Daily aspirin reduces estrogen receptor positive breast cancer risk

  A  report published online on April 30, 2008 in the journal Breast Cancer Research   concluded that the use of  aspirin on a daily basis reduced the risk of estrogen receptor-positive  breast cancer, which makes up 75 percent of breast cancer cases. These  cancers have receptors on their surface for female hormone estrogen, which  fuels the tumors’ growth.

Gretchen  L. Gierach and her colleagues at the National Cancer Institute evaluated  data from 127,383 women aged 51 to 72 who were enrolled in the National  Institutes of Health-AARP Diet and Health Study, which examined the  relationship between diet, health-related behaviors and cancer.  Questionnaires completed upon enrollment between1995 and 1996 provided  information on diet history, demographic characteristics and other data. A  second questionnaire completed between 1996 and 1997 collected information  concerning medication use, including aspirin and nonaspirin nonsteroidal  anti-inflammatory drugs (NSAIDs). Breast cancer cases were identified  through cancer registry information through the end of 2003.

Over  the period examined, 4,501 women developed breast cancer. Of the invasive  breast cancer cases for which estrogen receptor status was available,  1,439 were estrogen receptor positive and 280 estrogen receptor negative.  Although NSAID use was not linked to a reduction in overall breast cancer  risk, women who reported daily aspirin use had a 16 percent lower risk of  estrogen receptor positive breast cancer than women who did not use the  drug. There was also a significant reduction in risk in breast cancer in  situ (localized cancer) among daily aspirin users.

The  study is one of the largest to date to evaluate the association between  the type of NSAID used and breast cancer risk by tumor characteristics.  The authors remark that the association of a reduction in estrogen  receptor-positive breast cancer with aspirin is consistent with aspirin’s  ability to permanently inactivate cyclooxygenase-2 (COX-2), which  suppresses estrogen synthesis by decreasing aromatase activity, among  other pathways of risk reduction. COX-2 is expressed both in situ and  invasive breast cancer, and its upregulation may be an early event in  carcinogenesis.

“Our  results provide support for further evaluating relationships in  prospective studies with well-defined measures of NSAID use by NSAID type,  by breast cancer stage, and by estrogen receptor status,” the authors  conclude.