Regular Aspirin Use May Decrease Breast Cancer Risk
Marilie D. Gammon, Ph.D University of North Carolina, School of Public Health NIEHS Grant P30ES10126
Background: Aspirin has been used as a non-prescriptive pain reliever for over 100 years with current use equaling over 80 million tablets consumed in the United States every day. Not until the 1970's was the mechanism of action discovered. Aspirin was found to inhibit the production of proinflammatory prostaglandins.
In the past two decades, regular aspirin use has been shown to be protective for heart disease, stroke, and colorectal cancer. Research during this period has also suggested that inhibition of prostaglandin synthesis may prevent cancer. Cyclooxygenase (COX) is involved in the synthesis of prostaglandins. Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) are known to block the active site of COX and therefore, inhibit prostaglandin production. The final reaction in the synthesis of estrogen is dependent upon a cytochrome P450 enzyme that is stimulated by Prostaglandin E2. Therefore, inhibition of prostaglandin production will also decrease the production of estrogen. Given the importance of estrogen in the development of breast cancer, these investigators undertook an epidemiologic study to determine whether regular NSAID use protected against breast cancer.
Figure.
Prostaglandin E2 Produced by Tumor Cells Stimulates Expression of Cytochrome P450 Aromatase (CYP19) in Breast Adipose Stromal Cells.
Advance: Regular aspirin use was associated with a reduction in breast cancer risk in patients with hormone-responsive tumors. The results were stronger for women who took seven or more aspirin tablets per week. The results of Ibuprofen use were generally weaker. There was no reduction in risk among women who took acetaminophen, which does not inhibit prostaglandin synthesis.
Implication: This study adds to the growing body of data that supports the regular use of aspirin as an effective chemopreventive agent for hormone-responsive breast cancer tumors. This effect most likely occurs through the inhibition of prostaglandin and subsequent inhibition of estrogen biosynthesis. The reduced risk must be confirmed by other researchers before clinicians can make definite recommendations to women at risk for breast cancer, but this and other studies do provide evidence of a protective effect.
Citations:
Terry MB, Gammon MD, Zhang FF, Tawfik H, Teitelbaum SL, Britton JA, Subbaramaiah K, Dannenberg AJ, Neugut AI. Association of frequency and duration of aspirin use and hormone receptor status with breast cancer risk. JAMA. 2004 May 26;291(20):2433-40.
DuBois RN. Aspirin and breast cancer prevention: the estrogen connection. JAMA. 2004 May 26;291(20):2488-9.