{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["2(3)"],"submitter":["Hantschel O"],"pubmed_abstract":["We have identified differentially regulated genes in chronic myeloid leukemia (CML) cells upon short treatment with the broad-spectrum Bcr-Abl inhibitor dasatinib. The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells. Among the strongest downregulated genes, we have further validated the activation marker CD69 and the chemokine interleukin (IL)-8. Expression of both proteins is upregulated upon Bcr-Abl expression and inhibited by dasatinib and nilotinib. IL-8 may thus be a useful marker for the monitoring of CML inhibitor efficacy and play a potential pathophysiological r"],"journal":["Molecular oncology"],"pagination":["272-81"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5527809"],"repository":["biostudies-literature"],"pubmed_title":["The chemokine interleukin-8 and the surface activation protein CD69 are markers for Bcr-Abl activity in chronic myeloid leukemia."],"pmcid":["PMC5527809"],"pubmed_authors":["Gstoettenbauer A","Kaupe I","Hantschel O","Valent P","Burkard TR","Superti-Furga G","Colinge J","Bilban M"],"additional_accession":[]},"is_claimable":false,"name":"The chemokine interleukin-8 and the surface activation protein CD69 are markers for Bcr-Abl activity in chronic myeloid leukemia.","description":"We have identified differentially regulated genes in chronic myeloid leukemia (CML) cells upon short treatment with the broad-spectrum Bcr-Abl inhibitor dasatinib. The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells. Among the strongest downregulated genes, we have further validated the activation marker CD69 and the chemokine interleukin (IL)-8. Expression of both proteins is upregulated upon Bcr-Abl expression and inhibited by dasatinib and nilotinib. IL-8 may thus be a useful marker for the monitoring of CML inhibitor efficacy and play a potential pathophysiological r","dates":{"release":"2008-01-01T00:00:00Z","publication":"2008 Oct","modification":"2025-04-26T12:37:23.157Z","creation":"2019-03-27T02:51:40Z"},"accession":"S-EPMC5527809","cross_references":{"pubmed":["19383348"],"doi":["10.1016/j.molonc.2008.07.003"]}}