From Our 2009 Archives
Pregnancy Protein May Slow Breast Cancer
Researchers Say Early Research on Protein Called AFP Could Lead to Treatments
Reviewed By Louise Chang, MD
Investigators from the University of Albany linked the pregnancy protein alpha-fetoprotein (AFP) to slowed growth of breast cancer in rats exposed to pregnancy hormones such as estrogen, progesterone, or human chorionic gonadotropin.
These hormones were shown by the researchers to induce AFP during pregnancy.
They have also been shown to inhibit breast cancer growth in earlier rat studies, although estrogen and progesterone are known to fuel the growth of breast cancer in humans.
Study researcher Herbert Jacobson, PhD, who has been studying AFP in rats for more than two decades, strongly believes the protein is responsible for the pregnancy-related reduction in breast cancer risk.
"Twenty-five years ago I deduced that this must be the agent responsible for lowering breast cancer risk in women who have been pregnant," he tells WebMD. "And the research we have done since then supports this hypothesis."
AFP and Breast Cancer
Pregnancy, especially before the age of 30, is known to lower a woman's lifetime risk for developing breast cancer, and having more than one child is also protective.
Alpha-fetoprotein is made by the fetus, and measurement of the protein during pregnancy can help screen for birth defects.
Very high AFP levels, for example, suggest the presence of neural tube defects or an abdominal wall defect known as omphalocele, and very low levels are suggestive of Down syndrome.
The protein is usually undetectable in the blood of healthy men and healthy women who aren't pregnant. In these groups, elevated AFP levels suggest the presence of certain cancers.
In their new study, which appears in the December issue of Cancer Prevention Research, Jacobson and colleagues treated cancer-exposed rats that were not pregnant with estrogen, estrogen plus progesterone, or human chorionic gonadotropin (HCG).
As has been seen in previous studies, all three treatments were associated with a reduction in breast cancers in the high-risk rats.
All three of the hormone treatments were also associated with elevated AFP levels and AFP was found to directly inhibit the growth of breast cancer cells grown in lab cultures.
"Hormones in pregnancy, such as estrogen, all induce AFP, which directly inhibits the growth of breast cancer," Jacobson says in a news release.
But cancer specialist Powel Brown, MD, PhD, says the research does not prove this is the case.
Brown chairs the clinical cancer prevention department at the University of Texas M.D. Anderson Cancer Center and he serves as an editorial board member for Cancer Prevention Research.
He called the latest findings promising but preliminary in a statement released Tuesday.
"The researchers have not directly demonstrated the cancer preventive activity of AFP," he said, adding that the hormone treatment appeared to prevent or delay tumors in only 30% to 50% of the rats in the study.
"This study is promising and suggests that additional animal studies need to be done before translation to humans," he says.
Jacobson says AFP in its natural form is not appropriate for use in humans, but the research team has identified eight of the hundreds of amino acids in the protein that might be.
The researchers hope to win approval for early human studies of a modified version of AFP, which they call AFPep.
SOURCES: Cancer Prevention Research, December 2009; online edition.
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