Androgenetic Alopecia: Identification of Four Genetic Risk Loci and Evidence for the Contribution of WNT Signaling to Its Etiology
Publication year
2013Author(s)
Source
Journal of Investigative Dermatology, 133, 6, (2013), pp. 1489-1496ISSN
Related links
Publication type
Article / Letter to editor

Display more detailsDisplay less details
Organization
Human Genetics
Health Evidence
Urology
Former Organization
Epidemiology, Biostatistics & HTA
Journal title
Journal of Investigative Dermatology
Volume
vol. 133
Issue
iss. 6
Page start
p. 1489
Page end
p. 1496
Subject
NCEBP 1: Molecular epidemiology; NCEBP 1: Molecular epidemiology ONCOL 5: Aetiology, screening and detection; ONCOL 5: Aetiology, screening and detectionAbstract
The pathogenesis of androgenetic alopecia (AGA, male-pattern baldness) is driven by androgens, and genetic predisposition is the major prerequisite. Candidate gene and genome-wide association studies have reported that single-nucleotide polymorphisms (SNPs) at eight different genomic loci are associated with AGA development. However, a significant fraction of the overall heritable risk still awaits identification. Furthermore, the understanding of the pathophysiology of AGA is incomplete, and each newly associated locus may provide novel insights into contributing biological pathways. The aim of this study was to identify unknown AGA risk loci by replicating SNPs at the 12 genomic loci that showed suggestive association (5 x 10(-8)<P<10(-5)) with AGA in a recent meta-analysis. We analyzed a replication set comprising 2,759 cases and 2,661 controls of European descent to confirm the association with AGA at these loci. Combined analysis of the replication and the meta-analysis data identified four genome-wide significant risk loci for AGA on chromosomes 2q35, 3q25.1, 5q33.3, and 12p12.1. The strongest association signal was obtained for rs7349332 (P=3.55 x 10(-15)) on chr2q35, which is located intronically in WNT10A. Expression studies in human hair follicle tissue suggest that WNT10A has a functional role in AGA etiology. Thus, our study provides genetic evidence supporting an involvement of WNT signaling in AGA development.
This item appears in the following Collection(s)
- Academic publications [202802]
- Faculty of Medical Sciences [80020]
Upload full text
Use your RU credentials (u/z-number and password) to log in with SURFconext to upload a file for processing by the repository team.