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Search Result (502 REFERENCES)

2018

Circulating Folate, Vitamin B6, and Methionine in Relation to Lung Cancer Risk in the Lung Cancer Cohort Consortium (LC3)

Fanidi A., Muller D. C., Yuan J. M., Stevens V. L., Weinstein S. J., Albanes D., Prentice R., Thomsen C. A., Pettinger M., Cai Q., Blot W. J., Wu J., Arslan A. A., Zeleniuch-Jacquotte A., McCullough M. L., Le Marchand L., Wilkens L. R., Haiman C. A., Zhang X., Han J., Stampfer M. J., Smith-Warner S. A., Giovannucci E., Giles G. G., Hodge A. M., Severi G., Johansson M., Grankvist K., Langhammer A., Krokstad S., Naess M., Wang R., Gao Y. T., Butler L. M., Koh W. P., Shu X. O., Xiang Y. B., Li H., Zheng W., Lan Q., Visvanathan K., Bolton J. H., Ueland P. M., Midttun O., Ulvik A., Caporaso N. E., Purdue M., Ziegler R. G., Freedman N. D., Buring J. E., Lee I. M., Sesso H. D., Gaziano J. M., Manjer J., Ericson U., Relton C., Brennan P., Johansson M.

J Natl Cancer Inst; 2018; 110(1):

PMID:28922778

Abstract as provided by PubMed

Background: Circulating concentrations of B vitamins and factors related to one-carbon metabolism have been found to be strongly inversely associated with lung cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. The extent to which these associations are present in other study populations is unknown. Methods: Within 20 prospective cohorts from the National Cancer Institute Cohort Consortium, a nested case-control study was designed including 5364 incident lung cancer case patients and 5364 control subjects who were individually matched to case patients by age, sex, cohort, and smoking status. Centralized biochemical analyses were performed to measure circulating concentrations of vitamin B6, folate, and methionine, as well as cotinine as an indicator of recent tobacco exposure. The association between these biomarkers and lung cancer risk was evaluated using conditional logistic regression models. Results: Participants with higher circulating concentrations of vitamin B6 and folate had a modestly decreased risk of lung cancer risk overall, the odds ratios when comparing the top and bottom fourths (OR 4vs1 ) being 0.88 (95% confidence interval [CI] = 0.78 to 1.00) and 0.86 (95% CI = 0.74 to 0.99), respectively. We found stronger associations among men (vitamin B6: OR 4vs1 = 0.74, 95% CI = 0.62 to 0.89; folate: OR 4vs1 = 0.75, 95% CI = 0.61 to 0.93) and ever smokers (vitamin B6: OR 4vs1 = 0.78, 95% CI = 0.67 to 0.91; folate: OR 4vs1 = 0.87, 95% CI = 0.73 to 1.03). We further noted that the association of folate was restricted to Europe/Australia and Asia, whereas no clear association was observed for the United States. Circulating concentrations of methionine were not associated with lung cancer risk overall or in important subgroups. Conclusions: Although confounding by tobacco exposure or reverse causation cannot be ruled out, these study results are compatible with a small decrease in lung cancer risk in ever smokers who avoid low concentrations of circulating folate and vitamin B6.

Consumption of fruits, vegetables and fruit juices and differentiated thyroid carcinoma risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study

Zamora-Ros R., Beraud V., Franceschi S., Cayssials V., Tsilidis K. K., Boutron-Ruault M. C., Weiderpass E., Overvad K., Tjonneland A., Eriksen A. K., Bonnet F., Affret A., Katzke V., Kuhn T., Boeing H., Trichopoulou A., Valanou E., Karakatsani A., Masala G., Grioni S., Santucci de Magistris M., Tumino R., Ricceri F., Skeie G., Parr C. L., Merino S., Salamanca-Fernandez E., Chirlaque M. D., Ardanaz E., Amiano P., Almquist M., Drake I., Hennings J., Sandstrom M., Bueno-de-Mesquita H. B. A., Peeters P. H., Khaw K. T., Wareham N. J., Schmidt J. A., Perez-Cornago A., Aune D., Riboli E., Slimani N., Scalbert A., Romieu I., Agudo A., Rinaldi S.

Int J Cancer; 2018; 142(3): 449-459

PMID:28688112

Abstract as provided by PubMed

Fruit and vegetable (F&V) intake is considered as probably protective against overall cancer risk, but results in previous studies are not consistent for thyroid cancer (TC). The purpose of this study is to examine the association between the consumption of fruits, vegetables, fruit juices and differentiated thyroid cancer risk within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. The EPIC study is a cohort including over half a million participants, recruited between 1991 and 2000. During a mean follow-up of 14 years, 748 incident first primary differentiated TC cases were identified. F&V and fruit juice intakes were assessed through validated country-specific dietary questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression models adjusted for potential confounding factors. Comparing the highest versus lowest quartile of intake, differentiated TC risk was not associated with intakes of total F&V (HR: 0.89; 95% CI: 0.68-1.15; p-trend = 0.44), vegetables (HR: 0.89; 95% CI: 0.69-1.14; p-trend = 0.56), or fruit (HR: 1.00; 95% CI: 0.79-1.26; p-trend = 0.64). No significant association was observed with any individual type of vegetable or fruit. However, there was a positive borderline trend with fruit juice intake (HR: 1.23; 95% CI: 0.98-1.53; p-trend = 0.06). This study did not find any significant association between F&V intakes and differentiated TC risk; however a positive trend with fruit juice intake was observed, possibly related to its high sugar content.

2017

DNA methylome analysis identifies accelerated epigenetic ageing associated with postmenopausal breast cancer susceptibility

Ambatipudi S., Horvath S., Perrier F., Cuenin C., Hernandez-Vargas H., Le Calvez-Kelm F., Durand G., Byrnes G., Ferrari P., Bouaoun L., Sklias A., Chajes V., Overvad K., Severi G., Baglietto L., Clavel-Chapelon F., Kaaks R., Barrdahl M., Boeing H., Trichopoulou A., Lagiou P., Naska A., Masala G., Agnoli C., Polidoro S., Tumino R., Panico S., Dolle M., Peeters P. H., Onland-Moret N. C., Sandanger T. M., Nost T. H., Weiderpass E., Quiros J. R., Agudo A., Rodriguez-Barranco M., Huerta Castano J. M., Barricarte A., Fernandez A. M., Travis R. C., Vineis P., Muller D. C., Riboli E., Gunter M., Romieu I., Herceg Z.

Eur J Cancer; 2017; 299-307

PMID:28259012

Abstract as provided by PubMed

AIM OF THE STUDY: A vast majority of human malignancies are associated with ageing, and age is a strong predictor of cancer risk. Recently, DNA methylation-based marker of ageing, known as 'epigenetic clock', has been linked with cancer risk factors. This study aimed to evaluate whether the epigenetic clock is associated with breast cancer risk susceptibility and to identify potential epigenetics-based biomarkers for risk stratification. METHODS: Here, we profiled DNA methylation changes in a nested case-control study embedded in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort (n = 960) using the Illumina HumanMethylation 450K BeadChip arrays and used the Horvath age estimation method to calculate epigenetic age for these samples. Intrinsic epigenetic age acceleration (IEAA) was estimated as the residuals by regressing epigenetic age on chronological age. RESULTS: We observed an association between IEAA and breast cancer risk (OR, 1.04; 95% CI, 1.007-1.076, P = 0.016). One unit increase in IEAA was associated with a 4% increased odds of developing breast cancer (OR, 1.04; 95% CI, 1.007-1.076). Stratified analysis based on menopausal status revealed that IEAA was associated with development of postmenopausal breast cancers (OR, 1.07; 95% CI, 1.020-1.11, P = 0.003). In addition, methylome-wide analyses revealed that a higher mean DNA methylation at cytosine-phosphate-guanine (CpG) islands was associated with increased risk of breast cancer development (OR per 1 SD = 1.20; 95 %CI: 1.03-1.40, P = 0.02) whereas mean methylation levels at non-island CpGs were indistinguishable between cancer cases and controls. CONCLUSION: Epigenetic age acceleration and CpG island methylation have a weak, but statistically significant, association with breast cancer susceptibility.

Alcohol consumption and risk of urothelial cell bladder cancer in the European prospective investigation into cancer and nutrition cohort

Botteri E., Ferrari P., Roswall N., Tjonneland A., Hjartaker A., Huerta J. M., Fortner R. T., Trichopoulou A., Karakatsani A., La Vecchia C., Pala V., Perez-Cornago A., Sonestedt E., Liedberg F., Overvad K., Sanchez M. J., Gram I. T., Stepien M., Trijsburg L., Borje L., Johansson M., Kuhn T., Panico S., Tumino R., Bueno-de-Mesquita H. B. A., Weiderpass E.

Int J Cancer; 2017; 141(10): 1963-1970

PMID:28722206

Abstract as provided by PubMed

Findings on the association between alcohol consumption and bladder cancer are inconsistent. We investigated that association in the European Prospective Investigation into Cancer and Nutrition cohort. We included 476,160 individuals mostly aged 35-70 years, enrolled in ten countries and followed for 13.9 years on average. Hazard ratios (HR) for developing urothelial cell carcinoma (UCC; 1,802 incident cases) were calculated using Cox proportional hazards models. Alcohol consumption at baseline and over the life course was analyzed, as well as different types of beverages (beer, wine, spirits). Baseline alcohol intake was associated with a statistically nonsignificant increased risk of UCC (HR 1.03; 95% confidence interval (CI) 1.00-1.06 for each additional 12 g/day). HR in smokers was 1.04 (95% CI 1.01-1.07). Men reporting high baseline intakes of alcohol (>96 g/day) had an increased risk of UCC (HR 1.57; 95% CI 1.03-2.40) compared to those reporting moderate intakes (<6 g/day), but no dose-response relationship emerged. In men, an increased risk of aggressive forms of UCC was observed even at lower doses (>6 to 24 g/day). Average lifelong alcohol intake was not associated with the risk of UCC, however intakes of spirits > 24 g/day were associated with an increased risk of UCC in men (1.38; 95% CI 1.01-1.91) and smokers (1.39; 95% CI 1.01-1.92), compared to moderate intakes. We found no association between alcohol and UCC in women and never smokers. In conclusion, we observed some associations between alcohol and UCC in men and in smokers, possibly because of residual confounding by tobacco smoking.

Coffee, tea and melanoma risk: findings from the European Prospective Investigation into Cancer and Nutrition

Caini S., Masala G., Saieva C., Kvaskoff M., Savoye I., Sacerdote C., Hemmingsson O., Hammer Bech B., Overvad K., Tjonneland A., Petersen K. E., Mancini F. R., Boutron-Ruault M. C., Cervenka I., Kaaks R., Kuhn T., Boeing H., Floegel A., Trichopoulou A., Valanou E., Kritikou M., Tagliabue G., Panico S., Tumino R., Bueno-de-Mesquita H. B., Peeters P. H., Veierod M. B., Ghiasvand R., Lukic M., Quiros J. R., Chirlaque M. D., Ardanaz E., Salamanca Fernandez E., Larranaga N., Zamora-Ros R., Maria Nilsson L., Ljuslinder I., Jirstrom K., Sonestedt E., Key T. J., Wareham N., Khaw K. T., Gunter M., Huybrechts I., Murphy N., Tsilidis K. K., Weiderpass E., Palli D.

Int J Cancer; 2017; 140(10): 2246-2255

PMID:28218395

Abstract as provided by PubMed

In vitro and animal studies suggest that bioactive constituents of coffee and tea may have anticarcinogenic effects against cutaneous melanoma; however, epidemiological evidence is limited to date. We examined the relationships between coffee (total, caffeinated or decaffeinated) and tea consumption and risk of melanoma in the European Prospective Investigation into Cancer and Nutrition (EPIC). EPIC is a multicentre prospective study that enrolled over 500,000 participants aged 25-70 years from ten European countries in 1992-2000. Information on coffee and tea drinking was collected at baseline using validated country-specific dietary questionnaires. We used adjusted Cox proportional hazards regression models to calculate hazard ratios (HR) and 95% confidence intervals (95% CI) for the associations between coffee and tea consumption and melanoma risk. Overall, 2,712 melanoma cases were identified during a median follow-up of 14.9 years among 476,160 study participants. Consumption of caffeinated coffee was inversely associated with melanoma risk among men (HR for highest quartile of consumption vs. non-consumers 0.31, 95% CI 0.14-0.69) but not among women (HR 0.96, 95% CI 0.62-1.47). There were no statistically significant associations between consumption of decaffeinated coffee or tea and the risk of melanoma among both men and women. The consumption of caffeinated coffee was inversely associated with melanoma risk among men in this large cohort study. Further investigations are warranted to confirm our findings and clarify the possible role of caffeine and other coffee compounds in reducing the risk of melanoma.

Blood Metabolic Signatures of Body Mass Index: A Targeted Metabolomics Study in the EPIC Cohort

Carayol M., Leitzmann M. F., Ferrari P., Zamora-Ros R., Achaintre D., Stepien M., Schmidt J. A., Travis R. C., Overvad K., Tjonneland A., Hansen L., Kaaks R., Kuhn T., Boeing H., Bachlechner U., Trichopoulou A., Bamia C., Palli D., Agnoli C., Tumino R., Vineis P., Panico S., Quiros J. R., Sanchez-Cantalejo E., Huerta J. M., Ardanaz E., Arriola L., Agudo A., Nilsson J., Melander O., Bueno-de-Mesquita B., Peeters P. H., Wareham N., Khaw K. T., Jenab M., Key T. J., Scalbert A., Rinaldi S.

J Proteome Res; 2017; 16(9): 3137-3146

PMID:28758405

Abstract as provided by PubMed

Metabolomics is now widely used to characterize metabolic phenotypes associated with lifestyle risk factors such as obesity. The objective of the present study was to explore the associations of body mass index (BMI) with 145 metabolites measured in blood samples in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Metabolites were measured in blood from 392 men from the Oxford (UK) cohort (EPIC-Oxford) and in 327 control subjects who were part of a nested case-control study on hepatobiliary carcinomas (EPIC-Hepatobiliary). Measured metabolites included amino acids, acylcarnitines, hexoses, biogenic amines, phosphatidylcholines, and sphingomyelins. Linear regression models controlled for potential confounders and multiple testing were run to evaluate the associations of metabolite concentrations with BMI. 40 and 45 individual metabolites showed significant differences according to BMI variations, in the EPIC-Oxford and EPIC-Hepatobiliary subcohorts, respectively. Twenty two individual metabolites (kynurenine, one sphingomyelin, glutamate and 19 phosphatidylcholines) were associated with BMI in both subcohorts. The present findings provide additional knowledge on blood metabolic signatures of BMI in European adults, which may help identify mechanisms mediating the relationship of BMI with obesity-related diseases.

A prospective evaluation of plasma phospholipid fatty acids and breast cancer risk in the EPIC study

Chajes V., Assi N., Biessy C., Ferrari P., Rinaldi S., Slimani N., Lenoir G. M., Baglietto L., His M., Boutron-Ruault M. C., Trichopoulou A., Lagiou P., Katsoulis M., Kaaks R., Kuhn T., Panico S., Pala V., Masala G., Bueno-de-Mesquita H. B., Peeters P. H., van Gils C., Hjartaker A., Standahl Olsen K., Borgund Barnung R., Barricarte A., Redondo-Sanchez D., Menendez V., Amiano P., Wennberg M., Key T., Khaw K. T., Merritt M. A., Riboli E., Gunter M. J., Romieu I.

Ann Oncol; 2017; 28(11): 2836-2842

PMID:28950350

Abstract as provided by PubMed

Background: Intakes of specific fatty acids have been postulated to impact breast cancer risk but epidemiological data based on dietary questionnaires remain conflicting. Materials and methods: We assessed the association between plasma phospholipid fatty acids and breast cancer risk in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition study. Sixty fatty acids were measured by gas chromatography in pre-diagnostic plasma phospholipids from 2982 incident breast cancer cases matched to 2982 controls. Conditional logistic regression models were used to estimate relative risk of breast cancer by fatty acid level. The false discovery rate (q values) was computed to control for multiple comparisons. Subgroup analyses were carried out by estrogen receptor (ER) and progesterone receptor expression in the tumours. Results: A high level of palmitoleic acid [odds ratio (OR) for the highest quartile compared with the lowest OR (Q4-Q1) 1.37; 95% confidence interval (CI), 1.14-1.64; P for trend = 0.0001, q value = 0.004] as well as a high desaturation index (DI16) (16:1n-7/16:0) [OR (Q4-Q1), 1.28; 95% C, 1.07-1.54; P for trend = 0.002, q value = 0.037], as biomarkers of de novo lipogenesis, were significantly associated with increased risk of breast cancer. Levels of industrial trans-fatty acids were positively associated with ER-negative tumours [OR for the highest tertile compared with the lowest (T3-T1)=2.01; 95% CI, 1.03-3.90; P for trend = 0.047], whereas no association was found for ER-positive tumours (P-heterogeneity =0.01). No significant association was found between n-3 polyunsaturated fatty acids and breast cancer risk, overall or by hormonal receptor. Conclusion: These findings suggest that increased de novo lipogenesis, acting through increased synthesis of palmitoleic acid, could be a relevant metabolic pathway for breast tumourigenesis. Dietary trans-fatty acids derived from industrial processes may specifically increase ER-negative breast cancer risk.

A metabolomic study of biomarkers of meat and fish intake

Cheung W., Keski-Rahkonen P., Assi N., Ferrari P., Freisling H., Rinaldi S., Slimani N., Zamora-Ros R., Rundle M., Frost G., Gibbons H., Carr E., Brennan L., Cross A. J., Pala V., Panico S., Sacerdote C., Palli D., Tumino R., Kuhn T., Kaaks R., Boeing H., Floegel A., Mancini F., Boutron-Ruault M. C., Baglietto L., Trichopoulou A., Naska A., Orfanos P., Scalbert A.

Am J Clin Nutr; 2017; 105(3): 600-608

PMID:28122782

Abstract as provided by PubMed

Background: Meat and fish intakes have been associated with various chronic diseases. The use of specific biomarkers may help to assess meat and fish intake and improve subject classification according to the amount and type of meat or fish consumed.Objective: A metabolomic approach was applied to search for biomarkers of meat and fish intake in a dietary intervention study and in free-living subjects from the European Prospective Investigation into Cancer and Nutrition (EPIC) study.Design: In the dietary intervention study, 4 groups of 10 subjects consumed increasing quantities of chicken, red meat, processed meat, and fish over 3 successive weeks. Twenty-four-hour urine samples were collected during each period and analyzed by high-resolution liquid chromatography-mass spectrometry. Signals characteristic of meat or fish intake were replicated in 50 EPIC subjects for whom a 24-h urine sample and 24-h dietary recall were available and who were selected for their exclusive intake or no intake of any of the 4 same foods.Results: A total of 249 mass spectrometric features showed a positive dose-dependent response to meat or fish intake in the intervention study. Eighteen of these features best predicted intake of the 4 food groups in the EPIC urine samples on the basis of partial receiver operator curve analyses with permutation testing (areas under the curve ranging between 0.61 and 1.0). Of these signals, 8 metabolites were identified. Anserine was found to be specific for chicken intake, whereas trimethylamine-N-oxide showed good specificity for fish. Carnosine and 3 acylcarnitines (acetylcarnitine, propionylcarnitine, and 2-methylbutyrylcarnitine) appeared to be more generic indicators of meat and meat and fish intake, respectively.Conclusion: The meat and fish biomarkers identified in this work may be used to study associations between meat and fish intake and disease risk in epidemiologic studies. This trial was registered at clinicaltrials.gov as NCT01684917.

Endometrial cancer risk prediction including serum-based biomarkers: results from the EPIC cohort

Fortner R. T., Husing A., Kuhn T., Konar M., Overvad K., Tjonneland A., Hansen L., Boutron-Ruault M. C., Severi G., Fournier A., Boeing H., Trichopoulou A., Benetou V., Orfanos P., Masala G., Agnoli C., Mattiello A., Tumino R., Sacerdote C., Bueno-de-Mesquita H. B., Peeters P. H., Weiderpass E., Gram I. T., Gavrilyuk O., Quiros J. R., Maria Huerta J., Ardanaz E., Larranaga N., Lujan-Barroso L., Sanchez-Cantalejo E., Butt S. T., Borgquist S., Idahl A., Lundin E., Khaw K. T., Allen N. E., Rinaldi S., Dossus L., Gunter M., Merritt M. A., Tzoulaki I., Riboli E., Kaaks R.

Int J Cancer; 2017; 140(6): 1317-1323

PMID:27935083

Abstract as provided by PubMed

Endometrial cancer risk prediction models including lifestyle, anthropometric and reproductive factors have limited discrimination. Adding biomarker data to these models may improve predictive capacity; to our knowledge, this has not been investigated for endometrial cancer. Using a nested case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, we investigated the improvement in discrimination gained by adding serum biomarker concentrations to risk estimates derived from an existing risk prediction model based on epidemiologic factors. Serum concentrations of sex steroid hormones, metabolic markers, growth factors, adipokines and cytokines were evaluated in a step-wise backward selection process; biomarkers were retained at p < 0.157 indicating improvement in the Akaike information criterion (AIC). Improvement in discrimination was assessed using the C-statistic for all biomarkers alone, and change in C-statistic from addition of biomarkers to preexisting absolute risk estimates. We used internal validation with bootstrapping (1000-fold) to adjust for over-fitting. Adiponectin, estrone, interleukin-1 receptor antagonist, tumor necrosis factor-alpha and triglycerides were selected into the model. After accounting for over-fitting, discrimination was improved by 2.0 percentage points when all evaluated biomarkers were included and 1.7 percentage points in the model including the selected biomarkers. Models including etiologic markers on independent pathways and genetic markers may further improve discrimination.

Osteoprotegerin and breast cancer risk by hormone receptor subtype: a nested case-control study in the EPIC cohort

Fortner R. T., Sarink D., Schock H., Johnson T., Tjonneland A., Olsen A., Overvad K., Affret A., His M., Boutron-Ruault M. C., Boeing H., Trichopoulou A., Naska A., Orfanos P., Palli D., Sieri S., Mattiello A., Tumino R., Ricceri F., Bueno-de-Mesquita H. B., Peeters P. H., Van Gils C. H., Weiderpass E., Lund E., Quiros J. R., Agudo A., Sanchez M. J., Chirlaque M. D., Ardanaz E., Dorronsoro M., Key T., Khaw K. T., Rinaldi S., Dossus L., Gunter M., Merritt M. A., Riboli E., Kaaks R.

BMC Med; 2017; 15(1): 26

PMID:28173834

Abstract as provided by PubMed

BACKGROUND: Circulating osteoprotegerin (OPG), a member of the receptor activator of nuclear factor kappa-B (RANK) axis, may influence breast cancer risk via its role as the decoy receptor for both the RANK ligand (RANKL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Circulating OPG and breast cancer risk has been examined in only one prior study. METHODS: A case-control study was nested in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. A total of 2008 incident invasive breast cancer cases (estrogen receptor (ER)+, n = 1622; ER-, n = 386), matched 1:1 to controls, were included in the analysis. Women were predominantly postmenopausal at blood collection (77%); postmenopausal women included users and non-users of postmenopausal hormone therapy (HT). Serum OPG was quantified with an electrochemiluminescence assay. Relative risks (RRs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression. RESULTS: The associations between OPG and ER+ and ER- breast cancer differed significantly. Higher concentrations of OPG were associated with increased risk of ER- breast cancer (top vs. bottom tertile RR = 1.93 [95% CI 1.24-3.02]; p trend = 0.03). We observed a suggestive inverse association for ER+ disease overall and among women premenopausal at blood collection. Results for ER- disease did not differ by menopausal status at blood collection (p het = 0.97), and we observed no heterogeneity by HT use at blood collection (p het >/= 0.43) or age at breast cancer diagnosis (p het >/= 0.30). CONCLUSIONS: This study provides the first prospective data on OPG and breast cancer risk by hormone receptor subtype. High circulating OPG may represent a novel risk factor for ER- breast cancer.

Correlates of circulating ovarian cancer early detection markers and their contribution to discrimination of early detection models: results from the EPIC cohort

Fortner R. T., Vitonis A. F., Schock H., Husing A., Johnson T., Fichorova R. N., Fashemi T., Yamamoto H. S., Tjonneland A., Hansen L., Overvad K., Boutron-Ruault M. C., Kvaskoff M., Severi G., Boeing H., Trichopoulou A., Benetou V., La Vecchia C., Palli D., Sieri S., Tumino R., Matullo G., Mattiello A., Onland-Moret N. C., Peeters P. H., Weiderpass E., Gram I. T., Jareid M., Quiros J. R., Duell E. J., Sanchez M. J., Chirlaque M. D., Ardanaz E., Larranaga N., Nodin B., Brandstedt J., Idahl A., Khaw K. T., Allen N., Gunter M., Johansson M., Dossus L., Merritt M. A., Riboli E., Cramer D. W., Kaaks R., Terry K. L.

J Ovarian Res; 2017; 10(1): 20

PMID:28320479

Abstract as provided by PubMed

BACKGROUND: Ovarian cancer early detection markers CA125, CA15.3, HE4, and CA72.4 vary between healthy women, limiting their utility for screening. METHODS: We evaluated cross-sectional relationships between lifestyle and reproductive factors and these markers among controls (n = 1910) from a nested case-control study in the European Prospective Investigation into Cancer and Nutrition (EPIC). Improvements in discrimination of prediction models adjusting for correlates of the markers were evaluated among postmenopausal women in the nested case-control study (n = 590 cases). Generalized linear models were used to calculate geometric means of CA125, CA15.3, and HE4. CA72.4 above vs. below limit of detection was evaluated using logistic regression. Early detection prediction was modeled using conditional logistic regression. RESULTS: CA125 concentrations were lower, and CA15.3 higher, in post- vs. premenopausal women (p </= 0.02). Among postmenopausal women, CA125 was higher among women with higher parity and older age at menopause (ptrend </= 0.02), but lower among women reporting oophorectomy, hysterectomy, ever use of estrogen-only hormone therapy, or current smoking (p < 0.01). CA15.3 concentrations were higher among heavier women and in former smokers (p </= 0.03). HE4 was higher with older age at blood collection and in current smokers, and inversely associated with OC use duration, parity, and older age at menopause (</= 0.02). No associations were observed with CA72.4. Adjusting for correlates of the markers in prediction models did not improve the discrimination. CONCLUSIONS: This study provides insights into sources of variation in ovarian cancer early detection markers in healthy women and informs about the utility of individualizing marker cutpoints based on epidemiologic factors.

Coffee Drinking and Mortality in 10 European Countries: A Multinational Cohort Study

Gunter M. J., Murphy N., Cross A. J., Dossus L., Dartois L., Fagherazzi G., Kaaks R., Kuhn T., Boeing H., Aleksandrova K., Tjonneland A., Olsen A., Overvad K., Larsen S. C., Redondo Cornejo M. L., Agudo A., Sanchez Perez M. J., Altzibar J. M., Navarro C., Ardanaz E., Khaw K. T., Butterworth A., Bradbury K. E., Trichopoulou A., Lagiou P., Trichopoulos D., Palli D., Grioni S., Vineis P., Panico S., Tumino R., Bueno-de-Mesquita B., Siersema P., Leenders M., Beulens J. W. J., Uiterwaal C. U., Wallstrom P., Nilsson L. M., Landberg R., Weiderpass E., Skeie G., Braaten T., Brennan P., Licaj I., Muller D. C., Sinha R., Wareham N., Riboli E.

Ann Intern Med; 2017; 167(4): 236-247

PMID:28693038

Abstract as provided by PubMed

Background: The relationship between coffee consumption and mortality in diverse European populations with variable coffee preparation methods is unclear. Objective: To examine whether coffee consumption is associated with all-cause and cause-specific mortality. Design: Prospective cohort study. Setting: 10 European countries. Participants: 521 330 persons enrolled in EPIC (European Prospective Investigation into Cancer and Nutrition). Measurements: Hazard ratios (HRs) and 95% CIs estimated using multivariable Cox proportional hazards models. The association of coffee consumption with serum biomarkers of liver function, inflammation, and metabolic health was evaluated in the EPIC Biomarkers subcohort (n = 14 800). Results: During a mean follow-up of 16.4 years, 41 693 deaths occurred. Compared with nonconsumers, participants in the highest quartile of coffee consumption had statistically significantly lower all-cause mortality (men: HR, 0.88 [95% CI, 0.82 to 0.95]; P for trend < 0.001; women: HR, 0.93 [CI, 0.87 to 0.98]; P for trend = 0.009). Inverse associations were also observed for digestive disease mortality for men (HR, 0.41 [CI, 0.32 to 0.54]; P for trend < 0.001) and women (HR, 0.60 [CI, 0.46 to 0.78]; P for trend < 0.001). Among women, there was a statistically significant inverse association of coffee drinking with circulatory disease mortality (HR, 0.78 [CI, 0.68 to 0.90]; P for trend < 0.001) and cerebrovascular disease mortality (HR, 0.70 [CI, 0.55 to 0.90]; P for trend = 0.002) and a positive association with ovarian cancer mortality (HR, 1.31 [CI, 1.07 to 1.61]; P for trend = 0.015). In the EPIC Biomarkers subcohort, higher coffee consumption was associated with lower serum alkaline phosphatase; alanine aminotransferase; aspartate aminotransferase; gamma-glutamyltransferase; and, in women, C-reactive protein, lipoprotein(a), and glycated hemoglobin levels. Limitations: Reverse causality may have biased the findings; however, results did not differ after exclusion of participants who died within 8 years of baseline. Coffee-drinking habits were assessed only once. Conclusion: Coffee drinking was associated with reduced risk for death from various causes. This relationship did not vary by country. Primary Funding Source: European Commission Directorate-General for Health and Consumers and International Agency for Research on Cancer.

Helicobacter pylori infection, chronic corpus atrophic gastritis and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: A nested case-control study

Huang J., Zagai U., Hallmans G., Nyren O., Engstrand L., Stolzenberg-Solomon R., Duell E. J., Overvad K., Katzke V. A., Kaaks R., Jenab M., Park J. Y., Murillo R., Trichopoulou A., Lagiou P., Bamia C., Bradbury K. E., Riboli E., Aune D., Tsilidis K. K., Capella G., Agudo A., Krogh V., Palli D., Panico S., Weiderpass E., Tjonneland A., Olsen A., Martinez B., Redondo-Sanchez D., Chirlaque M. D., Hm Peeters P., Regner S., Lindkvist B., Naccarati A., Ardanaz E., Larranaga N., Boutron-Ruault M. C., Rebours V., Barre A., Bueno-de-Mesquita H. B., Ye W.

Int J Cancer; 2017; 140(8): 1727-1735

PMID:28032715

Abstract as provided by PubMed

The association between H. pylori infection and pancreatic cancer risk remains controversial. We conducted a nested case-control study with 448 pancreatic cancer cases and their individually matched control subjects, based on the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to determine whether there was an altered pancreatic cancer risk associated with H. pylori infection and chronic corpus atrophic gastritis. Conditional logistic regression models were applied to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs), adjusted for matching factors and other potential confounders. Our results showed that pancreatic cancer risk was neither associated with H. pylori seropositivity (OR = 0.96; 95% CI: 0.70, 1.31) nor CagA seropositivity (OR = 1.07; 95% CI: 0.77, 1.48). We also did not find any excess risk among individuals seropositive for H. pylori but seronegative for CagA, compared with the group seronegative for both antibodies (OR = 0.94; 95% CI: 0.63, 1.38). However, we found that chronic corpus atrophic gastritis was non-significantly associated with an increased pancreatic cancer risk (OR = 1.35; 95% CI: 0.77, 2.37), and although based on small numbers, the excess risk was particularly marked among individuals seronegative for both H. pylori and CagA (OR = 5.66; 95% CI: 1.59, 20.19, p value for interaction < 0.01). Our findings provided evidence supporting the null association between H. pylori infection and pancreatic cancer risk in western European populations. However, the suggested association between chronic corpus atrophic gastritis and pancreatic cancer risk warrants independent verification in future studies, and, if confirmed, further studies on the underlying mechanisms.

Hepcidin levels and gastric cancer risk in the EPIC-EurGast study

Jakszyn P., Fonseca-Nunes A., Lujan-Barroso L., Aranda N., Tous M., Arija V., Cross A., Bueno-de-Mesquita H. B. A., Weiderpass E., Kuhn T., Kaaks R., Sjoberg K., Ohlsson B., Tumino R., Palli D., Ricceri F., Fasanelli F., Krogh V., Mattiello A., Jenab M., Gunter M., Perez-Cornago A., Khaw K. T., Tjonneland A., Olsen A., Overvad K., Trichopoulou A., Peppa E., Vasilopoulou E., Boeing H., Sanchez-Cantalejo E., Huerta J. M., Dorronsoro M., Barricarte A., Quiros J. M., Peeters P. H., Agudo A.

Int J Cancer; 2017; 141(5): 945-951

PMID:28543377

Abstract as provided by PubMed

Hepcidin is the main regulator of iron homeostasis and dysregulation of proteins involved in iron metabolism has been associated with tumorogenesis. However, to date, no epidemiological study has researched the association between hepcidin levels and gastric cancer risk. To further investigate the relationship between hepcidin levels and gastric cancer risk, we conducted a nested case-control study (EURGAST) within the multicentric European Prospective Investigation into Cancer and Nutrition study. The study included 456 primary incident gastric adenocarcinoma cases and 900 matched controls that occurred during an average of 11 years of follow-up. We measured serum levels of hepcidin-25, iron, ferritin, transferrin and C-reactive protein. Odds ratios (ORs) and 95% confidence intervals (CIs) for the risk of gastric cancer by hepcidin levels were estimated from multivariable conditional logistic regression models. Mediation effect of the ferritin levels on the hepcidin-gastric cancer pathway was also evaluated. After adjusting for relevant confounders, we observed a statistically significant inverse association between gastric cancer and hepcidin levels (OR 5 ng/l = 0.96, 95% CI = 0.93-0.99). No differences were found by tumor localization or histological type. In mediation analysis, we found that the direct effect of hepcidin only represents a nonsignificant 38% (95% CI: -69%, 91%). In summary, these data suggest that the inverse association of hepcidin levels and gastric cancer risk was mostly accounted by ferritin levels. Further investigation including repeated measures of hepcidin is needed to clarify their role in gastric carcinogenesis.

Interaction between genes and macronutrient intake on the risk of developing type 2 diabetes: systematic review and findings from European Prospective Investigation into Cancer (EPIC)-InterAct

Li S. X., Imamura F., Ye Z., Schulze M. B., Zheng J., Ardanaz E., Arriola L., Boeing H., Dow C., Fagherazzi G., Franks P. W., Agudo A., Grioni S., Kaaks R., Katzke V. A., Key T. J., Khaw K. T., Mancini F. R., Navarro C., Nilsson P. M., Onland-Moret N. C., Overvad K., Palli D., Panico S., Quiros J. R., Rolandsson O., Sacerdote C., Sanchez M. J., Slimani N., Sluijs I., Spijkerman A. M., Tjonneland A., Tumino R., Sharp S. J., Riboli E., Langenberg C., Scott R. A., Forouhi N. G., Wareham N. J.

Am J Clin Nutr; 2017; 106(1): 263-275

PMID:28592605

Abstract as provided by PubMed

Background: Gene-diet interactions have been reported to contribute to the development of type 2 diabetes (T2D). However, to our knowledge, few examples have been consistently replicated to date.Objective: We aimed to identify existing evidence for gene-macronutrient interactions and T2D and to examine the reported interactions in a large-scale study.Design: We systematically reviewed studies reporting gene-macronutrient interactions and T2D. We searched the MEDLINE, Human Genome Epidemiology Network, and WHO International Clinical Trials Registry Platform electronic databases to identify studies published up to October 2015. Eligibility criteria included assessment of macronutrient quantity (e.g., total carbohydrate) or indicators of quality (e.g., dietary fiber) by use of self-report or objective biomarkers of intake. Interactions identified in the review were subsequently examined in the EPIC (European Prospective Investigation into Cancer)-InterAct case-cohort study (n = 21,148, with 9403 T2D cases; 8 European countries). Prentice-weighted Cox regression was used to estimate country-specific HRs, 95% CIs, and P-interaction values, which were then pooled by random-effects meta-analysis. A primary model was fitted by using the same covariates as reported in the published studies, and a second model adjusted for additional covariates and estimated the effects of isocaloric macronutrient substitution.Results: Thirteen observational studies met the eligibility criteria (n < 1700 cases). Eight unique interactions were reported to be significant between macronutrients [carbohydrate, fat, saturated fat, dietary fiber, and glycemic load derived from self-report of dietary intake and circulating n-3 (omega-3) polyunsaturated fatty acids] and genetic variants in or near transcription factor 7-like 2 (TCF7L2), gastric inhibitory polypeptide receptor (GIPR), caveolin 2 (CAV2), and peptidase D (PEPD) (P-interaction < 0.05). We found no evidence of interaction when we tried to replicate previously reported interactions. In addition, no interactions were detected in models with additional covariates.Conclusions: Eight gene-macronutrient interactions were identified for the risk of T2D from the literature. These interactions were not replicated in the EPIC-InterAct study, which mirrored the analyses undertaken in the original reports. Our findings highlight the importance of independent replication of reported interactions.

Biomarkers of folate and vitamin B12 and breast cancer risk: report from the EPIC cohort

Matejcic M., de Batlle J., Ricci C., Biessy C., Perrier F., Huybrechts I., Weiderpass E., Boutron-Ruault M. C., Cadeau C., His M., Cox D. G., Boeing H., Fortner R. T., Kaaks R., Lagiou P., Trichopoulou A., Benetou V., Tumino R., Panico S., Sieri S., Palli D., Ricceri F., Bueno-de-Mesquita H. B., Skeie G., Amiano P., Sanchez M. J., Chirlaque M. D., Barricarte A., Quiros J. R., Buckland G., van Gils C. H., Peeters P. H., Key T. J., Riboli E., Gylling B., Zeleniuch-Jacquotte A., Gunter M. J., Romieu I., Chajes V.

Int J Cancer; 2017; 140(6): 1246-1259

PMID:27905104

Abstract as provided by PubMed

Epidemiological studies have reported inconsistent findings for the association between B vitamins and breast cancer (BC) risk. We investigated the relationship between biomarkers of folate and vitamin B12 and the risk of BC in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Plasma concentrations of folate and vitamin B12 were determined in 2,491 BC cases individually matched to 2,521 controls among women who provided baseline blood samples. Multivariable logistic regression models were used to estimate odds ratios by quartiles of either plasma B vitamin. Subgroup analyses by menopausal status, hormone receptor status of breast tumors (estrogen receptor [ER], progesterone receptor [PR] and human epidermal growth factor receptor 2 [HER2]), alcohol intake and MTHFR polymorphisms (677C > T and 1298A > C) were also performed. Plasma levels of folate and vitamin B12 were not significantly associated with the overall risk of BC or by hormone receptor status. A marginally positive association was found between vitamin B12 status and BC risk in women consuming above the median level of alcohol (ORQ4-Q1 = 1.26; 95% CI 1.00-1.58; Ptrend = 0.05). Vitamin B12 status was also positively associated with BC risk in women with plasma folate levels below the median value (ORQ4-Q1 = 1.29; 95% CI 1.02-1.62; Ptrend = 0.03). Overall, folate and vitamin B12 status was not clearly associated with BC risk in this prospective cohort study. However, potential interactions between vitamin B12 and alcohol or folate on the risk of BC deserve further investigation.

Mediterranean diet and risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition cohort

Molina-Montes E., Sanchez M. J., Buckland G., Bueno-de-Mesquita H. B., Weiderpass E., Amiano P., Wark P. A., Kuhn T., Katzke V., Huerta J. M., Ardanaz E., Quiros J. R., Affret A., His M., Boutron-Ruault M. C., Peeters P. H., Ye W., Sund M., Boeing H., Iqbal K., Ohlsson B., Sonestedt E., Tjonneland A., Petersen K. E., Travis R. C., Skeie G., Agnoli C., Panico S., Palli D., Tumino R., Sacerdote C., Freisling H., Huybrechts I., Overvad K., Trichopoulou A., Bamia C., Vasilopoulou E., Wareham N., Khaw K. T., Cross A. J., Ward H. A., Riboli E., Duell E. J.

Br J Cancer; 2017; 116(6): 811-820

PMID:28170373

Abstract as provided by PubMed

BACKGROUND: The Mediterranean diet (MD) has been proposed as a means for cancer prevention, but little evidence has been accrued regarding its potential to prevent pancreatic cancer. We investigated the association between the adherence to the MD and pancreatic cancer risk within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. METHODS: Over half a million participants from 10 European countries were followed up for over 11 years, after which 865 newly diagnosed exocrine pancreatic cancer cases were identified. Adherence to the MD was estimated through an adapted score without the alcohol component (arMED) to discount alcohol-related harmful effects. Cox proportional hazards regression models, stratified by age, sex and centre, and adjusted for energy intake, body mass index, smoking status, alcohol intake and diabetes status at recruitment, were used to estimate hazard ratios (HRs) associated with pancreatic cancer and their corresponding 95% confidence intervals (CIs). RESULTS: Adherence to the arMED score was not associated with risk of pancreatic cancer (HR high vs low adherence=0.99; 95% CI: 0.77-1.26, and HR per increments of two units in adherence to arMED=1.00; 95% CI: 0.94-1.06). There was no convincing evidence for heterogeneity by smoking status, body mass index, diabetes or European region. There was also no evidence of significant associations in analyses involving microscopically confirmed cases, plausible reporters of energy intake or other definitions of the MD pattern. CONCLUSIONS: A high adherence to the MD is not associated with pancreatic cancer risk in the EPIC study.

Genetic variation in the ADIPOQ gene, adiponectin concentrations and risk of colorectal cancer: a Mendelian Randomization analysis using data from three large cohort studies

Nimptsch K., Song M., Aleksandrova K., Katsoulis M., Freisling H., Jenab M., Gunter M. J., Tsilidis K. K., Weiderpass E., Bueno-De-Mesquita H. B., Chong D. Q., Jensen M. K., Wu C., Overvad K., Kuhn T., Barrdahl M., Melander O., Jirstrom K., Peeters P. H., Sieri S., Panico S., Cross A. J., Riboli E., Van Guelpen B., Myte R., Huerta J. M., Rodriguez-Barranco M., Quiros J. R., Dorronsoro M., Tjonneland A., Olsen A., Travis R., Boutron-Ruault M. C., Carbonnel F., Severi G., Bonet C., Palli D., Janke J., Lee Y. A., Boeing H., Giovannucci E. L., Ogino S., Fuchs C. S., Rimm E., Wu K., Chan A. T., Pischon T.

Eur J Epidemiol; 2017; 32(5): 419-430

PMID:28550647

Abstract as provided by PubMed

Higher levels of circulating adiponectin have been related to lower risk of colorectal cancer in several prospective cohort studies, but it remains unclear whether this association may be causal. We aimed to improve causal inference in a Mendelian Randomization meta-analysis using nested case-control studies of the European Prospective Investigation into Cancer and Nutrition (EPIC, 623 cases, 623 matched controls), the Health Professionals Follow-up Study (HPFS, 231 cases, 230 controls) and the Nurses' Health Study (NHS, 399 cases, 774 controls) with available data on pre-diagnostic adiponectin concentrations and selected single nucleotide polymorphisms in the ADIPOQ gene. We created an ADIPOQ allele score that explained approximately 3% of the interindividual variation in adiponectin concentrations. The ADIPOQ allele score was not associated with risk of colorectal cancer in logistic regression analyses (pooled OR per score-unit unit 0.97, 95% CI 0.91, 1.04). Genetically determined twofold higher adiponectin was not significantly associated with risk of colorectal cancer using the ADIPOQ allele score as instrumental variable (pooled OR 0.73, 95% CI 0.40, 1.34). In a summary instrumental variable analysis (based on previously published data) with higher statistical power, no association between genetically determined twofold higher adiponectin and risk of colorectal cancer was observed (0.99, 95% CI 0.93, 1.06 in women and 0.94, 95% CI 0.88, 1.01 in men). Thus, our study does not support a causal effect of circulating adiponectin on colorectal cancer risk. Due to the limited genetic determination of adiponectin, larger Mendelian Randomization studies are necessary to clarify whether adiponectin is causally related to lower risk of colorectal cancer.

Identification of Urinary Polyphenol Metabolite Patterns Associated with Polyphenol-Rich Food Intake in Adults from Four European Countries

Noh H., Freisling H., Assi N., Zamora-Ros R., Achaintre D., Affret A., Mancini F., Boutron-Ruault M. C., Flogel A., Boeing H., Kuhn T., Schubel R., Trichopoulou A., Naska A., Kritikou M., Palli D., Pala V., Tumino R., Ricceri F., Santucci de Magistris M., Cross A., Slimani N., Scalbert A., Ferrari P.

Nutrients; 2017; 9(8):

PMID:28757581

Abstract as provided by PubMed

We identified urinary polyphenol metabolite patterns by a novel algorithm that combines dimension reduction and variable selection methods to explain polyphenol-rich food intake, and compared their respective performance with that of single biomarkers in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. The study included 475 adults from four European countries (Germany, France, Italy, and Greece). Dietary intakes were assessed with 24-h dietary recalls (24-HDR) and dietary questionnaires (DQ). Thirty-four polyphenols were measured by ultra-performance liquid chromatography-electrospray ionization-tandem mass spectrometry (UPLC-ESI-MS-MS) in 24-h urine. Reduced rank regression-based variable importance in projection (RRR-VIP) and least absolute shrinkage and selection operator (LASSO) methods were used to select polyphenol metabolites. Reduced rank regression (RRR) was then used to identify patterns in these metabolites, maximizing the explained variability in intake of pre-selected polyphenol-rich foods. The performance of RRR models was evaluated using internal cross-validation to control for over-optimistic findings from over-fitting. High performance was observed for explaining recent intake (24-HDR) of red wine (r = 0.65; AUC = 89.1%), coffee (r = 0.51; AUC = 89.1%), and olives (r = 0.35; AUC = 82.2%). These metabolite patterns performed better or equally well compared to single polyphenol biomarkers. Neither metabolite patterns nor single biomarkers performed well in explaining habitual intake (as reported in the DQ) of polyphenol-rich foods. This proposed strategy of biomarker pattern identification has the potential of expanding the currently still limited list of available dietary intake biomarkers.

Dietary and lifestyle determinants of acrylamide and glycidamide hemoglobin adducts in non-smoking postmenopausal women from the EPIC cohort

Obon-Santacana M., Lujan-Barroso L., Freisling H., Cadeau C., Fagherazzi G., Boutron-Ruault M. C., Kaaks R., Fortner R. T., Boeing H., Ramon Quiros J., Molina-Montes E., Chamosa S., Castano J. M., Ardanaz E., Khaw K. T., Wareham N., Key T., Trichopoulou A., Lagiou P., Naska A., Palli D., Grioni S., Tumino R., Vineis P., De Magistris M. S., Bueno-de-Mesquita H. B., Peeters P. H., Wennberg M., Bergdahl I. A., Vesper H., Riboli E., Duell E. J.

Eur J Nutr; 2017; 56(3): 1157-1168

PMID:26850269

Abstract as provided by PubMed

PURPOSE: Acrylamide was classified as 'probably carcinogenic' to humans in 1994 by the International Agency for Research on Cancer. In 2002, public health concern increased when acrylamide was identified in starchy, plant-based foods, processed at high temperatures. The purpose of this study was to identify which food groups and lifestyle variables were determinants of hemoglobin adduct concentrations of acrylamide (HbAA) and glycidamide (HbGA) in 801 non-smoking postmenopausal women from eight countries in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. METHODS: Biomarkers of internal exposure were measured in red blood cells (collected at baseline) by high-performance liquid chromatography/tandem mass spectrometry (HPLC/MS/MS) . In this cross-sectional analysis, four dependent variables were evaluated: HbAA, HbGA, sum of total adducts (HbAA + HbGA), and their ratio (HbGA/HbAA). Simple and multiple regression analyses were used to identify determinants of the four outcome variables. All dependent variables (except HbGA/HbAA) and all independent variables were log-transformed (log2) to improve normality. Median (25th-75th percentile) HbAA and HbGA adduct levels were 41.3 (32.8-53.1) pmol/g Hb and 34.2 (25.4-46.9) pmol/g Hb, respectively. RESULTS: The main food group determinants of HbAA, HbGA, and HbAA + HbGA were biscuits, crackers, and dry cakes. Alcohol intake and body mass index were identified as the principal determinants of HbGA/HbAA. The total percent variation in HbAA, HbGA, HbAA + HbGA, and HbGA/HbAA explained in this study was 30, 26, 29, and 13 %, respectively. CONCLUSIONS: Dietary and lifestyle factors explain a moderate proportion of acrylamide adduct variation in non-smoking postmenopausal women from the EPIC cohort.

Tall height and obesity are associated with an increased risk of aggressive prostate cancer: results from the EPIC cohort study

Perez-Cornago A., Appleby P. N., Pischon T., Tsilidis K. K., Tjonneland A., Olsen A., Overvad K., Kaaks R., Kuhn T., Boeing H., Steffen A., Trichopoulou A., Lagiou P., Kritikou M., Krogh V., Palli D., Sacerdote C., Tumino R., Bueno-de-Mesquita H. B., Agudo A., Larranaga N., Molina-Portillo E., Barricarte A., Chirlaque M. D., Quiros J. R., Stattin P., Haggstrom C., Wareham N., Khaw K. T., Schmidt J. A., Gunter M., Freisling H., Aune D., Ward H., Riboli E., Key T. J., Travis R. C.

BMC Med; 2017; 15(1): 115

PMID:28701188

Abstract as provided by PubMed

BACKGROUND: The relationship between body size and prostate cancer risk, and in particular risk by tumour characteristics, is not clear because most studies have not differentiated between high-grade or advanced stage tumours, but rather have assessed risk with a combined category of aggressive disease. We investigated the association of height and adiposity with incidence of and death from prostate cancer in 141,896 men in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. METHODS: Multivariable-adjusted Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). After an average of 13.9 years of follow-up, there were 7024 incident prostate cancers and 934 prostate cancer deaths. RESULTS: Height was not associated with total prostate cancer risk. Subgroup analyses showed heterogeneity in the association with height by tumour grade (P heterogeneity = 0.002), with a positive association with risk for high-grade but not low-intermediate-grade disease (HR for high-grade disease tallest versus shortest fifth of height, 1.54; 95% CI, 1.18-2.03). Greater height was also associated with a higher risk for prostate cancer death (HR = 1.43, 1.14-1.80). Body mass index (BMI) was significantly inversely associated with total prostate cancer, but there was evidence of heterogeneity by tumour grade (P heterogeneity = 0.01; HR = 0.89, 0.79-0.99 for low-intermediate grade and HR = 1.32, 1.01-1.72 for high-grade prostate cancer) and stage (P heterogeneity = 0.01; HR = 0.86, 0.75-0.99 for localised stage and HR = 1.11, 0.92-1.33 for advanced stage). BMI was positively associated with prostate cancer death (HR = 1.35, 1.09-1.68). The results for waist circumference were generally similar to those for BMI, but the associations were slightly stronger for high-grade (HR = 1.43, 1.07-1.92) and fatal prostate cancer (HR = 1.55, 1.23-1.96). CONCLUSIONS: The findings from this large prospective study show that men who are taller and who have greater adiposity have an elevated risk of high-grade prostate cancer and prostate cancer death.

Prediagnostic circulating concentrations of plasma insulin-like growth factor-I and risk of lymphoma in the European Prospective Investigation into Cancer and Nutrition

Perez-Cornago A., Appleby P. N., Tipper S., Key T. J., Allen N. E., Nieters A., Vermeulen R., Roulland S., Casabonne D., Kaaks R., Fortner R. T., Boeing H., Trichopoulou A., La Vecchia C., Klinaki E., Hansen L., Tjonneland A., Bonnet F., Fagherazzi G., Boutron-Ruault M. C., Pala V., Masala G., Sacerdote C., Peeters P. H., Bueno-de-Mesquita H. B., Weiderpass E., Dorronsoro M., Quiros J. R., Barricarte A., Gavrila D., Agudo A., Borgquist S., Rosendahl A. H., Melin B., Wareham N., Khaw K. T., Gunter M., Riboli E., Vineis P., Travis R. C.

Int J Cancer; 2017; 140(5): 1111-1118

PMID:27870006

Abstract as provided by PubMed

Insulin-like growth factor (IGF)-I has cancer promoting activities. However, the hypothesis that circulating IGF-I concentration is related to risk of lymphoma overall or its subtypes has not been examined prospectively. IGF-I concentration was measured in pre-diagnostic plasma samples from a nested case-control study of 1,072 cases of lymphoid malignancies and 1,072 individually matched controls from the European Prospective Investigation into Cancer and Nutrition. Odds ratios (ORs) and confidence intervals (CIs) for lymphoma were calculated using conditional logistic regression. IGF-I concentration was not associated with overall lymphoma risk (multivariable-adjusted OR for highest versus lowest third = 0.77 [95% CI = 0.57-1.03], ptrend = 0.06). There was no statistical evidence of heterogeneity in this association with IGF-I by sex, age at blood collection, time between blood collection and diagnosis, age at diagnosis, or body mass index (pheterogeneity for all >/= 0.05). There were no associations between IGF-I concentration and risk for specific BCL subtypes, T-cell lymphoma or Hodgkin lymphoma, although number of cases were small. In this European population, IGF-I concentration was not associated with risk of overall lymphoma. This study provides the first prospective evidence on circulating IGF-I concentrations and risk of lymphoma. Further prospective data are required to examine associations of IGF-I concentrations with lymphoma subtypes.

Fruit and vegetable intake and prostate cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC)

Perez-Cornago A., Travis R. C., Appleby P. N., Tsilidis K. K., Tjonneland A., Olsen A., Overvad K., Katzke V., Kuhn T., Trichopoulou A., Peppa E., Kritikou M., Sieri S., Palli D., Sacerdote C., Tumino R., Bueno-de-Mesquita H. B. A., Agudo A., Larranaga N., Molina-Portillo E., Ardanaz E., Chirlaque M. D., Lasheras C., Stattin P., Wennberg M., Drake I., Malm J., Schmidt J. A., Khaw K. T., Gunter M., Freisling H., Huybrechts I., Aune D., Cross A. J., Riboli E., Key T. J.

Int J Cancer; 2017; 141(2): 287-297

PMID:28419475

Abstract as provided by PubMed

Several dietary factors have been studied in relation to prostate cancer; however, most studies have not reported on subtypes of fruit and vegetables or tumor characteristics, and results obtained so far are inconclusive. This study aimed to examine the prospective association of total and subtypes of fruit and vegetable intake with the incidence of prostate cancer overall, by grade and stage of disease, and prostate cancer death. Lifestyle information for 142,239 men participating in the European Prospective Investigation into Cancer and Nutrition from 8 European countries was collected at baseline. Multivariable Cox regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). After an average follow-up time of 13.9 years, 7,036 prostate cancer cases were identified. Compared with the lowest fifth, those in the highest fifth of total fruit intake had a significantly reduced prostate cancer risk (HR = 0.91; 95% CI = 0.83-0.99; p-trend = 0.01). No associations between fruit subtypes and prostate cancer risk were observed, except for citrus fruits, where a significant trend was found (HR = 0.94; 95% CI = 0.86-1.02; p-trend = 0.01). No associations between total and subtypes of vegetables and prostate cancer risk were observed. We found no evidence of heterogeneity in these associations by tumor grade and stage, with the exception of significant heterogeneity by tumor grade (pheterogeneity <0.001) for leafy vegetables. No significant associations with prostate cancer death were observed. The main finding of this prospective study was that a higher fruit intake was associated with a small reduction in prostate cancer risk. Whether this association is causal remains unclear.

Fiber intake modulates the association of alcohol intake with breast cancer

Romieu I., Ferrari P., Chajes V., de Batlle J., Biessy C., Scoccianti C., Dossus L., Christine Boutron M., Bastide N., Overvad K., Olsen A., Tjonneland A., Kaaks R., Boeing H., Trichopoulou A., Lagiou P., Trichopoulos D., Palli D., Sieri S., Tumino R., Vineis P., Panico S., Bueno-de-Mesquita H. B., Gils C. H., Peeters P. H., Lund E., Skeie G., Weiderpass E., Ramon Quiros J., Chirlaque M. D., Ardanaz E., Sanchez M. J., Duell E. J., Amiano Etxezarreta P., Borgquist S., Hallmans G., Johansson I., Maria Nilsson L., Khaw K. T., Wareham N., Key T. J., Travis R. C., Murphy N., Wark P. A., Riboli E.

Int J Cancer; 2017; 140(2): 316-321

PMID:27599758

Abstract as provided by PubMed

Alcohol intake has been related to an increased risk of breast cancer (BC) while dietary fiber intake has been inversely associated to BC risk. A beneficial effect of fibers on ethanol carcinogenesis through their impact on estrogen levels is still controversial. We investigated the role of dietary fiber as a modifying factor of the association of alcohol and BC using data from the European Prospective Investigation into Cancer and Nutrition (EPIC). This study included 334,850 women aged 35-70 years at baseline enrolled in the ten countries of the EPIC study and followed up for 11.0 years on average. Information on fiber and alcohol intake at baseline and average lifetime alcohol intake were calculated from country-specific dietary and lifestyle questionnaires. Hazard ratios (HR) of developing invasive BC according to different levels of alcohol and fiber intake were computed. During 3,670,439 person-years, 11,576 incident BC cases were diagnosed. For subjects with low intake of fiber (<18.5 g/day), the risk of BC per 10 g/day of alcohol intake was 1.06 (1.03-1.08) while among subjects with high intake of fiber (>24.2 g/day) the risk of BC was 1.02 (0.99-1.05) (test for interaction p = 0.011). This modulating effect was stronger for fiber from vegetables. Our results suggest that fiber intake may modulate the positive association of alcohol intake and BC. Alcohol is well known to increase the risk for BC, while a fiber-rich diet has the opposite effect. Here the authors find a significant interaction between both lifestyle factors indicating that high fiber intake can ease the adverse effects associated with alcohol consumption. Consequently, women with high alcohol intake and low fiber intake (<18.5 g/day) had the highest risk for BC. Specific benefits were associated with fibers from vegetable, warranting further investigations into specific fiber sources and their mechanistic interactions with alcohol-induced BC risk.

Circulating RANKL and RANKL/OPG and Breast Cancer Risk by ER and PR Subtype: Results from the EPIC Cohort

Sarink D., Schock H., Johnson T., Overvad K., Holm M., Tjonneland A., Boutron-Ruault M. C., His M., Kvaskoff M., Boeing H., Lagiou P., Papatesta E. M., Trichopoulou A., Palli D., Pala V., Mattiello A., Tumino R., Sacerdote C., Bueno-de-Mesquita H. B. A., van Gils C. H., Peeters P. H., Weiderpass E., Agudo A., Sanchez M. J., Chirlaque M. D., Ardanaz E., Amiano P., Khaw K. T., Travis R., Dossus L., Gunter M., Rinaldi S., Merritt M., Riboli E., Kaaks R., Fortner R. T.

Cancer Prev Res (Phila); 2017; 10(9): 525-534

PMID:28701332

Abstract as provided by PubMed

Receptor activator of nuclear factor-kappa B (RANK)-RANK ligand (RANKL) signaling promotes mammary tumor development in experimental models. Circulating concentrations of soluble RANKL (sRANKL) may influence breast cancer risk via activation of RANK signaling; this may be modulated by osteoprotegerin (OPG), the decoy receptor for RANKL. sRANKL and breast cancer risk by hormone receptor subtype has not previously been investigated. A case-control study was nested in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. This study included 1,976 incident invasive breast cancer cases [estrogen receptor positive (ER+), n = 1,598], matched 1:1 to controls. Women were pre- or postmenopausal at blood collection. Serum sRANKL was quantified using an ELISA, serum OPG using an electrochemiluminescent assay. Risk ratios (RR) and 95% confidence intervals (95% CI) were calculated using conditional logistic regression. Associations between sRANKL and breast cancer risk differed by tumor hormone receptor status (Phet = 0.05). Higher concentrations of sRANKL were positively associated with risk of ER+ breast cancer [5th vs. 1st quintile RR 1.28 (95% CI, 1.01-1.63); Ptrend = 0.20], but not ER- disease. For both ER+ and estrogen and progesterone receptor positive (ER+PR+) breast cancer, results considering the sRANKL/OPG ratio were similar to those for sRANKL; we observed a suggestive inverse association between the ratio and ER-PR- disease [5th vs. 1st quintile RR = 0.60 (0.31-1.14); Ptrend = 0.03]. This study provides the first large-scale prospective data on circulating sRANKL and breast cancer. We observed limited evidence for an association between sRANKL and breast cancer risk. Cancer Prev Res; 10(9); 525-34. (c)2017 AACR.

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