Green Tea And Prostate Cancer
Prostate cancer is very scary thing and if you are a male over the age of 38 it should be on your radar. Prostate cancer is the most common form of non skin cancer in North America, it affects 1 in every 6 men. Age can be directly linked to the likelihood of being diagnosed with prostate cancer. Although only 1 in every 10,000 men under age of 40 will be diagnosed with prostate cancer, this rate rapidly rises to 1 in every 38 men for the ages of 40 to 59, and again 1 in every 15 for ages of 60 to 69. In fact, greater than 65% of all prostate cancer is diagnosed in men above the age of 65.
Green Tea however can help reduce your risk of being one of the unlucky that find themselves diagnosed with prostate cancer. Here are a few quick notes from the National Cancer Institute’s fact sheet:
The antioxidants found in tea–called catechins–may selectively inhibit the growth of cancer.- In lab studies using animals, catechins scavenged oxidants before cell damage occurred, reduced the number and size of tumors, and inhibited the growth of cancer cells.
- NCI researchers are investigating the therapeutic and preventive use of tea catechins against a variety of cancers.
Green Tea helps create a protective effect for advanced prostate cancer. This effect can be directly linked with the amount of green tea consumption, increasing intake is linked to reduced risk.
Effect of a prodrug of the green tea polyphenol (-)-epigallocatechin-3-gallate on the growth of androgen-independent prostate cancer in vivo.
Epigallocatechin-3-gallate (EGCG) is the major and most potent polyphenol compound of green tea that has been shown to have anticancer effects against various types of cancers. In this study, in addition to the EGCG compound, a synthetic derivative, the peracetate of EGCG (EGCG-P), was used to investigate the inhibitory effects on growth of androgen-independent prostate cancer in vivo. The advantage of EGCG-P is that it may act as a prodrug, leading to higher bioavailability than EGCG itself. The aim of our study was to compare the differences between EGCG and EGCG-P on their inhibitory effect on androgen-independent prostate cancer, CWR22R, xenograft model in nude mice. The mice were administrated daily with solvent dimethyl sulfoxide, EGCG, and EGCG-P separately through intraperitoneal injection for 20 days. Tumor volume and body weight of nude mice were recorded daily. Serum prostate-specific antigen (PSA) levels were also measured before and after the treatment. The effects of both EGCG and EGCG-P on tumor cell proliferation were assessed by immunohistochemical (IHC) method using antibodies against Ki-67 and proliferating cell nuclear antigen. The apoptotic effect was evaluated by IHC against B-cell non-Hodgkin lymphoma-2 and terminal deoxynucleotidyl transferase dUTP nick-end labeling assay by in situ apoptosis detection kit. Moreover, the potential suppression of angiogenesis by EGCG and EGCG-P on prostate cancer was examined by IHC against CD31. Our results revealed that treatment of EGCG and EGCG-P compounds suppressed the growth of CWR22R xenografts without causing any detectable side effects in nude mice. The suppression of growth of the tumor was correlated with the decrease of serum PSA level together with the reduction in tumor angiogenesis and an increase in apoptosis on prostate cancer cells. The results showed that treatment of EGCG and EGCG-P inhibited tumor growth and angiogenesis while promoting apoptosis of the prostate cancer cells in vivo. Our results suggest that EGCG-P may be a more stable and useful compound for increasing the therapeutic anticancer effects in androgen-independent prostate cancer.
Department of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, HKSAR, China.
Lee SC, Chan WK, Lee TW, Lam WH, Wang X, Chan TH, Wong YC.
