« Previous
Next »
Molecular Oncology
Volume 2, Issue 3
, Pages 272-281
, October 2008
The chemokine interleukin-8 and the surface activation protein CD69 are markers for Bcr–Abl activity in chronic myeloid leukemia
References
- . Targeting PIM kinases impairs survival of hematopoietic cells transformed by kinase inhibitor-sensitive and kinase inhibitor-resistant forms of Fms-like tyrosine kinase 3 and BCR/ABL. Cancer Res. 2006;66:3828–3835
- Quantitative chemical proteomics reveals mechanisms of action of clinical ABL kinase inhibitors. Nat. Biotechnol. 2007;25:1035–1044
- Deregulated expression of fat and muscle genes in B-cell chronic lymphocytic leukemia with high lipoprotein lipase expression. Leukemia. 2006;20:1080–1088
- Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases. Proc. Natl. Acad. Sci. U.S.A. 2005;102:11011–11016
- . Pim serine/threonine kinases regulate the stability of Socs-1 protein. Proc. Natl. Acad. Sci. U.S.A. 2002;99:2175–2180
- Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated phase chronic myelogenous leukemia. Blood. 2008;111:1834–1839
- . The development of imatinib as a therapeutic agent for chronic myeloid leukemia. Blood. 2005;105:2640–2653
- . DAVID: Database for Annotation, Visualization, and Integrated Discovery. Genome Biol. 2003;4:P3
- Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N. Engl. J. Med. 2006;355:2408–2417
- . The reciprocal role of Egr-1 and Sp family proteins in regulation of the PTP1B promoter in response to the p210 Bcr–Abl oncoprotein–tyrosine kinase. J. Biol. Chem. 2001;276:25512–25519
- The Btk tyrosine kinase is a major target of the Bcr–Abl inhibitor dasatinib. Proc. Natl. Acad. Sci. U.S.A. 2007;104:13283–13288
- . Target spectrum of the BCR-ABL inhibitors imatinib, nilotinib and dasatinib. Leuk. Lymphoma. 2008;49:615–619
- . Clarifying the role of Stat5 in lymphoid development and Abelson-induced transformation. Blood. 2006;107:4898–4906
- . Summaries of Affymetrix GeneChip probe level data. Nucleic Acids Res. 2003;31:e15
- Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib: a randomized phase-II trial. Blood. 2007;109:5143–5150
- . Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods. 2001;25:402–408
- Human protein reference database—2006 update. Nucleic Acids Res. 2006;34:D411–D414
- . Identification and functional signature of genes regulated by structurally different ABL kinase inhibitors. Oncogene. 2007;26:4179–4188
- . Targeted CML therapy: controlling drug resistance, seeking cure. Curr. Opin. Genet. Dev. 2006;16:92–99
- . Flying under the radar: the new wave of BCR-ABL inhibitors. Nat. Rev. Drug Discov. 2007;6:834–848
- . Mechanisms of BCR-ABL in the pathogenesis of chronic myelogenous leukaemia. Nat. Rev. Cancer. 2005;5:172–183
- Chemical proteomic profiles of the BCR-ABL inhibitors imatinib, nilotinib and dasatinib reveal novel kinase and non-kinase targets. Blood. 2007;110:4055–4063
- . Some aspects of IL-8 pathophysiology. III: Chemokine interaction with endothelial cells. J. Leukoc. Biol. 1996;59:39–44
- . CD69 is an immunoregulatory molecule induced following activation. Trends Immunol. 2005;26:136–140
- . Constitutive activation of STAT5 by the BCR-ABL oncogene in chronic myelogenous leukemia. Oncogene. 1996;13:247–254
- . c-Abl regulates early growth response protein (EGR1) in response to oxidative stress. Oncogene. 2005;24:8085–8092
- . Significance analysis of microarrays applied to the ionizing radiation response. Proc. Natl. Acad. Sci. U.S.A. 2001;98:5116–5121
- . Mechanisms of transformation by the BCR-ABL oncogene: new perspectives in the post-imatinib era. Leukemia Res. 28. Suppl. 2004;1:S21–S28
- . Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia. Nat. Rev. Cancer. 2007;7:345–356
- . The BCR-ABL Story: Bench to bedside and back. Annu. Rev. Immunol. 2004;22:247–306
- . STAT5 signaling is required for the efficient induction and maintenance of CML in mice. Blood. 2006;107:4917–4925
PII: S1574-7891(08)00093-8
doi: 10.1016/j.molonc.2008.07.003
© 2008 Federation of European Biochemical Societies. Published by Elsevier Inc. All rights reserved.
« Previous
Next »
Molecular Oncology
Volume 2, Issue 3
, Pages 272-281
, October 2008

