Study in mice reports success with drugs that inhibit estrogen,,
MONDAY, Nov. 9 (HealthDay News) -- Two drugs used to treat breast cancer and osteoporosis eliminated cervical cancer in mice, according to a new study.
The drugs also cleared precancerous growths in the cervix and vagina, and prevented the onset of cancer in mice with precancerous lesions.
The breast cancer drug fulvestrant and the breast cancer/osteoporosis drug raloxifene were given to mice genetically engineered to carry human papillomavirus (HPV) 16, which is strongly associated with cervical cancer. Both drugs prevent estrogen from working in cells. Fulvestrant is marketed for women as Faslodex, and raloxifene is marketed as Evista.
The study appears in this week's issue of the Proceedings of the National Academy of Sciences.
"We have begun to test whether the drugs are as effective in treating cervical cancer in human cells as they are in our mice," senior study author Dr. Paul F. Lambert, an oncology professor at the University of Wisconsin School of Medicine and Public Health, said in a university news release.
If the lab studies, expected to take one or two years, are successful, they could be followed quickly by clinical trials, the researchers said.
Nearly all cervical cancers test positive for HPV 16, Lambert said, but not all women infected with HPV get cervical cancer, which has led researchers to examine other factors.
"Since the cervix and other female reproductive organs are so responsive to estrogen, our lab and others began to focus on that hormone," he explained.
Fulvestrant and raloxifene block a receptor (estrogen receptor alpha) that mediates estrogen function in cells.
"We can't be sure how the science will translate from animals to humans, but we have faith in our mouse model," Lambert said. "There are many similarities in how cervical cancer develops and manifests itself in women and in mice."
The U.S. National Women's Health Information Center has more about cervical cancer.
-- Robert Preidt
SOURCE: University of Wisconsin, news release, Nov. 9, 2009
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