Chemical Carcinogenesis
This monograph provides a contemporary account of advances in chemical carcinogenesis. It promotes the view that it is alteration of the DNA by endogenous and exogenous carcinogens that ultimately leads to sporadic mutations which are a root cause of many
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Trevor M. Penning Editor
Chemical Carcinogenesis
Editor Trevor M. Penning Department of Pharmacology University of Pennsylvania School of Medicine Philadelphia, PA USA [email protected]
ISBN 978-1-61737-994-9 e-ISBN 978-1-61737-995-6 DOI 10.1007/978-1-61737-995-6 Springer New York Heidelberg London Dordrecht Library of Congress Control Number: 2011920809 © 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. Printed on acid-free paper Humana Press is part of Springer Science+Business Media (www.springer.com)
This monograph would not have been possible without the contributions of numerous scientists, too many to name individually, which have led to our understanding on how chemicals and environmental insults cause cancer. The monograph is also dedicated to my grandson “Trevor” who lights up my life with his smile.
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Preface
This volume will provide a contemporary account of advances in chemical carcinogenesis. It will promote the view that chemical alteration of DNA is the root cause of many cancers. This chemical alteration can result from exposure to biological reactive intermediates that may arise from the metabolism of endogenous and exogenous carcinogens. Furthermore, reactive metabolites can target 5¢-CpG’ islands and affect the epigenetic “footprinting” of tumor suppressor genes (leading to their silencing). Once the DNA is modified it is not predestined to cause mutations that may alter the function of critical growth control genes. Instead, eukaryotic cells have evolved sophisticated mechanisms for mutation avoidance using major DNA repair mechanisms including, but not limited to, nucleotide and base excision repair. If the ensuing DNA adducts escape repair, they can give rise to mutations during the replication phase. This often occurs as a result of a novel set of “by-pass” DNA polymerases, which can have low fidelity and processivity. It is faulty replication that leads to mutation of critical genes such as K-ras and p53. Knowledge of these events can identify critical genes and pathways involved in the carcinogenic process that can be exploited for cancer chemoprevention, intervention, and early diagnosis while an individual may be asymptomatic. This, in
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