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May 2, 2008

Daily aspirin reduces estrogen receptor positive breast cancer risk

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.

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Breast cancer

An important aspect in any reproductive cancer is whether the tumor growth is hormonally driven. Often breast tumors require hormones for growth, i.e., hormonally responsive tumor. The hormones attach to their receptor sites and promote cell proliferation. Hormone receptor-positive tumors consist of cancer cells with receptor sites for estrogen, progesterone, or both. The receptor status of a tumor is determined by testing tissue removed during a biopsy. Breast cancer can be categorized by its receptor status, which can be estrogen receptor-positive (ER+), estrogen receptor-negative (ER -), progesterone receptor-positive (PR+), progesterone receptor-negative (PR-) or any combination thereof. Both estrogen and progesterone are naturally occurring hormones that the body produces in varying amounts throughout one's lifetime. These hormones are essential for many other physiological functions, such as bone integrity.

Treatment to block the hormones from attaching to the tumor receptor sites may slow or stop the cancer's growth. The drug most often used in this type of treatment is tamoxifen, which is very effective against receptor-positive cancers.

Cancer cells have the ability to leave the original tumor site, travel to distant locations, and metastasize in organs such as the liver, lungs, or bones. The process of metastasis is dynamic and requires an optimal environment in order for a tumor cell to proliferate, invade surrounding tissues, be released into the circulation, adhere to blood vessels in the liver, invade the liver, proliferate, and establish its own blood supply (tumor angiogenesis). This complex process requires interaction of tumor cells with the microenvironment of the liver to the extent that the tumor cell can utilize the growth factors and blood vessels of the liver in order to grow.

Life Extension magazine May, 2008 issue now online!

Life Extension magazine May, 2008

 

 

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