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dc.contributor.authorLi, J-Len
dc.contributor.authorHarris, ALen
dc.date.accessioned2017-11-29T13:11:29Z
dc.date.available2017-11-29T13:11:29Z
dc.date.issued2005-07en
dc.identifier.issn1535-6108en
dc.identifier.urihttp://hdl.handle.net/10026.1/10344
dc.description.abstract

Notch signaling is an evolutionarily conserved pathway and plays key roles in embryonic vascular development and angiogenesis. Multiple components of the Notch pathway are expressed in vasculature, and mice deficient for a variety of these components display embryonic lethality with vascular remodeling defects. Alteration of Notch signaling in various endothelial cells generates profound effects on angiogenesis in vitro. New evidence shows that Notch signaling from tumor cells is able to activate endothelial cells and trigger tumor angiogenesis in vitro and in a xenograft mouse tumor model. Selective interruption of Notch signaling within tumors may provide an antiangiogenic strategy.

en
dc.format.extent1 - 3en
dc.languageengen
dc.language.isoengen
dc.subjectAngiogenesis Inhibitorsen
dc.subjectAnimalsen
dc.subjectHumansen
dc.subjectMembrane Proteinsen
dc.subjectNeoplasmsen
dc.subjectNeovascularization, Pathologicen
dc.subjectReceptors, Cell Surfaceen
dc.subjectReceptors, Notchen
dc.subjectSignal Transductionen
dc.titleNotch signaling from tumor cells: a new mechanism of angiogenesis.en
dc.typeJournal Article
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/16023591en
plymouth.issue1en
plymouth.volume8en
plymouth.publication-statusPublisheden
plymouth.journalCancer Cellen
dc.identifier.doi10.1016/j.ccr.2005.06.013en
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine/UoA01 Clinical Medicine
dc.publisher.placeUnited Statesen
dc.rights.embargoperiodNot knownen
rioxxterms.versionofrecord10.1016/j.ccr.2005.06.013en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.typeJournal Article/Reviewen


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