<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Dorfel D</submitter><funding>European Social Fund</funding><funding>Wilhelm Sander-Stiftung</funding><funding>Deutsche Krebshilfe</funding><pagination>775-783</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11028318</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>67(5)</volume><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</pubmed_abstract><journal>Cancer immunology, immunotherapy : CII</journal><pubmed_title>The BCR-ABL inhibitor nilotinib influences phenotype and function of monocyte-derived human dendritic cells.</pubmed_title><pmcid>PMC11028318</pmcid><funding_grant_id>109046</funding_grant_id><funding_grant_id>2013.148.1</funding_grant_id><pubmed_authors>Kopp HG</pubmed_authors><pubmed_authors>Geiger J</pubmed_authors><pubmed_authors>Maurer S</pubmed_authors><pubmed_authors>Rittig SM</pubmed_authors><pubmed_authors>Lechner CJ</pubmed_authors><pubmed_authors>Gutknecht M</pubmed_authors><pubmed_authors>Salih J</pubmed_authors><pubmed_authors>Salih HR</pubmed_authors><pubmed_authors>Dorfel D</pubmed_authors><pubmed_authors>Grunebach F</pubmed_authors><pubmed_authors>Funk T</pubmed_authors><pubmed_authors>Joas S</pubmed_authors><pubmed_authors>Kropp KN</pubmed_authors><pubmed_authors>Muller MR</pubmed_authors></additional><is_claimable>false</is_claimable><name>The BCR-ABL inhibitor nilotinib influences phenotype and function of monocyte-derived human dendritic cells.</name><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</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 May</publication><modification>2026-06-01T21:54:43.972Z</modification><creation>2025-04-06T03:15:21.014Z</creation></dates><accession>S-EPMC11028318</accession><cross_references><pubmed>29468363</pubmed><doi>10.1007/s00262-018-2129-9</doi></cross_references></HashMap>