@article{3166782,
    title = "Genome-wide association of polycystic ovary syndrome implicates
alterations in gonadotropin secretion in European ancestry populations",
    author = "Hayes, M. Geoffrey and Urbanek, Margrit and Ehrmann, David A. and and Armstrong, Loren L. and Lee, Ji Young and Sisk, Ryan and Karaderi, Tugce and and Barber, Thomas M. and McCarthy, Mark I. and Franks, Stephen and and Lindgren, Cecilia M. and Welt, Corrine K. and Diamanti-Kandarakis, and Evanthia and Panidis, Dimitrios and Goodarzi, Mark O. and Azziz, Ricardo and and Zhang, Yi and James, Roland G. and Olivier, Michael and Kissebah, and Ahmed H. and Stener-Victorin, Elisabet and Legro, Richard S. and Dunaif, and Andrea and Reprod Med Network",
    journal = "Nature Communications",
    year = "2015",
    volume = "6",
    publisher = "Nature Publishing Group",
    issn = "2041-1723",
    doi = "10.1038/ncomms8502",
    abstract = "Polycystic ovary syndrome (PCOS) is a common, highly heritable complex
disorder of unknown aetiology characterized by hyperandrogenism, chronic
anovulation and defects in glucose homeostasis. Increased luteinizing
hormone relative to follicle-stimulating hormone secretion, insulin
resistance and developmental exposure to androgens are hypothesized to
play a causal role in PCOS. Here we map common genetic susceptibility
loci in European ancestry women for the National Institutes of Health
PCOS phenotype, which confers the highest risk for metabolic
morbidities, as well as reproductive hormone levels. Three loci reach
genome-wide significance in the case-control meta-analysis, two novel
loci mapping to chr 8p32.1 and chr 11p14.1, and a chr 9q22.32 locus
previously found in Chinese PCOS. The same chr 11p14.1 SNP, rs11031006,
in the region of the follicle-stimulating hormone B polypeptide (FSHB)
gene strongly associates with PCOS diagnosis and luteinizing hormone
levels. These findings implicate neuroendocrine changes in disease
pathogenesis."
}