WASHINGTON -- For the first time, scientists have used a laboratory mouse model to mimic the development of human alcohol-induced breast cancer. The results are part of a new study, Chronic Alcohol Consumption Increases Tumor Growth and Amgiogenesis of Breast Cancer in Female Mice, conducted by Brandi Busby, Wei Tan, Jordan Covington, Emily Young, and Jian-Wei Gu, all of the University of Mississippi Medical Center, Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS. Dr. Gu will present the team's findings in detail during the American Physiological Society (APS; www.the-APS.org) annual meeting, which is being held as part of the Experimental Biology (EB '07) meeting. More than 12,000 scientists are attending the conference, being held April 28 - May 2, 2007 at the Washington, DC Convention Center.
Alcohol (EtOH) consumption -- even moderate -- is a well-established risk factor for breast cancer in women. A recent study showed that 60 percent of female breast cancers worldwide were attributable to alcohol consumption. Nevertheless, the mechanisms of alcohol-induced breast cancer are poorly understood.
The definitive biological effects and molecular mechanisms of EtOH on progression and malignancy of breast cancer have not been investigated using a mammalian breast cancer model that mimics the human disease. Scientists have suggested that the possible mechanisms involved include the agitation of estrogen metabolism and response; cell mutation by the EtOH metabolite acetaldehyde; oxidative damage; and one-carbon metabolism pathways through reduced folic acid.
To date, there has not been an animal model that faithfully mimics the human disease with respect to characteristics of breast cancer, immunocompetence, and physiologically relevant EtOH intake. The researchers addressed and overcame the obstacles and
Contact: Donna Krupa
American Physiological Society