dc.contributor.author | Engelsen, Agnete | |
dc.contributor.author | Wnuk-Lipinska, Katarzyna | |
dc.contributor.author | Bougnaud, Sébastien | |
dc.contributor.author | Vatter, Fanny A. Pelissier | |
dc.contributor.author | Tiron, Crina Elena | |
dc.contributor.author | Villadsen, René | |
dc.contributor.author | Miyano, Masaru | |
dc.contributor.author | Lotsberg, Maria Lie | |
dc.contributor.author | Madeleine, Noëlly | |
dc.contributor.author | Panahandeh, Pouda | |
dc.contributor.author | Dhakal, Sushil | |
dc.contributor.author | Tan, Tuan Zea | |
dc.contributor.author | Peters, Stacey D'Mello | |
dc.contributor.author | Grøndal, Sturla Magnus | |
dc.contributor.author | Aziz, Sura Mohammed | |
dc.contributor.author | Nord, Silje | |
dc.contributor.author | Herfindal, Lars | |
dc.contributor.author | Stampfer, Martha R. | |
dc.contributor.author | Sørlie, Therese | |
dc.contributor.author | Brekken, Rolf A | |
dc.contributor.author | Straume, Oddbjørn | |
dc.contributor.author | Halberg, Nils | |
dc.contributor.author | Gausdal, Gro | |
dc.contributor.author | Thiery, Jean Paul | |
dc.contributor.author | Akslen, Lars A. | |
dc.contributor.author | Petersen, Ole W. | |
dc.contributor.author | LaBarge, Mark A. | |
dc.contributor.author | Lorens, James | |
dc.date.accessioned | 2021-05-05T11:49:24Z | |
dc.date.available | 2021-05-05T11:49:24Z | |
dc.date.created | 2020-11-10T19:46:22Z | |
dc.date.issued | 2020 | |
dc.Published | iScience. 2020, 23 1-40. | |
dc.identifier.issn | 2589-0042 | |
dc.identifier.uri | https://hdl.handle.net/11250/2753692 | |
dc.description.abstract | The receptor tyrosine kinase AXL is associated with epithelial plasticity in several solid tumors including breast cancer and AXL-targeting agents are currently in clinical trials. We hypothesized that AXL is a driver of stemness traits in cancer by co-option of a regulatory function normally reserved for stem cells. AXL-expressing cells in human mammary epithelial ducts co-expressed markers associated with multipotency, and AXL inhibition abolished colony formation and self-maintenance activities while promoting terminal differentiation in vitro. Axl-null mice did not exhibit a strong developmental phenotype, but enrichment of Axl+ cells was required for mouse mammary gland reconstitution upon transplantation, and Axl-null mice had reduced incidence of Wnt1-driven mammary tumors. An AXL-dependent gene signature is a feature of transcriptomes in basal breast cancers and reduced patient survival irrespective of subtype. Our interpretation is that AXL regulates access to epithelial plasticity programs in MaSCs and, when co-opted, maintains acquired stemness in breast cancer cells. | en_US |
dc.language.iso | eng | en_US |
dc.publisher | Elsevier | en_US |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internasjonal | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/deed.no | * |
dc.title | AXL is a driver of stemness in normal mammary gland and breast cancer | en_US |
dc.type | Journal article | en_US |
dc.type | Peer reviewed | en_US |
dc.description.version | publishedVersion | en_US |
dc.rights.holder | Copyright 2020 The Authors | en_US |
dc.source.articlenumber | 101649 | en_US |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 1 | |
dc.identifier.doi | 10.1016/j.isci.2020.101649 | |
dc.identifier.cristin | 1846712 | |
dc.source.journal | iScience | en_US |
dc.source.40 | 23 | |
dc.identifier.citation | iScience. 2020, 23(11), 101649 | en_US |
dc.source.volume | 23 | en_US |
dc.source.issue | 11 | en_US |