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  • 301. Manning, Alisa K.
    et al.
    Hivert, Marie-France
    Scott, Robert A.
    Grimsby, Jonna L.
    Bouatia-Naji, Nabila
    Chen, Han
    Rybin, Denis
    Liu, Ching-Ti
    Bielak, Lawrence F.
    Prokopenko, Inga
    Amin, Najaf
    Barnes, Daniel
    Cadby, Gemma
    Hottenga, Jouke-Jan
    Ingelsson, Erik
    Jackson, Anne U.
    Johnson, Toby
    Kanoni, Stavroula
    Ladenvall, Claes
    Lagou, Vasiliki
    Lahti, Jari
    Lecoeur, Cecile
    Liu, Yongmei
    Martinez-Larrad, Maria Teresa
    Montasser, May E.
    Navarro, Pau
    Perry, John R. B.
    Rasmussen-Torvik, Laura J.
    Salo, Perttu
    Sattar, Naveed
    Shungin, Dmitry
    Umeå University, Faculty of Medicine, Department of Odontology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Strawbridge, Rona J.
    Tanaka, Toshiko
    van Duijn, Cornelia M.
    An, Ping
    de Andrade, Mariza
    Andrews, Jeanette S.
    Aspelund, Thor
    Atalay, Mustafa
    Aulchenko, Yurii
    Balkau, Beverley
    Bandinelli, Stefania
    Beckmann, Jacques S.
    Beilby, John P.
    Bellis, Claire
    Bergman, Richard N.
    Blangero, John
    Boban, Mladen
    Boehnke, Michael
    Boerwinkle, Eric
    Bonnycastle, Lori L.
    Boomsma, Dorret I.
    Borecki, Ingrid B.
    Boettcher, Yvonne
    Bouchard, Claude
    Brunner, Eric
    Budimir, Danijela
    Campbell, Harry
    Carlson, Olga
    Chines, Peter S.
    Clarke, Robert
    Collins, Francis S.
    Corbaton-Anchuelo, Arturo
    Couper, David
    de Faire, Ulf
    Dedoussis, George V.
    Deloukas, Panos
    Dimitriou, Maria
    Egan, Josephine M.
    Eiriksdottir, Gudny
    Erdos, Michael R.
    Eriksson, Johan G.
    Eury, Elodie
    Ferrucci, Luigi
    Ford, Ian
    Forouhi, Nita G.
    Fox, Caroline S.
    Franzosi, Maria Grazia
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Frayling, Timothy M.
    Froguel, Philippe
    Galan, Pilar
    de Geus, Eco
    Gigante, Bruna
    Glazer, Nicole L.
    Goel, Anuj
    Groop, Leif
    Gudnason, Vilmundur
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Hamsten, Anders
    Hansson, Ola
    Harris, Tamara B.
    Hayward, Caroline
    Heath, Simon
    Hercberg, Serge
    Hicks, Andrew A.
    Hingorani, Aroon
    Hofman, Albert
    Hui, Jennie
    Hung, Joseph
    Jarvelin, Marjo-Riitta
    Jhun, Min A.
    Johnson, Paul C. D.
    Jukema, J. Wouter
    Jula, Antti
    Kao, W. H.
    Kaprio, Jaakko
    Kardia, Sharon L. R.
    Keinanen-Kiukaanniemi, Sirkka
    Kivimaki, Mika
    Kolcic, Ivana
    Kovacs, Peter
    Kumari, Meena
    Kuusisto, Johanna
    Kyvik, Kirsten Ohm
    Laakso, Markku
    Lakka, Timo
    Lannfelt, Lars
    Lathrop, G. Mark
    Launer, Lenore J.
    Leander, Karin
    Li, Guo
    Lind, Lars
    Lindstrom, Jaana
    Lobbens, Stephane
    Loos, Ruth J. F.
    Luan, Jian'an
    Lyssenko, Valeriya
    Magi, Reedik
    Magnusson, Patrik K. E.
    Marmot, Michael
    Meneton, Pierre
    Mohlke, Karen L.
    Mooser, Vincent
    Morken, Mario A.
    Miljkovic, Iva
    Narisu, Narisu
    O'Connell, Jeff
    Ong, Ken K.
    Oostra, Ben A.
    Palmer, Lyle J.
    Palotie, Aarno
    Pankow, James S.
    Peden, John F.
    Pedersen, Nancy L.
    Pehlic, Marina
    Peltonen, Leena
    Penninx, Brenda
    Pericic, Marijana
    Perola, Markus
    Perusse, Louis
    Peyser, Patricia A.
    Polasek, Ozren
    Pramstaller, Peter P.
    Province, Michael A.
    Raikkonen, Katri
    Rauramaa, Rainer
    Rehnberg, Emil
    Rice, Ken
    Rotter, Jerome I.
    Rudan, Igor
    Ruokonen, Aimo
    Saaristo, Timo
    Sabater-Lleal, Maria
    Salomaa, Veikko
    Savage, David B.
    Saxena, Richa
    Schwarz, Peter
    Seedorf, Udo
    Sennblad, Bengt
    Serrano-Rios, Manuel
    Shuldiner, Alan R.
    Sijbrands, Eric J. G.
    Siscovick, David S.
    Smit, Johannes H.
    Small, Kerrin S.
    Smith, Nicholas L.
    Smith, Albert Vernon
    Stancakova, Alena
    Stirrups, Kathleen
    Stumvoll, Michael
    Sun, Yan V.
    Swift, Amy J.
    Toenjes, Anke
    Tuomilehto, Jaakko
    Trompet, Stella
    Uitterlinden, Andre G.
    Uusitupa, Matti
    Vikstrom, Max
    Vitart, Veronique
    Vohl, Marie-Claude
    Voight, Benjamin F.
    Vollenweider, Peter
    Waeber, Gerard
    Waterworth, Dawn M.
    Watkins, Hugh
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Wheeler, Eleanor
    Widen, Elisabeth
    Wild, Sarah H.
    Willems, Sara M.
    Willemsen, Gonneke
    Wilson, James F.
    Witteman, Jacqueline C. M.
    Wright, Alan F.
    Yaghootkar, Hanieh
    Zelenika, Diana
    Zemunik, Tatijana
    Zgaga, Lina
    Wareham, Nicholas J.
    McCarthy, Mark I.
    Barroso, Ines
    Watanabe, Richard M.
    Florez, Jose C.
    Dupuis, Josee
    Meigs, James B.
    Langenberg, Claudia
    A genome-wide approach accounting for body mass index identifies genetic variants influencing fasting glycemic traits and insulin resistance2012In: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 44, no 6, p. 659-669Article in journal (Refereed)
    Abstract [en]

    Recent genome-wide association studies have described many loci implicated in type 2 diabetes (T2D) pathophysiology and beta-cell dysfunction but have contributed little to the understanding of the genetic basis of insulin resistance. We hypothesized that genes implicated in insulin resistance pathways might be uncovered by accounting for differences in body mass index (BMI) and potential interactions between BMI and genetic variants. We applied a joint meta-analysis approach to test associations with fasting insulin and glucose on a genome-wide scale. We present six previously unknown loci associated with fasting insulin at P < 5 x 10(-8) in combined discovery and follow-up analyses of 52 studies comprising up to 96,496 non-diabetic individuals. Risk variants were associated with higher triglyceride and lower high-density lipoprotein (HDL) cholesterol levels, suggesting a role for these loci in insulin resistance pathways. The discovery of these loci will aid further characterization of the role of insulin resistance in T2D pathophysiology.

  • 302. Marcus, Claude
    et al.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Johansson, Gunnar
    Rothenberg, Elisabet
    Rössner, Stephan
    [High-fat diet intake can be questioned]2008In: Lakartidningen, ISSN 0023-7205, Vol. 105, no 24-25, p. 1864-6Article in journal (Refereed)
  • 303. McCormack, Valerie A
    et al.
    Agudo, Antonio
    Dahm, Christina C
    Overvad, Kim
    Olsen, Anja
    Tjonneland, Anne
    Kaaks, Rudolf
    Boeing, Heiner
    Manjer, Jonas
    Almquist, Martin
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology, Cariology.
    Chirlaque, Maria Dolores
    Barricarte, Aurelio
    Dorronsoro, Miren
    Rodriguez, Laudina
    Redondo, Maria Luisa
    Khaw, Kay-Tee
    Wareham, Nick
    Allen, Naomi
    Key, Tim
    Riboli, Elio
    Boffetta, Paolo
    Cigar and pipe smoking and cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC)2010In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 127, no 10, p. 2402-2411Article in journal (Refereed)
    Abstract [en]

    The carcinogenicity of cigar and pipe smoking is established but the effect of detailed smoking characteristics is less well defined. We examined the effects on cancer incidence of exclusive cigar and pipe smoking, and in combination with cigarettes, among 102,395 men from Denmark, Germany, Spain, Sweden and the United Kingdom in the EPIC cohort. Hazard ratios (HR) and their 95% confidence intervals (CI) for cancer during a median 9-year follow-up from ages 35 to 70 years were estimated using proportional hazards models. Compared to never smokers, HR of cancers of lung, upper aerodigestive tract and bladder combined was 2.2 (95% CI: 1.3, 3.8) for exclusive cigar smokers (16 cases), 3.0 (2.1, 4.5) for exclusive pipe smokers (33 cases) and 5.3 (4.4, 6.4) for exclusive cigarette smokers (1,069 cases). For each smoking type, effects were stronger in current smokers than in ex-smokers and in inhalers than in non-inhalers. Ever smokers of both cigarettes and cigars [HR 5.7 (4.4, 7.3), 120 cases] and cigarettes and pipes [5.1 (4.1, 6.4), 247 cases] had as high a raised risk as had exclusive cigarette smokers. In these smokers, the magnitude of the raised risk was smaller if they had switched to cigars or pipes only (i.e., quit cigarettes) and had not compensated with greater smoking intensity. Cigar and pipe smoking is not a safe alternative to cigarette smoking. The lower cancer risk of cigar and pipe smokers as compared to cigarette smokers is explained by lesser degree of inhalation and lower smoking intensity.

  • 304. McKay, James D.
    et al.
    Truong, Therese
    Gaborieau, Valerie
    Chabrier, Amelie
    Chuang, Shu-Chun
    Byrnes, Graham
    Zaridze, David
    Shangina, Oxana
    Szeszenia-Dabrowska, Neonila
    Lissowska, Jolanta
    Rudnai, Peter
    Fabianova, Eleonora
    Bucur, Alexandru
    Bencko, Vladimir
    Holcatova, Ivana
    Janout, Vladimir
    Foretova, Lenka
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Benhamou, Simone
    Bouchardy, Christine
    Ahrens, Wolfgang
    Merletti, Franco
    Richiardi, Lorenzo
    Talamini, Renato
    Barzan, Luigi
    Kjaerheim, Kristina
    Macfarlane, Gary J.
    Macfarlane, Tatiana V.
    Simonato, Lorenzo
    Canova, Cristina
    Agudo, Antonio
    Castellsague, Xavier
    Lowry, Ray
    Conway, David I.
    McKinney, Patricia A.
    Healy, Claire M.
    Toner, Mary E.
    Znaor, Ariana
    Curado, Maria Paula
    Koifman, Sergio
    Menezes, Ana
    Wuensch-Filho, Victor
    Neto, Jose Eluf
    Fernandez Garrote, Leticia
    Boccia, Stefania
    Cadoni, Gabriella
    Arzani, Dario
    Olshan, Andrew F.
    Weissler, Mark C.
    Funkhouser, William K.
    Luo, Jingchun
    Lubinski, Jan
    Trubicka, Joanna
    Lener, Marcin
    Oszutowska, Dorota
    Schwartz, Stephen M.
    Chen, Chu
    Fish, Sherianne
    Doody, David R.
    Muscat, Joshua E.
    Lazarus, Philip
    Gallagher, Carla J.
    Chang, Shen-Chih
    Zhang, Zuo-Feng
    Wei, Qingyi
    Sturgis, Erich M.
    Wang, Li-E
    Franceschi, Silvia
    Herrero, Rolando
    Kelsey, Karl T.
    McClean, Michael D.
    Marsit, Carmen J.
    Nelson, Heather H.
    Romkes, Marjorie
    Buch, Shama
    Nukui, Tomoko
    Zhong, Shilong
    Lacko, Martin
    Manni, Johannes J.
    Peters, Wilbert H. M.
    Hung, Rayjean J.
    McLaughlin, John
    Vatten, Lars
    Njolstad, Inger
    Goodman, Gary E.
    Field, John K.
    Liloglou, Triantafillos
    Vineis, Paolo
    Clavel-Chapelon, Francoise
    Palli, Domenico
    Tumino, Rosario
    Krogh, Vittorio
    Panico, Salvatore
    Gonzalez, Carlos A.
    Ramon Quiros, J.
    Martinez, Carmen
    Navarro, Carmen
    Ardanaz, Eva
    Larranaga, Nerea
    Khaw, Kay-Tee
    Key, Timothy
    Bueno-de-Mesquita, H. Bas
    Peeters, Petra H. M.
    Trichopoulou, Antonia
    Linseisen, Jakob
    Boeing, Heiner
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Overvad, Kim
    Tjonneland, Anne
    Kumle, Merethe
    Riboli, Elio
    Vaelk, Kristjan
    Voodern, Tonu
    Metspalu, Andres
    Zelenika, Diana
    Boland, Anne
    Delepine, Marc
    Foglio, Mario
    Lechner, Doris
    Blanche, Helene
    Gut, Ivo G.
    Galan, Pilar
    Heath, Simon
    Hashibe, Mia
    Hayes, Richard B.
    Boffetta, Paolo
    Lathrop, Mark
    Brennan, Paul
    A Genome-Wide Association Study of Upper Aerodigestive Tract Cancers Conducted within the INHANCE Consortium2011In: PLOS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 7, no 3, article id e1001333Article in journal (Refereed)
    Abstract [en]

    Genome-wide association studies (GWAS) have been successful in identifying common genetic variation involved in susceptibility to etiologically complex disease. We conducted a GWAS to identify common genetic variation involved in susceptibility to upper aero-digestive tract (UADT) cancers. Genome-wide genotyping was carried out using the Illumina HumanHap300 beadchips in 2,091 UADT cancer cases and 3,513 controls from two large European multi-centre UADT cancer studies, as well as 4,821 generic controls. The 19 top-ranked variants were investigated further in an additional 6,514 UADT cancer cases and 7,892 controls of European descent from an additional 13 UADT cancer studies participating in the INHANCE consortium. Five common variants presented evidence for significant association in the combined analysis (p <= 5 x 10(-7)). Two novel variants were identified, a 4q21 variant (rs1494961, p = 1 x 10(-8)) located near DNA repair related genes HEL308 and FAM175A (or Abraxas) and a 12q24 variant (rs4767364, p = 2 x 10(-8)) located in an extended linkage disequilibrium region that contains multiple genes including the aldehyde dehydrogenase 2 (ALDH2) gene. Three remaining variants are located in the ADH gene cluster and were identified previously in a candidate gene study involving some of these samples. The association between these three variants and UADT cancers was independently replicated in 5,092 UADT cancer cases and 6,794 controls non-overlapping samples presented here (rs1573496-ADH7, p = 5 x 10(-8); rs1229984-ADH1B, p = 7 x 10(-9); and rs698-ADH1C, p = 0.02). These results implicate two variants at 4q21 and 12q24 and further highlight three ADH variants in UADT cancer susceptibility.

  • 305.
    Melin, Beatrice
    et al.
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Dahlin, Anna M
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Andersson, Ulrika
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Wang, Zhaoming
    Henriksson, Roger
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Bondy, Melissa L
    Johansen, Christoffer
    Feychting, Maria
    Ahlbom, Anders
    Kitahara, Cari M
    Wang, Sophia S
    Ruder, Avima M
    Carreon, Tania
    Butler, Mary Ann
    Inskip, Peter D
    Purdue, Mark
    Hsing, Ann W
    Mechanic, Leah
    Gillanders, Elizabeth
    Yeager, Meredith
    Linet, Martha
    Chanock, Stephen J
    Hartge, Patricia
    Rajaraman, Preetha
    Known glioma risk loci are associated with glioma with a family history of brain tumours: a case-control gene association study2013In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 132, no 10, p. 2464-2468Article in journal (Refereed)
    Abstract [en]

    Familial cancer can be used to leverage genetic association studies. Recent genome-wide association studies have reported independent associations between seven single nucleotide polymorphisms (SNPs) and risk of glioma. The aim of this study was to investigate whether glioma cases with a positive family history of brain tumours, defined as having at least one first- or second-degree relative with a history of brain tumour, are associated with known glioma risk loci. One thousand four hundred and thirty-one glioma cases and 2,868 cancer-free controls were identified from four casecontrol studies and two prospective cohorts from USA, Sweden and Denmark and genotyped for seven SNPs previously reported to be associated with glioma risk in casecontrol designed studies. Odds ratios were calculated by unconditional logistic regression. In analyses including glioma cases with a family history of brain tumours (n = 104) and control subjects free of glioma at baseline, three of seven SNPs were associated with glioma risk: rs2736100 (5p15.33, TERT), rs4977756 (9p21.3, CDKN2A-CDKN2B) and rs6010620 (20q13.33, RTEL1). After Bonferroni correction for multiple comparisons, only one marker was statistically significantly associated with glioma risk, rs6010620 (ORtrend for the minor (A) allele, 0.39; 95% CI: 0.250.61; Bonferroni adjusted ptrend, 1.7 x 104). In conclusion, as previously shown for glioma regardless of family history of brain tumours, rs6010620 (RTEL1) was associated with an increased risk of glioma when restricting to cases with family history of brain tumours. These findings require confirmation in further studies with a larger number of glioma cases with a family history of brain tumours.

  • 306. Menvielle, Gwenn
    et al.
    Boshuizen, Hendriek
    Kunst, Anton E
    Dalton, Susanne O
    Vineis, Paolo
    Bergmann, Manuela M
    Hermann, Silke
    Ferrari, Pietro
    Raaschou-Nielsen, Ole
    Tjønneland, Anne
    Kaaks, Rudolf
    Linseisen, Jakob
    Kosti, Maria
    Trichopoulou, Antonia
    Dilis, Vardis
    Palli, Domenico
    Krogh, Vittorio
    Panico, Salvatore
    Tumino, Rosario
    Büchner, Frederike L
    van Gils, Carla H
    Peeters, Petra H M
    Braaten, Tonje
    Gram, Inger T
    Lund, Eiliv
    Rodriguez, Laudina
    Agudo, Antonio
    Sánchez, Maria-José
    Tormo, Maria-José
    Ardanaz, Eva
    Manjer, Jonas
    Wirfält, Elisabet
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Rasmuson, Torgny
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Bingham, Sheila
    Khaw, Kay-Tee
    Allen, Naomi
    Key, Tim
    Boffetta, Paolo
    Duell, Eric J
    Slimani, Nadia
    Gallo, Valentina
    Riboli, Elio
    Bueno-de-Mesquita, H Bas
    The role of smoking and diet in explaining educational inequalities in lung cancer incidence.2009In: Journal of the National Cancer Institute, ISSN 1460-2105, Vol. 101, no 5, p. 321-330Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Studies in many countries have reported higher lung cancer incidence and mortality in individuals with lower socioeconomic status. METHODS: To investigate the role of smoking in these inequalities, we used data from 391,251 participants in the European Prospective Investigation into Cancer and Nutrition study, a cohort of individuals in 10 European countries. We collected information on smoking (history and quantity), fruit and vegetable consumption, and education through questionnaires at study entry and gathered data on lung cancer incidence for a mean of 8.4 years. Socioeconomic status was defined as the highest attained level of education, and participants were grouped by sex and region of residence (Northern Europe, Germany, or Southern Europe). Relative indices of inequality (RIIs) of lung cancer risk unadjusted and adjusted for smoking were estimated using Cox regression models. Additional analyses were performed by histological type. RESULTS: During the study period, 939 men and 692 women developed lung cancer. Inequalities in lung cancer risk (RII(men) = 3.62, 95% confidence interval [CI] = 2.77 to 4.73, 117 vs 52 per 100,000 person-years for lowest vs highest education level; RII(women) = 2.39, 95% CI = 1.77 to 3.21, 46 vs 25 per 100,000 person-years) decreased after adjustment for smoking but remained statistically significant (RII(men) = 2.29, 95% CI = 1.75 to 3.01; RII(women) = 1.59, 95% CI = 1.18 to 2.13). Large RIIs were observed among men and women in Northern European countries and among men in Germany, but inequalities in lung cancer risk were reverse (RIIs < 1) among women in Southern European countries. Inequalities differed by histological type. Adjustment for smoking reduced inequalities similarly for all histological types and among men and women in all regions. In all analysis, further adjustment for fruit and vegetable consumption did not change the estimates. CONCLUSION: Self-reported smoking consistently explains approximately 50% of the inequalities in lung cancer risk due to differences in education.

  • 307. Michaud, Dominique S.
    et al.
    Bove, Gerald
    Gallo, Valentina
    Schlehofer, Brigitte
    Tjönneland, Anne
    Olsen, Anja
    Overvad, Kim
    Dahm, Christina C.
    Teucher, Brigit
    Boeing, Heiner
    Steffen, Annika
    Trichopoulou, Antonia
    Bamia, Christina
    Kyrozis, Andreas
    Sacerdote, Carlotta
    Agnoli, Claudia
    Palli, Domenico
    Tumino, Rosario
    Mattiello, Amalia
    Bueno-de-Mesquita, H. Bas
    Peeters, Petra H. M.
    May, Anne M.
    Barricarte, Aurelio
    Chirlaque, Maria-Dolores
    Dorronsoro, Miren
    Jose Sanchez, Maria
    Rodriguez, Laudina
    Duell, Eric J.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Melin, Beatrice S.
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Manjer, Jonas
    Borgquist, Signe
    Khaw, Kay-Tee
    Wareham, Nick
    Allen, Naomi E.
    Travis, Ruth C.
    Romieu, Isabelle
    Vineis, Paolo
    Riboli, Elio
    Anthropometric Measures, Physical Activity, and Risk of Glioma and Meningioma in a Large Prospective Cohort Study2011In: Cancer Prevention Research, ISSN 1940-6207, E-ISSN 1940-6215, Vol. 4, no 9, p. 1385-1392Article in journal (Refereed)
    Abstract [en]

    Body fatness has been associated with increased risk of a number of hormone-dependent cancers. Recent studies suggest that body mass index (BMI) may be related to meningiomas, which are more common in women than men, and for which estrogens are believed to play a role. Using data from a large European propective cohort, 203 incident cases of meningioma and 340 cases of glioma were included in the analysis for measures of body fat, height, and physical activity among 380,775 participants. All analyses were conducted using Cox proportional hazards model and controlling for age, sex, country, and education. A 71% increase in risk of meningioma was observed among men and women in the top quartile of waist circumference (HR = 1.71, 95% CI = 1.08-2.73, P(trend) = 0.01). A positive association was also observed for BMI and meningioma (HR = 1.48, 95% CI = 0.98-2.23, for BMI >= 30 compared with a BMI of 20-24.9, P(trend) = 0.05). An association with height and meningioma was also suggestive (HR = 1.24, 95% 0.96-1.51, for each 10 cm increase). In contrast, no associations were observed for height and different measures of body fat and risk of glioma. Physical activity was not related to either type of brain tumors. Results from this study support an increase in risk of meningioma with higher body fatness among both men and women. No association was observed between anthropometric measures and risk of glioma. Cancer Prev Res; 4(9); 1385-92. (C) 2011 AACR.

  • 308. Michaud, Dominique S
    et al.
    Gallo, Valentina
    Schlehofer, Brigitte
    Tjønneland, Anne
    Olsen, Anja
    Overvad, Kim
    Dahm, Christina C
    Kaaks, Rudolf
    Lukanova, Annekatrin
    Boeing, Heiner
    Schütze, Madlen
    Trichopoulou, Antonia
    Bamia, Christina
    Kyrozis, Andreas
    Sacerdote, Carlotta
    Agnoli, Claudia
    Palli, Domenico
    Tumino, Rosario
    Mattiello, Amalia
    Bueno-de-Mesquita, H Bas
    Ros, Martine M
    Peeters, Petra H M
    van Gils, Carla H
    Lund, Eiliv
    Bakken, Kjersti
    Gram, Inger T
    Barricarte, Aurelio
    Navarro, Carmen
    Dorronsoro, Miren
    Sánchez, Maria José
    Rodríguez, Laudina
    Duell, Eric J
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Melin, Beatrice
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Manjer, Jonas
    Borgquist, Signe
    Khaw, Kay-Tee
    Wareham, Nick
    Allen, Naomi E
    Tsilidis, Konstantinos K
    Romieu, Isabelle
    Rinaldi, Sabina
    Vineis, Paolo
    Riboli, Elio
    Reproductive factors and exogenous hormone use in relation to risk of glioma and meningioma in a large European cohort study2010In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 19, no 10, p. 2562-2569Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The etiologies of glioma and meningioma tumors are largely unknown. Although reproductive hormones are thought to influence the risk of these tumors, epidemiologic data are not supportive of this hypothesis; however, few cohort studies have published on this topic. We examined the relation between reproductive factors and the risk of glioma and meningioma among women in the European Prospective Investigation into Cancer and Nutrition (EPIC).

    METHODS: After a mean of 8.4 years of follow-up, 193 glioma and 194 meningioma cases were identified among 276,212 women. Information on reproductive factors and hormone use was collected at baseline. Cox proportional hazard regression was used to determine hazard ratios (HR) and 95% confidence intervals (95% CI).

    RESULTS: No associations were observed between glioma or meningioma risk and reproductive factors, including age at menarche, parity, age at first birth, menopausal status, and age at menopause. A higher risk of meningioma was observed among postmenopausal women who were current users of hormone replacement therapy (HR, 1.79; 95% CI, 1.18-2.71) compared with never users. Similarly, current users of oral contraceptives were at higher risk of meningioma than never users (HR, 3.61; 95% CI, 1.75-7.46).

    CONCLUSION: Our results do not support a role for estrogens and glioma risk. Use of exogenous hormones, especially current use, seems to increase meningioma risk. However, these findings could be due to diagnostic bias and require confirmation.

    IMPACT: Elucidating the role of hormones in brain tumor development has important implications and needs to be further examined using biological measurements.

  • 309. Miller, Anthony B
    et al.
    Altenburg, Hans-Peter
    Bueno-de-Mesquita, Bas
    Boshuizen, Hendriek C
    Agudo, Antonio
    Berrino, Franco
    Gram, Inger Torhild
    Janson, Lars
    Linseisen, Jacob
    Overvad, Kim
    Rasmuson, Torgny
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. Onkologi.
    Vineis, Paolo
    Lukanova, Annekatrin
    Allen, Naomi
    Amiano, Pilar
    Barricarte, Aurelio
    Berglund, Göran
    Boeing, Heiner
    Clavel-Chapelon, Francoise
    Day, Nicholas E
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Lund, Eiliv
    Martinez, Carmen
    Navarro, Carmen
    Palli, Domenico
    Panico, Salvatore
    Peeters, Petra H M
    Quirós, José Ramón
    Tjönneland, Anne
    Tumino, Rosario
    Trichopoulou, Antonia
    Trichopoulos, Dimitrios
    Slimani, Nadia
    Riboli, Elio
    Palli, Dominico
    Fruits and vegetables and lung cancer: Findings from the European Prospective Investigation into Cancer and Nutrition2004In: International Journal of Cancer, ISSN 0020-7136, Vol. 108, no 2, p. 269-276Article in journal (Refereed)
  • 310. Moazzami, Ali A.
    et al.
    Zhang, Jie-Xian
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Kamal-Eldin, Afaf
    Aman, Per
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Johansson, Jan-Erik
    Andersson, Sven-Olof
    Nuclear Magnetic Resonance-Based Metabolomics Enable Detection of the Effects of a Whole Grain Rye and Rye Bran Diet on the Metabolic Profile of Plasma in Prostate Cancer Patients2011In: Journal of Nutrition, ISSN 0022-3166, E-ISSN 1541-6100, Vol. 141, no 12, p. 2126-2132Article in journal (Refereed)
    Abstract [en]

    Prostate cancer (PC) is the most common cancer in the Western world and the second most important cancer causing male deaths, after lung cancer, in the United States and Britain. Lifestyle and dietary changes are recommended for men diagnosed with early-stage PC. It has been shown that a diet rich in whole grain (WG) rye reduces the progression of early-stage PC, but the underlying mechanism is not clear. This study sought to identify changes in the metabolic signature of plasma in patients with early-stage PC following intervention with a diet rich in WG rye and rye bran product (RP) compared with refined white wheat product (WP) as a tool for mechanistic investigation of the beneficial health effects of RP on PC progression. Seventeen PC patients received 485 g RP or WP in a randomized, controlled, crossover design during a period of 6 wk with a 2-wk washout period. At the end of each intervention period, plasma was collected after fasting and used for (1)H NMR-based metabolomics. Multilevel partial least squares discriminant analysis was used for paired comparisons of multivariate data. A metabolomics analysis of plasma showed an increase in 5 metabolites, including 3-hydroxybutyric acid, acetone, betaine, N,N-dimethylglycine, and dimethyl sulfone, after RP. To understand these metabolic changes, fasting plasma homocysteine, leptin, adiponectin, and glucagon were measured separately. The plasma homocysteine concentration was lower (P = 0.0171 and that of leptin tended to be lower (P = 0.07) after RP intake compared to WP intake. The increase in plasma 3-hydroxybutyric acid and acetone after RP suggests a shift in energy metabolism from anabolic to catabolic status, which could explain some of the beneficial health effects of WG rye, i.e., reduction in prostate-specific antigen and reduced 24-h insulin secretion. In addition, the increase in betaine and N,N-dimethylglycine and the decrease in homocysteine show a favorable shift in homocysteine metabolism after RP intake. J. Nutr. 141: 2126-2132, 2011.

  • 311.
    Myte, Robin
    et al.
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Gylling, Björn
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Häggström, Jenny
    Umeå University, Faculty of Social Sciences, Umeå School of Business and Economics (USBE), Statistics.
    Schneede, Jörn
    Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience.
    Löfgren-Burström, Anna
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Huyghe, Jeroen R.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Meyer, Klaus
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Ueland, Per Magne
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Van Guelpen, Bethany
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    One-carbon metabolism biomarkers and genetic variants in relation to colorectal cancer risk by KRAS and BRAF mutation status2018In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 13, no 4, article id e0196233Article in journal (Refereed)
    Abstract [en]

    Disturbances in one-carbon metabolism, intracellular reactions involved in nucleotide synthesis and methylation, likely increase the risk of colorectal cancer (CRC). However, results have been inconsistent. To explore whether this inconsistency could be explained by intertumoral heterogeneity, we evaluated a comprehensive panel of one-carbon metabolism biomarkers and some single nucleotide polymorphisms (SNPs) in relation to the risk of molecular subtypes of CRC defined by mutations in the KRAS and BRAF oncogenes. This nested case-control study included 488 CRC cases and 947 matched controls from two population-based cohorts in the Northern Sweden Health and Disease Study. We analyzed 14 biomarkers and 17 SNPs in prediagnostic blood and determined KRAS and BRAF mutation status in tumor tissue. In a multivariate network analysis, no variable displayed a strong association with the risk of specific CRC subtypes. A non-synonymous SNP in the CTH gene, rs1021737, had a stronger association compared with other variables. In subsequent univariate analyses, participants with variant rs1021737 genotype had a decreased risk of KRAS-mutated CRC (OR per allele = 0.72, 95% CI = 0.50, 1.05), and an increased risk of BRAF-mutated CRC (OR per allele = 1.56, 95% CI = 1.07, 2.30), with weak evidence for heterogeneity (Pheterogeneity = 0.01). This subtype-specific SNP association was not replicated in a case-case analysis of 533 CRC cases from The Cancer Genome Atlas (P = 0.85). In conclusion, we found no support for clear subtype-specific roles of one-carbon metabolism biomarkers and SNPs in CRC development, making differences in CRC molecular subtype distributions an unlikely explanation for the varying results on the role of one-carbon metabolism in CRC development across previous studies. Further investigation of the CTH gene in colorectal carcinogenesis with regards to KRAS and BRAF mutations or other molecular characteristics of the tumor may be warranted.

  • 312.
    Myte, Robin
    et al.
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Gylling, Björn
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Häggström, Jenny
    Umeå University, Faculty of Social Sciences, Umeå School of Business and Economics (USBE), Statistics.
    Schneede, Jörn
    Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience, Pharmacology.
    Ueland, Per Magne
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Van Guelpen, Bethany
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Untangling the role of one-carbon metabolism in colorectal cancer risk: a comprehensive Bayesian network analysis2017In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, article id 43434Article in journal (Refereed)
    Abstract [en]

    The role of one-carbon metabolism (1CM), particularly folate, in colorectal cancer (CRC) development has been extensively studied, but with inconclusive results. Given the complexity of 1CM, the conventional approach, investigating components individually, may be insufficient. We used a machine learning-based Bayesian network approach to study, simultaneously, 14 circulating one-carbon metabolites, 17 related single nucleotide polymorphisms (SNPs), and several environmental factors in relation to CRC risk in 613 cases and 1190 controls from the prospective Northern Sweden Health and Disease Study. The estimated networks corresponded largely to known biochemical relationships. Plasma concentrations of folate (direct), vitamin B6 (pyridoxal 5-phosphate) (inverse), and vitamin B2 (riboflavin) (inverse) had the strongest independent associations with CRC risk. Our study demonstrates the importance of incorporating B-vitamins in future studies of 1CM and CRC development, and the usefulness of Bayesian network learning for investigating complex biological systems in relation to disease.

  • 313.
    Myte, Robin
    et al.
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Gylling, Björn
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Schneede, Jörn
    Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience, Pharmacology.
    Ueland, Per Magne
    Häggström, Jenny
    Umeå University, Faculty of Social Sciences, Umeå School of Business and Economics (USBE), Statistics.
    Hultdin, Johan
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Van Guelpen, Bethany
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Components of One-carbon Metabolism Other than Folate and Colorectal Cancer Risk2016In: Epidemiology, ISSN 1044-3983, E-ISSN 1531-5487, Vol. 27, no 6, p. 787-796Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Despite extensive study, the role of folate in colorectal cancer remains unclear. Research has therefore begun to address the role of other elements of the folate-methionine metabolic cycles. This study investigated factors other than folate involved in one-carbon metabolism, i.e., choline, betaine, dimethylglycine, sarcosine, and methionine and relevant polymorphisms, in relation to the risk of colorectal cancer in a population with low intakes and circulating levels of folate.

    METHODS: This was a prospective case-control study of 613 case subjects and 1,190 matched control subjects nested within the population-based Northern Sweden Health and Disease Study. We estimated odds ratios (OR) by conditional logistic regression, and marginal risk differences with weighted maximum likelihood estimation using incidence data from the study cohort.

    RESULTS: Higher plasma concentrations of methionine and betaine were associated with modest colorectal cancer risk reductions (OR [95% confidence interval {CI}] for highest versus lowest tertile: 0.76 [0.57, 0.99] and 0.72 [0.55, 0.94], respectively). Estimated marginal risk differences corresponded to approximately 200 fewer colorectal cancer cases per 100,000 individuals on average. We observed no clear associations between choline, dimethylglycine, or sarcosine and colorectal cancer risk. The inverse association of methionine was modified by plasma folate concentrations (OR [95% CI] for highest/lowest versus lowest/lowest tertile of plasma methionine/folate concentrations 0.39 [0.24, 0.64], Pinteraction = 0.06).

    CONCLUSIONS: In this population-based, nested case-control study with a long follow-up time from baseline to diagnosis (median: 8.2 years), higher plasma concentrations of methionine and betaine were associated with lower colorectal cancer risk. See Video Abstract at http://links.lww.com/EDE/B83.

  • 314. Nagel, G
    et al.
    Concin, H
    Bjørge, T
    Rapp, K
    Manjer, J
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Diem, G
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Engeland, A
    Almquist, M
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Selmer, R
    Stocks, Tanja
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Tretli, S
    Ulmer, H
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Lukanova, A
    Metabolic syndrome and rare gynecological cancers in the Metabolic syndrome and Cancer project (Me-Can)2011In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 22, no 6, p. 1339-1345Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Risk factors for rare gynecological cancers are largely unknown. Initial research has indicated that the metabolic syndrome (MetS) or individual components could play a role. Materials and methods: The Metabolic syndrome and Cancer project cohort includes 288 834 women. During an average follow-up of 11 years, 82 vulvar, 26 vaginal and 43 other rare gynecological cancers were identified. Hazard ratios (HRs) were estimated fitting Cox proportional hazards regression models for tertiles and standardized z-scores [with a mean of 0 and a standard deviation (SD) of 1] of body mass index (BMI), blood pressure, glucose, cholesterol, triglycerides and MetS. Risk estimates were corrected for random error in the measurement of metabolic factors. RESULTS: The MetS was associated with increased risk of vulvar [HR 1.78, 95% confidence interval (CI) 1.30-2.41) and vaginal cancer (HR 1.87, 95% CI 1.07-3.25). Among separate MetS components, 1 SD increase in BMI was associated with overall risk (HR 1.43, 95% CI 1.23-1.66), vulvar (HR 1.36, 95% CI 1.11-1.69) and vaginal cancer (HR 1.79, 95% CI 1.30-2.46). Blood glucose and triglyceride concentrations were associated with increased risk of vulvar cancer (HR 1.98, 95% CI 1.10-3.58 and HR 2.09, 95% CI 1.39-3.15, respectively). CONCLUSION: The results from this first prospective study on rare gynecological cancers suggest that the MetS and its individual components may play a role in the development of these tumors.

  • 315. Nagel, G
    et al.
    Linseisen, J
    van Gils, C
    Peeters, P
    Boutron-Ruault, M
    Clavel-Chapelon, F
    Romieu, I
    Tjønneland, A
    Olsen, A
    Roswall, N
    Witt, P
    Overvad, K
    Rohrmann, S
    Kaaks, R
    Drogan, D
    Boeing, H
    Trichopoulou, A
    Stratigakou, V
    Zylis, D
    Engeset, D
    Lund, E
    Skeie, G
    Berrino, F
    Grioni, S
    Mattiello, A
    Masala, G
    Tumino, R
    Zanetti, R
    Ros, M
    Bueno-de-Mesquita, H
    Ardanaz, E
    Sánchez, M
    Huerta, J
    Amiano, P
    Rodríguez, L
    Manjer, J
    Wirfält, E
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Spencer, E
    Key, T
    Bingham, S
    Khaw, K
    Rinaldi, S
    Slimani, N
    Boffetta, P
    Gallo, V
    Norat, T
    Riboli, E
    Dietary beta-carotene, vitamin C and E intake and breast cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC).2010In: Breast cancer research and treatment, ISSN 1573-7217, Vol. 11, p. 753-765Article in journal (Refereed)
    Abstract [en]

    So far, studies on dietary antioxidant intake, including ss-carotene, vitamin C and vitamin E, and breast cancer risk are inconclusive. Thus, we addressed this question in the European Prospective Investigation into Cancer and Nutrition. During a median follow-up time of 8.8 years, 7,502 primary invasive breast cancer cases were identified. Cox proportional hazard models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI). All analyses were run stratified by menopausal status at recruitment and, additionally, by smoking status, alcohol intake, use of exogenous hormones and use of dietary supplements. In the multivariate analyses, dietary intake of beta-carotene, vitamin C and E was not associated with breast cancer risk in premenopausal [highest vs. lowest quintile: HR, 1.04 (95% CI, 0.85-1.27), 1.12 (0.92-1.36) and 1.10 (0.84-1.46), respectively] and postmenopausal women [0.93 (0.82-1.04), 0.98 (0.87-1.11) and 0.92 (0.77-1.11), respectively]. However, in postmenopausal women using exogenous hormones, high intake of beta-carotene [highest vs. lowest quintile; HR 0.79 (95% CI, 0.66-0.96), P (trend) 0.06] and vitamin C [0.88 (0.72-1.07), P (trend) 0.05] was associated with reduced breast cancer risk. In addition, dietary beta-carotene was associated with a decreased risk in postmenopausal women with high alcohol intake. Overall, dietary intake of beta-carotene, vitamin C and E was not related to breast cancer risk in neither pre- nor postmenopausal women. However, in subgroups of postmenopausal women, a weak protective effect between ss-carotene and vitamin E from food and breast cancer risk cannot be excluded.

  • 316. Nagel, Gabriele
    et al.
    Bjørge, T
    Stocks, Tanja
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Manjer, J
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Edlinger, M
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Engeland, A
    Johansen, D
    Kleiner, A
    Selmer, R
    Ulmer, H
    Tretli, S
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Concin, H
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Lukanova, A
    Metabolic risk factors and skin cancer in the Metabolic Syndrome and Cancer Project (Me-Can)2012In: British Journal of Dermatology, ISSN 0007-0963, E-ISSN 1365-2133, Vol. 167, no 1, p. 59-67Article in journal (Refereed)
    Abstract [en]

    Background  Little is known about the associations of metabolic aberrations with malignant melanoma (MM) and nonmelanoma skin cancer (NMSC). Objectives  To assess the associations between metabolic factors (both individually and combined) and the risk of skin cancer in the large prospective Metabolic Syndrome and Cancer Project (Me-Can). Methods  During a mean follow-up of 12 years of the Me-Can cohort, 1728 (41% women) incident MM, 230 (23% women) fatal MM and 1145 (33% women) NMSC were identified. Most NMSC cases (76%) were squamous cell carcinoma (SCC) (873, 33% women). Hazard ratios (HRs) were estimated by Cox proportional hazards regression for quintiles and standardized z-scores (with a mean of 0 and SD of 1) of body mass index (BMI), blood pressure, glucose, cholesterol, triglycerides and for a combined metabolic syndrome score. Risk estimates were corrected for random error in the measurements. Results  Blood pressure per unit increase of z-score was associated with an increased risk of incident MM cases in men and women [HR 1·17, 95% confidence interval (CI) 1·04-1·31 and HR 1·18, 95% CI 1·03-1·36, respectively] and fatal MM cases among women (HR 2·39, 95% CI 1·58-3·64). In men, all quintiles for BMI above the reference were associated with a higher risk of incident MM. In women, SCC NMSC risk increased across quintiles for glucose levels (P-trend 0·02) and there was a trend with triglyceride concentration (P-trend 0·09). Conclusion  These findings suggest that mechanisms linked to blood pressure may be involved in the pathogenesis of MM. SCC NMSC in women could be related to glucose and lipid metabolism.

  • 317. Nagel, Gabriele
    et al.
    Linseisen, Jakob
    Boshuizen, Hendriek C
    Pera, Guillem
    Del Giudice, Giuseppe
    Westert, Gert P
    Bueno-de-Mesquita, H Bas
    Allen, Naomi E
    Key, Timothy J
    Numans, Mattijs E
    Peeters, Petra Hm
    Sieri, Sabina
    Siman, Henrik
    Berglund, Goran
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Stenling, Roger
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology. Patologi.
    Martinez, Carmen
    Arriola, Larraitz
    Barricarte, Aurelio
    Chirlaque, M Dolores
    Quiros, Jose R
    Vineis, Paolo
    Masala, Giovanna
    Palli, Domenico
    Panico, Salvatore
    Tumino, Rosario
    Bingham, Sheila
    Boeing, Heiner
    Bergmann, Manuela M
    Overvad, Kim
    Boutron-Ruault, Marie-Christine
    Clavel-Chapelon, Francoise
    Olsen, Anja
    Tjonneland, Anne
    Trichopoulou, Antonia
    Bamia, Christina
    Soukara, Stavroula
    Sabourin, Jean-Christoph
    Carneiro, Fatima
    Slimani, Nadia
    Jenab, Mazda
    Norat, Teresa
    Riboli, Elio
    González, Carlos A
    Socioeconomic position and the risk of gastric and oesophageal cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST).2007In: International Journal of Epidemiology, ISSN 0300-5771, Vol. 36, no 1, p. 66-76Article in journal (Refereed)
  • 318. Nagel, Gabriele
    et al.
    Stocks, Tanja
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Spaeth, Daniela
    Hjartaker, Anette
    Lindkvist, Bjorn
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Bjorge, Tone
    Manjer, Jonas
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Engeland, Anders
    Ulmer, Hanno
    Selmer, Randi
    Concin, Hans
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Schlenk, Richard F.
    Metabolic factors and blood cancers among 578,000 adults in the metabolic syndrome and cancer project (Me-Can)2012In: Annals of Hematology, ISSN 0939-5555, E-ISSN 1432-0584, Vol. 91, no 10, p. 1519-1531Article in journal (Refereed)
    Abstract [en]

    We investigated associations between metabolic factors and blood cancer subtypes. Data on body mass index (BMI), blood pressure, blood glucose, total cholesterol, and triglycerides from seven prospective cohorts were pooled (n = 578,700; mean age = 44 years). Relative risks of blood cancers were calculated from Cox regression models. During mean follow-up of 12 years, 2,751 incident and 1,070 fatal cases of blood cancers occurred. Overall, higher BMI was associated with an increased blood cancer risk. In gender-specific subgroup analyses, BMI was positively associated with blood cancer risk (p = 0.002), lymphoid neoplasms (p = 0.01), and Hodgkin's lymphoma (p = 0.02) in women. Further associations with BMI were found for high-grade B-cell lymphoma (p = 0.02) and chronic lymphatic leukemia in men (p = 0.05) and women (p = 0.01). Higher cholesterol levels were inversely associated with myeloid neoplasms in women (p = 0.01), particularly acute myeloid leukemia (p = 0.003), and glucose was positively associated with chronic myeloid leukemia in women (p = 0.03). In men, glucose was positively associated with risk of high-grade B-cell lymphoma and multiple myeloma, while cholesterol was inversely associated with low-grade B-cell lymphoma. The metabolic syndrome score was related to 48 % increased risk of Hodgkin's lymphoma among women. BMI showed up as the most consistent risk factor, particularly in women. A clear pattern was not found for other metabolic factors.

  • 319. Neasham, David
    et al.
    Sifi, Ahlem
    Nielsen, Kaspar Rene
    Overvad, Kim
    Raaschou-Nielsen, Ole
    Tjønneland, Anne
    Barricarte, Aurelio
    González, Carlos A
    Navarro, Carmen
    Rodriguez Suarez, Laudina
    Travis, Ruth C
    Key, Tim
    Linseisen, Jakob
    Kaaks, Rudolf
    Crosignani, Paolo
    Berrino, Franco
    Rosso, Stefano
    Mattiello, Amalia
    Vermeulen, RCH
    Bueno-de-Mesquita, H Bas
    Berglund, Göran
    Manjer, Jonas
    Zackrisson, Sophia
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Malmer, Beatrice
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Bingham, Sheila
    Khaw, Kay Tee
    Bergmann, Manuela M
    Boeing, Heiner
    Trichopoulou, Antonia
    Masala, Giovanna
    Tumino, Rosario
    Lund, Eiliv
    Slimani, Nadia
    Ferrari, Pietro
    Boffetta, Paolo
    Vineis, Paolo
    Riboli, Elio
    Occupation and risk of lymphoma: a multicentre prospective cohort study (EPIC)2011In: Occupational and Environmental Medicine, ISSN 1351-0711, E-ISSN 1470-7926, Vol. 68, no 1, p. 77-81Article in journal (Refereed)
    Abstract [en]

    The findings in this current study of a higher risk of NHL among car repair workers and butchers and a higher risk of HL among gasoline station workers suggest a possible role from occupationally related exposures, such as solvents and zoonotic viruses, as risk factors for malignant lymphoma.

  • 320. Nelson, C. P.
    et al.
    Hamby, S. E.
    Saleheen, D.
    Hopewell, J. C.
    Zeng, L.
    Assimes, T. L.
    Kanoni, S.
    Willenborg, C.
    Burgess, S.
    Amouyel, P.
    Anand, S.
    Blankenberg, S.
    Boehm, B. O.
    Clarke, R. J.
    Collins, R.
    Dedoussis, G.
    Farrall, M.
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Department of Clinical Sciences, Lund University Diabetes Center, Skåne University Hospital; Department of Nutrition, Harvard School of Public Health, USA.
    Groop, L.
    Hall, A. S.
    Hamsten, A.
    Hengstenberg, C.
    Hovingh, G. Kees
    Ingelsson, E.
    Kathiresan, S.
    Kee, F.
    Koenig, I. R.
    Kooner, J.
    Lehtimaeki, T.
    Maerz, W.
    McPherson, R.
    Metspalu, A.
    Nieminen, M. S.
    O'Donnell, C. J.
    Palmer, C. N. A.
    Peters, A.
    Perola, M.
    Reilly, M. P.
    Ripatti, S.
    Roberts, R.
    Salomaa, V.
    Shah, S. H.
    Schreiber, S.
    Siegbahn, A.
    Thorsteinsdottir, U.
    Veronesi, G.
    Wareham, N.
    Willer, C. J.
    Zalloua, P. A.
    Erdmann, J.
    Deloukas, P.
    Watkins, H.
    Schunkert, H.
    Danesh, J.
    Thompson, J. R.
    Samani, N. J.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Genetically Determined Height and Coronary Artery Disease2015In: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 372, no 17, p. 1608-1618Article in journal (Refereed)
    Abstract [en]

    BACKGROUND The nature and underlying mechanisms of an inverse association between adult height and the risk of coronary artery disease (CAD) are unclear.

    METHODS We used a genetic approach to investigate the association between height and CAD, using 180 height-associated genetic variants. We tested the association between a change in genetically determined height of 1 SD (6.5 cm) with the risk of CAD in 65,066 cases and 128,383 controls. Using individual-level genotype data from 18,249 persons, we also examined the risk of CAD associated with the presence of various numbers of height-associated alleles. To identify putative mechanisms, we analyzed whether genetically determined height was associated with known cardiovascular risk factors and performed a pathway analysis of the height-associated genes.

    RESULTS We observed a relative increase of 13.5% (95% confidence interval [CI], 5.4 to 22.1; P<0.001) in the risk of CAD per 1-SD decrease in genetically determined height. There was a graded relationship between the presence of an increased number of height-raising variants and a reduced risk of CAD (odds ratio for height quar-tile 4 versus quartile 1, 0.74; 95% CI, 0.68 to 0.84; P<0.001). Of the 12 risk factors that we studied, we observed significant associations only with levels of low-density lipoprotein cholesterol and triglycerides (accounting for approximately 30% of the association). We identified several overlapping pathways involving genes associated with both development and atherosclerosis.

    CONCLUSIONS There is a primary association between a genetically determined shorter height and an increased risk of CAD, a link that is partly explained by the association between shorter height and an adverse lipid profile. Shared biologic processes that determine achieved height and the development of atherosclerosis may explain some of the association.

  • 321. Nettleton, Jennifer A
    et al.
    Follis, Jack L
    Ngwa, Julius S
    Smith, Caren E
    Ahmad, Shafqat
    Tanaka, Toshiko
    Wojczynski, Mary K
    Voortman, Trudy
    Lemaitre, Rozenn N
    Kristiansson, Kati
    Nuotio, Marja-Liisa
    Houston, Denise K
    Perälä, Mia-Maria
    Qi, Qibin
    Sonestedt, Emily
    Manichaikul, Ani
    Kanoni, Stavroula
    Ganna, Andrea
    Mikkilä, Vera
    North, Kari E
    Siscovick, David S
    Harald, Kennet
    Mckeown, Nicola M
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Rissanen, Harri
    Liu, Yongmei
    Lahti, Jari
    Hu, Frank B
    Bandinelli, Stefania
    Rukh, Gull
    Rich, Stephen
    Booij, Lisanne
    Dmitriou, Maria
    Ax, Erika
    Raitakari, Olli
    Mukamal, Kenneth
    Männistö, Satu
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Jula, Antti
    Ericson, Ulrika
    Jacobs, David R, Jr
    Van Rooij, Frank J A
    Deloukas, Panos
    Sjögren, Per
    Kähönen, Mika
    Djousse, Luc
    Perola, Markus
    Barroso, Inês
    Hofman, Albert
    Stirrups, Kathleen
    Viikari, Jorma
    Uitterlinden, André G
    Kalafati, Ioanna P
    Franco, Oscar H.
    Mozaffarian, Dariush
    Salomaa, Veikko
    Borecki, Ingrid B
    Knekt, Paul
    Kritchevsky, Stephen B
    Eriksson, Johan G
    Dedoussis, George V
    Qi, Lu
    Ferrucci, Luigi
    Orho-Melander, Marju
    Zillikens, M Carola
    Ingelsson, Erik
    Lehtimäki, Terho
    Renström, Frida
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Department of Clinical Sciences, Genetic and Molecular Epidemiology Unit, Lund University, Sweden.
    Cupples, L Adrienne
    Loos, Ruth J F
    Franks, Paul W
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Department of Clinical Sciences, Genetic and Molecular Epidemiology Unit, Lund University, Sweden; Department of Nutrition, Harvard Chan School of Public Health, Boston, MA, USA.
    Gene x dietary pattern interactions in obesity: analysis of up to 68 317 adults of European ancestry2015In: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 24, no 16, p. 4728-4738Article in journal (Refereed)
    Abstract [en]

    Obesity is highly heritable. Genetic variants showing robust associationswith obesity traits have been identified through genome wide association studies. We investigated whether a composite score representing healthy diet modifies associations of these variants with obesity traits. Totally, 32 body mass index (BMI)- and 14 waist-hip ratio (WHR)-associated single nucleotide polymorphismswere genotyped, and genetic risk scores (GRS) were calculated in 18 cohorts of European ancestry (n = 68 317). Diet score was calculated based on self-reported intakes of whole grains, fish, fruits, vegetables, nuts/seeds (favorable) and red/processed meats, sweets, sugar-sweetened beverages and fried potatoes (unfavorable). Multivariable adjusted, linear regression within each cohort followed by inverse variance-weighted, fixed-effects meta-analysis was used to characterize: (a) associations of each GRS with BMI and BMI-adjustedWHR and (b) diet score modification of genetic associations with BMI and BMI-adjusted WHR. Nominally significant interactions (P = 0.006-0.04) were observed between the diet score and WHR-GRS (but not BMI-GRS), two WHR loci (GRB14 rs10195252; LYPLAL1 rs4846567) and two BMI loci (LRRN6C rs10968576; MTIF3 rs4771122), for the respective BMI-adjustedWHR or BMI outcomes. Although the magnitudes of these select interactions were small, our data indicated that associations between genetic predisposition and obesity traits were stronger with a healthier diet. Our findings generate interesting hypotheses; however, experimental and functional studies are needed to determine their clinical relevance.

  • 322. Nettleton, Jennifer A
    et al.
    McKeown, Nicola M
    Kanoni, Stavroula
    Lemaitre, Rozenn N
    Hivert, Marie-France
    Ngwa, Julius
    van Rooij, Frank J A
    Sonestedt, Emily
    Wojczynski, Mary K
    Ye, Zheng
    Tanaka, Toshiko
    Garcia, Melissa
    Anderson, Jennifer S
    Follis, Jack L
    Djousse, Luc
    Mukamal, Kenneth
    Papoutsakis, Constantina
    Mozaffarian, Dariush
    Zillikens, M Carola
    Bandinelli, Stefania
    Bennett, Amanda J
    Borecki, Ingrid B
    Feitosa, Mary F
    Ferrucci, Luigi
    Forouhi, Nita G
    Groves, Christopher J
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Harris, Tamara
    Hofman, Albert
    Houston, Denise K
    Hu, Frank B
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Kritchevsky, Stephen B
    Langenberg, Claudia
    Launer, Lenore
    Liu, Yongmei
    Loos, Ruth J
    Nalls, Michael
    Orho-Melander, Marju
    Renström, Frida
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Rice, Kenneth
    Riserus, Ulf
    Rolandsson, Olov
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Rotter, Jerome I
    Saylor, Georgia
    Sijbrands, Eric JG
    Sjögren, Per
    Smith, Albert
    Steingrímsdóttir, Laufey
    Uitterlinden, André G
    Wareham, Nicholas J
    Prokopenko, Inga
    Pankow, James S
    van Duijn, Cornelia M
    Flores, Jose C
    Witteman, Jaqueline CM
    Dupuis, Josée
    Dedoussis, George V
    Ordovas, Jose M
    Ingelsson, Erik
    Cupples, L Adrienne
    Siscovick, David S
    Franks, Paul W
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Meigs, James B
    Interactions of dietary whole-grain intake with fasting glucose- and insulin-related genetic loci in individuals of European descent: a meta-analysis of 14 cohort studies2010In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 33, no 12, p. 2684-2691Article in journal (Refereed)
    Abstract [en]

    Our results support the favorable association of whole-grain intake with fasting glucose and insulin and suggest a potential interaction between variation in GCKR and whole-grain intake in influencing fasting insulin concentrations.

  • 323. Nieters, Alexandra
    et al.
    Rohrmann, Sabine
    Becker, Nikolaus
    Linseisen, Jakob
    Ruediger, Thomas
    Overvad, Kim
    Tjønneland, Anne
    Olsen, Anja
    Allen, Naomi E
    Travis, Ruth C
    Bingham, Sheila
    Khaw, Kay-Tee
    Ardanaz, Eva
    Redondo, M L
    Basterrechea, Mikel
    Martinez, Carmen
    Tormo, María-José
    Rosso, Stefano
    Tagliabue, Giovanna
    Masala, Giovanna
    Mattiello, Amalia
    Tumino, Rosario
    Boeing, Heiner
    Bergmann, Manuela
    Kaaks, Rudolf
    Trichopoulou, Antonia
    Trichopoulos, Dimitrios
    Peeters, Petra H
    Bueno-de-Mesquita, Bas
    Boffetta, Paolo
    Brennan, Paul
    Ferrari, Pietro
    Neasham, David
    Lund, Eiliv
    Berglund, Göran
    Manjer, Jonas
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Vineis, Paolo
    Riboli, Elio
    Smoking and Lymphoma Risk in the European Prospective Investigation into Cancer and Nutrition.2008In: Am J Epidemiol, ISSN 1476-6256Article in journal (Refereed)
    Abstract [en]

    Lymphomas are one of the few cancers that have been increasing in incidence over the past decades. So far, only a few established risk factors have been identified, including immunosuppression and viral infections. Recent evidence suggests etiologic heterogeneity of different lymphoma subtypes. Smoking may affect risk differently, depending on the lymphoma entity. The European Prospective Investigation into Cancer and Nutrition was used to study the role of smoking in the etiology of lymphomas and individual subtypes within a prospective study. Information on baseline and lifetime tobacco smoking by 478,590 participants was collected between 1992 and 2000. Cox proportional hazards regression was used to calculate multivariate-adjusted hazard ratios and 95% confidence intervals. During 3,567,410 person-years of follow-up, 1,371 lymphoma cases (1,304 non-Hodgkin's lymphomas and 67 Hodgkin's lymphomas) were identified. Relative risk for smokers at recruitment was more than twofold higher for Hodgkin's lymphoma (hazard ratio = 2.14, 95% confidence interval: 1.18, 3.87) but was not elevated for non-Hodgkin's lymphoma (hazard ratio = 1.06, 95% confidence interval: 0.94, 1.19) and individual B-cell non-Hodgkin's lymphoma subtypes. In this prospective study, smoking appeared to increase Hodgkin's lymphoma risk consistently in both genders, whereas B-cell non-Hodgkin's lymphoma risk was not associated. Future analysis should involve viral biomarkers and genetic susceptibility markers to elucidate potential mechanisms of smoking-induced carcinogenesis, particularly for Hodgkin's lymphoma.

  • 324.
    Nilsson, Lena Maria
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Winkvist, A
    Clinical Nutrition, University of Gothenburg.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Van Guelpen, Bethany
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Low-carbohydrate, high-protein score and cancer incidence and mortality in a northern swedish population2011In: Abstract Book: 2011 European Multidisciplinary Cancer Congress, Oxford: Elsevier, 2011, Vol. 47, p. S249-S249Conference paper (Refereed)
  • 325.
    Nilsson, Lena Maria
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Winkvist, Anna
    Göteborgs universitet.
    Eliasson, Mats
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Jansson, Jan-Håkan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology, Cariology.
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Van Guelpen, Bethany
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Low-carbohydrate, high-protein score and mortality in a northern Swedish population2012In: European Journal of Clinical Nutrition, ISSN 0954-3007, E-ISSN 1476-5640, Vol. 66, no 6, p. 694-700Article in journal (Refereed)
    Abstract [en]

    BACKGROUND/OBJECTIVE: Long-term effects of carbohydrate-restricted diets are unclear. We examined a low-carbohydrate, high-protein (LCHP) score in relation to mortality.

    SUBJECTS/METHODS: This is a population-based cohort study on adults in the northern Swedish county of Vasterbotten. In 37 639 men (1460 deaths) and 39 680 women (923 deaths) from the population-based Vasterbotten Intervention Program, deciles of energy-adjusted carbohydrate (descending) and protein (ascending) intake were added to create an LCHP score (2-20 points). Sex-specific hazard ratios (HR) were calculated by Cox regression.

    RESULTS: Median intakes of carbohydrates, protein and fat in subjects with LCHP scores 2-20 ranged from 61.0% to 38.6%, 11.3% to 19.2% and 26.6% to 41.5% of total energy intake, respectively. High LCHP score (14-20 points) did not predict all-cause mortality compared with low LCHP score (2-8 points), after accounting for saturated fat intake and established risk factors (men: HR for high vs low 1.03 (95% confidence interval (CI) 0.88-1.20), P for continuous 0.721; women: HR for high vs low 1.10 (95% CI 0.91-1.32), P for continuous 0.229). For cancer and cardiovascular disease, no clear associations were found. Carbohydrate intake was inversely associated with all-cause mortality, though only statistically significant in women (multivariate HR per decile increase 0.95 (95% CI 0.91-0.99), P = 0.010).

    CONCLUSION: Our results do not support a clear, general association between LCHP score and mortality. Studies encompassing a wider range of macronutrient consumption may be necessary to detect such an association.

  • 326.
    Nilsson, Lena Maria
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Arctic Research Centre at Umeå University.
    Winkvist, Anna
    Univ Gothenburg, Sahlgrenska Acad, Dept Internal Med & Clin Nutr, SE-40530 Gothenburg, Sweden.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology, Cariology.
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Van Guelpen, Bethany
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Low-carbohydrate, high-protein diet score and risk of incident cancer: a prospective cohort study2013In: Nutrition Journal, ISSN 1475-2891, E-ISSN 1475-2891, Vol. 12, p. 58-Article in journal (Refereed)
    Abstract [en]

    Background: Although carbohydrate reduction of varying degrees is a popular and controversial dietary trend, potential long-term effects for health, and cancer in specific, are largely unknown. Methods: We studied a previously established low-carbohydrate, high-protein (LCHP) score in relation to the incidence of cancer and specific cancer types in a population-based cohort in northern Sweden. Participants were 62,582 men and women with up to 17.8 years of follow-up (median 9.7), including 3,059 prospective cancer cases. Cox regression analyses were performed for a LCHP score based on the sum of energy-adjusted deciles of carbohydrate (descending) and protein (ascending) intake labeled 1 to 10, with higher scores representing a diet lower in carbohydrates and higher in protein. Important potential confounders were accounted for, and the role of metabolic risk profile, macronutrient quality including saturated fat intake, and adequacy of energy intake reporting was explored. Results: For the lowest to highest LCHP scores, 2 to 20, carbohydrate intakes ranged from median 60.9 to 38.9% of total energy intake. Both protein (primarily animal sources) and particularly fat (both saturated and unsaturated) intakes increased with increasing LCHP scores. LCHP score was not related to cancer risk, except for a non-dose-dependent, positive association for respiratory tract cancer that was statistically significant in men. The multivariate hazard ratio for medium (9-13) versus low (2-8) LCHP scores was 1.84 (95% confidence interval: 1.05-3.23; p-trend = 0.38). Other analyses were largely consistent with the main results, although LCHP score was associated with colorectal cancer risk inversely in women with high saturated fat intakes, and positively in men with higher LCHP scores based on vegetable protein. Conclusion: These largely null results provide important information concerning the long-term safety of moderate carbohydrate reduction and consequent increases in protein and, in this cohort, especially fat intakes. In order to determine the effects of stricter carbohydrate restriction, further studies encompassing a wider range of macronutrient intakes are warranted.

  • 327. Nilsson, Peter M
    et al.
    Pedersen, Nancy
    Lind, Lars
    Björkelund, Cecilia
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Söderkvist, Peter
    [Population studies are needed: also LifeGene!]2012In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 109, no 9-10, p. 484-Article in journal (Other academic)
  • 328.
    Nilsson Sommar, Johan
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Pettersson-Kymmer, Ulrika
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine. Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience, Pharmacology.
    Lundh, Thomas
    Svensson, Olle
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Orthopaedics.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Bergdahl, Ingvar A.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Hip Fracture Risk and Cadmium in Erythrocytes: A Nested Case-Control Study with Prospectively Collected Samples2014In: Calcified Tissue International, ISSN 0171-967X, E-ISSN 1432-0827, Vol. 94, no 2, p. 183-190Article in journal (Refereed)
    Abstract [en]

    Several studies have investigated the relation between bone mass density and cadmium exposure, but only few studies have been performed on fractures and biomarkers of cadmium. This study analyzed the association between hip fracture risk and cadmium in erythrocytes (Ery-Cd). Prospective samples from the Northern Sweden Health and Disease Study's biobank were used for 109 individuals who later in life had sustained a low-trauma hip fracture, matched with two controls of the same age and gender. The mean concentration of Ery-Cd (±SD) in case samples was 1.3 ± 1.4 versus 0.9 ± 1.0 μg/L in controls. The odds ratio (OR) was 1.63 [95 % confidence interval (CI) 1.10-2.42] for suffering a hip fracture for each microgram per liter increase in Ery-Cd. However, when taking smoking into consideration (never, former, or current), neither Ery-Cd nor smoking showed a statistically significant increase in fracture risk. Using multiple conditional logistic regression with BMI, height, and smoking, the estimated OR for a 1-μg/L increase in Ery-Cd was 1.52 (95 % CI 0.77-2.97). Subgroup analysis showed an increased fracture risk among women (OR = 1.94, 95 % CI 1.18-3.20, for a 1 μg/L increase), which also remained in the multiple analysis (OR = 3.33, 95 % CI 1.29-8.56). This study shows that fracture risk is associated with Ery-Cd. It is, however, not possible to draw firm conclusions on whether cadmium is the causal factor or whether other smoking-related factors cause this association. Subgroup analysis shows that cadmium is a risk factor for hip fracture among women.

  • 329.
    Nilsson Sommar, Johan
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Svensson, Maria K
    Department of Molecular and Clinical Medicine-Nephrology, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Björ, Bodil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Elmståhl, Sölve
    Department of Health Sciences, Division of Geriatric Medicine, Lund University, Lund, Sweden.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Lundh, Thomas
    Division of Occupational and Environmental Medicine, University Hospital, Lund, Sweden.
    Schön, Staffan Mi
    Diaverum Renal Services Group, Lund, Sweden & Swedish Renal Registry, Jönköping, Sweden.
    Skerfving, Staffan
    Division of Occupational and Environmental Medicine, University Hospital, Lund, Sweden.
    Bergdahl, Ingvar
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    End-stage renal disease and low level exposure to lead, cadmium and mercury: a population-based, prospective nested case-referent study in Sweden2013In: Environmental health, ISSN 1476-069X, E-ISSN 1476-069X, Vol. 12, no 9Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Cadmium (Cd), lead (Pb), and mercury (Hg) cause toxicological renal effects, but the clinical relevance at low-level exposures in general populations is unclear. The objective of this study is to assess the risk of developing end-stage renal disease in relation to Cd, Pb, and Hg exposure.

    METHODS: A total of 118 cases who later in life developed end-stage renal disease, and 378 matched (sex, age, area, and time of blood sampling) referents were identified among participants in two population-based prospective cohorts (130,000 individuals). Cd, Pb, and Hg concentrations were determined in prospectively collected samples.

    RESULTS: Erythrocyte lead was associated with an increased risk of developing end-stage renal disease (mean in cases 76 μg/L; odds ratio (OR) 1.54 for an interquartile range increase, 95% confidence interval (CI) 1.18-2.00), while erythrocyte mercury was negatively associated (2.4 μg/L; OR 0.75 for an interquartile range increase, CI 0.56-0.99). For erythrocyte cadmium, the OR of developing end-stage renal disease was 1.15 for an interquartile range increase (CI 0.99-1.34; mean Ery-Cd among cases: 1.3 μg/L). The associations for erythrocyte lead and erythrocyte mercury, but not for erythrocyte cadmium, remained after adjusting for the other two metals, smoking, BMI, diabetes, and hypertension. Gender-specific analyses showed that men carried almost all of the erythrocyte lead and erythrocyte cadmium associated risks.

    CONCLUSIONS: Erythrocyte lead is associated with end-stage renal disease but further studies are needed to evaluate causality. Gender-specific analyses suggest potential differences in susceptibility or in exposure biomarker reliability.

  • 330. Norat, Teresa
    et al.
    Bingham, Sheila
    Ferrari, Pietro
    Slimani, Nadia
    Jenab, Mazda
    Mazuir, Mathieu
    Overvad, Kim
    Olsen, Anja
    Tjonneland, Anne
    Clavel, Francoise
    Boutron-Ruault, Marie-Christine
    Kesse, Emmanuelle
    Boeing, Heiner
    Bergmann, Manuela M
    Nieters, Alexandra
    Linseisen, Jakob
    Trichopoulou, Antonia
    Trichopoulos, Dimitrios
    Tountas, Yannis
    Berrino, Franco
    Palli, Domenico
    Panico, Salvatore
    Tumino, Rosario
    Vineis, Paolo
    Bueno-de-Mesquita, H Bas
    Peeters, Petra H M
    Engeset, Dagrun
    Lund, Eiliv
    Skeie, Guri
    Ardanaz, Eva
    González, Carlos
    Navarro, Carmen
    Quirós, J Ramón
    Sanchez, Mariá José
    Berglund, Göran
    Mattisson, Irene
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology. Patologi.
    Day, Nicholas E
    Khaw, Kay-Tee
    Key, Timothy J
    San Joaquin, Miguel
    Hémon, Bertrand
    Saracci, Rodolfo
    Kaaks, Rudolf
    Riboli, Elio
    Meat, fish, and colorectal cancer risk: the European Prospective Investigation into cancer and nutrition.2005In: Journal of National Cancer Institute, ISSN 1460-2105, Vol. 97, no 12, p. 906-16Article in journal (Refereed)
  • 331.
    Norberg, Margareta
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Stenlund, Hans
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Andersson, Christer
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Weinehall, Lars
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Eriksson, Jan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Components of metabolic syndrome predicting diabetes: no role of inflammation or dyslipidemia.2007In: Obesity (Silver Spring), ISSN 1930-7381, Vol. 15, no 7, p. 1875-1885Article in journal (Refereed)
  • 332. Nyholm, Maria
    et al.
    Lissner, Lauren
    Hörnell, Agneta
    Umeå University, Faculty of Social Sciences, Department of Food and Nutrition.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology, School of Dentistry.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Weinehall, Lars
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Winkvist, Anna
    Exploring dietary patterns, obesity and sources of bias: the Västerbotten Intervention Programme (VIP)2013In: Public Health Nutrition, ISSN 1368-9800, E-ISSN 1475-2727, Vol. 16, no 4, p. 631-638Article in journal (Refereed)
    Abstract [en]

    Objective: Dietary patterns capture the overall diet and thereby provide information on how nutrients are consumed in combinations, and have been suggested to be a better method than studying single nutrients. The present study explored the relationship between dietary patterns at baseline and incidence of obesity at 10-year follow-up in women.

    Design: A longitudinal study using baseline measurements from 1992-1996, including food intake, medication, heredity, socio-economic status, lifestyle and measured body composition, and follow-up data collected in 2002-2006 including measured body composition.

    Setting: Data from the Västerbotten Intervention Programme (VIP) in Sweden.

    Subjects: A total of 6545 initially non-obese women aged 30-50 years.

    Results: Among women reporting plausible energy intakes, the 'Fruit and vegetables cluster' predicted the highest incidence of obesity (OR = 1·76, 95 % CI 1·11, 2·76; P = 0·015) compared with women in the other food pattern groups combined. When adjusting for metabolic factors and BMI at baseline, the risk for obesity in the 'Fruit and vegetables cluster' was attenuated to non-significance. In contrast, high intake of fruit per se was associated with a decreased risk of developing obesity (OR = 0·69, 95 % CI 0·51, 0·91; P = 0·010).

    Conclusions: Dietary pattern groups identified by cluster analysis are likely to reflect characteristics in addition to diet, including lifestyle, previous and current health status and risk factors for future disease, whereas intake of fruit per se was a stable indicator and less affected by baseline characteristics. These results underscore the need for complementary methods in understanding diet-disease relationships.

  • 333. Nöthlings, Ute
    et al.
    Schulze, Matthias B
    Weikert, Cornelia
    Boeing, Heiner
    van der Schouw, Yvonne T
    Bamia, Christina
    Benetou, Vasiliki
    Lagiou, Pagona
    Krogh, Vittorio
    Beulens, Joline W J
    Peeters, Petra H M
    Halkjaer, Jytte
    Tjønneland, Anne
    Tumino, Rosario
    Panico, Salvatore
    Masala, Giovanna
    Clavel-Chapelon, Francoise
    de Lauzon, Blandine
    Boutron-Ruault, Marie-Christine
    Vercambre, Marie-Noël
    Kaaks, Rudolf
    Linseisen, Jakob
    Overvad, Kim
    Arriola, Larraitz
    Ardanaz, Eva
    Gonzalez, Carlos A
    Tormo, Marie-Jose
    Bingham, Sheila
    Khaw, Kay-Tee
    Key, Tim J A
    Vineis, Paolo
    Riboli, Elio
    Ferrari, Pietro
    Boffetta, Paolo
    Bueno-de-Mesquita, H Bas
    van der A, Daphne L
    Berglund, Göran
    Wirfält, Elisabet
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology, Cariology.
    Lund, Eiliv
    Trichopoulo, Antonia
    Intake of vegetables, legumes, and fruit, and risk for all-cause, cardiovascular, and cancer mortality in a European diabetic population.2008In: Journal of Nutrition, ISSN 0022-3166, E-ISSN 1541-6100, Vol. 138, no 4, p. 775-81Article in journal (Refereed)
  • 334. Oei, Ling
    et al.
    Hsu, Yi-Hsiang
    Styrkarsdottir, Unnur
    Eussen, Bert H
    de Klein, Annelies
    Peters, Marjolein J
    Halldorsson, Bjarni
    Liu, Ching-Ti
    Alonso, Nerea
    Kaptoge, Stephen K
    Thorleifsson, Gudmar
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Hocking, Lynne J
    Husted, Lise Bjerre
    Jameson, Karen A
    Kruk, Marcin
    Lewis, Joshua R
    Patel, Millan S
    Scollen, Serena
    Svensson, Olle
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Orthopaedics.
    Trompet, Stella
    van Schoor, Natasja M
    Zhu, Kun
    Buckley, Brendan M
    Cooper, Cyrus
    Ford, Ian
    Goltzman, David
    González-Macías, Jesús
    Langdahl, Bente Lomholt
    Leslie, William D
    Lips, Paul
    Lorenc, Roman S
    Olmos, José M
    Pettersson-Kymmer, Ulrika
    Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience, Clinical Pharmacology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Reid, David M
    Riancho, José A
    Slagboom, P Eline
    Garcia-Ibarbia, Carmen
    Ingvarsson, Thorvaldur
    Johannsdottir, Hrefna
    Luben, Robert
    Medina-Gómez, Carolina
    Arp, Pascal
    Nandakumar, Kannabiran
    Palsson, Stefan Th
    Sigurdsson, Gunnar
    van Meurs, Joyce B J
    Zhou, Yanhua
    Hofman, Albert
    Jukema, J Wouter
    Pols, Huibert A P
    Prince, Richard L
    Cupples, L Adrienne
    Marshall, Christian R
    Pinto, Dalila
    Sato, Daisuke
    Scherer, Stephen W
    Reeve, Jonathan
    Thorsteinsdottir, Unnur
    Karasik, David
    Richards, J Brent
    Stefansson, Kari
    Uitterlinden, André G
    Ralston, Stuart H
    Ioannidis, John P A
    Kiel, Douglas P
    Rivadeneira, Fernando
    Estrada, Karol
    A genome-wide copy number association study of osteoporotic fractures points to the 6p25.1 locus2014In: Journal of Medical Genetics, ISSN 0022-2593, E-ISSN 1468-6244, Vol. 51, no 2, p. 122-131Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Osteoporosis is a systemic skeletal disease characterised by reduced bone mineral density and increased susceptibility to fracture; these traits are highly heritable. Both common and rare copy number variants (CNVs) potentially affect the function of genes and may influence disease risk.

    AIM: To identify CNVs associated with osteoporotic bone fracture risk.

    METHOD: We performed a genome-wide CNV association study in 5178 individuals from a prospective cohort in the Netherlands, including 809 osteoporotic fracture cases, and performed in silico lookups and de novo genotyping to replicate in several independent studies.

    RESULTS: A rare (population prevalence 0.14%, 95% CI 0.03% to 0.24%) 210 kb deletion located on chromosome 6p25.1 was associated with the risk of fracture (OR 32.58, 95% CI 3.95 to 1488.89; p=8.69×10(-5)). We performed an in silico meta-analysis in four studies with CNV microarray data and the association with fracture risk was replicated (OR 3.11, 95% CI 1.01 to 8.22; p=0.02). The prevalence of this deletion showed geographic diversity, being absent in additional samples from Australia, Canada, Poland, Iceland, Denmark, and Sweden, but present in the Netherlands (0.34%), Spain (0.33%), USA (0.23%), England (0.15%), Scotland (0.10%), and Ireland (0.06%), with insufficient evidence for association with fracture risk.

    CONCLUSIONS: These results suggest that deletions in the 6p25.1 locus may predispose to higher risk of fracture in a subset of populations of European origin; larger and geographically restricted studies will be needed to confirm this regional association. This is a first step towards the evaluation of the role of rare CNVs in osteoporosis.

  • 335. Opstelten, Jorrit L
    et al.
    Leenders, Max
    Dik, Vincent K
    Chan, Simon S M
    van Schaik, Fiona D M
    Khaw, Kay-Tee
    Luben, Robert
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Karling, Pontus
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Lindgren, Stefan
    Grip, Olof
    Key, Timothy J
    Crowe, Francesca L
    Boeing, Heiner
    Bergmann, Manuela M
    Overvad, Kim
    Palli, Domenico
    Masala, Giovanna
    Racine, Antoine
    Carbonnel, Franck
    Boutron-Ruault, Marie-Christine
    Tjønneland, Anne
    Olsen, Anja
    Andersen, Vibeke
    Kaaks, Rudolf
    Katzke, Verena A
    Tumino, Rosario
    Trichopoulou, Antonia
    Siersema, Peter D
    Bueno-de-Mesquita, H Bas
    Hart, Andrew R
    Oldenburg, Bas
    Dairy Products, Dietary Calcium, and Risk of Inflammatory Bowel Disease: Results From a European Prospective Cohort Investigation.2016In: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 22, no 6Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Dairy products may be involved in the etiology of inflammatory bowel disease by modulating gut microbiota and immune responses, but data from epidemiological studies examining this relationship are limited. We investigated the association between prediagnostic intake of these foods and dietary calcium, and the subsequent development of Crohn's disease (CD) and ulcerative colitis (UC).

    METHODS: In total, 401,326 participants were enrolled in the European Prospective Investigation into Cancer and Nutrition cohort. At recruitment, consumption of total and specific dairy products (milk, yogurt, and cheese) and dietary calcium was measured using validated food frequency questionnaires. Cases developing incident CD (n = 110) or UC (n = 244) during follow-up were matched with 4 controls. Conditional logistic regression analyses were used to calculate odds ratios (ORs) with 95% confidence intervals (CIs), adjusted for total energy intake and smoking.

    RESULTS: Compared with the lowest quartile, the ORs for the highest quartile of total dairy products and dietary calcium intake were 0.61 (95% CI, 0.32-1.19, p trend = 0.19) and 0.63 (95% CI, 0.28-1.42, p trend = 0.23) for CD, and 0.80 (95% CI, 0.50-1.30, p trend = 0.40) and 0.81 (95% CI, 0.49-1.34, p trend = 0.60) for UC, respectively. Compared with nonconsumers, individuals consuming milk had significantly reduced odds of CD (OR 0.30, 95% CI, 0.13-0.65) and nonsignificantly reduced odds of UC (OR 0.85, 95% CI, 0.49-1.47).

    CONCLUSIONS: Milk consumption may be associated with a decreased risk of developing CD, although a clear dose-response relationship was not established. Further studies are warranted to confirm this possible protective effect.

  • 336. Pala, Valeria
    et al.
    Krogh, Vittorio
    Berrino, Franco
    Sieri, Sabina
    Grioni, Sara
    Tjønneland, Anne
    Olsen, Anja
    Jakobsen, Marianne Uhre
    Overvad, Kim
    Clavel-Chapelon, Françoise
    Boutron-Ruault, Marie-Christine
    Romieu, Isabelle
    Linseisen, Jakob
    Rohrmann, Sabine
    Boeing, Heiner
    Steffen, Annika
    Trichopoulou, Antonia
    Benetou, Vassiliki
    Naska, Androniki
    Vineis, Paolo
    Tumino, Rosario
    Panico, Salvatore
    Masala, Giovanna
    Agnoli, Claudia
    Engeset, Dagrun
    Skeie, Guri
    Lund, Eiliv
    Ardanaz, Eva
    Navarro, Carmen
    Sánchez, Maria-José
    Amiano, Pilar
    Gonzalez Svatetz, Carlos Alberto
    Rodriguez, Laudina
    Wirfält, Elisabet
    Manjer, Jonas
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Peeters, Petra Hm
    van Gils, Carla H
    Bueno-de-Mesquita, H Bas
    van Duijnhoven, Fränzel Jb
    Key, Timothy J
    Spencer, Elizabeth
    Bingham, Sheila
    Khaw, Kay-Tee
    Ferrari, Pietro
    Byrnes, Graham
    Rinaldi, Sabina
    Norat, Teresa
    Michaud, Dominique S
    Riboli, Elio
    Meat, eggs, dairy products, and risk of breast cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.2009In: The American journal of clinical nutrition, ISSN 1938-3207, Vol. 90, no 3, p. 602-612Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: A Western diet is associated with breast cancer risk. OBJECTIVE: We investigated the relation of meat, egg, and dairy product consumption with breast cancer risk using data from the European Prospective Investigation into Cancer and Nutrition (EPIC). DESIGN: Between 1992 and 2003, information on diet was collected from 319,826 women. Disease hazard ratios were estimated with multivariate Cox proportional hazard models. RESULTS: Breast cancer cases (n = 7119) were observed during 8.8 y (median) of follow-up. No consistent association was found between breast cancer risk and the consumption of any of the food groups under study, analyzed by both categorical and continuous exposure variable models. High processed meat consumption was associated with a modest increase in breast cancer risk in the categorical model (hazard ratio: 1.10; 95% CI: 1.00, 1.20; highest compared with lowest quintile: P for trend = 0.07). Subgroup analyses suggested an association with butter consumption, limited to premenopausal women (hazard ratio: 1.28; 95% CI: 1.06, 1.53; highest compared with lowest quintile: P for trend = 0.21). Between-country heterogeneity was found for red meat (Q statistic = 18.03; P = 0.05) and was significantly explained (P = 0.023) by the proportion of meat cooked at high temperature. CONCLUSIONS: We have not consistently identified intakes of meat, eggs, or dairy products as risk factors for breast cancer. Future studies should investigate the possible role of high-temperature cooking in the relation of red meat intake with breast cancer risk.

  • 337. Palli, Domenico
    et al.
    Masala, Giovanna
    Del Giudice, Giuseppe
    Plebani, Mario
    Basso, Daniela
    Berti, Duccio
    Numans, Mattijs E
    E Numans, Mattijs
    Ceroti, Marco
    Peeters, Petra H M
    Bueno de Mesquita, H Bas
    Buchner, Frederike L
    Clavel-Chapelon, Francoise
    Boutron-Ruault, Marie-Christine
    Krogh, Vittorio
    Saieva, Calogero
    Vineis, Paolo
    Panico, Salvatore
    Tumino, Rosario
    Nyrén, Olof
    Simán, Henrik
    Berglund, Goran
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Sanchez, Maria-Jose
    Larrãnaga, Nerea
    Barricarte, Aurelio
    Navarro, Carmen
    Quiros, Jose R
    Key, Tim
    Allen, Naomi
    Bingham, Sheila
    Khaw, Kay Tee
    Boeing, Heiner
    Weikert, Cornelia
    Linseisen, Jakob
    Nagel, Gabriele
    Overvad, Kim
    Thomsen, Reimar W
    Tjonneland, Anne
    Olsen, Anja
    Trichoupoulou, Antonia
    Trichopoulos, Dimitrios
    Arvaniti, Athina
    Pera, Guillem
    Kaaks, Rudolf
    Jenab, Mazda
    Ferrari, Pietro
    Nesi, Gabriella
    Carneiro, Fatima
    Riboli, Elio
    Gonzalez, Carlos A
    CagA+ Helicobacter pylori infection and gastric cancer risk in the EPIC-EURGAST study.2007In: International Journal of Cancer, ISSN 0020-7136, Vol. 120, no 4, p. 859-67Article in journal (Refereed)
  • 338. Palmer, Nicholette D
    et al.
    McDonough, Caitrin W
    Hicks, Pamela J
    Roh, Bong H
    Wing, Maria R
    An, S Sandy
    Hester, Jessica M
    Cooke, Jessica N
    Bostrom, Meredith A
    Rudock, Megan E
    Talbert, Matthew E
    Lewis, Joshua P
    Ferrara, Assiamira
    Lu, Lingyi
    Ziegler, Julie T
    Sale, Michele M
    Divers, Jasmin
    Shriner, Daniel
    Adeyemo, Adebowale
    Rotimi, Charles N
    Ng, Maggie C Y
    Langefeld, Carl D
    Freedman, Barry I
    Bowden, Donald W
    Voight, Benjamin F
    Scott, Laura J
    Steinthorsdottir, Valgerdur
    Morris, Andrew P
    Dina, Christian
    Welch, Ryan P
    Zeggini, Eleftheria
    Huth, Cornelia
    Aulchenko, Yurii S
    Thorleifsson, Gudmar
    McCulloch, Laura J
    Ferreira, Teresa
    Grallert, Harald
    Amin, Najaf
    Wu, Guanming
    Willer, Cristen J
    Raychaudhuri, Soumya
    McCarroll, Steve A
    Langenberg, Claudia
    Hofmann, Oliver M
    Dupuis, Josée
    Qi, Lu
    Segrè, Ayellet V
    van Hoek, Mandy
    Navarro, Pau
    Ardlie, Kristin
    Balkau, Beverley
    Benediktsson, Rafn
    Bennett, Amanda J
    Blagieva, Roza
    Boerwinkle, Eric
    Bonnycastle, Lori L
    Boström, Kristina Bengtsson
    Bravenboer, Bert
    Bumpstead, Suzannah
    Burtt, Noël P
    Charpentier, Guillaume
    Chines, Peter S
    Cornelis, Marilyn
    Couper, David J
    Crawford, Gabe
    Doney, Alex S F
    Elliott, Katherine S
    Elliott, Amanda L
    Erdos, Michael R
    Fox, Caroline S
    Franklin, Christopher S
    Ganser, Martha
    Gieger, Christian
    Grarup, Niels
    Green, Todd
    Griffin, Simon
    Groves, Christopher J
    Guiducci, Candace
    Hadjadj, Samy
    Hassanali, Neelam
    Herder, Christian
    Isomaa, Bo
    Jackson, Anne U
    Johnson, Paul R V
    Jørgensen, Torben
    Kao, Wen H L
    Klopp, Norman
    Kong, Augustine
    Kraft, Peter
    Kuusisto, Johanna
    Lauritzen, Torsten
    Li, Man
    Lieverse, Aloysius
    Lindgren, Cecilia M
    Lyssenko, Valeriya
    Marre, Michel
    Meitinger, Thomas
    Midthjell, Kristian
    Morken, Mario A
    Narisu, Narisu
    Nilsson, Peter
    Owen, Katharine R
    Payne, Felicity
    Perry, John R B
    Petersen, Ann-Kristin
    Platou, Carl
    Proença, Christine
    Prokopenko, Inga
    Rathmann, Wolfgang
    Rayner, N William
    Robertson, Neil R
    Rocheleau, Ghislain
    Roden, Michael
    Sampson, Michael J
    Saxena, Richa
    Shields, Beverley M
    Shrader, Peter
    Sigurdsson, Gunnar
    Sparsø, Thomas
    Strassburger, Klaus
    Stringham, Heather M
    Sun, Qi
    Swift, Amy J
    Thorand, Barbara
    Tichet, Jean
    Tuomi, Tiinamaija
    van Dam, Rob M
    van Haeften, Timon W
    van Herpt, Thijs
    van Vliet-Ostaptchouk, Jana V
    Walters, G Bragi
    Weedon, Michael N
    Wijmenga, Cisca
    Witteman, Jacqueline
    Bergman, Richard N
    Cauchi, Stephane
    Collins, Francis S
    Gloyn, Anna L
    Gyllensten, Ulf
    Hansen, Torben
    Hide, Winston A
    Hitman, Graham A
    Hofman, Albert
    Hunter, David J
    Hveem, Kristian
    Laakso, Markku
    Mohlke, Karen L
    Morris, Andrew D
    Palmer, Colin N A
    Pramstaller, Peter P
    Rudan, Igor
    Sijbrands, Eric
    Stein, Lincoln D
    Tuomilehto, Jaakko
    Uitterlinden, Andre
    Walker, Mark
    Wareham, Nicholas J
    Watanabe, Richard M
    Abecasis, Goncalo R
    Boehm, Bernhard O
    Campbell, Harry
    Daly, Mark J
    Hattersley, Andrew T
    Hu, Frank B
    Meigs, James B
    Pankow, James S
    Pedersen, Oluf
    Wichmann, H-Erich
    Barroso, Inês
    Florez, Jose C
    Frayling, Timothy M
    Groop, Leif
    Sladek, Rob
    Thorsteinsdottir, Unnur
    Wilson, James F
    Illig, Thomas
    Froguel, Philippe
    van Duijn, Cornelia M
    Stefansson, Kari
    Altshuler, David
    Boehnke, Michael
    McCarthy, Mark I
    Soranzo, Nicole
    Wheeler, Eleanor
    Glazer, Nicole L
    Bouatia-Naji, Nabila
    Mägi, Reedik
    Randall, Joshua
    Johnson, Toby
    Elliott, Paul
    Rybin, Denis
    Henneman, Peter
    Dehghan, Abbas
    Hottenga, Jouke Jan
    Song, Kijoung
    Goel, Anuj
    Egan, Josephine M
    Lajunen, Taina
    Doney, Alex
    Kanoni, Stavroula
    Cavalcanti-Proença, Christine
    Kumari, Meena
    Timpson, Nicholas J
    Zabena, Carina
    Ingelsson, Erik
    An, Ping
    O'Connell, Jeffrey
    Luan, Jian'an
    Elliott, Amanda
    McCarroll, Steven A
    Roccasecca, Rosa Maria
    Pattou, François
    Sethupathy, Praveen
    Ariyurek, Yavuz
    Barter, Philip
    Beilby, John P
    Ben-Shlomo, Yoav
    Bergmann, Sven
    Bochud, Murielle
    Bonnefond, Amélie
    Borch-Johnsen, Knut
    Böttcher, Yvonne
    Brunner, Eric
    Bumpstead, Suzannah J
    Chen, Yii-Der Ida
    Chines, Peter
    Clarke, Robert
    Coin, Lachlan J M
    Cooper, Matthew N
    Crisponi, Laura
    Day, Ian N M
    de Geus, Eco J C
    Delplanque, Jerome
    Fedson, Annette C
    Fischer-Rosinsky, Antje
    Forouhi, Nita G
    Frants, Rune
    Franzosi, Maria Grazia
    Galan, Pilar
    Goodarzi, Mark O
    Graessler, Jürgen
    Grundy, Scott
    Gwilliam, Rhian
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Hammond, Naomi
    Han, Xijing
    Hartikainen, Anna-Liisa
    Hayward, Caroline
    Heath, Simon C
    Hercberg, Serge
    Hicks, Andrew A
    Hillman, David R
    Hingorani, Aroon D
    Hui, Jennie
    Hung, Joe
    Jula, Antti
    Kaakinen, Marika
    Kaprio, Jaakko
    Kesaniemi, Y Antero
    Kivimaki, Mika
    Knight, Beatrice
    Koskinen, Seppo
    Kovacs, Peter
    Kyvik, Kirsten Ohm
    Lathrop, G Mark
    Lawlor, Debbie A
    Le Bacquer, Olivier
    Lecoeur, Cécile
    Li, Yun
    Mahley, Robert
    Mangino, Massimo
    Manning, Alisa K
    Martínez-Larrad, María Teresa
    McAteer, Jarred B
    McPherson, Ruth
    Meisinger, Christa
    Melzer, David
    Meyre, David
    Mitchell, Braxton D
    Mukherjee, Sutapa
    Naitza, Silvia
    Neville, Matthew J
    Oostra, Ben A
    Orrù, Marco
    Pakyz, Ruth
    Paolisso, Giuseppe
    Pattaro, Cristian
    Pearson, Daniel
    Peden, John F
    Pedersen, Nancy L
    Perola, Markus
    Pfeiffer, Andreas F H
    Pichler, Irene
    Polasek, Ozren
    Posthuma, Danielle
    Potter, Simon C
    Pouta, Anneli
    Province, Michael A
    Psaty, Bruce M
    Rayner, Nigel W
    Rice, Kenneth
    Ripatti, Samuli
    Rivadeneira, Fernando
    Rolandsson, Olov
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Sandbaek, Annelli
    Sandhu, Manjinder
    Sanna, Serena
    Sayer, Avan Aihie
    Scheet, Paul
    Seedorf, Udo
    Sharp, Stephen J
    Shields, Beverley
    Sijbrands, Eric J G
    Silveira, Angela
    Simpson, Laila
    Singleton, Andrew
    Smith, Nicholas L
    Sovio, Ulla
    Swift, Amy
    Syddall, Holly
    Syvänen, Ann-Christine
    Tanaka, Toshiko
    Tönjes, Anke
    Uitterlinden, André G
    van Dijk, Ko Willems
    Varma, Dhiraj
    Visvikis-Siest, Sophie
    Vitart, Veronique
    Vogelzangs, Nicole
    Waeber, Gérard
    Wagner, Peter J
    Walley, Andrew
    Ward, Kim L
    Watkins, Hugh
    Wild, Sarah H
    Willemsen, Gonneke
    Witteman, Jaqueline C M
    Yarnell, John W G
    Zelenika, Diana
    Zethelius, Björn
    Zhai, Guangju
    Zhao, Jing Hua
    Zillikens, M Carola
    Borecki, Ingrid B
    Loos, Ruth J F
    Meneton, Pierre
    Magnusson, Patrik K E
    Nathan, David M
    Williams, Gordon H
    Silander, Kaisa
    Salomaa, Veikko
    Smith, George Davey
    Bornstein, Stefan R
    Schwarz, Peter
    Spranger, Joachim
    Karpe, Fredrik
    Shuldiner, Alan R
    Cooper, Cyrus
    Dedoussis, George V
    Serrano-Ríos, Manuel
    Lind, Lars
    Palmer, Lyle J
    Franks, Paul W
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Ebrahim, Shah
    Marmot, Michael
    Kao, W H Linda
    Pramstaller, Peter Paul
    Wright, Alan F
    Stumvoll, Michael
    Hamsten, Anders
    Buchanan, Thomas A
    Valle, Timo T
    Rotter, Jerome I
    Siscovick, David S
    Penninx, Brenda W J H
    Boomsma, Dorret I
    Deloukas, Panos
    Spector, Timothy D
    Ferrucci, Luigi
    Cao, Antonio
    Scuteri, Angelo
    Schlessinger, David
    Uda, Manuela
    Ruokonen, Aimo
    Jarvelin, Marjo-Riitta
    Waterworth, Dawn M
    Vollenweider, Peter
    Peltonen, Leena
    Mooser, Vincent
    Sladek, Robert
    A genome-wide association search for type 2 diabetes genes in African Americans.2012In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 7, no 1, p. e29202-Article in journal (Refereed)
    Abstract [en]

    African Americans are disproportionately affected by type 2 diabetes (T2DM) yet few studies have examined T2DM using genome-wide association approaches in this ethnicity. The aim of this study was to identify genes associated with T2DM in the African American population. We performed a Genome Wide Association Study (GWAS) using the Affymetrix 6.0 array in 965 African-American cases with T2DM and end-stage renal disease (T2DM-ESRD) and 1029 population-based controls. The most significant SNPs (n = 550 independent loci) were genotyped in a replication cohort and 122 SNPs (n = 98 independent loci) were further tested through genotyping three additional validation cohorts followed by meta-analysis in all five cohorts totaling 3,132 cases and 3,317 controls. Twelve SNPs had evidence of association in the GWAS (P<0.0071), were directionally consistent in the Replication cohort and were associated with T2DM in subjects without nephropathy (P<0.05). Meta-analysis in all cases and controls revealed a single SNP reaching genome-wide significance (P<2.5×10(-8)). SNP rs7560163 (P = 7.0×10(-9), OR (95% CI) = 0.75 (0.67-0.84)) is located intergenically between RND3 and RBM43. Four additional loci (rs7542900, rs4659485, rs2722769 and rs7107217) were associated with T2DM (P<0.05) and reached more nominal levels of significance (P<2.5×10(-5)) in the overall analysis and may represent novel loci that contribute to T2DM. We have identified novel T2DM-susceptibility variants in the African-American population. Notably, T2DM risk was associated with the major allele and implies an interesting genetic architecture in this population. These results suggest that multiple loci underlie T2DM susceptibility in the African-American population and that these loci are distinct from those identified in other ethnic populations.

  • 339. Peeters, Petra H M
    et al.
    Slimani, Nadia
    van der Schouw, Yvonne T
    Grace, Philip B
    Navarro, Carmen
    Tjonneland, Anne
    Olsen, Anja
    Clavel-Chapelon, Francoise
    Touillaud, Marina
    Boutron-Ruault, Marie-Christine
    Jenab, Mazda
    Kaaks, Rudolf
    Linseisen, Jakob
    Trichopoulou, Antonia
    Trichopoulos, Dimitrios
    Dilis, Vardis
    Boeing, Heiner
    Weikert, Cornelia
    Overvad, Kim
    Pala, Valeria
    Palli, Domenico
    Panico, Salvatore
    Tumino, Rosario
    Vineis, Paolo
    Bueno-de-Mesquita, H Bas
    van Gils, Carla H
    Skeie, Guri
    Jakszyn, Paula
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Berglund, Goran
    Key, Tim J
    Travis, Ruth
    Riboli, Elio
    Bingham, Sheila A
    Variations in plasma phytoestrogen concentrations in European adults.2007In: Journal of Nutrition, ISSN 0022-3166, Vol. 137, no 5, p. 1294-300Article in journal (Refereed)
  • 340. Pereira, Mark A
    et al.
    O'Reilly, Eilis
    Augustsson, Katarina
    Fraser, Gary E
    Goldbourt, Uri
    Heitmann, Berit L
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Knekt, Paul
    Liu, Simin
    Pietinen, Pirjo
    Spiegelman, Donna
    Stevens, June
    Virtamo, Jarmo
    Willett, Walter C
    Ascherio, Alberto
    Dietary fiber and risk of coronary heart disease: a pooled analysis of cohort studies.2004In: Arch Intern Med, ISSN 0003-9926, Vol. 164, no 4, p. 370-6Article in journal (Refereed)
  • 341. Peri, Suraj
    et al.
    de Cicco, Ricardo Lopez
    Santucci-Pereira, Julia
    Slifker, Michael
    Ross, Eric A
    Russo, Irma H
    Russo, Patricia A
    Arslan, Alan A
    Belitskaya-Levy, Ilana
    Zeleniuch-Jacquotte, Anne
    Bordas, Pal
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Åhman, Janet
    Afanasyeva, Yelena
    Johansson, Robert
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Sheriff, Fathima
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Toniolo, Paolo
    Russo, Jose
    Defining the genomic signature of the parous breast2012In: BMC Medical Genomics, ISSN 1755-8794, E-ISSN 1755-8794, Vol. 5, p. 46-Article in journal (Refereed)
    Abstract [en]

    Background: It is accepted that a woman's lifetime risk of developing breast cancer after menopause is reduced by early full term pregnancy and multiparity. This phenomenon is thought to be associated with the development and differentiation of the breast during pregnancy.

    Methods: In order to understand the underlying molecular mechanisms of pregnancy induced breast cancer protection, we profiled and compared the transcriptomes of normal breast tissue biopsies from 71 parous (P) and 42 nulliparous (NP) healthy postmenopausal women using Affymetrix Human Genome U133 Plus 2.0 arrays. To validate the results, we performed real time PCR and immunohistochemistry.

    Results: We identified 305 differentially expressed probesets (208 distinct genes). Of these, 267 probesets were up- and 38 down-regulated in parous breast samples; bioinformatics analysis using gene ontology enrichment revealed that up-regulated genes in the parous breast represented biological processes involving differentiation and development, anchoring of epithelial cells to the basement membrane, hemidesmosome and cell-substrate junction assembly, mRNA and RNA metabolic processes and RNA splicing machinery. The down-regulated genes represented biological processes that comprised cell proliferation, regulation of IGF-like growth factor receptor signaling, somatic stem cell maintenance, muscle cell differentiation and apoptosis.

    Conclusions: This study suggests that the differentiation of the breast imprints a genomic signature that is centered in the mRNA processing reactome. These findings indicate that pregnancy may induce a safeguard mechanism at post-transcriptional level that maintains the fidelity of the transcriptional process.

  • 342. Petersen, Gloria M
    et al.
    Amundadottir, Laufey
    Fuchs, Charles S
    Kraft, Peter
    Stolzenberg-Solomon, Rachael Z
    Jacobs, Kevin B
    Arslan, Alan A
    Bueno-de-Mesquita, H Bas
    Gallinger, Steven
    Gross, Myron
    Helzlsouer, Kathy
    Holly, Elizabeth A
    Jacobs, Eric J
    Klein, Alison P
    LaCroix, Andrea
    Li, Donghui
    Mandelson, Margaret T
    Olson, Sara H
    Risch, Harvey A
    Zheng, Wei
    Albanes, Demetrius
    Bamlet, William R
    Berg, Christine D
    Boutron-Ruault, Marie-Christine
    Buring, Julie E
    Bracci, Paige M
    Canzian, Federico
    Clipp, Sandra
    Cotterchio, Michelle
    de Andrade, Mariza
    Duell, Eric J
    Gaziano, J Michael
    Giovannucci, Edward L
    Goggins, Michael
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Hankinson, Susan E
    Hassan, Manal
    Howard, Barbara
    Hunter, David J
    Hutchinson, Amy
    Jenab, Mazda
    Kaaks, Rudolf
    Kooperberg, Charles
    Krogh, Vittorio
    Kurtz, Robert C
    Lynch, Shannon M
    McWilliams, Robert R
    Mendelsohn, Julie B
    Michaud, Dominique S
    Parikh, Hemang
    Patel, Alpa V
    Peeters, Petra H M
    Rajkovic, Aleksandar
    Riboli, Elio
    Rodriguez, Laudina
    Seminara, Daniela
    Shu, Xiao-Ou
    Thomas, Gilles
    Tjønneland, Anne
    Tobias, Geoffrey S
    Trichopoulos, Dimitrios
    Van Den Eeden, Stephen K
    Virtamo, Jarmo
    Wactawski-Wende, Jean
    Wang, Zhaoming
    Wolpin, Brian M
    Yu, Herbert
    Yu, Kai
    Zeleniuch-Jacquotte, Anne
    Fraumeni, Joseph F
    Hoover, Robert N
    Hartge, Patricia
    Chanock, Stephen J
    A genome-wide association study identifies pancreatic cancer susceptibility loci on chromosomes 13q22.1, 1q32.1 and 5p15.332010In: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 42, no 3, p. 224-228Article in journal (Refereed)
    Abstract [en]

    We conducted a genome-wide association study of pancreatic cancer in 3,851 affected individuals (cases) and 3,934 unaffected controls drawn from 12 prospective cohort studies and 8 case-control studies. Based on a logistic regression model for genotype trend effect that was adjusted for study, age, sex, self-described ancestry and five principal components, we identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.33. Two correlated SNPs, rs9543325 (P = 3.27 x 10(-11), per-allele odds ratio (OR) 1.26, 95% CI 1.18-1.35) and rs9564966 (P = 5.86 x 10(-8), per-allele OR 1.21, 95% CI 1.13-1.30), map to a nongenic region on chromosome 13q22.1. Five SNPs on 1q32.1 map to NR5A2, and the strongest signal was at rs3790844 (P = 2.45 x 10(-10), per-allele OR 0.77, 95% CI 0.71-0.84). A single SNP, rs401681 (P = 3.66 x 10(-7), per-allele OR 1.19, 95% CI 1.11-1.27), maps to the CLPTM1L-TERT locus on 5p15.33, which is associated with multiple cancers. Our study has identified common susceptibility loci for pancreatic cancer that warrant follow-up studies.

  • 343.
    Pettersson-Kymmer, Ulrika
    et al.
    Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Lacroix, Andrea
    Eriksson, Joel
    Bergström, Ulrica
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences.
    Melin, Beatrice
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Wibom, Carl
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Vandenput, Liesbeth
    Rajaraman, Preetha
    Hartge, Patricia
    Chanock, Stephen
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Duggan, David
    Kooperberg, Charles
    Handelman, Samuel
    Aragaki, Aaron
    Nethander, Maria
    Uitterlinden, Andre
    Rivadeneira, Fernando
    Jackson, Rebecca
    Ohlsson, Claes
    Genome-wide association study meta-analysis identifies the SOAT1/AXDND1 locus to be associated with hip and forearm fracture risk2013In: Bone Abstracts, 2013, Vol. 1Conference paper (Other academic)
    Abstract [en]

    Hip and forearm fractures are the two clinically most important non-vertebral fractures. Twin studies have demonstrated a high heritability of these fractures and the heritable component of fracture risk is largely independent of BMD. To identify common genetic variants associated with hip and forearm fractures, we performed a genome-wide association study (GWAS ~ 2.5 million SNPs) meta-analysis of two large fracture data sets within the well-characterized UFO cohort (UFO-hip; 1014 hip fractures and 862 controls, and UFO-forearm; 1060 forearm fractures and 1055 controls). All fractures were confirmed through radiographic reports. Replication was performed in the Women’s Health Initiative (WHI) cohort (1845 hip fractures verified by medical records and 2120 controls). We identified one SNP within the SOAT1/AXDND1 locus (1q25.2) that was associated with fracture risk at genome wide significance (OR per allele=1.33; P=3.1×10−8) in the UFO discovery meta-analysis. This SNP was associated with fracture risk both in the WHI replication cohort (OR 1.16, P=2.1×10−3) and in the combined analyses comprising 7956 subjects (3919 cases and 4037 controls; OR=1.24, P=5.6×10−10). However, it was not associated with BMD or biochemical bone markers, suggesting that its association with fractures is BMD-independent. A genetic score (GS), including information from 63 SNPs earlier shown to be reproducibly associated with BMD, was significantly associated with both hip (P=7.9×10−4) and forearm (P=8.6×10−5) fractures. Models including both the SNP in the SOAT1/AXDND1 locus and the GS demonstrated that the impact of the SNP in the SOAT1/AXDND1 locus on fracture risk was independent of the BMD-associated GS. In summary, both a BMD-associated GS and a non-BMD associated genetic variant in the SOAT1/AXDND1 locus are associated with hip and forearm fractures.

  • 344. Pischon, Tobias
    et al.
    Boeing, Heiner
    Weikert, Steffen
    Allen, Naomi
    Key, Tim
    Johnsen, Nina Føns
    Tjønneland, Anne
    Severinsen, Marianne Tang
    Overvad, Kim
    Rohrmann, Sabine
    Kaaks, Rudolf
    Trichopoulou, Antonia
    Zoi, Gitaki
    Trichopoulos, Dimitrios
    Pala, Valeria
    Palli, Domenico
    Tumino, Rosario
    Sacerdote, Carlotta
    Bueno-de-Mesquita, H Bas
    May, Anne
    Manjer, Jonas
    Wallström, Peter
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Buckland, Genevieve
    Larrañaga, Nerea
    Chirlaque, María Dolores
    Martínez, Carmen
    Redondo Cornejo, María L
    Ardanaz, Eva
    Bingham, Sheila
    Khaw, Kay-Tee
    Rinaldi, Sabina
    Slimani, Nadia
    Jenab, Mazda
    Riboli, Elio
    Body size and risk of prostate cancer in the European prospective investigation into cancer and nutrition2008In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 17, no 11, p. 3252-3261Article in journal (Refereed)
    Abstract [en]

    Background: Body size has been hypothesized to influence the risk of prostate cancer; however, most epidemiologic studies have relied on body mass index (BMI) to assess adiposity, whereas only a few studies have examined whether body fat distribution predicts prostate cancer.

    Methods: We examined the association of height, BMI, waist and hip circumference, and waist-hip ratio with prostate cancer risk among 129,502 men without cancer at baseline from 8 countries of the European Prospective Investigation into Cancer and Nutrition (EPIC), using Cox regression, with age as time metric, stratifying by study center and age at recruitment, and adjusting for education, smoking status, alcohol consumption, and physical activity.

    Results: During a mean follow-up of 8.5 years, 2,446 men developed prostate cancer. Waist circumference and waist-hip ratio were positively associated with risk of advanced disease. The relative risk of advanced prostate cancer was 1.06 (95% confidence interval, 1.01-1.1) per 5-cm-higher waist circumference and 1.21 (95% confidence interval, 1.04-1.39) per 0.1-unit-higher waist-hip ratio. When stratified by BMI, waist circumference and waist-hip ratio were positively related to risk of total, advanced, and high-grade prostate cancer among men with lower but not among those with higher BMI (Pinteraction for waist with BMI, 0.25, 0.02, and 0.05, respectively; Pinteraction for waist-hip ratio with BMI, 0.27, 0.22, and 0.14; respectively).

    Conclusions: These data suggest that abdominal adiposity may be associated with an increased risk of advanced prostate cancer. This association may be stronger among individuals with lower BMI; however, this finding needs confirmation in future studies.

  • 345. Pischon, Tobias
    et al.
    Lahmann, Petra H
    Boeing, Heiner
    Tjønneland, Anne
    Halkjaer, Jytte
    Overvad, Kim
    Klipstein-Grobusch, Kerstin
    Linseisen, Jakob
    Becker, Nikolaus
    Trichopoulou, Antonia
    Benetou, Vassiliki
    Trichopoulos, Dimitrios
    Sieri, Sabina
    Palli, Domenico
    Tumino, Rosario
    Vineis, Paolo
    Panico, Salvatore
    Monninkhof, Evelyn
    Peeters, Petra H M
    Bueno-de-Mesquita, H Bas
    Büchner, Frederike L
    Ljungberg, Börje
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Berglund, Göran
    Gonzalez, Carlos Alberto
    Dorronsoro, Miren
    Gurrea, Aurelio Barricarte
    Navarro, Carmen
    Martinez, Carmen
    Quirós, J Ramón
    Roddam, Andrew
    Allen, Naomi
    Bingham, Sheila
    Khaw, Kay-Tee
    Kaaks, Rudolf
    Norat, Teresa
    Slimani, Nadia
    Riboli, Elio
    Body size and risk of renal cell carcinoma in the European Prospective Investigation into Cancer and Nutrition (EPIC).2006In: International Journal of Cancer, ISSN 0020-7136, Vol. 118, no 3, p. 728-38Article in journal (Refereed)
  • 346. Poveda, Alaitz
    et al.
    Chen, Yan
    Brändström, Anders
    Umeå University, Faculty of Social Sciences, Centre for Demographic and Ageing Research (CEDAR).
    Engberg, Elisabeth
    Umeå University, Faculty of Social Sciences, Centre for Demographic and Ageing Research (CEDAR).
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Biobank Research.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Biobank Research.
    Renström, Frida
    Umeå University, Faculty of Medicine, Department of Biobank Research. Genetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Clinical Research Centre, Lund University, Jan Waldenströms gata 35, Building 91, Skåne University Hospital, SE-20502 Malmö, Sweden.
    Kurbasic, Azra
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Genetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Clinical Research Centre, Lund University, Jan Waldenströms gata 35, Building 91, Skåne University Hospital, SE-20502 Malmö, Sweden; Department of Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
    The heritable basis of gene-environment interactions in cardiometabolic traits2017In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 60, no 3, p. 442-452Article in journal (Refereed)
    Abstract [en]

    Aims/hypothesis Little is known about the heritable basis of gene-environment interactions in humans. We therefore screened multiple cardiometabolic traits to assess the probability that they are influenced by genotype-environment interactions.

    Methods Fourteen established environmental risk exposures and 11 cardiometabolic traits were analysed in the VIKING study, a cohort of 16,430 Swedish adults from 1682 extended pedigrees with available detailed genealogical, phenotypic and demographic information, using a maximum likelihood variance decomposition method in Sequential Oligogenic Linkage Analysis Routines software.

    Results All cardiometabolic traits had statistically significant heritability estimates, with narrow-sense heritabilities (h (2)) ranging from 24% to 47%. Genotype-environment interactions were detected for age and sex (for the majority of traits), physical activity (for triacylglycerols, 2 h glucose and diastolic BP), smoking (for weight), alcohol intake (for weight, BMI and 2 h glucose) and diet pattern (for weight, BMI, glycaemic traits and systolic BP). Genotype-age interactions for weight and systolic BP, genotype-sex interactions for BMI and triacylglycerols and genotype-alcohol intake interactions for weight remained significant after multiple test correction.

    Conclusion/hypothesis Age, sex and alcohol intake are likely to be major modifiers of genetic effects for a range of cardiometabolic traits. This information may prove valuable for studies that seek to identify specific loci that modify the effects of lifestyle in cardiometabolic disease.

  • 347. Poveda, Alaitz
    et al.
    Koivula, Robert W.
    Ahmad, Shafqat
    Barroso, Ines
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Biobank Research.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Renstrom, Frida
    Umeå University, Faculty of Medicine, Department of Biobank Research. Lund Univ, Dept Clin Sci, Genet & Mol Epidemiol Unit, Malmö, Sweden.
    Franks, Paul W.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Innate biology versus lifestyle behaviour in the aetiology of obesity and type 2 diabetes: the GLACIER Study2016In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 59, no 3, p. 462-471Article in journal (Refereed)
    Abstract [en]

    Aims/hypothesis We compared the ability of genetic (established type 2 diabetes, fasting glucose, 2 h glucose and obesity variants) and modifiable lifestyle (diet, physical activity, smoking, alcohol and education) risk factors to predict incident type 2 diabetes and obesity in a population-based prospective cohort of 3,444 Swedish adults studied sequentially at baseline and 10 years later. Methods Multivariable logistic regression analyses were used to assess the predictive ability of genetic and lifestyle risk factors on incident obesity and type 2 diabetes by calculating the AUC. Results The predictive accuracy of lifestyle risk factors was similar to that yielded by genetic information for incident type 2 diabetes (AUC 75% and 74%, respectively) and obesity (AUC 68% and 73%, respectively) in models adjusted for age, age2 and sex. The addition of genetic information to the lifestyle model significantly improved the prediction of type 2 diabetes (AUC 80%; p = 0.0003) and obesity (AUC 79%; p < 0.0001) and resulted in a net reclassification improvement of 58% for type 2 diabetes and 64% for obesity. Conclusions/interpretation These findings illustrate that lifestyle and genetic information separately provide a similarly high degree of long-range predictive accuracy for obesity and type 2 diabetes.

  • 348. Pukkala, Eero
    et al.
    Andersen, Aage
    Berglund, Göran
    Gislefoss, Randi
    Gudnason, Vilmundur
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Jellum, Egil
    Jousilahti, Pekka
    Knekt, Paul
    Koskela, Pentti
    Kyyrönen, P Pentti
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. Onkologi.
    Luostarinen, Tapio
    Löve, Arthur
    Ögmundsdóttir, Helga
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Tenkanen, Leena
    Tryggvadóttir, Laufey
    Virtamo, Jarmo
    Wadell, Göran
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology. Virologi.
    Widell, Anders
    Lehtinen, Matti
    Dillner, Joakim
    Nordic biological specimen banks as basis for studies of cancer causes and control - more than 2 million sample donors, 25 million person years and 100 000 prospective cancers.2007In: Acta Oncol, ISSN 0284-186X, Vol. 46, no 3, p. 286-307Article in journal (Refereed)
  • 349. Racine, A.
    et al.
    Carbonnel, F.
    Chan, S.
    Hart, A.
    de Mesquita, B. Bueno
    Oldenburg, B.
    VanSchaik, F.
    Tjonneland, A.
    Olsen, A.
    Dahm, C.
    Key, T.
    Luben, R.
    Kaw, K. -T
    Riboli, E.
    Grip, O.
    Lindgren, S.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Karling, Pontus
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Clavel-Chapelon, F.
    Bergman, M.
    Boeing, H.
    Buijsse, B.
    Kaaks, R.
    Katzke, V.
    Palli, D.
    Masala, G.
    Jantchou, P.
    Ruault, M. C. Boutron
    Dietary patterns and risk of Inflammatory Bowel Disease in Europe: Results from the EPIC study2015In: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 9, p. S26-S26Article in journal (Other academic)
  • 350. Racine, Antoine
    et al.
    Carbonnel, Franck
    Chan, Simon S. M.
    Hart, Andrew R.
    Bueno-de-Mesquita, H. Bas
    Oldenburg, Bas
    van Schaik, Fiona D. M.
    Tjønneland, Anne
    Olsen, Anja
    Dahm, Christina C.
    Key, Timothy
    Luben, Robert
    Khaw, Kay-Tee
    Riboli, Elio
    Grip, Olof
    Lindgren, Stefan
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Karling, Pontus
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Clavel-Chapelon, Francoise
    Bergman, Manuela M.
    Boeing, Heiner
    Kaaks, Rudolf
    Katzke, Verena A.
    Palli, Domenico
    Masala, G.
    Jantchou, Prevost
    Boutron-Ruault, Marie-Christine
    Dietary Patterns and Risk of Inflammatory Bowel Disease in Europe: Results from the EPIC Study2016In: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 22, no 2, p. 345-354Article in journal (Refereed)
    Abstract [en]

    Background: Specific nutrients or foods have been inconsistently associated with ulcerative colitis (UC) or Crohn’s disease (CD) risks. Thus, we investigated associations between diet as a whole, as dietary patterns, and UC and CD risks.

    Methods: Within the prospective EPIC (European Prospective Investigation into Cancer) study, we set up a nested matched case–control study among 366,351 participants with inflammatory bowel disease data, including 256 incident cases of UC and 117 of CD, and 4 matched controls per case. Dietary intake was recorded at baseline from validated food frequency questionnaires. Incidence rate ratios of developing UC and CD were calculated for quintiles of the Mediterranean diet score and a posteriori dietary patterns produced by factor analysis.

    Results: No dietary pattern was associated with either UC or CD risks. However, when excluding cases occurring within the first 2 years after dietary assessment, there was a positive association between a “high sugar and soft drinks” pattern and UC risk (incidence rate ratios for the fifth versus first quintile, 1.68 [1.00–2.82]; Ptrend ¼ 0.02). When considering the foods most associated with the pattern, high consumers of sugar and soft drinks were at higher UC risk only if they had low vegetables intakes.

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