Abstract
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Highlights
More attention is necessary on the issue of women and smoking because several epidemiological studies have indicated that for a given number of cigarettes smoked, females may be at higher risk of lung cancer compared with males [odds ratio (OR) of 1.2–1.7] [6,7,8]
Carcinogen metabolism is traditionally divided into two distinct phases: The Phase I metabolism, often involving the cytochrome P450 monooxygenase enzymes (CYP), creates reactive electrophiles that may serve as substrates for the second phase
The focus of this review will be on studies we have performed regarding: [1] Individual differences and sex differences in relation to carcinogen metabolism, polycyclic aromatic hydrocarbons (PAH)-DNA adduct levels in the lung, and mutations in the p53 tumor suppressor gene, and [2] p53 mutations as molecular biological markers for prognosis in lung cancer patients
Summary
Lung cancer is the most frequent cancer today and is expected to have a major impact on human health throughout the decades. The incidence of this epidemic increases by approximately 0.5% each year especially because of contributions from Eastern Europe and developing countries [1,2]. The role of tobacco smoking as a major etiologic factor of this malignancy is well established (85-90% of lung cancer cases are smokers), and smoking and lung cancer incidence shows a clear dose-response relationship [4,5]. Interactions between the environment and genetic risk factors (geneenvironment interactions) are involved in cancer, but in many multifactorial diseases (Figure 1)
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