Molecular Pathogenesis and Treatment of Chronic Myelogenous Leukemia
Molecular Pathogenesis and Treatment of Chronic Myelogenous Leukemia provides a comprehensive understanding of the recent molecular genetics of Chronic Myelogenous Leukemia (CML) and a characterization of the molecular targets for drug development. Includ
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Masahiro Kizaki Editor
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Molecular Pathogenesis and Treatment of Chronic Myelogenous Leukemia
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Masahiro Kizaki Editor
Molecular Pathogenesis and Treatment of Chronic Myelogenous Leukemia
Editor Masahiro Kizaki Department of Hematology, Saitama Medical Center Saitama Medical University Kawagoe, Saitama Japan
ISBN 978-4-431-55713-5 ISBN 978-4-431-55714-2 DOI 10.1007/978-4-431-55714-2
(eBook)
Library of Congress Control Number: 2015954659 Springer Tokyo Heidelberg New York Dordrecht London © Springer Japan 2016 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. Printed on acid-free paper Springer Japan KK is part of Springer Science+Business Media (www.springer.com)
Preface
Advances in treatment of chronic myeloid leukemia (CML) have been made over the past two decades thanks to research that has furthered our understanding of its molecular pathogenesis. CML is a clonal hematopoietic stem cell disorder characterized by the abnormal proliferation of myeloid cell lineages, which progresses through the chronic phase (CP) to the accelerated and blastic phases. CML is caused by the presence of the Philadelphia (Ph) chromosome in hematopoietic stem cells, which arises from the reciprocal translocation of chromosomes 9 and 22, t(9;22) (q34;q11), resulting in the development of the bcr-abl chimeric gene. This chimeric gene produces the BCR-ABL fusion protein that has oncogenic activity. The BCR-ABL fusion protein has constitutive tyrosine kinase (TK) activity that is stronger than that of the naı¨ve ABL protein, conferring a proliferative advantage and aberrant differentiation capacity to affected hematopoietic stem cells, resulting in the oncogenic event of leukemia development. Therefore, formation of the bcrabl chimeric gene and its encoded protein is a primary and central event in the molecular pathogenesis of CML. Until 2000, drug therapy for CML was limited to non-specific cytotoxic drugs such as busulfan and hydroxyurea, and then interferon
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