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Mendelian randomisation study of smoking exposure in relation to breast cancer risk

Park, Hanla A. ; Neumeyer, Sonja ; Michailidou, Kyriaki ; Bolla, Manjeet K. ; Wang, Qin ; Dennis, Joe ; Ahearn, Thomas U. ; Andrulis, Irene L. ; Anton-Culver, Hoda and Antonenkova, Natalia N. , et al. (2021) In British Journal of Cancer 125(8). p.1135-1145
Abstract

Background: Despite a modest association between tobacco smoking and breast cancer risk reported by recent epidemiological studies, it is still equivocal whether smoking is causally related to breast cancer risk. Methods: We applied Mendelian randomisation (MR) to evaluate a potential causal effect of cigarette smoking on breast cancer risk. Both individual-level data as well as summary statistics for 164 single-nucleotide polymorphisms (SNPs) reported in genome-wide association studies of lifetime smoking index (LSI) or cigarette per day (CPD) were used to obtain MR effect estimates. Data from 108,420 invasive breast cancer cases and 87,681 controls were used for the LSI analysis and for the CPD analysis conducted among ever-smokers... (More)

Background: Despite a modest association between tobacco smoking and breast cancer risk reported by recent epidemiological studies, it is still equivocal whether smoking is causally related to breast cancer risk. Methods: We applied Mendelian randomisation (MR) to evaluate a potential causal effect of cigarette smoking on breast cancer risk. Both individual-level data as well as summary statistics for 164 single-nucleotide polymorphisms (SNPs) reported in genome-wide association studies of lifetime smoking index (LSI) or cigarette per day (CPD) were used to obtain MR effect estimates. Data from 108,420 invasive breast cancer cases and 87,681 controls were used for the LSI analysis and for the CPD analysis conducted among ever-smokers from 26,147 cancer cases and 26,072 controls. Sensitivity analyses were conducted to address pleiotropy. Results: Genetically predicted LSI was associated with increased breast cancer risk (OR 1.18 per SD, 95% CI: 1.07–1.30, P = 0.11 × 10–2), but there was no evidence of association for genetically predicted CPD (OR 1.02, 95% CI: 0.78–1.19, P = 0.85). The sensitivity analyses yielded similar results and showed no strong evidence of pleiotropic effect. Conclusion: Our MR study provides supportive evidence for a potential causal association with breast cancer risk for lifetime smoking exposure but not cigarettes per day among smokers.

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type
Contribution to journal
publication status
published
subject
in
British Journal of Cancer
volume
125
issue
8
pages
1135 - 1145
publisher
Nature Publishing Group
external identifiers
  • pmid:34341517
  • scopus:85112658433
ISSN
0007-0920
DOI
10.1038/s41416-021-01432-8
language
English
LU publication?
yes
id
165ea89a-90df-4c82-b9ff-ba909ab51e05
date added to LUP
2021-09-23 15:32:34
date last changed
2023-09-13 01:25:57
@article{165ea89a-90df-4c82-b9ff-ba909ab51e05,
  abstract     = {{<p>Background: Despite a modest association between tobacco smoking and breast cancer risk reported by recent epidemiological studies, it is still equivocal whether smoking is causally related to breast cancer risk. Methods: We applied Mendelian randomisation (MR) to evaluate a potential causal effect of cigarette smoking on breast cancer risk. Both individual-level data as well as summary statistics for 164 single-nucleotide polymorphisms (SNPs) reported in genome-wide association studies of lifetime smoking index (LSI) or cigarette per day (CPD) were used to obtain MR effect estimates. Data from 108,420 invasive breast cancer cases and 87,681 controls were used for the LSI analysis and for the CPD analysis conducted among ever-smokers from 26,147 cancer cases and 26,072 controls. Sensitivity analyses were conducted to address pleiotropy. Results: Genetically predicted LSI was associated with increased breast cancer risk (OR 1.18 per SD, 95% CI: 1.07–1.30, P = 0.11 × 10<sup>–2</sup>), but there was no evidence of association for genetically predicted CPD (OR 1.02, 95% CI: 0.78–1.19, P = 0.85). The sensitivity analyses yielded similar results and showed no strong evidence of pleiotropic effect. Conclusion: Our MR study provides supportive evidence for a potential causal association with breast cancer risk for lifetime smoking exposure but not cigarettes per day among smokers.</p>}},
  author       = {{Park, Hanla A. and Neumeyer, Sonja and Michailidou, Kyriaki and Bolla, Manjeet K. and Wang, Qin and Dennis, Joe and Ahearn, Thomas U. and Andrulis, Irene L. and Anton-Culver, Hoda and Antonenkova, Natalia N. and Arndt, Volker and Aronson, Kristan J. and Augustinsson, Annelie and Baten, Adinda and Beane Freeman, Laura E. and Becher, Heiko and Beckmann, Matthias W. and Behrens, Sabine and Benitez, Javier and Bermisheva, Marina and Bogdanova, Natalia V. and Bojesen, Stig E. and Brauch, Hiltrud and Brenner, Hermann and Brucker, Sara Y. and Burwinkel, Barbara and Campa, Daniele and Canzian, Federico and Castelao, Jose E. and Chanock, Stephen J. and Chenevix-Trench, Georgia and Clarke, Christine L. and Børresen-Dale, Anne Lise and Grenaker Alnæs, Grethe I. and Sahlberg, Kristine K. and Ottestad, Lars and Kåresen, Rolf and Schlichting, Ellen and Holmen, Marit Muri and Sauer, Toril and Haakensen, Vilde and Engebråten, Olav and Naume, Bjørn and Fosså, Alexander and Kiserud, Cecile E. and Reinertsen, Kristin V. and Helland, Åslaug and Riis, Margit and Geisler, Jürgen and Olsson, Håkan}},
  issn         = {{0007-0920}},
  language     = {{eng}},
  month        = {{08}},
  number       = {{8}},
  pages        = {{1135--1145}},
  publisher    = {{Nature Publishing Group}},
  series       = {{British Journal of Cancer}},
  title        = {{Mendelian randomisation study of smoking exposure in relation to breast cancer risk}},
  url          = {{http://dx.doi.org/10.1038/s41416-021-01432-8}},
  doi          = {{10.1038/s41416-021-01432-8}},
  volume       = {{125}},
  year         = {{2021}},
}