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Abstract
After the menopausal transition, the ovaries cease to make estrogens, yet the incidence of breast cancer increases and the majority of these tumors are estrogen receptor positive. So, where is the estrogen driving this tumor development coming from? Several extragonadal sites, such as bone, brain and adipose tissue, synthesize estrogens from circulating C19 steroids. The largest of these depots is the adipose tissue, and increased BMI is associated with increased breast cancer risk as well as increased circulating estrogen levels. The mechanisms linking obesity to breast cancer risk are not yet completely understood, although it is widely assumed that estrogens produced in the fat play a role. This article aims to provide a comprehensive overview of the regulation of aromatase expression in the breast adipose tissue in response to fat and tumor-derived factors, as well as new evidence suggesting that breast-specific inhibition of aromatase may be possible.
Financial & competing interests disclosure
The work from the laboratory presented in this article was supported by the Victorian Breast Cancer Consortium Inc. and by Project Grant #494819 and Program Grant #494802 from the National Health and Medical Research Council. Kristy A Brown was supported by The Terry Fox Foundation through an award from the National Cancer Institute of Canada. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.