Vitamin E succinate inhibits prostate tumor growth in laboratory studies
A report published in the May 15, 2006 issue of the International Journal of Cancer revealed the findings of researchers at H. Lee Moffitt Cancer Center in Tampa, Florida and their colleagues at Southern Illinois University School of Medicine that a form of vitamin E (VE) known as vitamin E succinate (VES) suppressed prostate cancer cell growth in culture as well as in a mouse model of the disease.
Mokenge P. Malafa and his team used a rat prostate cancer cell line, and two androgen receptor-negative and one androgen receptor-positive human prostate cancer cell lines for the current study. The cells were incubated with various concentrations of vitamin E succinate, vitamin E (nonsuccinate), succinic acid, ethanol, or no additions, and cell activity was studied.
Vitamin E succinate significantly inhibited growth of the rat prostate cancer cells at 48 hours at a concentration for which vitamin E or succinic acid alone were ineffective. It was discovered that apoptosis, or programmed cell death, was the mechanism behind the growth inhibition. Vitamin E succinate also helped inhibit the growth of the human prostate cancer cells by the same mechanism.
In another experiment using mice who received prostate cancer tumor grafts, daily injections of 50 or 100 milligrams per kilogram vitamin E succinate were associated with tumor growth suppression compared to untreated mice. Although the 50 mg/kg dose appeared to be ineffective at preventing metastasis, mice who received the higher dose of vitamin E succinate had dramatically fewer metastatic nodules in the lungs than untreated mice.
“We have demonstrated for the first time that VES, a derivative of VE, is capable of inhibiting prostate cancer growth in vivo,” the authors announced. “Further studies of the antitumor effects of VES in vivo will aid in the design of clinical trials to incorporate the use of this micronutrient in the treatment of human prostate cancer,” they conclude.
Not all prostate cancer (PC) is systemic, anymore than all breast cancer or other tumor types are systemic. If they were, we would never cure any man or woman of PC, breast cancer, or any other malignancy. Physicians claiming that every man with PC needs androgen deprivation therapy (ADT) as primary and sole therapy are blindly ignoring the growing numbers of men who present 8 to 15 years after radical prostatectomy (RP) or radiation therapy (RT) with a flat PSA graph. Emphasis on the use of routine prostate specific antigen (PSA) monitoring starting annually at the age of 40 with PSA velocity and doubling time determinations as a standard part of PSA reporting will increase the numbers of men diagnosed earlier, with a lower tumor burden, and cured with local modalities of treatment (Labrie et al., J. Clin. Endocrinol. Metab., 1995; Labrie et al., Urology, 1996). PSA testing with these enhancements should start earlier, at age 35, in men with a familial history of PC.
The difference in treating early PC versus more advanced PC relates to the issue of cure as opposed to control. Early PC has the potential for cure via a local therapy combined with the use of ADT in situations where the tumor volume compromises the curative ability of local therapy such as RT (including seed implantation) or cryosurgery.
When PC spreads to the capsular interface and leaves the prostate gland, it reflects a change in the biologic nature of the cancer. The PC now is expressing its more aggressive nature in its ability to spread and metastasize. Why?
The aggressiveness of these tumors appears to directly correlate with the proportion of higher Gleason grade cells. This frequently involves multiple clones of PC cells-some androgen-sensitive, but others androgen-insensitive, and/or possibly androgen-altered (Aihara et al., Urology, 1994; Brawn, Cancer, 1983). This heterogeneity appears related to tumor size or burden. As the tumor burden increases by cell division, the chances of gene mutation increase, which in turn may lead to androgen or drug-resistant tumors. Such mutations likely result from the activation of oncogenes or the inhibition of tumor suppressor genes.
Prostate cancer cells would rather commit suicide than feel the burn of hot chili peppers (or, at least, one of chili peppers' components), according to a report published in the March 15, 2006 issue of Cancer Research. Scientists at the Samuel Oschin Comprehensive Cancer Institute at Cedars-Sinai Medical Center along with colleagues from the University of California at Los Angeles found that giving capsaicin, the compound in jalapeño chilies responsible for a burning sensation when consumed, to mice in whom human prostate cancer tumors were implanted caused approximately 80 percent of the cancerous cells to undergo apoptosis (programmed self-destruction). The dose given to the mice was the equivalent of giving a 200 pound man 400 milligrams capsaicin three times per week, which is the amount provided by three to eight fresh habañera peppers.
In separate studies using androgen-dependent and independent cell cultures, capsaicin reduced cell proliferation and lowered the production of prostate specific antigen (PSA), a protein produced by prostate tumors.
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