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dc.contributor.authorSletta, Kristine Yttersian
dc.contributor.authorMarin, Oriol Castells
dc.contributor.authorGjertsen, Bjørn Tore
dc.date.accessioned2022-04-20T07:34:40Z
dc.date.available2022-04-20T07:34:40Z
dc.date.created2021-05-06T12:16:35Z
dc.date.issued2021
dc.identifier.issn2234-943X
dc.identifier.urihttps://hdl.handle.net/11250/2991483
dc.description.abstractAcute myeloid leukemia (AML) is an aggressive heterogeneous blood cancer derived from hematopoietic stem cells. Tumor-stromal interactions in AML are of importance for disease development and therapy resistance, and bone marrow stroma seem like an attractive therapeutic target. Of particular interest is colony stimulating factor 1 receptor (CSF1R, M-CSFR, c-FMS, CD115) and its role in regulating plasticity of tumor-associated macrophages. We discuss first the potential of CSF1R-targeted therapy as an attractive concept with regards to the tumor microenvironment in the bone marrow niche. A second therapy approach, supported by preclinical research, also suggests that CSF1R-targeted therapy may increase the beneficial effect of conventional and novel therapeutics. Experimental evidence positioning inhibitors of CSF1R as treatment should, together with data from preclinical and early phase clinical trials, facilitate translation and clinical development of CSF1R-targeted therapy for AML.en_US
dc.language.isoengen_US
dc.publisherFrontiers Mediaen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleColony stimulating factor 1 receptor in acute myeloid leukemiaen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2021 Sletta, Castells and Gjertsenen_US
dc.source.articlenumber654817en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.doi10.3389/fonc.2021.654817
dc.identifier.cristin1908445
dc.source.journalFrontiers in Oncologyen_US
dc.identifier.citationFrontiers in Oncology. 2021, 11, 654817.en_US
dc.source.volume11en_US


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