Replication of prostate cancer risk loci on 8q24, 11q13, 17q12, 19q33, and Xp11 in African Americans

BACKGROUND Prostate cancer (Pca) is a common malignancy that disproportionately affects African American men (AA). Recently there have been several genome‐wide association studies (GWAS) implicating new prostate cancer risk loci along chromosomes 2, 3, 6, 7, 8, 10, 11, 12, 17, 19, and X in populatio...

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Published in:The Prostate 2010-02, Vol.70 (3), p.270-275
Main Authors: Hooker, Stanley, Hernandez, Wenndy, Chen, Hankui, Robbins, Christiane, Torres, Jada Benn, Ahaghotu, Chiledum, Carpten, John, Kittles, Rick A.
Format: Article
Language:English
Subjects:
African Americans - genetics
African-Americans
Aged
Case-Control Studies
Chromosome Mapping
Genetic Predisposition to Disease
genetic risk
Genome-Wide Association Study
GWAS
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide
prostate cancer
Prostatic Neoplasms - genetics
SNPs
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Summary:BACKGROUND Prostate cancer (Pca) is a common malignancy that disproportionately affects African American men (AA). Recently there have been several genome‐wide association studies (GWAS) implicating new prostate cancer risk loci along chromosomes 2, 3, 6, 7, 8, 10, 11, 12, 17, 19, and X in populations of European ancestry. Given the higher incidence and mortality for AAs, and differences in allele frequencies and haplotype structures between African and European descent populations, it is important to assess the impact of these candidate risk loci in AAs. METHODS Here we evaluated 20 single nucleotide polymorphisms (SNPs) associated with prostate cancer risk in recent GWAS studies, in AA prostate cancer cases and controls. RESULTS We replicated five of the SNPs in our AA population, rs10896449 on 11q13.2 (P = 0.009), rs2735839 on 19q33.33 region, (P = 0.04), rs443076 on chromosome 17q12 (P = 0.008), rs5945572 on Xp11.22 (P = 0.05), as well as the rare variant specific to west African ancestry, bd11934905 in region 2 of 8q24 (P = 1 × 10−4). CONCLUSIONS While we were able to replicate a few of the previous GWAS SNPs, we were not able to confirm the vast majority of these associations in our AA population. This finding further supports the need to perform GWAS and additional fine mapping in AAs to locate additional susceptibility loci. Prostate 70: 270–275, 2010. © 2009 Wiley‐Liss, Inc.
ISSN:0270-4137
1097-0045
DOI:10.1002/pros.21061