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      Androgenetic alopecia: identification of four genetic risk loci and evidence for the contribution of WNT signaling to its etiology.

      The Journal of Investigative Dermatology
      Adult, Alopecia, epidemiology, etiology, genetics, metabolism, Cholestanetriol 26-Monooxygenase, Chromosomes, Human, Pair 12, Chromosomes, Human, Pair 2, Chromosomes, Human, Pair 3, Chromosomes, Human, Pair 5, European Continental Ancestry Group, statistics & numerical data, Frizzled Receptors, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Risk Factors, Wnt Proteins, Wnt Signaling Pathway, physiology, Wnt3 Protein

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          Abstract

          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 × 10(-8)

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