Imperial College London

DrNeilMurphy

Faculty of MedicineSchool of Public Health

Honorary Senior Research Fellow
 
 
 
//

Contact

 

neil.murphy

 
 
//

Location

 

Norfolk PlaceSt Mary's Campus

//

Summary

 

Publications

Publication Type
Year
to

144 results found

Morgan E, Arnold M, Gini A, Lorenzoni V, Cabasag CJ, Laversanne M, Vignat J, Ferlay J, Murphy N, Bray Fet al., 2022, Global burden of colorectal cancer in 2020 and 2040: incidence and mortality estimates from GLOBOCAN, GUT, ISSN: 0017-5749

Journal article

Matta M, Deubler E, Chajes V, Vozar B, Gunter MJ, Murphy N, Gaudet MMet al., 2022, Circulating plasma phospholipid fatty acid levels and breast cancer risk in the Cancer Prevention Study-II Nutrition Cohort, INTERNATIONAL JOURNAL OF CANCER, Vol: 151, Pages: 2082-2094, ISSN: 0020-7136

Journal article

Tian Y, Kim AE, Bien SA, Lin Y, Qu C, Harrison T, Carreras-Torres R, Díez-Obrero V, Dimou N, Drew DA, Hidaka A, Huyghe JR, Jordahl KM, Morrison J, Murphy N, Obón-Santacana M, Ulrich CM, Ose J, Peoples AR, Ruiz-Narvaez EA, Shcherbina A, Stern M, Su Y-R, van Duijnhoven FJB, Arndt V, Baurley J, Berndt SI, Bishop DT, Brenner H, Buchanan DD, Chan AT, Figueiredo JC, Gallinger S, Gruber SB, Harlid S, Hoffmeister M, Jenkins MA, Joshi AD, Keku TO, Larsson SC, Le Marchand L, Li L, Giles GG, Milne RL, Nan H, Nassir R, Ogino S, Budiarto A, Platz EA, Potter JD, Prentice RL, Rennert G, Sakoda LC, Schoen RE, Slattery ML, Thibodeau SN, Van Guelpen B, Visvanathan K, White E, Wolk A, Woods MO, Wu AH, Campbell PT, Casey G, Conti DV, Gunter MJ, Kundaje A, Lewinger JP, Moreno V, Newcomb PA, Pardamean B, Thomas DC, Tsilidis KK, Peters U, Gauderman WJ, Hsu L, Chang-Claude Jet al., 2022, Genome-wide interaction analysis of genetic variants with menopausal hormone therapy for colorectal cancer risk, Journal of the National Cancer Institute, Vol: 114, Pages: 1135-1148, ISSN: 0027-8874

BACKGROUND: The use of menopausal hormone therapy (MHT) may interact with genetic variants to influence colorectal cancer (CRC) risk. METHODS: We conducted a genome-wide gene-environment interaction between single nucleotide polymorphisms and the use of any MHT, estrogen-only, and combined estrogen-progestogen therapy with CRC risk, among 28,486 postmenopausal women (11,519 cases and 16,967 controls) from 38 studies, using logistic regression, two-step method, and 2- or 3-degree-of-freedom (d.f.) joint test. A set-based score test was applied for rare genetic variants. RESULTS: The use of any MHT, estrogen-only and estrogen-progestogen were associated with a reduced CRC risk [odds ratio (OR) with 95% confidence interval (95% CI) of 0.71 (0.64-0.78), 0.65 (0.53-0.79), and 0.73 (0.59-0.90), respectively]. The two-step method identified a statistically significant interaction between a GRIN2B variant rs117868593 and MHT use, whereby MHT-associated CRC risk was significantly reduced in women with the GG genotype [0.68 (0.64-0.72)] but not within strata of GC or CC genotypes. A statistically significant interaction between a DCBLD1 intronic variant at 6q22.1 (rs10782186) and MHT use was identified by the 2-d.f. joint test. The MHT-associated CRC risk was reduced with increasing number of rs10782186-C alleles, showing ORs of 0.78 (0.70-0.87) for TT, 0.68 (0.63-0.73) for TC, and 0.66 (0.60-0.74) for CC genotypes. In addition, five genes in rare variant analysis showed suggestive interactions with MHT (two-sided P < 1.2x10-4). CONCLUSION: Genetic variants that modify the association between MHT and CRC risk were identified, offering new insights into pathways of CRC carcinogenesis and potential mechanisms involved.

Journal article

Dimou N, Omiyale W, Biessy C, Viallon V, Kaaks R, O'Mara TA, Aglago EK, Ardanaz E, Bergmann MM, Bondonno NP, Braaten T, Colorado-Yohar SM, Crous-Bou M, Dahm CC, Fortner RT, Gram IT, Harlid S, Heath AK, Idahl A, Kvaskoff M, Nøst TH, Overvad K, Palli D, Perez-Cornago A, Sacerdote C, Sánchez M-J, Schulze MB, Severi G, Simeon V, Tagliabue G, Tjønneland A, Truong T, Tumino R, Johansson M, Weiderpass E, Murphy N, Gunter MJ, Lacey B, Allen NE, Dossus Let al., 2022, Cigarette smoking and endometrial cancer risk: observational and mendelian randomization analyses, Cancer Epidemiology, Biomarkers &amp; Prevention, Vol: 31, Pages: OF1-OF10, ISSN: 1055-9965

Background:Current epidemiologic evidence indicates that smoking is associated with a lower endometrial cancer risk. However, it is unknown if this association is causal or confounded. To further elucidate the role of smoking in endometrial cancer risk, we conducted complementary observational and Mendelian randomization (MR) analyses.Methods:The observational analyses included 286,415 participants enrolled in the European Prospective Investigation into Cancer and Nutrition and 179,271 participants in the UK Biobank, and multivariable Cox proportional hazards models were used. In two-sample MR analyses, genetic variants robustly associated with lifetime amount of smoking (n = 126 variants) and ever having smoked regularly (n = 112 variants) were selected and their association with endometrial cancer risk (12,906 cancer/108,979 controls from the Endometrial Cancer Association Consortium) was examined.Results:In the observational analysis, lifetime amount of smoking and ever having smoked regularly were associated with a lower endometrial cancer risk. In the MR analysis accounting for body mass index, a genetic predisposition to a higher lifetime amount of smoking was not associated with endometrial cancer risk (OR per 1-SD increment: 1.15; 95% confidence interval: 0.91−1.44). Genetic predisposition to ever having smoked regularly was not associated with risk of endometrial cancer.Conclusions:Smoking was inversely associated with endometrial cancer in the observational analyses, although unsupported by the MR. Additional studies are required to better understand the possible confounders and mechanisms underlying the observed associations between smoking and endometrial cancer.Impact:The results from this analysis indicate that smoking is unlikely to be causally linked with endometrial cancer risk.

Journal article

Campbell PT, Newton CC, Jacobs EJ, McCullough ML, Wang Y, Rees-Punia E, Guinter MA, Murphy N, Koshiol J, Dehal AN, Rohan T, Strickler H, Petrick J, Gunter M, Zhang X, McGlynn KA, Pollak M, Patel AV, Gapstur SMet al., 2022, Prospective Associations of Hemoglobin A1c and c-peptide with Risk of Diabetes-related Cancers in the Cancer Prevention Study-II Nutrition Cohort, Cancer Research Communications, Vol: 2, Pages: 653-662

<jats:p>Self-reported type 2 diabetes mellitus (T2DM) is a risk factor for many cancers, suggesting its pathology relates to carcinogenesis. We conducted a case-cohort study to examine associations of hemoglobin A1c (HbA1c) and c-peptide with cancers associated with self-reported T2DM. This study was drawn from a prospective cohort of 32,383 women and men who provided blood specimens at baseline: c-peptide and HbA1c were assessed in 3,000 randomly selected participants who were cancer-free-at-baseline and an additional 2,281 participants who were cancer-free-at-baseline and subsequently diagnosed with incident colorectal, liver, pancreatic, female breast, endometrial, ovarian, bladder, or kidney cancers. Weighted Cox regression models estimated HRs and 95% confidence intervals (CI), adjusted for covariates. c-peptide was associated with higher risk of liver cancer [per SD HR: 1.80; 95% CI: 1.32–2.46]. HbA1c was associated with higher risk of pancreatic cancer (per SD HR: 1.21; 95% CI: 1.05–1.40) and with some suggestion of higher risks for all-cancers-of-interest (per SD HR: 1.05; 95% CI: 0.99–1.11) and colorectal (per SD HR: 1.09; 95% CI: 0.98–1.20), ovarian (per SD HR: 1.18; 95% CI: 0.96–1.45) and bladder (per SD HR: 1.08; 95% CI: 0.96–1.21) cancers. Compared with no self-reported T2DM and HbA1c &amp;lt; 6.5% (reference group), self-reported T2DM and HbA1c &amp;lt; 6.5% (i.e., T2DM in good glycemic control) was not associated with risk of colorectal cancer, whereas it was associated with higher risks of all-cancers-of-interest combined (HR: 1.28; 95% CI: 1.01–1.62), especially for breast and endometrial cancers. Additional large, prospective studies are needed to further explore the roles of hyperglycemia, hyperinsulinemia, and related metabolic traits with T2DM-associated cancers to better understand the mechanisms underlying the self-reported T2DM-cancer association and to identify persons at higher cancer

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., 2022, Metabolic signatures of healthy lifestyle patterns and colorectal cancer risk in a European cohort, Clinical Gastroenterology and Hepatology, Vol: 20, Pages: e1061-e1082, 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

Harlid S, Van Guelpen B, Qu C, Gylling B, Aglago EK, Amitay EL, Brenner H, Buchanan DD, Campbell PT, Cao Y, Chan AT, Chang-Claude J, Drew DA, Figueiredo JC, French AJ, Gallinger S, Giannakis M, Giles GG, Gunter MJ, Hoffmeister M, Hsu L, Jenkins MA, Lin Y, Moreno V, Murphy N, Newcomb PA, Newton CC, Nowak JA, Obon-Santacana M, Ogino S, Potter JD, Song M, Steinfelder RS, Sun W, Thibodeau SN, Toland AE, Ugai T, Um CY, Woods MO, Phipps A, Harrison T, Peters Uet al., 2022, Diabetes mellitus in relation to colorectal tumor molecular subtypes: A pooled analysis of more than 9000 cases, INTERNATIONAL JOURNAL OF CANCER, Vol: 151, Pages: 348-360, ISSN: 0020-7136

Journal article

Mariosa D, Smith-Byrne K, Richardson TG, Ferrari P, Gunter MJ, Papadimitriou N, Murphy N, Christakoudi S, Tsilidis KK, Riboli E, Muller D, Purdue MP, Chanock SJ, Hung RJ, Amos CI, O'Mara TA, Amiano P, Pasanisi F, Rodriguez-Barranco M, Krogh V, Tjønneland A, Halkjær J, Perez-Cornago A, Chirlaque M-D, Skeie G, Rylander C, Borch KB, Aune D, Heath AK, Ward HA, Schulze M, Bonet C, Weiderpass E, Smith GD, Brennan P, Johansson Met al., 2022, Body size at different ages and risk of six cancers: a Mendelian randomization and prospective cohort study, JNCI: Journal of the National Cancer Institute, Vol: 114, Pages: 1296-1300, ISSN: 0027-8874

It is unclear if body weight in early life affects cancer risk independently of adult body weight. To investigate this question for six obesity-related cancers, we performed univariable and multivariable analyses using i) Mendelian randomization (MR) analysis and ii) longitudinal analyses in prospective cohorts. Both the MR and longitudinal analyses indicated that larger body size at age 10 was associated with higher risk of endometrial (ORMR=1.61, 95%CI = 1.23–2.11) and kidney cancer (ORMR=1.40, 95%CI = 1.09–1.80). These associations were attenuated after accounting for adult body size in both the MR and cohort analyses. Early life BMI was not consistently associated with the other investigated cancers. The lack of clear independent risk associations suggests that early life BMI influences endometrial and kidney cancer risk mainly through pathways that are common with adult BMI.

Journal article

Archambault AN, Jeon J, Lin Y, Thomas M, Harrison TA, Bishop DT, Brenner H, Casey G, Chan AT, Chang-Claude J, Figueiredo JC, Gallinger S, Gruber SB, Gunter MJ, Guo F, Hoffmeister M, Jenkins MA, Keku TO, Le Marchand L, Li L, Moreno V, Newcomb PA, Pai R, Parfrey PS, Rennert G, Sakoda LC, Lee JK, Slattery ML, Song M, Win AK, Woods MO, Murphy N, Campbell PT, Su Y-R, Lansdorp-Vogelaar I, Peterse EFP, Cao Y, Zeleniuch-Jacquotte A, Liang PS, Du M, Corley DA, Hsu L, Peters U, Hayes RBet al., 2022, Risk Stratification for Early-Onset Colorectal Cancer Using a Combination of Genetic and Environmental Risk Scores: An International Multi-Center Study., J Natl Cancer Inst, Vol: 114, Pages: 528-539

BACKGROUND: The incidence of colorectal cancer (CRC) among individuals aged younger than 50 years has been increasing. As screening guidelines lower the recommended age of screening initiation, concerns including the burden on screening capacity and costs have been recognized, suggesting that an individualized approach may be warranted. We developed risk prediction models for early-onset CRC that incorporate an environmental risk score (ERS), including 16 lifestyle and environmental factors, and a polygenic risk score (PRS) of 141 variants. METHODS: Relying on risk score weights for ERS and PRS derived from studies of CRC at all ages, we evaluated risks for early-onset CRC in 3486 cases and 3890 controls aged younger than 50 years. Relative and absolute risks for early-onset CRC were assessed according to values of the ERS and PRS. The discriminatory performance of these scores was estimated using the covariate-adjusted area under the receiver operating characteristic curve. RESULTS: Increasing values of ERS and PRS were associated with increasing relative risks for early-onset CRC (odds ratio per SD of ERS = 1.14, 95% confidence interval [CI] = 1.08 to 1.20; odds ratio per SD of PRS = 1.59, 95% CI = 1.51 to 1.68), both contributing to case-control discrimination (area under the curve = 0.631, 95% CI = 0.615 to 0.647). Based on absolute risks, we can expect 26 excess cases per 10 000 men and 21 per 10 000 women among those scoring at the 90th percentile for both risk scores. CONCLUSIONS: Personal risk scores have the potential to identify individuals at differential relative and absolute risk for early-onset CRC. Improved discrimination may aid in targeted CRC screening of younger, high-risk individuals, potentially improving outcomes.

Journal article

Murphy N, Song M, Papadimitriou N, Carreras-Torres R, Langenberg C, Martin RM, Tsilidis KK, Barroso I, Chen J, Frayling T, Bull CJ, Vincent EE, Cotterchio M, Gruber SB, Pai RK, Newcomb PA, Perez-Cornago A, van Duijnhoven FJB, Van Guelpen B, Vodicka P, Wolk A, Wu AH, Peters U, Chan AT, Gunter MJet al., 2022, Associations Between Glycemic Traits and Colorectal Cancer: A Mendelian Randomization Analysis, JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, Vol: 114, Pages: 740-752, ISSN: 0027-8874

Journal article

Murphy N, Campbell PT, Gunter MJ, 2021, Are sugar-sweetened beverages contributing to the rising occurrence of colorectal cancer in young adults?, GUT, Vol: 70, Pages: 2222-2223, ISSN: 0017-5749

Journal article

Rothwell JA, Jenab M, Karimi M, Truong T, Mahamat-Saleh Y, Ferrari P, Dashti SG, Kühn T, Cross AJ, Severi G, Gunter MJ, Murphy Net al., 2021, Metabolic syndrome and risk of gastrointestinal cancers: an investigation using large-scale molecular data, Clinical Gastroenterology and Hepatology, Vol: 20, ISSN: 1542-3565

BACKGROUND AND AIMS: Gastrointestinal cancer risk is influenced by the presence of metabolic syndrome [MetS]. However, previous epidemiological studies lacked full serological biomarker data for the classification of MetS and the interaction of MetS with germline cancer risk variants is unknown. METHODS: We investigated the associations between MetS and gastrointestinal cancer risk (overall, colorectal, pancreatic, esophageal adenocarcinoma, esophageal squamous cell carcinoma, stomach cardia, stomach non-cardia, hepatocellular carcinoma, and intrahepatic bile duct cancer) in 366,016 UK Biobank participants with comprehensive serum biomarker and genotype data. MetS status was determined by three different definitions at baseline and, in 15,152 participants, at a repeat assessment after a median of 4.3 years of follow-up. Multivariable hazard ratios [HR] and 95% confidence intervals [CI] for cancer outcomes were estimated using Cox proportional hazards models. Analyses stratified by polygenic risk score [PRS] were conducted for colorectal and pancreatic cancers. RESULTS: During a median follow-up of 7.1 years, 4,238 incident cases of a gastrointestinal cancer occurred. MetS at baseline was associated with higher risk of overall gastrointestinal cancer by any definition (HR 1.21, 95% CI 1.13-1.29, harmonized definition). MetS was associated with increased risks of colorectal cancer, colon cancer, rectal cancer, hepatocellular carcinoma, pancreatic cancer in women, and esophageal adenocarcinoma in men. Associations for colorectal cancer and pancreatic cancer did not differ by PRS strata (P-heterogeneity 0.70 and 0.69, respectively), and 80% of participants with MetS at baseline retained this status at the repeat assessment. CONCLUSIONS: These findings underscore the importance of maintaining good metabolic health in reducing the burden of gastrointestinal cancers, irrespective of genetic predisposition.

Journal article

Rumgay H, Murphy N, Ferrari P, Soerjomataram Iet al., 2021, Alcohol and Cancer: Epidemiology and Biological Mechanisms, NUTRIENTS, Vol: 13

Journal article

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, BRITISH JOURNAL OF CANCER, Vol: 125, Pages: 1308-1317, ISSN: 0007-0920

Journal article

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

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

Journal article

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

Dimou N, Mori N, Harlid S, Harbs J, Martin RM, Smith-Byrne K, Papadimitriou N, Bishop DT, Casey G, Colorado-Yohar SM, Cotterchio M, Cross AJ, Le Marchand L, Lin Y, Offit K, Onland-Moret NC, Peters U, Potter JD, Rohan TE, Weiderpass E, Gunter MJ, Murphy Net al., 2021, Circulating Levels of Testosterone, Sex Hormone Binding Globulin and Colorectal Cancer Risk: Observational and Mendelian Randomization Analyses, CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION, Vol: 30, Pages: 1336-1348, ISSN: 1055-9965

Journal article

Hua X, Dai JY, Lindstrom S, Harrison TA, Lin Y, Alberts SR, Alwers E, Berndt S, Brenner H, Buchanan DD, Campbell PT, Casey G, Chang-Claude J, Gallinger S, Giles GG, Goldberg RM, Gunter MJ, Hoffmeister M, Jenkins MA, Joshi AD, Ma W, Milne RL, Murphy N, Pai RK, Sakoda LC, Schoen RE, Shi Q, Slattery ML, Song M, White E, Le Marchand L, Chan AT, Peters U, Newcomb PAet al., 2021, Genetically Predicted Circulating C-Reactive Protein Concentration and Colorectal Cancer Survival: A Mendelian Randomization Consortium Study, CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION, Vol: 30, Pages: 1349-1358, ISSN: 1055-9965

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

Seyed Khoei N, Wagner K-H, Carreras-Torres R, Gunter MJ, Murphy N, Freisling Het al., 2021, Associations between Prediagnostic Circulating Bilirubin Levels and Risk of Gastrointestinal Cancers in the UK Biobank, CANCERS, Vol: 13

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

Archambault AN, Lin Y, Jeon J, Harrison TA, Bishop DT, Brenner H, Casey G, Chan AT, Chang-Claude J, Figueiredo JC, Gallinger S, Gruber SB, Gunter MJ, Hoffmeister M, Jenkins MA, Keku TO, Le Marchand L, Li L, Moreno V, Newcomb PA, Pai R, Parfrey PS, Rennert G, Sakoda LC, Sandler RS, Slattery ML, Song M, Win AK, Woods MO, Murphy N, Campbell PT, Su Y-R, Zeleniuch-Jacquotte A, Liang PS, Du M, Hsu L, Peters U, Hayes RBet al., 2021, Nongenetic Determinants of Risk for Early-Onset Colorectal Cancer, JNCI CANCER SPECTRUM, Vol: 5

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

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

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

Kliemann N, Viallon V, Murphy N, Beeken RJ, Rothwell JA, Rinaldi S, Assi N, van Roekel EH, Schmidt JA, Borch KB, Agnoli C, Rosendahl AH, Sartor H, Huerta JM, Tjonneland A, Halkjaer J, Bueno-de-Mesquita B, Gicquiau A, Achaintre D, Aleksandrova K, Schulze MB, Heath AK, Tsilidis KK, Masala G, Panico S, Kaaks R, Fortner RT, Van Guelpen B, Dossus L, Scalbert A, Keun HC, Travis RC, Jenab M, Johansson M, Ferrari P, Gunter MJet al., 2021, Metabolic signatures of greater body size and their associations with risk of colorectal and endometrial cancers in the European Prospective Investigation into Cancer and Nutrition, BMC Medicine, Vol: 19, ISSN: 1741-7015

Background:The mechanisms underlying the obesity-cancer relationship are incompletely understood. This study aimed to characterise metabolic signatures of greater body size and to investigate their association with two obesity-related malignancies, endometrial and colorectal cancers, and with weight loss within the context of an intervention study.Methods:Targeted mass spectrometry metabolomics data from 4326 participants enrolled in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort and 17 individuals from a single-arm pilot weight loss intervention (Intercept) were used in this analysis. Metabolic signatures of body size were first determined in discovery (N = 3029) and replication (N = 1297) sets among EPIC participants by testing the associations between 129 metabolites and body mass index (BMI), waist circumference (WC), and waist-to-hip ratio (WHR) using linear regression models followed by partial least squares analyses. Conditional logistic regression models assessed the associations between the metabolic signatures with endometrial (N = 635 cases and 648 controls) and colorectal (N = 423 cases and 423 controls) cancer risk using nested case-control studies in EPIC. Pearson correlation between changes in the metabolic signatures and weight loss was tested among Intercept participants.Results:After adjustment for multiple comparisons, greater BMI, WC, and WHR were associated with higher levels of valine, isoleucine, glutamate, PC aa C38:3, and PC aa C38:4 and with lower levels of asparagine, glutamine, glycine, serine, lysoPC C17:0, lysoPC C18:1, lysoPC C18:2, PC aa C42:0, PC ae C34:3, PC ae C40:5, and PC ae C42:5. The metabolic signature of BMI (OR1-sd 1.50, 95% CI 1.30–1.74), WC (OR1-sd 1.46, 95% CI 1.27–1.69), and WHR (OR1-sd 1.54, 95% CI 1.33–1.79) were each associated with endometrial cancer risk. Risk of colorectal cancer was positively associated with

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

This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.

Request URL: http://wlsprd.imperial.ac.uk:80/respub/WEB-INF/jsp/search-html.jsp Request URI: /respub/WEB-INF/jsp/search-html.jsp Query String: respub-action=search.html&id=00583871&limit=30&person=true