-analyses

Author: Painter, Jodie N., O'Mara, Tracy A., Cheng, Timothy H.T., Gorman, Maggie, Martin, Lynn, Hodson, Shirley, Martin, Nicholas G., Henders, Anjali K., Attia, John, McEvoy, Mark, Holliday, Elizabeth G., Scott, Rodney J., Webb, Penelope M., Fasching, Peter A., Beckmann, Matthias W., Ekici, Arif B., Hein, Alexander, Rübner, Matthias, Hall, Per, Czene, Kamila, Dörk, Thilo, Dürst, Matthias, Hillemanns, Peter, Runnebaum, Ingo, Lambrechts, Diether, Amant, Frederic, Annibali, Daniela, Depreeuw, Jeroen, Vanderstichele, Adriaan, Goode, Ellen L., Cunningham, Julie M., Dowdy, Sean C., Winham, Stacey J., Trovik, Jone, Hoivik, Erling, Werner, Henrica M.J., Krakstad, Camilla, Ashton, Katie, Otton, Geoffrey, Proietto, Tony, Tham, Emma, Mints, Miriam, Ahmed, Shahana, Healey, Catherine S., Shah, Mitul, Pharoah, Paul D.P., Dunning, Alison M., Dennis, Joe, Bolla, Manjeet K., Michailidou, Kyriaki, Wang, Qin, Tyrer, Jonathan P., Hopper, John L., Peto, Julian, Swerdlow, Anthony J., Burwinkel, Barbara, Brenner, Hermann, Meindl, Alfons, Brauch, Hiltrud, Lindblom, Annika, Chang-Claude, Jenny, Couch, Fergus J., Giles, Graham G., Kristensen, Vessela N., Cox, Angela, Zondervan, Krina T., Nyholt, Dale R., MacGregor, Stuart, Montgomery, Grant W., Tomlinson, Ian, Easton, Douglas F., Thompson, Deborah J., Spurdle, Amanda B., Painter, Jodie N., O'Mara, Tracy A., Cheng, Timothy H.T., Gorman, Maggie, Martin, Lynn, Hodson, Shirley, Martin, Nicholas G., Henders, Anjali K., Attia, John, McEvoy, Mark, Holliday, Elizabeth G., Scott, Rodney J., Webb, Penelope M., Fasching, Peter A., Beckmann, Matthias W., Ekici, Arif B., Hein, Alexander, Rübner, Matthias, Hall, Per, Czene, Kamila, Dörk, Thilo, Dürst, Matthias, Hillemanns, Peter, Runnebaum, Ingo, Lambrechts, Diether, Amant, Frederic, Annibali, Daniela, Depreeuw, Jeroen, Vanderstichele, Adriaan, Goode, Ellen L., Cunningham, Julie M., Dowdy, Sean C., Winham, Stacey J., Trovik, Jone, Hoivik, Erling, Werner, Henrica M.J., Krakstad, Camilla, Ashton, Katie, Otton, Geoffrey, Proietto, Tony, Tham, Emma, Mints, Miriam, Ahmed, Shahana, Healey, Catherine S., Shah, Mitul, Pharoah, Paul D.P., Dunning, Alison M., Dennis, Joe, Bolla, Manjeet K., Michailidou, Kyriaki, Wang, Qin, Tyrer, Jonathan P., Hopper, John L., Peto, Julian, Swerdlow, Anthony J., Burwinkel, Barbara, Brenner, Hermann, Meindl, Alfons, Brauch, Hiltrud, Lindblom, Annika, Chang-Claude, Jenny, Couch, Fergus J., Giles, Graham G., Kristensen, Vessela N., Cox, Angela, Zondervan, Krina T., Nyholt, Dale R., MacGregor, Stuart, Montgomery, Grant W., Tomlinson, Ian, Easton, Douglas F., Thompson, Deborah J., and Spurdle, Amanda B.
Abstract: Epidemiological, biological, and molecular data suggest links between endometriosis and endometrial cancer, with recent epidemiological studies providing evidence for an association between a previous diagnosis of endometriosis and risk of endometrial cancer. We used genetic data as an alternative approach to investigate shared biological etiology of these two diseases. Genetic correlation analysis of summary level statistics from genomewide association studies (GWAS) using LD Score regression revealed moderate but significant genetic correlation (r g = 0.23, P = 9.3 × 10 −3 ), and SNP effect concordance analysis provided evidence for significant SNP pleiotropy (P = 6.0 × 10 −3 ) and concordance in effect direction (P = 2.0 × 10 −3 ) between the two diseases. Cross-disease GWAS meta-analysis highlighted 13 distinct loci associated at P ≤ 10 −5 with both endometriosis and endometrial cancer, with one locus (SNP rs2475335) located within PTPRD associated at a genomewide significant level (P = 4.9 × 10 −8 , OR = 1.11, 95% CI = 1.07–1.15). PTPRD acts in the STAT3 pathway, which has been implicated in both endometriosis and endometrial cancer. This study demonstrates the value of cross-disease genetic analysis to support epidemiological observations and to identify biological pathways of relevance to multiple diseases.
Published: 2018

102. Does Childhood Trauma Moderate Polygenic Risk for Depression? A Meta-analysis of 5765 Subjects From the Psychiatric Genomics Consortium

Author: Peyrot, Wouter J., Van der Auwera, Sandra, Milaneschi, Yuri, Dolan, Conor V., Madden, Pamela A.F., Sullivan, Patrick F., Strohmaier, Jana, Ripke, Stephan, Rietschel, Marcella, Nivard, Michel G., Mullins, Niamh, Montgomery, Grant W., Henders, Anjali K., Heat, Andrew C., Fisher, Helen L., Dunn, Erin C., Byrne, Enda M., Air, Tracy, Wray, Naomi R., Mattheisen, Manuel, Trzaskowski, Maciej, Abdellaoui, Abdel, Adams, Mark J., Agerbo, Esben, Andlauer, Till F.M., Bacanu, Silviu Alin, Bækvad-Hansen, Marie, Beekman, Aartjan T.F., Bigdeli, Tim B., Binder, Elisabeth B., Blackwood, Douglas H.R., Bryois, Julien, Buttenschøn, Henriette N., Bybjerg-Grauholm, Jonas, Cai, Na, Castelao, Enrique, Christensen, Jane Hvarregaard, Clarke, Toni Kim, Coleman, Jonathan R.I., Colodro-Conde, Lucía, Couvy-Duchesne, Baptiste, Craddock, Nick, Crawford, Gregory E., Davies, Gail, Deary, Ian J., Degenhardt, Franziska, Derks, Eske M., Direk, Nese, Eley, Thalia C., Escott-Price, Valentina, Farnush, Kiadeh, Farhadi Hassan, Finucane, Hilary K., Forstner, Andreas J., Frank, Josef, Gaspar, Héléna A., Gill, Michael, Goes, Fernando S., Gordon, Scott D., Grove, Jakob, Hall, Lynsey S., Hansen, Christine Søholm, Hansen, Thomas F., Herms, Stefan, Hicki, Ian B., Hoffmann, Per, Homuth, Georg, Horn, Carsten, Hottenga, Jouke Jan, Hougaard, David M., Ising, Marcus, Jansen, Rick, Jorgenson, Eric, Knowles, James A., Kraft, Julia, Kretzschmar, Warren W., Krogh, Jesper, Kutalik, Zoltán, Li, Yihan, Lind, Penelope A., MacIntyre, Donald J., MacKinnon, Dean F., Maier, Robert M., Maier, Wolfgang, Marchini, Jonathan, Mbarek, Hamdi, McGrath, Patrick, McGuffin, Peter, Medland, Sarah E., Mehta, Divya, Middeldorp, Christel M., Mihailov, Evelin, Milani, Lili, Mondimore, Francis M., Mostafavi, Sara, Nauck, Matthias, Ng, Bernard, O'Reilly, Paul F., Oskarsson, Hogni, Owen, Michael J., Painter, Jodie N., Pedersen, Carsten Bøcker, Pedersen, Marianne Giørtz, Peterson, Roseann E., Pettersson, Erik, Pistis, Giorgio, Posthuma, Danielle, Quiroz, Jorge A., Qvist, Per, Rice, John P., Riley, Brien P., Rivera, Margarita, Mirza, Saira Saeed, Schoevers, Robert, Schulte, Eva C., Shen, Ling, Shi, Jianxin, Shyn, Stanley I., Sigurdsson, Engilbert, Sinnamon, Grant C.B., Smit, Johannes H., Smith, Daniel J., Stefansson, Hreinn, Steinberg, Stacy, Streit, Fabian, Tansey, Katherine E., Teismann, Henning, Teumer, Alexander, Thompson, Wesley, Thomson, Pippa A., Thorgeirsson, Thorgeir E., Traylor, Matthew, Treutlein, Jens, Trubetskoy, Vassily, Uitterlinden, André G., Umbricht, Daniel, van Hemert, Albert M., Viktorin, Alexander, Visscher, Peter M., Wang, Yunpeng, Webb, Bradley T., Weinsheimer, Shantel Marie, Wellmann, Jürgen, Willemsen, Gonneke, Witt, Stephanie H., Wu, Yang, Xi, Hualin S., Yang, Jian, Zhang, Futao, Arolt, Volker, Baune, Bernhard T., Berger, Klaus, Boomsma, Dorret I., Cichon, Sven, Dannlowski, Udo, de Geus, E. J.C., DePaulo, J. Raymond, Domenici, Enrico, Domschke, Katharina, Esko, Tõnu, Grabe, Hans J., Hamilton, Steven P., Hayward, Caroline, Heath, Andrew C., Kendler, Kenneth S., Kloiber, Stefan, Lewis, Glyn, Li, Qingqin S., Lucae, Susanne, Magnusson, Patrik K., Martin, Nicholas G., McIntosh, Andrew M., Metspalu, Andres, Mors, Ole, Mortensen, Preben Bo, Müller-Myhsok, Bertram, Nordentoft, Merete, Nöthen, Markus M., O'Donovan, Michael C., Paciga, Sara A., Pedersen, Nancy L., Penninx, Brenda W.J.H., Perlis, Roy H., Porteous, David J., Potash, James B., Preisig, Martin, Schaefer, Catherine, Schulze, Thomas G., Smoller, Jordan W., Stefansson, Kari, Tiemeier, Henning, Uher, Rudolf, Völzke, Henry, Weissman, Myrna M., Werge, Thomas, Lewis, Cathryn M., Levinson, Douglas F., Breen, Gerome, Børglum, Anders D., Nelson, Elliot N., Peyrot, Wouter J., Van der Auwera, Sandra, Milaneschi, Yuri, Dolan, Conor V., Madden, Pamela A.F., Sullivan, Patrick F., Strohmaier, Jana, Ripke, Stephan, Rietschel, Marcella, Nivard, Michel G., Mullins, Niamh, Montgomery, Grant W., Henders, Anjali K., Heat, Andrew C., Fisher, Helen L., Dunn, Erin C., Byrne, Enda M., Air, Tracy, Wray, Naomi R., Mattheisen, Manuel, Trzaskowski, Maciej, Abdellaoui, Abdel, Adams, Mark J., Agerbo, Esben, Andlauer, Till F.M., Bacanu, Silviu Alin, Bækvad-Hansen, Marie, Beekman, Aartjan T.F., Bigdeli, Tim B., Binder, Elisabeth B., Blackwood, Douglas H.R., Bryois, Julien, Buttenschøn, Henriette N., Bybjerg-Grauholm, Jonas, Cai, Na, Castelao, Enrique, Christensen, Jane Hvarregaard, Clarke, Toni Kim, Coleman, Jonathan R.I., Colodro-Conde, Lucía, Couvy-Duchesne, Baptiste, Craddock, Nick, Crawford, Gregory E., Davies, Gail, Deary, Ian J., Degenhardt, Franziska, Derks, Eske M., Direk, Nese, Eley, Thalia C., Escott-Price, Valentina, Farnush, Kiadeh, Farhadi Hassan, Finucane, Hilary K., Forstner, Andreas J., Frank, Josef, Gaspar, Héléna A., Gill, Michael, Goes, Fernando S., Gordon, Scott D., Grove, Jakob, Hall, Lynsey S., Hansen, Christine Søholm, Hansen, Thomas F., Herms, Stefan, Hicki, Ian B., Hoffmann, Per, Homuth, Georg, Horn, Carsten, Hottenga, Jouke Jan, Hougaard, David M., Ising, Marcus, Jansen, Rick, Jorgenson, Eric, Knowles, James A., Kraft, Julia, Kretzschmar, Warren W., Krogh, Jesper, Kutalik, Zoltán, Li, Yihan, Lind, Penelope A., MacIntyre, Donald J., MacKinnon, Dean F., Maier, Robert M., Maier, Wolfgang, Marchini, Jonathan, Mbarek, Hamdi, McGrath, Patrick, McGuffin, Peter, Medland, Sarah E., Mehta, Divya, Middeldorp, Christel M., Mihailov, Evelin, Milani, Lili, Mondimore, Francis M., Mostafavi, Sara, Nauck, Matthias, Ng, Bernard, O'Reilly, Paul F., Oskarsson, Hogni, Owen, Michael J., Painter, Jodie N., Pedersen, Carsten Bøcker, Pedersen, Marianne Giørtz, Peterson, Roseann E., Pettersson, Erik, Pistis, Giorgio, Posthuma, Danielle, Quiroz, Jorge A., Qvist, Per, Rice, John P., Riley, Brien P., Rivera, Margarita, Mirza, Saira Saeed, Schoevers, Robert, Schulte, Eva C., Shen, Ling, Shi, Jianxin, Shyn, Stanley I., Sigurdsson, Engilbert, Sinnamon, Grant C.B., Smit, Johannes H., Smith, Daniel J., Stefansson, Hreinn, Steinberg, Stacy, Streit, Fabian, Tansey, Katherine E., Teismann, Henning, Teumer, Alexander, Thompson, Wesley, Thomson, Pippa A., Thorgeirsson, Thorgeir E., Traylor, Matthew, Treutlein, Jens, Trubetskoy, Vassily, Uitterlinden, André G., Umbricht, Daniel, van Hemert, Albert M., Viktorin, Alexander, Visscher, Peter M., Wang, Yunpeng, Webb, Bradley T., Weinsheimer, Shantel Marie, Wellmann, Jürgen, Willemsen, Gonneke, Witt, Stephanie H., Wu, Yang, Xi, Hualin S., Yang, Jian, Zhang, Futao, Arolt, Volker, Baune, Bernhard T., Berger, Klaus, Boomsma, Dorret I., Cichon, Sven, Dannlowski, Udo, de Geus, E. J.C., DePaulo, J. Raymond, Domenici, Enrico, Domschke, Katharina, Esko, Tõnu, Grabe, Hans J., Hamilton, Steven P., Hayward, Caroline, Heath, Andrew C., Kendler, Kenneth S., Kloiber, Stefan, Lewis, Glyn, Li, Qingqin S., Lucae, Susanne, Magnusson, Patrik K., Martin, Nicholas G., McIntosh, Andrew M., Metspalu, Andres, Mors, Ole, Mortensen, Preben Bo, Müller-Myhsok, Bertram, Nordentoft, Merete, Nöthen, Markus M., O'Donovan, Michael C., Paciga, Sara A., Pedersen, Nancy L., Penninx, Brenda W.J.H., Perlis, Roy H., Porteous, David J., Potash, James B., Preisig, Martin, Schaefer, Catherine, Schulze, Thomas G., Smoller, Jordan W., Stefansson, Kari, Tiemeier, Henning, Uher, Rudolf, Völzke, Henry, Weissman, Myrna M., Werge, Thomas, Lewis, Cathryn M., Levinson, Douglas F., Breen, Gerome, Børglum, Anders D., and Nelson, Elliot N.
Abstract: Background: The heterogeneity of genetic effects on major depressive disorder (MDD) may be partly attributable to moderation of genetic effects by environment, such as exposure to childhood trauma (CT). Indeed, previous findings in two independent cohorts showed evidence for interaction between polygenic risk scores (PRSs) and CT, albeit in opposing directions. This study aims to meta-analyze MDD-PRS × CT interaction results across these two and other cohorts, while applying more accurate PRSs based on a larger discovery sample. Methods: Data were combined from 3024 MDD cases and 2741 control subjects from nine cohorts contributing to the MDD Working Group of the Psychiatric Genomics Consortium. MDD-PRS were based on a discovery sample of ∼110,000 independent individuals. CT was assessed as exposure to sexual or physical abuse during childhood. In a subset of 1957 cases and 2002 control subjects, a more detailed five-domain measure additionally included emotional abuse, physical neglect, and emotional neglect. Results: MDD was associated with the MDD-PRS (odds ratio [OR] = 1.24, p = 3.6 × 10 −5 , R 2 = 1.18%) and with CT (OR = 2.63, p = 3.5 × 10 −18 and OR = 2.62, p = 1.4 ×10 −5 for the two- and five-domain measures, respectively). No interaction was found between MDD-PRS and the two-domain and five-domain CT measure (OR = 1.00, p =.89 and OR = 1.05, p =.66). Conclusions: No meta-analytic evidence for interaction between MDD-PRS and CT was found. This suggests that the previously reported interaction effects, although both statistically significant, can best be interpreted as chance findings. Further research is required, but this study suggests that the genetic heterogeneity of MDD is not attributable to genome-wide moderation of genetic effects by CT.
Published: 2018

103. Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics

Author: Beaumont, Robin N., Warrington, Nicole M., Cavadino, Alana, Tyrrell, Jessica, Nodzenski, Michael, Horikoshi, Momoko, Geller, Frank, Myhre, Ronny, Richmond, Rebecca C., Paternoster, Lavinia, Bradfield, Jonathan P., Kreiner-Moller, Eskil, Huikari, Ville, Metrustry, Sarah, Lunetta, Kathryn L., Painter, Jodie N., Hottenga, Jouke-Jan, Allard, Catherine, Barton, Sheila J., Espinosa, Ana, Marsh, Julie A., Potter, Catherine, Zhang, Ge, Ang, Wei, Berry, Diane J., Bouchard, Luigi, Das, Shikta, Hakonarson, Hakon, Heikkinen, Jani, Helgeland, Oyvind, Hocher, Berthold, Hofman, Albert, Inskip, Hazel M., Jones, Samuel E., Kogevinas, Manolis, Lind, Penelope A., Marullo, Letizia, Medland, Sarah E., Murray, Anna, Murray, Jeffrey C., Njolstad, Pal R., Nohr, Ellen A., Reichetzeder, Christoph, Ring, Susan M., Ruth, Katherine S., Santa-Marina, Loreto, Scholtens, Denise M., Sebert, Sylvain, Sengpiel, Verena, Tuke, Marcus A., Vaudel, Marc, Weedon, Michael N., Willemsen, Gonneke, Wood, Andrew R., Yaghootkar, Hanieh, Muglia, Louis J., Bartels, Meike, Relton, Caroline L., Pennell, Craig E., Chatzi, Leda, Estivill, Xavier, Holloway, John W., Boomsma, Dorret I., Montgomery, Grant W., Murabito, Joanne M., Spector, Tim D., Power, Christine, Jarvelin, Marjo-Ritta, Bisgaard, Hans, Grant, Struan F. A., Sørensen, Thorkild I. A., Jaddoe, Vincent W., Jacobsson, Bo, Melbye, Mads, McCarthy, Mark I., Hattersley, Andrew T., Hayes, M. Geoffrey, Frayling, Timothy M., Hivert, Marie-France, Felix, Janine F., Hypponen, Elina, Lowe, William L., Jr., Evans, David M., Lawlor, Debbie A., Feenstra, Bjarke, Freathy, Rachel M., Beaumont, Robin N., Warrington, Nicole M., Cavadino, Alana, Tyrrell, Jessica, Nodzenski, Michael, Horikoshi, Momoko, Geller, Frank, Myhre, Ronny, Richmond, Rebecca C., Paternoster, Lavinia, Bradfield, Jonathan P., Kreiner-Moller, Eskil, Huikari, Ville, Metrustry, Sarah, Lunetta, Kathryn L., Painter, Jodie N., Hottenga, Jouke-Jan, Allard, Catherine, Barton, Sheila J., Espinosa, Ana, Marsh, Julie A., Potter, Catherine, Zhang, Ge, Ang, Wei, Berry, Diane J., Bouchard, Luigi, Das, Shikta, Hakonarson, Hakon, Heikkinen, Jani, Helgeland, Oyvind, Hocher, Berthold, Hofman, Albert, Inskip, Hazel M., Jones, Samuel E., Kogevinas, Manolis, Lind, Penelope A., Marullo, Letizia, Medland, Sarah E., Murray, Anna, Murray, Jeffrey C., Njolstad, Pal R., Nohr, Ellen A., Reichetzeder, Christoph, Ring, Susan M., Ruth, Katherine S., Santa-Marina, Loreto, Scholtens, Denise M., Sebert, Sylvain, Sengpiel, Verena, Tuke, Marcus A., Vaudel, Marc, Weedon, Michael N., Willemsen, Gonneke, Wood, Andrew R., Yaghootkar, Hanieh, Muglia, Louis J., Bartels, Meike, Relton, Caroline L., Pennell, Craig E., Chatzi, Leda, Estivill, Xavier, Holloway, John W., Boomsma, Dorret I., Montgomery, Grant W., Murabito, Joanne M., Spector, Tim D., Power, Christine, Jarvelin, Marjo-Ritta, Bisgaard, Hans, Grant, Struan F. A., Sørensen, Thorkild I. A., Jaddoe, Vincent W., Jacobsson, Bo, Melbye, Mads, McCarthy, Mark I., Hattersley, Andrew T., Hayes, M. Geoffrey, Frayling, Timothy M., Hivert, Marie-France, Felix, Janine F., Hypponen, Elina, Lowe, William L., Jr., Evans, David M., Lawlor, Debbie A., Feenstra, Bjarke, and Freathy, Rachel M.
Abstract: Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P<5×10 -8. In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.
Published: 2018

104. Genetic Association of Major Depression With Atypical Features and Obesity-Related Immunometabolic Dysregulations

Author: Van Hemert, Albert M., Porteous, David J., O'Donovan, Michael C., McIntosh, Andrew M., Lewis, Glyn, Hayward, Caroline, Traylor, Matthew, Thomson, Pippa A., Tansey, Katherine E., Smith, Daniel J., Owen, Michael J., O'Reilly, Paul F., McGuffin, Peter, Marchini, Jonathan, MacIntyre, Donald J., Kretzschmar, Warren W., Hall, Lynsey S., Gaspar, Helena A., Escott-Price, Valentina, Eley, Thalia C., Deary, Ian J., Davies, Gail, Craddock, Nick, Coleman, Jonathan R.I., Clarke, Toni-Kim, Cai, Na, Blackwood, Douglas H.R., Adams, Mark J., Rivera, Margarita, Mullins, Niamh, Lewis, Cathryn, Kan, Carol, Dehghan, Abbas, Breen, Gerome, Sullivan, Patrick F., Borglum, Anders D., Levinson, Douglas F., Werge, Thomas, Weissman, Myrna M., Volzke, Henry, Uher, Rudolf, Tiemeier, Henning, Stefansson, Kari, Smoller, Jordan W., Schulze, Thomas G., Schaefer, Catherine, Potash, James B., Trubetskoy, Vassily, Treutlein, Jens, Thorgeirsson, Thorgeir E., Thompson, Wesley, Teismann, Henning, Steinberg, Stacy, Stefansson, Hreinn, Smit, Johannes H., Sinnamon, Grant C.B., Sigurdsson, Engilbert, Shyn, Stanley I., Shi, Jianxin, Shen, Ling, Schulte, Eva C., Schoevers, Robert, Mirza, Saira Saeed, Riley, Brien P., Rice, John P., Qvist, Per, Quiroz, Jorge A., Posthuma, Danielle, Pettersson, Erik, Peterson, Roseann E., Pedersen, Marianne Giortz, Pedersen, Carsten Bocker, Painter, Jodie N., Oskarsson, Hogni, Nyholt, Dale R., Nivard, Michel G., Ng, Bernard, Mostafavi, Sara, Montgomery, Grant W., Mondimore, Francis M., Milani, Lili, Mihailov, Evelin, Middeldorp, Christel M., Mehta, Divya, Medland, Sarah E., McGrath, Patrick, Mbarek, Hamdi, Maier, Wolfgang, Maier, Robert M., MacKinnon, Dean F., Lind, Penelope A., Li, Yihan, Kutalik, Zoltan, Krogh, Jesper, Kraft, Julia, Kohane, Isaac S., Knowles, James A., Jorgenson, Eric, Jansen, Rick, Ising, Marcus, Hougaard, David M., Hottenga, Jouke-Jan, Horn, Carsten, Hoffmann, Per, Hickie, Ian B., Herms, Stefan, Hansen, Thomas F., Hansen, Christine Soholm, Grove, Jakob, Gordon, Scott D., Goes, Fernando S., Frank, Josef, Finucane, Hilary K., Kiadeh, Farnush Farhadi Hassan, Dunn, Erin C., Dolan, Conor V., Direk, Nese, Derks, Eske M., Degenhardt, Franziska, Crawford, Gregory E., Couvy-Duchesne, Baptiste, Colodro-Conde, Lucia, Christensen, Jane Hvarregaard, Castelao, Enrique, Bybjerg-Grauholm, Jonas, Buttenschon, Henriette N., Bryois, Julien, Bigdeli, Tim B., Beekman, Aartjan T.F., Bakvad-Hansen, Marie, Bacanu, Silviu-Alin, Andlauer, Till F.M., Air, Tracy M., Agerbo, Esben, Abdellaoui, Abdel, Byrne, Enda M., Mattheisen, Manuel, Ripke, Stephan, Penninx, Brenda W.J.H., Boomsma, Dorret I., Wray, Naomi R., Van Der Auwera, Sandra, Teumer, Alexander, Strohmaier, Jana, Streit, Fabian, Rietschel, Marcella, Preisig, Martin, Pistis, Giorgio, Nauck, Matthias, Homuth, Georg, Grabe, Hans J., Forstner, Andreas J., Baune, Bernhard T., Peyrot, Wouter J., Lamers, Femke, Milaneschi, Yuri, Gill, Michael, Binder, Elisabeth B., Trzaskowski, Maciej, Perlis, Roy H., Pedersen, Nancy L., Paciga, Sara A., Nothen, Markus M., Nordentoft, Merete, Muller-Myhsok, Bertram, Mortensen, Preben Bo, Mors, Ole, Metspalu, Andres, Martin, Nicholas G., Magnusson, Patrik K., Madden, Pamela A.F., Lucae, Susanne, Li, Qingqin S., Kloiber, Stefan, Kendler, Kenneth S., Heath, Andrew C., Hamilton, Steven P., Esko, Tonu, Domschke, Katharina, Domenici, Enrico, DePaulo, J. Raymond, De Geus, E.J.C., Dannlowski, Udo, Cichon, Sven, Arolt, Volker, Zhang, Futao, Yang, Jian, Xi, Hualin S., Wu, Yang, Witt, Stephanie H., Willemsen, Gonneke, Wellmann, Jurgen, Weinsheimer, Shantel Marie, Webb, Bradley T., Wang, Yunpeng, Visscher, Peter M., Viktorin, Alexander, Umbricht, Daniel, Uitterlinden, Andre G., Berger, Klaus, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, APH - Mental Health, Psychiatry, APH - Digital Health, Biological Psychology, Clinical Psychology, APH - Methodology, Epidemiology, Urology, Child and Adolescent Psychiatry / Psychology, Internal Medicine, Medical Informatics, and Immunology
Subjects: Netherlands Twin Register (NTR), Adult, Male, medicine.medical_specialty, International Cooperation, Population, Genome-wide association study, Overweight, Weight Gain, behavioral disciplines and activities, Body Mass Index, 03 medical and health sciences, 0302 clinical medicine, SDG 3 - Good Health and Well-being, Internal medicine, mental disorders, medicine, Journal Article, Humans, Genetic Predisposition to Disease, Obesity, Psychiatry, education, Problem Solving, Depression (differential diagnoses), Original Investigation, Craving, Psychiatric Status Rating Scales, education.field_of_study, Depressive Disorder, Major, Odds ratio, medicine.disease, 030227 psychiatry, Multicenter Study, Diagnostic and Statistical Manual of Mental Disorders, Psychiatry and Mental health, C-Reactive Protein, Cohort, Major depressive disorder, Female, medicine.symptom, Psychology, Body mass index, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract: © 2017 American Medical Association. All rights reserved.IMPORTANCE The association between major depressive disorder (MDD) and obesitymay stem from shared immunometabolic mechanisms particularly evident in MDD with atypical features, characterized by increased appetite and/or weight (A/W) during an active episode. OBJECTIVE To determine whether subgroups of patients with MDD stratified according to the A/W criterion had a different degree of genetic overlap with obesity-related traits (body mass index [BMI] and levels of C-reactive protein [CRP] and leptin). DESIGN, SETTING, AND PATIENTS This multicenter study assembled genome-wide genotypic and phenotypic measures from 14 data sets of the Psychiatric Genomics Consortium. Data sets were drawn from case-control, cohort, and population-based studies, including 26 628 participants with established psychiatric diagnoses and genome-wide genotype data. Data on BMI were available for 15 237 participants. Data were retrieved and analyzed from September 28, 2015, through May 20, 2017. MAIN OUTCOMES AND MEASURES Lifetime DSM-IV MDDwas diagnosed using structured diagnostic instruments. Patients with MDD were stratified into subgroups according to change in the DSM-IV A/W symptoms as decreased or increased. RESULTS Data included 11 837 participants with MDD and 14 791 control individuals, for a total of 26 628 participants (59.1% female and 40.9%male). Among participants with MDD, 5347 (45.2%) were classified in the decreased A/W and 1871 (15.8%) in the increased A/W subgroups. Common genetic variants explained approximately 10% of the heritability in the 2 subgroups. The increased A/W subgroup showed a strong and positive genetic correlation (SE) with BMI (0.53 [0.15]; P = 6.3 × 10-4), whereas the decreased A/W subgroup showed an inverse correlation (-0.28 [0.14]; P = .06). Furthermore, the decreased A/W subgroup had a higher polygenic risk for increased BMI (odds ratio [OR], 1.18; 95%CI, 1.12-1.25; P = 1.6 × 10-10) and levels of CRP (OR, 1.08; 95%CI, 1.02-1.13; P = 7.3 × 10-3) and leptin (OR, 1.09; 95%CI, 1.06-1.12; P = 1.7 × 10-3). CONCLUSIONS AND RELEVANCE The phenotypic associations between atypical depressive symptoms and obesity-related traits may arise from shared pathophysiologic mechanisms in patients with MDD. Development of treatments effectively targeting immunometabolic dysregulations may benefit patients with depression and obesity, both syndromes with important disability.
Published: 2017
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105. Genome-wide association analyses identify 44 risk variants and refine the genetic architecture of major depressive disorder

Author: Wray, Naomi R, Ripke, Stephan, Mattheisen, Manuel, Trzaskowski, Maciej, Byrne, Enda M, Abdellaoui, Abdel, Adams, Mark J, Agerbo, Esben, Air, Tracy M, Andlauer, Till F M, Bacanu, Silviu-Alin, Bækvad-Hansen, Marie, Beekman, Aartjan T F, Bigdeli, Tim B, Binder, Elisabeth B, Blackwood, Douglas H R, Bryois, Julien, Buttenschøn, Henriette N, Bybjerg-Grauholm, Jonas, Cai, Na, Castelao, Enrique, Christensen, Jane Hvarregaard, Clarke, Toni-Kim, Coleman, Jonathan R I, Colodro-Conde, Lucía, Couvy-Duchesne, Baptiste, Craddock, Nick, Crawford, Gregory E, Crowley, Cheynna A, Dashti, Hassan S, Davies, Gail, Deary, Ian J, Degenhardt, Franziska, Derks, Eske M, Direk, Nese, Dolan, Conor V, Dunn, Erin C, Eley, Thalia C, Eriksson, Nicholas, Escott-Price, Valentina, Hassan Kiadeh, Farnush Farhadi, Finucane, Hilary K, Forstner, Andreas J, Frank, Josef, Gaspar, Héléna A, Gill, Michael, Giusti-Rorínguez, Paola, Goes, Fernando S, Gordon, Scott D, Grove, Jakob, Hall, Lynsey S, Hansen, Christine Søholm, Hansen, Thomas F, Herms, Stefan, Hickie, Ian B, Hoffmann, Per, Homuth, Georg, Horn, Carsten, Hottenga, Jouke-Jan, Hougaard, David M, Hu, Ming, Hyde, Craig L, Ising, Marcus, Jansen, Rick, Jin, Fulai, Jorgenson, Eric, Knowles, James A, Kohane, Isaac S, Kraft, Julia, Kretzschmar, Warren W., Krogh, Jesper, Kutalik, Zoltan, Lane, Jacqueline M, Li, Yihan, Li, Yun, Lind, Penelope A, Liu, Xiaoxiao, Lu, Leina, MacIntyre, Donald J, MacKinnon, Dean F, Maier, Robert M, Maier, Wolfgang, Marchini, Jonathan, Mbarek, Hamdi, McGrath, Patrick, McGuffin, Peter, Medland, Sarah E, Mehta, Divya, Middeldorp, Christel M, Mihailov, Evelin, Milaneschi, Yuri, Milani, Lili, Mondimore, Francis M, Montgomery, Grant W, Mostafavi, Sara, Mullins, Niamh, Nauck, Matthias, Ng, Bernard, Nivard, Michel G, Nyholt, Dale R, O’Reilly, Paul F, Oskarsson, Hogni, Owen, Michael J, Painter, Jodie N, Bøcker, Carsten, Pedersen, Marianne Giørtz, Peterson, Roseann E., Pettersson, Erik, Peyrot, Wouter J, Pistis, Giorgio, Posthuma, Danielle, Purcell, Shaun M, Quiroz, Jorge A, Qvist, Per, Rice, John P, Riley, Brien P., Rivera, Margarita, Mirza, Saira Saeed, Saxena, Richa, Schoevers, Robert, Schulte, Eva C, Shen, Ling, Shi, Jianxin, Shyn, Stanley I, Sigurdsson, Engilbert, Sinnamon, Grant C B, Smit, Johannes H, Smith, Daniel J, Stefansson, Hreinn, Steinberg, Stacy, Stockmeier, Craig A, Streit, Fabian, Strohmaier, Jana, Tansey, Katherine E, Teismann, Henning, Teumer, Alexander, Thompson, Wesley, Thomson, Pippa a, Thorgeirsson, Thorgeir E, Tian, Chao, Traylor, Matthew, Treutlein, Jens, Trubetskoy, Vassily, Uitterlinden, André G, Umbricht, Daniel, Auwera, Sandra Van der, Hemert, Albert M van, Viktorin, Alexander, Visscher, Peter M, Wang, Yunpeng, Webb, Bradley T., Weinsheimer, Shantel Marie, Wellmann, Jürgen, Willemsen, Gonneke, Witt, Stephanie H, Wu, Yang, Xi, Hualin S, Yang, Jian, Zhang, Futao, Arolt, Volker, Baune, Bernhard T, Berger, Klaus, Boomsma, Dorret I, Cichon, Sven, Dannlowski, udo, de Geus, EJC, DePaulo, J Raymond, Domenici, Enrico, Domschke, Katharina, Esko, Tönu, Grabe, Hans J, Hamilton, Steven P, Hayward, Caroline, Heath, Andrew C, Hinds, David A, Kendler, Kenneth S, Kloiber, Stefan, Lewis, Glyn, Li, Qingqin S, Lucae, Susanne, Madden, Pamela AF, Magnusson, Patrik K, Martin, Nicholas G, McIntosh, Andrew M, Metspalu, Andres, Mors, Ole, Mortensen, Preben Bo, Müller-Myhsok, Bertram, Nordentoft, Merete, Nöthen, Markus M, O’Donovan, Michael C, Paciga, Sara A, Pedersen, Nancy L, Penninx, Brenda WJH, Perlis, Roy H, Porteous, David J, Potash, James B, Preisig, Martin, Rietschel, Marcella, Schaefer, Catherine, Schulze, Thomas G, Smoller, Jordan W, Stefansson, Kari, Tiemeier, Henning, Uher, Rudolf, Völzke, Henry, Weissman, Myrna M, Werge, Thomas, Winslow, Ashley R, Lewis, Cathryn M, Levinson, Douglas F, Breen, Gerome, Børglum, Anders D, and Sullivan, Patrick F
Subjects: 0303 health sciences, business.industry, Genome-wide association study, medicine.disease, Bioinformatics, behavioral disciplines and activities, Genetic architecture, 3. Good health, 03 medical and health sciences, 0302 clinical medicine, medicine.anatomical_structure, Schizophrenia, mental disorders, medicine, Etiology, Autism, Major depressive disorder, business, 030217 neurology & neurosurgery, Depression (differential diagnoses), Anterior cingulate cortex, 030304 developmental biology
Abstract: Major depressive disorder (MDD) is a notably complex illness with a lifetime prevalence of 14%.1 It is often chronic or recurrent and is thus accompanied by considerable morbidity, excess mortality, substantial costs, and heightened risk of suicide.2-7 MDD is a major cause of disability worldwide.8 We conducted a genome-wide association (GWA) meta-analysis in 130,664 MDD cases and 330,470 controls, and identified 44 independent loci that met criteria for statistical significance. We present extensive analyses of these results which provide new insights into the nature of MDD. The genetic findings were associated with clinical features of MDD, and implicated prefrontal and anterior cingulate cortex in the pathophysiology of MDD (regions exhibiting anatomical differences between MDD cases and controls). Genes that are targets of antidepressant medications were strongly enriched for MDD association signals (P=8.5×10−10), suggesting the relevance of these findings for improved pharmacotherapy of MDD. Sets of genes involved in gene splicing and in creating isoforms were also enriched for smaller MDD GWA P-values, and these gene sets have also been implicated in schizophrenia and autism. Genetic risk for MDD was correlated with that for many adult and childhood onset psychiatric disorders. Our analyses suggested important relations of genetic risk for MDD with educational attainment, body mass, and schizophrenia: the genetic basis of lower educational attainment and higher body mass were putatively causal for MDD whereas MDD and schizophrenia reflected a partly shared biological etiology. All humans carry lesser or greater numbers of genetic risk factors for MDD, and a continuous measure of risk underlies the observed clinical phenotype. MDD is not a distinct entity that neatly demarcates normalcy from pathology but rather a useful clinical construct associated with a range of adverse outcomes and the end result of a complex process of intertwined genetic and environmental effects. These findings help refine and define the fundamental basis of MDD.
Published: 2017
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106. Genetic overlap between endometriosis and endometrial cancer: evidence from cross‐disease genetic correlation and GWAS meta‐analyses

Author: Painter, Jodie N., primary, O'Mara, Tracy A., additional, Morris, Andrew P., additional, Cheng, Timothy H. T., additional, Gorman, Maggie, additional, Martin, Lynn, additional, Hodson, Shirley, additional, Jones, Angela, additional, Martin, Nicholas G., additional, Gordon, Scott, additional, Henders, Anjali K., additional, Attia, John, additional, McEvoy, Mark, additional, Holliday, Elizabeth G., additional, Scott, Rodney J., additional, Webb, Penelope M., additional, Fasching, Peter A., additional, Beckmann, Matthias W., additional, Ekici, Arif B., additional, Hein, Alexander, additional, Rübner, Matthias, additional, Hall, Per, additional, Czene, Kamila, additional, Dörk, Thilo, additional, Dürst, Matthias, additional, Hillemanns, Peter, additional, Runnebaum, Ingo, additional, Lambrechts, Diether, additional, Amant, Frederic, additional, Annibali, Daniela, additional, Depreeuw, Jeroen, additional, Vanderstichele, Adriaan, additional, Goode, Ellen L., additional, Cunningham, Julie M., additional, Dowdy, Sean C., additional, Winham, Stacey J., additional, Trovik, Jone, additional, Hoivik, Erling, additional, Werner, Henrica M. J., additional, Krakstad, Camilla, additional, Ashton, Katie, additional, Otton, Geoffrey, additional, Proietto, Tony, additional, Tham, Emma, additional, Mints, Miriam, additional, Ahmed, Shahana, additional, Healey, Catherine S., additional, Shah, Mitul, additional, Pharoah, Paul D. P., additional, Dunning, Alison M., additional, Dennis, Joe, additional, Bolla, Manjeet K., additional, Michailidou, Kyriaki, additional, Wang, Qin, additional, Tyrer, Jonathan P., additional, Hopper, John L., additional, Peto, Julian, additional, Swerdlow, Anthony J., additional, Burwinkel, Barbara, additional, Brenner, Hermann, additional, Meindl, Alfons, additional, Brauch, Hiltrud, additional, Lindblom, Annika, additional, Chang‐Claude, Jenny, additional, Couch, Fergus J., additional, Giles, Graham G., additional, Kristensen, Vessela N., additional, Cox, Angela, additional, Zondervan, Krina T., additional, Nyholt, Dale R., additional, MacGregor, Stuart, additional, Montgomery, Grant W., additional, Tomlinson, Ian, additional, Easton, Douglas F., additional, Thompson, Deborah J., additional, and Spurdle, Amanda B., additional
Published: 2018
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107. Cohort Profile: Nausea and vomiting during pregnancy genetics consortium (NVP Genetics Consortium)

Author: Colodro-Conde, Lucia, Cross, Simone, Lind, Penelope, Painter, Jodie, Gunst, Annika, Jern, Patrick, Johansson, Ada, Maegbaek, Merete Lund, Munk-Olsen, Trine, Nyholt, Dale, other, and, Colodro-Conde, Lucia, Cross, Simone, Lind, Penelope, Painter, Jodie, Gunst, Annika, Jern, Patrick, Johansson, Ada, Maegbaek, Merete Lund, Munk-Olsen, Trine, Nyholt, Dale, and other, and
Abstract: Nausea and vomiting during pregnancy (NVP), commonly known as morning sickness, is very common and is typically self-limiting. However, more severe forms and the development of hyperemesis gravidarum (HG), defined as persistent and excessive vomiting, with dehydration, ketonuria and >5% bodyweight loss,1 may lead to health consequences for the mother and the offspring exposed in utero. Despite efforts towards understanding the causes of NVP and HG, they are not well established. The NVP Genetics Consortium is an open collaborative network of researchers integrating data on NVP of women who have been pregnant at least once, with the goal of investigating NVP, NVP severity and HG. Currently, the NVP Genetics Consortium brings together data from Australia, Finland, Spain, the UK and Denmark. The Consortium is actively recruiting new members...
Published: 2017

108. Genetic Risk Score Mendelian Randomization Shows that Obesity Measured as Body Mass Index, but not Waist:Hip Ratio, Is Causal for Endometrial Cancer

Author: Painter, Jodie N, O'Mara, Tracy A, Marquart, Louise, Webb, Penelope M, Attia, John, Medland, Sarah E, Cheng, Timothy, Dennis, Joe, Holliday, Elizabeth G, McEvoy, Mark, Scott, Rodney J, Ahmed, Shahana, Healey, Catherine S, Shah, Mitul, Gorman, Maggie, Martin, Lynn, Hodgson, Shirley V, Beckmann, Matthias W, Ekici, Arif B, Fasching, Peter A, Hein, Alexander, Rübner, Matthias, Czene, Kamila, Darabi, Hatef, Hall, Per, Li, Jingmei, Dörk, Thilo, Dürst, Matthias, Hillemanns, Peter, Runnebaum, Ingo B, Amant, Frederic, Annibali, Daniela, Depreeuw, Jeroen, Lambrechts, Diether, Neven, Patrick, Cunningham, Julie M, Dowdy, Sean C, Goode, Ellen L, Fridley, Brooke L, Winham, Stacey J, Njølstad, Tormund S, Salvesen, Helga B, Trovik, Jone, Werner, Henrica MJ, Ashton, Katie A, Otton, Geoffrey, Proietto, Anthony, Mints, Miriam, Tham, Emma, Bolla, Manjeet K, Michailidou, Kyriaki, Wang, Qin, Tyrer, Jonathan P, Hopper, John L, Peto, Julian, Swerdlow, Anthony J, Burwinkel, Barbara, Brenner, Hermann, Meindl, Alfons, Brauch, Hiltrud, Lindblom, Annika, Chang-Claude, Jenny, Couch, Fergus J, Giles, Graham G, Kristensen, Vessela N, Cox, Angela, Pharoah, Paul DP, Tomlinson, Ian, Dunning, Alison M, Easton, Douglas F, Thompson, Deborah J, Spurdle, Amanda B, AOCS Group, for RENDOCAS, National Study of Endometrial Cancer Genetics Group (NSECG), Australian National Endometrial Cancer Study Group (ANECS), Dennis, Joe [0000-0003-4591-1214], Wang, Jean [0000-0002-9139-0627], Tyrer, Jonathan [0000-0003-3724-4757], Pharoah, Paul [0000-0001-8494-732X], Dunning, Alison [0000-0001-6651-7166], Easton, Douglas [0000-0003-2444-3247], Thompson, Deborah [0000-0003-1465-5799], and Apollo - University of Cambridge Repository
Subjects: Waist-Hip Ratio, Humans, nutritional and metabolic diseases, Female, Genetic Predisposition to Disease, Obesity, Mendelian Randomization Analysis, Polymorphism, Single Nucleotide, Body Mass Index, Endometrial Neoplasms
Abstract: BACKGROUND: The strongest known risk factor for endometrial cancer is obesity. To determine whether SNPs associated with increased body mass index (BMI) or waist-hip ratio (WHR) are associated with endometrial cancer risk, independent of measured BMI, we investigated relationships between 77 BMI and 47 WHR SNPs and endometrial cancer in 6,609 cases and 37,926 country-matched controls. METHODS: Logistic regression analysis and fixed effects meta-analysis were used to test for associations between endometrial cancer risk and (i) individual BMI or WHR SNPs, (ii) a combined weighted genetic risk score (wGRS) for BMI or WHR. Causality of BMI for endometrial cancer was assessed using Mendelian randomization, with BMIwGRS as instrumental variable. RESULTS: The BMIwGRS was significantly associated with endometrial cancer risk (P = 3.4 × 10-17). Scaling the effect of the BMIwGRS on endometrial cancer risk by its effect on BMI, the endometrial cancer OR per 5 kg/m2 of genetically predicted BMI was 2.06 [95% confidence interval (CI), 1.89-2.21], larger than the observed effect of BMI on endometrial cancer risk (OR = 1.55; 95% CI, 1.44-1.68, per 5 kg/m2). The association attenuated but remained significant after adjusting for BMI (OR = 1.22; 95% CI, 1.10-1.39; P = 5.3 × 10-4). There was evidence of directional pleiotropy (P = 1.5 × 10-4). BMI SNP rs2075650 was associated with endometrial cancer at study-wide significance (P < 4.0 × 10-4), independent of BMI. Endometrial cancer was not significantly associated with individual WHR SNPs or the WHRwGRS. CONCLUSIONS: BMI, but not WHR, is causally associated with endometrial cancer risk, with evidence that some BMI-associated SNPs alter endometrial cancer risk via mechanisms other than measurable BMI. IMPACT: The causal association between BMI SNPs and endometrial cancer has possible implications for endometrial cancer risk modeling. Cancer Epidemiol Biomarkers Prev; 25(11); 1503-10. ©2016 AACR.
Published: 2016

109. Identifying the Genes Associated with Endometriosis Risk on Chromosomes 1 and 7

Author: Montgomery, Grant W., Nyholt, Dale R., Stuart MacGregor, Painter, Jodie N., Luong, Hien T. T., Dinger, Marcel E., Morris, Andrew P., Treloar, Susan A., Missmer, Stacey A., Rogers, Peter A. W., and Zondervan, Krina T.
Published: 2016

110. GWAS meta-analysis of 16 852 women identifies new susceptibility locus for endometrial cancer

Author: Chen, Maxine M, O'Mara, Tracy A, Thompson, Deborah J, Painter, Jodie N, Australian National Endometrial Cancer Study Group (ANECS), Attia, John, Black, Amanda, Brinton, Louise, Chanock, Stephen, Chen, Chu, Cheng, Timothy Ht, Cook, Linda S, Crous-Bou, Marta, Doherty, Jennifer, Friedenreich, Christine M, Garcia-Closas, Montserrat, Gaudet, Mia M, Gorman, Maggie, Haiman, Christopher, Hankinson, Susan E, Hartge, Patricia, Henderson, Brian E, Hodgson, Shirley, Holliday, Elizabeth G, Horn-Ross, Pamela L, Hunter, David J, Le Marchand, Loic, Liang, Xiaolin, Lissowska, Jolanta, Long, Jirong, Lu, Lingeng, Magliocco, Anthony M, Martin, Lynn, McEvoy, Mark, National Study Of Endometrial Cancer Genetics Group (NSECG), Olson, Sara H, Orlow, Irene, Pooler, Loreall, Prescott, Jennifer, Rastogi, Radhai, Rebbeck, Timothy R, Risch, Harvey, Sacerdote, Carlotta, Schumacher, Frederick, Wendy Setiawan, Veronica, Scott, Rodney J, Sheng, Xin, Shu, Xiao-Ou, Turman, Constance, Van Den Berg, David, Wang, Zhaoming, Weiss, Noel S, Wentzensen, Nicholas, Xia, Lucy, Xiang, Yong-Bing, Yang, Hannah P, Yu, Herbert, Zheng, Wei, Pharoah, Paul DP, Dunning, Alison M, Tomlinson, Ian, Easton, Douglas F, Kraft, Peter, Spurdle, Amanda B, De Vivo, Immaculata, Thompson, Deborah [0000-0003-1465-5799], Pharoah, Paul [0000-0001-8494-732X], Dunning, Alison [0000-0001-6651-7166], Easton, Douglas [0000-0003-2444-3247], and Apollo - University of Cambridge Repository
Subjects: Genotype, Humans, Chromosomes, Human, Pair 6, Female, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, White People, Endometrial Neoplasms, Genome-Wide Association Study
Abstract: Endometrial cancer is the most common gynecological malignancy in the developed world. Although there is evidence of genetic predisposition to the disease, most of the genetic risk remains unexplained. We present the meta-analysis results of four genome-wide association studies (4907 cases and 11 945 controls total) in women of European ancestry. We describe one new locus reaching genome-wide significance (P < 5 × 10 -8) at 6p22.3 (rs1740828; P = 2.29 × 10 -8, OR = 1.20), providing evidence of an additional region of interest for genetic susceptibility to endometrial cancer.
Published: 2016

111. CYP19A1 fine-mapping and Mendelian randomization

Author: Thompson, Deborah J, O'Mara, Tracy A, Glubb, Dylan M, Painter, Jodie N, Cheng, Timothy, Folkerd, Elizabeth J, Doody, Deborah, Dennis, Joe, Webb, Penelope M, Gorman, Maggie, Martin, Lynn, Hodgson, Shirley, Michailidou, Kyriaki, Tyrer, Jonathan P, Maranian, Mel J, Hall, Per, Czene, Kamila, Darabi, Hatef, Li, Jingmei, Fasching, Peter A, Hein, Alexander, Beckmann, Matthias W, Ekici, Arif B, Doerk, Thilo, Hillemanns, Peter, Durst, Matthias, Runnebaum, Ingo, Zhao, Hui, Depreeuw, Jeroen, Schrauwen, Stefanie, Amant, Frederic, Goode, Ellen L, Fridley, Brooke L, Dowdy, Sean C, Winham, Stacey J, Salvesen, Helga B, Trovik, Jone, Njolstad, Tormund S, Werner, Henrica M J, Ashton, Katie, Proietto, Tony, Otton, Geoffrey, Carvajal-carmona, Luis, Tham, Emma, Liu, Tao, Mints, Miriam, Scott, Rodney J, McEvoy, Mark G, Attia, John R, Holliday, Elizabeth G, Montgomery, Grant W., Martin, Nicholas G., Nyholt, Dale R, Henders, Anjali K, Hopper, John L, Traficante, Nadia, Ruebner, Matthias, Swerdlow, Anthony J, Burwinkel, Barbara, Brenner, Hermann, Meindl, Alfons, Brauch, Hiltrud, Lindblom, Annika, Lambrechts, Diether, Chang-Claude, Jenny, Couch, Fergus J, Giles, Graham, Kristensen, Vessela N, Cox, Angela, Bolla, Manjeet K, Wang, Qin, Bojesen, Stig E, Shah, Mitul, Luben, Robert, Khaw, Kay-Tee, Pharoah, Paul P D, Dunning, Alison M, Tomlinson, Ian, Dowsett, Mitch, Easton, Douglas F, and Spurdle, Amanda B
Abstract: Candidate gene studies have reported CYP19A1 variants to be associated with endometrial cancer and with estradiol (E2) concentrations. We analyzed 2937 single nucleotide polymorphisms (SNPs) in 6608 endometrial cancer cases and 37 925 controls and report the first genome wide-significant association between endometrial cancer and a CYP19A1 SNP (rs727479 in intron 2, P=4.8×10−11). SNP rs727479 was also among those most strongly associated with circulating E2 concentrations in 2767 post-menopausal controls (P=7.4×10−8). The observed endometrial cancer odds ratio per rs727479 A-allele (1.15, CI=1.11–1.21) is compatible with that predicted by the observed effect on E2 concentrations (1.09, CI=1.03–1.21), consistent with the hypothesis that endometrial cancer risk is driven by E2. From 28 candidate-causal SNPs, 12 co-located with three putative gene-regulatory elements and their risk alleles associated with higher CYP19A1 expression in bioinformatical analyses. For both phenotypes, the associations with rs727479 were stronger among women with a higher BMI (Pinteraction=0.034 and 0.066 respectively), suggesting a biologically plausible gene-environment interaction.
Published: 2016
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112. Identification of 55,000 Replicated DNA Methylation QTL

Author: McRae, Allan F, primary, Marioni, Riccardo E, additional, Shah, Sonia, additional, Yang, Jian, additional, Powell, Joseph E., additional, Harris, Sarah E, additional, Gibson, Jude, additional, Henders, Anjali K, additional, Bowdler, Lisa, additional, Painter, Jodie N., additional, Murphy, Lee, additional, Martin, Nicholas G, additional, Starr, John M, additional, Wray, Naomi R, additional, Deary, Ian J, additional, Visscher, Peter M, additional, and Montgomery, Grant W, additional
Published: 2017
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113. Comprehensive genetic assessment of the ESR1 locus identifies a risk region for endometrial cancer

Author: O'Mara, Tracy A, Glubb, Dylan M, Painter, Jodie N, Cheng, Timothy, Dennis, Joe, Australian National Endometrial Cancer Study Group (ANECS), Attia, John, Holliday, Elizabeth G, McEvoy, Mark, Scott, Rodney J, Ashton, Katie, Proietto, Tony, Otton, Geoffrey, Shah, Mitul, Ahmed, Shahana, Healey, Catherine S, Gorman, Maggie, Martin, Lynn, National Study of Endometrial Cancer Genetics Group (NSECG), Hodgson, Shirley, Fasching, Peter A, Hein, Alexander, Beckmann, Matthias W, Ekici, Arif B, Hall, Per, Czene, Kamila, Darabi, Hatef, Li, Jingmei, Dürst, Matthias, Runnebaum, Ingo, Hillemanns, Peter, Dörk, Thilo, Lambrechts, Diether, Depreeuw, Jeroen, Annibali, Daniela, Amant, Frederic, Zhao, Hui, Goode, Ellen L, Dowdy, Sean C, Fridley, Brooke L, Winham, Stacey J, Salvesen, Helga B, Njølstad, Tormund S, Trovik, Jone, Werner, Henrica MJ, Tham, Emma, Liu, Tao, Mints, Miriam, RENDOCAS, Bolla, Manjeet K, Michailidou, Kyriaki, Tyrer, Jonathan P, Wang, Qin, Hopper, John L, AOCS Group, Peto, Julian, Swerdlow, Anthony J, Burwinkel, Barbara, Brenner, Hermann, Meindl, Alfons, Brauch, Hiltrud, Lindblom, Annika, Chang-Claude, Jenny, Couch, Fergus J, Giles, Graham G, Kristensen, Vessela N, Cox, Angela, Pharoah, Paul DP, Dunning, Alison M, Tomlinson, Ian, Easton, Douglas F, Thompson, Deborah J, Spurdle, Amanda B, Dennis, Joe [0000-0003-4591-1214], Tyrer, Jonathan [0000-0003-3724-4757], Wang, Jean [0000-0002-9139-0627], Pharoah, Paul [0000-0001-8494-732X], Dunning, Alison [0000-0001-6651-7166], Easton, Douglas [0000-0003-2444-3247], Thompson, Deborah [0000-0003-1465-5799], and Apollo - University of Cambridge Repository
Subjects: Genotype, ESR1, fine-mapping analysis, Estrogen Receptor alpha, Computational Biology, Nuclear Proteins, Breast Neoplasms, Nerve Tissue Proteins, Prognosis, Polymorphism, Single Nucleotide, Endometrial Neoplasms, Cytoskeletal Proteins, Meta-Analysis as Topic, Genetic Loci, Risk Factors, Case-Control Studies, endometrial cancer, single-nucleotide polymorphisms, Databases, Genetic, Humans, Female, Genetic Predisposition to Disease, Promoter Regions, Genetic
Abstract: Excessive exposure to estrogen is a well-established risk factor for endometrial cancer (EC), particularly for cancers of endometrioid histology. The physiological function of estrogen is primarily mediated by estrogen receptor alpha, encoded by ESR1. Consequently, several studies have investigated whether variation at the ESR1 locus is associated with risk of EC, with conflicting results. We performed comprehensive fine-mapping analyses of 3633 genotyped and imputed single nucleotide polymorphisms (SNPs) in 6607 EC cases and 37 925 controls. There was evidence of an EC risk signal located at a potential alternative promoter of the ESR1 gene (lead SNP rs79575945, P=1.86×10(-5)), which was stronger for cancers of endometrioid subtype (P=3.76×10(-6)). Bioinformatic analysis suggests that this risk signal is in a functionally important region targeting ESR1, and eQTL analysis found that rs79575945 was associated with expression of SYNE1, a neighbouring gene. In summary, we have identified a single EC risk signal located at ESR1, at study-wide significance. Given SNPs located at this locus have been associated with risk for breast cancer, also a hormonally driven cancer, this study adds weight to the rationale for performing informed candidate fine-scale genetic studies across cancer types.
Published: 2015

114. Evidence of a Causal Association Between Insulinemia and Endometrial Cancer: A Mendelian Randomization Analysis

Author: Nead, Kevin T, Sharp, Stephen J, Thompson, Deborah J, Painter, Jodie N, Savage, David B, Semple, Robert K, Barker, Adam, Australian National Endometrial Cancer Study Group (ANECS), Perry, John RB, Attia, John, Dunning, Alison M, Easton, Douglas F, Holliday, Elizabeth, Lotta, Luca A, O'Mara, Tracy, McEvoy, Mark, Pharoah, Paul DP, Scott, Rodney J, Spurdle, Amanda B, Langenberg, Claudia, Wareham, Nicholas J, Scott, Robert A, Sharp, Stephen [0000-0003-2375-1440], Thompson, Deborah [0000-0003-1465-5799], Savage, David [0000-0002-7857-7032], Semple, Robert [0000-0001-6539-3069], Perry, John [0000-0001-6483-3771], Dunning, Alison [0000-0001-6651-7166], Easton, Douglas [0000-0003-2444-3247], Pharoah, Paul [0000-0001-8494-732X], Langenberg, Claudia [0000-0002-5017-7344], Wareham, Nicholas [0000-0003-1422-2993], and Apollo - University of Cambridge Repository
Subjects: Adult, Blood Glucose, Genotype, education, Fasting, Mendelian Randomization Analysis, Middle Aged, Polymorphism, Single Nucleotide, Risk Assessment, Body Mass Index, Endometrial Neoplasms, Diabetes Mellitus, Type 2, Risk Factors, Hyperinsulinism, Odds Ratio, Humans, Insulin, Female, health care economics and organizations, Aged
Abstract: BACKGROUND: Insulinemia and type 2 diabetes (T2D) have been associated with endometrial cancer risk in numerous observational studies. However, the causality of these associations is uncertain. Here we use a Mendelian randomization (MR) approach to assess whether insulinemia and T2D are causally associated with endometrial cancer. METHODS: We used single nucleotide polymorphisms (SNPs) associated with T2D (49 variants), fasting glucose (36 variants), fasting insulin (18 variants), early insulin secretion (17 variants), and body mass index (BMI) (32 variants) as instrumental variables in MR analyses. We calculated MR estimates for each risk factor with endometrial cancer using an inverse-variance weighted method with SNP-endometrial cancer associations from 1287 case patients and 8273 control participants. RESULTS: Genetically predicted higher fasting insulin levels were associated with greater risk of endometrial cancer (odds ratio [OR] per standard deviation = 2.34, 95% confidence internal [CI] = 1.06 to 5.14, P = .03). Consistently, genetically predicted higher 30-minute postchallenge insulin levels were also associated with endometrial cancer risk (OR = 1.40, 95% CI = 1.12 to 1.76, P = .003). We observed no associations between genetic risk of type 2 diabetes (OR = 0.91, 95% CI = 0.79 to 1.04, P = .16) or higher fasting glucose (OR = 1.00, 95% CI = 0.67 to 1.50, P = .99) and endometrial cancer. In contrast, endometrial cancer risk was higher in individuals with genetically predicted higher BMI (OR = 3.86, 95% CI = 2.24 to 6.64, P = 1.2x10(-6)). CONCLUSION: This study provides evidence to support a causal association of higher insulin levels, independently of BMI, with endometrial cancer risk.
Published: 2015

115. AB028. Identifying the functional role of VEZT gene for endometriosis risk

Author: Luong, Hien TT., Painter, Jodie N., Sapkota, Yadav, Nyholt, Dale R., Rogers, Peter A., and Montgomery, Grant W.
Subjects: Part 2: Symposium
Abstract: Endometriosis is a common, chronic gynaecological disease characterised by pelvic pain and sub-fertility. It is a complex genetic disease affecting of 6-10% women of reproductive age and up to 50% of women with infertility. Evidence from genomewide association (GWA) imputed and meta-analysis studies in women with and without endometriosis identified association on chromosome 12q22, located close to the putative candidate gene VEZT. Fine-mapping this region in our 1,029 Australian cases and 958 controls confirmed strong evidence of association for non-coding variants in the 12q22 GWA region with the best imputed SNP rs4762347 in the 3’UTR of VEZT (P=0.036; 95% CI, 1.01-1.38; OR =1.18) and four top imputed SNPs in high linkage disequilibrium (LD) with rs4762347. Bioinformatic analysis for potential functional roles for these SNPs using ENCODE data show rs4762347 is highly conserved and alters a regulatory motif for the transcription factor Nkx3. We conducted an initial experiment to evaluate gene expression of VEZT in 36 samples of endometrial tissue from endometriosis cases and controls using high-throughput gene expression RT-qPCR on a microfluidic dynamic array IFC 48x48 chip (Fluidigm Biomark). The results showed that VEZT was expressed in endometrial samples from cases and controls. There was a trend for increased expression levels of VEZT mRNAs in endometriosis cases compared to controls as well as during the secretory phase compared to proliferative phase of menstrual cycle, although these differences were not statistically significant. The top imputed SNP rs4762347 was chosen to test for its allelic effects on VEZT expression. There was suggestive evidence for differences in VEZT mRNA expression observed in allelic groups of rs4762347.
Published: 2015

116. Fine-mapping of the HNF1B multicancer locus identifies candidate variants that mediate endometrial cancer risk

Author: Painter, Jodie N., O'Mara, Tracy A., Batra, Jyotsna, Cheng, Timothy, Lose, Felicity A., Dennis, Joe, Michailidou, Kyriaki, Tyrer, Jonathan P., Ahmed, Shahana, Ferguson, Kaltin, Healey, Catherine S., Kaufmann, Susanne, Hillman, Kristine M., Walpole, Carina, Moya, Leire, Pollock, Pamela, Jones, Angela, Howarth, Kimberley, Martin, Lynn, Gorman, Maggie, Hodgson, Shirley, de Polanco, Ma Magdalena Echeverry, Sans, Monica, Carracedo, Angel, Castellvi-Bel, Sergi, Rojas-Martinez, Augusto, Santos, Erika, Teixeira, Manuel R., Carvajal-Carmona, Luis, Shu, Xiao-Ou, Long, Jirong, Zheng, Wei, Xiang, Yong-Bing, Montgomery, Grant W., Webb, Penelope M., Scott, Rodney J., McEvoy, Mark, Attia, John, Holliday, Elizabeth, Martin, Nicholas G., Nyholt, Dale R., Henders, Anjali K., Fasching, Peter A., Hein, Alexander, Beckmann, Matthias W., Renner, Stefan P., Dörk, Thilo, Hillemanns, Peter, Amant, Frederic, Other departments, and Graduate School
Abstract: Common variants in the hepatocyte nuclear factor 1 homeobox B (HNF1B) gene are associated with the risk of Type II diabetes and multiple cancers. Evidence to date indicates that cancer risk may be mediated via genetic or epigenetic effects on HNF1B gene expression. We previously found single-nucleotide polymorphisms (SNPs) at the HNF1B locus to be associated with endometrial cancer, and now report extensive fine-mapping and in silico and laboratory analyses of this locus. Analysis of 1184 genotyped and imputed SNPs in 6608 Caucasian cases and 37 925 controls, and 895 Asian cases and 1968 controls, revealed the best signal of association for SNP rs11263763 (P = 8.4 x 10(-14), odds ratio = 0.86, 95% confidence interval = 0.82-0.89), located within HNF1B intron 1. Haplotype analysis and conditional analyses provide no evidence of further independent endometrial cancer risk variants at this locus. SNP rs11263763 genotype was associated with HNF1B mRNA expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas. Genetic analyses prioritized rs11263763 and four other SNPs in high-to-moderate linkage disequilibrium as the most likely causal SNPs. Three of these SNPs map to the extended HNF1B promoter based on chromatin marks extending from the minimal promoter region. Reporter assays demonstrated that this extended region reduces activity in combination with the minimal HNF1B promoter, and that the minor alleles of rs11263763 or rs8064454 are associated with decreased HNF1B promoter activity. Our findings provide evidence for a single signal associated with endometrial cancer risk at the HNF1B locus, and that risk is likely mediated via altered HNF1B gene expression
Published: 2015

117. Genetic studies of body mass index yield new insights for obesity biology

Author: Locke, Adam E, Kahali, Bratati, Croteau-Chonka, Damien C, Doney, Alex S F, He, Bing, Heikkilä, Outi, Hietala, Kustaa, Kytö, Janne, Lahermo, Päivi, Lehto, Markku, Österholm, Anne-May, Parkkonen, Maija, Pitkäniemi, Janne, Rosengård-Bärlund, Milla, Eklund, Niina, Saraheimo, Markku, Sarti, Cinzia, Söderlund, Jenny, Soro-Paavonen, Aino, Syreeni, Anna, Thorn, Lena M, Tikkanen, Heikki, Tolonen, Nina, Tryggvason, Karl, Tuomilehto, Jaakko, Estrada, Karol, Wadén, Johan, Gill, Geoffrey V, Prior, Sarah, Guiducci, Candace, Mirel, Daniel B, Taylor, Andrew, Hosseini, Mohsen, Parving, Hans-Henrik, Rossing, Peter, Tarnow, Lise, Eury, Elodie, Ladenvall, Claes, Alhenc-Gelas, François, Lefebvre, Pierre, Rigalleau, Vincent, Roussel, Ronan, Tregouet, David-Alexandre, Maestroni, Anna, Maestroni, Silvia, Falhammar, Henrik, Gu, Tianwei, Folkersen, Lasse, Möllsten, Anna, Cimponeriu, Dan, Mihai, Ioana, Mota, Maria, Mota, Eugen, Serafinceanu, Cristian, Stavarachi, Monica, Hanson, Robert L, Nelson, Robert G, Kretzler, Matthias, Fraser, Ross M, Colhoun, Helen M, Panduru, Nicolae Mircea, Gu, Harvest F, Brismar, Kerstin, Zerbini, Gianpaolo, Hadjadj, Samy, Marre, Michel, Groop, Leif, Lajer, Maria, Bull, Shelley B, Garcia, Melissa E, Waggott, Daryl, Paterson, Andrew D, Savage, David A, Bain, Stephen C, Martin, Finian, Hirschhorn, Joel N, Godson, Catherine, Florez, Jose C, Groop, Per-Henrik, Maxwell, Alexander P, Geller, Frank, Willer, Cristen J, Schmidt, Ellen M, Sengupta, Sebanti, Peloso, Gina M, Gustafsson, Stefan, Kanoni, Stavroula, Ganna, Andrea, Chen, Jin, Buchkovich, Martin L, Mora, Samia, Giedraitis, Vilmantas, Beckmann, Jacques S, Bragg-Gresham, Jennifer L, Chang, Hsing-Y, Demirkan, Ayşe, Den Hertog, Heleen M, Do, Ron, Donnelly, Louise A, Ehret, Georg B, Esko, Tõnu, Feitosa, Mary F, Gigante, Bruna, Ferreira, Teresa, Fischer, Krista, Fontanillas, Pierre, Freitag, Daniel F, Gurdasani, Deepti, Heikkilä, Kauko, Hyppönen, Elina, Isaacs, Aaron, Jackson, Anne U, Esko, Tonu, Go, Alan S, Johansson, Åsa, Johnson, Toby, Kaakinen, Marika, Kettunen, Johannes, Kleber, Marcus E, Li, Xiaohui, Luan, Jian'an, Lyytikäinen, Leo-Pekka, Magnusson, Patrik K E, Mangino, Massimo, Golay, Alain, Mihailov, Evelin, Montasser, May E, Müller-Nurasyid, Martina, Nolte, Ilja M, O'Connell, Jeffrey R, Palmer, Cameron D, Perola, Markus, Petersen, Ann-Kristin, Sanna, Serena, Saxena, Richa, Goodall, Alison H, Service, Susan K, Shah, Sonia, Shungin, Dmitry, Sidore, Carlo, Song, Ci, Strawbridge, Rona J, Surakka, Ida, Tanaka, Toshiko, Teslovich, Tanya M, Thorleifsson, Gudmar, Gordon, Scott D, Van den Herik, Evita G, Voight, Benjamin F, Volcik, Kelly A, Waite, Lindsay L, Wong, Andrew, Wu, Ying, Zhang, Weihua, Absher, Devin, Asiki, Gershim, Barroso, Inês, Gorski, Mathias, Been, Latonya F, Bolton, Jennifer L, Bonnycastle, Lori L, Brambilla, Paolo, Burnett, Mary S, Cesana, Giancarlo, Dimitriou, Maria, Doring, Angela, Elliott, Paul, Grabe, Hans-Jörgen, Epstein, Stephen E, Eyjolfsson, Gudmundur Ingi, Goodarzi, Mark O, Grallert, Harald, Gravito, Martha L, Groves, Christopher J, Hallmans, Göran, Hartikainen, Anna-Liisa, Hayward, Caroline, Hernandez, Dena, Hicks, Andrew A, Holm, Hilma, Hung, Yi-Jen, Illig, Thomas, Jones, Michelle R, Kaleebu, Pontiano, Kastelein, John J P, Khaw, Kay-Tee, Kim, Eric, Grammer, Tanja B, Klopp, Norman, Komulainen, Pirjo, Kumari, Meena, Langenberg, Claudia, Lehtimaki, Terho, Lin, Shih-Yi, Lindstrom, Jaana, Loos, Ruth J F, Mach, François, McArdle, Wendy L, Gräßler, Jürgen, Meisinger, Christa, Mitchell, Braxton D, Muller, Gabrielle, Nagaraja, Ramaiah, Narisu, Narisu, Nieminen, Tuomo V M, Nsubuga, Rebecca N, Olafsson, Isleifur, Ong, Ken K, Palotie, Aarno, Grönberg, Henrik, Papamarkou, Theodore, Pomilla, Cristina, Pouta, Anneli, Rader, Daniel J, Reilly, Muredach P, Ridker, Paul M, Rivadeneira, Fernando, Rudan, Igor, Ruokonen, Aimo, Samani, Nilesh, Fall, Tove, Scharnagl, Hubert, Seeley, Janet, Silander, Kaisa, Stančáková, Alena, Stirrups, Kathleen, Swift, Amy J, Tiret, Laurence, Uitterlinden, Andre G, van Pelt, L Joost, Vedantam, Sailaja, Gusto, Gaëlle, Wainwright, Nicholas, Wijmenga, Cisca, Wild, Sarah H, Willemsen, Gonneke, Wilsgaard, Tom, Wilson, James F, Young, Elizabeth H, Zhao, Jing Hua, Adair, Linda S, Arveiler, Dominique, Haessler, Jeffrey, Assimes, Themistocles L, Bandinelli, Stefania, Bennett, Franklyn, Bochud, Murielle, Boehm, Bernhard O, Boomsma, Dorret I, Borecki, Ingrid B, Bornstein, Stefan R, Bovet, Pascal, Burnier, Michel, Hall, Per, Campbell, Harry, Chakravarti, Aravinda, Chambers, John C, Chen, Yii-Der Ida, Collins, Francis S, Cooper, Richard S, Danesh, John, Dedoussis, George, de Faire, Ulf, Feranil, Alan B, Haller, Toomas, Ferrieres, Jean, Ferrucci, Luigi, Freimer, Nelson B, Gieger, Christian, Groop, Leif C, Gudnason, Vilmundur, Gyllensten, Ulf, Hamsten, Anders, Harris, Tamara B, Hingorani, Aroon, Hallmans, Goran, Hofman, Albert, Hovingh, G Kees, Hsiung, Chao Agnes, Humphries, Steve E, Hunt, Steven C, Hveem, Kristian, Iribarren, Carlos, Jarvelin, Marjo-Riitta, Jula, Antti, Hartman, Catharina A, Kähönen, Mika, Kaprio, Jaakko, Kesäniemi, Antero, Kivimaki, Mika, Kooner, Jaspal S, Koudstaal, Peter J, Krauss, Ronald M, Kuh, Diana, Kuusisto, Johanna, Kyvik, Kirsten O, Hassinen, Maija, Laakso, Markku, Lakka, Timo A, Lind, Lars, Lindgren, Cecilia M, Martin, Nicholas G, März, Winfried, McCarthy, Mark I, McKenzie, Colin A, Meneton, Pierre, Metspalu, Andres, Moilanen, Leena, Morris, Andrew D, Munroe, Patricia B, Njølstad, Inger, Pedersen, Nancy L, Power, Chris, Pramstaller, Peter P, Price, Jackie F, Psaty, Bruce M, Quertermous, Thomas, Heard-Costa, Nancy L, Rauramaa, Rainer, Saleheen, Danish, Salomaa, Veikko, Sanghera, Dharambir K, Saramies, Jouko, Schwarz, Peter E H, Sheu, Wayne H-H, Shuldiner, Alan R, Siegbahn, Agneta, Spector, Tim D, Helmer, Quinta, Stefansson, Kari, Strachan, David P, Tayo, Bamidele O, Tremoli, Elena, Uusitupa, Matti, van Duijn, Cornelia M, Vollenweider, Peter, Wallentin, Lars, Wareham, Nicholas J, Hengstenberg, Christian, Whitfield, John B, Wolffenbuttel, Bruce H R, Ordovas, Jose M, Boerwinkle, Eric, Palmer, Colin N A, Thorsteinsdottir, Unnur, Chasman, Daniel I, Rotter, Jerome I, Franks, Paul W, Ripatti, Samuli, Holmen, Oddgeir, Cupples, L Adrienne, Sandhu, Manjinder S, Rich, Stephen S, Boehnke, Michael, Deloukas, Panos, Kathiresan, Sekar, Mohlke, Karen L, Ingelsson, Erik, Abecasis, Gonçalo R, Abecasis, Gonçalo, Hottenga, Jouke-Jan, Caulfield, Mark, Chasman, Dan, Ehret, Georg, Johnson, Andrew, Johnson, Louise, Larson, Martin, Levy, Daniel, James, Alan L, Munroe, Patricia, Newton-Cheh, Christopher, O'Reilly, Paul, Palmas, Walter, Psaty, Bruce, Rice, Kenneth, Smith, Albert, Snider, Harold, Tobin, Martin, Van Duijn, Cornelia, Jeff, Janina M, Verwoert, Germaine, Rice, Kenneth M, Johnson, Andrew D, Smith, Albert V, Tobin, Martin D, Verwoert, Germaine C, Hwang, Shih-Jen, Pihur, Vasyl, O'Reilly, Paul F, Amin, Najaf, Teumer, Alexander, Glazer, Nicole L, Launer, Lenore, Jolley, Jennifer, Aulchenko, Yurii, Heath, Simon, Sõber, Siim, Parsa, Afshin, Arora, Pankaj, Dehghan, Abbas, Zhang, Feng, Lucas, Gavin, Juliusdottir, Thorhildur, Peden, John F, Igl, Wilmar, Milaneschi, Yuri, Parker, Alex N, Fava, Cristiano, Kinnunen, Leena, Fox, Ervin R, Go, Min Jin, van der Harst, Pim, Kao, Wen Hong Linda, Sjögren, Marketa, Vinay, D. G., Alexander, Myriam, Tabara, Yasuharu, Shaw-Hawkins, Sue, Koenig, Wolfgang, Whincup, Peter H, Liu, Yongmei, Shi, Gang, Tayo, Bamidele, Seielstad, Mark, Sim, Xueling, Nguyen, Khanh-Dung Hoang, Lehtimäki, Terho, Matullo, Giuseppe, Koskenvuo, Markku, Gaunt, Tom R, Onland-Moret, N Charlotte, Cooper, Matthew N, Platou, Carl G P, Org, Elin, Hardy, Rebecca, Dahgam, Santosh, Palmen, Jutta, Vitart, Veronique, Kratzer, Wolfgang, Braund, Peter S, Kuznetsova, Tatiana, Uiterwaal, Cuno S P M, Adeyemo, Adebowale, Ludwig, Barbara, Tomaszewski, Maciej, Tzoulaki, Ioanna, Palmer, Nicholette D, Laitinen, Jaana, Aspelund, Thor, Garcia, Melissa, Chang, Yen-Pei C, Steinle, Nanette I, Grobbee, Diederick E, Arking, Dan E, Kardia, Sharon L, Morrison, Alanna C, Lamina, Claudia, Najjar, Samer, Hadley, David, Brown, Morris J, Connell, John M, Hingorani, Aroon D, Day, Ian N M, Lawlor, Debbie A, Beilby, John P, Lawrence, Robert W, Leander, Karin, Clarke, Robert, Collins, Rory, Hopewell, Jemma C, Ongen, Halit, Dreisbach, Albert W, Li, Yali, Young, J. H., Bis, Joshua C, Viikari, Jorma, Lee, Nanette R, Chen, Ming-Huei, Olden, Matthias, Pattaro, Cristian, Bolton, Judith A Hoffman, Köttgen, Anna, Bergmann, Sven, Mooser, Vincent, Chaturvedi, Nish, Lichtner, Peter, Frayling, Timothy M, Islam, Muhammad, Jafar, Tazeen H, Erdmann, Jeanette, Kulkarni, Smita R, Grässler, Jürgen, Howard, Philip, Guarrera, Simonetta, Ricceri, Fulvio, Emilsson, Valur, Plump, Andrew, Weder, Alan B, Lindström, Jaana, Sun, Yan V, Bergman, Richard N, Scott, Laura J, Stringham, Heather M, Peltonen, Leena, Vartiainen, Erkki, Brand, Stefan-Martin, Kutalik, Zoltán, Lo, Ken Sin, Staessen, Jan A, Wang, Thomas J, Burton, Paul R, Artigas, Maria Soler, Dong, Yanbin, Snieder, Harold, Wang, Xiaoling, Zhu, Haidong, Lohman, Kurt K, Rudock, Megan E, Lobbens, Stéphane, Heckbert, Susan R, Smith, Nicholas L, Wiggins, Kerri L, Doumatey, Ayo, Shriner, Daniel, Veldre, Gudrun, Viigimaa, Margus, Kinra, Sanjay, Prabhakaran, Dorairajan, Tripathy, Vikal, Lorbeer, Roberto, Langefeld, Carl D, Rosengren, Annika, Thelle, Dag S, Corsi, Anna Maria, Singleton, Andrew, Forrester, Terrence, Hilton, Gina, Salako, Tunde, Iwai, Naoharu, Lu, Yingchang, Kita, Yoshikuni, Ogihara, Toshio, Ohkubo, Takayoshi, Okamura, Tomonori, Ueshima, Hirotsugu, Umemura, Satoshi, Eyheramendy, Susana, Meitinger, Thomas, Wichmann, H-Erich, Cho, Yoon Shin, Kim, Hyung-Lae, Lee, Jong-Young, Scott, James, Sehmi, Joban S, Hedblad, Bo, Nilsson, Peter, Smith, George Davey, Raffel, Leslie J, Yao, Jie, O'Donnell, Chris, Schwartz, Stephen M, Ikram, M Arfan, Longstreth, W. T., Mosley, Thomas H, Seshadri, Sudha, Mahajan, Anubha, Shrine, Nick R G, Wain, Louise V, Morken, Mario A, Prokopenko, Inga, Zitting, Paavo, Cooper, Jackie A, Rasheed, Asif, Goel, Anuj, Watkins, Hugh, Bakker, Stephan J L, van Gilst, Wiek H, Janipalli, Charles S, Mani, K Radha, Yajnik, Chittaranjan S, McLachlan, Stela, Mattace-Raso, Francesco U S, Oostra, Ben A, Demirkan, Ayse, Lakatta, Edward G, Orru, Marco, Scuteri, Angelo, Ala-Korpela, Mika, Kangas, Antti J, Menni, Cristina, Soininen, Pasi, Tukiainen, Taru, Würtz, Peter, Ong, Rick Twee-Hee, Dörr, Marcus, Kroemer, Heyo K, Völker, Uwe, Völzke, Henry, Galan, Pilar, Merger, Sigrun, Hercberg, Serge, Lathrop, Mark, Zelenika, Diana, Zhai, Guangju, Meschia, James F, Nalls, Michael A, Sharma, Pankaj, Terzic, Janos, Kumar, M J Kranthi, Denniff, Matthew, Zukowska-Szczechowska, Ewa, Wagenknecht, Lynne E, Fowkes, F Gerald R, Charchar, Fadi J, Guo, Xiuqing, Milani, Lili, Rotimi, Charles, Bots, Michiel L, Brand, Eva, Samani, Nilesh J, Polasek, Ozren, Talmud, Philippa J, Nyberg, Fredrik, Laan, Maris, Moayyeri, Alireza, Palmer, Lyle J, van der Schouw, Yvonne T, Casas, Juan P, Vineis, Paolo, Raitakari, Olli, Ganesh, Santhi K, Wong, Tien Y, Tai, E Shyong, Monda, Keri L, Rao, Dabeeru C, Morris, Richard W, Dominiczak, Anna F, Marmot, Michael G, Miki, Tetsuro, Chandak, Giriraj R, Coresh, Josef, Navis, Gerjan, Han, Bok-Ghee, Zhu, Xiaofeng, Melander, Olle, Gyllensten, Ulf B, Mulas, Antonella, Wright, Alan F, Farrall, Martin, Elosua, Roberto, Soranzo, Nicole, Sijbrands, Eric J G, Altshuler, David, Müller, Gabriele, Rettig, Rainer, Uda, Manuela, Witteman, Jacqueline C M, Vasan, Ramachandran S, Larson, Martin G, Järvelin, Marjo-Riitta, Musk, Arthur W, Caulfield, Mark J, Alizadeh, Behrooz Z, de Boer, Rudolf A, Mägi, Reedik, Boezen, H Marike, Bruinenberg, Marcel, Franke, Lude, Hillege, Hans L, van der Klauw, Melanie M, Ormel, Johan, Postma, Dirkje S, Rosmalen, Judith G M, Nöthen, Markus M, Slaets, Joris P, Stolk, Ronald P, Scott, Robert 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EN., Warrington, NM., Alavere, H., Barroso, I., Berenson, GS., Blackburn, H., Busonero, F., Chen, W., Couper, D., Easton, DF., Eriksson, J., Foroud, T., Geller, F., Hernandez, DG., Kilpeläinen, TO., Li, S., Melbye, M., Murray, JC., Murray, SS., Nelis, M., Ness, AR., Northstone, K., Peacock, M., Pennell, CE., Pharoah, P., Rafnar, T., Rice, JP., Ring, SM., Schork, NJ., Segrè, AV., Sovio, U., Srinivasan, SR., Tammesoo, ML., Tyrer, J., van Meurs JB., Weedon, MN., Wichmann, H., Young, L., Bierut, LJ., Boyd, HA., Econs, MJ., Van T'Hooft, Ferdinand M., Njølstad, Inger, Abecasis, Gonçalo R., Barroso, Inɥ, The MIGEN Consortium, Investigator, Casari, GIORGIO NEVIO, Other departments, ACS - Amsterdam Cardiovascular Sciences, Vascular Medicine, Landsteiner Laboratory, Clinical Haematology, Damage and Repair in Cancer Development and Cancer Treatment (DARE), Guided Treatment in Optimal Selected Cancer Patients (GUTS), Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Life Course Epidemiology (LCE), Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Groningen Research Institute for Asthma and COPD (GRIAC), Groningen Institute for Organ Transplantation (GIOT), Lifestyle Medicine (LM), Groningen Kidney Center (GKC), Cardiovascular Centre (CVC), Center for Liver, Digestive and Metabolic Diseases (CLDM), Stem Cell Aging Leukemia and Lymphoma (SALL), Locke, A, Kahali, B, Berndt, S, Justice, A, Pers, T, Day, F, Powell, C, Vedantam, S, Buchkovich, M, Yang, J, Croteau-Chonka, D, Esko, T, Fall, T, Ferreira, T, Gustafsson, S, Kutalik, Z, Luan, J, Magi, R, Randall, J, Winkler, T, Wood, A, Workalemahu, T, Faul, J, Smith, J, Zhao, J, Zhao, W, Chen, J, Fehrmann, R, Hedman, A, Karjalainen, J, Schmidt, E, Absher, D, Amin, N, Anderson, D, Beekman, M, Bolton, J, Bragg-Gresham, J, Buyske, S, Demirkan, A, Deng, G, Ehret, G, Feenstra, B, Feitosa, M, Fischer, K, Goel, A, Gong, J, Jackson, A, Kanoni, S, Kleber, M, Kristiansson, K, Lim, U, Lotay, V, 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Investigators, The MuTHER Consortium, The MIGen Consortium, The PAGE Consortium, The ReproGen Consortium, The GENIE Consortium, The International Endogene Consortium, Berndt, Sonja I, Justice, Anne E, Hyppönen, Elina Tuulikki, Epidemiology and Data Science, NCA - Neurobiology of mental health, and EMGO - Lifestyle, overweight and diabetes
Subjects: Male, LOCI, Genome-wide association study, Continental Population Groups/genetics, VARIANTS, Body Mass Index, Insulin Secretion, Insulin, Age Factor, Adiposity, ddc:616, Adipogenesis, Genetic Predisposition to Disease/genetics, Synapse, 3. Good health, Continental Population Group, Urological cancers Radboud Institute for Health Sciences [Radboudumc 15], GENOME-WIDE ASSOCIATIONPROVIDES INSIGHTSGLYCEMIC TRAITSLOCIMETAANALYSISVARIANTSINDIVIDUALSHIPPOCAMPALARCHITECTURETOPIRAMATE, ddc:500, Adipogenesis/genetics, Single Nucleotide/genetics, Age Factors, Continental Population Groups, Energy Metabolism, Europe, Female, Genetic Predisposition to Disease, Glutamic Acid, Humans, Obesity, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Synapses, Genome-Wide Association Study, Multidisciplinary, genetics [Adiposity], Human, Socio-culturale, genetics [Energy Metabolism], ta3111, genetic, body mass index, obesity, SDG 3 - Good Health and Well-being, GLYCEMIC TRAITS, genetics [Continental Population Groups], Genetic variability, Polymorphism, GENOME-WIDE ASSOCIATION, genetics [Adipogenesis], METAANALYSIS, Genetic association, Adipogenesi, genetics [Quantitative Trait Loci], ta1184, metabolism [Glutamic Acid], ta1182, PATHWAYS, metabolism [Synapses], ta3121, medicine.disease, metabolism [Insulin], Adiposity/genetics, Clinical Medicine, Quantitative Trait Loci/genetics, Body mass index, HUMAN HEIGHT, BIO/12 - BIOCHIMICA CLINICA E BIOLOGIA MOLECOLARE CLINICA, Synapses/metabolism, Medizin, Obesity/genetics, Bioinformatics, genetic basis, Obesity/metabolism, genetics [Obesity], body mass index (BMI), genetics [Genetic Predisposition to Disease], ethnology [Europe], 2. Zero hunger, Genetics, ARCHITECTURE, Genetics of obesity, Medicine (all), Single Nucleotide, Polymorphism, Single Nucleotide/genetics, Insulin/metabolism/secretion, Glutamic Acid/metabolism, genetics [Polymorphism, Single Nucleotide], EXPRESSION, Insulin/metabolism, PROVIDES INSIGHTS, genetics [Racial Groups], Biology, Obesity/genetics/metabolism, Europe/ethnology, metabolism [Obesity], Mendelian randomization, medicine, Energy Metabolism/genetics, body mass, genetic analysis, obesity, Klinisk medicin
Abstract: Item does not contain fulltext Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 x 10(-8)), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for approximately 2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.
Published: 2015
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118. New genetic loci link adipose and insulin biology to body fat distribution

Author: Shungin, Dmitry, Winkler, Thomas W, Workalemahu, Tsegaselassie, Hartman, Catharina A, Duncan, Emma L, Ntzani, Evangelia E, Oei, Ling, Albagha, Omar M E, Amin, Najaf, Kemp, John P, Koller, Daniel L, Li, Guo, Liu, Ching-Ti, Minster, Ryan L, Hassinen, Maija, Moayyeri, Alireza, Vandenput, Liesbeth, Willner, Dana, Xiao, Su-Mei, Yerges-Armstrong, Laura M, Zheng, Hou-Feng, Alonso, Nerea, Eriksson, Joel, Kammerer, Candace M, Kaptoge, Stephen K, Hayward, Caroline, Leo, Paul J, Thorleifsson, Gudmar, Wilson, Scott G, Wilson, James F, Aalto, Ville, Alen, Markku, Aragaki, Aaron K, Aspelund, Thor, Center, Jacqueline R, Dailiana, Zoe, Heikkilä, Kauko, Duggan, David J, Garcia, Melissa, Garcia-Giralt, Natàlia, Giroux, Sylvie, Hallmans, Göran, Hocking, Lynne J, Husted, Lise Bjerre, Jameson, Karen A, Khusainova, Rita, Kim, Ghi Su, Herzig, Karl-Heinz, Kooperberg, Charles, Koromila, Theodora, Kruk, Marcin, Laaksonen, Marika, Lacroix, Andrea Z, Lee, Seung Hun, Leung, Ping C, Lewis, Joshua R, Masi, Laura, Mencej-Bedrac, Simona, Helmer, Quinta, Nguyen, Tuan V, Nogues, Xavier, Patel, Millan S, Prezelj, Janez, Rose, Lynda M, Scollen, Serena, Siggeirsdottir, Kristin, Smith, Albert V, Svensson, Olle, Trompet, Stella, Hillege, Hans L, Trummer, Olivia, van Schoor, Natasja M, Woo, Jean, Zhu, Kun, Balcells, Susana, Brandi, Maria Luisa, Buckley, Brendan M, Cheng, Sulin, Christiansen, Claus, Cooper, Cyrus, Holmen, Oddgeir, Dedoussis, George, Ford, Ian, Frost, Morten, Goltzman, David, González-Macías, Jesús, Kähönen, Mika, Karlsson, Magnus, Khusnutdinova, Elza, Koh, Jung-Min, Kollia, Panagoula, Hunt, Steven C, Langdahl, Bente Lomholt, Leslie, William D, Lips, Paul, Ljunggren, Östen, Lorenc, Roman S, Marc, Janja, Mellström, Dan, Obermayer-Pietsch, Barbara, Olmos, José M, Pettersson-Kymmer, Ulrika, Isaacs, Aaron, Reid, David M, Riancho, José A, Ridker, Paul M, Rousseau, François, Slagboom, P Eline, Tang, Nelson L S, Urreizti, Roser, Van Hul, Wim, Viikari, Jorma, Zarrabeitia, María T, Wu, 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Olivier, Mychaleckyj, Josyf C, Gräßler, Jürgen, Grewal, Jagvir, Curhan, Gary, Hallan, Stein, Shlipak, Michael G, Hallmans, Goran, Kao, W. H. 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Haessler, J., Kocarnik, J., Lin, Y., Jackson, R., Duggan, D., Kuller, L., Stolk, L., He, C., Sulem, P., Barbalic, M., Broer, L., Byrne, EM., Gudbjartsson, DF., McArdle, PF., Porcu, E., van Wingerden, S., Zhuang, W., Albrecht, E., Alizadeh, BZ., Lauc, LB., Broekmans, FJ., Burri, A., Chanock, SJ., Chen, C., Corre, T., Coviello, AD., d'Adamo, P., Davies, G., Deary, IJ., Ebrahim, S., Fauser, BC., Ferreli, L., Folsom, AR., Garcia, ME., Hall, P., Haller, T., Hankinson, SE., Hass, M., Heath, AC., Janssens, AC., Keyzer, J., Lahti, J., Lai, S., Laisk, T., Laven, JS., Liu, J., Lopez, LM., Louwers, YV., Marongiu, M., Klaric, IM., Masciullo, C., McKnight, B., Medland, SE., Melzer, D., Newman, AB., Paré, G., Peeters, PH., Plump, AS., Pop, VJ., Räikkönen, K., Salumets, A., Smith, JA., Stacey, SN., Starr, JM., Stathopoulou, MG., Tenesa, A., Thorand, B., Tryggvadottir, L., Tsui, K., van Dam RM., van Gils CH., van Nierop, P., Vink, JM., Voorhuis, M., Wallaschofski, H., Widen, E., Wijnands-van Gent CJ., Zgaga, L., Zygmunt, M., Arnold, AM., Buring, JE., Crisponi, L., Demerath, EW., Hunter, DJ., Schlessinger, D., Murray, A., Murabito, JM., Visser, JA., Lunetta, KL., Elks, CE., Cousminer, DL., Feenstra, B., Lin, P., van Wingerden SW., Smith, EN., Warrington, NM., Alavere, H., Barroso, I., Berenson, GS., Blackburn, H., Busonero, F., Chen, W., Couper, D., Easton, DF., Foroud, T., Geller, F., Hernandez, DG., Kilpeläinen, TO., Li, S., Melbye, M., Murray, JC., Murray, SS., Nelis, M., Ness, AR., Northstone, K., Pennell, CE., Pharoah, P., Rafnar, T., Rice, JP., Ring, SM., Schork, NJ., Segrè, AV., Sovio, U., Srinivasan, SR., Tammesoo, ML., Tyrer, J., Weedon, MN., Wichmann, H., Young, L., Zhuang, WV., Bierut, LJ., Boyd, HA., Department of Clinical Sciences, Lund University [Lund], Genetic Epidemiology and Clinical Research Group, Umea University Hospital, Department of Odontology, Umeå University, Signalisation et Transports Ioniques Membranaires (STIM), Université de Poitiers-Université de Tours (UT)-Centre National de la Recherche Scientifique (CNRS), Department of Medical Sciences, Center for Biological Sequence Analysis [Lyngby], Danmarks Tekniske Universitet = Technical University of Denmark (DTU), Laboratory of Image Science and Technology [Nanjing] (LIST), Southeast University [Jiangsu]-School of Computer Science and Engineering, Limnology, Ecology, Estonian Genome and Medicine, University of Tartu, Institute of Molecular and Cell Biology, Department of Medical Epidemiology and Biostatistics (MEB), Karolinska Institutet [Stockholm], Department of Medical Genetics, Université de Lausanne = University of Lausanne (UNIL), Institute of Medical Informatics, Biometry and Epidemiology, Universität Duisburg-Essen = University of Duisburg-Essen [Essen], Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Genetic Epidemiology Unit, Erasmus University Medical Center [Rotterdam] (Erasmus MC), Space Sciences Laboratory [Berkeley] (SSL), University of California [Berkeley] (UC Berkeley), University of California (UC)-University of California (UC), Department of Biostatistics and Center for Statistical Genetics, University of Michigan [Ann Arbor], University of Michigan System-University of Michigan System, Division of Statistical Genomics, Washington University School of Medicine, King‘s College London, Department of Medicine, University of Eastern Finland-Kuopio University Hospital, Molecular Genetics Section, University of Groningen [Groningen]-University Medical Centre Groningen, Metabolic functional (epi)genomics and molecular mechanisms involved in type 2 diabetes and related diseases - UMR 8199 - UMR 1283 (EGENODIA (GI3M)), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre National de la Recherche Scientifique (CNRS), Geriatric Rehabilitation Unit, Azienda Sanitaria Firenze, Department of Pharmacy Sciences, Creighton University Medical Center, Medical Department III, Universität Leipzig, Foie, métabolismes et cancer, Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Department of Epidemiology, Erasmus Medical Centre, Netherlands Genomics Initiative (NGI), Netherlands Genomics Initiative, Institute of Epidemiology [Neuherberg] (EPI), German Research Center for Environmental Health - Helmholtz Center München (GmbH), Department of Public Health and Clinical Medicine, Medstar Research Institute, Genetics and Pathology, Finnish Institute of Occupational Health, Epidemiology, University Medical Centre Groningen, Departments of Microbiology & Molecular Genetics and Molecular Biology & Biochemistry, University of California [Irvine] (UC Irvine), Department of Odontology, Cariology, Institute of Human Genetics, Helmholtz Zentrum München = German Research Center for Environmental Health, Génétique des maladies multifactorielles (GMM), Université de Lille, Droit et Santé-Centre National de la Recherche Scientifique (CNRS), Division of Cardiology, Geneva University Hospital (HUG), Department of Psychiatry and Psychotherapy, Rheinische Friedrich-Wilhelms-Universität Bonn, Department of Physics, Indian Institute of Technology Kanpur (IIT Kanpur), University of North Carolina [Chapel Hill] (UNC), University of North Carolina System (UNC)-University of North Carolina System (UNC), Department of Genomics, Life and Brain Center, Universität Bonn = University of Bonn, Anaesthesia and Intensive care, Royal Aberdeen Childrens Hospital, UCL Institute of neurology, UCL Institute of Neurology, Human Genetics, The Wellcome Trust Sanger Institute [Cambridge], Departments of Epidemiology and Nutrition, Harvard School of Public Health, Institute of Experimental Medicine, Czech Academy of Sciences [Prague] (CAS), Department of Medical Sciences and Uppsala Clinical Research Center, Uppsala University Hospital, Department of Genetics, University of Groningen [Groningen], deCODE Genetics, deCODE genetics [Reykjavik], Pediatric Pulmonology, Allergology & Epidemiology, University of Groningen [Groningen]-University Medical Center Groningen [Groningen] (UMCG)-Beatrix Children's Hospital-Groningen Research Institute for Asthma and COPD, Department of Nutrition-Dietetics, Harokopio University of Athens, Yale School of Medicine [New Haven, Connecticut] (YSM), National Heart and Lung Institute (NHLI), Imperial College London, Queensland Institute of Medical Research, Concord Hospital, Epidémiologie des maladies chroniques : impact des interactions gène environnement sur la santé des populations, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé, Dept. Atherosclerose, Kidney Center, University Medical Center Groningen [Groningen] (UMCG), Department of Public Health & Primary Care, University of Cambridge [UK] (CAM), Department of cardiology, The Wellcome Trust Centre for Human Genetics [Oxford], University of Oxford, Department of Internal Medicine, University of Pisa - Università di Pisa, MRC Epidemiology Unit, University of Cambridge [UK] (CAM)-Institute of Metabolic Science, Health Sciences Research Institute, Warwick, Department of Nephrology, University Medical Center, University of Groningen, Institute of Genetic Epidemiology, Icelandic Heart Association, Heart Preventive Clinic and Research Institute, University of Iceland [Reykjavik], Executive Board, Polycystic Kidney Disease Charity (PKD Charity)-Ciliopathy Alliance-International Alliance, Department of Zoology, University of Otago [Dunedin, Nouvelle-Zélande], Institute for Community Medicine, Department Epidemiology of Health Care and Community Health, Universität Greifswald - University of Greifswald, Interfaculty Institute for Genetics and Functional Genomics, 5 University Street, Centre for Paediatric Epidemiology and Biostatistics, University College of London [London] (UCL), MRC Centre for Epidemiology of Child Health, UCL Institute of Child Health, Unit for Molecular Epidemiology, Institute of Health Sciences and Biocenter Oulu, University of Oulu, Department of Epidemiology and Biostatistics, Department of Life Course and Services, National Institute for Health and Welfare [Helsinki], Department of Epidemiology and Public Health, Queen's University [Belfast] (QUB), Interdisciplinary Center of Clinical Research, Department of Physiology, University of Eastern Finland-Institute of Biomedicine, University of Hawai‘i [Mānoa] (UHM), Department of Clinical Chemistry, University of Tampere [Finland]-Tampere University Hospital, Chronic Disease Epidemiology and Prevention Unit, Université Laval [Québec] (ULaval), Centre for Bone and Arthritis Research, University of Gothenburg (GU)-Institute of Medicine, Interdisciplinary Center for Psychiatric Epidemiology, Medical Research Council Epidemiology Unit, Institute of Metabolic Science, Addenbrooke's Hospital, The Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Department of Clinical Physiology, Turku University Hospital (TYKS), Brigham and Women's Hospital [Boston], Department of Chronic Disease Prevention, Department of Cardiovascular Sciences [Leicester], University of Leicester, Leicester NIHR Biomedical Research Unit in Cardiovascular Disease, Maastricht University [Maastricht], Institute of Social and Preventive Medicine, Lausanne University Hospital, Carl Gustav Carus University Hospital, Recherches en Psychopathologie, nouveaux symptômes et lien social (EA 4050), Université de Poitiers-Université de Brest (UBO)-Université Catholique de l'Ouest (UCO)-Université de Rennes 2 (UR2), Institut de biologie de Lille - UMS 3702 (IBL), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Université de Lille-Centre National de la Recherche Scientifique (CNRS), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), HELIOS Klinikum Stralsund Hanseatic-Greifswald University Hospital, Department of child and adolescent psychiatry, Institute for Medical Informatics, Biometry, and Epidemiology, MRC National Survey of Health and Development, MRC Unit for Lifelong Health and Ageing, Clinical Institute of Medical and Chemical Laboratory Diagnostics, Karl-Franzens-Universität Graz, Peter MacCallum Cancer Center, Institute for Molecular Medicine Finland [Helsinki] (FIMM), Helsinki Institute of Life Science (HiLIFE), Helsingin yliopisto = Helsingfors universitet = University of Helsinki-Helsingin yliopisto = Helsingfors universitet = University of Helsinki, Unit of Genetic Epidemiology and Bioinformatics, Department of Epidemiology, University Medical Center Groningen, Department of Pediatrics, Augusta University - Medical College of Georgia, University System of Georgia (USG)-University System of Georgia (USG), Department of Public Health, South Ostrobothnia Central Hospital, Department of Clinical and Preventive Medicine, Danube-University Krems, Netherlands Consortium for Healthy Aging [Leiden, Netherlands] (NCHA), Institute of Public Health and Clinical Nutrition, University of Eastern Finland, MRC epidemiology Unit, Institute of Epidemiology, Clinical Genetics Branch, Division of Cancer Epidemiology & Genetics, National Institutes of Health [Bethesda] (NIH)-National Cancer Institute [Bethesda] (NCI-NIH), National Institutes of Health [Bethesda] (NIH), Department of Oncology, Queensland Brain Institute, University of Queensland [Brisbane], Harvard Reproductive Sciences Center and Reproductive Endocrine Unit, Massachusetts General Hospital [Boston], Divisions of Genetics and Endocrinology and Program in Genomics, Boston Children's Hospital, Metabolism Initiative and Program in Medical and Population Genetics, Broad Institute of MIT and Harvard (BROAD INSTITUTE), Harvard Medical School [Boston] (HMS)-Massachusetts Institute of Technology (MIT)-Massachusetts General Hospital [Boston]-Harvard Medical School [Boston] (HMS)-Massachusetts Institute of Technology (MIT)-Massachusetts General Hospital [Boston], University of North Carolina System (UNC)-University of North Carolina System (UNC)-UNC Gillings School of Global Public Health-Carolina Center for Genome Sciences, Metabolic Disease Group, University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Department of Epidemiology and Preventive Medicine, Regensburg University Medical Center, Epidemiology Unit, Addenbrooke's Hospital-Medical Research Council (MRC), Framingham Heart Study, Boston University [Boston] (BU)-National Heart, Lung, and Blood Institute [Bethesda] (NHLBI), Endocrinology and Metabolism, The Churchill Hospital-Oxford Centre for Diabetes, Landsteiner Laboratory, Clinical Haematology, Other departments, ACS - Amsterdam Cardiovascular Sciences, Vascular Medicine, Lund University Diabetes Centre-Lund University [Lund], Université de Tours-Centre National de la Recherche Scientifique (CNRS)-Université de Poitiers, Technical University of Denmark [Lyngby] (DTU), Université de Lausanne (UNIL), Universität Duisburg-Essen [Essen], Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), University of California [Berkeley], University of California-University of California, Génomique Intégrative et Modélisation des Maladies Métaboliques (EGID), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Universität Leipzig [Leipzig], Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), University of California [Irvine] (UCI), German Research Center for Environmental Health, University of Bonn, Czech Academy of Sciences [Prague] (ASCR), Yale University School of Medicine, University of Oxford [Oxford], German Research Center for Environmental Health-Helmholtz-Zentrum München (HZM), Laval University, Laval University [Québec], Turku University Hospital, Lausanne university hospital, Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), Institut de biologie de Lille - IBL (IBLI), Université de Lille, Sciences et Technologies-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Université de Lille, Droit et Santé-Centre National de la Recherche Scientifique (CNRS), University of Helsinki-University of Helsinki, Helmholtz-Zentrum München (HZM), National Heart, Lung, and Blood Institute [Bethesda] (NHLBI)-Boston University [Boston] (BU), Internal Medicine, Child and Adolescent Psychiatry / Psychology, Clinical Genetics, Medical Informatics, Obstetrics & Gynecology, Lund University [Lund]-Lund University Diabetes Centre, Metabolic functional (epi)genomics and molecular mechanisms involved in type 2 diabetes and related diseases - UMR 8199 - UMR 1283 (GI3M), Institute of Medicine-University of Gothenburg (GU), Signalisation et Transports Ioniques Membranaires ( STIM ), Université de Poitiers-Centre National de la Recherche Scientifique ( CNRS ), Technical University of Denmark [Lyngby] ( DTU ), Laboratory of Image Science and Technology [Nanjing] ( LIST ), Department of Medical Epidemiology and Biostatistics ( MEB ), University of Lausanne, Centre d'Immunologie de Marseille - Luminy ( CIML ), Aix Marseille Université ( AMU ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Erasmus MC, Space Sciences Laboratory [Berkeley] ( SSL ), Génomique Intégrative et Modélisation des Maladies Métaboliques ( EGID ), Université de Lille-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Institut Pasteur de Lille, Réseau International des Instituts Pasteur ( RIIP ) -Réseau International des Instituts Pasteur ( RIIP ) -Centre National de la Recherche Scientifique ( CNRS ) -Centre Hospitalier Régional Universitaire [Lille] ( CHRU Lille ), University of Leipzig, Université de Rennes 1 ( UR1 ), Université de Rennes ( UNIV-RENNES ) -Université de Rennes ( UNIV-RENNES ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Institute of Epidemiology [Neuherberg] ( EPI ), University of California [Irvine] ( UCI ), Génétique des maladies multifactorielles ( GMM ), Université de Lille, Droit et Santé-Centre National de la Recherche Scientifique ( CNRS ), Geneva University Hospital ( HUG ), Bonn Universität [Bonn], Indian Institute of Technology Kanpur ( IIT Kanpur ), The University of North Carolina at Chapel Hill, Université de Bonn, Wellcome Trust Sanger Institute, Harvard University School of Public Health, Czech Academy of Sciences [Prague] ( ASCR ), deCODE genetics, University of Groningen [Groningen]-University Medical Center Groningen-Beatrix Children's Hospital-Groningen Research Institute for Asthma and COPD, Yale School of Medicine, National Heart and Lung Institute ( NHLI ), Réseau International des Instituts Pasteur ( RIIP ) -Réseau International des Instituts Pasteur ( RIIP ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université de Lille, Droit et Santé, University Medical Center Groningen, University of Cambridge [UK] ( CAM ), Wellcome Trust Centre for Human Genetics, University of Pisa [Pisa], University of Cambridge [UK] ( CAM ) -Institute of Metabolic Science, German Research Center for Environmental Health-Helmholtz-Zentrum München ( HZM ), University of Otago, University of Greifswald, University College of London [London] ( UCL ), National Institute for Health and Welfare, Queen's University [Belfast] ( QUB ), University of Hawaii at Manoa ( UHM ), University of Gothenburg ( GU ) -Institute of Medicine, Recherches en Psychopathologie, nouveaux symptômes et lien social ( EA 4050 ), Université de Poitiers-Université de Brest ( UBO ) -Université Catholique de l'Ouest-Université de Rennes 2 ( UR2 ), Université de Rennes ( UNIV-RENNES ) -Université de Rennes ( UNIV-RENNES ), Institut de biologie de Lille - IBL ( IBLI ), Réseau International des Instituts Pasteur ( RIIP ) -Réseau International des Instituts Pasteur ( RIIP ) -Université de Lille, Droit et Santé-Centre National de la Recherche Scientifique ( CNRS ), Institut Cochin ( UM3 (UMR 8104 / U1016) ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), University Medicine Greifswald,-HELIOS Hospital Stralsund, Finland Institute for Molecular Medicine ( FIMM ), Georgia Prevention Institute, Netherlands Consortium for Healthy Aging, Helmholtz-Zentrum München ( HZM ), National Institutes of Health ( NIH ) -National Cancer Institute ( NIH ), Massachusetts General Hospital, Children's Hospital, Boston, Broad Institute, Cambridge, MA, The University of North Carolina at Chapel Hill-UNC Gillings School of Global Public Health-Carolina Center for Genome Sciences, Shungin D, Winkler TW, Adipogen, Consortium, Cardiogramplusc4d, Consortium, Ckdgen, Consortium, Gefos, Consortium, Genie, Consortium, Glgc, Icbp, International, Endogene Consortium, Lifelines, Cohort Study, Magic, Investigator, Muther, Consortium, Consortium, Page, ReproGen Consortium, Amouyel P, D'Adamo, ADAMO PIO, Gasparini, Paolo, Shungin, Dmitry, Winkler, Thomas W, Croteau-Chonka, Damien C, Ferreira, Teresa, Hypponen, Elina, Mohlke, Karen L, ADIPOGEN Consortium, Int Endogene Consortium, Lee Kong Chian School of Medicine (LKCMedicine), Epidemiologie, RS: CARIM - R3.02 - Hypertension and target organ damage, Université de Tours-Université de Poitiers-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Biological Psychology, Neuroscience Campus Amsterdam - Neurobiology of Mental Health, EMGO+ - Lifestyle, Overweight and Diabetes, Damage and Repair in Cancer Development and Cancer Treatment (DARE), Guided Treatment in Optimal Selected Cancer Patients (GUTS), Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Life Course Epidemiology (LCE), Cardiovascular Centre (CVC), Groningen Kidney Center (GKC), Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Groningen Research Institute for Asthma and COPD (GRIAC), Groningen Institute for Organ Transplantation (GIOT), Lifestyle Medicine (LM), Center for Liver, Digestive and Metabolic Diseases (CLDM), Stem Cell Aging Leukemia and Lymphoma (SALL), Shungin, D, Winkler, T, Croteau Chonka, D, Ferreira, T, Locke, A, Mägi, R, Strawbridge, R, Pers, T, Fischer, K, Justice, A, Workalemahu, T, Wu, J, Buchkovich, M, Heard Costa, N, Roman, T, Drong, A, Song, C, Gustafsson, S, Day, F, Esko, T, Fall, T, Kutalik, Z, Luan, J, Randall, J, Scherag, A, Vedantam, S, Wood, A, Chen, J, Fehrmann, R, Karjalainen, J, Kahali, B, Liu, C, Schmidt, E, Absher, D, Amin, N, Anderson, D, Beekman, M, Bragg Gresham, J, Buyske, S, Demirkan, A, Ehret, G, Feitosa, M, Goel, A, Jackson, A, Johnson, T, Kleber, M, Kristiansson, K, Mangino, M, Leach, I, Medina Gomez, C, Palmer, C, Pasko, D, Pechlivanis, S, Peters, M, Prokopenko, I, Stanca'Kova', A, Sung, Y, Tanaka, T, Teumer, A, Van Vliet Ostaptchouk, J, Yengo, L, Zhang, W, Albrecht, E, Ärnlöv, J, Arscott, G, Bandinelli, S, Barrett, A, Bellis, C, Bennett, A, Berne, C, Blüher, M, Böhringer, S, Bonnet, F, Böttcher, Y, Bruinenberg, M, Carba, D, Caspersen, I, Clarke, R, Daw, E, Deelen, J, Deelman, E, Delgado, G, Doney, A, Eklund, N, Erdos, M, Estrada, K, Eury, E, Friedrich, N, Garcia, M, Giedraitis, V, Gigante, B, Go, A, Golay, A, Grallert, H, Grammer, T, Gräsler, J, Grewal, J, Groves, C, Haller, T, Hallmans, G, Hartman, C, Hassinen, M, Hayward, C, Heikkilä, K, Herzig, K, Helmer, Q, Hillege, H, Holmen, O, Hunt, S, Isaacs, A, Ittermann, T, James, A, Johansson, I, Juliusdottir, T, Kalafati, I, Kinnunen, L, Koenig, W, Kooner, I, Kratzer, W, Lamina, C, Leander, K, Lee, N, Lichtner, P, Lind, L, Lindström, J, Lobbens, S, Lorentzon, M, Mach, F, Magnusson, P, Mahajan, A, Mcardle, W, Menni, C, Merger, S, Mihailov, E, Milani, L, Mills, R, Moayyeri, A, Monda, K, Mooijaart, S, Mühleisen, T, Mulas, A, Müller, G, Müller Nurasyid, M, Nagaraja, R, Nalls, M, Narisu, N, Glorioso, N, Nolte, I, Olden, M, Rayner, N, Renstrom, F, Ried, J, Robertson, N, Rose, L, Sanna, S, Scharnagl, H, Scholtens, S, Sennblad, B, Seufferlein, T, Sitlani, C, Smith, A, Stirrups, K, Stringham, H, Sundström, J, Swertz, M, Swift, A, Syvänen, A, Tayo, B, Thorand, B, Thorleifsson, G, Tomaschitz, A, Troffa, C, Van Oort, F, Verweij, N, Vonk, J, Waite, L, Wennauer, R, Wilsgaard, T, Wojczynski, M, Wong, A, Zhang, Q, Zhao, J, Brennan, E, Choi, M, Eriksson, P, Folkersen, L, Franco Cereceda, A, Gharavi, A, Hedman, A, Hivert, M, Huang, J, Kanoni, S, Karpe, F, Keildson, S, Kiryluk, K, Liang, L, Lifton, R, Ma, B, Mcknight, A, Mcpherson, R, Metspalu, A, Min, J, Moffatt, M, Montgomery, G, Murabito, J, Nicholson, G, Nyholt, D, Olsson, C, Perry, J, Reinmaa, E, Salem, R, Sandholm, N, Schadt, E, Scott, R, Stolk, L, Vallejo, E, Westra, H, Zondervan, K, Amouyel, P, Arveiler, D, Bakker, S, Beilby, J, Bergman, R, Blangero, J, Brown, M, Burnier, M, Campbell, H, Chakravarti, A, Chines, P, Claudi Boehm, S, Collins, F, Crawford, D, Danesh, J, De Faire, U, De Geus, E, Dörr, M, Erbel, R, Eriksson, J, Farrall, M, Ferrannini, E, Ferrières, J, Forouhi, N, Forrester, T, Franco, O, Gansevoort, R, Gieger, C, Gudnason, V, Haiman, C, Harris, T, Hattersley, A, Heliövaara, M, Hicks, A, Hingorani, A, Hoffmann, W, Hofman, A, Homuth, G, Humphries, S, Hyppönen, E, Illig, T, Jarvelin, M, Johansen, B, Jousilahti, P, Jula, A, Kaprio, J, Kee, F, Keinanen Kiukaanniemi, S, Kooner, J, Kooperberg, C, Kovacs, P, Kraja, A, Kumari, M, Kuulasmaa, K, Kuusisto, J, Lakka, T, Langenberg, C, Le Marchand, L, Lehtimäki, T, Lyssenko, V, Männistö, S, Marette, A, Matise, T, Mckenzie, C, Mcknight, B, Musk, A, Möhlenkamp, S, Morris, A, Nelis, M, Ohlsson, C, Oldehinkel, A, Ong, K, Palmer, L, Penninx, B, Peters, A, Pramstaller, P, Raitakari, O, Rankinen, T, Rao, D, Rice, T, Ridker, P, Ritchie, M, Rudan, I, Salomaa, V, Samani, N, Saramies, J, Sarzynski, M, Schwarz, P, Shuldiner, A, Staessen, J, Steinthorsdottir, V, Stolk, R, Strauch, K, Tönjes, A, Tremblay, A, Tremoli, E, Vohl, M, Völker, U, Vollenweider, P, Wilson, J, Witteman, J, Adair, L, Bochud, M, Boehm, B, Bornstein, S, Bouchard, C, Cauchi, S, Caulfield, M, Chambers, J, Chasman, D, Cooper, R, Dedoussis, G, Ferrucci, L, Froguel, P, Grabe, H, Hamsten, A, Hui, J, Hveem, K, Jöckel, K, Kivimaki, M, Kuh, D, Laakso, M, Liu, Y, März, W, Munroe, P, Njolstad, I, Oostra, B, Pedersen, N, Perola, M, Pe'Russe, L, Peters, U, Power, C, Quertermous, T, Rauramaa, R, Rivadeneira, F, Saaristo, T, Saleheen, D, Sinisalo, J, Slagboom, P, Snieder, H, Spector, T, Thorsteinsdottir, U, Stumvoll, M, Tuomilehto, J, Uitterlinden, A, Uusitupa, M, Van Der Harst, P, Veronesi, G, Walker, M, Wareham, N, Watkins, H, Wichmann, H, Abecasis, G, Assimes, T, Berndt, S, Boehnke, M, Borecki, I, Deloukas, P, Franke, L, Frayling, T, Groop, L, Hunter, D, Kaplan, R, O'Connell, J, Qi, L, Schlessinger, D, Strachan, D, Stefansson, K, Van Duijn, C, Willer, C, Visscher, P, Yang, J, Hirschhorn, J, Zillikens, M, Mccarthy, M, Speliotes, E, North, K, Fox, C, Barroso, I, Franks, P, Ingelsson, E, Heid, I, Loos, R, Cupples, L, Lindgren, C, Mohlke, K, Dastani, Z, Timpson, N, Yuan, X, Henneman, P, Kizer, J, Lyytikainen, L, Fuchsberger, C, Small, K, Coassin, S, Lohman, K, Pankow, J, Uh, H, Wu, Y, Bidulescu, A, Rasmussen Torvik, L, Greenwood, C, Ladouceur, M, Grimsby, J, Manning, A, Mooser, V, Kapur, K, Frants, R, Willemsvan vanDijk, K, Willems, S, Psaty, B, Tracy, R, Brody, J, Chen, I, Viikari, J, Kähönen, M, Evans, D, St Pourcain, B, Sattar, N, Carlson, O, Egan, J, van Heemst, D, Kedenko, L, Nuotio, M, Loo, B, Kanaya, A, Haun, M, Klopp, N, Katsareli, E, Couper, D, Duncan, B, Kloppenburg, M, Borja, J, Musani, S, Guo, X, Semple, R, Teslovich, T, Allison, M, Redline, S, Buxbaum, S, Meulenbelt, I, Ballantyne, C, Hu, F, Paulweber, B, Florez, J, Smith, G, Siscovick, D, Kronenberg, F, van Duijn, C, Waterworth, D, Meigs, J, Dupuis, J, Richards, J, Willenborg, C, Thompson, J, Erdmann, J, Goldstein, B, König, I, Cazier, J, Johansson, Å, Hall, A, Lee, J, Grundberg, E, Havulinna, A, Ho, W, Hopewell, J, Eriksson, N, Lundmark, P, Lyytikäinen, L, Rafelt, S, Tikkanen, E, Van Zuydam, N, Voight, B, Ziegler, A, Altshuler, D, Balmforth, A, Braund, P, Burgdorf, C, Cox, D, Dimitriou, M, Do, R, El Mokhtari, N, Fontanillas, P, Hager, J, Han, B, Kang, H, Kessler, T, Knowles, J, Kolovou, G, Langford, C, Lokki, M, Lundmark, A, Meisinger, C, Melander, O, Maouche, S, Nikus, K, Peden, J, Rasheed, A, Rosinger, S, Rubin, D, Rumpf, M, Schäfer, A, Sivananthan, M, Stewart, A, Tan, S, Thorgeirsson, G, van der Schoot, C, Wagner, P, Wells, G, Wild, P, Yang, T, Basart, H, Boerwinkle, E, Brambilla, P, Cambien, F, Cupples, A, de Faire, U, Dehghan, A, Diemert, P, Epstein, S, Evans, A, Ferrario, M, Gauguier, D, Goodall, A, Hazen, S, Holm, H, Iribarren, C, Jang, Y, Kim, H, Laaksonen, R, Ouwehand, W, Parish, S, Park, J, Rader, D, Shah, S, Stark, K, Trégouët, D, Virtamo, J, Wallentin, L, Zimmermann, M, Nieminen, M, Hengstenberg, C, Sandhu, M, Pastinen, T, Hovingh, G, Zalloua, P, Siegbahn, A, Schreiber, S, Ripatti, S, Blankenberg, S, O'Donnell, C, Reilly, M, Collins, R, Kathiresan, S, Roberts, R, Schunkert, H, Pattaro, C, Köttgen, A, Garnaas, M, Böger, C, Chen, M, Tin, A, Taliun, D, Li, M, Gao, X, Gorski, M, Yang, Q, Hundertmark, C, Foster, M, O'Seaghdha, C, Glazer, N, Struchalin, M, Li, G, Johnson, A, Gierman, H, Hwang, S, Atkinson, E, Cornelis, M, Chouraki, V, Holliday, E, Sorice, R, Deshmukh, H, Ulivi, S, Chu, A, Murgia, F, Trompet, S, Imboden, M, Kollerits, B, Pistis, G, Launer, L, Aspelund, T, Eiriksdottir, G, Mitchell, B, Schmidt, H, Cavalieri, M, Rao, M, de Andrade, M, Turner, S, Ding, J, Andrews, J, Freedman, B, Döring, A, Kolcic, I, Zemunik, T, Boban, M, Minelli, C, Wheeler, H, Igl, W, Zaboli, G, Wild, S, Wright, A, Ellinghaus, D, Nöthlings, U, Jacobs, G, Biffar, R, Endlich, K, Ernst, F, Kroemer, H, Nauck, M, Stracke, S, Völzke, H, Aulchenko, Y, Polasek, O, Hastie, N, Vitart, V, Helmer, C, Wang, J, Ruggiero, D, Bergmann, S, Nikopensius, T, Province, M, Ketkar, S, Colhoun, H, Robino, A, Giulianini, F, Krämer, B, Portas, L, Ford, I, Buckley, B, Adam, M, Thun, G, Sala, C, Metzger, M, Mitchell, P, Ciullo, M, Kim, S, Gasparini, P, Pirastu, M, Jukema, J, Probst Hensch, N, Toniolo, D, Coresh, J, Schmidt, R, Kardia, S, Curhan, G, Gyllensten, U, Franke, A, Rettig, R, Parsa, A, Goessling, W, Kao, W, de Boer, I, Peralta, C, Akylbekova, E, Kramer, H, van der Harst, P, Arking, D, Franceschini, N, Hernandez, D, Townsend, R, Lumley, T, Kestenbaum, B, Haritunians, T, Waeber, G, Lu, X, Leak, T, Aasarød, K, Skorpen, F, Baumert, J, Devuyst, O, Mychaleckyj, J, Hallan, S, Navis, G, Shlipak, M, Bull, S, Paterson, A, Rotter, J, Beckmann, J, Dreisbach, A, Styrkarsdottir, U, Evangelou, E, Hsu, Y, Duncan, E, Ntzani, E, Oei, L, Albagha, O, Kemp, J, Koller, D, Minster, R, Vandenput, L, Willner, D, Xiao, S, Yerges Armstrong, L, Zheng, H, Alonso, N, Kammerer, C, Kaptoge, S, Leo, P, Wilson, S, Aalto, V, Alen, M, Aragaki, A, Center, J, Dailiana, Z, Duggan, D, Garcia Giralt, N, Giroux, S, Hocking, L, Husted, L, Jameson, K, Khusainova, R, Kim, G, Koromila, T, Kruk, M, Laaksonen, M, Lacroix, A, Lee, S, Leung, P, Lewis, J, Masi, L, Mencej Bedrac, S, Nguyen, T, Nogues, X, Patel, M, Prezelj, J, Scollen, S, Siggeirsdottir, K, Svensson, O, Trummer, O, van Schoor, N, Woo, J, Zhu, K, Balcells, S, Brandi, M, Cheng, S, Christiansen, C, Cooper, C, Frost, M, Goltzman, D, González Macías, J, Karlsson, M, Khusnutdinova, E, Koh, J, Kollia, P, Langdahl, B, Leslie, W, Lips, P, Ljunggren, Ö, Lorenc, R, Marc, J, Mellström, D, Obermayer Pietsch, B, Olmos, J, 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Kaleebu, P, Kastelein, J, Kim, E, Komulainen, P, Lin, S, Nieminen, T, Nsubuga, R, Olafsson, I, Palotie, A, Papamarkou, T, Pomilla, C, Pouta, A, Ruokonen, A, Seeley, J, Silander, K, Stančáková, A, Tiret, L, van Pelt, L, Wainwright, N, Wijmenga, C, Willemsen, G, Young, E, Bennett, F, Boomsma, D, Bovet, P, Chen, Y, Feranil, A, Freimer, N, Hsiung, C, Järvelin, M, Kesäniemi, A, Koudstaal, P, Krauss, R, Kyvik, K, Martin, N, Meneton, P, Moilanen, L, Njølstad, I, Price, J, Sanghera, D, Sheu, W, Whitfield, J, Wolffenbuttel, B, Ordovas, J, Rich, S, Johnson, L, Larson, M, Levy, D, Newton Cheh, C, O'Reilly, P, Palmas, W, Rice, K, Snider, H, Tobin, M, Verwoert, G, Pihur, V, Heath, S, Sõber, S, Arora, P, Zhang, F, Lucas, G, Milaneschi, Y, Parker, A, Fava, C, Fox, E, Go, M, Sjögren, M, Vinay, D, Alexander, M, Tabara, Y, Shaw Hawkins, S, Whincup, P, Shi, G, Seielstad, M, Sim, X, Nguyen, K, Matullo, G, Gaunt, T, Onland Moret, N, Cooper, M, Platou, C, Org, E, Hardy, R, Dahgam, S, Palmen, J, Kuznetsova, T, Uiterwaal, C, Adeyemo, A, Ludwig, B, Tomaszewski, M, Tzoulaki, I, Palmer, N, Chang, Y, Steinle, N, Grobbee, D, Morrison, A, Najjar, S, Hadley, D, Connell, J, Day, I, Lawlor, D, Lawrence, R, Ongen, H, Li, Y, Young, J, Bis, J, Chaturvedi, N, Islam, M, Jafar, T, Kulkarni, S, Grässler, J, Howard, P, Guarrera, S, Ricceri, F, Emilsson, V, Plump, A, Weder, A, Sun, Y, Scott, L, Peltonen, L, Vartiainen, E, Brand, S, Wang, T, Burton, P, Artigas, M, Dong, Y, Wang, X, Zhu, H, Rudock, M, Heckbert, S, Smith, N, Wiggins, K, Doumatey, A, Shriner, D, Veldre, G, Viigimaa, M, Kinra, S, Prabhakaran, D, Tripathy, V, Langefeld, C, Rosengren, A, Thelle, D, Corsi, A, Singleton, A, Hilton, G, Salako, T, Iwai, N, Kita, Y, Ogihara, T, Ohkubo, T, Okamura, T, Ueshima, H, Umemura, S, Eyheramendy, S, Meitinger, T, Cho, Y, Scott, J, Sehmi, J, Hedblad, B, Nilsson, P, Stanèáková, A, Raffel, L, Yao, J, Schwartz, S, Ikram, M, Longstreth W., J, Mosley, T, Seshadri, S, Shrine, N, Wain, L, Morken, M, Laitinen, J, Zitting, P, Cooper, J, van Gilst, W, Janipalli, C, Mani, K, Yajnik, C, Mattace Raso, F, Lakatta, E, Orru, M, Scuteri, A, Ala Korpela, M, Kangas, A, Soininen, P, Tukiainen, T, Würtz, P, Ong, R, Galan, P, Hercberg, S, Lathrop, M, Zelenika, D, Zhai, G, Meschia, J, Sharma, P, Terzic, J, Kumar, M, Denniff, M, Zukowska Szczechowska, E, Wagenknecht, L, Fowkes, F, Charchar, F, Rotimi, C, Bots, M, Brand, E, Talmud, P, Nyberg, F, Laan, M, van der Schouw, Y, Casas, J, Vineis, P, Ganesh, S, Wong, T, Tai, E, Morris, R, Dominiczak, A, Marmot, M, Miki, T, Chandak, G, Zhu, X, Elosua, R, Soranzo, N, Sijbrands, E, Uda, M, Vasan, R, Anderson, C, Gordon, S, Guo, Q, Henders, A, Lambert, A, Kraft, P, Kennedy, S, Macgregor, S, Missmer, S, Painter, J, Roseman, F, Treloar, S, Wallace, L, Alizadeh, B, de Boer, R, Boezen, H, van der Klauw, M, Ormel, J, Postma, D, Rosmalen, J, Slaets, J, Lagou, V, Welch, R, Wheeler, E, Rehnberg, E, Lecoeur, C, Johnson, P, Hottenga, J, Salo, P, Bielak, L, Zhao, W, Horikoshi, M, Navarro, P, Chen, H, Rybin, D, Song, K, An, P, Marullo, L, Jansen, H, Edkins, S, Varga, T, Oksa, H, Antonella, M, Kong, A, Herder, C, Antti, J, Miljkovic, I, Atalay, M, Kiess, W, Smit, J, Campbell, S, Fowkes, G, Rathmann, W, Maerz, W, Watanabe, R, de Geus, E, Toenjes, A, Peyser, P, Körner, A, Cucca, F, Balkau, B, Bouatia Naji, N, Ahmadi, K, Ainali, C, Bataille, V, Bell, J, Buil, A, Dermitzakis, E, Dimas, A, Durbin, R, Glass, D, Hassanali, N, Hedman, Å, Ingle, C, Knowles, D, Krestyaninova, M, Lowe, C, Meduri, E, di Meglio, P, Montgomery, S, Nestle, F, Nica, A, Nisbet, J, O'Rahilly, S, Parts, L, Potter, S, Sekowska, M, Shin, S, Surdulescu, G, Travers, M, Tsaprouni, L, Tsoka, S, Wilk, A, Higashio, J, Williams, R, Nato, A, Ambite, J, Manolio, T, Hindorff, L, Heiss, G, Taylor, K, Avery, C, Graff, M, Lin, D, Quibrera, M, Cochran, B, Kao, L, Umans, J, Cole, S, Maccluer, J, Person, S, Gross, M, Fornage, M, Durda, P, Jenny, N, Patsy, B, Arnold, A, Buzkova, P, Haines, J, Murdock, D, Glenn, K, 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Smith, J, Stacey, S, Starr, J, Stathopoulou, M, Tenesa, A, Tryggvadottir, L, Tsui, K, van Dam, R, van Gils, C, van Nierop, P, Vink, J, Voorhuis, M, Wallaschofski, H, Widen, E, Wijnands van Gent, C, Zgaga, L, Zygmunt, M, Buring, J, Crisponi, L, Demerath, E, Murray, A, Visser, J, Lunetta, K, Elks, C, Cousminer, D, Feenstra, B, Lin, P, Smith, E, Warrington, N, Alavere, H, Berenson, G, Blackburn, H, Busonero, F, Chen, W, Easton, D, Foroud, T, Geller, F, Kilpeläinen, T, Li, S, Melbye, M, Murray, J, Murray, S, Ness, A, Northstone, K, Pennell, C, Pharoah, P, Rafnar, T, Rice, J, Ring, S, Schork, N, Segrè, A, Sovio, U, Srinivasan, S, Tammesoo, M, Tyrer, J, Weedon, M, Young, L, Bierut, L, Boyd, H, Psychiatry, NCA - Neurobiology of mental health, and EMGO - Lifestyle, overweight and diabetes
Subjects: Adipose Tissue/metabolism, Male, genetic association, subcutaneous fat, Transcription, Genetic, Adipocytes, Adipogenesis, Adipose Tissue, Age Factors, Body Mass Index, Continental Population Groups, Epigenesis, Genetic, Europe, Female, Genome, Human, Humans, Insulin, Insulin Resistance, Models, Biological, Neovascularization, Physiologic, Obesity, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Sex Characteristics, Waist-Hip Ratio, Body Fat Distribution, Genome-Wide Association Study, Multidisciplinary, Insulin Resistance/genetics, Genome-wide association study, Continental Population Groups/genetics, genetic analysis, heritability, gene cluster, Science::Biological sciences::Human anatomy and physiology [DRNTU], 0302 clinical medicine, high density lipoprotein cholesterol, Models, genetics [Insulin Resistance], histone modification, Age Factor, insulin receptor, 0303 health sciences, Adipocyte, Human/genetics, CARDIOGRAMplusC4D Consortium, ADIPOGENIC DIFFERENTIATION, genetic correlation, body fat, Continental Population Group, priority journal, 5 trisphosphate 3 phosphatase, GEFOS Consortium, meta analysis (topic), Science & Technology - Other Topics, ddc:500, transcription regulation, Adipogenesis/genetics, Single Nucleotide/genetics, Human, medicine.medical_specialty, Waist, phosphatidylinositol 3, European, ta3111, genetic regulation, Article, developmental biology, 03 medical and health sciences, MAGIC Investigators, transcription initiation site, SDG 3 - Good Health and Well-being, Genetic, genomics, GLYCEMIC TRAITS, genetics [Continental Population Groups], Polymorphism, GENOME-WIDE ASSOCIATION, Physiologic, genetics [Adipogenesis], Adipocytes/metabolism, Europe/ethnology, Genome, Human/genetics, Insulin/metabolism, Neovascularization, Physiologic/genetics, Obesity/genetics, Polymorphism, Single Nucleotide/genetics, Quantitative Trait Loci/genetics, Transcription, Genetic/genetics, Genetic/genetics, Adipogenesi, Science & Technology, adiponectin, [ SDV ] Life Sciences [q-bio], vasculotropin, genetics [Quantitative Trait Loci], ta1184, Racial Groups, ta1182, gene mapping, ta3121, triacylglycerol blood level, medicine.disease, Biological, major clinical study, amino acid sequence, metabolism [Insulin], Endocrinology, metabolism [Adipocytes], genetic loci, insulin, body fat, GLGC, International Endogene Consortium, metabolism [Adipose Tissue], Body mass index, HUMAN HEIGHT, Epigenesis, LifeLines Cohort Study, ReproGen Consortium, BIO/12 - BIOCHIMICA CLINICA E BIOLOGIA MOLECOLARE CLINICA, tissue level, Physiologic/genetics, [SDV]Life Sciences [q-bio], Medizin, Adipose tissue, low density lipoprotein cholesterol, PAGE Consortium, COMMON SNPS, angiogenesis, Waist–hip ratio, genetics [Obesity], MESH: Adipocytes/metabolism Adipogenesis/genetics Adipose Tissue/metabolism* Age Factors Body Fat Distribution* Body Mass Index Continental Population Groups/genetics Epigenesis, Genetic Europe/ethnology Female Genome, Human/genetics Genome-Wide Association Study* Humans Insulin/metabolism* Insulin Resistance/genetics Male Models, Biological Neovascularization, Physiologic/genetics Obesity/genetics Polymorphism, Single Nucleotide/genetics Quantitative Trait Loci/genetics* Sex Characteristics Transcription, Genetic/genetics Waist-Hip Ratio, single nucleotide polymorphism, fat, genetic variability, molecular biology, body mass index (BMI), ethnology [Europe], peroxisome proliferator activated receptor, 2. Zero hunger, Genetics, Genome, Single Nucleotide, waist circumference, insulin, phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase, triacylglycerol, vasculotropin, developmental biology, gene expression, genome, numerical model, adipocyte, adipose tissue, body fat distribution, body mass, female, gene locus, gene structure, hip circumference, human, insulin resistance, lipoprotein blood level, male, obesity, protein protein interaction, sex difference, waist hip ratio, Multidisciplinary Sciences, genetics [Transcription, Genetic], genetics [Polymorphism, Single Nucleotide], ADIPOGen Consortium, genetics [Neovascularization, Physiologic], Transcription, SUSCEPTIBILITY LOCI, General Science & Technology, ICBP, 030209 endocrinology & metabolism, Biology, adipocyte, MESH : Adipocytes/metabolism Adipogenesis/genetics Adipose Tissue/metabolism* Age Factors Body Fat Distribution* Body Mass Index Continental Population Groups/genetics Epigenesis, Genetic Europe/ethnology Female Genome, Human/genetics Genome-Wide Association Study* Humans Insulin/metabolism* Insulin Resistance/genetics Male Models, Biological Neovascularization, Physiologic/genetics Obesity/genetics Polymorphism, Single Nucleotide/genetics Quantitative Trait Loci/genetics* Sex Characteristics Transcription, Genetic/genetics Waist-Hip Ratio, MESENCHYMAL STEM-CELLS, GENIE Consortium, SEXUAL-DIMORPHISM, Insulin resistance, Internal medicine, medicine, genetics [Genome, Human], ABDOMINAL ADIPOSITY, Neovascularization, 030304 developmental biology, FALSE DISCOVERY, CKDGen Consortium, Sex Characteristic, MuTHER Consortium, numerical model
Abstract: Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P
Published: 2015
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119. A common variant at the 14q32 endometrial cancer risk locus activates AKT1 through YY1 binding

Author: Painter, Jodie, Kaufmann, Susanne, O'Mara, Tracy, Hillman, Kristine, Sivakumaran, Haran, Darabi, Hatef, Cheng, Timothy, Pearson, John, Kazakoff, Stephen, Waddell, Nicola, Hoivik, Erling, Goode, Ellen, Scott, Rodney, Tomlinson, Ian, Dunning, Alison, Easton, Douglas, French, Juliet, Salvesen, Helga, Pollock, Pamela, Thompson, Deborah, Spurdle, Amanda, Edwards, Stacey, Painter, Jodie, Kaufmann, Susanne, O'Mara, Tracy, Hillman, Kristine, Sivakumaran, Haran, Darabi, Hatef, Cheng, Timothy, Pearson, John, Kazakoff, Stephen, Waddell, Nicola, Hoivik, Erling, Goode, Ellen, Scott, Rodney, Tomlinson, Ian, Dunning, Alison, Easton, Douglas, French, Juliet, Salvesen, Helga, Pollock, Pamela, Thompson, Deborah, Spurdle, Amanda, and Edwards, Stacey
Abstract: A recent meta-analysis of multiple genome-wide association and follow-up endometrial cancer case-control datasets identified a novel genetic risk locus for this disease at chromosome 14q32.33. To prioritize the functional SNP(s) and target gene(s) at this locus, we employed an in silico fine-mapping approach using genotyped and imputed SNP data for 6,608 endometrial cancer cases and 37,925 controls of European ancestry. Association and functional analyses provide evidence that the best candidate causal SNP is rs2494737. Multiple experimental analyses show that SNP rs2494737 maps to a silencer element located within AKT1, a member of the PI3K/AKT/MTOR intracellular signaling pathway activated in endometrial tumors. The rs2494737 risk A allele creates a YY1 transcription factor-binding site and abrogates the silencer activity in luciferase assays, an effect mimicked by transfection of YY1 siRNA. Our findings suggest YY1 is a positive regulator of AKT1, mediating the stimulatory effects of rs2494737 increasing endometrial cancer risk. Identification of an endometrial cancer risk allele within a member of the PI3K/AKT signaling pathway, more commonly activated in tumors by somatic alterations, raises the possibility that well tolerated inhibitors targeting this pathway could be candidates for evaluation as chemopreventive agents in individuals at high risk of developing endometrial cancer.
Published: 2016

120. Five endometrial cancer risk loci identified through genome-wide association analysis

Author: Cheng, Timothy, Thompson, Deborah, O'Mara, Tracy, Painter, Jodie, Glubb, Dylan, Flach, Susanne, Lewis, Annabelle, French, Juliet, Freeman-Mills, Luke, Church, David, Nyholt, Dale, other, and, Cheng, Timothy, Thompson, Deborah, O'Mara, Tracy, Painter, Jodie, Glubb, Dylan, Flach, Susanne, Lewis, Annabelle, French, Juliet, Freeman-Mills, Luke, Church, David, Nyholt, Dale, and other, and
Abstract: We conducted a meta-analysis of three endometrial cancer genome-wide association studies (GWAS) and two follow-up phases totaling 7,737 endometrial cancer cases and 37,144 controls of European ancestry. Genome-wide imputation and meta-analysis identified five new risk loci of genome-wide significance at likely regulatory regions on chromosomes 13q22.1 (rs11841589, near KLF5), 6q22.31 (rs13328298, in LOC643623 and near HEY2 and NCOA7), 8q24.21 (rs4733613, telomeric to MYC), 15q15.1 (rs937213, in EIF2AK4, near BMF) and 14q32.33 (rs2498796, in AKT1, near SIVA1). We also found a second independent 8q24.21 signal (rs17232730). Functional studies of the 13q22.1 locus showed that rs9600103 (pairwise r2 = 0.98 with rs11841589) is located in a region of active chromatin that interacts with the KLF5 promoter region. The rs9600103[T] allele that is protective in endometrial cancer suppressed gene expression in vitro, suggesting that regulation of the expression of KLF5, a gene linked to uterine development, is implicated in tumorigenesis. These findings provide enhanced insight into the genetic and biological basis of endometrial cancer.
Published: 2016

121. Endometriosis risk alleles at 1p36.12 act through inverse regulation of CDC42 and LINC00339

Author: Powell, Joseph, Fung, Jenny, Shakhbazov, Konstantin, Sapkota, Yadav, Cloonan, Nicole, Hemani, Gibran, Hillman, Kristine, Kaufmann, Susanne, Luong, Hien, Bowdler, Lisa, Painter, Jodie, Holdsworth-Carson, Sarah, Visscher, Peter, Dinger, Marcel, Healey, Martin, Nyholt, Dale, French, Juliet, Edwards, Stacey, Rogers, Peter, Montgomery, Grant, Powell, Joseph, Fung, Jenny, Shakhbazov, Konstantin, Sapkota, Yadav, Cloonan, Nicole, Hemani, Gibran, Hillman, Kristine, Kaufmann, Susanne, Luong, Hien, Bowdler, Lisa, Painter, Jodie, Holdsworth-Carson, Sarah, Visscher, Peter, Dinger, Marcel, Healey, Martin, Nyholt, Dale, French, Juliet, Edwards, Stacey, Rogers, Peter, and Montgomery, Grant
Abstract: Free to read on publishers website Genome-wide association studies (GWAS) have identified markers within the WNT4 region on chromosome 1p36.12 showing consistent and strong association with increasing endometriosis risk. Fine mapping using sequence and imputed genotype data has revealed strong candidates for the causal SNPs within these critical regions; however, the molecular pathogenesis of these SNPs is currently unknown. We used gene expression data collected from whole blood from 862 individuals and endometrial tissue from 136 individuals from independent populations of European descent to examine the mechanism underlying endometriosis susceptibility. Association mapping results from 7,090 individuals (2,594 cases and 4,496 controls) supported rs3820282 as the SNP with the strongest association for endometriosis risk (P = 1.84 x 10-5, OR = 1.244 (1.126-1.375)). SNP rs3820282 is a significant eQTL in whole blood decreasing expression of LINC00339 (also known as HSPC157) and increasing expression of CDC42 (P = 2.0 x10-54 and 4.5x10-4 respectively). The largest effects were for two LINC00339 probes (P = 2.0 x10-54; 1.0 x 10-34). The eQTL for LINC00339 was also observed in endometrial tissue (P = 2.4 x10-8) with the same direction of effect for both whole blood and endometrial tissue. There was no evidence for eQTL effects for WNT4. Chromatin conformation capture provides evidence for risk SNPs interacting with the promoters of both LINC00339 and CDC4 and luciferase reporter assays suggest the risk SNP rs12038474 is located in a transcriptional silencer for CDC42 and the risk allele increases expression of CDC42. However, no effect of rs3820282 was observed in the LINC00339 expression in Ishikawa cells. Taken together, our results suggest that SNPs increasing endometriosis risk in this region act through CDC42, but further functional studies are required to rule out inverse regulation of both LINC00339 and CDC42.
Published: 2016

122. CYP19A1 fine-mapping and Mendelian randomization: estradiol is causal for endometrial cancer

Author: Thompson, Deborah, O'Mara, Tracy, Glubb, Dylan, Painter, Jodie, Cheng, Timothy, Folkerd, Elizabeth, Doody, Deborah, Dennis, Joe, Webb, Penelope, Gorman, Maggie, Nyholt, Dale, other, and, Thompson, Deborah, O'Mara, Tracy, Glubb, Dylan, Painter, Jodie, Cheng, Timothy, Folkerd, Elizabeth, Doody, Deborah, Dennis, Joe, Webb, Penelope, Gorman, Maggie, Nyholt, Dale, and other, and
Abstract: Candidate gene studies have reported CYP19A1 variants to be associated with endometrial cancer and with estradiol (E2) concentrations. We analyzed 2937 single nucleotide polymorphisms (SNPs) in 6608 endometrial cancer cases and 37 925 controls and report the first genome wide-significant association between endometrial cancer and a CYP19A1 SNP (rs727479 in intron 2, P=4.8x10(-11)). SNP rs727479 was also among those most strongly associated with circulating E2 concentrations in 2767 post-menopausal controls (P=7.4x10(-8)). The observed endometrial cancer odds ratio per rs727479 A-allele (1.15, CI=1.11-1.21) is compatible with that predicted by the observed effect on E2 concentrations (1.09, CI=1.03-1.21), consistent with the hypothesis that endometrial cancer risk is driven by E2. From 28 candidate-causal SNPs, 12 co-located with three putative gene-regulatory elements and their risk alleles associated with higher CYP19A1 expression in bioinformatical analyses. For both phenotypes, the associations with rs727479 were stronger among women with a higher BMI (Pinteraction=0.034 and 0.066 respectively), suggesting a biologically plausible gene-environment interaction.
Published: 2016

123. Adult body mass index and risk of ovarian cancer by subtype:a Mendelian randomization study

Author: Dixon, Suzanne C, Nagle, Christina M, Thrift, Aaron P, Pharoah, Paul Dp, Pearce, Celeste Leigh, Zheng, Wei, Painter, Jodie N, Chenevix-Trench, Georgia, Fasching, Peter A, Beckmann, Matthias W, Lambrechts, Diether, Vergote, Ignace, Lambrechts, Sandrina, Van Nieuwenhuysen, Els, Rossing, Mary Anne, Doherty, Jennifer A, Wicklund, Kristine G, Chang-Claude, Jenny, Rudolph, Anja, Moysich, Kirsten B, Odunsi, Kunle, Goodman, Marc T, Wilkens, Lynne R, Thompson, Pamela J, Shvetsov, Yurii B, Dörk, Thilo, Park-Simon, Tjoung-Won, Hillemanns, Peter, Bogdanova, Natalia, Butzow, Ralf, Nevanlinna, Heli, Pelttari, Liisa M, Leminen, Arto, Modugno, Francesmary, Ness, Roberta B, Edwards, Robert P, Kelley, Joseph L, Heitz, Florian, Karlan, Beth Y, Kjær, Susanne Krüger, Høgdall, Estrid Vilma Solyom, Jensen, Allan, Goode, Ellen L, Fridley, Brooke L, Cunningham, Julie M, Winham, Stacey J, Giles, Graham G, Bruinsma, Fiona, Milne, Roger L, Høgdall, Claus Kim, Dixon, Suzanne C, Nagle, Christina M, Thrift, Aaron P, Pharoah, Paul Dp, Pearce, Celeste Leigh, Zheng, Wei, Painter, Jodie N, Chenevix-Trench, Georgia, Fasching, Peter A, Beckmann, Matthias W, Lambrechts, Diether, Vergote, Ignace, Lambrechts, Sandrina, Van Nieuwenhuysen, Els, Rossing, Mary Anne, Doherty, Jennifer A, Wicklund, Kristine G, Chang-Claude, Jenny, Rudolph, Anja, Moysich, Kirsten B, Odunsi, Kunle, Goodman, Marc T, Wilkens, Lynne R, Thompson, Pamela J, Shvetsov, Yurii B, Dörk, Thilo, Park-Simon, Tjoung-Won, Hillemanns, Peter, Bogdanova, Natalia, Butzow, Ralf, Nevanlinna, Heli, Pelttari, Liisa M, Leminen, Arto, Modugno, Francesmary, Ness, Roberta B, Edwards, Robert P, Kelley, Joseph L, Heitz, Florian, Karlan, Beth Y, Kjær, Susanne Krüger, Høgdall, Estrid Vilma Solyom, Jensen, Allan, Goode, Ellen L, Fridley, Brooke L, Cunningham, Julie M, Winham, Stacey J, Giles, Graham G, Bruinsma, Fiona, Milne, Roger L, and Høgdall, Claus Kim
Abstract: BACKGROUND: Observational studies have reported a positive association between body mass index (BMI) and ovarian cancer risk. However, questions remain as to whether this represents a causal effect, or holds for all histological subtypes. The lack of association observed for serous cancers may, for instance, be due to disease-associated weight loss. Mendelian randomization (MR) uses genetic markers as proxies for risk factors to overcome limitations of observational studies. We used MR to elucidate the relationship between BMI and ovarian cancer, hypothesizing that genetically predicted BMI would be associated with increased risk of non-high grade serous ovarian cancers (non-HGSC) but not HGSC.METHODS: We pooled data from 39 studies (14 047 cases, 23 003 controls) in the Ovarian Cancer Association Consortium. We constructed a weighted genetic risk score (GRS, partial F-statistic = 172), summing alleles at 87 single nucleotide polymorphisms previously associated with BMI, weighting by their published strength of association with BMI. Applying two-stage predictor-substitution MR, we used logistic regression to estimate study-specific odds ratios (OR) and 95% confidence intervals (CI) for the association between genetically predicted BMI and risk, and pooled these using random-effects meta-analysis.RESULTS: Higher genetically predicted BMI was associated with increased risk of non-HGSC (pooled OR = 1.29, 95% CI 1.03-1.61 per 5 units BMI) but not HGSC (pooled OR = 1.06, 95% CI 0.88-1.27). Secondary analyses stratified by behaviour/subtype suggested that, consistent with observational data, the association was strongest for low-grade/borderline serous cancers (OR = 1.93, 95% CI 1.33-2.81).CONCLUSIONS: Our data suggest that higher BMI increases risk of non-HGSC, but not the more common and aggressive HGSC subtype, confirming the observational evidence.
Published: 2016

124. Candidate locus analysis of the TERT–CLPTM1L cancer risk region on chromosome 5p15 identifies multiple independent variants associated with endometrial cancer risk

Author: Carvajal-Carmona, Luis G., O’Mara, Tracy A., Painter, Jodie N., Lose, Felicity A., Dennis, Joe, Michailidou, Kyriaki, Tyrer, Jonathan P., Ahmed, Shahana, Ferguson, Kaltin, Healey, Catherine S., Pooley, Karen, Beesley, Jonathan, Cheng, Timothy, Jones, Angela, Howarth, Kimberley, Martin, Lynn, Gorman, Maggie, Hodgson, Shirley, Wentzensen, Nicholas, Fasching, Peter A., Hein, Alexander, Beckmann, Matthias W., Renner, Stefan P., Dörk, Thilo, Hillemanns, Peter, Dürst, Matthias, Runnebaum, Ingo, Lambrechts, Diether, Coenegrachts, Lieve, Schrauwen, Stefanie, Amant, Frederic, Winterhoff, Boris, Dowdy, Sean C., Goode, Ellen L., Teoman, Attila, Salvesen, Helga B., Trovik, Jone, Njolstad, Tormund S., Werner, Henrica M. J., Scott, Rodney J., Ashton, Katie, Proietto, Tony, Otton, Geoffrey, Wersäll, Ofra, Mints, Miriam, Tham, Emma, Hall, Per, Czene, Kamila, Liu, Jianjun, Li, Jingmei, Hopper, John L., Southey, Melissa C., Ekici, Arif B., Ruebner, Matthias, Johnson, Nichola, Peto, Julian, Burwinkel, Barbara, Marme, Frederik, Brenner, Hermann, Dieffenbach, Aida K., Meindl, Alfons, Brauch, Hiltrud, Lindblom, Annika, Depreeuw, Jeroen, Moisse, Matthieu, Chang-Claude, Jenny, Rudolph, Anja, Couch, Fergus J., Olson, Janet E., Giles, Graham G., Bruinsma, Fiona, Cunningham, Julie M., Fridley, Brooke L., Børresen-Dale, Anne-Lise, Kristensen, Vessela N., Cox, Angela, Swerdlow, Anthony J., Orr, Nicholas, Bolla, Manjeet K., Wang, Qin, Weber, Rachel Palmieri, Chen, Zhihua, Shah, Mitul, Pharoah, Paul D. P., Dunning, Alison M., Tomlinson, Ian, Easton, Douglas F., Spurdle, Amanda B., Thompson, Deborah J., and Other departments
Subjects: Models, Genetic, chromosome 5p15, Membrane Proteins, macromolecular substances, Polymorphism, Single Nucleotide, single-nucleotide polymorphisms (SNPs), Neoplasm Proteins, Gene Expression Regulation, Neoplastic, Medisinske fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710::Medisinsk genetikk: 714 [VDP], Haplotypes, Genetic Loci, Risk Factors, Midical sciences: 700::Basic medical, dental and veterinary sciences: 710::Medical genetics: 714 [VDP], Medisinske Fag: 700 [VDP], Genetics, Chromosomes, Human, Pair 5, Humans, Genetics(clinical), Female, Databases, Nucleic Acid, Promoter Regions, Genetic, multiple cancer types, Telomerase, Original Investigation
Abstract: Several studies have reported associations between multiple cancer types and single-nucleotide polymorphisms (SNPs) on chromosome 5p15, which harbours TERT and CLPTM1L, but no such association has been reported with endometrial cancer. To evaluate the role of genetic variants at the TERT–CLPTM1L region in endometrial cancer risk, we carried out comprehensive fine-mapping analyses of genotyped and imputed SNPs using a custom Illumina iSelect array which includes dense SNP coverage of this region. We examined 396 SNPs (113 genotyped, 283 imputed) in 4,401 endometrial cancer cases and 28,758 controls. Single-SNP and forward/backward logistic regression models suggested evidence for three variants independently associated with endometrial cancer risk (P = 4.9 × 10−6 to P = 7.7 × 10−5). Only one falls into a haplotype previously associated with other cancer types (rs7705526, in TERT intron 1), and this SNP has been shown to alter TERT promoter activity. One of the novel associations (rs13174814) maps to a second region in the TERT promoter and the other (rs62329728) is in the promoter region of CLPTM1L; neither are correlated with previously reported cancer-associated SNPs. Using TCGA RNASeq data, we found significantly increased expression of both TERT and CLPTM1L in endometrial cancer tissue compared with normal tissue (TERTP = 1.5 × 10−18, CLPTM1LP = 1.5 × 10−19). Our study thus reports a novel endometrial cancer risk locus and expands the spectrum of cancer types associated with genetic variation at 5p15, further highlighting the importance of this region for cancer susceptibility. Electronic supplementary material The online version of this article (doi:10.1007/s00439-014-1515-4) contains supplementary material, which is available to authorized users.
Published: 2014

125. Chapter 16 - Twins and Twinning

Author: Painter, Jodie N., Medland, Sarah J., Montgomery, Grant W., and Hall, Judith G.
Published: 2013
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126. Genetic Risk Score Mendelian Randomization Shows that Obesity Measured as Body Mass Index, but not Waist:Hip Ratio, Is Causal for Endometrial Cancer

Author: Painter, Jodie N., primary, O'Mara, Tracy A., additional, Marquart, Louise, additional, Webb, Penelope M., additional, Attia, John, additional, Medland, Sarah E., additional, Cheng, Timothy, additional, Dennis, Joe, additional, Holliday, Elizabeth G., additional, McEvoy, Mark, additional, Scott, Rodney J., additional, Ahmed, Shahana, additional, Healey, Catherine S., additional, Shah, Mitul, additional, Gorman, Maggie, additional, Martin, Lynn, additional, Hodgson, Shirley V., additional, Beckmann, Matthias W., additional, Ekici, Arif B., additional, Fasching, Peter A., additional, Hein, Alexander, additional, Rübner, Matthias, additional, Czene, Kamila, additional, Darabi, Hatef, additional, Hall, Per, additional, Li, Jingmei, additional, Dörk, Thilo, additional, Dürst, Matthias, additional, Hillemanns, Peter, additional, Runnebaum, Ingo B., additional, Amant, Frederic, additional, Annibali, Daniela, additional, Depreeuw, Jeroen, additional, Lambrechts, Diether, additional, Neven, Patrick, additional, Cunningham, Julie M., additional, Dowdy, Sean C., additional, Goode, Ellen L., additional, Fridley, Brooke L., additional, Winham, Stacey J., additional, Njølstad, Tormund S., additional, Salvesen, Helga B., additional, Trovik, Jone, additional, Werner, Henrica M.J., additional, Ashton, Katie A., additional, Otton, Geoffrey, additional, Proietto, Anthony, additional, Mints, Miriam, additional, Tham, Emma, additional, Bolla, Manjeet K., additional, Michailidou, Kyriaki, additional, Wang, Qin, additional, Tyrer, Jonathan P., additional, Hopper, John L., additional, Peto, Julian, additional, Swerdlow, Anthony J., additional, Burwinkel, Barbara, additional, Brenner, Hermann, additional, Meindl, Alfons, additional, Brauch, Hiltrud, additional, Lindblom, Annika, additional, Chang-Claude, Jenny, additional, Couch, Fergus J., additional, Giles, Graham G., additional, Kristensen, Vessela N., additional, Cox, Angela, additional, Pharoah, Paul D.P., additional, Tomlinson, Ian, additional, Dunning, Alison M., additional, Easton, Douglas F., additional, Thompson, Deborah J., additional, and Spurdle, Amanda B., additional
Published: 2016
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127. Endometriosis risk alleles at 1p36.12 act through inverse regulation ofCDC42andLINC00339

Author: Powell, Joseph E., primary, Fung, Jenny N., additional, Shakhbazov, Konstantin, additional, Sapkota, Yadav, additional, Cloonan, Nicole, additional, Hemani, Gibran, additional, Hillman, Kristine M., additional, Kaufmann, Susanne, additional, Luong, Hien T., additional, Bowdler, Lisa, additional, Painter, Jodie N., additional, Holdsworth-Carson, Sarah J., additional, Visscher, Peter M., additional, Dinger, Marcel E., additional, Healey, Martin, additional, Nyholt, Dale R., additional, French, Juliet D., additional, Edwards, Stacey L., additional, Rogers, Peter A. W., additional, and Montgomery, Grant W., additional
Published: 2016
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128. Genetic Evidence for Causal Relationships Between Maternal Obesity-Related Traits and Birth Weight

Author: Tyrrell, Jessica, primary, Richmond, Rebecca C., additional, Palmer, Tom M., additional, Feenstra, Bjarke, additional, Rangarajan, Janani, additional, Metrustry, Sarah, additional, Cavadino, Alana, additional, Paternoster, Lavinia, additional, Armstrong, Loren L., additional, De Silva, N. Maneka G., additional, Wood, Andrew R., additional, Horikoshi, Momoko, additional, Geller, Frank, additional, Myhre, Ronny, additional, Bradfield, Jonathan P., additional, Kreiner-Møller, Eskil, additional, Huikari, Ville, additional, Painter, Jodie N., additional, Hottenga, Jouke-Jan, additional, Allard, Catherine, additional, Berry, Diane J., additional, Bouchard, Luigi, additional, Das, Shikta, additional, Evans, David M., additional, Hakonarson, Hakon, additional, Hayes, M. Geoffrey, additional, Heikkinen, Jani, additional, Hofman, Albert, additional, Knight, Bridget, additional, Lind, Penelope A., additional, McCarthy, Mark I., additional, McMahon, George, additional, Medland, Sarah E., additional, Melbye, Mads, additional, Morris, Andrew P., additional, Nodzenski, Michael, additional, Reichetzeder, Christoph, additional, Ring, Susan M., additional, Sebert, Sylvain, additional, Sengpiel, Verena, additional, Sørensen, Thorkild I. A., additional, Willemsen, Gonneke, additional, de Geus, Eco J. C., additional, Martin, Nicholas G., additional, Spector, Tim D., additional, Power, Christine, additional, Järvelin, Marjo-Riitta, additional, Bisgaard, Hans, additional, Grant, Struan F. A., additional, Nohr, Ellen A., additional, Jaddoe, Vincent W., additional, Jacobsson, Bo, additional, Murray, Jeffrey C., additional, Hocher, Berthold, additional, Hattersley, Andrew T., additional, Scholtens, Denise M., additional, Davey Smith, George, additional, Hivert, Marie-France, additional, Felix, Janine F., additional, Hyppönen, Elina, additional, Lowe, William L., additional, Frayling, Timothy M., additional, Lawlor, Debbie A., additional, and Freathy, Rachel M., additional
Published: 2016
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129. Cohort Profile: Nausea and vomiting during pregnancy genetics consortium (NVP Genetics Consortium)

Author: Colodro-Conde, Lucía, primary, Cross, Simone M., additional, Lind, Penelope A., additional, Painter, Jodie N., additional, Gunst, Annika, additional, Jern, Patrick, additional, Johansson, Ada, additional, Lund Maegbaek, Merete, additional, Munk-Olsen, Trine, additional, Nyholt, Dale R., additional, Ordoñana, Juan R., additional, Paternoster, Lavinia, additional, Sánchez-Romera, Juan F., additional, Wright, Margaret J., additional, and Medland, Sarah E., additional
Published: 2016
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130. Genetic basis of a cognitive complexity metric

Author: Hansell, Narelle K, Halford, Graeme S, Andrews, Glenda, Shum, David H K, Harris, Sarah E, Davies, Gail, Franic, Sanja, Christoforou, Andrea, Zietsch, Brendan, Painter, Jodie, Medland, Sarah E, Ehli, Erik A, Davies, Gareth E, Steen, Vidar M, Lundervold, Astri J, Reinvang, Ivar, Montgomery, Grant W, Espeseth, Thomas, Hulshoff Pol, Hilleke E, Starr, John M, Martin, Nicholas G, Le Hellard, Stephanie, Boomsma, Dorret I, Deary, Ian J, Wright, Margaret J, Hansell, Narelle K, Halford, Graeme S, Andrews, Glenda, Shum, David H K, Harris, Sarah E, Davies, Gail, Franic, Sanja, Christoforou, Andrea, Zietsch, Brendan, Painter, Jodie, Medland, Sarah E, Ehli, Erik A, Davies, Gareth E, Steen, Vidar M, Lundervold, Astri J, Reinvang, Ivar, Montgomery, Grant W, Espeseth, Thomas, Hulshoff Pol, Hilleke E, Starr, John M, Martin, Nicholas G, Le Hellard, Stephanie, Boomsma, Dorret I, Deary, Ian J, and Wright, Margaret J
Published: 2015

131. Fine-mapping of the HNF1B multicancer locus identifies candidate variants that mediate endometrial cancer risk

Author: Painter, Jodie, O'Mara, Tracy, Batra, Jyotsna, Cheng, Timothy, Lose, Felicity, Dennis, Joe, Michailidou, Kyriaki, Tyrer, Jonathan, Ahmed, Shahana, Ferguson, Kaltin, Healey, Catherine, Kaufmann, Susanne, Hillman, Kristine, Walpole, Carina, Moya, Leire, Pollock, Pamela, other, and, Painter, Jodie, O'Mara, Tracy, Batra, Jyotsna, Cheng, Timothy, Lose, Felicity, Dennis, Joe, Michailidou, Kyriaki, Tyrer, Jonathan, Ahmed, Shahana, Ferguson, Kaltin, Healey, Catherine, Kaufmann, Susanne, Hillman, Kristine, Walpole, Carina, Moya, Leire, Pollock, Pamela, and other, and
Abstract: Common variants in the hepatocyte nuclear factor 1 homeobox B (HNF1B) gene are associated with the risk of Type II diabetes and multiple cancers. Evidence to date indicates that cancer risk may be mediated via genetic or epigenetic effects on HNF1B gene expression. We previously found single-nucleotide polymorphisms (SNPs) at the HNF1B locus to be associated with endometrial cancer, and now report extensive fine-mapping and in silico and laboratory analyses of this locus. Analysis of 1184 genotyped and imputed SNPs in 6608 Caucasian cases and 37 925 controls, and 895 Asian cases and 1968 controls, revealed the best signal of association for SNP rs11263763 (P = 8.4 × 10−14, odds ratio = 0.86, 95% confidence interval = 0.82–0.89), located within HNF1B intron 1. Haplotype analysis and conditional analyses provide no evidence of further independent endometrial cancer risk variants at this locus. SNP rs11263763 genotype was associated with HNF1B mRNA expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas. Genetic analyses prioritized rs11263763 and four other SNPs in high-to-moderate linkage disequilibrium as the most likely causal SNPs. Three of these SNPs map to the extended HNF1B promoter based on chromatin marks extending from the minimal promoter region. Reporter assays demonstrated that this extended region reduces activity in combination with the minimal HNF1B promoter, and that the minor alleles of rs11263763 or rs8064454 are associated with decreased HNF1B promoter activity. Our findings provide evidence for a single signal associated with endometrial cancer risk at the HNF1B locus, and that risk is likely mediated via altered HNF1B gene expression.
Published: 2015

132. Meta-analysis of genome-wide association studies identifies common susceptibility polymorphisms for colorectal and endometrial cancer near SH2B3 and TSHZ1

Author: Cheng, Timothy H. T., Thompson, Deborah, Painter, Jodie, O’Mara, Tracy, Gorman, Maggie, Martin, Lynn, Palles, Claire, Jones, Angela, Buchanan, Daniel D., Win, Aung Ko, Hopper, John, Jenkins, Mark, Lindor, Noralane M., Newcomb, Polly A., Gallinger, Steve, Conti, David, Schumacher, Fred, Casey, Graham, Giles, Graham G., Pharoah, Paul, Peto, Julian, Cox, Angela, Swerdlow, Anthony, Couch, Fergus, Cunningham, Julie M., Goode, Ellen L., Winham, Stacey J., Lambrechts, Diether, Fasching, Peter, Burwinkel, Barbara, Brenner, Hermann, Brauch, Hiltrud, Chang Claude, Jenny, Salvesen, Helga B., Kristensen, Vessela, Darabi, Hatef, Li, Jingmei, Liu, Tao, Lindblom, Annika, Hall, Per, Echeverry de Polanco, Magdalena, Sans, Monica, Carracedo, Angel, Castellvi Bel, Sergi, Rojas Martínez, Augusto, Aguiar Jnr, Samuel, Teixeira, Manuel R., Dunning, Alison M, Dennis, Joe, Otton, Geoffrey, Proietto, Tony, Holliday, Elizabeth, Attia, John, Ashton, Katie, Scott, Rodney J, McEvoy, Mark, Dowdy, Sean C, Fridley, Brooke L, Werner, Henrica MJ, Trovik, Jone, Njolstad, Tormund S, Tham, Emma, Mints, Miriam, Runnebaum, Ingo, Hillemanns, Peter, Dörk, Thilo, Amant, Frederic, Schrauwen, Stefanie, Hein, Alexander, Beckmann, Matthias W, Ekici, Arif, Czene, Kamila, Meindl, Alfons, Bolla, Manjeet K, Michailidou, Kyriaki, Tyrer, Jonathan P., Wang, Qin, Ahmed, Shahana, Healey, Catherine S., Shah, Mitul, Annibali, Daniela, Depreeuw, Jeroen, Al-Tassan, Nada A., Harris, Rebecca, Meyer, Brian F., Whiffin, Nicola, Hosking, Fay J, Kinnersley, Ben, Farrington, Susan M., Timofeeva, Maria, Tenesa, Albert, Campbell, Harry, Haile, Robert W., Hodgson, Shirley, Carvajal Carmona, Luis, Cheadle, Jeremy P., Easton, Douglas, Dunlop, Malcolm, Houlston, Richard, Spurdle, Amanda, Tomlinson, Ian, Cheng, Timothy H. T., Thompson, Deborah, Painter, Jodie, O’Mara, Tracy, Gorman, Maggie, Martin, Lynn, Palles, Claire, Jones, Angela, Buchanan, Daniel D., Win, Aung Ko, Hopper, John, Jenkins, Mark, Lindor, Noralane M., Newcomb, Polly A., Gallinger, Steve, Conti, David, Schumacher, Fred, Casey, Graham, Giles, Graham G., Pharoah, Paul, Peto, Julian, Cox, Angela, Swerdlow, Anthony, Couch, Fergus, Cunningham, Julie M., Goode, Ellen L., Winham, Stacey J., Lambrechts, Diether, Fasching, Peter, Burwinkel, Barbara, Brenner, Hermann, Brauch, Hiltrud, Chang Claude, Jenny, Salvesen, Helga B., Kristensen, Vessela, Darabi, Hatef, Li, Jingmei, Liu, Tao, Lindblom, Annika, Hall, Per, Echeverry de Polanco, Magdalena, Sans, Monica, Carracedo, Angel, Castellvi Bel, Sergi, Rojas Martínez, Augusto, Aguiar Jnr, Samuel, Teixeira, Manuel R., Dunning, Alison M, Dennis, Joe, Otton, Geoffrey, Proietto, Tony, Holliday, Elizabeth, Attia, John, Ashton, Katie, Scott, Rodney J, McEvoy, Mark, Dowdy, Sean C, Fridley, Brooke L, Werner, Henrica MJ, Trovik, Jone, Njolstad, Tormund S, Tham, Emma, Mints, Miriam, Runnebaum, Ingo, Hillemanns, Peter, Dörk, Thilo, Amant, Frederic, Schrauwen, Stefanie, Hein, Alexander, Beckmann, Matthias W, Ekici, Arif, Czene, Kamila, Meindl, Alfons, Bolla, Manjeet K, Michailidou, Kyriaki, Tyrer, Jonathan P., Wang, Qin, Ahmed, Shahana, Healey, Catherine S., Shah, Mitul, Annibali, Daniela, Depreeuw, Jeroen, Al-Tassan, Nada A., Harris, Rebecca, Meyer, Brian F., Whiffin, Nicola, Hosking, Fay J, Kinnersley, Ben, Farrington, Susan M., Timofeeva, Maria, Tenesa, Albert, Campbell, Harry, Haile, Robert W., Hodgson, Shirley, Carvajal Carmona, Luis, Cheadle, Jeremy P., Easton, Douglas, Dunlop, Malcolm, Houlston, Richard, Spurdle, Amanda, and Tomlinson, Ian
Published: 2015

133. Genetic basis of a cognitive complexity metric

Author: Onderzoeksgroep 1, Brain, Hansell, Narelle K, Halford, Graeme S, Andrews, Glenda, Shum, David H K, Harris, Sarah E, Davies, Gail, Franic, Sanja, Christoforou, Andrea, Zietsch, Brendan, Painter, Jodie, Medland, Sarah E, Ehli, Erik A, Davies, Gareth E, Steen, Vidar M, Lundervold, Astri J, Reinvang, Ivar, Montgomery, Grant W, Espeseth, Thomas, Hulshoff Pol, Hilleke E, Starr, John M, Martin, Nicholas G, Le Hellard, Stephanie, Boomsma, Dorret I, Deary, Ian J, Wright, Margaret J, Onderzoeksgroep 1, Brain, Hansell, Narelle K, Halford, Graeme S, Andrews, Glenda, Shum, David H K, Harris, Sarah E, Davies, Gail, Franic, Sanja, Christoforou, Andrea, Zietsch, Brendan, Painter, Jodie, Medland, Sarah E, Ehli, Erik A, Davies, Gareth E, Steen, Vidar M, Lundervold, Astri J, Reinvang, Ivar, Montgomery, Grant W, Espeseth, Thomas, Hulshoff Pol, Hilleke E, Starr, John M, Martin, Nicholas G, Le Hellard, Stephanie, Boomsma, Dorret I, Deary, Ian J, and Wright, Margaret J
Published: 2015

134. Fine mapping of variants associated with endometriosis in the WNT4 region on chromosome 1p36

Author: Luong, Hien Tt, Painter, Jodie N., Shakhbazov, Konstantin, Chapman, Brett, Henders, Anjali K., Powell, Joseph E., Dale Nyholt, and Montgomery, Grant W.
Subjects: Original Article
Abstract: Genome-wide association studies show strong evidence of association with endometriosis for markers on chromosome 1p36 spanning the potential candidate genes WNT4, CDC42 and LINC00339. WNT4 is involved in development of the uterus, and the expression of CDC42 and LINC00339 are altered in women with endometriosis. We conducted fine mapping to examine the role of coding variants in WNT4 and CDC42 and determine the key SNPs with strongest evidence of association in this region. We identified rare coding variants in WNT4 and CDC42 present only in endometriosis cases. The frequencies were low and cannot account for the common signal associated with increased risk of endometriosis. Genotypes for five common SNPs in the region of chromosome 1p36 show stronger association signals when compared with rs7521902 reported in published genome scans. Of these, three SNPs rs12404660, rs3820282, and rs55938609 were located in DNA sequences with potential functional roles including overlap with transcription factor binding sites for FOXA1, FOXA2, ESR1, and ESR2. Functional studies will be required to identify the gene or genes implicated in endometriosis risk.
Published: 2013

135. Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors

Author: Warrington, Nicole M., Beaumont, Robin N., Horikoshi, Momoko, Day, Felix R., Helgeland, Øyvind, Laurin, Charles, Bacelis, Jonas, Peng, Shouneng, Hao, Ke, Feenstra, Bjarke, Wood, Andrew R., Mahajan, Anubha, Tyrrell, Jessica, Robertson, Neil R., Rayner, N. William, Qiao, Zhen, Moen, Gunn-Helen, Vaudel, Marc, Marsit, Carmen J., Chen, Jia, Nodzenski, Michael, Schnurr, Theresia M., Zafarmand, Mohammad H., Bradfield, Jonathan P., Grarup, Niels, Kooijman, Marjolein N., Li-Gao, Ruifang, Geller, Frank, Ahluwalia, Tarunveer S., Paternoster, Lavinia, Rueedi, Rico, Huikari, Ville, Hottenga, Jouke-Jan, Lyytikäinen, Leo-Pekka, Cavadino, Alana, Metrustry, Sarah, Cousminer, Diana L., Wu, Ying, Thiering, Elisabeth, Wang, Carol A., Have, Christian T., Vilor-Tejedor, Natalia, Joshi, Peter K., Painter, Jodie N., Ntalla, Ioanna, Myhre, Ronny, Pitkänen, Niina, van Leeuwen, Elisabeth M., Joro, Raimo, Lagou, Vasiliki, Richmond, Rebecca C., Espinosa, Ana, Barton, Sheila J., Inskip, Hazel M., Holloway, John W., Santa-Marina, Loreto, Estivill, Xavier, Ang, Wei, Marsh, Julie A., Reichetzeder, Christoph, Marullo, Letizia, Hocher, Berthold, Lunetta, Kathryn L., Murabito, Joanne M., Relton, Caroline L., Kogevinas, Manolis, Chatzi, Leda, Allard, Catherine, Bouchard, Luigi, Hivert, Marie-France, Zhang, Ge, Muglia, Louis J., Heikkinen, Jani, Morgen, Camilla S., van Kampen, Antoine H. C., van Schaik, Barbera D. C., Mentch, Frank D., Langenberg, Claudia, Luan, Jian’an, Scott, Robert A., Zhao, Jing Hua, Hemani, Gibran, Ring, Susan M., Bennett, Amanda J., Gaulton, Kyle J., Fernandez-Tajes, Juan, van Zuydam, Natalie R., Medina-Gomez, Carolina, de Haan, Hugoline G., Rosendaal, Frits R., Kutalik, Zoltán, Marques-Vidal, Pedro, Das, Shikta, Willemsen, Gonneke, Mbarek, Hamdi, Müller-Nurasyid, Martina, Standl, Marie, Appel, Emil V. R., Fonvig, Cilius E., Trier, Caecilie, van Beijsterveldt, Catharina E. M., Murcia, Mario, Bustamante, Mariona, Bonas-Guarch, Sílvia, Hougaard, David M., Mercader, Josep M., Linneberg, Allan, Schraut, Katharina E., Lind, Penelope A., Medland, Sarah E., Shields, Beverley M., Knight, Bridget A., Chai, Jin-Fang, Panoutsopoulou, Kalliope, Bartels, Meike, Sánchez, Friman, Stokholm, Jakob, Torrents, David, Vinding, Rebecca K., Willems, Sara M., Atalay, Mustafa, Chawes, Bo L., Kovacs, Peter, Prokopenko, Inga, Tuke, Marcus A., Yaghootkar, Hanieh, Ruth, Katherine S., Jones, Samuel E., Loh, Po-Ru, Murray, Anna, Weedon, Michael N., Tönjes, Anke, Stumvoll, Michael, Michaelsen, Kim F., Eloranta, Aino-Maija, Lakka, Timo A., van Duijn, Cornelia M., Kiess, Wieland, Körner, Antje, Niinikoski, Harri, Pahkala, Katja, Raitakari, Olli T., Jacobsson, Bo, Zeggini, Eleftheria, Dedoussis, George V., Teo, Yik-Ying, Saw, Seang-Mei, Montgomery, Grant W., Campbell, Harry, Wilson, James F., Vrijkotte, Tanja G. M., Vrijheid, Martine, de Geus, Eco J. C. N., Hayes, M. Geoffrey, Kadarmideen, Haja N., Holm, Jens-Christian, Beilin, Lawrence J., Pennell, Craig E., Heinrich, Joachim, Adair, Linda S., Borja, Judith B., Mohlke, Karen L., Eriksson, Johan G., Widén, Elisabeth E., Hattersley, Andrew T., Spector, Tim D., Kähönen, Mika, Viikari, Jorma S., Lehtimäki, Terho, Boomsma, Dorret I., Sebert, Sylvain, Vollenweider, Peter, Sørensen, Thorkild I. A., Bisgaard, Hans, Bønnelykke, Klaus, Murray, Jeffrey C., Melbye, Mads, Nohr, Ellen A., Mook-Kanamori, Dennis O., Rivadeneira, Fernando, Hofman, Albert, Felix, Janine F., Jaddoe, Vincent W. V., Hansen, Torben, Pisinger, Charlotta, Vaag, Allan A., Pedersen, Oluf, Uitterlinden, André G., Järvelin, Marjo-Riitta, Power, Christine, Hyppönen, Elina, Scholtens, Denise M., Lowe, William L., Davey Smith, George, Timpson, Nicholas J., Morris, Andrew P., Wareham, Nicholas J., Hakonarson, Hakon, Grant, Struan F. A., Frayling, Timothy M., Lawlor, Debbie A., Njølstad, Pål R., Johansson, Stefan, Ong, Ken K., McCarthy, Mark I., Perry, John R. B., Evans, David M., and Freathy, Rachel M.
Abstract: Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n= 321,223) and offspring birth weight (n= 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight–blood pressure association is attributable to genetic effects, and not to intrauterine programming.
Published: 2019
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136. Meta-analysis of genome-wide association studies identifies common susceptibility polymorphisms for colorectal and endometrial cancer near SH2B3 and TSHZ1

Author: Cheng, Timothy HT, primary, Thompson, Deborah, additional, Painter, Jodie, additional, O’Mara, Tracy, additional, Gorman, Maggie, additional, Martin, Lynn, additional, Palles, Claire, additional, Jones, Angela, additional, Buchanan, Daniel D., additional, Win, Aung Ko, additional, Hopper, John, additional, Jenkins, Mark, additional, Lindor, Noralane M., additional, Newcomb, Polly A., additional, Gallinger, Steve, additional, Conti, David, additional, Schumacher, Fred, additional, Casey, Graham, additional, Giles, Graham G, additional, Pharoah, Paul, additional, Peto, Julian, additional, Cox, Angela, additional, Swerdlow, Anthony, additional, Couch, Fergus, additional, Cunningham, Julie M, additional, Goode, Ellen L, additional, Winham, Stacey J, additional, Lambrechts, Diether, additional, Fasching, Peter, additional, Burwinkel, Barbara, additional, Brenner, Hermann, additional, Brauch, Hiltrud, additional, Chang-Claude, Jenny, additional, Salvesen, Helga B., additional, Kristensen, Vessela, additional, Darabi, Hatef, additional, Li, Jingmei, additional, Liu, Tao, additional, Lindblom, Annika, additional, Hall, Per, additional, de Polanco, Magdalena Echeverry, additional, Sans, Monica, additional, Carracedo, Angel, additional, Castellvi-Bel, Sergi, additional, Rojas-Martinez, Augusto, additional, Aguiar Jnr, Samuel, additional, Teixeira, Manuel R., additional, Dunning, Alison M, additional, Dennis, Joe, additional, Otton, Geoffrey, additional, Proietto, Tony, additional, Holliday, Elizabeth, additional, Attia, John, additional, Ashton, Katie, additional, Scott, Rodney J, additional, McEvoy, Mark, additional, Dowdy, Sean C, additional, Fridley, Brooke L, additional, Werner, Henrica MJ, additional, Trovik, Jone, additional, Njolstad, Tormund S, additional, Tham, Emma, additional, Mints, Miriam, additional, Runnebaum, Ingo, additional, Hillemanns, Peter, additional, Dörk, Thilo, additional, Amant, Frederic, additional, Schrauwen, Stefanie, additional, Hein, Alexander, additional, Beckmann, Matthias W, additional, Ekici, Arif, additional, Czene, Kamila, additional, Meindl, Alfons, additional, Bolla, Manjeet K, additional, Michailidou, Kyriaki, additional, Tyrer, Jonathan P, additional, Wang, Qin, additional, Ahmed, Shahana, additional, Healey, Catherine S, additional, Shah, Mitul, additional, Annibali, Daniela, additional, Depreeuw, Jeroen, additional, Al-Tassan, Nada A., additional, Harris, Rebecca, additional, Meyer, Brian F., additional, Whiffin, Nicola, additional, Hosking, Fay J, additional, Kinnersley, Ben, additional, Farrington, Susan M., additional, Timofeeva, Maria, additional, Tenesa, Albert, additional, Campbell, Harry, additional, Haile, Robert W., additional, Hodgson, Shirley, additional, Carvajal-Carmona, Luis, additional, Cheadle, Jeremy P., additional, Easton, Douglas, additional, Dunlop, Malcolm, additional, Houlston, Richard, additional, Spurdle, Amanda, additional, and Tomlinson, Ian, additional
Published: 2015
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137. CYP19A1 fine-mapping and Mendelian randomization: estradiol is causal for endometrial cancer

Author: Thompson, Deborah J, primary, O'Mara, Tracy A, additional, Glubb, Dylan M, additional, Painter, Jodie N, additional, Cheng, Timothy, additional, Folkerd, Elizabeth, additional, Doody, Deborah, additional, Dennis, Joe, additional, Webb, Penelope M, additional, _, _, additional, Gorman, Maggie, additional, Martin, Lynn, additional, Hodgson, Shirley, additional, Michailidou, Kyriaki, additional, Tyrer, Jonathan P, additional, Maranian, Mel J, additional, Hall, Per, additional, Czene, Kamila, additional, Darabi, Hatef, additional, Li, Jingmei, additional, Fasching, Peter A, additional, Hein, Alexander, additional, Beckmann, Matthias W, additional, Ekici, Arif B, additional, Dörk, Thilo, additional, Hillemanns, Peter, additional, Dürst, Matthias, additional, Runnebaum, Ingo, additional, Zhao, Hui, additional, Depreeuw, Jeroen, additional, Schrauwen, Stefanie, additional, Amant, Frederic, additional, Goode, Ellen L, additional, Fridley, Brooke L, additional, Dowdy, Sean C, additional, Winham, Stacey J, additional, Salvesen, Helga B, additional, Trovik, Jone, additional, Njolstad, Tormund S, additional, Werner, Henrica M J, additional, Ashton, Katie, additional, Proietto, Tony, additional, Otton, Geoffrey, additional, Carvajal-Carmona, Luis, additional, Tham, Emma, additional, Liu, Tao, additional, Mints, Miriam, additional, Scott, Rodney J, additional, McEvoy, Mark, additional, Attia, John, additional, Holliday, Elizabeth G, additional, Montgomery, Grant W, additional, Martin, Nicholas G, additional, Nyholt, Dale R, additional, Henders, Anjali K, additional, Hopper, John L, additional, Traficante, Nadia, additional, Ruebner, Matthias, additional, Swerdlow, Anthony J, additional, Burwinkel, Barbara, additional, Brenner, Hermann, additional, Meindl, Alfons, additional, Brauch, Hiltrud, additional, Lindblom, Annika, additional, Lambrechts, Diether, additional, Chang-Claude, Jenny, additional, Couch, Fergus J, additional, Giles, Graham G, additional, Kristensen, Vessela N, additional, Cox, Angela, additional, Bolla, Manjeet K, additional, Wang, Qin, additional, Bojesen, Stig E, additional, Shah, Mitul, additional, Luben, Robert, additional, Khaw, Kay-Tee, additional, Pharoah, Paul D P, additional, Dunning, Alison M, additional, Tomlinson, Ian, additional, Dowsett, Mitch, additional, Easton, Douglas F, additional, and Spurdle, Amanda B, additional
Published: 2015
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138. Comprehensive genetic assessment of the ESR1 locus identifies a risk region for endometrial cancer

Author: O'Mara, Tracy A, primary, Glubb, Dylan M, additional, Painter, Jodie N, additional, Cheng, Timothy, additional, Dennis, Joe, additional, _, _, additional, Attia, John, additional, Holliday, Elizabeth G, additional, McEvoy, Mark, additional, Scott, Rodney J, additional, Ashton, Katie, additional, Proietto, Tony, additional, Otton, Geoffrey, additional, Shah, Mitul, additional, Ahmed, Shahana, additional, Healey, Catherine S, additional, Gorman, Maggie, additional, Martin, Lynn, additional, Hodgson, Shirley, additional, Fasching, Peter A, additional, Hein, Alexander, additional, Beckmann, Matthias W, additional, Ekici, Arif B, additional, Hall, Per, additional, Czene, Kamila, additional, Darabi, Hatef, additional, Li, Jingmei, additional, Dürst, Matthias, additional, Runnebaum, Ingo, additional, Hillemanns, Peter, additional, Dörk, Thilo, additional, Lambrechts, Diether, additional, Depreeuw, Jeroen, additional, Annibali, Daniela, additional, Amant, Frederic, additional, Zhao, Hui, additional, Goode, Ellen L, additional, Dowdy, Sean C, additional, Fridley, Brooke L, additional, Winham, Stacey J, additional, Salvesen, Helga B, additional, Njølstad, Tormund S, additional, Trovik, Jone, additional, Werner, Henrica M J, additional, Tham, Emma, additional, Liu, Tao, additional, Mints, Miriam, additional, Bolla, Manjeet K, additional, Michailidou, Kyriaki, additional, Tyrer, Jonathan P, additional, Wang, Qin, additional, Hopper, John L, additional, Peto, Julian, additional, Swerdlow, Anthony J, additional, Burwinkel, Barbara, additional, Brenner, Hermann, additional, Meindl, Alfons, additional, Brauch, Hiltrud, additional, Lindblom, Annika, additional, Chang-Claude, Jenny, additional, Couch, Fergus J, additional, Giles, Graham G, additional, Kristensen, Vessela N, additional, Cox, Angela, additional, Pharoah, Paul D P, additional, Dunning, Alison M, additional, Tomlinson, Ian, additional, Easton, Douglas F, additional, Thompson, Deborah J, additional, and Spurdle, Amanda B, additional
Published: 2015
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139. Genetic Basis of a Cognitive Complexity Metric

Author: Hansell, Narelle K., primary, Halford, Graeme S., additional, Andrews, Glenda, additional, Shum, David H. K., additional, Harris, Sarah E., additional, Davies, Gail, additional, Franic, Sanja, additional, Christoforou, Andrea, additional, Zietsch, Brendan, additional, Painter, Jodie, additional, Medland, Sarah E., additional, Ehli, Erik A., additional, Davies, Gareth E., additional, Steen, Vidar M., additional, Lundervold, Astri J., additional, Reinvang, Ivar, additional, Montgomery, Grant W., additional, Espeseth, Thomas, additional, Hulshoff Pol, Hilleke E., additional, Starr, John M., additional, Martin, Nicholas G., additional, Le Hellard, Stephanie, additional, Boomsma, Dorret I., additional, Deary, Ian J., additional, and Wright, Margaret J., additional
Published: 2015
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140. Common variants in the CYP2C19 gene are associated with susceptibility to endometriosis

Author: Painter, Jodie, Nyholt, Dale, Krause, Lutz, Zhao, Zhen Zhen, Chapman, Brett, Zhang, Christine, Medland, Sarah, Martin, Nicholas, Kennedy, Stephen, Treloar, Susan, Zondervan, Krina, Montgomery, Grant, Painter, Jodie, Nyholt, Dale, Krause, Lutz, Zhao, Zhen Zhen, Chapman, Brett, Zhang, Christine, Medland, Sarah, Martin, Nicholas, Kennedy, Stephen, Treloar, Susan, Zondervan, Krina, and Montgomery, Grant
Abstract: Objective: To follow-up previous studies highlighting a possible role for cytochrome P450, family 2, subfamily C, 19 (CYP2C19) in susceptibility to endometriosis by searching for additional variants in the CYP2C19 gene that may be associated with the disease. Design Case-control study. Setting Academic research. Subject(s) The cases comprised 2,271 women with surgically confirmed endometriosis; the controls comprised 939 women with self-report of no endometriosis and 1,770 unscreened population samples. Intervention(s) Sequencing of the CYP2C19 region and follow-up of 80 single nucleotide polymorphisms (SNPs) in two case-control samples. Main Outcome Measure(s) Allele frequency differences between cases and controls. Result(s) Sequencing of the CYP2C19 gene region resulted in the detection of a large number of known and novel SNPs. Genotyping of 80 polymorphic SNPs in 901 endometriosis cases and 939 controls resulted in study-wide significant association signals for SNPs in moderate or complete linkage disequilibrium with rs4244285, a functional SNP in exon 5 that abrogates CYP2C19 function through the creation of an alternative splice site. Evidence of association was also detected for another functional SNP in the CYP2C19 promoter, rs12248560, which was highlighted in our previous study. Conclusion(s) Functional variants in CYP2C19 may contribute to endometriosis susceptibility in both familial and sporadic cases. © 2014 by American Society for Reproductive Medicine.
Published: 2014

141. Contribution of genetic variation to transgenerational inheritance of DNA methylation

Author: McRae, Allan F, primary, Powell, Joseph E, additional, Henders, Anjali K, additional, Bowdler, Lisa, additional, Hemani, Gibran, additional, Shah, Sonia, additional, Painter, Jodie N, additional, Martin, Nicholas G, additional, Visscher, Peter M, additional, and Montgomery, Grant W, additional
Published: 2014
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142. Fine mapping of variants associated with endometriosis in the WNT4 region on chromosome 1p36

Author: Luong, Hien, Painter, Jodie, Shakhbazov, Konstantin, Chapman, Brett, Henders, Anjali, Powell, Joseph, Nyholt, Dale, Montgomery, Grant, Luong, Hien, Painter, Jodie, Shakhbazov, Konstantin, Chapman, Brett, Henders, Anjali, Powell, Joseph, Nyholt, Dale, and Montgomery, Grant
Abstract: Genome-wide association studies show strong evidence of association with endometriosis for markers on chromosome 1p36 spanning the potential candidate genes WNT4, CDC42 and LINC00339. WNT4 is involved in development of the uterus, and the expression of CDC42 and LINC00339 are altered in women with endometriosis. We conducted fine mapping to examine the role of coding variants in WNT4 and CDC42 and determine the key SNPs with strongest evidence of association in this region. We identified rare coding variants in WNT4 and CDC42 present only in endometriosis cases. The frequencies were low and cannot account for the common signal associated with increased risk of endometriosis. Genotypes for five common SNPs in the region of chromosome 1p36 show stronger association signals when compared with rs7521902 reported in published genome scans. Of these, three SNPs rs12404660, rs3820282, and rs55938609 were located in DNA sequences with potential functional roles including overlap with transcription factor binding sites for FOXA1, FOXA2, ESR1, and ESR2. Functional studies will be required to identify the gene or genes implicated in endometriosis risk.
Published: 2013

143. Genome-wide association analyses identify 44 risk variants and refine the genetic architecture of major depression

Author: Wray, Naomi, Ripke, Stephan, Mattheisen, Manuel, Trzaskowski, Maciej, Byrne, Enda, Abdellaoui, Abdel, Adams, Mark, Agerbo, Esben, Air, Tracy, Andlauer, Till, Bacanu, Silviu-Alin, Bækvad-Hansen, Marie, Beekman, Aartjan, Bigdeli, Tim, Binder, Elisabeth, Blackwood, Douglas, Bryois, Julien, Buttenschøn, Henriette, Bybjerg-Grauholm, Jonas, Cai, Na, Castelao, Enrique, Christensen, Jane, Clarke, Toni-Kim, Coleman, Jonathan, Colodro-Conde, Lucía, Couvy-Duchesne, Baptiste, Craddock, Nick, Crawford, Gregory, Crowley, Cheynna, Dashti, Hassan, Davies, Gail, Deary, Ian, Degenhardt, Franziska, Derks, Eske, Direk, Nese, Dolan, Conor, Dunn, Erin, Eley, Thalia, Eriksson, Nicholas, Escott-Price, Valentina, Kiadeh, Farnush, Finucane, Hilary, Forstner, Andreas, Frank, Josef, Gaspar, Héléna, Gill, Michael, Giusti-Rodríguez, Paola, Goes, Fernando, Gordon, Scott, Grove, Jakob, Hall, Lynsey, Hannon, Eilis, Hansen, Christine, Hansen, Thomas, Herms, Stefan, Hickie, Ian, Hoffmann, Per, Homuth, Georg, Horn, Carsten, Hottenga, Jouke-Jan, Hougaard, David, Hu, Ming, Hyde, Craig, Ising, Marcus, Jansen, Rick, Jin, Fulai, Jorgenson, Eric, Knowles, James, Kohane, Isaac, Kraft, Julia, Kretzschmar, Warren, Krogh, Jesper, Kutalik, Zoltán, Lane, Jacqueline, Li, Yihan, Li, Yun, Lind, Penelope, Liu, Xiaoxiao, Lu, Leina, MacIntyre, Donald, MacKinnon, Dean, Maier, Robert, Maier, Wolfgang, Marchini, Jonathan, Mbarek, Hamdi, McGrath, Patrick, McGuffin, Peter, Medland, Sarah, Mehta, Divya, Middeldorp, Christel, Mihailov, Evelin, Milaneschi, Yuri, Milani, Lili, Mill, Jonathan, Mondimore, Francis, Montgomery, Grant, Mostafavi, Sara, Mullins, Niamh, Nauck, Matthias, Ng, Bernard, Nivard, Michel, Nyholt, Dale, O’Reilly, Paul, Oskarsson, Hogni, Owen, Michael, Painter, Jodie, Pedersen, Carsten, Pedersen, Marianne, Peterson, Roseann, Pettersson, Erik, Peyrot, Wouter, Pistis, Giorgio, Posthuma, Danielle, Purcell, Shaun, Quiroz, Jorge, Qvist, Per, Rice, John, Riley, Brien, Rivera, Margarita, Saeed Mirza, Saira, Saxena, Richa, Schoevers, Robert, Schulte, Eva, Shen, Ling, Shi, Jianxin, Shyn, Stanley, Sigurdsson, Engilbert, Sinnamon, Grant, Smit, Johannes, Smith, Daniel, Stefansson, Hreinn, Steinberg, Stacy, Stockmeier, Craig, Streit, Fabian, Strohmaier, Jana, Tansey, Katherine, Teismann, Henning, Teumer, Alexander, Thompson, Wesley, Thomson, Pippa, Thorgeirsson, Thorgeir, Tian, Chao, Traylor, Matthew, Treutlein, Jens, Trubetskoy, Vassily, Uitterlinden, André, Umbricht, Daniel, Van der Auwera, Sandra, van Hemert, Albert, Viktorin, Alexander, Visscher, Peter, Wang, Yunpeng, Webb, Bradley, Weinsheimer, Shantel, Wellmann, Jürgen, Willemsen, Gonneke, Witt, Stephanie, Wu, Yang, Xi, Hualin, Yang, Jian, Zhang, Futao, Arolt, Volker, Baune, Bernhard, Berger, Klaus, Boomsma, Dorret, Cichon, Sven, Dannlowski, Udo, de Geus, E., DePaulo, J., Domenici, Enrico, Domschke, Katharina, Esko, Tõnu, Grabe, Hans, Hamilton, Steven, Hayward, Caroline, Heath, Andrew, Hinds, David, Kendler, Kenneth, Kloiber, Stefan, Lewis, Glyn, Li, Qingqin, Lucae, Susanne, Madden, Pamela, Magnusson, Patrik, Martin, Nicholas, McIntosh, Andrew, Metspalu, Andres, Mors, Ole, Mortensen, Preben, Müller-Myhsok, Bertram, Nordentoft, Merete, Nöthen, Markus, O’Donovan, Michael, Paciga, Sara, Pedersen, Nancy, Penninx, Brenda, Perlis, Roy, Porteous, David, Potash, James, Preisig, Martin, Rietschel, Marcella, Schaefer, Catherine, Schulze, Thomas, Smoller, Jordan, Stefansson, Kari, Tiemeier, Henning, Uher, Rudolf, Völzke, Henry, Weissman, Myrna, Werge, Thomas, Winslow, Ashley, Lewis, Cathryn, Levinson, Douglas, Breen, Gerome, Børglum, Anders, and Sullivan, Patrick
Abstract: Major depressive disorder (MDD) is a common illness accompanied by considerable morbidity, mortality, costs, and heightened risk of suicide. We conducted a genome-wide association meta-analysis based in 135,458 cases and 344,901 controls and identified 44 independent and significant loci. The genetic findings were associated with clinical features of major depression and implicated brain regions exhibiting anatomical differences in cases. Targets of antidepressant medications and genes involved in gene splicing were enriched for smaller association signal. We found important relationships of genetic risk for major depression with educational attainment, body mass, and schizophrenia: lower educational attainment and higher body mass were putatively causal, whereas major depression and schizophrenia reflected a partly shared biological etiology. All humans carry lesser or greater numbers of genetic risk factors for major depression. These findings help refine the basis of major depression and imply that a continuous measure of risk underlies the clinical phenotype. A genome-wide association meta-analysis of individuals with clinically assessed or self-reported depression identifies 44 independent risk loci. Comparisons with other psychiatric disorders and candidate gene analyses provide new insights into major depressive disorder.
Published: 2018
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144. No evidence for genetic association with the let-7 microRNA-binding site or other common KRAS variants in risk of endometriosis

Author: Luong, Hien, Nyholt, Dale, Painter, Jodie, Chapman, Brett, Kennedy, Stephen, Treloar, Susan, Zondervan, Krina, Montgomery, Grant, Luong, Hien, Nyholt, Dale, Painter, Jodie, Chapman, Brett, Kennedy, Stephen, Treloar, Susan, Zondervan, Krina, and Montgomery, Grant
Abstract: STUDY QUESTION Is there a contribution of the minor allele at the KRAS single nucleotide polymorphism (SNP) rs61764370 in the let-7 microRNA-binding site to endometriosis risk? SUMMARY ANSWER We found no evidence for association between endometriosis risk and rs61764370 or any other SNPs in KRAS. WHAT IS KNOWN ALREADY The rs61764370 SNP in the 3' untranslated region of the KRAS gene is predicted to disrupt a complementary binding site (LCS6) for the let-7 microRNA, and was recently reported to be at a high frequency (31%) in 132 women of varying ancestry with endometriosis compared with frequencies in a database of population controls (up to 7.6% depending on ancestry), suggesting a strong effect of this KRAS SNP in the aetiology of endometriosis. STUDY DESIGN, SIZE AND DURATION This was a case-control study with a total of 11 206 subjects. The study was performed between February 2012 and July 2012. PARTICIPANTS/MATERIALS, SETTINGAND METHODS We first investigated a possible association between common markers in KRAS and endometriosis risk from our genome-wide association (GWA) data in 3194 surgically confirmed endometriosis cases and 7060 controls of European ancestry. Although rs61764370 was not genotyped on the GWA arrays, five SNPs typed in the study were highly correlated with this variant. The rs61764370 and two SNPs highly correlated with rs61764370 were then genotyped in 933 endometriosis cases and 952 controls using the Sequenom MassARRAY platform. MAIN RESULTS AND THE ROLE OF CHANCE There was no evidence for an association between rs61764370 and endometriosis risk P = 0.411 and odds ratio = 1.10 (95% confidence intervals: 0.88-1.36). We also found no evidence for an association between the highly correlated SNP rs17387019 and endometriosis. Their minor allele frequencies in cases and controls were of 0.087-0.091 similar to the population frequency reported previously for this variant in controls. Analyses of endometriosis cases with revised American Fertil
Published: 2012

145. Genome-wide association meta-analysis identifies new endometriosis risk loci

Author: Nyholt, Dale, Low, Siew-Kee, Anderson, Carl, Painter, Jodie, Uno, Satoko, Morris, Andrew, Macgregor, Stuart, Gordon, Scott, Henders, Anjali, Martin, Nicholas, other, and, Nyholt, Dale, Low, Siew-Kee, Anderson, Carl, Painter, Jodie, Uno, Satoko, Morris, Andrew, Macgregor, Stuart, Gordon, Scott, Henders, Anjali, Martin, Nicholas, and other, and
Abstract: We conducted a genome-wide association meta-analysis of 4,604 endometriosis cases and 9,393 controls of Japanese and European ancestry. We show that rs12700667 on chromosome 7p15.2, previously found to associate with disease in Europeans, replicates in Japanese (P = 3.6 x 10(-3)), and we confirm association of rs7521902 at 1p36.12 near WNT4. In addition, we establish an association of rs13394619 in GREB1 at 2p25.1 with endometriosis and identify a newly associated locus at 12q22 near VEZT (rs10859871). Excluding cases of European ancestry of minimal or unknown severity, we identified additional previously unknown loci at 2p14 (rs4141819), 6p22.3 (rs7739264) and 9p21.3 (rs1537377). All seven SNP effects were replicated in an independent cohort and associated at P <5 x 10(-8) in a combined analysis. Finally, we found a significant overlap in polygenic risk for endometriosis between the genome-wide association cohorts of European and Japanese descent (P = 8.8 x 10(-11)), indicating that many weakly associated SNPs represent true endometriosis risk loci and that risk prediction and future targeted disease therapy may be transferred across these populations.
Published: 2012

146. Genome-wide linkage and association analyses implicate FASN in predisposition to uterine leiomyomata

Author: Eggert, Stacey, Huyck, Karen, Somasundaram, Priya, Kavalla, Raghava, Stewart, Elizabeth, Lu, Ake, Painter, Jodie, Montgomery, Grant, Medland, Sarah, Nyholt, Dale, other, and, Eggert, Stacey, Huyck, Karen, Somasundaram, Priya, Kavalla, Raghava, Stewart, Elizabeth, Lu, Ake, Painter, Jodie, Montgomery, Grant, Medland, Sarah, Nyholt, Dale, and other, and
Abstract: Full-text article is free to read on the publisher's website Uterine leiomyomata (UL), the most prevalent pelvic tumors in women of reproductive age, pose a major public health problem given their high frequency, associated morbidities, and most common indication for hysterectomies. A genetic component to UL predisposition is supported by analyses of ethnic predisposition, twin studies, and familial aggregation. A genome-wide SNP linkage panel was genotyped and analyzed in 261 white UL-affected sister-pair families from the Finding Genes for Fibroids study. Two significant linkage regions were detected in 10p11 (LOD = 4.15) and 3p21 (LOD = 3.73), and five additional linkage regions were identified with LOD scores > 2.00 in 2q37, 5p13, 11p15, 12q14, and 17q25. Genome-wide association studies were performed in two independent cohorts of white women, and a meta-analysis was conducted. One SNP (rs4247357) was identified with a p value (p = 3.05 x 10(-8)) that reached genome-wide significance (odds ratio = 1.299). The candidate SNP is under a linkage peak and in a block of linkage disequilibrium in 17q25.3, which spans fatty acid synthase (FASN), coiled-coil-domain-containing 57 (CCDC57), and solute-carrier family 16, member 3 (SLC16A3). By tissue microarray immunohistochemistry, we found elevated (3-fold) FAS levels in UL-affected tissue compared to matched myometrial tissue. FAS transcripts and/or protein levels are upregulated in various neoplasms and implicated in tumor cell survival. FASN represents the initial UL risk allele identified in white women by a genome-wide, unbiased approach and opens a path to management and potential therapeutic intervention.
Published: 2012

147. High-density fine-mapping of a chromosome 10q26 linkage peak suggests association between endometriosis and variants close to CYP2C19

Author: Painter, Jodie, Nyholt, Dale, Morris, Andrew, Zhao, Zhen Zhen, Henders, Anjali, Lambert, Ann, Wallace, Leanne, Martin, Nicholas, Kennedy, Stephen, Treloar, Susan, Zondervan, Krina, Montgomery, Grant, Painter, Jodie, Nyholt, Dale, Morris, Andrew, Zhao, Zhen Zhen, Henders, Anjali, Lambert, Ann, Wallace, Leanne, Martin, Nicholas, Kennedy, Stephen, Treloar, Susan, Zondervan, Krina, and Montgomery, Grant
Abstract: OBJECTIVE:To refine a previously reported linkage peak for endometriosis on chromosome 10q26, and conduct follow-up analyses and a fine-mapping association study across the region to identify new candidate genes for endometriosis. DESIGN:Case-control study. SETTING:Academic research. PATIENT(S):Cases=3,223 women with surgically confirmed endometriosis; controls=1,190 women without endometriosis and 7,060 population samples. INTERVENTION(S):Analysis of 11,984 single nucleotide polymorphisms on chromosome 10. MAIN OUTCOME MEASURE(S):Allele frequency differences between cases and controls. RESULT(S):Linkage analyses on families grouped by endometriosis symptoms (primarily subfertility) provided increased evidence for linkage (logarithm of odds score=3.62) near a previously reported linkage peak. Three independent association signals were found at 96.59 Mb (rs11592737), 105.63 Mb (rs1253130), and 124.25 Mb (rs2250804). Analyses including only samples from linkage families supported the association at all three regions. However, only rs11592737 in the cytochrome P450 subfamily C (CYP2C19) gene was replicated in an independent sample of 2,079 cases and 7,060 population controls. CONCLUSION(S):The role of the CYP2C19 gene in conferring risk for endometriosis warrants further investigation.
Published: 2011

148. Variation in BMPR1B, TGFRB1 and BMPR2 and control of dizygotic twinning

Author: Luong, Hien, Chaplin, Justin, McRae, Allan, Medland, Sarah, Willemsen, Gonneke, Nyholt, Dale, Henders, Anjali, Hoekstra, Chantal, Duffy, David, Martin, Nicholas, Boomsma, Dorret, Montgomery, Grant, Painter, Jodie, Luong, Hien, Chaplin, Justin, McRae, Allan, Medland, Sarah, Willemsen, Gonneke, Nyholt, Dale, Henders, Anjali, Hoekstra, Chantal, Duffy, David, Martin, Nicholas, Boomsma, Dorret, Montgomery, Grant, and Painter, Jodie
Abstract: Free to read Genes in the TGF9 signaling pathway play important roles in the regulation of ovarian follicle growth and ovulation rate. Mutations in three genes in this pathway, growth differentiation factor 9 (GDF9), bone morphogenetic protein 15 (BMP15) and the bone morphogenetic protein receptor B 1 (BMPRB1), influence dizygotic (DZ) twinning rates in sheep. To date, only variants in GDF9 and BMP15, but not their receptors transforming growth factor ss receptor 1 (TGFBR1), bone morphogenetic protein receptor 2 (BMPR2) and BMPR1B, have been investigated with respect to their roles in human DZ twinning. We screened for rare and novel variants in TGFBR1, BMPR2 and BMPR1B in mothers of dizygotic twins (MODZT) from twin-dense families, and assessed association between genotyped and imputed variants and DZ twinning in another large sample of MODZT. Three novel variants were found: a deep intronic variant in BMPR2, and one intronic and one non-synonymous exonic variant in BMPRB1 which would result in the replacement of glutamine by glutamic acid at amino acid position 294 (p.Gln294Glu). None of these variants were predicted to have major impacts on gene function. However, the p.Gln294Glu variant changes the same amino acid as a sheep BMPR1B functional variant and may have functional consequences. Six BMPR1B variants were marginally associated with DZ twinning in the larger case-control sample, but these were no longer significant once multiple testing was taken into account. Our results suggest that variation in the TGF9 signaling pathway type II receptors has limited effects on DZ twinning rates in humans.
Published: 2011

149. Association mapping

Author: Painter, Jodie, Nyholt, Dale, Montgomery, Grant, Painter, Jodie, Nyholt, Dale, and Montgomery, Grant
Abstract: Association mapping seeks to identify marker alleles present at significantly different frequencies in cases carrying a particular disease or trait compared with controls. Genome-wide association studies are increasingly replacing candidate gene-based association studies for complex diseases, where a number of loci are likely to contribute to disease risk and the effect size of each particular risk allele is typically modest or low. Good study design is essential to the success of an association study, and factors such as the heritability of the disease under investigation, the choice of controls, statistical power, multiple testing and whether the association can be replicated need to be considered before beginning. Likewise, thorough quality control of the genotype data needs to be undertaken prior to running any association analyses. Finally, it should be kept in mind that a significant genetic association is not proof positive that a particular genetic locus causes a disease, but rather an important first step in discovering the genetic variants underlying a complex disease.
Published: 2011

150. Genome-wide association study identifies a locus at 7p15.2 associated with endometriosis

Author: Painter, Jodie, Anderson, Carl, Nyholt, Dale, Macgregor, Stuart, Lin, Jianghai, Lee, Sang Hong, Lambert, Ann, Zhao, Zhen Zhen, Roseman, Fenella, Guo, Qun, other, and, Painter, Jodie, Anderson, Carl, Nyholt, Dale, Macgregor, Stuart, Lin, Jianghai, Lee, Sang Hong, Lambert, Ann, Zhao, Zhen Zhen, Roseman, Fenella, Guo, Qun, and other, and
Abstract: Endometriosis is a common gynecological disease associated with pelvic pain and subfertility. We conducted a genome-wide association study (GWAS) in 3,194 individuals with surgically confirmed endometriosis (cases) and 7,060 controls from Australia and the UK. Polygenic predictive modeling showed significantly increased genetic loading among 1,364 cases with moderate to severe endometriosis. The strongest association signal was on 7p15.2 (rs12700667) for 'all' endometriosis (P = 2.6 x 10(-)(7), odds ratio (OR) = 1.22, 95% CI 1.13-1.32) and for moderate to severe disease (P = 1.5 x 10(-)(9), OR = 1.38, 95% CI 1.24-1.53). We replicated rs12700667 in an independent cohort from the United States of 2,392 self-reported, surgically confirmed endometriosis cases and 2,271 controls (P = 1.2 x 10(-)(3), OR = 1.17, 95% CI 1.06-1.28), resulting in a genome-wide significant P value of 1.4 x 10(-)(9) (OR = 1.20, 95% CI 1.13-1.27) for 'all' endometriosis in our combined datasets of 5,586 cases and 9,331 controls. rs12700667 is located in an intergenic region upstream of the plausible candidate genes NFE2L3 and HOXA10.
Published: 2011

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