Author: "Hardie, Laura J." - Searchworks@Jio Institute Digital Library Search Results

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51. Prospective Study of Cyclin D1 Overexpression in Barrettʼs Esophagus: Association With Increased Risk of Adenocarcinoma

Author: Bani-Hani, Kamal, Martin, Iain G., Hardie, Laura J., Mapstone, Nicholas, Briggs, Jackie A., Forman, David, and Wild, Christopher P.
Published: 2000

52. Glutathione S-transferase M1 null genotype is associated with a decreased risk of myocardial infarction

Author: WILSON, MICHAEL H., GRANT, PETER J., HARDIE, LAURA J., and WILD, CHRISTOPHER PAUL
Published: 2000

53. Validity of an online 24-hour recall tool (myfood24) 1 for dietary assessment in 2 population studies: comparison with biomarkers and standard interviews

Author: Wark, Petra, Hardie, Laura J., Frost, Gary, Alwan, Nisreen, Carter, Michelle, Elliott, Paul, Ford, Heather E., Hancock, Neil, Morris, Michelle, Mulla, Umme Z., Noorwali, Essra A., Petropoulou, Katrina, Murphy, David, Potter, Gregory D.M., Riboli, Elio, Greenwood, Darren C., and Cade, Janet
Abstract: Background: Online dietary assessment tools can reduce administrative costs and facilitate repeated dietary assessment during follow-up in large-scale studies. However, information on bias due to measurement error of such tools is limited. We developed an online 24-hour recall (myfood24) and compared its performance with a traditional interviewer-administered multiple-pass 24-hour recall, assessing both against biomarkers. Methods: Metabolically stable adults were recruited and completed the new online dietary recall, an interviewer-based multiple pass recall and a suite of reference measures. Longer-term dietary intake was estimated from up to 3 x 24-hour recalls taken 2 weeks apart. Estimated intake of protein, potassium and sodium were compared with urinary biomarker concentrations. Estimated total sugar intake was compared with a predictive biomarker and estimated energy intake compared with energy expenditure measured by accelerometry and calorimetry. Nutrient intakes were also compared to those derived from an interviewer-administered multiple-pass 24-hour recall. Results: Biomarker samples were received from 212 participants on at least one occasion. Both self-reported dietary assessment tools led to attenuation compared to biomarkers. The online tools resulted in attenuation factors around 0.2 to 0.3 and partial correlation coefficients reflecting ranking intakes, of approximately 0.3 to 0.4. This was broadly similar to the more administratively burdensome interviewer-based tool. Other nutrient estimates derived from myfood24 were around 10-20% lower than from the interviewer-based tool, with wide limits of agreement. Intra-class correlation coefficients were approximately 0.4 to 0.5 indicating consistent moderate agreement. Conclusions: Our findings show that, whilst results from both measures of self-reported diet are attenuated compared to biomarker measures, the myfood24 online 24-hour recall is comparable to the more time-consuming and costly interviewer-based 24-hour recall across a range of measures.
Published: 2018

54. Validation of the Oxford WebQ Online 24-Hour Dietary Questionnaire Using Biomarkers

Author: Greenwood, Darren C, primary, Hardie, Laura J, primary, Frost, Gary S, primary, Alwan, Nisreen A, primary, Bradbury, Kathryn E, primary, Carter, Michelle, primary, Elliott, Paul, primary, Evans, Charlotte E L, primary, Ford, Heather E, primary, Hancock, Neil, primary, Key, Timothy J, primary, Liu, Bette, primary, Morris, Michelle A, primary, Mulla, Umme Z, primary, Petropoulou, Katerina, primary, Potter, Gregory D M, primary, Riboli, Elio, primary, Young, Heather, primary, Wark, Petra A, primary, and Cade, Janet E, primary
Published: 2019
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55. Maternal iodine status in a multi‐ethnic UK birth cohort: Associations with child cognitive and educational development.

Author: Threapleton, Diane E., Snart, Charles J. P., Keeble, Claire, Waterman, Amanda H., Taylor, Elizabeth, Mason, Dan, Reid, Stephen, Azad, Rafaq, Hill, Liam J. B., Meadows, Sarah, McKillion, Amanda, Alwan, Nisreen A., Cade, Janet E., Simpson, Nigel A. B., Stewart, Paul M., Zimmermann, Michael, Wright, John, Waiblinger, Dagmar, Mon‐Williams, Mark, and Hardie, Laura J.
Subjects: CHILD development, COGNITION, IODINE deficiency, PREGNANCY, NUTRITION in pregnancy
Abstract: Background: Maternal iodine requirements increase during pregnancy to supply thyroid hormones critical for fetal neurodevelopment. Iodine insufficiency may result in poorer cognitive or child educational outcomes but current evidence is sparse and inconsistent. Objectives: To quantify the association between maternal iodine status and child educational outcomes. Methods: Urinary iodine concentrations (UIC) and iodine/creatinine ratios (I:Cr) were measured in 6971 mothers at 26‐28 weeks' gestation participating in the Born in Bradford cohort. Maternal iodine status was examined in relation to child school achievement (early years foundation stage (EYFS), phonics, and Key Stage 1 (KS1)), other learning outcomes, social and behavioural difficulties, and sensorimotor control in 5745 children aged 4‐7 years. Results: Median (interquartile range) UIC was 76 µg/L (46, 120), and I:Cr was 83 µg/g (59, 121). Overall, there was no strong or consistent evidence to support associations between UIC or I:Cr and neurodevelopmental outcomes. For instance, predicted EYFS and phonics scores (primary outcomes) at the 25th vs 75th I:Cr percentiles (99% confidence intervals) were similar, with no evidence of associations: EYFS scores were 32 (99% CI 31, 33) and 33 (99% CI 32, 34), and phonics scores were 34 (99% CI 33, 35) and 35 (99% CI 34, 36), respectively. Conclusions: In the largest single study of its kind, there was little evidence of detrimental neurodevelopmental outcomes in children born to pregnant women with iodine insufficiency as defined by World Health Organization–outlined thresholds. Alternative functional biomarkers for iodine status in pregnancy and focused assessment of other health outcomes may provide additional insight. [ABSTRACT FROM AUTHOR]
Published: 2021
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56. Micronuclei in Cord Blood Lymphocytes and Associations with Biomarkers of Exposure to Carcinogens and Hormonally Active Factors, Gene Polymorphisms, and Gene Expression: The NewGeneris Cohort

Author: Merlo, Domenico Franco, Agramunt, Silvia, Anna, Lívia, Besselink, Harrie, Botsivali, Maria, Brady, Nigel J., Ceppi, Marcello, Chatzi, Leda, Chen, Bowang, Decordier, Ilse, Farmer, Peter B., Fleming, Sarah, Fontana, Vincenzo, Försti, Asta, Fthenou, Eleni, Gallo, Fabio, Georgiadis, Panagiotis, Gmuender, Hans, Godschalk, Roger W., Granum, Berit, Hardie, Laura J., Hemminki, Kari, Hochstenbach, Kevin, Knudsen, Lisbeth E., Kogevinas, Manolis, Kovács, Katalin, Kyrtopoulos, Soterios A., Løvik, Martinus, Nielsen, Jeanette K., Nygaard, Unni Cecilie, Pedersen, Marie, Rydberg, Per, Schoket, Bernadette, Segerbäck, Dan, Singh, Rajinder, Sunyer, Jordi, Törnqvist, Margareta, van Loveren, Henk, van Schooten, Frederik J., Vande Loock, Kim, von Stedingk, Hans, Wright, John, Kleinjans, Jos C, Kirsch Volders, Micheline, van Delft, Joost H. M., Marcos, R., Anderson, D., Stagi, E., Lukács, V., Mijal, R., Nomark, E., RS: GROW - Oncology, RS: NUTRIM - R4 - Gene-environment interaction, RS: GROW - R1 - Prevention, Farmacologie en Toxicologie, Promovendi ODB, Toxicogenomics, and Cell Genetics
Subjects: medicine.medical_specialty, Genotype, Health, Toxicology and Mutagenesis, Biomarkers, Carcinogens, Child, Cohort Studies, DNA Adducts, Europe, Female, Fetal Blood, Gene Expression Profiling, Gene Expression Regulation, Hormones, Humans, Leukemia, Malondialdehyde, Micronucleus Tests, Pregnancy, Prenatal Exposure Delayed Effects, T-Lymphocytes, Public Health, Environmental and Occupational Health, Embaràs, Environmental Health and Occupational Health, Sang -- Malalties, Single-nucleotide polymorphism, Genome-wide association study, EPHX1, Biology, Internal medicine, VDP::Midical sciences: 700::Clinical medical sciences: 750::Paediatrics: 760, medicine, CALUX, Toxicology and Mutagenesis, Leucèmia en els infants, Carcinogen, Cancer, Regulation of gene expression, Environmental and Occupational Health, VDP::Medisinske fag: 700::Klinisk medisinske fag: 750::Pediatri: 760, Toxicologia genètica, Gene expression profiling, Endocrinology, Health, Micronucleus test, Immunology, Children's Health, Public Health
Abstract: Background: Leukemia incidence has increased in recent decades among European children, suggesting that early-life environmental exposures play an important role in disease development. Objectives: We investigated the hypothesis that childhood susceptibility may increase as a result of in utero exposure to carcinogens and hormonally acting factors. Using cord blood samples from the NewGeneris cohort, we examined associations between a range of biomarkers of carcinogen exposure and hormonally acting factors with micronuclei (MN) frequency as a proxy measure of cancer risk. Associations with gene expression and genotype were also explored. Methods: DNA and protein adducts, gene expression profiles, circulating hormonally acting factors, and GWAS (genome-wide association study) data were investigated in relation to genomic damage measured by MN frequency in lymphocytes from 623 newborns enrolled between 2006 and 2010 across Europe. Results: Malondialdehyde DNA adducts (M1dG) were associated with increased MN frequency in binucleated lymphocytes (MNBN), and exposure to androgenic, estrogenic, and dioxin-like compounds was associated with MN frequency in mononucleated lymphocytes (MNMONO), although no monotonic exposure–outcome relationship was observed. Lower frequencies of MNBN were associated with a 1-unit increase expression of PDCD11, LATS2, TRIM13, CD28, SMC1A, IL7R, and NIPBL genes. Gene expression was significantly higher in association with the highest versus lowest category of bulky and M1dG–DNA adducts for five and six genes, respectively. Gene expression levels were significantly lower for 11 genes in association with the highest versus lowest category of plasma AR CALUX® (chemically activated luciferase expression for androgens) (8 genes), ERα CALUX® (for estrogens) (2 genes), and DR CALUX® (for dioxins). Several SNPs (single-nucleotide polymorphisms) on chromosome 11 near FOLH1 significantly modified associations between androgen activity and MNBN frequency. Polymorphisms in EPHX1/2 and CYP2E1 were associated with MNBN. Conclusion: We measured in utero exposure to selected environmental carcinogens and circulating hormonally acting factors and detected associations with MN frequency in newborns circulating T lymphocytes. The results highlight mechanisms that may contribute to carcinogen-induced leukemia and require further research. Citation: Merlo DF, Agramunt S, Anna L, Besselink H, Botsivali M, Brady NJ, Ceppi M, Chatzi L, Chen B, Decordier I, Farmer PB, Fleming S, Fontana V, Försti A, Fthenou E, Gallo F, Georgiadis P, Gmuender H, Godschalk RW, Granum B, Hardie LJ, Hemminki K, Hochstenbach K, Knudsen LE, Kogevinas M, Kovács K, Kyrtopoulos SA, Løvik M, Nielsen JK, Nygaard UC, Pedersen M, Rydberg P, Schoket B, Segerbäck D, Singh R, Sunyer J, Törnqvist M, van Loveren H, van Schooten FJ, Vande Loock K, von Stedingk H, Wright J, Kleinjans JC, Kirsch-Volders M, van Delft JHM, NewGeneris Consortium. 2014. Micronuclei in cord blood lymphocytes and associations with biomarkers of exposure to carcinogens and hormonally active factors, gene polymorphisms, and gene expression: The NewGeneris Cohort. Environ Health Perspect 122:193–200; http://dx.doi.org/10.1289/ehp.1206324
Published: 2014
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57. Bulky DNA adducts in cord blood, maternal fruit-and-vegetable consumption, and birth weight in a European mother-child study (NewGeneris)

Author: Pedersen, Marie, Schoket, Bernadette, Godschalk, Roger W., Wright, John, von Stedingk, Hans, Tornqvist, Margareta, Sunyer, Jordi, Nielsen, Jeanette K., Merlo, Domenico F., Mendez, Michelle A., Meltzer, Helle M., Lukacs, Viktoria, Landstrom, Anette, Kyrtopoulos, Soterios A., Kovacs, Katalin, Knudsen, Lisbeth E., Haugen, Margaretha, Hardie, Laura J., Gutzkow, Kristine B., Fleming, Sarah, Fthenou, Eleni, Farmer, Peter B., Espinosa, Aina, Chatzi, Leda, Brunborg, Gunnar, Brady, Nigel J., Botsivali, Maria, Arab, Khelifa, Anna, Livia, Alexander, Jan, Agramunt, Silvia, Kleinjans, Jos C., Segerback, Dan, and Kogevinas, Manolis
Subjects: Birth weight -- Genetic aspects, Fetal blood -- Genetic aspects -- Physiological aspects, Birth size -- Genetic aspects, Pregnant women -- Food and nutrition -- Health aspects -- Genetic aspects, Polycyclic aromatic hydrocarbons -- Genetic aspects -- Physiological aspects, Environmental issues, Health
Abstract: Background: Tobacco-smoke, airborne, and dietary exposures to polycyclic aromatic hydrocarbons (PAHs) have been associated with reduced prenatal growth. Evidence from biomarker-based studies of low-exposed populations is limited. Bulky DNA adducts in cord blood reflect the prenatal effective dose to several genotoxic agents including PAHs. OBJECTIVES: We estimated the association between bulky DNA adduct levels and birth weight in a multicenter study and examined modification of this association by maternal intake of fruits and vegetables during pregnancy. Methods: Pregnant women from Denmark, England, Greece, Norway, and Spain were recruited in 2006--2010. Adduct levels were measured by the [sup.32]P-postlabeling technique in white blood cells from 229 mothers and 612 newborns. Maternal diet was examined through questionnaires. Results: Adduct levels in maternal and cord blood samples were similar and positively correlated (median, 12.1 vs. 11.4 adducts in [10.sup.8]nucleotides; Spearman rank correlation coefficient = 0.66, p < 0.001). Cord blood adduct levels were negatively associated with birth weight, with an estimated difference in mean birth weight of -129 g (95% CI: -233, -25 g) for infants in the highest versus lowest tertile of adducts. The negative association with birth weight was limited to births in Norway, Denmark, and England, the countries with the lowest adduct levels, and was more pronounced in births to mothers with low intake of fruits and vegetables (-248 g; 95% CI: -405, -92 g) compared with those with high intake (-58 g; 95% CI: -206, 90 g). Conclusions: Maternal exposure to genotoxic agents that induce the formation of bulky DNA adducts may affect intrauterine growth. Maternal fruit and vegetable consumption may be protective., Introduction Environmental exposures in utero may have adverse effects on health both immediately and in later life. Measurement of biomarkers in cord blood improves exposure assessment and may improve our [...]
Published: 2013
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58. Recommended sleep duration is associated with higher consumption of fruits and vegetables; cross-sectional and prospective analyses from the UK Women’s Cohort Study

Author: Noorwali, Essra A., primary, Hardie, Laura J., additional, and Cade, Janet E., additional
Published: 2018
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59. Occurrence of deoxynivalenol in an elderly cohort in the UK: a biomonitoring approach

Author: Papageorgiou, Maria, primary, Wells, Liz, additional, Williams, Courtney, additional, White, Kay L.M., additional, De Santis, Barbara, additional, Liu, Yunru, additional, Debegnach, Francesca, additional, Miano, Brunella, additional, Moretti, Giorgio, additional, Greetham, Stephanie, additional, Brera, Carlo, additional, Atkin, Stephen L., additional, Hardie, Laura J., additional, and Sathyapalan, Thozhukat, additional
Published: 2018
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60. The relationship between sleep duration and fruit/vegetable intakes in UK adults: a cross-sectional study from the National Diet and Nutrition Survey

Author: Noorwali, Essra A, primary, Cade, Janet E, additional, Burley, Victoria J, additional, and Hardie, Laura J, additional
Published: 2018
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61. Expression of an inducible nitric oxide synthase gene in rainbow trout Oncorhynchus mykiss

Author: Laing, Kerry J, Hardie, Laura J, Aartsen, Wendy, Grabowski, Peter S, and Secombes, Christopher J
Published: 1999
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62. Large scale meta-analysis identifies new genetic risk loci for esophageal adenocarcinoma (EA) and the first EA risk locus independent of Barrett’s esophagus

Author: Gharahkhani, Puya, Fitzgerald, Rebecca C., Vaughan, Thomas L., Tomlinson, Ian, Gockel, Ines, Palles, Claire, 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, Bohmer, Anne C., Izbicki, Jakob R., Holscher, Arnulf H., Lang, Hauke, Lorenz, Dietmar, Schumacher, Brigitte, Hackelsberger, Andreas, Mayershofer, Rupert, Pech, Oliver, Vashist, Yogesh, Ott, Katja, Vieth, Michael, Weismuller, Josef, Nothen, Markus M., Attwood, Stephen, Barr, Hugh, Chegwidden, Laura, deCaestecker, John, Harrison, Rebecca, Love, Sharon B., MacDonald, David, Moayyedi, Paul, Prenen, Hans, Watson, RG 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, Rosch, Thomas, Ell, Christian, MacGregor, Stuart, Pharoah, Paul, Whiteman, David C., Jankowski, Janusz, Schumacher, Johannes, Gharahkhani, Puya, Fitzgerald, Rebecca C., Vaughan, Thomas L., Tomlinson, Ian, Gockel, Ines, Palles, Claire, 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, Bohmer, Anne C., Izbicki, Jakob R., Holscher, Arnulf H., Lang, Hauke, Lorenz, Dietmar, Schumacher, Brigitte, Hackelsberger, Andreas, Mayershofer, Rupert, Pech, Oliver, Vashist, Yogesh, Ott, Katja, Vieth, Michael, Weismuller, Josef, Nothen, Markus M., Attwood, Stephen, Barr, Hugh, Chegwidden, Laura, deCaestecker, John, Harrison, Rebecca, Love, Sharon B., MacDonald, David, Moayyedi, Paul, Prenen, Hans, Watson, RG 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, Rosch, Thomas, Ell, Christian, MacGregor, Stuart, Pharoah, Paul, Whiteman, David C., Jankowski, Janusz, and Schumacher, Johannes
Abstract: SUMMARY Background: Esophageal adenocarcinoma (EA) represents one of the fastest rising oncological diseases in western countries. Barrett’s Esophagus (BE) is the premalignant precursor of EA. However, only a subset of BE patients develop EA, which complicates the clinical management in the absence of valid predictors. Methods: Within an international consortium of groups involved in the genetics of BE/EA, we performed the first meta-analysis of all genome-wide association studies (GWAS) available (>10,000 BE/EA patients, >17,000 controls, all of European descent). The entire GWAS-data set was also analyzed using bioinformatics approaches in order to identify pathophysiologically relevant cellular pathways. Findings: We identified nine new disease loci for BE/EA (P<5×10-8) and thereby doubled the number of known risk loci. The strongest new risk locus implicates CFTR as BE/EA risk gene. Mutations in CFTR cause cystic fibrosis (CF), the most common recessive disorder in Europeans. Gastroesophageal reflux (GER) belongs to the phenotypic CF-spectrum and represents the main risk factor for BE/EA. Thus, the CFTR locus may trigger a common GER-mediated pathophysiology. The strongest disease pathways identified (P<10-6) belong to muscle cell differentiation and to mesenchyme development/differentiation, which fit with current pathophysiological BE/EA concepts. Furthermore, for the first time we identified an EA-specific association (P=1·6×10-8) near HTR3C/ABCC5 which is independent of BE development (P=0·45). Interpretation: The identified disease loci and pathways reveal new insights into the etiology of BE and EA. Furthermore, the EA-specific association at HTR3C/ABCC5 may constitute a novel genetic marker for the prediction of transition from BE to EA. Funding: US National Cancer Institute, US National Institutes of Health, National Health and Medical Research Council of Australia, Swedish Cancer Society, Medical Research Council of UK, Cambridge NIHR biomedical researc
Published: 2017

63. Longer sleep is associated with lower BMI and favorable metabolic profiles in UK adults: Findings from the National Diet and Nutrition Survey

Author: Potter, Gregory D. M., primary, Cade, Janet E., additional, and Hardie, Laura J., additional
Published: 2017
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64. Environmental, Dietary, Maternal, and Fetal Predictors of Bulky DNA Adducts in Cord Blood: A European Mother–Child Study (NewGeneris)

Author: de Hoogh, Kees, Merlo, Domenico F., Botsivali, Maria, Villanueva, Cristina M., Godschalk, Roger W., Meltzer, Helle Margrete, Hardie, Laura J., Anna, Lívia, Nielsen, Jeanette K., Smith, Rachel B., Wright, John, Alexander, Jan, Cirach, Marta, Chatzi, Leda, Fthenou, Eleni, Kovács, Katalin, Knudsen, Lisbeth E., Haugen, Margaretha, Brunborg, Gunnar, van Schooten, Frederik-Jan, Gutzkow, Kristine B., Pedersen, Marie, Toledano, Mireille B., Landström, Anette, Nieuwenhuijsen, Mark J., Hoek, Gerard, Ketzel, Matthias, Espinosa, Ana, Schoket, Bernadette, Gracia-Lavedan, Esther, Sunyer, Jordi, and Mendez, Michelle Ann
Abstract: Background:Bulky DNA adducts reflect genotoxic exposures, have been associated with lower birth weight, and may predict cancer risk.Objective:We selected factors known or hypothesized to affect in utero adduct formation and repair and examined their associations with adduct levels in neonates.Methods:Pregnant women from Greece, Spain, England, Denmark, and Norway were recruited in 2006–2010. Cord blood bulky DNA adduct levels were measured by the 32P-postlabeling technique (n = 511). Diet and maternal characteristics were assessed via questionnaires. Modeled exposures to air pollutants and drinking-water disinfection by-products, mainly trihalomethanes (THMs), were available for a large proportion of the study population.Results:Greek and Spanish neonates had higher adduct levels than the northern European neonates [median, 12.1 (n = 179) vs. 6.8 (n = 332) adducts per 108 nucleotides, p < 0.001]. Residence in southern European countries, higher maternal body mass index, delivery by cesarean section, male infant sex, low maternal intake of fruits rich in vitamin C, high intake of dairy products, and low adherence to healthy diet score were statistically significantly associated with higher adduct levels in adjusted models. Exposure to fine particulate matter and nitrogen dioxide was associated with significantly higher adducts in the Danish subsample only. Overall, the pooled results for THMs in water show no evidence of association with adduct levels; however, there are country-specific differences in results with a suggestion of an association in England.Conclusion:These findings suggest that a combination of factors, including unknown country-specific factors, influence the bulky DNA adduct levels in neonates.Citation:Pedersen M, Mendez MA, Schoket B, Godschalk RW, Espinosa A, Landström A, Villanueva CM, Merlo DF, Fthenou E, Gracia-Lavedan E, van Schooten FJ, Hoek G, Brunborg G, Meltzer HM, Alexander J, Nielsen JK, Sunyer J, Wright J, Kovács K, de Hoogh K, Gutzkow KB, Hardie LJ, Chatzi L, Knudsen LE, Anna L, Ketzel M, Haugen M, Botsivali M, Nieuwenhuijsen MJ, Cirach M, Toledano MB, Smith RB, Fleming S, Agramunt S, Kyrtopoulos SA, Lukács V, Kleinjans JC, Segerbäck D, Kogevinas M. 2015. Environmental, dietary, maternal, and fetal predictors of bulky DNA adducts in cord blood: a European mother–child study (NewGeneris). Environ Health Perspect 123:374–380; http://dx.doi.org/10.1289/ehp.1408613
Published: 2015
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65. Polymorphisms in genes in the androgen pathway and risk of Barrett's 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, Lagergren, Jesper, 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
Abstract: The strong male predominance in Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC) remains inadequately explained, but sex hormones might be involved. We hypothesized that single nucleotide polymorphisms (SNPs) in the androgen pathway influence risk of developing BE and EAC. This genetic-epidemiological analysis included 14 studies from Australia, Europe and North America. Polymorphisms in 16 genes coding for the androgen pathway were analyzed using a gene-based approach: versatile gene-based test association study. This method evaluates associations between a trait and all SNPs within a specific gene rather than each SNP marker individually as in a conventional GWAS. The data were stratified for sex, body-mass index, waist-to-hip ratio, tobacco smoking and gastroesophageal reflux status. Included were data from 1,508 EAC patients, 2,383 BE patients and 2,170 control participants. SNPs within the gene CYP17A1 were associated with risk of BE in the sexes combined (p = 0.002) and in males (p = 0.003), but not in females separately (p = 0.3). This association was found in tobacco smokers (p = 0.003) and in BE patients without reflux (p = 0.004), but not in nonsmokers (p = 0.2) or those with reflux (p = 0.036). SNPs within JMJD1C were associated with risk of EAC in females (p = 0.001). However, none of these associations replicated in a subsequent sample. Fourteen other genes studied did not reach statistically significant levels of association with BE, EAC or the combination of BE and EAC, after correcting for the number of genes included in the analysis. In conclusion, genetic variants in the androgen-related genes CYP17A1 and JMJD1C might be associated with risk of BE and EAC, respectively, but replication data with larger sample sizes are needed.
Published: 2016
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66. Large scale meta-analysis identifies new genetic risk loci for esophageal adenocarcinoma (EA) and the first EA risk locus independent of Barrett’s esophagus

Author: Gharahkhani, Puya, Fitzgerald, Rebecca C., Vaughan, Thomas L., Tomlinson, Ian, Gockel, Ines, Palles, Claire, 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, Bohmer, Anne C., Izbicki, Jakob R., Holscher, Arnulf H., Lang, Hauke, Lorenz, Dietmar, Schumacher, Brigitte, Hackelsberger, Andreas, Mayershofer, Rupert, Pech, Oliver, Vashist, Yogesh, Ott, Katja, Vieth, Michael, Weismuller, Josef, Nothen, Markus M., Attwood, Stephen, Barr, Hugh, Chegwidden, Laura, deCaestecker, John, Harrison, Rebecca, Love, Sharon B., MacDonald, David, Moayyedi, Paul, Prenen, Hans, Watson, RG 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, Rosch, Thomas, Ell, Christian, MacGregor, Stuart, Pharoah, Paul, Whiteman, David C., Jankowski, Janusz, Schumacher, Johannes, Gharahkhani, Puya, Fitzgerald, Rebecca C., Vaughan, Thomas L., Tomlinson, Ian, Gockel, Ines, Palles, Claire, 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, Bohmer, Anne C., Izbicki, Jakob R., Holscher, Arnulf H., Lang, Hauke, Lorenz, Dietmar, Schumacher, Brigitte, Hackelsberger, Andreas, Mayershofer, Rupert, Pech, Oliver, Vashist, Yogesh, Ott, Katja, Vieth, Michael, Weismuller, Josef, Nothen, Markus M., Attwood, Stephen, Barr, Hugh, Chegwidden, Laura, deCaestecker, John, Harrison, Rebecca, Love, Sharon B., MacDonald, David, Moayyedi, Paul, Prenen, Hans, Watson, RG 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, Rosch, Thomas, Ell, Christian, MacGregor, Stuart, Pharoah, Paul, Whiteman, David C., Jankowski, Janusz, and Schumacher, Johannes
Abstract: SUMMARY Background: Esophageal adenocarcinoma (EA) represents one of the fastest rising oncological diseases in western countries. Barrett’s Esophagus (BE) is the premalignant precursor of EA. However, only a subset of BE patients develop EA, which complicates the clinical management in the absence of valid predictors. Methods: Within an international consortium of groups involved in the genetics of BE/EA, we performed the first meta-analysis of all genome-wide association studies (GWAS) available (>10,000 BE/EA patients, >17,000 controls, all of European descent). The entire GWAS-data set was also analyzed using bioinformatics approaches in order to identify pathophysiologically relevant cellular pathways. Findings: We identified nine new disease loci for BE/EA (P<5×10-8) and thereby doubled the number of known risk loci. The strongest new risk locus implicates CFTR as BE/EA risk gene. Mutations in CFTR cause cystic fibrosis (CF), the most common recessive disorder in Europeans. Gastroesophageal reflux (GER) belongs to the phenotypic CF-spectrum and represents the main risk factor for BE/EA. Thus, the CFTR locus may trigger a common GER-mediated pathophysiology. The strongest disease pathways identified (P<10-6) belong to muscle cell differentiation and to mesenchyme development/differentiation, which fit with current pathophysiological BE/EA concepts. Furthermore, for the first time we identified an EA-specific association (P=1·6×10-8) near HTR3C/ABCC5 which is independent of BE development (P=0·45). Interpretation: The identified disease loci and pathways reveal new insights into the etiology of BE and EA. Furthermore, the EA-specific association at HTR3C/ABCC5 may constitute a novel genetic marker for the prediction of transition from BE to EA. Funding: US National Cancer Institute, US National Institutes of Health, National Health and Medical Research Council of Australia, Swedish Cancer Society, Medical Research Council of UK, Cambridge NIHR biomedical researc
Published: 2016

67. In Utero Exposure to Compounds with Dioxin-like Activity and Birth Outcomes

Author: Vafeiadi, Marina Agramunt, Silvia Pedersen, Marie Besselink, Harrie Chatzi, Leda Fthenou, Eleni Fleming, Sarah and Hardie, Laura J. Wright, John Knudsen, Lisbeth E. Nielsen, Jeanette K. S. Sunyer, Jordi Carreras, Ramon Brunborg, Gunnar Gutzkow, Kristine B. Nygaard, Unni C. Lovik, Martinus and Kyrtopoulos, Soterios A. Segerback, Dan Merlo, Domenico F. and Kleinjans, Jos C. Vrijheid, Martine Kogevinas, Manolis and NewGeneris Consortium
Abstract: Background: Maternal exposure to dioxins and dioxin-like compounds may affect fetal growth and development. We evaluated the association between in utero dioxin-like activity and birth outcomes in a prospective European mother-child study. Methods: We measured dioxin-like activity in maternal and cord blood plasma samples collected at delivery using the Dioxin-Responsive Chemically Activated LUciferase eXpression (DR CALUX) bioassay in 967 mother-child pairs, in Denmark, Greece, Norway, Spain, and England. Multiple linear regression models were used to investigate the associations with birth weight, gestational age, and head circumference. Results: Plasma dioxin-like activity was higher in maternal sample than in cord samples. Birth weight was lower with medium (-58 g [95% confidence interval (CI) = -176 to 62]) and high (-82 g [-216 to 53]) tertiles of exposure (cord blood) compared with the lowest tertile. Gestational age was shorter by approximately half a week in the highest compared with the lowest (-0.4 weeks [95% CI = -0.8 to -0.1]). This association was stronger in boys than in girls, although the statistical evidence for interaction was weak (P = 0.22). Analysis based on CALUX-toxic equivalents expressed per milliliter of plasma showed similar trends. We found no association between dioxin-like activity in maternal plasma and birth outcomes. Conclusions: Results from this international general population study suggest an association between low-level prenatal dioxin-like activity and shorter gestational age, particularly in boys, with weaker associations for birth weight.
Published: 2014

68. Micronuclei in Cord Blood Lymphocytes and Associations with Biomarkers of Exposure to Carcinogens and Hormonally Active Factors, Gene Polymorphisms, and Gene Expression: The NewGeneris Cohort

Author: Merlo, Domenico Franco Agramunt, Silvia Anna, Livia and Besselink, Harrie Botsivali, Maria Brady, Nigel J. Ceppi, Marcello Chatzi, Leda Chen, Bowang Decordier, Ilse and Farmer, Peter B. Fleming, Sarah Fontana, Vincenzo Foersti, Asta Fthenou, Eleni Gallo, Fabio Georgiadis, Panagiotis and Gmuender, Hans Godschalk, Roger W. Granum, Berit Hardie, Laura J. Hemminki, Kari Hochstenbach, Kevin Knudsen, Lisbeth E. Kogevinas, Manolis Kovacs, Katalin Kyrtopoulos, Soterios A. Lovik, Martinus Nielsen, Jeanette K. Nygaard, Unni Cecilie Pedersen, Marie Rydberg, Per Schoket, Bernadette and Segerback, Dan Singh, Rajinder Sunyer, Jordi Tornqvist, Margareta van Loveren, Henk van Schooten, Frederik J. vande Loock, Kim von Stedingk, Hans Wright, John Kleinjans, Jos C. and Kirsch-Volders, Micheline van Delft, Joost H. M. NewGeneris Consortium
Abstract: Background: Leukemia incidence has increased in recent decades among European children, -suggesting that early-life environmental exposures play an important role in disease development. Objectives: We investigated the hypothesis that childhood susceptibility may increase as a result of in utero exposure to carcinogens and hormonally acting factors. Using cord blood samples from the NewGeneris cohort, we examined associations between a range of biomarkers of carcinogen exposure and hormonally acting factors with micronuclei (MN) frequency as a proxy measure of cancer risk. Associations with gene expression and genotype were also explored. Methods: DNA and protein adducts, gene expression profiles, circulating hormonally acting factors, and GWAS (genome-wide association study) data were investigated in relation to genomic damage measured by MN frequency in lymphocytes from 623 newborns enrolled between 2006 and 2010 across Europe. Results: Malondialdehyde DNA adducts (M(1)dG) were associated with increased MN frequency in binucleated lymphocytes (MNBN), and exposure to androgenic, estrogenic, and dioxin-like compounds was associated with MN frequency in mononucleated lymphocytes (MNMONO), although no monotonic exposure-outcome relationship was observed. Lower frequencies of MNBN were associated with a 1-unit increase expression of PDCD11, LATS2, TRIM13, CD28, SMC1A, IL7R, and NIPBL genes. Gene expression was significantly higher in association with the highest versus lowest category of bulky and M(1)dG-DNA adducts for five and six genes, respectively. Gene expression levels were significantly lower for 11 genes in association with the highest versus lowest category of plasma AR CALUX (R) (chemically activated luciferase expression for androgens) (8 genes), ER alpha CALUX (R) (for estrogens) (2 genes), and DR CALUX (R) (for dioxins). Several SNPs (single-nucleotide polymorphisms) on chromosome 11 near FOLH1 significantly modified associations between androgen activity and MNBN frequency. Polymorphisms in EPHX1/ 2 and CYP2E1 were associated with MNBN. Conclusion: We measured in utero exposure to selected environmental carcinogens and circulating hormonally acting factors and detected associations with MN frequency in newborns circulating T lymphocytes. The results highlight mechanisms that may contribute to carcinogen-induced leukemia and require further research.
Published: 2014

69. 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 and Pedersen, Marie Besselink, Harrie Mendez, Michelle A. and Fleming, Sarah Hardie, Laura J. Knudsen, Lisbeth E. Wright, John Agramunt, Silvia Sunyer, Jordi Granum, Berit and Gutzkow, Kristine B. Brunborg, Gunnar Alexander, Jan and Meltzer, Helle Margrete Brantsaeter, Anne Lise Sarri, Katerina and Chatzi, Leda Merlo, Domenico F. Kleinjans, Jos C. and Haugen, Margaretha
Abstract: Maternal diet can result in exposure to environmental contaminants including dioxins which may influence foetal growth. We investigated the association between maternal diet and birth outcomes by defining a dioxin-rich diet. We used validated food frequency questionnaires to assess the diet of pregnant women from Greece, Spain, United Kingdom, Denmark and Norway and estimated plasma dioxin-like activity by the Dioxin-Responsive Chemically Activated LUciferase eXpression (DR-CALUX (R)) bioassay in 604 maternal blood samples collected at delivery. We applied reduced rank regression to identify a dioxin-rich dietary pattern based on dioxin-like activity (DR-CALUX (R)) levels in maternal plasma, and calculated a dioxin-diet score as an estimate of adherence to this dietary pattern. In the five country population, dioxin-diet score was characterised by high consumption of red and white meat, lean and fatty fish, low-fat dairy and low consumption of salty snacks and high-fat cheese, during pregnancy. The upper tertile of the dioxin-diet score was associated with a change in birth weight of -121 g (95% confidence intervals: -232, -10 g) compared to the lower tertile after adjustment for con-founders. A small non-significant reduction in gestational age was also observed (-1.4 days, 95% CI: -3.8, 1.0 days). Our results suggest that maternal diet might contribute to the exposure of the foetus to dioxins and dioxin-like compounds and may be related to reduced birth weight. More studies are needed to develop updated dietary guidelines for women of reproductive age, aiming to the reduction of dietary exposure to persistent organic pollutants as dioxins and dioxin-like compounds. (C) 2014 Elsevier B.V. All rights reserved.
Published: 2014

70. Circadian Rhythm and Sleep Disruption: Causes, Metabolic Consequences, and Countermeasures

Author: Potter, Gregory D. M., primary, Skene, Debra J., additional, Arendt, Josephine, additional, Cade, Janet E., additional, Grant, Peter J., additional, and Hardie, Laura J., additional
Published: 2016
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71. Germline variation in inflammation-related pathways and risk of Barrett's oesophagus and oesophageal adenocarcinoma

Author: Buas, Matthew F, primary, He, Qianchuan, additional, Johnson, Lisa G, additional, Onstad, Lynn, additional, Levine, David M, additional, Thrift, Aaron P, additional, Gharahkhani, Puya, additional, Palles, Claire, additional, Lagergren, Jesper, additional, Fitzgerald, Rebecca C, additional, Ye, Weimin, additional, Caldas, Carlos, additional, Bird, Nigel C, additional, Shaheen, Nicholas J, additional, Bernstein, Leslie, additional, Gammon, Marilie D, additional, Wu, Anna H, additional, Hardie, Laura J, additional, Pharoah, Paul D, additional, Liu, Geoffrey, additional, Iyer, Prassad, additional, Corley, Douglas A, additional, Risch, Harvey A, additional, Chow, Wong-Ho, additional, Prenen, Hans, additional, Chegwidden, Laura, additional, Love, Sharon, additional, Attwood, Stephen, additional, Moayyedi, Paul, additional, MacDonald, David, additional, Harrison, Rebecca, additional, Watson, Peter, additional, Barr, Hugh, additional, deCaestecker, John, additional, Tomlinson, Ian, additional, Jankowski, Janusz, additional, Whiteman, David C, additional, MacGregor, Stuart, additional, Vaughan, Thomas L, additional, and Madeleine, Margaret M, additional
Published: 2016
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72. Constrained Score Statistics Identify Genetic Variants Interacting with Multiple Risk Factors in Barrett’s Esophagus

Author: Dai, James Y., primary, Tapsoba, Jean de Dieu, additional, Buas, Matthew F., additional, Risch, Harvey A., additional, Vaughan, Thomas L., additional, Chow, Wong-Ho, additional, Shaheen, Nicholas J., additional, Anderson, Lesley, additional, Corley, Douglas A., additional, Gammon, Marilie D., additional, Hardie, Laura J., additional, Lagergren, Jesper, additional, and Whiteman, David C., additional
Published: 2016
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73. Nutrition and the circadian system

Author: Potter, Gregory D. M., primary, Cade, Janet E., additional, Grant, Peter J., additional, and Hardie, Laura J., additional
Published: 2016
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74. Erratum: “Environmental, Dietary, Maternal, and Fetal Predictors of Bulky DNA Adducts in Cord Blood: A European Mother–Child Study (NewGeneris)”

Author: Pedersen, Marie, primary, Mendez, Michelle A., additional, Schoket, Bernadette, additional, Godschalk, Roger W., additional, Espinosa, Ana, additional, Landström, Anette, additional, Villanueva, Cristina M., additional, Merlo, Domenico F., additional, Fthenou, Eleni, additional, Gracia-Lavedan, Esther, additional, van Schooten, Frederik-J., additional, Hoek, Gerard, additional, Brunborg, Gunnar, additional, Meltzer, Helle M., additional, Alexander, Jan, additional, Nielsen, Jeanette K., additional, Sunyer, Jordi, additional, Wright, John, additional, Kovács, Katalin, additional, de Hoogh, Kees, additional, Gutzkow, Kristine B., additional, Hardie, Laura J., additional, Chatzi, Leda, additional, Knudsen, Lisbeth E., additional, Anna, Lívia, additional, Ketzel, Matthias, additional, Haugen, Margaretha, additional, Botsivali, Maria, additional, Nieuwenhuijsen, Mark J., additional, Cirach, Marta, additional, Toledano, Mireille B., additional, Smith, Rachel B., additional, Fleming, Sarah, additional, Agramunt, Silvia, additional, Kyrtopoulos, Soterios A., additional, Lukács, Viktória, additional, Kleinjans, Jos C., additional, Segerbäck, Dan, additional, and Kogevinas, Manolis, additional
Published: 2016
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75. Polymorphisms in Genes of Relevance for Oestrogen and Oxytocin Pathways and Risk of Barrett's Oesophagus and Oesophageal Adenocarcinoma : A Pooled Analysis from the BEACON Consortium.

Author: Lagergren, Katarina, Ek, Weronica E, Levine, David, Chow, Wong-Ho, Bernstein, Leslie, Casson, Alan G, Risch, Harvey A, Shaheen, Nicholas J, Bird, Nigel C, Reid, Brian J, Corley, Douglas A, Hardie, Laura J, Wu, Anna H, Fitzgerald, Rebecca C, Pharoah, Paul, Caldas, Carlos, Romero, Yvonne, Vaughan, Thomas L, MacGregor, Stuart, Whiteman, David, Westberg, Lars, Nyren, Olof, Lagergren, Jesper, Lagergren, Katarina, Ek, Weronica E, Levine, David, Chow, Wong-Ho, Bernstein, Leslie, Casson, Alan G, Risch, Harvey A, Shaheen, Nicholas J, Bird, Nigel C, Reid, Brian J, Corley, Douglas A, Hardie, Laura J, Wu, Anna H, Fitzgerald, Rebecca C, Pharoah, Paul, Caldas, Carlos, Romero, Yvonne, Vaughan, Thomas L, MacGregor, Stuart, Whiteman, David, Westberg, Lars, Nyren, Olof, and Lagergren, Jesper
Abstract: BACKGROUND: The strong male predominance in oesophageal adenocarcinoma (OAC) and Barrett's oesophagus (BO) continues to puzzle. Hormonal influence, e.g. oestrogen or oxytocin, might contribute. METHODS: This genetic-epidemiological study pooled 14 studies from three continents, Australia, Europe, and North America. Polymorphisms in 3 key genes coding for the oestrogen pathway (receptor alpha (ESR1), receptor beta (ESR2), and aromatase (CYP19A1)), and 3 key genes of the oxytocin pathway (the oxytocin receptor (OXTR), oxytocin protein (OXT), and cyclic ADP ribose hydrolase glycoprotein (CD38)), were analysed using a gene-based approach, versatile gene-based test association study (VEGAS). RESULTS: Among 1508 OAC patients, 2383 BO patients, and 2170 controls, genetic variants within ESR1 were associated with BO in males (p = 0.0058) and an increased risk of OAC and BO combined in males (p = 0.0023). Genetic variants within OXTR were associated with an increased risk of BO in both sexes combined (p = 0.0035) and in males (p = 0.0012). We followed up these suggestive findings in a further smaller data set, but found no replication. There were no significant associations between the other 4 genes studied and risk of OAC, BO, separately on in combination, in males and females combined or in males only. CONCLUSION: Genetic variants in the oestrogen receptor alpha and the oxytocin receptor may be associated with an increased risk of BO or OAC, but replication in other large samples are needed., Shared first authorship
Published: 2015
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76. Pleiotropic Analysis of Cancer Risk Loci on Esophageal Adenocarcinoma Risk.

Author: Lee, Eunjung, Stram, Daniel O, Ek, Weronica E, Onstad, Lynn E, MacGregor, Stuart, Gharahkhani, Puya, Ye, Weimin, Lagergren, Jesper, Shaheen, Nicholas J, Murray, Liam J, Hardie, Laura J, Gammon, Marilie D, Chow, Wong-Ho, Risch, Harvey A, Corley, Douglas A, Levine, David M, Whiteman, David C, Bernstein, Leslie, Bird, Nigel C, Vaughan, Thomas L, Wu, Anna H, Lee, Eunjung, Stram, Daniel O, Ek, Weronica E, Onstad, Lynn E, MacGregor, Stuart, Gharahkhani, Puya, Ye, Weimin, Lagergren, Jesper, Shaheen, Nicholas J, Murray, Liam J, Hardie, Laura J, Gammon, Marilie D, Chow, Wong-Ho, Risch, Harvey A, Corley, Douglas A, Levine, David M, Whiteman, David C, Bernstein, Leslie, Bird, Nigel C, Vaughan, Thomas L, and Wu, Anna H
Abstract: BACKGROUND: Several cancer-associated loci identified from genome-wide association studies (GWAS) have been associated with risks of multiple cancer sites, suggesting pleiotropic effects. We investigated whether GWAS-identified risk variants for other common cancers are associated with risk of esophageal adenocarcinoma (EA) or its precursor, Barrett's esophagus. METHODS: We examined the associations between risks of EA and Barrett's esophagus and 387 SNPs that have been associated with risks of other cancers, by using genotype imputation data on 2,163 control participants and 3,885 (1,501 EA and 2,384 Barrett's esophagus) case patients from the Barrett's and Esophageal Adenocarcinoma Genetic Susceptibility Study, and investigated effect modification by smoking history, body mass index (BMI), and reflux/heartburn. RESULTS: After correcting for multiple testing, none of the tested 387 SNPs were statistically significantly associated with risk of EA or Barrett's esophagus. No evidence of effect modification by smoking, BMI, or reflux/heartburn was observed. CONCLUSIONS: Genetic risk variants for common cancers identified from GWAS appear not to be associated with risks of EA or Barrett's esophagus. IMPACT: To our knowledge, this is the first investigation of pleiotropic genetic associations with risks of EA and Barrett's esophagus. Cancer Epidemiol Biomarkers Prev; 24(11); 1801-3. ©2015 AACR.
Published: 2015
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77. Environmental, Dietary, Maternal, and Fetal Predictors of Bulky DNA Adducts in Cord Blood:A European Mother-Child Study (NewGeneris)

Author: Pedersen, Marie, Mendez, Michelle A, Schoket, Bernadette, Godschalk, Roger W, Espinosa, Ana, Landström, Anette, Villanueva, Cristina M, Merlo, Domenico F, Fthenou, Eleni, Gracia-Lavedan, Esther, van Schooten, Frederik-J, Hoek, Gerard, Brunborg, Gunnar, Meltzer, Helle M, Alexander, Jan, Nielsen, Jeanette Kolstrup Søgaard, Sunyer, Jordi, Wright, John, Kovács, Katalin, de Hoogh, Kees, Gutzkow, Kristine B, Hardie, Laura J, Chatzi, Leda, Knudsen, Lisbeth E., Anna, Lívia, Ketzel, Matthias, Haugen, Margaretha, Botsivali, Maria, Nieuwenhuijsen, Mark J, Cirach, Marta, Toledano, Mireille B, Smith, Rachel B, Fleming, Sarah, Agramunt, Silvia, Kyrtopoulos, Soterios A, Lukács, Viktória, Kleinjans, Jos C, Segerbäck, Dan, Kogevinas, Manolis, Pedersen, Marie, Mendez, Michelle A, Schoket, Bernadette, Godschalk, Roger W, Espinosa, Ana, Landström, Anette, Villanueva, Cristina M, Merlo, Domenico F, Fthenou, Eleni, Gracia-Lavedan, Esther, van Schooten, Frederik-J, Hoek, Gerard, Brunborg, Gunnar, Meltzer, Helle M, Alexander, Jan, Nielsen, Jeanette Kolstrup Søgaard, Sunyer, Jordi, Wright, John, Kovács, Katalin, de Hoogh, Kees, Gutzkow, Kristine B, Hardie, Laura J, Chatzi, Leda, Knudsen, Lisbeth E., Anna, Lívia, Ketzel, Matthias, Haugen, Margaretha, Botsivali, Maria, Nieuwenhuijsen, Mark J, Cirach, Marta, Toledano, Mireille B, Smith, Rachel B, Fleming, Sarah, Agramunt, Silvia, Kyrtopoulos, Soterios A, Lukács, Viktória, Kleinjans, Jos C, Segerbäck, Dan, and Kogevinas, Manolis
Abstract: BACKGROUND: Bulky DNA adducts reflect genotoxic exposures, have been associated with lower birth weight, and may predict cancer risk.OBJECTIVE: We selected factors known or hypothesized to affect in utero adduct formation and repair and examined their associations with adduct levels in neonates.METHODS: Pregnant women from Greece, Spain, England, Denmark, and Norway were recruited in 2006-2010. Cord blood bulky DNA adduct levels were measured by the 32P-postlabeling technique (n = 511). Diet and maternal characteristics were assessed via questionnaires. Modeled exposures to air pollutants and drinking-water disinfection by-products, mainly trihalomethanes (THMs), were available for a large proportion of the study population.RESULTS: Greek and Spanish neonates had higher adduct levels than the northern European neonates [median, 12.1 (n = 179) vs. 6.8 (n = 332) adducts per 108 nucleotides, p < 0.001]. Residence in southern European countries, higher maternal body mass index, delivery by cesarean section, male infant sex, low maternal intake of fruits rich in vitamin C, high intake of dairy products, and low adherence to healthy diet score were statistically significantly associated with higher adduct levels in adjusted models. Exposure to fine particulate matter and nitrogen dioxide was associated with significantly higher adducts in the Danish subsample only. Overall, the pooled results for THMs in water show no evidence of association with adduct levels; however, there are country-specific differences in results with a suggestion of an association in England.CONCLUSION: These findings suggest that a combination of factors, including unknown country-specific factors, influence the bulky DNA adduct levels in neonates.
Published: 2015

78. Bulky DNA Adducts in Cord Blood, Maternal Fruit-and-Vegetable Consumption, and Birth Weight in a European Mother–Child Study (NewGeneris)

Author: Botsivali, Maria, Hardie, Laura J., Chatzi, Leda, Brady, Nigel J., Schoket, Bernadette, Agramunt, Sylvia, Lukács, Viktória, Landström, Anette, Brunborg, Gunnar, Gützkow, Kristine B., Fleming, Sarah, Kovács, Katalin, Nielsen, Jeanette K., von Stedingk, Hans, Knudsen, Lisbeth E.., Haugen, Margaretha, Farmer, Peter B., Fthenou, Eleni, Alexander, Jan, Kleinjans, Jos C., Kyrtopoulos, Soterios A., Sunyer, Jordi, Merlo, Domenico Franco, Anna, Lívia, Arab, Khelifa, Godschalk, Roger W., Wright, John, Pedersen, Marie, Mendez, Michelle A., Espinosa, Aina, Törnqvist, Margareta, and Meltzer, Helle Margrete
Abstract: Background: Tobacco-smoke, airborne, and dietary exposures to polycyclic aromatic hydrocarbons (PAHs) have been associated with reduced prenatal growth. Evidence from biomarker-based studies of low-exposed populations is limited. Bulky DNA adducts in cord blood reflect the prenatal effective dose to several genotoxic agents including PAHs.
Published: 2013
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79. Assessment of Urinary Deoxynivalenol Biomarkers in UK Children and Adolescents.

Author: Papageorgiou, Maria, Wells, Liz, Williams, Courtney, White, Kay, De Santis, Barbara, Liu, Yunru, Debegnach, Francesca, Miano, Brunella, Moretti, Giorgio, Greetham, Stephanie, Brera, Carlo, Atkin, Stephen L, Hardie, Laura J, and Sathyapalan, Thozhukat
Subjects: DEOXYNIVALENOL, MYCOTOXINS, GLUCURONIDES, CREATININE, URINALYSIS
Abstract: Deoxynivalenol (DON), the mycotoxin produced mainly by Fusarium graminearum and found in contaminated cereal-based foodstuff, has been consistently detected in body fluids in adults. Available data in children and adolescents are scarce. This study assessed urinary DON concentrations in children aged 3-9 years (n = 40) and adolescents aged 10-17 years (n = 39) in the UK. Morning urine samples were collected over two consecutive days and analysed for free DON (un-metabolised form), DON-glucuronides (DON-GlcA), deepoxy deoxynivalenol (DOM-1), and total DON (sum of free DON, DON-GlcA, and DOM-1). Total DON was detected in the urine of >95% of children and adolescents on both days. Mean total DON concentrations (ng/mg creatinine) were 41.6 and 21.0 for children and adolescents, respectively. The greatest total DON levels were obtained in female children on both days (214 and 219 ng/mg creatinine on days 1 and 2, respectively). Free DON and DON-GlcA were detected in most urine specimens, whereas DOM-1 was not present in any sample. Estimation of dietary DON exposure suggested that 33-63% of children and 5-46% of adolescents exceeded current guidance regarding the maximum provisional tolerable daily intake (PMTDI) for DON. Although moderate mean urinary DON concentrations were shown, the high detection frequency of urinary DON, the maximum biomarker concentrations, and estimated dietary DON exposure are concerning. [ABSTRACT FROM AUTHOR]
Published: 2018
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80. Birth Weight, Head Circumference, and Prenatal Exposure to Acrylamide from Maternal Diet: The European Prospective Mother-Child Study (NewGeneris)

Author: Pedersen, Marie von Stedingk, Hans Botsivali, Maria and Agramunt, Silvia Alexander, Jan Brunborg, Gunnar Chatzi, Leda Fleming, Sarah Fthenou, Eleni Granum, Berit and Gutzkow, Kristine B. Hardie, Laura J. Knudsen, Lisbeth E. and Kyrtopoulos, Soterios A. Mendez, Michelle A. Merlo, Domenico F. and Nielsen, Jeanette K. Rydberg, Per Segerback, Dan Sunyer, Jordi Wright, John Tornqvist, Margareta Kleinjans, Jos C. and Kogevinas, Manolis NewGeneris Consortium
Abstract: BACKGROUND: Acrylamide is a common dietary exposure that crosses the human placenta. It is classified as a probable human carcinogen, and developmental toxicity has been observed in rodents. OBJECTIVES: We examined the associations between prenatal exposure to acrylamide and birth outcomes in a prospective European mother child study. METHODS: Hemoglobin (Hb) adducts of acrylamide and its metabolite glycidamide were measured in cord blood (reflecting cumulated exposure in the last months of pregnancy) from 1,101 singleton pregnant women recruited in Denmark, England, Greece, Norway, and Spain during 2006-2010. Maternal diet was estimated through food-frequency questionnaires. RESULTS: Both acrylamide and glycidamide Hb adducts were associated with a statistically significant reduction in birth weight and head circumference. The estimated difference in birth weight for infants in the highest versus lowest quartile of acrylamide Hb adduct levels after adjusting for gestational age and country was -132 g (95% CI: -207, -56); the corresponding difference for head circumference was -0.33 cm (95% CI: -0.61, -0.06). Findings were similar in infants of nonsmokers, were consistent across countries, and remained after adjustment for Factors associated with reduced birth weight. Maternal consumption of foods rich in acrylamide, such as fried potatoes, was associated with cord blood acrylamide adduct levels and with reduced birth weight. CONCLUSIONS: Dietary exposure to acrylamide was associated with reduced birth weight and head circumference. Consumption of specific foods during pregnancy was associated with higher acrylamide exposure in utero. IF confirmed, these findings suggest that dietary intake of acrylamide should be reduced among pregnant women.
Published: 2012

81. Pleiotropic Analysis of Cancer Risk Loci on Esophageal Adenocarcinoma Risk

Author: Lee, Eunjung, primary, Stram, Daniel O., additional, Ek, Weronica E., additional, Onstad, Lynn E., additional, MacGregor, Stuart, additional, Gharahkhani, Puya, additional, Ye, Weimin, additional, Lagergren, Jesper, additional, Shaheen, Nicholas J., additional, Murray, Liam J., additional, Hardie, Laura J., additional, Gammon, Marilie D., additional, Chow, Wong-Ho, additional, Risch, Harvey A., additional, Corley, Douglas A., additional, Levine, David M., additional, Whiteman, David C., additional, Bernstein, Leslie, additional, Bird, Nigel C., additional, Vaughan, Thomas L., additional, and Wu, Anna H., additional
Published: 2015
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82. A Newly Identified Susceptibility Locus nearFOXP1Modifies the Association of Gastroesophageal Reflux with Barrett's Esophagus

Author: Dai, James Y., primary, de Dieu Tapsoba, Jean, additional, Buas, Matthew F., additional, Onstad, Lynn E., additional, Levine, David M., additional, Risch, Harvey A., additional, Chow, Wong-Ho, additional, Bernstein, Leslie, additional, Ye, Weimin, additional, Lagergren, Jesper, additional, Bird, Nigel C., additional, Corley, Douglas A., additional, Shaheen, Nicholas J., additional, Wu, Anna H., additional, Reid, Brian J., additional, Hardie, Laura J., additional, Whiteman, David C., additional, and Vaughan, Thomas L., additional
Published: 2015
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83. Polymorphisms in genes in the androgen pathway and risk of Barrett's esophagus and esophageal adenocarcinoma

Author: Ek, Weronica E., primary, Lagergren, Katarina, additional, Cook, Michael, additional, Wu, Anna H., additional, Abnet, Christian C., additional, Levine, David, additional, Chow, Wong-Ho, additional, Bernstein, Leslie, additional, Risch, Harvey A., additional, Shaheen, Nicholas J., additional, Bird, Nigel C., additional, Corley, Douglas A., additional, Hardie, Laura J., additional, Fitzgerald, Rebecca C., additional, Gammon, Marilie D., additional, Romero, Yvonne, additional, Liu, Geoffrey, additional, Ye, Weimin, additional, Vaughan, Thomas L., additional, MacGregor, Stuart, additional, Whiteman, David C., additional, Westberg, Lars, additional, and Lagergren, Jesper, additional
Published: 2015
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84. Polymorphisms in Genes of Relevance for Oestrogen and Oxytocin Pathways and Risk of Barrett’s Oesophagus and Oesophageal Adenocarcinoma: A Pooled Analysis from the BEACON Consortium

Author: Lagergren, Katarina, primary, Ek, Weronica E., additional, Levine, David, additional, Chow, Wong-Ho, additional, Bernstein, Leslie, additional, Casson, Alan G., additional, Risch, Harvey A., additional, Shaheen, Nicholas J., additional, Bird, Nigel C., additional, Reid, Brian J., additional, Corley, Douglas A., additional, Hardie, Laura J., additional, Wu, Anna H., additional, Fitzgerald, Rebecca C., additional, Pharoah, Paul, additional, Caldas, Carlos, additional, Romero, Yvonne, additional, Vaughan, Thomas L., additional, MacGregor, Stuart, additional, Whiteman, David, additional, Westberg, Lars, additional, Nyren, Olof, additional, and Lagergren, Jesper, additional
Published: 2015
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85. MiRNA-Related SNPs and Risk of Esophageal Adenocarcinoma and Barrett’s Esophagus: Post Genome-Wide Association Analysis in the BEACON Consortium

Author: Buas, Matthew F., primary, Onstad, Lynn, additional, Levine, David M., additional, Risch, Harvey A., additional, Chow, Wong-Ho, additional, Liu, Geoffrey, additional, Fitzgerald, Rebecca C., additional, Bernstein, Leslie, additional, Ye, Weimin, additional, Bird, Nigel C., additional, Romero, Yvonne, additional, Casson, Alan G., additional, Corley, Douglas A., additional, Shaheen, Nicholas J., additional, Wu, Anna H., additional, Gammon, Marilie D., additional, Reid, Brian J., additional, Hardie, Laura J., additional, Peters, Ulrike, additional, Whiteman, David C., additional, and Vaughan, Thomas L., additional
Published: 2015
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86. Environmental, Dietary, Maternal, and Fetal Predictors of Bulky DNA Adducts in Cord Blood: A European Mother–Child Study (NewGeneris)

Author: Pedersen, Marie, primary, Mendez, Michelle A., additional, Schoket, Bernadette, additional, Godschalk, Roger W., additional, Espinosa, Ana, additional, Landström, Anette, additional, Villanueva, Cristina M., additional, Merlo, Domenico F., additional, Fthenou, Eleni, additional, Gracia-Lavedan, Esther, additional, van Schooten, Frederik-J., additional, Hoek, Gerard, additional, Brunborg, Gunnar, additional, Meltzer, Helle M., additional, Alexander, Jan, additional, Nielsen, Jeanette K., additional, Sunyer, Jordi, additional, Wright, John, additional, Kovács, Katalin, additional, de Hoogh, Kees, additional, Gutzkow, Kristine B., additional, Hardie, Laura J., additional, Chatzi, Leda, additional, Knudsen, Lisbeth E., additional, Anna, Lívia, additional, Ketzel, Matthias, additional, Haugen, Margaretha, additional, Botsivali, Maria, additional, Nieuwenhuijsen, Mark J., additional, Cirach, Marta, additional, Toledano, Mireille B., additional, Smith, Rachel B., additional, Fleming, Sarah, additional, Agramunt, Silvia, additional, Kyrtopoulos, Soterios A., additional, Lukács, Viktória, additional, Kleinjans, Jos C., additional, Segerbäck, Dan, additional, and Kogevinas, Manolis, additional
Published: 2015
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87. 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, Whiteman, David C, 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
Abstract: BACKGROUND: Data from observational studies suggest that body mass index (BMI) is causally related to esophageal adenocarcinoma (EAC) and its precursor, Barrett's esophagus (BE). However, the relationships may be affected by bias and confounding. METHODS: We used data from the Barrett's and Esophageal Adenocarcinoma Genetic Susceptibility Study: 999 patients with EAC, 2061 patients with BE, and 2169 population controls. We applied the two-stage control function instrumental variable method of the Mendelian randomization approach to estimate the unbiased, unconfounded effect of BMI on risk of EAC and BE. This was performed using a genetic risk score, derived from 29 genetic variants shown to be associated with BMI, as an instrument for lifetime BMI. A higher score indicates propensity to obesity. All tests were two-sided. RESULTS: The genetic risk score was not associated with potential confounders, including gastroesophageal reflux symptoms and smoking. In the instrumental variable analyses (IV), EAC risk increased by 16% (IV-odds ratio [OR] = 1.16, 95% confidence interval [CI] = 1.01 to 1.33) and BE risk increased by 12% (IV-OR = 1.12, 95% CI = 1.00 to 1.25) per 1kg/m(2) increase in BMI. BMI was statistically significantly associated with EAC and BE in conventional epidemiologic analyses. CONCLUSIONS: People with a high genetic propensity to obesity have higher risks of esophageal metaplasia and neoplasia than people with low genetic propensity. These analyses provide the strongest evidence to date that obesity is independently associated with BE and EAC, and is not due to confounding or bias inherent in conventional epidemiologic analyses.
Published: 2014
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88. In Utero Exposure to Compounds with Dioxin-like Activity and Birth Outcomes

Author: 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, Kogevinas, Manolis, 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
Abstract: BACKGROUND: Maternal exposure to dioxins and dioxin-like compounds may affect fetal growth and development. We evaluated the association between in utero dioxin-like activity and birth outcomes in a prospective European mother-child study.METHODS: We measured dioxin-like activity in maternal and cord blood plasma samples collected at delivery using the Dioxin-Responsive Chemically Activated LUciferase eXpression (DR CALUX) bioassay in 967 mother-child pairs, in Denmark, Greece, Norway, Spain, and England. Multiple linear regression models were used to investigate the associations with birth weight, gestational age, and head circumference.RESULTS: Plasma dioxin-like activity was higher in maternal sample than in cord samples. Birth weight was lower with medium (-58 g [95% confidence interval (CI) = -176 to 62]) and high (-82 g [-216 to 53]) tertiles of exposure (cord blood) compared with the lowest tertile. Gestational age was shorter by approximately half a week in the highest compared with the lowest (-0.4 weeks [95% CI = -0.8 to -0.1]). This association was stronger in boys than in girls, although the statistical evidence for interaction was weak (P = 0.22). Analysis based on CALUX-toxic equivalents expressed per milliliter of plasma showed similar trends. We found no association between dioxin-like activity in maternal plasma and birth outcomes.CONCLUSIONS: Results from this international general population study suggest an association between low-level prenatal dioxin-like activity and shorter gestational age, particularly in boys, with weaker associations for birth weight.
Published: 2014

89. Micronuclei in cord blood lymphocytes and associations with biomarkers of exposure to carcinogens and hormonally active factors, gene polymorphisms, and gene expression:the NewGeneris cohort

Author: Merlo, Domenico Franco, Agramunt, Silvia, Anna, Lívia, Besselink, Harrie, Botsivali, Maria, Brady, Nigel J, Ceppi, Marcello, Chatzi, Leda, Chen, Bowang, Decordier, Ilse, Farmer, Peter B, Fleming, Sarah, Fontana, Vincenzo, Försti, Asta, Fthenou, Eleni, Gallo, Fabio, Georgiadis, Panagiotis, Gmuender, Hans, Godschalk, Roger W, Granum, Berit, Hardie, Laura J, Hemminki, Kari, Hochstenbach, Kevin, Knudsen, Lisbeth E, Kogevinas, Manolis, Kovács, Katalin, Kyrtopoulos, Soterios A, Løvik, Martinus, Nielsen, Jeanette K, Nygaard, Unni Cecilie, Pedersen, Marie, Rydberg, Per, Schoket, Bernadette, Segerbäck, Dan, Singh, Rajinder, Sunyer, Jordi, Törnqvist, Margareta, van Loveren, Henk, van Schooten, Frederik J, Vande Loock, Kim, von Stedingk, Hans, Wright, Andrew John, Kleinjans, Jos C, Kirsch-Volders, Micheline, van Delft, Joost H M, Merlo, Domenico Franco, Agramunt, Silvia, Anna, Lívia, Besselink, Harrie, Botsivali, Maria, Brady, Nigel J, Ceppi, Marcello, Chatzi, Leda, Chen, Bowang, Decordier, Ilse, Farmer, Peter B, Fleming, Sarah, Fontana, Vincenzo, Försti, Asta, Fthenou, Eleni, Gallo, Fabio, Georgiadis, Panagiotis, Gmuender, Hans, Godschalk, Roger W, Granum, Berit, Hardie, Laura J, Hemminki, Kari, Hochstenbach, Kevin, Knudsen, Lisbeth E, Kogevinas, Manolis, Kovács, Katalin, Kyrtopoulos, Soterios A, Løvik, Martinus, Nielsen, Jeanette K, Nygaard, Unni Cecilie, Pedersen, Marie, Rydberg, Per, Schoket, Bernadette, Segerbäck, Dan, Singh, Rajinder, Sunyer, Jordi, Törnqvist, Margareta, van Loveren, Henk, van Schooten, Frederik J, Vande Loock, Kim, von Stedingk, Hans, Wright, Andrew John, Kleinjans, Jos C, Kirsch-Volders, Micheline, and van Delft, Joost H M
Abstract: Leukemia incidence has increased in recent decades among European children, suggesting that early-life environmental exposures play an important role in disease development.
Published: 2014

90. In Utero Exposure to Compounds with Dioxin-like Activity and Birth Outcomes

Author: Vafeiadi, Marina, primary, Agramunt, Silvia, additional, Pedersen, Marie, additional, Besselink, Harrie, additional, Chatzi, Leda, additional, Fthenou, Eleni, additional, Fleming, Sarah, additional, Hardie, Laura J., additional, Wright, John, additional, Knudsen, Lisbeth E., additional, Nielsen, Jeanette K.S., additional, Sunyer, Jordi, additional, Carreras, Ramon, additional, Brunborg, Gunnar, additional, Gutzkow, Kristine B., additional, Nygaard, Unni C., additional, Løvik, Martinus, additional, Kyrtopoulos, Soterios A., additional, Segerbäck, Dan, additional, Merlo, Domenico F., additional, Kleinjans, Jos C., additional, Vrijheid, Martine, additional, and Kogevinas, Manolis, additional
Published: 2014
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91. 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, MacGregor, Stuart, 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
Abstract: BACKGROUND: Esophageal adenocarcinoma (EA) is an increasingly common cancer with poor survival. Barrett's esophagus (BE) is the main precursor to EA, and every year 0.12% to 0.5% of BE patients progress to EA. BE typically arises on a background of chronic gastroesophageal reflux (GERD), one of the risk factors for EA. METHODS: We used genome-wide association data to investigate the genetic architecture underlying GERD, BE, and EA. We applied a method to estimate the variance explained (array heritability, h(2)g) and the genetic correlation (rg) between GERD, BE, and EA by considering all single nucleotide polymorphisms (SNPs) simultaneously. We also estimated the polygenic overlap between GERD, BE, and EA using a prediction approach. All tests were two-sided, except in the case of variance-explained estimation where one-sided tests were used. RESULTS: We estimated a statistically significant genetic variance explained for BE (h(2)g = 35%; standard error [SE] = 6%; one-sided P = 1 × 10(-9)) and for EA (h(2)g = 25 %; SE = 5%; one-sided P = 2 × 10(-7)). The genetic correlation between BE and EA was found to be high (rg = 1.0; SE = 0.37). We also estimated a statistically significant polygenic overlap between BE and EA (one-sided P = 1 × 10(-6)), which suggests, together with the high genetic correlation, that shared genes underlie the development of BE and EA. Conversely, no statistically significant results were obtained for GERD. CONCLUSIONS: We have demonstrated that risk to BE and EA is influenced by many germline genetic variants of small effect and that shared polygenic effects contribute to risk of these two diseases.
Published: 2013
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92. A genome-wide association study identifies new susceptibility loci for esophageal adenocarcinoma and Barrett's esophagus.

Author: Levine, David M, Ek, Weronica E, Zhang, Rui, Liu, Xinxue, Onstad, Lynn, Sather, Cassandra, Lao-Sirieix, Pierre, 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, Nyrén, Olof, Ye, Weimin, Liu, Geoffrey, Romero, Yvonne, Bernstein, Leslie, Wu, Anna H, Casson, Alan G, Chanock, Stephen J, Harrington, Patricia, Caldas, Isabel, Debiram-Beecham, Irene, Caldas, Carlos, Hayward, Nicholas K, Pharoah, Paul D, Fitzgerald, Rebecca C, Macgregor, Stuart, Whiteman, David C, Vaughan, Thomas L, Levine, David M, Ek, Weronica E, Zhang, Rui, Liu, Xinxue, Onstad, Lynn, Sather, Cassandra, Lao-Sirieix, Pierre, 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, Nyrén, Olof, Ye, Weimin, Liu, Geoffrey, Romero, Yvonne, Bernstein, Leslie, Wu, Anna H, Casson, Alan G, Chanock, Stephen J, Harrington, Patricia, Caldas, Isabel, Debiram-Beecham, Irene, Caldas, Carlos, Hayward, Nicholas K, Pharoah, Paul D, Fitzgerald, Rebecca C, Macgregor, Stuart, Whiteman, David C, and Vaughan, Thomas L
Abstract: Esophageal adenocarcinoma is a cancer with rising incidence and poor survival. Most such cancers arise in a specialized intestinal metaplastic epithelium, which is diagnostic of Barrett's esophagus. In a genome-wide association study, we compared esophageal adenocarcinoma cases (n = 2,390) and individuals with precancerous Barrett's esophagus (n = 3,175) with 10,120 controls in 2 phases. For the combined case group, we identified three new associations. The first is at 19p13 (rs10419226: P = 3.6 × 10(-10)) in CRTC1 (encoding CREB-regulated transcription coactivator), whose aberrant activation has been associated with oncogenic activity. A second is at 9q22 (rs11789015: P = 1.0 × 10(-9)) in BARX1, which encodes a transcription factor important in esophageal specification. A third is at 3p14 (rs2687201: P = 5.5 × 10(-9)) near the transcription factor FOXP1, which regulates esophageal development. We also refine a previously reported association with Barrett's esophagus near the putative tumor suppressor gene FOXF1 at 16q24 and extend our findings to now include esophageal adenocarcinoma.
Published: 2013
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93. Common variants at the MHC locus and at chromosome 16q24.1 predispose to Barrett's esophagus.

Author: Su, Zhan, Gay, Laura J, Strange, Amy, Palles, Claire, Band, Gavin, Whiteman, David C, Lescai, Francesco, Langford, Cordelia, Nanji, Manoj, Edkins, Sarah, van der Winkel, Anouk, Levine, David, Sasieni, Peter, Bellenguez, Céline, Howarth, Kimberley, Freeman, Colin, Trudgill, Nigel, Tucker, Art T, Pirinen, Matti, Peppelenbosch, Maikel P, van der Laan, Luc J W, Kuipers, Ernst J, Drenth, Joost P H, Peters, Wilbert H, Reynolds, John V, Kelleher, Dermot P, McManus, Ross, Grabsch, Heike, Prenen, Hans, Bisschops, Raf, Krishnadath, Kausila, Siersema, Peter D, van Baal, Jantine W P M, Middleton, Mark, Petty, Russell, Gillies, Richard, Burch, Nicola, Bhandari, Pradeep, Paterson, Stuart, Edwards, Cathryn, Penman, Ian, Vaidya, Kishor, Ang, Yeng, Murray, Iain, Patel, Praful, Ye, Weimin, Mullins, Paul, Wu, Anna H, Bird, Nigel C, Dallal, Helen, Shaheen, Nicholas J, Murray, Liam J, Koss, Konrad, Bernstein, Leslie, Romero, Yvonne, Hardie, Laura J, Zhang, Rui, Winter, Helen, Corley, Douglas A, Panter, Simon, Risch, Harvey A, Reid, Brian J, Sargeant, Ian, Gammon, Marilie D, Smart, Howard, Dhar, Anjan, McMurtry, Hugh, Ali, Haythem, Liu, Geoffrey, Casson, Alan G, Chow, Wong-Ho, Rutter, Matt, Tawil, Ashref, Morris, Danielle, Nwokolo, Chuka, Isaacs, Peter, Rodgers, Colin, Ragunath, Krish, MacDonald, Chris, Haigh, Chris, Monk, David, Davies, Gareth, Wajed, Saj, Johnston, David, Gibbons, Michael, Cullen, Sue, Church, Nicholas, Langley, Ruth, Griffin, Michael, Alderson, Derek, Deloukas, Panos, Hunt, Sarah E, Gray, Emma, Dronov, Serge, Potter, Simon C, Tashakkori-Ghanbaria, Avazeh, Anderson, Mark, Brooks, Claire, Blackwell, Jenefer M, Bramon, Elvira, Brown, Matthew A, Casas, Juan P, Corvin, Aiden, Duncanson, Audrey, Markus, Hugh S, Mathew, Christopher G, Palmer, Colin N A, Plomin, Robert, Rautanen, Anna, Sawcer, Stephen J, Trembath, Richard C, Viswanathan, Ananth C, Wood, Nicholas, Trynka, Gosia, Wijmenga, Cisca, Cazier, Jean-Baptiste, Atherfold, Paul, Nicholson, Anna M, Gellatly, Nichola L, Glancy, Deborah, Cooper, Sheldon C, Cunningham, David, Lind, Tore, Hapeshi, Julie, Ferry, David, Rathbone, Barrie, Brown, Julia, Love, Sharon, Attwood, Stephen, MacGregor, Stuart, Watson, Peter, Sanders, Scott, Ek, Weronica, Harrison, Rebecca F, Moayyedi, Paul, de Caestecker, John, Barr, Hugh, Stupka, Elia, Vaughan, Thomas L, Peltonen, Leena, Spencer, Chris C A, Tomlinson, Ian, Donnelly, Peter, Jankowski, Janusz A Z, Su, Zhan, Gay, Laura J, Strange, Amy, Palles, Claire, Band, Gavin, Whiteman, David C, Lescai, Francesco, Langford, Cordelia, Nanji, Manoj, Edkins, Sarah, van der Winkel, Anouk, Levine, David, Sasieni, Peter, Bellenguez, Céline, Howarth, Kimberley, Freeman, Colin, Trudgill, Nigel, Tucker, Art T, Pirinen, Matti, Peppelenbosch, Maikel P, van der Laan, Luc J W, Kuipers, Ernst J, Drenth, Joost P H, Peters, Wilbert H, Reynolds, John V, Kelleher, Dermot P, McManus, Ross, Grabsch, Heike, Prenen, Hans, Bisschops, Raf, Krishnadath, Kausila, Siersema, Peter D, van Baal, Jantine W P M, Middleton, Mark, Petty, Russell, Gillies, Richard, Burch, Nicola, Bhandari, Pradeep, Paterson, Stuart, Edwards, Cathryn, Penman, Ian, Vaidya, Kishor, Ang, Yeng, Murray, Iain, Patel, Praful, Ye, Weimin, Mullins, Paul, Wu, Anna H, Bird, Nigel C, Dallal, Helen, Shaheen, Nicholas J, Murray, Liam J, Koss, Konrad, Bernstein, Leslie, Romero, Yvonne, Hardie, Laura J, Zhang, Rui, Winter, Helen, Corley, Douglas A, Panter, Simon, Risch, Harvey A, Reid, Brian J, Sargeant, Ian, Gammon, Marilie D, Smart, Howard, Dhar, Anjan, McMurtry, Hugh, Ali, Haythem, Liu, Geoffrey, Casson, Alan G, Chow, Wong-Ho, Rutter, Matt, Tawil, Ashref, Morris, Danielle, Nwokolo, Chuka, Isaacs, Peter, Rodgers, Colin, Ragunath, Krish, MacDonald, Chris, Haigh, Chris, Monk, David, Davies, Gareth, Wajed, Saj, Johnston, David, Gibbons, Michael, Cullen, Sue, Church, Nicholas, Langley, Ruth, Griffin, Michael, Alderson, Derek, Deloukas, Panos, Hunt, Sarah E, Gray, Emma, Dronov, Serge, Potter, Simon C, Tashakkori-Ghanbaria, Avazeh, Anderson, Mark, Brooks, Claire, Blackwell, Jenefer M, Bramon, Elvira, Brown, Matthew A, Casas, Juan P, Corvin, Aiden, Duncanson, Audrey, Markus, Hugh S, Mathew, Christopher G, Palmer, Colin N A, Plomin, Robert, Rautanen, Anna, Sawcer, Stephen J, Trembath, Richard C, Viswanathan, Ananth C, Wood, Nicholas, Trynka, Gosia, Wijmenga, Cisca, Cazier, Jean-Baptiste, Atherfold, Paul, Nicholson, Anna M, Gellatly, Nichola L, Glancy, Deborah, Cooper, Sheldon C, Cunningham, David, Lind, Tore, Hapeshi, Julie, Ferry, David, Rathbone, Barrie, Brown, Julia, Love, Sharon, Attwood, Stephen, MacGregor, Stuart, Watson, Peter, Sanders, Scott, Ek, Weronica, Harrison, Rebecca F, Moayyedi, Paul, de Caestecker, John, Barr, Hugh, Stupka, Elia, Vaughan, Thomas L, Peltonen, Leena, Spencer, Chris C A, Tomlinson, Ian, Donnelly, Peter, and Jankowski, Janusz A Z
Abstract: Barrett's esophagus is an increasingly common disease that is strongly associated with reflux of stomach acid and usually a hiatus hernia, and it strongly predisposes to esophageal adenocarcinoma (EAC), a tumor with a very poor prognosis. We report the first genome-wide association study on Barrett's esophagus, comprising 1,852 UK cases and 5,172 UK controls in the discovery stage and 5,986 cases and 12,825 controls in the replication stage. Variants at two loci were associated with disease risk: chromosome 6p21, rs9257809 (Pcombined=4.09×10(-9); odds ratio (OR)=1.21, 95% confidence interval (CI)=1.13-1.28), within the major histocompatibility complex locus, and chromosome 16q24, rs9936833 (Pcombined=2.74×10(-10); OR=1.14, 95% CI=1.10-1.19), for which the closest protein-coding gene is FOXF1, which is implicated in esophageal development and structure. We found evidence that many common variants of small effect contribute to genetic susceptibility to Barrett's esophagus and that SNP alleles predisposing to obesity also increase risk for Barrett's esophagus.
Published: 2012
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94. Birth weight, head circumference, and prenatal exposure to acrylamide from maternal diet:the European prospective mother-child study (NewGeneris)

Author: 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, Kogevinas, Manolis, 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
Abstract: Acrylamide is a common dietary exposure that crosses the human placenta. It is classified as a probable human carcinogen, and developmental toxicity has been observed in rodents.
Published: 2012

95. A genome-wide association study identifies new susceptibility loci for esophageal adenocarcinoma and Barrett's esophagus

Author: Levine, David M, primary, Ek, Weronica E, additional, Zhang, Rui, additional, Liu, Xinxue, additional, Onstad, Lynn, additional, Sather, Cassandra, additional, Lao-Sirieix, Pierre, additional, Gammon, Marilie D, additional, Corley, Douglas A, additional, Shaheen, Nicholas J, additional, Bird, Nigel C, additional, Hardie, Laura J, additional, Murray, Liam J, additional, Reid, Brian J, additional, Chow, Wong-Ho, additional, Risch, Harvey A, additional, Nyrén, Olof, additional, Ye, Weimin, additional, Liu, Geoffrey, additional, Romero, Yvonne, additional, Bernstein, Leslie, additional, Wu, Anna H, additional, Casson, Alan G, additional, Chanock, Stephen J, additional, Harrington, Patricia, additional, Caldas, Isabel, additional, Debiram-Beecham, Irene, additional, Caldas, Carlos, additional, Hayward, Nicholas K, additional, Pharoah, Paul D, additional, Fitzgerald, Rebecca C, additional, MacGregor, Stuart, additional, Whiteman, David C, additional, and Vaughan, Thomas L, additional
Published: 2013
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96. MATERNAL, DIETARY AND ENVIRONMENTAL PREDICTORS OF BULKY DNA ADDUCTS IN CORD BLOOD: A EUROPEAN MOTHER–CHILD STUDY (NEWGENERIS).

Author: Pedersen, Marie, primary, Mendez, Michelle A, additional, Schoket, Bernadette, additional, Godschalk, Roger W, additional, Knudsen, Lisbeth E, additional, Brunborg, Gunnar, additional, Hardie, Laura J, additional, Chatzi, Leda, additional, and Kleinjans, Jos C, additional
Published: 2013
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97. Maternal dioxin-dietary patterns, prenatal exposure to dioxins and dioxin-like compounds, and birth outcomes in a European Mother-Child Study (NewGeneris)

Author: Papadopoulou, Eleni, primary, Vafeiadi, Marina, additional, Botsivali, Maria, additional, Pedersen, Marie, additional, Besselink, Harrie, additional, Chatzi, Leda, additional, Gutzkow, Kristine B, additional, Knudsen, Lisbeth E, additional, Hardie, Laura J, additional, Kogevinas, Manolis, additional, and Haugen, Margaretha, additional
Published: 2013
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98. Development of a New Branded UK Food Composition Database for an Online Dietary Assessment Tool.

Author: Carter, Michelle C., Hancock, Neil, Albar, Salwa A., Brown, Helen, Greenwood, Darren C., Hardie, Laura J., Frost, Gary S., Wark, Petra A., and Cade, Janet E.
Abstract: The current UK food composition tables are limited, containing ~3300 mostly generic food and drink items. To reflect the wide range of food products available to British consumers and to potentially improve accuracy of dietary assessment, a large UK specific electronic food composition database (FCDB) has been developed. A mapping exercise has been conducted that matched micronutrient data from generic food codes to "Back of Pack" data from branded food products using a semi-automated process. After cleaning and processing, version 1.0 of the new FCDB contains 40,274 generic and branded items with associated 120 macronutrient and micronutrient data and 5669 items with portion images. Over 50% of food and drink items were individually mapped to within 10% agreement with the generic food item for energy. Several quality checking procedures were applied after mapping including; identifying foods above and below the expected range for a particular nutrient within that food group and cross-checking the mapping of items such as concentrated and raw/dried products. The new electronic FCDB has substantially increased the size of the current, publically available, UK food tables. The FCDB has been incorporated into myfood24, a new fully automated online dietary assessment tool and, a smartphone application for weight loss. [ABSTRACT FROM AUTHOR]
Published: 2016
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99. Nuclear Magnetic Resonance Analysis of Glucose Levels in Weanling Piglets Plasma as a Function of Deoxynivalenol Exposure

Author: Hopton, Richard P., primary, Oswald, Isabelle P., additional, Hardie, Laura J., additional, Turner, Paul C., additional, and Fisher, Julie, additional
Published: 2012
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100. Use of information and communication technology to improve dietary assessment and tackle obesity

Author: Carter, Michelle, primary, Alwan, Nisreen A, additional, Burley, Victoria, additional, Wark, Petra A, additional, Evans, Charlotte E, additional, Greenwood, Darren C, additional, Hardie, Laura J, additional, Frost, Gary, additional, and Cade, Janet E, additional
Published: 2012
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