[Jackie07]

Marcia,

I think mine was also just 5% ER. I know, it sounds so tiny, but that's how ER+ is determined. Hope the information below helps:

The first molecular target for targeted cancer therapy was the cellular receptor for the female sex hormone estrogen, which many breast cancers require for growth. When estrogen binds to the estrogen receptor (ER) inside cells, the resulting hormone-receptor complex activates the expression of specific genes, including genes involved in cell growth and proliferation.

Research has shown that interfering with estrogen’s ability to stimulate the growth of breast cancer cells that have these receptors (ER-positive breast cancer cells) is an effective treatment approach.

Several drugs that interfere with estrogen binding to the ER have been approved by the FDA for the treatment of ER-positive breast cancer. Drugs called selective estrogen receptor modulators (SERMs), including tamoxifen and toremifene (Fareston®), bind to the ER and prevent estrogen binding. Another drug, fulvestrant (Faslodex®), binds to the ER and promotes its destruction, thereby reducing ER levels inside cells.

Another class of targeted drugs that interfere with estrogen’s ability to promote the growth of ER-positive breast cancers is called aromatase inhibitors (AIs). The enzyme aromatase is necessary to produce estrogen in the body. Blocking the activity of aromatase lowers estrogen levels and inhibits the growth of cancers that need estrogen to grow. AIs are used mostly in women who have reached menopause because the ovaries of premenopausal women can produce enough aromatase to override the inhibition. Three AIs have been approved by the FDA for the treatment of ER-positive breast cancer: Anastrozole (Arimidex®), exemestane (Aromasin®), and letrozole (Femara®).


www.cancer.gov/cancertopics/factsheet/Therapy/targeted

National Cancer Institute.