Helping Tamoxifen Help More Women

Study identifies possible mechanism for resistance to the breast cancer drug

Please note: This article was published more than one year ago. The facts and conclusions presented may have since changed and may no longer be accurate. And "More information" links may no longer work. Questions about personal health should always be referred to a physician or other health care professional.

En Español

WEDNESDAY, June 16, 2004 (HealthDayNews) -- Scientists are closer to solving the mystery of why some women aren't helped by tamoxifen, a drug widely used to prevent breast cancer or breast cancer recurrence.

Researchers at Baylor College of Medicine, in Houston, also found that another cancer drug -- gefitinib -- may be able to restore tamoxifen's ability to fight cancer.

The study is published in the June 16 issue of the Journal of the National Cancer Institute.

Tamoxifen can reduce the risk of death for women with invasive breast cancer by about 15 percent over 10 to 15 years. Still, experts have long known that a significant proportion of women don't seem to gain any preventive benefit from the drug.

Previous research found that women with estrogen receptor (ER)-positive tumors, which express high levels of compounds called HER2/neu and the ER coactivator AIB1, often develop a resistance to tamoxifen. But scientists had been unable to identify the mechanism that led to that resistance.

In this new study, the Houston researchers examined molecular interactions in breast cancer cells that expressed high levels of both HER2 and AIB1. The study found that, in these cells, tamoxifen actually stimulated tumor growth.

However, the researchers also found that gefitinib appears to reverse this effect. In cells treated with gefitinib, tamoxifen was once again effective in blocking tumor growth, they said in a prepared statement.

More information

The U.S. National Cancer Institute has more about tamoxifen.

SOURCE: Journal of the National Cancer Institute, news release, June 15, 2004

--

Last Updated:

Related Articles