Multilevel-analysis identify a cis -expression quantitative trait locus associated with risk of renal cell carcinoma
We conducted multilevel analyses to identify potential susceptibility loci for renal cell carcinoma (RCC), which may be overlooked in traditional genome-wide association studies (GWAS). A gene set enrichment analysis was performed utilizing a GWAS dataset comprised of 894 RCC cases and 1,516 control...
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| Published in | Oncotarget Vol. 6; no. 6; pp. 4097 - 4109 |
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| Main Authors | , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Impact Journals LLC
28.02.2015
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1949-2553 1949-2553 |
| DOI | 10.18632/oncotarget.3001 |
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| Abstract | We conducted multilevel analyses to identify potential susceptibility loci for renal cell carcinoma (RCC), which may be overlooked in traditional genome-wide association studies (GWAS). A gene set enrichment analysis was performed utilizing a GWAS dataset comprised of 894 RCC cases and 1,516 controls using GenGen, SNP ratio test, and ALIGATOR. The antigen processing and presentation pathway was consistently significant (P = 0.001, = 0.004, and < 0.001, respectively). Versatile gene-based association study approach was applied to the top-ranked pathway and identified the driven genes. By comparing the expression of the genes in RCC tumor and adjacent normal tissues, we observed significant overexpression of HLA genes in tumor tissues, which was also supported by public databases. We sought to validate genetic variants in antigen processing and presentation pathway in an independent GWAS dataset comprised of 1,311 RCC cases and 3,424 control subjects from the National Cancer Institute; one SNP, rs1063355, was significant in both populations (P(meta-analysis) = 9.15 × 10⁻⁴, P(heterogeneity) = 0.427). Strong correlation indicated that rs1063355 was a cis-expression quantitative trait loci which associated with HLA-DQB1 expression (Spearman's rank r = -0.59, p = 5.61 × 10⁻⁶). The correlation was further validated using a public dataset. Our results highlighted the role of immune-related pathway and genes in the etiology of RCC. |
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| AbstractList | We conducted multilevel analyses to identify potential susceptibility loci for renal cell carcinoma (RCC), which may be overlooked in traditional genome-wide association studies (GWAS). A gene set enrichment analysis was performed utilizing a GWAS dataset comprised of 894 RCC cases and 1,516 controls using GenGen, SNP ratio test, and ALIGATOR. The antigen processing and presentation pathway was consistently significant (P = 0.001, = 0.004, and < 0.001, respectively). Versatile gene-based association study approach was applied to the top-ranked pathway and identified the driven genes. By comparing the expression of the genes in RCC tumor and adjacent normal tissues, we observed significant overexpression of HLA genes in tumor tissues, which was also supported by public databases. We sought to validate genetic variants in antigen processing and presentation pathway in an independent GWAS dataset comprised of 1,311 RCC cases and 3,424 control subjects from the National Cancer Institute; one SNP, rs1063355, was significant in both populations (Pmeta-analysis = 9.15 × 10−4, Pheterogeneity = 0.427). Strong correlation indicated that rs1063355 was a cis-expression quantitative trait loci which associated with HLA-DQB1 expression (Spearman's rank r = −0.59, p = 5.61 × 10−6). The correlation was further validated using a public dataset. Our results highlighted the role of immune-related pathway and genes in the etiology of RCC. We conducted multilevel analyses to identify potential susceptibility loci for renal cell carcinoma (RCC), which may be overlooked in traditional genome-wide association studies (GWAS). A gene set enrichment analysis was performed utilizing a GWAS dataset comprised of 894 RCC cases and 1,516 controls using GenGen, SNP ratio test, and ALIGATOR. The antigen processing and presentation pathway was consistently significant (P = 0.001, = 0.004, and < 0.001, respectively). Versatile gene-based association study approach was applied to the top-ranked pathway and identified the driven genes. By comparing the expression of the genes in RCC tumor and adjacent normal tissues, we observed significant overexpression of HLA genes in tumor tissues, which was also supported by public databases. We sought to validate genetic variants in antigen processing and presentation pathway in an independent GWAS dataset comprised of 1,311 RCC cases and 3,424 control subjects from the National Cancer Institute; one SNP, rs1063355, was significant in both populations (P(meta-analysis) = 9.15 × 10⁻⁴, P(heterogeneity) = 0.427). Strong correlation indicated that rs1063355 was a cis-expression quantitative trait loci which associated with HLA-DQB1 expression (Spearman's rank r = -0.59, p = 5.61 × 10⁻⁶). The correlation was further validated using a public dataset. Our results highlighted the role of immune-related pathway and genes in the etiology of RCC.We conducted multilevel analyses to identify potential susceptibility loci for renal cell carcinoma (RCC), which may be overlooked in traditional genome-wide association studies (GWAS). A gene set enrichment analysis was performed utilizing a GWAS dataset comprised of 894 RCC cases and 1,516 controls using GenGen, SNP ratio test, and ALIGATOR. The antigen processing and presentation pathway was consistently significant (P = 0.001, = 0.004, and < 0.001, respectively). Versatile gene-based association study approach was applied to the top-ranked pathway and identified the driven genes. By comparing the expression of the genes in RCC tumor and adjacent normal tissues, we observed significant overexpression of HLA genes in tumor tissues, which was also supported by public databases. We sought to validate genetic variants in antigen processing and presentation pathway in an independent GWAS dataset comprised of 1,311 RCC cases and 3,424 control subjects from the National Cancer Institute; one SNP, rs1063355, was significant in both populations (P(meta-analysis) = 9.15 × 10⁻⁴, P(heterogeneity) = 0.427). Strong correlation indicated that rs1063355 was a cis-expression quantitative trait loci which associated with HLA-DQB1 expression (Spearman's rank r = -0.59, p = 5.61 × 10⁻⁶). The correlation was further validated using a public dataset. Our results highlighted the role of immune-related pathway and genes in the etiology of RCC. We conducted multilevel analyses to identify potential susceptibility loci for renal cell carcinoma (RCC), which may be overlooked in traditional genome-wide association studies (GWAS). A gene set enrichment analysis was performed utilizing a GWAS dataset comprised of 894 RCC cases and 1,516 controls using GenGen, SNP ratio test, and ALIGATOR. The antigen processing and presentation pathway was consistently significant (P = 0.001, = 0.004, and < 0.001, respectively). Versatile gene-based association study approach was applied to the top-ranked pathway and identified the driven genes. By comparing the expression of the genes in RCC tumor and adjacent normal tissues, we observed significant overexpression of HLA genes in tumor tissues, which was also supported by public databases. We sought to validate genetic variants in antigen processing and presentation pathway in an independent GWAS dataset comprised of 1,311 RCC cases and 3,424 control subjects from the National Cancer Institute; one SNP, rs1063355, was significant in both populations (P(meta-analysis) = 9.15 × 10⁻⁴, P(heterogeneity) = 0.427). Strong correlation indicated that rs1063355 was a cis-expression quantitative trait loci which associated with HLA-DQB1 expression (Spearman's rank r = -0.59, p = 5.61 × 10⁻⁶). The correlation was further validated using a public dataset. Our results highlighted the role of immune-related pathway and genes in the etiology of RCC. |
| Author | Pu, Xia Wu, Xifeng Diver, W. Ryan Tannir, Nizar M. Purdue, Mark P. Shu, Xiang Huang, Maosheng Stevens, Victoria L. Ye, Yuanqing Wood, Christopher G. Chow, Wong-Ho Chanock, Stephen J. Chen, Meng Virtamo, Jarmo Albanes, Demetrius Wang, Zhaoming Rothman, Nathaniel Gapstur, Susan M. Dinney, Colin P. |
| AuthorAffiliation | 5 Epidemiology Research Program, American Cancer Society, Atlanta, Georgia, USA 7 Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA 3 Urology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA 2 Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA 1 Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA 4 Cancer Genomics Research Laboratory, SAIC-Frederick Inc., National Cancer Institute-Frederick, Frederick, Maryland, USA 6 Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland |
| AuthorAffiliation_xml | – name: 4 Cancer Genomics Research Laboratory, SAIC-Frederick Inc., National Cancer Institute-Frederick, Frederick, Maryland, USA – name: 6 Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland – name: 7 Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA – name: 2 Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA – name: 5 Epidemiology Research Program, American Cancer Society, Atlanta, Georgia, USA – name: 1 Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA – name: 3 Urology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA |
| Author_xml | – sequence: 1 givenname: Xiang surname: Shu fullname: Shu, Xiang organization: Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA – sequence: 2 givenname: Mark P. surname: Purdue fullname: Purdue, Mark P. organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA – sequence: 3 givenname: Yuanqing surname: Ye fullname: Ye, Yuanqing organization: Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA – sequence: 4 givenname: Christopher G. surname: Wood fullname: Wood, Christopher G. organization: Urology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA – sequence: 5 givenname: Meng surname: Chen fullname: Chen, Meng organization: Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA – sequence: 6 givenname: Zhaoming surname: Wang fullname: Wang, Zhaoming organization: Cancer Genomics Research Laboratory, SAIC-Frederick Inc., National Cancer Institute-Frederick, Frederick, Maryland, USA – sequence: 7 givenname: Demetrius surname: Albanes fullname: Albanes, Demetrius organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA – sequence: 8 givenname: Xia surname: Pu fullname: Pu, Xia organization: Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA – sequence: 9 givenname: Maosheng surname: Huang fullname: Huang, Maosheng organization: Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA – sequence: 10 givenname: Victoria L. surname: Stevens fullname: Stevens, Victoria L. organization: Epidemiology Research Program, American Cancer Society, Atlanta, Georgia, USA – sequence: 11 givenname: W. Ryan surname: Diver fullname: Diver, W. Ryan organization: Epidemiology Research Program, American Cancer Society, Atlanta, Georgia, USA – sequence: 12 givenname: Susan M. surname: Gapstur fullname: Gapstur, Susan M. organization: Epidemiology Research Program, American Cancer Society, Atlanta, Georgia, USA – sequence: 13 givenname: Jarmo surname: Virtamo fullname: Virtamo, Jarmo organization: Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland – sequence: 14 givenname: Wong-Ho surname: Chow fullname: Chow, Wong-Ho organization: Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA – sequence: 15 givenname: Nizar M. surname: Tannir fullname: Tannir, Nizar M. organization: Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA – sequence: 16 givenname: Colin P. surname: Dinney fullname: Dinney, Colin P. organization: Urology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA – sequence: 17 givenname: Nathaniel surname: Rothman fullname: Rothman, Nathaniel organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA – sequence: 18 givenname: Stephen J. surname: Chanock fullname: Chanock, Stephen J. organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA – sequence: 19 givenname: Xifeng surname: Wu fullname: Wu, Xifeng organization: Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA |
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| SubjectTerms | Carcinoma, Renal Cell - genetics Case-Control Studies Female Genetic Predisposition to Disease Genome-Wide Association Study Humans Kidney Neoplasms - genetics Male Polymorphism, Single Nucleotide Quantitative Trait Loci Research Paper |
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| Title | Multilevel-analysis identify a cis -expression quantitative trait locus associated with risk of renal cell carcinoma |
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