The chemokine interleukin-8 and the surface activation protein CD69 are markers for Bcr-Abl activity in chronic myeloid leukemia

被引：25

作者：

Hantschel, Oliver ^{[1
]}

Gstoettenbauer, Agnes ^{[1
]}

Colinge, Jacques ^{[1
]}

Kaupe, Ines ^{[1
]}

Bilban, Martin ^{[2
,3
]}

Burkard, Thomas R. ^{[1
]}

Valent, Peter ^{[4
]}

Superti-Furga, Giulio ^{[1
]}

机构：

[1] Austrian Acad Sci, Ctr Mol Med, A-1090 Vienna, Austria

[2] Med Univ Vienna, Dept Lab Med, A-1090 Vienna, Austria

[3] Ludwig Boltzmann Inst Clin & Expt Oncol, A-1090 Vienna, Austria

[4] Med Univ Vienna, Dept Internal Med 1, Div Hematol & Hemostaseol, A-1090 Vienna, Austria

来源：

MOLECULAR ONCOLOGY | 2008年 / 2卷 / 03期

关键词：

Bcr-Abl; Chronic myeloid leukemia; Tyrosine kinase inhibitor; Biomarker; Imatinib;

D O I：

10.1016/j.molonc.2008.07.003

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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. (C) 2008 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：272 / 281

页数：10

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