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Aspirin use associated with decrease in hormone positive breast cancer risk
A study published in the May 26 2004 issue of the Journal of the American Medical Association has found a link between aspirin use and a lower incidence of hormone positive breast cancer. This study is the first to examine whether the protective effect of aspirin against breast cancer demonstrated by earlier research varies with hormone receptor status.
Researchers at Columbia University and the University of North Carolina at Chapel Hill examined data obtained from the Long Island Breast Cancer Study Project. One thousand four hundred forty-two participants with breast cancer were compared to 1420 women who did not have the disease.
The team found that the reduced risk of breast cancer associated with aspirin use was restricted to women with hormone-receptor positive tumors. Aspirin blocks the enzyme COX-2, which is responsible for the production of prostaglandin E2, a substance involved in inflammation that induces tumor-associated angiogenesis as well as aromatase expression. Blocking aromatase can lower estrogen levels, which may be a means by which aspirin helps prevent hormone-receptor positive breast cancer.
Lead investigator of the Long Island Breast Cancer Study Project and professor of epidemiology at the University of North Carolina at Chapel Hill, Dr Marilie D. Gammon, commented, "In this work, we confirm reports by others that aspirin reduces the risk of breast cancer by about 20 percent in some women. The risk reduction is most pronounced among daily aspirin users -- 27 percent. ER [estrogen-receptor]-positive breast cancer is the predominant type of breast cancer among postmenopausal women, and postmenopausal women make up about 75 percent of all newly diagnosed breast cancer cases in the United States. In contrast, ER-positive breast cancer is not prevalent among postmenopausal women in Japan, for example, where breast cancer rates are much lower than they are in the U.S. If we can reduce the risk of ER-positive breast cancer through such efforts as taking an aspirin-like chemopreventive, we could potentially reduce the incidence breast cancer among American women."
An important aspect in any reproductive cancer is whether the tumor growth is hormonally driven. Often breast cancer tumors require hormones for growth. This is known as a receptor-positive tumor. This type of cancer poses a unique problem because the hormones involved in tumor growth are either estrogen or progesterone or both. Estrogen and progesterone are naturally occurring hormones that the body produces in varying amounts throughout one's lifetime. To complicate the situation further, these hormones are essential for many other physiological functions, such as bone integrity, which will be discussed later in this protocol.
Hormone receptor-positive tumors consist of cancer cells with receptor sites for estrogen, progesterone, or both. The hormones attach to these receptor sites and promote cell proliferation. 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.
In 1991, researchers at the Institute for Hormone Research announced that they had been able to induce the body to convert the stronger form of estrogen (estradiol) into the weaker form (estriol) without using drugs. Estriol is considered to be a more desirable form of estrogen. It is less active than estradiol, so when it occupies the estrogen receptor, it blocks estradiol's strong "grow" signals. It took only 1 week to prove that the conversion of estradiol to estriol could be accomplished without drugs. Using a natural substance, researchers were able to increase the conversion of estradiol to estriol by 50% in 12 healthy people (Michnovicz et al. 1991).
Next, they tested the natural substance in female mice prone to developing breast cancer. The incidence of cancer and the number of tumors fell significantly. The substance was indole-3-carbinol (I3C), a phytochemical isolated from cruciferous vegetables (broccoli, cauliflower, Brussels sprouts, turnips, kale, green cabbage, mustard seed, etc.). I3C was then given to 17 men and women for 2 months. Again, levels of strong estrogen declined, and levels of weak estrogen increased. But more importantly, the level of an estrogen metabolite associated with breast and endometrial cancer (16,alpha-hydroxyestrone) fell (Bradlow et al. 1991).
In 1997, researchers at Strang Cancer Research Laboratory at Rockefeller University discovered that when I3C changes "strong" estrogen to "weak" estrogen, the growth of human cancer cells is inhibited by 54-61% (Telang et al. 1997). More important to breast cancer patients, this study demonstrated that I3C provoked cancer cells to self-destruct (apoptosis). A prime goal of cytotoxic chemotherapy is to induce apoptosis. If future studies show that nontoxic I3C can reliably facilitate apoptosis, this phytonutrient may become a standard adjunct in).