<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>2(3)</volume><submitter>Hantschel O</submitter><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</pubmed_abstract><journal>Molecular oncology</journal><pagination>272-81</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5527809</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The chemokine interleukin-8 and the surface activation protein CD69 are markers for Bcr-Abl activity in chronic myeloid leukemia.</pubmed_title><pmcid>PMC5527809</pmcid><pubmed_authors>Gstoettenbauer A</pubmed_authors><pubmed_authors>Kaupe I</pubmed_authors><pubmed_authors>Hantschel O</pubmed_authors><pubmed_authors>Valent P</pubmed_authors><pubmed_authors>Burkard TR</pubmed_authors><pubmed_authors>Superti-Furga G</pubmed_authors><pubmed_authors>Colinge J</pubmed_authors><pubmed_authors>Bilban M</pubmed_authors></additional><is_claimable>false</is_claimable><name>The chemokine interleukin-8 and the surface activation protein CD69 are markers for Bcr-Abl activity in chronic myeloid leukemia.</name><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</description><dates><release>2008-01-01T00:00:00Z</release><publication>2008 Oct</publication><modification>2025-04-26T12:37:23.157Z</modification><creation>2019-03-27T02:51:40Z</creation></dates><accession>S-EPMC5527809</accession><cross_references><pubmed>19383348</pubmed><doi>10.1016/j.molonc.2008.07.003</doi></cross_references></HashMap>