• Tocotrienols inhibit proliferation & growth of both estrogen receptor-negative MDA-MB-435 and receptor-positive MCF-7 human breast cancer cells in culture.
• Palm based tocotrienols had been proven to inhibit human breast cancer cells irrespective of estrogen receptor status.
• Alpha-tocotrienols when used together with Tamoxifen, the combination was found to be 60 times more potent.
• Delta - tocotrienols was found to be the most effective tocotrienols in inducing apoptosis (cell death) in estrogen-responsive and estrogen-non responsive human breast cancer cells.
• Alpha-tocotrienols and gamma-tocotrienols have shown to prolong the life span of cancer-infected mice.
• Gamma-tocotrienols is 3 times more potent in inhibiting growth of human breast cancer cultured cells than Tamoxifen.
• Tocotrienols confer anti-cancer properties.
• Tocotrienols inhibit tumor growth of certain cancers.
• Combined low dose treatment of gamma-tocotrienols with individual statins may have potential value in the treatment of breast cancer without causing myotoxicity that is associated with high dose statin treatment.
• A blend of lovastatin (1 microM) and d-gamma-tocotrienols (5 microM) totally blocked cell growth, an impact far exceeding the sum of inhibitions induced by lovastatin (12%) and d-gamma-tocotrienols (8%) individually.
• The higher adipose tissue concentrations of tocotrienols in benign patients provide support for the idea that tocotrienols may provide protection against breast cancer.
• 6-O-carboxypropyl-alpha-tocotrienols (T3E) shows more potential anti-carcinogenic property than alpha-tocotrienols T3 in a lung cancer cell (A549 cell).
• Tocotrienols ameliorate the fibrogenesis associated with chronic pancreatitis.
• Tocotrienols induce apoptosis and autophagy in rat pancreatic stellate cells through the mitochondrial death pathway.

Tocotrienols are shown to be effective antiproliferating agent. It also contributes to immunoregulation, antibody production and resistance to implanted tumors. Tocotrienols have the abilities to affect cell homeostasis.

Oral administration of tocotrienols resulted in significant suppression of liver and lung carcinogenesis in mice. In cases of human breast cancer, the antiproliferative activity of tocotrienols has been shown to be enhanced with Tamoxifen, a synthetic estrogen antagonist. Tocotrienols might potentially serve as a synergistic chemotherapeutic agent, perhaps rendering it possible to reduce the dosage of more toxic chemotherapies, in turn minimizing adverse effect.

Tocotrienols has been reported to induce apoptosis. When apoptosis is induced in mammalian cells, various types of caspases are activated. These caspases are considered to be executive factors for apoptosis. It is believed that the activation of caspase is induced through two pathways. In the first pathway, binding of cytochrome c released from mitochondria to Apf-1 participates in the activation of caspase-9. In the second pathway, binding of death ligand to death receptors such as Fas and TNF receptor participates in the activation of caspase-8. Caspase-8 and caspase-9 activate caspase-3, and activated caspase-3 cleaves poly (ADP-ribose) polymerase (PARP). The cleavage of PARP is used as an indicator of apoptosis. Tocotrienols induced apoptosis in human hepatoma Hep3B cells and that caspase-8 and caspase-9 were involved in apoptosis induction.

The selective effect of tocotrienols-rich fraction of palm oil causes cell cycle arrest and apoptosis in prostate cancer cells without affecting normal cells.(22)

High telomerase activity is detected in most cancer cells.Inhibition of telomerase by drug or dietary food components is a new strategy for cancer prevention. Tocotrienols exhibited the inhibitory effect on cellular telomerase activity and the inhibitory potency of tocotrienols is much superior to that of tocopherol. Tocotrienols modulated telomerase by repressing hTERT and c-myc expression via inhibition of PKC activity.