Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/22534
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dc.contributor.authorPoh, Ashleigh R-
dc.contributor.authorDwyer, Amy R-
dc.contributor.authorEissmann, Moritz F-
dc.contributor.authorChand, Ashwini L-
dc.contributor.authorBaloyan, David-
dc.contributor.authorBoon, Louis-
dc.contributor.authorMurrey, Michael W-
dc.contributor.authorWhitehead, Lachlan-
dc.contributor.authorO'Brien, Megan-
dc.contributor.authorLowell, Clifford A-
dc.contributor.authorPutoczki, Tracy L-
dc.contributor.authorPixley, Fiona J-
dc.contributor.authorO'Donoghue, Robert Jj-
dc.contributor.authorErnst, Matthias-
dc.date2020-
dc.date.accessioned2020-02-04T03:22:14Z-
dc.date.available2020-02-04T03:22:14Z-
dc.date.issued2020-01-28-
dc.identifier.citationCancer immunology research 2020-01-28-
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/22534-
dc.description.abstractPersistent activation of the latent transcription factor STAT3 is observed in gastric tumor epithelial and immune cells and is associated with a poor patient prognosis. Although targeting STAT3-activating upstream kinases offers therapeutically viable targets with limited specificity, direct inhibition of STAT3 remains challenging. Here we provide functional evidence that myeloid-specific hematopoietic cell kinase (HCK) activity can drive STAT3-dependent epithelial tumor growth in mice and is associated with alternative macrophage activation alongside matrix remodeling and tumor cell invasion. Accordingly, genetic reduction of HCK expression in bone marrow-derived cells or systemic pharmacologic inhibition of HCK activity suppresses alternative macrophage polarization, epithelial STAT3 activation, and impairs tumor growth. These data validate HCK as a molecular target for the treatment of human solid tumors harboring excessive STAT3 activity.-
dc.language.isoeng-
dc.titleInhibition of the SRC kinase HCK impairs STAT3-dependent gastric tumor growth in mice.-
dc.typeJournal Article-
dc.identifier.journaltitleCancer immunology research-
dc.identifier.affiliationCancer and Inflammation, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine at La Trobe University-
dc.identifier.affiliationSchool of Biomedical Sciences, University of Western Australiaen
dc.identifier.affiliationMasonic Cancer Center, University of Minnesota-
dc.identifier.affiliationCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute-
dc.identifier.affiliationCancer and Inflammation, Olivia Newton-John Cancer Research Institute and School of Cancer Medicine at La Trobe University-
dc.identifier.affiliationCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine-
dc.identifier.affiliationBioceros, CM Utrecht-
dc.identifier.affiliationMedical Biology, The Walter and Eliza Hall Institute-
dc.identifier.affiliationCancer and Inflammation Laboratory, Olivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine-
dc.identifier.affiliationLaboratory Medicine, University of California, San Francisco-
dc.identifier.affiliationInflammation Division, Walter and Eliza Hall Institute of Medical Research-
dc.identifier.affiliationDepartment of Pharmacology and Therapeutics, University of Melbourne-
dc.identifier.doi10.1158/2326-6066.CIR-19-0623-
dc.identifier.orcid0000-0002-1245-729X-
dc.identifier.orcid0000-0002-4388-9642-
dc.identifier.orcid0000-0002-1571-2532-
dc.identifier.orcid0000-0002-6399-1177-
dc.identifier.pubmedid31992566-
Appears in Collections:Journal articles

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