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dc.contributor.authorFletcher, Michael NCen
dc.contributor.authorCastro, Mauro AAen
dc.contributor.authorWang, Xinen
dc.contributor.authorde, Santiago Inesen
dc.contributor.authorO'Reilly, Martinen
dc.contributor.authorChin, Suet-Feungen
dc.contributor.authorRueda, Oscar Men
dc.contributor.authorCaldas, Carlosen
dc.contributor.authorPonder, Bruceen
dc.contributor.authorMarkowetz, Florianen
dc.contributor.authorMeyer, Kerstinen
dc.date.accessioned2014-09-10T15:36:47Z
dc.date.available2014-09-10T15:36:47Z
dc.date.issued2013-09-17en
dc.identifier.citation(2013) Nature Communications 4: 2464en
dc.identifier.issn2041-1723
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/245908
dc.description.abstractThe fibroblast growth factor receptor 2 (FGFR2) locus has been consistently identified as a breast cancer risk locus in independent genome-wide association studies. However, the molecular mechanisms underlying FGFR2-mediated risk are still unknown. Using model systems we show that FGFR2-regulated genes are preferentially linked to breast cancer risk loci in expression quantitative trait loci analysis, supporting the concept that risk genes cluster in pathways. Using a network derived from 2,000 transcriptional profiles we identify SPDEF, ERa, FOXA1, GATA3 and PTTG1 as master regulators of fibroblast growth factor receptor 2 signalling, and show that ERa occupancy responds to fibroblast growth factor receptor 2 signalling. Our results indicate that ERa, FOXA1 and GATA3 contribute to the regulation of breast cancer susceptibility genes, which is consistent with the effects of antioestrogen treatment in breast cancer prevention, and suggest that fibroblast growth factor receptor 2 signalling has an important role in mediating breast cancer risk.
dc.languageen_USen
dc.language.isoen_USen
dc.publisherNPG
dc.rightsAttribution-NonCommercial-ShareAlike 2.0 UK: England & Wales*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/2.0/uk/*
dc.titleMaster regulators of FGFR2 signalling and breast cancer risken
dc.typeArticle
dc.description.versionThis is the final version of the article. It was originally published in Nature Communications here: http://www.nature.com/ncomms/2013/130917/ncomms3464/full/ncomms3464.html.en
prism.publicationDate2013en
prism.publicationNameNature Communicationsen
prism.startingPage2464
prism.volume4en
dc.rioxxterms.funderCancer Research UK National Institute for Health Research Cambridge Biomedical Research Centre Hutchison Whampoa Ltd
dcterms.dateAccepted2013-08-16en
rioxxterms.versionofrecord10.1038/ncomms3464en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2013-09-17en
dc.contributor.orcidChin, Suet-Feung [0000-0001-5697-1082]
dc.contributor.orcidCaldas, Carlos [0000-0003-3547-1489]
dc.contributor.orcidMarkowetz, Florian [0000-0002-2784-5308]
dc.contributor.orcidMeyer, Kerstin [0000-0001-5906-1498]
dc.identifier.eissn2041-1723
rioxxterms.typeJournal Article/Reviewen


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Attribution-NonCommercial-ShareAlike 2.0 UK: England & Wales
Except where otherwise noted, this item's licence is described as Attribution-NonCommercial-ShareAlike 2.0 UK: England & Wales