الفهرس 
Review of literature
SmokingOnly 14 pages are availabe for public view
 |  | from | 242 |  |  |
| | | from | 242 | | |
Abstract
Lung cancer is the leading cause of cancer-related mortality worldwide and is thus a major public health problem. Exposures to environmental carcinogens, such as tobacco smoke, can result in various types of DNA damage and subsequently lead to the development of cancer. Cigarette smoking may induce DNA damage and individuals with a reduced capacity of DNA repair would be expected to have more carcinogen-DNA adducts in their tissue. Indeed, lung cancer patients may have lower capacity of DNA repair when compared with healthy subjects and this may modulate the risk of lung cancer associated with smoking. Polymorphisms of DNA repair genes that impair their function should theoretically predispose an individual to development of tobacco-related cancers such as those in the lung. Thus, lung cancer is a genetic disease that is associated with the accumulation of genetic damage induced by carcinogen exposure.
Most chemical carcinogens present in cigarette smoke exist in a pro-carcinogen form and require metabolic activation to form electrophilic species that covalently bind to DNA, resulting in DNA adduct formation. If DNA adducts are not repaired efficiently before DNA replication, they may cause mutations, DNA strand breaks, and other genetic alterations. Hence, carcinogen-DNA adduct formation is thought to play a central role in the early stages of chemical carcinogenesis and to contribute to tumor development through accumulated genetic damage.