The researchers analysed information on smoking habits and symptoms of nicotine dependence, gathered from almost 1200 grade 7 students in 10 schools.
Blood samples were taken to identify genetic profiles, and 228 students who smoked, but were not yet addicted were subsequently monitored for around two years.
During this period, 67 students became addicted to nicotine. Dependency was significantly more likely among those students with the "inactive" gene variants of the CYP2A6 gene (CYP2A6*2 or CYP2A6*4).
They were almost three times as likely to become addicted to tobacco as those with the normal variants of the gene. Those with partially inactive variants of the CYP2A6 gene were not at increased risk of becoming addicted.
Students with the normal gene smoked an average of 29 cigarettes a week. Those with the partially inactive variant smoked 17. But those with the inactive variant, which slowed down nicotine clearance the most, smoked around 12 cigarettes a week.
The authors suggest that slow clearance prolongs the exposure of the brain to nicotine and is likely to make it more intense. This may boost the effects of the physiological processes which lead to dependence/addiction, and result in the requirement for fewer cigarettes to achieve it.
It also means that while young smokers with the slowest variant are likely to smoke less, they are also likely to get hooked more easily than light smokers, say the authors. Previous research has shown that it is much harder for those who become chemically dependent on nicotine to quit smoking.
Contact: Carmen Kinniburgh, Communications Officer, National Cancer Institute of Canada For Dr Jennifer O'Loughlin, Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Quebec, Canada Tel: + 1 416 934 5684 Email: ckinniburghcancer
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Researchers found mutations in EPHB2 gene in 8% of prostate cancer patients, particularly in the metastatic tumors. The discovery is hoped to facilitate the development of novel therapeutics for prostate cancer. The researches aim to develop the novel NMD-CGH microarray method further and apply it for new tumor-suppressor gene discovery approaches in prostate cancer and other cancer types.
Launched three years ago at the National Institutes of Health (NIH) in the United States, the research was continued in Finland at VTT in the Medical Biotechnology Department, in collaboration with a research team at the Translational Genomics Research institute in the US.
Prostate cancer is the most common cancer in men, the incidence of which has shown an increasing trend over the past few years. The origins of prostate cancer remain largely unknown, however, researchers believe that genetic errors occurring in prostate cells during the aging process have a significant impact. The loss of function of the tumor-suppressor genes plays a major role in the development of cancer. So far approximately twenty such genes have been identified in the human genome. Their normal function ensures the correct growth of cells and prevents the proliferation of cancer cells in the body.
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