{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Dorfel D"],"funding":["European Social Fund","Wilhelm Sander-Stiftung","Deutsche Krebshilfe"],"pagination":["775-783"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11028318"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["67(5)"],"pubmed_abstract":["In chronic myeloid leukemia (CML), the translocation t(9;22) results in the fusion protein BCR-ABL (breakpoint cluster region-abelson murine leukemia), a tyrosine kinase mediating oncogenic signaling which is successfully targeted by treatment with BCR-ABL inhibitors like imatinib. However, BCR-ABL inhibitors may also affect antitumor immunity. For instance, it was reported that imatinib impairs the function of dendritic cells (DCs) that play a central role in initiating and sustaining T cell responses. Meanwhile, second generation BCR-ABL inhibitors like nilotinib, which inhibits BCR-ABL with enhanced potency have become standard of treatment, at least in patients with BCR-ABL kinase domain mutations. In this study we analyzed the influence of therapeutic concentrations of nilotinib on hu"],"journal":["Cancer immunology, immunotherapy : CII"],"pubmed_title":["The BCR-ABL inhibitor nilotinib influences phenotype and function of monocyte-derived human dendritic cells."],"pmcid":["PMC11028318"],"funding_grant_id":["109046","2013.148.1"],"pubmed_authors":["Kopp HG","Geiger J","Maurer S","Rittig SM","Lechner CJ","Gutknecht M","Salih J","Salih HR","Dorfel D","Grunebach F","Funk T","Joas S","Kropp KN","Muller MR"],"additional_accession":[]},"is_claimable":false,"name":"The BCR-ABL inhibitor nilotinib influences phenotype and function of monocyte-derived human dendritic cells.","description":"In chronic myeloid leukemia (CML), the translocation t(9;22) results in the fusion protein BCR-ABL (breakpoint cluster region-abelson murine leukemia), a tyrosine kinase mediating oncogenic signaling which is successfully targeted by treatment with BCR-ABL inhibitors like imatinib. However, BCR-ABL inhibitors may also affect antitumor immunity. For instance, it was reported that imatinib impairs the function of dendritic cells (DCs) that play a central role in initiating and sustaining T cell responses. Meanwhile, second generation BCR-ABL inhibitors like nilotinib, which inhibits BCR-ABL with enhanced potency have become standard of treatment, at least in patients with BCR-ABL kinase domain mutations. In this study we analyzed the influence of therapeutic concentrations of nilotinib on hu","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 May","modification":"2026-06-01T21:54:43.972Z","creation":"2025-04-06T03:15:21.014Z"},"accession":"S-EPMC11028318","cross_references":{"pubmed":["29468363"],"doi":["10.1007/s00262-018-2129-9"]}}