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Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies
Accumulating evidences have indicated that the functional -94 ins/del ATTG polymorphism in the promoter region of human nuclear factor-kappa B1 (NFKB1) gene may be associated with cancer risk. However, some studies yielded conflicting results. To clarify precise association, we performed a comprehen...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4957149/ https://www.ncbi.nlm.nih.gov/pubmed/27443693 http://dx.doi.org/10.1038/srep30220 |
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author | Wang, Duan Xie, Tianhang Xu, Jin Wang, Haoyang Zeng, Weinan Rao, Shuquan Zhou, Kai Pei, Fuxing Zhou, Zongke |
author_facet | Wang, Duan Xie, Tianhang Xu, Jin Wang, Haoyang Zeng, Weinan Rao, Shuquan Zhou, Kai Pei, Fuxing Zhou, Zongke |
author_sort | Wang, Duan |
collection | PubMed |
description | Accumulating evidences have indicated that the functional -94 ins/del ATTG polymorphism in the promoter region of human nuclear factor-kappa B1 (NFKB1) gene may be associated with cancer risk. However, some studies yielded conflicting results. To clarify precise association, we performed a comprehensive meta-analysis of 42 case-control studies involving 43,000 subjects (18,222 cases and 24,778 controls). The overall results suggested that the -94 ins/del ATTG polymorphism had a decreased risk for cancer, reaching significant levels in five genetic models (dominant model: OR = 0.86, 95% CI = 0.79–0.95, P = 0.002; recessive model: OR = 0.84, 95% CI = 0.74–0.94, P = 0.003; homozygous model: OR = 0.77, 95% CI = 0.66–0.90, P = 0.001; heterozygous model: OR = 0.90, 95% CI = 0.83–0.98, P = 0.011; allelic model: OR = 0.89, 95% CI = 0.83–0.96, P = 0.002). Furthermore, the -94 ins/del ATTG polymorphism could confer a decreased or increased risk for cancer development among Asians and Caucasians, respectively. Additionally, the stratification analysis revealed a significant association between the variant and decreased risk of oral, ovarian, and nasopharyngeal cancer in Asians. After we adjusted p values using the Benjamini-Hochberg false discovery rate method to account for multiple comparisons, these associations remained. |
format | Online Article Text |
id | pubmed-4957149 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-49571492016-07-26 Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies Wang, Duan Xie, Tianhang Xu, Jin Wang, Haoyang Zeng, Weinan Rao, Shuquan Zhou, Kai Pei, Fuxing Zhou, Zongke Sci Rep Article Accumulating evidences have indicated that the functional -94 ins/del ATTG polymorphism in the promoter region of human nuclear factor-kappa B1 (NFKB1) gene may be associated with cancer risk. However, some studies yielded conflicting results. To clarify precise association, we performed a comprehensive meta-analysis of 42 case-control studies involving 43,000 subjects (18,222 cases and 24,778 controls). The overall results suggested that the -94 ins/del ATTG polymorphism had a decreased risk for cancer, reaching significant levels in five genetic models (dominant model: OR = 0.86, 95% CI = 0.79–0.95, P = 0.002; recessive model: OR = 0.84, 95% CI = 0.74–0.94, P = 0.003; homozygous model: OR = 0.77, 95% CI = 0.66–0.90, P = 0.001; heterozygous model: OR = 0.90, 95% CI = 0.83–0.98, P = 0.011; allelic model: OR = 0.89, 95% CI = 0.83–0.96, P = 0.002). Furthermore, the -94 ins/del ATTG polymorphism could confer a decreased or increased risk for cancer development among Asians and Caucasians, respectively. Additionally, the stratification analysis revealed a significant association between the variant and decreased risk of oral, ovarian, and nasopharyngeal cancer in Asians. After we adjusted p values using the Benjamini-Hochberg false discovery rate method to account for multiple comparisons, these associations remained. Nature Publishing Group 2016-07-22 /pmc/articles/PMC4957149/ /pubmed/27443693 http://dx.doi.org/10.1038/srep30220 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Wang, Duan Xie, Tianhang Xu, Jin Wang, Haoyang Zeng, Weinan Rao, Shuquan Zhou, Kai Pei, Fuxing Zhou, Zongke Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies |
title | Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies |
title_full | Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies |
title_fullStr | Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies |
title_full_unstemmed | Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies |
title_short | Genetic association between NFKB1 −94 ins/del ATTG Promoter Polymorphism and cancer risk: a meta-analysis of 42 case-control studies |
title_sort | genetic association between nfkb1 −94 ins/del attg promoter polymorphism and cancer risk: a meta-analysis of 42 case-control studies |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4957149/ https://www.ncbi.nlm.nih.gov/pubmed/27443693 http://dx.doi.org/10.1038/srep30220 |
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