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Identification of susceptibility pathways for the role of chromosome 15q25.1 in modifying lung cancer risk

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  • Xuemei Ji
  • Yohan Bossé
  • Maria Teresa Landi
  • Jiang Gui
  • Xiangjun Xiao
  • David Qian
  • Philippe Joubert
  • Maxime Lamontagne
  • Yafang Li
  • Ivan Gorlov
  • Mariella de Biasi
  • Younghun Han
  • Olga Gorlova
  • Rayjean J Hung
  • Xifeng Wu
  • James McKay
  • Xuchen Zong
  • Robert Carreras-Torres
  • David C Christiani
  • Neil Caporaso
  • Mattias Johansson
  • Geoffrey Liu
  • Stig E Bojesen
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  • M Dawn Teare
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  • Aage Haugen
  • Stephen Lam
  • Matthew B Schabath
  • Angeline S Andrew
  • Hongbing Shen
  • Yun-Chul Hong
  • Jian-Min Yuan
  • Pier A Bertazzi
  • Angela C Pesatori
  • Yuanqing Ye
  • Nancy Diao
  • Li Su
  • Ruyang Zhang
  • Yonathan Brhane
  • Natasha Leighl
  • Jakob S Johansen
  • Anders Mellemgaard
  • Walid Saliba
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  • Ana Fernandez-Somoano
  • Guillermo Fernandez-Tardon
  • Erik H F M van der Heijden
  • Jin Hee Kim
  • Juncheng Dai
  • Zhibin Hu
  • Michael P A Davies
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  • Hans Brunnström
  • Jonas Manjer
  • Olle Melander
  • David C Muller
  • Kim Overvad
  • Antonia Trichopoulou
  • Rosario Tumino
  • Jennifer Doherty
  • Gary E Goodman
  • Angela Cox
  • Fiona Taylor
  • Penella Woll
  • Irene Brüske
  • Judith Manz
  • Thomas Muley
  • Angela Risch
  • Albert Rosenberger
  • Kjell Grankvist
  • Mikael Johansson
  • Frances Shepherd
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  • John McLaughlin
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  • David C Nickle
  • Ma'en Obeidat
  • Wim Timens
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  • María Soler Artigas
  • Martin D Tobin
  • Louise V Wain
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Vis graf over relationer

Genome-wide association studies (GWAS) identified the chromosome 15q25.1 locus as a leading susceptibility region for lung cancer. However, the pathogenic pathways, through which susceptibility SNPs within chromosome 15q25.1 affects lung cancer risk, have not been explored. We analyzed three cohorts with GWAS data consisting 42,901 individuals and lung expression quantitative trait loci (eQTL) data on 409 individuals to identify and validate the underlying pathways and to investigate the combined effect of genes from the identified susceptibility pathways. The KEGG neuroactive ligand receptor interaction pathway, two Reactome pathways, and 22 Gene Ontology terms were identified and replicated to be significantly associated with lung cancer risk, with P values less than 0.05 and FDR less than 0.1. Functional annotation of eQTL analysis results showed that the neuroactive ligand receptor interaction pathway and gated channel activity were involved in lung cancer risk. These pathways provide important insights for the etiology of lung cancer.

OriginalsprogEngelsk
TidsskriftNature Communications
Vol/bind9
Udgave nummer1
Sider (fra-til)3221
ISSN2041-1723
DOI
StatusUdgivet - 13 aug. 2018

ID: 56576353