Dec. 1 (Xinhuanet) -- American scientists caution that their research is still
in the exploratory stages, but recent results have shown the abortion drug
RU-486 prevented tumors in mice bred with a breast cancer gene.
Although no one is suggesting women use the abortion
pill to prevent breast cancer, the experiment did show that RU-486 blocks a
hormone called progesterone, which activates the breast cancer gene BRCA1.
"All of us have to be cautious," said cell biologist
Eva Lee of the University of California, Irvine, who led the research published
in Friday's edition of the journal Science. "But I do think if there is a better
anti-progesterone available, hopefully there will be other options in the future
for these women."
Women today have few options to prevent breast
cancer, and if researchers could produce a safer hormone blocker it would offer
a viable alternative for women with the BRCA1 gene.
not involved with the experiment praised the work, even as they warned women not
to get their hopes up.
"This is an avenue worth pursuing on a research
level," said Dr. Claudine Isaacs, an oncologist at Georgetown University
Hospital who works closely with carriers of BRCA1 and a related gene.
"This is work in a mouse," she added. "It's clearly
too early to start recommending use of this agent."
Dr. Len Lichtenfeld, the American Cancer Society's
deputy chief medical officer, said researchers and patients will "take interest
in this topic and explore it further."
He called the paper "elegant research," but stressed
that "it would not be appropriate in any way, shape or form that women start
taking RU-486 for this purpose."
Long-term use of RU-486 could suppress the immune
system and cause other side effects.
Some 212,000 women in the United States will be
diagnosed with breast cancer this year. Only 5 percent to 10 percent will have a
hereditary form. Women who inherit mutations in the BRCA1 gene are at far
greater risk of cancer than the average woman. By age 70, more than half of
those gene carriers develop either breast or ovarian cancer.
In their research, Lee and colleagues created mice
whose mammary glands only harbor the BRCA1 mutation.
The scientists found the bad gene made
breast tissue have too-high levels of progesterone receptors. That leads to
excessive cell growth because the hormone stays longer than it should.
In fact, the mice's breast tissue looked like it
should have during pregnancy, when temporarily high progesterone levels cause
breast growth as the gland prepares to make milk.
The final evidence came from RU-486, also called
mifepristone. It causes human abortions by suppressing progesterone, a hormone
crucial to sustaining pregnancy.
Instead of a human pill, Lee implanted some of the
cancer-prone mice with an RU-486 pellet designed to slowly emit the drug into
their bodies over two months.
By 8 months of age, each of the untreated
gene-defective mice had developed tumors. But none of the mice given RU-486 had
developed tumors by 12 months, when the study stopped.
Lee cautioned that RU-486 is not a good candidate for
such long-term use in people. She said more targeted progesterone blockers
already are being developed.