Bazedoxifene, a drug approved for osteoporosis treatment in Europe, has also shown good results in fighting hard-to-kill breast cancer cells.
The study was conducted by researchers at Duke Cancer Institute who found that the drug was equally effective against cancer cells that had become resistant to other medications.
The drug fights cancer cells on two fronts- one, it prevents estrogen from helping the cell grow and two, it points out the estrogen receptor on the cell, which makes it easier to destroy the receptor.
Breast cancer is one of the most common cancers diagnosed in women in the U.S. Despite its high prevalence, researchers aren't sure why normal breast cells turn cancerous. According to most experts, breast cancer is caused by a combination of genetic, hormonal and environmental factors. According to estimates by the National Cancer Institute, 232,340 new cases of female breast cancer are expected to be detected in 2013 and nearly 40,000 women could die due to breast cancer.
The new study shows that Bazedoxifene can be used to kill the toughest cancer cells.
"We found bazedoxifene binds to the estrogen receptor and interferes with its activity, but the surprising thing we then found was that it also degrades the receptor; it gets rid of it," said Donald McDonnell, PhD, chair of Duke's Department of Pharmacology and Cancer Biology and senior author of the study.
The drug was tested on animal models which effectively inhibited growth in estrogen-dependent cancer cells as well as those cells that had become resistant to anti-cancer drugs such as tamoxifen or aromatase inhibitors. Today, most patients with treatment-resistant cancers are put on toxic chemotherapy agents, which have significant side-effects.
Bazedoxifene belongs to a class of drugs called specific estrogen receptor modulators (SERMs). These drugs behave like estrogen in some tissues, but block estrogen receptors in other tissues. However, unlike other drugs in the class such as tamoxifen, bazedoxifene is a selective estrogen receptor degrader (or SERDs) drug that can target an estrogen receptor for destruction.
"Because the drug is removing the estrogen receptor as a target by degradation, it is less likely the cancer cell can develop a resistance mechanism because you are removing the target," said Suzanne Wardell, PhD, a research scientist working in McDonnell's lab and lead author of the study, according to a news release.
The study findings were presented at the annual Endocrine Society meeting in San Francisco on June 15, 2013.
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