Accumulating evidence suggests that obesity is a high risk factor for breast cancer among post-menopausal women, which can at least partially be explained by the contribution of adipose tissue to local and circulating estrogen.In response to tumor cell-secreted cytokines, adipose stromal cells (ASCs) express a large amount of aromatase, a key enzyme in estrogen biosynthesis and a clinically proven target for breast cancer therapy.Increased estrogen production from ASCs in turn stimulates hormone-dependent tumor growth, thus creating a "vicious cycle" between estrogendependent tumor cells and estrogen-producing ASCs that is conducive to mammary tumorigenesis.In contrast to our knowledge of aromatase expression in tumor-associated ASCs, relatively little is known about its regulation in ASCs under disease-free conditions.