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dc.contributor.authorEissmann, Moritz F-
dc.contributor.authorDijkstra, Christine-
dc.contributor.authorJarnicki, Andrew-
dc.contributor.authorPhesse, Toby-
dc.contributor.authorBrunnberg, Jamina-
dc.contributor.authorPoh, Ashleigh R-
dc.contributor.authorEtemadi, Nima-
dc.contributor.authorTsantikos, Evelyn-
dc.contributor.authorThiem, Stefan-
dc.contributor.authorHuntington, Nicholas D-
dc.contributor.authorHibbs, Margaret L-
dc.contributor.authorBoussioutas, Alex-
dc.contributor.authorGrimbaldeston, Michele A-
dc.contributor.authorBuchert, Michael-
dc.contributor.authorO'Donoghue, Robert J J-
dc.contributor.authorMasson, Frederick-
dc.contributor.authorErnst, Matthias-
dc.identifier.citationNature communications 2019; 10(1): 2735-
dc.description.abstractThe contribution of mast cells in the microenvironment of solid malignancies remains controversial. Here we functionally assess the impact of tumor-adjacent, submucosal mast cell accumulation in murine and human intestinal-type gastric cancer. We find that genetic ablation or therapeutic inactivation of mast cells suppresses accumulation of tumor-associated macrophages, reduces tumor cell proliferation and angiogenesis, and diminishes tumor burden. Mast cells are activated by interleukin (IL)-33, an alarmin produced by the tumor epithelium in response to the inflammatory cytokine IL-11, which is required for the growth of gastric cancers in mice. Accordingly, ablation of the cognate IL-33 receptor St2 limits tumor growth, and reduces mast cell-dependent production and release of the macrophage-attracting factors Csf2, Ccl3, and Il6. Conversely, genetic or therapeutic macrophage depletion reduces tumor burden without affecting mast cell abundance. Therefore, tumor-derived IL-33 sustains a mast cell and macrophage-dependent signaling cascade that is amenable for the treatment of gastric cancer.-
dc.titleIL-33-mediated mast cell activation promotes gastric cancer through macrophage mobilization.-
dc.typeJournal Article-
dc.typeResearch Support, Non-U.S. Gov't-
dc.identifier.journaltitleNature communications-
dc.identifier.affiliationTeam 5, Centre of Physiopathology Toulouse-Purpan, INSERM UMR 1043/CNRS UMR 5282, University Toulouse III, CHU Purpan, 31024, Toulouse, Franceen
dc.identifier.affiliationCell Signalling and Cell Death Division, Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Melbourne, VIC, 3052, Australiaen
dc.identifier.affiliationInstitute of Biochemistry, Goethe University Frankfurt, Frankfurt am Main, 60438, Frankfurt, Germanyen
dc.identifier.affiliationDepartment of Pharmacology and Therapeutics, University of Melbourne, Melbourne, VIC, 3010, Australiaen
dc.identifier.affiliationCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, 5000, Australiaen
dc.identifier.affiliationOMNI-Biomarker Development, Genentech Inc., South San Francisco, CA, 94080, USAen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Melbourne, VIC, 3050, Australiaen
dc.identifier.affiliationDepartment of Immunology and Pathology, Monash University, Melbourne, VIC, 3004, Australiaen
dc.identifier.affiliationMolecular Immunology Division, The Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Melbourne, VIC, 3052, Australiaen
dc.identifier.affiliationCell Signaling and Cancer Laboratory, European Cancer Stem Cell Research Institute and Cardiff University, Cardiff, CF24 4HQ, UKen
dc.identifier.affiliationCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationSchool of Cancer Medicine, La Trobe University, Heidelberg, VIC, 3084, Australia-
Appears in Collections:Journal articles

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