Selenium and vitamin E supplements for prostate cancer: evidence or embellishment?

Moyad, Mark A.

doi:10.1016/s0090-4295(01)01190-6

Cited by 72 publications

(32 citation statements)

References 54 publications

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“…In addition, DNA hypermethylation, DNA hypomethylation, and histone acetylation are thought to contribute to prostatic tumorigenesis. Hypermethylation of DNA damage repair genes glutathione S-transferase 1 and O 6 -methylguanine DNA methyltransferase has been reported in CaP, with methylation of glutathione S-transferase 1 gene promoter detected in greater that 70% of CaP specimens (4).…”

Section: Introductionmentioning

confidence: 99%

“…In addition, particular nutrients may be effective only in subgroups defined by genotypes or by nutritional status of another nutrient. In this respect, a closer analysis of trials under way for selenium and vitamin E, probably two of the most popular dietary supplements against CaP, reveals that selenium supplements provided benefit only for those individuals who had lower levels of baseline plasma selenium, whereas subjects with normal or higher levels did not benefit and may have an increased risk for CaP (6). In addition, although vitamin E reduced the risk of CaP in smokers and those with low levels of this vitamin, vitamin E supplements in higher doses (z100 IU) were associated with a higher risk of aggressive or fatal CaP in nonsmokers.…”

Section: Introductionmentioning

confidence: 99%

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Chemoprevention of Prostate Cancer through Dietary Agents: Progress and Promise

Syed

Khan

Afaq

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

164

124

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Prostate cancer (CaP) is second only to lung cancer as the cause of cancer-related deaths in American men and is responsible for over 29,000 deaths per year. One promising approach to reduce the incidence of CaP is through chemoprevention, which has been recognized as a plausible and cost-effective approach to reduce cancer morbidity and mortality by inhibiting precancerous events before the occurrence of clinical disease. Indeed, CaP is an ideal candidate disease for chemoprevention because it is typically diagnosed in the elderly population with a relatively slower rate of growth and progression, and therefore, even a modest delay in the development of cancer, achieved through pharmacologic or nutritional intervention, could result in substantial reduction in the incidence of clinically detectable disease. In this review, we have summarized the recent investigations and mechanistic studies on CaP chemoprevention using dietary agents, such as selenium, vitamins D and E, lycopene, phytoestrogens, flavonoids, and green tea polyphenols. Well-designed trials are required to delineate the potential clinical usefulness of these agents through issues, such as determining the optimal period and route of administration, systemic bioavailability, optimal dosing and toxicity of the agent, and single or combinatorial approach. It is hoped that, combining the knowledge based on agents with targets, effective approaches for CaP chemoprevention can be established. (Cancer Epidemiol Biomarkers Prev 2007;16(11):2193 -203)

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chemoprevention of Prostate Cancer through Dietary Agents: Progress and Promise

Syed

Khan

Afaq

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

164

124

View full text Add to dashboard Cite

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“…Among them, ␣T is the predominant form of vitamin E in plasma and tissues and is the form that has drawn most attention in the past. Benefit from ␣T for cancer prevention has been suggested in some studies (1), but contradictory results exist in both animal and human intervention studies (2)(3)(4)(5). Recently, studies by us and others have indicated that other forms of vitamin E appear to have unique properties that are not shared by ␣T but may be important to human health (6).…”

mentioning

confidence: 99%

γ-Tocopherol or combinations of vitamin E forms induce cell death in human prostate cancer cells by interrupting sphingolipid synthesis

Jiang

Wong

Fyrst

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

186

147

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␥-Tocopherol (␥T), the predominant form of vitamin E in diets, but not ␣-tocopherol, the major vitamin E form in tissues and supplements, inhibits proliferation of prostate cancer cells (LNCaP and PC-3) and lung cancer cells (A549). In contrast, at similar concentrations, ␥T has no effect on normal prostate epithelial cells. Combinations of some vitamin E forms, such as ␥T and ␦-tocopherol, exhibit additive or synergistic inhibitory effects. In this study, ␥T or its combination with ␦-tocopherol induced apoptosis in androgen-sensitive prostate LNCaP, but not in androgenresistant PC-3 cells, by the induction of cytochrome c release, activation of caspase 9 and caspase 3, cleavage of poly-ADP-ribose polymerase (PARP), and involvement of caspase-independent pathways. Myriocin and fumonisin B1, specific inhibitors of key enzymes (serine palmitoyltransferase and dihydroceramide synthase, respectively) in de novo synthesis of sphingolipids, significantly protected cells from ␥T-induced DNA fragmentation, cytochrome c release, PARP cleavage, and the formation of active caspase 3. Compared with vehicle-treated controls, ␥T treatment led to pronounced dihydroceramide and dihydrosphingosine accumulation, which preceded morphological and biochemical manifestations of apoptosis. In contrast, ceramide and shpingosine levels did not increase until day 3, when substantial cell death took place. Our study demonstrates that ␥T and mixed vitamin E forms induce cell death by interrupting the de novo sphingolipid pathway in a prostate cancer cell line. Thus, certain vitamin E forms may be valuable as anticancer agents.

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“…Fifth, the ATBC study suggested obesity as a confounding factor, since the data from this trial demonstrated that the negative impact of extreme obesity was greater than the positive impact (32% decrease in risk) of taking the vitamin E supplement (104). Thus, obesity should also be taken into consideration when conducting future PCa trials.…”

Section: Why Select Failed: Potential Reasonsmentioning

confidence: 96%

“…During the experimental design procedure, it was acknowledged that more data on selenium and vitamin E would have been helpful, but it was felt the time was right to proceed with the study, and regardless of limited data, selenium and vitamin E represented the best possible options among promising PCa chemoprevention agents (103). However, several investigators were skeptical and voiced a concern that preclinical studies do not support the rationale and design of SELECT (104).…”

Section: Select: the Details And The Rise And Fall Of The Trialmentioning

confidence: 99%