Lab Study Looks at Why Cancers Become Resistant to Tamoxifen

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Breast cancers that are hormone-receptor-positive usually respond to hormonal therapy medicine (tamoxifen or an aromatase inhibitor). An early study was research done in a lab on individual cells, not on people. The researchers found that hormone-receptor-positive invasive lobular breast cancer cells may not respond or may stop responding to tamoxifen because the cells develop a protein receptor that stops tamoxifen from blocking estrogen.

Invasive lobular carcinoma (ILC) is breast cancer that begins in the milk-producing lobules that empty into ducts that carry milk to the nipple. ILC is the second most common type of invasive breast cancer. Invasive ductal carcinoma (IDC), which begins in the ducts that carry milk from the lobules to the nipple, is the most common type of invasive breast cancer.

Both invasive lobular and invasive ductal cancer cells usually have hormone receptors, which make these cancers likely to be hormone-receptor-positive. ILC cells are more likely than IDC cells to have hormone receptors. But invasive lobular breast cancer is more likely to have a poor response or no response at all to tamoxifen compared to invasive ductal breast cancer.

This study suggests that ILC's lack of response to tamoxifen might be because some ILC cells produce too many receptors that act like estrogen receptors but aren't really estrogen receptors. These receptors are called estrogen-related receptor gamma (ERR-gamma). ERR-gamma appears to block tamoxifen's effect on estrogen receptors. The genes HMGCS2 and FASN may help make ILC cells produce too many ERR-gamma.

Identifying receptors such as ERR-gamma and the genes that make cells produce these receptors can help researchers and doctors working to find new, better ways to treat breast cancer that doesn't respond well or at all to available treatments. Based on this research, ERR-gamma, as well as the HMGCS2 and FASN genes, may guide the development of new targeted therapies. This type of research led to the development of the targeted therapy Herceptin (chemical name: trastuzumab). Researchers first discovered that certain breast cancer cells produce too many HER2-neu receptors. These cancers are known as HER2-positive cancers. Scientists then began trying to develop medicine that could target the HER2-neu receptor and Herceptin was the result.

Stay tuned to Breastcancer.org for the latest research findings that may lead to new, better ways to prevent, diagnose, and treat breast cancer.

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