The Mechanism of Lung Carcinogenesis and Smoking Cessation
作者:
John,
期刊:
Epidemiology
(OVID Available online 1990)
卷期:
Volume 1,
issue 4
页码: 314-317
ISSN:1044-3983
年代: 1990
出版商: OVID
关键词: ex-smoker;lung cancer;mechanisms;carcinogenesis;genotoxicity;promotion;nutrition;prevention
数据来源: OVID
摘要:
Mathematical modeling of risk of lung cancer upon smoking cessation suggests increasing risk, whereas the facts show decreasing mortality. This discordance is resolved by taking into account the mechanistically distinct steps in chemical carcinogenesis: (1) neoplastic conversion hygenotoxic carcinogens and (2) neoplastic growth and development by agents with epigenetic and promoting effects. Tobacco smoke contains relatively small amounts of several types of genotoxic carcinogens, the effect of which is considerably and vitally enhanced by nongenotoxic promoting factors. Upon smoking cessation, the effect of the second type of agent is abruptly eliminated. Therefore, any preneoplastic lesions remain static or regress, whereas in the continuing smoker they progress. These sequences also apply, with different chemicals involved, in nutritional carcinogenesis. (Epidemiology 1990;1:314–317)
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