457 results on '"Katzke V."'
Search Results
2. Dietary fatty acids and endometrial cancer risk within the European Prospective Investigation into Cancer and Nutrition
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Yammine, S. G., Huybrechts, I., Biessy, C., Dossus, L., Panico, S., Sánchez, M. J., Benetou, V., Turzanski-Fortner, R., Katzke, V., Idahl, A., Skeie, G., Olsen, K. Standahl, Tjønneland, A., Halkjaer, J., Colorado-Yohar, S., Heath, A. K., Sonestedt, E., Sartor, H., Schulze, M. B., Palli, D., Crous-Bou, M., Dorronsoro, A., Overvad, K., Gurrea, A. Barricarte, Severi, G., Vermeulen, R. C.H., Sandanger, T. M., Travis, R. C., Key, T., Amiano, P., Van Guelpen, B., Johansson, M., Sund, M., Tumino, R., Wareham, N., Sacerdote, C., Krogh, V., Brennan, P., Riboli, E., Weiderpass, E., Gunter, M. J., and Chajès, V.
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- 2023
- Full Text
- View/download PDF
3. Lifestyle changes in middle age and risk of cancer: evidence from the European Prospective Investigation into Cancer and Nutrition
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Botteri, E, Peveri, G, Berstad, P, Bagnardi, V, Hoff, G, Heath, A, Cross, A, Vineis, P, Dossus, L, Johansson, M, Freisling, H, Matta, K, Huybrechts, I, Chen, S, B. Borch, K, Sandanger, T, H. Nost, T, Dahm, C, Antoniussen, C, Tin Tin, S, Fournier, A, Marques, C, Artaud, F, Sanchez, M, Guevara, M, Santiuste, C, Agudo, A, Bajracharya, R, Katzke, V, Ricceri, F, Agnoli, C, Bergmann, M, Schulze, M, Panico, S, Masala, G, Tjonneland, A, Olsen, A, Stocks, T, Manjer, J, Aizpurua-Atxega, A, Weiderpass, E, Riboli, E, Gunter, M, Ferrari, P, Botteri E., Peveri G., Berstad P., Bagnardi V., Hoff G., Heath A. K., Cross A. J., Vineis P., Dossus L., Johansson M., Freisling H., Matta K., Huybrechts I., Chen S. L. F., B. Borch K., Sandanger T. M., H. Nost T., Dahm C. C., Antoniussen C. S., Tin Tin S., Fournier A., Marques C., Artaud F., Sanchez M. -J., Guevara M., Santiuste C., Agudo A., Bajracharya R., Katzke V., Ricceri F., Agnoli C., Bergmann M. M., Schulze M. B., Panico S., Masala G., Tjonneland A., Olsen A., Stocks T., Manjer J., Aizpurua-Atxega A., Weiderpass E., Riboli E., Gunter M. J., Ferrari P., Botteri, E, Peveri, G, Berstad, P, Bagnardi, V, Hoff, G, Heath, A, Cross, A, Vineis, P, Dossus, L, Johansson, M, Freisling, H, Matta, K, Huybrechts, I, Chen, S, B. Borch, K, Sandanger, T, H. Nost, T, Dahm, C, Antoniussen, C, Tin Tin, S, Fournier, A, Marques, C, Artaud, F, Sanchez, M, Guevara, M, Santiuste, C, Agudo, A, Bajracharya, R, Katzke, V, Ricceri, F, Agnoli, C, Bergmann, M, Schulze, M, Panico, S, Masala, G, Tjonneland, A, Olsen, A, Stocks, T, Manjer, J, Aizpurua-Atxega, A, Weiderpass, E, Riboli, E, Gunter, M, Ferrari, P, Botteri E., Peveri G., Berstad P., Bagnardi V., Hoff G., Heath A. K., Cross A. J., Vineis P., Dossus L., Johansson M., Freisling H., Matta K., Huybrechts I., Chen S. L. F., B. Borch K., Sandanger T. M., H. Nost T., Dahm C. C., Antoniussen C. S., Tin Tin S., Fournier A., Marques C., Artaud F., Sanchez M. -J., Guevara M., Santiuste C., Agudo A., Bajracharya R., Katzke V., Ricceri F., Agnoli C., Bergmann M. M., Schulze M. B., Panico S., Masala G., Tjonneland A., Olsen A., Stocks T., Manjer J., Aizpurua-Atxega A., Weiderpass E., Riboli E., Gunter M. J., and Ferrari P.
- Abstract
In this study, we aimed to provide novel evidence on the impact of changing lifestyle habits on cancer risk. In the EPIC cohort, 295,865 middle-aged participants returned a lifestyle questionnaire at baseline and during follow-up. At both timepoints, we calculated a healthy lifestyle index (HLI) score based on cigarette smoking, alcohol consumption, body mass index and physical activity. HLI ranged from 0 (most unfavourable) to 16 (most favourable). We estimated the association between HLI change and risk of lifestyle-related cancers—including cancer of the breast, lung, colorectum, stomach, liver, cervix, oesophagus, bladder, and others—using Cox regression models. We reported hazard ratios (HR) with 95% confidence intervals (CI). Median time between the two questionnaires was 5.7 years, median age at follow-up questionnaire was 59 years. After the follow-up questionnaire, we observed 14,933 lifestyle-related cancers over a median follow-up of 7.8 years. Each unit increase in the HLI score was associated with 4% lower risk of lifestyle-related cancers (HR 0.96; 95%CI 0.95–0.97). Among participants in the top HLI third at baseline (HLI > 11), those in the bottom third at follow-up (HLI ≤ 9) had 21% higher risk of lifestyle-related cancers (HR 1.21; 95%CI 1.07–1.37) than those remaining in the top third. Among participants in the bottom HLI third at baseline, those in the top third at follow-up had 25% lower risk of lifestyle-related cancers (HR 0.75; 95%CI 0.65–0.86) than those remaining in the bottom third. These results indicate that lifestyle changes in middle age may have a significant impact on cancer risk.
- Published
- 2024
4. A pleiotropy scan to discover new susceptibility loci for pancreatic ductal adenocarcinoma
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Giaccherini, M, primary, Rende, M, additional, Gentiluomo, M, additional, Corradi, C, additional, Archibugi, L, additional, Ermini, S, additional, Maiello, E, additional, Morelli, L, additional, van Eijck, C H J, additional, Cavestro, G M, additional, Schneider, M, additional, Mickevicius, A, additional, Adamonis, K, additional, Basso, D, additional, Hlavac, V, additional, Gioffreda, D, additional, Talar-Wojnarowska, R, additional, Schöttker, B, additional, Lovecek, M, additional, Vanella, G, additional, Gazouli, M, additional, Uno, M, additional, Malecka-Wojciesko, E, additional, Vodicka, P, additional, Goetz, M, additional, Bijlsma, M F, additional, Petrone, M C, additional, Bazzocchi, F, additional, Kiudelis, M, additional, Szentesi, A, additional, Carrara, S, additional, Nappo, G, additional, Brenner, H, additional, Milanetto, A C, additional, Soucek, P, additional, Katzke, V, additional, Peduzzi, G, additional, Rizzato, C, additional, Pasquali, C, additional, Chen, X, additional, Capurso, G, additional, Hackert, T, additional, Bueno-de-Mesquita, B, additional, Uzunoglu, F G G, additional, Hegyi, P, additional, Greenhalf, W, additional, Theodoropoulos, G E E, additional, Sperti, C, additional, Perri, F, additional, Oliverius, M, additional, Mambrini, A, additional, Tavano, F, additional, Farinella, R, additional, Arcidiacono, P G, additional, Lucchesi, M, additional, Bunduc, S, additional, Kupcinskas, J, additional, Di Franco, G, additional, Stocker, S, additional, Neoptolemos, J P, additional, Bambi, F, additional, Jamroziak, K, additional, Testoni, S G G, additional, Aoki, M N, additional, Mohelnikova-Duchonova, B, additional, Izbicki, J R, additional, Pezzilli, R, additional, Lawlor, R T, additional, Kauffmann, E F, additional, López de Maturana, E, additional, Malats, N, additional, Canzian, F, additional, and Campa, D, additional
- Published
- 2024
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5. Dietary intake of advanced glycation end products (AGEs) and changes in body weight in European adults
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Cordova, R., Knaze, V., Viallon, V., Rust, P., Schalkwijk, C. G., Weiderpass, E., Wagner, K-H., Mayen-Chacon, A-L., Aglago, E. K., Dahm, C. C., Overvad, K., Tjønneland, A., Halkjær, J., Mancini, F. R., Boutron-Ruault, M-C., Fagherazzi, G., Katzke, V., Kühn, T., Schulze, M. B., Boeing, H., Trichopoulou, A., Karakatsani, A., Thriskos, P., Masala, G., Krogh, V., Panico, S., Tumino, R., Ricceri, F., Spijkerman, A., Boer, J., Skeie, G., Rylander, C., Borch, K. B., Quirós, J. R., Agudo, A., Redondo-Sánchez, D., Amiano, P., Gómez-Gómez, J-H., Barricarte, A., Ramne, S., Sonestedt, E., Johansson, I., Esberg, A., Tong, T., Aune, D., Tsilidis, K. K., Gunter, M. J., Jenab, M., and Freisling, Heinz
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- 2020
- Full Text
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6. Changes in Lifestyle and Risk of Colorectal Cancer in the European Prospective Investigation Into Cancer and Nutrition
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Botteri, E, Peveri, G, Berstad, P, Bagnardi, V, Chen, S, Sandanger, T, Hoff, G, Dahm, C, Antoniussen, C, Tjonneland, A, Eriksen, A, Skeie, G, Perez-Cornago, A, Huerta, J, Jakszyn, P, Harlid, S, Sundstrom, B, Barricarte, A, Monninkhof, E, Derksen, J, Schulze, M, Bueno-De-Mesquita, B, Sanchez, M, Cross, A, Tsilidis, K, De Magistris, M, Kaaks, R, Katzke, V, Rothwell, J, Laouali, N, Severi, G, Amiano, P, Contiero, P, Sacerdote, C, Goldberg, M, Touvier, M, Freisling, H, Viallon, V, Weiderpass, E, Riboli, E, Gunter, M, Jenab, M, Ferrari, P, Botteri E., Peveri G., Berstad P., Bagnardi V., Chen S. L. F., Sandanger T. M., Hoff G., Dahm C. C., Antoniussen C. S., Tjonneland A., Eriksen A. K., Skeie G., Perez-Cornago A., Huerta J. M., Jakszyn P., Harlid S., Sundstrom B., Barricarte A., Monninkhof E. M., Derksen J. W. G., Schulze M. B., Bueno-De-Mesquita B., Sanchez M. -J., Cross A. J., Tsilidis K. K., De Magistris M. S., Kaaks R., Katzke V., Rothwell J. A., Laouali N., Severi G., Amiano P., Contiero P., Sacerdote C., Goldberg M., Touvier M., Freisling H., Viallon V., Weiderpass E., Riboli E., Gunter M. J., Jenab M., Ferrari P., Botteri, E, Peveri, G, Berstad, P, Bagnardi, V, Chen, S, Sandanger, T, Hoff, G, Dahm, C, Antoniussen, C, Tjonneland, A, Eriksen, A, Skeie, G, Perez-Cornago, A, Huerta, J, Jakszyn, P, Harlid, S, Sundstrom, B, Barricarte, A, Monninkhof, E, Derksen, J, Schulze, M, Bueno-De-Mesquita, B, Sanchez, M, Cross, A, Tsilidis, K, De Magistris, M, Kaaks, R, Katzke, V, Rothwell, J, Laouali, N, Severi, G, Amiano, P, Contiero, P, Sacerdote, C, Goldberg, M, Touvier, M, Freisling, H, Viallon, V, Weiderpass, E, Riboli, E, Gunter, M, Jenab, M, Ferrari, P, Botteri E., Peveri G., Berstad P., Bagnardi V., Chen S. L. F., Sandanger T. M., Hoff G., Dahm C. C., Antoniussen C. S., Tjonneland A., Eriksen A. K., Skeie G., Perez-Cornago A., Huerta J. M., Jakszyn P., Harlid S., Sundstrom B., Barricarte A., Monninkhof E. M., Derksen J. W. G., Schulze M. B., Bueno-De-Mesquita B., Sanchez M. -J., Cross A. J., Tsilidis K. K., De Magistris M. S., Kaaks R., Katzke V., Rothwell J. A., Laouali N., Severi G., Amiano P., Contiero P., Sacerdote C., Goldberg M., Touvier M., Freisling H., Viallon V., Weiderpass E., Riboli E., Gunter M. J., Jenab M., and Ferrari P.
- Abstract
Introduction: We investigated the impact of changes in lifestyle habits on colorectal cancer (CRC) risk in a multicountry European cohort. Methods: We used baseline and follow-up questionnaire data from the European Prospective Investigation into Cancer cohort to assess changes in lifestyle habits and their associations with CRC development. We calculated a healthy lifestyle index (HLI) score based on smoking status, alcohol consumption, body mass index, and physical activity collected at the 2 time points. HLI ranged from 0 (most unfavorable) to 16 (most favorable). We estimated the association between HLI changes and CRC risk using Cox regression models and reported hazard ratios (HR) with 95% confidence intervals (CI). Results: Among 295,865 participants, 2,799 CRC cases were observed over a median of 7.8 years. The median time between questionnaires was 5.7 years. Each unit increase in HLI from the baseline to the follow-up assessment was associated with a statistically significant 3% lower CRC risk. Among participants in the top tertile at baseline (HLI > 11), those in the bottom tertile at follow-up (HLI ≤ 9) had a higher CRC risk (HR 1.34; 95% CI 1.02-1.75) than those remaining in the top tertile. Among individuals in the bottom tertile at baseline, those in the top tertile at follow-up had a lower risk (HR 0.77; 95% CI 0.59-1.00) than those remaining in the bottom tertile. Discussion: Improving adherence to a healthy lifestyle was inversely associated with CRC risk, while worsening adherence was positively associated with CRC risk. These results justify and support recommendations for healthy lifestyle changes and healthy lifestyle maintenance for CRC prevention.
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- 2023
7. A body shape index (ABSI) is associated inversely with post-menopausal progesterone-receptor-negative breast cancer risk in a large European cohort
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Christakoudi, S, Tsilidis, KK, Dossus, L, Rinaldi, S, Weiderpass, E, Antoniussen, CS, Dahm, CC, Tjønneland, A, Mellemkjær, L, Katzke, V, Kaaks, R, Schulze, MB, Masala, G, Grioni, S, Panico, S, Tumino, R, Sacerdote, C, May, AM, Monninkhof, EM, Quirós, JR, Bonet, C, Sánchez, M-J, Amiano, P, Chirlaque, M-D, Guevara, M, Rosendahl, AH, Stocks, T, Perez-Cornago, A, Tin Tin, S, Heath, AK, Aglago, EK, Peruchet-Noray, L, Freisling, H, and Riboli, E
- Subjects
Breast Neoplasms/complications ,Somatotypes ,Hip Size ,Triple Negative Breast Neoplasms/complications ,Waist Size ,Middle Aged ,Body Mass Index ,Postmenopause ,ABSI ,Body shape ,Breast cancer ,Risk Factors ,Humans ,Female ,Prospective Studies ,Obesity ,Progesterone - Abstract
BACKGROUND: Associations of body shape with breast cancer risk, independent of body size, are unclear because waist and hip circumferences are correlated strongly positively with body mass index (BMI).METHODS: We evaluated body shape with the allometric "a body shape index" (ABSI) and hip index (HI), which compare waist and hip circumferences, correspondingly, among individuals with the same weight and height. We examined associations of ABSI, HI, and BMI (per one standard deviation increment) with breast cancer overall, and according to menopausal status at baseline, age at diagnosis, and oestrogen and progesterone receptor status (ER+/-PR+/-) in multivariable Cox proportional hazards models using data from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.RESULTS: During a mean follow-up of 14.0 years, 9011 incident breast cancers were diagnosed among 218,276 women. Although there was little evidence for association of ABSI with breast cancer overall (hazard ratio HR = 0.984; 95% confidence interval: 0.961-1.007), we found borderline inverse associations for post-menopausal women (HR = 0.971; 0.942-1.000; n = 5268 cases) and breast cancers diagnosed at age ≥ 55 years (HR = 0.976; 0.951-1.002; n = 7043) and clear inverse associations for ER + PR- subtypes (HR = 0.894; 0.822-0.971; n = 726) and ER-PR- subtypes (HR = 0.906; 0.835-0.983 n = 759). There were no material associations with HI. BMI was associated strongly positively with breast cancer overall (HR = 1.074; 1.049-1.098), for post-menopausal women (HR = 1.117; 1.085-1.150), for cancers diagnosed at age ≥ 55 years (HR = 1.104; 1.076-1.132), and for ER + PR + subtypes (HR = 1.122; 1.080-1.165; n = 3101), but not for PR- subtypes.CONCLUSIONS: In the EPIC cohort, abdominal obesity evaluated with ABSI was not associated with breast cancer risk overall but was associated inversely with the risk of post-menopausal PR- breast cancer. Our findings require validation in other cohorts and with a larger number of PR- breast cancer cases.
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- 2023
8. Dietary fatty acids and endometrial cancer risk within the European Prospective Investigation into Cancer and Nutrition
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IRAS OH Epidemiology Chemical Agents, Yammine, S G, Huybrechts, I, Biessy, C, Dossus, L, Panico, S, Sánchez, M J, Benetou, V, Turzanski-Fortner, R, Katzke, V, Idahl, A, Skeie, G, Olsen, K Standahl, Tjønneland, A, Halkjaer, J, Colorado-Yohar, S, Heath, A K, Sonestedt, E, Sartor, H, Schulze, M B, Palli, D, Crous-Bou, M, Dorronsoro, A, Overvad, K, Gurrea, A Barricarte, Severi, G, Vermeulen, R C H, Sandanger, T M, Travis, R C, Key, T, Amiano, P, Van Guelpen, B, Johansson, M, Sund, M, Tumino, R, Wareham, N, Sacerdote, C, Krogh, V, Brennan, P, Riboli, E, Weiderpass, E, Gunter, M J, Chajès, V, IRAS OH Epidemiology Chemical Agents, Yammine, S G, Huybrechts, I, Biessy, C, Dossus, L, Panico, S, Sánchez, M J, Benetou, V, Turzanski-Fortner, R, Katzke, V, Idahl, A, Skeie, G, Olsen, K Standahl, Tjønneland, A, Halkjaer, J, Colorado-Yohar, S, Heath, A K, Sonestedt, E, Sartor, H, Schulze, M B, Palli, D, Crous-Bou, M, Dorronsoro, A, Overvad, K, Gurrea, A Barricarte, Severi, G, Vermeulen, R C H, Sandanger, T M, Travis, R C, Key, T, Amiano, P, Van Guelpen, B, Johansson, M, Sund, M, Tumino, R, Wareham, N, Sacerdote, C, Krogh, V, Brennan, P, Riboli, E, Weiderpass, E, Gunter, M J, and Chajès, V
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- 2023
9. Baseline and lifetime alcohol consumption and risk of skin cancer in the European Prospective Investigation into Cancer and Nutrition cohort (EPIC).
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Mahamat-Saleh, Y, Al-Rahmoun, M, Severi, G, Ghiasvand, R, Veierod, MB, Caini, S, Palli, D, Botteri, E, Sacerdote, C, Ricceri, F, Lukic, M, Sánchez, MJ, Pala, V, Tumino, R, Chiodini, P, Amiano, P, Colorado-Yohar, S, Chirlaque, M-D, Ardanaz, E, Bonet, C, Katzke, V, Kaaks, R, Schulze, MB, Overvad, K, Dahm, CC, Antoniussen, CS, Tjønneland, A, Kyrø, C, Bueno-de-Mesquita, B, Manjer, J, Jansson, M, Esberg, A, Mori, N, Ferrari, P, Weiderpass, E, Boutron-Ruault, M-C, Kvaskoff, M, Mahamat-Saleh, Y, Al-Rahmoun, M, Severi, G, Ghiasvand, R, Veierod, MB, Caini, S, Palli, D, Botteri, E, Sacerdote, C, Ricceri, F, Lukic, M, Sánchez, MJ, Pala, V, Tumino, R, Chiodini, P, Amiano, P, Colorado-Yohar, S, Chirlaque, M-D, Ardanaz, E, Bonet, C, Katzke, V, Kaaks, R, Schulze, MB, Overvad, K, Dahm, CC, Antoniussen, CS, Tjønneland, A, Kyrø, C, Bueno-de-Mesquita, B, Manjer, J, Jansson, M, Esberg, A, Mori, N, Ferrari, P, Weiderpass, E, Boutron-Ruault, M-C, and Kvaskoff, M
- Abstract
Experimental evidence suggests that alcohol induces cutaneous carcinogenesis, yet epidemiological studies on the link between alcohol intake and skin cancer have been inconsistent. The European Prospective Investigation into Cancer and Nutrition (EPIC) is a prospective cohort initiated in 1992 in 10 European countries. Alcohol intake at baseline and average lifetime alcohol intake were assessed using validated country-specific dietary and lifestyle questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated in Cox models. A total of 14 037 skin cancer cases (melanoma: n = 2457; basal-cell carcinoma (BCC): n = 8711; squamous-cell carcinoma (SCC): n = 1928; unknown: n = 941) were identified among 450 112 participants (average follow-up: 15 years). Baseline alcohol intake was positively associated with SCC (>15 vs 0.1-4.9 g/day: HR = 1.44, 95% CI = 1.17-1.77; Ptrend = .001), BCC (HR = 1.12, 95% CI = 1.01-1.23; Ptrend = .04), and melanoma risks in men (HR = 1.17, 95% CI = 0.95-1.44; Ptrend = .17), while associations were more modest in women (SCC: HR = 1.09, 95% CI = 0.90-1.30; Ptrend = .13; BCC: HR = 1.08, 95% CI = 1.00-1.17, Ptrend = .03; melanoma: HR = 0.93, 95% CI = 0.80-1.08, Ptrend = .13). Associations were similar for lifetime alcohol intake, with an attenuated linear trend. Lifetime liquor/spirit intake was positively associated with melanoma (fourth vs first quartile: HR = 1.47, 95% CI = 1.08-1.99; Ptrend = .0009) and BCC risks in men (HR = 1.17, 95% CI = 1.04-1.31; Ptrend = .14). Baseline and lifetime intakes of wine were associated with BCC risk (HR = 1.25 in men; HR = 1.11-1.12; in women). No statistically significant associations were found between beverage types and SCC risk. Intake of beer was not associated with skin cancer risk. Our study suggests positive relationships between alcohol intake and skin cancer risk, which may have important implications for the primary prevention of skin cancer.
- Published
- 2023
10. Lipopolysaccharide-binding protein and future Parkinson's disease risk: a European prospective cohort.
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Zhao, Yujia, Walker, D.I., Lill, C.M., Bloem, B.R., Darweesh, S.K.L., Pinto-Pacheco, B., McNeil, B., Miller, G.W., Heath, A.K., Frissen, M.N., Petrova, D., Sánchez, M.J., Chirlaque, M.D., Guevara, M., Zibetti, M., Panico, S., Middleton, L., Katzke, V., Kaaks, R., Riboli, E., Masala, G., Sieri, S., Zamora-Ros, R., Amiano, P., Jenab, M., Peters, Susan, Vermeulen, R., Zhao, Yujia, Walker, D.I., Lill, C.M., Bloem, B.R., Darweesh, S.K.L., Pinto-Pacheco, B., McNeil, B., Miller, G.W., Heath, A.K., Frissen, M.N., Petrova, D., Sánchez, M.J., Chirlaque, M.D., Guevara, M., Zibetti, M., Panico, S., Middleton, L., Katzke, V., Kaaks, R., Riboli, E., Masala, G., Sieri, S., Zamora-Ros, R., Amiano, P., Jenab, M., Peters, Susan, and Vermeulen, R.
- Abstract
Item does not contain fulltext, INTRODUCTION: Lipopolysaccharide (LPS) is the outer membrane component of Gram-negative bacteria. LPS-binding protein (LBP) is an acute-phase reactant that mediates immune responses triggered by LPS and has been used as a blood marker for LPS. LBP has recently been indicated to be associated with Parkinson's disease (PD) in small-scale retrospective case-control studies. We aimed to investigate the association between LBP blood levels with PD risk in a nested case-control study within a large European prospective cohort. METHODS: A total of 352 incident PD cases (55% males) were identified and one control per case was selected, matched by age at recruitment, sex and study center. LBP levels in plasma collected at recruitment, which was on average 7.8 years before diagnosis of the cases, were analyzed by enzyme linked immunosorbent assay. Odds ratios (ORs) were estimated for one unit increase of the natural log of LBP levels and PD incidence by conditional logistic regression. RESULTS: Plasma LBP levels were higher in prospective PD cases compared to controls (median (interquartile range) 26.9 (18.1-41.0) vs. 24.7 (16.6-38.4) µg/ml). The OR for PD incidence per one unit increase of log LBP was elevated (1.46, 95% CI 0.98-2.19). This association was more pronounced among women (OR 2.68, 95% CI 1.40-5.13) and overweight/obese subjects (OR 1.54, 95% CI 1.09-2.18). CONCLUSION: The findings suggest that higher plasma LBP levels may be associated with an increased risk of PD and may thus pinpoint to a potential role of endotoxemia in the pathogenesis of PD, particularly in women and overweight/obese individuals.
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- 2023
11. Long-term ovarian function in women treated with CHOP or CHOP plus etoposide for aggressive lymphoma
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Meissner, J., Tichy, D., Katzke, V., Kühn, T., Dietrich, S., Schmitt, T., Ziepert, M., Kuhnt, E., Rixecker, T., Zorn, M., Witzens-Harig, M., Pfreundschuh, M., and Ho, A.D.
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- 2015
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12. Association of Mediterranean diet with survival after breast cancer diagnosis in women from nine European countries: results from the EPIC cohort study
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Castro-Espin, C, Bonet, C, Crous-Bou, M, Nadal-Zaragoza, N, Tjønneland, A, Mellemkjær, L, Hajji-Louati, M, Truong, T, Katzke, V, Le Cornet, C, Schulze, MB, Jannasch, F, Masala, G, Sieri, S, Panico, S, Di Girolamo, C, Skeie, G, Borch, KB, Olsen, KS, Sánchez, M-J, Amiano, P, Chirlaque, M-D, Guevara, M, Sund, M, Bodén, S, Gunter, MJ, Gonzalez-Gil, EM, Weiderpass, E, Aguilera-Buenosvinos, I, Tsilidis, KK, Heath, AK, Aune, D, Dossus, L, and Agudo, A
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Näringslära ,Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi ,Nutrition and Dietetics ,Breast cancer ,Cancer survivors ,Mediterranean diet ,Public Health, Global Health, Social Medicine and Epidemiology ,Dietary patterns ,Prospective studies - Abstract
BACKGROUND: The Mediterranean diet has been associated with lower risk of breast cancer (BC) but evidence from prospective studies on the role of Mediterranean diet on BC survival remains sparse and conflicting. We aimed to investigate whether adherence to Mediterranean diet prior to diagnosis is associated with overall and BC-specific mortality. METHODS: A total of 13,270 incident breast cancer cases were identified from an initial sample of 318,686 women in 9 countries from the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Adherence to Mediterranean diet was estimated through the adapted relative Mediterranean diet (arMED), a 16-point score that includes 8 key components of the Mediterranean diet and excludes alcohol. The degree of adherence to arMED was classified as low (score 0-5), medium (score 6-8), and high (score 9-16). Multivariable Cox proportional hazards models were used to analyze the association between the arMED score and overall mortality, and Fine-Gray competing risks models were applied for BC-specific mortality. RESULTS: After a mean follow-up of 8.6 years from diagnosis, 2340 women died, including 1475 from breast cancer. Among all BC survivors, low compared to medium adherence to arMED score was associated with a 13% higher risk of all-cause mortality (HR 1.13, 95%CI 1.01-1.26). High compared to medium adherence to arMED showed a non-statistically significant association (HR 0.94; 95% CI 0.84-1.05). With no statistically significant departures from linearity, on a continuous scale, a 3-unit increase in the arMED score was associated with an 8% reduced risk of overall mortality (HR3-unit 0.92, 95% CI: 0.87-0.97). This result sustained when restricted to postmenopausal women and was stronger among metastatic BC cases (HR3-unit 0.81, 95% CI: 0.72-0.91). CONCLUSIONS: Consuming a Mediterranean diet before BC diagnosis may improve long-term prognosis, particularly after menopause and in cases of metastatic breast cancer. Well-designed dietary interventions are needed to confirm these findings and define specific dietary recommendations.
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- 2023
13. No association of alcohol use and the risk of ulcerative colitis or Crohn’s disease: data from a European Prospective cohort study (EPIC)
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Bergmann, M M, Hernandez, V, Bernigau, W, Boeing, H, Chan, S S M, Luben, R, Khaw, K-T, van Schaik, F, Oldenburg, B, Bueno-de-Mesquita, B, Overvad, K, Palli, D, Masala, G, Carbonnel, F, Boutron-Ruault, M-C, Olsen, A, Tjonneland, A, Kaaks, R, Katzke, V, Riboli, E, and Hart, A R
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- 2017
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14. Eating at restaurants, at work or at home. Is there a difference? A study among adults of 11 European countries in the context of the HECTOR* project
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Orfanos, P, Naska, A, Rodrigues, S, Lopes, C, Freisling, H, Rohrmann, S, Sieri, S, Elmadfa, I, Lachat, C, Gedrich, K, Boeing, H, Katzke, V, Turrini, A, Tumino, R, Ricceri, F, Mattiello, A, Palli, D, Ocké, M, Engeset, D, Oltarzewski, M, Nilsson, L M, Key, T, and Trichopoulou, A
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- 2017
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15. SCORE2 risk prediction algorithms: new models to estimate 10-year risk of cardiovascular disease in Europe
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Hageman, S., Pennells, L., Ojeda, F., Kaptoge, S., Kuulasmaa, K., Vries, T. de, Xu, Z., Kee, F., Chung, R., Wood, A., McEvoy, J.W., Veronesi, G., Bolton, T., Dendale, P., Ference, B.A., Halle, M., Timmis, A., Vardas, P., Danesh, J., Graham, I., Salomaa, V., Visseren, F., Bacquer, D. de, Blankenberg, S., Dorresteijn, J., Angelantonio, E. di, Achenbach, S., Aleksandrova, K., Amiano, P., Amouyel, P., Andersson, J., Bakker, S.J.L., Costa, R.B.D., Beulens, J.W.J., Blaha, M., Bobak, M., Boer, J.M.A., Bonet, C., Bonnet, F., Boutron-Ruault, M.C., Braaten, T., Brenner, H., Brunner, F., Brunner, E.J., Brunstrom, M., Buring, J., Butterworth, A.S., Capkova, N., Cesana, G., Chrysohoou, C., Colorado-Yohar, S., Cook, N.R., Cooper, C., Dahm, C.C., Davidson, K., Dennison, E., Castelnuovo, A. di, Donfrancesco, C., Dorr, M., Dorynska, A., Eliasson, M., Engstrom, G., Ferrari, P., Ferrario, M., Ford, I., Fu, M., Gansevoort, R.T., Giampaoli, S., Gillum, R.F., Camara, A.G. de la, Grassi, G., Hansson, P.O., Huculeci, R., Hveem, K., Iacoviello, L., Ikram, M.K., Jorgensen, T., Joseph, B., Jousilahti, P., Jukema, J.W., Kaaks, R., Katzke, V., Kavousi, M., Kiechl, S., Klotsche, J., Konig, W., Kronmal, R.A., Kubinova, R., Kucharska-Newton, A., Lall, K., Lehmann, N., Leistner, D., Linneberg, A., Pablos, D.L., Lorenz, T., Lu, W.T., Luksiene, D., Lyngbakken, M., Magnussen, C., Malyutina, S., Ibanez, A.M., Masala, G., Mathiesen, E.B., Matsushita, K., Meade, T.W., Melander, O., Meyer, H.E., Moons, K.G.M., Moreno-Iribas, C., Muller, D., Munzel, T., Nikitin, Y., Nordestgaard, B.G., Omland, T., Onland, C., Overvad, K., Packard, C., Pajak, A., Palmieri, L., Panagiotakos, D., Panico, S., Perez-Cornago, A., Peters, A., Pietila, A., Pikhart, H., Psaty, B.M., Quarti-Trevano, F., Garcia, J.R.Q., Riboli, E., Ridker, P.M., Rodriguez, B., Rodriguez-Barranco, M., Rosengren, A., Roussel, R., Sacerdote, C., Sans, S., Sattar, N., Schiborn, C., Schmidt, B., Schottker, B., Schulze, M., Schwartz, J.E., Selmer, R.M., Shea, S., Shipley, M.J., Sieri, S., Soderberg, S., Sofat, R., Tamosiunas, A., Thorand, B., Tillmann, T., Tjonneland, A., Tong, T.Y.N., Trichopoulou, A., Tumino, R., Tunstall-Pedoe, H., Tybjaerg-Hansen, A., Tzoulaki, J., Heijden, A. van der, Schouw, Y.T. van der, Verschuren, W.M.M., Volzke, H., Waldeyer, C., Wareham, N.J., Weiderpass, E., Weidinger, F., Wild, P., Willeit, J., Willeit, P., Wilsgaard, T., Woodward, M., Zeller, T., Zhang, D.D., Zhou, B., SCORE2 Working Grp, ESC Cardiovasc Risk Collaboration, collaboration, SCORE2 working group and ESC Cardiovascular risk, Groningen Institute for Organ Transplantation (GIOT), Groningen Kidney Center (GKC), Cardiovascular Centre (CVC), Epidemiology, Neurology, Achenbach, S, Aleksandrova, K, Amiano, P, San Sebastian, D, Amouyel, P, Andersson, J, Bakker, S, Da Providencia Costa, R, Beulens, J, Blaha, M, Bobak, M, Boer, J, Bonet, C, Bonnet, F, Boutron-Ruault, M, Braaten, T, Brenner, H, Brunner, F, Brunner, E, Brunström, M, Buring, J, Butterworth, A, Capkova, N, Cesana, G, Chrysohoou, C, Colorado-Yohar, S, Cook, N, Cooper, C, Dahm, C, Davidson, K, Dennison, E, Di Castelnuovo, A, Donfrancesco, C, Dörr, M, Doryńska, A, Eliasson, M, Engström, G, Ferrari, P, Ferrario, M, Ford, I, Fu, M, Gansevoort, R, Giampaoli, S, Gillum, R, Gómez de la Cámara, A, Grassi, G, Hansson, P, Huculeci, R, Hveem, K, Iacoviello, L, Ikram, M, Jørgensen, T, Joseph, B, Jousilahti, P, Wouter Jukema, J, Kaaks, R, Katzke, V, Kavousi, M, Kiechl, S, Klotsche, J, König, W, Kronmal, R, Kubinova, R, Kucharska-Newton, A, Läll, K, Lehmann, N, Leistner, D, Linneberg, A, Pablos, D, Lorenz, T, Lu, W, Luksiene, D, Lyngbakken, M, Magnussen, C, Malyutina, S, Ibañez, A, Masala, G, Mathiesen, E, Matsushita, K, Meade, T, Melander, O, Meyer, H, Moons, K, Moreno-Iribas, C, Muller, D, Münzel, T, Nikitin, Y, Nordestgaard, B, Omland, T, Onland, C, Overvad, K, Packard, C, Pająk, A, Palmieri, L, Panagiotakos, D, Panico, S, Perez-Cornago, A, Peters, A, Pietilä, A, Pikhart, H, Psaty, B, Quarti-Trevano, F, Garcia, J, Riboli, E, Ridker, P, Rodriguez, B, Rodriguez-Barranco, M, Rosengren, A, Roussel, R, Sacerdote, C, S, S, Sattar, N, Schiborn, C, Schmidt, B, Schöttker, B, Schulze, M, Schwartz, J, Selmer, R, Shea, S, Shipley, M, Sieri, S, Söderberg, S, Sofat, R, Tamosiunas, A, Thorand, B, Tillmann, T, Tjønneland, A, Tong, T, Trichopoulou, A, Tumino, R, Tunstall-Pedoe, H, Tybjaerg-Hansen, A, Tzoulaki, J, van der Heijden, A, van der Schouw, Y, Verschuren, W, Völzke, H, Waldeyer, C, Wareham, N, Weiderpass, E, Weidinger, F, Wild, P, Willeit, J, Willeit, P, Wilsgaard, T, Woodward, M, Zeller, T, Zhang, D, Zhou, B, and Apollo - University of Cambridge Repository
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Male ,Cardiology ,RATIONALE ,Blood Pressure ,Disease ,030204 cardiovascular system & hematology ,PROFILE ,ACUTE CORONARY EVENTS ,VALIDATION ,Europe/epidemiology ,03 medical and health sciences ,0302 clinical medicine ,SDG 3 - Good Health and Well-being ,DESIGN ,Clinical Research ,Risk Factors ,Diabetes mellitus ,medicine ,PARTICIPANTS ,Humans ,030212 general & internal medicine ,Risk factor ,Aged ,Primary prevention ,business.industry ,10-year CVD risk ,Incidence (epidemiology) ,Cardiovascular Diseases/epidemiology ,Risk Prediction ,Cardiovascular Disease ,Primary Prevention ,10-year Cvd Risk ,External validation ,PRIMARY-CARE ,Middle Aged ,medicine.disease ,Cardiovascular disease ,Risk prediction ,3. Good health ,Europe ,Prediction algorithms ,Blood pressure ,Cardiovascular Diseases ,Smoking status ,Female ,Cardiology and Cardiovascular Medicine ,business ,Algorithms ,Demography - Abstract
Aims The aim of this study was to develop, validate, and illustrate an updated prediction model (SCORE2) to estimate 10-year fatal and non-fatal cardiovascular disease (CVD) risk in individuals without previous CVD or diabetes aged 40-69 years in Europe.Methods and results We derived risk prediction models using individual-participant data from 45 cohorts in 13 countries (677 684 individuals, 30 121 CVD events). We used sex-specific and competing risk-adjusted models, including age, smoking status, systolic blood pressure, and total- and HDL-cholesterol. We defined four risk regions in Europe according to country-specific CVD mortality, recalibrating models to each region using expected incidences and risk factor distributions. Region-specific incidence was estimated using CVD mortality and incidence data on 10 776 466 individuals. For external validation, we analysed data from 25 additional cohorts in 15 European countries (1 133 181 individuals, 43 492 CVD events). After applying the derived risk prediction models to external validation cohorts, C-indices ranged from 0.67 (0.65-0.68) to 0.81 (0.76-0.86). Predicted CVD risk varied several-fold across European regions. For example, the estimated 10-year CVD risk for a 50-year-old smoker, with a systolic blood pressure of 140 mmHg, total cholesterol of 5.5 mmol/L, and HDL-cholesterol of 1.3 mmol/L, ranged from 5.9% for men in low- risk countries to 14.0% for men in very high-risk countries, and from 4.2% for women in low-risk countries to 13.7% for women in very high-risk countries.Conclusion SCORE2-a new algorithm derived, calibrated, and validated to predict 10-year risk of first-onset CVD in European populations-enhances the identification of individuals at higher risk of developing CVD across Europe. Acknowledgements We thank investigators and participants of the several studies that contributed data to the Emerging Risk Factors Collaboration (ERFC). This research has been conducted using the UK Biobank Resource under Application Number 26865. Data from the Clinical Practice Research Datalink (CPRD) were obtained under licence from the UK Medicines and Healthcare products Regulatory Agency (protocol 162RMn2). CPRD uses data provided by patients and collected by the NHS as part of their care and support. We thank all EPIC participants and staff for their contribution to the study, the laboratory teams at the Medical Research Council Epidemiology Unit for sample management and Cambridge Genomic Services for genotyping, Sarah Spackman for data management and the team at the EPIC-CVD Coordinating Centre for study co-ordination and administration. Funding The ERFC co-ordinating centre was underpinned by programme grants from the British Heart Foundation (SP/09/002; RG/13/13/30194; RG/18/13/33946), BHF Centre of Research Excellence (RE/18/1/34212), the UK Medical Research Council (MR/L003120/1), and the National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre (BRC1215-20014), with project-specific support received from the UK NIHR [*], British United Provident Association UK Foundation and an unrestricted educational grant from GlaxoSmithKline. A variety of funding sources have supported recruitment, follow-up, and laboratory measurements in the studies contributing data to the ERFC, which are listed on the ERFC website (www.phpc.cam.ac.uk/ceu/erfc/list-of-studies). *The views expressed are those of the author(s) and not necessarily those of the NIHR or the Department of Health and Social Care. This work was supported by Health Data Research UK, which is funded by the UK Medical Research Council, Engineering and Physical Sciences Research Council, Economic and Social Research Council, Department of Health and Social Care (England), Chief Scientist Office of the Scottish Government Health and Social Care Directorates, Health and Social Care Research and Development Division (Welsh Government), Public Health Agency (Northern Ireland), British Heart Foundation, and Wellcome. The MORGAM Project has received funding from EU projects MORGAM (Biomed BMH4-CT98-3183), GenomEUtwin (FP5, QLG2-CT-2002-01254), ENGAGE (FP7, HEALTH-F4-2007-201413),CHANCES (FP7, HEALTH-F3-2010-242244), BiomarCaRE (FP7,HEALTH-F2-2011-278913), euCanSHare (Horizon 2020, No. 825903) and AFFECT-EU (Horizon 2020, No. 847770); and Medical Research Council, London (G0601463, No. 80983: Biomarkers in the MORGAM Populations). This has supported central coordination, workshops and part of the activities of the MORGAM Data Centre, the MORGAM Laboratories and the MORGAM Participating Centres EPIC-CVD was funded by the European Research Council (268834), and the European Commission Framework Programme 7 (HEALTH-F2-2012-279233). This work was supported by the Estonian Research Council grant PUTs (PRG687, PUT1660, PUT1665, PRG184), by European Union through the European Regional Development Fund project no. MOBERA5 (Norface Network project no 462.16.107), by the Green ICT programme under Norway Grants 2014 – 2021 (grant number EU53928), by the European Union through Horizon 2020 grant no. 810645 and through the European Regional Development Fund (Project No. 2014-2020.4.01.16-0125) and by the PRECISE4Q consortium. PRECISE4Q project has received funding from the European Union’s Horizon 2020 Research and Innovation Programme under Grant agreement 777107. This work was partly funded through the CoMorMent project. CoMorMent has received funding from the European Union’s Horizon 2020 Research and Innovation Programme under Grant agreement 847776. The KORA study was initiated and financed by the Helmholtz Zentrum Mu¨nchen—German Research Center for Environmental Health, which is funded by the German Federal Ministry of Education and Research (BMBF) and by the State of Bavaria. The KORA study was supported by a research grant from the Virtual Institute of Diabetes Research (Helmholtz Zentrum Mu¨nchen), the Clinical Cooperation Group Diabetes between Ludwig-Maximilians-Universita¨t Mu¨nchen and Helmholtz Zentrum Mu¨nchen, and by the German Diabetes Center (DDZ). The HAPIEE project, Institute, was supported by grants from the Wellcome Trust (064947/Z/01/Z; WT081081) and US National Institute on Aging (1R01 and AG23522). The co-ordination of EPIC is financially supported by International Agency for Research on Cancer (IARC) and also by the Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, which has additional infrastructure support provided by the NIHR Imperial Biomedical Research Centre (BRC). The national cohorts are supported by: Danish Cancer Society (Denmark); Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Ge´ne´rale de l’Education Nationale, Institut National de la Sante´ et de la Recherche Me´dicale (INSERM) (France); German Cancer Aid, German Cancer Research Center (DKFZ), German Institute of Human Nutrition Potsdam Rehbruecke (DIfE), Federal Ministry of Education and Research (BMBF) (Germany); Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy, Compagnia di SanPaolo and National Research Council (Italy); Dutch 2448 SCORE2 working group and ESC Cardiovascular Risk Collaboration Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Netherlands); Health Research Fund (FIS)—Instituto de Salud Carlos III (ISCIII), Regional Governments of Andalucı´a, Asturias, Basque Country, Murcia and Navarra, and the Catalan Institute of Oncology—ICO (Spain); Swedish Cancer Society, Swedish Research Council and County Councils of Ska˚ne and Va¨sterbotten (Sweden); Cancer Research UK (14136 to EPIC-Norfolk; C8221/A29017 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk; MR/M012190/1 to EPIC-Oxford) (United Kingdom)
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- 2021
16. Metabolic Signatures of Healthy Lifestyle Patterns and Colorectal Cancer Risk in a European Cohort.
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Rothwell, JA, Murphy, N, Bešević, J, Kliemann, N, Jenab, M, Ferrari, P, Achaintre, D, Gicquiau, A, Vozar, B, Scalbert, A, Huybrechts, I, Freisling, H, Prehn, C, Adamski, J, Cross, AJ, Pala, VM, Boutron-Ruault, M-C, Dahm, CC, Overvad, K, Gram, IT, Sandanger, TM, Skeie, G, Jakszyn, P, Tsilidis, KK, Aleksandrova, K, Schulze, MB, Hughes, DJ, van Guelpen, B, Bodén, S, Sánchez, M-J, Schmidt, JA, Katzke, V, Kühn, T, Colorado-Yohar, S, Tumino, R, Bueno-de-Mesquita, B, Vineis, P, Masala, G, Panico, S, Eriksen, AK, Tjønneland, A, Aune, D, Weiderpass, E, Severi, G, Chajès, V, Gunter, MJ, Rothwell, JA, Murphy, N, Bešević, J, Kliemann, N, Jenab, M, Ferrari, P, Achaintre, D, Gicquiau, A, Vozar, B, Scalbert, A, Huybrechts, I, Freisling, H, Prehn, C, Adamski, J, Cross, AJ, Pala, VM, Boutron-Ruault, M-C, Dahm, CC, Overvad, K, Gram, IT, Sandanger, TM, Skeie, G, Jakszyn, P, Tsilidis, KK, Aleksandrova, K, Schulze, MB, Hughes, DJ, van Guelpen, B, Bodén, S, Sánchez, M-J, Schmidt, JA, Katzke, V, Kühn, T, Colorado-Yohar, S, Tumino, R, Bueno-de-Mesquita, B, Vineis, P, Masala, G, Panico, S, Eriksen, AK, Tjønneland, A, Aune, D, Weiderpass, E, Severi, G, Chajès, V, and Gunter, MJ
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BACKGROUND & AIMS: Colorectal cancer risk can be lowered by adherence to the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) guidelines. We derived metabolic signatures of adherence to these guidelines and tested their associations with colorectal cancer risk in the European Prospective Investigation into Cancer and Nutrition cohort. METHODS: Scores reflecting adherence to the WCRF/AICR recommendations (scale, 1-5) were calculated from participant data on weight maintenance, physical activity, diet, and alcohol among a discovery set of 5738 cancer-free European Prospective Investigation into Cancer and Nutrition participants with metabolomics data. Partial least-squares regression was used to derive fatty acid and endogenous metabolite signatures of the WCRF/AICR score in this group. In an independent set of 1608 colorectal cancer cases and matched controls, odds ratios (ORs) and 95% CIs were calculated for colorectal cancer risk per unit increase in WCRF/AICR score and per the corresponding change in metabolic signatures using multivariable conditional logistic regression. RESULTS: Higher WCRF/AICR scores were characterized by metabolic signatures of increased odd-chain fatty acids, serine, glycine, and specific phosphatidylcholines. Signatures were inversely associated more strongly with colorectal cancer risk (fatty acids: OR, 0.51 per unit increase; 95% CI, 0.29-0.90; endogenous metabolites: OR, 0.62 per unit change; 95% CI, 0.50-0.78) than the WCRF/AICR score (OR, 0.93 per unit change; 95% CI, 0.86-1.00) overall. Signature associations were stronger in male compared with female participants. CONCLUSIONS: Metabolite profiles reflecting adherence to WCRF/AICR guidelines and additional lifestyle or biological risk factors were associated with colorectal cancer. Measuring a specific panel of metabolites representative of a healthy or unhealthy lifestyle may identify strata of the population at higher risk of colorectal cancer.
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- 2022
17. Pre-diagnostic C-reactive protein concentrations, CRP genetic variation and mortality among individuals with colorectal cancer in Western European populations
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Nimptsch, K., Aleksandrova, K., Fedirko, V., Jenab, M., Gunter, M.J., Siersema, P.D., Wu, K., Katzke, V., Kaaks, R., Panico, S., Palli, D., May, A.M., Sieri, S., Bueno-de-Mesquita, B., Standahl, K., Sánchez, M.J., Perez-Cornago, A., Olsen, A., Tjønneland, A., Bonet, C.B., Dahm, C.C., Chirlaque, M.D., Fiano, V., Tumino, R., Gurrea, A.B., Boutron-Ruault, M.C., Menegaux, F., Severi, G., Guelpen, B. van, Lee, Y.A., Pischon, T., Nimptsch, K., Aleksandrova, K., Fedirko, V., Jenab, M., Gunter, M.J., Siersema, P.D., Wu, K., Katzke, V., Kaaks, R., Panico, S., Palli, D., May, A.M., Sieri, S., Bueno-de-Mesquita, B., Standahl, K., Sánchez, M.J., Perez-Cornago, A., Olsen, A., Tjønneland, A., Bonet, C.B., Dahm, C.C., Chirlaque, M.D., Fiano, V., Tumino, R., Gurrea, A.B., Boutron-Ruault, M.C., Menegaux, F., Severi, G., Guelpen, B. van, Lee, Y.A., and Pischon, T.
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Contains fulltext : 252185.pdf (Publisher’s version ) (Open Access), BACKGROUND: The role of elevated pre-diagnostic C-reactive protein (CRP) concentrations on mortality in individuals with colorectal cancer (CRC) remains unclear. METHODS: We investigated the association between pre-diagnostic high-sensitivity CRP concentrations and CRP genetic variation associated with circulating CRP and CRC-specific and all-cause mortality based on data from 1,235 individuals with CRC within the European Prospective Investigation into Cancer and Nutrition cohort using multivariable-adjusted Cox proportional hazards regression. RESULTS: During a median follow-up of 9.3 years, 455 CRC-specific deaths were recorded, out of 590 deaths from all causes. Pre-diagnostic CRP concentrations were not associated with CRC-specific (hazard ratio, HR highest versus lowest quintile 0.92, 95% confidence interval, CI 0.66, 1.28) or all-cause mortality (HR 0.91, 95% CI 0.68, 1.21). Genetic predisposition to higher CRP (weighted score based on alleles of four CRP SNPs associated with higher circulating CRP) was not significantly associated with CRC-specific mortality (HR per CRP-score unit 0.95, 95% CI 0.86, 1.05) or all-cause mortality (HR 0.98, 95% CI 0.90, 1.07). Among four investigated CRP genetic variants, only SNP rs1205 was significantly associated with CRC-specific (comparing the CT and CC genotypes with TT genotype, HR 0.54, 95% CI 0.35, 0.83 and HR 0.58, 95% CI 0.38, 0.88, respectively) and all-cause mortality (HR 0.58, 95% CI 0.40, 0.85 and 0.64, 95% CI 0.44, 0.92, respectively). CONCLUSIONS: The results of this prospective cohort study do not support a role of pre-diagnostic CRP concentrations on mortality in individuals with CRC. The observed associations with rs1205 deserve further scientific attention.
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- 2022
18. Pre-diagnostic C-reactive protein concentrations, CRP genetic variation and mortality among individuals with colorectal cancer in Western European populations.
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Nimptsch, K, Aleksandrova, K, Fedirko, V, Jenab, M, Gunter, MJ, Siersema, PD, Wu, K, Katzke, V, Kaaks, R, Panico, S, Palli, D, May, AM, Sieri, S, Bueno-de-Mesquita, B, Standahl, K, Sánchez, M-J, Perez-Cornago, A, Olsen, A, Tjønneland, A, Bonet, CB, Dahm, CC, Chirlaque, M-D, Fiano, V, Tumino, R, Gurrea, AB, Boutron-Ruault, M-C, Menegaux, F, Severi, G, van Guelpen, B, Lee, Y-A, Pischon, T, Nimptsch, K, Aleksandrova, K, Fedirko, V, Jenab, M, Gunter, MJ, Siersema, PD, Wu, K, Katzke, V, Kaaks, R, Panico, S, Palli, D, May, AM, Sieri, S, Bueno-de-Mesquita, B, Standahl, K, Sánchez, M-J, Perez-Cornago, A, Olsen, A, Tjønneland, A, Bonet, CB, Dahm, CC, Chirlaque, M-D, Fiano, V, Tumino, R, Gurrea, AB, Boutron-Ruault, M-C, Menegaux, F, Severi, G, van Guelpen, B, Lee, Y-A, and Pischon, T
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BACKGROUND: The role of elevated pre-diagnostic C-reactive protein (CRP) concentrations on mortality in individuals with colorectal cancer (CRC) remains unclear. METHODS: We investigated the association between pre-diagnostic high-sensitivity CRP concentrations and CRP genetic variation associated with circulating CRP and CRC-specific and all-cause mortality based on data from 1,235 individuals with CRC within the European Prospective Investigation into Cancer and Nutrition cohort using multivariable-adjusted Cox proportional hazards regression. RESULTS: During a median follow-up of 9.3 years, 455 CRC-specific deaths were recorded, out of 590 deaths from all causes. Pre-diagnostic CRP concentrations were not associated with CRC-specific (hazard ratio, HR highest versus lowest quintile 0.92, 95% confidence interval, CI 0.66, 1.28) or all-cause mortality (HR 0.91, 95% CI 0.68, 1.21). Genetic predisposition to higher CRP (weighted score based on alleles of four CRP SNPs associated with higher circulating CRP) was not significantly associated with CRC-specific mortality (HR per CRP-score unit 0.95, 95% CI 0.86, 1.05) or all-cause mortality (HR 0.98, 95% CI 0.90, 1.07). Among four investigated CRP genetic variants, only SNP rs1205 was significantly associated with CRC-specific (comparing the CT and CC genotypes with TT genotype, HR 0.54, 95% CI 0.35, 0.83 and HR 0.58, 95% CI 0.38, 0.88, respectively) and all-cause mortality (HR 0.58, 95% CI 0.40, 0.85 and 0.64, 95% CI 0.44, 0.92, respectively). CONCLUSIONS: The results of this prospective cohort study do not support a role of pre-diagnostic CRP concentrations on mortality in individuals with CRC. The observed associations with rs1205 deserve further scientific attention.
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- 2022
19. Mild-to-Moderate Kidney Dysfunction and Cardiovascular Disease: Observational and Mendelian Randomization Analyses
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Gaziano, L, Sun, L, Arnold, M, Bell, S, Cho, K, Kaptoge, SK, Song, RJ, Burgess, S, Posner, DC, Mosconi, K, Cohen, CR, Mason, AM, Bolton, TR, Tao, R, Allara, E, Schubert, P, Chen, L, Staley, JR, Staplin, N, Altay, S, Amiano, P, Arndt, PV, Arnlov, J, Barr, ELM, Bjorkelund, C, Boer, JMA, Brenner, H, Casiglia, E, Chiodini, P, Cooper, JA, Coresh, J, Cushman, M, Dankner, R, Davidson, KW, de Jongh, RT, Donfrancesco, C, Engstrom, G, Freisling, H, de la Camara, AG, Gudnason, V, Hankey, GJ, Hansson, P, Heath, AK, Hoorn, EJ, Imano, H, Jassal, SK, Kaaks, R, Katzke, V, Kauhanen, J, Kiechl, S, Koenig, W, Kronmal, RA, Kyro, C, Lawlor, DA, Ljungberg, B, MacDonald, C, Masala, G, Meisinger, C, Melander, O, Iribas, CM, Ninomiya, T, Nitsch, D, Nordestgaard, BG, OnlandMoret, C, Palmieri, L, Petrova, D, Garcia, JRQ, Rosengren, A, Sacerdote, C, Sakurai, M, Santiuste, C, Schulze, MB, Sieri, S, Sundstrom, J, Tikhonoff, V, Tjonneland, A, Tong, T, Tumino, R, Tzoulaki, I, van der Schouw, YT, Verschuren, WMM, Volzke, H, Wallace, RB, Wannamethee, SG, Weiderpass, E, Willeit, P, Woodward, M, Yamagishi, K, ZamoraRos, R, Akwo, EA, Pyarajan, S, Gagnon, DR, Tsao, PS, Muralidhar, S, Edwards, TL, Damrauer, SM, Joseph, J, Pennells, L, Wilson, PWF, Harrison, S, Gaziano, TA, Inouye, M, Baigent, C, Casas, JP, Langenberg, C, Wareham, N, Riboli, E, Gaziano, JM, Danesh, J, Hung, AM, Butterworth, AS, Wood, AM, Di Angelantonio, E, Gaziano, L, Sun, L, Arnold, M, Bell, S, Cho, K, Kaptoge, SK, Song, RJ, Burgess, S, Posner, DC, Mosconi, K, Cohen, CR, Mason, AM, Bolton, TR, Tao, R, Allara, E, Schubert, P, Chen, L, Staley, JR, Staplin, N, Altay, S, Amiano, P, Arndt, PV, Arnlov, J, Barr, ELM, Bjorkelund, C, Boer, JMA, Brenner, H, Casiglia, E, Chiodini, P, Cooper, JA, Coresh, J, Cushman, M, Dankner, R, Davidson, KW, de Jongh, RT, Donfrancesco, C, Engstrom, G, Freisling, H, de la Camara, AG, Gudnason, V, Hankey, GJ, Hansson, P, Heath, AK, Hoorn, EJ, Imano, H, Jassal, SK, Kaaks, R, Katzke, V, Kauhanen, J, Kiechl, S, Koenig, W, Kronmal, RA, Kyro, C, Lawlor, DA, Ljungberg, B, MacDonald, C, Masala, G, Meisinger, C, Melander, O, Iribas, CM, Ninomiya, T, Nitsch, D, Nordestgaard, BG, OnlandMoret, C, Palmieri, L, Petrova, D, Garcia, JRQ, Rosengren, A, Sacerdote, C, Sakurai, M, Santiuste, C, Schulze, MB, Sieri, S, Sundstrom, J, Tikhonoff, V, Tjonneland, A, Tong, T, Tumino, R, Tzoulaki, I, van der Schouw, YT, Verschuren, WMM, Volzke, H, Wallace, RB, Wannamethee, SG, Weiderpass, E, Willeit, P, Woodward, M, Yamagishi, K, ZamoraRos, R, Akwo, EA, Pyarajan, S, Gagnon, DR, Tsao, PS, Muralidhar, S, Edwards, TL, Damrauer, SM, Joseph, J, Pennells, L, Wilson, PWF, Harrison, S, Gaziano, TA, Inouye, M, Baigent, C, Casas, JP, Langenberg, C, Wareham, N, Riboli, E, Gaziano, JM, Danesh, J, Hung, AM, Butterworth, AS, Wood, AM, and Di Angelantonio, E
- Abstract
BACKGROUND: End-stage renal disease is associated with a high risk of cardiovascular events. It is unknown, however, whether mild-to-moderate kidney dysfunction is causally related to coronary heart disease (CHD) and stroke. METHODS: Observational analyses were conducted using individual-level data from 4 population data sources (Emerging Risk Factors Collaboration, EPIC-CVD [European Prospective Investigation into Cancer and Nutrition-Cardiovascular Disease Study], Million Veteran Program, and UK Biobank), comprising 648 135 participants with no history of cardiovascular disease or diabetes at baseline, yielding 42 858 and 15 693 incident CHD and stroke events, respectively, during 6.8 million person-years of follow-up. Using a genetic risk score of 218 variants for estimated glomerular filtration rate (eGFR), we conducted Mendelian randomization analyses involving 413 718 participants (25 917 CHD and 8622 strokes) in EPIC-CVD, Million Veteran Program, and UK Biobank. RESULTS: There were U-shaped observational associations of creatinine-based eGFR with CHD and stroke, with higher risk in participants with eGFR values <60 or >105 mL·min-1·1.73 m-2, compared with those with eGFR between 60 and 105 mL·min-1·1.73 m-2. Mendelian randomization analyses for CHD showed an association among participants with eGFR <60 mL·min-1·1.73 m-2, with a 14% (95% CI, 3%-27%) higher CHD risk per 5 mL·min-1·1.73 m-2 lower genetically predicted eGFR, but not for those with eGFR >105 mL·min-1·1.73 m-2. Results were not materially different after adjustment for factors associated with the eGFR genetic risk score, such as lipoprotein(a), triglycerides, hemoglobin A1c, and blood pressure. Mendelian randomization results for stroke were nonsignificant but broadly similar to those for CHD. CONCLUSIONS: In people without manifest cardiovascular disease or diabetes, mild-to-moderate kidney dysfunction is causally related to risk of CHD, highlighting the potential value of preventive approaches th
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- 2022
20. Pan-cancer analysis of pre-diagnostic blood metabolite concentrations in the European Prospective Investigation into Cancer and Nutrition.
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Breeur, M, Ferrari, P, Dossus, L, Jenab, M, Johansson, M, Rinaldi, S, Travis, RC, His, M, Key, TJ, Schmidt, JA, Overvad, K, Tjønneland, A, Kyrø, C, Rothwell, JA, Laouali, N, Severi, G, Kaaks, R, Katzke, V, Schulze, MB, Eichelmann, F, Palli, D, Grioni, S, Panico, S, Tumino, R, Sacerdote, C, Bueno-de-Mesquita, B, Olsen, KS, Sandanger, TM, Nøst, TH, Quirós, JR, Bonet, C, Barranco, MR, Chirlaque, M-D, Ardanaz, E, Sandsveden, M, Manjer, J, Vidman, L, Rentoft, M, Muller, D, Tsilidis, K, Heath, AK, Keun, H, Adamski, J, Keski-Rahkonen, P, Scalbert, A, Gunter, MJ, Viallon, V, Breeur, M, Ferrari, P, Dossus, L, Jenab, M, Johansson, M, Rinaldi, S, Travis, RC, His, M, Key, TJ, Schmidt, JA, Overvad, K, Tjønneland, A, Kyrø, C, Rothwell, JA, Laouali, N, Severi, G, Kaaks, R, Katzke, V, Schulze, MB, Eichelmann, F, Palli, D, Grioni, S, Panico, S, Tumino, R, Sacerdote, C, Bueno-de-Mesquita, B, Olsen, KS, Sandanger, TM, Nøst, TH, Quirós, JR, Bonet, C, Barranco, MR, Chirlaque, M-D, Ardanaz, E, Sandsveden, M, Manjer, J, Vidman, L, Rentoft, M, Muller, D, Tsilidis, K, Heath, AK, Keun, H, Adamski, J, Keski-Rahkonen, P, Scalbert, A, Gunter, MJ, and Viallon, V
- Abstract
BACKGROUND: Epidemiological studies of associations between metabolites and cancer risk have typically focused on specific cancer types separately. Here, we designed a multivariate pan-cancer analysis to identify metabolites potentially associated with multiple cancer types, while also allowing the investigation of cancer type-specific associations. METHODS: We analysed targeted metabolomics data available for 5828 matched case-control pairs from cancer-specific case-control studies on breast, colorectal, endometrial, gallbladder, kidney, localized and advanced prostate cancer, and hepatocellular carcinoma nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. From pre-diagnostic blood levels of an initial set of 117 metabolites, 33 cluster representatives of strongly correlated metabolites and 17 single metabolites were derived by hierarchical clustering. The mutually adjusted associations of the resulting 50 metabolites with cancer risk were examined in penalized conditional logistic regression models adjusted for body mass index, using the data-shared lasso penalty. RESULTS: Out of the 50 studied metabolites, (i) six were inversely associated with the risk of most cancer types: glutamine, butyrylcarnitine, lysophosphatidylcholine a C18:2, and three clusters of phosphatidylcholines (PCs); (ii) three were positively associated with most cancer types: proline, decanoylcarnitine, and one cluster of PCs; and (iii) 10 were specifically associated with particular cancer types, including histidine that was inversely associated with colorectal cancer risk and one cluster of sphingomyelins that was inversely associated with risk of hepatocellular carcinoma and positively with endometrial cancer risk. CONCLUSIONS: These results could provide novel insights for the identification of pathways for cancer development, in particular those shared across different cancer types.
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- 2022
21. A longitudinal evaluation of alcohol intake throughout adulthood and colorectal cancer risk
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Mayen, A, Viallon, V, Botteri, E, Proust-Lima, C, Bagnardi, V, Batista, V, Cross, A, Laouali, N, Macdonald, C, Severi, G, Katzke, V, Bergmann, M, Schulze, M, Tjonneland, A, Eriksen, A, Dahm, C, Antoniussen, C, Jakszyn, P, Sanchez, M, Amiano, P, Colorado-Yohar, S, Ardanaz, E, Travis, R, Palli, D, Sabina, S, Tumino, R, Ricceri, F, Panico, S, Bueno-de-Mesquita, B, Derksen, J, Sonestedt, E, Winkvist, A, Harlid, S, Braaten, T, Gram, I, Lukic, M, Jenab, M, Riboli, E, Freisling, H, Weiderpass, E, Gunter, M, Ferrari, P, Mayen, A, Viallon, V, Botteri, E, Proust-Lima, C, Bagnardi, V, Batista, V, Cross, A, Laouali, N, Macdonald, C, Severi, G, Katzke, V, Bergmann, M, Schulze, M, Tjonneland, A, Eriksen, A, Dahm, C, Antoniussen, C, Jakszyn, P, Sanchez, M, Amiano, P, Colorado-Yohar, S, Ardanaz, E, Travis, R, Palli, D, Sabina, S, Tumino, R, Ricceri, F, Panico, S, Bueno-de-Mesquita, B, Derksen, J, Sonestedt, E, Winkvist, A, Harlid, S, Braaten, T, Gram, I, Lukic, M, Jenab, M, Riboli, E, Freisling, H, Weiderpass, E, Gunter, M, and Ferrari, P
- Abstract
Background: Alcohol intake is an established risk factor for colorectal cancer (CRC); however, there is limited knowledge on whether changing alcohol drinking habits during adulthood modifies CRC risk. Objective: Leveraging longitudinal exposure assessments on alcohol intake at different ages, we examined the relationship between change in alcohol intake and subsequent CRC risk. Methods: Within the European Prospective Investigation into Cancer and Nutrition, changes in alcohol intake comparing follow-up with baseline assessments were investigated in relation to CRC risk. The analysis included 191,180, participants and 1530 incident CRC cases, with exclusion of the first three years of follow-up to minimize reverse causation. Trajectory profiles of alcohol intake, assessed at ages 20, 30, 40, 50 years, at baseline and during follow-up, were estimated using latent class mixed models and related to CRC risk, including 407,605 participants and 5,008 incident CRC cases. Results: Mean age at baseline was 50.2 years and the follow-up assessment occurred on average 7.1 years later. Compared to stable intake, a 12 g/day increase in alcohol intake during follow-up was positively associated with CRC risk (HR = 1.15, 95%CI 1.04, 1.25), while a 12 g/day reduction was inversely associated with CRC risk (HR = 0.86, 95%CI 0.78, 0.95). Trajectory analysis showed that compared to low alcohol intake, men who increased their alcohol intake from early- to mid- and late-adulthood by up to 30 g/day on average had significantly increased CRC risk (HR = 1.24; 95%CI 1.08, 1.42), while no associations were observed in women. Results were consistent by anatomical subsite. Conclusions: Increasing alcohol intake during mid-to-late adulthood raised CRC risk, while reduction lowered risk.
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- 2022
22. Dietary Folate Intake and Breast Cancer Risk: European Prospective Investigation Into Cancer and Nutrition
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de Batlle, J., Ferrari, P., Chajes, V., Park, J. Y., Slimani, N., McKenzie, F., Overvad, K., Roswall, N., Tjønneland, A., Boutron-Ruault, M. C., Clavel-Chapelon, F., Fagherazzi, G., Katzke, V., Kaaks, R., Bergmann, M. M., Trichopoulou, A., Lagiou, P., Trichopoulos, D., Palli, D., Sieri, S., Panico, S., Tumino, R., Vineis, P., Bueno-de-Mesquita, H. B., Peeters, P. H., Hjartåker, A., Engeset, D., Weiderpass, E., Sánchez, S., Travier, N., Sánchez, M. J., Amiano, P., Chirlaque, M. D., Barricarte Gurrea, A., Khaw, K. T., Key, T. J., Bradbury, K. E., Ericson, U., Sonestedt, E., Van Guelpen, B., Schneede, J., Riboli, E., and Romieu, I.
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- 2015
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23. Associations between dietary amino acid intakes and blood concentration levels
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Iguacel, I., Perez-Cornago, A., Van Puyvelde, H., Travis, R., Stepien, M., Scalbert, A., Casagrande, C., Weiderpass, E., Riboli, E., Schulze, M.B., Skeie, G., Bodén, S., Boeing, H., Cross, A.J., Harlid, S., Jensen, T.E., Huerta, J.M., Katzke, V., Kühn, T., Lujan-Barroso, L., Masala, G., Rodriguez-Barranco, M., Rostgaard-Hansen, A.L., van der Schouw, Y.T., Vermeulen, R., Tagliabue, G., Tjønneland, A., Trevisan, M., Ferrari, P., Gunter, M.J., Huybrechts, I., IRAS OH Epidemiology Chemical Agents, and dIRAS RA-2
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Dietary questionnaire ,Nutrition and Dietetics ,Blood levels ,Dietary intake ,Amino acids ,Critical Care and Intensive Care Medicine ,24-H dietary recall - Abstract
Background and aims: Emerging evidence suggests a role of amino acids (AAs) in the development of various diseases including renal failure, liver cirrhosis, diabetes and cancer. However, mechanistic pathways and the effects of dietary AA intakes on circulating levels and disease outcomes are unclear. We aimed to compare protein and AA intakes, with their respective blood concentrations in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Methods: Dietary protein and AA intakes were assessed via the EPIC dietary questionnaires (DQ) and 24-h dietary recalls (24-HDR). A subsample of 3768 EPIC participants who were free of cancer had blood AA concentrations measured. To investigate how circulating levels relate to their respective intakes, dietary AA intake was examined in quintiles and ANOVA tests were run. Pearson correlations were examined for continous associations between intakes and blood concentrations. Results: Dietary AA intakes (assessed with the DQ) and blood AA concentrations were not strongly correlated (−0.15 ≤ r ≤ 0.17) and the direction of the correlations depended on AA class: weak positive correlations were found for most essential AAs (isoleucine, leucine, lysine, methionine, threonine, tryptophan, and valine) and conditionally essential AAs (arginine and tyrosine), while negative associations were found for non-essential AAs. Similar results were found when using the 24-HDR. When conducting ANOVA tests for essential AAs, higher intake quintiles were linked to higher blood AA concentrations, except for histidine and phenylalanine. For non-essential AAs and glycine, an inverse relationship was observed. Conditionally-essential AAs showed mixed results. Conclusions: Weak positive correlations and dose responses were found between most essential and conditionally essential AA intakes, and blood concentrations, but not for the non-essential AAs. These results suggest that intake of dietary AA might be related to physiological AA status, particularly for the essential AAs. However, these results should be further evaluated and confirmed in large-scale prospective studies.
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- 2021
24. Dietary intake and plasma phospholipid concentrations of saturated, monounsaturated and trans fatty acids and colorectal cancer risk in the EPIC cohort
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Aglago, EK, Murphy, N, Huybrechts, I, Nicolas, G, Casagrande, C, Fedirko, V, Weiderpass, E, Rothwell, JA, Dahm, CC, Olsen, A, Tjønneland, A, Kaaks, R, Katzke, V, Schulze, MB, Masala, G, Agnoli, C, Panico, S, Tumino, R, Sacerdote, C, Bueno‐de‐Mesquita, BH, Derksen, JWG, Skeie, G, Gram, IT, Brustad, M, Jakszyn, P, Sánchez, M, Amiano, P, Huerta, JM, Ericson, U, Wennberg, M, Perez‐Cornago, A, Heath, AK, Jenab, M, Chajes, V, and Gunter, MJ
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Science & Technology ,colorectal cancer ,ASSOCIATION ,fatty acids ,DISEASE ,Oncology ,COLON ,biomarker ,1112 Oncology and Carcinogenesis ,Oncology & Carcinogenesis ,dietary intake ,Life Sciences & Biomedicine ,2 SIDES ,LIPIDS - Abstract
Epidemiologic studies examining the association between specific fatty acids and colorectal cancer (CRC) risk are inconclusive. We investigated the association between dietary estimates and plasma levels of individual and total saturated (SFA), monounsaturated (MUFA), industrial‐processed trans (iTFA), and ruminant‐sourced trans (rTFA) fatty acids, and CRC risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). Baseline fatty acid intakes were estimated in 450,112 participants (6,162 developed CRC, median follow‐up=15 years). In a nested case‐control study, plasma phospholipid fatty acids were determined by gas chromatography in 433 colon cancer cases and 433 matched controls. Multivariable‐adjusted hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (CIs) were computed using Cox and conditional logistic regression, respectively. Dietary total SFA (highest vs. lowest quintile, HRQ5vs.Q1=0.80; 95%CI:0.69‐0.92), myristic acid (HRQ5vs.Q1=0.83, 95%CI:0.74‐0.93) and palmitic acid (HRQ5vs.Q1=0.81, 95%CI:0.70‐0.93) were inversely associated with CRC risk. Plasma myristic acid was also inversely associated with colon cancer risk (highest vs. lowest quartile, ORQ4vs.Q1=0.51; 95%CI:0.32‐0.83), whereas a borderline positive association was found for plasma stearic acid (ORQ4vs.Q1=1.63; 95%CI:1.00‐2.64). Dietary total MUFA was inversely associated with colon cancer (per one‐standard deviation increment, HR1‐SD=0.92, 95%CI: 0.85‐0.98), but not rectal cancer (HR1‐SD=1.04, 95%CI:0.95‐1.15, Pheterogeneity=0.027). Dietary iTFA, and particularly elaidic acid, was positively associated with rectal cancer (HR1‐SD =1.07, 95%CI:1.02‐1.13). Our results suggest that total and individual saturated fatty acids and fatty acids of industrial origin may be relevant to the aetiology of CRC. Both dietary and plasma myristic acid levels were inversely associated with colon cancer risk, which warrants further investigation.
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- 2021
25. Plant foods, dietary fibre and risk of ischaemic heart disease in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort
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Perez-Cornago, A. Crowe, F.L. Appleby, P.N. Bradbury, K.E. Wood, A.M. Jakobsen, M.U. Johnson, L. Sacerdote, C. Steur, M. Weiderpass, E. Würtz, A.M.L. Kühn, T. Katzke, V. Trichopoulou, A. Karakatsani, A. La Vecchia, C. Masala, G. Tumino, R. Panico, S. Sluijs, I. Skeie, G. Imaz, L. Petrova, D. Quirós, J.R. Yohar, S.M.C. Jakszyn, P. Melander, O. Sonestedt, E. Andersson, J. Wennberg, M. Aune, D. Riboli, E. Schulze, M.B. Di Angelantonio, E. Wareham, N.J. Danesh, J. Forouhi, N.G. Butterworth, A.S. Key, T.J.
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food and beverages - Abstract
Background: Epidemiological evidence indicates that diets rich in plant foods are associated with a lower risk of ischaemic heart disease (IHD), but there is sparse information on fruit and vegetable subtypes and sources of dietary fibre. This study examined the associations of major plant foods, their subtypes and dietary fibre with risk of IHD in the European Prospective Investigation into Cancer and Nutrition (EPIC). Methods: We conducted a prospective analysis of 490 311 men and women without a history of myocardial infarction or stroke at recruitment (12.6 years of follow-up, n cases = 8504), in 10 European countries. Dietary intake was assessed using validated questionnaires, calibrated with 24-h recalls. Multivariable Cox regressions were used to estimate hazard ratios (HR) of IHD. Results: There was a lower risk of IHD with a higher intake of fruit and vegetables combined [HR per 200 g/day higher intake 0.94, 95% confidence interval (CI): 0.90-0.99, P-trend = 0.009], and with total fruits (per 100 g/day 0.97, 0.95-1.00, P-trend = 0.021). There was no evidence for a reduced risk for fruit subtypes, except for bananas. Risk was lower with higher intakes of nuts and seeds (per 10 g/day 0.90, 0.82-0.98, P-trend = 0.020), total fibre (per 10 g/day 0.91, 0.85-0.98, P-trend = 0.015), fruit and vegetable fibre (per 4 g/day 0.95, 0.91-0.99, P-trend = 0.022) and fruit fibre (per 2 g/day 0.97, 0.95-1.00, P-trend = 0.045). No associations were observed between vegetables, vegetables subtypes, legumes, cereals and IHD risk. Conclusions: In this large prospective study, we found some small inverse associations between plant foods and IHD risk, with fruit and vegetables combined being the most strongly inversely associated with risk. Whether these small associations are causal remains unclear. © 2020 The Author(s) 2020. Published by Oxford University Press on behalf of the International Epidemiological Association.
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- 2021
26. Genome-wide association study data reveal genetic susceptibility to chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma risk.
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Wang X., Yuan F., Hung R.J., Walsh N., Zhang H., Platz E.A., Wheeler W., Song L., Arslan A.A., Beane Freeman L.E., Bracci P., Canzian F., Du M., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Shi J., Duell E.J., Amundadottir L.T., Li D., Petersen G.M., Wolpin B.M., Risch H.A., Yu K., Klein A.P., Stolzenberg-Solomon R., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Rosendahl J., Scelo G., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Amiano P., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Chanock S.J., Fuchs C.S., Michael Gaziano J., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Katzke V., Kirsten H., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Ng K., Oberg A.L., Porta M., Rabe K.G., Real F.X., Rothman N., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., Wentzensen N., Wang X., Yuan F., Hung R.J., Walsh N., Zhang H., Platz E.A., Wheeler W., Song L., Arslan A.A., Beane Freeman L.E., Bracci P., Canzian F., Du M., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Shi J., Duell E.J., Amundadottir L.T., Li D., Petersen G.M., Wolpin B.M., Risch H.A., Yu K., Klein A.P., Stolzenberg-Solomon R., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Rosendahl J., Scelo G., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Amiano P., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Chanock S.J., Fuchs C.S., Michael Gaziano J., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Katzke V., Kirsten H., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Ng K., Oberg A.L., Porta M., Rabe K.G., Real F.X., Rothman N., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., and Wentzensen N.
- Abstract
Registry-based epidemiologic studies suggest associations between chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma (PDAC). As genetic susceptibility contributes to a large proportion of chronic inflammatory intestinal diseases, we hypothesize that the genomic regions surrounding established genome-wide associated variants for these chronic inflammatory diseases are associated with PDAC. We examined the association between PDAC and genomic regions (+500 kb) surrounding established common susceptibility variants for ulcerative colitis, Crohn's disease, inflammatory bowel disease, celiac disease, chronic pancreatitis, and primary sclerosing cholangitis. We analyzed summary statistics from genome-wide association studies data for 8,384 cases and 11,955 controls of European descent from two large consortium studies using the summary data-based adaptive rank truncated product method to examine the overall association of combined genomic regions for each inflammatory disease group. Combined genomic susceptibility regions for ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis were associated with PDAC at P values < 0.05 (0.0040, 0.0057, 0.011, and 3.4 x 10-6, respectively). After excluding the 20 PDAC susceptibility regions (+500 kb) previously identified by GWAS, the genomic regions for ulcerative colitis, Crohn disease, and inflammatory bowel disease remained associated with PDAC (P 1/4 0.0029, 0.0057, and 0.0098, respectively). Genomic regions for celiac disease (P 1/4 0.22) and primary sclerosing cholangitis (P 1/4 0.078) were not associated with PDAC. Our results support the hypothesis that genomic regions surrounding variants associated with inflammatory intestinal diseases, particularly, ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis are associated with PDAC.Copyright © 2020 American Association for Cancer Research.
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- 2021
27. Associations between genetically predicted blood protein biomarkers and pancreatic cancer risk.
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Haiman C.A., Bracci P., Katzke V., Neale R.E., Gallinger S., van Den Eeden S.K., Arslan A.A., Canzian F., Kooperberg C., Beane Freeman L.E., Scelo G., Visvanathan K., Li D., Le Marchand L., Yu H., Petersen G.M., Stolzenberg-Solomon R., Klein A.P., Cai Q., Long J., Shu X.-O., Zheng W., Wu L., Shu X., Guo X., Liu D., Bao J., Milne R.L., Giles G.G., Wu C., Du M., White E., Risch H.A., Malats N., Duell E.J., Goodman P.J., Zhu J., Haiman C.A., Bracci P., Katzke V., Neale R.E., Gallinger S., van Den Eeden S.K., Arslan A.A., Canzian F., Kooperberg C., Beane Freeman L.E., Scelo G., Visvanathan K., Li D., Le Marchand L., Yu H., Petersen G.M., Stolzenberg-Solomon R., Klein A.P., Cai Q., Long J., Shu X.-O., Zheng W., Wu L., Shu X., Guo X., Liu D., Bao J., Milne R.L., Giles G.G., Wu C., Du M., White E., Risch H.A., Malats N., Duell E.J., Goodman P.J., and Zhu J.
- Abstract
Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, with few known risk factors and biomarkers. Several blood protein biomarkers have been linked to PDAC in previous studies, but these studies have assessed only a limited number of biomarkers, usually in small samples. In this study, we evaluated associations of circulating protein levels and PDAC risk using genetic instruments. Method(s): To identify novel circulating protein biomarkers of PDAC, we studied 8,280 cases and 6,728 controls of European descent from the Pancreatic Cancer Cohort Consortium and the Pancreatic Cancer Case-Control Consortium, using genetic instruments of protein quantitative trait loci. Result(s): We observed associations between predicted concentrations of 38 proteins and PDAC risk at an FDR of < 0.05, including 23 of those proteins that showed an association even after Bonferroni correction. These include the protein encoded by ABO, which has been implicated as a potential target gene of PDAC risk variant. Eight of the identified proteins (LMA2L, TM11D, IP-10, ADH1B, STOM, TENC1, DOCK9, and CRBB2) were associated with PDAC risk after adjusting for previously reported PDAC risk variants (OR ranged from 0.79 to 1.52). Pathway enrichment analysis showed that the encoding genes for implicated proteins were significantly enriched in cancer-related pathways, such as STAT3 and IL15 production. Conclusion(s): We identified 38 candidates of protein biomarkers for PDAC risk. Impact: This study identifies novel protein biomarker candidates for PDAC, which if validated by additional studies, may contribute to the etiologic understanding of PDAC development.Copyright © 2020 American Association for Cancer Research.
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- 2021
28. Blood polyphenol concentrations and differentiated thyroid carcinoma in women from the European Prospective Investigation into Cancer and Nutrition (EPIC) study
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IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Zamora-Ros, R., Lujan-Barroso, L., Achaintre, D., Franceschi, S., Kyrø, C., Overvad, K., Tjønneland, A., Truong, T., Lecuyer, L., Boutron-Ruault, M.-C., Katzke, V., Johnson, T.S., Schulze, M.B., Trichopoulou, A., Peppa, E., La Vechia, C., Masala, G., Pala, V., Panico, S., Tumino, R., Ricceri, F., Skeie, G., Ramón Quirós, J., Rodriguez-Barranco, M., Amiano, P., Chirlaque, M.-D., Ardanaz, E., Almquist, M., Hennings, J., Vermeulen, R., Wareham, N.J., Tong, T.Y.N., Aune, D., Byrnes, G., Weiderpass, E., Scalbert, A., Rinaldi, S., Agudo, A., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Zamora-Ros, R., Lujan-Barroso, L., Achaintre, D., Franceschi, S., Kyrø, C., Overvad, K., Tjønneland, A., Truong, T., Lecuyer, L., Boutron-Ruault, M.-C., Katzke, V., Johnson, T.S., Schulze, M.B., Trichopoulou, A., Peppa, E., La Vechia, C., Masala, G., Pala, V., Panico, S., Tumino, R., Ricceri, F., Skeie, G., Ramón Quirós, J., Rodriguez-Barranco, M., Amiano, P., Chirlaque, M.-D., Ardanaz, E., Almquist, M., Hennings, J., Vermeulen, R., Wareham, N.J., Tong, T.Y.N., Aune, D., Byrnes, G., Weiderpass, E., Scalbert, A., Rinaldi, S., and Agudo, A.
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- 2021
29. Associations between dietary amino acid intakes and blood concentration levels
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IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Iguacel, I., Perez-Cornago, A., Van Puyvelde, H., Travis, R., Stepien, M., Scalbert, A., Casagrande, C., Weiderpass, E., Riboli, E., Schulze, M.B., Skeie, G., Bodén, S., Boeing, H., Cross, A.J., Harlid, S., Jensen, T.E., Huerta, J.M., Katzke, V., Kühn, T., Lujan-Barroso, L., Masala, G., Rodriguez-Barranco, M., Rostgaard-Hansen, A.L., van der Schouw, Y.T., Vermeulen, R., Tagliabue, G., Tjønneland, A., Trevisan, M., Ferrari, P., Gunter, M.J., Huybrechts, I., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Iguacel, I., Perez-Cornago, A., Van Puyvelde, H., Travis, R., Stepien, M., Scalbert, A., Casagrande, C., Weiderpass, E., Riboli, E., Schulze, M.B., Skeie, G., Bodén, S., Boeing, H., Cross, A.J., Harlid, S., Jensen, T.E., Huerta, J.M., Katzke, V., Kühn, T., Lujan-Barroso, L., Masala, G., Rodriguez-Barranco, M., Rostgaard-Hansen, A.L., van der Schouw, Y.T., Vermeulen, R., Tagliabue, G., Tjønneland, A., Trevisan, M., Ferrari, P., Gunter, M.J., and Huybrechts, I.
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- 2021
30. Circulating tryptophan metabolites and risk of colon cancer: Results from case-control and prospective cohort studies
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Papadimitriou, N., Papadimitriou, N., Gunter, M.J., Murphy, N., Gicquiau, A., Achaintre, D., Brezina, S., Gumpenberger, T., Baierl, A., Ose, J., Geijsen, A.J.M.R., van Roekel, E.H., Gsur, A., Gigic, B., Habermann, N., Ulrich, C.M., Kampman, E., Weijenberg, M.P., Ueland, P.M., Kaaks, R., Katzke, V., Krogh, V., Bueno-de-Mesquita, B., Ardanaz, E., Travis, R.C., Schulze, M.B., Sanchez, M.J., Colorado-Yohar, S.M., Weiderpass, E., Scalbert, A., Keski-Rahkonen, P., Papadimitriou, N., Papadimitriou, N., Gunter, M.J., Murphy, N., Gicquiau, A., Achaintre, D., Brezina, S., Gumpenberger, T., Baierl, A., Ose, J., Geijsen, A.J.M.R., van Roekel, E.H., Gsur, A., Gigic, B., Habermann, N., Ulrich, C.M., Kampman, E., Weijenberg, M.P., Ueland, P.M., Kaaks, R., Katzke, V., Krogh, V., Bueno-de-Mesquita, B., Ardanaz, E., Travis, R.C., Schulze, M.B., Sanchez, M.J., Colorado-Yohar, S.M., Weiderpass, E., Scalbert, A., and Keski-Rahkonen, P.
- Abstract
Dysregulation of tryptophan metabolism has been linked to colorectal tumorigenesis; however, epidemiological studies investigating tryptophan metabolites in relation to colorectal cancer risk are limited. We studied associations of plasma tryptophan, serotonin and kynurenine with colon cancer risk in two studies with cancer patients and controls, and in one prospective cohort: ColoCare Study (110 patients/153 controls), the Colorectal Cancer Study of Austria (CORSA; 46 patients/390 controls) and the European Prospective Investigation into Cancer and Nutrition (EPIC; 456 matched case-control pairs). Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for colon cancer risk. Tryptophan was inversely associated with colon cancer risk in ColoCare (OR per 1-SD = 0.44; 95% CI, 0.31-0.64) and EPIC (OR per 1-SD = 0.86; 95% CI, 0.74-0.99). Comparing detectable vs nondetectable levels, serotonin was positively associated with colon cancer in CORSA (OR = 6.39; 95% CI, 3.61-11.3) and EPIC (OR = 2.03; 95% CI, 1.20-3.40). Kynurenine was inversely associated with colon cancer in ColoCare (OR per 1-SD = 0.74; 95% CI, 0.55-0.98), positively associated in CORSA (OR per 1-SD = 1.79; 95% CI, 1.27-2.52), while no association was observed in EPIC. The kynurenine-to-tryptophan ratio was positively associated with colon cancer in ColoCare (OR per 1-SD = 1.38; 95% CI, 1.03-1.84) and CORSA (OR per 1-SD = 1.44; 95% CI, 1.06-1.96), but not in EPIC. These results suggest that higher plasma tryptophan may be associated with lower colon cancer risk, while increased serotonin may be associated with a higher risk of colon cancer. The kynurenine-to-tryptophan ratio may also reflect altered tryptophan catabolism during colon cancer development.
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- 2021
31. Dietary Intake of Advanced Glycation End Products (AGEs) and Mortality among Individuals with Colorectal Cancer
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Mao, Z, Aglago, EK, Zhao, Z, Schalkwijk, C, Jiao, L, Freisling, H, Weiderpass, E, Hughes, DJ, Eriksen, AK, Tjonneland, A, Severi, G, Rothwell, J, Boutron-Ruault, M-C, Katzke, V, Kaaks, R, Schulze, MB, Birukov, A, Krogh, V, Panico, S, Tumino, R, Ricceri, F, Bueno-de-Mesquita, HB, Vermeulen, RCH, Gram, IT, Skeie, G, Sandanger, TM, Quiros, JR, Crous-Bou, M, Sanchez, M-J, Amiano, P, Chirlaque, M-D, Barricarte Gurrea, A, Manjer, J, Johansson, I, Perez-Cornago, A, Jenab, M, Fedirko, V, Mao, Z, Aglago, EK, Zhao, Z, Schalkwijk, C, Jiao, L, Freisling, H, Weiderpass, E, Hughes, DJ, Eriksen, AK, Tjonneland, A, Severi, G, Rothwell, J, Boutron-Ruault, M-C, Katzke, V, Kaaks, R, Schulze, MB, Birukov, A, Krogh, V, Panico, S, Tumino, R, Ricceri, F, Bueno-de-Mesquita, HB, Vermeulen, RCH, Gram, IT, Skeie, G, Sandanger, TM, Quiros, JR, Crous-Bou, M, Sanchez, M-J, Amiano, P, Chirlaque, M-D, Barricarte Gurrea, A, Manjer, J, Johansson, I, Perez-Cornago, A, Jenab, M, and Fedirko, V
- Abstract
Advanced glycation end-products (AGEs) may promote oxidative stress and inflammation and have been linked to multiple chronic diseases, including cancer. However, the association of AGEs with mortality after colorectal cancer (CRC) diagnosis has not been previously investigated. Multivariable Cox proportional hazards models were used to calculate hazard ratios and corresponding 95% confidence intervals for associations between dietary intake of AGEs with CRC-specific and all-cause mortality among 5801 participant cases diagnosed with CRC in the European Prospective Investigation into Cancer and Nutrition study between 1993 and 2013. Dietary intakes of AGEs were estimated using country-specific dietary questionnaires, linked to an AGE database, that accounted for food preparation and processing. During a median of 58 months of follow-up, 2421 cases died (1841 from CRC). Individually or combined, dietary intakes of AGEs were not associated with all-cause and CRC-specific mortality among cases. However, there was a suggestion for a positive association between AGEs and all-cause or CRC-specific mortality among CRC cases without type II diabetes (all-cause, Pinteraction = 0.05) and CRC cases with the longest follow-up between recruitment and cancer diagnosis (CRC-specific, Pinteraction = 0.003; all-cause, Pinteraction = 0.01). Our study suggests that pre-diagnostic dietary intakes of AGEs were not associated with CRC-specific or all-cause mortality among CRC patients. Further investigations using biomarkers of AGEs and stratifying by sex, diabetes status, and timing of exposure to AGEs are warranted.
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- 2021
32. Urinary Concentrations of (+)-Catechin and (-)-Epicatechin as Biomarkers of Dietary Intake of Flavan-3-ols in the European Prospective Investigation into Cancer and Nutrition (EPIC) Study
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Almanza-Aguilera, E, Ceballos-Sanchez, D, Achaintre, D, Rothwell, JA, Laouali, N, Severi, G, Katzke, V, Johnson, T, Schulze, MB, Palli, D, Gargano, G, de Magistris, MS, Tumino, R, Sacerdote, C, Scalbert, A, Zamora-Ros, R, Almanza-Aguilera, E, Ceballos-Sanchez, D, Achaintre, D, Rothwell, JA, Laouali, N, Severi, G, Katzke, V, Johnson, T, Schulze, MB, Palli, D, Gargano, G, de Magistris, MS, Tumino, R, Sacerdote, C, Scalbert, A, and Zamora-Ros, R
- Abstract
This study examines the correlation of acute and habitual dietary intake of flavan-3-ol monomers, proanthocyanidins, theaflavins, and their main food sources with the urinary concentrations of (+)-catechin and (-)-epicatechin in the European Prospective Investigation into Cancer and Nutrition study (EPIC). Participants (N = 419, men and women) provided 24-h urine samples and completed a 24-h dietary recall (24-HDR) on the same day. Acute and habitual dietary data were collected using a standardized 24-HDR software and a validated dietary questionnaire, respectively. Intake of flavan-3-ols was estimated using the Phenol-Explorer database. Concentrations of (+)-catechin and (-)-epicatechin in 24-h urine were analyzed using tandem mass spectrometry after enzymatic deconjugation. Simple and partial Spearman's correlations showed that urinary concentrations of (+)-catechin, (-)-epicatechin and their sum were more strongly correlated with acute than with habitual intake of individual and total monomers (acute rpartial = 0.13-0.54, p < 0.05; and habitual rpartial = 0.14-0.28, p < 0.01), proanthocyanidins (acute rpartial = 0.24-0.49, p < 0.001; and habitual rpartial = 0.10-0.15, p < 0.05), theaflavins (acute rpartial = 0.22-0.31, p < 0.001; and habitual rpartial = 0.20-0.26, p < 0.01), and total flavan-3-ols (acute rpartial = 0.40-0.48, p < 0.001; and habitual rpartial = 0.23-0.33, p < 0.001). Similarly, urinary concentrations of flavan-3-ols were weakly correlated with both acute (rpartial = 0.12-0.30, p < 0.05) and habitual intake (rpartial = 0.10-0.27, p < 0.05) of apple and pear, stone fruits, berries, chocolate and chocolate products, cakes and pastries, tea, herbal tea, wine, red wine, and beer and cider. Moreover, all comparable correlations were stronger for urinary (-)-epicatechin than for (+)-catechin. In conclusion, our data support the use of urinary concentrations of (+)-catechin and (-)-epicatechin, especially as short-term nutritional biomarkers of dietary ca
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- 2021
33. Lifestyle correlates of eight breast cancer-related metabolites: a cross-sectional study within the EPIC cohort
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His, M, Viallon, V, Dossus, L, Schmidt, JA, Travis, RC, Gunter, MJ, Overvad, K, Kyro, C, Tjonneland, A, Lecuyer, L, Rothwell, JA, Severi, G, Johnson, T, Katzke, V, Schulze, MB, Masala, G, Sieri, S, Panico, S, Tumino, R, Macciotta, A, Boer, JMA, Monninkhof, EM, Olsen, KS, Nost, TH, Sandanger, TM, Agudo, A, Sanchez, M-J, Amiano, P, Colorado-Yohar, SM, Ardanaz, E, Vidman, L, Winkvist, A, Heath, AK, Weiderpass, E, Huybrechts, I, Rinaldi, S, His, M, Viallon, V, Dossus, L, Schmidt, JA, Travis, RC, Gunter, MJ, Overvad, K, Kyro, C, Tjonneland, A, Lecuyer, L, Rothwell, JA, Severi, G, Johnson, T, Katzke, V, Schulze, MB, Masala, G, Sieri, S, Panico, S, Tumino, R, Macciotta, A, Boer, JMA, Monninkhof, EM, Olsen, KS, Nost, TH, Sandanger, TM, Agudo, A, Sanchez, M-J, Amiano, P, Colorado-Yohar, SM, Ardanaz, E, Vidman, L, Winkvist, A, Heath, AK, Weiderpass, E, Huybrechts, I, and Rinaldi, S
- Abstract
BACKGROUND: Metabolomics is a promising molecular tool for identifying novel etiological pathways leading to cancer. In an earlier prospective study among pre- and postmenopausal women not using exogenous hormones, we observed a higher risk of breast cancer associated with higher blood concentrations of one metabolite (acetylcarnitine) and a lower risk associated with higher blood concentrations of seven others (arginine, asparagine, phosphatidylcholines (PCs) aa C36:3, ae C34:2, ae C36:2, ae C36:3, and ae C38:2). METHODS: To identify determinants of these breast cancer-related metabolites, we conducted a cross-sectional analysis to identify their lifestyle and anthropometric correlates in 2358 women, who were previously included as controls in case-control studies nested within the European Prospective Investigation into Cancer and Nutrition cohort and not using exogenous hormones at blood collection. Associations of each metabolite concentration with 42 variables were assessed using linear regression models in a discovery set of 1572 participants. Significant associations were evaluated in a validation set (n = 786). RESULTS: For the metabolites previously associated with a lower risk of breast cancer, concentrations of PCs ae C34:2, C36:2, C36:3, and C38:2 were negatively associated with adiposity and positively associated with total and saturated fat intakes. PC ae C36:2 was also negatively associated with alcohol consumption and positively associated with two scores reflecting adherence to a healthy lifestyle. Asparagine concentration was negatively associated with adiposity. Arginine and PC aa C36:3 concentrations were not associated to any of the factors examined. For the metabolite previously associated with a higher risk of breast cancer, acetylcarnitine, a positive association with age was observed. CONCLUSIONS: These associations may indicate possible mechanisms underlying associations between lifestyle and anthropometric factors, and risk of breast cance
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- 2021
34. Prediagnostic Blood Selenium Status and Mortality among Patients with Colorectal Cancer in Western European Populations
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Baker, JR, Umesh, S, Jenab, M, Schomburg, L, Tjonneland, A, Olsen, A, Boutron-Ruault, M-C, Rothwell, JA, Severi, G, Katzke, V, Johnson, T, Schulze, MB, Masala, G, Agnoli, C, Simeon, V, Tumino, R, Bueno-de-Mesquita, HB, Gram, IT, Skeie, G, Bonet, C, Rodriguez-Barranco, M, Houerta, JM, Gylling, B, Van Guelpen, B, Perez-Cornago, A, Aglago, E, Freisling, H, Weiderpass, E, Cross, AJ, Heath, AK, Hughes, DJ, Fedirko, V, Baker, JR, Umesh, S, Jenab, M, Schomburg, L, Tjonneland, A, Olsen, A, Boutron-Ruault, M-C, Rothwell, JA, Severi, G, Katzke, V, Johnson, T, Schulze, MB, Masala, G, Agnoli, C, Simeon, V, Tumino, R, Bueno-de-Mesquita, HB, Gram, IT, Skeie, G, Bonet, C, Rodriguez-Barranco, M, Houerta, JM, Gylling, B, Van Guelpen, B, Perez-Cornago, A, Aglago, E, Freisling, H, Weiderpass, E, Cross, AJ, Heath, AK, Hughes, DJ, and Fedirko, V
- Abstract
A higher selenium (Se) status has been shown to be associated with lower risk for colorectal cancer (CRC), but the importance of Se in survival after CRC diagnosis is not well studied. The associations of prediagnostic circulating Se status (as indicated by serum Se and selenoprotein P (SELENOP) measurements) with overall and CRC-specific mortality were estimated using multivariable Cox proportional hazards regression among 995 CRC cases (515 deaths, 396 from CRC) in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Se and SELENOP serum concentrations were measured on average 46 months before CRC diagnosis. Median follow-up time was 113 months. Participants with Se concentrations in the highest quintile (≥100 µg/L) had a multivariable-adjusted hazard ratio (HR) of 0.73 (95% CI: 0.52-1.02; Ptrend = 0.06) for CRC-specific mortality and 0.77 (95% CI: 0.57-1.03; Ptrend = 0.04) for overall mortality, compared with the lowest quintile (≤67.5 µg/L). Similarly, participants with SELENOP concentrations in the highest (≥5.07 mg/L) compared with the lowest quintile (≤3.53 mg/L) had HRs of 0.89 (95% CI: 0.64-1.24; Ptrend = 0.39) for CRC-specific mortality and 0.83 (95% CI: 0.62-1.11; Ptrend = 0.17) for overall mortality. Higher prediagnostic exposure to Se within an optimal concentration (100-150 µg/L) might be associated with improved survival among CRC patients, although our results were not statistically significant and additional studies are needed to confirm this potential association. Our findings may stimulate further research on selenium's role in survival among CRC patients especially among those residing in geographic regions with suboptimal Se availability.
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- 2021
35. SCORE2 risk prediction algorithms: new models to estimate 10-year risk of cardiovascular disease in Europe
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Achenbach, S, Aleksandrova, K, Amiano, P, San Sebastian, D, Amouyel, P, Andersson, J, Bakker, S, Da Providencia Costa, R, Beulens, J, Blaha, M, Bobak, M, Boer, J, Bonet, C, Bonnet, F, Boutron-Ruault, M, Braaten, T, Brenner, H, Brunner, F, Brunner, E, Brunström, M, Buring, J, Butterworth, A, Capkova, N, Cesana, G, Chrysohoou, C, Colorado-Yohar, S, Cook, N, Cooper, C, Dahm, C, Davidson, K, Dennison, E, Di Castelnuovo, A, Donfrancesco, C, Dörr, M, Doryńska, A, Eliasson, M, Engström, G, Ferrari, P, Ferrario, M, Ford, I, Fu, M, Gansevoort, R, Giampaoli, S, Gillum, R, Gómez de la Cámara, A, Grassi, G, Hansson, P, Huculeci, R, Hveem, K, Iacoviello, L, Ikram, M, Jørgensen, T, Joseph, B, Jousilahti, P, Wouter Jukema, J, Kaaks, R, Katzke, V, Kavousi, M, Kiechl, S, Klotsche, J, König, W, Kronmal, R, Kubinova, R, Kucharska-Newton, A, Läll, K, Lehmann, N, Leistner, D, Linneberg, A, Pablos, D, Lorenz, T, Lu, W, Luksiene, D, Lyngbakken, M, Magnussen, C, Malyutina, S, Ibañez, A, Masala, G, Mathiesen, E, Matsushita, K, Meade, T, Melander, O, Meyer, H, Moons, K, Moreno-Iribas, C, Muller, D, Münzel, T, Nikitin, Y, Nordestgaard, B, Omland, T, Onland, C, Overvad, K, Packard, C, Pająk, A, Palmieri, L, Panagiotakos, D, Panico, S, Perez-Cornago, A, Peters, A, Pietilä, A, Pikhart, H, Psaty, B, Quarti-Trevano, F, Garcia, J, Riboli, E, Ridker, P, Rodriguez, B, Rodriguez-Barranco, M, Rosengren, A, Roussel, R, Sacerdote, C, S, S, Sattar, N, Schiborn, C, Schmidt, B, Schöttker, B, Schulze, M, Schwartz, J, Selmer, R, Shea, S, Shipley, M, Sieri, S, Söderberg, S, Sofat, R, Tamosiunas, A, Thorand, B, Tillmann, T, Tjønneland, A, Tong, T, Trichopoulou, A, Tumino, R, Tunstall-Pedoe, H, Tybjaerg-Hansen, A, Tzoulaki, J, van der Heijden, A, van der Schouw, Y, Verschuren, W, Völzke, H, Waldeyer, C, Wareham, N, Weiderpass, E, Weidinger, F, Wild, P, Willeit, J, Willeit, P, Wilsgaard, T, Woodward, M, Zeller, T, Zhang, D, Zhou, B, Bakker, SJL, Da Providencia Costa, RB, Beulens, JWJ, Boer, JMA, Boutron-Ruault, MC, Brunner, EJ, Butterworth, AS, Cook, NR, Dahm, CC, Gansevoort, RT, Gillum, RF, Hansson, PO, Ikram, MK, Kronmal, RA, Pablos, DL, Malyutina, So, Ibañez, AM, Mathiesen, EB, Meade, TW, Meyer, HE, Moons, KGM, Nordestgaard, BG, Psaty, BM, Garcia, JRQ, Ridker, PM, C Sans, Schwartz, JE, Selmer, RM, Shipley, MJ, Tong, TYN, van der Schouw, YT, Verschuren, WMM, Wareham, NJ, Achenbach, S, Aleksandrova, K, Amiano, P, San Sebastian, D, Amouyel, P, Andersson, J, Bakker, S, Da Providencia Costa, R, Beulens, J, Blaha, M, Bobak, M, Boer, J, Bonet, C, Bonnet, F, Boutron-Ruault, M, Braaten, T, Brenner, H, Brunner, F, Brunner, E, Brunström, M, Buring, J, Butterworth, A, Capkova, N, Cesana, G, Chrysohoou, C, Colorado-Yohar, S, Cook, N, Cooper, C, Dahm, C, Davidson, K, Dennison, E, Di Castelnuovo, A, Donfrancesco, C, Dörr, M, Doryńska, A, Eliasson, M, Engström, G, Ferrari, P, Ferrario, M, Ford, I, Fu, M, Gansevoort, R, Giampaoli, S, Gillum, R, Gómez de la Cámara, A, Grassi, G, Hansson, P, Huculeci, R, Hveem, K, Iacoviello, L, Ikram, M, Jørgensen, T, Joseph, B, Jousilahti, P, Wouter Jukema, J, Kaaks, R, Katzke, V, Kavousi, M, Kiechl, S, Klotsche, J, König, W, Kronmal, R, Kubinova, R, Kucharska-Newton, A, Läll, K, Lehmann, N, Leistner, D, Linneberg, A, Pablos, D, Lorenz, T, Lu, W, Luksiene, D, Lyngbakken, M, Magnussen, C, Malyutina, S, Ibañez, A, Masala, G, Mathiesen, E, Matsushita, K, Meade, T, Melander, O, Meyer, H, Moons, K, Moreno-Iribas, C, Muller, D, Münzel, T, Nikitin, Y, Nordestgaard, B, Omland, T, Onland, C, Overvad, K, Packard, C, Pająk, A, Palmieri, L, Panagiotakos, D, Panico, S, Perez-Cornago, A, Peters, A, Pietilä, A, Pikhart, H, Psaty, B, Quarti-Trevano, F, Garcia, J, Riboli, E, Ridker, P, Rodriguez, B, Rodriguez-Barranco, M, Rosengren, A, Roussel, R, Sacerdote, C, S, S, Sattar, N, Schiborn, C, Schmidt, B, Schöttker, B, Schulze, M, Schwartz, J, Selmer, R, Shea, S, Shipley, M, Sieri, S, Söderberg, S, Sofat, R, Tamosiunas, A, Thorand, B, Tillmann, T, Tjønneland, A, Tong, T, Trichopoulou, A, Tumino, R, Tunstall-Pedoe, H, Tybjaerg-Hansen, A, Tzoulaki, J, van der Heijden, A, van der Schouw, Y, Verschuren, W, Völzke, H, Waldeyer, C, Wareham, N, Weiderpass, E, Weidinger, F, Wild, P, Willeit, J, Willeit, P, Wilsgaard, T, Woodward, M, Zeller, T, Zhang, D, Zhou, B, Bakker, SJL, Da Providencia Costa, RB, Beulens, JWJ, Boer, JMA, Boutron-Ruault, MC, Brunner, EJ, Butterworth, AS, Cook, NR, Dahm, CC, Gansevoort, RT, Gillum, RF, Hansson, PO, Ikram, MK, Kronmal, RA, Pablos, DL, Malyutina, So, Ibañez, AM, Mathiesen, EB, Meade, TW, Meyer, HE, Moons, KGM, Nordestgaard, BG, Psaty, BM, Garcia, JRQ, Ridker, PM, C Sans, Schwartz, JE, Selmer, RM, Shipley, MJ, Tong, TYN, van der Schouw, YT, Verschuren, WMM, and Wareham, NJ
- Abstract
Aims: The aim of this study was to develop, validate, and illustrate an updated prediction model (SCORE2) to estimate 10-year fatal and non-fatal cardiovascular disease (CVD) risk in individuals without previous CVD or diabetes aged 40-69 years in Europe. Methods and results : We derived risk prediction models using individual-participant data from 45 cohorts in 13 countries (677 684 individuals, 30 121 CVD events). We used sex-specific and competing risk-adjusted models, including age, smoking status, systolic blood pressure, and total- and HDL-cholesterol. We defined four risk regions in Europe according to country-specific CVD mortality, recalibrating models to each region using expected incidences and risk factor distributions. Region-specific incidence was estimated using CVD mortality and incidence data on 10 776 466 individuals. For external validation, we analysed data from 25 additional cohorts in 15 European countries (1 133 181 individuals, 43 492 CVD events). After applying the derived risk prediction models to external validation cohorts, C-indices ranged from 0.67 (0.65-0.68) to 0.81 (0.76-0.86). Predicted CVD risk varied several-fold across European regions. For example, the estimated 10-year CVD risk for a 50-year-old smoker, with a systolic blood pressure of 140 mmHg, total cholesterol of 5.5 mmol/L, and HDL-cholesterol of 1.3 mmol/L, ranged from 5.9% for men in low-risk countries to 14.0% for men in very high-risk countries, and from 4.2% for women in low-risk countries to 13.7% for women in very high-risk countries. Conclusion : SCORE2-a new algorithm derived, calibrated, and validated to predict 10-year risk of first-onset CVD in European populations-enhances the identification of individuals at higher risk of developing CVD across Europe.
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- 2021
36. Genetic determinants of telomere length and risk of pancreatic cancer: A PANDoRA study
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Campa, D, Matarazzi, M, Greenhalf, W, Bijlsma, M, Saum, K-U, Pasquali, C, Van Laarhoven, H, Szentesi, A, Federici, F, Vodicka, P, Funel, N, Pezzilli, R, Bueno-De-Mesquita, HB, Vodickova, L, Basso, D, Obazee, O, Hackert, T, Soucek, P, Cuk, K, Kaiser, J, Sperti, C, Lovecek, M, Capurso, G, Mohelnikova-Duchonova, B, Khaw, K-T, König, A-K, Kupcinskas, J, Kaaks, R, Bambi, F, Archibugi, L, Mambrini, A, Cavestro, GM, Landi, S, Hegyi, P, Izbicki, JR, Gioffreda, D, Zambon, CF, Tavano, F, Talar-Wojnarowska, R, Jamroziak, K, Key, TJ, Fave, GD, Strobel, O, Jonaitis, L, Andriulli, A, Lawlor, RT, Pirozzi, F, Katzke, V, Valsuani, C, Vashist, YK, Brenner, H, Canzian, F, Campa, D., Matarazzi, M., Greenhalf, W., Bijlsma, M., Saum, K. -U., Pasquali, C., van Laarhoven, H., Szentesi, A., Federici, F., Vodicka, P., Funel, N., Pezzilli, R., Bueno-de-Mesquita, H. B., Vodickova, L., Basso, D., Obazee, O., Hackert, T., Soucek, P., Cuk, K., Kaiser, J., Sperti, C., Lovecek, M., Capurso, G., Mohelnikova-Duchonova, B., Khaw, K. -T., Konig, A. -K., Kupcinskas, J., Kaaks, R., Bambi, F., Archibugi, L., Mambrini, A., Cavestro, G. M., Landi, S., Hegyi, P., Izbicki, J. R., Gioffreda, D., Zambon, C. F., Tavano, F., Talar-Wojnarowska, R., Jamroziak, K., Key, T. J., Fave, G. D., Strobel, O., Jonaitis, L., Andriulli, A., Lawlor, R. T., Pirozzi, F., Katzke, V., Valsuani, C., Vashist, Y. K., Brenner, H., Canzian, F., Center of Experimental and Molecular Medicine, CCA - Cancer biology and immunology, Radiotherapy, Oncology, and AGEM - Re-generation and cancer of the digestive system
- Subjects
Male ,Cancer Research ,pancreatic ductal adenocarcinoma ,Polymorphism, Single Nucleotide ,lymphocyte telomere length ,genetic polymorphisms ,association ,Mendelian randomization ,Oncology ,Humans ,genetic polymorphism ,Lymphocytes ,Telomerase ,Telomere Shortening ,Aged ,Pancreatic Neoplasm ,Ribonucleoprotein ,Middle Aged ,Telomere ,Pancreatic Neoplasms ,Europe ,Ribonucleoproteins ,Case-Control Studies ,Female ,Lymphocyte ,Case-Control Studie ,Carcinoma, Pancreatic Ductal ,Genome-Wide Association Study ,Human - Abstract
Telomere deregulation is a hallmark of cancer. Telomere length measured in lymphocytes (LTL) has been shown to be a risk marker for several cancers. For pancreatic ductal adenocarcinoma (PDAC) consensus is lacking whether risk is associated with long or short telomeres. Mendelian randomization approaches have shown that a score built from SNPs associated with LTL could be used as a robust risk marker. We explored this approach in a large scale study within the PANcreatic Disease ReseArch (PANDoRA) consortium. We analyzed 10 SNPs (ZNF676-rs409627, TERT-rs2736100, CTC1-rs3027234, DHX35-rs6028466, PXK-rs6772228, NAF1-rs7675998, ZNF208-rs8105767, OBFC1-rs9420907, ACYP2-rs11125529 and TERC-rs10936599) alone and combined in a LTL genetic score (“teloscore”, which explains 2.2% of the telomere variability) in relation to PDAC risk in 2,374 cases and 4,326 controls. We identified several associations with PDAC risk, among which the strongest were with the TERT-rs2736100 SNP (OR = 1.54; 95%CI 1.35–1.76; p = 1.54 × 10 −10 ) and a novel one with the NAF1-rs7675998 SNP (OR = 0.80; 95%CI 0.73–0.88; p = 1.87 × 10 −6 , p trend = 3.27 × 10 −7 ). The association of short LTL, measured by the teloscore, with PDAC risk reached genome-wide significance (p = 2.98 × 10 −9 for highest vs. lowest quintile; p = 1.82 × 10 −10 as a continuous variable). In conclusion, we present a novel genome-wide candidate SNP for PDAC risk (TERT-rs2736100), a completely new signal (NAF1-rs7675998) approaching genome-wide significance and we report a strong association between the teloscore and risk of pancreatic cancer, suggesting that telomeres are a potential risk factor for pancreatic cancer.
- Published
- 2019
37. Polyphenol intake and differentiated thyroid cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort
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Zamora-Ros, R., Cayssials, V., Franceschi, S., Kyrø, C., Weiderpass, E., Hennings, J., Sandström, M., Tjønneland, A., Olsen, A., Overvad, K., Boutron-Ruault, M.-C., Truong, T., Mancini, F.R., Katzke, V., Kühn, T., Boeing, H., Trichopoulou, A., Karakatsani, A., Martimianaki, G., Palli, D., Krogh, V., Panico, S., Tumino, R., Sacerdote, C., Lasheras, C., Rodríguez-Barranco, M., Amiano, P., Colorado-Yohar, S.M., Ardanaz, E., Almquist, M., Ericson, U., Bueno-de-Mesquita, H.B., Vermeulen, R., Byrnes, G., Scalbert, A., Agudo, A., Rinaldi, S., IRAS OH Epidemiology Chemical Agents, and dIRAS RA-2
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flavonoids ,thyroid cancer ,cohort ,EPIC ,intake ,polyphenols - Abstract
Polyphenols are bioactive compounds with several anticarcinogenic activities; however, human data regarding associations with thyroid cancer (TC) is still negligible. Our aim was to evaluate the association between intakes of total, classes and subclasses of polyphenols and risk of differentiated TC and its main subtypes, papillary and follicular, in a European population. The European Prospective Investigation into Cancer and Nutrition cohort included 476,108 men and women from 10 European countries. During a mean follow-up of 14 years, there were 748 incident differentiated TC cases, including 601 papillary and 109 follicular tumors. Polyphenol intake was estimated at baseline using validated center/country-specific dietary questionnaires and the Phenol-Explorer database. In multivariable-adjusted Cox regression models, no association between total polyphenol and the risks of overall differentiated TC (HRQ4 vs. Q1 = 0.99, 95% confidence interval [CI] 0.77–1.29), papillary (HRQ4 vs. Q1 = 1.06, 95% CI 0.80–1.41) or follicular TC (HRQ4 vs. Q1 = 1.10, 95% CI 0.55–2.22) were found. No associations were observed either for flavonoids, phenolic acids or the rest of classes and subclasses of polyphenols. After stratification by body mass index (BMI), an inverse association between the intake of polyphenols (p-trend = 0.019) and phenolic acids (p-trend = 0.007) and differentiated TC risk in subjects with BMI ≥ 25 was observed. In conclusion, our study showed no associations between dietary polyphenol intake and differentiated TC risk; although further studies are warranted to investigate the potential protective associations in overweight and obese individuals.
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- 2020
38. Selbstberichtete Krebserkrankungen in der NAKO Gesundheitsstudie: Erfassungsmethoden und erste Ergebnisse [Self-reported cancer in the German National Cohort (NAKO Gesundheitsstudie): assessment methods and first results]
- Author
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Nimptsch, K., Jaeschke, L., Chang-Claude, J., Kaaks, R., Katzke, V., Michels, K.B., Franzke, C.W., Obi, N., Becher, H., Kuß, O., Schikowski, T., Schulze, M.B., Gastell, S., Hoffmann, W., Schipf, S., Ahrens, W., Günther, K., Krist, L., Keil, T., Jöckel, K.H., Schmidt, B., Brenner, H., Holleczek, B., Fischer, B., Leitzmann, M., Lieb, W., Berger, K., Krause, G., Löffler, M., Schmidt-Pokrzywniak, A., Mikolajczyk, R., Linseisen, J., Greiser, K.H., and Pischon, T.
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Cardiovascular and Metabolic Diseases - Abstract
BACKGROUND: In the German National Cohort (NAKO Gesundheitsstudie), the largest prospective cohort study in Germany, data on self-reported cancer diagnoses are now available for the first half of participants. OBJECTIVES: Description of the methods to assess self-reported cancer diagnoses and type of cancer in the NAKO and presentation of first results. MATERIALS AND METHODS: In a computer-assisted, standardized personal interview, 101,787 participants (54,526 women, 47,261 men) were asked whether they had ever been diagnosed with cancer (malignant tumors including in situ) by a physician and how many cancer diagnoses they had. The type of cancer was classified with a list. Absolute and relative frequencies of self-reported cancer diagnoses and types of cancer were calculated and compared with cancer registry data. RESULTS: A physician-diagnosed cancer was reported by 9.4% of women and 7.0% of men. Of the participants who reported a cancer diagnosis, 88.3% reported to have had only one cancer diagnosis. In women, the most frequent malignancies were breast cancer, cervical cancer, and melanoma. In men, the most frequent malignancies were prostate cancer, melanoma, and colorectal cancer. Comparing the frequencies of cancer diagnoses reported by 45- to 74-year-old NAKO participants within the last five years to cancer registry-based 5‑year prevalences, most types of cancer were less frequent in the NAKO, with the exception of melanoma in men and women, cervical cancer and liver cancer in women, and bladder cancer and breast cancer in men. CONCLUSIONS: The NAKO is a rich data basis for future investigations of incident cancer.
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- 2020
39. Plasma polyphenols associated with lower high-sensitivity C-reactive protein concentrations: A cross-sectional study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort
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Harms, L.M., Scalbert, A., Zamora-Ros, R., Rinaldi, S., Jenab, M., Murphy, N., Achaintre, D., Tjønneland, A., Olsen, A., Overvad, K., Romana Mancini, F., Mahamat-Saleh, Y., Boutron-Ruault, M.-C., Kühn, T., Katzke, V., Trichopoulou, A., Martimianaki, G., Karakatsani, A., Palli, D., Panico, S., Sieri, S., Tumino, R., Sacerdote, C., Bueno-De-Mesquita, B., Vermeulen, R.C.H., Weiderpass, E., Nøst, T.H., Lasheras, C., Rodríguez-Barranco, M., Huerta, J.M., Barricarte, A., Dorronsoro, M., Hultdin, J., Gunter, M., Riboli, E., Aleksandrova, K., IRAS OH Epidemiology Chemical Agents, and dIRAS RA-2
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Plasma measurements ,Inflammation ,Chronic diseases ,Polyphenols ,C-reactive protein - Abstract
Experimental studies have reported on the anti-inflammatory properties of polyphenols. However, results from epidemiological investigations have been inconsistent and especially studies using biomarkers for assessment of polyphenol intake have been scant. We aimed to characterise the association between plasma concentrations of thirty-five polyphenol compounds and low-grade systemic inflammation state as measured by high-sensitivity C-reactive protein (hsCRP). A cross-sectional data analysis was performed based on 315 participants in the European Prospective Investigation into Cancer and Nutrition cohort with available measurements of plasma polyphenols and hsCRP. In logistic regression analysis, the OR and 95 % CI of elevated serum hsCRP (>3 mg/l) were calculated within quartiles and per standard deviation higher level of plasma polyphenol concentrations. In a multivariable-adjusted model, the sum of plasma concentrations of all polyphenols measured (per standard deviation) was associated with 29 (95 % CI 50, 1) % lower odds of elevated hsCRP. In the class of flavonoids, daidzein was inversely associated with elevated hsCRP (OR 0·66, 95 % CI 0·46, 0·96). Among phenolic acids, statistically significant associations were observed for 3,5-dihydroxyphenylpropionic acid (OR 0·58, 95 % CI 0·39, 0·86), 3,4-dihydroxyphenylpropionic acid (OR 0·63, 95 % CI 0·46, 0·87), ferulic acid (OR 0·65, 95 % CI 0·44, 0·96) and caffeic acid (OR 0·69, 95 % CI 0·51, 0·93). The odds of elevated hsCRP were significantly reduced for hydroxytyrosol (OR 0·67, 95 % CI 0·48, 0·93). The present study showed that polyphenol biomarkers are associated with lower odds of elevated hsCRP. Whether diet rich in bioactive polyphenol compounds could be an effective strategy to prevent or modulate deleterious health effects of inflammation should be addressed by further well-powered longitudinal studies.
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- 2020
40. Plasma polyphenols associated with lower high-sensitivity C-reactive protein concentrations: A cross-sectional study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort
- Author
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Harms, L.M. Scalbert, A. Zamora-Ros, R. Rinaldi, S. Jenab, M. Murphy, N. Achaintre, D. Tjønneland, A. Olsen, A. Overvad, K. Romana Mancini, F. Mahamat-Saleh, Y. Boutron-Ruault, M.-C. Kühn, T. Katzke, V. Trichopoulou, A. Martimianaki, G. Karakatsani, A. Palli, D. Panico, S. Sieri, S. Tumino, R. Sacerdote, C. Bueno-De-Mesquita, B. Vermeulen, R.C.H. Weiderpass, E. Nøst, T.H. Lasheras, C. Rodríguez-Barranco, M. Huerta, J.M. Barricarte, A. Dorronsoro, M. Hultdin, J. Schmidt, J.A. Gunter, M. Riboli, E. Aleksandrova, K.
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food and beverages - Abstract
Experimental studies have reported on the anti-inflammatory properties of polyphenols. However, results from epidemiological investigations have been inconsistent and especially studies using biomarkers for assessment of polyphenol intake have been scant. We aimed to characterise the association between plasma concentrations of thirty-five polyphenol compounds and low-grade systemic inflammation state as measured by high-sensitivity C-reactive protein (hsCRP). A cross-sectional data analysis was performed based on 315 participants in the European Prospective Investigation into Cancer and Nutrition cohort with available measurements of plasma polyphenols and hsCRP. In logistic regression analysis, the OR and 95 % CI of elevated serum hsCRP (>3 mg/l) were calculated within quartiles and per standard deviation higher level of plasma polyphenol concentrations. In a multivariable-adjusted model, the sum of plasma concentrations of all polyphenols measured (per standard deviation) was associated with 29 (95 % CI 50, 1) % lower odds of elevated hsCRP. In the class of flavonoids, daidzein was inversely associated with elevated hsCRP (OR 0·66, 95 % CI 0·46, 0·96). Among phenolic acids, statistically significant associations were observed for 3,5-dihydroxyphenylpropionic acid (OR 0·58, 95 % CI 0·39, 0·86), 3,4-dihydroxyphenylpropionic acid (OR 0·63, 95 % CI 0·46, 0·87), ferulic acid (OR 0·65, 95 % CI 0·44, 0·96) and caffeic acid (OR 0·69, 95 % CI 0·51, 0·93). The odds of elevated hsCRP were significantly reduced for hydroxytyrosol (OR 0·67, 95 % CI 0·48, 0·93). The present study showed that polyphenol biomarkers are associated with lower odds of elevated hsCRP. Whether diet rich in bioactive polyphenol compounds could be an effective strategy to prevent or modulate deleterious health effects of inflammation should be addressed by further well-powered longitudinal studies. © The Authors 2019.
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- 2020
41. 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
42. Healthy lifestyle and the risk of pancreatic cancer in the EPIC study
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Naudin, S. Viallon, V. Hashim, D. Freisling, H. Jenab, M. Weiderpass, E. Perrier, F. McKenzie, F. Bueno-de-Mesquita, H.B. Olsen, A. Tjønneland, A. Dahm, C.C. Overvad, K. Mancini, F.R. Rebours, V. Boutron-Ruault, M.-C. Katzke, V. Kaaks, R. Bergmann, M. Boeing, H. Peppa, E. Karakatsani, A. Trichopoulou, A. Pala, V. Masala, G. Panico, S. Tumino, R. Sacerdote, C. May, A.M. van Gils, C.H. Rylander, C. Borch, K.B. Chirlaque López, M.D. Sánchez, M.-J. Ardanaz, E. Quirós, J.R. Amiano Exezarreta, P. Sund, M. Drake, I. Regnér, S. Travis, R.C. Wareham, N. Aune, D. Riboli, E. Gunter, M.J. Duell, E.J. Brennan, P. Ferrari, P.
- Abstract
Pancreatic cancer (PC) is a highly fatal cancer with currently limited opportunities for early detection and effective treatment. Modifiable factors may offer pathways for primary prevention. In this study, the association between the Healthy Lifestyle Index (HLI) and PC risk was examined. Within the European Prospective Investigation into Cancer and Nutrition cohort, 1113 incident PC (57% women) were diagnosed from 400,577 participants followed-up for 15 years (median). HLI scores combined smoking, alcohol intake, dietary exposure, physical activity and, in turn, overall and central adiposity using BMI (HLIBMI) and waist-to-hip ratio (WHR, HLIWHR), respectively. High values of HLI indicate adherence to healthy behaviors. Cox proportional hazard models with age as primary time variable were used to estimate PC hazard ratios (HR) and 95% confidence intervals (CI). Sensitivity analyses were performed by excluding, in turn, each factor from the HLI score. Population attributable fractions (PAF) were estimated assuming participants’ shift to healthier lifestyles. The HRs for a one-standard deviation increment of HLIBMI and HLIWHR were 0.84 (95% CI: 0.79, 0.89; ptrend = 4.3e−09) and 0.77 (0.72, 0.82; ptrend = 1.7e−15), respectively. Exclusions of smoking from HLIWHR resulted in HRs of 0.88 (0.82, 0.94; ptrend = 4.9e−04). The overall PAF estimate was 19% (95% CI: 11%, 26%), and 14% (6%, 21%) when smoking was removed from the score. Adherence to a healthy lifestyle was inversely associated with PC risk, beyond the beneficial role of smoking avoidance. Public health measures targeting compliance with healthy lifestyles may have an impact on PC incidence. © 2019, Springer Nature B.V.
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- 2020
43. Plasma polyphenols associated with lower high-sensitivity C-reactive protein concentrations:a cross-sectional study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort
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Harms, L.M., Scalbert, A., Zamora-Ros, R., Rinaldi, S., Jenab, M., Murphy, N., Achaintre, D., Tjønneland, A., Olsen, A., Overvad, K., Romana Mancini, F., Mahamat-Saleh, Y., Boutron-Ruault, M.-C., Kühn, T., Katzke, V., Trichopoulou, A., Martimianaki, G., Karakatsani, A., Palli, D., Panico, S., Sieri, S., Tumino, R., Sacerdote, C., Bueno-De-Mesquita, B., Vermeulen, R.C.H., Weiderpass, E., Nøst, T.H., Lasheras, C., Rodríguez-Barranco, M., Huerta, J.M., Barricarte, A., Dorronsoro, M., Hultdin, J., Gunter, M., Riboli, E., Aleksandrova, K., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Centre de recherche en épidémiologie et santé des populations (CESP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), PI13/00061, PI13/01162 RD06/0020 6236 Kræftens Bekæmpelse, DCS Deutsches Krebsforschungszentrum, DKFZ Centre International de Recherche sur le Cancer, CIRC College of Environmental Science and Forestry, State University of New York, ESF National Research Council, NRC Medical Research Council, MRC: CP15/00100, MR/M012190/1 Cancer Research UK, CRUK: C8221/A19170 World Cancer Research Fund, WCRF: ERC-2009-AdG 232997 European Commission, EC Institut National de la Santé et de la Recherche Médicale, Inserm Bundesministerium für Bildung und Forschung, BMBF Cancerfonden Ministerie van Volksgezondheid, Welzijn en Sport, VWS Ligue Contre le Cancer VetenskapsrÃ¥det, VR Instituto de Salud Carlos III, ISCIII NordForsk European Social Fund, ESF Associazione Italiana per la Ricerca sul Cancro, AIRC Deutsche Krebshilfe Mutuelle Générale de l'Education Nationale, MGEN, The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by Danish Cancer Society (Denmark), Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l’Education Nationale and Institut National de la Santé et de la Recherche Médicale (INSERM) (France), German Cancer Aid, German Cancer Research Center (DKFZ), Federal Ministry of Education and Research (BMBF), Deutsche Krebshilfe, Deutsches Krebsforschungszentrum and Federal Ministry of Education and Research (Germany), the Hellenic Health Foundation (Greece), Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy), Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Netherlands), ERC-2009-AdG 232997 and Nordforsk, Nordic Centre of Excellence Programme on Food, Nutrition and Health (Norway), Health Research Fund (FIS), PI13/00061 to Granada, PI13/01162 to EPIC-Murcia), Regional Governments of Andalucía, Asturias, Basque Country, Murcia (no. 6236) and Navarra, ISCIII RETIC (RD06/0020) (Spain), Swedish Cancer Society, Swedish Research Council and County Councils of Skåne and Västerbotten (Sweden), Cancer Research UK (14136 to EPIC-Norfolk, and C8221/A19170 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk, MR/M012190/1 to EPIC-Oxford) (UK). R. Z.-R. is supported by the ‘Miguel Servet’ programme (CP15/00100) from the Institute of Health Carlos III and the European Social Fund (ESF).
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Male ,0301 basic medicine ,Medicine (miscellaneous) ,Gastroenterology ,Cohort Studies ,chronic diseases ,chemistry.chemical_compound ,0302 clinical medicine ,Risk Factors ,Neoplasms ,Caffeic acid ,Medicine ,Malalties cròniques ,odds ratio ,Prospective Studies ,Prospective cohort study ,Nutrition and Dietetics ,VDP::Medisinske Fag: 700::Helsefag: 800::Samfunnsmedisin, sosialmedisin: 801 ,biology ,food and beverages ,Full Papers ,Middle Aged ,3. Good health ,European Prospective Investigation into Cancer and Nutrition ,Näringslära ,Europe ,hormone replacement therapy ,Polifenols ,Cohort ,Female ,standard deviation ,Human and Clinical Nutrition ,Cohort study ,Adult ,Plasma measurements ,medicine.medical_specialty ,030209 endocrinology & metabolism ,body mass index ,Diet Surveys ,C-reactive protein ,03 medical and health sciences ,Internal medicine ,Humans ,polyphenols ,Aged ,Inflammation ,030109 nutrition & dietetics ,business.industry ,Daidzein ,Polyphenols ,Diet ,cardiovascular diseases ,Cross-Sectional Studies ,Nutrition Assessment ,chemistry ,confidence interval ,Polyphenol ,plasma measurements ,inflammation ,Chronic diseases ,randomized controlled trial ,biology.protein ,high-sensitivity C-reactive protein ,VDP::Medical disciplines: 700::Health sciences: 800::Community medicine, Social medicine: 801 ,business ,[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition ,Biomarkers - Abstract
Experimental studies have reported on the anti-inflammatory properties of polyphenols. However, results from epidemiological investigations have been inconsistent and especially studies using biomarkers for assessment of polyphenol intake have been scant. We aimed to characterise the association between plasma concentrations of thirty-five polyphenol compounds and low-grade systemic inflammation state as measured by high-sensitivity C-reactive protein (hsCRP). A cross-sectional data analysis was performed based on 315 participants in the European Prospective Investigation into Cancer and Nutrition cohort with available measurements of plasma polyphenols and hsCRP. In logistic regression analysis, the OR and 95 % CI of elevated serum hsCRP (>3 mg/l) were calculated within quartiles and per standard deviation higher level of plasma polyphenol concentrations. In a multivariable-adjusted model, the sum of plasma concentrations of all polyphenols measured (per standard deviation) was associated with 29 (95 % CI 50, 1) % lower odds of elevated hsCRP. In the class of flavonoids, daidzein was inversely associated with elevated hsCRP (OR 0 center dot 66, 95 % CI 0 center dot 46, 0 center dot 96). Among phenolic acids, statistically significant associations were observed for 3,5-dihydroxyphenylpropionic acid (OR 0 center dot 58, 95 % CI 0 center dot 39, 0 center dot 86), 3,4-dihydroxyphenylpropionic acid (OR 0 center dot 63, 95 % CI 0 center dot 46, 0 center dot 87), ferulic acid (OR 0 center dot 65, 95 % CI 0 center dot 44, 0 center dot 96) and caffeic acid (OR 0 center dot 69, 95 % CI 0 center dot 51, 0 center dot 93). The odds of elevated hsCRP were significantly reduced for hydroxytyrosol (OR 0 center dot 67, 95 % CI 0 center dot 48, 0 center dot 93). The present study showed that polyphenol biomarkers are associated with lower odds of elevated hsCRP. Whether diet rich in bioactive polyphenol compounds could be an effective strategy to prevent or modulate deleterious health effects of inflammation should be addressed by further well-powered longitudinal studies.
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- 2020
44. Alcohol Consumption and Risk of Parkinson's Disease: Data From a Large Prospective European Cohort
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Peters, S. Gallo, V. Vineis, P. Middleton, L.T. Forsgren, L. Sacerdote, C. Sieri, S. Kyrozis, A. Chirlaque, M.-D. Zamora-Ros, R. Hansson, O. Petersson, J. Katzke, V. Kühn, T. Mokoroa, O. Masala, G. Ardanaz, E. Panico, S. Bergmann, M.M. Key, T.J. Weiderpass, E. Ferrari, P. Vermeulen, R.
- Abstract
Background: Parkinson's disease (PD) etiology is not well understood. Reported inverse associations with smoking and coffee consumption prompted the investigation of alcohol consumption as a risk factor, for which evidence is inconclusive. Objective: To assess the associations between alcohol consumption and PD risk. Methods: Within NeuroEPIC4PD, a prospective European population-based cohort, 694 incident PD cases were ascertained from 209,998 PD-free participants. Average alcohol consumption at different time points was self-reported at recruitment. Cox regression hazard ratios were estimated for alcohol consumption and PD occurrence. Results: No associations between baseline or lifetime total alcohol consumption and PD risk were observed. Men with moderate lifetime consumption (5–29.9 g/day) were at ~50% higher risk compared with light consumption (0.1–4.9 g/day), but no linear exposure–response trend was observed. Analyses by beverage type also revealed no associations with PD. Conclusion: Our data reinforce previous findings from prospective studies showing no association between alcohol consumption and PD risk. © 2020 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society. © 2020 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
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- 2020
45. 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
46. Association between nutritional profiles of foods underlying Nutri-Score front-of-pack labels and mortality: EPIC cohort study in 10 European countries
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Deschasaux, M. Huybrechts, I. Julia, C. Hercberg, S. Egnell, M. Srour, B. Kesse-Guyot, E. Latino-Martel, P. Biessy, C. Casagrande, C. Murphy, N. Jenab, M. Ward, H.A. Weiderpass, E. Overvad, K. Tjønneland, A. Rostgaard-Hansen, A.L. Boutron-Ruault, M.-C. Mancini, F.R. Mahamat-Saleh, Y. Kühn, T. Katzke, V. Bergmann, M.M. Schulze, M.B. Trichopoulou, A. Karakatsani, A. Peppa, E. Masala, G. Agnoli, C. De Magistris, M.S. Tumino, R. Sacerdote, C. Boer, J.M.A. Monique Verschuren, W.M. Van Der Schouw, Y.T. Skeie, G. Braaten, T. Luisa Redondo, M. Agudo, A. Petrova, D. Colorado-Yohar, S.M. Barricarte, A. Amiano, P. Sonestedt, E. Ericson, U. Otten, J. Sundström, B. Wareham, N.J. Forouhi, N.G. Vineis, P. Tsilidis, K.K. Knuppel, A. Papier, K. Ferrari, P. Riboli, E. Gunter, M.J. Touvier, M.
- Abstract
Objective To determine if the Food Standards Agency nutrient profiling system (FSAm-NPS), which grades the nutritional quality of food products and is used to derive the Nutri-Score front-of-packet label to guide consumers towards healthier food choices, is associated with mortality. Design Population based cohort study. Setting European Prospective Investigation into Cancer and Nutrition (EPIC) cohort from 23 centres in 10 European countries. Participants 521 324 adults; at recruitment, country specific and validated dietary questionnaires were used to assess their usual dietary intakes. A FSAm-NPS score was calculated for each food item per 100 g content of energy, sugars, saturated fatty acids, sodium, fibre, and protein, and of fruit, vegetables, legumes, and nuts. The FSAm-NPS dietary index was calculated for each participant as an energy weighted mean of the FSAm-NPS score of all foods consumed. The higher the score the lower the overall nutritional quality of the diet. Main outcome measure Associations between the FSAm-NPS dietary index score and mortality, assessed using multivariable adjusted Cox proportional hazards regression models. Results After exclusions, 501 594 adults (median follow-up 17.2 years, 8 162 730 person years) were included in the analyses. Those with a higher FSAm-NPS dietary index score (highest versus lowest fifth) showed an increased risk of all cause mortality (n=53 112 events from non-external causes; hazard ratio 1.07, 95% confidence interval 1.03 to 1.10, P
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- 2020
47. Intake of individual fatty acids and risk of prostate cancer in the European prospective investigation into cancer and nutrition
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Perez-Cornago, A. Huybrechts, I. Appleby, P.N. Schmidt, J.A. Crowe, F.L. Overvad, K. Tjønneland, A. Kühn, T. Katzke, V. Trichopoulou, A. Karakatsani, A. Peppa, E. Grioni, S. Palli, D. Sacerdote, C. Tumino, R. Bueno-de-Mesquita, H.B. Larrañaga, N. Sánchez, M.-J. Quirós, J.R. Ardanaz, E. Chirlaque, M.-D. Agudo, A. Bjartell, A. Wallström, P. Chajes, V. Tsilidis, K.K. Aune, D. Riboli, E. Travis, R.C. Key, T.J.
- Abstract
The associations of individual dietary fatty acids with prostate cancer risk have not been examined comprehensively. We examined the prospective association of individual dietary fatty acids with prostate cancer risk overall, by tumor subtypes, and prostate cancer death. 142,239 men from the European Prospective Investigation into Cancer and Nutrition who were free from cancer at recruitment were included. Dietary intakes of individual fatty acids were estimated using center-specific validated dietary questionnaires at baseline and calibrated with 24-h recalls. Multivariable Cox regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). After an average follow-up of 13.9 years, 7,036 prostate cancer cases and 936 prostate cancer deaths were ascertained. Intakes of individual fatty acids were not related to overall prostate cancer risk. There was evidence of heterogeneity in the association of some short chain saturated fatty acids with prostate cancer risk by tumor stage (pheterogeneity < 0.015), with a positive association with risk of advanced stage disease for butyric acid (4:0; HR1SD = 1.08; 95%CI = 1.01–1.15; p-trend = 0.026). There were no associations with fatal prostate cancer, with the exception of a slightly higher risk for those who consumed more eicosenoic acid (22:1n-9c; HR1SD = 1.05; 1.00–1.11; p-trend = 0.048) and eicosapentaenoic acid (20:5n-3c; HR1SD = 1.07; 1.00–1.14; p-trend = 0.045). There was no evidence that dietary intakes of individual fatty acids were associated with overall prostate cancer risk. However, a higher intake of butyric acid might be associated with a higher risk of advanced, whereas intakes of eicosenoic and eicosapentaenoic acids might be positively associated with fatal prostate cancer risk. © 2019 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC
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- 2020
48. Correlations between urinary concentrations and dietary intakes of flavonols in the European Prospective Investigation into Cancer and Nutrition (EPIC) study
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Garro-Aguilar, Y. Cayssials, V. Achaintre, D. Boeing, H. Mancini, F.R. Mahamat-Saleh, Y. Boutron-Ruault, M.-C. Kühn, T. Katzke, V. Trichopoulou, A. Karakatsani, A. Thriskos, P. Masala, G. Grioni, S. Santucci de Magistris, M. Tumino, R. Ricceri, F. Huybrechts, I. Agudo, A. Scalbert, A. Zamora-Ros, R.
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food and beverages - Abstract
Purpose: In this study, we aimed to study the correlation between acute and habitual intakes of flavonols, their main food sources and their 24-h urinary concentrations in an European population. Methods: A 24-h dietary recall (24-HDR) and 24-h urine samples were collected on the same day from a convenience subsample of 475 men and women from four countries (France, Italy, Greece and Germany) of the European Prospective Investigation into Cancer and Nutrition (EPIC) study. A standardized 24-HDR software and a country/centre-specific validated dietary questionnaire (DQ) were used to collect acute and habitual dietary data, respectively. The intake of dietary flavonols was estimated using the Phenol-Explorer database. Urinary flavonols (quercetin, isorhamnetin, and kaempferol) were analysed using tandem mass spectrometry with a previous enzymatic hydrolysis. Results: Weak partial Spearman correlations between both dietary acute and habitual intake and urinary concentrations of quercetin (both Rpartial ~ 0.3) and total flavonols (both Rpartial ~ 0.2) were observed. No significant correlations were found for kaempferol and isorhamentin. Regarding flavonol-rich foods, weak correlations were found between urinary concentrations of quercetin and total flavonols and the acute intake of onions and garlics, fruits, tea, and herbal tea (all Rpartial ~ 0.2). For habitual intake, statistically significant correlations were only found between urinary quercetin concentration and herbal tea (Rpartial = 0.345) and between urinary total flavonol concentration and tea, and herbal tea consumption (Rpartial ~ 0.2). Conclusions: Our results suggest that urinary quercetin level can be used as potential concentration biomarkers of both acute and habitual quercetin intake, while urinary concentrations of flavonols are unlikely to be useful biomarkers of individual flavonol-rich foods. © 2019, Springer-Verlag GmbH Germany, part of Springer Nature.
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- 2020
49. Consumption of nuts and seeds and pancreatic ductal adenocarcinoma risk in the European Prospective Investigation into Cancer and Nutrition
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Obón-Santacana, M., Luján-Barroso, L., Freisling, H., Naudin, S., Boutron-Ruault, M.-C., Mancini, F.R., Rebours, V., Kühn, T., Katzke, V., Boeing, H., Tjønneland, A., Olsen, A., Overvad, K., Lasheras, C., Rodríguez-Barranco, M., Amiano, P., Santiuste, C., Ardanaz, E., Khaw, K.-T., Wareham, N.J., Aune, D., Trichopoulou, A., Thriskos, P., Peppa, E., Masala, G., Grioni, S., Tumino, R., Panico, S., Bueno-de-Mesquita, B., Sciannameo, V., Vermeulen, R., Sonestedt, E., Sund, M., Weiderpass, E., Skeie, G., Riboli, E., Duell, E.J., IRAS OH Epidemiology Chemical Agents, and dIRAS RA-2
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prospective cohort study ,pancreatic cancer ,nuts ,seeds ,diet ,EPIC ,intake - Abstract
Four epidemiologic studies have assessed the association between nut intake and pancreatic cancer risk with contradictory results. The present study aims to investigate the relation between nut intake (including seeds) and pancreatic ductal adenocarcinoma (PDAC) risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Cox proportional hazards models were used to estimate hazards ratio (HR) and 95% confidence intervals (95% CI) for nut intake and PDAC risk. Information on intake of nuts was obtained from the EPIC country-specific dietary questionnaires. After a mean follow-up of 14 years, 476,160 participants were eligible for the present study and included 1,283 PDAC cases. No association was observed between consumption of nuts and PDAC risk (highest intake vs nonconsumers: HR, 0.89; 95% CI, 0.72–1.10; p-trend = 0.70). Furthermore, no evidence for effect-measure modification was observed when different subgroups were analyzed. Overall, in EPIC, the highest intake of nuts was not statistically significantly associated with PDAC risk.
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- 2020
50. Polyphenol intake and differentiated thyroid cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort
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Zamora-Ros, R. Cayssials, V. Franceschi, S. Kyrø, C. Weiderpass, E. Hennings, J. Sandström, M. Tjønneland, A. Olsen, A. Overvad, K. Boutron-Ruault, M.-C. Truong, T. Mancini, F.R. Katzke, V. Kühn, T. Boeing, H. Trichopoulou, A. Karakatsani, A. Martimianaki, G. Palli, D. Krogh, V. Panico, S. Tumino, R. Sacerdote, C. Lasheras, C. Rodríguez-Barranco, M. Amiano, P. Colorado-Yohar, S.M. Ardanaz, E. Almquist, M. Ericson, U. Bueno-de-Mesquita, H.B. Vermeulen, R. Schmidt, J.A. Byrnes, G. Scalbert, A. Agudo, A. Rinaldi, S.
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food and beverages - Abstract
Polyphenols are bioactive compounds with several anticarcinogenic activities; however, human data regarding associations with thyroid cancer (TC) is still negligible. Our aim was to evaluate the association between intakes of total, classes and subclasses of polyphenols and risk of differentiated TC and its main subtypes, papillary and follicular, in a European population. The European Prospective Investigation into Cancer and Nutrition cohort included 476,108 men and women from 10 European countries. During a mean follow-up of 14 years, there were 748 incident differentiated TC cases, including 601 papillary and 109 follicular tumors. Polyphenol intake was estimated at baseline using validated center/country-specific dietary questionnaires and the Phenol-Explorer database. In multivariable-adjusted Cox regression models, no association between total polyphenol and the risks of overall differentiated TC (HRQ4 vs. Q1 = 0.99, 95% confidence interval [CI] 0.77–1.29), papillary (HRQ4 vs. Q1 = 1.06, 95% CI 0.80–1.41) or follicular TC (HRQ4 vs. Q1 = 1.10, 95% CI 0.55–2.22) were found. No associations were observed either for flavonoids, phenolic acids or the rest of classes and subclasses of polyphenols. After stratification by body mass index (BMI), an inverse association between the intake of polyphenols (p-trend = 0.019) and phenolic acids (p-trend = 0.007) and differentiated TC risk in subjects with BMI ≥ 25 was observed. In conclusion, our study showed no associations between dietary polyphenol intake and differentiated TC risk; although further studies are warranted to investigate the potential protective associations in overweight and obese individuals. © 2019 UICC
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- 2020
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