Tobacco use, cancer causation and public health impact.

This review describes global patterns of tobacco use and the mechanisms by which tobacco use is involved in carcinogenesis. A second part will discuss the association between tobacco use and risk of specific cancer types. Tobacco use has traditionally been a practice of high-income countries, but it has recently been taken up in low-income countries and it is particularly common in men. A wide variety of tobacco products exist, of which cigarettes are most frequently consumed. Tobacco products contain more than 50 established or identified carcinogens and these may increase risk of cancer by causing mutations that disrupt cell cycle regulation, or through their effect on the immune or endocrine systems. Certain factors such as genes, diet and environmental exposures may alter susceptibility to cancer in tobacco users. Today at least 15% of all cancers are estimated to be attributable to smoking, but this figure is expected to increase because of the uptake of tobacco use in low-income countries

Antioxidant defense markers modulated by glutathione S-transferase genetic polymorphism: results of lung cancer case–control study

Oxidative stress and xenobiotic metabolizing enzymes are suspected to be related to carcinogenesis by different cellular mechanisms. Hence, our study aimed at identifying potential relationships between antioxidant defense parameters measured in blood and glutathione S-transferase (GST) genetic polymorphisms of four GST izoenzymes in lung cancer patients and reference individuals. The case–control study included 404 lung cancer patients and 410 non-cancer subjects as controls, matched by age, gender and place of living (central Poland). In control subjects with GSTM3*A/*A, GSTT1 null, GSTM1 null + GSTT1 null, GSTM3*A/*A + GSTT1 null genotype, glutathione peroxidase activity was significantly higher (P < 0.05) than in controls possessing respective potential protective GST genotypes. Controls with GSTM3*A/*A + GSTP1*B genotype presented significantly higher ceruloplasmin activity (P < 0.05) than GSTM3*B + GSTP1*A/*A carriers. Zinc level was significantly higher (P < 0.05) in controls and cases with GSTP1*B + GSTT1 null genotype and in cases with GSTM1 null + GSTP1*B genotype, when compared with respective potential protective GST genotypes. This case–control study indicates that particular defective GST genotypes may enhance the defense against oxidative stress. The potential relationship between the investigated antioxidative enzymes and microelements, and common functional genetic polymorphism of GST was observed mostly in control subjects