Imperial College London

DrNeilMurphy

Faculty of MedicineSchool of Public Health

Honorary Senior Research Fellow
 
 
 
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Contact

 

neil.murphy

 
 
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Location

 

Norfolk PlaceSt Mary's Campus

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Summary

 

Publications

Publication Type
Year
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125 results found

Mullee A, Dimou N, Allen N, O'Mara T, Gunter MJ, Murphy Net al., 2021, Testosterone, sex hormone-binding globulin, insulin-like growth factor-1 and endometrial cancer risk: observational and Mendelian randomization analyses., Br J Cancer

BACKGROUND: Dysregulation of endocrine pathways related to steroid and growth hormones may modify endometrial cancer risk; however, prospective data on testosterone, sex hormone-binding globulin (SHBG) and insulin-like growth factor (IGF)-1 are limited. To elucidate the role of these hormones in endometrial cancer risk we conducted complementary observational and Mendelian randomization (MR) analyses. METHODS: The observational analyses included 159,702 women (80% postmenopausal) enrolled in the UK Biobank. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. For MR analyses, genetic variants associated with hormone levels were identified and their association with endometrial cancer (12,906 cases/108,979 controls) was examined using two-sample MR. RESULTS: In the observational analysis, higher circulating concentrations of total (HR per unit inverse normal scale = 1.38, 95% CI = 1.22-1.57) and free testosterone (HR per unit log scale = 2.07, 95% CI = 1.66-2.58) were associated with higher endometrial cancer risk. An inverse association was found for SHBG (HR per unit inverse normal scale = 0.76, 95% CI = 0.67-0.86). Results for testosterone and SHBG were supported by the MR analyses. No association was found between genetically predicted IGF-1 concentration and endometrial cancer risk. CONCLUSIONS: Our results support probable causal associations between circulating concentrations of testosterone and SHBG with endometrial cancer risk.

Journal article

Papadimitriou N, Gunter MJ, Murphy N, Gicquiau A, Achaintre D, Brezina S, Gumpenberger T, Baierl A, Ose J, Geijsen AJMR, van Roekel EH, Gsur A, Gigic B, Habermann N, Ulrich CM, Kampman E, Weijenberg MP, Ueland PM, Kaaks R, Katzke V, Krogh V, Bueno-de-Mesquita B, Ardanaz E, Travis RC, Schulze MB, Sanchez M-J, Colorado-Yohar SM, Weiderpass E, Scalbert A, Keski-Rahkonen Pet al., 2021, Circulating tryptophan metabolites and risk of colon cancer: Results from case-control and prospective cohort studies, INTERNATIONAL JOURNAL OF CANCER, Vol: 149, Pages: 1659-1669, ISSN: 0020-7136

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

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

Dimou N, Yarmolinsky J, Bouras E, Tsilidis KK, Martin RM, Lewis SJ, Gram IT, Bakker MF, Brenner H, Figueiredo JC, Fortner RT, Gruber SB, Van Guelpen B, Hsu L, Kaaks R, Kweon S-S, Lin Y, Lindor NM, Newcomb PA, Sanchez-Perez M-J, Severi G, Tindle HA, Tumino R, Weiderpass E, Gunter MJ, Murphy Net al., 2021, Causal effects of lifetime smoking on breast and colorectal cancer risk: Mendelian randomization study, Cancer Epidemiology, Biomarkers and Prevention, Vol: 30, Pages: 953-964, ISSN: 1055-9965

BACKGROUND: Observational evidence has shown that smoking is a risk factor for breast and colorectal cancer. We used Mendelian randomization (MR) to examine causal associations between smoking and risks of breast and colorectal cancer. METHODS: Genome-wide association study summary data were used to identify genetic variants associated with lifetime amount of smoking (n=126 variants) and ever having smoked regularly (n=112 variants). Using two-sample MR, we examined these variants in relation to incident breast (122,977 cases/105,974 controls) and colorectal cancer (52,775 cases/45,940 controls). RESULTS: In inverse-variance weighted models, a genetic predisposition to higher lifetime amount of smoking was positively associated with breast cancer risk [odds ratio [OR] per 1-standard deviation (SD) increment: 1.13 (95% confidence interval [CI]: 1.00-1.26); P: 0.04]; although heterogeneity was observed. Similar associations were found for estrogen receptor-positive and estrogen receptor-negative tumors. Higher lifetime amount of smoking was positively associated with colorectal cancer [OR per 1-SD increment: 1.21 (95% CI: 1.04-1.40); P: 0.01], colon cancer [OR: 1.31 (95% CI: 1.11-1.55); P: <0.01], and rectal cancer [OR: 1.36 (95% CI: 1.07-1.73); P: 0.01]. Ever having smoked regularly was not associated with risks of breast [OR: 1.01 (95% CI: 0.90-1.14); P: 0.85] or colorectal cancer [OR: 0.97 (95% CI: 0.86-1.10); P: 0.68]. CONCLUSIONS: These findings are consistent with prior observational evidence and support a causal role of higher lifetime smoking amount in the development of breast and colorectal cancer. IMPACT: The results from this comprehensive MR analysis indicate that lifetime smoking is a causal risk factor for these common malignancies.

Journal article

Murphy N, Campbell PT, Gunter MJ, 2021, Unraveling the Etiology of Early-Onset Colorectal Cancer, JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, Vol: 113, Pages: 505-506, ISSN: 0027-8874

Journal article

Watts EL, Fensom GK, Byrne KS, Perez-Cornago A, Allen NE, Knuppel A, Gunter MJ, Holmes M, Martin RM, Murphy N, Tsilidis KK, Yeap BB, Key TJ, Travis RCet al., 2021, Circulating insulin-like growth factor-I, total and free testosterone concentrations and prostate cancer risk in 200 000 men in UK Biobank, International Journal of Cancer, Vol: 148, Pages: 2274-2288, ISSN: 0020-7136

Insulin‐like growth factor‐I (IGF‐I) and testosterone have been implicated in prostate cancer aetiology. Using data from a large prospective full‐cohort with standardised assays and repeat blood measurements, and genetic data from an international consortium, we investigated the associations of circulating IGF‐I, sex hormone‐binding globulin (SHBG), and total and calculated free testosterone concentrations with prostate cancer incidence and mortality. For prospective analyses, risk was estimated using multivariable‐adjusted Cox regression in 199 698 male UK Biobank participants. Hazard ratios (HRs) were corrected for regression dilution bias using repeat hormone measurements from a subsample. Two‐sample Mendelian randomisation (MR) analysis of IGF‐I and risk used genetic instruments identified from UK Biobank men and genetic outcome data from the PRACTICAL consortium (79 148 cases and 61 106 controls). We used cis‐ and all (cis and trans) SNP MR approaches. A total of 5402 men were diagnosed with and 295 died from prostate cancer (mean follow‐up 6.9 years). Higher circulating IGF‐I was associated with elevated prostate cancer diagnosis (HR per 5 nmol/L increment = 1.09, 95% CI 1.05‐1.12) and mortality (HR per 5 nmol/L increment = 1.15, 1.02‐1.29). MR analyses also supported the role of IGF‐I in prostate cancer diagnosis (cis‐MR odds ratio per 5 nmol/L increment = 1.34, 1.07‐1.68). In observational analyses, higher free testosterone was associated with a higher risk of prostate cancer (HR per 50 pmol/L increment = 1.10, 1.05‐1.15). Higher SHBG was associated with a lower risk (HR per 10 nmol/L increment = 0.95, 0.94‐0.97), neither was associated with prostate cancer mortality. Total testosterone was not associated with prostate cancer. These findings implicate IGF‐I and free testosterone in prostate cancer development and/or progression.

Journal article

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, BuenodeMesquita BH, Derksen JWG, Skeie G, Gram IT, Brustad M, Jakszyn P, Sánchez M, Amiano P, Huerta JM, Ericson U, Wennberg M, PerezCornago A, Heath AK, Jenab M, Chajes V, Gunter MJet al., 2021, Dietary intake and plasma phospholipid concentrations of saturated, monounsaturated and trans fatty acids and colorectal cancer risk in the EPIC cohort, International Journal of Cancer, Vol: 149, Pages: 865-882, ISSN: 0020-7136

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.

Journal article

Fuhrman BJ, Moore SC, Byrne C, Makhoul I, Kitahara CM, de Gonzalez AB, Linet MS, Weiderpass E, Adami H-O, Freedman ND, Liao LM, Matthews CE, Stolzenberg-Solomon RZ, Gaudet MM, Patel AV, Lee I-M, Buring JE, Wolk A, Larsson SC, Prizment AE, Robien K, Spriggs M, Check DP, Murphy N, Gunter MJ, Van Dusen HL, Ziegler RG, Hoover RNet al., 2021, Association of the Age at Menarche with Site-Specific Cancer Risks in Pooled Data from Nine Cohorts, CANCER RESEARCH, Vol: 81, Pages: 2246-2255, ISSN: 0008-5472

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

Matta M, Huybrechts I, Biessy C, Casagrande C, Yammine S, Fournier A, Olsen KS, Lukic M, Gram IT, Ardanaz E, Sánchez M-J, Dossus L, Fortner RT, Srour B, Jannasch F, Schulze MB, Amiano P, Agudo A, Colorado-Yohar S, Quirós JR, Tumino R, Panico S, Masala G, Pala V, Sacerdote C, Tjønneland A, Olsen A, Dahm CC, Rosendahl AH, Borgquist S, Wennberg M, Heath AK, Aune D, Schmidt J, Weiderpass E, Chajes V, Gunter MJ, Murphy Net al., 2021, Dietary intake of trans fatty acids and breast cancer risk in 9 European countries, BMC Medicine, Vol: 19, Pages: 1-11, ISSN: 1741-7015

BackgroundTrans fatty acids (TFAs) have been hypothesised to influence breast cancer risk. However, relatively few prospective studies have examined this relationship, and well-powered analyses according to hormone receptor-defined molecular subtypes, menopausal status, and body size have rarely been conducted.MethodsIn the European Prospective Investigation into Cancer and Nutrition (EPIC), we investigated the associations between dietary intakes of TFAs (industrial trans fatty acids [ITFAs] and ruminant trans fatty acids [RTFAs]) and breast cancer risk among 318,607 women. Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models, adjusted for other breast cancer risk factors.ResultsAfter a median follow-up of 8.1 years, 13,241 breast cancer cases occurred. In the multivariable-adjusted model, higher total ITFA intake was associated with elevated breast cancer risk (HR for highest vs lowest quintile, 1.14, 95% CI 1.06–1.23; P trend = 0.001). A similar positive association was found between intake of elaidic acid, the predominant ITFA, and breast cancer risk (HR for highest vs lowest quintile, 1.14, 95% CI 1.06–1.23; P trend = 0.001). Intake of total RTFAs was also associated with higher breast cancer risk (HR for highest vs lowest quintile, 1.09, 95% CI 1.01–1.17; P trend = 0.015). For individual RTFAs, we found positive associations with breast cancer risk for dietary intakes of two strongly correlated fatty acids (Spearman correlation r = 0.77), conjugated linoleic acid (HR for highest vs lowest quintile, 1.11, 95% CI 1.03–1.20; P trend = 0.001) and palmitelaidic acid (HR for highest vs lowest quintile, 1.08, 95% CI 1.01–1.16; P trend = 0.028). Similar associations were found for total ITFAs and RTFAs with breast cancer risk according to menopausal status, body mass index, and bre

Journal article

NCD Risk Factor Collaboration NCD-RisC, Iurilli N, 2021, Heterogeneous contributions of change in population distribution of body-mass index to change in obesity and underweight, eLife, Vol: 10, ISSN: 2050-084X

From 1985 to 2016, the prevalence of underweight decreased, and that of obesity and severe obesity increased, in most regions, with significant variation in the magnitude of these changes across regions. We investigated how much change in mean body mass index (BMI) explains changes in the prevalence of underweight, obesity, and severe obesity in different regions using data from 2896 population-based studies with 187 million participants. Changes in the prevalence of underweight and total obesity, and to a lesser extent severe obesity, are largely driven by shifts in the distribution of BMI, with smaller contributions from changes in the shape of the distribution. In East and Southeast Asia and sub-Saharan Africa, the underweight tail of the BMI distribution was left behind as the distribution shifted. There is a need for policies that address all forms of malnutrition by making healthy foods accessible and affordable, while restricting unhealthy foods through fiscal and regulatory restrictions.

Journal article

Thomas M, Sakoda LC, Hoffmeister M, Rosenthal EA, Lee JK, van Duijnhoven FJB, Platz EA, Wu AH, Dampier CH, de la Chapelle A, Wolk A, Joshi AD, Burnett-Hartman A, Gsur A, Lindblom A, Castells A, Kowin A, Namjou B, Van Guelpen B, Tangen CM, He Q, Li CI, Schafmayer C, Joshu CE, Ulrich CM, Bishop DT, Buchanan DD, Schaid D, Drew DA, Muller DC, Duggan D, Crosslin DR, Albanes D, Giovannucci EL, Larson E, Qu F, Mentch F, Giles GG, Hakonarson H, Hampel H, Stanaway IB, Figueiredo JC, Huyghe JR, Minnier J, Chang-Claude J, Hampe J, Harley JB, Visvanathan K, Curtis KR, Offit K, Li L, Le Marchand L, Vodickova L, Gunter MJ, Jenkins MA, Slattery ML, Lemire M, Woods MO, Song M, Murphy N, Lindor NM, Dikilitas O, Pharoah PDP, Campbell PT, Newcomb PA, Milne RL, MacInnis RJ, Castellvi-Bel S, Ogino S, Berndt SI, Bezieau S, Thibodeau SN, Gallinger SJ, Zaidi SH, Harrison TA, Keku TO, Hudson TJ, Vymetalkova V, Moreno V, Martin V, Arndt V, Wei W-Q, Chung W, Su Y-R, Hayes RB, White E, Vodicka P, Casey G, Gruber SB, Schoen RE, Chan AT, Potter JD, Brenner H, Jarvik GP, Corley DA, Peters U, Hsu Let al., 2021, Age dependency of the polygenic risk score for colorectal cancer Response, AMERICAN JOURNAL OF HUMAN GENETICS, Vol: 108, Pages: 527-529, ISSN: 0002-9297

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Guo X, Lin W, Wen W, Huyghe J, Bien S, Cai Q, Harrison T, Chen Z, Qu C, Bao J, Long J, Yuan Y, Wang F, Bai M, Abecasis GR, Albanes D, Berndt S, Bezieau S, Bishop DT, Brenner H, Buch S, Burnett-Hartman A, Campbell PT, Castellvi-Bel S, Chan AT, Chang-Claude J, Chanock SJ, Cho SH, Conti D, de la Chapelle A, Feskens EJM, Gallinger SJ, Giles GG, Goodman PJ, Gsur A, Guinter M, Gunter MJ, Hampe J, Hampel H, Hayes RB, Hoffmeister M, Kampman E, Kang HM, Keku TO, Kim HR, Le Marchand L, Lee SC, Li C, Li L, Lindblom A, Lindor N, Milne RL, Moreno V, Murphy N, Newcomb PA, Nickerson DA, Offit K, Pearlman R, Pharoah PDP, Platz EA, Potter JD, Rennert G, Sakoda LC, Schafmayer C, Schmit SL, Schoen RE, Schumacher FR, Slattery ML, Su Y-R, Tangen CM, Ulrich CM, van Duijnhoven FJB, Van Guelpen B, Visvanathan K, Vodicka P, Vodickova L, Vymetalkova V, Wang X, White E, Wolk A, Woods MO, Casey G, Hsu L, Jenkins MA, Gruber SB, Peters U, Zheng Wet al., 2021, Identifying Novel Susceptibility Genes for Colorectal Cancer Risk From a Transcriptome-Wide Association Study of 125,478 Subjects, GASTROENTEROLOGY, Vol: 160, Pages: 1164-+, ISSN: 0016-5085

Journal article

Khoei NS, Carreras-Torres R, Murphy N, Gunter MJ, Brennan P, Smith-Byrne K, Mariosa D, Mckay J, O'Mara TA, Jarrett R, Hjalgrim H, Smedby KE, Cozen W, Onel K, Diepstra A, Wagner K-H, Freisling Het al., 2021, Genetically Raised Circulating Bilirubin Levels and Risk of Ten Cancers: A Mendelian Randomization Study, CELLS, Vol: 10

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Papadimitriou N, Dimou N, Gill D, Tzoulaki I, Murphy N, Riboli E, Lewis SJ, Martin RM, Gunter MJ, Tsilidis KKet al., 2021, Genetically predicted circulating concentrations of micro-nutrients and risk of breast cancer: A Mendelian randomization study, International Journal of Cancer, Vol: 148, Pages: 646-653, ISSN: 0020-7136

The epidemiological literature reports inconsistent associations between consumption or circulating concentrations of micro-nutrients and breast cancer risk. We investigated associations between genetically predicted concentrations of 11 micro-nutrients (beta-carotene, calcium, copper, folate, iron, magnesium, phosphorus, selenium, vitamin B6, vitamin B12 and zinc) and breast cancer risk using Mendelian randomization (MR). A two-sample MR study was conducted using 122,977 women with breast cancer and 105,974 controls from the Breast Cancer Association Consortium. MR analyses were conducted using the inverse variance weighted approach, and sensitivity analyses were conducted to assess the impact of potential violations of MR assumptions. One standard deviation (SD: 0.08 mmol/L) higher genetically predicted concentration of magnesium was associated with a 17% (odds ratio [OR]: 1.17, 95% confidence interval [CI]: 1.10 to 1.25, P-value=9.1 ×10-7 ) and 20% (OR: 1.20, 95% CI: 1.08 to 1.34, P-value=3.2×10-6 ) higher risk of overall and ER+ve breast cancer, respectively. An inverse association was observed for a SD (0.5 mg/dL) higher genetically predicted phosphorus concentration and ER-ve breast cancer (OR: 0.84, 95% CI: 0.72 to 0.98, P-value=0.03). There was little evidence that any other nutrient was associated with breast cancer. The results for magnesium were robust under all sensitivity analyses and survived correction for multiple comparisons. Higher circulating concentrations of magnesium and potentially phosphorus may affect breast cancer risk. Further work is required to replicate these findings and investigate underlying mechanisms.

Journal article

Campbell PT, Lin Y, Bien SA, Figueiredo JC, Harrison TA, Guinter MA, Berndt S, Brenner H, Chan AT, Chang-Claude J, Gallinger SJ, Gapstur SM, Giles GG, Giovannucci E, Gruber SB, Gunter M, Hoffmeister M, Jacobs EJ, Jenkins MA, Le Marchand L, Li L, McLaughlin JR, Murphy N, Milne RL, Newcomb PA, Newton C, Ogino S, Potter JD, Rennert G, Rennert HS, Robinson J, Sakoda LC, Slattery ML, Song Y, White E, Woods MO, Casey G, Hsu L, Peters Uet al., 2021, Association of Body Mass Index With Colorectal Cancer Risk by Genome-Wide Variants, JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, Vol: 113, Pages: 38-47, ISSN: 0027-8874

Journal article

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 MJet al., 2020, Metabolic Signatures of Healthy Lifestyle Patterns and Colorectal Cancer Risk in a European Cohort, Clinical Gastroenterology and Hepatology, ISSN: 1542-3565

Background & AimsColorectal 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 cohort.MethodsScores 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 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.ResultsHigher 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.ConclusionsMetabolite 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.

Journal article

Bull CJ, Bell JA, Murphy N, Sanderson E, Davey Smith G, Timpson NJ, Banbury BL, Albanes D, Berndt SI, Bezieau S, Bishop DT, Brenner H, Buchanan DD, Burnett-Hartman A, Casey G, Castellvi-Bel S, Chan AT, Chang-Claude J, Cross AJ, de la Chapelle A, Figueiredo JC, Gallinger SJ, Gapstur SM, Giles GG, Gruber SB, Gsur A, Hampe J, Hampel H, Harrison TA, Hoffmeister M, Hsu L, Huang W-Y, Huyghe JR, Jenkins MA, Joshu CE, Keku TO, Kuhn T, Kweon S-S, Le Marchand L, Li CI, Li L, Lindblom A, Martin V, May AM, Milne RL, Moreno V, Newcomb PA, Offit K, Ogino S, Phipps AI, Platz EA, Potter JD, Qu C, Quiros JR, Rennert G, Riboli E, Sakoda LC, Schafmayer C, Schoen RE, Slattery ML, Tangen CM, Tsilidis KK, Ulrich CM, van Duijnhoven FJB, van Guelpen B, Visvanathan K, Vodicka P, Vodickova L, Wang H, White E, Wolk A, Woods MO, Wu AH, Campbell PT, Zheng W, Peters U, Vincent EE, Gunter MJet al., 2020, Adiposity, metabolites, and colorectal cancer risk: Mendelian randomization study, BMC Medicine, Vol: 18, ISSN: 1741-7015

BackgroundHigher adiposity increases the risk of colorectal cancer (CRC), but whether this relationship varies by anatomical sub-site or by sex is unclear. Further, the metabolic alterations mediating the effects of adiposity on CRC are not fully understood.MethodsWe examined sex- and site-specific associations of adiposity with CRC risk and whether adiposity-associated metabolites explain the associations of adiposity with CRC. Genetic variants from genome-wide association studies of body mass index (BMI) and waist-to-hip ratio (WHR, unadjusted for BMI; N = 806,810), and 123 metabolites from targeted nuclear magnetic resonance metabolomics (N = 24,925), were used as instruments. Sex-combined and sex-specific Mendelian randomization (MR) was conducted for BMI and WHR with CRC risk (58,221 cases and 67,694 controls in the Genetics and Epidemiology of Colorectal Cancer Consortium, Colorectal Cancer Transdisciplinary Study, and Colon Cancer Family Registry). Sex-combined MR was conducted for BMI and WHR with metabolites, for metabolites with CRC, and for BMI and WHR with CRC adjusted for metabolite classes in multivariable models.ResultsIn sex-specific MR analyses, higher BMI (per 4.2 kg/m2) was associated with 1.23 (95% confidence interval (CI) = 1.08, 1.38) times higher CRC odds among men (inverse-variance-weighted (IVW) model); among women, higher BMI (per 5.2 kg/m2) was associated with 1.09 (95% CI = 0.97, 1.22) times higher CRC odds. WHR (per 0.07 higher) was more strongly associated with CRC risk among women (IVW OR = 1.25, 95% CI = 1.08, 1.43) than men (IVW OR = 1.05, 95% CI = 0.81, 1.36). BMI or WHR was associated with 104/123 metabolites at false discovery rate-corrected P ≤ 0.05; several metabolites were associated with CRC, but not in directions that were consistent with the mediation of positive adiposity-CRC relatio

Journal article

Ghoneim DH, Zhu J, Zheng W, Long J, Murff HJ, Ye F, Setiawan VW, Wilkens LR, Khankari NK, Haycock P, Antwi SO, Yang Y, Arslan AA, Freeman LEB, Bracci PM, Canzian F, Du M, Gallinger S, Giles GG, Goodman PJ, Kooperberg C, Le Marchand L, Neale RE, Scelo G, Visvanathan K, White E, Albanes D, Amiano P, Andreotti G, Babic A, Bamlet WR, Berndt SI, Brais LK, Brennan P, Bueno-De-Mesquita B, Buring JE, Campbell PT, Rabe KG, Chanock SJ, Duggal P, Fuchs CS, Gaziano JM, Goggins MG, Hackert T, Hassan MM, Helzlsouer KJ, Holly EA, Hoover RN, Katske V, Kurtz RC, Lee I-M, Malats N, Milne RL, Murphy N, Oberg AL, Porta M, Rothman N, Sesso HD, Silverman DT, Thompson IM, Wactawski-Wende J, Wang X, Wentzensen N, Yu H, Zeleniuch-Jacquotte A, Yu K, Wolpin BM, Jacobs EJ, Duell EJ, Risch HA, Petersen GM, Amundadottir LT, Kraft P, Klein AP, Stolzenberg-Solomon RZ, Shu X-O, Wu Let al., 2020, Mendelian Randomization Analysis of n-6 Polyunsaturated Fatty Acid Levels and Pancreatic Cancer Risk, CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION, Vol: 29, Pages: 2735-2739, ISSN: 1055-9965

Journal article

Rodriguez-Martinez A, Zhou B, Sophiea MK, Bentham J, Paciorek CJ, Iurilli ML, Carrillo-Larco RM, Bennett JE, Di Cesare M, Taddei C, Bixby H, Stevens GA, Riley LM, Cowan MJ, Savin S, Danaei G, Chirita-Emandi A, Kengne AP, Khang YH, Laxmaiah A, Malekzadeh R, Miranda JJ, Moon JS, Popovic SR, Sørensen TI, Soric M, Starc G, Zainuddin AA, Gregg EW, Bhutta ZA, Black R, Abarca-Gómez L, Abdeen ZA, Abdrakhmanova S, Abdul Ghaffar S, Abdul Rahim HF, Abu-Rmeileh NM, Abubakar Garba J, Acosta-Cazares B, Adams RJ, Aekplakorn W, Afsana K, Afzal S, Agdeppa IA, Aghazadeh-Attari J, Aguilar-Salinas CA, Agyemang C, Ahmad MH, Ahmad NA, Ahmadi A, Ahmadi N, Ahmed SH, Ahrens W, Aitmurzaeva G, Ajlouni K, Al-Hazzaa HM, Al-Othman AR, Al-Raddadi R, Alarouj M, AlBuhairan F, AlDhukair S, Ali MM, Alkandari A, Alkerwi A, Allin K, Alvarez-Pedrerol M, Aly E, Amarapurkar DN, Amiri P, Amougou N, Amouyel P, Andersen LB, Anderssen SA, Ängquist L, Anjana RM, Ansari-Moghaddam A, Aounallah-Skhiri H, Araújo J, Ariansen I, Aris T, Arku RE, Arlappa N, Aryal KK, Aspelund T, Assah FK, Assunção MCF, Aung MS, Auvinen J, Avdicová M, Azevedo A, Azimi-Nezhad M, Azizi F, Azmin M, Babu BV, Bæksgaard Jørgensen M, Baharudin A, Bahijri S, Baker JL, Balakrishna N, Bamoshmoosh Met al., 2020, Height and body-mass index trajectories of school-aged children and adolescents from 1985 to 2019 in 200 countries and territories: a pooled analysis of 2181 population-based studies with 65 million participants, The Lancet, Vol: 396, Pages: 1511-1524, ISSN: 0140-6736

SummaryBackgroundComparable global data on health and nutrition of school-aged children and adolescents are scarce. We aimed to estimate age trajectories and time trends in mean height and mean body-mass index (BMI), which measures weight gain beyond what is expected from height gain, for school-aged children and adolescents.MethodsFor this pooled analysis, we used a database of cardiometabolic risk factors collated by the Non-Communicable Disease Risk Factor Collaboration. We applied a Bayesian hierarchical model to estimate trends from 1985 to 2019 in mean height and mean BMI in 1-year age groups for ages 5–19 years. The model allowed for non-linear changes over time in mean height and mean BMI and for non-linear changes with age of children and adolescents, including periods of rapid growth during adolescence.FindingsWe pooled data from 2181 population-based studies, with measurements of height and weight in 65 million participants in 200 countries and territories. In 2019, we estimated a difference of 20 cm or higher in mean height of 19-year-old adolescents between countries with the tallest populations (the Netherlands, Montenegro, Estonia, and Bosnia and Herzegovina for boys; and the Netherlands, Montenegro, Denmark, and Iceland for girls) and those with the shortest populations (Timor-Leste, Laos, Solomon Islands, and Papua New Guinea for boys; and Guatemala, Bangladesh, Nepal, and Timor-Leste for girls). In the same year, the difference between the highest mean BMI (in Pacific island countries, Kuwait, Bahrain, The Bahamas, Chile, the USA, and New Zealand for both boys and girls and in South Africa for girls) and lowest mean BMI (in India, Bangladesh, Timor-Leste, Ethiopia, and Chad for boys and girls; and in Japan and Romania for girls) was approximately 9–10 kg/m2. In some countries, children aged 5 years started with healthier height or BMI than the global median and, in some cases, as healthy as the best performing countries, but they became

Journal article

Dimou NL, Papadimitriou N, Mariosa D, Johansson M, Brennan P, Peters U, Chanock SJ, Purdue M, Bishop DT, Gago-Dominquez M, Giles GG, Moreno V, Platz EA, Tangen CM, Wolk A, Zheng W, Wu X, Campbell PT, Giovannucci E, Lin Y, Gunter MJ, Murphy Net al., 2020, Circulating adipokine concentrations and risk of five obesity-related cancers: A Mendelian randomization study, INTERNATIONAL JOURNAL OF CANCER, Vol: 148, Pages: 1625-1636, ISSN: 0020-7136

Journal article

Sanikini H, Muller DC, Chadeau-Hyam M, Murphy N, Gunter MJ, Cross AJet al., 2020, Anthropometry, body fat composition and reproductive factors and risk of oesophageal and gastric cancer by subtype and subsite in the UK Biobank cohort, PLoS One, Vol: 15, Pages: 1-22, ISSN: 1932-6203

BackgroundObesity has been positively associated with upper gastrointestinal cancers, but prospective data by subtype/subsite are limited. Obesity influences hormonal factors, which may play a role in these cancers. We examined anthropometry, body fat and reproductive factors in relation to oesophageal and gastric cancer by subtype/subsite in the UK Biobank cohort.MethodsAmong 458,713 UK Biobank participants, 339 oesophageal adenocarcinomas, 124 oesophageal squamous cell carcinomas, 137 gastric cardia and 92 gastric non-cardia cancers were diagnosed during a mean of 6.5 years follow-up. Cox models estimated multivariable hazard ratios (HRs) and 95% confidence intervals (CIs).ResultsBody mass index (BMI), hip circumference, waist circumference, waist-to-hip ratio, waist-to-height ratio, total body fat and trunk fat were positively associated with oesophageal adenocarcinoma (highest vs lowest category: HR = 2.33, 95%-CI:1.65–3.28; HR = 1.56, 95%-CI:1.15–2.13; HR = 2.30, 95%-CI:1.47–3.57; HR = 1.71, 95%-CI:1.01–2.90; HR = 2.87, 95%-CI:1.88–4.38; HR = 1.96, 95%-CI:1.30–2.96; HR = 2.34, 95%-CI:1.70–3.22, respectively). Although there were no statistically significant associations in combined sex analyses, BMI (HR = 1.83, 95%-CI:1.00–3.37), waist circumference (HR = 2.21, 95%-CI:1.27–3.84) and waist-to-hip ratio (HR = 1.92, 95%-CI:1.11–3.29) were associated with gastric cardia cancer in men; however, mutual adjustment attenuated the associations for BMI and waist-to-hip ratio. For oesophageal squamous cell carcinoma, statistically significant inverse associations were observed among women for BMI, hip circumference, waist circumference, waist-to-height ratio, total body fat and trunk fat, although they were based on small numbers. In addition, older age at first (HR = 0.44, 95%-CI:0.22–0.88) and last live birth (HR = 0.44, 95%-CI:0.22–0.87) were inversely associated with oesophageal squamous cell carc

Journal article

Labadie JD, Harrison TA, Banbury B, Amtay EL, Bernd S, Brenner H, Buchanan DD, Campbell PT, Cao Y, Chan AT, Chang-Claude J, English D, Figueiredo JC, Gallinger SJ, Giles GG, Gunter MJ, Hoffmeister M, Hsu L, Jenkins MA, Lin Y, Milne RL, Moreno V, Murphy N, Ogino S, Phipps A, Sakoda LC, Slattery ML, Southey MC, Sun W, Thibodeau SN, Van Guelpen B, Zaidi SH, Peters U, Newcomb PAet al., 2020, Postmenopausal Hormone Therapy and Colorectal Cancer Risk by Molecularly Defined Subtypes and Tumor Location, JNCI CANCER SPECTRUM, Vol: 4

Journal article

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 HA, Weiderpass E, Overvad K, Tjønneland A, Rostgaard-Hansen AL, Boutron-Ruault M-C, Mancini FR, Mahamat-Saleh Y, Kühn T, Katzke V, Bergmann MM, Schulze MB, Trichopoulou A, Karakatsani A, Peppa E, Masala G, Agnoli C, De Magistris MS, Tumino R, Sacerdote C, Boer JM, Verschuren WM, van der Schouw YT, Skeie G, Braaten T, Redondo ML, Agudo A, Petrova D, Colorado-Yohar SM, Barricarte A, Amiano P, Sonestedt E, Ericson U, Otten J, Sundström B, Wareham NJ, Forouhi NG, Vineis P, Tsilidis KK, Knuppel A, Papier K, Ferrari P, Riboli E, Gunter MJ, Touvier Met al., 2020, Association between nutritional profiles of foods underlying Nutri-Score front-of-pack labels and mortality: EPIC cohort study in 10 European countries., BMJ, Vol: 370, Pages: 1-13, ISSN: 1759-2151

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<0.001 for trend) and mortality from cancer (1.08, 1.03 to 1.13, P<0.001 for trend) and diseases of the circulatory (1.04, 0.98 to 1.11, P=0.06 for trend), respiratory (1.39, 1.22 to 1.59, P<0.001), and digestive (1.22, 1.02 to 1.45, P=0.03 for trend) systems. The age standardised absolute rates for all cause mortality per 10 000 persons over 10 years were 760 (men=1237; women=563) for those in the highest fifth of the FSA

Journal article

Yuan F, Hung RJ, Walsh N, Zhang H, Platz EA, Wheeler W, Song L, Arslan AA, Freeman LEB, Bracci P, Canzian F, Du M, Gallinger S, Giles GG, Goodman PJ, Kooperberg C, Le Marchand L, Neale RE, Rosendahl J, Scelo G, Shu X-O, Visvanathan K, White E, Zheng W, Albanes D, Amiano P, Andreotti G, Babic A, Bamlet WR, Berndt SI, Brennan P, Bueno-de-Mesquita B, Buring JE, Campbell PT, Chanock SJ, Fuchs CS, Gaziano JM, Goggins MG, Hackert T, Hartge P, Hassan MM, Holly EA, Hoover RN, Katzke V, Kirsten H, Kurtz RC, Lee I-M, Malats N, Milne RL, Murphy N, Ng K, Oberg AL, Porta M, Rabe KG, Real FX, Rothman N, Sesso HD, Silverman DT, Thompson IM, Wactawski-Wende J, Wang X, Wentzensen N, Wilkens LR, Yu H, Zeleniuch-Jacquotte A, Shi J, Duell EJ, Amundadottir LT, Li D, Petersen GM, Wolpin BM, Risch HA, Yu K, Klein AP, Stolzenberg-Solomon Ret al., 2020, Genome-Wide Association Study Data Reveal Genetic Susceptibility to Chronic Inflammatory Intestinal Diseases and Pancreatic Ductal Adenocarcinoma Risk, CANCER RESEARCH, Vol: 80, Pages: 4004-4013, ISSN: 0008-5472

Journal article

Knuppel A, Fensom GK, Watts EL, Gunter MJ, Murphy N, Papier K, Perez-Cornago A, Schmidt JA, Byrne KS, Travis RC, Key TJet al., 2020, Circulating Insulin-like Growth Factor-I Concentrations and Risk of 30 Cancers: Prospective Analyses in UK Biobank, CANCER RESEARCH, Vol: 80, Pages: 4014-4021, ISSN: 0008-5472

Journal article

Thomas M, Sakoda LC, Hoffmeister M, Rosenthal EA, Lee JK, van Duijnhoven FJB, Platz EA, Wu AH, Dampier CH, de la Chapelle A, Wolk A, Joshi AD, Burnett-Hartman A, Gsur A, Lindblom A, Castells A, Win AK, Namjou B, Van Guelpen B, Tangen CM, He Q, Li C, Schafmayer C, Joshu CE, Ulrich CM, Bishop DT, Buchanan DD, Schaid D, Drew DA, Muller DC, Duggan D, Crosslin DR, Albanes D, Giovannucci EL, Larson E, Qu F, Mentch F, Giles GG, Hakonarson H, Hampel H, Stanaway IB, Figueiredo JC, Huyghe JR, Minnier J, Chang-Claude J, Hampe J, Harley JB, Visvanathan K, Curtis KR, Offit K, Li L, Le Marchand L, Vodickova L, Gunter MJ, Jenkins MA, Slattery ML, Lemire M, Woods MO, Song M, Murphy N, Lindor NM, Dikilitas O, Pharoah PDP, Campbell PT, Newcomb PA, Milne RL, MacInnis RJ, Castellvi-Bel S, Ogino S, Berndt S, Bezieau S, Thibodeau SN, Gallinger SJ, Zaidi SH, Harrison TA, Keku TO, Hudson TJ, Vymetalkova V, Moreno V, Martin V, Arndt V, Wei W-Q, Chung W, Su Y-R, Hayes RB, White E, Vodicka P, Casey G, Gruber SB, Schoen RE, Chan AT, Potter JD, Brenner H, Jarvik GP, Corley DA, Peters U, Hsu Let al., 2020, Genome-wide Modeling of Polygenic Risk Score in Colorectal Cancer Risk, AMERICAN JOURNAL OF HUMAN GENETICS, Vol: 107, Pages: 432-444, ISSN: 0002-9297

Journal article

Bueno-de-Mesquita B, Cross A, Aune D, Tsilidis Ket al., 2020, Circulating bilirubin levels and risk of colorectal cancer: serological and Mendelian randomization analyses, BMC Medicine, Vol: 18, Pages: 1-15, ISSN: 1741-7015

BACKGROUND: Bilirubin, a byproduct of hemoglobin breakdown and purported antioxidant, 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, 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 < 5x10-8) 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 (Pheterogeneity=0.008). Among men, higher levels of UCB were positively associated with CRC risk (odds ratio [OR] = 1.19, 95% confidence interval [CI] = 1.04-1.36; per 1-SD increment of log-UCB). In women, an inverse association was observed (OR = 0.86 (0.76-0.97)). In the MR analysis of the main UGT1A1 SNP (rs6431625), genetically predicted higher levels of total bilirubin, were associated with a 7% increase in CRC risk in men (OR = 1.07 (1.02-1.12); P=0.006; per 1-SD increment of total bilirubin), while there was no association in women (OR = 1.01 (0.96-1.06); P=0.73). Raised bilirubin levels, predicted by instrumental variables excluding rs6431625, were

Journal article

Stepien M, Keski-Rahkonen P, Kiss A, Robinot N, Duarte-Salles T, Murphy N, Perlemuter G, Viallon V, Tjonneland A, Rostgaard-Hansen AL, Dahm CC, Overvad K, Boutron-Ruault M-C, Mancini FR, Mahannat-Saleh Y, Aleksandrova K, Kaaks R, Kuehn T, Trichopoulou A, Karakatsani A, Panico S, Tumino R, Palli D, Tagliabue G, Naccarati A, Vermeulen RCH, Bueno-de-Mesquita HB, Weiderpass E, Skeie G, Ramon Quiros J, Ardanaz E, Mokoroa O, Sala N, Sanchez M-J, Maria Huerta J, Winkvist A, Harlid S, Ohlsson B, Sjoberg K, Schmidt JA, Wareham N, Khaw K-T, Ferrari P, Rothwell JA, Gunter M, Riboli E, Scalbert A, Jenab Met al., 2020, Metabolic perturbations prior to hepatocellular carcinoma diagnosis: Findings from a prospective observational cohort study, INTERNATIONAL JOURNAL OF CANCER, Vol: 148, Pages: 609-625, ISSN: 0020-7136

Journal article

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