Estrogen Receptor Status Does Not Affect Response to Herceptin in Breast Cancer

Estrogen Receptor Status Does Not Affect Response to Herceptin in Breast Cancer Patients

Estrogen receptor (ER) status in breast cancers does not affect responses to Herceptin®, according to recent results presented at the 37th Annual Meeting of the American Society of Clinical Oncology.

HER2 positive breast cancer refers to a specific type of breast cancer in which the cancer cells display an overabundance of small proteins on their outer surface called human epidermal growth factor receptor 2 protein (HER2). HER2 proteins possess exclusive selectivity to bind with other proteins called growth factors. The binding action between HER2 and growth factors facilitates cancer cells to replicate and grow in an uncontrolled manner.

Herceptin® is the first monoclonal antibody that has been approved by the FDA for the treatment of breast cancer. Monoclonal antibodies are proteins that can be made in the laboratory and are designed to recognize and bind to very specific sites on a cell. Herceptin® is a monoclonal antibody that binds to the HER2 protein and achieves anti-cancer benefits through two distinct processes. First, the binding of Herceptin® blocks growth factors from being able to bind to HER2, eliminating the stimulating effects on cancer cells. Second, the binding action of Herceptin® stimulates the immune system to attack and kill the cancer cells to which Herceptin® is bound.

Herceptin® has proven effective in the treatment of HER2 positive metastatic breast cancer and has been used in combination with chemotherapy. Women treated with Herceptin and chemotherapy have achieved better survival rates than those treated with chemotherapy alone.

Estrogen receptor-positive breast cancer is a type of cancer that is stimulated to grow by a naturally occurring female hormone called estrogen. Specific proteins, called estrogen receptors, cover the surface of these cancer cells, enabling estrogen to enter into the cell, ultimately facilitating cancer growth. Currently, many women with estrogen receptor-positive breast cancer are treated with drugs that either inhibit estrogen synthesis or block estrogen from entering into the cancer cell.

Recently, a study was performed to determine if ER status affected responses to Herceptin® in patients with advanced breast cancer. Data was analyzed from 3 institutions in the U.S., involving over 800 patients who had been treated for advanced breast cancer. All patients were HER2 positive, with 50% being ER-positive, 40% ER-negative, and 10% unknown ER status. When Herceptin® was combined with chemotherapy, response rates were 53% for ER-positive patients and 49% for ER-negative patients. Median survival was 25.4 months for ER+ patients and 24.1 months for ER- patients. For patients receiving Herceptin® alone, response rates were 25% for ER+ patients and 29% for ER- patients, with an average survival of 26 months for ER+ patients and 20 months for ER- patients.

These results indicate that ER status does not appear to affect responses to Herceptin® in patients with breast cancer. Although ER status is important in determining optimal treatment strategies for breast cancer patients, it is not an independent predictor of a patients response to Herceptin®. (Proceedings from the 37thAnnual Meeting of the American Society of Clinical Oncology, abstract 172, San Francisco, CA, May, 2001)

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