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dc.contributor.authorScheel, Christina
dc.contributor.authorEaton, Elinor Ng
dc.contributor.authorChaffer, Christine L.
dc.contributor.authorReinhardt, Ferenc
dc.contributor.authorKah, Kong-Jie
dc.contributor.authorBell, George
dc.contributor.authorGuo, Wenjun
dc.contributor.authorRubin, Jeffrey
dc.contributor.authorRichardson, Andrea L.
dc.contributor.authorWeinberg, Robert A.
dc.contributor.authorLi, Sophia
dc.contributor.authorWeinberg, Robert A
dc.date.accessioned2014-12-10T19:33:28Z
dc.date.available2014-12-10T19:33:28Z
dc.date.issued2011-06
dc.date.submitted2011-02
dc.identifier.issn00928674
dc.identifier.issn1097-4172
dc.identifier.urihttp://hdl.handle.net/1721.1/92261
dc.description.abstractThe epithelial-mesenchymal transition (EMT) has been associated with the acquisition of motility, invasiveness, and self-renewal traits. During both normal development and tumor pathogenesis, this change in cell phenotype is induced by contextual signals that epithelial cells receive from their microenvironment. The signals that are responsible for inducing an EMT and maintaining the resulting cellular state have been unclear. We describe three signaling pathways, involving transforming growth factor (TGF)-β and canonical and noncanonical Wnt signaling, that collaborate to induce activation of the EMT program and thereafter function in an autocrine fashion to maintain the resulting mesenchymal state. Downregulation of endogenously synthesized inhibitors of autocrine signals in epithelial cells enables the induction of the EMT program. Conversely, disruption of autocrine signaling by added inhibitors of these pathways inhibits migration and self-renewal in primary mammary epithelial cells and reduces tumorigenicity and metastasis by their transformed derivatives.en_US
dc.description.sponsorshipNational Cancer Institute (U.S.) (CA12515)en_US
dc.description.sponsorshipNational Cancer Institute (U.S.) (DE020817)en_US
dc.description.sponsorshipMassachusetts Institute of Technology. Ludwig Center for Molecular Oncologyen_US
dc.description.sponsorshipBreast Cancer Research Foundationen_US
dc.description.sponsorshipDana-Farber/Harvard Cancer Center. SPOREen_US
dc.description.sponsorshipUnited States. Dept. of Defense. Congressionally Directed Medical Research Programs. Breast Cancer Research Program (Idea Award)en_US
dc.description.sponsorshipSamuel Waxman Foundationen_US
dc.language.isoen_US
dc.publisherElsevieren_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.cell.2011.04.029en_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.sourceElsevieren_US
dc.titleParacrine and Autocrine Signals Induce and Maintain Mesenchymal and Stem Cell States in the Breasten_US
dc.typeArticleen_US
dc.identifier.citationScheel, Christina, Elinor Ng Eaton, Sophia Hsin-Jung Li, Christine L. Chaffer, Ferenc Reinhardt, Kong-Jie Kah, George Bell, et al. “Paracrine and Autocrine Signals Induce and Maintain Mesenchymal and Stem Cell States in the Breast.” Cell 145, no. 6 (June 2011): 926–940. © 2011 Elsevier Inc.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biological Engineeringen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.departmentWhitehead Institute for Biomedical Researchen_US
dc.contributor.departmentLudwig Center for Molecular Oncology (Massachusetts Institute of Technology)en_US
dc.contributor.mitauthorLi, Sophiaen_US
dc.contributor.mitauthorKah, Kong-Jieen_US
dc.contributor.mitauthorWeinberg, Robert A.en_US
dc.relation.journalCellen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsScheel, Christina; Eaton, Elinor Ng; Li, Sophia Hsin-Jung; Chaffer, Christine L.; Reinhardt, Ferenc; Kah, Kong-Jie; Bell, George; Guo, Wenjun; Rubin, Jeffrey; Richardson, Andrea L.; Weinberg, Robert A.en_US
dc.identifier.orcidhttps://orcid.org/0000-0002-0895-3557
mit.licensePUBLISHER_POLICYen_US


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