作者: Peter G Shields , Curtis C Harris
DOI: 10.1001/JAMA.1991.03470050081027
关键词:
摘要: Environmental, occupational, and recreational exposures to carcinogens contribute cancer risk in humans. Cancer formation is a multistage process involving tumor initiation, promotion, conversion, progression. Carcinogens can affect any of these stages through genetic epigenetic mechanisms. The association suspected carcinogenic exposure be studied populations with classic epidemiologic techniques. However, techniques are not applicable the assessment individuals. Molecular epidemiology, contrast, field that integrates molecular biology, vitro vivo laboratory models, biochemistry, epidemiology infer individual risk. Carcinogen-macromolecular adduct levels, somatic cell mutations measured determine biologically effective dose carcinogen. also explores host susceptibilities, such as carcinogen metabolic activation, DNA repair, endogenous mutation rates, inheritance mutated suppressor genes. Substantial interindividual variation for each biologic end points has been shown and, therefore, highlights need assessing on an basis. Given pace last decade, it feasible next 10 years will allow epidemiologists develop cancer-risk profile includes number factors. This help focus preventive strategies strengthen quantitative assessments. ( JAMA . 1991;266:681-687)