The study, led by Robert Clarke, Ph.D., D.Sc., professor of oncology, shows that there may be an association between the gene IRF 1 (Interferon Regulatory Factor) and breast tumor resistance to tamoxifen or other antiestrogen treatment. IRF 1 is a tumor suppressor gene not previously associated with breast cancer.
"We hope that by pinpointing the connection between IRF 1 and breast cancer, we may be able to better identify which patients will respond to antiestrogen treatment and which patients will ultimately develop antiestrogen resistance," said Clarke.
Antiestrogen therapy is currently the most effective means to manage hormone-dependent breast cancer and has the fewest serious side effects. Hormone-dependent breast cancer accounts for approximately one-third of all breast cancer cases. The most widely prescribed antiestrogen therapy is tamoxifen, which blocks the activity of the estrogen hormone in breast tissue and can increase patients' overall survival. However about a third of breast tumors that might be expected to respond (because they express receptors for estrogen) are resistant to antiestrogens from the onset of treatment, and many initially responsive tumors sooner or later become resistant.
The Lombardi researchers studied a series of antiestrogen-sensitive and antiestrogen-resistant human breast cells using a variety of different microarray technologies.
"The logical implication of our work is that by adding the protein interferon to antiestrogen therapy, we should be able to turn on the IRF 1 gene to make these tumors sensitive to antiestrogen therapy, hopefully inhibiting new breast cancers or reoccurrences
Contact: Elizabeth McDonald
Georgetown University Medical Center