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      Association of three 8q24 polymorphisms with prostate cancer susceptibility: evidence from a meta-analysis with 50,854 subjects

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          Abstract

          The 8q24 polymorphisms have been implicated in various cancers. Three 8q24 polymorphisms (rs1447295 C>A, rs16901979 C>A, and rs6983267 T>G) have been extensively investigated for their association with prostate cancer (PCa) susceptibility, yet conclusions are contradictory. We conducted a comprehensive meta-analysis to reevaluate the associations between those polymorphisms and PCa susceptibility, according to the latest meta-analysis guidelines (PRISMA). Eligible publications were searched from MEDLINE, EMBASE and CBM. False positive report possibility analysis was performed. We totally collected 20184 cases and 20439 controls from 20 studies for the rs1447295 C>A, 1850 cases and 2090 controls from 7 studies for the rs16901979 C>A, and 12233 cases and 7582 controls from 17 studies for the rs6983267 T>G. Overall, each of studied 8q24 polymorphisms was significantly associated with PCa risk individually. Significant associations were also observed in stratified analysis by ethnicity, source of control, and quality score. Interestingly, the effect of rs1447295 on PCa risk was observed among Caucasians and Asians, but not Africa-Americans. The effect of rs16901979 was more prominent among Africa-Americans than Asians. Likewise, rs6983267 conferred a higher Pca risk among Caucasians than Asians. Collectively, these 8q24 variant(s) may modulate PCa risk in an ethnic-specific manner.

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          Most cited references 39

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          Genome-wide association study identifies five new breast cancer susceptibility loci.

          Breast cancer is the most common cancer in women in developed countries. To identify common breast cancer susceptibility alleles, we conducted a genome-wide association study in which 582,886 SNPs were genotyped in 3,659 cases with a family history of the disease and 4,897 controls. Promising associations were evaluated in a second stage, comprising 12,576 cases and 12,223 controls. We identified five new susceptibility loci, on chromosomes 9, 10 and 11 (P = 4.6 x 10(-7) to P = 3.2 x 10(-15)). We also identified SNPs in the 6q25.1 (rs3757318, P = 2.9 x 10(-6)), 8q24 (rs1562430, P = 5.8 x 10(-7)) and LSP1 (rs909116, P = 7.3 x 10(-7)) regions that showed more significant association with risk than those reported previously. Previously identified breast cancer susceptibility loci were also found to show larger effect sizes in this study of familial breast cancer cases than in previous population-based studies, consistent with polygenic susceptibility to the disease.
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            Genome-wide association study of prostate cancer identifies a second risk locus at 8q24.

            Recently, common variants on human chromosome 8q24 were found to be associated with prostate cancer risk. While conducting a genome-wide association study in the Cancer Genetic Markers of Susceptibility project with 550,000 SNPs in a nested case-control study (1,172 cases and 1,157 controls of European origin), we identified a new association at 8q24 with an independent effect on prostate cancer susceptibility. The most significant signal is 70 kb centromeric to the previously reported SNP, rs1447295, but shows little evidence of linkage disequilibrium with it. A combined analysis with four additional studies (total: 4,296 cases and 4,299 controls) confirms association with prostate cancer for rs6983267 in the centromeric locus (P = 9.42 x 10(-13); heterozygote odds ratio (OR): 1.26, 95% confidence interval (c.i.): 1.13-1.41; homozygote OR: 1.58, 95% c.i.: 1.40-1.78). Each SNP remained significant in a joint analysis after adjusting for the other (rs1447295 P = 1.41 x 10(-11); rs6983267 P = 6.62 x 10(-10)). These observations, combined with compelling evidence for a recombination hotspot between the two markers, indicate the presence of at least two independent loci within 8q24 that contribute to prostate cancer in men of European ancestry. We estimate that the population attributable risk of the new locus, marked by rs6983267, is higher than the locus marked by rs1447295 (21% versus 9%).
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              Genome-wide association study identifies five susceptibility loci for glioma.

              To identify risk variants for glioma, we conducted a meta-analysis of two genome-wide association studies by genotyping 550K tagging SNPs in a total of 1,878 cases and 3,670 controls, with validation in three additional independent series totaling 2,545 cases and 2,953 controls. We identified five risk loci for glioma at 5p15.33 (rs2736100, TERT; P = 1.50 x 10(-17)), 8q24.21 (rs4295627, CCDC26; P = 2.34 x 10(-18)), 9p21.3 (rs4977756, CDKN2A-CDKN2B; P = 7.24 x 10(-15)), 20q13.33 (rs6010620, RTEL1; P = 2.52 x 10(-12)) and 11q23.3 (rs498872, PHLDB1; P = 1.07 x 10(-8)). These data show that common low-penetrance susceptibility alleles contribute to the risk of developing glioma and provide insight into disease causation of this primary brain tumor.
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                Author and article information

                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group
                2045-2322
                10 July 2015
                2015
                : 5
                Affiliations
                [1 ]Department of Pathology, First Affiliated Hospital, Xinjiang Medical University , 137 Liyushan Road, Urumqi, Xinjiang, 830054, China
                [2 ]Department of Oncology, First affiliated Hospital of Sun Yat-Sen University , 58 Zhongshan Er Road, Guangzhou, Guangdong, 510080, China
                [3 ]Department of Uorology, First Affiliated Hospital, Xinjiang Medical University , 137 Liyushan Road, Urumqi, Xinjiang, 830054, China
                [4 ]Molecular Epidemiology Laboratory and Department of Laboratory Medicine, Harbin Medical University Cancer Hospital , 150 Haping Road, Harbin, Heilongjang, 150040, China
                Author notes
                [*]

                These authors contributed equally to this work.

                Article
                srep12069
                10.1038/srep12069
                4498192
                26159557
                Copyright © 2015, Macmillan Publishers Limited

                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/

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