Dietary vitamin E, highly expressed in palm oil, exists as either tocopherols or tocotrienols. Evidence indicates that vitamin Es may be potent cancer preventive agents. In this study, the γ- and δ- isoforms of vitamin E were found to be the most effective at cancer cell growth inhibition, with the tocotrienols being more effective than the tocopherols in androgen-independent PC-3 prostate cancer cells. To assure that these compounds were selective toward cancer cells, the growth arrest of PrEC normal prostate cells was compared to PC-3 cells. At concentrations of ≤30 μM dietary, γ-vitamin Es showed no significant growth arrest on PrEC cell growth, but selectively inhibited growth in the PC-3 cancer cells. Moreover γ-tocotrienol demonstrated a greater potential to inhibit growth in cancer cells at these lower concentrations than did γ-tocopherol. Two independent pathways important in carcinogenesis were tested: PPAR γ and NFκB. The PPAR γ was up regulated by both dietary γ-vitamin Es by the modulation of the endogenous ligand 15-S-HETE, while NFκB was only regulated by γ-tocotrienol. The modulation of NFκB was confirmed by the down regulation of the pro-apoptotic proteins cIAP, xIAP, and BcL-2 which potentiate apoptosis and are down stream effectors of NFκB.