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Genome-wide associations for benign prostatic hyperplasia reveal a genetic correlation with serum levels of PSA

Genome-wide associations for benign prostatic hyperplasia reveal a genetic correlation with serum levels of PSA


Title: Genome-wide associations for benign prostatic hyperplasia reveal a genetic correlation with serum levels of PSA
Author: Gudmundsson, Julius   orcid.org/0000-0003-2517-4763
Sigurðsson, Jón K.
Stefánsdóttir, Lilja
Agnarsson, Bjarni A.
Ísaksson, Helgi J.
Stefánsson, Ólafur A.
Guðjónsson, Sigurjón Axel
Gudbjartsson, Daniel   orcid.org/0000-0002-5222-9857
Másson, Gísli   orcid.org/0000-0003-0493-8242
Frigge, Michael L.
... 18 more authors Show all authors
Date: 2018-11-08
Language: English
Scope: 4568
University/Institute: Háskóli Íslands (HÍ)
University of Iceland (UI)
School: School of Health Sciences (UI)
Heilbrigðisvísindasvið (HÍ)
School of Engineering and Natural Sciences (UI)
Verkfræði- og náttúruvísindasvið (HÍ)
Department: Faculty of Medicine (UI)
Læknadeild (HÍ)
Biomedical Center (UI)
Lífvísindasetur (HÍ)
Series: Nature Communications;9(1)
ISSN: 2041-1723
DOI: 10.1038/s41467-018-06920-9
Subject: Cancer; Genetics; Krabbamein; Blöðruhálskirtilskrabbamein; Erfðafræði; Rannsóknir
URI: https://hdl.handle.net/20.500.11815/1385

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Citation:

Gudmundsson, J., Sigurdsson, J.K., Stefansdottir, L. et al. Genome-wide associations for benign prostatic hyperplasia reveal a genetic correlation with serum levels of PSA. Nat Commun 9, 4568 (2018) doi:10.1038/s41467-018-06920-9

Abstract:

Benign prostatic hyperplasia and associated lower urinary tract symptoms (BPH/LUTS) are common conditions affecting the majority of elderly males. Here we report the results of a genome-wide association study of symptomatic BPH/LUTS in 20,621 patients and 280,541 controls of European ancestry, from Iceland and the UK. We discovered 23 genome-wide significant variants, located at 14 loci. There is little or no overlap between the BPH/LUTS variants and published prostate cancer risk variants. However, 15 of the variants reported here also associate with serum levels of prostate specific antigen (PSA) (at a Bonferroni corrected P < 0.0022). Furthermore, there is a strong genetic correlation, r g = 0.77 (P = 2.6 × 10 −11 ), between PSA and BPH/LUTS, and one standard deviation increase in a polygenic risk score (PRS) for BPH/LUTS increases PSA levels by 12.9% (P = 1.6×10 −55 ). These results shed a light on the genetic background of BPH/LUTS and its substantial influence on PSA levels.

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