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Scripta Scientifica Medica


N. Temnyalov


Investigations under in vitro and in vivo conditions prove the role of certain components of more than 4000 chemical compounds isolated from tobacco smoke in the molecular mechanisms of cancerogenesis. One of the most difficult tasks is to evaluate the degree of increasing of the individual risk for cancer. Recent studies by Cascorbi et al of the hereditary susceptibility factors of bronchogenic carcinoma reveal the advantages of molecular-epidermiologic studies to estimate the extent of an individual's risk. Gene mutation frequencies of the phase-I enzyme CYPIA1 and the phase-II enzyme arylamine N-acetyltransferase 2 (NAT2) are determined by PCR/RFLP among 155 lung cancer patients and 310 matched controls. The high activity of NAT2 catalyzing the O-acetylation of arylamines contained in cigarette smoke is identified. The enhanced inducibility of some alleles and the deficiency of the detoxifying enzyme can increase the risk of cancer among smokers. Until recently, it has been accepted that the number of cigarettes smoked per day and the duration of smoking could represent the main risks for cancer and first of all for lung cancer. A complex approach is required including parameters of genetic mutations and metabolic enzymes for assessment of the degree of individual risk.


Lung cancer; tobacco; risk factors; carcinogenesis; molecular epidemiology


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N. Temnyalov

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