Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/17200
Full metadata record
DC FieldValueLanguage
dc.contributor.authorSchmidt, Stefanie-
dc.contributor.authorSchumacher, Neele-
dc.contributor.authorSchwarz, Jeanette-
dc.contributor.authorTangermann, Simone-
dc.contributor.authorKenner, Lukas-
dc.contributor.authorSchlederer, Michaela-
dc.contributor.authorSibilia, Maria-
dc.contributor.authorLinder, Markus-
dc.contributor.authorAltendorf-Hofmann, Annelore-
dc.contributor.authorKnösel, Thomas-
dc.contributor.authorGruber, Elisabeth S-
dc.contributor.authorOberhuber, Georg-
dc.contributor.authorBolik, Julia-
dc.contributor.authorRehman, Ateequr-
dc.contributor.authorSinha, Anupam-
dc.contributor.authorLokau, Juliane-
dc.contributor.authorArnold, Philipp-
dc.contributor.authorCabron, Anne-Sophie-
dc.contributor.authorZunke, Friederike-
dc.contributor.authorBecker-Pauly, Christoph-
dc.contributor.authorPreaudet, Adele-
dc.contributor.authorNguyen, Paul-
dc.contributor.authorHuynh, Jennifer-
dc.contributor.authorAfshar-Sterle, Shoukat-
dc.contributor.authorChand, Ashwini L-
dc.contributor.authorWestermann, Jürgen-
dc.contributor.authorDempsey, Peter J-
dc.contributor.authorGarbers, Christoph-
dc.contributor.authorSchmidt-Arras, Dirk-
dc.contributor.authorRosenstiel, Philip-
dc.contributor.authorPutoczki, Tracy-
dc.contributor.authorErnst, Matthias-
dc.contributor.authorRose-John, Stefan-
dc.date2018-
dc.date.accessioned2018-03-12T21:50:35Z-
dc.date.available2018-03-12T21:50:35Z-
dc.date.issued2018-02-22-
dc.identifier.citationThe Journal of experimental medicine 2018; 215(4): 1205-1225-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/17200-
dc.description.abstractColorectal cancer is treated with antibodies blocking epidermal growth factor receptor (EGF-R), but therapeutic success is limited. EGF-R is stimulated by soluble ligands, which are derived from transmembrane precursors by ADAM17-mediated proteolytic cleavage. In mouse intestinal cancer models in the absence of ADAM17, tumorigenesis was almost completely inhibited, and the few remaining tumors were of low-grade dysplasia. RNA sequencing analysis demonstrated down-regulation of STAT3 and Wnt pathway components. Because EGF-R on myeloid cells, but not on intestinal epithelial cells, is required for intestinal cancer and because IL-6 is induced via EGF-R stimulation, we analyzed the role of IL-6 signaling. Tumor formation was equally impaired in IL-6-/-mice and sgp130Fc transgenic mice, in which only trans-signaling via soluble IL-6R is abrogated. ADAM17 is needed for EGF-R-mediated induction of IL-6 synthesis, which via IL-6 trans-signaling induces β-catenin-dependent tumorigenesis. Our data reveal the possibility of a novel strategy for treatment of colorectal cancer that could circumvent intrinsic and acquired resistance to EGF-R blockade.-
dc.language.isoeng-
dc.titleADAM17 is required for EGF-R-induced intestinal tumors via IL-6 trans-signaling.-
dc.typeJournal Article-
dc.identifier.journaltitleThe Journal of experimental medicine-
dc.identifier.affiliationBiochemisches Institut, Christian Albrechts Universität Kiel, Kiel, Germany-
dc.identifier.affiliationUnit of Laboratory Animal Pathology, University of Veterinary Medicine, Vienna, Austria-
dc.identifier.affiliationLudwig Boltzmann Institute for Cancer Research, Vienna, Austria-
dc.identifier.affiliationDepartment of Experimental and Laboratory Animal Pathology, Medical University Vienna, Vienna, Austria-
dc.identifier.affiliationInstitute of Cancer Research, Department of Medicine I, Medical University of Vienna, Comprehensive Cancer Center, Vienna, Austria-
dc.identifier.affiliationDepartment of General, Visceral and Vascular Surgery, Jena University Hospital, Jena, Germany-
dc.identifier.affiliationInstitute of Pathology, Ludwig-Maximilians-University, Munich, Germany-
dc.identifier.affiliationDepartment of General Surgery, Division of Surgery and Comprehensive Cancer Center, Medical University Vienna, Vienna, Austria-
dc.identifier.affiliationInstitute of Clinical Molecular Biology, Christian Albrechts Universität Kiel, Kiel, Germany-
dc.identifier.affiliationAnatomisches Institut, Christian Albrechts Universität Kiel, Kiel, Germany-
dc.identifier.affiliationThe Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria, Australia-
dc.identifier.affiliationDepartment of Medical Biology, The University of Melbourne, Melbourne, Victoria, Australia-
dc.identifier.affiliationOlivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australia-
dc.identifier.affiliationInstitut für Anatomie, Universität zu Lübeck, Lübeck, Germany-
dc.identifier.affiliationDepartment of Pediatrics, University of Colorado School of Medicine, Aurora, CO-
dc.identifier.affiliationSchool of Cancer Medicine, La Trobe University, Melbourne, Victoria, Australia-
dc.identifier.doi10.1084/jem.20171696-
dc.identifier.orcid0000-0002-6471-5473-
dc.identifier.orcid0000-0002-8646-1865-
dc.identifier.orcid0000-0002-5100-9916-
dc.identifier.orcid0000-0002-1245-729X-
dc.identifier.orcid0000-0001-9054-8755-
dc.identifier.orcid0000-0003-4151-799X-
dc.identifier.orcid0000-0003-4939-6950-
dc.identifier.orcid0000-0002-1072-7495-
dc.identifier.orcid0000-0002-9692-8828-
dc.identifier.orcid0000-0002-7519-3279-
dc.identifier.pubmedid29472497-
dc.type.austinJournal Article-
local.name.researcherAfshar-Sterle, Shoukat
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
Appears in Collections:Journal articles
Show simple item record

Page view(s)

28
checked on Mar 28, 2024

Google ScholarTM

Check


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.