Technique May Let More Women Use Tamoxifen

Feb. 24 -- MONDAY, Feb. 23 (HealthDay News) -- Researchers have found a way to "switch on" estrogen sensitivity in breast tumor cells, thereby making them vulnerable to the breast cancer drug tamoxifen.

If successful, the technique might someday allow breast cancer patients who don't respond to tamoxifen to benefit from the drug.

"We're excited by the results," said study author Caroline Ford, a member of the department of cell and experimental pathology at Lund University in Malmo, Sweden. "This has implications for the 30 percent of breast cancer patients who are estrogen-receptor negative who currently have a poor prognosis."

Not only might these tumors become amenable to tamoxifen, but they may also respond to other "endocrine" treatments such as aromatase inhibitors, which also interfere with estrogen production in the body.

"We are currently investigating this," Ford said.

The findings may also provide alternatives for the group of women who start out estrogen receptor-positive but later become negative and for whom treatments stop working.

The findings are published in this week's issue of the Proceedings of the National Academy of Sciences.

As Ford noted, a large minority of patients have breast cancer tumors that do not express estrogen receptors. Not only does this make them unresponsive to a variety of treatments now available for estrogen receptor-positive malignancies, but it indicates a more aggressive cancer in general.

Tamoxifen, which has been a gold standard of breast cancer treatment for decades, works by binding to the estrogen receptor. If there is no receptor, however, tamoxifen becomes useless.

Any means of allowing the three out of 10 women whose cancers don't respond to tamoxifen and other endrocrine therapies would be a big advance, experts say.

"[Research] groups have been looking to restore positivity, to open the door to treatment with tamoxifen and aromatase inhibitors," said Dr. Minetta Liu, a translational researcher and breast oncologist at Georgetown University's Lombardi Comprehensive Cancer Center in Washington, D.C. The Swedish team now "have a molecule suggested that may, in fact, succeed. The findings are very exciting," he said.