Beyond Tamoxifen: Osteoporosis Drug Shown to Fight Breast Cancer
Will bazedoxifene be the new tamoxifen? Will it replace Arimidex? A drug currently used in the EU for relief of postmenopausal issues, including osteoporosis and osteopenia, has been found to stop the growth of breast cancer cells – even in women whose cancer has proved resistant to traditional treatments.
If you’ve been diagnosed with hormone-receptive breast cancer (ER/PR+) – one that depends on estrogen to grow – join the crowd: about 70% of breast cancers are hormone-receptive.
Thankfully, there are effective drugs on the market to help prevent recurrence of these types of cancers: tamoxifen (for pre-menopausal women), and aromatase inhibitors (AIs) – Arimidex, Femara, and Aromasin – for those past menopause.
Once active treatment has ended, women with ER+/PR+ cancers generally undergo long-term hormone therapy, taking either tamoxifen or an AI for 5 to 10 years. These drugs have a proven track record of working to prevent recurrence: tamoxifen has been on the market for over 30 years, the AIs for more than a decade.
How do these drugs work, exactly? By depriving cancer cells of estrogen, critical to their growth.
Tamoxifen is a SERM (selective estrogen-receptor modulator). It works by blocking estrogen from attaching itself to the special receptors on cancer cells. Think of a department store parking lot during a big sale: there are plenty of parking places, but they’re all full, so you’re forced to drive away. A SERM “fills” a cell’s estrogen receptors, leaving no room for estrogen.
And how does an AI work? Aromatase is an enzyme that turns the hormone androgen into estrogen. No aromatase = no estrogen. No estrogen = breast cancer cells can't grow.
Sadly, some women develop resistance to these drugs over time; their cancer cells adapt, and figure a way around hormone therapy’s blocking mechanisms.
And when that happens, and cancer recurs, doctors have no choice but to put the woman through chemotherapy – with its miserable and destructive side effects.
But now, potentially, there’s a new drug in town. A Duke Cancer Institute study, presented June 15 at the annual Endocrine Society meeting in San Francisco, indicates that bazedoxifene “not only prevents estrogen from fueling breast cancer cell growth, [it] flags the estrogen receptor for destruction.” (Boltz, 2013).
Like tamoxifen, bazedoxifene is a SERM, preventing the estrogen receptors on breast cancer cells from doing their job.
But this SERM also has an important attribute from another, newer class of drugs known as SERDs: selective estrogen receptor destroyers. Bazedoxifene doesn’t just block the cancer cells’ estrogen receptors; it destroys them. The hope is that survivors no longer responding to tamoxifen or an AI could see their cancer slowed by bazedoxifene.
Bazedoxifene is currently used in the European Union for osteoporosis treatment. And it’s been slowly winding its way through the FDA approval process in this country for at least 6 years.
With this just-released information about its efficacy not just as an osteoporosis treatment, but as a possible new and more effective breast cancer drug, the urgency to get bazedoxifene onto the market may make it an option for survivors in the near – rather than far – future.
Boltz, K. (2013, July 04). Osteoporosis drug stops growth of breast cancer cells, including resistant cells. Retrieved from http://www.oncologynurseadvisor.com/osteoporosis-drug-stops-growth-of-breast-cancer-cells-including-resistant-cells/article/301543/
Duke Medicine (2013, June 15). Osteoporosis drug stops growth of breast cancer cells, even in resistant tumors, study suggests. ScienceDaily. Retrieved July 8, 2013, from http://www.sciencedaily.com /releases/2013/06/130615152341.htm