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dc.contributor.authorPetridis, C
dc.contributor.authorBrook, MN
dc.contributor.authorShah, V
dc.contributor.authorKohut, K
dc.contributor.authorGorman, P
dc.contributor.authorCaneppele, M
dc.contributor.authorLevi, D
dc.contributor.authorPapouli, E
dc.contributor.authorOrr, N
dc.contributor.authorCox, A
dc.contributor.authorCross, SS
dc.contributor.authorDos-Santos-Silva, I
dc.contributor.authorPeto, J
dc.contributor.authorSwerdlow, A
dc.contributor.authorSchoemaker, MJ
dc.contributor.authorBolla, MK
dc.contributor.authorWang, Q
dc.contributor.authorDennis, J
dc.contributor.authorMichailidou, K
dc.contributor.authorBenitez, J et al
dc.date.accessioned2017-02-15T07:34:48Z
dc.date.available2017-02-15T07:34:48Z
dc.date.issued2016
dc.identifier10.1186/s13058-016-0675-7fi_FI
dc.identifier.issn1465-542X
dc.identifier.urihttps://erepo.uef.fi/handle/123456789/277
dc.descriptionArticle
dc.description.abstractBackground Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer. It is often associated with invasive ductal carcinoma (IDC), and is considered to be a non-obligate precursor of IDC. It is not clear to what extent these two forms of cancer share low-risk susceptibility loci, or whether there are differences in the strength of association for shared loci. Methods To identify genetic polymorphisms that predispose to DCIS, we pooled data from 38 studies comprising 5,067 cases of DCIS, 24,584 cases of IDC and 37,467 controls, all genotyped using the iCOGS chip. Results Most (67 %) of the 76 known breast cancer predisposition loci showed an association with DCIS in the same direction as previously reported for invasive breast cancer. Case-only analysis showed no evidence for differences between associations for IDC and DCIS after considering multiple testing. Analysis by estrogen receptor (ER) status confirmed that loci associated with ER positive IDC were also associated with ER positive DCIS. Analysis of DCIS by grade suggested that two independent SNPs at 11q13.3 near CCND1 were specific to low/intermediate grade DCIS (rs75915166, rs554219). These associations with grade remained after adjusting for ER status and were also found in IDC. We found no novel DCIS-specific loci at a genome wide significance level of P < 5.0x10-8. Conclusion In conclusion, this study provides the strongest evidence to date of a shared genetic susceptibility for IDC and DCIS. Studies with larger numbers of DCIS are needed to determine if IDC or DCIS specific loci exist.fi_FI
dc.language.isoENGfi_FI
dc.publisherSpringer Naturefi_FI
dc.relation.ispartofseriesBREAST CANCER RESEARCH
dc.relation.urihttp://doi.org/10.1186/s13058-016-0675-7fi_FI
dc.rightsCC BY http://creativecommons.org/licenses/by/4.0/
dc.subjectDuctal carcinoma in situfi_FI
dc.subjectAssociation studyfi_FI
dc.subjectGenetic predispositionfi_FI
dc.subjectCommon variantsfi_FI
dc.titleGenetic predisposition to ductal carcinoma in situ of the breastfi_FI
dc.typehttp://purl.org/eprint/type/JournalArticle
dc.description.versionpublisher's pdffi_FI
dc.contributor.departmentSchool of Medicine / Clinical Medicine
uef.solecris.id41738359
eprint.statushttp://purl.org/eprint/status/PeerReviewedfi_FI
dc.type.publicationinfo:eu-repo/semantics/article
dc.rights.accessrights© Authors
uef.citationinfo.issue18(22)
dc.relation.doi10.1186/s13058-016-0675-7
dc.description.reviewstatushttp://purl.org/eprint/status/PeerReviewed
dc.relation.articlenumber22
dc.relation.issn1465-542X
dc.relation.volume18
dc.rights.accesslevelopenAccess


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