Clinical studies suggest and obesity increases the risk for breast cancer and there is convincing evidence that post-menopausal breast cancer risk is highly correlated with serum estrogen levels. One potential link between obesity and breast cancer risk is increased estrogen production by the adipose tissue itself. The adipose tissue produces the enzyme aromatase which catalyses the biosynthesis of estrogen from androgen and also 17-β-hydroxysteroid dehydrogenase (17-βHSD) important for the conversion of estrone to estradiol. In spite of this the mechanisms regulating the adipose expression of aromatase and 17-βHSD is however currently unknown. Identifying the mediators in obesity that regulate aromatase and 17-βHSD synthesis in adipose tissues and in adipocytes may provide a unique therapeutic preventive strategy to reduce systemic estrogen levels and thereby reduce post-menopausal breast cancer risk associated with obesity.

Dr. Samad's lab has identified two key molecules (insulin and leptin) in obesity that regulates aromatase and 17-beta HSD synthesis in adipose tissues and in adipocytes. The identification of these target molecules that may ultimately induce estrogen production in the setting of obesity may provide a unique therapeutic preventive strategy to reduce systemic estrogen levels and thereby reduce post-menopausal breast cancer risk associated with obesity.

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