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Green tea may negate the effects of a common cancer therapy
Date:2/3/2009

(WASHINGTON, February 3, 2009) Green tea products have become regarded as a valuable health supplement, as studies have shown evidence of its benefit against a variety of diseases, including cancer. However, a new study suggests that some components of green tea may counteract the anticancer effects of one cancer therapy, bortezomib (Velcade), and may be contraindicated for patients taking this medicine to ensure its maximum therapeutic benefit. This study is being prepublished online today in Blood, the official journal of the American Society of Hematology.

Because of its increasing popularity and availability to the public in many formulations, green tea has been increasingly studied to understand its effect on cancer, heart disease, and other conditions. In animal studies, an antioxidant compound in green tea called the EGCG polyphenol (epigallocatechin gallate) has been shown to be a potent anticancer agent, with effects demonstrated against leukemia, as well as lung, prostate, colon, and breast cancer. Among other properties, EGCG binds to a common protein in tumors called GRP78 (which is responsible for preventing cell death) and inhibits its function, thereby assisting in the death of tumor cells.

We know that cancer patients look to green tea extracts among other natural supplements to complement their therapeutic regimens. We wanted to better understand how the compounds in green tea interact with a cytotoxic chemical therapy and how that may affect patient outcomes, said Axel Schnthal, PhD, of the University of Southern California Keck School of Medicine and senior study author.

In this study, researchers evaluated whether the combination of green tea and bortezomib would improve outcomes against multiple myeloma, a blood cancer, and glioblastoma, a malignant brain tumor. Bortezomib, an anticancer therapy approved to tre
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Contact: Patrick C. Irelan
pirelan@hematology.org
202-292-0253
American Society of Hematology
Source:Eurekalert

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