Study Sheds New Light on Mechanism of Breast Cancer Treatment Resistance
A study by researchers at Dana-Farber Cancer Institute has illuminated a specific mechanism by which estrogen receptor-positive (ER+) breast cancers can become resistant to standard therapies and metastasize.
The scientists say the mechanism explains why breast cancers with mutations in the ER gene itself – the target of drugs such as aromatase inhibitors and tamoxifen – become resistant to these therapies and are prone to become metastatic. Resistance to therapy for ER-positive breast cancer is a common cause of breast cancer mortality and a major unmet need.
Myles Brown, MD, director of the Center for Functional Cancer Epigenetics at Dana-Farber, and Rinath Jeselsohn, MD, of Dana-Farber's Susan F. Smith Center for Women's Cancers, led the research team reporting their findings in the journal Cancer Cell.
A majority of women with breast cancer have tumors that are fueled by the hormone estrogen. Most are treated with therapies that prevent estrogen production or block the estrogen receptor in cancer cells to prevent binding by estrogen, with the goal of starving the tumor of estrogen and interrupting cancer growth.