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Updated analysis of vitamin D receptor gene FokI polymorphism and prostate cancer susceptibility
INTRODUCTION: Polymorphisms of the vitamin D receptor (VDR) gene have been investigated in various case-control studies to evaluate prostate cancer susceptibility; however, published data on the association between vitamin D receptor gene FokI polymorphism and prostate cancer risk are inconclusive....
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Termedia Publishing House
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5701687/ https://www.ncbi.nlm.nih.gov/pubmed/29181077 http://dx.doi.org/10.5114/aoms.2016.61793 |
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author | Mi, Yuan-Yuan Chen, Yang-Zhi Chen, Jing Zhang, Li-Feng Zuo, Li Zou, Jian-Gang |
author_facet | Mi, Yuan-Yuan Chen, Yang-Zhi Chen, Jing Zhang, Li-Feng Zuo, Li Zou, Jian-Gang |
author_sort | Mi, Yuan-Yuan |
collection | PubMed |
description | INTRODUCTION: Polymorphisms of the vitamin D receptor (VDR) gene have been investigated in various case-control studies to evaluate prostate cancer susceptibility; however, published data on the association between vitamin D receptor gene FokI polymorphism and prostate cancer risk are inconclusive. MATERIAL AND METHODS: To assess the impact of vitamin D receptor gene FokI polymorphism, we performed a meta-analysis of eligible studies including 9,720 patients and 9,710 control subjects. RESULTS: The overall results indicated no obvious association of this variant on prostate cancer risk. However, in subgroup analysis by ethnicity, positive associations existed in Caucasian descendents for allelic contrast (OR = 1.03, 95% CI: 1.00–1.06, p(heterogeneity) = 0.552, p = 0.026) and the dominant genetic model (OR = 1.03, 95% CI: 1.00–1.05, p(heterogeneity) = 0.856, p = 0.032). In the subgroup analysis by tumor stage, there was a significant association between this variant and advanced prostate cancer under the recessive genetic model (OR = 1.15, 95% CI: 1.01–1.32, p(heterogeneity) = 0.469, p = 0.032). In the subgroup analysis by source of control, association of the VDR FokI polymorphism and prostate cancer susceptibility was also found in population-based studies under homozygote comparison and the recessive genetic model. CONCLUSIONS: The VDR FokI polymorphism may contribute to the risk of developing prostate cancer in Caucasian and population-based studies. Further large, well-designed studies are warranted to confirm this conclusion in more detail. |
format | Online Article Text |
id | pubmed-5701687 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Termedia Publishing House |
record_format | MEDLINE/PubMed |
spelling | pubmed-57016872017-11-27 Updated analysis of vitamin D receptor gene FokI polymorphism and prostate cancer susceptibility Mi, Yuan-Yuan Chen, Yang-Zhi Chen, Jing Zhang, Li-Feng Zuo, Li Zou, Jian-Gang Arch Med Sci Clinical Research INTRODUCTION: Polymorphisms of the vitamin D receptor (VDR) gene have been investigated in various case-control studies to evaluate prostate cancer susceptibility; however, published data on the association between vitamin D receptor gene FokI polymorphism and prostate cancer risk are inconclusive. MATERIAL AND METHODS: To assess the impact of vitamin D receptor gene FokI polymorphism, we performed a meta-analysis of eligible studies including 9,720 patients and 9,710 control subjects. RESULTS: The overall results indicated no obvious association of this variant on prostate cancer risk. However, in subgroup analysis by ethnicity, positive associations existed in Caucasian descendents for allelic contrast (OR = 1.03, 95% CI: 1.00–1.06, p(heterogeneity) = 0.552, p = 0.026) and the dominant genetic model (OR = 1.03, 95% CI: 1.00–1.05, p(heterogeneity) = 0.856, p = 0.032). In the subgroup analysis by tumor stage, there was a significant association between this variant and advanced prostate cancer under the recessive genetic model (OR = 1.15, 95% CI: 1.01–1.32, p(heterogeneity) = 0.469, p = 0.032). In the subgroup analysis by source of control, association of the VDR FokI polymorphism and prostate cancer susceptibility was also found in population-based studies under homozygote comparison and the recessive genetic model. CONCLUSIONS: The VDR FokI polymorphism may contribute to the risk of developing prostate cancer in Caucasian and population-based studies. Further large, well-designed studies are warranted to confirm this conclusion in more detail. Termedia Publishing House 2016-08-16 2017-10 /pmc/articles/PMC5701687/ /pubmed/29181077 http://dx.doi.org/10.5114/aoms.2016.61793 Text en Copyright: © 2016 Termedia & Banach http://creativecommons.org/licenses/by-nc-sa/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license. |
spellingShingle | Clinical Research Mi, Yuan-Yuan Chen, Yang-Zhi Chen, Jing Zhang, Li-Feng Zuo, Li Zou, Jian-Gang Updated analysis of vitamin D receptor gene FokI polymorphism and prostate cancer susceptibility |
title | Updated analysis of vitamin D receptor gene FokI polymorphism and prostate cancer susceptibility |
title_full | Updated analysis of vitamin D receptor gene FokI polymorphism and prostate cancer susceptibility |
title_fullStr | Updated analysis of vitamin D receptor gene FokI polymorphism and prostate cancer susceptibility |
title_full_unstemmed | Updated analysis of vitamin D receptor gene FokI polymorphism and prostate cancer susceptibility |
title_short | Updated analysis of vitamin D receptor gene FokI polymorphism and prostate cancer susceptibility |
title_sort | updated analysis of vitamin d receptor gene foki polymorphism and prostate cancer susceptibility |
topic | Clinical Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5701687/ https://www.ncbi.nlm.nih.gov/pubmed/29181077 http://dx.doi.org/10.5114/aoms.2016.61793 |
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