WEDNESDAY, Sept. 6, 2006 (HealthDay News) -- Overexpression of a cell-regulating gene called cyclin D1 occurs in 30 percent to 50 percent of breast cancer patients and is associated with increased sensitivity to anti-cancer drugs and improved chance of survival, U.S. researchers report.
A team at Mount Sinai School of Medicine in New York City has found that cyclin D1 suppresses the activity of a gene called STAT3, which promotes cell overgrowth and prevents harmful cells from dying.
The findings were published in the Sept. 6 issue of the Journal of the National Cancer Institute.
The results surprised the researchers, because previous findings suggested that overexpression of cyclin D1 was associated with poor outcomes in patients with other kinds of cancer.
"Tumors occur because of a lack of control over cellular division. Cyclin D1 promotes cell growth, so you would think it would be an advantage to the tumor. But instead, we found that when cyclin D1 is overexpressed, it blocks STAT3. So, cyclin D1 is inhibiting STAT3, which in turn, keeps the cancer from developing further," Doris Germain, assistant professor of medicine at Mount Sinai, said in a prepared statement.
The researchers also found that high levels of cyclin D1 increased sensitivity to the drug bortezomib (Velcade), which was recently approved in the United States as a treatment for multiple myeloma.
The finding suggests that checking levels of cyclin D1 may help doctors predict which breast cancer patients would respond well to bortezomib.
The American Cancer Society has more about breast cancer.