A byproduct of cholesterol may function like the hormone estrogen to fuel the growth of breast cancer in mice, and perhaps in people, according to a U.S. study. The study, which was released Thursday, shed light on the link between high cholesterol and breast cancer for the first time, especially in post-menopausal women. "A lot of studies have shown a connection between obesity and breast cancer, and specifically that elevated cholesterol is associated with breast cancer risk, but no mechanism has been identified," said senior author Donald McDonnell of Duke University, in a statement. "What we have now found is a molecule - - not cholesterol itself, but an abundant metabolite of cholesterol -- called 27HC that mimics the hormone estrogen and can independently drive the growth of breast cancer." According to the researchers, the hormone estrogen feeds an estimated 75 percent of all breast cancers, and they found that 27- hydroxycholesterol, or 27HC, behaved similarly to estrogen in animals. Using mouse models that are highly predictive of what occurs in humans, McDonnell and colleagues demonstrated the direct involvement of 27HC in breast tumor growth, as well as the aggressiveness of the cancer to spread to other organs. They also found that the activity of this cholesterol metabolite was inhibited when the animals were treated with antiestrogens or when supplementation of 27HC was stopped. To further explore the role of 27HC in tumor growth, the researchers turned to human breast cancer samples and found the most aggressive tumors had the highest levels of the enzyme that converts cholesterol to 27HC. They also noted that 27HC could be made in other places in the body and transported to the tumor. McDonnell said the findings suggest there may be a simple way to reduce the risk of breast cancer by keeping cholesterol in check, either with anti-cholesterol drugs such as statins or a healthy diet. The next steps for research include clinical studies to verify those potential outcomes, as well as studies to determine if 27HC plays a role in other cancers, McDonnell added. The findings were published in the U.S. journal Science.