Do variants associated with susceptibility to pancreatic cancer and type 2 diabetes reciprocally affect risk?

OBJECTIVES:Although type 2 diabetes mellitus is a known risk factor for pancreatic cancer, the existence of shared genetic susceptibility is largely unknown. We evaluated whether any reported genetic risk variants of either disease found by genome-wide association studies reciprocally confer suscept...

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Main Authors: Lang Wu, Kari G Rabe, Gloria M Petersen
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2015-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4319943?pdf=render
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spelling doaj-82eb7ecea48649d0a86621a8e8baaa7f2020-11-24T22:00:06ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-01102e011723010.1371/journal.pone.0117230Do variants associated with susceptibility to pancreatic cancer and type 2 diabetes reciprocally affect risk?Lang WuKari G RabeGloria M PetersenOBJECTIVES:Although type 2 diabetes mellitus is a known risk factor for pancreatic cancer, the existence of shared genetic susceptibility is largely unknown. We evaluated whether any reported genetic risk variants of either disease found by genome-wide association studies reciprocally confer susceptibility. METHODS:Data that were generated in previous genome-wide association studies (GENEVA Type 2 Diabetes; PanScan) were obtained through the National Institutes of Health database of Genotypes and Phenotypes (dbGaP). Using the PanScan datasets, we tested for association of 38 variants within 37 genomic regions known to be susceptibility factors for type 2 diabetes. We further examined whether type 2 diabetes variants predispose to pancreatic cancer risk stratified by diabetes status. Correspondingly, we examined the association of fourteen pancreatic cancer susceptibility variants within eight genomic regions in the GENEVA Type 2 Diabetes dataset. RESULTS:Four plausible associations of diabetes variants and pancreatic cancer risk were detected at a significance threshold of p = 0.05, and one pancreatic cancer susceptibility variant was associated with diabetes risk at threshold of p = 0.05, but none remained significant after correction for multiple comparisons. CONCLUSION:Currently identified GWAS susceptibility variants are unlikely to explain the potential shared genetic etiology between Type 2 diabetes and pancreatic cancer.http://europepmc.org/articles/PMC4319943?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Lang Wu
Kari G Rabe
Gloria M Petersen
spellingShingle Lang Wu
Kari G Rabe
Gloria M Petersen
Do variants associated with susceptibility to pancreatic cancer and type 2 diabetes reciprocally affect risk?
PLoS ONE
author_facet Lang Wu
Kari G Rabe
Gloria M Petersen
author_sort Lang Wu
title Do variants associated with susceptibility to pancreatic cancer and type 2 diabetes reciprocally affect risk?
title_short Do variants associated with susceptibility to pancreatic cancer and type 2 diabetes reciprocally affect risk?
title_full Do variants associated with susceptibility to pancreatic cancer and type 2 diabetes reciprocally affect risk?
title_fullStr Do variants associated with susceptibility to pancreatic cancer and type 2 diabetes reciprocally affect risk?
title_full_unstemmed Do variants associated with susceptibility to pancreatic cancer and type 2 diabetes reciprocally affect risk?
title_sort do variants associated with susceptibility to pancreatic cancer and type 2 diabetes reciprocally affect risk?
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2015-01-01
description OBJECTIVES:Although type 2 diabetes mellitus is a known risk factor for pancreatic cancer, the existence of shared genetic susceptibility is largely unknown. We evaluated whether any reported genetic risk variants of either disease found by genome-wide association studies reciprocally confer susceptibility. METHODS:Data that were generated in previous genome-wide association studies (GENEVA Type 2 Diabetes; PanScan) were obtained through the National Institutes of Health database of Genotypes and Phenotypes (dbGaP). Using the PanScan datasets, we tested for association of 38 variants within 37 genomic regions known to be susceptibility factors for type 2 diabetes. We further examined whether type 2 diabetes variants predispose to pancreatic cancer risk stratified by diabetes status. Correspondingly, we examined the association of fourteen pancreatic cancer susceptibility variants within eight genomic regions in the GENEVA Type 2 Diabetes dataset. RESULTS:Four plausible associations of diabetes variants and pancreatic cancer risk were detected at a significance threshold of p = 0.05, and one pancreatic cancer susceptibility variant was associated with diabetes risk at threshold of p = 0.05, but none remained significant after correction for multiple comparisons. CONCLUSION:Currently identified GWAS susceptibility variants are unlikely to explain the potential shared genetic etiology between Type 2 diabetes and pancreatic cancer.
url http://europepmc.org/articles/PMC4319943?pdf=render
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AT karigrabe dovariantsassociatedwithsusceptibilitytopancreaticcancerandtype2diabetesreciprocallyaffectrisk
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