#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

The relationship between circulating lipids and breast cancer risk: A Mendelian randomization study


Autoři: Kelsey E. Johnson aff001;  Katherine M. Siewert aff002;  Derek Klarin aff003;  Scott M. Damrauer aff006;  ;  Kyong-Mi Chang aff006;  Philip S. Tsao aff009;  Themistocles L. Assimes aff009;  Kara N. Maxwell aff008;  Benjamin F. Voight aff006
Působiště autorů: Cell and Molecular Biology Graduate Group, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States of America aff001;  Genomics and Computational Biology Graduate Group, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, United States of America aff002;  Boston VA Healthcare System, Boston, Massachusetts, United States of America aff003;  Center for Genomic Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States of America aff004;  Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, United States of America aff005;  Corporal Michael Crescenz VA Medical Center, Philadelphia, Pennsylvania, United States of America aff006;  Department of Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America aff007;  Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America aff008;  VA Palo Alto Health Care System, Palo Alto, California, United States of America aff009;  Department of Medicine, Stanford University School of Medicine, Stanford, California, United States of America aff010;  Department of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America aff011;  Department of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America aff012;  Institute for Translational Medicine and Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America aff013
Vyšlo v časopise: The relationship between circulating lipids and breast cancer risk: A Mendelian randomization study. PLoS Med 17(9): e32767. doi:10.1371/journal.pmed.1003302
Kategorie: Research Article
doi: https://doi.org/10.1371/journal.pmed.1003302

Souhrn

Background

A number of epidemiological and genetic studies have attempted to determine whether levels of circulating lipids are associated with risks of various cancers, including breast cancer (BC). However, it remains unclear whether a causal relationship exists between lipids and BC. If alteration of lipid levels also reduced risk of BC, this could present a target for disease prevention. This study aimed to assess a potential causal relationship between genetic variants associated with plasma lipid traits (high-density lipoprotein, HDL; low-density lipoprotein, LDL; triglycerides, TGs) with risk for BC using Mendelian randomization (MR).

Methods and findings

Data from genome-wide association studies in up to 215,551 participants from the Million Veteran Program (MVP) were used to construct genetic instruments for plasma lipid traits. The effect of these instruments on BC risk was evaluated using genetic data from the BCAC (Breast Cancer Association Consortium) based on 122,977 BC cases and 105,974 controls. Using MR, we observed that a 1-standard–deviation genetically determined increase in HDL levels is associated with an increased risk for all BCs (HDL: OR [odds ratio] = 1.08, 95% confidence interval [CI] = 1.04–1.13, P < 0.001). Multivariable MR analysis, which adjusted for the effects of LDL, TGs, body mass index (BMI), and age at menarche, corroborated this observation for HDL (OR = 1.06, 95% CI = 1.03–1.10, P = 4.9 × 10−4) and also found a relationship between LDL and BC risk (OR = 1.03, 95% CI = 1.01–1.07, P = 0.02). We did not observe a difference in these relationships when stratified by breast tumor estrogen receptor (ER) status. We repeated this analysis using genetic variants independent of the leading association at core HDL pathway genes and found that these variants were also associated with risk for BCs (OR = 1.11, 95% CI = 1.06–1.16, P = 1.5 × 10−6), including locus-specific associations at ABCA1 (ATP Binding Cassette Subfamily A Member 1), APOE-APOC1-APOC4-APOC2 (Apolipoproteins E, C1, C4, and C2), and CETP (Cholesteryl Ester Transfer Protein). In addition, we found evidence that genetic variation at the ABO locus is associated with both lipid levels and BC. Through multiple statistical approaches, we minimized and tested for the confounding effects of pleiotropy and population stratification on our analysis; however, the possible existence of residual pleiotropy and stratification remains a limitation of this study.

Conclusions

We observed that genetically elevated plasma HDL and LDL levels appear to be associated with increased BC risk. Future studies are required to understand the mechanism underlying this putative causal relationship, with the goal of developing potential therapeutic strategies aimed at altering the cholesterol-mediated effect on BC risk.

Klíčová slova:

Breast cancer – Cancer risk factors – Genetic loci – Genetics – Cholesterol – Lipid analysis – Lipids – Lipoproteins


Zdroje

1. Torre LA, Siegel RL, Ward EM, Jemal A. Global Cancer Incidence and Mortality Rates and Trends—An Update. Cancer Epidemiol Biomarkers Prev. 2016;25: 16–27. doi: 10.1158/1055-9965.EPI-15-0578 26667886

2. Rose D, Gracheck P, Vona-Davis L, Rose DP, Gracheck PJ, Vona-Davis L. The Interactions of Obesity, Inflammation and Insulin Resistance in Breast Cancer. Cancers (Basel). 2015;7: 2147–2168. 26516917

3. Kuzu OF, Noory MA, Robertson GP. The role of cholesterol in cancer. Cancer Research. 2016;76(8): 2063–2070. doi: 10.1158/0008-5472.CAN-15-2613 27197250

4. Touvier M, Fassier P, His M, Norat T, Chan DSM, Blacher J, et al. Cholesterol and breast cancer risk: a systematic review and meta-analysis of prospective studies. Br J Nutr. 2015;114: 347–357. doi: 10.1017/S000711451500183X 26173770

5. Ni H, Liu H, Gao R. Serum Lipids and Breast Cancer Risk: A Meta-Analysis of Prospective Cohort Studies. Singh S, editor. PLoS ONE. 2015;10: e0142669. doi: 10.1371/journal.pone.0142669 26554382

6. Martin LJ, Melnichouk O, Huszti E, Connelly PW, Greenberg CV., Minkin S, et al. Serum Lipids, Lipoproteins, and Risk of Breast Cancer: A Nested Case-Control Study Using Multiple Time Points. JNCI J Natl Cancer Inst. 2015;107: djv032–djv032. doi: 10.1093/jnci/djv032 25817193

7. Zhong S, Zhang X, Chen L, Ma T, Tang J, Zhao J. Statin use and mortality in cancer patients: Systematic review and meta-analysis of observational studies. Cancer Treatment Reviews. 2015;41(6): 554–567. doi: 10.1016/j.ctrv.2015.04.005 25890842

8. Borgquist S, Giobbie-Hurder A, Ahern TP, Garber JE, Colleoni M, Láng I, et al. Cholesterol, Cholesterol-Lowering Medication Use, and Breast Cancer Outcome in the BIG 1–98 Study. J Clin Oncol. 2017;35: 1179–1188. doi: 10.1200/JCO.2016.70.3116 28380313

9. Orho-Melander M, Hindy G, Borgquist S, Schulz C-A, Manjer J, Melander O, et al. Blood lipid genetic scores, the HMGCR gene and cancer risk: a Mendelian randomization study. Int J Epidemiol. 2018;47(2): 495–505. Epub 2017 Nov 20. doi: 10.1093/ije/dyx237 29165714

10. Nowak C, Ärnlöv J. A Mendelian randomization study of the effects of blood lipids on breast cancer risk. Nat Commun. 2018;9(1): 3957. doi: 10.1038/s41467-018-06467-9 30262900

11. Michailidou K, Lindström S, Dennis J, Beesley J, Hui S, Kar S, et al. Association analysis identifies 65 new breast cancer risk loci. Nature. 2017;551: 92–94. doi: 10.1038/nature24284 29059683

12. Global Lipids Genetics Consortium, Willer CJ, Schmidt EM, Sengupta S, Peloso GM, Gustafsson S, Kanoni S, et al. Discovery and Refinement of Loci Associated with Lipid Levels. Nat Genet. 2013;45: 1274–1283. doi: 10.1038/ng.2797 24097068

13. Qi G, Chatterjee N. Mendelian randomization analysis using mixture models for robust and efficient estimation of causal effects. Nat Commun. 2019;10: 1941. doi: 10.1038/s41467-019-09432-2 31028273

14. Neuhouser ML, Aragaki AK, Prentice RL, Manson JE, Chlebowski R, Carty CL, et al. Overweight, Obesity, and Postmenopausal Invasive Breast Cancer Risk. JAMA Oncol. 2015;1: 611. doi: 10.1001/jamaoncol.2015.1546 26182172

15. Bulik-Sullivan B, Finucane HK, Anttila V, Gusev A, Day FR, Loh PR, et al. An atlas of genetic correlations across human diseases and traits. Nat Genet. 2015;47: 1236–1241. doi: 10.1038/ng.3406 26414676

16. Lindström S, Finucane H, Bulik-Sullivan B, Schumacher FR, Amos CI, Hung RJ, et al. Quantifying the genetic correlation between multiple cancer types. Cancer Epidemiol Biomarkers Prev. 2017;26: 1427–1435. doi: 10.1158/1055-9965.EPI-17-0211 28637796

17. Day FR, Thompson DJ, Helgason H, Chasman DI, Finucane H, Sulem P, et al. Genomic analyses identify hundreds of variants associated with age at menarche and support a role for puberty timing in cancer risk. Nat Genet. 2017;49: 834–841. doi: 10.1038/ng.3841 28436984

18. Burgess S, Thompson DJ, Rees JMB, Day FR, Perry JR, Ong KK. Dissecting causal pathways using mendelian randomization with summarized genetic data: Application to age at menarche and risk of breast cancer. Genetics. 2017;207: 481–487. doi: 10.1534/genetics.117.300191 28835472

19. Feng Y, Hong X, Wilker E, Li Z, Zhang W, Jin D, et al. Effects of age at menarche, reproductive years, and menopause on metabolic risk factors for cardiovascular diseases. Atherosclerosis. 2008;196: 590–597. doi: 10.1016/j.atherosclerosis.2007.06.016 17675039

20. Hamajima N, Hirose K, Tajima K, Rohan T, Friedenreich CM, Calle EE, et al. Menarche, menopause, and breast cancer risk: Individual participant meta-analysis, including 118 964 women with breast cancer from 117 epidemiological studies. Lancet Oncol. 2012;13: 1141–1151. doi: 10.1016/S1470-2045(12)70425-4 23084519

21. Jiang X, Finucane HK, Schumacher FR, Schmit SL, Tyrer JP, Han Y, et al. Shared heritability and functional enrichment across six solid cancers. Nat Commun. 2019;10: 431. doi: 10.1038/s41467-018-08054-4 30683880

22. Klarin D, Damrauer SM, Cho K, Sun Y V., Teslovich TM, Honerlaw J, et al. Genetics of blood lipids among ~300,000 multi-ethnic participants of the Million Veteran Program. Nat Genet. 2018;50: 1514–1523. doi: 10.1038/s41588-018-0222-9 30275531

23. Yengo L, Sidorenko J, Kemper KE, Zheng Z, Wood AR, Weedon MN, et al. Meta-analysis of genome-wide association studies for height and body mass index in ~700000 individuals of European ancestry. Hum Mol Genet. 2018;27: 3641–3649. doi: 10.1093/hmg/ddy271 30124842

24. Purcell S, Neale B, Todd-Brown K, Thomas L, Ferreira MAR, Bender D, et al. PLINK: A Tool Set for Whole-Genome Association and Population-Based Linkage Analyses. Am J Hum Genet. 2007;81: 559–575. doi: 10.1086/519795 17701901

25. Hemani G, Zheng J, Elsworth B, Wade KH, Haberland V, Baird D, et al. The MR-Base platform supports systematic causal inference across the human phenome. Elife. 2018;7: e34408. doi: 10.7554/eLife.34408 29846171

26. Bowden J, Davey Smith G, Burgess S. Mendelian randomization with invalid instruments: effect estimation and bias detection through Egger regression. Int J Epidemiol. 2015;44: 512–525. doi: 10.1093/ije/dyv080 26050253

27. Bowden J, Davey Smith G, Haycock PC, Burgess S. Consistent Estimation in Mendelian Randomization with Some Invalid Instruments Using a Weighted Median Estimator. Genet Epidemiol. 2016;40: 304–314. doi: 10.1002/gepi.21965 27061298

28. Hartwig FP, Smith GD, Bowden J. Robust inference in summary data Mendelian randomization via the zero modal pleiotropy assumption. Int J Epidemiol. 2017;46(6): 1985–1998. doi: 10.1093/ije/dyx102 29040600

29. Walter K, Min JL, Huang J, Crooks L, Memari Y, McCarthy S, et al. The UK10K project identifies rare variants in health and disease. Nature. 2015;526: 82–90. doi: 10.1038/nature14962 26367797

30. Voight BF. MR-predictor: A simulation engine for Mendelian Randomization studies. Bioinformatics. 2014;30: 3432–3434. doi: 10.1093/bioinformatics/btu564 25165093

31. Burgess S. Sample size and power calculations in Mendelian randomization with a single instrumental variable and a binary outcome. Int J Epidemiol. 2014;43: 922–929. doi: 10.1093/ije/dyu005 24608958

32. Burgess S, Thompson SG. Multivariable Mendelian randomization: The use of pleiotropic genetic variants to estimate causal effects. Am J Epidemiol. 2015;181: 251–260. doi: 10.1093/aje/kwu283 25632051

33. Burgess S, Dudbridge F, Thompson SG. Re: “Multivariable Mendelian randomization: The use of pleiotropic genetic variants to estimate causal effects.” Am J Epidemiol. 2015;181: 290–291. doi: 10.1093/aje/kwv017 25660081

34. Sanderson E, Davey Smith G, Windmeijer F, Bowden J. An examination of multivariable Mendelian randomization in the single-sample and two-sample summary data settings. Int J Epidemiol. 2019;48: 713–727. doi: 10.1093/ije/dyy262 30535378

35. Schwarzer G. meta: An R package for meta-analysis. R News. 2007;7: 40–45.

36. Shi H, Mancuso N, Spendlove S, Pasaniuc B. Local Genetic Correlation Gives Insights into the Shared Genetic Architecture of Complex Traits. Am J Hum Genet. 2017;101: 737–751. doi: 10.1016/j.ajhg.2017.09.022 29100087

37. Berisa T, Pickrell JK. Approximately independent linkage disequilibrium blocks in human populations. Bioinformatics. 2016;32: 283–5. doi: 10.1093/bioinformatics/btv546 26395773

38. The GTEx Consortium, Aguet F, Ardlie KG, Cummings BB, Gelfand ET, Getz G, et al. Genetic effects on gene expression across human tissues. Nature. 2017;550: 204–213. doi: 10.1038/nature24277 29022597

39. von Elm E, Altman DG, Egger M, Pocock SJ, Gøtzsche PC, Vandenbroucke JP. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) Statement: Guidelines for Reporting Observational Studies. PLoS Med. 2007;4: e296. doi: 10.1371/journal.pmed.0040296 17941714

40. Davey Smith G, Davies N, Dimou N, Egger M, Gallo V, Golub R, et al. STROBE-MR: Guidelines for strengthening the reporting of Mendelian randomization studies. PeerJ Preprints 27857 [Preprint]. 2019 [cited 2020 May 18]. https://peerj.com/preprints/27857/

41. Pickrell JK, Berisa T, Liu JZ, Ségurel L, Tung JY, Hinds DA. Detection and interpretation of shared genetic influences on 42 human traits. Nat Genet. 2016;48: 709–717. doi: 10.1038/ng.3570 27182965

42. Hemani G, Tilling K, Davey Smith G. Orienting the causal relationship between imprecisely measured traits using GWAS summary data. Li J, editor. PLoS Genet. 2017;13: e1007081. doi: 10.1371/journal.pgen.1007081 29149188

43. Guo Y, Warren Andersen S, Shu XO, Michailidou K, Bolla MK, Wang Q, et al. Genetically Predicted Body Mass Index and Breast Cancer Risk: Mendelian Randomization Analyses of Data from 145,000 Women of European Descent. PLoS Med. 2016;13. doi: 10.1371/journal.pmed.1002105 27551723

44. Renehan AG, Tyson M, Egger M, Heller RF, Zwahlen M. Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet. 2008;371: 569–78. doi: 10.1016/S0140-6736(08)60269-X 18280327

45. Borgquist S, Butt T, Almgren P, Shiffman D, Stocks T, Orho-Melander M, et al. Apolipoproteins, lipids and risk of cancer. Int J Cancer. 2016;138: 2648–2656. doi: 10.1002/ijc.30013 26804063

46. Melvin JC, Seth D, Holmberg L, Garmo H, Hammar N, Jungner I, et al. Lipid profiles and risk of breast and ovarian cancer in the swedish AMORIS study. Cancer Epidemiol Biomarkers Prev. 2012;21: 1381–1384. doi: 10.1158/1055-9965.EPI-12-0188 22593241

47. Zhang B-L, He N, Huang Y-B, Song F-J, Chen K-X. ABO blood groups and risk of cancer: a systematic review and meta-analysis. Asian Pac J Cancer Prev. 2014;15: 4643–50. doi: 10.7314/apjcp.2014.15.11.4643 24969898

48. Beeghly-Fadiel A, Khankari NK, Delahanty RJ, Shu X-O, Lu Y, Schmidt MK, et al. A Mendelian randomization analysis of circulating lipid traits and breast cancer risk. Int J Epidemiol. Epub 2019 Dec 23. doi: 10.1093/ije/dyz242 31872213

49. Madsen CM, Varbo A, Nordestgaard BG. Extreme high high-density lipoprotein cholesterol is paradoxically associated with high mortality in men and women: two prospective cohort studies. Eur Heart J. 2017;38: 2478–2486. doi: 10.1093/eurheartj/ehx163 28419274

50. Hamer M, O’Donovan G, Stamatakis E. High-Density Lipoprotein Cholesterol and Mortality: Too Much of a Good Thing? Arterioscler Thromb Vasc Biol. 2018;38: 669–672. doi: 10.1161/ATVBAHA.117.310587 29326314

51. Burgess S, Davey Smith G. Mendelian Randomization Implicates High-Density Lipoprotein Cholesterol–Associated Mechanisms in Etiology of Age-Related Macular Degeneration. Ophthalmology. 2017;124: 1165–1174. doi: 10.1016/j.ophtha.2017.03.042 28456421

52. Fan Q, Maranville JC, Fritsche L, Sim X, Cheung CMG, Chen LJ, et al. HDL-cholesterol levels and risk of age-related macular degeneration: a multiethnic genetic study using Mendelian randomization. Int J Epidemiol. 2017;46: 1891–1902. doi: 10.1093/ije/dyx189 29025108

53. Bonovas S, Filioussi K, Tsavaris N, Sitaras NM. Use of Statins and Breast Cancer: A Meta-Analysis of Seven Randomized Clinical Trials and Nine Observational Studies. J Clin Oncol. 2005;23: 8606–8612. doi: 10.1200/JCO.2005.02.7045 16260694

54. Llewellyn-Bennett R, Edwards D, Roberts N, Hainsworth AH, Bulbulia R, Bowman L. Post-trial follow-up methodology in large randomised controlled trials: a systematic review. Trials. 2018;19: 298. doi: 10.1186/s13063-018-2653-0 29843774

55. VanderWeele TJ, Tchetgen Tchetgen EJ, Cornelis M, Kraft P. Methodological challenges in mendelian randomization. Epidemiology. 2014;25: 427–35. doi: 10.1097/EDE.0000000000000081 24681576

56. O’Connor LJ, Price AL. Distinguishing genetic correlation from causation across 52 diseases and complex traits. Nat Genet. 2018;50: 1728–1734. doi: 10.1038/s41588-018-0255-0 30374074

57. Haycock PC, Burgess S, Wade KH, Bowden J, Relton C, Davey Smith G. Best (but oft-forgotten) practices: the design, analysis, and interpretation of Mendelian randomization studies. Am J Clin Nutr. 2016;103: 965–978. doi: 10.3945/ajcn.115.118216 26961927

58. Silvente-Poirot S, Poirot M. Cancer. Cholesterol and cancer, in the balance. Science. 2014;343(6178): 1445–1446. doi: 10.1126/science.1252787 24675946

59. Nelson ER. The significance of cholesterol and its metabolite, 27-hydroxycholesterol in breast cancer. Mol Cell Endocrinol. 2018;466: 73–80. doi: 10.1016/j.mce.2017.09.021 28919300


Článek vyšel v časopise

PLOS Medicine


2020 Číslo 9
Nejčtenější tento týden
Nejčtenější v tomto čísle
Kurzy

Zvyšte si kvalifikaci online z pohodlí domova

Aktuální možnosti diagnostiky a léčby litiáz
nový kurz
Autoři: MUDr. Tomáš Ürge, PhD.

Střevní příprava před kolonoskopií
Autoři: MUDr. Klára Kmochová, Ph.D.

Závislosti moderní doby – digitální závislosti a hypnotika
Autoři: MUDr. Vladimír Kmoch

Aktuální možnosti diagnostiky a léčby AML a MDS nízkého rizika
Autoři: MUDr. Natália Podstavková

Jak diagnostikovat a efektivně léčit CHOPN v roce 2024
Autoři: doc. MUDr. Vladimír Koblížek, Ph.D.

Všechny kurzy
Přihlášení
Zapomenuté heslo

Zadejte e-mailovou adresu, se kterou jste vytvářel(a) účet, budou Vám na ni zaslány informace k nastavení nového hesla.

Přihlášení

Nemáte účet?  Registrujte se

#ADS_BOTTOM_SCRIPTS#