Investigation of the Interplay between Circulating Lipids and IGF-I and Relevance to Breast Cancer Risk: An Observational and Mendelian Randomization Study
Circulating lipids and insulin-like growth factor 1 (IGF-I) have been reliably associated with breast cancer. Observational studies suggest an interplay between lipids and IGF-I, however, whether these relationships are causal and if pathways from these phenotypes to breast cancer overlap is unclear...
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| Vydáno v: | Cancer epidemiology, biomarkers & prevention Ročník 30; číslo 12; s. 2207 |
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| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
01.12.2021
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| ISSN: | 1538-7755, 1538-7755 |
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| Abstract | Circulating lipids and insulin-like growth factor 1 (IGF-I) have been reliably associated with breast cancer. Observational studies suggest an interplay between lipids and IGF-I, however, whether these relationships are causal and if pathways from these phenotypes to breast cancer overlap is unclear.
Mendelian randomization (MR) was conducted to estimate the relationship between lipids or IGF-I and breast cancer risk using genetic summary statistics for lipids (low-density lipoprotein cholesterol, LDL-C; high-density lipoprotein cholesterol, HDL-C; triglycerides, TGs), IGF-I and breast cancer from GLGC/UKBB (
= 239,119), CHARGE/UKBB (
= 252,547), and Breast Cancer Association Consortium (
= 247,173), respectively. Cross-sectional observational and MR analyses were conducted to assess the bi-directional relationship between lipids and IGF-I in SHIP (
= 3,812) and UKBB (
= 422,389), and using genetic summary statistics from GLGC (
= 188,577) and CHARGE/UKBB (
= 469,872).
In multivariable MR (MVMR) analyses, the OR for breast cancer per 1-SD increase in HDL-C and TG was 1.08 [95% confidence interval (CI), 1.04-1.13] and 0.94 (95% CI, 0.89-0.98), respectively. The OR for breast cancer per 1-SD increase in IGF-I was 1.09 (95% CI, 1.04-1.15). MR analyses suggested a bi-directional TG-IGF-I relationship (TG-IGF-I
per 1-SD: -0.13; 95% CI, -0.23 to -0.04; and IGF-I-TG
per 1-SD: -0.11; 95% CI, -0.18 to -0.05). There was little evidence for a causal relationship between HDL-C and LDL-C with IGF-I. In MVMR analyses, associations of TG or IGF-I with breast cancer were robust to adjustment for IGF-I or TG, respectively.
Our findings suggest a causal role of HDL-C, TG, and IGF-I in breast cancer. Observational and MR analyses support an interplay between IGF-I and TG; however, MVMR estimates suggest that TG and IGF-I may act independently to influence breast cancer.
Our findings should be considered in the development of prevention strategies for breast cancer, where interventions are known to modify circulating lipids and IGF-I. |
|---|---|
| AbstractList | Circulating lipids and insulin-like growth factor 1 (IGF-I) have been reliably associated with breast cancer. Observational studies suggest an interplay between lipids and IGF-I, however, whether these relationships are causal and if pathways from these phenotypes to breast cancer overlap is unclear.
Mendelian randomization (MR) was conducted to estimate the relationship between lipids or IGF-I and breast cancer risk using genetic summary statistics for lipids (low-density lipoprotein cholesterol, LDL-C; high-density lipoprotein cholesterol, HDL-C; triglycerides, TGs), IGF-I and breast cancer from GLGC/UKBB (
= 239,119), CHARGE/UKBB (
= 252,547), and Breast Cancer Association Consortium (
= 247,173), respectively. Cross-sectional observational and MR analyses were conducted to assess the bi-directional relationship between lipids and IGF-I in SHIP (
= 3,812) and UKBB (
= 422,389), and using genetic summary statistics from GLGC (
= 188,577) and CHARGE/UKBB (
= 469,872).
In multivariable MR (MVMR) analyses, the OR for breast cancer per 1-SD increase in HDL-C and TG was 1.08 [95% confidence interval (CI), 1.04-1.13] and 0.94 (95% CI, 0.89-0.98), respectively. The OR for breast cancer per 1-SD increase in IGF-I was 1.09 (95% CI, 1.04-1.15). MR analyses suggested a bi-directional TG-IGF-I relationship (TG-IGF-I
per 1-SD: -0.13; 95% CI, -0.23 to -0.04; and IGF-I-TG
per 1-SD: -0.11; 95% CI, -0.18 to -0.05). There was little evidence for a causal relationship between HDL-C and LDL-C with IGF-I. In MVMR analyses, associations of TG or IGF-I with breast cancer were robust to adjustment for IGF-I or TG, respectively.
Our findings suggest a causal role of HDL-C, TG, and IGF-I in breast cancer. Observational and MR analyses support an interplay between IGF-I and TG; however, MVMR estimates suggest that TG and IGF-I may act independently to influence breast cancer.
Our findings should be considered in the development of prevention strategies for breast cancer, where interventions are known to modify circulating lipids and IGF-I. Circulating lipids and insulin-like growth factor 1 (IGF-I) have been reliably associated with breast cancer. Observational studies suggest an interplay between lipids and IGF-I, however, whether these relationships are causal and if pathways from these phenotypes to breast cancer overlap is unclear.BACKGROUNDCirculating lipids and insulin-like growth factor 1 (IGF-I) have been reliably associated with breast cancer. Observational studies suggest an interplay between lipids and IGF-I, however, whether these relationships are causal and if pathways from these phenotypes to breast cancer overlap is unclear.Mendelian randomization (MR) was conducted to estimate the relationship between lipids or IGF-I and breast cancer risk using genetic summary statistics for lipids (low-density lipoprotein cholesterol, LDL-C; high-density lipoprotein cholesterol, HDL-C; triglycerides, TGs), IGF-I and breast cancer from GLGC/UKBB (N = 239,119), CHARGE/UKBB (N = 252,547), and Breast Cancer Association Consortium (N = 247,173), respectively. Cross-sectional observational and MR analyses were conducted to assess the bi-directional relationship between lipids and IGF-I in SHIP (N = 3,812) and UKBB (N = 422,389), and using genetic summary statistics from GLGC (N = 188,577) and CHARGE/UKBB (N = 469,872).METHODSMendelian randomization (MR) was conducted to estimate the relationship between lipids or IGF-I and breast cancer risk using genetic summary statistics for lipids (low-density lipoprotein cholesterol, LDL-C; high-density lipoprotein cholesterol, HDL-C; triglycerides, TGs), IGF-I and breast cancer from GLGC/UKBB (N = 239,119), CHARGE/UKBB (N = 252,547), and Breast Cancer Association Consortium (N = 247,173), respectively. Cross-sectional observational and MR analyses were conducted to assess the bi-directional relationship between lipids and IGF-I in SHIP (N = 3,812) and UKBB (N = 422,389), and using genetic summary statistics from GLGC (N = 188,577) and CHARGE/UKBB (N = 469,872).In multivariable MR (MVMR) analyses, the OR for breast cancer per 1-SD increase in HDL-C and TG was 1.08 [95% confidence interval (CI), 1.04-1.13] and 0.94 (95% CI, 0.89-0.98), respectively. The OR for breast cancer per 1-SD increase in IGF-I was 1.09 (95% CI, 1.04-1.15). MR analyses suggested a bi-directional TG-IGF-I relationship (TG-IGF-I β per 1-SD: -0.13; 95% CI, -0.23 to -0.04; and IGF-I-TG β per 1-SD: -0.11; 95% CI, -0.18 to -0.05). There was little evidence for a causal relationship between HDL-C and LDL-C with IGF-I. In MVMR analyses, associations of TG or IGF-I with breast cancer were robust to adjustment for IGF-I or TG, respectively.RESULTSIn multivariable MR (MVMR) analyses, the OR for breast cancer per 1-SD increase in HDL-C and TG was 1.08 [95% confidence interval (CI), 1.04-1.13] and 0.94 (95% CI, 0.89-0.98), respectively. The OR for breast cancer per 1-SD increase in IGF-I was 1.09 (95% CI, 1.04-1.15). MR analyses suggested a bi-directional TG-IGF-I relationship (TG-IGF-I β per 1-SD: -0.13; 95% CI, -0.23 to -0.04; and IGF-I-TG β per 1-SD: -0.11; 95% CI, -0.18 to -0.05). There was little evidence for a causal relationship between HDL-C and LDL-C with IGF-I. In MVMR analyses, associations of TG or IGF-I with breast cancer were robust to adjustment for IGF-I or TG, respectively.Our findings suggest a causal role of HDL-C, TG, and IGF-I in breast cancer. Observational and MR analyses support an interplay between IGF-I and TG; however, MVMR estimates suggest that TG and IGF-I may act independently to influence breast cancer.CONCLUSIONSOur findings suggest a causal role of HDL-C, TG, and IGF-I in breast cancer. Observational and MR analyses support an interplay between IGF-I and TG; however, MVMR estimates suggest that TG and IGF-I may act independently to influence breast cancer.Our findings should be considered in the development of prevention strategies for breast cancer, where interventions are known to modify circulating lipids and IGF-I.IMPACTOur findings should be considered in the development of prevention strategies for breast cancer, where interventions are known to modify circulating lipids and IGF-I. |
| Author | Bull, Caroline J Dudding, Tom Timpson, Nicholas J Perks, Claire M Rotter, Jerome I Biernacka, Kalina M Friedrich, Nele Teumer, Alexander Sanderson, Eleanor Qi, Qibin Mayerle, Julia Holly, Jeff M P Kaplan, Robert C Tan, Vanessa Y Richardson, Tom G Völker, Uwe Corbin, Laura J |
| Author_xml | – sequence: 1 givenname: Vanessa Y orcidid: 0000-0001-7938-127X surname: Tan fullname: Tan, Vanessa Y organization: Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom – sequence: 2 givenname: Caroline J orcidid: 0000-0002-2176-5120 surname: Bull fullname: Bull, Caroline J organization: Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom – sequence: 3 givenname: Kalina M orcidid: 0000-0001-6344-7449 surname: Biernacka fullname: Biernacka, Kalina M organization: IGFs & Metabolic Endocrinology Group, School of Translational Health Sciences, Learning & Research Building, Southmead Hospital, Bristol, United Kingdom – sequence: 4 givenname: Alexander orcidid: 0000-0002-8309-094X surname: Teumer fullname: Teumer, Alexander organization: Department of Population Medicine and Lifestyle Diseases Prevention, Medical University of Bialystok, Bialystok, Poland – sequence: 5 givenname: Tom G orcidid: 0000-0002-7918-2040 surname: Richardson fullname: Richardson, Tom G organization: Novo Nordisk Research Centre, Headington, Oxford, United Kingdom – sequence: 6 givenname: Eleanor surname: Sanderson fullname: Sanderson, Eleanor organization: Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom – sequence: 7 givenname: Laura J orcidid: 0000-0002-4032-9500 surname: Corbin fullname: Corbin, Laura J organization: Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom – sequence: 8 givenname: Tom orcidid: 0000-0003-3756-040X surname: Dudding fullname: Dudding, Tom organization: Bristol Dental School, University of Bristol, Bristol, United Kingdom – sequence: 9 givenname: Qibin surname: Qi fullname: Qi, Qibin organization: Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York – sequence: 10 givenname: Robert C surname: Kaplan fullname: Kaplan, Robert C organization: Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington – sequence: 11 givenname: Jerome I orcidid: 0000-0001-7191-1723 surname: Rotter fullname: Rotter, Jerome I organization: The Institute for Translational Genomics and Population Sciences, Department of Pediatrics, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, California – sequence: 12 givenname: Nele surname: Friedrich fullname: Friedrich, Nele organization: Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald, Greifswald, Germany – sequence: 13 givenname: Uwe surname: Völker fullname: Völker, Uwe organization: Interfaculty Institute for Genetics and Functional Genomics, University Medicine Greifswald, Greifswald, Germany – sequence: 14 givenname: Julia surname: Mayerle fullname: Mayerle, Julia organization: Department of Medicine II, University Hospital, LMU Munich, Munich, Germany – sequence: 15 givenname: Claire M orcidid: 0000-0003-1562-891X surname: Perks fullname: Perks, Claire M organization: IGFs & Metabolic Endocrinology Group, School of Translational Health Sciences, Learning & Research Building, Southmead Hospital, Bristol, United Kingdom – sequence: 16 givenname: Jeff M P surname: Holly fullname: Holly, Jeff M P organization: IGFs & Metabolic Endocrinology Group, School of Translational Health Sciences, Learning & Research Building, Southmead Hospital, Bristol, United Kingdom – sequence: 17 givenname: Nicholas J surname: Timpson fullname: Timpson, Nicholas J email: N.J.Timpson@bristol.ac.uk organization: Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom |
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| SubjectTerms | Breast Neoplasms - blood Breast Neoplasms - genetics Causality Cholesterol, HDL - blood Cholesterol, LDL - blood Cross-Sectional Studies Female Genome-Wide Association Study Humans Insulin-Like Growth Factor I - genetics Mendelian Randomization Analysis Triglycerides - blood |
| Title | Investigation of the Interplay between Circulating Lipids and IGF-I and Relevance to Breast Cancer Risk: An Observational and Mendelian Randomization Study |
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