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Alcohol related cancers and genetic susceptibility in europe

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There were a total of 2467 cases and 2366 controls recruited and interviewed with the lifestyle questionnaire. For smoking tobacco products (cigarettes, cigars, pipes), current smokers had an increase in risk of 6.23 (95%CI=5.06-7.67), whereas former smokers had an approximately 2-fold increase in risk (95%CI=1.68-2.56; Table 3). Smoking immediately after waking up, an indicator of the level of addiction to cigarette smoking, increased the UADT cancer risk significantly. There was also a clear dose-response trend with the years of cigarette smoking; individuals who smoked for 41 years or more had an odds ratio of 5.11 (95%CI=3.98-6.55). Our results confirm that tobacco is the main causes of UADT cancers cancer in Europe. The carcinogenic risk of tobacco smoking was recently re-evaluated by the IARC monographs (1), and the average relative risk across the studies reviewed was estimated as 10-fold for laryngeal cancer, 4-5 fold for oral and pharyngeal cancers and 2-5 fold for esophageal cancers (17). The magnitude of risk observed in our study is comparable, with a 6-fold increase in risk of laryngeal cancer among current smokers and a 2-fold increase among ex-smokers. For alcohol drinking, our risk estimates were moderate, with an approximately 1.5 - 2.0 fold increase in UADT cancer risk for. Furthermore, we identified an independent effect of alcohol consumption. Although ethanol itself is not suggested as a carcinogen in experimental animals, ethanol as a solvent may damage the oral cells and increase the mucosal penetration of oral carcinogens, in particular those contained in tobacco smoke. In addition, alcohol may reduce nutrient absorption and levels, for instance folate levels (18), and thus reduce the protective effects of vegetables and fruits against oral cancer and its premalignant lesions, and it may suppress the immune system, in combination with nutrient deficiency (19).

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