905 results on '"Severi G"'
Search Results
2. ARID1B-related disorder in 87 adults: Natural history and self-sustainability
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van der Sluijs, P.J., Gösgens, M., Dingemans, A.J.M., Striano, P., Riva, A., Mignot, C., Faudet, A., Vasileiou, G., Walther, M., Schrier Vergano, S.A., Alders, M., Alkuraya, F.S., Alorainy, I., Alsaif, H.S., Anderlid, B., Bache, I., van Beek, I., Blanluet, M., van Bon, B.W., Brunet, T., Brunner, H., Carriero, M.L., Charles, P., Chatron, N., Coccia, E., Dubourg, C., Earl, R.K., Eichler, E.E., Faivre, L., Foulds, N., Graziano, C., Guerrot, A.M., Hashem, M.O., Heide, S., Heron, D., Hickey, S.E., Hopman, S.M.J., Kattentidt-Mouravieva, A., Kerkhof, J., Klein Wassink-Ruiter, J.S., Kurtz-Nelson, E.C., Kušíková, K., Kvarnung, M., Lecoquierre, F., Leszinski, G.S., Loberti, L., Magoulas, P.L., Mari, F., Maystadt, I., Merla, G., Milunsky, J.M., Moortgat, S., Nicolas, G., Leary, M.O.’, Odent, S., Ozmore, J.R., Parbhoo, K., Pfundt, R., Piccione, M., Pinto, A.M., Popp, B., Putoux, A., Rehm, H.L., Reis, A., Renieri, A., Rosenfeld, J.A., Rossi, M., Salzano, E., Saugier-Veber, P., Seri, M., Severi, G., Sonmez, F.M., Strobl-Wildemann, G., Stuurman, K.E., Uctepe, E., Van Esch, H., Vitetta, G., de Vries, B.B.A., Wahl, D., Wang, T., Zacher, P., Heitink, K.R., Ropers, F.G., Steenbeek, D., Rybak, T., and Santen, G.W.E.
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- 2024
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3. Analgesic use and the risk of renal cell carcinoma – Findings from the Consortium for the Investigation of Renal Malignancies (CONFIRM) study
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Bruinsma, F.J., Jordan, S., Bassett, J.K., Severi, G., MacInnis, R.J., Walsh, J., Aitken, T., Jenkins, M., Carroll, R., Jefford, M., Davis, I.D., Tucker, K., Dudding-Byth, T., English, D.R., Giles, G.G., Winship, I., and Milne, R.L.
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- 2021
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4. Associations between smoking and blood-group, and the risk of dyslipidaemia amongst French women
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MacDonald, C. J., Madika, A. L., Severi, G., Fournier, A., and Boutron-Ruault, M. C.
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- 2021
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5. Association between menopausal hormone therapy, mammographic density and breast cancer risk: results from the E3N cohort study
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Fornili, M., Perduca, V., Fournier, A., Jérolon, A., Boutron-Ruault, M. C., Maskarinec, G., Severi, G., and Baglietto, L.
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- 2021
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6. Vitamin B6 catabolism and lung cancer risk: results from the Lung Cancer Cohort Consortium (LC3)
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Zuo, H., Ueland, P.M., Midttun, Ø, Tell, G.S., Fanidi, A., Zheng, W., Shu, X., Xiang, Y., Wu, J., Prentice, R., Pettinger, M., Thomson, C.A., Giles, G.G., Hodge, A., Cai, Q., Blot, W.J., Johansson, M., Hultdin, J., Grankvist, K., Stevens, V.L., McCullough, M.L., Weinstein, S.J., Albanes, D., Ziegler, R.G., Freedman, N.D., Caporaso, N.E., Langhammer, A., Hveem, K., Næss, M., Buring, J.E., Lee, I., Gaziano, J.M., Severi, G., Zhang, X., Stampfer, M.J., Han, J., Zeleniuch-Jacquotte, A., Marchand, L.L., Yuan, J., Wang, R., Koh, W., Gao, Y., Ericson, U., Visvanathan, K., Jones, M.R., Relton, C., Brennan, P., and Ulvik, A.
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- 2019
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7. No association between circulating concentrations of vitamin D and risk of lung cancer: an analysis in 20 prospective studies in the Lung Cancer Cohort Consortium (LC3)
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Muller, D.C., Hodge, A.M., Fanidi, A., Albanes, D., Mai, X.M., Shu, X.O., Weinstein, S.J., Larose, T.L., Zhang, X., Han, J., Stampfer, M.J., Smith-Warner, S.A., Ma, J., Gaziano, J.M., Sesso, H.D., Stevens, V.L., McCullough, M.L., Layne, T.M., Prentice, R., Pettinger, M., Thomson, C.A., Zheng, W., Gao, Y.T., Rothman, N., Xiang, Y.B., Cai, H., Wang, R., Yuan, J.M., Koh, W.P., Butler, L.M., Cai, Q., Blot, W.J., Wu, J., Ueland, P.M., Midttun, Ø., Langhammer, A., Hveem, K., Johansson, M., Hultdin, J., Grankvist, K., Arslan, A.A., Le Marchand, L., Severi, G., and Brennan, P.
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- 2018
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8. Evidence of Gene-Environment Interactions between Common Breast Cancer Susceptibility Loci and Established Environmental Risk Factors
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Nickels, S, Truong, T, Hein, R, Stevens, K, Buck, K, Behrens, S, Eilber, U, Schmidt, M, Häberle, L, Vrieling, A, Gaudet, M, Figueroa, J, Schoof, N, Spurdle, AB, Rudolph, A, Fasching, PA, Hopper, JL, Makalic, E, Schmidt, DF, Southey, MC, Beckmann, MW, Ekici, AB, Fletcher, O, Gibson, L, dos Santos Silva, I, Peto, J, Humphreys, MK, Wang, J, Cordina-Duverger, E, Menegaux, F, Nordestgaard, BG, Bojesen, SE, Lanng, C, Anton-Culver, H, Ziogas, A, Bernstein, L, Clarke, CA, Brenner, H, Müller, H, Arndt, V, Stegmaier, C, Brauch, H, Brüning, T, Harth, V, Mannermaa, A, Kataja, V, Kosma, VM, Hartikainen, JM, Lambrechts, D, Smeets, D, Neven, P, Paridaens, R, Flesch-Janys, D, Obi, N, Wang-Gohrke, S, Couch, FJ, Olson, JE, Vachon, CM, Giles, GG, Severi, G, Baglietto, L, Offit, K, John, EM, Miron, A, Andrulis, IL, Knight, JA, Glendon, G, Mulligan, AM, Chanock, SJ, Lissowska, J, Liu, J, Cox, A, Cramp, H, Connley, D, Balasubramanian, S, Dunning, AM, Shah, M, Trentham-Dietz, A, Newcomb, P, Titus, L, Egan, K, Cahoon, EK, and Rajaraman, P
- Abstract
Various common genetic susceptibility loci have been identified for breast cancer; however, it is unclear how they combine with lifestyle/environmental risk factors to influence risk. We undertook an international collaborative study to assess gene-environment interaction for risk of breast cancer. Data from 24 studies of the Breast Cancer Association Consortium were pooled. Using up to 34,793 invasive breast cancers and 41,099 controls, we examined whether the relative risks associated with 23 single nucleotide polymorphisms were modified by 10 established environmental risk factors (age at menarche, parity, breastfeeding, body mass index, height, oral contraceptive use, menopausal hormone therapy use, alcohol consumption, cigarette smoking, physical activity) in women of European ancestry. We used logistic regression models stratified by study and adjusted for age and performed likelihood ratio tests to assess gene-environment interactions. All statistical tests were two-sided. We replicated previously reported potential interactions between LSP1-rs3817198 and parity (Pinteraction= 2.4×10-6) and between CASP8-rs17468277 and alcohol consumption (Pinteraction= 3.1×10-4). Overall, the per-allele odds ratio (95% confidence interval) for LSP1-rs3817198 was 1.08 (1.01-1.16) in nulliparous women and ranged from 1.03 (0.96-1.10) in parous women with one birth to 1.26 (1.16-1.37) in women with at least four births. For CASP8-rs17468277, the per-allele OR was 0.91 (0.85-0.98) in those with an alcohol intake of
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- 2013
9. PREDICT Plus: development and validation of a prognostic model for early breast cancer that includes HER2
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Wishart, GC, Bajdik, CD, Dicks, E, Provenzano, E, Schmidt, MK, Sherman, M, Greenberg, DC, Green, AR, Gelmon, KA, Kosma, V-M, Olson, JE, Beckmann, MW, Winqvist, R, Cross, SS, Severi, G, Huntsman, D, Pylkäs, K, Ellis, I, Nielsen, TO, Giles, G, Blomqvist, C, Fasching, PA, Couch, FJ, Rakha, E, Foulkes, WD, Blows, FM, Bégin, LR, van't Veer, LJ, Southey, M, Nevanlinna, H, Mannermaa, A, Cox, A, Cheang, M, Baglietto, L, Caldas, C, Garcia-Closas, M, and Pharoah, PDP
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Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Breast Cancer ,Clinical Research ,Cancer ,4.2 Evaluation of markers and technologies ,Detection ,screening and diagnosis ,Adult ,Aged ,Breast Neoplasms ,Cohort Studies ,Female ,Humans ,Middle Aged ,Models ,Statistical ,Prognosis ,Proportional Hazards Models ,Receptor ,ErbB-2 ,Reproducibility of Results ,Young Adult ,breast cancer ,HER2 ,prognostic model ,Receptor ,erbB-2 ,Public Health and Health Services ,Oncology & Carcinogenesis ,Oncology and carcinogenesis - Abstract
Predict (www.predict.nhs.uk) is an online, breast cancer prognostication and treatment benefit tool. The aim of this study was to incorporate the prognostic effect of HER2 status in a new version (Predict+), and to compare its performance with the original Predict and Adjuvant!. The prognostic effect of HER2 status was based on an analysis of data from 10 179 breast cancer patients from 14 studies in the Breast Cancer Association Consortium. The hazard ratio estimates were incorporated into Predict. The validation study was based on 1653 patients with early-stage invasive breast cancer identified from the British Columbia Breast Cancer Outcomes Unit. Predicted overall survival (OS) and breast cancer-specific survival (BCSS) for Predict+, Predict and Adjuvant! were compared with observed outcomes. All three models performed well for both OS and BCSS. Both Predict models provided better BCSS estimates than Adjuvant!. In the subset of patients with HER2-positive tumours, Predict+ performed substantially better than the other two models for both OS and BCSS. Predict+ is the first clinical breast cancer prognostication tool that includes tumour HER2 status. Use of the model might lead to more accurate absolute treatment benefit predictions for individual patients.
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- 2012
10. Evaluation of variation in the phosphoinositide-3-kinase catalytic subunit alpha oncogene and breast cancer risk
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Stevens, KN, Garcia-Closas, M, Fredericksen, Z, Kosel, M, Pankratz, VS, Hopper, JL, Dite, GS, Apicella, C, Southey, MC, Schmidt, MK, Broeks, A, Van ‘t Veer, LJ, Tollenaar, RAEM, Fasching, PA, Beckmann, MW, Hein, A, Ekici, AB, Johnson, N, Peto, J, dos Santos Silva, I, Gibson, L, Sawyer, E, Tomlinson, I, Kerin, MJ, Chanock, S, Lissowska, J, Hunter, DJ, Hoover, RN, Thomas, GD, Milne, RL, Pérez, JI Arias, González-Neira, A, Benítez, J, Burwinkel, B, Meindl, A, Schmutzler, RK, Bartrar, CR, Hamann, U, Ko, YD, Brüning, T, Chang-Claude, J, Hein, R, Wang-Gohrke, S, Dörk, T, Schürmann, P, Bremer, M, Hillemanns, P, Bogdanova, N, Zalutsky, JV, Rogov, YI, Antonenkova, N, Lindblom, A, Margolin, S, Mannermaa, A, Kataja, V, Kosma, V-M, Hartikainen, J, Chenevix-Trench, G, Chen, X, Peterlongo, P, Bonanni, B, Bernard, L, Manoukian, S, Wang, X, Cerhan, J, Vachon, CM, Olson, J, Giles, GG, Baglietto, L, McLean, CA, Severi, G, John, EM, Miron, A, Winqvist, R, Pylkäs, K, Jukkola-Vuorinen, A, Grip, M, Andrulis, I, Knight, JA, Glendon, G, Mulligan, AM, Cox, A, Brock, IW, Elliott, G, Cross, SS, Pharoah, PP, Dunning, AM, Pooley, KA, Humphreys, MK, Wang, J, Kang, D, Yoo, K-Y, Noh, D-Y, Sangrajrang, S, Gabrieau, V, Brennan, P, McKay, J, Anton-Culver, H, Ziogas, A, and Couch, FJ
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Biomedical and Clinical Sciences ,Oncology and Carcinogenesis ,Prevention ,Genetics ,Cancer ,Breast Cancer ,Human Genome ,2.1 Biological and endogenous factors ,Aetiology ,Breast Neoplasms ,Case-Control Studies ,Class I Phosphatidylinositol 3-Kinases ,Female ,Genetic Predisposition to Disease ,Genetic Variation ,Humans ,Phosphatidylinositol 3-Kinases ,genetic susceptibility ,neoplasms ,association study ,GENICA Network ,kConFab Investigators ,Australian Ovarian Cancer Study Group ,Public Health and Health Services ,Oncology & Carcinogenesis ,Oncology and carcinogenesis - Abstract
BackgroundSomatic mutations in phosphoinositide-3-kinase catalytic subunit alpha (PIK3CA) are frequent in breast tumours and have been associated with oestrogen receptor (ER) expression, human epidermal growth factor receptor-2 overexpression, lymph node metastasis and poor survival. The goal of this study was to evaluate the association between inherited variation in this oncogene and risk of breast cancer.MethodsA single-nucleotide polymorphism from the PIK3CA locus that was associated with breast cancer in a study of Caucasian breast cancer cases and controls from the Mayo Clinic (MCBCS) was genotyped in 5436 cases and 5280 controls from the Cancer Genetic Markers of Susceptibility (CGEMS) study and in 30 949 cases and 29 788 controls from the Breast Cancer Association Consortium (BCAC).ResultsRs1607237 was significantly associated with a decreased risk of breast cancer in MCBCS, CGEMS and all studies of white Europeans combined (odds ratio (OR)=0.97, 95% confidence interval (CI) 0.95-0.99, P=4.6 × 10(-3)), but did not reach significance in the BCAC replication study alone (OR=0.98, 95% CI 0.96-1.01, P=0.139).ConclusionCommon germline variation in PIK3CA does not have a strong influence on the risk of breast cancer.
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- 2011
11. Assessing interactions between the associations of common genetic susceptibility variants, reproductive history and body mass index with breast cancer risk in the breast cancer association consortium: A combined case-control study
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Milne, RL, Gaudet, MM, Spurdle, AB, Fasching, PA, Couch, FJ, Benítez, J, Arias Pérez, JI, Zamora, MP, Malats, N, dos Santos Silva, I, Gibson, LJ, Fletcher, O, Johnson, N, Anton-Culver, H, Ziogas, A, Figueroa, J, Brinton, L, Sherman, ME, Lissowska, J, Hopper, JL, Dite, GS, Apicella, C, Southey, MC, Sigurdson, AJ, Linet, MS, Schonfeld, SJ, Freedman, DM, Mannermaa, A, Kosma, VM, Kataja, V, Auvinen, P, Andrulis, IL, Glendon, G, Knight, JA, Weerasooriya, N, Cox, A, Reed, MWR, Cross, SS, Dunning, AM, Ahmed, S, Shah, M, Brauch, H, Ko, YD, Brüning, T, Lambrechts, D, Reumers, J, Smeets, A, Wang-Gohrke, S, Hall, P, Czene, K, Liu, J, Irwanto, AK, Chenevix-Trench, G, Holland, H, Fab, KC, Giles, GG, Baglietto, L, Severi, G, Bojensen, SE, Nordestgaard, BG, Flyger, H, John, EM, West, DW, Whittemore, AS, Vachon, C, Olson, JE, Fredericksen, Z, Kosel, M, Hein, R, Vrieling, A, Flesch-Janys, D, Heinz, J, Beckmann, MW, Heusinger, K, Ekici, AB, Haeberle, L, Humphreys, MK, Morrison, J, Easton, DF, and Pharoah, PD
- Abstract
Introduction: Several common breast cancer genetic susceptibility variants have recently been identified. We aimed to determine how these variants combine with a subset of other known risk factors to influence breast cancer risk in white women of European ancestry using case-control studies participating in the Breast Cancer Association Consortium.Methods: We evaluated two-way interactions between each of age at menarche, ever having had a live birth, number of live births, age at first birth and body mass index (BMI) and each of 12 single nucleotide polymorphisms (SNPs) (10q26-rs2981582 (FGFR2), 8q24-rs13281615, 11p15-rs3817198 (LSP1), 5q11-rs889312 (MAP3K1), 16q12-rs3803662 (TOX3), 2q35-rs13387042, 5p12-rs10941679 (MRPS30), 17q23-rs6504950 (COX11), 3p24-rs4973768 (SLC4A7), CASP8-rs17468277, TGFB1-rs1982073 and ESR1-rs3020314). Interactions were tested for by fitting logistic regression models including per-allele and linear trend main effects for SNPs and risk factors, respectively, and single-parameter interaction terms for linear departure from independent multiplicative effects.Results: These analyses were applied to data for up to 26,349 invasive breast cancer cases and up to 32,208 controls from 21 case-control studies. No statistical evidence of interaction was observed beyond that expected by chance. Analyses were repeated using data from 11 population-based studies, and results were very similar.Conclusions: The relative risks for breast cancer associated with the common susceptibility variants identified to date do not appear to vary across women with different reproductive histories or body mass index (BMI). The assumption of multiplicative combined effects for these established genetic and other risk factors in risk prediction models appears justified. © 2010 Milne et al.; licensee BioMed Central Ltd.
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- 2010
12. Risk of Prostate Cancer Associated with a Family History in an Era of Rapid Increase in Prostate Cancer Diagnosis (Australia)
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Staples, M. P., Giles, G. G., English, D. R., McCredie, M. R. E., Severi, G., Cui, J. S., and Hopper, J. L.
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- 2003
13. Alternative umbrella arches: The use of composite pile roofs
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Lopez, F., primary, von Havranek, F., additional, and Severi, G., additional
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- 2019
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14. Cohort Profile: The Melbourne Collaborative Cohort Study (Health 2020)
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Milne, R L, Fletcher, A S, MacInnis, R J, Hodge, A M, Hopkins, A H, Bassett, J K, Bruinsma, F J, Lynch, B M, Dugué, P A, Jayasekara, H, Brinkman, M T, Popowski, L V, Baglietto, L, Severi, G, OʼDea, K, Hopper, J L, Southey, M C, English, D R, and Giles, G G
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- 2017
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15. Dietary inflammatory index, Mediterranean diet score, and lung cancer : a prospective study
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Hodge, A. M., Bassett, J. K., Shivappa, N., Hébert, J. R., English, D. R., Giles, G. G., and Severi, G.
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- 2016
16. Cigarette Smoking and Endometrial Cancer Risk:Observational and Mendelian Randomization Analyses
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Dimou, N, Omiyale, W, Biessy, C, Viallon, V, Kaaks, R, O'Mara, TA, Aglago, EK, Ardanaz, E, Bergmann, MM, Bondonno, NP, Braaten, T, Colorado-Yohar, SM, Crous-Bou, M, Dahm, CC, Fortner, RT, Gram, IT, Harlid, S, Heath, AK, Idahl, A, Kvaskoff, M, Nøst, TH, Overvad, K, Palli, D, Perez-Cornago, A, Sacerdote, C, Sánchez, M-J, Schulze, MB, Severi, G, Simeon, V, Tagliabue, G, Tjønneland, A, Truong, T, Tumino, R, Johansson, M, Weiderpass, E, Murphy, N, Gunter, MJ, Lacey, B, Allen, NE, Dossus, L, Dimou, N., Omiyale, W., Biessy, C., Viallon, V., Kaaks, R., O'Mara, T. A., Aglago, E. K., Ardanaz, E., Bergmann, M. M., Bondonno, N. P., Braaten, T., Colorado-Yohar, S. M., Crous-Bou, M., Dahm, C. C., Fortner, R. T., Gram, I. T., Harlid, S., Heath, A. K., Idahl, A., Kvaskoff, M., Nost, T. H., Overvad, K., Palli, D., Perez-Cornago, A., Sacerdote, C., Sanchez, M. -J., Schulze, M. B., Severi, G., Simeon, V., Tagliabue, G., Tjonneland, A., Truong, T., Tumino, R., Johansson, M., Weiderpass, E., Murphy, N., Gunter, M. J., Lacey, B., Allen, N. E., and Dossus, L.
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Epidemiology ,ESTROGENS ,Polymorphism, Single Nucleotide ,BREAST ,Article ,Cigarette Smoking ,Risk Factors ,GENETIC-VARIANTS ,REGRESSION ,Humans ,Genetic Predisposition to Disease ,Prospective Studies ,11 Medical and Health Sciences ,INDEX ,Cancer och onkologi ,IDENTIFICATION ,WOMEN ,Public Health, Global Health, Social Medicine and Epidemiology ,Mendelian Randomization Analysis ,Endometrial Neoplasms ,OVERLAP ,Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi ,Oncology ,Cancer and Oncology ,OBESITY ,Female ,SEX-HORMONES ,Genome-Wide Association Study - Abstract
Background: Current epidemiologic evidence indicates that smoking is associated with a lower endometrial cancer risk. However, it is unknown if this association is causal or confounded. To further elucidate the role of smoking in endometrial cancer risk, we conducted complementary observational and Mendelian randomization (MR) analyses. Methods: The observational analyses included 286,415 participants enrolled in the European Prospective Investigation into Cancer and Nutrition and 179,271 participants in the UK Biobank, and multivariable Cox proportional hazards models were used. In twosampleMR analyses, genetic variants robustly associated with lifetime amount of smoking (n ¼ 126 variants) and ever having smoked regularly (n ¼ 112 variants) were selected and their association with endometrial cancer risk (12,906 cancer/108,979 controls from the Endometrial Cancer Association Consortium) was examined. Results: In the observational analysis, lifetime amount of smoking and ever having smoked regularly were associated with a lower endometrial cancer risk. In the MR analysis accounting for body mass index, a genetic predisposition to a higher lifetime amount of smoking was not associated with endometrial cancer risk (OR per 1-SD increment: 1.15; 95% confidence interval: 0.91–1.44). Genetic predisposition to ever having smoked regularly was not associated with risk of endometrial cancer. Conclusions: Smoking was inversely associated with endometrial cancer in the observational analyses, although unsupported by the MR. Additional studies are required to better understand the possible confounders and mechanisms underlying the observed associations between smoking and endometrial cancer. Impact: The results from this analysis indicate that smoking is unlikely to be causally linked with endometrial cancer risk., World Health Organization, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, NIHR Imperial Biomedical Research Centre (BRC), Danish Cancer Society, Ligue Contre le Cancer (France) Institut Gustave Roussy (France) MutuelleGenerale de l'Education Nationale (France), Institut National de la Sante et de la Recherche Medicale (Inserm), Deutsche Krebshilfe German Cancer Research Center (DKFZ) (Germany) German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE) (Germany) Federal Ministry of Education & Research (BMBF), Fondazione AIRC per la ricerca sul cancro Compagnia di San Paolo Consiglio Nazionale delle Ricerche (CNR), Netherlands Government Netherlands Government, World Cancer Research Fund International (WCRF), Netherlands Government, Health Research Fund (FIS) - Instituto de Salud Carlos III (ISCIII) (Spain), Junta de Andalucia, Principality of Asturias Regional Government of Basque Country (Spain) Regional Government of Murcia (Spain) Regional Government of Navarra (Spain) Catalan Institute of Oncology - ICO (Spain), Swedish Cancer Society Swedish Research Council County Council of Skane (Sweden) County Council of Vasterbotten (Sweden), Cancer Research UK 14136 C8221/A29017, UK Research & Innovation (UKRI), Medical Research Council UK (MRC) 1000143 MR/M012190/1 MR/N003284/1 MC-UU_12015/1 MC_UU_00006/ 1, Cancer Research UK C864/A14136 C18281/A29019
- Published
- 2022
17. Trust in sources of information on COVID-19 at the beginning of the pandemic first wave and incident persistent symptoms: A prospective population-based cohort study
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Matta, J., Wiernik, E., Robineau, O., Severi, G., Touvier, M., Gouraud, C., Ouazana-Vedrines, C., Pitron, V., Ranque, B., Hoertel, N., Van Den Bergh, O., Witthöft, M., Kab, S., Goldberg, M., Zins, M., and Lemogne, C.
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- 2023
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18. Total and beverage-specific alcohol intake and the risk of aggressive prostate cancer: a case–control study
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Papa, N P, MacInnis, R J, Jayasekara, H, English, D R, Bolton, D, Davis, I D, Lawrentschuk, N, Millar, J L, Pedersen, J, Severi, G, Southey, M C, Hopper, J L, and Giles, G G
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- 2017
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19. 127 - Consommation d'alcool et méthylation de l'ADN dans le sang : une revue systématique
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Dragic, D., primary, Chang, S.-L., additional, Ennour-Idrissi, K., additional, Durocher, F., additional, Severi, G., additional, and Diorio, C., additional
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- 2022
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20. An epigenome-wide association study meta-analysis of educational attainment
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Linnér, R Karlsson, Marioni, R E, Rietveld, C A, Simpkin, A J, Davies, N M, Watanabe, K, Armstrong, N J, Auro, K, Baumbach, C, Bonder, M J, Buchwald, J, Fiorito, G, Ismail, K, Iurato, S, Joensuu, A, Karell, P, Kasela, S, Lahti, J, McRae, A F, Mandaviya, P R, Seppälä, I, Wang, Y, Baglietto, L, Binder, E B, Harris, S E, Hodge, A M, Horvath, S, Hurme, M, Johannesson, M, Latvala, A, Mather, K A, Medland, S E, Metspalu, A, Milani, L, Milne, R L, Pattie, A, Pedersen, N L, Peters, A, Polidoro, S, Räikkönen, K, Severi, G, Starr, J M, Stolk, L, Waldenberger, M, Consortium, B IOS, Eriksson, J G, Esko, T, Franke, L, Gieger, C, Giles, G G, Hägg, S, Jousilahti, P, Kaprio, J, Kähönen, M, Lehtimäki, T, Martin, N G, van Meurs, J BC, Ollikainen, M, Perola, M, Posthuma, D, Raitakari, O T, Sachdev, P S, Taskesen, E, Uitterlinden, A G, Vineis, P, Wijmenga, C, Wright, M J, Relton, C, Smith, G Davey, Deary, I J, Koellinger, P D, and Benjamin, D J
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- 2017
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21. Application de deux approches statistiques pour évaluer l'association entre l'exposition aux mélanges de retardateurs de flamme bromés et substances perfluoroalkylées et le risque de cancer du sein dans la cohorte E3N
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Freno, P., primary, Perduca, V., additional, Cano-Sancho, G., additional, Antignac, J., additional, Severi, G., additional, and Mancini, F., additional
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- 2022
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22. Alimentation et risque d’infection par le SARS-CoV-2 : étude prospective dans la cohorte NutriNet-Santé
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Deschasaux-Tanguy, M., primary, Srour, B., additional, Bourhis, L., additional, Arnault, N., additional, Druesne-Pecollo, N., additional, Esseddik, Y., additional, Szabo De Edelenyi, F., additional, Allègre, J., additional, Allès, B., additional, Andreeva, V.A., additional, Baudry, J., additional, Fezeu, L.K., additional, Galan, P., additional, Julia, C., additional, Kesse-Guyot, E., additional, Péneau, S., additional, Hercberg, S., additional, Bajos, N., additional, Severi, G., additional, Zins, M., additional, De Lamballerie, X., additional, Carrat, F., additional, and Touvier, M., additional
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- 2022
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23. Association between transportation noise exposure ans hypertension risk in the french E3N cohort
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Faure, E., primary, Houeto, A., additional, Boileau, A., additional, Perrin, C., additional, Gelot, A., additional, Correia, E., additional, Artaud, F., additional, Jamard, P., additional, Perez Munoz, A., additional, Mietlicki, F., additional, Quenez, M., additional, Gissinger, V., additional, Domergue, C., additional, Janillon, V., additional, Vincent, B., additional, Mohamed, F., additional, Godet, K., additional, Giorgis-Allemand, L., additional, Leduc, J., additional, Evrard, A.-S., additional, and Severi, G., additional
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- 2022
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24. Risk of Cardiometabolic Disease in Adults Exposed to Transportation Noise: a Systematic Review and Meta- Analysis
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Leduc, J., primary, Faure, E., additional, Severi, G., additional, and Evrard, A.-S., additional
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- 2022
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25. A new pipeline for the normalization and pooling of metabolomics data
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Viallon, V., His, M., Rinaldi, S., Breeur, M., Gicquiau, A., Hemon, B., Overvad, K., Tjønneland, A., Rostgaard-Hansen, A.L., Rothwell, J.A., Lecuyer, L., Severi, G., Kaaks, R., Johnson, T., Schulze, M.B., Palli, D., Agnoli, C., Panico, S., Tumino, R., Ricceri, F., Monique Verschuren, W.M., Engelfriet, P., Onland-Moret, C., Vermeulen, R., Nøst, T.H., Urbarova, I., Zamora-Ros, R., Rodriguez-Barranco, M., Amiano, P., Huerta, J.M., Ardanaz, E., Melander, O., Ottoson, F., Vidman, L., Rentoft, M., Schmidt, J.A., Travis, R.C., Weiderpass, E., Johansson, M., Dossus, L., Jenab, M., Gunter, M.J., Bermejo, J.L., Scherer, D., Salek, R.M., Keski-Rahkonen, P., Ferrari, P., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Sub Inorganic Chemistry and Catalysis, IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, and Sub Inorganic Chemistry and Catalysis
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Normalization (statistics) ,Pooling ,Computer science ,Pipeline (computing) ,Endocrinology, Diabetes and Metabolism ,computer.software_genre ,Microbiology ,Biochemistry ,Generalized linear mixed model ,Statistical power ,Article ,03 medical and health sciences ,Endocrinology ,0302 clinical medicine ,Cancer epidemiology ,Metabolites ,Metabolomics ,Imputation (statistics) ,Càncer ,Molecular Biology ,030304 developmental biology ,Cancer ,0303 health sciences ,Cancer och onkologi ,Bioinformatics (Computational Biology) ,Normalization ,Technical variability ,VDP::Medisinske Fag: 700::Helsefag: 800::Samfunnsmedisin, sosialmedisin: 801 ,Missing data ,QR1-502 ,3. Good health ,Diabetes and Metabolism ,Metabolòmica ,030220 oncology & carcinogenesis ,Cancer and Oncology ,Outlier ,Bioinformatik (beräkningsbiologi) ,Data mining ,VDP::Medical disciplines: 700::Health sciences: 800::Community medicine, Social medicine: 801 ,computer - Abstract
Pooling metabolomics data across studies is often desirable to increase the statistical power of the analysis. However, this can raise methodological challenges as several preanalytical and analytical factors could introduce differences in measured concentrations and variability between datasets. Specifically, different studies may use variable sample types (e.g., serum versus plasma) collected, treated, and stored according to different protocols, and assayed in different laboratories using different instruments. To address these issues, a new pipeline was developed to normalize and pool metabolomics data through a set of sequential steps: (i) exclusions of the least informative observations and metabolites and removal of outliers, imputation of missing data, (ii) identification of the main sources of variability through principal component partial R-square (PC-PR2) analysis, (iii) application of linear mixed models to remove unwanted variability, including samples’ originating study and batch, and preserve biological variations while accounting for potential differences in the residual variances across studies. This pipeline was applied to targeted metabolomics data acquired using Biocrates AbsoluteIDQ kits in eight case-control studies nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Comprehensive examination of metabolomics measurements indicated that the pipeline improved the comparability of data across the studies. Our pipeline can be adapted to normalize other molecular data, including biomarkers as well as proteomics data, and could be used for pooling molecular datasets, for example in international consortia, to limit biases introduced by inter-study variability. This versatility of the pipeline makes our work of potential interest to molecular epidemiologists.
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- 2021
26. Interval to biochemical recurrence following radical prostatectomy does not affect survival in men with low-risk prostate cancer
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Bolton, D. M., Ta, A., Bagnato, M., Muller, D., Lawrentschuk, N. L., Severi, G., Syme, R. R., and Giles, G. G.
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- 2014
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27. Red blood cell fatty acids and risk of colorectal cancer in the European Prospective investigation into cancer and nutrition (EPIC)
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Linseisen, J., Grundmann, N., Zoller, D., Kuhn, T., Chajes, V., Fedirko, V., Weiderpass, E., Dahm, C.C., Overvad, K., Tjønneland, A., Boutron-Ruault, M.-C., Rothwell, J.A., Severi, G., Kaaks, R., Schulze, M.B., Aleksandrova, K., Sieri, S., Panico, S., Tumino, R., Masala, G., de Marco, L., Bueno-De-Mesquita, B., Vermeulen, R., Gram, I.T., Skeie, G., Chirlaque, M.-D., Ardanaz, E., Agudo, A., Sánchez, M.-J., Amiano, P., Wennberg, M., Bodén, S., Perez-Cornago, A., Aglago, E.K., Gunter, M.J., Jenab, M., Heath, A.K., Nieters, A., IRAS OH Epidemiology Chemical Agents, and dIRAS RA-2
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Oncology ,Epidemiology - Abstract
Background: A growing body of evidence suggests that alterations of dietary fatty acid (FA) profiles are associated with colorectal cancer risk. However, data from large-scale epidemiologic studies using circulating FA measurements to objectively assess individual FA and FA categories are scarce. Methods: We investigate the association between red blood cell (RBC) membrane FAs and risk of colorectal cancer in a case–control study nested within a large prospective cohort. After a median follow-up of 6.4 years, 1,069 incident colorectal cancer cases were identified and matched to 1,069 controls among participants of the European Prospective Investigation into Cancer and Nutrition (EPIC). The FA composition of RBC phospholipids (in mol%) was analyzed by gas chromatography, and their association with risk of colorectal cancer was estimated by multivariable adjusted conditional logistic regression models. Results: After correction for multiple testing, subjects with higher concentrations of RBC stearic acid were at higher risk for colorectal cancer (OR ¼ 1.23; 95% CI ¼ 1.07–1.42, per 1 mol%). Conversely, colorectal cancer incidence decreased with increasing proportions of RBC n-3 PUFA, particularly eicosapentaenoic acid (0.75; 0.62–0.92, per 1 mol%). The findings for the n-6 PUFA arachidonic acid were inconsistent. Conclusions: The positive association between prediagnostic RBC stearic acid and colorectal cancer reflects putative differences in FA intake and metabolism between cancer cases and matched controls, which deserve further investigation. The inverse relationship between EPA and colorectal cancer is in line with the repeatedly reported protective effect of fish consumption on colorectal cancer risk. Impact: These findings add to the evidence on colorectal cancer prevention.
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- 2021
28. 238MO Long-term residential and workplace exposure to air pollution and breast cancer risk: A case-control study nested in the French E3N cohort from 1990 to 2011
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Fervers, B., Duboeuf, M., Amadou, A., Coudon, T., Grassot, L., Faure, E., Severi, G., Mancini, F., Salizzoni, P., Gulliver, J., and Praud, D.
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- 2023
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29. Physical activity and stroke among women - A non-linear relationship
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MACDONALD, C. J., MADIKA, A. L., Gomes, R., SEVERI, G., Sibon, I., Debette, Stephanie, Boutron-Ruault, M. C., Bordeaux population health (BPH), and Université de Bordeaux (UB)-Institut de Santé Publique, d'Épidémiologie et de Développement (ISPED)-Institut National de la Santé et de la Recherche Médicale (INSERM)
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Stroke ,Epidemiology ,Physical exercise ,[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie ,cardiovascular diseases - Abstract
Studies have identified non-linear inverse relationships between physical activity and the risk of stroke. A U-shaped response has been observed between haemorrhagic stroke and physical activity. The objective of this study was to investigate the associations between physical activities on stroke. We used data from the E3N cohort study, a French prospective study of women initiated in 1990. From the women in the study, we included those without cardiovascular disease or cancer at baseline, resulting in 94,169 women. We assessed total physical activity in 1993, grouped as quartiles. Cox models adjusted for potential confounders were used to assess the relationship with stroke, considering cases until 2008. Splines were used to assess the shape of the response. Similarly, we then considered high and low-intensity physical activity grouped as tertiles. Among the included women, with a mean age of 51.2 ± 6.7 years, 592 cases of stroke were identified over an average follow-up time of 16.2 years. Total physical activity was associated with a lower stroke risk (HR(Q1-Q4) = 0.38 [0.30, 0.49]). An inverse relationship was observed between physical activity and all stroke sub-types. A non-linear (L-shaped) relationship was observed for all-stroke, and ischemic stroke, and a U-shaped response for sub-arachnoid and intracerebral haemorrhage. High-intensity activities were associated with a U-shaped response for haemorrhagic stroke types. Low-intensity activities were associated with a linear response for all stroke types. Our results support other observations that physical activity may reduce stroke risk. U-shaped responses were observed between physical activity and haemorrhagic stroke.
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- 2021
30. Development and validation of a lifestyle-based model for colorectal cancer risk prediction: the LiFeCRC score
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Aleksandrova, K. Reichmann, R. Kaaks, R. Jenab, M. Bueno-de-Mesquita, H.B. Dahm, C.C. Eriksen, A.K. Tjønneland, A. Artaud, F. Boutron-Ruault, M.-C. Severi, G. Hüsing, A. Trichopoulou, A. Karakatsani, A. Peppa, E. Panico, S. Masala, G. Grioni, S. Sacerdote, C. Tumino, R. Elias, S.G. May, A.M. Borch, K.B. Sandanger, T.M. Skeie, G. Sánchez, M.-J. Huerta, J.M. Sala, N. Gurrea, A.B. Quirós, J.R. Amiano, P. Berntsson, J. Drake, I. van Guelpen, B. Harlid, S. Key, T. Weiderpass, E. Aglago, E.K. Cross, A.J. Tsilidis, K.K. Riboli, E. Gunter, M.J.
- Abstract
Background: Nutrition and lifestyle have been long established as risk factors for colorectal cancer (CRC). Modifiable lifestyle behaviours bear potential to minimize long-term CRC risk; however, translation of lifestyle information into individualized CRC risk assessment has not been implemented. Lifestyle-based risk models may aid the identification of high-risk individuals, guide referral to screening and motivate behaviour change. We therefore developed and validated a lifestyle-based CRC risk prediction algorithm in an asymptomatic European population. Methods: The model was based on data from 255,482 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) study aged 19 to 70 years who were free of cancer at study baseline (1992–2000) and were followed up to 31 September 2010. The model was validated in a sample comprising 74,403 participants selected among five EPIC centres. Over a median follow-up time of 15 years, there were 3645 and 981 colorectal cancer cases in the derivation and validation samples, respectively. Variable selection algorithms in Cox proportional hazard regression and random survival forest (RSF) were used to identify the best predictors among plausible predictor variables. Measures of discrimination and calibration were calculated in derivation and validation samples. To facilitate model communication, a nomogram and a web-based application were developed. Results: The final selection model included age, waist circumference, height, smoking, alcohol consumption, physical activity, vegetables, dairy products, processed meat, and sugar and confectionary. The risk score demonstrated good discrimination overall and in sex-specific models. Harrell’s C-index was 0.710 in the derivation cohort and 0.714 in the validation cohort. The model was well calibrated and showed strong agreement between predicted and observed risk. Random survival forest analysis suggested high model robustness. Beyond age, lifestyle data led to improved model performance overall (continuous net reclassification improvement = 0.307 (95% CI 0.264–0.352)), and especially for young individuals below 45 years (continuous net reclassification improvement = 0.364 (95% CI 0.084–0.575)). Conclusions: LiFeCRC score based on age and lifestyle data accurately identifies individuals at risk for incident colorectal cancer in European populations and could contribute to improved prevention through motivating lifestyle change at an individual level. © 2020, The Author(s).
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- 2021
31. The blood metabolome of incident kidney cancer: A case-control study nested within the MetKid consortium
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Guida, F., Tan, V.Y., Corbin, L.J., Smith-Byrne, K., Alcala, K., Langenberg, C., Stewart, I.D., Butterworth, A.S., Surendran, P., Achaintre, D., Adamski, J., Exezarreta, P.A., Bergmann, M.M., Bull, C.J., Dahm, C.C., Gicquiau, A., Giles, G.G., Gunter, M.J., Haller, T., Langhammer, A., Larose, T.L., Ljungberg, B., Metspalu, A., Milne, R.L., Muller, D.C., Nøst, T.H., Sørgjerd, E.P., Prehn, C., Riboli, E., Rinaldi, S., Rothwell, J.A., Scalbert, A., Schmidt, J.A., Severi, G., Sieri, S., Vermeulen, R., Vincent, E.E., Waldenberger, M., Timpson, N.J., Johansson, M., Afd. Theologie, Sub Inorganic Chemistry and Catalysis, IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Langenberg, Claudia [0000-0002-5017-7344], Butterworth, Adam [0000-0002-6915-9015], Apollo - University of Cambridge Repository, Cancer Research UK, Guida, Florence [0000-0002-9652-2430], Tan, Vanessa Y. [0000-0001-7938-127X], Corbin, Laura J. [0000-0002-4032-9500], Alcala, Karine [0000-0003-2308-9880], Adamski, Jerzy [0000-0001-9259-0199], Bull, Caroline J. [0000-0002-2176-5120], Dahm, Christina C. [0000-0003-0481-2893], Giles, Graham G. [0000-0003-4946-9099], Langhammer, Arnulf [0000-0001-5296-6673], Ljungberg, Börje [0000-0002-4121-3753], Milne, Roger L. [0000-0001-5764-7268], Nøst, Therese H. [0000-0001-6805-3094], Pettersen Sørgjerd, Elin [0000-0002-5995-2386], Prehn, Cornelia [0000-0002-1274-4715], Riboli, Elio [0000-0001-6795-6080], Rothwell, Joseph A. [0000-0002-6927-3360], Scalbert, Augustin [0000-0001-6651-6710], Schmidt, Julie A. [0000-0002-7733-8750], Severi, Gianluca [0000-0001-7157-419X], Sieri, Sabina [0000-0001-5201-172X], Vincent, Emma E. [0000-0002-8917-7384], Timpson, Nicholas J. [0000-0002-7141-9189], Johansson, Mattias [0000-0002-3116-5081], Tan, Vanessa Y [0000-0001-7938-127X], Corbin, Laura J [0000-0002-4032-9500], Bull, Caroline J [0000-0002-2176-5120], Dahm, Christina C [0000-0003-0481-2893], Giles, Graham G [0000-0003-4946-9099], Milne, Roger L [0000-0001-5764-7268], Muller, David C [0000-0002-2350-0417], Nøst, Therese H [0000-0001-6805-3094], Rothwell, Joseph A [0000-0002-6927-3360], Schmidt, Julie A [0000-0002-7733-8750], Vincent, Emma E [0000-0002-8917-7384], Timpson, Nicholas J [0000-0002-7141-9189], Afd. Theologie, Sub Inorganic Chemistry and Catalysis, IRAS OH Epidemiology Chemical Agents, and dIRAS RA-2
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Male ,Epidemiology ,Single Nucleotide Polymorphisms ,Physiology ,Biochemistry ,Body Mass Index ,0302 clinical medicine ,Risk Factors ,Metabolites ,Medicine ,Prospective Studies ,Prospective cohort study ,11 Medical and Health Sciences ,2. Zero hunger ,Medicine(all) ,0303 health sciences ,Cancer Risk Factors ,Incidence ,Neurochemistry ,General Medicine ,Neurotransmitters ,Middle Aged ,Kidney Neoplasms ,3. Good health ,Europe ,Oncology ,Nephrology ,030220 oncology & carcinogenesis ,Renal Cancer ,Metabolome ,Female ,Metabolic Pathways ,Metabolic Labeling ,ICEP ,Glutamate ,Research Article ,Victoria ,Risk Assessment ,03 medical and health sciences ,General & Internal Medicine ,Genetics ,Xenobiotic Metabolism ,Humans ,Metabolomics ,Obesity ,Risk factor ,Molecular Biology Techniques ,Molecular Biology ,030304 developmental biology ,Aged ,Medicine and health sciences ,Cancer och onkologi ,Biology and life sciences ,business.industry ,Case-control study ,Cancer ,Odds ratio ,Mendelian Randomization Analysis ,medicine.disease ,Research and analysis methods ,Metabolism ,Cell Labeling ,Medical Risk Factors ,Cancer and Oncology ,Case-Control Studies ,business ,Kidney cancer ,Body mass index ,Biomarkers ,Neuroscience - Abstract
Background Excess bodyweight and related metabolic perturbations have been implicated in kidney cancer aetiology, but the specific molecular mechanisms underlying these relationships are poorly understood. In this study, we sought to identify circulating metabolites that predispose kidney cancer and to evaluate the extent to which they are influenced by body mass index (BMI). Methods and findings We assessed the association between circulating levels of 1,416 metabolites and incident kidney cancer using pre-diagnostic blood samples from up to 1,305 kidney cancer case–control pairs from 5 prospective cohort studies. Cases were diagnosed on average 8 years after blood collection. We found 25 metabolites robustly associated with kidney cancer risk. In particular, 14 glycerophospholipids (GPLs) were inversely associated with risk, including 8 phosphatidylcholines (PCs) and 2 plasmalogens. The PC with the strongest association was PC ae C34:3 with an odds ratio (OR) for 1 standard deviation (SD) increment of 0.75 (95% confidence interval [CI]: 0.68 to 0.83, p = 2.6 × 10−8). In contrast, 4 amino acids, including glutamate (OR for 1 SD = 1.39, 95% CI: 1.20 to 1.60, p = 1.6 × 10−5), were positively associated with risk. Adjusting for BMI partly attenuated the risk association for some—but not all—metabolites, whereas other known risk factors of kidney cancer, such as smoking and alcohol consumption, had minimal impact on the observed associations. A mendelian randomisation (MR) analysis of the influence of BMI on the blood metabolome highlighted that some metabolites associated with kidney cancer risk are influenced by BMI. Specifically, elevated BMI appeared to decrease levels of several GPLs that were also found inversely associated with kidney cancer risk (e.g., −0.17 SD change [ßBMI] in 1-(1-enyl-palmitoyl)-2-linoleoyl-GPC (P-16:0/18:2) levels per SD change in BMI, p = 3.4 × 10−5). BMI was also associated with increased levels of glutamate (ßBMI: 0.12, p = 1.5 × 10−3). While our results were robust across the participating studies, they were limited to study participants of European descent, and it will, therefore, be important to evaluate if our findings can be generalised to populations with different genetic backgrounds. Conclusions This study suggests a potentially important role of the blood metabolome in kidney cancer aetiology by highlighting a wide range of metabolites associated with the risk of developing kidney cancer and the extent to which changes in levels of these metabolites are driven by BMI—the principal modifiable risk factor of kidney cancer., In a case-control study, Florence Guida and colleagues identify metabolites associated with risk of kidney cancer, and use Mendelian randomization techniques to study the role of body mass index in this relationship., Author summary Why was this study done? Several modifiable risk factors have been established for kidney cancer, among which elevated body mass index (BMI) and obesity are central. The biological mechanisms underlying these relationships are poorly understood, but obesity-related metabolic perturbations may be important. What did the researchers do and find? We looked at the association between kidney cancer and the levels of 1,416 metabolites measured in blood on average 8 years before the disease onset. The study included 1,305 kidney cancer cases and 1,305 healthy controls. We found 25 metabolites robustly associated with kidney cancer risk. Specifically, multiple glycerophospholipids (GPLs) were inversely associated with risk, while several amino acids were positively associated with risk. Accounting for BMI highlighted that some—but not all—metabolites associated with kidney cancer risk are influenced by BMI. What do these findings mean? These findings illustrate the potential utility of prospectively measured metabolites in helping us to understand the aetiology of kidney cancer. By examining overlap between the metabolomic profile of prospective risk of kidney cancer and that of modifiable risk factors for the disease—in this case BMI—we can begin to identify biological pathways relevant to disease onset.
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- 2021
32. Monitoring the proportion of the population infected by SARS-CoV-2 using age-stratified hospitalization and serological data: a modelling study
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Hoze N, Paireau J, Lapidus N, Tran Kiem C, Salje H, Severi G, Touvier M, Zins M, de Lamballerie X, Lévy-Bruhl D, Carrat F, Cauchemez S
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- 2021
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33. Long-term exposure to fine particle elemental components and lung cancer incidence in the ELAPSE pooled cohort
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Hvidtfeldt, U.A. Chen, J. Andersen, Z.J. Atkinson, R. Bauwelinck, M. Bellander, T. Brandt, J. Brunekreef, B. Cesaroni, G. Concin, H. Fecht, D. Forastiere, F. van Gils, C.H. Gulliver, J. Hertel, O. Hoek, G. Hoffmann, B. de Hoogh, K. Janssen, N. Jørgensen, J.T. Katsouyanni, K. Jöckel, K.-H. Ketzel, M. Klompmaker, J.O. Lang, A. Leander, K. Liu, S. Ljungman, P.L.S. Magnusson, P.K.E. Mehta, A.J. Nagel, G. Oftedal, B. Pershagen, G. Peter, R.S. Peters, A. Renzi, M. Rizzuto, D. Rodopoulou, S. Samoli, E. Schwarze, P.E. Severi, G. Sigsgaard, T. Stafoggia, M. Strak, M. Vienneau, D. Weinmayr, G. Wolf, K. Raaschou-Nielsen, O.
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complex mixtures - Abstract
Background: An association between long-term exposure to fine particulate matter (PM2.5) and lung cancer has been established in previous studies. PM2.5 is a complex mixture of chemical components from various sources and little is known about whether certain components contribute specifically to the associated lung cancer risk. The present study builds on recent findings from the “Effects of Low-level Air Pollution: A Study in Europe” (ELAPSE) collaboration and addresses the potential association between specific elemental components of PM2.5 and lung cancer incidence. Methods: We pooled seven cohorts from across Europe and assigned exposure estimates for eight components of PM2.5 representing non-tail pipe emissions (copper (Cu), iron (Fe), and zinc (Zn)), long-range transport (sulfur (S)), oil burning/industry emissions (nickel (Ni), vanadium (V)), crustal material (silicon (Si)), and biomass burning (potassium (K)) to cohort participants’ baseline residential address based on 100 m by 100 m grids from newly developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). Results: The pooled study population comprised 306,550 individuals with 3916 incident lung cancer events during 5,541,672 person-years of follow-up. We observed a positive association between exposure to all eight components and lung cancer incidence, with adjusted HRs of 1.10 (95% CI 1.05, 1.16) per 50 ng/m3 PM2.5 K, 1.09 (95% CI 1.02, 1.15) per 1 ng/m3 PM2.5 Ni, 1.22 (95% CI 1.11, 1.35) per 200 ng/m3 PM2.5 S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m3 PM2.5 V. Effect estimates were largely unaffected by adjustment for nitrogen dioxide (NO2). After adjustment for PM2.5 mass, effect estimates of K, Ni, S, and V were slightly attenuated, whereas effect estimates of Cu, Si, Fe, and Zn became null or negative. Conclusions: Our results point towards an increased risk of lung cancer in connection with sources of combustion particles from oil and biomass burning and secondary inorganic aerosols rather than non-exhaust traffic emissions. Specific limit values or guidelines targeting these specific PM2.5 components may prove helpful in future lung cancer prevention strategies. © 2020 Elsevier Inc.
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- 2021
34. Lifetime alcohol intake, drinking patterns over time and risk of stomach cancer: A pooled analysis of data from two prospective cohort studies
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Jayasekara, H. MacInnis, R.J. Lujan-Barroso, L. Mayen-Chacon, A.-L. Cross, A.J. Wallner, B. Palli, D. Ricceri, F. Pala, V. Panico, S. Tumino, R. Kühn, T. Kaaks, R. Tsilidis, K. Sánchez, M.-J. Amiano, P. Ardanaz, E. Chirlaque López, M.D. Merino, S. Rothwell, J.A. Boutron-Ruault, M.-C. Severi, G. Sternby, H. Sonestedt, E. Bueno-de-Mesquita, B. Boeing, H. Travis, R. Sandanger, T.M. Trichopoulou, A. Karakatsani, A. Peppa, E. Tjønneland, A. Yang, Y. Hodge, A.M. Mitchell, H. Haydon, A. Room, R. Hopper, J.L. Weiderpass, E. Gunter, M.J. Riboli, E. Giles, G.G. Milne, R.L. Agudo, A. English, D.R. Ferrari, P.
- Abstract
Alcohol consumption is causally linked to several cancers but the evidence for stomach cancer is inconclusive. In our study, the association between long-term alcohol intake and risk of stomach cancer and its subtypes was evaluated. We performed a pooled analysis of data collected at baseline from 491 714 participants in the European Prospective Investigation into Cancer and Nutrition and the Melbourne Collaborative Cohort Study. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated for incident stomach cancer in relation to lifetime alcohol intake and group-based life course intake trajectories, adjusted for potential confounders including Helicobacter pylori infection. In all, 1225 incident stomach cancers (78% noncardia) were diagnosed over 7 094 637 person-years; 984 in 382 957 study participants with lifetime alcohol intake data (5 455 507 person-years). Although lifetime alcohol intake was not associated with overall stomach cancer risk, we observed a weak positive association with noncardia cancer (HR = 1.03, 95% CI: 1.00-1.06 per 10 g/d increment), with a HR of 1.50 (95% CI: 1.08-2.09) for ≥60 g/d compared to 0.1 to 4.9 g/d. A weak inverse association with cardia cancer (HR = 0.93, 95% CI: 0.87-1.00) was also observed. HRs of 1.48 (95% CI: 1.10-1.99) for noncardia and 0.51 (95% CI: 0.26-1.03) for cardia cancer were observed for a life course trajectory characterized by heavy decreasing intake compared to light stable intake (Phomogeneity =.02). These associations did not differ appreciably by smoking or H pylori infection status. Limiting alcohol use during lifetime, particularly avoiding heavy use during early adulthood, might help prevent noncardia stomach cancer. Heterogeneous associations observed for cardia and noncardia cancers may indicate etiologic differences. © 2021 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.
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- 2021
35. Modeling multi-level survival data in multi-center epidemiological cohort studies: Applications from the ELAPSE project
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Samoli, E. Rodopoulou, S. Hvidtfeldt, U.A. Wolf, K. Stafoggia, M. Brunekreef, B. Strak, M. Chen, J. Andersen, Z.J. Atkinson, R. Bauwelinck, M. Bellander, T. Brandt, J. Cesaroni, G. Forastiere, F. Fecht, D. Gulliver, J. Hertel, O. Hoffmann, B. de Hoogh, K. Janssen, N.A.H. Ketzel, M. Klompmaker, J.O. Liu, S. Ljungman, P. Nagel, G. Oftedal, B. Pershagen, G. Peters, A. Raaschou-Nielsen, O. Renzi, M. Kristoffersen, D.T. Severi, G. Sigsgaard, T. Vienneau, D. Weinmayr, G. Hoek, G. Katsouyanni, K.
- Abstract
Background: We evaluated methods for the analysis of multi-level survival data using a pooled dataset of 14 cohorts participating in the ELAPSE project investigating associations between residential exposure to low levels of air pollution (PM2.5 and NO2) and health (natural-cause mortality and cerebrovascular, coronary and lung cancer incidence). Methods: We applied five approaches in a multivariable Cox model to account for the first level of clustering corresponding to cohort specification: (1) not accounting for the cohort or using (2) indicator variables, (3) strata, (4) a frailty term in frailty Cox models, (5) a random intercept under a mixed Cox, for cohort identification. We accounted for the second level of clustering due to common characteristics in the residential area by (1) a random intercept per small area or (2) applying variance correction. We assessed the stratified, frailty and mixed Cox approach through simulations under different scenarios for heterogeneity in the underlying hazards and the air pollution effects. Results: Effect estimates were stable under approaches used to adjust for cohort but substantially differed when no adjustment was applied. Further adjustment for the small area grouping increased the effect estimates’ standard errors. Simulations confirmed identical results between the stratified and frailty models. In ELAPSE we selected a stratified multivariable Cox model to account for between-cohort heterogeneity without adjustment for small area level, due to the small number of subjects and events in the latter. Conclusions: Our study supports the need to account for between-cohort heterogeneity in multi-center collaborations using pooled individual level data. © 2021 The Authors
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- 2021
36. Dietary intake of B vitamins and methionine and risk of lung cancer
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Bassett, J K, Hodge, A M, English, D R, Baglietto, L, Hopper, J L, Giles, G G, and Severi, G
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- 2012
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37. Identification of a novel prostate cancer susceptibility variant in the KLK3 gene transcript
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Kote-Jarai, Z., Amin Al Olama, A., Leongamornlert, D., Tymrakiewicz, M., Saunders, E., Guy, M., Giles, G. G., Severi, G., Southey, M., Hopper, J. L., Sit, K. C., Harris, J. M., Batra, J., Spurdle, A. B., Clements, J. A., Hamdy, F., Neal, D., Donovan, J., Muir, K., Pharoah, P. D. P., Chanock, S. J., Brown, N., Benlloch, S., Castro, E., Mahmud, N., O’Brien, L., Hall, A., Sawyer, E., Wilkinson, R., Easton, D. F., and Eeles, R. A.
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- 2011
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38. Consumption of animal products, their nutrient components and postmenopausal circulating steroid hormone concentrations
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Brinkman, M T, Baglietto, L, Krishnan, K, English, D R, Severi, G, Morris, H A, Hopper, J L, and Giles, G G
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- 2010
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39. HDAC8 Loss of Function and SHOX Haploinsufficiency: Two Independent Genetic Defects Responsible for a Complex Phenotype
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Severi G., Bonora E., Perri A., Scarano E., Mazzanti L., Isidori F., Zuntini R., Menabo S., Graziano C., Severi G., Bonora E., Perri A., Scarano E., Mazzanti L., Isidori F., Zuntini R., Menabo S., and Graziano C.
- Subjects
Haploinsufficiency ,Osteochondrodysplasias ,Whole Exome Sequencing ,Histone Deacetylases ,Brachydactyly-mental retardation syndrome ,Short Stature Homeobox Protein ,Growth Disorder ,Histone Deacetylase ,De Lange Syndrome ,Exome Sequencing ,Humans ,Osteochondrodysplasia ,Child ,Frameshift Mutation ,Growth Disorders ,Comparative Genomic Hybridization ,Repressor Protein ,Dual molecular diagnosi ,Pedigree ,Repressor Proteins ,Phenotype ,HDAC8 ,Female ,Gene Deletion ,SHOX ,Human - Abstract
We report a patient with developmental delay, brachydactyly type E, short stature, and tetralogy of Fallot. Brachydactyly-mental retardation syndrome (BDMR) was suspected based on the phenotype; however, array CGH excluded a 2q37 deletion, but identified a deletion encompassing the SHOX gene. BDMR is characterized by cognitive impairment, skeletal abnormalities involving hands and feet, short stature, and overweight. Most affected individuals carry relatively large 2q37 deletions encompassing HDAC4. This gene encodes a histone deacetylase involved in epigenetic regulation of cell growth and differentiation, specifically during endochondral bone formation in chondrocyte hypertrophy. Since SHOX haploinsufficiency can cause skeletal defects and short stature but would not fully explain the clinical picture of this patient, exome sequencing was performed, and a heterozygous HDAC8 frameshift mutation was identified. HDAC8 is a distinct histone deacetylase involved in cohesin recycling and is responsible for an X-linked dominant Cornelia de Lange-like phenotype. A new blended clinical phenotype may be explained by the result of a dual molecular diagnosis, which represents a combination of 2 independent genetic defects, with relevant implications for genetic counseling, clinical management, and prognosis.
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- 2018
40. A metabolomic study of red and processed meat intake and acylcarnitine concentrations in human urine and blood
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Wedekind, R., Kiss, A., Keski-Rahkonen, P., Viallon, V., Rothwell, J.A., Cross, A.J., Rostgaard-Hansen, A.L., Sandanger, T.M., Jakszyn, P., Pala, V., Vermeulen, R., Schulze, M.B., Kühn, T., Johnson, T., Trichopoulou, A., Peppa, E., Vechia, C.L., Masala, G., Tumino, R., Sacerdote, C., Wittenbecher, C., de Magistris, M.S., Dahm, C.C., Severi, G., Mancini, F.R., Weiderpass, E., Gunter, M.J., Huybrechts, I., Scalbert, A., IRAS OH Epidemiology Chemical Agents, and dIRAS RA-2
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acylcarnitines ,blood ,meat intake ,red and processed meat ,metabolomics ,urine - Abstract
Background Acylcarnitines (ACs) play a major role in fatty acid metabolism and are potential markers of metabolic dysfunction with higher blood concentrations reported in obese and diabetic individuals. Diet, and in particular red and processed meat intake, has been shown to influence AC concentrations but data on the effect of meat consumption on AC concentrations is limited. Objectives To investigate the effect of red and processed meat intake on AC concentrations in plasma and urine using a randomized controlled trial with replication in an observational cohort. Methods In the randomized crossover trial, 12 volunteers successively consumed 2 different diets containing either pork or tofu for 3 d each. A panel of 44 ACs including several oxidized ACs was analyzed by LC-MS in plasma and urine samples collected after the 3-d period. ACs that were associated with pork intake were then measured in urine (n = 474) and serum samples (n = 451) from the European Prospective Investigation into Cancer and nutrition (EPIC) study and tested for associations with habitual red and processed meat intake derived from dietary questionnaires. Results In urine samples from the intervention study, pork intake was positively associated with concentrations of 18 short- and medium-chain ACs. Eleven of these were also positively associated with habitual red and processed meat intake in the EPIC cross-sectional study. In blood, C18:0 was positively associated with red meat intake in both the intervention study (q = 0.004, Student's t-test) and the cross-sectional study (q = 0.033, linear regression). Conclusions AC concentrations in urine and blood were associated with red meat intake in both a highly controlled intervention study and in subjects of a cross-sectional study. Our data on the role of meat intake on this important pathway of fatty acid and energy metabolism may help understanding the role of red meat consumption in the etiology of some chronic diseases. This trial was registered at Clinicaltrials.gov as NCT03354130.
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- 2020
41. Exogenous hormone use and cutaneous melanoma risk in women: The European Prospective Investigation into Cancer and Nutrition
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Cervenka, I. Al Rahmoun, M. Mahamat-Saleh, Y. Fournier, A. Boutron-Ruault, M.-C. Severi, G. Caini, S. Palli, D. Ghiasvand, R. Veierod, M.B. Botteri, E. Tjønneland, A. Olsen, A. Fortner, R.T. Kaaks, R. Schulze, M.B. Panico, S. Trichopoulou, A. Dessinioti, C. Niforou, K. Sieri, S. Tumino, R. Sacerdote, C. Bueno-de-Mesquita, B. Sandanger, T.M. Colorado-Yohar, S. Sánchez, M.J. Gil Majuelo, L. Lujan-Barroso, L. Ardanaz, E. Merino, S. Isaksson, K. Butt, S. Ljuslinder, I. Jansson, M. Travis, R.C. Khaw, K.-T. Weiderpass, E. Dossus, L. Rinaldi, S. Kvaskoff, M.
- Abstract
Evidence suggests an influence of sex hormones on cutaneous melanoma risk, but epidemiologic findings are conflicting. We examined the associations between use of oral contraceptives (OCs) and menopausal hormone therapy (MHT) and melanoma risk in women participating in the European Prospective Investigation into Cancer and Nutrition (EPIC). EPIC is a prospective cohort study initiated in 1992 in 10 European countries. Information on exogenous hormone use at baseline was derived from country-specific self-administered questionnaires. We used Cox proportional hazards regression models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). Over 1992–2015, 1,696 melanoma cases were identified among 334,483 women, whereof 770 cases among 134,758 postmenopausal women. There was a positive, borderline-significant association between OC use and melanoma risk (HR = 1.12, 95% CI = 1.00–1.26), with no detected heterogeneity across countries (phomogeneity = 0.42). This risk increased linearly with duration of use (ptrend = 0.01). Among postmenopausal women, ever use of MHT was associated with a nonsignificant increase in melanoma risk overall (HR = 1.14, 95% CI = 0.97–1.43), which was heterogeneous across countries (phomogeneity = 0.05). Our findings do not support a strong and direct association between exogenous hormone use and melanoma risk. In order to better understand these relations, further research should be performed using prospectively collected data including detailed information on types of hormone, and on sun exposure, which may act as an important confounder or effect modifier on these relations. © 2019 UICC
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- 2020
42. Consumption of Fish and Long-chain n-3 Polyunsaturated Fatty Acids Is Associated With Reduced Risk of Colorectal Cancer in a Large European Cohort
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Aglago, E.K. Huybrechts, I. Murphy, N. Casagrande, C. Nicolas, G. Pischon, T. Fedirko, V. Severi, G. Boutron-Ruault, M.-C. Fournier, A. Katzke, V. Kühn, T. Olsen, A. Tjønneland, A. Dahm, C.C. Overvad, K. Lasheras, C. Agudo, A. Sánchez, M.-J. Amiano, P. Huerta, J.M. Ardanaz, E. Perez-Cornago, A. Trichopoulou, A. Karakatsani, A. Martimianaki, G. Palli, D. Pala, V. Tumino, R. Naccarati, A. Panico, S. Bueno-de-Mesquita, B. May, A. Derksen, J.W.G. Hellstrand, S. Ohlsson, B. Wennberg, M. Van Guelpen, B. Skeie, G. Brustad, M. Weiderpass, E. Cross, A.J. Ward, H. Riboli, E. Norat, T. Chajes, V. Gunter, M.J.
- Abstract
Background & Aims: There is an unclear association between intake of fish and long-chain n-3 polyunsaturated fatty acids (n-3 LC-PUFAs) and colorectal cancer (CRC). We examined the association between fish consumption, dietary and circulating levels of n-3 LC-PUFAs, and ratio of n-6:n-3 LC-PUFA with CRC using data from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Methods: Dietary intake of fish (total, fatty/oily, lean/white) and n-3 LC-PUFA were estimated by food frequency questionnaires given to 521,324 participants in the EPIC study; among these, 6291 individuals developed CRC (median follow up, 14.9 years). Levels of phospholipid LC-PUFA were measured by gas chromatography in plasma samples from a sub-group of 461 CRC cases and 461 matched individuals without CRC (controls). Multivariable Cox proportional hazards and conditional logistic regression models were used to calculate hazard ratios (HRs) and odds ratios (ORs), respectively, with 95% CIs. Results: Total intake of fish (HR for quintile 5 vs 1, 0.88; 95% CI, 0.80–0.96; Ptrend = .005), fatty fish (HR for quintile 5 vs 1, 0.90; 95% CI, 0.82–0.98; Ptrend = .009), and lean fish (HR for quintile 5 vs 1, 0.91; 95% CI, 0.83–1.00; Ptrend = .016) were inversely associated with CRC incidence. Intake of total n-3 LC-PUFA (HR for quintile 5 vs 1, 0.86; 95% CI, 0.78–0.95; Ptrend = .010) was also associated with reduced risk of CRC, whereas dietary ratio of n-6:n-3 LC-PUFA was associated with increased risk of CRC (HR for quintile 5 vs 1, 1.31; 95% CI, 1.18–1.45; Ptrend < .001). Plasma levels of phospholipid n-3 LC-PUFA was not associated with overall CRC risk, but an inverse trend was observed for proximal compared with distal colon cancer (Pheterogeneity = .026). Conclusions: In an analysis of dietary patterns of participants in the EPIC study, we found regular consumption of fish, at recommended levels, to be associated with a lower risk of CRC, possibly through exposure to n-3 LC-PUFA. Levels of n-3 LC-PUFA in plasma were not associated with CRC risk, but there may be differences in risk at different regions of the colon. © 2020 AGA Institute
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- 2020
43. Prediagnostic Plasma Bile Acid Levels and Colon Cancer Risk: A Prospective Study
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Kühn, T. Stepien, M. López-Nogueroles, M. Damms-Machado, A. Sookthai, D. Johnson, T. Roca, M. Hüsing, A. Maldonado, S.G. Cross, A.J. Murphy, N. Freisling, H. Rinaldi, S. Scalbert, A. Fedirko, V. Severi, G. Boutron-Ruault, M.-C. Mancini, F.R. Sowah, S.A. Boeing, H. Jakszyn, P. Sánchez, M.J. Merino, S. Colorado-Yohar, S. Barricarte, A. Khaw, K.T. Schmidt, J.A. Perez-Cornago, A. Trichopoulou, A. Karakatsani, A. Thriskos, P. Palli, D. Agnoli, C. Tumino, R. Sacerdote, C. Panico, S. Bueno-De-Mesquita, B. Van Gils, C.H. Heath, A.K. Gunter, M.J. Riboli, E. Lahoz, A. Jenab, M. Kaaks, R.
- Abstract
Background: Bile acids have been proposed to promote colon carcinogenesis. However, there are limited prospective data on circulating bile acid levels and colon cancer risk in humans. Methods: Associations between prediagnostic plasma levels of 17 primary, secondary, and tertiary bile acid metabolites (conjugated and unconjugated) and colon cancer risk were evaluated in a nested case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Bile acid levels were quantified by tandem mass spectrometry in samples from 569 incident colon cancer cases and 569 matched controls. Multivariable logistic regression analyses were used to estimate odds ratios (ORs) for colon cancer risk across quartiles of bile acid concentrations. Results: Positive associations were observed between colon cancer risk and plasma levels of seven conjugated bile acid metabolites: the primary bile acids glycocholic acid (ORquartile 4 vs quartile 1= 2.22, 95% confidence interval [CI] = 1.52 to 3.26), taurocholic acid (OR = 1.78, 95% CI = 1.23 to 2.58), glycochenodeoxycholic acid (OR = 1.68, 95% CI = 1.13 to 2.48), taurochenodeoxycholic acid (OR = 1.62, 95% CI = 1.11 to 2.36), and glycohyocholic acid (OR = 1.65, 95% CI = 1.13 to 2.40), and the secondary bile acids glycodeoxycholic acid (OR = 1.68, 95% CI = 1.12 to 2.54) and taurodeoxycholic acid (OR = 1.54, 95% CI = 1.02 to 2.31). By contrast, unconjugated bile acids and tertiary bile acids were not associated with risk. Conclusions: This prospective study showed that prediagnostic levels of certain conjugated primary and secondary bile acids were positively associated with risk of colon cancer. Our findings support experimental data to suggest that a high bile acid load is colon cancer promotive. © 2020 The Author(s) 2019. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.
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- 2020
44. Circulating bilirubin levels and risk of colorectal cancer: serological and Mendelian randomization analyses
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Seyed Khoei, N., Jenab, M., Murphy, N., Banbury, B.L., Carreras-Torres, R., Viallon, V., Kühn, T., Bueno-de-Mesquita, B., Aleksandrova, K., Cross, A.J., Weiderpass, E., Stepien, M., Bulmer, A., Tjønneland, A., Boutron-Ruault, M.C., Severi, G., Carbonnel, F., Katzke, V., Boeing, H., Bergmann, M.M., Trichopoulou, A., Karakatsani, A., Martimianaki, G., Palli, D., Tagliabue, G., Panico, S., Tumino, R., Sacerdote, C., Skeie, G., Merino, S., Bonet, C., Rodríguez-Barranco, M., Gil, L., Chirlaque, M.D., Ardanaz, E., Myte, R., Hultdin, J., Perez-Cornago, A., Aune, D., Tsilidis, K.K., Albanes, D., Baron, J.A., Berndt, S.I., Bézieau, S., Brenner, H., Campbell, P.T., Casey, G., Chang-Claude, J., Chanock, S.J., Cotterchio, M., Gallinger, S., Gruber, S.B., Haile, R.W., Hampe, J., Hoffmeister, M., Hopper, J.L., Hsu, L., Huyghe, J.R., Jenkins, M.A., Joshi, A.D., Kampman, E., Larsson, S.C., Le Marchand, L., Li, C.I., Li, L., Lindblom, A., Lindor, N.M., Martín, V., Moreno, V., Newcomb, P.A., Offit, K., Ogino, S., Parfrey, P.S., Pharoah, P.D.P., Rennert, G., Sakoda, L.C., Schafmayer, C., Schmit, S.L., Schoen, R.E., Slattery, M.L., Thibodeau, S.N., Ulrich, C.M., van Duijnhoven, F.J.B., Weigl, K., Weinstein, S.J., White, E., Wolk, A., Woods, M.O., Wu, A.H., Zhang, X., Ferrari, P., Anton, G., Peters, A., Peters, U., Gunter, M.J., Wagner, K.H., and Freisling, H.
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Bilirubin ,Cancer ,Colorectal Cancer ,Anti-oxidants ,Mendelian Randomization Analysis - Abstract
Background Bilirubin, a byproduct of hemoglobin breakdown and purported anti-oxidant, is thought to be cancer preventive. We conducted complementary serological and Mendelian randomization (MR) analyses to investigate whether alterations in circulating levels of bilirubin are associated with risk of colorectal cancer (CRC). We decided a priori to perform analyses separately in men and women based on suggestive evidence that associations may differ by sex. Methods In a case-control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC), pre-diagnostic unconjugated bilirubin (UCB, the main component of total bilirubin) concentrations were measured by high-performance liquid chromatography in plasma samples of 1386 CRC cases and their individually matched controls. Additionally, 115 single-nucleotide polymorphisms (SNPs) robustly associated (P < 5 x 10(-8)) with circulating total bilirubin were instrumented in a 2-sample MR to test for a potential causal effect of bilirubin on CRC risk in 52,775 CRC cases and 45,940 matched controls in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), the Colon Cancer Family Registry (CCFR), and the Colorectal Transdisciplinary (CORECT) study. Results The associations between circulating UCB levels and CRC risk differed by sex (P-heterogeneity = 0.008). Among men, higher levels of UCB were positively associated with CRC risk (odds ratio [OR] = 1.19, 95% confidence interval [CI] = 1.04-1.36; per 1-SD increment of log-UCB). In women, an inverse association was observed (OR = 0.86 (0.76-0.97)). In the MR analysis of the mainUGT1A1SNP (rs6431625), genetically predicted higher levels of total bilirubin were associated with a 7% increase in CRC risk in men (OR = 1.07 (1.02-1.12);P = 0.006; per 1-SD increment of total bilirubin), while there was no association in women (OR = 1.01 (0.96-1.06);P = 0.73). Raised bilirubin levels, predicted by instrumental variables excluding rs6431625, were suggestive of an inverse association with CRC in men, but not in women. These differences by sex did not reach formal statistical significance (P-heterogeneity >= 0.2). Conclusions Additional insight into the relationship between circulating bilirubin and CRC is needed in order to conclude on a potential causal role of bilirubin in CRC development.
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- 2020
45. Lifestyle factors and risk of multimorbidity of cancer and cardiometabolic diseases: A multinational cohort study
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Freisling, H. Viallon, V. Lennon, H. Bagnardi, V. Ricci, C. Butterworth, A.S. Sweeting, M. Muller, D. Romieu, I. Bazelle, P. Kvaskoff, M. Arveux, P. Severi, G. Bamia, C. Kühn, T. Kaaks, R. Bergmann, M. Boeing, H. Tjønneland, A. Olsen, A. Overvad, K. Dahm, C.C. Menéndez, V. Agudo, A. Sánchez, M.-J. Amiano, P. Santiuste, C. Gurrea, A.B. Tong, T.Y.N. Schmidt, J.A. Tzoulaki, I. Tsilidis, K.K. Ward, H. Palli, D. Agnoli, C. Tumino, R. Ricceri, F. Panico, S. Picavet, H.S.J. Bakker, M. Monninkhof, E. Nilsson, P. Manjer, J. Rolandsson, O. Thysell, E. Weiderpass, E. Jenab, M. Riboli, E. Vineis, P. Danesh, J. Wareham, N.J. Gunter, M.J. Ferrari, P.
- Abstract
Background: Although lifestyle factors have been studied in relation to individual non-communicable diseases (NCDs), their association with development of a subsequent NCD, defined as multimorbidity, has been scarcely investigated. The aim of this study was to investigate associations between five lifestyle factors and incident multimorbidity of cancer and cardiometabolic diseases. Methods: In this prospective cohort study, 291,778 participants (64% women) from seven European countries, mostly aged 43 to 58 years and free of cancer, cardiovascular disease (CVD), and type 2 diabetes (T2D) at recruitment, were included. Incident multimorbidity of cancer and cardiometabolic diseases was defined as developing subsequently two diseases including first cancer at any site, CVD, and T2D in an individual. Multi-state modelling based on Cox regression was used to compute hazard ratios (HR) and 95% confidence intervals (95% CI) of developing cancer, CVD, or T2D, and subsequent transitions to multimorbidity, in relation to body mass index (BMI), smoking status, alcohol intake, physical activity, adherence to the Mediterranean diet, and their combination as a healthy lifestyle index (HLI) score. Cumulative incidence functions (CIFs) were estimated to compute 10-year absolute risks for transitions from healthy to cancer at any site, CVD (both fatal and non-fatal), or T2D, and to subsequent multimorbidity after each of the three NCDs. Results: During a median follow-up of 11 years, 1910 men and 1334 women developed multimorbidity of cancer and cardiometabolic diseases. A higher HLI, reflecting healthy lifestyles, was strongly inversely associated with multimorbidity, with hazard ratios per 3-unit increment of 0.75 (95% CI, 0.71 to 0.81), 0.84 (0.79 to 0.90), and 0.82 (0.77 to 0.88) after cancer, CVD, and T2D, respectively. After T2D, the 10-year absolute risks of multimorbidity were 40% and 25% for men and women, respectively, with unhealthy lifestyle, and 30% and 18% for men and women with healthy lifestyles. Conclusion: Pre-diagnostic healthy lifestyle behaviours were strongly inversely associated with the risk of cancer and cardiometabolic diseases, and with the prognosis of these diseases by reducing risk of multimorbidity. © 2020 The Author(s).
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- 2020
46. Blood pressure and risk of cancer in the European Prospective Investigation into Cancer and Nutrition
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Christakoudi, S. Kakourou, A. Markozannes, G. Tzoulaki, I. Weiderpass, E. Brennan, P. Gunter, M. Dahm, C.C. Overvad, K. Olsen, A. Tjønneland, A. Boutron-Ruault, M.-C. Madika, A.-L. Severi, G. Katzke, V. Kühn, T. Bergmann, M.M. Boeing, H. Karakatsani, A. Martimianaki, G. Thriskos, P. Masala, G. Sieri, S. Panico, S. Tumino, R. Ricceri, F. Agudo, A. Redondo-Sánchez, D. Colorado-Yohar, S.M. Mokoroa, O. Melander, O. Stocks, T. Häggström, C. Harlid, S. Bueno-de-Mesquita, B. van Gils, C.H. Vermeulen, R.C.H. Khaw, K.-T. Wareham, N.J. Tong, T.Y.N. Freisling, H. Johansson, M. Lennon, H. Aune, D. Riboli, E. Trichopoulos, D. Trichopoulou, A. Tsilidis, K.K.
- Abstract
Several studies have reported associations of hypertension with cancer, but not all results were conclusive. We examined the association of systolic (SBP) and diastolic (DBP) blood pressure with the development of incident cancer at all anatomical sites in the European Prospective Investigation into Cancer and Nutrition (EPIC). Hazard ratios (HRs) (95% confidence intervals) were estimated using multivariable Cox proportional hazards models, stratified by EPIC-participating center and age at recruitment, and adjusted for sex, education, smoking, body mass index, physical activity, diabetes and dietary (in women also reproductive) factors. The study included 307,318 men and women, with an average follow-up of 13.7 (standard deviation 4.4) years and 39,298 incident cancers. We confirmed the expected positive association with renal cell carcinoma: HR = 1.12 (1.08–1.17) per 10 mm Hg higher SBP and HR = 1.23 (1.14–1.32) for DBP. We additionally found positive associations for esophageal squamous cell carcinoma (SCC): HR = 1.16 (1.07–1.26) (SBP), HR = 1.31 (1.13–1.51) (DBP), weaker for head and neck cancers: HR = 1.08 (1.04–1.12) (SBP), HR = 1.09 (1.01–1.17) (DBP) and, similarly, for skin SCC, colon cancer, postmenopausal breast cancer and uterine adenocarcinoma (AC), but not for esophageal AC, lung SCC, lung AC or uterine endometroid cancer. We observed weak inverse associations of SBP with cervical SCC: HR = 0.91 (0.82–1.00) and lymphomas: HR = 0.97 (0.93–1.00). There were no consistent associations with cancers in other locations. Our results are largely compatible with published studies and support weak associations of blood pressure with cancers in specific locations and morphologies. © 2019 UICC
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- 2020
47. Circulating bilirubin levels and risk of colorectal cancer: Serological and Mendelian randomization analyses
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Seyed Khoei, N. Jenab, M. Murphy, N. Banbury, B.L. Carreras-Torres, R. Viallon, V. Kühn, T. Bueno-De-Mesquita, B. Aleksandrova, K. Cross, A.J. Weiderpass, E. Stepien, M. Bulmer, A. Tjønneland, A. Boutron-Ruault, M.-C. Severi, G. Carbonnel, F. Katzke, V. Boeing, H. Bergmann, M.M. Trichopoulou, A. Karakatsani, A. Martimianaki, G. Palli, D. Tagliabue, G. Panico, S. Tumino, R. Sacerdote, C. Skeie, G. Merino, S. Bonet, C. Rodríguez-Barranco, M. Gil, L. Chirlaque, M.-D. Ardanaz, E. Myte, R. Hultdin, J. Perez-Cornago, A. Aune, D. Tsilidis, K.K. Albanes, D. Baron, J.A. Berndt, S.I. Bézieau, S. Brenner, H. Campbell, P.T. Casey, G. Chan, A.T. Chang-Claude, J. Chanock, S.J. Cotterchio, M. Gallinger, S. Gruber, S.B. Haile, R.W. Hampe, J. Hoffmeister, M. Hopper, J.L. Hsu, L. Huyghe, J.R. Jenkins, M.A. Joshi, A.D. Kampman, E. Larsson, S.C. Le Marchand, L. Li, C.I. Li, L. Lindblom, A. Lindor, N.M. Martín, V. Moreno, V. Newcomb, P.A. Offit, K. Ogino, S. Parfrey, P.S. Pharoah, P.D.P. Rennert, G. Sakoda, L.C. Schafmayer, C. Schmit, S.L. Schoen, R.E. Slattery, M.L. Thibodeau, S.N. Ulrich, C.M. Van Duijnhoven, F.J.B. Weigl, K. Weinstein, S.J. White, E. Wolk, A. Woods, M.O. Wu, A.H. Zhang, X. Ferrari, P. Anton, G. Peters, A. Peters, U. Gunter, M.J. Wagner, K.-H. Freisling, H.
- Abstract
Background: Bilirubin, a byproduct of hemoglobin breakdown and purported anti-oxidant, is thought to be cancer preventive. We conducted complementary serological and Mendelian randomization (MR) analyses to investigate whether alterations in circulating levels of bilirubin are associated with risk of colorectal cancer (CRC). We decided a priori to perform analyses separately in men and women based on suggestive evidence that associations may differ by sex. Methods: In a case-control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC), pre-diagnostic unconjugated bilirubin (UCB, the main component of total bilirubin) concentrations were measured by high-performance liquid chromatography in plasma samples of 1386 CRC cases and their individually matched controls. Additionally, 115 single-nucleotide polymorphisms (SNPs) robustly associated (P < 5 × 10-8) with circulating total bilirubin were instrumented in a 2-sample MR to test for a potential causal effect of bilirubin on CRC risk in 52,775 CRC cases and 45,940 matched controls in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), the Colon Cancer Family Registry (CCFR), and the Colorectal Transdisciplinary (CORECT) study. Results: The associations between circulating UCB levels and CRC risk differed by sex (P heterogeneity = 0.008). Among men, higher levels of UCB were positively associated with CRC risk (odds ratio [OR] = 1.19, 95% confidence interval [CI] = 1.04-1.36; per 1-SD increment of log-UCB). In women, an inverse association was observed (OR = 0.86 (0.76-0.97)). In the MR analysis of the main UGT1A1 SNP (rs6431625), genetically predicted higher levels of total bilirubin were associated with a 7% increase in CRC risk in men (OR = 1.07 (1.02-1.12); P = 0.006; per 1-SD increment of total bilirubin), while there was no association in women (OR = 1.01 (0.96-1.06); P = 0.73). Raised bilirubin levels, predicted by instrumental variables excluding rs6431625, were suggestive of an inverse association with CRC in men, but not in women. These differences by sex did not reach formal statistical significance (P heterogeneity ≥ 0.2). Conclusions: Additional insight into the relationship between circulating bilirubin and CRC is needed in order to conclude on a potential causal role of bilirubin in CRC development. © 2020 The Author(s).
- Published
- 2020
48. Mitochondrial DNA copy-number variation and pancreatic cancer risk in the prospective EPIC cohort
- Author
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Gentiluomo, M. Katzke, V.A. Kaaks, R. Tjønneland, A. Severi, G. Perduca, V. Boutron-Ruault, M.-C. Weiderpass, E. Ferrari, P. Johnson, T. Schulze, M.B. Bergmann, M. Trichopoulou, A. Karakatsani, A. Vecchia, C.L. Palli, D. Grioni, S. Panico, S. Tumino, R. Sacerdote, C. Bueno-De-Mesquita, B. Vermeulen, R. Sandanger, T.M. Ramón Quirós, J. Rodriguez-Barranco, M. Amiano, P. Colorado-Yohar, S. Ardanaz, E. Sund, M. Khaw, K.-T. Wareham, N.J. Schmidt, J.A. Jakszyn, P. Morelli, L. Canzian, F. Campa, D.
- Abstract
Background: Mitochondrial DNA (mtDNA) copy number in peripheral blood has been found to be associated with risk of developing several cancers. However, data on pancreatic ductal adenocarcinoma (PDAC) are very limited. Methods: To further our knowledge on this topic, we measured relative mtDNA copy number by a quantitative real-time PCR assay in peripheral leukocyte samples of 476 PDAC cases and 357 controls nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Results: We observed lower mtDNA copy number with advancing age (P = 6.54 x 10-5) and with a high body mass index (BMI) level (P = 0.004) and no association with sex, smoking behavior, and alcohol consumption. We found an association between increased mtDNA copy number and decreased risk of developing PDAC with an odds ratios (OR) of 0.35 [95% confidence interval (CI), 0.16-0.79; P = 0.01] when comparing the fifth quintile with the first using an unconditional logistic regression and an OR of 0.19 (95% CI, 0.07-0.52; P = 0.001) with a conditional analysis. Analyses stratified by BMI showed an association between high mtDNA copy number and decreased risk in the stratum of normal weight, consistent with the main analyses. Conclusions: Our results suggest a protective effect of a higher number of mitochondria, measured in peripheral blood leukocytes, on PDAC risk. Impact: Our findings highlight the importance of understanding the mitochondrial biology in pancreatic cancer. © 2020 American Association for Cancer Research.
- Published
- 2020
49. Association analysis of oestrogen receptor beta gene (ESR2) polymorphisms with female pattern hair loss
- Author
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Yip, L., Zaloumis, S., Irwin, D., Severi, G., Hopper, J., Giles, G., Harrap, S., Sinclair, R., and Ellis, J.
- Published
- 2012
- Full Text
- View/download PDF
50. A whole-of-population, multi-user series of High-Intensity Focused Ultrasound (HIFU) for management of localised prostate cancer: outcomes and implications: 23
- Author
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ONG, K., ROYCE, P., WOO, H., GILES, G., SEVERI, G., DEAN, T., APPU, S., TROY, A., LAWRENTSCHUK, N., and BOLTON, D.
- Published
- 2012
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