Targeted Therapies Mechanisms of Resistance
This volume explores the mechanisms of resistance to targeted therapeutics. The focus is on the cancer cell signaling network, although other mechanisms of resistance including target mutation, and new areas of study such as cancer stem cel
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Series Editors William B. Coleman Gregory J. Tsongalis
For further volumes: http://www.springer.com/series/8176
Daniel Gioeli Editor
Targeted Therapies Mechanisms of Resistance
Editor Daniel Gioeli, Ph.D. Department of Microbiology and Cancer Center University of Virginia Charlottesville, VA USA [email protected]
ISBN 978-1-60761-477-7 e-ISBN 978-1-60761-478-4 DOI 10.1007/978-1-60761-478-4 Springer New York Dordrecht Heidelberg London Library of Congress Control Number: 2011928683 © Springer Science+Business Media, LLC 2011 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Humana Press, c/o Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein. Printed on acid-free paper Humana Press is part of Springer Science+Business Media (www.springer.com)
Foreword
The spectacular success of the first tyrosine kinase inhibitor imatinib, approved just 10 years ago, has transformed oncology drug development. Nearly all drug discovery efforts today have shifted away from conventional cytotoxic therapies toward the development of molecularly-targeted agents. Much of the emphasis is on finding drugs that inhibit “driver” oncogenes in tumors, with the expectation that these new compounds will have single agent activity in appropriately selected patients whose tumors contain “driver” mutations in the gene or pathway targeted by the new agent. The list of successes using this approach continues to grow, including two examples in the past year – BRAF-mutant melanoma and ALK-mutant lung cancer – that are likely to result in two new drug approvals. Yet all these successes are accompanied by the problem of drug resistance, which has plagued cancer drug development beginning with the very first success using antimetabolites to treat childhood acute lymphocytic leukemia. The drug resistance problem in acute lymphocytic leukemia, as well as other chemotherapysensitive tumors such as Hodgkin’s lymphoma and testicular cancer, was overcome through the use of combination of chemotherapy agents with nonoverlapping toxicities. But this success required decades of clinical trials –
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