scholarly journals Mendelian randomisation analysis of circulating adipokines and C‐reactive protein on breast cancer risk

2020 ◽  
Vol 147 (6) ◽  
pp. 1597-1603 ◽  
Author(s):  
Timothy Robinson ◽  
Richard M. Martin ◽  
James Yarmolinsky
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Mendelian Randomisation ◽  
C Reactive Protein ◽  
Reactive Protein

C-reactive protein and postmenopausal breast cancer risk: results from the E3N cohort study

2014 ◽  
Vol 25 (4) ◽  
pp. 533-539 ◽  
Author(s):  
Laure Dossus ◽  
Aida Jimenez-Corona ◽  
Isabelle Romieu ◽  
Marie-Christine Boutron-Ruault ◽  
Anne Boutten ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cohort Study ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Postmenopausal Breast Cancer ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Postmenopausal Breast Cancer Risk

Pre-diagnostic high-sensitive C-reactive protein and breast cancer risk, recurrence, and survival

2016 ◽  
Vol 155 (2) ◽  
pp. 345-354 ◽  
Author(s):  
H. Frydenberg ◽  
I. Thune ◽  
T. Lofterød ◽  
E. S. Mortensen ◽  
A. E. Eggen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Risk Recurrence

scholarly journals Genetically Predicted C-Reactive Protein Associated With Postmenopausal Breast Cancer Risk: Interrelation With Estrogen and Cancer Molecular Subtypes Using Mendelian Randomization

2021 ◽  
Vol 10 ◽  
Author(s):  
Su Yon Jung ◽  
Jeanette C. Papp ◽  
Eric M. Sobel ◽  
Matteo Pellegrini ◽  
Herbert Yu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Mendelian Randomization ◽  
Postmenopausal Breast Cancer ◽  
Nucleotide Polymorphisms ◽  
Reverse Causality ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Increased Risk

BackgroundImmune-related etiologic pathways that influence breast cancer risk are incompletely understood and may be confounded by lifestyles or reverse causality. Using a Mendelian randomization (MR) approach, we investigated the potential causal relationship between genetically elevated C-reactive protein (CRP) concentrations and primary invasive breast cancer risk in postmenopausal women.MethodsWe used individual-level data obtained from 10,179 women, including 537 who developed breast cancer, from the Women’s Health Initiative Database for Genotypes and Phenotypes Study, which consists of five genome-wide association (GWA) studies. We examined 61 GWA single-nucleotide polymorphisms (SNPs) previously associated with CRP. We employed weighted/penalized weighted–medians and MR gene–environment interactions that allow instruments’ invalidity to some extent and attenuate the heterogeneous estimates of outlying SNPs.ResultsIn lifestyle-stratification analyses, genetically elevated CRP decreased risk for breast cancer in exogenous estrogen-only, estrogen + progestin, and past oral contraceptive (OC) users, but only among relatively short-term users (<5 years). Estrogen-only users for ≥5 years had more profound CRP-decreased breast cancer risk in dose–response fashion, whereas past OC users for ≥5 years had CRP-increased cancer risk. Also, genetically predicted CRP was strongly associated with increased risk for hormone-receptor positive or human epidermal growth factor receptor-2 negative breast cancer.ConclusionsOur findings may provide novel evidence on the immune-related molecular pathways linking to breast cancer risk and suggest potential clinical use of CRP to predict the specific cancer subtypes. Our findings suggest potential interventions targeting CRP–inflammatory markers to reduce breast cancer risk.

scholarly journals Genetically predicted C-reactive protein associated with breast cancer risk: interrelation with estrogen and cancer molecular subtypes using a Mendelian randomization

2020 ◽  
Author(s):  
Su Yon Jung ◽  
Jeanette C. Papp ◽  
Eric M. Sobel ◽  
Matteo Pellegrini ◽  
Herbert Yu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Mendelian Randomization ◽  
Molecular Subtypes ◽  
C Reactive Protein ◽  
Reactive Protein

Abstract The authors have withdrawn this preprint due to erroneous posting.

scholarly journals Genetically predicted C-reactive protein associated with breast cancer risk: interrelation with estrogen and cancer molecular subtypes using a Mendelian randomization

2020 ◽  
Author(s):  
Su Yon Jung ◽  
Jeanette C. Papp ◽  
Eric M. Sobel ◽  
Matteo Pellegrini ◽  
Herbert Yu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Mendelian Randomization ◽  
Inflammatory Marker ◽  
Postmenopausal Breast Cancer ◽  
Reverse Causality ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Increased Risk

Abstract Background: Immune-related etiologic pathways that influence breast cancer risk are incompletely understood and may be confounded by lifestyles or reverse causality. Using a Mendelian randomization (MR) approach, we investigated the potential causal relationship between genetically elevated C-reactive protein (CRP) concentrations and primary invasive breast cancer risk in postmenopausal women.Methods: We used individual-level data obtained from 10,170 women, including 537 who developed breast cancer, from the Women’s Health Initiative Database for Genotypes and Phenotypes Study, which consists of 5 genome-wide association (GWA) studies. We examined 61 GWA single-nucleotide polymorphisms (SNPs) previously associated with CRP. We employed weighted/penalized weighted–medians and MR gene–environment interactions that allow instruments’ invalidity to some extent and attenuate the heterogeneous estimates of outlying SNPs.Results: In lifestyle-stratification analyses, genetically elevated CRP decreased risk for breast cancer in exogenous estrogen-only, estrogen + progestin, and past oral contraceptive (OC) users, but only among relatively short-term users (< 5 years). Estrogen-only users for ≥ 5 years had more profound CRP-decreased breast cancer risk in dose-response fashion, whereas past OC users for ≥ 5 years had CRP-increased cancer risk. Also, genetically predicted CRP was strongly associated with increased risk for hormone-receptor positive or human epidermal growth factor receptor-2 negative breast cancer.Conclusions: Our findings may provide novel evidence on the immune-related pathways linking to breast cancer risk, and suggest potential clinical use of CRP to predict the specific cancer subtypes and CRP–inflammatory marker targeting interventions to reduce postmenopausal breast cancer risk.

scholarly journals Investigating causal relations between sleep traits and risk of breast cancer in women: mendelian randomisation study

BMJ ◽  
2019 ◽  
pp. l2327 ◽  
Author(s):  
Rebecca C Richmond ◽  
Emma L Anderson ◽  
Hassan S Dashti ◽  
Samuel E Jones ◽  
Jacqueline M Lane ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Protective Effect ◽  
Sleep Duration ◽  
Breast Cancer Diagnosis ◽  
Mendelian Randomisation ◽  
Uk Biobank ◽  
Multivariable Regression ◽  
Insomnia Symptoms

Abstract Objective To examine whether sleep traits have a causal effect on risk of breast cancer. Design Mendelian randomisation study. Setting UK Biobank prospective cohort study and Breast Cancer Association Consortium (BCAC) case-control genome-wide association study. Participants 156 848 women in the multivariable regression and one sample mendelian randomisation (MR) analysis in UK Biobank (7784 with a breast cancer diagnosis) and 122 977 breast cancer cases and 105 974 controls from BCAC in the two sample MR analysis. Exposures Self reported chronotype (morning or evening preference), insomnia symptoms, and sleep duration in multivariable regression, and genetic variants robustly associated with these sleep traits. Main outcome measure Breast cancer diagnosis. Results In multivariable regression analysis using UK Biobank data on breast cancer incidence, morning preference was inversely associated with breast cancer (hazard ratio 0.95, 95% confidence interval 0.93 to 0.98 per category increase), whereas there was little evidence for an association between sleep duration and insomnia symptoms. Using 341 single nucleotide polymorphisms (SNPs) associated with chronotype, 91 SNPs associated with sleep duration, and 57 SNPs associated with insomnia symptoms, one sample MR analysis in UK Biobank provided some supportive evidence for a protective effect of morning preference on breast cancer risk (0.85, 0.70, 1.03 per category increase) but imprecise estimates for sleep duration and insomnia symptoms. Two sample MR using data from BCAC supported findings for a protective effect of morning preference (inverse variance weighted odds ratio 0.88, 95% confidence interval 0.82 to 0.93 per category increase) and adverse effect of increased sleep duration (1.19, 1.02 to 1.39 per hour increase) on breast cancer risk (both oestrogen receptor positive and oestrogen receptor negative), whereas evidence for insomnia symptoms was inconsistent. Results were largely robust to sensitivity analyses accounting for horizontal pleiotropy. Conclusions Findings showed consistent evidence for a protective effect of morning preference and suggestive evidence for an adverse effect of increased sleep duration on breast cancer risk.

scholarly journals The association between weight at birth and breast cancer risk revisited using Mendelian randomisation

2019 ◽  
Vol 34 (6) ◽  
pp. 591-600 ◽  
Author(s):  
Siddhartha P. Kar ◽  
Irene L. Andrulis ◽  
Hermann Brenner ◽  
Stephen Burgess ◽  
Jenny Chang-Claude ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Mendelian Randomisation

scholarly journals The association between weight at birth and breast cancer risk revisited using Mendelian randomisation

2018 ◽  
Author(s):  
Siddhartha P. Kar ◽  
Irene L. Andrulis ◽  
Hermann Brenner ◽  
Stephen Burgess ◽  
Jenny Chang-Claude ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Adult Life ◽  
Data Availability ◽  
Alternative Methods ◽  
Sensitivity Analyses ◽  
Mendelian Randomisation ◽  
Age At Menarche ◽  
Increased Risk

AbstractObservational studies suggest that higher birth weight (BW) is associated with increased risk of breast cancer in adult life. We conducted a two-sample Mendelian randomisation (MR) study to assess whether this association is causal. Sixty independent single nucleotide polymorphisms (SNPs) known to be associated at P < 5 × 10-8 with BW were used to construct (1) a 41-SNP instrumental variable (IV) for univariable MR after removing SNPs with pleiotropic associations with other breast cancer risk factors and (2) a 49-SNP IV for multivariable MR after filtering SNPs for data availability. BW predicted by the 41-SNP IV was not associated with overall breast cancer risk in inverse-variance weighted (IVW) univariable MR analysis of genetic association data from 122,977 breast cancer cases and 105,974 controls (odds ratio = 0.86 per 500 g higher BW; 95% confidence interval: 0.73—1.01). Sensitivity analyses using four alternative methods and three alternative IVs, including an IV with 59 of the 60 BW-associated SNPs, yielded similar results. Multivariable MR adjusting for the effects of the 49-SNP IV on birth length, adult height, adult body mass index, age at menarche, and age at menopause using IVW and MR-Egger methods provided estimates consistent with univariable analyses. Results were also similar when all analyses were repeated after restricting to estrogen receptor-positive or -negative breast cancer cases. Point estimates of the odds ratios from most analyses performed indicated an inverse relationship between genetically-predicted BW and breast cancer. Thus, there is little evidence from MR to suggest that the previously observed association between higher BW and increased risk of breast cancer in adult life is causal.

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

2021 ◽  
Author(s):  
Hanla A. Park ◽  
Sonja Neumeyer ◽  
Kyriaki Michailidou ◽  
Manjeet K. Bolla ◽  
Qin Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Causal Effect ◽  
Association Studies ◽  
Sensitivity Analyses ◽  
Mendelian Randomisation ◽  
Genome Wide Association Studies ◽  
Nucleotide Polymorphisms ◽  
Smoking Exposure

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 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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