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NEW YORK (Reuters Health) - Scientists from the University of South Florida in Tampa say they have a new understanding of the mechanisms underlying nicotine's ability to trigger tumor progression.
Their studies, reported online in the Journal of Clinical Investigation, suggest that nicotine functions like a growth factor, by binding to nicotine receptors on bronchial cells as well as on lung cancer cells.
"While there is no evidence that nicotine contributes to the induction of tumors, it has been demonstrated that nicotine promotes the growth of solid tumors in vivo, suggesting that nicotine might be contributing to the progression of tumors already initiated," note Dr. Piyali Dasgupta and colleagues. But until now it has been unclear which molecules mediate these events.
Dasgupta's team showed that stimulation of lung cancer cells, as well as bronchial cells, with doses of nicotine leads to robust cell proliferation that is dependent on nicotine receptors.
Nicotine's effects -- triggering a cascade of molecular activity in the cells and leading to tumor growth -- are "analogous to those of growth factors," the researchers report.
Dasgupta's group concludes that "while tobacco carcinogens can initiate and promote tumorigenesis, the results of the present study raise the possibility that exposure to nicotine, by either cigarette substitutes or nicotine supplements, might confer a proliferative advantage to tumors already initiated."
On the other hand, the findings "may open new avenues for targeting cancer therapy," since some of the interactions triggered by nicotine could be interrupted in the researchers' experiments.
SOURCE: Journal of Clinical Investigation, July 20, 2006.
NEW YORK (Reuters Health) - Scientists from the University of South Florida in Tampa say they have a new understanding of the mechanisms underlying nicotine's ability to trigger tumor progression.
Their studies, reported online in the Journal of Clinical Investigation, suggest that nicotine functions like a growth factor, by binding to nicotine receptors on bronchial cells as well as on lung cancer cells.
"While there is no evidence that nicotine contributes to the induction of tumors, it has been demonstrated that nicotine promotes the growth of solid tumors in vivo, suggesting that nicotine might be contributing to the progression of tumors already initiated," note Dr. Piyali Dasgupta and colleagues. But until now it has been unclear which molecules mediate these events.
Dasgupta's team showed that stimulation of lung cancer cells, as well as bronchial cells, with doses of nicotine leads to robust cell proliferation that is dependent on nicotine receptors.
Nicotine's effects -- triggering a cascade of molecular activity in the cells and leading to tumor growth -- are "analogous to those of growth factors," the researchers report.
Dasgupta's group concludes that "while tobacco carcinogens can initiate and promote tumorigenesis, the results of the present study raise the possibility that exposure to nicotine, by either cigarette substitutes or nicotine supplements, might confer a proliferative advantage to tumors already initiated."
On the other hand, the findings "may open new avenues for targeting cancer therapy," since some of the interactions triggered by nicotine could be interrupted in the researchers' experiments.
SOURCE: Journal of Clinical Investigation, July 20, 2006.
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