Imperial College London

ProfessorElioRiboli

Faculty of MedicineSchool of Public Health

Chair in Cancer Epidemiology and Prevention
 
 
 
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Contact

 

e.riboli Website CV

 
 
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Assistant

 

Ms Julieta Dourado +44 (0)20 7594 3426

 
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Location

 

152Medical SchoolSt Mary's Campus

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Summary

 

Publications

Publication Type
Year
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1248 results found

Chan SSM, Chen Y, Casey K, Olen O, Ludvigsson JF, Carbonnel F, Oldenburg B, Gunter MJ, Tjønneland A, Grip O, DEFINe-IBD Investigators, Lochhead P, Chan AT, Wolk A, Khalili Het al., 2022, Obesity is associated with increased risk of Crohn's disease, but not ulcerative colitis: a pooled analysis of five prospective cohort studies, Clinical Gastroenterology and Hepatology, Vol: 20, Pages: 1048-1058, ISSN: 1542-3565

BACKGROUND AND AIMS: It is unclear whether obesity is associated with the development of inflammatory bowel disease despite compelling data from basic science studies. We therefore examined the association between obesity and risk of Crohn's disease (CD) and ulcerative colitis (UC). METHODS: We conducted pooled analyses of 5 prospective cohorts with validated anthropometric measurements for body mass index (BMI) and waist-hip ratio and other lifestyle factors. Diagnoses of CD and UC were confirmed through medical records or ascertained using validated definitions. We used Cox proportional hazards modeling to calculate pooled multivariable-adjusted HRs (aHRs) and 95% confidence intervals (CIs). RESULTS: Among 601,009 participants (age range, 18-98 years) with 10,110,018 person-years of follow-up, we confirmed 563 incident cases of CD and 1047 incident cases of UC. Obesity (baseline BMI ≥30 kg/m2) was associated with an increased risk of CD (pooled aHR, 1.34; 95% CI, 1.05-1.71, I2 = 0%) compared with normal BMI (18.5 to <25 kg/m2). Each 5 kg/m2 increment in baseline BMI was associated with a 16% increase in risk of CD (pooled aHR, 1.16; 95% CI, 1.05-1.22; I2 = 0%). Similarly, with each 5 kg/m2 increment in early adulthood BMI (age, 18-20 years), there was a 22% increase in risk of CD (pooled aHR, 1.22; 95% CI, 1.05-1.40; I2 = 13.6%). An increase in waist-hip ratio was associated with an increased risk of CD that did not reach statistical significance (pooled aHR across quartiles, 1.08; 95% CI, 0.97-1.19; I2 = 0%). No associations were observed between measures of obesity and risk of UC. CONCLUSIONS: In an adult population, obesity as measured by BMI was associated with an increased risk of older-onset CD but not UC.

Journal article

Fortuin-de Smidt MC, Sewe MO, Lassale C, Weiderpass E, Andersson J, Huerta JM, Ekelund U, Aleksandrova K, Tong TYN, Dahm CC, Tjønneland A, Kyrø C, Steindorf K, Schulze MB, Katzke V, Sacerdote C, Agnoli C, Masala G, Tumino R, Panico S, Boer JMA, Onland-Moret NC, Wendel-Vos GCW, van der Schouw YT, Borch KB, Agudo A, Petrova D, Chirlaque M-D, Conchi M-I, Amiano P, Melander O, Heath AK, Aune D, Forouhi NG, Langenberg C, Brage S, Riboli E, Wareham NJ, Danesh J, Butterworth AS, Wennberg Pet al., 2022, Physical activity attenuates but does not eliminate coronary heart disease risk amongst adults with risk factors: EPIC-CVD case-cohort study, European Journal of Preventive Cardiology, ISSN: 2047-4873

AimsThis study aimed to evaluate the association between physical activity and the incidence of coronary heart disease (CHD) in individuals with and without CHD risk factors.Methods and resultsEPIC-CVD is a case-cohort study of 29 333 participants that included 13 582 incident CHD cases and a randomly selected sub-cohort nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Self-reported physical activity was summarized using the Cambridge physical activity index (inactive, moderately inactive, moderately active, and active). Participants were categorized into sub-groups based on the presence or the absence of the following risk factors: obesity (body mass index ≥30 kg/m2), hypercholesterolaemia (total cholesterol ≥6.2 mmol/L), history of diabetes, hypertension (self-reported or ≥140/90 mmHg), and current smoking. Prentice-weighted Cox regression was used to assess the association between physical activity and incident CHD events (non-fatal and fatal).Compared to inactive participants without the respective CHD risk factor (referent), excess CHD risk was highest in physically inactive and lowest in moderately active participants with CHD risk factors. Corresponding excess CHD risk estimates amongst those with obesity were 47% [95% confidence interval (CI) 32–64%] and 21% (95%CI 2–44%), with hypercholesterolaemia were 80% (95%CI 55–108%) and 48% (95%CI 22–81%), with hypertension were 80% (95%CI 65–96%) and 49% (95%CI 28–74%), with diabetes were 142% (95%CI 63–260%), and 100% (95%CI 32–204%), and amongst smokers were 152% (95%CI 122–186%) and 109% (95%CI 74–150%).ConclusionsIn people with CHD risk factors, moderate physical activity, equivalent to 40 mins of walking per day, attenuates but does not completely offset CHD risk.

Journal article

Clasen JL, Heath AK, Van Puyvelde H, Huybrechts I, Park JY, Ferrari P, Scelo G, Ulvik A, Midttun Ø, Ueland PM, Overvad K, Eriksen AK, Tjønneland A, Kaaks R, Katzke V, Schulze MB, Palli D, Agnoli C, Chiodini P, Tumino R, Sacerdote C, Zamora-Ros R, Rodriguez-Barranco M, Santiuste C, Ardanaz E, Amiano P, Schmidt JA, Weiderpass E, Gunter M, Riboli E, Cross AJ, Johansson M, Muller DCet al., 2022, Biomarkers of the transsulfuration pathway and risk of renal cell carcinoma in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, International Journal of Cancer, ISSN: 0020-7136

Previous studies have suggested that components of one-carbon metabolism, particularly circulating vitamin B6, have an etiological role in renal cell carcinoma (RCC). Vitamin B6 is a cofactor in the transsulfuration pathway. We sought to holistically investigate the role of the transsulfuration pathway in RCC risk. We conducted a nested case-control study (455 RCC cases and 455 matched controls) within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Plasma samples from the baseline visit were analyzed for metabolites of the transsulfuration pathway, including pyridoxal 5'-phosphate (PLP, the biologically active form of vitamin B6), homocysteine, serine, cystathionine, and cysteine, in addition to folate. Bayesian conditional logistic regression was used to estimate associations of metabolites with RCC risk as well as interactions with established RCC risk factors. Circulating PLP and cysteine were inversely associated with RCC risk, and these association were not attenuated after adjustment for other transsulfuration metabolites (odds ratio (OR) and 90% credible interval (CrI) per 1 SD increase in log concentration: 0.76 [0.66, 0.87]; 0.81 [0.66, 0.96], respectively). A comparison of joint metabolite profiles suggested substantially greater RCC risk for the profile representative of low overall transsulfuration function compared with high function (OR 2.70 [90% CrI 1.26, 5.70]). We found some statistical evidence of interactions of cysteine with body mass index, and PLP and homocysteine with smoking status, on their associations with RCC risk. In conclusion, we found evidence suggesting that the transsulfuration pathway may play a role in metabolic dysregulation leading to RCC development. This article is protected by copyright. All rights reserved.

Journal article

Papadimitriou N, Bouras E, van den Brandt PA, Muller DC, Papadopoulou A, Heath AK, Critselis E, Gunter MJ, Vineis P, Ferrari P, Weiderpass E, Boeing H, Bastide N, Merritt MA, Lopez DS, Bergmann MM, Perez-Cornago A, Schulze M, Skeie G, Srour B, Eriksen AK, Boden S, Johansson I, Nøst TH, Lukic M, Ricceri F, Ericson U, Huerta JM, Dahm CC, Agnoli C, Amiano PE, Tjønneland A, Gurrea AB, Bueno-de-Mesquita B, Ardanaz E, Berntsson J, Sánchez M-J, Tumino R, Panico S, Katzke V, Jakszyn P, Masala G, Derksen JWG, Quirós JR, Severi G, Cross AJ, Riboli E, Tzoulaki I, Tsilidis KKet al., 2022, A prospective diet-wide association study for risk of colorectal cancer in EPIC, Clinical Gastroenterology and Hepatology, Vol: 20, Pages: 864-873.e13, ISSN: 1542-3565

BACKGROUND & AIMS: Evidence regarding the association of dietary exposures with colorectal cancer (CRC) risk is not consistent with a few exceptions. Therefore, we conducted a diet-wide association study (DWAS) in the European Prospective Investigation into Cancer and Nutrition (EPIC) to evaluate the associations between several dietary exposures with CRC risk. METHODS: The association of 92 food and nutrient intakes with CRC risk was assessed in 386,792 participants, 5,069 of whom developed incident CRC. Correction for multiple comparisons was performed using the false discovery rate, and emerging associations were examined in the Netherlands Cohort Study (NLCS). Multiplicative gene-nutrient interactions were also tested in EPIC based on known CRC-associated loci. RESULTS: In EPIC, alcohol, liquor/spirits, wine, beer/cider, soft drinks, and pork were positively associated with CRC, whereas milk, cheese, calcium, phosphorus, magnesium, potassium, riboflavin, vitamin B6, beta-carotene, fruit, fibre, non-white bread, banana, and total protein intakes were inversely associated. Of these 20 associations, 13 were replicated in NLCS, for which a meta-analysis was performed, namely alcohol (summary HR per 1 SD increment in intake: 1.07; 95%CI:1.04-1.09), liquor/spirits (1.04; 1.02-1.06), wine (1.04;1.02-1.07), beer/cider (1.06;1.04-1.08), milk (0.95;0.93-0.98), cheese (0.96;0.94-0.99), calcium (0.93;0.90-0.95), phosphorus (0.92;0.90-0.95), magnesium (0.95;0.92-0.98), potassium (0.96;0.94-0.99), riboflavin (0.94;0.92-0.97), beta-carotene (0.96;0.93-0.98), and total protein (0.94;0.92-0.97). None of the gene-nutrient interactions were significant after adjustment for multiple comparisons. CONCLUSIONS: Our findings confirm a positive association for alcohol and an inverse association for dairy products and calcium with CRC risk, and also suggest a lower risk at higher dietary intakes of phosphorus, magnesium, potassium, riboflavin, beta-carotene and total protein.

Journal article

Dam V, Onland-Moret NC, Burgess S, Chirlaque M-D, Peters SAE, Schuit E, Tikk K, Weiderpass E, Oliver-Williams C, Wood AM, Tjonneland A, Dahm CC, Overvad K, Boutron-Ruault M-C, Schulze MB, Trichopoulou A, Ferrari P, Masala G, Krogh V, Tumino R, Matullo G, Panico S, Boer JMA, Verschuren WMM, Waaseth M, Sanchez Perez MJ, Amiano P, Imaz L, Moreno-Iribas C, Melander O, Harlid S, Nordendahl M, Wennberg P, Key TJ, Riboli E, Santiuste C, Kaaks R, Katzke V, Langenberg C, Wareham NJ, Schunkert H, Erdmann J, Willenborg C, Hengstenberg C, Kleber ME, Delgado G, Marz W, Kanoni S, Dedoussis G, Deloukas P, Nikpay M, McPherson R, Scholz M, Teren A, Butterworth AS, van der Schouw YTet al., 2022, Genetically Determined Reproductive Aging and Coronary Heart Disease: A Bidirectional 2-sample Mendelian Randomization, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, ISSN: 0021-972X

Journal article

Zheng B, Su B, Udeh-Momoh C, Price G, Tzoulaki I, Vamos EP, Majeed A, Riboli E, Ahmadi-Abhari S, Middleton LTet al., 2022, Associations of cardiovascular and non-cardiovascular comorbidities with dementia risk in patients with diabetes: results from a large UK cohort study, JPAD-JOURNAL OF PREVENTION OF ALZHEIMERS DISEASE, Vol: 9, Pages: 86-91, ISSN: 2274-5807

BackgroundType 2 diabetes (T2D) is an established risk factor for dementia. However, it remains unclear whether the presence of comorbidities could further increase dementia risk in diabetes patients.ObjectivesTo examine the associations between cardiovascular and non-cardiovascular comorbidities and dementia risk in T2D patients.DesignPopulation-based cohort study.SettingThe UK Clinical Practice Research Datalink (CPRD).Participants489,205 T2D patients aged over 50 years in the UK CPRD.MeasurementsMajor cardiovascular and non-cardiovascular comorbidities were extracted as time-varying exposure variables. The outcome event was dementia incidence based on dementia diagnosis or dementia-specific drug prescription.ResultsDuring a median of six years follow-up, 33,773 (6.9%) incident dementia cases were observed. Time-varying Cox regressions showed T2D patients with stroke, peripheral vascular disease, atrial fibrillation, heart failure or hypertension were at higher risk of dementia compared to those without such comorbidities (HR [95% CI] = 1.64 [1.59–1.68], 1.37 [1.34–1.41], 1.26 [1.22–1.30], 1.15 [1.11–1.20] or 1.10 [1.03–1.18], respectively). Presence of chronic obstructive pulmonary disease or chronic kidney disease was also associated with increased dementia risk (HR [95% CI] = 1.05 [1.01–1.10] or 1.11 [1.07–1.14]).ConclusionsA range of cardiovascular and non-cardiovascular comorbidities were associated with further increases of dementia risk in T2D patients. Prevention and effective management of these comorbidities may play a significant role in maintaining cognitive health in T2D patients.

Journal article

Iguacel I, Perez-Cornago A, Schmidt JA, Van Puyvelde H, Travis R, Casagrande C, Nicolas G, Riboli E, Weiderpass E, Ardanaz E, Barricarte A, Boden S, Bruno E, Ching-Lopez A, Aune D, Jensen TE, Ericson U, Johansson I, Huerta JM, Katzke V, Kuehn T, Sacerdote C, Schulze MB, Skeie G, Ramne S, Ward H, Gunter MJ, Huybrechts Iet al., 2021, Evaluation of protein and amino acid intake estimates from the EPIC dietary questionnaires and 24-h dietary recalls using different food composition databases, NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES, Vol: 32, Pages: 80-89, ISSN: 0939-4753

Journal article

Ellingjord-Dale M, Christakoudi S, Weiderpass E, Panico S, Dossus L, Olsen A, Tjønneland A, Kaaks R, Schulze MB, Masala G, Gram IT, Skeie G, Rosendahl AH, Sund M, Key T, Ferrari P, Gunter M, Heath AK, Tsilidis KK, Riboli E, Additional Authorset al., 2021, Long-term weight change and risk of breast cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, International Journal of Epidemiology, Vol: 50, Pages: 1914-1926, ISSN: 0300-5771

BACKGROUND: The role of obesity and weight change in breast-cancer development is complex and incompletely understood. We investigated long-term weight change and breast-cancer risk by body mass index (BMI) at age 20 years, menopausal status, hormone replacement therapy (HRT) and hormone-receptor status. METHODS: Using data on weight collected at three different time points from women who participated in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, we investigated the association between weight change from age 20 years until middle adulthood and risk of breast cancer. RESULTS: In total, 150 257 women with a median age of 51 years at cohort entry were followed for an average of 14 years (standard deviation = 3.9) during which 6532 breast-cancer cases occurred. Compared with women with stable weight (±2.5 kg), long-term weight gain >10 kg was positively associated with postmenopausal breast-cancer risk in women who were lean at age 20 [hazard ratio (HR) = 1.42; 95% confidence interval 1.22-1.65] in ever HRT users (HR = 1.23; 1.04-1.44), in never HRT users (HR = 1.40; 1.16-1.68) and in oestrogen-and-progesterone-receptor-positive (ER+PR+) breast cancer (HR = 1.46; 1.15-1.85). CONCLUSION: Long-term weight gain was positively associated with postmenopausal breast cancer in women who were lean at age 20, both in HRT ever users and non-users, and hormone-receptor-positive breast cancer.

Journal article

Steur M, Johnson L, Sharp S, Imamura F, Heath A, Riboli Eet al., 2021, Dietary fatty acids, macronutrient substitutions and food sources and incidence of coronary heart disease: findings from the EPIC-CVD case-cohort study across nine European countries, Journal of the American Heart Association, Vol: 10, Pages: 1-37, ISSN: 2047-9980

Background: There is controversy about associations between total dietary fatty acids, their classes (saturated, monounsaturated, polyunsaturated fatty acids; SFAs, MUFAs, PUFAs, respectively) and risk of coronary heart disease (CHD). Specifically, the relevance of food sources of SFAs to CHD associations is uncertain.Methods and Results: We conducted a case-cohort study involving 10,529 incident CHD cases and a random subcohort of 16,730 adults selected from a cohort of 385,747 participants in nine countries of the European Prospective Investigation into Cancer and Nutrition study. We estimated multivariable adjusted country-specific hazard ratios (HRs) and 95% confidence intervals (CIs) per 5% of energy intake from dietary fatty acids, with and without isocaloric macronutrient substitutions, using Prentice-weighted Cox regression models and pooled results using random-effects meta-analysis. We found no evidence for associations of the consumption of total or fatty acid classes with CHD, regardless of macronutrient substitutions. In analyses considering food sources, CHD incidence was lower per 1% higher energy intake of SFAs from yoghurt (HRs [95% CIs]: 0.93 [0.88-0.99]), cheese (0.98 [0.96-1.00]), and fish (0.87 [0.75-1.00]), but higher for SFAs from red meat (1.07 [1.02-1.12]) and butter (1.02 [1.00-1.04]).Conclusions: This observational study found no strong associations of total fatty acids, SFAs, MUFAs, and PUFAs, with incident CHD. By contrast, we found associations of SFAs with CHD in opposite directions dependent on the food source. These findings should be further confirmed, but support public health recommendations to consider food sources alongside the macronutrients they contain, and suggest the importance of the overall food matrix.

Journal article

Laine J, Huybrechts I, Gunter M, Ferrari P, Weiderpass E, Tsilidis K, Dagfinn A, Schulze M, Bergmann M, Temme E, Boer JMA, Agnoli C, Ericson U, Stubbendorff A, Ibsen DB, Dahm CC, Deschasaux M, Touvier M, Kesse-Guyot E, Sánchez M-J, Barranco MR, Tong TYN, Papier K, Knuppel A, Boutron-Ruault M-C, Mancini F, Severi G, Srour B, Kühn T, Masala G, Agudo A, Skeie G, Rylander C, Sandanger TM, Riboli E, Vineis Pet al., 2021, Co-benefits from sustainable dietary shifts for population and environmental health: an assessment from a large European cohort study, The Lancet Planetary Health, Vol: 5, Pages: e786-e796, ISSN: 2542-5196

Background: Unhealthy diets, the rise of non-communicable diseases, and the declining health of the planet are highly intertwined, where food production and consumption are major drivers of increases in greenhouse gas (GHG) emissions, substantial land use, (LU) and adverse health outcomes such as cancer and mortality. Methods: In the European Prospective Investigation into Cancer and Nutrition (EPIC), a multi-centre prospective cohort study (n=443,991), we estimated associations between dietary contributions to GHG emissions and LU and all-cause and cause-specific mortality and incident cancers using Cox proportional-hazard regression models. Co-benefits, encompassing the potential effects of alternative diets on all-cause mortality and cancer and potential reduction in GHG emissions and LU, were estimated using counterfactual attributable fraction (AF) intervention models, simulating potential effects from dietary shifts based on the EAT-Lancet reference diet. Findings: There was an association between levels of dietary-based GHG emissions and LU and all-cause mortality, with a Hazard Ratio and 95% Confidence Interval (CI) of 1.13 (1.10, 1.16) and 1.18 (95% CI: 1.15, 1.21), respectively, comparing the fourth quartile to the first (HRQ4 vs Q1). Similar associations were observed for cause-specific mortality. There were also associations between overall cancer rates and GHG emissions (HRQ4 vs Q1: 1.11, 95% CI: 1.09, 1.14) and LU (HRQ4 vs Q1: 1.13, 95% CI: 1.10, 1.15); however, estimates differed by cancer type. Through counterfactual AF modelling of shifts in diets, we find that between 19 to 63% of deaths and 10 to 39% of cancers could be prevented, over a 20-year risk period, from adhering to different scores of the EAT-Lancet reference diet. Additionally, switching from a lower score of the EAT-Lancet reference diet to a higher score could reduce food-associated GHG and LU levels by 50% and 62%, respectively.Interpretation: Our results support shifts in diets that

Journal article

Vissers LET, Sluijs I, Burgess S, Forouhi NG, Freisling H, Imamura F, Nilsson TK, Renstroem F, Weiderpass E, Aleksandrova K, Dahm CC, Perez-Cornago A, Schulze MB, Tong TYN, Aune D, Bonet C, Boer JMA, Boeing H, Chirlaque MD, Conchi M, Imaz L, Jaeger S, Krogh V, Kyro C, Masala G, Melander O, Overvad K, Panico S, Sanches MJ, Sonestedt E, Tjonneland A, Tzoulaki I, Verschuren WMM, Riboli E, Wareham NJ, Danesh J, Butterworth AS, van der Schouw YTet al., 2021, Milk intake and incident stroke and CHD in populations of European descent: a Mendelian randomisation study, BRITISH JOURNAL OF NUTRITION, ISSN: 0007-1145

Journal article

Hanley-Cook GT, Huybrechts I, Biessy C, Remans R, Kennedy G, Deschasaux-Tanguy M, Murray KA, Touvier M, Skeie G, Kesse-Guyot E, Argaw A, Casagrande C, Nicolas G, Vineis P, Millett CJ, Weiderpass E, Ferrari P, Dahm CC, Bueno-de-Mesquita HB, Sandanger TM, Ibsen DB, Freisling H, Ramne S, Jannasch F, van der Schouw YT, Schulze MB, Tsilidis KK, Tjonneland A, Ardanaz E, Boden S, Cirera L, Gargano G, Halkjaer J, Jakszyn P, Johansson I, Katzke V, Masala G, Panico S, Rodriguez-Barranco M, Sacerdote C, Srour B, Tumino R, Riboli E, Gunter MJ, Jones AD, Lachat Cet al., 2021, Food biodiversity and total and cause-specific mortality in 9 European countries: An analysis of a prospective cohort study, PLoS Medicine, Vol: 18, ISSN: 1549-1277

BackgroundFood biodiversity, encompassing the variety of plants, animals, and other organisms consumed as food and drink, has intrinsic potential to underpin diverse, nutritious diets and improve Earth system resilience. Dietary species richness (DSR), which is recommended as a crosscutting measure of food biodiversity, has been positively associated with the micronutrient adequacy of diets in women and young children in low- and middle-income countries (LMICs). However, the relationships between DSR and major health outcomes have yet to be assessed in any population.Methods and findingsWe examined the associations between DSR and subsequent total and cause-specific mortality among 451,390 adults enrolled in the European Prospective Investigation into Cancer and Nutrition (EPIC) study (1992 to 2014, median follow-up: 17 years), free of cancer, diabetes, heart attack, or stroke at baseline. Usual dietary intakes were assessed at recruitment with country-specific dietary questionnaires (DQs). DSR of an individual’s yearly diet was calculated based on the absolute number of unique biological species in each (composite) food and drink. Associations were assessed by fitting multivariable-adjusted Cox proportional hazards regression models. In the EPIC cohort, 2 crops (common wheat and potato) and 2 animal species (cow and pig) accounted for approximately 45% of self-reported total dietary energy intake [median (P10–P90): 68 (40 to 83) species consumed per year]. Overall, higher DSR was inversely associated with all-cause mortality rate. Hazard ratios (HRs) and 95% confidence intervals (CIs) comparing total mortality in the second, third, fourth, and fifth (highest) quintiles (Qs) of DSR to the first (lowest) Q indicate significant inverse associations, after stratification by sex, age, and study center and adjustment for smoking status, educational level, marital status, physical activity, alcohol intake, and total energy intake, Mediterranean diet score, red

Journal article

Christakoudi S, Tsilidis K, Evangelou E, Riboli Eet al., 2021, Association of body-shape phenotypes with imaging measures of body composition in the UK Biobank cohort: relevance to colon cancer risk, BMC Cancer, Vol: 21, Pages: 1-15, ISSN: 1471-2407

BackgroundBody mass index (BMI), waist and hip circumference are strongly correlated and do not reflect body composition. A Body Shape Index (ABSI) and Hip Index (HI) define waist and hip size among individuals with the same weight and height and would thus reflect body density. We examined differences in body composition between body-shape phenotypes defined with ABSI and HI and used this information to propose explanations for associations between body-shape phenotypes and colon cancer risk.MethodsWe used data from the UK Biobank Resource for 15,520 men, 16,548 women with dual-emission X-ray absorptiometry (DXA) measurements; 3997 men, 4402 women with magnetic resonance imaging (MRI) measurements; 200,289 men, 230,326 women followed-up for colon cancer. We defined body-shape phenotypes as: large-ABSI-small-HI (“apple”), small-ABSI-large-HI (“pear”), small-ABSI-small-HI (“slim”), large-ABSI-large-HI (“wide”). We evaluated differences in body composition in linear models and associations with colon cancer risk in Cox proportional hazards models adjusted for confounders and explored heterogeneity by BMI.ResultsAmong individuals with the same height and weight, visceral adipose tissue (VAT) was lowest for “pear” and highest for “apple”, while abdominal subcutaneous adipose tissue (ASAT) was lowest for “slim” and highest for “wide” phenotype. In the gynoid region, differences between “apple” and “pear” phenotypes were accounted for mainly by fat mass in women but by lean mass in men. In men, lean mass was inversely associated with waist size, while the pattern of gynoid fat resembled ASAT in women. Lean and fat mass were higher for higher BMI, but not hand grip strength. Compared to normal weight “pear”, the risk of colon cancer in men (1029 cases) was higher for “apple” phenotype for normal weight (hazard ratio HR =&thi

Journal article

Guida F, Tan VY, Corbin LJ, Smith-Byrne K, Alcala K, Langenberg C, Stewart ID, Butterworth AS, Surendran P, Achaintre D, Adamski J, Amiano Exezarreta P, Bergmann MM, Bull CJ, Dahm CC, Gicquiau A, Giles GG, Gunter MJ, Haller T, Langhammer A, Larose TL, Ljungberg B, Metspalu A, Milne RL, Muller DC, Nøst TH, Pettersen Sørgjerd E, Prehn C, Riboli E, Rinaldi S, Rothwell JA, Scalbert A, Schmidt JA, Severi G, Sieri S, Vermeulen R, Vincent EE, Waldenberger M, Timpson NJ, Johansson Met al., 2021, The blood metabolome of incident kidney cancer: A case-control study nested within the MetKid consortium, PLoS Medicine, Vol: 18, ISSN: 1549-1277

BACKGROUND: Excess bodyweight and related metabolic perturbations have been implicated in kidney cancer aetiology, but the specific molecular mechanisms underlying these relationships are poorly understood. In this study, we sought to identify circulating metabolites that predispose kidney cancer and to evaluate the extent to which they are influenced by body mass index (BMI). METHODS AND FINDINGS: We assessed the association between circulating levels of 1,416 metabolites and incident kidney cancer using pre-diagnostic blood samples from up to 1,305 kidney cancer case-control pairs from 5 prospective cohort studies. Cases were diagnosed on average 8 years after blood collection. We found 25 metabolites robustly associated with kidney cancer risk. In particular, 14 glycerophospholipids (GPLs) were inversely associated with risk, including 8 phosphatidylcholines (PCs) and 2 plasmalogens. The PC with the strongest association was PC ae C34:3 with an odds ratio (OR) for 1 standard deviation (SD) increment of 0.75 (95% confidence interval [CI]: 0.68 to 0.83, p = 2.6 × 10-8). In contrast, 4 amino acids, including glutamate (OR for 1 SD = 1.39, 95% CI: 1.20 to 1.60, p = 1.6 × 10-5), were positively associated with risk. Adjusting for BMI partly attenuated the risk association for some-but not all-metabolites, whereas other known risk factors of kidney cancer, such as smoking and alcohol consumption, had minimal impact on the observed associations. A mendelian randomisation (MR) analysis of the influence of BMI on the blood metabolome highlighted that some metabolites associated with kidney cancer risk are influenced by BMI. Specifically, elevated BMI appeared to decrease levels of several GPLs that were also found inversely associated with kidney cancer risk (e.g., -0.17 SD change [ßBMI] in 1-(1-enyl-palmitoyl)-2-linoleoyl-GPC (P-16:0/18:2) levels per SD change in BMI, p = 3.4 × 10-5). BMI was also associated with increased levels of glutamate (&sz

Journal article

Clasen J, Heath AK, Van Puyvelde H, Huybrechts I, Johansson M, Ferrari P, Park JY, Brennan P, Riboli E, Muller DCet al., 2021, Vitamin B6 intake, its active form pyridoxal 5'phosphate, and markers of B6 activity and catabolism, IEA WORLD CONGRESS OF EPIDEMIOLOGY 2021, Publisher: Oxford University Press, Pages: 1-1, ISSN: 0300-5771

BackgroundSeveral biological pathways implicated in cancer risk rely on vitamin B6, which can be measured in its active form pyridoxal 5’-phosphate (PLP). Functional markers of B6 enzymatic activity have been proposed, including the homocysteine:cysteine ratio (Hcy:Cys, a marker of transsulfuration), 3-hydroxykynurenine ratio (HKr, a marker of tryptophan catabolism), and the 4-pyridoxic acid ratio (PAr, a marker of B6 catabolism). We investigated the extent to which these markers are associated with B6 intake.MethodsData from 4,750 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) study were included. We estimated the expected percentage change in each of the markers (PLP, Hcy:Cys, HKr, and PAr) for a doubling in B6 intake using log-linear Bayesian hierarchical regression models with log-transformed intake and biomarker data.ResultsThe percent change (posterior mean [95% Credible Interval (CrI)]) for a doubling of B6 intake was 61.0 [51.2, 71.8] for PLP, -12.7 [-15.2, -9.9] for Hcy:Cys, -12.9 [-15.7, -9.9] for HKr, and 1.3 [-3.5, 6.2] for PAr.ConclusionsB6 intake is most strongly associated with PLP, but is also associated with functional markers of transsulfuration and tryptophan catabolism, in the direction of increased activity in these pathways. There is no evidence of a linear association between vitamin B6 intake and catabolism.Key messagesOur results show differing sensitivity of PLP, markers of tryptophan catabolism and transsulfuration, and vitamin B6 catabolism to B6 intake.

Conference paper

Christakoudi S, Tsilidis K, Evangelou E, Riboli Eet al., 2021, A Body Shape Index (ABSI), hip index and risk of cancer in the UK Biobank cohort, Cancer Medicine, Vol: 10, Pages: 5614-5628, ISSN: 2045-7634

Abdominal size is associated positively with the risk of some cancers but the influence of body mass index (BMI) and gluteofemoral size is unclear because waist and hip circumference are strongly correlated with BMI. We examined associations of 33 cancers with A Body Shape Index (ABSI) and hip index (HI), which are independent of BMI by design, and compared these with waist and hip circumference, using multivariable Cox proportional hazards models in UK Biobank. During a mean follow up of seven years, 14,682 incident cancers were ascertained in 200,289 men and 12,965 cancers in 230,326 women. In men, ABSI was associated positively with cancers of the head and neck (hazard ratio HR=1.14; 95% confidence interval 1.03-1.26 per one standard deviation increment), oesophagus (adenocarcinoma, HR=1.27; 1.12-1.44), gastric cardia (HR=1.31; 1.07-1.61), colon (HR=1.18; 1.10-1.26), rectum (HR=1.13; 1.04-1.22), lung (adenocarcinoma, HR=1.16; 1.03-1.30; squamous-cell carcinoma (SCC), HR=1.33; 1.17-1.52), and bladder (HR=1.15; 1.04-1.27), while HI was associated inversely with cancers of the oesophagus (adenocarcinoma, HR=0.89; 0.79-1.00), gastric cardia (HR=0.79; 0.65-0.96), colon (HR=0.92; 0.86-0.98), liver (HR=0.86; 0.75-0.98), and multiple myeloma (HR=0.86; 0.75-1.00). In women, ABSI was associated positively with cancers of the head and neck (HR=1.27; 1.10-1.48), oesophagus (SCC, HR=1.37; 1.07-1.76), colon (HR=1.08; 1.01-1.16), lung (adenocarcinoma, HR=1.17; 1.06-1.29; SCC, HR=1.40; 1.20-1.63; small-cell, HR=1.39; 1.14-1.69), kidney (clear-cell, HR=1.25; 1.03-1.50), and post-menopausal endometrium (HR=1.11; 1.02-1.20), while HI was associated inversely with skin SCC (HR=0.91; 0.83-0.99), post-menopausal kidney cancer (HR=0.77; 0.67-0.88) and post-menopausal melanoma (HR=0.90; 0.83-0.98). Unusually, ABSI was associated inversely with melanoma in men (HR=0.89; 0.82-0.96) and pre-menopausal women (HR=0.77; 0.65-0.91). Waist and hip circumference reflected associations with BMI

Journal article

Porta M, Gasull M, Pumarega J, Kiviranta H, Rantakokko P, Raaschou-Nielsen O, Bergdahl IA, Sandanger TM, Agudo A, Rylander C, Nøst TH, Donat-Vargas C, Aune D, Heath AK, Cirera L, Goñi-Irigoyen F, Alguacil J, Giménez-Robert À, Tjønneland A, Sund M, Overvad K, Mancini FR, Rebours V, Boutron-Ruault M-C, Kaaks R, Schulze MB, Trichopoulou A, Palli D, Grioni S, Tumino R, Naccarati A, Panico S, Vermeulen R, Quirós JR, Rodríguez-Barranco M, Colorado-Yohar SM, Chirlaque M-D, Ardanaz E, Wareham N, Key T, Johansson M, Murphy N, Ferrari P, Huybrechts I, Chajes V, Gonzalez CA, de-Mesquita BB, Gunter M, Weiderpass E, Riboli E, Duell EJ, Katzke V, Vineis Pet al., 2021, Plasma concentrations of persistent organic pollutants and pancreatic cancer risk, International Journal of Epidemiology, Vol: 00, Pages: 1-12, ISSN: 0300-5771

BackgroundFindings and limitations of previous studies on persistent organic pollutants (POPs) and pancreatic cancer risk support conducting further research in prospective cohorts.MethodsWe conducted a prospective case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Participants were 513 pancreatic cancer cases and 1020 matched controls. Concentrations of 22 POPs were measured in plasma collected at baseline.ResultsSome associations were observed at higher concentrations of p, p’-DDT, trans-nonachlor, β-hexachlorocyclohexane and the sum of six organochlorine pesticides and of 16 POPs. The odds ratio (OR) for the upper quartile of trans-nonachlor was 1.55 (95% confidence interval 1.06-2.26; P for trend = 0.025). Associations were stronger in the groups predefined as most valid (participants having fasted >6 h, with microscopic diagnostic confirmation, normal weight, and never smokers), and as most relevant (follow-up ≥10 years). Among participants having fasted >6 h, the ORs were relevant for 10 of 11 exposures. Higher ORs were also observed among cases with microscopic confirmation than in cases with a clinical diagnosis, and among normal-weight participants than in the rest of participants. Among participants with a follow-up ≥10 years, estimates were higher than in participants with a shorter follow-up (for trans-nonachlor: OR = 2.14, 1.01 to 4.53, P for trend = 0.035). Overall, trans-nonachlor, three PCBs and the two sums of POPs were the exposures most clearly associated with pancreatic cancer risk.ConclusionsIndividually or in combination, most of the 22 POPs analysed did not or only moderately increased the risk of pancreatic cancer.

Journal article

Clasen J, Heath A, Van Puyvelde H, Huybrechts I, Young Park J, Ferrari P, Johansson M, Scelo G, Midttun Ø, Magne Ueland P, Dahm C, Halkjær J, Olsen A, Johnson T, Katzke V, Schulze M, Masala G, Segrado F, Santucci de Magistris M, Sacerdote C, Ocké M, Luján-Barroso L, Ching-López A, Huerta JM, Ardanaz E, Amiano P, Ericson U, Manjer J, Gylling B, Johansson I, Schmidt J, Weiderpass E, Riboli E, Cross A, Muller Det al., 2021, A comparison of complementary measures of vitamin B6 status, function, and metabolism in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, American Journal of Clinical Nutrition, Vol: 114, Pages: 338-347, ISSN: 0002-9165

BackgroundVitamin B6 insufficiency has been linked to increased risk of cancer and other chronic diseases. The circulating concentration of pyridoxal 5′-phosphate (PLP) is a commonly used measure of vitamin B6 status. Ratios of substrates indicating PLP coenzymatic function and metabolism may be useful complementary measures to further explore the role of vitamin B6 in health.ObjectivesWe explored the sensitivity of 5 outcomes, namely PLP concentration, homocysteine:cysteine (Hcy:Cys), cystathionine:cysteine (Cysta:Cys), the 3´-hydroxykynurenine ratio (HKr), and the 4-pyridoxic acid ratio (PAr) to vitamin B6 intake as well as personal and lifestyle characteristics.MedthodsDietary intake and biomarker data were collected from participants from 3 nested case-control studies within the European Prospective Investigation into Cancer and Nutrition (EPIC). Bayesian regression models assessed the associations of the 5 biomarker outcomes with vitamin B6 intake and personal and lifestyle covariates. Analogous models examined the relations of Hcy:Cys, Cysta:Cys, and HKr with PLP.ResultsIn total, 4608 participants were included in the analyses. Vitamin B6 intake was most strongly associated with PLP, moderately associated with Hcy:Cys, Cysta:Cys, and HKr, and not associated with PAr (fold change in marker given a doubling of vitamin B6 intake: PLP 1.60 [95% credible interval (CrI): 1.50, 1.71]; Hcy:Cys 0.87 [95% CrI: 0.84, 0.90]; Cysta:Cys 0.89 [95% CrI: 0.84, 0.94]; HKr 0.88 [95% CrI: 0.85, 0.91]; PAr 1.00 [95% CrI: 0.95, 1.05]). PAr was most sensitive to age, and HKr was least sensitive to BMI and alcohol intake. Sex and menopause status were strongly associated with all 5 markers.ConclusionsWe found that 5 different markers, capturing different aspects of vitamin B6–related biological processes, varied in their associations with vitamin B6 intake and personal and lifestyle predictors.

Journal article

Agudo A, Cayssials V, Bonet C, Tjønneland A, Overvad K, Boutron-Ruault M-C, Affret A, Fagherazzi G, Katzke V, Schubel R, Trichopoulou A, Karakatsani A, La Vecchia C, Palli D, Grioni S, Tumino R, Ricceri F, Panico S, Bueno-de-Mesquita B, Peeters PH, Weiderpass E, Skeie G, Nøst TH, Lasheras C, Rodríguez-Barranco M, Amiano P, Chirlaque M-D, Ardanaz E, Ohlsson B, Dias JA, Nilsson LM, Myte R, Khaw K-T, Perez-Cornago A, Gunter M, Huybrechts I, Cross AJ, Tsilidis K, Riboli E, Jakszyn Pet al., 2021, Inflammatory potential of the diet & risk of gastric cancer in the European Investigation into Cancer & Nutrition, American Journal of Clinical Nutrition, Vol: 36, Pages: 953-964, ISSN: 1938-3207

The role of chronic inflammation on breast cancer (BC) risk remains unclear beyond as an underlying mechanism of obesity and physical activity. We aimed to evaluate the association between the inflammatory potential of the diet and risk of BC overall, according to menopausal status and tumour subtypes. Within the European Prospective Investigation into Cancer and Nutrition cohort, 318,686 women were followed for 14 years, among whom 13,246 incident BC cases were identified. The inflammatory potential of the diet was characterized by an inflammatory score of the diet (ISD). Multivariable Cox regression models were used to assess the potential effect of the ISD on BC risk by means of hazard ratios (HR) and 95% confidence intervals (CI). ISD was positively associated with BC risk. Each increase of one standard deviation (1-Sd) of the score increased by 4% the risk of BC (HR = 1.04; 95% CI 1.01–1.07). Women in the highest quintile of the ISD (indicating a most pro-inflammatory diet) had a 12% increase in risk compared with those in the lowest quintile (HR = 1.12; 95% CI 1.04–1.21) with a significant trend. The association was strongest among premenopausal women, with an 8% increased risk for 1-Sd increase in the score (HR = 1.08; 95% CI 1.01–1.14). The pattern of the association was quite homogeneous by BC subtypes based on hormone receptor status. There were no significant interactions between ISD and body mass index, physical activity, or alcohol consumption. Women consuming more pro-inflammatory diets as measured by ISD are at increased risk for BC, especially premenopausal women.

Journal article

Hageman S, Pennells L, Ojeda F, Kaptoge S, Kuulasmaa K, de Vries T, Xu Z, Kee F, Chung R, Wood A, McEvoy JW, Veronesi G, Bolton T, Dendale P, Ference BA, Halle M, Timmis A, Vardas P, Danesh J, Graham I, Salomaa V, Visseren F, De Bacquer D, Blankenberg S, Dorresteijn J, Di Angelantonio E, Achenbach S, Aleksandrova K, Amiano P, Amouyel P, Andersson J, Bakker SJL, Costa RBDP, Beulens JWJ, Blaha M, Bobak M, Boer JMA, Bonet C, Bonnet F, Boutron-Ruault M-C, Braaten T, Brenner H, Brunner F, Brunner EJ, Brunstrom M, Buring J, Butterworth AS, Capkova N, Cesana G, Chrysohoou C, Colorado-Yohar S, Cook NR, Cooper C, Dahm CC, Davidson K, Dennison E, Di Castelnuovo A, Donfrancesco C, Doerr M, Dorynska A, Eliasson M, Engstrom G, Ferrari P, Ferrario M, Ford I, Fu M, Gansevoort RT, Giampaoli S, Gillum RF, de la Camara AG, Grassi G, Hansson P-O, Huculeci R, Hveem K, Iacoviello L, Ikram MK, Jorgensen T, Joseph B, Jousilahti P, Jukema JW, Kaaks R, Katzke V, Kavousi M, Kiechl S, Klotsche J, Koenig W, Kronmal RA, Kubinova R, Kucharska-Newton A, Lall K, Lehmann N, Leistner D, Linneberg A, Lora Pablos D, Lorenz T, Lu W, Luksiene D, Lyngbakken M, Magnussen C, Malyutina S, Marin Ibanez A, Masala G, Mathiesen EB, Matsushita K, Meade TW, Melander O, Meyer HE, Moons KGM, Moreno-Iribas C, Muller D, Muenzel T, Nikitin Y, Nordestgaard BG, 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 BM, Quarti-Trevano F, Quiros Garcia JR, Riboli E, Ridker PM, Rodriguez B, Rodriguez-Barranco M, Rosengren A, Roussel R, Sacerdote C, Sans S, Sattar N, Schiborn C, Schmidt B, Schoettker B, Schulze M, Schwartz JE, Selmer RM, Shea S, Shipley MJ, Sieri S, Soderberg S, Sofat R, Tamosiunas A, Thorand B, Tillmann T, Tjonneland A, Tong TYN, Trichopoulou A, Tumino R, Tunstall-Pedoe H, Tybjaerg-Hansen A, Tzoulaki J, van der Heijden A, van der Schouw YT, Verschuren WMM, Voelzke H, Waldeyer C, Wareham NJ, Weiderpass E, Weidinger F Wet al., 2021, SCORE2 risk prediction algorithms: new models to estimate 10-year risk of cardiovascular disease in Europe, EUROPEAN HEART JOURNAL, Vol: 42, Pages: 2439-2454, ISSN: 0195-668X

Journal article

Huyghe JR, Harrison TA, Bien SA, Hampel H, Figueiredo JC, Schmit SL, Conti DV, Chen S, Qu C, Lin Y, Barfield R, Baron JA, Cross AJ, Diergaarde B, Duggan D, Harlid S, Imaz L, Kang HM, Levine DM, Perduca V, Perez-Cornago A, Sakoda LC, Schumacher FR, Slattery ML, Toland AE, van Duijnhoven FJB, Van Guelpen B, Agudo A, Albanes D, Alonso MH, Anderson K, Arnau-Collell C, Arndt V, Banbury BL, Bassik MC, Berndt SI, Bézieau S, Bishop DT, Boehm J, Boeing H, Boutron-Ruault M-C, Brenner H, Brezina S, Buch S, Buchanan DD, Burnett-Hartman A, Caan BJ, Campbell PT, Carr PR, Castells A, Castellví-Bel S, Chan AT, Chang-Claude J, Chanock SJ, Curtis KR, de la Chapelle A, Easton DF, English DR, Feskens EJM, Gala M, Gallinger SJ, Gauderman WJ, Giles GG, Goodman PJ, Grady WM, Grove JS, Gsur A, Gunter MJ, Haile RW, Hampe J, Hoffmeister M, Hopper JL, Hsu W-L, Huang W-Y, Hudson TJ, Jenab M, Jenkins MA, Joshi AD, Keku TO, Kooperberg C, Kühn T, Küry S, Le Marchand L, Lejbkowicz F, Li CI, Li L, Lieb W, Lindblom A, Lindor NM, Männistö S, Markowitz SD, Milne RL, Moreno L, Murphy N, Nassir R, Offit K, Ogino S, Panico S, Parfrey PS, Pearlman R, Pharoah PDP, Phipps AI, Platz EA, Potter JD, Prentice RL, Qi L, Raskin L, Rennert G, Rennert HS, Riboli E, Schafmayer C, Schoen RE, Seminara D, Song M, Su Y-R, Tangen CM, Thibodeau SN, Thomas DC, Trichopoulou A, Ulrich CM, Visvanathan K, Vodicka P, Vodickova L, Vymetalkova V, Weigl K, Weinstein SJ, White E, Wolk A, Woods MO, Wu AH, Abecasis GR, Nickerson DA, Scacheri PC, Kundaje A, Casey G, Gruber SB, Hsu L, Moreno V, Hayes RB, Newcomb PA, Peters Uet al., 2021, Genetic architectures of proximal and distal colorectal cancer are partly distinct, Gut, Vol: 70, Pages: 1325-1334, ISSN: 0017-5749

OBJECTIVE: An understanding of the etiologic heterogeneity of colorectal cancer (CRC) is critical for improving precision prevention, including individualized screening recommendations and the discovery of novel drug targets and repurposable drug candidates for chemoprevention. Known differences in molecular characteristics and environmental risk factors among tumors arising in different locations of the colorectum suggest partly distinct mechanisms of carcinogenesis. The extent to which the contribution of inherited genetic risk factors for CRC differs by anatomical subsite of the primary tumor has not been examined. DESIGN: To identify new anatomical subsite-specific risk loci, we performed genome-wide association study (GWAS) meta-analyses including data of 48 214 CRC cases and 64 159 controls of European ancestry. We characterised effect heterogeneity at CRC risk loci using multinomial modelling. RESULTS: We identified 13 loci that reached genome-wide significance (p<5×10-8) and that were not reported by previous GWASs for overall CRC risk. Multiple lines of evidence support candidate genes at several of these loci. We detected substantial heterogeneity between anatomical subsites. Just over half (61) of 109 known and new risk variants showed no evidence for heterogeneity. In contrast, 22 variants showed association with distal CRC (including rectal cancer), but no evidence for association or an attenuated association with proximal CRC. For two loci, there was strong evidence for effects confined to proximal colon cancer. CONCLUSION: Genetic architectures of proximal and distal CRC are partly distinct. Studies of risk factors and mechanisms of carcinogenesis, and precision prevention strategies should take into consideration the anatomical subsite of the tumour.

Journal article

Mocci E, Kundu P, Wheeler W, Arslan AA, Beane-Freeman LE, Bracci PM, Brennan P, Canzian F, Du M, Gallinger S, Giles GG, Goodman PJ, Kooperberg C, Le Marchand L, Neale RE, Shu X-O, Visvanathan K, White E, Zheng W, Albanes D, Andreotti G, Babic A, Bamlet WR, Berndt S, Blackford AL, Bueno-de-Mesquita B, Buring JE, Campa D, Chanock SJ, Childs EJ, Duell EJ, Fuchs CS, Gaziano JM, Giovannucci EL, Goggins MG, Hartge P, Hassan MM, Holly EA, Hoover RN, Hung RJ, Kurtz RC, Lee I-M, Malats N, Milne RL, Ng K, Oberg AL, Panico S, Peters U, Porta M, Rabe KG, Riboli E, Rothman N, Scelo G, Sesso HD, Silverman DT, Stevens VL, Strobel O, Thompson IM, Tjonneland A, Trichopoulou A, Van den Eeden SK, Wactawski-Wende J, Wentzensen N, Wilkens LR, Yu H, Yuan F, Zeleniuch-Jacquotte A, Amundadottir LT, Li D, Jacobs EJ, Petersen GM, Wolpin BM, Risch HA, Kraft P, Chatterjee N, Klein AP, Stolzenberg-Solomon Ret al., 2021, Smoking Modifies Pancreatic Cancer Risk Loci on 2q21.3, CANCER RESEARCH, Vol: 81, Pages: 3134-3143, ISSN: 0008-5472

Journal article

Tsilidis KK, Papadimitriou N, Dimou N, Gill D, Lewis SJ, Martin RM, Murphy N, Markozannes G, Zuber V, Cross AJ, Burrows K, Lopez DS, Key TJ, Travis RC, Perez-Cornago A, Hunter DJ, van Duijnhoven FJB, Albanes D, Arndt V, Berndt SI, Bézieau S, Bishop DT, Boehm J, Brenner H, Burnett-Hartman A, Campbell PT, Casey G, Castellví-Bel S, Chan AT, Chang-Claude J, de la Chapelle A, Figueiredo JC, Gallinger SJ, Giles GG, Goodman PJ, Gsur A, Hampe J, Hampel H, Hoffmeister M, Jenkins MA, Keku TO, Kweon S-S, Larsson SC, Le Marchand L, Li CI, Li L, Lindblom A, Martín V, Milne RL, Moreno V, Nan H, Nassir R, Newcomb PA, Offit K, Pharoah PDP, Platz EA, Potter JD, Qi L, Rennert G, Sakoda LC, Schafmayer C, Slattery ML, Snetselaar L, Schenk J, Thibodeau SN, Ulrich CM, Van Guelpen B, Harlid S, Visvanathan K, Vodickova L, Wang H, White E, Wolk A, Woods MO, Wu AH, Zheng W, Bueno-de-Mesquita B, Boutron-Ruault M-C, Hughes DJ, Jakszyn P, Kühn T, Palli D, Riboli E, Giovannucci EL, Banbury BL, Gruber SB, Peters U, Gunter MJet al., 2021, Genetically predicted circulating concentrations of micronutrients and risk of colorectal cancer among individuals of European descent: a Mendelian randomization study, American Journal of Clinical Nutrition, Vol: 113, Pages: 1490-1502, ISSN: 0002-9165

BACKGROUND: The literature on associations of circulating concentrations of minerals and vitamins with risk of colorectal cancer is limited and inconsistent. Evidence from randomized controlled trials (RCTs) to support the efficacy of dietary modification or nutrient supplementation for colorectal cancer prevention is also limited. OBJECTIVES: To complement observational and RCT findings, we investigated associations of genetically predicted concentrations of 11 micronutrients (β-carotene, calcium, copper, folate, iron, magnesium, phosphorus, selenium, vitamin B-6, vitamin B-12, and zinc) with colorectal cancer risk using Mendelian randomization (MR). METHODS: Two-sample MR was conducted using 58,221 individuals with colorectal cancer and 67,694 controls from the Genetics and Epidemiology of Colorectal Cancer Consortium, Colorectal Cancer Transdisciplinary Study, and Colon Cancer Family Registry. Inverse variance-weighted MR analyses were performed with sensitivity analyses to assess the impact of potential violations of MR assumptions. RESULTS: Nominally significant associations were noted for genetically predicted iron concentration and higher risk of colon cancer [ORs per SD (ORSD): 1.08; 95% CI: 1.00, 1.17; P value = 0.05] and similarly for proximal colon cancer, and for vitamin B-12 concentration and higher risk of colorectal cancer (ORSD: 1.12; 95% CI: 1.03, 1.21; P value = 0.01) and similarly for colon cancer. A nominally significant association was also noted for genetically predicted selenium concentration and lower risk of colon cancer (ORSD: 0.98; 95% CI: 0.96, 1.00; P value = 0.05) and similarly for distal colon cancer. These associations were robust to sensitivity analyses. Nominally significant inverse associations were observed for zinc and risk of colorectal and distal colon cancers, but sensitivity analyses could not be performed. None of these findings survived correction for multiple testing. Genetica

Journal article

Iguacel I, Schmidt JA, Perez-Cornago A, Van Puyvelde H, Travis R, Stepien M, Scalbert A, Casagrande C, Weiderpass E, Riboli E, Schulze MB, Skeie G, Bodén S, Boeing H, Cross AJ, Harlid S, Jensen TE, Huerta JM, Katzke V, Kühn T, Lujan-Barroso L, Masala G, Rodriguez-Barranco M, Rostgaard-Hansen AL, van der Schouw YT, Vermeulen R, Tagliabue G, Tjønneland A, Trevisan M, Ferrari P, Gunter MJ, Huybrechts Iet al., 2021, Associations between dietary amino acid intakes and blood concentration levels, Clinical Nutrition, Vol: 40, Pages: 3772-3779, ISSN: 0261-5614

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 b

Journal article

Dianatinasab M, Wesselius A, de Loeij T, Salehi-Abargouei A, Yu EYW, Fararouei M, Brinkman M, van den Brandt P, White E, Weiderpass E, Le Calvez-Kelm F, Gunter MJ, Huybrechts I, Liedberg F, Skeie G, Tjonneland A, Riboli E, Zeegers MPet al., 2021, The association between meat and fish consumption and bladder cancer risk: a pooled analysis of 11 cohort studies, EUROPEAN JOURNAL OF EPIDEMIOLOGY, Vol: 36, Pages: 781-792, ISSN: 0393-2990

Journal article

Aredo JV, Luo SJ, Gardner RM, Sanyal N, Choi E, Hickey TP, Riley TL, Huang W-Y, Kurian AW, Leung AN, Wilkens LR, Robbins HA, Riboli E, Kaaks R, Tjonneland A, Vermeulen RCH, Panico S, Marchand LL, Amos CI, Hung RJ, Freedman ND, Johansson M, Cheng I, Wakelee HA, Han SSet al., 2021, Tobacco Smoking and Risk of Second Primary Lung Cancer, JOURNAL OF THORACIC ONCOLOGY, Vol: 16, Pages: 968-979, ISSN: 1556-0864

Journal article

Christakoudi S, Evangelou E, Riboli E, Tsilidis Ket al., 2021, GWAS of allometric body-shape indices in UK Biobank identifies loci suggesting associations with morphogenesis, organogenesis, adrenal cell renewal and cancer, Scientific Reports, Vol: 11, Pages: 1-18, ISSN: 2045-2322

Genetic studies have examined body-shape measures adjusted for body mass index (BMI), while allometric indices are additionally adjusted for height. We performed the first genome-wide association study of A Body Shape Index (ABSI), Hip Index (HI) and the new Waist-to-Hip Index and compared these with traditional indices, using data from the UK Biobank Resource for 219,872 women and 186,825 men with white British ancestry and Bayesian linear mixed-models (BOLT-LMM). One to two thirds of the loci identified for allometric body-shape indices were novel. Most prominent was rs72959041 variant in RSPO3 gene, expressed in visceral adipose tissue and regulating adrenal cell renewal. Highly ranked were genes related to morphogenesis and organogenesis, previously additionally linked to cancer development and progression. Genetic associations were fewer in men compared to women. Prominent region-specific associations showed variants in loci VEGFA and HMGA1 for ABSI and KLF14 for HI in women, and C5orf67 and HOXC4/5 for ABSI and RSPO3, VEGFA and SLC30A10 for HI in men. Although more variants were associated with waist and hip circumference adjusted for BMI compared to ABSI and HI, associations with height had previously been reported for many of the additional variants, illustrating the importance of adjusting correctly for height.

Journal article

Aune D, Sen A, Norat T, Riboli E, Folseraas Tet al., 2021, Primary sclerosing cholangitis and the risk of cancer, cardiovascular disease, and all-cause mortality: a systematic review and meta-analysis of cohort studies, Scientific Reports, Vol: 11, ISSN: 2045-2322

A diagnosis of primary sclerosing cholangitis (PSC) has been associated with increased risk of hepatobiliary cancers, colorectal cancer and all-cause mortality in several studies, while associations with cardiovascular disease have been inconsistent. We conducted a systematic review and meta-analysis of published cohort studies on the topic to summarize these associations. PubMed and Embase databases were searched up to January 13th, 2020. Cohort studies on PSC and risk of cancer, cardiovascular disease, or mortality were included. Summary relative risks (RRs) and 95% confidence intervals (95% CIs) were estimated using random effects models. The summary RR (95% CI) comparing persons with PSC to persons without PSC was 584.37 (269.42–1267.51, I2 = 89%, n = 4) for cholangiocarcinoma (CCA), 155.54 (125.34–193.02, I2 = 0%, n = 3) for hepatobiliary cancer, 30.22 (11.99–76.17, I2 = 0%, n = 2) for liver cancer, 16.92 (8.73–32.78, I2 = 88%, n = 4) for gastrointestinal cancer, 7.56 (2.42–23.62, I2 = 0%, n = 3) for pancreatic cancer, 6.10 (4.19–8.87, I2 = 14%, n = 7) for colorectal cancer (CRC), 4.13 (2.99–5.71, I2 = 80%, n = 5) for total cancer, 3.55 (2.94–4.28, I2 = 46%, n = 5) for all-cause mortality, and 1.57 (0.25–9.69, I2 = 79%, n = 2) for cardiovascular disease. Strong positive associations were observed between PSC and risk of CCA, hepatobiliary cancer, liver cancer, gastrointestinal cancer, pancreatic cancer, CRC, total cancer, and all-cause mortality, but not for cardiovascular disease.

Journal article

Heath A, Clasen J, Jayanth N, Jenab M, Tjønneland A, Petersen K, Overvad K, Srour B, Katzke V, Bergmann M, Schulze M, Masala G, Krogh V, Tumino R, Catalano A, Pasanisi F, Brustad M, Standahl Olsen K, Skeie G, Luján-Barroso L, Rodríguez Barranco M, Amiano P, Santiuste C, Barricarte Gurrea A, Axelson H, Ramne S, Ljungberg B, Watts E, Huybrechts I, Weiderpass E, Riboli E, Muller Det al., 2021, Soft drink and juice consumption and renal cell carcinoma incidence and mortality in the European Prospective Investigation into Cancer and Nutrition, Cancer Epidemiology, Biomarkers and Prevention, Vol: 30, Pages: 1270-1274, ISSN: 1055-9965

Background: Renal cell carcinoma (RCC) accounts for more than 80% of kidney cancers in adults, and obesity is a known risk factor. Regular consumption of sweetened beverages has been linked to obesity and several chronic diseases, including some types of cancer. It is uncertain whether soft drink and juice consumption is associated with risk of RCC. We investigated the associations of soft drink and juice consumption with RCC incidence and mortality in the European Prospective Investigation into Cancer and Nutrition (EPIC).Methods: A total of 389,220 EPIC participants with median age of 52 years at recruitment (1991–2000) were included. Cox regression yielded adjusted HRs and 95% confidence intervals (CI) for RCC incidence and mortality in relation to intakes of juices and total, sugar-sweetened, and artificially sweetened soft drinks.Results: A total of 888 incident RCCs and 356 RCC deaths were identified. In models including adjustment for body mass index and energy intake, there was no higher risk of incident RCC associated with consumption of juices (HR per 100 g/day increment = 1.03; 95% CI, 0.97–1.09), total soft drinks (HR = 1.01; 95% CI, 0.98–1.05), sugar-sweetened soft drinks (HR = 0.99; 95% CI, 0.94–1.05), or artificially sweetened soft drinks (HR = 1.02; 95% CI, 0.96–1.08). In these fully adjusted models, none of the beverages was associated with RCC mortality (HR, 95% CI per 100 g/day increment 1.06, 0.97–1.16; 1.03, 0.98–1.09; 0.97, 0.89–1.07; and 1.06, 0.99–1.14, respectively).Conclusions: Consumption of juices or soft drinks was not associated with RCC incidence or mortality after adjusting for obesity.

Journal article

Christakoudi S, Pagoni P, Ferrari P, Cross AJ, Tzoulaki I, Muller DC, Weiderpass E, Freisling H, Murphy N, Dossus L, Fortner RT, Agudo A, Overvad K, Perez-Cornago A, Key TJ, Brennan P, Johansson M, Tjønneland A, Halkjær J, Boutron-Ruault M-C, Artaud F, Severi G, Kaaks R, Schulze MB, Bergmann MM, Masala G, Grioni S, Simeon V, Tumino R, Sacerdote C, Skeie G, Rylander C, Borch KB, Quirós JR, Rodriguez-Barranco M, Chirlaque M-D, Ardanaz E, Amiano P, Drake I, Stocks T, Häggström C, Harlid S, Ellingjord-Dale M, Riboli E, Tsilidis KKet al., 2021, Weight change in middle adulthood and risk of cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, International Journal of Cancer, Vol: 148, Pages: 1637-1651, ISSN: 0020-7136

Obesity is a risk factor for several major cancers. Associations of weight change in middle adulthood with cancer risk, however, are less clear. We examined the association of change in weight and body mass index (BMI) category during middle adulthood with 42 cancers, using multivariable Cox proportional hazards models in the European Prospective Investigation into Cancer and Nutrition cohort. Of 241,323 participants (31% men), 20% lost and 32% gained weight (>0.4 to 5.0 kg/year) during 6.9 years (average). During 8.0 years of follow-up after the second weight assessment, 20,960 incident cancers were ascertained. Independent of baseline BMI, weight gain (per one kg/year increment) was positively associated with cancer of the corpus uteri (hazard ratio HR=1.14; 95% confidence interval: 1.05-1.23). Compared to stable weight (+/-0.4 kg/year), weight gain (>0.4 to 5.0 kg/year) was positively associated with cancers of the gallbladder and bile ducts (HR=1.41; 1.01-1.96), post-menopausal breast (HR=1.08, 1.00-1.16) and thyroid (HR=1.40; 1.04-1.90). Compared to maintaining normal weight, maintaining overweight or obese BMI (World Health Organization categories) was positively associated with most obesity-related cancers. Compared to maintaining the baseline BMI category, weight gain to a higher BMI category was positively associated with cancers of the post-menopausal breast (HR=1.19; 1.06-1.33), ovary (HR=1.40; 1.04-1.91), corpus uteri (HR=1.42; 1.06-1.91), kidney (HR=1.80; 1.20-2.68) and pancreas in men (HR=1.81; 1.11-2.95). Losing weight to a lower BMI category, however, was inversely associated with cancers of the corpus uteri (HR=0.40; 0.23-0.69) and colon (HR=0.69; 0.52-0.92). Our findings support avoiding weight gain and encouraging weight loss in middle adulthood.

Journal article

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