000164358 001__ 164358
000164358 005__ 20181203022328.0
000164358 0247_ $$2doi$$a10.1016/j.molonc.2008.07.003
000164358 022__ $$a1878-0261
000164358 037__ $$aARTICLE
000164358 245__ $$aThe chemokine interleukin-8 and the surface activation protein CD69 are markers for Bcr-Abl activity in chronic myeloid leukemia
000164358 269__ $$a2008
000164358 260__ $$c2008
000164358 336__ $$aJournal Articles
000164358 520__ $$aWe have identified differentially regulated genes in chronic myeloid leukemia (CML) cells upon short treatment with the broad-spectrum Bcr-Abl inhibitor dasatinib. The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells. Among the strongest downregulated genes, we have further validated the activation marker CD69 and the chemokine interleukin (IL)-8. Expression of both proteins is upregulated upon Bcr-Abl expression and inhibited by dasatinib and nilotinib. IL-8 may thus be a useful marker for the monitoring of CML inhibitor efficacy and play a potential pathophysiological role in CML.
000164358 700__ $$0245280$$g209845$$aHantschel, Oliver
000164358 700__ $$aGstoettenbauer, Agnes
000164358 700__ $$aColinge, Jacques
000164358 700__ $$aKaupe, Ines
000164358 700__ $$aBilban, Martin
000164358 700__ $$aBurkard, Thomas R.
000164358 700__ $$aValent, Peter
000164358 700__ $$aSuperti-Furga, Giulio
000164358 773__ $$j2$$tMolecular oncology$$k3$$q272-81
000164358 909C0 $$xU12375$$0252328$$pUPHAN
000164358 909CO $$pSV$$particle$$ooai:infoscience.tind.io:164358
000164358 917Z8 $$x182396
000164358 937__ $$aEPFL-ARTICLE-164358
000164358 973__ $$rREVIEWED$$sPUBLISHED$$aOTHER
000164358 980__ $$aARTICLE