Tobacco smoke and radioactive radon gas impose a high risk for lung cancer. The radon-derived ionizing radiation and some components\r\nof cigarette smoke induce oxidative stress by generating reactive oxygen species (ROS). Respiratory lung cells are subject to\r\nthe ROS that causes DNA breaks, which subsequently bring about DNAmutagenesis and are intimately linked with carcinogenesis.\r\nThe damaged cells by oxidative stress are often destroyed through the active apoptotic pathway. However, the ROS also perform\r\ncritical signaling functions in stress responses, cell survival, and cell proliferation. Some molecules enhance radiation-induced\r\ntumor cell killing via the reduction in DNA repair levels. Hence the DNA repair levels may be a novel therapeutic modality in overcoming\r\ndrug resistance in lung cancer. Either survival or apoptosis, which is determined by the balance between DNA damage and\r\nDNA repair levels, may lender the major problems in cancer therapy. The purpose of this paper is to take a closer look at risk factor\r\nand at therapy modulation factor in lung cancer relevant to the ROS.
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