Potency and Molecular Signatures of Tobacco Carcinogens in the Early Development of Human Breast Cancer
Hwa-Chain Robert Wang
D.V.M. equivalent, National Chung-Hsing University, Taiwan
MS, Auburn University
Ph.D., University of Virginia Cancer Center
Associate Professor
After lung cancer, breast cancer ranks second among cancer deaths in women. In the United States, one out of eight women will develop breast cancer during her lifetime – a new case is diagnosed every three minutes. Researchers have identified several factors, including age, family history, and obesity, that increase the risk of developing breast cancer.
Researchers know that cigarette smoke contains many potent cancer-causing chemicals; however, numerous investigations into the potential link between smoking and breast cancer have produced conflicting results. Epidemiological studies have suggested that exposure to tobacco substances increases the risk of developing breast cancer, but more research is required to precisely identify the tobacco carcinogens involved and the exact roles they might play in the development of breast cancer.
NNK, a tobacco-specific nitrosamine, is one of the most potent carcinogens found in cigarette smoke. Studies have shown that NNK induces lung tumors in rodents. Most studies involving tobacco carcinogens use high doses of the carcinogen to induce tumors in animals; however, such studies have not been successful in elucidating the role tobacco carcinogens play in the induction of mammary tumors in animals.
In a recent study, Dr. Wang’s group treated human breast epithelial cells with the same concentrations of NNK commonly detected in smokers. The results of their study showed, for the first time, that NNK can induce noncancerous cells to acquire cancerous properties. Dr. Wang’s group is currently working to identify the molecular signatures of NNK-induced breast cancer cells.
Based on the molecular signature of cancerous cells, researchers will be able to determine the stage of cancers, and identify molecular targets for choosing agents that prevent cancer by interfering with the biological processes underlying cancer development.
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