A familial predisposition to lung cancer has been recognized and supports a

A familial predisposition to lung cancer has been

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A familial predisposition to lung cancer has been recognized and supports a genetic association. The genetic trait is apparently best expressed, however, in the presence of its major predisposing factor—cigarette smoking. Recent research has localized a region on the long arm of chromosome 6 that contains a gene that confers an increased susceptibility to the development of lung cancer in smokers. High levels of air pollution (believed to cause approximately 1% of all lung cancer deaths) are considered a significant risk factor. Certain diseases are also associated with an increased risk, including pulmonary fibrosis, tuberculosis, chronic obstructive pulmonary disease (up to six-fold increased risk), and sarcoidosis. Furthermore, anyone who has previ- ously been diagnosed with lung cancer is more likely to develop a new lung cancer than the average person is to develop an initial lung cancer. Epidemiologic studies have shown a reduction in the rate of lung cancer among people who consume large amounts of fruit and vegetables, a benefit theoretically related to high levels of -carotene, vitamin A, and other antioxidants. Disease Summary Question 1. Can cigarette smokers ever decrease their risk for developing lung cancer if they stop smoking? Disease Summary Question 2. Do pipe and cigar smoking also cause lung cancer? Disease Summary Question 3. Does smoking filtered, low-tar, or low-nicotine tobacco products offer protection against the development of lung cancer? Pathophysiology Cancer of the lung, like all cancers, results from a stepwise accumulation of genetic muta- tions in the body’s basic unit of life—the cell. Normally, the body maintains a system of checks and balances on cell growth so that cells divide to produce new cells only when needed (e.g., when cells get old and die). Disruption of this system of checks and balances on
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DS16-4 Case Study 16 Lung Cancer cell growth by repeated exposures to carcinogens, like cigarette smoke or radon gas, results in an uncontrolled division and proliferation of cells that eventually forms a mass known as a tumor . As cells continue to divide, they undergo a genetic transformation that both alters their appearance and permits them to spread to nearby lymph nodes or through the blood- stream to other organs. As cancer cells spread and continue to divide, they deprive normal healthy cells of oxygen and vital nutrients and cause widespread tissue damage. At the molecular level, transformation of a normal cell into a cancerous one involves the activation of multiple oncogenes (i.e., genes that promote uncontrolled cell division) and the inactivation of several tumor suppressor genes (i.e., genes that inhibit proliferation of cells). Inherited mutations also facilitate the transformation process. Once the development of lung cancer has been initiated by carcinogen-induced and inherited mutations, tumor develop- ment is sustained by a variety of tumor growth factors (e.g., epidermal growth factor).
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  • Summer '10
  • RECKTENWALD
  • bronchogenic carcinoma

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