A protein relationship that may be an ideal treatment target for ER+ breast cancer has been identified by researchers from the Kimmel Cancer Center at Jefferson. The study was reported in the July 15 issue of Cancer Research.
DACH1, a cell fate determination factor protein, prevents cancer cell proliferation by repressing the function of estrogen receptorsin breast cancer, the researchers found. However, they also found that as the presence of DACH1 decreases in breast cancer, the presence of estrogen receptors increases, and vice versa.
Approximately 70% of breast cancers are ER+. Treatment for ER+ breast cancer usually consists of hormone therapy, which includes lowering the natural estrogen levels in the body or using synthetic drugs like tamoxifen, which compete with natural estrogen. However, this treatment only works for a few years.
DACH1 is expressed in normal breast tissue. As breast cancer develops and becomes more invasive, the expression of DACH1 decreases. In a previous study of more than 2,000 breast cancer patients, Jefferson researchers found that a lack of DACH1 expression was associated with a poor prognosis. Patients who did express DACH1 lived an average of 40 months longer.
"Many more studies need to be done, but there is strong evidence that DACH1 is a promising marker of survival and therapeutic target in patients with breast cancer," said the study's senior researcher Richard Pestell, M.D., Ph.D, who is director of the Kimmel Cancer Center and chair of the Cancer Biology department at Jefferson.