Researchers in the US found that the decline in use of postmenopausal hormone therapy may partly explain the fall in incidence of a known risk factor for breast cancer, atypical ductal hyperplasia. They also said their findings support the idea that low and high grade breast cancers develop via different pathways and thereby clarify the role that hormone therapy may play in increasing the rates of breast cancer.

The study was the work of first author Dr Tehillah Menes, and colleagues and is published in the November issue of Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research.

Menes, who during the study was the chief of breast service in the Department of Surgery at Elmhurst Hospital Center, New York, told the press that:

“Postmenopausal hormone treatment is associated with increased rates of benign breast biopsies, and early and late stages of cancer.”

“Atypical ductal hyperplasia is associated with the use of postmenopausal hormone treatment and its rates have decreased with the decline in use of this treatment,” she added.

Atypical ductal hyperplasia occurs when abnormal cells start to grow in the milk ducts of the breast and other studies suggest the condition is linked to a three to five-fold increased risk of developing breast cancer.

For this investigation, Menes and colleagues used data from more than 2.4 million mammography studies with and without breast cancer taken between 1996 and 2005. The data came from the Breast Cancer Surveillance Consortium, which gathers information from a network of seven mammography registries with links to tumor and/or pathology registries in various parts of the US.

Their aim was to examine risk factors and rates of atypical ductal hyperplasia with and without associated breast cancer over time. They also looked at tumor characteristics of breast cancer with and without associated atypical ductal hyperplasia in women previously screened with mammography.

The results showed that:

  • A total of 2,453,483 screening mammograms were linked to 1,064 biopsies with atypical ductal hyperplasia (ADH), 833 breast cancers with ADH, and 8,161 cancers with no ADH.
  • Postmenopausal hormone therapy use decreased significantly from 35 per cent to 11 per cent over the study period.
  • Rates of ADH decreased from a peak of 5.5 per 10,000 mammograms in 1999 to 2.4 per 10,000 in 2005.
  • Rates of cancer with ADH decreased from a peak of 4.3 per 10,000 mammograms in 2003 to 3.3 per 10,000 in 2005.
  • ADH and breast cancer were significantly linked to postmenopausal use of hormone therapy.
  • Cancer linked with ADH was of lower grade and stage and more estrogen receptor positive than cancer without ADH.

Menes and colleagues concluded that postmenopausal hormone therapy is linked with an increased risk of ADH with or without cancer, and that:

“Rates of ADH have decreased over the past decade, which may be partially explained by the significant reduction in use of postmenopausal HT [hormone therapy].”

Co-author Dr Karla Kerlikowske, who is professor of medicine and epidemiology and biostatistics at University of California, San Francisco, said:

“The rate of atypical hyperplasia declined, which we didn’t expect to see with the increased use of mammography to identify abnormal lesions.”

“We did not expect to find a decline in rate of atypical ductal hyperplasia with a decline in postmenopausal hormone treatment use,” she added.

The finding that cancer linked with atypical ductal hyperplasia is usually of lower grade and stage supports the theory that low and high grade cancers develop via separate pathways, said Menes.

“These findings help clarify the different pathways to the development of breast cancer and the role of postmenopausal hormone treatment in increasing the rates of breast cancer,” she concluded.

Kerlikowske suggested future research should concentrate on the effect of hormone therapy on benign proliferative breast lesions.

“Rates of Atypical Ductal Hyperplasia Have Declined with Less Use of Postmenopausal Hormone Treatment: Findings from the Breast Cancer Surveillance Consortium.”
Tehillah S. Menes, Karla Kerlikowske, Shabnam Jaffer, Deborah Seger, and Diana L. Miglioretti.
Cancer Epidemiol Biomarkers Prev, November 2009 18:2822-2828
DOI:10.1158/1055-9965.EPI-09-0745

Source: American Association for Cancer Research.

Written by: Catharine Paddock, PhD