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      Therapeutic options for chronic myeloid leukemia: focus on imatinib (Glivec ®, Gleevec™)

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          Abstract

          Treatment options for chronic myeloid leukemia (CML) have changed dramatically during the last decades. Interferon-α treatment and stem cell transplantation (SCT) clearly improved survival over conventional chemotherapy and offered the possibility of complete and durable responses. With the advent of the small molecule inhibitor imatinib mesylate (Glivec ®, Gleevec™) targeting the causative Bcr-Abl oncoprotein, the era of molecular cancer therapy began with remarkable success especially in chronic phase patients. Today, imatinib is the first-line treatment for CML. However, imatinib does not appear to be capable to eliminate all leukemia cells in the patients and pre-existing as well as acquired resistance to the drug has been increasingly recognized. To overcome these problems, several strategies involving dose escalation, combinations with other agents, and novel Bcr-Abl inhibitors have been developed.

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          Most cited references 276

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          Pericyte loss and microaneurysm formation in PDGF-B-deficient mice.

          Platelet-derived growth factor (PDGF)-B-deficient mouse embryos were found to lack microvascular pericytes, which normally form part of the capillary wall, and they developed numerous capillary microaneurysms that ruptured at late gestation. Endothelial cells of the sprouting capillaries in the mutant mice appeared to be unable to attract PDGF-Rbeta-positive pericyte progenitor cells. Pericytes may contribute to the mechanical stability of the capillary wall. Comparisons made between PDGF null mouse phenotypes suggest a general role for PDGFs in the development of myofibroblasts.
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            Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining.

             Jodi Rowley (1973)
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              Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells.

              The bcr-abl oncogene, present in 95% of patients with chronic myelogenous leukemia (CML), has been implicated as the cause of this disease. A compound, designed to inhibit the Abl protein tyrosine kinase, was evaluated for its effects on cells containing the Bcr-Abl fusion protein. Cellular proliferation and tumor formation by Bcr-Abl-expressing cells were specifically inhibited by this compound. In colony-forming assays of peripheral blood or bone marrow from patients with CML, there was a 92-98% decrease in the number of bcr-abl colonies formed but no inhibition of normal colony formation. This compound may be useful in the treatment of bcr-abl-positive leukemias.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                February 2008
                February 2008
                : 4
                : 1
                : 163-187
                Affiliations
                [1 ]2nd Department of Internal Medicine, Oncology and Hematology, Robert Bosch Hospital Auerbachstr. 110, Stuttgart, Germany
                [2 ]Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology Auerbachstr. 112, Stuttgart, and University of Tuebingen, Germany
                Author notes
                Correspondence: Heiko van der Kuip Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology, Auerbachstr. 112, 70376 Stuttgart, Germany Tel +49 711 8101 3730 Fax +49 711 829 295 Email heiko.van-der-kuip@ 123456ikp-stuttgart.de
                Article
                2503652
                18728706
                © 2008 Dove Medical Press Limited. All rights reserved
                Categories
                Review

                Medicine

                novel kinase inhibitors, sct, imatinib, cml therapy

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