TAILIEUCHUNG - Báo cáo sinh học : "Exploiting the promiscuity of imatinib"

Tuyển tập các báo cáo nghiên cứu về sinh học được đăng trên tạp chí sinh học Journal of Biology đề tài: Exploiting the promiscuity of imatinib. | Journal of Biology BioMed Central Minireview Exploiting the promiscuity of imatinib Shun J Lee 1 and Jean YJ Wang 1 Address Department of Medicine and Division of Hematology-Oncology tMoores Cancer Center and Division of Biological Sciences 3855 Health Sciences Drive University of California San Diego La Jolla CA 92093 USA. Correspondence Jean YJ Wang. Email jywang@ Published 15 April 2009 Journal of Biology 2009 8 30 doi jbiol134 The electronic version of this article is the complete one and can be found online at http content 8 3 30 2009 BioMed Central Ltd Abstract The protein kinase inhibitor imatinib also known as Gleevec has been a notable success in treating chronic myelogenous leukemia. A recent paper in BMC Structural Biology reports a A crystal structure of imatinib bound to the oxidoreductase NQO2 and reveals insights into the binding specificity and the off-target effects of the inhibitor. Imatinib also known as STI571 or Gleevec is one of the great success stories of cancer therapy and is a milestone in small-molecule drug discovery and molecular targeted therapies. Imatinib is the current first-line therapy for all stages of chronic myelogenous leukemia CML in which the chronic phase of the disease is characterized by the increased proliferation of the myeloid lineage and which is cytogenetically diagnosed by the presence of the Philadelphia chromosome. This contains a fusion gene encoding the oncoprotein BCR-ABL in which a part of the BCR protein is fused to the non-receptor ABL tyrosine kinase causing it to become constitutively active. The deregulated kinase activity of BCR-ABL accounts for the oncogenicity of the protein and is inhibited by imatinib. Since the approval of imatinib by the US Food and Drug Administration in May 2001 there has been a dramatic reduction in the number of bone marrow transplants for CML in the US imatinib monotherapy has also been used successfully to induce a complete cytogenetic response

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