Celebrex Could Help Fight Breast Cancer
Arthritis drug appears to regulate cell's use of estrogen, small study finds
FRIDAY, Dec. 10, 2004 (HealthDayNews) -- Celebrex, the popular arthritis drug, might reduce a woman's risk of developing breast cancer.
That's the preliminary finding of a small study presented Dec. 10 at the San Antonio Breast Cancer Symposium in San Antonio.
"If this drug is shown to be beneficial, then a high-risk woman could actually take this drug, but we obviously need further, larger studies to verify this," said lead researcher Dr. Banu Arun, an associate professor in the Department of Breast Medical Oncology at the University of Texas M.D. Anderson Cancer Center.
The National Cancer Institute (NCI) and Pfizer Inc., which makes Celebrex, funded the study, part of a larger investigation examining alternatives to the breast cancer drug tamoxifen.
Patients with advanced breast cancer and women at high risk of developing the disease are prescribed tamoxifen to prevent new and recurrent breast cancers; it is considered highly effective. Yet for all of its benefits, it has some unpleasant side effects, Arun explained, including an increased risk for uterine cancer and hot flashes. "So we are trying to find other drugs at least as effective, or better, with less side effects," Arun said.
Celebrex (celecoxib) is part of a class of painkillers known as cox-2 inhibitors. Lately, the entire family of stomach-friendly pain medicines has come under scrutiny following Merck & Co.'s decision to pull its cox-2 drug Vioxx off the market when a trial showed users had nearly twice the risk of heart attack and stroke.
The news has been more positive for Celebrex. In one study reported earlier this week, researchers at the University of Pennsylvania found the Pfizer drug to be safer for the heart than Vioxx.
As for its cancer-fighting properties, Celebrex has been shown to reduce tumor mass by encouraging cell death. It also discourages cell proliferation and the sprouting of new blood vessels to feed tumor growth, according to researchers at Mayo Clinic in Scottsdale, Ariz., whose findings were reported last month in Molecular Cancer Research.
Pinku Mukherjee, director of the Cellular Immunology Laboratory at the clinic and senior author of that report, said Arun's study "adds another interesting piece to the already known anti-proliferation effects of cox-2 inhibition."
The University of Texas team focused on the expression of "estrogen receptors," which are protein molecules found in cells that target mainly the breast and uterus. Estrogen, the female sex hormone, binds to these receptors.
In breast tissue, estrogen promotes the proliferation of cells lining the milk glands, readying the breast for nursing should the woman become pregnant, according to the NCI. Estrogen also benefits women by controlling the buildup of plaque in the arteries and preserving bone strength.
At the same time, estrogen can promote the proliferation of mutant cells, which can become cancerous, the NCI explains.
Arun and her colleagues wanted to see whether Celebrex could prevent breast cancer in women at high risk of the disease. Forty high-risk women agreed to participate in the study. After six months of drug therapy, breast biopsies revealed a drop in the level of estrogen-receptor expression -- to 21.8 percent from 30.8 percent.
"These findings show that there is a modest, albeit statistical, effect on estrogen receptor (ER) expression in breast issue with celecoxib treatment. However, the clinical significance of this finding remains completely unknown, particularly due to vary small sample size and a modest effect on ER expression," Mukherjee observed. What's more, estrogen-receptor expression may not the best marker for breast cancer proliferation, he added.
"I found this study provocative, but would wait for other proliferation indexes to confirm possibilities," he added.
Arun's team, in fact, is examining the impact of Celebrex on other cancer risk markers in breast cells as part of the larger study.
The National Cancer Institute can explain the role of estrogen receptors.