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January 8, 2010

Pomegranate inhibits hormone-dependent breast cancer cell growth

Pomegranate inhibits hormone-dependent breast cancer cell growth

A report published in the January, 2010 issue of the American Association for Cancer Research journal Cancer Prevention Research reveals the discovery by researchers at City of Hope Hospital in Duarte, California of a suppressive effect for compounds found in pomegranate on the proliferation of breast cancer cells. Prior research has demonstrated that ellagic acid in pomegranates inhibits the enzyme known as aromatase that converts androgen to estrogen hormones which fuel a common type of breast cancer.

City of Hope Division of Tumor Cell Biology director and Breast Cancer Research Program co-leader Shiuan Chen, PhD, along with Beckman Research Institute fellow Lynn Adams and their associates found that ten ellagitannins occurring in pomegranates had the potential to prevent estrogen-responsive breast cancer, with a metabolite of ellagic acid called urolithin B significantly inhibiting the growth of cultured breast cancer cells.

"Phytochemicals suppress estrogen production that prevents the proliferation of breast cancer cells and the growth of estrogen-responsive tumors," Dr Chen explained.

"We were surprised by our findings," he remarked. "We previously found other fruits, such as grapes, to be capable of the inhibition of aromatase. But, phytochemicals in pomegranates and in grapes are different."

University of Texas M.D. Anderson Center Clinical Cancer Prevention Department Chairman Powel Brown, MD, PhD is intrigued by the study's results. "More research on the individual components and the combination of chemicals is needed to understand the potential risks and benefits of using pomegranate juice or isolated compounds for a health benefit or for cancer prevention," he stated. "This study does suggest that studies of the ellagitannins from pomegranates should be continued."

He suggested that people "might consider consuming more pomegranates to protect against cancer development in the breast and perhaps in other tissues and organs."

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Health Concern Life Extension Highlight

Breast cancer

Breast tumors often require hormones for growth, which poses a unique problem because the hormones involved in tumor growth are either estrogen, progesterone, or both. Estrogen and progesterone are naturally occurring and necessary hormones, produced mainly in the ovaries and adrenal glands in varying amounts throughout a woman's lifetime. These hormones are essential for many physiological functions, such as bone integrity.

Hormone receptor-positive tumors can consist of cancer cells with receptor sites for estrogen, progesterone, or both. The hormones attach to receptor sites and promote cell proliferation. Hormone therapy blocks the hormones from attaching to the tumor receptor sites and may slow or stop the cancer's growth. The drug most often used in this type of endocrine therapy is tamoxifen, with a response rate from 30-60%. Other therapies are sometimes used, such as aromatase inhibitors (that inhibit the conversion of precursors to estrogens) or oophorectomy (the removal of the ovaries).

The stronger form of estrogen, estradiol, can be converted into the weaker form, estriol, in the body 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 "growth" signals. Using a natural substance, the conversion of estradiol to estriol increased by 50% in 12 healthy people (Michnovicz et al. 1991). Furthermore, in female mice prone to developing breast cancer the natural substance reduced the incidence of cancer and the number of tumors significantly. The natural substance was indole-3-carbinol (I3C).

Indole-3-carbinol (I3C) is a phytochemical isolated from cruciferous vegetables (broccoli, cauliflower, Brussels sprouts, turnips, kale, green cabbage, mustard seed, etc.). I3C given to 17 men and women for 2 months reduced the levels of strong estrogen, and increased the levels of weak estrogen. But more importantly, the level of an estrogen metabolite associated with breast and endometrial cancer, 16-a-hydroxyestrone, was reduced by I3C (Bradlow et al. 1991).

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