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  1. Article ; Online: Native American ancestry and breast cancer risk in Colombian and Mexican women: ruling out potential confounding through ancestry-informative markers.

    Zollner, Linda / Torres, Diana / Briceno, Ignacio / Gilbert, Michael / Torres-Mejía, Gabriela / Dennis, Joe / Bolla, Manjeet K / Wang, Qin / Hamann, Ute / Lorenzo Bermejo, Justo

    Breast cancer research : BCR

    2023  Volume 25, Issue 1, Page(s) 111

    Abstract: Background: Latin American and Hispanic women are less likely to develop breast cancer (BC) than women of European descent. Observational studies have found an inverse relationship between the individual proportion of Native American ancestry and BC ... ...

    Abstract Background: Latin American and Hispanic women are less likely to develop breast cancer (BC) than women of European descent. Observational studies have found an inverse relationship between the individual proportion of Native American ancestry and BC risk. Here, we use ancestry-informative markers to rule out potential confounding of this relationship, estimating the confounder-free effect of Native American ancestry on BC risk.
    Methods and study population: We used the informativeness for assignment measure to select robust instrumental variables for the individual proportion of Native American ancestry. We then conducted separate Mendelian randomization (MR) analyses based on 1401 Colombian women, most of them from the central Andean regions of Cundinamarca and Huila, and 1366 Mexican women from Mexico City, Monterrey and Veracruz, supplemented by sensitivity and stratified analyses.
    Results: The proportion of Colombian Native American ancestry showed a putatively causal protective effect on BC risk (inverse variance-weighted odds ratio [OR] = 0.974 per 1% increase in ancestry proportion, 95% confidence interval [CI] 0.970-0.978, p = 3.1 × 10
    Conclusions: The present results point to an unconfounded protective effect of Native American ancestry on BC risk in both Colombian and Mexican women which appears to be stronger for familial and ER-positive BC. These findings provide a rationale for personalised prevention programmes that take genetic ancestry into account, as well as for future admixture mapping studies.
    MeSH term(s) Female ; Humans ; American Indian or Alaska Native/ethnology ; American Indian or Alaska Native/genetics ; American Indian or Alaska Native/statistics & numerical data ; Breast ; Breast Neoplasms/epidemiology ; Breast Neoplasms/ethnology ; Breast Neoplasms/genetics ; Colombia/epidemiology ; Mexico/epidemiology ; Triple Negative Breast Neoplasms/epidemiology ; Triple Negative Breast Neoplasms/ethnology ; Triple Negative Breast Neoplasms/genetics
    Language English
    Publishing date 2023-10-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2015059-3
    ISSN 1465-542X ; 1465-5411
    ISSN (online) 1465-542X
    ISSN 1465-5411
    DOI 10.1186/s13058-023-01713-5
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  2. Article ; Online: Disentangling the relationships of body mass index and circulating sex hormone concentrations in mammographic density using Mendelian randomization.

    Haas, Cameron B / Chen, Hongjie / Harrison, Tabitha / Fan, Shaoqi / Gago-Dominguez, Manuela / Castelao, Jose E / Bolla, Manjeet K / Wang, Qin / Dennis, Joe / Michailidou, Kyriaki / Dunning, Alison M / Easton, Douglas F / Antoniou, Antonis C / Hall, Per / Czene, Kamila / Andrulis, Irene L / Mulligan, Anna Marie / Milne, Roger L / Fasching, Peter A /
    Haeberle, Lothar / Garcia-Closas, Montserrat / Ahearn, Thomas / Gierach, Gretchen L / Haiman, Christopher / Maskarinec, Gertraud / Couch, Fergus J / Olson, Janet E / John, Esther M / Chenevix-Trench, Geogia / de Gonzalez, Amy Berrington / Jones, Michael / Stone, Jennifer / Murphy, Rachel / Aronson, Kristan J / Wernli, Karen J / Hsu, Li / Vachon, Celine / Tamimi, Rulla M / Lindström, Sara

    Breast cancer research and treatment

    2024  

    Abstract: Purpose: Mammographic density phenotypes, adjusted for age and body mass index (BMI), are strong predictors of breast cancer risk. BMI is associated with mammographic density measures, but the role of circulating sex hormone concentrations is less clear. ...

    Abstract Purpose: Mammographic density phenotypes, adjusted for age and body mass index (BMI), are strong predictors of breast cancer risk. BMI is associated with mammographic density measures, but the role of circulating sex hormone concentrations is less clear. We investigated the relationship between BMI, circulating sex hormone concentrations, and mammographic density phenotypes using Mendelian randomization (MR).
    Methods: We applied two-sample MR approaches to assess the association between genetically predicted circulating concentrations of sex hormones [estradiol, testosterone, sex hormone-binding globulin (SHBG)], BMI, and mammographic density phenotypes (dense and non-dense area). We created instrumental variables from large European ancestry-based genome-wide association studies and applied estimates to mammographic density phenotypes in up to 14,000 women of European ancestry. We performed analyses overall and by menopausal status.
    Results: Genetically predicted BMI was positively associated with non-dense area (IVW: β = 1.79; 95% CI = 1.58, 2.00; p = 9.57 × 10
    Conclusion: Our findings support a positive causal association between BMI and mammographic non-dense area and an inverse association between BMI and dense area. Evidence was weaker and inconsistent for a causal effect of circulating sex hormone concentrations on mammographic density phenotypes. Based on our findings, associations between circulating sex hormone concentrations and mammographic density phenotypes are weak at best.
    Language English
    Publishing date 2024-04-24
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 604563-7
    ISSN 1573-7217 ; 0167-6806
    ISSN (online) 1573-7217
    ISSN 0167-6806
    DOI 10.1007/s10549-024-07306-w
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  3. Article: Body mass index and type 2 diabetes and breast cancer survival: a Mendelian randomization study.

    Liu, Yi-Shian / Wu, Pei-Ei / Chou, Wen-Cheng / Vikram, Rajeev / Chen, Wei-Ting / Yang, Show-Ling / Bolla, Manjeet K / Wang, Qin / Dennis, Joe / Chan, Tsun L / Choi, Ji-Yeob / Hou, Ming-Feng / Ito, Hidemi / Kang, Daehee / Kim, Sung-Won / Kwong, Ava / Matsuo, Keitaro / Park, Sue K / Shu, Xiao-Ou /
    Zheng, Wei / Dunning, Alison M / Easton, Douglas F / Shen, Chen-Yang

    American journal of cancer research

    2021  Volume 11, Issue 8, Page(s) 3921–3934

    Abstract: The causal relationship between body mass index (BMI) and type 2 diabetes (T2D) and breast cancer prognosis is still ambiguous. The aim of this study was to investigate the prognostic effect of BMI and T2D on breast cancer disease-free survival (DFS) ... ...

    Abstract The causal relationship between body mass index (BMI) and type 2 diabetes (T2D) and breast cancer prognosis is still ambiguous. The aim of this study was to investigate the prognostic effect of BMI and T2D on breast cancer disease-free survival (DFS) among Asian individuals. In this two-sample Mendelian randomization (MR) study, the instrumental variables (IVs) were identified using a genome-wide association study (GWAS) among 24,000 participants in the Taiwan Biobank. Importantly, the validity of these IVs was confirmed with a previous large-scale GWAS (Biobank Japan Project, BBJ). In this study, we found that a genetic predisposition toward higher BMI (as indicated by BMI IVs, F = 86.88) was associated with poor breast cancer DFS (hazard ratio [HR] = 6.11; P < 0.001). Furthermore, higher level of genetically predicted T2D (as indicated by T2D IVs) was associated with an increased risk of recurrence of and mortality from breast cancer (HR = 1.43; P < 0.001). Sensitivity analyses, including the weighted-median approach, MR-Egger regression, Radial regression and Mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) supported the consistency of our findings. Finally, the causal relationship between BMI and poor breast cancer prognosis was confirmed in a prospective cohort study. Our MR analyses demonstrated the causal relationship between the genetic prediction of elevated BMI and a greater risk of T2D with poor breast cancer prognosis. BMI and T2D have important clinical implications and may be used as prognostic indicators of breast cancer.
    Language English
    Publishing date 2021-08-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2589522-9
    ISSN 2156-6976
    ISSN 2156-6976
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Authors' response: Associations of obesity and circulating insulin and glucose with breast cancer risk.

    Shu, Xiang / Wu, Lang / Khankari, Nikhil K / Shu, Xiao-Ou / Wang, Thomas J / Michailidou, Kyriaki / Bolla, Manjeet K / Wang, Qin / Dennis, Joe / Milne, Roger L / Schmidt, Marjanka K / Pharoah, Paul / Andrulis, Irene L / Hunter, David J / Simard, Jacques / Easton, Douglas F / Zheng, Wei

    International journal of epidemiology

    2019  Volume 48, Issue 3, Page(s) 1016–1017

    MeSH term(s) Breast Neoplasms ; Glucose ; Humans ; Insulin ; Mendelian Randomization Analysis ; Obesity
    Chemical Substances Insulin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2019-06-20
    Publishing country England
    Document type Letter ; Comment
    ZDB-ID 187909-1
    ISSN 1464-3685 ; 0300-5771
    ISSN (online) 1464-3685
    ISSN 0300-5771
    DOI 10.1093/ije/dyz015
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  5. Article ; Online: Targeted Resequencing of the Coding Sequence of 38 Genes Near Breast Cancer GWAS Loci in a Large Case-Control Study.

    Decker, Brennan / Allen, Jamie / Luccarini, Craig / Pooley, Karen A / Shah, Mitul / Bolla, Manjeet K / Wang, Qin / Ahmed, Shahana / Baynes, Caroline / Conroy, Don M / Brown, Judith / Luben, Robert / Ostrander, Elaine A / Pharoah, Paul D P / Dunning, Alison M / Easton, Douglas F

    Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

    2019  Volume 28, Issue 4, Page(s) 822–825

    Abstract: Background: Genes regulated by breast cancer risk alleles identified through genome-wide association studies (GWAS) may harbor rare coding risk alleles.: Methods: We sequenced the coding regions for 38 genes within 500 kb of 38 lead GWAS SNPs in 13, ... ...

    Abstract Background: Genes regulated by breast cancer risk alleles identified through genome-wide association studies (GWAS) may harbor rare coding risk alleles.
    Methods: We sequenced the coding regions for 38 genes within 500 kb of 38 lead GWAS SNPs in 13,538 breast cancer cases and 5,518 controls.
    Results: Truncating variants in these genes were rare, and were not associated with breast cancer risk. Burden testing of rare missense variants highlighted 5 genes with some suggestion of an association with breast cancer, although none met the multiple testing thresholds:
    Conclusions: There was no evidence that rare coding variants in these genes confer substantial breast cancer risks. However, more modest effect sizes could not be ruled out.
    Impact: We tested the hypothesis that rare variants in 38 genes near breast cancer GWAS loci may mediate risk. These variants do not appear to play a major role in breast cancer heritability.
    MeSH term(s) Breast Neoplasms/genetics ; Case-Control Studies ; Female ; Gene Frequency/genetics ; Genetic Predisposition to Disease ; Genome-Wide Association Study/methods ; Humans
    Language English
    Publishing date 2019-01-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1153420-5
    ISSN 1538-7755 ; 1055-9965
    ISSN (online) 1538-7755
    ISSN 1055-9965
    DOI 10.1158/1055-9965.EPI-18-0298
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Assessment of interactions between 205 breast cancer susceptibility loci and 13 established risk factors in relation to breast cancer risk, in the Breast Cancer Association Consortium.

    Kapoor, Pooja Middha / Lindström, Sara / Behrens, Sabine / Wang, Xiaoliang / Michailidou, Kyriaki / Bolla, Manjeet K / Wang, Qin / Dennis, Joe / Dunning, Alison M / Pharoah, Paul D P / Schmidt, Marjanka K / Kraft, Peter / García-Closas, Montserrat / Easton, Douglas F / Milne, Roger L / Chang-Claude, Jenny

    International journal of epidemiology

    2019  Volume 49, Issue 1, Page(s) 216–232

    Abstract: Background: Previous gene-environment interaction studies of breast cancer risk have provided sparse evidence of interactions. Using the largest available dataset to date, we performed a comprehensive assessment of potential effect modification of 205 ... ...

    Abstract Background: Previous gene-environment interaction studies of breast cancer risk have provided sparse evidence of interactions. Using the largest available dataset to date, we performed a comprehensive assessment of potential effect modification of 205 common susceptibility variants by 13 established breast cancer risk factors, including replication of previously reported interactions.
    Methods: Analyses were performed using 28 176 cases and 32 209 controls genotyped with iCOGS array and 44 109 cases and 48 145 controls genotyped using OncoArray from the Breast Cancer Association Consortium (BCAC). Gene-environment interactions were assessed using unconditional logistic regression and likelihood ratio tests for breast cancer risk overall and by estrogen-receptor (ER) status. Bayesian false discovery probability was used to assess the noteworthiness of the meta-analysed array-specific interactions.
    Results: Noteworthy evidence of interaction at ≤1% prior probability was observed for three single nucleotide polymorphism (SNP)-risk factor pairs. SNP rs4442975 was associated with a greater reduction of risk of ER-positive breast cancer [odds ratio (OR)int = 0.85 (0.78-0.93), Pint = 2.8 x 10-4] and overall breast cancer [ORint = 0.85 (0.78-0.92), Pint = 7.4 x 10-5) in current users of estrogen-progesterone therapy compared with non-users. This finding was supported by replication using OncoArray data of the previously reported interaction between rs13387042 (r2 = 0.93 with rs4442975) and current estrogen-progesterone therapy for overall disease (Pint = 0.004). The two other interactions suggested stronger associations between SNP rs6596100 and ER-negative breast cancer with increasing parity and younger age at first birth.
    Conclusions: Overall, our study does not suggest strong effect modification of common breast cancer susceptibility variants by established risk factors.
    MeSH term(s) Alleles ; Breast Neoplasms/genetics ; Case-Control Studies ; Europe ; Factor XIII ; Female ; Gene-Environment Interaction ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study ; Genotype ; Humans ; Polymorphism, Single Nucleotide/genetics ; Receptors, Estrogen/genetics ; Risk Factors ; White People
    Chemical Substances Receptors, Estrogen ; Factor XIII (9013-56-3)
    Language English
    Publishing date 2019-10-11
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 187909-1
    ISSN 1464-3685 ; 0300-5771
    ISSN (online) 1464-3685
    ISSN 0300-5771
    DOI 10.1093/ije/dyz193
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  7. Article ; Online: Polymorphisms in genes of melatonin biosynthesis and signaling support the light-at-night hypothesis for breast cancer.

    Wichert, Katharina / Hoppe, Reiner / Ickstadt, Katja / Behrens, Thomas / Winter, Stefan / Herold, Robert / Terschüren, Claudia / Lo, Wing-Yee / Guénel, Pascal / Truong, Thérèse / Bolla, Manjeet K / Wang, Qin / Dennis, Joe / Michailidou, Kyriaki / Lush, Michael / Andrulis, Irene L / Brenner, Hermann / Chang-Claude, Jenny / Cox, Angela /
    Cross, Simon S / Czene, Kamila / Eriksson, Mikael / Figueroa, Jonine D / García-Closas, Montserrat / Goldberg, Mark S / Hamann, Ute / He, Wei / Holleczek, Bernd / Hopper, John L / Jakubowska, Anna / Ko, Yon-Dschun / Lubiński, Jan / Mulligan, Anna Marie / Obi, Nadia / Rhenius, Valerie / Shah, Mitul / Shu, Xiao-Ou / Simard, Jacques / Southey, Melissa C / Zheng, Wei / Dunning, Alison M / Pharoah, Paul D P / Hall, Per / Easton, Douglas F / Brüning, Thomas / Brauch, Hiltrud / Harth, Volker / Rabstein, Sylvia

    European journal of epidemiology

    2023  Volume 38, Issue 10, Page(s) 1053–1068

    Abstract: Light-at-night triggers the decline of pineal gland melatonin biosynthesis and secretion and is an IARC-classified probable breast-cancer risk factor. We applied a large-scale molecular epidemiology approach to shed light on the putative role of ... ...

    Abstract Light-at-night triggers the decline of pineal gland melatonin biosynthesis and secretion and is an IARC-classified probable breast-cancer risk factor. We applied a large-scale molecular epidemiology approach to shed light on the putative role of melatonin in breast cancer. We investigated associations between breast-cancer risk and polymorphisms at genes of melatonin biosynthesis/signaling using a study population of 44,405 women from the Breast Cancer Association Consortium (22,992 cases, 21,413 population-based controls). Genotype data of 97 candidate single nucleotide polymorphisms (SNPs) at 18 defined gene regions were investigated for breast-cancer risk effects. We calculated adjusted odds ratios (ORs) and 95% confidence intervals (CI) by logistic regression for the main-effect analysis as well as stratified analyses by estrogen- and progesterone-receptor (ER, PR) status. SNP-SNP interactions were analyzed via a two-step procedure based on logic regression. The Bayesian false-discovery probability (BFDP) was used for all analyses to account for multiple testing. Noteworthy associations (BFDP < 0.8) included 10 linked SNPs in tryptophan hydroxylase 2 (TPH2) (e.g. rs1386492: OR = 1.07, 95% CI 1.02-1.12), and a SNP in the mitogen-activated protein kinase 8 (MAPK8) (rs10857561: OR = 1.11, 95% CI 1.04-1.18). The SNP-SNP interaction analysis revealed noteworthy interaction terms with TPH2- and MAPK-related SNPs (e.g. rs1386483
    MeSH term(s) Humans ; Female ; Breast Neoplasms/genetics ; Breast Neoplasms/epidemiology ; Melatonin/genetics ; Melatonin/metabolism ; Bayes Theorem ; Polymorphism, Single Nucleotide ; Logistic Models ; Case-Control Studies ; Genetic Predisposition to Disease
    Chemical Substances Melatonin (JL5DK93RCL)
    Language English
    Publishing date 2023-10-03
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 632614-6
    ISSN 1573-7284 ; 0393-2990
    ISSN (online) 1573-7284
    ISSN 0393-2990
    DOI 10.1007/s10654-023-01048-7
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  8. Article ; Online: Associations of obesity and circulating insulin and glucose with breast cancer risk: a Mendelian randomization analysis.

    Shu, Xiang / Wu, Lang / Khankari, Nikhil K / Shu, Xiao-Ou / Wang, Thomas J / Michailidou, Kyriaki / Bolla, Manjeet K / Wang, Qin / Dennis, Joe / Milne, Roger L / Schmidt, Marjanka K / Pharoah, Paul D P / Andrulis, Irene L / Hunter, David J / Simard, Jacques / Easton, Douglas F / Zheng, Wei

    International journal of epidemiology

    2018  Volume 48, Issue 3, Page(s) 795–806

    Abstract: Background: In addition to the established association between general obesity and breast cancer risk, central obesity and circulating fasting insulin and glucose have been linked to the development of this common malignancy. Findings from previous ... ...

    Abstract Background: In addition to the established association between general obesity and breast cancer risk, central obesity and circulating fasting insulin and glucose have been linked to the development of this common malignancy. Findings from previous studies, however, have been inconsistent, and the nature of the associations is unclear.
    Methods: We conducted Mendelian randomization analyses to evaluate the association of breast cancer risk, using genetic instruments, with fasting insulin, fasting glucose, 2-h glucose, body mass index (BMI) and BMI-adjusted waist-hip-ratio (WHRadj BMI). We first confirmed the association of these instruments with type 2 diabetes risk in a large diabetes genome-wide association study consortium. We then investigated their associations with breast cancer risk using individual-level data obtained from 98 842 cases and 83 464 controls of European descent in the Breast Cancer Association Consortium.
    Results: All sets of instruments were associated with risk of type 2 diabetes. Associations with breast cancer risk were found for genetically predicted fasting insulin [odds ratio (OR) = 1.71 per standard deviation (SD) increase, 95% confidence interval (CI) = 1.26-2.31, p  =  5.09  ×  10-4], 2-h glucose (OR = 1.80 per SD increase, 95% CI = 1.3 0-2.49, p  =  4.02  ×  10-4), BMI (OR = 0.70 per 5-unit increase, 95% CI = 0.65-0.76, p  =  5.05  ×  10-19) and WHRadj BMI (OR = 0.85, 95% CI = 0.79-0.91, p  =  9.22  ×  10-6). Stratified analyses showed that genetically predicted fasting insulin was more closely related to risk of estrogen-receptor [ER]-positive cancer, whereas the associations with instruments of 2-h glucose, BMI and WHRadj BMI were consistent regardless of age, menopausal status, estrogen receptor status and family history of breast cancer.
    Conclusions: We confirmed the previously reported inverse association of genetically predicted BMI with breast cancer risk, and showed a positive association of genetically predicted fasting insulin and 2-h glucose and an inverse association of WHRadj BMI with breast cancer risk. Our study suggests that genetically determined obesity and glucose/insulin-related traits have an important role in the aetiology of breast cancer.
    MeSH term(s) Adult ; Aged ; Blood Glucose/genetics ; Body Mass Index ; Breast Neoplasms/epidemiology ; Diabetes Mellitus, Type 2/epidemiology ; Female ; Humans ; Insulin/blood ; Insulin/genetics ; Mendelian Randomization Analysis ; Middle Aged ; Obesity/genetics ; Obesity, Abdominal/genetics ; Waist-Hip Ratio
    Chemical Substances Blood Glucose ; Insulin
    Language English
    Publishing date 2018-10-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187909-1
    ISSN 1464-3685 ; 0300-5771
    ISSN (online) 1464-3685
    ISSN 0300-5771
    DOI 10.1093/ije/dyy201
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  9. Article ; Online: A Mendelian randomization analysis of circulating lipid traits and breast cancer risk.

    Beeghly-Fadiel, Alicia / Khankari, Nikhil K / Delahanty, Ryan J / Shu, Xiao-Ou / Lu, Yingchang / Schmidt, Marjanka K / Bolla, Manjeet K / Michailidou, Kyriaki / Wang, Qin / Dennis, Joe / Yannoukakos, Drakoulis / Dunning, Alison M / Pharoah, Paul D P / Chenevix-Trench, Georgia / Milne, Roger L / Hunter, David J / Per, Hall / Kraft, Peter / Simard, Jacques /
    Easton, Douglas F / Zheng, Wei

    International journal of epidemiology

    2019  Volume 49, Issue 4, Page(s) 1117–1131

    Abstract: Background: Conventional epidemiologic studies have evaluated associations between circulating lipid levels and breast cancer risk, but results have been inconsistent. As Mendelian randomization analyses may provide evidence for causal inference, we ... ...

    Abstract Background: Conventional epidemiologic studies have evaluated associations between circulating lipid levels and breast cancer risk, but results have been inconsistent. As Mendelian randomization analyses may provide evidence for causal inference, we sought to evaluate potentially unbiased associations between breast cancer risk and four genetically predicted lipid traits.
    Methods: Previous genome-wide association studies (GWAS) have identified 164 discrete variants associated with high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), triglycerides and total cholesterol. We used 162 of these unique variants to construct weighted genetic scores (wGSs) for a total of 101 424 breast cancer cases and 80 253 controls of European ancestry from the Breast Cancer Association Consortium (BCAC). Unconditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for associations between per standard deviation increase in genetically predicted lipid traits and breast cancer risk. Additional Mendelian randomization analysis approaches and sensitivity analyses were conducted to assess pleiotropy and instrument validity.
    Results: Corresponding to approximately 15 mg/dL, one standard deviation increase in genetically predicted HDL-C was associated with a 12% increased breast cancer risk (OR: 1.12, 95% CI: 1.08-1.16). Findings were consistent after adjustment for breast cancer risk factors and were robust in several sensitivity analyses. Associations with genetically predicted triglycerides and total cholesterol were inconsistent, and no association for genetically predicted LDL-C was observed.
    Conclusions: This study provides strong evidence that circulating HDL-C may be associated with an increased risk of breast cancer, whereas LDL-C may not be related to breast cancer risk.
    MeSH term(s) Breast Neoplasms/epidemiology ; Breast Neoplasms/genetics ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Lipids ; Mendelian Randomization Analysis ; Polymorphism, Single Nucleotide ; Risk Factors ; Triglycerides
    Chemical Substances Lipids ; Triglycerides
    Language English
    Publishing date 2019-12-23
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 187909-1
    ISSN 1464-3685 ; 0300-5771
    ISSN (online) 1464-3685
    ISSN 0300-5771
    DOI 10.1093/ije/dyz242
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  10. Article ; Online: Author Correction: Exome sequencing identifies breast cancer susceptibility genes and defines the contribution of coding variants to breast cancer risk.

    Wilcox, Naomi / Dumont, Martine / González-Neira, Anna / Carvalho, Sara / Joly Beauparlant, Charles / Crotti, Marco / Luccarini, Craig / Soucy, Penny / Dubois, Stéphane / Nuñez-Torres, Rocio / Pita, Guillermo / Gardner, Eugene J / Dennis, Joe / Alonso, M Rosario / Álvarez, Nuria / Baynes, Caroline / Collin-Deschesnes, Annie Claude / Desjardins, Sylvie / Becher, Heiko /
    Behrens, Sabine / Bolla, Manjeet K / Castelao, Jose E / Chang-Claude, Jenny / Cornelissen, Sten / Dörk, Thilo / Engel, Christoph / Gago-Dominguez, Manuela / Guénel, Pascal / Hadjisavvas, Andreas / Hahnen, Eric / Hartman, Mikael / Herráez, Belén / Jung, Audrey / Keeman, Renske / Kiechle, Marion / Li, Jingmei / Loizidou, Maria A / Lush, Michael / Michailidou, Kyriaki / Panayiotidis, Mihalis I / Sim, Xueling / Teo, Soo Hwang / Tyrer, Jonathan P / van der Kolk, Lizet E / Wahlström, Cecilia / Wang, Qin / Perry, John R B / Benitez, Javier / Schmidt, Marjanka K / Schmutzler, Rita K / Pharoah, Paul D P / Droit, Arnaud / Dunning, Alison M / Kvist, Anders / Devilee, Peter / Easton, Douglas F / Simard, Jacques

    Nature genetics

    2023  Volume 55, Issue 11, Page(s) 2009

    Language English
    Publishing date 2023-09-26
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/s41588-023-01549-x
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