Open AccessThe chemokine interleukin‐8 and the surface activation protein CD69 are markers for Bcr–Abl activity in chronic myeloid leukemia
Author(s) -
Hantschel Oliver,
Gstoettenbauer Agnes,
Colinge Jacques,
Kaupe Ines,
Bilban Martin,
Burkard Thomas R.,
Valent Peter,
Superti-Furga Giulio
Publication year - 2008
Publication title -
molecular oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.332
H-Index - 88
eISSN - 1878-0261
pISSN - 1574-7891
DOI - 10.1016/j.molonc.2008.07.003
Subject(s) - dasatinib , myeloid leukemia , nilotinib , cancer research , breakpoint cluster region , imatinib , abl , chemokine , chronic myelogenous leukemia , biology , immunology , leukemia , tyrosine kinase , signal transduction , gene , microbiology and biotechnology , inflammation , biochemistry
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 role in CML.