Study Suggests Timing Is Important In Cancer Chemoprevention

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January 7, 2011

Study suggests timing is important in cancer chemoprevention

Study suggests timing is important in cancer chemoprevention

An article published online on December 24, 2010 in the journal Carcinogenesis reports the outcome of a rodent study which found a protective benefit for vitamin E and selenium against esophageal cancer, particularly if administered early after exposure to a carcinogenic substance.

Scientists at the Chinese Center for Disease Control and Prevention in Beijing gave five groups of rats a diet that contained reduced amounts of vitamin E and selenium, which was designed to mimic the diet of some human populations. All but one group were administered the carcinogen NMBzA 3 times per week for 5 weeks. One of the carcinogen-treated groups received the diet supplemented with vitamin E and selenium for the first 10 weeks of the study, while a second group was supplemented between 11 and 25 weeks. A third group received a supplemented diet throughout the 25 week experiment.

Blood samples were collected at the beginning of the study and at week 5, 15 and 25. Although a benefit for late supplementation was observed at the end of the study, rats that received diets containing sufficient vitamin E and selenium throughout the course of the study and those that received diets supplemented with the vitamins for the first ten weeks had a significantly lower number of visible tumors and esophageal squamous cell carcinomas compared with the other carcinogen-treated animals. Supplementation was associated with a reduction in cell proliferation, angiogenesis, oxidative stress and inflammation.

"Vitamin E/selenium supplementation at the early stage of esophageal carcinogenesis had a relatively stronger effect than that at the late stage," the authors remark. The findings support the results of a clinical trial of supplementation with vitamin E and selenium which found a significant reduction in esophageal cancer deaths among younger participants, but not among older subjects who are likelier to have precancerous lesions.

"This present study in an animal model and the human studies support the hypothesis that marginal deficiencies or lower status in micronutrients enhance the risk for esophageal cancer caused by environmental carcinogens such as dietary nitrosamines or their precursor, as well as genetic susceptibility factors," the authors conclude.

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Complementary alternative cancer therapies

Selenium supplements have cancer-preventive properties (Combs GF, Jr. 2005), particularly in reducing the occurrence of lung, colorectal, esophageal, and prostate cancers (Mark SD et al 2000). Indeed, low selenium levels are associated with a four- to fivefold increase in the risk of developing prostate cancer (Brooks JD et al 2001). Higher selenium levels are associated with a reduced risk of prostate cancer (Brooks JD et al 2001). Because selenium levels decline with age, selenium supplements may be of particular benefit to elderly men (Brooks JD et al 2001).

However, the benefits of selenium supplements in preventing cancer appear to be cancer-specific, as some clinical studies have shown supplementation to be ineffective in protecting against basal and squamous cell carcinomas of the skin (Clark LC et al 1996).

Clinical studies have shown that vitamin E can reduce the risk of prostate and lung cancers, particularly when used in combination with selenium supplements (Helzlsouer KJ et al 2000; Woodson K et al 1999). Regular and long-term (over 10 years) use of vitamin E reduces the risk of death from bladder cancer (Jacobs EJ et al 2002). Similarly, the use of vitamin E supplements for longer than three years slightly reduces the risk of recurrence among breast cancer survivors (Fleischauer AT et al 2003).

In addition, animal studies indicate that vitamin E may have activity against colon cancer and melanoma (Barnett KT et al 2002; Malafa MP et al 2002b; Malafa MP et al 2002a). Larger clinical studies are currently underway to further assess vitamin E’s protective role against prostate cancer (Fleshner N et al 2005; Lippman SM et al 2005).

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