Investigating the possible causal role of coffee consumption with prostate cancer risk and progression using Mendelian randomization analysis

Amy E Taylor; Richard M Martin; Milan S Geybels; Janet L Stanford; Irene Shui; Rosalind Eeles; Doug Easton; Zsofia Kote-Jarai; Ali Amin Al Olama; Sara Benlloch; Kenneth Muir; Graham G Giles; Fredrik Wiklund; Henrik Gronberg; Christopher A Haiman; Johanna Schleutker; Børge G Nordestgaard; Ruth C Travis; David Neal; Nora Pashayan; Kay-Tee Khaw; William Blot; Stephen Thibodeau; Christiane Maier; Adam S Kibel; Cezary Cybulski; Lisa Cannon-Albright; Hermann Brenner; Jong Park; Radka Kaneva; Jyotsna Batra; Manuel R Teixeira; Hardev Pandha; PRACTICAL consortium; Jenny Donovan; Marcus R Munafò

doi:10.1002/ijc.30462

Investigating the possible causal role of coffee consumption with prostate cancer risk and progression using Mendelian randomization analysis

Amy E Taylor, Richard M Martin, Milan S Geybels, Janet L Stanford, Irene Shui, Rosalind Eeles, Doug Easton, Zsofia Kote-Jarai, Ali Amin Al Olama, Sara Benlloch, Kenneth Muir, Graham G Giles, Fredrik Wiklund, Henrik Gronberg, Christopher A Haiman, Johanna Schleutker, Børge G Nordestgaard, Ruth C Travis, David Neal, Nora PashayanKay-Tee Khaw, William Blot, Stephen Thibodeau, Christiane Maier, Adam S Kibel, Cezary Cybulski, Lisa Cannon-Albright, Hermann Brenner, Jong Park, Radka Kaneva, Jyotsna Batra, Manuel R Teixeira, Hardev Pandha, PRACTICAL consortium, Jenny Donovan, Marcus R Munafò

Institut for Klinisk Medicin

11 Citationer (Scopus)

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Abstract

Coffee consumption has been shown in some studies to be associated with lower risk of prostate cancer. However, it is unclear if this association is causal or due to confounding or reverse causality. We conducted a Mendelian randomisation analysis to investigate the causal effects of coffee consumption on prostate cancer risk and progression. We used two genetic variants robustly associated with caffeine intake (rs4410790 and rs2472297) as proxies for coffee consumption in a sample of 46,687 men of European ancestry from 25 studies in the PRACTICAL consortium. Associations between genetic variants and prostate cancer case status, stage and grade were assessed by logistic regression and with all-cause and prostate cancer-specific mortality using Cox proportional hazards regression. There was no clear evidence that a genetic risk score combining rs4410790 and rs2472297 was associated with prostate cancer risk (OR per additional coffee increasing allele: 1.01, 95% CI: 0.98,1.03) or having high-grade compared to low-grade disease (OR: 1.01, 95% CI: 0.97,1.04). There was some evidence that the genetic risk score was associated with higher odds of having nonlocalised compared to localised stage disease (OR: 1.03, 95% CI: 1.01, 1.06). Amongst men with prostate cancer, there was no clear association between the genetic risk score and all-cause mortality (HR: 1.00, 95% CI: 0.97,1.04) or prostate cancer-specific mortality (HR: 1.03, 95% CI: 0.98,1.08). These results, which should have less bias from confounding than observational estimates, are not consistent with a substantial effect of coffee consumption on reducing prostate cancer incidence or progression.

Originalsprog	Engelsk
Tidsskrift	International Journal of Cancer
Vol/bind	140
Udgave nummer	2
Sider (fra-til)	322-328
Antal sider	7
ISSN	0898-6924
DOI	https://doi.org/10.1002/ijc.30462
Status	Udgivet - 15 jan. 2017

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10.1002/ijc.30462Licens: CC BY

Investigating the possible causal role of coffee consumption with prostate cancer risk and progression using Mendelian randomization analysisForlagets udgivne version, 394 KBLicens: CC BY

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Taylor, A. E., Martin, R. M., Geybels, M. S., Stanford, J. L., Shui, I., Eeles, R., Easton, D., Kote-Jarai, Z., Amin Al Olama, A., Benlloch, S., Muir, K., Giles, G. G., Wiklund, F., Gronberg, H., Haiman, C. A., Schleutker, J., Nordestgaard, B. G., Travis, R. C., Neal, D., ... Munafò, M. R. (2017). Investigating the possible causal role of coffee consumption with prostate cancer risk and progression using Mendelian randomization analysis. International Journal of Cancer, 140(2), 322-328. https://doi.org/10.1002/ijc.30462

Taylor, AE, Martin, RM, Geybels, MS, Stanford, JL, Shui, I, Eeles, R, Easton, D, Kote-Jarai, Z, Amin Al Olama, A, Benlloch, S, Muir, K, Giles, GG, Wiklund, F, Gronberg, H, Haiman, CA, Schleutker, J, Nordestgaard, BG, Travis, RC, Neal, D, Pashayan, N, Khaw, K-T, Blot, W, Thibodeau, S, Maier, C, Kibel, AS, Cybulski, C, Cannon-Albright, L, Brenner, H, Park, J, Kaneva, R, Batra, J, Teixeira, MR, Pandha, H, PRACTICAL consortium, Donovan, J & Munafò, MR 2017, 'Investigating the possible causal role of coffee consumption with prostate cancer risk and progression using Mendelian randomization analysis', International Journal of Cancer, bind 140, nr. 2, s. 322-328. https://doi.org/10.1002/ijc.30462

@article{ecf226a57e8b41a391d43e2dfc41fdf9,

title = "Investigating the possible causal role of coffee consumption with prostate cancer risk and progression using Mendelian randomization analysis",

abstract = "Coffee consumption has been shown in some studies to be associated with lower risk of prostate cancer. However, it is unclear if this association is causal or due to confounding or reverse causality. We conducted a Mendelian randomisation analysis to investigate the causal effects of coffee consumption on prostate cancer risk and progression. We used two genetic variants robustly associated with caffeine intake (rs4410790 and rs2472297) as proxies for coffee consumption in a sample of 46,687 men of European ancestry from 25 studies in the PRACTICAL consortium. Associations between genetic variants and prostate cancer case status, stage and grade were assessed by logistic regression and with all-cause and prostate cancer-specific mortality using Cox proportional hazards regression. There was no clear evidence that a genetic risk score combining rs4410790 and rs2472297 was associated with prostate cancer risk (OR per additional coffee increasing allele: 1.01, 95% CI: 0.98,1.03) or having high-grade compared to low-grade disease (OR: 1.01, 95% CI: 0.97,1.04). There was some evidence that the genetic risk score was associated with higher odds of having nonlocalised compared to localised stage disease (OR: 1.03, 95% CI: 1.01, 1.06). Amongst men with prostate cancer, there was no clear association between the genetic risk score and all-cause mortality (HR: 1.00, 95% CI: 0.97,1.04) or prostate cancer-specific mortality (HR: 1.03, 95% CI: 0.98,1.08). These results, which should have less bias from confounding than observational estimates, are not consistent with a substantial effect of coffee consumption on reducing prostate cancer incidence or progression.",

keywords = "Aged, Alleles, Coffee/adverse effects, Disease Progression, Genetic Variation/genetics, Humans, Male, Mendelian Randomization Analysis/methods, Middle Aged, Prostatic Neoplasms/etiology, Risk Factors",

author = "Taylor, {Amy E} and Martin, {Richard M} and Geybels, {Milan S} and Stanford, {Janet L} and Irene Shui and Rosalind Eeles and Doug Easton and Zsofia Kote-Jarai and {Amin Al Olama}, Ali and Sara Benlloch and Kenneth Muir and Giles, {Graham G} and Fredrik Wiklund and Henrik Gronberg and Haiman, {Christopher A} and Johanna Schleutker and Nordestgaard, {B{\o}rge G} and Travis, {Ruth C} and David Neal and Nora Pashayan and Kay-Tee Khaw and William Blot and Stephen Thibodeau and Christiane Maier and Kibel, {Adam S} and Cezary Cybulski and Lisa Cannon-Albright and Hermann Brenner and Jong Park and Radka Kaneva and Jyotsna Batra and Teixeira, {Manuel R} and Hardev Pandha and {PRACTICAL consortium} and Jenny Donovan and Munaf{\`o}, {Marcus R}",

note = "{\textcopyright} 2016 The Authors International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.",

year = "2017",

month = jan,

day = "15",

doi = "10.1002/ijc.30462",

language = "English",

volume = "140",

pages = "322--328",

journal = "International Journal of Cancer. Supplement",

issn = "0898-6924",

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TY - JOUR

T1 - Investigating the possible causal role of coffee consumption with prostate cancer risk and progression using Mendelian randomization analysis

AU - Taylor, Amy E

AU - Martin, Richard M

AU - Geybels, Milan S

AU - Stanford, Janet L

AU - Shui, Irene

AU - Eeles, Rosalind

AU - Easton, Doug

AU - Kote-Jarai, Zsofia

AU - Amin Al Olama, Ali

AU - Benlloch, Sara

AU - Muir, Kenneth

AU - Giles, Graham G

AU - Wiklund, Fredrik

AU - Gronberg, Henrik

AU - Haiman, Christopher A

AU - Schleutker, Johanna

AU - Nordestgaard, Børge G

AU - Travis, Ruth C

AU - Neal, David

AU - Pashayan, Nora

AU - Khaw, Kay-Tee

AU - Blot, William

AU - Thibodeau, Stephen

AU - Maier, Christiane

AU - Kibel, Adam S

AU - Cybulski, Cezary

AU - Cannon-Albright, Lisa

AU - Brenner, Hermann

AU - Park, Jong

AU - Kaneva, Radka

AU - Batra, Jyotsna

AU - Teixeira, Manuel R

AU - Pandha, Hardev

AU - PRACTICAL consortium

AU - Donovan, Jenny

AU - Munafò, Marcus R

PY - 2017/1/15

Y1 - 2017/1/15

N2 - Coffee consumption has been shown in some studies to be associated with lower risk of prostate cancer. However, it is unclear if this association is causal or due to confounding or reverse causality. We conducted a Mendelian randomisation analysis to investigate the causal effects of coffee consumption on prostate cancer risk and progression. We used two genetic variants robustly associated with caffeine intake (rs4410790 and rs2472297) as proxies for coffee consumption in a sample of 46,687 men of European ancestry from 25 studies in the PRACTICAL consortium. Associations between genetic variants and prostate cancer case status, stage and grade were assessed by logistic regression and with all-cause and prostate cancer-specific mortality using Cox proportional hazards regression. There was no clear evidence that a genetic risk score combining rs4410790 and rs2472297 was associated with prostate cancer risk (OR per additional coffee increasing allele: 1.01, 95% CI: 0.98,1.03) or having high-grade compared to low-grade disease (OR: 1.01, 95% CI: 0.97,1.04). There was some evidence that the genetic risk score was associated with higher odds of having nonlocalised compared to localised stage disease (OR: 1.03, 95% CI: 1.01, 1.06). Amongst men with prostate cancer, there was no clear association between the genetic risk score and all-cause mortality (HR: 1.00, 95% CI: 0.97,1.04) or prostate cancer-specific mortality (HR: 1.03, 95% CI: 0.98,1.08). These results, which should have less bias from confounding than observational estimates, are not consistent with a substantial effect of coffee consumption on reducing prostate cancer incidence or progression.

AB - Coffee consumption has been shown in some studies to be associated with lower risk of prostate cancer. However, it is unclear if this association is causal or due to confounding or reverse causality. We conducted a Mendelian randomisation analysis to investigate the causal effects of coffee consumption on prostate cancer risk and progression. We used two genetic variants robustly associated with caffeine intake (rs4410790 and rs2472297) as proxies for coffee consumption in a sample of 46,687 men of European ancestry from 25 studies in the PRACTICAL consortium. Associations between genetic variants and prostate cancer case status, stage and grade were assessed by logistic regression and with all-cause and prostate cancer-specific mortality using Cox proportional hazards regression. There was no clear evidence that a genetic risk score combining rs4410790 and rs2472297 was associated with prostate cancer risk (OR per additional coffee increasing allele: 1.01, 95% CI: 0.98,1.03) or having high-grade compared to low-grade disease (OR: 1.01, 95% CI: 0.97,1.04). There was some evidence that the genetic risk score was associated with higher odds of having nonlocalised compared to localised stage disease (OR: 1.03, 95% CI: 1.01, 1.06). Amongst men with prostate cancer, there was no clear association between the genetic risk score and all-cause mortality (HR: 1.00, 95% CI: 0.97,1.04) or prostate cancer-specific mortality (HR: 1.03, 95% CI: 0.98,1.08). These results, which should have less bias from confounding than observational estimates, are not consistent with a substantial effect of coffee consumption on reducing prostate cancer incidence or progression.

KW - Aged

KW - Alleles

KW - Coffee/adverse effects

KW - Disease Progression

KW - Genetic Variation/genetics

KW - Humans

KW - Male

KW - Mendelian Randomization Analysis/methods

KW - Middle Aged

KW - Prostatic Neoplasms/etiology

KW - Risk Factors

U2 - 10.1002/ijc.30462

DO - 10.1002/ijc.30462

M3 - Journal article

C2 - 27741566

SN - 0898-6924

VL - 140

SP - 322

EP - 328

JO - International Journal of Cancer. Supplement

JF - International Journal of Cancer. Supplement

IS - 2

ER -

Investigating the possible causal role of coffee consumption with prostate cancer risk and progression using Mendelian randomization analysis

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