ArticleFrontiers in oncology2014
Evidence of differential effects of vitamin d receptor variants on epithelial ovarian cancer risk by predicted vitamin d status.
Article in Frontiers in oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Vitamin D and Ovarian Cancer: Systematic Review of the Literature with a Focus on Molecular Mechanisms.Cells · 2020Pooled it
- The role of vitamin D in ovarian cancer: epidemiology, molecular mechanism and prevention.Journal of ovarian research · 2018Review
- Epidemiology of ovarian cancer: a review.Cancer biology & medicine · 2017Article
- Association of vitamin D levels and risk of ovarian cancer: a Mendelian randomization study.International journal of epidemiology · 2016Article
- Commentary: Vitamin D and Pancreatic Cancer: A Pooled Analysis from the Pancreatic Cancer Case-Control Consortium.Frontiers in oncology · 2015Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
introductionExperimental studies suggest vitamin D inhibits ovarian carcinogenesis. Yet, epidemiologic studies of ovarian cancer risk and lifestyle correlates of vitamin D status, plasma 25-hydroxyvitamin D [25(OH)D], or vitamin D receptor (VDR) variants have been inconsistent.
objectiveTo evaluate VDR genetic associations by high vs. low predicted 25(OH)D, scores derived from known determinants of plasma 25(OH)D. To assess ovarian cancer associations with variants identified in genome-wide association studies (GWAS) of plasma 25(OH)D.
methodsWe genotyped up to seven VDR and eight 25(OH)D GWAS variants in the Nurses' Health Studies (562 cases, 1,553 controls) and New England Case-Control study (1,821 cases, 1,870 controls). We estimated haplotype scores using expectation-maximization-based algorithms. We used unconditional logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CI). We combined study results using DerSimonian and Laird meta-analysis.
resultsOvarian cancer risk increased per A allele of rs7975232 (VDR; OR = 1.12, 95% CI = 1.01-1.25) among all women. When stratified by predicted 25(OH)D, ovarian cancer was associated with rs731236 (VDR; per C allele OR = 1.31) and rs7975232 (OR = 1.38) among women with high predicted 25(OH)D, but not among women with low levels (P ≤ 0.009). We also observed heterogeneity by predicted 25(OH)D for the ovarian cancer association with VDR 3' end haplotypes (P = 0.009). Of 25(OH)D-associated GWAS loci, rs7041 was associated with reduced ovarian cancer risk (per T allele OR = 0.92, 95% CI = 0.85-0.99), which did not differ by predicted 25(OH)D status.
conclusionOur study suggests an influence of VDR 3' end variants on ovarian cancer risk may be observed in women with high predicted 25(OH)D, which remained even after taking multiple comparisons into consideration. Future studies are needed to confirm our results and explore further the relation between vitamin D exposure, genetic variants, and ovarian cancer risk.
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