Publications
1312 results found
Gunter MJ, Alhomoud S, Arnold M, et al., 2019, International cancer seminars:a focus on colorectal cancer, Annals of Oncology, ISSN: 0923-7534
Despite significant progress in our understanding of the etiology, biology and genetics of colorectal cancer, as well as important clinical advances, it remains the third most frequently diagnosed cancer worldwide and is the second leading cause of cancer death. Based on demographic projections, the global burden of colorectal cancer would be expected to rise by 72% from 1.8 million new cases in 2018 to over 3 million in 2040 with substantial increases anticipated in low and middle income countries. In this meeting report, we summarize the content of a joint workshop led by the National Cancer Institute (NCI) and the International Agency for Research on Cancer (IARC) which was held to summarize the important achievements that have been made in our understanding of colorectal cancer etiology, genetics, early detection and treatment and to identify key research questions that remain to be addressed.
Matejcic M, Saunders EJ, Dadaev T, et al., 2019, Author Correction: Germline variation at 8q24 and prostate cancer risk in men of European ancestry, Nature Communications, Vol: 10, ISSN: 2041-1723
Correction to: Nature Communications; https://doi.org/10.1038/s41467-018-06863-1, published online 5 November 2018.The original version of this Article contained an error in the spelling of the author Manuela Gago-Dominguez, which was incorrectly given as Manuela G. Dominguez. This has now been corrected in both the PDF and HTML versions of the Article.
Sen A, Papadimitriou N, Lagiou P, et al., 2019, Coffee and tea consumption and risk of prostate cancer in the European Prospective Investigation into Cancer and Nutrition, International Journal of Cancer, Vol: 144, Pages: 240-250, ISSN: 0020-7136
The epidemiological evidence regarding the association of coffee and tea consumption with prostate cancer risk is inconclusive, and few cohort studies have assessed these associations by disease stage and grade. We examined the associations of coffee (total, caffeinated and decaffeinated) and tea intake with prostate cancer risk in the European Prospective Investigation into Cancer and Nutrition. Among 142,196 men, 7,036 incident prostate cancer cases were diagnosed over 14 years of follow-up. Data on coffee and tea consumption were collected through validated country-specific food questionnaires at baseline. We used Cox proportional hazards regression models to compute hazard ratios (HRs) and 95% confidence intervals (CI). Models were stratified by center and age, and adjusted for anthropometric, lifestyle and dietary factors. Median coffee and tea intake were 375 mL/day and 106 mL/day, respectively, but large variations existed by country. Comparing the highest (median of 855 mL/day) versus lowest (median of 103 mL/day) consumers of coffee and tea (450 mL/day versus 12 mL/day) the HRs were 1.02 (95% CI, 0.94-1.09) and 0.98 (95% CI, 0.90-1.07) for risk of total prostate cancer, and 0.97 (95% CI, 0.79-1.21) and 0.89 (95% CI, 0.70-1.13) for risk of fatal disease, respectively. No evidence of association was seen for consumption of total, caffeinated or decaffeinated coffee or tea and risk of total prostate cancer or cancer by stage, grade or fatality in this large cohort. Further investigations are needed to clarify whether an association exists by different preparations or by concentrations and constituents of these beverages. This article is protected by copyright. All rights reserved.
Nichols HB, Schoemaker MJ, Cai J, et al., 2019, Breast cancer risk after recent childbirth: A pooled analysis of 15 prospective studies, Annals of Internal Medicine, Vol: 170, Pages: 22-30, ISSN: 1539-3704
Background: Parity is widely recognized as protective for breast cancer, but breast cancer risk may be increased shortly after childbirth. Whether this risk varies with breastfeeding, family history of breast cancer, or specific tumor subtype has rarely been evaluated. Objective: To characterize breast cancer risk in relation to recent childbirth. Design: Pooled analysis of individual-level data from 15 prospective cohort studies. Setting: The international Premenopausal Breast Cancer Collaborative Group. Participants: Women younger than 55 years. Measurements: During 9.6 million person-years of follow-up, 18 826 incident cases of breast cancer were diagnosed. Hazard ratios (HRs) and 95% CIs for breast cancer were calculated using Cox proportional hazards regression. Results: Compared with nulliparous women, parous women had an HR for breast cancer that peaked about 5 years after birth (HR, 1.80 [95% CI, 1.63 to 1.99]) before decreasing to 0.77 (CI, 0.67 to 0.88) after 34 years. The association crossed over from positive to negative about 24 years after birth. The overall pattern was driven by estrogen receptor (ER)-positive breast cancer; no crossover was seen for ER-negative cancer. Increases in breast cancer risk after childbirth were pronounced when combined with a family history of breast cancer and were greater for women who were older at first birth or who had more births. Breastfeeding did not modify overall risk patterns. Limitations: Breast cancer diagnoses during pregnancy were not uniformly distinguishable from early postpartum diagnoses. Data on human epidermal growth factor receptor 2 (HER2) oncogene overexpression were limited. Conclusion: Compared with nulliparous women, parous women have an increased risk for breast cancer for more than 20 years after childbirth. Health care providers should consider recent childbirth a risk factor for breast cancer in young women. Primary Funding Source: The Avon Foundation, the National Institute of Environme
Huyghe JR, Bien SA, Harrison TA, et al., 2019, Discovery of common and rare genetic risk variants for colorectal cancer, Nature Genetics, Vol: 51, Pages: 76-87, ISSN: 1061-4036
To further dissect the genetic architecture of colorectal cancer (CRC), we performed whole-genome sequencing of 1,439 cases and 720 controls, imputed discovered sequence variants and Haplotype Reference Consortium panel variants into genome-wide association study data, and tested for association in 34,869 cases and 29,051 controls. Findings were followed up in an additional 23,262 cases and 38,296 controls. We discovered a strongly protective 0.3% frequency variant signal at CHD1. In a combined meta-analysis of 125,478 individuals, we identified 40 new independent signals at P < 5 × 10−8, bringing the number of known independent signals for CRC to ~100. New signals implicate lower-frequency variants, Krüppel-like factors, Hedgehog signaling, Hippo-YAP signaling, long noncoding RNAs and somatic drivers, and support a role for immune function. Heritability analyses suggest that CRC risk is highly polygenic, and larger, more comprehensive studies enabling rare variant analysis will improve understanding of biology underlying this risk and influence personalized screening strategies and drug development.
Li K, Anderson G, Viallon V, et al., 2018, Risk prediction for estrogen receptor-specific breast cancers in two large prospective cohorts, Breast Cancer Research, Vol: 20, ISSN: 1465-5411
Background: Few published breast cancer (BC) risk prediction models consider the heterogeneity of predictor variables between estrogen-receptor positive (ER+) and negative (ER-) tumors. Using data from two large cohorts, we examined whether modeling this heterogeneity could improve prediction. Methods: We built two models, for ER+ (ModelER+) and ER- tumors (ModelER-), respectively, in 281,330 women (51% postmenopausal at recruitment) from the European Prospective Investigation into Cancer and Nutrition cohort. Discrimination (C-statistic) and calibration (the agreement between predicted and observed tumor risks) were assessed both internally and externally in 82,319 postmenopausal women from the Women's Health Initiative study. We performed decision curve analysis to compare ModelER+ and the Gail model (ModelGail) regarding their applicability in risk assessment for chemoprevention. Results: Parity, number of full-term pregnancies, age at first full-term pregnancy and body height were only associated with ER+ tumors. Menopausal status, age at menarche and at menopause, hormone replacement therapy, postmenopausal body mass index, and alcohol intake were homogeneously associated with ER+ and ER- tumors. Internal validation yielded a C-statistic of 0.64 for ModelER+ and 0.59 for ModelER-. External validation reduced the C-statistic of ModelER+ (0.59) and ModelGail (0.57). In external evaluation of calibration, ModelER+ outperformed the ModelGail: the former led to a 9% overestimation of the risk of ER+ tumors, while the latter yielded a 22% underestimation of the overall BC risk. Compared with the treat-all strategy, ModelER+ produced equal or higher net benefits irrespective of the benefit-to-harm ratio of chemoprevention, while ModelGail did not produce higher net benefits unless the benefit-to-harm ratio was below 50. The clinical applicability, i.e. the area defined by the net benefit curve and the treat-all and treat-none strategies, was 12.7 × 10- 6 for Mod
Aune D, Snekvik I, Schlesinger S, et al., 2018, Body mass index, abdominal fatness, weight gain and the risk of psoriasis: a systematic review and dose-response meta-analysis of prospective studies, European Journal of Epidemiology, Vol: 33, Pages: 1163-1178, ISSN: 0393-2990
Greater body mass index (BMI) has been associated with increased risk of psoriasis in case-control and cross-sectional studies, however, the evidence from prospective studies has been limited. We conducted a systematic review and dose-response meta-analysis of different adiposity measures and the risk of psoriasis to provide a more robust summary of the evidence based on data from prospective studies. PubMed and Embase databases were searched for relevant studies up to August 8th 2017. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using a random effects model. The summary relative risk (RR) for a 5 unit increment in BMI was 1.19 (95% CI 1.10-1.28, I2 = 83%, n = 7). The association appeared to be stronger at higher compared to lower levels of BMI, pnonlinearity < 0.0001, and the lowest risk was observed at a BMI around 20. The summary RR was 1.24 (95% CI 1.17-1.31, I2 = 0%, pheterogeneity = 0.72, n = 3) per 10 cm increase in waist circumference, 1.37 (95% CI 1.23-1.53, I2 = 0%, pheterogeneity = 0.93, n = 3) per 0.1 unit increase in waist-to-hip ratio, and 1.11 (95% CI 1.07-1.16, I2 = 47%, pheterogeneity = 0.15, n = 3) per 5 kg of weight gain. Adiposity as measured by BMI, waist circumference, waist-to-hip ratio, and weight gain is associated with increased risk of psoriasis.
Chadeau M, Campanella G, Gunter MJ, et al., 2018, Epigenome-wide association study of adiposity and future risk of obesity-related diseases, International Journal of Obesity, Vol: 42, Pages: 2022-2035, ISSN: 0307-0565
BackgroundObesity is an established risk factor for several common chronic diseases such as breast and colorectal cancer, metabolic and cardiovascular diseases; however, the biological basis for these relationships is not fully understood. To explore the association of obesity with these conditions, we investigated peripheral blood leucocyte (PBL) DNA methylation markers for adiposity and their contribution to risk of incident breast and colorectal cancer and myocardial infarction.MethodsDNA methylation profiles (Illumina Infinium® HumanMethylation450 BeadChip) from 1941 individuals from four population-based European cohorts were analysed in relation to body mass index, waist circumference, waist-hip and waist-height ratio within a meta-analytical framework. In a subset of these individuals, data on genome-wide gene expression level, biomarkers of glucose and lipid metabolism were also available. Validation of methylation markers associated with all adiposity measures was performed in 358 individuals. Finally, we investigated the association of obesity-related methylation marks with breast, colorectal cancer and myocardial infarction within relevant subsets of the discovery population.ResultsWe identified 40 CpG loci with methylation levels associated with at least one adiposity measure. Of these, one CpG locus (cg06500161) in ABCG1 was associated with all four adiposity measures (P = 9.07×10−8 to 3.27×10−18) and lower transcriptional activity of the full-length isoform of ABCG1 (P = 6.00×10−7), higher triglyceride levels (P = 5.37×10−9) and higher triglycerides-to-HDL cholesterol ratio (P = 1.03×10−10). Of the 40 informative and obesity-related CpG loci, two (in IL2RB and FGF18) were significantly associated with colorectal cancer (inversely, P < 1.6×10−3) and one intergenic locus on chromosome 1 was inversely associa
Aune D, Schlesinger S, Norat T, et al., 2018, Diabetes mellitus and the risk of abdominal aortic aneurysm: A systematic review and meta-analysis of prospective studies, Journal of Diabetes and its Complications, Vol: 32, Pages: 1169-1174, ISSN: 1056-8727
BACKGROUND: Diabetes mellitus has been associated with reduced risk of abdominal aortic aneurysm in a number of epidemiological studies, however, until recently little data from prospective studies have been available. We therefore conducted a systematic review and meta-analysis of prospective studies to quantify the association. MATERIAL AND METHODS: Two investigators searched the PubMed and Embase databases for studies of diabetes and abdominal aortic aneurysm up to May 8th 2018. Prospective studies were included if they reported adjusted relative risk (RR) estimates and 95% confidence intervals (95% CIs) of abdominal aortic aneurysm associated with a diabetes diagnosis. Summary relative risks were estimated by use of a random effects model. RESULTS: We identified 16 prospective studies with 16,572 cases among 4,563,415 participants that could be included in the meta-analysis. The summary RR for individuals with diabetes compared to individuals without diabetes was 0.58 (95% CI: 0.51-0.66, I2 = 40.4%, pheterogeneity = 0.06). The results persisted when stratified by sex, duration of follow-up, and in most of the other subgroup analyses. There was no evidence of publication bias with Egger's test, p = 0.64 or by inspection of the funnel plots. CONCLUSIONS: These results suggest that individuals with diabetes mellitus are at a reduced risk of abdominal aortic aneurysm, however, whether pharmacological agents for diabetes mellitus explain this observation needs to be clarified in future studies.
Bottazzi B, Riboli E, Mantovani A, 2018, Aging, inflammation and cancer, SEMINARS IN IMMUNOLOGY, Vol: 40, Pages: 74-82, ISSN: 1044-5323
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Aune D, Keum N, Giovannucci E, et al., 2018, Dietary intake and blood concentrations of antioxidants and the risk of cardiovascular disease, total cancer, and all-cause mortality: a systematic review and dose-response meta-analysis of prospective studies, American Journal of Clinical Nutrition, Vol: 108, Pages: 1069-1091, ISSN: 1938-3207
Background: High dietary intake or blood concentrations (as biomarkers of dietary intake) of vitamin C, carotenoids, and vitamin E have been associated with reduced risk of cardiovascular disease, cancer, and mortality, but these associations have not been systematically assessed. Objective: We conducted a systematic review and meta-analysis of prospective studies of dietary intake and blood concentrations of vitamin C, carotenoids, and vitamin E in relation to these outcomes. Design: We searched PubMed and Embase up to 14 February 2018. Summary RRs and 95% CIs were calculated with the use of random-effects models. Results: Sixty-nine prospective studies (99 publications) were included. The summary RR per 100-mg/d increment of dietary vitamin C intake was 0.88 (95% CI: 0.79, 0.98, I2 = 65%, n = 11) for coronary heart disease, 0.92 (95% CI: 0.87, 0.98, I2 = 68%, n = 12) for stroke, 0.89 (95% CI: 0.85, 0.94, I2 = 27%, n = 10) for cardiovascular disease, 0.93 (95% CI: 0.87, 0.99, I2 = 46%, n = 8) for total cancer, and 0.89 (95% CI: 0.85, 0.94, I2 = 80%, n = 14) for all-cause mortality. Corresponding RRs per 50-μmol/L increase in blood concentrations of vitamin C were 0.74 (95% CI: 0.65, 0.83, I2 = 0%, n = 4), 0.70 (95% CI: 0.61, 0.81, I2 = 0%, n = 4), 0.76 (95% CI: 0.65, 0.87, I2 = 56%, n = 6), 0.74 (95% CI: 0.66, 0.82, I2 = 0%, n = 5), and 0.72 (95% CI: 0.66, 0.79, I2 = 0%, n = 8). Dietary intake and/or blood concentrations of carotenoids (total, β-carotene, α-carotene, β-cryptoxanthin, lycopene) and α-tocopherol, but not dietary vitamin E, were similarly inversely associated with coronary heart disease, stroke, cardiovascular disease, cancer, and/or all-cause mortality. Conclusions: Higher dietary intake and/or blood concentrations of vitamin C
Matejcic M, Lesueur F, Biessy C, et al., 2018, Circulating plasma phospholipid fatty acids and risk of pancreatic cancer in a large European cohort, International Journal of Cancer, Vol: 143, Pages: 2437-2448, ISSN: 0020-7136
There are both limited and conflicting data on the role of dietary fat and specific fatty acids in the development of pancreatic cancer. In this study, we investigated the association between plasma phospholipid fatty acids and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. The fatty acid composition was measured by gas chromatography in plasma samples collected at recruitment from 375 incident pancreatic cancer cases and 375 matched controls. Associations of specific fatty acids with pancreatic cancer risk were evaluated using multivariable conditional logistic regression models with adjustment for established pancreatic cancer risk factors. Statistically significant inverse associations were found between pancreatic cancer incidence and levels of heptadecanoic acid (ORT3-T1 [odds ratio for highest versus lowest tertile] =0.63; 95%CI[confidence interval]=0.41-0.98; Ptrend =0.036), n-3 polyunsaturated α-linolenic acid (ORT3-T1 =0.60; 95%CI=0.39-0.92; Ptrend =0.02) and docosapentaenoic acid (ORT3-T1 =0.52; 95%CI=0.32-0.85; Ptrend =0.008). Industrial trans-fatty acids were positively associated with pancreatic cancer risk among men (ORT3-T1 =3.00; 95%CI=1.13-7.99; Ptrend =0.029), while conjugated linoleic acids were inversely related to pancreatic cancer among women only (ORT3-T1 =0.37; 95%CI=0.17-0.81; Ptrend =0.008). Among current smokers, the long-chain n-6/n-3 polyunsaturated fatty acids ratio was positively associated with pancreatic cancer risk (ORT3-T1 =3.40; 95%CI=1.39-8.34; Ptrend =0.007). Results were robust to a range of sensitivity analyses. Our findings suggest that higher circulating levels of saturated fatty acids with an odd number of carbon atoms and n-3 polyunsaturated fatty acids may be related to lower risk of pancreatic cancer. The influence of some fatty acids on the development of pancreatic cancer may be sex-specific and modulated by smoking. This article is protected by copyright
Matejcic M, Saunders EJ, Dadaev T, et al., 2018, Germline variation at 8q24 and prostate cancer risk in men of European ancestry, NATURE COMMUNICATIONS, Vol: 9
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Aune D, Mahamat-Saleh Y, Norat T, et al., 2018, Body fatness, diabetes, physical activity and risk of kidney stones: a systematic review and meta-analysis of cohort studies, European Journal of Epidemiology, Vol: 33, Pages: 1033-1047, ISSN: 0393-2990
We conducted a systematic review and meta-analysis to clarify the association between adiposity, diabetes, and physical activity and the risk of kidney stones. PubMed and Embase were searched up to April 22nd 2018 for relevant studies. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random effects models. Thirteen cohort studies were included. The summary relative risk was 1.21 (95% CI 1.12-1.30, I2 = 76%, n = 8) per 5 unit increment in BMI, 1.16 (95% CI 1.12-1.19, I2 = 0%, n = 5) per 10 cm increase in waist circumference, 1.06 (95% CI 1.04-1.08, I2 = 67%, n = 3) per 5 kg increase in weight and 1.12 (95% CI 1.06-1.18, I2 = 86%, n = 3) per 5 kg of weight gain. The summary RR was 1.16 (95% CI 1.03-1.31, I2 = 51%, n = 10) for participants with diabetes compared to participants without diabetes, and 0.93 (95% CI 0.78-1.10, I2 = 80%, n = 4) for high vs. low physical activity. These results suggest a positive association between adiposity and diabetes and the risk of kidney stones, but no association with physical activity.
Schoemaker MJ, Nichols HB, Wright LB, et al., 2018, Association of Body Mass Index and Age With Subsequent Breast Cancer Risk in Premenopausal Women, JAMA ONCOLOGY, Vol: 4, ISSN: 2374-2437
Aune D, Schlesinger S, Neuenschwander M, et al., 2018, Diabetes mellitus, blood glucose and the risk of heart failure: A systematic review and meta-analysis of prospective studies, Nutrition, Metabolism and Cardiovascular Diseases, Vol: 28, Pages: 1081-1091, ISSN: 0939-4753
BACKGROUND AND AIM: The strength of the association between diabetes and risk of heart failure has differed between previous studies and the available studies have not been summarized in a meta-analysis. We therefore quantified the association between diabetes and blood glucose and heart failure in a systematic review and meta-analysis. METHODS AND RESULTS: PubMed and Embase databases were searched up to May 3rd 2018. Prospective studies on diabetes mellitus or blood glucose and heart failure risk were included. A random effects model was used to calculate summary relative risks (RRs) and 95% confidence intervals (CIs). Seventy seven studies were included. Among the population-based prospective studies, the summary RR for individuals with diabetes vs. no diabetes was 2.06 (95% CIs: 1.73-2.46, I2 = 99.8%, n = 30 studies, 401495 cases, 21416780 participants). The summary RR was 1.23 (95% CI: 1.15-1.32, I2 = 78.2%, n = 10, 5344 cases, 91758 participants) per 20 mg/dl increase in blood glucose and there was evidence of a J-shaped association with nadir around 90 mg/dl and increased risk even within the pre-diabetic blood glucose range. Among the patient-based studies the summary RR was 1.69 (95% CI: 1.57-1.81, I2 = 85.5%, pheterogeneity<0.0001) for diabetes vs. no diabetes (n = 41, 100284 cases and >613925 participants) and 1.25 (95% CI: 0.89-1.75, I2 = 95.6%, pheterogeneity<0.0001) per 20 mg/dl increase in blood glucose (1016 cases, 34309 participants, n = 2). In the analyses of diabetes and heart failure there was low or no heterogeneity among the population-based studies that adjusted for alcohol intake and physical activity and among the patient-based studies there was no heterogeneity among studies with ≥10 years follow-up. CONCLUSIONS: These results suggest that individuals with diabetes are at an increased risk of developing heart failure and there is eviden
Scelo G, Muller DC, Riboli E, et al., 2018, KIM-1 as a blood-based marker for early detection of kidney cancer: a prospective nested case-control study, Clinical Cancer Research, Vol: 24, ISSN: 1078-0432
Purpose: Renal cell carcinoma (RCC) has the potential for cure with surgery when diagnosed at an early stage. Kidney injury molecule-1 (KIM-1) has been shown to be elevated in the plasma of RCC patients. We aimed to test whether plasma KIM-1 could represent a means of detecting RCC prior to clinical diagnosis. Experimental Design: KIM-1 concentrations were measured in pre-diagnostic plasma from 190 RCC cases and 190 controls nested within a population-based prospective cohort study. Cases had entered the cohort up to five years before diagnosis, and controls were matched on cases for date of birth, date at blood donation, sex, and country. We applied conditional logistic regression and flexible parametric survival models to evaluate the association between plasma KIM-1 concentrations and RCC risk and survival. Results: The incidence rate ratio (IRR) of RCC for a doubling in KIM-1 concentration was 1.71 (95% confidence interval [CI]: 1.44-2.03, p-value = 4.1x10-23), corresponding to an IRR of 63.3 (95% CI: 16.2-246.9) comparing the 80th to the 20th percentile of the KIM-1 distribution in this sample. Compared with a risk model including known risk factors of RCC (age, sex, country, body mass index and tobacco smoking status), a risk model additionally including KIM-1 substantially improved discrimination between cases and controls (area under the receiver operating characteristic curve of 0.8 compared to 0.7). High plasma KIM-1 concentrations were also associated with poorer survival (p=0.0053). Conclusions: Plasma KIM-1 concentrations could predict RCC incidence up to 5 years prior to diagnosis and were associated with poorer survival.
Gunter MJ, Riboli E, 2018, Obesity and gastrointestinal cancers - where do we go from here?, Nature Reviews Gastroenterology and Hepatology, Vol: 15, Pages: 651-652, ISSN: 1759-5045
Obesity is an established risk factor for gastrointestinal cancers. Interventions that reduce the burden of obesity at both the societal and individual level and targeted interventions among those at higher risk of cancer should be developed, supported by advances in understanding of the biology that underpins the obesity–cancer link.
Sarink D, Schock H, Johnson T, et al., 2018, Receptor activator of nuclear factor kB ligand, osteoprotegerin, and risk of death following a breast cancer diagnosis: results from the EPIC cohort, BMC Cancer, Vol: 18, ISSN: 1471-2407
BackgroundReceptor activator of nuclear factor kappa-B (RANK)-signaling is involved in tumor growth and spread in experimental models. Binding of RANK ligand (RANKL) to RANK activates signaling, which is inhibited by osteoprotegerin (OPG). We have previously shown that circulating soluble RANKL (sRANKL) and OPG are associated with breast cancer risk. Here we extend these findings to provide the first data on pre-diagnosis concentrations of sRANKL and OPG and risk of breast cancer-specific and overall mortality after a breast cancer diagnosis.MethodsTwo thousand six pre- and postmenopausal women with incident invasive breast cancer (1620 (81%) with ER+ disease) participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort were followed-up for mortality. Pre-diagnosis concentrations of sRANKL and OPG were quantified in baseline serum samples using an enzyme-linked immunosorbent assay and electrochemiluminescent assay, respectively. Hazard ratios (HRs) and 95% confidence intervals (CIs) for breast cancer-specific and overall mortality were calculated using Cox proportional hazards regression models.ResultsEspecially in women with ER+ disease, higher circulating OPG concentrations were associated with higher risk of breast cancer-specific (quintile 5 vs 1 HR 1.77 [CI 1.03, 3.04]; ptrend 0.10) and overall mortality (q5 vs 1 HR 1.39 [CI 0.94, 2.05]; ptrend 0.02). sRANKL and the sRANKL/OPG ratio were not associated with mortality following a breast cancer diagnosis.ConclusionsHigh pre-diagnosis endogenous concentrations of OPG, the decoy receptor for RANKL, were associated with increased risk of death after a breast cancer diagnosis, especially in those with ER+ disease. These results need to be confirmed in well-characterized patient cohorts.
Guida F, Sun N, Bantis L, et al., 2018, Assessment of lung cancer risk based on a biomarker panel of circulating proteins, JAMA Oncology, Vol: 4, ISSN: 2374-2445
Importance: There is an urgent need to improve lung cancer risk assessment as current screening criteria miss a large proportion of cases.Objective: To determine if a panel of selected circulating protein biomarkers can contribute to lung cancer risk assessment and outperform current US screening criteria.Design, Setting and Participants: Pre-diagnostic samples from ever-smoking cases diagnosed within one year of blood collection and smoking-matched controls from the Carotene and Retinol Efficacy Trial (CARET) cohort were used to develop a biomarker risk-score based on 4 proteins (CA125, CEA, CYFRA 21-1 and Pro-SFTPB). The biomarker score was subsequently validated blindly using absolute risk-estimates in ever-smoking cases diagnosed within one year of blood collection and matched controls from two large European population-based cohorts; the European Prospective Investigation into Cancer and nutrition (EPIC) study and the Northern Sweden Health and Disease Study (NSHDS). Main Outcome and Measures: Model validity in discriminating between future lung cancer cases and controls. Discrimination estimates were weighted to reflect the background populations of EPIC and NSHDS validation studies (area under receiver-operating characteristics curve [AUC], sensitivity and specificity).Results: In the validation study, an integrated risk-prediction model combining smoking exposure with the biomarker score yielded an AUC of 0.83 (95% CI: 0.76-0.90) compared to 0.73 (95% CI: 0.64-0.82) for a model based on smoking exposure alone (P=0.003 for difference in AUC). At an overall specificity of 0.83 based on the USPSTF screening criteria, the sensitivity of the integrated risk-prediction model (biomarker) model was 0.63 compared to 0.43 for the smoking model. Conversely, at an overall sensitivity of 0.42 (USPSTF), the integrated risk-prediction model yielded a specificity of 0.95 compared to 0.86 for the smoking model. Conclusions and Relevance: This study provided a proof-of-prin
Aune D, Schlesinger S, Norat T, et al., 2018, Tobacco smoking and the risk of abdominal aortic aneurysm: A systematic review and meta-analysis of prospective studies, Scientific Reports, Vol: 8, ISSN: 2045-2322
Several studies have found that smoking increases the risk of abdominal aortic aneurysm, however, the strength of the association has differed between studies and data from cohort studies have not yet been summarized. A systematic review and meta-analysis was therefore conducted to clarify this association. We searched PubMed and Embase databases up to May 2nd 2018. A random effects model was used to estimate summary relative risks (RRs) and 95% confidence intervals (CIs). Twenty three prospective studies were included. Comparing current, former and ever smokers with never smokers the summary RRs were 4.87 (95% CI: 3.93–6.02, I2 = 92%, n = 20), 2.10 (95% CI: 1.76–2.50, I2 = 71%, n = 15) and 3.28 (95% CI: 2.60–4.15, I2 = 96%, n = 18), respectively. The summary RR was 1.87 (95% CI: 1.45–2.40, I2 = 97%) per 10 cigarettes per day, 1.78 (95% CI: 1.54–2.06, I2 = 83%) per 10 pack-years was and 0.45 (95% CI: 0.32–0.63, I2 = 92.3%) per 10 years of smoking cessation. There was evidence of nonlinearity for cigarettes per day and pack-years (pnonlinearity < 0.0001 and pnonlinearity = 0.02, respectively), but not for smoking cessation, pnonlinearity = 0.85. Among smokers who quit, the RR was similar to that of never smokers by 25 years of smoking cessation. These findings confirm a strong association between smoking and the risk of developing abdominal aortic aneurysms.
Cairat M, Fournier A, Murphy N, et al., 2018, Nonsteroidal anti-inflammatory drug use and breast cancer risk in a European prospective cohort study, International Journal of Cancer, Vol: 143, Pages: 1688-1695, ISSN: 0020-7136
Experimental studies have shown a protective effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on breast cancer development. However, results from epidemiological cohort studies are less consistent. Our objective was to assess the association between NSAID use and breast cancer risk within the European Prospective Investigation into Cancer and Nutrition (EPIC). EPIC is a prospective cohort study initiated in 1992 in 10 European countries. Self-reported information on NSAID use at baseline has been collected in five EPIC countries. Multivariable Cox regression models were used to estimate hazard ratios for the association of NSAID use with breast cancer incidence with adjustment for potential confounders. We also assessed effect modification by breast cancer risk factors and examined the associations within specific breast cancer subtypes. Among the 140,981 women included in the analysis, 7% were regularly using NSAIDs at baseline. During a median follow-up time period of 13 years, 7,379 incident breast cancer cases were diagnosed (816 in situ and 6,563 invasive). There were no statistically significant associations between NSAID use and breast cancer risk, overall and by subtypes. However, a statistically significant interaction was observed for invasive cases between NSAID use and ever use of menopausal hormonal therapy (MHT) among postmenopausal women [MHT users: HRNSAID use =0.84 (0.73 - 0.96); non MHT users: HRNSAID use = 1.08 (0.93 - 1.25); Pinteraction = 0.05]. Our results indicate potential effect modification of MHT use on the association between use of NSAIDs and breast cancer risk which deserves in-depth investigation in studies with accurate data on both NSAID and MHT use.
Deschasaux M, Huybrechts I, Murphy N, et al., 2018, Nutritional quality of food as represented by the FSAm-NPS nutrient profiling system underlying the Nutri-Score label and cancer risk in Europe: results from the EPIC prospective cohort study, PLoS Medicine, Vol: 15, ISSN: 1549-1277
BackgroundHelping consumers make healthier food choices is a key issue for the prevention of cancer and other diseases. In many countries, political authorities are considering the implementation of a simplified labelling system to reflect the nutritional quality of food products. The Nutri-Score, a five-colour nutrition label, is derived from the Nutrient Profiling System of the British Food Standards Agency (modified version) (FSAm-NPS). How the consumption of foods with high/low FSAm-NPS relates to cancer risk has been studied in national/regional cohorts but has not been characterized in diverse European populations.Methods and findingsThis prospective analysis included 471,495 adults from the European Prospective Investigation into Cancer and Nutrition (EPIC, 1992–2014, median follow-up: 15.3 y), among whom there were 49,794 incident cancer cases (main locations: breast, n = 12,063; prostate, n = 6,745; colon-rectum, n = 5,806). Usual food intakes were assessed with standardized country-specific diet assessment methods. The FSAm-NPS was calculated for each food/beverage using their 100-g content in energy, sugar, saturated fatty acid, sodium, fibres, proteins, and fruits/vegetables/legumes/nuts. The FSAm-NPS scores of all food items usually consumed by a participant were averaged to obtain the individual FSAm-NPS Dietary Index (DI) scores. Multi-adjusted Cox proportional hazards models were computed. A higher FSAm-NPS DI score, reflecting a lower nutritional quality of the food consumed, was associated with a higher risk of total cancer (HRQ5 versus Q1 = 1.07; 95% CI 1.03–1.10, P-trend < 0.001). Absolute cancer rates in those with high and low (quintiles 5 and 1) FSAm-NPS DI scores were 81.4 and 69.5 cases/10,000 person-years, respectively. Higher FSAm-NPS DI scores were specifically associated with higher risks of cancers of the colon-rectum, upper aerodigestive tract and stomach, lung for men, and liver and postmenopausal breast for women (all
de Pablo P, Romaguera D, Panico S, et al., 2018, Lower Educational level is associated with Higher risk of developing rheumatoid arthritis, Arthritis and Rheumatology, Vol: 70, Pages: 1905-1905, ISSN: 2326-5205
Forman D, Bauld L, Bonanni B, et al., 2018, Time for a European initiative for research to prevent cancer: A manifesto for Cancer Prevention Europe (CPE), JOURNAL OF CANCER POLICY, Vol: 17, Pages: 15-23, ISSN: 2213-5383
Aune D, Schlesinger S, Norat T, et al., 2018, Tobacco smoking and the risk of atrial fibrillation: a systematic review and meta-analysis of prospective studies, European Journal of Preventive Cardiology, Vol: 25, Pages: 1437-1451, ISSN: 2047-4873
Background Epidemiological studies on smoking and atrial fibrillation have been inconsistent, with some studies showing a positive association while others have found no association. It is also unclear whether there is a dose-response relationship between the number of cigarettes smoked or pack-years and the risk of atrial fibrillation. We conducted a systematic review and meta-analysis to clarify the association. Design Systematic review and meta-analysis. Methods We searched the PubMed and Embase databases for studies of smoking and atrial fibrillation up to 20 July 2017. Prospective studies and nested case-control studies within cohort studies reporting adjusted relative risk estimates and 95% confidence intervals (CIs) of atrial fibrillation associated with smoking were included. Summary relative risks (95% CIs) were estimated using a random effects model. Results Twenty nine prospective studies (22 publications) were included. The summary relative risk was 1.32 (95% CI 1.12-1.56, I2 = 84%, n = 11 studies) for current smokers, 1.09 (95% CI 1.00-1.18, I2 = 33%, n = 9) for former smokers and 1.21 (95% CI 1.12-1.31, I2 = 80%, n = 14) for ever smokers compared to never smokers. Comparing current versus non-current smokers the summary relative risk was 1.33 (95% CI 1.14-1.56, I2 = 78%, n = 10). The summary relative risk was 1.14 (95% CI 1.10-1.20, I2 = 0%, n = 3) per 10 cigarettes per day and 1.16 (95% CI 1.09-1.25, I2 = 49%, n = 2) per 10 pack-years and there was no evidence of a non-linear association for cigarettes per day, Pnon-linearity = 0.17. Conclusions The current meta-analysis suggests that smoking is associated with an increased risk of atrial fibrillation in a dose-dependent matter, but the association is weaker among former smokers compared to current smokers.
Naudin S, Li K, Jaouen T, et al., 2018, Lifetime and baseline alcohol intakes and risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition study, International Journal of Cancer, Vol: 143, Pages: 801-812, ISSN: 0020-7136
Recent evidence suggested a weak relationship between alcohol consumption and pancreatic cancer (PC) risk. In this study, the association between lifetime and baseline alcohol intakes and the risk of PC was evaluated, including the type of alcoholic beverages and potential interaction with smoking. Within the European Prospective Investigation into Cancer and Nutrition (EPIC) study, 1,283 incident PC (57% women) were diagnosed from 476,106 cancer-free participants, followed up for 14 years. Amounts of lifetime and baseline alcohol were estimated through lifestyle and dietary questionnaires, respectively. Cox proportional hazard models with age as primary time variable were used to estimate PC hazard ratios (HR) and their 95% confidence interval (CI). Alcohol intake was positively associated with PC risk in men. Associations were mainly driven by extreme alcohol levels, with HRs comparing heavy drinkers (>60 g/day) to the reference category (0.1-4.9 g/day) equal to 1.77 (95% CI: 1.06, 2.95) and 1.63 (95% CI: 1.16, 2.29) for lifetime and baseline alcohol, respectively. Baseline alcohol intakes from beer (>40 g/day) and spirits/liquors (>10 g/day) showed HRs equal to 1.58 (95% CI: 1.07, 2.34) and 1.41 (95% CI: 1.03, 1.94), respectively, compared to the reference category (0.1-2.9 g/day). In women, HR estimates did not reach statistically significance. The alcohol and PC risk association was not modified by smoking status. Findings from a large prospective study suggest that baseline and lifetime alcohol intakes were positively associated with PC risk, with more apparent risk estimates for beer and spirits/liquors than wine intake. This article is protected by copyright. All rights reserved.
Wark PA, Hardie LJ, Frost GS, et al., 2018, Validity of an online 24-h recall tool (myfood24) for dietary assessment in population studies: comparison with biomarkers and standard interviews, BMC Medicine, Vol: 16, ISSN: 1741-7015
BackgroundOnline dietary assessment tools can reduce administrative costs and facilitate repeated dietary assessment during follow-up in large-scale studies. However, information on bias due to measurement error of such tools is limited. We developed an online 24-h recall (myfood24) and compared its performance with a traditional interviewer-administered multiple-pass 24-h recall, assessing both against biomarkers.MethodsMetabolically stable adults were recruited and completed the new online dietary recall, an interviewer-based multiple pass recall and a suite of reference measures. Longer-term dietary intake was estimated from up to 3 × 24-h recalls taken 2 weeks apart. Estimated intakes of protein, potassium and sodium were compared with urinary biomarker concentrations. Estimated total sugar intake was compared with a predictive biomarker and estimated energy intake compared with energy expenditure measured by accelerometry and calorimetry. Nutrient intakes were also compared to those derived from an interviewer-administered multiple-pass 24-h recall.ResultsBiomarker samples were received from 212 participants on at least one occasion. Both self-reported dietary assessment tools led to attenuation compared to biomarkers. The online tools resulted in attenuation factors of around 0.2–0.3 and partial correlation coefficients, reflecting ranking intakes, of approximately 0.3–0.4. This was broadly similar to the more administratively burdensome interviewer-based tool. Other nutrient estimates derived from myfood24 were around 10–20% lower than those from the interviewer-based tool, with wide limits of agreement. Intraclass correlation coefficients were approximately 0.4–0.5, indicating consistent moderate agreement.ConclusionsOur findings show that, whilst results from both measures of self-reported diet are attenuated compared to biomarker measures, the myfood24 online 24-h recall is comparable to the more time-consuming a
Wark P, Frost G, Elliott P, et al., 2018, An online 24-hour recall tool (myfood24) is valid for dietary assessment in population studies: comparison with biomarkers and standard interviews., BMC Medicine, Vol: 16, ISSN: 1741-7015
BackgroundOnline dietary assessment tools can reduce administrative costs and facilitate repeated dietary assessment during follow-up in large-scale studies. However, information on bias due to measurement error of such tools is limited. We developed an online 24-h recall (myfood24) and compared its performance with a traditional interviewer-administered multiple-pass 24-h recall, assessing both against biomarkers.MethodsMetabolically stable adults were recruited and completed the new online dietary recall, an interviewer-based multiple pass recall and a suite of reference measures. Longer-term dietary intake was estimated from up to 3 × 24-h recalls taken 2 weeks apart. Estimated intakes of protein, potassium and sodium were compared with urinary biomarker concentrations. Estimated total sugar intake was compared with a predictive biomarker and estimated energy intake compared with energy expenditure measured by accelerometry and calorimetry. Nutrient intakes were also compared to those derived from an interviewer-administered multiple-pass 24-h recall.ResultsBiomarker samples were received from 212 participants on at least one occasion. Both self-reported dietary assessment tools led to attenuation compared to biomarkers. The online tools resulted in attenuation factors of around 0.2–0.3 and partial correlation coefficients, reflecting ranking intakes, of approximately 0.3–0.4. This was broadly similar to the more administratively burdensome interviewer-based tool. Other nutrient estimates derived from myfood24 were around 10–20% lower than those from the interviewer-based tool, with wide limits of agreement. Intraclass correlation coefficients were approximately 0.4–0.5, indicating consistent moderate agreement.ConclusionsOur findings show that, whilst results from both measures of self-reported diet are attenuated compared to biomarker measures, the myfood24 online 24-h recall is comparable to the more time-consuming a
Aune D, Schlesinger S, Norat T, et al., 2018, Body mass index, abdominal fatness, and the risk of sudden cardiac death: a systematic review and dose-response meta-analysis of prospective studies, European Journal of Epidemiology, Vol: 33, Pages: 711-722, ISSN: 0393-2990
Although overweight and obesity are established risk factors for some types of heart disease including ischemic heart disease, heart failure and atrial fibrillation, less is known about the association between adiposity and sudden cardiac death. We conducted a systematic review and meta-analysis of prospective studies to clarify the association between adiposity and risk of sudden cardiac death. PubMed and Embase databases were searched up to July 20th 2017. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random effects models. The summary RR was 1.16 (95% CI 1.05-1.28, I2 = 68%, n = 14) per 5 unit increment in BMI, and 1.82 (95% CI 1.61-2.07, I2 = 0%, n = 3) per 0.1 unit increase in waist-to-hip ratio, and 1.03 (95% CI 0.93-1.15, I2 = 0%, n = 2) per 10 cm increase in waist circumference. The heterogeneity in the analysis of BMI and sudden cardiac death persisted across most subgroup analyses. The association was stronger among studies with longer follow-up compared to short follow-up and was observed in the European and American studies, but not in the Asian studies. There was a J-shaped association between BMI and sudden cardiac death and the lowest risk was observed in the normal weight range, however, the increased risk with a low BMI was attenuated among studies with a longer duration of follow-up. This meta-analysis suggest an increased risk of sudden cardiac death with increasing BMI and waist-to-hip ratio, however, further studies with stratification for smoking status are needed of waist circumference, weight changes and adiposity at younger ages.
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