Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12590
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dc.contributor.authorVella, Laura Jen
dc.contributor.authorAndrews, Miles Cen
dc.contributor.authorPasam, Anupamaen
dc.contributor.authorWoods, Katherineen
dc.contributor.authorBehren, Andreasen
dc.contributor.authorCebon, Jonathan Sen
dc.date.accessioned2015-05-16T02:18:23Z
dc.date.available2015-05-16T02:18:23Z
dc.date.issued2014-07-03en
dc.identifier.citationOncoimmunology 2014; 3(7): e946367en
dc.identifier.govdoc25610732en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/12590en
dc.description.abstractMetastatic melanoma is frequently fatal. Optimal treatment regimens require both rapid and durable disease control, likely best achieved by combining targeted agents with immunotherapeutics. In order to accomplish this, a detailed understanding of the immune consequences of the kinase inhibitors used to treat melanoma is required.en
dc.language.isoenen
dc.subject.otherBRAFen
dc.subject.otherMEKen
dc.subject.otherT-lymphocytesen
dc.subject.otherdendritic cellsen
dc.subject.othermelanomaen
dc.titleThe kinase inhibitors dabrafenib and trametinib affect isolated immune cell populations.en
dc.typeJournal Articleen
dc.identifier.journaltitleOncoimmunologyen
dc.identifier.affiliationLudwig Institute for Cancer Research; Melbourne-Austin Branch; Cancer Immuno-biology Laboratory ; Heidelberg, Australiaen
dc.identifier.doi10.4161/21624011.2014.946367en
dc.description.pagese946367en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/25610732en
dc.type.austinJournal Articleen
item.languageiso639-1en-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
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