According to an article recently published in the New England Journal of Medicine, status of the human epidermal growth factor receptor-2 (HER2) determines whether treatment with the chemotherapy agent Taxol® (paclitaxel) is effective in early breast cancer.
Early breast cancer, or cancer that has not spread past the lymph nodes under the arms, has high cure rates following standard therapies. Much of this is attributed to improvements in treatment, including chemotherapy. Standard treatment for early breast cancer typically includes surgical removal of the cancer, followed by radiation, chemotherapy, and/or hormone therapy.
The majority of breast cancers are referred to as hormone-positive, or estrogen-receptor positive (ER-positive), cancer. This means that the cancer cells are stimulated to grow from exposure to the female hormone estrogen. Patients with ER-positive breast cancer are treated with hormone therapy, which blocks the growth-stimulating effects of hormones on cancer cells.
Approximately 25–30% of breast cancers are also referred to HER2-positive cancers. The HER2 is a protein that is part of biologic pathways involved in cellular replication and growth. If patients have an overabundance of HER2 or a mutation within a gene affecting HER2, they are classified as having HER2-positive cancer. These patients now have an option to be treated with the targeted agent Herceptin® (trastuzumab), which binds to HER2 and decreases or prevents cellular growth through this pathway.
Chemotherapy also remains a cornerstone of treatment for patients with early breast cancer. A common chemotherapy agent used in combination with other chemotherapy agents is Taxol. Chemotherapy is often used in combination with either Herceptin and/or hormone therapy.
Research has been moving toward establishing more individualized treatment approaches for patients. Genetic analysis and biomarkers are increasingly assessed in individual patients for their association in outcomes with specific types of therapy. Goals of such individualized approaches include improving disease outcomes and allowing more patients to avoid side effects caused by unnecessary therapy.
Researchers affiliated with the Cancer and Leukemia Group B (CALGB) recently conducted a clinical study to evaluate the benefits of Taxol in patients with early breast cancer. This study included data from over 1,320 women with breast cancer that had spread to the lymph nodes under the arms (node-positive). All patients had been treated with chemotherapy consisting of Adriamycin® (doxorubicin) plus Cytoxan® (cyclophosphamide). One group of patients was then treated with Taxol, while the other group received no further chemotherapy.
- Patients who were HER2-negative and ER-positive derived no benefit from the addition of Taxol.
- Patients who were HER2-positive and either ER-positive or ER-negative had a 40% reduced risk of a cancer recurrence with the use of Taxol.
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The researchers concluded: “[HER2-positive ] breast cancer is associated with a benefit from the addition of paclitaxel after adjuvant treatment with doxorubicin (<60 mg per square meter) plus cyclophosphamide in node-positive breast cancer, regardless of estrogen-receptor status. Patients with HER2-negative, estrogen-receptor–positive, node-positive breast cancer may gain little benefit from the administration of paclitaxel after adjuvant chemotherapy with doxorubicin plus cyclophosphamide.”
An accompanying editorial states: “This is nota call to abandon [Taxol] for this group of patients,” as there are several different treatment options that include Taxol. However, it is important for both physicians and patients to be aware of this data. The authors also state: “Thedays of ‘one size fits all’ therapy for patients with breastcancer are coming to an end.”
Patients diagnosed with breast cancer may wish to discuss their ER status and HER2 status with their physician, as well as discuss their individual risks and benefits of all treatment options.
Hayes D, Thor A, Dressler L, et al. HER2 and response to paclitaxel in node-positive breast cancer. New England Journal of Medicine. 2007;357:1496-1506.
Moore A. Breast cancer therapy-looking back to the future. New England Journal of Medicine. 2007;357:1547-1549.
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