COX-2 expression is marker for cancer development in some benign breast biopsies

The researchers calculated that, among the women in the study group, the absolute risk of developing breast cancer 15 years after a diagnosis of atypical hyperplasia was 13 percent in biopsies with little or no COX-2 expression, 19 percent with moderate COX-2 expression, and 25 percent with strong COX-2 expression. In women who had been followed for 20 years or more, the association was more definitive: stratification of risk was 14 percent, 24 percent, and 31 percent, respectively. (Because the participants had atypical hyperplasia, they were all at increased baseline risk of developing breast cancer.)

The finding that risk of later breast cancer was associated with increasing levels of COX-2 expression was of borderline statistical significance (p=.07), likely due to the small sample size Dr. Hartmann says. “But higher expression levels were tightly linked to an increased number of abnormal foci in the biopsy, which we had earlier found to be a strong risk factor for breast cancer.”

The researchers also assessed the relative risk of developing breast cancer, based on COX-2 expression in atypical hyperplasia, compared to a “control” population of unaffected women, and found that little COX-2 expression was associated with 2.6 times the risk, moderate COX-2 expression increased risk by 3.5 times, and a strong expression of COX-2 elevated risk by more than 5.6 times, compared to women in the general population.

“COX-2 appears to be a biomarker that further stratifies breast cancer risk among women with atypia and may be a relevant target for chemoprevention strategies,” says Dr. Hartmann.

Other Mayo Clinic researchers included V. Shane Pankratz, Ph.D.; Marta Santisteban, M.D., Ph.D.; Carol Reynolds, M.D.; Robert Vierkant; Wilma Lingle, Ph.D.; and Marlene Frost, Ph.D. Additional contributors included Daniel Visscher, M.D., from the University of Michigan, Ann Arbor and Ari Ristimaki, M.D., from the University of Helsinki, Finland.

Funding for the study was provided by the U.S. Department of Defense, and grants from Martha and H. Bruce Atwater Jr. and the Regis Foundation for Breast Cancer Research.

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