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A comprehensive meta-analysis of case-control association studies to evaluate polymorphisms associated with the risk of differentiated thyroid carcinoma

Figlioli, Gisella ; Elisei, Rossella ; Romei, Cristina ; Melaiu, Ombretta ; Cipollini, Monica ; Bambi, Franco ; Chen, Bowang LU ; Kohler, Aleksandra ; Cristaudo, Alfonso and Hemminki, Kari LU , et al. (2016) In Cancer Epidemiology Biomarkers & Prevention 25(4). p.700-713
Abstract

Background: Linkage analyses and association studies suggested that inherited genetic variations play a role in the development of differentiated thyroid carcinoma (DTC). Methods: We combined the results from a genome-wide association study (GWAS) performed by our group and frompublished studies onDTC. With a first approach, we evaluated whether a SNP published as associated with the risk of DTC could replicate in our GWAS (using FDR as adjustment for multiple comparisons). With the second approach, meta-analyses were performed between literature and GWAS when both sources suggested an association, increasing the statistical power of the analysis. Results: rs1799814 (CYP1A1), rs1121980 (FTO), and 3 SNPs within 9q22 (rs965513, rs7048394,... (More)

Background: Linkage analyses and association studies suggested that inherited genetic variations play a role in the development of differentiated thyroid carcinoma (DTC). Methods: We combined the results from a genome-wide association study (GWAS) performed by our group and frompublished studies onDTC. With a first approach, we evaluated whether a SNP published as associated with the risk of DTC could replicate in our GWAS (using FDR as adjustment for multiple comparisons). With the second approach, meta-analyses were performed between literature and GWAS when both sources suggested an association, increasing the statistical power of the analysis. Results: rs1799814 (CYP1A1), rs1121980 (FTO), and 3 SNPs within 9q22 (rs965513, rs7048394, and rs894673) replicated the associations described in the literature. In addition, the meta-analyses between literature and GWAS revealed 10 more SNPs within 9q22, six within FTO, two within SOD1, and single variations within HUS1, WDR3, UGT2B7, ALOX12, TICAM1, ATG16L1, HDAC4, PIK3CA, SULF1, IL11RA, VEGFA, and 1p31.3, 2q35, 8p12, and 14q13. Conclusion: This analysis confirmed several published risk loci that could be involved in DTC predisposition. Impact: These findings provide evidence for the role of germline variants in DTC etiology and are consistent with a polygenic model of the disease.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cancer Epidemiology Biomarkers & Prevention
volume
25
issue
4
pages
14 pages
publisher
American Association for Cancer Research
external identifiers
  • scopus:84962433786
  • wos:000373485900019
  • pmid:26843521
ISSN
1055-9965
DOI
10.1158/1055-9965.EPI-15-0652
language
English
LU publication?
yes
id
9cb6051a-14e7-41df-bdb0-5aa3c9e87265
date added to LUP
2016-06-01 15:23:55
date last changed
2024-01-04 07:50:52
@article{9cb6051a-14e7-41df-bdb0-5aa3c9e87265,
  abstract     = {{<p>Background: Linkage analyses and association studies suggested that inherited genetic variations play a role in the development of differentiated thyroid carcinoma (DTC). Methods: We combined the results from a genome-wide association study (GWAS) performed by our group and frompublished studies onDTC. With a first approach, we evaluated whether a SNP published as associated with the risk of DTC could replicate in our GWAS (using FDR as adjustment for multiple comparisons). With the second approach, meta-analyses were performed between literature and GWAS when both sources suggested an association, increasing the statistical power of the analysis. Results: rs1799814 (CYP1A1), rs1121980 (FTO), and 3 SNPs within 9q22 (rs965513, rs7048394, and rs894673) replicated the associations described in the literature. In addition, the meta-analyses between literature and GWAS revealed 10 more SNPs within 9q22, six within FTO, two within SOD1, and single variations within HUS1, WDR3, UGT2B7, ALOX12, TICAM1, ATG16L1, HDAC4, PIK3CA, SULF1, IL11RA, VEGFA, and 1p31.3, 2q35, 8p12, and 14q13. Conclusion: This analysis confirmed several published risk loci that could be involved in DTC predisposition. Impact: These findings provide evidence for the role of germline variants in DTC etiology and are consistent with a polygenic model of the disease.</p>}},
  author       = {{Figlioli, Gisella and Elisei, Rossella and Romei, Cristina and Melaiu, Ombretta and Cipollini, Monica and Bambi, Franco and Chen, Bowang and Kohler, Aleksandra and Cristaudo, Alfonso and Hemminki, Kari and Gemignani, Federica and Forsti, Asta and Landi, Stefano}},
  issn         = {{1055-9965}},
  language     = {{eng}},
  month        = {{04}},
  number       = {{4}},
  pages        = {{700--713}},
  publisher    = {{American Association for Cancer Research}},
  series       = {{Cancer Epidemiology Biomarkers & Prevention}},
  title        = {{A comprehensive meta-analysis of case-control association studies to evaluate polymorphisms associated with the risk of differentiated thyroid carcinoma}},
  url          = {{http://dx.doi.org/10.1158/1055-9965.EPI-15-0652}},
  doi          = {{10.1158/1055-9965.EPI-15-0652}},
  volume       = {{25}},
  year         = {{2016}},
}