Green tea boosts production of detox enzymes, rendering cancerous chemicals harmless

PHILADELPHIA − Concentrated chemicals derived from green tea dramatically boosted production of a group of key detoxification enzymes in people with low levels of these beneficial proteins, according to researchers at Arizona Cancer Center.

These findings, published in the August issue of Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research, suggest that a green tea concentrate might help some people strengthen their metabolic defense against toxins capable of causing cancer.

In a study of 42 people, the concentrate − composed of chemicals known as green tea catechins in amounts equal to that found in 8-16 cups of green tea − boosted production of the enzymes, which belong to the glutathione S-transferase (GST) family, by as much as 80 percent in some participants.

GST enzymes are believed to be crucial to the body’s defense against cancer-causing chemicals and other toxins, according to the study’s lead investigator, H.-H. Sherry Chow, Ph.D., a research associate professor at the University of Arizona. They modify the cancer-causing molecules that would otherwise damage cellular DNA, thus rendering them inert.

“They actually convert known carcinogens to non-toxic chemicals, and studies have shown a correlation between deficient expression of these enzymes and increased risk of developing some cancers,” Chow said.

“Expression of this enzyme varies dramatically in people due to genetic variation and environmental factors,” Chow added. “Green tea catechins somehow increase gene expression of these enzymes, which can be an advantage to people with low levels to start with.”

Green tea has long been of interest to researchers given studies that have shown populations in which it is often consumed, such as the Chinese and Japanese, generally have lower rates of cancer. To find out if green tea can protect against cancer, the NCI has sponsored a number of rigorous scientific studies testing capsules of the extract, Polyphenon E, that have been prepared in Japan to meet exact specifications. These pills contain epigallocatechin gallate (EGCG), a catechin known for its potent antioxidant activity, and are currently being tested against a variety of cancers in clinical trials.

This study was designed to see if green tea catechin concentrate had any effect on the levels of GST enzymes in healthy individuals − research that could explain the tea’s anti-cancer properties. Healthy volunteers were asked to abstain from consuming any tea or tea-related products for four weeks. At the end of this “washout period,” blood was drawn and baseline GST enzyme levels were determined for each participant. Then, the volunteers were asked to take four Polyphenon E capsules, for a total of 800 milligrams of EGCG, each morning on an empty stomach for four weeks and to abstain from drinking tea or eating many cruciferous vegetables, which contain other beneficial chemicals. Another blood sample was taken after four weeks, and GST activity was determined.

Researchers found that use of Polyphenon E enhanced GST activity when data from all participants were included for analysis. But it had its most significant effect in volunteers whose baseline blood measurements showed low GST activity − an 80 percent increase compared to baseline GST activity. Activity did not change in volunteers with medium GST expression, or in those with the highest levels, GST seemed to decrease slightly although researchers believe that decline was due to random variation.

“This is the first clinical study to show proof that chemicals in green tea can increase detoxification enzymes in humans,” Chow said. “There may be other mechanism in play by which green tea may protect against cancer development, but this is a good place to start.”

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The NCI supported the study and researchers from NCI also participated in conducting the study.

The mission of the American Association for Cancer Research is to prevent and cure cancer. Founded in 1907, AACR is the world’s oldest and largest professional organization dedicated to advancing cancer research. The membership includes nearly 26,000 basic, translational, and clinical researchers; health care professionals; and cancer survivors and advocates in the United States and more than 70 other countries. AACR marshals the full spectrum of expertise from the cancer community to accelerate progress in the prevention, diagnosis and treatment of cancer through high-quality scientific and educational programs. It funds innovative, meritorious research grants. The AACR Annual Meeting attracts more than 17,000 participants who share the latest discoveries and developments in the field. Special Conferences throughout the year present novel data across a wide variety of topics in cancer research, treatment, and patient care. AACR publishes five major peer-reviewed journals: Cancer Research; Clinical Cancer Research; Molecular Cancer Therapeutics; Molecular Cancer Research; and Cancer Epidemiology, Biomarkers & Prevention. Its most recent publication, CR, is a magazine for cancer survivors, patient advocates, their families, physicians, and scientists. It provides a forum for sharing essential, evidence-based information and perspectives on progress in cancer research, survivorship, and advocacy.

Contact: Greg Lester
lester@aacr.org
267-646-0554
American Association for Cancer Research

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Gene variations directly link inflammation to an increased risk for lung cancer

Contact: Greg Lester
lester@aacr.org
267-646-0554
American Association for Cancer Research

Variations in two genes related to inflammation may be a major risk factor for developing lung cancer, according to a team of scientists from the National Cancer Institute and the University of Texas M. D. Anderson Cancer Center. The effect of these genes is especially strong among heavy smokers, suggesting that the inflammatory response is important in modulating the damage caused by tobacco smoke.

Their study, published in the July 1 issue of Cancer Research, a publication of the American Association for Cancer Research, is the first to pinpoint the mechanism by which damage to the lung might trigger an overzealous inflammatory response by the immune system, leading to lung cancer. The variants, or polymorphisms, were found in genes for interleukin 1A and interleukin 1B, two signaling molecules that immune system cells secrete in response to infection or tissue damage.

“Our findings help explain how heavy smoking, for example, combines with a genetic predisposition to create a besieged environment within the lungs,” said lead author Eric Engels, M.D., MPH, researcher at the Viral Epidemiology Branch of the NCI’s Division of Cancer Epidemiology and Genetics. “Essentially, sustained inflammation alters the microenvironment of the lung tissue, damaging cells and altering DNA.”

Inflammation is part of the immune system’s arsenal to combat the effects of infection and cell damage. However, prolonged or intense inflammation could lead to conditions within the lung environment that foster cancer, Engels said. Previous studies have shown that diseases associated with lung damage, such as tuberculosis and asthma, increase the risk of developing lung cancer. Likewise, exposure to tissue-damaging substances like silica and asbestos, inhaled into the lungs, has also been shown to increases lung cancer risk.

“Inflammation has long been thought to be a factor in many cancers, including lung cancer, and could provide an explanation how damage to lung tissue leads to cancer,” Engels said. “Knowing more about the downstream effects of these polymorphisms, and discovering others like them, will increase our understanding of how some people are predisposed to developing cancer.”

To examine the relationship between inflammation and lung cancer risk, the researchers compared differences in genes related to inflammation between more than 1,500 lung cancer patients and 1,700 controls at M. D. Anderson Cancer Center in Houston, Texas. More than 80 percent of the cancer patients in the study were current or former smokers. Among the 59 variations in 37 inflammation-related genes studied, the researchers discovered that some variants in the genes for interleukin (IL) 1A and 1B, are found more frequently in patients with lung cancer — and especially among heavy smokers. The effect was most profound in polymorphisms in IL1B, which is central to the inflammation process, the researchers said.

According to Engels, the IL1B protein is an integral part of the chemical cascade by which cell signals moderate the response to inflammation. Variations in the gene may lead to greater expression of the protein, which is more likely to turn on the cascade and sustain the damaging effects of inflammation. Over time, the constant damage of inflammation could lead to genetic damage and cancer, Engels said.

The researchers believe their findings will provide the basis for further lung cancer research as well as a model for examining the nature of inflammation in other types of cancer.

“While smoking is still the greatest risk factor, we still do not understand how other factors play a role,” Engels said. “A better understanding of the risks involving inflammation will lead to a better understanding of cancer prevention.”

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