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dc.contributor.authorOliemuller, E
dc.contributor.authorNewman, R
dc.contributor.authorTsang, SM
dc.contributor.authorFoo, S
dc.contributor.authorMuirhead, G
dc.contributor.authorNoor, F
dc.contributor.authorHaider, S
dc.contributor.authorAurrekoetxea-Rodríguez, I
dc.contributor.authorVivanco, MD
dc.contributor.authorHoward, BA
dc.date.accessioned2020-09-16T13:32:28Z
dc.date.issued2020-09-10
dc.identifier.citationeLife, 2020, 9
dc.identifier.issn2050-084X
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/4070
dc.identifier.eissn2050-084X
dc.identifier.doi10.7554/elife.58374
dc.description.abstractSOX11 is an embryonic mammary epithelial marker that is normally silenced prior to birth. High SOX11 levels in breast tumours are significantly associated with distant metastasis and poor outcome in breast cancer patients. Here, we show that SOX11 confers distinct features to ER-negative DCIS.com breast cancer cells, leading to populations enriched with highly plastic hybrid epithelial/mesenchymal cells, which display invasive features and alterations in metastatic tropism when xenografted into mice. We found that SOX11+DCIS tumour cells metastasize to brain and bone at greater frequency and to lungs at lower frequency compared to cells with lower SOX11 levels. High levels of SOX11 leads to the expression of markers associated with mesenchymal state and embryonic cellular phenotypes. Our results suggest that SOX11 may be a potential biomarker for breast tumours with elevated risk of developing metastases and may require more aggressive therapies.
dc.formatElectronic
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleSOX11 promotes epithelial/mesenchymal hybrid state and alters tropism of invasive breast cancer cells.
dc.typeJournal Article
dcterms.dateAccepted2020-09-09
rioxxterms.versionofrecord10.7554/elife.58374
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2020-09-10
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfeLife
pubs.notesNo embargo
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Endocrine control mechanisms
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Endocrine control mechanisms
pubs.publication-statusPublished
pubs.volume9
pubs.embargo.termsNo embargo
icr.researchteamEndocrine control mechanismsen_US
dc.contributor.icrauthorHoward, Beatriceen


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