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Cover

Alcohol, Tobacco and Cancer

Editor(s): Cho C.H. (Hong Kong) 
Purohit V. (Bethesda, Md.) 
Table of Contents
No. , 2006
Section title:
Cho CH, Purohit V (eds): Alcohol, Tobacco and Cancer. Basel, Karger, 2006, pp 48-62
(DOI:10.1159/000095014)

Interaction of Alcohol and Tobacco in Upper Aerodigestive Tract and Stomach Cancer

Salaspuro M.a · Salaspuro V.a · Seitz H.b
aResearch Unit of Substance Abuse Medicine, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland; bDepartment of Medicine, Salem Medical Center Heidelberg and Laboratory of Alcohol Research, Liver Disease and Nutrition, Heidelberg, Germany

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Article / Publication Details

First-Page Preview
Abstract of

Published online: August 10, 2006
Cover Date: 2006

Number of Print Pages: 15
Number of Figures: 0
Number of Tables: 0

ISBN: 978-3-8055-8107-3 (Print)
eISBN: 978-3-318-01338-2 (Online)

Abstract

There is increasing epidemiological, biochemical, and genetic evidence supporting the role of the first metabolite of alcohol oxidation - acetaldehyde - as a common denominator in the pathogenesis of upper aerodigestive tract cancers. Accordingly, acetaldehyde derived either from ethanol or tobacco appear to act in the digestive tract as a local carcinogen in a dose-dependent and synergistic way. Alcohol is metabolized to acetaldehyde locally in the oral cavity mainly by microbes representing normal oral flora. Also tobacco smoke contains high levels of acetaldehyde, which during smoking is dissolved in the saliva. Via swallowing salivary acetaldehyde of either origin will be distributed further to the pharynx, esophagus, and stomach. However, strongest evidence for the local carcinogenic action of acetaldehyde provide biochemical studies with individuals who have either a decreased ability to detoxify acetaldehyde or an enhanced ability to produce it. ALDH2-deficient Asian heavy drinkers and Caucasian alcoholics homozygous for the fast ADH1C*1 allele have markedly increased risk for aerodigestive tract cancers. Both of these groups also have markedly higher salivary acetaldehyde levels after drinking of alcohol than in those with the normal enzymes. In affected individuals the cells of the salivary glands and/or mucous membranes, obviously contribute in addition to the microbes to the local production of acetaldehyde in the saliva. On this basis, these genetic variants form an exceptional human model for long-term acetaldehyde exposure. With regard to cancer prevention, it is important to characterize all those factors that regulate the concentration of acetaldehyde in the upper aerodigestive tract. In addition to the hereditary factors, these include smoking and drinking habits, individual differences in the gut microflora, salivary ethanol levels, and some acetaldehyde-binding agents.


Article / Publication Details

First-Page Preview
Abstract of

Published online: August 10, 2006
Cover Date: 2006

Number of Print Pages: 15
Number of Figures: 0
Number of Tables: 0

ISBN: 978-3-8055-8107-3 (Print)
eISBN: 978-3-318-01338-2 (Online)


Copyright / Drug Dosage / Disclaimer

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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