scholarly journals Depression and prostate cancer risk: A Mendelian randomization study

2020 ◽  
Vol 9 (23) ◽  
pp. 9160-9167
Author(s):  
Xiong Chen ◽  
Jianqiu Kong ◽  
Xiayao Diao ◽  
Jiahao Cai ◽  
Junjiong Zheng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Mendelian Randomization ◽  
Prostate Cancer Risk

scholarly journals Circulating Selenium and Prostate Cancer Risk: A Mendelian Randomization Analysis

2018 ◽  
Vol 110 (9) ◽  
pp. 1035-1038 ◽  
Author(s):  
James Yarmolinsky ◽  
Carolina Bonilla ◽  
Philip C Haycock ◽  
Ryan J Q Langdon ◽  
Luca A Lotta ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Mendelian Randomization ◽  
Prostate Cancer Risk ◽  
Mendelian Randomization Analysis ◽  
Randomization Analysis

scholarly journals Appraising causal relationships of dietary, nutritional and physical-activity exposures with overall and aggressive prostate cancer: two-sample Mendelian-randomization study based on 79 148 prostate-cancer cases and 61 106 controls

2019 ◽  
Vol 49 (2) ◽  
pp. 587-596 ◽  
Author(s):  
Nabila Kazmi ◽  
Philip Haycock ◽  
Konstantinos Tsilidis ◽  
Brigid M Lynch ◽  
Therese Truong ◽  
...  
Keyword(s):  
Physical Activity ◽  
Prostate Cancer ◽  
Risk Factors ◽  
Cancer Risk ◽  
Serum Iron ◽  
Mendelian Randomization ◽  
Prostate Cancer Risk ◽  
Uk Biobank ◽  
Monounsaturated Fat ◽  
Aggressive Prostate Cancer

Abstract Background Prostate cancer is the second most common male cancer worldwide, but there is substantial geographical variation, suggesting a potential role for modifiable risk factors in prostate carcinogenesis. Methods We identified previously reported prostate cancer risk factors from the World Cancer Research Fund (WCRF)’s systematic appraisal of the global evidence (2018). We assessed whether each identified risk factor was causally associated with risk of overall (79 148 cases and 61 106 controls) or aggressive (15 167 cases and 58 308 controls) prostate cancer using Mendelian randomization (MR) based on genome-wide association-study summary statistics from the PRACTICAL and GAME-ON/ELLIPSE consortia. We assessed evidence for replication in UK Biobank (7844 prostate-cancer cases and 204 001 controls). Results WCRF identified 57 potential risk factors, of which 22 could be instrumented for MR analyses using single nucleotide polymorphisms. For overall prostate cancer, we identified evidence compatible with causality for the following risk factors (odds ratio [OR] per standard deviation increase; 95% confidence interval): accelerometer-measured physical activity, OR = 0.49 (0.33–0.72; P = 0.0003); serum iron, OR = 0.92 (0.86–0.98; P = 0.007); body mass index (BMI), OR = 0.90 (0.84–0.97; P = 0.003); and monounsaturated fat, OR = 1.11 (1.02–1.20; P = 0.02). Findings in our replication analyses in UK Biobank were compatible with our main analyses (albeit with wide confidence intervals). In MR analysis, height was positively associated with aggressive-prostate-cancer risk: OR = 1.07 (1.01–1.15; P = 0.03). Conclusions The results for physical activity, serum iron, BMI, monounsaturated fat and height are compatible with causality for prostate cancer. The results suggest that interventions aimed at increasing physical activity may reduce prostate-cancer risk, although interventions to change other risk factors may have negative consequences on other diseases.

scholarly journals Mendelian randomization does not support serum calcium in prostate cancer risk

2018 ◽  
Author(s):  
James Yarmolinsky ◽  
Katie Berryman ◽  
Ryan Langdon ◽  
Carolina Bonilla ◽  
George Davey Smith ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Causal Inference ◽  
Serum Calcium ◽  
Observational Studies ◽  
Advanced Prostate Cancer ◽  
Mendelian Randomization ◽  
Prostate Cancer Risk ◽  
A Genome ◽  
Increased Risk

AbstractBackground: Observational studies suggest that dietary and serum calcium are risk factors for prostate cancer. However, such studies suffer from residual confounding (due to unmeasured or imprecisely measured confounders), undermining causal inference. Mendelian randomization uses randomly assigned (hence unconfounded and pre-disease onset) germline genetic variation to proxy for phenotypes and strengthen causal inference in observational studies.Objective: We tested the hypothesis that serum calcium is associated with an increased risk of overall and advanced prostate cancer.Design: A genetic instrument was constructed using 5 single nucleotide polymorphisms robustly associated with serum calcium in a genome-wide association study (N ≤ 61,079). This instrument was then used to test the effect of a 0.5 mg/dL increase (1 standard deviation, SD) in serum calcium on risk of prostate cancer in 72,729 men in the PRACTICAL (Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome) Consortium (44,825 cases, 27,904 controls) and risk of advanced prostate cancer in 33,498 men (6,263 cases, 27,235 controls).Results: We found weak evidence for a protective effect of serum calcium on prostate cancer risk (odds ratio [OR] per 0.5 mg/dL increase in calcium: 0.83, 95% CI: 0.63-1.08; P=0.12). We did not find strong evidence for an effect of serum calcium on advanced prostate cancer (OR per 0.5 mg/dL increase in calcium: 0.98, 95% CI: 0.57-1.70; P=0.93).Conclusions: Our Mendelian randomization analysis does not support the hypothesis that serum calcium increases risk of overall or advanced prostate cancer.

scholarly journals Appraising causal relationships of dietary, nutritional and physical-activity exposures with overall and aggressive prostate cancer: two-sample Mendelian randomization study based on 79,148 prostate cancer cases and 61,106 controls

2019 ◽  
Author(s):  
Nabila Kazmi ◽  
Philip Haycock ◽  
Konstantinos Tsilidis ◽  
Brigid M. Lynch ◽  
Therese Truong ◽  
...  
Keyword(s):  
Physical Activity ◽  
Prostate Cancer ◽  
Risk Factors ◽  
Cancer Research ◽  
Cancer Risk ◽  
Serum Iron ◽  
Mendelian Randomization ◽  
Prostate Cancer Risk ◽  
Uk Biobank ◽  
Unsaturated Fat

SummaryBackgroundProstate cancer is the second most common male cancer worldwide, but there is substantial geographical variation suggesting a potential role for modifiable risk factors in prostate carcinogenesis.MethodsWe identified previously reported prostate cancer risk factors from the World Cancer Research Fund’s (WCRF) systematic appraisal of the global evidence (2018). We assessed whether each identified risk factor was causally associated with risk of overall (79,148 cases and 61,106 controls) or aggressive (15,167 cases and 58,308 controls) prostate cancer using Mendelian randomization (MR) based on genome wide association study (GWAS) summary statistics from the PRACTICAL and GAME-ON/ELLIPSE consortia. We assessed evidence for replication in UK Biobank (7,844 prostate cancer cases and 204,001 controls).FindingsWCRF identified 57 potential risk factors, of which 22 could be instrumented for MR analyses using single nucleotide polymorphisms (SNPs). In MR analyses for overall prostate cancer, we identified evidence compatible with causality for the following risk factors (odds ratio [OR] per standard deviation increase; 95% confidence interval): accelerometer-measured physical-activity, OR=0.49 (0.33-0.72; p=0.0003); serum iron, OR=0.92 (0.86-0.98; p=0.007); body mass index (BMI), OR=0.90 (0.84-0.97; p=0.003); and mono-unsaturated fat, OR=1.11 (1.02-1.20; p=0.02). Findings in our replication analyses in UK Biobank were compatible with our main analyses (albeit with wide confidence intervals). In MR analysis, height was positively associated with aggressive prostate cancer risk: OR=1.07 (1.01-1.15; p=0.03).InterpretationThe results for physical-activity, serum iron, BMI, mono-unsaturated fat and height are compatible with causality for prostate cancer but more research is needed to rule out violations of MR assumptions for some risk factors. The results suggest that interventions aimed at increasing physical activity may reduce prostate cancer risk, but the direction of effects of BMI, and iron are at odds with their effects on other diseases, so the overall public health impact of intervening on these need to be considered.FundingWorld Cancer Research Fund International (2015/1421), Cancer Research UK program grant (C18281/A19169), National Institute for Health Research, Bristol Biomedical Research Centre, and Victorian Cancer Agency (MCRF18005).

scholarly journals Pubertal development and prostate cancer risk: Mendelian randomization study in a population-based cohort

BMC Medicine ◽  
2016 ◽  
Vol 14 (1) ◽  
Author(s):  
Carolina Bonilla ◽  
◽  
Sarah J. Lewis ◽  
Richard M. Martin ◽  
Jenny L. Donovan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Mendelian Randomization ◽  
Pubertal Development ◽  
Prostate Cancer Risk ◽  
Population Based

Genetically predicted levels of circulating cytokines and prostate cancer risk: A Mendelian randomization study

2020 ◽  
Vol 147 (9) ◽  
pp. 2469-2478
Author(s):  
Xiaohui Sun ◽  
Ding Ye ◽  
Lingbin Du ◽  
Yu Qian ◽  
Xia Jiang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Mendelian Randomization ◽  
Prostate Cancer Risk ◽  
Circulating Cytokines

scholarly journals Coffee Consumption and Prostate Cancer Risk: Results from National Health and Nutrition Examination Survey 1999–2010 and Mendelian Randomization Analyses

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2317
Author(s):  
Menghua Wang ◽  
Zhongyu Jian ◽  
Chi Yuan ◽  
Xi Jin ◽  
Hong Li ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Observational Study ◽  
Mendelian Randomization ◽  
Prostate Cancer Risk ◽  
Nutrition Examination Survey ◽  
Causal Association ◽  
Coffee Intake ◽  
Health And Nutrition ◽  
Genetic Instruments

The aim of this study was to examine the association between coffee and prostate cancer. Firstly, we conducted an observational study using data from National Health and Nutrition Examination Survey (NHANES) 1999–2010. Coffee intake was derived from 24 h dietary recalls. Weighted multivariable-adjusted logistic regression was applied to evaluate the association. Then, we performed Mendelian randomization (MR) to explore the possible causal effect of coffee on prostate cancer risk. Primary and secondary genetic instruments were obtained from genome-wide association studies among 375,833 and 91,462 individuals separately. Prostate cancer summary statistics were extracted from Prostate Cancer Association Group to Investigate Cancer-Associated Alterations in the Genome (PRACTICAL) (79,194 cases and 61,112 controls) and FinnGen project (4754 cases and 63,465 controls). Inverse variance weighted (IVW) was the primary analytical method. Through selection, we enrolled 8336 individuals (weighted number = 58,796,070) for our observational study in NHANES. Results suggested that there was no association between coffee and prostate cancer. MR analyses with primary genetic instruments also did not support a causal association between coffee intake and prostate cancer risk, whether using summary data from PRACTICAL (IVW: OR 1.001, 95% CI 0.997–1.005) or FinnGen (IVW: OR 1.005, 95% CI 0.998–1.012). Similar results were observed when using secondary genetic instruments. Therefore, our study did not support a causal association between coffee intake and prostate cancer risk. Further studies with a larger sample size are needed to examine if an association exists by different coffee bean types, roasting procedures, and brewing methods.

scholarly journals Circulating selenium and prostate cancer risk: a Mendelian randomization analysis

2017 ◽  
Author(s):  
James Yarmolinsky ◽  
Carolina Bonilla ◽  
Philip C Haycock ◽  
Ryan JQ Langdon ◽  
Luca A Lotta ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Type 2 Diabetes ◽  
Cancer Risk ◽  
Mendelian Randomization ◽  
Prostate Cancer Risk ◽  
Selenium Supplementation ◽  
High Grade ◽  
Mendelian Randomization Analysis ◽  
Randomization Analysis

AbstractIn the Selenium and Vitamin E Cancer Prevention Trial (SELECT), selenium supplementation (causing a median 114 μg/L increase in circulating selenium) did not lower overall prostate cancer risk, but increased risk of high-grade prostate cancer and type 2 diabetes. Mendelian randomization analysis uses genetic variants to proxy modifiable risk factors and can strengthen causal inference in observational studies. We constructed a genetic risk score comprising eleven single-nucleotide polymorphisms robustly (P<5x10−8) associated with circulating selenium in genome-wide association studies. In a Mendelian randomization analysis of 72,729 men in the PRACTICAL Consortium (44,825 cases, 27,904 controls), 114 μg/L higher genetically-elevated circulating selenium was not associated with prostate cancer (OR: 1.01; 95% CI: 0.89-1.13). Concordant with findings from SELECT, selenium was weakly associated with advanced (including high-grade) prostate cancer (OR: 1.21; 95% CI: 0.98-1.49) and type 2 diabetes (OR: 1.18; 95% CI: 0.97-1.43; in a type 2 diabetes GWAS meta-analysis with up to 49,266 cases, 249,906 controls). Mendelian randomization mirrored the outcome of selenium supplementation in SELECT and may offer an approach for the prioritization of interventions for follow-up in large-scale randomized controlled trials.

scholarly journals Mendelian randomization does not support serum calcium in prostate cancer risk

2018 ◽  
Vol 29 (11) ◽  
pp. 1073-1080
Author(s):  
James Yarmolinsky ◽  
◽  
Katie Berryman ◽  
Ryan Langdon ◽  
Carolina Bonilla ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Serum Calcium ◽  
Mendelian Randomization ◽  
Prostate Cancer Risk
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