Title: "Mammary tumorigenesis in a Rat Model of Early Onset Diet Induced Obesity "
Speaker: Dr. Ignacio Camarillo, Department of Biological Sciences, Purdue University
Place: Smith Hall (SMTH) 108; Tuesday, February 15, 2005, 4:30pm


Obesity is a major health problem around the world and is positively associated with breast cancer incidence and mortality. Recent rapid increases in the prevalence of childhood obesity indicate the adverse effects of obesity will be a concern for decades to come. The mechanisms involved in obesity-associated breast cancer have not been delineated. Obesity is characterized by increased circulating levels of Leptin, an adipocyte-derived hormone known to regulate body weight and energy expenditure. Recent evidence demonstrates leptin also plays an important role in normal mammary gland development and in mammary tumor formation. These studies support that adipose tissue, through its production of hormones such as leptin, is an important regulator of mammary tumorigenesis. The establishment of adipose tissue as a novel endocrine organ justifies studies that evaluate the function of mammary gland adipocytes during obesity and breast cancer. The goal of our studies is to identify the changes in mammary adipocyte gene expression that occur during obesity and breast cancer and determine how these changes are involved in mammary tumorigenesis. To accomplish our goals we chemically induce mammary tumors in a rat model of early onset Diet Induced Obesity (DIO). Subsequently, individual adipocyte cells are isolated from tumor-free or tumor-containing mammary tissue via laser capture microdissection. Cells from lean and obese animals are then used to generate Affymetrix microarray gene expression profiles. Overall, this work will allow us to better understand mammary adipocyte-epithelial interactions and to identify novel potential targets for obesity-associated cancer therapies.

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