Hantschel, OliverGstoettenbauer, AgnesColinge, JacquesKaupe, InesBilban, MartinBurkard, Thomas R.Valent, PeterSuperti-Furga, Giulio2011-03-212011-03-212011-03-21200810.1016/j.molonc.2008.07.003https://infoscience.epfl.ch/handle/20.500.14299/65502We 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 role in CML.text::journal::journal article::research article