Checkpoint Controls and Targets in Cancer Therapy
There is no question that loss of cell cycle checkpoint regulation is an intrinsic characteristic of cancer. However, many tumors retain parallel checkpoint pathways that are activated by antitumor agents and facilitate therapeutic response. Failur
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Cancer Drug Discovery and Development Series Beverly A. Teicher, PhD, Series Editor
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Checkpoint Controls and Targets in Cancer Therapy Edited by
Zahid H. Siddik University of Texas, M.D. Anderson Cancer Center, Houston, Texas, USA
Editor Zahid H. Siddik Department of Experimental Therapeutics The University of Texas M.D. Anderson Cancer Center 1515 Holcombe Boulevard Houston, TX 77030 USA [email protected]
Series Editor Beverly A. Teicher, PhD Department of Oncology Research Genzyme Corporation Framingham, MA, USA
ISBN 978-1-60761-177-6 e-ISBN 978-1-60761-178-3 DOI 10.1007/978-1-60761-178-3 Springer Dordrecht Heidelberg London New York Library of Congress Control Number: 2009933775 © Humana Press, a part of Springer Science+Business Media, LLC 2010 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, 999 Riverview Drive, Suite 208, Totowa, NJ 07512 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 Springer is part of Springer Science+Business Media (www.springer.com)
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Preface
Much work over the last two decades has firmly established that loss of cell cycle checkpoint regulation, and resultant unabated cellular proliferation, is an inherent characteristic of cancer. This loss can occur through aberration in any one single component of the many signal transduction pathways that orchestrate checkpoint regulation, and results in either a failure to activate the checkpoint or a failure to respond to the activated checkpoint. In normal cells, checkpoint pathways are activated when genetic or cellular homeostasis is compromised, and signals are then transduced to re-establish basal conditions, and, failing this, to activate the apoptotic machinery to induce a cellular suicidal response. This implies that both survival and cell death pathways are induced following checkpoint activation, and that the final decision by the cell to live or die is dependent on the net result from integrating two opposing se
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