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dc.contributor.authorJonsdottir, Asta Bjork
dc.contributor.authorStefansson, Olafur Andri
dc.contributor.authorBjornsson, Johannes
dc.contributor.authorJonasson, Jon G
dc.contributor.authorOgmundsdottir, Helga M
dc.contributor.authorEyfjord, Jorunn E
dc.date.accessioned2013-08-27T11:45:23Z
dc.date.available2013-08-27T11:45:23Z
dc.date.issued2012-02
dc.date.submitted2013-08-27
dc.identifier.citationEur. J. Cancer 2012, 48(3):305-10en_GB
dc.identifier.issn1879-0852
dc.identifier.pmid22133571
dc.identifier.doi10.1016/j.ejca.2011.11.008
dc.identifier.urihttp://hdl.handle.net/2336/299937
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links field.en_GB
dc.description.abstractTetraploidy and aneuploidy can be caused by cell division errors and are frequently observed in many human carcinomas. We have recently reported delayed cytokinesis in primary human fibroblasts from BRCA2 mutation carriers, implying a function for the BRCA2 tumour suppressor in completion of cell division. Here, we address ploidy aberrations in breast tumours derived from BRCA2 germline mutation carriers. Ploidy aberrations were evaluated from flow cytometry histograms on selected breast tumour samples (n=236), previously screened for local BRCA mutations. The ploidy between BRCA2-mutated (n=71) and matched sporadic (n=165) cancers was compared. Differences in ploidy distribution were examined with respect to molecular tumour subtypes, previously defined by immunohistochemistry on tissue microarray sections. Tetraploidy was significantly 3 times more common in BRCA2 breast cancers than sporadic. However, no differences were found in the overall ploidy distribution between BRCA2-mutation carriers and non-carriers. In BRCA2 cancers, tetraploidy was associated with luminal characteristics. The increased frequency of tetraploidy in BRCA2 associated cancers may be linked to cell division errors, particularly cytokinesis. Additionally, tetraploidy emerges predominantly in BRCA2 breast cancers displaying luminal rather than triple-negative phenotypes.
dc.description.sponsorshipUniversity of Iceland Soroptimist International of Europeen_GB
dc.language.isoenen
dc.publisherElsevier Scienceen_GB
dc.relation.urlhttp://dx.doi.org/10.1016/j.ejca.2011.11.008en_GB
dc.rightsArchived with thanks to European journal of cancer (Oxford, England : 1990)en_GB
dc.subject.meshAneuploidyen_GB
dc.subject.meshBreast Neoplasmsen_GB
dc.subject.meshFemaleen_GB
dc.subject.meshFlow Cytometryen_GB
dc.subject.meshGenes, BRCA2en_GB
dc.subject.meshGenetic Markersen_GB
dc.subject.meshGerm-Line Mutationen_GB
dc.subject.meshHumansen_GB
dc.subject.meshImmunohistochemistryen_GB
dc.subject.meshMolecular Sequence Dataen_GB
dc.subject.meshPhenotypeen_GB
dc.subject.meshTetraploidyen_GB
dc.titleTetraploidy in BRCA2 breast tumours.en
dc.typeArticleen
dc.contributor.departmentCancer Research Laboratory, Faculty of Medicine, University of Iceland, Reykjavik, Iceland.en_GB
dc.identifier.journalEuropean journal of cancer (Oxford, England : 1990)en_GB
dc.rights.accessNational Consortium - Landsaðganguren
html.description.abstractTetraploidy and aneuploidy can be caused by cell division errors and are frequently observed in many human carcinomas. We have recently reported delayed cytokinesis in primary human fibroblasts from BRCA2 mutation carriers, implying a function for the BRCA2 tumour suppressor in completion of cell division. Here, we address ploidy aberrations in breast tumours derived from BRCA2 germline mutation carriers. Ploidy aberrations were evaluated from flow cytometry histograms on selected breast tumour samples (n=236), previously screened for local BRCA mutations. The ploidy between BRCA2-mutated (n=71) and matched sporadic (n=165) cancers was compared. Differences in ploidy distribution were examined with respect to molecular tumour subtypes, previously defined by immunohistochemistry on tissue microarray sections. Tetraploidy was significantly 3 times more common in BRCA2 breast cancers than sporadic. However, no differences were found in the overall ploidy distribution between BRCA2-mutation carriers and non-carriers. In BRCA2 cancers, tetraploidy was associated with luminal characteristics. The increased frequency of tetraploidy in BRCA2 associated cancers may be linked to cell division errors, particularly cytokinesis. Additionally, tetraploidy emerges predominantly in BRCA2 breast cancers displaying luminal rather than triple-negative phenotypes.


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