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Vitamin D-related gene polymorphisms, plasma 25-hydroxyvitamin D, and breast cancer risk.
Cancer Causes Control. 2015 Feb; 26(2):187-203.CC

Abstract

PURPOSE

Studies of vitamin D-pathway genetic variants in relation to cancer risk have been inconsistent. We examined the associations between vitamin D-related genetic polymorphisms, plasma 25-hydroxyvitamin D [25(OH)D], and breast cancer risk.

METHODS

In a population-based case-control study of 967 incident breast cancer cases and 993 controls, we genotyped 25 polymorphisms encoding the vitamin D receptor (VDR) gene, 1α-hydroxylase (CYP27B1), 24-hydroxylase (CYP24A1), and vitamin D-binding protein (GC) and measured plasma 25(OH)D. We used multivariable logistic regression to estimate adjusted odds ratios (ORs) and 95 % confidence intervals (CIs).

RESULTS

Among CYP24A1 polymorphisms, rs6068816 was associated with a 72 % reduction in breast cancer risk (TT vs. CC, OR 0.28, 95 % CI 0.10-0.76; p trend = 0.01), but for rs13038432, the 46 % decrease included the null value (GG vs. AA, OR 0.54, 95 % CI 0.17-1.67; p trend = 0.03). Increased risk that included the null value was noted for CYP24A1 rs3787557 (CC vs. TT, OR 1.34, 95 % CI 0.92-1.89). The VDR polymorphism, TaqI (rs731236), was associated with a 26 % risk reduction (TT vs. CC, OR 0.74, 95 % CI 0.56-0.98; p trend = 0.01). For other polymorphisms, ORs were weak and included the null value. The inverse association for plasma 25(OH)D with breast cancer was more pronounced (OR 0.43, 95 % CI 0.27-0.68) among women with the common allele for CYP24A1, rs927650 (p for interaction on a multiplicative scale = 0.01).

CONCLUSION

Breast cancer risk may be associated with specific vitamin D-related polymorphisms, particularly CYP24A1. Genetic variation in the vitamin D pathway should be considered when designing potential intervention strategies with vitamin D supplementation.

Authors+Show Affiliations

Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 W 168th St, 7th Floor, New York, NY, 10032, USA. llr2124@columbia.edu.Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 W 168th St, 7th Floor, New York, NY, 10032, USA. Department of Medicine, Columbia University, New York, NY, USA. Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY, USA.Department of Nutrition, University of North Carolina, Chapel Hill, NC, USA.Department of Environmental Health, Columbia University, New York, NY, USA. Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY, USA.Department of Epidemiology and Biostatistics, University of South Carolina, Columbia, SC, USA.Department of Environmental Health, Columbia University, New York, NY, USA.Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 W 168th St, 7th Floor, New York, NY, 10032, USA. Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY, USA.Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 W 168th St, 7th Floor, New York, NY, 10032, USA. Department of Medicine, Columbia University, New York, NY, USA. Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY, USA.Department of Medicine, Columbia University, New York, NY, USA.Department of Medicine, Columbia University, New York, NY, USA.Department of Medicine, Columbia University, New York, NY, USA.Department of Preventive Medicine, Mt. Sinai School of Medicine, New York, NY, USA.Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 W 168th St, 7th Floor, New York, NY, 10032, USA. Department of Medicine, Columbia University, New York, NY, USA. Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY, USA.Department of Epidemiology, University of North Carolina, Chapel Hill, NC, USA.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25421379

Citation

Reimers, Laura L., et al. "Vitamin D-related Gene Polymorphisms, Plasma 25-hydroxyvitamin D, and Breast Cancer Risk." Cancer Causes & Control : CCC, vol. 26, no. 2, 2015, pp. 187-203.
Reimers LL, Crew KD, Bradshaw PT, et al. Vitamin D-related gene polymorphisms, plasma 25-hydroxyvitamin D, and breast cancer risk. Cancer Causes Control. 2015;26(2):187-203.
Reimers, L. L., Crew, K. D., Bradshaw, P. T., Santella, R. M., Steck, S. E., Sirosh, I., Terry, M. B., Hershman, D. L., Shane, E., Cremers, S., Dworakowski, E., Teitelbaum, S. L., Neugut, A. I., & Gammon, M. D. (2015). Vitamin D-related gene polymorphisms, plasma 25-hydroxyvitamin D, and breast cancer risk. Cancer Causes & Control : CCC, 26(2), 187-203. https://doi.org/10.1007/s10552-014-0497-9
Reimers LL, et al. Vitamin D-related Gene Polymorphisms, Plasma 25-hydroxyvitamin D, and Breast Cancer Risk. Cancer Causes Control. 2015;26(2):187-203. PubMed PMID: 25421379.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vitamin D-related gene polymorphisms, plasma 25-hydroxyvitamin D, and breast cancer risk. AU - Reimers,Laura L, AU - Crew,Katherine D, AU - Bradshaw,Patrick T, AU - Santella,Regina M, AU - Steck,Susan E, AU - Sirosh,Iryna, AU - Terry,Mary Beth, AU - Hershman,Dawn L, AU - Shane,Elizabeth, AU - Cremers,Serge, AU - Dworakowski,Elzbieta, AU - Teitelbaum,Susan L, AU - Neugut,Alfred I, AU - Gammon,Marilie D, Y1 - 2014/11/25/ PY - 2014/05/20/received PY - 2014/11/13/accepted PY - 2014/11/26/entrez PY - 2014/11/26/pubmed PY - 2016/3/30/medline SP - 187 EP - 203 JF - Cancer causes & control : CCC JO - Cancer Causes Control VL - 26 IS - 2 N2 - PURPOSE: Studies of vitamin D-pathway genetic variants in relation to cancer risk have been inconsistent. We examined the associations between vitamin D-related genetic polymorphisms, plasma 25-hydroxyvitamin D [25(OH)D], and breast cancer risk. METHODS: In a population-based case-control study of 967 incident breast cancer cases and 993 controls, we genotyped 25 polymorphisms encoding the vitamin D receptor (VDR) gene, 1α-hydroxylase (CYP27B1), 24-hydroxylase (CYP24A1), and vitamin D-binding protein (GC) and measured plasma 25(OH)D. We used multivariable logistic regression to estimate adjusted odds ratios (ORs) and 95 % confidence intervals (CIs). RESULTS: Among CYP24A1 polymorphisms, rs6068816 was associated with a 72 % reduction in breast cancer risk (TT vs. CC, OR 0.28, 95 % CI 0.10-0.76; p trend = 0.01), but for rs13038432, the 46 % decrease included the null value (GG vs. AA, OR 0.54, 95 % CI 0.17-1.67; p trend = 0.03). Increased risk that included the null value was noted for CYP24A1 rs3787557 (CC vs. TT, OR 1.34, 95 % CI 0.92-1.89). The VDR polymorphism, TaqI (rs731236), was associated with a 26 % risk reduction (TT vs. CC, OR 0.74, 95 % CI 0.56-0.98; p trend = 0.01). For other polymorphisms, ORs were weak and included the null value. The inverse association for plasma 25(OH)D with breast cancer was more pronounced (OR 0.43, 95 % CI 0.27-0.68) among women with the common allele for CYP24A1, rs927650 (p for interaction on a multiplicative scale = 0.01). CONCLUSION: Breast cancer risk may be associated with specific vitamin D-related polymorphisms, particularly CYP24A1. Genetic variation in the vitamin D pathway should be considered when designing potential intervention strategies with vitamin D supplementation. SN - 1573-7225 UR - https://www.unboundmedicine.com/medline/citation/25421379/Vitamin_D_related_gene_polymorphisms_plasma_25_hydroxyvitamin_D_and_breast_cancer_risk_ L2 - https://doi.org/10.1007/s10552-014-0497-9 DB - PRIME DP - Unbound Medicine ER -