The right form of Vit E -Tocotrienols a potential anticancer agent!!http://www.lef.org/LEFCMS/aspx/PrintVer ... sID=112391
This brand has ALL 4 kinds of TOCOTRIENOLS. You need all 4. Go light on the tocopherols.
jackDTocotrienol as a potential anticancer agent.
Ling MT, Luk SU, Al-Ejeh F, Khanna KK.
SourceAustralian Prostate Cancer Research Centre-Queensland, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Qld 4102, Australia.
Vitamin E is composed of two structurally similar compounds: tocopherols (TPs) and tocotrienols (T3).
Despite being overshadowed by TP over the past few decades, T3 is now considered to be a promising anticancer agent due to its potent effects against a wide range of cancers.
A growing body of evidence suggests that in addition to its antioxidative and pro-apoptotic functions, T3 possesses a number of anticancer properties that make it superior to TP. These include the inhibition of epithelial-to-mesenchymal transitions, the suppression of vascular endothelial growth factor tumor angiogenic pathway and the induction of antitumor immunity.More recently, T3, but not TP, has been shown to have chemosensitization and anti-cancer stem cell effects, further demonstrating the potential of T3 as an effective anticancer therapeutic agent. With most of the previous clinical studies on TP producing disappointing results, research has now focused on testing T3 as the next generation vitamin E for chemoprevention and cancer treatment.
This review will summarize recent developments in the understanding of the anticancer effects of T3. We will also discuss current progress in clinical trials involving T3 as an adjuvant to conventional cancer therapy.
PMID:22095072[PubMed - in process]
J Nutr Biochem. 2009 Feb;20(2):79-86. Epub 2008 Dec 13.Antiangiogenic and anticancer potential of unsaturated vitamin E (tocotrienol).
Miyazawa T, Shibata A, Sookwong P, Kawakami Y, Eitsuka T, Asai A, Oikawa S, Nakagawa K.
SourceFood and Biodynamic Chemistry Laboratory, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan. email@example.com
and endothelial cells, have been implicated in such anticancer action of T3, while the in vivo potency and exact intracellular mechanisms for the anticancer properties of T3 remain not fully unSeveral lines of evidence support the beneficial effect of tocotrienol (T3; an unsaturated vitamin E) on inhibition of tumor development. Many factors, including decrease in oxidative stress and modulation of cell signaling pathways in tumor derstood.
We have hypothesized that the inhibitory effect of T3 on cancer may be attributable to the antiangiogenic activity of T3, and we found that T3 acts as a potent regulator of growth-factor-dependent signaling in endothelial cells and as an antiangiogenic agent minimizing tumor growth. In this work, we review the history and biological action (i.e., anticancer) of vitamin E and describe current research on the antiangiogenic effects of T3 and its mechanisms.
PMID:19071006[PubMed - indexed for MEDLINE]
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Nutr Cancer. 2012 Jan;64(1):136-52. Epub 2011 Dec 15.
Induction of DNA damage and caspase-independent programmed cell death by vitamin e.
Constantinou C, Neophytou CM, Vraka P, Hyatt JA, Papas KA, Constantinou AI.
Sourcea Yasoo Health, Ltd. , Nicosia , Cyprus.
Vitamin E comprises 8 functionally unique isoforms and may be a suitable candidate for the adjuvant treatment of prostate cancer. In this study, we examined the ability of 2 vitamin E isoforms [α-tocotrienol (γ-TT) and δ-tocotrienol (δ-TT)] and 4 synthetic derivatives [γ- and δ-tocotrienol succinate (γ-TS, δ-TS), α-tocopheryl polyethylene glycol succinate (TPGS), and α-tocopheryl polyethylene glycol ether (TPGS-e)] of vitamin E to induce cell death in AR- (DU145 and PC-3) and AR+ (LNCaP) prostate cancer cell lines. Our results show that δ-TT and TPGS-e are the most effective isoform and synthetic derivative, respectively, of all compounds examined. Overall, the results of our study suggest that isoforms and synthetic derivatives of vitamin E have the potency to trigger both caspase-dependent and -independent DNA damage and dominant caspase-independent programmed cell death. The capacity of vitamin E to trigger caspase-independent programmed cell death suggests that it may be useful in the chemotherapy of prostate cancer since it may prevent the tumor resistance commonly associated with the use of classical chemotherapeutic agents that trigger caspase-dependent programmed cell death.
PMID:22172208[PubMed - in process]
Nutr Cancer. 2010;62(6):789-94.Mixed tocotrienols inhibit prostate carcinogenesis in TRAMP mice.
Barve A, Khor TO, Reuhl K, Reddy B, Newmark H, Kong AN.
SourceRutgers, The State University of New Jersey, 160 Frelinghuysen Road, Piscataway, NJ 08854, USA.
The biological activities of tocotrienols are receiving increasing attention. Herein, we report the efficacy of a mixed-tocotrienol diet against prostate tumorigenesis in the transgenic adenocarcinoma mouse prostate (TRAMP) mouse model.
Male TRAMP mice, 8 wk old, were fed 0.1%, 0.3%, or 1% mixed tocotrienols in AIN-76A diet up to 24 wk old. Likewise, a positive control group consisting of male TRAMP mice and a negative control group consisting of wild-type nontransgenic mice were fed regular AIN-76A diet up to 24 wk old.
Our results show that mixed-tocotrienol-fed groups had a lower incidence of tumor formation along with a significant reduction in the average wet weight of genitourinary apparatus. Furthermore, mixed tocotrienols significantly reduced the levels of high-grade neoplastic lesions as compared to the positive controls.
This decrease in levels of high-grade neoplastic lesions was found to be associated with increased expression of proapoptotic proteins BAD (Bcl(2) antagonist of cell death) and cleaved caspase-3 and cell cycle regulatory proteins cyclin dependent kinase inhibitors p21 and p27.
In contrast, the expression of cyclins A and E were found to be decreased in mixed-tocotrienol groups. Taken together, our results show that by modulating cell cycle regulatory proteins and increasing expression of proapoptotic proteins, mixed tocotrienols suppress prostate tumorigenesis in the TRAMP mice.
PMID:20661828[PubMed - indexed for MEDLINE]
Genes Nutr. 2012 Jan;7(1):43-52. Epub 2011 Apr 9.Tocotrienols fight cancer by targeting multiple cell signaling pathways.
Kannappan R, Gupta SC, Kim JH, Aggarwal BB.
SourceCytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Cancer cells are distinguished by several distinct characteristics, such as self-sufficiency in growth signal, resistance to growth inhibition, limitless replicative potential, evasion of apoptosis, sustained angiogenesis, and tissue invasion and metastasis. Tumor cells acquire these properties due to the dysregulation of multiple genes and associated cell signaling pathways, most of which are linked to inflammation. For that reason, rationally designed drugs that target a single gene product are unlikely to be of use in preventing or treating cancer. Moreover, targeted drugs can cause serious and even life-threatening side effects. Therefore, there is an urgent need for safe and effective promiscuous (multitargeted) drugs. "Mother Nature" produces numerous such compounds that regulate multiple cell signaling pathways, are cost effective, exhibit low toxicity, and are readily available. One among these is tocotrienol, a member of the vitamin E family, which has exhibited anticancer properties.
This review summarizes data from in vitro and in vivo studies of the effects of tocotrienol on nuclear factor-κB, signal transducer and activator of transcription (STAT) 3, death receptors, apoptosis, nuclear factor (erythroid-derived 2)-like 2 (Nrf2), hypoxia-inducible factor (HIF) 1, growth factor receptor kinases, and angiogenic pathways.
PMID:21484157[PubMed - in process] PMCID:PMC3250528