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(HealthDay News) -- Declining use of hormone replacement therapy may be driving down rates of a condition called "atypical ductal hyperplasia," a known risk factor for breast cancer, new research suggests.
This is the first time a link has been found between atypical ductal hyperplasia -- abnormal cells in the breast's milk ducts -- and hormone therapy, said Diana Miglioretti, senior author of a paper published in the November issue of Cancer Epidemiology, Biomarkers & Prevention.
"It sounds like another reason not to take hormones," said Dr. Jay Brooks, chairman of hematology/oncology at Ochsner Health System in Baton Rouge.
"This is part of a pattern that combined use of hormone therapy with both estrogen and progesterone does something to a woman's breast that predisposes them to atypical ductal hyperplasia, which is felt to be a precursor to certain types of malignancies," Brooks added.
If atypical ductal hyperplasia does turn out to be a precursor to breast cancer, this link would be a good indicator of how use of hormone therapy -- often used for menopausal symptoms such as hot flashes -- can help spur malignancy.
The findings are in keeping with other recent research showing a decline in breast cancer rates since the release of results from the Women's Health Initiative, a major trial that caused many women to stop taking combined (estrogen plus progesterone) hormone therapy.
The Women's Health Initiative was halted in July of 2002 after researchers found higher risks of heart attacks and breast cancer in women taking the hormone supplements compared with placebo.
Since that time, use of hormone replacement therapy (HRT) has experienced a precipitous decline.
According to experts, women diagnosed with atypical ductal hyperplasia have a three to five times increased risk of developing breast cancer, either in the same breast or the opposite breast.
Atypical ductal hyperplasia "is a benign condition but it is a risk factor for breast cancer. It's not clear if it's a precursor to breast cancer," said Miglioretti, who is a senior investigator with the Group Health Research Institute in Seattle. "This sheds light on more of the breast process, how HRT affects breast cancer."
Miglioretti and her co-authors analyzed almost 2.5 million screening mammographies from samples provided by the Breast Cancer Surveillance Consortium. The mammograms were done between 1996 and 2005.
In 1999, atypical ductal hyperplasia was found in 5.5 per 10,000 mammograms but by 2005 had declined to only 2.4 per 10,000, a drop of more than half. This occurred despite an increase over time of rates of mammography, which tend to pick up the abnormality.
Meanwhile, breast cancer cases in women with atypical ductal hyperplasia declined from 4.3 per 10,000 mammograms in 2003 to 3.3 per 10,000 mammograms in 2005.
And postmenopausal use of hormone therapy dropped from 35 percent to 11 percent.
The study also revealed that cancers associated with atypical ductal hyperplasia tend to be less aggressive, lending support to the theory that less aggressive and more aggressive cancers develop differently, the authors stated.
One breast cancer expert said the new study dovetails with recent trends in breast cancer incidence.
"The finding they report is consistent with [previous] observations that suggested there was a drop in incidence of breast cancer in about 2003 and it coincided with when the Women's Health Initiative reported that estrogen-plus-progesterone use was associated with an increased risk of heart attacks as well as a slight increased incidence of breast cancer risk," said Dr. James Liu, chairman of obstetrics and gynecology at MacDonald Women's Hospital, Case Medical Center, University Hospitals in Cleveland. "The association caused many women to either question their need to be on [hormone therapy] or stopping it."
But, cautioned Liu, "the data is not strong enough to say this observation was caused by [a decline in hormone use] but it is a very strong association."
There's more on hormone therapy and cancer at the U.S. National Cancer Institute.