Interaction between dietary acrylamide intake and genetic variants for estrogen receptor-positive breast cancer risk

Janneke G F Hogervorst,Leo J Schouten,Piet A Van Den Brandt,Roger W L Godschalk,Frederik-Jan Van Schooten

doi:10.1007/s00394-018-1619-z

Janneke G F Hogervorst, Leo J Schouten + Show 3 more

Open Access

https://doi.org/10.1007/s00394-018-1619-z

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Abstract

PurposeThe association between dietary acrylamide intake and estrogen receptor-positive (ER+) breast cancer risk in epidemiological studies is inconsistent. By analyzing gene-acrylamide interactions for ER+ breast cancer risk, we aimed to clarify the role of acrylamide intake in ER+ breast cancer etiology.MethodsThe prospective Netherlands Cohort Study on diet and cancer includes 62,573 women, aged 55–69 years. At baseline, a random subcohort of 2589 women was sampled from the total cohort for a case–cohort analysis approach. Dietary acrylamide intake of subcohort members (n = 1449) and ER+ breast cancer cases (n = 844) was assessed with a food frequency questionnaire. We genotyped single nucleotide polymorphisms (SNPs) in genes in acrylamide metabolism, sex steroid systems, oxidative stress and DNA repair. Multiplicative interaction between acrylamide intake and SNPs was assessed with Cox proportional hazards analysis, based on 20.3 years of follow-up.ResultsUnexpectedly, there was a statistically non-significant inverse association between acrylamide and ER+ breast cancer risk among all women but with no clear dose–response relationship, and no association among never smokers. Among the results for 57 SNPs and 2 gene deletions, rs1056827 in CYP1B1, rs2959008 and rs7173655 in CYP11A1, the GSTT1 gene deletion, and rs1052133 in hOGG1 showed a statistically significant interaction with acrylamide intake for ER+ breast cancer risk.ConclusionsThis study did not provide evidence for a positive association between acrylamide intake and ER+ breast cancer risk. If anything, acrylamide was associated with a decreased ER+ breast cancer risk. The interaction with SNPs in CYP1B1 and CYP11A1 suggests that acrylamide may influence ER+ breast cancer risk through sex hormone pathways.

Highlights

Acrylamide, a probable human carcinogen (IARC class 2A), was discovered in 2002 in various heat-treated carbohydraterich foods, such as cookies, potato crisps, French fries and coffee
There was a statistically non-significant inverse association between acrylamide and ER+ breast cancer risk after 20.3 years of follow-up in all women (HR of highest versus the lowest quintile of intake: 0.85 and 0.94 (0.88–1.00) per 10 μg/day increment of intake) but with no clear dose–response relationship
There was no association in never-smoking women (HR of highest versus the lowest quintile of intake: 1.18 and 1.02 (0.93–1.11) per 10 μg/day increment of intake) (Table 2)

Summary

Introduction

Acrylamide, a probable human carcinogen (IARC class 2A), was discovered in 2002 in various heat-treated carbohydraterich foods, such as cookies, potato crisps, French fries and coffee. Acrylamide is a small hydrophilic compound that is distributed throughout the body with the blood. In theory, it can cause cancer everywhere in the body. Acrylamide is a multisite carcinogen in rodents, in which it causes, among other, mammary gland tumors in females [1]. The mechanisms by which acrylamide causes mammary gland tumors in rodents are hypothesized to be genotoxicity and endocrine effects [1]. Since 2002, a few epidemiological studies have investigated the impact of dietary acrylamide intake on human cancer risks.

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