877 . 318 . 8728    Contact Us    Login

Please download the most recent Flash Player, here...

Get Adobe Flash player
News - October is National Breast Cancer Awareness Month

US BioTek Laboratories - News

October is National Breast Cancer Awareness Month

Thursday, October 8th, 2009

In a recently published prospective cohort study of over 50,000 African-American women(1), researchers found a significant inverse association of a “prudent” dietary pattern, defined as one consisting of whole grains, cruciferous and other vegetables, fruit, low-fat dairy products, fish and poultry with estrogen receptor-negative breast cancer risk in thin young women (premenopausal women with a BMI <25). These women were thirty percent less likely to develop breast cancer over the twelve year study period compared to their counterparts who maintained a “Western” dietary pattern of refined grains, high-fat dairy products, processed meats and sweets.
Many studies have shown that dietary patterns, rich in antioxidants, isothiocyanates, flavonoids, folate and phytoestrogens are associated with a decreased cancer risk. This study by Agurs-Collins et al., is cited as especially important being a first to look at dietary patterns and risk of breast cancer in African American women who are noted to have a higher prevalence of hormone receptor-negative tumors than their white female counterparts.(2) Hormone receptor-negative tumors are clinically aggressive. It is important to note that a significant percentage of breast cancer cases may be the result of faulty genes and not linked to lifestyle.

Hormone receptor-positive tumors on the other hand, for example estrogen receptor positive tumors of the breast, ovaries, uterus, cervix and prostate, depend on the presence of unopposed estrogen for ongoing proliferation.

How does the body metabolize estrogen?

The detoxification of estrogens for their eventual elimination involves the cytochrome P-450 system, a class of enzymes found throughout the body tissues including the liver. It is through this detoxification process that yields the 2- or 16α-hydroxylated estrogen products. Genetic polymorphisms of the cytochrome P450 enzymes, affecting the transformation of the estrogens have and continue to be identified as playing an integral role in hormone-sensitive cancer etiology.(3)

The ratio of 2:16α hydroxyestrone has been utilized to assess estrogen metabolism.
The hydroxylation of estrogen at the C-16, or carbon-16 position, produces the biologically strong 16α-OHE1 metabolite. This metabolite has been shown to exert a proliferative or stimulatory activity on human cancer cell lines.(4)(5)(6) Hydroxylation at the C-2 position, on the other hand, yields the biologically weaker estrogen metabolite, 2-OHE1. This metabolite has been shown to exert anti-proliferative properties on human cancer cells with little to no estrogenic activity.(7)

Although the optimal level for the ratio is not known, an increase in the ratio of 2-hydroxyestrone relative to 16α-hydroxyestrone is considered to be an indicator of favorable estrogen metabolism. Currently there are no published human data on the effects of very high ratios or what can be considered reasonable upper limits.

Certain factors have been shown to influence estrogen metabolism and the 2:16α ratio favouring 2-hydroxylation. These include but are not limited to; a diet rich in cruciferous vegetables, phytoestrogens, lignans and marine fatty acids. Maintaining a healthy weight, being physically active, eliminating smoking and limiting alcohol intake may be wise preventive measures overall in modifying cancer risk.

US BioTek Laboratories Comprehensive Urinary Steroid Hormone Profile measures the 2- and 16α-hydroxylated estrogen metabolites from a 24-hour urine sample collection.

To view complete test profile information please click here.

Helpful Links:

http://www.breastcancer.org/

http://www.nbcam.org/

http://www.dietandcancerreport.org/

__________________________
1 Collins-Agurs, T., Rosenberg, L., Makambi, K. et al. (2009). Dietary patterns and breast cancer risk in women participating in the Black Women’s Health Study. Am J Clin Nutr, 90:621-628.
2 Amend, K,. Hicks, D, Ambrosone, C.B. Breast cancer in African-American women: difference in tumor biology from European-American women. Cancer Res, 2006; 66:8327-8330.
3 Tworoger, S.S., Chubak, J., Aiello, E.J., et al. (2004). Association of CYP17, CYP19, CYP1B1, and COMT polymorphisms with serum and urinary sex hormone concentrations in postmenopausal women. Canc Epid Biomarkers & Prevention, 13:94-101.
4 Yager, J.D., Davidson, N.E. (2006). Estrogen carcinogenesis in breast cancer. N Eng J Med, 354:270-282.
5 Lottering, M.L., Haag, M., Seegers, J.C. (1992).  Effects of 17b-estradiol metabolites on cell cycle events in MCF-7 cells. Cancer Res, 52:5926-5932.
6 Lippert, C., Seeger, H., Mueck, A.O. (2003). The effect of endogenous estradiol metabolites on the proliferation of human breast cancer cells. Life Sciences, 72:877-883.
7 Lippert, C., Seeger, H., Mueck, A.O. (2003). The effect of endogenous estradiol metabolites on the proliferation of human breast cancer cells. Life Sciences, 72:877-883.

Back to Top            Back to previous page


13500 Linden Ave North, Seattle, WA 98133 USA, Phone: 206.365.1256 Fax: 206.363.8790 Toll Free: 877.318.8728