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2. Dose–Response Associations Between Diet and Risk of Rheumatoid Arthritis: A Meta-Analysis of Prospective Cohort Studies.

Author

Dong, Yuanyuan, Greenwood, Darren C., Webster, James, Uzokwe, Chinwe, Tao, Jinhui, Hardie, Laura J., and Cade, Janet E.

Abstract

To provide a systematic and quantitative summary of dietary factors and rheumatoid arthritis (RA) risk. A systematic review and meta-analysis included prospective cohort studies from 2000 to 2024 reporting relative risks (RRs) with 95% confidence intervals (CIs) for RA incidence relating to 32 different dietary exposures. Linear and non-linear dose–response analyses were conducted. Thirty studies were included, involving 2,986,747 participants with 9,677 RA cases. Linear dose–response analysis suggested that each 2-unit per week increase in total alcohol intake was linked to 4% risk reduction (RR (95%-CI), heterogeneity (I2), NutriGrade score: 0.96 (0.94, 0.98), 58%, moderate certainty), and beer consumption was associated with a 10% reduction per 2 units/week increase (0.90 (0.84, 0.97), 0%, very low certainty). Each 2-unit/week increase in total alcohol intake was associated with a 3% decrease in seropositive RA risk (0.97 (0.96, 0.99), 28%, moderate certainty). Increased intakes of fruit (per 80 g/day) and cereals (per 30 g/day) were associated with 5% (0.95 (0.92, 0.99), 57%, moderate certainty) and 3% (0.97 (0.96, 0.99), 20%, moderate certainty) reduced risk, respectively. Conversely, tea consumption showed a 4% increased risk per additional cup/day (1.04 (1.02, 1.05), 0%, moderate certainty). Non-linear associations were observed for total coffee, vegetables, oily fish, and vitamin D supplementation. Data on dietary patterns and specific micronutrients were limited. The findings suggest that moderate alcohol consumption and a higher intake of fruits, oily fish, and cereals are associated with a reduced risk of RA, while tea and coffee may be linked to an increased risk. Optimising dietary intake of certain food components may reduce RA risk, despite moderate-quality evidence. [ABSTRACT FROM AUTHOR]

Published
2024
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4. Association Between Levels of Sex Hormones and Risk of Esophageal Adenocarcinoma and Barrett’s Esophagus

Author

Xie, Shao-Hua, Fang, Rui, Huang, Mingtao, Dai, Juncheng, Thrift, Aaron P., Anderson, Lesley A., Chow, Wong-Ho, Bernstein, Leslie, Gammon, Marilie D., Risch, Harvey A., Shaheen, Nicholas J., Reid, Brian J., Wu, Anna H., Iyer, Prasad G., Liu, Geoffrey, Corley, Douglas A., Whiteman, David C., Caldas, Carlos, Pharoah, Paul D., Hardie, Laura J., Fitzgerald, Rebecca C., Shen, Hongbing, Vaughan, Thomas L., and Lagergren, Jesper

Published
2020
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7. Interactions Between Genetic Variants and Environmental Factors Affect Risk of Esophageal Adenocarcinoma and Barrett’s Esophagus

Author

Dong, Jing, Levine, David M., Buas, Matthew F., Zhang, Rui, Onstad, Lynn, Fitzgerald, Rebecca C., Corley, Douglas A., Shaheen, Nicholas J., Lagergren, Jesper, Hardie, Laura J., Reid, Brian J., Iyer, Prasad G., Risch, Harvey A., Caldas, Carlos, Caldas, Isabel, Pharoah, Paul D., Liu, Geoffrey, Gammon, Marilie D., Chow, Wong-Ho, Bernstein, Leslie, Bird, Nigel C., Ye, Weimin, Wu, Anna H., Anderson, Lesley A., MacGregor, Stuart, Whiteman, David C., Vaughan, Thomas L., and Thrift, Aaron P.

Published
2018
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8. Determining Risk of Barrett’s Esophagus and Esophageal Adenocarcinoma Based on Epidemiologic Factors and Genetic Variants

Author

Dong, Jing, Buas, Matthew F., Gharahkhani, Puya, Kendall, Bradley J., Onstad, Lynn, Zhao, Shanshan, Anderson, Lesley A., Wu, Anna H., Ye, Weimin, Bird, Nigel C., Bernstein, Leslie, Chow, Wong-Ho, Gammon, Marilie D., Liu, Geoffrey, Caldas, Carlos, Pharoah, Paul D., Risch, Harvey A., Iyer, Prasad G., Reid, Brian J., Hardie, Laura J., Lagergren, Jesper, Shaheen, Nicholas J., Corley, Douglas A., Fitzgerald, Rebecca C., Whiteman, David C., Vaughan, Thomas L., and Thrift, Aaron P.

Published
2018
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9. Maternal iodine status in a multi-ethnic UK birth cohort: associations with autism spectrum disorder

Author

Cromie, Kirsten Jade, Threapleton, Diane Erin, Snart, Charles Jonathan Peter, Taylor, Elizabeth, Mason, Dan, Wright, Barry, Kelly, Brian, Reid, Stephen, Azad, Rafaq, Keeble, Claire, Waterman, Amanda H., Meadows, Sarah, McKillion, Amanda, Alwan, Nisreen A., Cade, Janet Elizabeth, Simpson, Nigel A. B., Stewart, Paul M., Zimmermann, Michael, Wright, John, Waiblinger, Dagmar, Mon-Williams, Mark, Hardie, Laura J., and Greenwood, Darren Charles

Published
2020
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10. Maternal iodine status, intrauterine growth, birth outcomes and congenital anomalies in a UK birth cohort

Author

Snart, Charles Jonathan Peter, Threapleton, Diane Erin, Keeble, Claire, Taylor, Elizabeth, Waiblinger, Dagmar, Reid, Stephen, Alwan, Nisreen A., Mason, Dan, Azad, Rafaq, Cade, Janet Elizabeth, Simpson, Nigel A. B., Meadows, Sarah, McKillion, Amanda, Santorelli, Gillian, Waterman, Amanda H., Zimmermann, Michael, Stewart, Paul M., Wright, John, Mon-Williams, Mark, Greenwood, Darren Charles, and Hardie, Laura J.

Published
2020
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11. Genome-wide association studies in oesophageal adenocarcinoma and Barrett's oesophagus: a large-scale meta-analysis

Author

Gharahkhani, Puya, Fitzgerald, Rebecca C, Vaughan, Thomas L, Palles, Claire, Gockel, Ines, Tomlinson, Ian, Buas, Matthew F, May, Andrea, Gerges, Christian, Anders, Mario, Becker, Jessica, Kreuser, Nicole, Noder, Tania, Venerito, Marino, Veits, Lothar, Schmidt, Thomas, Manner, Hendrik, Schmidt, Claudia, Hess, Timo, Böhmer, Anne C, Izbicki, Jakob R, Hölscher, Arnulf H, Lang, Hauke, Lorenz, Dietmar, Schumacher, Brigitte, Hackelsberger, Andreas, Mayershofer, Rupert, Pech, Oliver, Vashist, Yogesh, Ott, Katja, Vieth, Michael, Weismüller, Josef, Nöthen, Markus M, Attwood, Stephen, Barr, Hugh, Chegwidden, Laura, de Caestecker, John, Harrison, Rebecca, Love, Sharon B, MacDonald, David, Moayyedi, Paul, Prenen, Hans, Watson, R G Peter, Iyer, Prasad G, Anderson, Lesley A, Bernstein, Leslie, Chow, Wong-Ho, Hardie, Laura J, Lagergren, Jesper, Liu, Geoffrey, Risch, Harvey A, Wu, Anna H, Ye, Weimin, Bird, Nigel C, Shaheen, Nicholas J, Gammon, Marilie D, Corley, Douglas A, Caldas, Carlos, Moebus, Susanne, Knapp, Michael, Peters, Wilbert H M, Neuhaus, Horst, Rösch, Thomas, Ell, Christian, MacGregor, Stuart, Pharoah, Paul, Whiteman, David C, Jankowski, Janusz, and Schumacher, Johannes

Published
2016
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13. Supplementary Figure legends from A Newly Identified Susceptibility Locus near FOXP1 Modifies the Association of Gastroesophageal Reflux with Barrett's Esophagus

Author

Dai, James Y., primary, de Dieu Tapsoba, Jean, primary, Buas, Matthew F., primary, Onstad, Lynn E., primary, Levine, David M., primary, Risch, Harvey A., primary, Chow, Wong-Ho, primary, Bernstein, Leslie, primary, Ye, Weimin, primary, Lagergren, Jesper, primary, Bird, Nigel C., primary, Corley, Douglas A., primary, Shaheen, Nicholas J., primary, Wu, Anna H., primary, Reid, Brian J., primary, Hardie, Laura J., primary, Whiteman, David C., primary, and Vaughan, Thomas L., primary

Published
2023
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14. Supplementary figure 1 from A Newly Identified Susceptibility Locus near FOXP1 Modifies the Association of Gastroesophageal Reflux with Barrett's Esophagus

Author

Dai, James Y., primary, de Dieu Tapsoba, Jean, primary, Buas, Matthew F., primary, Onstad, Lynn E., primary, Levine, David M., primary, Risch, Harvey A., primary, Chow, Wong-Ho, primary, Bernstein, Leslie, primary, Ye, Weimin, primary, Lagergren, Jesper, primary, Bird, Nigel C., primary, Corley, Douglas A., primary, Shaheen, Nicholas J., primary, Wu, Anna H., primary, Reid, Brian J., primary, Hardie, Laura J., primary, Whiteman, David C., primary, and Vaughan, Thomas L., primary

Published
2023
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15. Data from Pleiotropic Analysis of Cancer Risk Loci on Esophageal Adenocarcinoma Risk

Author

Lee, Eunjung, primary, Stram, Daniel O., primary, Ek, Weronica E., primary, Onstad, Lynn E., primary, MacGregor, Stuart, primary, Gharahkhani, Puya, primary, Ye, Weimin, primary, Lagergren, Jesper, primary, Shaheen, Nicholas J., primary, Murray, Liam J., primary, Hardie, Laura J., primary, Gammon, Marilie D., primary, Chow, Wong-Ho, primary, Risch, Harvey A., primary, Corley, Douglas A., primary, Levine, David M., primary, Whiteman, David C., primary, Bernstein, Leslie, primary, Bird, Nigel C., primary, Vaughan, Thomas L., primary, and Wu, Anna H., primary

Published
2023
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16. Data from A Newly Identified Susceptibility Locus near FOXP1 Modifies the Association of Gastroesophageal Reflux with Barrett's Esophagus

Author

Dai, James Y., primary, de Dieu Tapsoba, Jean, primary, Buas, Matthew F., primary, Onstad, Lynn E., primary, Levine, David M., primary, Risch, Harvey A., primary, Chow, Wong-Ho, primary, Bernstein, Leslie, primary, Ye, Weimin, primary, Lagergren, Jesper, primary, Bird, Nigel C., primary, Corley, Douglas A., primary, Shaheen, Nicholas J., primary, Wu, Anna H., primary, Reid, Brian J., primary, Hardie, Laura J., primary, Whiteman, David C., primary, and Vaughan, Thomas L., primary

Published
2023
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18. Polymorphisms Near TBX5 and GDF7 Are Associated With Increased Risk for Barrett’s Esophagus

Author

Palles, Claire, Chegwidden, Laura, Li, Xinzhong, Findlay, John M., Farnham, Garry, Castro Giner, Francesc, Peppelenbosch, Maikel P., Kovac, Michal, Adams, Claire L., Prenen, Hans, Briggs, Sarah, Harrison, Rebecca, Sanders, Scott, MacDonald, David, Haigh, Chris, Tucker, Art, Love, Sharon, Nanji, Manoj, deCaestecker, John, Ferry, David, Rathbone, Barrie, Hapeshi, Julie, Barr, Hugh, Moayyedi, Paul, Watson, Peter, Zietek, Barbara, Maroo, Neera, Gay, Laura, Underwood, Tim, Boulter, Lisa, McMurtry, Hugh, Monk, David, Patel, Praful, Ragunath, Krish, Al Dulaimi, David, Murray, Iain, Koss, Konrad, Veitch, Andrew, Trudgill, Nigel, Nwokolo, Chuka, Rembacken, Bjorn, Atherfold, Paul, Green, Elaine, Ang, Yeng, Kuipers, Ernst J., Chow, Wu, Paterson, Stuart, Kadri, Sudarshan, Beales, Ian, Grimley, Charles, Mullins, Paul, Beckett, Conrad, Farrant, Mark, Dixon, Andrew, Kelly, Sean, Johnson, Matthew, Wajed, Shahjehan, Dhar, Anjan, Sawyer, Elinor, Roylance, Rebecca, Onstad, Lynn, Gammon, Marilie D., Corley, Douglas A., Shaheen, Nicholas J., Bird, Nigel C., Hardie, Laura J., Reid, Brian J., Ye, Weimin, Liu, Geoffrey, Romero, Yvonne, Bernstein, Leslie, Wu, Anna H., Casson, Alan G., Fitzgerald, Rebecca, Whiteman, David C., Risch, Harvey A., Levine, David M., Vaughan, Tom L., Verhaar, Auke P., van den Brande, Jan, Toxopeus, Eelke L., Spaander, Manon C., Wijnhoven, Bas P.L., van der Laan, Luc J.W., Krishnadath, Kausilia, Wijmenga, Cisca, Trynka, Gosia, McManus, Ross, Reynolds, John V., O’Sullivan, Jacintha, MacMathuna, Padraic, McGarrigle, Sarah A., Kelleher, Dermot, Vermeire, Severine, Cleynen, Isabelle, Bisschops, Raf, Tomlinson, Ian, and Jankowski, Janusz

Published
2015
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19. The effects of dietary vitamins, lipids and temperature on teleost immunity

Author

Hardie, Laura J.

Subjects
590, Fish immunology
Abstract

Singular or dual dietary depletions of vitamins C and E in Atlantic salmon parr increased susceptibility to Aeromonas salmonicida challenge. An array of immune parameters were evaluated to identify the involvement of these vitamin depletions on the immune response. Dietary vitamin E levels in salmon had no impact on haematological parameters, total serum protein or lysozyme levels. Similarly, dietary vitamin E levels did not affect leucocyte antibody production, macrophage activating factor (MAF) release and respiratory burst (RB) phenomena. However, haemolytic and opsonic properties of complement were compromised in vitamin E depleted salmon. Parenteral administration of vitamin E to vitamin E depleted carp did not elevate phytohaemagglutinin (PHA) lymphocyte proliferation responses or complement activity. In vitro additions of vitamin E to lymphocytes from carp fed a commercial diet did not elevate PHA proliferation responses either. The increased disease susceptibility provoked by dietary vitamin C restriction in Atlantic salmon was not correlated with serum protein levels, differential leucocyte numbers or phagocyte functions as tested by RB activity or phagocytosis by macrophages. Lymphocyte functions were operational in these fish as examined by MAF secretion and antibody production. Analogous to vitamin E depletion, dietary vitamin C restriction in salmon compromised complement haemolytic activity. Elevating the vitamin C content of diets above normal levels enhanced complement activity in salmon. Vitamin C was a potent modulator of rainbow trout leucocyte functions. In vitro supplementation of vitamin C in the sodium (NaAsc) or polyphosphate (PPAsc) form was required for PHA-proliferation responses. MAF secretion was also augmented by in vitro additions of NaAsc to leucocytes obtained from vitamin C depleted trout. Injecting NaAsc into depleted fish elevated PHA proliferation responses compared with saline-injected controls. Leucocytes from the latter group could recover proliferative responses to levels associated with NaAsc-injected fish with in vitro additions of 1x10-3 and 1x10-4M PPAsc. Increased disease susceptibility, reduced complement activity and haematocrit values were symptomatic of combined dietary vitamin C and E depletion in salmon parr. Total and differential leucocyte numbers, or serum parameters including antiprotease activity and total protein level were unaffected by this dietary regime. Although poorly adherent, macrophages obtained from dually depleted salmon had similar RB values and expressed greater responsiveness to a MAF-containing supernatant than vitamin sufficient counterparts. Lymphocyte functions were impervious to dual vitamin depletion as antibody and MAF production responses were intact. In vitro additions of NaAsc and PPAsc were shown to elevate RB responses in macrophages from vitamin-restricted and -adequate salmon. MAF secretion was demonstrated to be a temperature-dependent phenomenon in rainbow trout leucocytes. After 48h acclimation at low in vitro temperatures (6 C), leucocytes obtained from trout at 14C expressed impoverished MAF production. Acclimation of trout to 7 C did riot rescue MAF production. Also, normal RB activity was reduced in macrophages obtained from fish at 14 C after 48h at 6 C in vitro. However, if allowed to acclimate, these macrophages become more responsive to MAF and recovered RB activity to levels associated with macrophages held at 10 and 18C. RB responses of macrophages from fish at 7 C functioned equally well across a wide range of in vitro temperature regimes. Phagocytic activity of macrophages obtained from fish at 14 C and placed at 6 C in vitro for 48h expressed temperature sensitivity. This was especially apparent in fish fed a dietary ?-3/?-6 fatty acid ratio of 2.0. However, this dietary regime also elevated phagocytic activity of these macrophages to such an extent, that their response surpassed that of macrophages from fish fed commercial diets or ?-3/?-6 ratios of 0.5 and 1 even at low in vitro temperatures.

Published
1991

20. Risk of Esophageal Adenocarcinoma Decreases With Height, Based on Consortium Analysis and Confirmed by Mendelian Randomization

Author

Thrift, Aaron P., Risch, Harvey A., Onstad, Lynn, Shaheen, Nicholas J., Casson, Alan G., Bernstein, Leslie, Corley, Douglas A., Levine, David M., Chow, Wong–Ho, Reid, Brian J., Romero, Yvonne, Hardie, Laura J., Liu, Geoffrey, Wu, Anna H., Bird, Nigel C., Gammon, Marilie D., Ye, Weimin, Whiteman, David C., and Vaughan, Thomas L.

Published
2014
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21. Maternal diet, prenatal exposure to dioxin-like compounds and birth outcomes in a European prospective mother–child study (NewGeneris)

Author

Papadopoulou, Eleni, Kogevinas, Manolis, Botsivali, Maria, Pedersen, Marie, Besselink, Harrie, Mendez, Michelle A., Fleming, Sarah, Hardie, Laura J., Knudsen, Lisbeth E., Wright, John, Agramunt, Silvia, Sunyer, Jordi, Granum, Berit, Gutzkow, Kristine B., Brunborg, Gunnar, Alexander, Jan, Meltzer, Helle Margrete, Brantsæter, Anne Lise, Sarri, Katerina, Chatzi, Leda, Merlo, Domenico F., Kleinjans, Jos C., and Haugen, Margaretha

Published
2014
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22. In Utero Exposure to Compounds with Dioxin-like Activity and Birth Outcomes

Author

The NewGeneris Consortium, Vafeiadi, Marina, Agramunt, Silvia, Pedersen, Marie, Besselink, Harrie, Chatzi, Leda, Fthenou, Eleni, Fleming, Sarah, Hardie, Laura J., Wright, John, Knudsen, Lisbeth E., Nielsen, Jeanette K.S., Sunyer, Jordi, Carreras, Ramon, Brunborg, Gunnar, Gutzkow, Kristine B., Nygaard, Unni C., Løvik, Martinus, Kyrtopoulos, Soterios A., Segerbäck, Dan, Merlo, Domenico F., Kleinjans, Jos C., Vrijheid, Martine, and Kogevinas, Manolis

Published
2014

23. Validity of an online 24-h recall tool (myfood24) for dietary assessment in population studies: comparison with biomarkers and standard interviews

Author

Wark, Petra A., Hardie, Laura J., Frost, Gary S., Alwan, Nisreen A., Carter, Michelle, Elliott, Paul, Ford, Heather E., Hancock, Neil, Morris, Michelle A., Mulla, Umme Z., Noorwali, Essra A., Petropoulou, K., Murphy, David, Potter, Gregory D. M., Riboli, Elio, Greenwood, Darren C., and Cade, Janet E.

Published
2018
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24. eQTL Set-Based Association Analysis Identifies Novel Susceptibility Loci for Barrett Esophagus and Esophageal Adenocarcinoma

Author

Wang, Xiaoyu, Gharahkhani, Puya, Levine, David M., Fitzgerald, Rebecca C., Gockel, Ines, Corley, Douglas A., Risch, Harvey A., Bernstein, Leslie, Chow, Wong-Ho, Onstad, Lynn, Shaheen, Nicholas J., Lagergren, Jesper, Hardie, Laura J., Wu, Anna H., Pharoah, Paul D. P., Liu, Geoffrey, Anderson, Lesley A., Iyer, Prasad G., Gammon, Marilie D., Caldas, Carlos, Ye, Weimin, Barr, Hugh, Moayyedi, Paul, Harrison, Rebecca, Watson, R. G. Peter, Attwood, Stephen, Chegwidden, Laura, Love, Sharon B., MacDonald, David, DeCaestecker, John, Prenen, Hans, Ott, Katja, Moebus, Susanne, Venerito, Marino, Lang, Hauke, Mayershofer, Rupert, Knapp, Michael, Veits, Lothar, Gerges, Christian, Weismueller, Josef, Reeh, Matthias, Noethen, Markus M., Izbicki, Jakob R., Manner, Hendrik, Neuhaus, Horst, Roesch, Thomas, Boehmer, Anne C., Hoelscher, Arnulf H., Anders, Mario, Pech, Oliver, Schumacher, Brigitte, Schmidt, Claudia, Schmidt, Thomas, Noder, Tania, Lorenz, Dietmar, Vieth, Michael, May, Andrea, Hess, Timo, Kreuser, Nicole, Becker, Jessica, Ell, Christian, Tomlinson, Ian, Palles, Claire, Jankowski, Janusz A., Whiteman, David C., MacGregor, Stuart, Schumacher, Johannes, Vaughan, Thomas L., Buas, Matthew F., Dai, James Y., Wang, Xiaoyu, Gharahkhani, Puya, Levine, David M., Fitzgerald, Rebecca C., Gockel, Ines, Corley, Douglas A., Risch, Harvey A., Bernstein, Leslie, Chow, Wong-Ho, Onstad, Lynn, Shaheen, Nicholas J., Lagergren, Jesper, Hardie, Laura J., Wu, Anna H., Pharoah, Paul D. P., Liu, Geoffrey, Anderson, Lesley A., Iyer, Prasad G., Gammon, Marilie D., Caldas, Carlos, Ye, Weimin, Barr, Hugh, Moayyedi, Paul, Harrison, Rebecca, Watson, R. G. Peter, Attwood, Stephen, Chegwidden, Laura, Love, Sharon B., MacDonald, David, DeCaestecker, John, Prenen, Hans, Ott, Katja, Moebus, Susanne, Venerito, Marino, Lang, Hauke, Mayershofer, Rupert, Knapp, Michael, Veits, Lothar, Gerges, Christian, Weismueller, Josef, Reeh, Matthias, Noethen, Markus M., Izbicki, Jakob R., Manner, Hendrik, Neuhaus, Horst, Roesch, Thomas, Boehmer, Anne C., Hoelscher, Arnulf H., Anders, Mario, Pech, Oliver, Schumacher, Brigitte, Schmidt, Claudia, Schmidt, Thomas, Noder, Tania, Lorenz, Dietmar, Vieth, Michael, May, Andrea, Hess, Timo, Kreuser, Nicole, Becker, Jessica, Ell, Christian, Tomlinson, Ian, Palles, Claire, Jankowski, Janusz A., Whiteman, David C., MacGregor, Stuart, Schumacher, Johannes, Vaughan, Thomas L., Buas, Matthew F., and Dai, James Y.

Abstract

Background: Over 20 susceptibility single-nucleotide poly-morphisms (SNP) have been identified for esophageal adenocarcinoma (EAC) and its precursor, Barrett esophagus (BE), explaining a small portion of heritability.Methods: Using genetic data from 4,323 BE and 4,116 EAC patients aggregated by international consortia including the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON), we conducted a comprehensive transcriptome-wide association study (TWAS) for BE/EAC, leveraging Genotype Tissue Expression (GTEx) gene-expression data from six tissue types of plausible relevance to EAC etiology: mucosa and muscularis from the esophagus, gastroesophageal (GE) junction, stomach, whole blood, and visceral adipose. Two analytical approaches were taken: standard TWAS using the predicted gene expression from local expression quantitative trait loci (eQTL), and set-based SKAT association using selected eQTLs that predict the gene expression. Results: Although the standard approach did not identify significant signals, the eQTL set-based approach identified eight novel associations, three of which were validated in independent external data (eQTL SNP sets for EXOC3, ZNF641, and HSP90AA1). Conclusions: This study identified novel genetic susceptibility loci for EAC and BE using an eQTL set-based genetic association approach.Impact: This study expanded the pool of genetic susceptibility loci for EAC and BE, suggesting the potential of the eQTL set-based genetic association approach as an alternative method for TWAS analysis.

Published
2022

25. Germline variation in inflammation-related pathways and risk of Barrettʼs oesophagus and oesophageal adenocarcinoma

Author

Buas, Matthew F, He, Qianchuan, Johnson, Lisa G, Onstad, Lynn, Levine, David M, Thrift, Aaron P, Gharahkhani, Puya, Palles, Claire, Lagergren, Jesper, Fitzgerald, Rebecca C, Ye, Weimin, Caldas, Carlos, Bird, Nigel C, Shaheen, Nicholas J, Bernstein, Leslie, Gammon, Marilie D, Wu, Anna H, Hardie, Laura J, Pharoah, Paul D, Liu, Geoffrey, Iyer, Prassad, Corley, Douglas A, Risch, Harvey A, Chow, Wong-Ho, Prenen, Hans, Chegwidden, Laura, Love, Sharon, Attwood, Stephen, Moayyedi, Paul, MacDonald, David, Harrison, Rebecca, Watson, Peter, Barr, Hugh, deCaestecker, John, Tomlinson, Ian, Jankowski, Janusz, Whiteman, David C, MacGregor, Stuart, Vaughan, Thomas L, and Madeleine, Margaret M

Published
2017
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26. Birth Weight, Head Circumference, and Prenatal Exposure to Acrylamide from Maternal Diet: The European Prospective Mother—Child Study (NewGeneris)

Author

NewGeneris Consortium, Pedersen, Marie, von Stedingk, Hans, Botsivali, Maria, Agramunt, Silvia, Alexander, Jan, Brunborg, Gunnar, Chatzi, Leda, Fleming, Sarah, Fthenou, Eleni, Granum, Berit, Gutzkow, Kristine B., Hardie, Laura J., Knudsen, Lisbeth E., Kyrtopoulos, Soterios A., Mendez, Michelle A., Merlo, Domenico F., Nielsen, Jeanette K., Rydberg, Per, Segerbäck, Dan, Sunyer, Jordi, Wright, John, Törnqvist, Margareta, Kleinjans, Jos C., and Kogevinas, Manolis

Published
2012

27. eQTL Set–Based Association Analysis Identifies Novel Susceptibility Loci for Barrett Esophagus and Esophageal Adenocarcinoma

Author

Wang, Xiaoyu, primary, Gharahkhani, Puya, additional, Levine, David M., additional, Fitzgerald, Rebecca C., additional, Gockel, Ines, additional, Corley, Douglas A., additional, Risch, Harvey A., additional, Bernstein, Leslie, additional, Chow, Wong-Ho, additional, Onstad, Lynn, additional, Shaheen, Nicholas J., additional, Lagergren, Jesper, additional, Hardie, Laura J., additional, Wu, Anna H., additional, Pharoah, Paul D.P., additional, Liu, Geoffrey, additional, Anderson, Lesley A., additional, Iyer, Prasad G., additional, Gammon, Marilie D., additional, Caldas, Carlos, additional, Ye, Weimin, additional, Barr, Hugh, additional, Moayyedi, Paul, additional, Harrison, Rebecca, additional, Watson, R.G. Peter, additional, Attwood, Stephen, additional, Chegwidden, Laura, additional, Love, Sharon B., additional, MacDonald, David, additional, deCaestecker, John, additional, Prenen, Hans, additional, Ott, Katja, additional, Moebus, Susanne, additional, Venerito, Marino, additional, Lang, Hauke, additional, Mayershofer, Rupert, additional, Knapp, Michael, additional, Veits, Lothar, additional, Gerges, Christian, additional, Weismüller, Josef, additional, Reeh, Matthias, additional, Nöthen, Markus M., additional, Izbicki, Jakob R., additional, Manner, Hendrik, additional, Neuhaus, Horst, additional, Rösch, Thomas, additional, Böhmer, Anne C., additional, Hölscher, Arnulf H., additional, Anders, Mario, additional, Pech, Oliver, additional, Schumacher, Brigitte, additional, Schmidt, Claudia, additional, Schmidt, Thomas, additional, Noder, Tania, additional, Lorenz, Dietmar, additional, Vieth, Michael, additional, May, Andrea, additional, Hess, Timo, additional, Kreuser, Nicole, additional, Becker, Jessica, additional, Ell, Christian, additional, Tomlinson, Ian, additional, Palles, Claire, additional, Jankowski, Janusz A., additional, Whiteman, David C., additional, MacGregor, Stuart, additional, Schumacher, Johannes, additional, Vaughan, Thomas L., additional, Buas, Matthew F., additional, and Dai, James Y., additional

Published
2022
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28. Polymorphisms in genes in the androgen pathway and risk of Barrettʼs esophagus and esophageal adenocarcinoma

Author

Ek, Weronica E., Lagergren, Katarina, Cook, Michael, Wu, Anna H., Abnet, Christian C., Levine, David, Chow, Wong-Ho, Bernstein, Leslie, Risch, Harvey A., Shaheen, Nicholas J., Bird, Nigel C., Corley, Douglas A., Hardie, Laura J., Fitzgerald, Rebecca C., Gammon, Marilie D., Romero, Yvonne, Liu, Geoffrey, Ye, Weimin, Vaughan, Thomas L., MacGregor, Stuart, Whiteman, David C., Westberg, Lars, and Lagergren, Jesper

Published
2016
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30. Obesity and Risk of Esophageal Adenocarcinoma and Barrett’s Esophagus: A Mendelian Randomization Study

Author

Thrift, Aaron P., Shaheen, Nicholas J., Gammon, Marilie D., Bernstein, Leslie, Reid, Brian J., Onstad, Lynn, Risch, Harvey A., Liu, Geoffrey, Bird, Nigel C., Wu, Anna H., Corley, Douglas A., Romero, Yvonne, Chanock, Stephen J., Chow, Wong-Ho, Casson, Alan G., Levine, David M., Zhang, Rui, Ek, Weronica E., MacGregor, Stuart, Ye, Weimin, Hardie, Laura J., Vaughan, Thomas L., and Whiteman, David C.

Published
2014
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32. A comprehensive re-assessment of the association between vitamin D and cancer susceptibility using Mendelian randomization

Author

Ong, Jue-Sheng, Dixon-Suen, Suzanne C., Han, Xikun, An, Jiyuan, Liyanage, Upekha, Dusingize, Jean-Cluade, Schumacher, Johannes, Gockel, Ines, Böhmer, Anne, Jankowski, Janusz, Palles, Claire, O’Mara, Tracy, Spurdle, Amanda, Law, Matthew H., Iles, Mark M., Pharoah, Paul, Berchuck, Andrew, Zheng, Wei, Thrift, Aaron P., Olsen, Catherine, Neale, Rachel E., Gharahkhani, Puya, Webb, Penelope M., MacGregor, Stuart, Fitzgerald, Rebecca, Buas, Matt, Gammon, Marilie D., Corley, Douglas A., Shaheen, Nicholas J., Hardie, Laura J., Bird, Nigel C., Reid, Brian J., Chow, Wong-Ho, Risch, Harvey A., Ye, Weimin, Liu, Geoffrey, Romero, Yvonne, Bernstein, Leslie, Wu, Anna H., Whiteman, David E., Vaughan, Thomas, Agee, M., Alipanahi, B., Auton, A., Bell, R. K., Bryc, K., Elson, S. L., Fontanillas, P., Furlotte, N. A., Hinds, D. A., Huber, K. E., Kleinman, A., Litterman, N. K., McIntyre, M. H., Mountain, J. L., Noblin, E. S., Northover, C. A. M., Pitts, S. J., Sathirapongsasuti, J. Fah, Sazonova, O. V., Shelton, J. F., Shringarpure, S., Tian, C., Tung, J. Y., Vacic, V., Wilson, C. H., Ong, Jue-Sheng [0000-0002-6062-710X], Dixon-Suen, Suzanne C. [0000-0003-3714-8386], Han, Xikun [0000-0002-3823-7308], Gockel, Ines [0000-0001-7423-713X], Böhmer, Anne [0000-0002-5716-786X], O’Mara, Tracy [0000-0002-5436-3232], Spurdle, Amanda [0000-0003-1337-7897], Law, Matthew H. [0000-0002-4303-8821], Iles, Mark M. [0000-0002-2603-6509], Pharoah, Paul [0000-0001-8494-732X], Zheng, Wei [0000-0003-1226-070X], Thrift, Aaron P. [0000-0002-0084-5308], Olsen, Catherine [0000-0003-4483-1888], Gharahkhani, Puya [0000-0002-4203-5952], Webb, Penelope M. [0000-0003-0733-5930], MacGregor, Stuart [0000-0001-6731-8142], and Apollo - University of Cambridge Repository

Subjects
631/67/68, 45/43, article, 692/699/67/2195, 692/4028/67/2324
Abstract

Previous Mendelian randomization (MR) studies on 25-hydroxyvitamin D (25(OH)D) and cancer have typically adopted a handful of variants and found no relationship between 25(OH)D and cancer; however, issues of horizontal pleiotropy cannot be reliably addressed. Using a larger set of variants associated with 25(OH)D (74 SNPs, up from 6 previously), we perform a unified MR analysis to re-evaluate the relationship between 25(OH)D and ten cancers. Our findings are broadly consistent with previous MR studies indicating no relationship, apart from ovarian cancers (OR 0.89; 95% C.I: 0.82 to 0.96 per 1 SD change in 25(OH)D concentration) and basal cell carcinoma (OR 1.16; 95% C.I.: 1.04 to 1.28). However, after adjustment for pigmentation related variables in a multivariable MR framework, the BCC findings were attenuated. Here we report that lower 25(OH)D is unlikely to be a causal risk factor for most cancers, with our study providing more precise confidence intervals than previously possible.

Published
2021
Full Text
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33. Germline variation in the insulin-like growth factor pathway and risk of Barrett's esophagus and esophageal adenocarcinoma

Author

Dighe, Shruti G., Chen, Jianhong, Yan, Li, He, Qianchuan, Gharahkhani, Puya, Onstad, Lynn, Levine, David M., Palles, Claire, Ye, Weimin, Gammon, Marilie D., Iyer, Prasad G., Anderson, Lesley A., Liu, Geoffrey, Wu, Anna H., Dai, James Y., Chow, Wong-Ho, Risch, Harvey A., Lagergren, Jesper, Shaheen, Nicholas J., Bernstein, Leslie, Corley, Douglas A., Prenen, Hans, DeCaestecker, John, MacDonald, David, Moayyedi, Paul, Barr, Hugh, Love, Sharon B., Chegwidden, Laura, Attwood, Stephen, Watson, Peter, Harrison, Rebecca, Ott, Katja, Moebus, Susanne, Venerito, Marino, Lang, Hauke, Mayershofer, Rupert, Knapp, Michael, Veits, Lothar, Gerges, Christian, Weismueller, Josef, Gockel, Ines, Vashist, Yogesh, Noethen, Markus M., Izbicki, Jakob R., Manner, Hendrik, Neuhaus, Horst, Roesch, Thomas, Boehmer, Anne C., Hoelscher, Arnulf H., Anders, Mario, Pech, Oliver, Schumacher, Brigitte, Schmidt, Claudia, Schmidt, Thomas, Noder, Tania, Lorenz, Dietmar, Vieth, Michael, May, Andrea, Hess, Timo, Kreuser, Nicole, Becker, Jessica, Ell, Christian, Ambrosone, Christine B., Moysich, Kirsten B., MacGregor, Stuart, Tomlinson, Ian, Whiteman, David C., Jankowski, Janusz, Schumacher, Johannes, Vaughan, Thomas L., Madeleine, Margaret M., Hardie, Laura J., Buas, Matthew F., Dighe, Shruti G., Chen, Jianhong, Yan, Li, He, Qianchuan, Gharahkhani, Puya, Onstad, Lynn, Levine, David M., Palles, Claire, Ye, Weimin, Gammon, Marilie D., Iyer, Prasad G., Anderson, Lesley A., Liu, Geoffrey, Wu, Anna H., Dai, James Y., Chow, Wong-Ho, Risch, Harvey A., Lagergren, Jesper, Shaheen, Nicholas J., Bernstein, Leslie, Corley, Douglas A., Prenen, Hans, DeCaestecker, John, MacDonald, David, Moayyedi, Paul, Barr, Hugh, Love, Sharon B., Chegwidden, Laura, Attwood, Stephen, Watson, Peter, Harrison, Rebecca, Ott, Katja, Moebus, Susanne, Venerito, Marino, Lang, Hauke, Mayershofer, Rupert, Knapp, Michael, Veits, Lothar, Gerges, Christian, Weismueller, Josef, Gockel, Ines, Vashist, Yogesh, Noethen, Markus M., Izbicki, Jakob R., Manner, Hendrik, Neuhaus, Horst, Roesch, Thomas, Boehmer, Anne C., Hoelscher, Arnulf H., Anders, Mario, Pech, Oliver, Schumacher, Brigitte, Schmidt, Claudia, Schmidt, Thomas, Noder, Tania, Lorenz, Dietmar, Vieth, Michael, May, Andrea, Hess, Timo, Kreuser, Nicole, Becker, Jessica, Ell, Christian, Ambrosone, Christine B., Moysich, Kirsten B., MacGregor, Stuart, Tomlinson, Ian, Whiteman, David C., Jankowski, Janusz, Schumacher, Johannes, Vaughan, Thomas L., Madeleine, Margaret M., Hardie, Laura J., and Buas, Matthew F.

Abstract

Genome-wide association studies (GWAS) of esophageal adenocarcinoma (EAC) and its precursor, Barrett's esophagus (BE), have uncovered significant genetic components of risk, but most heritability remains unexplained. Targeted assessment of genetic variation in biologically relevant pathways using novel analytical approaches may identify missed susceptibility signals. Central obesity, a key BE/EAC risk factor, is linked to systemic inflammation, altered hormonal signaling and insulin-like growth factor (IGF) axis dysfunction. Here, we assessed IGF-related genetic variation and risk of BE and EAC. Principal component analysis was employed to evaluate pathway-level and gene-level associations with BE/EAC, using genotypes for 270 single-nucleotide polymorphisms (SNPs) in or near 12 IGF-related genes, ascertained from 3295 BE cases, 2515 EAC cases and 3207 controls in the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON) GWAS. Gene-level signals were assessed using Multi-marker Analysis of GenoMic Annotation (MAGMA) and SNP summary statistics from BEACON and an expanded GWAS meta-analysis (6167 BE cases, 4112 EAC cases, 17 159 controls). Global variation in the IGF pathway was associated with risk of BE (P = 0.0015). Gene-level associations with BE were observed for GHR (growth hormone receptor; P = 0.00046, false discovery rate q = 0.0056) and IGF1R (IGF1 receptor; P = 0.0090, q = 0.0542). These gene-level signals remained significant at q < 0.1 when assessed using data from the largest available BE/EAC GWAS metaanalysis. No significant associations were observed for EAC. This study represents the most comprehensive evaluation to date of inherited genetic variation in the IGF pathway and BE/EAC risk, providing novel evidence that variation in two genes encoding cell-surface receptors, GHR and IGF1R, may influence risk of BE.

Published
2021

34. A comprehensive re-assessment of the association between vitamin D and cancer susceptibility using Mendelian randomization

Author

Ong, Jue Sheng, Dixon-Suen, Suzanne C., Han, Xikun, An, Jiyuan, Fitzgerald, Rebecca, Buas, Matt, Gammon, Marilie D., Corley, Douglas A., Shaheen, Nicholas J., Hardie, Laura J., Bird, Nigel C., Reid, Brian J., Chow, Wong Ho, Risch, Harvey A., Ye, Weimin, Liu, Geoffrey, Romero, Yvonne, Bernstein, Leslie, Wu, Anna H., Whiteman, David E., Vaughan, Thomas, Agee, M., Alipanahi, B., Auton, A., Bell, R. K., Bryc, K., Elson, S. L., Fontanillas, P., Furlotte, N. A., Hinds, D. A., Huber, K. E., Kleinman, A., Litterman, N. K., McIntyre, M. H., Mountain, J. L., Noblin, E. S., Northover, C. A.M., Pitts, S. J., Sathirapongsasuti, J. Fah, Sazonova, O. V., Shelton, J. F., Shringarpure, S., Tian, C., Tung, J. Y., Vacic, V., Wilson, C. H., Liyanage, Upekha, Dusingize, Jean Cluade, Schumacher, Johannes, Gockel, Ines, Böhmer, Anne, Jankowski, Janusz, Palles, Claire, O’Mara, Tracy, Spurdle, Amanda, Law, Matthew H., Iles, Mark M., Pharoah, Paul, Berchuck, Andrew, Zheng, Wei, Thrift, Aaron P., Olsen, Catherine, Neale, Rachel E., Gharahkhani, Puya, Webb, Penelope M., MacGregor, Stuart, other, and, Ong, Jue Sheng, Dixon-Suen, Suzanne C., Han, Xikun, An, Jiyuan, Fitzgerald, Rebecca, Buas, Matt, Gammon, Marilie D., Corley, Douglas A., Shaheen, Nicholas J., Hardie, Laura J., Bird, Nigel C., Reid, Brian J., Chow, Wong Ho, Risch, Harvey A., Ye, Weimin, Liu, Geoffrey, Romero, Yvonne, Bernstein, Leslie, Wu, Anna H., Whiteman, David E., Vaughan, Thomas, Agee, M., Alipanahi, B., Auton, A., Bell, R. K., Bryc, K., Elson, S. L., Fontanillas, P., Furlotte, N. A., Hinds, D. A., Huber, K. E., Kleinman, A., Litterman, N. K., McIntyre, M. H., Mountain, J. L., Noblin, E. S., Northover, C. A.M., Pitts, S. J., Sathirapongsasuti, J. Fah, Sazonova, O. V., Shelton, J. F., Shringarpure, S., Tian, C., Tung, J. Y., Vacic, V., Wilson, C. H., Liyanage, Upekha, Dusingize, Jean Cluade, Schumacher, Johannes, Gockel, Ines, Böhmer, Anne, Jankowski, Janusz, Palles, Claire, O’Mara, Tracy, Spurdle, Amanda, Law, Matthew H., Iles, Mark M., Pharoah, Paul, Berchuck, Andrew, Zheng, Wei, Thrift, Aaron P., Olsen, Catherine, Neale, Rachel E., Gharahkhani, Puya, Webb, Penelope M., MacGregor, Stuart, and other, and

Abstract

Previous Mendelian randomization (MR) studies on 25-hydroxyvitamin D (25(OH)D) and cancer have typically adopted a handful of variants and found no relationship between 25(OH)D and cancer; however, issues of horizontal pleiotropy cannot be reliably addressed. Using a larger set of variants associated with 25(OH)D (74 SNPs, up from 6 previously), we perform a unified MR analysis to re-evaluate the relationship between 25(OH)D and ten cancers. Our findings are broadly consistent with previous MR studies indicating no relationship, apart from ovarian cancers (OR 0.89; 95% C.I: 0.82 to 0.96 per 1 SD change in 25(OH)D concentration) and basal cell carcinoma (OR 1.16; 95% C.I.: 1.04 to 1.28). However, after adjustment for pigmentation related variables in a multivariable MR framework, the BCC findings were attenuated. Here we report that lower 25(OH)D is unlikely to be a causal risk factor for most cancers, with our study providing more precise confidence intervals than previously possible.

Published
2021

35. Birth weight, head circumference, and prenatal exposure to acrylamide from maternal diet: the European prospective mother-child study (NewGeneris)

Author

Pedersen, Marie, Stedingk, Hans von, Botsivali, Maria, Agramunt, Silvia, Alexander, Jan, Brunborg, Gunnar, Chatzi, Leda, Fleming, Sarah, Fthenou, Eleni, Granum, Berit, Gutzkow, Kristine B., Hardie, Laura J., Knudsen, Lisbeth E., Kyrtopoulos, Soterios A., Mendez, Michelle A., Merlo, Domenico F., Nielsen, Jeanette K., Rydberg, Per, Segerback, Dan, Sunyer, Jordi, Wright, John, Tornqvist, Margareta, Kleinjans, Jos C., and Kogevinas, Manolis

Subjects
Birth weight -- Measurement, Acrylamide -- Health aspects, Birth size -- Measurement, Cephalometry -- Methods, Diet -- Physiological aspects, Prenatal influences -- Physiological aspects, Environmental issues, Health
Abstract

Acrylamide is neurotoxic in humans and animals, and is classified as a probable human carcinogen [International Agency for Research on Cancer (IARC) 1994]. Occupational expo-sure and smoking were originally regarded [...]

Published
2012

36. Integrative post-genome-wide association analysis of CDKN2A and TP53 SNPs and risk of esophageal adenocarcinoma

Author

Buas, Matthew F., Levine, David M., Makar, Karen W., Utsugi, Heidi, Onstad, Lynn, Li, Xiaohong, Galipeau, Patricia C., Shaheen, Nicholas J., Hardie, Laura J., Romero, Yvonne, Bernstein, Leslie, Gammon, Marilie D., Casson, Alan G., Bird, Nigel C., Risch, Harvey A., Ye, Weimin, Liu, Geoffrey, Corley, Douglas A., Blount, Patricia L., Fitzgerald, Rebecca C., Whiteman, David C., Wu, Anna H., Reid, Brian J., and Vaughan, Thomas L.

Published
2014
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37. eQTL Set-Based Association Analysis Identifies Novel Susceptibility Loci for Barrett Esophagus and Esophageal Adenocarcinoma.

Author

Xiaoyu Wang, Gharahkhani, Puya, Levine, David M., Fitzgerald, Rebecca C., Gockel, Ines, Corley, Douglas A., Risch, Harvey A., Bernstein, Leslie, Wong-Ho Chow, Onstad, Lynn, Shaheen, Nicholas J., Lagergren, Jesper, Hardie, Laura J., Wu, Anna H., Pharoah, Paul D. P., Liu, Geoffrey, Anderson, Lesley A., Iyer, Prasad G., Gammon, Marilie D., and Caldas, Carlos

Abstract

Background: Over 20 susceptibility single-nucleotide polymorphisms (SNP) have been identified for esophageal adenocarcinoma (EAC) and its precursor, Barrett esophagus (BE), explaining a small portion of heritability. Methods: Using genetic data from 4,323 BE and 4,116 EAC patients aggregated by international consortia including the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON), we conducted a comprehensive transcriptome-wide association study (TWAS) for BE/EAC, leveraging Genotype Tissue Expression (GTEx) gene-expression data from six tissue types of plausible relevance to EAC etiology: mucosa and muscularis from the esophagus, gastroesophageal (GE) junction, stomach, whole blood, and visceral adipose. Two analytical approaches were taken: standard TWAS using the predicted gene expression from local expression quantitative trait loci (eQTL), and set-based SKAT association using selected eQTLs that predict the gene expression. Results: Although the standard approach did not identify significant signals, the eQTL set-based approach identified eight novel associations, three of which were validated in independent external data (eQTL SNP sets for EXOC3, ZNF641, and HSP90AA1). Conclusions: This study identified novel genetic susceptibility loci for EAC and BE using an eQTL set-based genetic association approach. [ABSTRACT FROM AUTHOR]

Published
2022
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38. Additional file 1 of Maternal iodine status, intrauterine growth, birth outcomes and congenital anomalies in a UK birth cohort

Author

Snart, Charles Jonathan Peter, Threapleton, Diane Erin, Keeble, Claire, Taylor, Elizabeth, Waiblinger, Dagmar, Reid, Stephen, Nisreen A. Alwan, Mason, Dan, Rafaq Azad, Cade, Janet Elizabeth, Simpson, Nigel A. B., Meadows, Sarah, McKillion, Amanda, Santorelli, Gillian, Waterman, Amanda H., Zimmermann, Michael, Stewart, Paul M., Wright, John, Mon-Williams, Mark, Greenwood, Darren Charles, and Hardie, Laura J.

Abstract

Additional file 1: Table S1. Details of socioeconomic position categories and maternal education levels. Table S2. Details of model covariates, sample exclusions, sensitivity analyses and subgroup analyses for each of the different outcomes. Table S3. Pairwise correlations between each of the growth measures. Table S4. Predicted estimates (continuous outcomes) and percent at the threshold (binary outcomes) (99% CIs) at the 25th, 50th and 75th centiles of iodine concentration and p-overall* for ‘average’ participants†. Figure S1. A directed acyclic graph used to identify confounders and competing exposures in the association between maternal iodine concentration and birth or pregnancy outcomes. Figure S2. Flow chart of participant inclusions and exclusions. Figure S3. Estimated APGAR score at 1 minute and percent with congenital anomalies, using imputed datasets for the full sample. Figure S4. Estimated biparietal diameter, femur length and abdominal circumference, from ultrasound scans at 34 weeks’ gestation, across the range of maternal I:Cr concentrations using imputed datasets for the full sample. Figure S5. Estimated birthweight centile in all participants, sensitivity analysis and subgroups. Figure S6. Estimated birthweight in grams in all participants, sensitivity analysis and subgroups. Figure S7. Probability of being small for gestational age in all participants, sensitivity analysis and subgroups. Figure S8. Probability of low birthweight in all participants, sensitivity analysis and subgroups. Figure S9. Apgar score at 5 minutes after birth in all participants, sensitivity analysis and subgroups. Figure S10. Estimated head circumference at birth in all participants, sensitivity analysis and subgroups. Figure S11. Estimated head circumference from 34 week ultrasound scan in all participants, sensitivity analysis and subgroups. Figure S12. Estimated weight from 34 week ultrasound scan in all participants, sensitivity analysis and subgroups. Figure S13. Probability of preterm birth in all participants, sensitivity analysis and subgroups. Figure S14. Probability of congenital anomalies in all participants, sensitivity analysis and subgroups.

Published
2020
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40. Prenatal and Postpartum Maternal Iodide Intake from Diet and Supplements, Urinary Iodine and Thyroid Hormone Concentrations in a Region of the United Kingdom with Mild-to-Moderate Iodine Deficiency

Author

Threapleton, Diane E., primary, Waiblinger, Dagmar, additional, Snart, Charles J.P., additional, Taylor, Elizabeth, additional, Keeble, Claire, additional, Ashraf, Samina, additional, Bi, Shazia, additional, Ajjan, Ramzi, additional, Azad, Rafaq, additional, Hancock, Neil, additional, Mason, Dan, additional, Reid, Stephen, additional, Cromie, Kirsten J., additional, Alwan, Nisreen A., additional, Zimmermann, Michael, additional, Stewart, Paul M., additional, Simpson, Nigel A.B., additional, Wright, John, additional, Cade, Janet E., additional, Hardie, Laura J., additional, and Greenwood, Darren C., additional

Published
2021
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41. Germline Genetic Contributions to Risk for Esophageal Adenocarcinoma, Barrett’s Esophagus, and Gastroesophageal Reflux

Author

Ek, Weronica E., Levine, David M., D’Amato, Mauro, Pedersen, Nancy L., Magnusson, Patrik K. E., Bresso, Francesca, Onstad, Lynn E., Schmidt, Peter T., Törnblom, Hans, Nordenstedt, Helena, Romero, Yvonne, Chow, Wong-Ho, Murray, Liam J., Gammon, Marilie D., Liu, Geoffrey, Bernstein, Leslie, Casson, Alan G., Risch, Harvey A., Shaheen, Nicholas J., Bird, Nigel C., Reid, Brian J., Corley, Douglas A., Hardie, Laura J., Ye, Weimin, Wu, Anna H., Zucchelli, Marco, Spector, Tim D., Hysi, Pirro, Vaughan, Thomas L., Whiteman, David C., and MacGregor, Stuart

Published
2013
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45. Germline variation in the insulin-like growth factor pathway and risk of Barrett’s esophagus and esophageal adenocarcinoma

Author

Dighe, Shruti G, primary, Chen, Jianhong, additional, Yan, Li, additional, He, Qianchuan, additional, Gharahkhani, Puya, additional, Onstad, Lynn, additional, Levine, David M, additional, Palles, Claire, additional, Ye, Weimin, additional, Gammon, Marilie D, additional, Iyer, Prasad G, additional, Anderson, Lesley A, additional, Liu, Geoffrey, additional, Wu, Anna H, additional, Dai, James Y, additional, Chow, Wong-Ho, additional, Risch, Harvey A, additional, Lagergren, Jesper, additional, Shaheen, Nicholas J, additional, Bernstein, Leslie, additional, Corley, Douglas A, additional, Prenen, Hans, additional, deCaestecker, John, additional, MacDonald, David, additional, Moayyedi, Paul, additional, Barr, Hugh, additional, Love, Sharon B, additional, Chegwidden, Laura, additional, Attwood, Stephen, additional, Watson, Peter, additional, Harrison, Rebecca, additional, Ott, Katja, additional, Moebus, Susanne, additional, Venerito, Marino, additional, Lang, Hauke, additional, Mayershofer, Rupert, additional, Knapp, Michael, additional, Veits, Lothar, additional, Gerges, Christian, additional, Weismüller, Josef, additional, Gockel, Ines, additional, Vashist, Yogesh, additional, Nöthen, Markus M, additional, Izbicki, Jakob R, additional, Manner, Hendrik, additional, Neuhaus, Horst, additional, Rösch, Thomas, additional, Böhmer, Anne C, additional, Hölscher, Arnulf H, additional, Anders, Mario, additional, Pech, Oliver, additional, Schumacher, Brigitte, additional, Schmidt, Claudia, additional, Schmidt, Thomas, additional, Noder, Tania, additional, Lorenz, Dietmar, additional, Vieth, Michael, additional, May, Andrea, additional, Hess, Timo, additional, Kreuser, Nicole, additional, Becker, Jessica, additional, Ell, Christian, additional, Ambrosone, Christine B, additional, Moysich, Kirsten B, additional, MacGregor, Stuart, additional, Tomlinson, Ian, additional, Whiteman, David C, additional, Jankowski, Janusz, additional, Schumacher, Johannes, additional, Vaughan, Thomas L, additional, Madeleine, Margaret M, additional, Hardie, Laura J, additional, and Buas, Matthew F, additional

Published
2020
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46. Maternal iodine status in a multi‐ethnic UK birth cohort: Associations with child cognitive and educational development

Author

Threapleton, Diane E., primary, Snart, Charles J. P., additional, Keeble, Claire, additional, Waterman, Amanda H., additional, Taylor, Elizabeth, additional, Mason, Dan, additional, Reid, Stephen, additional, Azad, Rafaq, additional, Hill, Liam J. B., additional, Meadows, Sarah, additional, McKillion, Amanda, additional, Alwan, Nisreen A., additional, Cade, Janet E., additional, Simpson, Nigel A. B., additional, Stewart, Paul M., additional, Zimmermann, Michael, additional, Wright, John, additional, Waiblinger, Dagmar, additional, Mon‐Williams, Mark, additional, Hardie, Laura J., additional, and Greenwood, Darren C., additional

Published
2020
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48. Gastroesophageal reflux GWAS identifies risk loci that also associate with subsequent severe esophageal diseases

Author

An, Jiyuan, Gharahkhani, Puya, Law, Matthew H., Ong, Jue-Sheng, Han, Xikun, Olsen, Catherine M., Neale, Rachel E., Lai, John, Vaughan, Tom L., Gockel, Ines, Thieme, René, Böhmer, Anne C., Jankowski, Janusz, Fitzgerald, Rebecca C., Schumacher, Johannes, Palles, Claire, Whiteman, David C., MacGregor, Stuart, Gammon, Marilie D., Corley, Douglas A., Shaheen, Nicholas J., Bird, Nigel C., Hardie, Laura J., Murray, Liam J., Reid, Brian J., Chow, Wong-Ho, Risch, Harvey A., Ye, Weimin, Liu, Geoffrey, Romero, Yvonne, Bernstein, Leslie, Wu, Anna H., Agee, M., Alipanahi, B., Auton, A., Bell, R. K., Bryc, K., Elson, S. L., Fontanillas, P., Furlotte, N. A., Hinds, D. A., Huber, K. E., Kleinman, A., Litterman, N. K., McIntyre, M. H., Mountain, J. L., Noblin, E. S., Northover, C. A. M., Pitts, S. J., Sathirapongsasuti, J. Fah, Sazonova, O. V., Shelton, J. F., Shringarpure, S., Tian, C., Tung, J. Y., Vacic, V., Wilson, C. H., Gharahkhani, Puya [0000-0002-4203-5952], Law, Matthew H. [0000-0002-4303-8821], Ong, Jue-Sheng [0000-0002-6062-710X], Han, Xikun [0000-0002-3823-7308], Olsen, Catherine M. [0000-0003-4483-1888], Böhmer, Anne C. [0000-0002-5716-786X], Fitzgerald, Rebecca C. [0000-0002-3434-3568], MacGregor, Stuart [0000-0001-6731-8142], and Apollo - University of Cambridge Repository

Subjects
631/67/1504/1477, 631/208/205/2138, 45/43, article, 38/39, 631/208/68, 692/699/1503/1476/196, health care economics and organizations, humanities, digestive system diseases
Abstract

Funder: The Swedish Esophageal Cancer Study was funded by grants (R01 CA57947-03) from the National Cancer Institute he California Tobacco Related Research Program (3RT-0122; and; 10RT-0251) Marit Peterson Fund for Melanoma Research. CIDR is supported by contract HHSN268200782096C, Gastroesophageal reflux disease (GERD) is caused by gastric acid entering the esophagus. GERD has high prevalence and is the major risk factor for Barrett’s esophagus (BE) and esophageal adenocarcinoma (EA). We conduct a large GERD GWAS meta-analysis (80,265 cases, 305,011 controls), identifying 25 independent genome-wide significant loci for GERD. Several of the implicated genes are existing or putative drug targets. Loci discovery is greatest with a broad GERD definition (including cases defined by self-report or medication data). Further, 91% of the GERD risk-increasing alleles also increase BE and/or EA risk, greatly expanding gene discovery for these traits. Our results map genes for GERD and related traits and uncover potential new drug targets for these conditions.

Published
2019

49. Postnatal development of the ob gene system: elevated leptin levels in suckling fa/fa rats

Author

Rayner, D.V., Dalgliesh, Gillian D., Duncan, Jacqueline S., Hardie, Laura J., Hoggard, Nigel, and Trayhurn, Paul

Subjects
Rats -- Physiological aspects, Leptin -- Physiological aspects, Metabolic regulation -- Research, Biological sciences
Abstract

Researchers have investigated the postnatal development of the leptin system in the rat in order to establish the stage of development at which the potential for energy balance regulation by leptin first arises. This involved taking white adipose tissue from rats aged between one day and 28 days. It was found that the leptin system is operational shortly after birth in the rat in terms of ob gene expression and leptin production.

Published
1997

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