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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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

The association between adult attained height and sitting height with mortality in the European Prospective Investigation into Cancer and Nutrition (EPIC)

Sawada N., Wark P. A., Merritt M. A., Tsugane S., Ward H. A., Rinaldi S., Weiderpass E., Dartois L., His M., Boutron-Ruault M. C., Turzanski-Fortner R., Kaaks R., Overvad K., Redondo M. L., Travier N., Molina-Portillo E., Dorronsoro M., Cirera L., Ardanaz E., Perez-Cornago A., Trichopoulou A., Lagiou P., Valanou E., Masala G., Pala V., Hm Peeters P., T. van der Schouw Y, Melander O., Manjer J., da Silva M., Skeie G., Tjonneland A., Olsen A., J. Gunter M, Riboli E., J. Cross A

PLoS ONE; 2017; 12(3): e0173117

PMID:28257491

Abstract as provided by PubMed

Adult height and sitting height may reflect genetic and environmental factors, including early life nutrition, physical and social environments. Previous studies have reported divergent associations for height and chronic disease mortality, with positive associations observed for cancer mortality but inverse associations for circulatory disease mortality. Sitting height might be more strongly associated with insulin resistance; however, data on sitting height and mortality is sparse. Using the European Prospective Investigation into Cancer and Nutrition study, a prospective cohort of 409,748 individuals, we examined adult height and sitting height in relation to all-cause and cause-specific mortality. Height was measured in the majority of participants; sitting height was measured in ~253,000 participants. During an average of 12.5 years of follow-up, 29,810 deaths (11,931 from cancer and 7,346 from circulatory disease) were identified. Hazard ratios (HR) with 95% confidence intervals (CI) for death were calculated using multivariable Cox regression within quintiles of height. Height was positively associated with cancer mortality (men: HRQ5 vs. Q1 = 1.11, 95%CI = 1.00-1.24; women: HRQ5 vs. Q1 = 1.17, 95%CI = 1.07-1.28). In contrast, height was inversely associated with circulatory disease mortality (men: HRQ5 vs. Q1 = 0.63, 95%CI = 0.56-0.71; women: HRQ5 vs. Q1 = 0.81, 95%CI = 0.70-0.93). Although sitting height was not associated with cancer mortality, it was inversely associated with circulatory disease (men: HRQ5 vs. Q1 = 0.64, 95%CI = 0.55-0.75; women: HRQ5 vs. Q1 = 0.60, 95%CI = 0.49-0.74) and respiratory disease mortality (men: HRQ5 vs. Q1 = 0.45, 95%CI = 0.28-0.71; women: HRQ5 vs. Q1 = 0.60, 95%CI = 0.40-0.89). We observed opposing effects of height on cancer and circulatory disease mortality. Sitting height was inversely associated with circulatory disease and respiratory disease mortality.

Pre-diagnostic metabolite concentrations and prostate cancer risk in 1077 cases and 1077 matched controls in the European Prospective Investigation into Cancer and Nutrition

Schmidt J. A., Fensom G. K., Rinaldi S., Scalbert A., Appleby P. N., Achaintre D., Gicquiau A., Gunter M. J., Ferrari P., Kaaks R., Kuhn T., Floegel A., Boeing H., Trichopoulou A., Lagiou P., Anifantis E., Agnoli C., Palli D., Trevisan M., Tumino R., Bueno-de-Mesquita H. B., Agudo A., Larranaga N., Redondo-Sanchez D., Barricarte A., Huerta J. M., Quiros J. R., Wareham N., Khaw K. T., Perez-Cornago A., Johansson M., Cross A. J., Tsilidis K. K., Riboli E., Key T. J., Travis R. C.

BMC Med; 2017; 15(1): 122

PMID:28676103

Abstract as provided by PubMed

BACKGROUND: Little is known about how pre-diagnostic metabolites in blood relate to risk of prostate cancer. We aimed to investigate the prospective association between plasma metabolite concentrations and risk of prostate cancer overall, and by time to diagnosis and tumour characteristics, and risk of death from prostate cancer. METHODS: In a case-control study nested in the European Prospective Investigation into Cancer and Nutrition, pre-diagnostic plasma concentrations of 122 metabolites (including acylcarnitines, amino acids, biogenic amines, glycerophospholipids, hexose and sphingolipids) were measured using targeted mass spectrometry (AbsoluteIDQ p180 Kit) and compared between 1077 prostate cancer cases and 1077 matched controls. Risk of prostate cancer associated with metabolite concentrations was estimated by multi-variable conditional logistic regression, and multiple testing was accounted for by using a false discovery rate controlling procedure. RESULTS: Seven metabolite concentrations, i.e. acylcarnitine C18:1, amino acids citrulline and trans-4-hydroxyproline, glycerophospholipids PC aa C28:1, PC ae C30:0 and PC ae C30:2, and sphingolipid SM (OH) C14:1, were associated with prostate cancer (p < 0.05), but none of the associations were statistically significant after controlling for multiple testing. Citrulline was associated with a decreased risk of prostate cancer (odds ratio (OR1SD) = 0.73; 95% confidence interval (CI) 0.62-0.86; p trend = 0.0002) in the first 5 years of follow-up after taking multiple testing into account, but not after longer follow-up; results for other metabolites did not vary by time to diagnosis. After controlling for multiple testing, 12 glycerophospholipids were inversely associated with advanced stage disease, with risk reduction up to 46% per standard deviation increase in concentration (OR1SD = 0.54; 95% CI 0.40-0.72; p trend = 0.00004 for PC aa C40:3). Death from prostate cancer was associated with higher concentrations of acylcarnitine C3, amino acids methionine and trans-4-hydroxyproline, biogenic amine ADMA, hexose and sphingolipid SM (OH) C14:1 and lower concentration of glycerophospholipid PC aa C42:4. CONCLUSIONS: Several metabolites, i.e. C18:1, citrulline, trans-4-hydroxyproline, three glycerophospholipids and SM (OH) C14:1, might be related to prostate cancer. Analyses by time to diagnosis indicated that citrulline may be a marker of subclinical prostate cancer, while other metabolites might be related to aetiology. Several glycerophospholipids were inversely related to advanced stage disease. More prospective data are needed to confirm these associations.

Vasectomy and Prostate Cancer Risk in the European Prospective Investigation Into Cancer and Nutrition (EPIC)

Smith K., Byrne, Castano J. M., Chirlaque M. D., Lilja H., Agudo A., Ardanaz E., Rodriguez-Barranco M., Boeing H., Kaaks R., Khaw K. T., Larranaga N., Navarro C., Olsen A., Overvad K., Perez-Cornago A., Rohrmann S., Sanchez M. J., Tjonneland A., Tsilidis K. K., Johansson M., Riboli E., Key T. J., Travis R. C.

J Clin Oncol; 2017; 35(12): 1297-1303

PMID:28375714

Abstract as provided by PubMed

Purpose Vasectomy is a commonly used form of male sterilization, and some studies have suggested that it may be associated with an increased risk of prostate cancer, including more aggressive forms of the disease. We investigated the prospective association of vasectomy with prostate cancer in a large European cohort, with a focus on high-grade and advanced-stage tumors, and death due to prostate cancer. Patients and Methods A total of 84,753 men from the European Prospective Investigation into Cancer and Nutrition (EPIC), aged 35 to 79 years, provided information on vasectomy status (15% with vasectomy) at recruitment and were followed for incidence of prostate cancer and death. We estimated the association of vasectomy with prostate cancer risk overall, by tumor subtype, and for death due to prostate cancer, using multivariable-adjusted Cox proportional hazards models. Results During an average follow-up of 15.4 years, 4,377 men were diagnosed with prostate cancer, including 641 who had undergone a vasectomy. Vasectomy was not associated with prostate cancer risk (hazard ratio [HR], 1.05; 95% CI, 0.96 to 1.15), and no evidence for heterogeneity in the association was observed by stage of disease or years since vasectomy. There was some evidence of heterogeneity by tumor grade ( P = .02), with an increased risk for low-intermediate grade (HR, 1.14; 95% CI, 1.01 to 1.29) but not high-grade prostate cancer (HR, 0.83; 95% CI, 0.64 to 1.07). Vasectomy was not associated with death due to prostate cancer (HR, 0.88; 95% CI, 0.68 to 1.12). Conclusion These findings from a large European prospective study show no elevated risk for overall, high-grade or advanced-stage prostate cancer, or death due to prostate cancer in men who have undergone a vasectomy compared with men who have not.

Circulating copper and zinc levels and risk of hepatobiliary cancers in Europeans

Stepien M., Hughes D. J., Hybsier S., Bamia C., Tjonneland A., Overvad K., Affret A., His M., Boutron-Ruault M. C., Katzke V., Kuhn T., Aleksandrova K., Trichopoulou A., Lagiou P., Orfanos P., Palli D., Sieri S., Tumino R., Ricceri F., Panico S., Bueno-de-Mesquita H. B., Peeters P. H., Weiderpass E., Lasheras C., Bonet Bonet C., Molina-Portillo E., Dorronsoro M., Huerta J. M., Barricarte A., Ohlsson B., Sjoberg K., Werner M., Shungin D., Wareham N., Khaw K. T., Travis R. C., Freisling H., Cross A. J., Schomburg L., Jenab M.

Br J Cancer; 2017; 116(5): 688-696

PMID:28152549

Abstract as provided by PubMed

BACKGROUND: Copper and zinc are essential micronutrients and cofactors of many enzymatic reactions that may be involved in liver-cancer development. We aimed to assess pre-diagnostic circulating levels of copper, zinc and their ratio (Cu/Zn) in relation to hepatocellular carcinoma (HCC), intrahepatic bile duct (IHBD) and gall bladder and biliary tract (GBTC) cancers. METHODS: A nested case-control study was conducted within the European Prospective Investigation into Cancer and Nutrition cohort. Serum zinc and copper levels were measured in baseline blood samples by total reflection X-ray fluorescence in cancer cases (HCC n=106, IHDB n=34, GBTC n=96) and their matched controls (1:1). The Cu/Zn ratio, an indicator of the balance between the micronutrients, was computed. Multivariable adjusted odds ratios and 95% confidence intervals (OR; 95% CI) were used to estimate cancer risk. RESULTS: For HCC, the highest vs lowest tertile showed a strong inverse association for zinc (OR=0.36; 95% CI: 0.13-0.98, Ptrend=0.0123), but no association for copper (OR=1.06; 95% CI: 0.45-2.46, Ptrend=0.8878) in multivariable models. The calculated Cu/Zn ratio showed a positive association for HCC (OR=4.63; 95% CI: 1.41-15.27, Ptrend=0.0135). For IHBC and GBTC, no significant associations were observed. CONCLUSIONS: Zinc may have a role in preventing liver-cancer development, but this finding requires further investigation in other settings.

Measured Adiposity in Relation to Head and Neck Cancer Risk in the European Prospective Investigation into Cancer and Nutrition

Ward H. A., Wark P. A., Muller D. C., Steffen A., Johansson M., Norat T., Gunter M. J., Overvad K., Dahm C. C., Halkjaer J., Tjonneland A., Boutron-Ruault M. C., Fagherazzi G., Mesrine S., Brennan P., Freisling H., Li K., Kaaks R., Trichopoulou A., Lagiou P., Panico S., Grioni S., Tumino R., Vineis P., Palli D., Peeters P. H. M., Bueno-de-Mesquita H. B., Weiderpass E., Agudo A., Quiros J. R., Larranaga N., Ardanaz E., Huerta J. M., Sanchez M. J., Laurell G., Johansson I., Westin U., Wallstrom P., Bradbury K. E., Wareham N. J., Khaw K. T., Pearson C., Boeing H., Riboli E.

Cancer Epidemiol Biomarkers Prev; 2017; 26(6): 895-904

PMID:28183827

Abstract as provided by PubMed

Background: Emerging evidence from cohort studies indicates that adiposity is associated with greater incidence of head and neck cancer. However, most studies have used self-reported anthropometry which is prone to error.Methods: Among 363,094 participants in the European Prospective Investigation into Cancer and Nutrition study (EPIC) with measured anthropometry, there were 837 incident cases of head and neck cancer. Head and neck cancer risk was examined in relation to body mass index (BMI) [lean: <22.5 kg/m2, normal weight (reference): 22.5-24.9 kg/m2, overweight 25-29.9 kg/m2, obese: >/=30 kg/m2], waist circumference (WC), hip circumference (HC), and waist-to-hip ratio (WHR) using Cox proportional hazards models.Results: Among men, a BMI < 22.5 kg/m2 was associated with higher head and neck cancer risk [HR 1.62; 95% confidence interval (CI), 1.23-2.12)]; BMI was not associated with head and neck cancer among women. WC and WHR were associated with greater risk of head and neck cancer among women (WC per 5 cm: HR, 1.08; 95% CI, 1.02-1.15; WHR per 0.1 unit: HR, 1.64; 95% CI, 1.38-1.93). After stratification by smoking status, the association for WHR was present only among smokers (Pinteraction = 0.004). Among men, WC and WHR were associated with head and neck cancer only upon additional adjustment for BMI (WC per 5 cm: HR 1.16; 95% CI, 1.07-1.26; WHR per 0.1 unit: HR, 1.42; 95% CI, 1.21-1.65).Conclusions: Central adiposity, particularly among women, may have a stronger association with head and neck cancer risk than previously estimated.Impact: Strategies to reduce obesity may beneficially impact head and neck cancer incidence. Cancer Epidemiol Biomarkers Prev; 26(6); 895-904. (c)2017 AACR.

Evaluation of urinary resveratrol as a biomarker of dietary resveratrol intake in the European Prospective Investigation into Cancer and Nutrition (EPIC) study

Zamora-Ros R., Rothwell J. A., Achaintre D., Ferrari P., Boutron-Ruault M. C., Mancini F. R., Affret A., Kuhn T., Katzke V., Boeing H., Kuppel S., Trichopoulou A., Lagiou P., La Vecchia C., Palli D., Contiero P., Panico S., Tumino R., Ricceri F., Noh H., Freisling H., Romieu I., Scalbert A.

Br J Nutr; 2017; 117(11): 1596-1602

PMID:28637522

Abstract as provided by PubMed

In vitro studies have shown several beneficial properties of resveratrol. Epidemiological evidence is still scarce, probably because of the difficulty in estimating resveratrol exposure accurately. The current study aimed to assess the relationships between acute and habitual dietary resveratrol and wine intake and urinary resveratrol excretion in a European population. A stratified random subsample of 475 men and women from four countries participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) cross-sectional study, who had provided 24-h urine samples and completed a 24-h dietary recall (24-HDR) on the same day, were included. Acute and habitual dietary data were collected using standardised 24-HDR software and a validated country-specific dietary questionnaire, respectively. Phenol-Explorer was used to estimate the intake of resveratrol and other stilbenes. Urinary resveratrol was analysed using tandem MS. Spearman's correlation coefficients between estimated dietary intakes of resveratrol and other stilbenes and consumption of wine, their main food source, were very high (r>0.9) when measured using dietary questionnaires and were slightly lower with 24-HDR (r>0.8). Partial Spearman's correlations between urinary resveratrol excretion and intake of resveratrol, total stilbenes or wine were found to be higher when using the 24-HDR (R 2 partial approximately 0.6) than when using the dietary questionnaires (R 2 partial approximately 0.5). Moderate to high correlations between dietary resveratrol, total stilbenes and wine, and urinary resveratrol concentrations were observed. These support the earlier findings that 24-h urinary resveratrol is an effective biomarker of both resveratrol and wine intakes. These correlations also support the validity of the estimation of resveratrol intake using the dietary questionnaire and Phenol-Explorer.

Consumption of Fish Is Not Associated with Risk of Differentiated Thyroid Carcinoma in the European Prospective Investigation into Cancer and Nutrition (EPIC) Study

Zamora-Ros R., Castaneda J., Rinaldi S., Cayssials V., Slimani N., Weiderpass E., Tsilidis K. K., Boutron-Ruault M. C., Overvad K., Eriksen A. K., Tjonneland A., Kuhn T., Katzke V., Boeing H., Trichopoulou A., La Vecchia C., Kotanidou A., Palli D., Grioni S., Mattiello A., Tumino R., Sciannameo V., Lund E., Merino S., Salamanca-Fernandez E., Amiano P., Huerta J. M., Barricarte A., Ericson U., Almquist M., Hennings J., Sandstrom M., Bueno-de-Mesquita H. B., Peeters P. H., Khaw K. T., Wareham N. J., Schmidt J. A., Cross A. J., Riboli E., Scalbert A., Romieu I., Agudo A., Franceschi S.

J Nutr; 2017; 147(7): 1366-1373

PMID:28592517

Abstract as provided by PubMed

Background: Differentiated thyroid cancer (TC) is the most common endocrine cancer. Fish can be an important source of iodine and other micronutrients and contaminants that may affect the thyroid gland and TC risk.Objective: We prospectively evaluated the relations between the consumption of total fish and different fish types and shellfish and TC risk in the EPIC (European Prospective Investigation into Cancer and Nutrition) study.Methods: EPIC is a cohort of >500,000 men and women, mostly aged 35-70 y, who were recruited in 10 European countries. After a mean follow-up of 14 y, 748 primary differentiated TC cases were diagnosed; 666 were in women and 601 were papillary TC. Data on intakes of lean fish, fatty fish, fish products, and shellfish were collected by using country-specific validated dietary questionnaires at recruitment. Multivariable Cox regression was used to calculate HRs and 95% CIs adjusted for many potential confounders, including dietary and nondietary factors.Results: No significant association was observed between total fish consumption and differentiated TC risk for the highest compared with the lowest quartile (HR: 1.03; 95% CI: 0.81, 1.32; P-trend = 0.67). Likewise, no significant association was observed with the intake of any specific type of fish, fish product, or shellfish. No significant heterogeneity was found by TC subtype (papillary or follicular tumors), by sex, or between countries with low and high TC incidence.Conclusion: This large study shows that the intake of fish and shellfish was not associated with differentiated TC risk in Europe, a region in which iodine deficiency or excess is rare.

Dietary flavonoid intake and colorectal cancer risk in the European prospective investigation into cancer and nutrition (EPIC) cohort

Zamora-Ros R., Barupal D. K., Rothwell J. A., Jenab M., Fedirko V., Romieu I., Aleksandrova K., Overvad K., Kyro C., Tjonneland A., Affret A., His M., Boutron-Ruault M. C., Katzke V., Kuhn T., Boeing H., Trichopoulou A., Naska A., Kritikou M., Saieva C., Agnoli C., Santucci de Magistris M., Tumino R., Fasanelli F., Weiderpass E., Skeie G., Merino S., Jakszyn P., Sanchez M. J., Dorronsoro M., Navarro C., Ardanaz E., Sonestedt E., Ericson U., Maria Nilsson L., Boden S., Bueno-de-Mesquita H. B., Peeters P. H., Perez-Cornago A., Wareham N. J., Khaw K. T., Freisling H., Cross A. J., Riboli E., Scalbert A.

Int J Cancer; 2017; 140(8): 1836-1844

PMID:28006847

Abstract as provided by PubMed

Flavonoids have been shown to inhibit colon cancer cell proliferation in vitro and protect against colorectal carcinogenesis in animal models. However, epidemiological evidence on the potential role of flavonoid intake in colorectal cancer (CRC) development remains sparse and inconsistent. We evaluated the association between dietary intakes of total flavonoids and their subclasses and risk of development of CRC, within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. A cohort of 477,312 adult men and women were recruited in 10 European countries. At baseline, dietary intakes of total flavonoids and individual subclasses were estimated using centre-specific validated dietary questionnaires and composition data from the Phenol-Explorer database. During an average of 11 years of follow-up, 4,517 new cases of primary CRC were identified, of which 2,869 were colon (proximal = 1,298 and distal = 1,266) and 1,648 rectal tumours. No association was found between total flavonoid intake and the risk of overall CRC (HR for comparison of extreme quintiles 1.05, 95% CI 0.93-1.18; p-trend = 0.58) or any CRC subtype. No association was also observed with any intake of individual flavonoid subclasses. Similar results were observed for flavonoid intake expressed as glycosides or aglycone equivalents. Intake of total flavonoids and flavonoid subclasses, as estimated from dietary questionnaires, did not show any association with risk of CRC development.

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