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dc.contributor.authorOliemuller, E-
dc.contributor.authorKogata, N-
dc.contributor.authorBland, P-
dc.contributor.authorKriplani, D-
dc.contributor.authorDaley, F-
dc.contributor.authorHaider, S-
dc.contributor.authorShah, V-
dc.contributor.authorSawyer, EJ-
dc.contributor.authorHoward, BA-
dc.identifier.citationThe Journal of Pathology, (2017)en_US
dc.description.abstractHere, we show that SOX11, an embryonic mammary marker that is normally silent in postnatal breast cells, is expressed in many oestrogen receptor-negative preinvasive ductal carcinoma in situ (DCIS) lesions. Mature mammary epithelial cells engineered to express SOX11 showed alterations in progenitor cell populations, including an expanded basal-like population with increased aldehyde dehydrogenase (ALDH) activity, and increased mammosphere-forming capacity. cells engineered to express SOX11 showed increased ALDH activity, which is a feature of cancer stem cells. The CD44+/CD24–/ALDH+ cell population was increased in cells that expressed SOX11. Upregulating SOX11 expression in cells led to increased invasive growth both in vitro and when they were injected intraductally in a mouse model of DCIS that recapitulates human disease. Invasive lesions formed sooner and tumour growth was augmented in vivo, suggesting that SOX11 contributes to the progression of DCIS to invasive breast cancer. We identified potential downstream effectors of SOX11 during both microinvasive and invasive tumour growth stages, including several with established links to regulation of progenitor cell function and prenatal developmental growth. Our findings suggest that SOX11 is a potential biomarker for DCIS lesions containing cells harbouring distinct biological features that are likely to progress to invasive breast cancer.en_US
dc.publisherWiley Open Accessen_US
dc.subjectEmbryonic mammary markeren_US
dc.subjectMammary progenitor/stem cellsen_US
dc.titleSOX11 promotes invasive growth and ductal carcinoma in situ progressionen_US
dc.relation.isPartOfThe Journal of Pathology-
pubs.publication-statusPublished online-
Appears in Collections:Dept of Life Sciences Research Papers

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