{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shu ST"],"funding":["NCI NIH HHS","NIH HHS"],"pagination":["174"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11697302"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["Overexpression of the myeloid Src-family kinases Fgr and Hck has been linked to the development of acute myeloid leukemia (AML). Here we characterized the contribution of active forms of these kinases to AML cell cytokine dependence, inhibitor sensitivity, and AML cell engraftment in vivo. The human TF-1 erythroleukemia cell line was used as a model system as it does not express endogenous Hck or Fgr. To induce constitutive kinase activity, Hck and Fgr were fused to the coiled-coil (CC) oligomerization domain of the breakpoint cluster region protein associated with the Bcr-Abl tyrosine kinase in chronic myeloid leukemia. Expression of CC-Hck or CC-Fgr transformed TF-1 cells to a granulocyte-macrophage colony-stimulating factor (GM-CSF)-independent phenotype that correlated with enhanced ph"],"journal":["Scientific reports"],"pubmed_title":["Constitutive activation of the Src-family kinases Fgr and Hck enhances the tumor burden of acute myeloid leukemia cells in immunocompromised mice."],"pmcid":["PMC11697302"],"funding_grant_id":["R01 CA233576","CA233576"],"pubmed_authors":["Shu ST","Smithgall TE","Chen L","Gonzalez-Areizaga G"],"additional_accession":[]},"is_claimable":false,"name":"Constitutive activation of the Src-family kinases Fgr and Hck enhances the tumor burden of acute myeloid leukemia cells in immunocompromised mice.","description":"Overexpression of the myeloid Src-family kinases Fgr and Hck has been linked to the development of acute myeloid leukemia (AML). Here we characterized the contribution of active forms of these kinases to AML cell cytokine dependence, inhibitor sensitivity, and AML cell engraftment in vivo. The human TF-1 erythroleukemia cell line was used as a model system as it does not express endogenous Hck or Fgr. To induce constitutive kinase activity, Hck and Fgr were fused to the coiled-coil (CC) oligomerization domain of the breakpoint cluster region protein associated with the Bcr-Abl tyrosine kinase in chronic myeloid leukemia. Expression of CC-Hck or CC-Fgr transformed TF-1 cells to a granulocyte-macrophage colony-stimulating factor (GM-CSF)-independent phenotype that correlated with enhanced ph","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2026-06-01T11:07:13.376Z","creation":"2025-04-04T12:02:10.433Z"},"accession":"S-EPMC11697302","cross_references":{"pubmed":["39747387"],"doi":["10.1038/s41598-024-83740-6"]}}