Imperial College London

DrNeilMurphy

Faculty of MedicineSchool of Public Health

Honorary Senior Research Fellow
 
 
 
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neil.murphy

 
 
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Norfolk PlaceSt Mary's Campus

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Summary

 

Publications

Publication Type
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198 results found

Zhou B, Carrillo-Larco RM, Danaei G, Riley LM, Paciorek CJ, Stevens GA, Gregg EW, Bennett JE, Solomon B, Singleton RKet al., 2021, Worldwide trends in hypertension prevalence and progress in treatment and control from 1990 to 2019: a pooled analysis of 1201 population-representative studies with 104 million participants, The Lancet, Vol: 398, Pages: 957-980, ISSN: 0140-6736

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

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

Dashti SG, Viallon V, Simpson JA, Karahalios A, Moreno-Betancur M, English DR, Gunter MJ, Murphy Net al., 2020, Explaining the link between adiposity and colorectal cancer risk in men and postmenopausal women in the UK Biobank: A sequential causal mediation analysis, INTERNATIONAL JOURNAL OF CANCER, Vol: 147, Pages: 1881-1894, ISSN: 0020-7136

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

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

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

Kliemann N, Murphy N, Viallon V, Freisling H, Tsilidis KK, Rinaldi S, Mancini FR, Fagherazzi G, Boutron-Ruault M-C, Boeing H, Schulze MB, Masala G, Krogh V, Sacerdote C, Santucci de Magistris M, Bueno-de-Mesquita B, Weiderpass E, Kühn T, Kaaks R, Jakszyn P, Redondo-Sánchez D, Amiano P, Chirlaque M-D, Barricarte Gurrea A, Ericson U, Drake I, Nøst TH, Aune D, May AM, Tjønneland A, Dahm CC, Overvad K, Tumino R, Ramón Quirós J, Trichopoulou A, Karakatsani A, La Vecchia C, Nilsson LM, Riboli E, Huybrechts I, Gunter MJet al., 2020, Predicted Basal metabolic rate and cancer risk in the European Prospective Investigation into Cancer and Nutrition (Epic), International Journal of Cancer, Vol: 147, Pages: 648-661, ISSN: 0020-7136

Emerging evidence suggests that a metabolic profile associated with obesity may be a more relevant risk factor for some cancers than adiposity per se. Basal metabolic rate (BMR) is an indicator of overall body metabolism and may be a proxy for the impact of a specific metabolic profile on cancer risk. Therefore, we investigated the association of estimated BMR with incidence of 13 obesity-related cancers in the European Prospective Investigation into Cancer and Nutrition. Estimated BMR at baseline was calculated using the WHO/FAO/UNU equations and the relationships between BMR and cancer risk were investigated using multivariable Cox proportional hazards regression models. A total of 141,295 men and 317,613 women, with a mean follow-up of 14 years were included in the analysis. Overall, higher BMR was associated with a greater risk for most cancers that have been linked with obesity. However, among normal weight participants, higher BMR was associated with elevated risks of esophageal adenocarcinoma (Hazard Ratio per 1-standard deviation change in BMR [HR1-sd ]: 2.46; 95%CI 1.20; 5.03), and distal colon cancer (HR1-sd : 1.33; 95%CI 1.001; 1.77) among men, and with proximal colon (HR1-sd : 1.16; 95%CI 1.01; 1.35), pancreatic (HR1-sd : 1.37; 95%CI 1.13; 1.66), thyroid (HR1-sd : 1.65; 95%CI 1.33; 2.05), postmenopausal breast (HR1-sd : 1.17; 95%CI 1.11; 1.22), and endometrial (HR1-sd : 1.20; 95%CI 1.03; 1.40) cancers in women. These results indicate that higher BMR may be an indicator of a metabolic phenotype associated with risk of certain cancer types, and may be a useful predictor of cancer risk independent of body fatness. This article is protected by copyright. All rights reserved.

Journal article

Lujan-Barroso L, Botteri E, Caini S, Ljungberg B, Roswall N, Tjønneland A, Bueno-de-Mesquita B, Gram IT, Tumino R, Kiemeney LA, Liedberg F, Stocks T, Gunter MJ, Murphy N, Cervenka I, Fournier A, Kvaskoff M, Häggström C, Overvad K, Lund E, Waaseth M, Fortner RT, Kühn T, Menéndez V, Sánchez M-J, Santiuste C, Perez-Cornago A, Zamora-Ros R, Cross AJ, Trichopoulou A, Karakatsani A, Peppa E, Palli D, Krogh V, Sciannameo V, Mattiello A, Panico S, van Gils CH, Onland-Moret NC, Barricarte A, Amiano P, Khaw K-T, Boeing H, Weiderpass E, Duell EJet al., 2020, Menstrual factors, reproductive history, hormone use, and urothelial carcinoma risk: a prospective study in the EPIC cohort, Cancer Epidemiology, Biomarkers and Prevention, Vol: 29, Pages: 1654-1664, ISSN: 1055-9965

BACKGROUND: Urothelial carcinoma is the predominant (95%) bladder cancer subtype in industrialized nations. Animal and epidemiologic human studies suggest that hormonal factors may influence urothelial carcinoma risk. METHODS: We used an analytic cohort of 333,919 women from the European Prospective Investigation into Cancer and Nutrition Cohort. Associations between hormonal factors and incident urothelial carcinoma (overall and by tumor grade, tumor aggressiveness, and non-muscle-invasive urothelial carcinoma) risk were evaluated using Cox proportional hazards models. RESULTS: During a mean of 15 years of follow-up, 529 women developed urothelial carcinoma. In a model including number of full-term pregnancies (FTP), menopausal status, and menopausal hormone therapy (MHT), number of FTP was inversely associated with urothelial carcinoma risk (HR≥5vs1 = 0.48; 0.25-0.90; Ptrend in parous women = 0.010) and MHT use (compared with nonuse) was positively associated with urothelial carcinoma risk (HR = 1.27; 1.03-1.57), but no dose response by years of MHT use was observed. No modification of HRs by smoking status was observed. Finally, sensitivity analyses in never smokers showed similar HR patterns for the number of FTP, while no association between MHT use and urothelial carcinoma risk was observed. Association between MHT use and urothelial carcinoma risk remained significant only in current smokers. No heterogeneity of the risk estimations in the final model was observed by tumor aggressiveness or by tumor grade. A positive association between MTH use and non-muscle-invasive urothelial carcinoma risk was observed. CONCLUSIONS: Our results support that increasing the number of FTP may reduce urothelial carcinoma risk. IMPACT: More detailed studies on parity are needed to understand the possible effects of perinatal hormone changes in urothelial cells.

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, Arndt V, Agudo A, Albanes D, Alonso MH, Anderson K, Arnau-Collell C, Banbury B, 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 P, 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, Kuhn 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., 2020, Genetic architectures of proximal and distal colorectal cancer are partly distinct

<jats:title>ABSTRACT</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>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 sporadic CRC differs by anatomical subsite of the primary tumor has not been examined.</jats:p></jats:sec><jats:sec><jats:title>Design</jats:title><jats:p>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 characterized effect heterogeneity at CRC risk loci using multinomial modeling.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>We identified 13 loci that reached genome-wide significance <jats:italic>(P</jats:italic>&lt;5×10<jats:sup>−8</jats:sup>) and that were not reported by previous GWAS 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.</jats:p></jats:sec><jats:sec>&

Journal article

Murphy N, Knuppel A, Papadimitriou N, Martin RM, Tsilidis KK, Smith-Byrne K, Fensom G, Perez-Cornago A, Travis RC, Key TJ, Gunter MJet al., 2020, Insulin-like growth factor-1, insulin-like growth factor-binding protein-3, and breast cancer risk: observational and Mendelian randomization analyses with ∼430 000 women, Annals of Oncology, Vol: 31, Pages: 641-649, ISSN: 0923-7534

BACKGROUND: Epidemiological evidence supports a positive association between circulating insulin-like growth factor-1 (IGF-1) concentrations and breast cancer risk, but both the magnitude and causality of this relationship are uncertain. We conducted observational analyses with adjustment for regression dilution bias, and Mendelian randomization (MR) analyses allowed for causal inference. PATIENTS AND METHODS: We investigated the associations between circulating IGF-1 concentrations and incident breast cancer risk in 206 263 women in the UK Biobank. Multivariable hazard ratios (HRs) and 95% confidence intervals (CI) were estimated using Cox proportional hazards models. HRs were corrected for regression dilution using repeat IGF-1 measures available in a subsample of 6711 women. For the MR analyses, genetic variants associated with circulating IGF-1 and IGF-binding protein-3 (IGFBP-3) levels were identified and their association with breast cancer was examined with two-sample MR methods using genome-wide data from 122 977 cases and 105 974 controls. RESULTS: In the UK Biobank, after a median follow-up of 7.1 years, 4360 incident breast cancer cases occurred. In the multivariable-adjusted models corrected for regression dilution, higher IGF-1 concentrations were associated with a greater risk of breast cancer (HR per 5 nmol/l increment of IGF-1 = 1.11, 95% CI = 1.07-1.16). Similar positive associations were found by follow-up time, menopausal status, body mass index, and other risk factors. In the MR analyses, a 5 nmol/l increment in genetically-predicted IGF-1 concentration was associated with a greater breast cancer risk (odds ratio = 1.05, 95% CI = 1.01-1.10; P = 0.02), with a similar effect estimate for estrogen-positive (ER+) tumours, but no effect found for estrogen-negative (ER-) tumours. Genetically-predicted IGFBP-3 concentrations were not associated with breast cancer risk (odds ratio per 1-standard deviation increment = 1.00, 9

Journal article

Xia Z, Su Y-R, Petersen P, Qi L, Kim AE, Figueiredo JC, Lin Y, Nan H, Sakoda LC, Albanes D, Berndt SI, Bezieau S, Bien S, Buchanan DD, Casey G, Chan AT, Conti DV, Drew DA, Gallinger SJ, Gauderman WJ, Giles GG, Gruber SB, Gunter MJ, Hoffmeister M, Jenkins MA, Joshi AD, Le Marchand L, Lewinger JP, Li L, Lindor NM, Moreno V, Murphy N, Nassir R, Newcomb PA, Ogino S, Rennert G, Song M, Wang X, Wolk A, Woods MO, Brenner H, White E, Slattery ML, Giovannucci EL, Chang-Claude J, Pharoah PDP, Hsu L, Campbell PT, Peters Uet al., 2020, Functional informed genome-wide interaction analysis of body mass index, diabetes and colorectal cancer risk, CANCER MEDICINE, Vol: 9, Pages: 3563-3573, ISSN: 2045-7634

Journal article

Murphy N, Carreras-Torres R, Song M, Chan AT, Martin RM, Papadimitriou N, Dimou N, Tsilidis KK, Banbury B, Bradbury KE, Besevic J, Rinaldi S, Riboli E, Cross AJ, Travis RC, Agnoli C, Albanes D, Berndt SI, Bézieau S, Bishop DT, Brenner H, Buchanan DD, Onland-Moret NC, Burnett-Hartman A, Campbell PT, Casey G, Castellví-Bel S, Chang-Claude J, Chirlaque M-D, Chapelle ADL, English D, Figueiredo JC, Gallinger SJ, Giles GG, Gruber SB, Gsur A, Hampe J, Hampel H, Harrison TA, Hoffmeister M, Hsu L, Huang W-Y, Huyghe JR, Jenkins MA, Keku TO, Kühn T, Kweon S-S, Le Marchand L, Li CI, Li L, Lindblom A, Martín V, Milne RL, Moreno V, Newcomb PA, Offit K, Ogino S, Ose J, Perduca V, Phipps AI, Platz EA, Potter JD, Qu C, Rennert G, Sakoda LC, Schafmayer C, Schoen RE, Slattery ML, Tangen CM, Ulrich CM, van Duijnhoven FJ, Van Guelpen B, Visvanathan K, Vodicka P, Vodickova L, Vymetalkova V, Wang H, White E, Wolk A, Woods MO, Wu AH, Zheng W, Peters U, Gunter MJet al., 2020, Circulating levels of insulin-like growth factor 1 and insulin-like growth factor binding protein 3 associate with risk of colorectal cancer based on serologic and mendelian randomization analyses, Gastroenterology, Vol: 158, Pages: 1300-1312.e20, ISSN: 0016-5085

BACKGROUND AIMS: Human studies examining associations between circulating levels of insulin-like growth factor 1 (IGF1) and insulin-like growth factor binding protein 3 (IGFBP3) and colorectal cancer risk have reported inconsistent results. We conducted complementary serologic and Mendelian randomization (MR) analyses to determine whether alterations in circulating levels of IGF1 or IGFBP3 are associated with colorectal cancer development. METHODS: Serum levels of IGF1 and other proteins were measured in blood samples collected from 397,380 participants from the UK Biobank, from 2006 through 2010. Incident cancer cases and cancer cases recorded first in death certificates were identified through linkage to national cancer and death registries. Complete follow up was available through March 31, 2016. For the MR analyses, we identified genetic variants associated with circulating levels of IGF1 and IGFBP3. The association of these genetic variants with colorectal cancer was examined with 2-sample MR methods using genome-wide association study consortia data (52,865 cases with colorectal cancer and 46,287 individuals without [controls]) RESULTS: After a median follow-up period of 7.1 years, 2665 cases of colorectal cancer were recorded. In a multivariable-adjusted model, circulating level of IGF1 level associated with colorectal cancer risk (hazard ratio per 1 standard deviation increment of IGF1, 1.11; 95% CI, 1.05-1.17). Similar associations were found by sex, follow-up time, and tumor subsite. In the MR analyses, a 1 standard deviation increment in IGF1 level, predicted based on genetic factors, was associated with a higher risk of colorectal cancer risk (odds ratio, 1.08; 95% CI, 1.03-1.12; P=3.3 x 10-4). Level of IGFBP3, predicted based on genetic factors, was associated with colorectal cancer risk (odds ratio per 1 standard deviation increment, 1.12; 95% CI, 1.06-1.18; P =4.2 x 10-5). Colorectal cancer risk was associated with only 1 variant in IGFBP3 (rs11977526

Journal article

Archambault AN, Su Y-R, Jeon J, Thomas M, Lin Y, Conti DV, Win AK, Sakoda LC, Lansdorp-Vogelaar I, Peterse EF, Zauber AG, Duggan D, Holowatyj AN, Huyghe JR, Brenner H, Cotterchio M, Bézieau S, Schmit SL, Edlund CK, Southey MC, MacInnis RJ, Campbell PT, Chang-Claude J, Slattery ML, Chan AT, Joshi AD, Song M, Cao Y, Woods MO, White E, Weinstein SJ, Ulrich CM, Hoffmeister M, Bien SA, Harrison TA, Hampe J, Li CI, Schafmayer C, Offit K, Pharoah PD, Moreno V, Lindblom A, Wolk A, Wu AH, Li L, Gunter MJ, Gsur A, Keku TO, Pearlman R, Bishop DT, Castellví-Bel S, Moreira L, Vodicka P, Kampman E, Giles GG, Albanes D, Baron JA, Berndt SI, Brezina S, Buch S, Buchanan DD, Trichopoulou A, Severi G, Chirlaque M-D, Sánchez M-J, Palli D, Kühn T, Murphy N, Cross AJ, Burnett-Hartman AN, Chanock SJ, Chapelle ADL, Easton DF, Elliott F, English DR, Feskens EJ, FitzGerald LM, Goodman PJ, Hopper JL, Hudson TJ, Hunter DJ, Jacobs EJ, Joshu CE, Küry S, Markowitz SD, Milne RL, Platz EA, Rennert G, Rennert HS, Schumacher FR, Sandler RS, Seminara D, Tangen CM, Thibodeau SN, Toland AE, van Duijnhoven FJ, Visvanathan K, Vodickova L, Potter JD, Männistö S, Weigl K, Figueiredo J, Martín V, Larsson SC, Parfrey PS, Huang W-Y, Lenz H-J, Castelao JE, Gago-Dominguez M, Muñoz-Garzón V, Mancao C, Haiman CA, Wilkens LR, Siegel E, Barry E, Younghusband B, Van Guelpen B, Harlid S, Zeleniuch-Jacquotte A, Liang PS, Du M, Casey G, Lindor NM, Le Marchand L, Gallinger SJ, Jenkins MA, Newcomb PA, Gruber SB, Schoen RE, Hampel H, Corley DA, Hsu L, Peters U, Hayes RBet al., 2020, Cumulative burden of colorectal cancer-associated genetic variants is more strongly associated with early-onset vs late-onset cancer, Gastroenterology, Vol: 158, Pages: 1274-1286.e12, ISSN: 0016-5085

BACKGROUND & AIMS: Early-onset colorectal cancer (CRC, in persons younger than 50 years old) is increasing in incidence; yet, in the absence of a family history of CRC, this population lacks harmonized recommendations for prevention. We aimed to determine whether a polygenic risk score (PRS) developed from 95 CRC-associated common genetic risk variants was associated with risk for early-onset CRC. METHODS: We studied risk for CRC associated with a weighted PRS in 12,197 participants younger than 50 years old vs 95,865 participants 50 years or older. PRS was calculated based on single-nucleotide polymorphisms associated with CRC in a large-scale genome-wide association study as of January 2019. Participants were pooled from 3 large consortia that provided clinical and genotyping data: the Colon Cancer Family Registry, the Colorectal Transdisciplinary study, and the Genetics and Epidemiology of Colorectal Cancer Consortium and were all of genetically defined European descent. Findings were replicated in an independent cohort of 72,573 participants. RESULTS: Overall associations with CRC per standard deviation of PRS were significant for early-onset cancer, and were stronger compared with late-onset cancer (P for interaction=.01); when we compared the highest PRS quartile with the lowest, risk increased 3.7-fold for early-onset CRC (95% CI, 3.28-4.24) vs 2.9-fold for late-onset CRC (95% CI, 2.80-3.04). This association was strongest for participants without a first-degree family history of CRC (P for interaction=5.61x10-5). When we compared the highest with the lowest quartiles in this group, risk increased 4.3-fold for early-onset CRC (95% CI, 3.61-5.01) vs 2.9-fold for late-onset CRC (95% CI, 2.70-3.00). Sensitivity analyses were consistent with these findings. CONCLUSIONS: In an analysis of associations with CRC per standard deviation of PRS, we found the cumulative burden of CRC-associated common genetic variants to associate with early-onset cancer, and to be

Journal article

Watts EL, Fensom GK, Byrne KS, Perez-Cornago A, Allen NE, Knuppel A, Gunter MJ, Holmes MV, Martin RM, Murphy N, Tsilidis KK, Yeap BB, Key TJ, Travis RCet al., 2020, Circulating insulin-like growth factor-I, total and free testosterone concentrations and prostate cancer risk in 200,000 men in UK Biobank

<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Insulin-like growth factor-I (IGF-I) and testosterone have been implicated in prostate cancer aetiology. Using newly available data from a large prospective full-cohort with standardised assays and repeat blood measurements, and genetic data from an international consortium, we aimed to investigate the associations of circulating concentrations of IGF-I, sex hormone-binding globulin (SHBG), total and calculated free testosterone with prostate cancer risk.</jats:p></jats:sec><jats:sec><jats:title>Patients and methods</jats:title><jats:p>For prospective analyses of prostate cancer incidence and mortality, we studied 199,698 male UK Biobank participants using Cox proportional hazards models. Multivariable-adjusted hazard ratios (HRs) were corrected for regression dilution bias using repeat hormone measurements from a subsample of up to 7,776 men. A 2-sample Mendelian randomization (MR) analysis of IGF-I and risk used genetic instruments identified from UK Biobank men and genetic outcome data from 79,148 cases and 61,106 controls from the PRACTICAL consortium. We used <jats:italic>cis</jats:italic>- and all (<jats:italic>cis</jats:italic> and <jats:italic>trans</jats:italic>) SNP MR approaches.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>After a mean follow-up of 6.9 years, 5,402 men were diagnosed with and 295 died from prostate cancer. Higher circulating IGF-I was associated with an elevated risk (HR per 5 nmol/L increment=1.09, 95% CI 1.05-1.12) and prostate cancer mortality (HR per 5 nmol/L increment=1.15,1.02-1.29) in observational analyses. <jats:italic>Cis</jats:italic>- and all SNPs MR analyses also supported the role of IGF-I in prostate cancer diagnosis (<jats:italic>cis</jats:italic>-M

Journal article

Bull CJ, Bell JA, Murphy N, Sanderson E, Smith GD, Timpson NJ, Banbury BL, Albanes D, Berndt SI, Bézieau S, Bishop DTT, Brenner H, Buchanan DD, Burnett-Hartman A, Casey G, Castellví-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, Kühn T, Kweon S-S, Le Marchand L, Li CI, Li L, Lindblom A, Martín V, May AM, Milne RL, Moreno V, Newcomb PA, Offit K, Ogino S, Phipps AI, Platz EA, Potter JD, Qu C, Quirós 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

<jats:title>Abstract</jats:title><jats:sec><jats:title>Importance</jats:title><jats:p>Evidence on adiposity altering colorectal cancer (CRC) risk differently among men and women, and on metabolic alterations mediating effects of adiposity on CRC, is unclear.</jats:p></jats:sec><jats:sec><jats:title>Objective</jats:title><jats:p>To examine sex- and site-specific associations of adiposity with CRC risk, and whether adiposity-associated metabolites explain associations of adiposity with CRC.</jats:p></jats:sec><jats:sec><jats:title>Design</jats:title><jats:p>Two-sample Mendelian randomization (MR) study.</jats:p></jats:sec><jats:sec><jats:title>Setting</jats:title><jats:p>Genetic variants from expanded genome-wide association studies of body mass index (BMI) and waist-to-hip ratio (WHR, unadjusted for BMI; N=806,810), and 123 metabolites (mostly lipoprotein subclass-specific lipids) from targeted nuclear magnetic resonance metabolomics (N=24,925), were used as instruments. Sex-combined and sex-specific MR was conducted for BMI and WHR with CRC risk; 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.</jats:p></jats:sec><jats:sec><jats:title>Participants</jats:title><jats:p>58,221 cases and 67,694 controls (Genetics and Epidemiology of Colorectal Cancer Consortium; Colorectal Cancer Transdisciplinary Study; Colon Cancer Family Registry).</jats:p></jats:sec><jats:sec><jats:title>Main outcome measures</jats:title><jats:p>Incident CRC (overall and site-specific).</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Among men, higher BMI (per 4.2 kg/m<jats:sup>2</jats:sup>) was associated with 1.23 (9

Journal article

Aglago EK, Huybrechts I, Murphy N, Casagrande C, Nicolas G, Pischon T, Fedirko V, Severi G, Boutron-Ruault M-C, Fournier A, Katzke V, Kühn T, Olsen A, Tjønneland A, Dahm CC, Overvad K, Lasheras C, Agudo A, Sánchez M-J, Amiano P, Huerta JM, Ardanaz E, Perez-Cornago A, Trichopoulou A, Karakatsani A, Martimianaki G, Palli D, Pala V, Tumino R, Naccarati A, Panico S, Bueno-de-Mesquita B, May A, Derksen JWG, Hellstrand S, Ohlsson B, Wennberg M, Van Guelpen B, Skeie G, Brustad M, Weiderpass E, Cross AJ, Ward H, Riboli E, Norat T, Chajes V, Gunter MJet al., 2020, Consumption of fish and long-chain n-3 polyunsaturated fatty acids is associated with reduced risk of colorectal cancer in a large European cohort, Clinical Gastroenterology and Hepatology, Vol: 18, Pages: 654-666.e6, ISSN: 1542-3565

BACKGROUND & AIMS: There is an unclear association between intake of fish and long-chain n-3 polyunsaturated fatty acids (n-3 LC-PUFAs) and colorectal cancer (CRC). We examined the association between fish consumption, dietary and circulating levels of n-3 LC-PUFAs, and ratio of n-6:n-3 LC-PUFA with CRC using data from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. METHODS: Dietary intake of fish (total, fatty/oily, lean/white) and n-3 LC-PUFA were estimated by food frequency questionnaires given to 521,324 participants in the EPIC study; among these, 6291 individuals developed CRC (median follow up, 14.9 years). Levels of phospholipid LC-PUFA were measured by gas chromatography in plasma samples from a sub-group of 461 CRC cases and 461 matched individuals without CRC (controls). Multivariable Cox proportional hazards and conditional logistic regression models were used to calculate hazard ratios (HRs) and odds ratios (ORs), respectively, with 95% CIs. RESULTS: Total intake of fish (HR for quintile 5 vs 1, 0.88; 95% CI, 0.80-0.96; Ptrend=.005), fatty fish (HR for quintile 5 vs 1, 0.90; 95% CI, 0.82-0.98; Ptrend=.009), and lean fish (HR for quintile 5 vs 1, 0.91; 95% CI, 0.83-1.00; Ptrend=.016) were inversely associated with CRC incidence. Intake of total n-3 LC-PUFA (HR for quintile 5 vs 1, 0.86; 95% CI, 0.78-0.95; Ptrend=.010) was also associated with reduced risk of CRC, whereas dietary ratio of n-6:n-3 LC-PUFA was associated with increased risk of CRC (HR for quintile 5 vs 1, 1.31; 95% CI, 1.18-1.45; Ptrend<.001). Plasma levels of phospholipid n-3 LC-PUFA was not associated with overall CRC risk, but an inverse trend was observed for proximal compared with distal colon cancer (Pheterogeneity=.026). CONCLUSIONS: In an analysis of dietary patterns of participants in the EPIC study, we found regular consumption of fish, at recommended levels, to be associated with a lower risk of CRC, possibly through exposure to n-3 LC-PUFA.

Journal article

Sanikini H, Muller DC, Sophiea M, Rinaldi S, Agudo A, Duell EJ, Weiderpass E, Overvad K, Tjønneland A, Halkjaer J, Boutron-Ruault M-C, Carbonnel F, Cervenka I, Boeing H, Kaaks R, Kühn T, Trichopoulou A, Martimianaki G, Karakatsani A, Pala V, Palli D, Mattiello A, Tumino R, Sacerdote C, Skeie G, Rylander C, López MDC, Sánchez M-J, Ardanaz E, Regnér S, Stocks T, Bueno-de-Mesquita B, Vermeulen RCH, Aune D, Tong TYN, Kliemann N, Murphy N, Chadeau-Hyam M, Gunter MJ, Cross AJet al., 2020, Anthropometric and reproductive factors and risk of esophageal and gastric cancer by subtype and subsite: results from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, International Journal of Cancer, Vol: 146, Pages: 929-942, ISSN: 0020-7136

Obesity has been associated with upper gastrointestinal cancers; however, there are limited prospective data on associations by subtype/subsite. Obesity can impact hormonal factors, which have been hypothesized to play a role in these cancers. We investigated anthropometric and reproductive factors in relation to esophageal and gastric cancer by subtype and subsite for 476,160 participants from the European Prospective Investigation into Cancer and Nutrition cohort. Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox models. During a mean follow‐up of 14 years, 220 esophageal adenocarcinomas (EA), 195 esophageal squamous cell carcinomas, 243 gastric cardia (GC) and 373 gastric noncardia (GNC) cancers were diagnosed. Body mass index (BMI) was associated with EA in men (BMI ≥30 vs. 18.5–25 kg/m2: HR = 1.94, 95% CI: 1.25–3.03) and women (HR = 2.66, 95% CI: 1.15–6.19); however, adjustment for waist‐to‐hip ratio (WHR) attenuated these associations. After mutual adjustment for BMI and HC, respectively, WHR and waist circumference (WC) were associated with EA in men (HR = 3.47, 95% CI: 1.99–6.06 for WHR >0.96 vs. <0.91; HR = 2.67, 95% CI: 1.52–4.72 for WC >98 vs. <90 cm) and women (HR = 4.40, 95% CI: 1.35–14.33 for WHR >0.82 vs. <0.76; HR = 5.67, 95% CI: 1.76–18.26 for WC >84 vs. <74 cm). WHR was also positively associated with GC in women, and WC was positively associated with GC in men. Inverse associations were observed between parity and EA (HR = 0.38, 95% CI: 0.14–0.99; >2 vs. 0) and age at first pregnancy and GNC (HR = 0.54, 95% CI: 0.32–0.91; >26 vs. <22 years); whereas bilateral ovariectomy was positively associated with GNC (HR = 1.87, 95% CI: 1.04–3.36). These findings support a role for hormonal pathways in upper gastrointestinal cancers.

Journal article

Mullee A, Gunter MJ, Murphy N, 2020, Hypertension and Unlikely Causality in the Association Between Soft Drink Consumption and Mortality Reply, JAMA INTERNAL MEDICINE, Vol: 180, Pages: 336-337, ISSN: 2168-6106

Journal article

Bradbury KE, Murphy N, Key TJ, 2020, Diet and colorectal cancer in UK Biobank: a prospective study, INTERNATIONAL JOURNAL OF EPIDEMIOLOGY, Vol: 49, Pages: 246-258, ISSN: 0300-5771

Journal article

Papadimitriou N, Dimou N, Tsilidis KK, Banbury B, Martin RM, Lewis SJ, Kazmi N, Robinson TM, Albanes D, Aleksandrova K, Berndt SI, Timothy Bishop D, Brenner H, Buchanan DD, Bueno-de-Mesquita B, Campbell PT, Castellví-Bel S, Chan AT, Chang-Claude J, Ellingjord-Dale M, Figueiredo JC, Gallinger SJ, Giles GG, Giovannucci E, Gruber SB, Gsur A, Hampe J, Hampel H, Harlid S, Harrison TA, Hoffmeister M, Hopper JL, Hsu L, María Huerta J, Huyghe JR, Jenkins MA, Keku TO, Kühn T, La Vecchia C, Le Marchand L, Li CI, Li L, Lindblom A, Lindor NM, Lynch B, Markowitz SD, Masala G, May AM, Milne R, Monninkhof E, Moreno L, Moreno V, Newcomb PA, Offit K, Perduca V, Pharoah PDP, Platz EA, Potter JD, Rennert G, Riboli E, Sánchez M-J, Schmit SL, Schoen RE, Severi G, Sieri S, Slattery ML, Song M, Tangen CM, Thibodeau SN, Travis RC, Trichopoulou A, Ulrich CM, van Duijnhoven FJB, Van Guelpen B, Vodicka P, White E, Wolk A, Woods MO, Wu AH, Peters U, Gunter MJ, Murphy Net al., 2020, Physical activity and risks of breast and colorectal cancer: a Mendelian randomisation analysis, Nature Communications, Vol: 11, ISSN: 2041-1723

Physical activity has been associated with lower risks of breast and colorectal cancer in epidemiological studies; however, it is unknown if these associations are causal or confounded. In two-sample Mendelian randomisation analyses, using summary genetic data from the UK Biobank and GWA consortia, we found that a one standard deviation increment in average acceleration was associated with lower risks of breast cancer (odds ratio [OR]: 0.51, 95% confidence interval [CI]: 0.27 to 0.98, P-value = 0.04) and colorectal cancer (OR: 0.66, 95% CI: 0.48 to 0.90, P-value = 0.01). We found similar magnitude inverse associations for estrogen positive (ER+ve) breast cancer and for colon cancer. Our results support a potentially causal relationship between higher physical activity levels and lower risks of breast cancer and colorectal cancer. Based on these data, the promotion of physical activity is probably an effective strategy in the primary prevention of these commonly diagnosed cancers.

Journal article

Harms LM, Scalbert A, Zamora-Ros R, Rinaldi S, Jenab M, Murphy N, Achaintre D, Tjonneland A, Olsen A, Overvad K, Mancini FR, Mahamat-Saleh Y, Boutron-Ruault M-C, Kuehn T, Katzke V, Trichopoulou A, Martimianaki G, Karakatsani A, Palli D, Panico S, Sieri S, Tumino R, Sacerdote C, Bueno-de-Mesquita B, Vermeulen RCH, Weiderpass E, Nost TH, Lasheras C, Rodriguez-Barranco M, Maria Huerta J, Barricarte A, Dorronsoro M, Hultdin J, Schmidt JA, Gunter M, Riboli E, Aleksandrova Ket al., 2020, Plasma polyphenols associated with lower high-sensitivity C-reactive protein concentrations: a cross-sectional study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, BRITISH JOURNAL OF NUTRITION, Vol: 123, Pages: 198-208, ISSN: 0007-1145

Journal article

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