Spivack S D, Fasco M J, Walker V E, Kaminsky L S
Laboratory of Human Toxicology and Molecular Epidemiology, New York State Department of Health, Albany, NY 12201-0509, USA.
Crit Rev Toxicol. 1997 Jul;27(4):319-65. doi: 10.3109/10408449709089898.
One in ten tobacco smokers develops bronchogenic carcinoma over a lifetime. The study of susceptibility of an individual and a population to lung cancer traditionally has been limited to the study of tobacco smoke dose and family history of cancer. New insights into lung carcinogenesis have made the study of molecular markers of risk possible in human populations in the emerging field of molecular epidemiology. This review summarizes data addressing the relationships of human lung cancer to polymorphisms of phase I procarcinogen-activating and phase II-deactivating enzymes and intermediate biomarkers of DNA mutation, such as DNA adducts, oncogene and tumor suppressor gene mutation, and polymorphisms. These parameters are reviewed as they relate to tobacco smoke exposure, procarcinogen metabolizing polymorphisms, and the presence of lung cancer. Problem areas in biomarker validation, such as cross-sectional data interpretation; tissue source, race, statistical power, and ethical implications are addressed.
每十名吸烟人群中就有一人在一生中会患上支气管源性癌。传统上,对个体和人群肺癌易感性的研究仅限于烟草烟雾剂量和癌症家族史的研究。肺癌发生机制的新见解使得在新兴的分子流行病学领域对人群中风险分子标志物的研究成为可能。本综述总结了有关人类肺癌与I期前致癌物激活酶和II期失活酶的多态性以及DNA突变的中间生物标志物(如DNA加合物、癌基因和肿瘤抑制基因突变及多态性)之间关系的数据。这些参数将根据它们与烟草烟雾暴露、前致癌物代谢多态性以及肺癌存在情况的相关性进行综述。还将讨论生物标志物验证中的问题领域,如横断面数据解释、组织来源、种族、统计效力和伦理问题。